Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology 1 > Potassium balance > Flashcards

Potassium balance Flashcards

1
Q

What is our daily intake of potassium?

A

A typical daily intake in the UK is 50-125mmol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where do we obtain potassium from?

A
  • Potassium is found particularly in leafy vegetables and most fruit and fruit juice, and in potatoes, especially if they are fried* or baked.
  • high salt content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe potassium homeostasis

A

On image

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does regulation of potassium homeostasis imply?

A

Acute regulation:
- Distribution of K+ through ICF and ECF compartments
Chronic regulation:
- Achieved by the kidney adjusting K+ excretion & reabsorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does a sodium-potassium pump work?

A

On image

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When does ECF pool change?

A

ECF pool will change more dramatically with changes in body K distribution e.g. after a meal, get slight increase in plasma [K+], which is shifted into ICF compartment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When does internal balance and acute regulation shift?

A 
Shift mainly subject to hormonal control:
Insulin
Adrenaline
Aldosterone
pH changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define Hyperkalaemia and Hypokalaemia

A

Hyperkalaemia = plasma [K+] > 5.5mM

Hypokalaemia = plasma [K+] < 3.5mM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What creates a resting membrane potential?

A

Ionic gradients (i.e. combination of chemical & electrical gradients)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the Nerst equation determine?

A

Resting membrane potential of the ions (potassium and sodium)

These ions determine resting membrane potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens when plasma [K+] is altered above or below normal (its effect on the membrane potential)

A

Normal: [K]o=3.5mM and [K]i=140mM ⇒ EK = -98.5

Hyperkalemia: [K]o=7mM and [K]i=140mM ⇒ EK = -80

Hypokalemia: [K]o=1.5mM and [K]i=140mM ⇒ EK = -121.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What can changes in potassium cause?

A

Can severely affect the heart - cardiac cell membrane potential (depolarisations/hyperporlarisations) producing characteristic changes in ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is cell membrane hyperpolarisation and depolarisation?

A

Cell membrane hyperpolarization – increased negativity of voltage across membrane, hence decreased excitability of neurones & muscle cells

Cell membrane depolarization – decreased negativity of voltage, hence threshold approached quicker, increased excitability & muscle contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What effect does Hyperkalaemia and Hypokalaemia have on the ECG?

A

Hyperkalaemia: ↑QRS complex, ↑amplitude T-wave, eventual loss P-wave

Hypokalaemia: ↓amplitude T-wave, prolong Q-U interval, prolong P-wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

When can Hypokalaemia caused by renal or extra-renal loss of K+ or by restricted intake occur and cause?

A 
Long-standing use of diuretics w/out KCl compensation
Hyperaldosteronism/Conn’s Syndrome
(increases aldosterone secretion)
Prolonged vomiting → Na+ loss → aldosterone secretion → K+ excretion in kidneys
Profuse diarrhoea (diarrhoea fluid contains 50mM K+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What does Hypokalaemia result in?

A

Hypokalaemia results in ↓release of adrenaline, aldosterone & insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When does acute hyperkalaemia normally occur?

A

Acute hyperkalaemia normal following prolonged exercise → normal kidneys excrete K+ easily

18
Q

What disease states can occur as a result of Hyperkalaemia?

A

Insufficient renal excretion
Increased release from damaged body cells eg. during chemotherapy, long-lasting hunger, prolonged exercise or severe burns
Long-term use of Potassium-sparing diuretics
Addison’s disease (adrenal insufficiency)

19
Q

When plasma concentration of potassium is greater than 7mM what can it cause?

A

asystolic - > cardiac arrest

20
Q

How does insulin and glucose drive potassium back into cells?

A

Insulin extremely important – mechanism unclear, may stimulate Na-K-ATPase. Why is glucose given with it?

21
Q

What other hormones stimulate the Na+-K+ pump?

A

Other hormones (aldosterone, adrenaline) stimulate Na+-K+ pump -> cellular K+ influx

22
Q

What is external balance of potassium maintained by?

A

The kidney

23
Q

How is potassium involved in the treatment of CVD?

A

Drugs like β-blockers, ACE inhibitors etc raise serum [K] →risk of hyperkalaemia

Conversely loop diuretics, used to treat heart failure, enhance risk of hypokalaemia

K+ excretion in the stools is not under regulatory control ⇒large amounts can be lost by extra-renal routes

24
Q

What is the concentration of soidum and potassium in the BC

A

On image

25
Q

What percentage of Na/+K+ is reabsorbed in the PCT?

A

60-70%

Fraction that is reabsorbed in PCT is ~ constant
Although absolute amount reabsorbed varies with GFR

26
Q

Describe potassium movement on PCT

What happens if this Na+/ K+ pump is inhibited by dopamine?

A
  1. Potassium diffuses from the sodium-potassium pump from the epithelial cell into the capillaries
  2. Also passive across by passive and paracellular mechanisms (K+, Cl-, Na+)

If this is inhibited (by for eg dopamine, digitalis) then the Na gradient is dissipated, eventually loose primary Na transport and the associated secondary active solute transport and also NO osmotic gradient for water transport.

27
Q

What determines K+ secretion in DCT?

How is this achieved?

A
  1. Increased K+ intake
  2. Changes in blood pH
    - Alkalosis ⇒ ↑excretion of K+ ⇒ ↓serum [K+]
    - *Acute Acidosis ⇒ ↓excretion of K+ ⇒ ↑serum [K+]
  3. activity of Na-K-ATPase pump
  4. electrochemical gradient
  5. permeability of luminal membrane channel
28
Q

What does aldosterone do?

A

Aldosterone is major regulator of K balance in the body. It acts to:
↑activity of Na+/K+ pump -> ↑K+ influx -> ↑[K+]i -> cell-lumen concentration gradient
↑ENaC channels -> ↑Na+ reabsorption -> ↓cell negativity and ↑lumen negativity -> voltage gradient
Redistributes ENaC from intracellular localization to membrane
↑permeability of luminal membrane to K+

On image

29
Q

How does an ↑Plasma [K] increases K secretion?

A

slows exit from basolateral membrane -> ↑[K+]i -> cell-lumen concentration gradient

↑activity of Na+/K+ ATPase -> ↑[K+] within cell

↑Plasma [K] -> stimulates aldosterone secretion

On image

30
Q

Describe the pathway that leads to an increase in potassium excretion

A

On image

31
Q

How does alkalosis and acidosis effect secretion of potassium ions?

A

On image

32
Q

What other factors can cause an increase in potassium excretion?

A

↑Flow rate by:
↑GFR
Inhibition of re-absorption
K-wasting diuretics

33
Q

How are alpha-intercalated cells of late DCT/ CD involved in severe hypokalemia?

A
  1. Activation of potassium-hydrogen ATPase increases reabsorption into peritubular capillary
34
Q

Dependence of potassium secretion on sodium and flow poses problems

WHY?

A

Changing effects of sodium or potassium may have unwanted effects on one of these but wanted effects on the other

35
Q

How does a decrease in ECFV cause secretion/ excretion of potassium ions?

A

On image

36
Q

Describe the RAAS cascade

A

On image

37
Q

What factors shift K+ into cells and what factors shift potassium out of cells?

A

On table

38
Q

Describe addisons disease

What does the cortex produce?

What can damage to the cortex cause?

What does a deficiency in aldosterone cause?

What treatment option is available for people with Addison’s disease?

A 
Cortex produces:
glucocorticoid hormones (e.g. Cortisol)
Mineralocorticoid hormones (e.g. Aldosterone)
Sex hormones (androgens &amp; estrogens)

Primary Adrenal Insufficiency aka Addison’s disease (very rare ) as opposed to secondary adrenal insufficiency

Damage to cortex -> ↓↓ hormone production -> numerous symptoms

Deficiency in aldosterone ->
body secreting large amounts Na ->
low serum Na levels
body retaining K-> hyperkalaemia

Treatment usually involves corticosteroid (steroid) replacement therapy for life.

39
Q

What does secondary adrenal insufficiency cause?

A

Pituitary ACTH -> Cortisol Decrease-> Adrenal glands shrink

40
Q

What causes Primary Aldosteronism aka Conn’s Syndrome?

What does it cause?

A

Primary Aldosteronism aka Conn’s Syndrome
due to aldosterone-producing adenoma of ZG of adrenal gland
usually <3cm, unilateral & renin-unresponsive

Hyperaldosteronism (excess release of aldosterone) due to variety chronic disease

Most common (50-60%) due to Conn’s syndrome, remaining 40-50% due to bilateral adrenal hyperplasia
Aldosterone release in absence of stimulation by Angiotensin II

↑↑↑ Plasma Aldosterone -> kidneys to stimulate Na+ reabsorption & K+ excretion -> develop hypertension* -> ↑fluid volume -> hypokalaemia (↓[K+]), hypernatremia and alkalosis
*↑bp & Na delivery to macula densa -> ↓↓release of renin -> renin-independent cause of hypertension (very difficult to control)
Treatment:
surgical removal of tumour-containing adrenal gland
hypertension & hypokalaemia controlled with K+-sparing agents e.g spironolactone

Physiology 1 (72 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions