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USMLE S1 > Kidney, Urinary Tract and Electrolytes > Flashcards

Kidney, Urinary Tract and Electrolytes Flashcards

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USMLE® Step 1 flashcards
1
Q

subendothelial immune complex deposition is which pathology?

A

type I membranoproliferative glomerulonephritis

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2
Q

what is bethanechol?

A

mAChR agonist used for acute neurogenic urinary retention

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3
Q

pathophysiology of acute interstitial nephritis?

A

drug-induced hypersensitivity reaction involving the interstitium and tubules in the kidney, leads to AKI

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4
Q

what molecules do you use to estimate GFR and RPF?

A

GFR = inulin, freely filtered and neither secreted nor resorbed

RPF = para-aminohippuric acid (PAH), combination of filtration and secretion means that all PAH entering the kidney is lost to the urine

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5
Q

which disease predisposes to angiomyolipoma? what is this tumour?

A

tuberous sclerosis hamartoma of connective tissue

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6
Q

2 classes of aetiology for acute tubular necrosis?

A
  • nephrotoxic
  • ischaemic –> consequence of prerenal AKI
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7
Q

non-enzymatic glycosylation occurs preferentially at which site of the glomerulus in DM?

A

efferent arteriole leads to hyaline arteriolosclerosis, increased pressure in the glomerulus leading to hyperfiltration

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8
Q

Minimal change disease histological findings? Immune fluorescence?

A

nil on light microscopy effacement of the podocyte foot processes on EM nil on IF

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9
Q

what are the two main embryonic structues giving rise to kidey and what do they turn out to become?

A
  1. ureteric bud - ureters, calyx, pelvis, collecting ducts
  2. metanephric mesenchyme - glomerulus through DCT
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10
Q

which diuretics lead to low urine Ca++

A

thiazides

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11
Q

pathoG - muddy brown casts

A

acute tubular necrosis

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12
Q

6 aetiologies of nephrotic sydnrome

A
  1. minimal change disease 2. focal segmental glomerulonephritis 3. membranous nephropathy 4. MPGN 5. diabetes mellitus 6. systemic amyloidosis
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13
Q

what is the effect of ACE-I on glomerular filtration rate?

A

inhibit ACE, decrease AT II, prevent constriction of efferent arteriole

decreases GFR

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14
Q

location of immune complex in membranoproliferative glomerulonephritis type 2 - ‘dense deposit disease’

associated condition

A

intramembranous

positive C3 nephritic factor (autoantibody), constituent conversion of C3, leading to nephritic syndrome

(lab finding = decreased circulating C3)

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15
Q

a shrunken, cystic kidney suggests what pathology?

A

end-stage renal failure on dialysis

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16
Q

association with horseshoe kidneys (2)

A

ureteropelvic junction obstruction and hydronephrosis

stones and infection

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17
Q

focal segmental glomerular sclerosis disease association(s)

A

HIV, sickle cell disease, heroin abuse

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18
Q

what is this?

underlying condition?

A

renal angiomyolipoma

associated with tuberous sclerosis

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19
Q

nephrolithiasis shape = coffin lid, rectangular prism radio opaque

A

Magnesium ammonium phosphate (MAP)

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20
Q

site of action of mannitol?

A

where the tubule is permeable to water freely

PCT and dLH

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21
Q

in a woman, ureter passes infront of what artery and underneath what artery in the pelvis?

A

infront - internal iliac

behind - uterine (within uterosacral ligament)

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22
Q

focal segmental glomerular sclerosis race association

A

Hispanic and African-American

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23
Q

Churg-Strauss features (4)

A
  1. RPGN 2. asthma 3. eosinophilia 4. granulomatous inflammation
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24
Q

nephrolithiasis shape = diamond or rhombus non radio opaque

A

urate

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25
Q

a heroin addict presents with nephrotic syndrome - what is the most likely pathology?

A

focal segmental glomerulonephritis

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26
Q

crystalisation of urate crystals occurs where in the nephron? why?

A

collecting ducts low pH

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27
Q

blood supply to the proximal ureters

blood supply to the distal ureteres

A

renal arteries

superior vesical arteries

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28
Q

spike and dome appearance on IF is suggestive of what pathology?

A

membranous nephropathy

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29
Q

patient with SLE develops nephritic syndrome. what is the most likely pathology?

A

diffuse proliferative glomerulonephritis which is one of the Rapidly Progressive Glomerulonephritides

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30
Q

RPGN IF findings = granular (2)

A

Immune complex mediated PSGN or diffuse proliferative glomerulonephritis

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31
Q

equation for filtration fraction?

A

FF = GFR/RPF

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32
Q

major complication of PSGN?

A

rapidly progressive glomerulonephritis - renal failure in weeks to months

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33
Q

metolazone is what?

A

thiazide diuretic

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34
Q

what is the normal handling of potassium along the nephron?

A

free filtration at the glomerulus, 70% isotonic resporption at PCT

20-25% resorption across NKCC in TALH

point of control = DCT and collecting duct

excretion through principal cells (Na/K ATPase), resorption in alpha-intercalated cells

increase excretion = high extracellular K+, aldosterone, alkalosis

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35
Q

nephrolithiasis shape = hexagon radio opaque

A

cystine

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36
Q

3 diseases associated with Wilms tumour

A
  1. WAGR 2. Denys-Drash syndrome 3. Beckwith-Wiedemann syndrome
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37
Q

5 nephrotoxins that can cause acute tubular necrosis?

A

uric acid - tumour lysis syndrome

aminoglycosides

ethylene glycol (associated oxalate crystals in urine)

heavy metals - lead

myoglobin (crush injury)

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38
Q

what are the nephrotoxic effects of amphotericin B?

A

decreased GFR and direct toxicity to the epithelium

results in anaemia (decreased EPO), hypokalaemia/hypoMg++

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39
Q

asymptomatic with one hypertrophied kidney at birth?

A

congential solitary functioning kidney

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40
Q

EPO is produced by which cells?

A

renal peritubular interstitial cells

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41
Q

what is normal GFR?

A

125 mL/min

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42
Q

2 clinical features of renal papillary necrosis?

A

gross haematuria and flank pain

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43
Q

what is the final structure of the developing kidney to canalize?

A

uteropelvic junction - detected on USS as hydronephrosis

most common site of obstruction

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44
Q

what is the benefit of ARB over ACE-I?

A

does not give bradykinin symptoms

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45
Q

functional definition of nephrotic syndrome

A

> 3.5 g/day protein in 24 hour urine collection

46
Q

4 causes of renal papillary necrosis

A
  1. analgesic abuse (aspirin or pheacetin) 2. diabetes mellitus 3. sickle cell disease (or trait) 4. severe, acute pyelonephritis
47
Q

isolated haematuria & hearing loss suggest?

A

Alport syndrome (also ocular disturbance and X-linked inheritance pattern)

48
Q

which diuretics lead to acidaemia?

A
  1. carbonic anhydrase inhibitors (acteazolamide)
  2. potassium sparing diuretics

reduced secretion of K+/H+ in DCT/CD; hyperkalaemia forces protons out of cells through K+/H+ antiporter

49
Q

which diuretics cause an increase in urine potassium?

A

mostly loop and thiazide diuretics, hence hypoK+

50
Q

what is the site of action of acetazolamine in the nephron?

A

PCT and dLH

51
Q

which diuretics lead to alkalosis and what are the 3 mechanisms?

A

loop diuretics and thiazides

  1. contraction alkalosis - total volume decrease, RAAS activation, Na+/H+ resorption in PCT, HCO3- follows, total body bicarb increases
  2. loss of K+, hypokalaemia pulls K+ out of cells forcing H+ into cells out of plasma
  3. paradoxical aciduria - hypokalaemia means H+ rather then K+ is secreted for Na+ resorption in DCT/CD across Na+/K+ transporter
52
Q

RPGN IF findings = linear (1)

A

Goodpasture IgA bound in a line to GBM

53
Q

prenatal hydronephrosis and thickened bladder wall suggests…?

A

posterior urethral valve

only in males, most common bladder outlet obstruction

54
Q

patient with SLE develops nephrotic syndrome. what is the most likely pathology?

A

membranous nephropathy

55
Q

4 blood findings with nephrotic syndrome

A
  1. hypoalbuminaemia 2. hypogammaglobulinaemia 3. hypercholesterolaemia 4. hypercoagulability - selective loss of antithrombin III
56
Q

subepithelial immune complex deposition is which pathology?

A

membranous nephropathy

57
Q

renal blood flow = 1.0

GFR = 0.1

haematocrit = 0.5

what is the filtration fraction?

A

FF = GFR/RPF; RPF = RBF * (1 - Hct)

FF = (0.1) / (1.0 - 0.5) = 0.2

58
Q

bugs causing cystitis

A

E Coli (80%) Staph saprophyticus (young, sexually active women) Klebs pneumoniae Proteus - alkaline urine Enterococcus faecalis

59
Q

what is the site and mechanism of action of potassium sparing diuretics?

A

DCT and collecting duct

Na+ channel blockers/reduce expression

60
Q

where is the site of PTH action in the nephron? what channel and what is the net result?

A

proximal CT

inhibits NaPi cotransport, increasing PO43- excretion

distal CT

stimulates Na+/Ca++ exchange at the basolateral surface, increasing Ca++ resorption

61
Q

how long following an episode of acute tubular necrosis does normal kidney function return?

A

3 weeks

62
Q

location of immune complex in membranoproliferative glomerulonephritis type 1

associated condition

A

subendothelial

Hepatitis B & C

63
Q

what’s the formula for clearance of substance in the kidney?

A

clearance of ‘x’ = [x]urine * (urine flow)/[x]plasma

urine flow usually in mL/min, just make sure units for concentration are equivalent

64
Q

pathoG Kimmelstiel-Wilson

A

Diabetes mellitus sclerotic nodules formed in the glomerular mesangium

65
Q

what are the adverse effects of potassium sparing diuretics?

A

hyperkalaemia

spironolactone = anti-androgen effects (gynaecomastia)

66
Q

where does horseshoe kidney get stuck?

A

inferior mesenteric artery

67
Q

pathoG - eosinophil in urine

A

acute interstitial nephritis

68
Q

caudal end of mesonephric duct (mesoderm) produces what structure?

A

bladder trigone

where the rest of the bladder is endoderm

69
Q

what are the metabolic effects of loop diuretics?

A
  1. hypokalaemia
  2. contraction alkalosis (activation of RAAS following contraction dumps H+ in exchange for Na+)
70
Q

which kidney do you take in transplant donation and why?

A

left kidney b/c longer renal vein

71
Q

membranous nephropathy is associated with which 4 conditions?

A

SLE HBV HCV solid tumours

72
Q

what does mesonephros do?

A

interim kidney for 1st trimester then degenerates

forms part of male genital system

73
Q

focal segmental glomerular sclerosis histological findings? EM/Immune fluorescence?

A

sclerosis (collagen deposition) of only a segment of the glomerulus (H&E)

effacement of the podocyte foot processes on EM

nil on IF

74
Q

complications of duplex collecting system

A

viscoureteric reflux and ureteral obstruction (UTIs)

75
Q

pathoG - white blood cell cast

A

pyelonephritis

76
Q

RPGN IF findings = negative (3)

A

Wegener’s granulomatosis (cANCA) microscopic polyangiitis (pANCA) Churg-Strauss syndrome (pANCA)

77
Q

tumour lysis syndrome prophylaxis

A
  1. adequate hydration (good GFR, less likely to build up toxins in tubule) 2. allopurinol - limit the conversion of amino acids to uric acid all in one go
78
Q

the classic triad of RCC

A

haematuria palpable mass flank pain

79
Q

what is the most common cause of nephrotic syndrome in otherwise healthy Caucasian adults?

A

membranous nephropathy

80
Q

immune signalling mechanism leading to glomerular inflammation in nephritic syndrome

A
  1. immune complex deposition
  2. activation of complement C5a
  3. activation attracts neutrophils (hypercellular on H&E)
  4. neutrophils mediate inflammation and damage
81
Q

a large, cystic kidney suggests what pathology?

A

polycystic kidney disease

82
Q

what is the mechanism of acyclovir nephrotoxicity?

A

renal excretion

if concentration builds up in collecting duct then crystalisation and renal tubular damage will occur

prophylaxis with aggressive IV fluids

83
Q

what is the site and mechanism of action for thiazide diuretics?

A

inhibit NaCl reabsorption in DCT

reduces Ca+ excretion

84
Q

pathoG waxy casts

A

chronic pyelonephritis, chronic kidney disease, end-stage renal failure

85
Q

what are the adverse effects of foscarnet and what are the mechanisms?

A

hypocalaemia and hypomagnesaemia

  1. direct chelator of calcium
  2. renal wasting of magnesium, decrease PTH, exacerbate hypoCa++
86
Q

nephrolithiasis shape = octahedron radio opaque

A

calcium oxalate

87
Q

pathoG subepithelial hump

A

post streptococcal glomerulonephritis

88
Q

what are the adverse effects of loop diuretics?

think: direct effect, metabolic disturbance, hypersensitivity

A

ototoxicity

hypoK+/Mg++, metabolic alkalosis

sulfa allergy/interstitial nephritis

89
Q

which drug therapy is best management to prevent development of renal failure in a diabetic?

A

ACE inhibitor

90
Q

what is the effect of the sympathetic nervous system on RAAS?

A

sympathetic action on beta1-adrenoceptors on macula densa increases renin secretion

beta-blockers main action on hypertension is through decreasing RAAS

91
Q

failure of the ureteric bud to induce proper differentiation of the metanephric mesenchyme results in what disease?

A

multicystic dysplastic kidney

92
Q

gold standard for UTI diagnosis

A

>100,000 colony forming units on urine culture

93
Q

what embryonic tissue gives rise to the kidneys?

A

metanephros

94
Q

brown, granular casts in the urine suggests what pathology?

A

acute tubular necrosis necrotic cells plug the tubule, casting into shape and obstructing flow, decreasing GFR. eventually pass through into the urine

95
Q

chlorthialidone is what?

A

thiazide diuretic

96
Q

when does pronephros degenerate?

A

by week 4

97
Q

what is the site and mechanism of action of loop diuretics?

2 examples

A

thick ascending LH

inhibit NKCC cotransport, natriuresis.
increase excretion of Ca++ ‘loops lose Ca++’

furosemide, bumetanide, torsemide, ethacrynic acid (nonsulfa drug)

98
Q

presence of ‘M protein’ refers to which organism? what is the clinical relevance?

A

group A beta-haemolytic streptococcus increases the chance of developing PSGN following skin or pharynx infection

99
Q

what are the benefits and risks of using ethacrynic acid over furosemide?

A

cannot induce sulpha allergy

more ototoxic

100
Q

pathoG red cell cast

A

nephritic syndrome glomerular bleeding

101
Q

what are the histopathologic findings in membranous nephropathy?

A

light microscopy = thickened GBM EM = subepithelial immune complex deposit with ‘spike & dome’ appearance IF = granular deposits

102
Q

biopsy - uniform, diffuse thickening of the basement membrane without an increase in cellularity suggests which pathology?

A

membranous glomerulopathy

103
Q

what are the adverse effects of thiazide diuretics?

A

hypoK+/Na+ metabolic alkalosis

hyperGLUC -glycaemia, lipidaemia, uraemia, calcaemia

104
Q

triamterene is what?

A

Na+ channel blocker in cortical collecting duct, K+-sparing diuretic

same action as amiloride

105
Q

acetazolamide causes alkalosis or acidosis?

A

reduces resorbtion of bicarb, so you lose total body HCO3-
Resulting in acidosis

106
Q

decreased kidney perfusion causing pre-renal AKI affects which portion(s) of the nephron first?

A

proximal convoluted tubule and thick ascending limb of loop of henlé - both in renal medulla which has poor oxygen supply even in physiological conditions

107
Q

glomerular sclerosis and hyalinosis would suggest which pathology?

A

diabetic nephropathy

108
Q

intramembranous immune complex deposition is which pathology?

A

type II membranoproliferative glomerulonephritis

109
Q

eplerenone is what?

A

aldosterone antagonist, K+-sparing diuretic

110
Q

nonfunctional kidney consisting of cysts and connective tissue..

diagnosis?

A

mutlicystic dysplastic kidney

111
Q

which diuretics lead to loss of Ca++

A

loop diuretics

112
Q

renin is released by which cells in the kidney?

A

juxtaglomerular cells which are modified smooth muscle cells located around the wall of the afferent arteriole

USMLE S1 (16 decks)

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