Exam 2: Renal Disease Flashcards Preview

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Flashcards in Exam 2: Renal Disease Deck (97):
1

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

glomeruli

2

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

tubules

3

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

interstitium

4

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

azotemia

5

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

Uremia

6

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

acute nephritic syndrome

7

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

nephrotic syndrome

8

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

acute renal failure

9

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

polycystic kidney disease

10

What are the clinical manifestations of polycystic kidney disease

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

11

What is the etiology of polycystic kidney disease

defective PKD1 gene located on chromosome 16
encoding for polycystin

12

What are the extrarenal pathologies of polycystic kidney disease

1/3 of patients have cysts in the liver
saccular aneurysms may develop in the circle of Willis

13

What is the gross pathology of polycystic kidney disease

large kidneys (4g) predominated by numerous cysts

14

What is the histopathology of polycystic kidney disease

cysts derive from all levels of the nephron

15

What is the etiology of polycystic kidney disease in childhood

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

16

What is the extrarenal pathology of polycystic kidney disease in children

almost all have liver cysts and progressive liver fibrosis

17

What is the pathology of polycystic kidney disease in children

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

18

What are three mechanisms of glomerular disease

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

19

What are three ways in which to examine kidney biopsies

light microscopy
immunofluorescence
electron microscopy

20

This is caused by increased glomerular capillary permeability to plasma proteins

nephrotic syndromes

21

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

minimal change disease

22

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

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

23

What kind of treatment is there for minimal change disease

corticosteroid treatment, which produces a good response in children

24

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

focal and segmental glomerulosclerosis

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