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USMLE Step 1 Physiology
The document contains a comprehensive overview of various cardiovascular and respiratory mechanisms, including blood flow dynamics, pressures, and gas exchange principles. It discusses concepts such as cardiac output, stroke volume, and the effects of different factors on vascular resistance and compliance. Additionally, it covers renal function, hormonal influences on metabolism, and the physics behind capillary filtration and reabsorption.
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USMLE Step 1 Physiology
- 2. 𝑉 = 𝐴 𝐶 𝑂𝑆𝑀 =2 𝑁𝑎 + 𝐵𝑈𝑁 2.8 + 𝐺𝑙𝑢𝑐𝑜𝑠𝑒 18 𝑄𝑓 = 𝑘 𝑃 𝑐 + 𝜋𝑖𝑓 − (𝑃𝑖𝑓 + 𝜋 𝑐) 𝐵𝑙𝑜𝑜𝑑 𝑉𝑜𝑙𝑢𝑚𝑒 = 𝑃𝑙𝑎𝑠𝑚𝑎 𝑉𝑜𝑙𝑢𝑚𝑒 1 − 𝐻𝑒𝑚𝑎𝑡𝑜𝑐𝑟𝑖𝑡 ∆𝑃 = 𝑃1 − 𝑃2 P1= Upstream pressure P2= Pressure at the end 𝑄 = ∆𝑃 𝑅𝑒𝑠𝑖𝑠𝑡. Q= Flow ∆𝑃= Pressure Gradient 𝑆𝑉 = 𝐸𝐷𝑉 − 𝐸𝑆𝑉 EDV= End diastolic volume ESV= End systolic volume 𝑅𝑒𝑦𝑛𝑜𝑙𝑑′ 𝑠 # = (𝐷𝑖𝑎𝑚𝑒𝑡𝑒𝑟)(𝑉𝑒𝑙)(𝐷𝑒𝑛𝑠𝑖𝑡𝑦) 𝑉𝑖𝑠𝑐𝑜𝑠𝑖𝑡𝑦 >2000 = Turbulent flow <2000 = Laminar flow 𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 = 𝑣𝐿 𝑟4 V= Viscosity R= Radius 50% = 16x 𝐶𝑂 = 𝑀𝐴𝑃 𝑇𝑃𝑅 MAP= Mean arterial pressure TPR= Total Peripheral Resistance 𝐶 = ∆𝑉 ∆𝑃 C = Compliance ∆ = Change veins arteries
- 3. 𝐹𝑙𝑜𝑤 = 𝑂𝑥𝑦𝑔𝑒𝑛 𝑈𝑝𝑡𝑎𝑘𝑒 𝐴𝑟𝑡𝑒𝑟𝑦𝑂2 − 𝑉𝑒𝑖𝑛 𝑂2 Blood flow in an organ 𝐶𝑎𝑟𝑑𝑖𝑎𝑐 𝐼𝑛𝑑𝑒𝑥 = 𝐶𝑂 𝐵𝑆𝐴 BSA= Body Surface Area 𝑉 𝐸 = 𝑉𝑇 × 𝑓 VE= Total Ventilation VT= Tidal volume F= Respiratory rate 𝑉 𝐴 = 𝑉 𝑇 − 𝑉𝐷 𝑓 VA= Alveolar ventilation VD= Dead space 𝑃𝐼𝑂2 = (𝑃𝑎𝑡𝑚 − 𝑃𝐻2 𝑂)𝑓𝑂2 PIO2 = Partial pressure of inspired gas PH2O = Partial pressure of H2O vapor (47) 47 𝐷𝑖𝑓𝑓𝑢𝑠𝑖𝑜𝑛 = 𝑆𝐴 × ∆𝑃 × 𝑆𝑜𝑙 𝑇√𝑚𝑊 SA = Surface Area Sol = Solubility T= Membrane thickness mW= Molecular weight 𝑃 𝐴 𝐶𝑂2 = 𝑀𝑒𝑡𝑎𝑏𝑜𝑙𝑖𝑠𝑚 𝐴. 𝑉𝑒𝑛𝑡𝑖𝑙𝑎𝑡𝑖𝑜𝑛 𝑃 𝐴 𝑂2 = 𝑃𝑎𝑡𝑚 − 47 𝑓𝑂2 − 𝑃𝐶𝑂2 𝑅 Patm= Atmospheric pressure f= fraction of Oxygen in the air (21%) R= Gas constant (0.8-1) 𝐹𝐹 = 𝐺𝐹𝑅 𝑅𝑃𝐹 FF= Filtration fraction GFR= Glomerular Filtrat. RPR= Renal Plasma Flow 600 12020% 𝐹𝑖𝑙𝑡𝑒𝑟𝑒𝑑 𝐿𝑜𝑎𝑑 = 𝐺𝐹𝑅 × 𝑃𝑥 Px = Free concentration of substance in plasma
- 4. Concentration of Solute VolumeVolume HYPO-osmolar HYPER-osmolar ECFICFPlasma 300 mOsm/L 300 mOsm/L Cell Dehydration
- 5. Loss of IsotonicFluid Hemorrhage Loss of Hypotonic Fluid Diabetes Insipidus, Sweating or Dehydration Gain of Isotonic Fluid Gain of Hypotonic Fluid Gain of Hypertonic FluidLoss of Hypertonic Fluid Adrenal Insufficiency
- 6. FILTRATION Hydrostatic Pressure Pc= CAPILLARY push out Oncotic force π = INTERSTITIUM pull out ABSORPTION Oncotic force π = CAPILLARY pull IN Hydrostatic Pressure Pc= INTERSTITIUM push IN Capillary Interstitium Interstitium 𝑄𝑓 = 𝑘 𝑃 𝑐 + 𝜋𝑖𝑓 − (𝑃𝑖𝑓 + 𝜋 𝑐) Forces of Filtration -Hydrostatic pressure If is opposing filtration
- 7. V Pc Increased blood flow,venous pressure Elevated blood volume, Left ventricle failure Pulmonary edema –Wedge up (cardiogenic) πif Thyroid dysfunction Fluid accumulation Non-pitting edema πc Liver failure (Cirrhosis) Nephrotic syndrome Congestive Heart Failure K (capillary permeability) Circulating agents, eg. TNF-alpha, bradykinin, histamine, cytokines Increase fluid filtration - edema 𝑉 = 𝐴 𝐶 𝑉 = 300𝑚𝑔 0.05 𝑚𝑔 𝑚𝑙 = 6000 𝑚𝑙 TRACERS Plasma: Albumin ECF: Inulin Total body water: Urea
- 8. • Follow theconcentration gradient. • Continuous. • Not affected by action potential. • ALWAYS open (K+) • Depends on + or – charges • Creates and affected by action potential. • Create concentration differences. • FAST (Na+) Closed at rest • SLOW (K+ and Ca++) • Protein transporter • Neuromuscular junction Ca+ • It’ll take an electrical stimulus and turn it into a chemical stimulus. Ungated
- 9. Low Cl- High K+ LowNa+ -90mV High Cl- Low K+ High Na+ Na K ATP
- 10. Depolarization: Rapid fluxof Na+ into the cell Repolarization: Na+/K+ ATPase pump Hyperpolarization: K+ leaves the cell, becomes more negative 2- Absolute Refractory Period – NOTHING will incite a response 4- Relative Refractory Period – needs GREATER than normal stimulus Na+ channels close
- 11. SA node ActionPotential 4 4 0 3 OR Slow influx of Ca+
- 12.
- 13. 25mm/sec P Q R S T PR QRS QT ST T Atrium Depolarization Ventricular Depolarization Repolarization SAto AV 0.12 sec 0.35-0.44 - Arrythmias Phase 0 Phase 3 200 ms 300 150 100 75 60 50 40 40 ms
- 14. Lead-AVF Lead-I Lead+I Lead+AVF Lead-AVF Lead-I Lead+I Lead+AVF Lead-AVF Lead-ILead+I Lead+AVF Lead-AVF Lead-I Lead+I Lead+AVF Voltages: Lead +I Lead +AVF Normal axis Voltages: Lead +I Lead -AVF Left axis Voltages: Lead -I Lead +AVF Right axis Extreme right axis Left axis deviation Right axis deviation Normal
- 15. PR progressively lengthensand drops PR Drops all of a sudden Atrium (60-100) and Ventricle (30-40) have a complete dissociation, beat independently. Bradycardia
- 16.
- 17. Determined by Venousreturn and End Diastolic Volume 120 ml of Blood = Optimally filled
- 18. X Ventricular Preload SystolicPerformance C A N B E D F IVIII Decreasespreload and performance - Preload but + performance = + contractility All points in the same line (D, C, E) have the same contractility Increase contractility Decrease contractility On different lines CO = Preload + Contractility + Preload and + performance = - contractility.
- 19. Heart Dysfunction Diastolic Filling dysfunction (Venous return) Hemorrhage Preload defects Hypertrophic Restrictive Systolic Pressurefactors Increased TPR Increased afterload Hypertension = Concentric Hypertrophy Obstruction Aortic Stenosis Volume factors Increased End Diastolic Volume Aortic insufficiency Mitral insufficiency Eccentric Hypertrophy Increased backflow
- 20.
- 21. Pulmonary circuit hasa high compliance and low resistance. CO % Lungs: 100% Liver: 25% Kidneys: 20% Brain: 15% Heart: 5% Cardiac AV difference is very large = Large extraction.
- 22. Flow equal atALL points. Total resistance is equal to the SUM. Adding resistances will increase the total. Within organs Flow is independent from each other NOT equal at all times, it varies. There is no summation of resistances. Total is always LESS than any of the resistances Between organs (if subtracts one, R increases) 1 𝑅𝑇 = 1 𝑅1 + 1 𝑅2 + 1 𝑅3 𝑅𝑇 = 𝑅1 + 𝑅2 + 𝑅3
- 23. Pulse Pressure Systolic Cardiac Output HeartRate Stroke volume Compliance Diastolic TPR Radius Compliance ACEIs Alpha blocker Calcium channel blocker Increases as you go DISTALLY from the heart.
- 24. Intrinsic Regulation -Metabolites Coronary Circulation Adenosine Vasodilates Cerebral Circulation Pa Co2 Exercising Skeletal Muscle Lactic Acid - Vasodilates Systolic Diastolic MAP Kidneys Under normal circumstances. Eg. Hemorrhage
- 25. Extrinsic Regulation SkinResting Muscle CNS– alpha receptors Other – Angiotensin and Beta 2
- 26.
- 27. System Blood flow MAP TPRBlood volume # Perfused capillary Capillary surface area PO2 PCO2 Temp pH Preload Pulmonary Circuit Gas exchange Arterial system Severe Venous system Exercising muscle Filtration Pressure Skin Coronary / Heart Severe Cerebral Renal and GI
- 28. Normal Pressure tracing 80 Diastole (VFilling) Systole S1 S2 15
- 29. EKG Event ValveSound Sound abnormality P Atrial depolarization Mitral Opening S3 and S4 S3 – Volume overload S4 – Stiff ventricle QRS Ventricular depolarization Mitral Closure S1 PR interval AV node conduction None None T wave Ventricular repolarization Aortic Valve (1st), Pulmonary valve closure (2nd) S2 Widening – Pulmonic stenosis, Right bundle branch block. Fixed – ASD, L-R shunt Paradoxical – Left Bundle branch block, Aortic stenosis. ST interval Ejection phase Aortic Opening None
- 30. . A P. 2-3rd 5-6th . Aortic Pulmonary Tricuspid Mitral Close at beginning of S Open at beginning of D Close at beginning of D Open at beginning of S Sounds are generated at the time of closure. S1 beginning of systole S2 beginning of diastole Stenosis – Anterograde Insufficiency – Retrograde MT A: Systolic – Aortic stenosis P: Systolic – Mitral insufficiency T: Systolic – Tricuspid insufficiency T: Diastolic – Tricuspid stenosis M: Diastolic – Mitral stenosis and aortic insufficiency T P
- 31. Murmur Systolic Patent Ductus arteriosus Holosystolic Machine like murmur Bicuspidaortic valve Early systolic High-frequency click Right 2nd interspace Hypertrophic Cardiomyopathy Crescendo- decrescendo murmur Between apex and left sternal Radiates to the suprasternal notch Louder standing up Aortic Stenosis Early Systolic Click, ejection Crescendo- decrescendo murmur Pulse late and weak Old age / Rheumatic F. Congenital Bicuspid valve Angina, syncope, CHF Pulmonary Stenosis Tetralogy of Fallot Harsh ejection murmur Systolic thrill Mitral Regurgitation Pansystolic blowing Louder w/ squatting Radiates to axilla Increases After load Acute Rheumatic Fever MV Prolapse complication Libman-Sacks endocarditis Mitral Valve Prolapse Myxoid degeneration Late-systolic Click Marfan syndrome Ehlers-Danlos Decreases w/squatting Tricuspid Regurgitation Pansystolic Increase right heart Flow Taking a Deep breath IV drug users w/ endocarditis Dilated cardiomyopathy Septal Defects Ventricular Harsh Holosystolic Atrial Fixed Splitting of S2 (Aortic and Pulmonary closure) Diastolic Aortic Regurgitation Blowing murmur Widened pulse pressure Aortic root dilation Infectious Endocarditis Aortic root aneurysm Decreases in intensity Pulmonary Regurgitation Mitral Stenosis Opening snap Chronic Rheumatic Fever Diastolic Rumble Mid-late murmur Gradual decrease in mid-late Tricuspid Stenosis Mid-late murmur
- 32. A: Right atrialcontraction - depolarization C: Bulging of tricuspid valve during right ventricular contraction (uncommon) X: Right atrial relaxation (filling) V: Inflow of venous blood into the atrium during ventricular systole. Y: Filling of the right ventricle, after opening the tricuspid. Jugular Venous Tracing
- 33. Normal Tracing AtrialFibrillation Tricuspid Insufficiency Tricuspid Stenosis Loss of x descent – Not enough time for veins to empty Blood backs up into the RA, increases pressure. Loss of x descent – Pressure in the atrium will increase
- 34. Volume Pressure Ejection Isovolumetric ContractionIsovolumetric relaxation Filling Aortic valve closes Aortic valve opens Mitralvalve opens Mitral valve closes Stroke Volume ESV EDV Pressure Volume Loops Aortic Insufficiency: Increased preload, increased SV, increased pressure. Systolic Heart Failure: Increased preload, decreased pressure. Essential Hypertension: Increased pressure, little change in preload. Increased Contractility: Decreased preload, increased ejection fraction, increased pressure. Exercise: Increased preload, increased ejection fraction, increased pressure. Preload Afterload Aortic Stenosis: Increased afterload, little increase in EDV, increased pressure, little increase in SV
- 35. >120 Aortic valve pathology +PressureGradient = Aortic stenosis -Pressure Gradient= Aortic Insufficiency >15 Mitral valve pathology Diastole (V Filling) Systole When? Diastole = Mitral stenosis Systole = Mitral Insufficiency S1 S2
- 36. 𝑇𝐿𝐶 = 𝑉𝐶+ 𝑅𝑉 𝑇𝐿𝐶 = 𝐹𝑅𝐶 + 𝐼𝐶 RATE DEPTH Conducting More CO2 Less O2 Low pH Respiratory Less CO2 More O2 High pH
- 37. DEAD SPACE CONDUCTING PO2 =100 PCO2 = 40 PN2 = 600 PH2O = 47 RESPIRATORY ZONE PO2 = 100 PCO2 = 40 PN2 = 600 PH2O = 47 End of Expiration End of Inspiration Same composition as respiratory zone (CO2) O2, N2, H20. NO CO2 in normal atmosphere Patm = 0Patm = 0 PA = +1 PA = 0 PA = -1 During mid-Inspiration P = -4 P = -8 Recoil = +8Recoil = +5 RESTRICTIVE diseases OBSTRUCTIVE diseases
- 38. Pressure is inverseto Volume Ventilation: Blood Flow: Increased O2 Ventilation: Blood Flow: Increased CO2
- 39. 𝐶 = ∆𝑉 ∆𝑃 A B Ageing RD Syndrome /Atelectasis
- 40.
- 42.
- 43. Alveolar Ventilation Chemoreceptors Central Medulla of the brain Maindrive of VA in normal circumstances Monitor PaCO2 H+ ions Peripheral Around the carotid sinus and Aortic arch Take over in severe decrease in PaO2 Monitor PaO2 PaCO2 (less) Excess in Meningitis Suppressed in Opiates OD Room air 21% of O2 <1% of CO2
- 44. PAO2 - PaO2difference = 0-5 mmHg Hypoxia Hypoventilation Decreased PaO2 A-a = 0 Decrease in Alveolar vent. TX= Oxygen Diffusion Impairment Decreased PaO2 A-a = > 0 Lung Fibrosis Give 100% O2 and redo. Perfusion Limited Situation Decreased PaO2 A-a = > 0 Pulmonary Shunt (Atelectasis) Equilibrium capillary – interstitium Significant Increase (>10) = Diffusion Impairment No Significant Increase (<10) = Pulmonary Shunt
- 45. If Glomerular CapillaryPressure goes up = Increase in GFR, if it goes down = decrease in GFR PGC PBS πGC πBS 8 mmHg 45 mmHg 0 mmHg24 mmHg - + - Freely filtered (1.0) Electrolytes (Na+,Cl-,K+,HCO3) Metabolic waste (urea) Metabolites (glucose, aa) Non-natural substances (inulin, PAH) Low-weight proteins (insulin)
- 47. If the substancehas the same dynamics or use the same transporter but nothing changes while adding one or other, they have to be transported by simple diffusion. Facilitated transport FASTER TM = Transport Maximum Secondary active transport: Depends indirectly on ATP as a source of energy. Eg. Cotransport of Na-glucose in PCT ATP is consumed directly by the protein UREA is freely filtered, flow dependent.
- 48. (mg/ml) GFR= 120 ml/min Ifyou decrease GFR, you decrease the filter load of glucose and increases the threshold. In pregnancy GFR is elevated, so T is lower. Glucose will appear in the urine at a lower concentration. 𝐹𝐿 = 𝐺𝐹𝑅 × 𝑃𝐺𝐶 FL = Filter load PGC = Plasma Glucose Concentration 𝐸 = 𝑈𝑥 × 𝑉 E = Excretion Ux = Urine concentration of substance V = Urine flow rate
- 49. 20% 120 ml/min 80% 480 ml/min 100% 600ml/min Protein Inulin = GFR Na, K, Urea PAHGlucose, Bicarbonate Creatinine
- 50. 600 200 100 0 Inulin PAH Creatinine Glucose Volume filtered in Bowman’sCapsule 80% delivered to peritubular capillaries Plasma Concentration (mg/dl) Zero clearance at lower concentrations Carrier Saturation, no longer 100% filtered
- 51. 60% Retained at thePCT Osmotic Gradient Diluting segment – Greatly decreases Osm K+ Na+ H+ 5a 5b Aldosterone Lithium Clearance Na+ K+ 40 ml/min Urea PTH Phosphate Vitamin D Ca++ Inhibits K+ Inhibits
- 52.
- 53. Acidosis Alkalosis Compensation pHLow High Respiratory PCO2 High Low Only Renal Metabolic HCO3 Low High Ac. Hyperventilation Alk. Hypoventilation Renal If both present: Mixed pH: 7.4 HCO3: 24 mEq/L PCO2: 40 mmHg Renal Compensation: Lowers plasma HCO3 by excreting it Raises HCO3 by generating new 𝑁𝑎 + = 𝐶𝑙 − +𝐻𝐶𝑂3 − Plasma Anion Gap 140 108 24 132
- 55.
- 56. 1. Fast –Short half-life 2. Non-protein bound (except IGF) 3. Excreted in urine 4. Activates a protein 5. Have second messengers 1. Slow – Long half-life 2. Protein bound (except for DHEA) 3. Not excreted 4. Makes a protein 5. Pulsatile (except Thyroid) Regulated Feedback Inhibition Effect on an organ
- 57. Permissive Action Growth HormoneThyroid Glucagon,CatecholaminesCortisol Fast, Arginine and hypoglycemia stimulates it. Elevated during sleep Overnight Dexamethasone suppression test Elevated in the morning TRH Thyrotrophs (10%) TSH CRH Corticotrophs (10-25%) ACTH GnRH Gonadotrophs (10-15%) LH, FSH GHRH Somatotrophs (50%) GH SST Dopamine Lactotrophs (10-15%) Prolactin TRH (elevated) + + + + + - -
- 58. Stress Hormones 1. GrowthHormone – Increases protein formation from A.A. 2. Glucagon – Takes aminoacids and uses for gluconeogenesis 3. Epinephrine – No effect on proteins 4. Cortisol – Promotes degradation on proteins Anabolic Hormones 1. Thyroid hormone 2. Growth Hormone 3. Insulin 4. Sex Steroids (mainly Testosterone) Raises: Glucose Free fatty acids Lipolysis
- 59. Zona Glomerulosa Zona Fasciculata ZonaReticularis Capsule Medulla ACTH Cortisol and Androgens Aldosterone 80% Epinephrine 20% Norepinephrine Angiotensin II, K+ ANS REGION HORMONES CONTROLLED BY
- 60. Cholesterol Pregnenolone Mineralocorticoid (11-deoxycorticosterone) Cortisol Sex Steroids Mineralocorticoid (Aldosterone) 21-h21-h11-h 11-h 21-hydroxylase deficiency VS 11-hydroxylase deficiency SALT-WASTING sx with Hyperkalemia and Hypovolemia, Hypertension 17-h LDL Acetate Glomerulosa Fasciculata Reticularis Conn Syndrome – Hypertension + Hypokalemia Deficient in ALL of them. Lack of feedback inhibition leads to Increased ACTH
- 61. Plasma Osm UrineOsm Plasma ADH Urine Osm Post- desmopressin Normal 297 814 Elevated 815 Central Diabetes Insipidus 342 102 Decreased 622 Nephrogenic 327 106 Elevated 118 1 mg overnight dexamethasone High dose dexamethasone ACTH level Suppressed Normal Pituitary source Adrenal source (feedback inh) Not Suppressed Hypercortisolism Ectopic ACTH, adrenal tumor Pituitary or Ectopic source
- 63. Insulin • Protein Synthesis •Glycogenesis • Lipogenesis • Glucose Oxidation (muscle) • Increases glucose • Increases fatty acids • Increases IGF – make proteins Glucagon • Ureagenesis (protein metabolism) • Glycogenolysis • Lipolysis • Gluconeogenesis • Ketogenesis (fatty acids metabolism) • Insulin secretion Growth Hormone
- 64. Dihydrotestosterone in thebaby: Makes penis, prostate and scrotum Dihydrotestosterone in the adult: Male pattern baldness and BPH Testosterone in the baby: Vas deferens, seminal vesicle, epididymis. Testosterone in the adult: Maintains Sertoli cells - semen Leydig Sertoli / Semen Leydig Both Müllerian Inhibiting Factor: Inhibits growth of female internal structures. Leydig makes Estradiol
- 65. Variable 14 Days Yellow LH- - Estrogen + - β-HCG rescues corpusluteum during pregnancy
- 66. Hormone Source StimulusStomach Motility and Secretion Pancreas Gallbladder Secretin S cells lining duodenum Acid entering duodenum, activates CFTR via Gs Inhibits Stimulates fluid secretion (HCO3) and Bile into bile canalicular ducts. CCK Cells lining duodenum Fat, peptides and amino acids entering duodenum Inhibits emptying Stimulates enzyme secretion (Amylase, lipase, protease) 1. Contraction 2. Relaxation of Oddi Sphincter Gastrin (ACh) Feedback inhibition with acid or SST G cells of the stomach Stomach distension (stretch) Stimulates motility Antrum Parasympathetic (GRP), Peptides (protein) Activates Pepsin, acid production Duodenum Stomach and acid inhibits GIP (Gastric inhibitory peptide) GLP Duodenum Fat, Carbohydrates, amino acids Inhibits High increase of insulin, decreases glucagon All four hormones stimulate Insulin release. CCK, GIP and Secretin increase pyloric constriction, slow stomach emptying.
- 67. Duodenum – Fluidremains isotonic. Absorption of ions and water-soluble vitamins begin. Iron (ferritin) and Ca+ absorption (calbinding and calcitriol). Jejunum –Net reabsorption of ions and water- soluble vitamins. Ileum – Net reabsorption of water, Na+, Cl- and K+. Secretion of HCO3 Distal Ileum – Reabsorption of bile salts and Intrinsic factor with Vitamin B12 Colon – Doesn’t have digestive enzymes. Net reabsorption of water and NaCl. Target for Aldosterone, increases Na+ and water reabsorption and K+ secretion.