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CR4 > renal path flashcards (BAD DECK) > Flashcards

renal path flashcards (BAD DECK)

1
Q

Autosomal dominant Polycystic Kidney Disease (associated with accelerated disease in black patients with sickle cell trait) and Real Medullary Carcinoma

A

Pathology

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2
Q

90% of cases have fusion of upper pole - patients are usually asymptomatic/normally functioning

A

Pathology

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3
Q

Cysts not present at birth, renal function intact until the 4th or 5th decade when patients become symptomatic. Inscidious onset of hematuria (1st symptom) followed by polyuria and hypertension (Kiddos- HTN and hematuria)

A

Pathology

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4
Q

ADPKD

A

Pathology

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5
Q

ADPKD

A

Pathology

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6
Q

PKD1 (85%) and PKD2- PKD2 presents later than PKD1

A

Pathology

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7
Q

ADPKD= dilation of all parts of the nephron ARPKD= dilation of the collecting tubules

A

Pathology

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8
Q

RCC R/O based on the fact that ADPKD is bilateral rather than unilateral and the cysts are NONuniform

A

Pathology

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9
Q

ADPKD

A

Pathology

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10
Q

ARPKD

A

Pathology

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11
Q

ARPKD. Pulmonary Hyperplasia is secondary to oligohydramnios

A

Pathology

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12
Q

Liver and Kidney most often involved (lungs in neonates) , most present before age 20, Hypertension in almost all cases, liver disease predominates in older children and adults (portal hypertension and splenomegaly)

A

Pathology

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13
Q

ARPKD

A

Pathology

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14
Q

ARPKD

A

Pathology

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15
Q

Multicystic Dysplastic Kidney

A

Pathology

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16
Q

Multicystic Dysplastic Kidney

A

Pathology

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17
Q

Medullary sponge kidney

A

Pathology

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18
Q

Medullary sponge has intersitial fibrosis

A

Pathology

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19
Q

Nephrophthisis

A

Pathology

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20
Q

Polycystic Kidney Hepatic Disease gene (PKHD1)

A

Pathology

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21
Q

Familial (juvenile) - becomes clinically evident in childhoood or adolescence.

A

Pathology

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22
Q

Nephrophthisis

A

Pathology

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23
Q

Nephrophthisis

A

Pathology

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24
Q

nephrophthisis

A

Pathology

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25
Q

Present in 3rd -4th decade with polyuria and polydipsia, may also have hyperuricemia and gout

A

Pathology

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26
Q

Adult onset medullary cystic disease

A

Pathology

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27
Q

Acquired cystic renal disease

A

Pathology

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28
Q

acquired cystic renal disease

A

Pathology

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29
Q

Simple Cyst

A

Pathology

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30
Q

Acute proliferative glomerularnephritis, Rapid progressive glomerular nephritis, IgA nephropathy, Alport Syndrome Membranoproliferative Glomerulonephritis

A

Pathology

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31
Q

Acute proliferative glomerulonephritis

A

Pathology

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32
Q

Acute proliferative glomerulonephritis MCC = Group A strep pharyngitis

A

Pathology

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33
Q

Acute proliferative glomerulonephritis

A

Pathology

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34
Q

Rapid progressive Glomerular nephritis

A

Pathology

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35
Q

kidney is large and pale with petichial hemorrage

A

Pathology

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36
Q

IgA nephropathy

A

Pathology

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37
Q

IgA nephropathy

A

Pathology

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38
Q

igA nephropathy

A

Pathology

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39
Q

iga nephropathy

A

Pathology

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40
Q

Alport Syndrome “Cant see, cant pee, cant hear a bee”

A

Pathology

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41
Q

will always have microscopic hematuria with Alport syndrome. Microscopic hematuria will be abscent between illnesses in IgA nephropathy

A

Pathology

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42
Q

Alport Syndrome

A

Pathology

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43
Q

Membranoproliferative Glomerulonephritis

A

Pathology

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44
Q

Membranoproliferative Glomerulonephritis

A

Pathology

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45
Q

Subendithelual deposits between duplicated membranes

A

Pathology

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46
Q

Intramembranous dense deposits = Ribbon like deposits

A

Pathology

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47
Q

Membranous Nephropathy, Focal Segmental GN, Diabetic nephropathy Minimal change

A

Pathology

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48
Q

membranous GN

A

Pathology

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49
Q

membranous GN

A

Pathology

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50
Q

membranous GN

A

Pathology

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51
Q

Focal segmental GN

A

Pathology

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52
Q

Obesisty and anabolic steroid use

53
Q

Hyalin insudation and lipid vacuoles in sclerotic areas

54
Q

Diabetic Glomerulonephropathy

55
Q

Diabetic Glomerulonephropathy

56
Q

Minimal change disease

57
Q

Acute tubular injury (tubular necrosis)

58
Q

straight portions of the proximal tubule and medullary thick ascending loop of henle

59
Q

Acute Tubular injury (tubular necrosis)

60
Q

ballooning and hydrophobic or vacuolar degeneration of proximal convoluted tubules. Calcium oxide crystals in tubular lumen

61
Q

Acute pyelonephritis

62
Q

Chronic pyelonephrits

63
Q

drug and toxin induced tublointersitial nephritis

64
Q

lasts 36 hours - period when patient exposed to ischemia/toxin and parenchymal injury is developing but not yet established.

65
Q

Uremia, salt and water overload, rising BUN, HYPERkalemia, metabolic acidosis

66
Q

diuretic phase large amount of salt and water lost, HYPOkalemia becomes a problem

67
Q

Acute: Leukocyte infiltration (mainly neutrophils and eosinophils) Chronic: inflammation mainly monocytes

68
Q

Ascending infection (usually E.coli)

69
Q

Papillary Necrosis, Pyonephrosis, Perinephric abscess

70
Q

complication of acute pyelonephritis seen in people with diabetes, sickle cell disease, urinary obstruction, also seen in NSAIDs

71
Q

tips or distal 2/3 of the pyramids have areas of gray/white to yellow necrosis

72
Q

suppurative exudatecannot drain (due to obstruction) and fills the renal pelvis, calyces, and ureter with pus

73
Q

precipitation of uric acid in renal tubules and development of acute renal failure - seen in leukemic patients undergoing chemotherapy (cancer cell is killed and uric acid us released- tumor lysis syndrome)

74
Q

Acute Uric Acid nephropathy

75
Q

Gouty nephropathy- monosodium urates deposit in the distal tubules and collecting ducts and interstitium and form birifringent needle like cysts

76
Q

Medullary Sponge Kidney and Hypercalcemia and Nephrocalcinosis

77
Q

Light chain cast nephropathy (myeloma kidney)

78
Q

Light chain cast nephropathy (myeloma kidney)

79
Q

Sclerosis of renal arterioles and small arteries usually in the setting of HTN that results in parenchymal ischemia and glomerulosclerosis that ultimately shrinks the kidney

80
Q

Nephrosclerosis (fine even granularity)

81
Q

fibromuscular dysplasia havs the lumen still in the center

82
Q

Inflammation is in response to the necrosis NOT the cause of the necrosis

83
Q

Thrombotic Microangiopathies - result from shearing of red blood cells

84
Q

Wims (Nephroblastoma)

85
Q

Renal Papillary Adenoma, Renal oncocytoma, Angiomyolipoma

86
Q

Clear cell renal cell carcinoma, Papillary renal cell carcinoma, Chromophobe renal cell carcinoma, Collecting duct (Bellini duct) carcinoma, renal medullary carcinoma, urothelial carcinomal or the renal pelvis

87
Q

coronary atherosclerosis (90%)

88
Q

Angina pectoris

89
Q

middle aged men and women after menopause

90
Q

Stable Angina

91
Q

False

92
Q

Stable angina

93
Q

disruption of a plaque and superimposed partial thrombus, and probably embolis or vasospasm (or both)

94
Q

within seconds - lactate levels rise and ATP falls (due to lact of oxygen and cessation of aerobic metabolism)

95
Q

within 60 seconds

96
Q

20-30 minutes - ischemia > 1 hour causes damage to cardiac microvasculature

97
Q

Transmural

98
Q

Necrosis begins in small zone of myocardium beneath the endocardial surface in the center of the ischemic zone. VERY NARROW ZONE OF MYOCARDIUM BENEATH THE ENDOCARDIUM IS SPARED FROM NECROSIS DUE TO DIFFUSION OF OXYGEN FROM THE VENTRICLE

99
Q

MI

100
Q

12-24 hours: Dark Mottling of infarct and central pallor

101
Q

1-3 days

102
Q

7-10 days

103
Q

begins at 2 weeks and is complete at 8 weeks

104
Q

indicative of reperfusion injury post MI

105
Q

CKMB

106
Q

appears 2-4 hours after MI, peaks at 24 hours and returns to baseline at 36

107
Q

Troponin (T and I)

108
Q

appears 2-4 hours after MI, peaks at 48 hours, and persists for 10-14 days post MI

109
Q

left ventricular hypertorphy and ventricular dilation

110
Q

3-8 weeks gestation

111
Q

sporadic genetic abnormalities

112
Q

bacterial endocarditis - abnormalities cause turbulent flowt that can damage endocardium

113
Q

Ventricular septal defect

114
Q

Right to left

115
Q

left to right

116
Q

“all have a D in them” ASD, VSD, PDA, AVDS

117
Q

foramen ovale

118
Q

ASD

119
Q

“All have a T in them” Tetrology of fallot, transposition of the great vessels, tricupsid atresia, patent truncus arteriosus, total anomolous venous connection/reutrun

120
Q

AVSD

121
Q

1: VSD 2: Overriding Aorta 3: RVH 4: Pulmonic stenosis

122
Q

tetrology of fallot

123
Q

tetrology of fallot

124
Q

tetrology of fallot - squatting increases venous return to the heart

125
Q

coartation of the aorta

126
Q

congenital aortic stenosis, congenital pulmonic stenosis, coarctation of the aorta

127
Q

coartation of the aorta

128
Q

Right to left shunts - clubbing fo fingers (tips of fingers expand and blunt)

CR4 (2 decks)

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