Case study tutorials on clinical chemistry Flashcards
Case 1: - 56 M referred liver clinic - malaise and pruritis - increasingly unwell over last few weeks - past few days developed jaundice - urine has gone dark Blood tests: - Bilirubin = 97 (1-22) - ALT = 108 (<35) - AST = 97 (<31) - ALP = 396 (45-105) - Albumin = 32 (35-45) - gamma-GT = 750 (<55)
What is the best description of this pattern of results?
cholestatic
- due to the bilirubin being 97 this means the conjugated bilirubin fraction will be more than the unconjugated bilirubin
What causes cholestatic jaundice and what are the key signs?
caused by bile duct obstruction
- malignancy (cholangiocarcinoma, pancreatic carcinoma)
- gallstones
- sclerosing cholangitis
painful (galllstones, pancreatitis) vs painless (malignancy
bilirubin clinically detectable at >50
pale stools and dark urine
ALP»ALT
conjugated bilirubin>unconjugated bilirubin
When is ALT/ AST higher than ALP?
in hepatitis - ALP and gamma GT will only be slightly raised
Case 1: - 56 M referred liver clinic - malaise and pruritis - increasingly unwell over last few weeks - past few days developed jaundice - urine has gone dark Blood tests: - Bilirubin = 97 (1-22) - ALT = 108 (<35) - AST = 97 (<31) - ALP = 396 (45-105) - Albumin = 32 (35-45) - gamma-GT = 750 (<55)
Based on the Hx and exam what is the most likely cause?
carcinoma of the head of the pancreas= painless
- a pancreatic mass causing extrahepatic obstructionn and there were multiple hypoechoic lesions in the liver suspicious of metastatic deposits
referred to oncology for possible palliative chemo and ERCP with stenting
Case 2: - 68 retired secretary - tiredness and SOB - no pmhx but smoked 50 pack year history Blood test results: - free T4 = 3.2 (10-22) - free T3 = 0.2 (3.1-7.7) - TSH = 41 (0.4-4.5)
What is the biochemical abnormality?
What is the most likely cause of this biochemical abnormality?
primary hypothyroidism
- autoimmune thyroid disease - commonest cause of hypothyroidism
What is the earliest time at which repeat thyroid function testing is indicated i.e. full effects of levothyroxine treatment will be seen?
4 weeks - full time to take its affect
Case 3: - 71 F known hx of breast cancer- treated with oral anastrozole - after a wide local clearance 6 months earlier, presents with nausea, vomiting and widespread pains Blood results: - Ca2+ = 2.88 (2.2-2.6) - Albumin = 24 (35-45) - Phosphate = 0.96 (0.8-1.4) - ALP = 102 (45-105) - PTH = <1 (1.05-6.83)
What is the calculated adjusted calcium concentration ?
3.20 mmol/L = higher than the reported Ca2+
plasma Ca and albumin correction
= plasma Ca + [40-plasma albumin] x0.02
Why do you have to correct the calcium concentration based on albumin level?
calcium is present in 2 main forms:
- calcium bound to proteins (principally albumin)
- free ionised calcium
changes in plasma protein concentration alter the commonly measures plasma total calcium concentration
most labs report adjusted calcium conc
if albumin is low the Ca2+ will be high
Case 3: - 71 F known hx of breast cancer- treated with oral anastrozole - after a wide local clearance 6 months earlier, presents with nausea, vomiting and widespread pains Blood results: - Ca2+ = 2.88 (2.2-2.6) - Albumin = 24 (35-45) - Phosphate = 0.96 (0.8-1.4) - ALP = 102 (45-105) - PTH = <1 (1.05-6.83)
What is the most likely diagnosis?
hypercalcaemia of malignancy
- if you have a high calcium and a low PTH think malignancy
- high ca in blood suppresses PTH
What malignancies is hypercalcaemia associated with?
bony metastases e.g. breast, lung, prostate, kidney, thyroid
solid tumours with humoral effects
haematological tumours (multiple myeloma)
Clinically what does bony metastases look like?
hypercalcaemia associated with a rise in phosphate concentration and a rise in plasma ALP (usually due to osteoclast activity)
What is humoral hypercalcaemia of malignancy caused by?
synthesis of parathyroid hormone related peptide
- secreted in breast and certain lung tumours
- not detected by PTH assay
Which of the following clinical features is NOT associated with hypercalcaemia?
- constipation
- depression
- diabetes mellitus
- short QT interval on ECG
- thirst and polyuria
diabetes mellitus - can occur in insipidus but not mellitus
Case 4: - 15 F 10 day hx lethargy, thirst and polyuria - abdominal pain and been vomiting for last 2 days - clinically unwell, deep sighing breathing and dry mucous membrane - GCS 14/15 - BP 85/42 - 104 bpm Blood results - Na= 131 (135-145) - K = 6.3 (3.5-5.5) - Urea = 14.2 (4-8) - creatinine = 120 (75-105) - bicarbonate= 15 (22-28) - glucose = 35 (4-5)
What does the low bicarbonate prompt?
An ABG to be carried out
Case 4: - 15 F 10 day hx lethargy, thirst and polyuria - abdominal pain and been vomiting for last 2 days - clinically unwell, deep sighing breathing and dry mucous membrane - GCS 14/15 - BP 85/42 - 104 bpm Blood results - Na= 131 (135-145) - K = 6.3 (3.5-5.5) - Urea = 14.2 (4-8) - creatinine = 120 (75-105) - bicarbonate= 15 (22-28) - glucose = 35 (4-5)
Blood gas
- pH = 7.21
- pO2 = 18
- PCO2= 2.8
- HCO3= 12
What is the best description of this abnormality ?
What is the most likely diagnosis?
metabolic acidosis with partial respiratory compensation
- bringing CO2 down by deep sighing breathing = kusmal’s breathing
- only partial because although the CO2 is low the patient is still acidotic
Diabetic ketoacidosis
- resuscited with fluids and IV insulin infusion
- at risk of hypokalaemia
What is the treatment for diabetic ketoacidosis?
Aggressive fluid resuscitation - initially saline
- hyperglycaemia causes osmotic diuresis = dehydration can be severe
- fluid overload unlikely in young person with previously normal kidney function
- fluid balance should be carefully monitored
Intravenous infusion of insulin
- insulin co-prescribed with IV fluids
- weight based fixed rate IV infusion insulin
- hypoglycaemia should be preventable if protocol correctly followed
Monitor U/E
- lack of insulin => hyperkalaemia
- osmotic diuresis causes total body depletion of electrolytes including potassium and sodium
- insulin treatment drives potassium uptake causing hypokalaemia
Case 5: - 67 M presents to A&E - central crushing chest pain, radiates down L arm - hx exertional angina, smoking and DM ECG - ST elevation in inferior leads high sensitivity troponin T is 53 and 3 hours later its 244 What is the likely diagnosis?
acute MI - undergoes primary angioplasty with stenting of his RCA
Case 5:
- 67 M presents to A&E
- central crushing chest pain, radiates down L arm
- hx exertional angina, smoking and DM
ECG
- ST elevation in inferior leads
high sensitivity troponin T is 53 and 3 hours later its 244
Recovering well but then he has palpatations 3 days later:
- Na 131
- K 7.1
- Urea 9.8
- creatinine 184
- eGFR 34
- Glucose 12.1
What is the most immediately life threatening abnormality?
Then what biochemical investigation should be done?
hyperkalaemia
bicarbonate measurement based on renal failure
Which of the following ECG abnormalities is NOT associated with hyperkalaemia?
- broad QRS
- Flat P waves
- Prolonged QT interval
- Sinusoidal pattern
- Tented T waves
prolonged QT interval = associated with hypokalaemia
What are the common causes of AKI?
IV contrast agents ABX - aminoglycosides NSAIDs ACE inhibitors infection hypovolaemia
What are the main risk factors for AKI?
DM HF history of chronic kidney failure or liver impairment hypovolaemia sepsis drugs (NSAIDs, ACEi, contrast agents) symptoms of urinary obstruction
Case 6:
- 63 M acute confusion
- shallow breathing, RR 28
- early finger clubbing
- absent R sided breath sound and dullness to percussion
- not oedematous
Bloods
- Na 116
- K 3.7
- urea 2.2
- creatinine 92
- bilirubin 13
- ALP 376
- ALT 41
- albumin 28
CXR confirms R sided pleural effusion and an opacity in the R lower zone
- on bendroflumethiazide for hypertension and has a 40 pack yr smoking hx
What is the most likely cause of his hyponatraemia?
syndrome of inappropriate ADH secretion - most likely caused by ADH secreting lung tumour
Why is it important not to correct hyponatraemia rapidly?
rapid correction with twice normal saline can cause pontine demyelination which can be fatal
What does SIADH cause?
intravascular fluid retention/haemodilution leading to low serum osmolality with high urine osmolality
hyponatraemia is caused by haemodilution rather than total body sodium depletion
What commonly causes SIADH?
UNDERLYING CAUSE: intracranial pathology - infections (meningitis, abscess) - subarachnoid haemorrhage - tumours
Lung pathology
- infections (pneumonia, abscess)
- malignancy
- sarcoidosis
Drugs
- SSRIs, carbamezepine, amitriptyline
How is SIADH treated?
fluid restriction +/- demeclocyline or similar
What level of hyponatraemia is potentially life threatening?
<115 - can be if its rapid
correction with IV saline is only necessary if its a total body sodium depletion
correction should always be done slowly
