AKI Flashcards

1
Q

AKI due to scleroderma (scleroderma renal crisis) should be treated with

A

ACE inhibitors.

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

for hepatorenal syndrome:
Bridge therapies that have shown promise include terlipressin (a vasopressin analog), combination therapy with octreotide (a somatostatin analog) and midodrine (an a1-adrenergic agonist), and norepinephrine, in combination with what intravenous fluid?

A

albumin (25–50 g, maximum 100 g/d)

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

Idiopathic TTP-HUS is a medical emergency and should be treated promptly with

A

plasma exchange

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

Early and aggressive volume repletion is mandatory in patients with rhabdomyolysis, who may initially require

A

10 L of fluid per day

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

Alkaline fluids may be beneficial in preventing tubular injury and cast formation, but carry the risk of worsening _______.

A
  • 75 mmol/L sodium bicarbonate added to 0.45% saline

* hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

According to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines, patients with AKI should achieve a total energy intake of

A

20–30 kcal/kg per day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Protein intake should vary depending on the severity of AKI: 0.8–1.0 g/kg per day in noncatabolic AKI without the need for dialysis; 1.0–1.5 g/kg per day in patients on dialysis; and up to a maximum of ______ if hypercatabolic and receiving continuous renal replacement therapy.

A

1.7 g/kg per day

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

a technology similar to hemodialysis except at lower blood flow and dialysate flow rates.

A

CRRT Continuous renal replacement therapy can also be performed by diffusive clearance (continuous venovenous hemodialysis [CVVHD]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

in which large volumes of plasma water (and accompanying solutes) are forced across the semipermeable membrane by means of hydrostatic pressure;

A

Continuous renal replacement therapy (CRRT) can be performed by convective clearance (continuous venovenous hemofiltration [CVVH]

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

A hybrid therapy combines both diffusive and convective clearance

A

continuous venovenous hemodiafiltration [CVVHDF]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

To achieve some of the advantages of CRRT without the need for 24-h staffing of the procedure, some physicians favor _____ or extended daily dialysis (EDD).
In this therapy, blood flow and dialysate flow are higher than in CVVHD, but the treatment time is reduced to ≤12 h.

A

slow low-efficiency dialysis (SLED)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

If available, is often preferred in patients with severe hemodynamic instability, cerebral edema, or significant volume overload.

A

CRRT

Continuous renal replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Common causes of community-acquired AKI include

A
volume depletion
heart failure
adverse effects of medications
obstruction of the urinary tract
malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The most common clinical settings for hospital-acquire AKI are

A

sepsis
major surgical procedures
critical illness involving Heart or liver failure
nephrotoxic medication administration

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

is the most common form of AKI. It is the designation for a rise in SCr or BUN concentration due to inadequate renal plasma flow and intraglomerular hydrostatic pressure to support normal glomerular filtration

A

Prerenal azotemia

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

Prolonged periods of prerenal azotemia May lead to ischemic injury, often termed

A

acute tubular necrosis (ATN)

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

Glomerular filtration can be maintained despite reduced renal bloodflow by _____, which-maintains glomerular capillary hydrostatic pressure closer to normal and thereby prevents marked reductions in GFR if renal blood flow reduction is not excessive

A

angiotensin II–mediated renal efferent vasoconstriction

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

Intrarenal biosynthesis of vasodilators such as____

increase in response to low renal Perfusion pressure

A

prostaglandins(prostacyclin, prostaglandin E2), kallikrein and kinins,and possibly nitric oxide (NO)

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

Even in healthy adults, renal autoregulation usually fails once the systolic blood pressure falls below

A

80 mmHg

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

can also occur following percutaneous catheterization of the aorta, or spontaneously, is due to cholesterol crystal embolizationresulting in partial or total occlusion of multiple small arteries withinthe kidney.

A

AKI from atheroembolic disease

21
Q

Individuals undergoing massive fluid resuscitation for trauma, burns, and acute pancreatitis can also develop _______, where markedly elevated intraabdominal pressures, usually >20 mmHg, lead to renal vein compression and reduced GFR

A

the abdominal compartment syndrome

22
Q

The most common clinical course of contrast nephropathy is characterized by a rise in SCr beginning ___ following exposure, peaking within 3–5 days, and resolving within 1 week

A

24–48 h

1-2days (nor exceeding 2 days and after 1 day post exposure)

23
Q

transient tubule obstruction with precipitated contrast material agents implicated as a cause of AKI are

A
  1. high-dose gadolinium used for magnetic resonance imaging (MRI) and
  2. oral sodium Phosphate solutions used as bowel purgatives.
  3. Iodinated contrast agents use din CV CT SCANS
24
Q

Antibiotics that cause AKI

A

Vancomycin
Aminoglycosides and amphotericin B
Acyclovir

25
Q

Clinical features of amphotericin B nephrotoxicity include

A

polyuria,
hypomagnesemia
hypocalcemia,
non-gap metabolic acidosis.

26
Q

Antibiotic that can precipitate in tubules and cause AKI by tubular “obstructions” particularly when given as an intravenous bolus at high doses (500 mg/m2) or in the setting of hypovolemia.

A

Acyclovir

27
Q

are also frequently associated withAKI due to tubular toxicity

A
Acyclovir
Foscarnet
pentamidine
tenofovir
cidofovir
28
Q

may Cause hemorrhagic cystitis and tubular toxicity, manifested as type II renal tubular acidosis (Fanconi’s syndrome), polyuria, hypokalemia,and a modest decline in GFR.

A

Ifosfamide

29
Q

Chemotherapeutic agents casing AKI

A

Ifosfamide
Cisplatin and carboplatin
bevacizumab

30
Q

Toxic Ingestions causing AKI

A

Ethylene glycol
HEAA
Diethylene glycol
Aristolochic acid

31
Q

the most common protein in urine and produced in the thick ascending limb of the loop of Henle

A

uromodulin

32
Q

may follow initiation of cytotoxic therapy in patients with high-grade lymphomas and acute lymphoblastic leukemia; massive release of uric acid (with serum levels often exceeding15 mg/dL) leads to precipitation of uric acid in the renal tubules and AKI (Other features include hyperkalemia and hyperphosphatemia

A

Tumor lysis syndrome

33
Q

contamination of foodstuffs has led to nephrolithiasis and AKI, eitherthrough intratubular obstruction or possibly direct tubular toxicit

A

Melamine

34
Q

distinctions-of ckd to AKI ,clues suggestive of CKD can come from

A

radiologic studies (small,shrunken kidneys with cortical thinning on renal ultrasound, or evidence of renal osteodystrophy)
or
laboratory tests such as normocytic anemia in the absence of blood loss or secondary hyperparathyroidism with hyperphosphatemia and hypocalcemia

35
Q

Prerenal azotemia should be suspected in the setting of

A

vomiting, diarrhea, glycosuria causing polyuria, and several medications including diuretics, NSAIDs, ACE inhibitors, and ARBs.

Physical signs of orthostatic hypotension, tachycardia, reduced jugular venous pressure, decreased skin turgor, and dry mucous membranes

36
Q

Recent manipulation of the aorta or other large vessels; may occur spontaneously or after anticoagulation;retinal plaques, palpable purpura,livedo reticularis, GI bleed
Labs: Hypocomplementemia, eosinophiluria(variable), variable amounts ofproteinuria

A

Atheroembolic disease

37
Q

Complete anuria early in the course of AKI is uncommon except in thefollowing situations:

A
complete urinary tract obstruction, 
renal artery Occlusion, 
overwhelming septic shock, 
severe ischemia (often with cortical necrosis), or severe proliferative glomerulonephritis 
or vasculitis
38
Q

In CKD, kidneys are usually smaller unless the patient has

A

diabetic nephropathy,
HIV-associated nephropathy,
or infiltrative diseases.

39
Q

In cases-of oliguric AKI, the urinary flow rate in response to bolus intravenous furosemide 1.0–1.5 mg/kg can be used a prognostic test: urine outputof less than ____ after intravenous furosemide may identify patients at higher risk of progression to more severe AKI, and the need for renal replacement therapy.

A

200 mL over 2 h

40
Q

The definitive treatment of the hepatorenal syndrome is

A

orthotopic liver transplantation

41
Q

AKI due to scleroderma(scleroderma renal crisis) should be treated with

A

ACE inhibitors

42
Q

Early and aggressive volume repletion is mandatory in patients withrhabdomyolysis, who may initially require

A

10 L of fluid per day

Alkaline diuretics

Alkaline fluids (e.g., 75 mmol/L sodium bicarbonate added to 0.45% saline

Diuretics may be used if fluid repletion is adequate but unsuccessful in achieving urinary flow rates of 200–300 mL/h.

43
Q

Management of Tumor lysis syndrome:

A

aggressive intravenous fluids and allopurinol or rasburicase

44
Q

Management for Volume overload

A

Salt and water restriction
Diuretics
Ultrafiltration

45
Q

In severe cases of volume overload, furosemide may be given as a bolus

A

(200 mg) followed by an intravenous drip (10–40 mg/h), with or without a thiazide diuretic

46
Q

Hyperphosphatemia is commonin AKI and can usually be treated by limiting intestinal absorption of phosphate using phosphate binders:

A
calcium carbonate
calcium acetate
lanthanum
sevelamer
or 
aluminum hydroxide
47
Q

According to the Kidney Disease Improving Global Outcomes(KDIGO) guidelines, patients with AKI should achieve a total energy intake of

A

20–30 kcal/kg per day

48
Q

According to the Kidney Disease Improving Global Outcomes(KDIGO) guidelines, patients with AKI should achieve a total protein intake of

A

1.7 g/kg per day if hypercatabolic and Receiving continuous renal replacement therapy