CV System-Fung Flashcards
1
Q
What do arteries have more of in their media than veins?
A
smooth muscle
2
Q
What is the weight of a female heart?
Male heart?
What is the ventricular wall thickness of the right ventricle?
Left ventricle?
A
250-300 grams
300-350 grams
right: 0.3-0.5 cm
left: 1.3-1.5 cm
3
Q
What are the four major components of cardiac muscle?
A
tropomyosin
troponin
actin
myosin
4
Q
Where do you find the SA node?
AV node?
Accessory pathway connection?
Bundle of his?
A
Right atrium
interatrial septum
Right side atrioventricular septum
interventricular septum
5
Q
What are the four major components of cardiac muscle?
A
tropomyosin
troponin
actin
myosin
6
Q
Where do you find the SA node?
AV node?
Accessory pathway connection?
Bundle of his?
A
Right atrium
interatrial septum
Right side atrioventricular septum
Ventricular septum
7
Q
What does the left coronary artery branch into?
A
the circumflex, LAD, Large marginal artery
8
Q
What does the right coronary artery branch into?
A
right (acute) marginal artery and posterior descending artery
9
Q
What do endothelial cells due for the structure of the vascular system?
A
- maintain non-thrombogenic blood-tissue interface
- modulate vascular resistance
- metabolize hormones
- regulate inflammation
- regulate cell growth
10
Q
What do the smooth muscle cells of the vascular system do?
A
- proliferate when stimulated
- synthesize collagen, elastin, proteoglycans
- Elaborate growth factors and cytokines
11
Q
What is found within the ECM of the vascular system?
A
- Elastin
- Collagen
- Glycosoaminoglycans
12
Q
What are the layers of the vascular system?
A
intima
media
adventitia
13
Q
What kind of arteries are the radial and femoral arteries?
A
muscular arteries
14
Q
Where do you find elastin in muscular arteries?
A
internal and external elastic lamina
15
Q
What are the six mechanisms of dysfunction in cardiovascular disease and what is the major mechanism of dysfunction?
A
Failure of the pump
Obstruction to flow
Regurgitant flow
Shunted flow (congenital heart disease)
Disorders of cardiac conduction (bundle branch blocks)
Rupture of the heart or a major blood vessel (dissection of aorta)
FAILURE OF PUMP
16
Q
What happens when there is endothelial cell loss or dysfunction?
A
stimulates smooth muscle cell growth/proliferation and extracellular matrix synthesisi leading to intimal thickening
17
Q
Sustained increased BP is associated with increased risk of (blank X 5)
A
- atherosclerosis
- hypertensive heart disease
- multi-infarct dementia
- aortic dissection
- renal failure
18
Q
When you have decreased blood pressure what will your peripheral resistance look like and why?
What will your cardiac output look like and why?
A
Decreased resistance i.e dilation
-increased NO,prostacyclin, kinins, ANP, and decreased neural factors
Decreased CO-> due to decreased BV, HR, Contactility
19
Q
How do you increased BP?
A
renin released from kidney, converts angiotensinogen from liver into angiotensin in lung which makes adrenal glands secrete aldosterone which will make the kidneys resorb Na and water which will increase your BV and thus your BP. and you will vasconstrict
20
Q
How do you lower blood volume?
A
kidney excretes sodium and water and you vasodilate
21
Q
Whats normal systolic and diastolic?
Whats prehypertensive?
Whats abnormal?
Whats malignant?
A
- less than 120, less than 80
- 120-139, 80-89
- greater than 140, greater than 89
- greater than 200, greater than 120
22
Q
What is essential HTN?
A
idiopathic without any real known cause
23
Q
What are the Contributing factors of essential HTN?
A
single gene defects
polymorphisms
vascular
environmental factors
24
Q
What are some single gene defects that cause essential HTN?
Polymorphisms?
Vascular?
Environmental Factors?
A
- aldosterone metabolism, sodium reabsorption
- angiotensinogen locus, angiotensin receptor locus, renin-angiotensin system
- vasoconstriction, structural changes
- diet, stress, obesity, smoking, physical inactivity
25
What are the causes of secondary hypertension?
- renal
- endocrine
- CV
- Neuroogic
26
What are the renal causes of secondary htn?
- acute glomerulonephritis
- chronic renal disease
- polycystic disease
- renal artery stenosis
- renal vasculitis
- renin-producing tumors
27
What are the endocrine causes of secondary htn?
- adrenocortical dysfunction
- exogenous hormones
- pheochromocytoma
- acromegaly
- hypothyroidism
- hyperthyroidism
- pregnancy-induced
28
What are the CV causes of secondary HTN?
- coarctation of aorta
- polyarteritis nodosa
- increased intravascular volume
- increased CO
- rigidity of aorta
29
What are the neurologic causes of secondary HTN?
- psychogenic
- increased ICP
- sleep apnea
- acute stress
30
What is this:
an eosinophilic deposition of material around arterioles in the kidney, looks like a rough kidney and is associated with benign essential htn
hyaline arteriosclerosis
31
What is this:
| deposition of smooth muscle cells around the arterioles of the kidney. Associated with malignant htn.
Hyperplastic arteriosclerosis
32
Atheromas protrude into the vessel lumen and can.....?
- obstruct blood flow
- rupture and cause vessel thrombosis
- lead to aneurysm formation
33
What are atheromas?
raised lesions with a soft yellow core of lipid covered with a fibrous cap
34
What all makes up an atheroma?
SM cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, calcium
35
What are the constitutional risk factors of atherosclerosis?
What are the modifiable risk factors?
What are other risk factors?
- age, gender, genetics
- hyperlipidemia, HTN, cigarette smoking, diabetes
- inflammation, hyperhomocystinemia, metabolic syndrome, lipoprotein a, hemostatic factors, sedentary life style, type A personality, obesity
36
What is the risky age for females to have atherosclerosis?
| For males?
above 55
| above 45
37
(blank) is a chronic inflammatory and healing response to arterial wall and endothelial injury
Atherosclerosis
38
What are the pathologic events that lead to atherosclerosis?
-endothelial injury-> lipoprotein accumulation (in media) -> monocyte adhesion and formation of foam cells->platelet adhesion-> smooth muscle cell recruitment-> smooth muscle cell proliferation and ECM production-> lipid accumulation
39
Where do you get lipoprotein accumulation in the formation of atherosclerosis?
in media
40
How do you get monocyte adhesion and formation of foam cells?
Through scavenger pathway and LDL breakdown
41
What are ways you can get endothelial injury?
- Mechanical denudation (wearing down)
- immune complex deposition
- irridiation
- chemicals
42
What are causes of endothelial dysfunction?
- hemodynamic disturbances
- hypercholesterolemia
- hypertension
- smoking
- infectious agents
- homocysteine
43
Plaques tend to occur at areas of disturbed blood flow... such as?
- ostia of exiting vessels
- branch points
- posterior wall of abdominal aorta
44
Why kind of flow protects against atherosclerosis?
non-turbulent, laminar flow
45
What are the dominant lipids in plaques?
cholesterol and cholesterol esters
46
Genetic (blank) is associated with accelerated atherosclerosis
hyperlipoproteinemia
47
What 2 diseases are associated with hypercholesterolemia?
DM and hypothyroidism
48
Lower serum (blank) slows the rate of atherosclerosis
cholesterol
49
Lipid accumulation reduces (blank) ability of vessels. Why?
vasodilation
| -because hyperlipidemia increases oxygen free radical production which then accelerates nitric oxide decay
50
Atherosclerosis increases production of foam cells. Explain why?
oxygen free radicals (created by hyperlipidemia) oxidizes LDL which is then ingested by macrophages through a scavenger receptor.
51
What will oxidized LDL increase release of? what will this recruit?
growth factors, cytokines, and chemokines
-monocytes!!!!!
52
Atherosclerotic lesions are in a chronic (blank) state
inflammatory state (t-lymphocytes)
53
What promotes smooth muscle cell proliferation and ECM synthesis? How will this affect the fatty streak?
Chemokines and growth factors
| It will convert the fatty streak into a mature atheroma
54
What are the major consequences of atherosclerosis?
- MI
- Cerebral Infarction
- Aortic Aneurysm
- Peripheral vascular disease
55
Critical stenosis occurs at (blank) occlusion
70%
56
With stenosis, you get decreased profusion which leads to .....?
- Bowel Ischemia
- Chronic IHD
- Ischemic encephalopathy
- Intermittent Claudication
57
What are acute plaque changes?
- Rupture exposing plaque contents to blood
- Erosion or ulceration exposing BM to blood
- Rupture and hemmorhage into atheroma
58
What are the pre-clinical phases of atherosclerosis?
- fatty streak
- fibrofatty plaque
- advanced vulnerable plaque
59
What are the clinical phases of atherosclerosis?
Aneurysm and Rupture
Occlusion by Thrombus
Critical stenosis
60
What is this:
| generic designation for a group of pathologically related syndromes resulting from myocardial ischemia :)
Ischemic Heart Disease
61
(blank) is an imbalance between the supply and demand of the heart for oxygenated blood. What is this frequently referred to as?
Myocardial ischemia
| -coronary artery disease
62
90% of the time ischemic heart disease results from (blank)
obstructive atherosclerotic lesions in the coronary arteries
63
What are minor causes of ischemic heart disease?
- Tachycardia
- Myocardial Hypertrophy
- Hypoxemia
- Coronary Emboli
- Blockage of coronary arteries
- Severe hypotension
64
What are some acute coronary syndromes that cause ischemic heart disease?
- angina pectoris
- myocardial infarction
- chronic IHD with heart failure
- sudden cardiac death
65
What is angina pectoris?
| What is it caused by?
Paroxysmal and recurrent attacks of substernal and precordial chest discomfort
-Caused by transient myocardial ischemia that falls short of inducing myocyte necrosis
66
What are the three variants of angina?
- stable (typical)
- prinzmetal
- unstable (crescendo)
67
What causes stable angina?
caused by an imbalance of perfusion (75% occlusion) relative to myocardial demand
-physical activity, emotional excitement or increased cardiac workload causes it.
68
What percentage of occlusion can cause stable angina?
75%
69
What relieves stable angina?
rest or vasodilators
70
What causes prinzmetal angina?
| What relieves this?
- coronary artery spasm unrelated to physical activity, heart rate or BP
- vasodilators and calcium channel blockers
71
What is unstable angina?
pattern of increasingly frequent pain of prolonged duration that is precipitated at low levels or activity or at rest
72
What percent of artery occlusion do you have to have for unstable angina to occur?
90% or greater
73
What is unstable angina caused by?
Unstable angina gives you a warning for an impending (blank)
- acute plaque change with superimposed thrombosis/embolism
- vasospasm
-acute MI
74
What is this;
| Death of cardiac muscle due to prolonged severe ischemia
Myocardial infarction
75
What is the typical sequence of an MI?
- atheromatous plaque exposes thrombogenic contents
- platelets adhere to plaque and degranulate and initiate vasospasms
- tissue factor activates the coagulation cascade adding to the bulk of the thrombus
- thrombus completely occludes the lumen of the vessel
76
10% of MI can occur without (blank)
coronary vascular pathology
77
What can cause vasospasm with/without atherosclerosis resulting in MI?
cocaine abuse
| platelet aggregation
78
What can cause emboli resulting in MI?
- atrial fibrillation of left atrium
- vegatations from infective endocarditis
- left sided mural thrombus
- paradoxical right sided emboli
79
What can cause ischemia without atherosclerosis or thrombosis ?
```
vasculitis
sickle cell disease
amyloid deposition
vascular dissection
severe hypotension (shock)
```
80
MI can be divided into phases of (blank) and (blank) injury
reversible and irreversible
81
Reversible injury is ischemia lasting no more than (blank) minutes.
20-30
82
Reversible injury is ischemia lasting no more than 20-30 minutes. What will happen within seconds? What will happen within 60 seconds?
- cessation of aerobic metabolism within seconds
| - loss of contractility within 60 seconds
83
Irreversible injury is when you have prolonged severe ischemia leading to myocyte necrosis. Necrosis is complete within (blank) hours of onset
6
84
The morphologic features of a myocardial infarction depends on ....?
- 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 02 saturation
85
Myocardial ischemia proceeds from the (blank) outward
endocardium
86
What is a transmural infarction?
- necrosis involves the full thickness
| - associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
87
What causes a transmural infarction?
| What will it look like on an EKG?
- associated with chronic atherosclerosis, acute plaque change, superimposed thrombus
- ST elevation infarcts
88
What is a subendocardial infarction?
What is this due to?
What does it look like on an EKG?
- Necrosis limited to the inner 1/3-1/2 of the ventricular wall
- any reduction in coronary flow (plaque disruption with lysed thrombus, global hypotension)
- non-ST elevation infarcts
89
What does the LAD supply?
apex
anterior wall of LV
anterior 2/3 of ventricular septum
90
What does the Right coronary artery supply?
posterior 1/3 of septum (dominant)
RV free wall
Posterobasal wall of LV
91
What does the Left circumflex artery supply?
LV myocardium
92
What happens within hours of an infarction?
within days?
Within weeks?
Within months?
- Coagulative necrosis
- Neutrophils then macrophages
- granulation tissue
- scarring
93
What are the clinical features of an MI?
rapid, weak pulse
diaphoresis
dyspnea
asymptomatic
94
When do you get a rise in myoglobin, CK-MB, Troponin I and T
0-2 hours
2-4 hrs
2-4 hrs
95
When do you have peak levels of myoglobin, CK-MB, Troponin I and T?
Myoglobin: 6-8 hrs
CK-MB: 24 hrs
Troponins: 48 hrs
96
What test is sensitive but not specific?
| What test is sensitive and specific?
CK-MB
| Troponin I and T
97
Whats awesome about troponins besides they are specific and sensitive?
their levels persist for 7-10 days post MI so you can tell if someone had a heart attack days ago
98
What is the treatment of MI?
```
aspirin (inhibits platelets)
heparin (inhibits coag)
oxygen (higher O2 sat)
nitrates (vasodilate)
beta-adrenergic inhibitors
ACE inhibitors
Reperfusion
```
99
What does reperfusion do and how do you do this?
- thrombolysis
- angioplasty
- stent placement
- coronary artery bypass graft (CABG)
100
What is reperfusion limited by?
- rapidity of alleviating the obstruction
| - extent of the correction and the underlying causal lesion
101
What are the adverse complication 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)
102
What are complications of 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
```
103
What is chronic ischemic heart disease?
| What is this commonly called?
progressive heart failure as a consequence of ischemic myocardial damage
-ischemic cardiomyopathy
104
How can sudden cardiac death occur?
consequence of lethal arrhythmia normally triggered by myocardial ischemia.
105
What are 2 types of lethal arrhythmias?
asystole
| ventricular fibrillation
106
arrhythmia normally occurs at a site (blank) from the conduction system
distant
**also found adjacent to scars of previous MI
107
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
Systemic metabolic and hemodynamic alterations
Catecholamines
108
What are hereiditary or acquired cardiac arrhythmias that can cause sudden cardiac death?
```
Long QT
Short QT
WPW
Sick sinus syndrome
Catecholamine polymorphic VT
```
109
When does heart failure occur?
- when the heart is unable to pump blood sufficiently to meet the demands of the tissue
- When the heart can only pump blood sufficiently at elevated filling pressures
110
Why will heart failure develop?
- chronic or acute valve disease
- long standing htn
- ischemic heart disease with MI
- Fluid overload
111
What is forward heart failure characterized by?
decreased cardiac output and tissue perfusion
112
What is backward heart failure characterized by?
pooling of blood in the venous system (pulmonary and/or peripheral edema)
113
What is the frank-starling mechanism?
dilation and increased filling pressure INCREASES contractility
114
What are adaptive mechanisms for heart failure?
- frank starling mechanism
- ventricular remodeling (hypertrophy with or without dilation)
- neurohomonal mechanisms
115
What are the neurohormonal mechanisms of the heart that are adaptive in the case of heart failure?
- norepinephrine release to increase heart rate
- activation of renin-angiotensin-aldosterone system to adjust filling volumes and pressures
- release of ANP to adjust filling volumes and pressures
116
What is this:
increased mechanical work due to pressure or volume overload or due to trophic signals causes the myocytes to increase in size
Hypertrophy
117
What will myocytes due in heart failure?
- increase protein synthesis to increase sarcomeres
- increase mitrochondria to gain more energy
- increase nuclear size due to ploidy
118
In heart failure, you will get pressure overload hypertrophy and volume overload hypertrophy, what will this result in?
increased cardiac weight
sarcomeres increase in parallel and in series
ventricle wall thickness changes (increases, decreases, or no change)
119
In volume or pressure overload hypertrophy will you get sarcomeres increasing in parallel to long axes of cells?
What about in series?
- Pressure overload hypertrophy
| - Volume overload hypertrophy
120
In pressure overload hypertrophy what will your heart look like?
In volume overload?
- Concentric increase in wall thickness
| - Ventricular dilation
121
THe changes in the heart used to compensate for hypertrophied hearts can end up damaging the heart, why?
- hypertrophy isnt accompanied by increase in capillaries
- change in myocardial metabolism
- alteration in calcium homeo
- apoptosis of myocytes
- reprogramming of gene expression
122
What causes left sided heart failure?
-Ischemic heart disease
-Hypertension
-Aortic and valvular diseases
-Myocardial disease
Systolic and Diastolic failure
123
How do you get systolic failure?
| How do you get diastolic failure?
insuffiicient cadiact output (pump failure)
| stiff ventricle that cannot expand and increase its output
124
Why do symptoms develop from left sided heart failure?
BECAUSE YOU GET:
- congestion of pulmonary circulation
- stasis of blood in left chambers
- hypoperfusion of tissues
125
What are the symptoms of left sided heart failure?
```
Cough
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Renal failure
Loss of attention span, restlessness
```
126
What causes right sided heart failure (cor pulmonale)?
Left sided heart failure and its causes and pulmonary hypertension.
127
WHat causes pulmonary htn?
parenchymal disease of the lung
pulmonary vasculature disease
pulmonary thromboembolism
hypoxic conditions
128
What is the general symptom of cor pulmonale (right sided heart failure)?
What are the specific symptoms?
Systemic and Venous congestion
- Hepatosplenomegaly
- Peripheral edema
- Pleural effusions
- Ascites
- Abnormal mental function
- Renal failure
129
In heart failure, pnts frequently present with (blank) with symptoms of both right and left sided heart failure.
How do you treat this?
biventricular
- Diuretics
- Renin-angiotensin-aldosterone blockers (ACE inhibitors)
- Beta-blockers (lower adrenergic tone)
130
What will sustained htn cause?
| How do you classify it?
```
pressure overload and ventricular hypertrophy i.e hypertensive heart disease (HHD)
Left sided (systemic) HHD or Right sided (cor pulmonale) HHD.
```
131
What is the diagnostic criteria for systemic HHD (left sided)?
- Left ventricular hypertrophy without any other cardiovascular pathology
- History or pathologic evidence of HTN
132
What is the diagnostic criteria for pulmonary HHD (right sided)?
- Characterized by right ventricular hypertrophy and dilation
- can be acute (pulmonary embolism) or chronic
133
How can you have acute pulmonary HHD?
pulmonary embolism
134
What do you find on the AV valves?
| What do you find on the semilunar valves?
papillary muscles/chordae tendineae
cusps
135
What is this:
Failure of a valve to open completely, which impedes flow
Leads to pressure overload
Stenosis
136
What is this:
Failure of a valve to close completely, allowing reversed flow
Leads to volume overload
Functional regurgitation
Insufficiency/Regurgitation
137
What disease will you see mitral stenosis?
rheumatic heart disease
138
What diseases will you see mitral regurgitation?
```
Rheumatic fever
Infective endocarditis
Mitral valve prolapse
Drugs
Rupture of papillary muscle
Papillary muscle dysfunction
Rupture of chordae tendinae
LVH
Calcification
```
139
What diseases will you see aortic stenosis?
Rheumatic heart disease
Senile calcifications
Calcification of a congenitally deformed valve
140
What disease will you see aortic regurgitation?
```
Rheumatic heart disease
Infective endocarditis
Marfan syndrome
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
Rheumatoid arthritis
Marfan syndrome
```
141
What is a valvular disease associated with calcification of the aorta?
What is it due to?
Who is it present in?
What can this result in?
- Calcific aortic stenosis
- Normal wear and tear
- Normally presents in the 7th to 9th decades of life
- Obstruction results in pressure overload and LVH
142
What is the most frequent congenital CV malformation?
What is it due to?
When does it present?
Calcific stenosis of congenitally bicuspid aortic valve
- normal wear and tear
- 5th to 7th decades of life
143
How does mitral annular calcification present? HOw does it affect valvular function?
What are some rare complications of mitral annular calcification?
- with calcifications in the peripheral fibrous ring.
- It doesn't affect it and is thus not clinically important.
- Regurgitation, Stenosis, Arrhythmias and sudden cardiac death
144
What is this:
mitral valve leaflet are floppy and prolapse into the left atrium during systole
-myxomatous degeneration (weakening of CT)
-most patients are asymptomatic and associated with a midsystolic click
Mitral valve prolapse
145
What are the rare complications associated with mitral valve prolapse?
Infective endocarditis
Mitral insufficiency
Stroke
Arrhythmias
146
What is this:
Acute, immunologically mediated multisystem inflammatory disease that occurs a few weeks after group (blank) streptococcal pharyngitis
What is a frequent consequence?
Rheumatic fever
Group A
Acute rheumatic carditis
147
What are clinical features of rheumatic heart disease?
How do you diagnose it?
```
Migratory polyarthritis of large joints
Pancarditis
Subcutaneous nodules
Erythema marginatum of the skin
Sydenham chorea
```
Jones criteria
148
What is the jones criteria?
There are five major criteria:
- carditis
- polyarthritis
- chorea
- erythema marginatum
- subcutaneous nodules
149
Acute rheumatic heart disease is characterized by (blank). What is this composed of?
Aschoff bodies
inflammation (plasma and lymphocytes), Antischkow cells (reactive histiocytes with slender, wavy nuclei)
Giant cells
Fibrinoid material
150
What layer can aschoff bodies be found?
any layer (pancarditis)
151
Vegetations with underling fibrinoid necrosis is found in what type of RHD?
Acute rheumatic heart disease
152
(blank) plaques within the left atrium are found in acute rheumatic heart diseease
MacCallum plaques
153
What is this:
a deforming fibrotic valvular disease which is the only cause of mitral stenosis.
Other valves can be involved.
Aschoff bodies not identified
Chronic rheumatic heart disease
154
In chronic rheumatic heart disease what does the mitral valve show?
- leaflet thinkening
- commissural fusion and shortening
- thickening and fusion of tendinous cords
155
What is this:
| serious condition characterized by colonization or invasion of the heart valves or mural endocardium by a microbe.
Infective endocarditis
156
What are the vegetations made up in infective endocarditis?
thrombotic debris and organisms
157
What are the 2 forms of infective endocarditis?
acute or subacute
158
How do you diagnose infective endocarditis?
duke criteria
| pathologic criteria, major clinical criteria, minor clinical criteria
159
What is this:
previously normal heart valve infected by a highly virulent organism.
Necrotizing, ulcerative, destructive lesions
Is it easy to cure?
Acute infective endocarditis
| No, it is difficult to cure with antiobiotics
160
What is this:
Insidious infections of deformed valves by organisms of lower virulence
Less destructive lesion
Is it easy to cure?
Subacute infective endocarditis
Yes, cure produced with antibiotics
161
What organism is most commonly seen in subacute infective endocarditis?
S. viridans
| native but attacks previously damaged or abnormal valves
162
What organism is most commonly seen in acute infective endocarditis and is the most virulent?
S. aureus
| attacks healthy or deformed valves
163
What organism is seen in prosthetic valves?
S. epidermis (coagulase (-) staph)
164
What are the other organisms that can cause infective endocarditis organisms?
- HACEK (Hemophilus, Actinobaccilus, Cardiobacterium, Eikenella, Kingella)
- Enterococci
- Gram negative bacilli
- Fungi
165
What is this:
| non-infected (sterile) vegetations caused by non-bacterial thrombotic endocarditis.
Non-infective endocarditis (Libman-Sacks endocarditis (SLE)
166
What is this:
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.
Non-bacterial thrombotic endocarditis (previously referred as marantic endocarditis)
167
Who does non-bacterial thrombotic endocarditis appear in?
patients with cancer (mucinous adenocarcinoma), sepsis, or hypercoagulable state
168
What is this:
Patients have systemic lupus erythematosus and have vegetations located on the mitral and tricuspid valves, valvular endocardium, chords, and mural endocardium of the atria
Libman-Sacks disease
169
What are the vegetations made up of in Libman-Sacks disease?
composed of finely granular, fibrinous eosinophilc material with hematoxylin bodies
170
In libman-sacks disease you have intense (blank) with (blank) necrosis of the valve
valvulitis
| fibrinoid
171
What are the complications associated with artificial valves (mechanical prostheses, tissue valves)?
- thromboembolism
- infective endocarditis with ring abscess
- structural deterioration
172
What is this:
| Lesions are firm and plaque like endocardial fibrous thickenings found at the tricuspid and pulmonary valves
Carcinoid heart disease
173
What is carcinoid heart disease due to?
carcinoid syndrome that results in carcinoids emptying into the IVC
174
What are the three primary cardiomyopathies (disorders confined to the heart muscle)?
- Dilated
- Hypertrophic
- Restrictive
175
What are secondary cardiomyopathies?
myocardial involvement as a component of a systemic or multiorgan disorder
176
What is the most common form of primary cardiomyopathy?
| What is it characterized by?
Dilated cardiomyopathy (90%)
Progressive cardiac dilation and contractile dysfunction
177
What is hypertrophic cardiomyopathy characterized by?
- myocardial hypertrophy
- poorly compliant LV myocardium
- abnormal diastolic filling
- intermittent ventricular outflow obstruction
178
What is the leading cause of unexplained LVH?
hypertrophic cardiomyopathy (caused by gene mutation, seen in HS athletes)
179
What is restrictive cardiomyopathy characterized by?
decreased ventricular compliance resulting in impaired filling during diastole
180
What is the mechanism of impairment of dilated cardiomyopathy?
contractility (systolic dysfunction)
181
What is the mechanism of impairment of hypertrophic cardiomyopathy?
compliance (diastolic dysfunction)
182
What is the mechanism of impairment of restrictive cardiomyopathy?
compliance (diastolic dysfunction)
183
What are the causes of dilated cardiomyopathy?
```
Genetic
Myocarditis
Alcohol abuse
Childbirth
Chronic anemia
Medications
Hemochromatosis
```
184
What are the causes of hypertrophic cardiomyopathy?
Genetics
185
What are the causes of restrictive cardiomyopathy?
idiopathic
amyloidosis
radiation induced
fibrosis
186
What is arrhythmogenic right ventricular cardiomyopathy?
An inherited disorder (autosomal dominant) that breaks down the myocardium increasing risk of abnormal heartbeat (arrhythmia) and sudden death.
187
What will arrhythmogenic right ventricular cardiomyopathy cause?
right ventricular failure and various rhythm disturbances (ventricular tachycardia, ventricular fibrillation)
Thinned right ventricular wall
188
Why is the right ventricle wall severely thinned in arrhythmogenic right ventricular cardiomyopathy?
loss of myocytes, fatty infiltration and fibrosis
189
Arrhythmogenic right ventricular cardiomyopathy is related to defective (blank) in the desmosomes that link adjacent myocytes
cell adhesion proteins
190
What is this:
Thickened interventricular wall
Enlarged myofibrils with big nuclei
Myofibral disarray
Cardiomyopathy
191
What will you see on a histogram of restrictive cardiomyopathy?
amyloid deposition
192
What will a histogram look like of arrhthmogenic right ventricular cardiomyopathy?
fatty deposits due to a genetic mutation that causes a fatty mutation of the myocardium which causes expansion
193
What is myocarditis?
infectious or inflammatory processes that cause myocardial injury
194
What are the infectious processes that cause myocardial injury?
```
Viruses
Bacteria
Fungus
Protozoa (trypanosoma)
Helminths
```
195
What are the viruses that cause myocardial injury?
Coxsackie A/B
Enterovirus
HIV
CMV
196
What are the bacteria that cause myocardial injury?
Chlamydia
Neisseria
Borrelia
Rickettsia
197
What are the causes of immune-mediated myocarditis?
```
post-viral
poststreptococcal
SLE
Drug Hypersensitivity
-methyldopa
-sulfoamides
Transplant rejection
```
198
What are 2 other cause of myocarditis?
sarcoidosis
| giant cell myocarditis
199
The normal pericardial space contains (blank) mL of thin, clear, straw colored fluid.
30-50
200
Chronic pressure allows effusion of up to (blank) mL in the pericardial space.
Rapid effusion allows up to (blank) mL
500
| 200-300
201
What is this:
| pericardial space distended by serous fluid
Pericardial effusion
202
What is this:
| pericardial space distended by blood
Hemopericardium
203
What is this:
| Pericardial space distended by pus
Purulent pericarditis
204
What are types of acute pericarditis?
```
Serous pericarditis
Fibrinous/serofibrinous pericarditis
Purulent pericarditis
Hemorrhagic pericarditis
Caseous pericarditis
```
205
What are types of chronic pericarditis?
adhesive pericarditis
| constructive pericarditis
206
What is serous pericarditis produced by? What is the infiltrate like and where is it found?
- non-infectious inflammatory disease
| - mild lymphocytic infiltrate in the epipericardial fat
207
What is the most frequent type of acute pericarditis?
Fibrinous/ serofibrinous
208
What is characteristic of fibrinous/serofibrinous acute pericarditis?
loud pericardial friction rub
209
What is this:
| composed of serous fluid mixed with fibrinous exudate
fibrinous/serofibrinous acute pericarditis
210
What is fibrinous/serofibrinous acute pericarditis associated with?
acute MI, postinfarction syndrome, uremia, chest radiation, Rheumatoid Factor, systemic lupus erythematosus, trauma
211
What causes acute purulent pericarditis?
invasion of microbes into the pericardial space by direct extension, seeding from the blood, lymphatic extension, introduction during cardiotomy
212
Acute purulent pericarditis is an acute inflammatory reaction that can produce a (blank). What can occur after this and what type of pericarditis is that associated with?
mediastinopericarditis
Scarring and re-organization which results in constrictive pericarditis.
213
What is the appearance of hemorrhagic acute pericarditis?
blood with a fibrinous or suppurative effusion
214
What causes hemorrhagic acute pericarditis?
metastatic malignant neoplasm
| also found in TB and bacterial infections and post-cardiac surgery
215
What does caseous acute pericarditis lead to?
a disabling, fibrocalcific, chronic constrictive pericarditis
216
What is caseous acute pericarditis due to and is it common?
due to TB by direct spread, but sometimes fungus
| -rare
217
What are the four types of chronic pericarditis?
- no clinical consequence
- adhesive pericarditis
- adhesive mediastinopericarditis
- constrictive pericarditis
218
When do you get adhesive mediastinopericarditis?
| What is it?
- following infectious pericarditis, cardiac surgery, radiation
- pericardial sac is obliterated and pericardium adheres to surrounding structures
219
What is constrictive pericarditis?
heart is encased in a fibrous/ fibrocalcific scar that limits diastolic expansion and cardiac output
220
What does constrictive pericarditis mimic?
| What are the heart sounds like in constrictive pericarditis?
restrictive cardiomyopathy
| muffled or distant
221
What is the most common primary cardiac tumor in adults? Are they malignant or benign
What chromosomes are abnormal?
Where do these arise from?
What part of the heart are they found?
10% of these are associated with (blank) complex
- myxoma
- benign
- 12 & 17
- primitive multipotent mesenchymal cells
- atria but can arise in any chamber
- Carney complex
222
What is the most common cardiac tumor in children? What is it associated with? what are they considered?
```
Rhabdomyoma
tuberous sclerosis (disease that causes benign tumor growth in essential organs and skin)
hamartomas (normally present cells with abnormal structure but is benign and resembles a tumor)
```
223
What is this:
A cardiac benign tumor of mature adipose tissue
most often located in the LV, RA or atrial septum
Lipoma
224
What is this:
A cardiac benign neoplasm often discovered at autopsy
Resemble Lambl excrescences (filiform fronds that occur at sites of valve closure)
Papillary fibroelastoma
