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Histo (VM1 Fall) > Exam 3 - Lecture 36 (Glomerular Filtration and its Regulation) > Flashcards

Exam 3 - Lecture 36 (Glomerular Filtration and its Regulation) Flashcards

1
Q

What % of blood leaves the glomerulus as filtrate?

A

15-20%

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2
Q

The filtration barrier separates on basis of _____ and _____.

A

size and charge

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3
Q

What is the size and charge of the fenestrated epithelium?

A 
Size = Large pores (60-80 nm)
Charge = polyanionic glycoprotein glycocalyx (neg. charge)
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4
Q

What is the size and charge of the lamina rara interna and externa?

A 
Size = does not filter based on size
Charge = Polyanionic non-collagenous proteins (neg. charge)
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5
Q

What is the size and charge of the lamina rara densa?

A 
Size = Collagenous proteins
Charge = Does not filter based on charge
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6
Q

What is the size and charge of the slit diaphragm?

A 
Size = Perforated with small pores
Charge = Podocytes are covered with polyanionic glycoprotein glycocalyx (neg. charged)
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7
Q

What size and charge does the glomerulus prefer for filtration?

A

Positively charged and small

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8
Q

Between anionic and cationic molecules, which is harder for the glomerulus to filter?

A

anionic (esp. when large)

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9
Q

When would a cationic molecule be hard for the glomerulus to filter?

A

If it is large in size

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10
Q

How are neutral molecules filtered by the glomerulus?

A

Only based on size

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11
Q

Filtration is designed to exclude _____.

A

most proteins

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12
Q

Which molecule will most easily cross the filtration barrier?

A) Na+ (small and pos. charged)
B) Cl- (small and neg. charged)
C) Gamma globulin (large [150 kDa] and neg. charged)
D) Dextran-70 (large [70 kDa] and neutral)

A

A) Na+ (small and pos. charged)

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13
Q

Where do Starling’s Forces operate?

A

At any capillary bed

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14
Q

What are the two types of hydrostatic pressure?

A
  1. Capillary HS pressure (Pc)

2. Bowman’s space HS pressure (Pbs)

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15
Q

What are the two types of oncotic pressure?

A
  1. Capillary oncotic pressure (πc)

2. Bowman’s space oncotic pressure (πbs)

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16
Q

What is capillary hydrostatic pressure?

A

Pressure of the glomerulus pushing out

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17
Q

What is Bowman’s space hydrostatic pressure?

A

Pressure of Bowman’s space pushing back on the glomerulus

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18
Q

What is capillary oncotic pressure?

A

Pressure into the glomerulus by capillaries

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19
Q

What is Bowman’s space oncotic pressure?

A

Pressure out of Bowman’s space by small amount of proteins getting through; is usually NEGLIGIBLE

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20
Q

What is oncotic pressure?

A

Osmotic pressure generated by plasma proteins

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21
Q

How do you calculate the magnitude of the force favoring glomerular filatration and what is the meaning of the result?

A

Pc - (Pbs + πc); net pressure moving OUT

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22
Q

What is Kf?

A

Filtration constant

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23
Q

Which Starling’s force is negligible and almost always 0?

A

πbs

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24
Q

Changes in resistance to blood flow in afferent/efferent arterioles changes _____ and therefore _____.

A

Pc; GFR

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25
Q

Increased resistance in efferent arteriole _____ Pc and GFR.

A

increases

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26
Q

What happens if the efferent arteriole narrows?

A

Easier for blood to enter thru afferent arteriole and GFR increases.

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27
Q

Constriction of the afferent arteriole combined with dilation of the efferent arteriole will produce which effect?

A) Increased Pc, Increased GFR
B) Increased Pc, decreased GFR
C) Decreased Pc, increased GFR
D) Decreased Pc, decreased GFR

A

D) Decreased Pc, decreased GFR

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28
Q

Why do disease states alter GFR?

A

Because they change Starling’s Forces

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29
Q

What happens when you feed a dog grapes or raisins?

A

necrosis of the tubules –> renal failure

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30
Q

Kf = _____ x _____

A

permeability of capillary X filtration SA

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31
Q

Most disease states _____ Kf and SA for filtration

A

Decrease

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32
Q

What is an example of a human disease state that alters GFR?

A

Glomerular disease caused by Schistosoma mansoni (human blood fluke); leads to renal failure

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33
Q

What are 2 examples of veterinary disease states that alter GFR and what does each lead to?

A
  1. Lyme disease (Borreliosis) –> chronic renal disease

2. Ethylene glycol toxicity –> acute renal failure

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34
Q

What is an example of disease state that changes Kf?

A

Glomerular disease

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35
Q

What is an example of a disease state that changes Pc?

A

Acute renal failure

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36
Q

In acute renal failure, Pc can _____ due to impaired renal perfusion; this causes _____ in GFR.

A

decrease; decrease

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37
Q

What is an example of a disease state that changes πc?

A

Plasma protein levels increase and decrease

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38
Q

If πc increases, GFR _____.

A

decreases

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39
Q

If πc decreases, GFR _____.

A

increases

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40
Q

What is an example of a disease state that changes Pbs?

A

Obstructions such as uroliths or plugs that increase Pbs.

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41
Q

If Pbs increases, GFR _____.

A

decreases

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42
Q

If Pbs decreases, GFR _____.

A

increases

43
Q

GFR is the sum of _____.

A

filtration rates over all functioning glomeruli (SNGFR X total # of nephrons)

44
Q

GFR is the _____ of renal function.

A

main descriptor

45
Q

What is acute renal failure/

A

Rapid (hrs/wks) but partially reversible decline in GFR.

46
Q

What is clearance?

A

How efficiently the kidney can get rid of a substance.

47
Q

When does clearance = GFR?

A

If substance is freely filtered by glomerulus and isn’t secreted or absorbed in the tubules

48
Q

The tone of the afferent and efferent arterioles is important in regulating GFR. Which of the following statements is true?

A) Dilated afferent arteriole and normal efferent arteriole increases GFR
B) Normal afferent arteriole and constricted efferent arteriole decreases GFR
C) Constricted afferent arteriole and normal efferent arteriole increases GFR
D) Normal afferent arteriole and dilated efferent arteriole increases GFR

A

A) Dilated afferent arteriole and normal efferent arteriole increases GFR

49
Q

What are the two types of markers used to measure clearance?

A
  1. Exogenous

2. Endogenous

50
Q

What is the exogenous marker used for measuring clearance?

A

Inulin

51
Q

What are the endogenous markers used for measuring clearance?

A
  1. Creatinine

2. BUN

52
Q

What is an exogenous marker?

A

Something that is introduced

53
Q

What is an endogenous marker?

A

Things we know are present in the ECF

54
Q

What is the most commonly used endogenous marker?

A

Creatinine

55
Q

How is creatinine filtered by the glomerulus?

A

Freely

56
Q

Presence of creatinine in the blood is _____ proportional to GFR.

A

indirectly

57
Q

What are the normal serum creatinine levels in dogs?

A

0.3 - 1.3 mg/dL

58
Q

What are the normal serum creatinine levels in cats?

A

0.8 - 1.8 mg/dL

59
Q

Why is BUN not as reliable as creatinine as a guide to renal function?

A

Up to 40% may be reabsorbed by the tubules

60
Q

What do increases in BUN/creatinine mean?

A

At least 75% of nephrons are not functioning, but up to this point the kidney can still function

61
Q

Which of Starling’s forces is the most important?

A

Pc (capillary hydrostatic pressure)

62
Q

What is general autoregulation?

A

Intrinsic ability of an organ to maintain blood flow at a nearly constant rate despite changes in arterial perfusion pressure (systemic BP change)

63
Q

What is renal autoregulation?

A

Point/range where changes in systemic BP do not affect the renal blood flow or the GFR (between 80 and 180 mm Hg).

64
Q

What are the two goals of renal autoregulation?

A
  1. Prevent damage to glomeruli caused by spiking BP

2. Prevent fluctuations in BP from changing delivery of filtrate to tubules

65
Q

What are the 2 mechanisms that the kidney uses for autoregulation?

A
  1. Myogenic mechanism

2. Tubuloglomerular feedback

66
Q

What is the goal of the myogenic mechanism?

A

Prevent damage to glomeruli

67
Q

What triggers the myogenic mechanism?

A

Fluctuations in BP changing transmural pressure in the AFFERENT arteriole

68
Q

In the myogenic mechanism, increased BP elicits _____ and _____ blood flow.

A

vasoconstriction; decreased

69
Q

In the myogenic mechanism, decreased BP elicits _____ and _____ blood flow.

A

vasodilation; increased

70
Q

What is the speed of the myogenic mechanism?

A

Rapid changes (1-2 sec) in response to rapid BP changes

71
Q

Which statement about the myogenic mechanism is true?

A) It is a slow acting response
B) The main effect is to constrict the efferent arteriole
C) It helps to protect the glomerulus
D) It is triggered in the efferent arteriole wall
E) It will reduce GFR in response to low BP

A

C) It helps to protect the glomerulus

72
Q

What is the goal of tubuloglomerular feedback?

A

“Fine-tuning”; we don’t want too much or too little solute getting dumped into the nephron when the GFR changes

73
Q

What is the trigger for tubuloglomerular feedback?

A

Fluctuations in BP change GFR meaning DT fluid composition is altered

74
Q

What are the 3 steps to tubuloglomerular feedback?

A
  1. Low/High GFR produces low/high ultrafiltrate
  2. Low/High [ion] sensed by macula densa
  3. JGA changes arteriole resistance to autoregulate GFR
75
Q

What is the speed of tubuloglomerular feedback?

A

Slower changes (10-12 sec) in response to slower BP changes

76
Q

What cells are the macula densa cells directly connected to?

A

Juxtaglomerular cells of the afferent arteriole

77
Q

What is the role of the extraglomerular mesangial cells?

A

Promote info transfer between MD and JG

78
Q

What type of muscle are JG cells?

A

smooth

79
Q

What do JG cells contain/produce?

A

renin

80
Q

What are the 3 steps of the Renin-Angiotensin system?

A
  1. Liver releases Angiotensinogen
  2. JG cells produce Renin which catalyzes angiotensinogen –> Angiotensin I
  3. Angiotensin I is converted to Angiotensin II by Angiotensin Converting Enzyme (ACE)
81
Q

Where does angiotensin converting enzyme come from?

A

lung

82
Q

What 4 things does angiotensin II do?

A
  1. Systemic arteriolar vasoconstriction to increase BP
  2. Increases aldosterone secretion (adrenal cortex)
  3. Promotes ADH secretion (pituitary) and thirst
  4. Increases tubular NaCl uptake
83
Q

What do you WANT to do to GFR when BP is high?

A

reduce it

84
Q

How does tubuloglomerular feedback work to reduce GFR when BP is high (6 steps)?

A
  1. High Na+, K+, and Cl- sensed by NKCC2 on apical surface of MD
  2. MD releases ATP and/or adenosine
  3. ATP/adenosine activate receptors on EG mesangial cells
  4. Increased IC Ca2+ in EG mesangial cells causes same response in afferent arteriole smooth muscle and JG cells
  5. Afferent art. smooth muscle contracts (REDUCES GFR)
  6. JG cells are inhibited from releasing renin (REDUCES GFR)
85
Q

What is released by the MD during tubuloglomerular feedback?

A

Adenosine/ATP when BP is high to lower GFR

PGE2 when BP is low to increase GFR

86
Q

What does NKCC2 transport?

A

1 Na+
1 K+
2 Cl-

87
Q

What effect does caffeine have on adenosine Rs?

A

Blocks Rs –> acts as diuretic

88
Q

How does tubuloglomerular feedback work to increase GFR when BP is low (5 steps)?

A
  1. Low Na+, K+, and Cl- sensed by NKCC2 on apical surface of MD
  2. MD releases PGE2
  3. PGE2 causes afferent art. vasodilation (INCREASES GFR)
  4. PGE2 stimulates JG to release renin, increasing angiotensin II
  5. Angiotensin II causes 4 things to happen in the bloodstream that increase GFR
89
Q

What 4 things does angiotensin II do in the bloodstream during tubuloglomerular feedback?

A
  1. Causes systemic vasoconstriction (INCREASES GFR)
  2. Preferentially contracts efferent over afferent arteriole (INCREASES GFR)
  3. Increases PGE2 production from MD
  4. Negatively feedbacks onto contralateral kidney to stop renin release
90
Q

Tubuloglomerular feedback regulates GFR. When a high GFR is lowered by TGF, which of the following statements is accurate?

A) The trigger is low Na+, K+, and Cl- sensed by the macula densa
B) A key intermediate step is decreased IC Ca2+ in EG mesangial cells
C) Afferent arteriole smooth muscle contracts
D) JG cells release renin
E) Macula densa releases PGE2

A

C) Afferent arteriole smooth muscle contracts

91
Q

How can chronic use of NSAIDs affect the kidney?

A

Can lead to acute renal failure

92
Q

How do NSAIDs (esp. prolonged use) affect the autoregulation pathway?

A

They inhibit PGE2 production, so GFR cannot be raised when BP drops; leads to ischemic injury, acute renal failure, vomiting, and anorexia.

93
Q

What is the sensor in the myogenic mechanism?

A

BP changes in afferent arteriole

94
Q

What is the effector in the myogenic mechanism?

A

Afferent arteriole

95
Q

What is the role of the myogenic mechanism?

A

Protection against injury

96
Q

What is the response time of the myogenic mechanism?

A

Fast - adapts to changes up to 6 Hz

97
Q

What is the importance of the myogenic mechanism?

A

No mechanism = no autoregulation

98
Q

What is the sensor in TGF?

A

Ionic changes in the DT

99
Q

What is the effector in TGF?

A

Afferent AND efferent arterioles

100
Q

What is the role of TGF?

A

Regulation of GFR

101
Q

What is the response time of TGF?

A

Slower - adapts to changes less than 0.1 Hz

102
Q

What is the importance of TGF?

A

Less important than the myogenic mechanism; works with other mechanisms to control GFR and fluid homeostasis

103
Q

Captopril is an angiotensin converting enzyme (ACE) inhibitor. Bases on what you know about the renin-angiotensin system, which of the following statements is correct?

A) Captopril reduces Angiotensin II and increases GFR
B) Captopril reduces Angiotensin II and decreases GFR
C) Captopril increases Angiotensin II and increases GFR
D) Captopril increases Angiotensin II and decreases GFR

A

B) Captopril reduces Angiotensin II and decreases GFR

Histo (VM1 Fall) (27 decks)

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