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Cardio > Valvular Heart Disease > Flashcards

Valvular Heart Disease Flashcards

1
Q

Define Stenosis

A

failure to open completely. Usually due to a chronic process affecting valve cusps

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2
Q

Insufficiency: define

2 kinds

A

Failure to close completely.
Functional regurgitation-incompentence due to supporting structure
Intrinsic valve cusp abnormality

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3
Q

Valvular Diseases
2 major categories
Subcategories

A
  1. congenital
    -Bicuspid aortic valve is most common
  2. Acquired
    -aortic: stenosis –senile calcific aortic stenosis
    Insufficiency-dilation of ascending aorta due to HTN or age
    -Mitral: Stenosis RHD; insufficiency Myxomatous degeneration
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4
Q

Stenosis vs. insufficiency. which is more common?

A

stenosis

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5
Q

Dystrophic calcifications

  • 2 examples
  • cause?
  • risk factors (3)
A
  • calcific aortic stenosis
  • mitral annular calcification
  • caused by wear tear plus complications from calcium phosphate deposition
  • Hyperlipidemia, hypertension, inflammation
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6
Q

What is the most common valvular abnormality

A

calcific aortic stenosis

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7
Q

Calcific Aortic stenosis (AS)
when does it occur normally, when does it occure in predisposed population?
-what is the genetic abnormality for predisposition?

A

8-9th decade of life.

Notch mutation patients could experience CAS in 5-6th decade of life.

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8
Q

Calcific AS
-clinical symptoms: 4
-key clinical finding of heart?
treatment?

A

angina, ischemia, CHF

  • LVH
  • valve replacement
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9
Q

What does cacific aortic stenosis look like morphologically?
2 key findings

A

the leaflets are heaped up with calcified masses at the base of cusp

  • no fusion of commissures
  • free cuspal edges are not involved
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10
Q

Mitral annular calcification

  • define/explain
  • patient population
  • risk factors
  • valvular function?
  • mitral annular calcification puts patients at risk for what?
A

-degenerative deposition of calcium to the fibrous ring at the base of valve
-patient population is women >60 y/o
-myxomatous valves; elevated LV pressure
-usually does not involve function of valves
but pts are at greater risk for thrombi/infection

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11
Q

Myxomatous Degeneration of Mitral Valve

  • What’s another name for this
  • patient population (2)
  • complication?
  • PEx findings?
  • pathogenesis?
A
  • prolapse
  • young females; and marfan pts
  • no serious complications
  • mid systolic click
  • pathogenesis not clear, maybe anomaly in devo of connective tissue. Plus deposition of mucoid material in valves
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12
Q

Complications of myxomatous degeration of mitral

A
  1. Regurgitation ( late systolic/holosystolic murmur)
  2. uncommon ones
    - infective endocarditis
    - mitral insufficiency
    - thrombi on atrial surfaces–>stroke/infarcts
    - arrhythmias –>sudden death (most common in mitral insufficiency)
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13
Q

What is a serious complication of mitral insufficiency?

A

sudden death

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14
Q

Rheumatic Heart Disease

  • cause
  • most important complication?
A
  • strep pyogenes

- chronic valvular dysfunction AKA mitral stenosis

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15
Q

Acute Rheumatic heart disease

Where is the infection located?
Presentation in each layer of the heart? (be specific)

A

Disseminated infection that starts with strep pharyngitis
it presents as pancarditis…
Endocarditis is characterized with vegetation on valve leaflets
Myocarditis is characterized by Auschoff bodies–fibrinous material with Anitchkow bodies (aka catepillar nuclei cells)
Pericarditis results in “bread/butter” texture

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16
Q

Chronic rheumatic heart disease

what is this?
what are the key findings? (3)

A

Prolonged inflammation/repeated infection resulting in fibrosis and inflammatory changes of the heart. Usually decades after the initial attack

  • Thicked leaflets
  • Fused leaflets–resulting in a fish mouth valve
  • thickened chordae tendinae
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17
Q

What are some longterm serious consequences of chronic rheumatic heart disease?

  • What is the major effect?
  • What does this do to the heart?
A

mitral stenosis leads to L atrial dilation… inorder to increase CO of the LV

  • thrombus formation on L atrium
  • pulmonary congestion
  • R ventricular hypertrophy— and eventually R sided failure.
18
Q

Rheumatic Heart Disease

  • Which valve is affected the most?
  • Which the second affected?
A

Mitral alone
Mitral PLUS aortic.

MITRAL is ALWAYS first affected.

19
Q

Pathogenesis of rheumatic heart disease

  • organism
  • pathogenic factor? What does it do.
  • How likely is rheumatic fever?
A

Strep pyogenes (group A strep)
protein M cross links to the glycoproteins on the heart myocytes and causes hypersensitivity
-only 3% of people with strep pharyngitis will develop rheumatic fever.

20
Q

Criteria for dx rheumatic fever?

A
  1. sx onset must follow Group A Strep infection
  2. JONES criteria–migratory large joint pain, carditis, subQ nodules, Erythema marginatum, and sydenham’s chorea
  3. minor criterias- Fever, arthralgia, elevated CRP

Must have two major or 1 major and 2 minor. number 1 is obligatory

21
Q

Clinical course of Acute rheumatic fever

  • when does it start?
  • patient population?
  • blood test positive for what? (2)
  • prognosis?
A

1-4 weeks after strep pharyngitis

  • 5-15- year old children
  • blood test is positive for ASO and DNase B
  • prognosis is good, but are more likely to have repeat attacks
22
Q

Chronic rheumatic carditis

  • onset?
  • what is the main complication?
  • prognosis?
A

years/decades post initial episode

  • valvulitis
  • probably will need valve replacement
23
Q 
Infective Endocarditis
2 basic forms
-characteristics of the organisms
-characteristics of the valves
-patient survival?
-characteristics of the disease
A

Acute Infective Endocarditis

  • very virulent
  • attacks normal valve
  • 50% mortality
  • very destructive, so requires surgery

Subacute Infective Endocarditis

  • not as virulent
  • attacks deformed valves
  • good survival with abx
  • less destruction
24
Q

Name two patient factors that makes infective endocarditis more likely?

A
  1. deformed valve

2. immunocompromised (neutropenia, malignancy, DM, alcoholic, IV drug user)

25
Q

Agents of endocarditis.

Name 3

A

Strep Viridans-most common
Staph Aureus-Most common in IVDA
Staph Epidermidis- most common in prosthesis

26
Q

Morphology of endocarditis– acute? subacute?

What valves are most affected? What about in IVDA?

A

large friable chunks of vegetation (fibrin, inflammatory cells, and bacteria) on valves–> may lead to myocardial erosion (RING ABSCESS)

  • subacute has less destruction, fibrosis, and gradulation tissue at the base of vegetation.
  • mitral and aortic are most affected; Tricuspid most affected in IVDA
27
Q

What will you see on histology in infective endocarditis?

A

neutrophils!!! and chunks of bacteria

28
Q

Diagnosing infective endocarditis

A 
Duke Criteria
Major
-positive blood culture
-enchocardiogram findings
-New valvular regurgitation
Minor
-fever
predisposition to heart lesions or IVDA
-uncommon septic emboli findings 
--Splinter Hemorrhage, Roth's spots (retina), Janeway lesions (palm/sole), petechiae, Osler nodes
29
Q

Complications of Bacterial Endocarditis (4)

A
  • valvular insufficiency/stenosis/heart failure
  • myocardial abscess/perforation
  • embolic complications due to breaking off vegetations
  • glomerulonephritis
30
Q

Bacterial Endocarditis

treatments

A

IV abx, replacement of valve if necessary

-prophylactic abx after valve damage

31
Q

Name 2 noninfective vegetation causes

A
  • non-bacterial thrombotic endocarditis

- Libman-sacks endocarditis

32
Q

Nonbacterial thrombotic endocarditis

  • patient population
  • possible causes (3)
  • clinical findings
  • possible complication
A
  • debilitated patients (cancer, sepsis…etc)
  • hypercoagulation, mucin producing adenocarcinomas (DVTs, Trousseau syndrome), Endocardial trauma via Swan Ganz catheters
  • deposition of small masses of fibrin, platelets
  • —sterile, nondestructive, non inflammatory, small 1-5 mm, along lines of closure
  • emboli are potential complications
33
Q

Libman Sacks Endocarditis (AKA…?)

  • cause
  • valves involved
  • blood test findings?
  • morphology
A

AKA primary antiphospholipid syndrome

  • SLE
  • mitral and tricuspid are most involved
  • antiphospholipid abs found in blood
  • vegetation are present on either or both sides of valve…. 1-4 mm verrucae with fibrinous material.
  • -COULD CAUSE INTENSE INFLAMMATION
34
Q

Carcinoid Syndrome

  • What is it? What are produced (6)
  • Where is it usually located?
  • symptoms (5)
A
  • tumors that produce serotonin, kalikrein, bradykinin, histamine,prostaglandin, and tachykinins
  • Usually located in lungs or GI tract
  • Symptoms: flushing, abd cramps, N/V/D
35
Q

Cardiac manifestation of carcinoid syndrome

  • cause
  • clinical finding
  • which side of the heart is affected? and why?
A
  • cause unknown…possibly due to endothelial damage caused by vasoactive factors
  • plaque like fibrosis of RIGHT heart endocardium/valves
  • Right side is affected, because the factors are usually inactivated by MAO in the lungs before passing to the L
36
Q

carcinoid heart disease occurs with pts with what (2)

A
  • GI carcinoids with hepatic mets
  • carcinoids outside of the portal system of venous drainage (esp ovaries and testes–draining directly to caval system) OR (primary carcinoid syndrome of the lungs, so that the agents are not inactiviated)
37
Q

carcinoid heart disease

  • morphology
  • which valves are most affected?
A
  • smooth muscle cells/collagen embedded in mucopolysaccharide matrix (endocardial plaque like thickeings)
  • tricuspid (insufficiency) and pulmonic (stenosis)most affected
38
Q

Name two types of artificial valves

A

mechanical and bioprosthesis

39
Q

Name two complications of mechanical prosthesis?

A

thromboembolic, and infectious endocarditis

40
Q

Name two complications of bioprosthesis?

A

structural deterioration (50% pts need replacement by 15 years); infective endocarditis

Cardio (6 decks)

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