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Physiology > Integrative Physiology II > Flashcards

Integrative Physiology II Flashcards

1
Q

ECF K+ tightly regulated

at — meq/L.

A

4.2

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2
Q

Increase of only 3 to 4

mEq/L can cause (3)

A

cardiac
arrhythmias, cardiac
arrest, or fibrillation.

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3
Q

Mechanisms controlling K+

Homeostasis (2)

A
  1. Control of K+ distribution
    between the ECF and ICF
  2. To keep [K+]ECF constant; rate of K+ excretion must equal rate of K+ input.
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4
Q

High [K+ ]ECF:

A

Hyperkalemia

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5
Q

Low [K+ ]ECF:

A

Hypokalemia

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6
Q

Factors That Shift K+ Into Cells (decrease [K+]ECF) (7)

A 
insulin
aldosterone 
beta2 adrenergic stimulation
alkalosis
decrease ECF osm 
increase na/k ATPase activity 
dilute ICF, decrease ΔEC for diffusion out of K+ cell
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7
Q

Factors That Shift K+ Out of Cells (increase [K+]ECF) (8)

A 
increased insulin deficiency 
aldosterone deficiency
beta2 adrenergic antagonists 
acidosis
increase ECF osm 
strenuous exercise 
decrease Na+/K+ ATPase Activity
concentrate ICF, increase ΔEC for diffusion out of cell
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8
Q

Acidosis =

A

Hyperkalemia

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9
Q

Alkalosis =

A

Hypokalemia

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10
Q

Three Factors in Tubular Processing of K+

A

(Filtration; Reabsorption; Secretion)

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11
Q

Day to Day regulation of [K+]ECF is function of

A

late Distal Tubule/Collecting Duct

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12
Q

High K+ intake increases

A

K+ secretion (principal cells)

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13
Q

Low K+ intake increases

A

K+ reabsorption (alpha intercalated cells)

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14
Q

Factors that Determine Rate of K+

Secretion by Principal Cells (3)

A
  1. Na+/K+ ATPase Activity
  2. Transepithelial potential difference
    (TEPD) between blood and lumen
  3. Permeability of apical membrane for K+
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15
Q

Factors that Control Principal Cell K+ Secretion

 Results in increased K+ Secretion (4)

A
  1. increase [K+]ECF
  2. increase Aldosterone
  3. increase Distal Tubule Flow Rate
  4. Acid/Base Status
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16
Q

Alkalosis –

A

increase K+ Secretion

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17
Q

Acidosis –

A

decrease K+ secretion

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18
Q

↑[K+]ECF Increases K+ Secretion

Mechanisms (4)

A
  1. increase Na+/K+ ATPase activity
  2. TEPD is more lumen
    negative (due to increased
    Na+ reabsorption) which
    favors K+ secretion
  3. increase # K+ channels in apical
    membrane
  4. Stimulates aldosterone
    secretion.
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19
Q

Increased Distal Tubule Flow Rate: increase K+ Secretion

Causes (3)

A

 increase ECF volume
 Na+ loading
 Some Diuretics

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20
Q

Increased Distal Tubule Flow Rate: increase K+ Secretion

Mechanisms (2)

A 
1. Increased tubule flow rate keeps 
luminal K+ lower, maintaining ΔC for 
secretion
2. Increases #BK channels in apical 
membrane
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21
Q

Causes of Hyperkalemia (5)

A

Renal failure
 Decreased distal nephron flow (heart failure, severe
volume depletion, NSAID, etc.)
 Decreased aldosterone or decreased effect of
aldosterone
 Metabolic acidosis (hyperkalemia is mild)
Diabetes (kidney disease, acidosis, decreased insulin)

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22
Q

Decreased aldosterone or decreased effect of

aldosterone: (3)

A
  • adrenal insufficiency
  • resistance to aldosterone
  • K+ sparing diuretics (spironolactone)
23
Q

Causes of Hypokalemia (6)

A 
Very low intake of K +
GI loss of K+ - diarrhea
Metabolic alkalosis
Excess insulin
Increased distal tubular flow
Excess aldosterone
24
Q

Increased distal tubular flow: (3)

A
  • salt wasting nephropathies
  • osmotic diuretics
  • loop diuretics
25
Q

Diuretic is a

A

drug that increases urine volume output.

26
Q

Most diuretics act by

A

decreasing Na+ reabsorption from some

part of the nephron.

27
Q

Natriuresis causes

A

diuresis by an osmotic mechanism.

28
Q

Natriuresis also affects reabsorption of (3)

A

Cl-, K+, and other

electrolytes.

29
Q

Most common reason for use of diuretics is to (3)

A

reduce ECFV (extracellular fluid volume).

– Reduces edema
– Reduces MAP (mean arterial pressure)

30
Q

Diuretics Increase
Solute and H2O
Excretion until

A

Compensatory
Mechanisms Re-
establishes
Balance

31
Q

— Transport is a Target

for many Diuretics

A

Na+
(Where goes the Na+
goes the H2O)

32
Q

Osmotic Diuretics

A

Nonabsorbable substance is filtered (ex. mannitol,

sucrose).

33
Q

Osmols in tubular fluid require —.

A

water

34
Q

Osmotic Diuretics

Similar to effects of

A

endogenous substances
(glucose, urea).
- Diuresis caused by hyperglycemia.

35
Q

Osmotic Diuretics

May increase excretion of

A

other solutes.

36
Q

Carbonic Anhydrase Inhibitors (3)

A 
Acetazolamide.
More than 80% of HCO3- reabsorption and H+ 
secretion occurs in 
proximal tubule.
CA inhibitors block Na+ 
reabsorption (and H+ 
secretion) indirectly.
37
Q

Loop Diuretics

 ex (3)

A

Furosemide, ethacrynic acid,

bumetanide

38
Q

Loop Diuretics

Inhibit

A

Na+-K+-2Cl- - cotransport
pump on luminal membrane of
TAL of Henle.

39
Q

Loop Diuretics

Most powerful

A

diuretics
available (30% of GFR may
appear in urine!).

40
Q

Loop Diuretics
Overwhelm downstream
— capacity.

A

absorptive

41
Q

Loop Diuretics

Disrupt

A

countercurrent

multiplier.

42
Q

Thiazide Diuretics

 ex (2)

A

Hydrochlorothiazide,

chlorthalidone, etc.

43
Q

Thiazide Diuretics

Block

A

Na+-Cl- cotransport
mechanism in early distal
tubule

44
Q

Thiazide Diuretics
More distal tubular
segments have limited
ability to

A

respond to
increased load of Na+, Cl-,
H2O.

45
Q

class: Osmotic (mannitol)
mechanism:
site of aciton:

A

↑ osmolarity of tubular
fluid

Mainly proximal tubule

46
Q

class: Loop (furosemide)
mechanism:
site of aciton:

A

↓ Na-K-2Cl cotransport

TAL of Henle

47
Q

class: Carbonic anhydrase inhibitor
(acetazolamide)
mechanism:
site of aciton:

A

↓ H+ secretion, HCO3- ab-
sorption (↓Na-H exchange)

Proximal tubule

48
Q

class: Thiazide (hydrochlorothiazide)
mechanism:
site of aciton:

A

↓ Na-Cl cotransport

Early distal tubule

49
Q

class: Aldosterone antagonists
(spironolactone)
mechanism:
site of aciton:

A

↓ Na+ absorption & K+
secretion

Late distal & Collecting
tubule

50
Q

class: Na channel blocker
(triamterene)
mechanism:
site of aciton:

A

Block ENaC & ↓ K+
secretion
Late distal & Collecting
tubule

51
Q

K+ Sparing Diuretics (2)

A

Aldosterone antagonists
(spironolactone)
Na channel blocker
(triamterene)

52
Q

Many Diuretics Cause K+ Loss (Hypokalemia) (3)

A 
 Increasing flow rate of filtrate through distal 
nephron decreases K+ reabsorption.
 Keeps luminal K+ concentration low 
supporting secretion
 Hypokalemia may result.
53
Q 
Aldosterone 
antagonists reduce 
levels of (3)
A

Na+/K+ ATPase,

ENaC, K+ channel.

54
Q

ENaC blockers reduce

3

A

Na+ uptake, Na+/K+

activity, K+ secretion

Physiology (53 decks)

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