Renal pathology, diuretics and anesthesia- week 5 Flashcards

(34 cards)

1
Q

What is natriuretic peptide?

A

involved in long-term regulation of sodium and water balance

blood volume

arterial pressure

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2
Q

what are the actions of natriuretic peptides?

A

vasodilator effects- directly dilate veins
-decrease CVP
-Decrease CO
-Decrease preload

dilate arteries- decrease SVR
- increasing GFR and filtration fraction =
-naturesis (increase sodium excretion)
-diuresis

decrease renin release = decreased angiotensin 2 and aldosterone

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3
Q

Natriuretic peptides serve as a:

A

counter-regulatory system for the RAAS

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4
Q

What is atrial natriuretic peptide?

A

-produced by atrial myocytes

functions:
-relax smooth muscle
-promote NaCl and water excretion by kidney

Stimuli for release:
-atrial stretch (increased extracellular volume)

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5
Q

What are the actions of ANP

A

-inhibit renin release

-increased GFR via vasodilation of afferent arteriole and constriction of efferent arteriole

-inhibits aldosterone secretion

-acts directly on collecting duct to decrease sodium chloride reabsorption

-inhibits ADH release from posterior pituitary

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6
Q

What is Brain Natriuretic peptide

A
  • synthesized largely by the ventricles (as well as the brain)

-BNP is released by the same mechanisms that release ANP and has similar physiologic actions

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7
Q

What are the cv and renal actions of natriuretic peptides?

A

natiuresis
diuresis
improved GFR
inhibit renin release
decrease angiotensin 2
decrease aldosterone
systemic vasodilation
arterial hypotension
reduced venous pressure
reduced pulm. cap. wedge pressure

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8
Q

What is the definition of diuretics?

A

a substance that increases the rate of urine volume output

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9
Q

how do diuretics work?

A

Act by decreasing the rate of sodium reabsorption from the tubules which causes sodium output to increase natriuresis which then results in water output

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10
Q

what are the common clinical uses of diuretics?

A

decrease ecf volume
treat edema
chf
HTN

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11
Q

why do diuretics stop working?

A

decreased ECF= decreased MAP = decreased GFR= increased renin= angiotensin 2

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12
Q

Most diuretics produce diuresis by:

A

inhibiting the reabsorption of sodium at different segments of the renal tubular system

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13
Q

what diuretics work in PCT?

A

carbonic anhydrase inhibitors

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14
Q

where do loop diuretics work?

A

TAL

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15
Q

where do K+ sparing diuretics work?

A

collecting duct

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16
Q

Where do thiazides work?

17
Q

What are osmotic diuretics?

A

urea or mannitol

draw fluid into tubules

18
Q

what are loop diuretics?

A

furosemide
bumetanide
ethacrynic acid

action: inhibit the na-k-2cl co-transporter in the TAL

countercurrent multiplier system is disrupted and the interstitium cannot become hyperosmolar

19
Q

What are the thiazide diuretics?

A

hydrochlorathiazide (HCTZ)

most used diuretic

action inhibit sodium chloride reabsorption in early distal convoluted tubule

-hypokalemia
-metabolic alkalosis

20
Q

What are carbonic anhydrase inhibitors?

A

acetazolamide (diamox)

action: reduce reabsorpton of Na+ in the PCT by decreasing HCO3- reabsorption

  • main use is tx of glucoma

disadvantage: causes acidosis through bicarb loss in urine

21
Q

what are aldosterone antagonists?

A

spironolactone

action: potassium-sparing diuretic

decreases reabsorption of Na+ and K+ secretion by competing for aldosterone binding sites in the distal segment of the distal tubule *

-do not produce hypokalemia (like loop and thiazide)

The reason for this is that by inhibiting aldosterone-sensitive sodium reabsorption, less potassium and hydrogen ion are exchanged for sodium by this transporter and therefore less potassium and hydrogen are lost to the urine.

22
Q

Na+ channel blockers

A

amiloride and triamterene

action: decrease activity of na/K atpase in collecting tubules and thereby decrease Na+ reabsorption

-spare potassium

23
Q

What is the leading cause of end-stage renal disease (ESRD)

A

Diabetes mellitus

HTN

24
Q

How does kidney disease happen?

A

-decrease number of nephrons
-hypertrophy of surviving nephrons
-increase glomerular pressure
-glomerular sclerosis

25
what is AKI?
abrupt loss of kidney function within a few days severe AKI where the kidneys may abruptly stop working entirely or almost entirely pts w AKI may eventually recover
26
What is chronic kidney disease?
irreversible decrease in number of functional nephrons
27
categories of acute renal failure
pre-renal intra-renal post-renal
28
what is pre-renal
kidney not getting enough blood flow and becomes ischemia ex HF, hypovolemia
29
What is intra-renal?
damage to kidney itself ex: toxins, infections, autoimmune, direct renal injury
30
what is post-renal?
obstruction of the collecting system ex: stones, urethral valves, tied off ureter, kinked foley
31
when do symptoms of chronic kidney disease occur?
Symptoms often don't occur until the number of functioning nephrons decreases to at least 70% below normal
32
what is CKD defined as?
presence of kidney damage or decreased kidney function for at least 3 months
33
when can normal blood concentrations and electrolytes no longer be maintained?
until the number of functioning nephrons decreases below 20-25% of normal
34