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5. ADV PHYS > Potassium homeostasis > Flashcards

Potassium homeostasis Flashcards

1
Q

normal range of K+ in ECF plasma:

A

3.8-5mM

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2
Q

[K+] cell conc:

A

~140mM

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3
Q

resting potential of nn and mm cell determined by:

A

ratio of ECF and cellular K conc

- when cells at rest (btw APs) cell membrane has greater permeability to K than any ion

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4
Q

[K] ECF: 3 mM

A
  • hypokalemia (-103 mV Nernst potential (Ek))

- membrane potential (Em) hyperpolarised

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5
Q

[K] ECF: 4 mM

A
  • normal (Ek= -94 mV)

- membrane potential (Em) normal

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6
Q

[K] ECF: 7 mM

A
  • hyperkalemia (Ek= -80mV)

- membrane potential (Em) depolarised

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7
Q

[K] ECF: if below 3 mM or above 7 mM chances increase of

A
  • potentially fatal arrhythmias

- when [K] ECF outside normal range, heart produces abnormal ECG traces

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8
Q

symptoms: hypokalaemia

A
  • skipped heart beats/ palpitations
  • fatigue
  • mm weakness
  • spasms, tingling, numbness
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9
Q

symptoms: hyperkalaemia

A
  • nausea
  • slow/ weak irreg pulse
  • sudden colapse due to arrhythmias
  • esp dangerous
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10
Q

K: overview

A
  • K from food moves rapidly from GIT to ECF
  • exercise releases K into ECF during repolarisation phase of AP in skeletal mm
  • K ECF is low, addition of K in meal during whole body exercise/ meal dangerous changes to mem potential
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11
Q

K: meal rich in fruits/ veggies

A
  • K in ECF ~65-70 mM
  • rich meal may 2x this
  • need rapid mechanism to combat
  • shift K into cells as soon as enter GIT
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12
Q

K: sink for K

A
  • most of body K in skeletal mm
  • liver also important site for K buffering
  • K conc inside cells v high, K entering from ECF will make lil diff to mem potential
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13
Q

K: btw meals

A
  • K released from cells, excreted by kidneys
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14
Q

K: kidneys sig

A
  • control body content of K, is too slow to stop rapid entry of K into mm
  • rapid moving K into cells + slower excretion by kidneys = K homeostasis
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15
Q

K: fasting/ v low K diet

A
  • all K entering in kidney will be reabsorbed
  • but K still lost in stools and sweat
  • then skeletal mm will donate K to ECF to maintain [K]ECF
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16
Q

translocation of K: btw ECF and cells

A
  • Na/K exchange pumps on all cells
  • move 3x Na out/ 2 K into cell
  • both ions moving up electrochemical gradient = ATP needed
  • pump protein also acts as ATPase, energy from 1x ATP is used to power each exchange cycle
  • exchange is highly regulated to maintain constant [K]ECF
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17
Q

translocation of K: feedback/foward sys?

A
  • feedback relied on error signal to change controlled variable

= feedforward as don’t need error, fast effect as dangerous is change in [K] ECF

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18
Q

translocation of K: during a meal, insulin

A
  • special nutrients (esp glucose) and electrolytes
  • detected by GIT ‘taste receptors’ release incretins (GLP-1: glucose dependent insulin tropic hormone) signal for insulin release before glucose enters blood
  • insulin: uptake of glucose into cells, stimulated Na/K pump
  • feedforward activates translocation of K into cells before bulk of K from meal enters ECF
  • insulin release when glucose rises in plasma further increases K uptake
  • high plasma K conc will directly stimulate insulin release: depolarisation of membrane of pancreatic ß cells
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19
Q

translocation of K: short term K deprivation

A
  • inhibits ability of insulin to promote cellular K uptake by pump
  • good for preventing hypokalaemia after carb rich, K poor meal
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20
Q

translocation of K: high [K]ECF and aldosterone

A
  • also stimulate Na/K pump

- only in extreme conditions when normal feedforward sys failed to maintain normal lvls of K conc in ECF

21
Q

translocation of K: whole body exercise

A
  • at high work rate
  • K conc ECF increases, stimulates Na/K exchange pump
  • increased plasma Ad conc during exercise also stimulate pump
  • counteract loss of K from contracting mm cells
22
Q

control whole body K: by kidney

A
  • input: diet
  • output: digestive tract, sweat, kidneys
  • ## only renal excretion of K is controlled, kidneys ensure K output = input so whole body K constant
23
Q

control whole body K: rate of excretion equation and wat is reg?

A

excretion rate = filtration rate - reabsorption rate + secretion rate

  • reabsorption, secretion reg
24
Q

control whole body K: why controlled secretion vital

A
  • K filtered at low rate
  • due to low conc in plasma
  • normal-high K diets, lrg amounts must be excreted
25
Q

control whole body K: K depletion of filtered load where, un/reg? and excretion

A

~85% of load absorbed into proximal tubule, LOH, process largely unreg
- almost all rest absorbed by distal tubule, collecting duct so ~1% of K in filtered load excreted

26
Q

control whole body K: reabsorption of K

A
  • highly reg, by intercalated cells
  • make up wall of nephron w Na/K pumps on BASOlateral mem
  • K transported into cells
27
Q

control whole body K: K into cells

A
  • from tubular fluid by K/H antiport (2º active transport) on LUMINAL mem
  • K moves DOWN electrochemical grad through channel into ECF
28
Q

control whole body K: when is secretion not present

A
  • when K conc in body lower than normal
29
Q

control whole body K: normal/high K intake

A
  • 85% filtered load still reabsorbed in proximal tubule and LOH
  • reabsorption greatly reduced
  • amount of K =15-80% in glomerular filtrate secreted into distal tubule, collecting duct and excreted
30
Q

control whole body K: principal cells have, secretion

A
  • of collecting duct have K channels (ROMK) on LUMINAL mem
  • secretion from active transportation via ROMK channels in principal DOWN electrochemical grad via ROMK channels
  • K shifted from ECF to tubular fluid for excretion
31
Q

control whole body K: aldosterone

A
  • stimulates K secretion into tubular fluid by principal cells of distal tubule, collecting duct
  • high [K]ECF depolarises plasma mem of aldosterone prod cells in adrenal cortex
  • opens voltage gated Ca channels
  • Ca activates Ca-calmodulin-dependant protein kinases that stimulate aldosterone prod
  • is steroid hormone, can’t be stored in cell
  • release directly related to rate of prod
32
Q

control whole body K: membrane transport in distal tubule, collecting duct reg by

A
  • aldosterone
  • travels in blood bound to carrier protein
  • crosses basolateral mem of cell: distal tubule, collecting duct
  • hormone bind to receptor within cell of distal tubule, collecting duct
33
Q

control whole body K: when aldosterone binds in cell

A
  • hormone binds to receptor in cell, moved into nucleus to bind to HRE of several genes
  • rate of transcription of RNA of many proteins increased (eg. Na/Cl cotransport (NCC) of distal tubule, Na (ENaC) and K (ROMK) channels on LUMINAL mem of principal cells of collecting tubule, collecting duct)
  • prod of Na/K exchange pumps, proteins involved in ATP prod within mitochondria also upreg
34
Q

control whole body K: result of aldosterone changes

A
  • changes to increase reab of Na and secretion of K
  • these processes not directly linked entry of Na into cells of collecting duct produces electrical grad facilitating exit of K so effective secretion of K required reab of Na in region of nephron
  • aldosterone inhibits K reab by intercalated cells of collecting duct
35
Q

regulation of K secretion, reabsorption: when [K]ECF is increased

A
  • aldosterone lvls rise
  • causing changes in transport processes in connecting tubule, collecting duct
  • would promote both K secretion through ROMK channels, Na reab through ENaC
36
Q

regulation of K secretion, reabsorption: problem w K secretion and Na reabsorption

A
  • when K is secreted, body Na and ECF vol would be altered (aldosterone paradox)
  • but if upstream (distal tubule) NCC was inhibited, less Na would be reab in distal tubule, balancing increased reab through ENaC in collecting duct
  • Na reab, water follows (osmosis) slowing Na reab through NCC would increase flow rate in collecting duct
  • favouring K secretion through ROMK
37
Q

regulation of K secretion, reabsorption: for K secretion but no excess Na reab

A
  • NCC needs to be inhibited
  • but aldosterone stimulated NCC vs inhibiting it
  • but studies: effect of aldosterone on NCC overriden by high [K]ECF acting via WNK protein kinases within cells of distal tubule
38
Q

regulation of K secretion, reabsorption: low K diet

A
  • aldosterone lvls drop
  • K secretion stopped
  • aldosterone inhibits reab of K by intercalated cels (collecting duct) so falling lvls aldosterone allow cells resume function of reab K, so virtually all K filtered into nephron reab
39
Q

combined reg of ECF vol and whole body K by kidney: total body Na determines?

A
  • plasma vol

- bP

40
Q

combined reg of ECF vol and whole body K by kidney: low plasma vol activates and effect

A
  • RAAS sys
  • prod of angiotensin II -> cause release of aldosterone
  • both these hormones affect Na, K transport in distal nephron
  • angiotensin II and aldosterone stim reab of Na through NCC
  • angiotensin II overrides activation of ROMK by aldosterone
  • despite elevated aldosterone lvls, lack of open ROMK channels reduce flow of water, Na in collecting duct = ensure K secretion not increased while Na reab by NCC
  • opposes fall in plasma vol
41
Q

combined reg of ECF vol and whole body K by kidney: plasma vol low, [K]ECF increased

A
  • both changes reinforce to cause lrg release of aldosterone
  • aldosterone overrides inhibitory effect of angiotensin II on ROMK and NCC inhibited directly by high [K]ECF and increased secretion of K through ROMK
42
Q

combined reg of ECF vol and whole body K by kidney: constant values of total body Na, K maintained by, which transporters

A
  • aldosterone
  • angiotensin II
direct effect of [K]ECF on:
- NCC
- ENaC
- ROMK
in distal nephron
43
Q

diuretics: most common, effective class to treat hypertension

A
  • thiazides
44
Q

diuretics: thiazides features

A
  • promote diuresis (decrease ECF vol) by inhibiting NCC in distal tubules =less Na reab
  • water remains in tubular fluid w Na -> excreted
45
Q

diuretics: increased flow in tubules result

A
  • to ENaC, ROMK in collecting duct
  • reduction in ECF vol, increase release of aldosterone
  • secretion of K through ROMK stimulated potentially leading to hypokalaemia
46
Q

diuretics: prevent loss of K?

A
  • thiazides diuretics often used in combo w K sparing agents that block ENaC and/or Na/K pump
  • mineralocorticoid receptor antagonist prevent aldosterone promoting K secretion in collecting duct
  • aldosterone is mineralocorticoid
47
Q

nernst potential for K:

A

-94 mV

48
Q

Em for cardiac mm cells:

A

-90 mV

5. ADV PHYS (10 decks)

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