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Physio II (Exam 2) > Topic 7: Glomerular Filtration and Renal Bllod Flow 2 > Flashcards

Topic 7: Glomerular Filtration and Renal Bllod Flow 2 Flashcards

1
Q

GFR = equation

A

Kf x Net filtration pressure

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2
Q

Kf

A

is the glomerular capillary filtration coefficient

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3
Q

GFR is determined by what?

A
  1. the sum of the hydrostatic and colloid osmotic forces across the glomerular membrane which gives the Net Filtration Pressure
  2. the glomerular capillary filtration coefficient Kf
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4
Q

Net Filtration Pressure

A

represents the sum of the hydrostatic and colloid osmotic forces that either favor or oppose filtration across the glomerular capillaries

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5
Q

Net Filtration Pressure promotes what?

A

Promotes filtration

  • Glomerular hydrostatic pressure (60 mmHg)
  • Bowman’s capsule oncotic pressure (0 mmHg) (factor with disease)
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6
Q

Net Filtration Pressure inhibits what?

A

Inhibits filtration

  • Glomerular oncotic pressure (32 mmHg)
  • Bowman’s capsule hydrostatic pressure (18 mmHg)
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7
Q

Kf= equation

A

GFR / Net filtration pressure

estimated way to find Kf bc we cant measure directly

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8
Q

Kf affected by what ?

A

Affected by overall hydraulic conductivity and surface area of the glomerular capillaries
Not able to measure directly

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9
Q

measure of the product of the hydraulic conductivity and SA of the glomerular capillaries

A

Kf

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10
Q

Net Filtration Pressure equation

A

Pg-Pb-Pieg+Pieb

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11
Q

Normal Kf other capillaries compared to glomerular capillaries

A

Glomerular capillaries Kf is 400x as high as other capillaries.
glomerular capillaries = 4.2 mls/min/mmHg/100 grams of tissue
normal capillaries = 0.01 mls/min/mmHg/100 gm

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12
Q

Filtration Coefficient and GFR have what kind of relationship

A

direct positive relationship

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13
Q

Increase in Hydrostatic Pressure in Bowmans Capsule (Pb) - does what to GFR

A

Decrease GFR

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14
Q

Decrease in Hydrostatic Pressure in Bowmans Capsule (Pb) - does what to GFR

A

Increase GFR

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15
Q

Pb a direct means for affecting GFR

A
  • Pb is not a primary means for regulating GFR

- Usually not part of day-to-day control of GFR

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16
Q

Increase Kf does what to GFR?

A

Increase GFR

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17
Q

Chronic uncontrolled HTN and diabetes mellitus do what to Kf

A

decrease Kf

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18
Q

Chronic uncontrolled HTN and diabetes mellitus decrease Kf how?

A

increasing the thickness of glomerular capillary basement membrane and eventually damaging the capillary so severely that there is loss of capillary function

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19
Q

Increased glomerular oncotic pressure = does what to GFR

A

Decreased GFR

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20
Q

How does Increased glomerular oncotic pressure decrease GFR?

A

as blood passes from afferent arteriole through the glomerular capillaries to the efferent arterioles the plasma protein concentration increases 25%. bc 1/5th of the fluid in the capillaries filters into Bowmans capsule concentrating proteins

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21
Q

Decreased glomerular oncotic pressure = what GFR?

A

Increased GFR

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22
Q

As blood passes through glomerulus plasma oncotic pressure will what?

A

pressure will increase ≈ 20%

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23
Q

Plasma oncotic pressure entering and exiting the glomerulus

A

28 mmHg entering glomerulus and 36 mmHg as blood leaves glomerulus
Average 32

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24
Q

Factors Affecting Glomerular Oncotic Pressure

A

1) the arterial plasma colloid osmotic pressure

2) Filtration Fraction

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25
Q

Filtration Fraction

A

the fraction of plasma filtered by the glomerular capillaries

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26
Q

Increased plasma protein concentration will _____glomerular oncotic pressure which will _____ GFR

A

Increase glomerular oncotic pressure

decrease GRF

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27
Q

Increased filtration fraction means more whatis being filtered from each ml of blood in the glomerulus

A

plasma

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28
Q

Filtration fraction = equation

A

GFR / RBF

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29
Q

A decrease in RBF (no initial change in GFR) will do what to FF and GFR?

A

will increase the filtration fraction thus producing a decrease in GFR

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30
Q

Increased RBF – __ Filtration Fraction – __ glomerular oncotic pressure – __ GFR

A

Increased RBF – Decreased Fraction – Decreased glomerular oncotic pressure – Increased GFR

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31
Q

Changing RBF with constant glomerular hydrostatic pressure thus has an effect on GFR?

A

Increase RBF = Increased GFR

Decrease RBF = Decrease GFR

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32
Q

Increased Pg = does what to GFR

A

Increased GFR

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33
Q

Decreased Pg = does what to GFR?

A

Decreased GFR

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34
Q

Pg primary means of changing GFR by? (3)

A
  1. Arterial Pressure
  2. Afferent arterial resistance
  3. Efferent arterial resistance
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35
Q

Increased MAP = what happens to GFR?

A

Increased

[Buffered by autoregulation of flow to keep consistent glomerular pressure]

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36
Q

Increased Art Pressure does what to Pg and GFR

A

Increases Pg and Increased GFR

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37
Q

Increased constriction (increased Afferent arteriole Resistance) = what happens to pressure (Pg) and GFR ?

A

Decreased pressure (Pg) = Decreased GFR

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38
Q

Decreased constriction (decreased Afferent arteriole Resistance) = what to pressure Pg and GFR

A

Increased pressure (Pg) = Increased GFR

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39
Q

Increased constriction (Efferent Arteriole Resistance) = what happens to Pg and GFR

A

Increased pressure (Pg)= Increased GFR (slightly)

as long as RBF doesnt reduce too much

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40
Q

Increased constriction (Efferent Arteriole Resistance) = what happens to FF and Glomerular Osmotic Oncotic Pressure

A

Increased FF and Glomerular Osmotic Oncotic Pressure because of Decreased RBF

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41
Q

If Efferent Arteriole Resistance constricts renal blood flow too much what happens?

A

if constricts too much, GFR decreases bc Renal BF decreases or stops which Increases Glomerularr Colliod Pressure > Pg

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42
Q

If Efferent Arteriole Resistance constricts renal blood flow too much what happens to filtration fraction?

A

Filtration fraction increases (decreased blood flow, increased GFR) which results in higher glomerular colloid oncotic pressure which decreases GFR

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43
Q

Increased Bowman hydrostatic pressure (Pb) = does what to GFR?

A

Decreased GFR

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44
Q

Decreased Bowman hydrostatic pressure (Pb) = does what to GFR?

A

Increase GFR

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45
Q

Does Pb normally play a role in controlling GFR?

A

Normally does not play a primary role in controlling GFR

46
Q

How does an obstruction of the urinary tract cause hydronephrosis?

A

Bowmans capsule pressure can increase causing serious reduction in GFR a precipitation of the Ca or Uric Acid may lead to stones that lodge in Urinary Tract, that ⬆️ Pb which ⬇️GFR and cause hydronephrosis

47
Q

Obstruction of urinary tract block Pb and GFR?

A

Could produce big increase in Pb pressure with big decrease in GFR

48
Q

⬇️Kf ➡️⬇️GFR causes

A

renal disease, diabetes mellitus, HTN

49
Q

⬆️Pb➡️⬇️GFR

A

urinary tract obstruction

50
Q

⬆️Pie g➡️⬇️ GFR

A

⬇️ renal BF, increases plasma proteins

51
Q

⬇️Pg➡️⬇️GFR

A

⬇️ arterial pressure (has only small effect due to autoregulation)

52
Q

⬇️ Efferent arteriolar resistance ➡️⬇️Pg

A

⬇️ Angiotensin II (drugs that block angiotensin II formation)

53
Q

⬆️Afferent arteriolar resistance ➡️ decreases Pg

A

⬆️ Sympathetic activity, vasoconstrictor hormones (nori, endothelin)

Decease GFR

54
Q

RBF provides flow for what? (2)

A
  • basic metabolic needs of kidneys

- excess flow for plasma filtration

55
Q

Renal O2 consumption and blood flow compared to the brain.

A

O2 consumption is 2x that of the brain

but blood flow is 7x of the brain

56
Q

Most of O2 consumed by the kidneys is due to what?

A

supports sodium reabsorption–consumption directly related to rate of sodium reabsorption

57
Q

Renal Oxy consumption is proportional to what?

A

renal tubular Na reabsorption

58
Q

renal tubular Na reabsorption is related to what?

A

GFR and rate Na filtered

59
Q

RBF = equation

A

(Renal artery pressure–Renal vein pressure) / Total renal resistance

60
Q

Percentage of total renal vascular resistance:

Renal artery ?

A

100 - 100 = 0%

61
Q

Percentage of total renal vascular resistance:

Afferent Arteriole ?

A

~85-60 = 26%

62
Q

Percentage of total renal vascular resistance:

Efferent Arteriole ?

A

59-18 = 43%

63
Q

Percentage of total renal vascular resistance:

Interlobar, arcuate, and interlobular arteries?

A

8-4= 16%

64
Q

Pg and Glomerular Osmotic oncotic pressure

A

Resistance of these three areas controlled by sympathetic nervous system, hormones, local control within kidneys

65
Q

% Renal flow going to the renal cortex?

A

98-99%

66
Q

% Renal flow going to the renal medulla?

A

only 1-2% of BF, supplied by Vasa Recta (concentrates Urine)

67
Q

Strong Sympathetic Nervous System activation – what effect on renal arterioles ?

A

can cause constriction to renal arterioles thus

Decrease RBF and GFR

68
Q

Mild to moderate Sympathetic Nervous System activation - what effect on renal arterioles?

A

Little effect on RBF or GFR

moderate decrease in BP with corresponding baroreceptor response

69
Q

When does SNS innervation have the largest effect?

A

during acute issues, like Brain ischemis and Severe Hemorrage

70
Q

Epinephrine and Norepinephrine effect on RBF?

A

constrict afferent and efferent arterioles

Cause decrease in RBF and GFR

71
Q

Endothelium released by what?

A

-Released by damaged vascular endothelial cells of kidneys and other tissue–
(play role in hemostasis - by vasoconstrict to keep damaged bld in)

72
Q

Endothelium is what? and has what effect on RBF?

A
  • autacoid
  • Concentration increased during toxemia of pregnancy, acute renal failure, chronic uremia
  • Powerful vasoconstrictor
73
Q

Endothelium does what to GFR?

A

decreases - bc constriction - ⬇️RBF thus ⬇️GFR .

74
Q

Angiotensin II is what?

A

circulating hormone and autacoid

powerful vasocanstrictor

75
Q

Angiotensin II and afferent arterioles (preglomerular vessels)?

A 
afferent arterioles (preglomerular vessels) are relatively protected from angiotensin II constriction in most situations associated w/the renin-angiotensin system.
this protection is due to the release of vasodilators (NO and prostaglandins) which counteract that vasoconstriction.
76
Q

Angiotensin II and efferent arterioles?

A

Very sensitive to Angiotensin II
⬆️Angiotensin II -> ⬆️Pg while ⬇️RBF
Enhanced tubular reabsorption because of decreased flow thru peritubular capillaries

77
Q

When is angiotensin II usually formed?

A

in times where there is ⬇️MAP or ⬇️ Vol which would ⬇️GFR but Angiotensin II prevents the ⬇️GFR by Vasoconstricting.

78
Q

Nitric Oxide basal level important for what?

A

basal level of NO secreted that helps maintain dilation of renal vessels, to allow kidneys to secrete normal amounts of Na and H2O

79
Q

Nitric Oxide is a what? effect on Resistance and GFR?

A

autacoid - endothelial derived

⬇️ Renal Vascular resistance and ⬆️GFR and urinary excretion of Na

80
Q

Endothelial derived NO

A

autacoid - that⬇️ Renal Vascular resistance and is released by vascular endothelium throughout the body

81
Q

A NO inhibitor drug does what to GFR and Resistance?

A

⬆️ Renal Vascular resistance and ⬇️ GFR and urinary Na excretion, The ⬆️Na levels - due to lack of excretion will eventually causing high BP/MAP.

82
Q

Bradykinin & Prostaglandins - impact on RBF and GFR?

A
  • autacoids and hormones
  • Potent vasodilators
  • Tend to increase RBF and GFR
  • Do not appear to have major impact during normal conditions
83
Q

Prostaglandins effect on afferent arterioles

A

opposing vasoconstriction effect of sympathetic nerves or angiotensin II on the afferent arterioles
May help prevent excessive decreases in RBF and GFR

84
Q

When to Administer nonsteroidal anti-inflammatory agents (ex aspirin)?

A

-under stressful conditions/bld loss/surgery - -giving this may inhibit prostagladin synthesis may cause significant reduction in GFR

85
Q

Bradykinin & Prostaglandins inhibited by what?

A

nonsteroidal anti-inflammatory agents

86
Q

Autoregulation of GFR and RBF

A
  • Purpose is to maintain NORMAL GFR and allow control of renal excretion of water and solutes
  • Prevents big changes in water / solute excretion with normal changes in blood pressure
87
Q

Autoregulation can last between what MAP pressure ranges?

A

Decreasing MAP to 75 mmHg or increasing to 160 mmHg results in a small change in GFR (<10% change)

88
Q

If no autoregulation in place and

Increase MAP 100 to 125 mmHg GFR would do what?

A

GFR would go from 180 L/day to 225 L/day

89
Q

But urine output and solute excretion DOES what with an increase in MAP

A

INCREASE

Pressure diuresis and pressure natriuresis

90
Q

Large increase in urine output prevented by

A

Autoregulation

Changes in tubular reabsorption

91
Q

Tubuloglomerular Feedback Mechanism

A

Links autoregulation of GFR and RBF to the amount of NaCl entering the distal tubule

92
Q

Tubuloglomerular Feedback Mechanism

A

Regulates RBF and GFR in parallel

—GFR regulation rather than RBF regulation plays larger role in maintaining constant delivery of NaCl to distal tubule

93
Q

Tubuloglomerular Feedback Mechanism Components: (3)

A

Afferent arteriole feedback mechanism
Efferent arteriole feedback mechanism
Juxtaglomerular complex

94
Q

Macula densa cells - where? and what?

A

Epithelial cells located initial part of distal tubule

Sense changes in NaCl concentration in the tubular fluid

95
Q

Juxtaglomerular cells surround what?

in contact with what?

A
  • Surround afferent arteriole where it enters the glomerulus
  • Surround efferent arteriole where it leaves glomerulus
  • In contact with portion of distal tubule that contains macula densa
96
Q

Juxtaglomerular cells storage site for what?

A

-Major storage site for renin

97
Q

Juxtaglomerular cells operation

A

Believed that macula densa monitors amount of volume delivered to distal tubule via NaCl concentration

98
Q

Response from macula densa has two effects

A

–Dilation of afferent arteriole
Results in an increase in glomerular hydrostatic pressure
–Stimulation of increased renin release from juxtaglomerular cells
Results in an increased constriction of efferent arteriole which produces an increase in glomerular hydrostatic pressure

99
Q

Response from macula densa (decreased concentration of Na Cl in macula densa) has two effects in arterioles:

A
  1. Resistance to BF to afferent arterioles. (Dilation) which increases Pg
  2. Increase renin release from the juxtaglomerular cells of the efferent and afferent arterioles.
100
Q

Macula Densa cells sense what?

A

Sense changes in NaCl concentration in the distal tubular fluid
monitors amount of volume delivered to distal tubule via NaCl concentration

101
Q

GFR decreases - affects Loop of Henle how?
(Flow?
Reabsorption?
Thus concentration in macula densa?)

A

Flow rate through Loop Henle also decreases
Reabsorption of Na+ and Cl-in loop increases
Concentration Na+ and Cl-at macula densa decreases
Decreased concentration elicits response from macula densa

102
Q

Dilation of afferent arteriole - what happens to Pg?

A

Results in an increase in glomerular hydrostatic pressure

103
Q

Stimulation of increased renin release from juxtaglomerular cells results in what effect on Pg? (this is a macula densa response)

A

Results in an increased constriction of efferent arteriole which produces an increase in glomerular hydrostatic pressure

104
Q

An increase in MAP have what reaction to the smooth muscle of small arterioles?

A

An increase in MAP will cause an increase in smooth muscle contraction especially of small arterioles
BC - MAP increases which cause the vessel walls to stretch thus increasing wall tension. The increased stretch results in movement of additional calcium into the smooth muscle cells which increases the overall level of contraction

105
Q

afferent arterioles show strong or weak myogenic response

A

afferent arterioles show a strong myogenic response to sudden increase in arterial pressure
(Dont know if this is that important to the kidneys)

106
Q

Result of increased afferent constriction is a reduction in what two things?

A

reduction in RBF (due to increased resistance) and a decrease in GFR (due to decreased glomerular hydrostatic pressure)

107
Q

Juxtaglomerular Feedback Mechanism

A
  • Feedback mechanism designed to maintain consistent delivery of NaCl to the distal tubule
  • Any problem that increases NaCl reabsorption in the proximal tubule will trigger the feedback mechanism
108
Q

Juxtaglomerular Feedback Mechanism:

two examples?

A

High protein intake

Increase in Blood Glucose

109
Q

High protein intake

A

Higher than normal amino acid concentration in the blood–Sodium and amino acid reabsorption linked, so an increase in amino acid reabsorption — results in an increase in sodium reabsorption and stimulation of the Juxtaglomerular feedback mechanism

110
Q

High protein intake can increase GFR how much?

A

20 to 30% increase in GFR 1 to 2 hours after eating a high-protein meal

111
Q

Increase in blood glucose

A

Again, glucose reabsorption tied to sodium reabsorption
–
As concentration of glucose in the blood increases, glucose and sodium reabsorption also increase thus stimulating the feedback
mechanism which ultimately results in an increase in GFR

Physio II (Exam 2) (6 decks)

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