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Physiology - Block 3 - Part 1

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davidwurbel7's version from 2015-11-19 22:02

Microcirculation

Question Answer
Almost entirely controlled via adrenergic nervesCutaneous Circulation
Increased skin temperature directly causes this, which increases heat lossVasodilatation
No significant change in PO2 & PCO2 . No change or slight decrease in pHArterial System During Exercise
Decrease in PO2 & increase in PCO2Venous System During Exercise
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Heart As A Pump

Question Answer
Volume of blood ejected by the ventricle depends on the volume of blood present in the ventricle at the end of diastoleFrank-Starling Law
The driving force for venous returnPressure Gradient
Negative intrathoracic pressure (Inspiration). Increase in total blood volume. Contraction of skeletal muscles, Increased venomotor tone. Lying postureFactors Increasing Venous Return
Relationship between right atrial pressure (RAP) and venous return (VR)Inverse Relationship
Point at which venous return equals 0Mean Circulatory (Mean Systemic) Filling Pressure
With 5 liters of blood circulating, the mean circulatory (mean systemic) filling pressure is equal to+7
Venous return with negative atrial pressure does not increase past 7L/minute due toCollapse of Veins
The collapse of veins connected to the atrial is due toNegative Atrial Pressure
Positive inotropic agents shifts the steady stateLeft and Up
Increased blood volume (IV infusion) shifts the steady stateRight and Up
Decrease blood volume (hemorrhage or dehydration) shifts the steady stateLeft and Down
Beta blockers and MI shifts the steady stateRight and Down
Increase in preload results in an increase inStroke Volume
There is an increase in this volume after ventricular filling because of an increase in preloadEDV
Decrease in preload results in an decrease inStroke Volume
There is an decrease in this volume after ventricular filling because of an decrease in preloadEDV
An increase in afterload results in an increase in this due to an increase in resistanceVentricular Pressure
An increase in afterload results in a decrease inSV
An increase in afterload results in an increase inESV
An increase in myocardial contractility results in an increase in this due to a greater force of contraction of the ventricularVentricular Pressure
An increase in myocardial contractility results in an increase inSV
An increase in myocardial contractility results in a decrease inESV
An increase in myocardial contractility results in an increase inEjection Fraction
Immediate effect of reduced contractility, there is a reduction inCO
Blood volume expansion has partially restored the CO by Starling’s mechanism; This gradually progresses to massive volume expansionCompensated Heart Failure
There is severe reduction in contractility despite extreme increase in preload, due to overstretching of ventricleDecompensated Heart Failure
ACE inhibitors, diuretics and beta blockers are administered forDecompensated Heart Failure
Cardiac output = O2 consumed by the whole body per minute / O2 content of systemic artery-O2 content of pulmonary arteryFick's Principle
This is likely to be present at a PCWP of >20mmHgAcute Pulmonary Edema
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EKG

Question Answer
Lead I, Lead II and Lead III aVR, aVL and aVFFrontal Leads
V1, V2, V3, V4, V5 and V6Horizontal Leads
The first part of the heart that undergoes depolarization firstEndocardium
The first part of the heart that undergoes repolarization firstEpicardium
Term for when a wave has half of the wave being positive deflection and half being negative deflectionEqualphasic
A depolarization wave is this type of wavePositive Wave
A repolarization wave is this type of waveNegative Wave
A positive wave moving toward the positivePositive Deflection
A positive wave moving away from the positiveNegative Deflection
A negative wave moving toward the positiveNegative Deflection
A negative wave moving away from the positivePositive Deflection
Inferior wall leadsLead I, II, and aVF
Lateral wall leadsLead I, aVL, V5 and V6
Septal leadsV1 and V2
Anterior wall leadsV3 and V4
The normal interval lasts 0.12 to 0.2 secondsPR Interval
Increase parasympathetic activity, use of beta blockers and Ca+2 channel blockers prolongs thisPR Interval
Wave with <0.04s duration and <25% the amplitude of the R waveNormal Q Wave
Wave is 25% or more of the height of the partner R wave and/or they are greater than 0.04 seconds in widthPathological Q Waves
Duration of 0.08 to 0.10 secondsQRS Complex
Usually horizontal or gently up-sloping in all leads. End of ventricular depolarization to start of ventricular repolarizationST Segment
Ventricular repolarization. Largely passive with high energy expenditure. Susceptible to both cardiac and non cardiac influences and therefore variable in appearanceT Wave
Start of atrial depolarization to start of ventricular depolarizationPR interval
End of atrial depolarization to the start of ventricular depolarizationPR segment
End of ventricular depolarization to start of ventricular repolarizationST segment
Start of ventricular depolarization to end of ventricular repolarizationQT interval
Time of ventricular depolarizationQRS interval
Normal 0.12-0.20 secPR interval
Normal 0.08-0.10 secQRS interval
Normal 0.32-0.43 secQT interval
Lead I positive, aVF positiveNormal Axis
Lead I positive, aVF negativeLAD
Lead I negative, aVF positiveRAD
Lead I negative, aVF negativeExtreme RAD
P wave greater than 2.5 mm wideP Mitrale
P mitrale is suggestive of thisLeft Atrial Enlargement
P wave greater than 2.5 mm highP Pulmonale
P pulmonale is suggestive of thisRight Atrial Enlargement
S wave in V1 is greater than or equal to 25 mmLVH
R wave in V6 is greater than or equal to 25 mmLVH
Sum of the height of the S wave in V1 and R V5 is greater than 35 mm is suggestive ofLeft Ventricular Hypertrophy
R wave in V1 is greater than or equal to 7 mmRVH
S wave in V6 is greater than or equal to 7 mmRVH
Sum of the height of the R wave in V1 and V6 is greater than 35 mm is suggestive ofRight Ventricular Hypertrophy
Prolonged PR interval (> 0.20 s). Slowed conduction through the AV node1st Degree Heart Block
Progressive lengthening of PR interval ending in one dropped beat2nd Degree Mobitz-Wenckebach Heart Block
No measurable lengthening of PR interval2nd Degree Mobitz-II Heart Block
No correlation between P waves & QRS complexes3rd Degree Heart Block
Sycopal episodes due to 3rd degree heart blockStokes-Adams Syndrome
Multiple foci of impulse generation in atria. ECG shows multiple, low voltage, irregular P waves. A few impulses reach ventricle producing QRS waves. Produces an irregular rateAtrial Fibrillation
This determines the ventricular rate in A-fibAV Refractory Period
Complications of A-fibEmbolization
Treatment for this includes rate control and cardioversion with drugs or electricityAtrial Fibrillation
Depression of ST segment; T wave inversionAngina Pectoris
Tall T waves (defective repolarization). Long PR interval (increased AV delay). Prolonged QRS (altered excitability)Hyperkalemia
Flat or low amplitude T waveHypokalemia
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Renal BF & GFR

Question Answer
Red cells in urineHaematuria
Protein in urineProteinuria
Albumin in urineAlbuminuria
Large volume of urine, >3L/dayPolyuria
Small volume of urine, < 400ml/dayOliguria
Less than 50ml/dayAnuria
Generalized edemaAnasarca
Accumulation of nitrogenous wastesUremia
Renal insufficiencyRenal Failure
Build up of azole groups or nitrogen in the bloodAzotemia
Syndrome of very severe renal failure in which there is a need for dialysisUremia
Mainly contains glomeruli & tubulesRenal Cortex
Mainly contains long loops of Henle, terminal regions of collecting ducts & vasa rectaMedulla
Functional unit of kidneyNephron
Filtration of plasma occurs hereRenal Corpuscle
Reabsorption, Secretion occurs hereRenal Tubule
Carry the reabsorbed substances back to general circulation. Secrete substances into tubules. Provide blood supply like in any other organ. Helps to maintain the osmotic gradient in medullary interstitiumPeritubular Capillaries
Branch off of the interlobular arteryAfferent Arteriole
Continuation of the efferent arteriole that terminates in the interlobar veinPeriitubular Capillaries
7/8 of all nephrons. Glomeruli in outer cortex. Short loops of Henle that descend only till outer medullaCortical nephron
Tubules in cortex supplied by peritubular capillaries. Peritubular capillaries are essential for tubular transportCortical Nephron
1/8 of all nephrons. Glomeruli at corticomedullary junction. Long loops of Henle that descend deep into inner medullaJuxtamedullary Nephron
Have vasa recta in addition to peritubular capillaries. Vasa recta lie parallel to LOH & have a hairpin turn. Vasa recta serve as counter-current exchangers essential for production of concentrated urine. Essential for urine concentrationJuxtamedullary Nephron
Structure consisting of glomerular capillaries and Bowman's capsuleRenal Corpuscle
Plasma filtered into the Bowman's spaceGlomerular Filtrate
Fluid within the tubulesTubular Fluid
Persons with long standing diabetes, these cells can die offJuxtaglomerular Cell
Function is ultrafiltration of bloodGlomerulus
Concentration of small solutes in the filtrate in the glomerulus is equal to the concentration of small solutes herePlasma
Granular cells, Extraglomerular mesangial cells and Macula densa are components ofJuxtaglomerular Apparatus (JGA)
Modified epithelial cells of early DCTMacula Densa
Cell located in the afferent arterioleGranular Cells
Autoregulation of the glomerular filtration of the single nephron byTubuloglomerular Feedback
The rate at which plasma is filtered into Bowman’s capsules of all functioning nephrons of both the kidneysGlomerular filtration rate (GFR)
115 -125 mL/minNormal GFR per Minute
180 L/dayNormal GFR per Day
Basement membrane repels negatively charged large solutes such proteins becauseNegative Charge
Loss of negative charges, causes leakage of proteins into filtrate resulting in proteinuria, hypoalbuminemia & edemaMinimal Change Disease
Proteinuria greater than 3.5 g/dayNephrotic Syndrome
Most important factor favoring filtrationHydrostatic Pressure in Glomerular Capillary
Kf (P[gc] - [P[bs]) - (π[gc] - π[bs]) GFR
Increases when there is obstruction to urine flowHydrostatic Pressure in Bowman’s Space (P[bs])
Determined by the plasma protein concentration of glomerular capillary blood and is the force opposes filtrationGlomerular Capillary Oncotic Pressure (π[gc])
Agents that relax mesangial cells that increases GFRANP and Dopamine
Agents contract mesangial cells that decreases GFRA-II, NE, and Arginine Vasopressin (AVP)
Potent vasoconstrictor of both afferent & efferent arterioles. But Efferent arterioles are more sensitiveAngiotensin II
Increase RBF by vasodilation locallyProstaglandins
Increases RBF by causing renal vasodilation, but at high doses also constricts skeletal muscle & cutaneous arteriolesDopamine
An increase in Na+ Cl- flow through the DCT cause these cells to secrete adenosineMacula densa
An increase in Na+ Cl- flow through the DCT cause macula densa to secrete thisAdenosine
GFR / RPFFiltration Fraction
0.15 to 0.20Normal Filtration Fraction
15% - 20% Normal Filtration Fraction
Decreases RPF and increases GFR & therefore, increases FFEfferent arteriolar constriction
Decreases RPF and decreases GFR & therefore, same FFAfferent arteriolar constriction
Decrease in both RBF & GFR. Decrease in RPF is more than the decrease in GFR, increases FFSympathetic Stimulation
Increase P[bs] and decreases GFR. RPF is unaffected. Overall decrease in FFConstriction / Obstruction of the Ureter
Increase π[gc] and decreases GFR. RPF is unaffected. Overall decrease in FFIncreased Plasma Protein Concentration
Decrease in π[gc] and increase GFR. RPF is unaffected. Overall increase in FFDecreased Plasma Protein Concentration
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