Brainscape's Knowledge GenomeTM

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


See full index

Block 9 week 1 > Cardiovascular System - Fung > Flashcards

Cardiovascular System - Fung Flashcards

1
Q

What are the layers of a blood vessel?

A
  1. the tunica intima
  2. the tunica media
  3. the tunica adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How are the layers of a blood vessel related to the heart?

A

The major blood vessels that connect to the heart are continuous with the heart.

  1. the intima becomes endocardium
  2. the media is made up of cardiac myocytes
  3. the adventitia becomes epicardium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What two characteristics of the heart are most important in heart pathology?

A
  1. cardiac weight

2. ventricular wall thickness

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

What is the average weight of a female heart?

A

250-300 grams

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

What is the average weight of a male heart?

A

300-350 grams

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

What is the typical thickness of the ventricular wall in females?

A

0.3-0.5 cm

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

What is the typical thickness of the ventricular wall in males?

A

1.3-1.5 cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is cardiac muscle different from striated muscle?

A

It has centrally located nuclei.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the functions of vascular endothelial cells?

A
  1. maintain non-thrombogenic blood-tissue interface
  2. modulate vascular resistance
  3. metabolize hormones
  4. regulate inflammation
  5. regulate cell growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the function of smooth vascular smooth muscle cells?

A
  1. synthesize collagen, elastin and proteoglycans

2. produce growth factors and cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the components of of vascular extracellular matrix?

A
  1. elastin
  2. collagen
  3. gycosaminoglycans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the two types of arteries?

A
  1. elastic arteries

2. muscular arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What layer of vasculature contain smooth muscle cells?

A

The tunica media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which cells of vasculature are responsible for homeostasis of the vessel?

A

The endothelial cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does an artery have more smooth muscle in it’s tunica media?

A

Yes. Arteries have to work under higher pressure than veins.

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

What is the vasa vasorum and why do we need it?

A

The vasa vasorum are tiny blood vessels that supply other larger vessels. We need them because nutrients and oxygen can only diffuse so far. The vasa vasorum supplies part of the tunica media and the tunica adventitia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which types of vessels have more elastic tissue?

A

Elastic arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Do muscular arteries have elastic tissue?

A

Yes. They have elastic tissue in the internal and external elastic lamina. They have less elastic tissue than elastic arteries.

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

Give a couple examples of elastic arteries.

A
  1. aorta

2. common carotids

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

Give a couple examples of muscular arteries.

A
  1. radial artery

2. femoral artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the two types of vascular systems?

A
  1. blood vascular system

2. lymph vascular system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Do lymph vessels have muscular walls?

A

No. Lymph moves due to contraction of surrounding muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does gas and nutrient exchange take place?

A

Capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Veins are not very muscular. How do they get blood back to the heart?

A

Contraction of skeletal muscle helps blood flow back to heart and one way valves keep the blood from flowing backwards.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Most cardiovascular disease results from….?

A

“a complex interplay of genetics and environmental factors that disrupt networks of genes and signaling pathways that control morphogenesis, myocyte survival and response to injury, biochemical stress responses, contractility or electrical conduction”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the six mechanisms of cardiac dysfunction?

A
  1. failure of pump
  2. obstruction of flow
  3. regurgitant flow
  4. shunted flow
  5. disorders of cardiac conduction
  6. rupture of the heart or a major blood vessel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Cardiovascular disease is most commonly related to what?

A

Atherosclerosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the stereotypical response of blood vessels to injury.

A
  1. recruitment of smooth muscle cells or smooth muscle precursor cells to the tunica intima
  2. smooth muscle cells undergo mitosis and proliferation
  3. elaboration of smooth muscle cell extracellular matrix
  4. inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Endothelial cell loss or dysfunction does what…?

A

Stimulates smooth muscle cell growth and extracellular matrix synthesis leading to intimal thickening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is hypertension?

A

Sustained increased blood pressure associated with increased risks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Sustained increased blood pressure is associated with risk of…?

A
  1. atherosclerosis
  2. hypertensive heart disease
  3. multi-infarct dementia
  4. aortic dissection
  5. renal failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the normal blood pressure range?

A

less than 120/less than 80 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is prehypertension?

A

Blood pressure between 120-139/ 80-89 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the blood pressure range for hypertension?

A

greater than 140/greater than 89 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the blood pressure range associated with malignant hypertension?

A

greater than 200/ greater than 120 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are some broad categories of causes of essential hypertension?

A
  1. single gene defects
  2. polymorphisms
  3. vascular - vasoconstricion, structural changes
  4. environmental factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Single gene defects that cause essential hypertension are usually involved in what functions?

A
  1. aldosterone
  2. metabolism
  3. sodium reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Polymorphisms associated with essential hypertension are usually involved with what systems?

A
  1. angiotensinogen locus
  2. angiotensin receptor locus
  3. renin-angiotensin system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are some environmental factors associated with essential hypertension?

A
  1. diet
  2. stress
  3. obesity
  4. smoking
  5. physical inactivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Most commonly, the cause of essential hypertension is what?

A

Idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are systems that if effected could cause secondary hypertension?

A
  1. renal system
  2. endocrine system
  3. cardiovascular system
  4. neurologic system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What kinds of conditions affecting the renal system could lead to secondary hypertension?

A
  1. acute glomerulonephritis
  2. chronic renal disease
  3. polycystic disease
  4. renal artery stenosis
  5. renal vasculitis
  6. renin-producing tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What kinds of conditions affecting the endocrine system could lead to secondary hypertension?

A
  1. adrenocortical dysfunction
  2. exogenous hormones
  3. pheochromocytoma
  4. acromegaly
  5. hypothyroidism
  6. hyperthyroidism
  7. pregnancy-induced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What kinds of conditions affecting the cardiovascular system can lead to secondary hypertension?

A
  1. coarctation of the aorta
  2. polyarteritis nodosa
  3. increased vascular volume
  4. increased cardiac output
  5. rigidity of aorta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What kinds of conditions affecting the neurologic system can lead to secondary hypertension?

A
  1. psychogenic
  2. increased intracranial pressure
  3. sleep apnea
  4. acute stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Hyperplastic arteriosclerosis is associated with what type of hypertension?

A

Malignant hypertension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are atheromas?

A

Raised lesions that protrude into a vessel lumen. They consist of a sod yellow core of lipid and are covered by a fibrous cap.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What does a fibrous cap consist of?

A
  1. smooth muscle cells
  2. macrophages
  3. foam cells
  4. lymphocytes
  5. collagen
  6. elastin
  7. proteoglycans
  8. they are also neovascularized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does the necrotic center of an atheroma consist of?

A
  1. cell debris
  2. cholesterol crystals
  3. foam cells
  4. calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Atheromas can cause…..?

A
  1. obstruction of blood flow
  2. they can rupture and cause vessel thrombosis
  3. can lead to formation of an aneurysm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Does atherosclerosis start in childhood?

A

Yes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is one consequence of an atheroma?

A

Because they protrude out from the vessel wall and into the lumen, they increase the distance with which nutrients have to diffuse to get to the layers of the vessel wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the constitutional risk factors for atherosclerosis?

A
  1. age
  2. gender (male)
  3. genetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the modifiable risk factors for atherosclerosis?

A
  1. hyperlipidemia
  2. hypertension
  3. smoking
  4. diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are some other risk factors for atherosclerosis?

A
  1. inflammation
  2. hyperhomocysteinemia
  3. metabolic syndrome
  4. Lipoprotein A
  5. hemostatic factors
  6. sedentary life style
  7. Type A personality/stress
  8. obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the response to injury hypothesis of athersclerosis?

A

This theory states that atherosclerosis is a chronic inflammatory and healing response to arterial wall and endothelial injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the steps leading to atherosclerosis according to the injury response hypothesis?

A
  1. endothelial injury
  2. lipoprotein accumulation
  3. monocyte adhesion and formation of foam cells
  4. platelet adhesion
  5. smooth muscle cell recruitment
  6. smooth muscle cell proliferation and ECM production
  7. lipid accumulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the two main causes of endothelial injury?

A
  1. hemodynamic disturbances

2. hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What are some ways that endothelium can be injured?

A
  1. mechanical denudation
  2. immune complex deposition
  3. irradiation
  4. chemicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are some things that can cause endothelial dysfunction?

A
  1. hemodynamic disturbances
  2. hypercholesterolemia
  3. hypertension
  4. smoking
  5. infectious agents
  6. homocysteine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Where do atherosclerotic plaques tend to occur?

A

At areas of disturbed blood flow or areas of hemodynamic disturbance. Including - branch points, ostia of exiting vessels, and the posterior wall of the abdominal aorta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What type of blood flow is protective against atherosclerosis?

A

Non-turbulent, laminar flow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the dominant types of lipids in atherosclerotic plaques?

A
  1. cholesterol

2. cholesterol esters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Describe the relationship between lipids and atherosclerosis.

A
  1. Genetic hyperlipoproteinemia is associated with accelerated atherosclerosis
  2. DM and hypothyroidism is associated with hypercholesterolemia
  3. Lowering serum cholesterol slows the rate of atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What affect does lipid accumulation have on vessels?

A

It reduces their ability to dilate. Hyperlipidemia increases ROS production which then accelerates decay of nitric oxide so that vessels cannot vasodilate very well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Lipid accumulation increases the production of what type of cells?

A

Foam cells. The ROS’s oxidize LDL which is then ingested by macrophages through a scavenger receptor. Also, oxidized LDL increases release of growth factors, cytokines and chemokines that lead to monocyte recruitment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

LDL is cytotoxic to what?

A

Endothelial cells and smooth muscle cells of the vessel wall. This injures the endothelium and leads to plaque formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Atherosclerotic lesions cause what?

A

Chronic inflammation with T-cell proliferation. It also leads to release of chemokines and growth factors that promote smooth muscle cell proliferation and ECM synthesis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the major consequences of atherosclerosis?

A
  1. MI
  2. cerebral infarction
  3. aortic aneurysm
  4. peripheral vascular disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Atheroma’s project into the lumen of a vessels and cause….?

A

Stenosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What percentage of stenosis of a vessel is critical and causes chronically decreased perfusion?

A

70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Chronically decreased perfusion leads to…..?

A
  1. bowel ischemia
  2. chronic ischemic heart disease
  3. ischemic encephalopathy
  4. intermittent claudication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Unstable atherosclerotic plaques can undergo what changes?

A
  1. they can rupture, fissure, erode or ulcerate
  2. if any of the above happen then thrombogenic plaque contents or the thrombogenic sub endothelial basement membrane is exposed to blood and can lead to thrombus formation
  3. plaques can also hemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe the progression of atherosclerosis.

A

Pre-clinical phase - usually younger age:
1. lesion prone areas start to form fatty streaks or undergo endothelial injury or dysfunction
2. endothelial injury/dysfunction leads to formation of plaques
3. over time plaques remodel and grow and may become unstable
Clinical phase - usually middle age to elderly:
1. plaques/atheroma’s begin to cause clinical symptoms
2. They can cause thrombosis, emboli and vessel wall weakening leading to aneurysm and rupture
3. atheroma’s can rupture, erode, hemorrhage leading to thrombus formation and occlusion
4. atheroma’s can grow and cause critical stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Describe ischemic heart disease.

A

This term is a generic designation for a group of pathologically related syndromes resulting from myocardial ischemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is myocardial ischemia?

A

An imbalance between the supply and demand of the heart for oxygenated blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Ischemic heart disease is also called what?

A

Coronary artery disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Ischemic heart disease results from what?

A
  1. a greater than 90% obstructive atherosclerotic lesion in the coronary arteries
  2. coronary emboli
  3. blockage of coronary arteries
  4. severe hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What are some results of ischemic heart disease?

A
  1. tachycardia
  2. myocardial hypertrophy
  3. hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Name some ischemic heart diseases?

A
  1. angina pectoris
  2. MI
  3. chronic ischemic heart disease with heart failure
  4. sudden cardiac death (usually due to arrythmias)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe angina pectoris.

A
  1. Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
  2. Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the variants of angina pectoris?

A
  1. stable (most common)
  2. prinzmetal
  3. unstable (crescendo)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Describe Stable angina.

A
  1. Caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
  2. Physical activity, emotional excitement or increased cardiac workload
  3. Relieved by rest or vasodilators
84
Q

Describe Prinzmetal angina.

A
  1. Caused by coronary artery spasm unrelated to physical activity, heart rate or BP
  2. Relieved by vasodilators and calcium channel blockers
85
Q

Describe Unstable angina.

A
  1. Pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest
  2. Seen in artery occlusion of 90% or greater
  3. Caused by:
    Acute plaque change with superimposed thrombosis/embolism or vasospasm
  4. Warning of impending acute MI
86
Q

What is MI?

A

Myocardial infarction - death of cardiac muscle due to prolonged severe ischemia.

87
Q

Describe the typical sequence of an MI.

A
  1. Acute change of an atheromatous plaque exposes very thrombogenic contents
  2. Platelets adhere to the exposed plaque and degranulate and initiate vasospasm
  3. Tissue factor activates the coagulation cascade adding to the bulk of the thrombus
  4. Thrombus completely occludes the lumen of the vessel
88
Q

What is the time frame in which ischemia may occur but in which myocardium can still be saved?

A

Transient myocardial ischemia can last for about 20-30 minutes. After this time there will be myocardial death and an MI has occurred.

89
Q

90% of MI’s are caused by what?

A

Atherosclerosis. The other 10% occur without accompanying coronary vascular pathology.

90
Q

What are some ways for MI to occur without vascular pathology?

A
  1. cocaïne abuse can cause vasospasm
  2. A-fib, infective endocarditis with vegetations, left sided mural thrombus, paradoxical right sided emboli can all cause occlusion via an emboli
  3. vasculitis, sickle cell disease, amyloid deposition, vascular dissection and hypotensive shock can all cause MI without atherosclerosis or thrombosis
91
Q

Describe when irreversible and reversible injury occur during ischemia/MI.

A
  1. reversible injury occurs when ischemia lasts no more than 20-30 minutes
  2. irreversible injury occurs with severe and prolonged ischemia (longer than 30 minutes) leading to myocyte necrosis
92
Q

Necrosis after an MI is complete within……?

A

6 hours

93
Q

What happens to cardiac myocytes during ischemia?

A
  1. within seconds there will be cessation of aerobic metabolism
  2. there will be loss of contractility within 60 seconds
94
Q

The morphologic features of an MI depend on what factors?

A
  1. Location and severity of the atherosclerosis
  2. Size of the vascular bed perfused by the obstructed vessel
  3. Duration of the occlusion
  4. Oxygen demands of the affected myocardium
  5. Extent of collateral circulation
  6. Heart rate, cardiac rhythm and 7. O2 saturation
95
Q

Myocardial ischemia proceeds….?

A

From the endocardium outward.

96
Q

Name two types of infarctions.

A
  1. transmural infarction

2. subendocardial infarction

97
Q

Describe a transmural infarction.

A
  1. Necrosis involves the full thickness
  2. Associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
  3. ST elevation infarcts
98
Q

Describe subendocardial infarction.

A
  1. Necrosis limited to the inner 1/3-1/2 of the ventricular wall
  2. Due to any reduction in coronary flow: plaque disruption with lysed thrombus, global hypotension
  3. Non-ST elevation infarcts
99
Q

The LAD supplies what areas of the heart?

A
  1. apex
  2. anterior wall of the left ventricle
  3. anterior 2/3 of the ventricular septum
100
Q

The Right coronary artery supplies what areas of the heart?

A
  1. posterior 1/3 of the septum
  2. free wall of right ventricle
  3. posterolateral wall of the left ventricle
101
Q

The left circumflex artery supplies what area of the heart?

A

The myocardium of the left ventricle.

102
Q

Describe some of the changes that occur in myocardium after an MI.

A
  1. in the first two days there will be coagulative necrosis
  2. in 3-4 days there is recruitment of acute inflammatory cells and the myocardium begins healing
  3. in 1-2 weeks granulation tissue, lots of macrophages and new blood vessels will be present
  4. eventually there will be scarring and once there is scarring you cannot tell when the MI occurred
103
Q

What are the clinical features of an MI?

A
  1. rapid, weak pulse
  2. diaphoresis
  3. dyspnea
  4. can also be asymptomatic
104
Q

Name three cardiac markers in the blood.

A
  1. myoglobin
  2. CK-MB
  3. Troponin I and T
105
Q

When does Myoglobin appear in the blood after an MI?

A

0-2 hours and it peaks at about 6-8 hours.

106
Q

Is the myoglobin marker specific and/or sensitive for an MI?

A

No. It can be found in the blood after cardiac or skeletal muscle injury.

107
Q

When does CK-MB appear in the blood after an MI?

A

2-4 hours and it peaks at about 24 hours.

108
Q

Is the CK-MB marker specific and/or sensitive for an MI?

A

It is sensitive but not specific. It is mainly found in cardiac muscle but can be found in some skeletal muscle.

109
Q

When does Troponin appear in the blood after an MI?

A

2-4 hours and it peaks at about 48 hours. Levels persist for 7-10 days post MI.

110
Q

Is the Troponin marker specific and/or sensitive for an MI?

A

It is both sensitive and specific. It is more sensitive than CK-MB.

111
Q

What is given to treat MI’s?

A 
Aspirin
Heparin
Oxygen
Nitrates
Beta-adrenergic inhibitors
ACE inhibitors
Reperfusion
112
Q

How does repercussion help treat an MI?

A 
1. Rescues ischemic myocardium and limits infarct size and can be done via:
Thrombolysis 
Angioplasty
Stent placement
Coronary artery bypass graft (CABG)
  1. Is limited by:
    Rapidity of alleviating the obstruction
    Extent of the correction and the underlying causal lesion
113
Q

What are some adverse complications that can occur after reperfusion?

A
  1. Arrhythmias
  2. Myocardial hemorrhage with contraction bands
  3. Irreversible cell damage superimposed on the original injury (reperfusion injury)
  4. Microvascular injury
  5. Prolonged ischemic dysfunction (myocardial stunning)
114
Q

What are some complications of an MI?

A 
Contractile dysfunction
Arrhythmias
Myocardial rupture
Pericarditis
Right ventricular infarctionInfarct extension
Infarct expansion
Mural thrombus
Ventricular aneurysm
Papillary muscle dysfunction
Progressive late heart failure
115
Q

Describe chronic ischemic heart disease.

A
  1. Progressive heart failure as a consequence of ischemic myocardial damage
  2. Also referred as ischemic cardiomyopathy
  3. Appears due to function decompensation of hypertrophied noninfarcted myocardium
116
Q

Sudden cardiac death can be caused by what?

A

Congenital structural or coronary arterial abnormalities
Aortic valve stenosis
Mitral valve prolapse
Myocarditis
Cardiomyopathies
Pulmonary hypertension
Drug abuse (cocaine, meth)
Hereditary or acquired cardiac arrhythmias
Systemic metabolic and hemodynamic alterations
Catecholamines

117
Q

What are some hereditary or acquired arrhythmias that can cause sudden cardiac death?

A
  1. long QT
  2. short QT
  3. WPW
  4. sick sinus syndrome
  5. catecholamine polymorphic VT
118
Q

Sudden cardiac death can also be caused by what complication of atherosclerosis and ischemia?

A
  1. formation of a lethal arrhythmia such as Asystole or V-fib
  2. arrhythmia normally occurs at a site distant from the conduction system such as adjacent to scars of previous MI’s
119
Q

Heart failure occurs when….?

A
  1. Heart is unable to pump blood sufficiently to meet the demands of the tissue
  2. Heart can only pump blood sufficiently at elevated filling pressures
120
Q

Heart failure develops due to….?

A
  1. Chronic or acute valve disease
  2. Long standing hypertension
  3. Ischemic heart disease with myocardial infarction
  4. Fluid overload
121
Q

Heart failure is characterized by….?

A
  1. Forward failure: decreased cardiac output and tissue perfusion (often associated with left-sided heart failure)
  2. Backward failure: pooling of blood in the venous system (pulmonary and/or peripheral edema and liver congestion) - often associated with right sided heart failure
122
Q

The body adapts to heart failure by what types of adaptive mechanisms?

A
  1. Frank-starling mechanism - dilation and increased filling pressure
  2. ventricular remodeling such as hypertrophy (with or without dilation)
  3. neurohormonal mechanisms
123
Q

Describe some neurohormonal mechanisms of adaption to heart failure.

A
  1. Norepinephrine release to increase the heart rate
  2. Activation of renin-angiotensin-aldosterone system to adjust filling volumes and pressures
  3. Release of atrial natriuretic peptide to adjust filling volumes and pressures
124
Q

What is hypertrophy in relation to heart failure?

A

Increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size.

125
Q

How do myocytes increase in size during hypertrophy?

A
  1. Protein synthesis to increase sarcomeres
  2. Mitochondria increased to gain more energy
  3. Nuclear size increased due to ploidy
126
Q

Describe pressure overload hypertrophy.

A
  1. Cardiac weight is increased
  2. Sarcomeres increase in parallel to the long axes of cells, there is concentric increase in wall thickness
  3. ventricular chamber size is normal
127
Q

Describe volume overload hypertrophy.

A
  1. Cardiac weight is increased
  2. Sarcomeres increase in series with existing cells
  3. Ventricle wall thickness may be increased, normal or less than normal
  4. ventricles may dilate so that the ventricular chamber is increased in size
128
Q

Adaptive changes of heart muscle in response to heart failure may themselves contribute to heart failure. By what mechanisms?

A
  1. Hypertrophy isn’t accompanied by increase in capillaries
  2. Change in myocardial metabolism
  3. Alteration in intracellular handing of calcium ions
  4. Apoptosis of myocytes
  5. Reprogramming of gene expression
129
Q

Left sided heart failure is caused by……?

A

Ischemic heart disease
Hypertension
Aortic and valvular diseases
Myocardial diseases

130
Q

Describe the systolic and diastolic failure associated with left sided heart failure.

A
  1. Systolic failure caused by insufficient cardiac output (basically pump failure)
  2. Diastolic failure caused by stiff ventricles that cannot expand to increase output
131
Q

What are the symptoms of left sided heart failure?

A 
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
132
Q

Symptoms develop because of what in left sided heart failure?

A

Congestion of pulmonary circulation
Stasis of blood in left chambers
Hypoperfusion of tissues

133
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure.

134
Q

Right sided heart failure (Cor Pulmonale) is caused by what?

A
  1. Left sided heart failure and its causes
  2. Pulmonary hypertension resulting from:
    Parenchymal disease of the lung
    Pulmonary vasculature disorders
    Pulmonary thromboembolism
    Hypoxic conditions
135
Q

What are the symptoms of right sided heart failure?

A

Systemic and venous congestion dominate and cause:

Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites 
Abnormal mental function
Renal failure
136
Q

Patients with heart failure frequently present with what?

A

Biventricular heart failure with symptoms of both right and left sided heart failure.

137
Q

What meds are used to treat heart failure?

A
  1. Diuretics
  2. Renin-angiotensin-aldosterone blockers (ACE inhibitors)
  3. β-blockers (lower adrenergic tone)
138
Q

Hypertensive heart disease results from….?

A

Sustained increased hypertension that causes pressure overload and ventricular hypertrophy.

139
Q

How is hypertensive heart disease (HHD) classified?

A
  1. Left-sided (systemic) HHD

2. Right-side (cor pulmonale or pulmonary) HHD

140
Q

What is the diagnostic criteria for Systemic HHD?

A
  1. Left ventricular hypertrophy without any other cardiovascular pathology
  2. History or pathologic evidence of hypertension
141
Q

Describe pulmonary HHD.

A
  1. Characterized by right ventricular hypertrophy and dilation
  2. Can be acute (pulmonary embolism) or chronic
142
Q

What is stenosis in relation to valvular heart disease?

A
  1. Failure of a valve to open completely, which impedes flow

2. Leads to pressure overload

143
Q

What is insufficiency/regurgitation in relation to valvular heart disease?

A
  1. Failure of a valve to close completely, allowing reversed flow
  2. Leads to volume overload
  3. Functional regurgitation - failure in another component that then effects the valves
144
Q

What causes mitral stenosis?

A

Rheumatic heart disease.

145
Q

What are some causes of mitral regurgitation?

A
  1. Rheumatic heart disease
  2. infective endocarditis
  3. mitral valve prolapse
  4. drugs
  5. rupture of papillary muscles
  6. papillary muscle dysfunction
  7. rupture of chordae tendineae
  8. LVH
  9. calcification
146
Q

What are some causes of aortic valve stenosis?

A
  1. rheumatic heart disease
  2. senile calcifications
  3. calcification of a congenitally deformed valve
147
Q

What are some causes of aortic regurgitation?

A
  1. rheumatic heart disease
  2. infective endocarditis
  3. marfan syndrome
  4. degenerative aortic dilation
  5. syphilitic aortitis
  6. ankylosing spondylitis
  7. rheumatoid arthritis
148
Q

Describe Calcific aortic stenosis.

A
  1. Due to normal wear and tear
  2. Normally presents in the seventh to ninth decades of life
  3. Obstruction results in pressure overload and LVH
  4. the calcium that is deposited is made in fibroelastic cells of the valve itself
149
Q

Describe calcific stenosis of a congenitally bicuspid aortic valve.

A
  1. Most frequent congenital cardiovascular malformation
  2. Due to normal wear and tear
  3. Presents in the fifth to seventh decades of life, presents earlier in those with a bicuspid aortic valve because there are two cusps instead of three so wear and tear occurs faster
150
Q

Describe mitral annular calcification.

A
  1. Calcifications in the peripheral fibrous ring - NOT in valve itself
  2. Does not affect valvular function or become clinically important
  3. Rare complications include:
    Regurgitation
    Stenosis
    Arrhythmias and sudden cardiac death
151
Q

Describe mitral valve prolapse.

A
  1. Mitral valve leaflets are floppy and prolapse into the left atrium during systole
  2. Histologic change is myxomatous degeneration by an unknown mechanism
  3. Most patients are asymptomatic and associated with a midsystolic click
152
Q

What are some rare complications of mitral valve prolapse?

A

Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias

153
Q

Describe Rheumatic fever.

A
  1. Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis (antibodies to Group A strep attack antigens in heart that are similar in structure to Group A strep antigens)
  2. Acute rheumatic carditis is a frequent consequence
154
Q

What are the clinical features of Rheumatic fever?

A 
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
155
Q

How is Rheumatic fever diagnosed?

A

The Jones criteria - According to revised Jones criteria, the diagnosis of rheumatic fever can be made when two of the major criteria, or one major criterion plus two minor criteria, are present along with evidence of streptococcal infection: elevated or rising antistreptolysin O titre or DNAase”

156
Q

What are the major criteria in Jones criteria?

A
  1. polyarthritis
  2. carditis
  3. erythema marginatum
  4. sydenham’s chorea
  5. subacute nodules
157
Q

What are the minor criteria in Jones criteria?

A
  1. fever
  2. arthralgia
  3. leukocytosis
  4. abnormal ECG
  5. previous episodes of rheumatic fever
  6. raised erythrocyte sedimentation rate of C-reactive protein
158
Q

Acute rheumatic heart disease is characterized by…..?

A
  1. Aschoff bodies (can be found in any layer - called pancarditis)
  2. vegetations with underlying fibrinoid necrosis
  3. MacCallum plaques within the left atrium
159
Q

What types of cells are included in Aschoff bodies?

A

Aschoff bodies are granulomatous nodules found in the heart with Rheumatic disease, they are caused by inflammation and contain:

  1. lymphocytes
  2. plasma cells
  3. Anitschkow cells ( are enlarged macrophages called Caterpillar cells because of the appearance of their chromatin)
160
Q

Describe chronic Rheumatic heart disease.

A
  1. A deforming fibrotic valvular disease
  2. Only cause of mitral stenosis
  3. Other valves can be involved
  4. Aschoff bodies not identified
161
Q

What happens to the mitral valve in chronic Rheumatic heart disease?

A
  1. Leaflet thickening
  2. Commissural fusion and shortening
  3. Thickening and fusion of tendinous cords
162
Q

Describe infective endocarditis.

A
  1. Serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe
  2. Vegetations composed of thrombotic debris and organisms
  3. Acute or subacute forms
163
Q

How is infective endocarditis diagnosed?

A

Via the Duke criteria which has pathologic, major and minor criteria. To diagnose you must have pathologic criteria, 2 major criteria, 5 minor criteria or 1 major plus three minor criteria.

164
Q

What is the pathologic criteria of the Duke criteria?

A
  1. vegetation or intracardiac abscess present - confirmed by histology
  2. bacteria demonstrated by culture or histology in a vegetation, a emboli zed vegetation or an intracardiac abscess
165
Q

What is the major criteria of the Duke criteria?

A
  1. supportive lab evidence - such as typical bacteria for infective endocarditis in two separate blood cultures or community acquired enterococci in the absence of a primary focus.
  2. evidence of endocardial involvement such as an echocardiogram
  3. new valvular regurgitation - increase or change in pre-existing murmur not sufficient
166
Q

What is the minor criteria of the Duke criteria?

A
  1. predisposing heart condition or IV drug use
  2. Fever greater than 38.0 C
  3. vascular phenomenon such as a major arterial emboli
  4. immunologic phenomena such as glomerulonephritis
  5. positive blood culture that does not meet criterion of the major criteria.
167
Q

What are two types of infective endocarditis?

A
  1. acute

2. subacute

168
Q

Describe acute infective endocarditis.

A
  1. Previously normal heart valve by a highly virulent organism
  2. Necrotizing, ulcerative, destructive lesions
  3. Difficult to cure with antibiotics - especially because valves are not very vascular
169
Q

Describe subacute infective endocarditis.

A
  1. Insidious infections of deformed valves by organisms of lower virulence
  2. Less destructive lesion
  3. Cures produced with antibiotics
170
Q

List some organisms that can cause infective endocarditis.

A
  1. S. viridans effects mainly
    native but previously damaged or abnormal valves
  2. S. aureus effects mainly
    healthy or deformed valves
  3. S. epidermis (coagulase (-) Staph) effects mainly
    prosthetic valves
  4. HACEK - (Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
  5. Enterococci
  6. Gram negative bacilli
  7. Fungi
171
Q

What are the two most common organisms causing infective endocarditis?

A
  1. Staph aureus

2. S. viridans

172
Q

What can cause non-infective endocarditis?

A
  1. Systemic Lupus - called Libman-Sacks endocarditis

2. non-bacterial vegetations

173
Q

Describe non-bacterial thrombotic endocarditis.

A
  1. Previously referred as marantic endocarditis
  2. Characterized by deposition of small sterile thrombi on the leaflets of cardiac valves
  3. Vegetations are thrombi that do not invade or elicit an inflammatory reaction
  4. May be the source of systemic thrombi
  5. Occurs in patients with cancer (mucinous adenocarcinoma), sepsis or hypercoagulable state
174
Q

Describe Libman-Sacks endocarditis.

A
  1. Patients have systemic lupus erythematosus
  2. Vegetations located:
    mitral and tricuspid valves,
    valvular endocardium, chords, or
    mural endocardium of the atria
  3. Vegetations composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies
  4. Intense valvulitis with fibrinoid necrosis of the valve
175
Q

What are some possible complications of receiving artificial heart valves?

A

Thromboembolism
Infective endocarditis with ring abscess
Structural deterioration

176
Q

Describe Carcinoid heart disease.

A
  1. Cardiac manifestation of carcinoid syndrome
  2. Lesions are firm plaque-like endocardial fibrous thickenings and the tricuspid and pulmonary valves
  3. Due to carcinoids that occur outside the portal system that empty directly into the IVC
177
Q

What are primary cardiomyopathies?

A

Heart muscle disorders classified as dilated (most common), hypertrophic or restrictive.

178
Q

What are secondary cardiomyopathies?

A

Heart muscle disorders that are components of a systemic or multi-organ disorder.

179
Q

Describe dilated cardiomyopathy.

A

Characterized by progressive cardiac dilation and contractile or systolic dysfunction

180
Q

Describe hypertrophic cardiomyopathy.

A
  1. Characterized by myocardial hypertrophy, poorly compliant LV myocardium leading to abnormal diastolic filling and intermittent ventricular outflow obstruction
  2. Leading cause of unexplained LVH
181
Q

Describe restrictive cardiomyopathy.

A

Characterized by primary decreased ventricular compliance resulting in impaired filling during diastole

182
Q

What are some causes of dilated cardiomyopathy?

A 
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
183
Q

What causes hypertrophic cardiomyopathy?

A

Genetics.

184
Q

What are some causes of restrictive cardiomyopathy.

A

Idiopathic
Amyloidosis
Radiation induced
Fibrosis

185
Q

Describe Arrhythmogenic right ventricular cardiomyopathy.

A
  1. Inherited (autosomal dominant, variable penetrance) disease of the cardiac muscle causing:
    Right ventricular failure
    Various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)
  2. Right ventricular wall is severely thinned due to:
    loss of myocytes, fatty infiltration and fibrosis
  3. Disease is related to defective cell adhesion proteins in the desmosomes that link adjacent myocytes
186
Q

What is myocarditis?

A

Infectious or inflammatory processes that cause myocardial injury.

187
Q

What types of organisms cause myocarditis?

A
  1. Viruses:
    Coxsackie A/B (most common), Enterovirus, HIV, CMV
  2. Bacteria:
    Chlamydia, Neisseria, Borrelia, Rickettsia
  3. Fungus
  4. Protozoa (Tyrpanosoma)
  5. Helminths
188
Q

What are some immune mediated causes of myocarditis?

A
  1. Post-viral
  2. Poststreptococcal
  3. SLE
  4. Drug hypersensitivity:
    Methyldopa
    Sulfonamides
  5. Transplant rejection
189
Q

What else can cause myocarditis?

A

Sarcoidosis

Giant cell myocarditis

190
Q

What do you see with myocarditis?

A
  1. chronic inflammatory reaction/infiltration - histologically
  2. punctate hemorrhages grossly
191
Q

What are some types of pericardial diseases?

A
  1. Pericardial effusion: pericardial space distended by serous fluid
  2. Hemopericardium: pericardial space distended by blood
  3. Purulent pericarditis: pericardial space distended by pus
192
Q

The normal pericardial space contains how much fluid?

A

30-50 mL of thin, serous fluid. With chronic pressure there can be up to 500 mL of effusion and with rapid effusion - up to 200-300 mL.

193
Q

Name the types of acute pericarditis.

A 
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
194
Q

Name the types of chronic pericarditis.

A

Adhesive pericarditis

Constrictive pericarditis

195
Q

Describe serous acute pericarditis.

A
  1. Produced by non-infectious inflammatory diseases

2. Mild lymphocytic infiltrate in the epipericardial fat

196
Q

Describe fibrinous/Serofibrinous pericarditis.

A
  1. Most frequent type with a loud pericardial friction rub
  2. Composed of serous fluid mixed with fibrinous exudate
  3. Associated with acute MI, postinfarction syndrome, uremia, chest radiation, RF, SLE, trauma
197
Q

Describe acute purulent pericarditis.

A
  1. Caused by invasion of microbes into the pericardial space by:
    Direct extension
    Seeding from the blood
    Lymphatic extension
    Introduction during craniotomy
  2. Acute inflammatory reaction that can produce a mediastinopericarditis
  3. Organization and scarring usual outcome with constrictive pericarditis
198
Q

Describe acute hemorrhagic pericarditis.

A
  1. Blood with a fibrinous or suppurative effusion
  2. Most commonly caused by a metastatic malignant neoplasm
  3. Also found in TB and bacterial infections and post-cardiac surgery
199
Q

Describe acute caseous pericarditis.

A
  1. Rare
  2. Almost always due to TB by direct spread, but sometimes fungus
  3. Leads to a disabling, fibrocalcific, chronic constrictive pericarditis
200
Q

Describe chronic adhesive pericarditis.

A
  1. Follows infectious pericarditis, cardiac surgery, radiation
  2. Pericardial sac is obliterated and pericardium adheres to surrounding structures
201
Q

Describe chronic constrictive pericarditis.

A
  1. Heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
  2. Mimic restrictive cardiomyopathy
  3. Heart sounds are muffled or distant
202
Q

What is a myxoma?

A

A cardiac tumor. The most common primary cardiac tumor in adults.

203
Q

Describe Myxomas.

A
  1. Benign neoplasm with abnormalities of chr 12 & 17
  2. Arise from primitive multipotent mesenchymal cells
  3. Most often in the atria, but can arise in any chamber
  4. 10% associated with Carney complex
204
Q

What is a rhabdomyoma?

A

A cardiac tumor. The most frequent primary cardiac timor in children. Is considered a harmartoma.

205
Q

What disease are rhabdomyoma’s associated with?

A

Tuberous sclerosis.

206
Q

What are Lipomas?

A

Benign tumors of mature adipose tissue. Can occur in heart - most often in LV, RA or atrial septum.

207
Q

What are papillary fibroelastoma’s?

A

Benign neoplasm often discovered at autopsy. Resembles a Lambl excrescence (filiform fronds that occur at sites of valve closure. They originate as small thrombi on endocardial surfaces (where the valve margins contact) and have the potential to embolize to distant organs).

Block 9 week 1 (8 decks)

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