K & Mg physiology Flashcards

1
Q

role of Mg

A
  • bone formation
  • enzyme co-factor = ATP metabolism, muscle contraction/relaxation, neurological function
  • regulation of vascular tone
  • cardiac rhythm
  • platelet activation
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2
Q

Mg reabsorption

A

glomerulus
- freely filtered
proximal tubule
- 15% reabsorption
Loop of Henle
- 70% reabsorption in thick ascending limb
- paracellular channel formed by claudin
Distal tubule
- 10% reabsorption
- by transient receptor potential channels (TRPC6)
- mutations give hypomagnesaemia & hypercalcaemia

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3
Q

Assessing Mg

A
  • serum Mg
  • red cell Mg
  • 24 hour excretion
  • Mg retention test
  • isotope analysis
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4
Q

causes of hypomagnesemia

A
  1. decreased dietary intake
  2. GI malabsorption
  3. endocrine (hyperaldosterone, SIADH)
  4. renal loss (congenital, drug-induced)
    - proton pump inhibits, amphotericin B
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5
Q

symptoms of hypomagnesemia

A
  • weakness, fatigue
  • fasciculations, cramps, tetany
  • numbness
  • seizures
  • arrhythmias
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6
Q

treatment for hypomagnesemia

A
  • oral (most cases)

- IV magnesium sulphate

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7
Q

hypermagnesaemia

A
  • less common
  • cause = excessive oral administration of Mg / Mg-containing drugs (in GORD drugs)
    - advanced CKD possible, less common
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8
Q

homeostasis of K

A
  • initial changes buffered by movement in/out of skeletal m (regulated by insulin, catecholamines)
  • hyperglycemia & acidosis cause K efflux from cell
  • serum K affected by intake, losses, redistribution from ECF/cells
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9
Q

K reabsorption

A

glomerulus
- freely filtered

proximal tubule

- 60% reabsorption
- passive paracellular movement with water (due to Na/K exchanger)

Loop of Henle

- 30% reabsorption in thick ascending limb
- active reabsorption by NKCC2 channel
- ROMK channel & Na/K/ATPase also involved 

Distal tubule & CD

- variable reabsorption/secertion
- influenced by aldosterone, angiotensin
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10
Q

hypokalaemia and its symptoms

A
  • serum K <3.5mmol/L

- symptoms = muscle weakness, paralysis, cramps, cardiac conduction abnormalities, constipation

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11
Q

causes of hypokalaemia

A

GI loss
-vomiting, diarrhea, laxatives, ileostomy

renal loss

  • hyperaldosterone
  • diuretics (e.g. loop diuretics - furosemide)
  • renal tubular acidosis
  • liquorice (produces enzymes w/ aldosterone-like effect)
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12
Q

treatment for hypokalaemia

A
  • treat underlying cause
  • mild hypokalemia (3-3.5) = use oral K
  • sever (<3) = use IV replacement
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13
Q

hyperkalemia and its symptoms

A
  • serum K > 5mmol/L
  • symptoms = fatigue, weakness, paresthesia, nausea, vomiting, dyspnoea, palpitations
  • pseudo-hyperkalemia = breakdown of RBCs in sample raises K
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14
Q

causes of hyperkalemia

A
  • increased intake (usually in kidney disease)
  • disruption of cell intake
    - acidosis
    - beta blockers
    - rhabdomyolysis
  • decreased excretion
    - renal failure
    - hypoaldosteronism (spironolactone)
    - drugs = ACEi, AIIA
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15
Q

Addison’s disease

A
  • deficient adrenal cortex hormones (aldosterone, cortisol)
  • gives characteristic hyper-pigmentation (excessive ACTH & MSH production)
  • lethargy, weakness, weight loss, low BP
  • electrolytes = low Na, high K
  • diagnosis by synacthen test
  • treated w/ synthetic hormones (e.g. dexamethasone)
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16
Q

ECG changes with hyperkalemia

A
  • prolonged PR, wide QRS

- progressing to peaked T waves, loss of QRS complex -> VF

17
Q

treatment for hyperkalemia (if abnormal ECG)

A

short term = drive K into cells to stabilise AP:

  • IV Ca
  • salbutamol nebuliser
  • insulin w/ dextrose

after that:

  • reduce K absorption
  • increase elimination (K losing diuretics e.g. furosemide, dialysis)

fix underlying problem
- acidosis = give oral bicarbonate tablets or IV in emergency