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review course > 7 - renal physiology > Flashcards

7 - renal physiology Flashcards

1
Q

renal blood flow - % CO

A

20-25% cardiac output (1.2L/min)

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2
Q

renal blood flow - regulated by

A

renal vascular resistance

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3
Q

what is renal plasma flow

A

RPF = RBF x (1-hct). More concentrated blood has lower RPF

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4
Q

para-aminohippuric acid is what

A

used to measure RPF

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5
Q

nl RPF #?

A

670

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6
Q

filtration fraction def

A

blood actually filtered by glomerulus

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7
Q

filtration fraction - RBF and RPF

A

10% RBF and 20% RPF (80% unfiltered)

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8
Q

what happens to unfiltered renal plasma flow

A

leaves glomerulus via efferent arterioles to become peritubular circulation

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9
Q

2 types of nephrons and main diff

A

cortical (short tubule) and juxtamedullary (long tubule) nephron

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10
Q

2 types of nephrons and % of all nephrons

A

cortical (85%) and juxtamedullary (15%) nephron

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11
Q

loop of henley - which side is thick/thin

A

descending - thin, ascending - thick

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12
Q

how is net filtration pressure for glomerulus calculated

A

net filtration pressure = glomerular hydrostatic pressure (55mmhg) - colloid osmotic pressure (30 mmg ) - capsular hydrostatic pressure

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13
Q

what is net filtration pressure #?

A

10-15mmhg

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14
Q

what is def of renal clearance (creatinine)

A

volume of plasma cleared of a substance in a specific time (cc/minute)

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15
Q

nl creatinine clearance

A

1mg/kg/hr or 1 mg/min

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16
Q

by what % does creatinine overestimate GFR

A

15-20%

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17
Q

what is nl decline in GFR with age

A

7cc/min/decade

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18
Q

prox tubule - % na reabsorbed

A

70%

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19
Q

thin descending loop - % na reabsorbed

A

0 - permeable to water only

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20
Q

thin limb - effect of permeability

A

increased concentration

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21
Q

thick ascending loop - % na reabsorbed

A

20%

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22
Q

2 things that augment sodium reabsorbtion in thick ascendin limb

A

aldosterone and ADH

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23
Q

thick ascending loop permeable to?

A

solutes, not water

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24
Q

thick ascending loop works how?

A

sodium pumped out, resulting in hypotonic fluid at end of tubule

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25
Q

distal convoluted tubule - % na reabsorbed

A

10%

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26
Q

primary driver of reabsorbtion in PCT

A

Na-K ATPase pump out

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27
Q

primary driver of reabsorbtion in PCT - why

A

secondary active transport and passive reabsorbtion are dependent on co-transport of sodium in or ion gradient, respectively

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28
Q

what is secondary active transport

A

absorbtion of things co transported with sodium

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29
Q

what is passive reabsorbtion

A

negatively charged ions travel along electrical gradient created by na active transport

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30
Q

concentration gradient in kidney

A

300-1200

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31
Q

what type of nephrons are involved in countercurrent mech

A

juxtamedullary nephrons

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32
Q

what is countercurrent mech

A

interraction btw filtrate flow through loop of henle of JG nephrons and blood flow through vasa recta

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33
Q

how is na reabsorbed in PCT - 2

A

NA-H and Na-solute active transporters

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34
Q

glucose reabsorbtion in PCT

A

100% reabsorbed in PCT via na-gucose co-transporter

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35
Q

HCO3 and prox tubule

A

generated in cell and absorbed with sodium

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36
Q

aa, peptides, vitamins in PCT

A

90% reabs via 2ndary active transport w na

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37
Q

cations in PCT

A

passive transport along e-gradient

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38
Q

anions in PCT

A

passive transport along e-gradient for cl- and 2ndary transport w na

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39
Q

H2O in PCT

A

osmotically driven, aquaporins

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40
Q

where is ca reabsorbed

A

prox and distal tubules

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41
Q

where does PTH have effect on ca

A

DCT

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42
Q

where does aldosterone have effect

A

DCT and collecting duct

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43
Q

reabsorbtion via primary active transport in collecting duct

A

primary active transport by na, regulated by aldosterone, and medullary gradient allows for passive transport of cl- and HCO2 for reabsorbtion

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44
Q

where is ammonia secreted

A

PCT

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45
Q

how is NH4+ reabsorbed

A

NH3- secreted into lumen, traps H+

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46
Q

where is tubular secretion most active

A

PCT (also happens in DCT and collecting duct)

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47
Q

what gets secreted in collecting duct and what stimulates it - 3

A

K by aldosterone, NH3 to trap H+, and H based on blood pH

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48
Q

how to make dilute urine

A

ascending loop filtrate is allowed to pass to renal pelvis with no modification. Passive

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49
Q

how to make concentrated urine

A

ADH - makes collecting ducts permeable to water and increases water uptake from urine.

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50
Q

where is ADH made

A

hypothalamus

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51
Q

where is ADH stored

A

posterior pituitary

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52
Q

ADH secondary effect

A

makes collecting ducts more permeable to urea, promoting concentration gradient in inner medulla

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53
Q

atrial natiuretic peptide effect on urine

A

makes dilute urine

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54
Q

atrial natiuretic peptide effect on kidney

A

vasodilation of afferent arterioles –> inc GFR –> more na reaches macula densa and ANP opposes RAS therefore naturesis (loss of na)

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55
Q

ANP made/stored/released where

A

atrial myocytes in response to stretch (HTN, hypervolemia)

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56
Q

osmotic substances and diuresis

A

osmotic substances inc osmolality and hold water in filtrate

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57
Q

loop diuretics MOA

A

inhibit na/k/cl cotransporter on lumina membrane of thisk ascending loop of henle, reducing medullary solute content and impair urinary concentrating ability.

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58
Q

loop diuretics increase excretion of what 5 electrolytes

A

na, k, cl, ca, mg

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59
Q

thiazide MOA

A

inhibit na-cl exchanger in DISTAL convoluted tubule. More na in filtrate and more water excreted

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60
Q

thiazide effect on electrolites

A

decreaed serum [na/k], increased serum [ca]

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61
Q

kidney role in acid-base balance - 2

A

excrete non-volatile acids (lungs excrete volatile acids (esp CO2)), and reabsorb all HCO3

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62
Q

net effect of metabolism is to create

A

acid

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63
Q

nl urine pH

A

6

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64
Q

blood [HCO3-]

A

24 mM

65
Q

blood PCO2

A

40 mmHg

66
Q

anion gap calc

A

na-[cl+HCO3-]

67
Q

nl anion gap

A

(10-12)

68
Q

sources of net H+ gain - 4

A

CO2, nonvolatile acids (lcatic acid), loss of HCO3- in diarrhea, loss of HCO3- in urine

69
Q

sources of net H+ loss - 4

A

loss in urine, loss in GI secretions, hyperventilation (blow off CO2), use of H+ in metabolism of organic anions

70
Q

how do kidneys affect serum [H+]

A

by altering [HCO3-]

71
Q

nl % HCO# reabsorbed

A

100%

72
Q

how is HCO3- reabsorbed

A

HCO3- + H+ -(CA 1)-> CO2 + H2O - (CA2) –> HCO3- (to plasma) + H+ (back to tubule). CA= carbonic anhydrase

73
Q

how to add HCO3 to serum

A

H+ combines with phosphate in tubule, CA2 still makes HCO3 from CO2 and H2O

74
Q

metabolic acidosis - compensation

A

hyperventilation

75
Q

metabolic alkalosis - compensation

A

hypoventilation

76
Q

respiratory acidosis - compensation

A

renal HCO3- reabsorbtion

77
Q

respiratory alkalosis - compensation

A

renal HCO3- excretion

78
Q

3 hormone functions of kidney

A

erythropoetin, vit D ACTIVATION, endothelin production

79
Q

where in kidney erythropoetin made

A

interstitial cells in kidney

80
Q

what stimulates erythropoetin release

A

hypoxia and anemia

81
Q

vit D as it passes through kidney

A

25-vit D –> 1,25 vit D

82
Q

what are endothelins

A

made by kidney - work in vasoconstriction and salt retention. Functionally similar to RAS

83
Q

def of renovascular disease

A

renin dependent HTN cured by correction of renal vasc HTN

84
Q

nephrosclerosis

A

microvascular dz of kidney

85
Q

% with refractory HTN who have RAS

A

3%

86
Q

3 main categories of RAS

A

atherosclerosis, fibromuscular, secondary lesinos

87
Q

% RAS lesions atherosclerosis

A

70%

88
Q

% RAS lesions fibromuscular disease

A

20%

89
Q

3 types of fibromuscular dysplasia

A

intimal, fibromuscular, perimedial

90
Q

who gets intimal hyperplasia

A

kids < 18 yo

91
Q

intimal hyperplasia characterized by

A

collagen inside elastic membrane

92
Q

how does perimedial fibroplasia happen

A

collagen deposition in outer media within external elastica

93
Q

what does perimedial fibropalsia angiogram look like

A

beaded with COLLATERALS

94
Q

intimal hyperplasia on angiogram

A

smooth focal stenosis

95
Q

what makes medial fibroplasia different

A

non-progressive.

96
Q

medial fibroplasia on angiogram

A

string of beads

97
Q

who is at risk of aneurysm rupture

A

women of child bearing age

98
Q

what size aneurisms rupture

A

> 2-3 cm (la place law - wall tension is function of radius)

99
Q

type of aneurism that is at higher risk of rupture

A

saccular

100
Q

pathophys of ischemic renal artery disease

A

juxtaglomerular aparatus responds to decreased blood flow and low [sodium] (macula densa cells) releases renin –> inc BP, inc Na retention

101
Q

what % stenosis is clinically significant

A

70% (bernuli principle - 70% decrease in diameter = 50% flow decrease)

102
Q

where are macula densa

A

distal tubule

103
Q

what does macula densa do

A

senses BP and releases renin when increased BP

104
Q

path of RAS

A

angiotensinogen (liver) -(renin)-> angiotensin 1 -(ACE in lung)-> angiotensin 2

105
Q

effects of angiotensin 2 (5)

A

inc central symp activity, tubular nacl retention K excretion, aldosterone release (hold nacl, release k), arterial constriction, ADH secretion (H2O absorbtion)

106
Q

receptor for angiotensin 2

A

AT1

107
Q

net effect of angiotensin 2

A

inc intracellular Ca –> vasocontriction and aldosterone adrenal

108
Q

AT1 antagonists

A

sartans (ARB’s)

109
Q

how does angiotensin affect GFR

A

constricts efferent arteriole to maintain hydrostatic pressure

110
Q

ACE inhibitor in RAS

A

cr goes up because decreased hydrostatic pressure

111
Q

clinical char of renal vasc HTN (5)

A
  1. abrupt onset HTN < 30 yo (fibromuscular lesions) or > 50 yo (atherosclerosis), 2. severe/refractory HTN, 3. HTN < 2 yrs, 4. hypokalemia, 5. progressive azotemia w meds for HTN
112
Q

when does captopril renogram not work

A

GFR < 50

113
Q

best imaging study for RAS

A

duplex renal us - only detects > 60% stenosis. Cant quantify stenosis. CT/MRA not sensitive enough

114
Q

criteria for renal salvage in ischemic nephropathy - 4

A

kidney > 9 cm, function on mag 3, cr < 30, 50% glomerulosclerosis on biopsy

115
Q

principles to limit morbidity in surgery for surgical correction of RAS - 2

A

avoid badly diseased aorta’s, correct extra-renal vasc disease prior to renal surg

116
Q

when is nephrectomy best choicefor RAS- 6

A
  1. branch disease/ occlusion/Infarction, 2. severe atrophy < 9 cm, 3.segmental hypoplasia, 4. non correctable lesions, 5. failed prior revasc, 6. good contralat function
117
Q

best surgical correction for RAS

A

aortorenal bypass

118
Q

surgery vs angioplasty - fibromuscular dz - 5

A

surgery for failed PTA, branch disease, total occlusion, aneurysms, dissections

119
Q

surgery vs angioplasty - artherosclerosis

A

same as fibromuscular including simultaneous aortic repair

120
Q

what have RCT’s shown for RAS tx

A

surgery, stents, PTA are no better than medical therapy

121
Q

contributing factors to kidney concentrating mechanism - 4

A
  1. countercurrent multiplier, 2. urea diffussion by DCT, 3. vasa recta cycling salt to inner medulla, 4. aquaporin water channels (ADH)
122
Q

3 parts to countercurrent mech (concentrating effect of kidney)

A

H2O diffusion through loop of henle, urea diffusion, vasa recta

123
Q

loop of henle and counter current mech - AKA

A

aka countercurrent multiplier

124
Q

loop of henle and counter current mech - mech

A

descending thin limb permeable to H2O, [filtrate] increases as H2O reabsorbed. Thick ascending limb permeable to solutes, not H2O

125
Q

urea diffusion and countercurrent mech

A

deep medullary gradient bolstered by passive diffusion of urea through colelcting duct

126
Q

vasa recta and countercurrent mech

A

facilitate [gradient] by cycling salt to inner medulla via efferents and out

127
Q

hyponatremia usu results from what defect

A

renal water handling

128
Q

primary defect in hypernatremia

A

impaired water intake in the setting of increased water loss

129
Q

why r geriatric pts more at risk of hypernatremia - 2

A

decreased thirst response and decreased renal concentrating ability

130
Q

first step when you see metabolic acidosis

A

calculate anion gap to look for missing anions

131
Q

cardiac findings in hypokalemia - 4

A

tachycardia, prolonged QT interval, st depression, u waves

132
Q

4 medical causes of hyperkalemia

A

drugs, hyperaldosteronism, chronic acidosis, renal failure

133
Q

3 drugs causing hyperkalemia

A

ace inhibitor, K sparing diuretics, beta blockers

134
Q

3 EKG findings in hyperkalemia

A

peaked t waves, shortened QT, ST segment depression,

135
Q

3 signs of advanced hyperkalemia on EKG

A

widened QRS, increased PR interval, decreased p wave amplitude

136
Q

when is calcium gluconate indicated in hyperkalemia

A

EKG shows signifcant abnormalities (QRS widening, loss of p wave, arrythmia)

137
Q

high sodium concentration sx - 4

A

lethargy, weakness, irritability, twitching

138
Q

low calcium sx - 4

A

tetany, depression, papilledema, seizures

139
Q

high calcium sx - 3

A

abd pain, constipation, fatigue

140
Q

low mg - 5

A

weakness, anorexia, tetany, delrium, coma

141
Q

high phos sx - 3

A

tumor lysis syndrome, rhabdo, renal failure

142
Q

where is calcium absorbed

A

majority in PCT and ascending loop, fine tuning (15%) in DCT and collecting duct

143
Q

primary defect in RTA type 1

A

failure of H+ secretion in distal nephron

144
Q

ammonium chloride test

A

provocative test for RTA type 1

145
Q

RTA type 2 defect

A

failure of BICARB reabsorbtion in PCT

146
Q

RTA type 2 finding

A

kid with growth retardation and metabolic bone disease (tiny tim)

147
Q

2 ways to treat alkalosis with gastric substitution

A

PPI and acidificaiton with dilute HCL solution

148
Q

metabolic problem in addition to K, Cl in jejunum

A

HYPOnatremia

149
Q

treatment for jejunal metabolic abnormalities

A

nacl tabs, thiazide

150
Q

why do ppl have acidois with ileum

A

inability to secrete acid as ammonium (reabsorbed) depeltes buffers

151
Q

what happens with B12 deficiency

A

anemia and neurologic degeneration

152
Q

why does postobstructive diuresis happen

A

urea is osmotic diuretic - loss of concentrating ability from urea washout from medulla

153
Q

renal duplex criteria for renal vascular HTN

A

peak systolic velocity > 1.8 cm/sec = > 60% stenosis

154
Q

renal vascular disease 1 kidney 1 clip vs 2 kidney 1 clip and plasma renin activity

A

1 kidney 1 clip = bilateral RAS and unchanged plasma renin activity, however na retained due to low perfusion pressure and water retention/HTN occurs. 2 kidney 1 clip - stenotic kidney rleases renin to increase perfusion pressure, resulting in ACE responsive HTN with nl bloodvolume

155
Q

renal us resistive index prognostic significance

A

if > 0.8 then revascularization unlikely to help renal function

156
Q

where is renal artery angioplasty helpful

A

fibromuscular dysplasia

157
Q

2 groups who get renal artery senosis surgical repair

A
  1. surgical aortic repair, 2. pts with renal artery aneurism (@ risk for rupture, > 2 cm, no calcifications, expanding, HTN, pregnancy)
158
Q

renal fuction after surgical/endovascular renal artery repair

A

no change usually

159
Q

signs of RAS reversibility with stenting

A

progressive occlsion, collaterals, retrograde arterial filling, size > 7 cm, cr < 4, preservation of glomeruli on biopsy

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