Oral replacement.
Administration of active Vitamin D (Calcitriol).
To stimulate or suppress a particular hormonal axis and observe the appropriate hormonal response.
Anorexia, nausea, polyuria, polydipsia, muscle weakness/paralysis, respiratory distress, arrhythmia, ECG changes, paralytic ileus, constipation.
Due to the discrepancy between intracellular and extracellular potassium levels.
Facial muscle spasm on tapping the facial nerve.
To decrease sample antigen concentration.
Myeloma, CA Breast, CA Lung (SCC), CA Head & Neck (SCC), CA Prostate, CA Kidney (RCC), Lymphoma.
1kg, with 98% in bone as Hydroxyapatite crystal.
1. Exclusion of exogenous Glucocorticoid exposure. 2. Perform 24h UFC, Overnight 1 mg DST, or Late-night salivary cortisol tests. 3. Exclude physiologic cause of Hypercortisolism. 4. Consult endocrinologist. 5. Perform 1 or 2 other studies above (repeating abnormal study, Dex-CRH, or Midnight serum Cortisol). 6. No discrepancy in findings leads to Cushing syndrome diagnosis.
Cerebral oedema.
In normal subjects, dexamethasone suppresses ACTH and therefore adrenal Cortisol secretion. In Cushing syndrome, the suppression is incomplete.
Fatigue, Muscle weakness, Constipation, Anorexia, Nausea.
Water replacement.
IV Insulin/ Dextrose (DI drip).
Hypotonic (0.45%) Saline Replacement.
TTKG = (Urine [K] x serum osm.) / (Serum [K] x urine osm.)
Enzymes (e.g., PSA), hormones (e.g., hCG), onco-foetal antigens (e.g., AFP, CEA), and carbohydrates.
HyperG (Actual Na = Na + G/4) and IV Mannitol.
K loading and renal impairment.
It decreases Serum Calcium and Phosphate, reduces Bone resorption, and increases Renal excretion of both Calcium and Phosphate.
K loading, premenopausal women, renal impairment, PHA-2 (Gordon), high dietary Na, advanced age, and renin inhibitors.
Total Ca (mmol/L) + 0.02 x (40 - Serum Albumin in g/L) or Total Ca (mg/dL) + 0.8 x (4.0 - Serum Albumin in g/L).
Normal foetus (from 15w of gestation to 2yo), pregnancy, HCC, germ cell tumour, ovarian cancer, non-HCC GI tumours, and benign liver diseases.
Replacement of plasma volume with solids such as Glucose, Mannitol, Lipid, Protein, Cells.
Reduced reflexes, muscle cramps, convulsion, coma.
High ECF volume, high total body Na.
Aldosterone, with minor action by cortisol.
Large amount of water excreted by kidney = Water depletion by Renal loss.
Maximal increase of 12 mmol/L/d (or <0.5 mmol/L/hr).
Elevated JVP, oedema.
HyperCa > 3.0 mmol/L, Urine Ca > 10 mmol/d.
Plasma HCO3, Anion Gap, SCr, ACTH stimulation test, Renin, Aldosterone.
IV Calcium Gluconate and monitoring of Serum Ca level Q6-8h.
The difference in concentration between measured cations and measured anions.
Too old, too young, no access to water, unconsciousness, dysphagia, severe nausea/vomiting.
It is part of the differential diagnosis (Ddx) for Hypokalaemia.
Paired spot urine Na.
IV Calcium glucuronate.
3.5 - 4.5
Renal loss of potassium, vomiting, apparent mineralocorticoid excess syndrome (AMES), gentamicin, magnesium depletion, leukaemia, and drug-induced causes.
Bone density, muscle contraction, NMJ excitability, blood coagulation, hormone secretion, enzymatic reactions.
It is a glycoprotein synthesized during embryonic development by the foetal liver and yolk sac.
Non-renal loss with acidosis and renal loss with acidosis, including Type I and Type II Renal Tubular Acidosis (RTA) and carbonic anhydrase inhibitors.
Cation-exchange Resin (e.g. Resonium).
Greater than 145 mmol/L.
Only 70% of HCC cases have elevated AFP.
Dehydration, Venous stasis during Venipuncture.
Low sensitivity, low specificity, and low positive predictive value despite high sensitivity and specificity.
Check Urine/Serum osmolality ratio (normally, U>S), and then ECF volume.
DKA, Tumour lysis syndrome, Tissue necrosis, Hyperkalaemic Periodic Paralysis, Thyrotoxic Hypokalaemic Periodic Paralysis, Acute Kidney Injury.
Renal loss of both Water and Na (Osmotic Diuresis).
1/3 in 1st 8h; 1/3 in 2nd 16h; 1/3 in 3rd 24h.
It indicates Pseudo-HypoNa, which can be caused by substances like Mannitol, Lipid, and Protein.
Increases renal excretion of Ca, decreases bone resorption by interfering with Osteoclast maturation.
Biliary tract obstruction, cholangitis, pancreatitis, CRC, HCC.
Heterophile antibodies in serum due to surgery/chemotherapy of gestational trophoblastic disease.
Carpal spasm on inflating a BP cuff over the brachium.
Muscle cramps, carpopedal spasm, laryngeal spasm.
Presence of extra organic acids, such as lactic acid and keto-acid.
Sweating, burns, evaporation, hyperventilation, osmotic diarrhoea, fistulas.
1%, with 0.5% in teeth, 0.5% in soft tissue, and 0.3% in muscle.
Central diabetes insipidus, nephrogenic diabetes insipidus, chronic renal disease, electrolyte disorders, drug-induced factors, miscellaneous factors.
By BP, CVP, etc.
Mineralocorticoid Receptor Antagonist (MRA) (Spironolactone, Eplerenone etc).
CASR gene mutation (that encodes CaSR); AD inheritance.
Inadequate potassium intake, extra-renal loss, and intracellular shift.
Cerebral oedema (osmosis across BBB).
4-10.
Mainly intracellular fluid (ICF).
High CCD [K], i.e. Renal loss of K.
1. Biochemical diagnosis (from lab report) 2. Clinical diagnosis/ confirmation (by Hx taking and P/E) 3. Further investigations.
It is characterized by high serum osmolality and can be treated with interventions like HyperG and IV Mannitol.
Mineralocorticoid activity, e.g. Secondary Hypertension due to Mineralocorticoid excess.
Adrenaline stimulates cellular K uptake. High adrenaline can lead to Hypokalaemia.
Primary Hypercalcaemia (feedback on PTH), Malignancy, Vitamin D excess, Immobilisation, Sarcoidosis, Milk alkali syndrome, Thyrotoxicosis, Vitamin A excess, Thiazide diuretics, Addison’s disease, Malignancy.
Rare, AD trait, Acute weakness + Hyperkalemia, Resolves in hours, Triggered by Exercise, Cold, Hyperkalemia.
Osmotic agents (retain water) and non-osmotic agents (doesn’t retain water).
Hypertension and Hypokalaemia.
It is important to consider the patient's drug history.
In patients with Myeloma, Leukaemia, Lymphoma, Sarcoidosis, and Vitamin D intoxication.
Paired urine potassium.
Local Bone metastasis, Distal Bone metastasis, Ectopic PTH production, Ectopic Vitamin D, Lymphokine production, Vitamin D-mediated.
Asymptomatic usually associated with primary HyperPTH.
Steroid, Hyperparathyroidism (Primary and Tertiary).
0.1%.
Intellectual disability, basal ganglia calcification, skeletal malformations, poor teeth formation, dermatitis, cataracts.
Ca, Mg.
Serum osmolality.
Biomarkers found in blood, human excretions, or body tissues that elevate in patients with tumours.
Plasma K > 5.0 mmol/L or Plasma K > 5.5 mmol/L (higher due to release of K from PLTs).
Always treat the primary cause.
Intranasal 10-20ug Desmopressin (DDAVP®) q.d. or b.d.
Parathyroid hormone (PTH), Vitamin D, Calcitonin.
It pumps 3Na out and 2K in. If the pump fails, it can lead to HyperKalemia, K deficit (intracellular), and possibly HypoNatremia.
Urine osm. > Serum osm., Urine Na > 40 mmol/L, No K supplement given.
Insulin promotes cellular uptake of glucose, accompanied by K, Mg, and PO4. High insulin can lead to Hypokalaemia, thus insulin must be given together with K.
Epithelial CA Ovary, ascites, fibroids, endometriosis, adenomyosis, pregnancy, menstruation, acute PID, benign/borderline ovarian tumours.
Mineralocorticoid deficiency (e.g. Congenital Adrenal Hyperplasia, Addison’s disease), Diabetic Ketoacidosis (DKA), Hyperosmolar Hyperglycaemic Syndrome (HHS).
Adsorbs to surface of bone hydroxyapatite, cytotoxic to osteoclasts, decreases Ca release from bone, and slows bone resorption.
Low salt intake, extra-renal loss (GI loss, skin loss), renal loss (CKD, salt losing nephritis, renal tubular acidosis, etc.), glucocorticoid and mineralocorticoid deficiency (Addison’s disease), CSWS.
Hypertonic dialysis, Hypertonic saline infusion, IV NHCO3 overdose, Hypertonic tube feeding/TPN.
Post-operation.
It indicates True HypoNa and can be assessed based on hydration status, ECF status, and fluid status.
IV replacement (also if cannot tolerate oral route).
Wash step.
Stone (Renal stone, Ureteric Colic), Bone (Bone pain esp. for HyperPTH), Groans (Abdominal cramping, Constipation), Morning Moans (Depression)/ Psychiatric overtone.
AFP, Ferritin, Prolactin, β-hCG, Other tumour markers.
Prolactin binds to IgG, forming 'big' prolactin and even 'big big' prolactin, protecting prolactin from metabolism, resulting in falsely high prolactin.
It is part of the differential diagnosis (Ddx) for Hypokalaemia.
Measuring individual mineralocorticoids like Serum Aldosterone, Urine metabolites, Cortisol, Cortisone, Deoxycorticosterone. Measuring mineralocorticoid function by assessing Serum K, Urine K, and Transtubular Potassium Gradient (TTKG). Screening test using Aldosterone-Renin Ratio (ARR).
Transtubular Potassium Gradient.
Oral Sodium Loading Test, Saline Infusion Test, Fludrocortisone Suppression Test, Captopril Challenge Test.
Phosphate, Protein, Organic anions (e.g. Ketone, Lactic acid, Drug).
Frusemide Stimulation Test.
Urgent HD (Hemodialysis).
Moderate: Plasma K < 5.5 mmol/L, Severe: Plasma K > 6.5 mmol/L.
Indicated in both Hypovolaemic HypoNa and Hypovolaemic HyperNa.
1/3 in 1st 8h; 1/3 in 2nd 16h; 1/3 in 3rd 24h.
When USG findings are inconclusive of nature in premenopausal women with ovarian cyst.
Technical artefacts, Renal failure, K-sparing diuretics (Aldosterone inhibitor) e.g. Spironolactone.
Fluid restriction (0.8-1L/d), low dose Frusemide, Demeclocycline, V2R Antagonist.
Excess Na, Water Depletion, and Water + Na deficit.
HCC.
PTH, Calcitriol/1,25-(OH)2 Vitamin D3, and Calcitonin.
Acute phase reaction, renal toxicity, AVN of Jaw, nausea, and hypocalcemia (common mistake is repeated Bisphosphonate given when serum Ca does not drop in first few days).
Cellular dehydration leading to neurological symptoms such as restlessness, irritability, lethargy, muscle twitching, hyperreflexia, spasticity, confusion, coma, irreversible neurological damage, sunken cheeks and eyes, weakness, loss of skin turgor, and weight loss.
Normal saline.
Brain cell shrinkage leading to tearing of cerebral vessels, haemorrhage, venous sinus thrombosis, postural hypotension, tachycardia, low JVP, and reduced skin turgor.
Hypoalbuminaemia, Chronic Kidney Disease, Drug-induced, Hungry bone syndrome, Extra-skeletal sequestration, Pseudo-HypoPTH, Hypomagnesaemia, Vitamin D deficiency, Type I and Type II Vitamin D dependent Rickets.
To trigger ADH secretion and reabsorb water.
They affect Renin more than Aldosterone.
Excessive Vitamin D or Calcium administration, Increased sensitivity to Vitamin D, Decreased urine excretion, Other drugs, Non-PTH Hormone, Immobilisation.
Abdominal Pain, Vomiting, Polyuria, Dehydration, Thirst, Polydipsia, Arrhythmia, Short QT, Pancreatitis.
3.7 - 5.2
Impaired Consciousness, Coma usually associated with CA of 298-614.
Diet, e.g. meat, fish, fruit.
Vitamin D.
Regeneration of liver tissue in liver diseases, especially HCC, and acute hepatitis.
Hypervolaemic (e.g., Congestive Heart failure, Cirrhosis w/ Ascites, Nephrotic syndrome), Euvolaemic (e.g., Acute water overload, Chronic water overload), and Hypovolaemic (e.g., Estimation of severity, Extra-Renal, Renal).
Loop Diuretics if not oliguric.
About 1-3%.
Lethargy, confusion, nausea, vomiting, respiratory depression.
Normal saline, inhibition of PCT and Loop Na reabsorption, and monitoring fluid and electrolyte balance.
It is characterized by normal serum osmolality and can be associated with conditions like HyperLipid and Protein.
True [Na] = Na divided by WATER.
99.8%.
6-7 mmol/L: Peaked T waves, 8-10 mmol/L: Wide QRS complex, Loss of P, Gradual bradycardia, 10-12 mmol/L: Ventricular Fibrillation, 11 mmol/L: Fusion of QRS and T.
No Renal loss of water.
Inappropriate renal response to Hyperkalemia.
ECF volume, and then Urine Na and Urine osmolality.
Diabetes Insipidus, Osmotic Diuresis.
Addison’s disease (1° Hypoaldosteronism), CYP21 deficiency (Congenital Adrenal Hyperplasia).
Diuretics, vomiting, diarrhea, magnesium deficiency.
Mineralocorticoid excess, glucocorticoid excess, renal tubular acidosis, hypokalaemic periodic paralysis, dialysis.
≥ 1 hour.
Perioral numbness.
Anion Gap = [Na] - [Cl] - [HCO3] OR [Na] + [K] - [Cl] - [HCO3] (K is optionally omitted for practical reasons).
Severe HT, Drug-resistant HT, Spontaneous or Diuretic-related HT, Early onset HT or Stroke at young age, FHx of Primary hyperaldosteronism.
Loss of bicarbonate, with electrical positivity compensation by reabsorption of Cl (Hyperchloraemic acidosis).
Very young and very old individuals.
Endogenous heterophile antibody attacks the reagent antibody, e.g., Human Against Animal Ab (HAMA), associated with previous contacts with animals.
Usually hospital-acquired or iatrogenic cases.
Potassium (K) levels.
It increases Serum Calcium and decreases Phosphate.
35 u/ml (Low specificity).
Cortisol-corrected-Aldosterone Ratios and Imaging like CT Adrenal to exclude cancers or guide surgery.
tPSA, %fPSA, PHI for prostate; AFP, Lectin-binding AFP for liver; CEA, CYFRA21-1, NSE, proGRP for lung; CA15-3, PR, ER, HER2 for breast; CA125, HE4 for ovary; CA19-9 for pancreas; hCG, AFP for germ cell; Thyroglobulin for thyroid; Calcitonin, Procalcitonin for thyroid (MTC).
Order ECG (+ Urine K +/- other blood samples before Tx).
Cerebral oedema (osmosis across BBB).
(Current [Na] - 140) x TBF.
Renin inhibitors, K-wasting diuretics, ACEI, ARB, CCB (Dihydropyridine), K-sparing diuretics, low dietary Na, pregnancy, renovascular HT, and malignant HT.
When there are confusing Serum Protein levels, e.g. low Albumin or high Globulin, and in neonates.
Water intoxication.
It is identified by true hypoNa through Osmol Gap (OG) and can be further classified into high OG (Pseudo-HypoNa) and normal OG (True HypoNa).
Months to years.
Low sensitivity.
Rare in 1° HyperPTH, frequent in other cases.
Any causes including concussion, and in the respiratory system: lung cancer, respiratory infection (including TB).
Self-limiting symptoms such as malaise, lethargy, headache, anorexia, nausea, vomiting, abdominal pain.
For Hypercalcemia of malignancy refractory to bisphosphonate.
Long QT, T wave abnormalities.
In the extracellular fluid (ECF) only.
Renal loss (osmotic diuresis, post-obstruction diuresis, hyperglycemia, IV mannitol), extra-renal loss (excessive sweating, diarrhea in children).
50%.
Shifts potassium into cells, with an effect within 30 minutes and lasting for several hours.
HyperLipid (TAG > 50mmol/L) and HyperProtein (TP > 150g/L).
Normal salt diet.
It increases Serum Calcium and Phosphate, and enhances Intestinal Calcium absorption.
Postmenopausal women.
Adjusted Plasma Ca, PTH, 24 Urine Ca & Creatinine.
Screening, diagnostic, guiding treatment, monitoring therapeutic response/surveillance, and prognostic.
Clinical Pathology and Nephrology.
Technical Artefacts, Pseudo-hyperkalemia, EDTA contamination, Haemolysis, Thrombocytosis, Leukocytosis.
Non-PTH related causes.
Cirrhosis, pancreatitis.
Non-specific: Malaise, Vomit, Nausea, Vague muscle weakness, Flaccid paralysis, Paresthesia, Arrhythmia - ECG changes.
It is a glycoprotein secreted by trophoblastic cells of the placenta.
Thirst, weakness, apathy, cramps, anorexia, nausea, postural hypotension, low pulse volume, reduced JVP, decreased skin turgor, peripheral vasoconstriction.
Pregnancy and some germ cell tumors (choriocarcinoma, embryonal CA, 10% of seminoma).
Primary aldosteronism (Conn's syndrome), Cushing syndrome, Ectopic ACTH syndrome, Glucocorticoid resistance, 11-hydroxylase deficiency, 17-hydroxylase deficiency, Pheochromocytoma.
It suggests organ failure and is associated with fluid overload.
Direct effect on Osteoclast, slow bone resorption, and maximal fall occurs in 2-5 days.
Neuromuscular symptoms due to intracellular oedema.
Interstitial nephritis, Obstructive uropathy, Amyloidosis, SLE, Pseudohypoaldosteronism (Gordon Syndrome).
AD inheritance genetic disorder involving fusion of 5’ of CYP11B1 and 3’ of CYP11B2, leading to abnormal stimulation of aldosterone production by ACTH.
Iatrogenic (e.g., Thyroidectomy, Neck irradiation, CA Neck, Amyloid infiltration), Familial (Genetic), Idiopathic (Autoimmune).
Rare, AD trait, Male, Flaccid paralysis lasting 6-24h + Hypokalemia, Resolves.
Normal Na, Normal ECF volume (or slightly reduced due to diuresis).
Regularly, especially if it falls below 280 mmol/L or rises above 614 mmol/L.
SIADH: euvolaemic, high urine [Na], oliguria, normotension. CSWS: hypovolaemic, high urine [Na], polyuria (diuresis), (postural) hypotension, low JVP.
Measuring Anti-Tg Ab with every serum Tg, and knowing if [Tg] is measured after TSH stimulation.
Diuretics, Water Replacement, Hypotonic saline.
Life-threatening symptoms such as seizures, coma.
Hyperphosphataemia can conjugate ionised Ca.
Low ECF volume, Low Total body Na.
Excess Na.
Less than 2.0 mmol/L.
Temporary Apparent Mineralocorticoid Excess Syndrome (AMES) by blocking 11 β-hydroxylase.
Tumour, Trauma, Infection, Others.
Low PTH (Hypoparathyroidism), PTH Resistance (Pseudo-HypoPTH), PTH Inhibition (HypoMg).
Central acting: Narcotics, Sulphonylureas, Clofibrate, Carbamazepine. Renal acting: Diuretics, Sulphonylureas, Biguanides, NSAID.
Adrenal neoplasm, adrenal hyperplasia, adrenal adenoma, adrenal cortex carcinoma, mineralocorticoid receptor defect, Liddle syndrome, Glucocorticoid Remediable Aldosteronism (GRA), Gordon Syndrome.
It suggests fluid loss and can be assessed based on chronicity, with acute and chronic classifications.
Nephrotic Syndrome, Liver Failure, Malabsorption, Malnutrition, Protein-losing Enteropathy.
Low/Normal (usu. not intact) or High of 299-614.
Pure Water Depletion.
Loss of both Water and Na.
Alkalosis leads to low ionised Ca, and citrate use can also be a factor.
Impaired Ca reabsorption, PO4 retention leading to soft tissue precipitation, impaired 1-hydroxylase function, and Uraemia causing anorexia & PTH-resistance of bone.
It suggests fluid overload and can be indicative of certain medical conditions.
Agitation, confusion, hallucination, impaired mental function, incontinence.
Genetic ENaC dysregulation leading to excessive sodium reabsorption, resulting in hypernatraemia, hypokalaemia, and hypertension.
Dietary deficiency and malabsorption.
It presents with fewer symptoms even when [Na] < 110, and rapid correction can lead to complications like Central Pontine Myelinolysis.
Vitamin D deficiency (Dietary, Malabsorption) and Poor Vitamin D activation (Chronic Liver Disease, CKD).
It presents with more symptoms, severe effects when [Na] < 120, and rapid correction leads to fewer complications.
Pseudohypoaldosteronism, characterized by aldosterone resistance, biochemical hyperaldosteronism, and clinical hypoaldosteronism.
Severe HypoMg < 0.3 mmol/L, inhibits PTH action, causes HypoK & HypoCa, and is refractory to K and Ca replacement treatment.
