MUHS 2nd MBBS important questions Microbiology Pathology Pharmacology exam 2024 2025

MUHS Maharashtra 2nd MBBS frequently asked questions microbiology pathology pharmacology previous year

mkdir -p /home/daytona/workspace/muhs-study-guide && ls /home/daytona/workspace/…

~/muhs-study-guide/generate_pdf.py

#!/usr/bin/env python3
"""
MUHS 2nd MBBS Clinical Q&A Study Guide PDF Generator
Uses ReportLab for professional PDF generation
"""

from reportlab.lib.pagesizes import A4
from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle
from reportlab.lib.colors import HexColor, white, black, Color
from reportlab.lib.units import cm, mm
from reportlab.platypus import (
    SimpleDocTemplate, Paragraph, Spacer, Table, TableStyle,
    PageBreak, HRFlowable, KeepTogether
)
from reportlab.lib.enums import TA_CENTER, TA_LEFT, TA_JUSTIFY
from reportlab.platypus import BaseDocTemplate, PageTemplate, Frame
from reportlab.lib import colors
import datetime

# ── Color Palette ──────────────────────────────────────────────
DARK_BLUE    = HexColor("#1a237e")   # Cover / subject headers
MED_BLUE     = HexColor("#1565c0")
LIGHT_BLUE   = HexColor("#e3f2fd")
RED_ACCENT   = HexColor("#c62828")
GREEN_ACCENT = HexColor("#2e7d32")
ORANGE       = HexColor("#e65100")
PURPLE       = HexColor("#6a1b9a")
TEAL         = HexColor("#00695c")
GOLD         = HexColor("#f9a825")
LIGHT_GOLD   = HexColor("#fff9c4")
LIGHT_GREEN  = HexColor("#e8f5e9")
LIGHT_RED    = HexColor("#ffebee")
LIGHT_PURPLE = HexColor("#f3e5f5")
LIGHT_TEAL   = HexColor("#e0f2f1")
GRAY_BG      = HexColor("#f5f5f5")
DARK_GRAY    = HexColor("#424242")
MID_GRAY     = HexColor("#757575")

# ── Document Setup ─────────────────────────────────────────────
OUTPUT_PATH = "/home/daytona/workspace/muhs-study-guide/MUHS_2ndMBBS_Clinical_QA_StudyGuide.pdf"

def get_styles():
    styles = getSampleStyleSheet()

    styles.add(ParagraphStyle(
        name='CoverTitle',
        fontSize=28, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_CENTER,
        spaceAfter=8, leading=34
    ))
    styles.add(ParagraphStyle(
        name='CoverSubtitle',
        fontSize=14, fontName='Helvetica',
        textColor=HexColor("#bbdefb"), alignment=TA_CENTER,
        spaceAfter=6, leading=18
    ))
    styles.add(ParagraphStyle(
        name='SubjectHeader',
        fontSize=16, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_CENTER,
        spaceAfter=6, leading=20
    ))
    styles.add(ParagraphStyle(
        name='SectionTitle',
        fontSize=13, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, alignment=TA_LEFT,
        spaceAfter=4, spaceBefore=10, leading=16
    ))
    styles.add(ParagraphStyle(
        name='QuestionNum',
        fontSize=11, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_LEFT,
        spaceAfter=0, leading=15
    ))
    styles.add(ParagraphStyle(
        name='QuestionText',
        fontSize=10.5, fontName='Helvetica',
        textColor=HexColor("#1a237e"), alignment=TA_JUSTIFY,
        spaceAfter=4, leading=14
    ))
    styles.add(ParagraphStyle(
        name='SubQ',
        fontSize=10, fontName='Helvetica',
        textColor=DARK_GRAY, alignment=TA_LEFT,
        spaceAfter=2, leading=13, leftIndent=12
    ))
    styles.add(ParagraphStyle(
        name='AnswerLabel',
        fontSize=10, fontName='Helvetica-Bold',
        textColor=GREEN_ACCENT, alignment=TA_LEFT,
        spaceAfter=2, leading=13
    ))
    styles.add(ParagraphStyle(
        name='AnswerText',
        fontSize=10, fontName='Helvetica',
        textColor=DARK_GRAY, alignment=TA_JUSTIFY,
        spaceAfter=3, leading=13, leftIndent=12
    ))
    styles.add(ParagraphStyle(
        name='BulletPoint',
        fontSize=9.5, fontName='Helvetica',
        textColor=DARK_GRAY, alignment=TA_LEFT,
        spaceAfter=2, leading=13, leftIndent=20, bulletIndent=10
    ))
    styles.add(ParagraphStyle(
        name='KeyBox',
        fontSize=9.5, fontName='Helvetica-Bold',
        textColor=ORANGE, alignment=TA_LEFT,
        spaceAfter=2, leading=13
    ))
    styles.add(ParagraphStyle(
        name='TipText',
        fontSize=9.5, fontName='Helvetica-Oblique',
        textColor=HexColor("#4a148c"), alignment=TA_LEFT,
        spaceAfter=2, leading=13
    ))
    styles.add(ParagraphStyle(
        name='TableHeader',
        fontSize=9, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_CENTER, leading=12
    ))
    styles.add(ParagraphStyle(
        name='TableCell',
        fontSize=9, fontName='Helvetica',
        textColor=DARK_GRAY, alignment=TA_LEFT, leading=12
    ))
    styles.add(ParagraphStyle(
        name='PageNum',
        fontSize=8, fontName='Helvetica',
        textColor=MID_GRAY, alignment=TA_CENTER
    ))
    styles.add(ParagraphStyle(
        name='TOCEntry',
        fontSize=11, fontName='Helvetica',
        textColor=DARK_BLUE, alignment=TA_LEFT,
        spaceAfter=5, leading=14, leftIndent=20
    ))
    styles.add(ParagraphStyle(
        name='TOCHeader',
        fontSize=13, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, alignment=TA_LEFT,
        spaceAfter=3, spaceBefore=8, leading=16
    ))
    return styles


def header_footer(canvas, doc):
    canvas.saveState()
    w, h = A4
    # Header bar
    canvas.setFillColor(DARK_BLUE)
    canvas.rect(0, h - 22*mm, w, 22*mm, fill=1, stroke=0)
    canvas.setFillColor(white)
    canvas.setFont("Helvetica-Bold", 9)
    canvas.drawString(1.5*cm, h - 13*mm, "MUHS 2nd MBBS  |  Clinical Q&A Study Guide")
    canvas.setFont("Helvetica", 8)
    canvas.drawRightString(w - 1.5*cm, h - 13*mm,
                           "Microbiology  |  Pathology  |  Pharmacology")
    # Footer bar
    canvas.setFillColor(DARK_BLUE)
    canvas.rect(0, 0, w, 12*mm, fill=1, stroke=0)
    canvas.setFillColor(GOLD)
    canvas.setFont("Helvetica-Bold", 8)
    canvas.drawCentredString(w/2, 4*mm, f"Page {doc.page}")
    canvas.setFillColor(white)
    canvas.setFont("Helvetica", 7)
    canvas.drawString(1.5*cm, 4*mm, "For Educational Use Only")
    canvas.drawRightString(w - 1.5*cm, 4*mm, f"Generated: {datetime.date.today().strftime('%B %Y')}")
    canvas.restoreState()


def colored_box(text, bg_color, text_color=white, style_name='SubjectHeader'):
    """Return a 1-cell table acting as a colored section header."""
    s = get_styles()
    p = Paragraph(text, ParagraphStyle(
        'tmp', fontSize=13, fontName='Helvetica-Bold',
        textColor=text_color, alignment=TA_CENTER, leading=18
    ))
    t = Table([[p]], colWidths=[17*cm])
    t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), bg_color),
        ('ROWPADDING', (0,0), (-1,-1), 8),
        ('BOX', (0,0), (-1,-1), 0, white),
        ('TOPPADDING', (0,0), (-1,-1), 7),
        ('BOTTOMPADDING', (0,0), (-1,-1), 7),
    ]))
    return t


def question_block(num, scenario, sub_questions, answers, styles, accent_color, light_color):
    """Build a full Q&A block with scenario, sub-questions, and answers."""
    elems = []

    # Question header bar
    q_header_p = Paragraph(f"Q{num}. Clinical Scenario", ParagraphStyle(
        'qh', fontSize=10, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_LEFT, leading=14
    ))
    q_header_t = Table([[q_header_p]], colWidths=[17*cm])
    q_header_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), accent_color),
        ('TOPPADDING', (0,0), (-1,-1), 5),
        ('BOTTOMPADDING', (0,0), (-1,-1), 5),
        ('LEFTPADDING', (0,0), (-1,-1), 10),
    ]))
    elems.append(q_header_t)

    # Scenario box
    sc_p = Paragraph(scenario, ParagraphStyle(
        'sc', fontSize=10, fontName='Helvetica',
        textColor=HexColor("#1a237e"), alignment=TA_JUSTIFY, leading=14
    ))
    sc_t = Table([[sc_p]], colWidths=[17*cm])
    sc_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), light_color),
        ('TOPPADDING', (0,0), (-1,-1), 7),
        ('BOTTOMPADDING', (0,0), (-1,-1), 7),
        ('LEFTPADDING', (0,0), (-1,-1), 12),
        ('RIGHTPADDING', (0,0), (-1,-1), 12),
        ('BOX', (0,0), (-1,-1), 0.5, accent_color),
    ]))
    elems.append(sc_t)

    # Sub-questions
    sq_data = []
    for sq in sub_questions:
        sq_data.append([Paragraph(sq, ParagraphStyle(
            'sqp', fontSize=9.5, fontName='Helvetica',
            textColor=DARK_GRAY, leading=13
        ))])
    sq_t = Table(sq_data, colWidths=[17*cm])
    sq_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), GRAY_BG),
        ('TOPPADDING', (0,0), (-1,-1), 4),
        ('BOTTOMPADDING', (0,0), (-1,-1), 4),
        ('LEFTPADDING', (0,0), (-1,-1), 16),
        ('RIGHTPADDING', (0,0), (-1,-1), 12),
        ('LINEBELOW', (0,0), (-1,-2), 0.3, HexColor("#e0e0e0")),
    ]))
    elems.append(sq_t)

    # Answers header
    ans_hdr = Paragraph("ANSWERS", ParagraphStyle(
        'ah', fontSize=9, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_LEFT, leading=13
    ))
    ans_hdr_t = Table([[ans_hdr]], colWidths=[17*cm])
    ans_hdr_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), GREEN_ACCENT),
        ('TOPPADDING', (0,0), (-1,-1), 4),
        ('BOTTOMPADDING', (0,0), (-1,-1), 4),
        ('LEFTPADDING', (0,0), (-1,-1), 10),
    ]))
    elems.append(ans_hdr_t)

    # Answer content
    ans_data = []
    for ans in answers:
        ans_data.append([Paragraph(ans, ParagraphStyle(
            'ansp', fontSize=9.5, fontName='Helvetica',
            textColor=DARK_GRAY, leading=13, alignment=TA_LEFT
        ))])
    ans_t = Table(ans_data, colWidths=[17*cm])
    ans_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), LIGHT_GREEN),
        ('TOPPADDING', (0,0), (-1,-1), 4),
        ('BOTTOMPADDING', (0,0), (-1,-1), 4),
        ('LEFTPADDING', (0,0), (-1,-1), 16),
        ('RIGHTPADDING', (0,0), (-1,-1), 12),
        ('LINEBELOW', (0,0), (-1,-2), 0.3, HexColor("#c8e6c9")),
        ('BOX', (0,0), (-1,-1), 0.5, GREEN_ACCENT),
    ]))
    elems.append(ans_t)
    elems.append(Spacer(1, 8))
    return elems


def key_point_box(points, styles, title="KEY POINTS TO REMEMBER"):
    data = [[Paragraph(title, ParagraphStyle(
        'kph', fontSize=10, fontName='Helvetica-Bold',
        textColor=white, leading=14
    ))]]
    for p in points:
        data.append([Paragraph(f"• {p}", ParagraphStyle(
            'kp', fontSize=9.5, fontName='Helvetica',
            textColor=DARK_GRAY, leading=13
        ))])
    t = Table(data, colWidths=[17*cm])
    style = [
        ('BACKGROUND', (0,0), (0,0), ORANGE),
        ('BACKGROUND', (0,1), (-1,-1), LIGHT_GOLD),
        ('TOPPADDING', (0,0), (-1,-1), 5),
        ('BOTTOMPADDING', (0,0), (-1,-1), 5),
        ('LEFTPADDING', (0,0), (-1,-1), 12),
        ('RIGHTPADDING', (0,0), (-1,-1), 12),
        ('BOX', (0,0), (-1,-1), 0.5, ORANGE),
    ]
    t.setStyle(TableStyle(style))
    return t


def comparison_table(headers, rows, col_widths, accent):
    data = [[Paragraph(h, ParagraphStyle(
        'th', fontSize=9, fontName='Helvetica-Bold',
        textColor=white, alignment=TA_CENTER, leading=12
    )) for h in headers]]
    for i, row in enumerate(rows):
        data.append([Paragraph(str(c), ParagraphStyle(
            'tc', fontSize=9, fontName='Helvetica',
            textColor=DARK_GRAY, leading=12
        )) for c in row])
    t = Table(data, colWidths=col_widths)
    style = [
        ('BACKGROUND', (0,0), (-1,0), accent),
        ('ROWBACKGROUNDS', (0,1), (-1,-1), [white, GRAY_BG]),
        ('GRID', (0,0), (-1,-1), 0.4, HexColor("#bdbdbd")),
        ('TOPPADDING', (0,0), (-1,-1), 5),
        ('BOTTOMPADDING', (0,0), (-1,-1), 5),
        ('LEFTPADDING', (0,0), (-1,-1), 6),
        ('RIGHTPADDING', (0,0), (-1,-1), 6),
        ('ALIGN', (0,0), (-1,-1), 'LEFT'),
        ('VALIGN', (0,0), (-1,-1), 'TOP'),
    ]
    t.setStyle(TableStyle(style))
    return t


# ═══════════════════════════════════════════════════════════════
#  CONTENT DATA
# ═══════════════════════════════════════════════════════════════

MICRO_QUESTIONS = [
    {
        "scenario": "<b>A 30-year-old male</b> presents with fever for 3 weeks, relative bradycardia, rose spots on the abdomen, and splenomegaly. Stool culture grows a lactose-non-fermenting, H2S-producing, motile gram-negative bacillus. Blood culture in week 1 was positive.",
        "sub_qs": [
            "(a) What is the most likely diagnosis?",
            "(b) Name the causative organism and its virulence factors.",
            "(c) How will you confirm the diagnosis in each week of illness?",
            "(d) Name the culture media used and describe colonial characteristics.",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Enteric Fever (Typhoid Fever) caused by Salmonella typhi.",
            "<b>(b) Causative Organism & Virulence Factors:</b> Salmonella typhi. Virulence factors: Vi antigen (anti-phagocytic capsule), Endotoxin (LPS - causes fever/shock), Flagella (motility, invasion), Type III secretion system (cell invasion), Biofilm formation in gallbladder.",
            "<b>(c) Week-wise Diagnosis:</b> Week 1 - Blood culture (most sensitive, 80-90% positive). Week 2 - Blood + Urine culture. Week 3 - Stool culture + Widal test (titre ≥1:160 for O antigen = significant). Week 4 - Widal test (rising titre is diagnostic).",
            "<b>(d) Culture Media:</b> Blood: Brain Heart Infusion broth. Stool/Urine: MacConkey agar (pale/non-lactose fermenting colonies), Bismuth sulfite agar (black colonies due to H2S), SS agar. Colonial characters: Pale non-lactose fermenting smooth colonies on MacConkey; black metallic sheen on BS agar.",
        ],
    },
    {
        "scenario": "<b>A 2-year-old child</b> presents with sudden-onset high fever, severe headache, neck stiffness (nuchal rigidity), photophobia, and a non-blanching petechial rash. Lumbar puncture reveals turbid CSF with gram-negative intracellular diplococci on smear.",
        "sub_qs": [
            "(a) Name the organism and its virulence factors.",
            "(b) What specific lab investigations will you perform on CSF?",
            "(c) What is the treatment of choice?",
            "(d) Mention chemoprophylaxis for close contacts.",
        ],
        "answers": [
            "<b>(a) Organism:</b> Neisseria meningitidis (Meningococcus). Virulence factors: Polysaccharide capsule (antiphagocytic, antigen for serotyping A,B,C,Y,W135), Pili (attachment to nasopharynx), Outer membrane proteins (OMP), IgA1 protease (cleaves mucosal IgA), Endotoxin (LPS - causes DIC and Waterhouse-Friderichsen syndrome).",
            "<b>(b) CSF Investigations:</b> Microscopy: Gram stain (Gram-negative diplococci), Biochemistry: Glucose ↓, Protein ↑, Cell count: >1000 WBC (mostly neutrophils), Culture: Chocolate agar/Mueller-Hinton agar at 37°C with 5-10% CO2, Latex agglutination test (rapid antigen detection), PCR for N. meningitidis DNA.",
            "<b>(c) Treatment:</b> IV Benzylpenicillin (Penicillin G) - drug of choice. Alternative: Ceftriaxone (for penicillin allergy or empirical treatment). Dexamethasone (to reduce inflammation). ICU monitoring for DIC and septic shock.",
            "<b>(d) Chemoprophylaxis:</b> Rifampicin 10 mg/kg BD x 2 days (drug of choice for contacts). Alternative: Single dose Ciprofloxacin 500 mg (adults) or Ceftriaxone 250 mg IM. Vaccine: Quadrivalent meningococcal vaccine (A,C,Y,W135) for epidemic control.",
        ],
    },
    {
        "scenario": "<b>A 45-year-old male</b> returns from a coastal area with profuse rice-water diarrhea (10-15 L/day), severe dehydration, sunken eyes, skin tenting, and voice hoarseness. Stool shows rapidly motile comma-shaped organisms on dark-field microscopy.",
        "sub_qs": [
            "(a) Identify the organism and the toxin responsible.",
            "(b) Explain the mechanism of toxin action.",
            "(c) What are the culture media used?",
            "(d) Mention the treatment and preventive measures.",
        ],
        "answers": [
            "<b>(a) Organism:</b> Vibrio cholerae O1 (El Tor biotype). Toxin: Cholera toxin (CT) - an enterotoxin (AB5 type). Colonization factor: TCP pilus (Toxin Co-regulated Pilus).",
            "<b>(b) Mechanism of Toxin:</b> B subunit binds GM1 ganglioside receptors on enterocytes. A subunit (ADP-ribosyl transferase) activates Gs alpha subunit. Adenylate cyclase permanently activated → cAMP ↑↑. Cl- secretion ↑ and Na+ absorption ↓ via CFTR channels. Result: Massive isotonic fluid loss (rice-water stool = shed enterocytes + mucus).",
            "<b>(c) Culture Media:</b> Alkaline peptone water (pH 8.6) - enrichment medium. TCBS agar (Thiosulfate-Citrate-Bile salts-Sucrose): Yellow flat colonies (V. cholerae ferments sucrose). Bile salts agar: flat translucent colonies. String test positive (mucoid colonies in 0.5% sodium desoxycholate).",
            "<b>(d) Treatment:</b> PRIMARY = Aggressive ORS/IV Ringer's Lactate. Antibiotics (shorten duration): Doxycycline 300 mg single dose (adults), Azithromycin (children/pregnant). Prevention: Safe water, sanitation, cholera vaccine (Shanchol/OCV), notification to health authorities.",
        ],
    },
    {
        "scenario": "<b>A 22-year-old male</b> presents with jaundice, dark urine (tea-colored), clay-colored stools, right upper quadrant pain, anorexia, and malaise for 2 weeks. Lab: HBsAg positive, IgM anti-HBc positive, HBeAg positive, ALT markedly elevated.",
        "sub_qs": [
            "(a) Interpret the serological markers.",
            "(b) Differentiate acute vs chronic Hepatitis B using markers.",
            "(c) What is the 'window period' in HBV infection?",
            "(d) Mention the vaccines available and schedule.",
        ],
        "answers": [
            "<b>(a) Interpretation:</b> HBsAg +ve: Active HBV infection (surface antigen). IgM anti-HBc +ve: ACUTE HBV infection (IgM = recent). HBeAg +ve: Active viral replication, HIGH infectivity. ALT markedly ↑: Hepatocyte damage. Diagnosis = ACUTE Hepatitis B with high infectivity.",
            "<b>(b) Acute vs Chronic HBV:</b> Acute: HBsAg +ve (resolves by 6 months), IgM anti-HBc +ve, HBeAg +ve (temporary), ALT spikes then normalizes. Chronic: HBsAg +ve for >6 months, IgG anti-HBc +ve, HBeAg may be +ve or -ve (precore mutant), ALT persistently elevated or fluctuating. HBV DNA by PCR confirms replication.",
            "<b>(c) Window Period:</b> Period between disappearance of HBsAg and appearance of anti-HBs antibody. During this period: HBsAg is negative, Anti-HBs is negative, Only IgM anti-HBc is POSITIVE. Diagnostic importance: Window period blood is INFECTIOUS but HBsAg test is negative - hence risk in blood transfusion. Duration: 3-6 weeks.",
            "<b>(d) Vaccines:</b> Recombinant HBsAg vaccine (Engerix-B, Recombivax HB). Schedule: 0, 1, 6 months (3 doses). Neonatal: 0, 6, 10, 14 weeks under UIP. HBIG (Hepatitis B Immunoglobulin): For post-exposure prophylaxis (needlestick injury, neonate of HBsAg+ve mother) - gives passive immunity.",
        ],
    },
    {
        "scenario": "<b>A tribal patient from Maharashtra</b> presents with cyclical fever every 48 hours (tertian), severe headache, chills, rigor, splenomegaly, and pallor. Peripheral blood smear shows ring forms with multiple rings per RBC, banana-shaped gametocytes, and Maurer's clefts.",
        "sub_qs": [
            "(a) Identify the Plasmodium species.",
            "(b) What is the fever pattern for each Plasmodium species?",
            "(c) Name the rapid diagnostic test (RDT) used.",
            "(d) What is the drug of choice, and why is chloroquine resistance a concern?",
        ],
        "answers": [
            "<b>(a) Species:</b> Plasmodium falciparum. Diagnostic features: Multiple rings per RBC (double/triple infections), Applique (accolé) position of ring forms, Banana-shaped (crescent) gametocytes, Maurer's clefts in RBC, Small ring forms (1/5 of RBC diameter). Only rings + gametocytes seen in peripheral blood (mature trophozoites sequester in deep vessels).",
            "<b>(b) Fever Patterns:</b> P. falciparum: Malignant tertian (irregular/continuous fever, every 48 hrs). P. vivax: Benign tertian (every 48 hrs, schizogony). P. malariae: Quartan malaria (every 72 hrs, 4th day fever). P. ovale: Benign tertian (every 48 hrs, like vivax). Note: Falciparum fever is often irregular due to multiple broods.",
            "<b>(c) Rapid Diagnostic Test:</b> ICT (Immunochromatographic test) / RDT: OptiMAL (detects pLDH - parasite lactate dehydrogenase), HRP-2 based RDT (detects P. falciparum-specific HRP-2 antigen), ParaHIT-f (HRP-2 antigen). Thick blood smear remains gold standard. Thin smear for species identification.",
            "<b>(d) Drug of Choice:</b> Artemisinin-based Combination Therapy (ACT): Artesunate + Sulfadoxine-Pyrimethamine (in India, NMP). OR Artemether-Lumefantrine. Chloroquine Resistance: Pfcrt (chloroquine resistance transporter) gene mutation → accumulation of chloroquine blocked in parasite food vacuole → drug cannot act on heme detoxification. Primaquine added for P. vivax/P. ovale to kill hypnozoites and prevent relapse.",
        ],
    },
]

PATH_QUESTIONS = [
    {
        "scenario": "<b>A 55-year-old hypertensive male</b> presents to the emergency with severe crushing chest pain radiating to the left arm and jaw, profuse sweating, and hypotension. ECG shows ST elevation in leads II, III, aVF. Troponin I is markedly elevated.",
        "sub_qs": [
            "(a) What is the diagnosis?",
            "(b) Describe the macroscopic and microscopic changes at 6 hrs, 24 hrs, 5 days, and 8 weeks.",
            "(c) Name the cardiac biomarkers and their time course.",
            "(d) Mention the complications of MI.",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Acute ST-Elevation Myocardial Infarction (STEMI), inferior wall (RCA territory - leads II, III, aVF). Cause: Atherosclerotic plaque rupture → coronary thrombosis → ischemic necrosis of myocardium.",
            "<b>(b) Morphological Changes:</b> 0-6 hrs: Microscopy: No change (wavy fiber change after 1-2 hrs). Macro: No gross change. 6-24 hrs: Macro: Pale/mottled area. Micro: Coagulative necrosis begins, contraction band necrosis, loss of nuclei. 1-5 days: Macro: Yellow-tan infarct with hyperemic border. Micro: Neutrophil infiltration (peak 3-4 days), complete coagulative necrosis. 1-3 weeks: Macro: Yellow-tan softening, hyperemic border. Micro: Macrophage infiltration, granulation tissue (fibroblasts + capillaries) at periphery. >2 months (8 wks): Macro: Gray-white scar. Micro: Dense collagenous scar (healed infarct).",
            "<b>(c) Cardiac Biomarkers:</b> Troponin I/T: Rises 3-6 hrs, PEAKS 24-48 hrs, remains elevated 7-10 days. MOST SPECIFIC AND SENSITIVE. CK-MB: Rises 3-6 hrs, peaks 18-24 hrs, returns normal 2-3 days (best for reinfarction). Myoglobin: Rises 1-3 hrs (earliest), NOT specific. LDH: Rises 24 hrs, peaks 3-5 days (useful when late presentation).",
            "<b>(d) Complications:</b> Early (1-3 days): Arrhythmias (VF - most common cause of early death), Cardiogenic shock, Rupture of free wall (hemopericardium). Day 3-5: Papillary muscle rupture (MR), Interventricular septal rupture. Late: Pericarditis (Dressler's syndrome), Left ventricular aneurysm, Mural thrombus → embolism, Congestive cardiac failure.",
        ],
    },
    {
        "scenario": "<b>A 35-year-old female</b> presents with a painless lump in the right breast for 3 months. Biopsy shows malignant ductal cells in gland-like structures with stromal desmoplasia (scirrhous appearance), lymphovascular invasion, and 3 out of 5 axillary lymph node metastases. ER+, PR+, HER2/neu negative.",
        "sub_qs": [
            "(a) What is the diagnosis?",
            "(b) Differentiate between ductal and lobular carcinoma of breast.",
            "(c) Explain the significance of ER, PR, and HER2/neu receptors.",
            "(d) What is DCIS (Ductal Carcinoma In Situ)?",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Invasive Ductal Carcinoma (IDC) / Infiltrating Ductal Carcinoma NOS (Not Otherwise Specified) - the most common type (~70-80% of breast cancers). Stage: pT2N2M0 (Stage IIIA based on 3 nodes +ve). Scirrhous variant due to desmoplastic stromal reaction.",
            "<b>(b) Ductal vs Lobular Carcinoma:</b> IDC: Arises from ductal epithelium, Firm/gritty texture (desmoplasia), Gland-like structures on microscopy, E-cadherin POSITIVE, Most common type, Often unicentric. ILC (Invasive Lobular): Arises from lobular units, Indian file / single file pattern, E-cadherin NEGATIVE (mutation), Often bilateral and multicentric, Better prognosis overall but difficult to detect on mammography.",
            "<b>(c) Receptor Significance:</b> ER+/PR+: Responsive to anti-estrogen therapy (Tamoxifen - premenopausal; Aromatase inhibitors - postmenopausal). Better prognosis than hormone receptor negative. HER2/neu overexpression: Poor prognosis, treated with Trastuzumab (Herceptin). Triple Negative (ER-, PR-, HER2-): Worst prognosis, no targeted therapy, treated with chemotherapy only. BRCA1/2 mutations: Familial breast cancer, bilateral risk.",
            "<b>(d) DCIS:</b> Ductal Carcinoma In Situ = malignant ductal epithelial cells confined within the basement membrane (no invasion). Pre-invasive lesion. Types: Comedo DCIS (central necrosis = comedo pattern, most aggressive), Non-comedo (cribriform, micropapillary, solid). Treatment: Lumpectomy + radiation; mastectomy in extensive cases. 30% progress to invasive carcinoma if untreated.",
        ],
    },
    {
        "scenario": "<b>A 50-year-old chronic alcoholic male</b> presents with massive abdominal distension (ascites), jaundice (bilirubin 8 mg/dL), hematemesis (variceal bleeding), and confusion (hepatic encephalopathy). Liver biopsy shows nodular regeneration with thick fibrous bands.",
        "sub_qs": [
            "(a) What is the diagnosis? Name the types and their causes.",
            "(b) Explain the pathogenesis of portal hypertension and ascites.",
            "(c) What are the major complications of liver cirrhosis?",
            "(d) What are the lab findings in cirrhosis?",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Liver Cirrhosis (Alcoholic). Types: Micronodular (<3mm): Alcoholic, Hemochromatosis, Wilson's disease. Macronodular (>3mm): Post-hepatitic (HBV/HCV), Wilson's disease, Alpha-1-AT deficiency. Mixed: Common in advanced disease. Alcoholic liver disease progression: Fatty liver → Alcoholic hepatitis (Mallory-Denk bodies) → Cirrhosis.",
            "<b>(b) Pathogenesis of Portal Hypertension & Ascites:</b> Portal hypertension: Fibrous bands + regenerative nodules → increased resistance to portal blood flow → portal venous pressure >12 mmHg. Ascites pathogenesis: Portal HTN → splanchnic vasodilation (NO↑) → decreased effective circulating volume → RAAS activation → Na+ and water retention → ascites. Low serum albumin (liver failure) → reduced oncotic pressure → ascites. Lymph formation exceeds drainage. SAAG (serum-ascites albumin gradient) >1.1 g/dL confirms portal HTN.",
            "<b>(c) Complications:</b> Hepatic encephalopathy: NH3 accumulation → cerebral edema. Portal hypertension → Esophageal varices (variceal hemorrhage), Splenomegaly (hypersplenism → thrombocytopenia). Spontaneous Bacterial Peritonitis (SBP): E. coli, Klebsiella. Hepatorenal syndrome: Type 1 (acute), Type 2 (chronic). Hepatocellular Carcinoma (HCC): Especially HBV/HCV cirrhosis. Coagulopathy: Reduced clotting factor synthesis.",
            "<b>(d) Lab Findings:</b> LFT: ↑ Bilirubin, ↑ ALT/AST (AST:ALT ratio >2 in alcoholic), ↑ ALP, ↑ GGT. Synthetic function: ↓ Albumin (<3.5), ↑ PT/INR, ↓ clotting factors. CBC: Thrombocytopenia (hypersplenism), Macrocytic anemia (B12/folate deficiency). Child-Pugh score (Bilirubin, Albumin, PT, Ascites, Encephalopathy) used for prognosis. Alpha-fetoprotein ↑ suggests HCC.",
        ],
    },
    {
        "scenario": "<b>A 10-year-old child</b> develops periorbital puffiness (especially morning), gross proteinuria (6g/day), hypoalbuminemia (serum albumin 1.8 g/dL), hyperlipidemia, and lipiduria. Blood pressure is normal. No hematuria. Renal biopsy shows effacement of podocyte foot processes on electron microscopy (normal light microscopy).",
        "sub_qs": [
            "(a) What is the diagnosis?",
            "(b) Differentiate nephrotic syndrome vs nephritic syndrome.",
            "(c) Name the causes of nephrotic syndrome in children vs adults.",
            "(d) What is the treatment and prognosis?",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Nephrotic Syndrome due to Minimal Change Disease (MCD) / Nil disease / Lipoid nephrosis. Most common cause of nephrotic syndrome in children. Electron microscopy shows diffuse effacement of podocyte foot processes (fusion) with NO immune deposits (unlike other GN).",
            "<b>(b) Nephrotic vs Nephritic Syndrome:</b> Nephrotic: Proteinuria >3.5g/day, Hypoalbuminemia <3.5g/dL, Edema (massive), Hyperlipidemia, Lipiduria, NO/mild hematuria, NO hypertension usually. Nephritic: Hematuria (RBC casts), Oliguria, Hypertension, Mild-moderate proteinuria, Azotemia. Causes of Nephritic: PSGN, IgA nephropathy, SLE, Goodpasture's.",
            "<b>(c) Causes by Age:</b> Children (<15 yrs): Minimal Change Disease (80%), FSGS, Membranoproliferative GN. Adults: Membranous nephropathy (most common primary), FSGS, Diabetic nephropathy, Amyloidosis, SLE (secondary). Secondary causes overall: Diabetes, Amyloidosis, SLE, Drugs (NSAIDs, gold, penicillamine), Infections (malaria, HBV, HCV).",
            "<b>(d) Treatment & Prognosis:</b> MCD: Responds dramatically to corticosteroids (prednisolone 60 mg/m2/day x 4-6 wks) - hence also called 'steroid-sensitive nephrotic syndrome'. >90% of children achieve complete remission. Cyclophosphamide for frequent relapsers. General: Dietary Na+ restriction, Diuretics (furosemide + spironolactone), ACE inhibitors (reduce proteinuria), Statins (hyperlipidemia), Anticoagulation (DVT prophylaxis - AT-III lost in urine). Prognosis: Excellent in MCD. Poor in FSGS.",
        ],
    },
    {
        "scenario": "<b>A 25-year-old female</b> presents with painless neck swelling (anterior, moves with swallowing), fatigue, cold intolerance, weight gain, constipation, and dry skin. TSH: 45 mIU/L (very high), Free T4: low. FNAC shows Hurthle cell change with lymphocytic infiltration and germinal center formation.",
        "sub_qs": [
            "(a) What is the diagnosis?",
            "(b) Compare Hashimoto's thyroiditis and Graves' disease.",
            "(c) What is the risk of malignancy? What type?",
            "(d) Describe the antibodies involved.",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Hashimoto's Thyroiditis (Autoimmune/Chronic Lymphocytic Thyroiditis). Most common cause of hypothyroidism in iodine-sufficient areas. Autoimmune destruction of thyroid follicles by CD8+ cytotoxic T cells and anti-thyroid antibodies. Pathology: Dense lymphocytic infiltration with germinal center formation, Hurthle (Askanazy) cell metaplasia of follicular epithelium, Fibrous bands in advanced disease.",
            "<b>(b) Hashimoto's vs Graves' Disease:</b> Hashimoto's: Hypothyroidism, Anti-TPO + Anti-TG antibodies (destructive), Lymphocytic infiltration, Germinal centers, Hurthle cells, Goiter (firm), TSH ↑, T3/T4 ↓, Radioiodine uptake ↓. Graves': Hyperthyroidism, TSI/TRAb (stimulating antibodies), Diffuse hyperplasia, Tall follicular cells, Exophthalmos, Pretibial myxedema, TSH ↓, T3/T4 ↑, Radioiodine uptake ↑.",
            "<b>(c) Malignancy Risk:</b> Increased risk of: Primary thyroid lymphoma (B-cell NHL) - rare but specifically associated with Hashimoto's. Papillary thyroid carcinoma: Slightly increased risk. Psammoma bodies and nuclear features of PTC may coexist. FNAC important to exclude malignancy (PTC shows Orphan Annie eye nuclei, nuclear grooves, pseudo-inclusions).",
            "<b>(d) Antibodies:</b> Anti-TPO (Anti-thyroid peroxidase): Most sensitive marker, present in 95% cases. Causes complement-mediated destruction. Anti-Thyroglobulin (Anti-TG): Present in ~60%. Less specific. These lead to progressive follicular destruction → hypothyroidism. Note: Transient hyperthyroidism ('Hashitoxicosis') may occur early due to release of stored T3/T4 from damaged follicles.",
        ],
    },
]

PHARMA_QUESTIONS = [
    {
        "scenario": "<b>A 60-year-old diabetic hypertensive male</b> is started on enalapril. One week later, he develops a dry, irritating, non-productive cough that disturbs his sleep. His serum creatinine rises from 1.0 to 1.4 mg/dL. Serum potassium is 5.2 mEq/L.",
        "sub_qs": [
            "(a) Name the drug class. What is causing the cough?",
            "(b) Explain the mechanism of antihypertensive action.",
            "(c) What alternative drug class is preferred to avoid cough?",
            "(d) Why is this class the preferred drug in diabetic nephropathy?",
        ],
        "answers": [
            "<b>(a) Drug Class & Cough:</b> ACE Inhibitors (Enalapril, Lisinopril, Ramipril). Cough is caused by accumulation of Bradykinin and Substance P. ACE normally inactivates bradykinin; when ACE is inhibited → bradykinin accumulates in lungs → stimulates C-fibers → dry cough. Occurs in 10-15% patients (more common in Asians/Indians ~30%). Management: Switch to ARB (no bradykinin accumulation).",
            "<b>(b) Mechanism of ACE Inhibitors:</b> ACE inhibitors block conversion of Angiotensin I → Angiotensin II (by inhibiting ACE enzyme). Effects: ↓ Angiotensin II → arteriolar vasodilation (↓ afterload). ↓ Aldosterone secretion → ↓ Na+ and water retention (↓ preload). ↓ Bradykinin breakdown → vasodilation (additional BP lowering). Mild rise in serum creatinine in 1st 2 weeks is acceptable (functional - due to efferent arteriole dilation). K+ retention (hyperkalemia risk) - monitor.",
            "<b>(c) Alternative - ARBs:</b> Angiotensin Receptor Blockers (ARBs): Losartan, Valsartan, Telmisartan. Block AT1 receptors directly. Do NOT inhibit ACE → no bradykinin accumulation → NO COUGH. Same renoprotective benefit as ACE inhibitors in diabetic nephropathy. First choice in patients intolerant to ACE inhibitors. Note: ACE inhibitors + ARBs COMBINATION is contraindicated (hyperkalemia, renal failure).",
            "<b>(d) Renoprotection in Diabetic Nephropathy:</b> Intraglomerular hypertension is the key mechanism of diabetic nephropathy. ACE inhibitors/ARBs selectively dilate the efferent arteriole > afferent → ↓ glomerular filtration pressure → ↓ proteinuria. Reduce progression from microalbuminuria to macroalbuminuria. Delay onset of end-stage renal disease (ESRD). Indicated even in normotensive diabetics with microalbuminuria. Additional benefit: Prevent cardiac remodeling (post-MI).",
        ],
    },
    {
        "scenario": "<b>A 70-year-old male with atrial fibrillation</b> on digoxin 0.25 mg/day is started on furosemide for heart failure. Three days later, he presents with nausea, vomiting, seeing yellow-green halos around lights (xanthopsia), and his HR is 42/min with PVCs on ECG.",
        "sub_qs": [
            "(a) What is the diagnosis?",
            "(b) Why did furosemide precipitate this condition?",
            "(c) How will you manage this emergency?",
            "(d) Name the antidote and its mechanism.",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Digoxin Toxicity (Digitalis toxicity). Classic triad: GI symptoms (nausea/vomiting), Visual disturbances (xanthopsia - yellow-green vision, halos), Cardiac arrhythmias (bradycardia, PVCs, AV block). Narrow therapeutic index drug (therapeutic: 0.8-2 ng/mL; toxic: >2 ng/mL).",
            "<b>(b) Furosemide Precipitation:</b> Furosemide → loop diuretic → causes HYPOKALEMIA (K+ wasting). Hypokalemia sensitizes the heart to digoxin toxicity because: K+ and digoxin compete for the SAME binding site on Na+/K+ ATPase pump. Low K+ → MORE digoxin binding → INCREASED toxicity at normal digoxin levels. Other factors increasing digoxin toxicity: Hypomagnesemia, Hypercalcemia, Hypothyroidism, Renal failure (reduced excretion), Old age, Drug interactions (amiodarone, verapamil, quinidine increase digoxin levels).",
            "<b>(c) Management:</b> STOP digoxin immediately. Correct hypokalemia: IV KCl (not in AV block). Correct hypomagnesemia: IV MgSO4. Monitor ECG continuously (ICU). For life-threatening arrhythmias: Lidocaine / Phenytoin (for ventricular arrhythmias - DO NOT use DC cardioversion - may → VF). Atropine for severe bradycardia/AV block. Administer Digibind (specific antidote).",
            "<b>(d) Antidote:</b> Digoxin-specific antibody fragments (Fab fragments) - Digibind / DigiFab. Mechanism: Fab fragments bind free digoxin molecules with high affinity (> Na+/K+ ATPase affinity). Forms Digoxin-Fab complex (inactive, renally excreted). Rapidly reverses toxicity within 30-60 minutes. Indications: Life-threatening arrhythmias, K+ >5.5 mEq/L, Serum digoxin >10-15 ng/mL.",
        ],
    },
    {
        "scenario": "<b>A 25-year-old male</b> is brought unconscious with pin-point pupils (miosis), bradycardia (HR 45), bradypnea (RR 6/min), hypotension, and cyanosis after suspected heroin injection. The classic triad is present.",
        "sub_qs": [
            "(a) What is the diagnosis? Name the classic triad.",
            "(b) Name the antidote and its mechanism of action.",
            "(c) Explain opioid receptor types and their effects.",
            "(d) What is the treatment of opioid withdrawal syndrome?",
        ],
        "answers": [
            "<b>(a) Diagnosis:</b> Acute Opioid Toxicity / Heroin Overdose. Classic Triad (Opioid Toxidrome): 1) Pin-point pupils (miosis) - mu receptor mediated, 2) CNS depression (coma/unconsciousness), 3) Respiratory depression (bradypnea) - MOST DANGEROUS complication causing death. Additional: Bradycardia, Hypotension, Decreased GI motility (constipation). Note: Tramadol overdose may cause SEIZURES (different from pure opioids).",
            "<b>(b) Antidote - Naloxone:</b> Naloxone (Narcan) - Pure competitive opioid ANTAGONIST. Mechanism: Competitively blocks all opioid receptors (mu, kappa, delta) with higher affinity than opioids. Reverses all features: miosis, CNS depression, respiratory depression. Route: IV/IM/Intranasal (fastest IV). Duration: 30-90 min (SHORTER than opioids - repeated doses needed as opioid may outlast naloxone - 'renarcotization'). Dose: 0.4-2 mg IV, repeat every 2-3 min if needed (max 10 mg). Note: Naltrexone = oral, long-acting version (for opioid/alcohol dependence).",
            "<b>(c) Opioid Receptors:</b> Mu (µ) receptors: Analgesia, euphoria, respiratory depression, miosis, constipation, physical dependence - MOST IMPORTANT. Kappa (κ): Analgesia, sedation, miosis, dysphoria (no euphoria). Delta (δ): Analgesia, mood, spinal analgesia. Sigma (σ): Dysphoria, hallucinations, tachycardia (NOT blocked by naloxone). Morphine acts mainly on µ receptors. Pentazocine: kappa agonist + weak mu antagonist.",
            "<b>(d) Opioid Withdrawal Treatment:</b> Opioid withdrawal is NOT life-threatening (unlike alcohol withdrawal) but very distressing. Symptoms: Yawning, lacrimation, rhinorrhea, piloerection (goosebumps), mydriasis, diarrhea, tachycardia, hypertension, cramps, anxiety. Treatment: Methadone maintenance therapy (long-acting oral opioid agonist - reduces cravings). Buprenorphine/Naloxone (Suboxone) - partial mu agonist. Clonidine (alpha-2 agonist): Reduces autonomic symptoms (not cravings). Naltrexone: After detox for relapse prevention.",
        ],
    },
    {
        "scenario": "<b>A 28-year-old epileptic female</b> on phenytoin 300 mg/day for 2 years wants to conceive. Her OCP (combined oral contraceptive pill) has been 'failing' with irregular cycles. She asks about switching medications.",
        "sub_qs": [
            "(a) What is the drug interaction between phenytoin and OCP?",
            "(b) Name the teratogenic effects of phenytoin.",
            "(c) What antiepileptic drugs are relatively safer in pregnancy?",
            "(d) What other adverse effects does long-term phenytoin use cause?",
        ],
        "answers": [
            "<b>(a) Phenytoin-OCP Interaction:</b> Phenytoin is a potent ENZYME INDUCER of CYP450 (CYP3A4, 2C9). Induces metabolism of ethinyl estradiol and progestins in OCP → rapidly inactivated → REDUCED OCP efficacy → contraceptive failure. Other enzyme inducers that reduce OCP efficacy: Carbamazepine, Phenobarbital, Rifampicin (most potent), Topiramate, Primidone. Management: Use higher-dose OCP (≥50 mcg estrogen) + barrier method, OR switch to enzyme non-inducing AED (lamotrigine, levetiracetam, valproate).",
            "<b>(b) Phenytoin Teratogenicity - Fetal Hydantoin Syndrome:</b> Occurs in ~10% of fetuses exposed to phenytoin. Features: Craniofacial anomalies (cleft palate, broad flat nose, hypertelorism), Digit/nail hypoplasia (hypoplastic distal phalanges), Prenatal growth retardation, Mental retardation/cognitive deficits, Cardiac defects. Mechanism: Toxic epoxide metabolite + oxidative stress damages fetal tissue. Folic acid supplementation (5 mg/day pre-conception and through pregnancy) reduces risk.",
            "<b>(c) Safer AEDs in Pregnancy:</b> No AED is completely safe. Relatively safer: Lamotrigine (drug of choice in pregnancy - least teratogenic, no enzyme induction), Levetiracetam (increasing use in pregnancy). Avoid: Valproate (HIGHEST teratogenicity - neural tube defects, spina bifida, autism spectrum disorder - avoid if possible). Phenytoin, Carbamazepine (neural tube defects). Principle: Use monotherapy at lowest effective dose, supplement folic acid 5 mg/day.",
            "<b>(d) Other Phenytoin Adverse Effects:</b> Dose-related: Nystagmus (earliest sign), Ataxia, Diplopia, Cognitive impairment, Sedation. Chronic use: Gingival hyperplasia (most characteristic - seen in 50%), Hirsutism, Acne, Coarsening of facial features, Peripheral neuropathy, Osteomalacia (CYP induction → Vit D metabolism ↑ → Ca2+ absorption ↓), Megaloblastic anemia (folate metabolism). Idiosyncratic: Steven-Johnson syndrome, Hepatotoxicity, Agranulocytosis. Zero-order kinetics: Phenytoin has saturable metabolism → small dose increase → disproportionate toxicity.",
        ],
    },
    {
        "scenario": "<b>A 10-year-old child</b> is given chloramphenicol for a multidrug-resistant typhoid fever. Two days later, the child develops abdominal distension, vomiting, hypothermia, and ashen-gray cyanosis followed by circulatory collapse.",
        "sub_qs": [
            "(a) What is this reaction? Why does it occur in neonates/children?",
            "(b) What enzyme is deficient, and what metabolite accumulates?",
            "(c) Name other significant adverse effects of chloramphenicol.",
            "(d) Name alternative drugs for typhoid and other indications.",
        ],
        "answers": [
            "<b>(a) Gray Baby Syndrome:</b> This is 'Gray Baby Syndrome' - a potentially fatal reaction to chloramphenicol in neonates and young infants (rarely in children). Features: Ashen-gray cyanosis (hallmark), Vomiting and abdominal distension (paralytic ileus), Hypothermia, Cardiovascular collapse (vasodilation + myocardial depression), 40% mortality if untreated. Why neonates/children: Immature/deficient hepatic UDP-glucuronyl transferase enzyme. Immature renal tubular secretion for chloramphenicol glucuronide.",
            "<b>(b) Enzyme & Metabolite:</b> Deficient Enzyme: UDP-glucuronyl transferase (glucuronidation pathway in liver). Normal adults conjugate chloramphenicol to inactive glucuronide → renally excreted. In neonates: Conjugation is minimal → FREE chloramphenicol accumulates to toxic levels → Inhibits mitochondrial protein synthesis in myocardium → cardiotoxicity. Prevention: Avoid chloramphenicol in neonates; if essential, use doses ≤25 mg/kg/day with drug level monitoring.",
            "<b>(c) Other Chloramphenicol ADRs:</b> Bone marrow suppression (two types): Dose-related reversible aplasia (common, reversible on stopping). Idiosyncratic irreversible aplastic anemia (rare 1:40,000 but FATAL - occurs even with eye drops). Blood dyscrasias: Neutropenia, thrombocytopenia, anemia. Optic neuritis (with prolonged use). Drug interactions: Inhibits CYP2C9 and CYP3A4 → increases levels of warfarin, phenytoin, sulfonylureas. Herxheimer reaction in typhoid (rare).",
            "<b>(d) Alternatives:</b> For Typhoid: Ceftriaxone (IV, drug of choice for MDR typhoid), Azithromycin (oral MDR typhoid, especially in children), Fluoroquinolones (ciprofloxacin - if susceptible; reduced efficacy against nalidixic acid-resistant strains). Chloramphenicol still used for: Bacterial meningitis (H. influenzae, N. meningitidis) when penicillin/cephalosporin not available. Rickettsial infections (Rocky Mountain Spotted Fever - though doxycycline preferred). Brain abscess (good CNS penetration).",
        ],
    },
]

# ─── Answer Structure Tips ─────────────────────────────────────
ANSWER_TIPS = [
    "State the DIAGNOSIS clearly in the FIRST sentence - examiners look for this first.",
    "Use organism/drug names precisely - genus and species for organisms (e.g., Salmonella typhi, not just 'Salmonella').",
    "Structure answers: Diagnosis → Mechanism/Pathogenesis → Lab Diagnosis → Treatment → Complications.",
    "Draw DIAGRAMS wherever applicable - life cycles, flowcharts, time-course graphs fetch extra marks.",
    "Use COMPARISON TABLES for paired topics (Nephrotic vs Nephritic, Acute vs Chronic, Ductal vs Lobular).",
    "Under CBME, always add a line of clinical relevance: 'This explains why patient presents with...'",
    "For Pharmacology: Always write MOA → Uses → ADRs → Contraindications → Drug Interactions.",
    "For Microbiology: Always include culture media + staining technique + specific test for each organism.",
    "Mention DRUG OF CHOICE explicitly - examiners specifically look for this in treatment sections.",
    "Under MUHS MCQ section: watch for 'EXCEPT' and 'NOT' type questions - read carefully before marking.",
]


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    # ── TABLE OF CONTENTS ───────────────────────────────────────
    story.append(Paragraph("Table of Contents", ParagraphStyle(
        'toc_main', fontSize=16, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, alignment=TA_CENTER, spaceAfter=10
    )))
    story.append(HRFlowable(width=W, thickness=2, color=DARK_BLUE))
    story.append(Spacer(1, 0.2*cm))

    sections = [
        ("MICROBIOLOGY", TEAL, [
            "Q1 - Enteric Fever / Salmonella typhi",
            "Q2 - Bacterial Meningitis / N. meningitidis",
            "Q3 - Cholera / Vibrio cholerae",
            "Q4 - Hepatitis B - Serological Markers",
            "Q5 - Malaria / Plasmodium falciparum",
        ]),
        ("PATHOLOGY", RED_ACCENT, [
            "Q1 - Myocardial Infarction",
            "Q2 - Carcinoma Breast",
            "Q3 - Liver Cirrhosis",
            "Q4 - Nephrotic Syndrome / Minimal Change Disease",
            "Q5 - Hashimoto's Thyroiditis",
        ]),
        ("PHARMACOLOGY", PURPLE, [
            "Q1 - ACE Inhibitors / Diabetic Nephropathy",
            "Q2 - Digoxin Toxicity",
            "Q3 - Opioid Toxicity / Naloxone",
            "Q4 - Phenytoin / Drug Interactions in Pregnancy",
            "Q5 - Gray Baby Syndrome / Chloramphenicol",
        ]),
    ]
    for sec_name, sec_color, items in sections:
        sec_hdr = Paragraph(sec_name, ParagraphStyle(
            'toc_sh', fontSize=11, fontName='Helvetica-Bold',
            textColor=white, alignment=TA_LEFT
        ))
        toc_hdr_t = Table([[sec_hdr]], colWidths=[W])
        toc_hdr_t.setStyle(TableStyle([
            ('BACKGROUND', (0,0), (-1,-1), sec_color),
            ('TOPPADDING', (0,0), (-1,-1), 6),
            ('BOTTOMPADDING', (0,0), (-1,-1), 6),
            ('LEFTPADDING', (0,0), (-1,-1), 12),
        ]))
        story.append(toc_hdr_t)
        for item in items:
            story.append(Paragraph(f"&#x25B6; &nbsp; {item}", ParagraphStyle(
                'tocitem', fontSize=10, fontName='Helvetica',
                textColor=DARK_GRAY, leftIndent=20, spaceAfter=3, leading=14
            )))
        story.append(Spacer(1, 0.15*cm))

    # Answer tips in TOC
    story.append(Spacer(1, 0.2*cm))
    story.append(Paragraph("+ Exam Answer Structure Tips (Page: Appendix)", ParagraphStyle(
        'toc_app', fontSize=10, fontName='Helvetica-Oblique',
        textColor=ORANGE, leftIndent=20, spaceAfter=5
    )))
    story.append(PageBreak())

    # ── SUBJECT SECTIONS ───────────────────────────────────────

    subject_config = [
        ("MICROBIOLOGY", "Bacteriology | Virology | Parasitology | Immunology",
         TEAL, LIGHT_TEAL, MICRO_QUESTIONS),
        ("PATHOLOGY", "General Pathology | Systemic Pathology",
         RED_ACCENT, LIGHT_RED, PATH_QUESTIONS),
        ("PHARMACOLOGY", "General Pharmacology | Chemotherapy | Systemic Pharmacology",
         PURPLE, LIGHT_PURPLE, PHARMA_QUESTIONS),
    ]

    for subj_name, subj_sub, subj_color, subj_light, questions in subject_config:
        # Subject cover band
        subj_cover = Table([
            [Paragraph(subj_name, ParagraphStyle(
                'scn', fontSize=18, fontName='Helvetica-Bold',
                textColor=white, alignment=TA_CENTER, leading=24
            ))],
            [Paragraph(subj_sub, ParagraphStyle(
                'scs', fontSize=10, fontName='Helvetica-Oblique',
                textColor=HexColor("#e0e0e0"), alignment=TA_CENTER, leading=14
            ))],
        ], colWidths=[W])
        subj_cover.setStyle(TableStyle([
            ('BACKGROUND', (0,0), (-1,-1), subj_color),
            ('TOPPADDING', (0,0), (0,0), 14),
            ('BOTTOMPADDING', (0,1), (0,1), 14),
            ('TOPPADDING', (0,1), (0,1), 4),
            ('LEFTPADDING', (0,0), (-1,-1), 10),
        ]))
        story.append(subj_cover)
        story.append(Spacer(1, 0.3*cm))

        for i, q in enumerate(questions):
            block = question_block(
                i + 1,
                q["scenario"],
                q["sub_qs"],
                q["answers"],
                styles,
                subj_color,
                subj_light,
            )
            story.extend(block)

        story.append(PageBreak())

    # ── APPENDIX: EXAM TIPS ─────────────────────────────────────
    story.append(colored_box("APPENDIX: EXAM ANSWER STRUCTURE TIPS", DARK_BLUE))
    story.append(Spacer(1, 0.2*cm))
    story.append(key_point_box(ANSWER_TIPS, styles, "GOLDEN RULES FOR MUHS CLINICAL ANSWERS"))
    story.append(Spacer(1, 0.4*cm))

    # Comparison: Nephrotic vs Nephritic
    story.append(Paragraph("Quick Reference: Nephrotic vs Nephritic Syndrome", ParagraphStyle(
        'qr', fontSize=11, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, spaceAfter=4
    )))
    nt_headers = ["Feature", "Nephrotic Syndrome", "Nephritic Syndrome"]
    nt_rows = [
        ["Proteinuria", ">3.5 g/day (massive)", "<3.5 g/day (mild-moderate)"],
        ["Hematuria", "Absent / minimal", "Present (RBC casts)"],
        ["Edema", "Massive (anasarca)", "Mild-moderate"],
        ["Hypertension", "Absent / mild", "Present"],
        ["Serum Albumin", "Low (<3.5 g/dL)", "Normal/mildly reduced"],
        ["Hyperlipidemia", "Present (lipiduria)", "Absent"],
        ["Classic Cause", "MCD (children), Membranous (adults)", "PSGN, IgA nephropathy"],
    ]
    story.append(comparison_table(nt_headers, nt_rows, [4*cm, 6.5*cm, 6.5*cm], TEAL))
    story.append(Spacer(1, 0.4*cm))

    # Comparison: Acute vs Chronic Hepatitis B
    story.append(Paragraph("Quick Reference: HBV Serological Markers", ParagraphStyle(
        'qr2', fontSize=11, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, spaceAfter=4
    )))
    hbv_headers = ["Marker", "Acute HBV", "Chronic HBV", "Resolved HBV", "Vaccinated"]
    hbv_rows = [
        ["HBsAg", "+", "+(>6 months)", "-", "-"],
        ["Anti-HBs", "-", "-", "+", "+"],
        ["IgM anti-HBc", "+", "-", "-", "-"],
        ["IgG anti-HBc", "-", "+", "+", "-"],
        ["HBeAg", "+(early)", "+/-", "-", "-"],
        ["Anti-HBe", "-", "+/-", "+", "-"],
    ]
    story.append(comparison_table(hbv_headers, hbv_rows,
                                  [3.5*cm, 3.2*cm, 3.2*cm, 3.6*cm, 3.5*cm], MED_BLUE))
    story.append(Spacer(1, 0.4*cm))

    # Cardiac biomarkers timeline table
    story.append(Paragraph("Quick Reference: Cardiac Biomarkers in MI", ParagraphStyle(
        'qr3', fontSize=11, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, spaceAfter=4
    )))
    bio_headers = ["Biomarker", "Rises", "Peaks", "Returns Normal", "Note"]
    bio_rows = [
        ["Myoglobin", "1-3 hrs", "6-9 hrs", "24-36 hrs", "Earliest, NOT specific"],
        ["CK-MB", "3-6 hrs", "18-24 hrs", "2-3 days", "Best for reinfarction"],
        ["Troponin I/T", "3-6 hrs", "24-48 hrs", "7-10 days", "MOST specific & sensitive"],
        ["LDH", "24 hrs", "3-5 days", "10-14 days", "Late presentation marker"],
        ["AST", "8-12 hrs", "24-48 hrs", "3-4 days", "Non-specific"],
    ]
    story.append(comparison_table(bio_headers, bio_rows,
                                  [3.2*cm, 2.5*cm, 2.8*cm, 3.2*cm, 5.3*cm], RED_ACCENT))
    story.append(Spacer(1, 0.4*cm))

    # Opioid receptors quick table
    story.append(Paragraph("Quick Reference: Opioid Receptors", ParagraphStyle(
        'qr4', fontSize=11, fontName='Helvetica-Bold',
        textColor=DARK_BLUE, spaceAfter=4
    )))
    opi_headers = ["Receptor", "Key Effects", "Example Agonist", "Clinical Note"]
    opi_rows = [
        ["Mu (µ)", "Analgesia, euphoria, resp. depression, miosis, constipation, dependence",
         "Morphine, Heroin, Fentanyl", "Most important - basis of opioid toxicity"],
        ["Kappa (κ)", "Analgesia, sedation, miosis, DYSPHORIA",
         "Pentazocine, Buprenorphine (partial)", "No euphoria - less abuse potential"],
        ["Delta (δ)", "Analgesia, mood modulation",
         "Enkephalins", "Spinal analgesia"],
        ["Sigma (σ)", "Dysphoria, hallucinations, tachycardia",
         "Ketamine (partial)", "NOT blocked by Naloxone"],
    ]
    story.append(comparison_table(opi_headers, opi_rows,
                                  [2.5*cm, 5.5*cm, 4*cm, 5*cm], PURPLE))
    story.append(Spacer(1, 0.3*cm))

    # Final note
    fn_data = [[Paragraph(
        "<b>Disclaimer:</b> This guide is for educational purposes only. Always refer to "
        "standard textbooks (Ananthanarayan, Robbins, KD Tripathi) and the official MUHS "
        "CBME syllabus. Drug dosages and clinical guidelines should be verified from current "
        "references before clinical application.",
        ParagraphStyle('fn', fontSize=8.5, fontName='Helvetica-Oblique',
                       textColor=DARK_GRAY, alignment=TA_CENTER, leading=13)
    )]]
    fn_t = Table(fn_data, colWidths=[W])
    fn_t.setStyle(TableStyle([
        ('BACKGROUND', (0,0), (-1,-1), GRAY_BG),
        ('BOX', (0,0), (-1,-1), 0.5, MID_GRAY),
        ('TOPPADDING', (0,0), (-1,-1), 8),
        ('BOTTOMPADDING', (0,0), (-1,-1), 8),
        ('LEFTPADDING', (0,0), (-1,-1), 12),
        ('RIGHTPADDING', (0,0), (-1,-1), 12),
    ]))
    story.append(fn_t)

    # Build
    doc.build(story)
    print(f"PDF generated successfully: {OUTPUT_PATH}")


if __name__ == "__main__":
    build_pdf()

cd /home/daytona/workspace/muhs-study-guide && python3 generate_pdf.py 2>&1

ls -lh /home/daytona/workspace/muhs-study-guide/MUHS_2ndMBBS_Clinical_QA_StudyGu…