Cv System - Viral Myocarditis/chagas Disease By Blue/jackson

Front 1

What is the target for viral myocarditis.

Back 1

myocytes. that's where you get the damage, inflammation, edema, swelling. this will cause difficulty pumping, pain, etc. because of the thickened myocardium.

Front 2

the primary viral causative agents of myocarditis?

Back 2

Major Causes:
Coxackievirus B
Adenovirus
*90% combined cause of myocarditis

Minor Causes:
Coxackievirus A
HIV
Herpes Simplex Virus
Echovirus
Influenza A and B viruses

Front 3

What is the CAR receptor?

Back 3

Coxackievirus/Adenovirus Receptor:
The specific receptor that allows attachment and eventual infection of heart myocytes. It's the direct receptor for coxackie B Virus and adenovirus. CVB3 just needs the CAR to bind to the myocyte, but the adenovirus needs the CAR as well as a coreceptor in order for successful infection.

Front 4

Where are CAR receptors?

Back 4

On a wide variety of tissues. There's a broad spectrum of disease that CVB can attach, but since the adenovirus needs that coreceptor, it's limited primarily to respiratory tract infections and myocyte infections.

Front 5

What determines the severity of the disease?

Back 5

the abundance of the CAR receptor and the susceptibility of the host in terms.

Front 6

Compare neonatal myocarditis to adolescent/adult seriousness and why the difference.

Back 6

neonatal is far more serious. this is because there's an abundance of CAR receptor on the myocytes right after birth. As time goes on, the amount of CAR receptor diminishes, so you become less susceptible to infection of the myocytes by CVB.

Front 7

Which viruses and numbers are responsible most for neonatal myocarditis?

Back 7

Coxackievirus B types 2-5 (3,4 are 80%)

adenovirus 2,5 (20%)

HSV-2 (in neonatal herpes)- will see multiple syndromes of diseases.

Front 8

For newborns...What percent of viruses is acquired from the mother? nosocomially (hospital staff)?

Back 8

mother- 60-70%

nosocomially- 30-40%

*most often from common cold

Front 9

Again, why is neonatal viral myocarditis worse?

Back 9

1. heavy receptor density in newborn
2. insufficient specific and non-specific immune responses
3. rapid, extensive necrosis
4. timing of maternal infection (and transfer) probably critical. Summer/fall you see CVB

*worst in the first 7 days. infants will appear listless, anorexic, and with resp. distress. myocarditis can be alone or couple with encephalitis or hepatitis. Mortality rate is 50-75%.

Front 10

What diagnostic techniques are useful for identifying the viral causative agents?

Back 10

-Symptoms (tachypnea, tachycardia, anorexia, diaphoresis)
-EKG
-Isolate, detect virus/nucleic acid from any site (post-mortem)
-differentiate from congenital heart disease, HSV-2 neonatal infection, bacterial sepsis.

Treatment is supportive, fluid management, digoxin, diuretics, ACE-I.
*ribavirin (antiviral) is too toxic.

Front 11

Adolescent and Adult pathogenesis

Back 11

75% CVB
Often following respiratory or GI infection, rash.

1. infection of heart myocytes
2. unsually limited and transient necrosis. outcomes:
-asymptomatic
-transient inflammatory, full recovery
-chronic
-auto-immune damage, mediated by CYTOTOXIC T LYMPHOCYTES, Ab and macrophages

Front 12

Etiology for adolescents/adults

Back 12

Viremia- resp tract infection, virus carried to lymph nodes where there's replication, release into blood stream, direct access to heart, and infection by that way.
Receptors- less receptors, so limited damage.
Auto-immune component-seriousness of the disease is dependent upon the reaction/overreaction of the immune system to the initial incident damage and the immune system carrying on the damage to the heart. that's why it can become chronic and possible need for heart transplant.

Front 13

Epidemiology

Back 13

likely preceded by a cold, flu-like or GI symptoms.
-sporadic
-male incidence twice that of females
-incidence decrease with age.

Front 14

Describe myosin's involvement in all of this.

Back 14

When myocyte is damaged, myosin is released. Myosin is known as a sequestered antigen, which means it is not recognized as self. So when myosin is released, this stimulates the immune system by cell-mediated and antibody production to attack it. The immune system takes over, so there's continuous attack of the myocytes through this priming by myosin.

Front 15

Treatment for adults

Back 15

supportive, bed rest, antiarrhythmic agents. usually it'll resolve on it's own.

Front 16

What organism causes chagas?

Back 16

trypanosoma cruzi, a single celled organism. they have a stage with flagella and undulating membrane (protozoan).

Front 17

What is acute chagas?

Back 17

signs/symptoms of arrhythmia or cardiac failure along with chagoma, Romana's sign, with history of presence in South or Central America.

Front 18

What is chronic chagas?

Back 18

signs/symptoms of arrhythmia or cardiac failure, along with signs of megaesophagus or megacolon, with history in South/Central America.

Front 19

What cell type do these organisms target once in the blood?

Back 19

muscle cells (cardiac and others). also will attack leukocytes, cells in spleen/liver.

Front 20

Once they get into the cell, what happens?

Back 20

Once they get into the cell, they change their morphology. They get round and smaller. they multiply out of control and lyse the cell, causing damage.

Front 21

How do you pass this small organism to humans?

Back 21

via an insect vector. The bug is called triatomid insect. aka Kissing Bug. it feeds around the face, bites, scratches, then defecates on your FACE! So you rub it in, gets in the blood stream, and then the organisms are loose in the system. people in rural, poorer socioeconomic areas have to worry about these bugs.

Front 22

Whats an important cause of cardiomyopathy particularly in South and Central America?

Back 22

Chagas Disease.