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Family Med/Geriatrics rotation > Cardio part 3 > Flashcards

Cardio part 3 Flashcards

1
Q

Effects of bile acid resins on lipid profile

A

Moderate reduction in LDL
Increase or no change in triglycerides (do not use for people who already have triglyceride issues)
Modest increase in HDL

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2
Q

Effects of niacin on lipid profile

A

Modest reduction in LDL
Significant reduction in TG
Significant increase in HDL

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3
Q

Considerations of niacin

A

Hepatotoxicity
Increased uric acid levels
Caution in pts with renal dysfunction

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4
Q

Effects of fibrates on lipid profile

A

Can increase or decrease LDL
Significant reduction in TG
Significant increase in HDL

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5
Q

What is considered part of clinical ASCVD?

A 
Acute coronary syndromes
H/o MI
Stable or unstable angina
Coronary revascularization
Stroke
TIA of atherosclerotic origin
PAD
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6
Q

Which statins are considered high-intensity?

A

Atorvastatin

Rosuvastatin

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7
Q

Which statins are considered moderate intensity?

A 
Atorvastatin
Rosuvastatin
Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin
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8
Q

What is considered a low-intensity statin?

A 
Simvastatin
Pravastatin
Lovastatin
Fluvastatin
Pitavastatin
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9
Q

Pathophys of peripheral vascular dz

A

Primarily the result of atherosclerosis
The process may gradually progress to complete occlusion of medium-sized and large arteries
May manifest acutely when thrombi, emboli, or acute trauma compromises perfusion

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10
Q

What are some factors that can predispose pts to thrombosis?

A 
Sepsis
Hypotension
Low cardiac output
Aneurysms
Aortic dissection
Bypass grafts
Underlying atherosclerotic narrowing of the arterial lumen
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11
Q

What are conditions that often coexist with PVD

A 
Primary factor: atherosclerosis
CAD
AFib
Cerebrovascular dz
Renal dz
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12
Q

RFs for PVD

A

Smoking
HLD
DM
Hyperviscosity

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13
Q

Hx manifestations of PVD

A

Intermittent claudication may be the sole manifestation of early symptomatic PVD
Aortoiliac dz- pain the thigh and buttock
Femoropopliteal dz-pain in the calf
Sx are precipitated by walking a predictable distance and are relieved by rest
Claudication may also present as the hip or leg “giving out” after a certain period of exertion and may not demonstrate the typical symptom of pain on exertion
The pain of claudication usually does not occur with sitting or standing
Erectile dysfunction has been linked as a potential early indicator

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14
Q

Leriche syndrome

A

Intermittent claudication
Impotence
Significantly decreased or absent femoral pulses

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15
Q

PE of PVD

A 
Pulselessness
Paralysis
Paresthesia
Pain
Pallor
Assess for murmurs or other heart abnormalities
Investigate all peripheral vessels
Skin may have an atrophic, shiny appearance and may demonstrate trophic changes:
Alopecia
Dry, scaly, or erythematous skin
Chronic pigmentation changes 
Brittle nails
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16
Q

Presentation of advanced PVD

A

Mottling in a “fishnet pattern”
Pulselessness
Numbness
Cyanosis

17
Q

Workup of PVD

A 
CBC
BUN
Creatinine
Electrolyte studies
D-dimer
CRP
Interleukin-6
Homocysteine
Arteriography- could have more risks than gains
Doppler u/s
ABI
18
Q

Tx of PVD

A

Counsel pts regarding the potential effects of various activities and medications on the course of their illness
Counsel on smoking cessation
Avoid cold exposures and medications that can lead to vasoconstriction
Anticoagulants

19
Q

Pathophys of aortic stenosis

A

When the valve becomes stenotic, resistance to systolic ejection occurs and a systolic pressure gradient develops between the left ventricle and the aorta

20
Q

Etiology of aortic stenosis requiring surgery

A 
Common causes <70 yo in order in order from most common to least common:
Bicuspid AV
Postinflammatory
Degenerative
Unicommisural
Hypoplastic
Indeterminate
Common causes >70 yo in order:
Degenerative
Bicuspid
Postinflammatory
Hypoplastic
21
Q

H/o aortic stenosis

A 
Usually has an asymptomatic latent period of 10-20 years
MC initial complaint is dyspnea
CP
Heart failure
Syncope
22
Q

PE of aortic stenosis

A

Carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude and gradual downslope (pulsus parvus et tardus)
Jugular venous pulse may show prominent a waves
A2 usually diminished or absent
Paradoxical splitting of the S2
Prominent S4 can be present
Crescendo-decrescendo systolic murmur
Rough low-pitched sound that is best heard at the second intercostal space in right upper sternal border
Radiates to carotid artery

23
Q

Workup of aortic stenosis

A 
EKG
CXR
CMP
Cardiac markers
CBC
TTE
Cardiac cath and coronary arteriography
BNP
24
Q

Tx of aortic stenosis

A

Address ABCs
Perform CPR if in cardiac arrest
With acute sx, hospital admission, telemetry/ICU admission, and cardiology consultation should be considered
Heart failure- oxygen, cardiac and oximetry monitoring, IV access, loop diuretics, nitrates, morphine, and ventilatory support
Percutaneous balloon valvuloplasty is used as a palliative measure
Aortic valve replacement

25
Q

Pathophys of aortic regurgitation

A

Acute- the LV does not have sufficient time to dilate in response to the sudden increase in volume
As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure and altering coronary flow dynamics
Chronic- gradual LV volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy
There is greater capacity to deliver a large stroke volume that can compensate for the regurgitant volume

26
Q

Etiology of acute aortic regurgitation

A 
Infective endocarditis
Bulky vegetation
Chest trauma
Post-TAVR
LVAD implantation
Aortic dissection (type A)
27
Q

Etiology of chronic aortic regurgitation

A 
Bicuspid aortic vavle- MCC of isolated AR
Certain wt loss medications
Rheumatic fever
Ankylosing spondylitis
Behcet dz
Giant cell arteritis
RA
SLE
Takayasu arteritis
Whipple disease
28
Q

Connective tissue d/os that can cause significant AR

A 
Marfan
Ehlers-Danlos
Floppy aortic valve
Aortic valve prolapse
Sinus of Valsalva aneurysm
Aortic annular fistula
29
Q

Hx of acute aortic regurgitation

A

Sudden, severe SOB
Rapidly developing heart failure
CP if myocardial perfusion pressure is decreased or an aortic dissection is present

30
Q

Hx of chronic aortic regurgitation

A

Often have a long-standing asymptomatic period that may last for several years
Compensatory tachycardia
Severe chronic AR:
Palpitations
SOB
CP
Sudden cardiac death: uncommon in asymptomatic pts with preserved LV function

31
Q

PE of acute aortic regurgitation

A

May be fulminant and lead to cardiogenic shock
Pts with CHF or shock associated often appear gravely ill
Other sx:
Tachycardia
Peripheral vasoconstriction
Cyanosis
Pulmonary edema
Alterial pulsus alternans
Austin-Flint murmur (Lower piched and short in duration)
Decrescendo diastolic murmur that is heard best with the pt leaning forward

32
Q

Chronic aortic regurgitation PE: signs

A

Widened pulse pressure
Becker sign- visible systolic pulsations of the retinal arterioles
Corrigan pulse- abrupt distention and quick collapse on palpation of the peripheral arterial pulse
de Musset sign- bobbing motion of the pt’s head with each heartbeat
Hill sign- popliteal cuff SBP 40 mm higher than brachial cuff systolic BP
Droziez sign- systolic murmur over the femoral artery with proximal compression of the artery, and diastolic murmur over the femoral artery with distal compression of the artery
Muller sign- visible systolic pulsations of the uvula
Quincke sign-visible pulsations of the fingernail bed with light compression of the fingernail
Traube sign- booming systolic and diastolic sounds auscultated over the femoral artery

33
Q

Chronic AR PE: distention/sx

A

PMI may be diffuse or hyperdynamic but is often displaced inferiorly and toward the axilla
Peripheral pulses are prominent or bounding
S3 gallop if LV dysfunction is present
High-pitched sound in diastole that is loudest at the left sternal border

34
Q

Workup of AR

A 
Should be guided by clinical scenario
Could also include:
CBC
PT/aPTT
Type and screen
Electrolytes
VDRL
LDH
TTE
CXR
Radionuclide imaging
Aortic angiography
EKG
Cardiac cath
35
Q

Tx of AR

A

Severe chronic AR- vasodilator therapy
Valve replacement
With HTN or hypervolemia, salt restriction
Ongoing clinical surveillance with periodic echocardiogarphy for
After initial study, clinical eval and a repeat echo are recommended in 3 mos
When to subsequently followup is determined based on the stability of the LV end-systolic dimension and LV end-diastolic dimension
Consider hydralazine or nifedipine

36
Q

Pathophys of pulmonic stenosis

A

Can be due to isolated valvular, subvalvular or peripheral obstruction or it may be found in association with more complicated congenital heart disorders
Valvular- valve commissures are partially fused and the 3 leaflets are thin and pliant, resulting in a conical or dome-shaped structure with a narrowed central orifice
Subvalvular- narrowing of the infundibular or subinfundibular region, often with a normal pulmonic valve
Peirpheral- can cause obstruction at the level of the main pulmonary artery, at its bifurcation, or at the more distal branches

37
Q

Hx of pulmonary stenosis

A

Mos with mild-to-moderately severe PS are asymptomatic
Severe: exertional dyspnea and fatigue
Right heart failure: peripheral edema and other typical sx
Significant right-to-left shunt: cyanosis

38
Q

PE of pulmonary stenosis

A

Precordial heave or a palpable impulse from the RV along the left parasternal border

Family Med/Geriatrics rotation (6 decks)

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