Cardiac Pathology Flashcards
1
Q
What happens to the myocytes with unstable angina?
A
Reversible injury to the myocytes (cellular swelling)
2
Q
What percent of stenosis of the arteries with atheromas does stable angina develop?
A
Greater than 70%
3
Q
What are the s/sx of stable angina? How long does it last for?
A
Chest pain that lasts less than 20 minutes, and is brought on by exercise
4
Q
How long does the chest pain last in stable angina? What is the significance of this time?
A
Less than 20 minutes How long that myocytes can tolerate reduced blood flow
5
Q
Which cell layer of the heart is affected with myocardial ischemia? What are the characteristic EKG findings with this?
A
- Subendocardial layer
- ST segment depression
6
Q
What is the MOA by which NTG relieves stable angina?
A
Decreases venous return (preload) via NO production
7
Q
What are the characteristics of unstable angina?
A
Chest pain at rest due to rupture of an atherosclerotic plaque
8
Q
What causes unstable angina?
A
Rupture of an atheroscleotic plaque with thrombosis and an incomplete occlusion of a coronary artery
9
Q
Is the injury to the myocytes in unstable angina reversible?
A
Yes
10
Q
What are the EKG changes with unstable angina?
A
ST segment depression
11
Q
What is Prinzmetal angina?
A
Spasm of the coronary artery, causing chest pain that is unrelated to exertion
12
Q
What are the EKG findings with Prinzmetal angina? Why?
A
- ST elevation
- Complete loss of blood supply to all layers of the myocardium
13
Q
What are the meds that are used in Prinzmetal angina, and how do they relieve chest pain?
A
NTG- vasodilation
CCB- vasodilation + stop spasms
14
Q
What is the cause of an MI?
A
Complete occlusion of a coronary artery by plaque or spasm
15
Q
How long does the chest pain last with an MI?
A
Greater than 20 minutes
16
Q
Is the chest pain with an MI relieved by NTG administration?
A
No
17
Q
What is the most common artery that is occluded in an MI? What does this cause in terms of heart wall damage?
A
- LAD
- Anterior wall of the LV infarction
18
Q
What is the artery that supplies the inferior wall of the ventricle?
A
RCA
19
Q
What is the artery that supplies the left lateral wall of the LV?
A
LCX
20
Q
Which layer of the heart is undergoes necrosis first in an MI? What will will the EKG show?
A
- Subendocardium
- ST depression
21
Q
What is the most sensitive test for an MI? When does this rise, and for how long?
A
- Troponin I
- Rises 2-4 hours after infarction, peaking at 24 hours, and returning to normal at 7 days
22
Q
What is the use of CK-MB?
A
Rises 4-6 hours, but returns to normal after 72 hours. Thus can be used to r/o a reinfarction after a recent MI
23
Q
What is the treatment for an MI?
A
- ASA/heparin
- Supplemental O2
- Nitrates
- Beta blocker
- ACEI
24
Q
What is the use of beta blockers in an MI?
A
Lower oxygen demand by decreasing contractility
Lower BP
25
What is the basis of using an ACEI in an MI? (2)
- Inhibit volume increase via aldosterone
| - Lower BP rise with angiotensin
26
What causes the contraction band contraction after fibrinolysis?
Return of blood flow returns Ca to a dead myocytes, causing contraction
27
What is the cause of reperfusion injury?
Release of oxygenated blood to myocytes that do not have Enzymes to catalyze it
28
What are the myocyte changes that are seen within four hours after onset of an MI?
None
29
What are the changes in myocytes that occurs within 4-24 hours? (color, necrosis type)
Dark discoloration
| Coagulative necrosis
30
What are the changes in myocytes that occurs within 1-3 days? (color, cellular infiltration)
Yellow pallor
| PMN infiltration
31
What are the changes in myocytes that occurs within 4-7 days? (color, cellular infiltration)
Yellow pallor with macrophage infiltration
32
What are the changes in myocytes that occurs within 7+ days? (color, tissue changes)
Red border emerges as granulation tissue enters from the edge of infarct
Granulation tissue with plump fibroblasts
33
What are the myocytes changes that occur months after an MI?
White scar
| Fibrosis
34
How long does it takes for arrhythmias to occur during an MI? Why?
4-24 hours
| If hits the tracts, then will appear in this timeframe
35
What are the changes that result when macrophages/PMNs infiltrate myocytes?
Yellow discoloration
36
What must happen for pericarditis to occur with an MI, and when does this occur?
Transmural infarction
PMN phase--1-3 days
37
What is the key complication that occurs with the macrophage phase of myocyte infiltration?
Rupture of the ventricles or septum
38
What artery is occluded that risks papillary muscle rupture?
RCA
39
What are the three characteristics of the granulation tissue that forms within myocytes?
Plump fibroblasts
Collagen
Blood vessels
40
What causes the red border of the granulation tissue in dead myocytes?
Neovascularization
41
What is the major long term complication of the white scar left behind from an MI? Why?
- Aneurysm = thombus formation
| - Weaker wall
42
What is Dressler syndrome? When does this occur after an MI?
Inflammation of the pericardium, causing an autoimmune pericarditis
6-8 weeks once immune system revs up
43
What is the collagen type that is found within the white scar post MI?
Type I collagen
44
What causes sudden cardiac death?
Fatal ventricular arrhythmia, from severe preexisting atherosclerosis
45
---What is chronic ischemic heart disease?---
---Poor myocardial function d/t chronic ischemic damage, leading to CHF---
46
What are the major causes of left sided heart failure?
- Ischemia
- HTN
- Dilated cardiomyopathy
- MI
- Restrictive cardiomyopathy
47
Why does hypertrophy of the heart lead to damage?
Ischemia secondary to lack of oxygenation from increase in muscle tissue
48
What are heart failure cells? What causes these?
Hemosiderin laden macrophages from consuming blood from ruptured capillaries
49
Why does LV failure lead to congestion failure?
Buildup of fluid backward
50
What happens in the kidney during LV failure?
Activation of the renin-angiotensin system leads to increased BP and aldosterone release, causing Na (and water) resorption
51
What is the mainstay of treatment for CHF? Why?
- ACEI
| - Reduces TPR and blood volume
52
What is the most common cause of RV failure? What are the two other major examples?
- LV failure
- VSD
- COPD
53
How does COPD lead to RV failure?
hypoxia throughout the lung causing vasoconstriction, and increased pulmonary resistance
54
----What causes cardiac cirrhosis (liver cirrhosis 2/2 HF)? How does this appear grossly?----
---RV failure leads to backup of fluid into the liver
Nutmeg liver----
55
When do heart defects generally form in gestation? What percent of births do these occur in?
3-8 weeks
| 1% of live birth
56
True or false: most congenital heart defects are sporadic
True
57
What is the most common CHD? What is it associated with?
- VSD
| - Fetal alcohol syndrome
58
What is the long term sequale with a VSD?
L to R shunt will cause pulmonary HTN until there is lower pressure in the LV, forcing deoxygenated blood to the systemic system
59
True or false: small VSDs are usually asymptomatic
True
60
What is Eisenmenger syndrome? What may the kidneys do to counteract the hypoxemia
RVH from chronic stress of excess blood
Polycythemia d/t chronic hypoxia from a VSD
61
What is the most common type of an ASD? What genetic disorder is this highly associated with?
Ostium secundum
Down syndrome (THIS IS PRIMUM, thus this card is half-incorrect)
62
What is the treatment for small and large VSDs?
Large need surgical closure, small usually regress on their own
63
What is the cause of a paradoxical embolus?
ASD allows a thrombus to cross over to the systemic circulation as opposed to the pulmonary
64
What infectious disease is PDA associated with? What are the other s/sx of this congenital infection?
Congenital rubella
- PDA
- Cataracts
- Sensorineural deafness
65
What is the natural history of a PDA (specifically before and after the pulmonary artery changes occur)?
shunting of blood from the pulmonary artery to the aorta initially causes pulmonary overload, and pHTN.
The shunt reverses when this gets high enough, causing deoxygenated blood to flow to the aorta, resulting in peripheral cyanosis
66
What is the murmur that is found with PDA?
Holosystolic, machine-like murmur
67
What is the basis for using indomethacin for closing a PDA?
Decreases PGE, resulting in PDA closure
68
What are the four components of the TOF?
1. VSD
2. Pulmonary stenosis
3. Overriding aorta
4. RVH
69
What is the way in which kids with TOF increase blood flow to the pulmonary circuit? How does this work?
- Squat down
| - Increasing arterial vascular pressure increases afterload
70
What determines that degree of shunting in TOF?
Degree of pulmonary artery stenosis
71
What is the classic finding on CXR with TOF?
Boot-shaped heart
72
What is transposition of the great vessels?
- Aorta connects to the RV
| - Pulmonary artery connects to the LV
73
What is the drug that can be administered to maintain an open PDA?
PGE
74
Transposition of the great vessels is associated with what maternal condition?
Maternal DM
75
How do kids with TGA present?
Pulmonary and systemic circuits do not mix, thus fast onset of cyanosis
76
What is the immediate treatment for transposition of the great vessels?
PGE to maintain PDA
77
What is the pathophysiology of persistent truncus arteriosus?
Single large vessel arising from both ventricles d/t failure of the truncus to divide.
This causes inappropriate mixing of blood = cyanosis
78
What occurs in the heart with tricuspid atresia?
Failure of the tricuspid valve to develop, leading to RV hypoplasia. ASD leads to a R to L shunt
79
What is the infantile form of coarctation of the aorta?
Coarctation lies distal to the aortic arch, but proximal to the PDA
80
What genetic disease is the infantile form of coarctation of the aorta associated with?
Turner syndrome
81
How does the infantile form of coarctation of the aorta usually present?
Lower extremity cyanosis
82
What is the major cause of cyanosis in infantile coarctation of the aorta?
Lower pressure after the coarctation allows PDA to shunt deoxygenated blood to the systemic circuit
83
What is the adult form of coarctation of the aorta?
Not associated with a PDA, but coarctation lead to HTN in the upper extremities, and hypotension in the lower extremities
84
What is the classical sign of the adult form of coarctation of the aorta?
Major SBP difference between upper and lower extremities d/t coarctation cutting off blood to the lower part of the body
85
What other congenital condition of the adult form of coarctation of the aorta associated with?
Bicuspid aortic valve
86
---What is the classical findings on CXR with the adult form of coarctation of the aorta?---
---Engorged arteries cause notching of ribs---
87
What is the agent that causes acute rheumatic fever? When does it occur?
Group A strep pharyngitis complication that occurs 2-3 weeks after strep throat
88
How does Strep cause rheumatic fever?
molecular mimicry from the bacterial M protein
89
What is the criteria (eponym) for rheumatic fever infection?
Evidence of a prior group A strep infection
Fever + elevated ESR
And a major criteria
90
What are the two lab markers of a prior group A strep infection?
ASO
| Anti-DNase B titer
91
What are the major criteria for the Jones criteria of acute rheumatic fever?
- Joint infection (migratory)
- O (pancarditis)
- Nodules of skin
- Erythema marginatum
- Sydenham chorea
92
What is the preferential area affected with endocarditis secondary to rheumatic fever?
Endocardium (usually Mitral valve or sometime Aortic)
93
What is the key histological finding of rheumatic fever affecting the mitral valve? What are these made of?
Aschoff bodies
| Collagen, giant cells, and *Anitschkow cells*
94
What are Aschoff bodies?
Collections of collagen, giant cells, and anitschkow cells found in rheumatic fever
95
What are Anitschkow cells?
Histiocytes with slender, wavy nuclei in the center found in myocarditis in acute rheumatic fever
96
What happens with chronic rheumatic fever upon reexposure to strep A?
results in relapse of the acute phase, and increases the risk for chronic valvular disease
97
What is chronic rheumatic valve disease?
Valve scarring that results from rheumatic fever that usually results in stenosis with a "fish-like" appearance
98
What is the hallmark appearance of the aortic valve stenosis in chronic rheumatic fever?
"fish-like"
99
What happens to the chordae tendineae and cusps of the mitral valve in chronic rheumatic fever?
Thickening
100
What happens if the mitral valve is affected in chronic rheumatic fever?
Fusion of the commissures, causing stenosis
101
What is the cause of aortic stenosis?
Wear and tear on the valve
102
When does aortic stenosis usually present?
Late adult life
103
What particular congenital disorder increases the risk of developing aortic stenosis? Why?
Bicuspid aortic valve
| now two cusps are doing the work of three
104
How do you differentiate aortic stenosis secondary to rheumatic valve disease, and the "wear and tear" etiology?
Rheumatic valve disease has coexisting mitral valve stenosis
Aortic valve with have fusion of the commissures with rheumatic heart disease
105
What does the compensation of aortic stenosis (of any etiology) lead to?
Systolic ejection click, crescendo-decrescendo followed by a murmur.
LV hypertrophy
106
Why are angina and syncope common with aortic stenosis?
Inability to get blood across the valve to the heart and coronaries
107
What is the anemia that is caused by aortic stenosis? How does it cause this?
Microangiopathic hemolytic anemia
Rupture of the RBCs as they pass the stenotic area
108
What is the treatment for aortic stenosis? When is this performed?
Valve replacement after the onset of complications
109
When in the heart cycle does aortic regurgitation occur?
Diastole
110
What are the two causes of aortic regurgitation?
Aortic root dilation (increases space between the valves) or valve damage
111
What are the sounds of an aortic regurg murmur?
Early, blowing diastolic murmur
112
What are the hyperdynamic findings of aortic regurgitation? Why does these occur?
bounding pulses, pulsating nail bed, head bobbing
Large increase in SBP
113
What causes the increase in wedge pressure with aortic regurg?
Large increase in SBP d/t LVH, lower DBP d/t backflow of blood
114
What happens to the LV in aortic regurgitation?
Dilation and *eccentric* hypertrophy
115
What is the treatment for aortic regurg?
Valve replacement when LV dysfunction develops
116
What is the cause of mitral valve prolapse?
Degeneration of the mitral valve, making it more floppy than usual
117
What inherited diseases is mitral valve prolapse associated with?
Ehlers-Danlos syndrome or Marfan's
118
What causes the click heard in mitral valve prolapse?
Ballooning back of the mitral valve into the atrium
119
What are the characteristics of the murmur produced from mitral valve prolapse?
Mid-Systolic click
120
What are the complications of mitral valve prolapse?
Infectious endocarditis
Arrhythmia
Severe mitral regurg
121
What is the treatment for mitral valve prolapse?
Valve replacement
122
What, usually, is the cause of mitral regurg?
Complication secondary to mitral valve prolapse
Or can be from LV dilation
123
What muscles, when damaged during an MI, can lead to mitral valve prolapse?
Papillary muscles
124
What are the characteristics of the murmur found in mitral valve regurgitation? What can increase the intensity of the sound?
Holosystolic "blowing" murmur, with squatting and expiration increasing the sound
125
What causes the increase in intensity of a mitral regurgitation murmur with expiration?
Expiration leads to increased venous return to the LA and LV, meaning more blood is regurgitated
126
What is the usual cause of mitral stenosis?
Chronic rheumatic valve disease
127
What are the characteristics of the murmur heard in mitral stenosis?
Opening snap, followed by a diastolic rumble
128
---What are the three major complications associated with mitral stenosis?----
- ----
- Pulmonary congestion
- Pulmonary HTN
- A-fib
- ----
129
What is endocarditis?
Inflammation of the endocardium that lines the cardiac valves, usually due to a bacterial infection
130
What infectious agent is the most common overall cause of endocarditis? How virulent is this and why?
- Strep viridans
| - Low virulence, since it only infects previously damaged valve
131
What is the end result of endocarditis infection with Strep Viridans?
Small vegetations that do not destroy the valve
132
What about damaged valve leads to the development of endocarditis?
Damaged endocardial surface develops thrombotic vegetations, allowing for the trapping of bacteria within the vegetations
133
What is the most common infectious agent that causes endocarditis in IV drug abusers? How virulent is this and why?
- Staph Aureus
| - High virulence, since it can infect normal valve, and results in large vegetations that destroy the valve
134
Which valve is the one classically infected by staph Aureus?
tricuspid
135
What is the key bacteria that causes endocarditis of prosthetic valves?
Staph Epidermidis
136
What is the infectious agent that causes endocarditis in patient with underlying colorectal carcinoma?
Strep Bovis
Bovis in the blood, cancer in the colon
137
What are the HACEK organisms that cause endocarditis? What is characteristic of the blood cultures of these organisms?
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella
All will grow negative blood cultures
138
What are the clinical features of endocarditis?
- Fever
- Murmur
- Janeway lesions
- Osler nodes
- Anemia of chronic disease
139
What causes the murmur in endocarditis?
Vegetation of the valves disrupts flow
140
What causes the emboli found with endocarditis?
break off pieces of the vegetations
141
What are Janeway lesions?
Erythematous, non-tender lesions on the palms and soles of the feet due to septic emboli
142
What are Osler nodes?
Painful lesions on the fingers or toes secondary to septic emboli from endocarditits
143
What hematologic abnormality may occur with endocarditis?
-Anemia of chronic disease
144
What type of anemia is the anemia of chronic disease?
- Microcytic anemia
| - Hepcidin release, forcing Fe into storage ferritin
145
What is the best method to diagnose endocarditis?
Transesophageal echocardiogram (TEE)
146
What is nonbacterial thrombotic endocarditis? What valve do the vegetations usually form on?
Sterile vegetations that arise with hypercoagulable state or underlying adenocarcinoma
Mitral valve along the lines of closure
147
---What is Libman-Sacks endocarditis?---
---Sterile vegetations associated with SLE, the results on vegetations present on both sides of the mitral valve---
148
What is the most common form of cardiomyopathy?
Dilated cardiomyopathy
149
What is dilated cardiomyopathy? What type of dysfunction does it cause (systolic or diastolic)?
- Dilation of all four chambers of the heart
| - Systolic dysfunction, leading to biventricular CHF
150
What are the complications of dilated cardiomyopathy?
Mitral and tricuspid valve regurgitation and arrhythmia d/t stretching of valves
151
What causes the regurgitation in dilated cardiomyopathy?
Stretching of the valves
152
What are the factors that are thought to play a role in the development of dilated cardiomyopathy? (5)
- Genetic mutations
- Myocarditis
- Alcohol abuse
- Drugs
- Pregnancy
153
What virus is the most common cause of myocarditis?
Coxsackie virus
154
What is the treatment for dilated cardiomyopathy?
Transplant
155
What is the most common cause of hypertrophic cardiomyopathy?
AD mutations in sarcomere proteins
156
What is the most common form of hypertrophic cardiomyopathy?
LVH
157
Why is there decreased CO with hypertrophic cardiomyopathy?
-Decreased compliance of the ventricle walls
158
What are the clinical features of hypertrophic cardiomyopathy?
- Sudden death
- Decreased CO
- Syncope with exercise
159
What is the classic histological finding with hypertrophic cardiomyopathy?
Fibrillar and myocyte disarray
160
What is restrictive cardiomyopathy?
Decreased compliance of ventricular endocardium
161
What type of dysfunction is seen with restrictive cardiomyopathy (systolic or diastolic)?
Diastolic
162
What are the causes of restrictive cardiomyopathy? (5)
- Amyloidosis
- Sarcoidosis
- Hemochromatosis
- Endocardial fibroelastosis
- Loeffler syndrome
163
What is Loeffler syndrome? What type of cardiomyopathy does it cause?
- Eosinophilic infiltration of the endo and myocardium
| - Leads to restrictive cardiomyopathy
164
What is Endocardial fibroelastosis? Who does this usually occur in?
Fibrous and elastic tissue build up in the heart--usually in children
165
How do patients with restrictive cardiomyopathy present (what late complication)? EKG findings?
- CHF
| - Low voltage EKG with diminished QRS amplitudes
166
What is a myxoma? Where is this usually found?
Benign mesenchymal proliferation with a gelatinous appearance that grows as a pedunculated mass in the LA
167
What are the histological characteristics of a myxoma?
Abundant ground substance
168
What is the most common primary cardiac tumor in adults? Children?
Myxoma -adults
| Rhabdomyomas - children
169
What causes the syncope commonly seen with a myxoma?
Syncope d/t obstruction of the mitral valve
170
What are rhabdomyomas? Where do they usually arise? What are they associated with?
Benign hamartoma of cardiac muscle that usually arise in the ventricles, and are associated with tuberous sclerosis
171
True or false: mets to the heart are more common than primary tumors
true
172
What are the common mets that go to the heart? (4)
Breast and lung carcinoma, melanoma, and lymphoma
173
Metastases that go to the heart usually involve what layer? What does this result in?
Pericardium
| Pericardial effusion
174
What type of cardiac hypertrophy is had with chronic HTN? (concentric or eccentric)
Concentric
175
What happens to the heart sounds with ASDs? Why?
Fixed splitting of S1 and S2, since LA has a consistent volume, regardless of inspiration or not
