Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path Fall > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are 3 layers of blood vessels?

A

Intima- endothelial cells and elastic lamina
Media- smooth muscle and extracellular matrix.
Adventitia- collagen and elastic fibers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are 8 properties/functions of endothelial cells in the vasculature?

A
  1. Maintenance of permeability barrier.
  2. Elaboration of anti-coagulant, anti-thrombotic, fibrinolytic regulators.
  3. Elaboration of prothrombotic molecules.
  4. Modulation of blood flow and vascular reactivity
  5. Regulation of inflammation and immunity.
  6. Regulation of cell growth
  7. Oxidation of LDL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are 4 properties/functions of smooth muscle in the vasculature?

A
  1. Participate in normal vascular repair and pathologic process.
  2. Proliferate
  3. Upregulate extra-cellular matrix collagen, elastin, and proteoglycan production.
  4. Mediate vasoconstriction and vasodilation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is cardiac output and how is it regulated?

A

CO= HR x SV
Regulated by:
1. Heart rate and contractility regulated by alpha and beta adrenergic systems.
2. Blood volume: renal sodium excretion/resorption (aldosterone vs. atrial naturetic peptide), mineralocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Peripheral vascular resistance and how is it regulated?

A

Resistance to blood flow inside the arteries.
Regulated by-
1. Humoral factors: constrictors (angiotensin II, catecholamines, thromboxane, leukotrienes, endothelin), Dilators (prostaglandins, kinins, nitrous oxide)
2. Neural factors: Constrictors (alpha adrenergic), dilators (beta adrenergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the difference between primary and secondary hypertension?

A

Primary: 90-95% of all cases, multifactorial disorder involving environmental and genetic causes and risk factors.

Secondary: Hypertension caused by underlying problem such as renal/adrenal/endocrine/neurologic disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What 4 mechanisms are most commonly believed to contribute to essential hypertension?

A
  1. Reduced renal sodium excretion.
  2. Vasoconstriction or structural changes in vessel walls.
  3. Genetic factors.
  4. Environmental factors (stress, obesity, smoking, diet)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the structure of a typical atherosclerotic plaque (3 things)

A
  1. Raised lesion
  2. Necrotic debris and lipid core (cholesterol, calcium)
  3. fibrous caps (smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, neovascularization)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the nonmodifiable (4) and modifiable (5) risk factors for atherosclerosis?

A

Nonmodifiable:

  1. Genetic abnormalities
  2. Family history
  3. Increasing age
  4. Male gender

Modifiable:

  1. hyperlipidemia
  2. hypertension
  3. Smoking
  4. Diabetes
  5. Inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 5 steps in the response-to-injury hypothesis regarding pathogenesis of atherosclerotic plaques?

A
  1. Endothelial injury
  2. Endothelial dysfunction (increased permeability, leukocyte adhesion), monocyte adhesion and migration.
  3. Macrophage activation, smooth muscle recruitment, accumulation of lipids in vessel wall.
  4. Macrophages and smooth muscle cells engulf lipids.
  5. Smooth muscle cell proliferation, Extracellular matrix deposition, extracellular lipid accumulation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are 5 morphological changes in development of atherosclerosis?

A
  1. Chronic endothelial inury, increased permeability, leukocyte adhesion.
  2. Fatty spots, earliest lesion of atherosclerosis, composed of lipid-filled foam cells.
  3. Fatty streak containing T lymphocytes, macrophages and extracellular lipids.
  4. Fibrofatty plaque (a.k.a. atheroma), plaque filled with fibrin, collagen, calcification.
  5. Advanced calcification: calcification and fibrosis continues, lipid rich core surrounding fibrous capsule, lumen narrowing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 3 categories of atherosclerotic plaque changes that can trigger thrombosis?

A
  1. Rupture/fissuring: exposes the highly thrombogenic plaque constituents.
  2. Erosion/ulceration: exposes the thrombogenic, subendothelial basement membrane to blood.
  3. Hemorrhage into the atheroma: expand volume of plaque
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are characteristics of vulnerable plaques/ high risk for rupture?

A
  1. Lots of foam cells
  2. Lots of extracellular lipids
  3. thin fibrous caps
  4. clusters of inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are characteristics of stable plaques?

A
  1. Thick collagenized fibrous cap.
  2. Minimal lipid accumulation.
  3. Little inflammation.
  4. Little to no underlying lipid core.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between a true aneurysm and false aneurysm?

A

True: involve all three layers (intima/media/adventitia) or the attenuated wall of the heart.
False: When a wall defect leads to formation of an extravascular hematoma (contained by extravascular connective tissue) that communicates with the intravascular space. “pulsating hematoma”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is pathogenesis and risk factors for aortic dissection?

A

Pathogenesis: blood splays apart the laminar planes of the media to form a blood-filled channel with the artery wall.

Risk factors:

  1. Hypertension
  2. men 40-60 yrs
  3. Marfan’s syndrome
  4. Iatrogenic
  5. Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 3 subtypes of abdominal aortic aneurysm?

A
  1. Inflammatory: dense periaortic fibrosis containing abundant lymphoplasmacytic inflammation with many macrophages and giant cells.
  2. Immunoglobulin G4: subtype of inflammatory, tissue fibrosis associated with frequent infiltrating IgG4 expressing plasma cells.
  3. Mycotic: circulating microorgansisms seed the aneurysm wall/associated thrombus; results in accelerating medial destruction and may lead to rapid dilation and rupture.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is vasculitis?

A

General term for vessel wall inflammation. Most commonly caused by immune-mediated inflammation or infectious pathogens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is giant cell temporal arteritis?

A

Chronic inflammatory disorder, granulomatous inflammation, principally affects arteries in the head.
T-cell mediated.
Symptoms: fever, weight loss, head pain, tenderness with palpation of temporal artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are varicose veins?

A

Abnormally dilated tortuous veins produced by chronically increased intraluminal pressures and weakened vessel wall support.

21
Q

What is pathogenesis of esophageal varices?

A

Caused by portal vein hypertension from liver cirrhosis. Porto-systemic shunts open and increase blood flow to veins at the gastroesophageal junction.

22
Q

What is pathogenesis of hemorrhoids?

A

Varicose dilations of the venous plexus at anorectal junction due to prolonged pelvic vascular congestions. Associated with pregnancy, straining to defecate. Prone to thrombosis and painful ulceration.

23
Q

What are 10 risk factors for DVT?

A
  1. Prolonged immobilization resulting in venous stasis.
  2. Postoperative state.
  3. CHF
  4. Pregnancy
  5. Oral contraceptives
  6. Malignancy
  7. Obesity
  8. Males
  9. > 50 years
  10. Inherited defects in coagulation factors
24
Q

Define Congestive Heart Failure.

A

CHF occurs when the heart cannot generate sufficient output to meet the metabolic demands of the tissues, or can only do so at higher-than-normal filling pressures.

25
Q

What is the difference between systolic and diastolic CHF?

A

Systolic: Results from inadequate myocardial contractile function, usually as a consequence of ischemic heart disease or hypertension.
Diastolic: Inability of the heart to adequately relax and fill, which may be a consequence of massive left ventricular hypertrophy, myocardial fibrosis, amyloid deposition, constrictive pericarditis.

26
Q

Define ischemic heart disease.

A

Broad term encompassing several closely related syndromes caused by myocardial ischemia. Causes include atherosclerotic vascular disease, increased heart rate or blood pressure, hypotension, shock, pneumonia, CHF, anemia, carbon monoxide poisoning.

27
Q

Define angina pectoris.

A

Intermittent chest pain caused by transient, reversible myocardial ischemia.
Stable: predictable episodic and associated with exertion/tachycardia.
Unstable: increasingly frequent, occurring at rest.
Prinzmetal: caused by coronary artery spasm.

28
Q

Define acute myocardial infarction.

A

Necrosis of heart muscle resulting from ischemia. Caused by acute thrombosis within coronary arteries.

29
Q

What is chronic ischemic heart disease with CHF?

A

Progressive heart failure secondary to ischemic myocardial damage, usually with known history of MI

30
Q

What is acute coronary syndrome (ACS)?

A

term applied to any of the 3 catastrophic manifestations of ischemic heart disease: MI, sudden cardiac death, unstable angina.

31
Q

Describe progression of plaque change/thrombosis in acute coronary syndrome.

A

Sudden disruption (erosion or rupture) of partially occlusive plaque, leading to rapid thrombosis. Also, hemorrhage into core of plaque can expand plaque volume and exacerbate luminal occlusion.

32
Q

What is the typical sequence of events for an MI?

A
  1. Atheromatous plaque is eroded or suddenly disrupted, exposing subendothelial contents to blood.
  2. Platelets adhere and aggregate.
  3. Activation of coagulation by exposure of tissue factor.
33
Q

What are functional and biochemical consequences of myocardial ischemia?

A
  1. Aerobic metabolism stops, decrease of ATP and increase in lactic acid.
  2. Loss of contractility (non-contractile state)
  3. Electrical instability (arrhythmia)
  4. Tissue edema
34
Q

List the factors that determine the pattern of injury in an infarction.

A
  1. Size and distribution of involved vessel.
  2. Rate of development and duration of the occlusion.
  3. Metabolic demands of myocardium.
  4. Extent of collateral supply.
35
Q

What are 2 patterns of myocardial infarctions?

A
  1. Transmural infarctions (full thickness of ventricle, ST-elevation)
  2. Subendocardial infarctions (inner third of myocardium, ST- depression or T wave abnormalities)
36
Q

What are the cardiac markers and describe timing of release/metabolism?

A
  1. Troponin- slowest to release, lasts longest.
  2. Creatine kinase- middle of the 3 in terms of timing and metabolism.
  3. Myoglobin- fastest to release and fastest to metabolize.
37
Q

List potential complications associated with acute MI.

A
  1. Arrhythmias.
  2. Congestive heart failure
  3. Mitral valve chorda tendinea rupture.
  4. Cardiogenic shock.
  5. Thromboembolism
  6. Cardiac tamponade.
  7. Ventricular aneurysm
38
Q

Describe relationship of hypertension to left ventricular hypertrophy and ventricular failure.

A

Chronic pressure overload of systemic hypertension causes left ventricular hypertrophy, associated with left atrial dilation. Persistent pressure overload can cause ventricular failure with dilation.

39
Q

Define cor pulmonale and its causes.

A

Right ventricle hypertrophy and dilation, accompanied by right sided heart failure and pulmonary hypertension.
Causes: lung diseases, disorders of pulmonary vasculature, pulmonary embolism, sleep apnea.

40
Q

Describe general effects of valvular stenosis and regurgitation.

A

Valvular stenosis: failure of a valve to open completely, obstructing forward flow.
Regurgitation (insufficiency): failure of a valve to close completely allowing regurgitation of blood.

41
Q

What is calcified aortic stenosis?

A

Heaped calcified masses form on the outflow side of the cusps and mechanically impede valve opening. Caused by atherosclerosis.
Can lead to left ventricle hypertrophy.

42
Q

What is mitral valve prolapse (myxomatous mitral valve)?

A

Intrinsic defect of connective tissue or remodeling. Genetic condition, can occur with Marfan’s syndrome. Mostly asymptomatic, increased risk for endocarditis.

43
Q

What is rheumatic valvular disease?

A

Hypersensitivity reaction attributed to antibodies directed against group A strep. Causes mitral valve stenosis.

44
Q

What is infective endocarditis?

A

Microbial infection of heart valves or mural endocardium that leads to formation of vegetations composed of thrombotic debris and organisms. Symptoms include fever, flu-like prodrome, splenomegaly, splinter hemorrhages

45
Q

What are features of dilated cardiomyopathy?

A
  1. Impairment of contractility.
  2. Progressive cardiac dilation (all chambers)
  3. Hypertrophy
46
Q

What are features of restrictive cardiomyopathy?

A
  1. Least common type of cardiomyopathy.
  2. Impaired compliance/ filling.
  3. Diastolic dysfunction (stiffness).
47
Q

What are features of hypertrophic cardiomyopathy?

A
  1. Impairment of compliance (diastolic dysfunction).
  2. Myocardial hypertrophy.
  3. Defective diastolic filling.
  4. Ventricular outflow obstruction.
  5. Decreased stroke volume.
48
Q

Compare pericardial effusion with pericarditis.

A
  1. Pericardial effusion: Pericardial sac distended by serous fluid. Caused by CHF, trauma, MI, aortic dissection.
  2. Pericarditis: Swelling of pericardium due to infection. Typically secondary to MI or thoracic surgery.

Path Fall (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions