Lecture 18 - Renal Physiology: Potassium & Magnesium Flashcards

1
Q

Key roles of the kidney?

A

elimination of waste products, control of fluid balance, control of minerals, regulate acid-base balance, produce hormones

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2
Q

Mg Physiology?

A

bone formation, cofactor in copious amounts of reactions, regulation of vascular tone, cardiac rhythm, platelet-activated thrombosis

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3
Q

Mg Absorption?

A

10-20% PCT, 60-70% thich ascending LoH, 10% DCT

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4
Q

Mg reabsorption - LoH?

A

active transport through Claudin 16-19 receptors

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5
Q

Assessments of Mg?

A

serum Mg, red cell Mg, 24hr excretion, Mg retention test, isotope analysis

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6
Q

Symptom of hypomagnesaemia?

A

fatigue, cramps, tetany spasm, numbness, seizures, arrhythmias

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7
Q

Causes of hypomagnesaemia?

A

common condition; diet, malabsorption and loss, hyperaldosteronism, diabetes, SIADH, renal loss

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8
Q

Hypomagnesaemia treatment?

A

typically oral magnesium, otherwise IV magnesium sulphate

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9
Q

Causes of hypermagnesaemia?

A

advanced CKD, excessive magnesium salt or drugs, Iatrogenic

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10
Q

Internal balance of K?

A

buffered by movement of K into or out of skeletal muscles regulated by insulin and catecholamines

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11
Q

pH and K?

A

acidosis leads to K efflux (as well as hyperglycaemia), alkalosis vice versa

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12
Q

K reabsorption?

A

60% PCT, 30% thick ascending LoH, variable in collecting ducts

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13
Q

Symptoms of hypokalaemia?

A

muscle weakness, paralysis, cardiac conduction abnormalities, cramps, constipation

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14
Q

Hypokalaemic Periodic Paralysis?

A

inherited (rare) or thyrotoxic origin, abnormal K channels, triggered by high carbs (insulin) or SNS activation (stress), excessive K influx -> weakness

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15
Q

K losses - renal?

A

hyperaldosteronism, licorice, diuretics, renal tubular acidosis

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16
Q

K losses - gut?

A

vomiting, diarrhoea, laxatives, ileostomy

17
Q

Conns syndrome?

A

adrenal adenoma, secretes aldosterone -> hypertension and hyperkalaemia

18
Q

Symptoms of hyperkalaemia?

A

fatigue, paraesthesia, nausea, dyspnoea, palpitations

19
Q

Heart attack?

A

hyperkalaemia -> ventricular fibrillation -> cardiac arrest

20
Q

Psuedohyperkalaemia?

A

caused by haemolysis

21
Q

Causes of hyperkalaemia?

A

increased intake, disruption of cell intake (beta blockers, acidosis), decreased excretion (renal failure, hypoaldosteronism)

22
Q

Addison’s disease?

A

deficient secretion of aldosterone and cortisol, hyperpigmentation due to excessive ACTH excretion stimulating melanocytes, symptoms: lethargy, weakness, weight loss, hypotension

23
Q

Addison’s - diagnosis and treatment?

A

hyperkalaemia, hyponatraemia; use of short synacthen test; treatment: dexamethasome or fludrocortisone

24
Q

Treatment of hyperkalaemic MI?

A

stabilise AP, push K into cells, reduce K reabsorption, increase elimination, fix underlying problem

25
Q

Stabilising AP?

A

calcium, normalises membrane excitability, lasts 30min, prolongs cardiac arrest

26
Q

Beta agonists?

A

ventolin nebuliser, reduces K via influx, 30-60min to work, lasts 6 hr (combine w insulin w dextrose)

27
Q

Treating acidosis?

A

oral bicarbonate (IV if emergency)

28
Q

Reducing K absorption?

A

cation exchange products, calcium resonium

29
Q

Increasing K elimination?

A

K losing diuretic, or dialysis if already dialysis patient or Rhabdomyolysis