Di

Fever is part of:

A. defense mechanism of our body

B. A cellular activated response
C. A T lymphocyte activation
D. All of the above
E. A and C
What is the most common
cardiovascular manifestation of
thyrotoxicosis?

A. Sinus Tachycardia
B. Atrial Fibrillation
C. Atrial Flutter
D. Ventricular tachycardia
The following are causes of high
output failure except
• A.thyrotoxicosis
• B.hypothyroidism
• C.Fever
• D.arteriovenous fistula
The following are uremic
manifestations except:

A. Vomiting
B. Anorexia
C. Difficulty of breathing
D. None of the above
Diabetes

• The macrovascular complication of

Diabetes is:
• A. Nephropathy
• B. Retinopathy
• C. coronary artery disease
• D. Neuropathy
Pathogenesis (COPD):

1. Chronic exposure to cigarette smoke

may lead to inflammatory cell
recruitment within the terminal airspaces
of the lungs.
2. Inflammatory cells release elastolytic
proteinases which damage the
extracellular matrix of the lung
 Acute ST elevation MI
• Pathogenesis: thrombotic occlusion of a coronary
artery previously affected by atherosclerosis
• Pathology: disrupted atherosclerotic plaque
 thrombogenesis (platelet activation 
coagulation cascade )  coronary artery
occlusion
• Pathophysiology: coronary artery occlusion 
sudden decrease in oxygen supply  myocardial
damage
Diagnosis of Acute ST elevation MI
ECG Cardiac biomarkers imaging

ST segment elevation Troponin T and 2Decho- wall motion

Troponin I  20x abnormality;
higher than upper decreased LV
reference limit; function; RV infarction
elevated up to 7-10
days

Presence of Q waves CKMB- increased up to Myocardial perfusion

4-8 hours; return to imaging
normal in 48-72H;
lacks specificity
Loss of R waves Cardiac MRI
Treatment of Acute ST elevation MI

• emergency treatment: ASA, sublingual

NTG, O2 inhalation, morphine, IV beta
blockers
• Reperfusion: PCI vs fibrinolytics
(streptokinase, r-TPA, glycoprotein IIb-
IIIa inhibitors) vs CABG
• Antithrombotics: UFH, LMWH
• Others: beta blockers, ACE-I, ARBs
Prevention of Acute STEMI

• Primary : Control of risk factors:

- Smoking, hypertension, dyslipidemia,
diabetes, stress and/or weight
management
- Secondary/ Tertiary : ASA , statins, beta
blockers, ACE-I/ARBS
Pathogenesis:

3. Loss of matrix-cell attachment leads to

apoptosis of structural cells of the lungs.
4. Ineffective repair of elastin and other
extracellular matrix components result in
airspace enlargement that defines
pulmonary emphysema.
Pathogenesis (CAD):

Inadequate supply of blood and oxygen

to a portion of myocardium
Atherosclerosis of epicardial coronary
artery