B5-042 CBCL: Kidney Failure Flashcards

1
Q

developed in less than 3 months

A

acute

greater than 3 is chronic

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2
Q

prerenal vascular problems cause low blood flow/perfusion which leads to changes in

A

glomerular filtrating pressure

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3
Q

when the hydrostatic pressure in the glomerulus is lower, what happens to the net ultrafiltration pressure and GFR?

A

both lower

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4
Q

what type of kidney failure does renal artery stenosis cause?

A

prerenal

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5
Q

causes of intra-renal tubular injury

A

ischemia, toxins (ATN)
inflammatory (pyelonephritis)

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6
Q

pyelonephritis causes the inability to concentrate urine, leading to […]uria

A

polyuria

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7
Q

acute tubular necrosis (ATN) causes an intial phase of […]uria

A

oligouria

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8
Q

heavy proteinuria (>3.5 g/day)

nephrotic or nephritic

A

nephrotic

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9
Q

hypoalbuminemia with pitting edema

nephrotic or nephritic

A

nephrotic

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10
Q

hyperlipidemia and hypercholesterolemia

nephrotic or nephritic

A

nephrotic

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11
Q

hematuria

nephrotic or nephritic

A

nephritic

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12
Q

oligouria and azotemia

nephrotic or nephritic

A

nephritic

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13
Q

RBC casts and dismorphic RBCs in urine

nephrotic or nephritic

A

nephritic

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14
Q

proteinuria below 3.5 g/day

A

nephritic

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15
Q

what is the first thing that happens when the kidneys don’t function properly?

A

volume overload

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16
Q

what is the most important reason volume overload occurs?

A

sodium retention

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17
Q

how does kidney insufficiency cause acidosis?

A

low acid excretion –> accumulates

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18
Q

what type of anemia accompanies kidney insufficiency?

A

normocytic, normochromic anemia

kidneys can’t make EPO

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19
Q

treatment for anemia caused by renal insufficiency

A

EPO
iron supplement
B12 and folate supplements

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20
Q

signs of bone disease in kidney insufficiency

A
  • bone pain
  • increased risk of fracture
  • osteomalacia
  • rickets (kids)
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21
Q

how does renal insufficiency cause bone disease?

3

A
  • kidneys activate vitamin D, which is necessary to increase/maintain calcium levels in plasma
  • reduced GFR –> less phosphate excretion —> stimulates PTH secretion
  • metabolic acidosis
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22
Q

treatment for bone disease in renal insufficiency

A

calcitriol
calcium supplement

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23
Q

how do you measure function of the tubules?

A

using fractional excretion of sodium

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24
Q

the clearance of […] is used to measure GFR

A

creatinine

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25
Q

as kidney function decreases, plasma creatinine

A

increases

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26
Q

normal value of FE Na

A

1-3%

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27
Q

indicator of both glomerular and tubular function

A

BUN/creatinine ratio

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28
Q

filtered and reabsorbed in the tubules and provides an estimate of GFR and tubular function

A

urea

BUN

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29
Q

normal BUN/Cr

A

15-20

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30
Q

useful to differentiate the origin of kidney failure (prerenal, intrarenal, postrenal)

A

BUN/Cr

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31
Q

glomerular function impaired
tubular function intially maintained

prerenal, intrarenal, or postrenal

A

prerenal

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32
Q

glomerular function intially maintained
tubular function impaired

prerenal, intrarenal, or postrenal

A

intrarenal

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33
Q

glomerular pressure and function impaired
tubular function impaired at late stages

prerenal, intrarenal, or postrenal

A

postrenal

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34
Q
  • decreased GFR
  • Azotemia, oliguria
  • increased BUN
  • Normal FE Na
  • Normal osmolarity

prerenal, intrarenal, or postrenal

A

prerenal

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35
Q
  • azotemia
  • oliguria with brown casts
  • decreased BUN/Cr
  • elevated FE Na
  • low osmolarity

prerenal, intrarenal, or postrenal

A

intrarenal

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36
Q
  • azotemia, oliguria
  • decreased GFR
  • decreased BUN/Cr or normal
  • elevated FE Na
  • low osmolarity

prerenal, intrarenal, or postrenal

A

postrenal

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37
Q

treatments to control hypertension

A
  • sodium restriction
  • diuretics
  • ACE/ARBS
  • beta blockers
  • calcium channel blockers
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38
Q

treatment of patients with renal insufficiency should aim to control

4

A
  • hypertension
  • electrolytes
  • pH
  • anemia
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39
Q

involves more than 50% of glomerulus

A

diffuse

less than 50% = focal

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40
Q

portions of the glomerulus affected

A

segmental

all = global

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41
Q

thickening of capillary wall

A

membranous

combination of membranous and proliferative = membranoproliferative

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42
Q

hypercellularity in glomerulus, mesangial expansion

A

proliferative

combination of membranous and proliferative = membranoproliferative

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43
Q

sclerosis with capillary collapse

A

glomerulosclerosis

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44
Q

nephrotic triad

A
  • proteinuria
  • hypoalbuminuria
  • hyperlipidemia/cholesterolemia
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45
Q
  • most common in children
  • usually idiopathic
  • podocyte effacement
  • excellent response to corticoids
A

minimal change glomerulonephritis

46
Q
  • most common in hispanic or AA
  • idiopathic or associated with sickle cell and HIV
  • partial sclerosis of some glomeruli
  • podocyte effacement
A

focal segmental glomerulosclerosis

47
Q
  • most common in white adults
  • idiopathic or associated with NSAID, malignancy, chronic antigenic stimulation
  • thickening of GBM
  • granular IgG and C3
  • sub-epithelial deposits
A

membranous glomerulonephritis

48
Q
  • most common cause of ERSD in US
  • sclerosis of mesangium, KW nodules
  • hyaline artherosclerosis of arterioles
A

diabetic nephropathy

49
Q
  • amyloid in mesangium/expanded mesangium
  • green birefringence under polarized light with Congo Red
A

amyloidosis

50
Q

characteristics of glomerulonephritis

5

A
  • glomerular inflammation/hematuria
  • oliguria
  • azotemia
  • RBC casts/dysmorphic RBCs in urine
  • proteinuria below 3.5
51
Q
  • after Group A hemolytic strep infection
  • reduced C3-C4 in first 6-8 weeks
  • hypercellular inflammed glomeruli
  • immunocomplex deposition (sub-epithelial humps)
A

post-streptococcal glomerulonephritis

52
Q
  • progresses rapidly to renal failure
  • ANCA
  • presents with rapidly progressive glomerulonephritis
  • cresents of fibrin in Bowman’s space
A

ANCA-associated glomerulonephritis
ANCA-associated vasculitis

53
Q
  • inherited alteration of type IV collagen
  • thinning and splitting of GBM
A

Alport syndrome

54
Q
  • anti-GBM antibodies
  • IgG deposition along glomerular capillary loops
  • fibrin in crescents
  • linear or diffuse IgG staining of GBM
  • responds to corticosteroids
A

Goodpasture syndrome

55
Q

diseases that cause glomerulonephritis and can lead to both nephrotic/nephritic syndromes

3

A
  • membrane proliferative glomerulonephritis
  • IgA nephropathy (Berger)
  • Lupus nephropathy
56
Q
  • Ig+ with chronic antigenemia or Ig- with alternative complement antibodies
  • double contours and lobular hypercellularity
  • sub-endothelial deposits
A

membrane proliferative glomerulonephritis

57
Q
  • common in young white males and asians
  • IgA granular deposit in mesangium and hypercellularity
A

IgA nephropathy (Berger)

58
Q
  • “full house” (IgG, IgA, IgM, C3, C1q)
  • deposits everywhere, GB may show dense depositis
A

lupus nephropathy

59
Q
  • episodic hematuria after infection
  • Henoch-Shein purpura
  • proteinuria –> nephritic syndrome
  • rarely progress to nephrotic syndrome
A

IgA nephropathy (Berger)

60
Q
  • focal or segmental glomerular mesangial expansion
  • deposits of IgA in glomerular membrane
  • healing lesions may lead to sclerosis
A

IgA nephropathy

61
Q

genetic or acquired abnormality of immune regulation with abnormal increase in the polymeric form of secretory IgA in blood

A

IgA nephropathy

62
Q

in IgA nephropathy, IgA is abnormally […]

A

glycosylated

63
Q

IgA trapped in glomerular mesangium causing it to proliferate

A

IgA nephropathy

64
Q

diagnosis of IgA nephropathy

A
  • urine test for blood or protein
  • kidney biopsy for IgA
65
Q

treatment of IgA nephropathy

A
  • HTN medications
  • inmunosuppressants (steroids)
  • omega-3 fatty acids
66
Q
  • fatigue, headaches, malaise
  • nausea, vomiting, lack of appetite
  • itchy skin, leg swelling
A

diabetic nephropathy

67
Q

microalbuminuria at first, then progresses to heavy proteinuria

A

diabetic nephropathy

68
Q
  • GBM thickening
  • mesangial widening with KW nodules
  • intracapillary glomerulosclerosis
  • hyalinosis
  • tubulointerstitium
A

diabetic nephropathy

69
Q

caused by high glucose levels and protein glycosylation

A

diabetic nephropathy

70
Q

diagnosis of diabetic nephropathy

A
  • urine test for microalbuminuria or proteinuria
  • US of kidneys
71
Q

treatment of diabetic nephropathy

A
  • HTN medications
  • control ESRD
72
Q

what amount of urine is associated with oliguria?

A

< 400 mL/day

73
Q

common skin symptom of patients in ESRD

A

pruritis

related to high BUN levels

74
Q

what indicates recovery in nephrotic syndrome?

A

disappearance of protein from urine

75
Q

characterized by hematuria, proteinuria, edema, oliguria, azotemia

A

nephritic syndrome

76
Q

sudden reduction in renal function after infectious glomerulonephritis will present with

3

A
  • hypertension
  • oliguria
  • fatigue
77
Q
  • back pain
  • nausea
  • vomiting

associated with

A

renal calculi

78
Q
  • dysuria
  • frequent urinating

symptoms of

A

UTI

79
Q

diabetic nephropathy progresses into

A

nephrotic syndrome

80
Q

what filtration pressure does hydronephrosis increase?

A

hydrostatic pressure in Bowman’s capsule

81
Q

which filtration pressure would multiple myeloma impact?

A

increase oncotic pressure in glomerular capillaries

82
Q

hypotensive hospitalized patients are the most common antecedent to

A

acute tubular necrosis

83
Q

earliest event in glomerulonephritis

A

loss of negative charge of GBM

84
Q

extreme pruritis and crystallized white deposits are associated with

A

increased urea

85
Q

what type of diet is best for ESRD?

A

low protein
low sodium
low potassium
low phosphate

86
Q

chronic kidney diease, DM, and vomiting all can lead to

A

primary metabolic acidosis

87
Q

as kidney disease progresses, the distal nephron loses its ability to secrete K+ leading to

A

hyperkalemia

88
Q

renal insufficiency is accompanied by […] retention

A

sodium

89
Q

most common manifestation of acute renal failure secondary to NSAIDs

A

hyperkalemia

90
Q

in ESRD, lack of activation of vitamin D causes

A

spontaneous fractures

91
Q

broad and waxy casts

A

chronic renal failure

92
Q

muddy brown granular casts

A

acute tubular necrosis

93
Q

red blood cell casts

A

nephritis

94
Q

white blood cell casts

2

A
  • interstitial nephritis
  • pyelonephritis
95
Q

renal insufficiency is accompanied by

4

A
  • anemia
  • low bone density
  • hypervolemia
  • hyperkalemia
96
Q

three most common causes of CKD

A
  • DM
  • HTN
  • glomerulonephritis
97
Q

urinary casts indicate

A

tubular damage

98
Q

does renal insufficiency cause hypo or hyper kalemia?

A

hyperkalemia

99
Q

does renal insufficiency cause hypo or hyper natremia?

A

hypernatremia

100
Q

does renal insufficiency cause hypo or hyper calcemia?

A

hypocalcemia

101
Q

does renal insufficiency cause hypo or hyper phosphatemia?

A

hyperphosphatemia

102
Q

renal damage accompanying DM leads to excessive release of

2

A

renin and aldosterone

103
Q

filtration in the glomerulus is […] in renal insufficiency

decreased or increased

A

decreased

104
Q

plasma sodium is […] in renal insufficiency

increased or decreased

A

increased

105
Q

fibromuscular dysplasa and renal artery stenosis cause […] kidney insufficiency

A

pre renal

106
Q

kidney stones cause […] kidney insufficiency

A

post renal

107
Q

commonly presents after an infection of the respiratory tract

A

Berger (IgA nephropathy)

108
Q

first sign of Berger

A

hematuria

109
Q

brown cell casts and urine sediment

A

acute tubular necrosis

110
Q

consequences of renal failure

A

Metabolic Acidosis
Dyslipidemia
High potassium
Uremia
Na+/H2O retention
Growth retardation
Erythropoietin deficiency
Renal osteodystrophy

MAD HUNGER