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Flashcards in renal path flashcards (BAD DECK) Deck (128)
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1

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

Pathology

2

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

Pathology

3

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)

Pathology

4

ADPKD

Pathology

5

ADPKD

Pathology

6

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

Pathology

7

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

Pathology

8

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

Pathology

9

ADPKD

Pathology

10

ARPKD

Pathology

11

ARPKD. Pulmonary Hyperplasia is secondary to oligohydramnios

Pathology

12

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)

Pathology

13

ARPKD

Pathology

14

ARPKD

Pathology

15

Multicystic Dysplastic Kidney

Pathology

16

Multicystic Dysplastic Kidney

Pathology

17

Medullary sponge kidney

Pathology

18

Medullary sponge has intersitial fibrosis

Pathology

19

Nephrophthisis

Pathology

20

Polycystic Kidney Hepatic Disease gene (PKHD1)

Pathology

21

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

Pathology

22

Nephrophthisis

Pathology

23

Nephrophthisis

Pathology

24

nephrophthisis

Pathology

25

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

Pathology

26

Adult onset medullary cystic disease

Pathology

27

Acquired cystic renal disease

Pathology

28

acquired cystic renal disease

Pathology

29

Simple Cyst

Pathology

30

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

Pathology

31

Acute proliferative glomerulonephritis

Pathology

32

Acute proliferative glomerulonephritis MCC = Group A strep pharyngitis

Pathology

33

Acute proliferative glomerulonephritis

Pathology

34

Rapid progressive Glomerular nephritis

Pathology

35

kidney is large and pale with petichial hemorrage

Pathology

36

IgA nephropathy

Pathology

37

IgA nephropathy

Pathology

38

igA nephropathy

Pathology

39

iga nephropathy

Pathology

40

Alport Syndrome "Cant see, cant pee, cant hear a bee"

Pathology

41

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

Pathology

42

Alport Syndrome

Pathology

43

Membranoproliferative Glomerulonephritis

Pathology

44

Membranoproliferative Glomerulonephritis

Pathology

45

Subendithelual deposits between duplicated membranes

Pathology

46

Intramembranous dense deposits = Ribbon like deposits

Pathology

47

Membranous Nephropathy, Focal Segmental GN, Diabetic nephropathy Minimal change

Pathology

48

membranous GN

Pathology

49

membranous GN

Pathology

50

membranous GN

Pathology

51

Focal segmental GN

Pathology

52

Obesisty and anabolic steroid use

Pathology

53

Hyalin insudation and lipid vacuoles in sclerotic areas

Pathology

54

Diabetic Glomerulonephropathy

Pathology

55

Diabetic Glomerulonephropathy

Pathology

56

Minimal change disease

Pathology

57

Acute tubular injury (tubular necrosis)

Pathology

58

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

Pathology

59

Acute Tubular injury (tubular necrosis)

Pathology

60

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

Pathology

61

Acute pyelonephritis

Pathology

62

Chronic pyelonephrits

Pathology

63

drug and toxin induced tublointersitial nephritis

Pathology

64

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

Pathology

65

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

Pathology

66

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

Pathology

67

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

Pathology

68

Ascending infection (usually E.coli)

Pathology

69

Papillary Necrosis, Pyonephrosis, Perinephric abscess

Pathology

70

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

Pathology

71

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

Pathology

72

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

Pathology

73

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)

Pathology

74

Acute Uric Acid nephropathy

Pathology

75

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

Pathology

76

Medullary Sponge Kidney and Hypercalcemia and Nephrocalcinosis

Pathology

77

Light chain cast nephropathy (myeloma kidney)

Pathology

78

Light chain cast nephropathy (myeloma kidney)

Pathology

79

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

Pathology

80

Nephrosclerosis (fine even granularity)

Pathology

81

fibromuscular dysplasia havs the lumen still in the center

Pathology

82

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

Pathology

83

Thrombotic Microangiopathies - result from shearing of red blood cells

Pathology

84

Wims (Nephroblastoma)

Pathology

85

Renal Papillary Adenoma, Renal oncocytoma, Angiomyolipoma

Pathology

86

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

Pathology

87

coronary atherosclerosis (90%)

Pathology

88

Angina pectoris

Pathology

89

middle aged men and women after menopause

Pathology

90

Stable Angina

Pathology

91

False

Pathology

92

Stable angina

Pathology

93

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

Pathology

94

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

Pathology

95

within 60 seconds

Pathology

96

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

Pathology

97

Transmural

Pathology

98

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

Pathology

99

MI

Pathology

100

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

Pathology

101

1-3 days

Pathology

102

7-10 days

Pathology

103

begins at 2 weeks and is complete at 8 weeks

Pathology

104

indicative of reperfusion injury post MI

Pathology

105

CKMB

Pathology

106

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

Pathology

107

Troponin (T and I)

Pathology

108

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

Pathology

109

left ventricular hypertorphy and ventricular dilation

Pathology

110

3-8 weeks gestation

Pathology

111

sporadic genetic abnormalities

Pathology

112

bacterial endocarditis - abnormalities cause turbulent flowt that can damage endocardium

Pathology

113

Ventricular septal defect

Pathology

114

Right to left

Pathology

115

left to right

Pathology

116

"all have a D in them" ASD, VSD, PDA, AVDS

Pathology

117

foramen ovale

Pathology

118

ASD

Pathology

119

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

Pathology

120

AVSD

Pathology

121

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

Pathology

122

tetrology of fallot

Pathology

123

tetrology of fallot

Pathology

124

tetrology of fallot - squatting increases venous return to the heart

Pathology

125

coartation of the aorta

Pathology

126

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

Pathology

127

coartation of the aorta

Pathology

128

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

Pathology