Exam 2: Renal Flashcards

1
Q

Kidneys maintain homeostasis: Regulatory function

A

Control composition and volume of blood - maintain stable conc of cations (Na, K, Ca)
Maintain acid-base balance

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2
Q

Kidneys maintain homeostasis: Excretory function

A

Produce urine

Remove metabolic waste (urea and other waste products)

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3
Q

Kidneys maintain homeostasis: Hormone function

A

Produce renin for BP control
Produce erythropoietin which stimulates marrow production of RBC
Activate 25(OH)-D (inactive vit d) to 1,25(OH)D (active vit D)

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4
Q

Kidneys maintain homeostasis: Metabolic function

A

Gluconeogenesis

Metabolize drugs and endogenous substances (insulin)

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5
Q

Kidneys maintain homeostasis: BP function

A

Decrease kidney perfusion stimulates the release of renin from juxtaglomerular cells of the kidneys
Renin converts angiotensinogen to AT1
AT2 a potent vasoconstrictive agent
- stimulates Na retention in the nephron (particularly in PCT)
- stimulates release of aldosterone from the adrenal gland to increase Na

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6
Q

Kidney primary functions

A

Filtration (glomerulus)

Reabsorption and secretion (tubule)

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7
Q

If tubular cells are damaged, ____ will be wasted and increase _____

A

sodium/electrolytes and increase urine sodium (normally reabsorbed but tubule cells damaged and unable to)

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8
Q

Explain relationship with BUN and low perfusion pressure

A

If perfusion pressure is low (CHF, dehydration, hypotension, then tubular cells will reabsorb sodium and water to maintain homeostasis and urea will follow sodium

reabsorption of urea increases BUN

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9
Q

Creatinine is ___% filtered and ____ secreted

A

80-90 and 10-20

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10
Q

Synonym of prerenal AKI

A

Prerenal azotemia

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11
Q

Doubling of ___ is evidence of AKI

A

SCr

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12
Q

Def: Azotemia

A

Increase in waste products (Cr and urea)

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13
Q

What does AIN stand for

A

Acute interstitial nephritis

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14
Q

What does ATN stand for

A

Acute tubular necrosis

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15
Q

What are 3 types of intrinsic/intrarenal AKI?

A

acute interstitial nephritis (AIN), acute tubular necrosis (ATN), and glomerulonephritis

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16
Q

Def: Nonoliguria

A

> 500 ml/day

17
Q

Def: oliguria

A

100-500ml/day

18
Q

Def: anuria

A

<100ml/day

19
Q

Key determinants of AKI

A
x2 SCr
Decrease UO (<0.5ml/kg/hr over 12 hrs)
Abrupt change over short period of time (hours to days) and sustained for over 24 hrs
20
Q

AKI cases in hospital is a/w increased ____, ____, and _____

A

risk of death (7x), length of stay (4x) and risk of transfer to ICU (x4)

21
Q

What are non-modifiable risk factors of AKI

A
CKD
DM
Older age
Chronic liver disease (cirrhosis) 
CHF
Renal artery stenosis
Peripheral vascular disease
22
Q

What are modifiable risk factors of AKI?

A
Volume depletion
HTN/Hypotension
Hypoalbuminemia 
sepsis/shock
Nephrotoxic meds
Major surgery/anesthesia
23
Q

Prerenal AKI: Results of hypoperfusion of the kidneys

A

Volume depletion (burns, hemorrhage, GI loss like diarrhea)
HYPOtension (sepsis, shock)
Renal artery stenosis

24
Q

Prerenal AKI: What are the effects of ACEI/ARBS?

A

Vasodilation of efferent arteriole

25
Q

Prerenal AKI: What are the effects of epinephrine?

A

Vasoconstriction of afferent arteriole

26
Q

Prerenal AKI: What are the effects of high-dose dopamine?

A

Vasoconstriction afferent arteriole

27
Q

Prerenal AKI: Diagnostic parameters

A

BUN/SCr 20:1 ratio (Scr x2, BUN rapidly increase, usually faster than Cr)
UO usually decrease to conserve (dark urine, more concentrated)
Urine sediment/RBC/WBC/protein - none
Urina Na <20 mEq/L
FeNa <1% (conserving Na)

28
Q

What is the relation between cirrhosis and low flow

A

decrease in albumin production and water cannot be stored in bloodstream so intravascular volume depletion

29
Q

Prerenal AKI: 3 causes

A

Low volume, flow, and drug-induced

30
Q

DIKD: Prerenal: Agents

A

NSAIDs, ACEI/ARBs, Radioconstrast media, loop diuretics and metolazone