Renal Flashcards

(39 cards)

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

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

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

24
Q

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

25
Effects of efferent constriction
Small constriction = increased GFR | Excessive constriction = decreased GFR and RBF
26
Normal BUN
10-20
27
What IS BUN?
Primary metabolite of protein metabolism in the liver | amino acids --> ammonia --> urea
28
What does a 100% increase in serum creatinine represent?
A 50% reduction in GFR
29
BUN:Cr ratio
Should be 10:1 >20:1 suggests preener azotemia
30
Fractional excretion of sodium
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
Spec grav analysis
1.010-1.015 = ATN (loss of concentrating ability) > 1.015 = Pre-renal oliguria > 1.024 = Physiologic oliguria
32
Which is a better test of tubular function, spec grav or urine osmolality?
Urine osmolality
33
How can the risk of preener azotemia be reduced?
Maintaining MAP > 65 and giving adequate hydration
34
What is prerenal azotemia?
Basically, prerenal kidney injury that results in azotemia (buildup of BUN and other nitrogenous waste products)
35
Effect of A1 agonists on RBF
Causes a decrease in RBF Septic patients will benefit though because increasing the MAP will outweigh the renal vasoconstrictive effects
36
This medication is better at increasing GFR and UO than phenylephrine or NE
Vasopressin | Preferentially constricts the efferent arteriole
37
Top causes of CKD
1) DM | 2) HTN
38
1st line treatment for uremic coagulopathy
Desmopressin to increase vWF and Factor VIII Cryo can be given for this reason too, but carries risk of viral transmission
39
ADH mech of action
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