Pharmacology of CV Disease Flashcards
What can hypertension cause?
End organ damage
Brain - strokes, heart failure, renal failure, hypertensive retniopathy
How tx hypertension?
- Non-pharmacologically - lifestyle (less fat, salt, alcohol, smoking cessation)
- Antihypertensives (CAB TA)
Name 5 anti-hypertensives?
Ca channel blocker, ACE inhibition, beta blockers, thiazide, ARBs
Explain use of thiazide diuretics in hypertension
Inhibit reabsorption of NaCl in proximal/ early distal tubule
Cheap and used first line
E.g bendroflumethiazide
Explain use of ACE inhibitors in hypertension
Inhibit conversion angiotensin I –> AG2
Side effect: prevent bradykinin breakdown = dry cough
e.g Ramapril
Explain renin-angiotensin pathway - what does the end product cause?
Angiotensinogen –> angiotensin I (renin)
Angiotensin I –> Angiotensin II (ACE)
Angiotensin II –> Receptors (A2R)
Aldoesterone production -reabsorb H20/ Na = raise BP
Explain use of ARBs in hypertension?
Angiotensin II receptor antagonist - similar to ACE but doesn’t involve bradykinin - no dry cough
e.g Losartan
Explain use of Ca Channel blockers in hypertension?
Cause vasodilation by decreasing systemic vascular tone
- dipine e.g amlodipine
How do atherosclerotic plaque form?
- Defect in blood vessel lining
- Fatty streak form - lipid accumulation in foamy macrophage in tunica intima
- Fibrolipid plaque formed as collagen deposited = fibrous cap that bulge into lumen
- Cause lymphocyte accumulation
- If cap become unstable - plaque can be exposed to blood = thrombosis
How does atherosclerosis progress to thrombosis?
Virchow triad: stasis, hyper coagulability, endothelium injury
- Fatty steak enlarge = atherosclerosis
- Increase turbulence due to protrusion - loss endothelium and collagen exposure
- Platelet activation and adherence of fibrin meshwork to trap RBC
- Further increase turbulence
What is a thrombosis made from?
Layer platelet, fibrin and entrapped RBC
What drugs can be used for angina?
NPCB
Nitrates, potassium channel activator, ca channel blockers, beta blockers
Use of beta blockers in angina?
Lower myocardial O2 demand by decreasing HR and contractibility
Can’t be withdrawn suddenly
Use of nitrates in angina?
Oral or sublingual - quicker access to systemic circulation
Nitric oxide produced on endothelial surface = smooth muscle relaxation and arterial and venous dilation
Decrease myocardial demand
Some problem with tolerance
Use of potassium channel blockers in angina?
Cause arterial and venous dilation
Second line therapy - mucocutaneous ulceration but no prob with tolerance
