H, K, Ca & Mg Flashcards

1
Q

Why does the kidney try to conserve all/generate excess bicarb?

A

For every bicarb lost in urine an H+ is generated

Therefore need to re-absorb all bicarb before we can excrete excess H+

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2
Q

Acidosis and alkalosis, which can we withstand better?

A

Alkalosis

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3
Q

The pH is 6.7 at the end of the PCT, why?

A

Re-absorption of bicarb

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4
Q

The pH in the CD can vary between 4.5-8, why such a large range?

A

pH will reflex how much acid needed to maintain serum pH

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5
Q

How is the acid-base balance effected in vomiting?

A

Loss of H+

Loss of K+

Metabolic alkalosis

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6
Q

How is the acid-base balance effected in diarrhoea?

A

Loss of K+

Loss of bicarb

Metabolic acidosis

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7
Q

K+ intake from food (and therefore serum levels) can be quite high, how is death prevented?

A

K+ uptake into cells (quick)

K+ excretion in urine (6-8hrs)

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8
Q

What 3 things increase the activity of Na/K ATPase? (Decreasing extracellular [K])

A

K+ conc in plasma

Insulin

Noradrenaline effect on beta2-adrenoceptors

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9
Q

How is K+ excreted?

A

Small amounts in faeces and sweat

800 mmol by normal kidneys

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10
Q

What factors increase K+ secretion?

A

Increased intracellular [K+] = larger gradient (raised by aldosterone)

Increased electro-ve lumen = large pull for K+ (raised by aldosterone)

Increased permeability of the luminal mem (raised by aldosterone)

Decreased luminal [K+]

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11
Q

What is hypokalaemias effect on membrane potential?

A

Bigger gradient between intracellular and extracellular compartment

Depolarisation lead to increased excitability

Risk of arrhythmias

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12
Q

What is hyperkalaemias effect on membrane potential?

A

Smaller gradient between intracellular and extracellular compartment

Decreased membrane excitability

Risk of cardiac arrhythmias

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13
Q

Outline the symptoms of hypokalaemia

A

Weakness

Polyuria = low K causes ADH resistance

Constipation = smooth muscle dysfunction

Arrhythmias

U wave on ECG

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14
Q

What are the causes of hypokalaemia?

A

Reduced dietary intake

Increased entry into cells = met alkalosis, increased beta-adrenergic activity

Increased GI loss = vomiting, diarrhoea

Increased urine loss = increased aldosterone, increased urine flow, renal tubular acidosis

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15
Q

Ca reabsorption is under what kind of control?

A

Hormonal and vitD

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16
Q

What inhibits the precipitation of Ca and therefore the formation of stones?

A

Magnesium

17
Q

What happens in the presence to hypercalcaemia?

A

Activation of Ca sensing receptors

Decreased PTH and increased calcitonin release =
1) increased renal excretion

2) less active vit D = decreased calcitriol synthesis = decreased mobilisation of Ca from skeleton and soft tissues

= normal plasma Ca

18
Q

What happens in the presence of hypocalcaemia?

A

Inactivation of Ca sensing receptors

Increased in PTH release =

1) decreased in renal excretion
2) more active vit D = increase in calcitriol synthesis = increased mobilisation of Ca from skeleton and soft tissue

= normal plasma Ca

19
Q

What part of the tubules is under PTH and vit D control?

A

DCT

20
Q

What are the symptoms of hypocalcaemia?

A

Paraesthesia = pins and needles

Tetany

Laryngospasm

Reduced myocardial contractility

Memory loss

Confusion

Hallucination

21
Q

Outline the causes of hypocalcaemia?

A

Vit D def

Lack of PTH

Reduced intake

Malabsorption

Hypomagneasaemia = interferes with PTH

22
Q

Outline the functions of magnesium

A

Intracellular signalling

Cofactor for protein and DNS synthesis

Control of neural activity in the brain

Cardiac excitability

Neuromuscular transmission

Osteoblast proliferation and bone strength

23
Q

In the tubule where does the majority of magnesium reabsorption take place?

A

TAL 50-70%

24
Q

Name some causes of hypomagnesaemia

A

Malnutrition

Prolonged fasting

IV feeding

Loop diuretics

Thiazide diuretics

25
Q

What symptoms occur with hypomagnesaemia?

A

Fatigue

Muscle spasms

Anxiety

Headache

Cardiac dysrhythmias

Tetany

Seizures

Hypocalaemia