Renal Flashcards

1
Q

Is the kidney capable of metabolism?

A

Yes, it’s capable of phase I and phase II biotransformations

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2
Q

Hormones made by the kidney

A

EPO
Calcitriol
Prostaglandins

Kidneys are also able to perform gluconeogenesis (from amino acids) about as well as the liver

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3
Q

Prostaglandins and their effects on renal arteries

A

Dilators: PGE2 and PGI2

Constrictor: Thromboxane A2 (TXA2)

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4
Q

This % of blood that reaches the kidney is actually filtered by the glomerulus

A

20%

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5
Q

Part of the kidney most sensitive to drops in PaO2

A

Medulla, because it only receives 10% of RBF to begin with

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6
Q

MAP range of kidney auto regulation

A

50-180

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7
Q

UO is linearly related to what?

A

MAP > 50

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8
Q

How is renal auto regulation performed?

A
  • Myogenic mechanisms**
  • JG apparatus and tuboglomerular feedback**
  • RAAS
  • Prostaglandins
  • ANP
  • SNS
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9
Q

Where is the JG apparatus located?

A

Distal tubule as it passes through the afferent and efferent arterioles

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10
Q

ANS influence in kidney

A

SNS (from T8-L1) innervates afferent and efferent arterioles. Very little PSNS present.

Internal autoregulatory mechanisms overrise SNS effects.

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11
Q

Renin is released in response to these 3 things

A

Reduced renal perfusion
B1 stimulation
Decreased NaCl delivery to distal tubule (decreased delivery means flow is slow and perfusion is thus poor)

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12
Q

What does the JG apparatus monitor?

A

2 things:

  • Renal perfusion
  • Solute concentration

Feedback about NaCl composition of tubular fluid affects arteriolar tone

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13
Q

Angiotensin II affects which arteriole?

A

It constricts the efferent arteriole

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14
Q

How does aldosterone exert it’s effects

A

Activates the Na/K/ATP pump in the principal cells of the distal tubules and collecting ducts

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15
Q

RAAS stimulates aldosterone secretion from the adrenal gland, but what else does as well?

A

Hyponatremia and hyperkalemia

b/c aldosterone will fix both of these things

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16
Q

2 mechanisms that control ADH release

A

1) Increased osmolarity of ECF
- Shrinks the osmoreceptors in hypothalamus (supraoptic an paraventricular nuclei), resulting in ADH release

2) Decreased blood volume
- Baroreceptors in carotid bodies, transverse aortic arch, great veins, and RA stimulate ADH release

17
Q

1/2 life of ADH

A

5-15 minutes

18
Q

What is fenoldopam?

A

DA1 agonist that increases RBF

19
Q

3 general things that promote renal vasodilation

A

1) Prostaglandins
2) ANP
3) DA agonism

20
Q

Where are prostaglandins made in the nephron?

A

Afferent arteriole

21
Q

RAAS has this effect on RBF

A

decreases

22
Q

The afferent arteriole makes prostaglandins in response to what?

A

Ischemia
NE
Angiotensin II

Helps promote a balance!

23
Q

Leukotrienes have this effect on renal vasculature

A

Constriction

24
Q

Only DA1 agonist that may reduce mortality and dialysis requirement and outcomes in aortic surgery and CPB

A

Fenoldopam

25
Q

Effects of efferent constriction

A

Small constriction = increased GFR

Excessive constriction = decreased GFR and RBF

26
Q

Normal BUN

A

10-20

27
Q

What IS BUN?

A

Primary metabolite of protein metabolism in the liver

amino acids –> ammonia –> urea

28
Q

What does a 100% increase in serum creatinine represent?

A

A 50% reduction in GFR

29
Q

BUN:Cr ratio

A

Should be 10:1

> 20:1 suggests preener azotemia

30
Q

Fractional excretion of sodium

A

Relates sodium clearance to Cr clearance

If Fe(Na+) 3%, then more sodium was excreted relative to the amount of Cr cleared, and it suggests impaired tubular function

31
Q

Spec grav analysis

A

1.010-1.015 = ATN (loss of concentrating ability)

> 1.015 = Pre-renal oliguria

> 1.024 = Physiologic oliguria

32
Q

Which is a better test of tubular function, spec grav or urine osmolality?

A

Urine osmolality

33
Q

How can the risk of preener azotemia be reduced?

A

Maintaining MAP > 65 and giving adequate hydration

34
Q

What is prerenal azotemia?

A

Basically, prerenal kidney injury that results in azotemia (buildup of BUN and other nitrogenous waste products)

35
Q

Effect of A1 agonists on RBF

A

Causes a decrease in RBF

Septic patients will benefit though because increasing the MAP will outweigh the renal vasoconstrictive effects

36
Q

This medication is better at increasing GFR and UO than phenylephrine or NE

A

Vasopressin

Preferentially constricts the efferent arteriole

37
Q

Top causes of CKD

A

1) DM

2) HTN

38
Q

1st line treatment for uremic coagulopathy

A

Desmopressin to increase vWF and Factor VIII

Cryo can be given for this reason too, but carries risk of viral transmission

39
Q

ADH mech of action

A

stimulates V2 receptors (increased cAMP) in the collecting ducts –> increased aquaporins –> increased water re-absorption –> decreases blood oSm and plasma volume

Stimulates V1 receptors in the vasculature (increased IP3, DAG, Ca+) –> vasoconstriction