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CVPR > CVPR Week 7: Hemodynamics > Flashcards

CVPR Week 7: Hemodynamics Flashcards

1
Q

Objectives

A
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2
Q

Question 1

A

D. Angiotensin

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3
Q

Question 2

A

A. β adrenergic receptors

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4
Q

Question 3

A

I think it is B but not 100%

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5
Q

Identify

A
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6
Q

Identify

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7
Q

Identify

A
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8
Q

Determinants of renal blood flow

A
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9
Q

Renal blood flow % of CO

A

20%

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10
Q

Pressure in renal arteries

A
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11
Q

Renal capillaries properties

A
  • Highly fenestrated capillaries have a high degree of permeability
  • Two distinctly different capillary beds arranged in series
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12
Q

Distinct capillary beds of the renal system

A
  • Glomerular capillaries
  • Peritubular capillaries
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13
Q

Glomerular capillaries function

A

Filtration

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14
Q

PEritubular capillaries function

A

Reabsorption

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15
Q

Juxtoglomerular cells location

A
  • Afferent arteriole
  • abut closely to the distal tubule
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16
Q

Identify

A
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17
Q

Juxtaglomerular cells structure

A

Modified smooth muscle cells

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18
Q

Juxtaglomerular cells function

A

Produce and secrete renin

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19
Q

Identify

A
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20
Q

Identify

A
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21
Q

Vasa Recta Capillaries function

A
  • Supply medullary blood flow
  • maintain concentration gradient in the renal medulla
  • Delivers nutrients
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22
Q

Vasa Recta Capillaries location

A

Form long loops paralleling loops of Henle

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23
Q

Identify

A

Vasa Recta Capillaries

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24
Q

Vasa Recta Capillaries % of renal blood flow

A

10% of renal blood flow

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25
Q

Control mechanisms of renal blood flow

2 listed

A
  • Intrarenal (Autoregulation)
  • Extrarenal (extrinsic regulation)
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26
Q

Intrarenal regulation AKA

A

Autoregulation

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27
Q

Autoregulation of renal blood flow AKA

A

Intrarenal

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28
Q

Autoregulation of renal blood flow mechanisms and effects

A
  • Myogenic tone
  • Tubuloglomerular feedback

Maintain constant RBF & GFR almost constant when arterial pressure changes

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29
Q

Extrinsic regulation of renal blood flow AKA

A

Extrarenal

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30
Q

Extrarenal regulation of renal blood flow AKA

A

Extrinsic regulation

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31
Q

Extrinsic regulation of renal blood flow mediators & effects

A
  • Sympathetic nerves
  • Renin-angiotensin system
  • Other hormone regulators

Regulate renal function to maintain whole body fluid homeostasis

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32
Q

Renal autoregulation

A
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33
Q

Myogenic tone

34
Q

Myogenic tone is affected by?

A
  • Myogenic tone is independent of extrarenal forces
  • Stretch stimulates VSMC contraction
36
Q

Identify

37
Q

Identify

38
Q

Identify

40
Q

Role of the sympathetic nerves in renal extrinsic regulation

41
Q

Vascular smooth muscle cells sympathetic receptors for renal vasculature

A

α adrenergic receptors

42
Q

Identify

43
Q

Juxtaglomerular cells sympathetic receptors

A

Juxtaglomerularcells contain β1 adrenergic receptors

44
Q

sympathetic effects on juxtaglomerular cells

A

Stimulate renin release

Leads to formation of angiotensin II

45
Q

Identify

46
Q

Identify

47
Q

Hypoxia activation of SNSA does what?

A

Affects renal function

48
Q

Organ systems affected by SNSA

A
  • Kidneys
  • Vascular smooth muscle
  • Endocrine
49
Q

Kidney effects of SNSA

A
  • Constricts afferent and efferent arterioles t decrease renal blood flow
  • Potently increases Na+ reabsorption in the proximal tubule
  • Large activation decreases GFR
50
Q

Vascular smooth muscle effects on SNSA

A
  • Constricts arteries to decrease renal blood flow
51
Q

Endocrine effects of SNSA

A

Stimulates renin secretion (β1 receptors) to increase levels of angiotensin II and vasopressin

52
Q

Describe the Renin-Angiotensin System

53
Q

Effects of activating the Renin-Angiotensin system

5 listed

A
  • Thrist
  • Vasoconstriction
  • Water reabsorption
  • Sodium reabsorption

results in increased extracellular fluid volume

54
Q

Summary of the Renin-Angiotensin system

55
Q

Describe the juxtaglomerular apparatus

56
Q

Mediators of the RAS

A
  • SNSA
  • Aldosterone
  • ADH
57
Q

SNSA AKA

A

Sympathetic nervous system activation

58
Q

RAS AKA

A

Renin-Angiotensin System

59
Q

Aldosterone effects on RAS

A

Aldosterone increases distal tubulue Na+ reabsorption

  • Increases Na/K-ATPase activity in distal tubule basolateral membrane
  • Increases lumiinal membrane Na+ and K+ permeability
60
Q

ADH effects on the RAS

A

ADH causes water reabsorption

  • Stimulates water reabsorption in the collecting duct
  • Increases urea reabsorption in the collecting duct
61
Q

Effects of Angiotensin on vascular smooth muscle

A

Causes constriction of arteries increasing peripheral resistance resulting in increased arterial blood pressure

62
Q

Effects of Angiotensin on the central and peripheral nervous systems

A

Facilitate sympathetic transmission resulting in:

  • constriction of arteries leading to increased peripheral resistance leading to increased arterial blood pressure
  • increased cardiac output resulting in increased arterial blood pressure
63
Q

Effects of Angiotensin on Adrenal cortex

A

increased aldosterone secretion leading to increased sodium reabsorption leading to increased sodium & water reabsorption leading to increased cardiac output resulting in increased arterial blood pressure

64
Q

Effects of Angiotensin on direct effects on the kidneys on the tubules and arterioles

A
  • increased sodium reabsorption and decreased GFR leading to sodium and water retention leading to increased cardiac output resulting in increased arterial blood pressure
65
Q

Effects of Angiotensin on the brain

A

Causes increased thirst leading to increased water reabsorption and Increased ADH leading to increased water reabsorption causing sodium and water retention causing increased cardiac output resulting in increased arterial blood pressure

66
Q

Angiotensin II effects on vascular smooth muscle

67
Q

Angiotensin II effects on central and peripheral nervous systems

68
Q

Angiotensin II effects on adrenal cortex

69
Q

Angiotensin II effects on renal tubules and arterioles

70
Q

Angiotensin II effects on the brain

71
Q

Prostaglandins effect on renal blood flow

A
  • Typically do not regulate renal blood flow or GFR under normal conditions (i.e. cyclo-oxygenase inhibition does not alter renal blood flow)
  • Vasodilator PG’s limit constriction of afferent arteriole
  • PG-induced vasodilation maintains glomerular blood flow during volume or sodium depletion
  • Cyclo-oxygenase inhibitors can cause acute renal failure during dehydration or following a stress such as surgery
72
Q

Cyclo-oxygenase inhibitors and renal function

A

Acute renal failure during dehydration or following a stress such as surgery

73
Q

Atrial natriuretic peptide is secreted from?

A

atria in response to stretch

74
Q

Atrial natriuretic peptide effects on GFR

A

Dilates afferent arteriole and also constricts efferent arteriole to increase GFR

75
Q

Atrial natriuretic peptide effects on urine production

A

Decreases Na reabsorption in medullary collecting to cause diuresis and natriuresis

76
Q

Diuresis description

A

increased urine production

77
Q

Natriuresis description

A

excretion of sodium in the urine

78
Q

Brain natriuretic peptide secreted from

A

ventricles

79
Q

Atrial natriuretic peptide and Brain natriuretic peptide levels in renal failure

A

increased levels in renal failure

80
Q

ANP and BNP effects in renal failure

A

Increased levels in renal failure resulting in

  • reduced renal clearance
  • increased synthesis

CVPR (93 decks)

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