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Exam 3 physio > Lecture 4 Renal > Flashcards

Lecture 4 Renal Flashcards

1
Q

what are the main uses of diuretics

A

to INHIBIT reabsorption of Na and WATER, thus causing an increase in urine volume and dropping blood volume thus dropping BP

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2
Q

reasons for use of diuretics

A

CHF: Leads to dec GFR, INC aldosterone, INC Na and H2o Reabsorption, INC ECV and edema
HYPERtension: INC ECV, INC plasma volume thus INC BP
Diuretics aim to treat these symptoms and thus dec the effects of these diseases

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3
Q

Osmotic diuretics action and site of action

A

Osmotic diuretics act in PCT and descending LoH

retain water by INC osmotic pressure, go in the tubule by filtration

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4
Q

CA inhibitors action and site of action

A

CA inhibitors DEC Na reabsorption and act in PCT

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5
Q

Loop diuretics action and site of action

A

loop diuretics act in THICK ASCENDING LIMB to inhibit Na reabsorption VIA NaKCl2 symporter

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6
Q

Thiazide action and site of action

A

thiazides act in DCT by blocking NaCl symporter

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7
Q

K sparing action and site of action

A

K sparing act in collecting ducts and DCT to inhibit Na reabsorption and INHIBIT K secretion

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8
Q

2 classes of K sparing diuretics

A

aldosterone antagonists

ENaC blockers

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9
Q

aqueretics site of action and action

A

aqueretics act in collecting duct and are aldosterone receptor antagonists

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10
Q

what is the only diuretic that gains access to the tubules thru filtration

A

Osmotic diuretics only one!

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11
Q

osmotic diuretics do what

2 examples
absorbed or poorly absorbed?
effects what part of tubule
results in excretion of how much filtered Na?

A

INC osmotic pressure in tubular fluid thus INHIBITING Na reabsorption
mannitol and elevated glucose
poorly absorbed
actions where tubule is permeable to water
10% INC in excretion of filtered Na

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12
Q

If osmotic diuretics DEC water reabsorption what happens to Ca absorption

A

Ca absorption is DEC due to solvent drag

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13
Q 
CA inhibitors act how
example
gain access to tubule how?
most of diuretic effect is where?
INC Na excretion how much
A 
CA inhibitors DEC Na absorption by INHIBITING CA thus reducing H for Na/H antiporter 
example: acetazolamide
gain accès to PCT by secretion
most of diuretic effect in PCT 
INC Na excretion 5-10%
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14
Q 
Loop diuretics act how
act where? 
example?
secreted of filtered?
INC Na excretion how much
A 
loops: Inhibit Na absorption inhibiting Na K 2Cl symporter hus causing urine to leave loop diluted
Loops act in THICK ascending limb
example: furosemide (lasix)
secreted!
INC Na secretion by 25%!
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15
Q

what do loop diuretics prevent from forming causing urine to be diluted

A

Loops prevent osmotic gradient from forming in medullae interstitium so water is NOT reabsorbed in collecting duct

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16
Q

what is the most powerful diuretic?

A

LOOPS = most powerful for failing kidney and CHF

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17
Q 
Thiazides act how 
act where? 
secreted or filtered
example
how much Na secreted bc of thiazides
A

Thiazides inhibit NaCl transporter thus inhibits Na absorption - diminishes kidneys ability to dilute urine
act in early DCT
example: chlorothiazide
INC Na secretion of 5-20%

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18
Q

K sparing diuretics act how
act where and on what specifically?
secreted or filtered

A

act by aldosterone antagonists or inhibiting ENaC this inhibiting Na absorption
secreted into fluid
act on principal cells in DCT and collecting ducts

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19
Q

what do aldosterone antagonist K sparing drugs do

A

blocks aldosterone ability to INC Na transporters in principal cells

20
Q

what do ENaC inhibitor K sparing diuretics do

A

block Na absorption across apical membrane, act on membrane proteins

21
Q

Aquatics developed why
act how
act where

A

aquatics developed to prevent loss of Na and only INC excretion of H2O
act by blocking action of ADH this INC secretion of water but allowing Na to be absorbed
act in DCT and collecting duct

22
Q

explain the 2nd effect of diuretics called diuretic braking phenomenon

A

continued use of diuretics becomes less effective BC Volume contraction counteracts the effects of the diuretic
IE: diuretics DEC ECV so compensatory mechs involved

23
Q

what compensatory mechanisms are involved with diuretic braking phenomenon (x4)

A

INC simp activity in RED BP > DEC GFR > INC PT and renin
DEC natruiretic peptides
DEC Na excretion bc INC Renin
INC ADH thus DEC water excretion

24
Q

what does aldosterone do

A

INC Na reabsorption thus dec WATER excretion

25
Q

another secondary effect of diuretics is INC secretion of K why? (2x)
what drug prevents K secretion and loss

A

diuretics INC flow of tubular fluid which INC K secretion
reduce ECV > INC aldosterone > INC K secretion

Use K sparing diuretics to dec K loss

26
Q

how does acid base balance become affected by diuretics? specifically talk about 4 drugs

A

CA inhibitors= metabolic acidosis
Loops and Thiazide= DEC ECV > metabolic ALKALOSIS
K sparing= metabolic acidosis bc H secretion is inhibited

27
Q

what drugs cause metabolic acidosis

A

CA inhibitors and K sparing = acidosis

28
Q

what drugs cause metabolic alkalosis

A

Loops and thiazides= alkalosis

29
Q

what is the only drug that does NOT alter Ca excretion?

A

K sparing diuretics has NO effect on Ca

30
Q

What do osmotic and CA inhibitors due to Ca

A

Osmotic and CAIs RED Ca absorption this INC Ca excretion

31
Q

what do loops do to Ca levels and how

A

Loops INC Ca excretion by affecting the transepithelial voltage

32
Q

what do thiazides do to Ca levels?

A

Thiazides INC Ca REABSORPTION!!! reduce excretion of Ca

33
Q

when is hemodialysis needed and what is it

A

Hemodialysis is the removal of waste products from blood when kidney is impaired. demand is on the rise!

34
Q

how are dialysis fluid and plasma similar and what does the cause

A

both have similar concentrations of NaCl so urea, K, and phosphatase diffuse from blood into dialysis fluid

35
Q

what is high in dialysis fluid to flow into blood to reduce blood acidity

A

dialysis fluid has high bicarbonate

36
Q

methods to access blood for dialysis

pros and cons of the 3 methods

A

catheter: venous blood access for short term TX, scarring, vessel narrowing or occlusion can occur
AV fistula: Long term TX, creates an anastomosis between A and V, takes out arterial blood and returns blood to vein
AV graft: artificial vessel to join and A and V when there are vascular problems, cons: narrowing, clotting and infection

37
Q

what can dialysis prescription be based on (3x)

typical TX

A

dialysis depends on frequency, type of fluid, size of dialyzer
typical TX: 3-4 hours per 3x a week

38
Q

side effects of hemodialysis
short term
long term

A

vascular access problems
fatigue, chest pain, cramps, naussea, headaches due to acute change in blood chemistry
THE DIALYSIS HANGOVER
Long term: sepsis, endocarditis, osteomyelitis
amyloid deposits in joints from build up of minerals in dialysis fluid

39
Q

patients with ESRD are always diagnosed with what and why

A

ESRD = anemia bc DEC secretion of EPO and DEC of RBCs

40
Q

what is EPO

A

hormone produced by kidneys that stimulates bone marrow to make red blood cells

41
Q

what is EPO made by and controlled by

A

EPO made by interstitial fibroblasts in renal cortex and is controlled at transcription level

42
Q

when is EPO production INC?

A

EPO production stimulated when PO2 is low

43
Q

what transcription factors regulate production of EPO in DEC PO2

A

hypoxia inducible factors 1 and 2

HIF 1 and HIF 2

44
Q

Describe the life of HIF 1 and HIF2

A

HIF 1 and HIF 2 are continually made but degraded when PO2 is normal

45
Q

what does EPO stimulate

A

EPO stimulates differentiation of RBC progenitor cells in bone marrow

46
Q

treat of anemia by using EPO uses what

A

use Procrit to stimulate erythropoiesis

47
Q

side effects of Procrit

A

flu like symptoms, headaches, high BP, cardio problems

Exam 3 physio (4 decks)

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