Notes

Mini Problem 3 :Myocardial infarction
1. What is Ms. Nora suffering from?
Familial Combined Hyperlipidemia (FCH)

2. What is familial combined hyperlipidemia?
Inherited condition which individuals have high TGI + high cholesterol level. D/T genetic abnormalities.

3. How common is FCH?
1% of the population, most common genetic cause of hyperlipidemia. People with FCH had increased risk of CVD

4. Name two differences between familial combined hyperlipidemia (FCH) and familial hypercholesterolemia (FH)?
FCH: caused by Several loci, as well as environmental factors. The diagnosis of FCH by an increase in apolipoprotein B, together with elevated numbers of small, dense LDL particles. 
FH: is autosomal dominant and associated with early vascular disease diagnosis based on high LDL-cholesterol levels (usually 250 mg/dl) in untreated adults and frequent tendinous xanthomas. 

5. What is the treatment of FCH?
• A healthy lifestyle: reducing saturated fats
• Medication: depend on the individual’s levels of TGI and cholesterol:
Statins, ezetimibe,bile acid-sequestering resins, Fibrates ,Nicotinic acid and a newer class PCSK9 inhibitors

Which type of anti-lipidemic drugs you would chose for patients with FCH?
Drugs that reduce cholesterolemia and triglyceridemia ???

6. WHY THE DOCTOR DID ORDERED ALL CARDIAC BIOMARKERS AND NOT JUST ONE?
• Glycogen phosphorylase isoenzyme BB (GPBB): specific to heart muscle ,so most specific for myocardial infarction
• Troponin: The most sensitive and specific test for myocardial damage and stay raised for longer time up to 7 days.
• creatine kinase CK-MB : raised fast and go down fast ,back to normal within 2–3 days..


7. What is the mechanism of Niacin action? Niacin affects apolipoprotein B-containing lipoproteins (VLDL,LDL and lipoprotein a) so increases HDL and Inhibit triglycerides (TG) synthesis 


8. What are the side effects of Niacin? And what is the second line of drugs that can be used?
Flushing or redness of the skin. All are prostaglandin mediated side effects so aspirin (30 min before the Niacin) will reduce them.


9. What is the action of aspirin in MI?
Inhibits platelet generation effect d/t TXA2 = antithrombotic effect.

10. After 3 months therapy with Pravastatin the result of Ms. Nora lipid profile was as follow.. 

11. Comment on the two result?
Still high

12. What is the rational for using GPBB as biomarker for MI?
It is specific for MI , since it is found only in the heart and brain , but due to blood brain barrier that it can’t pass, so the presence of GPBB would indicate myocardial infarction .


13. What is the type of pain experienced by the patient?
Visceral pain d/t ischemia

14.Which nerves carry the pain sensation from the heart?
Sympathetic nerve fibers from the sympathetic trunk in the thoracic and cervical trunk

15. Which spinal cord segments are involved in pain transmission?
T1-T4

16.Which coronary artery involved in this type of infarction?
RCA or the circumflex since she has a posterior infarction where the two arteries meet, but in inferior infarct ,the involved one is RCA and LCA if lateral infarct

17.Which part of heart is supplied by the affected artery?
Posterior wall, basal part of the LV, posterior third interventricular septum.

18. Is there any possible that the SA node might be affected by the occlusion of the artery? Why?
Yes, because the right coronary artery supplies right atrium in 60% of cases 
19 What are the changes seen in this ECG?what is your diagnosis?
ST segment elevation, Inverted T waves
the diagnosis is posterior MI.