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MBCHB3 RBF > Lecture 21: Mg and K > Flashcards

Lecture 21: Mg and K Flashcards

1
Q

Describe the distribution of Mg:

A
  • ECF contains 1%
  • Mostly in Bone, muscle and soft tissue
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2
Q

What is the role of Mg in the bodies physiology?

A
  • Bone formation
  • Cofactor for many enzymatic reactions
  • Regulation of vascular tone
  • Cardiac rhythm
  • Platelet activated thrombosis
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3
Q

Whats the role of the kidneys in Mg regulation?

A
  • Serum Mg is controlled by renal excretion
  • 95% reabsorbed ~5% secreted - throughout the kidney but mainly the ascending LOH (usually paracellularly) DCT has transporter.
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4
Q

How do you assess Mg status?

A
  • Serum Mg (poor indicator of upstream stores)
  • Red cell Mg
  • 24hr excretion
  • Mg retention test
  • Isotope analysis
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5
Q

What are the causes of hypomagnesamia?

A

1) Decrease diet
2) Gi malsorption or loss
3) Endocrine - Hypoaldosteroneism, DM, SIADH
4) Renal loss

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6
Q

What drugs can induce renal loss of Mg?

A
  • Aminoglycosides
  • Omeprazole
  • Pentamidine
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7
Q

What are the Sx of hypomagnesaemia?

A
  • Weakness and fatigue
  • Fasciculations/cramps
  • Tetany
  • Seizures
  • Arrhythmias
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8
Q

How do you treat hypomagnesium?

A
  • Oral tabs
  • Could use IV
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9
Q

When is hypermagnesaemia seen?

A

Rare

  • CKD compensatory mechanisms fail might cause it
  • Addisons or hypothyroidism
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10
Q

Sx of hypermagnesium?

A
  • Hypotension
  • Cutaneous flushing
  • N&V
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11
Q

Describe the normal K levels in the body:

A

3.5->5.0mmol/L in plasma

ICF ~150mmol.L

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12
Q

What does daily K homeostasis rely on?

A

Daily K oral intake, most of which is excreted in the kidneys

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13
Q

Describe the internal balance of K:

A

Initial changes in ECF K are intially buffered by movement of K into or out of skeletal muscle regulated by insulin and catecholamines.

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14
Q

Describe how tonicity influences K:

A

Hyperglyceamia will lead to a K efflux from the cell.

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15
Q

Describe how pH influences K:

A
  • Acidosis can also drive K efflux
  • Alkalosis will lead to K influx
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16
Q

Where is K reabsorbed? and secreted

A
  • 60% PCT (Paracellular)
  • 30% Asc. LoH (Paracellular) but ROMK also pumping it out.
  • Aldo promotes Na/KATPase, K in cell is secreted) (and ENAC for Na reabsorption)
17
Q

What affects serum K?

A
  • K intake
  • K losses
  • K redistributed from ECF in/out of cells
18
Q

What are the Sx of hypokalaemia?

A

Serum <3.5mmol

  • Muscle weakness if not paralysis
  • Cramps
  • Constipation
  • Cardiac conduction abnormalities
19
Q

What is hypokalaemic periodic paralysis?

A
  • Autosomal dominant or thyrotoxic
  • Abnormal K channels on cell membrane
  • High carb meal (Inuslin) or SNS activation i.e exercise or anxiety
    = Excessive movement of K into cells = extreme weakness
20
Q

What are the causes of K loss?

A

Renal:
- Hyperaldosteronism (tumor)
- Licorice
- Diuretics that arent K sparring
- Renal tubular acidosis

Gut
- V&D
- Laxitives
- Ileostomy

21
Q

Whats conns syndrome?

A

Adrenal adenoma
- Secretes aldosterone
Presents with:
- Hypertension
- Hypokalaemia

22
Q

How does licorice cause hypokalaemia?

A

Acts on mineralcorticoids receptor = psuedohyperaldosteroneism

23
Q

Which diuretics influence K?

A

PCT: Mannitol
Asc LOH: Fruosemide
DCT: Metolozone
CD: Spironolactone or amiloride

24
Q

How is hypokalaemia treated?

A
  • Treat the underlying problem
  • Use oral K for mild and IV for severe
25
Q

What are the Sx of hyperkalaemia?

A

K > 5.2mmol/L

Symptoms
- Fatigue or weakness
- Paraesthesia
- Nausea and vomiting
- Dyspnoea
- Palpitations

26
Q

What is the risk of hyperkalaemia?

A

Ventricular fibrillation and cardiac arrest

Prolonged P-P

27
Q

What can cause psuedohyperkalamia?

A

When a lab sample is heamolysed

28
Q

What are the causes of hyperkalaemia?

A

Increased intake

Disruption of cell intake
- Beta blockers
- Acidosis
- Rhabdomyolysis

Decreased excretion
- Renal failure
- Hypoaldosteronism
- ACEi/ARB

29
Q

Whats happening in addisons?

A
  • Deficient secretion of aldosterone and cortisol

Bronzed because heightened ACTH causes melanocyte sitmulation

30
Q

How is addisons diagnosed and treated?

A

Lab: Hyperkalaemia, Hyponatrreamia

Diagosis: Short synacthen test

Treated: Dexamethasone, fludrocortisone

31
Q

How is hyperkalaemia treated?

VIP

A
  • Stabilise AP
  • Push K into cells (beta agonists or insulin (need dextrose too)
  • Reduce K absorption (Cation exchange i.e Ca resonium binds K in gut and eliminates)
  • Treat acidosis (Bicarb)
  • Increase elimination (K losing diuretic or dialysis)
  • Fix underlying casues
32
Q

How is the AP stabilised?

A
  • Ca stabilises AP
  • Normalises membrane excitability
  • Lasts 30 mins
  • Prevents cardiac arrest while you sort the rest out
33
Q

What are the cells of the kidney mainly involved with K secretion?

A

Principle (ROMK) and intercalated cells (K/H exchanger)

MBCHB3 RBF (39 decks)

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