Week 3 - Acute Kidney Injury Flashcards
(53 cards)
1
Q
what is prerenal kidney dsease
A
- problem with blood flow into the kidney
2
Q
what is intrarenal kidney disease
A
- damage to the kidney
3
Q
what is postrenal kidney disease
A
- obstruction of the urinary tract
4
Q
in pre and post renal disease is the kidney itself damaged? what does this mean?
A
- no it is not
- means we have time to act to prevent damage to the kidney itself
5
Q
what is acute kidney injury
A
- represents a group of disorders that cause a rapid deterioration in renal function & resulting in azotemia
6
Q
how does AKI present (2)
A
- rapid rising BUN and creatinine
2. diminished urine volume (oliguria)
7
Q
what is one of the most common causes of AKI
A
- sepsis
8
Q
how does sepsis cause AKI (2)
A
- sepsis causes hypotension thru systemic vasodilation = kidneys are not perfused
- patients with sepsis are often exposed to nephrotoxic antibiotics to treat the infection
9
Q
list 4 causes of prerenal disease
A
- hypovolemia
- septicemia & septic shock
- heart failure
- interruption of renal blood flow caused by surgery or other causes
10
Q
how does hypovolemia cause prerenal disease
A
- decreased blood vol = blood is diverted away from the kidneys to keep vital organs perfused
11
Q
list 4 things that can cause hypovolemia
A
- dehydration
- loss of GI fluid
- hemorrhage
- fluid seqeuestration
12
Q
what is fluid sequestration? how could this cause prerenal injury?
A
- fluid shift from blood space to a 3rd space
ex. ascites - although you still have the same volume of fluid in the body, there is less fluid available to circulate
13
Q
how does heart failure cause prerenal disease
A
- if the heart is not pumping enough blood it will cause decreased blood flow to the kidneys
14
Q
list 2 examples of causes of postrenal disease
A
- ureteral obstruction
- bladder outlet obstruction
15
Q
list 2 examples of ureteral obstruction
A
- calculi
- tumours
16
Q
list 2 examples of bladder outlet obstruction
A
- prostatic hyperplasia
- ureteral structures
17
Q
list 7 causes of intrarenal disease
A
- acute tubular necrosis
- prolonged renal ischemia
- exposure to nephrotoxic drugs
- exposure to heavy metals
- exposure to organic solvents
- acute glomerulonephritis
- acute pyelonephritis
18
Q
list 3 examples of nephrotoxic drugs
A
- aminoglycosides
- radiocontrast agents
- NSAIDs
19
Q
what is an example of an aminoglycoside
A
- gentamycin
20
Q
what are 3 examples of conditions that cause preexisting renal hypoperfusion
A
- HF
- diabetes
- renal stenosis
21
Q
what is the effect of NSAIDs and ACE inhibtors on people with preexisting renal hypoperfusion? why does this occur?
A
- may cause them to develop AKI
- bc prostaglandins dilate the afferent arteriole
- and angiotensin 2 acts to constrict the efferent artiole
and both of these are blocked by the meds
22
Q
describe the effect of heme-containing molecules on the renal tubules
A
- heme is small enough to be filtered = toxic & cause damage to the tubules
23
Q
list 3 things that can cause AKI thru the release of heme
A
- eclampsia
- hemolysis
- muscle damage due to trauma
24
Q
describe how hemolysis can cause AKI
A
- breakdown of RBC = released hgb = heme-containing group is filtered & causes damage to the kidney
25
describe how muscle damage can cause AKI
- damage to muscle causes release of myoglobin which contains heme
26
list 1 examples of muscle damage
- hypermyoglobinemia / rhabdomyolysis
27
what is eclampsia
- seizures during or shortly after birth
- follows preeclampsia: systemic vasoconstriction and HTN
not rlly sure how this contributes to heme being filtered
28
what occurs in the early stages of prerenal disease? what does this result in?
- GFR is decreased due to renal hypoperfussion
| = prerenal azotemia
29
manifestations of AKI are a result of what??
- tubule obstruction by necrotic tissue
30
what does tubule obstruction by necrotic tissue in AKI cause?
- increases the intratubular pressure
| = offsets the glomerular filtration pressure = dramatic reduction in GFR
31
what 2 things does acute tubular necrosis result in?
- loss of tubular function (reabsorb & secrete)
| - failure to conc. urine
32
describe the effects of nephortoxins on the kidney (6)
1. meds enter the filtrate & become v conc
2. concentrated nephrotoxin causes the tubule wall to become swollen & necrotic
3. lumen becomes shrunken = increased resistance
4. filtrate has high back pressire
5. = decreased GFR
6. oliguria
33
what are casts?
- cell debris & protein that combine together within the tubule & are excreted in the urine
34
what are the early signs of AKI (4)
1. elevated BUN and creatinine
2. oliguria
3. hyperkalemia
4. fatigue & malaise
35
what causes elevated BUN and creatine in the early signs of AKI
- decreased GFR (due to the high back pressure in the filtrate)
36
describe the ratio of BUN:creatinine during prerenal azotemia; what causes this?
- high ratio
- during prerenal azotemia, the tubules still function properly
- urea is filtered & reabsorbed while creatinine is only filtered
- since urea is still being reabsorbed, the BUN is higher
37
what might cause BUN to increase rapidly? include 2 examples
- increased protein catabolism
| ex. during fever & sepsis
38
what might cause creatinine to be unusually high
- if rhabdomyolysis is the cause
39
what causes oliguria during early AKI
- decreased GFR and/or tubule obstruction
40
what % of patients do not have oliguria? this will occur especially when it is caused by???
- 25% of patients will not have oliguria
| - especially if AKI is caused by nephrotoxins
41
what causes hyperkalemia during early AKI (2)
- if GFR is significantly reduced
| - & there is significant acidosis
42
what can hyperkalemia cause during early AKI (2)
- ECG changes
| - arrhythmias
43
list 4 things that can treat hyperkalemia during early AKI
- insulin/glucose
- salbuterol
- Kayexalate
- furosemide
44
what causes fatigue & malaise during early AKI (4)
- water intoxication & hyponatremia
- hyperkalemia
- acidosis
- elevated metabolic wastes
45
list late symptoms of AKI (5)
- low ratio of BUN:creatinine
- pulmonary/CVS effects
- edema
- altered mental status
- urinalysis abnormalities
46
why is there now a low ratio of BUN; creatinine during late AKI
- during acute tubular necrosis, the tubules are now damaged so it is no longer reabsorbing urea
47
what pulmonary manifestations occur with late AKI? what causes them?
- dyspnea
- orthopnea
- rales & crackles
- 3rd heart sound
due to fluid overload
48
what causes edema in late AKI
- fluid overload
49
what causes altered mental status in late AKI (3)
- when metabolic wastes become increasing elevated in the blood
- altered electrolytes
- acidosis
50
what is a good indicator of toxicity
- BUN
51
what might the urinalysis show during late AKI
- hematuria
- proteinuria
- pyuris
- with acute tubular necrosis: casts & very dilute urine
52
what is pyuris? what is it a sign of?
- pus in the urine
| - sign of infection
53
regardless of eitology, AKI will likely result in what? why?
- this will result in necrotic death of the tubule epithelial cells bc they are furthest away (=acute tubular necrosis) without successful treatment
