Rheumatic Heart Disease_patho.diagram

Predisposing Factors: • Familial tendency • 5-15 years old • Female • Poor living conditions

Etiology: Group A-beta hemolytic streptococcus

Activated antigenpresenting cells present the bacterial antigen to helper T-cells

Helper T-cells subsequently activate Bcells

Induce the production of antibodies against the cell wall of the streptococcus

M-protein in the cell wall of the streptococcus induces cross-reactivity

Antibodies cross-react with cardiac myosin, and antigens of tissue glycoprotein in the joints, skin, brain, and other connective tissues

A

•

Precipitating Factor: History of group Abeta hemolytic streptococcus pharyngeal infection (strep throat)

A

Induces cytokine release S/Sx: Syndenham chorea Carditis Polyarthritis Erythema marginatum Subcutaneous nodules Arthralgia Fever Elevated ESR Prolonged PR interval

• Diagnostic Tests: • JONES criteria • Strep throat culture • ESR • WBC • ECG

Induce the expression of E-selectin

Inflammatory response If unmanaged and if there is subsequent exposure to the antigen

• • • • • • • •

Subsequent re-infiltration by lymphocytes and cycle of scarring

Fibroid necrosis and verrucae formation along the lines of closure of the left sided heart valves Diagnostic Tests: • ECG • Doppler investigation

Leaflet thickening, commissural fusion, shortening and thickening of tendinous chords

• • •

Mgt.: Percutaneous mitral balloon valvotomy Open mitral commissurotomy Mitral valve replacement

•

•

Mgt.: Antiinflammatory medications such as aspirin and corticosteroi ds Low-dose antibiotics such as penicillin, erythromycin and sulfadiazine

B B

Decrease blood flow from the left atrium into the left ventricle during diastole

Increase blood volume and pressure in the left atrium

•

Mgt.: Digitalis

Decrease cardiac output Stimulates SNS

Decrease blood flow from the pulmonary vessels

Release of epinephrine and norepinephrine

Increase pulmonary venous blood flow and pressure

Diagno stic Test:

Pulmonary congestion

• Chest radiography

S/Sx: • Dyspnea • Cough • Pulmonary crackles

• •

Mgt.: Avoidance of excessive fluid intake Oxygen therapy

Continuous response causes loss of beta 1-adrenergic receptor cells

Further damage to the heart muscles

Pulmonary edema

Impairs gas exchange

•

S/Sx: Lower-thannormal oxygen saturation levels

•

Mgt.: Oxygen therapy

Decreases renal perfusion

Release of renin by the kidneys

C D

C

D

Pulmonary hypertension

Formation of angiotensin

Respiratory failure

ACE converts angiotensin I to angiotensin II

Right ventricular failure

Promotes the release of aldosterone

Congestion of the viscera and peripheral tissues

• •

S/Sx: JVD Edema

Blood backs up in the hepatic veins

Liver becomes engorged

Increase pressure within the portal vessels

Portal hypertension

G

•

Mgt.: Diuretics

Promotes sodium and water retention

Increases preload and afterload

•

S/Sx: Hepatomegaly

Further increases the stress on ventricular wall

Further increase in the workload of the heart

E

F

E

F

Force fluid into the abdominal cavity

• • •

•

Mgt.: Diuretics Paracentesi s Sodium restriction Mgt.: Antibiotics

Ascites

•

If unmanaged

• •

Spontaneous bacterial peritonitis

• • •

G

S/Sx: Abdomina l pain Anorexia Nausea

Further increases ventricular pressure and resistance to ventricular filling

Venous collaterals develop Abnormal varicoid vessels

S/Sx: n/v Abdominal pain Fever

Subsequent decrease in cardiac output

Prone to rupture and bleeding

If unmanaged Bleeding

Diagnostic Sepsis

Increases the thickness of the heart muscle

Development of high pressure gradient between portal vein and inferior vena cava

Test:

If unmanaged

Mgt.: • Vasopress in • Balloon Tamponade

Hemorrhagic shock

DEATH • •

Mgt.: Dialysis Renal

transplantati

• • • • • • • •

S/Sx: HPN Edema Hyperkalemia Anemia Acidosis Osteodystrophi es Hypocalcemia Hyper-

Successive decrease in renal perfusion

S/Sx: S har p in u.o. • in BU N •

Decreases GFR Further decrease in GFR

Accumulation of nitrogenous wastes; alterations in water, electrolyte, and acidbase balance; inactivation of Vitamin D; disruption in erythropoietin production

Increase risk of infection

I I

Actual Infection If unmanaged Sepsis

DEATH

•

Mgt.: Antibiotics