ls -la /tmp/workspace/ 2>/dev/null || mkdir -p /tmp/workspace && echo "created"

mkdir -p /tmp/workspace/physiology-viva && cat > /tmp/workspace/physiology-viva/build_pptx.py << 'PYEOF' from pptx import Presentation from pptx.util import Inches, Pt, Emu from pptx.dml.color import RGBColor from pptx.enum.text import PP_ALIGN, MSO_ANCHOR from pptx.util import Inches, Pt from io import BytesIO # ── Color Palette ────────────────────────────────────────────── DARK_BLUE = RGBColor(0x0D, 0x2B, 0x55) # deep navy MED_BLUE = RGBColor(0x1A, 0x5F, 0x9C) # section header ACCENT_GOLD = RGBColor(0xF0, 0xA5, 0x00) # accent / Q label WHITE = RGBColor(0xFF, 0xFF, 0xFF) LIGHT_GRAY = RGBColor(0xF2, 0xF4, 0xF7) DARK_TEXT = RGBColor(0x1C, 0x1C, 0x1C) ANSWER_GREEN = RGBColor(0x0A, 0x7A, 0x3E) # answer text prs = Presentation() prs.slide_width = Inches(13.333) prs.slide_height = Inches(7.5) blank = prs.slide_layouts[6] # ── Helpers ──────────────────────────────────────────────────── def add_rect(slide, x, y, w, h, fill_color, alpha=None): shape = slide.shapes.add_shape(1, Inches(x), Inches(y), Inches(w), Inches(h)) shape.fill.solid() shape.fill.fore_color.rgb = fill_color shape.line.fill.background() return shape def add_text(slide, text, x, y, w, h, font_size=18, bold=False, color=DARK_TEXT, align=PP_ALIGN.LEFT, wrap=True, italic=False, font_name="Calibri"): tb = slide.shapes.add_textbox(Inches(x), Inches(y), Inches(w), Inches(h)) tf = tb.text_frame tf.word_wrap = wrap tf.margin_left = Pt(4) tf.margin_right = Pt(4) tf.margin_top = Pt(2) tf.margin_bottom= Pt(2) p = tf.paragraphs[0] p.alignment = align run = p.add_run() run.text = text run.font.name = font_name run.font.size = Pt(font_size) run.font.bold = bold run.font.italic= italic run.font.color.rgb = color return tb def add_multiline(slide, lines, x, y, w, h, font_size=15, color=DARK_TEXT, font_name="Calibri", bullet=True, line_spacing=1.2): """lines = list of (text, bold, color_override)""" from pptx.oxml.ns import qn from lxml import etree tb = slide.shapes.add_textbox(Inches(x), Inches(y), Inches(w), Inches(h)) tf = tb.text_frame tf.word_wrap = True tf.margin_left = Pt(4) tf.margin_right = Pt(4) tf.margin_top = Pt(2) tf.margin_bottom = Pt(2) for i, (txt, bold, col) in enumerate(lines): p = tf.paragraphs[0] if i == 0 else tf.add_paragraph() p.alignment = PP_ALIGN.LEFT run = p.add_run() run.text = txt run.font.name = font_name run.font.size = Pt(font_size) run.font.bold = bold run.font.color.rgb = col if col else color return tb # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ # SLIDE BUILDERS # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ def make_title_slide(prs): slide = prs.slides.add_slide(blank) # Full background add_rect(slide, 0, 0, 13.333, 7.5, DARK_BLUE) # Gold accent bar add_rect(slide, 0, 3.0, 13.333, 0.07, ACCENT_GOLD) # decorative side strip add_rect(slide, 0, 0, 0.3, 7.5, MED_BLUE) # Title add_text(slide, "Physiology Viva Questions", 0.6, 1.5, 12.0, 1.4, font_size=44, bold=True, color=WHITE, align=PP_ALIGN.CENTER) # Subtitle add_text(slide, "Frequently Asked Questions for 1st Year MBBS", 0.6, 3.2, 12.0, 0.8, font_size=22, bold=False, color=ACCENT_GOLD, align=PP_ALIGN.CENTER, italic=True) # Topics line topics = "General Physiology • Hematology • Biophysics • Endocrine System\nThyroid • Parathyroid • Anterior Pituitary" add_text(slide, topics, 0.6, 4.3, 12.0, 1.2, font_size=16, bold=False, color=LIGHT_GRAY, align=PP_ALIGN.CENTER) # Footer add_text(slide, "1st Year MBBS | Physiology Department", 0.6, 6.7, 12.0, 0.5, font_size=13, color=RGBColor(0xAA, 0xBB, 0xCC), align=PP_ALIGN.CENTER) def make_section_divider(prs, section_num, title, subtitle=""): slide = prs.slides.add_slide(blank) add_rect(slide, 0, 0, 13.333, 7.5, MED_BLUE) add_rect(slide, 0, 0, 0.5, 7.5, ACCENT_GOLD) add_rect(slide, 0, 6.8, 13.333, 0.7, DARK_BLUE) # Section number circle add_rect(slide, 1.2, 2.5, 1.2, 1.2, ACCENT_GOLD) add_text(slide, str(section_num), 1.2, 2.5, 1.2, 1.2, font_size=36, bold=True, color=DARK_BLUE, align=PP_ALIGN.CENTER) add_text(slide, title, 2.7, 2.5, 10.0, 1.1, font_size=38, bold=True, color=WHITE, align=PP_ALIGN.LEFT) if subtitle: add_text(slide, subtitle, 2.7, 3.7, 10.0, 0.7, font_size=18, bold=False, color=LIGHT_GRAY, align=PP_ALIGN.LEFT, italic=True) def make_qa_slide(prs, section_tag, slide_title, qa_pairs, tip=None): """qa_pairs = list of (question_str, answer_str)""" slide = prs.slides.add_slide(blank) # Top header bar add_rect(slide, 0, 0, 13.333, 0.75, DARK_BLUE) # Gold left strip add_rect(slide, 0, 0, 0.18, 7.5, ACCENT_GOLD) # Section tag add_text(slide, section_tag, 0.35, 0.1, 3.0, 0.55, font_size=12, bold=True, color=ACCENT_GOLD, align=PP_ALIGN.LEFT) # Slide title add_text(slide, slide_title, 0.35, 0.1, 12.5, 0.55, font_size=18, bold=True, color=WHITE, align=PP_ALIGN.CENTER) # Light background body add_rect(slide, 0.18, 0.75, 13.133, 6.75, LIGHT_GRAY) # Layout: up to 3 Q&A pairs per slide n = len(qa_pairs) box_h = 5.9 / n for i, (q, a) in enumerate(qa_pairs): y_start = 0.85 + i * box_h # Q box add_rect(slide, 0.3, y_start, 12.7, box_h * 0.42, DARK_BLUE) add_text(slide, "Q " + q, 0.45, y_start + 0.03, 12.4, box_h * 0.38, font_size=14, bold=True, color=ACCENT_GOLD, align=PP_ALIGN.LEFT, wrap=True) # A box add_rect(slide, 0.3, y_start + box_h * 0.44, 12.7, box_h * 0.50, WHITE) add_text(slide, "A " + a, 0.45, y_start + box_h * 0.46, 12.4, box_h * 0.46, font_size=13, bold=False, color=DARK_TEXT, align=PP_ALIGN.LEFT, wrap=True) # Optional tip banner at bottom if tip: add_rect(slide, 0.18, 6.9, 13.133, 0.5, DARK_BLUE) add_text(slide, "💡 Examiner Tip: " + tip, 0.35, 6.92, 12.8, 0.4, font_size=12, bold=False, color=ACCENT_GOLD, align=PP_ALIGN.LEFT) # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ # CONTENT DATA # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ slides_data = [ # ── SECTION 1: GENERAL PHYSIOLOGY ────────────────────────── ("GENERAL PHYSIOLOGY", "1", "General Physiology", "Cell physiology, homeostasis, membrane transport"), ("GENERAL PHYSIOLOGY", None, "Cell Membrane & Transport", [ ("What is the fluid mosaic model?", "The cell membrane is a phospholipid bilayer with embedded proteins that can move laterally — proposed by Singer & Nicolson (1972). Phospholipid head is hydrophilic; tail is hydrophobic."), ("What is the resting membrane potential of a neuron?", "-70 mV (inside negative). Maintained by Na⁺/K⁺-ATPase pump (3Na⁺ out, 2K⁺ in) and differential permeability — K⁺ leakage channels dominate at rest."), ("Difference between diffusion and osmosis?", "Diffusion: movement of solute from high to low concentration. Osmosis: movement of WATER across a semipermeable membrane from low solute to high solute concentration."), ], "Always state the value (e.g., -70 mV), the ion responsible, and the pump maintaining it."), ("GENERAL PHYSIOLOGY", None, "Membrane Transport Types", [ ("What is active transport? Give an example.", "Movement of substances against their concentration gradient using energy (ATP). Example: Na⁺/K⁺-ATPase pump moves Na⁺ out and K⁺ in against gradients."), ("What is facilitated diffusion?", "Passive transport of substances down concentration gradient via specific carrier proteins or channel proteins. No energy required. Example: glucose entry into RBCs via GLUT-1."), ("What is secondary active transport?", "Uses the electrochemical gradient of Na⁺ (created by Na⁺/K⁺ pump) to drive another molecule. If both move same direction — co-transport (symport). Opposite — counter-transport (antiport)."), ], "Examiners often ask you to classify a given transport mechanism — know the energy requirement and direction."), ("GENERAL PHYSIOLOGY", None, "Homeostasis & Cell Communication", [ ("Define homeostasis. Give an example.", "Maintenance of a stable internal environment despite external changes. Example: blood glucose maintained at 70–110 mg/dL by insulin/glucagon feedback loops."), ("What is a negative feedback loop?", "The response opposes the original stimulus, restoring equilibrium. Example: High body temp → sweating → temp falls back to normal. Most homeostatic mechanisms use negative feedback."), ("What are gap junctions?", "Protein channels (connexins) that directly connect cytoplasm of adjacent cells, allowing ions and small molecules to pass. Important in cardiac muscle (electrical coupling) and smooth muscle."), ], "Positive feedback amplifies the stimulus (e.g., childbirth, blood clotting) — contrast with negative feedback."), # ── SECTION 2: HEMATOLOGY ────────────────────────────────── ("HEMATOLOGY", "2", "Hematology", "Blood cells, hemoglobin, coagulation, blood groups"), ("HEMATOLOGY", None, "Red Blood Cells & Hemoglobin", [ ("What are normal RBC values?", "Male: 4.5–5.5 million/µL | Female: 3.8–4.8 million/µL. RBC lifespan: 120 days. Destroyed in spleen. Produced in red bone marrow (erythropoiesis)."), ("Describe the structure of hemoglobin.", "Hb is a tetramer: 2α + 2β globin chains (HbA). Each chain has 1 heme group (porphyrin ring + Fe²⁺). Fe²⁺ binds O₂ reversibly. Molecular weight: 68,000 Da. Normal Hb: Male 14–17 g/dL; Female 12–15 g/dL."), ("What is the Bohr effect?", "↑CO₂ or ↓pH shifts O₂-Hb dissociation curve to the RIGHT, decreasing Hb's affinity for O₂ — facilitating O₂ release to tissues. Opposite shifts curve left (↑O₂ affinity)."), ], "Always know the curve shift directions and what causes them (CADET: CO₂, Acid, 2,3-DPG, Exercise, Temp)."), ("HEMATOLOGY", None, "WBCs & Platelets", [ ("What is the normal WBC count and differential?", "Total WBC: 4,000–11,000/µL. Differential: Neutrophils 60–70%, Lymphocytes 20–30%, Monocytes 2–8%, Eosinophils 1–4%, Basophils 0–1%. Mnemonic: Never Let Monkeys Eat Bananas."), ("What is the function of platelets?", "Platelets (thrombocytes) have a lifespan of 8–10 days; normal count 1.5–4 lakh/µL. Function: Primary hemostasis — platelet plug formation via adhesion (vWF), activation (ADP/TXA₂), and aggregation (GPIIb/IIIa + fibrinogen)."), ("What is erythropoietin (EPO) and where is it produced?", "EPO is a glycoprotein hormone produced mainly by peritubular cells of the kidney (90%) in response to hypoxia. It stimulates RBC production (erythropoiesis) in bone marrow."), ], "For platelets always mention: count, lifespan, and the 3 phases of primary hemostasis."), ("HEMATOLOGY", None, "Coagulation & Blood Groups", [ ("What are the intrinsic and extrinsic pathways of coagulation?", "Intrinsic (contact): XII→XI→IX→X. Extrinsic (tissue factor): VII+TF→X. Both converge at Factor X → common pathway → prothrombin→thrombin→fibrinogen→fibrin clot. PT tests extrinsic; aPTT tests intrinsic."), ("What are the ABO blood groups?", "Type A: antigen A on RBC, anti-B antibody. Type B: antigen B, anti-A. Type AB: both antigens, no antibodies (universal recipient). Type O: no antigens, both antibodies (universal donor). Determined by gene on chromosome 9."), ("What is the Rh factor? Why is it clinically important?", "Rh factor (D antigen) — present in Rh+ (85%), absent in Rh-. If Rh- mother carries Rh+ fetus, sensitization occurs in 1st pregnancy; 2nd pregnancy → maternal anti-D IgG crosses placenta → hemolytic disease of newborn (HDN)."), ], "Coagulation cascade is very frequently asked — draw it if given the chance."), # ── SECTION 3: BIOPHYSICS ────────────────────────────────── ("BIOPHYSICS", "3", "Biophysics", "Physical principles applied to biological systems"), ("BIOPHYSICS", None, "Membrane Potentials & Bioelectricity", [ ("What is an action potential? Describe its phases.", "Rapid change in membrane potential: ① Resting: -70 mV ② Depolarization: Na⁺ channels open, rises to +30 mV ③ Repolarization: Na⁺ inactivates, K⁺ channels open ④ Hyperpolarization (after-potential): K⁺ channels close slowly ⑤ Return to -70 mV."), ("What is the all-or-none law?", "Once a threshold stimulus is reached (~-55 mV), an action potential fires at full magnitude regardless of stimulus strength. Subthreshold stimuli produce no AP. Amplitude does NOT increase with stronger stimuli."), ("What are refractory periods?", "Absolute refractory period (ARP): no stimulus can fire another AP (Na⁺ channels inactivated). Relative refractory period (RRP): stronger-than-normal stimulus can fire AP (some Na⁺ channels recovering, K⁺ channels still open)."), ], "Draw the action potential curve — it takes 30 seconds and impresses examiners greatly."), ("BIOPHYSICS", None, "Surface Tension & Osmosis", [ ("What is surface tension in the context of alveoli?", "Surface tension = force at air-liquid interface tending to collapse alveoli. Surfactant (DPPC, produced by Type II pneumocytes) reduces surface tension, preventing alveolar collapse. By Laplace law: P = 2T/r (smaller alveoli need more pressure)."), ("Define osmolarity and osmolality.", "Osmolarity: number of osmoles of solute per LITRE of solution (mOsm/L). Osmolality: osmoles per KG of solvent (mOsm/kg). Normal plasma osmolality: 285–295 mOsm/kg. Osmolality is more clinically used (measured by freezing point depression)."), ("What is the Donnan equilibrium?", "When a membrane is impermeable to one ion (e.g., large proteins), the diffusible ions distribute unequally to maintain electrical neutrality. Result: protein-containing compartment has slightly higher total osmolarity — contributes to oncotic pressure."), ], "Laplace's Law (P = 2T/r) is frequently asked in context of both alveoli and blood vessels."), # ── SECTION 4: ENDOCRINE - INTRODUCTION ──────────────────── ("ENDOCRINE SYSTEM", "4", "Endocrine System — Introduction", "Hormones, receptors, feedback mechanisms"), ("ENDOCRINE SYSTEM", None, "Hormone Classification & Mechanisms", [ ("How are hormones classified based on chemistry?", "① Peptide/Protein hormones: insulin, GH, PTH — water-soluble, act on surface receptors, use cAMP/IP₃ as second messengers. ② Steroid hormones: cortisol, sex hormones — lipid-soluble, cross membrane, act on nuclear receptors. ③ Amine hormones: adrenaline (surface receptor), thyroid hormones (nuclear receptor)."), ("What is a second messenger? Give examples.", "An intracellular signaling molecule that carries signal from receptor to effector. Examples: cAMP (adenylyl cyclase pathway — glucagon, adrenaline), IP₃/DAG (phospholipase C — angiotensin II, GnRH), Ca²⁺, cGMP (ANP, NO)."), ("What is a negative feedback in the endocrine system?", "High levels of an end-hormone suppress the upstream axis. Example: High cortisol → inhibits CRH (hypothalamus) and ACTH (pituitary) → reduces cortisol production. This prevents hormonal excess and is the basis of steroid therapy tapering."), ], "Always mention the receptor type (surface vs. nuclear) and second messenger when discussing peptide vs. steroid hormones."), # ── SECTION 5: THYROID GLAND ─────────────────────────────── ("THYROID GLAND", "5", "Thyroid Gland", "Synthesis, secretion, and actions of thyroid hormones"), ("THYROID GLAND", None, "Thyroid Hormone Synthesis", [ ("Describe the steps of thyroid hormone synthesis.", "① Iodide trapping (NIS symporter) ② Oxidation of I⁻ to I₀ by thyroid peroxidase (TPO) ③ Organification: iodination of tyrosine residues on thyroglobulin → MIT, DIT ④ Coupling: MIT+DIT→T₃; DIT+DIT→T₄ ⑤ Stored as colloid ⑥ TSH stimulates endocytosis, proteolysis, release of T₃/T₄."), ("What is the ratio of T3 to T4 secreted and which is more active?", "T4:T3 secreted ratio = 20:1. T4 (thyroxine) is the prohormone — converted to active T3 (triiodothyronine) in peripheral tissues by 5'-deiodinase. T3 is 3–5× more potent than T4 and has shorter half-life (1 day vs 7 days for T4)."), ("What is the role of TSH?", "TSH (thyrotropin) from anterior pituitary: stimulates all steps of thyroid hormone synthesis and secretion, promotes thyroid cell growth and vascularity. Acts via cAMP second messenger. Controlled by TRH (hypothalamus) and negative feedback by T₃/T₄."), ], "The synthesis steps (trapping → oxidation → organification → coupling → storage → release) are very commonly asked."), ("THYROID GLAND", None, "Actions & Clinical Relevance", [ ("What are the physiological effects of thyroid hormones?", "① Calorigenic: ↑BMR, ↑O₂ consumption ② Growth: essential for brain development, bone maturation ③ Cardiovascular: ↑HR, ↑CO, ↑Na⁺/K⁺ ATPase ④ Metabolic: ↑glucose absorption, ↑lipolysis, ↑protein synthesis (physiological) ⑤ Permissive for action of catecholamines."), ("What is the difference between primary and secondary hypothyroidism?", "Primary: thyroid gland failure → ↓T₃/T₄, ↑TSH (loss of negative feedback). Example: Hashimoto's thyroiditis, iodine deficiency. Secondary: pituitary failure → ↓TSH → ↓T₃/T₄. Distinguishing factor: TSH level (high in primary, low in secondary)."), ("What is cretinism vs. myxedema?", "Cretinism: hypothyroidism in infancy/childhood — mental retardation, dwarfism, coarse features, protruding tongue. Myxedema: hypothyroidism in adults — non-pitting edema (glycosaminoglycan accumulation), bradycardia, cold intolerance, constipation."), ], "TSH is the best single test for thyroid function — always mention this in clinical questions."), # ── SECTION 6: PARATHYROID GLAND ─────────────────────────── ("PARATHYROID GLAND", "6", "Parathyroid Gland", "PTH, calcium regulation, Vitamin D"), ("PARATHYROID GLAND", None, "PTH — Synthesis & Actions", [ ("What stimulates PTH secretion?", "LOW serum Ca²⁺ is the primary stimulus (sensed by calcium-sensing receptor, CaSR). Also stimulated by ↑phosphate and ↓Mg²⁺. HIGH Ca²⁺, calcitriol (1,25-VitD), and high Mg²⁺ suppress PTH. PTH is an 84 amino acid peptide hormone."), ("What are the actions of PTH on bone, kidney, and gut?", "Bone: ↑osteoclast activity → Ca²⁺ and phosphate released (bone resorption). Kidney: ↑Ca²⁺ reabsorption (DCT), ↓phosphate reabsorption (proximal tubule → phosphaturia), ↑1α-hydroxylase (activates Vit D). Gut: indirect — via activated Vit D → ↑Ca²⁺ absorption."), ("What is the net effect of PTH on serum calcium and phosphate?", "PTH → ↑serum Ca²⁺ (hypercalcemia) and ↓serum phosphate (hypophosphatemia). This is key to distinguishing hyperparathyroidism (high Ca, low PO₄) from other hypercalcemic states."), ], "Mnemonic for PTH action on kidney: Ca REABSORBED, Phosphate EXCRETED (opposite directions)."), ("PARATHYROID GLAND", None, "Vitamin D & Calcium Disorders", [ ("Describe the activation pathway of Vitamin D.", "Skin: UV light converts 7-dehydrocholesterol → cholecalciferol (Vit D₃). Liver: 25-hydroxylase → 25-OH-D₃ (storage form). Kidney: 1α-hydroxylase (stimulated by PTH, hypocalcemia) → 1,25-(OH)₂-D₃ = calcitriol (active form). Acts on nuclear receptors."), ("What is hypoparathyroidism? What are its features?", "↓PTH → ↓serum Ca²⁺ (hypocalcemia) + ↑phosphate. Features: tetany, Chvostek's sign (facial muscle twitch on tapping facial nerve), Trousseau's sign (carpal spasm on BP cuff inflation), perioral tingling, seizures, prolonged QT on ECG."), ("What is pseudohypoparathyroidism?", "Normal or elevated PTH but target organs are RESISTANT to PTH (receptor defect — Gs protein mutation). Features of hypoparathyroidism (hypocalcemia, hyperphosphatemia) but PTH is HIGH. Short 4th metacarpal, round face (Albright's hereditary osteodystrophy)."), ], "Chvostek & Trousseau signs are EXAM FAVORITES — know how to elicit and what they indicate."), # ── SECTION 7: ANTERIOR PITUITARY ────────────────────────── ("ANTERIOR PITUITARY", "7", "Anterior Pituitary", "Hormones, regulation, clinical correlations"), ("ANTERIOR PITUITARY", None, "Hormones of Anterior Pituitary", [ ("Name the hormones secreted by the anterior pituitary.", "Mnemonic: FLAT PEG — FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH. Cell types: Somatotrophs (GH), Corticotrophs (ACTH), Thyrotrophs (TSH), Gonadotrophs (FSH/LH), Lactotrophs (Prolactin). Anterior pituitary is derived from Rathke's pouch (oral ectoderm)."), ("What controls anterior pituitary hormone secretion?", "Hypothalamus releases RELEASING hormones (CRH→ACTH, TRH→TSH, GHRH→GH, GnRH→FSH/LH) and INHIBITING hormones (somatostatin inhibits GH; dopamine inhibits prolactin) via hypothalamo-hypophyseal PORTAL system."), ("What is special about prolactin regulation?", "Prolactin is UNIQUE — under predominant INHIBITORY control by dopamine (PIH) from hypothalamus. All other anterior pituitary hormones are predominantly under stimulatory control. Dopamine antagonists (e.g., metoclopramide, antipsychotics) → ↑prolactin → galactorrhea."), ], "FLAT PEG mnemonic covers all 6 major anterior pituitary hormones — and remember prolactin is uniquely inhibited."), ("ANTERIOR PITUITARY", None, "Growth Hormone", [ ("What are the physiological actions of growth hormone?", "Direct effects: ↑lipolysis, ↑blood glucose (anti-insulin), ↑protein synthesis. Indirect effects (via IGF-1/somatomedin-C produced by liver): ↑bone growth (epiphyseal plates), ↑muscle mass, ↑organ growth. GH is a 191 amino acid single-chain polypeptide."), ("What stimulates and inhibits GH secretion?", "Stimulate: sleep (peak in slow-wave sleep), exercise, hypoglycemia, stress, GHRH, ghrelin, amino acids. Inhibit: somatostatin, IGF-1 (negative feedback), obesity, hyperglycemia, free fatty acids, glucocorticoids."), ("What is acromegaly vs. gigantism?", "Both due to GH excess. Gigantism: GH excess BEFORE epiphyseal fusion (childhood) → proportionate tall stature. Acromegaly: GH excess AFTER epiphyseal fusion (adult) → enlarged hands, feet, jaw (prognathism), coarse facial features, frontal bossing. Diagnosed by ↑IGF-1 + GH non-suppressible by glucose."), ], "IGF-1 is the best screening test for GH excess (acromegaly) — more stable than GH itself."), ("ANTERIOR PITUITARY", None, "ACTH, FSH, LH & TSH", [ ("What is the HPA axis?", "Hypothalamus → CRH → Anterior pituitary → ACTH → Adrenal cortex → Cortisol. Cortisol exerts NEGATIVE feedback on both hypothalamus (↓CRH) and pituitary (↓ACTH). ACTH also stimulates adrenal androgen (DHEA) production and promotes adrenal gland growth."), ("What are the functions of FSH and LH?", "In males: FSH → Sertoli cells (spermatogenesis, inhibin). LH → Leydig cells (testosterone). In females: FSH → follicle development, ↑estrogen. LH → ovulation trigger (LH surge), corpus luteum formation, progesterone production. Both controlled by pulsatile GnRH."), ("What is panhypopituitarism?", "Deficiency of ALL anterior pituitary hormones. Causes: Sheehan's syndrome (postpartum pituitary necrosis), tumors, radiation. Order of hormone loss: GH first → then FSH/LH → TSH → ACTH last. Presents with short stature, hypothyroidism, adrenal insufficiency, hypogonadism."), ], "In Sheehan's syndrome, failure to lactate and absent menstruation postpartum are the first clues."), ] # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ # BUILD THE PRESENTATION # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ make_title_slide(prs) for item in slides_data: if len(item) == 4 and isinstance(item[1], str) and item[1].isdigit(): # Section divider: (tag, num, title, subtitle) make_section_divider(prs, item[1], item[2], item[3]) elif len(item) == 4 and isinstance(item[2], str) and isinstance(item[3], list): # Q&A slide: (tag, None, title, qa_pairs) make_qa_slide(prs, item[0], item[2], item[3]) elif len(item) == 5: # Q&A slide with tip: (tag, None, title, qa_pairs, tip) make_qa_slide(prs, item[0], item[2], item[3], tip=item[4]) # Save out_path = "/tmp/workspace/physiology-viva/Physiology_Viva_Questions.pptx" prs.save(out_path) print(f"Saved: {out_path}") print(f"Slides: {len(prs.slides)}") PYEOF echo "Script written"

cd /tmp/workspace/physiology-viva && python build_pptx.py

which libreoffice 2>/dev/null || which soffice 2>/dev/null || echo "LibreOffice not found"

cat > /tmp/workspace/physiology-viva/build_pdf.py << 'PYEOF' from reportlab.lib.pagesizes import landscape, A4 from reportlab.lib import colors from reportlab.lib.units import inch, cm from reportlab.pdfgen import canvas from reportlab.lib.utils import simpleSplit import textwrap PAGE_W, PAGE_H = landscape(A4) # 841 x 595 pt # Colors (R,G,B 0-1) C_DARK_BLUE = colors.HexColor("#0D2B55") C_MED_BLUE = colors.HexColor("#1A5F9C") C_GOLD = colors.HexColor("#F0A500") C_WHITE = colors.white C_LIGHT_GRAY = colors.HexColor("#F2F4F7") C_DARK_TEXT = colors.HexColor("#1C1C1C") C_GREEN = colors.HexColor("#0A7A3E") def rect(c, x, y, w, h, fill_color, stroke=False): c.setFillColor(fill_color) if stroke: c.setStrokeColor(fill_color) else: c.setStrokeColor(fill_color) c.rect(x, y, w, h, stroke=0, fill=1) def draw_text(c, text, x, y, max_w, font="Helvetica", size=12, color=C_DARK_TEXT, align="left", line_height=None, max_lines=None): c.setFont(font, size) c.setFillColor(color) if line_height is None: line_height = size * 1.3 # Wrap text lines = [] for para in text.split('\n'): wrapped = simpleSplit(para, font, size, max_w) lines.extend(wrapped if wrapped else ['']) if max_lines: lines = lines[:max_lines] cur_y = y for line in lines: if align == "center": text_w = c.stringWidth(line, font, size) c.drawString(x + (max_w - text_w) / 2, cur_y, line) elif align == "right": text_w = c.stringWidth(line, font, size) c.drawString(x + max_w - text_w, cur_y, line) else: c.drawString(x, cur_y, line) cur_y -= line_height return cur_y # return y after last line def make_title_slide(c): # Full background rect(c, 0, 0, PAGE_W, PAGE_H, C_DARK_BLUE) # Gold divider line rect(c, 0, PAGE_H*0.42, PAGE_W, 3, C_GOLD) # Left strip rect(c, 0, 0, 18, PAGE_H, C_MED_BLUE) # Main title draw_text(c, "Physiology Viva Questions", 30, PAGE_H*0.72, PAGE_W-60, "Helvetica-Bold", 38, C_WHITE, "center") # Subtitle draw_text(c, "Frequently Asked Questions — 1st Year MBBS", 30, PAGE_H*0.58, PAGE_W-60, "Helvetica-Oblique", 20, C_GOLD, "center") # Topics topics = "General Physiology • Hematology • Biophysics • Endocrine System • Thyroid • Parathyroid • Anterior Pituitary" draw_text(c, topics, 30, PAGE_H*0.46, PAGE_W-60, "Helvetica", 13, colors.HexColor("#AABBCC"), "center") # Footer rect(c, 0, 0, PAGE_W, 28, colors.HexColor("#0A1F3D")) draw_text(c, "1st Year MBBS | Physiology Department", 30, 9, PAGE_W-60, "Helvetica", 11, colors.HexColor("#AABBCC"), "center") def make_section_slide(c, num, title, subtitle): rect(c, 0, 0, PAGE_W, PAGE_H, C_MED_BLUE) rect(c, 0, 0, 28, PAGE_H, C_GOLD) rect(c, 0, 0, PAGE_W, 30, C_DARK_BLUE) # Number box rect(c, 70, PAGE_H*0.48, 65, 65, C_GOLD) c.setFont("Helvetica-Bold", 34) c.setFillColor(C_DARK_BLUE) c.drawCentredString(103, PAGE_H*0.48 + 18, str(num)) # Title draw_text(c, title, 155, PAGE_H*0.60, PAGE_W-185, "Helvetica-Bold", 34, C_WHITE) if subtitle: draw_text(c, subtitle, 155, PAGE_H*0.43, PAGE_W-185, "Helvetica-Oblique", 16, C_LIGHT_GRAY) # Footer draw_text(c, "PHYSIOLOGY VIVA | 1ST YEAR MBBS", 30, 9, PAGE_W-60, "Helvetica", 10, colors.HexColor("#CCDDEE"), "center") def make_qa_slide(c, section_tag, slide_title, qa_pairs, tip=None): # Background rect(c, 0, 0, PAGE_W, PAGE_H, C_LIGHT_GRAY) # Top header rect(c, 0, PAGE_H-46, PAGE_W, 46, C_DARK_BLUE) # Left accent strip rect(c, 0, 0, 10, PAGE_H, C_GOLD) # Header texts draw_text(c, section_tag, 20, PAGE_H-32, 200, "Helvetica-Bold", 10, C_GOLD) draw_text(c, slide_title, 20, PAGE_H-32, PAGE_W-40, "Helvetica-Bold", 16, C_WHITE, "center") # Bottom tip bar tip_h = 32 if tip else 0 if tip: rect(c, 0, 0, PAGE_W, tip_h, C_DARK_BLUE) draw_text(c, "Examiner Tip: " + tip, 20, 8, PAGE_W-40, "Helvetica-Oblique", 10, C_GOLD) # Q&A boxes n = len(qa_pairs) body_top = PAGE_H - 50 body_bot = tip_h + 8 body_h = body_top - body_bot slot_h = body_h / n margin = 14 for i, (q, a) in enumerate(qa_pairs): slot_y = body_bot + (n - 1 - i) * slot_h q_h = slot_h * 0.40 a_h = slot_h * 0.52 gap = slot_h * 0.04 # Q box rect(c, margin, slot_y + a_h + gap*2, PAGE_W - margin*2, q_h, C_DARK_BLUE) draw_text(c, "Q " + q, margin+10, slot_y + a_h + gap*2 + q_h - 14, PAGE_W - margin*2 - 20, "Helvetica-Bold", 11, C_GOLD, max_lines=3) # A box rect(c, margin, slot_y, PAGE_W - margin*2, a_h, C_WHITE) draw_text(c, "A " + a, margin+10, slot_y + a_h - 14, PAGE_W - margin*2 - 20, "Helvetica", 10, C_DARK_TEXT, max_lines=5) def build_pdf(slides_data, out_path): c = canvas.Canvas(out_path, pagesize=landscape(A4)) c.setTitle("Physiology Viva Questions — 1st Year MBBS") # Title slide make_title_slide(c) c.showPage() for item in slides_data: if len(item) == 4 and isinstance(item[1], str) and item[1].isdigit(): make_section_slide(c, item[1], item[2], item[3]) c.showPage() elif len(item) == 4 and item[1] is None: make_qa_slide(c, item[0], item[2], item[3]) c.showPage() elif len(item) == 5: make_qa_slide(c, item[0], item[2], item[3], tip=item[4]) c.showPage() c.save() print(f"PDF saved: {out_path}") # ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━ slides_data = [ # ── GENERAL PHYSIOLOGY ────────────────────────────────────── ("GENERAL PHYSIOLOGY", "1", "General Physiology", "Cell physiology, homeostasis, membrane transport"), ("GENERAL PHYSIOLOGY", None, "Cell Membrane & Transport", [ ("What is the fluid mosaic model?", "The cell membrane is a phospholipid bilayer with embedded proteins that can move laterally - proposed by Singer & Nicolson (1972). Phospholipid head is hydrophilic; tail is hydrophobic."), ("What is the resting membrane potential of a neuron?", "-70 mV (inside negative). Maintained by Na+/K+-ATPase pump (3Na+ out, 2K+ in) and differential permeability - K+ leakage channels dominate at rest."), ("Difference between diffusion and osmosis?", "Diffusion: movement of solute from high to low concentration. Osmosis: movement of WATER across a semipermeable membrane from low solute to high solute concentration."), ], "Always state the value (e.g., -70 mV), the ion responsible, and the pump maintaining it."), ("GENERAL PHYSIOLOGY", None, "Active vs Passive Transport", [ ("What is active transport? Give an example.", "Movement against concentration gradient using energy (ATP). Example: Na+/K+-ATPase pump moves Na+ out and K+ in against gradients. Primary active transport uses ATP directly."), ("What is facilitated diffusion?", "Passive transport down concentration gradient via specific carrier or channel proteins. No energy required. Example: glucose entry into RBCs via GLUT-1 transporter."), ("What is secondary active transport?", "Uses electrochemical gradient of Na+ (created by Na+/K+ pump) to drive another molecule. Same direction = co-transport (symport). Opposite direction = counter-transport (antiport). e.g., Na+-glucose symport in intestine."), ], "Examiners often ask: classify a transport mechanism by energy requirement and direction."), ("GENERAL PHYSIOLOGY", None, "Homeostasis & Cell Communication", [ ("Define homeostasis with an example.", "Maintenance of a stable internal environment despite external changes. Example: blood glucose maintained at 70-110 mg/dL by insulin/glucagon feedback loops in the body."), ("What is negative feedback? Why is it important?", "The response opposes the original stimulus, restoring equilibrium. Example: High body temperature -> sweating -> temp falls back to normal. Most homeostatic mechanisms use negative feedback."), ("What are gap junctions?", "Protein channels (connexins) directly connecting cytoplasm of adjacent cells, allowing ions and small molecules to pass. Important in cardiac muscle (electrical coupling) and smooth muscle."), ], "Positive feedback AMPLIFIES the stimulus (childbirth, blood clotting) - contrast with negative feedback."), # ── HEMATOLOGY ────────────────────────────────────────────── ("HEMATOLOGY", "2", "Hematology", "Blood cells, hemoglobin, coagulation, blood groups"), ("HEMATOLOGY", None, "Red Blood Cells & Hemoglobin", [ ("What are normal RBC values?", "Male: 4.5-5.5 million/uL | Female: 3.8-4.8 million/uL. RBC lifespan: 120 days. Destroyed in spleen. Produced in red bone marrow (erythropoiesis). No nucleus or mitochondria in mature RBC."), ("Describe the structure of hemoglobin.", "Hb is a tetramer: 2alpha + 2beta globin chains (HbA). Each chain has 1 heme group (porphyrin ring + Fe2+). Fe2+ binds O2 reversibly. Normal Hb: Male 14-17 g/dL; Female 12-15 g/dL. MW: 68,000 Da."), ("What is the Bohr effect?", "Increased CO2 or decreased pH shifts O2-Hb dissociation curve to the RIGHT, decreasing Hb affinity for O2 - facilitating O2 release to tissues. Mnemonic: CADET (CO2, Acid, 2,3-DPG, Exercise, Temp) shift right."), ], "Always know the O2-Hb dissociation curve shifts (CADET shifts right = releases more O2 to tissues)."), ("HEMATOLOGY", None, "WBCs, Platelets & EPO", [ ("What is the normal WBC count and differential?", "Total WBC: 4,000-11,000/uL. Differential: Neutrophils 60-70%, Lymphocytes 20-30%, Monocytes 2-8%, Eosinophils 1-4%, Basophils 0-1%. Mnemonic: Never Let Monkeys Eat Bananas."), ("What is the function of platelets?", "Lifespan: 8-10 days. Normal count: 1.5-4 lakh/uL. Function: Primary hemostasis - platelet plug via adhesion (vWF), activation (ADP/TXA2), and aggregation (GPIIb/IIIa + fibrinogen)."), ("What is erythropoietin (EPO)?", "Glycoprotein hormone produced mainly by peritubular cells of kidney (90%) in response to hypoxia. Stimulates RBC production (erythropoiesis) in bone marrow. Used clinically in renal anemia."), ], "For platelets: always mention count, lifespan, and the 3 phases of primary hemostasis."), ("HEMATOLOGY", None, "Coagulation & Blood Groups", [ ("What are intrinsic and extrinsic pathways?", "Intrinsic (contact): XII->XI->IX->X. Extrinsic (tissue factor): VII+TF->X. Both converge at Factor X -> common pathway -> prothrombin->thrombin->fibrinogen->fibrin. PT tests extrinsic; aPTT tests intrinsic."), ("What are the ABO blood groups?", "Type A: antigen A, anti-B antibody. Type B: antigen B, anti-A. Type AB: both antigens, NO antibodies (universal recipient). Type O: no antigens, BOTH antibodies (universal donor). Determined by chromosome 9."), ("What is the Rh factor? Why is it clinically important?", "Rh+ (85% population) has D antigen; Rh- lacks it. If Rh- mother carries Rh+ fetus: sensitization in 1st pregnancy; in 2nd pregnancy maternal anti-D IgG crosses placenta causing Hemolytic Disease of the Newborn (HDN)."), ], "Coagulation cascade is frequently asked - draw it if possible. Remember PT=extrinsic, aPTT=intrinsic."), # ── BIOPHYSICS ─────────────────────────────────────────────── ("BIOPHYSICS", "3", "Biophysics", "Physical principles applied to biological systems"), ("BIOPHYSICS", None, "Action Potential & Refractory Periods", [ ("What is an action potential? Describe its phases.", "1) Resting: -70 mV 2) Depolarization: Na+ channels open, membrane rises to +30 mV 3) Repolarization: Na+ inactivates, K+ channels open 4) After-hyperpolarization: K+ channels close slowly 5) Return to -70 mV."), ("What is the all-or-none law?", "Once a threshold stimulus is reached (~-55 mV), an action potential fires at FULL magnitude regardless of stimulus strength. Subthreshold stimuli produce no AP. Amplitude does NOT increase with stronger stimuli."), ("What are absolute and relative refractory periods?", "Absolute RP: No stimulus can fire another AP (Na+ channels inactivated). Relative RP: Stronger-than-normal stimulus CAN fire AP (some Na+ channels recovering, K+ channels still open and membrane hyperpolarized)."), ], "Drawing the AP curve takes 30 seconds and impresses examiners greatly - always offer to draw it."), ("BIOPHYSICS", None, "Surface Tension, Osmosis & Donnan", [ ("What is surface tension in alveoli? What prevents collapse?", "Surface tension = force at air-liquid interface tending to collapse alveoli. Surfactant (DPPC, produced by Type II pneumocytes) reduces surface tension, preventing collapse. Laplace law: P = 2T/r."), ("Define osmolarity vs osmolality.", "Osmolarity: osmoles of solute per LITRE of solution (mOsm/L). Osmolality: osmoles per KG of solvent (mOsm/kg). Normal plasma osmolality: 285-295 mOsm/kg. Osmolality is clinically measured (freezing point depression)."), ("What is Donnan equilibrium?", "When a membrane is impermeable to one ion (e.g., large proteins), diffusible ions distribute unequally to maintain electrical neutrality. Protein-containing compartment has higher total osmolarity - contributes to oncotic pressure."), ], "Laplace's Law (P = 2T/r) is frequently asked in context of both alveoli and blood vessels."), # ── ENDOCRINE INTRODUCTION ─────────────────────────────────── ("ENDOCRINE SYSTEM", "4", "Endocrine System - Introduction", "Hormones, receptors, feedback mechanisms"), ("ENDOCRINE SYSTEM", None, "Hormone Classification & Mechanisms", [ ("How are hormones classified based on chemistry?", "1) Peptide/Protein: insulin, GH, PTH - water-soluble, surface receptors, cAMP/IP3 messengers. 2) Steroid: cortisol, sex hormones - lipid-soluble, nuclear receptors. 3) Amines: adrenaline (surface), thyroid hormones (nuclear)."), ("What is a second messenger? Examples?", "Intracellular signaling molecule carrying signal from receptor to effector. Examples: cAMP (adenylyl cyclase - glucagon, adrenaline), IP3/DAG (phospholipase C - angiotensin II, GnRH), Ca2+, cGMP (ANP, nitric oxide)."), ("What is negative feedback in the endocrine system?", "High levels of an end-hormone suppress the upstream axis. Example: High cortisol -> inhibits CRH (hypothalamus) and ACTH (pituitary) -> reduces cortisol. Basis of gradual tapering when stopping steroid therapy."), ], "Mention receptor type (surface vs. nuclear) and second messenger for peptide vs. steroid hormones."), # ── THYROID GLAND ──────────────────────────────────────────── ("THYROID GLAND", "5", "Thyroid Gland", "Synthesis, secretion, and actions of thyroid hormones"), ("THYROID GLAND", None, "Thyroid Hormone Synthesis", [ ("Describe steps of thyroid hormone synthesis.", "1) Iodide trapping (NIS symporter) 2) Oxidation by TPO 3) Organification: MIT, DIT on thyroglobulin 4) Coupling: MIT+DIT=T3; DIT+DIT=T4 5) Stored in colloid 6) TSH -> endocytosis -> proteolysis -> T3/T4 release."), ("T3 vs T4 - which is more active?", "T4:T3 secreted ratio = 20:1. T4 (thyroxine) is the PROHORMONE - converted to active T3 by 5'-deiodinase in peripheral tissues. T3 is 3-5x more potent. T3 half-life = 1 day; T4 half-life = 7 days."), ("What is the role of TSH?", "TSH (thyrotropin) from anterior pituitary: stimulates all steps of TH synthesis and secretion, promotes thyroid cell growth and vascularity. Acts via cAMP. Controlled by TRH (hypothalamus) and negative feedback by T3/T4."), ], "Synthesis steps (trapping->oxidation->organification->coupling->storage->release) are very commonly asked."), ("THYROID GLAND", None, "Actions & Clinical Disorders", [ ("What are the physiological effects of thyroid hormones?", "1) Calorigenic: increased BMR, O2 consumption 2) Growth: brain dev, bone maturation 3) CVS: increased HR, CO, Na+/K+ ATPase 4) Metabolic: increased glucose absorption, lipolysis, protein synthesis 5) Permissive for catecholamines."), ("Primary vs secondary hypothyroidism?", "Primary: thyroid failure -> decreased T3/T4, INCREASED TSH (loss of neg feedback). e.g., Hashimoto's, iodine deficiency. Secondary: pituitary failure -> decreased TSH -> decreased T3/T4. Key: TSH is HIGH in primary, LOW in secondary."), ("What is cretinism vs. myxedema?", "Cretinism: hypothyroidism in infancy/childhood - mental retardation, dwarfism, coarse features, protruding tongue. Myxedema: hypothyroidism in adults - non-pitting edema (glycosaminoglycans), bradycardia, cold intolerance, constipation."), ], "TSH is the single BEST test for thyroid function - always mention this in clinical questions."), # ── PARATHYROID GLAND ──────────────────────────────────────── ("PARATHYROID GLAND", "6", "Parathyroid Gland", "PTH, calcium regulation, Vitamin D"), ("PARATHYROID GLAND", None, "PTH - Synthesis & Actions", [ ("What stimulates PTH secretion?", "LOW serum Ca2+ is the primary stimulus (sensed by calcium-sensing receptor, CaSR). Also: increased phosphate, decreased Mg2+. HIGH Ca2+, calcitriol, and high Mg2+ suppress PTH. PTH is an 84 amino acid peptide."), ("Actions of PTH on bone, kidney, and gut?", "Bone: increased osteoclast activity -> Ca2+ and phosphate released. Kidney: increased Ca2+ reabsorption (DCT), DECREASED phosphate reabsorption (phosphaturia), increased 1alpha-hydroxylase (activates Vit D). Gut: indirect via Vit D -> Ca2+ absorption."), ("Net effect of PTH on serum Ca2+ and phosphate?", "PTH causes HYPERCALCEMIA and HYPOPHOSPHATEMIA. This distinguishes hyperparathyroidism (high Ca, low PO4) from other causes of hypercalcemia. Key exam fact: Ca and phosphate move in OPPOSITE directions with PTH."), ], "Mnemonic: PTH on kidney - Ca REABSORBED, Phosphate EXCRETED (opposite directions)."), ("PARATHYROID GLAND", None, "Vitamin D & Calcium Disorders", [ ("Describe Vitamin D activation pathway.", "Skin: UV light -> 7-dehydrocholesterol -> cholecalciferol (D3). Liver: 25-hydroxylase -> 25-OH-D3 (storage form). Kidney: 1alpha-hydroxylase (stimulated by PTH, hypocalcemia) -> 1,25-(OH)2-D3 = calcitriol (ACTIVE form)."), ("Features of hypoparathyroidism?", "Decreased PTH -> decreased Ca2+ (hypocalcemia) + increased phosphate. Features: tetany, Chvostek's sign (facial twitch on tapping facial nerve), Trousseau's sign (carpal spasm with BP cuff), perioral tingling, seizures, prolonged QT."), ("What is pseudohypoparathyroidism?", "Normal or HIGH PTH but target organs are RESISTANT (Gs protein mutation). Features of hypoparathyroidism (hypocalcemia, hyperphosphatemia) but PTH is HIGH. Associated with Albright's hereditary osteodystrophy (short 4th metacarpal, round face)."), ], "Chvostek and Trousseau signs are EXAM FAVORITES - know how to elicit them and what they indicate."), # ── ANTERIOR PITUITARY ─────────────────────────────────────── ("ANTERIOR PITUITARY", "7", "Anterior Pituitary", "Hormones, regulation, clinical correlations"), ("ANTERIOR PITUITARY", None, "Hormones of the Anterior Pituitary", [ ("Name all anterior pituitary hormones.", "Mnemonic FLAT PEG: FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH. Cell types: Somatotrophs(GH), Corticotrophs(ACTH), Thyrotrophs(TSH), Gonadotrophs(FSH/LH), Lactotrophs(Prolactin). Embryological origin: Rathke's pouch (oral ectoderm)."), ("How is anterior pituitary controlled by hypothalamus?", "Hypothalamus releases hormones into hypothalamo-hypophyseal PORTAL system. Releasing: CRH->ACTH, TRH->TSH, GHRH->GH, GnRH->FSH/LH. Inhibiting: somatostatin inhibits GH; DOPAMINE inhibits prolactin."), ("What is special about prolactin regulation?", "Prolactin is UNIQUE - under predominant INHIBITORY control by dopamine (PIH). All others are stimulated. Dopamine antagonists (metoclopramide, antipsychotics) increase prolactin -> galactorrhea, amenorrhea (hyperprolactinemia)."), ], "FLAT PEG covers all 6 anterior pituitary hormones. Remember: prolactin is uniquely inhibited by dopamine."), ("ANTERIOR PITUITARY", None, "Growth Hormone", [ ("Actions of growth hormone?", "Direct: increased lipolysis, increased blood glucose (anti-insulin), increased protein synthesis. Indirect (via IGF-1/somatomedin-C from liver): increased bone growth (epiphyseal plates), increased muscle mass, increased organ growth."), ("What stimulates and inhibits GH secretion?", "Stimulate: sleep (peak in slow-wave sleep), exercise, hypoglycemia, stress, GHRH, ghrelin, amino acids. Inhibit: somatostatin, IGF-1 (neg feedback), obesity, hyperglycemia, free fatty acids, glucocorticoids."), ("Acromegaly vs. gigantism?", "Both due to GH excess. Gigantism: GH excess BEFORE epiphyseal fusion (childhood) -> proportionate tall stature. Acromegaly: GH excess AFTER fusion (adult) -> large hands/feet/jaw, coarse features, frontal bossing. Diagnosed: raised IGF-1 + GH not suppressed by glucose."), ], "IGF-1 is the best SCREENING TEST for acromegaly (more stable than GH itself)."), ("ANTERIOR PITUITARY", None, "ACTH, FSH, LH & Panhypopituitarism", [ ("What is the HPA axis?", "Hypothalamus -> CRH -> Anterior pituitary -> ACTH -> Adrenal cortex -> Cortisol. Cortisol exerts NEGATIVE feedback on both hypothalamus (reduces CRH) and pituitary (reduces ACTH). ACTH also stimulates adrenal androgen (DHEA) production."), ("Functions of FSH and LH?", "Males: FSH -> Sertoli cells (spermatogenesis, inhibin). LH -> Leydig cells (testosterone). Females: FSH -> follicle development, estrogen. LH -> ovulation trigger (LH surge), corpus luteum, progesterone. Both controlled by pulsatile GnRH."), ("What is panhypopituitarism?", "Deficiency of ALL anterior pituitary hormones. Causes: Sheehan's syndrome (postpartum necrosis), tumors, radiation. Order of hormone loss: GH first -> FSH/LH -> TSH -> ACTH last. Features: short stature, hypothyroidism, adrenal insufficiency, hypogonadism."), ], "In Sheehan's syndrome: failure to lactate + absent menstruation postpartum are the first clues."), ] build_pdf(slides_data, "/tmp/workspace/physiology-viva/Physiology_Viva_Questions.pdf") PYEOF python /tmp/workspace/physiology-viva/build_pdf.py

ls -lh /tmp/workspace/physiology-viva/