Part 1 Viva Flashcards
Causes of respiratory alkalosis
Hypoxia - altitude, anaemia, R-L shunts
Drugs – salicylate, catecholamines etc.
Pulmonary – pneumothorax, haemothorax, pulmonary oedema, pulmonary embolism, aspiration, COPD
Endocrine – pregnancy, hyperthyroidism
CNS – pain, hyperventilation, anxiety, fever, trauma, tumour, meningitis etc.
Causes of a low urea
Hepatobiliary disease due to dec synthesis – acute liver failure, alcohol abuse
Overhydration
Starvation
SIADH
Causes of a high urea
High protein diet
Increased protein catabolism
Dehydration
Renal dysfunction
Shock
Haemorrhage
GI bleed
Causes of hypokalaemia
Inadequate intake - alcoholic, anorexia etc.
Transcellular shift - insulin, ventolin, periodic paralysis etc.
Renal loss - diuretics, vomiting, RTA, Bartter’s syndrome etc.
Extra-renal loss - diarrhoea, laxitives, cancer etc.
Misc – Mg depletion etc.
Further investigation of hypokalaemia
Urine [K], [Cl], plasma [HCO3-], aldo:renin
Bartter syndrome lab findings
Hypokalemic alkalosis
Hypercalciuria/nephrocalcinosis
Increased levels of plasma renin and aldosterone
Biochemical investigation of hyperammonaemia
Mild - exclude artefactual increase and repeat
Exclude heaptic causes (LFTs)
U&E, glucose, Ca, lactate, urine ketones, INR, ABG
Plasma amino acids, urine amino acids, organic acids, orotate, plasma acylcarnitines
Gitelman syndrome lab findings
Hypokalaemic metabolic alkalosis in combination with significant hypomagnesaemia and low urinary calcium excretion
Biochemical investigation of a patient with renal calculi
Single calcium calculus - serum calcium, ionised calcium, and PTH
Recurrent - MC&S, pH, 24 h urinary calcium, phosphate, urate, oxalate, citrate, cystine, creatinine
Stone analysis for components (Fourier Transform InfraRed Spectroscopy)
Causes of low magnesiumm
- Low albumin – biologically active serum Mg is normal
- Electrolyte loss
- GI (malabsorption, diarrhoea, short bowel)
- renal tubular disease, e.g. chronic pyelonephritis, glomerulonephritis, recovery from acute tubular necrosis, post-transplantation - Poor intake - inadequate parenteral nutrition, malabsorption, starvation
- Drugs - thiazides, loop diuretics, aminoglycosides, amphotericin B, cytotoxics, cyclosporine, pentamidine, laxative abuse, proton pump inhibitors, e.g. omeprazole (rare)
- Alcoholism - common (1/3), multiple causes: diet, diarrhoea, renal tubular losses
- Endocrine - hyperthyroidism, hyperparathyroidism, poorly controlled diabetes (osmotic diuresis), hyperaldosteronism, SIADH
- Redistribution - alkalosis, correction of acidosis, severe stress, ‘hungry bone’ syndrome after parathyroid surgery
- Chelation - acute pancreatitis, post-transfusion, foscarnet therapy
- Genetic causes - Bartter, Gitelman syndromes
- Late pregnancy - combination of low albumin and respiratory alkalosis
- High fat diet - up to 10% of patients (mechanism unclear)
Causes of hypoglycaemia in an infant/newborn
- Idiopathic ketotic hypoglycaemia
- Hormonal abnormalities
Insulin excess (non-ketotic)
Counter-regulatory hormone deficiency (ketotic)
eg deficiency of growth hormone or cortisol - Hepatic enzyme deficiencies (ketotic), eg
o Involving glycogen breakdown or synthesis - Glucose-6-phosphatase deficiency, Debrancher deficiency, etc
o Involving gluconeogenesis - Fructose-1,6-diphosphatase deficiency, etc - Other enzyme deficiencies, eg
o Fatty acid oxidation defects (non-ketotic – but not all cases)
o Congenital disorders of glycosylation (phosphomannose isomerase deficiency) - Reaction to drugs or toxins
- Secondary to other systemic disease
Liver failure
Gastroenteritis
CNS disorders
Reye’s syndrome, etc - Iatrogenic – following fundoplication, with gastric tube feeding
Investigation of neonatal hypoglycaemia
o Glucose
o Insulin
o Cortisol
o Growth hormone
o Plasma β-hydroxybutyrate and free fatty acids
o Lactate
o Acylcarnitines (elevated in fatty acid oxidation defects)
o Urine metabolic profile (looking for abnormal patterns of organic acid excretion which may be seen in fatty acid oxidation defects, etc)
o Urine drug screen
o Ammonia (rare possibility of the hyperammonaemia, hypoglycaemia syndrome – activating mutation in glutamate dehydrogenase)
o Other tests – electrolytes and acid-base studies
What substances within the RBC cause interference by haemolysis?
Hb
AST
K
Mg
LDH
Phosphate
Adenylate kinase
Proteases
Rule of thumb: resp compensation for met acidosis?
Winter’s formula: pCO2 = 1.5HCO3 + 8 (+/-2)
Rule of thumb: resp compensation for met alkalosis?
For every 10 mmol/L increase in HCO3, pCO2 should increase by 7 mmHg (by 24 hours)
Expected changes in acute diarrhoea
Expected changes in chronic diarrhoea
Rule of thumb: compensation for acute respiratory acidosis
Every 10mmHg rise in pCO2, 1mmol/L rise in HCO3
Rule of thumb: compensation for chronic resp acidosis
Every 10mmHg rise in pCO2, 3.5 mmol/L rise in HCO3
Rule of thumb: compensation for acute respiratory alkalosis
Every 10mmHg fall in pCO2, 2 mmol/L fall in HCO3
Rule of thumb: compensation for chronic respiratory alkalosis
Every 10mmHg fall in pCO2, 5 mmol/L fall in HCO3
Diagnostic test for protein losing enteropathy
Faecal alpha-1-AT - spot or 24hr clearance
(why - A1AT shows minimal degradation and secretion by GIT, and has similar MW to albumin)
Calculation of 24hr clearance A1AT?
(stool vol x stool [A1AT])/serum [A1AT]
Causes of protein-losing enteropathy
Non GI vs GI
NonGI causes (Lymphatic obstruction vs Cardiac):
Lymphangiectasia
Portal hypertension
Fontan procedure (for univentricular heart)
Congenital heart disease
Congestive heart failure esp RHF
Pericarditis
GI causes (Erosive vs Non-erosive)
Erosive:
IBD primarily Crohn’s
NSAID abuse
Gut malignancy
GVHD
Sarcoidosis
Non-erosive:
Amyloidosis
Collagenous colitis
Sprue
Eosinophilc gastroenteritis
Lupus and ANCA vasculitis, Sjogrens
