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35 Cards in this Set
- Front
- Back
define myocarditis
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inflammation of the myocardium; infectious microorgs, toxins or autoimmune inflammatory processes cause myocardial injury
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adult incidence of myocarditis
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10/100,000 - 5/100
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neonatal incidence
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60-70% acquired from mother; 30-40% acquired from hospital staff (nosocomial); Mortality rate is 50-75% with death within 1 week
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myocarditis etiological agents
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-adenovirus
-coxsackie virus (enterovirus) -trypanosoma cruzi |
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most common cause of myocarditis in kids
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adenovirus
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most common cause of myocarditis in adults
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coxsackie virus
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cinical presentation of myocarditis
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protean Sx: fatigue, dyspnea; Diffuse mononuclear inflammatory infiltrate is most common; acute, subacute or chronic; Survival: inflammatory lesions resolve or heal by progressive fibrosis
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Viral myocarditis - Pathophys Phase 1: Viral
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Adenovirus and coxsackievirus enter via the GI or respiratory system by binding the coxsackie-adenoviral receptor (CAR), a junctional protein that is highly expressed in the heart, brain and gut
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Viral myocarditis - Pathophys Phase 2: Immune Response
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Virus or the immune response (innate immune response and CTLs) cause acute injury leading to cardiac damage
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Viral myocarditis - Pathophys Phase 3: Cardiac Remodeling
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virus-mediated cardiac injury and the immune response may destroy heart tissue acutely or linger and produce cardiac remodeling leading to cardiomyopathies, heart failure or death
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myocarditis most likely outcome for otherwise healthy patients
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typically resolves without complication
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myocarditis diagnostics
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PCR and in situ hybridization (molecular tools to detect viral nucleic acid); newer imaging techniques such as PET-CT (detects inflammation of the myocardium). Cardiac magnetic resonance imaging (CMR) allows visualization of the entire myocardium (pre/post contrast)
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myocarditis therapeutics
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Type I interferons exert anti-viral activity; immunoglobulins (IVIG to block the autoimmune component) and antiviral agents. Immunosuppressants - unclear if useful; the immune response is as much protective as it is harmful
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Why are the unrelated coxsackie and adenoviruses both major causes of myocarditis?
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both enter via the GI or respiratory system by binding the *coxsackie-adenoviral receptor (CAR)*, a junctional protein that is highly expressed in the heart, brain and gut
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What type of patients have poor prognosis with myocarditis?
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Less common viral causes occur mostly in immunocompromised patients: CMV, HIV (HIV-associated myocarditis = poor prognosis)
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picornaviruses
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literally means small RNA virus;
Non-enveloped RNA viruses with an icosahedral capsid- enteroviruses, Hep A and Rhinoviruses. |
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Myocarditis - Non-viral causes
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Virtually any bacterial agent can cause myocardial damage due to release of inflammatory mediators (activation of Toll-like receptors and production of inflammatory cytokines such as TNF-a)
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Toxic myocarditis
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may occur in diptheria
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Myocarditis occurs in 5% of ______ disease patients (Borrelia burgdorferi)
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Lyme Dz
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diptheria
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is an acute infectious disease caused by the bacteria Corynebacterium diphtheriae
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myocarditis morphological features
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-Lymphocytic myocarditis
-Hypersensitivity myocarditis -Giant-cell myocarditis -The myocarditis of Chagas disease |
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In situ hydridization
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detects presence of viral
DNA (blue stain) |
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viral myocarditis antigenic mimicry
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T cells and antibodies can react with viral proteins that mimic those of the host (ex. cardiac myosin) - this is termed molecular or antigenic mimicry and it can trigger autoimmunity [don't forget APC involvement; look at slides 26-28]
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A 6-day old baby is brought to the emergency department with a 2-day history of tachypnea, tachycardia and diaphoresis. The baby has a fever, is anorexic and is in acute respiratory distress. The baby’s mother has a runny nose, headache and sore throat. The most likely etiology of the baby’s symptoms is:
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adenovirus infection
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Myocarditis - Diagnosis
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auscultation: rarely audilbe
ECG: rule out Blood: increase in creatine kinase or appearance of troponin may indicate myocyte necrosis (myocytolysis); autoantibodies may appear only later in the disease process Heart biopsy: detect presence of inflammatory cells simultaneous with evidence of myocyte degeneration or necrosis on same section of the biopsy specimen. Serology is of limited value |
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Myocarditis - Treatment
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supportive care, bed rest, cardiac monitoring, anti-arrhythmic agents, fluid management, drugs to treat heart failure
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A 20-year old man with no previous cardiac history presents with severe acute chest pain, fatigue, dyspnea and palpitations. He appears healthy, denies narcotic use and has not traveled outside of the US in the past year. The most likely etiology is:
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Most of these can cause myocarditis but the most common cause, especially as the patient has not traveled outside the US, is Coxsackievirus.
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In the previous case a cardiac biopsy is performed and analyzed by the polymerase chain reaction (PCR) to detect:
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Viral nucleic acid-PCR detects nucleic acid by amplifying specific genomes of a given virus. Viral antibodies may be present but this does not definitively indicate a viral cause of myocarditis. In addition, antibodies may arise a few weeks following the onset of symptoms and thus may not be detected when serology is performed.
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In the previous case, if the patient’s blood showed elevated anti-viral antibodies, the mechanism involved in the patient’s disease would most likely be due to virus activation of:
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Toll-like receptors- Viruses, like all microbes, bear pathogen-associated molecular patterns, such as viral nucleic acid, that activate toll-like receptors resulting in the activation of innate immune responses.
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Chagas Dz
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[American trypanosomiasis]
Infectious agent : Trypanosoma cruzi (flagellated protozoan) |
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Diseases of Trypanosomes
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Chagas disease – American trypanosomiasis (kissing bug vector)
African sleeping sickness – African trypanosomiasis (tsetse fly vector) |
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Triatomid insect = reduviid = “Kissing bug”
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Bloodsucker, likes faces… bites and then poops out a parasite which you scratch and cause bodily entrance. Parasite likes heart and nerves. Morphology of parasite changes to round form and multiply within cells, change to flagelated form and spread to other areas.
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Chagas Acute Phase
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-1-2 weeks
-Usually mild; weeks to month -Fever, fatigue, rash -Swelling at infection site; Chagoma -Rarely, myocarditis |
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Chagas chronic phase
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-10-30 years
-Palpitations, dyspnea, syncope due to enlarged heart, altered heart rate or rhythm (may be fatal) -Dysphagia or constipation → due to mega-esophagus, mega-colon |
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Key factors for Dx of Chagas
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Romanas sign (one swollen-shut eye) and recent trip to South America
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