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(J2) CPR II Test 1 (Cardiovascular) > Valvular Disease > Flashcards

Valvular Disease Flashcards

1
Q

What is the most common valvular disease?

A

calcific aortic stenosis

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2
Q

What are the mechanisms of aortic stenosis?

A
  • aortic valve sclerosis
  • bicuspid aortic valve
  • rheumatic fever -> aquired bicuspid aortic valve
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3
Q

What is aortic valve scleoris?

A

calcification and fibrosis of the aortic valve preventing full opening of the valve

mechanisms similar to those of athersclerosis and with similar risk factors:

  • age
  • HTN
  • hyperlipidemia
  • inflammation
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4
Q

When is aortic valve sclerosis seen?

A

age 60-80

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5
Q

What is a bicuspid aortic valve?

A

congenital fusion of 2 of the 3 arotic valve leaflets

-predisposes to valve calcification (seen earlier)

can be aquired as a result of rheumatic heart disease

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6
Q

What changes occur in the heart due to aortic stenosis?

A

increased resistance of the aortic opening -> increased pressure -> LVH

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7
Q

What is the clinical presentation of aortic stenosis?

A

initially asymptomatic

progression may lead to symptoms with exertion and eventually at rest

Presentation:

  • systolic ejection murmur (crescendo-decrescendo)
  • > angina -> syncope -> CHF
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8
Q

What is the prognosis and treatment for aortic stenosis?

A

prognosis worsens with progression of symptoms

-angina -> syncope -> CHF = approx. 5, 3, and 2 years respectively until death

threatment is surgical aortic valve replacement/repair:

-in symptomatic or functionally deficient pts

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9
Q

What is mitral annular calcification?

A

calcification of the mitral annulus at the base of the mitral leaftlets

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10
Q

What is the epidemiology of mitral annular calcification?

A
  • females
  • >60
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11
Q

How does mitral annular calcification present?

Complications?

A

normally remains asymptomatic

Complications:

  • mitral regurgitaiton
  • mitral stenosis
  • arrhythmia
  • thrombus formation
  • infective endocarditis
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12
Q

What is mitral valve prolapse?

(causes)

A

mitral valve leaflets prolapse into LA during LV contraction

Causes:

  • mostly idiopathic
  • connective tissue diseases (Marfan and Ehlers-Danlos)
  • ischemia; chordae tendinae damage
  • rheumatic heart disease
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13
Q

What structural findings are associated with mitral valve prolapse?

A
  • thick and rubbery leaflets; deposition of GAGs -> myxomatous degeneration
  • “hooding” of leaflets
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14
Q

What is the epidemiology of mitral valve prolapse?

A
  • relatively common 2-3% of adults
  • 7:1 female predominance
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15
Q

How does mitral valve prolapse present?

Complications?

A

asymptomatic with mid-systolic click; murmur if reguritaiton is present

Complicaitons:

-mitral regurgitation; most common cause in developed countries

Rare:

  • infective endocarditis
  • mitral insufficiency (possible chordal rupture)
  • arrhythmia (typically atrial, rarely ventricular)
  • thromboembolism
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16
Q

What is the prognosis and treatment for mitral valve prolapse?

A

very good prognosis; serious complications are rare

generally does not require treatment itself beyond treatment of complications

17
Q

What is rheumatic fever?

A

autoimmune condition triggered by molecular mimicry of M streptococcal Ag of group A streptococcus

Ab and cell-mediated reaction to heart, joints, soft tissue, skin, and nervous system

18
Q

What is the clinical presentation of rheumatic fever?

A

occurs 2-4 weeks after group A strep infection

Presentation:

  • fever >101 + J♥(O)NES criteria
  • Joints: migratory polyarthritis (mostly large joints)
  • ♥: pancarditis (endo, myo, and pericarditis)
  • Nodules: subcutaneous nodules
  • Erythema marginatum (ring-shaped macular rash)
  • Sydenham chorea (ballismus occasionally w/ behavorial changes)
19
Q

What tests are used to diagnose rheumatic fever?

A
  • antistreptolysin O (ASO)
  • antistreptococcal DNAse B (ADB)

cannot culture for strep as inciting infeciton has likely resolved

20
Q

What are complications of rheumatic fever?

A

collectively refered to as rheumatic heart disease

Acute (inflammation):

  • pancarditis
  • verrcurae, valvular vegetations
  • MacCallum plaque (thickened posterior LA wall)

Chronic (valvular changes):

  • valvular lesions -> regurgitaiton/stenosis
  • affects mitral > aortic > tricuspid (rarely pulmonary); MAT

-LAE -> A-fib

-infective endocarditis

21
Q

What pathologic findings are associated with the heart in rheumatic fever?

A

Aschoff bodies:

-lesions in the heart consisting of T-cells, plasma cells, and Anitschkow cells

Anitschkow cells:

  • **pathognomonic** for rheumatic fever
  • macrophage
  • caterpilar-like chromatin
  • owl-eye apperance
22
Q

What is infective endocarditits?

(risk factors)

A

infection of damaged cardiac valves or structural anomalies in the heart

Risk factors:

  • male
  • age >60
  • IVDU
  • body peircings
  • poor dentition; dental procedures
23
Q

What organisms are responsible for infective endocarditits?

A

native, structurally abnormal valves -> Streptococcus viridians

poor dentition -> HACEK (Heomphilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

prosthetic valves -> Staphylococcus epidermidis

IVD -> Staphylococcus aureus

24
Q

What valves does infective endocarditis normally effect?

A

mitral > aortic > tricuspid > pulmonary (same order as rheumatic heart disease)

IVD particularlly affects the right sided valves -> tricuspid/pulmonary

25
Q

What is the clinical presentation of infective endocarditis?

A

Acute endocarditits:

  • rapid onset of high fever + extracardiac manifestations
  • typically S. aureus

Subacute endocarditis:

-slow onset of low fever + extracardiac manifestations

Extracardiac manifestations:

  • splinter hemorraghes
  • Osler nodes (painful nodules on pads of fingers/toes)
  • Roth spots (retinal hemorrhages with pale center)
  • Janeway lesions (non-tender, macules on palms and soles)
26
Q

What is nonbacterial thrombotic endocarditis?

(cause)

A

sterile valvular thrombi

caused by procoagulative states:

  • sepsis
  • cancer
  • antiphospholipid syndrome
  • SLE -> Libman-Sacks
27
Q

What is carcinoid heart disease?

(pathophysiology)

A

caused by mediators released by carcinoid tumors; most commonly serotonin

liver clears excess serotonin from carcinoid tumors, progression of tumor growth can produce too much serotonin for the liver to clear or metastasis to the liver can occur allowing serotonin to enter hepatic vein and reach heart

serotonin stimulates fibrosis of the cardiac valves

28
Q

What valves are typically affected in carcinoid heart disease?

A

right sided valves, tricuspid > pulmonary

pulmonary tissue also clears serotonin, protecting left valves

29
Q

How does carcinoid syndrome/carcinoid heart disease present?

A

Systemic/carcinoid syndrome:

  • flushing
  • dermatitis
  • bronchoconstriction
  • diarrhea

Heart:

-tricuspid insufficiency -> right sided heart failure

(J2) CPR II Test 1 (Cardiovascular) (18 decks)

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