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PANCE Review > Nephrology & Urology > Flashcards

Nephrology & Urology Flashcards

1
Q

Characterize nephrotic syndrome

A
  • proteinuria
  • hypoalbuminemia
  • hyperlipidemia
  • edema*
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2
Q

what is nephrotic syndrome (anatomy)

A

damage to the glomerular causes PROTEIN loss in urine –> hyPOalbuminemia –> *EDEMA

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3
Q

name 3 primary idiopathic causes of nephrotic syndrome

A

1) minimal change disease
2) focal segmental glomerulosclerosis (FSGS)
3) membranous nephropathy

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4
Q

80% of children that have nephrotic syndrome present with this type

A

minimal change disease

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5
Q

Tx of choice for minimal change disease

A

Prednisone

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6
Q

what is seen on electron microscope in minimal change disease

A

podocyte damage

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7
Q

what is focal segmental glomerlosclerosis

A

fibrosis within the glomerulus

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8
Q

causes of focal segmental glomerlosclerosis

A
  • Htn (esp African Americans)
  • IV heroin abuse
  • HIV
  • reflux nephropathy
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9
Q

what is membranous nephropathy

A

thickening of the golmerulur basement membrane

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10
Q

how does membranou nephropathy usually present as

A

nephritic- nephrotic picture

-MC in Caucasian men >40 y/o

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11
Q

clinical manifestations of nephrotic syndrome

A

1) EDEMA (esp periorbital edema)
2) anemia
3) DVT
4) frothy urine
5) pulmonary edema
6) pleural effusion

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12
Q

Gold standard dx for nephrotic syndrome

A

24 hour urine protein collection

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13
Q

what is the diagnosis for nephrotic syndrome for a 24 hr urine protein collection

A

> 3.5g/day**

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14
Q

Diagnosis work up for nephrotic syndrome

A
  • 24 hour urine protein collection
  • UA
  • Serum albumin/lipids
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15
Q

management of nephrotic syndrome: address these

  • Minimal change dz
  • FSGS
  • edema reduction
  • proteinuria
  • hyperlipidemia
A
  • Minimal change dz –> corticosteroids
  • FSGS –> corticosteroids
  • edema reduction –> diuretics
  • proteinuria–> ACEI, ARB
  • hyperlipidemia –> diet and meds
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16
Q

characteristic of UA of nephrotic syndrome

A

**oval fat bodies “maletese cross shaped”

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17
Q

what is acute glomerulonephritis

A

immunologic inflammation of the glomeruli causing PROTEIN** AND RBC** leakage into the urine

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18
Q

hallmark characteristics of glomerulonephritis

A
  • HTN
  • HEMATURIA (RBC CASTS)
  • DEPENDEPENT EDEMA (PROTEINURIA)
  • AZOTEMIA
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19
Q

name different etiologies of acute glomerular nephritis

A
  • IgA nephropathy (Berger’s disease)
  • Post infectious
  • Membranoproliferative/mesangiocapillary
  • Goodpasture’s disease
  • vasculitis
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20
Q

which are etiologies of rapidly progressive glomerulonephritis (RPGN)

A
  • Goodpasture’s disease

- Vasculitis

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21
Q

another name for IgA nephropathy

A

Bergers disease

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22
Q

what is the MC cause of acute glomerulonephritis in adults worldwide

A

IgA nephropathy

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23
Q

Pt usually presents with this type of AGN after a URI or GI infection, often affects young males within 24-48 hours

A

IgA nephropathy

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24
Q

how do you diagnose IgA nephropathy

A

+ IgA mesangial deposits

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25
Q

management of IgA nephropathy (Bergers disease)

A

ACE +/- corticosteroids

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26
Q

this type of AGN happens after GABHS

A

post infectious AGN

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27
Q

coca cola colored/dark urine

A

post infectious AGN

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28
Q

dx workup of post infectious AGN

A
  • ASO titers

- Low serum complement (C3)

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29
Q

management of post infectious AGN

A

-supportive

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30
Q

how does membranoproliferative/mesangiocapillary AGN present

A

mixed nephritic /nephrotic picture

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31
Q

cresent formation on bx

A

rapidly progressive glomerulonephritis

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32
Q

management of RPGN

A

corticosteroids + cyclophosphamide

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33
Q

+anti-GBM antibodies

A

Goodpastures disease

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34
Q

dx of Goodpasture’s disease

A

linear IgG deposits

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35
Q

management of goodpasture’s disease

A

high dose corticosteroids* + cyclophosphamide* plus plasmapheresis

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36
Q

Microscopic polyangiitis dx

A

+ P-ANCA

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37
Q

granulomatosis w/ polyangiitis (wegnener’s) dx

A

+ C-ANCA

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38
Q

clinical manifestations of acute glomerulonephritis

A
  • Hallmark- **hematuria (*coca colored/dark urine)
  • Edema (85%): peripheral, periorbital (esp in children)
  • Htn* (80%)
  • *fever, abdominal pain, flank pain
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39
Q

management of Bergers disease/proteinuria

A

ACE inhibitors +/- corticosteroids

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40
Q

Tx of Lupus nephritis

A

steroids or cyclophosphamide

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41
Q

Tx for rapidly progressive AGN or severe disease

A

***corticosteroids PLUS cyclophosphamide

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42
Q

What happens in acute kidney injury in terms of creatinine and BUN

A
  • increased serum creatinine >50%

- increased blood urea nitrogen/BUN (azotemia)

43
Q

what is the most common type of AKI

A

pr-renal

44
Q

what can prerenal AKI often lead to

A

acute tubular necrosis

45
Q

what can prerenal AKI be caused by

A

reduced renal perfusion (hypovolemia)

46
Q

examples of postrenal AKI

A

obstruction (BPH)

47
Q

what type of AKI causes direct kidney damage

A

intrinsic

48
Q

what causes intrinsic AKI

A

nephrotoxic, cytotoxic, prolonged ischemic

49
Q

cellular cast formation

A

intrinsic AKI

50
Q

what are the types of intrinsic AKI

A
  • acute tubular necrosis (ATN)
  • acute tubulointerstitial nephritis (AIN)
  • glomerulur (acute glomerulonephritis-AGN)
51
Q

what medications/ substances can cause nephrotoxic ATN

A
  • *aminoglycosides, contrast dye, cyclosporine

- endogenous- crystal precipitation, myoglobuinuiria, lymphoma, leukemia

52
Q

MC type of ATN

A

nephrogenic

53
Q

muddy brown casts

A

acute tubular necrosis

54
Q

epithelial cell casts

A

acute tubular necrosis

55
Q

Labs values of K and Phosphate

A
  • Hyperkalemia

- Increase phosphatemia

56
Q

tx of AKI

A
  • stop offending agent

- IV fluids

57
Q

most causes of acute tubulointerstitial nephritis (AIN) is…

A

drug hypersensitivities

58
Q

drug hypersensitivity that cause acute tubulointerstitial nephritis (AIN)

A
  • PCNs*
  • NSAIDs*
  • Sulfa drugs*
  • cephalosporins
  • cipro
  • rifampin
  • allopurinol
59
Q

clinical manifestations of acute tubulointerstitial nephritis (AIN)

A
  • **fever
  • *****esosinophila
  • **maculopapular rash
  • arthralgia
60
Q

pathopneumonic UA from acute tubulointerstitial nephritis (AIN)

A

WBC CASTS, increased serum IgE

61
Q

management of acute tubulointerstitial nephritis (AIN)

A

stop offending agent

62
Q

tx for acute glomerulonephritis (AGN)

A

high dose corticosteroids

63
Q

clinical manifestations of AGN

A
  • *hematuria
  • *HTN
  • *azotemia
  • *proteinuria
64
Q

what are the two types of vascular AKI

A
  • microvascular (TTP, HELLP syndrome, DIC)
  • macrovascular (AA, renal artery dissection/thrombosis, malignant htn, atheroembolic disease-associated with ischemic digits/blue to syndrome esp. post cath, CABG or AAA repair)
65
Q

Pre-renal AKI labs values:

  • Creatinine
  • Urine Na/FeNa
  • UA
  • Response to volume replacement
  • BUN/Cr
A
  • Creatinine: increases slower than 0.3mg/day
  • Urine Na: <20 /FeNa: <1%
  • UA: normal, HIGH specific gravity
  • Response to volume replacement: *creatinine rapidly improves
  • BUN/Cr: increased *>20:1
66
Q

Acute tubular necrosis (ATN) lab values:

  • Creatinine
  • Urine Na/FeNa
  • UA
  • Response to volume replacement
  • BUN/Cr
A
  • Creatinine: increases AT 0.3-0.5 mg/dL/day
  • Urine Na: >40 /FeNa: >2%
  • UA: *epithelial cells, granular casts, LOW specific gravity
  • Response to volume replacement: creatinine WONT improve
  • BUN/Cr: 10-15:1
67
Q

how is adult polycystic kidney disease inherited

A

autosomal DOMINANT

68
Q

what is adult polycystic kidney disease

A

multisystemic progressive enlarged and formation of kidney cysts AND cysts in other organs

69
Q

where can cysts from polycystic kidney disease be in other places of the body

A
  • liver
  • spleen
  • pancreas
70
Q

what does vasopressin stimulate to cause ESRD in polycystic kidney disease

A

cytogenesis

71
Q

clinical manifestations of polycystic kidney disease

A
  • abdominal/flank pain
  • palpable flank mass
  • HTN
  • hematuria
72
Q

what are EXTRArenal manifestations of polycystic kidney disease

A
  • ****CEREBRAL BERRY ANEURYSMS
  • ***MITRAL VALVE PROLAPSE
  • *HEPATIC CYSTS
  • *COLONIC DIVERTICULA
73
Q

most widely used 1st dx for polycystic kidney disease

A

renal US

74
Q

dx work up of polycystic kidney disease

A
  • renal US

- CT scan/MRI (more sensitive than US)

75
Q

management of simple AND multiple cysts in polycystic kidney disease

A
  • simple: observation, ACE for htn

- multiple: supportive, *increase fluid intake (decreases vasopressin)

76
Q

clinical manifestation of hypophophatemia

A
  • DIFFUSE muscle weakness

- flaccid paralysis (due to decreased ATP)

77
Q

clinical manifestations of hyperphosphatemia

A
  • most asymptomatic
  • heart block
  • *soft tissue calcifications
78
Q

what are the stages of CKD

A 
stage 1: >90 w/ proteinuria/abnormal urine
stage 2: 60-89
stage 3a: 45-59
stage 3b: 30-44
stage 4: 15-29
stage 5: <15 ESRD
79
Q

what is the MC cause of ESRD

A

DM

80
Q

what is the 2nd MC cause of ESRD

A

htn

81
Q

single best predictor of renal disease progression

A

proteinuria

82
Q

what is the best test to measure CKD

A

spot Ualbumin/Ucreatinine ratio (ACR)

83
Q

what is the second best test to measure ckd

A

24 hour urine collection

84
Q

broad waxy casts

A

ESRD

85
Q

salt and pepper appearance of the skill on x-ray

A

osteitis fibrosis cystica

86
Q

what is the biggest electrolyte abnormality is SIADH

A

hypOnatermia (becuase the blood is becoming diluted by the excess amount of water)

87
Q

what is SIADH

A

excess increased in ADH causing the inability to dilute the urine (increases free water retention)

88
Q

what is the MC cause of SIADH from CNS

A

stroke

89
Q

what pulmonary ca can secrete ectopic ADH causing SIADH

A

small cell lung cancer

90
Q

in isovolemic hypotonic hyponatremia is the serum osmolarity increased to decreased

A

DECREASED

91
Q

is the urine osmolarity increased or decreased in SIADH

A

INCREASED

92
Q

mainstay tx of SIADH

A

H2O restriction

93
Q

how do you tx severe cases of SIADH that are refractory to H2O restriction

A

demecycline

94
Q

why do you want to only correct hyponatermia no faster thatn 0.5mEq/L per hour

A

dont want to have central pontine myelinolysis

95
Q

what is diabetes insipidis

A

inability of the kidney to concentrate urine –> large prodcution of DILUTE urine

96
Q

central DI vs nephrogenic DI

A

central: decreased ADH production (MC type)
nephrogenic: partial or complete INSENSITIVITY to ADH

97
Q

what is the MC type of DI

A

central

98
Q

what are the MC manifestations of DI

A
  • polydipsia
  • polyuria
  • nocturia
99
Q

how do you dx DI

A

fluid deprivation test*

100
Q

what is a + fluid deprivation test for DI

A

continued production of dilute urine

101
Q

what test allows us to differentiate between nephrogenic and central DI

A

desmopressin (ADH) stimulation test

102
Q

what would be the desmopressin test result of a central vs nephrogenic DI

A

central: reduction in urine output**
nephrogenic: NO reponse to desmopressin, continued urine output

103
Q

tx for central DI

A

desmopressive/DDAVP or carbamazepine

104
Q

tx for nephrogenic DI

A

HCTZ

PANCE Review (2 decks)

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