Do you know , for my MD Psychiatry university exam, MUHS university, Neurology case is of 100 marks?
MUHS MD Psychiatry university exam pattern neurology case 100 marks
MUHS Maharashtra University Health Sciences MD Psychiatry exam scheme marks distribution
| Component | Marks |
|---|---|
| Psychiatry Long Case | 100 marks |
| Neurology Case | 50 marks |
| Short Case (Psychiatry) | 60 marks |
| Viva Voce | 40 marks |
| Internal Assessment | 50 marks |
| Clinical Exam + Internal Assessment Total | 300 marks |
So the Neurology case is 50 marks, not 100, according to the IPS PG Training Guidelines that MUHS follows. The Long Case (Psychiatry) is 100 marks.
| Paper | Topic | Marks |
|---|---|---|
| Paper I | Basic Sciences as related to Psychiatry | 100 |
| Paper II | Clinical Psychiatry | 100 |
| Paper III | Psychiatric Specialties & Applied Psychiatry | 100 |
| Paper IV | Neuropsychiatry and Behavioural Neurology | 100 |
Consider you are my external examiner and ask me questions on my case of left hemiparesis having history of hypertension and hypertonia , brisk reflex and 2/5 power on left side with angle of mouth is deviated to right side. You are external examiner. Make a pdf of questions that you are going to ask me from must know, normal , brilliant and distinction level wise
mkdir -p /tmp/workspace/muhs-neurology-exam && ls /tmp/workspace/
cat << 'PYEOF' > /tmp/workspace/muhs-neurology-exam/generate_pdf.py from reportlab.lib.pagesizes import A4 from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib.units import cm from reportlab.lib import colors from reportlab.platypus import ( SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle, HRFlowable, KeepTogether ) from reportlab.lib.enums import TA_CENTER, TA_LEFT, TA_JUSTIFY from reportlab.platypus import PageBreak # ── Output path ────────────────────────────────────────────────────────────── OUTPUT = "/tmp/workspace/muhs-neurology-exam/MUHS_Neurology_Viva_Questions.pdf" # ── Document setup ─────────────────────────────────────────────────────────── doc = SimpleDocTemplate( OUTPUT, pagesize=A4, leftMargin=2*cm, rightMargin=2*cm, topMargin=2.5*cm, bottomMargin=2*cm, title="MUHS MD Psychiatry – Neurology Case Viva Questions", author="External Examiner (Orris AI)" ) # ── Colour palette ─────────────────────────────────────────────────────────── NAVY = colors.HexColor("#1a237e") DARK_BLUE = colors.HexColor("#283593") TEAL = colors.HexColor("#00695c") AMBER = colors.HexColor("#e65100") PURPLE = colors.HexColor("#4a148c") GOLD = colors.HexColor("#f9a825") LIGHT_GREY = colors.HexColor("#f5f5f5") WHITE = colors.white RED_DARK = colors.HexColor("#b71c1c") LEVEL_COLORS = { "MUST KNOW": (colors.HexColor("#e3f2fd"), colors.HexColor("#0d47a1")), "NORMAL": (colors.HexColor("#e8f5e9"), colors.HexColor("#1b5e20")), "BRILLIANT": (colors.HexColor("#fff8e1"), colors.HexColor("#e65100")), "DISTINCTION": (colors.HexColor("#f3e5f5"), colors.HexColor("#4a148c")), } # ── Styles ─────────────────────────────────────────────────────────────────── styles = getSampleStyleSheet() title_style = ParagraphStyle( "TitleStyle", parent=styles["Title"], fontSize=18, leading=24, textColor=NAVY, spaceAfter=4, alignment=TA_CENTER, fontName="Helvetica-Bold" ) subtitle_style = ParagraphStyle( "SubTitle", parent=styles["Normal"], fontSize=11, leading=16, textColor=DARK_BLUE, spaceAfter=2, alignment=TA_CENTER, fontName="Helvetica" ) case_header_style = ParagraphStyle( "CaseHeader", parent=styles["Normal"], fontSize=10, leading=14, textColor=WHITE, spaceBefore=0, spaceAfter=0, leftIndent=6, fontName="Helvetica-Bold" ) case_body_style = ParagraphStyle( "CaseBody", parent=styles["Normal"], fontSize=9.5, leading=14, textColor=colors.HexColor("#212121"), spaceBefore=0, spaceAfter=0, leftIndent=6, fontName="Helvetica" ) level_heading_style = ParagraphStyle( "LevelHeading", parent=styles["Normal"], fontSize=13, leading=18, textColor=WHITE, spaceBefore=2, spaceAfter=2, fontName="Helvetica-Bold", alignment=TA_CENTER ) question_style = ParagraphStyle( "Question", parent=styles["Normal"], fontSize=9.5, leading=15, textColor=colors.HexColor("#212121"), spaceBefore=0, spaceAfter=0, fontName="Helvetica", leftIndent=4 ) note_style = ParagraphStyle( "Note", parent=styles["Normal"], fontSize=8.5, leading=13, textColor=colors.HexColor("#5d4037"), spaceBefore=0, spaceAfter=0, fontName="Helvetica-Oblique", leftIndent=4 ) footer_style = ParagraphStyle( "Footer", parent=styles["Normal"], fontSize=8, textColor=colors.grey, alignment=TA_CENTER, fontName="Helvetica" ) # ── Data ───────────────────────────────────────────────────────────────────── CASE_SUMMARY = [ ("Patient:", "Adult with Left Hemiparesis"), ("History:", "Hypertension (known case)"), ("Tone:", "Hypertonia on left side"), ("Reflexes:", "Brisk / Hyperreflexia on left side"), ("Power:", "2/5 on left side (upper and lower limb)"), ("Cranial Nerve:", "Angle of mouth deviated to RIGHT side (left LMNF of VII spared; right side droop = central VII)"), ("Localization:", "Right-sided UMN lesion (corticospinal + corticobulbar tract involvement)"), ("Likely Dx:", "Right-sided Ischaemic / Haemorrhagic Stroke (Hypertensive)"), ] QUESTIONS = { "MUST KNOW": { "badge": "PASS LEVEL", "intro": "Every MD Psychiatry candidate MUST answer these correctly. Failure here = fail in clinical.", "items": [ ("Q1", "What is your diagnosis in this patient? Justify with clinical findings.", "Right-sided UMN lesion causing left hemiparesis. Evidence: contralateral weakness, hypertonia, hyperreflexia, central VII palsy (mouth deviated away from lesion side)."), ("Q2", "Differentiate UMN vs LMN lesion on clinical examination.", "UMN: spasticity, hyperreflexia, Babinski +ve, no significant atrophy, clasp-knife rigidity. LMN: flaccidity, hyporeflexia/areflexia, fasciculations, significant wasting."), ("Q3", "Why is the mouth deviated to the RIGHT in this patient who has LEFT-sided weakness?", "Central (UMN) facial palsy spares the upper face (forehead). The RIGHT mouth droop = left corticobulbar tract lesion. But here mouth is deviated to right = LEFT side is weak facially. Ipsilateral to weakness = LMN? Examiner tests your reasoning. Correct: in UMN VII palsy, the WEAK side droops/deviates AWAY from the midline, so mouth corner falls on the weak side. The intact side pulls the mouth to the right. Left face is weak → mouth deviates to right."), ("Q4", "What is the MRC power scale? What does 2/5 mean?", "0=no movement; 1=flicker; 2=movement with gravity eliminated; 3=movement against gravity; 4=movement against some resistance; 5=normal power. 2/5 = can move limb only when gravity is eliminated."), ("Q5", "Name 4 investigations you would order immediately for this patient.", "1. Non-contrast CT brain (rule out haemorrhage). 2. MRI brain DWI (ischaemic stroke). 3. ECG (AF as embolic cause). 4. Blood: CBC, RBS, S. electrolytes, coagulation profile, lipid profile."), ("Q6", "What is Babinski's sign? How do you elicit it and what does it indicate?", "Elicited by firm stroking of lateral plantar surface. Positive = extension of big toe + fanning of other toes. Indicates UMN lesion (corticospinal tract involvement)."), ("Q7", "What are the psychiatric complications of stroke relevant to a psychiatrist?", "Post-stroke depression (most common ~33%), post-stroke anxiety, emotionalism (pathological crying/laughing), post-stroke psychosis, vascular dementia, delirium, apathy, anosognosia."), ] }, "NORMAL": { "badge": "GOOD PASS", "intro": "Questions for a solid pass. Candidate should answer 70-80% correctly.", "items": [ ("Q1", "Localize the lesion: where exactly in the neuraxis is this lesion likely to be?", "Right side: internal capsule (posterior limb) OR right MCA territory cortex. Internal capsule lesion = pure motor hemiplegia without cortical signs. Cortical lesion = may have sensory loss, homonymous hemianopia, aphasia (if dominant hemisphere)."), ("Q2", "What is clasp-knife rigidity? How does it differ from cogwheel and lead-pipe rigidity?", "Clasp-knife = velocity-dependent resistance that suddenly gives way (UMN/spasticity). Cogwheel = ratchety resistance throughout ROM (Parkinsonism). Lead-pipe = uniform resistance throughout (extrapyramidal)."), ("Q3", "What are the vascular territories of the brain and which is most commonly involved in hypertensive stroke?", "MCA (most common), ACA, PCA, vertebrobasilar. Hypertensive bleeds: basal ganglia (putamen most common), thalamus, pons, cerebellum. Lacunar infarcts: posterior limb of internal capsule (pure motor hemiplegia)."), ("Q4", "Explain the anatomical basis of why upper face is SPARED in UMN VII palsy.", "Frontalis/orbicularis oculi receive bilateral cortical representation (both hemispheres project to their nuclei). Lower face receives predominantly contralateral cortical input only. So UMN lesion affects lower face but spares forehead."), ("Q5", "What is the NIHSS? Name 5 items assessed in it.", "National Institutes of Health Stroke Scale. Items: level of consciousness, gaze, visual fields, facial palsy, motor arm, motor leg, limb ataxia, sensory, language, dysarthria, extinction/neglect. Max score 42."), ("Q6", "What antihypertensives are used in acute stroke and what targets are recommended?", "In ischaemic stroke: do NOT aggressively lower BP; target <185/110 if thrombolysis planned; otherwise permissive hypertension up to 220/120 for first 24h. In haemorrhagic stroke: target SBP <140. Preferred agents: labetalol, nicardipine IV."), ("Q7", "What is post-stroke depression (PSD)? What is its timeframe and treatment?", "Occurs in ~33% of stroke survivors. Can appear acutely or at 3-6 months. Linked to lesions in left frontal lobe, basal ganglia. Treatment: SSRIs (sertraline, escitalopram) preferred. Nortriptyline also studied. Psychotherapy + rehabilitation important."), ("Q8", "What is hemineglect? How would you test for it?", "Failure to attend to stimuli on the side contralateral to the lesion (usually right hemisphere lesion causing left neglect). Tests: line bisection test, cancellation test, clock drawing test, double simultaneous stimulation."), ] }, "BRILLIANT": { "badge": "MERIT / DISTINCTION BORDER", "intro": "For candidates aiming above average. Demonstrates depth of neuropsychiatric knowledge.", "items": [ ("Q1", "Describe the complete course of the corticospinal tract from cortex to spinal cord and explain why this patient has contralateral weakness.", "Origin: primary motor cortex (area 4), premotor (area 6), somatosensory cortex. Passes through corona radiata → posterior limb of internal capsule → cerebral peduncle → basis pontis → medullary pyramid → decussates at cervicomedullary junction → lateral corticospinal tract. Decussation explains contralateral weakness."), ("Q2", "What is the locked-in syndrome? How does it differ from this patient's presentation?", "Locked-in syndrome: bilateral ventral pontine lesion interrupting corticospinal and corticobulbar tracts bilaterally. Patient is quadriplegic, anarthric but CONSCIOUS with preserved vertical eye movements. This patient has unilateral lesion with preserved consciousness and speech."), ("Q3", "What is the concept of diaschisis? How is it relevant in stroke recovery?", "Von Monakow's concept: remote functional depression of areas connected to but not directly damaged by the lesion (e.g., contralateral cerebellar depression after supratentorial stroke = crossed cerebellar diaschisis). Relevant because recovery partly involves resolution of diaschisis and neural reorganisation."), ("Q4", "Discuss the neurobiology of post-stroke depression. Which lesion locations are associated?", "Disruption of frontal-subcortical circuits (especially left frontal lobe, basal ganglia, thalamus). Monoamine depletion (serotonin, norepinephrine pathways). Inflammatory cytokines (IL-6, TNF-alpha) post-infarction. HPA axis dysregulation. Left dorsolateral prefrontal cortex lesions most associated with PSD."), ("Q5", "What is emotionalism (pathological laughing and crying) post-stroke? What is its neural basis?", "Involuntary, uncontrollable episodes of laughing or crying disproportionate/incongruent to emotional state. Neural basis: damage to pathways modulating brainstem emotional motor control (corticobulbar, cerebellar-brainstem circuits). Treated with SSRIs (sertraline, fluoxetine) or TCAs (nortriptyline)."), ("Q6", "Explain the role of NMDA receptors in ischaemic neuronal death (excitotoxicity).", "Ischaemia → ATP depletion → failure of Na/K-ATPase → cell depolarisation → mass glutamate release → NMDA receptor overactivation → Ca2+ influx → activation of lipases, proteases, endonucleases → free radical generation → mitochondrial dysfunction → apoptosis/necrosis."), ("Q7", "What is vascular cognitive impairment (VCI)? Distinguish it from Alzheimer's disease.", "VCI: cognitive impairment from cerebrovascular disease. Subcortical type (small vessel disease) = executive dysfunction, slowed processing, gait disturbance, urinary urgency, less prominent memory loss. Alzheimer's = predominantly episodic memory failure early, insidious onset, no focal signs initially. VCI: stepwise progression, focal signs, vascular risk factors, neuroimaging changes (white matter hyperintensities, lacunes)."), ] }, "DISTINCTION": { "badge": "DISTINCTION LEVEL", "intro": "High-order reasoning questions. Expected only from the top 5-10% of candidates. Demonstrates mastery.", "items": [ ("Q1", "If this patient instead had LEFT hemisphere lesion with right hemiplegia — what additional neuropsychiatric features would you expect and why?", "Broca's aphasia (non-fluent, effortful speech) or Wernicke's aphasia (fluent but nonsensical) depending on lesion location. Apraxia (ideomotor). Post-stroke depression even more likely (left anterior lesion). Anosognosia less common than with right hemisphere lesions. Right hemisphere lesion more commonly causes neglect, anosognosia, prosody disturbance, visuospatial deficits."), ("Q2", "What is the difference between spasticity and rigidity at a neurophysiological level? Which spinal circuits are involved?", "Spasticity: velocity-dependent increase in tonic stretch reflexes; caused by loss of descending inhibition (reticulospinal pathways) → hyperexcitable muscle spindle Ia afferents via reduced presynaptic inhibition and reduced Ib interneuron inhibition. Rigidity: non-velocity-dependent; caused by excessive gamma motor neuron drive from basal ganglia loop disruption (loss of dopaminergic inhibition of indirect pathway → excessive pallidal output → thalamic suppression → loss of cortical modulation of gamma drive)."), ("Q3", "Discuss neuroplasticity mechanisms relevant to recovery after stroke. How can a psychiatrist contribute to rehabilitation?", "Axonal sprouting, dendritic remodelling, unmasking of latent pathways, contralateral hemisphere recruitment, synaptogenesis. BDNF plays key role. Constraint-induced movement therapy exploits neuroplasticity. Psychiatrist's role: treat PSD (untreated depression worsens rehabilitation outcomes significantly), manage anxiety, cognitive rehabilitation, motivational interviewing, family psychoeducation, manage emotionalism, screen and treat vascular dementia."), ("Q4", "What is the thalamic pain syndrome (Dejerine-Roussy syndrome)? How would you manage it?", "Central post-stroke pain following thalamic infarct (VPL nucleus). Contralateral hemibody burning/aching pain, allodynia, hyperalgesia, sometimes spontaneous. Management: tricyclic antidepressants (amitriptyline), anticonvulsants (gabapentin, pregabalin, lamotrigine), opioids for refractory cases, thalamic deep brain stimulation in refractory cases. SSRIs have limited efficacy."), ("Q5", "If this patient develops acute psychosis 2 weeks post-stroke, how would you approach it? What organic causes would you rule out?", "Organic causes to rule out: delirium (metabolic, infection, drug-induced), post-stroke psychosis (lesion location: right temporal/parietal), new haemorrhage, non-convulsive status epilepticus (post-stroke seizures), steroid-induced psychosis (if on dexamethasone), hyponatremia, UTI in elderly. Approach: MRI brain (new lesion?), EEG, metabolic panel, urine culture, review medications. Treatment: low-dose atypical antipsychotic (quetiapine preferred in elderly) + treat underlying cause."), ("Q6", "How does the concept of 'cerebral autoregulation' relate to this hypertensive patient's stroke, and what are the implications for BP management?", "Normal autoregulation maintains CBF constant over MAP 60-160 mmHg. Chronic hypertension shifts the autoregulation curve rightward (brain acclimates to higher pressures). After stroke, autoregulation may be impaired in the ischaemic penumbra. Aggressive BP lowering can reduce perfusion in penumbra → extend infarct. Hence permissive hypertension in first 24-48h unless thrombolysis planned or haemorrhagic transformation suspected."), ] } } # ── Build story ─────────────────────────────────────────────────────────────── story = [] # ── Title block ────────────────────────────────────────────────────────────── story.append(Spacer(1, 0.3*cm)) story.append(Paragraph("MUHS MD PSYCHIATRY EXAMINATION", title_style)) story.append(Paragraph("Neurology Case — External Examiner Question Bank", subtitle_style)) story.append(Paragraph("Prepared by: External Examiner | Date: July 2026", subtitle_style)) story.append(Spacer(1, 0.4*cm)) story.append(HRFlowable(width="100%", thickness=2, color=NAVY)) story.append(Spacer(1, 0.3*cm)) # ── Case Summary Box ───────────────────────────────────────────────────────── case_rows = [[ Paragraph("CLINICAL CASE SUMMARY", case_header_style), "" ]] for label, value in CASE_SUMMARY: case_rows.append([ Paragraph(f"<b>{label}</b>", case_body_style), Paragraph(value, case_body_style) ]) case_table = Table(case_rows, colWidths=[4.5*cm, 12.5*cm]) case_table.setStyle(TableStyle([ ("BACKGROUND", (0, 0), (-1, 0), NAVY), ("SPAN", (0, 0), (-1, 0)), ("ALIGN", (0, 0), (-1, 0), "CENTER"), ("BACKGROUND", (0, 1), (-1, -1), LIGHT_GREY), ("ROWBACKGROUNDS", (0, 1), (-1, -1), [colors.HexColor("#eceff1"), colors.HexColor("#fafafa")]), ("GRID", (0, 0), (-1, -1), 0.5, colors.HexColor("#b0bec5")), ("TOPPADDING", (0, 0), (-1, -1), 5), ("BOTTOMPADDING",(0, 0), (-1, -1), 5), ("LEFTPADDING", (0, 0), (-1, -1), 6), ("RIGHTPADDING",(0, 0), (-1, -1), 6), ("FONTNAME", (0, 1), (0, -1), "Helvetica-Bold"), ("VALIGN", (0, 0), (-1, -1), "TOP"), ])) story.append(case_table) story.append(Spacer(1, 0.5*cm)) # ── Level sections ──────────────────────────────────────────────────────────── LEVEL_ORDER = ["MUST KNOW", "NORMAL", "BRILLIANT", "DISTINCTION"] LEVEL_ICONS = { "MUST KNOW": "⚡ MUST KNOW [Pass Level]", "NORMAL": "✓ NORMAL [Good Pass]", "BRILLIANT": "★ BRILLIANT [Merit / Distinction Border]", "DISTINCTION": "◆ DISTINCTION [Top Performer]", } for level in LEVEL_ORDER: bg, fg = LEVEL_COLORS[level] data = QUESTIONS[level] # Level header row header_para = Paragraph(f"<b>{LEVEL_ICONS[level]}</b>", level_heading_style) header_table = Table([[header_para]], colWidths=[17*cm]) header_table.setStyle(TableStyle([ ("BACKGROUND", (0, 0), (-1, -1), fg), ("TOPPADDING", (0, 0), (-1, -1), 8), ("BOTTOMPADDING", (0, 0), (-1, -1), 8), ("LEFTPADDING", (0, 0), (-1, -1), 8), ("ROUNDEDCORNERS", [4]), ])) story.append(KeepTogether([header_table])) story.append(Spacer(1, 0.15*cm)) # Intro blurb intro_para = Paragraph(f"<i>{data['intro']}</i>", note_style) story.append(intro_para) story.append(Spacer(1, 0.25*cm)) # Questions q_rows = [ [ Paragraph("<b>No.</b>", ParagraphStyle("QH", parent=styles["Normal"], fontSize=9, fontName="Helvetica-Bold", textColor=WHITE, alignment=TA_CENTER)), Paragraph("<b>Question</b>", ParagraphStyle("QH", parent=styles["Normal"], fontSize=9, fontName="Helvetica-Bold", textColor=WHITE)), Paragraph("<b>Key Points Expected</b>", ParagraphStyle("QH", parent=styles["Normal"], fontSize=9, fontName="Helvetica-Bold", textColor=WHITE)), ] ] for qnum, question, keypoints in data["items"]: q_rows.append([ Paragraph(f"<b>{qnum}</b>", ParagraphStyle("QN", parent=styles["Normal"], fontSize=9.5, fontName="Helvetica-Bold", alignment=TA_CENTER)), Paragraph(question, question_style), Paragraph(f"<i>{keypoints}</i>", note_style), ]) q_table = Table(q_rows, colWidths=[1.1*cm, 7.3*cm, 8.6*cm]) q_table.setStyle(TableStyle([ ("BACKGROUND", (0, 0), (-1, 0), fg), ("TEXTCOLOR", (0, 0), (-1, 0), WHITE), ("ROWBACKGROUNDS",(0, 1), (-1, -1), [bg, WHITE]), ("GRID", (0, 0), (-1, -1), 0.4, colors.HexColor("#cfd8dc")), ("TOPPADDING", (0, 0), (-1, -1), 6), ("BOTTOMPADDING", (0, 0), (-1, -1), 6), ("LEFTPADDING", (0, 0), (-1, -1), 5), ("RIGHTPADDING", (0, 0), (-1, -1), 5), ("VALIGN", (0, 0), (-1, -1), "TOP"), ("ALIGN", (0, 0), (0, -1), "CENTER"), ])) story.append(q_table) story.append(Spacer(1, 0.6*cm)) # ── Marking guidance ───────────────────────────────────────────────────────── story.append(HRFlowable(width="100%", thickness=1.5, color=NAVY)) story.append(Spacer(1, 0.2*cm)) story.append(Paragraph("<b>EXAMINER'S MARKING GUIDANCE</b>", ParagraphStyle( "MG", parent=styles["Normal"], fontSize=11, fontName="Helvetica-Bold", textColor=NAVY, spaceAfter=4))) marking_data = [ ["Level", "Expected Performance", "Marks Range (out of 50)"], ["Must Know", "Answers all 7 correctly with clear reasoning", "20 – 25"], ["Normal", "Answers 6-8 correctly with adequate depth", "26 – 35"], ["Brilliant", "Answers 5-7 with depth and clinical correlation", "36 – 42"], ["Distinction","Answers 4-6 with original insight and integration", "43 – 50"], ] m_table = Table(marking_data, colWidths=[3.5*cm, 9.5*cm, 4*cm]) m_table.setStyle(TableStyle([ ("BACKGROUND", (0, 0), (-1, 0), NAVY), ("TEXTCOLOR", (0, 0), (-1, 0), WHITE), ("FONTNAME", (0, 0), (-1, 0), "Helvetica-Bold"), ("ROWBACKGROUNDS",(0, 1), (-1, -1), [colors.HexColor("#e3f2fd"), colors.HexColor("#e8f5e9"), colors.HexColor("#fff8e1"), colors.HexColor("#f3e5f5")]), ("GRID", (0, 0), (-1, -1), 0.5, colors.HexColor("#b0bec5")), ("TOPPADDING", (0, 0), (-1, -1), 6), ("BOTTOMPADDING", (0, 0), (-1, -1), 6), ("LEFTPADDING", (0, 0), (-1, -1), 6), ("ALIGN", (2, 0), (2, -1), "CENTER"), ("FONTNAME", (0, 1), (-1, -1), "Helvetica"), ("FONTSIZE", (0, 0), (-1, -1), 9), ("VALIGN", (0, 0), (-1, -1), "MIDDLE"), ])) story.append(m_table) story.append(Spacer(1, 0.4*cm)) story.append(Paragraph( "Note: In MUHS MD Psychiatry clinical examination, the Neurology case is worth 50 marks. " "The candidate must demonstrate neurological localization, clinical reasoning, and " "neuropsychiatric correlation. Marks are awarded for accuracy, depth, and clinical relevance.", ParagraphStyle("NoteBottom", parent=styles["Normal"], fontSize=8.5, fontName="Helvetica-Oblique", textColor=colors.HexColor("#5d4037")) )) story.append(Spacer(1, 0.2*cm)) story.append(HRFlowable(width="100%", thickness=1, color=colors.grey)) story.append(Spacer(1, 0.1*cm)) story.append(Paragraph( "Generated by Orris AI | MUHS MD Psychiatry Neurology Viva | July 2026 | For Educational Use Only", footer_style )) # ── Build PDF ───────────────────────────────────────────────────────────────── doc.build(story) print(f"PDF created: {OUTPUT}") PYEOF python3 /tmp/workspace/muhs-neurology-exam/generate_pdf.py
MUHS Neurology Viva Questions
PDF Document · PDF
| Feature | Finding |
|---|---|
| Diagnosis | Right-sided UMN lesion → Left Hemiparesis |
| History | Hypertension (known case) |
| Tone | Hypertonia on left side |
| Reflexes | Brisk / Hyperreflexia on left side |
| Power | 2/5 left side |
| Cranial nerve | Mouth deviated to RIGHT = left upper motor neuron VII palsy |
| Likely etiology | Right-sided hypertensive ischaemic/haemorrhagic stroke |
| Q | Question | Key Points |
|---|---|---|
| Q1 | What is your diagnosis? Justify. | Right UMN lesion: contralateral weakness + hypertonia + hyperreflexia + central VII palsy |
| Q2 | Differentiate UMN vs LMN clinically | UMN: spasticity, hyperreflexia, Babinski +ve, no wasting. LMN: flaccidity, fasciculations, atrophy |
| Q3 | Why is the mouth deviated to the RIGHT in a LEFT hemiparesis? | UMN VII palsy - left face is weak, intact right side pulls mouth to right |
| Q4 | What is MRC power scale? What does 2/5 mean? | Movement with gravity eliminated only |
| Q5 | Name 4 immediate investigations | CT brain, MRI DWI, ECG, blood workup (CBC/RBS/lipids/coagulation) |
| Q6 | What is Babinski's sign? How to elicit? | Lateral plantar stroke → extensor plantar = UMN lesion |
| Q7 | Psychiatric complications of stroke? | PSD, anxiety, emotionalism, psychosis, vascular dementia, delirium, anosognosia |
Can you make similar questions that can be asked by external examiner for the case of schizophrenia patient having delusion of persecution, auditory hallucinations, continuous illness and having family history of bipolar mood disorder . Ask questions in similar 4 sets, must know, good to know , brilliant and distinction . Ask around 50-60 questions in total
cat << 'PYEOF' > /tmp/workspace/muhs-neurology-exam/schizophrenia_viva.py from reportlab.lib.pagesizes import A4 from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib.units import cm from reportlab.lib import colors from reportlab.platypus import ( SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle, HRFlowable, KeepTogether, PageBreak ) from reportlab.lib.enums import TA_CENTER, TA_LEFT, TA_JUSTIFY OUTPUT = "/tmp/workspace/muhs-neurology-exam/MUHS_Schizophrenia_Viva_Questions.pdf" doc = SimpleDocTemplate( OUTPUT, pagesize=A4, leftMargin=1.8*cm, rightMargin=1.8*cm, topMargin=2.2*cm, bottomMargin=2*cm, title="MUHS MD Psychiatry – Schizophrenia Case Viva Questions", author="External Examiner (Orris AI)" ) # Colours NAVY = colors.HexColor("#1a237e") DARK_BLUE = colors.HexColor("#283593") TEAL = colors.HexColor("#00695c") AMBER = colors.HexColor("#e65100") PURPLE = colors.HexColor("#4a148c") GOLD = colors.HexColor("#f9a825") LIGHT_GREY = colors.HexColor("#f5f5f5") WHITE = colors.white LEVEL_COLORS = { "MUST KNOW": (colors.HexColor("#e3f2fd"), colors.HexColor("#0d47a1")), "GOOD TO KNOW": (colors.HexColor("#e8f5e9"), colors.HexColor("#1b5e20")), "BRILLIANT": (colors.HexColor("#fff8e1"), colors.HexColor("#e65100")), "DISTINCTION": (colors.HexColor("#f3e5f5"), colors.HexColor("#4a148c")), } styles = getSampleStyleSheet() title_style = ParagraphStyle("TS", parent=styles["Title"], fontSize=17, leading=22, textColor=NAVY, alignment=TA_CENTER, fontName="Helvetica-Bold", spaceAfter=3) subtitle_style = ParagraphStyle("SS", parent=styles["Normal"], fontSize=10.5, leading=15, textColor=DARK_BLUE, alignment=TA_CENTER, fontName="Helvetica", spaceAfter=2) case_header_style = ParagraphStyle("CH", parent=styles["Normal"], fontSize=10, leading=14, textColor=WHITE, leftIndent=6, fontName="Helvetica-Bold") case_body_style = ParagraphStyle("CB", parent=styles["Normal"], fontSize=9.5, leading=14, textColor=colors.HexColor("#212121"), leftIndent=6, fontName="Helvetica") level_heading_style = ParagraphStyle("LH", parent=styles["Normal"], fontSize=12, leading=17, textColor=WHITE, fontName="Helvetica-Bold", alignment=TA_CENTER) question_style = ParagraphStyle("QS", parent=styles["Normal"], fontSize=9, leading=14, textColor=colors.HexColor("#1a1a1a"), fontName="Helvetica", leftIndent=4) note_style = ParagraphStyle("NS", parent=styles["Normal"], fontSize=8.5, leading=13, textColor=colors.HexColor("#4e342e"), fontName="Helvetica-Oblique", leftIndent=4) footer_style = ParagraphStyle("FS", parent=styles["Normal"], fontSize=8, textColor=colors.grey, alignment=TA_CENTER, fontName="Helvetica") section_tag_style = ParagraphStyle("STG", parent=styles["Normal"], fontSize=8, leading=11, textColor=WHITE, fontName="Helvetica-Bold", alignment=TA_CENTER) # ─── CASE SUMMARY ──────────────────────────────────────────────────────────── CASE_SUMMARY = [ ("Patient:", "Adult (likely young adult male, late teens to 30s)"), ("Presenting complaint:", "Delusion of persecution + Auditory hallucinations"), ("Illness course:", "Continuous illness (no periods of remission)"), ("Family history:", "Bipolar mood disorder in a first-degree relative"), ("Key clinical issue:", "Diagnosis, differential (schizoaffective?), treatment, long-term prognosis"), ("Exam significance:", "Tests clinical reasoning, psychopathology, pharmacology, and neuropsychiatric insight"), ] # ─── QUESTIONS ─────────────────────────────────────────────────────────────── QUESTIONS = { "MUST KNOW": { "badge": "PASS LEVEL — Every candidate must answer these", "color_key": "MUST KNOW", "items": [ ("Q1", "What is your diagnosis in this patient? State the criteria you are using.", "Schizophrenia (DSM-5-TR / ICD-11). Criteria: ≥2 of: delusions, hallucinations, disorganized speech, disorganized/catatonic behaviour, negative symptoms — present for ≥1 month active phase + ≥6 months total including prodrome. Functioning impaired. Not attributable to substances or medical condition."), ("Q2", "What type of delusion does this patient have? Define it.", "Delusion of persecution (paranoid delusion). A fixed, false, unshakeable belief that one is being harmed, harassed, cheated, or conspired against — not consistent with cultural norms and not amenable to counter-argument."), ("Q3", "What is an auditory hallucination? How do you differentiate it from illusions and pseudohallucinations?", "Hallucination: perception without external stimulus, with full force of reality. Illusion: misperception of a real stimulus. Pseudohallucination: vivid, involuntary, perceived in inner space (mind's eye/ear), patient recognises it as not real. Schizophrenia: true hallucinations, perceived externally."), ("Q4", "Name and describe Schneider's First Rank Symptoms. Which are present in this case?", "FRS: (1) Thought insertion/withdrawal/broadcasting, (2) Made feelings/impulses/actions (passivity phenomena), (3) Somatic passivity, (4) Delusional perception, (5) Third-person running commentary, (6) Voices arguing/discussing. In this case: auditory hallucinations (likely 3rd person) + delusion of persecution may indicate delusional perception."), ("Q5", "What is the difference between positive and negative symptoms of schizophrenia? Give 4 examples of each.", "Positive (excess/distortion): hallucinations, delusions, disorganized speech, disorganized behaviour. Negative (diminution/absence): alogia, avolition, anhedonia, affective flattening, asociality."), ("Q6", "What does 'continuous illness' mean in the context of schizophrenia? What is its prognostic significance?", "Continuous course = no discrete episodes with return to baseline; persistent psychotic or residual symptoms. Prognostically poor: associated with more negative symptoms, cognitive decline, treatment resistance, and significant functional impairment."), ("Q7", "What first-line antipsychotic would you start in this patient and at what dose?", "Atypical (2nd generation) antipsychotic: Olanzapine 5-20mg/day, Risperidone 2-6mg/day, or Aripiprazole 10-30mg/day. Or FGA: Haloperidol 5-15mg/day. Start low, titrate. Prefer atypical for better tolerability. Monitor metabolic parameters (olanzapine)."), ("Q8", "What is the significance of the family history of bipolar disorder in this case?", "Raises differential diagnosis of schizoaffective disorder or bipolar disorder with psychotic features. Also has genetic/heritability significance: schizophrenia and bipolar share genetic risk loci (DISC1, NRG1, CACNA1C). Family history of bipolar increases risk of mood episodes in this patient."), ("Q9", "How long must symptoms be present to diagnose schizophrenia as per DSM-5?", "At least 6 months (including ≥1 month of active-phase symptoms i.e., Criterion A). Before 6 months = Schizophreniform disorder. Before 1 month = Brief Psychotic Disorder."), ("Q10", "What is the difference between schizophrenia, schizophreniform disorder, and brief psychotic disorder?", "Brief Psychotic Disorder: 1 day to <1 month. Schizophreniform Disorder: 1-6 months. Schizophrenia: >6 months. Social/occupational dysfunction required for schizophrenia diagnosis but not the other two."), ("Q11", "Name 4 important physical investigations you would order before starting antipsychotics.", "1. CBC (baseline, clozapine monitoring). 2. Fasting blood glucose + lipid profile (metabolic syndrome risk). 3. LFT, RFT. 4. ECG (QTc prolongation risk with antipsychotics). Also: thyroid function, urine drug screen, pregnancy test in females."), ("Q12", "What is the dopamine hypothesis of schizophrenia? Which pathway is involved in positive symptoms?", "Mesolimbic HYPERDOPAMINERGIA → positive symptoms (hallucinations, delusions). Mesocortical HYPODOPAMINERGIA → negative symptoms and cognitive deficits. Antipsychotics work mainly by D2 blockade in mesolimbic pathway."), ("Q13", "What are the extrapyramidal side effects of antipsychotics? Name 4.", "1. Acute dystonia (within hours-days). 2. Akathisia (restlessness, within days-weeks). 3. Drug-induced Parkinsonism (bradykinesia, tremor, rigidity). 4. Tardive dyskinesia (after months-years of use — orofacial involuntary movements)."), ] }, "GOOD TO KNOW": { "badge": "GOOD PASS — Demonstrates clinical competence", "color_key": "GOOD TO KNOW", "items": [ ("Q1", "How would you differentiate schizophrenia from schizoaffective disorder in this patient?", "Schizoaffective disorder requires: (a) uninterrupted period with major mood episode concurrent with Criterion A symptoms of schizophrenia, AND (b) delusions/hallucinations for ≥2 weeks WITHOUT prominent mood symptoms, AND (c) mood symptoms present for majority of total illness duration. If family history of bipolar and mood features emerge, reconsider diagnosis longitudinally."), ("Q2", "What is delusional disorder? How does it differ from schizophrenia?", "Delusional disorder: non-bizarre delusions, ≥1 month, functioning NOT markedly impaired, no prominent hallucinations, no Criterion A schizophrenia symptoms. Schizophrenia: broader psychopathology (hallucinations, disorganisation, negative symptoms), functional impairment, longer duration."), ("Q3", "Classify auditory hallucinations. Which type is most characteristic of schizophrenia?", "Elementary (tinnitus-like), verbal (voices). Types: 2nd person (commands/insults), 3rd person (running commentary or two voices discussing patient). 3rd-person auditory hallucinations = Schneiderian FRS, highly characteristic of schizophrenia. Command hallucinations carry risk of violence/self-harm."), ("Q4", "What is thought broadcasting? How would a patient describe it?", "Patient believes their thoughts are being broadcast to others (radio, TV, can be heard by strangers). A Schneiderian FRS. Patient may say: 'My thoughts are going out on the radio' or 'People around me can hear what I think.'"), ("Q5", "What psychosocial interventions are evidence-based in schizophrenia?", "1. Cognitive Behavioural Therapy for psychosis (CBTp). 2. Family therapy/psychoeducation (reduces expressed emotion, reduces relapse rate by ~50%). 3. Social skills training. 4. Supported employment (Individual Placement and Support model). 5. Assertive Community Treatment (ACT). 6. Cognitive remediation therapy for cognitive deficits."), ("Q6", "What is Neuroleptic Malignant Syndrome (NMS)? How is it managed?", "NMS: hyperthermia, severe rigidity, autonomic instability (BP fluctuations, tachycardia, diaphoresis), altered consciousness + markedly raised CK. Management: STOP antipsychotic immediately, supportive care (cooling, IV fluids), dantrolene (muscle relaxant), bromocriptine/amantadine (dopamine agonists), ICU if severe. Do NOT restart same antipsychotic for at least 2 weeks."), ("Q7", "What is tardive dyskinesia? How do you manage it?", "Tardive dyskinesia (TD): late-onset, involuntary repetitive movements — mainly orofacial (lip smacking, tongue protrusion, chewing), also limb/trunk choreiform movements. Caused by D2 receptor supersensitivity after prolonged blockade. Management: Reduce/switch antipsychotic, VMAT2 inhibitors (valbenazine, deutetrabenazine) — FDA-approved for TD. Clonazepam may help. Switch to clozapine (low TD risk)."), ("Q8", "What is the role of clozapine in schizophrenia? When is it indicated?", "Clozapine: gold standard for treatment-resistant schizophrenia (TRS) = failure of ≥2 antipsychotics at adequate dose/duration. Also for suicidality (FDA-approved indication). Mechanism: low D2 affinity + high 5HT2A, alpha, H1, M antagonism. Serious risk: agranulocytosis (1-2%) — mandatory WBC/ANC monitoring. Metabolic syndrome, seizures, hypersalivation, myocarditis."), ("Q9", "What is expressed emotion (EE)? How does it affect schizophrenia outcomes?", "High expressed emotion (EE) in families = high levels of criticism, hostility, emotional over-involvement. High EE families → 2-3x higher relapse rate compared to low EE families. Family therapy aims to reduce EE. Key studies: Brown, Vaughn & Leff. Psychoeducation for family is a cornerstone of management."), ("Q10", "What is the concept of 'insight' in psychiatry? How would you assess it in this patient?", "Insight = patient's awareness of their illness. Use David's Insight Scale / Schedule for Assessment of Insight (SAI). Dimensions: (1) awareness of mental illness, (2) recognition that symptoms are due to illness, (3) compliance with treatment. Most schizophrenia patients have impaired insight (anosognosia), which is a major driver of non-compliance."), ("Q11", "What is the genetic basis of schizophrenia? What is the heritability?", "Heritability ~80%. Multifactorial polygenic. Risk: MZ twin concordance 40-50%, DZ ~15%, first-degree relative ~10%, general population ~1%. Key genes: DISC1, NRG1, DTNBP1, COMT (Val158Met). Copy number variants: 22q11.2 deletion (DiGeorge syndrome) → 20-30% develop schizophrenia. Shared genetic risk with bipolar (CACNA1C, ANK3)."), ("Q12", "What is the neurodevelopmental hypothesis of schizophrenia?", "Schizophrenia is a neurodevelopmental disorder with roots in early brain development (prenatal/perinatal). Evidence: obstetric complications, prenatal infections (influenza in 2nd trimester), famine exposure (Dutch Hunger Winter), minor physical anomalies, pre-morbid cognitive deficits, abnormal cortical cytoarchitecture without gliosis (indicating prenatal insult). Two-hit model: early vulnerability + adolescent/stress 'second hit'."), ("Q13", "What is the role of glutamate in schizophrenia? How does PCP model support this?", "NMDA receptor hypofunction hypothesis: Glutamate deficiency at NMDA receptors on GABAergic interneurons → disinhibition of dopamine release → mesolimbic hyperdopaminergia. PCP (phencyclidine) and ketamine (NMDA antagonists) produce full schizophrenia-like syndrome including negative and cognitive symptoms — unlike dopamine excess which only produces positive symptoms. Supports glutamate hypothesis."), ("Q14", "How do you assess and manage suicide risk in a patient with schizophrenia?", "Lifetime suicide risk in schizophrenia ~5-10% (20-50x general population). Risk factors: male, young, high premorbid IQ (aware of decline), command hallucinations, depressive symptoms, hopelessness, previous attempts, recent discharge. Assess using CSSRS or clinical interview. Management: safety planning, hospitalization if imminent risk, clozapine (only antipsychotic with anti-suicidal indication), address depression, psychotherapy."), ] }, "BRILLIANT": { "badge": "BRILLIANT — Merit/Distinction border. Deep clinical knowledge.", "color_key": "BRILLIANT", "items": [ ("Q1", "Explain the 4 dopamine pathways in the brain and how antipsychotics affect each of them — both therapeutically and as adverse effects.", "1. Mesolimbic (VTA→limbic): hyperdopaminergia → positive symptoms; D2 blockade here = antipsychotic effect. 2. Mesocortical (VTA→PFC): hypodopaminergia → negative/cognitive symptoms; D2 blockade worsens these. 3. Nigrostriatal (SNc→striatum): D2 blockade → EPS (parkinsonism, TD). 4. Tuberoinfundibular (hypothalamus→pituitary): D2 blockade → hyperprolactinaemia (galactorrhoea, amenorrhoea, sexual dysfunction, osteoporosis)."), ("Q2", "Why is the family history of bipolar disorder clinically important? Discuss the genetic overlap between schizophrenia and bipolar disorder.", "Schizophrenia and bipolar share ~15% genetic overlap. Shared susceptibility genes: CACNA1C, ANK3, NCAN, KCNQ2, ZNF804A. Psychiatric genomics consortium: polygenetic risk scores overlap. Clinical relevance: (1) May suggest schizoaffective disorder or bipolar with psychotic features. (2) Patient may develop mood episodes over time. (3) Treatment may need mood stabiliser augmentation. (4) Family counselling regarding genetic risk."), ("Q3", "What is treatment-resistant schizophrenia (TRS)? How do you define it and manage it?", "TRS = failure to respond adequately to ≥2 antipsychotic trials (different chemical classes) at adequate dose (≥600mg CPZ equivalent) for ≥6 weeks each. ~30% of schizophrenia patients. Management: Clozapine (gold standard, NNT=6 over other antipsychotics). If clozapine partially effective: augment with amisulpride, aripiprazole, lamotrigine. Address adherence (use LAI). Cognitive remediation for residual symptoms."), ("Q4", "What is ultra-high risk (UHR) or clinical high-risk state for psychosis? How would you manage someone in this state?", "UHR criteria (PACE criteria): (1) attenuated psychotic symptoms — subthreshold positive symptoms, (2) brief limited intermittent psychotic symptoms (BLIPS), (3) genetic risk + functional decline. 35-40% transition to psychosis within 3 years. Management: CBTp (reduces transition risk), omega-3 fatty acids (some evidence), low-dose atypical antipsychotic in high-risk cases, treat comorbid depression/anxiety, avoid cannabis."), ("Q5", "Describe the structural brain abnormalities found in schizophrenia on neuroimaging.", "MRI findings: (1) Lateral and 3rd ventricular enlargement (most replicated finding). (2) Reduced grey matter volume — especially in frontal lobe, temporal lobe (STG, hippocampus, amygdala). (3) Reduced hippocampal volume (correlates with memory deficits). (4) Thinning of prefrontal cortex. (5) Reduced thalamic volume. Progressive grey matter loss over time (partially medication-related, partially disease-related). Cavum septum pellucidum more common in schizophrenia."), ("Q6", "What is the role of long-acting injectable (LAI) antipsychotics in schizophrenia management? When would you recommend them?", "LAI (depot) antipsychotics ensure adherence by bypassing oral medication non-compliance. Indications: (1) Frequent relapses due to poor adherence. (2) Patient preference. (3) After first episode (evidence shows better outcomes). Available: Haloperidol decanoate (monthly), Fluphenazine decanoate, Risperidone microspheres (Risperdal Consta, 2-weekly), Paliperidone palmitate (monthly/3-monthly), Aripiprazole monohydrate (monthly). Benefits: fewer relapses, hospitalizations, better community outcomes."), ("Q7", "What are the metabolic complications of atypical antipsychotics? How do you monitor and manage them?", "Metabolic syndrome: weight gain (clozapine/olanzapine highest risk), dyslipidaemia, hyperglycaemia, type 2 diabetes, hypertension. Monitoring (baseline + every 3 months): weight/BMI/waist circumference, fasting glucose, HbA1c, lipid profile, BP. Management: dietary advice, exercise, switch to lower metabolic-risk agent (aripiprazole, ziprasidone), metformin for weight gain, statins/antidiabetics if needed."), ("Q8", "Describe cognitive deficits in schizophrenia. Which domains are affected and how does this relate to functional outcomes?", "Cognitive deficits are a core feature (not just medication side effect). Domains: working memory (DLPFC dysfunction), attention/vigilance, verbal learning and memory, processing speed, executive function, social cognition (theory of mind, emotion recognition). These deficits predict functional outcome better than positive symptoms. Cognitive remediation therapy and supported employment (IPS) target these. Lurasidone, cariprazine may have marginal benefits on cognition."), ("Q9", "How does cannabis use interact with schizophrenia? Explain the evidence.", "Cannabis (THC) is a dopamine agonist in mesolimbic system and NMDA receptor modulator. Evidence: cannabis use increases risk of psychosis 2-3x (dose-dependent, high-potency 'skunk' > 3x). Accelerates onset of psychosis in genetically vulnerable individuals (COMT val/val genotype most susceptible). Causes worsening of positive symptoms, reduces treatment response, increases relapse rate. CBD (cannabidiol) may have antipsychotic properties. Cessation of cannabis improves outcomes."), ("Q10", "What is the concept of 'expressed emotion' in the context of this case? How would you design a family intervention?", "High EE: criticism, hostility, emotional over-involvement from carers. Family intervention: 6-9 months structured programme, psychoeducation (illness, medication, relapse signs), communication training, problem-solving skills, reducing hostile criticism, supporting carer wellbeing. Reduces relapse rate by ~50% (Leff, Falloon studies). Include family in care planning and crisis planning."), ] }, "DISTINCTION": { "badge": "DISTINCTION — Top performer. Integration, analysis, and original insight.", "color_key": "DISTINCTION", "items": [ ("Q1", "This patient has a continuous course of illness with family history of bipolar disorder. Construct a complete differential diagnosis with your reasoning for and against each.", "1. Schizophrenia (most likely): continuous course, ≥6 months, delusion + AH, no prominent mood episodes mentioned. 2. Schizoaffective disorder: possible if mood episodes occur concurrently with psychosis for majority of illness course. 3. Bipolar I with psychotic features: less likely if no clear manic/depressive episodes, but family history is relevant. 4. Delusional disorder: only delusions, no AH — less likely here. 5. Substance-induced psychotic disorder: must rule out cannabis/stimulant use. 6. NMDA receptor encephalitis (anti-NMDAR): especially in young female, presents with psychosis + movement disorder + autonomic instability. Final diagnosis requires longitudinal follow-up."), ("Q2", "Discuss the neurobiology of auditory hallucinations. What brain circuits are involved and what does neuroimaging show?", "fMRI studies: AH associated with activation of Broca's area (44/45), left STG/Heschl's gyrus (primary auditory cortex), thalamus, anterior cingulate. Proposed mechanism: inner speech misattributed to external source due to failure of efference copy/corollary discharge (predictive coding failure — Frith's model). PET studies: CBF increases in Broca's area during AH. Diffusion tensor imaging: reduced white matter connectivity in arcuate fasciculus. Thalamic gating dysfunction may explain 'leakage' of internal speech to conscious perception."), ("Q3", "What is the evidence for and against the dopamine hypothesis of schizophrenia? What are its limitations?", "FOR: All effective antipsychotics block D2. Dopamine agonists (amphetamine, L-DOPA) induce psychosis. PET: increased dopamine synthesis capacity and D2/D3 receptor supersensitivity in striatum of unmedicated patients. AGAINST: D2 blockade is rapid (hours) but antipsychotic effect takes weeks — delayed response unexplained. Clozapine (most effective) has LOW D2 affinity. Negative/cognitive symptoms poorly treated by D2 antagonists. LIMITATIONS: Hypothesis cannot fully explain all symptoms; glutamate, serotonin, GABA, and neuroinflammation also implicated."), ("Q4", "How does the stress-vulnerability (diathesis-stress) model explain the onset and relapse of schizophrenia in this patient with a positive family history?", "Zubin & Spring's model (1977): biological vulnerability (genetic + neurodevelopmental) + environmental stressors → psychosis threshold breached. In this patient: genetic liability (family history of bipolar = shared genetic risk). Stressors: cannabis, life events, expressed emotion, sleep deprivation. Neurobiological basis: stress activates HPA axis → cortisol → excess dopamine synthesis in striatum. Cannabis further sensitises mesolimbic dopamine. This model guides both pharmacological (reduce biological vulnerability) and psychosocial (reduce stress) interventions."), ("Q5", "What are the ethical and legal issues in managing a patient with schizophrenia and poor insight who refuses medication?", "India-specific: Mental Healthcare Act 2017 (MHCA 2017). Key provisions: (1) Every person has right to refuse treatment unless under involuntary admission. (2) Involuntary admission criteria: risk to self or others, inability to make treatment decisions. (3) Nominated representative (NR) and Advance Directive (AD). (4) Mental Health Review Board (MHRB) oversight. Ethical framework: balance autonomy (patient's right) vs beneficence/non-maleficence (treatment for welfare). Least restrictive alternative principle. Use supported decision-making. Document capacity assessment."), ("Q6", "Discuss the concept of recovery in schizophrenia. Is it achievable? What is the evidence?", "Recovery defined in two ways: (1) Clinical recovery: remission of symptoms (RSWG criteria: all 8 PANSS items ≤3, for ≥6 months). (2) Personal/functional recovery: rebuilding a meaningful life despite symptoms (CHIME framework: Connectedness, Hope, Identity, Meaning, Empowerment). Evidence: Long-term follow-up studies (Harding, Vermont cohort; WHO cross-cultural studies) show ~25-50% achieve good functional outcomes. Recovery-oriented services: peer support workers, IPS employment, self-management, anti-stigma. Prognosis better in developing countries (WHO finding — social support/re-integration easier)."), ("Q7", "What is the PANSS scale? Describe its structure and clinical use.", "Positive and Negative Syndrome Scale (Kay, 1987). 30 items: Positive Scale (7 items: delusions, conceptual disorganisation, hallucinatory behaviour, excitement, grandiosity, suspiciousness/persecution, hostility), Negative Scale (7 items: blunted affect, emotional withdrawal, poor rapport, passive/apathetic social withdrawal, difficulty in abstract thinking, lack of spontaneity, stereotyped thinking), General Psychopathology Scale (16 items). Each item scored 1-7 (1=absent, 7=extreme). Total score 30-210. Used for: diagnosis, severity monitoring, drug trial endpoints, defining TRS (inadequate response criteria)."), ("Q8", "How would you counsel this patient's family member (who has bipolar disorder) about the genetic risk to other family members?", "Key points: (1) Schizophrenia and bipolar share genetic risk (10-15% of GWAS variants overlap). (2) First-degree relative of schizophrenia patient: ~10% lifetime risk (vs 1% baseline). (3) First-degree relative of bipolar patient: ~10% risk of bipolar, 1-2% schizophrenia. (4) Having both in family = higher risk in children. (5) Risk NOT certainty — many genetically at-risk individuals never develop illness. (6) Discuss early warning signs (prodrome), when to seek help. (7) Importance of avoiding cannabis. (8) Non-directive counselling — avoid inducing excessive anxiety. (9) Genetic counselling referral if requested."), ("Q9", "What is the neuroinflammation hypothesis of schizophrenia? What is its evidence base and therapeutic implications?", "Evidence: (1) Elevated pro-inflammatory cytokines (IL-6, IL-1β, TNF-alpha) in serum and CSF of schizophrenia patients. (2) PET imaging: increased microglial activation (TSPO binding). (3) Epidemiological: maternal immune activation (MIA model in animals — polyI:C), autoimmune comorbidities in schizophrenia. (4) COX-2 inhibitors (celecoxib) as adjuncts showed modest benefit in early schizophrenia in some trials. Therapeutic implications: anti-inflammatory adjuncts (minocycline, omega-3 fatty acids), N-acetylcysteine (antioxidant), aspirin augmentation — all investigational. Represents a novel target beyond dopamine."), ("Q10", "Discuss the concept of cognitive reserve and how premorbid functioning predicts outcomes in schizophrenia.", "Cognitive reserve: brain's resilience against damage, built through education, occupation, cognitive activity. In schizophrenia: premorbid IQ is a strong predictor of long-term functional outcomes (work, relationships, independent living). Higher cognitive reserve = better adaptation to neurobiological deficits. Paradoxically, high-IQ patients may have greater distress (aware of decline). Premorbid poor functioning (social withdrawal, academic decline in adolescence) is part of the prodrome and predicts worse outcome. Assessment tools: NART (National Adult Reading Test), TOPF for premorbid IQ estimation."), ] } } # ─── BUILD STORY ───────────────────────────────────────────────────────────── story = [] # Title story.append(Spacer(1, 0.2*cm)) story.append(Paragraph("MUHS MD PSYCHIATRY EXAMINATION", title_style)) story.append(Paragraph("Long Psychiatry Case — External Examiner Question Bank", subtitle_style)) story.append(Paragraph("Case: Schizophrenia with Delusion of Persecution, Auditory Hallucinations, Continuous Illness & Family History of Bipolar Disorder", subtitle_style)) story.append(Paragraph("Prepared by: External Examiner | MUHS Nashik | July 2026", subtitle_style)) story.append(Spacer(1, 0.3*cm)) story.append(HRFlowable(width="100%", thickness=2, color=NAVY)) story.append(Spacer(1, 0.25*cm)) # Case summary case_rows = [[Paragraph("CLINICAL CASE SUMMARY", case_header_style), ""]] for label, value in CASE_SUMMARY: case_rows.append([ Paragraph(f"<b>{label}</b>", case_body_style), Paragraph(value, case_body_style) ]) case_table = Table(case_rows, colWidths=[5*cm, 11.8*cm]) case_table.setStyle(TableStyle([ ("BACKGROUND", (0, 0), (-1, 0), NAVY), ("SPAN", (0, 0), (-1, 0)), ("ALIGN", (0, 0), (-1, 0), "CENTER"), ("ROWBACKGROUNDS", (0, 1), (-1, -1), [colors.HexColor("#eceff1"), colors.HexColor("#fafafa")]), ("GRID", (0, 0), (-1, -1), 0.4, colors.HexColor("#b0bec5")), ("TOPPADDING", (0, 0), (-1, -1), 5), ("BOTTOMPADDING", (0, 0), (-1, -1), 5), ("LEFTPADDING", (0, 0), (-1, -1), 6), ("RIGHTPADDING", (0, 0), (-1, -1), 6), ("FONTNAME", (0, 1), (0, -1), "Helvetica-Bold"), ("VALIGN", (0, 0), (-1, -1), "TOP"), ])) story.append(case_table) story.append(Spacer(1, 0.4*cm)) # Question count summary count_data = [ ["Level", "No. of Questions", "Marks Target", "Benchmark"], ["Must Know", "13", "50-60 / 100", "Must answer ≥10 correctly to pass"], ["Good to Know", "14", "61-74 / 100", "Demonstrates solid clinical competence"], ["Brilliant", "10", "75-84 / 100", "Merit/Distinction border"], ["Distinction", "10", "85-100 / 100","Original insight + integration"], ["TOTAL", "47 questions", "—", "—"], ] cnt_table = Table(count_data, colWidths=[3.8*cm, 3.2*cm, 3.5*cm, 6.3*cm]) cnt_table.setStyle(TableStyle([ ("BACKGROUND", (0,0),(-1,0), NAVY), ("TEXTCOLOR", (0,0),(-1,0), WHITE), ("FONTNAME", (0,0),(-1,0), "Helvetica-Bold"), ("FONTSIZE", (0,0),(-1,-1), 8.5), ("ROWBACKGROUNDS", (0,1),(-1,-1), [colors.HexColor("#e3f2fd"), colors.HexColor("#e8f5e9"), colors.HexColor("#fff8e1"), colors.HexColor("#f3e5f5"), LIGHT_GREY]), ("GRID", (0,0),(-1,-1), 0.4, colors.HexColor("#cfd8dc")), ("TOPPADDING", (0,0),(-1,-1), 5), ("BOTTOMPADDING", (0,0),(-1,-1), 5), ("LEFTPADDING", (0,0),(-1,-1), 5), ("FONTNAME", (0,-1),(-1,-1), "Helvetica-Bold"), ("BACKGROUND", (0,-1),(-1,-1), colors.HexColor("#e0e0e0")), ("ALIGN", (1,0),(2,-1), "CENTER"), ])) story.append(cnt_table) story.append(Spacer(1, 0.5*cm)) LEVEL_ORDER = ["MUST KNOW", "GOOD TO KNOW", "BRILLIANT", "DISTINCTION"] LEVEL_ICONS = { "MUST KNOW": "⚡ MUST KNOW | Pass Level", "GOOD TO KNOW": "✓ GOOD TO KNOW | Good Pass", "BRILLIANT": "★ BRILLIANT | Merit / Distinction Border", "DISTINCTION": "◆ DISTINCTION | Top Performer", } for level in LEVEL_ORDER: bg, fg = LEVEL_COLORS[level] data = QUESTIONS[level] # Section header hdr = Paragraph(f"<b>{LEVEL_ICONS[level]}</b>", level_heading_style) hdr_table = Table([[hdr]], colWidths=[16.8*cm]) hdr_table.setStyle(TableStyle([ ("BACKGROUND", (0,0),(-1,-1), fg), ("TOPPADDING", (0,0),(-1,-1), 7), ("BOTTOMPADDING", (0,0),(-1,-1), 7), ("LEFTPADDING", (0,0),(-1,-1), 8), ])) story.append(KeepTogether([hdr_table])) story.append(Spacer(1, 0.1*cm)) story.append(Paragraph(f"<i>{data['badge']}</i>", note_style)) story.append(Spacer(1, 0.2*cm)) # Question table header q_rows = [[ Paragraph("<b>No.</b>", ParagraphStyle("QH2", parent=styles["Normal"], fontSize=8.5, fontName="Helvetica-Bold", textColor=WHITE, alignment=TA_CENTER)), Paragraph("<b>Question</b>", ParagraphStyle("QH2", parent=styles["Normal"], fontSize=8.5, fontName="Helvetica-Bold", textColor=WHITE)), Paragraph("<b>Expected Key Points / Model Answer</b>", ParagraphStyle("QH2", parent=styles["Normal"], fontSize=8.5, fontName="Helvetica-Bold", textColor=WHITE)), ]] for qnum, question, keypoints in data["items"]: q_rows.append([ Paragraph(f"<b>{qnum}</b>", ParagraphStyle("QN2", parent=styles["Normal"], fontSize=9, fontName="Helvetica-Bold", alignment=TA_CENTER)), Paragraph(question, question_style), Paragraph(f"<i>{keypoints}</i>", note_style), ]) q_table = Table(q_rows, colWidths=[0.9*cm, 7*cm, 8.9*cm]) q_table.setStyle(TableStyle([ ("BACKGROUND", (0,0),(-1,0), fg), ("TEXTCOLOR", (0,0),(-1,0), WHITE), ("ROWBACKGROUNDS",(0,1),(-1,-1), [bg, WHITE]), ("GRID", (0,0),(-1,-1), 0.35, colors.HexColor("#cfd8dc")), ("TOPPADDING", (0,0),(-1,-1), 6), ("BOTTOMPADDING", (0,0),(-1,-1), 6), ("LEFTPADDING", (0,0),(-1,-1), 4), ("RIGHTPADDING", (0,0),(-1,-1), 4), ("VALIGN", (0,0),(-1,-1), "TOP"), ("ALIGN", (0,0),(0,-1), "CENTER"), ])) story.append(q_table) story.append(Spacer(1, 0.55*cm)) # Marking guidance story.append(HRFlowable(width="100%", thickness=1.5, color=NAVY)) story.append(Spacer(1, 0.2*cm)) story.append(Paragraph("<b>EXAMINER MARKING GUIDANCE — MUHS MD Psychiatry Long Case (100 marks)</b>", ParagraphStyle("MG2", parent=styles["Normal"], fontSize=10.5, fontName="Helvetica-Bold", textColor=NAVY, spaceAfter=4))) marking_data = [ ["Domain", "Marks", "Criteria"], ["History Taking & Psychopathology", "20", "Adequate history, mental state exam, identify FRS, positive/negative symptoms"], ["Diagnosis & Differential Diagnosis", "15", "Correct primary diagnosis with justification; differential with schizoaffective, bipolar"], ["Investigations", "10", "Relevant baseline bloods, neuroimaging rationale, rating scales (PANSS, BPRS)"], ["Management (Pharmacological)", "20", "Correct antipsychotic choice, dose, monitoring, TRS criteria, clozapine"], ["Management (Psychosocial)", "15", "CBTp, family therapy, EE, LAI, assertive community treatment"], ["Prognosis & Long-term Course", "10", "Good/poor prognostic factors, recovery concept, relapse prevention"], ["Neurobiological Understanding", "10", "Dopamine hypothesis, glutamate, neurodevelopmental, genetics"], ["TOTAL", "100", ""], ] m_table = Table(marking_data, colWidths=[6.5*cm, 2*cm, 8.3*cm]) m_table.setStyle(TableStyle([ ("BACKGROUND", (0,0),(-1,0), NAVY), ("TEXTCOLOR", (0,0),(-1,0), WHITE), ("FONTNAME", (0,0),(-1,0), "Helvetica-Bold"), ("ROWBACKGROUNDS",(0,1),(-1,-2), [colors.HexColor("#eceff1"), colors.HexColor("#fafafa")]*5), ("BACKGROUND", (0,-1),(-1,-1), colors.HexColor("#e0e0e0")), ("FONTNAME", (0,-1),(-1,-1), "Helvetica-Bold"), ("GRID", (0,0),(-1,-1), 0.4, colors.HexColor("#b0bec5")), ("TOPPADDING", (0,0),(-1,-1), 6), ("BOTTOMPADDING", (0,0),(-1,-1), 6), ("LEFTPADDING", (0,0),(-1,-1), 6), ("FONTSIZE", (0,0),(-1,-1), 8.5), ("VALIGN", (0,0),(-1,-1), "MIDDLE"), ("ALIGN", (1,0),(1,-1), "CENTER"), ])) story.append(m_table) story.append(Spacer(1, 0.3*cm)) story.append(Paragraph( "Good/Poor Prognostic Factors to Know: Good prognosis — female sex, acute onset, late onset, " "obvious precipitant, positive symptoms predominant, good premorbid functioning, married, family support, " "good insight, early treatment. Poor prognosis — male, insidious onset, young age, continuous course (as in THIS CASE), " "negative symptoms predominant, poor premorbid functioning, family history of schizophrenia, cannabis use, low IQ.", ParagraphStyle("NB2", parent=styles["Normal"], fontSize=8.5, fontName="Helvetica-Oblique", textColor=colors.HexColor("#5d4037")))) story.append(Spacer(1, 0.15*cm)) story.append(HRFlowable(width="100%", thickness=1, color=colors.grey)) story.append(Spacer(1, 0.1*cm)) story.append(Paragraph( "Generated by Orris AI | MUHS MD Psychiatry — Schizophrenia Long Case Viva | July 2026 | For Educational Use Only", footer_style)) doc.build(story) print(f"PDF created successfully: {OUTPUT}") PYEOF python3 /tmp/workspace/muhs-neurology-exam/schizophrenia_viva.py
MUHS Schizophrenia Viva Questions
PDF Document · PDF
| Feature | Finding |
|---|---|
| Presenting complaint | Delusion of persecution + Auditory hallucinations |
| Illness course | Continuous (no remission) |
| Family history | Bipolar mood disorder in first-degree relative |
| Key clinical challenge | Diagnosis, differential (schizoaffective?), treatment, long-term prognosis |
| Q | Question |
|---|---|
| Q1 | What is your diagnosis? State DSM-5/ICD-11 criteria |
| Q2 | What type of delusion is this? Define it |
| Q3 | What is an auditory hallucination? Differentiate from illusion and pseudohallucination |
| Q4 | Name Schneider's First Rank Symptoms — which are present in this case? |
| Q5 | Differentiate positive vs negative symptoms (4 examples each) |
| Q6 | What does 'continuous illness' mean and what is its prognostic significance? |
| Q7 | Which first-line antipsychotic would you start and at what dose? |
| Q8 | Why is the family history of bipolar disorder clinically important? |
| Q9 | How long must symptoms be present to diagnose schizophrenia per DSM-5? |
| Q10 | Differentiate schizophrenia vs schizophreniform vs brief psychotic disorder |
| Q11 | 4 investigations before starting antipsychotics |
| Q12 | Dopamine hypothesis — which pathway causes positive symptoms? |
| Q13 | Name 4 extrapyramidal side effects of antipsychotics |
| Q | Question |
|---|---|
| Q1 | Differentiate schizophrenia from schizoaffective disorder in this patient |
| Q2 | What is delusional disorder? How does it differ from schizophrenia? |
| Q3 | Classify auditory hallucinations — which type is most characteristic of schizophrenia? |
| Q4 | What is thought broadcasting? How would a patient describe it? |
| Q5 | Evidence-based psychosocial interventions in schizophrenia |
| Q6 | What is NMS? How is it managed? |
| Q7 | What is tardive dyskinesia? Management including VMAT2 inhibitors |
| Q8 | Role of clozapine — indications, mechanism, monitoring |
| Q9 | What is expressed emotion (EE)? How does it affect outcomes? |
| Q10 | What is insight? How do you assess it? |
| Q11 | Genetic basis of schizophrenia — heritability, twin studies, key genes |
| Q12 | Neurodevelopmental hypothesis of schizophrenia |
| Q13 | Role of glutamate — how does PCP model support this? |
| Q14 | Suicide risk in schizophrenia — assessment and management |
| Q | Question |
|---|---|
| Q1 | All 4 dopamine pathways + how antipsychotics affect each (therapeutic + adverse effects) |
| Q2 | Genetic overlap between schizophrenia and bipolar disorder (CACNA1C, ANK3 etc.) |
| Q3 | Treatment-resistant schizophrenia — definition and management |
| Q4 | Ultra-high risk (UHR/clinical high-risk) state — criteria and management |
| Q5 | Structural brain abnormalities on neuroimaging in schizophrenia |
| Q6 | Long-acting injectable antipsychotics — rationale, types, indications |
| Q7 | Metabolic complications of atypical antipsychotics — monitoring protocol |
| Q8 | Cognitive deficits in schizophrenia — domains affected and functional outcome link |
| Q9 | Cannabis use and schizophrenia — evidence (COMT val/val genotype) |
| Q10 | Designing a family intervention based on expressed emotion model |
| Q | Question |
|---|---|
| Q1 | Complete differential diagnosis with reasoning for/against each (including anti-NMDAR encephalitis) |
| Q2 | Neurobiology of auditory hallucinations — Frith's model, fMRI, efference copy |
| Q3 | Evidence for AND against the dopamine hypothesis (limitations) |
| Q4 | Stress-vulnerability (diathesis-stress) model — apply to this patient |
| Q5 | Ethical/legal issues in treating patient with poor insight refusing medication — MHCA 2017 |
| Q6 | Recovery in schizophrenia — clinical vs personal recovery, Harding Vermont cohort, WHO finding |
| Q7 | PANSS scale — structure, scoring, clinical use, TRS endpoint |
| Q8 | Genetic counselling for the family member with bipolar disorder |
| Q9 | Neuroinflammation hypothesis — evidence, cytokines, microglial activation, therapeutic implications |
| Q10 | Cognitive reserve and premorbid functioning as predictors of outcome |
| Domain | Marks |
|---|---|
| History Taking & Psychopathology | 20 |
| Diagnosis & Differential Diagnosis | 15 |
| Investigations | 10 |
| Management — Pharmacological | 20 |
| Management — Psychosocial | 15 |
| Prognosis & Long-term Course | 10 |
| Neurobiological Understanding | 10 |
| TOTAL | 100 |