Chem Path: Potassium and electrolytes Flashcards

1
Q

What is the serum level for K+

A

3.5 to 5

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2
Q

Explain how the RAAS system works

A

Low perfusion pressure or low serum sodium triggers renin release from JGA, which in turn converts angiotensinogen from the liver to angio 1, which is converted to angio 2 in the lungs via ACE. This triggers aldosterone release from the adrenals

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3
Q

What does aldosterone do

A

Increased Na channels in the kidneys to reabsorb water and Na and excrete K via ROMK channels

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4
Q

What receptor does aldosterone work on

A

Mineralocortocid receptor

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5
Q

How can you classify the reasons for hyperK

A
Renal
Reduced Renin
Drugs
Cellular secretion 
Low aldosterone
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6
Q

Explain the renal causes of hyperK

A

Due to low egfr (low gradient between efferent and afferent), there is need to increase the gradient between the afferent and efferent arterioles. Therefore, you need to dilate afferent. This is done by reducing the angio 2 as it is a vasoconstrictor.

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7
Q

Why can you have reduced renin?

A

Type 4 renal tubular acidosis seen in diabetic nephropathy

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8
Q

Name which drugs can cause hyperK

A

NSAIDS, ACEi, ARB, Aldosterone antagonists

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9
Q

How does NSAID cause it

A

Chronic NSAID use reduces renin and aldosterone

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10
Q

Name some ACEi

A

Ramipril and lisinopril

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11
Q

Name some ARBs

A

Losartan and candesartan

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12
Q

Name some aldosterone rec blockers

A

Spironolactone

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13
Q

What causes low aldosterone?

A

Addison’s

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14
Q

How does Addison’s present in terms of symptoms?

A

Dizziness and nausea, tanned and postural hypotension

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15
Q

How is Addisons diagnosed

A

Short synthacten test

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16
Q

How is Addisons treated?

A

Hydrocortisone and fludrocortisone

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17
Q

When is K released from cells?

A

Rhabdomyosis and in acidotic states

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18
Q

What are the ecg changes you can see in hyperK

A

Peaked T waves

19
Q

How is hyperK managed?

A

First, 10ml 10% calcium gluconate. Next 100ml 20% dextrose with 10 units of insulin and insulin drives K+ into cells. Next nebulised salbutamol. Treat underlying cause

20
Q

What are the causes of hypoK+

A
GI Loss due to D&V
Renal
Cells (HypoMg and alkalosis)
Excess cortisol 
Thiazide and loop diuretics
21
Q

Which drugs cause hypoK

A

Thiazide diuretics and loop diuretics

22
Q

How do the diuretics cause hypoK?

A

Prevents reabsorption of Na at the loop, therefor more Na reaches the distal nephron, this means more Na is crossing the channels, and more K+ is being lost.

23
Q

What are the 2 syndromes that also prevent Na reabsorption at the loop?

A

Gitelman and Bartter

24
Q

How does excess cortisol cause hypoK

A

It binds to the MR receptors, mimicing aldosterone

25
Q

What are the cellular/metabolic causes of hypo K

A

Alkalosis and hypoMg

26
Q

Symptoms of hypoK+

A

Muscle weakness, cardiac arryhtmias, polyurea and polkydipsia

27
Q

What are the ecg changes of hypoK

A

U waves, torsades de pointes and increased risk of VT

28
Q

Why is there polyurea and polydipsia?

A

HypoK can cause nephrogenic DI due to resistance to ADH

29
Q

How to test for hypoK with hypertension

A

Aldosterone:renin ratio

30
Q

How to manage hypoK?

A

Depends on K+ levels,

If between 3 and 3.5 - PO KCL (2 sandoK tables TDS for 48 hours)

If less than 3 - IV KCL max 10mmol per hour

31
Q

How do you manage hypovolaemic hypoNa

A

Volume replacement with 0.9% saline

32
Q

What are the features of hypervolaemia

A

Raised JVP, odoema

33
Q

What can cause hypervolaemia?

A

Heart failure, nephrotic syndrome, cirrhosis

34
Q

Why does heart failure cause low Na?

A

In HF there is low CO, so BP is low, this stimulates osmorecetpors which in turn increases ADH production, which retains more water

35
Q

How do you manage hypercvolaemia?

A

Fluid restrict

36
Q

How does cirrhosis cause hypervolaemia?

A

In cirrhosis, there is vasodilation due to disrupted NO action escpecially in the splachnic circulation. So BP drops and the osmoreceptors cause ADH release.

37
Q

What can cause SIADH?

A

Lung cancer releasing ADH

38
Q

How do you diagnose SIADH and what are the parameters?

A

Measure plasma and urine osmolality. There will be reduced plasma osmolality and increased urine osmolality

39
Q

What do you do before diagnosing SIADH?

A

Rule out hypovolaemia, hypothyroid and adrenal insufficiency (check cortisol)

40
Q

What drugs can cause SIADH

A

SSRIs, TCA, opiates, PPIs, carbamazepine

41
Q

What are features of central DI

A

Polyuria, polydipsia and may have bitemporal hemianopia

42
Q

How is DI diagnosed?

A

High plasma osmolality and reduced urine osmolality (opposite to SIADH)

43
Q

What would you exclude before DI?

A

Diabetes, hypoK, hyperCa,