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Urinary > Week 6 - Potassium control > Flashcards

Week 6 - Potassium control Flashcards

1
Q

Why does small shifts of K result in such a big increase in ECF concentrations?

A

-The ECF is kept at such a low conc (approx 4.5mmol) that a shift of 1% of ICF results in a 50% rise in ECF

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2
Q

What maintains the difference between ECF and ICF?

A

-NaKATPase

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3
Q

What effect does K have on the resting membrane potential during normal, decreased ECF and increased ECF?

A

-K+ establishes a gradient across the cell membrane which sets up the RMP
normal -> steady RMP
decreased ->increases the gradient across the cell and hyperpolarises
increased -> decreases the gradient across the cell and depolarises

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4
Q

By what two mechanisms is potassium regulated?

A

-Internal and external balance

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5
Q

What is the purpose of internal balance?

A

-To have an immediate effect by shifting K between ECF and ICF -> does not solve the problem only helps cope with it

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6
Q

What is the function of external balance?

A

-To adjust renal K excretion to correct K imbalance

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7
Q

Describe the events which occur to deal with K after ingestion of a meal

A

1)Intestine and colon absorb dietary K -> large amount of K enters ECF
2)4/5ths of ingested K moved into cells within minutes
3)After a slight delay kidneys begin to excrete K and K is slowly released from cells
Excretion is complete within 6-12 hours.

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8
Q

By what mechanism is ECF shifted to ICF in internal balance?

A

-Mediated via NaKATPase

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9
Q

By what mechanism is K shifted from ICF to ECF in internal balance?

A

-Through ROMK

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10
Q

What are the three factors which increase K uptake by cells?

A
  • Hormones
  • Increased [K] in ECF
  • Alkalosis
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11
Q

What hormones cause cellular uptake of K?

A
  • Insulin
  • Aldosterone
  • Catecholamines
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12
Q

How does alkalosis cause cellular uptake of K?

A

-ECF K is exchanged for H+ in order to correct alkalosis

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13
Q

How do hormones promote cellular uptake of K?

A

-Increase NaKATPase activity

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14
Q

What factors influence K to be shifted out of cells?

A
  • Exercise
  • Cell Lysis
  • Increased ECF osmolarity
  • Low ECF [K]
  • Acidosis
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15
Q

How does exercise promote K to be released from cells? How is this corrected?

A
  • Skeletal muscle contraction releases K in proportion to intensity of exercise
  • Surrounding non-contracting tissues uptake K and prevent hyperkalaemia
  • Exercise also increases catecholamines to offset increase in ECF [K]
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16
Q

Give 3 examples of clinical conditions/treatments which cause cell lysis

A
  • Rhabdomyolysis
  • Intravascular haemolysis
  • Cancer chemotherapy
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17
Q

How does increase in plasma osmolarity effect K?

A
  • Water moves from ICF to ECF to decrease osmolarity

- Increases [K] in ICF so K leaves down conc gradient

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18
Q

Describe the renal handling of potassium

A
  • K is freely filtered at the glomerulus
  • Most reabsorbed in PCT and LoH
  • Control occurs in DCT and CD where potassium secretion/absorbtion is altered to match ingestion
19
Q

From which cells in the nephron is potassium secreted?

A

-Principal cells of DCT and cortical CD

20
Q

Describe K secretion in principal cels off DCT/CD

A
  • NaKATPase basolateral activity maintains high ICF [K]
  • this creates a chemical gradient for secretion
  • Na influx produces a high electrical gradient
  • K leaves the cell down the electro-chemical gradient via apical K channels
21
Q

How does [K] ECF effect K secretion by principle cell

A

-high [K] ECF stimulates NaKATPase, increases permeability of apical K channels and stimulates aldosterone

22
Q

How does aldosterone affect K secretion by principle cells?

A

-Aldosterone increases expression of NaKATPase, K channels and ENaC thus increasing secretion

23
Q

How does acid base status influence K secretion by principle cells?

A
  • Acid base status -> acidosis decreases secretion via inhibition of NaKATPase and decreased K channel permeability
  • > alkalosis increases secretion via stimulating NaKATPase and increasing K channel permeability
24
Q

What luminal factors affect K secretion by principal cells?

A
  • Increased DCT flow rate washes away luminal K -> Increased gradient = increased secretion
  • Increased Na delivery to distal tubule -> more Na resorbed, more K secreted
25
Q

Which cells of the DCT and CD resorb K?

A

-Intercalated cells

26
Q

Describe K resorption by intercalated cells

A

-Active process mediated by H+K+ATPase in apical membrane

27
Q

When is hyperkalaemia defined?

A

-[K]>5.0mmol/L

28
Q

When can increased intake cause hyperkalaemia?

A

-When there is renal dysfunction

29
Q

What can cause decreased renal excretion of potassium?

A
  • Acute/chronic injury
  • Drugs which block potassium excretion eg ACEI, K sparing diuretics
  • Low aldosterone states eg addisons
30
Q

How can diabetic ketoacidosis cause hyperkalaemia?

A
  • No insulin ->Decreased internal balance shifting K from ECF to ICF
  • Increased plasma osmolarity
  • Metabolic acidosis
31
Q

What are the clinical features of hyperkalaemia?

A
  • Altered excitability of the heart -> arrhythmias or heart block
  • Gastrointestinal neuromuscular dysfunction -> paralytic ileus
  • Acidosis
32
Q

How does hyperkalaemia cause arrhythmias?

A

-Increased ECF conc -> decreased gradient -> depolarisation of cardiac tissue -> more fast Na channels remain inactive -> heart less excitable

33
Q

Describe the ECG changes seen in hyperkalaemia

A
  • Tented T wave
  • Prolonged PR interval
  • Depressed ST
  • Absent P wave
  • Ventricular fibrillation
34
Q

What is the emergency treatment of hyperkalaemia?

A
  • IV calcium gluconate
  • Glucose + insulin IV
  • Nebulised Salbutamol
35
Q

Describe long term treatment of hyperkalaemia

A
  • Treat cause eg stop medications, treat DKA etc
  • Reduce intake
  • Measures to removes excess K -> dialysis, binding resins
36
Q

When is hypokalaemia defined?

A

-[K] less than 3.5mmol/L

37
Q

What problems with external balance can lead to hypokalaemia?

A
  • Excessive GI loss via diarrhoea, bulimia, vomiting

- Renal loss via diuretic drugs, high aldosterone

38
Q

What problems with internal balance can cause hypokalaemia?

A
  • excess insulin, aldosterone and catecholamines
  • low ICF
  • Metabolic alkalosis
39
Q

Describe the clinical features of hypokalaemia

A
  • Arrthymias
  • Paralytic ileus
  • Muscle weakness
40
Q

Why does hypokalaemia cause arrhythmias?

A
  • Increased gradient between ICF and ECF
  • Hyperpolarisation of cell
  • More fast Na channels in active form
  • Heart more excitable
41
Q

What is the main ECG change in hypokalaemia?

A

-Low T wave

42
Q

How do you treat hypokalaemia?

A
  • Treat cause
  • K replacement via IV/oral
  • potassium sparing diuretics if due to increased aldosterone
43
Q

Where is most of the bodys K?

A

-ICF (98%) mostly skeletal muscle

Urinary (21 decks)

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