Chem Path Flashcards
Osmolarity=
2(Na + K) + Urea + Glucose
Osmolar gap=
Osmolality (measured) - Osmolarity (calculated)
Normal less than 2
Anion Gap=
(Na + K) - (Cl +HCO3)
Normal= 14-18
Normal range of Na
135-145
Hyponatraemia Sx
N+V
Confusion
Seizures
Coma
True Hyponatraemia
Low osmolality
Causes of True Hyponatraemia
Hypervolaemic - Organ failure (CCF, Cirrhosis, Neophrotic)
Euvolaemic - Endocrine (HoTy, Adrenal insuf., SIADH)
Hypovolaemic - Loss (D+V, Salt losing neph., Diuretics)
Differentiating causes of Hypovolaemic HoNa
Urinary Na >20= renal (diuretic, Addison’s, Salt losing neph.)
Urinary Na less than 20= non renal (D+V)
SIADH feats
True, euvolaemic HoNa w/ Urinary Na >20
Urine osm >100! (usually > serum osm)
No adrenal, renal or thyroid dysfunction
Hypernatraemia Sx
Thirst
Confusion
Seizures + ataxia
Coma
Hypernatraemia causes
Hypovolaemic
Euvolaemic
Hypervolaemic
Hypovolaemic HyperNa causes
GI loss (D+V) Skin loss (sweating, burns) Renal loss (loop diuretics, osmotic diuresis, renal disease)
Euvolaemic HyperNa causes
Resp loss (tachypnoea) Skin loss (sweating, fever) Renal loss (Diabetes insipidus)
Hypervolaemic HyperNa causes
Mineralocorticoid excess (Conn's) Hypertonic saline infusion
Diabetes insipidus
Polyuria, polydipsia + dilute urine (osm less than 2)
8 hour fluid deprivation test
Normal - Concentrate urine >600 osm/kg
Primary polydipsia - Concentrate urine >400-600
Cranial DI - Concentrate urine after desmopressin
Nephrogenic DI - No urine concentration
Potassium normal range
3.5-5
Hypokalaemia causes
GI loss (vomiting) Renal loss (hyperaldosteronism, excess cortisol, osmotic diuresis) Redistribution into cells (insulin, alkalosis) Rare (Tubular acidosis T1+2, Bartter's, Liddle's, Gitelman's)
Hyperkalaemia causes
Excessive intake (oral, parenteral, blood transfusion) Transcellular movement (acidosis, insulin shortage, tissue damage/catabolic state) Decreased excretion (ARF, CRF, Sprionolactone, Addison's NSAIDs, ACEi)
Adult maintenance fluid requirement
25-30ml/kg/day
Paediatric maintenance fluid requirement
1st 10 kg: 100ml/kg/day
2nd 10kg: 50ml/kg/day
Each kg after: 20ml/kg/day
Normal serum osmolality
275-295
Causes of HoNa w/ normal osmolality
Spurious, Drip arm sample, PseudoHoNa (hyperlipidaemia/paraproteinaemia) - everything normal except Na + Hx of DM or metabolic synd.
TURP syndrome
Hyponatraemia from water absorbed through damaged prostate
Differentiating Causes of Hypervolaemic HoNa
Urinary Na >20= Renal (ARF, CRF)
Urinary Na less than 20= Non renal (CCF, Cirrhosis)
Central pontine myelinosis
Pseudobulbar palsy, Paraparesis, Locked in syndrome due to Correcting HoNa too quickly
Increase Na by no more than 12mmol/L in 1st 24h
SIADH causes
Malignancy (SCLC, pancreas, prostate, lymphoma)
CNS disorders (meningoenceph., haem, abscess)
Resp (TB, pneumonia, abscess)
Drugs (opiates, SSRIs, Carbamazepine)
Addison’s bloods
HypoNa, HyperK, HypoGly, Urine Na >20
Bartter syndrome
Autosomal recessive
HypoK, Alkalosis + HoTN
Hypercalciuria + Nephrocalcinosis
Short SynACTHen
Cortisol measured at 0, ACTH given at 30mins + Cortisol measured at 60 mins
Final Cortisol less than 550= production defect
Long SynACTHen
1mg ACTH given and measure cortisol at 24h
>900= Secondary (Pituitary problem)
NB Secondary also has HypoK NOT HyperK
less than 900= Primary
OGTT for Acromegaly
75mg Glucose should decrease GH to 2 = Acromegaly
Schmidst’s syndrome
AI polyendocrine syndrome
Addison’s, HoTy + T1DM
Kallman’s syndrome
Hypogonadotrophic Hypogonadism
Low LH + FSH + Anosmia
Renal Tubular Acidosis
HypoK w/ Acidosis
T1 - Distal tubule (HypoCa)
T2 - Proximal Tubule (Fanconi -> HyperPhos -> Ricketts)
T3 - Both
T4 - Defect in adrenals (HyperK - deficiency of Aldosterone)
Drugs that causes nephrogenic DI
Lithium, Demeclocycline (used to Tx SIADH!)
Causes of conn’s
ABCD Adrenal Adenoma Bilateral nodular hyperplasia Ca of adrenals Defective gene (GRA)
Causes of Elevated anion gap Metabolic acidosis
MUDPILES Methanol Uraemia DKA Propylene glycol Isoniazid Lactic acidosis Ethylene glycol Salicylates
Causes of HoNa w/ high osmolality
Glucose, Mannitol, EtOH
Gilbert’s
Isolated unconj bili
Crigler-Najjar
Isolated unconj bili (more constant and severe than Gilbert’s)
Alcoholic liver disease LFTs
High AST> High ALT (AST:ALT>1) High GGT (chronic)
Hepatitis LFTs
High AST=High ALT
Cholestatic LFTs
High GGT + ALP then Increased AST, ALT + Bili (conj)