Renal physiology - magnesium and potassium Flashcards

1
Q

Magnesium

  • how is it absorbed?
  • where is it absorbed?
A

is often bound to water, cannot get it absorbed without removing it from water first

  • and is hard to get intracellular absorption
  • it is absorbed in the thick ascnedign limb of loop of henle after water is absorbed from descending limb - increases conc of electrolytes
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2
Q

Hypomagnesimia

A
  • Can occur in some of the transporters for magneisium in kidney so dont get reabsorpition
  • present in childhood
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3
Q

How to test this?

A
  • serum Mg
  • red cell Mg
  • 24 hour excretion
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4
Q

Causes of hypomagneisa

A
  • decreased dietary intake
  • GI malabsorption and loss
  • endocrine - hyperaldosterronism , SIADH
  • renal loss - congential, aquired, drug
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5
Q

Symptoms of hypomagnesia

and treatment

A
  • weakness and fatigue
  • teetany
  • seizures, arrhythmias

-IV - magensium sulphate

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6
Q

Hypermagnesaemia

A

in advanced CKD - the compensatory mechanism start to become inadequate and hypermagnesaemia may develop
-excessive oral administration of magnesium salts or magnesium containing drugs

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7
Q

Initial changes in potassium into extracellular compartment

A

-extracellular K are initially buffered by movement of K into or out of skeletal muscle regulated by insulin and catecholamines

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8
Q

Hyperglycaemia what can this do to potassium

A

-can lead to K efflux from the cell

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9
Q

Acidosis and alkalosis on potassium

A
  • acidosis can drive K effulux (hydrogen will be pushed into cells and K out)
  • alkalosis - (H will be pushed out of cells and K will go in)
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10
Q

How is it absorbed

A

active reabsoprtion of potassium with sodium potassium chloride channel

  • also has aROMK channel
  • also a sodium potassium atapse pump
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11
Q

Aldosterone

A

-works on principle cells in the distal tubule and collecting duct
will increase absorption of sodium and increase secretion of potassium via sodium ptoassium atpase
-is stimulated by having increased potassium or by angiotensin 2 due to reduced extracellular volume

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12
Q

Hypokalaemia

A
-muscle weakness
paralysis
cardiac conduction abnormalities
cramps 
constipation 

K loses
Renal - hyperaldosteronism (aldosterone secreting turour) , liquorice, diuretics (some cause increase K some caused decreased) , renal tubular acidosis

Gut
-vomiting, diarrhoea, laxatinves, ileostomy

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13
Q

Conns syndrome

A
  • adrenal adenoma
  • secretes aldosterone
  • hypertension
  • hypokalaemia
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14
Q

Licorice

A

contains glycyrrhizin, acts like aldosterone by activiating mineralcorticoid receptors in the kdiney

  • results in hypokalaemia and HTN
  • psudohyperaldosteronism
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15
Q

Sprinolactone

A
  • mineralocorticoid antagonist (stops action of aldosterone)
  • will reduce amount of sodium absorption and result in a decrease in potassium secretion
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16
Q

Treatment

A
  • treat underlying problme
  • oral tablets
  • sever - IV replacement
17
Q

Hyperkalemia

A

-symptoms - fatigue or weakness
parasthesia, nausea or vomitign, palpatatiosn
-can get ventricular fibrilaiton and cardiac arrest

Causes - ncrease intake
disruption of cell intake - beta blockers, acidosis

Decrease exceriton - renal failure, hypoaldosternoism, ACEi/arb

-adisons disease

18
Q

psuedo-hyperkalemia

A

-can get false result due to haemolysed sample

19
Q

Addisons disease

A

Deficient secretion of adrenocortical hormones - aldosterone and cortisol

  • tanned skin appearance
  • symptoms- lethargy, waekness, weight loss, low BP
  • hyperkalaemia, hyponatraemia
  • can get VF

Treatment - stabilise AP

  • push K into cells
  • reduce K absorption
  • increase elemination
  • fix underlying problem
20
Q

Treatment for hyperkalemia resutling in VF

A
  • IV calcium can stabilise the AP
  • want reduced potassium absorption , increase elemination , fix underlying probleme
  • can give insulin - drive potassium to get into cells (also give dextrose so dont make patient hypoglyacemic)
  • treat acidosi s- bicarbonate
  • can give somethign to bidn to K so get more elimination