1. Thought broadcast - Schneider's first-rank symptoms include thought insertion, thought withdrawal, thought broadcast, made feelings/impulses/actions, somatic passivity, delusional perception, and third-person auditory hallucinations.
2. Depression - Depression is by far the most common psychiatric disorder in primary care settings.
3. Delusion of reference - The belief that external stimuli (TV, radio, newspapers) are sending special messages to oneself is a classic delusion of reference.
4. Dopamine - Antipsychotics block D2 receptors in the nigrostriatal pathway, causing Parkinsonian side effects (tremor, rigidity, bradykinesia).
5. SSRI - SSRIs (e.g., sertraline, paroxetine) are first-line pharmacotherapy for panic disorder per all major guidelines.
6. Thought blocking - Thought blocking is a negative/formal thought disorder symptom, NOT a feature of mania. The others (grandiosity, increased goal-directed activity, flight of ideas) are all classic manic symptoms.
7. Alcohol - Alcohol is the most widely abused substance globally by prevalence and burden of disease.
8. Neuroleptic Malignant Syndrome (NMS) - The tetrad of hyperthermia, rigidity, autonomic instability, and elevated CPK following antipsychotic use = NMS.
9. Sublimation - Sublimation (channeling unacceptable impulses into socially acceptable behavior) is a mature/adaptive defense mechanism. Projection, denial, and splitting are immature/primitive.
10. Disturbance of attention and awareness - Delirium is defined by acute fluctuating disturbance in attention and awareness (DSM-5), not by clear consciousness or stable deficits.
11. Phenelzine - Phenelzine is an MAOI. MAOIs + tyramine-rich foods = hypertensive crisis ("cheese reaction"). SSRIs like fluoxetine, sertraline, and escitalopram do not carry this risk.
12. Intrusive thoughts recognized as one's own - The hallmark of OCD is ego-dystonic obsessions - intrusive, unwanted thoughts the patient recognizes as their own but cannot control.
13. Naloxone - Naloxone is the immediate antidote for opioid overdose (competitive opioid receptor antagonist). Naltrexone is for relapse prevention, not acute reversal.
14. Fine tremors - Fine hand tremors are the most common side effect of lithium. Hypothyroidism (not hyperthyroidism) and nephrogenic diabetes insipidus are other important side effects.
15. ADHD - Persistent inattention and hyperactivity/impulsivity in multiple settings (school AND home) in a child is the classic presentation of ADHD.
16. Avolition - Avolition (lack of motivation/goal-directed behavior) is a negative symptom. Delusions, hallucinations, and thought insertion are positive symptoms.
17. Compulsion - Repetitive, purposeful behavior performed in response to an obsession (checking the door) despite recognizing it as irrational = compulsion.
18. Lorazepam/Diazepam - Benzodiazepines are the drug of choice for delirium tremens, as they enhance GABA activity and prevent seizures/autonomic instability.
19. Borderline Personality Disorder - Recurrent self-harm and suicidal gestures are a hallmark feature of BPD (DSM-5 criterion 5).
20. ECT (Electroconvulsive Therapy) - ECT is the gold standard for severe depression with psychotic features, catatonia, or high suicidal risk due to its rapid onset of action.
21. Attention span and working memory - The Digit Span Test (forward and backward) primarily assesses immediate attention and working memory.
22. Running commentary hallucinations - Voices that discuss or comment on the patient's actions in third person = running commentary, which is also a Schneiderian first-rank symptom.
23. Naltrexone - Naltrexone (opioid antagonist) is FDA-approved for alcohol use disorder relapse prevention (reduces craving/reward). Acamprosate and disulfiram are also approved options.
24. Cognitive impairment - The MMSE is a standardized screening tool for cognitive impairment and dementia (max score 30; <24 suggests impairment).
25. Bipolar I disorder - Bipolar I = at least one full manic episode (with or without depressive episodes). Bipolar II = hypomanic + major depressive episodes, with NO full mania.

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Management of Stroke - Detailed Overview

---

1. Overview and Classification

• Ischemic stroke (~80-85%): Thrombotic or embolic occlusion of a cerebral artery
• Hemorrhagic stroke (~15-20%): Intracerebral hemorrhage (ICH) or subarachnoid hemorrhage (SAH)
• Transient Ischemic Attack (TIA): Transient focal neurological deficit without infarction

---

2. Initial Emergency Assessment (Both Types)

Immediate ABCs

• Airway: Protect airway; if GCS ≤8, intubate (use fentanyl 2-3 mcg/kg IV first to prevent ICP spike from tracheal stimulation)
• Breathing: Pulse oximetry; supplemental O2 if SpO2 < 94%; assisted ventilation if needed
• Circulation: IV access, cardiac monitoring for ≥48 hours; immediate 12-lead ECG and troponin (concomitant MI occurs in 3-20% of strokes)

Neurological Assessment

• NIH Stroke Scale (NIHSS): Quantify deficits; NIHSS >15 indicates large infarct
• Assess consciousness, language, cranial nerves, visual fields, motor/sensory function, cerebellar function

Emergency Labs

Emergency Imaging

• Non-contrast CT head: First-line; rules out hemorrhage (takes <5 minutes)
• CT Angiography (CTA): If thrombectomy is being considered (large vessel occlusion)
• CT Perfusion or MRI/DWI: Distinguishes infarcted core from viable penumbra; guides late window treatment

---

3. Management of Acute Ischemic Stroke

A. Stroke Unit Admission

• Bradley and Daroff's Neurology in Clinical Practice, p. 1405

B. IV Thrombolysis (Alteplase / rt-PA)

• 10% as IV bolus over 1 minute
• Remaining 90% as infusion over 60 minutes

• BP must be <185/110 mmHg before giving alteplase (lower first with labetalol or nicardipine if needed)
• Blood glucose >50 mg/dL
• No intracranial hemorrhage on CT

From Rosen's Emergency Medicine (Table 87.5, 2019 AHA/ASA guidelines), p. 1435

C. Mechanical Thrombectomy (Endovascular Therapy)

• Recommended up to 24 hours from last-known-well in selected patients (DAWN, DEFUSE-3 criteria based on CT perfusion mismatch)
• Can be performed in addition to or instead of IV alteplase
• Stent retrievers and aspiration catheters are used
• For symptomatic high-grade intracranial stenosis, aggressive medical management is superior to stenting (SAMMPRIS trial - 14% stroke/death with stenting vs. 5.8% with medical therapy at 30 days)

D. Blood Pressure Management in Ischemic Stroke

• Nicardipine (first-line): Start 5 mg/h, titrate by 2.5 mg/h every 5-15 min, max 15 mg/h
• Labetalol: 10 mg IV over 1-2 min, repeat/double every 10-20 min, max 300 mg
• Avoid: Sublingual/immediate-release nifedipine (unpredictable drops); sodium nitroprusside (cerebral vasodilation worsens edema)

E. Blood Glucose Management

• Avoid hyperglycemia (worsens ischemic injury in animal models; associated with hematoma expansion in ICH)
• Avoid hypoglycemia (causes neuronal injury independent of ischemia)
• Target: Maintain near-euglycemia, but intensive glucose control (SHINE, GIST-UK trials) did NOT improve outcomes and increased hypoglycemia risk
• Regular glucose checks; insulin infusion if consistently >180 mg/dL

F. Temperature

• Hyperthermia worsens ischemic injury; treat aggressively with antipyretics
• Mild therapeutic hypothermia is neuroprotective in models but not yet standard practice for ischemic stroke

G. Cerebral Edema Management

1. Elevate head of bed 20-30 degrees
2. Mannitol 0.25-1 g/kg IV over 30 minutes; repeat every 6 hours (max 2 g/kg); controversial in ischemic edema
3. Hypertonic saline (alternative)
4. Hyperventilation: Rapid ICP reduction but only transient; avoid prolonged use
5. Decompressive hemicraniectomy + durotomy: For malignant MCA infarction - proven to improve survival and functional outcome in select patients (Fig. 65.32 - right frontal infarct with subfalcine herniation)
6. Steroids are NOT indicated in ischemic stroke - ineffective and worsen hyperglycemia/BP

• Bradley and Daroff's Neurology in Clinical Practice, pp. 1406-1408

H. DVT/VTE Prophylaxis

• DVT in hemiparetic limb is common; risk persists into post-stroke period
• LMWH preferred: Enoxaparin 40 mg SC once daily (superior to UFH in the PREVAIL trial, though small increase in extracranial hemorrhage)
• Unfractionated heparin (UFH): 5,000 units SC twice daily if LMWH unavailable
• If heparin is contraindicated: Intermittent pneumatic compression (IPC) of lower limbs (CLOTS-3 trial validated)
• Prophylactic heparin can be given safely alongside aspirin

I. Aspiration and Nutrition

• Aspiration pneumonia kills 15-25% of stroke patients
• Formal swallowing evaluation before any oral intake (video-fluoroscopic modified barium swallow)
• Aspiration occurs in >33% of brainstem strokes, 25% bilateral hemispheric, 10% unilateral hemispheric strokes
• If dysphagia present: Nasogastric tube (NGT) feeding; NPO until swallow confirmed safe
• Urinary catheter: Avoid unless urinary retention; remove at earliest opportunity to prevent urosepsis

J. Antiplatelet Therapy (Acute Phase)

• Aspirin 160-325 mg within 24-48 hours of stroke onset (after ruling out hemorrhage, and if not receiving alteplase within 24 hours)
• IST and CAST trials established a modest but significant reduction in early recurrence and mortality
• Dual antiplatelet therapy (DAPT - aspirin + clopidogrel): For minor stroke/TIA with high recurrence risk (ABCD2 score based risk):
  • CHANCE trial (China): 75-300 mg clopidogrel + aspirin for 21 days - reduced 90-day recurrence, no increase in intracranial hemorrhage
  • POINT trial: Similar benefit in non-Asian populations; slight increase in systemic bleeding when extended to 90 days
  • DAPT not appropriate if thrombolysis, thrombectomy, or anticoagulation is planned

---

4. Management of Intracerebral Hemorrhage (ICH)

A. Initial Stabilization

• Secure airway: Intubate if GCS ≤8 (pre-treat with fentanyl 2-3 mcg/kg to blunt ICP rise)
• Emergent CT head to establish location, size, hemorrhage volume
• Neurosurgical consultation immediately
• Labs: CBC, coagulation (PT/INR, aPTT), toxicology, glucose, type & screen

B. Blood Pressure Management in ICH

• Rapid lowering does NOT appear to reduce peri-hematomal perfusion or worsen neurological status
• Preferred agent: IV nicardipine or labetalol (same agents as ischemic stroke)

C. Reversal of Coagulopathy

D. Prevention of Hematoma Expansion

• Tranexamic acid (TICH-2 trial): 1 g IV bolus then 1 g over 8 hours within 8 hours of onset - safe, reduced early deaths and hematoma expansion, but did NOT improve 90-day functional outcomes
• rFVIIa (recombinant activated Factor VII): Phase II showed hematoma growth reduction; Phase III FAST trial showed NO clinical benefit at 90 days and increased arterial thromboembolic complications (10% vs 5%) - not currently recommended
• FASTEST trial is ongoing (targeting very early ICH within 2 hours)

E. Surgical Management of ICH

• Bradley and Daroff's Neurology in Clinical Practice, p. 1438 (eFig 66.20: midline cerebellar hemorrhage with brainstem distortion and hydrocephalus)

F. ICP Management in ICH

---

5. Secondary Prevention (Long-Term)

Antiplatelet Therapy

• Aspirin monotherapy: Modestly reduces recurrent stroke and mortality
• Clopidogrel monotherapy: Modest benefit; not dramatically superior to aspirin alone
• Aspirin + clopidogrel long-term: NOT recommended - excess major bleeding outweighs benefit (ACTIVE trial)

Anticoagulation

• For non-cardioembolic ischemic stroke: warfarin is NOT superior to aspirin (WARSS, WASID trials)

Statins

• High-dose statin therapy reduces subsequent stroke by ~2% over 5 years (SPARCL trial)
• Target LDL <70 mg/dL for secondary stroke prevention
• Guidelines recommend statin initiation in all ischemic stroke patients

Carotid Intervention

• Symptomatic carotid stenosis ≥70%: Carotid endarterectomy (CEA) within 2 weeks (best outcomes)
• Symptomatic stenosis 50-69%: CEA may benefit, especially in men
• <50% stenosis: Medical management

Blood Pressure (Long-Term)

• Target BP <130/80 mmHg (or stricter in hemorrhagic stroke)
• Begin antihypertensive therapy once neurological deficit has stabilized (typically after several days in acute stroke)

Lifestyle

• Smoking cessation, physical activity, Mediterranean diet, weight management, alcohol reduction

---

6. Rehabilitation

• Rehabilitation should begin as soon as diagnosis is established and life-threatening complications are stabilized
• Multidisciplinary team: Neurology, physiotherapy, occupational therapy, speech therapy, nutrition, social services
• Screen all patients for rehabilitation candidacy early
• Address shoulder subluxation in hemiplegic patients early
• Fall risk assessment at regular intervals
• Pressure sore prevention: Frequent repositioning, skin inspection, special mattresses

---

7. Complication Prevention Summary

---

Key Management Algorithms

SUSPECTED STROKE
      |
   ABCs + IV access + ECG
      |
   NIHSS assessment
      |
   URGENT CT head (non-contrast)
     /          \
HEMORRHAGE      NO HEMORRHAGE (Ischemic)
    |                  |
ICH/SAH protocol    Check time from onset
Reverse coagulopathy     |
Control BP               |
Neurosurgery consult    <4.5 hrs?    Yes → Assess alteplase eligibility
                         |                  BP <185/110? → Give alteplase 0.9 mg/kg
                        LVO?         No → Antiplatelet + supportive care
                         |
                    Thrombectomy (up to 24h with perfusion imaging)
                         |
              ----STROKE UNIT ADMISSION----
              BP management, glucose control,
              DVT prophylaxis, swallow assessment,
              antiplatelet/anticoagulation, statin,
              rehabilitation

---

---

Transient Ischemic Attack (TIA) - Detailed Overview

---

1. Definition

This is important: a patient whose symptoms resolve in 30 minutes but who has a DWI-positive lesion on MRI is classified as having a stroke, not a TIA. Most TIAs last less than 1 hour in practice.

• Harrison's Principles of Internal Medicine, 22e, p. 3491
• Rosen's Emergency Medicine, p. 1423

---

2. Epidemiology and Importance

• Stroke risk after TIA is ~10% at 2 days and 15% at 90 days (up to 22% for ABCD2 score of 7)
• Most strokes occur in the first 2 days after TIA - this is the window where intervention matters most
• TIA is therefore a medical emergency requiring same-day urgent evaluation
• In the US, a stroke occurs every 40 seconds; TIA is a critical warning event preceding many of these
• Frameworks for Internal Medicine, p. 574

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3. Pathophysiology / Causes

Mechanisms:

---

4. Clinical Features

Features by Vascular Territory:

Anterior Circulation (Carotid Territory - MCA/ACA)

Posterior Circulation (Vertebrobasilar Territory)

---

5. Differential Diagnosis

• Frameworks for Internal Medicine, p. 574

---

6. Risk Stratification - The ABCD2 Score

ABCD2 Score Table (Harrison's Principles of Internal Medicine, 22e)

Risk Interpretation and 3-Month Stroke Rate:

Caution: More recent studies have found the ABCD2 score alone does not always provide accurate stroke risk estimation. The ABCD2-I (adding MRI findings) and ABCD3-I (adding dual imaging) improve predictive accuracy but are not yet universally validated.

• Harrison's, Table 438-5; Rosen's, Table 87.6

---

7. Investigations

Immediate (Emergency) Workup

---

8. Management of TIA

A. Admission vs. Outpatient Management

• Rosen's Emergency Medicine, p. 1423

B. Antiplatelet Therapy (Cornerstone of Treatment)

Thrombolysis (alteplase) is CONTRAINDICATED in TIA - the deficit has already resolved. However, the patient should be admitted so thrombolysis can be rapidly administered if symptoms recur.

Dual Antiplatelet Therapy (DAPT) - First-Line for TIA/Minor Stroke

• CHANCE trial (China): DAPT for 21 days reduced 90-day recurrent stroke vs. aspirin alone, no increase in intracranial hemorrhage
• POINT trial (US/international): Similar benefit; slightly increased systemic hemorrhage when extended to 90 days
• Pooled analysis: DAPT most beneficial in first 21 days after TIA/minor stroke
• After 21-90 days: Switch to single antiplatelet (aspirin or clopidogrel monotherapy) to reduce bleeding risk

• Rosen's Emergency Medicine, p. 1423-1424; Harrison's, p. 3492

C. Anticoagulation (for Cardioembolic TIA)

• For new-onset AF: Immediate anticoagulation unless CHA2DS2-VASc score = 0 (men) or 1 (women) with self-terminating paroxysms

D. Statin Therapy

• All TIA patients should receive high-intensity statin (atorvastatin 40-80 mg or rosuvastatin 20-40 mg)
• Target LDL <70 mg/dL for secondary prevention
• SPARCL trial: High-dose statin reduced 5-year recurrent stroke by ~2%

E. Blood Pressure Management

• After TIA, begin antihypertensive therapy once neurological status is stable
• Target: <130/80 mmHg long-term
• First-line agents: ACE inhibitors or ARBs (especially with diabetes); thiazide diuretics; calcium channel blockers
• Do NOT aggressively lower BP acutely in the first 24-48 hours (same rationale as ischemic stroke - impaired autoregulation)

F. Carotid Revascularization

• CEA should be performed by surgeons with <6% perioperative stroke/death rate
• Carotid artery stenting (CAS): Alternative to CEA in high surgical-risk patients
• For symptomatic intracranial stenosis: Aggressive medical management is superior to stenting (SAMMPRIS trial)
• Tintinalli's Emergency Medicine, p. 2286

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9. Secondary Prevention (Long-Term)

---

10. Stroke Center Classification and Systems of Care

• Acute Stroke-Ready Hospital (ASRH): Smaller hospitals; initial diagnosis and stabilization; telemedicine link to larger center
• Primary Stroke Center (PSC): Full stroke infrastructure (stroke team, stroke unit, CT/MRI, protocols)
• Comprehensive Stroke Center (CSC): All of the above + advanced imaging, surgery, endovascular thrombectomy

• Rosen's Emergency Medicine, p. 1443

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11. TIA vs. Stroke - Quick Comparison

---

Summary Flowchart

SUSPECTED TIA (resolved focal deficits)
           |
    Urgent CT head (rule out hemorrhage)
           |
    MRI with DWI (preferred - detect silent infarction)
           |
    ABCD2 Score + Vascular imaging (CTA/carotid Doppler) + ECG + Echo
           |
    ┌──────┴──────┐
  High risk      Low risk
  (score ≥4)    (score 0-3)
    Admit         Rapid TIA clinic within 24h
           |
    Initiate DAPT (aspirin + clopidogrel) x 21 days
    Statin (atorvastatin 40-80 mg)
    AF? → DOAC
    Carotid stenosis ≥70%? → CEA within 2 weeks
           |
    Long-term single antiplatelet + risk factor control

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Management of Migraine - Detailed Overview

---

1. Definition and Overview

---

2. Classification (ICHD-III)

• Harrison's Principles of Internal Medicine 22e, Table 441-1

---

3. Diagnostic Criteria (ICHD-III)

Migraine WITHOUT Aura (≥5 attacks required):

1. Headache lasting 4-72 hours
2. At least 2 of the following:
   • Unilateral location
   • Pulsating/throbbing quality
   • Moderate or severe intensity (inhibits or prohibits daily activities)
   • Aggravated by routine physical activity (walking, climbing stairs)
3. During headache, at least 1 of:
   • Nausea and/or vomiting
   • Photophobia AND phonophobia

Migraine WITH Aura (≥2 attacks required):

• Same as above PLUS aura symptoms (fully reversible):
  • Visual: Zigzag lines (fortification spectra), scintillating scotoma, flashing lights - most common aura type (occurs in only 20-25% of migraineurs)
  • Sensory: Ipsilateral arm or periorbital paresthesias/numbness with a "marching" characteristic
  • Motor: Weakness spreading from one area to another (hemiplegic migraine)
  • Speech: Mild dysphasia
• Aura typically lasts 20-60 minutes and precedes the headache

Phases of a Migraine Attack:

• Harrison's Principles of Internal Medicine 22e

---

4. Pathophysiology

1. Cortical spreading depression (CSD): A wave of neuronal/glial depolarization that spreads across the cortex at 3-5 mm/min, believed to be the neural substrate of the aura
2. Trigeminovascular activation: CSD activates trigeminal nerve fibers surrounding meningeal blood vessels → release of vasoactive neuropeptides:
   • CGRP (Calcitonin Gene-Related Peptide) - causes vasodilation and sensitizes pain fibers
   • PACAP (Pituitary Adenylate Cyclase-Activating Polypeptide) - similar role
   • These neuropeptides cause neurogenic inflammation and central sensitization
3. Serotonin (5-HT) role:
   • Plasma/platelet 5-HT levels fluctuate with migraine phases
   • 5-HT-releasing agents (reserpine, fenfluramine) can precipitate migraine
   • Triptans (5-HT1B/1D agonists) abort attacks
   • 5-HT₁B/1D receptor activation: (a) cranial vessel constriction + (b) inhibition of sensory neuropeptide release from perivascular trigeminal afferents + (c) attenuation of TNC (trigeminal nucleus caudalis) excitability
4. Dopamine: Premonitory symptoms (yawning, nausea, hypotension) are dopaminergic; dopamine receptor antagonists (metoclopramide, prochlorperazine) are effective in treatment
5. Ion channel mutations (FHM genes): Mutations in calcium, sodium, and potassium channels alter membrane excitability and predispose to migraine aura

• Harrison's 22e; Goodman & Gilman's Pharmacology

---

5. Triggers

• Hormonal: Menstruation, oral contraceptives, hormone replacement
• Sleep: Too much or too little sleep
• Stress/letdown from stress
• Dietary: Alcohol (red wine), caffeine or caffeine withdrawal, nitrates (processed meats), chocolate, aged cheese, MSG, fasting/missed meals
• Environmental: Barometric pressure changes, strong scents, bright lights, loud noise
• Physical exertion

---

6. Management Overview

┌─────────────────────────────────────────┐
│         MIGRAINE MANAGEMENT             │
├──────────────┬──────────────────────────┤
│  1. Non-     │  Identify & avoid        │
│ Pharmacologic│  triggers; lifestyle     │
│              │  modification            │
├──────────────┼──────────────────────────┤
│  2. Acute    │  Abort the attack when   │
│  (Abortive)  │  it occurs               │
├──────────────┼──────────────────────────┤
│  3.          │  Reduce frequency/       │
│ Prophylactic │  severity (daily meds)   │
└──────────────┴──────────────────────────┘

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7. Non-Pharmacological Management

• Trigger identification and avoidance: Headache diary is invaluable
• Stress management and relaxation techniques (biofeedback, CBT)
• Regular sleep schedule: Avoid excessive or insufficient sleep
• Regular meals: Avoid fasting; maintain consistent meal times
• Regular aerobic exercise: Reduces frequency and severity
• Physical therapy: For cervicogenic component
• Limit caffeine intake: Avoid rebound
• Avoid hormonal triggers: Consider alternative contraception in women with hormonal migraines

---

8. Acute (Abortive) Treatment

Key Principles:

• Treat as early as possible in the attack - once the attack is fully established, oral drugs are less effective due to reduced GI motility and poor absorption
• Use non-oral routes (intranasal, SC injection, rectal) if severe nausea/vomiting is present
• Stratified care is superior to step care: match drug potency to attack severity upfront (randomized trial evidence) rather than always starting NSAIDs first
• Rational polytherapy (combining agents with different mechanisms - e.g., NSAID + triptan + antiemetic) is more effective than monotherapy
• Bradley and Daroff's Neurology, p. 350

Step 1: Mild-to-Moderate Attacks

• Bradley and Daroff's Neurology (Table 102.4)

Step 2: Moderate-to-Severe Attacks - Triptans (Drug of Choice)

• Begin as soon as possible after headache onset (NOT during aura - sumatriptan SC may be ineffective in the aura phase)
• Not for use in prophylaxis - acute treatment ONLY
• Contraindicated in: hemiplegic migraine, basilar/brainstem migraine, uncontrolled hypertension, ischemic heart disease, Prinzmetal's angina, history of stroke/TIA, pregnancy (relative)
• Not effective if taken during aura (controversy exists)

Step 3: Ergot Derivatives (Alternative to Triptans)

Step 4: Antiemetics / Adjuncts

Step 5: CGRP Receptor Antagonists - Gepants (Newer Acute Agents)

• No vasoconstriction → safe in cardiovascular disease
• Safe in hemiplegic/basilar migraine
• Rimegepant can serve dual purpose (acute + prevention)

Step 6: Ditans (5-HT1F Agonists)

• No vasoconstriction → cardiovascular safety
• Oral: 50-200 mg as needed
• Side effects: dizziness, sedation (CNS-active); driving restriction for 8 hours after use

Special Situation: Status Migrainosus (>72 hours)

• IV fluids (rehydration if vomiting)
• IV prochlorperazine or chlorpromazine (first-line in ED)
• IV ketorolac 15-30 mg q6h (parenteral NSAID)
• IV dihydroergotamine (DHE) - highly effective; pretreat with metoclopramide for nausea
• IV dexamethasone 4-8 mg (single dose - reduces recurrence within 24-72 hours)
• IV magnesium sulfate 1-2 g (particularly useful in migraine with aura)
• Opioids: AVOID if possible - risk of rebound headache and habituation; reserved for when all else fails

Intranasal Lidocaine

---

9. Prophylactic (Preventive) Treatment

Indications for Prophylaxis:

• ≥4 migraine days/month OR attacks so severe that acute treatment is consistently insufficient
• Increasing frequency over time / possible medication overuse
• Acute therapy overuse (risk of rebound/medication overuse headache - MOH)
• Chronic migraine (≥15 headache days/month with ≥8 being migraine)
• Specific migraine subtypes: hemiplegic migraine, migraine with prolonged aura, migrainous infarction
• Patient preference / significant disability

Class 1: Beta-Blockers (Best Evidence - First Line)

Class 2: Antiepileptic Drugs (Level A Evidence)

Class 3: Antidepressants

Class 4: Calcium Channel Blockers

Class 5: OnabotulinumtoxinA (Botox) - For Chronic Migraine

• FDA approved specifically for chronic migraine (≥15 headache days/month)
• 155-195 units injected across 31-39 sites in head and neck muscles every 12 weeks
• Very effective for chronic migraine; not indicated for episodic migraine
• Mechanism: Inhibits CGRP and SP release from peripheral trigeminal afferents

Class 6: CGRP Monoclonal Antibodies (Newest - Most Targeted Therapy)

• Harrison's 22e; Goldman-Cecil Medicine; Kaplan & Sadock's Psychiatry

Summary Table: Prophylactic Agents with Evidence Levels

• Textbook of Family Medicine 9e; Kaplan & Sadock's Psychiatry (Table 2.11-5)

---

10. Special Situations

Menstrual Migraine

• Occurs perimenstrually (day -2 to +3 of menstruation)
• Short-term prophylaxis (when regular prophylaxis is not desired):
  • NSAIDs: Naproxen sodium 550 mg BID (days -3 to +3) OR mefenamic acid 250 mg TID OR ketoprofen 75 mg TID
  • Frovatriptan or naratriptan (longer-acting triptans) taken days -3 to +3 - specifically recommended for menstrual migraine prevention
  • Ergots (days -3 to +3) - alternative
• Hormonal approaches: Transdermal estrogen supplementation during menses; changing to continuous OCP without pill-free intervals

Migraine in Pregnancy

• Triptans: Use with caution (Category C); sumatriptan has most safety data
• Ergotamine: Contraindicated (fetal vasoconstriction/harm)
• Valproate: Contraindicated (teratogenic)
• Safe options: Paracetamol, beta-blockers (propranolol), low-dose aspirin, magnesium
• Migraine often improves in the 2nd and 3rd trimesters due to stable estrogen levels

Medication Overuse Headache (MOH / Rebound Headache)

• Develops with regular use of acute medications >10-15 days/month
• Worst with opioids and butalbital (>10 days/month); also triptans and ergotamines (>10 days/month); NSAIDs (>15 days/month)
• Management: Withdrawal of overused medication + bridging therapy (NSAIDs, corticosteroids, DHE) + initiate prophylaxis

---

11. Stepped Approach Summary

ACUTE MIGRAINE ATTACK
         |
   Mild-Moderate?
         |
   Yes → NSAIDs ± antiemetic ± caffeine combination
         |
   Insufficient → TRIPTAN (oral/nasal/SC based on severity/nausea)
         |
   + Antiemetic (metoclopramide / prochlorperazine) if nausea
         |
   Refractory/Severe → DHE IV or SC + antiemetic
         |
   Status migrainosus → ED: IV prochlorperazine + ketorolac ± DHE ± dexamethasone
         |
   No vascular risk? → Gepants (ubrogepant/rimegepant) or lasmiditan as alternatives

PROPHYLAXIS (if ≥4 attacks/month):
   First-line → Propranolol OR topiramate OR amitriptyline
   Refractory/chronic → Add OnabotulinumtoxinA (if chronic migraine)
   Or switch to → CGRP monoclonal antibody (erenumab/fremanezumab/galcanezumab)

---

Recent Evidence Alert (2025): European evidence-based guidelines (Ornello et al., Cephalalgia 2025, PMID 40277319/40277321) confirm CGRP-targeted therapies (both gepants and monoclonal antibodies) as effective first-line options for both acute and preventive treatment. A 2024 network meta-analysis (Karlsson et al., BMJ, PMID 39293828) comparing acute migraine drugs found triptans remain the most effective class for acute treatment overall.

SECTION - 2 ANSWERS

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Q1. Acute Coronary Syndromes (ACS) (15 marks: 3+4+4+4)

Part 1: What are Acute Coronary Syndromes? (3 marks)

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Part 2: Etiology and Pathogenesis (4 marks)

Etiology / Risk Factors:

• Modifiable: Hypertension, dyslipidemia (↑LDL, ↓HDL), diabetes mellitus, smoking, obesity, physical inactivity, metabolic syndrome
• Non-modifiable: Age (>45 men, >55 women), male sex, family history of premature CAD (<55 male relatives, <65 female relatives)
• Other: Cocaine use, vasculitis, coronary spasm (Prinzmetal's angina)

Pathogenesis:

• Platelet adhesion (via GPIb-vWF), activation (TxA2, ADP release), aggregation (GPIIb/IIIa - fibrinogen bridges)
• Coagulation cascade: thrombin generation → fibrin clot
• Partial occlusion → UA/NSTEMI; Complete occlusion → STEMI

• Ischemia begins within seconds of occlusion
• Irreversible cell death begins after 20 minutes of complete ischemia
• "Wavefront phenomenon": Infarction spreads from subendocardium (most vulnerable - highest oxygen demand, lowest supply) outward to epicardium over 4-6 hours
• Necrotic myocardium releases Troponin I and T (most specific), CK-MB, myoglobin

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Part 3: Clinical Presentations (4 marks)

Classic Presentation:

• Chest pain: Severe, crushing/pressure/squeezing, retrosternal, lasting >20 minutes (UA: <20 min, relieved by rest/nitrates)
• Radiation: Left arm, jaw, neck, shoulder, epigastrium
• Associated symptoms: Diaphoresis, nausea, vomiting, dyspnea, palpitations, sense of impending doom
• No relief with antacids or rest (unlike angina)

Atypical Presentations (especially in elderly, women, diabetics):

• Epigastric pain mistaken for indigestion
• Isolated dyspnea (equivalent)
• Fatigue, syncope, altered consciousness
• Silent MI (in diabetics due to autonomic neuropathy)

Physical Examination:

• Anxiety, pallor, diaphoresis
• Hypotension or hypertension
• Tachycardia or bradycardia
• S3/S4 gallop (heart failure)
• New murmur (papillary muscle rupture, VSD)
• Elevated JVP (right heart failure in inferior MI)
• Signs of cardiogenic shock in severe cases

ECG Changes:

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Part 4: Emergency Management - 55-year-old Hemodynamically Stable Male with ACS (4 marks)

Immediate (First 10 minutes - "TIME IS MUSCLE"):

• Morphine: 2-4 mg IV (if chest pain severe; use with caution - may worsen outcomes in NSTEMI)
• Oxygen: Only if SpO2 <90% or respiratory distress (avoid hyperoxia)
• Nitrates: Sublingual nitroglycerin 0.4 mg q5 min × 3 (if SBP >90, no PDE5 inhibitor use in last 24-48 hrs, no inferior/RV MI); IV nitroglycerin for persistent pain
• Aspirin: 300 mg loading dose chewed immediately (irreversible COX-1 inhibitor)

12-lead ECG within 10 minutes - determines pathway:

If STEMI:

• Primary PCI (percutaneous coronary intervention) within 90 minutes of first medical contact - GOLD STANDARD
• If PCI not available within 120 minutes: Fibrinolysis (Streptokinase or tPA) within 30 minutes of hospital arrival
• Anti-platelet: Aspirin 300 mg + P2Y12 inhibitor (ticagrelor 180 mg or clopidogrel 300-600 mg loading)
• Anti-coagulation: Heparin UFH 60 units/kg IV bolus (max 4000 units) + infusion

If NSTE-ACS (NSTEMI/UA):

• Risk stratify with TIMI score or GRACE score
• Antiplatelets: Aspirin + Ticagrelor (180 mg then 90 mg BD) or Clopidogrel (300 mg then 75 mg OD)
• Anticoagulation: Enoxaparin 1 mg/kg SC BD OR fondaparinux 2.5 mg SC OD (preferred - less bleeding)
• Early invasive strategy (angiography within 24-48 hrs) for high-risk NSTEMI
• Beta-blocker: Metoprolol 25-50 mg oral (if heart rate >60, no contraindication) - reduces infarct size, prevents arrhythmias
• High-dose statin: Atorvastatin 80 mg immediately

Monitoring:

• Continuous ECG monitoring (detect arrhythmias: VF, heart block)
• IV access, pulse oximetry
• Serial troponins at 0, 3, 6 hours
• Echocardiography (assess LV function, wall motion abnormality)
• Maintain SBP >90 mmHg; Hemodynamically stable so avoid aggressive fluid loading

Subsequent Management:

• Dual antiplatelet (aspirin + P2Y12 inhibitor) for 12 months post-ACS
• Beta-blocker long-term (reduces mortality)
• ACE inhibitor/ARB (especially if EF <40%, hypertension, diabetes)
• Statin (target LDL <70 mg/dL)
• Cardiac rehabilitation, lifestyle modification

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Q2. Diagnosis, Evaluation and Management - Ascites Case (10 marks: 3+3+4)

Clinical Analysis of the Case:

Part 1: Diagnosis (3 marks)

• SAAG ≥1.1 g/dL confirms portal hypertension (cirrhosis, Budd-Chiari, cardiac)
• Low ascitic protein (<2.5 g/dL) with high SAAG = cirrhotic ascites (vs. cardiac ascites which has high protein)
• PMN ≥250 cells/mm³ = DIAGNOSTIC of SBP (even before culture results)
• Low ascitic glucose (<50 mg/dL vs. serum) and elevated cell count support infection
• Jaundice + ascites + edema in 40-year-old male → decompensated liver cirrhosis

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Part 2: Further Evaluation (3 marks)

To Confirm Cirrhosis:

• LFTs: Bilirubin (↑↑ in jaundice), ALT/AST (↑ - hepatocellular), ALP/GGT (↑ - cholestatic), albumin (↓ - synthetic function), PT/INR (↑ - coagulation factor deficiency)
• CBC: Anemia (pallor), thrombocytopenia (hypersplenism), leukocytosis (infection)
• Serum albumin: Low in cirrhosis; calculate SAAG = serum albumin - ascitic albumin
• Serum creatinine, electrolytes, BUN: Detect hepatorenal syndrome (feared complication)
• Serum bilirubin + conjugated/unconjugated ratio: Type of jaundice

To Identify Etiology of Cirrhosis:

• HBsAg, Anti-HBc, Anti-HCV: Viral hepatitis
• Alcohol history + GGT: Alcoholic liver disease (AST:ALT ratio >2:1 in ALD)
• ANA, anti-smooth muscle antibody: Autoimmune hepatitis (less likely)
• Serum ferritin + transferrin saturation: Hemochromatosis
• Ceruloplasmin + urine copper: Wilson's disease (in young patients)

Imaging:

• Ultrasound abdomen with Doppler: Liver size, echogenicity, portal vein diameter, splenomegaly, ascites volume, hepatic vein flow (exclude Budd-Chiari)
• Upper GI Endoscopy: Esophageal varices (grading), gastric varices (risk stratification)
• FIBROSCAN (Transient Elastography): Non-invasive liver fibrosis assessment
• CT abdomen: If HCC suspected (AFP level)

To Further Evaluate SBP:

• Ascitic fluid culture (bedside inoculation into blood culture bottles - highest sensitivity): Identify organism (E. coli, Klebsiella, Streptococcus pneumoniae most common)
• Ascitic fluid pH, LDH (secondary peritonitis if LDH > serum LDH, protein >1 g/dL, glucose <50 mg/dL - "Runyon's criteria")

Assess Severity and Complications:

• Child-Pugh score (bilirubin, albumin, PT, ascites, encephalopathy) → Grades A/B/C
• MELD score (bilirubin, creatinine, INR) → Predicts 3-month mortality
• Serum-ascites albumin gradient (already calculated = 1.2)
• Chest X-ray: Pleural effusion (hepatic hydrothorax)
• EEG/clinical assessment: Hepatic encephalopathy

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Part 3: Management (4 marks)

A. Immediate Treatment of SBP:

• Cefotaxime 2g IV every 8 hours × 5 days (drug of choice for SBP)
• Alternative: Amoxicillin-clavulanate IV or ciprofloxacin 400 mg IV BD
• IV Albumin infusion: 1.5 g/kg on Day 1 + 1 g/kg on Day 3 → Prevents hepatorenal syndrome (reduces mortality from 29% to 10% - NEJM landmark trial)
• Repeat paracentesis at 48 hours: PMN should decrease by >25% to confirm response

B. Management of Ascites:

• Sodium restriction: 1500-2000 mg/day (5-6 g table salt)
• Fluid restriction: Only if serum Na <125 mEq/L
• Diuretics (first-line for cirrhotic ascites):
  • Spironolactone 100 mg/day (aldosterone antagonist - drug of choice) → up to 400 mg/day
  • Add Furosemide 40 mg/day → up to 160 mg/day (maintain 100:40 ratio spiro:furo)
  • Monitor weight loss: aim 0.5 kg/day (no edema) or 1 kg/day (with edema)
• Therapeutic paracentesis (large volume - >5L): Give albumin replacement (8g per liter removed) to prevent paracentesis-induced circulatory dysfunction

C. Prophylaxis Against SBP Recurrence:

• Norfloxacin 400 mg/day oral (primary and secondary prophylaxis) OR ciprofloxacin 500 mg/day
• Indicated after first SBP episode AND in patients with ascitic protein <1.5 g/dL + renal impairment or Child-Pugh ≥9

D. Management of Jaundice / Underlying Liver Disease:

• Alcohol cessation (if ALD) - most important intervention; can achieve partial recovery
• Antiviral therapy if HBV/HCV-related cirrhosis (Tenofovir for HBV; DAAs for HCV)
• Nutritional support: High-calorie, high-protein diet (1.2-1.5 g/kg protein); BCAA supplements for encephalopathy-prone patients
• Lactulose 30 mL BD-TDS (prevents hepatic encephalopathy by reducing ammonia absorption)
• Beta-blockers (propranolol or carvedilol): Primary prophylaxis of variceal bleeding if large varices present

E. Monitoring and Complications:

• Monitor: Daily weight, abdominal girth, urine output, electrolytes, renal function
• Watch for: Hepatorenal syndrome (rising creatinine), hepatic encephalopathy, variceal bleed, hepatocellular carcinoma (6-monthly AFP + USS surveillance)
• Liver transplant evaluation: If MELD score >15 or decompensated despite medical therapy

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Q3. Short Answer Questions (5 marks each)

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Q3A: HAART in India (5 marks)

Definition:

How HAART Works:

Standard First-Line Regimen in India (NACO Guidelines):

How Employed in India (NACO - National AIDS Control Organisation):

• Free ART programme through government ART centers and Link ART centers
• Initiated when: CD4 count <350 cells/mm³ OR AIDS-defining illness regardless of CD4, OR co-infection with TB, OR pregnancy
• India now follows "Test and Treat" policy (treat ALL HIV-positive persons regardless of CD4 count)
• Monitoring: CD4 count every 6 months, viral load annually, liver function, renal function
• PMTCT (Prevention of Mother-to-Child Transmission): ART for all HIV-positive pregnant women
• PrEP (Pre-Exposure Prophylaxis): TDF + FTC for high-risk uninfected individuals
• Goals: Achieve undetectable viral load (<50 copies/mL) → "U=U" (Undetectable = Untransmittable)

Key Benefits of HAART:

• Reduces viral load to undetectable levels
• Increases CD4 count (immune reconstitution)
• Prevents AIDS-defining opportunistic infections
• Reduces transmission
• Near-normal life expectancy with adherence

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Q3B: CVA - Classification, Clinical Features, Etiology/Risk Factors in 35-Year-Old (5 marks)

Classification of CVA (Cerebrovascular Accident / Stroke):

CVA
├── Ischemic Stroke (~80%)
│   ├── Thrombotic (large vessel atherosclerosis)
│   ├── Embolic (cardioembolic - AF, valves)
│   ├── Lacunar (small vessel disease)
│   └── Cryptogenic
└── Hemorrhagic Stroke (~20%)
    ├── Intracerebral Hemorrhage (ICH)
    └── Subarachnoid Hemorrhage (SAH)

Clinical Features by Territory:

Etiology and Risk Factors Specific to a 35-Year-Old:

• Rheumatic heart disease with mitral stenosis (common in India) + AF
• Patent foramen ovale (PFO) - paradoxical embolism
• Infective endocarditis (IVDU, rheumatic)
• Dilated cardiomyopathy, atrial myxoma

• Antiphospholipid antibody syndrome (APAS) - young women
• Polycythemia vera, thrombocytosis
• Sickle cell disease, factor V Leiden, protein C/S deficiency, antithrombin III deficiency
• Hyperhomocysteinemia

• Spontaneous arterial dissection (carotid or vertebral) - trauma, neck manipulation
• Fibromuscular dysplasia
• Moyamoya disease (common in Asian young adults)
• Vasculitis (CNS vasculitis, SLE, Takayasu's arteritis)

• Cocaine, amphetamines (vasoconstriction/vasculitis)
• Oral contraceptive pills (especially combined OCP) + smoking in young women

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Q3C: Inflammatory vs Non-Inflammatory Joint Pain + RA Management (5 marks)

Differentiation: Inflammatory vs Non-Inflammatory Arthritis

Management of Rheumatoid Arthritis in a 30-Year-Old Lady:

• Joint involvement, serology (RF, anti-CCP), acute phase reactants, duration

Principles: "Treat to Target" - aim for remission or low disease activity (DAS28 score)

• Patient education, physiotherapy, occupational therapy
• Joint protection techniques, splinting (wrist)
• Regular low-impact exercise
• Smoking cessation
• Folic acid supplementation (with methotrexate)

• Ibuprofen 400-800 mg TID or Diclofenac 50 mg BD with meals and PPI cover
• Use lowest effective dose; NOT disease-modifying

• Methotrexate (MTX) - anchor drug; 7.5-25 mg weekly + folic acid 5 mg weekly (reduces toxicity)
  • Monitor: LFTs, CBC monthly (hepatotoxicity, myelosuppression)
  • Contraindicated in pregnancy (teratogenic) - use reliable contraception in this 30-year-old woman
• Hydroxychloroquine 200-400 mg/day (eye check every 6-12 months - retinopathy)
• Sulfasalazine 1-3 g/day
• Triple therapy (MTX + HCQ + SSZ) very effective

• Anti-TNF agents: Etanercept, adalimumab, infliximab
• IL-6 inhibitors: Tocilizumab
• CTLA-4-Ig: Abatacept
• Anti-CD20: Rituximab
• Screen for TB, hepatitis B before starting biologics (immune suppression)

• Tofacitinib, baricitinib - oral; important for young women planning pregnancy (counseling needed)

• Low-dose prednisolone 5-10 mg/day as bridging therapy while waiting for DMARDs to take effect
• Intra-articular triamcinolone for acutely inflamed joints
• Avoid long-term high-dose steroids (osteoporosis, diabetes - especially important in young woman)
• Add calcium + Vitamin D + bisphosphonate if on long-term steroids

• Contraceptive counseling (MTX, leflunomide, biologics - teratogenic)
• Bone protection (young women on steroids - osteoporosis risk)
• Pregnancy planning: Can use HCQ + sulfasalazine safely; switch from MTX; anti-TNF generally safe until 3rd trimester
• Mental health support (chronic pain, functional disability in young person)

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Q3D: DKA - Clinical Features and Management (5 marks)

Clinical Scenario Context:

• Type 2 DM on oral hypoglycaemic agents (OHAs) - DKA is LESS common in T2DM but occurs during severe physiological stress
• Precipitating factor: UTI (infection is the most common precipitant of DKA)
• Why: Infection → ↑counter-regulatory hormones (glucagon, cortisol, catecholamines) → ↑gluconeogenesis, lipolysis → DKA

Clinical Features of DKA:

• Polyuria, polydipsia, polyphagia (osmotic symptoms from hyperglycemia)
• Nausea, vomiting, abdominal pain (from ketosis, ileus)
• Weakness, fatigue
• Symptoms of UTI: dysuria, frequency, suprapubic pain, fever

• Kussmaul breathing: Deep, rapid respirations (compensatory respiratory alkalosis for metabolic acidosis)
• Fruity/acetone breath (ketones)
• Dehydration: Dry mucous membranes, sunken eyes, skin turgor loss, tachycardia, hypotension
• Altered consciousness: Drowsiness, confusion, coma (in severe cases)
• Fever (from underlying UTI)
• Abdominal tenderness (may mimic acute abdomen - due to ketoacidosis itself)

Management of DKA (Rosen's Emergency Medicine - Box 115.1):

1. IV Fluid Resuscitation (Most Important First Step):

• Normal Saline (0.9% NaCl) 1-2 L IV over first 1-3 hours (rapid rehydration)
• Then 0.45% NaCl 250-500 mL/hour based on hydration status
• When glucose ≤250 mg/dL: Switch to D5W/0.45% NaCl (prevent hypoglycemia while continuing insulin for ketosis clearance)
• Goal: Replace deficit over 24-48 hours (avoid too-rapid correction - cerebral edema risk, especially in children)

2. Insulin:

• IMPORTANT: Do NOT start insulin until K+ ≥3.3 mEq/L (risk of fatal hypokalemia)
• Regular insulin 0.1 units/kg/hour IV continuous infusion (NOT SC in DKA - erratic absorption)
• Target: Glucose fall by 50-75 mg/dL/hour; if not falling, double infusion rate
• When glucose <250 mg/dL: Reduce to 0.05 units/kg/hour and switch IV fluid to D5W
• Continue insulin infusion until anion gap closes (NOT until glucose normalizes) - DKA resolution: pH >7.3 + HCO3 >18 + anion gap normal

3. Potassium Replacement:

• Paradox: Serum K+ is HIGH initially but total body K+ is LOW
• As insulin and fluids are given → K+ shifts intracellularly → RAPID hypokalemia
• If K+ 3.3-5.5 mEq/L: Add 20-40 mEq KCl to each liter of IV fluid
• If K+ <3.3: Give IV potassium BEFORE starting insulin
• If K+ >5.5: No potassium supplementation; reassess every 2 hours

4. Treat Precipitant (UTI in this case):

• Urine culture and sensitivity before starting antibiotics
• Start empirical antibiotics: Ceftriaxone 1g IV BD or oral ciprofloxacin/nitrofurantoin (if uncomplicated)
• Cover for gram-negative organisms (E. coli, Klebsiella)
• Continue specific antibiotics based on culture/sensitivity

5. Bicarbonate:

• Generally NOT recommended (even if pH <7.0) - may worsen hypokalemia, paradoxical CNS acidosis
• Consider only if pH <6.9 with hemodynamic compromise: Sodium bicarbonate 50 mEq in 200 mL sterile water over 2 hours

6. Other:

• NGT if altered consciousness (prevent aspiration)
• Urinary catheter for accurate urine output monitoring
• Hourly vitals, glucose monitoring; 2-hourly electrolytes
• Meticulous flow sheets
• Address OHA management: Metformin should be withheld until patient is stable and eating (risk of lactic acidosis)

Transition to SC Insulin:

• Once patient eating, anion gap closed, mentally alert → start SC insulin
• Overlap SC with IV insulin for 1-2 hours before stopping infusion

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Q3E: Conflict of Interest in Patient Care (5 marks)

Definition:

Types of Conflict of Interest:

Illustration Using a Clinical Example:

1. The evidence does not support PCI over medical therapy in stable CAD (COURAGE trial, ISCHEMIA trial)
2. Dr. Sharma receives a consultancy fee and procedural incentive from Company X
3. The patient undergoes an unnecessary, high-cost procedure with associated procedural risks (bleeding, contrast nephropathy, restenosis)

• The physician's financial relationship with Company X has compromised his obligation to recommend evidence-based, patient-centered care
• The patient is exposed to unnecessary risk and financial burden
• The decision was not made in the patient's best interest

How to Manage Conflict of Interest:

• Disclosure: Declare all financial relationships to patients and institutions
• Recusal: Step aside from decisions where COI exists
• Institutional oversight: Ethics committees, COI policies
• Ban on gifts: MCI/NMC guidelines in India prohibit accepting gifts, paid travel from pharma companies
• Informed consent: Patients must know if their doctor has a financial stake in recommended treatment
• Transparency in research: Declare funding sources in all publications

In India, the Medical Council of India (MCI) Code of Medical Ethics 2002 and now the National Medical Commission (NMC) explicitly prohibits physicians from accepting gifts, hospitality, or payments from pharmaceutical companies that could influence prescribing behavior.

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Quick Summary of All Answers

• ACS = UA + NSTEMI + STEMI spectrum; caused by plaque rupture → thrombosis
• Pathogenesis: Atherosclerosis → vulnerable plaque → rupture → platelet activation → thrombosis → ischemia/infarction
• Clinical: Crushing central chest pain >20 min, radiation, diaphoresis, dyspnea
• Emergency Rx: MONA + Aspirin 300 mg + P2Y12 inhibitor + STEMI → Primary PCI within 90 min / NSTEMI → Anticoagulation + early angiography + beta-blocker + high-dose statin

• Diagnosis: Spontaneous Bacterial Peritonitis (SBP) complicating decompensated cirrhosis (SAAG ≥1.1 + PMN ≥250 cells/mm³ = SBP)
• Evaluation: LFTs, viral markers, ultrasound Doppler, endoscopy, ascitic culture, Child-Pugh/MELD
• Management: Cefotaxime IV + IV albumin (Day 1: 1.5 g/kg, Day 3: 1 g/kg) + diuretics + SBP prophylaxis with norfloxacin