Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

FA17 Nephrology > AKI 2 > Flashcards

AKI 2 Flashcards

1
Q

renal failure

A

kidney fails to remove end products of metabolism from blood, regulate fluid, electrolyte and pH balance of extracellular fluid

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

AKI is _____ risk factor for…

A

independent risk factor for MORBIDITY and MORTALITY of hospitalized patients

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

diagnostic criteria of AKI

A

abrupt reduction in kidney function (48hrs) , on e of:

  1. increase in serum Cr by 0.3 mg/dL+ in 48hrs
  2. increased serum Cr by 150% + in 48hrs
  3. Oliguria less than 0.5 mL/kg/hr for more than 6 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

when is serum Cr unreliable

A
  1. when pt is not in steady state (hasn’t accumulated properly)
  2. Dialysis patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pre-renal azotemia def + cause (5)

A

decrease in renal blood flow - kidney is STILL being perfused, just not filtered

  1. Heart failure
  2. blood loss (surgery, trauma, GI)
  3. shock
  4. renal artery stenosis
  5. dehydration (vomiting, diarrhea, sweat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

renal azotemia

A

disease of renal parenchyma (Kidney is also not being perfused)

tubular necrosis , caused by
1. HoTN (severe decrease in blood flow)

  1. Nephrotoxins
  2. glomerulonephritis and acute interstitial nephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

most cases of intrinsic AKI are due to

A

acute tubular necrosis

caused by ischemia and nephrotoxins

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

post renal azotemia

A

diseases that involve remainder of urinary tract excluding kidney (down stream obstruction)

  1. kidney stone
  2. BPH
  3. neurogenic bladder
  4. retroperitoneal fibrosis
  5. tumor (pelvis - cancers)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

best way to diagnose AKI

A

good history and PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

history questions (7)

A
  1. hx of renal fxn and labs
  2. urinary output (amnt, color, incontinence)
  3. infection
  4. HoTN, volume loss
  5. nephrotoxic agents
  6. recent sx, anesthesia
  7. evidence of obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PE findings indicative of AKI

A
  1. orthostasis (pre-renal, severe intrinsic)
  2. fluid overload
  3. weight loss
  4. palpable, full bladder (post renal)
  5. rectal exam/prostate (post renal)
  6. post void straight cath or bladder scan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

s/s of aki

specific for kidney

A
  1. decreased/absent urine output
  2. flank pain
  3. edema
  4. HoTN
  5. discolored urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

General S/s of AKI

A

weakness/easy fatiguability

anorexia, n/v

mental status change

systemic: fever, arthralgia, pulmonary lesions, lived reticularis

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

symptoms of AKI suggesting vasculitis

A

fever, arthralgia, pulmonary lesions

this indicates systemic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of livedo reticularis in AKI

A

aortic cat or atheromatous or cholesterol emboli

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

diagnostic eval of of AKI

A

plasma CR

serum bicarb, K

urine volume (anuria, can be oliguric, non-oliguric)

urine sediments (cells and casts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pre-renal azotemia casts

A

moderate hyaline and finely granular casts but cellular casts are infrequent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ATN casts

A

dirty brown granular casts

renal tubular epithelial cells, free and in casts

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

urinary indicies use

A

helpful in distinguishing ATN and pre-renal azotemia

urine sodium, urine CR, urine osmolarity, FE Na)

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

urinary indices in prerenal azotemia

A

can’t filter, so decreased volume therefore

Urine Na = LOW (not as much water out)
Urine Cr = HIGH
Urine osmolarity = HIGH (more concentration)

Fe Na = < 1

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

urinary indices in ATN

A

not enough blood flow, decreased function (unable to pull the water in so diluted)

Urine Na = HIGH
Urine Cr = LOW
Urine osmolarity = LOW

Fe Na = > 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

when are imaging tests indicated in AKI ?

A
  1. obstructive pathology
  2. determine if renal failure is acute or chronic

ultrasound of Kidney or CT scan of abdomen/pelvis

if CKD: small, shrunken kidney

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

when is a renal biopsy indicated in AKI?

A
  1. vascular pathology suspected
  2. progressive AKI and no reason why (non responsive to meds)
  3. oliguria greater than 4 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

early renal bx looks for

A

vasculitis, TTP, glomerulonephritis, HUS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what might suggest duration of disease if previous labs are unavailable?
1. recent onset of symptoms 2. little to no urine 3. progressively increasing Cr 4. rate of rise in Cr (ATN = 0.3-0.5/day, rapid) 5. small, echogenic kidney on US (chronic dz)
26
lab abnormalities of AKI
Hyperkalemia (K > 5.5) BUN > 80 bicarb levels fall (< 15)
27
emergent action in AKI deadly complications
arrhythmias (due to hyperK) fluid overload acidosis
28
emergent AKI complications (8)
1. cogaulopathy 2. confusion, coma 3. pericarditis 4. severe itching 5. infection 6. seizures 7. drug toxicity 8. nausea/vomiting
29
indications for "urgent" hemodialysis
1. metabolic acidosis 2. fluid overload (unresponsive to med) 3. hyperkalemia 4. affects of uremia (pericarditis, confusion, coma, seizures, coagulopathy, n/v, GIB
30
pre-renal AKI tx
drop in perfusion pressure fluids (0.9 NS, LR) pressers (dobutamine)
31
post renal AKI tx
imagining and restoration of urine flow foley cath stent urethra nephrostomy tube placement
32
stages of ATN
ignition phase mantainence phase recovery phase
33
pathophysiology of ATN
due to initiation and injury of tubular cells 1. loss of barrier, back leak of filtrate 2. damage to Na+/K+ ATPase pump 3. sloughing of tubular cells = granular casts 4. decreased vasodilator production 5. increased free radicals
34
maintenance phase
stabilization of GFR at low level (1-2 weeks) uremic complications
35
recovery phase
cells regenerate abnormal diuresis can occur - salt and water loss
36
ischemic ATN cause
low perfusion to parenchyma can be due to progression of prerenal phase caused by HoTN, hypoxemia, shock, sepsis, dehydration, hypovolemia
37
effects of major surgical procedures and ischemia ATN
prolonged hypoperfusion worsened by vasodilation anesthetic agents and narcotics
38
when is ATN most likely to occur?
surgery shock (esp. sepsis) contrast
39
which patients are susceptible to ATN
underlying CKD elderly people on medications (ACE, ARB, diuretics, metformin) dehydration
40
how to prevent ATN
correct underlying electrolyte abnormalities hydration avoid nephrotoxic drugs
41
antibiotics that likely cause ATN (class and drug names)
aminoglycosides Gentamycin Tobramycin Amacaine/Neomycin
42
aminoglycosides and ATN
older patients and those with renal disease are concerns occurs 5-10 days after exposure (mild and non oliguric)
43
treatment of ATN caused by aminoglycosides
stop medications hydrate gently monitor renal function
44
NSAIDs/COX-2 and ATN
inhibit prostaglandin synthesis by endothelial cells not an issue in people with normal function, but some patients depend on constant prostaglandin induced vasodilation of renal arterioles
45
patients depending on prostaglandin for normal kidney function
``` HTN Stage III CKD Chronic arteriosclerotic dz volume depletion nephrotic syndrome ESLD severe hypercalcemia ```
46
treatment of ATN due to NSAIDs/COX-2
improve in 3-7 days following drug d/c
47
acute interstitial nephritis
allergy to NSAIDS (ibuprofen, naproxen, fenoprofen) reaction occurs in the kidney causes renal insufficiency and nephrotic range proteinuria
48
other drugs causing ATN
amphotericin B (Antifungal) vancomycin acyclovir cephalosporins ACE inhibitors/ARBs Foscarnet Antivirals synthetic cannabinoids
49
contrast dye and ATN
occurs w/in 24-96 hrs of administration renal function returns in 7-10 days no effective treatment
50
risk factors for contrast induced ATN
``` CKD (stage 3+) DM >65 y/o Volume depletion large volumes/repeated doses ```
51
prevention of contrast induced ATN
lower doses IV hydration before and after avoid nephrotoxic agents 224-48hrs before and after mucomyst/m-acetylcystine
52
exogenous nephrotoxins
cyclosporin immunosuppressant (dose dependent, biopsy needed) antineoplastics, cisplatin organic solvents heavy metals (mercury, cadmium, arsenic)
53
endogenous nephrotoxins
myoglobin | hemoblogbin
54
myoglobin and nephrotoxin
from rhabdo released into blood causing damage to renal tubules complain of muscular pain (show signs of muscle injury)
55
myoglobin urine
dark brown without RBCs serum CPK and myoglobin elevated dark brown and false positive for RBCs (not on dipstick)
56
clinical situations where Rhbadomyolysis is seen
statins elderly people/drugs = fall can't get up extreme exercise crush injuries
57
clinically relevant CK levels
20k-50k or more
58
side effects of muscle cell lysis
ATN hyperkalemia, hyperphostphatemia, hyperuricemia
59
treatment of ATN due to rhabdo
hydration at high rate may do alkaline IV must monitor urine output
60
alkaline IV in rhabdo
sodium bicarb in D5 forces metabolic alkalosis that protects kidney and body from hyperkalemia and prevents AKI
61
hemoglobin
causes direct injury due to massive intravascular hemolysis treament: reversal of cause and hydration
62
causes of massive hemolysis
wrong match blood transfusions hemolytic anemia
63
uric acid as a nephrotoxin
occurs in rapid cell turnover and lysis (neoplastic diseases) esp. in chemo precipitation of uric acid crystals in tubules (+ hyper K and PO4)
64
prevention of uric acid ATN
UOP of 3l/day prophylactic allopurinol
65
multiple myeloma and ATN
nephrotoxicity due to excretion of light chain Igs into urine light chains are not found on UA so must diagnose with serum electrophoresis hydration and MM treatment
66
treatment goals of ATN
avoid volume overload and hyper kalmia (volume restriction and loop diuretics) nutritional support (catholic state, keep weight up)
67
indications for hemodialysis in AKI
1. life threating electrolyte issue (hyperK) 2. volume overload 3. worsening acidosis 4. avoidance of uremic complications (BUN > 80)
68
treatment of ATN
correct anemia if symptomatic (don't want to fluid overload) appropriately dose drugs be sure to monitor for infection (decrease number of lines)

FA17 Nephrology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions