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M2 Renal/FEK > 20. Acute Kidney Injury > Flashcards

20. Acute Kidney Injury Flashcards

1
Q

what does a small amount of highly concentrated urine with low Na mean?

A

warning that irreversible cell damage is imminent.
reason: water has been reabsorbed due to ADH, and salt has been reabsorbed due to aldosterone. Both were upreg’d due to sympathetic stimulation

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2
Q

definition of acute kidney injury?

A

reduction in GFR by 25% or more

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3
Q

how is GFR measured?

A

serum creatinine concentration. accumulates in serum if not cleared by kidneys

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4
Q

which artery supplies the tubular structures?

A

efferent. but decr blood flow in either will cause possible ischemia to the nephron blood supply

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5
Q

generally, a decrease in circulating blood (ECV) supply activates what?

What causes decr. in ECV?

A

sympathetics!
tachy, vasoconstriction, RAAS system, thirst, ADH
also aldo, AtII –> incr reabsorption of Na

causes: CHF, cirrhosis, sepsis, vasodilators, nephrotic syndrome, RAS, ACEi - anything that decreases GFR

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6
Q

define pre-renal azotemia

A

moderate decrease in renal perfusion (GFR decreases)

renal sympathetics activate, sodium is reabsorbed –> low urine Na concentration

water is reab –> concentrated urine

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7
Q

define acute tubular necrosis (ATN)

What do you see on labs?

A

severe/sustained fall in renal perfusion (sustained decr. ECV) –> cell death; tubular fluid is not processed, results in accumulation of toxins/electrolytes, may result in isothenuria (urine = plasma osmolarity)

incr. serum creatinine/BUN in the setting of decr ECV (incr. HR, decr. BP, cool skin, diaphoresis)

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8
Q

what marks the transition point between pre-renal azotemia and ATN?

A

urine osmolality approach PLASMA values (i.e., tubular fluid not altered much by action of tubular cells) = ISOTHENURIA

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9
Q

at the point of ATN, what is the significance clinically?

A

past the point of being able to restore renal function by restoring circulating volume

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10
Q

Pre-renal AKI treatment:

ATN treatment

A

pre-renal: restore ECV to maintain perfusion

ATN: decr. fluid intake, K, correct A/B balance, dialysis (basically maintain homeostasis until the tubules regenerate)

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11
Q

ATN: what will be seen on urine microscopy?

A

muddy brown casts

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12
Q

ATN clinical labs demonstrate:

A

FENa: if 2% (since tubules aren’t working properly and are unable to respond to aldosterone/AII and are excreting too much Na)

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13
Q

how should I monitor patients with Pre-renal AKI?

A

monitor serum creatinine, minimize blood loss, restore ECV

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14
Q

calculation for FENa?

What does FENa 1?

A

(USPC)/(UCPS) x 100

1 = tubules aren’t reabsorbing Na properly

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15
Q

What is intrinsic AKI? Where can it happen? 3

A

toxic or immunologic injury within the kidney compartment.

can be glomerular, tubulo-interstitial, or vascular

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16
Q

with a tubular injury, will I see proteinuria?

A

no, will see proteinuria with a glomerular injury

17
Q

What would you see with glomerular AKI?

A

oliguria with HTN
cola-colored urine
hematuria (dysmorphic RBC + casts)

18
Q

What is tubular-interstitial AKI caused by? 3 broad categories

A 
Allergic Interstitial nephritis (AIN)
Endogenous toxins (myoglobin, light chains, uric acid)
Exogenous toxins (nsaids, contrast, Calcineurin inhibitors, Aminoglycosides, crystals, acetaminophen, ETOH, Lithium)
19
Q

What is allergic interstitial nephritis?

labs?
creatinine?
oliguric or non-oliguric?
urine findings?
bx findings?
systemic findings?

trmt:

A

hypersensitivity rxn to exogenous chemicals/meds that can act as haptens (penicillin, cephalosporin, PPIs, sulfur-based Rx, NSAIDs, etc)

Labs:
incr serum creatinine
non-oliguric (>0.5ml/kg/hr)
urine: sterile pyuria (+WBC)
bx: lymphocytes + eosinophils
systemic: rash

discontinue offending agent

20
Q

How does myoglobin cause AKI?

causes?
labs?
creatinine?
oliguric or non-oliguric?
urine findings?
bx findings?
systemic findings?

Trmt?
contraindications?

A

myoglobin released from muscle damage (crush injury, rhabdomyolysis, NMS) cause VASOCONSTRICTION of afferent arteriole and direct toxicity to RTE

labs:
incr. CPK
can be oliguric or non-oliguric
pink urine + pink plasma
systemic: edematous

trmt: hydration, alkalinazation, dialysis
contraindications: diuretics

21
Q

How does light chains cause AKI?

causes?
labs?
creatinine?
oliguric or non-oliguric?
urine findings?
bx findings?
systemic findings?

Trmt?
contraindications?

A

Multiple myeloma, plasma cell dyscrasias produce light chains that accumulate in the PCT –> toxic

Insidious loss of GFR over days-months
Non-oliguric
May have RTA Type II
decr. AG (due to incr serum globulins, which are + charge)
incr. risk of AKI in response to minor changes in ECV
urine dipstick = NEGATIVE
Urine microscopy: no cells, casts, or crystals

Trmt:
Alkylating agents (melphalan) & Prednisone
Velcade/Bortezomib
Thalidomide and lenalidomide (Revlamid)
Autologous transplantation
22
Q

How does uric acid cause AKI?

causes?
labs?
oliguric or non-oliguric?
urine findings?

Trmt?
contraindications?

A

Tumor lysis syndrome or defects in purine metabolism (Lesch-Nyhan Syndrome); Uric acid accumulates in peri-tubular fluid and precipitate into uric acid crystals -> inflammatory response

Labs:
Hyperuricemia
Urine sediment: bland, urate crystals
Oliguric or non-oliguric
High FENa
phosphate & LDH (due to cell lysis)
Trmt:
Hydration
Alkalination 
Allopurinol + Febuxostat
Recombinant IV uricase
23
Q

Exogenous toxins that can cause AKI?

A 
NSAIDs
Iodinated Contrast
Calcineurin Inhibitors
Aminoglycosides
Crystals
Acetaminophen
ETOH
Lithium
24
Q

How does NSAIDs cause AKI?

Lab findings?

A

Inhibit vasodilator prostaglandins -> afferent arteriole vasoconstriction -> medullary ischemia

low FENa (due to afferent arteriolar vasoconstriction)
high K + metabolic acidosis due to distal inhibition of K/H secretion
25
Q

How does iodinated contrast cause AKI?

Lab findings?

A

afferent arteriole vasoconstriction
Viscous –> impedes tubular flow
Directly toxic to renal tubule cells

incr. creatinine 24-48 hours after contrast administration
non-oliguric
low FENa (due to vasoconstriction)
urine sediment: no casts, cells, crystals

26
Q

How does calcineurin inhibitors cause AKI?

A

afferent arteriole vasoconstriction

Directly toxic to renal tubular cells

27
Q

How does aminoglycosides cause AKI?

Lab findings?

A

Interferes with mitochondria function and IP3 signal transduction in proximal RTE and cochlear hair cells
Ex: Gentamycin, Streptomyosin, tobramycin

Non-oliguric
Urine microscopy: no casts, cells, crystals
Possible RTA Type I or Type II
3-5 days after dosing

28
Q

How does lithium cause AKI?

A

block ADH mediated actions in DCT -> diuresis

29
Q

How does acetaminophen cause AKI?

A

causes chronic interstitial nephritis, papillary necrosis, calcifications

30
Q

How does ETOH cause AKI?

Lab findings?

A

blocks ADH release from pituitary -> diuresis

31
Q

Hoes does RAS cause AKI?

findings?

Trmt?

A

Atherosclerotic renal artery stenosis - occlusion by thrombus or embolus

Urine sediment: no cells, casts
Unilateral: incr Serum Cr with rapid compensation by incr RBF and GFR in contralateral kidney;

non-oliguric AKI
Bilateral: Anuric AKI

32
Q

Hoes does renal vein thrombosis cause AKI?

findings?

Trmt?

A

Renal vein thrombosis - due to hypercoagulable states: protein C/S deficiency, anti-heparin antibodies (HIT), antiphospholipid syndrome, malignancy, nephrotic syndrome, severe sepsis

Bilateral
Dull loin ache or no pain
Oliguria with gross hematuria (due to damage from back pressure)

33
Q

What is post-renal AKI? What causes it? How does it cause AKI?

findings?

trmt?

A

Obstruction to outflow of urine

  • Congenital (posterior urethral valves)
  • Acquired (prostatic hypertrophy, radiation damage to trigone, nephrolithiasis, single kidney)

decr. flow in the medullary capillary bed -> decr. GFR via TG feedback
- > ischemic flow at the distal tubule and CD
- > decr. effectiveness of ADH action at the CD
- > accumulation of toxins in the blood + urine composition = plasma composition

results in Type IV RTA (Hyperkalemia, Non-AG acidosis)

Non-oliguric – urine is dilute and contains less K/H
Hyperkalemia + Non-AG acidosis (Type IV RTA)
distended bladder (dullness to percussion)

Process:

  1. Urinary catheter
  2. Ultrasound – most sensitive for detecting obstruction
  3. CT w/o contrast – best for finding kidney stone
34
Q

How do you relieve a post-obstructive AKI? What must you be careful of?

A

Catheter – relieves obstruction; be careful of

  • over-rapid decompression of chronically obstructed bladder, which may result in tearing of the venous plexus lining the bladder
  • restoration of GFR may produce large amounts of urine, which may result in decr. ECV, hypokalemia, and hypomagnesemia
    solution: match 1:1 urine output

Cystoscopy – remove stones

M2 Renal/FEK (20 decks)

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