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Step 1 > F 6/2 > Flashcards

F 6/2 Flashcards

1
Q

Where do horseshoe kidneys get “caught?”

A

On IMA

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2
Q

How does AR PCKD present?

A

Infants w worsening RF and HTN
Newborns may present w Potter sequence
Assoc w cong hep fibrosis (leads to portal HTN) and hepatic cysts

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3
Q

How does AD PCKD present?

A

Young adults w HTN (inc renin), hematuria and worsening RF

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4
Q

What is the gene in AD PCKD?

A

APKD1, APKD2

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5
Q

What are non-renal associations w AD PCKD?

A

Berry aneurysm (COD), hepatic cysts, MV prolapse

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6
Q

What is medullary cystic kidney disease and how is it inherited?

A

Cysts in medullary CD
Parenchymal fibrosis - shrunken kidneys, RF
AD

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7
Q

How is azotemia defined?

A

Inc BUN, Inc Cr

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8
Q

What causes prerenal azotemia

A

Dec BF to kidneys

Dec GFR, azotemia, oliguria

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9
Q

What is the BUN:Cr in pre-renal azotemia?

A

> 15

Reabs of fluid and BUN - tubular function intact

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10
Q

What causes postrenal azotemia?

A

Downstream obstruction of UT

Dec GFR, azotemia, oliguria

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11
Q

What is the BUN:Cr in longstanding postrenal azotemia?

A

<15

Tubular damage

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12
Q

What is the most common cause of acture renal failure?

A

ATN

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13
Q

Which areas of the nephron are particularly susceptible to ischemia?

A

PT

Medullary segment of TAL

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14
Q

What area of the nephron is particularly susceptible to toxins?

A

PT

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15
Q

What are the lab findings in ATN?

A

Oliguria w brown granular casts
Inc BUN, Inc Cr
HK (dec renal exc)
Met acidosis (inc anion gap)

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16
Q

What is acute interstitial nephritis?

A

Drug-induced hypersensitivity involving interstitiom and tubules?

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17
Q

What are causes of AIN?

A

NSAIDs, penicillin, diuretics

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18
Q

How does AIN present?

A

Oliguria, fever, rash - days to wks after starting drug

Eosinophils in urine

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19
Q

What is renal papillary necrosis and how does it present?

A

Necrosis of renal papillae

Gross hematuria, flank pain

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20
Q

What are some causes of RPN?

A

Chronic analgesic use (phenacetin, aspiriin)
DM
SCT or SCD
severe acute pyelonephritis

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21
Q

What are the features of nephrotic syndrome?

A 
Proteinuria > 3.5 g/d
hypoalbuminemia - pitting edema
hypogammaglobulinemia - risk inf
hypercoaguable state - loss of AT III
HL, Hchol - fatty casts in urine
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22
Q

What is the most common cause of nephrotic syndrome in children? What is its cause?

A

MCD
Usually idiopathic
may be associated w HL

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23
Q

How does MCD appear on HE, EM, IF?

A

HE - N
EM - effacement of foot processes
IF - N

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24
Q

How does MCD respond to steroids?

A

well

damage is mediated by cytokines from T cells

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25
Q

Is there inc risk of inf in MCD?

A

No - selective proteinuria

loss of albumin but not Ig

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26
Q

What is the most common cause of nephrotic syndrome in Hispanics and AAs?

A

FSGS

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27
Q

What causes FSGS?

A

Usually idiopathic

may be assoc w HIV, heroin use, SCD

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28
Q

What are the findings in FSGS on HE, EM, IF?

A

HE - focal and segmental sclerosis
EM - effacement of foot processes
IF - N

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29
Q

How does FSGS respond to steroids?

A

Not well; progresses to CRF

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30
Q

What is the most common cause of nephrotic syndrome in caucasian adults?

A

Membranous nephropathy

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31
Q

What causes MN?

A

Usually idiopathic

assoc w HBV, HCV, solid tumors, SLE, drugs (NSAID, penicillamine)

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32
Q

MN - HE, IF, EM

A

HE - thick GBM
IF - granular (IC depo)
EM - subepithelial deposits w spike and dome appearance

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33
Q

How does MPGN look on HE and IF?

A

HE - Thick GBM w tram-track appearance

IF - granular (IC depo)

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34
Q

Where are the IC deposits located in Type I and II MPGN?

A

Type I - subendothelial
Assoc w HBV, HCV
Type II = dense deposit disease - intramembranous
assoc w C3 nephritic factor

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35
Q

What is C3 nephritic factor?

A

AutoAb that stabilizes C3 convertase, leading to overactivation of complement, inflammation, and low levels of circulation C3

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36
Q

What happens to the kidney in DM?

A

NEG of vasc BM leads to hyaline arteriolosclerosis

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37
Q

What is more affects in DM - aff or eff arteriole?

A

Efferent
Leads to high GFP
Hyperfiltration injury leads to microalbuminuria

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38
Q

What is the first indication of kidney damage in DM?

A

Albuminuria

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39
Q

What are Kimmelstiel-Wilson nodules?

A

Sclerosis of the mesangium in diabetic nephropathy

40
Q

What is the most commonly involved organ in systemic amyloidosis?

A

Kidney

41
Q

Where does amyloid deposit in the kidney?

A

Mesangium

42
Q

What are the features of nephritic syndrome?

A 
proteinuria < 3.5 g/d
Oliguria, azotemia
salt retention - periorbital edema, HTN
RBC casts/dysmorphic RBCs in urine
Hypercellular, inflamed glomeruli
43
Q

What is the inciting event for PSGN?

A

GAS skin inf or pharyngitis

44
Q

What are the histological findings of PSGN?

A

IC depo - granular IF

subepitheial humps - EM

45
Q

What is the IF patterin in Goodpasture?

A

Linear (anti-BM Ab)

46
Q

What causes Goodpasture?

A

Ab against collagen in glomerular and alveolar BM

47
Q

How does Goodpasture present?

A

Hematuria

Hemoptysis young adult males

48
Q

What is the most common type of renal disease in SLE?

A

Diffuse proliferative GN

49
Q

How does Wegener present on IF, what is it associated w?

A

Negative (pauci-immune)

c-ANCA

50
Q

How do Churg-Strauss and microscopic polyangiitis present on IF, what is it associated w?

A 
Negative IF (pauci-immune)
p-ANCA
51
Q

What distinguishes Churg-Strauss from microscopic polyangiitis?

A

Granulomatous inflammation, eosinophilia, arthma

52
Q

What is RPGN?

A

Nephritic syndrome that progresses to RF in w to m

53
Q

What is found in Bowman space in RPGN? What are they composed of?

A

Crescents

Fibrin and macrophages

54
Q

What is the most common nephropathy worldwide?

A

Iga ( Berger)

55
Q

How does IgA nephropathy present?

A

During childhood as episodic gross or microscopic hematuria w RBC casts
Usually following mucosal infection

56
Q

Where does IgA deposit in IgA nephropathy?

A

Mesangium

57
Q

What is Alport syndrome?

A 
Inherited defect in type IV collagen
Most commonly X-linked
Thinning, splitting GBM
Isolated hematuria
sensory hearing loss
ocular disturbances
58
Q

What causes “thyroidization” of the kidney?

A

Chronic pyelonephritis

59
Q

Scarring at what location is characteristic of VER?

A

Upper and lower poles

60
Q

What is the most common type of nephrolithiasis?

A

Calcium oxalate/phosphate

61
Q

What are causes of Ca stones?

A

Idiopathic hypercalciuria
HyperCa
Crohn disease

62
Q

What is tx for Ca stones?

A

HCT

63
Q

What is the most common cause of Ammonium Mg PO4 stones?

A

Inf w urease pos organisms (Proteus, Klebsiella)

alkaline urine leads to formation of stone

64
Q

What type of stone is radiolucent?

A

Uric acid

65
Q

What are risk factors for uric acid stones?

A 
hot arid climates
low urine vol
acidic pH
gout
hyperuricemia (leukemia, MPD)
66
Q

What is the tx for uric acid stones?

A

Hydration

alkalinization of urine (K bicarb)

67
Q

What type of nephrolithiasis is mostly seen in children?

A

Cystine

68
Q

What is the result of loss of VHL tumor suppressor gene

A

Increased IGF-1
Inc HIF TF
Increased VEGF, PDGF

69
Q

What is Wilms tumor?

A

Malignant kidney tumor
comprised of blastema (immature kidney mesenchyme)
primitive glomeruli and tubules
stromal cells
Most common malignant renal tumor in children
avg age = 3y

70
Q

How does Wilms tumor present?

A

Lg, unilateral flank mass w hematuria and HTN

71
Q

What is WAGR syndrome?

A 
Wilms tumor
Aniridia
Genital abN
Mental and motor retardation
del of WT1 tumor suppressor gene
72
Q

What is Denys-Drash syndrome?

A

Wilms tumor
Prog glomerular disease
male pseudohermaphroditism
assoc w muts of WT1

73
Q

What is Beckwith-Wiedemann syndrome?

A 
Wilms tumor
neonatal hypoglycemia
muscular hemihypertrophy
organomegaly
assoc w muts in WT2 gene cluster, particularly IGF1
74
Q

What are the 2 types of urothelial carcinomas and their progression?

A

Flat - high grade, invades, early p53 muts

Papillary - low grade, prog to high grade then invades

75
Q

What is nimodipine and what is used for following subarachnoid hemorrhage?

A

CCB

Prevent cerebral vascular spasm

76
Q

What is the most common primary cerebral neoplasm in adults?

A

Glioblastoma

77
Q

What does cleft 1 become?

A

External auditory meatus

78
Q

What CNs are associate with arch 1?

A

V2, V3

79
Q

What CNs are associated with arch 2?

A

VII

80
Q

What CNs are associated w arch 3?

A

IX - stylopharyngeus

81
Q

What CNs are associated w arch 4 (and 6)

A

X

82
Q

What does pouch 3 become

A

Thymus and inferior PTs

83
Q

What does pouch 4 become?

A

Super PT

84
Q

What does pouch 5 become/

A

C cells of thyroid

85
Q

What are the clefts derived from?

A

Ectoderm

86
Q

What are the arches derived from?

A

Mesoderm and neural crests

87
Q

What are the pouches derived from?

A

Endoderm

88
Q

What is a branchial cleft cyst?

A

Cleft 2, lateral neck

Can have pharyngeal fistula

89
Q

What pharyngeal arches are disrupted in MEN 2A?

A

PT - 3rd, 4th

Parafollicular cells of thyroid - 4th, 5th

90
Q

What is aberrand in Digeorge?

A

Aberrant 3rd and 4th pouch deveopment
T cell deficiency (athymic)
hCa (aPT)

91
Q

What pharyngeal arch is associated with the carotid arteries?

A

3

92
Q

What pharyngeal arch is associated with the aortic arch?

A

4

93
Q

What is a cleft lip?

A

Failure of the fusion of the maxillary and medial nasal processes to fuse

94
Q

What is cleft palate?

A

Failrue of fusion of lateral palatine process, nasal septum, and/or median palatine process

95
Q

What is Treacher-Collins syndrome?

A

Failure of the 1st arch to migrate

Mandibular hypoplasia, facial abN

96
Q

What is the msot common congenital malformation of the head and neck?

A

Unilateral cleft

97
Q

What is the most common arterial malformation in infants?

A

PDA

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