pathophysiology-of-tuberculosis-02

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Pathophysiology of Koch’s Disease (Tuberculosis) Predisposing Factors: Precipitating Factors: Age - Occupation (e.g Health Workers) Immunosuppression - Repeated close contact w/ infected persons o Prolonged corticosteroid therapy - Indefinite substance abuse via IV Systemic Infection: - recurrence of infection o Diabetes Mellitus o End-stage Renal Disease o HIV or AIDS infection Exposure or inhalation of infected Aerosol through droplet nuclei (exposure to infected clients by coughing, sneezing, talking) Tubercle bacilli invasion in the apices of the Lungs or near the pleurae of the lower lobes Bronchopneumonia develops in the lung tissue (Phagocytosed tubercle bacilli are ingested by macrophages) bacterial cell wall binds with macrophages arrest of a phagosome which results to bacilli replication Necrotic Degeneration occurs (production of cavities filled with cheese-like mass of tubercle bacilli, dead WBCs, necrotic lung tissue) drainage of necrotic materials into the tracheobronchial tree (eruption of coughing, formation of lesions) PRIMARY INFECTION Lesions may calcify (Ghon’s Complex) and form scars and may heal over a period of time Tubercle bacilli immunity develops

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Page 1: Pathophysiology-of-Tuberculosis-02

Pathophysiology of Koch’s Disease(Tuberculosis)

Predisposing Factors: Precipitating Factors:

Age - Occupation (e.g Health Workers) Immunosuppression - Repeated close contact w/ infected persons

o Prolonged corticosteroid therapy - Indefinite substance abuse via IV Systemic Infection: - recurrence of infection

o Diabetes Mellituso End-stage Renal Diseaseo HIV or AIDS infection

Exposure or inhalation of infectedAerosol through droplet nuclei

(exposure to infected clients by coughing,sneezing, talking)

Tubercle bacilli invasion in the apices of the Lungs or near the pleurae of the lower lobes

Bronchopneumonia develops in the lung tissue(Phagocytosed tubercle bacilli are ingested by macrophages)

bacterial cell wall binds with macrophages arrest of a phagosome which results to bacilli replication

Necrotic Degeneration occurs(production of cavities filled with cheese-like

mass of tubercle bacilli, dead WBCs, necrotic lung tissue)

drainage of necrotic materials into the tracheobronchial tree

(eruption of coughing, formation of lesions) PRIMARY INFECTION

Lesions may calcify (Ghon’s Complex)and form scars and may heal

over a period of time

Tubercle bacilli immunity develops(2 to 6 weeks after infection)

(maintains in the body as long as living bacilli remains in the body)

Acquired immunity leads to further growthOf bacilli and development of ACTIVE INFECTION

Page 2: Pathophysiology-of-Tuberculosis-02

SIGNS AND SYMPTOMS

Pulmonary Symptoms: General Symptoms:

Dyspnea - Fatigue Non-productive or productive cough - anorexia Hemoptysis (blood tinge sputum) - Weight loss Chest pain that may be pleuritic or dull - low grade fever with chills and Chest tightness sweats (often at night) Crackles may be present on auscultation

With Medical Intervention Without Medical intervention

Early detection/ diagnosis of the dse Reactivation of the tubercle bacilli Multi-antibacterial therapy (Due to repeated exposure to infected Fixed- dose therapy Individuals, Immunosuppression) TB DOTS (Direct Observed Therapy) SECONDARY INFECTION BCG vaccination

Severe occurrence of lesions in the lungs No Recurrence Recurrence

Cavitation in the lungs occurs Good Prognosis Bad Prognosis

Active infection is spread throughout the body systems (infiltration of tubercle bacilli in other organs)

TB of the Bones Pott’s Disease Renal TB

SEVERE OCCURRENCE OF INFECTION Client becomes clinically ill

BAD PROGNOSIS

DEATH