lecture 6 Flashcards

1
Q

sodium

A

most prevalent and important solute in ECF

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2
Q

effect of high Na+

A

retain more water so weight increases

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3
Q

high Na+ intake in diet

A

increased osmolarity (body won’t allow), so increased ECF volume, (increased water reabsorption) increasing blood volume and pressure

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4
Q

where is Na+ reabsorbed

A

65% proximal (to aid in reabsorbing other nutrients), 25% thick ascending loop of Henle (create hyper-osmolar fluid), 8% distal, 2% collecting

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5
Q

if high GFR

A

increase Na reabsorption as more fluid in; if low, lower Na reabsorption; always reabsorbing same proportion

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6
Q

change amount of Na excreted

A

change amount put in tubular system (by chaning pressure and GFR)

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7
Q

if low BP

A

increased sympathetic activity (also stimulates granular cells for renin so ang II to reduce BP and Na+ uptake in PCT) and reduced GFR; PCT reabsorb more Na+; sympathetic causes aldosterone release increasing Na+ uptake in distal and collecting duct; if low tubular Na+ at juxtaglomerular apparatus, renin produced

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8
Q

if high BP

A

atrial naturietic peptide, suppresses activity so decreases Na reabsorption

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9
Q

JGA of kidney

A

produces renin due to Na+/K+/Cl- channel. amount of Na+ in goes down, so low osmolarity vs environment so water leaves cells, shrinking them and they produce NO and PGE2 - stimulate granular cells to secrete renin

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10
Q

RAAS

A

liver - angiotensinogen - angiotensin I (renin) - angiotensin II (ACE in lung - greater epithelial SA; causes vasoconstriction) - aldosterone (adrenal) - feeds back to kidney for Na+ and water reabsorption

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11
Q

effects of ang II

A

proximal: increase Na+ and water reabsorption, increasing ECF and BP; vascular: vasoconstriction and increased BP; causes aldosterone synthesis

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12
Q

aldosterone

A

works on principal cells of collecting duct, stimulares Na+ absorption, K+ and H+ secretion; excess causes hypokalaemic alkalosis

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13
Q

how does aldosterone work

A

induces expression of apical Na channel of collecting duct; induces formation of Na+/K+ ATPase pumps by increasing transcription of corresponding mRNA; Na+ reabsorbed into blood and K+ secreted

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14
Q

hypoaldosteronism

A

reduced Na reabsorption in distal, increasing urinary Na loss; ECF volume falls, increasing renin angII and ADH; causes dizziness, low BP, salt craving and palpitations

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15
Q

hyperaldosteronism

A

increased Na reabsorption in distal, decreasing urinary Na loss; ECF volume rises (high BP), reduced renin angII and ADH; increased ANP and BNP; causes high BP, muscle weakness, polyuria, thirst

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16
Q

Liddle’s syndrome

A

inherited hypertension as mutation in aldosterone activated Na+ channel (always on), causing Na+ retention and hypertension

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17
Q

reabsorbing water when high Na+, causing polyuria and polydypsia

A

thirst as higher osmolarity than should have; as more water in, more urine out

18
Q

baroreceptors

A

low pressure side: heart (atria, right ventricle), high pressure side: vascular (carotid sinus, aortic arch, JGA)

19
Q

low pressure side

A

can respond to low or high BP; if lowm afferent to brainstem for sympathetic activity and ADH release; if high pressure, atrial stretch so ANP, BNP released

20
Q

high pressure side

A

slide 29

21
Q

atrial natriuretic peptide (ANP)

A

small made in atria (also make BNP); released in response to atrial stretch

22
Q

actions of ANP

A

slide 30

23
Q

slide 31: high GFR

A

decent diagram

24
Q

slide 32: low GFR

A

another cracking diagram

25
Q

ACE inhibitors

A

reduce ang II so reduces vasoconstriction and aldosterone production (less Na+ reabsorption in DCT)

26
Q

osmotic diuretics

A

glucose (increases osmolarity in tubular fluid, acting as osmotic component so lesser osmotic gradient - diabetes mellitus), mannitol

27
Q

need to ensure more solute gets to dct and collecting duct if high BP to get rid of more water

A

loop, thiazides, K+ sparing (don’t lose as much K+) - slide 36

28
Q

carbonic anhydrase inhibitors

A

export H+ at expense of Na+, so if inhibit production of H+ in PCT, so less Na+ can come in, so more Na+ excreted as reaches dct

29
Q

loop diuretics e.g. furosemide

A

potent; block triple transporter (Na+/K+/Cl-) in ascending limb of loop of Henle; more Na+ in tubular fluid so less in interstitial space also

30
Q

thiazides

A

block Na+/Cl- symporter in dct

31
Q

K+ sparing diuretics

A

distal ct; reduce Na+ in from lumen so reduce amount of Na+ pumped out into blood

32
Q

spiralmalactone (inhibits aldosterone)

A

inhibits Na+/K+ ATPase to blood and Na+ channel in dct (similar to K+ sparing diuretic)

33
Q

high K+

A

depolarises membranes - action potentials, heart arrhythmias; low also causes heart arrhythmias

34
Q

meal

A

increase K+ absorption, increase plasma K+, increased tissue uptake quickly (na/k pump) so K+ doesnt rise (stimulated by insulin; reduced by aldosterone and adrenaline)

35
Q

K+ absorption

A

30% reaches descending loop of henle; anywhere between 1-80% secreted

36
Q

k+ secretion

A

stimulated by high plasma K+, pH, high aldosterone, high tubular flow rate

37
Q

K+ secetion by principal cells

A

slide 45

38
Q

aldosterone stimulates K+ into cell and out into lumen

A

slide 46

39
Q

collecting tube cells

A

cilia so as flow increase, stimulate PDK1 activity, cascade so increases IC Ca2+ - activates K+ channels to release more K+

40
Q

hypokalaemia

A

common; diuretics (increases tubular flow rates and K+ excretion), surreptitious vomiting, diarrhoea, genetic mutations (reduced Na+ inport so increased flow rate)

41
Q

hyperkalaemia

A

response to K+ sparing diuretics, ACE inhibitors; elderly