Renal exam - physiology Flashcards
(123 cards)
1
Q
How much body weight is ICF
A
40%
2
Q
How much body weight is ECF
A
20%
3
Q
how much body weight is total body water
A
60%
4
Q
what fraction of TBW is ICF
A
2/3
5
Q
what fraction of TBW is ECF
A
1/3
6
Q
is calcium primarily intracellular or extracellular
A
extracellular
7
Q
ECF is divided into what 2 compartments
A
plasma and interstitial
8
Q
when volume changes occur, which compartment is affected first
A
ECF
9
Q
Normal serum osmolarity
A
280-300
10
Q
example of isosmotic volume contraction
A
diarrhea
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
12
Q
example of isosmotic volume expansion
A
administration of isotonic saline solution
13
Q
what occurs with isosmotic volume expansion
A
isotonic fluid increases ECF volume with no fluid shifts and no changes in osmolarity
14
Q
example of hyperosmotic volume contraction
A
sweating
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
16
Q
example of hyperosmotic volume expansion
A
drinking a hyperosmotic sports drink
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.
18
Q
example of hyposmotic volume contraction
A
loss of salt (hypoaldosteronism)
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
20
Q
example of hyposmotic volume expansion
A
drinking water
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.
22
Q
what % of renal bloodflow goes to cortex
A
90%
23
Q
2 categories of control mechanisms of renal bloodflow
A
autoregulation, extrarenal
24
Q
components of autoregulation of renal blood flow
A
myogenic mechanism, tubuloglomerular feedback
25
explain myogenic mechanism
stretch of blood vessels causes them to constrict to reduce blood flow (reflex)
26
explain tubuloglomerular feedback
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
27
what does the extrarenal mechanism of controlling renal blood flow consist of
SNS, RAAS, other hormones
28
what can stimulate renin release
SNS stimulation of B1 receptors in JG cells, low Na at macula densa, decreased afferent arteriole BP
29
main goal of RAAS
to increase extracellular fluid volume
30
layers of the barrier between glomerulus and capsule
capillary endothelium, basement membrane, podocytes
31
which layer of the glomerular filter barrier has fenestrations and which has nephrin
endothelial cells; podocytes
32
low-moderate levels of SNS stimulation constrict ____
efferent arteriole
33
greater constriction of efferent arteriole does what to GFR
increases, then decreases as constriction continues
34
greater constriction of afferent arteriole does what to GFR
decreases
35
where does water leave the loop of henle
descending
36
where does salt leave the loop of henle
ascending
37
osmolarity of fluid leaving the PCT
isosmotic
38
goal of the counter-current multiplier
decrease osmolarity in tubule (pumps) and increase interstitial osmolarity, allowing water to flow out of the descending limb
39
limit of urinary concentration/osmolarity at bottom of loop of henle
1200 mOsm
40
what is vasa recta
vascular source for medulla
41
osmolarity of urine when it reaches collecting duct
120 mOsm
42
how is urine concentrated once it leaves the ascending loop
ADH forms aquaporins in DT/CD to allow water to leave the tubule and concentrate urine
43
what stimulates release of ADH
SNS stimulation, increased plasma osmolality (sensed by osmoreceptors in hypothalamus) and decreased blood pressure, sensed by baroreceptors (aortic arch, carotid sinus, LA, pulmonary vessels)
44
what releases ADH
posterior pituitary
45
effects of ADH on water, urine, plasma
increased water reabsorption/total body water, decreased urine volume, lower plasma osmolarity, increased blood volume
46
physiological response to osmoregulation
water excretion, retention or intake (via ADH/thirst)
47
physiological response to volume regulation
urinary sodium excretion or retention (via RAAS, SNS, ANP, ADH)
48
major anion of ICF
phosphates
49
major anions of ECF
Cl, HCO3, albumin
50
major cation of ICF
potassium
51
major cation of ECF
sodium
52
major buffer system of ECF
bicarbonate
53
major buffer systems of ICF
hemoglobin, proteins, phosphate
54
addition of strong acid to bicarbonate buffer system leads to
prevention of sudden change in pH, depletion of HCO3-, accumulation of CO2
55
addition of strong base to bicarbonate buffer system leads to
prevention of sudden change in pH, depletion of CO2, depletion of H2CO3
56
what two substances regulate pH
HCO3, pCO2
57
requirements of efficient functioning of the bicarbonate buffer system
removal of CO2 by lungs, addition of new HCO3 by kidneys
58
formula for determining expected pCO2 in metabolic acidosis
[HCO3-] +15 +/-2
59
formula for determining expected pCO2 in metabolic alkalosis
[HCO3-]+10 +/-5
60
formula for determining expected HCO3- in respiratory acidosis, acute phase
rise in [HCO3-] = (rise in pCO2)/10
61
formula for determining expected HCO3- in respiratory acidosis, chronic phase
rise in [HCO3-] = 4*(rise in pCO2)/10
62
formula for determining expected HCO3- in respiratory alkalosis, acute phase
drop in [HCO3-] = 2*(drop in pCO2)/10
63
formula for determining expected HCO3 in respiratory alkalosis, chronic phase
change in [HCO3-] = 4*(drop in pCO2)/10
64
steps of reabsorption of bicarb in PCT
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
how much filtered bicarb is reabsorbed
all of it
66
steps of creation of new HCO3- in PCT
glutamine metabolizes into ammonium and bicarb
67
factors that increase glutamine metabolism
acidosis and hypokalemia
68
2 main mechanisms of metabolic acidosis
loss of HCO3-, gain of acid
69
what mechanism of metabolic acidosis is usually associated with an increase in anion gap
gain of acid
70
2 areas where HCO3- can be lost
kidneys, GI tract
71
anion gap formula
Serum Na- (Cl+HCO3)
72
normal anion gap
8-12 mEq/L
73
mnemonic for high anion gap metabolic acidosis
MUDPILESCAT
74
what does MUDPILESCAT stand for
```
Methanol
Uremia
DKA
Propylene glycol
INH/Iron
Lactic acid
Ethylene glycol/Ethanol
Salicylates
CO2/cyanide
Aminoglycosides
Toluene
```
75
what is delta/delta
change in anion gap/change in HCO3-
76
what is the purpose of the delta/delta
to see if the change in anion gap is appropriate for the change in HCO3-, helps identify mixed disorder
77
delta/delta of 1-2
pure AG metabolic acidosis
78
delta/delta <1
AG metabolic acidosis with non-AG metabolic acidosis
79
delta/delta >2
AG metabolic acidosis with metabolic alkalosis
80
non-anion gap metabolic acidosis AKA
hyperchloremic acidosis
81
causes of non-anion gap metabolic acidosis
GI: diarrhea
Renal: RTA, carbonic anhydrase inhibitor, post-hypocapnia
82
why is anion gap normal in RTA and diarrhea
chloride is also elevated
83
if pCO2 is less than expected in metabolic acidosis
concomitant respiratory alkalosis
84
if pCO2 is greater than expected in metabolic acidosis
concomitant respiratory acidosis
85
what is osmolal gap for
to find out where there is a substance that may be causing acidosis in ECF
86
what does an osmolal gap greater than 10 mean
points towards the presence of a toxic alcohol
87
what does a positive urinary anion gap mean
kidneys are not making NH4: renal failure, RTA
88
what does a negative urinary anion gap mean
kidneys are making NH4: GI HCO3 loss due to diarrhea
89
stimuli for aldosterone release
hyperkalemia, volume depletion
90
where is aldosterone made
zona glomerulosa in adrenal cortex
91
if pCO2 is less than expected in metabolic alkalosis
concomitant respiratory alkalosis
92
if pCO2 is greater than expected pCO2 in metabolic alkalosis
concomitant respiratory acidosis
93
what is necessary for metabolic alkalosis to persist
aldosterone
94
2 major types of metabolic alkalosis
volume/saline/chloride sensitive and resistant
95
urine cl less than 10
volume/saline/chloride sensitive metabolic alkalosis: Hypotension
96
urine cl greater than 10
volume/saline/chloride resistant metabolic alkalosis: Hypertension, caused by renal artery stenosis, hyperaldosteronism
97
alkalosis is associated with what electrolyte derangement
hypokalemia
98
what does proteinuria signify
damage to glomerulus
99
why is creatinine clearance an estimation of GFR
amount filtered = amount cleared
100
GFR =
[urine]/[plasma] * urine flow rate
101
if amount excreted is greater than filtered
substance must have been secreted as well as filtered
102
amount of substance excreted =
urine concentration * urine flow rate OR filtered + secreted - reabsorbed
103
amount of substance filtered =
plasma concentration * GFR
104
if amount excreted is < filtered
the substance was reabsorbed or metabolized
105
small increase in angiotensin 2 effects
efferent arteriole constriction and increased GFR with an unchanged Kf
106
large increase in angiotensin 2 effects
increased arteriole resistance and decreased GFR with a decreased Kf
107
net effect of Na/K/ATPase
3 Na+ out, 2 K+ in
108
mechanism of secondary active transport
requires energy but the energy is derived from a different ATPase pump
109
example of carrier-mediated transport
glucose
110
at what plasma level does reduced glucose absorption occur`
200 mg/dl
111
at what plasma level are all glucose co-transports saturated
>350 mg/dl
112
what is fanconi syndrome
loss of proximal tubule function (polyuria, polydipsia, glycosuria with normal BGL)
113
target of furosemide
Na/K/2Cl in thick ascending loop of Henle
114
how much sodium is reabsorbed in thick ascending loop
25%
115
hormones released or produced by kidneys
EPO, renin, calcitriol
116
hormones acting on kidneys
angiotensin II, ANP, ADH, aldosterone, PTH
117
effects of angiotensin II
vasoconstriction, stimulate thirst, simulate aldosterone/ADH release, increase Na/H20 reabsorption in proximal tubule
118
overall effects of aldosterone
increased Na/H20 reabsorption, increased effective circulating volume, increased K/H+ exretion
119
PTH release stimulated by
hypocalcemia and hyperphosphatemia
120
PTH mechanisms
increase Ca reabsorption in DCT, decreases Ph reabsorption in PCT, increases conversion to active vitamin D
121
furosemide effect on calcium
increase calcium excretion in loop of henle
122
thiazide effect on calcium
decrease calcium excretion in DCT
123
which type of hyperparathyroidism is seen in CKD
secondary
