Pick the section to prepare first as concise GK Pal-style exam notes/PDF.

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physiology education AND systematic review

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mkdir -p "/tmp/workspace/physiology-paper1-crash-notes/src" "/tmp/workspace/physiology-paper1-crash-notes/output"

WHO physiology learning study tips active recall medical students

python - <<'PY' from pathlib import Path p=Path('/tmp/workspace/physiology-paper1-crash-notes/src/create_pdf.py') p.write_text(r'''from reportlab.lib.pagesizes import A4 from reportlab.platypus import SimpleDocTemplate, Paragraph, Spacer, PageBreak, Table, TableStyle, KeepTogether from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib import colors from reportlab.lib.units import cm from reportlab.pdfbase.pdfmetrics import stringWidth from reportlab.pdfbase.ttfonts import TTFont from reportlab.pdfbase import pdfmetrics from reportlab.lib.enums import TA_CENTER from reportlab.pdfgen import canvas from xml.sax.saxutils import escape OUT='/tmp/workspace/physiology-paper1-crash-notes/output/Physiology_Paper_1_Last_Night_Crash_Notes.pdf' class NumberedCanvas(canvas.Canvas): def __init__(self,*args,**kwargs): canvas.Canvas.__init__(self,*args,**kwargs); self.pages=[] def showPage(self): self.pages.append(dict(self.__dict__)); self._startPage() def save(self): n=len(self.pages) for st in self.pages: self.__dict__.update(st); self.setFont('Helvetica',8); self.setFillColor(colors.HexColor('#4B5563')) self.drawString(1.6*cm,1.1*cm,'Physiology Paper 1 - Last-night crash notes') self.drawRightString(A4[0]-1.6*cm,1.1*cm,f'Page {self._pageNumber} of {n}') canvas.Canvas.showPage(self) canvas.Canvas.save(self) styles=getSampleStyleSheet() styles.add(ParagraphStyle(name='Title2',parent=styles['Title'],fontName='Helvetica-Bold',fontSize=21,leading=25,textColor=colors.HexColor('#12355B'),alignment=TA_CENTER,spaceAfter=12)) styles.add(ParagraphStyle(name='Sub',parent=styles['Normal'],fontSize=10,leading=14,alignment=TA_CENTER,textColor=colors.HexColor('#4B5563'),spaceAfter=12)) styles.add(ParagraphStyle(name='H1x',parent=styles['Heading1'],fontName='Helvetica-Bold',fontSize=16,leading=20,textColor=colors.white,backColor=colors.HexColor('#12355B'),borderPadding=6,spaceBefore=12,spaceAfter=8)) styles.add(ParagraphStyle(name='H2x',parent=styles['Heading2'],fontName='Helvetica-Bold',fontSize=12.5,leading=15,textColor=colors.HexColor('#0F4C5C'),spaceBefore=9,spaceAfter=4)) styles.add(ParagraphStyle(name='Bodyx',parent=styles['BodyText'],fontSize=9.1,leading=12.2,spaceAfter=4)) styles.add(ParagraphStyle(name='Sm',parent=styles['BodyText'],fontSize=8.25,leading=10.4,spaceAfter=2)) styles.add(ParagraphStyle(name='Box',parent=styles['BodyText'],fontSize=9,leading=12,backColor=colors.HexColor('#EAF3F8'),borderColor=colors.HexColor('#8DB9CA'),borderWidth=.5,borderPadding=6,spaceBefore=5,spaceAfter=7)) def P(t,style='Bodyx'): return Paragraph(t,styles[style]) def bullets(items): return [P('• '+x) for x in items] def sec(title): story.append(P(title,'H1x')) def topic(title,items,extra=None): story.append(P(title,'H2x')); story.extend(bullets(items)); if extra: story.append(P('<b>Write in exam:</b> '+extra,'Box')) def table(headers, rows, widths=None): data=[[P('<b>'+escape(x)+'</b>','Sm') for x in headers]]+[[P(escape(x),'Sm') for x in r] for r in rows] t=Table(data,colWidths=widths,repeatRows=1,hAlign='LEFT') t.setStyle(TableStyle([('BACKGROUND',(0,0),(-1,0),colors.HexColor('#0F4C5C')),('TEXTCOLOR',(0,0),(-1,0),colors.white),('GRID',(0,0),(-1,-1),.35,colors.HexColor('#9CA3AF')),('VALIGN',(0,0),(-1,-1),'TOP'),('ROWBACKGROUNDS',(0,1),(-1,-1),[colors.white,colors.HexColor('#F5FAFC')]),('LEFTPADDING',(0,0),(-1,-1),5),('RIGHTPADDING',(0,0),(-1,-1),5),('TOPPADDING',(0,0),(-1,-1),4),('BOTTOMPADDING',(0,0),(-1,-1),4)])) story.append(t); story.append(Spacer(1,6)) story=[] story += [Spacer(1,2*cm),P('PHYSIOLOGY PAPER 1','Title2'),P('Last-night High-yield Crash Notes','Title2'),P('CVS | Respiratory | GI | Blood & Immunity | Renal','Sub'),P('<b>How to use:</b> Learn the bolded headings as answer skeletons. Draw a simple flowchart or graph wherever stated. Write definition first, then mechanism, regulation, functions/clinical relevance. This is concise revision material, not a substitute for your prescribed textbook.','Box'),P('<b>Pass plan:</b> CVS (2 h) → Respiratory (2 h) → Renal (2 h) → Blood (1.5 h) → GI (1.5 h). Before sleep, revise comparison tables, normal values and flow arrows.','Box'),PageBreak()] sec('1. CARDIOVASCULAR SYSTEM') topic('Nerve supply of heart',[ '<b>Sympathetic:</b> T1-T5 segments → cervical and upper thoracic sympathetic ganglia → cardiac nerves. Increases heart rate, conduction, contractility and coronary flow.', '<b>Parasympathetic:</b> vagus nerves. Decreases SA rate and AV conduction; slight reduction of atrial contractility. Ventricles have sparse vagal supply.', '<b>Afferents:</b> pain fibers travel with sympathetics to T1-T5; reflex afferents travel mainly in vagus. Cardiac plexus lies at base of heart.' ],'Draw a cardiac plexus flowchart and state sympathetic versus vagal effects.') topic('Frank-Starling law',[ '<b>Law:</b> within physiological limits, force of ventricular contraction is proportional to initial length of myocardial fibers, hence to end-diastolic volume (preload).', 'Mechanism: increased fiber length → better actin-myosin overlap and increased Ca2+ sensitivity → increased stroke volume.', 'Importance: matches right and left ventricular output, adjusts output to venous return, provides cardiac reserve. <b>Heterometric regulation.</b>' ],'Draw ventricular function curve: stroke volume/cardiac output rises with EDV or right atrial pressure.') topic('Properties of cardiac muscle',[ '<b>Automaticity/rhythmicity:</b> spontaneous impulse generation, maximum in SA node. <b>Excitability:</b> response to stimulus. <b>Conductivity:</b> impulse transmission.', '<b>Contractility:</b> force at a given initial length. <b>All-or-none law:</b> whole myocardium behaves as functional syncytium. <b>Long refractory period:</b> prevents tetanus and allows filling.', '<b>Treppe:</b> increased force with repeated stimulation after rest. Staircase effect occurs partly due to Ca2+ accumulation.' ]) topic('Pacemaker potential and conducting system',[ '<b>SA node:</b> normal pacemaker 60-100/min. Phase 4 slow diastolic depolarization due to funny current (If, Na+), reduced K+ efflux and Ca2+ entry. Phase 0: L-type Ca2+ influx. Phase 3: K+ efflux. No phases 1 and 2.', 'Intrinsic rates: SA 60-100/min; AV node 40-60/min; Purkinje 15-40/min. Vagus shifts phase 4 slope down; sympathetic increases it.', 'Pathway: SA node → atrial pathways/Bachmann bundle → AV node (physiological delay about 0.1 s) → bundle of His → right/left bundle branches → Purkinje fibers → ventricles. AV delay permits atrial emptying before ventricular systole.' ],'Draw the conduction pathway. Mention AV nodal delay and intrinsic rates.') topic('ECG: definition, leads, waves and intervals',[ '<b>Definition:</b> graphic recording of electrical activity of heart from body surface.', '<b>Leads:</b> bipolar limb I, II, III; augmented limb aVR, aVL, aVF; precordial V1-V6. Lead II is from right arm to left leg and usually shows upright P, R and T.', '<b>P wave:</b> atrial depolarization. <b>QRS:</b> ventricular depolarization, duration <0.12 s. <b>T:</b> ventricular repolarization. Atrial repolarization is hidden in QRS.', '<b>PR interval:</b> start P to start QRS, 0.12-0.20 s: atrial depolarization plus AV nodal/His conduction. Prolonged in first-degree AV block. <b>QT:</b> ventricular electrical systole, rate dependent. <b>ST segment:</b> normally isoelectric.' ],'Draw Lead II and label P, QRS, T, PR, ST, QT and RR.') topic('Cardiac cycle and LV pressure-volume changes',[ 'Phases: (1) atrial systole, completes ventricular filling; (2) isovolumetric ventricular contraction, AV valves close, S1; (3) rapid ejection; (4) reduced ejection; (5) isovolumetric relaxation, semilunar valves close, S2; (6) rapid filling; (7) reduced filling/diastasis.', 'At end-diastole LV volume is about 120 mL. During isovolumetric contraction volume constant and pressure rises. Ejection reduces volume to ESV about 50 mL. Stroke volume about 70 mL; ejection fraction about 60%.', 'PV loop: mitral opens at low pressure after relaxation; mitral closes at EDV; aortic opens when LV pressure exceeds aortic pressure; aortic closes at end systole.' ],'Draw Wiggers diagram and a LV pressure-volume loop. Label valve events and heart sounds.') topic('JVP waves',[ '<b>a wave:</b> right atrial contraction. <b>c wave:</b> bulging of tricuspid into atrium in early ventricular systole. <b>x descent:</b> atrial relaxation and downward tricuspid movement.', '<b>v wave:</b> venous filling of RA against closed tricuspid. <b>y descent:</b> rapid RA emptying after tricuspid opens.', 'Absent a: atrial fibrillation. Giant a: tricuspid stenosis/pulmonary hypertension. Cannon a: AV dissociation. Raised JVP: right heart failure, tamponade, fluid overload.' ]) topic('Cardiac output: regulation and determination',[ '<b>CO = HR × SV</b>. Normal resting CO about 5 L/min; cardiac index about 3 L/min/m2. SV depends on preload, contractility and afterload.', 'Increase CO: exercise, sympathetic activity, thyroxine, pregnancy. Decrease CO: hemorrhage, heart failure, vagal stimulation.', '<b>Fick principle:</b> CO = O2 consumption ÷ (arterial O2 content - mixed venous O2 content). Other methods: indicator dilution, thermodilution, Doppler echocardiography.', '<b>Venous return equals CO</b> in steady state. Factors raising venous return: muscle pump, respiratory pump, sympathetic venoconstriction, increased blood volume.' ]) topic('Short-term regulation of arterial BP',[ '<b>MAP ≈ DBP + one-third pulse pressure; MAP = CO × TPR.</b> Baroreceptor reflex is fastest: carotid sinus via IX and aortic arch via X → medulla. Increased BP raises firing → ↓sympathetic, ↑vagus → reduced HR, contractility, TPR and venous tone.', 'Chemoreceptor reflex responds to severe hypotension, hypoxia, hypercapnia and acidosis; increases sympathetic vasoconstriction. CNS ischemic response occurs in severe cerebral hypoperfusion.', 'Other rapid influences: cardiopulmonary receptors, adrenal catecholamines, stress and exercise. Baroreceptors reset in chronic hypertension.' ]) topic('Coronary circulation, triple response and shock',[ '<b>Coronary flow:</b> left coronary flow mainly occurs in diastole because systolic LV compression reduces flow. Local metabolic control dominates: adenosine, low O2, high CO2/H+, K+ and NO cause vasodilation. Subendocardium is most vulnerable to ischemia.', '<b>Triple response of Lewis:</b> red line (capillary dilatation), flare (axon reflex arteriolar dilatation), wheal (increased permeability/edema) after firm skin stroke.', '<b>Shock:</b> acute circulatory failure causing inadequate tissue perfusion. Types: hypovolemic, cardiogenic, distributive (septic/anaphylactic/neurogenic), obstructive. Stages: compensated → progressive → irreversible. Key features: hypotension, tachycardia except neurogenic, cold clammy skin in hypovolemic/cardiogenic shock, oliguria, altered sensorium.' ]) sec('2. RESPIRATORY SYSTEM') topic('Functions of upper respiratory tract',[ 'Conducts air; filters particles by hairs, mucus and cilia; warms and humidifies inspired air; olfaction; voice resonance; defense by cough/sneeze, IgA and lymphoid tissue. Nose causes turbulent airflow and conditions air.' ]) topic('Mechanism of inspiration and expiration',[ '<b>Quiet inspiration:</b> active. Diaphragm contracts and descends, external intercostals elevate ribs → thoracic volume rises → intrapleural pressure becomes more negative → alveolar pressure falls → air enters.', '<b>Quiet expiration:</b> passive elastic recoil of lungs/chest wall. Forced expiration uses internal intercostals and abdominal muscles.', 'Compliance = ΔV/ΔP. Surfactant lowers surface tension, increases compliance, prevents alveolar collapse and reduces work of breathing.' ],'Draw pressure changes: intrapleural pressure stays negative; alveolar pressure becomes slightly negative in inspiration and positive in expiration.') topic('Dead space and V/Q ratio',[ '<b>Anatomical dead space:</b> conducting airways, about 150 mL. <b>Alveolar dead space:</b> ventilated alveoli not perfused. Physiological dead space = anatomical + alveolar.', '<b>V/Q ratio:</b> total ventilation about 4 L/min and perfusion 5 L/min, average V/Q about 0.8. Apex: high V/Q (more ventilation relative to perfusion); base: low V/Q.', 'V/Q = 0 is shunt; V/Q → infinity is dead space. Hypoxic pulmonary vasoconstriction diverts blood from poorly ventilated alveoli.' ]) topic('O2 and CO2 transport, chloride shift',[ '<b>O2:</b> about 98-99% bound to Hb, 1-2% dissolved. Each gram Hb carries about 1.34 mL O2 when fully saturated. O2 content = 1.34 × Hb × saturation + 0.003 × PaO2.', '<b>CO2:</b> about 70% as bicarbonate, 20-23% carbamino compounds, 7% dissolved. In RBC: CO2 + H2O ⇌ H2CO3 ⇌ H+ + HCO3- via carbonic anhydrase.', '<b>Chloride shift:</b> in tissues HCO3- leaves RBC in exchange for Cl- entering. Reverse shift occurs in lungs.' ]) topic('Oxygen dissociation curve, Bohr and Haldane effects',[ 'Sigmoid curve due to cooperative Hb binding. P50 about 26-27 mmHg. Plateau supports loading in lungs; steep portion supports unloading in tissues.', '<b>Right shift:</b> increased H+, PCO2, temperature, 2,3-BPG, exercise: reduced affinity and enhanced unloading. <b>Left shift:</b> opposite, fetal Hb, CO poisoning.', '<b>Bohr effect:</b> increased CO2/H+ decreases Hb affinity for O2, promoting O2 unloading in tissues. <b>Haldane effect:</b> oxygenation of Hb in lungs reduces its CO2/H+ binding, enhancing CO2 unloading; deoxygenated Hb carries more CO2/H+ in tissues.' ],'Draw the sigmoid curve with right and left shift factors.') topic('Regulation of respiration, acclimatization and periodic breathing',[ 'Medullary dorsal respiratory group generates inspiratory rhythm; ventral group assists forced breathing. Pontine centers modify pattern.', '<b>Central chemoreceptors:</b> medulla, respond mainly to increased CO2 through CSF H+. <b>Peripheral chemoreceptors:</b> carotid (IX) and aortic bodies (X), stimulated by PaO2 <60 mmHg, increased CO2 and H+.', '<b>High altitude acclimatization:</b> hyperventilation, renal HCO3- excretion, increased 2,3-BPG, increased EPO/RBC mass, increased pulmonary diffusion capacity and tissue capillaries.', '<b>Periodic breathing:</b> cyclic waxing and waning ventilation with apneic periods. Cheyne-Stokes occurs in heart failure, CNS disease and high altitude.' ]) topic('Hypoxia, oxygen therapy and artificial ventilation',[ '<b>Hypoxic hypoxia:</b> low PaO2, e.g., altitude, hypoventilation, V/Q mismatch. <b>Anemic:</b> low O2 content with normal PaO2. <b>Stagnant/circulatory:</b> reduced blood flow. <b>Histotoxic:</b> cells cannot use O2, e.g., cyanide.', 'O2 therapy: give supplemental oxygen for documented hypoxemia and treat cause. In chronic CO2 retainers, oxygen is titrated with monitoring rather than withheld. CO poisoning needs high-flow oxygen; hyperbaric oxygen is considered in selected severe cases.', 'Artificial ventilation supplies positive-pressure breaths when spontaneous ventilation is inadequate. Risks include barotrauma, hypotension and ventilator-associated infection. <b>Cyanosis:</b> bluish discoloration from increased deoxygenated Hb, generally >5 g/dL; absent in severe anemia and may be marked in polycythemia.' ]) sec('3. GASTROINTESTINAL PHYSIOLOGY') topic('Saliva and CCK',[ '<b>Saliva:</b> 1-1.5 L/day, hypotonic; water, mucins, HCO3-, K+, amylase, lingual lipase, IgA, lysozyme. Functions: lubrication, taste, speech, oral hygiene, starch digestion, buffering. Parasympathetic stimulation causes copious watery secretion; sympathetic causes smaller viscous secretion.', '<b>CCK:</b> secreted by I cells of duodenum/jejunum in response to fatty acids and amino acids. Contracts gallbladder, relaxes sphincter of Oddi, stimulates enzyme-rich pancreatic secretion, potentiates secretin action, slows gastric emptying and promotes satiety.' ]) topic('Stomach, HCl and peptic ulcer',[ '<b>Stomach functions:</b> reservoir, mixing/grinding, controlled emptying, secretion of HCl, pepsinogen, intrinsic factor, mucus/HCO3- and gastrin; begins protein digestion.', '<b>HCl secretion:</b> parietal cell H+/K+ ATPase secretes H+. Carbonic anhydrase produces H+ and HCO3-; HCO3- enters blood causing alkaline tide. Stimulators: ACh (M3), gastrin (CCK-B), histamine (H2). Inhibitors: somatostatin, prostaglandins, low antral pH, secretin.', 'Cephalic, gastric and intestinal phases regulate secretion. <b>Peptic ulcer:</b> imbalance of acid-pepsin injury versus mucosal defense, commonly H. pylori or NSAIDs. Mucosal barrier depends on mucus-HCO3-, prostaglandins, epithelial repair and blood flow.' ]) topic('Pancreatic and biliary secretion, enterohepatic circulation',[ '<b>Exocrine pancreas:</b> acinar cells release enzymes (amylase, lipase, protease zymogens, nucleases); duct cells release HCO3--rich fluid. CCK stimulates enzymes; secretin stimulates bicarbonate; vagus potentiates.', '<b>Bile:</b> bile salts, phospholipids, cholesterol, bilirubin, electrolytes. Functions: fat emulsification and micelle formation, excretion of bilirubin/cholesterol, alkaline medium. Secretin increases watery bile; CCK empties gallbladder.', '<b>Enterohepatic circulation:</b> bile salts absorbed mainly in terminal ileum → portal blood → liver → resecreted. Conserves bile salts and maintains bile salt pool.' ]) topic('Jaundice, large intestine, swallowing, intestinal movements and defecation',[ '<b>Jaundice:</b> bilirubin > about 2 mg/dL. Prehepatic/hemolytic: unconjugated bilirubin ↑, urine bilirubin absent, urine urobilinogen ↑, stools dark. Hepatic: mixed pattern. Posthepatic/obstructive: conjugated bilirubin ↑, dark urine, pale clay stool, urobilinogen absent, pruritus.', '<b>Large intestine:</b> absorbs water and electrolytes, forms/stores feces, bacterial synthesis of vitamin K and some B vitamins; movements include haustral contractions and mass movements.', '<b>Deglutition:</b> oral voluntary; pharyngeal involuntary phase: soft palate closes nasopharynx, larynx elevates and glottis closes, upper esophageal sphincter relaxes, pharyngeal constrictors propel bolus. <b>Achalasia:</b> failure of LES relaxation due to myenteric plexus dysfunction; dysphagia and dilated esophagus.', 'Small intestine movements: segmentation for mixing; peristalsis for propulsion; migrating motor complex in fasting. <b>Defecation:</b> rectal stretch → sacral parasympathetic reflex (S2-S4) → rectal contraction/internal anal sphincter relaxation; voluntary external sphincter control via pudendal nerve.' ]) sec('4. BLOOD AND IMMUNITY') topic('Plasma proteins, erythropoiesis and anemia',[ 'Plasma proteins: albumin (oncotic pressure, transport, buffer), globulins (transport/immunity), fibrinogen (clotting). Normal total about 6-8 g/dL; albumin about 3.5-5 g/dL.', '<b>Erythropoiesis:</b> stem cell → erythroid progenitors → proerythroblast → normoblasts → reticulocyte → RBC. EPO is mainly from renal peritubular interstitial cells in response to hypoxia. Requires iron, B12, folate, protein, B6 and EPO.', '<b>Anemia:</b> decreased Hb/O2-carrying capacity. Morphological: microcytic hypochromic (iron deficiency, thalassemia), normocytic normochromic (acute blood loss, hemolysis, chronic disease), macrocytic (B12/folate deficiency). Symptoms: fatigue, dyspnea, tachycardia, pallor.' ]) topic('Fate of RBC, polycythemia and reticuloendothelial system',[ 'RBC life span about 120 days. Senescent RBCs are phagocytosed in spleen, liver and marrow. Globin → amino acids; iron recycled via transferrin/ferritin; heme → biliverdin → unconjugated bilirubin → liver conjugation → bile → urobilinogen → stercobilin (stool) and urobilin (urine).', '<b>Polycythemia:</b> raised RBC mass/hematocrit. Relative: dehydration. Absolute primary: polycythemia vera; secondary: hypoxia or excess EPO. Consequences: hyperviscosity, thrombosis, headache.', '<b>RES/mononuclear phagocyte system:</b> tissue macrophages in liver (Kupffer), spleen, lymph nodes, marrow, lung. Functions: phagocytosis, antigen presentation, cytokine secretion, RBC breakdown and iron recycling.' ]) topic('ABO/Rh grouping, cross-match and transfusion reactions',[ 'ABO antigens are on RBCs; naturally occurring IgM antibodies are in plasma. Group A: A antigen/anti-B; B: B/anti-A; AB: both antigens/no anti-A or anti-B; O: no antigens/both antibodies. For RBC transfusion, group O is commonly emergency donor and AB common recipient only when compatibility rules are followed.', '<b>Cross-match:</b> recipient serum + donor RBCs to detect incompatibility. Major cross-match is most important.', '<b>Incompatible transfusion:</b> acute intravascular hemolysis, fever/chills, hypotension, hemoglobinuria, DIC, renal failure and shock. Stop transfusion immediately and maintain IV access/supportive management.', '<b>Rh:</b> D antigen is most important. Rh-negative mother carrying Rh-positive fetus can be sensitized; subsequent fetus risks hemolytic disease. Anti-D immunoglobulin prophylaxis prevents sensitization.' ]) topic('T lymphocytes and cell-mediated immunity',[ '<b>T cells:</b> mature in thymus. CD4 helper cells coordinate immunity through cytokines; CD8 cytotoxic cells kill virus-infected/tumor cells; Treg cells suppress excessive responses; memory T cells enable rapid secondary response.', '<b>Cell-mediated immunity:</b> antigen presented on MHC activates T cells. CD8 recognizes MHC I and kills by perforin-granzyme/Fas pathways. CD4 Th1 activates macrophages. Important against intracellular microbes, tumors and graft rejection; mediates delayed hypersensitivity.' ]) topic('Platelets, purpura, coagulation, anticoagulants and hemophilia',[ '<b>Platelet plug:</b> adhesion via vWF-GpIb, activation/release of ADP, TXA2, Ca2+, aggregation via GpIIb/IIIa-fibrinogen. Platelets also provide phospholipid surface for coagulation. <b>Purpura:</b> skin/mucosal bleeding from thrombocytopenia or platelet/vascular defects, usually with prolonged bleeding time.', '<b>Extrinsic pathway:</b> tissue factor + VII → X; tested by PT/INR. <b>Intrinsic:</b> XII, XI, IX, VIII → X; tested by aPTT. <b>Common:</b> X, V, II (prothrombin), I (fibrinogen) → fibrin. Thrombin converts fibrinogen to fibrin; XIII stabilizes fibrin.', 'Natural anticoagulants: antithrombin, protein C/S, TFPI. Heparin potentiates antithrombin, rapidly inhibits IIa/Xa; monitor aPTT. Warfarin blocks vitamin K-dependent II, VII, IX, X synthesis; monitor INR. Citrate chelates Ca2+ in stored blood. <b>Hemophilia A:</b> factor VIII deficiency; B: IX deficiency; deep bleeding/hemarthroses and prolonged aPTT.' ]) sec('5. RENAL PHYSIOLOGY') topic('JGA, renal blood flow and GFR',[ '<b>JGA:</b> macula densa (distal tubule NaCl sensor), juxtaglomerular/granular cells (renin), extraglomerular mesangial cells. Low renal perfusion, low NaCl at macula densa and β1 stimulation release renin → angiotensin II → aldosterone.', 'Renal blood flow about 1.2 L/min, 20-25% of CO. Autoregulation at MAP roughly 80-180 mmHg by myogenic response and tubuloglomerular feedback. Sympathetic activity and angiotensin II decrease renal blood flow, particularly in severe hemorrhage.', '<b>GFR about 125 mL/min or 180 L/day.</b> GFR = Kf[(Pgc - Pbs) - (πgc - πbs)]. Increased by higher glomerular capillary pressure; reduced by increased Bowman space pressure or plasma oncotic pressure. Creatinine clearance estimates GFR; inulin clearance is ideal measurement.' ]) topic('Urine formation, concentration and countercurrent mechanism',[ 'Urine formation: glomerular filtration → tubular reabsorption → tubular secretion → excretion. PCT reabsorbs about 65% Na+/water, all glucose and amino acids normally. Loop, DCT and collecting duct fine-tune composition.', '<b>Countercurrent multiplier:</b> loop of Henle creates medullary gradient. Descending limb is water permeable; thick ascending limb actively reabsorbs Na-K-2Cl and is water impermeable. <b>Vasa recta:</b> countercurrent exchanger preserves gradient. Urea recycling augments inner medullary osmolality.', '<b>Concentrated urine:</b> high ADH → aquaporin-2 insertion in collecting duct → water reabsorption down medullary gradient. <b>Dilute urine:</b> low ADH, solute reabsorption continues while water remains in tubule.' ]) topic('Water reabsorption, diuresis and acidification',[ 'Water reabsorption: PCT obligatory isotonic reabsorption; descending limb; collecting ducts under ADH. ADH rises with increased plasma osmolality or low effective circulating volume. Thirst also protects water balance.', '<b>Diuresis:</b> water diuresis from low ADH/excess water; osmotic diuresis from nonreabsorbed solute such as glucose; pressure diuresis from raised arterial pressure.', '<b>Urine acidification:</b> H+ secreted in PCT, distal tubule and collecting duct. HCO3- is reclaimed; new HCO3- generated as H+ excreted as titratable acid (phosphate) and NH4+. Minimum urine pH about 4.5. Type A intercalated cells secrete H+; type B secrete HCO3-.' ]) topic('Cystometrogram and micturition',[ '<b>Cystometrogram:</b> plot of intravesical pressure against bladder volume. Initial slight rise then plateau due to stress relaxation; marked pressure rise near capacity. First desire around 150 mL, normal desire about 300-400 mL, capacity about 400-600 mL.', '<b>Micturition reflex:</b> bladder stretch receptors → pelvic nerves → sacral S2-S4 center → parasympathetic pelvic nerves contract detrusor and relax internal sphincter. Pontine micturition center coordinates voiding. External sphincter is voluntary via pudendal nerve.', 'Sympathetic hypogastric nerve promotes storage: β3 relaxes detrusor, α1 contracts internal sphincter. In infants reflex is automatic; cortical control develops later. Spinal lesions cause characteristic neurogenic bladder patterns.' ]) sec('LAST 20-MINUTE REVISION') table(['Formula / fact','Remember'],[ ['CO','HR × SV; normal about 5 L/min'],['MAP','DBP + 1/3 pulse pressure; equals CO × TPR'],['SV','EDV - ESV; normal about 70 mL'],['EF','SV/EDV × 100; around 60%'],['PR interval','0.12-0.20 s'],['GFR','about 125 mL/min; about 180 L/day'],['RBF','about 1.2 L/min; 20-25% CO'],['Dead space','anatomical about 150 mL'],['V/Q','average about 0.8'],['P50','about 26-27 mmHg'],['RBC life span','about 120 days'],['Platelet plug','vWF-GpIb adhesion; GpIIb/IIIa aggregation'],['PT / aPTT','extrinsic / intrinsic'],['Micturition','S2-S4 parasympathetic; pudendal external sphincter']], [4.4*cm,11.5*cm]) story.append(P('<b>Exam answer rule:</b> Definition → labeled diagram/flowchart → mechanism → regulation → functions/clinical relevance. Underline headings. Never leave a diagram unlabeled.','Box')) story.append(P('Prepared as concise revision notes from standard physiology principles. For exact wording and additional details, compare with your prescribed G.K. Pal text after the examination.','Sub')) doc=SimpleDocTemplate(OUT,pagesize=A4,rightMargin=1.45*cm,leftMargin=1.45*cm,topMargin=1.35*cm,bottomMargin=1.65*cm,title='Physiology Paper 1 Last-night Crash Notes',author='Orris') doc.build(story,canvasmaker=NumberedCanvas) print(OUT) ''') PY python "/tmp/workspace/physiology-paper1-crash-notes/src/create_pdf.py" python - <<'PY' from pypdf import PdfReader p='/tmp/workspace/physiology-paper1-crash-notes/output/Physiology_Paper_1_Last_Night_Crash_Notes.pdf' r=PdfReader(p) print('pages',len(r.pages),'size',__import__('os').path.getsize(p)) print((r.pages[0].extract_text() or '')[:300]) PY

python - <<'PY' from pypdf import PdfReader p='/tmp/workspace/physiology-paper1-crash-notes/output/Physiology_Paper_1_Last_Night_Crash_Notes.pdf' r=PdfReader(p) assert len(r.pages)==7 text='\n'.join(page.extract_text() or '' for page in r.pages) for term in ['CARDIOVASCULAR SYSTEM','RESPIRATORY SYSTEM','GASTROINTESTINAL PHYSIOLOGY','BLOOD AND IMMUNITY','RENAL PHYSIOLOGY','LAST 20-MINUTE REVISION']: assert term in text, term print('verified: 7 pages, all five modules and revision page present') PY