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46 Cards in this Set

  • Front
  • Back
What is arteriosclerosis?
A thickening & hardening of the arteries, involving the intimal layer & leading to HTN.
What is atherosclerosis?
A form of arteriosclerosis, that begins w/endothelial injury & progresses through several stages to become a fibrotic plaque.
What is the leading contributor to CAD & CVD?
Atherosclerosis
What causes HTN?
Increases in cardiac output or/& total peripheral resistance.
What are the risk factors for HTN?
Family hx, male gender, advancing age, black race, obesity, high Na intake, Low magnesium, K or Ca intake, DM, labile blood pressure, smoking, heavy ETOH use.
What is the pathophysiology of HTN?
Damage & inflammation of the vessel walls that stimulate the vessels to thicken, harden & become narrow, Narrowing causes vasoconstriction & increases the permeability of the vessel walls, leading to influx of Na, Ca, H2O, plasma proteins. Ca increases smooth muscle contraction.
What are the hypothesis of the cause of primary HTN?
1.Overactivity of the sympathetic nervous system. 2.Overactivity of the renin-angiotensin-aldosterone system. 3.Na & H2O retention by the kidneys 4. Hormonal inhibition of Na-K transport across cell walls. 5. Complex interactions involving insulin resistance & endothelial function.
What causes the clinical manifestations of HTN?
Damage of organs & tissues outside the vascular system. (Hrt Dz, Renal Dz, CNS problems, Musculoskeletal dysfunction)
What is orthostatic hypotension?
A drop in BP that occurs on standing.
What causes the acute form of orthostatic Hypotension?
A delay in the normal regulatory mechanisms.
What causes the chronic form of orthostatic Hypotension?
They are secondary to specific dzs or are idiopathic.
What are the clinical manifestations of orthostatic Hypotension?
Fainting & may involvecardiovascular sx as well as impotence & bowel & bladder dysfunction.
What is an aneurysm?
A localized dilation of a vessel wall (the aorta is particularly susceptible)
What is a thrombus?
A clot that remains attached to a vascular wall.
How can arteriosclerosis generate thrombus formation?
Through roughening of the intima that activates the clotting cascade.
What is the most common source of arterial thrombotic emboli?
The heart, as a result of mitral & aortic valvular dz & Afib, followed by myxomas
What is a myxoma?
Tumor composed of mucous connective tissue similar to that present in the embryo or umbilical cord. Cells are stellate or spindle-shaped and separated by mucoid tissue.
What are the tissues affected by a emboli that starts in the heart?
The lower extremities, the brain & the heart.
What is a embolus?
A mobile aggregate of a variety of substances that occludes the vasculature.
What are some common sources of emboli?
Clots, air amniotic fluid, bacteria, fat & foreign matter.
What does an air emboli require?
A connection between the vascular compartment & a source of air.
What are the main causes of fat emboli?
Trauma to the long bones, either through defective fat metabolism p trauma or through the release of fat globules from bone marrow exposed by fx.
Vasoplastic disorders include what dzs?
Raynaud dz (involving arterioles of the extremities), Prinzmetal angina (involving coronary arteries), Buerger dz (involving arteries of the hands & feet).
Name the possible cause of diabetic lesions of the arteries?
A defect in glycoprotein metabolism that involves the capillary basement membranes in kidneys, retinas, & extremities.
What are varicosities?
Areas of veins in which blood has pooled (usually in the saphenous veins).
What can cause varicosities?
Damaged valves due to trauma or by chronic venous distention involving gravity & venous constriction.
What is chronic venous insufficiency?
Inadequate venous return over a long period of time that causes pathologic ischemic changes in the vasculature, skin, & supporting tissues.
What can follow the development of chronic venous insufficiency?
Venous stasis ulcers.
What is a possible cause of venous stasis ulcers?
Borderline metabolic state of the cells in the affected extremities.
Is the pathophysiology of thrombus formation in the veins the sames as thrombus formation in the arteries?
Yes
What is superior vena cava syndrome?
A progressive occlusion of the superior vena cava that leads to venous distention in the upper extremities & head.
What is usually the cause of superior vena cava syndrome?
Bronchogenic cancer
What is usually the cause of Coronary artery dz (CAD)?
Atherosclerosis.
What are the risk factors of CAD?
Dyslipidemia, smoking, HTN, DM, advancing age, obesity, sedentary life-style, psychosocial factors, hyperhomocystimemia & heavy ETOH use.
What are the 3 risk factors most predictive of CAD?
Hypercholesterolemia, smoking & HTN.
What is usually the cause of ischemic heart dz?
CAD & the resultant decrease in cyocardial blood supply.
What is angina pectoris?
CP caused by myocardial ischemia.
What are some therapeutic interventions for CAD?
Vasodilators & meds to reduce cardia workload (eg Bblockers), Surgical procedures.
What are the 3 types of cardiomyopathies?
Dilated cardiomyopathy, Hypertrophic cardiomyopathy & Restrictive cardiomyopathy.
What are the 3 clinically useful ways to classify infective endocarditis?
1. Clinical Course,
2. Host substrate,
3. The specific interfering microorganism.
Acute bacterial endocarditis?
Presents as an acute, fulminating infection, is highly virulent & an invasive organism is implicated, may occur on previously healthy hrt valves.
Subacute bacterial endocarditis?
Less virulent organisms involved, usually occurs in pts w/previous underlying valvular damage.
What Infective Endocarditis' are classified by clinical course?
Acute bacterial endocarditis & Subacute bacterial endocarditis.
What Infective Endocarditis' are classified by Host Substrate?
Native valve endocarditis (60-80% of host substrate IE), Prosthetic valve endocarditis & in IE caused by intravenous drug abuse.
What is the most common cause of endothelial injury?
Turbulent blood flow resulting from underlying valvular abnormalities.
70% of pts w/endocarditis have?
Evidence of underlying structural or hemodynamic abnormalities.