Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ADPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ADPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

ADPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ARPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ARPKD. Pulmonary Hyperplasia is secondary to oligohydramnios

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ARPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ARPKD

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Multicystic Dysplastic Kidney

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Multicystic Dysplastic Kidney

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Medullary sponge kidney

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Medullary sponge has intersitial fibrosis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Nephrophthisis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Polycystic Kidney Hepatic Disease gene (PKHD1)

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Nephrophthisis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Nephrophthisis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

nephrophthisis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Adult onset medullary cystic disease

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Acquired cystic renal disease

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

acquired cystic renal disease

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Simple Cyst

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Acute proliferative glomerulonephritis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Acute proliferative glomerulonephritis MCC = Group A strep pharyngitis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Acute proliferative glomerulonephritis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Rapid progressive Glomerular nephritis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

kidney is large and pale with petichial hemorrage

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

IgA nephropathy

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

IgA nephropathy

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

igA nephropathy

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

iga nephropathy

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Alport Syndrome

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Membranoproliferative Glomerulonephritis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Membranoproliferative Glomerulonephritis

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Subendithelual deposits between duplicated membranes

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Intramembranous dense deposits = Ribbon like deposits

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Membranous Nephropathy, Focal Segmental GN, Diabetic nephropathy Minimal change

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

membranous GN

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

membranous GN

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

membranous GN

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Focal segmental GN

A

Pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Obesisty and anabolic steroid use

A

Pathology

53
Q

Hyalin insudation and lipid vacuoles in sclerotic areas

A

Pathology

54
Q

Diabetic Glomerulonephropathy

A

Pathology

55
Q

Diabetic Glomerulonephropathy

A

Pathology

56
Q

Minimal change disease

A

Pathology

57
Q

Acute tubular injury (tubular necrosis)

A

Pathology

58
Q

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

A

Pathology

59
Q

Acute Tubular injury (tubular necrosis)

A

Pathology

60
Q

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

A

Pathology

61
Q

Acute pyelonephritis

A

Pathology

62
Q

Chronic pyelonephrits

A

Pathology

63
Q

drug and toxin induced tublointersitial nephritis

A

Pathology

64
Q

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

A

Pathology

65
Q

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

A

Pathology

66
Q

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

A

Pathology

67
Q

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

A

Pathology

68
Q

Ascending infection (usually E.coli)

A

Pathology

69
Q

Papillary Necrosis, Pyonephrosis, Perinephric abscess

A

Pathology

70
Q

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

A

Pathology

71
Q

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

A

Pathology

72
Q

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

A

Pathology

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)

A

Pathology

74
Q

Acute Uric Acid nephropathy

A

Pathology

75
Q

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

A

Pathology

76
Q

Medullary Sponge Kidney and Hypercalcemia and Nephrocalcinosis

A

Pathology

77
Q

Light chain cast nephropathy (myeloma kidney)

A

Pathology

78
Q

Light chain cast nephropathy (myeloma kidney)

A

Pathology

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

A

Pathology

80
Q

Nephrosclerosis (fine even granularity)

A

Pathology

81
Q

fibromuscular dysplasia havs the lumen still in the center

A

Pathology

82
Q

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

A

Pathology

83
Q

Thrombotic Microangiopathies - result from shearing of red blood cells

A

Pathology

84
Q

Wims (Nephroblastoma)

A

Pathology

85
Q

Renal Papillary Adenoma, Renal oncocytoma, Angiomyolipoma

A

Pathology

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

A

Pathology

87
Q

coronary atherosclerosis (90%)

A

Pathology

88
Q

Angina pectoris

A

Pathology

89
Q

middle aged men and women after menopause

A

Pathology

90
Q

Stable Angina

A

Pathology

91
Q

False

A

Pathology

92
Q

Stable angina

A

Pathology

93
Q

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

A

Pathology

94
Q

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

A

Pathology

95
Q

within 60 seconds

A

Pathology

96
Q

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

A

Pathology

97
Q

Transmural

A

Pathology

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

A

Pathology

99
Q

MI

A

Pathology

100
Q

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

A

Pathology

101
Q

1-3 days

A

Pathology

102
Q

7-10 days

A

Pathology

103
Q

begins at 2 weeks and is complete at 8 weeks

A

Pathology

104
Q

indicative of reperfusion injury post MI

A

Pathology

105
Q

CKMB

A

Pathology

106
Q

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

A

Pathology

107
Q

Troponin (T and I)

A

Pathology

108
Q

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

A

Pathology

109
Q

left ventricular hypertorphy and ventricular dilation

A

Pathology

110
Q

3-8 weeks gestation

A

Pathology

111
Q

sporadic genetic abnormalities

A

Pathology

112
Q

bacterial endocarditis - abnormalities cause turbulent flowt that can damage endocardium

A

Pathology

113
Q

Ventricular septal defect

A

Pathology

114
Q

Right to left

A

Pathology

115
Q

left to right

A

Pathology

116
Q

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

A

Pathology

117
Q

foramen ovale

A

Pathology

118
Q

ASD

A

Pathology

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

A

Pathology

120
Q

AVSD

A

Pathology

121
Q

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

A

Pathology

122
Q

tetrology of fallot

A

Pathology

123
Q

tetrology of fallot

A

Pathology

124
Q

tetrology of fallot - squatting increases venous return to the heart

A

Pathology

125
Q

coartation of the aorta

A

Pathology

126
Q

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

A

Pathology

127
Q

coartation of the aorta

A

Pathology

128
Q

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

A

Pathology

CR4 (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions