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
2
Q
90% of cases have fusion of upper pole - patients are usually asymptomatic/normally functioning
A
Pathology
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
4
Q
ADPKD
A
Pathology
5
Q
ADPKD
A
Pathology
6
Q
PKD1 (85%) and PKD2- PKD2 presents later than PKD1
A
Pathology
7
Q
ADPKD= dilation of all parts of the nephron ARPKD= dilation of the collecting tubules
A
Pathology
8
Q
RCC R/O based on the fact that ADPKD is bilateral rather than unilateral and the cysts are NONuniform
A
Pathology
9
Q
ADPKD
A
Pathology
10
Q
ARPKD
A
Pathology
11
Q
ARPKD. Pulmonary Hyperplasia is secondary to oligohydramnios
A
Pathology
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
13
Q
ARPKD
A
Pathology
14
Q
ARPKD
A
Pathology
15
Q
Multicystic Dysplastic Kidney
A
Pathology
16
Q
Multicystic Dysplastic Kidney
A
Pathology
17
Q
Medullary sponge kidney
A
Pathology
18
Q
Medullary sponge has intersitial fibrosis
A
Pathology
19
Q
Nephrophthisis
A
Pathology
20
Q
Polycystic Kidney Hepatic Disease gene (PKHD1)
A
Pathology
21
Q
Familial (juvenile) - becomes clinically evident in childhoood or adolescence.
A
Pathology
22
Q
Nephrophthisis
A
Pathology
23
Q
Nephrophthisis
A
Pathology
24
Q
nephrophthisis
A
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
