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Flashcards in Biochemistry Potassium Deck (54)
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1
Q

Intracellular Potassium

A

98% - 2940 mmol

2
Q

Extracellular

A

2% 60 mmol

3
Q

Plasma (extracellular)

A

0.5%-15 mmol (sampling this proportion)

4
Q

Transport out/into cells via

A

Na/K ATPase

5
Q

Potassium (plasma) maintains the

A

resting membrane potential

6
Q

Determine via

A

Potassium inside cells vs. extracellular

7
Q

Resting potential of

A

-70mV

8
Q

Disturbing potassium problem

A

Disturbs resting potential and therefore leading to the clinical symptoms of hypo or hyper

9
Q

The Na+ and K+ gradients are maintained by

A

by the sodium-potassium pump

10
Q

Intake

A

100 mmol per day

11
Q

Output

A
30 mmol/day
	Skin – 10 mmnol
	Faeces – 10 mmol
	Urine >10 mmol
Minimum loss – 7 mmoll/litre in urine
12
Q

Patient on IV fluids

A

The patient would start to build up a hypo as no input but still output therefore supplementing input with potassium however must be observed.

13
Q

Potassium – Renal Potassium Handling: Filtered

A

800 mmnol/day

14
Q

Potassium – Renal Potassium Handling: Reabsorption

A

100% in proximal nephron

15
Q

Potassium – Renal Potassium Handling: Secretion via

A

Controlled Na/K exchanger in distal convoluted tubule regulated by aldosterone – regulates potassium excretion to maintain potassium balance

16
Q

Potassium – Renal Potassium Handling: Urine potassium excretion depends on

A
  • Availability of sodium for exchange –
  • Plasma aldosterone concentration
  • Relative intracellular [K+] and [H+]
17
Q

Potassium – Renal Potassium Handling: Output

A

• Input – other losses

18
Q

Potassium – Renal Potassium Handling: Availability of sodium for exchange

A

Cant excrete potassium unless exchanged for sodium. Acute renal failure – less potassium being filtrerd but the main factor is reduced filtration of sodium (most reabsorb in proximal nephron. Little sodium gets to distal tubule therefore limited capacity for potassium xcretion = severe hyperalaemia in acute kidney injury

19
Q

Metabolic acidosis:

A

Kidney is required to excrete more H+ - less capacity for K= excretion as H+ being excreted in lieu of potassium. Hyperkalaemia in these patients.

20
Q

Potassium depleted –

A

Hypokalaemia alkalosis With an increased plasma bicarb concentration.
→ Reduction in intracellular potassium. Less potassium needing to be excreted. Potassium depletion there is enhanced H+ loss.
Also bicarb generation produced.

21
Q

Catecholamine effect on potassium/hydrogen

A

Salbutamol to treat hyperkalaemia as it stimulates Potassium excretion.

22
Q

Insulin →

A

diabetic ketoacidosis: one effects after treatment (as normal high potassium with acidosis observed rapid reduction in plasma potassium.

23
Q

Re-feeding syndrome –

A

redistribution of electrolytes post starving and start eating. When carbohydrate delivered exaggerated insulin and catecholamines (stress) response and get redistribution of potassium magnesium etc.
→ If a patient has not had a normal diet for +10 days feeding must be at a low dose. Monitor carefully.

24
Q

Causes of Hypokalaemia

A

Renal Loss

Extra-renal loss

25
Q

Renal loss hypokalameia

A
Alkalosis – favours potassium loss in kidney.
Drugs – diuretics (thiazides and loop)
Mineralcorticoid excess
•	1o hyperaldosteronism
•	2o hyperaldosteronism
•	Cushing’s syndrome
•	Ectopic ACTH
Renal disease
•	Renal tubular acidosis
•	Interstitial nephritis
•	Polyuric ATH
Miscellaneous
•	Hypomagnesaemia
•	Hypercalcaemia
26
Q

Extra-renal loss hypokalaemia

A
GI loss
•	Diarrhoea
•	Villous adenoma (sigmoid)
•	Pancreatic fistula
EC to IC shift
•	Insulin
•	Catecholamines
•	Refeeding syndrome
Inadequate intake
•	Alcoholism
•	Anorexia nervosa
27
Q

Alkalosis

A

Reciprocal relation with potassium nd hydrogen
Alkalosis – favours potassium loss
Acidosis – inhibits potassium loss (getting rid of H+ ions)

Hypokalaemia – may causes alkalosis

28
Q

Diuretics

A

Most common cause
Block sodium reabsorption and therefore increased water loss.
Work in first half of nephron – causes increased delivery of sodium to distal nephron. So more sodium being reabsorb and encourages/enhances potassium/hydroden loss
→Hypokalaemia alkalosis

29
Q

Mineralcorticoid excess

A

Driving Sodium reabsorption
Hall mark of primary aldosteronism – hypokalaemia
Clinical picture → Resistant hypertension with low potassium (unless diuretics causing it) - suspicious for conn’s syndrome.

30
Q

Cushing’s

A

Excess cortisol – glucocorticoids. Sufficiently high levels of cortisol leading to cross reactivity.

31
Q

Ectopic ACTH

A

Stimulates adrenal gland.
Biochemical pattern just like conn’s syndrome. But aldostere is normal.
Treat people with a longtime
Case:28:00 mins re-listen.
→ Hypokalaemia alkalosis often with a relatively high sodium

32
Q

Renal tubular disease

A

Renal tubular acidosis → acidosis of renal tubular origin. The defect in the ability of the kidney to excrete hydrogen ions. Therefore the kidney favours potassium loss in exchange of sodium.
Proximal tubule dysfunction – loss of potassium as failure to reabsorb.

33
Q

Hypomagnesium

A

Magnesium is a vital cofactor with ATP. So with magnesium depletion ATP cant work and cant fuel pump/receptor mechanisms. Therefore if leakage of Potassium out of cells and leaking out of kidney because pumps not working.
Causes of low magnesium
 Gut → diarrhoea
 Renal tubular toxicity (platinum chemo drugs)
 Sigmoid adenoma
Exocrine pancreatic fistula (electrolyte rich loss in intestine) – bicarb rich also. Acidosis with a low potassium Hypokalaemia with low bicarb (atypical but points towards these causes)

34
Q

Anorexia Nervosa

A

Potassium intake low

Vomiting

35
Q

Acidosis with low potassium →

A
Hypokalaemia with low bicarb – atypical (gastrointestinal loss) or renal tubular acidosis.
•	Diarrhoea
•	Villous adenoma (sigmoid)
•	Pancreatic fistula
•	Renal tubular acidosis
36
Q

Clinical Features of Hypokalaemia →

A
  1. Muscle weakness/ hypotonia
  2. Paralytic ileus
  3. Exacerbation of hepatic encephalopathy
  4. Enhanced sensitivity to digoxin
  5. Polyuria (renal tubular vacuolation)
  6. Cardiac dysrhythmias
37
Q

Cardiac dysrhythmias in hypokalaemia

A

a. Low T wave
b. ST segment depression (pathopneumonic)
c. Prominent U waves (pathopneumonic)
d. Wide OT interval

38
Q

Causes of Hyperkalaemia →

A

Renal Cause

Extra-renal cause

39
Q

Renal Cause

A
Renal Failure
•	Acute
•	End-stage chronic
Drugs
•	Potassium-sparing diuretics
→ Amiloride
→ Spironolacetone
•	ACE inhibitors

Mineralocorticoid deficiency
• Addison’s disease
• Hyporeninaemia hypoaldosteronism

40
Q

Extra-renal cause hyperkalaemia

A
Pseudohyperkalaemia
•	Haemolysis – blood sample
•	Leukocytosis – WCC/platelets release more potassium
•	Thrombocytosis
Increased potassium input
•	Exogenous
•	Endogenous
→ Tissue necrosis
             → Haemolysis
             →  Malignancy
              → Chemotherapy

IC to EC shift
 Acidosis
 Hypoxia
 Insulin deficiency

41
Q

Renal Failure

A

If potassium is above 6/rising rapidly concenring feature for cardiac problems.

42
Q

Chronic renal failure

A

Potassium usually normal until late

43
Q

Spironolacetone

A

Blocks Potassium excretion in distal tubule via blocking Na-K channel.

44
Q

ACE inhibitors and angtiotensin II blockers

A

If a patient has renal artery stenosis. Relying on high renin levels to drive function of kidney. If you suddenly inhibit that system. Causes an acute rise in potassium.

45
Q

Pseudo Hypokalaemia

A

Artefact. Traumatise blood cells e.h. haemolyses blood samples.

46
Q

Leukocytosis

A

High WCC/Platelets release potassium more than normal. Always check FBC with unexplained hyperpotassium.

47
Q

Malignancy

A

Large amount of tissue being killed by chemo – tumourlysis (rapid release of potassium).

48
Q

Hypoxia

A

Can operate sodium/potassium pump

49
Q

Insulin deficiency

A

Results in deficient uptake of NA (DKA)

50
Q

Clinical Features of Hyperkalaemia →

A

Tall peaked tented T waves [T wave larger than R wave in more than 1 lead]

Prolonged PR interval
Flattened or about P waves

Widened QRS [greater than 0.12 seconds]
Sine wave pattern (S and T waves merging)
Bradycardia
Ventricular tachycardia

51
Q

Treatment hyperkalaemia

A
Calcium Gluconate
Salbutamol
Insulin + 50% dextrose
Na HCO3 (not used_
Calcium resonium
Haemofiltration or Dialysis
52
Q

Hypokalaemia treatment

A

Oral

Intravenous

53
Q

Oral treatment

A

Sando-K
Bananas
Tomato juice

54
Q

Intravenous

A

a. Only if oral supplementation impossible
b. Concentration less than 40 mmol/L (peripherally)
c. Rate less than 20 mmol/h
d. Frequent monitoring of serum potassium concentration
e. Consider ECG monitoring

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