Renal pathology, diuretics and anesthesia- week 5 Flashcards

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?

A

DCT

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
Q

what is AKI?

A

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
Q

What is chronic kidney disease?

A

irreversible decrease in number of functional nephrons

27
Q

categories of acute renal failure

A

pre-renal

intra-renal

post-renal

28
Q

what is pre-renal

A

kidney not getting enough blood flow and becomes ischemia

ex HF, hypovolemia

29
Q

What is intra-renal?

A

damage to kidney itself

ex: toxins, infections, autoimmune, direct renal injury

30
Q

what is post-renal?

A

obstruction of the collecting system

ex: stones, urethral valves, tied off ureter, kinked foley

31
Q

when do symptoms of chronic kidney disease occur?

A

Symptoms often don’t occur until the number of functioning nephrons decreases to at least 70% below normal

32
Q

what is CKD defined as?

A

presence of kidney damage or decreased kidney function for at least 3 months

33
Q

when can normal blood concentrations and electrolytes no longer be maintained?

A

until the number of functioning nephrons decreases below 20-25% of normal

34
Q
A