Path II Flashcards

1
Q

What are the two types of Valvular Heart disease (VHD)

A
  • STENOSIS = failure of valve to open competely

–> leads to PRESSURE OVERLOAD of the heart

  • INSUFFICIENCY = failure of the valve to close completely, thereby allowing reversed flow

–> leads to VOLUME OVERLOAD

**EITHER WAY THE HEART HAS TO DO MORE WORK**

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2
Q

define aortic stenosis

A
  • Aortic stenosis = calcification of anatomically normal and congenitally bicuspid aortic valve
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3
Q

define aortic insufficiency

A
  • Dialtion of the ascending aorta, usually related to hypertension and aging
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4
Q

define mitral stenosis

A
  • often caused by rheumatic heart disease
  • mitral ring calcification
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5
Q

define mitral insufficiency

A
  • caused by myxomatous degeneration (mitral valve prolapse)
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6
Q

Describe aortic stenosis

A
  • usually a cosnequence of ageing of anatomically normal or congenitally bicuspid balbes
  • senile cacific aortic stenosis occurs in the seventh to ninth decade, whereas stenotic bicuspid tend to present in patients 50-70 years of age
  • causes LEFT VENTRICULAR (PRESSURE OVERLOAD) HYPERTROPHY
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7
Q

Aortic valve insufficiency (AI)

A
  • leaking of the aortic valve of the ehart causes blood to flow in reverse direction during ventricular diastole, from the aorta into the left ventricle

–> results in aortic backflow and massive Left ventricle hypertrophy with DILATION and Left ventricle failure

  • ETIOLOGY: rheumatic or aging (most common)
  • AORTIC ROOT DILATION PULLS LEAFLETS APART causing insuffiencey
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8
Q

Rheumatic fever and rheumatic heart disease

A
  • Multisystem inflammatory disease that occurs few weeks after an episode of GROUP A STREP. PHARYNGITIS
  • antigenic mimicry causes immune system to target human tissue such as heart valves, myosin and tropomyosin
  • CHARACTERIZED BY:

–> migratory polyarthritis of large joints

–> pancarditis

–> subcutaneous nodules

–> erythema marginatum of the skin

–> Sydenham chorea

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9
Q

What are the early lesions of RHD

A
  • EARLY = VERRUCAE on leaflets of valves
  • LATE

–> thickening of alve occurs

–> fusion of commisures

–> also can have calcification along with RHD leadign to sclerosis and stenosis

  • TARGETS MITRAL > AORTIC > TRICUSPID > PULMONIC in order
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10
Q

MITRAL VALVE STENOSIS

A
  • Left atrium has to pump hard so it becomes dilated and enlarged
  • so it backs up into the pulmonary arteries and lungs leading to Right heart failrue eventually
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11
Q

Calcified Mitral annulus

A
  • degenerative calcific deposits can develop in the annulus of the mitral valve
  • LEADS TO:

–> regurgitation by interfereing with phsyiologic contraction of valve ring

–> stenosis by impairing opening of mitral leaflets

–> arrhythmias and occasionally sudden death by penetration of calcium deposits to a depth sufficient to impinge on atroventricular conductions ystem

–> site for thombi that can embolize

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12
Q

MITRAL VALVE PROLAPSE

A
  • One or both mitral valve leaflets are FLOPPY and prolapse, or BALLOON BACK, into the left atrium during systole (PARACUITES)

–>KEY HISTOLOGICAL CHANGE = MYXOMATOUS DEGERNATION

–> Cuases a MID SYSTOLIC CLICK

  • Associated with MARFANS syndrome
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13
Q

describe clinical findings of mitral valve prolapse

A
  • Most patients are asymptomatic
  • Midsystolic click: diagnosis can be confirmed by echocardiography
  • MINORITY OF PATIENTS have chest pain mimicking angina, dyspnea and fatigue
  • SMALL PERCENTAGE CAN DEVELOP

–> infective endocarditis

–> chordal rupture

–> thromboembolism

–> Arrhythmias

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14
Q

Define ACUTE INFECTIVE ENDOCARDITIS

A
  • Organisms HIGH VIRULUENCE
  • STAPH AUREUS
  • produces necrotizing, ulcerative, destructive lesions of normal or deformed valves
  • Difficult to cure with antibiotics
  • HIGH MORALITY
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15
Q

DESCRIBE SUBACUTE INFECTIVE ENDOCARDITIS

A
  • Organisms lower virulence (low virulence think viridands
  • STREP. VIRIDANS
  • insidious infectiosn of deformed valves that are less destructive
  • may pursue a protracted course of weeks to months, and cures are often produced with antibiotics
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16
Q

What are some signs of infective endocarditis

A
  • splinter hemorrhages
  • janeway lesions
  • osler nodes
  • roth spots
17
Q

describe some complications of infective endocarditis

A
  • septic emboli –> peripheral infarcts and abscessess
  • Mural endocarditis = infection of non-valvular endocardium
  • IVDA increase susceptible and will have tricuspid valve involvement more often
18
Q

MYOCARDITIS

A
  • MOST COMMON IS COXSACKIEVIRUSES A and B
  • More chronic, lymphocytic type infection (compared to ischemic heart disease)
  • Pathologic changes (gross heart may appear normal or dilated and flabby)

–> inflammatory destruction of myocardial fibers –> may heal with fibrosis

19
Q

describe stages of Lyme disease (BORRELIA)

A

-Stage 1

–> early localized infection with flu-like symptoms and BULLSEYE RASH

  • STAGE 2

–> early disseminated infection with bacteria spreading through bloodstream with meningitis and migratory artheritis

  • Stage 3

–> Late persistent infection (severe and chronic symptoms)

–> myocarditis in heart

20
Q

describe dilated cardiomyopathy (DCM)

A
  • Left ventricle becomes really dilated and WEAK (also left atrium because it can’t pump blood out of heart

–> SYSTOLIC FAILURE

  • ASSOCIATED WITH:

–> Toxins = alchohol, catecholamines, CO, drugs

–> Metabolic = Increase/decrease thyroid hormones, potassium or nutritional deficiency

21
Q

Hypertrophic cardiomyopathy

A
  • ASYMPTOMATIC THICKENING (more in septum)
  • Hard to pump blood into left ventricle
  • DIASTOLIC FAILURE
  • ASSOCIATED WITH:

–> Neuromuscular disease (muscular dystorphy

–> storage disorders = glycogen storage disease, lysosomal storage disaease

22
Q

REstictive cardiomyopathy

A
  • Diastolic failure
  • blood backs up to left atrium because of a blockage
  • Associated wtih:

–> Depositions = amyloidosis

–> infiltrative = cancer, radiation-induced fibrosis

23
Q

describe the clincial course of Dialted cardiomyopathy

A
  • most common age is 20-50
  • slowly progessive signs and symptoms of CHF such as shortness of breath, easy fatigability, and poor exertion
  • Ejection fractions of less than 25%
  • secondary mitral regurgitation and abnormal cardiac rhythms are common
24
Q

describe pathogenesis of hypertrophic cardiomyopathy

A
  • poorly compliant left ventricular myocardium leading to abnormal diastolic filling
  • Reduced stroke volume due to impaired diastolic filling, which results from reduced chamber size and compliance of massively hyptrophied left ventricle
  • Classic pattern of disproportionate thickening of ventricular septum compaired with free wall
25
Q

describe the clinical course of Hypertrophy cardiomyopathy

A
  • lmitation of cardiac output and secondary increase in pulmonary venous pressure cause EXERTIONAL DYSPNEA
  • Anginal pain is frequent
  • atrial fibrillation, mural thrombus formation leading to embolization and possible stroke, intractable cardiac fialure, ventricular arrhythmias
26
Q

describethe pathology of restrictive cardiomyopathy

A
  • ventricles are of approximately normal size or slightly enalrged, the cavities are not dilated, and the myocardium is firm and noncpliant
  • biatrial dilation is commonly observed
27
Q

describe the cardiomyopathy and how it relates to ejection fraction and mechanisms of heart failure

A