Electrolyes Flashcards by Jen Gaffney

Treatment of SIADH

Demeclocycline
TolvAptan
Conivaptan
Lithium
Urea

Vaptans are V2 receptor antagonists
- specific and work reliably

Demeclocycline and lithium both cause nephrogenic DI, but take several days to be effective

Urea causes an osmotic diuresis and enhances water excretion

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Na corrected for glucose

Correct na = na + BSL/3

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Na deficit equation

Na deficit = 0.6x body wt x (desired na - current na)

Women - 0.5

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Causes of SIADH

Neoplastic - SCLC, mesothelioma, sarcoma, leukaemia, lymphoma, pancreas, bladder, prostate

Pulmonary - infection, asthma, CF

CNS - infections, sah, subdue all, CVA, TBI, MS, GBS

Drugs - vasopressin, deamopressin, oxytocin
SSRI, TCA, NSAIDs, opioids, anticonvulsants, PPI, amioderone

Other - post surgical stress response

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Adverse effects of hypertonic Saline

Hyperosmolality
Overshoot Na
CCF and pull oedema
Low K
NAGMA
Phlebitis
Coagulopathy
Renal failure
Reduced LOC
rebound increase ICP
Seizures
Central pontine myelinolysis

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Patients at risk of central pontine myelinolysis

Alcoholics
Malnourished of
Low K
Burns
Elderly (esp if on thiazides)
Liver Tx

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symptoms of central pontine myelinolysis

Initially dysarthria and dysphasia
Then confusion, delirium, hallucinations, tremor

Flaccid quadraparesia

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Diagnostic requirements of SIADH

Hypotonic hyponatraemia
Urine osmolality > plasma
Urine na >20
Normal renal, hepatic, pituitary, adrenal and thyroid function
Absence of low BP, hypovolaemia, oedema, drugs affecting ADH secretion
Correction by water restriction

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Causes of hypotonic hyponatraemia with low urine osmolality and Na

Beer potomania
Psychogenic polydipsia
Excess 5% dextrose

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Clinical features of hypernatramia

When Na >155 and osmolality >330mosm/kg

Increased temp
Restlessness
Irritability
Drowsiness
Lethargy
Confusion
Coma

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Causes of cranial DI

Idiopathic
Head injury/neurosurgery
Neoplastic - pituitary tumour, hypothalamic mets
Infections - meningitis, encephalitis
Granulomatois disease - sarcoidosis
Vascular - aneurysm, sickle cell anaesmia, Sheehan syndrome
Drugs - ADH suppressed by naloxone, phenytoin

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Causes of hypernatraemia

Extrarenal - burns, gastric loss

Salt gain - infusion of bicarbonate, hypertonic saline, ingestion of sea water

Nephrogenic DI - lithium, pyelonephritis, multiple myeloma, amyloid, sarcoidosis

Central DI - TBI, pituitary tumour, meningitis, encephalitis, TB

Renal losses - mannitol, urea, loop diuretics, hyperaldoesteronism

May occur in the recovery phase of an illness as there is more rapid clearance of free water than sodium

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Water deficit

Total body water x (1- [ 140/Na] )

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Issues needed to be addressed in DI post TBI

Hypernatraemia - give DDAVP if euvolaemic, replace only last hours u/o, avoid fall >0.5/hr

Total body water deficit - replace rapidly if associated with shock, need to use extreme caution - use both isotonic and hypertonic saline to avoid rapid drop

Associated anterior pituitary dysfunction - give hydrocortisone if shocked (will worsen diuresis but improve CVS stability)

Underlying ADH deficiency - DDAVP; selective v2 receptor agonist

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Types of DI

Nephrogenic - congenital/acquired

lithium associated most common
hypercalcaemia and hypokalaemia also cause

Central - cogential or acquired
Acquired may be transient (inflammation) or permanent (transaction) and absolute or relative
- TBI especially import - seen in up to 70% patients

Gestational - may be associated with HELLP Anand PET

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Causes of polydipsia

Psychiatric disorder
Drugs that give sensation of dry mouth eg oxygen, anticholinergics
Hypothalamic lesions that disturb thirst centre
Appropriate detection by osmoreceptors of raised osmolality eg glucose, na, alcohol

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How to determine solute diuresis from water diuresis

One off urine osmolality - >300mOsm/kg indicate solute

Commonest cause is glycosuria

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Causes of polyuria following head injury

DI
CSW
appropriate post-resus diuresis
Appropriate natriuresis following hypertonic saline
Mannitol induced
Hypothermic diuresis

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Metabolic factors that influence calcium

Protein - calcium increases with decreasing albumin
- often unwell hypoalbuminaemic cancer patients have much higher ca

pH - acidosis -> increased iCa

Phosphate

Causes of hypercalcaemia

Primary endocrine; PTH increase, thyrotoxicosis, adrenal insufficiency

Paraneoplastic;

PTH secretion - lung, head and neck, breast, ovarian, bladder
lytic bone - MM, Breast, harm
phaeochromocytoma

Granulomatous - sarcoidosis, TB

Drug induced - thiazides, lithium, HRT/oestrogen, TPN

Random causes - immobilisation, rhabdo, milk alkali syndrome

Effects of hypercalcaemia

Polyuria and polydipsia
Dyspepsia
Depression
Muscle weakness
Constipation
Fatigue
Short QT
vomiting and diarrhoea
Coma
Pancreatitis
Renal failure (due to vasoconstriction)

Treatment of hypercalcaemia

Fluid +/- frusemide
Bisphosphonates
Calcitreol
Steroids (reduce absorption from gut)
Loop diuretics (reduce absorption from renal tubule)
NSAIDs

Causes of hypocalcaemia

Citrate
Hypoparathyroidism
Alkalosis
Pancreatitis
Tumour lysis
Rhabdo  - ca may be very low initially, can then become very high
Drugs - phenytoin

Instances of hypocalcaemia and acidosis

Acute renal failure
Rumour lysis
Rhabdo
Pancreatitis
Ethylene glycol poisoning
Hydrofluoric acid poisoning

Clinical manifestations of hypocalcaemia

``` Cirimoral and peripheral paraesthesia Tetany Seizures Tremor and ataxia Proximal myopathy Hypotension non responsive to unit ropes Long Qt Loss of digitalis effect Apnoea Larygospasm/bronchospasm ``` Symptoms exacerbated if K and Mg also low

Indications for calcium administration

Symptomatic hypocalcaemia iCa <0.8n Hyperkalaemia Ca channel overdose ``` Relative indications - Beta blocker od Hypermagnesaemia Hypocalcaemia in the fact of Inotrope requirement MBT ```

Clinical features of hypokalaemia

``` Weakness Constipation Ileus Torsades/VT/atrial tachycardia Coma ``` Prolonged severe hypo can -> rhabdo and nephrogenic DI ECG changes - Long PR TWI U wave

Aetiology of hypokalaemia

``` Inadequate diet GI losses Renal losses - - endocrine; conns, cushings, bartters - drugs - diuretics, steroids - RTA - Mg deficiency Compartmental shifts - - alkalosis - insulin - beta adrenergic stimulation - hypothermia - post blood transfusion (delayed) - poisoning - barium, touline ```

Clinical features of jyperkalaemia

``` Paraesthesia Weakness Flaccid paralysis Hypotension Bradycardia ``` ECG - peaked T, flat p, long PR, wide QRS, deep s, sine wave

Aeitiology of hyperkalaemia

Artefactual Increase from somewhere - transfusion, tissues damage (burns, rhabdo, trauma, tumour lysis) Decreased renal excretion - renal failure, addisons, drugs (spironolactone. ACEi) Compartmental shifts - Acidosis, insulin deficiency, toxins (digoxin, sux)

Causes of hypomagnesaemia

GI disorders - malabsorption, GIT fistula, short bowel, prolonged NG suction, diarrhoea, pancreatitis, parenteral nutrition Endocrine - hyperparathyroidism, hyperthyroidism, Conns, DM, hyperaldosteronism Renal disease - RTA, diuretic phase of ATN Drugs - alcohol, aminoglycosides, amphoteracin B diuretics

Clinical features of hypomagnaesaemia

Physical - - confusion - delerium - tremors - seizures - tetany (as with hypo calcaemia) ECG - - wide QRS - peaked T waves (disappear when very severe) - long PR Associated biochemical abnormalities - - Hypokalaemia, refractory to replacement - hypocalcaemia - low PTH (in spite of low ca) - low vit D

Characteristic changes with adrenal insufficicney

``` low Na high K NAGMA low BSL high Ca ```

Characteristic changes with hyperaldosteronism

high Na low K met alkalosis

Characteristic changes with refeeding syndrome

low K low PO4 low Mg low BSL

Characteristic changes with administration of TPN

high BSL high lipids NAGMA

Characteristic changes with rhabdo

high K high PO4 high LDH and CK myoglobinuria

Characteristic changes with TLS

``` high PO4 high K high uric acid low Ca HAGMA raised LDH ```

Characteristic changes with toxic alcohols

HAGMA High serum osmolar gap low Ca

Characteristic changes with lithium toxicity

negative anion gap | high Na

Characteristic changes with salycilate toxicity

HAGMA low K high urinary K

Causes of hypermagnesaemia

Increased intake - infusion, oral tablets, unregulated absorption (ulcer), milk alkali syndrome Compartment shift or leak - TLS, rhabdo, acidosis DEcreased loss - renal failure, primary hyperparathyroidism, lithium therapy, hypoaldosteronism

Clinical features of hyperMg

1.8 - 2 mmol/l - hypocalcaemia, ileus, antiarrhythmic effects 2 - 4mmol/l - hyporeflexia ,muscle weakness, nausea, flushing, headache, lethargy 4 - 6 - resp failure, hypotension, bradycardia, decreased LOC 6 - 10 - apnoe, coma, CHB -> asystole >10 - non survivable

Management of hyperMg

usually rapidly corrects with no intervention can give calcium to antagonise insulin/dex will promote entry into cells haemodialysis

HyperPO4 - causes

INcreased inake - TPN, enema Tissue breakdown - rhabdo, TLS, haemolysis Decreased excretion - acute or chronic renal failure Increased tubular reabsorption - hypoparathyroidism, acromegaly, bisphophonates, vit D toxicity Compartmental shift - carb infusion, hormonal effects (insulin,, glucagon, refeeding), alkalosis Suprious - hyperlipidaemia, hyperglobulinaemia (MM, waldenstroms), haemolysis

clinical feaures of hypO PO4

neuro - irritablility, hallucination, seizures, coma CVS - imparied contractility, arrythmias MSSK - weakness, proximal myopathy, dysphagia, slow vent weaning, rhabdo Haem - decreased 23DPG (left shift), increased RBC fragility -> haemolysis, thrombocytopaenia