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Physio Exam 3 > Jackson 8 > Flashcards

Jackson 8 Flashcards

1
Q

Diuresis =

A

excessive urine ouput

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2
Q

Reasons for use of diuretics

A

congestive heart failure
heart weakens → ↓ cardiac output → ↓ GFR → ↑ aldosterone → ↑ Na+ and H2O reabsorption → ↑ ECV and edema

hypertension
↑ ECV → ↑ plasma volume → ↑ blood pressure

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3
Q

Different diuretics act on different segments of the nephron. They gain access to tubules either by

A

filtration or secretion.

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4
Q

Osmotic diuretics - retain water by

A

increasing osmotic pressure; act in water-permeable segments of the nephron (PT & descending loop of Henle)

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5
Q

CA inhibitors – reduce

A

Na+ reabsorption; proximal tubule is major site of action

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6
Q

Loop diuretics – act in

A

thick ascending limb to inhibit Na+ reabsorption via the Na+ K+ 2Cl- symporter

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7
Q

Thiazides – block

A

Na+Cl- symporter in early distal tubule

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8
Q

K+ - sparing – two classes that both act in

A

late distal tubule and cortical collecting duct to inhibit sodium reabsorption AND potassium secretion

  1. aldosterone antagonists
  2. ENaC blockers
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9
Q

Aquaretics –

A

ADH receptor antagonists

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10
Q

Osmotic diuretics increase the osmotic pressure in the

A

tubular fluid, and, thus, impair Na+ reabsorption.

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11
Q

Osmotic diuretics

Examples include

A

mannitol and pathologically elevated glucose.

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12
Q

Osmotic diuretics

A

gain access to tubule by glomerular filtration

are poorly reabsorbed

will have an effect where tubule is freely permeable to water

some of what’s not reabsorbed in PT and DL can be reabsorbed downstream, but typically results in excretion of 10% of filtered Na+

note: ↓ water reabsorption → ↓ Ca2+ reabsorption by solvent drag

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13
Q

Carbonic anhydrase inhibitors reduce

A

Na+ reabsorption by inhibiting CA, thus reducing the H+ available for the Na+/H+ antiporter.

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14
Q

Acetazolamide is an example of a

A

CA inhibitor.

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15
Q

CA inhibitors gain access to the

A

proximal tubule via secretion

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16
Q

CA inhibitors

Most of the diuretic effect is in the

A

proximal tubule where ~1/3 of Na+ reabsorption relies on the Na+/H+ antiporter

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17
Q

CA inhibitors

Diuretic effect is

A

not large
downstream segments will increase Na+ reabsorption when tubular Na+ increases

typically increases Na+ excretion to 5-10% of filtered load

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18
Q

Loop diuretics are the most

A

powerful of all diuretics; they inhibit Na+ reabsorption in the ascending limb of the loop of Henle.

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19
Q

Furosemide (lasix) is an example of a

A

loop diuretic.

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20
Q

Loop diuretics are secreted into the

A

proximal tubule (not filtered)

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21
Q

LOOP DIURETICS:

Inhibit

A

Na+K+2Cl- symporter in the thick ascending limb which inhibits Na+ reabsorption

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22
Q

Loop diuretics

urine leaving loop is not

A

dilute

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23
Q

Loop diuretics

no osmotic gradient established in the

A

medulla interstitium so water is not reabsorbed along collecting duct → urine is dilute (500 mOsm instead of 1400 mOsm)

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24
Q

Loop diuretics

Can increase

A

Na+ excretion to as much as 25% of filtered load, because Na+ reabsorption capacities downstream of their site of action are limited.

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25
Q

Thiazide diuretics

Thiazide diuretics like

A

chlorothiazide are secreted into the proximal tubules, and they act in the early distal tubule to block the Na+Cl- transporter

26
Q

Thiazide diuretics

kidney’s ability to dilute urine is

A

diminished

27
Q

Thiazide diuretics

reabsorption of water in the collecting duct still occurs, but

A

5-20% of the filtered Na+ is excreted

28
Q

K+-sparing diuretics

K+ - sparing diuretics act where

A

K+ is normally secreted into the tubular fluid by the principal cells. There are two types of K+- sparing diuretics

29
Q

K+-sparing diuretics
1. aldosterone antagonists, e.g. spironolactone
block

A

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

must get inside tubular cells to block aldosterone receptors

30
Q

K+-sparing diuretics
2. ENaC blockers, e.g. amiloride
block

A

Na+ reabsorption across the apical membrane

these act on a membrane protein so can gain access by secretion into the proximal tubule

31
Q

Aquaretics

Aquaretics, e.g. tolvaptan, increase excretion of water by blocking the action of

A

ADH in the late distal tubules and collecting duct. Water is eliminated without the loss of solutes.

32
Q

Secondary effects of diuretics
Diuretic braking phenomenon
Continued use of diuretics becomes

A

less effective because volume contraction counteracts the effects of the diuretic, i.e. diuretics decrease ECV so compensatory mechanisms activated

33
Q

diuretic braking

1. increased sympathetic activity in response to reduced BP —>

A

decrease GFR à increase PT reabsorption & increase renin

34
Q

diuretic braking

2. decrease

A

natriuretic peptides

35
Q

diuretic braking

3. secrete renin from

A

juxtaglomerular apparatus à increase angiotensin II and aldosterone à decrease Na+ excretion

36
Q

diuretic braking

4. stimulate ADH release —->

A

decrease water excretion

37
Q

Side effects of Procrit ® treatment include

A

flu-like symptoms, headaches, high BP, and cardiovascular problems

38
Q

Using EPO to treat anemia in dialysis patients

Treatment of anemia typically uses

A

Procrit ® to stimulate erythropoiesis (rather than rely on transfusions).

39
Q

Increased excretion of K+

Diuretics increase Na+ reabsorption, so they secondarily influence

A

renal processing of other solutes (and water)

40
Q

K+ excretion increases because……

A

diurectics increase the flow of tubular fluid which stimulates K+ secretion

diuretics reduce ECV à increase aldosterone à stimulate K+ secretion

K+ -sparing diuretics are used to prevent an increase in K+ secretion

41
Q

Disruption of acid-base balance
Acid-base balance is affected by all diuretics
CA inhibitors —>

A

metabolic acidosis

42
Q

Loop and thiazide diuretics —>

A

reduced ECV à metabolic alkalosis

43
Q

potassium-sparing diuretics —->

A

metabolic acidosis because H+ secretion in distal tubule and cortical collecting duct is inhibited

44
Q

Except for the K+ sparing diuretics, all other diuretics

A

alter calcium excretion.

45
Q

Osmotic and CA inhibitors both act in

A

proximal tubule and reduce reabsorption of calcium in this segment (so excretion is increased).

46
Q

Loop diuretics increase calcium excretion by affecting the

A

transepithelial voltage that normally provides the driving force for paracellular transport of calcium.

47
Q

Thiazide diuretics stimulate calcium reabsorption in the distal tubule and thus reduce

A

excretion.

Normally, distal tubule reabsorbs 9% of filtered calcium via active transport.

48
Q

The concentration of NaCl in the dialysis fluid is similar to that in

A

plasma.

Urea, potassium, phosphate diffuse from blood into dialysis fluid.

49
Q

Bicarbonate is high in the dialysis fluid so it

A

diffuses into blood to correct blood acidity

50
Q

Methods of accessing the blood for dialysis: pros & cons

catheter –

A

used to access venous blood for short-term treatment; scarring, vessel narrowing or occlusion can occur

51
Q

Methods of accessing the blood for dialysis: pros & cons

AV fistula –

A

preferred for long-term treatment; creates an anastomosis between artery and vein. Arterial blood is withdrawn, and blood is returned to the vein after dialysis.

52
Q

Methods of accessing the blood for dialysis: pros & cons

AV graft –

A

uses an artificial/synthetic vessel to join an artery and vein when vascular problems do not permit using a fistula; can become narrowed which can lead to clotting and/or infections.

53
Q

Dialysis treatment requires a prescription and can vary based on

A

type of solution, frequency, and size of dialyzer – typically 3-4 hours per treatment, three times per week

54
Q

Side effects and complications of hemodialysis

Short-term side effects:

A

fatigue, chest pains, cramps, nausea, headaches

often called “dialysis hangover”

due to acute, dramatic changes in blood chemistry.

55
Q

Long-term consequences of hemodialysis

A

sepsis, endocarditis & osteomyelitis (secondary infections)

56
Q

amyloid deposits in joints (like amyloid plaques that form in neural tissue) can result from the

A

build-up of trace minerals (e.g. copper, zinc, and aluminum) that might be in the dialysis fluid.

57
Q

Patients with chronic renal failure are almost always diagnosed with anemia due

A

inadequate secretion of erythropoietin (EPO) and loss of erythrocytes.

58
Q

EPO is produced by

A

interstitial fibroblasts in the renal cortex, and its production is controlled at the transcriptional level.

59
Q

EPO production is stimulated when

A

PO2 is low due to activity of transcription factors that regulate EPO synthesis (hypoxia-inducible factors 1 and 2 or HIF-1 and HIF-2)

60
Q

HIFs are continually produced, but are targeted for degradation when

A

O2 is normal.

61
Q

When O2 is low, they function as

A

transcription factors to increase EPO synthesis and secretion.

62
Q

EPO stimulates differentiation of

A

erythrocyte progenitor cells in the bone marrow

Physio Exam 3 (19 decks)

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