7 - renal physiology Flashcards
(159 cards)
1
Q
renal blood flow - % CO
A
20-25% cardiac output (1.2L/min)
2
Q
renal blood flow - regulated by
A
renal vascular resistance
3
Q
what is renal plasma flow
A
RPF = RBF x (1-hct). More concentrated blood has lower RPF
4
Q
para-aminohippuric acid is what
A
used to measure RPF
5
Q
nl RPF #?
A
670
6
Q
filtration fraction def
A
blood actually filtered by glomerulus
7
Q
filtration fraction - RBF and RPF
A
10% RBF and 20% RPF (80% unfiltered)
8
Q
what happens to unfiltered renal plasma flow
A
leaves glomerulus via efferent arterioles to become peritubular circulation
9
Q
2 types of nephrons and main diff
A
cortical (short tubule) and juxtamedullary (long tubule) nephron
10
Q
2 types of nephrons and % of all nephrons
A
cortical (85%) and juxtamedullary (15%) nephron
11
Q
loop of henley - which side is thick/thin
A
descending - thin, ascending - thick
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
13
Q
what is net filtration pressure #?
A
10-15mmhg
14
Q
what is def of renal clearance (creatinine)
A
volume of plasma cleared of a substance in a specific time (cc/minute)
15
Q
nl creatinine clearance
A
1mg/kg/hr or 1 mg/min
16
Q
by what % does creatinine overestimate GFR
A
15-20%
17
Q
what is nl decline in GFR with age
A
7cc/min/decade
18
Q
prox tubule - % na reabsorbed
A
70%
19
Q
thin descending loop - % na reabsorbed
A
0 - permeable to water only
20
Q
thin limb - effect of permeability
A
increased concentration
21
Q
thick ascending loop - % na reabsorbed
A
20%
22
Q
2 things that augment sodium reabsorbtion in thick ascendin limb
A
aldosterone and ADH
23
Q
thick ascending loop permeable to?
A
solutes, not water
24
Q
thick ascending loop works how?
A
sodium pumped out, resulting in hypotonic fluid at end of tubule
25
distal convoluted tubule - % na reabsorbed
10%
26
primary driver of reabsorbtion in PCT
Na-K ATPase pump out
27
primary driver of reabsorbtion in PCT - why
secondary active transport and passive reabsorbtion are dependent on co-transport of sodium in or ion gradient, respectively
28
what is secondary active transport
absorbtion of things co transported with sodium
29
what is passive reabsorbtion
negatively charged ions travel along electrical gradient created by na active transport
30
concentration gradient in kidney
300-1200
31
what type of nephrons are involved in countercurrent mech
juxtamedullary nephrons
32
what is countercurrent mech
interraction btw filtrate flow through loop of henle of JG nephrons and blood flow through vasa recta
33
how is na reabsorbed in PCT - 2
NA-H and Na-solute active transporters
34
glucose reabsorbtion in PCT
100% reabsorbed in PCT via na-gucose co-transporter
35
HCO3 and prox tubule
generated in cell and absorbed with sodium
36
aa, peptides, vitamins in PCT
90% reabs via 2ndary active transport w na
37
cations in PCT
passive transport along e-gradient
38
anions in PCT
passive transport along e-gradient for cl- and 2ndary transport w na
39
H2O in PCT
osmotically driven, aquaporins
40
where is ca reabsorbed
prox and distal tubules
41
where does PTH have effect on ca
DCT
42
where does aldosterone have effect
DCT and collecting duct
43
reabsorbtion via primary active transport in collecting duct
primary active transport by na, regulated by aldosterone, and medullary gradient allows for passive transport of cl- and HCO2 for reabsorbtion
44
where is ammonia secreted
PCT
45
how is NH4+ reabsorbed
NH3- secreted into lumen, traps H+
46
where is tubular secretion most active
PCT (also happens in DCT and collecting duct)
47
what gets secreted in collecting duct and what stimulates it - 3
K by aldosterone, NH3 to trap H+, and H based on blood pH
48
how to make dilute urine
ascending loop filtrate is allowed to pass to renal pelvis with no modification. Passive
49
how to make concentrated urine
ADH - makes collecting ducts permeable to water and increases water uptake from urine.
50
where is ADH made
hypothalamus
51
where is ADH stored
posterior pituitary
52
ADH secondary effect
makes collecting ducts more permeable to urea, promoting concentration gradient in inner medulla
53
atrial natiuretic peptide effect on urine
makes dilute urine
54
atrial natiuretic peptide effect on kidney
vasodilation of afferent arterioles --> inc GFR --> more na reaches macula densa and ANP opposes RAS therefore naturesis (loss of na)
55
ANP made/stored/released where
atrial myocytes in response to stretch (HTN, hypervolemia)
56
osmotic substances and diuresis
osmotic substances inc osmolality and hold water in filtrate
57
loop diuretics MOA
inhibit na/k/cl cotransporter on lumina membrane of thisk ascending loop of henle, reducing medullary solute content and impair urinary concentrating ability.
58
loop diuretics increase excretion of what 5 electrolytes
na, k, cl, ca, mg
59
thiazide MOA
inhibit na-cl exchanger in DISTAL convoluted tubule. More na in filtrate and more water excreted
60
thiazide effect on electrolites
decreaed serum [na/k], increased serum [ca]
61
kidney role in acid-base balance - 2
excrete non-volatile acids (lungs excrete volatile acids (esp CO2)), and reabsorb all HCO3
62
net effect of metabolism is to create
acid
63
nl urine pH
6
64
blood [HCO3-]
24 mM
65
blood PCO2
40 mmHg
66
anion gap calc
na-[cl+HCO3-]
67
nl anion gap
(10-12)
68
sources of net H+ gain - 4
CO2, nonvolatile acids (lcatic acid), loss of HCO3- in diarrhea, loss of HCO3- in urine
69
sources of net H+ loss - 4
loss in urine, loss in GI secretions, hyperventilation (blow off CO2), use of H+ in metabolism of organic anions
70
how do kidneys affect serum [H+]
by altering [HCO3-]
71
nl % HCO# reabsorbed
100%
72
how is HCO3- reabsorbed
HCO3- + H+ -(CA 1)-> CO2 + H2O - (CA2) --> HCO3- (to plasma) + H+ (back to tubule). CA= carbonic anhydrase
73
how to add HCO3 to serum
H+ combines with phosphate in tubule, CA2 still makes HCO3 from CO2 and H2O
74
metabolic acidosis - compensation
hyperventilation
75
metabolic alkalosis - compensation
hypoventilation
76
respiratory acidosis - compensation
renal HCO3- reabsorbtion
77
respiratory alkalosis - compensation
renal HCO3- excretion
78
3 hormone functions of kidney
erythropoetin, vit D ACTIVATION, endothelin production
79
where in kidney erythropoetin made
interstitial cells in kidney
80
what stimulates erythropoetin release
hypoxia and anemia
81
vit D as it passes through kidney
25-vit D --> 1,25 vit D
82
what are endothelins
made by kidney - work in vasoconstriction and salt retention. Functionally similar to RAS
83
def of renovascular disease
renin dependent HTN cured by correction of renal vasc HTN
84
nephrosclerosis
microvascular dz of kidney
85
% with refractory HTN who have RAS
3%
86
3 main categories of RAS
atherosclerosis, fibromuscular, secondary lesinos
87
% RAS lesions atherosclerosis
70%
88
% RAS lesions fibromuscular disease
20%
89
3 types of fibromuscular dysplasia
intimal, fibromuscular, perimedial
90
who gets intimal hyperplasia
kids < 18 yo
91
intimal hyperplasia characterized by
collagen inside elastic membrane
92
how does perimedial fibroplasia happen
collagen deposition in outer media within external elastica
93
what does perimedial fibropalsia angiogram look like
beaded with COLLATERALS
94
intimal hyperplasia on angiogram
smooth focal stenosis
95
what makes medial fibroplasia different
non-progressive.
96
medial fibroplasia on angiogram
string of beads
97
who is at risk of aneurysm rupture
women of child bearing age
98
what size aneurisms rupture
> 2-3 cm (la place law - wall tension is function of radius)
99
type of aneurism that is at higher risk of rupture
saccular
100
pathophys of ischemic renal artery disease
juxtaglomerular aparatus responds to decreased blood flow and low [sodium] (macula densa cells) releases renin --> inc BP, inc Na retention
101
what % stenosis is clinically significant
70% (bernuli principle - 70% decrease in diameter = 50% flow decrease)
102
where are macula densa
distal tubule
103
what does macula densa do
senses BP and releases renin when increased BP
104
path of RAS
angiotensinogen (liver) -(renin)-> angiotensin 1 -(ACE in lung)-> angiotensin 2
105
effects of angiotensin 2 (5)
inc central symp activity, tubular nacl retention K excretion, aldosterone release (hold nacl, release k), arterial constriction, ADH secretion (H2O absorbtion)
106
receptor for angiotensin 2
AT1
107
net effect of angiotensin 2
inc intracellular Ca --> vasocontriction and aldosterone adrenal
108
AT1 antagonists
sartans (ARB's)
109
how does angiotensin affect GFR
constricts efferent arteriole to maintain hydrostatic pressure
110
ACE inhibitor in RAS
cr goes up because decreased hydrostatic pressure
111
clinical char of renal vasc HTN (5)
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
when does captopril renogram not work
GFR < 50
113
best imaging study for RAS
duplex renal us - only detects > 60% stenosis. Cant quantify stenosis. CT/MRA not sensitive enough
114
criteria for renal salvage in ischemic nephropathy - 4
kidney > 9 cm, function on mag 3, cr < 30, 50% glomerulosclerosis on biopsy
115
principles to limit morbidity in surgery for surgical correction of RAS - 2
avoid badly diseased aorta's, correct extra-renal vasc disease prior to renal surg
116
when is nephrectomy best choicefor RAS- 6
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
best surgical correction for RAS
aortorenal bypass
118
surgery vs angioplasty - fibromuscular dz - 5
surgery for failed PTA, branch disease, total occlusion, aneurysms, dissections
119
surgery vs angioplasty - artherosclerosis
same as fibromuscular including simultaneous aortic repair
120
what have RCT's shown for RAS tx
surgery, stents, PTA are no better than medical therapy
121
contributing factors to kidney concentrating mechanism - 4
1. countercurrent multiplier, 2. urea diffussion by DCT, 3. vasa recta cycling salt to inner medulla, 4. aquaporin water channels (ADH)
122
3 parts to countercurrent mech (concentrating effect of kidney)
H2O diffusion through loop of henle, urea diffusion, vasa recta
123
loop of henle and counter current mech - AKA
aka countercurrent multiplier
124
loop of henle and counter current mech - mech
descending thin limb permeable to H2O, [filtrate] increases as H2O reabsorbed. Thick ascending limb permeable to solutes, not H2O
125
urea diffusion and countercurrent mech
deep medullary gradient bolstered by passive diffusion of urea through colelcting duct
126
vasa recta and countercurrent mech
facilitate [gradient] by cycling salt to inner medulla via efferents and out
127
hyponatremia usu results from what defect
renal water handling
128
primary defect in hypernatremia
impaired water intake in the setting of increased water loss
129
why r geriatric pts more at risk of hypernatremia - 2
decreased thirst response and decreased renal concentrating ability
130
first step when you see metabolic acidosis
calculate anion gap to look for missing anions
131
cardiac findings in hypokalemia - 4
tachycardia, prolonged QT interval, st depression, u waves
132
4 medical causes of hyperkalemia
drugs, hyperaldosteronism, chronic acidosis, renal failure
133
3 drugs causing hyperkalemia
ace inhibitor, K sparing diuretics, beta blockers
134
3 EKG findings in hyperkalemia
peaked t waves, shortened QT, ST segment depression,
135
3 signs of advanced hyperkalemia on EKG
widened QRS, increased PR interval, decreased p wave amplitude
136
when is calcium gluconate indicated in hyperkalemia
EKG shows signifcant abnormalities (QRS widening, loss of p wave, arrythmia)
137
high sodium concentration sx - 4
lethargy, weakness, irritability, twitching
138
low calcium sx - 4
tetany, depression, papilledema, seizures
139
high calcium sx - 3
abd pain, constipation, fatigue
140
low mg - 5
weakness, anorexia, tetany, delrium, coma
141
high phos sx - 3
tumor lysis syndrome, rhabdo, renal failure
142
where is calcium absorbed
majority in PCT and ascending loop, fine tuning (15%) in DCT and collecting duct
143
primary defect in RTA type 1
failure of H+ secretion in distal nephron
144
ammonium chloride test
provocative test for RTA type 1
145
RTA type 2 defect
failure of BICARB reabsorbtion in PCT
146
RTA type 2 finding
kid with growth retardation and metabolic bone disease (tiny tim)
147
2 ways to treat alkalosis with gastric substitution
PPI and acidificaiton with dilute HCL solution
148
metabolic problem in addition to K, Cl in jejunum
HYPOnatremia
149
treatment for jejunal metabolic abnormalities
nacl tabs, thiazide
150
why do ppl have acidois with ileum
inability to secrete acid as ammonium (reabsorbed) depeltes buffers
151
what happens with B12 deficiency
anemia and neurologic degeneration
152
why does postobstructive diuresis happen
urea is osmotic diuretic - loss of concentrating ability from urea washout from medulla
153
renal duplex criteria for renal vascular HTN
peak systolic velocity > 1.8 cm/sec = > 60% stenosis
154
renal vascular disease 1 kidney 1 clip vs 2 kidney 1 clip and plasma renin activity
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
renal us resistive index prognostic significance
if > 0.8 then revascularization unlikely to help renal function
156
where is renal artery angioplasty helpful
fibromuscular dysplasia
157
2 groups who get renal artery senosis surgical repair
1. surgical aortic repair, 2. pts with renal artery aneurism (@ risk for rupture, > 2 cm, no calcifications, expanding, HTN, pregnancy)
158
renal fuction after surgical/endovascular renal artery repair
no change usually
159
signs of RAS reversibility with stenting
progressive occlsion, collaterals, retrograde arterial filling, size > 7 cm, cr < 4, preservation of glomeruli on biopsy
