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Physio Exam 3 > Sweep 1.2 > Flashcards

Sweep 1.2 Flashcards

1
Q

K+ - sparing diuretics act where

A

K+ is normally secreted into the tubular fluid by the principal cells.

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2
Q

K+ sparing

  1. aldosterone antagonists,
A

e.g. spironolactone
block aldosterone’s ability to increase Na+ transporters in principal cells

must get inside tubular cells to block aldosterone receptors

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3
Q

K+ sparing

2. ENaC blockers,

A

e.g. amiloride
block Na+ reabsorption across the apical membrane

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

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4
Q

Aquaretics, e.g. tolvaptan, increase excretion of

A

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

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5
Q

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

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6
Q
  1. increased sympathetic activity in response to reduced BP –> decrease —– —-> increase
A

GFR

PT reabsorption & increase renin

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7
Q

Secondary effects of diuretics

2. decrease

A

natriuretic peptides

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8
Q

Increased excretion of K+

Diuretics increase ——–, so they secondarily influence renal processing of other solutes (and water)

A

Na+ reabsorption

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9
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

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10
Q

Loop and thiazide diuretics —>

A

reduced ECV à metabolic alkalosis

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11
Q

potassium-sparing diuretics —–> ———- because H+ secretion in distal tubule and cortical collecting duct is -=——

A

metabolic acidosis

inhibited

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12
Q

Except for ———-, all other diuretics alter calcium excretion.

A

the K+ sparing diuretics

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13
Q

Calcium reabsorption in the nephron

in proximal tubule –

A

mostly by paracellular transport/solvent drag

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14
Q

Calcium reabsorption in the nephron

in thick ascending limb –

A

transcellular and paracellular transport (paracellular not solvent drag)

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15
Q

Calcium reabsorption in the nephron

in distal tubule –

A

transcellular reabsorption of calcium

transport here can be regulated because expression of Ca2+ transporters is regulated by PTH

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16
Q

Calcium reabsorption in the nephron

the collecting duct is not significantly involved with

A

Ca2+ reabsorption

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17
Q

• calcitonin
released in response to ———-

increases ————

A

hypercalcaemia

bone deposition

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18
Q

• calcitriol (1,25 dihydroxyvitamin D)

metabolism of vitamin D to calcitriol is stimulated by

A

hypocalcaemia and/or hypophosphatemia (and further stimulated by PTH, see above)

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19
Q

• calcitriol (1,25 dihydroxyvitamin D)

stimulates active transport mechanism for

A

Ca2+ absorption in the small intestine

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20
Q

• calcitriol (1,25 dihydroxyvitamin D)

facilitates action of ——- and increases ——

A

PTH

renal Ca2+ transport

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21
Q

• parathyroid hormone (PTH)

released in response to

A

hypocalcaemia

22
Q

• parathyroid hormone (PTH)

increases ———–, increases renal —– reabsorption, and stimulates ——–

A

bone resorption

Ca+

calcitriol production

23
Q

Calcium is regulated by three hormones all of which are regulated by a

A

calcium sensing receptor (CaSR)

24
Q

Osmotic and CA inhibitors both act in ——— and reduce reabsorption of ————

A

proximal tubule

calcium in this segment (so excretion is increased).

25
Q

Loop diuretics increase calcium excretion by affecting the

A

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

26
Q

Thiazide diuretics stimulate

A

calcium reabsorption in the distal tubule and thus reduce excretion.

27
Q

Normally, distal tubule reabsorbs —- of filtered calcium via active transport.

A

9%

28
Q

catheter – used to access

A

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

29
Q

AV fistula – preferred for

A

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

30
Q

AV graft – uses an

A

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.

31
Q

Long-term consequences of hemodialysis

A

sepsis, endocarditis & osteomyelitis (secondary infections)

amyloid deposits in joints (like amyloid plaques that form in neural tissue) can result from the build-up of trace minerals (e.g. copper, zinc, and aluminum) that might be in the dialysis fluid.

32
Q

Patients with chronic renal failure are almost always diagnosed with

A

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

33
Q

EPO is produced by ———— in the renal cortex, and its production is controlled at the transcriptional level.

A

interstitial fibroblasts

34
Q

HIFs are continually produced, but are targeted for degradation when

A

O2 is normal.

35
Q

HIFs

When O2 is low, they function as

A

transcription factors to increase EPO synthesis and secretion.

36
Q

EPO stimulates differentiation of ——— in the bone marrow

A

erythrocyte progenitor cells

37
Q

transcellular – molecules move

A

through tubular cells

38
Q

paracellular – molecules move

A

between tubular cells

39
Q

solvent drag results from solutes being carried by water in

A

paracellular transport

40
Q

rate of water diffusion can be regulated by

A

aquaporins

41
Q

Note that a decrease in plasma pH will increase the amount of ———- which can be filtered and excreted, so alkalosis can lead to ———-.

A

free Ca2+

hypocalcemia

42
Q

Why is it important to regulate calcium?

hypocalcemia increases

A

excitability of neural and muscle tissue; tetany

43
Q

Why is it important to regulate calcium?

hypercalcemia can cause

A

cardiac arrhythmia and disorientation; can lead to death

44
Q

only a little more than ½ of ECF calcium is

A

free or complexed with anions, and, therefore, can be filtered in the glomerulus

45
Q

Metabolic alkalosis – hi

A

pH due to excess HCO3-

46
Q

Metabolic alkalosis

respiratory compensatory response –

A

hypoventilate (how does this work?) – increase CO2, increase CA reaction, increase acidity

47
Q

Metabolic alkalosis

renal compensatory response —>

A

excrete HCO3-

48
Q

Metabolic acidosis - low pH due to low

A

HCO3-

49
Q

Metabolic acidosis

causes include

A

diabetic ketosis, diarrhea, renal failure

50
Q

Metabolic acidosis

respiratory compensatory response —->

A

hyperventilate

51
Q

Metabolic acidosis

renal compensatory response —> produce

A

new HCO3-

Physio Exam 3 (19 decks)

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