Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
Describe the difference between atherosclerosis and arteriosclerosis? (P640-642)
|
- Arteriosclerosis – Abnormal Thickening of Vessel Walls; Thickening of Tunica Intima;
- Atherosclerosis – Deposits of Fat and Fibrin Build on Vessel Walls; Stages of: Fatty Streak; Fibrous Plaque; and Complicated Lesion |
|
Describe the Etiology of Atherosclerosis and Arteriosclerosis? (P.640)
|
- Arteriosclerosis – Part of Normal Aging Process
- Atherosclerosis – Endothelial Injury from Smoking, Hypertension, Diabetes |
|
In Atherosclerosis at what % of Occlusion does Symptoms Generally Appear? (P.641)
|
- Typically No Symptoms Until 60% of Vessel is Occluded
|
|
Explain how Arteriosclerosis Raises Blood Pressure?
|
- Decreases Distencibility
- Decreases Lumen Diameter |
|
Define Normal Blood Pressure for Adults Age 18 or Older? (P.646)
|
- Normal <120, <80
- Prehypertension <139, <89 - Stage 1 < 159, <99 - Stage 2 >159, >99 |
|
Differentiate Between Primary and Secondary Hypertension? (P.646)
|
- Primary Is Most Common Form
- Overactivity Sympathetic Nervous System - Overavtivity Renin/Angiotensin/Aldosterone System - Salt & Water Retention of Kidneys - Secondary is Caused By Systemic Disease Process - Tumors - Contraceptives - Corticosteriods - Antihistamines - Blood Pressure Returns to Normal If Treated Early |
|
Describe the Mechanisms of Organ Damage Secondary to Sustained Hypertension? (P.649)
|
- Myocardium – Increased Work Load; Diminished Blood Flow in Coronary Arteries
- Coronary Arteries – Accelerated Atherosclerosis - Kidneys – Renin Aldosterone Secretion Stimulation; Reduced Oxygen Supply - Essentially a Reduce in Blood Flow is the Mechanism of Injury |
|
Describe Etiology, Manifestations of Orthostatic Hypotension? (P.650)
|
- Decrease in Systolic & Diastolic on Standing
- Baroreceptor Mediates Increase in Heart Rate & Constricts Arterioles - Acute - Normal Regulatory Mechanisms Become Sluggish - Drugs, Starvation, Loss of Fluid - Most Common in Elderly - Chronic – Secondary to a Disease, Endocrine Disorders, Disease of CNS |
|
Discuss Aneurysms; Including Location of Majority, Types Requiring Emergency Surgeries? (P.651)
|
- Most Occur in Lower Abdomial Aorta (75%)
- True Aneurysms (Fusiform Circumfrential, Fusiform Saccular) - Involve All Three Layers - False Extravascular Hematoma Communicates with Extravascular Space - Typically Between Vascular Graft & Artery - Dissecting Saccular – Weakness or Separation of Vascular Layers - Requires Emergency Treatment |
|
Explain the Difference Between a Thrombus, Embolus and Thromboembolus? (P.652)
|
- Thrombus – Blood Clot Remains Attached to a Vessel
- Thromboembolus – Detached Thrombus - Embolus – Bolus of Matter Circulating in Blood Stream - Embolism – Obstruction of a Blood Vessel by Embolus |
|
Explain the Pathophysiology of Thrombus Formation? (P.652)
|
- Conditions Promote Coagulation or Clotting
- Roughening, Inflammation, Trauma, Pooling of Blood |
|
Discuss Pulmonary Embolism; Including Etiology, S/S, Most Likely Originating Site? (P.652??)
|
- Venous Side (Typically Deep Veins of Legs)
- Dislodged Thrombus -Dyspnea; Unexplained Anxiety |
|
Discuss Raynauds Disease; Including Pathophysiology, Trigger Events, S/S? (P.653)
|
- Characterized by Attacks of Vasospam in Small Arteries
- Secondry to a Disease Such as Collagen Vascular Disease - Caused By Long Term Exposure to Cold, Vibrating Machinery - Effects Hands; Pale Skin, Numbness |
|
Discuss Varicose Veins; Including Common Etiologies? (P.654)
|
- Vein in Blood Has Pooled Producing Tortuous, and Palpable Vessels
- Caused by Trauma to Saphenous Veins; Distention Caused By Standing for Long Periods - Crossing Legs |
|
Discuss Chronic Venous Insufficiency; Including Etiology and Manifestations? (P.654)
|
- Inadequate Venous Returns Over Long Periods
- Trauma or Pressure Can Lower Blood Supply Leading to Venous Stasis Ulcers |
|
. Differentiate Between Myocardial Ischemia, Necrosis and Hypertrophy and Etiologies of All? (P.655, 663???)
|
- Ischemia – Local State When Cells are Temporarily Deprived of Blood Supply (Atherosclerosis)
- Hypertrophy – Angiotensin Released in Ischemia Promotes Growth of Smooth Muscle - Necrosis – After 20 mins of Myocardial Ischemia |
|
Describe Modifiable and Non-Modifiable Risk Factors for CAD?
|
Modifiable:
- Hyperlipidemia - Hypertension - Cigarette Smoking - Obesity - Alcohol Non-Modifiable: - Gender - Genetic Predisposition - Age |
|
Describe what is happening in the Heart that Causes Angina Pectoris? (P.658)
|
- Symptoms of Chest Pain, Myocardial Ischemia
- Caused by Gradual Luminal Narrowing & Hardening of Arterial Walls - Vessels Cannot Dilate In Response to Increased Myocardial Demand - Relieved by Rest and Nitrates - Discomfort Lasts 3 to 5 Minutes |
|
Differentiate Between Stable, Unstable and Prinzmetal Angina? (P.658)
|
Stable:
- Lasts 3 to 5 Minutes - Not Tissue Damage - Relieved By Nitrates & Rest Prinzmental: - Transient Ischemia of Myocardium at Rest - Vasospasms of One or More Coronary Arteries - Occurs in REM Sleep Triggered by Sympathetic Nervous System Unstable: - Between Reversible Myocardial Ischemia and Infarction - Atherosclerotic Plaque has become Complicated - Occlusion Occurs for 10 to 20 Min With Return to Perfusion |
|
How long can Cardiac Cells Withstand Ischemic Conditions Before Damage is Permanent? (P.663)
|
- Cardiac Cells Can Withstand 20 Minutes of Ischemic Conditions Before
Cellular Death Takes Place |
|
Describe the Goal(s) of Therapy in Managing Myocardial Ischemia (P.661)
|
- Reduce Myocardial Oxygen Consumption
- Control Factors Such As: Blood Pressure, Heart Rate, Contractility, and Left Ventricular Volume |
|
Describe how Myocardial Infarction can lead to Ventricular Impairment? (P.???)
|
- Scar Tissue Does Not Function Like Original Tissue
|
|
Explain why Fever Often Occurs soon after Myocardial Infarction? (P.664)
|
- Inflammatory Activity Within Myocardium
|
|
Discuss Pericarditis; Including Complications of Pericardial Effusion, Related Condtions? (P.667)
|
Pericarditis – Pericardial Response to Injury (Acute Pericarditis, Pericardial Effusion, Constrictive Percarditis)
- Accumulation of Fluid in Pericardial Cavity - Indicates underlying disorder such as Lupus, Erythematosus - Serious Condition can cause Tamponade (Fluid Can Cause Cardiac Compression) - Can be Caused by Tuberculosis |
|
Describe Complication that is Possibility in all forms of Heart Valve Dysfunction? (P.671)
|
- Myocardial Hypertrophy
|
|
Differentiate Between Valvular Regurgitation, Insufficiency, and Stenosis? (P.671)
|
- Valvular Stenosis – Orifice is Constricted So Blood Cannot Flow Forward; Pressure & Work Increase
- Valvular Regurgitation (Insufficiency) – Valve Fails to Close; Permitting Blood to Flow When Closed |
|
Identify the Valve Disorder Commonly Resulting in R Sided Heart Failure? (P.673)
|
- Tricuspid Regurgitation
|
|
Identify the Most Common Cardiac Valve Disease Most Prevalent in Young Women? (P.703)
|
-Mitral Valve Prolapse
|
|
Describe the Etiology, Pathophysiology and S/S of Rheumatic Heart Disease? (P.674)
|
- Group A Streptococcus (B-Hemolytic)
- Typically Occurs in Children 5 – 15 years |
|
Define the type of Microbe Most Often Responsible for Infective Endocarditis? (P.677)
|
- Endocarditis is Inflammation of Endocardium
- Staphylococcus Aureus |
|
Describe how Chronic HTN can Lead to L Heart Failure? (P.684)
|
- Increased Afterload Leads To Hypertrophy
|
|
Describe how Decreased Perfusion to Kidneys from Heart Failure Can Aggravate the Problem? (P.687)
|
- Decreased Cardiac Output Decreases Renal Perfusion Activating Renin-Angiotesnion-Aldosterone System
|
|
In Heart Failure what is the Pathophysiology that Results in Pulmonary Symptoms? (P.687-688)
|
- Left Heart Failure
- Pulmonary Vascular Congestion & Inadequate Profusion of Systemic Circulation |
|
Identify the Common Cause of R Heart Failure? (P.688)
|
- Left Heart Failure
- COPD, Cystic Fibrosis, ARDS (Adult Respiratory Distress Syndrome) |
|
Differentiate Between the S/S of R and L Heart Failure? (Notes)
|
- Right: Edema, Asceitis, JVD, Fatigue, Liver/Spleen Engorgement
- Left: Active & Sleeping Dyspnea; Orthopnea, Cough, Bloody Speutum, Cyanonsis, Decereased Uringary Output; S3 Gallop |
|
In Shock What Leads to the Impairment in Cellular Metabolism? (P.689, 691)
|
- Oxygen & Glucose Depletion
|
|
Differentiate Between the Etiology and Patho, S/S of Cardiogenic, Hypovolemic, Anaphylactic and Septic Shock? (P.691)
|
- Cardiogenic: Typically Myocardial Infarction, Pericardial Infections, Drug Toxicity
- Hypovolemic: Loss of Whole Blood |
|
What Major Injury Can Result in 3rd Spacing. What Type of Shock is This? (P.109)
|
- Burns, Hypovolemic Shock
- Fluids Travel From Vessel to Interstitial Space |
|
What is the Underlying Process Occurring that Results in the Pale Cool Skin that Often Occurs in Hypovolemic Shock?
|
- Blood Travels From Peripherals To Core
|
|
Describe the Etiology of Neurogenic Shock?
|
- Spinal Cord Injury
|
|
Describe the Most Common Cause of Multiple Organ Dysfunction Syndrome (MODS)? (P.698)
|
- Sepsis and Septic Shock (Most Common)
- Any Disease Process that Causes Systemic Inflammatory Response - Trauma, Burns, Acute Pancreatitis |
|
Which Organ of the Body is Often the First to Fail in MODS? (P.700)
|
- Lung (Resulting in Adult Respiratory Distress Syndrome)
- Liver and Kidney Failures Then Appear |