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Pathology > Chapter 10 - Heart Pathology > Flashcards

Chapter 10 - Heart Pathology Flashcards

1
Q

Congestive Heart Failure

A

Multisystem derangement occurring when the heart is unable to eject the blood delivered to it by the venous system, “forward failure”

Caused by: Left - systemic hypertension, mitral/aortic valvular disease, ischemic heart disease, primary cardiomyopathies
Right - 2 to L heart failure, pulmonary hypertension

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2
Q

Stages of Congestive Heart Failure

A

1 - compensated failure: increased catecholamines (improve contractility), hypertrophy of myocytes and chamber dilation
2 - uncompensated failure: clinical signs of venous congestion appear (pulmonary edema, peripheral edema, congestion of abdominal viscera), cyanosis & acidosis due to decreased tissue perfusion

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3
Q

Clinical signs of Left heart failure

A 
pulmonary edema
pleural effusions
dyspnea
dyspnea lying down
"orthopnea"
fatigue, tachycardia
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4
Q

Clinical signs of Right heart failure

A 
systemic venous congestion
soft tissue edema
distended neck veins
enlarged liver
inc. deep vein thromboses/pulmonary emboli
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5
Q

Hypertensive heart disease

A

left ventricular hypertrophy in an indiv w/ history of hypertension
*Concentric ventricular thickening rather than eccentric

Clinical features: CO normal = asymptomatic
L heart failure appears with ischemia (angina pectoris)

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6
Q

Cor Pulmonale

A

R ventricular hypertrophy secondary to pulmonary arterial hypertension (lung disease, esp w/ scarring, multiple small pulmonary emboli)

Both reduce vascular bed, inc pulmonary arterial pressure

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7
Q

Congenital heart disease

A

atrial septal defects, ventricular septal defects, patent (persistent) ductus arteriosus, tetralogy of Fallot, transposition of the great arteries, coarctation of aorta

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8
Q

Shunts

A

small hole or passage which allows movement of fluids from one part of the body to another

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9
Q

Left to right shunt

A

pressure higher in left heart than in right heart, no cyanosis initially, late cyanosis when shunt reverses due to pulmonary hypertension

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10
Q

Atrial septal defect

A

*Most common congenital cardiac malformation first diagnosed in adults, no symptoms in childhood, pulmonary hypertension may reverse shunt and produce cyanosis

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11
Q

Ventricular Septal Defect (VSD)

A

Most common congenital heart disease (CHD) diagnosed at birth (most are small and close spontaneously)

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12
Q

Patent Ductus Arteriosus

A

Ductus arteriosus normally closes shortly after birth, Patent ductus arteriosus usually identified early on the corrected w/ medication or surgery, eventually shunt reverses due to pulmonary hypertension and cyanosis develops

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13
Q

Right to left shunt

A

pressure higher in right heart than in left heart
**Cyanosis initially since blood is shunted away from lungs (reduced oxygenation)

Tetralogy of Fallot

Blood is diverted from pulmonary circulation to systemic thus reducing oxygenation, cyanosis at or near birth

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14
Q

Tetralogy of Fallot

A

1 - Pulmonary Artery Stenosis
2 - Overriding aorta
3 - Ventriculoseptal defect
4 - Right ventricular hypertrophy

May also have a patent ductus which helps oxygenate the blood

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15
Q

Transposition of the Great Arteries

A

Second leading cause of congenital cyanosis

abnormal truncal septation, aorta arises from R ventricle and the pulmonary artery arises from L ventricle

*Cyanosis is the main clinical sign

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16
Q

Coarcation of Aorta

A

Abnormal narrowing of the aortic lumen (blood pressure higher in arms than legs)

Cerebral hemorrhages common due to inc intracranial arterial pressure

Weak pulses in the lower extremities with signs and symptoms of intermittent claudication (ischemic leg pain)

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17
Q

Ischemic Heart Disease

A

imbalance between myocardial supply (perfusion) and cardia demand for oxygenated blood

most common cause: atherosclerotic narrowing of coronary arteries

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18
Q

4 forms or manifestations of ischemic heart disease

A

1) angina pectoris (ischemic chest pain)
2) myocardial infarction (MI)
3) sudden cardiac death (SCD)
4) chronic ischemic heart disease w/ heart failure

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19
Q

“Acute Coronary Syndrome”

A

an umbrella term for 3 acute conditions resulting from coronary artery disease

1 - unstable angina pectoris
2 - acute myocardial infarction
3 - sudden cardiac death

**All 3 result from acute changes in the morphology of coronary atherosclerotic plaques

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20
Q

Etiology of Coronary Artery Disease

A

Hypertension, Diabetes (type I and II), Smoking, High levels of LDL, Low levels of HDL, Poorly understood hereditary factors

21
Q

Coronary Artery plaque

A

critical stenosis

> 75% luminal reduction of 1+ coronary arteries,
compensatory vasodilation is insufficient to compensate

22
Q

Acute Plaque Changes

A

abrupt changes in plaque followed by thrombosis (fissuring, hemorrhage into plaque, overt plaque rupture w/ embolization of atheromatous debris)

may occur w/ plaques less than 75% occlusive and in prev asymptomatic individuals

23
Q

Coronary Artery Thrombosis

A

1 - plaque rupture exposes thrombogenic lipids and subendothelial collagen initiating thrombosis
2 - if vessel completely occluded, infarction occurs

If vessel incompletely occluded, unstable angina or lethal ventricular arrhythmia results

24
Q

Angina Pectoris

A

Intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia

25
Q

Stable Angina Pectoris

A

Associated with fixed atherosclerotic narrowing of 1+ coronary arteries
Discomfort in chest described as deep, poorly localized pressure, squeezing or burning sensation
Produces by physical activity, emotional excitement, or physiological stress
Pain relieved by rest and/or nitroglycerin or calcium channel blockers

26
Q

Prinzmetal Angina Pectoris

A

Anginal pain occurring at rest or awakening patient from sleep
Usually associated with coronary artery spasm often adjacent to a site of atherosclerotic plaque
Mechanism underlying spasm poorly misunderstood

27
Q

Unstable Angina Pectoris

A

Increased frequency of angina episodes
Precipitated by progressively less exertion
Described as intense pain
More intense - last longer than “stable anginga” (>20 min)
Induced by acute plaque change w/ a superimposed partial thrombosis or vasospasm or both

28
Q

Myocardial Infarction

A

development of an area of myocardial necrosis caused by localized ischemia
Risk factors are same as atherosclerosis

Myocardial necrosis begins w/ 20-30 min reaching full size within 3-6 hours
Begins in subendocardium extending toward epicardium

Thrombolytic agents may limit size of infarct during this time frame

29
Q

Clinical complications of Acute MI

A

sudden death, cardia arrhythmias, left heart failure, cardiogenic shock, myocardial rupture w/ hemopericardium and cardia tamponade, thromboembolism

30
Q

Anatomic Complications of MI

A

Infarcted papillary muscle and mitral valve insufficiency
External rupture of the infarct w/ cardia tamponade
Mural thrombus giving rise to systemic arterial emboli
Ventricular aneurysms

31
Q

Sudden Cardiac Death

A

Most common cause: ischemic heart disease (coronary artery atherosclerosis) (acute “cor pulmonale” due to massive pulmonary artery thromboembolism

32
Q

Valvular Heart Disease

A

Mitral valve stenosis

Regurgitation

33
Q

Calcific Aortic Stenosis

A

age related degeneration, most common cause of isolated aortic stenosis in USA, L ventricular hypertrophy and dec aortic outflow lead to myocardial ischemia, death within 3-4 years unless treated

34
Q

Mitral Valve Prolapse

A

results in mitral regurgitation, common cardiac disorder, prone to infective endocarditis/ arrhythmias/ emboli from L atrium

*most cases are sporadic; may be seen with Marfan syndrome

35
Q

Rheumatic Fever

A

acute, immunologically-mediated, multisystem inflammatory disease usually following group A streptococcal pharyngitis after an interval of a few weeks
Pharyngitis severity not related to risk of developing RF

Pathogenesis: Hypersensitivity reaction induced by group A streptococci, antibodies developed against “M” proteins of group A strep cross-react w/ similar epitopes in heart, joints, skin, and other, comprised of **“Anitschkow cells”

Acute RF - rarely causes heart failure due to myocarditis and valvular injury
Chronic RF - irreversible valvular deformity (Mitral valve 95%, Mitral+Aortic 25%)

36
Q

Infective Endocarditis

A

Infection of cardiac valves or mural surfaces of endocardium

Gradual onset or explosive onset depending upon the virulence of the organism (Low - low-grade fever, malaise, weight loss) (High - high ever, shaking chills, overt septicemia)

37
Q

Acute Infective Endocarditis

A

Organisms of high virulence Staph aureus
Often involves normal valves
Intravenous drug use
Often tricuspid and pulmonic valves rather than left heart valves

38
Q

Subacute Infective Endocarditis

A

Organisms of low virulence
50-60% of cases of endocarditis occurring on damaged valves are caused by Strep viridans
Pre-existing cardiac abnormalities, especially valvular disease (small ventriculoseptal defects, chronic rheumatic valvular disease, calcific aortic stenosis, mitral valve prolapse

39
Q

Noninfective Endocarditis

A

Systemic Lupus Erythematosus: Endocarditis Usually mitral valve “Libman-Sacks disease”

40
Q

Dilated Cardiomyopathy

A

4 chamber dilation and hypertrophy
Idiopathic
Fundamental defect is ineffective contraction: ejection fraction < than 25%. Normal = 55-70%
Some association w/ alcoholism and prior viral myocarditis
Occur at any age, more often in men, 20-30% due to inherited genetic disorders

41
Q

Hypertrophic Cardiomyopathy

A

“Idiopathic hypertrophic subaortic stenosis”
Heavy, muscular, hypercontracting heart
Genetic basis of 50% of cases; AD
One of most common causes of sudden unexpected death in young athletes

42
Q

Myocarditis

A

Inflammatory process of the myocardium resulting in injury to cardiac myocytes
Causes: viral, bacterial, parasitic, fungal, immune-mediated myocardial injury

43
Q

Pericarditis

A

Inflammatory process involving the pericardium as a result of a systemic disease or a primary pericardium disorder

Morphologically classified in 5 types: fibrinous, serous, purulent, hemorrhagic, caseous

44
Q

Fibrinous Pericarditis “Bread & Butter” pericarditis

A

most frequent type
pericardium opaque and granular
associated w/ acute myocardial infarction, SLE, chest irradiation and trauma
May develop a loud pericardial friction rub
Can compromise cardiac output due to fluid accumulation in pericardial sac
Histology shows the deposition of fibrin and leukocytic exudate

45
Q

Bacterial (purulent) Pericarditis

A

Occurs by direct infection during trauma, thoracic surgery, or catheter drainage, by spread from an intrathoracic, myocardial, or subdiaphragmatic focus, and by hematogenous dissemination
Frequent causes are staph, Haemophilus, and M. tuberculosis

46
Q

Hemorrhagic pericarditis

A

Involves blood mixed w/ a fibrinous or suppurative effusion
Most commonly caused by tuberculosis or direct neoplastic invasion
Can occur in sever bacterial infections or in patients w/ a bleeding diathesis

47
Q

Pericardial effusions

A

Fluid accumulation in the pericardial space
Nature of fluid varies with the cause of the effusion
-Serous: congestive heart failure, hypoalbuminemia
-Serosanguineous (watery, blood tinged): blunt chest trauma, malignancy
-Chylous (milky) mediastinal lymphatic obstruction, usually by mediastinal neoplasm

Clinical features: Cardiac tamponade (heart unable to expand during diastole due to fluid in sac)

48
Q

Hemopericardium

A

Ruptured infarction
Penetrating cardiac trauma
Cardiac tamponade results

49
Q

Atrial Fibrillation

A

a disease of the heart characterized by irregular and often faster heartbeat
Predisposes the patient to thromboemboli from the left heart resulting in ischemic strokes
Most patients on long-term anticoagulation are being treated for this reason

Clinical Features:
may be asymptomatic, dizziness, light-headness, syncope, tachycardia, stroke,

Treatment: Warfarin and Factor X/ Thrombin antagonists

Pathology (13 decks)

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