• levels can be elevated due to non-renal failure causes
  • increased ingestion: big meat eaters, protein supplements
  • assay interference: DKA, fasting, hyper-lipidaemia, haemolysis and drugs eg. cephalosporins, barbiturates and some chemoRx
  • reduced tubular secretion: trimethoprim, H2 antagonists

• Primary hyperparathyroidism and malignancy are the two most common causes of increased serum calcium levels. If PTH levels are detectable, generally speaking the cause of hyper Ca++ is primary hyperparathyroidism
• other causes include sarcoidosis, thyrotoxicosis
• severe hypercalcaemia (>3.5 mmol/L) requires emergency management
• can cause:
  • nephrogenic diabetes insipidus
  • abdo pain - constipation, ileus, pancreatitis
  • fatigue and even coma, Muscle weakness
• Emergency Mx - IV saline, IV bisphosphonate if no success.
  • Other agents: calcitonin (100U SC per 6-8/24 or ≤10U/kg IV over 6/24 in emergency), dialysis, mithramycin and also anti-resorptive agent denosumab

• acquired or hereditary. Acquired causes include:
  • hypoparathyroidism
  • liver disease
  • kidney disease
  • pancreatitis, COVID-19
  • hyperphosphataemia, hypomagnesaemia, vit D deficiency
  • diet, medication, and surgery

• Severe (ionized Ca⁺⁺ <1 mmol/L) - 10-20ml of 10% calcium gluconate over 10mins and repeated per hour until tetany, seizure or laryngospasm resolves
• Without seizure or tetany: 10ml 10% over 1/24
• 10ml of 10% solution (100mg/ml) = 1g = 2.2mmol

• recurrent vomiting, gastric acid loss
• diuretic-induced alkalosis (loop or thiazide diuretics)
• posthypercapnic metabolic alkalosis.
• CLD, cystic fibrosis, and laxative abuse are also potential causes.

• acute or chronic AKI/CKD
• DKA
• drug causes

ECG changes in rough order of appearance:

• Peaked T waves with a shortened QT interval
• prolonged PR and QRS complex
• disappearance of p wave
• widening of QRS eventually progressing to a sine wave before asystole

rqia guidelines for Hyperkalaemia 2021

• Increased GI losses
  • vomiting & diarrhoeal causes
  • bowel preps
• tumour related - intestinal adenomas
• Renal losses
  • Diuretics, amphotericin
  • hypomagnesaemia
  • renal tubular acidosis
  • other salt wasting nephropathies
• Skin losses - sweating, CF, other skin conditions including burns

*Dialysis and other transfusion related conditions

• Chronic alcoholism
• hyperaldosteronism
• associated with DKA

Requires treatment when severe - eg <2.5mmol/L or symptomatic

• severe muscle weakness, paralysis
• DKA
• cardiac arrhythmias

• usually in elderly with mental or physical disability exacerbated by acute infection
• as a result of impaired thirst or access to adequate water or increased losses
• water losses - diuretics, osmotic diuresis (eg hyperglycaemia), acute tubular necrosis, GI losses and sweating

• represents water excess
• often related to loop diuretics but also associated with other disease processes which have been recognised to initiate SIADH

• redistribution - associated with major surgery fluid shifts, insulin/glucagon/adrenaline use, respiratory alkalosis
  • beware esp in Rx of hyperglycaemia, DKA (osmotic losses + redistribution with insulin)
• decreased absorption - malnutrition, alcohol Xs, anorexia
• increased renal loss - associated with diuretics
• renal replacement therapies - loss in effluent with large fluid shifts
• Clinical - muscle weakness, CNS changes, poor WCC function reducing resistance to infection, arrhythmias
• Treatment - depends on level
  • <0.64mmol/l & asymptomatic - preferably enteral replacement (Phosphate Sandoz tablets contain 500mg elemental phosphorous - 4-6 tablets daily for adults, 2-3 for kids)
  • <0.32mmol/l or symptomatic - parenteral replacement

C-reactive protein - increases with age and BMI

• synthesised in liver in response to inflammatory stimuli, usually peaking in 2/7
• both pro and anti-inflammatory actions
• exact mechanism of actin unknown but triggers complement pathway and others
• also produced in endothelium, smooth M and adipose tissue
• t_1/2 = 20/24
• raised in response to any inflammatory stimulus - infection (viral, TB, fungal etc), trauma, auto-immune diseases (Crohn disease, rheumatoid arthritis, juvenile idiopathic arthritis, vasculitis, autoimmune hepatitis), necrosis, ischaemia, malignancy etc
  • Causes and outcomes of markedly raised CPR 2017
• high sensitivity CRP (hs-CRP) useful in high risk coronary disease

Lipase is found in most parts of the GI tract but has also has been found in liver, heart, lungs and leukocytes

• acute pancreatitis usually associated with 2-3x rise in lipase
• less significant rise in lipase associated with many illnesses
• more specific than amylase for pancreatitis
• significant increases in lipase (>3x upper limit) can be seen with:
  • reduced clearance of lipase caused by renal impairment or macrolipase formation
  • other hepatobiliary, gastroduodenal, intestinal and neoplastic causes
  • critical illness, including neurosurgical pathology
  • alternative pancreatic diagnoses, such as non-pathological pancreatic hyperenzymaemia
  • miscellaneous causes such as diabetes, drugs and infections. (esp. Narcotics, thiazide diuretics, oral contraceptives, adrenocorticotropic hormone, cholinergics but many others as well have been associated with rise)
  • Multi trauma without head injury can also cause 3x rise in lipase

non pancreatic causes of raised lipase

• considerable variation but 50% women will have values as below within 3/7 of value shown
• tend to plateau and begin to decline around d60 (ie. ~9/40)

http://pathology.royalberkshire.nhs.uk/HCGrange.php

ProBNP in the ED, AmCollege of Cardiology 2018

• Practically all PCT formed in thyroid C cells is converted to calcitonin so that no PCT is released into the circulation. Hence, the PCT level in healthy subjects is very low (0.05 ng/mL)
• inflammatory release of PCT is independent. During inflammation, PCT is produced mainly by two alternative mechanisms; direct pathway induced by lipopolysaccharide (LPS) or other toxic metabolite from microbes and indirect pathway induced by various inflammatory mediators like IL-6, TNF-a, etc
• PCT is generally elevated by bacterial infection but not viral
• not usually raised with PE and therefore may be useful in differentiating pneumonia and PE particularly when associated with fever

• patients with a 5 mL/min/1.73 m2 lower mean eGFR had 13% higher levels of mean hs‐cTnT.
• patients with pre-existing CHF had a 34% higher level of hs‐cTnT, history of hypertension (34%), myocardial infarct (33%), angina pectoris (31%), atrial fibrillation (26%), of male sex (24%), diabetes mellitus (24%), and patients with lower hemoglobin (4% per 10 g/L).
• reason for raised Trop is unclear in CKD - may be related to reduced clearance although small molecules are able to pass through glomerular membrane. May be due to chronic stress assoc with CKD

Assoc b/w Troponin and renal function - AHA 2019

troponin is known to rise post neurological insult eg. SAH, but is also associated with seizures ESocJ seizures

Venous Blood Gas