chap 19 Flashcards
Acute Pericarditis
Acute pericarditis is most often of viral origin
It may occur in several forms:
less thn 2 weeks duration
increased capillary peremeability
Serous pericarditis :
slowly accumulating exudates - 50 to 200 ml of
produced by nonbacterial involvement RHD, LES, tumours, uremia and primary viral infection (Coxsackie).
inflammatory reaction in the epicardial and pericardial surfaces - scant numbers of PMN, lymphocytes, and macrophages
Fibrinous and serofibrinous pericarditis
the most frequent type of pericarditis
causes: acute MI, the postinfarction (Dressler) sdr. and cardiac surgery
the surface is dry, with a fine granular roughening
an increased inflammatory process thicker fluid, yellow and cloudy owing to leukocytes and erythrocytes
exudate may be completely resolved or be organized causing adhesive pericarditis
Purulent or Suppurative Pericarditis
due to bacteria (Staphylococci, Streptococci, and Pneumococci), fungus or parasitic infection.
by direct extension, by hematogenous or lymphatic route from the neighbouring areas of infection (pneumonia, subphrenic abscess)
thin to creamy pus - 400 to 500 ml
erythematous, granular serous surfaces
may produce mediastinopericarditis
it usually organizes constrictive pericarditis
Hemorrhagic pericarditis:
exudates of blood admixed with fibrinous to suppurative effusion
follows cardiac surgery or is associated with tuberculosis or malignancy.
It usually organizes with or without calcification.
Caseous pericarditis:
This form is due to tuberculosis (by direct extension from neighbouring lymphnodes) or less commonly, mycotic infection.
causes fibrocalcific constrictive
Chronic pericarditis
Organization produces plaque-like fibrous thickenings of the serosal membranes (“soldier’s plaque”) or thin, delicate adhesions
Types: Adhesive pericarditis (in rheumatic disease) Adhesive mediastinopericarditis (the pericardial sac is obliterated ) Constrictive pericarditis (pericardial space is obliterated by a dense fibrous tissue, often calcified)
cardiac tamponade
compression of the heart due to accumulation of fluid or blood in the peridacial sac. limitaion of ventricular diastolic filling, red of SV amd CO
METABOLITES
MEDIATORS FOR THE VASODLATIONthat accompies increased cardiac work. other shit like adenosine has the greatest vasodilator effect
Congenital Heart Disease
Abnormalities of the heart or great vessels that are present from birth.
The most common type of heart disease among children.
The incidence is higher in premature infants and in stillborns.
Some forms of produce manifestations soon after birth, others not become evident until adulthood
Atrial septal defect
A heart condition called Atrial Septal Defect is characterized by an opening between the atria. This allows extra blood flow and leads to an enlargement of the right heart and pulmonary arteries.
Tetralogy of Fallot
Heart condition called Tetralogy of Fallot can lead to insufficient blood flow to the lungs and a weakening of the right ventricle.
Ventricular septal defect
also called a hole in the heart, is a common heart defect that’s present at birth (congenital). The defect involves an opening (hole) in the heart forming between the heart’s lower chambers, allowing oxygen-rich and oxygen-poor blood to mix.
Most CommonCongenital Heart Diseases arise from
Most arise from faulty embryogenesis during gestational weeks 3 through 8, when major cardiovascular structures develop.
Defects compatible with embryologic maturation and birth are morphogenetic defects of individual chambers or regions of the heart, with the remainder of the heart developing relatively normally
ventricular septal defect
Are classified according to size and location
Most are about the size of the aortic valve orifice
Ischemic Heart Disease
Common Health problem. High Mortality & Morbidity. Etiology – common Atherosclerosis (next 4 slides) Patterns: -Angina Pectoris -Acute Myocardial Infarction Sudden cardiac death Risk factors: -Hypertension (2d) -Hypercholesterolemia -Diabetes -Smoking, Life style, Diet, Genetic
Congestive heart failure:
an inability of theheartto provide sufficient pump action to distributeblood flowto meet the needs of the body.
Pathogenesis of Ischemic Heart Disease
Obstruction to blood flow. -Atheroma, Thrombosis Diminished coronary perfusion Ischemia Angina Infarction Necrosis -Inflammation -Granulation tissue -Fibrous scarring.
Atheroma
is an accumulation and swelling in artery walls made up of (mostly) macrophage cells, or debris, and containing lipids (cholesterol)
Angina
is a chest pain or discomfort that occurs if an area of your heart muscle doesn’t get enough oxygen-rich blood
Thrombosis
is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system
Myocardial Infarction-MI
“Death of heart tissue due to lack of blood supply”
Atherosclerosis is the common cause
Coagulative necrosis – intact cell shape
Severe chest pain, breathlessness & sweating
Complications – cardiogenic shock, Death or Cardiac failure.
Cardiogenic shock:
a condition in which a suddenly weakened heart isn’t able to pump enough blood to meet the body’s needs
Cellular changes in MI
Reversible
• Glycogen depletion
• Mitochondrial swelling
Irreversible
• Myofibril disruption
• Sarcolemmal disruption
• Mitochondrial deposits
Progression of myocardial necrosis after coronary artery occlusion
Necrosis begins in a small zone of the myocardium.
This entire region of myocardium (shaded) depends on the occluded vessel for perfusion and is the area at risk.
The end result of the obstruction to blood flow is necrosis of the muscle that was dependent on perfusion from the coronary artery obstructed.
Nearly the entire area at risk loses viability. The process is called myocardial infarction, and the region of necrotic muscle is a myocardial infarct.
Complications of MI
Cardiogenic shock, death Arrhythmias and conduction defects Congestive heart failure (pulmonary edema) Mural thrombosis Myocardial wall rupture Ventricular aneurysm
OUTCOME OF MYOCARDIAL INFATRACT
1ST DAY= sudden death and arrhythmia
first week= arrhythmia, chf, shock, heart rupture
first year= chf, arrhythmia, aneurysm
chronic left heart weakness= chf, infarcts, arrhythmia
Congestive Heart Failure
Cardiac output insufficient for metabolic requirements of the body
Systolic dysfunction – decreased myocardial contractility
Diastolic dysfunction – insufficient expansion for ventricular volume
Problems are accentuated by increased demand – high output heart failure
Rheumatic fever (RF)
acute, immunologically mediated, multisystem inflammatory
occurs a few weeks following an episode of group A streptococcal pharyngitis (not skin infection)
Acute rheumatic carditis may progress to chronic rheumatic heart disease (RHD) chronic valvular deformities (mitral stenosis )
Chronic Rheumatic Heart Disease
organization of the acute inflammation and subsequent fibrosis
mitral valve is virtually always abnormal
irregular thickening and calcification of its leaflets,
often with fusion of its commissures
aortic valve, the 2nd most commonly involved valve stenosis or insufficiency
–RHD is overwhelmingly the most frequent cause of mitral stenosis (99% of cases).
Stenosis
“narrowing” is an abnormal narrowing in a blood vessel or other tubular organ or structure
Infectious Diseases of the Heart
Endocarditis
Myocarditis
Pericarditis
Endocarditis
Microbial infection of the endocardial surface
The characteristic lesion, a vegetation*, is composed of a collection of platelets, fibrin, microorganisms, and inflammatory cells
Involves most commonly heart valves
Endocarditis may develop on:
- Previously normal valves
- Deformed valves
- Artificial (prosthetic) valves
Predisposing influences - host factors
- neutropenia, immunodeficiency, malignancy, therapeutic -immunosuppression,
- diabetes mellitus
- alcohol
- intravenous drug abuse
Bacterial Endocarditis
vegetation is composed of a collection of platelets, fibrin, microorganisms, and inflammatory cells
Causes of Infectious Myocarditis
Viruses (most common)
Bacteria (immunosuppressed persons or in sepsis)
Parasites & protozoa (e.g., Trypanosoma cruzi)
Causes of Pericarditis
Viruses (most common) Bacteria Fungi (rare) Rheumatic heart disease Open heart surgery
Cardiac Tumors
Rare
Most common primary tumor: atrial myxoma, which is benign; can be removed surgically
Metastases: most often from lung cancer; involve pericardium
Diseases of Veins
Varicose veins
Thrombi
Thrombophlebitis
Myocardial diseases
Infectious / Inflammatory (myocarditis) Metabolic Developmental / Degenerative Toxic-metabolic Neoplastic
Clinical, functional, and pathologic patterns
Types:
Dilated cardiomyopathy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
The dilated form is most common (90% of cases)
Each of these patterns can be either idiopathic or due to a specific identifiable cause
Dilated cardiomyopathy
LEFT VENT EJECTION FRACTION=
Hypertrophic cardiomyopathy
Restrictive
LEFT VENT EJECTION FRACTION=50-80%, diastolic dysfunction, genetic,
Restrictive cardiomyopathy
LEFT VENT EJECTION FRACTION= 45-90%, DIASTOLIC DYSFUNCTION, idiopathic , pericardial constriction
Myocarditis morphology
Dilated cardiomyopathy pattern- Gross –dilated, flabby heart, pale patches with hemorrhage
Microscopic – interstitial inflammatory infiltrate with myocyte necrosis, fibrosis
Mononuclear cells – idiopathic or viral
Neutrophils – bacterial
Eosinophils –hypersensitivity or protozoa
Granulomatous – TB or sarcoid
Diphtheria myocarditis –
due to a toxin rather than bacterial invasion. There is
some inflammation, myocyte changes
Giant Cell Myocarditis
Myocyte necrosis
Multinucleated giant cells
Lymphocytes, plasma cells, macrophages, eosinophils, and neutrophils
Often fulminant, rapid progression to death
Differential diagnosis – cardiac sarcoidosis
Dilated Cardiomyopathy
Gross – increased weight, dilatation, endocardial fibrosis, normal valves and coronary arteries
Microscopic – myocyte hypertrophy, myofibrillar loss and interstitial fibrosis
Etiology – viral, genetic, toxins
Clinical significance – heart failure & death
Cardiomyopathy –
trichrome stain showing extensive fibrosis (blue) between
the myocytes. The myocytes also vary in size, and some have partial loss of
myofibrils.
Hypertrophic Cardiomyopathy
Etiology – hereditary, mostly autosomal dominant, can appear sporadically
Clinical significance – syncope, arrhythmias and sudden death with a risk of 2-6% per year
Cannot equate with hypertrophy alone!
Hypertrophic Cardiomyopathy
Hypertrophy of ventricular septum (95%) Disarray of myofibers (100%) Volume reduction of ventricles (90%) Endocardial thickening of LV (75%) Mitral valve leaflet thickening (75%) Dilated atria (100%) Abnormal intramural coronaries (50%)
myofiber dysarray
– not all fibers are pulling the same direction
>contraction is ineffective.
However, the cardiac
conduction system can have these same problems, which might cause the
arrhythmias and sudden death these patients tend to die of.
Restrictive Cardiomyopathy
Amyloidosis
Endomyocardial fibrosis – subendocardial fibrosis
Loeffler’s endocarditis – eosinophilic infiltrate
Endocardial fibroelastosis
Amyloidosis –
this heart is thickened, pale, and has a rubbery consistency that
interferes with cardiac expansion during diastole.
Specific Heart Muscle Diseases
Toxic – alcohol, catecholamines, cocaine, Adriamycin
Metabolic – hemochromatosis, hyperthyroidism, hyper/hypoK-emie
Neuromuscular – muscular dystrophy
Storage disease – glycogen, Fabry’s disease
Infiltrative - sarcoidosis
- Becker’s muscular dystrophy
fibrosis and loss of myofibrils in some cells.
Pericarditis
Usually secondary to disorders involving the heart, or adjacent mediastinal structures
Classification on the basis of etiological factors:
Acute nonspecific (idiopathic)
Infective : a) Bacterial b) Viral c) Other infections
Immunologic : a) Rheumatic fever b) Other connective tissue disorder
Neoplastic
Metabolic : a) Uremic b) Myxedema c) Gout.
Traumatic (including after cardiac surgery)
Associated with myocardial infarction
Tumors of the Heart
80% to 90% of primary tumors of the heart are benign
Myxoma
the most common primary tumor of the heart in adults
90% are located in the atria- predilection to fossa ovalis
majority are attached to the endocardium by broad based or pedunculated stalk, ¼ sesile
can be:
-Firm surface and lobular
-Myxoid and gelatinous
-Friable and irregular
Histologically (myoixa)
covered on the surface by endothelium
stellate or globular myxoma (“lepidic”) cells, endothelial cells, smooth muscle cells, and undifferentiated cells
embedded within an abundant acid MPZ ground substance and
peculiar structures ~ glands or vessels are characteristic.
hemorrhage and mononuclear inflammation are usually present.
Papillary fibroelastoma
incidental, lesions, most often identified at autopsy
occurs on endocardial surfaces – sites of greatest hemodynamic stress
cluster of hair-like projections up to 1 cm in diameter
avascular myxoid connective tissue containing abundant MPZ matrix and elastic fibers covered by endothelium,
Lipoma
- Rare (~3% of primary cardiac tumors)
- Predominantly adults
- Occur in the subendocardium, myocardium and subepicardium
- Symptoms related to local tissue encroachment (arrhythmia, heart block, and sudden death)
- Circumscribed, spherical or elliptical mass
- Composed of mature adipocytes
- Differ from lipomatous hypertrophy of IAS=interatrial septum:
- -Usually encapsulated
- -No brown fat cells
- -No myocytes found
Lipomatous septal hypertrophy
Not a true tumor Exaggerated growth of normal fat in IAS Up to 2cm in thickness Seen in elderly and obese people Only consider surger if symptomatic: Atrial arrhythmias and Heart block
Rhabdomyomas
Primarily pediatric
Usually age
Fibromas
Second most common tumor in children
Firm, white, bulging well circumscribed mass
Usually involves ventricle
Calcification is common
May markedly cellular in young patients – DDx fibrosarcoma
Cardiac arrhythmias,
heart failure
Teratoma
Obviously a pediatric issue
Arise within pericardium
Benign in nature but cause drastic complications via tamponade
High risk of death in-utero or after birth
Hemangiomas
Found at any age but tend to occur in adults
Two basic pathologic type
circumscribed type - cavernous vascular spaces with a myxoid background
Infiltrating type - more symptoms
Symptoms: arrhythmias, pericardial effusions, congestive heart failure
Associated with GI tract or skin hemangioma (Kasabach-Merritt syndrome)
Paraganglioma
Extremely rare
Arise from chromaffin cells, mainly in atria
Majority produce catecholamines
Positive biomarkers similar to pheocromocytoma
20% of patients also have extracardiac tumor
Surgical excision is definitive treatment
chief cells arranged in clusters, “zellballen” surrounded by capillary network
most common malignant tumors
in adults=angiosarcoma= 28%
rhabdomyosarcoma, children 41%, infants, 50%
Sarcomas
Constitute most of all malignant tumors
Overall, 2nd most common cardiac tumor
Virtually all cell types have been reported
Clinical presentation depends on location, rather than its histopathology.
Angiosarcoma
Composed of malignant cells that form vascular channels
Predominantly in the right atrium
Leiomyosarcomas
Spindle-celled, high-grade tumors
Arise in the left atrium
High rate of local recurrence and systemic spread
Lymphoma
Very rare Typically non-Hodgkin type Mostly occur in the immunocompromised Presentation: progressive heart failure, chest pain, tamponade,SVC syndrome Can be multiple, firm white nodules Can be fish-flesh homogenous appearance More than one cardiac chamber Pericardiac effusion is common
