glomerular problems (W3) Flashcards

1
Q

what is the functional unit of the kidney?

A

the nephron

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2
Q

glomerulonephritis

A

a variety of conditions that cause the inflammation of glomeruli
can be focal or diffuse
affects both/either or
3rd leading cause of kidney failure, about 1/4 of ESRD cases
primarily an immune-mediated response

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3
Q

where does damage occur?

A

glomerulus- delicate network of arterioles within bowmans capsule
tubules- massive oxygen consumer

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4
Q

glomerular d/o

A

alterations in glomerular capillary

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5
Q

glomerulus (3 layers of the capillary membrane)

A
  1. endothelium layer
  2. basement membrane
  3. podocytes (special epithelial cells)
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6
Q

how to classify glomerulonephritis

A

etiology:
primary- isolated to kidneys
secondary- caused by systemic disease

damage to glomeruli:
focal- only some glomeruli
local- an area of glomeruli

disease progression

clinical presentation

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7
Q

type 2

A

occurs on the cell surface and results in direct cell death/malfunction

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8
Q

type 3

A

immune complexes are deposited into tissues and the resulting inflammation destroys tissues

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9
Q

type 2 and 3- what do they have in common?

A

immune complexes

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10
Q

two types of injury

A
  1. AB attack to antigens of the glomerular basement membrane, direct attack via “anti-GBM AB” (> 5%)
  2. antibodies react with circulating antigens that are deposited in the GBM (> 90%)
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11
Q

both types of injury- what do they have in common?

A
  1. accumulation of antigens, AB, complement
  2. complement activation results in tissue injury
  3. inflammation
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12
Q

acute glomerulonephritis

A

abrupt onset
“HARP”
H- hematuria, blood in urine
A- azotemia, buildup of wast products
R- retention, sodium/water/oliguria/leads to htn and edema
P- proteinuria, protein in urine

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13
Q

AG triggers

A

post-infection: strep/non-strep/bacterial/viral/parasitic
primary disease: berger disease
multisystem disease: good pasture syndrome, systemic lupus (SLE), vasculititis

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14
Q

anti-GBM AB

A

think about the disease good pasture syndrome
similar to lungs
hemoptysis
results in renal and respiratory problems

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15
Q

acute glomerulonephritis pathogenesis

A
  1. trigger
  2. immune complex formation
  3. complement activation
  4. release mediators
  5. tissue injury
  6. hematuria, proteinuria, decreaed GFR
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16
Q

chronic glomerulonephritis

A

LT inflammaton- weeks to months
buildup of scar tissue, results in non-functional kidney
similar s/s of acute
progression- s/s renal failure
slow
eventually ESRD- dialysis

17
Q

pharm

A

corticosteroids
diuretics
immunosuppressants
anti-hypertensives

18
Q

other treatment

A

dialysis
diet (< protein, salt, potassium)

19
Q

S/S of glomerular problems

A

hematuria- coffee/cola-colored
oliguria
fluid retention
labs (increased BUN/creatinine- ratio 20:1, positive protein in the urine, hypoproteinemia, low albumin)

20
Q

loss of albumin

A

hypoproteinemia

21
Q

glomerulopathy

A

diabetes
hypertension

22
Q

diabetic glomerulopathy

A

major complication
gross thickening of GBM

23
Q

hypertension glomerulopathy

A

decreased renal perfussion
scarring
sclerotic glomerular changes

24
Q

nephrotic syndrome

A

damage causes glomeruli to be too permeable to plasma proteins, eliminates > 3 grams of protein each day

etiology:
1. glomerulonephritis
2. diabetes

25
Q

patho of nephrotic syndrome

A

increased glomeruli permeability
proteinuria
hypo-abluminemia

26
Q

nephrotic syndrome- clinical manifestations

A

edema (decreased albumin)
hypertension (compensates)
liver (hyperlipidemia, hypercoagulation because of loss of antithrombin 3 and plasminogen)

27
Q

why does edema occur in nephrotic syndrome?

A

due to decrease in serum osmotic pressure caused by loss of serum albumin