Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal > SM 195 > Flashcards

SM 195 Flashcards

1
Q

What are the effects of AKI on renal function?

A

AKI is responsible for:

Excretion of nitrogenous waste products
Maintain fluid balance
Maintain electrolyte balance

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

What populations are AKI more common in?

A

Hospitalized patients who are septic and critically ill are more likely to develop AKI

Especially those with pre-existing CKD

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

What changes in serum creatinine define AKI?

A

Serum creatinine increases of 0.3 mg/dL within 48hrs or an increase in serum creatinine by 1.5x baseline within 7 days

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

What changes in urine volume define AKI?

A

Urine volume decreases of 0.5mL for 6 hours

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

What defines oliguria?

A

< 500 mL urine output over 24hrs

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

What defines anuria?

A

< 50 mL urine output over 24hrs

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

What systemic manifestations effect AKI?

A

Hyperkalemia due to Metabolic Acidosis inhibiting the Na/K ATPase
Anemia due to decreased EPO from kidney injury
ECV expansion such as HTN, CHF

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

What defines prerenal AKI?

A

Reduced GFR from decreased renal perfusion that can be reversed with a restoration of renal perfusion

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

How does a loss of renal perfusion setup prerenal AKI?

A

RAAS is activated in response to decreased NaCl delivery to the Macula Densa from lower perfusion, causing vasoconstriction to the Kidney in an attempt to restore perfusion to the heart and brain

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

What can cause prerenal AKI?

A

DHPS

Decreased CO
Hypovolemia
Peripheral Vasodilation
Selective Renal Ischemia

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

How can prerenal AKI be diagnosed, in terms of history and PE.?

A

HPI: diarrhea, diuretics
PE: signs of dehydration

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

How can prerenal AKI be diagnosed, in terms of labs?

A

BUN:Cr > 20:1

FENa < 1%

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

What FENa suggests prerenal disease?

A

FENa < 1% suggests prerenal disease

FENa > 2% suggests ATN

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

What are limitations of the FENa?

A

FENa only suggests a disease and is not diagnostic

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

What is postrenal kidney failure?

A

Obstruction in the urinary tract that causes renal failure, due increased capsule hydrostatic pressure lowering GFR

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

What can cause postrenal kidney failure?

A

Bladder obstruction from prostate hypertrophy, uretrhal obstruction, ureter obstruction

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

What are the HPI and PE for a patient with postrenal kidney failure?

A

Distended bladder, enlarged prostate

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

How is postrenal kidney failure managed?

A

Rapid diagnosis and relief of urinary obstruction leading to postobstructive diuresis is essential to preserve kidney function

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

What can cause intrinsic renal failure?

A

ATN (tubular), interstitial vascular, and glomerular issues can cause intrinsic renal failure

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

What do muddy brown casts in urinalysis suggest?

A

Acute Tubular Necrosis

21
Q

What do red blood cell casts in urinalysis suggest?

A

Glomerulonephritis

22
Q

What do white blood cell casts in urinalysis suggest?

A

Infection, allergies

23
Q

How should acidosis be managed?

A

Bicarbonate therapy

24
Q

How should hyperkalemia be managed?

A 
Modify Diet (low K)
Insulin and Epinephrine
Kalexylate to promote Na/K exchange in the gut
25
Q

How should hyperphosphatemia be managed?

A

Calcium Containing Binders

Sevelamer (anti-phosphatemia drug)

26
Q

How do creatinine levels compare during the initial injury period and while the injury is ongoing?

A

Creatinine levels increase as GFR falls during the injury itself

After the injury, a steady state of constant Creatinine level is re-established with elevated GFR and an increased Serum Creatinine, relative to before the injury

27
Q

How does AKI vary among stages?

A

AKI at higher stages has higher increases in serum creatinine and lower urine output for longer periods of time

28
Q

What are the 4 possible outcomes of AKI?

A

AKI can progress to:

Full recovery
AKI to CKD
Acute on Chronic Kidney Disease (AKI on pre-existing CKD)
AKI to ESRD

29
Q

How can AKI present?

A

Most people are asymptomatic, but:

Malaise, flank pain, edema, HTN, and SOB are possible

30
Q

What type of AKI is produced by abnormalities of renal perfusion?

A

Pre-renal AKI

31
Q

What type of AKI is produced by abnormalities within the kidney?

A

Intrinsic AKI

32
Q

What type of AKI is produced by abnormalities of urine output?

A

Post-renal AKI

33
Q

Does pre-renal AKI involve structural injury to the kidney?

A

No, the Kidney is just hypoperfused, so it recovers quickly after perfusion is restored

34
Q

What can cause hypovolemia?

A

Intravascular volume depletion
Third Spacing
Decreased CO

35
Q

How do prostaglandins and angiotensin II regulate GFR?

A

Prostaglandins dilate the afferent arteriole to increase blood flow to the glomerulus and raise GFR

Antiogensin II constricts the efferent arteriole to decrease blood flow

36
Q

How does aldosterone effect glomerular filtration?

A

Aldosterone stimulates sodium reabsorption in the CD, raising the ECV

37
Q

How does ADH effect glomerular filtration?

A

ADH prevents the insertion of sodium channels in the CD, lowering sodium reabsorption and promoting fluid loss

38
Q

Orthostatic hypotension, poor skin turgor, dry mucosa and edema suggest which type of AKI?

A

Pre-renal AKI

39
Q

What is Hepatorenal Syndrome?

A

Liver failure that causes AKI due to systemic vasodilation that is compensated by profound vasoconstriction in the Kidneys, leading to impaired sodium/water handling and oliguria that does not respond to volume repletion

40
Q

What are the types of ATN?

A

Ischemic and Toxic ATN

41
Q

What is the most common cause of Intrinsic AKI?

A

ATN, due to reduced oxygen supply causing ischemia and cell death of tubular cells

42
Q

What class of drugs can cause Tubular ATN?

A

Aminoglycosides

43
Q

What syndromes can cause Tubular ATN?

A

Rhabdomyolysis, Hemolysis, Tumor Lysis Syndrome, Myeloma drugs

44
Q

What type of sediment does ATN produce on urinalysis?

A

Dark, muddy brown sediment = ATN

45
Q

What can cause Interstitial ATN?

A

Autoimmune diseases (Sjorgens, Lupus, Sarcoid)
HIV
Penicillins, Rifampin, NSAIDS

46
Q

What is glomerulonephropathy?

A

A type of Intrinsic AKI (like ATN)

47
Q

What are the types of glomeruloneprhapthy?

A 
Rapidly Progressive Glomerulonephritis (RPGN)
IgA Nephropathy
Post Infection (PIGN after Strep)
Immune-complex mediated
FSGS
Minimal Change Disease
48
Q

What does the ANA test diagnose?

A

Lupus

49
Q

What can cause Vascular Intrinsic AKI?

A

Small or medium vessel inflammation due to:

Cholesterol atheroembolisms
Hemolytic Uremic Syndrome (E coli infections)
Scleroderma

Renal (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions