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33 Cards in this Set
- Front
- Back
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GFR proportional to |
Glomerular Filtration Pressure (GFP) |
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GFP formula |
GCP - CP - COP GCP = glomerular capillary blood pressure CP = Bowman's capsule hyrdostatic pressure COP = plasma colloid osmotic pressure (plasma oncotic pressure) |
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Factors affecting GFR |
Glomerular capillary blood pressure (depends largely on this) Capillary surface area Membrane permeability |
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Filtration coeffcient |
f(glomerular surface area, membrane permeability) |
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Main method of adjusting glomerular capillary pressure |
Changes in diameters of afferent and efferent arterioles |
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3 basic mechanisms for capillary blood pressure |
Autoregulation Sympathetic control Hormonal regulation |
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Autoregulation defn and function |
Intrinsic mechanism allowing kidneys to regulate own functions Function: to maintain constant capillary pressure in spite of changing arterial blood pressure i.e. to maintain relatively constant GFR and renal blood flow |
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Major site of autoregulation |
Afferent arteriole |
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Effective range of autoregulation |
90 - 180 mmHg |
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Two ways to adjust diameter of afferent arterioles |
Myogenic Tubularglomerular feedback |
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Myogenic method description |
Arteriole muscle can contract when stretched, resisting the increased aterial blood pressure |
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Tubuloglomerular feedback defn |
NaCl concentration dependent (detected at macula densa) Controls tone of afferent aretriole |
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GFR GCP feedback loop |
Reduced GFR = reduced NaCl detected at macula densa -> dilation of afferent arteriole -> increased GCP |
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Paracrine release by macula densa description |
ATP and adenosine cause constriction of afferent arteriole Reduces GFR Stimulates calcium release in afferent areteriole smooth muscle cells Part of tubuloglomerular feedback mechanism |
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When does sympathetic affect GFR |
Intense stimulation (circulatory shock or intense exercise) |
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Hormonal regulation method |
RAAS |
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RAAS involves homeostatis of: |
Na+ concentration Blood volume Blood pressure |
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Triggers for renin |
Decrease in Na+, blood volume, or blood pressure Sympathetic stimulation |
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Site of renin release |
Granular cells (juxtaglomerular cells) |
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RAAS pathway |
Renin enhances conversion of angiontensinogen from liver into angiotensin I ANG I is converted to ANG II by the lungs (ACE in pulmonary capillaries) ANG II is a potent vasoconstrictor |
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Vasopressin stimulated by |
Angiotensin |
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Angiotensin secreted/stored by |
Secreted by hypothalamus, stored and released from posterior pituitary |
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Angiotensin effects |
Increase vasopressing Increase thirst by osmoreceptors at supraoptic nucleus within hypothalamus Increases aldosterone release by adrenal cortex |
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Aldosterone increase results in |
Enhanced Na+ reabsorption in the DT and collecting duct |
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ANP activation |
Stretching of the atria |
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ANP effect |
Inhibits Na+ and H2O reabsorption by proximal tubule and collecting duct Inhibits aldosterone Causes relaxation of glomerular mesangial cells (contractile cells) (increases suface area of glomerulus) |
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ANG II effect on each arteriole |
@ low concentration: efferent have higher degree of constriction @ high concentration: equally potent to both afferent and efferent arterioles Due to limited receptors at efferent |
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Prostaglandin effect |
Minimal on GFR in healthy people When under stress and dehydration, PGE2 produced by kidneys PGE2 reduces vasoconstrictor effect to enhance blood flow and prevent damage |
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Medullary concentration depends on |
How loop of Henle functions Vasa recta circulation (countercurrent mechanism) Urea recycling |
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Factors increasing ADH |
Low water intake -> reduced blood volume -> reduced BP; increased osmolarity |
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Effect of ADH |
Increase water reabsorption at distal tubule and collecting duct |
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Arterial pressure sensed in |
Baroreceptors in carotid sinus and aortic arch |
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Why no NSAIDs for patient with renal ischemia |
Blocks prostaglandins, which reduces vasoconstrictive effect in afferent arterioles |
