UNIT 6 Flashcards
1
Q
Describe Anemias
A
- Characterized by a reduced O2 carrying capacity of blood
- Results from low levels of hemoglobin (Hb) in blood (definition of anemia)
- Reasons underlying low hemoglobinemia include: decreased/abnormal RBC production, decreased/abnormal hemoglobin synthesis, increased TBC destruction and loss of RBC (ex: hemorrhage)
2
Q
Describe Anemia- Signs and Symptoms
A
Related to the adaptive responses to hypoxia:
- Low energy and fatigue due to under perfusion of tissues
- Pallor from hypoxia –> peripheral vasoconstriction
- Tachycardia (increased heart rate) due to sympathetic reflex response needed to increase cardiac output
- Dyspena (increase in berating) result of hypoxia –> increase respiration to increase ventilation
- Epithelial tissue ulceration (mouth, GI) due to decreased tissue regeneration
3
Q
Types of Anemia (5 types)
A
- Iron deficiency anemia
- Pernicious anemia
- Aplastic anemia
- Hemolytic anemia
- Sickle cell anemia
4
Q
Describe Coronary Artery Disease
A
- Also called ischemic heart disease
- Basic pathophysiology is related to insufficient O2 supply to heart muscle
5
Q
4 Types of Coronary Artery Disease
A
- Arteriosclerosis
- Atherosclerosis
- Angina Pectoris
- Myocardial Infarction (heart attack)
6
Q
Describe Arteriosclerosis
A
- Refers to degenerative changes occurring in arteries
- Involves small arteries and arterioles
- Known colloquially as ‘hardening of the arteries’ because of changes that occur in blood vessels walls: loss of elasticity, thickening and hardening and narrowing of lumen
- End result is ischemia
7
Q
Describe Atherosclerosis
A
- Occurs in large arteries, particularly at regions of bifurcation
- Changes include build-up of atheromas (plaque): composed of fat, cells, cell debris, fibrin and thrombi
8
Q
Atherosclerosis- Risk Factors
A
-Hypertension
-Ratio of low-density to high density lipoproteins (LDL:HDL ration):
LDL = bad cholesterol (transport cholesterol to cells)
HDL = good cholesterol (transports cholesterol to liver)
-Atherosclerosis is the result of an inflammatory process occurring in the artery walls
9
Q
Atherosclerosis- Pathophysiology
A
- Arterial endothelium injury (break in epithelium), resulting in local inflammation: monocytes/macrophages, lipids accumulate in inner lining of artery and in middle muscle layer
- Smooth muscle cells undergo hyperplasia
- Fatty plaque forms
- Platelets adhere to damaged surface: thrombus (clot) forms, partial obstruction of lumen and more platelets adhere releasing prostaglandins (PG): vascular response and platelet aggregation
- Result in large growing thrombus: blood flow becomes turbulent, promoting further clot formation
- Plaque may ulcerate promoting more tissue damage and more clot formation. Vicious cycle, with unhappy ending
- Obstruction may be partial
- Eventually, BV’s may close completely resulting schema or necrosis of distal tissue
- Recall: atheromas typically form in larger vessels: requires much build-up to close artery completely
- If heart vessel narrows, get symptoms of angina
- Piece of thrombus may break off (resulting in embolus)
- Embolus circulates and may block smaller vessel: if blockage is complete, distal tissue dies
10
Q
Atherosclerosis- Risk Factors Cont’: non-modifiable
A
- Age greater than 40 years
- Male sex (women protected by estrogen)
- Genetic predispositions (ex: high lipid levels)
- Family lifestyle
11
Q
Atherosclerosis- Risk Factors Cont’: Modifiable Risk Factors
A
- Obesity
- Diets high in animal fat
- Smoking (increase LDG, decrease HDL, promotes clotting processes)
- Sedentary lifestyle
- Diabetes (increase serum lipid, endothelial damage)
- Smoking together with some oral contraceptives
- Stress (increase serum cholesterol)
12
Q
Atherosclerosis- Therapy
A
- Reduce or eliminate modifiable risk factors
- Lower cholesterol (diet and medication)
- Control diabetes and hypertension
- Oral anticoagulants
- Surgical intervention: angioplasty, laser angioplasty, bypass surgery and stents
13
Q
Describe Angina Pectoris
A
- Chest pain due to cardiac muscle hypoxia: imbalance between O2 supply and demand and increase demand or increase supply or combination of both
- Signs of angina manifest during incidences of increased cardiac O2 demand
- Angina is heart muscle simply making a protest statement: unless angina is severe, frequency or prolonged permanent heart damage is unlikely
- Healthy coronary arteries: : increased O2 demand is my by increased O2 supply and vasodilation of coronary arteries
- Narrowed coronary arteries (several causes): O2 demands or normal activity are not met by O2 supply and/or damaged or hard arteries cannot vasodilate adequately
- Severe coronary artery narrowing: O2 supply cannot meet basic O2 demands therefore Ischemia results
14
Q
Three Patterns of Angina Pectoris
A
Exertional Angina:
- Most common presentation of angina
- Pain occurs upon sudden increased demand (exertion)
Variant Angina:
- Pain occurs at rest
- Coronary artery narrowed by vasospasm
Unstable Angina:
- Pain occurs at rest
- Signs are relatively recent in onset
- May reflect arterial crisis (ex: fragmentation of atheroma)
- May be harbinger of heart attack
15
Q
Angina Pectoris- Etiology
A
- Atherosclerosis: narrowing of lumen
- Arteriosclerosis: narrowing of lumen
- Vasospasm: local constriction of coronary arterioles
- Cardiac muscle hypertrophy: increased cardiac muscle mass resulting in a higher O2 demand
- Chronic tachycardia: accelerated heart rate (ex: arrhythmia, hyperthyroidism) resulting in a higher O2 demand
- Chronic Hypertension: need to pump blood against arterial resistance therefore heart must work harder and a result of a higher O2 demand is needed
