Jan4 M2-Sodium Homeostasis Flashcards

1
Q

what’s the cause for the variations in our U Na

A

changes in dietary Na intake

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2
Q

what senses body sodium

A

PRESSURE receptors in the vascular wall, the renal AA and the heart

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3
Q

pressure receptors (baroreceptors) activation leads to changes in what

A

RAAS, SS, ADH and ANPs

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4
Q

impact of SS activation on the kidney (2)

A

SS stimulates juxtaglomerular cells to secrete renin

NE stimulates Na reabso in the PCT

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5
Q

diuretics mainly for what 2 conditions

A

edema and hypertension

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6
Q

Na in the PCT: %, mechanisms (3) and regulatory factors (3)

A

65%. Na channels + Na-H exchange + NaK ATPase drives Na+glucose,a.a,PO4 cotransporters.
AT2, NE and GFR

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7
Q

Na in loop of Henle: %, mechanisms (3) and regulatory factor

A

No reabso in the DL. TAL: 25%. NaK ATPase (baso), Na-K-2Cl cotransporter, Na-H exchanger, paracellular (tight junctions). flow-dependent

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8
Q

Na in the DCT: %, mechanism and regulatory factor

A

5%. NaK ATPase (baso), Na-Cl cotransporter. flow-dependent

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9
Q

Na in the collecting tubules: %, mechanism and regulatory factors (2)

A

3%, Na channels. aldo and ANP

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10
Q

other ion coming in with Na in CCD (CT) and how

A

Cl- paracellularly bc cation needs its anion

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11
Q

what goes outside CT to compensate on Na entry and how

A

K through K channel

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12
Q

aldosterone: hormone type, exact mode of action and on what exact cell

A

steroid hormone, binds aldoR in the nucleus of principal cells (CCD). aldoR acts as TF. more Na and K channels are made

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13
Q

AT2 and NE exact mode of action on the tubule in volume depletion

A

enhance Na reabso in PCT by increasing the activity of the Na-H exchanger

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14
Q

feedback loop in the RAAS

A

aldosterone feeds back on renin and suppresses it (baroreceptor feedback)

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15
Q

aldo produced where exactly, stimulus for its release and what exact molecule stimulates it + exact site of action of aldo

A

hypovolemia and AT2. zona glomerulosa. acts on CCD (CT)

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16
Q

aldo makes Na reabso vary by how much

A

0 to 2%. no aldo. 2% filtered load is excreted. with aldo: 0% filtered load is excreted

17
Q

adrenal layers + fct and which are in cortex/medulla

A

cortex: zona glomerulosa (salt), zona fasciculata (sugar), zona reticularis (sex)
medulla: panic (catecholamines)

18
Q

3 mechanisms by which renin is stimulated in hypovolemia

A

SS activity, drop in arterial P (less stretch on AA), less NaCl delivery to the macula densa

19
Q

why does Na = volume

A

it is the main extracellular ion

20
Q

2 things doing the opposite of aldo on Na excretion (2 other factors)

A

ANP and BP

21
Q

how ANP acts to increase Na excretion (3)

A
  • acts on CT (CCD) to stop eNac channels and decrease Na reabso
  • GFR (AA dilation and EA constriction)
  • inhibits aldo release
22
Q

how BP acts on increase Na excretion

A

pressure natriuresis

23
Q

what’s the result if all ingested Na is not excreted

A

increase in ECF volume (interstitial and intravascular)

24
Q

what happens to IV volume if give 1L saline and why

A

increases by 250 ml because Na can’t cross cells. extra Na to the body always in ECF. contributes to ECF volume

25
good strategy to control BP
lower dietary Na intake
26
euvolemic % Na reabso in the tubule
``` PCT: 65% TAL: 25% DCT: 5% CCD: 3% 1% excreted ```
27
main changes in tubular Na reabso in hypovolemia
- 80% abso in PCT (AT2 and NE enhance Na-H exchanger) | - 0% excreted
28
main changes in tubular Na reabso in hypervolemia
50% reabso PCT 12% reabso DCT 6% excreted
29
4 volume regulation systems
SS, RAAS, ANPs, ADH
30
SS effects on kidneys in very low BP (severe hemorrhage, severe hypovolemia, ..)
- constricts renal arterioles to drop GFR (overrides renal autoregulation (of GFR)) - activates renin (RAAS)
31
tubules reaction in severe drop in BP
increase Na reabsorption