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step 1 - physiology > renal > Flashcards

renal Flashcards

1
Q

what do you use to measure plasma volume?

A

radiolabeled albumin

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2
Q

what do you use to measure extracellular volume?

A

inulin

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3
Q

normal osmolality?

A

285-295 mOsm/kg H2O

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4
Q

what does the fenestrated capillary endothelium of the glomerulus do?

A

acts as a size barrier

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5
Q

what does the basement membrane of the glomerulus do?

A

acts as a negative charge barrier

** has heparan sulfate

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6
Q

what component of the glomerulus is lost in nephrotic syndrome?

A

charge barrier

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7
Q

formula for renal clearance?

A

Cx = UxV/Px

where V = urine flow rate (mL/min)

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8
Q

what can you use to calculate GFR?

A 
inulin clearance (neither reabsorbed nor secreted)
creatinine clearance - slightly overestimates bc of moderate tubular secretion
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9
Q

what is normal GFR?

A

100 mL/min

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10
Q

what can you use to estimate effective renal plasma flow?

A

PAH - filtered and secreted in PCT, near 100% excretion

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11
Q

formula for eRPF?

A

eRPF = U(PAH) * V/P(PAH)
in other words, eRPF = PAH clearance

** understimates RPF by 10%

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12
Q

formula for renal blood flow?

A

RBF = RPF/(1 - Hct)

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13
Q

formula for filtration fraction?

A

FF = GFR/RPF

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14
Q

what is normal FF?

A

20%

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15
Q

formula for filtered load?

A

filtered load (mg/min) = GFR * plasma concentration

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16
Q

how do prostaglandins affect RPF, GFR, FF?

A

dilate afferent arteriole –> increased RPF and GFR, so FF remains the same

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17
Q

how does ATII affect RPF, GFR, FF?

A

constrict efferent arteriole –> decreased RPF and increased GFR –> increased FF

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18
Q

how does a change in plasma protein affect RPF, GFR, FF?

A

increase: decreased GFR, RPF remains same –> FF decreases
decrease: increased GFR, RPF remains same –> FF increases

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19
Q

how does constriction of the ureter affect RPF, GFR, FF?

A

decreases GFR, no change in RPG –> FF decreases

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20
Q

formula for excretion rate?

A

excretion rate = V * Ux

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21
Q

how to calculate reabsorption and secretion rates?

A 
reabsorption = filtered - excreted = (GFR * Px) - (V * Ux)
secretion = excreted - filtered
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22
Q

how is glucose reabsorbed in the kidneys?

A

in PCT

Na/glucose cotransport

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23
Q

what are thresholds of glucose reabsorption?

A

200 mg/dL - begin to have glucosuria

375 mg/dL - all transporters saturated (reached Tm)

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24
Q

pregnancy and glucose/AA reabsorption?

A

decrease PCT ability to reabsorb

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25
Q

how are AAs reabsorbed in kidneys?

A

PCT

Na-dependent transporters

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26
Q

Hartnup dz?

A

AR
deficiency in neutral AA transporters in PCT and enterocytes –> decreased tryptophan –> decreased niacin production –> pellagra

** tx: high-protein diet and niacin

27
Q

what happens in the PCT?

A

all glucose and AA reabsorption
most reabsorption of other electrolytes
secretion of NH3 - buffer for H+ secretion

** isotonic absorption

28
Q

where does PTH act on the kidney?

A

PCT: inhibits Na/P cotransport –> increases P excretion
DCT: increases Na/Ca exchange –> increases Ca reabsorption

29
Q

where does ATII act on the kidney?

A

PCT: stimulates Na/H exchange –> increased Na, H2O, HCO3 reabsorption

** contraction alkalosis!

30
Q

where does acetazolamide act on the kidney?

A

PCT: inhibits carbonic anhydrase, increases HCO3 excretion in urine

31
Q

what happens in the thin descending loop of Henle?

A

passive reabsorption of water
concentration of urine –> hypertonic

** impermeable to Na

32
Q

what happens in the thick ascending loop of Henle?

A

Na/K/Cl reabsorption via cotransporter
paracellular reabsorption of Ca and Mg (via K+ backleak–>membrane potential)

    • impermeable to H2O
    • urine becomes less concentrated
33
Q

where do loop diuretics act on the kidney?

A

thick ascending LOH

inhibit Na/K/Cl transporter

34
Q

what happens in the DCT?

A

Na, Cl reabsorption (via cotransporter)
Ca reabsorption
urine becomes hypotonic

35
Q

where do thiazide diuretics act on the kidney?

A

DCT - inhibit Na/Cl transporter

36
Q

what happens in the collecting tubule?

A
  • principal cells: Na reabsorbed in exchange for K and H secretion via Na/K pump, ENaC, apical K loss
  • H2O reabsorption via aquaporins (apical side of principal cells)
  • alpha-intercalated cells: HCO3/Cl exchange via H+ ATPase, H/K exchanger
37
Q

where does aldosterone act on the kidney?

A

collecting tubule

1) principal: upregulates apical K, Na/K pump, ENaC
2) alpha-intercalated: upregulates H+ ATPase –> increases HCO3/Cl exchanger activity

38
Q

where does ADH act on the kidney?

A

V2 receptor of collecting tubule

insertion of AQP on apical side

39
Q

generalized reabsorptive defect in PCT?

A

Fanconi syndrome
increased excretion of AAs, glucose, HCO3, Phos
may cause RTA2

** causes: hereditary, ischemia, MM, nephrotoxins/drugs, lead poisoning

40
Q

reabsorptive defect in thick ascending LOH?

A

Bartter syndrome - AR
affects Na/K/Cl cotransporter

** hypokalemia, metabolic alkalosis with hypercalciuria

41
Q

reabsorptive defect in DCT?

A

Gitelman - AR
affects Na/Cl cotransporter

** hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

42
Q

gain of function mutation in collecting tubule?

A

Liddle syndrome - AD
affects ENaC channel

    • HTN, hypokalemia, metabolic alkalosis, low aldosterone
    • tx: amiloride
43
Q

where do amiloride and triamterene act on the kidney?

A

collecting tubule - block ENac

K sparing diuretics

44
Q

syndrome of apparent mineralocorticoid excess?

A

11beta-hydroxysteroid DH deficiency - can’t convert cortisol to cortisone
excess cortisol –> increased mineralocorticoid receptor activity
HTN, hypokalemia, metabolic alkalosis; low aldosterone

45
Q

what does glycyrrhetic acid do to you?

A

(found in licorice)

blocks 11beta-hydroxysteroid DH –> gives you syndrome of apparent mineralocorticoid excess

46
Q

why does tubular inulin concentration increase along PCT?

A

bc of water reabsorption

47
Q

which solutes are reabsorbed at about the same rate as water in the PCT?

A

Na, K

48
Q

how does Cl concentration change in PCT?

A

initially reabsorbed slower than Na –> relative concentration in PCT increases
then rate increases to match Na rate –> concentration plateaus

49
Q

what makes angiotensinogen?

A

the liver

50
Q

what makes ACE?

A

the lungs

51
Q

what activates RAAS?

A

JG cells sense BP decrease
macula densa cells sense decreased Na delivery
B1 receptors sense increased sympathetic tone

52
Q

what cells make renin?

A

JG cells (in afferent arteriole)

53
Q

functions of ATII?

A

1) AT1 receptor on vascular smooth mm –> constriction
2) constriction of efferent arteriole –> increased FF
3) stimulates aldosterone and ADH release
4) increases PCT Na/H activity
5) stimulates thirst center in hypothalamus

54
Q

how do ANP and BNP interact with RAAS?

A

may act as “check” - relax vascular smooth mm via cGMP, causing increase in GFR without concurrent absorption of Na/H2O

55
Q

where is the macula densa?

A

DCT

56
Q

what do macula densa cells do?

A

sense decreased Na delivery to DCT

release renin –> vasoconstriction

57
Q

where is EPO made?

A

interstitial cells in peritubular capillary bed

released in response to hypoxia

58
Q

where is vitD converted to active form?

A

PCT

** enzyme: 1alpha hydroxylase

59
Q

Henderson Hasselbach?

A

pH = 6.1 + log ([HCO3-]/(0.03*PCO2))

60
Q

Winters formula?

A

PCO2 = 1.5[HCO3] + 8 +/- 2

61
Q

metabolic acidosis, hypokalemia, calcium phosphate kidney stones?

A

type I RTA
- distal: alpha intercalated cells can’t secrete H+ so no HCO3 generated

** causes: amphoB, analgesic nephropathy, congenital anomalies (e.g. obstruction)

62
Q

metabolic acidosis, hypokalemia, hypophosphatemic rickets?

A

type II RTA
- proximal: PCT can’t reabsorb HCO3

** causes: Fanconi, carbonic anhydrase inhibitors

63
Q

hypoaldo, hyperkalemia, decreased ammonia in urine?

A

type IV RTA
- decreased aldo –> hyperkalemia –> decreased PCT NH3 synthesis

** causes: decreased aldo production (diabetes, mx, adrenal insufficiency), aldo resistance (K+ sparing diuretics, obstructive nephropathy, bactrim)

step 1 - physiology (8 decks)

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