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EOR Exam - Internal Medicine > Cardiovascular Part 1 > Flashcards

Cardiovascular Part 1 Flashcards

1
Q

Describe the pathophysiology of angina pectoris.

A

Insufficient oxygen supply to myocardium s/p atherosclerotic narrowing or vasospasm.

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2
Q

What is the most common cause of angina pectoris?

A

CAD

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3
Q

Differentiate stable angina from unstable angina.

A

Stable: transient and predictable ischemic S/S
Unstable: Pain less responsive to NTG/rest or pain occurs at rest or after less exertion than normal.

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4
Q

What are the most useful tests performed in stable and unstable angina?

A

Stable: exercise stress testing
Unstable: angiography

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5
Q

What treatment is 1st line in the management of chronic angina and why?

A

BBs –> prolong life in patients with CAD

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6
Q

Define prinzmetal angina.

A

Angina S/S from coronary artery vasospasm

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7
Q

What is the #1 risk factor for prinzmetal angina?

A

smoking

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8
Q

What is the gold-standard imaging study in the diagnosis of prinzmetal angina?

A

coronary angiography with injection of provoking agents

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9
Q

What is the treatment for prinzmetal angina and what medication is contraindicated?

A

Treatment: Nitrates, CCBs

C/I: propranolol

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10
Q

How should a patient be counseled when long-acting nitrate therapy is prescribed?

A

Have an 8-10 hour treatment free window each day to avoid the development of tolerance.

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11
Q

Describe the parameters of the CHAD-VASC score for atrial fibrillation.

A 
C: History of CHF = 1 point
H: History of HTN = 1 point
A: Age > 75 = 2 points
D: History of DM = 1 point
S: History of TIA or stroke = 2 points
V: History of vascular disease = 1 point
A: Age 65 - 74 = 1 point
Sc: Female gender = 1 point
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12
Q

Describe how results of the CHAD-VASC scoring system for atrial fibrillation should be interpreted.

A

Used to assess stroke risk of patients with a-fib.
Score of 0 = no indication for PO anticoagulants
Score of 1 = consider PO anticoagulant or ASA
Score of 2+ = prescribe PO anticoagulant

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13
Q

What are treatment options for conversion of atrial fibrillation to a sinus rhythm?

A

Rate control: CCBs or BBs

Conversion: < 48 hours old = cardioversion, 48+ hours old = amiodarone.

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14
Q

For a patient that has been in a-fib more than 48 hours, how long should anticoagulants be used before cardioversion is performed?

A

21 days of anticoagulants.

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15
Q

What is the name for the accessory conduction pathway present in WPW?

A

bundle of Kent

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16
Q

What ECG finding is indicative of WPW?

A

delta wave –> early depolarization leading into QRS

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17
Q

What are the treatment options for SVT?

A

Stable: adenosine
Unstable: cardioversion
Definitive: radiofrequency ablation

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18
Q

What is the definitive treatment for sick sinus syndrome?

A

pacemaker

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19
Q

What are the common causes of and treatment for torsades de pointes?

A

Causes: hypoMg or hypoK most common
Treatment: IV magnesium

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20
Q

What is the treatment for ventricular tachycardia?

A

Stable: amiodarone or lidocaine
Unstable: cardioversion

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21
Q

What is the most common type of cardiomyopathy?

A

dilated

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22
Q

Describe the pathophysiology of dilated cardiomyopathy.

A

Dilation of the LV leads to decreased strength of contraction –> AKA systolic heart failure

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23
Q

What physical exam findings will likely be present in dilated cardiomyopathy?

A

Dyspnea, rales, JVD, S3 gallop, enlarged heart on imaging.

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24
Q

What are treatment recommendations for dilated or restrictive cardiomyopathy?

A

ACEIs, diuretic, CCBs –> alcohol cessation

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25
Q

Describe the pathophysiology of restrictive cardiomyopathy.

A

LV thickens and stiffens leading to reduced filling volume –> AKA diastolic heart failure

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26
Q

What physical exam findings will likely be present in restrictive cardiomyopathy?

A

pulmonary HTN, normal EF, normal heart size, enlarged atria, S4 heart sound.

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27
Q

Describe the pathophysiology of hypertrophic cardiomyopathy.

A

Thickening of the LV septum which leads to obstruction of the LV outflow tract.

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28
Q

What is the most common presentation of a patient with hypertrophic cardiomyopathy?

A

Young athlete with HPI of sudden syncope and family history of sudden death or syncope.

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29
Q

Describe the abnormal heart sounds likely present in a patient with hypertrophic cardiomyopathy.

A

S4 gallop; high pitched mid-systolic murmur at LLSB increased with Valsalva and standing (less blood in chamber) and decreased with squatting.

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30
Q

What treatment options are considered for hypertrophic cardiomyopathy?

A

Refrain from physical activity, CCB or BB, ICD, surgical ablation or myectomy of hypertrophied septum.

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31
Q

List four common causes of heart failure.

A

CAD, HTN, MI, DM

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32
Q

Describe the pathophysiology of heart failure.

A

LV remodeling leads to dilation, thinning, mitral valve incompetence, RV remodeling.

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33
Q

Describe S/S associated with heart failure.

A

exertional dyspnea, nonproductive cough, fatigue, orthopnea, PND, nocturia, edema, rales, extra heart sound, cyanosis, hepatomegaly, JVD > 8cm.

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34
Q

Which type of heart failre is associated with preserved EF and which is associated with reduced EF?

A

Diastolic HF = preserved EF = restrictive cardiomyopathy

Systolic HF = reduced EF = dilated cardiomyopathy

35
Q

Differentiate common heart sound findings present in systolic and diastolic heart failure.

A

Systolic: S3 heart sound
Diastolic: S4 heart sound

36
Q

Describe the four classifications in the NY Heart Failure Classification System.

A

1: no limitations on physical activity
2: comfortable at rest with slight physical limitations
3: comfortable at rest with marked physical limitations
4: symptoms at rest with severe physical limitations

37
Q

What tests are used in the diagnosis of CHF and which is the gold standard test?

A

BNP, ECG, CXR (Kerley B Lines)

Gold Standard = echocardiogram

38
Q

What medication treatment options are available for CHF?

A

Class 1: manage risk factors –> HTN, lipids, DM, obesity, smoke cessation
Class 2: Primarily managed with ACEI and BBs
Class 3: ACEI/ARB, BB, Diuretic considered
Class 4: Same as 3 with consideration for assist devices and/or transplant

39
Q

What is the mainstay pharmacological treatment for chronic heart failure?

A

loop diuretics

40
Q

Which BBs may be used in heart failure? Which is most common and what must be evaluated prior to initiation?

A

Carvedilol, bisoprolol, metoprolol (most common)

Patients should be euvolemic before starting BBs

41
Q

List and describe two newer medications used in the treatment of heart failure.

A

Entresto: increase Na/water clearance –> performed better than ACEI in a study
Ivabradine: for patients with EF < 35% and poorly controlled HR

42
Q

T/F: Mortality rates for CAD have deceased since 1968.

A

True: still the number 1 killer in US and worldwide

43
Q

List modifiable and non-modifiable risk factors for CAD.

A

Mod: smoking, DM, dyslipidemia, HTN

Non-mod: family history, men > 55, women > 65

44
Q

Differentiate between primary prevention and secondary prevention options for CAD.

A

1: platelet inhibitors (ASA)
2: ASA, BBs, ACEI/ARB, statins, NTG if symptomatic

45
Q

Describe the pathophysiology of CAD and plaque development.

A

LDL accumulates under the endothelial cell layer of the intima –> LDL particles taken up by macrophages and become foam cells –> fatty streak develops –> fibroblasts from collagen cap over lipid pool.

46
Q

Describe foam cells and state the age at which they begin to form.

A

Foam cells are macrophages that chew up lipids. Once they die, they remain in place and release cytokines that attract more macrophages to the area. This process begins at about age 10.

47
Q

Differentiate a stable plaque from an unstable plaque.

A

Stable: thick and difficult to rupture –> may narrow vessel.
Unstable: fissures develop in endothelium exposing lipids to circulation which triggers a thrombus formation.

48
Q

List the valves in descending order from most commonly affected by endocarditis to least common.

A

Mitral –> Aortic –> Tricuspid –> Pulmonic

49
Q

What pathogen and valve are most commonly affected by endocarditis from IV drug use.

A

Staph Aureus and tricuspid valve

50
Q

In what three circumstances does a patient most commonly develop endocarditis?

A

Direct inoculation during surgery
IV drug users
Late stage HIV

51
Q

List 4 common generalized S/S seen in endocarditis.

A

Fever, ECG abnormalities, anorexia, weight loss.

52
Q

List 5 specific peripheral sequelae that can result from endocarditis.

A
  1. Janeway lesions: painless erythematous macules on palms/soles
  2. Roth spots: retinal hemorrhage with pale center
  3. Osler nodes: tender nodules on pads of digits
  4. Splinter hemorrhages of proximal nail bed
  5. Septic emboli in CNS, kidneys, spleen, joints
53
Q

What is the key diagnostic test that needs to be performed in evaluating for endocarditis and what is the timing/when should it be repeated?

A

Blood cultures obtained three times at least one hour apart from one another. Should be done before abx are administered.

54
Q

What imaging study is best to evaluate for endocarditis?

A

Echo –> transthoracic first, but transesophageal is more sensitive.

55
Q

What are the two major criteria used in the diagnosis of endocarditis?

A
  1. Two or more positive blood cultures

2. Echo showing new valvular regurgitation or vegetations/abscesses on endocardium

56
Q

What are the six minor criteria used in the diagnosis of endocarditis?

A
  1. Predisposing condition (IV Drugs, Catheter)
  2. Fever > 100.4
  3. Vascular finding: janeways, septic emboli, etc.
  4. Immunologic findings: Osler’s, Roth, positive RF
  5. Single positive blood culture
  6. Positive echo not meeting major criteria
57
Q

What major and minor findings are required to make a diagnosis of endocarditis?

A

2 major …or…
1 major and 3 minor …or…
5 minor

58
Q

What abx are recommended in empiric treatment of endocarditis?

A

Native valve subacute endo: PCN/ampicillin plus Gentamicin –> Vancomycin in IV drug users
Prosthetic: vancomycin, gentamicin and rifampin
Fungal: ampho B –> caspofungin if severe

59
Q

How long is abx therapy continued in the treatment of endocarditis?

A

4 - 6 weeks

60
Q

What are the indications for surgical treatment of endocarditis?

A

Refractory CHF, persistent or refractory infection, invasive infection, prosthetic valve, recurrent systemic emboli, fungal infection.

61
Q

What are the HACEK bacteria associated with vegetations resulting from endocarditis?

A 
H: H. flu
A: Antinobacillus
C: Cardiobacterium
E: Eikenella
K: Klingella
62
Q

Describe the murmurs and key S/S associated with aortic stenosis and regurgitation.

A

AS: harsh systolic ejection crescendo-decrescendo at RUS border with radiation to neck and apex. Squatting increases intensity, split S2, syncope on exertion.
AR: soft high pitched, blowing, crescendo-decrescendo along LUS border. Louder squatting, water-hammer pulse.

63
Q

Describe the murmurs and key S/S associated with mitral stenosis, regurgitation, and prolapse.

A

MS: diastolic low pitched decrescendo rumbling with opening snap heard best at apex with pt. lying left lateral decubitus position.
MR: blowing holosystolic murmur at apex with split S2 radiating to left axilla.
MVP: midsystolic ejection click heard best at apex

64
Q

Describe the murmurs and key S/S associated with tricuspid stenosis and regurgitation.

A

TS: mid diastolic rumbling murmur at LLSB with opening snap. Rare condition.
TR: high pitched holostystolic murmur at LLSB radiates to sternum and increases with inspiration.

65
Q

Describe the murmurs and key S/S associated with pulmonic stenosis and regurgitation.

A

PS: harsh, loud systolic murmur heard best at 2nd/3rd left IC space that may increase with inspiration. Will also have widely split S2.
PR: high pitched early diastolic decrescendo murmur at LUSB that increases with inspiration.

66
Q

Open space for podcast murmurs question

A

Open

67
Q

Open space for podcast murmurs question

A

Open

68
Q

Open space for podcast murmurs question

A

Open

69
Q

Open space for podcast murmurs question

A

Open

70
Q

Define a xanthoma and describe its association with hyperlipidemia.

A

Def: lipid buildup under the skin - most commonly at eyelids and achilles tendon.
Usually indicate a genetic cause when associated with hyperlipidemia. However, 2/3 with xanthelasmas (eyelids) have normal serum lipids.

71
Q

Describe LDL level treatment goals in all patients, patients with CVD, and patients with no CVD but risk factors present.

A

CVD: Start meds at LDL < 130. Goal is LDL < 100 but LDL < 70 is optimal.
RFs: Meds at LDL > 160, goal is LDL < 130
All others: Meds at LDL > 190, goal is LDL < 160

72
Q

Describe the USPSTF recommendations for lipid screening.

A

Screening should begin at age 35 for males and 45 for females if no evidence of CVD or other risk factors. High risk patients should start at 25 ad 35.

73
Q

When screening what are the lipid level goals?

A

Total cholesterol < 200, HDL > 45, Triglycerides < 150, LDL < 160 (if no risk factors)

74
Q

Name and describe the primary therapeutic method used to manage hyperlipidemia.

A

Lifestyle changes - weight reduction, exercise, reduce cholesterol, carbs, and trans fats in diet, increase fruits (antioxidants) and vegetables (fiber), smoke cessation.

75
Q

What drug should not be used in DM patients and why? What other options would be used in its place?

A

Niacin causes hyperglycemia. Use fibrates and statins instead.

76
Q

What are the primary affects of statin medications?

A

Decrease LDL (best drug to dec LDL), increase HDL, decrease triglycerides.

77
Q

Describe the MOA of statin medications.

A

HMGcoA reductase inhibitor - rate limiting step in cholesterol synthesis in the liver. Also increases LDL receptors which helps remove cholesterol from the blood.

78
Q

When should statin medications be taken?

A

At night when cholesterol synthesis is at its highest. Less important with newer statins - atorvastatin, pitavastatin, rosuvastatin.

79
Q

What are the two primary affects of niacin?

A

Inc HDL and dec triglycerides –> mild dec in LDL

80
Q

What are the effects of fibrate meds?

A

Primarily dec triglycerides –> minimal inc in HDL and dec in LDL.

81
Q

What are the affects of bile acid sequestering agents?

A

Dec LDL –> especially when combined with statins
May inc TGs –> Pt must have normal triglycerides
Mild inc HDL

82
Q

What is the best use of bile acid sequestering agents?

A

In combination with statins or niacin.

83
Q

What is the MOA of ezetemibe?

A

Blocks cholesterol transporter which inhibits gastric absorption of cholesterol.

84
Q

What is the best use of ezetemibe?

A

In combination with a statin to lower LDL.

EOR Exam - Internal Medicine (9 decks)

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