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Renal Urinary System and Electrolytes > Renal Urinary System part 2 > Flashcards

Renal Urinary System part 2 Flashcards

1
Q

Lupus Nephritis (SLE-systemimc lupus erythematosus with renal involvement)

A

x

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2
Q

syx

A

x

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3
Q

what are signs?

A

proteinuria, active urine sediment-(hematuria, RBC casts, RBC cells,) declining renal function

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4
Q

dx

A

x

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5
Q

what is required prior to guiding therapy?

A

kidney biopsy

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6
Q

signficant kidney involvement would show what?

A

proteinuria, active urine sediment-(hematuria, RBC casts, RBC cells,) declining renal function

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7
Q

what would complement levels show?

A

low serum complement (C3 and C4)

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8
Q

subtypes of lupus nephritis

A

x

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9
Q

what class is minimal mesangial involvemement, usually asyx, trx?

A

class I, no trx

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10
Q

what class is mesangial proliferative, with microscopic hematuria and proteinuria, trx?

A

class II, no trx

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11
Q

what class is focal with hematuria proteinuria, possible HTN, decreased GFR, variable prognosis, trx?

A

class III, immunosuppression with steroids (eg methylprednisolone, prednisone) and cyclophosphamide or mycophenolate mofetil

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12
Q

what class is diffuse histo pattern with poor prognosis , trx?

A

class IV, immunosuppression with steroids (eg methylprednisolone, prednisone) and cyclophosphamide or mycophenolate mofetil

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13
Q

what class is membranous and has nephrotic syndrome involved, trx?

A

class V, immunosuppression with steroids (eg methylprednisolone, prednisone) and cyclophosphamide or mycophenolate mofetil

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14
Q

what class is advanced sclerosing with progressive CKD with bland urinary sediment, trx?

A

class VI, no immunosupression

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15
Q

management

A

x

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16
Q

how do you track renal involvement and renal improvement with lupus nephritis?

A

anti-dsDNA (immune complexes that deposit on membrane) and complement levels (correlate well with disease activity)

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17
Q

Rhabdomyolysis

A

x

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18
Q

cause

A

x

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19
Q

what is the cause ?

A

muscular injury, PCP, trauma, toxin exposure

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20
Q

dx

A

x

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21
Q

what do the lab show?

A

elevated CK >10,000

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22
Q

what does the UA show?

A

blood with no RBCs (indicating myoglobinuria)

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23
Q

complications

A

x

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24
Q

what is a major complication of rhabdomyolysis?

A

AKI from myoglobinuria

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25
Q

trx

A

x

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26
Q

what is the major trx?

A

IV isotonic saline

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27
Q

Orthostatic Proteinuria

A

x

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28
Q

epid

A

x

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29
Q

most common cause of proetinuria in what age group?

A

adolescents

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30
Q

define

A

x

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31
Q

what is it?

A

abnoramlly high protein excretion during the day (when upright) but normal protein excertion at night (when supine)

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32
Q

dx

A

x

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33
Q

how do you ensure dx?

A

UA shows proteinuria and excludes hematuria, AKI

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34
Q

what makes you suspect orthostatic proteinuria?

A

24 h urine collection showing protien excretion, but not >3.5g/24 hr to make you think nephrotic syndrome

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35
Q

what is the test to dx orhtostatic proteinuria?

A

split (day and night) 24 hour urine collection , showing elevated daytime but normal nighttime protein excretion rates

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36
Q

management

A

x

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37
Q

what is the best management for orthostatic proteinuria?

A

benign condition, no further intervention, resolves with age

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38
Q

Hepatorenal Syndrome

A

x

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39
Q

pathophys

A

x

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40
Q

what is the pathophys?

A

cirrhosis develop decreased peripheral vascular resistance secondary to splanchnic vasodilation, which can cause the decreased renal perfusion of hepatorenal syndrome

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41
Q

cause

A

x

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42
Q

what is the cause ?

A

patients with cirrhosis

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43
Q

dx

A

x

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44
Q

what do you see on CMP?

A

elevated LFTs, acute elevated BUN and Cr

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45
Q

how do you dx?

A

by exclusion,

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46
Q

risk

A

x

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47
Q

what is a frequent percipitent of hepatorenal syndrome?

A

SBP (spontaneous bacterial peritonitis)

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48
Q

management

A

x

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49
Q

if patient has ascites and PMN>250, what do you do trx of hepatorenal?

A

paracentesis

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50
Q

Alcoholic Ketoacidosis

A

x

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51
Q

syx

A

x

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52
Q

what are symptoms?

A

AMS, confused, disoriented, generalized abd pain and thirst

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53
Q

dx

A

x

54
Q

how do you diagnose it?

A

Anion gap acidosis, increased osmol gap, ketonemia, ketonuria , variable blood glucose

55
Q

what is the plasma glucose level?

A

variable, <250 usually (as >250 indicates DKA)

56
Q

risk

A

x

57
Q

who are the risks of alcoholic ketoacidosis?

A

homeless, alcoholics

58
Q

pathophys

A

x

59
Q

what causes elevated glucose?

A

impaired insuline secretion and increased insulin resistance

60
Q

management

A

x

61
Q

what should be management?

A

IV dextrose containing normal saline and thiamine, insulin is generally not required

62
Q

why do you need IV dextrose?

A

leads to increase in insulin secretion, which leads to the metabolism of ketone bodies to bicarb

63
Q

Autosomal Dominant Polycystic Kidney Disease (ADPCKD)

A

x

64
Q

syx

A

x

65
Q

what are syx?

A

asyx but may develop HTN, hematuria, proteinuria, renal insufficiency, and/or flank pain.

66
Q

PE

A

x

67
Q

what are physical exam findings?

A

flank pain

68
Q

what might be appreciated on exam?

A

palpable abd mass (usually bilateral)

69
Q

dx

A

x

70
Q

what do you see on U/S ? what is alternate imaging?

A

multiple bilateral renal cysts; CT or MRI

71
Q

what do you see on UA?

A

hematuria, protenuria

72
Q

association

A

x

73
Q

what are other associated factors?

A

LVH and displaced PMI, associated with HTN

74
Q

complications

A

x

75
Q

what are the complications of ADPKD?

A

ESRD, HTN

76
Q

what are some extra renal features?

A 
Cerebral aneurysms
Hepatic &amp; pancreatic cysts
Cardiac valve disorders (mitral valve prolapse, aortic regurgitation)
Colonic diverticulosis
Ventral &amp; inguinal hernias
77
Q

management

A

x

78
Q

what is the best management?

A
  • Follow blood pressure & renal function
  • Aggressive control of cardiovascular risk factors, including hypertension
  • ACE inhibitors preferred for high blood pressure
  • End-stage renal disease: Dialysis, renal transplant
79
Q

screening

A

x

80
Q

what consequences can occur from a positive screening ADPKD and what must be done first prior to screening?

A

counseling is required prior to testing as a diagnosis of ADPKD often can result in psychological, insurability, and employment consequences.

81
Q

patients with a fam hx of ADPCKD should get screened after >=18 y.o. with?

A

renal ultrasound

82
Q

Acute kidney injury (AKI)

A

x

83
Q

types

A

x

84
Q

what are the types of AKI?

A

prerenal, ATN, postrenal

85
Q

Prerenal

A

x

86
Q

mechanism

A

x

87
Q

what is the mechanism of action of prerenal ?

A

Decreased renal perfusion from volume depletion (eg, hypovolemia, hemorrhage) or decreased effective circulating volume (eg, heart failure)

88
Q

association

A

x

89
Q

what are associated conditions of prerenal AKI?

A

CHF

90
Q

dx

A

x

91
Q

what does BUN/Cr ratio show for prerenal AKI?

A

Typically >20

92
Q

what does FeNa show for prerenal AKI?

A

<1%

93
Q

what does urine osmolality for prerenal AKI show?

A

> 500 mOsm/kg

94
Q

what does microscopy show for prerenal AKI?

A

Bland

95
Q

management

A

x

96
Q

what is the management of prerenal AKI?

A

Intravenous fluids (responds to fluid challenge)

97
Q

ATN

A

x

98
Q

mechanism

A

x

99
Q

what is the mechanism of action of ATN ?

A

Tubular injury from renal ischemia, sepsis, or nephrotoxins (eg, aminoglycosides, tenofovir, radiocontrast media)

other etiopathology generally involves a perfusion deficit due to hypovolemia, hypotension, shock, sepsis, or low cardiac output states.

100
Q

association

A

x

101
Q

what are associated conditions of ATN?

A

aminoglycosides, tenofovir, radiocontrast media

102
Q

dx

A

x

103
Q

what does BUN/Cr ratio show for ATN AKI?

A

Typically normal (~10-15)

104
Q

what does FeNa show for ATN AKI?

A

> 2%

105
Q

what does urine osmolality for ATN AKI show?

A

~300 mOsm/kg

106
Q

what does microscopy show for ATN AKI?

A

Muddy brown casts

107
Q

management

A

x

108
Q

what is the management of ATN AKI?

A

Supportive care, treatment of underlying cause &/or removal of offending agent

109
Q

Postrenal

A

x

110
Q

mechanism

A

x

111
Q

what is the mechanism of action of Postrenal ?

A

Obstruction (eg, benign prostatic hypertrophy, renal stones, malignancy)

112
Q

association

A

x

113
Q

what are associated conditions of Postrenal AKI?

A

benign prostatic hypertrophy, renal stones, malignancy)

114
Q

dx

A

x

115
Q

what does BUN/Cr ratio show for Postrenal AKI?

A

Variable

116
Q

what does FeNa show for Postrenal AKI?

A

Variable

117
Q

what does urine osmolality for Postrenal AKI show?

A

Variable

118
Q

what does microscopy show for Postrenal AKI?

A

bland

119
Q

management

A

x

120
Q

what is the management of Postrenal AKI?

A

Relief of obstruction

121
Q

Prerenal Azotemia/Prerenal AKI

A

x

122
Q

dx

A

x

123
Q

what do labs show for prerenal azotemia?

A

decreased fractional excretion of sodium; however, once ATN sets in, the fractional excretion of sodium increases (usually >2).

124
Q

what is the gold standard in distinguishing prerenal azotemia from ATN?

A

fluid challenge , as prerenal azotemia responds to a fluid challenge with improved urine output, where ATN does not

125
Q

hyperchloremic non-anion gap metabolic acidosis

A

x

126
Q

cause

A

x

127
Q

what is the cause of hyperchloremic non-anion gap metabolic acidosis?

A

excess IV Normal Saline

128
Q

Dialysis

A

x

129
Q

indications

A

x

130
Q

what are indications of dialysis?

A

intractable hyperkalemia, hypervolemia, severe metabolic acidosis (eg, pH <7.1), and marked uremic symptoms

Renal Urinary System and Electrolytes (2 decks)

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