Cardio-boards Flashcards

1
Q

A Anitschkow cell is hallmark for?

A

Acute Rheumatic Fever

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2
Q

What are the Diagnosis Major criteria for Acute Rheumatic Fever?

A

JONES; J = joints O= heart, N= subQ nodules, E= Erythema marginatum, S= Sydenham chorea

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3
Q

What is the key clinical problem with acute rheumatic fever?

A

Heart problems (pancarditis- each of the heart layers are inflamed)

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4
Q

What is molecular mimicry in reference to Acute rheumatic fever?

A

The way in which the M protein (VF in rheumatic fever), resembles a human tissue

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5
Q

What is Infantile coarctation of the aorta associated with?

A

Turner’s Syndrome and a PDA

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6
Q

How will someone with adult coarctation of the aorta present clinically?

A

They will present with HTN in the UE and hypotension in the LE. Also on X-ray you will see “RIB NOTCHING” due to engorged intercostal vessels receiving excess blood.

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7
Q

What is Tricuspid atresia associated with?

A

ASD

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8
Q

What is Truncus arteriosus?

A

Where there is a large vessel arising from both ventricles (there is not separate aortic or pulmonic artery)

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9
Q

How do you maintain a PDA until you can surgically repair it?

A

PGE (alprostadil, etc.)

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10
Q

What is transposition of the great vessels?

A

where the pulmonary artery arises from the L. ventricle, and the aorta arises from the R. ventricle

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11
Q

What is associated with transposition of the great vessels?

A

Maternal diabetes

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12
Q

How do you close a PDA?

A

Indomethacin

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13
Q

What is Patent Ductus Arteriosus associated with?

A

Congenital Rubella

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14
Q

How will the heart sound in someone with a PDA?

A

continuous “machine-like” murmur

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15
Q

What is tetralogy of Fallot?

A

PROV; P= pulmonary artery stenosis, R= Right ventricular hypertrophy, O= overriding aorta, V= VSD

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16
Q

How do patients with a Tetralogy of Fallot present?

A

Early cyanosis (due to a R–> L shunt), the patient learns to squat in response to the cyanotic spell

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17
Q

How will you be able to tell on X-ray that someone has a Tetralogy of Fallot?

A

It will appear “Boot-shaped” on x-ray

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18
Q

What is the most common ASD?

A

Ostium secundum

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19
Q

What is associated with a Ostium primum ASD?

A

Down syndrome

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20
Q

What is a paradoxical emboli?

A

Where the embolus forms on the R. side of the heart and due to a ASD can cross and lodge on the L. side of the heart

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21
Q

What is the most common congenital heart defect?

A

VSD

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22
Q

What is associated with a VSD?

A

Fetal Alcohol syndrome

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23
Q

How do you treat a VSD?

A

Small defects may close spontaneously, Large defects need surgery

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24
Q

What is Eisenmenger syndrome?

A

This is where you have a VSD which causes a Left to Right shunt. This in turn increases the blood flow to the lungs resulting in pulmonary HTN. This pulmonary HTN will then result in a Right to Left shunt and you get deoxygenated blood mixing with oxygenated blood and being sent out to the body resulting in cyanosis.

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25
What is the most common cause of Right sided heart failure?
Left sided heart failure
26
What are some clinical features of Right sided heart failure?
JVD, "nutmeg" liver, dependent pitting edema
27
What is the main way to treat Left sided heart failure?
ACE inhibitor
28
Where do you see "heart failure" cells (hemosiderin laden macrophages)
Left-sided heart failure
29
What is Dressler syndrome?
where you get autoimmune antibodies against the pericardium. This occurs 6-8 weeks post MI and results in pericarditis.
30
What is the Gold standard cardiac enzyme for MI?
Troponin I
31
What is CK-MB useful for as a cardiac enzyme?
Detects reinfarction (because it disappears in 72 hours while Troponin I stays for 7-10 days, it is possible to see if it is the same MI or a reinfarction)
32
Why can the patient appear worse hours after treatment for a MI?
Reperfusion injury (due to free radicals further damaging the myocytes) and Contraction band necrosis (damaged cells cause Ca+ influx and contraction)
33
How will the initial phase of the MI appear on the EKG?
ST segment depression (subendocardial necrosis--> hasn't involved the whole wall yet)
34
How will the continued ischemia of an MI appear on the EKG?
ST segment elevation ( transmural necrosis--> involving the whole wall)
35
What will you see microscopically 4-24 hours post MI?
Coagulative necrosis (pyknosis, karrohlexis, karyolysis)
36
How will the heart appear 4-24 hours post MI?
Dark discoloration (complications can be arrhythmic)
37
How will the heart appear 1-3 days post MI? | What microscopic changes will be seen?
- Yellow | - Neutrophils
38
What will the microscopic changes be 4-7 days post MI? | What will the heart look like?
Macrophages | Yellow
39
What will the heart look like 1-3 weeks post MI? | What microscopic changes will be seen?
Red border emerging from the edge of infarct | Granulation tissue
40
What will the heart look like months post MI? | What microscopic changes are occurring?
White scar | Fibrosis
41
What is a possible complication of the white scar post MI?
Aneurysm, mural thrombus, dressler syndrome
42
What is a possible complication of 4-7 days post MI with macrophages?
Rupture of the ventricular free wall, IV septum, or papillary muscle (papillary muscle rupture is associated with Right coronary artery infarction)
43
What is the most commonly involved artery in MI?
LAD
44
what is the 2nd most common artery involved in an MI?
RCA (right coronary artery)
45
What is stable angina? | How will it appear on EKG?
Chest pain arising with exertion or emotional stress | ST segment depression
46
How do you treat stable angina?
Rest or nitroglycerin
47
How will stable angina present?
chest pain <20 minutes radiating to the left arm or jaw
48
What is unstable angina?
Chest pain occurring at rest
49
What causes unstable angina?
Rupture of the atherosclerotic plaque with thrombus (which occurs due to the collagen of the basement membrane being exposed). It is an INCOMPLETE occlusion of the coronary artery
50
How will the EKG look when someone has unstable angina? | How do you treat it?
ST segment depression | Nitroglycerin
51
What is prinzmetal angina
episodic chest pain unrelated to exertion (due to coronary artery vasospasm)
52
How will the EKG look on someone with prinzmetal angina?
ST segment elevation
53
How do you treat prinzmetal angina?
Nitroglycerin or CCB's
54
What is an MI?
Necrosis of cardiac myocytes (irreversible injury and cell death)
55
What usually causes an MI?
rupture of atherosclerotic plaque with thrombis and COMPLETE occlusion of the coronary artery
56
How will someone with an MI present?
severe crushing chest pain lasting >20 minutes hat radiates to the left arm or jaw
57
What is chronic rheumatic heart disease?
scarring that arises as a consequence of repeated exposure to Group A strep
58
How does the valve appear in someone with chronic rheumatic heart disease?
"fish mouth" appearance
59
What is the valve that is almost always involved with chronic rheumatic heart disease?
Mitral valve (occasionally the aortic valve)
60
How can you tell aortic stenosis by itself from chronic rheumatic heart disease?
Chronic rheumatic heart disease ALWAYS has mitral stenosis and can have aortic as well, whereas aortic stenosis by itself won't have mitral stenosis
61
What complication can arise from acute rheumatic disease ? | What complication can arise from chronic rheumatic disease?
Mitral regurgitation | Mitral stenosis
62
What bug is the most common overall cause of endocarditis?
Strep Viridans
63
What bug is the most common cause of endocarditis in IV drug users?
Staph Aureus
64
What bug is associated with endocarditis of prosthetic valves?
Staph Epidermidis
65
What Bug is associated with endocarditis in patients with underlying colorectal cancer?
Strep Bovis
66
What bug(s) are associated with endocarditis and have a negative blood culture?
HACEK; H= haemophilus, A= actinobacillus, C= cardiobacterium, E= eiknella, K= kingella sx's= Osler nodes, Janeway lesions and splinter hemorrhages
67
What is the difference in endocarditis caused by Strep Viridans vs Staph aureus?
Endocarditis with Strep Viridans= low-virulence organism that infects previously damaged valves (doesn't destroy valves); Endocarditis with Staph Aureus= High-virulence organism that infects normal valves (tricuspid) (destroys the valve)
68
What is Libman-Sacks endocarditis?
Endocarditis where you get sterile vegetations that arise in association with SLE **(on both sides the surface and undersurface)**
69
What is the test to detect endocarditis lesions on the valves?
TEE (transesophageal echocardiogram)
70
What is the most common form of cardiomyopathy?
Dilated Cardiomyopathy
71
This cardiac tumor appears gelatinous and has abundant ground substance on histology
Myxoma
72
What area of the heart does a myxoma affect?
It is a pedunculated mass in the LEFT ATRIUM and causes obstruction of the mitral valve
73
What is the most common primary cardiac tumor in children?
Rhabdomyoma
74
What is the most common primary cardiac tumor in adults
Myxoma
75
What is associated with rhabdomyoma?
Tuberous sclerosis (it arises in the ventricles)
76
This is more common than primary tumors in the heart?
Metastasis
77
What tumors like to metastasize to the heart?
Breast, lung, melanoma, lymphoma
78
What part of the heart is usually affected by metastasis?
pericardium
79
What is the usual cause of Hypertrophic cardiomyopathy?
Genetic mutations in SARCOMERE PROTEINS
80
This disease usually presents as sudden death in young athletes
Hypertrophic cardiomyopathy
81
How will someone's heart with hypertrophic cardiomyopathy look histologically?
Myofiber disarray
82
What type of dysfunction will hypertrophic cardiomyopathy cause?
diastolic dysfunction (can't fill the heart)
83
What can cause dilated cardiomyopathy?
genetic (AD), coxsackie A or B, Alcohol abuse, doxorubicin & cocaine, pregnancy, hemochromatosis
84
What is restrictive cardiomyopathy?
Decreased compliance of ventricular endomyocardium
85
What is restrictive cardiomyopathy in kids called?
endomyocardial fibrosis
86
backflow of blood from aorta into L. ventricle during diastole
aortic regurgitation
87
What is the most common cause of aortic regurgitation?
Isolated root dilation
88
Clinical features of aortic regurgitation
Wide pulse pressure (systolic increases, diastolic decreases), water hammer pulse, Austin flint characteristic, head bobbing, pulsating nail bed
89
what is mitral valve prolapse?
ballooning of mitral valve into left atrium during systole
90
what type of pts can you see mitral valve prolapse with?
Ehlers-danlos and Marfans
91
Mid systolic click followed by regurgitation murmur (becomes softer with squatting)
Mitral valve prolapse
92
Holosystolic "blowing murmur" (louder with squatting and expiration)
Mitral regurgitation
93
Acute rheumatic heart disease can cause
Mitral regurgitation
94
Volume overload resulting in dilation of the L. atrium (usually due to chronic rheumatic heart disease)
Mitral stenosis