Year 3 Disease Index

221 diseases · 135 criteria across all four modules. Pick a module, then Disease Index or Criteria. Slide-sourced only · Special = pathognomonic-only.

C/P

Inves

Mng

Special — pathognomonic

Perioperative, Shock & Surgical Infection

26 entries

Cell injury, hypoxia & inflammation (concept)

C/P

systemic inflammation signs: fever + sweating/chills (hypothalamic); tachycardia HR>90 (sympathetic); tachypnoea RR>20 (hyperventilation vs metabolic acidosis); constitutional (anorexia, tiredness, weakness, drowsiness); leucocytosis + ↑ESR
reversible injury (mild, reverts after removal) vs irreversible (nuclear appearance changes + cell membrane rupture); difference mostly quantitative
inflammation components: vascular + cellular + humoral (mediators)

Inves

ESR = rough measure of altered plasma protein composition (albumin + acute-phase reactants: CRP, α1-antitrypsin, ceruloplasmin, fibrinogen, serum amyloid)
CRP = sensitive biochemical test, used instead of standard ESR
leukocytosis: accelerated marrow release via IL-1 + TNF; if persists → macrophages + T-lymphocytes make CSFs

Mng

Special

O2 deficiency = MOST important cause of cell injury; hypoxia = relative O2 deficiency (need vs availability), complete block of supply = anoxia
anaerobic respiration product = lactic acid → systemic METABOLIC acidosis (aerobic product CO2, cleared by lungs)
inflammation CANNOT occur in isolated single cells/amoeba/tissue culture (needs vascularised multicellular tissue); cell injury CAN

Neuroendocrine–metabolic stress response to injury (concept)

C/P

graded/proportional to injury; metabolism + nitrogen excretion ∝ degree of stress; modifiable (ICU)
phases: Ebb (hypometabolic, first ~12h = clinically shock) → catabolic Flow (hypermetabolic, days) → anabolic Flow/recovery (weeks)
pyrexia, tachycardia, tachypnoea, hypermetabolism; water + salt retention; coagulation hypercoagulability → hypocoagulability; catabolism → muscle wasting + insulin resistance → ↓functional recovery
pituitary = "leader of endocrine orchestra"; injury → afferent spinal cord → hypothalamus → CRF → pituitary ACTH + GH ("fight or flight"); pancreas ↑glucagon; thyroid/gonads minor
stressors: major trauma (fractures/burns/head/abdo/chest), infection/sepsis, major ops (head-down + pneumoperitoneum, tissue trauma, blood/fluid loss), major CV events (MI/PE/stroke), haemorrhage, hypoxia

Inves

stress hyperglycaemia (counterregulatory hormones + insulin resistance; catecholamine + cortisol suppress insulin; glucagon → glycogenolysis + gluconeogenesis) = "stress-induced diabetes" → risk sepsis/renal impairment/polyneuropathy

Mng

tight glucose control + IV insulin sliding scale ↓ morbidity/mortality
general aim: ↑ circulating glucose/FFA/amino acids for energy + healing; ↓ periphery (muscle) → protects but ↓functional recovery

Special

mediators = neural + endocrine + inflammatory; complement = earliest humoral (C3a + C5a anaphylatoxins); TNF-α + IL-1 key; IL-6 induces T & B cells; IL-8 recruits inflammatory cells; IL-10 = key anti-inflammatory
TNF-α from macrophages + NK cells (NOT leukocytes); unchecked → multiorgan failure; anti-TNF antibody trials (NORASEPT, INTERSEPT) no significant benefit
stress hormones: Stress = catecholamines; Storage = insulin; Permissive = glucocorticoids/glucagon/GH; cortisol up to 6-fold ↑ free in severe sepsis, sensitises receptors to catecholamines, binds INTRAcellular steroid receptors
catecholamines: epinephrine mainly adrenal (hormone); most norepinephrine from synaptic clefts (neurotransmitter); enteric organs produce ~37% NE + >50% dopamine
fuel: brain/liver/RBCs no insulin needed for glucose; muscle + adipocytes insulin-dependent; glycogenolysis ~8h (up to 18h) → hepatic gluconeogenesis (lactate, pyruvate, α-ketoacids, glycerol); ketogenesis in prolonged starvation → β-hydroxybutyrate (protein-sparing) + acetone (fruity breath); BCAAs = leucine/isoleucine/valine; 45% body protein structural

Hypovolaemic / haemorrhagic (traumatic) shock

C/P

tachycardia (HR↑) then hypotension; early = normal systolic/↑diastolic (narrowed pulse pressure), late = BP↓
cold sweaty skin; flat neck veins; ↓CVP; ↓urine output
tolerate ~1000 ml loss if quiet; won't survive untreated after ≥1500 ml loss
haemodynamic signature: HR↑, CVP↓, SVR↑, CO↓, PCWP↓, SvO2↓, (CaO2–CvO2)↑
source = trauma (penetrating/blunt/blast), GI/vascular bleed, burns (plasma loss)

Inves

labs: Hb + HCT, blood grouping/typing, blood gases, serum lactate
bedside imaging: FAST + CXR
monitoring: CVP + serum lactate; base deficit = surrogate for lactate (less specific — renal failure, alcohol, bicarbonate loss)
non-sustained responder → check CVP: LOW = sustained bleeding → explore

Mng

crystalloid fluid challenge until blood products available; permissive hypotension guided by serum lactate; blood products + control source
damage-control surgery if prolonged; control lethal triad (acidosis, hypothermia, coagulopathy)
debride entry stab wound to reduce inflammatory load

Special

cold sweaty skin distinguishes from septic (cool, not sweaty) shock
referred left shoulder pain from left diaphragm irritation (splenic haematoma)

Cardiogenic shock

C/P

hypotension with RAISED CVP (distended neck veins); tachycardia
haemodynamic signature: HR↑, BP↓, CVP↑, SVR↑, CO↓, PCWP↑, SvO2↓, a-vO2↑, VO2↓

Inves

non-sustained responder with HIGH CVP → obstructive/cardiogenic shock

Mng

manage before anaesthesia; fluid resuscitation + vasopressors

Special

hypotension + high CVP/PCWP distinguishes from hypovolaemic (low CVP)

Obstructive shock

C/P

hypotension with raised CVP; tachycardia
haemodynamic signature: HR↑, BP↓, CVP↑, SVR↑, CO↓, PCWP↑ or ↓, SvO2↓, a-vO2↑, VO2↓ (specifics depend on type)

Inves

HIGH CVP in non-responder → obstructive/cardiogenic

Mng

manage cause before anaesthesia

Special

sudden BP drop after bleeding control from ruptured emphysematous bulla during ventilation → CVP RISES

Neurogenic shock

C/P

hypotension WITHOUT tachycardia (HR normal or ↓); warm periphery (↓SVR)
haemodynamic signature: HR normal/↓, BP↓, CVP↓, SVR↓, CO↓, PCWP↓, SvO2 normal/↓, a-vO2 normal/↑, VO2 normal/↓

Inves

Mng

Special

hypotension with normal/low heart rate + low SVR (loss of sympathetic tone) distinguishes from all other shock types

Hypoadrenal (adrenal-crisis) shock

C/P

chronic steroid user (e.g. asthmatic on corticosteroids) → immunocompromised + liable to hypoadrenal shock under surgical stress; profound hypotension

Inves

LOW CVP, unresponsive to volume + vasopressors

Mng

Special

refractory hypotension with low CVP unresponsive to fluids/pressors in a chronic-steroid patient under stress

Sepsis / SIRS / septic shock

C/P

fever/hypothermia, tachycardia, tachypnoea, hypotension, altered mental status (somnolence/difficulty arousing)
cool skin (NOT cold sweaty) = septic/distributive shock; hyperdynamic circulation
two haemodynamic patterns — hypovolaemic (early, HR↑ CVP↓ SVR↓ CO↓ SvO2↓) and euvolaemic hyperdynamic (HR↑, SVR↓, CO↑, PCWP normal/↑, SvO2↑, VO2↑)
septic shock = sepsis needing vasopressors to keep MAP >65 despite adequate fluid resus + lactate >2.0 mmol/L
flat neck veins + hypotension excludes cardiogenic; distension + diffuse tenderness with NO guarding/percussion tenderness = no peritonitis (localises source e.g. colon)

Inves

lactate = marker of metabolic acidosis + tissue hypoperfusion; hypotension + lactate ≥4 → ↑mortality vs either alone; monitor to guide resuscitation
WBC (24 = ongoing infection); creatinine (renal dysfunction); ScvO2 (55% = sepsis); ABG/base deficit
cultures BEFORE antibiotics; give within 1h; if cultures would delay >1h, give antibiotics first
score with SIRS (early screen), qSOFA, SOFA

Mng

Sepsis Six within 1 hour (O2, cultures + source control, IV antibiotics, IV fluid, lactate, urinary catheter)
early empiric broad-spectrum antibiotics within 1h (no need to identify organism first); each hour of delay ↑ mortality
goal-directed therapy within 6h (CVP 8–12, MAP 65, UO 0.5 mL/kg/h, ScvO2 ≥70%/SvO2 ≥65%)
Surviving Sepsis: crystalloid boluses 1000 mL to CVP 8–12; NOREPINEPHRINE first-line (central); dobutamine for myocardial dysfunction; dopamine NOT for renal protection; phenylephrine not recommended
IV hydrocortisone 300 mg/day if hypotension responds poorly to fluids + vasopressors
transfuse RBC when Hb <7.0 g/dL; lung-protective ventilation (TV 6 mL/kg, plateau ≤30); glucose target ≤180 mg/dL; stress-ulcer + DVT prophylaxis

Special

warm vasodilated hyperdynamic circulation with ↑CO / ↓SVR / ↑SvO2 (only shock with raised CO + SvO2) = distributive/septic signature

Multi-organ dysfunction syndrome (MODS)

C/P

sequential organ failure; bimodal — early <3 days + late 6–8 days
step from death; SIRS controlled by endogenous cytokine antagonists — if inadequate → MODS

Inves

SOFA per-organ scoring

Mng

prevent/at-risk (MODS prevention): rapid CV resuscitation + prevent shock (minimise splanchnic ischaemia); optimise O2 delivery (measure arterial PO2 + pH, correct metabolic acidosis); nutritional support via ENTERAL route (nourish enterocytes)

Special

"two-event"/two-hit model; does NOT require documented infection; increased incidence (from improved initial survival); blood transfusion immunomodulatory/may be detrimental

Major burns

C/P

3rd-degree 45% BSA → hypovolaemia (plasma loss + evaporation from denuded skin); MOST intensive hypermetabolism of any injury
skin loss → secondary infection → more catabolism

Inves

Mng

fluid resuscitation; operations (escharotomies, tangential excision) with blood loss + anaesthesia

Special

highest hypermetabolism + protein catabolism of all injury sources; evaporative loss from denuded skin

Acute (biliary) pancreatitis

C/P

vomiting + epigastric pain radiating to back (e.g. 4 days); can deteriorate to ARDS (hypoxia + bilateral infiltrates)

Inves

↑amylase/lipase; US = small gallstones + biliary mud (biliary aetiology)
follow Ranson's criteria every 48h
dynamic/contrast-enhanced CT pancreas from 1 week post-presentation (detect fluid collections/necrosis, infected or not)

Mng

conservative; analgesics; fluid resuscitation
nasojejunal tube blenderised formula beyond gastric outlet obstruction if vomiting persists
gradual TPN if ICU/ventilated; repeated debridement for infected pancreatic necrosis (sepsis source)
severe stress 1.5–2 g/kg protein; sepsis calorie factor 1.3–1.35

Special

infected pancreatic necrosis of body/tail on CECT = local complication driving debridement

Perioperative malnutrition / nutritional depletion

C/P

weight loss, ↓ food intake, low BMI, poor performance status; impaired preoperative status + disease severity

Inves

NRS-2002 nutrition risk score (see Criteria); total ≥3 → at risk; <3 → weekly rescreen

Mng

most surgical patients need NO supplementation (adequate reserves ≥1 week partial starvation) — give IV fluids + electrolytes + ≥100 g glucose/day to minimise protein catabolism
total ≥3 → nutritional care plan; enteral preferred (nourish enterocytes); fast-track + early enteral in GIT surgery
route by scenario: oral/blenderised (if swallows fluids) → nasojejunal elemental/blenderised (past outlet obstruction, jejunal absorption despite diarrhoea) → short preop IV hyperalimentation/TPN → early postop IV hyperalimentation for anastomotic healing then enteral fortification
protein/calorie targets by stress level (see Criteria)

Special

feeding gastrostomy avoided when it interferes with future stomach mobilisation (oesophageal ca) or colon-bypass adhesions; aspiration of saliva = disadvantage of feeding gastrostomy

Surgical site infection (SSI)

C/P

within 30 days of surgery (1 year if implant/foreign body); onset usually 12h–7 days postop
superficial incisional (skin + subcutaneous) + deep incisional (fascia/muscle): calor, rubor, tumour, dolor, purulent drainage
organ space (any structure opened/manipulated): systemic signs (fever, ileus, shock) ± imaging
examine if fever 39°C <12h: foul-smelling serous discharge, painful ± crepitus
most common source after groin hernia repair = patient's own skin; endogenous (large-bowel reservoir) vs exogenous/HAI (theatre/hands)

Inves

wound infection = >100,000 organisms/gram tissue; Gram stain (gram-positive rods = clostridial)
blood cultures + urine + sputum Gram/culture; CT/US-guided for deep space

Mng

DRAINAGE first (reopen wound; image-guided for deep/organ space); antibiotics for cellulitis/generalised sepsis empirically until cultures
superficial → open + local care (antibiotics only if erythema beyond margin or systemic signs); deeper → exploration + debridement
irrigation with tap water (↓bacterial load, promotes healing); avoid alcohol/Dakin/H2O2 (kill fibroblasts); VAC for sternal/abdominal dehiscence/perineal/grafts
prevention: hand scrub, prophylactic antibiotics (see Criteria), normothermia, glucose control, STOP SMOKING (leading preventable factor, ↑SSI 6-fold), gentle handling, eliminate dead space, minimise foreign material
antibiotic choice: cefazolin (1st-gen) for clean; tailor to organ flora if contaminated (gut → enterobacteriaceae + anaerobes; biliary/oesophageal → + enterococci; urinary/vaginal → group D strep/Pseudomonas/Proteus); intranasal mupirocin for S. aureus nasal carriage; elective colon → oral + IV superior to IV alone

Special

crepitus + foul discharge + gram-positive rods on Gram stain within 12h = clostridial SSI

Wound dehiscence / evisceration

C/P

serosanguineous leakage = first sign; absence of healing ridge (normally ~0.5 cm each side within 1 week) predicts breakdown
sensation of tearing/popping with coughing/retching; sudden evisceration; most common days 5–10 (wound strength minimum)
predisposing: age >60, obesity, ↑intra-abdominal pressure, malnutrition, renal/hepatic insufficiency, DM, corticosteroids, cytotoxics, irradiation, infection (>half); MOST important = adequacy of closure

Inves

Mng

no infection → elective reclosure; unfit patient/wound → heal by second intention (later scar/hernia repair)
evisceration = surgical emergency (mortality 10–20%): resuscitate + protect viscera with moist towels + prompt closure (lavage, return bowel, close wall, pack skin open ± VAC)

Special

evisceration = rupture of abdominal wall + extrusion of viscera; serosanguineous herald leak precedes it

Ventilator-associated / hospital-acquired pneumonia (VAP / HAP)

C/P

VAP = pneumonia 48–72h after endotracheal intubation; most common ICU infection in surgical/trauma patients
HAP/VAP = 2nd most common nosocomial infection AFTER UTI ("most common" is FALSE)
usually aerobic gram-negative bacilli (P. aeruginosa, E. coli, K. pneumoniae, Acinetobacter); gram-positive cocci (S. aureus/MRSA) more common in diabetics/head trauma/ICU; S. aureus = 40% of VAP

Inves

sputum Gram/culture; CXR

Mng

early-onset VAP (<5 days): antibiotic-SENSITIVE bacteria (MSSA, S. pneumoniae, H. influenzae); trauma-prone, gastric aspiration
late-onset VAP (≥5 days): MDR pathogens (MRSA, Pseudomonas, Acinetobacter) → cover
empiric (no MDR suspicion) = ceftriaxone/fluoroquinolone/ampicillin-sulbactam/ertapenem; MRSA → linezolid; P. aeruginosa most common gram-neg MDR (some only susceptible to polymyxin B)

Special

5-day cut-off (early vs late onset) drives pathogen resistance + antibiotic choice

Catheter-associated urinary tract infection (CAUTI)

C/P

UTI = most common nosocomial infection; longer Foley → more likely; by 5–7 days most patients have infected urine; urinary catheter >2 weeks → infection

Inves

urine culture >100,000 bacteria/ml + WBC on urinalysis

Mng

remove catheter ("Water" of the 5 Ws)

Special

germs crawl up the OUTSIDE of the catheter (ascending)

Catheter-related bloodstream infection (CLABSI / catheter sepsis)

C/P

risk ↑ with central vein, indwelling >3–5 days, blood sampling; septic thrombophlebitis = late postop fever (~2 weeks) at IV line
bacteraemia = mostly indwelling vascular catheters

Inves

blood cultures; inspect old + current IV sites

Mng

full sterile barrier at insertion + strict care + prompt removal; remove/replace suboptimal-barrier central catheters

Special

septic thrombophlebitis at an IV site as source of late unexplained fever

Intra-abdominal infection / peritonitis (IAI)

C/P

community-associated (CA-IAI) vs hospital-associated (HA-IAI, e.g. colon anastomotic dehiscence)
uncomplicated (uIAI: contained to single organ, no perforation, rarely serious) vs complicated (cIAI: perforation → peritoneal cavity → greater SIRS; contained = abscess, uncontained = diffuse peritonitis)
postoperative anastomotic leak (e.g. day 7 after anterior resection) → generalised peritonitis, hyperdynamic septic shock, 2nd hit, more virulent/resistant organisms
Hinchey 4 = perforated diverticular disease with faeculant peritonitis

Inves

prompt imaging to confirm/localise source

Mng

source control immediately after initial resuscitation (drainage / urgent celiotomy); CA-IAI = narrow pathogen-specific; cIAI/HA-IAI/high-risk = broad-spectrum empirical (MDR risk); diversion/difficult closure for colonic injury

Special

healthcare-associated NON-postoperative IAI (e.g. acute acalculous cholecystitis) = particularly poor prognosis (delayed diagnosis)

Necrotising soft-tissue infection (NSTI)

C/P

PAIN out of proportion = most consistent/constant finding (due to ischaemia)
skin initially deceiving (minimal erythema/oedema, spared by collaterals); later blistering, crepitus, bullae, haemorrhagic blebs, necrosis = "hard signs" → immediate debridement
can present with SIRS/sepsis/shock/MOF; mortality up to 25% (one series)
encompasses necrotizing cellulitis/fasciitis/myositis (by depth); Fournier's gangrene = perineum/genitourinary; Ludwig angina = submandibular/sublingual; clostridial = muscle myonecrosis/gas gangrene

Inves

GOLD STANDARD = clinical diagnosis confirmed by operative exploration: pasty gray necrotic tissue, thin "dishwater" purulent fluid, positive finger test (lack of resistance to digital pressure), lack of bleeding, thrombosed vessels, muscle not contracting to electrocautery; equivocal → 2-cm bedside incision to superficial fascia under LA
labs none specifically diagnostic; WBC <15,400/µL or Na >135 mEq/L → NPV 99% (90% sensitivity); LRINEC ≥6 highly suspicious (see Criteria)
plain X-ray gas (subcutaneous emphysema 17–30%, specific not sensitive, ~25% cases); CT (gas high specificity/low sensitivity, ~80% sensitivity); MRI most useful to differentiate necrotizing vs non (T2 hyperintense) but low specificity 50% + time delay; POCUS operator-dependent

Mng

immediate debridement = single most important survival determinant; >24h delay → 9-fold ↑ death; excise all necrotic skin/subcutaneous/fascia/muscle to healthy viable bleeding tissue; second-look 12–24h; serial debridements; VAC then graft/rotational flap; amputation if limb not viable; diverting colostomy for perineal soilage
broad-spectrum antibiotics (gram-neg + gram-pos + anaerobic) + empiric MRSA; clindamycin attenuates toxins; Vibrio/Aeromonas → add doxycycline/tetracycline; ~14 days IV after source control; continue ≥48–72h after resolution + source control
rising WBC + lactate on antibiotics = progression → SECOND-LOOK operation
IVIG (INSTINCT RCT no survival benefit) + hyperbaric O2 (no proven benefit) NOT routine

Special

pain out of proportion + "dishwater" pus + positive finger test + gas/crepitus; liquefaction of fascia = diagnostic feature; fascia avascular → susceptible; IV antibiotics ALONE → mortality ~100% (thrombosis blocks penetration — never a replacement for surgery)

Non-necrotizing cellulitis

C/P

erythema, oedema, tenderness (non-necrotizing)

Inves

Mng

most frequent = Streptococcus pyogenes (also H. influenzae, pneumococcus); parenteral penicillin = treatment of choice
severe → protein synthesis inhibitors ± cell-wall agents (macrolide resistance ↑); alternatives antistaphylococcal penicillins, cefazolin, ceftaroline, ceftriaxone

Special

Diabetic foot infection

C/P

chronic ulcer (probing/tracking), malodor, oedematous/erythematous foot in diabetic with neuropathy/PVD; chronic wounds resistant

Inves

obtain tissue cultures

Mng

gram-positive cocci most common (also gram-negative bacilli + anaerobes); empirical per local susceptibility + prior exposure
regimens: cefazolin, ceftriaxone, cefoxitin, ceftaroline, ampicillin-sulbactam, piperacillin-tazobactam, carbapenem; daptomycin/linezolid + gram-negative cover; MRSA → vancomycin, telavancin, ceftaroline, daptomycin, tigecycline, linezolid

Special

NSTI risk factors present: DM, CKD, existing midfoot ulcer, impaired vascularity

Complicated skin / soft-tissue infection

C/P

abscess ± cellulitis; polymicrobial

Inves

Mng

S. aureus most common isolate; CA-MRSA increasingly common; simple abscess → I&D alone; complex/abscess+cellulitis → adjuvant antibiotics; cover CA-MRSA + enteric gram-negatives + anaerobes if polymicrobial

Special

Toxic shock syndrome (TSS)

C/P

~48h after surgery (e.g. total mastectomy): high fever, diarrhoea, vomiting, whole-body redness (erythroderma), hypotension → then diffuse desquamation; resembles severe scarlet fever; wound often unremarkable; half present <48h

Inves

Mng

wound drainage + antibiotics + clindamycin (inhibits exotoxin)

Special

diffuse desquamation following erythroderma; S. aureus TSST-1 + enterotoxin B/C (superantigen); originally tampon-associated; rarely S. pyogenes

Pseudomembranous colitis (C. difficile)

C/P

diarrhoea + abdominal pain after prolonged antibiotics (e.g. recent 2-week course); previous diverticulitis → resistant residual flora

Inves

Mng

metronidazole (anaerobic cover); hand hygiene with soap + water

Special

alcohol gel does NOT kill C. difficile spores → must use soap + water

Malignant hyperthermia

C/P

rare life-threatening response to inhaled anaesthetics/some muscle relaxants; core >40°C; heat, acidosis, hypokalemia, muscle rigidity, coagulopathy, circulatory collapse

Inves

Mng

Special

abnormal Ca metabolism in skeletal muscle; triggered by inhaled anaesthetics/muscle relaxants

Postoperative fever (concept)

C/P

fever = pathologic systemic inflammation, core >38 rarely >40°C; macrophages release IL-1/TNF/interferon → reset hypothalamic thermoregulatory centre
early (1–3 days): most common = atelectasis (sterile, not infected; total pneumothorax does NOT cause fever)
late (~2 weeks): septic thrombophlebitis (IV line) + occult intra-abdominal abscess
5 Ws: Wind (atelectasis/pneumonia), Water (UTI), Walk (thrombophlebitis), Wound

Inves

inspect incisions; old/current IV sites; blood cultures + urine Gram/culture + sputum Gram/culture; CXR if breath sounds worrisome

Mng

aspirin/acetaminophen/ibuprofen (COX inhibitors block PGE2); treating controversial (no outcome benefit) — investigate = yes

Special

atelectasis = commonest early cause; total pneumothorax does NOT cause fever

Perioperative, Shock & Surgical Infection

21 entries

SIRS (Sepsis-1)

≥2 of: RR >20 or PaCO2 <4.25 kPa (32 mmHg); HR >90; temp >38 or <36°C; WBC >12,000/mm³ or <3,000/mm³ or bandaemia >10%. Use for EARLY screening.

qSOFA (Sepsis-3)

2 of 3: RR ≥22/min = 1; altered mental status = 1; SBP <100 mmHg = 1. Poor sensitivity → not for early screening.

Sepsis definitions

septic shock = sepsis requiring vasopressors to keep MAP >65 despite adequate fluid resuscitation + lactate >2.0 mmol/L. (Admission readings before resuscitation don't yet qualify.)

SOFA score (per organ, 0 → 4)

Organ	0	1	2	3	4
Respiratory PO2/FiO2 mmHg (kPa)	≥400 (53.3)	<400 (53.3)	<300 (40)	<200 (26.7) + resp support	<100 (13.3) + resp support
Coagulation platelets/mm³	≥150,000	<150,000	<100,000	<50,000	<20,000
Liver bilirubin mg/dl	<1.2	1.2–1.9	2.0–5.9	6.0–11.9	>12.0
Cardiovascular	MAP ≥70	MAP <70	dopamine <5 or dobutamine (any)	dopamine 5.1–15 or epi ≤0.1 or norepi ≤0.1	dopamine >15 or epi >0.1 or norepi >0.1
CNS (GCS)	15	13–14	10–12	6–9	<6
Renal creatinine mg/dl (UO ml/d)	<1.2	1.2–1.9	2.0–3.4	3.5–4.9 (<500)	>5.0 (<200)

Sepsis Six (all within 1 hour)

high-flow O2 non-rebreathe; blood cultures + source control; IV antibiotics per local protocol; IV fluid resuscitation (Hartmann's/equivalent); check lactate; urinary catheter for hourly urine output.

Early goal-directed therapy / Surviving Sepsis resuscitation goals (within 6h)

CVP 8–12 mmHg (12–15 if ventilated); MAP 65 mmHg; urine output 0.5 mL/kg/hr; ScvO2 ≥70% or SvO2/mixed venous ≥65%; normalise lactate; no arbitrary systolic BP goal. Antibiotics IV within first hour; reassess daily + de-escalate; discontinue 7–10 days most infections.

Shock haemodynamic profile (printed table)

(↑ up, ↓ down)

Type	HR	BP	CVP	SVR	CO	PCWP	SvO2	a-vO2	VO2
Hypovolaemic (early)	↑	normal syst/↑ diast	↓	↑	↓	↓	↓	↑	normal
Hypovolaemic (late)	↑	↓	↓	↑	↓	↓	↓	↑	↓
Cardiogenic	↑	↓	↑	↑	↓	↑	↓	↑	↓
Neurogenic	normal/↓	↓	↓	↓	↓	↓	normal/↓	normal/↑	normal/↓
Septic (hypovolaemic)	↑	↓	↓	↓	↓	↓	↓	↑	↓
Septic (euvolaemic)	↑	normal/↓	normal/↓	↓	↑	normal/↑	↑	↓	↑
Obstructive	↑	↓	↑	↑	↓	↑ or ↓	↓	↑	↓

(BP change depends on % blood volume lost; obstructive specifics depend on type of obstruction.)

Principles of shock treatment

control inciting process; optimise cardiovascular dynamics; restore perfusion; control lethal triad (hypothermia, acidosis, coagulopathy); support organs at risk (lung, kidney, liver).

Ebb–flow model (Sir David Cuthbertson, 1930)

Ebb/early = holding pattern first 12h (clinically = shock, hypometabolic) → catabolic Flow (days, hypermetabolic) → anabolic Flow / recovery-repair (weeks, hypermetabolic).

Metabolic response — starvation vs stress (REE)

Parameter	Starvation	Stress
Resting energy expenditure	↓	↑
Mediator activation	↓	↑
Branched-chain oxidation	+	+++
Hepatic protein synthesis	+	+++
Ureagenesis	+	+++
Urinary N loss	+	+++
Gluconeogenesis	+	+++
Ketone body production	++++	+
Proteolysis	+	+++
Primary fuel	fat	mixed

NRS-2002 nutrition risk score

Impaired nutrition (food intake last week): 1 = ↓ to 50–70% of req; 2 = 25–60%; 3 = 0–25%
Impaired nutrition (weight loss / BMI): 1 = >5% loss in 3 months (or BMI 18.5–25 + impaired general condition); 2 = >5% loss in 2 months; 3 = >5% loss in 1 month (or BMI <18.5 + impaired general condition)
Severity of disease: 1 = diabetes, oncology, chronic (COPD/cirrhosis esp. with acute complication), chronic haemodialysis, hip fracture; 2 = major surgery, stroke, severe pneumonia, haematological malignancy; 3 = ICU, head injury, bone-marrow transplant
Age >70 → add 1 (age-adjusted total)
Total ≥3 → nutritionally at risk → nutritional care plan; <3 → weekly rescreen; major op scheduled → preventive plan

Protein / calorie needs by stress

Normal (unstressed): 0.8 g protein/kg/day + 20 kcal/kg/day
Moderate stress: 1.2–1.4 g/kg/day (sepsis calorie stress factor 1.3–1.35)
Severe stress: 1.5–2 g/kg/day

Surgical wound classification

Clean/I (hernia, breast biopsy) 2.1%; Clean-contaminated/II (cholecystectomy, elective GI) 3.3%; Contaminated/III (bowel injury/enterotomy) 6.4%; Dirty/IV (perforated appendicitis, diverticulitis, NSTI) 7.1%. (Herniorrhaphy 2%, cholecystectomy 3%, appendectomy 5%, thoracotomy 6%, colectomy 12%.)

SSI definitions & thresholds

must occur within 30 days of surgery (1 year if implant/foreign body); depth = superficial incisional (skin + subcutaneous) / deep incisional (fascia/muscle) / organ space (structure opened). Wound infection = >100,000 organisms/gram tissue. Inoculum for infection: intact skin 8 million; violated skin 1 million; foreign material present only 100. Decisive period = host defences take up to 4h to mobilise after breach (prophylaxis must cover it, tissue levels above MIC90).

NNIS risk index

ASA >2; wound class III/IV; operation duration >75th percentile.

NSTI types (population / pathogen / antibiotics)

Type	Population	Pathogen	Antibiotics
I (55–80%, most common)	DM/CKD/cirrhosis/obesity	mixed aerobic (streptococcus) + anaerobic (bacteroides)	gram-neg + gram-pos incl. MRSA + anaerobic
II (10–15%)	trauma/postoperative/IVDA	β-haemolytic Streptococcus ± S. aureus (M proteins → cytokine release → septic shock)	above + clindamycin
III	marine organisms (warm coastal water/raw oysters, Asia; mortality 30–40%)	Clostridium spp + Vibrio vulnificus	above + tetracycline
IV	immunocompromised/penetrating trauma (rare/aggressive/high mortality)	Aeromonas hydrophila + fungi (Candida if immunocompromised, zygomycetes if immunocompetent)	above + antifungal

LRINEC score (Wong 2004)

components: WBC, haemoglobin, sodium, glucose, creatinine, CRP. ≥6 highly suspicious (PPV 92%, NPV 96%); <6 does NOT exclude.

Antibiotic surgical prophylaxis standards

dose within 1h before incision (2h for vancomycin/fluoroquinolone; slide also states within 30 min before incision); approved agent; discontinue within 24h (48h cardiac); redose during long operations per drug half-life; clindamycin if β-lactam allergy; single-dose = multiple-dose; not after wound closed unless contamination; IV <1h before incision (late = don't give). Glucose (cardiac) <200 mg/dL first 2 days (measure closest to 6am POD1+2); hair removal by clippers/depilatory immediately preop (NO razors); colorectal normothermia core 96.8–100.4°F within first hour after leaving OR.

Antibiotic categories by mechanism

cell-wall active (β-lactams: penicillins, cephalosporins, monobactams, carbapenems ± β-lactamase inhibitors — inhibit final cell-wall step via transpeptidases/PBPs); protein synthesis inhibitors (aminoglycosides + tetracyclines → 30S; linezolid/macrolides/chloramphenicol → 50S; clindamycin → aminoacyl-tRNA); nucleic-acid disruptors (fluoroquinolones, metronidazole [anaerobes only, needs reduction], TMP-SMX). Empirical: gram-positive (vancomycin/telavancin, daptomycin [NOT pneumonia], linezolid); gram-negative (3rd-gen cephalosporin not ceftriaxone, monobactam, polymyxin B/colistin); antianaerobic (metronidazole, carbapenems, β-lactam/β-lactamase combos, tigecycline); broad-spectrum (piperacillin-tazobactam, carbapenems, fluoroquinolones, tigecycline + antipseudomonal). Metronidazole → peripheral neuropathy with prolonged use; disulfiram-like reaction.

Ranson's criteria

referenced (followed every 48h in acute pancreatitis to grade severity); individual components NOT printed in source.

Safe prescribing standards (VM045)

Legal responsibility = the practitioner who SIGNS; write per BNF + local practice
Patient ID on all charts/TTAs: surname + given name, DOB, admission date, Consultant; document WEIGHT if weight-dependent (paediatrics, LMWH, under/overweight)
Allergy box: document BOTH positive and negative histories; describe symptoms if positive
Drug names: approved names, legible, correctly spelt, NO abbreviations
Dose rules: NO trailing zeroes (5mg not 5.0mg); ≥1g in grams; <1g in milligrams (500mg not 0.5g); <1mg in micrograms (100micrograms not 0.1mg); decimal must be preceded by a figure (0.5mls not .5mls); "micrograms/nanograms/units" NOT abbreviated; millilitre = ml (not cc/cm³)
Frequency: dose + frequency; PRN → specify MINIMUM dose interval (6 hours not qds) + indication
Start date = date first prescribed on this admission (not chart-rewrite date); dose change → rewrite with NEW start date
Signature: indelible ballpoint + bleep/contact number
Controlled-drug TTAs: entirely in doctor's OWN handwriting; name + address (or unit no.); form + strength; total dose units in BOTH words AND figures; the dose
IV: continuous infusion on IV Fluid prescription (drug + quantity, diluent, rate in mls/min or mls/hr)
Unusual regimens: cross out non-due dose boxes with large X (weekly alendronate, 3×/week erythropoietin)
Discontinuing: cross off BOTH prescribing + administration sections diagonally, sign + date
Insulin + warfarin on separate charts; doses must NOT appear on two charts concurrently; one drug chart at a time (label '1 of 2'/'2 of 2' if overflow)

C/P

Inves

Mng

Special — pathognomonic

Cardiology

17 entries

Acute Coronary Syndrome (STEMI / NSTEMI / Unstable Angina)

C/P

nocturnal chest pain waking from sleep (~0200), ~20–25 min, sweaty, eased with rest
acute chest pain + sweating, distressed
ischaemic symptoms: pain chest/arms/back/jaw >15 min (over 20 min)
chest pain + nausea/vomiting, marked sweating or breathlessness, or haemodynamic instability
new-onset pain OR abrupt deterioration of stable angina — recurrent, little/no exertion, >15 min
CV risk factors: smoking (40 yrs), HTN, DM, dyslipidaemia
cardiac-pain assessment: pain history; CV risk factors; prior IHD + treatment; previous chest-pain investigations

Inves

resting 12-lead ECG; serial ECGs; review previous ECGs; additional leads
ECG no regional ST-elevation / no presumed LBBB, no ST-depression / deep T-inversion → NSTEMI or stable angina
Troponin T 0.02 initially → repeat troponin 10–12 h after symptom onset → 0.15 µg/L at 12 h = diagnose ACS
cardiac enzymes incl Troponin I; CBC, blood glucose, urea, creatinine; coagulation profile
pulse oximetry
DDx to consider: PE, aortic dissection, pneumonia

Mng

pain relief: GTN and/or IV opioid
single loading dose aspirin 300 mg (unless allergic) → continue aspirin indefinitely
other antiplatelets only in hospital
O₂ if SpO₂ <94% → aim 94–98%; COPD/hypercapnic-risk aim 88–92% until ABG
monitor: pain, pulse/BP, rhythm, SpO₂, serial ECGs, pain-relief efficacy
STEMI / inferior MI: antiplatelet loading dose → transfer for urgent percutaneous angiography + angioplasty

Special

regional ST-elevation or new LBBB = STEMI; no ST-elevation + troponin rise = NSTEMI; no rise = unstable angina
culprit artery: inferior wall MI → RCA; anterior STEMI → LAD

Prinzmetal (Vasospastic) Angina

C/P

L pectoral pain → lower jaw
at rest / before sleep / wakes from sleep
~1 month, ~10 min episodes, relieved spontaneously
none on daily activity (no exertional trigger); smoker

Inves

ECG during attack = ST-elevation anterior leads, resolves when pain gone
echo, stress ECG, CT coronary angiography
labs: CBC, lipid profile, DM detection
goal: confirm ischaemia + risk-stratify

Mng

calcium-channel blockers
nitroglycerine
statin
smoking cessation + lifestyle modification

Special

transient ST-elevation during attack that fully resolves; rest pain, not exertional

Chronic Coronary Syndrome (Effort / Stable Angina)

C/P

L pectoral pain → both arms
on effort, at ~900 m walk, ~7 min, relieved by rest
~2 months; smoker 35 yrs, HTN, no FHx IHD
normal exam / resting ECG, BP 140/90

Inves

labs: CBC, lipid profile, DM workup, kidney + liver function
stress ECG, echo, coronary CT angiography

Mng

aspirin, beta-blocker, ACEI (if echo abnormality), oral nitroglycerine or K⁺-channel openers, statins
smoking cessation + lifestyle
if severe ischaemia + failed medical Rx → coronary angiography + stenting (NOT first line)

Special

exertional pain relieved by rest with normal resting ECG (distinguishes from ACS / Prinzmetal)

Atypical Chest Pain (Inflammatory / Musculoskeletal)

C/P

central stitching pain lasting hours–whole day
worse with chest movement / cough / walking
~3 days; central chest tender
non-smoker / non-HTN / non-DM, no FHx
normal exam / resting ECG, BP 130/90

Inves

CBC, chest X-ray, echo

Mng

reassurance
anti-inflammatory drugs + antacids
follow-up 1 week

Special

reproducible chest-wall tenderness, pain worse with movement/cough → inflammatory, not ischaemia

Infective Endocarditis

C/P

fever, constitutional symptoms
history of murmur; history of teeth extraction
palpable spleen
2 factors needed: predisposing endocardial abnormality + bacteraemia
endocardial predisposers: congenital heart defects, rheumatic valvular disease, bicuspid/calcific aortic valve, MVP, HCM, prior endocarditis, prosthetic valves/intracardiac devices
organisms: streptococci + Staph aureus = 80–90%; rest = enterococci, gram-neg bacilli, HACEK (Haemophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae), fungi
toothbrushing/chewing → viridans strep bacteraemia in gingivitis
3 stages: bacteraemia → adhesion → colonization (mature vegetation); biofilms shield from immunity/antibiotics
distribution: left-sided most common (mitral/aortic); 10–20% right-sided (tricuspid/pulmonic); IVDU 30–70% right-sided
local consequences: myocardial abscess (conduction abnormalities esp low septal abscess); sudden severe valvular regurgitation → HF/death; aortitis
systemic: embolization + immune-mediated; right-sided → septic pulmonary emboli (infarction, pneumonia, empyema); left-sided → kidneys, spleen, CNS; mycotic aneurysms; diffuse (immune-complex) glomerulonephritis
risk factors: prior IE; prosthetic heart valves; certain congenital heart disease; post-heart-transplant valvulopathy

Inves

blood culture: 2–3 samples from different sites over 1 hour BEFORE antibiotics
blood C&S; Echo ± TTE; CT brain; serology
CBC; serum chemistry panel with glucose; urinalysis
elevated inflammatory markers
consider: rheumatoid factor, ESR, complement levels, CT

Mng

IV antibiotics (organism + susceptibility) ± valve debridement/repair/replacement
dental evaluation + treatment; remove source of bacteraemia (catheters/devices)
course 2–8 weeks (often home IV)
empiric native valve: Vancomycin 15–20 mg/kg IV q8–12h (max 2 g/dose)
empiric prosthetic valve: Vancomycin 15–20 mg/kg IV q8–12h + gentamicin 1 mg/kg q8h + either cefepime 2 g IV q8h OR imipenem 1 g IV q6–8h (max 4 g/day)
left-sided IE: 6 weeks parenteral; oral switch after min 10 days parenteral = non-inferior (uncomplicated)
surgery: heart failure; uncontrolled infection (persistent, fungal/resistant, recurrent prosthetic, or heart block/abscess/aneurysm/fistula/enlarging vegetation); embolism risk (vegetations >10 mm US or recurrent emboli)
worsening HF with S. aureus/gram-neg/fungus → surgery after only 24–72 h
right-sided usually medical; if surgery needed, repair preferred over replacement
delay surgery 1 month after intracranial haemorrhage / major ischaemic stroke
response: penicillin-susceptible strep improves + fever ↓ in 3–7 days; staph slower; relapse usually within 4 weeks; recrudescence after 6 weeks usually = new infection

Special

peripheral signs: splinter haemorrhages, Osler's nodes, Janeway lesions, conjunctival haemorrhage, Roth spots

Acute Heart Failure / Acute Pulmonary Oedema

C/P

AHF = worsening signs/symptoms, heart cannot pump at rate for body's needs at normal filling pressure
severe dyspnoea + pulmonary congestion, cough
bilateral LL pitting oedema to knees (right HF)
severely distressed + cyanosed; BP 160/100, HR 130, RR 30
bilateral crepitations lung bases → midzone; diminished breath sounds + diffuse crackles posterior fields
JVD 9 cm (normal ≤3)
HF picture: exertional dyspnoea, orthopnoea, PND, pink frothy sputum, tachypnoea/tachycardia, bilateral crackles + wheeze (cardiac asthma), JVP + pitting ankle oedema
aetiology: IHD, valvular heart disease, AF, hypertension, acute kidney disease; left-sided (ischaemic + HTN) vs right-sided (2° to left → pulmonary HTN)
pulmonary oedema = fluid extravasation from pulmonary vasculature into interstitium/alveoli
pathophysiology: imbalance of Starling forces (↑ pulmonary capillary hydrostatic pressure, ↓ plasma oncotic pressure, ↑ negative interstitial pressure); alveolar–capillary barrier damage; lymphatic obstruction; idiopathic
types: cardiogenic (sudden ↑ pulmonary venous pressure) vs non-cardiogenic (↑ capillary permeability); other = high-altitude, neurogenic, rapid aspiration of massive pleural effusion / unilateral pneumothorax, post-cardiopulmonary bypass

Inves

labs: CBC, LFT, RFT, ABG, cardiac enzymes, Pro-BNP
ECG for coronary ischaemia
imaging: echo + CXR
Echo EF 32%, anterior-wall hypokinesia
CXR bilateral moderate pleural effusion + cardiomegaly

Mng

stabilize; establish dx/aetiology/precipitants; symptomatic relief
emergency: hospitalization + high-flow O₂ 100%; O₂ if SpO₂ <90%
NIPPV / non-invasive ventilation (avoids intubation; ↓ intubation rate, hospital mortality, mechanical ventilation)
diuretics = cornerstone; IV furosemide preferred initially 40 mg, bolus or continuous infusion; assess response 2–4 h; ↑ dose/frequency if inadequate
vasodilators: nitrates (venodilator ↓ preload/LV filling pressure), hydralazine, ACEI/ARB; sodium nitroprusside (arterial dilator ↓ afterload), nitroglycerin, nesiritide; IV most common route
IV nitrates GTN infusion; morphine IV 5 mg (pain control if present)
neurohormonal inhibition (mortality drugs): ACEI/ARB, beta-blockers, aldosterone antagonists, SGLT2
loop diuretics + digoxin = symptomatic only
inotropes / mechanical circulatory support if organ hypoperfusion/shock; ultrafiltration option

Special

pink frothy sputum + cardiac asthma (bilateral crackles + wheeze) of acute pulmonary oedema

Congestive Heart Failure

C/P

progressive SOB; 4-month exertional SOB; fatigue + anorexia
PND (woke, dry cough, better sitting edge of bed ~1 h)
orthopnoea (2–3 pillows)
cough productive of pink frothy sputum
undernourished, cyanotic lips; BP 98/82 (narrow pulse pressure), HR 110, RR 26
dullness to percussion both bases, bilateral inspiratory crackles lower fields, distended neck veins, bilateral LL pitting oedema
common aetiologies: ischaemic heart disease, hypertension, valvular heart disease, cardiomyopathies

Inves

labs: WBC 8,400 (normal diff), Hb 14.6, Hct 40%, Plt 290k; glucose 112 (non-fasting), BUN 33, creatinine 1.6, total bili 1.9, direct bili 0.3, albumin 3.1, Na 136, K 4.0
CXR: bilateral prominent pulmonary vascular shadows, bilateral pleural effusions, ↑ haziness/↓ radiolucency of parenchyma, ↑ transverse cardiac diameter (cardiomegaly)
ECG, echo

Mng

inotropes ↑ CO: dobutamine, dopamine, digoxin (immediate onset); norepinephrine inotropic but aggravates HF
preload ↓: diuretics; furosemide (loop + acute venodilator); nitroglycerine venodilation
afterload ↓: nitroprusside (arteriolar + venodilator)

Special

orthopnoea + PND + leg oedema triad distinguishes CHF from pulmonary DDx

Iron-Deficiency Anaemia (hidden case dx — SOB/palpitation workup)

C/P

SOB + palpitation, no PMH; SOB on stairs/exercise
heavy menstrual periods; hair fall
BP 90/60, HR 100, RR 14, T 36.7; conjunctival pallor

Inves

CBC, iron profile, TFTs
low ferritin + iron, high TIBC, Hb 9, normal thyroid

Mng

iron supplementation

Special

low ferritin/iron + high TIBC with menstrual blood loss source

Aortic Regurgitation

C/P

wide pulse pressure
hyperdynamic pulse + head bobbing when severe/chronic
progresses to left HF
aetiology: aortic-root dilation / bicuspid aortic valve / endocarditis / rheumatic fever

Inves

Mng

Special

high-pitched "blowing" early diastolic decrescendo murmur; long diastolic murmur

Mitral Stenosis

C/P

late highly-specific sequela of rheumatic fever
LA >> LV pressure in diastole
chronic MS → LA dilatation → dysphagia/hoarseness (oesophagus / left recurrent laryngeal nerve compression)

Inves

Mng

Special

follows opening snap (OS = abrupt halt in leaflet motion, leaflet-tip fusion); delayed rumbling mid-to-late diastolic murmur; ↓ S2–OS interval correlates with ↑ severity; heard better with the bell

Mitral Regurgitation

C/P

Inves

Mng

Special

pansystolic (isointensity S1→S2) murmur

Tricuspid Regurgitation

C/P

Inves

Mng

Special

pansystolic (isointensity S1→S2) murmur

Ventricular Septal Defect (VSD)

C/P

Inves

Mng

Special

pansystolic (isointensity S1→S2) murmur; also listed among ejection systolic murmurs

Aortic Stenosis

C/P

Inves

Mng

Special

ejection systolic crescendo–decrescendo / diamond-shaped murmur

Pulmonary Stenosis

C/P

Inves

Mng

Special

ejection systolic crescendo–decrescendo / diamond-shaped murmur

Atrial Septal Defect (ASD)

C/P

Inves

Mng

Special

ejection systolic crescendo–decrescendo / diamond-shaped murmur

Mitral Valve Prolapse

C/P

Inves

Mng

Special

grade 2–3 loud mid/late systolic murmur following a mid-systolic click

Respiratory

29 entries

Asthma

C/P

heterogeneous disease, chronic airway inflammation; variable chest symptoms + variable expiratory airflow limitation
cough, SOB, wheeze, chest tightness; >1 symptom, variable over time (even within a day) + varying intensity
worse at night/on waking, viral infection, exercise, laughing, cold air, allergen
supportive (not essential): onset since childhood, other allergies (sinusitis, eczema), FHx asthma/allergy; exam may be normal, wheezes, nasal polyps
LESS likely if: isolated cough, chronic sputum, chest pain, dyspnea + dizziness/paresthesia, dyspnea + stridor
two presentations: uncontrolled asthma vs acute exacerbation
exercise-induced (EIA): wheeze after exercise
occupational asthma: symptoms improve on holidays/away from work (e.g. gasoline factory worker, PEFR 40% diurnal variability)
GERD as exacerbator: worsens when PPI stopped
acute exacerbation: acute flare-up (hours–days) of symptoms + airflow limitation beyond usual; at risk if prior exacerbations/ICU-MV, incorrect inhaler technique, frequent SABA, inadequate ICS, high Th2 inflammation, comorbidities

Inves

confirm dx physiologically before treating: spirometry, PEF meter, bronchial provocation
spirometry: may be normal if not in attack; FEV1/FVC <80%, FEV1 <80% predicted (required ≥once for dx) + reversibility
reversibility: salbutamol 200–400 mcg, recheck FEV1 at 10–15 min → +200 mL AND +12% = positive
PEF meter: daily diurnal variability >10% = asthma; ≥2×/day, best of 3 trials; variability% = (highest−lowest)/mean ×100
acute: spirometry usually not possible (too dyspneic); ABG only if SpO2 <92%, life-threatening asthma, or other dx (DKA); CXR not routine unless suspect pneumothorax/pneumonia, life-threatening, or failure to respond
Th2 markers (severe asthma phenotyping): sputum eosinophil ≥2%, and/or FeNO ≥20 ppb, and/or blood eosinophil ≥150/µL

Mng

controller (fixed dose, must contain ICS) vs reliever (as-needed; ICS-formoterol preferred; prophylaxis before exercise in EIA)
anti-inflammatory: ICS budesonide (mainstay), OCS prednisolone, LTRA montelukast
bronchodilators: SABA salbutamol 4–6h, LABA formoterol 12h, ultra-long indacaterol 24h; SAMA ipratropium 4–6h, LAMA tiotropium 24h
other: biologicals (anti-IgE omalizumab, anti-IL5/5r, anti-IL4r, anti-TSLP), azithromycin, bronchial thermoplasty
regimens: AIR = anti-inflammatory reliever; MART = maintenance + reliever therapy
EIA prophylaxis = inhaled ICS-formoterol; never LABA alone (controller must contain ICS)
occupational asthma → change job; GERD trigger → restart PPI
severe asthma add-on: Th2 → biological (omalizumab, benralizumab)/azithromycin/high ICS/OCS; non-Th2 → LAMA/azithromycin/bronchial thermoplasty; azithromycin 250 mg every other day × 6 months
review response after 2–3 months; step down once good control maintained 3 months
acute exacerbation: OCS early, SABA, SAMA nebulizer, ICS, IV magnesium sulfate?; O2 to keep SpO2 >93%; prednisolone 20–40 mg daily ×5–7 days; antibiotics NOT routine
discharge after acute: symptoms improved/no SABA need, PEF >60–80% predicted, SpO2 >94% RA, adequate home resources; follow-up 2–7 days (1–2 wk), step up controller, check inhaler technique

Special

— (dx is physiological reversibility/variability; severity + step ladder in Criteria)

COPD / AECOPD

C/P

acute chest tightness + productive cough (×6 days); heavy smoker (15 cig/day ×40 yr), no atopy
unable to talk full sentences; congested neck veins, no LL edema
harsh vesicular breathing + prolonged expiration + scattered bilateral wheeze
rhonchi (low-pitched, snoring-like) from large-airway obstruction/secretions

Inves

ABG, CXR, CBC
ABG (RA): pH 7.38, PaCO2 55, PaO2 58, HCO3 32, BE +6.2, SpO2 86% → compensated respiratory acidosis
CXR = hyper-expanded chest

Mng

target SpO2 88–92% (type II resp failure); O2 via Venturi mask (controlled)
antibiotics: amoxicillin/clavulanic acid OR macrolide OR tetracycline
frequent exacerbations / on ventilator → sputum C&S to exclude resistant/unusual bacteria (Pseudomonas aeruginosa)

Special

compensated respiratory acidosis on ABG; hyper-expanded chest on CXR

Wheeze (approach / differentials)

C/P

wheeze: continuous musical sound; vibration of opposing walls of narrowed airway; high/low pitched, inspiration or expiration; all wheezes = obstruction
extra-thoracic obstruction limits INSPIRATION; intra-thoracic limits EXPIRATION
stridor: high-pitched; supraglottis/glottis/subglottis/trachea (e.g. vocal cord dysfunction); often heard without stethoscope
rhonchi: low-pitched, snoring-like; large-airway obstruction/secretions (COPD, bronchiectasis)
causes upper airway: post-nasal drip, vocal cord dysfunction, anaphylaxis (angioedema), foreign body, tracheal tumors
causes lower airway: bronchial asthma, COPD, bronchiectasis, aspiration, heart failure (cardiac asthma), bronchogenic carcinoma (localized wheeze)

Inves

history, exam, spirometry (+reversibility), bronchial challenge, radiology (CXR, CT chest, CT neck), bronchoscopy

Mng

treat underlying cause

Special

localized/monophonic wheeze → bronchogenic carcinoma or tracheal lesion

Tracheal tumour

C/P

75yo, 20 pack-yr, 6-wk worsening wheeze/cough/green sputum + exertional dyspnea
inspiratory stridor + expiratory wheeze

Inves

CXR = right paratracheal mass shifting trachea to left

Mng

Special

localized wheeze + stridor with paratracheal mass shifting trachea

Community-Acquired Pneumonia (CAP)

C/P

acute infection with clinical and/or radiological signs of consolidation, part(s) of one/both lungs
transmission: inhalation, aspiration, colonization, blood spread
fever, tachycardia, hypotension (shock), tachypnea, low SpO2 (resp failure); cyanosis, accessory muscles, dullness to percussion, bronchial breathing, crackles
elderly = vague: GI upset, confusion, absent fever (GI upset → hyponatremia → confusion); atypical pattern
microbiology: Strep pneumoniae 35%, H. influenzae 12%, atypicals 22%, others 31%
pleurisy (pleuritic pain worse with deep breathing/coughing) may complicate pneumonia
aspiration/anaerobic (oral cavity bacteria): foul-smelling sputum; complications = lung abscess + empyema

Inves

routine: CXR, lung US (LUS), CT chest; CBC, ABG, BUN
FiO2 = 0.21 room air, +0.04 per L O2; PaO2/FiO2 e.g. 51.4/0.21 = 244.8 (<250)
risk factors for resistant bacteria: recent hospitalization + IV abx in 90 days; prior Pseudomonas/MRSA; comorbidities (chronic heart/lung [bronchiectasis, CF]/liver/renal [dialysis], DM, alcoholism, malignancy, asplenia)
further Ix (sputum Gram stain, sputum C&S, blood C&S) ONLY if hospitalized AND (severe by IDSA/ATS OR resistance risk); intubated → endotracheal aspirate
clinical resolution: fever 2–4 d, leukocytosis 3–4 d, crackles 3–6 d, cough 4–9 d
radiological resolution lags: Legionella 2–6 mo, Staph 3–5 mo, S. pneumoniae + shock 3–5 mo, Mycoplasma 2–4 wk; don't image before 3 wk; symptoms resolved in 5–7 d → no routine follow-up imaging

Mng

site of care by CURB-65: 0–1 home; 2 ward; 3–5 (or severe by IDSA/ATS) ICU
outpatient, no comorbidity: amoxicillin OR doxycycline OR macrolide
outpatient + comorbidity: amox/clav (or ceftriaxone/3rd-gen ceph) + macrolide/doxycycline; OR monotherapy fluoroquinolone
inpatient non-severe: β-lactam + macrolide OR fluoroquinolone
inpatient severe: β-lactam + macrolide OR β-lactam + fluoroquinolone; + anti-MRSA and/or anti-Pseudomonas if risk factors; de-escalate by culture
examples: β-lactam amoxicillin/ceftriaxone; macrolide azithromycin; fluoroquinolone levofloxacin; Pseudomonas → pip-tazo, meropenem; MRSA → vancomycin, linezolid
aspiration/anaerobic: add anti-anaerobic (clindamycin) ONLY if lung abscess/empyema suspected
influenza (molecular test +) → antiviral (oseltamivir/Tamiflu, favipiravir)
corticosteroid ONLY in severe CAP + septic shock, OR resp failure (P:F <300), OR rapid progression (severe CAP ≤3 days from onset)
duration: non-severe + stable 3–4 days; severe or deteriorating ≥5 days (Egypt clinical practice ≥7 days)
non-responding pneumonia: organism (Pseudomonas/MDR/TB), doctor (wrong abx or wrong dx: HF/PE/cancer/vasculitis/ILD), patient (comorbidity, abscess, non-adherence, aggressive host inflammation)
prevention: influenza vaccine annually (by end of October; IIV/RIV/LAIV); pneumococcal polysaccharide vaccine ≥65 or 2–64 high-risk
LAIV contraindicated: prior vaccine allergy, severe egg allergy, adults >65, immunosuppression, pregnancy

Special

Legionella pneumonia (Legionnaires')

C/P

common atypical CAP; aerosolized water (contaminated AC/nebulizers); variable severity → multiorgan failure
1/3 have hemoptysis; extra-thoracic = confusion, diarrhea, bradycardia; + hyponatremia

Inves

radiological resolution 2–6 mo

Mng

Special

extra-pulmonary confusion + diarrhea + relative bradycardia + hyponatremia

Klebsiella pneumonia (Friedländer's)

C/P

rare CAP, common in DM/alcoholics; high severity/mortality; high antibiotic resistance
lobar pneumonia, RUL common = apical pneumonia

Inves

CXR = bulging fissure sign (downward bulge of minor fissure from RUL enlargement)

Mng

Special

bulging fissure sign on CXR

Acute bronchitis

C/P

productive cough/fever but no consolidation on CXR → CAP criteria not fulfilled

Inves

CXR: no consolidation

Mng

treat at home; broad-spectrum antibiotic (e.g. ampicillin) + antipyretic (paracetamol)

Special

Sarcoidosis

C/P

systemic, unknown cause; non-caseating granulomas in lung + other organs
↑incidence in blacks, age 20–40, female preponderance; pulmonary involvement most common (>90%)
bilateral hilar + left paratracheal adenopathy = most common presentation (positive despine sign)
asymptomatic (only hilar adenopathy on imaging) or symptoms of affected organ; dyspnea + dry cough, bilateral crepitations
Löfgren's syndrome (v good prognosis): fever, arthralgia, erythema nodosum, bilateral hilar adenopathy (painful erythematous papules over anterior legs + symmetric knee/PIP/MCP joint swelling)
Heerfordt-Waldenström (v good prognosis): anterior uveitis, fever, parotid enlargement, facial palsy
other systems: ocular, cutaneous (25%), cardiac, rheumatologic, GI, neurologic

Inves

CXR = initial staging modality; HRCT = parenchymal assessment
HRCT: septal beading + nodules abutting bronchovascular bundles (perilymphatic); peribronchovascular nodules + bilateral hilar LAD
FBC: mild normochromic normocytic anemia (chronic disease) + raised ESR; hypercalcemia 10–20%, hypercalciuria 30–50% (↑vit D from macrophages)
serum ACE elevated >75% untreated (non-specific; screening + monitors activity/response)
PFT = restrictive with reduced gas transfer if parenchymal involvement/fibrosis
BAL lymphocytosis CD4:CD8 >2.5 = diagnostic; transbronchial biopsy positive up to 90%
definitive dx = biopsy non-caseating granulomas ("tissue is the issue")

Mng

1st line prednisolone (or equiv) 0.5 mg/kg × 4–6 wk, taper to maintenance ≥12 months
immunosuppressants (add to prednisolone): methotrexate, azathioprine, hydroxychloroquine
Löfgren's: no investigation needed, symptomatic only (bed rest, antipyretics, NSAIDs)

Special

non-caseating granulomas; BAL CD4:CD8 >2.5; Löfgren's & Heerfordt-Waldenström syndromes; bilateral hilar + left paratracheal adenopathy

Idiopathic Pulmonary Fibrosis (IPF)

C/P

70yo M, gradual progressive dyspnea + dry cough ×1 yr; clubbing 2nd degree; Velcro rales at bases

Inves

HRCT: bilateral basal honeycombing + traction bronchiectasis
BAL: ↑neutrophils; ABG hypoxemia
PFT severe restrictive (↓VC/TLC/RV, normal FEV1/FVC, ↓DLCO)

Mng

pirfenidone

Special

basal honeycombing + traction bronchiectasis; Velcro rales

Radiation pneumonitis

C/P

dyspnea + dry cough; H/O radiotherapy (post-mastectomy for breast cancer); unilateral crackles on irradiated side

Inves

HRCT: GGOs on irradiated side (right-sided GGOs)

Mng

Special

GGOs confined to the radiation field (unilateral)

Diffuse Alveolar Hemorrhage (DAH)

C/P

severe acute dyspnea ×2 days; known GPA (granulomatosis with polyangiitis) — pulmonary vasculitis

Inves

HRCT: bilateral diffuse alveolar filling
BAL: increasing RBC count on sequential BALs >20% + hemosiderin-laden macrophages; hypoxemia

Mng

plasmapheresis + immunosuppression

Special

sequentially bloodier BAL + hemosiderin-laden macrophages

Lymphangioleiomyomatosis (LAM)

C/P

25yo F childbearing age, gradual dyspnea + dry cough ×8 mo

Inves

HRCT: bilateral diffuse cystic changes with normal intervening lung; hypoxemia

Mng

sirolimus (Rapamune); avoid pregnancy

Special

diffuse cysts with normal intervening lung, woman of childbearing age

Pulmonary Langerhans Cell Histiocytosis (PLCH)

C/P

50yo M, gradual dyspnea + dry cough ×2 yr; heavy smoker (3P/day)

Inves

HRCT: bilateral bizarre-shaped variable-sized cystic changes
BAL: Langerhans' cells >3% total, CD1a + S100 positive

Mng

smoking cessation + cladribine

Special

bizarre-shaped cysts; BAL Langerhans cells CD1a + S100 positive

Pulmonary Alveolar Proteinosis (PAP)

C/P

22yo M, acute dyspnea + dry cough ×5 days

Inves

HRCT: bilateral diffuse alveolar filling + GGOs with interlobular thickening (crazy paving)
BAL: milky fluid with debris + foamy macrophages; hypoxemia

Mng

whole-lung lavage + GM-CSF

Special

crazy paving on HRCT; milky BAL with foamy macrophages

Hypersensitivity Pneumonitis (HP)

C/P

gradual dyspnea + dry cough; antigen exposure (breeds pigeons ×11 yr); clubbing 2nd degree; late-inspiratory crackles
SpO2 90%→73% on 6-min walk

Inves

CXR: bilateral upper-zone veiling (patchy opacities)
HRCT: bilateral GGOs predominantly upper zones (headcheese sign)
BAL: ↑lymphocytes, CD4/CD8 <1; hypoxemia

Mng

Special

headcheese sign; BAL CD4/CD8 <1; bird-fancier (pigeon) exposure

Chronic Eosinophilic Pneumonia

C/P

42yo M, gradual dyspnea + dry cough ×2 mo

Inves

HRCT: bilateral basal honeycombing + traction bronchiectasis
BAL: eosinophils >50%

Mng

Special

BAL eosinophils >50%

Drug-induced ILD

C/P

gradual dyspnea + dry cough; bilateral basal crepitations; on culprit drug
culprits: amiodarone (for AF), methotrexate (for RA)
DDx with HP (pigeon breeding) + radiation (post-mastectomy RT)

Inves

Mng

Special

amiodarone / methotrexate exposure

TB (ILD-mimic)

C/P

44yo African-American F, childhood asthma + T2DM, SOB; treated as asthma exacerbation with prednisone → worsening dyspnea, night sweats, weight loss

Inves

CXR: hilar LAD
not responding to prednisolone (sarcoid/lymphoma would improve) → consider TB

Mng

Special

hilar LAD worsening on steroids (unlike sarcoid/lymphoma) → TB

Asbestosis (asbestos-related lung disease)

C/P

prolonged asbestos dust inhalation; H/O exposure needed (mining/milling primary; manufacturing/insulation/brake linings/roofing/WWII shipbuilding secondary)
parenchymal fibrosis in lower lung fields; onset 20–30 yr after constant exposure (<10 yr if very heavy)
dyspnea, cough, clubbing, cor pulmonale, respiratory failure; bilateral inspiratory rales
spectrum: pleural disease (most common), asbestosis, bronchogenic carcinoma (synergistic with cigarette smoking)
pleural plaques = localized thickening + calcification at diaphragm level (asymptomatic, most common asbestos effect)
rounded atelectasis: visceral+parietal pleura fold over/fuse trapping lung → atelectasis; comet-tail sign; DDx lung cancer (pseudotumor)

Inves

CXR: bilateral diffuse reticulonodular opacities + honeycombing
ABG: hypoxemia + ↑A-a gradient
PFT: restrictive (↓lung volumes, ↓DLCO); airflow obstruction NOT characteristic
biopsy: barbell-shaped fiber / golden-brown fusiform rods = ferruginous bodies; sputum stained by Prussian blue

Mng

no specific Rx; symptomatic; smoking cessation (lung cancer risk 75× normal)
general pneumoconiosis measures: influenza + pneumococcal vaccines, bronchodilators for airflow limitation, antibiotics for infection, supplemental O2 for hypoxemia

Special

ferruginous bodies (barbell / golden-brown rods, Prussian blue); comet-tail sign of rounded atelectasis; pleural plaques at diaphragm

Mesothelioma

C/P

80yo, central chest pain + progressive dyspnea + dry cough ×1 yr; asbestos exposure (pipe work, sewage/water treatment); may never smoke
constant central chest pain = chest wall invasion

Inves

Mng

Special

constant central chest pain (chest-wall invasion) in asbestos-exposed patient

Silicosis

C/P

inhaled silica dust (mining, quarrying, drilling, tunneling, sandblasting, cement/concrete, glass/pottery)
chronic: symptoms like asbestosis, latency >15 yr
acute: within months, massive inhalation → rapid severe hypoxemic ventilatory failure + death
(case) concrete production + sandblasting; tachypneic RR 24, SpO2 91%, bilateral crackles

Inves

CXR chronic: nodules 1–10 mm prominent in upper lobes → coalesce >10 mm → progressive massive fibrosis (PMF); eggshell calcification of LNs (characteristic)
CXR acute: diffuse alveolar filling, lower-zone predominance
pathology: silicotic nodule (concentric hyalinized collagen surrounded by connective tissue)
dx: history of exposure + lung biopsy

Mng

no effective therapy; symptomatic
TB may complicate all forms → yearly tuberculin test
case measures: avoid silica, smoking cessation, influenza/pneumococcal vaccine, supplemental O2, tuberculin skin test

Special

eggshell calcification of hilar LNs; silicotic nodule

Coal Worker's Pneumoconiosis (CWP / black lung)

C/P

inhalation/deposition of coal mine dust + tissue reaction; ↑risk of COPD
clubbing + crackles NOT features (if present → investigate further)

Inves

CXR: simple CWP = small rounded opacities <1 cm in upper zones; PMF = large opacities >1 cm, upper-lobe predominance
biopsy/pathology: coal macule (primary lesion; focal coal dust in pigment-laden macrophages around respiratory bronchioles, not palpable); coal nodule (larger, palpable); emphysema adjacent to dust macule

Mng

no cure; symptomatic only

Special

coal macule; Caplan syndrome (rheumatoid pneumoconiosis) = nodular opacities in Welsh coal miners + RA + circulating RF among miners with PMF; Rx as PMF + RA

Bronchogenic Carcinoma

C/P

65yo M, change in morning cough; heavy smoker (2P/day ×30 yr); weight loss 10 kg/3 mo + anorexia + dysphagia; recent voice change; hemoptysis then blood-tinged sputum
mediastinal invasion: recurrent laryngeal nerve → voice change; esophagus → dysphagia
central (hilar): more common; squamous cell or small cell; spreads to mediastinum early; cough, dyspnea, hemoptysis; visible early on bronchoscopy
peripheral: less common; adenocarcinoma; spreads to pleura early; pleurisy, chest pain; hardly visible on bronchoscopy

Inves

labs: CBC, liver/kidney function, coagulation; ESR markedly elevated; serum calcium/glucose/ACTH/sodium (endocrine disturbance); sputum cytology; pleural fluid analysis if present
radiology: CXR; CT chest with contrast (not high-res — high-res is for parenchyma)
CXR: opacity (hetero/homogeneous) or cavitation (thick wall → malignant)
metastasis search: abdominal US/CT, CT brain, bone scan, PET-CT; common distant sites = adrenal, brain, liver, bone
biopsy ("tissue is the issue"): bronchoscopy (endobronchial/transbronchial biopsy, TBNA ± US) for central; image-guided true-cut needle (CT/US) for peripheral; LN biopsy (supraclavicular excision); thoracoscopy for mass + pleural effusion

Mng

NSCLC: surgery if resectable + no metastasis; radiotherapy; chemotherapy; 5-yr survival 3–60% (~20% overall)
SCLC: metastases usual at presentation; surgery contraindicated in most; chemotherapy (highly sensitive initially); radiotherapy only if SVC obstruction; survival 10–20 mo treated, 2–4 mo untreated

Special

cavitation with thick wall → malignant; localized wheeze; hoarseness (recurrent laryngeal) + dysphagia (esophagus) from mediastinal invasion

Pleural Effusion

C/P

fluid accumulation in pleural space (normal 1–15 mL, 0.2 mL/kg); disruption of hydrostatic/oncotic balance + lymphatic drainage
dyspnea (most common), dry cough
pleuritic pain → PE or inflammatory process; constant dull-aching pain → chest wall invasion by bronchogenic carcinoma/mesothelioma
signs (>300 mL): stony dullness, ↓breath sounds, ↓vocal resonance; mediastinal shift AWAY if >1000 mL
shift TOWARD effusion = lobar bronchus obstruction by endobronchial lesion (malignancy/foreign body)
transudate causes (low LDH+protein): CHF, constrictive pericarditis, cirrhosis (hepatic hydrothorax), hypoalbuminemia, nephrotic syndrome, SVC syndrome
exudate causes (high LDH+protein): parapneumonic, tuberculous, malignancy (carcinoma, mesothelioma), collagen-vascular (RA, SLE), PE, asbestos, pancreatitis, trauma, esophageal perforation, radiation pleuritis, drugs

Inves

CXR PA upright: small effusion blunts costophrenic angle; large = shift away; minimal detected PA 200–300 mL, lateral decubitus 75–100 mL (layering ≥1 cm = >200 mL); US most sensitive
pleural fluid analysis = only diagnostic: gross (transudate = dilute-urine transparent; exudate = concentrated urine; chylothorax = white; hemothorax = red), chemistry, cytology (+ve malignancy), cell count, bacterial C&S (+ve 60% infected fluid)
pleural biopsy: closed-needle, medical thoracoscopy, open (thoracotomy)
thoracentesis (dx or therapeutic): sit upright; puncture 2 rib interspaces below level of dullness, on upper border of lower rib; US/CT-guided; betadine + 1% lidocaine; confirm via 25-gauge before larger bore; supplemental O2; post-procedure expiratory CXR (exclude PTX) + inspiratory CXR (baseline)
- relative CI: <1 cm on lateral decubitus, bleeding disorder/anticoagulation, mechanical ventilation, cutaneous disease over site
- complications: pain, bleeding, pneumothorax, empyema, spleen/liver puncture; limit 1–1.5 L (re-expansion pulmonary edema)
differential cell count: lymphocyte >85% → TB, lymphoma; eosinophil >10% → PE with infarction, parasitic (paragonimiasis), medications; WBC transudate <1000, exudate >1000/mm³

Mng

treat underlying cause, therapeutic thoracentesis, tube thoracostomy drainage, indwelling tunneled catheter (pigtail), pleurodesis, surgical care + decortication

Special

D-shaped opacity → empyema; effusion in lung cancer may be transudate/exudate/hemorrhagic/chylothorax/pyothorax; malignant effusion = hemorrhagic, massive, rapidly accumulating, mediastinum may shift to same side

Empyema

C/P

purulent pleural fluid (pyothorax); complicates pneumonia/aspiration

Inves

gross purulent; D-shaped opacity on imaging
LDH >1000 IU/L; glucose <30 mg/dl; pH <7.2

Mng

always drain pus regardless of contraindication; large-bore ICT (20 French)

Special

pH <7.2 / glucose <30 / D-shaped opacity

Chylothorax

C/P

milky pleural fluid; lymphatic obstruction by malignancy or thoracic duct injury

Inves

gross white/milky; triglyceride >110 mg/dl

Mng

Special

milky fluid, triglyceride >110 mg/dl

Hemothorax

C/P

causes: chest trauma (usually blunt); iatrogenic (cardiac surgery, chest drain insertion, CVP catheter — most common); spontaneous rare even in clotting disorders
signs: stony dullness, ↓breath sounds, hypovolemia + collapse if large

Inves

erect CXR (serial — blunting of hemidiaphragm, progressive loss of basal lung field)
needle aspiration confirms blood; pleural fluid hematocrit >50% of peripheral = hemothorax

Mng

cross-match for urgent transfusion; correct coagulopathy FFP ± platelets
small → observe with serial X-rays; significant/symptomatic → large-bore chest drain
drainage >1000 mL or >200 mL/h for 3h despite correcting coagulopathy → contact thoracic surgeon

Special

pleural fluid hematocrit >50% of peripheral

Pneumothorax (incl. tension)

C/P

causes: spontaneous, traumatic, iatrogenic
primary: no underlying lung disease; thin young adults; M>F; hereditary (Marfan, Ehlers-Danlos); pleural pressure < atmospheric
secondary: underlying lung disease (COPD, asthma, CF); pleural pressure = atmospheric
tension: pleural pressure > atmospheric (one-way valve)
symptoms: asymptomatic, pleuritic chest pain, dyspnea
signs: asymmetric chest expansion (limited affected side), hyper-resonance, absent/↓breath sounds affected side

Inves

CXR: absent lung markings lateral to well-defined lung border
tension: hyperlucent areas devoid of lung markings

Mng

assess 3 Qs: age >50, smoking history, evidence of underlying lung disease (exam/CXR)
small-bore (8–14 French) chest tube
tension → needle decompression 2nd rib space MCL (rush of air converts tension → simple), then tube thoracostomy

Special

tension: mediastinal shift (trachea + heart), JVD, hypotension, difficulty ventilating; needle decompression 2nd ICS MCL

Vascular Surgery

11 entries

Acute Limb Ischaemia

C/P

sudden-onset limb pain + coldness (heavy smoker)
most present sudden pain + pallor (thrombus-in-situ or embolus)
6 P's referenced on slide (not individually enumerated)
aetiology — embolism (AF, mural thrombus, vegetations from endocarditis/valvular disease, proximal aneurysms, atherosclerotic plaque thrombosis)
thrombosis (atherosclerosis, popliteal aneurysm thrombosis, bypass graft occlusion)
traumatic (blunt, penetrating, iatrogenic)
thrombotic conditions (hypercoagulable state, low-flow state)

Inves

Duplex = first line
then CTA/MRA
gold-standard inv = angiogram — anatomical location of occlusion, state of distal vessels, decides operative approach (femoral vs popliteal incision)

Mng

ABCDE; resuscitation — O2, IV fluids, heparin, analgesia; call vascular review
best time to manage = within first 6 hours
definitive by cause — embolus → embolectomy; thrombus → thrombolysis; either → bypass; trauma → end-to-end anastomosis / autologous vein graft
treatment depends on cause, regional anatomy, comorbid status
complications — mortality, amputation, reperfusion injury, compartment syndrome

Special

— (viability categories → CRITERIA)

Aneurysms (AAA + Popliteal)

C/P

popliteal aneurysm — prominent wide popliteal pulse; can compress popliteal vein → oedema; tendency to thrombose + distal embolisation; 50% bilateral; 30% assoc. AAA
acute arterio-arterial embolic ischaemia (popliteal aneurysm as embolic source) — swollen pale cold leg, intact femoral pulse, lost pedal pulses
types — true vs false (pseudo) aneurysm; common sites = abdominal aorta + popliteal artery
AAA — modifiable risk factors for progression/rupture = smoking, hyperlipidaemia, hypertension
ischaemic colitis (post-EVAR day 1) — L upper abdo pain + PR bleeding (mesenteric/pelvic circulation compromise)
aorto-enteric fistula — hx open aortic graft, painless PR bleed → haemodynamic instability

Inves

popliteal aneurysm — duplex confirms; then further imaging for distal runoff
CT angiography — assess distal runoff + plan operation (esp. if raised creatinine); CTA = surgical planning
US = screening + AAA surveillance (follow-up gold standard = ultrasound, looking for increase in aneurysm size)
revise general exam = palpate abdomen for AAA (30% popliteal aneurysms assoc.); revise local exam = contralateral popliteal fossa (50% bilateral)
ischaemic colitis — after resuscitation, first-line inv = colonoscopy/sigmoidoscopy (visualise ischaemic mucosa)

Mng

popliteal aneurysm — exclusion (not excision) of aneurysm + in-situ saphenous vein bypass graft (in-situ overcomes anastomotic size discrepancy); local thrombolysis may improve distal runoff until definitive therapy (recent recommendation)
acutely ischaemic limb treated first; asymptomatic AAA → surveillance; asymptomatic contralateral popliteal aneurysm → elective repair
AAA 4 cm → surveillance; 5 cm (grew from 4 cm) → elective EVAR; elective repair = open vs EVAR
factor NOT affecting open-vs-EVAR = size of aneurysm (relevant = marked comorbidity, previous abdominal surgery, anatomy of graft take-off + landing)
aorto-enteric fistula → resuscitate + urgent surgery

Special

blue-toe syndrome — with popliteal aneurysms

Chronic Arterial Ischaemia / PAD (incl. intermittent claudication, critical limb ischaemia)

C/P

symptomatic chronic atherosclerotic ischaemia — all chronic risk factors, no acute event
intermittent claudication — leg-muscle pain on walking (thigh/buttock/calf/foot), stops walking, relieved by rest; cramping after fixed distance (e.g. 150 m, 400 m) relieved by 2–3 min rest
rest pain — interferes with sleep, positional relief
occlusion site by symptom — thigh/buttock cramping = aorto-iliac
most limb-threatening multilevel combo = aorto-iliac + tibioperoneal disease (loss of distal runoff → no bypass target)
non-healing ulcers (pulses unchanged) → new distal lesion (multilevel disease)
critical limb ischaemia / digital gangrene on PAD background
life-threatening element = progression of disease elsewhere (e.g. coronary artery disease)
most serious limb-threatening risk factor = smoking (direct toxic effect on vascular endothelium)
diabetes threatens ulcerated limb — macroangiopathy (multilevel), microangiopathy, ulcers easily infected, Charcot's joint impedes healing
Buerger's disease (differential) — young male (~40), heavy smoker; claudication + Raynaud's phenomenon + thrombophlebitis migrans

Inves

conservative decided after duplex + ABI
risk assessment — carotid duplex, ECG/echo, stress thallium coronary perfusion (if claudication distance allows); NOT direct carotid arteriography in all (too invasive for screening)
most important pre-op inv = digital subtraction angiography (DSA)

Mng

surgical intervention not immediately needed if not limb/life-threatening + not incapacitating
conservative — limb care (podology, nail/foot care) + regular exercise (improves collateral circulation) + life care (risk assessment/management); reassurance alone insufficient
bypass — fem-fem crossover bypass; fem-popliteal bypass w/ reversed saphenous vein; graft choice depends on site of occlusion + size discrepancy, NOT length of occlusive lesion
occluded graft (2 yrs) cause = intimal hyperplasia → transcatheter thrombolysis (anticoagulants → limb lost; open redo too invasive)
critical limb ischaemia — revascularisation (angioplasty or surgery) unless foot healing; diabetes control; debridement/amputation

Special

Leriche's syndrome — buttock claudication + loss of penile erection (ED) → occlusion of abdominal aorta or internal iliac artery
Buerger's test — named in ILOs (angle/values not printed on slides)
Raynaud's — limb colour white→blue→red in response to cold
Charcot's (neuropathic) joint — dislocation, pathologic fractures, debilitating deformities

Compartment Syndrome (limb)

C/P

post arterial/venous repair or reperfusion — increasing leg/foot swelling, foot pain, can't move toes
pedal pulses may still be palpable

Inves

clinical (pulses may still be present)

Mng

immediate step = fasciotomy

Special

pulses may still be present despite compartment syndrome

Mesenteric Ischaemia

C/P

post-prandial GI pain + weight loss → ischaemia of celiac artery / SMA / IMA

Inves

Mng

Special

DVT / Venous Thromboembolism (VTE)

C/P

leg pain + swelling (calf→thigh), skin erythema, warm tender calf, low-grade temp, tachycardia, normal foot pulses
most cases silent; symptomatic 3rd–4th day post-op
pelvic/femoral vein involvement → massive whole-limb swelling
differentials — cellulitis, lymphoedema, ruptured Baker's cyst, lymphangitis, haematoma
risk factors — age, bed rest, pregnancy, OCP, major surgery, major trauma, burns, lower-limb fractures, thrombocytosis, thrombophilia (hereditary/acquired), protein S/protein C deficiency, factor V Leiden, antithrombin III deficiency, antiphospholipid syndrome
complications — immediate PE + sudden death; post-thrombotic leg (eczema, pigmentation, lipodermatosclerosis); venous ulceration; phlegmasia alba dolens; phlegmasia cerulea dolens
VTE = most common direct cause of death in surgical patients (autopsy studies)

Inves

venous duplex US = inv of choice
CTV/MRV; CBC, D-dimer, PT/PTT/INR; LFT/KFT

Mng

anticoagulation = mainstay (prevents thrombus extension + reduces PE risk)
therapeutic LMWH + warfarin/NOAC started together; heparin stopped once INR therapeutic (if warfarin); target INR 2–3
prophylaxis — early mobilisation, post-op hydration, intraop intermittent calf compression (inflatable cushions), elastic stockings + leg elevation, SC LMWH started pre-op continued while at risk
PE — morphine, oxygen, thrombolytics, anticoagulant, embolectomy; IVC filter if anticoagulation contraindicated (prevents recurrent PE)

Special

Homan's sign — obsolete
phlegmasia alba dolens / phlegmasia cerulea dolens
Virchow's triad (components → CRITERIA)

Varicose Veins

C/P

leg pain on prolonged standing + distended/dilated tortuous veins; commoner in women; prolonged standing ↑ venous hydrostatic pressure → distension + valve incompetence
primary/idiopathic (majority); secondary = pelvic masses (pregnancy, fibroids, ovarian mass, tumour), pelvic venous abnormalities (post pelvic surgery/irradiation, previous DVT)
red patch = venous eczema
complications if untreated — pain, leg swelling, bleeding, eczema, skin ulceration; also superficial thrombophlebitis, lipodermatosclerosis
venous system holds ~60% of total blood volume, avg pressure ~5–10 mmHg

Inves

duplex ultrasound (standard) — identifies all reflux/obstruction, superficial + deep
examine patient while STANDING

Mng

graded compression stockings (minor varicosities, elderly, pregnant, unfit for intervention; graduated — higher pressure at ankle than thigh)
sclerotherapy (small/medium varices below knee; compress 2 days; complications = bruising, phlebitis, ulceration)
endovenous laser ablation (replacing surgery/sclerotherapy; laser heat ablates endothelium → thrombose)
surgery — high ligation (disconnect GSV from femoral vein) + tributary ligation ± GSV stripping groin→knee ± perforator ligation/avulsion

Special

Trendelenburg test — confirms deep→superficial reflux + level of incompetent connection; high-thigh tourniquet controls veins if SFJ incompetence; move tourniquet lower to locate connection
thrill/cough impulse at SFJ on coughing

Venous Ulcer (+ arterial / neuropathic contrast)

C/P

ulcer lower leg after minor trauma, growing; slough + exudate base, surrounding dark pigmentation; assoc. LSV varicose veins
causes of leg ulceration — arterial (ischaemic), venous, mixed, vasculitic (RA, pyoderma gangrenosum), malignant (Marjolin), infective (TB, syphilis, leprosy), traumatic, diabetic (neuropathic), haemolytic anaemia (sickle cell, pernicious anaemia)
sites — venous = gaiter area, just above medial malleolus (medial calf perforators); arterial = distal foot (toe tips, between toes, ball of foot, lateral malleolus, bony prominences); neuropathic = pressure areas (beneath metatarsal heads)
characteristics — venous: irregular, sloping, white edges (+ oedema, stasis eczema, pigmentation, lipodermatosclerosis, ankle flare, atrophie blanche); arterial: well-defined, deep, punched-out edges (+ cold pale limb, poor cap refill, absent/weak pulses, atrophic dry shiny hairless skin); neuropathic: thick keratinised raised edges (+ decreased sensation)
venous disease = ~85% of all chronic lower-limb ulcers; 15–30% of venous ulcer patients have concomitant arterial disease = mixed ulcer

Inves

palpate peripheral pulses
duplex (SFJ/SPJ competence, perforators, deep system)
CBC/ESR/CRP, fasting lipids, blood glucose
ABPI to exclude arterial disease if in doubt

Mng

mobilise; leg elevation
compression therapy = most important (safe if ABPI >0.8; inspect ulcer each dressing change; bandages changed by experienced nurse)
once healed → graduated class I/II elastic stockings (prevent recurrence)
varicose vein surgery if caused by superficial varicosities w/ no deep incompetence
surgical debridement if necrotic

Special

Marjolin ulcer — malignant transformation
atrophie blanche / ankle flare — venous
punched-out edges — arterial

Lymphoedema

C/P

unilateral limb swelling, slowly progressive; iatrogenic post axillary clearance + chest-wall/axilla radiotherapy (breast cancer)
early warning — achiness/tingling/warmth in hand/arm/chest/breast/underarm; "bursting"/shooting pain or pins-and-needles; puffiness + pitting (temporary indentation on pressure); veins/tendons harder to see, less pronounced knuckles, smoother skin; clothing/bra/jewellery tighter; skin texture changes (tightness, redness, hardening), rash/itch/warmth
congenital lymphatic dysplasia types — congenita / praecox / tarda (full breakdown → CRITERIA)
SOURCE DISCREPANCY — same 16F post-menarche, unilateral-to-knee case labelled "lymphoedema praecox" in [45.1] but "congenital lymphoedema" in [045]
exclude breast cancer recurrence — neoplastic axillary infiltration → arm swelling (lymphatic + venous blockage) + pain (brachial plexus involvement) → deceiving

Inves

bloods
duplex US (venous + arterial systems)
lymphoscintigraphy (radionuclide lymphatic imaging — dye through lymph vessels, highlights blockages)
scans for underlying cause (pelvic US, CT, MRI)

Mng

written skin-care instructions (oedematous limb prone to bacterial infection), limb elevation, elastic arm stockings / compression garments, pneumatic compression, antibiotics if superimposed infection
light exercises; limb bandaging/wrapping; manual lymph drainage massage (avoid if skin infection/clots/active disease)
complete decongestive therapy (CDT) — avoid in HTN, diabetes, paralysis, heart failure, clots, acute infection
surgery for severe — excise excess tissue, or lymphatic-to-venous anastomosis / lymph node transplant
prevention (post-op) — protect skin (gloves, no barefoot, electric razor, treat cuts, insect repellent, sun block, ± prophylactic antibiotics on holiday); protect arm from extremes (heat, exercise, pressure); gentle graded exercise plan; lose weight; no injections/bloods/BP on affected arm

Special

Stemmer's sign — named distinguishing sign
lymphangiosarcoma — rare late complication (many yrs post-treatment); multiple subcutaneous nodules upper limb; distinguish from recurrent breast carcinoma; prognosis poor, some respond to cytotoxics/irradiation
mechanism — Starling's forces imbalance + impaired lymphatic drainage

Post-Thrombotic Syndrome (PTS)

C/P

hx DVT (post major surgery for rectal mass); years later discolouration, swelling, itching
exam — bluish skin, dilated veins at groin + lower leg/thigh, venous ulcer on medial leg
symptoms/signs — chronic aching pain + heaviness; itching; oedema; secondary varicose veins; brown discolouration (hyperpigmentation) around ankle; ulceration (severe)
risk factors — rectal mass (pelvic malignancy), DVT (venous hypertension)
varicose vein type = secondary (predisposing factors, irregular pattern, crossing veins at groin, venous ulcer = deep-system failure)

Inves

duplex scan = inv of choice (state of deep veins, missed DVT, perforators) + clotting bloods

Mng

mobilisation, leg elevation, compression therapy (treat ulcer), antibiotics if infected, continue compression stockings once healed

Special

Diabetic Foot

C/P

acute diabetic foot infection (cellulitis) — red swollen foot, fever, ↑WCC/CRP, palpable foot pulses (pulses present → not primarily ischaemic); DD = acute Charcot foot (also red/hot/swollen)
neuropathic (diabetic) foot ulcer — chronic wound, enlarging/deepening after tight footwear (sensory neuropathy + pressure)
critical limb ischaemia / digital gangrene — black toe, claudication ~200 m, T2DM/HTN/ex-smoker (neuro-ischaemic foot)
2 main reasons diabetics prone = neuropathy + ischaemia
sensory neuropathy → can't appreciate damage (ill-fitting footwear); motor → weak short flexors → clawed toes + prominent metatarsal heads → weight-bearing ulceration; autonomic → ↓ sweating, dry cracking skin
diabetics = 4× increased PAD risk; DM + PAD = greatest amputation risk
microcirculation — thickened basement membrane, ↑ capillary permeability, ↑ platelet adherence
foot complications — ~10% ischaemic, 45–60% neuropathic, 25–45% neuro-ischaemic; infection = common final presenting factor (hyperglycaemia immunosuppressive)
highest risk for ulceration = diabetic peripheral neuropathy (neuropathy = 45–60% of foot complications)
ulcer sites = weight-bearing/pressure points (metatarsal heads, heel, Charcot bony prominences e.g. navicular); least likely = medial malleolus (venous-ulcer site)
amputation relative risk 13× vs non-diabetic; 85% of amputations avoidable with adequate care; 15% of diabetics develop foot ulcer yearly; >40% of PAD patients have diabetes

Inves

cultures + wound swabs; deep-tissue aspiration more accurate than superficial swabs
plain X-ray (osteomyelitis, gas in tissues)
vascular status — absent pedal pulses + low ankle BP = high-risk foot; duplex + CT angiogram
screening — 10 g monofilament test + peripheral pulse palpation + ankle BP measurement

Mng

acute infection — first line control diabetes (sliding scale / correct ketoacidosis); IV antibiotics (cover Staph aureus, Streptococcus, Pseudomonas, anaerobes); surgical drainage + debridement of collection within 24h; leg elevation
diabetic foot ulcer management (6) — off-loading, debridement, wound dressings, antibiotics, revascularisation, amputation; multidisciplinary (ortho, vascular surgery, endocrinology, podiatry, infectious disease)
critical limb ischaemia — revascularisation (angioplasty or surgery) unless foot healing; diabetes control; debridement/amputation of toe
wounds not sutured → heal by secondary intention; negative-pressure wound therapy; total contact casts (window for inspection) for early mobilisation

Special

Charcot's foot — bone/joint fragmentation + deformity, loss of normal joint connections → serious foot deformity; chronic-phase mgmt (7): assessment (ulcer, vascularity, neuropathy, bloods, X-ray, MRI); acute foot (antibiotics, drainage, debridement); off-loading; VAC dressing; larvae therapy; risk-factor management; arterial reconstruction

Haematology

5 entries

Factor V Leiden thrombophilia

C/P

28M, DVT after long flight
FHx: father sudden death 46, sister DVT in pregnancy
homozygous FVL

Inves

Doppler confirmed DVT
thrombophilia screen delayed ≥1 month post-anticoagulation (acute post-thrombotic state + anticoagulants distort tests; dx doesn't change acute mng)
initial screen normal: PT 13 / APTT 36 / TT 14; protein C 131, AT 95, protein S 105
PCR panel: Factor V G1691A (Leiden), prothrombin G20210A, MTHFR C677T/A1298C

Mng

anticoagulation (screen deferred until ≥1 month after)
advise sister → offer thrombophilia screening

Special

autosomal dominant; Arg506Gln (G→A at G1691A) → factor V less cleaved by activated protein C (APC resistance)
heterozygous ~4× VTE risk, homozygous ~20×

Antiphospholipid syndrome (APLS)

C/P

32F, 3 recurrent spontaneous abortions at 9th gestational week, no anatomic/hormonal cause

Inves

lupus anticoagulant weakly positive (sensitive PTT / dRVVT) = suggestive not diagnostic
order anticardiolipin + beta-2 glycoprotein-1 antibodies: cardiolipin IgG 45 (0–10, high), B2GP1 strong positive
must repeat after 12 weeks; still-positive high titre = diagnostic

Mng

anticoagulant therapy as soon as she falls pregnant

Special

Autoimmune haemolytic anaemia (AIHA)

C/P

cold-agglutinin type: 44F, fatigue/weakness 4wk, jaundiced
secondary to CLL (warm): 68M, tiredness + lymphadenopathy + splenomegaly

Inves

CBC: Hb 7 low, Hct 21% low, MCV 97 N → normocytic normochromic + jaundice → haemolysis
confirm: bilirubin, haptoglobin, reticulocytes → retics 13% high, total bili 4.2 high, haptoglobin low
urine pinkish-red haemoglobinuria → intravascular haemolysis
film: spherocytes + RBC agglutination (cold agglutinins)
DAT 3+ = diagnostic; serum antibody = cold agglutinin
CLL-associated: MCV 115 macrocytic (reticulocytosis raises MCV), retic 23%, polychromasia; direct Coombs +ve (also seen in SLE)

Mng

corticosteroids for autoimmune haemolysis (CLL-associated case)

Special

cold type usually IgM, life-threatening haemolysis; half secondary (lymphoproliferative/lymphoma or viral), rest idiopathic
spherocytes + RBC agglutination; DAT/direct Coombs +ve

Thrombotic thrombocytopenic purpura (TTP)

C/P

27F pregnant 36wk; fever, purpura, declining consciousness, no HTN (increased frequency in pregnancy)
pentad: fever + fragmented RBCs + renal affection + neurological (declined consciousness) + thrombocytopenia

Inves

Hb 7.5 low, MCV 102 high, retics 12% high, WBC 11, platelets 40 low, urea 67 high
film: fragmented red cells → microangiopathic haemolytic anaemia (MAHA)
normal coag profile excludes DIC; normal LFTs exclude HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets)

Mng

early daily plasma exchange with FFP (crucial)
untreated → high mortality (multi-organ failure); relapse 30–60% (most in first month)
newer = recombinant ADAMTS13 or rituximab

Special

antibodies to ADAMTS13 (cleaves VWF) → high-MW VWF multimers; rare inherited ADAMTS13 deficiency
schistocytes / fragmented RBCs (MAHA)

Disseminated intravascular coagulation (DIC)

C/P

in pregnancy: sepsis, amniotic-fluid embolism, antepartum haemorrhage, retained dead fetus

Inves

abnormal coag profile (normal coag profile excludes it — vs TTP)

Mng

Special

Toxicology & Psychiatry

7 entries

Poisoning — general approach

C/P

Dx from history (sudden illness, food/drink/chemical/gas/bite exposure, empty bottle/syringe), exam (vitals/toxidromes, systemic)

Inves

Routine labs: CBC, electrolytes, ABG, renal/hepatic, glucose
Anion gap (raised in MUDPILES); toxicology screen (qualitative color test; quantitative GC/HPLC)
ECG + cardiac monitoring (sympathomimetics); CXR (chemical/aspiration pneumonia); AXR radiopaque = CHIPES

Mng

Supportive/1st aid (coma cocktail = dextrose, naloxone, thiamine) → GI decontamination (gastric lavage early ~3h; emesis not preferred, no saline; CI to lavage: coma, corrosives, hydrocarbons, convulsions) → antidotes → elimination → symptomatic

Special

— (see CRITERIA: anion gap, MUDPILES, CHIPES, coma cocktail)

Scorpion sting (envenomation)

C/P

Case 1: 5y child agitated, BP 130/95, tachypnoeic, tremors, sweating, no local sign; after 1.5h → vomiting, tachy 140, breathless, cyanosed, stupor
Autonomic storm: venom = potent autonomic stimulant → massive release endogenous catecholamines + acetylcholine
Complications: dehydration/vomiting/diarrhoea/gastritis; CVS HTN/dysrhythmia/MI/acute HF; pulmonary oedema; CNS agitation/convulsions; metabolic hyperK/hyperglycaemia/acidosis

Inves

ABG (oxygenation/metabolic acidosis); electrolytes (hyperK); RBS (hyperglycaemia); ECG (sinus tachy/brady, arrhythmia, ischaemic changes); CXR (pulmonary oedema)

Mng

Scorpion antivenom — best first 4h, still up to 24h; 3–5 ampoules initial slow IV/IM; more q30 min if progressing/not regressing; skin test, if +ve premedicate hydrocortisone; dose same for children + adults

Special

Autonomic storm (catecholamine + ACh surge); no local sign

Snake bite

C/P

Viper: severe local (fang marks, pain/bleeding, rapid oedema, tender regional nodes, ecchymosis, blistering, necrosis/dry gangrene) + general (coagulopathy, bleeding, haemolysis, hypotension/shock, myotoxicity → myoglobinuria → renal failure, hyperK)
Cobra: minimal local; neurotoxic general (facial/neck fasciculation → descending skeletal paralysis, delayed up to 12h; consciousness + sensation spared)

Inves

Mng

1st aid: rest/reassurance/immobilise limb/remove constricting objects; incision-suction/cryotherapy/electric shock = harmful, obsolete
Polyvalent antivenom — all systemic envenomation; best within 2h but never too late; slow IV; 3–5 vials initial; 10 vials if still progressing
Tetanus prophylaxis; debridement of necrotic tissue

Special

Viper = local necrosis + coagulopathy; Cobra = descending paralysis with spared consciousness/sensation

Organophosphate poisoning

C/P

Case 2: 40M spraying fruit trees; confused, diaphoretic, BP 100/70, pulse 40, small pupils, crepitations, vomiting/diarrhoea, O2→70%, pink frothy sputum
OP inhibits acetylcholinesterase → ACh accumulates → muscarinic + nicotinic + CNS stimulation; irreversible after 24–36h (carbamates = reversible, rarely fatal)
Muscarinic = DUMBELS; nicotinic = MATCH; central = vertigo/confusion/tremor/agitation/convulsions/coma
Deterioration (atropine overdose) = anticholinergic toxidrome: dry skin/mucosa, dilated non-reactive pupils, hyperthermia, hallucinations, urinary retention, decreased bowel sounds, tachycardia (Case 2: BP 170/90, pulse 135, warm/dry/pink, pupils 7mm unreactive, temp 38.5)
Complications: intermediate syndrome (2–3 days, proximal-limb/neck-flexor/respiratory paralysis, oximes may prevent); cardiomyopathy; delayed neuropathy (2–3 weeks, mixed sensory-motor, demyelination, usually permanent)

Inves

ABG/electrolytes/glucose/urea/creatinine; ECG + cardiac monitoring
True (RBC) + pseudo (plasma) AChE — pseudocholinesterase decreased; CXR (aspiration pneumonia/bronchospasm)

Mng

ABC, decontamination
Atropine 2–5 mg IV q15 min until bronchospasm relief + dry chest secretions (don't rely on HR/pupil size); keep atropinized 1–2 days; slide table: 0.02 mg/kg IV then double q5–15 min till full atropinization
Obidoxime 250 mg amp IV/day ×3 days; slide table: toxogonin 250mg/5ml loading 4–8 mg/kg then 10 mg/kg/day infusion
Atropine overdose = symptomatic (cold compresses, IV fluids, BZD)
Atropine = competitive muscarinic antagonist (not nicotinic); oximes = reactivate AChE (give first 24–48h before enzyme aging)

Special

Pinpoint miosis + bradycardia + bronchorrhoea (DUMBELS); pink frothy sputum; spray/insecticide exposure

Carbon monoxide poisoning

C/P

Case 3: 64F fire smoke inhalation; coma GCS 5, RR 7, BP 50/30, pulse 40, wheezes+creps
Throbbing headache, dizziness/nausea, cognitive impairment/ataxia/confusion/convulsions/coma; CVS tachy/hypotension/arrhythmia/angina→MI; pulmonary oedema; cherry-red skin (rare); rhabdomyolysis → myoglobinuria/renal failure; delayed neuropsychiatric sequelae (lucid interval 2–40 days; recovery only 50%)
Mechanism: binds Hb 200–250× affinity of O2; leftward shift oxyHb curve; binds myoglobin (40–60×); inhibits cytochrome oxidase; displaces NO

Inves

ABG pH 6.90, PaO2 55, PCO2 50, HCO3 8; Na 136, K 4, Cl 92; anion gap (136+4)−(8+92)=40, high
Confirm carboxyhaemoglobin; CXR bilateral infiltrates/alveolar filling

Mng

ABC 1st aid; 100% O2 (CO t½ 5h→1h); hyperbaric O2 (2 atm → t½ 20 min) if altered mental status/confusion, COHb >25%, or fetal distress
Cerebral oedema = prednisolone 1mg/kg IV q4h + mannitol 20% 1mg/kg over 20 min

Special

Cherry-red skin (rare); COHb; leftward oxyHb shift

Cyanide poisoning

C/P

Hydrocyanic/Prussic acid; volatile colourless liquid, bitter-almond smell
Blocks cytochrome oxidase (binds ferric ion) → histotoxic anoxia (red asphyxia, no cyanosis; arterial O2 = venous O2) → lactic acidosis, ↓ATP
Large dose = sudden death 1–2 min; small dose = CNS (headache→seizures/coma), CVS (initial brady+HTN → hypotension+reflex tachy → terminal brady+hypotension), respiratory (tachypnoea→bradypnoea+pulmonary oedema, no cyanosis), metabolic acidosis

Inves

Confirm cyanohaemoglobin; DDx red asphyxia: CO, cyanide, cold (hypothermia)

Mng

100% O2 artificial respiration, GI decontamination
Cyanide kit = amyl nitrite + sodium nitrite + sodium thiosulfate + reducing agent (vit C or methylene blue)
Dicobalt EDTA (Kelocyanor — chelates circulating not intracellular); hydroxocobalamin (Vit B12a → cyanocobalamin, renally excreted)
Sodium nitrite induces methaemoglobinaemia (ferric iron binds cyanide → cyanmethaemoglobin); thiosulfate → thiocyanate; hydroxocobalamin → cyanocobalamin

Special

Bitter-almond smell; red asphyxia (no cyanosis, arterial O2 = venous O2); histotoxic anoxia

Disturbed behaviour — acute presentations (VM031; scenario-implied, NOT printed)

C/P

Inves

Mng

Special

Cardiology

9 entries

Auscultation areas

Aortic = 2nd ICS right sternal border (heard in S2); Pulmonary = 2nd ICS left sternal border (S2); Tricuspid = 5th ICS left sternal border (S1); Mitral = 5th ICS mid-clavicular line (S1).

Heart sounds

S1 = mitral + tricuspid closure, loudest at mitral area; S2 = aortic + pulmonary closure, loudest at left upper sternal border. Physiological S2 splitting: inspiration → ↓ intrathoracic pressure → ↑ venous return → ↑ RV filling → ↑ RV stroke volume → ↑ RV ejection time → delayed pulmonic closure (↓ pulmonary impedance also delays).

Murmur timing

starts WITH carotid pulse → systolic; starts AFTER carotid pulse → diastolic. Types: systolic, diastolic, continuous.

Systolic murmur types

Pansystolic (isointensity S1→S2) = MR, TR, VSD; Ejection systolic (crescendo–decrescendo / diamond-shaped) = AS, PS, ASD, VSD; Mid/late systolic (grade 2–3, following a mid-systolic click) = MVP.

Diastolic murmur types

Early diastolic decrescendo (high-pitched "blowing") = AR; Mid-to-late diastolic rumbling (follows opening snap) = MS (mid-diastolic also tricuspid stenosis).

S3 vs S4

S3 (ventricular gallop, "Ken-Tuc-KY"): early diastole; passive LV filling; may be normal; needs very compliant LV; sign of systolic HF; heard only with bell. S4 (atrial gallop, "TE-Nuh-See"): late diastole; active LV filling; almost always abnormal; needs non-compliant LV; sign of diastolic HF. Both heard only at apex; S3 only with the bell.

ACS diagnostic criteria

rise/fall of cardiac biomarker (troponin) ≥1 value >99th percentile URL (local >0.03 µg/L suggests ischaemia) PLUS ≥1 of: ischaemic symptoms; chest pain >15 min + sweatiness; new ST-T changes or new LBBB; pathological Q waves; imaging new loss of viable myocardium / new regional wall-motion abnormality. Troponin: repeat 10–12 h after symptom onset.

Ischaemic symptoms flagging ACS

pain chest/arms/back/jaw >15 min (over 20 min); chest pain + nausea/vomiting, marked sweating or breathlessness, or haemodynamic instability; new-onset pain OR abrupt deterioration of stable angina with recurrent pain, little/no exertion, >15 min.

MI localisation (culprit artery)

inferior wall MI → right coronary artery; anterior STEMI → LAD. (Task 7 = localizing MI on ECG.)

Respiratory

13 entries

GINA assess-control triad (selects the step)

(1) daytime symptom frequency, (2) night symptoms, (3) FEV1.

GINA stepwise ladder (ICS-formoterol track)

Step	Trigger	Treatment
1–2 (AIR)	symptoms <3–5 days/wk + normal/mildly-reduced lung function	as-needed-only low-dose ICS-formoterol
3 (MART)	symptoms most days OR night-waking ≥1/wk OR low lung function	low-dose MART (ICS-formoterol)
4 (MART)	daily symptoms + night-waking ≥1/wk + low lung function OR recent exacerbation	medium-dose MART
5	severe asthma	refer for expert assessment/phenotyping + add-on

Reliever throughout = as-needed low-dose ICS-formoterol.

Asthma acute-severity (→ ICU/MV features)

confusion, low BP, RR >30, SpO2 <90%, silent chest. (DDx: heart failure, PE, upper airway obstruction.)

Asthma dx thresholds

Spirometry: FEV1/FVC <80%, FEV1 <80% predicted. Reversibility: post-salbutamol FEV1 +200 mL AND +12%. PEF: diurnal variability >10%.

Severe-asthma Th2 phenotype

sputum eosinophil ≥2%, and/or FeNO ≥20 ppb, and/or blood eosinophil ≥150/µL.

IDSA/ATS Severe Pneumonia

1 major OR 3 minor.

Major: (1) septic shock needing vasopressors; (2) respiratory failure requiring mechanical ventilation.
Minor: (1) RR ≥30; (2) hypotension corrected by IV fluid; (3) hypothermia; (4) confusion/disorientation; (5) leukopenia <4,000; (6) thrombocytopenia <100,000/mL; (7) uremia BUN ≥20 mg/dl; (8) PaO2/FiO2 ≤250; (9) multilobar infiltrates.
FiO2 = 0.21 room air, +0.04 per L O2.

CURB-65 (site of care)

score 0–1 = home; 2 = ward; 3–5 (or severe CAP by IDSA/ATS) = ICU.

Responsive-pneumonia criteria (72h follow-up)

T ≤37.8, HR ≤100, RR ≤24, SBP ≥90, SpO2 ≥90% RA, normal mental status, normal oral intake.

Sarcoidosis CXR staging (not progressive)

Stage	Findings
1	bilateral hilar LAD
2	bilateral hilar LAD + pulmonary disease
3	only pulmonary disease (reticulonodular)
4	irreversible fibrosis + honeycombing

Light's criteria (exudate if ANY)

pleural/serum protein >0.5; pleural/serum LDH >0.6; pleural LDH >2/3 upper limit of normal serum. Requires simultaneous pleural + serum protein & LDH.

Pleural-fluid chemical thresholds

Marker	Threshold → meaning
Protein	>2.9 g/dl = exudate
LDH	>1000 IU/L = empyema, malignant effusion
Glucose	30–50 mg/dl = malignant, TB; <30 = empyema
Triglyceride	>110 mg/dl = chylothorax
pH	<7.2 = empyema (pyothorax; always drain)
Hematocrit	>50% of peripheral = hemothorax
WBC	transudate <1000/mm³, exudate >1000/mm³
Cell diff	lymphocyte >85% → TB/lymphoma; eosinophil >10% → PE-infarction/parasitic/drugs

Lung cancer TNM (NSCLC, 8th edition)

T1 ≤3 cm no invasion (T1a ≤1, T1b >1–2, T1c >2–3 cm)
T2 >3 to ≤5 cm OR main bronchus (not carina)/visceral pleura/atelectasis or obstructive pneumonitis (T2a >3–4, T2b >4–5 cm)
T3 >5 to ≤7 cm OR chest wall/parietal pleura, phrenic nerve, parietal pericardium, or separate nodule same lobe
T4 >7 cm OR carina, diaphragm, esophagus, great vessels, heart, mediastinum, trachea, recurrent laryngeal nerve, vertebral body, or nodule in different ipsilateral lobe
N0 none; N1 ipsilateral peribronchial/hilar/intrapulmonary; N2 ipsilateral mediastinal/subcarinal; N3 contralateral mediastinal/hilar, or any scalene/supraclavicular
M0 none; M1a nodule contralateral lobe / pleural or pericardial nodule / malignant pleural or pericardial effusion; M1b single extrathoracic met; M1c multiple extrathoracic mets

SCLC staging

(TNM not used — metastatic at presentation)

Limited: confined to ipsilateral thorax (incl. supraclavicular fossa + pleural effusion) → median survival 1–2 yr.
Extensive: all others → 6–12 mo.

Vascular Surgery

7 entries

ALI viability categories

Reversible / Partially reversible / Irreversible (non-viable/dead limb).

ABPI cutoffs

compression bandaging/therapy safe if ABPI >0.8; used to exclude arterial disease as ulcer cause; low ankle pressure + absent pedal pulses = high-risk (diabetic) foot.

Virchow's triad

(1) blood contact with abnormal surface (endothelial damage); (2) abnormal flow (stasis); (3) abnormal blood (thrombophilia).

Lymphoedema — congenital lymphatic dysplasia types

congenita: onset shortly after birth / within 2 yrs, more common males, mostly bilateral whole-limb · praecox: onset 2–35 yrs, more common females, peak after menarche, unilateral, limb affected to knee · tarda: onset >35 yrs, assoc. obesity.

Varicose vein distribution

long saphenous ≈60% (medial thigh/calf) · short saphenous ≈20% (posterolateral calf) · anterolateral thigh/calf = proximal anterolateral LSV tributary.

Leg ulcer differentiation (venous / arterial / neuropathic)

venous: gaiter area, just above medial malleolus; irregular, sloping, white edges · arterial: distal foot (toe tips, between toes, ball of foot, lateral malleolus, bony prominences); well-defined, deep, punched-out edges · neuropathic: pressure areas (beneath metatarsal heads); thick keratinised raised edges.

Pack-year

20 cigarettes (1 pack)/day for 1 year.

Haematology

8 entries

Coagulation factor names

I fibrinogen; II prothrombin; III tissue factor; V labile; VII proconvertin; VIII antihaemophilic; IX Christmas; X Stuart-Prower; XI plasma thromboplastin antecedent; XII Hageman/contact; XIII fibrin-stabilizing (transglutaminase); prekallikrein (Fletcher); HMWK (Fitzgerald)

Vitamin-K-dependent factors

II, VII, IX, X + protein C & S
warfarin = oral anticoagulant, vit K antagonist (blocks vit K reductase)

Naturally occurring anticoagulants

Prostacyclin (PGI2) — healthy endothelium; inhibits platelet aggregation + phospholipid release
Antithrombin III (heparin cofactor I): inactivates II, IX, X, XI, XII; principal inhibitor of thrombin AND factor Xa; facilitated by heparin
Protein C system: inactivates factors V and VIII

PT (prothrombin time)

extrinsic pathway efficiency; normal 11–16 s (rabbit thromboplastin), 10–12 s (human recombinant); monitors oral anticoagulant (warfarin); anticoag = trisodium citrate

INR

= (PT patient / mean normal PT) raised to ISI; ISI = international sensitivity index (standardises thromboplastin sensitivity vs reference)

APTT

intrinsic pathway; normal 26–40 s; monitors unfractionated heparin

TT (thrombin time)

thrombin added; affected by fibrinogen concentration + inhibitors (incl heparin)

Platelet reference range (adult)

150–410 ×10⁹/L

Toxicology & Psychiatry

6 entries

Anion gap

([VM030])

AG = (Na⁺+K⁺) − (Cl⁻+HCO3⁻) = 20±8 mmol/L
Alt slide: (Na) − (Cl+HCO3) = 7±4
Raised in MUDPILES

MUDPILES

(raised anion-gap metabolic acidosis) ([VM030])

Methanol, Uraemia, DKA, Paraldehyde, Iron, Lactic acidosis, Ethylene glycol, Salicylates

CHIPES

(radiopaque on AXR) ([VM030])

Chloral hydrate, Heavy metal, Iron, Phenothiazine, Enteric-coated/Sustained-release

Coma cocktail

([VM030])

Dextrose + Naloxone + Thiamine

DUMBELS

(OP muscarinic effects) ([VM030])

Diarrhoea, Urination, Miosis (pinpoint), Bradycardia/hypotension/Bronchospasm/Bronchorrhoea, Emesis, Lacrimation, Salivation/Sweating

MATCH

(OP nicotinic effects) ([VM030])

Muscle fasciculations, Adrenal medullary hyperactivity, Tachycardia/arrhythmia, Cramping, Hypertension

C/P

Inves

Mng

Special — pathognomonic

GI & Hepatobiliary Surgery

23 entries

Peritonitis

C/P

Localized: sudden RLQ/RIF pain + sickening sensation + one vomit at onset; steadily ↑ over 24h, continuous, analgesia unhelpful; tender RIF mass; ↑pain on flexion + int/ext rotation of right hip; DRE tender right-sided rockable mass
Generalized: sudden continuous pain epigastric → whole abdomen over few hours; vomiting not prominent; abdomen distended + marked tenderness
Perforated viscus features: sudden onset; abdominal rigidity / board-like rigidity
Acute biliary pancreatitis as cause: sudden onset; Hx repeated biliary colic; non-prominent vomiting; generalized distension + tenderness
Perforated peptic ulcer as cause: sudden onset; board-like rigidity; generalized distension + tenderness; Hx NSAID intake; air under diaphragm
DDx of generalized peritonitis: perforated transverse colon; perforated peptic ulcer; acute biliary pancreatitis

Inves

Localized (not in shock, gynae DDx): transvaginal ultrasonography = most suitable + sensitive Ix
Generalized, most specific lab for aetiology: raised serum lipase (biliary pancreatitis)
Air under diaphragm = perforated peptic ulcer

Mng

Generalized: crystalloid fluid resuscitation = main priority (before imaging/analgesia/drainage); working dx assigned after resuscitation

Special

Grey Turner / Cullen = distractors for perforated viscus (NOT features)

Acute appendicitis

C/P

Continuous lower right quadrant pain; one vomit at start of pain a day ago; palpable mass RLQ
Against appendicitis (in 32F case): her age; continuous pain; sudden onset; presence of a mass

Inves

Appendicular mass, before conservative Rx → baseline HCT; baseline CRP; glycaemic control in diabetics; baseline ESR

Mng

Appendicular mass → conservative Rx (labs as above baseline)

Special

Asymptomatic (silent) gallstones

C/P

Incidental / antenatal scan; small mobile stones; no colic; non-thickened GB wall
Natural history: 80% asymptomatic; biliary colic in 1–2% of asymptomatic pts/yr; complications in 3–5% of symptomatic pts/yr
Asymptomatic → symptomatic conversion: 5yr 10%, 10yr 15%, 15yr 18%

Inves

US: non-thickened GB wall (thickened wall from fibrosis = chronic calcular cholecystitis, NOT silent stones)

Mng

Observation / reassurance, NO cholecystectomy (risk of observation ≤ risk of operation)
Prophylactic cholecystectomy beneficial: congenital haemolytic anaemia w/ stones at splenectomy; obese undergoing bariatric surgery w/ existing stones; pre-organ-transplant w/ asymptomatic cholelithiasis (future immunosuppression)
Pregnancy: most acute biliary colic attacks resolve spontaneously → lap chole after delivery (avoid surgically-induced abortion); if necessary (non-resolving acute cholecystitis) → 2nd trimester preferred

Special

Biliary colic (symptomatic gallstone)

C/P

Severe epigastric pain radiating under ribs + to back/right scapula; builds over 1h; lasts up to 4h; nauseated, no vomiting; temp 37.2; no tenderness
Visceral + referred pain w/ fatty meals (foregut → epigastrium); vomiting uncommon; no fever; no jaundice; no abdominal signs; <6h
Trigger: fatty acids in duodenum → CCK → GB contraction + sphincter of Oddi relaxation → free stone impacts in GB neck
Relief: disimpaction of stone (spontaneous or antispasmodic)

Inves

Normal bloods (stone in secondary biliary tract)
Abdominal US = diagnostic: multiple gallstones; impacted stone in GB neck; normal thin GB wall (arrows = acoustic shadows)

Mng

Elective laparoscopic cholecystectomy after relief

Special

Acute cholecystitis

C/P

Acute severe RUQ pain radiating to infrascapular, 24h; nausea + vomiting; temp 38, BP 144/88, HR 76; RUQ tenderness + guarding + inspiratory arrest on deep RUQ palpation
Pain w/ fatty meals; vomiting more frequent; fever; no jaundice; RUQ tenderness + parietal pain; >6h
Acute calcular: intense/prolonged pain radiating to back/interscapular; anorexia/nausea/vomiting; maybe fever; tenderness; maybe mass
From impaction of stone in neck / cystic duct obstruction

Inves

HIDA / radioisotope scan (Tc-99m iminodiacetic acid, taken up by liver RE cells, excreted in bile): non-visualization of GB = acute cholecystitis; GB seen within 30min in 90% normal (1h remainder), bowel within 1h; absent GB filling also in acalculous cholecystitis; can diagnose bile leaks / iatrogenic obstruction

Mng

Cholecystectomy = best Rx of complicated acute cholecystitis
Unstable → percutaneous cholecystostomy under LA

Special

+ve Murphy's sign (inspiratory arrest on deep RUQ palpation)

Emphysematous cholecystitis

C/P

70M diabetic; localized RUQ pain; temp 38.7; WBC 18,000; normal LFTs
Rare acute cholecystitis w/ anaerobic infection → gas in GB lumen + wall; begins as acute cholecystitis (calculous/acalculous) → ischaemia/gangrene → gas-producing organisms
Most frequent in elderly men + diabetics; gallstones in 28–80%
Organisms: clostridia, anaerobic streptococci, gas-forming E. coli

Inves

US: gallstones + pericholecystic fluid + air in GB wall; confirmed by CT; CBD 4.5mm
Diagnosis usually on abdominal X-ray

Mng

Prompt surgical drainage + antibiotics mandatory; cholecystectomy = best Rx
Unstable → percutaneous cholecystostomy under LA

Special

Air in GB wall; gas in lumen dissecting in wall = gaseous ring; or gas in pericholecystic tissue

GB mucocele / empyema (fate of persistently-impacted stone)

C/P

After first acute cholecystitis attack, persistently impacted stone:
Good immunity + strong antibiotics → mucocele of GB (mucus, NOT bile/pus) → subsidence → palpable slightly-tender GB mass
If not controlled → septic cholecystitis → empyema (GB full of pus) → perforation → subphrenic abscess
If relieved medically → impacted stone returns toward fundus; if GB wall inflamed, smaller stones escape into biliary tract → choledocholithiasis

Inves

Mng

Special

Chronic (calcular) cholecystitis

C/P

Less intense pain w/ fatty meals; no physical findings; mild tenderness; no lab changes

Inves

US: thickened GB wall from fibrosis

Mng

Special

Choledocholithiasis

C/P

Stones in CBD; smaller stones escaped from inflamed GB into biliary tract
Complicated (jaundice/cholangitis/pancreatitis): RUQ pain; fever + rigors (cholangitis); obstructive jaundice (mild in cholangitis); tender liver

Inves

Mng

Special

Acute cholangitis

C/P

48F; 24h RUQ pain + nausea/vomiting; prior greasy-food episodes; slightly confused; dark urine; temp 38.5, HR 110, BP 90/60; RUQ tender (not Murphy's); scleral icterus
Obstructive picture = confusion + dark urine + fever + icterus
Infection of biliary tree from obstruction (secondary to choledocholithiasis)

Inves

WBC 20k; total bilirubin 4.0 (0.1–1.2); ALP 350 (33–131); AST 300, ALT 280; GGT 330 (8–88); amylase 100 (normal); urine +ve bilirubin
Normal amylase rules out pancreatitis

Mng

1) resuscitation + intensive antibiotics; 2) CBD drainage, preferably ERCP + stone extraction; 3) interval cholecystectomy

Special

Acute pancreatitis

C/P

29F; severe continuous epigastric pain 24h radiating straight through to back, relieved leaning forward; progressive nausea + bile-stained vomiting; prior brief fatty-meal episodes; afebrile, HR 115, BP 128/86; epigastric tenderness, NO guarding/rebound; hypoactive bowel sounds
Against biliary colic: continuous pain 24h (colic intermittent max 4–6h); progressive bile-stained vomiting; marked epigastric tenderness; leucocytosis
Against acute cholecystitis: no fever, no +ve Murphy's

Inves

WBC 17.2k; amylase 1,545 (30–110); lipase 1,134 (7–60); ALT 245; AST 263; glucose 156; LDH 180
Glucose >200 = severe
Raised serum lipase = most specific
AXR: gas throughout small + large bowel; focal dilated proximal small-bowel loop (sentinel loop) w/o air-fluid levels; no free air under diaphragm; AXR not diagnostic (rules out perforation)
AP AXR signs: air-fluid levels (ileus); colon cutoff sign (splenic flexure spasm); widened duodenal C-loop (head oedema)

Mng

(Mng not printed separately in source)

Special

Cullen's sign = periumbilical bruising (delayed, days, severe pancreatitis, extensive peripancreatic inflammation)
Grey Turner's sign = left flank bruising (haemorrhagic pancreatitis)
Sentinel loop; colon cutoff sign; widened duodenal C-loop

Abdominal trauma — penetrating

C/P

Stab / impalement (kitchen knife RUQ); HR 140, SBP 80, RR 20
Verbally clear = airway patent + breathing not severely compromised + no major ↓consciousness
Low-velocity penetrating at RUQ can traverse diaphragm → check breathing for tension pneumothorax + haemothorax
Shock aetiology: haemorrhage (hypovolaemia) OR cardiac tamponade / tension pneumothorax (obstructive shock)
Spinal cord injury unlikely (commoner w/ higher-velocity)
Tension pneumothorax: mediastinal shift + kinking of caval vessels → impeded venous return → obstructive shock; shifted trachea, ↓respiration affected side, hyper-resonance, engorged neck veins
Cardiac tamponade: central trachea, muffled heart sounds
Empty neck veins = hypovolaemia
Organs at risk — intraperitoneal: hollow (small intestine, transverse colon, stomach → peritonism not haemorrhagic shock), solid (liver commonest/largest, spleen more severe/left-side stabs), mesenteric; extraperitoneal: hollow (duodenum ± pancreas), solid (kidney), great vessels zone I retroperitoneum

Inves

Only imaging in unstable = FAST bedside + portable CXR (don't transport unstable patient)
FAST: pericardial fluid / tamponade; portable CXR: haemo/pneumothorax needing chest tube; ECG: cardiac injury
Most important lab: blood typing + cross-match (type-specific or O-negative); Hb/HCT falsely affected by crystalloid volume/rate
FAST -ve pericardial + CXR no haemo/pneumothorax → obstructive shock excluded → haemorrhagic shock

Mng

Tension pneumothorax suspected → needle in 2nd space, do NOT wait for X-ray
Resuscitation: don't delay for definitive dx; if doubt assume hypovolaemia, start fluids, assess response
Fluid challenge: 2 L lactated Ringer until blood transfused
Retained weapon removed in OR (may be tamponading a lacerated vessel)
Clear indication for immediate operative intervention (impalement + retained agent)

Special

Abdominal trauma — blunt

C/P

High-speed MVC driver; distended mildly tender abdomen; moderate hypovolaemia (~1500cc loss); blood at urethral meatus
Wide impact (transportation accidents, fall from height) vs limited impact (assaults)
Wide-impact regions: head/neck (CNS, spinal), maxillofacial; torso (thoracic, abdomen, pelvic); extremities
Passenger-space intrusion + steering-wheel deformity
Expect cervical spine injury in capsize / impact / ejection
Suspected pelvic fracture: PR may reveal floating prostate

Inves

ECG: arrhythmia due to myocardial contusion
CXR: flail chest; mediastinal shift; widening of mediastinum (thoracic aortic rupture → shock); massive haemothorax (→shock); solitary rib fracture (explains shallow respiration)
FAST if unstable (lower rib # → hepatic/splenic injury)
Contraindicated adjunct: per-urethral urinary catheter (blood at meatus); don't attempt classical catheterization in suspected pelvic #

Mng

Resuscitate w/ fluid challenge + prepare blood; suspected pelvic # → pelvic immobilization by hammock (helps venous pelvic bleeding)
Non-responders w/ pelvic #: check abdomen (FAST) + chest (CXR); check coagulopathy from excess transfusion; both -ve → embolize arterial pelvic bleeding
Non-responders without pelvic #: FAST +ve → exploration
Sustained responders: no peritonism → imaging for grading + observation (± external fixator if pelvic #); peritonism early/late → laparotomy
Decompensation after response: persistent loss → manage as non-responder; late (weeks) → delayed splenic rupture → laparotomy; haemobilia → embolization

Special

Widening of mediastinum = thoracic aortic rupture
Blood at urethral meatus = pelvic/urethral injury (contraindicates catheter)

Small bowel obstruction (SBO)

C/P

51F; intermittent gripping pain → continuous last 2h; central abdominal distension; vomited twice; passed flatus but no bowel motion; unwell, obese; BP 106/70, HR 108, temp 38; tender esp RIF; hyperactive bowel sounds
Dynamic obstruction (simple or complicated); obstruction symptoms = vomiting, distension, pain, constipation (maybe absolute)
Adhesive SBO = simple band obstruction of small bowel (op finding)
Most relevant past Hx: previous abdominal surgery
With visible groin/ventral swelling → hernia (e.g. femoral); without swelling → strangulated/obstructed or intussusception mass
Alarming signs: obesity; tachycardia; fever; localized tenderness; hyperaudible sounds

Inves

AXR: dilated small bowel (valvulae conniventes / plicae circulares crossing full lumen width); collapsed distal small bowel + large bowel; erect = multiple dilated loops + fluid levels; prolonged = thickened wall (space between loops)
CT: dilated fluid-filled loops + transition point + intraperitoneal free fluid
Water-soluble contrast follow-through: failure to reach caecum = obstruction needs surgery; contrast reaching colon by 4h = no surgery (adhesive SBO resolving)

Mng

Contrast to colon by 4h → conservative (resolving); failure to reach caecum → surgery

Special

Valvulae conniventes crossing full lumen width (AXR)

Large bowel obstruction (LBO)

C/P

65M diabetic hypertensive; 3 days constipation + distension; tachycardic, BP 130/100, temp 37; peripheral distension; mild diffuse tenderness; no guarding/percussion tenderness; no leucocytosis
Late vomiting; peripheral marked distension; intermittent less-frequent pain; early constipation
Adynamic (pseudo-obstruction, no pain, post-op narcotics) vs dynamic (with pain)
Dynamic LBO: intermittent non-gripping pain; bearing-down + spurious diarrhoea = faecal impaction (PR full of soft stools, palpable indentable faecula mass LIF)
Causes: sigmoid volvulus; inflammatory strictures (complicated diverticulitis, Crohn's colon); malignant strictures

Inves

(Cause-specific: see colonic stricture differentiation in CRITERIA)

Mng

Special

Sigmoid volvulus

C/P

Dynamic LBO cause; dilates + twists at mesentery root

Inves

Typical plain film; Omega sign on plain film
CT "swirl sign" of mesenteric vessels (loop twisted around internal hernia; untwisting restores flow)
Colonoscopy = temporary therapeutic role

Mng

Special

Omega sign (plain film); swirl sign of mesenteric vessels (CT)

Caecal volvulus

C/P

Marked caecal dilatation; closed-loop

Inves

CT: caecum twisting at mesentery ± transmural necrosis

Mng

Special

Intussusception

C/P

Mass as lead point; vascular compromise cause

Inves

CT "target sign" (spindle cell tumour / GIST as lead point)

Mng

Special

Target sign (CT)

Closed-loop obstruction

C/P

Competent ileocaecal valve + LBO → closed-loop, high perforation risk; caecal dilatation w/ loss of haustration
Obstruction near splenic flexure (carcinoma) → absent left colonic gas + caecal perforation (extraperitoneal gas)
Perforation site: at pathology site; on top of closed-loop (usually caecum if competent ileocaecal valve); stercoral ulcer in hugely dilated colon

Inves

Mng

Special

Inguinal hernia

C/P

Commonest abdominal hernia at all ages; indirect = most common type
65M farmer, bilateral groin swellings; mild discomfort lifting; disappear on rest; heavy smoker; urinary frequency + dysuria (prostatic → post-op urine retention risk)
Above + medial to pubic tubercle
Reducibility; expansile cough impulse; resonance/gurgling if intestine content

Inves

Internal ring test: finger 1cm above middle of inguinal ligament (midway pubic tubercle–ASIS), press + cough → identifies direct vs indirect

Mng

(Repair; not detailed separately in source)

Special

Femoral hernia

C/P

More common in multipara / old females
56F; severe left groin pain + nausea/vomiting 4h; prior small reducible painless left groin swelling 6mo → suspected complicated (strangulated/obstructed) femoral hernia
Below + lateral to pubic tubercle
Groin swelling below + lateral to pubic tubercle, irreducible, red, no cough impulse (from SBO case)

Inves

Routine cases: none needed; if uncertain → US or CT
Emergency: bowel obstruction usual, plain radiograph shows SBO; all unexplained SBO → examine for femoral hernia; CT can identify obstructing femoral hernia missed clinically

Mng

Special

Pubic tubercle = landmark: femoral below + lateral vs inguinal above + medial

Incisional / ventral hernia (VIH)

C/P

74M smoker, diabetic, obese, HTN; intermittent periumbilical pain 3mo; BMI 41; midline scar + 5×6cm VIH, partially reducible, tender to deep palpation; PSH perforated diverticulitis → colectomy + colostomy reversed w/ wound infection
Extrusion of peritoneum + abdominal contents through weak scar / accidental wound = partial wound dehiscence with intact skin
Distinguish from rectus diastasis; distinguish reducible/chronically incarcerated from acutely incarcerated (urgent surgery — obstruction, acutely tender bulge, erythema if strangulated)
Complications: intestinal obstruction (often intermittent); incarceration; strangulation; skin excoriation; persistent pain
Predisposing — preop: age, immunocompromise (renal failure, diabetes, steroids), obesity, malignancy, abdominal distension; operative: poor closure (small bites/wrong suture), drains through wounds; postop: wound infection, haematoma, early mobilization, atelectasis + chest infection

Inves

LFTs, amylase, WBC (normal); plain abdominal films; RUQ US (normal); CT (no obstruction, demonstrates hernia defect); ECG + echocardiography

Mng

Surgical repair, laparoscopic or open with mesh (if gap >2cm)
Repair usually for pain/discomfort + loss of domain > for incarceration/strangulation
Laparoscopic: safe, fewer wound complications, shorter stay, equivalent/lower recurrence

Special

Foodborne & waterborne infections

C/P

Illness from food/water contaminated w/ bacteria/toxins, parasites, viruses, or chemicals; outbreak = similar (GI) illness in ≥2 people + food-source evidence
Mode usually viral; children = Rotavirus; adults = Norovirus + Campylobacter
Present: nausea, vomiting, fever, abdominal pain, diarrhoea
Non-inflammatory: enterotoxins impair small-intestine secretion without invasion → large-volume watery stool, no blood/pus/severe pain, dehydration
Inflammatory: cytotoxins invade + destroy mucosa (colon/distal small bowel) → bloody mucoid diarrhoea + leukocytes, febrile/toxic, dehydration less likely (small volumes)
Vomiting predominant → Staph aureus, B. cereus, Norovirus
Fever = invasive disease; blood/mucus stool = mucosal invasion
Reactive arthritis: Salmonella, Shigella, Campylobacter, Yersinia
Rice-water stool → cholera; bloating → giardiasis; Yersinia may mimic appendicitis
Proctitis (shigellosis): frequent painful BMs w/ blood/pus/mucus, tenesmus, rectal discomfort
Acute <2 weeks; persistent 2–4 weeks; chronic >4 weeks
Non-GI: botulism (paralysis); ciguatera/scombroid (headache + tingling); amnesic shellfish (amnesia); hepatitis A/E; Listeria (meningitis / spontaneous abortion)

Inves

Gram + Loeffler methylene blue stain of stool for WBCs (invasive vs non-invasive); faecal leukocytes / +ve stool lactoferrin = inflammatory; sheets of leukocytes = colitis
Microscopy for ova + parasites; bacterial culture (mandatory if WBC/blood +ve, fever, or symptoms >3–4 days); blood culture if febrile; CBC + differential, electrolytes, BUN/creatinine; C. difficile assay if recent antibiotics
Flat + upright abdominal radiographs if bloating, severe pain, obstruction, or suspected perforation
Sigmoidoscopy/colonoscopy + biopsy, EGD + duodenal aspirate (nondiagnostic stool, esp immunocompromised); sigmoidoscopy in bloody diarrhoea
Rectal exam always: visualize stool, occult blood, palpate mucosa

Mng

Fluids: oral rehydration solution (water, salts, sugar) mild/moderate; IV fluids severe
Antibiotics generally NOT needed; recommended only for fever + bloody diarrhoea
STEC: antibiotics may increase HUS risk (avoid empiric antibiotics)
Life-threatening (C. botulinum, L. monocytogenes, V. vulnificus) → speedy therapy lifesaving
Prevention: handwashing, clean water, human-waste disposal, fly control; Rotavirus vaccine in children; continued breastfeeding in babies

Special

Rose spots on upper abdomen + hepatosplenomegaly = S. typhi
Erythema nodosum + exudative pharyngitis = Yersinia
Cellulitis + otitis media = V. vulnificus / V. alginolyticus

Rheumatology & Spine

24 entries

Rheumatoid arthritis

C/P

38F, bilateral hand swelling 3wk — wrists + MCPs + PIPs tender; malaise/fatigue; pale lips
45M, bilateral hand + wrist pain/swelling worse AM ~1hr, improves with movement
symmetrical small-joint (wrists/MCPs/PIPs); morning stiffness improving with movement

Inves

CBC = hypochromic anaemia + thrombocytosis; normal liver/kidney/urine
anti-CCP↑ + RF↑
RF = autoantibody vs Fc portion of IgG
anti-CCP = more specific than RF (early + established RA); predicts progression in undifferentiated arthritis; marker of erosive disease; may appear years before clinical RA
CXR + echo to exclude chest/cardiac; fundus exam before antimalarials
X-ray wrist — carpal ankylosis at 8yr

Mng

treat early (within 12wk, "window of opportunity") — ~30% less pain at 36mo if <12wk
antimalarials (hydroxychloroquine) — fundus exam before starting
methotrexate = most effective DMARD (mono + combo); once weekly + folic acid 1mg/day
other conventional: leflunomide, sulfasalazine
step-wise: conventional DMARDs → if fail biologic/tsDMARD; low-dose steroid/NSAID bridging only
biologics: anti-TNF, anti-IL-1 (anakinra), anti-IL-6 (tocilizumab), abatacept, rituximab (seropositive); JAK inhibitors (refractory)

Special

anti-CCP (specific; erosive-disease marker; precedes clinical RA)

Ankylosing spondylitis

C/P

24M, gradual backache + morning stiffness improved by exercise; ↓spinal mobility; occiput doesn't touch wall

Inves

MRI SIJ with STIR = sacroiliitis

Mng

sulfasalazine (seronegative SpA); anti-TNF (AS); JAK inhibitors (axial SpA); methotrexate (peripheral arthritis)

Special

MRI SIJ STIR — sacroiliitis

Psoriatic arthritis

C/P

45M, 20yr hand pain/deformity, 1hr AM stiffness improving w/ movement; 2 swollen toes (dactylitis); DIP joints painful/deformed bilaterally; Achilles enthesitis; father had psoriasis

Inves

(Ix asked, not printed)

Mng

sulfasalazine, leflunomide, methotrexate, anti-TNF, abatacept (active PsA), JAK inhibitors, cyclosporine

Special

dactylitis + bilateral DIP involvement + enthesitis pattern

Enteropathic (IBD-associated) arthropathy

C/P

35F, 3mo alternating buttock pain, fatigue, oral ulcers, recurrent abdo pain + bloody diarrhoea, erythema nodosum (tender red shin bumps), now R knee + L ankle swelling

Inves

(Ix asked, not printed)

Mng

sulfasalazine (seronegative SpA — enteropathic); methotrexate (peripheral arthritis)

Special

erythema nodosum + IBD (bloody diarrhoea) association

Reactive arthritis

C/P

22M returned from Thailand, swollen R knee + dysuria; key Q = recent sexual history
triggers: GI (campylobacter/salmonella/shigella/yersinia); GU (chlamydia)

Inves

Mng

sulfasalazine (seronegative SpA — reactive)

Special

post-GI or post-GU (chlamydia) trigger

Systemic sclerosis (diffuse + limited/CREST + scleroderma renal crisis)

C/P

40F: Raynaud's (cold colour change pallor→cyanosis→rubor), hand puffiness + skin tightness, dysphagia, exertional dyspnoea + dry cough, constipation
exam: skin tightness proximal to elbows/knees, finger contractures, hard swelling extensor elbows, fine basal inspiratory creps
55F: dysphagia + finger discoloration on cold (Raynaud's) + facial change
limited/CREST = Calcinosis, Raynaud's, Oesophageal dysfunction, Sclerodactyly, Telangiectasia
diffuse = widespread skin + internal-organ disease
complication → interstitial pulmonary fibrosis
scleroderma renal crisis (1yr later) = malignant HTN 200/120 + ↑creatinine 2.5

Inves

ANA +ve 90% (nucleolar pattern); anti-dsDNA normal
anti-Scl-70 +ve → diffuse SSc (40% progressive; widespread skin + internal organ; oesophageal dysmotility; pulmonary fibrosis/HTN)
anti-centromere → limited SSc/CREST (80-90% CREST)
nail-fold capillaroscopy

Mng

SSc-ILD: mycophenolate mofetil, cyclophosphamide, rituximab; mild → azathioprine

Special

anti-Scl-70 (diffuse); anti-centromere (limited/CREST); nucleolar ANA

Dermatomyositis (anti-synthetase syndrome)

C/P

33F: nocturnal fever 39°C + 4kg wt loss, Raynaud's, proximal myalgia + polyarthralgia, can't raise arms to comb hair, difficulty climbing stairs, dysphagia, violaceous eyelid rash, dry cracked hands
exam: proximal weakness grade III hips/shoulders (distal gr V), heliotrope rash, Gottron's papules, mechanic's hands

Inves

↑CPK, ALT, AST, aldolase
EMG = ↑spontaneous activity + polyphasic small-amplitude short-duration MUAPs
ANA +ve; anti-Jo-1 (anti-histidyl-tRNA-synthetase) +ve

Mng

steroids (high-dose start, then taper) + immunosuppressives
myositis DMARDs: methotrexate / azathioprine; cyclosporine; JAK inhibitors

Special

anti-Jo-1 (anti-histidyl-tRNA-synthetase); heliotrope rash; Gottron's papules; mechanic's hands

Systemic lupus erythematosus (SLE)

C/P

28F: hand/wrist pain, hair loss, oral ulcers, puffy eyelid, swollen non-tender legs (± nephrotic/renal involvement)

Inves

ANA very sensitive for SLE (>95% +ve), specificity low (57%), PPV 11%; negative helps rule out; does NOT reflect activity / not for monitoring
ANA patterns: homogenous, speckled, cytoplasmic, centromere, nucleolar; low titre <1:160 minimal significance
anti-dsDNA — less sensitive but more specific than ANA; rare in normals; 50-80% untreated SLE; correlates with renal disease + activity (with complement); monitors lupus nephritis
ENA: anti-Smith, anti-U1 RNP, anti-Ro (SS-A), anti-La (SS-B)
APS antibodies: lupus anticoagulant, anti-cardiolipin IgG/IgM, anti-β2 glycoprotein IgG/IgM
CRP preferred over ESR EXCEPT in SLE + cancer; don't serially repeat labs except cANCA + dsDNA

Mng

hydroxychloroquine + sun protection for ALL (prevents flares)
organ-specific: arthritis MTX/leflunomide; myositis MTX/AZA; cutaneous MMF/MTX; severe LN or neuropsychiatric cyclophosphamide/MMF; biologics if conventional fails
lupus nephritis: Induction = cyclophosphamide OR MMF; Maintenance = azathioprine OR MMF; MMF preferred if ovarian reserve to preserve (>30yr, single, no offspring)
rituximab (SLE); cyclosporine (refractory LN, membranous)
NOT anti-TNF (can cause lupus)
drug-induced lupus = mild + anti-histone (anti-TNF, isoniazid, procainamide, minocycline); anti-TNF induces ANA + anti-dsDNA but complement not depleted, ESR + CRP rise together, antibodies disappear when drug stopped

Special

anti-dsDNA (specific; monitors lupus nephritis); anti-Smith (ENA)

Sjögren's syndrome

C/P

autoimmune salivary + lacrimal → dry eyes / dry mouth

Inves

high IgG → persistently very high ESR but normal CRP
ANA + anti-Ro + anti-La; RF often +ve but anti-CCP -ve; no erosive arthritis

Mng

rituximab; hydroxychloroquine; corticosteroids (collagen disorder)

Special

anti-Ro + anti-La; very high ESR / normal CRP dissociation

Complex regional pain syndrome (CRPS)

C/P

continuing regional pain after inciting event, distal limbs, disproportionate; spontaneous + evoked pain, autonomic/motor/trophic changes
Type I = no definable nerve lesion; Type II (causalgia) = definable nerve lesion
triggers: fractures 45%, sprain 18%, elective surgery 12%, spontaneous <10%
epi: 30-50yr, F:M 3:1, upper:lower 2:1, 75% resolve within 1yr
Stage 1 (1-3mo): burning/throbbing pain (not single-nerve), warm+red, ↑sweating, localised oedema
Stage 2 (3-6mo): soft-tissue oedema, skin/soft-tissue thickening, muscle wasting + osteoporosis, cold cyanotic sweaty
Stage 3: contractures of digits, severe osteoporosis, waxy trophic skin, brittle ridged nails, allodynia + hyperalgesia

Inves

clinical (disproportionate regional pain); no test of sufficient sensitivity/specificity; exclude other causes

Mng

physiotherapy (single most important) + TENS, OT, psychology
drugs: paracetamol/codeine/tramadol/NSAIDs; morphine (severe); amitriptyline/duloxetine; bisphosphonates; capsaicin; lidocaine patches; sympathetic nerve blocks; steroids (early)

Special

3-stage progression; Type I vs Type II (causalgia)

Fibromyalgia

C/P

chronic widespread muscular pain; NOT inflammatory/degenerative, no permanent damage
triggers: viral infection, physical/mental trauma, stress
Sx: chronic fatigue, diffuse pain, restless legs, TMJ disorder, headache, IBS, ± hypothyroidism; sleep disturbance (loss of deep sleep, vicious cycle)

Inves

Mng

multidisciplinary; non-pharm = aerobic/aquatic exercise, resistance training, CBT, relaxation, acupuncture
TCAs (low-dose amitriptyline, dosulepin — 2-3h before bed); SSRIs (fluoxetine, paroxetine); SNRI (duloxetine); pregabalin/gabapentin (6wk trial)

Special

Benign joint hypermobility syndrome (BJHS)

C/P

movement beyond normal range; common cause of generalised pain in young; more common in girls, ↓ with age; may co-exist with fibromyalgia; pain cause unknown (instability/microtrauma/central sensitisation); ↓muscle strength + balance

Inves

Mng

reassurance (most important — benign, lessens with age), supportive footwear, muscle reconditioning, evening acetaminophen/NSAID

Special

Septic arthritis

C/P

medical emergency, most serious cause of acute monoarthritis; mortality 10%, long-term sequelae 30%
painful swollen red joint; 85% monoarthritis; knee most common; fever only in 50%; subacute over 1-2wk
55M diabetic/HTN/IHD, 2d red swollen tender L knee → first to exclude in acute monoarthritis
RFs: immunocompromised, underlying joint disease, prosthetic joints, IA steroid injection, extremes of age, low socioeconomic status, cutaneous ulcers, IVDU

Inves

aspirate native joint (colour/clarity/pus, Gram stain, WCC, C&S, crystals) BEFORE antibiotics = single most important / first Ix = joint aspiration
blood cultures; markers may be absent; X-ray limited value acutely; refer prosthetic joints to ortho

Mng

sepsis management; IV antibiotics AFTER aspiration (modify to Gram/culture; typically 2wk IV then 4wk oral); arthroscopic washout or daily aspiration; remove prosthesis; analgesia

Special

organisms: Staph aureus (~50%, most common), MRSA, Staph epidermidis, Strep spp, Gram-negative spp

Acute gout

C/P

rapid onset, severe pain/heat/swelling/erythema, exquisite tenderness, skin desquamation
1st attack 1st MTPJ in 50-70% (1st MTPJ acute monoarthritis likely gout — podagra)

Inves

crystal ID = gold standard (not needed w/ classic podagra)
serum uric acid = acute-phase reactant (normal during attack 25-49%; hyperuricaemia ≠ gout; useful for monitoring)
WCC/ESR/CRP usually elevated
MSU crystals: needle-shaped, strong birefringence, yellow parallel to axis

Mng

acute: NSAIDs, colchicine, corticosteroids
prophylaxis: allopurinol, febuxostat, probenecid, benzbromarone — must cover with NSAID/colchicine/steroid during initiation/escalation
do NOT combine azathioprine with gout meds (xanthine-oxidase inhibition → fatal)

Special

MSU crystals — needle-shaped, strong birefringence, yellow parallel to axis

Pseudogout

C/P

features similar to gout, sites vary; commonest cause of cartilage calcification

Inves

CPPD crystals: rhomboid, weak birefringence, blue parallel to axis

Mng

symptomatic relief only, no prophylaxis

Special

CPPD crystals — rhomboid, weak birefringence, blue parallel to axis; cartilage calcification

Haemophilic arthropathy (haemophilias)

C/P

1/10,000 males; haemarthrosis
A = factor VIII deficiency; B = factor IX deficiency; vWD = factor V deficiency (as printed on slide — slide error)
acquired minor joint bleeding from heparin/warfarin + minor trauma

Inves

Mng

replace deficient factor, rest joint in extension, ice, analgesics, NSAIDs; severe → arthroscopic synovectomy

Special

Pigmented villonodular synovitis

C/P

locally invasive neoplasm; knees; bloody effusion

Inves

X-ray / radionuclide / MRI

Mng

Special

bloody effusion

Palindromic rheumatism

C/P

recurring acute arthritis with symptom-free months

Inves

Mng

hydroxychloroquine

Special

Osteoarthritis

C/P

degenerative joint disease (DDx of pain — degenerative)

Inves

Mng

NSAIDs; intra-articular corticosteroid injection

Special

Giant cell arteritis (GCA)

C/P

large-vessel/temporal arteritis; risk of blindness

Inves

temporal artery duplex — turbulent flow, narrowed lumen, hypoechoic halo

Mng

pulse corticosteroids 250mg ×1-few days (life-threatening emergency, avoid blindness), hospitalise

Special

hypoechoic halo on temporal artery duplex

Prolapsed lumbar disc

C/P

23M accountant, acute mechanical LBP 3d; 2wk later burning pain shooting down R leg + paraesthesia (radiculopathy/sciatica)

Inves

lumbar X-ray (initial); lumbar MRI = disc herniation

Mng

lumbar decompression (laminectomy + discectomy + fusion/interbody grafts + pedicle screws)

Special

Spondylolysis (± spondylolisthesis)

C/P

15F gymnast, LBP

Inves

oblique lumbar X-ray "Scottie dog" with collar/broken-neck sign

Mng

Special

Scottie dog sign (pars interarticularis defect) — collar/broken-neck on oblique X-ray

Cervical spondylotic myelopathy

C/P

45M, progressive bilateral upper-limb weakness, long-standing neck pain refractory to medical Rx + physio

Inves

cervical MRI = cord compression

Mng

cervical decompression (anterior/posterior)

Special

Cauda equina syndrome

C/P

50F, bilateral lower-limb weakness + urine & stool incontinence (emergency)

Inves

MRI (lumbar)

Mng

urgent surgical decompression

Special

GI & Hepatobiliary Surgery

19 entries

Biliary colic vs Acute cholecystitis

Feature	Biliary colic	Cholecystitis
Pain site	Epigastric	RUQ
Duration	4h (<6h)	24h (>6h)
Nausea/vomiting	Nausea, no vomiting	Nausea + vomiting
Fever	No fever	Feverish 38
Tenderness	No tenderness	+ve Murphy's sign
WBC	Normal	Leucocytosis

Acute vs Chronic calcular cholecystitis

Acute: more intense/prolonged pain, radiates to back/interscapular; anorexia/nausea/vomiting; maybe fever; +ve Murphy; tenderness; maybe mass
Chronic: less intense pain w/ fatty meals; no physical findings; mild tenderness; no lab changes

Biliary disease spectrum (recap definitions)

Cholelithiasis = GB stones (symptomatic → biliary colic)
Cholecystitis = GB inflammation from stone impaction in neck / cystic duct obstruction
Choledocholithiasis = stones in CBD
Cholangitis = infection of biliary tree from obstruction (secondary to choledocholithiasis)
Biliary colic: visceral + referred pain w/ fatty meals; vomiting uncommon; no fever; no jaundice; no abdominal signs; <6h
Cholecystitis: pain w/ fatty meals; vomiting more frequent; fever; no jaundice; RUQ tenderness + parietal pain + +ve Murphy; >6h
Complicated choledocholithiasis (jaundice/cholangitis/pancreatitis): RUQ pain; fever + rigors (cholangitis); obstructive jaundice (mild in cholangitis); tender liver

Shock class (trauma)

Hypotension in supine position = blood loss 1500–2000 ml (classes I–IV)

Fluid-challenge response (moderate/severe shock)

2 L lactated Ringer until blood transfused
Definite improvement → continue
No improvement + low CVP = continued losses → exploration
No improvement + rising CVP = "the killers": tension pneumothorax, cardiac tamponade, cardiac failure

Retroperitoneum zones

Zone 1 central; zone 2 lateral; zone 3 pelvic
Solitary-injury order: great vessels zone 1 (loss of retroperitoneal tamponade); right renal zone 2 (vascular pedicle); liver (portal triad / left-lobe transfixion / hepatic vein); mesenteric (middle colic vessel)

Blunt abdominal trauma types

Wide impact: transportation accidents, fall from height — pedestrian (adult/child), passenger high-speed vehicle, insecure vehicles (tuk-tuk), motorcycle driver
Limited impact: assaults

Penetrating abdominal injury algorithm

Impalement + retained agent → resuscitate + explore anyway
Low velocity (knife) → resuscitate + look for peritoneal irritation signs
Intermediate velocity (shotgun) → resuscitate + CT + look for peritoneal irritation
High velocity (bullet) → resuscitate + explore anyway
Low-velocity + evisceration → resuscitate + explore
Anterior wall, no peritonism → local wound exploration → if penetrating → diagnostic laparoscopy (remember diaphragm)
Posterior wall penetration, no peritonism → wound exploration unreliable → triple-contrast CT
Intermediate velocity + peritonism → resuscitate + explore; no shock/peritonism → CT; solid-organ injury → observe for delayed intestinal injury

Blunt trauma management algorithm

Resuscitate w/ fluid challenge + prepare blood; suspected pelvic # → pelvic immobilization by hammock
Non-responders w/ pelvic #: FAST + CXR; check coagulopathy; both -ve → embolize arterial pelvic bleeding
Non-responders without pelvic #: FAST +ve → exploration
Sustained responders: no peritonism → imaging for grading + observation (± external fixator if pelvic #); peritonism early/late → laparotomy
Decompensation: persistent loss → manage as non-responder; late (weeks) → delayed splenic rupture → laparotomy; haemobilia → embolization

Levels of obstruction

Level	Vomiting	Distension	Pain	Constipation
High small bowel	Profuse	None	Intermittent gripping, frequent	Late
Low small bowel	Present	Central	Intermittent gripping, frequent	Earlier than high
Large bowel	Late	Peripheral, marked	Intermittent, less frequent	Early

Categories of obstruction

Adynamic: almost no pain
Neuromuscular incoordination: Hirschsprung — no relaxation + proximal dilatation
Dynamic: simple or complicated

Complications of obstruction

Vascular compromise: pain becomes continuous; fever; localized tenderness; leucocytosis (causes = strangulation of hernia contents, volvulus, intussusception)
Perforation: pain continuous; fever; tenderness maybe generalized; leucocytosis; air under diaphragm

Colonic stricture differentiation (dynamic LBO)

Cause	Features	Ix
Complicated diverticulitis	Repeated LIF pain + fever → progressive constipation + ribbon stools; maybe LIF phlegmon	CT (diverticulae); sigmoidoscopy + biopsy
Crohn's colonic stricture	Diarrhoea + limited PR bleeding → progressive constipation + ribbon stools; skip lesions in rectum, recurrent anal fistula + skin tags	CT (hard to differentiate from malignancy); sigmoidoscopy + biopsy
Malignancy	Progressive constipation + ribbon stools; maybe liver masses	CT diagnostic in some; sigmoidoscopy + biopsy

Commonest abdominal hernias

Inguinal (commonest at all ages); umbilical/paraumbilical; femoral (more common in multipara females); incisional (over previous scars); obturator
Indirect inguinal = most common type; femoral more common in old females

Hernia classification

Evident (external): groin/ventral, incisional outside rectus sheath, Spigelian
Non-evident (needs CT): internal hernia (recess, mesenteric defect, complicated vitellointestinal duct), obturator/sciatic, hiatal/diaphragmatic

DDx of groin swelling

Hernial orifices (inguinal, femoral); testicular apparatus (hydrocele of cord, ectopic testis); vein (saphena varix); artery (femoral aneurysm); lymph nodes (infection/neoplasm/lymphoma); psoas sheath (psoas abscess); skin/subcutaneous (lipoma)

Foodborne/waterborne organism → presentation → food → treatment

Organism	Presentation	Food/source	Notes / Rx
Bacillus cereus	Diarrhoea + cramping (or emetic: vomiting 1–6h)	Preformed toxin, starchy foods — rice, reheated fried rice/noodles	Self-limited 24–48h
Staphylococcus aureus	Vomiting + abdominal pain, diarrhoea not typical, rapid onset	Preformed heat-stable toxin; foods left at room temp — dairy, produce, meat, eggs, salads, mayonnaise	Clinical dx; self-limited 24–48h
Cl. perfringens	Watery diarrhoea	Spores germinate in meats/poultry/gravy; toxin in host GI	—
Salmonella	Watery diarrhoea, cramps, fever, vomiting	Undercooked/unrefrigerated food, esp poultry + eggs; nontyphoidal incubation 1–3 days	Antibiotics only for severe or immunocompromised; stool cultures
S. typhi/paratyphi (typhoidal)	Systemic illness, little diarrhoea; rose spots	Human colonizer	—
Vibrio vulnificus	Vomiting, diarrhoea, abdominal pain; skin infection → bacteraemia	Raw/undercooked shellfish	Deadly in immunocompromised / liver disease; incubation 1–7 days; special culture media
Vibrio (parahaemolyticus)	Watery diarrhoea	Raw shellfish prior 48h	Specific lab request/culture
E. coli (EHEC/STEC O157:H7)	Watery → bloody diarrhoea, no fever (commonest bloody diarrhoea w/o fever)	Undercooked beef / bovine-feces food, unpasteurized juice, raw fruit/veg	Causes HUS; Shiga-toxin assay (better than sorbitol MacConkey); antibiotics ↑ HUS risk; incubation ~1 day–1 week
ETEC	Watery (traveller's diarrhoea)	—	Enterotoxin-mediated
Shigella	Bloody diarrhoea + fever + bacteraemia; proctitis	Contaminated food/water, travel, salads/raw veg/dairy/poultry	Routinely isolated
Campylobacter	Abdominal pain + bloody diarrhoea	Raw/undercooked meats	Highest in children + young adults
Vibrio cholera	Rice-water stool	—	Enterotoxin made in intestine
Yersinia enterocolitica	May mimic appendicitis; erythema nodosum + pharyngitis	Undercooked pork, unpasteurized milk, contaminated water	—
Cryptosporidium parvum	Persistent chronic diarrhoea in immunocompromised	Cattle-endemic; water/produce/unpasteurized milk/person-to-person	Incubation ~1 week (up to 28d); acid-fast stain / IF / EIA
Cyclospora cayetanensis	Watery diarrhoea	Faecally contaminated water, fresh basil	Acid-fast microscopy; treat w/ trimethoprim-sulfamethoxazole
Giardia lamblia	Bloating	Faecal-oral	—
Entamoeba histolytica	Amoebic dysentery	—	—
Tapeworms (Taenia saginata/solium, Diphyllobothrium latum)	—	Undercooked beef/pork/fish	—
Botulism (Cl. botulinum)	Visual disturbance + descending paralysis	Home-canned foods, fermented fish, herb-infused oils, warm-held foods	Life-threatening; test stool + serum for toxin
Ciguatera toxin	N/V/D/pain 2–6h → paraesthesia, weakness, hot/cold reversal; CVS 2–5 days	Large reef fish (grouper, red snapper, amberjack, barracuda)	Heat-stable ciguatoxin from dinoflagellates
Scombroid	Minutes–hours: flushing, burning, urticaria, dizziness, paraesthesia	Blue fish, tuna, mackerel, marlin (or cheese); biogenic amines (histamine)	—
Listeria monocytogenes	Meningitis / spontaneous abortion; mortality ~20%	Deli meat, raw hot dogs, unpasteurized soft cheese	Immunocompromised/elderly/pregnant; incubation up to 6 weeks; blood/CSF culture (stool unhelpful)
Hepatitis A virus	Acute hepatitis up to acute liver failure, no chronicity	Raw shellfish, produce, infected food handler	Incubation 15–50 days; serology
Brucellosis (B. melitensis/abortus/suis/canis)	Fever + weight loss, malaise, night sweats, arthralgias	Unpasteurized dairy / undercooked meat	—
Rotavirus	Localized gastroenteritis (children)	Faecal-oral	Short incubation; immunity IgA; vaccine
Norovirus	Acute gastroenteritis; cruise-ship/institutional outbreaks	—	48–72h self-limited; no long-lasting immunity

Major foodborne mechanisms

Mechanism	Organisms	Onset / stool
Enterotoxin ingested (preformed)	Staph aureus, B. cereus	Quick 1–6h; vomiting predominant
Enterotoxin made in intestine	Cl. perfringens, ETEC/STEC, Vibrio cholera	Delayed >1 day; watery/bloody diarrhoea
Bacterial epithelial invasion	Campylobacter jejuni, nontyphoidal Salmonella, Listeria	Variable onset; watery/bloody diarrhoea, fever, systemic (Listeria)

Food clues → organism

Undercooked meat/poultry → Salmonella, Campylobacter, STEC, C. perfringens
Raw seafood → Norwalk virus, Vibrio, hep A
Home-canned → C. botulinum
Unpasteurized soft cheese → Listeria, Salmonella, Campylobacter, STEC, Yersinia
Deli meats → Listeria
Unpasteurized milk/juice → Campylobacter, Salmonella, STEC, Yersinia
Raw eggs → Salmonella

Rheumatology & Spine

13 entries

Polarised-light crystal microscopy — MSU vs CPPD

	Crystal	Shape	Birefringence	Colour parallel to axis
Gout	MSU	needle	strong	yellow
Pseudogout	CPPD	rhomboid	weak	blue

Corticosteroid dose bands

(prednisone equivalent/day)

low <7.5mg (maintenance)
medium 7.5-30
high 30-100
very high >100
pulse 250mg ×1-few days (life-threatening emergency e.g. avoid blindness in GCA; hospitalise)
max normally 1mg/kg
MOA: transactivation → side effects; transrepression → anti-inflammatory

NSAID classes

(slide: "only know the classes")

acetic acids
COX-2 inhibitors
fenamates
oxicam derivatives
propionic acids
salicylates

Autoantibody → disease associations

Antibody	Association / notes
RF	vs Fc portion of IgG; RA; Sjögren's often +ve
Anti-CCP	RA — more specific than RF (early + established); predicts progression; erosive marker; may precede clinical RA
ANA	SLE — very sensitive (>95%), low specificity (57%), PPV 11%; negative rules out; not for monitoring; patterns homogenous/speckled/cytoplasmic/centromere/nucleolar; low titre <1:160 minimal
Anti-dsDNA	SLE — more specific, less sensitive than ANA; 50-80% untreated; correlates renal + activity; monitors lupus nephritis
ENA (4 main)	anti-Smith, anti-U1 RNP, anti-Ro (SS-A), anti-La (SS-B); diagnosis not monitoring
Anti-Ro + anti-La	Sjögren's (with ANA; anti-CCP -ve)
Anti-centromere	limited SSc / CREST (80-90%)
Anti-Scl-70	diffuse SSc (40% progressive)
Anti-Jo-1 (anti-histidyl-tRNA-synthetase)	dermatomyositis / anti-synthetase
Anti-histone	drug-induced lupus (anti-TNF, isoniazid, procainamide, minocycline)
APS	lupus anticoagulant, anti-cardiolipin IgG/IgM, anti-β2 glycoprotein IgG/IgM
cANCA (+ dsDNA)	only antibodies worth serial repeat

Systemic sclerosis antibody table

ANA +ve 90%; anti-dsDNA normal
Anti-centromere → limited SSc/CREST (80-90% CREST — Calcinosis, Raynaud's, Oesophageal dysfunction, Sclerodactyly, Telangiectasia)
Anti-Scl-70 → diffuse SSc (40% progressive; widespread skin + internal organ; oesophageal dysmotility; pulmonary fibrosis/HTN)

Acute swollen joint — joint-count & tempo definitions

mono = 1 joint; oligo = 2-4; poly = ≥5
acute <14d; subacute 2-6wk; chronic >6wk

Sensitivity vs specificity

Sensitivity = proportion WITH disease testing +ve → high sensitivity, negative rules out (screening, low false -ve)
Specificity = proportion WITHOUT disease testing -ve → high specificity, positive rules in (confirmation, low false +ve)

CRP vs ESR

CRP = acute-phase protein, made in hepatocytes by IL-6/IL-1/INF/TNF; reflects disease activity (Crohn's, RA, vasculitis, bacterial infection); NOT affected by pregnancy/age
ESR = reflects fibrinogen/globulins + immunoglobulins; affected by age, sex, anaemia, pregnancy

DMARDs safe in pregnancy/lactation

corticosteroids, hydroxychloroquine, azathioprine, sulfasalazine, cyclosporine

Blood-donation deferral criteria

(Egypt: volunteer, unpaid donors only; every donation ABO + Rh-D typed; mandatory tests HBsAg, anti-HIV 1&2, anti-HCV, syphilis antibody; NAT = nucleic acid testing) (BTC = uses NAT)

Age: usually 18-60
Occupation: HCW needlestick/splash exposure → defer 6-12mo (per incubation); hazardous jobs (emergency services, heights) → no work ≥24h post-donation (delayed vasovagal)
Donation interval: min 12wk males (16wk females per WHO)
Surgery: major 6mo, minor 3mo; dental 6mo (3mo if NAT)
Tattoo/acupuncture/piercing/needle prick: 6mo (3mo if NAT)
Received blood <12mo: defer 6mo (recipients + sexual contacts); 3mo if NAT
Viral hepatitis: Hep A/E/unknown → 12mo post-recovery (6mo contacts); HBV/HCV → permanent (contacts 6mo, 3mo if NAT); AIDS/HIV → patient permanent, contact 6mo
Pregnancy: defer until delivery; normal labour/CS accepted 6mo post-delivery unless breastfeeding; breastfeeding → 1yr post-delivery
Vaccination: killed/toxoid accepted (cholera, typhoid, rabies-no-bite, pertussis, injected polio, influenza, tetanus, HAV); live attenuated → defer 4wk (BCG, yellow fever, MMR, oral polio, typhoid, varicella, cholera); HBV vaccine 1mo; HBV Ig / post-bite rabies / anti-D Rhogam / non-specific IgG → 1yr
Drugs: injecting drug use → permanent; aspirin 7d; other NSAIDs 48h; antibiotics 7d post-completion; warfarin/heparin accepted 1wk after last dose; human pituitary-derived GH → permanent; retinoids — etretinate permanent, acitretin 12mo-3yr, isotretinoin 4wk
Measles/chickenpox contact: measles/mumps accepted 3wk post-recovery (patient + contact); herpes viruses → defer until recovery (HHV-8 / active → permanent), contacts 1mo
HTN: accepted if stable/controlled on meds; defer if recently started/changed until 28d after BP stable; permanent if hypertensive heart/renal disease
DM: accepted if diet/oral controlled; permanent if on insulin
TB: defer patient + contact 2yr after confirmed cure
CVD: permanent for CHD — symptomatic IHD, symptomatic PVD/arterial thrombosis, MI, severe arrhythmia, RF with chronic heart disease, valvular stenosis/regurgitation, valve replacement, HCM, uncorrected congenital HD
Asthma: mild (<7 attacks/wk) + moderate (7-14) accepted; severe (>14) or on steroids → permanent; acute exacerbation defer 14d post-recovery
Bilharziasis: active → defer 1mo post-recovery; past treated by tablets → accepted; past treated by injections → permanent
Thyroid: euthyroid accepted (asymptomatic goitre, past viral thyroiditis); defer if under investigation / hypothyroid / malignant thyroid tumour history; Graves' thyrotoxicosis → permanent
Malaria: travel to endemic no fever → 12mo from return; travel + febrile → permanent; lived in endemic first 5yr of life or ≥6mo continuous → permanent; ever diagnosed → permanent
Sexual/STI: high-risk behaviour → deferral; syphilis ever → permanent; gonorrhoea → 12mo post-treatment + assess high-risk
Constitutional: fever/diarrhoea/weight loss → defer permanently until underlying diagnosis

Blood-donation physical-exam thresholds

weight ≥45kg to donate 350ml (≤13% blood volume)
BP systolic 100-140 / diastolic 60-90
febrile if oral temp >37.5°C
pulse 60-100 regular
Hb ≥12 g/dl females, ≥13 g/dl males

Blood-bag testing (WHO minimum)

HIV-1&2, HBsAg, HCV, syphilis (treponemal Ab); only bags negative for all released; positives → donor notified

Acute haemolytic transfusion reaction — protocol

(crush-injury case, 20min in → chest pain, tachycardia, rigors)

immediate: stop transfusion (keep cannula in), assess/manage vitals, contact transfusion service (reaction form)
send STAT: blood bag + set + IV fluids, post-transfusion EDTA + chemistry sample, post-transfusion urine
workup: clerical check; visual plasma for haemolysis; check bag; compare types pre/post; DAT on post-reaction sample (pre -ve + post +ve → haemolytic reaction possible); urine dipstick for Hb; compare Hb/haptoglobin/bilirubin (repeat 4-6h)
SHOT = Serious Hazards of Transfusion (UK) — anonymised adverse-event surveillance, annual safety recommendations
alloimmunisation = immune response to foreign antigens after exposure to genetically different cells/tissues (pregnancy, transfusion, transplant)

C/P

Inves

Mng

Special — pathognomonic

Endocrinology & Nephrology

34 entries

Addisonian crisis (acute adrenal insufficiency)

C/P

50M repeated syncope/fatigue/anorexia, prev TB
weight loss + episodic abdo pain
generalised skin darkening, buccal pigmentation + bronze skin
BP 80/50 supine + postural drop, HR 103, Temp 38.4, BMI 17
commonest cause: Addison's (autoimmune primary hypoadrenalism)
DD: TB, rapid long-term steroid withdrawal, sepsis/stress on chronic adrenal dysfunction, adrenal haemorrhage (heparin/warfarin, DIC), postpartum infarction, bacteraemia, trauma/mets/amyloid/haemochromatosis/lymphoma, pituitary secondary

Inves

ER: CBC, RBG, Na⁺, K⁺, ABG
confirm: ACTH stimulation (Synacthen) test; serum cortisol + ACTH 9 am

Mng

IV cortisone + fluids on suspicion (treat first, confirm later)
no mineralocorticoid in acute attack

Special

buccal pigmentation + bronze skin (absent in secondary/pituitary — no pigmentation)
meningococcal adrenal haemorrhage = Waterhouse-Friderichsen

Hypoglycaemic coma

C/P

17F athlete, unresponsive after sudden LOC during basketball, no head trauma
T1DM 7y on insulin, GCS 7/15, low glucometer glucose
conscious symptoms: headache, difficulty problem-solving, altered behaviour, coma, seizures, anxiety, tachycardia, sweating, cool clammy skin
causes in DM: small/delayed/skipped meals, renal/liver disease, ↑physical activity, insulin or secretagogues (sulfonylureas)

Inves

Whipple triad; plasma glucose <70 mg/dl (see Criteria)
severity levels L1/L2/L3 (see Criteria)

Mng

intubate to protect airway; correct w/ IV glucose 25%
conscious: 15-20 g oral rapidly-acting carb, recheck 15 min, retreat if CBG <70
glucagon IM/SC
prevention: patient education, no insulin/OSU if exercising or missing meal, home glucagon pen

Special

Whipple triad diagnostic

DKA (newly diagnosed T1DM)

C/P

18M diffuse abdo pain + nausea/vomiting 2d, weight loss/polyuria/polydipsia
drowsy + dehydrated, rapid deep breathing, BP 100/60, HR 110

Inves

RBG, ABG (pH, HCO3, PO2, PCO2), Na⁺/K⁺, urea/creatinine, urine ketone dipstick

Mng

initial ER: fluids (normal saline) + IV regular insulin together, careful monitoring
IV NS 0.9% till BG <250 → shift Dextrose 5%
IV insulin 0.1×BW×hr till BG <250 → decrease to 0.05×BW×hr
IV KCl 40 mg per 1 L fluid if K⁺ 5.5→3.5; if K⁺ <3.3 mEq/L give fluid + K before insulin (prevent worsening hypokalaemia)
IV bicarbonate if pH <6.9 (controversial)
shift IV→SC insulin when anion gap <18 w/ 1 h overlap
discharge: insulin replacement (basal-bolus or pump) + CGM

Special

HHS (uncontrolled T2DM)

C/P

60F confusion/anorexia/nausea 2d, T2DM 10y on orals, last HbA1c 13%, refused insulin
confused/agitated, BP 140/90, HR 95, Temp 38, ↓skin turgor + dry mucosa
swollen painful hyperaemic left big toe (precipitant infection)

Inves

RBG, ABG, Na/K, urea/creatinine, serum osmolality, urine ketone dipstick, CBC

Mng

initial ER: IV fluids + IV insulin + treat underlying cause (antibiotics for toe)
rehydrate maintaining electrolyte homeostasis, correct hyperglycaemia, treat underlying
monitor CV/pulm/renal/CNS; prevent arterial/venous thrombosis + cerebral oedema
shift when serum osmolality + hyperglycaemia corrected
discharge: tight glycaemic control (protocols), foot-care education

Special

serum osmolality is the shift/monitoring marker

Thyroid storm (thyrotoxic crisis on Graves')

C/P

25F agitated, months irritability/nervousness/behavioural change (lost job)
↑appetite w/ weight loss, episodic diarrhoea, heat intolerance
BP 90/60, HR 120, Temp 39.5, RR 18, moist skin, bilateral fine tremor
bilateral proptosis, diffuse goitre w/ thrill + bruit

Inves

clinical dx + TSH, free T4, free T3, RAIU, thyroid scan

Mng

general: fluids/electrolytes/vasopressors as indicated; cooling blanket + acetaminophen for pyrexia
propranolol (β-block + ↓peripheral T4→T3, watch CHF): IV 1 mg/min till blockade then oral/NG 60-80 mg q4h
specific: PTU high-dose = 1000 mg PO/crushed-NG load then 250 mg PO q6h (alt methimazole 30 mg PO q6h)
iodide 1 h AFTER PTU load (inhibits release): Lugol's 2-3 drops q8h OR SSKI 5 drops q8h
dexamethasone 2 mg IV q6h first 24-48h (↓temp + inhibits T4→T3)
identify/treat precipitants
definitive: total thyroidectomy, RAI (caution in Graves' orbitopathy), medical

Special

iodide given only 1 h AFTER PTU load (sequence)

Graves' disease

C/P

45F 4mo irritability + frequent bowel movements, 6.8 kg weight loss w/o appetite change
HR 112, moist palms, diffuse goitre no nodules
orbital proptosis + pretibial myxoedema
pregnant variant: 21F primigravid 10wk, weight loss despite ↑appetite, HR 120, prominent globes, firm diffuse goitre, fine tremor

Inves

TSH 0.2 (low), T4 22 (high); confirm anti-TSH-receptor Ab
RAIU: increased uptake, diffuse pattern
ECG sinus tachycardia

Mng

acute: β-blocker (propranolol) + antithyroid (carbimazole or PTU)
definitive: RAI or surgery
surgery over RAI when: pregnancy, large goitre w/ severe compressive symptoms
pregnancy: PTU 1st trimester, carbimazole 2nd/3rd; no improvement → thyroidectomy in 2nd trimester
re-pregnant later on thyroxine → increase thyroxine dose by 30%

Special

orbital proptosis + pretibial myxoedema = most specific vs other hyperthyroidism
RAI complication = worsening ophthalmopathy (CI in moderate-severe/sight-threatening orbitopathy; avoid, cover w/ steroids)
PTU hepatotoxic; carbimazole agranulocytosis + teratogenic

Toxic multinodular goitre

C/P

40F 3mo hand tremors + SOB, anxious
neck swelling moves on swallowing, sinus tachycardia

Inves

TSH 0.006 (low) → free T3, free T4, thyroid US, uptake scan
US: diffuse enlargement w/ multiple nodules + retrosternal extension
retrosternal extension = commonest obstructive-goitre symptom (30-60%)

Mng

start propranolol + refer surgery after euthyroid
best mng: total thyroidectomy

Special

Hashimoto's thyroiditis / hypothyroidism

C/P

44F 1mo fatigue + dysphagia, dry skin/thinning hair/facial rounding
T1DM + RA; father had papillary-cancer thyroidectomy
HR 62, painless diffusely enlarged thyroid

Inves

TFT + thyroid US → high TSH, low free T3/T4, US diffuse no nodules
confirm: anti-thyroglobulin, anti-TPO, anti-microsomal Ab

Mng

thyroxine
monitor: first few weeks by symptom improvement, after 6 weeks by TSH

Special

rapid thyroid enlargement over months → thyroid lymphoma

Thyroid lymphoma

C/P

rapid thyroid enlargement over months on Hashimoto background

Inves

primary thyroid lymphoma = FNA-malignant non-epithelial category

Mng

surgical mng (malignant FNA category)

Special

arises from Hashimoto chronic lymphocytic thyroiditis

De Quervain's (subacute) thyroiditis

C/P

40F neck pain days after common cold
tachycardia + diarrhoea, tender thyroid + fine tremor

Inves

TFT + ESR → low TSH, high free T3/T4, high ESR
RAIU: decreased uptake (distinguishes from Graves')

Mng

NSAIDs and/or steroids for pain; propranolol for symptoms

Special

tender thyroid after viral URTI + decreased RAIU
prognosis: 90% resolve self-limited, 10% overt hypothyroidism

Tertiary hyperparathyroidism

C/P

53F on hospital haemodialysis 10y, acutely unwell at session
Ca 3.70 mmol/L (high), alb 35

Inves

PTH, phosphate, CBC, U&E, ECG

Mng

Special

patho: renal failure → chronic hypocalcaemia → 2° hyperPTH → autonomous PTH secretion → tertiary

Primary hyperparathyroidism

C/P

45F 1mo fatigue/polyuria/headache, normal glucose no glycosuria
MEN2A component: kidney stones, pancreatitis, ulcers, osteoporosis

Inves

Ca 3.20 (high), alb 38, phosphate 0.61 (low), creatinine 130, PTH 19.0 (high)
hypercalcaemia + hypophosphataemia + high PTH → probable parathyroid adenoma
ECG, neck US, sestamibi scan

Mng

MEN2A: usually hyperplastic glands → subtotal resection w/ cryopreservation or implantation (neck/forearm)

Special

hypercalcaemia + hypophosphataemia + HIGH PTH (vs malignancy = high Ca, NORMAL PTH)

Hypercalcaemia of malignancy (metastatic bone disease)

C/P

57F known breast carcinoma

Inves

Ca 3.00 (high), alb 37, phosphate 0.85, ALP 133 (>122, high), PTH 1.7 (1.3-7.6, normal/low)
hypercalcaemia w/ NORMAL PTH; ECG, bone scan

Mng

Special

hypercalcaemia w/ NORMAL/suppressed PTH
mechanisms: (1) PTHrP (non-metastatic solid tumours), (2) osteolytic mets w/ local cytokines (solid tumours + multiple myeloma), (3) tumour 1,25-diOH vit D (lymphoma)

Sarcoidosis (hypercalcaemia)

C/P

36M routine screen, asymptomatic

Inves

Ca 2.75 (high), alb 42, phosphate 0.72, creatinine 90, PTH 6.2 (normal)
CXR bilateral hilar lymphadenopathy

Mng

Special

hypercalcaemia w/ normal PTH + bilateral hilar lymphadenopathy

Thyroid nodule / thyroid cancer

C/P

nodules frequent, ↑ with age; <5% palpable nodules malignant (>90% benign)
50% of clinically solitary nodules prove multinodular
concomitant-cancer risk in longstanding MNG ≈ solitary nodule (<5%)
benign (>90%): adenomas (follicular/microfollicular/Hurthle), colloid nodule, granulomatous (Hashimoto, De Quervain); rare cyst, infection (bacterial/TB), infiltrative (sarcoid/amyloid)

Inves

which to evaluate: palpable solitary >1cm euthyroid; MNG dominant nodule >1.5-2cm (largest or recent growth); incidentaloma = focal FDG-PET uptake (33.2% carcinoma)
ACR TI-RADS ultrasound risk score (see Criteria)
FNA + classification / histology correlation (see Criteria)
clinical malignancy risk factors (most specific): thyroid-cancer FHx, MEN2, rapid growth, neck irradiation before adolescence, age <20/>60, male, hard nodule, fixed to neck structures, vocal-cord paralysis, enlarged regional LN*

Mng

FNA benign macrofollicular → clinical follow-up
FNA malignant → surgical mng
microfollicular (follicular neoplasm) → hemithyroidectomy (lobectomy)
inadequate → repeat FNA
WDTC operative recommendations by size (see Criteria)
nodal disease: palpable LN → FNA node; positive → total thyroidectomy + central LN dissection + modified radical neck dissection (removes ipsilateral cervical LN II-V; preserves IJV, SCM, spinal accessory nerve); no palpable LN → total thyroidectomy + central LN dissection

Special

histology distribution: papillary 80%, follicular 15%, medullary <5%, anaplastic <2%, poorly diff <1% (see Criteria)

Medullary thyroid cancer

C/P

part of MEN2; MTC ~5% of thyroid malignancies, inherited in up to 20%

Inves

RET proto-oncogene testing (positive = hereditary/MEN2)
serum calcitonin >100 pg/l = 100% PPV for MTC; >400 pg/l suspect distant mets (FDG-PET if CT/MRI negative)
also secretes CEA (adjunct for disease extent)

Mng

RET positive: genetic counselling + prophylactic thyroidectomy for asymptomatic offspring
primary: total thyroidectomy (treat proven MTC + prevent in MEN2 carriers)
MEN2A prophylactic thyroidectomy: no cervical LN dissection needed
proven cancer: total extracapsular thyroidectomy + bilateral central neck dissection; lateral compartments only if FNA-proven spread

Special

calcitonin >100 pg/l = 100% PPV; secretes CEA
RET on chromosome 10

MEN2

C/P

MTC + phaeochromocytoma
MEN2A adds primary hyperparathyroidism
MEN2B = mucosal/musculoskeletal: mouth/lip mucosal neuromas, marfanoid habitus, bowel ganglioneuromatosis; + congenital hip dislocation, pes cavus, pectus excavatum, kyphosis

Inves

RET proto-oncogene (chromosome 10)

Mng

per component (MTC → thyroidectomy; phaeo → adrenalectomy; hyperPTH → subtotal parathyroid resection)

Special

AD ~100% penetrance
MEN2B mucosal neuromas + marfanoid habitus

Phaeochromocytoma (in MEN2)

C/P

clues: anxiety/tremor/panic attacks; FHx young-onset HTN or sudden death
severe headache + anxiety alongside MTC → suspect synchronous phaeo
up to 24% at thyroid dx; may be bilateral or extra-adrenal (organ of Zuckerkandl)

Inves

24h urine catecholamines pre-op
MIBG scan (extra-adrenal)

Mng

pre-op α-blockade (phenoxybenzamine)
if present w/ MTC → treat phaeo FIRST
unilateral laparoscopic adrenalectomy (contralateral normal) or cortical-sparing (MEN prone to bilateral, up to 50%)

Special

treat phaeo before MTC
organ of Zuckerkandl (extra-adrenal) → MIBG scan

Acute Kidney Injury (overview)

C/P

AKI vs CKD: AKI = recent normal creatinine, kidney normal size 10-12 cm, acute symptoms (dyspnoea, nausea, vomiting, diarrhoea); anaemia/high-PTH/hyperphosphataemia/hypocalcaemia less common
CKD = previous high creatinine, small kidney (except diabetics normal/large), long history (fatigue, nausea, nocturia, itching)
at risk: blood loss, fluid loss (vomiting/diarrhoea/DI), burns, hospitalized, critically ill, older

Inves

phases: onset / oliguric-anuric / diuretic / recovery (see Criteria)
AKI staging KDIGO (see Criteria)
oliguria classification + AKI chemistry (see Criteria)
with no kidney function creatinine ↑ 100 µmol/L/day

Mng

per cause (see subtype entries)

Special

Prerenal AKI

C/P

70M disturbed consciousness, severe diarrhoea + vomiting 3d, HTN/DM
dehydration signs: ↓skin elasticity, hypotension, rapid pulse, collapsed neck veins

Inves

creatinine 1.8 1mo ago → 4.2, urea 280, UOP 300 mL/d
US kidney 11 cm normal echogenicity, no hydronephrosis; urine pus 2-3/RBC 1-2
FeNa, urine Na, osmolality; ACR, HbA1c

Mng

measure glucose (exclude hypoglycaemia); antibiotics for GE
stop ACE + diuretics; balanced crystalloids + follow-up

Special

prerenal on top of chronic (baseline 1.8)
prognosis: if prolonged/untreated → ATN, function may not return to baseline

Acute tubular necrosis (ATN)

C/P

Task 1 DD: 65F diabetic, NSAID (ibuprofen) for OA, nausea/vomiting 4d
Task 4 sepsis-ATN: oliguria + congested neck veins + bilateral basal creps + drowsy

Inves

Task 1: creatinine 5 (normal 1mo ago), urea 100, UOP 200 mL/d; FeNa 3%, urinary Na 30; Hb 12.5/MCV 92/Ca 9/phos 4.8/Na 135/K 4.5 → DD oliguric ATN vs AIN
Task 4: creatinine 10, K 7, HCO3 18, CRP 300, D-dimer positive

Mng

Task 1: stop ACEi/thiazides/ibuprofen/nephrotoxics; balanced crystalloids (Ringer's) if dehydrated; close monitoring
Task 4 (sepsis): treat septic shock, IV sodium bicarbonate, manage hyperkalaemia, dialysis (CRRT)

Special

FeNa 3% (>2%, vs prerenal)

Acute interstitial nephritis (AIN)

C/P

80F admitted CAP on IV antibiotics (penicillin + garamycin) + diclofenac + IV fluids
drug-induced (antibiotics, NSAID)

Inves

creatinine rose to 3.1 over 3d
urine eosinophiluria + pus 12/HPF, proteinuria 800 mg/24h
Hb 10.1, TLC 25000, PLT 100000, CRP 80, Ca 9, pH 4.5, HCO3 22

Mng

stop offending drug (first line)

Special

urine eosinophiluria

Contrast-associated AKI (contrast nephropathy)

C/P

65M post emergency coronary angiogram for MI; creatinine rise 3d later

Inves

creatinine 2.5 (pre 1.1), no overload, HCO3 25, K 4.5, UOP 300 mL/24h
no renal-biopsy indication

Mng

prevention: pre-procedure stop ACE/metformin/diuretics; adequate hydration w/ isotonic saline before + after; lowest contrast dose

Special

creatinine rise ~3d post contrast

Obstructive / post-renal AKI (BPH)

C/P

85M suprapubic pain in agony, low UOP 3d w/ hesitancy + frequency
no loin pain, no analgesics/nephrotoxics

Inves

abdominal exam; US abdomen/pelvis for obstruction + hydronephrosis; urinary catheter

Mng

urinary catheter; refer urosurgery to relieve obstruction

Special

Acute hyperuricaemic nephropathy (tumour lysis)

C/P

54M lymphoma post-chemo

Inves

creatinine 8, uric acid 25, K 7

Mng

allopurinol before + throughout radio/cytotoxic therapy
oral/parenteral fluids
febuxostat (if allopurinol not tolerated + eGFR >30)
rasburicase (recombinant urate oxidase)
urine alkalinisation w/ sodium bicarbonate in acidosis
manage hyperkalaemia

Special

post-chemo lymphoma; uric acid 25

Conn's syndrome / primary hyperaldosteronism

C/P

25F newly HTN, muscle fatigue/weakness, no meds, BP 160/100
picture: HTN + hypernatraemia + hypokalaemia + metabolic alkalosis

Inves

Na 150 (high), K 2.2 (low), creatinine 1, pH 7.5, HCO3 30, PCO2 51
primary disturbance = metabolic alkalosis; compensation by hypoventilation
HTN differentiation: Conn's + Cushing's = low renin/aldosterone ratio; renal artery stenosis = increased renin/aldosterone ratio
ECG: arrhythmias, flat T wave, U wave (hypokalaemia)

Mng

hypokalaemia: treat cause + IV potassium infusion
hypernatraemia: diuretics + water intake (5% dextrose or oral water) + treat cause

Special

low renin/aldosterone ratio (vs renal artery stenosis = increased)

Hyperkalaemia

C/P

74M syncope, now alert, muscle weakness; CKD 10y (missed 6mo follow-up)
BP 100/60, HR 45

Inves

Na 140, K 6.9, creatinine 7.8 → cause = renal failure (CKD)
ECG: peaked T wave + heart block

Mng

immediate: IV calcium gluconate
further: sodium bicarbonate, insulin + dextrose, β2-agonists, loop diuretics, cation-exchange resin, dialysis

Special

other causes: K-sparing diuretics, Addison's, renal failure, rhabdomyolysis
ECG peaked T wave + heart block

SIADH (hyponatraemia)

C/P

58M diabetic, RTA head injury; Na 140 on admission → confused next afternoon
cause: head injury

Inves

Na 122, K 4, creatinine 1.1, BP 130/80; euvolaemic
confirm SIADH: low serum osmolality <275 mosm/kg, increased urine osmolality >100 mosm/kg, no other cause of euvolaemic hyponatraemia (e.g. hypothyroidism)
urine output low

Mng

3% hypertonic saline + water restriction + diuretics + treat cause

Special

euvolaemic + low serum / high urine osmolality

Nephrogenic diabetes insipidus (lithium)

C/P

58F bipolar on lithium 9y, restlessness/agitation
day 2 polyuria (24h UOP 7L)

Inves

BP 156/76, RR 23, SpO2 91%, HR 101, Hb 12.1, BUN 26, creatinine 1.1
Na 151 (high), lithium 0.9, MRI brain normal, serum osmolality 327 (high)
urine output high
confirm: water deprivation test

Mng

water intake (5% dextrose or oral water) + treat cause (replace lithium w/ another medication)

Special

lithium-induced; high serum osmolality + polyuria

Chronic Kidney Disease (CKD)

C/P

65F CKD/DM/HTN, mild leg oedema; long history fatigue/nausea/nocturia/itching
small kidneys (except diabetics — normal/large)

Inves

GFR = volume filtered from glomerular capillaries into Bowman's capsule per unit time
eGFR (CKD-EPI creatinine) or Cockcroft-Gault (see Criteria)
CKD stages by eGFR G1-5 + ACR categories (see Criteria)
US 8-cm kidneys; ACR 320 (rising from 120), urea 85, creatinine 3
biochemistry: linear ↓GFR, ↑nitrogenous waste; K maintained until GFR <5; impaired H⁺ excretion if GFR <30; low Ca w/ high PTH (2° hyperPTH); high Mg + phosphate
order CBC, iron profile, Ca, Ph, PTH; assess vascular calcification

Mng

control BP w/ ACE or ARB to 130-140/70-79
change gliclazide → SGLT2i (dapagliflozin); add statin
stage 5: Na + K dietary restriction, diuretics, avoid NSAIDs, sodium bicarbonate, manage hyperkalaemia
nephrotoxic drugs to avoid: IV contrast, NSAIDs, aminoglycosides
hand-vein precaution: don't cannulate/sample from non-dominant arm — save for AV fistula

Special

progression = eGFR decline >5 mL/min/1.73m² within 1 year

CKD anaemia

C/P

52M CKD stage 4 (diabetic), lethargy/fatigue/breathlessness, pale

Inves

Hb 8, normal WBC/PLT, iron 20, TIBC 450, ferritin 200
TSAT = 20/450×100 = 4%
causes: ↓erythropoietin, absolute iron deficiency, blood loss, folate deficiency, B12 deficiency, CKD mineral+bone disorder, marrow suppression by uraemia

Mng

iron supplement (trial oral ferrous sulphate)
after store correction start epoetin (or longer-acting darbepoetin)

Special

TSAT = iron/TIBC ×100

Renal osteodystrophy (CKD-MBD)

C/P

55M CKD stage 5, generalised bony aches

Inves

Ca 7.5 (low), alb 3.2, phosphate 8 (high), PTH 210 (high)
corrected Ca = 7.5 + 0.8×(4−3.2) = 8.14 mg/dl; Ca×PO4 = 8.14×8 = 65.12 (elevated)
mechanism: ↓vit D activation, ↓Ca, phosphate retention/↑phosphate, ↑FGF-23

Mng

first step: phosphate dietary restriction + phosphate gut binder (calcium acetate during/immediately after meal; sevelamer)
ESRD on HD: calcium carbonate 1 h after meal + alfacalcidol or calcitriol

Special

Ca×PO4 product elevated (65.12)

Nephrotic syndrome

C/P

30M unwell 6 weeks, bilateral pitting LL oedema; dipstick severe proteinuria
oedema (Na/water retention by tubules > oncotic drop; liver ↑albumin production)

Inves

proteinuria >3.5 g/24h, hypoalbuminaemia + oedema
dipstick severe proteinuria

Mng

admitted (source minimal)

Special

defining: proteinuria >3.5 g/24h + hypoalbuminaemia + oedema

Renal tubular acidosis (RTA)

C/P

metabolic acidosis from reduced H⁺ excretion; urine not maximally/appropriately acid

Inves

types 1/2/4 (see Criteria)

Mng

Special

Type 1 distal, Type 2 proximal (Fanconi), Type 4 hyporeninaemic hypoaldosteronism (diabetic nephropathy)

Haematology

21 entries

Aplastic anaemia

C/P

22F, 6wk easy bruising + recurrent infections (otitis externa, vaginal thrush, URTI, gum infection) + heavy periods
pale, 0.5cm neck nodes, oedematous/inflamed gums

Inves

pancytopenia (diff neuts 9% low, lymphs 88% high), retic 0.1% (low, N 0.2–2%), B12/folate normal
BM aspirate: hypocellular, reduced erythroid + myeloid precursors, majority lymphocytes
trephine: grossly hypocellular, scattered eosinophils/plasma cells/lymphocytes, no erythroid precursors or megakaryocytes

Mng

transfuse blood + platelets, IUCD removed, norethisterone, metronidazole for gingivitis
ALG + cyclosporin + prednisolone
complication: serum sickness 10 days post-ALG (pyrexia 38.5, arthralgia, erythematous rash) → settled with steroids

Special

Anaemia of chronic disease

C/P

46M long-standing RA on sulfasalazine + naproxen; Hb 9

Inves

cause: anaemia of chronic disease; GI-tract bleeding
iron stores by BM aspirate (not routine), upper GI endoscopy, CRP/ESR

Mng

better arthritis control; less commonly EPO or transfusion (doesn't need — Hb 9)

Special

Anaemia in chronic liver disease (alcohol)

C/P

54F alcoholic, haematemesis, jaundiced, palpable liver + moderate splenomegaly

Inves

haematemesis causes: varices, peptic ulcer, Mallory-Weiss + clotting defect if liver decompensated
anaemia causes: bleeding, folate deficiency, direct toxic effect of alcohol

Mng

resuscitate (ABC), blood, FFP to correct clotting, endoscopy + primary mng of varices/ulcer

Special

Anaemia of chronic renal failure (renal anaemia)

C/P

46M poorly-controlled long-standing IDDM, increasing lethargy, exam unremarkable

Inves

probable chronic renal failure from poorly-controlled diabetes; anaemia from inadequate EPO production by kidneys
measure plasma EPO

Mng

recombinant EPO

Special

Myelodysplasia (MDS)

C/P

63M known myelodysplasia, 48h painless haematuria, pale
urine frank haematuria + proteinuria ++

Inves

dx = BM exam showing dysplastic blood cells
haematuria: image renal tract, cystoscopy

Mng

refer urology, platelet transfusion, treat underlying cause

Special

Leukoerythroblastic reaction

C/P

31M mechanic, L chest pain worse on breathing/movement 24h + dry cough; smoker 40/day
precipitant here: pneumococcal lobar pneumonia (severe infection)

Inves

diff: neut 88% high, metamyelocytes 4%, myelocytes 2%, NRBC 1/100 WBC
film: toxic granulation + left shift; ESR 85 → leukoerythroblastic blood picture
causes: severe infection, bone marrow infiltration

Mng

treat underlying cause

Special

leukoerythroblastic film = left shift (metamyelocytes/myelocytes) + NRBCs + toxic granulation

Reactive lymphadenitis (benign lymphadenopathy)

C/P

lymphadenopathy causes: inflammation (reactive lymphadenitis), lymphoma/leukaemia, metastasis
acute non-specific: pain/tenderness/enlargement; swollen grey-red engorged nodes

Inves

acute non-specific: large germinal centres + numerous mitoses; pyogenic → neutrophil infiltrate around follicles + in sinuses; severe → follicle-centre necrosis/abscess; dx clinical
chronic non-specific 3 patterns: follicular hyperplasia (B-cell activation; RA, toxoplasmosis, early HIV), paracortical hyperplasia (T-cell reactions), sinus histiocytosis (nodes draining cancers)
follicular hyperplasia: reactive follicles w activated B cells, tingible-body macrophages, follicular dendritic cells

Mng

Special

reactive follicular hyperplasia: tingible-body macrophages PRESENT, sharply-defined mantle interface, heterogeneous (vs follicular lymphoma)
CD3+/CD20+ = reactive hyperplasia

Acute lymphoblastic leukaemia (ALL)

C/P

neoplasm of immature pre-B or pre-T lymphoblasts
~85% B-ALL (childhood leukaemia, peak age ~3); T-ALL (adolescent males, thymic/mediastinal mass in 50–70% ± lymphadenopathy/splenomegaly)
most common cancer of children; white:black 3:1; boys>girls

Inves

morphology: scant basophilic cytoplasm, high N/C, numerous mitoses, finely-stippled chromatin, inconspicuous nucleoli
IHC: CD20 (B), CD3 (T), TdT +ve in 95%
B-cell markers: early pre-B-ALL CD19/CD10/TdT; mature B-ALL CD10±/CD19/CD20/CD22/surface IgM

Mng

(lymphoblastic lymphoma → treat as ALL + CNS prophylaxis)

Special

TdT +ve in 95%; lymphoblasts high N/C, finely-stippled chromatin, inconspicuous nucleoli

Chronic lymphocytic leukaemia (CLL)

C/P

commonest leukaemia in West, elderly; commonest cause of lymphocytosis in middle-aged/elderly
68M tiredness, cervical + axillary lymphadenopathy, spleen 3cm
generalized lymphadenopathy, splenomegaly; hypogammaglobulinaemia → infection risk

Inves

smear cells; >95% B-cell (CD19, surface Ig, CD5); T-cell type worse prognosis
clonal absolute lymphocytosis >5000; BM infiltration
Case 6: WBC 88, Hb 7.3, MCV 115 macrocytic, lymphs 75%, smear cells, polychromasia, retic 23% (with autoimmune haemolysis)
immunophenotype CD5/19/23 + light-chain restriction

Mng

often no Rx
cytotoxic when symptomatic/marrow failure — chlorambucil/cyclophosphamide (young: COP/CHOP; fludarabine)
corticosteroids for autoimmune haemolysis; chemoimmunotherapy for clone

Special

smear cells; CD5/19/23 +, light-chain restriction

Hairy cell leukaemia

C/P

elderly males, massive splenomegaly

Inves

B-cell with cytoplasmic projections; monocytopenia

Mng

splenectomy for cytopenias, interferon, deoxycoformycin

Special

B-cell cytoplasmic (hairy) projections; monocytopenia

Prolymphocytic leukaemia (PLL)

C/P

usually B-cell; massive splenomegaly, high WCC, commoner in males

Inves

prolymphocyte = intermediate between lymphoblast and mature lymphocyte (single prominent nucleolus, voluminous cytoplasm)

Mng

leucopheresis

Special

prolymphocyte: single prominent nucleolus, voluminous cytoplasm

Plasma cell leukaemia

C/P

rare; primitive plasma cells released into blood; few seen in advanced myeloma; bad prognosis

Inves

primitive plasma cells in blood

Mng

Special

primitive plasma cells circulating

Hodgkin lymphoma

C/P

incidence 2.4/100,000, peak early adulthood
lymphadenopathy esp neck, usually painless, contiguous spread (mediastinum often involved)
B symptoms (fever, night sweats, weight loss, lassitude) = worse prognosis; pruritus common but no prognostic significance; alcohol-related node pain; anaemia in ~1/3
advanced: lymphocytopenia, hypoalbuminaemia, raised ESR
Case 1: 24F cough + exertional wheeze (treated as asthma 3mo), severe pruritus + excoriations, 15×10mm R supraclavicular node
Case 2: 17F fever + fatigue, enlarged R cervical nodes only

Inves

Case 1: CXR superior mediastinal mass 7cm; biopsy nodular sclerosing HL; CT R supraclavicular + axillary + superior mediastinal → Stage IIA
Case 2: node nodular grey-tan cut, nodular architecture + intervening collagen, classic binucleate RS owl-eye, polymorphic background (eosinophils, lymphocytes, macrophages); IHC CD15+, CD20−, CD30+
classic HL IHC: CD15+, CD30+, CD20−; NLPHL: CD20+, CD15−/CD30−

Mng

stage IA/IIA historically radiotherapy alone (mantle field upper-half, inverted-Y lower-half) → now short combination chemo + involved-field RT
localised-with-B-symptoms + advanced → 6–8 courses ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) — replaced MOPP (mustine, vincristine, procarbazine, prednisolone): better efficacy, less infertility, fewer secondary leukaemias
progression → high-dose chemo + stem cell transplant
Case 1: 4× ABVD + involved-field RT (alt 6–8 cycles chemo alone); follow-up monthly ×3 → 3-monthly → 6-monthly for 5yr; watch relapse/secondary NHL, lung fibrosis, cardiomyopathy; advice node self-exam, regular ECHO, sperm/ova banking pre-therapy
prognosis: 5-yr survival ~90%

Special

RS giant cell, arises from germinal-centre B cells; EBV role (identical genome in all RS cells → infection precedes transformation); RS cells liberate cytokines → recruit non-neoplastic infiltrate (>90% of tumour)
subtypes: nodular sclerosis (65–75%, cervical/supraclavicular/mediastinal, uncommonly EBV, excellent prognosis, collagen bands + lacunar + classic RS); mixed cellularity (20–25%, older, EBV 70%, classic + mononuclear RS plentiful, excess eosinophils, good prognosis); NLPHL (~5%, isolated cervical/axillary, no EBV, excellent prognosis, L&H popcorn cells, typical RS rare); lymphocyte-rich; lymphocyte-depletion
classic HL CD15+/CD30+/CD20−

Non-Hodgkin lymphoma (NHL)

C/P

incidence ~12/100,000, rising ~5%/yr
non-contiguous spread; hepatosplenomegaly + BM involvement commoner than HL
B symptoms commoner in high-grade; autoimmune haemolytic anaemia in low-grade + some T-cell
risk factors: immunodeficiency (primary/secondary), autoimmune (Sjogren, RA, Hashimoto), viruses (HIV, EBV, KSHV/HHV8, HTLV-1), H. pylori, radiation, chemotherapy

Inves

gross: multiple enlarged rubbery nodes, fleshy tan cut; spleen single mass or diffuse tiny nodules; extranodal mass/diffuse
micro: diffuse effacement of follicular architecture by sheets of neoplastic lymphocytes (small/intermediate/large); lack normal admixture; infiltrate capsule + perinodal tissue
diagnosis: clinical, gross, H&E, immunophenotyping, cytogenetics; clonality = antigen-receptor gene rearrangement (all daughter cells identical)
CD45/LCA +ve in lymphoid cells

Mng

low-grade: localised → RT (may cure); advanced incurable relapsing-remitting; asymptomatic → watch & wait; symptoms/organ dysfunction → chemo (oral chlorambucil, CVP [cyclophosphamide, vincristine, prednisolone], fludarabine, anthracycline, anti-CD20 mAb); gastric MALT → H. pylori eradication → remission ~90%
high-grade → CHOP (cyclophosphamide, adriamycin/hydroxydaunorubicin, vincristine/oncovin, prednisolone) 6–8 cycles 3-weekly
very high-grade: lymphoblastic → treat as ALL + CNS prophylaxis; Burkitt's → 4-month intensive + CNS prophylaxis
poor prognostic factors: age >60, stage III/IV, poor performance status, raised LDH
prognosis: low-grade median survival ~8yr (no survival-curve plateau); high-grade combined 10-yr survival ~45% (most cured)

Special

Follicular lymphoma

C/P

Case 1: 58M neck swelling + fever/night sweats/weight loss, cervical + inguinal nodes, mediastinal + para-aortic lymphadenopathy, elevated LDH
mature germinal-centre B cell, 2nd commonest NHL, M:F 1:1.7, median 60–65, cervical/inguinal, indolent (5yr PFS ~60%), localized in 10–20%, can transform to DLBCL / B-lymphoblastic
Case 3: 52M persistently blocked nose (dx sinusitis), lymphadenopathy neck/axillae/groin (largest 1cm), neutropenic → follicular small cell lymphoma

Inves

morphology: partial/complete nodal effacement by neoplastic follicles — similarly sized, non-polarized, absent mantle zones, no tingible-body macrophages, infrequent mitoses
IHC CD20+/CD3−, CD10+, BCL2+
FL vs reactive follicular hyperplasia: FL monomorphic (centrocyte predominance), lacks tingible-body macrophages, fuzzy follicle edge, absent/attenuated mantle zone, closely-packed uniform follicles, infrequent mitoses
Case 3 further Ix: CT / PET-CT, immunohistochemistry, BM exam, LFT/RFT

Mng

Case 3: nodes both sides diaphragm = stage 3A, no B symptoms, small nodes → may not need current Rx; neutropenia → possible BM infiltration → if proven, combination chemo

Special

CD20+/CD3−, CD10+, BCL2+; neoplastic follicles lack tingible-body macrophages

Diffuse large B-cell lymphoma (DLBCL)

C/P

61F malaise/nausea/abdo pain/diarrhoea/fever 39, then L abdo tenderness + L basal crepitations

Inves

Hb 10, WBC 23.2, neuts 78%, ESR 52, raised ALP/ALT/GGT, urate 620 high, LDH 1021 high
BM normocellular, large foamy-blue-cytoplasm cells, no light-chain restriction (probable lymphoma)
CT abdo: gross para-aortic glandular enlargement + borderline splenomegaly
needle biopsy → DLBCL
light chain restriction = clonal B cells express single kappa OR lambda = monoclonal
prognostic group bad: Stage 4 (abdo nodes + spleen + lung + BM ± liver), possible B symptoms, advanced age, high-grade DLBCL, high LDH, non-response to 1st line

Mng

CHOP → progressed after 2 cycles → cisplatinum regimen → no response, died 4mo
CHOP side effects: general tumour lysis syndrome + pancytopenia; cyclophosphamide renal; adriamycin cardiac arrhythmia + liver; vincristine neuropathy; steroids HTN/DM/gastric

Special

Mycosis fungoides / Sézary syndrome

C/P

commonest cutaneous T-cell lymphoma; mature post-thymic T; median 50s; clinical dx of exclusion
Sézary: T-cell (CD4+), skin-trophic, erythroderma

Inves

MF stages: patch (epidermotropism, string-of-pearls basal lymphocytes, halos), plaque (Pautrier microabscesses, cerebriform/hyperconvoluted nuclei, lichenoid dermal infiltrate), tumour (dermal pleomorphic infiltrate ± blast transformation)
IHC CD3+/CD20−; clonal TCR rearrangement
Sézary: cerebriform nucleus, Pautrier microabscesses

Mng

Sézary: chemo / electron-beam RT / PUVA / extracorporeal photopheresis

Special

Pautrier microabscesses; cerebriform/hyperconvoluted (Sézary) nuclei; CD4+ T-cell, CD3+/CD20−

Multiple myeloma

C/P

bone pain (OAF → osteolytic axial lesions, back pain/fractures/cord compression), marrow failure, infection (immune paresis), hypercalcaemia + renal failure, hyperviscosity (esp IgA), AL amyloidosis
Case 4: 67M fall → R humerus fracture (proximal 3rd) + lytic lesions ribs/clavicle

Inves

Case 4: Hb 10.3, ESR 140, serum electrophoresis monoclonal band IgG kappa (immunofixation)
further: BM exam + immunophenotyping, renal function
monoclonal band = monoclonal Ig from expanded plasma-cell clone; immunofixation = detects + types monoclonal Ig in serum/urine

Mng

supportive: hydration + bisphosphonates for hypercalcaemia, surgery for cord compression/fractures, RT for bone pain, plasmapheresis for hyperviscosity
cytotoxic melphalan/cyclophosphamide + prednisolone; younger → VAD (vincristine, adriamycin, dexamethasone); high-dose melphalan + autologous SCT; bisphosphonates
Case 4: localised RT to painful lesions (palliation post pathological fracture), bisphosphonates, supportive (pain, anaemia/EPO), targeted (proteasome inhibitors, immunomodulators, corticosteroids)

Special

osteolytic axial lesions from OAF; IgG kappa monoclonal band; plasma-cell clone

MGUS

C/P

no myeloma features

Inves

low paraprotein, preserved other Ig, static paraprotein, <10% plasma cells in BM
1%/yr → myeloma

Mng

Special

Plasmacytoma

C/P

localised malignant plasma cells; RT may cure; many → myeloma
Case 5: 42M 4wk severe back pain + unsteady walking; brisk equal LL reflexes, upgoing plantars, sensory level below umbilicus (cord compression)

Inves

mass at T11 = sheets of plasma cells, lambda+ kappa−, amyloid deposition
serum electrophoresis normal; urine Bence Jones 0.2g/l; BM + skeletal survey normal
light-chain staining shows monoclonal restriction → malignancy
AL amyloidosis: myeloma cells secrete amyloid → systemic (kidney → renal failure, cardiomyopathy; may reverse w anti-myeloma Rx)

Mng

surgical removal if possible + local RT; close follow-up for myeloma

Special

single region, otherwise normal BM; monoclonal light-chain restriction

Waldenström's macroglobulinaemia

C/P

IgM paraprotein → hyperviscosity (weakness/tiredness → confusion/coma), oedema, HF, nosebleeds, purpura
unlike myeloma: no bone pain / hypercalcaemia / renal failure

Inves

IgM paraprotein

Mng

plasmapheresis if hyperviscosity, else as CLL

Special

IgM paraprotein; hyperviscosity without bone pain/hypercalcaemia/renal failure

Neurology

24 entries

Bacterial meningitis

C/P

Fever, headache, neck stiffness ± altered conscious level
CN involvement (deafness, imbalance); focal/generalized seizures
Meningism (neck spasm, photophobia); raised ICP (headache, blurry vision, nausea, projectile vomiting)
Infection of subarachnoid space + meninges, PMN in CSF
Organisms: Strep pneumoniae + Neisseria meningitidis (most common)
Non-neuro complications: endocarditis, thrombocytopenia, acute adrenal failure
Case 4: RTA 1wk ago (skull fissure fracture), GTC convulsion, fever 39, +Kernig/+Brudzinski, GCS 11/15, TLC 15000 neutrophils, CRP 78

Inves

LP + CSF: turbid, protein 2g/l, 2000 PMN, low chloride, CSF/plasma glucose 34% (Case 4)
Blood/nasopharynx/respiratory/urine/skin cultures + antigen/PCR; CT head + MRI brain

Mng

3rd-gen cephalosporin (ceftriaxone, cefotaxime, cefepime); penicillin G if meningococci confirmed
Notify Health Protection Unit (all ABM)
Close-contact prophylaxis: single-dose ciprofloxacin OR rifampicin 600mg bd ×2 days
Prevention: vaccines N. meningitidis C + ACYW135, S. pneumoniae, Hib
Anticonvulsants, osmotic diuretics/corticosteroids if impending herniation

Special

CSF turbid + PMN predominant + low glucose ratio; +Kernig/+Brudzinski

Brain abscess

C/P

General infection symptoms + raised ICP + focal signs
Paroxysmal headache worse on exertion → constant/severe; neck stiffness (associated meningitis); disturbed conscious level
Case 5: 54M diabetic, R ear infection 1.5mo, headache worse on exertion→constant, unsteady gait + L-body weakness, dysphasic, L hemiparesis, bilateral grade-II papilledema
Case 2: flu-like + headache, then unresponsive, L weakness + hypothesia

Inves

MRI brain w contrast or CT; MRV if venous thrombosis
LP contraindicated (raised ICP/papilledema)

Mng

Empirical 3rd-gen cephalosporin (aerobic G−/G+) + metronidazole (anaerobes)
Surgical excision/stereotactic aspiration; corticosteroids + hyperosmolar agents for oedema/raised ICT

Special

LP CONTRAINDICATED (raised ICP); contrast ring lesion

Viral encephalitis

C/P

Prodrome (fever, malaise, myalgia); leptomeningeal irritation (headache, fever, neck stiffness); disturbed conscious level; generalized/focal fits
Organisms usually HSV, chickenpox, measles, enterovirus
Case 3: 28F feverish/agitated/mumbling, L focal fits, temp 38 + neck stiffness

Inves

LP protein 1g/l (rest normal); EEG right focal temporal epileptiform discharges; MRI

Mng

Control fever; antiviral (acyclovir or ganciclovir) 14–21 days; antiepileptic

Special

EEG focal temporal epileptiform discharges (HSV temporal predilection)

Fungal meningoencephalitis

C/P

Chronic meningitis ± encephalitis (weeks–months; headache, neck stiffness, mental changes)
Venous sinus thrombosis, infarction/mycotic aneurysm, granuloma/abscess
Organisms: candidiasis, aspergillosis, cryptococcosis
Case 6: 40M kidney transplant 5yr, pan-sinusitis 2wk, L-eye vision loss + pain, L ophthalmoplegia, diplopia, facial hypothesia, GCS 12/15

Inves

CSF turbid, raised opening pressure, 500 lymphocytes, CSF/plasma glucose 20%, protein 0.3g/l

Mng

Amphotericin B + symptomatic (fits, oedema, raised ICT)

Special

Immunocompromised host (transplant); CSF lymphocytic + very low glucose ratio

Rabies

C/P

Rabies virus, inoculated via saliva through broken skin; IP 3wk–3mo/years; 80% bite history
First: flu-like malaise/fever/chills/myalgia/headache/GI + tingling at bite site
Cerebral within days (hallucinations, nightmares, agitation, delirium, fits)
Hydrophobia (pharyngeal/laryngeal spasm at sound of water); paralysis of bitten limb
Case 7: 32M dog bite 1mo untreated, fever/agitation/dysphagia, muscle spasms + rigidity

Inves

Clinical + bite hx; virus antigen from saliva/skin/urine/CSF by fluorescent antibody; Ab serum/CSF; PCR CSF
Case 7: CSF protein 61mg/dL + WBC 1/L, CT normal, cultures negative (Rabies vs Herpes for PCR)

Mng

Wound cleaned w detergent + water; passive immunity (human rabies Ig); active (human diploid-cell vaccine); anticonvulsants + muscle relaxants

Special

Hydrophobia (pharyngeal/laryngeal spasm at sound of water); bite history

Tetanus

C/P

Clostridium tetani; IP 24h–1–3wk
Entry: contaminated cuts/burns/animal bites, childbirth/abortion (umbilicus), IV drug abuse/piercings/surgery
Local tetanus (localized rigidity/spasm near wound)
Generalized: malaise, spasm + trismus, risus sardonicus, abdominal/paraspinal rigidity, fractures
Sympathetic hyperactivity (tachycardia, HTN, dysrhythmia ± sudden death)
Case 8: 36M from Mexico, jaw pain 3 days, difficulty opening mouth + dysphonia, no tetanus prophylaxis/never vaccinated

Inves

Mng

Wound cleaning + debridement; muscle relaxants; human tetanus Ig; active immunization

Special

Trismus + risus sardonicus; sympathetic hyperactivity

PML (progressive multifocal leukoencephalopathy)

C/P

Only neuro disorder caused by JC virus; dormant → activated when immunocompromised (HIV, CLL, natalizumab)
Oligodendrocytes loaded → destruction → patchy demyelination
Progressive behavioural changes, seizures, focal deficit; insidious onset, rapid course, death within a couple of months

Inves

MRI: multifocal subcortical white-matter lesions

Mng

No specific treatment

Special

JC virus (only neuro disorder it causes); fatal, 25% mortality in MS (treat plasma exchange)

HIV neuro

C/P

RNA virus, any part of neuroaxis; transmission sexual/blood transfusion/infected needles
Mechanism: direct (HAND — HIV-associated neurodegenerative disorder), immunocompromise, PNS

Inves

Mng

Special

Friedreich's ataxia

C/P

Case 1: presented age 6, poor balance + bumping into things + deformed feet; parents 2nd-degree cousins, maternal relatives wheelchair-bound died in 30s
Bilateral pes cavus + hammer toes; dysarthric cerebellar speech; glove-and-stocking hypothesia + reduced vibration/joint-position LL
Globally reduced tone + mild scoliosis; power proximal 5/5 distal 3/5; areflexia + positive Babinski; dysdiadochokinesia/dysmetria/intention tremor; high-steppage gait
<5yr from onset: progressive gait ataxia, LL areflexia, extensor plantar
>5yr: pyramidal leg weakness, ↓vibration/joint-position LL, dysarthria, generalized areflexia
>50%: scoliosis + cardiomyopathy. <50%: optic atrophy, nystagmus, deafness (10%), distal weakness, DM (10%), pes cavus

Inves

Exclude Wilson's: serum ceruloplasmin / 24h urine copper / KF rings
NCS (sensory axonal polyneuropathy); vitamin E level (normal); VEP (normal); central motor conduction (pyramidal dysfunction)
CT/MRI brain (NAD); MRI cervical cord (atrophic); DNA testing → GAA trinucleotide expansion

Mng

Supportive (physio); speech/language therapy; avoid recumbency complications (DVT, bed sores); treat cardiac failure

Special

GAA trinucleotide expansion; areflexia WITH extensor plantar; pes cavus + hammer toes; dorsal column (worse cervical) + spinocerebellar degeneration, DRG loss

Parkinson's disease

C/P

Case 2: 52M resting tremor R middle 3 fingers worse with stress; hypomimia + infrequent blinking; micrographia; reduced arm swing; difficulty turning in bed
Flexed posture, sialorrhea, monotonous speech, lead-pipe rigidity, power 4/5, Myerson's sign (glabellar reflex fails to habituate), shuffling gait
Pathology: degeneration of substantia nigra pars compacta → ↓dopamine

Inves

Exclude secondary: levodopa challenge, MRI brain, PET/SPECT (dopamine terminal dysfunction)

Mng

Anticholinergics (SE cognitive decline in elderly); dopamine agonist; L-dopa (cumulative SE); amantadine (NMDA antagonist for postural symptoms/bradykinesia)

Special

Myerson's sign (glabellar reflex fails to habituate); lead-pipe rigidity; substantia nigra pars compacta degeneration

Huntington's disease (chorea)

C/P

Case 3: 47F involuntary uncontrollable movements (hands/legs/head); difficulty speech/holding/swallowing/chewing; unable to stand/walk unsupported + mild behavioural change
Started 4yr ago neck twitching → jerky limb movements, progressive; father died age 48 similar
Personality change, depressive mood, slow thought; slow saccades (III/IV/VI), unable to open jaw (V), abnormal tongue (XII); rigidity + spasticity; power 3/5; brisk reflexes; wide-based swaying/staggering (marionette) gait
Pathology: atrophy of caudate + putamen

Inves

Genetic testing: expanded CAG repeats on huntingtin gene (>40 = clinical HD)
MRI caudate atrophy; PET ↓basal-ganglia metabolism

Mng

Special

CAG repeats >40; caudate + putamen atrophy; marionette gait; AD anticipation (father died age 48)

Primary idiopathic generalized dystonia

C/P

Case 4: 24F spasm L leg muscles since age 6, age 12 both LL, now includes trunk; father had neck spasms age 30 that self-resolved
Neurologically free aside from spasms both LL + trunk
Started focal → generalized (generalization in 80% of early-onset dystonia)
Pathology: abnormal basal-ganglia circuitry → imbalance direct/indirect pathways → loss cortical inhibition; loss of motor-inhibition (spinal/brainstem/cortical) → co-contraction agonist + antagonist

Inves

Mng

Special

Co-contraction of agonist + antagonist; generalization in 80% early-onset

Optic neuritis

C/P

Case 1: 31F pain + visual loss R eye (grey/blurred, worse over 2 days, painful on eye movement, washed-out colours); R eye VA 6/60, scotoma, swollen disc; L normal

Inves

MRI brain + cervical spine w contrast; MRI optic nerve; VEP; CSF

Mng

IV methylprednisolone first line (0.5–1g daily, 3–5 days); 2nd line IVIG / plasmapheresis

Special

Painful visual loss + washed-out colours; swollen disc

Multiple sclerosis (CIS / RRMS / SPMS / PPMS)

C/P

CIS: Case 1 at 3mo — vision normal, blurs in hot bath (Uhthoff phenomenon, not true relapse), R disc pale; MRI few lesions no enhancement; CSF negative OCBs → Clinically isolated syndrome (DIS, no DIT)
RRMS: Case 1 — 3yr later numbness + paraesthesia R then L leg over days, difficulty feeling floor, ~3wk then improved over 2mo → RRMS. Case 2 — numbness + weakness both legs over 4 days (walk ~10m) + urinary urgency/frequency, then 18mo later vertigo/imbalance/diplopia (brainstem/cerebellar), walking 'drunk'
SPMS: Case 3 — presented 30yr ago LL weakness, remained well, then dragging leg + numb/tingling feet + urinary urgency; pale fundi, broken pursuit, ankle clonus, brisk reflexes + extensor plantars, loss of vibration to knees → SPMS (mild)
PPMS: Case 4 — numbness L foot + hand 10yr ago, scuffing toes, gradual worsening over 2yr, then crutches + leg spasms + urge incontinence + constipation + choking + slurred speech + forgetful (bulbar); wheelchair outdoors → PPMS. DDx cord compression, other myelopathy (B12), rare (PLS, MSA, HSP)
Uhthoff phenomenon: heat-worsened (hot bath) blurring, not a true relapse

Inves

MRI: periventricular WM lesions + cord lesion
LP: oligoclonal bands in CSF not serum (intrathecal synthesis); Case 2 — 8 lymphocytes, normal glucose/protein; ANA + ACE normal (exclude sarcoidosis)
PPMS CSF: normal cells, protein slightly high, glucose normal; OCBs in CSF fewer in serum; SSEP delay
VEP

Mng

Relapse: IV methylprednisolone 1g/day ×3 OR PO 500mg/day ×5; exclude infection (mimics relapse); reserve for disabling relapses (SE osteoporosis, avascular necrosis, sleep/mood)
DMT: beta-interferon or Copaxone; Avonex (IM once-weekly beta-interferon 1a); beta-interferon considered if further attack within 2yr
Escalate Natalizumab (Tysabri): indications = 2 disabling relapses/year, disabling relapse on beta-interferon, MRI activity (Gad enhancement / new lesions 3mo apart); humanized mAb blocks α4-integrin (VLA4) → prevents VCAM-1 binding → stops migration; monthly IV; rare PML (JC virus)
Poor course predictors → high-efficacy DMD (natalizumab, fingolimod, ocrelizumab) or induction (alemtuzumab); PPMS with activity → ocrelizumab; PPMS otherwise no DMT benefit
Symptomatic: spasticity — baclofen/tizanidine/clonazepam, botox/intrathecal phenol/intrathecal baclofen pump; bladder — oxybutynin if residual <100ml, ISC/SPC, catheters; pain — gabapentin/pregabalin/amitriptyline; paroxysmal tonic spasms — carbamazepine; fatigue — amantadine/modafinil (Case 2: residual urinary → oxybutynin, fatigue → modafinil)

Special

Uhthoff phenomenon (heat-worsened vision, NOT a relapse); oligoclonal bands in CSF not serum (intrathecal synthesis); PML on natalizumab (JC virus, ~25% mortality)

Vasovagal / neurocardiogenic syncope

C/P

Case 1: 18F past febrile convulsion, recurrent LOC + collapse; precipitants hot day/dehydrated, standing; prodrome vision/hearing/paraesthesia/clammy/nausea; no chest pain/palpitations/seizure markers
Syncope features: circumstances, pallor, hot/sweaty, nausea ± vomiting, change in vision/hearing, long onset, floppy dead weight
Syncope = transient loss of awareness from cerebral hypoperfusion; 50% experience an episode of transient LOC; vasovagal commoner in adolescence; cardiac in elderly (annual incidence 6%, recurrence 30%)
Myoclonic jerks common in syncope (multifocal, non-rhythmic)

Inves

Reflex/vasovagal → tilt-table
Structural heart disease (aortic stenosis, cardiomyopathy, RV dysplasia) → ECHO; arrhythmia (VT, Brugada, long-QT, AV block) → ECG routine/prolonged

Mng

Special

Prodrome + floppy dead weight; multifocal non-rhythmic myoclonic jerks

Reflex anoxic event

C/P

May sound syncopal but seizure-like features (shaking, twitching, stiffening); usually brief; may occur if kept upright

Inves

Mng

Special

Dissociative (non-epileptic) seizures / NEAD

C/P

Case 2: 25F no antecedent hx, recurrent LOC + collapse, PMH asthma; attacks no warning, sudden collapse, no precipitants, 5–15 min, tongue biting/incontinence/carpet burns/injuries, mild psychiatric co-morbidity

Inves

EEG/MRI/ECG unremarkable; captured on mobile-phone recording/VT

Mng

Special

Tongue-tip bite / carpet burns; alpha on EEG (unresponsive); wax-and-wane flailing/thrashing/pelvic thrusting

Epilepsy (simple partial seizures)

C/P

Case 4: 18M recurrent limb jerking during sleep + wakefulness, precipitated by sleep deprivation, unilateral + mouth involved
Case 5: 40M recurrent limb jerking during sleep with some recollection, precipitated by sleep deprivation (same category)

Inves

Mng

Special

Unilateral jerking with retained awareness; sleep-deprivation precipitant

Sleep disorders

C/P

Case 3: 50F recurrent LOC + collapse, PMH migraine, prior sleep studies, blank spells lasting seconds, no witness
Excessive daytime somnolence (OSA, narcolepsy); parasomnias — NREM sleepwalking, REM behaviour disorder; cataplexy

Inves

Mng

Special

Ischaemic stroke

C/P

Case 1 (Amir): 62M diabetic + hypertensive, 2h slurred speech + R hemiplegia; BP 180/90, CBG 340; mild dysarthria, R hemiplegia, R UMN facial palsy, R hemihypothesia

Inves

CT brain to exclude haemorrhagic infarction; hyperdense MCA sign → MCA occlusion

Mng

Lower BP + IV tPA if no contraindications; mechanical thrombectomy (MCA occlusion)

Special

Hyperdense MCA sign → MCA occlusion

TIA

C/P

Case 3: 75M, 2 episodes — sudden L-eye blindness (curtain, 3 min) then R weakness + difficulty talking 2h; HTN, DM, smoker
Case 3(b) (Samira): 40F diabetic + CKD, L weakness + numbness since day before, twice before (3mo + 1mo, same side, resolved in hours); BP 180/90, HR 50, L VII UMN + L hemiparesis grade 3

Inves

MRI brain (confirm); HbA1c, lipid profile, cardiac echo, carotid duplex

Mng

Antiplatelets, statins, lifestyle modification, diabetic control

Special

Amaurosis fugax (curtain-like transient monocular blindness)

Intracerebral haemorrhage

C/P

Case 4 (Ahmed): 60M acute deteriorating GCS, severe headache + vomited twice + generalized shaking 2 min; BP 250/100; global aphasia, R hemiplegia, hemineglect, forced gaze to left
DDx: intracerebral haemorrhage, ischaemic stroke, status epilepticus
2 days later fever + basal crepitations → aspiration pneumonia

Inves

CT brain

Mng

Special

Forced gaze to left + BP 250/100

Subarachnoid haemorrhage

C/P

Case 5 (Amira): 20F sudden severe headache after sneezing → collapse, photophobia, double vision, drowsy but conscious; BP 180/90

Inves

CT brain + CT angiography head/neck; daily transcranial Doppler for intracranial vasospasm

Mng

Coiling of aneurysm + Ca-channel blockers

Special

Thunderclap headache after sneezing; vasospasm monitored by transcranial Doppler

Stroke from infective endocarditis

C/P

Case 2 (Ahmed): 59M hypertensive, mitral valve replacement on warfarin; difficulty speaking + unsteady gait, wants blanket + myalgia; temp 38, BP 190/80

Inves

MRI brain; CBC, coagulation profile, blood cultures; confirm ECHO + blood cultures

Mng

Special

Prosthetic valve + fever → embolic (IE) source of stroke

Endocrinology & Nephrology

21 entries

Normal reference ranges (source)

TSH 0.5-5 U/mL; T4 total 5-12 g/dL, free 0.9-2.4 ng/dl · albumin 3.5-5.5 g/dL (35-55 g/L); total Ca 9-10.5 mg/dL (2.2-2.6 mmol/L) · serum creatinine 60-110 µmol/L (0.7-1.2 mg/dl) men, 45-90 (0.5-1.0) women; urea 7-20 mg/dl.

Corrected calcium formulas

mg/dl: corrected Ca = serum Ca + 0.8×(4 − albumin g/dl); e.g. Ca 7, alb 2.6 → 8.12
mmol/L: corrected Ca = Ca + 0.02×(40 − albumin g/L); e.g. Ca 2.0, alb 30 → 2.2
worked: alb 26 + Ca 2.0 → 2.28 mmol/L; alb 50 + Ca 3.2 → 3 mmol/L; alb 2.5 + Ca 6.5 mg/dL → 7.7 mg/dL

Whipple triad (hypoglycaemia dx)

hypoglycaemia symptoms + plasma glucose <70 mg/dl + resolution after glucose raised.

Hypoglycaemia severity levels

L1: glucose <70 & >54 · L2: <54 · L3: severe event w/ altered mental/physical status requiring assistance.

ACR TI-RADS (2017) — ultrasound risk score

sum 5 features:

Feature	Points
Composition	0–2
Echogenicity	0–3
Shape (taller-than-wide = 3)	0 / 3
Margin (extrathyroidal extension = 3)	0–3
Echogenic foci (punctate = 3)	0–3

Level	Points	Category	FNA / follow-up	Malignancy risk
TR1	0	benign	no FNA	0.3%
TR2	2	not suspicious	no FNA	1.5%
TR3	3	mildly suspicious	follow ≥1.5cm at 1/3/5y; FNA ≥2.5cm	4.8%
TR4	4–6	moderately suspicious	follow ≥1cm; FNA ≥1.5cm	9.1%
TR5	≥7	highly suspicious	follow ≥0.5cm annually ×5y; FNA ≥1cm	35%

Which nodule to evaluate for malignancy

palpable solitary >1cm in euthyroid; MNG dominant nodule >1.5-2cm (largest or recent significant growth); incidentaloma = focal FDG-PET uptake (33.2% proved carcinoma).

FNA cytology classification → management

benign macrofollicular → clinical follow-up
malignant (papillary/follicular/oncocytic-Hurthle/anaplastic/medullary/thyroid lymphoma) → surgical mng
microfollicular = follicular neoplasm → hemithyroidectomy (lobectomy)
inadequate material → repeat FNA

FNA–histology correlation

benign macrofollicular ~70% → >97% benign; malignant ~5% → >97% malignant; microfollicular (suspicious) ~20% → 10-20% malignant; repeated inadequate ~5% (risk = initial nodule risk).

Thyroid malignancy histology distribution

epithelial: papillary 80%, follicular 15%, poorly differentiated <1%, anaplastic <2%; non-epithelial: medullary <5%, primary thyroid lymphoma, metastatic (renal/breast/lung/colon/melanoma).

Well-differentiated thyroid ca — operative recommendations by size

<1cm, no extrathyroidal extension, no apparent LN → thyroid lobectomy + isthmusectomy
1-4cm, no extension, no apparent LN → total thyroidectomy OR lobectomy + isthmusectomy
>4cm → total thyroidectomy + central LN dissection
any size w/ extrathyroidal extension + clinically apparent LN → total thyroidectomy + central LN dissection

Medullary thyroid ca — calcitonin cutoffs

>100 pg/l = 100% PPV for MTC; >400 pg/l suspect distant mets.

AKI phases

1. Onset — ↓renal blood flow, UOP <0.5 mL/kg/h, no change in creatinine/electrolytes/acid-base

2. Oliguric/anuric — ↓kidney oxygenation, oliguria <400 mL/d or anuria <100 mL/d, fluid overload/oedema, ↑BUN, ↑serum K, metabolic acidosis

3. Diuretic — UOP >400 mL/d, near-normal creatinine, possible electrolyte depletion, acid-base near normal

4. Recovery — normal, full renal recovery (may leave tubule scarring/oedema)

AKI staging (creatinine relative rise from baseline OR urine output)

Stage	Creatinine	Urine output
1	×1.5	6h <0.5 mL/kg/h
2	×2	—
3	×3	12h <0.5 mL/kg/h OR 24h <0.3 mL/kg/h OR 12h anuria

Oliguria classification

prerenal (severe dehydration, kidney reacting effectively, not failure unless progresses to hypovolaemic shock); post-renal (ureteric obstruction, can progress to back-pressure damage).

AKI (oliguric) chemistry

serum Na + HCO3 low; urea/creatinine/K high; phosphate/urate/Mg high; urine Na >20 mmol/L; urinary urea <500 mmol/L. Polyuric phase: urea/creatinine returning to normal, Na + K lost in urine (replace losses).

CKD stages by eGFR

Stage	eGFR (mL/min/1.73m²)	Description
1	>90	normal / minimal damage
2	60-89	mild
3	30-59	moderate (3a from Task = 30-59 range)
4	15-29	severe
5	<15	kidney failure

normal eGFR >90; progression = decline >5 mL/min/1.73m² within 1 year
eGFR uses 4 variables: serum creatinine, age, sex, race; not valid <18y, ARF, pregnancy, oedematous, muscle wasting, amputees, malnourished

GFR estimation formulas

Cockcroft-Gault: CrCl = (140−age)×wt(kg)×1.23 / (serum creatinine µmol/l), ×0.85 for women (unreliable if unstable renal function, very obese, or oedematous)
Creatinine clearance (ml/min) = (urinary creatinine × urine volume) / (plasma creatinine × collection period)

Proteinuria / albuminuria thresholds

proteinuria >150 mg/24h abnormal (>500 mg/24h → treat); dipstick 1+ = 200-300 mg/L; detects albumin, insensitive to Bence-Jones
albuminuria/ACR: microalbuminuria ACR 3.5 mg/mmol (F) / 2.5 (M) or 30-300 mg/g; moderately increased 30-300 mg/g; severely increased >300 mg/g; two positive tests over 3+ months = principal marker of kidney damage; clinically significant non-diabetic ACR >30 mg/mmol, diabetics >3 mg/mmol

Nephrotic syndrome definition

proteinuria >3.5 g/24h + hypoalbuminaemia + oedema.

Renal tubular acidosis types

Type 1 distal — fails to maintain H⁺ gradient (autoimmune or hypercalcaemia)
Type 2 proximal — bicarbonate leak (Fanconi)
Type 4 — hyporeninaemic hypoaldosteronism (diabetic nephropathy)

TSAT

transferrin saturation = iron/TIBC ×100 (e.g. 20/450 = 4%).

Haematology

12 entries

Coagulation — three complexes

Extrinsic Xase (tenase): VIIa + TF + PL + Ca → Xa — initiation phase (small amount can't make fibrin but activates V, VIII, platelets, XI)
Intrinsic Xase (tenase): IXa + VIIIa + PL + Ca → Xa — amplification phase
Prothrombinase: Xa + Va + PL + Ca → IIa (thrombin) — thrombin burst; converts prothrombin (II) → thrombin (IIa)

Platelet plug — adhesion receptors

high shear (arterioles): subendothelial VWF via GPIb-IX-V → activates GPIIb/IIIa
low/static shear: subendothelial collagen via GPIa/IIa
aggregation: crosslinking via active GPIIb/IIIa + fibrinogen bridges
ADP (dense granules) + TXA2 = positive-feedback amplification (TXA2 also vasoconstrictor)

Pancytopenia — cytopenia thresholds

pancytopenia = reduction in all blood cells (WBC, red cells/Hb, platelets)
platelets: no significant spontaneous bleeding until <50; prophylactic transfusion when <10
neutrophils: severe infection unusual until <0.5; bacterial then fungal common with prolonged (>5 days) neutropenia <0.1

Blood-film reaction causes

leukoerythroblastic: severe infection, bone marrow infiltration
thrombocytosis: inflammation, chronic bleeding, essential thrombocythaemia

Ann Arbor staging (HL + NHL)

I: single node region (single extralymphatic = IE)
II: ≥2 node regions same side of diaphragm (± contiguous extralymphatic = IIE)
III: both sides of diaphragm (± spleen = IIIS, extralymphatic = IIIE)
IV: disseminated / extralymphatic (liver, BM)
Suffix A = absence of B symptoms; B = present (fever, night sweats, >10% weight loss)

HL vs NHL

HL: localized single axial group (cervical/mediastinal/para-aortic), orderly contiguous spread, mesenteric/Waldeyer rarely involved, extranodal uncommon
NHL: multiple peripheral nodes, non-contiguous spread, mesenteric/Waldeyer common, extranodal common

HL immunohistochemistry

classic: CD15+, CD30+, CD20−
NLPHL: CD20+, CD15−/CD30−

Reed-Sternberg cell variants

(1) classic diagnostic RS: >45µm, multilobate/mirror-image binucleate (owl-eye), eosinophilic nucleoli + eosinophilic cytoplasm
(2) mononuclear: single nucleus + inclusion-like nucleolus — classic HL
(3) lacunar: folded nucleus in retracted-cytoplasm lacune — nodular sclerosis
(4) L&H / popcorn — NLPHL

Lymphoma split

NHL 90% (B-cell 80–85%, T-cell 15–20%); Hodgkin 10% (classic + NLPHL)

NHL grades (REAL/WHO)

low: small lymphocytic/CLL, follicular, marginal (incl MALT), mantle cell
high: diffuse large B-cell, anaplastic large cell, peripheral T-cell
very high (CNS-dissemination risk): lymphoblastic, Burkitt's

NHL WHO classes

B-cell (85%), null/stem, T-cell (15%); precursor (immature) vs peripheral (mature)
B-cell: precursor B-ALL; peripheral SLL/CLL, follicular, mantle zone, marginal zone, Burkitt, DLBCL
T-cell: precursor T-ALL; peripheral anaplastic large cell, mycosis fungoides/Sézary, peripheral T-cell

Immunophenotype markers (lineage)

CD45/LCA +ve in lymphoid cells (node CD45− = metastasis; extranodal CD45+ = lymphoma)
CD3 = T marker; CD20 = B marker
CD3+/CD20+ = reactive hyperplasia; CD3+/CD20− = T-cell lymphoma; CD3−/CD20+ = B-cell lymphoma
TdT +ve in 95% of ALL / lymphoblasts
T-cell markers: earliest CD7, most specific CD3
B-cell markers: early pre-B-ALL CD19/CD10/TdT; mature B-ALL CD10±/CD19/CD20/CD22/surface IgM
CLL immunophenotype: CD5/19/23 + light-chain restriction + BM infiltration

Neurology

6 entries

CSF findings — Normal / Viral / Bacterial / Fungal

([149], as printed)

	Normal	Viral	Bacterial	Fungal
Opening pressure	<20 cm	Normal or increased	Raised	Raised
Colour	clear	clear	turbid	turbid/clear
Cells/mm³	<5	Normal–1000	>1000	Normal or raised up to 1000
Predominant WBC	lymphocytes	lymphocytes	PMN	lymphocytes
CSF/plasma glucose ratio	<66%	Normal	Low	Normal/low
Protein g/l	<0.5	Normal (0.5–1)	>1	N or (0.2–5)

MS dissemination (DIS/DIT), as referenced

([049], only as framed — no full McDonald table printed)

CIS = DIS (dissemination in space), no DIT (dissemination in time)
RRMS diagnosed when additional lesion appears on repeat imaging (adds DIT)

Dystonia classification

([041])

Age: early-onset / adult-onset
Distribution: focal = 1 region; segmental = ≥2 contiguous; hemidystonia = whole side; multifocal = ≥2 non-contiguous; generalized = trunk + 2 other parts
Etiology: primary isolated / dystonia-plus / secondary

Fits/faints/funny turns — DDx by system

([044])

Head: seizures, migraine, TIA, transient global amnesia, narcolepsy (rare — colloid cyst of 3rd ventricle)
Heart: syncope, reflex anoxic event, arrhythmia, structural (valvular), muscle, hypotension
Metabolic: hypoglycaemia, hyponatraemia, hypokalaemia, hypomagnesaemia
Psychological: panic attacks, hyperventilation, dissociative attacks
Sleep: hypnic jerks, parasomnia, narcolepsy, obstructive sleep apnoea

Syncope vs GTCS

([044], as printed)

Feature	Syncope	GTCS
Duration	usually <30s	1–2 min
Precipitant	50%	None
Falls	flaccid/stiff	tonic
Jerking	20–80%	always
Hypersalivation	none	common
Incontinence	quite common	common
Tongue bite	rare	common
Post-ictal confusion	<30s	2–30 min

Epilepsy vs NEAD

([044], as printed)

Feature	Epilepsy	NEAD
Precipitant	rare	common (emotion/stress)
Onset	rapid	gradual
Aura	various	panic/altered mental state
Consciousness	complete/incomplete	unresponsive (alpha on EEG)
Movement	tonic/clonic/automatisms	flailing/thrashing/pelvic thrusting/wax-and-wane
Injury	tongue bite + fall	tongue-tip bite/carpet burns
Duration	few minutes	often prolonged/variable recovery