GNUR 293 Exam 3 | Questions And Answers | Verified
Updates
Risk 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
Differentiate between anti-platelet, anticoagulant, and thrombolytic drugs ANS Anti-platelet:
Aspirin, Prevent platelet aggregation or adhesion
Anticoagulant:
Heparin, Prevents clots, prevents clots from getting bigger
Thrombolytic:
Dissolve clots; increased risk of bleeding
Updates
Risk 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
Differentiate between anti-platelet, anticoagulant, and thrombolytic drugs ANS Anti-platelet:
Aspirin, Prevent platelet aggregation or adhesion
Anticoagulant:
Heparin, Prevents clots, prevents clots from getting bigger
Thrombolytic:
Dissolve clots; increased risk of bleeding
