Cardiac Flashcards

1
Q

Definition of Atherosclerosis

A

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

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2
Q

Stages of Atherosclerosis

A
  1. Fatty streak: Earliest lesion. Composed of lipids
  2. Fibrous plaque: Advanced lesion. Composed of lipids, collagen, smooth muscle cells, debris from cellular necrosis. Protrude into lumen of vessel
  3. Complicated lesion: Plaques rupture due to release of macrophage degradative enzymes. Known as “unstable” plaques
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3
Q

Common risk factors for atherosclerosis

A

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)

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4
Q

Pathogenesis of Atherosclerosis

A

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

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5
Q

Clinical Manifestations of Atherosclerosis

A

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

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6
Q

Thrombus formation

A

an abnormal clot that is formed in a vessel

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7
Q

Embolus formation

A

floating clot that lodges somewhere

Emboli usually break off from thrombi

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8
Q

Deep vein thrombosis

A

Thrombi in deep veins

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9
Q

Virchow’s Triad

A
  1. Endothelial damage–>transudate–>hemoconcentration
  2. Flow/Stasis
  3. Hypercoagulable state–>thrombosis
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10
Q

Risk factors for venous thrombosis

A

Venous stasis, hyperreactivity of blood coagulation, vascular trauma

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11
Q

Patho of DVT

A

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)
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12
Q

Definition of HTN

A

Sustained SBP of 140 mmHg or greater or DBP of 90 mmHg or greater

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13
Q

Primary (Essential HTN)

A

No identifiable cause; modifiable

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14
Q

Secondary HTN

A

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

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15
Q

Malignant HTN (Hypertensive crisis)

A

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

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