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HES 311 > week 7 part 2 > Flashcards

week 7 part 2 Flashcards

1
Q

arteriosclerosis

A

hardening and thickening of the arterial wall

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2
Q

why arteriosclerosis

A

An inflammatory response to endothelial cell injury
* Characterized by the build-up of atherosclerotic
‘plaques’ (atheroma) within the vessel wall
* Made up of lipids (mainly cholesterol), cell debris, fibrin, thrombus

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3
Q

most common

A
  1. abdomial aorta and iliac arteries
  2. proximal coronary arteries
    3.thoracic aorta femoral and popliteal arteries
    4.internal carotid arteries
  3. vertebral basilar and middle cerebral arteies
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4
Q

LDL

A
  • low-density lipoprotein
    -has low levels of cholesterol
  • Transports cholesterol from liver to cells
  • Major factor contributing to atheroma
    formation
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5
Q

HDL

A

-high-density lipoprotein
-Transports cholesterol away from the
peripheral cells to liver—“good”
lipoprotein
-Breakdown in liver and excretion

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6
Q

transport of lipids

A
  1. dietary intake of cholesterol and triglycerides
  2. chylomicrons absorbed into blood and lymph
  3. lipid uptake by adipose and skeletal ,muscle
  4. remnant to liver
  5. liver synthesize lipoprotein
  6. LDL transport cholesterol to cell
  7. LDL attaches to LDL receptors in smooth muscles and endothelial tissue
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7
Q

steps to atherosclerosis

A

1.Physical or chemical stress imposed against the arterial wall
2.Endothelial cells become injured
3.LDL particles leak into the intimal layer and become oxidized
4.Immune/Inflammatory response  Macrophages, Monocytes, cytokines
5.Macrophages eat up the LDL Particles  Foam cells  Creates a Fatty
Streak
6.Platelets are recruited and activated  release growth factors
7.Smooth muscle cell proliferation & migration from the tunica media
into the tunica intima
8.Growth of extracellular matrix (fibroblasts)  formation of a fibrous
cap over a lipid core = Fibrous Plaque

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8
Q

atherosclerosis over time

A
  1. the foam cells within lipids undergo necrosis
    2.Release of enzymes that eat at the fibrous cap
    3.Eventual rupture  Atheroma is now exposed into the
    lumen of the blood vessel
    4.More platelets activated
    5.Fibrin clot forms at the site of the rupture
    6.Clot occludes the lumen of the artery even more AND can
    detach and travel to occlude a distal artery
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9
Q

atherosclerosis over time consequences

A
  • Ischemia (at least 70% of the lumen occluded)
  • Angina pectoris if coronary arteries are involved (Coronary
    Artery Disease)
  • Claudication if peripheral arteries are involved (Peripheral
    Artery Disease)
  • Total Occlusion / Plaque rupture  clot detachment
  • Myocardial Infarction, Ischemic Stroke
  • Atheroma can weaken the wall of the vessel
  • Aneurism
  • Cholesterol embolism: the plaque itself dislodges and blocks a
    distal artery
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10
Q

Atherosclerosis diagnosis

A

Screening tests: Assessing risk
* Blood cholesterol level (HDL, LDL)
* Blood Pressure
* C-reactive protein level (inflammatory marker)
* Exercise Stress testing
Imaging
* Coronary angiography – Visualize blood flow in coronary arteries
* Ultrasound –Visualize blood flow in peripheral vessels

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11
Q

Atherosclerosis treatment

A

Risk Reduction
* Dietary / lifestyle intervention
* Pharmaceutical measures: anti-hypertensives, cholesterol-lowering, anticoagulants
Maintenance of existing conditions
* Diabetes, hypertension
Surgical intervention
* Angioplasty
* Bypass

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12
Q

Balloon Angioplasty:

A

Catheter with an inflatable balloon that flattens
the atheroma when inflated
- balloon flattens the plague around

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13
Q

Laser Angioplasty:

A

Catheter with a laser  inserted into the
narrowed part of the artery  Laser
disintegrates the plaque

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14
Q

Coronary Artery Bypass Graft

A
  • Open heart surgery
  • Heart is arrested and cooled
  • Circulation bypassed using a heart-lung machine
  • Artery with plaque physically removed
  • Replaced with piece of saphenous vein from leg or
    mammary artery
  • Very invasive
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15
Q

Angina Pectoris

A
  • Chest pain due to myocardial ischemia
  • When the Oxygen Supply does not meet the Oxygen Demand
  • Due to vessel occlusion and/or inability to vasodilate to meet
    perfusion demand
  • Atherosclerosis, vasospasm, myocardial hypertrophy
  • Stable (transient and usually due to a vasospasm or exertion) or unstable (prolonged
    pain at rest)
  • Does not usually cause permanent damage unless episodes are extended or severe
  • Angina can be treated with rest, lifestyle modification, nitroglycerin, surgical
    intervention
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16
Q

3 ways to develop infarction

A
  • Thrombus build up and obstructs artery
  • Vasospasm in an area of partial occlusion
  • Thrombus breaks away and lodges in small branch
17
Q

Size, location & duration determine the severity of damage

A
  • Most are transmural (affect all three layers of the heart)
  • Enzymes are released from the damaged/dead myocardial
    cells  released into the blood
  • Damage may be reversible if blood supply is restored within
    20 minutes (thrombolytic therapy)
18
Q

Myocardial Infarction – Signs &
Symptoms

A
  • Pain:
  • Sudden, Severe, Crushing - Substernal chest pain with radiation to left arm,
    shoulder, jaw, or neck
  • Can also be milder and present as indigestion
  • Pallor, Sweating
  • Nausea, Dizziness, Weakness, Dyspnea
  • Anxiety and fear
  • Hypotension, rapid and week pulse to due decreased cardiac output
  • Low-grade fever
19
Q

Myocardial Infarction Diagnosis

A
  • ECG: ST-elevation
  • Enzymes and other markers in the blood
  • LDH-1: Lactate dehydrogenase
  • AST: Aspartate Aminotransferase
  • CPK-MB: Creatine Phosphokinase
20
Q

Myocardial Infarction complications

A
  • Sudden Death due to fibrillation
  • Dysrhythmias
  • Cardiogenic shock: severely low cardiac output
  • Heart Failure
21
Q

Myocardial Infarction treatment

A
  • Anticoagulation, antithrombotic
  • Defibrillation, Surgery
  • Reduce risks
  • Cardiac Rehabilitation programs: exercise, diet, stress reduction
22
Q

Peripheral Artery Disease

A

Due to Atherosclerosis in peripheral arteries (most common) or inflammation that leads to stenosis
- often in the legs

23
Q

Peripheral Artery Disease signs and symptoms

A
  • Fatigue and weakness in the legs
  • Intermittent claudication (often with exertion)
  • Weak peripheral pulse
  • Skin appearance – pallor, cyanotic, dry, hairless, thick toenails
24
Q

Peripheral Artery Disease treatment

A
  • Reduce risk factors (blood glucose, cholesterol, BMI, smoking, etc)
  • Anticoagulants, peripheral vasodilators
  • Increased physical activity
25
Q

Venous Disorders

A
  • Irregular, dilated, tortuous areas of superficial or deep veins
  • Risks factors: Increased body mass index, pregnancy, weight lifting, family history
26
Q

Venous Disorders treatment

A
  • Keep legs elevated, support stockings
  • Intermittent voluntary muscle contractions when sitting for longer periods
  • Can be surgically removed
27
Q

Venous Disorders – Thrombophlebitis

A
  • Thrombus development in vein where inflammation is present (e.g., IV site)
     Platelets adhere to inflamed site  Thrombus develops
28
Q

Venous Disorders phlebothrombosis

A
  • Phlebothrombosis
  • Thrombus forms spontaneously without prior inflammation; attached loosely.
  • Factors for thrombus development
  • Stasis of blood or sluggish blood flow
  • Endothelial injury
  • Increased blood coagulability
29
Q

Venous Thrombosis – Signs/Symptoms

A
  • Aching, burning, tenderness in affected area
  • Warmth, redness
  • Edema as blood pools distal to obstructed thrombus
  • Homan’s Sign: pain in the calf muscle upon foot dorsiflexion
30
Q

Venous Thrombosis Treatment

A
  • Prevention:
  • Compression stockings
  • Exercise to improve muscle tone, reduce stasis
  • Pharmaceuticals: Anticoagulants, Fibrinolytics
  • Surgical intervention: Thrombectomy

HES 311 (23 decks)

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