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physiology > renal 4 > Flashcards

renal 4 Flashcards

1
Q

what is diuresis

A

excessive urine output

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2
Q

what is a diuretic

A

a drug that increases urine output due to action in th ekidney (increase water out and excretion of others)

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3
Q

why use diuretics

A

congestive heart failure

hypertension

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4
Q

why use a diuretic for congestive heart failure

A 
heart weakens
decreased Cardiac output
decreased GFR
increase aldosterone
increased Na and H2O reabsorption
increased ECV and edema
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5
Q

why use a diuretic for hypertension

A

increased ECV
increased plasma volume
increased Blood pressure

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6
Q

how to diuretics gain access to tubules

A

Filtration

secretion

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7
Q

where do osmotic diuretics work

A

in water permeable segments of the nephron (PT and descending loop of henle

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8
Q

where do Ca inhibitors act

A

proximal tubule

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9
Q

what are loop diuretics

A

inhibit Na reabsorption via the NaK2Cl symporter

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10
Q

where do loop diuretics work

A

act in the thick ascnending limb

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11
Q

what is the action of Thiazides

A

block NaCl symptoer

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12
Q

where do thiazides work

A

early distal tubule

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13
Q

what are the types of K sparing diuretics

A

Aldosterone Antagonists

ENaC Blockers

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14
Q

where do K Sparing diuretics work

A

late distal tubule

cortical collecting duct

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15
Q

what is the action of K sparing diuretics

A

inhibit sodium reabsortpion and Potassium secretion

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16
Q

what are Aquaretics

A

ADH antagonists

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17
Q

what is the action of Osmotic diuretics

A

increase osmotic pressure in tubular fluid, therefore impairing Na reabsorption

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18
Q

what are examples of osmotic diuretics

A

mannitol

Pathologicallyy elevated glucose

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19
Q

how do osmotic diuretics get into the tubule

A

via glomerular filtration and are poorly reabsorbed

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20
Q

where do osmotic diuretics have an effect

A

in tubule freely permeable to water

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21
Q

where do osmotic diuretics tend to get reabsorbed

A

PT and DL

- rest reabsorbed downstream

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22
Q

what happens when Osmotic diuretics are reabsorbed downstream

A

results in excretion of 10% of filtered Na

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23
Q

what is the effect on Ca due to osmotic diuretics

A

decrease Ca reabsorption from a decreased solvent drag

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24
Q

what is the action of Carbonic Anhydrase inhibitors

A

reduce Na reabsorption by inhibiting Ca

- reduces H available for Na/H antiporter

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25
Q

what is a CA inhibitor

A

Acetazolamide

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26
Q

how do Ca Inhibitors gain access to the proximal tubule

A

secretion

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27
Q

why does CA inhibitors affect mostly the proximal tubule

A

1/3 of Na reabsortpion relies on the Na/H antiporter there

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28
Q

how large of an effect does CA inhibitors have on excreteion

A

not large

- increase Na excretion to 5-10% filtered load

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29
Q

why does CA inhibitors have not a large effect downstream

A

downstream segments increase Na reabsoprtion when tubular Na increases

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30
Q

what is the most powerful diuretic

A

Loop diuretics

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31
Q

what is the action of loop diuretics

A

inhibit Na reabsoprtion

  • inhibit NaK2CL symptorer in thick ascending limb creating not dilute urine
  • no osmotic gradient estabilished in the medulla interstitum so water is not reabsorbed along collecting duct
32
Q

where do loop diuretics work

A

in the loop of henle

33
Q

how does the urine change in loop diuretics

A

starts out not dilute, but then very diluted

- increases Na excretion to 25% of filtered load because Na reabsorption capacity is limited downstream

34
Q

can ADH compensate for loop diuretisc

A

Nope

35
Q

what is a type of Thiazide diuretic

A

Chlorothiazine

36
Q

where are thiazide diuretics secreted

A

into the proximal tubules

37
Q

where do thiazide diuretics act

A

in the early distal tubule

38
Q

what is the action of thiazide diuretics

A

block the NaCl transporter

- the kidneys ability to dilute urine is dimished

39
Q

net effect of thiazide diuretics

A

reabsorption of water in collecting duct occures

- 5-20% of filtered Na is excreted

40
Q

where do K sparing diuretics work

A

act where K is normally secred into tubular fluid by principal cells

41
Q

what is the action of aldosterone antagonists

A

blok aldosterone’s ability to increase Na transporters in principal cells

42
Q

where must aldosterone antagonists go

A

must get inside tubular cells to block aldosterone receptors

43
Q

what is an examples of an aldosterone antagnoists

A

spironolactone

44
Q

what do ENaC blockers do

A

block Na reabsorption across the apical membrane

45
Q

how do ENaC blockers get to their target

A

act on membrane protein so gain acess by secretion into proximal tubule

46
Q

what happens to the effectiveness of Diuretics over time

A

become less effective due to volume contraction counteracting the effects of the diuretics

47
Q

how does increased sympathetic activty in response to reduced blood pressure from diurestics manifest

A

decrease GFR

increase PT reabsorption and increased renin

48
Q

what does secretion of renin from juxtaglomerular apparatus manifest as

A

increase angiotensin II and aldosterone

- decrease Na excretion

49
Q

what is the diuretic braking phnomenon

A

the body’s response to lots of diuretics that decrease their effectiveness

50
Q

what are the secondary effects of diuretics

A 
Diuretic braking phenomenon:
 - increased sympa in response to reduced BP
 - decreased natriuretic peptides
 - secrete renin 
 - stimulate ADH release
 Increased excreteion of K
Disrutpion of acid-base balance
disrupt calcium homeostasis
51
Q

why does the use of diretics increase Excretion of K

A
  • diuretics increase flow of tubular fluid, stimulating K secretion
  • Diuretics reduce ECV-> increase aldosterone-> stimulate K secretion
52
Q

what is used to stop the increased excretion of K from prolonged diuretics

A

K sparing diuretics

53
Q

what does CA inhibitors do to acid base balance

A

metabolic acidosis

54
Q

what does Loop and Thiazide diuretics do to acid base balance

A

reduced ECV

metabolic alkalosis

55
Q

what do K sparing diuretics do to acid-base balance

A

metabolic acidosis due to H secretion in distal tubule and cortical collectin duct is inhibited

56
Q

what diuretic doesn’t affect calcium homeostasis

A

K sparing diuretics

57
Q

what do osmotic and Ca inhibitors do to Ca homeostasis

A

reduce reabsorption of CA in the proximal tubule

58
Q

what do loop diuretics do to Ca homeostasis

A

increase CA excretion by affecting transepithelial voltage that normally is the driving force fro transprot of calcium

59
Q

what do Thiazide diuretics do to Ca Homeostatis

A

stimulate Ca reabsorption in the distal tubule and reduce excretion

60
Q

how Much Ca does the distal tubule usually reabsorb

A

9% of filtered calcum via active transportretion

61
Q

what is hemodialysis

A

removal of waste produces from the blood when kidney function has been impaired

62
Q

is the need for hemodialysis/transplant increasing

A

Yes

63
Q

how is hemodialysis done in a kidney failure patient

A

blood briefly removed from the body to be circulated through a dialyzer

64
Q

how does a dialysizer work

A

A cylindrical bundle of fibers that allows small modcules to diffuse into dialysis fluid

65
Q

what direction do the fluid and blood move in a dialyzer

A

in countercurrent direction to remove nitrogenous and other waste
- adjust osmolarity before blood is returned to the body

66
Q

what is the concentration of NaCL in dialysis fluid

A

Similar to that of plasma

67
Q

what diffuses from the blood into dialysis fluid

A

urea
Potassium
Phosphate

68
Q

what flows from dialysis fluid to the blood

A

Bicarbonate

69
Q

how often is dialysis done

A

3-4 hours 3 times per week

70
Q

side effects of hemodilaysis

A
  • Vascular access problems
  • short term: Fatigue, chest pain, cramps, nausea, headaches (dialysis hangover)
  • long term: sepsis, endocarditis, osteomyelitis (sec infections)
    • amyloid deposites in joints
71
Q

what causes a dialysis hangover

A

Acute, dramatic changes in blood chem

72
Q

what causes amyloid depsoites in joints from hemodialsis

A

build up of trace minerals in dialysis fliud

73
Q

why do patients with chronic renal failure get anemia

A

Inadequate secretion of EPO and loss of erythrocytes

74
Q

what cells produce EPO

A

Interstitial fibroblasts in the renal cortex

75
Q

where is EPO production control

A

Transcriptional level

76
Q

what stimulates EPO production

A

PO2 is low

77
Q

how do Transcription factors work for EPO

A

Hypoxia inducible factors are continually produced but are targeted for degradation when O2 is normal

physiology (32 decks)

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