Coronary Heart Diesase and Thromboembolic CV pathologies Flashcards
Oxygen supply to myocardium
- Hearts myocardium receives high levels of oxygen during diastole as blood is entering heart
- When there is no contraction heart receives high amount of blood supply
Coronary circulation
- Two tiny arteries leaving out of the aorta
- Profuse blood to the myocardium
- Handles high BP
Myocardial ischemia
- Thickening of internal surfaces of arteries or progression of atherosclerosis lesions occlude oxygen supply cause CVD
Coronary artery flow angina
- Atherosclerosis lesions narrow coronary artery and reduce ability for dilation
- Lesions rupture and stimulate platelet aggregation causing thrombus to occlude artery restrict blood supply
Symptoms of angina
- Reduced capacity in artery causes stress chest pains no change in troponin ECG
Unstable angina
- Rapid reduction of blood flow due to rupture severe chest pain requiring urgent treatment
- No change in troponin some ST depression in ECG
Antianginal drugs
- Nitrates for acute attacks/ preventative measures - sublingual glyceryl trinitite
Nitric acid cytoplasmic guanylyl cyclase receptor
- Nitric oxide endothelium derived vasodilator factor
- Stimulate cytoplasmic guanylyl cyclase
- Activate protein kinase G causing smooth muscle dilation
- PDE isoform breaks down cGMP
Nitrates
- Acute angina attacks/ Preventative measure
- Isosorbide dinitrate (organic)
- Isosorbide mononitrate (organic)
- nitroglycerin
The effects of nitrates on Systemic vasculature
- Increased venous dilation
- decrease venous pressure
- Decrease arterial pressure
The effects of nitrates on cardiac
- Reduced preload and afterload
- Decrease oxygen demand
The effects of nitrates on coronary
- Prevents reverse vasospasm
- Vasodilation
- Improves subendocardial perfusion
- Increased oxygen delivery
Beta-Blockers
- Cardio specific depression of sympathetic activity
- Reduce heart rate & lengthened diastole
- Increased oxygen supply to myocardium
- Patient with variant angina or HF are contraindicated
Calcium- Channel blocker
- Verapamil and diltiazem cardiac specific
- Amlodipine effective for patient with Prinzmetal angina
Second line inhibitors
- Ivabradine selectively block hyperpolarization activated cyclic nucleotide gate in SA node
- Lowers heart rate without effecting contractility of cardiac muscle
Class ID sodium channel blocker
- Ranolazine blocks late inward sodium currents occurring during phase II of ventricular action potentials
Potassium channel activator
- Nicorandil activate ATP sensitive K+ channels to enhance K+ efflux and hyperpolarization of vascular smooth muscle
- Decrease calcium ion entry reduce cardiac contraction
Progressive CVD
- Narrowing transient occlusion or microembolization of thrombus
Non-ST segment elevation MI
- Myocardial ischemia and necrosis changes in troponin and no change in ECG
Extreme CVD
- Complete and prolonged exclusion of epicardial coronary blood vessel
ST Segment elevation MI extreme
- Dysfunction and death of cardiac myocytes
- Troponin levels increase and elevation of ST levels and ECG
Thrombosis
- Blood clotting in artery
Embolism
- Blood clot materials moving in the blood vessel obstruct flow
Cardiovascular atherosclerosis
- Fat deposit and aggregation of thrombus ruptures and reaches small arteries causing ischemia
Risk factors that lead to thrombus formation
- Endothelial dysfunction - Smoking and hypertension
- Hypercoagulability - Hereditary - Factor V Leiden, Protein C and S deficiency, Cancer
Stasis - immobility polycythemia
Artery
- Thrombocytes (Platelets)
- Contain no nucleus/ mitochondria and blood clotting
Haemostasias - Vascular spasm
- Rupture in Artery
- Vascular spasm occurs prevent blood loss
- Create signal for clotting factors chemicals and mediators released at sight of injury
- Damage to collogen, endothelial cells and vascular smooth muscle cells
Platelet activation plug
- Platelet stick to exposed collogen
- Platelets stimulate ADP, Thromboxane A2 and serotonin
- Van-Wilbur factor stabilizes collogen and platelet adhesion
Coagulation patch
- Clotting factors in the liver, vitamin K and the biosynthesis of I to XIII
- Prothrombin Activator to Prothrombin to Thrombin to fibrinogen to fibrin insoluble to fibrin mesh
Platelet endothelial interaction
- thrombin activate platelet by PAR
- Platelets stick on exposed collogen
- Protease activated receptor is mediated by the thrombin for platelets to interact with cell surface
Clot regulation in a healthy individual
- Endothelial cells in plasma membrane release heparin
- Work as anticoagulant recruit antithrombin in circulation AT-III binding negatively inhibits thrombin activation on platelet
- Clot formation prevented
Atherosclerosis
- Thrombin mediated platelet activation become abrupt and accelerated due to endothelial dysfunction and damage
Platelet endothelial interaction (ADP - mediated process)
- Activated platelets stimulates release of ADP which acts on P2Y 12 receptors activate positive feedback change platelet to start shape
Negative feedback of ADP during Haemostasias
- ADP binds P2Y1 receptor stimulates the release of prostacyclin and nitric oxide from endothelial cells to prevent plug formation
Atherosclerosis
- ADP meditated platelet formation become accelerated due to endothelial dysfunction damage
- Smoking and hyperlipidemia damage endothelial and challenge negative feedback more clot
Platelet fibrin plug formation
- Von-Wilber factor bridge between collogen exposed in damaged blood vessels & glycoprotein receptor GPIIb expressed in activated platelets
- GPIIb receptor binds fibrinogen and form platelet fibrin plug
Clot and vessel healing
- Clot retraction occurs actin and myosin in platelet contract pulls fibrin
Platelet derived growth factor
Stimulate smooth muscle and fibroblast division
Vascular endothelial growth factor
- Rebuilds endothelial lining by multiplying endothelial cells
Fibrinolysis
- Plasminogen plasma protein trapped in clot converted and plasmin digest fibrin