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

OUTPUT = "/tmp/workspace/physiology-exam/Physiology_Model_Exam_QA.pdf"

# ── Colors ──────────────────────────────────────────────────────────────────
DARK_BLUE   = HexColor("#1a237e")   # deep navy
MID_BLUE    = HexColor("#1565c0")   # section header bg
LIGHT_BLUE  = HexColor("#e3f2fd")   # Q background
TEAL        = HexColor("#00796b")   # answer accent
TEAL_LIGHT  = HexColor("#e0f2f1")   # A background
ORANGE      = HexColor("#e65100")   # key-point label
ORANGE_LT   = HexColor("#fff3e0")   # key-point bg
GREY_LINE   = HexColor("#b0bec5")
GREY_TEXT   = HexColor("#37474f")
WHITE       = white

# ── Document ─────────────────────────────────────────────────────────────────
doc = SimpleDocTemplate(
    OUTPUT,
    pagesize=A4,
    leftMargin=1.8*cm, rightMargin=1.8*cm,
    topMargin=2.2*cm, bottomMargin=2*cm,
    title="Physiology Model Exam – Important Q&A",
    author="Orris AI Study Assistant"
)

# ── Styles ────────────────────────────────────────────────────────────────────
base = getSampleStyleSheet()

cover_title = ParagraphStyle("cover_title",
    fontSize=28, fontName="Helvetica-Bold",
    textColor=WHITE, alignment=TA_CENTER,
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cover_sub = ParagraphStyle("cover_sub",
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    textColor=HexColor("#bbdefb"), alignment=TA_CENTER,
    spaceAfter=6, leading=18)

section_title = ParagraphStyle("section_title",
    fontSize=14, fontName="Helvetica-Bold",
    textColor=WHITE, alignment=TA_CENTER,
    spaceAfter=0, leading=18)

q_style = ParagraphStyle("q_style",
    fontSize=10.5, fontName="Helvetica-Bold",
    textColor=MID_BLUE, leading=14,
    leftIndent=6, rightIndent=6,
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a_style = ParagraphStyle("a_style",
    fontSize=10, fontName="Helvetica",
    textColor=GREY_TEXT, leading=13,
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bullet_style = ParagraphStyle("bullet_style",
    fontSize=9.5, fontName="Helvetica",
    textColor=GREY_TEXT, leading=13,
    leftIndent=14, bulletIndent=6,
    spaceBefore=1, spaceAfter=1)

kp_label = ParagraphStyle("kp_label",
    fontSize=9, fontName="Helvetica-Bold",
    textColor=ORANGE, leading=12)

kp_text = ParagraphStyle("kp_text",
    fontSize=9.5, fontName="Helvetica",
    textColor=HexColor("#4e342e"), leading=13,
    leftIndent=4)

footer_style = ParagraphStyle("footer",
    fontSize=8, fontName="Helvetica",
    textColor=HexColor("#90a4ae"), alignment=TA_CENTER)

# ── Helpers ───────────────────────────────────────────────────────────────────
def section_header(title, color=MID_BLUE):
    tbl = Table([[Paragraph(title, section_title)]], colWidths=[17.2*cm])
    tbl.setStyle(TableStyle([
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    ]))
    return tbl

def qna_block(number, question, answer_paras, key_point=None):
    """Returns a KeepTogether block for one Q&A."""
    items = []
    # Question row
    q_tbl = Table(
        [[Paragraph(f"Q{number}. {question}", q_style)]],
        colWidths=[17.2*cm]
    )
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        ("BOTTOMPADDING",(0,0),(-1,-1),6),
    ]))
    items.append(q_tbl)
    items.append(Spacer(1, 2))

    # Answer rows
    ans_cells = [[Paragraph("Ans:", ParagraphStyle("alabel",
        fontSize=9, fontName="Helvetica-Bold", textColor=TEAL, leading=12))]]
    ans_content = []
    for para in answer_paras:
        ans_content.append(Paragraph(para, a_style))
    a_tbl = Table(
        [[Paragraph("Ans:", ParagraphStyle("alabel",
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    )
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        ("VALIGN", (0,0),(-1,-1), "TOP"),
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        ("BOTTOMPADDING",(0,0),(-1,-1),5),
        ("LEFTPADDING",(0,0),(-1,-1),6),
    ]))
    items.append(a_tbl)

    # Key point
    if key_point:
        kp_tbl = Table(
            [[Paragraph("★ KEY POINT: ", kp_label),
              Paragraph(key_point, kp_text)]],
            colWidths=[2.2*cm, 15*cm]
        )
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            ("BOTTOMPADDING",(0,0),(-1,-1),4),
            ("LEFTPADDING",(0,0),(-1,-1),6),
            ("ROUNDEDCORNERS",[4]),
        ]))
        items.append(Spacer(1,2))
        items.append(kp_tbl)

    items.append(Spacer(1, 7))
    return KeepTogether(items)


# ══════════════════════════════════════════════════════════════════════════════
# CONTENT DATA
# ══════════════════════════════════════════════════════════════════════════════
sections = [
    {
        "title": "❤  SECTION 1: CARDIOVASCULAR SYSTEM",
        "color": HexColor("#1565c0"),
        "qna": [
            {
                "q": "What is Cardiac Output and how is it calculated? What are normal values?",
                "a": [
                    "Cardiac output (CO) is the total volume of blood ejected by the ventricle per unit time.",
                    "Formula: CO = Stroke Volume (SV) × Heart Rate (HR)",
                    "Normal values: SV ≈ 70 mL, HR ≈ 72 beats/min → CO ≈ 5000 mL/min (5 L/min) in a 70-kg man.",
                    "Cardiac index = CO / Body Surface Area (BSA) — normalises CO for body size.",
                ],
                "kp": "CO = SV × HR. Normal CO ≈ 5 L/min. Both SV and HR independently regulate CO."
            },
            {
                "q": "Define Stroke Volume, Ejection Fraction, End-Diastolic Volume, and End-Systolic Volume.",
                "a": [
                    "Stroke Volume (SV): Volume ejected per beat = EDV − ESV. Normal ≈ 70 mL.",
                    "End-Diastolic Volume (EDV): Volume in ventricle before ejection ≈ 135 mL.",
                    "End-Systolic Volume (ESV): Volume remaining after ejection ≈ 65 mL.",
                    "Ejection Fraction (EF) = SV / EDV. Normal EF ≈ 55–65%.",
                    "EF is an indicator of contractility — ↑EF = ↑contractility; ↓EF in heart failure.",
                ],
                "kp": "EF = SV/EDV × 100%. Normal ≥55%. EF <40% = systolic heart failure."
            },
            {
                "q": "State and explain the Frank-Starling Law of the heart.",
                "a": [
                    "The Frank-Starling Law states: The volume of blood ejected by the ventricle in systole depends on the volume present in the ventricle at the end of diastole (EDV).",
                    "Mechanism: ↑ venous return → ↑ EDV → ↑ stretching of cardiac muscle fibers → optimal overlap of actin-myosin filaments → ↑ force of contraction → ↑ SV.",
                    "This ensures cardiac output equals venous return in steady state.",
                    "Positive inotropic agents (e.g., digoxin, catecholamines) shift the Frank-Starling curve upward — greater SV for same EDV.",
                    "Negative inotropic agents (e.g., heart failure, acidosis) shift the curve downward.",
                ],
                "kp": "Starling's Law = the heart pumps whatever blood it receives. Intrinsic mechanism ensuring CO = venous return."
            },
            {
                "q": "Describe the Cardiac Cycle — all phases, valve events, and heart sounds.",
                "a": [
                    "The cardiac cycle has 7 phases:",
                    "A. Atrial Systole: P wave on ECG; atria contract; mitral valve open; S4 (if present) heard. Final ventricular filling.",
                    "B. Isovolumetric Ventricular Contraction: QRS complex; ventricles contract; all valves CLOSED; pressure rises but volume unchanged. S1 = mitral valve closure.",
                    "C. Rapid Ventricular Ejection: ST segment; aortic valve opens; pressure reaches maximum; ventricular volume falls rapidly.",
                    "D. Reduced Ventricular Ejection: T wave; slower ejection; ventricle reaches minimum volume.",
                    "E. Isovolumetric Ventricular Relaxation: aortic valve closes → S2; all valves closed; ventricular pressure drops but volume unchanged.",
                    "F. Rapid Ventricular Filling: mitral valve opens; ventricles fill passively. S3 (physiologic in children) may occur.",
                    "G. Reduced Ventricular Filling: slow passive filling before next atrial systole.",
                ],
                "kp": "S1 = mitral valve closure (start of systole). S2 = aortic valve closure (start of diastole). S3 = rapid filling. S4 = atrial contraction into stiff ventricle."
            },
            {
                "q": "What are the determinants of Stroke Volume? How does preload, afterload, and contractility affect it?",
                "a": [
                    "SV is determined by three factors:",
                    "1. PRELOAD: The ventricular volume at end-diastole (EDV). ↑ Preload → ↑ SV (Starling's law). Increased by ↑ venous return, fluid load.",
                    "2. AFTERLOAD: The resistance against which the ventricle ejects blood (= aortic pressure / systemic vascular resistance). ↑ Afterload → ↓ SV (more difficult to eject).",
                    "3. CONTRACTILITY (Inotropy): Intrinsic ability of myocardium to contract independent of preload/afterload. ↑ Contractility (catecholamines, digoxin) → ↑ SV. ↓ Contractility (heart failure, β-blockers) → ↓ SV.",
                ],
                "kp": "Preload ↑→ SV ↑; Afterload ↑ → SV ↓; Contractility ↑ → SV ↑"
            },
            {
                "q": "Describe the action potential of a ventricular myocyte — all phases.",
                "a": [
                    "Phase 0 (Upstroke): Rapid depolarization due to fast Na+ channel opening (INa). Membrane potential rises from −90 mV to +30 mV.",
                    "Phase 1 (Early repolarization): Fast Na+ channels inactivate; transient outward K+ current (Ito) causes slight repolarization.",
                    "Phase 2 (Plateau): Ca²+ enters via L-type Ca²+ channels (ICaL); balanced by K+ outflow. Unique to cardiac muscle — responsible for sustained contraction.",
                    "Phase 3 (Repolarization): L-type Ca²+ channels close; K+ outflow (IK) predominates → repolarization to resting potential.",
                    "Phase 4 (Resting potential): −90 mV maintained by IK1 (inward rectifier K+ current). Stable in ventricular muscle (no spontaneous depolarization).",
                ],
                "kp": "The PLATEAU (Phase 2) distinguishes cardiac from nerve AP. Ca²+ entry during plateau triggers Ca²+-induced Ca²+ release from SR → contraction."
            },
            {
                "q": "What is the ECG? Explain the waves, intervals, and what each represents.",
                "a": [
                    "The ECG records the electrical activity of the heart from the body surface.",
                    "P wave: Atrial depolarization (SA node → atria). Duration <0.12 s.",
                    "PR interval: Time from atrial depolarization to ventricular depolarization (through AV node). Normal 0.12–0.20 s.",
                    "QRS complex: Ventricular depolarization. Normal duration <0.12 s (120 ms).",
                    "ST segment: Period of ventricular depolarization plateau (no net electrical activity). Normally isoelectric.",
                    "T wave: Ventricular repolarization. Normally upright in most leads.",
                    "QT interval: Total ventricular electrical systole (depolarization + repolarization). Normal ≤0.44 s (corrected).",
                    "U wave: Repolarization of Purkinje fibers (or papillary muscles) — seen especially in hypokalemia.",
                ],
                "kp": "P = atrial depol. QRS = ventricular depol. T = ventricular repol. PR interval = AV conduction time."
            },
            {
                "q": "What is the baroreceptor reflex? Describe its mechanism and importance.",
                "a": [
                    "Baroreceptors are stretch-sensitive mechanoreceptors located in the carotid sinus (CN IX) and aortic arch (CN X).",
                    "When blood pressure ↑: Baroreceptors fire more → signals to NTS (nucleus tractus solitarius) in medulla → ↑ parasympathetic output + ↓ sympathetic output → ↓ HR, ↓ contractility, ↓ SVR → BP falls back to normal.",
                    "When blood pressure ↓: Baroreceptors fire less → ↓ parasympathetic + ↑ sympathetic output → ↑ HR, ↑ SV, ↑ SVR → BP rises.",
                    "This is a rapid (seconds) short-term blood pressure control mechanism.",
                    "Clinical: Baroreceptor reflex mediates orthostatic hypotension compensation; failure causes labile hypertension.",
                ],
                "kp": "Baroreceptors = short-term BP regulators. Carotid sinus (CN IX) + aortic arch (CN X) → medulla → ANS output."
            },
            {
                "q": "Describe the regulation of Heart Rate by the autonomic nervous system.",
                "a": [
                    "The SA node (pacemaker) sets the intrinsic HR at ~100 bpm. Vagal tone normally slows this to ~70 bpm.",
                    "SYMPATHETIC: NE acts on β1-adrenergic receptors → ↑ If (funny current) in SA node → faster depolarization → ↑ HR (positive chronotropy). Also ↑ AV conduction (positive dromotropy).",
                    "PARASYMPATHETIC (Vagus): ACh acts on M2 muscarinic receptors → opens K+ channels (IKACh) → hyperpolarization → slower spontaneous depolarization → ↓ HR (negative chronotropy).",
                    "Intrinsic HR ≈ 100 bpm (when denervated). Resting HR ≈ 70 bpm due to dominant vagal tone.",
                ],
                "kp": "Sympathetic → β1 → ↑HR. Parasympathetic → M2 → ↓HR. Dominant resting tone is PARASYMPATHETIC (vagal)."
            },
            {
                "q": "What is mean arterial pressure (MAP)? How is it calculated?",
                "a": [
                    "MAP is the average pressure in the arterial system during one cardiac cycle.",
                    "MAP = Diastolic BP + 1/3 (Pulse Pressure) where Pulse Pressure = Systolic BP − Diastolic BP.",
                    "Or: MAP ≈ DBP + (SBP − DBP)/3",
                    "Example: BP = 120/80 → MAP = 80 + 40/3 ≈ 93 mmHg",
                    "MAP = CO × Total Peripheral Resistance (TPR)",
                    "MAP is closer to DBP because diastole lasts longer than systole.",
                ],
                "kp": "MAP = DBP + 1/3 PP. Normal MAP = 70–100 mmHg. MAP = CO × TPR."
            },
        ]
    },
    {
        "title": "🫁  SECTION 2: RESPIRATORY SYSTEM",
        "color": HexColor("#00695c"),
        "qna": [
            {
                "q": "Define and list all lung volumes and capacities with normal values.",
                "a": [
                    "LUNG VOLUMES (4 primary — cannot be added together to make a capacity individually):",
                    "• Tidal Volume (TV/Vt): Volume of air in/out per normal breath ≈ 500 mL",
                    "• Inspiratory Reserve Volume (IRV): Extra air inspired above TV ≈ 3000 mL",
                    "• Expiratory Reserve Volume (ERV): Extra air expired below TV ≈ 1200 mL",
                    "• Residual Volume (RV): Air remaining after maximal expiration ≈ 1200 mL (NOT measurable by spirometry)",
                    "",
                    "LUNG CAPACITIES (combinations of volumes):",
                    "• Inspiratory Capacity (IC) = TV + IRV ≈ 3500 mL",
                    "• Functional Residual Capacity (FRC) = ERV + RV ≈ 2400 mL (equilibrium volume)",
                    "• Vital Capacity (VC) = IRV + TV + ERV ≈ 4700 mL",
                    "• Total Lung Capacity (TLC) = VC + RV ≈ 5900 mL",
                    "",
                    "FRC and TLC include RV — NOT measurable by spirometry. Measured by helium dilution or body plethysmography.",
                ],
                "kp": "RV cannot be measured by spirometry → FRC and TLC also cannot. FRC = resting/equilibrium volume of lungs."
            },
            {
                "q": "What is Dead Space? Distinguish anatomical, alveolar, and physiological dead space.",
                "a": [
                    "Dead Space is the volume of inspired air that does NOT participate in gas exchange.",
                    "ANATOMICAL dead space: Volume of conducting airways (trachea, bronchi, bronchioles) = ~150 mL. No gas exchange occurs here.",
                    "ALVEOLAR dead space: Ventilated alveoli that receive no blood flow (V/Q = ∞). Normally near zero in healthy lungs. ↑ in pulmonary embolism.",
                    "PHYSIOLOGICAL dead space = Anatomical dead space + Alveolar dead space.",
                    "Calculated by Bohr equation: Vd/Vt = (PaCO2 − PeCO2) / PaCO2",
                    "• PaCO2 = arterial CO2 tension; PeCO2 = mixed expired CO2 tension",
                    "In health: Physiological ≈ Anatomical dead space (~150 mL or ~30% of TV).",
                ],
                "kp": "Physiological dead space = anatomical + alveolar. In disease (e.g., PE), alveolar dead space ↑ → physiological dead space ↑."
            },
            {
                "q": "Explain Ventilation-Perfusion (V/Q) ratio. What happens when V/Q = 0, normal, and infinity?",
                "a": [
                    "V/Q ratio = Alveolar ventilation (V) / Pulmonary blood flow (Q). Normal average ≈ 0.8.",
                    "V/Q = INFINITY (Dead Space): Ventilation present but NO perfusion. E.g., pulmonary embolism. Alveolar gas = inspired air (PO2 ↑, PCO2 ≈ 0). No gas exchange.",
                    "V/Q = 0 (Shunt): Perfusion present but NO ventilation. E.g., pneumonia, atelectasis. Blood passes unventilated alveoli → deoxygenated blood reaches systemic circulation. Causes hypoxemia NOT corrected by supplemental O2.",
                    "V/Q = NORMAL (~0.8): Ideal matching. Blood becomes fully oxygenated.",
                    "Regional variation: Apex of lung has higher V/Q (better ventilated, less perfused). Base has lower V/Q (better perfused). This causes slight regional PO2 differences.",
                ],
                "kp": "Shunt (V/Q=0) → hypoxemia not corrected by O2. Dead space (V/Q=∞) → wasted ventilation. V/Q mismatch = most common cause of hypoxemia."
            },
            {
                "q": "Describe Oxygen transport in blood. What is the oxyhemoglobin dissociation curve?",
                "a": [
                    "O2 is carried in blood in two forms:",
                    "1. DISSOLVED O2: ~2% of total O2. Only dissolved O2 exerts partial pressure. Concentration = 0.003 mL O2/100mL/mmHg × PaO2.",
                    "2. BOUND TO HEMOGLOBIN: ~98% of total O2. Hemoglobin (Hb) has 4 subunits, each binding 1 O2 → 4 O2 per Hb molecule. Adult Hb = α2β2.",
                    "O2 content of blood (CaO2) = (Hb × 1.34 × SaO2) + (0.003 × PaO2)",
                    "Oxyhemoglobin dissociation curve: S-shaped (sigmoidal). Relates PO2 to % Hb saturation.",
                    "RIGHT shift (↓ O2 affinity → O2 unloading in tissues): ↑ Temperature, ↑ PCO2, ↑ H+ (↓ pH), ↑ 2,3-DPG",
                    "LEFT shift (↑ O2 affinity → O2 loading in lungs): ↓ Temperature, ↓ PCO2, ↓ H+, ↓ 2,3-DPG, fetal Hb (HbF), CO poisoning",
                    "P50 = PO2 at which Hb is 50% saturated. Normal P50 = 26–27 mmHg.",
                ],
                "kp": "Hb carries ~98% of O2. Right shift = O2 unloading (CADET: CO2, Acid, 2,3-DPG, Exercise, Temperature ↑). HbF has LEFT shift → better O2 from placenta."
            },
            {
                "q": "How is CO2 transported in blood? Explain the Haldane effect and Chloride shift.",
                "a": [
                    "CO2 is transported in three forms:",
                    "1. Dissolved CO2: ~7% (CO2 is 20× more soluble than O2 in blood).",
                    "2. Carbaminohemoglobin (CO2 bound to Hb): ~23%. CO2 binds to amino groups of globin chains.",
                    "3. As bicarbonate (HCO3−): ~70%. CO2 + H2O → H2CO3 (catalyzed by carbonic anhydrase in RBCs) → H+ + HCO3−. HCO3− exits RBC via Cl−/HCO3− exchanger (CHLORIDE SHIFT / Hamburger shift). H+ is buffered by Hb.",
                    "HALDANE EFFECT: Deoxygenated Hb (deoxyhemoglobin) has greater affinity for CO2 and H+ than oxyhemoglobin. This enhances CO2 carriage in venous blood and CO2 release in the lungs (when Hb is oxygenated).",
                ],
                "kp": "70% CO2 as HCO3−. Chloride shift: HCO3− leaves RBC in exchange for Cl−. Haldane effect: deoxyHb binds more CO2."
            },
            {
                "q": "Explain the control of breathing. What are central and peripheral chemoreceptors?",
                "a": [
                    "Respiratory rhythm is generated by the respiratory center in the medulla (pre-Bötzinger complex).",
                    "CENTRAL CHEMORECEPTORS: Located on the ventrolateral surface of the medulla. Respond to changes in CSF pH (which reflects arterial PCO2). CO2 crosses blood-brain barrier → CSF CO2 ↑ → ↑ [H+] → stimulates ventilation. Most important regulator of ventilation in normal conditions.",
                    "PERIPHERAL CHEMORECEPTORS: Carotid bodies (CN IX) and aortic bodies (CN X).",
                    "• Respond primarily to ↓ PaO2 (hypoxia) — stimulated when PaO2 < 60 mmHg.",
                    "• Also respond to ↑ PaCO2 and ↑ [H+].",
                    "• In COPD with chronic CO2 retention, the hypoxic drive (peripheral chemoreceptors) becomes the primary stimulus — reason why high-flow O2 in COPD must be used with caution.",
                ],
                "kp": "CO2/pH → central chemoreceptors (main driver). Hypoxia (PaO2 <60) → peripheral chemoreceptors (carotid bodies). COPD: hypoxic drive is primary stimulus."
            },
            {
                "q": "Distinguish between Obstructive and Restrictive lung disease using spirometry.",
                "a": [
                    "OBSTRUCTIVE: Airway narrowing → difficulty expelling air. FEV1 ↓, FVC normal or slightly ↓, FEV1/FVC ratio < 0.70 (hallmark). TLC ↑, RV ↑. Examples: COPD, Asthma, Bronchiectasis.",
                    "RESTRICTIVE: Reduced lung expansion → smaller lung volumes. FEV1 ↓, FVC ↓↓, FEV1/FVC ratio NORMAL or ↑ (>0.80). TLC ↓, RV ↓. Examples: Pulmonary fibrosis, pleural effusion, neuromuscular disease, obesity.",
                    "Key test: FEV1/FVC (Tiffeneau index).",
                    "• <70% = Obstructive.",
                    "• ≥80% (with ↓ FVC and ↓ TLC) = Restrictive.",
                ],
                "kp": "Obstructive: FEV1/FVC <70%, TLC ↑. Restrictive: FEV1/FVC normal/>80%, TLC ↓. FEV1/FVC is the key discriminator."
            },
        ]
    },
    {
        "title": "🧠  SECTION 3: NERVOUS SYSTEM",
        "color": HexColor("#4527a0"),
        "qna": [
            {
                "q": "What is the Resting Membrane Potential? What maintains it?",
                "a": [
                    "The resting membrane potential (RMP) is the electrical potential difference across the cell membrane at rest. Normal RMP ≈ −70 to −90 mV (inside negative).",
                    "It is established by DIFFUSION POTENTIALS — created because cell membranes have selective permeability to ions:",
                    "• High resting K+ permeability: K+ diffuses OUT down concentration gradient → negative potential inside.",
                    "• Low resting Na+ permeability: Na+ contribution is minimal.",
                    "• Cl− is near electrochemical equilibrium at rest.",
                    "RMP ≈ K+ equilibrium potential (≈ −94 mV) because K+ permeability dominates.",
                    "The Na+-K+ ATPase pump (3 Na+ out, 2 K+ in) has two roles:",
                    "  1. Small direct electrogenic contribution (−3 to −5 mV)",
                    "  2. Maintains K+ gradient (indirect, more important role)",
                ],
                "kp": "RMP ≈ −70 to −90 mV. Dominated by K+ permeability. Na+/K+ ATPase maintains the ionic gradients needed."
            },
            {
                "q": "Describe the Action Potential in a nerve fiber — all phases, ion movements, and pharmacology.",
                "a": [
                    "An action potential is an all-or-none, rapid depolarization followed by repolarization of excitable cells.",
                    "PHASES:",
                    "1. Resting state: −70 mV. Na+ channels closed (activation gate closed, inactivation gate open). K+ channels open.",
                    "2. Threshold: ~−60 mV. Must be reached for AP to occur (all-or-none).",
                    "3. Upstroke (Depolarization): Voltage-gated Na+ channels open rapidly → Na+ rushes in → membrane potential rises to ~+30 mV.",
                    "4. Repolarization: Na+ channel inactivation gates close (stop Na+ entry) + voltage-gated K+ channels open (K+ rushes out) → repolarization.",
                    "5. After-hyperpolarization (undershoot): K+ channels remain briefly open → membrane more negative than RMP.",
                    "6. Return to RMP: K+ channels close.",
                    "PHARMACOLOGY:",
                    "• Tetrodotoxin (TTX), Lidocaine (local anesthetics): Block voltage-gated Na+ channels → block AP.",
                    "• Tetraethylammonium (TEA): Blocks K+ channels → prolongs AP.",
                ],
                "kp": "Upstroke = Na+ IN (fast). Repolarization = K+ OUT + Na+ channel inactivation. TTX blocks Na+ channels."
            },
            {
                "q": "Compare the sympathetic and parasympathetic divisions of the autonomic nervous system.",
                "a": [
                    "SYMPATHETIC (Thoracolumbar — T1 to L2/L3):",
                    "• Short preganglionic (ACh, nicotinic), long postganglionic (NE, adrenergic receptors α and β)",
                    "• Paravertebral ganglia chain (close to spinal cord)",
                    "• Exception: Adrenal medulla — preganglionic directly innervates → releases Epinephrine",
                    "• Effect: 'Fight or flight' — ↑ HR, ↑ BP, bronchodilation, mydriasis, ↓ GI motility, glycogenolysis",
                    "",
                    "PARASYMPATHETIC (Craniosacral — CN III, VII, IX, X + S2-S4):",
                    "• Long preganglionic (ACh, nicotinic), short postganglionic (ACh, muscarinic receptors)",
                    "• Ganglia near or in target organs",
                    "• Effect: 'Rest and digest' — ↓ HR, ↑ GI motility, miosis, lacrimation, micturition",
                    "",
                    "NEUROTRANSMITTERS SUMMARY:",
                    "• All preganglionic: ACh (nicotinic)",
                    "• Sympathetic postganglionic: NE (except sweat glands → ACh)",
                    "• Parasympathetic postganglionic: ACh (muscarinic)",
                ],
                "kp": "PARASYMPATHETIC: ACh → muscarinic. SYMPATHETIC: NE → adrenergic. Exception: sweat glands get sympathetic ACh."
            },
            {
                "q": "What is a synapse? Describe synaptic transmission at a chemical synapse.",
                "a": [
                    "A synapse is a junction between two neurons (or neuron and effector) where information is transmitted.",
                    "Steps of chemical synaptic transmission:",
                    "1. Action potential arrives at presynaptic terminal.",
                    "2. Depolarization opens voltage-gated Ca²+ channels → Ca²+ enters presynaptic terminal.",
                    "3. Ca²+ triggers exocytosis of neurotransmitter-containing vesicles into synaptic cleft.",
                    "4. Neurotransmitter diffuses across cleft and binds to postsynaptic receptors.",
                    "5. Receptor activation opens ion channels → EPSP (excitatory) or IPSP (inhibitory).",
                    "6. Neurotransmitter is removed by: reuptake, enzymatic degradation (e.g., AChE breaks down ACh), or diffusion.",
                    "EPSP: Depolarization (Na+ influx). IPSP: Hyperpolarization (K+ efflux or Cl− influx).",
                    "Temporal summation: Multiple EPSPs in rapid succession. Spatial summation: EPSPs from multiple neurons at same time.",
                ],
                "kp": "Synaptic transmission: AP → Ca²+ entry → vesicle exocytosis → NT release → postsynaptic receptor → EPSP/IPSP."
            },
            {
                "q": "Describe the neuromuscular junction (NMJ) and how neuromuscular blocking drugs work.",
                "a": [
                    "The NMJ is the synapse between a motor neuron and skeletal muscle.",
                    "Normal transmission:",
                    "1. AP in motor neuron → Ca²+ entry → ACh release from vesicles",
                    "2. ACh binds nicotinic ACh receptors (NnACh receptors) on motor end plate",
                    "3. Na+ influx → end plate potential (EPP) → muscle AP → contraction",
                    "4. ACh degraded by acetylcholinesterase (AChE)",
                    "",
                    "PHARMACOLOGY at NMJ:",
                    "• Non-depolarizing blockers (Tubocurarine, Vecuronium, Atracurium): Competitive antagonists at nicotinic receptor → block ACh binding → paralysis. Reversed by neostigmine (AChE inhibitor).",
                    "• Depolarizing blockers (Succinylcholine): Acts like ACh but is not broken down quickly → persistent depolarization → initial fasciculations → flaccid paralysis. NOT reversed by neostigmine.",
                    "• Myasthenia Gravis: Autoantibodies destroy nicotinic ACh receptors → muscle weakness. Treated with AChE inhibitors.",
                ],
                "kp": "NMJ: ACh → nicotinic receptor → EPP → muscle AP. Non-depolarizing blockers reversed by neostigmine. Succinylcholine = depolarizing — NOT reversible."
            },
            {
                "q": "What are the functions of the cerebellum and basal ganglia?",
                "a": [
                    "CEREBELLUM — coordination, not initiation of movement:",
                    "• Coordinates smooth, precise voluntary movement",
                    "• Maintains posture and balance (vestibulocerebellum)",
                    "• Motor learning / skill acquisition (cerebrocerebellum)",
                    "• Controls eye movements (flocculonodular lobe)",
                    "• Cerebellar damage → ipsilateral deficits: ataxia, intention tremor, dysmetria, dysdiadochokinesis, nystagmus, hypotonia",
                    "",
                    "BASAL GANGLIA — filter and modulate cortical motor output:",
                    "• Components: Striatum (caudate + putamen), globus pallidus, substantia nigra, subthalamic nucleus",
                    "• Direct pathway: facilitates desired movements (↑ motor cortex activity)",
                    "• Indirect pathway: suppresses unwanted movements (↓ motor cortex activity)",
                    "• Hypokinetic disorder: Parkinson's disease — dopamine deficiency from substantia nigra → rigidity, bradykinesia, resting tremor, postural instability",
                    "• Hyperkinetic disorder: Huntington's disease — striatal degeneration → chorea (involuntary, dance-like movements)",
                ],
                "kp": "Cerebellum: coordination (ipsilateral). Basal ganglia: movement filtering. Parkinson's = ↓ dopamine → hypokinesia. Huntington's = striatum → hyperkinesia."
            },
        ]
    },
    {
        "title": "👁  SECTION 4: SPECIAL SENSES",
        "color": HexColor("#c62828"),
        "qna": [
            {
                "q": "Describe the structures of the eye and the properties of rods vs cones.",
                "a": [
                    "The eye wall has 3 layers: Outer (fibrous) = cornea + sclera; Middle (vascular) = iris + choroid; Inner (neural) = retina.",
                    "Important structures:",
                    "• Macula: Area of highest visual acuity on the retina",
                    "• Fovea: Central depression in macula; packed with cones; highest acuity",
                    "• Optic disc (blind spot): Head of optic nerve; no photoreceptors",
                    "• Aqueous humor: Fills anterior chamber (between cornea and lens)",
                    "• Vitreous humor: Fills posterior chamber (between lens and retina)",
                    "",
                    "RODS vs CONES:",
                    "• RODS: Low threshold; sensitive to dim light; night vision; low acuity; no color vision; not at fovea; dark-adapt SLOWLY",
                    "• CONES: High threshold; daylight vision; high acuity; color vision (3 types: red, green, blue); concentrated at fovea; dark-adapt RAPIDLY",
                ],
                "kp": "Fovea = cones only = highest acuity. Rods = night vision. Optic disc = blind spot. Cones adapt fast to dark; rods adapt slowly but more sensitive."
            },
            {
                "q": "Explain phototransduction — how light is converted to a neural signal in the retina.",
                "a": [
                    "Phototransduction in RODS (using rhodopsin):",
                    "1. Dark: Rod is DEPOLARIZED (−40 mV). cGMP keeps Na+/Ca²+ channels open (dark current). Rod releases glutamate continuously.",
                    "2. Light hits rhodopsin (retinal + opsin): Retinal changes from 11-cis to all-trans → activates rhodopsin",
                    "3. Activated rhodopsin activates Transducin (G protein) → activates Phosphodiesterase (PDE)",
                    "4. PDE breaks down cGMP → cGMP falls → Na+ channels CLOSE → rod HYPERPOLARIZES",
                    "5. Hyperpolarized rod ↓ glutamate release → signals downstream retinal cells",
                    "Dark adaptation: Regeneration of 11-cis retinal (slow, ~20 min). Vitamin A deficiency → night blindness (cannot regenerate 11-cis retinal).",
                ],
                "kp": "Light → rhodopsin → transducin → PDE → ↓ cGMP → Na+ channels close → HYPERPOLARIZATION. Dark adaptation requires Vitamin A."
            },
            {
                "q": "Describe the pathway of the visual system from the retina to cortex. What are visual field defects?",
                "a": [
                    "Visual pathway: Retina → Optic nerve (CN II) → Optic chiasm → Optic tract → Lateral Geniculate Nucleus (LGN) → Optic radiation → Primary visual cortex (V1, occipital lobe, Area 17)",
                    "",
                    "AT THE OPTIC CHIASM: Nasal fibers (from nasal retina = temporal visual field) CROSS to opposite side. Temporal fibers (from temporal retina = nasal visual field) remain ipsilateral.",
                    "",
                    "VISUAL FIELD DEFECTS:",
                    "• Optic nerve lesion (before chiasm): Monocular blindness (one eye loses vision entirely)",
                    "• Optic chiasm lesion (e.g., pituitary tumor): BITEMPORAL HEMIANOPIA — loss of both temporal visual fields (tunnel vision)",
                    "• Optic tract / LGN / optic radiation / cortex lesion (after chiasm): HOMONYMOUS HEMIANOPIA — loss of same visual field in both eyes (e.g., right optic tract → left homonymous hemianopia)",
                    "• Macular sparing: Cortical lesions often spare the macula (foveal representation = large cortical area with dual blood supply)",
                ],
                "kp": "Chiasm: nasal fibers cross. Pituitary tumor → bitemporal hemianopia. Post-chiasmal lesion → homonymous hemianopia."
            },
            {
                "q": "Describe the structures of the ear and the mechanism of hearing.",
                "a": [
                    "EAR STRUCTURES:",
                    "• Outer ear: Pinna + external auditory canal → collects sound",
                    "• Tympanic membrane: Vibrates with sound waves",
                    "• Middle ear: Ossicles (malleus → incus → stapes) amplify sound ~20×; stapes footplate vibrates oval window",
                    "• Inner ear: Cochlea (hearing) + Vestibular apparatus (balance)",
                    "",
                    "COCHLEA: Fluid-filled coiled structure. Contains three scalae:",
                    "• Scala vestibuli (perilymph, above)",
                    "• Scala media / Cochlear duct (endolymph — high K+, unique)",
                    "• Scala tympani (perilymph, below)",
                    "• Organ of Corti sits on basilar membrane (in scala media); contains inner and outer hair cells",
                    "",
                    "MECHANISM OF HEARING:",
                    "1. Sound → vibrates tympanic membrane → ossicles → oval window",
                    "2. Oval window vibration → fluid waves in perilymph",
                    "3. Basilar membrane vibrates — high frequency sounds vibrate BASE; low frequency sounds vibrate APEX (Tonotopy)",
                    "4. Hair cell stereocilia deflect → K+ channels open (K+ enters from endolymph) → depolarization → NT release → spiral ganglion → CN VIII (cochlear branch)",
                ],
                "kp": "Tonotopy: Base = high freq; Apex = low freq. Endolymph is HIGH K+. Hair cell depolarization = K+ influx from endolymph."
            },
            {
                "q": "Describe the vestibular system and the sense of balance. What is nystagmus?",
                "a": [
                    "The vestibular apparatus (inner ear) detects head position and movement:",
                    "• Semicircular canals (3): Detect angular/rotational acceleration. Each canal is in a different plane (horizontal, anterior, posterior).",
                    "• Utricle: Detects horizontal linear acceleration (forward-backward) and static head tilt",
                    "• Saccule: Detects vertical linear acceleration (up-down) and gravity",
                    "• Contains hair cells with stereocilia embedded in otolith membrane (crystals of calcium carbonate — otoliths/otoconia)",
                    "",
                    "Vestibular pathway: CN VIII → vestibular nuclei (medulla) → cerebellum, spinal cord, and eye muscles (via MLF)",
                    "",
                    "NYSTAGMUS: Involuntary rhythmic eye movement. Has a SLOW phase (vestibular) and a FAST phase (corrective — cortex). Direction of nystagmus is defined by FAST phase.",
                    "Caloric testing: Cold water in ear → nystagmus AWAY from that ear. Warm water → nystagmus TOWARD that ear. (Mnemonic: COWS = Cold Opposite, Warm Same)",
                ],
                "kp": "Semicircular canals = angular acceleration. Utricle/saccule = linear acceleration + gravity. COWS = Cold Opposite, Warm Same (nystagmus direction)."
            },
            {
                "q": "Describe the sense of smell (olfaction) and taste (gustation).",
                "a": [
                    "OLFACTION (Smell):",
                    "• Olfactory receptor neurons are in the olfactory epithelium (roof of nasal cavity)",
                    "• Unique: neurons are directly exposed to the environment AND regenerate throughout life",
                    "• Odorant binds receptor → G protein (Golf) → ↑ cAMP → opens Na+/Ca²+ channels → depolarization",
                    "• Axons of olfactory neurons = CN I (olfactory nerve) → pierce cribriform plate → olfactory bulb → olfactory cortex (piriform cortex, amygdala)",
                    "• Only sense that does NOT pass through thalamus before reaching cortex",
                    "• Anosmia: Loss of smell (e.g., cribriform plate fracture, COVID-19, Parkinson's, Alzheimer's)",
                    "",
                    "GUSTATION (Taste):",
                    "• Five primary tastes: Sweet, Salty, Sour, Bitter, Umami",
                    "• Taste buds on tongue (fungiform, circumvallate, foliate papillae) and palate/epiglottis",
                    "• Bitter and sweet via G protein → 2nd messengers. Salty and sour via direct ion channels.",
                    "• CN VII (anterior 2/3 tongue via chorda tympani), CN IX (posterior 1/3), CN X (epiglottis) → NTS (medulla) → thalamus → gustatory cortex (insula)",
                ],
                "kp": "Olfaction is the ONLY sense bypassing the thalamus. CN I → olfactory bulb → piriform cortex. Taste: CN VII (anterior 2/3), CN IX (posterior 1/3)."
            },
        ]
    }
]


# ══════════════════════════════════════════════════════════════════════════════
# BUILD DOCUMENT
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# ── COVER PAGE ────────────────────────────────────────────────────────────────
cover_bg = Table(
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     [Paragraph("Model Exam Preparation — July 2026", cover_sub)],
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     [Paragraph("Cardiovascular System  •  Respiratory System", cover_sub)],
     [Paragraph("Nervous System  •  Special Senses", cover_sub)],
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story.append(Spacer(1, 2*cm))
story.append(cover_bg)
story.append(PageBreak())

# ── QUICK REFERENCE TABLE ─────────────────────────────────────────────────────
story.append(section_header("⚡  QUICK REFERENCE — NORMAL VALUES", HexColor("#4e342e")))
story.append(Spacer(1, 6))

ref_data = [
    ["Parameter", "Normal Value"],
    ["Cardiac Output", "5 L/min (5000 mL/min)"],
    ["Heart Rate", "60–100 bpm"],
    ["Stroke Volume", "~70 mL"],
    ["Ejection Fraction", "≥55%"],
    ["Blood Pressure", "120/80 mmHg"],
    ["MAP", "70–100 mmHg"],
    ["Tidal Volume", "~500 mL"],
    ["Total Lung Capacity", "~5900 mL"],
    ["Vital Capacity", "~4700 mL"],
    ["FRC", "~2400 mL"],
    ["Residual Volume", "~1200 mL"],
    ["FEV1/FVC (normal)", "≥70%"],
    ["PaO2", "80–100 mmHg"],
    ["PaCO2", "35–45 mmHg"],
    ["pH (arterial)", "7.35–7.45"],
    ["P50 of Hb", "26–27 mmHg"],
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story.append(ref_tbl)
story.append(PageBreak())

# ── SECTIONS ─────────────────────────────────────────────────────────────────
q_count = 1
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# ── BUILD ──────────────────────────────────────────────────────────────────────
doc.build(story)
print(f"PDF created: {OUTPUT}")