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GNUR 293 Exam 3
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Exam of 28 pages for the course Anatomy Condensed Final Exam Review - GNUR 155 at Anatomy Condensed Final Exam Review - GNUR 155 (GNUR 293 Exam 3)
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GNUR 293 Exam 3Risk Factors for DVT - ANS-Most frequently due to thrombus in deep vein of lower
extremity
Prolonged inactivity
venous constriction
Virchow's triad
Previous DVT
Virchow's triad - ANS-Stasis of blood flow
Endothelial injury
Hypercoagulability
What life threatening complication can be caused by a DVT? - ANS-Pulmonary
Embolism
DVT Prevention - ANS-Anticoagulant Therapy (Prevent clots, prevent clots from getting
any bigger) - Heparin
Antiplatelet Therapy (Block platelet activation/ aggregation) - Aspirin
Antiembolic Stockings (Promotes venous return)
Sequential compression devices (massages, promotes venous return)
Ambulation as soon as possible (ROM exercises in bed if patient cannot walk yet)
Smoking Cessation
DVT Treatment - ANS-Anticoagulant Therapy (Prevent clot from getting any bigger,
body will dissolve it itself) - Heparin
Thrombolytic Therapy (Dissolves clots) - Increased risk of bleeding; do not do if patient
is post-op or had CPR
Surgery to remove thrombus (Only in severe cases)
Non-modifiable Risks of Peripheral Arterial Disease - ANS-Age
Gender: Post-Menopause in females
Family History
Ethnicity: African American
Modifiable Risks of Peripheral Arterial Disease - ANS-Smoking (#1)
Metabolic Syndrome
High Cholesterol
Obesity
,Physical Inactivity
Glucose Intolerance/ Diabetes - Especially prevalent due to damaged vessels
HTN
Stress and Mental Illness
Clinical Manifestations of Deep Vein Thrombosis vs. Peripheral Arterial Disease -
ANS-Deep Vein Thrombosis:
Unilateral edema
Increase in Hydrostatic Pressure
Fluid accumulation below the clot
Aching, dull pain
Redness
Warm below the clot
Should have a pulse
Peripheral Arterial Disease:
Distal Ischemia
No blood flow beyond the clot
Sharp Pain
Necrosis in tissue
Intermittent Claudication
Cyanotic
Cold beyond the obstruction
Lack of O2- Hypoxemia
Weak pulse
Dry, waxy, shedding skin
Hairless, shiny skin
Pathogenesis of Atherosclerosis - ANS-Damage to intima
LDL enters intima through intact endothelium
Intimal LDL is oxidized into pro-inflammatory lipids
Oxidized LDL causes adhesion and entry of monocytes and T-lymphocytes across
endothelium
Monocytes differentiate into macrophages and then consume large amounts of LDL,
transforming into foam cells (bad)
Foam cells release growth factors (cytokines) that encourage atherosclerosis (Foam
cells die and build up to form plaque)
Stable vs. Unstable Plaque - ANS-Stable Plaque:
, Chance of rupture is low, Tend to have dense fibrous cap, minimal lipid accumulation,
and little inflammation
Unstable Plaque:
Chance of rupture is higher, can cause a complete obstruction which could lead to a
heart attack; have thin caps, large lipid cores, and relatively dense inflammatory
infiltrates
Non-modifiable Risks for Atherosclerosis - ANS-Age
Gender: Post-menopause in females
Family History
Ethnicity: African American
Modifiable Risks of Atherosclerosis - ANS-Tobacco (#1)
Metabolic Syndrome
High Cholesterol
Obesity
Physical Inactivity
Glucose Intolerance/ Diabetes: Damaged vessels
HTN
Stress and Mental Illness
What are the effects of smoking on the vessels of systemic circulation - ANS-Injures
endothelium
Nicotine: Vasoconstriction
Elevates LDL, cholesterol, triglycerides
Decreases HDL
Produces Vasospasm
Increases platelet aggregation
Increases BP and HR
Increases risk of coronary heart disease
Complications of atherosclerosis - ANS-HTN: plaque leads to smaller lumen (hole),
higher pressure
Cardiac disease
Myocardial Infarction
Peripheral Arterial Disease
Stroke
Renal Disease
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