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CICM > Electrolyes > Flashcards

Electrolyes Flashcards

1
Q

Treatment of SIADH

A 
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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2
Q

Na corrected for glucose

A

Correct na = na + BSL/3

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3
Q

Na deficit equation

A

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

Women - 0.5

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4
Q

Causes of SIADH

A

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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5
Q

Adverse effects of hypertonic Saline

A 
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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6
Q

Patients at risk of central pontine myelinolysis

A 
Alcoholics
Malnourished of
Low K
Burns
Elderly (esp if on thiazides)
Liver Tx
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7
Q

symptoms of central pontine myelinolysis

A

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

Flaccid quadraparesia

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8
Q

Diagnostic requirements of SIADH

A

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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9
Q

Causes of hypotonic hyponatraemia with low urine osmolality and Na

A

Beer potomania
Psychogenic polydipsia
Excess 5% dextrose

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10
Q

Clinical features of hypernatramia

A

When Na >155 and osmolality >330mosm/kg

Increased temp
Restlessness
Irritability
Drowsiness
Lethargy
Confusion
Coma
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11
Q

Causes of cranial DI

A

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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12
Q

Causes of hypernatraemia

A

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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13
Q

Water deficit

A

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

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14
Q

Issues needed to be addressed in DI post TBI

A

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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15
Q

Types of DI

A

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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16
Q

Causes of polydipsia

A

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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17
Q

How to determine solute diuresis from water diuresis

A

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

Commonest cause is glycosuria

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18
Q

Causes of polyuria following head injury

A 
DI
CSW
appropriate post-resus diuresis
Appropriate natriuresis following hypertonic saline
Mannitol induced
Hypothermic diuresis
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19
Q

Metabolic factors that influence calcium

A

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

pH - acidosis -> increased iCa

Phosphate

Mg

20
Q

Causes of hypercalcaemia

A

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

21
Q

Effects of hypercalcaemia

A 
Polyuria and polydipsia
Dyspepsia
Depression
Muscle weakness
Constipation
Fatigue
Short QT
vomiting and diarrhoea
Coma
Pancreatitis
Renal failure (due to vasoconstriction)
22
Q

Treatment of hypercalcaemia

A 
Fluid +/- frusemide
Bisphosphonates
Calcitreol
Steroids (reduce absorption from gut)
Loop diuretics (reduce absorption from renal tubule)
NSAIDs
23
Q

Causes of hypocalcaemia

A 
Citrate
Hypoparathyroidism
Alkalosis
Pancreatitis
Tumour lysis
Rhabdo  - ca may be very low initially, can then become very high
Drugs - phenytoin
24
Q

Instances of hypocalcaemia and acidosis

A 
Acute renal failure
Rumour lysis
Rhabdo
Pancreatitis
Ethylene glycol poisoning
Hydrofluoric acid poisoning
25
Q

Clinical manifestations of hypocalcaemia

A 
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

26
Q

Indications for calcium administration

A

Symptomatic hypocalcaemia
iCa <0.8n
Hyperkalaemia
Ca channel overdose

Relative indications -
Beta blocker od
Hypermagnesaemia
Hypocalcaemia in the fact of
Inotrope requirement 
MBT
27
Q

Clinical features of hypokalaemia

A 
Weakness
Constipation
Ileus
Torsades/VT/atrial tachycardia
Coma

Prolonged severe hypo can -> rhabdo and nephrogenic DI

ECG changes -
Long PR
TWI
U wave

28
Q

Aetiology of hypokalaemia

A 
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
29
Q

Clinical features of jyperkalaemia

A 
Paraesthesia
Weakness
Flaccid paralysis
Hypotension
Bradycardia

ECG - peaked T, flat p, long PR, wide QRS, deep s, sine wave

30
Q

Aeitiology of hyperkalaemia

A

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)

31
Q

Causes of hypomagnesaemia

A

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

32
Q

Clinical features of hypomagnaesaemia

A

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
33
Q

Characteristic changes with adrenal insufficicney

A 
low Na
high K
NAGMA
low BSL
high Ca
34
Q

Characteristic changes with hyperaldosteronism

A

high Na
low K
met alkalosis

35
Q

Characteristic changes with refeeding syndrome

A

low K
low PO4
low Mg
low BSL

36
Q

Characteristic changes with administration of TPN

A

high BSL
high lipids
NAGMA

37
Q

Characteristic changes with rhabdo

A

high K
high PO4
high LDH and CK
myoglobinuria

38
Q

Characteristic changes with TLS

A 
high PO4
high K
high uric acid
low Ca
HAGMA
raised LDH
39
Q

Characteristic changes with toxic alcohols

A

HAGMA
High serum osmolar gap
low Ca

40
Q

Characteristic changes with lithium toxicity

A

negative anion gap

high Na

41
Q

Characteristic changes with salycilate toxicity

A

HAGMA
low K
high urinary K

42
Q

Causes of hypermagnesaemia

A

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

43
Q

Clinical features of hyperMg

A

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

44
Q

Management of hyperMg

A

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

45
Q

HyperPO4 - causes

A

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

46
Q

clinical feaures of hypO PO4

A

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

CICM (20 decks)

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