Contorl Of Potassium Flashcards

1
Q

Describe the distribution o K+ in body fluids

A

98% in ICF, only 2% in ECF Mainly in skeletal muscle cells (also liver, red cells, bone)
Shift of 1% of ICF K+ to ECF would raise ECF [K+] by 50%
Difference between ICF & ECF [K+] maintained by Na-K-ATPase Maintaining ECF [K+] is critical

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2
Q

Why is maintaining [K+] critical?

A
  • Because of its effect on the resting membrane potential
  • Hence its effects on excitability of cardiac tissue
  • Hence risk of life threatening arrhythmias with hyperkalaemia and hypokalaemia
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3
Q

How is ECF K+ regulated

A
– Immediate Control
By internal balance  Moves K+ between ECF and ICF
– Longer term, overall K+ balance
By external balance
adjusting renal K+ excretion
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4
Q

What are potassium rich foods

A

Raisins, honey dew, banana, orange, tomato, potato chips, baked potato, milk

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5
Q

Describe he events following an average meal

A

• Intestine and colon absorb dietary K+
• E.g. If 28 mmol K+ absorbed
— ECF K+ will increase by 2mmol/L
— If pre-meal K+ was 5 mmol/L could rise to 7 mmol/L (which is a dangerous level)
• But 4/5ths moves into cells within minutes
• After slight delay kidneys begin to excrete K+
Excretion complete in 6 -12 hours

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6
Q

Describe K+ balance following a K+ load eg average meal

A

See slide

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7
Q

Decsribe the internal balance of K+

A

Is the net result of
1. Movement of K+ from ECF -> into cells
mediated via Na-K-ATPase
2. Movement of K+ out of cells into ECF
Via K+ channels (channels which determine the K+ permeability of the cell membrane)

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8
Q

What increases K+ uptake by cells

A
1. Hormones (Act via Na-K-ATPase)
• Insulin,
• Aldosterone
• Catecholamines
2. Increased [K+ ] in ECF 
3. Alkalosis - low ECF [H+] K+ shift -> into cells
(more later)
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9
Q

What promote K+ shift out of cells

A
  1. Exercise
  2. Cell lysis
  3. Increase in ECF Osmolality
  4. Low ECF [K+ ]
  5. Acidosis - increase ECF [H+]
    — K+ shift -> out of cells
    (more later)
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10
Q

Describe the effect of K= o insulin

A

• K+ in splanchnic blood stimulates insulin secretion by pancreas
• Insulin increases Na-K-ATPase activity -> increases K+ uptake by
muscle cells and liver
Clinical Use: I.V. insulin + Dextrose used treat hyperkalaemia

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11
Q

Describ ethe effect of K+ on aldosterone

A

Aldosterone
– K+ in blood stimulates Aldosterone secretion
– stimulates uptake of K+ via Na-K-ATPase

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12
Q

Desctibe the relation between k+ and catecholamines

A

Catecholamines
– Acts via B2 adrenoceptors
– Which stimulate Na-K-ATPase and cellular uptake of K+

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13
Q

Describe excerciese and K+

A

• Net release of K+ during recovery phase of action potential, K+ exits cell (K+ channels open)
• Also skeletal muscle damage during exercise releases K+
• -> increase in plasma [K+] is proportional to the intensity of exercise
• Uptake by non-contracting tissues prevents dangerously high
hyperkalaemia
• Exercise (& trauma) also increase catecholamines, which
offset ECF [K+] rise by increasing K+ uptake by other cells
• Cessation of exercise results in a rapid ↓plasma [K+], often to
<3mmol/L

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14
Q

Describe the acid base disturbances to K+

A

• Affect several acid-base, Na+ and K+ transport pathways across
cell membrane
• Final result is as if there is a reciprocal shift of H+ and K+
between the cells and ECF

— acidosis shift of H+ into cells, reciprocal shift o K+ out of cells leading to hyperkalaemia
— alkalosis shift of H+ out of cells, reciprocal shift of K+ into cells, leading to hypokalaemia

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15
Q

How can changes in [K+] affect pH

A

Hypo & Hyperkalaemia Similarly, changes in ECF [K+] causes reciprocal shifts in K+ and H+ between the ECF & ICF
Hyperkalaemia, shift of K+ into cells
Reciprocal H+ shift out of the cells
Hyperkalaemia leads to acidosis
Hypokalaemia  shift of K+ out of cells Reciprocal H+ shift  into the cells
Hypokalaemia causes alkalosis

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16
Q

Describe the external balance of K+

A

• Slower • 6 -12 hours to excrete a load of K+
• Controls total body potassium content over the Longer term
• By regulated K+ secretion in late DT & cortical collecting ducts
Around 90-95% Gi absorption, rest is lost

17
Q

Describe the renal handling of K+

A

K+ freely filtered at glomerulus
K+ reabsorbed at PCT, Thick AL, DCT, CCD, MCD
K+ also secreted at DCT and CCD (principal cells)

18
Q

Describe K+ secretion in DCT and CCD

A

By principal cells Na-K ATPase activity in Basolateral membrane:
High intracellular K+ & low Na+
high intracellular K+ creates chemical gradient for secretion
Na+ moves from lumen into cell down its concentration gradient (via apical ENaC ) creating an electrical gradient - negative potential outside cell
Together create a favourable electro chemical gradient for K+ secretion via apical K+ channels

19
Q

What are the tubular factors affecting K+ secretion by principal cells

A

• ECF [K+]
– Directly stimulates Na-K-ATPase &
Increases permeability of apical K+ channels
– Also stimulates aldosterone secretion

• Aldosterone
— increases  transcription of relevant proteins:- 
— increase Na-K-ATPase 
— increase  K+ channels &amp; 
— increase  ENaC in apical membrane
• Acid base status
- Acidosis decreases K+ secretion:
inhibits Na-K-ATPase, decreased K+ channel permeability
- Alkalosis ↑ K+ secretion:
stimulates Na-K-ATPase,
Increase  K+ channel permeability
20
Q

Describe luminal factors affecting K+ secretion by principal cell

A

• Increased distal tubular flow rate washes away luminal K+, increases K+ loss
• Increased Na delivery to distal tubule
More Na absorbed; classic example eg furosemide, blocks Na reabsorption upstream (in tal) so more is available here
results in more K+ loss

21
Q

Describe k+ absorption in DCT and CCD

A
  • K+ absorbed by intercalated cells
  • Active process
  • Mediated by H+ K+ ATPase in apical membrane
22
Q

What are the effects of changing in ECF K+

A

— Alter cell membrane resting potential
— Alter neuro muscular excitability
• Problems with cardiac conduction & pacemaker automaticity
• Alter neuronal function
• Alter skeletal muscle function
• Alter smooth muscle function
— Result in arrhythmias, cardiac arrest, muscle paralysis

Dont pick it up until quite late

23
Q

What are the causes of hyperkalaemia rom external balance

A

Important to know causes bc hard to pick up
May be due to
– Increased intake (unlikely)
only if renal dysfunction is also present Unless: inappropriate doses of IV K+ (dangerous)
– Decreased renal excretion
• Acute or Chronic kidney injury
• Drugs which block potassium excretion
– ACE inhibitors
– K+ sparing diuretics
• Low aldosterone state (addison’s disease) - addisonian crisis - monitor potassium

24
Q

What are internal shifts that can cause hyperkalaemia

A
May also be due to internal shifts
1. Diabetic ketoacidosis 
no insulin; - insulin promotes k+ into cells 
&amp; plasma hyper osmolarity &amp;  metabolic acidosis)
2. Cell lysis
muscle-crush injuries, Tumour lysis 
3. Metabolic Acidosis 
4. (Exercise)
25
Q

What are the clinical features of kyperkalaemia

A
  1. Heart
    altered excitability → arrhythmias, heart block
    Hyperkalaemia depolarises cardiac tissue - initial increase in excitability, but as time goes on, more fast Na channels remain in inactive form – heart less excitable
  2. Gastro Intestinal
    neuromuscular dysfunction
    → paralytic ileus
  3. Acidosis
26
Q

What are the ECG changes seen in hyperkalaemia

A

7 mEq/L - HIgh T wave
8 mEq/L - Prolonged PR interval, depressed ST segment, high T wave
9 mEq/L - Atrial standstill, P wave absent, intraventricular block
10 mEq/L - Ventricular fibrillation

27
Q

What are emergency treatments for hyperkalaemia

A
1. Reduce  K+ effect on heart - prevent arrhythmias
IV calcium gluconate – immediate effect
2. Also Shift K+ into ICF by:– 
– glucose +insulin IV
(action in ≈ 30 mins) 
– Nebulised Beta agonists (Salbutamol) (catecholamines also push K+ into cell)
3.  Remove excess K+
– Dialysis
28
Q

What are the longer term treatments for hyperkalaemia

A
  1. Treat cause
    stop medications, treat DKA, etc
  2. Reduce intake
  3. Measures to remove excess K+
    – Dialysis ( in acute or chronic kidney injury)
    – Oral K+ binding resins to bind K+ in gut (CKI)
29
Q

What are the causes of hypokalaemia

A
May be due to 1. problems of external balance
– Excessive loss
• GI – diarrhoea/ Bulimia /vomiting
• Renal loss of potassium can cause loss of K+
Diuretic drugs,
Osmotic diuresis (Diabetes)
High aldosterone levels
2. Problems of internal balance
– shifts of potassium into ICF
E.g.  Metabolic Alkalosis
30
Q

What are the clinical features of hypokalaemia

A
1. Heart :  altered excitability →
arrhythmias
Hypokalaemia hyperpolarised  RMP
more fast Na channels available in active form → heart more excitable
2. Gastro Intestinal :
neuromuscular dysfunction →
paralytic ileus
3. Skeletal Muscle:
neuromuscular dysfunction →
muscle weakness
4. Renal :  unresponsive to ADH
→nephrogenic DI
Polyuria and polydipsia
31
Q

What are the ECG changes in hypokalaemia

A

2.5 - Low T wave, high U wave, low ST segment
3 - Low T wave, Hugh U wave
3.5 - Low T wave

32
Q

What is the treatment for hypokalaemia

A
  • Treat cause
  • Potassium replacement - IV /oral
  • If due to increased mineralocorticoid activity — potassium sparing diuretics which block action of aldosterone on principal cells