Cardiac Flashcards
Definition of Atherosclerosis
Thickening and hardening of vessel are caused by accumulation of lipid-laden macrophages within arterial wall, which leads to formation of a lesion called a plaque
Classified as an inflammatory disease
Stages of Atherosclerosis
- Fatty streak: Earliest lesion. Composed of lipids
- Fibrous plaque: Advanced lesion. Composed of lipids, collagen, smooth muscle cells, debris from cellular necrosis. Protrude into lumen of vessel
- Complicated lesion: Plaques rupture due to release of macrophage degradative enzymes. Known as “unstable” plaques
Common risk factors for atherosclerosis
Non-modifiable: Age, gender, hormones, family history
Modifiable: Tobacco, HTN, dyslipidemia, DM, obesity, sedentary lifestyle, alcohol, atherogenic diet
Non-traditional: Hyperhomocystinemia, Infection (cytomegalovirus, chlamydia pneumonia, H. Pylori as marked by C-reactive proteins)
Pathogenesis of Atherosclerosis
Risk factor–>injury–>inflammation–>
Macrophages release oxygen radicals & growth factors. Oxidation of LDLs & smooth muscle cell proliferation–>
Engulfment of oxidized LDL & smooth muscle cells by macrophages–>
Fatty streak–>
Continued inflammation, increased release of oxygen free radicals, more smooth muscle cell proliferation, fibroblast proliferation, fibrous plaque–>
Continued inflammation, plaque ruptures, complicated lesion. Plaque hemorrhages, platelets adhere, clotting cascade, thrombus formation
Clinical Manifestations of Atherosclerosis
Occur due to ischemia occuring distal from the site of occlusion. Atherosclerosis in:
Carotid Artery: CVA (stroke)
Femoral artery: Peripheral vascular disease (PVD)
Coronary artery: Angina and Myocardial Infarction (MI)
Renal artery: HTN, ESRD
Thrombus formation
an abnormal clot that is formed in a vessel
Embolus formation
floating clot that lodges somewhere
Emboli usually break off from thrombi
Deep vein thrombosis
Thrombi in deep veins
Virchow’s Triad
- Endothelial damage–>transudate–>hemoconcentration
- Flow/Stasis
- Hypercoagulable state–>thrombosis
Risk factors for venous thrombosis
Venous stasis, hyperreactivity of blood coagulation, vascular trauma
Patho of DVT
Vascular trauma–>stasis–>platelets adhere
Platelets adhere to collagen–>ADP released–>additional platelets attracted–>platelet plug
Coagulation cascade
Pulmonary embolus (if dislodges) OR Inflammation (if deep vein obstructed)-->Pain, erythema, fever, unilateral sweling, Homan's sign-->Venous insufficiency (if inflammation destroys valves)
Definition of HTN
Sustained SBP of 140 mmHg or greater or DBP of 90 mmHg or greater
Primary (Essential HTN)
No identifiable cause; modifiable
Secondary HTN
Non-modifiable risks
Kidneys: Renal failure, renal artery stenosis
Hormonal changes: Hyperaldosteronism, Cushing’s syndrome, hyperthyroidism, pheochromocytoma (E/NE), pregnancy induced
Changes in arteries: Vasculitis
Drugs: Oral contraceptives, corticosteroids
Malignant HTN (Hypertensive crisis)
Sudden increase in SBP and/or DBP
SBP greater or equal to 210 and/or
DBP greater or equal to 120
Medical emergency
Most cases caused by secondary HTN (e.g., Guillian Barre syndrome, autonomic dysreflexia, withdrawal from beta blockers) or poorly controlled primary HTN