1. CASE STUDY ON ACUTE MYOCARDIAL
(DEPARTMENT OF CARDIOLOGY)
2. CASE HISTORY
• 46 years old, male patient was brought to hospital on
Cardiology OPD; he was having the symptom of
• shortness of breath
• chest pain (angina)
• discomfort in back
• fatigue from last few weeks
Based on the interaction with patient family
• the patient was diagnosed with hypertension previously
• none of the family member has any issues related to CVD.
• he used to be an active smoker.
3. DISEASE JUSTIFICATION BY PATIENT SYMPTOMS
TEST & REPORTS
TESTS REPORT NORMAL
1 KFT: UREA
122 [mg/dl] High↑
2 LFT: SGPT
160 [U/L] High↑
3 BLOOD PRESSURE every three days Report
170/80 mm/hg HR: 110 b/m
160/ 80 mm/hg HR: 107b/m
160/80 mm/hg HR:106b/m
160/70 mm/hg HR: 103b/m
150/70 mm/hg HR: 95b/m
4. ECG Report
From observing the patient symptoms and above test report it was found
out that our patient is diagnosed with Acute Myocardial Infraction.
5. ACUTE MYOCARDIAL INFARCTION
• Acute Myocardial infarction (heart attack) occurs when blood flows
stop or decreases to the coronary artery of the heart
• Symptoms include chest pain (angina), shortness of breath, fatigue,
discomfort in back, arm and shoulder.
• major risk factor to develop atherosclerosis like hypertension,
diabetes mellitus, cigarette smoking and dyslipidemia.
• Male are at the significantly higher risk of developing MI as compared
females probably due to the protective influence of estrogen.
8. JUSTIFICATION OF PRESCRIBED DRUG WITH MECHANISM
SI NO DRUGS DOSE MECHANISM OF ACTION CLASS
1g IV The beta lactam ring inhibits the final transpeptidation step of
peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell
2 Aspirin 300mg It is NSAID which inhibits cycloxygenase which leads to formation
of prostaglandins that cause inflammation
20mg IV Inhibition of Na+-k+-2 cotranspoter. It preventing the transport of
sodium ions from the luminal site into the basolateral site for
40mg Telmisartan interferes with the binding of angiotensin II to the
angiotensin II AT1-receptor by binding reversibly and selectively to
the receptors in vascular smooth muscle
NTG is converted to nitric oxide (NO), an active substance which
then activates the enzyme guanylate cyclase. The activation of this
enzyme convert GTP to (cGMP), activating a cascade of protein
kinase-dependent phosphorylation events in smooth muscles.
9. PHARMACEUTICAL CARE
Educating the patient.
Adopting a new good dietary pattern, advised to avoided some
herbs as they are blood thinner.
Check Electrolyte (Na+) balance in body, if found high, control
Consult the doctor if any sever adverse effect is caused observed
due to the prescribe medication
staying away from potential risk factors including smoking and