Cardiovascular-Fung Flashcards
1
Q
How much does a female heart weigh? Male heart weight?
A
Female heart: 250-300 grams
Male heart: 300-350 grams
2
Q
What is the vascular wall thickness of the right atrium & left atrium?
A
RA: 0.3-0.5 cm
LA: 1.3-1.5 cm
3
Q
What are the 3 layers of cardiac tissue?
A
intima: endocardium w/ endocardial cells
media: cardiac myocytes w/ centrally located nuclei & striations
adventita: epicardium
4
Q
What is the main distinguishing feature b/w cardiac muscle & skeletal muscle on histo?
A
cardiac: has intercalated discs & centrally located nuclei
skeletal: has peripherally located nuclei
5
Q
What causes the striations in muscle?
A
myosin & actin
myosin-heavy chains
actin-light chains
6
Q
Which valves have leaflets & chordae tendinae attached? Which side of the heart?
A
Tricuspid valve–right side
bicuspid valve-left side
the cuspids are the leaflets…
7
Q
The chordae tendiae that attach to the tricuspid & bicuspid valves attach to what structure?
A
papillary muscles in the ventricular wall
8
Q
T/F Semilunar valves have chordae tendinae which attach them to the ventricular wall of the heart.
A
False. Only the tricuspid & bicuspid valves.
9
Q
Which are the semilunar valves?
A
aortic & pulmonic
10
Q
Briefly describe the coronary arteries supplying the heart.
A
L has a short main branch & then divides into L circumflex & L anterior descending
R takes longer to branch
11
Q
Where do the L & R coronary arteries pop off from?
A
the aorta!
12
Q
What is the function of the endothelial cells in blood vessels?
A
Maintain non-thrombogenic blood-tissue interface Modulate vascular resistance Metabolize hormones Regulate inflammation Regulate cell growth
13
Q
What is the fcn of smooth muscle cells in blood vessels?
A
Proliferate when stimulated Synthesize Collagen Elastin Proteoglycans Growth factors Cytokines
14
Q
What is the ECM of blood vessels composed of?
A
elastin
collagen
glycosaminoglycan
15
Q
Describe the structure of veins v. arteries.
A
arteries:
intima-endothelial lining
media-thick b/c they need to handle blood at high pressure-lots of smooth muscle!
adventitia-contains vaso vasorum to deliver nutrients to bv
veins:
same except media thinner
16
Q
What are the main types of arteries?
A
Elastic artery–common carotid, aorta etc. Need recoil & resistance–lots of elastin
Muscular artery-radial artery etc. not as much elastin
Arteriole
17
Q
Where does gas & nutrient exchange occur?
A
at the level of the capillaries…
18
Q
Although muscular arteries have less elastin than elastic ones, they still have some in strategic places. Describe.
A
found in the internal & external elastic lamina
external elastic lamina separates the media from the adventitia
19
Q
What is the vascular system besides the blood system?
A
the lymphatic system
uses skeletal muscle as its pump
includes lymph nodes
returns extra fluid to the cardiovascular system
20
Q
How do veins get blood to move?
A
thru contraction of skeletal muscle
one-way valves prevent backflow
21
Q
What are 6 mechanisms of dysfunction seen in cardiovascular disease?
A
Failure of the pump (heart)
Obstruction to flow
Regurgitant flow (regurgitant valve)
Shunted flow
Disorders of cardiac conduction (bundle branch blocks)
Rupture of the heart or a major blood vessel
22
Q
What would be some ways to get failure of the pump?
A
MI
cardiac hypertrophy
23
Q
What would be some ways to get obstruction of flow?
A
stenosis of a valve
24
Q
What would be a way to get shunted flow?
A
congenital heart disease
25
How might you get a rupture of the heart or a major blood vessel?
aortic dissection
| massive MI
26
What is the stereotypical response of cardiovascular disease?
intimal thickening after injury
smooth muscle cell recruitment to intima
macrophages & T cells get in there
deposition of matrix intima
27
What is the role of the kidney in HTN?
juxtaglomerular apparatus senses blood volume
if it senses it is too low-->will release renin
renin ultimately leads to increased BP via increased blood volume via increased sodium reabsorption
28
What exactly does renin do?
converts angiotensinogen to angiotensin I
in the lungs & other places w/ ACE, Ang I is converted to Ang II.
Ang II causes vasoconstriction.
Ang II also goes to the adrenal glands & causes the secretion of aldosterone.
THis prompts the reabsorption of sodium. Therefore, blood volume increases.
29
What happens if you get volume overload & your BP is too high?
get atrial natriuretic peptide released from the heart.
This causes the excretion of sodium & water.
also causes vasodilation.
30
What is considered a normal BP?
less than 120/80
31
What is considered pre-HTN?
over 120/80
32
What is considered HTN?
over 140/90
33
What is considered malignant HTN?
200/120 & above
34
What is essential HTN?
HTN w/ a primary identifiable cause.
35
What are some genetic causes of essential HTN?
gene defects of aldosterone metabolism
| defects of sodium reabsorption
36
What are some polymorphisms that can cause essential HTN?
at the loci of...
angiotensin
angiotensin receptor
RAAS
37
What are some vascular causes of essential HTN?
vasoconstriction
| structural changes
38
What are some environmental factors that can cause essential HTN?
```
Diet
Stress
Obesity
Smoking
Physical inactivity
```
39
What is secondary hypertension?
HTN that is secondary to some disease process
| Happens only 5-10% of the time
40
What are some renal causes of secondary HTN?
```
Acute glomerulonephritis
Chronic renal disease
Polycystic disease
Renal artery stenosis
Renal vasculitis
Renin-producing tumors
```
41
What are some endocrine causes of secondary HTN?
```
Adrenocortical dysfunction
Exogenous hormones
Pheochromocytoma
Acromegaly
Hypothyroidism
Hyperthyroidism
Pregnancy-induced
```
42
What are some cardiovascular causes of secondary HTN?
```
Coarctation of aorta
Polyarteritis nodosa
Increased intravascular volume
Increased cardiac output
Rigidity of aorta
```
43
What are some neurologic causes of secondary HTN?
Psychogenic
Increased intracranial pressure
Sleep apnea
Acute stress
44
When would you see hyaline arteriolosclerosis? What would you see?
benign essential HTN
see: Eosinophilic deposition around the arterioles in the kidney. Kidney would look blown up. Kidney would have a rough outer surface b/c of the hyaline arteriosclerosis.
45
When would you see hyperplastic arteriolosclerosis? What would you see?
malignant HTN
proliferation of the smooth muscle cells around the arterioles of the kidney.
more smooth muscle cells in the media
see hemorrhages along the outside of the kidney
46
What is an atheroma? What are its 3 main parts?
raised lesions w/ a soft, yellow core of lipid covered with a fibrous cap
1. media
2. necrotic center
3. fibrous cap
47
What are 3 negative consequences of atheromas in the lumen of a blood vessel?
1. obstruct blood flow-stenosis
2. rupture & cause vessel thrombosis
3. lead to aneurysm formation
48
What is found in the necrotic center of an atheroma?
cell debris
cholesterol crystals
foam cells
calcium
49
What is found in the center of a fibrous cap?
```
smooth muscle cells
macrophages
foam cells
lymphocytes
collagen
elastin
proteoglycans
neovascularization
```
50
What are some constitutional risk factors for the development of atherosclerosis?
1. age
2. genetics
3. gender
51
What are some modifiable risk factors for the development of atherosclerosis?
1. Hyperlipidemia
2. HTN
3. Cigarette Smoking
4. Diabetes
52
What are some other risk factors for the development of atherosclerosis?
```
Inflammation
Hyperhomocystinemia
Metabolic syndrome
Lipoprotein a
Hemostatic factors
Sedentary life style
Type A personality
Obesity
```
53
What is the response to injury hypothesis for atherosclerosis?
atherosclerosis is a chronic inflammatory and healing response to arterial wall and endothelial injury
54
What are some of the pathological events leading to atherosclerosis?
```
Endothelial injury
Lipoprotein accumulation
monocyte adhesion
Formation of foam cells
platelet adhesion
smooth muscle cell recruitment
smooth muscle cell proliferation & ECM production
lipid accumulation
```
55
SO...the first step in atherosclerosis is endothelial injury. What are some possible causes of injury?
Mechanical denudation
Immune complex deposition
Irradiation
Chemicals
56
What are some possible causes of endothelial dysfunction?
```
Hemodynamic disturbances
Hypercholesterolemia
Hypertension
Smoking
Infectious agents
Homocysteine
```
57
What are hemodynamic disturbances? How do they contribute to the formation of endothelial dysfunction and atherosclerosis?
principle of plaques being deposited at areas of disturbed blood flow, like branch points and ostia of exiting vessels
ALSO the posterior wall of the abdominal aorta
58
What is a protective hemodynamic factor against atherosclerosis?
non-turbulent laminar flow
59
What are the dominant lipids found in plaques?
cholesterols & cholesterol esters
60
What are 2 conditions that predispose to hyperlipidemia, and therefore increased risk of atherosclerosis?
diabetes type II
| hypothyroidism
61
HOw do lipids lead to atherosclerosis?
1. lipids increase oxygen free radical formation--which decrease NO & the ability of a bv to vasodilate.
2. oxygen free radicals make LDL oxidized. THis is eaten by macrophages=foam cells.
3. Oxidized LDL increases release of growth factors, cytokines, chemokines--more monocytes!
4. Oxidized LDL causes endothelial dysfunction (also bad for smooth muscle cells).
62
What does it take to convert a fatty streak into a mature atheroma?
smooth muscle cell proliferation & extracellular matrix synthesis.
promoted by chemokines & growth factors
63
What are 4 serious possible consequences of atherosclerosis?
1. MI
2. Cerebral infarction
3. aortic aneurysm
4. peripheral vascular disease
64
HOw can atherosclerosis lead to an aortic aneurysm?
with the atheroma formation, increased distance is created b/w the lumen where the nutrients are & the media...necrosis ensues with time
the medial wall gets thinner
rupture becomes possible-aneurysm formation.
called cystic medial degeneration
65
T/F Females' estrogen levels are protective for a time against atherosclerosis.
True. The process is delayed longer. More common in men, therefore.
66
How does peripheral vascular disease from atherosclerosis present?
patients will get pain when they walk b/c their legs don't get enough oxygen
67
When has atherosclerosis accomplished stenosis of a blood vessel?
Critical stenosis when the blood vessel is 70% occluded from the atheroma.
68
What are some possible negative consequences that result from chronic decreased perfusion ?
Bowel ischemia
Chronic Ischemic Heart Disease
Ischemic encephalopathy
Intermittent claudication
69
What is an acute plaque change?
Rupture or fissure exposing highly thombogenic plaque contents
Erosion or ulceration exposing the thrombogenic subendothelial basement membrane to blood
Hemorrhage into the atheroma
70
What is the process of atherosclerosis at the preclinical stage? What age group does this usu occur in?
usu younger people
1. normal artery
2. fatty streak
3. fibrofatty plaque
4. advanced/vulnerable plaque
71
In which step of atherosclerosis formation does the organization of a thrombus & calcification occur?
b/w fibrofatty plaque & advanced vulnerable plaque
72
What are some possible outcomes at the clinical stage once you have an advanced vulnerable plaque? Which age group does this occur in?
1. Aneurysm & Rupture
2. Occlusion by Thrombus
3. Critical STenosis
73
What is ischemic heart disease? What is it also known as?
syndromes involving myocardial ischemia
| aka coronary artery disease
74
What is myocardial ischemia?
Myocardial ischemia is an imbalance between the supply and demand of the heart for oxygenated blood
75
What are some things that can cause ischemic heart disease?
>90% blockage of coronary arteries with plaque
coronary emboli
blockage of coronary arteries
severe hypotension
76
What are some of the symptoms of IHD?
Tachycardia
Myocardial hypertrophy
Hypoxemia
77
What are some acute coronary syndromes that fall within ischemic heart disease?
Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death
78
What is angina pectoris? WHat are its 3 variants?
Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis
Variants:
Stable
Prinzmetal
Unstable
79
What is stable angina? What provokes & alleviates the symptoms?
Caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
Physical activity, emotional excitement or increased cardiac workload
Relieved by rest or vasodilators
80
What is prinzmetal angina? What provokes and alleviates those symptoms?
Caused by coronary artery spasm unrelated to physical activity, heart rate or BP
Relieved by vasodilators and calcium channel blockers
COCAINE ABUSE
81
WHat is unstable angina? What can it indicate?
Pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest
Seen in artery occlusion of 90% or greater
Warning of impending acute MI
82
What is unstable angina caused by?
Acute plaque change with superimposed thrombosis/embolism
| Vasospasm
83
What is an MI?
Death of cardiac muscle due to prolonged severe ischemia
84
What is the sequence like leading up to an MI ?
Acute change of an atheromatous plaque exposes very thrombogenic contents
Platelets adhere to the exposed plaque and degranulate and initiate vasospasm
Tissue factor activates the coagulation cascade adding to the bulk of the thrombus
Thrombus completely occludes the lumen of the vessel
85
10% of MIs are caused w/o the typical coronary vascular pathology. What are some of these causes?
```
vasospasm-cocaine, platelet aggregation
emboli
Vasculitis
Sickle cell disease
Amyloid deposition
Vascular dissection
Severe hypotension (shock)
```
86
What are some sources of emboli that can cause MI?
Atrial fibrillation of left atrium
Vegetations from infective endocarditis
Left sided mural thrombus
Paradoxical right sided emboli
87
WHat is reversible injury with MIs?
Reversible injury is ischemia lasting no more than 20-30 minutes
Cessation of aerobic metabolism within seconds
Loss of contractility within 60 seconds
88
What is irreversible injury with MIs?
Prolonged severe ischemia leads to myocyte necrosis
| Necrosis is complete within 6 hours of onset
89
The morphologic features of an MI depend on which factors?
Location and severity of the atherosclerosis
Size of the vascular bed perfused by the obstructed vessel
Duration of the occlusion
Oxygen demands of the affected myocardium
Extent of collateral circulation
Heart rate, cardiac rhythm and O2 saturation
90
What is the direction of myocardial ischemia?
inside outward!
| starts in the endocardium
91
What are 2 types of infarctions?
Transmural
| Subendocardial
92
What is a transmural infarction? What would the EKG show?
Necrosis involves the full thickness
Associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
ST elevation infarcts
93
What is a subendocardial infarct? What would the EKG show?
Necrosis limited to the inner 1/3-1/2 of the ventricular wall
Due to any reduction in coronary flow: plaque disruption with lysed thrombus, global hypotension
Non-ST elevation infarcts
94
WHich part of the heart does the LAD supply?
Apex
Anterior wall of LV
Anterior 2/3 of ventricular septum
95
Which part of the heart does the right coronary artery supply?
Posterior 1/3 of septum (dominant)
RV free wall
Posterobasal wall of LV
96
Which part of the heart does the Left Circumflex artery supply?
LV myocardium
97
WHat are the clinical features seen in ischemic heart disease?
Rapid, weak pulse
Diaphoresis
Dyspnea
Asymptomatic sometimes
98
Myoglobin
When do you see the rise in levels?
Peak of levels?
Other info?
Rise: 0-2 hours; first biomarker to rise
Peak: 6-8 hrs
found in skeletal & cardiac muscle, so not specific
99
```
CK-MB
When do you see the rise in levels?
Peak of levels?
Sensitive, specific?
Other info?
```
```
Rises w/i 2-4 hours
Peak: 24 hours
sensitive, but not specific
CK-MB is also found in skeletal muscle
there is also CK-MM & CK-BB
```
100
Where are CK-MM & CK-BB found?
CK-MM: cardiac & skeletal muscle
| CK-BB: brain & lung
101
```
Troponin I & T
When do you see the rise in levels?
Peak of levels?
Sensitive, specific?
Other info?
```
```
Rise: 2-4 hours
Peak: 48 hours
last to show up, but also longest lasting
most sensitive & specific
Levels persist for 7-10 days
```
102
WHat is the medical treatment for an MI, ischemic heart disease?
```
Aspirin
Heparin
Oxygen
Nitrates
Beta-adrenergic inhibitors
ACE inhibitors
Reperfusion
```
103
WHat is involved in reperfusion? What are some different ways to do that?
```
Rescues ischemic myocardium and limits infarct size
Thrombolysis
Angioplasty
Stent placement
Coronary artery bypass graft (CABG)
```
104
What are some limitations to reperfusion?
Rapidity of alleviating the obstruction
| Extent of the correction and the underlying causal lesion
105
What are some adverse complications of reperfusion?
Arrhythmias
Myocardial hemorrhage with contraction bands
Irreversible cell damage superimposed on the original injury (reperfusion injury)
Microvascular injury
Prolonged ischemic dysfunction (myocardial stunning)
106
What are some complications involved in MI?
```
Contractile dysfunction
Arrhythmias
Myocardial rupture
Pericarditis
Right ventricular infarction
Infarct extension
Infarct expansion
Mural thrombus
Ventricular aneurysm
Papillary muscle dysfunction
Progressive late heart failure
```
107
What is ischemic cardiomyopathy ?
Progressive heart failure as a consequence of ischemic myocardial damage
Appears due to function decompensation of hypertrophied noninfarcted myocardium
108
What are 2 types of arrhythmia that can result from MI? Where do these arrhythmias usu originate?
Asystole
Ventricular fibrillation
**Arrhythmia normally occurs at a site distant from the conduction system
Adjacent to scars of previous myocardial infarction
109
What are some nonatherosclerotic conditions that can cause sudden cardiac death?
```
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
Long QT
Short QT
WPW
Sick sinus syndrome
Catecholamine polymorphic VT
Systemic metabolic and hemodynamic alterations
Catecholamines
```
110
What is heart failure?
Heart is unable to pump blood sufficiently to meet the demands of the tissue
Heart can only pump blood sufficiently at elevated filling pressures
111
What are some causes of heart failure?
Chronic or acute valve disease
Long standing hypertension
Ischemic heart disease with myocardial infarction
Fluid overload
112
What are the 2 types of heart failure?
Forward Failure
| Backward Failure
113
What is forward failure?
decreased cardiac output and tissue perfusion
| Left sided heart failure
114
What is backward failure?
pooling of blood in the venous system (pulmonary and/or peripheral edema). Liver congestion
Right sided heart failure
115
What are some adaptive mechanisms to deal with heart failure?
```
Frank Starling mechanism: the more stretch by fluid, the greater contractility
Ventricular Remodeling-hypertrophy
Neurohormonal mechanisms:
NE-HR increases
RAAS-BV & BP increases
ANP-decreases BP
```
116
What is hypertrophy really? What are the changes involved for the myocytes?
```
Increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size
Myocytes increase:
Protein synthesis to increase sarcomeres
Mitochondria to gain more energy
Nuclear size increases due to ploidy
```
117
What is pressure overload hypertrophy?
Concentric increase in the wall thickness crazy hypertrophied LV. Usu still a normal chamber size.
Cardiac weight is increased
Sarcomeres increase in parallel to the long axes of cells
118
What is volume overload hypertrophy?
Get dilation of the ventricle. Larger chamber. Ventricular wall thickness probably hasn’t really increased.
Cardiac weight is increased
Sarcomeres increase in series with existing cells
Ventricle wall thickness may be increased, normal or less than normal
119
Why does hypertrophy eventually fail as a compensatory mechanism?
Eventually fails b/c there is no increase in capillaries to supply the new muscle. Do increase sarcomeres & nuclei.
120
What are other reasons that hypertrophy eventually fails?
Change in myocardial metabolism
Alteration in intracellular handing of calcium ions
Apoptosis of myocytes
Reprogramming of gene expression
121
What are the 2 types of left sided heart failure?
Systolic failure-Insufficient cardiac output (pump failure)
| diastolic failure-Stiff ventricle that cannot expand and increase its output
122
What are some causes of left sided heart failure?
Ischemic heart disease
Hypertension
Aortic and valvular diseases
Myocardial diseases
123
What are the main problems with left sided heart failure that give rise to its main symptoms?
Congestion of pulmonary circulation
Stasis of blood in left chambers
Hypoperfusion of tissues
124
What are the main symptoms of left sided heart failure?
```
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
```
125
What is another name for right sided heart failure? What are its 2 main causes?
Cor Pulmonale
Caused by:
Left sided heart failure
Pulmonary HTN
126
What are possible causes of Pulmonary HTN that could lead to right sided heart failure?
Parenchymal disease of the lung
Pulmonary vasculature disorders
Pulmonary thromboembolism
Hypoxic conditions
127
WHat are the symptoms of right sided heart failure?
```
Systemic and venous congestion
Hepatosplenomegaly
Peripheral edema
Pleural effusions
Ascites
Abnormal mental function
Renal failure
```
128
What are the medical treatments for heart failure?
Diuretics
Renin-angiotensin-aldosterone blockers (ACE inhibitors)
β-blockers (lower adrenergic tone)
129
What is hypertensive heart disease?
Results from sustained increased hypertension that causes pressure overload and ventricular hypertrophy
Classified as
Left-sided (systemic) HHD
Right-side (cor pulmonale) HHD
130
What is the diagnostic criteria for systemic hypertensive heart disease?
Left ventricular hypertrophy without any other cardiovascular pathology
History or pathologic evidence of hypertension
131
What is the diagnostic criteria for pulmonary hypertensive heart disease?
Characterized by right ventricular hypertrophy and dilation
| Can be acute (pulmonary embolism) or chronic
132
What are some forms of valvular heart disease?
```
Mitral Stenosis
Mitral Regurgitation
Mitral annular calcification
mitral valve prolapse
Aortic stenosis
aortic reguritation
Calcific aortic stenosis
Calcific stenosis of congenitally bicuspid aortic valve
Rheumatic fever
Acute Rheumatic heart disease
Chronic Rheumatic heart disease
Infective Endocarditis
Non-infective endocarditis: Nonbacterial thrombotic endocarditis, Libman Sacks Endocarditis
Carcinoid Heart Disease
```
133
What is stenosis? What does it lead to?
Failure of a valve to open completely, which impedes flow
| Leads to pressure overload
134
What is insufficiency/regurgitation?
Failure of a valve to close completely, allowing reversed flow
Leads to volume overload
Functional regurgitation
135
Rheumatic heart disease can lead to which forms of valvular heart disease?
mitral stenosis
mitral regurgitation
aortic stenosis
aortic regurgitation
136
Infective endocarditis can lead to which forms of valvular heart disease?
mitral regurgitation
| aortic regurgitation
137
What can calcification of a valve lead to in terms of valvular heart disease?
mitral regurgitation
| aortic stenosis
138
What can messing with the chordae tendinae or papillary muscles lead to?
mitral regurgitation
139
What are some other things that can cause mitral regurgitation?
drugs
| LVH
140
Aside from rheumatic heart disease & infective endocarditis, what else can cause aortic regurgitation?
```
Marfan syndrome
Syphilis
Ankylosing spondilitis
Rheumatoid arthritis
degenerative aortic dilation
```
141
Calcific aortic stenosis is another form of valvular heart disease. What causes it? When does it present? What are the complications of it?
caused by normal wear & tear
presents in 7th-9th decades of life
complications: LVH, pressure overload
142
What is the mechanism involved in creating calcific aortic stenosis?
Valves have “osteoblast like cells” that cause the deposition of calcium. Ca++ is made inside the fibroelastic tissue of the valve.
143
What is calcific stenosis of congenitally bicuspid aortic valve? When does it present?
form of valvular heart disease
Most frequent congenital cardiovascular malformation
Due to normal wear and tear
Presents in the fifth to seventh decades of life
144
What is mitral annular calcification? What can that lead to?
Calcifications in the peripheral fibrous ring of the mitral valve
Does not affect valvular function or become clinically important
Rare complications:
Regurgitation
Stenosis
Arrhythmias and sudden cardiac death
145
What is mitral valve prolapse? What does it look like on histo?
Mitral valve leaflets are floppy and prolapse into the left atrium during systole
Histologic change is myxomatous degeneration by an unknown mechanism
146
What might be a physical exam finding in a patient with mitral valve prolapse? What are some rare complications of this?
Most patients are asymptomatic and associated with a midsystolic click
```
Rare complications:
Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias
```
147
What is rheumatic fever? What is a frequent consequence of it?
Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group A streptococcal pharyngitis
Acute rheumatic carditis is a frequent consequence
148
What are some important clinical features of rheumatic fever?
```
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
```
149
What is a special histo feature of rheumatic fever? Where is it found?
Aschoff bodies-include lymphocytes, plasma cells, Anitschkow cells.
Aschoff looks like granulomatous reaction. Surrounds a blood vessel. Inflammatory reaction—macrophages w/ prominent nucleoli—bodies.
found in any layer of the heart (pancarditis)
150
Aside from aschoff bodies, what are other distinguishing features of acute rheumatic disease?
Vegetations with underlying fibrinoid necrosis
| MacCallum plaques within the left atrium
151
T/F Aschoff bodies are an important distinguishing feature of chronic rheumatic disease.
F. This form of rheumatic disease does not include aschoff bodies.
152
What is chronic rheumatic disease?
A deforming fibrotic valvular disease
Only cause of mitral stenosis
Other valves can be involved
153
What does the mitral valve look like in a patient with chronic rheumatic disease?
Leaflet thickening
Commissural fusion and shortening
Thickening and fusion of tendinous cords
154
Another form of valvular heart disease is endocarditis. What is thiS? What are the 2 major forms?
Serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe
Vegetations composed of thrombotic debris and organisms
Acute or subacute forms
155
What is acute endocarditis?
Previously NORMAL heart valve by a highly virulent organism
Necrotizing, ulcerative, destructive lesions
Difficult to cure with antibiotics
156
What is subacute endocarditis?
Insidious infections of deformed valves by organisms of lower virulence
Less destructive lesion
Cures produced with antibiotics
157
What is an organism that can infect native but deformed valves, producing ____ endocarditis?
strep viridans
| subacute endocarditis
158
What is an organism that can infect healthy valves, producing ____ endocarditis?
staph aureus
| acute endocarditis
159
What is an organism that can infect prosthetic heart valves? Other organisms that can infect valves in general?
staph epidermis (coagulase -)
```
Other:
HACEK
Enterococci
Gram negative bacilli
Fungi
```
160
What does HACEK stand for?
Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
161
Why can it be a challenged to cure endocarditis with antibiotics?
b/c heart valves are not very vascular, for the delivery of antibiotics
162
Non infective endocarditis is caused by which 2 conditions?
Non-infected (sterile) vegetations caused by:
Non-bacterial thrombotic endocarditis
Libman-Sacks endocarditis (SLE)
163
What is nonbacterial thrombotic endocarditis?
Previously referred as marantic endocarditis
Characterized by deposition of small sterile thrombi on the leaflets of cardiac valves
Vegetations are thrombi that do not invade or elicit an inflammatory reaction
May be the source of systemic thrombi
164
Which patients experience nonthrombotic endocarditis?
cancer (mucinous adenocarcinoma), sepsis or hypercoagulable state
165
What is Libman-Sacks disease?
occurs in patients with SLE
patients have vegetations
Get Intense valvulitis with fibrinoid necrosis of the valve
166
Where are the vegetations located in Libman-Sacks disease?
mitral and tricuspid valves
Valvular endocardium
Chords
Mural endocardium of the atria
167
What do the vegetations look like on histo in Libman-Sacks disease?
Vegetations composed of finely granular, fibrinous eosinophilic material with hematoxylin bodies
168
What are 2 types of artificial heart valves? What are possible complications of this?
mechanical, tissue
complications:
Thromboembolism
Infective endocarditis with ring abscess
Structural deterioration
169
What's the deal with carcinoid heart disease?
carcinoid tumors can often occur in the GI tract
if they occur outside the portal system & dump into the IVC they will go into the RA & plaques will form on the tricuspid & pulmonary valves
Note: these plaques are endocardial fibrous thickenings
170
What are primary & secondary cardiomyopathies?
primary: disorder confined to heart muscle, 3 subtypes
secondary: myocardial involvement in a multiorgan disorder
171
What are the 3 subtypes of primary cardiomyopathies?
dilated
hypertrophic
restrictive
172
What is dilated cardiomyopathy?
Characterized by progressive cardiac dilation and contractile dysfunction
173
What is hypertrophic cardiomyopathy?
Characterized by myocardial hypertrophy, poorly compliant LV myocardium leading to abnormal diastolic filling and intermittent ventricular outflow obstruction
174
What is restrictive cardiomyopathy?
Characterized by primary decreased ventricular compliance resulting in impaired filling during diastole
175
What is the leading cause of unexplained LVH?
hypertrophic cardiomyopathy
176
What is the mechanism of impairment for the the following:
| dilated, hypertrophic, restrictive cardiomyopathy?
dilated: contractility (systole)
| hypertrophic & restrictive: compliance (diastole)
177
What are some possible causes of dilated cardiomyopathy?
```
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
```
178
What are some possible causes of hypertrophic & restrictive cardiomyopathy?
hypertrophic;
genetics
```
restrictive:
Idiopathic
Amyloidosis
Radiation induced
Fibrosis
```
179
What is Arrhythmogenic right ventricular cardiomyopathy? What cause it?
Disease is related to defective cell adhesion proteins in the desmosomes that link adjacent myocytes
Aut Dom
thin RV wall: loss of myocytes, fatty infiltration, fibrosis
Right ventricular failure
Various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)
180
What is myocarditis?
Infectious or inflammatory processes that cause myocardial injury
181
What are some different types of myocarditis?
Infectious
Immune-mediated
Sarcoidosis
Giant Cell Myocarditis
182
What are some infectious agents that can cause infectious myocarditis?
```
Viruses
Bacteria
Fungus
Protozoa
Helminths
```
183
What are some viruses that can cause infectious myocarditis?
Coxsackie A/B, Enterovirus, HIV, CMV
184
What are some bacteria that can cause infectious myocarditis?
Chlamydia, Neisseria, Borrelia, Rickettsia
185
What are some causes of immune mediated myocarditis?
```
Post-viral
Poststreptococcal
SLE
Drug hypersensitivity
Methyldopa
Sulfonamides
Transplant rejection
```
186
What is pericardial disease? How much fluid should usu be in the pericardial sac?
this is when extra fluid gets stuck in the pericardial space
| should only be 20-30 mL normally...w/ thin clear straw colored fluid
187
With chronic pressure how much fluid can get stuck in there? With rapid effusion?
Chronic: up to 500 mL!
Rapid: 200-300 mL
188
What do the following mean?
pericardial effusion
hemopericardium
purulent pericarditis
pericardial effusion: distended by serous fluid
hemo: distended by blood
purulent: pus
189
What are some different forms of acute pericarditis?
```
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
```
190
What are some different forms of chronic pericarditis?
Adhesive pericarditis
| Constrictive pericarditis
191
What does serous acute pericarditis look like?
Produced by non-infectious inflammatory diseases
| Mild lymphocytic infiltrate in the epipericardial fat
192
What does fibrinous/serofibrinous pericarditis look like?
Most frequent type with a loud pericardial friction rub
| Composed of serous fluid mixed with fibrinous exudate
193
What is fibrinous/serofibrinous pericarditis associated with?
Associated with acute MI, postinfarction syndrome, uremia, chest radiation, RF, SLE, trauma
194
What causes acute purulent pericarditis?
```
Caused by invasion of microbes into the pericardial space by
Direct extension
Seeding from the blood
Lymphatic extension
Introduction during cardiotomy
```
195
What are possible end results of acute purulent pericarditis?
Acute inflammatory reaction that can produce a mediastinopericarditis
Organization and scarring usual outcome with constrictive pericarditis
196
What causes acute pericarditis-hemmorhagic? What is it?
Blood with a fibrinous or suppurative effusion
Most commonly caused by a metastatic malignant neoplasm
Also found in TB and bacterial infections and post-cardiac surgery
197
What's the deal with acute pericarditis-caseous?
Rare
Almost always due to TB by direct spread, but sometimes fungus
Leads to a disabling, fibrocalcific, chronic constrictive pericarditis
198
What is adhesive mediastinopericarditis? What category does it fall into?
Follow infectious pericarditis, cardiac surgery, radiation
Pericardial sac is obliterated and pericardium adheres to surrounding structures
**falls into the category of chronic pericarditis
199
What is constrictive pericarditis? How do the heart sounds present?
Heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
Mimic restrictive cardiomyopathy
Heart sounds are muffled or distant
200
Give 4 cardiac tumors.
myxoma
rhabdomyoma
lipoma
papillary fibroelastoma
201
What is a myxoma?
Most common primary tumor in adults
BENIGN
Most often in the atria, but can arise in any chamber
10% associated with Carney complex
202
Which chromosomal abnormalities can cause a myxoma? Which cell type do they originate from?
Arise from primitive multipotent mesenchymal cells
| chromosomes 12 & 17
203
What pop are rhabdomyomas common in? Also called? Associated with what?
Most frequent primary tumor in children
Associated with tuberous sclerosis
Considered hamartomas
204
T/F Rhabdomyomas are the most common primary tumor in adults.
FALSE
in children...
myxoma is most common primary in adult
205
Is a lipoma benign or malignant? Which tissue is it found in?
Benign tumor of mature adipose tissue
206
Where are lipomas most often located?
Most often located in the LV, RA or atrial septum
207
What's the deal with a papillary fibroelastoma?
Benign neoplasm often discovered at autopsy
| Resemble Lambl excrescences
