StudyFix ICC-1 Disease Index
Deck-derived triage sheet — Psychiatry · Toxicology · Tropical Medicine · Ophthalmology
Disease Index
Criteria & Scores
C/P
Obsessions: intrusive, repetitive thoughts / images / impulses → anxiety
Common themes: contamination, harm to family, job loss, being a bad person
Compulsions: ritualistic washing / checking / ordering; mental acts (praying, counting)
Cycle: Obsessions → Anxiety → Compulsions → Relief
Insight preserved (thoughts recognised as own)
Inves
Clinical diagnosis (ICD-11 / DSM-5)
Mng
3 pillars: psycho-education + psychotherapy + medication
1st-line meds: SSRIs (e.g. Sertraline)
2nd-line: Clomipramine (TCA)
Psychotherapy: CBT (1st), MCT, MBT, psychodynamic
Time threshold: >1h/day OR significant distress/impairment
Special
Hyperactive CSTC loop (cortico-striato-thalamo-cortical) — DLPFC ↔ striatum
Orbitofronto-striatal hyperactivity drives compulsivity
Caudate / OFC / anterior cingulate implicated
Serotonergic pathway dysregulation
PANDAS (immunological, paediatric)
5-7× risk if first-degree relative; 80% concordance in identical twins
C/P
Trigger: extremely threatening / horrific event
Emotional: sadness, anxiety, anger, despair
Somatic: daze, confusion
Cognitive: amnesia, depersonalisation, derealisation, stupor
Behavioural: overactivity, inactivity, social withdrawal
Autonomic: tachycardia, sweating, flushing
Onset hours-days; subsides within days of removal from situation
Inves
Clinical; rule out physical cause
Mng
Social support + information (1st-line)
Psychoeducation, normalisation, practical support
Little evidence for routine medication
NOT CBT acutely; NOT benzodiazepines
Special
NOT a mental disorder in ICD-11 — listed as reason for clinical encounter
C/P
DSM-5 only
Symptom categories: intrusion + negative mood + dissociation + avoidance + arousal
Exposure: directly experienced / witnessed / learned of close family / repeated extreme
Inves
Clinical (DSM-5 criteria)
Mng
Psychoeducation + practical support
Trauma-focused CBT if persistent
Special
Duration 3 days to 1 month after trauma; beyond 1 month → PTSD
C/P
Maladaptive reaction to identifiable psychosocial stressor
Preoccupation with stressor, excessive worry, rumination, recurrent distressing thoughts
Significant impairment in functioning
Mng
Address the stressor
Psychological support
Special
Onset within 1 month of stressor; resolves within 6 months of stressor ending
C/P
4 core clusters: intrusion + persistent avoidance + negative alterations in cognition/mood + alterations in arousal/reactivity
Intrusion: flashbacks, distressing memories, recurrent dreams
Arousal: hypervigilance, exaggerated startle, sleep disturbance, poor concentration
Negative cognition: guilt, detachment, impaired memory
Co-morbidities: substance misuse, affective + anxiety disorders, somatisation, violence
Lifetime prevalence 7.8% (F > M)
Mng
Psychological: CBT, EMDR, psychodynamic, hypnotherapy
Pharmacological: SSRIs (1st-line)
Special
Duration >1 month required
Biological signature: ↑ catecholamines + low cortisol (hypersuppression of HPA)
Loss of function predicts PTSD better than physical injury severity
Intentional harm + harm to children = high-risk stressors
C/P
Subjectively unpleasant inner restlessness + compulsion to move
Foot stamping, leg crossing/uncrossing, rocking, pacing
Prevalence ~25%
Less common with atypical antipsychotics
Weakly linked with suicide
Inves
Clinical (recognise drug history)
Mng
Reduce / change antipsychotic
Propranolol
Clonazepam
5-HT2 antagonists (e.g. mirtazapine)
Special
Side-effect of antipsychotic medication (organic risk factor for disturbed behaviour)
C/P
Contraction of muscles to maximum limits
Oculogyric crisis (eyes rolling upwards)
Torticollis (head/neck twisted)
Unable to speak / swallow
Back arching; jaw dislocation (extreme)
Prevalence 10%
Mng
Oral / IM procyclidine (anticholinergic)
Special
Risk: young neuroleptic-naïve males; high-potency drugs (e.g. haloperidol)
C/P
Tetrad: fever + muscular rigidity + altered mental status + autonomic dysfunction
Incidence 0.1%; mortality 5-10%
Mortality causes: respiratory failure, CV collapse, myoglobinuric renal failure, arrhythmias / DIC
Inves
Massively elevated CK (↑↑CK)
Leukocytosis
Altered LFTs
Mng
Stop causative agent
Supportive: O&sub2;, rehydration, cooling
Reduce rigidity: bromocriptine + dantrolene
Sedation: benzodiazepines
Supported ventilation if needed
Wait ≥5 days before cautious re-start with structurally unrelated antipsychotic
Special
Pathophys: dopamine antagonism + impaired Ca²⁺ mobilisation in muscle + SNS dysfunction
Rare but potentially life-threatening effect of all antipsychotics
C/P
Heroin = mu-receptor agonist; smoked / snorted / injected
Sedative + analgesic
Physical dependence
Withdrawal: sweaty, tremor, muscle aches/jerks, abdominal cramps, diarrhoea, piloerection, dilated pupils, runny nose, yawning, nausea
Inves
Urine drug screen (opiates / methadone)
COWS (Clinical Opiate Withdrawal Scale)
Verify community scripts with treatment agency + pharmacy
Screen Hep B / Hep C / HIV
Mng
A&E: symptomatic — diazepam, loperamide, buscopan (no methadone in A&E)
AMU: methadone substitution per local protocol
Methadone protocol: 10 mg up to QDS, max 40 mg in first 24h (titration)
Naloxone if overdose (short half-life → observation)
Discharge: link to local drug service early
Always write "OMIT IF SEDATED OR INTOXICATED"
Avoid doses after 18:00; oral solution 1mg/ml only
Special
Co-ingestion with benzos / alcohol = poly-drug overdose risk
Fatal respiratory depression possible at ≥30 mg methadone in non-tolerant individuals
C/P
GBL = gamma-butyrolactone; GHB = gamma-hydroxybutyric acid
Liquid; weak action at GABA-B receptors
Sedative effects
Severe respiratory depression with alcohol
Short half-life → intoxication rapidly progresses to withdrawal
Withdrawal: anxiety → confusion / agitation, tremor, cramps, insomnia, combativeness, delirium, delusions, paranoia + hallucinations (auditory/tactile/visual), tachycardia, hypotension
Mng
Withdrawal: benzodiazepines + baclofen
May need ITU admission
Special
Repeated use → physical dependence
Benzodiazepine withdrawal: anxiety, depersonalisation/derealisation, light/sound sensitivity, fits → diazepam detoxification
C/P
Stimulant — affects dopamine
Binge pattern of use
High-dose complications: fits, hypertension, ischaemia (MI / ischaemic stroke / intestinal infarction), rhabdomyolysis
Inves
Urine drug screen
ECG, troponin if chest pain
Mng
Supportive
Benzodiazepines for agitation
Avoid β-blockers (unopposed α effect)
Special
Hallucinogens (e.g. LSD) → acute psychotic symptoms
C/P
BAC <0.06: mild euphoria, ↓ concentration
BAC 0.06-0.09: disinhibition, ↓ reasoning / depth perception (UK drive limit 0.08)
BAC 0.10-0.19: emotional lability, slurred speech, gross motor impairment
BAC 0.20-0.29: stupor, memory blackout, severe motor impairment
BAC 0.30-0.49: severe CNS depression, ↓ HR / breathing / bladder
BAC >0.50: poisoning, death
Chronic GI/liver: gastritis, alcoholic hepatitis, fatty liver → fibrosis → cirrhosis → decompensated cirrhosis, oesophageal varices, encephalopathy
Chronic CNS: dementia, peripheral neuropathy, mood/personality changes
Withdrawal: sweating, tremor, tachycardia, anxiety, N&V, seizures
Drink-drive limit UK: 80 mg/100 mL blood; 35 µg/100 mL breath
Inves
FBC, U&Es, LFTs, GGT, amylase, clotting
SADQ score (mild <16 / moderate 16-30 / severe >30)
AUDIT / AUDIT-C / FAST / PAT / CAGE screening
Deranged LFTs: raised GGT + ALP, raised bilirubin
Mng
A&E: ABCDE, check blood sugar, IV fluids; airway protection (vomit aspiration risk)
AMU detox: chlordiazepoxide reducing regimen (per SADQ)
Thiamine: 100 mg PO TDS; Pabrinex I + II IM/IV for 3-5 days
DTs: haloperidol 5-10 mg PO or 5 mg IM (max 30 mg/24h PO, 18 mg/24h IM)
Seizures: diazepam 10 mg PR
Primary care: brief intervention, AA/NA referral, shared care
Discharge planning early; refer to local drug & alcohol service
Special
3rd biggest lifestyle risk factor for disease / death in UK (after smoking + obesity)
Alcohol dependence criteria (ICD): ≥3 of 6 features over past year
Alcoholic hallucinosis = chronic psychiatric effect
Fetal alcohol syndrome: small head, brain damage, retarded growth/development
C/P
Triad: disorientation + visual hallucinations + signs of alcohol withdrawal
Clouding of consciousness, amnesia for recent events
Tactile / auditory / visual hallucinations
Severe: fear, paranoid delusions, sudden cardiovascular collapse
Mortality 5-10%
Inves
Clinical
ABG, electrolytes, glucose
Mng
Medical emergency
Benzodiazepines (chlordiazepoxide)
Haloperidol 5-10 mg PO or 5 mg IM (lower in elderly)
IV thiamine (Pabrinex)
Correct hypoglycaemia + magnesium
Special
Also occurs in benzodiazepine and cocaine withdrawal
C/P
Classic triad + 1: ophthalmoplegia + nystagmus + ataxia + confusion
Caused by thiamine (B1) deficiency
Petechial haemorrhages in brain stem
Inves
Clinical
Check magnesium, glucose
Mng
IV thiamine (medical emergency)
Correct magnesium deficiency + hypoglycaemia
Special
Untreated → Korsakoff's syndrome (irreversible)
C/P
Loss of short-term memory (cannot register / recall new information)
Sequellae of untreated Wernicke's
Mng
IV thiamine
Supportive (deficit largely irreversible)
Special
Caused by thiamine deficiency
C/P
Toxic dose ≥150-250 mg/kg single dose
Stage I (0-24h): asymptomatic / non-specific symptoms; LFTs normal
Stage II (24-72h): AST elevation precedes overt dysfunction
Stage III (72-96h): maximal hepatotoxicity → encephalopathy, coma, haemorrhage, cerebral oedema, ARF, pancreatitis
Stage IV (up to 3 wk): recovery with complete hepatic regeneration in survivors
Inves
Serum paracetamol level (validated prognostic indicator)
Serum AST + ALT
Arterial pH + lactate
PT / INR, U&Es, glucose, serum salicylate
Abnormalities of PT, bilirubin, glucose, lactate, pH > aminotransferases for prognosis (predict need for transplant)
Mng
<1h ingestion: activated charcoal 50g
IV N-acetylcysteine (NAC) — glutathione precursor / substitute
NAC nearly 100% hepatoprotective if within 8h
Indications: toxic dose history / staggered dose / above Rumack-Matthews treatment line / hepatotoxicity / high risk
Special
Mechanism: CYP450 minor pathway → NAPQI → glutathione depletion → hepatotoxicity
Risk factors: alcohol, chronic liver disease, malnutrition, old age, CYP-inducing drugs (carbamazepine, phenytoin)
Rumack-Matthews nomogram: starts at 4h, applied if entire ingestion within 4h
C/P
CNS early: restlessness, agitation, seizures → late: coma
Anticholinergic: dry skin, dilated pupil, sinus tachycardia, urinary retention, ↓ bowel movement, constipation, hyperthermia
CVS: sinus tachycardia, prolonged QT, dysrhythmias, hypotension
Inves
ECG: QRS >100 ms = sensitive indicator of toxicity
Continuous cardiac monitoring
Mng
Emergency measures (ABCD)
Continuous cardiac monitoring
Gastric lavage useful even after several hours (anticholinergic delays gastric emptying)
MDAC (enterohepatic circulation)
Serum alkalinisation: indications = conduction defects, dysrhythmias, hypotension, acidosis correction
Alkalinisation threshold: QRS >100 ms
Special
Mechanism: ↓ reuptake of NE + 5-HT; blocks muscarinic (anticholinergic), H1 (sedation), α1 (orthostatic hypotension)
Direct quinidine-like → conduction defects, dysrhythmias
Antidote: sodium bicarbonate
C/P
N&V, gastric irritation
Hyperventilation / acute lung injury
Tinnitus, reversible hearing loss
Acid-base disturbances, hypokalaemia, hypocalcaemia, hypo-prothrombinaemia
Prerenal failure
Confusion, delirium
Terminal: cardiac arrest
Fluid loss: hypermetabolic state, tachypnoea, vomiting, fever, diuresis
Inves
Serum salicylate level (BSL)
ABG (mixed acid-base)
U&Es, glucose
Mng
Correct to euvolaemia
Gastric lavage useful even after several hours (concretions, delayed absorption)
MDAC
Urinary alkalinisation if BSL >35 mg/dL → target serum pH 7.3-7.5, urine pH 7.5-8
Cooling for hyperthermia; antacid for ulcer; vit K / blood for hypoprothrombinaemia
Haemodialysis if acute BSL >100 mg/dL OR severe acid-base / electrolyte imbalance / deterioration / renal failure / ALI / persistent CNS / coagulopathy
Special
Mechanism: uncoupling oxidative phosphorylation
Initial respiratory alkalosis (resp centre stimulation) → metabolic acidosis with compensatory resp alkalosis → severe: respiratory acidosis (CNS/resp depression)
Antidote: sodium bicarbonate
C/P
Ingestion of "packets" of drugs for smuggling (condoms / cellophane; often opiates or cocaine)
Complications: intestinal obstruction OR breakage + leak → toxidrome
Sympathomimetic (cocaine leak): sweating, hypertension, tachycardia
Inves
AXR and/or CT — multiple radio-opaque foreign bodies in GIT
Urine / plasma toxicological screen for leakage
Mng
No leak features: lactulose + observe
Leak / obstruction: surgical intervention
Special
Whole bowel irrigation is indicated for body packers / stuffers (CI in ileus, coma, convulsions unless airway protected)
C/P
Bradycardia + AV block + dysrhythmias (most frequent cardiac manifestations)
GI symptoms = first to evolve
Hyperkalaemia (early predictor of need for antidote)
Inves
Serum digoxin concentration (SDC) — measure 6h post-ingestion (therapeutic 0.6-2.1 ng/ml; >15 ng/ml = serious)
Electrolytes (K, Ca, Mg)
Renal function
ECG: bradycardia, AV block, atrial/ventricular tachydysrhythmias, nonspecific ST sagging, peaked T (if hyperK)
Mng
Emergency measures
Continuous cardiac monitoring
MDAC (enterohepatic circulation)
Digibind (digoxin immune Fab) — indications: K >5 mEq/L, SDC >10 ng/ml adults (>5 children), ingestion ≥10 mg adults (≥4 mg children), life-threatening dysrhythmias, haemodynamically significant bradycardia unresponsive to atropine, suspected toxicity with unavailable SDC
Monitor K after Fab (hypoK may occur from Na/K-ATPase reactivation)
If Fab unavailable → correct hyperK
Special
Mechanism: inhibits Na/K-ATPase → ↑ intracellular Na → reverses NCX → intracellular Ca²⁺ overload
HypoK exacerbates chronic toxicity
HyperCa, hypoMg exacerbate cardiac glycoside toxicity
C/P
Triad: sedation/coma + respiratory depression + pin-point pupil
Shallow respiration, cyanosis, low SaO&sub2;
Loud snoring / unrousable
Needle tracks
Respiratory depression → death
Inves
ABG
CXR
Consider co-ingestions (benzos, alcohol)
Mng
ABC, airway, breathing
IV access
Naloxone (opiate antagonist) — titrate; infusion if responds to initial dose
CXR
Observe (naloxone half-life shorter than most opioids → rebound coma risk)
Special
Opioid toxidrome: BP ↓, P ↓, RR ↓, T ↓, depressed mental status, pin-point pupils, ↓ peristalsis, hyporeflexia
C/P
Cholinergic crisis onset shortly after ingestion
Muscarinic (DUMBELS): diarrhoea, urination, miosis (pin-point), bradycardia/bronchospasm/bronchorrhoea, emesis, lacrimation, salivation, sweating
Nicotinic (MATCH): muscle fasciculations, adrenal medullary hyperactivity, tachycardia/arrhythmias, cramping of skeletal muscles, hypertension
CNS: vertigo, confusion, tremors, agitation, convulsions, coma
Intermediate syndrome (2-3 days): proximal limb / neck flexor / respiratory muscle paralysis (muscle fibre necrosis) — prevented by early oximes
Delayed neuropathy (2-3 weeks): mixed sensorimotor neuropathy (demyelination) — usually permanent
Cardiomyopathy
Inves
True AChE (RBC membranes)
Pseudo AChE (plasma)
ABG, electrolytes, glucose, U&Cr
ECG + cardiac monitoring
CXR (aspiration pneumonia / bronchospasm)
Mng
ABC + decontamination + continuous cardiac monitoring
Atropine 2-5 mg IV every 15 min (or double every 5-15 min) until atropinisation
Atropine endpoints: relief of bronchospasm + dryness of chest secretions (NOT HR, NOT pupil size)
Atropinisation for 1-2 days (prevent relapse)
Obidoxime (Toxogonin): 4-8 mg/kg loading → 10 mg/kg/day infusion × 3 days
Critical oxime window: first 24-48h (before enzyme aging)
Atropine overdose: cold compresses + IV fluids + benzodiazepines
Special
Mechanism: inhibits AChE → ACh accumulates at muscarinic + nicotinic + CNS
Irreversible after 24-36h ("aging")
Carbamates: reversible, shorter duration, low dermal toxicity, rarely fatal
Atropine = muscarinic antagonist only (does NOT block nicotinic)
Oximes = reactivate AChE → correct all 3 (muscarinic + nicotinic + CNS)
Anticholinergic toxidrome from atropine overshoot: warm dry pink skin + dilated non-reactive pupils + hyperthermia + tachycardia + urinary retention + ↓ bowel sounds + hallucinations
C/P
Colourless, odourless, tasteless, non-irritating ("silent killer")
Throbbing headache (reflex cerebral vasodilatation 2° hypoxia)
Minor: dizziness, nausea
Significant: cognitive impairment, ataxia, visual/auditory abnormalities, confusion/convulsions, coma
CVS: tachycardia/hypotension, arrhythmias, conduction abnormalities, angina → MI
Pulmonary: tachypnoea, pulmonary oedema (cardiogenic or non-cardiogenic)
Cherry-red skin (rare, after excessive exposure)
Rhabdomyolysis → myoglobinuria → acute renal failure
Delayed neuropsychiatric sequelae (DNS): 2-40 day lucid period → behavioural changes, learning difficulties, memory problems, psychosis, gait disturbance, parkinsonism, paralysis, chorea, peripheral neuropathy, incontinence — recovery in only 50%
Inves
Carboxyhaemoglobin level
ABG
ECG / cardiac monitoring
CXR
Mng
ABC
100% O&sub2; (decreases CO t½ from 5h to 1h)
Hyperbaric oxygen (2 atm) — decreases t½ to 20 min
HBO indications: altered mental status / confusion, COHb >25%, fetal distress in pregnancy
Cerebral oedema: prednisolone (1 mg/kg IV q4h) + mannitol 20% (1 mg/kg over 20 min)
Treat seizures, arrhythmias (antiarrhythmics), pulmonary oedema, acidosis/coma
Smoke inhalation: consider co-existing cyanide exposure
Special
CO Hb affinity 200-250× O&sub2; → leftward shift of OxyHb dissociation curve
Binds myoglobin (40-60× affinity) → cardiac depression / arrhythmias
Binds cytochrome oxidase → tissue anoxia
Displaces NO from platelet heme → vasodilatation / hypotension (correlates with neurological effects)
Fetal Hb has increased CO affinity + slow elimination + leftward fetal curve → neonates/fetuses more vulnerable
Antidote: hyperbaric oxygen
C/P
Bitter almond smell; volatile colourless liquid
Large dose: sudden death within 1-2 min
Small dose CNS: headache, anxiety, agitation, confusion, lethargy, seizures, coma
CVS: initial bradycardia + hypertension → hypotension + reflex tachycardia → terminal bradycardia/hypotension
Resp: initial tachypnoea → bradypnoea + pulmonary oedema
Cyanosis NOT apparent (red asphyxia — blood stays bright red)
Metabolic acidosis
Inves
Cyanohemoglobin level
ABG (severe metabolic acidosis with raised AG)
Mng
Care of respiration (100% O&sub2;, intubation + mechanical ventilation)
GIT decontamination
Cyanide kit: amyl nitrite + sodium nitrite + sodium thiosulfate
Reducing agents: vit C, methylene blue
Dicobalt EDTA (Kelocyanor) — chelates circulating cyanide (does NOT bind intracellular)
Hydroxycobalamin (vit B12a) — cobalt binds cyanide → cyanocobalamin (vit B12) → urine excretion
IV NaHCO&sub3; for acidosis
Special
Mechanism: blocks cytochrome oxidase (binds ferric Fe³⁺) → halts aerobic metabolism → cellular asphyxia (histotoxic anoxia)
O&sub2; arterial = O&sub2; venous (no consumption)
Sodium nitrite: induces methaemoglobinaemia → Fe³⁺ pulls cyanide from cytochrome oxidase
Thiosulfate: provides sulfur → thiocyanate (renal elimination, minimally toxic)
Causes of red asphyxia: CO poisoning, cyanide poisoning, cold exposure (hypothermia)
Antidote: cyanide kit
C/P
May have NO apparent local manifestations
Autonomic storm: agitation, hypertension, tachypnoea, generalised tremors, sweating
Delayed (~1.5h): vomiting, tachycardia, breathless, cyanosis, stupor
General/GI: dehydration, vomiting, diarrhoea, acute gastritis
CVS: hypertension, dysrhythmias, MI, acute heart failure
Pulmonary: respiratory distress, pulmonary oedema
CNS: agitation, convulsions
Metabolic: hyperkalaemia, stress hyperglycaemia, metabolic acidosis
Inves
ABG (impaired oxygenation / metabolic acidosis)
Serum electrolytes (hyperK)
RBS (hyperglycaemia)
ECG (sinus tachy or brady, arrhythmias, ischaemic changes)
CXR (pulmonary oedema)
Mng
Scorpion antivenom — ideal within first 4h (max window 24h)
Initial dose 3-5 ampoules slow IV or IM
Repeat every 30 min if progressing
Pre-administration: hypersensitivity skin test (premedicate with hydrocortisone if positive)
Treat complications (fluid, inotropes, ventilation, anticonvulsants)
Special
Egypt habitat: Cairo suburban / Upper Egypt
Pathophys: venom = potent autonomic stimulant → sudden pouring of endogenous catecholamines AND acetylcholine simultaneously → autonomic storm + cardiogenic shock
Antivenom dose same for children and adults (dose based on venom amount)
C/P
1-2 fang marks
Local: severe pain, bleeding from fang marks, oedema (whole limb), enlarged tender regional LNs, ecchymosis, blistering, skin necrosis / dry gangrene
General: anxiety (sweating, N&V, rigors, tachycardia, chest tightness), coagulopathy, bleeding, haemolysis, hypotension/shock
Myotoxicity: muscle pain/tenderness/weakness, myoglobinuria → renal failure, hyperkalaemia → arrhythmias
Inves
Coagulation profile
U&Es, CK
ECG (hyperK)
Mng
ABC priority
Polyvalent antivenom (slow IV or IV infusion) — best within 2h
Initial dose 3-5 vials; 10 additional if progressing; no absolute max
Treat hypotension, hemostatic abnormalities
Tetanus prophylaxis
Debridement of necrotic tissue
Special
Egypt habitat: most Egyptian deserts
Hemotoxic + vasculotoxic venom
First aid: rest, reassurance, immobilisation, remove constricting objects
Harmful: incision, suction, cryotherapy, electric shock
C/P
1-2 fang marks
Minimal local pain + oedema (unlike vipers)
General: anxiety, sweating, N&V, rigors, tachycardia (within hours, may delay up to 12h)
Neuromuscular: fasciculation of face/neck → paralysis of skeletal muscles whole body
Inves
Clinical
Monitor respiratory function
Mng
ABC (airway protection critical)
Polyvalent antivenom IV
Ventilatory support
Special
Egypt habitat: humid environment (around Nile Valley)
Neurotoxic (not hemotoxic)
Consciousness + sensation spared
C/P
Few (1-2) lesions, <10 cm
Sharply demarcated hypopigmented macule (ovoid / circular / serpiginous)
Elevated edges, dry scaly centre, erythematous borders
Anaesthetic lesion
Sites: face, extensor surfaces of limbs
Uninvolved: perineum, scalp, axilla (too warm)
Nerves thickened + palpable + sometimes tender
Loss of sensation, sweating (rough dry hairless skin), deformity
Palpable nerves: great auricular, common peroneal, median, ulnar
Inves
Lepromin test positive (>5 mm induration)
Skin smear: absent organisms
Skin biopsy: granulomas, giant cells, mononuclear cell infiltration of nerve bundles
PCR (most specific)
Mng
WHO Paucibacillary regimen: Dapsone 100 mg daily + Rifampicin 600 mg monthly × 6 months
Side effects: haemolysis (G6PD), allergy, hepatitis, red urine
Special
Stable form; highest cell-mediated immunity; lowest bacterial load
Non-infectious
Mucosa + internal organs NOT affected
Early nerve affection (anaesthesia)
C/P
Multiple, bilateral, symmetrical, widespread lesions
Poorly defined hypopigmented + erythematous
Macules / patches / papules / plaques / nodules
Normal sensation in lesions
Worst on cooler body parts
Leonine facies: thickened forehead, madarosis (loss of eyebrows/eyelashes), thickened earlobes, nasal septum perforation → collapse
Symmetric peripheral neuropathy — glove and stocking sensory loss
Ocular: corneal anaesthesia, keratitis, corneal ulceration, uveitis/glaucoma, irreversible blindness
Testicular: orchitis, atrophy, sterility
Hepatic: hepatitis, hepatic amyloidosis
Renal: glomerulonephritis, renal amyloidosis
Bone: osteoporosis, resorption of digits
Inves
Lepromin test NEGATIVE (no response)
Skin smear: numerous acid-fast bacilli
Skin biopsy: dense dermal infiltrates with fat-laden macrophages, paucity of lymphocytes
PCR (most specific)
Sites: ear lobes, elbows, knees, typical lesions
Mng
WHO Multibacillary regimen: Dapsone 100 mg + Clofazimine 50 mg daily; Rifampicin 600 mg + Clofazimine 300 mg monthly × 12-24 months
Side effects: red skin, ichthyosis
Post-exposure prophylaxis: single dose rifampicin → ↓ paucibacillary by 50%
Special
Stable form; lowest cell-mediated immunity; highest bacterial load
Infectious
Mucosa + internal organs affected
Late nerve affection
M. leprae doubling time 12-14 days; obligate intracellular acid-fast bacillus; not cultured in vitro; armadillo + mouse footpad reservoirs
C/P
Mid-borderline (BB): rarely seen, transient, unstable; multiple lesions of varying size/shape/distribution; skin-coloured or erythematous; "inverted saucer" / "Swiss cheese" lesions with sloping edges + punched-out centre
Borderline Tuberculoid (BT): larger, more numerous (5-20), less well-defined, less anaesthesia than TT; asymmetric; satellite lesions; asymmetric peripheral nerve involvement
Borderline Lepromatous (BL): widespread bilaterally symmetric macules / papules / nodules; sensation + hair growth normal within lesion; widespread peripheral nerve involvement
Mng
WHO classification: ≥5 skin lesions = multibacillary (BB, BL → MB regimen); BT may fall in paucibacillary (≤5 lesions → PB regimen)
Special
Unstable forms (can shift along spectrum)
C/P
Asymptomatic microfilaremia → acute adenolymphangitis (ADL) → chronic lymphoedema
ADL: sudden onset febrile painful lymphadenopathy (inguinal LNs, testis, spermatic cord); resolves in 1 week; recurrent; retrograde lymphangitis (distinguishes from bacterial)
Filarial fever: fever without adenitis
Tropical pulmonary eosinophilia (TPE): dry paroxysmal nocturnal cough, wheezing, dyspnoea, anorexia, malaise, weight loss; peripheral eosinophilia; diffuse pulmonary infiltrates on CXR
Chronic lymphoedema grades I-IV
Chyluria
Inves
Nocturnal blood smear (10pm-2am) — microfilariae
W. bancrofti: anucleate tail tip, clear end of nuclear column
B. malayi: subterminal + terminal tail nuclei
Circulating filarial antigen (CFA) — W. bancrofti only
Filarial antibodies (recombinant antigen)
PCR (research mostly)
Lymph ultrasonography: "filarial dance" sign (viable worms in continuous motion)
CXR for TPE: diffuse pulmonary infiltrates
Mng
Diethylcarbamazine (DEC) — treatment of choice
Monoinfection: DEC 6 mg/kg × 12 days
Doxycycline 200 mg/d × 6 weeks (targets Wolbachia endosymbiont)
Lymphoedema: steroids (soften + ↓ swelling), bed rest, limb elevation, compression bandages
Chyluria: low-fat high-protein diet + medium-chain triglycerides
Secondary infection prevention: hygiene, antiseptic creams, footwear, limb exercise
Surgery: hydrocele + scrotal elephantiasis; gross limb less successful (may need grafting)
Special
Causative: Wuchereria bancrofti, Brugia malayi, B. timori
Vectors: Aedes, Anopheles, Culex, Mansonia mosquitoes
Pathophys: Th2 inflammatory response (IgE + IgG4) + Wolbachia endosymbiont → lymphatic endothelial hyperplasia → fibrosis
Egypt = first Eastern Mediterranean country to eliminate as public health problem (WHO milestone March 2018)
Once fibrosis established → irreversible (DEC does not change prognosis)
C/P
Progressive inflammatory eye + skin disease
Pruritus (microfilariae migrating through skin)
Subcutaneous nodules (onchocercomas)
Lymphadenitis
Blindness due to corneal fibrosis
Alternative names: Hanging groins, Leopard skin, River blindness, Sowda
Inves
Skin snips — definitive diagnosis (microfilariae from multiple body sites)
African: gluteal + thigh
American: scapula + iliac crest
Slit-lamp: microfilariae in cornea + anterior chamber
ICT card tests for IgG4 (recombinant antigen)
Mazzotti test: oral DEC 50-100 mg → intense pruritic rash + fever + oedema if positive
DEC 10% patch test (more localised reaction)
Mng
Ivermectin 150 mcg/kg every 3 months until symptoms resolve
Nonendemic areas: doxycycline 200 mg/d × 4-6 weeks (targets Wolbachia) followed by ivermectin
Moxidectin (FDA-approved 2018, ≥12 years)
Special
Causative: Onchocerca volvulus
Vector: Black flies (Simulium damnosum / Buffalo fly)
99% in sub-Saharan Africa
2nd leading infectious cause of blindness worldwide
Adult macrofilariae in subcutaneous nodules; ovoviviparous females release L1 microfilariae
C/P
Subcutaneous swellings on extremities
Localised pain, pruritus, urticaria
Microfilaremia phase usually asymptomatic
Calabar swellings (local hypersensitivity reaction — named after Nigerian city)
Migrating worm visible in subconjunctival + subcutaneous tissues
Inves
Diurnal blood smear (10am-2pm)
Adult worm in subcutaneous / conjunctiva
Serology for travellers to endemic areas
Mng
DEC is primary treatment
Mandatory microfilarial count before therapy (threshold 2500/mL)
Low count: DEC 8-10 mg/kg/d × 21 days
High count + symptomatic: pre-treat with albendazole 200 mg bid × 3 weeks → then DEC
Apheresis to lower counts pre-DEC
Special
Causative: Loa loa
Risk of severe encephalopathy with DEC if high microfilarial load
Diurnal periodicity (unlike W. bancrofti nocturnal)
Particular concern for MDA programmes for lymphatic filariasis in co-endemic regions
C/P
NPDR (Stage I): microaneurysms, retinal haemorrhages (dot and blot), hard exudates
Severe NPDR (Stage II): cotton wool spots (nerve fibre layer infarcts), venous beading, IRMA (intraretinal micro-vascular abnormalities), deep haemorrhages
Proliferative DR (Stage III): neovascularisation on disc (NVD) + elsewhere (NVE), fibro-vascular proliferation
Advanced eye disease: vitreous haemorrhage, tractional retinal detachment, neovascular glaucoma
Inves
Fundus examination
Fluorescein angiography
OCT
Mng
Strict blood glucose control (primary systemic)
Mild NPDR: observation + treat macular oedema
Severe NPDR: pan-retinal photocoagulation (PRP) laser
PDR: PRP
Advanced: vitrectomy + endolaser
Anti-VEGF (e.g. intravitreal Lucentis) for diabetic oedema → protects wall integrity, ↓ leakage
PRP side-effects: loss of peripheral vision, ↓ night vision
Special
Commonest cause of blindness in economically active population
Microangiopathy = microvascular occlusion + leakage
Pathogenesis: ↓ pericytes → microaneurysms → capillary closure → ischaemia → VEGF release → neovascularisation
Risk factors: duration of disease, hypertension, poor DM control, renal disease
C/P
Leakage from unhealthy capillary bed at macula
Most common cause of visual loss in NPDR
Can occur at any stage of DR
Mng
Intravitreal anti-VEGF (treatment of choice)
Special
Anti-VEGF mechanism: protect integrity of wall → ↓ leakage
C/P
Grade 0: no changes
Grade 1: barely detectable arterial narrowing
Grade 2: obvious arterial narrowing + focal irregularities
Grade 3: Grade 2 + retinal haemorrhages ± exudates
Grade 4: Grade 3 + disc swelling
Fundus signs: blot haemorrhage, AV nicking, cotton wool spots, arteriolar narrowing, disc oedema, copper wiring, exudates
Inves
Fundus examination
Systemic BP
Mng
Urgent BP control if Grade 4 (malignant HTN emergency)
Special
Grade 4 = malignant hypertension emergency
C/P
Sudden painless loss of vision
Preceded by amaurosis fugax (similar to TIA — temporary vision loss)
CRAO: profound ↓ visual acuity + RAPD
BRAO: field defect; pale ischaemic zone in distribution of blocked branch artery
Fundus: cherry-red spot at fovea, pale retina, attenuated vessels (embolus may be seen)
Inves
BP, lipid profile, fasting glucose, FBC, U&Es, LFTs, CRP/ESR
Carotid Doppler, ECG, ECHO
Mng
Emergency: first 15 min → 1 hour
Lower IOP → vascular dilatation: massage, IV mannitol, anterior chamber paracentesis
Vasodilatation: sublingual nitrates, breathing 5% CO&sub2; (in a bag)
Special
Cherry-red spot: fovea has dual blood supply + supplied by choroid; no coagulative necrosis (no ganglion cells at fovea)
Pale retina = coagulative necrosis of ganglion cells (surrounding retina)
Ophthalmic emergency ("stroke of the eye")
C/P
Sudden painless loss of vision (variable severity)
CRVO: profound ↓ VA + RAPD; extensive haemorrhages throughout fundus ("blood and thunder")
BRVO: field loss OR asymptomatic; confined to quadrant
Fundus: extensive flame-shaped retinal haemorrhages, cotton wool spots + exudates, disc swelling, macular oedema, engorged tortuous vessels
Inves
BP, lipid profile, smoking, fasting glucose, FBC, U&Es, LFTs, CRP/ESR
Carotid Doppler, ECG, ECHO
Mng
Anti-VEGF for macular oedema (early)
Pan-retinal photocoagulation for neovascularisation (late, ~3 months)
Special
Variable vision loss depending on macular involvement
C/P
30% of >70 years
Dry (non-exudative): asymptomatic OR gradual loss of central vision; early sign = macular drusen; late sign = geographic atrophy (sclera visible, choroid + retina atrophied)
Wet (exudative): choroidal neovascular membrane (CNVM) — abnormal vessels from choroid into subretinal space → can bleed / leak lipids → scar
Amsler grid defects: metamorphopsia (distortion), scotoma (blind spot)
Inves
Amsler grid
Slit-lamp
Fluorescein angiography (IV dye)
OCT (cut section of retina)
Mng
General (both): education + Amsler grid, smoking cessation, sunglasses, vitamin supplements (C+E, Zinc, beta-carotene)
Wet AMD: intravitreal anti-VEGF, photodynamic therapy (PDT)
Special
Lipophilic drusen deposits in Bruch's membrane
Risk factors: aging, smoking, UV light, +ve family history
CNVM causes: age-related (Wet AMD), idiopathic (<50 years), degenerative myopia, trauma, iatrogenic (intense laser burn)
Core Requirement
Persistent obsessions and/or compulsions Obsessions
Repetitive and persistent thoughts, images, or impulses/urges experienced as intrusive and unwanted
Examples: thoughts (contamination), images (violent scenes), impulses/urges (to stab someone)
Commonly associated with anxiety
Patient attempts to ignore / suppress / neutralise by performing compulsions
Compulsions
Repetitive behaviours or rituals, including repetitive mental acts
Performed in response to obsession
Examples: repetitive washing, checking, ordering of objects
Threshold
>1 hour per day OR significant distress / impairment
Core Requirement
Presence of obsessions, compulsions, or both Obsession Criteria (both)
Experienced as intrusive + unwanted; cause marked anxiety / distress
Attempts to ignore / suppress / neutralise with another thought or action
Compulsion Criteria (both)
Repetitive behaviours (hand washing, ordering, checking) OR mental acts (praying, counting, repeating words silently)
Driven to perform in response to obsession
Aimed at preventing or reducing anxiety
Severity (Criterion B)
>1 hour per day OR clinically significant distress / impairment
Criterion A — Exposure (1 of 4)
Directly experiencing
Witnessing
Learning it occurred to close family / friend
Repeated extreme exposure
Criterion B — Symptom Categories (5)
Intrusion
Negative mood
Dissociation
Avoidance
Arousal
Criterion C — Duration
3 days to 1 month after trauma exposure
DSM-IIIR
A traumatic event outside the range of usual human experience that would be markedly distressing to almost anyone
Limitation: too restrictive
DSM-5 — Types of Exposure (4)
Directly experiencing
Witnessing in person
Learning about close family / friend (event must be violent or accidental)
Repeated / extreme exposure to aversive details (e.g. first responders collecting remains; police repeatedly exposed to child abuse details)
ICD-11
Exposure to event/situation of extremely threatening or horrific nature (short- or long-lasting)
Examples directly experienced: natural / human-made disasters, acute life-threatening illness (e.g. heart attack)
Witnessing/learning: sudden, unexpected, violent manner
Specific Events That Can Cause PTSD (7)
Military combat
Serious road accidents
Terrorist attacks
Natural disasters
Being held hostage
Witnessing violent deaths
Violent personal assaults
Duration
Core Symptom Categories (4)
Intrusion symptoms (flashbacks, intrusive memories, recurrent distressing dreams)
Persistent avoidance
Negative alterations in cognition / mood (impaired memory, guilt, detachment)
Alterations in arousal / reactivity (startle response, ↓ concentration, sleep disturbance)
Diagnostic Requirement
≥3 features over past year: Features (6)
(a) Strong desire or compulsion to drink
(b) Difficulty controlling drinking (onset / termination / level)
(c) Physiological withdrawal symptoms or drinking to relieve them
(d) Tolerance
(e) Neglect of alternative interests / time spent recovering
(f) Persisting drinking despite clear evidence of harmful consequences
4 Components
Understand information
Retain information
Weigh information & reach decision
Communicate the decision
5 Core Principles
Presumption of capacity unless proved otherwise
Capacity is task- and time-specific
Individuals supported as much as possible to make own decisions
Unwise decisions do not necessarily indicate lack of capacity
Best interests + least restrictive decisions on behalf of incapacitated
Categories of Incapacity (3)
Temporarily lacks capacity (e.g. unconscious after an accident)
Permanently lacks capacity (formerly had it — dementia, severe injury)
Never had capacity (severe learning difficulties)
Score Severity
<16 Mild dependence 16-30 Moderate dependence >30 Severe dependence
Clinical Domains (3)
Hazardous alcohol use
Dependence symptoms
Harmful alcohol use
AUDIT-C Threshold
Parameters Assessed (7)
Resting pulse rate
Sweating
Restlessness (observation)
Pupil size
Bone or joint aches
Runny nose or tearing
GI upset
Type Stability Cell-mediated immunity Bacterial load
Tuberculoid (TT) Stable Highest Lowest Borderline Tuberculoid (BT) Unstable Decreasing — Borderline (BB) Unstable Middle Middle Borderline Lepromatous (BL) Unstable — Increasing Lepromatous (LL) Stable Lowest Highest
Purpose
Simplify diagnosis
Promote rapid implementation of treatment
Type Lesions Ridley-Jopling overlap
Paucibacillary 1-5 skin lesions TT, BT Multibacillary >5 skin lesions BB, BL, LL
Group Species
Lymphatic Wuchereria bancrofti, Brugia malayi, B. timori Cutaneous Loa loa, Onchocerca volvulus, Mansonella streptocerca Body-cavity Mansonella perstans, M. ozzardi
Grade Features
I Reversible on elevation (pitting oedema) II Does not reverse on elevation (pitting or non-pitting); no skin changes III Not reversible (non-pitting); thickening of skin IV Non-pitting, not reversible, thickened skin with nodular / warty excrescences (stage of elephantiasis)
Stage Features
NPDR (Background) Microaneurysms, dot/blot haemorrhages, hard exudates Severe NPDR Cotton wool spots, venous beading, IRMA, deep haemorrhages Proliferative DR Neovascularisation (NVD, NVE), fibro-vascular proliferation Advanced Diabetic Eye Disease Vitreous haemorrhage, tractional retinal detachment, neovascular glaucoma
Grade Features
0 No changes 1 Barely detectable arterial narrowing 2 Obvious arterial narrowing + focal irregularities 3 Grade 2 + retinal haemorrhages ± exudates 4 Grade 3 + disc swelling (malignant HTN emergency)
Disorder pH Primary Secondary
Metabolic acidosis ↓ ↓ HCO₃⁻ ↓ pCO&sub2; Metabolic alkalosis ↑ ↑ HCO₃⁻ ↑ pCO&sub2; Respiratory acidosis ↓ ↑ pCO&sub2; ↑ HCO₃⁻ Respiratory alkalosis ↑ ↓ pCO&sub2; ↓ HCO₃⁻
Formula
Normal Range
8-12 mEq/L (without potassium)
12-16 mEq/L (with potassium)
7 ± 4 mmol/L (alternative deck value)
BAC Behavioural Impairment
<0.06 Mild euphoria, relaxation Concentration 0.06-0.09 Disinhibition, extroversion Reasoning, depth perception (UK drive limit 0.08) 0.10-0.19 Emotional lability, anger / sadness, ↓ libido Reaction time, gross motor, slurred speech 0.20-0.29 Stupor, loss of understanding Severe motor, LOC, memory blackout 0.30-0.49 Severe CNS depression Bladder, breathing, HR >0.50 High risk of poisoning, death —
Drink-Drive Limit UK
80 mg / 100 mL blood
35 µg / 100 mL breath
Toxidrome BP P RR T Mental status Pupils Other
Anticholinergic -/↑ ↑ ↑ ↑ Delirium ↑ Dry mucous membranes, flushing, urinary retention Cholinergic ± ± -/↓ - Normal to depressed ± Salivation, lacrimation, urination, bronchorrhoea, fasciculation, paralysis Ethanol / sedative-hypnotic ↓ ↓ ↓ -/↓ Depressed, agitated ± Hyporeflexia, ataxia Opioid ↓ ↓ ↓ ↓ Depressed ↓ Hyporeflexia Sympathomimetic ↑ ↑ ↑ ↑ Agitated ↑ Tremor, seizures Withdrawal — EtOH / sedative ↑ ↑ ↑ ↑ Agitated, disoriented, hallucinations ↑ Tremor, seizures Withdrawal — opioid ↑ ↑ - - Normal, anxious ↑ Vomiting, rhinorrhoea, piloerection, diarrhoea, yawning
Diarrhoea
Urination
Miosis (pin-point pupil)
Bradycardia (and bronchospasm / bronchorrhoea)
Emesis
Lacrimation
Salivation
Sweating
Muscle fasciculations
Adrenal medullary hyperactivity
Tachycardia (and arrhythmias)
Cramping of skeletal muscles
Hypertension
Methanol
Uremia
Diabetic ketoacidosis
Paraldehyde
Iron / Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
Chloral hydrate
Heavy metal
Iron
Phenothiazine
Enteric coated
Sustained-release
Dextrose
Naloxone
Thiamine
5 Stages (in order)
1. Verbal de-escalation
2. Time out
3. Rapid tranquilisation
4. Physical restraint
5. Seclusion
Behavioural Progression
Antecedents (A)
Behaviour (B)
Consequences (C)
Intervention Hierarchy
Prevention → Management → Harm reduction
Act Grounds Scope
Mental Health Act (MHA) (Possibly) suffering from a mental disorder Assessment / treatment of mental illness only Mental Capacity Act (MCA) Lack of capacity in dissenting patient; condition severe / life-threatening Treatment in patient's best interests
Level Frequency Clothing Movement
Constant monitoring Within hand reach (staff sitting with patient) — — Level 1 Every 15 min Hospital pyjamas Can wander, cannot leave unit Level 2 Every 30 min Own clothes Can leave unit with responsible adult Level 3 Every hour (acute unit) Own clothes Can leave unit, accounts for whereabouts
Hold Duration
Max initial hold by psychiatrist: 72 hours Criteria (any of 3)
Danger to self
Danger to others
Unable to take care of self
Treatment During Hold
No treatment without consent (except emergency) Notification
Regional Council for Mental Health Extension
≤1 week if hold reasons continue + no independent assessment obtained
Authorised Applicants
Parents, guardian, trustee Notification Within 2 Business Days
Social worker
Regional Mental Health Council
Guardian Rights
May request discharge at any time (unless involuntary admission applies)
Mandatory (all 3)
Psychiatrist approval
Clear indication of severe mental illness
Patient refusing admission
Conditional (≥1 of 2)
Imminent deterioration of psychiatric condition
Serious + imminent threat to safety / health / life of self or others
Notify Within 24h
Parents
Director of facility
National / Regional Council for Mental Health
Hold Duration
Max for evaluation: 48 hours Accepted Written Request From (6)
Relative ≤2nd degree
Police officer
Social worker
Specialised health inspector
Foreign consul
Unrelated external psychiatry specialist
Notification
Public prosecutor within 24h
Trigger
Assessment Requirements
2 psychiatric assessments required
One external, one from facility
At least one government employee
Paperwork Deadline
To Regional Council within 7 days
If deadline missed → involuntary admission ends; facility bears consequences
Urgent Transfer
Notify Regional Council for Mental Health within 24h Non-Urgent Transfer
Public Prosecution assigns evaluating psychiatrist Escapes
Inform Police + Public Prosecution
Psychiatrist may compel treatment
Review every 4 weeks at most
New independent assessment required if forced treatment >3 months
Maximum Duration
Indications (2)
Prevent imminent deterioration of mental/physical condition
Prevent imminent grave danger to others' life/health
Standard Requirements (3)
General anaesthetic
Muscle relaxer
Written free-willed informed consent
Involuntary Patient Refusing
Independent medical evaluation required
Max 2 emergency sessions while awaiting assessment
Definitions
Seclusion: confining person in room from which they cannot exit freely
Restraint forms (3): physical force, mechanical devices, chemicals (sedation)
Indications (4)
Agitated / uncontrollable patient
Restrained for hospital admission
Medication given against will
Long-term complete movement control needed by staff
Use Principles
Non-therapeutic — last resort
Least possible duration
Risk of further physical or psychosocial trauma