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Renal exam - physiology Flashcards

1
Q

How much body weight is ICF

A

40%

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2
Q

How much body weight is ECF

A

20%

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3
Q

how much body weight is total body water

A

60%

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4
Q

what fraction of TBW is ICF

A

2/3

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5
Q

what fraction of TBW is ECF

A

1/3

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6
Q

is calcium primarily intracellular or extracellular

A

extracellular

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7
Q

ECF is divided into what 2 compartments

A

plasma and interstitial

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8
Q

when volume changes occur, which compartment is affected first

A

ECF

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9
Q

Normal serum osmolarity

A

280-300

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10
Q

example of isosmotic volume contraction

A

diarrhea

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11
Q

what occurs with isosmotic volume contraction

A

isotonic fluid is lost leading to a reduced ECF volume and no fluid shifts and no changes in osmolarity

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12
Q

example of isosmotic volume expansion

A

administration of isotonic saline solution

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13
Q

what occurs with isosmotic volume expansion

A

isotonic fluid increases ECF volume with no fluid shifts and no changes in osmolarity

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14
Q

example of hyperosmotic volume contraction

A

sweating

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15
Q

what occurs with hyperosmotic volume contraction

A

hyposmotic fluid is lost from ECF, increasing the osmolarity of ECF. Fluid shifts from ICF to ECF to compensate, causing the osmolarity of both to be higher and the volume of both to be lower

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16
Q

example of hyperosmotic volume expansion

A

drinking a hyperosmotic sports drink

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17
Q

what occurs with hyperosmotic volume expansion

A

the ECF volume and osmolarity increase, causing the ICF to flow into the ECF. The ECF volume increases, the ICF volume decreases, and the osmolarities of both increase.

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18
Q

example of hyposmotic volume contraction

A

loss of salt (hypoaldosteronism)

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19
Q

what occurs with hyposmotic volume contraction

A

the solute loss leaves the ECF hyposmotic, so fluid shifts from ECF to ICF. The osmolarity of both decrease, the ICF volume increases, and the ECF volume decreases

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20
Q

example of hyposmotic volume expansion

A

drinking water

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21
Q

what occurs with hyposmotic volume expansion

A

osmolarity decreases in ECF so fluid shifts from ECF to ICF. Osmolarity of both is decreased and volume of both is increased.

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22
Q

what % of renal bloodflow goes to cortex

A

90%

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23
Q

2 categories of control mechanisms of renal bloodflow

A

autoregulation, extrarenal

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24
Q

components of autoregulation of renal blood flow

A

myogenic mechanism, tubuloglomerular feedback

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25
Q

explain myogenic mechanism

A

stretch of blood vessels causes them to constrict to reduce blood flow (reflex)

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26
Q

explain tubuloglomerular feedback

A

Macula densa senses increase in NaCl in tubule. Low NaCl is interpreted as a signal of low GFR, so afferent arteriole dilates to increase GFR, and RAAS in stimulated to increase Na reabsorption to increase ECV and restore GFR

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27
Q

what does the extrarenal mechanism of controlling renal blood flow consist of

A

SNS, RAAS, other hormones

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28
Q

what can stimulate renin release

A

SNS stimulation of B1 receptors in JG cells, low Na at macula densa, decreased afferent arteriole BP

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29
Q

main goal of RAAS

A

to increase extracellular fluid volume

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30
Q

layers of the barrier between glomerulus and capsule

A

capillary endothelium, basement membrane, podocytes

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31
Q

which layer of the glomerular filter barrier has fenestrations and which has nephrin

A

endothelial cells; podocytes

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32
Q

low-moderate levels of SNS stimulation constrict ____

A

efferent arteriole

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33
Q

greater constriction of efferent arteriole does what to GFR

A

increases, then decreases as constriction continues

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34
Q

greater constriction of afferent arteriole does what to GFR

A

decreases

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35
Q

where does water leave the loop of henle

A

descending

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36
Q

where does salt leave the loop of henle

A

ascending

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37
Q

osmolarity of fluid leaving the PCT

A

isosmotic

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38
Q

goal of the counter-current multiplier

A

decrease osmolarity in tubule (pumps) and increase interstitial osmolarity, allowing water to flow out of the descending limb

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39
Q

limit of urinary concentration/osmolarity at bottom of loop of henle

A

1200 mOsm

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40
Q

what is vasa recta

A

vascular source for medulla

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41
Q

osmolarity of urine when it reaches collecting duct

A

120 mOsm

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42
Q

how is urine concentrated once it leaves the ascending loop

A

ADH forms aquaporins in DT/CD to allow water to leave the tubule and concentrate urine

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43
Q

what stimulates release of ADH

A

SNS stimulation, increased plasma osmolality (sensed by osmoreceptors in hypothalamus) and decreased blood pressure, sensed by baroreceptors (aortic arch, carotid sinus, LA, pulmonary vessels)

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44
Q

what releases ADH

A

posterior pituitary

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45
Q

effects of ADH on water, urine, plasma

A

increased water reabsorption/total body water, decreased urine volume, lower plasma osmolarity, increased blood volume

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46
Q

physiological response to osmoregulation

A

water excretion, retention or intake (via ADH/thirst)

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47
Q

physiological response to volume regulation

A

urinary sodium excretion or retention (via RAAS, SNS, ANP, ADH)

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48
Q

major anion of ICF

A

phosphates

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49
Q

major anions of ECF

A

Cl, HCO3, albumin

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50
Q

major cation of ICF

51
Q

major cation of ECF

52
Q

major buffer system of ECF

A

bicarbonate

53
Q

major buffer systems of ICF

A

hemoglobin, proteins, phosphate

54
Q

addition of strong acid to bicarbonate buffer system leads to

A

prevention of sudden change in pH, depletion of HCO3-, accumulation of CO2

55
Q

addition of strong base to bicarbonate buffer system leads to

A

prevention of sudden change in pH, depletion of CO2, depletion of H2CO3

56
Q

what two substances regulate pH

A

HCO3, pCO2

57
Q

requirements of efficient functioning of the bicarbonate buffer system

A

removal of CO2 by lungs, addition of new HCO3 by kidneys

58
Q

formula for determining expected pCO2 in metabolic acidosis

A

[HCO3-] +15 +/-2

59
Q

formula for determining expected pCO2 in metabolic alkalosis

A

[HCO3-]+10 +/-5

60
Q

formula for determining expected HCO3- in respiratory acidosis, acute phase

A

rise in [HCO3-] = (rise in pCO2)/10

61
Q

formula for determining expected HCO3- in respiratory acidosis, chronic phase

A

rise in [HCO3-] = 4*(rise in pCO2)/10

62
Q

formula for determining expected HCO3- in respiratory alkalosis, acute phase

A

drop in [HCO3-] = 2*(drop in pCO2)/10

63
Q

formula for determining expected HCO3 in respiratory alkalosis, chronic phase

A

change in [HCO3-] = 4*(drop in pCO2)/10

64
Q

steps of reabsorption of bicarb in PCT

A

bicarb is freely filtered in glomerulus and then enters PCT, where there is H+. Carbonic anhydrase 2 catalyzes a reaction of H+ with bicarb to form H2CO3, which then dissociates into H20 and CO2. The CO2 enters the PCT cell where carbonic anhydrase 4 catalyzes a reaction with OH- to form bicarb, which then enters bloodstream

65
Q

how much filtered bicarb is reabsorbed

66
Q

steps of creation of new HCO3- in PCT

A

glutamine metabolizes into ammonium and bicarb

67
Q

factors that increase glutamine metabolism

A

acidosis and hypokalemia

68
Q

2 main mechanisms of metabolic acidosis

A

loss of HCO3-, gain of acid

69
Q

what mechanism of metabolic acidosis is usually associated with an increase in anion gap

A

gain of acid

70
Q

2 areas where HCO3- can be lost

A

kidneys, GI tract

71
Q

anion gap formula

A

Serum Na- (Cl+HCO3)

72
Q

normal anion gap

A

8-12 mEq/L

73
Q

mnemonic for high anion gap metabolic acidosis

A

MUDPILESCAT

74
Q

what does MUDPILESCAT stand for

A 
Methanol
Uremia
DKA
Propylene glycol
INH/Iron
Lactic acid
Ethylene glycol/Ethanol
Salicylates
CO2/cyanide
Aminoglycosides
Toluene
75
Q

what is delta/delta

A

change in anion gap/change in HCO3-

76
Q

what is the purpose of the delta/delta

A

to see if the change in anion gap is appropriate for the change in HCO3-, helps identify mixed disorder

77
Q

delta/delta of 1-2

A

pure AG metabolic acidosis

78
Q

delta/delta <1

A

AG metabolic acidosis with non-AG metabolic acidosis

79
Q

delta/delta >2

A

AG metabolic acidosis with metabolic alkalosis

80
Q

non-anion gap metabolic acidosis AKA

A

hyperchloremic acidosis

81
Q

causes of non-anion gap metabolic acidosis

A

GI: diarrhea
Renal: RTA, carbonic anhydrase inhibitor, post-hypocapnia

82
Q

why is anion gap normal in RTA and diarrhea

A

chloride is also elevated

83
Q

if pCO2 is less than expected in metabolic acidosis

A

concomitant respiratory alkalosis

84
Q

if pCO2 is greater than expected in metabolic acidosis

A

concomitant respiratory acidosis

85
Q

what is osmolal gap for

A

to find out where there is a substance that may be causing acidosis in ECF

86
Q

what does an osmolal gap greater than 10 mean

A

points towards the presence of a toxic alcohol

87
Q

what does a positive urinary anion gap mean

A

kidneys are not making NH4: renal failure, RTA

88
Q

what does a negative urinary anion gap mean

A

kidneys are making NH4: GI HCO3 loss due to diarrhea

89
Q

stimuli for aldosterone release

A

hyperkalemia, volume depletion

90
Q

where is aldosterone made

A

zona glomerulosa in adrenal cortex

91
Q

if pCO2 is less than expected in metabolic alkalosis

A

concomitant respiratory alkalosis

92
Q

if pCO2 is greater than expected pCO2 in metabolic alkalosis

A

concomitant respiratory acidosis

93
Q

what is necessary for metabolic alkalosis to persist

A

aldosterone

94
Q

2 major types of metabolic alkalosis

A

volume/saline/chloride sensitive and resistant

95
Q

urine cl less than 10

A

volume/saline/chloride sensitive metabolic alkalosis: Hypotension

96
Q

urine cl greater than 10

A

volume/saline/chloride resistant metabolic alkalosis: Hypertension, caused by renal artery stenosis, hyperaldosteronism

97
Q

alkalosis is associated with what electrolyte derangement

A

hypokalemia

98
Q

what does proteinuria signify

A

damage to glomerulus

99
Q

why is creatinine clearance an estimation of GFR

A

amount filtered = amount cleared

100
Q

GFR =

A

[urine]/[plasma] * urine flow rate

101
Q

if amount excreted is greater than filtered

A

substance must have been secreted as well as filtered

102
Q

amount of substance excreted =

A

urine concentration * urine flow rate OR filtered + secreted - reabsorbed

103
Q

amount of substance filtered =

A

plasma concentration * GFR

104
Q

if amount excreted is < filtered

A

the substance was reabsorbed or metabolized

105
Q

small increase in angiotensin 2 effects

A

efferent arteriole constriction and increased GFR with an unchanged Kf

106
Q

large increase in angiotensin 2 effects

A

increased arteriole resistance and decreased GFR with a decreased Kf

107
Q

net effect of Na/K/ATPase

A

3 Na+ out, 2 K+ in

108
Q

mechanism of secondary active transport

A

requires energy but the energy is derived from a different ATPase pump

109
Q

example of carrier-mediated transport

110
Q

at what plasma level does reduced glucose absorption occur`

111
Q

at what plasma level are all glucose co-transports saturated

A

> 350 mg/dl

112
Q

what is fanconi syndrome

A

loss of proximal tubule function (polyuria, polydipsia, glycosuria with normal BGL)

113
Q

target of furosemide

A

Na/K/2Cl in thick ascending loop of Henle

114
Q

how much sodium is reabsorbed in thick ascending loop

115
Q

hormones released or produced by kidneys

A

EPO, renin, calcitriol

116
Q

hormones acting on kidneys

A

angiotensin II, ANP, ADH, aldosterone, PTH

117
Q

effects of angiotensin II

A

vasoconstriction, stimulate thirst, simulate aldosterone/ADH release, increase Na/H20 reabsorption in proximal tubule

118
Q

overall effects of aldosterone

A

increased Na/H20 reabsorption, increased effective circulating volume, increased K/H+ exretion

119
Q

PTH release stimulated by

A

hypocalcemia and hyperphosphatemia

120
Q

PTH mechanisms

A

increase Ca reabsorption in DCT, decreases Ph reabsorption in PCT, increases conversion to active vitamin D

121
Q

furosemide effect on calcium

A

increase calcium excretion in loop of henle

122
Q

thiazide effect on calcium

A

decrease calcium excretion in DCT

123
Q

which type of hyperparathyroidism is seen in CKD

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