What is the management approach for mild hypokalemia?
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Oral replacement.
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What is the management approach for mild hypokalemia?
Oral replacement.
What is the recommended management for mild hypocalcaemia if there is no response to oral replacement?
Administration of active Vitamin D (Calcitriol).
What is the purpose of Diagnostic/Dynamic Function Tests?
To stimulate or suppress a particular hormonal axis and observe the appropriate hormonal response.
What are the clinical presentations of Hypokalaemia?
Anorexia, nausea, polyuria, polydipsia, muscle weakness/paralysis, respiratory distress, arrhythmia, ECG changes, paralytic ileus, constipation.
Why is the exact amount of K needed for replacement difficult to calculate?
Due to the discrepancy between intracellular and extracellular potassium levels.
What is Chvostek's sign in the context of acute hypocalcemia?
Facial muscle spasm on tapping the facial nerve.
What is the purpose of diluting suspect samples in prevention?
To decrease sample antigen concentration.
What are the high-risk cancers associated with Hypercalcaemia?
Myeloma, CA Breast, CA Lung (SCC), CA Head & Neck (SCC), CA Prostate, CA Kidney (RCC), Lymphoma.
What is the total body store of calcium?
1kg, with 98% in bone as Hydroxyapatite crystal.
What are the steps involved in diagnosing Cushing Syndrome?
What can result from inappropriate treatment of Hypernatraemia, such as rapid over-rehydration?
Cerebral oedema.
What is the principle of Overnight 1mg Dexamethasone Suppression Test (DST)?
In normal subjects, dexamethasone suppresses ACTH and therefore adrenal Cortisol secretion. In Cushing syndrome, the suppression is incomplete.
What are the symptoms associated with moderate hypercalcemia?
Fatigue, Muscle weakness, Constipation, Anorexia, Nausea.
What is the management approach for pure water loss in Hypernatremia?
Water replacement.
Which emergency treatment for hyperkalemia involves shifting potassium into cells and has an effect within 1 hour, lasting for only 5-6 hours?
IV Insulin/ Dextrose (DI drip).
What is the management approach for water + Na deficit in Hypernatremia?
Hypotonic (0.45%) Saline Replacement.
What is the formula for TTKG?
TTKG = (Urine [K] x serum osm.) / (Serum [K] x urine osm.)
What types of biomarkers can be used as tumour markers?
Enzymes (e.g., PSA), hormones (e.g., hCG), onco-foetal antigens (e.g., AFP, CEA), and carbohydrates.
What is used to diagnose Hypertonic Pseudo-Hyponatremia?
HyperG (Actual Na = Na + G/4) and IV Mannitol.
What factors should be considered for ARR testing in premenopausal women?
K loading and renal impairment.
What are the effects of Calcitonin on Serum Calcium and Phosphate?
It decreases Serum Calcium and Phosphate, reduces Bone resorption, and increases Renal excretion of both Calcium and Phosphate.
Which factors result in a positive interpretation of ARR testing?
K loading, premenopausal women, renal impairment, PHA-2 (Gordon), high dietary Na, advanced age, and renin inhibitors.
How is Plasma Albumin adjusted Calcium calculated?
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).
What are the causes of high serum AFP?
Normal foetus (from 15w of gestation to 2yo), pregnancy, HCC, germ cell tumour, ovarian cancer, non-HCC GI tumours, and benign liver diseases.
What is Pseudo-Hyponatraemia associated with?
Replacement of plasma volume with solids such as Glucose, Mannitol, Lipid, Protein, Cells.
What are the symptoms of Hypovolaemic HypoNa?
Reduced reflexes, muscle cramps, convulsion, coma.
What are the causes of Excess Na in Hypernatraemia?
High ECF volume, high total body Na.
What is the major mineralocorticoid in the body?
Aldosterone, with minor action by cortisol.
What does U<S indicate in the Clinical Pathology algorithm for Hypernatraemia diagnosis?
Large amount of water excreted by kidney = Water depletion by Renal loss.
What is the maximal increase of Na level per day for slow replacement in Chronic HypoNa?
Maximal increase of 12 mmol/L/d (or <0.5 mmol/L/hr).
What are the clinical presentations of HypoNa in hypervolaemia?
Elevated JVP, oedema.
What are the levels of HyperCa and Urine Ca in the diagnosis of Hypercalcaemia?
HyperCa > 3.0 mmol/L, Urine Ca > 10 mmol/d.
What are the components used to diagnose High Anion Gap Metabolic Acidosis?
Plasma HCO3, Anion Gap, SCr, ACTH stimulation test, Renin, Aldosterone.
What is the initial management for severe or symptomatic hypocalcaemia?
IV Calcium Gluconate and monitoring of Serum Ca level Q6-8h.
What is the Anion Gap?
The difference in concentration between measured cations and measured anions.
What are some causes of decreased water intake?
Too old, too young, no access to water, unconsciousness, dysphagia, severe nausea/vomiting.
What is the significance of plasma HCO3 in the diagnosis of Hypokalaemia?
It is part of the differential diagnosis (Ddx) for Hypokalaemia.
What is the recommended test before sodium replacement (e.g. NS) for the diagnosis of Hyponatremia?
Paired spot urine Na.
What is the emergency treatment for hyperkalemia to increase action potential threshold and have a cardioprotective effect within minutes?
IV Calcium glucuronate.
What is the normal range of plasma potassium (K)?
3.5 - 4.5
What are the causes of Hypokalaemia when the urine potassium is normal or raised?
Renal loss of potassium, vomiting, apparent mineralocorticoid excess syndrome (AMES), gentamicin, magnesium depletion, leukaemia, and drug-induced causes.
What are the physiological roles of calcium?
Bone density, muscle contraction, NMJ excitability, blood coagulation, hormone secretion, enzymatic reactions.
What is Serum Alpha Fetoprotein (AFP)?
It is a glycoprotein synthesized during embryonic development by the foetal liver and yolk sac.
What are the causes of Hypokalaemia when it is caused by acidosis?
Non-renal loss with acidosis and renal loss with acidosis, including Type I and Type II Renal Tubular Acidosis (RTA) and carbonic anhydrase inhibitors.
What is the non-emergency treatment for hyperkalemia involving the use of cation-exchange resin to remove potassium in the gut and excrete in stool?
Cation-exchange Resin (e.g. Resonium).
What is the plasma Na concentration in Hypernatraemia?
Greater than 145 mmol/L.
Why is high serum AFP not sensitive for HCC?
Only 70% of HCC cases have elevated AFP.
What are the causes of increased Plasma Albumin in the diagnosis of Hypercalcaemia?
Dehydration, Venous stasis during Venipuncture.
What are the problems associated with tumour markers?
Low sensitivity, low specificity, and low positive predictive value despite high sensitivity and specificity.
What is the first step in the Clinical Pathology algorithm for Hypernatraemia diagnosis?
Check Urine/Serum osmolality ratio (normally, U>S), and then ECF volume.
What are the important conditions associated with Hyperkalemia?
DKA, Tumour lysis syndrome, Tissue necrosis, Hyperkalaemic Periodic Paralysis, Thyrotoxic Hypokalaemic Periodic Paralysis, Acute Kidney Injury.
What does U~S indicate in the Clinical Pathology algorithm for Hypernatraemia diagnosis?
Renal loss of both Water and Na (Osmotic Diuresis).
What is the rate of replacement for HypoNa based on the 1/3 rule?
1/3 in 1st 8h; 1/3 in 2nd 16h; 1/3 in 3rd 24h.
What does a high Osmol Gap (OG) indicate in hyponatremia?
It indicates Pseudo-HypoNa, which can be caused by substances like Mannitol, Lipid, and Protein.
What is the mechanism of action of Calcitonin in the management of Hypercalcemia?
Increases renal excretion of Ca, decreases bone resorption by interfering with Osteoclast maturation.
What are the causes of high serum CA19-9 related to the pancreas?
Biliary tract obstruction, cholangitis, pancreatitis, CRC, HCC.
What is Phantom hCG in serum?
Heterophile antibodies in serum due to surgery/chemotherapy of gestational trophoblastic disease.
What is Trousseau's sign of late tetany in the context of acute hypocalcemia?
Carpal spasm on inflating a BP cuff over the brachium.
What are the muscle symptoms associated with acute hypocalcemia?
Muscle cramps, carpopedal spasm, laryngeal spasm.
What does a high Anion Gap indicate?
Presence of extra organic acids, such as lactic acid and keto-acid.
What are some causes of increased water loss through extra-renal mechanisms?
Sweating, burns, evaporation, hyperventilation, osmotic diarrhoea, fistulas.
What percentage of calcium is in the exchangeable pool?
1%, with 0.5% in teeth, 0.5% in soft tissue, and 0.3% in muscle.
What are some causes of increased water loss through renal mechanisms?
Central diabetes insipidus, nephrogenic diabetes insipidus, chronic renal disease, electrolyte disorders, drug-induced factors, miscellaneous factors.
How is Effective Circulatory Volume (ECV) determined?
By BP, CVP, etc.
Which anti-hypertensive drug must be withdrawn for at least 4 weeks prior to testing Aldosterone-Renin Ratio (ARR)?
Mineralocorticoid Receptor Antagonist (MRA) (Spironolactone, Eplerenone etc).
What is the cause of Familial Hypocalciuric Hypercalcaemia?
CASR gene mutation (that encodes CaSR); AD inheritance.
What are the causes of Hypokalaemia when the urine potassium is less than 20 mmol/L?
Inadequate potassium intake, extra-renal loss, and intracellular shift.
What are the complications of a rapid drop in Osmolarity?
Cerebral oedema (osmosis across BBB).
What is the normal range for TTKG?
4-10.
What is the main location of potassium (K) distribution in the body?
Mainly intracellular fluid (ICF).
What does a high TTKG indicate?
High CCD [K], i.e. Renal loss of K.
What are the steps to diagnose Hyponatraemia?
How is hypertonic hyponatremia characterized?
It is characterized by high serum osmolality and can be treated with interventions like HyperG and IV Mannitol.
What clinical application does TTKG reflect?
Mineralocorticoid activity, e.g. Secondary Hypertension due to Mineralocorticoid excess.
What effect does adrenaline have on potassium (K) levels?
Adrenaline stimulates cellular K uptake. High adrenaline can lead to Hypokalaemia.
What conditions are associated with low PTH in the diagnosis of Hypercalcaemia?
Primary Hypercalcaemia (feedback on PTH), Malignancy, Vitamin D excess, Immobilisation, Sarcoidosis, Milk alkali syndrome, Thyrotoxicosis, Vitamin A excess, Thiazide diuretics, Addison’s disease, Malignancy.
What is the characteristic of Hyperkalaemic Periodic Paralysis?
Rare, AD trait, Acute weakness + Hyperkalemia, Resolves in hours, Triggered by Exercise, Cold, Hyperkalemia.
What are the two types of agents causing Hypertonic Plasma?
Osmotic agents (retain water) and non-osmotic agents (doesn’t retain water).
What are the most common presentations of mineralocorticoid excess/hyperaldosteronism?
Hypertension and Hypokalaemia.
What is the importance of drug history in the context of Hyperkalaemia?
It is important to consider the patient's drug history.
When is Corticosteroids considered useful in the management of Hypercalcemia?
In patients with Myeloma, Leukaemia, Lymphoma, Sarcoidosis, and Vitamin D intoxication.
What must be used before potassium replacement in the diagnosis of Hypokalaemia?
Paired urine potassium.
What are the pathogenesis factors contributing to Hypercalcaemia?
Local Bone metastasis, Distal Bone metastasis, Ectopic PTH production, Ectopic Vitamin D, Lymphokine production, Vitamin D-mediated.
What are the symptoms associated with mild hypercalcemia?
Asymptomatic usually associated with primary HyperPTH.
What are the treatable causes of Hypercalcaemia?
Steroid, Hyperparathyroidism (Primary and Tertiary).
What percentage of calcium is in the extracellular fluid (ECF)?
0.1%.
What are the chronic symptoms of hypocalcemia?
Intellectual disability, basal ganglia calcification, skeletal malformations, poor teeth formation, dermatitis, cataracts.
What are examples of unmeasured cations?
Ca, Mg.
What is used to determine Volume status/ ECV in the diagnosis of Hyponatremia?
Serum osmolality.
What are tumour markers?
Biomarkers found in blood, human excretions, or body tissues that elevate in patients with tumours.
What are the criteria for diagnosing Hyperkalaemia based on plasma K levels?
Plasma K > 5.0 mmol/L or Plasma K > 5.5 mmol/L (higher due to release of K from PLTs).
What is the primary management approach for HypoNa?
Always treat the primary cause.
What is the specific treatment for Central Diabetes Insipidus?
Intranasal 10-20ug Desmopressin (DDAVP®) q.d. or b.d.
What controls the renal reabsorption of calcium?
Parathyroid hormone (PTH), Vitamin D, Calcitonin.
What is the function of Na/K-ATPase in potassium (K) distribution?
It pumps 3Na out and 2K in. If the pump fails, it can lead to HyperKalemia, K deficit (intracellular), and possibly HypoNatremia.
What are the prerequisites for interpreting TTKG?
Urine osm. > Serum osm., Urine Na > 40 mmol/L, No K supplement given.
How does insulin affect potassium (K) levels?
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.
What are the causes of high serum CA125 related to the ovary?
Epithelial CA Ovary, ascites, fibroids, endometriosis, adenomyosis, pregnancy, menstruation, acute PID, benign/borderline ovarian tumours.
What are the important causes of Hyperkalaemia?
Mineralocorticoid deficiency (e.g. Congenital Adrenal Hyperplasia, Addison’s disease), Diabetic Ketoacidosis (DKA), Hyperosmolar Hyperglycaemic Syndrome (HHS).
What is the mechanism of action of Bisphosphonate in the management of Hypercalcemia?
Adsorbs to surface of bone hydroxyapatite, cytotoxic to osteoclasts, decreases Ca release from bone, and slows bone resorption.
What are the aetiologies of Hypovolaemic HypoNa?
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.
Name some Iatrogenic causes of Excess Na in Hypernatraemia.
Hypertonic dialysis, Hypertonic saline infusion, IV NHCO3 overdose, Hypertonic tube feeding/TPN.
What is the commonest cause of Euvolaemic Hyponatraemia in hospitalised patients?
Post-operation.
What does a normal Osmol Gap (OG) indicate in hyponatremia?
It indicates True HypoNa and can be assessed based on hydration status, ECF status, and fluid status.
What is the management approach for moderate to severe hypokalemia (≤ 2.5 mmol/L)?
IV replacement (also if cannot tolerate oral route).
What is the common step prior to the addition of a second antibody in the 2-step sequence approach?
Wash step.
What are the clinical presentations of hypercalcemia?
Stone (Renal stone, Ureteric Colic), Bone (Bone pain esp. for HyperPTH), Groans (Abdominal cramping, Constipation), Morning Moans (Depression)/ Psychiatric overtone.
Which common analyses are prone to high-dose hook effect?
AFP, Ferritin, Prolactin, β-hCG, Other tumour markers.
What is the mechanism of macroprolactinaemia?
Prolactin binds to IgG, forming 'big' prolactin and even 'big big' prolactin, protecting prolactin from metabolism, resulting in falsely high prolactin.
What is the significance of urine potassium in the diagnosis of Hypokalaemia?
It is part of the differential diagnosis (Ddx) for Hypokalaemia.
What are the investigations for Primary Hyperaldosteronism?
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).
What does TTKG stand for?
Transtubular Potassium Gradient.
What are the confirmatory tests for Primary vs Secondary Hyperaldosteronism?
Oral Sodium Loading Test, Saline Infusion Test, Fludrocortisone Suppression Test, Captopril Challenge Test.
What are examples of unmeasured anions?
Phosphate, Protein, Organic anions (e.g. Ketone, Lactic acid, Drug).
What is the screening test for Frusemide Stimulation Test for Primary Hyperaldosteronism or Hyporeninaemic Hypoaldosteronism?
Frusemide Stimulation Test.
What is the most effective non-emergency treatment for removing potassium in hyperkalemia?
Urgent HD (Hemodialysis).
What is the severity classification for Hyperkalaemia based on plasma K levels?
Moderate: Plasma K < 5.5 mmol/L, Severe: Plasma K > 6.5 mmol/L.
What are the indications for fluid and electrolyte replacement in HypoNa?
Indicated in both Hypovolaemic HypoNa and Hypovolaemic HyperNa.
What is the volume of water deficit replacement based on the 1/3 rule?
1/3 in 1st 8h; 1/3 in 2nd 16h; 1/3 in 3rd 24h.
When is the measurement of serum CA125 recommended in premenopausal women?
When USG findings are inconclusive of nature in premenopausal women with ovarian cyst.
What are the common causes of Hyperkalaemia?
Technical artefacts, Renal failure, K-sparing diuretics (Aldosterone inhibitor) e.g. Spironolactone.
What is the new treatment for Dilutional HypoNa (e.g., SIADH, CHF)?
Fluid restriction (0.8-1L/d), low dose Frusemide, Demeclocycline, V2R Antagonist.
What are the three major mechanisms leading to Hypernatraemia?
Excess Na, Water Depletion, and Water + Na deficit.
What is Lectin-binding AFP more specific to?
HCC.
What are the 3 principal hormones involved in the regulation of Plasma Calcium and Free Ionised Calcium?
PTH, Calcitriol/1,25-(OH)2 Vitamin D3, and Calcitonin.
What are the adverse drug reactions (ADR) associated with Bisphosphonate treatment for Hypercalcemia?
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).
What are the major manifestations of Hypernatraemia?
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.
What should be used to dilute IV KCl?
Normal saline.
What are the clinical characteristics of hypovolaemia in Hypernatraemia?
Brain cell shrinkage leading to tearing of cerebral vessels, haemorrhage, venous sinus thrombosis, postural hypotension, tachycardia, low JVP, and reduced skin turgor.
What are the differential diagnoses for hypocalcaemia?
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.
What is the purpose of the Water Deprivation Test in the diagnosis of Diabetes Insipidus?
To trigger ADH secretion and reabsorb water.
What is the effect of majority of anti-hypertensive drugs on Renin and Aldosterone?
They affect Renin more than Aldosterone.
What are the other rarer causes of Hypercalcaemia?
Excessive Vitamin D or Calcium administration, Increased sensitivity to Vitamin D, Decreased urine excretion, Other drugs, Non-PTH Hormone, Immobilisation.
What are the symptoms associated with severe/crisis hypercalcemia?
Abdominal Pain, Vomiting, Polyuria, Dehydration, Thirst, Polydipsia, Arrhythmia, Short QT, Pancreatitis.
What is the normal range of serum potassium (K)?
3.7 - 5.2
What are the symptoms associated with dangerous hypercalcemia?
Impaired Consciousness, Coma usually associated with CA of 298-614.
What is the main source of potassium (K) for the body?
Diet, e.g. meat, fish, fruit.
What controls the absorption of calcium in the gastrointestinal tract (GIT)?
Vitamin D.
What are the common causes of elevated serum AFP?
Regeneration of liver tissue in liver diseases, especially HCC, and acute hepatitis.
What conditions lead to Hypotonic True Hyponatremia?
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).
Apart from cation-exchange resin, what other non-emergency treatment can be used to remove potassium in hyperkalemia?
Loop Diuretics if not oliguric.
What is the incidence of Hypernatraemia in the hospitalised population?
About 1-3%.
What are the symptoms of Euvolaemic HypoNa?
Lethargy, confusion, nausea, vomiting, respiratory depression.
What is the management approach for Hypercalcemia involving fluid replacement?
Normal saline, inhibition of PCT and Loop Na reabsorption, and monitoring fluid and electrolyte balance.
What defines normotonic hyponatremia?
It is characterized by normal serum osmolality and can be associated with conditions like HyperLipid and Protein.
What is the true measure of sodium concentration in the blood?
True [Na] = Na divided by WATER.
What is the specificity of serum CA19-9 for CA Pancreas when the level is ≥ 1,000?
99.8%.
What are the ECG changes associated with Hyperkalaemia at different plasma K levels?
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.
What does U>S (normal) indicate in the Clinical Pathology algorithm for Hypernatraemia diagnosis?
No Renal loss of water.
What does a TTKG value of less than 6 indicate in the diagnosis of Hyperkalemia?
Inappropriate renal response to Hyperkalemia.
What does the Nephrology algorithm for Hypernatraemia diagnosis check first?
ECF volume, and then Urine Na and Urine osmolality.
What are the renal causes of Hypernatraemia?
Diabetes Insipidus, Osmotic Diuresis.
What are the possible causes of Primary Adrenal Insufficiency?
Addison’s disease (1° Hypoaldosteronism), CYP21 deficiency (Congenital Adrenal Hyperplasia).
What are the common causes of Hypokalaemia?
Diuretics, vomiting, diarrhea, magnesium deficiency.
What are the important causes of Hypokalaemia?
Mineralocorticoid excess, glucocorticoid excess, renal tubular acidosis, hypokalaemic periodic paralysis, dialysis.
What is the minimum time gap that should be maintained between Thyroxine and Calcium replacement?
≥ 1 hour.
What are the paraesthesia symptoms associated with acute hypocalcemia?
Perioral numbness.
How is Anion Gap calculated?
Anion Gap = [Na] - [Cl] - [HCO3] OR [Na] + [K] - [Cl] - [HCO3] (K is optionally omitted for practical reasons).
What are the risk factors for Primary Hyperaldosteronism?
Severe HT, Drug-resistant HT, Spontaneous or Diuretic-related HT, Early onset HT or Stroke at young age, FHx of Primary hyperaldosteronism.
What does a non-Anion Gap/Normal Anion Gap Acidosis indicate?
Loss of bicarbonate, with electrical positivity compensation by reabsorption of Cl (Hyperchloraemic acidosis).
Who are the usual outpatients affected by Hypernatraemia?
Very young and very old individuals.
What is the mechanism of heterophile antibody interference?
Endogenous heterophile antibody attacks the reagent antibody, e.g., Human Against Animal Ab (HAMA), associated with previous contacts with animals.
Who are the usual inpatients affected by Hypernatraemia?
Usually hospital-acquired or iatrogenic cases.
What factors significantly affect Aldosterone and must be corrected prior to testing?
Potassium (K) levels.
What effect does Parathyroid Hormone (PTH) have on Serum Calcium and Phosphate?
It increases Serum Calcium and decreases Phosphate.
What is the cut-off for serum CA125 in premenopausal women?
35 u/ml (Low specificity).
What is used for localisation in Primary Hyperaldosteronism?
Cortisol-corrected-Aldosterone Ratios and Imaging like CT Adrenal to exclude cancers or guide surgery.
Give examples of tumour markers for different types of cancer.
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).
What is the recommended action when Plasma K > 6.5 mmol/L?
Order ECG (+ Urine K +/- other blood samples before Tx).
What complications can arise from a rapid drop in osmolarity in HypoNa?
Cerebral oedema (osmosis across BBB).
What is the volume of replacement for combined water & Na deficit in Hypernatremia?
(Current [Na] - 140) x TBF.
Which factors result in a negative interpretation of ARR testing?
Renin inhibitors, K-wasting diuretics, ACEI, ARB, CCB (Dihydropyridine), K-sparing diuretics, low dietary Na, pregnancy, renovascular HT, and malignant HT.
When is Free Ionised Ca most useful?
When there are confusing Serum Protein levels, e.g. low Albumin or high Globulin, and in neonates.
What are the complications of using hypertonic saline in HypoNa management?
Water intoxication.
How is hypotonic hyponatremia identified?
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).
What is the duration of 1° HyperPTH in the diagnosis of Hypercalcaemia?
Months to years.
What limits the use of CA19-9 as a screening tool?
Low sensitivity.
What are the characteristics of renal calculi in the diagnosis of Hypercalcaemia?
Rare in 1° HyperPTH, frequent in other cases.
What are the potential causes of SIADH (Syndrome of Inappropriate Antidiuretic Hormone) in the CNS?
Any causes including concussion, and in the respiratory system: lung cancer, respiratory infection (including TB).
What are the symptoms of mild HypoNa?
Self-limiting symptoms such as malaise, lethargy, headache, anorexia, nausea, vomiting, abdominal pain.
When is Denosumab FDA approved for the management of Hypercalcemia?
For Hypercalcemia of malignancy refractory to bisphosphonate.
What ECG abnormalities are associated with acute hypocalcemia?
Long QT, T wave abnormalities.
What is the initial distribution of K when administered intravenously?
In the extracellular fluid (ECF) only.
What are some causes of water and sodium deficit with low extracellular fluid (ECF) volume and low total body sodium?
Renal loss (osmotic diuresis, post-obstruction diuresis, hyperglycemia, IV mannitol), extra-renal loss (excessive sweating, diarrhea in children).
What percentage of calcium is free ionised and biologically active?
50%.
What is the effect of NaHCO3 infusion in the emergency treatment of hyperkalemia?
Shifts potassium into cells, with an effect within 30 minutes and lasting for several hours.
What are the causes of Pseudo-Hyponatremia in the diagnosis of Hyponatremia?
HyperLipid (TAG > 50mmol/L) and HyperProtein (TP > 150g/L).
What dietary condition should be maintained for investigation of Aldosterone via Renin?
Normal salt diet.
What is the role of Vitamin D in relation to Serum Calcium and Phosphate?
It increases Serum Calcium and Phosphate, and enhances Intestinal Calcium absorption.
In which group of women is serum CA125 more sensitive and specific?
Postmenopausal women.
What are the methods used for the diagnosis of Hypercalcaemia?
Adjusted Plasma Ca, PTH, 24 Urine Ca & Creatinine.
What are the roles of tumour markers?
Screening, diagnostic, guiding treatment, monitoring therapeutic response/surveillance, and prognostic.
What are the two algorithms used for the diagnosis of Hypernatraemia?
Clinical Pathology and Nephrology.
What are the possible exclusions for the diagnosis of Hyperkalemia?
Technical Artefacts, Pseudo-hyperkalemia, EDTA contamination, Haemolysis, Thrombocytosis, Leukocytosis.
What does an inappropriately normal PTH level indicate in the diagnosis of Hypercalcaemia?
Non-PTH related causes.
What are the causes of high serum CA125 related to other conditions?
Cirrhosis, pancreatitis.
What are the clinical presentations of Hyperkalaemia?
Non-specific: Malaise, Vomit, Nausea, Vague muscle weakness, Flaccid paralysis, Paresthesia, Arrhythmia - ECG changes.
What is Serum Human Chorionic Gonadotropin (hCG)?
It is a glycoprotein secreted by trophoblastic cells of the placenta.
What are the clinical presentations of HypoNa in hypovolaemia?
Thirst, weakness, apathy, cramps, anorexia, nausea, postural hypotension, low pulse volume, reduced JVP, decreased skin turgor, peripheral vasoconstriction.
In which conditions is Serum Human Chorionic Gonadotropin (hCG) elevated?
Pregnancy and some germ cell tumors (choriocarcinoma, embryonal CA, 10% of seminoma).
What are the differential diagnoses of secondary hypertension related to adrenal causes?
Primary aldosteronism (Conn's syndrome), Cushing syndrome, Ectopic ACTH syndrome, Glucocorticoid resistance, 11-hydroxylase deficiency, 17-hydroxylase deficiency, Pheochromocytoma.
What does hypervolaemic hyponatremia suggest?
It suggests organ failure and is associated with fluid overload.
What is the mechanism of action of Mithramycin or Plicamycin in the management of Hypercalcemia?
Direct effect on Osteoclast, slow bone resorption, and maximal fall occurs in 2-5 days.
What are the symptoms of severe Water Intoxication?
Neuromuscular symptoms due to intracellular oedema.
What are the possible causes of Mineralocorticoid resistance (2° Hyperaldosteronism)?
Interstitial nephritis, Obstructive uropathy, Amyloidosis, SLE, Pseudohypoaldosteronism (Gordon Syndrome).
What is Glucocorticoid Remediable Aldosteronism (GRA) caused by?
AD inheritance genetic disorder involving fusion of 5’ of CYP11B1 and 3’ of CYP11B2, leading to abnormal stimulation of aldosterone production by ACTH.
What are the potential causes of Primary HypoPTH (PhPT)?
Iatrogenic (e.g., Thyroidectomy, Neck irradiation, CA Neck, Amyloid infiltration), Familial (Genetic), Idiopathic (Autoimmune).
What is the characteristic of Thyrotoxic Hypokalaemic Periodic Paralysis?
Rare, AD trait, Male, Flaccid paralysis lasting 6-24h + Hypokalemia, Resolves.
What are the causes of Water Depletion in Hypernatraemia?
Normal Na, Normal ECF volume (or slightly reduced due to diuresis).
How should [Na] be monitored in HypoNa management?
Regularly, especially if it falls below 280 mmol/L or rises above 614 mmol/L.
What are the differences in clinical presentation between SIADH and CSWS in HypoNa?
SIADH: euvolaemic, high urine [Na], oliguria, normotension. CSWS: hypovolaemic, high urine [Na], polyuria (diuresis), (postural) hypotension, low JVP.
What precautions are important for Serum Thyroglobulin (Tg) measurement?
Measuring Anti-Tg Ab with every serum Tg, and knowing if [Tg] is measured after TSH stimulation.
What is the treatment for Hypernatraemia?
Diuretics, Water Replacement, Hypotonic saline.
What are the symptoms of dangerous HypoNa?
Life-threatening symptoms such as seizures, coma.
What is the impact of Phosphate disturbance on Hypocalcaemia?
Hyperphosphataemia can conjugate ionised Ca.
What are the causes of Water + Na Deficit in Hypernatraemia?
Low ECF volume, Low Total body Na.
What does high ECFV indicate in the Nephrology algorithm for Hypernatraemia diagnosis?
Excess Na.
What is the plasma Ca level in Hypocalcaemia?
Less than 2.0 mmol/L.
What is Liquorice associated with in the context of primary hyperaldosteronism?
Temporary Apparent Mineralocorticoid Excess Syndrome (AMES) by blocking 11 β-hydroxylase.
What are the causes of Central DI according to the U:S ratio?
Tumour, Trauma, Infection, Others.
What are the potential causes of Hypocalcaemia related to the PTH pathway?
Low PTH (Hypoparathyroidism), PTH Resistance (Pseudo-HypoPTH), PTH Inhibition (HypoMg).
What are the potential drug-induced causes of Hyponatraemia?
Central acting: Narcotics, Sulphonylureas, Clofibrate, Carbamazepine. Renal acting: Diuretics, Sulphonylureas, Biguanides, NSAID.
What are the differential diagnoses of primary hyperaldosteronism?
Adrenal neoplasm, adrenal hyperplasia, adrenal adenoma, adrenal cortex carcinoma, mineralocorticoid receptor defect, Liddle syndrome, Glucocorticoid Remediable Aldosteronism (GRA), Gordon Syndrome.
What does hypovolaemic hyponatremia suggest?
It suggests fluid loss and can be assessed based on chronicity, with acute and chronic classifications.
What condition can lead to Pseudo-hypoCa due to low Albumin?
Nephrotic Syndrome, Liver Failure, Malabsorption, Malnutrition, Protein-losing Enteropathy.
What are the levels of Plasma intact PTH (iPTH) in the diagnosis of Hypercalcaemia?
Low/Normal (usu. not intact) or High of 299-614.
What does normal ECFV indicate in the Nephrology algorithm for Hypernatraemia diagnosis?
Pure Water Depletion.
What does low ECFV indicate in the Nephrology algorithm for Hypernatraemia diagnosis?
Loss of both Water and Na.
How does pH disturbance contribute to Hypocalcaemia?
Alkalosis leads to low ionised Ca, and citrate use can also be a factor.
What is the pathogenesis of Hypocalcaemia in Chronic Kidney Disease (CKD)?
Impaired Ca reabsorption, PO4 retention leading to soft tissue precipitation, impaired 1-hydroxylase function, and Uraemia causing anorexia & PTH-resistance of bone.
What does euvolaemic hyponatremia suggest?
It suggests fluid overload and can be indicative of certain medical conditions.
What are the symptoms of severe HypoNa?
Agitation, confusion, hallucination, impaired mental function, incontinence.
What is Liddle Syndrome characterized by?
Genetic ENaC dysregulation leading to excessive sodium reabsorption, resulting in hypernatraemia, hypokalaemia, and hypertension.
What are the potential causes of Hypocalcaemia related to calcium deficiency?
Dietary deficiency and malabsorption.
What are the characteristics of chronic hyponatremia?
It presents with fewer symptoms even when [Na] < 110, and rapid correction can lead to complications like Central Pontine Myelinolysis.
What are the potential causes of Hypocalcaemia related to the Vitamin D pathway?
Vitamin D deficiency (Dietary, Malabsorption) and Poor Vitamin D activation (Chronic Liver Disease, CKD).
What are the characteristics of acute hyponatremia?
It presents with more symptoms, severe effects when [Na] < 120, and rapid correction leads to fewer complications.
What is Gordon Syndrome also known as?
Pseudohypoaldosteronism, characterized by aldosterone resistance, biochemical hyperaldosteronism, and clinical hypoaldosteronism.
What are the characteristics of Hypomangesaemia (HypoMg)?
Severe HypoMg < 0.3 mmol/L, inhibits PTH action, causes HypoK & HypoCa, and is refractory to K and Ca replacement treatment.