electrolytes Flashcards

(26 cards)

1
Q

hypomagnesia

A

causes arrythmias icn risk of torsdade de pointes
neurological symptoms
more excitable nervous system as calcium

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2
Q

what do we give in hyper magnesium

A

ca gluconate

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3
Q

whats included in a bone profile l

A

ca
phosphate
ALP
albumin

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4
Q

tx for hypocalcemia

A

aggressive fluid resuscitation and if refractory then biphosphanates

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5
Q

why would yo order a bone profile test

A

if you suspect bony pathology

osteoporosis
osteomalacia
pagets disease
metastasis

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6
Q

primary hyperparathyroid

A

Primary hyperparathyroidism is when there’s a problem within the parathyroid gland itself, usually a benign (non-cancerous) tumour of the gland.

So causes high levels of calcium in blood and pee
Reciprocal with phosphate

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7
Q

secondary hyperpathyroidism(table)

A

Key word here is REACtIVe
Secondary hyperparathyroidism is when the glands are fine but a condition, like kidney failure, or low vit d lowers calcium levels and causes the body to react by producing extra parathyroid hormone.

Calcium levels can be normal or low

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8
Q

tertiary hyperparathyroidism

A

ertiary hyperparathyroidism is when long-standing secondary hyperparathyroidism starts to behave like primary hyperparathyroidism. often associated with kidney failure

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9
Q

whats an important complication of hypercalcemia

A

pancreatitis (qute rare and the mechanism is not well understaoon)

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10
Q

symproms of hyper calcemia

A

stones : kidney damage
bones -pathological fractures
psychiatric moans- mood
groans - kidney stones, pancreatitis and constipation

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11
Q

hypocalcemia signs and treatment

A

muscle weakness/cramps
tetany
perioral anesthesia

orally like calcichew
iv - calcium gluconate

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12
Q

ALP marker is a sign of

A

cholestasis or bone disease or liver

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13
Q

so how would you tell the difference between cholsetatis or bone disease in reference to ALP

A

do a GGT, if thats raise most likely liver

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14
Q

An ALP rise with normal GGT suggests increased bone turnover
An ALP rise with associated GGT rise is more suggestive of cholestasis

A
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15
Q

causes of isolated ALP (normal GGT)

A

healing bone fracturs
pagets disease
metasisis

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16
Q

causes of Paget disease

A

osteoclasts are overactive

17
Q

what can casue hyperkalemia

A
  1. medications like ace inhibitors and ARBS
  2. taking too many k +sparing diuertics like spironotone
  3. CKD
  4. a lack of aldosterone(mineralcorticoid ) addisons
  5. over supplementation
18
Q

with hyperkalemia what could the heart rate be

19
Q

what drugs can cause low sodium

A

dieretics
thiazides
carbamazepine is a well known cause
antidepressants- SSRIS(sertraline, escitalopram, fluoxetine) - cause the brain to release ADH esp in the first few months

20
Q

euvolaemic hyponatraemia

A

more dilutional in nature so actual sodium is normal but appears less

21
Q

what blood tests to order for low sodium

A

TSH - test for hypothryoidsim
CORTISOL - test for addiosns

22
Q

After how much non-responsive fluid resuscitation should a patient be considered fluid unresponsive?

23
Q

What is the expect pattern of serum and urine osmolalities is seen in SIADH?

A

urine osmolitiy will be high - very concentrated (think desert)

serum will be low

24
Q

How is hyponatraemia treated in the emergency setting?

A

IV 3% saline in a critical care setting

25
What are the treatment options for SIADH?
Fluid restriction ADH receptor antagonists (e.g. tolvaptan, deomeclocycline) Oral sodium and furosemide
26
signs of hyponatremia
vomiting headaches muscle weakness seizures coma arrythmias confusion