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SP15 Pathology > Exam 2: Renal Disease > Flashcards

Exam 2: Renal Disease Flashcards

1
Q

This is a network of capillaries between afferent arteriole and efferent arteriole

A

glomeruli

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2
Q

The filtrate from the glomeruli travels through a system of what; these resorb some substances and secretes others

A

tubules

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3
Q

This is formed by collagen and blood vessels between the tubules and glomeruli

A

interstitium

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4
Q

This is elevation of the blood urea nitrogen (BUN) and creatine levels, due to decreased filtration of the blood through the glomeruli

A

azotemia

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5
Q

This is elevation of blood urea nitrogen and creatine levels due to decreased filtration of the blood through the glomeruli as well as gastroenteritis, peripheral neuropathy, pericarditis, dermatitis, hyperkalemia, and lipiduria

A

Uremia

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6
Q

This results from glomerular injury and is characterized by actue onset of hematuria, mild to moderate proteinuria, azotemia, and hypertension

A

acute nephritic syndrome

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7
Q

This is a glomerular syndrome characterized by heavy proteinuria (>3.5 grams/day), hypoalbuminemia, severe edema, hyperlipidemia, and lipiduria

A

nephrotic syndrome

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8
Q

This is the acute onset of azotemia with oliguria (abnormally small amounts of urine) or anuria (no urine)

A

acute renal failure

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9
Q

This autosomal dominant disease is seen in 1 out of every 500-1000 people and is characterized by multiple expanding cysts in both kidneys

A

polycystic kidney disease

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10
Q

What are the clinical manifestations of polycystic kidney disease

A 
gradual onset of renal failure
urinary tract hemorrhage
flank pain around the 4th decade
hypertension
UTI
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11
Q

What is the etiology of polycystic kidney disease

A

defective PKD1 gene located on chromosome 16

encoding for polycystin

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12
Q

What are the extrarenal pathologies of polycystic kidney disease

A

1/3 of patients have cysts in the liver

saccular aneurysms may develop in the circle of Willis

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13
Q

What is the gross pathology of polycystic kidney disease

A

large kidneys (4g) predominated by numerous cysts

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14
Q

What is the histopathology of polycystic kidney disease

A

cysts derive from all levels of the nephron

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15
Q

What is the etiology of polycystic kidney disease in childhood

A

autosomal recessive due to a mutation in PKDH-1 - fibrocystin
1:20,000 live births

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16
Q

What is the extrarenal pathology of polycystic kidney disease in children

A

almost all have liver cysts and progressive liver fibrosis

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17
Q

What is the pathology of polycystic kidney disease in children

A

numerous small uniform-size cysts from collecting tubules in cortex and medulla

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18
Q

What are three mechanisms of glomerular disease

A

immune complex deposits in glomerular basement membrane or mesangium
anti-GBM antibody
epithelial and endothelial injury

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19
Q

What are three ways in which to examine kidney biopsies

A

light microscopy
immunofluorescence
electron microscopy

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20
Q

This is caused by increased glomerular capillary permeability to plasma proteins

A

nephrotic syndromes

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21
Q

This nephrotic syndrome is the most common cause if nephrotic syndrome in children (2/3rds of all cases)

A

minimal change disease

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22
Q

What is the pathology of minimal change disease as sen in LM, IF, and EM

A

LM - normal appearing glomeruli
IF - no immune complex deposits
EM - foot processes effacement

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23
Q

What kind of treatment is there for minimal change disease

A

corticosteroid treatment, which produces a good response in children

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24
Q

This is a common cause of adult nephrotic syndrome, may be primary or secondary to other glomerular diseases and is some cases, familial

A

focal and segmental glomerulosclerosis

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25
What is the pathology (LM, IF, and EM) of focal and segmental glomerulosclerosis
LM - focal and segmental sclerosis with obliteration of capillary lips IF and EM - no immune complex deposits in the PRIMARY form
26
What is the response to treatment of focal and segmental glomerulosclerosis
poor response to corticoid treatment | renal failure after 10 years
27
This nephrotic syndrome is most common in adults, but may affect children and may be primary or secondary to infection, malignancy, SLE, or drugs
membranous nephropathy
28
What is the pathology (LM, IF, EM) of membranous nephropathy
LM - nearly normal IF - immune complex deposits M - deposits in sub epithelial side of the GBM
29
What is the response to treatment of membranous nephropathy
poor response to corticoid steroid treatment
30
Renal failure is 2nd only to MI as what
cause of death in diabetes patients
31
What is the pathology (LM, IF, EM) of glomerular disease in diabetes mellitus
LM - nodular glomerulosclerosis IF - no immune complex deposits EM - thick GBM
32
This is a glomerular disease characterized proteinuria progresses over 10-15 years to severe proteinuria
glomerular disease in diabetes mellitus
33
What are the clinical manifestations of glomerular disease in diabetes mellitus
thick basement membranes | diffuse increase in mesangial matrix and formation of mesangial nodules (Kimmelstiel-Wilson lesion)
34
The a glomerular disease nephrotic syndrome is characterized by
the acute onset of hematuria, oliguria and azotemia, and hypertension
35
There is proliferation of what regarding nephritic syndrome
cells within the glomeruli accompanied by inflammatory cells
36
Inflammation associated with nephritis syndrome severely injures what
capillary walls
37
What does nephritis syndrome result in
in blood passing into urine as well as reduced GFR
38
This usually follows (1-4 weeks) streptococcal pharyngitis; other infections may also cause this problem; common in children
acute postinfectious glomerulonephritis
39
What are the pathologic (LM, IF, EM) of acute postinfectious glomerulonephritis
LM - proliferation of endothelial and mesangial cells, inflammatory cells, may develop cellular crescents IF - immune complex deposition, granular EM - immune complexes at GBM and/or mesangium
40
This affects children and young adults and is characterized by hematuria 1-2 dats post-URT incfection
IgA nephropathy
41
When globular disease is associated with systemic manifestations (prurpuric skin rash/arthritis) this is called what
Henoch-Schönlein purpura
42
What are the pathologic (LM, IF, EM) of IgA nephroapathy
LM - variable mesangial cell proliferation | IF and EM - immune IgA complexes within the mesangium
43
This may be associated with antibodies directed against a globular basement antigen, deposition of immune complexes, or lack of immune complex deposition
crescentic or rapidly progressive glomerulonephritis
44
This is a progressive loss of renal function, lab finding nephritic syndrome, severe oligouria
rapidly progressive glomerulonephritis
45
Death from renal failure associated with rapidly progressive glomerulonephritis is in how long if left untreated
weeks to months
46
What is the characteristic finding of rapidly progressive glomerulonephritis
crescentic glomerulonephritis due to proliferation of epithelial cells with infiltration of histiocytes
47
What are the components of the several different disorders associated with rapidly progressive glomerulonephritis
12% - anti-GBM antibody disease 44% - immune complex disease 44% pauci-immune, lack of anti-GBM or immune complexes
48
Untreated glomerular disease leads to what
loss of glomeruli and tubules with fibrosis
49
By the time this is diagnosed, the original renal disease often cannot be identified
chronic glomerulonephritis
50
How may chronic, end stage, renal disease be detected
routine exam by findings of proteinuria, hypertension, and azotemia
51
This is also known as tubulointerstitial nephritis with suppurative inflammation of kidney and renal pelvis caused by bacterial infection
acute pyelonephritits
52
How acute pyleonephritis spread
the bacterial infection may spread from the urinary bladder, up the ureters and into the renal pelvis and kidney (ascending) - most common or to the kidney from the blood
53
What is characteristic of the cells involved with acute pyleonephritis
neutrophil infiltration of the interstitum and tubules | clusters of neutrophils in the tubular lumens
54
What is the clinical manifestation of acute pyelonephritits
sudden one of pain at the costovertebral angle and systemic evidence of infection often accompanying dysuria, frequency and urgency
55
What are the etiologies of acute pyelonephritits
``` UT obstruction vesicoureteral reflux pregnancy gender and age diabetes immunosuppression catheters ```
56
Repeated bouts of acute inflammation associated with acute pyelonephritis may lead to what
chronic pyelonephritis | mononuclear inflammatory infiltration and irregular scarring
57
What is the treatment for acute pyelonephritis
treat the bacterial infection
58
What is the etiology of drug-induced interstitial nephritis
antibitoics NSAIDs diuretics
59
What is the pathogenesis of drug-induced interstitial nephritis
hypersensitivity reaction to the drugs | drugs may bind to tubular or interstitial cells and act as hapten with immunogenic response
60
What are the clinical symptoms of drug-induced interstitial nephritis
rapid onset (2-40) days of fever eosinophila renal dysfunction with hematuria little to no proteinuria
61
What are the pathologic findings of drug-induced interstitial nephritis
interstitial mononuclear cell infiltration and edema often with many eosinophils occasionally with non-necortizing granulomas
62
What is the treatment for drug-induced interstitial nephritis
withdrawal of the offending drug and corticoid steroids
63
What is the prognosis of drug-induced interstitial nephritis
generally good with full recovery in 6-8 weeks
64
This is a clinical and pathologic condition where renal function declines rapidly with evidence of tubular epithelial damage/necrosis
acute tubular necrosis
65
What results from acute tubular necrosis
acute kidney injury decreased GFR oliguria (small amounts of urine) electrolyte abnormalities
66
True or False | acute tubular necrosis is permanent and leads to intense scarring
False, recovery of renal function is possible as tubular epithelium regenerates
67
What are four causes of acute tubular necrosis
severe trauma ischemia (shock) septicemia toxins
68
What are the pathologic findings of acute tubular necrosis
dilation of tubules interstitial edema necrosis of tubular epithelium often very focal and subtle with ischemic injury and is more diffuse with injury from a toxin
69
What is the treatment for acute tubular necrosis
supportive care and dialysis
70
What is typically the prognosis for acute tubular necrosis
in the absence of preexisting kidney disease, most patients fully recover renal function
71
This is the thickening and sclerosing of renal arteries associated with benign hypertension
arterionephrosclerosis
72
arterionephrosclerosis is associated with what specific gene
apolipoprotein LI gene; found in African Americans | has the same linkage as focal and segmental glomerular sclerosis (FSGS)
73
What is the pathology of arterionephrosclerosis
grossly small kidneys with granular surface hyaline ateriolosclerosis/fibroelastic hyperplasia tubular atrophy and fibrosis global sclerosis of glomeruli
74
What are two contributing factors of arterionephrosclerosis
hypertension and diabetes
75
What are the clinical manifestations of arterionephrosclerosis
associated with malignant hypertension about 5% of benign hypertension (but also de novo) increased cranial pressure (headache, visual impairment, nausea) proteinuria ischemia leading to acute kidney injury
76
What is the pathology of arterionephrosclerosis when it is associated with malignant hypertension
hyperplastic arteriosclerosis
77
This is an acquired defect in metalloproteinase that degrades vWD (or inherited ADAMTS 13 defect)
thrombotic thrombyctyopenia purport (TTP)
78
This is an endothelial cell injury which, in most cases, is due to the Shiga toxin from E. coli leading to platelet activation
hemolytic-uremic syndrome (HUS)
79
TTP and HUS are related to the activation, aggregations, and consumption of what
platelets
80
What is the pathology of TTP and HUS
widespread micro thrombi in capillaries with RBC damage (schistocytes)
81
Which one, TTP or HUS, is more associated with renal involvement and occurs most in children
HUS
82
Which one, TTP or HUS, is there more widespread involvement of other organs
TTP
83
What is the prevalence of Urolithiasis
by the age of 70, affects 11% of men and 6% of women
84
What are the clinical manifestations of urolithiasis
``` asymptomatic UT obstruction intense pain infection hematuria ```
85
What is the pathology of urolithiasis
stones are unilateral in 80% of patients site or formation is within the calyces and pelvis large stones are referred to as "stag horn calculi" forming a cast of the pelvis and calycal system
86
In which patients would you see calcium based urolithiasis
patients that have increased Ca in the urine
87
In which patients would you see magnesium ammonium phosphate urolithiasis
patients that have persistently alkaline urine; infection with proteus
88
In which patients would you see uric acid urolithiasis
patients with gout, leukemia (high cell turnover) or persistently acidic urine
89
This is dilation of the renal plevis/calyces with parenchymal atrophy secondary to obstruction caused by renal tones, UT obstruction, enlarged prostate, neoplasms, neurogenic bladder, pregnancy
hydronephrosis
90
What are some risk factors for renal cell carcinoma
``` older adult males (2:1) smoking hypertension/obesity acquired politic disease due to chronic dialysis von Hippel-Lindeau syndrome ```
91
What are the clinical manifestations of renal cell carcinoma
``` hematuria mass pain fever polycythemia (tumor produced erythropoietin) ```
92
What is the pathology of renal cell carcinoma
tumor often invades renal vein pale/clear cells common carcinomas typically travel via lymphatics (this is an exception
93
What is the treatment of renal cell carcinoma
surgery +/- radiation
94
What is the prognosis of renal cell carcinoma dependent upon
Staging Five year survival stage 1: 81% stage 4: 8%
95
What are the clinical manifestations of Wilms Tumor
one or more common cancers in children (2-5) abdominal mass pain
96
What are the clinical manifestations of Wilms tumor
triphasic proliferation of cells, with epithelial, stream, and blastemal components (Its trying to form a kidney, but no)
97
What is the treatment and prognosis of Wilms tumor
surgery and chemotherapy | prognosis is very good

SP15 Pathology (17 decks)

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