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Clinical Medicine 2 > Exam 1: Cardiomyopathies > Flashcards

Exam 1: Cardiomyopathies Flashcards

1
Q

What is cardiomyopathy?

A

A myocardial disorder in which the heart muscle is structurally and functionally abnormal in the absence of CAD, HTN, valvular disease, and CHD sufficient to explain the abnormality

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2
Q

What are the 3 main types of cardiomyopathy (CM)?

A

Dilated, hypertrophic, and restrictive

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3
Q

What is dilated CM pathophysiology?

A

Symmetric LV dilation and impaired LV systolic function.

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4
Q

What is the presentation of dilated CM (DCM)?

A

Exertional intolerance with SOB and fatigue, chest pain, palpitations, and peripheral edema

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5
Q

What are some possible PE findings in DCM?

A

Mitral/tricuspid regurg, s3 gallop, increased JVP, and basal crackles

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6
Q

What is idiopathic DCM?

A

When there is no identifiable cause, accounts for up to 50% of all DCM cases

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7
Q

What is the primary indication for cardiac transplant?

A

Idiopathic DCM

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8
Q

What is infectious DCM?

A

Myocarditis: an inflammatory process secondary to infectious or non infectious causes. Most commonly viral in the US.

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9
Q

What is the gold standard for diagnosis of infectious DCM?

A

Endomyocardial biopsy, although not always required because a general work up is completed first

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10
Q

What is the presentation of pericardium DCM?

A
  • generally at 36 weeks of gestation though 5 months postpartum.
  • Dyspnea, orthopnea, PND, pedal edema, cough, and hemoptysis
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11
Q

What are the risk factors for pericardium DCM?

A

> 30 yo, African descent, multifarious, history of preeclampsia, material cocaine abuse, and >4 wks of oral tocolytic

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12
Q

What is the presentation of alcoholic DCM?

A

HF symptoms in conjunction with signs of long term alcohol abuse

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13
Q

What is the prognosis of alcoholic DCM?

A
  • Abstinence can lead to significant improvement in heart failure
  • if continued use, poor prognosis with mortality of 50% at 3-6 yrs
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14
Q

What causes DCM in cocaine use?

A
  • toxic effects to the myocardium and myocarditis

- cessation of cocaine may reverse myocardial dysfunction

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15
Q

What drug is a common cause of chemotherapy induced DCM?

A

Anthracyclines, dose dependent

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16
Q

When starting a patient on anthracyclines for chemotherapy, what should you do to prevent DCM?

A

Obtain a baseline echo to measure EF and continue to monitor

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17
Q

What 3 things cause endocrine dysfunction DCM?

A

DM, thyroid dysfunction, and pheochromocytoma

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18
Q

How does DM cause DCM?

A

Initially myocardial fibrosis and diastolic dysfunction (restrictive CM) and later stages have systolic dysfunction

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19
Q

When a patient has endocrine dysfunction DCM, cardiac dysfunction can be reverse by **

A

Correction of the endocrine disorder

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20
Q

What two nutritional deficiencies can cause DCM?

A

Thiamine (B1) and carnitine deficiency

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21
Q

How does carnitine deficiency cause DCM?

A

There is impaired oxidation of fatty acids, resulting in lipid accumulation in myocyte cytoplasm

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22
Q

What is the diagnostic study of choice for DCM?

A

Echo

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23
Q

What might you see on CXR of a patient with DCM?

A

Cardiomegaly and pleural effusions

24
Q

What is the first line medication for DCM?

A

ACE inhibitors- reduced afterload by vasodilation and reduces BP

25
Q

What medications can be given for DCM?

A

ACE, diuretics, B blockers, digoxin, antiarrhythmics, and anticoagulants

26
Q

What are the two surgical options for DCM?

A

Implanted cardioverter defibrillator or cardiac transplantation

27
Q

What is the pathophysiology of HCM?

A

Left ventricular hypertrophy in the absence of a cause

28
Q

What is the histological hallmark in HCM?

A

Myocyte hypertrophy and disarray with interstitial fibrosis

29
Q

What is the leading cause of sudden cardiac death in young people?

A

HCM

30
Q

What is the etiology of HCM?

A

Familial

31
Q

What factors worsen left ventricular outflow in obstructive HCM?

A

Tachycardia, hypovolemic, standing, valsalva, positive inotropes, diuretics, and vasodilators

32
Q

What are potential PE finding on LVOT obstruction HCM?

A

Brisk bifid carotid pulse, audible S4, crescendo decrescendo ejection murmur that increases with valsalva and standing, but decreases with squatting and isometric handgrip

33
Q

What is the diagnostic study of choice for HCM?

A

Echo, showing Increased LV wall thickness.

34
Q

What changes will you see on EKG in a patient with HCM?

A

LVH with strain

35
Q

What is the management for asymptomatic HCM?

A

No prophylactic therapy

36
Q

What is the management for symptomatic HCM?

A
  • Beta blockers or non-dihydropyridine CCBs (- inotrope)
  • Diuretisc with caution if significant LVOT obstruction
  • Manage arrhythmias
  • ICD implantation if high risk for sudden cardiac death
37
Q

When is surgery for HCM indicated? What are the surgical options?

A
  • Indicated for symptomatic LVOT obstruction with advanced HF refractory to medical therapy
  • Surgical septal myectomy, EtOH ablation, or mitral valve surgery
38
Q

What is the pathophysiology of RCM?

A
  • Non-dilated, rigid ventricles with diastolic dysfunction and restrictive filling
  • Preserved systolic function (HFpEF)
39
Q

What can RCM resemble?

A

Constrictive pericarditis

40
Q

What is constrictive pericarditis?

A

Scarring and consequential loss of the normal elasticity of the pericardial sac, impaired ventricular filling

41
Q

What is the least common CM?

A

Restrictive

42
Q

What are the etiologies of RCM?

A
  • Infiltrative: Amyloidosis and sarcoidosis
  • Storage disease: hemochromatosis, glycogen storage disease
  • other: idiopathic, scleroderma, and fibrosis secondary to chemo/radiation
43
Q

What is the most common cause of RCM?

A

Amyloidosis

44
Q

What are the common symptoms of RCM?

A
  • Right > left heart failure (edema, abdominal discomfort, and ascites)
  • Angina, syncope, and dyspnea
45
Q

What are the PE findings of RCM?

A

S3 gallop (Not heard in constrictive pericarditis!!), prominent JCP, possibly kussmauls sign, and possible MR/TR murmur

46
Q

What is the presentation of Cardiac Amyloidosis?

A
  • Periorbital purpura with HF is pathognomonic

- Hepatomegaly, ascites, and elevated JVP

47
Q

What is the diagnostic study that gives a definitive diagnosis of cardiac Amyloidosis?

A

Endomyocardial biopsy

48
Q

What will you see on an echo in a patient with cardiac Amyloidosis?

A

Increased left ventricular wall thickness with diastolic dysfunction, later RV diastolic dysfunction develops

49
Q

What is the management for RCM?

A
  • treat underlying cause
  • low dose loop diuretics
  • transplant consideration
  • Poor prognosis
50
Q

What is takotsubo CM (TCM) also known as?

A

Stress CM, apical ballooning syndrome, and broken heart syndrome

51
Q

What is TCM?

A

Transient LV systolic and diastolic dysfunction in the absence of attributable CAD
-often precede by emotional or physical trigger

52
Q

What is the presentation of TCM?

A
  • abrupt onset
  • similar to ACS with substernal CP, SOB, and syncope
  • Symptoms of HF
53
Q

Is Troponin elevated in TCM?

A

Yes

54
Q

What will you see on EKG of TCM?

A

ST segment elevation, deep anterior T wave inversions which gradually resolve

55
Q

What is the management of TCM?

A
  • Immediate and similar to any acute MI including cath lab

- resolve trigger

Clinical Medicine 2 (22 decks)

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