Muscle and cardiac markers Flashcards
1
Q
What is myoglobin
A
- Haem like and has iron
- Extracts O2 very well and stores it for muscles
- Found in cytoplasm of muscle cells
- Small molecule so when damaged will leak into bloodstream and be filtered by glomerulus
- Brown urine= excess myoglobin- this can damage renal tubules and cause AKI
2
Q
What is creatinine kinase
A
- Things that increase myoglobin also increase this
- More specific to muscle damage as is used when muscle contracts to generate ATP
- Has 2 subunits M/B
- Skeletal muscle= CKMM
- 30% Cardiac muscle muscle= CK-MB (if increased indicates cardiac damage)
- Plasma CK= mainly CKMM
3
Q
What is aspartate aminotransferase
A
- Less muscle specific
- Highest conc in liver
- High levels and no liver abnormality - could be cardiac
4
Q
What is lactate dehydrogenase
A
- Found in all cells
- Marker of cell breakdown (will increase with high number of cells or a quick increase in cells)
- Can indicate tumour growth in some leukaemia/ lymphomas
5
Q
What is CK-MB
A
- After ischaemia it will increase for 4-9 hrs and back to baseline at 48-72 hours (helpful at looking for reinfarction)
- Not cardiac specific
- Used alongside ECG changes
6
Q
How can you tell the difference between myositis and rhambomyolysis
A
- Myositis will have mild increase in CK with increased level of muscle breakdown
- Rhabdomyolysis will have increased CK 5-10 times the upper limit with catastrophic rapid muscle breakdown and dark urine
7
Q
Discuss the features of Rhabdomyolysis
A
- Increased CK and myoglobin
- AKI caused from increased myoglobin (high urea, creat, eGFR)
- High potassium and phosphate (rapid cell breakdown- watch for arrhythmia with K)
- Metabolic acidosis - (AKI or acids release from muscle- lactic acidosis- muscle ischaemia)
- Increased uric acid - protein/ purine release when muscles are broken down
- Calcium- falls first then increased in recovery phase -binds to protein in damaged muscle cells
8
Q
List the various causes of skeletal muscle disease
A
- Physical injury- crush syndrome, ischaemia, hypothermia, post seizure
- Inflam- autoimmune, ploymyosisitis, viral
- Electrolyte: Hypo/hyperkalaemia , hypocalcaemia, hypophosphateamia, hypomagnesia
- Endocrine- Hypo/hyper thyroid, hypo/hyper andrenalism
- Genetic metabolic- mitochondrial disorders
- Genetic- non metabolic, muscular dystrophies, malignant hyperpyrexia
- Paraneoplastic
9
Q
What is troponin and how does it relate to cardiac damage
A
- A regulatory protein for contractile mechanism - actin and myosin
- Tropomyosin binds to actin and prevents contraction
- Troponin changes the binding of tropomyosin allows contraction
- Specific cardiac troponin complex - troponin T and troponin I
- Troponin I = inhibitory protein
- Troponin T= anchors tropomyosin complex
- Troponin C= binds to calcium - causes change in tropomyosin binding- allows muscle contraction
- Changes in Trop I and Trop T in someone with chest pain = mI
- Rise after infarct can take 7 days to come back down- can’t detect reinfarct
10
Q
What are the steps in the chest pain pathway
A
- ECG and baseline troponin and changes at 1 hr and 3 hrs
11
Q
What are other causes of increased troponin that are not an MI
A
Non cardiac
- Acute illness
- PE
- Sub arachnoid haemorrhage
- Stroke
- CKD
- Sepsis
- Severe exertion
Cardiac
- Acute myocarditis (viral/autoimmune)
- Post-cardiac surgery
- Aortic dissection
- Cardiomyopathy
12
Q
What is BNP
A
- Causes loss of sodium and water and relaxes smooth muscle
- Mainly for diagnosing chronic/ acute heart failure
- Main source- left ventricle, secreted from myocytes
- BNP will increase in blood with age so need reference ranges
- Measure BNP in no history of IHD
13
Q
What are other causes of raised BNP and NT pro BNP
A
- PE
- Septic shock
- Liver cirrhosis
- Kidney injury
- COPD, Cor pulmonale
- Subarachnoid haemorrhage
- Stroke
- Hyperthyroid
- IHD
- AF
