Brainscape's Knowledge GenomeTM

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


See full index

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

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

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

A

tubules

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

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

A

interstitium

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

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

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

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

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

A

nephrotic syndrome

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

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

A

acute renal failure

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

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

What is the etiology of polycystic kidney disease

A

defective PKD1 gene located on chromosome 16

encoding for polycystin

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

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

What is the gross pathology of polycystic kidney disease

A

large kidneys (4g) predominated by numerous cysts

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

What is the histopathology of polycystic kidney disease

A

cysts derive from all levels of the nephron

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

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

What is the extrarenal pathology of polycystic kidney disease in children

A

almost all have liver cysts and progressive liver fibrosis

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

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

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

What are three ways in which to examine kidney biopsies

A

light microscopy
immunofluorescence
electron microscopy

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

This is caused by increased glomerular capillary permeability to plasma proteins

A

nephrotic syndromes

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

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

A

minimal change disease

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

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

What kind of treatment is there for minimal change disease

A

corticosteroid treatment, which produces a good response in children

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

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

What is the pathology (LM, IF, and EM) of focal and segmental glomerulosclerosis

A

LM - focal and segmental sclerosis with obliteration of capillary lips
IF and EM - no immune complex deposits in the PRIMARY form

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

What is the response to treatment of focal and segmental glomerulosclerosis

A

poor response to corticoid treatment

renal failure after 10 years

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

This nephrotic syndrome is most common in adults, but may affect children and may be primary or secondary to infection, malignancy, SLE, or drugs

A

membranous nephropathy

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

What is the pathology (LM, IF, EM) of membranous nephropathy

A

LM - nearly normal
IF - immune complex deposits
M - deposits in sub epithelial side of the GBM

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

What is the response to treatment of membranous nephropathy

A

poor response to corticoid steroid treatment

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

Renal failure is 2nd only to MI as what

A

cause of death in diabetes patients

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

What is the pathology (LM, IF, EM) of glomerular disease in diabetes mellitus

A

LM - nodular glomerulosclerosis
IF - no immune complex deposits
EM - thick GBM

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

This is a glomerular disease characterized proteinuria progresses over 10-15 years to severe proteinuria

A

glomerular disease in diabetes mellitus

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

What are the clinical manifestations of glomerular disease in diabetes mellitus

A

thick basement membranes

diffuse increase in mesangial matrix and formation of mesangial nodules (Kimmelstiel-Wilson lesion)

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

The a glomerular disease nephrotic syndrome is characterized by

A

the acute onset of hematuria, oliguria and azotemia, and hypertension

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

There is proliferation of what regarding nephritic syndrome

A

cells within the glomeruli accompanied by inflammatory cells

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

Inflammation associated with nephritis syndrome severely injures what

A

capillary walls

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

What does nephritis syndrome result in

A

in blood passing into urine as well as reduced GFR

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

This usually follows (1-4 weeks) streptococcal pharyngitis; other infections may also cause this problem; common in children

A

acute postinfectious glomerulonephritis

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

What are the pathologic (LM, IF, EM) of acute postinfectious glomerulonephritis

A

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
Q

This affects children and young adults and is characterized by hematuria 1-2 dats post-URT incfection

A

IgA nephropathy

41
Q

When globular disease is associated with systemic manifestations (prurpuric skin rash/arthritis) this is called what

A

Henoch-Schönlein purpura

42
Q

What are the pathologic (LM, IF, EM) of IgA nephroapathy

A

LM - variable mesangial cell proliferation

IF and EM - immune IgA complexes within the mesangium

43
Q

This may be associated with antibodies directed against a globular basement antigen, deposition of immune complexes, or lack of immune complex deposition

A

crescentic or rapidly progressive glomerulonephritis

44
Q

This is a progressive loss of renal function, lab finding nephritic syndrome, severe oligouria

A

rapidly progressive glomerulonephritis

45
Q

Death from renal failure associated with rapidly progressive glomerulonephritis is in how long if left untreated

A

weeks to months

46
Q

What is the characteristic finding of rapidly progressive glomerulonephritis

A

crescentic glomerulonephritis due to proliferation of epithelial cells with infiltration of histiocytes

47
Q

What are the components of the several different disorders associated with rapidly progressive glomerulonephritis

A

12% - anti-GBM antibody disease
44% - immune complex disease
44% pauci-immune, lack of anti-GBM or immune complexes

48
Q

Untreated glomerular disease leads to what

A

loss of glomeruli and tubules with fibrosis

49
Q

By the time this is diagnosed, the original renal disease often cannot be identified

A

chronic glomerulonephritis

50
Q

How may chronic, end stage, renal disease be detected

A

routine exam by findings of proteinuria, hypertension, and azotemia

51
Q

This is also known as tubulointerstitial nephritis with suppurative inflammation of kidney and renal pelvis caused by bacterial infection

A

acute pyelonephritits

52
Q

How acute pyleonephritis spread

A

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
Q

What is characteristic of the cells involved with acute pyleonephritis

A

neutrophil infiltration of the interstitum and tubules

clusters of neutrophils in the tubular lumens

54
Q

What is the clinical manifestation of acute pyelonephritits

A

sudden one of pain at the costovertebral angle and systemic evidence of infection
often accompanying dysuria, frequency and urgency

55
Q

What are the etiologies of acute pyelonephritits

A 
UT obstruction
vesicoureteral reflux
pregnancy
gender and age
diabetes
immunosuppression
catheters
56
Q

Repeated bouts of acute inflammation associated with acute pyelonephritis may lead to what

A

chronic pyelonephritis

mononuclear inflammatory infiltration and irregular scarring

57
Q

What is the treatment for acute pyelonephritis

A

treat the bacterial infection

58
Q

What is the etiology of drug-induced interstitial nephritis

A

antibitoics
NSAIDs
diuretics

59
Q

What is the pathogenesis of drug-induced interstitial nephritis

A

hypersensitivity reaction to the drugs

drugs may bind to tubular or interstitial cells and act as hapten with immunogenic response

60
Q

What are the clinical symptoms of drug-induced interstitial nephritis

A

rapid onset (2-40) days of fever
eosinophila
renal dysfunction with hematuria
little to no proteinuria

61
Q

What are the pathologic findings of drug-induced interstitial nephritis

A

interstitial mononuclear cell infiltration and edema
often with many eosinophils
occasionally with non-necortizing granulomas

62
Q

What is the treatment for drug-induced interstitial nephritis

A

withdrawal of the offending drug and corticoid steroids

63
Q

What is the prognosis of drug-induced interstitial nephritis

A

generally good with full recovery in 6-8 weeks

64
Q

This is a clinical and pathologic condition where renal function declines rapidly with evidence of tubular epithelial damage/necrosis

A

acute tubular necrosis

65
Q

What results from acute tubular necrosis

A

acute kidney injury
decreased GFR
oliguria (small amounts of urine)
electrolyte abnormalities

66
Q

True or False

acute tubular necrosis is permanent and leads to intense scarring

A

False, recovery of renal function is possible as tubular epithelium regenerates

67
Q

What are four causes of acute tubular necrosis

A

severe trauma
ischemia (shock)
septicemia
toxins

68
Q

What are the pathologic findings of acute tubular necrosis

A

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
Q

What is the treatment for acute tubular necrosis

A

supportive care and dialysis

70
Q

What is typically the prognosis for acute tubular necrosis

A

in the absence of preexisting kidney disease, most patients fully recover renal function

71
Q

This is the thickening and sclerosing of renal arteries associated with benign hypertension

A

arterionephrosclerosis

72
Q

arterionephrosclerosis is associated with what specific gene

A

apolipoprotein LI gene; found in African Americans

has the same linkage as focal and segmental glomerular sclerosis (FSGS)

73
Q

What is the pathology of arterionephrosclerosis

A

grossly small kidneys with granular surface
hyaline ateriolosclerosis/fibroelastic hyperplasia
tubular atrophy and fibrosis
global sclerosis of glomeruli

74
Q

What are two contributing factors of arterionephrosclerosis

A

hypertension and diabetes

75
Q

What are the clinical manifestations of arterionephrosclerosis

A

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
Q

What is the pathology of arterionephrosclerosis when it is associated with malignant hypertension

A

hyperplastic arteriosclerosis

77
Q

This is an acquired defect in metalloproteinase that degrades vWD (or inherited ADAMTS 13 defect)

A

thrombotic thrombyctyopenia purport (TTP)

78
Q

This is an endothelial cell injury which, in most cases, is due to the Shiga toxin from E. coli leading to platelet activation

A

hemolytic-uremic syndrome (HUS)

79
Q

TTP and HUS are related to the activation, aggregations, and consumption of what

A

platelets

80
Q

What is the pathology of TTP and HUS

A

widespread micro thrombi in capillaries with RBC damage (schistocytes)

81
Q

Which one, TTP or HUS, is more associated with renal involvement and occurs most in children

A

HUS

82
Q

Which one, TTP or HUS, is there more widespread involvement of other organs

A

TTP

83
Q

What is the prevalence of Urolithiasis

A

by the age of 70, affects 11% of men and 6% of women

84
Q

What are the clinical manifestations of urolithiasis

A 
asymptomatic
UT obstruction
intense pain
infection
hematuria
85
Q

What is the pathology of urolithiasis

A

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
Q

In which patients would you see calcium based urolithiasis

A

patients that have increased Ca in the urine

87
Q

In which patients would you see magnesium ammonium phosphate urolithiasis

A

patients that have persistently alkaline urine; infection with proteus

88
Q

In which patients would you see uric acid urolithiasis

A

patients with gout, leukemia (high cell turnover) or persistently acidic urine

89
Q

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

A

hydronephrosis

90
Q

What are some risk factors for renal cell carcinoma

A 
older adult males (2:1)
smoking
hypertension/obesity
acquired politic disease due to chronic dialysis
von Hippel-Lindeau syndrome
91
Q

What are the clinical manifestations of renal cell carcinoma

A 
hematuria
mass
pain
fever
polycythemia (tumor produced erythropoietin)
92
Q

What is the pathology of renal cell carcinoma

A

tumor often invades renal vein
pale/clear cells common
carcinomas typically travel via lymphatics (this is an exception

93
Q

What is the treatment of renal cell carcinoma

A

surgery +/- radiation

94
Q

What is the prognosis of renal cell carcinoma dependent upon

A

Staging
Five year survival
stage 1: 81%
stage 4: 8%

95
Q

What are the clinical manifestations of Wilms Tumor

A

one or more common cancers in children (2-5)
abdominal mass
pain

96
Q

What are the clinical manifestations of Wilms tumor

A

triphasic proliferation of cells, with epithelial, stream, and blastemal components
(Its trying to form a kidney, but no)

97
Q

What is the treatment and prognosis of Wilms tumor

A

surgery and chemotherapy

prognosis is very good

SP15 Pathology (17 decks)

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