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NUR326: exam 2 > urologic problems: glomerular disease > Flashcards

urologic problems: glomerular disease Flashcards

1
Q

azotemia

A

increase BUN and Cr in urine

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2
Q

glomerular filtration rate (GFR)

A

blood test to check kidney function –> blood filtered per hour

calculated of blood metabolic panel

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3
Q

glomerular disorders

A

glomerulonephritis

nephrotic syndrome

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4
Q

glomerulonephritis

A

a variety of conditions that cause inflammation of glomeruli
-primarily an immune response
-focal or diffused
-affects BOTH kidneys equally

**3rd leading cause of kidney failure in US (25% of ESRD cases)

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5
Q

where does the damage of glomerulonephritis occur?

A

glomerulus - delicate network of arterioles within the Bowman’s capsule

tubules - massive consumer of oxygen

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6
Q

glomerular disorders

A

alterations in glomerular capillary

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7
Q

glomerulus layers

A

capillary membranes have 3 layers:
1. endothelium
2. basement membrane
3. podocytes (special epithelial cells)

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8
Q

primary vs. secondary glomerulonephritis

A

primary - isolated to kidneys
secondary - caused by systemic disease

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9
Q

type II immune complex

A

reactions occur on the cell surface and result in direct cell death or malfunction

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10
Q

type III immune complex

A

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

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11
Q

what are the 2 type of glomerulonephritis injuries?

A
  1. antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) –> 5%
  2. antibodies react with circulating antigens and are deposited as immune complex in the GBM –> 90%
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12
Q

what do BOTH types of glomerulonephritis have in common?

A

-accumulation of antigens, antibodies, and complement

-complement activation results in tissue injury

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13
Q

acute glomerulonephritis characterized by…

A

ABRUPT ONSET

HARP
H- hematuria
A- azotemia
R- retention (sodium & water retention; leads to oliguria, edema and HTN)
P- proteinuria

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14
Q

triggers of acute glomerulonephritis

A

post-infectious:
-post-streptococcal infection
-non-streptococcal infection (bacterial, viral, parasitic)

primary disease
(ex: Berger disease)

multisystem disease:
(ex: goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis)

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15
Q

anti-GBM antibodies

A
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16
Q

acute glomerulonephritis patho

A
  1. trigger
  2. immune complexs form
  3. complement activated
  4. release of mediators
  5. tissue injury
  6. hematuria, proteinuria, decreased GFR
17
Q

chronic glomerulonephritis

A

longer term complication build up of scar tissue – scar tissue can’t filter/produce urine effectively
*inflammatory process
*can lasts months - years

18
Q

clinical manifestations of chronic glomerulonephritis

A

similar to acute –>

HARP
H- hematuria
A- azotemia
R- retention (sodium & water retention; leads to oliguria, edema and HTN)
P- proteinuria

*dependent of severity of damage to kidney’s

19
Q

prognosis of chronic glomerulonephritis

A

slow progressive destruction of glomerular tissue

ENDS with ESRD and REQUIRES dialysis

20
Q

pharmacotherapy for glomerulonephritis

A

corticosteroids (predisone) - reduce inflammation

diuretics - reduce swelling

immunosuppressants
anti-hypertensives (ACE or ARB)

21
Q

other treatment (aside from meds)

A

dialysis
diet (less PRO, salt, potassium)

22
Q

common S/S of glomerulonephritis

A

hematuria (coffee colored urine)
oliguria (<400mL/day)
fluid retention (edema, HTN)
labs
- elevated BUN, Cr (>20:1 BUN:Cr ratio)
-++proteinuria
-hypoproteinemia

23
Q

glomerulopathy: DM

A

diabetic neuropathy
-major complication
-underlying pathology (gross thickening of GBM–> poor filtration)
END RESULT:

24
Q

glomerulopathy: HTN

A

hypertensive glomerular disease
-decreased renal perfusion
-sclerotic glomerular changes

25
Q

nephrotic syndrome

A

the glomerulus is too permeable to plasma proteins
elimination > 3 grams of protein per day

26
Q

cause of nephrotic syndrome

A

glomerulonephritis
DM

27
Q

nephrotic syndrome PATHO

A

increased glomerular permeability –> proteinuria –> hypoalbuminemia

28
Q

clinical manifestations of nephrotic syndrome

A

edema
HTN
hyperlipidemia
hyper coagulation (DVT, PE) – loss of antithrombin III and plasminogen

29
Q

antithrombin III fxn

A

keeps balance between clots and free flowing blood

30
Q

plasminogen

A

percursor to plasmin which helps breakdown clots that do form

NUR326: exam 2 (12 decks)

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