1. Diagnosis for TB
1.1. Screening for latent TB
1.1.1. TST
1.1.1.1. False positive
1.1.1.1.1. BCG vaccine
1.1.2. Interferon- gamma release assay
1.2. Microbiologic testing
1.2.1. Direct smear examination
1.2.1.1. Ziehl-Nelsen stain
1.2.1.2. Fluorecent microscopy
1.2.1.2.1. By Auramine stain
1.2.2. Culture
1.2.2.1. Solid
1.2.2.1.1. Lowenstein - Jensen media
1.2.2.1.2. Result within 1 month
1.2.2.1.3. Less prone to contamination
1.2.2.2. Liquid
1.2.2.2.1. Results within 7 days
1.2.2.2.2. 10% more sen. Than solid
1.2.2.2.3. Prone to contamination
1.2.3. Molecular
1.2.3.1. NAA test
1.3. TB radiological changes
1.3.1. Primary TB
1.3.1.1. consolidation
1.3.1.2. with ipsilateral hilar enlargement due to lymphadenopathy
1.3.1.3. Ghon focus: well-defined focus of calcific density is also seen
1.3.2. Secondary TB
1.3.2.1. Consolidation of upper lobe
1.3.2.2. cavitation of upper lobes
1.3.2.3. with fibro-calcific changes post immune response
1.3.3. Miliary TB
1.3.3.1. Very fine nodules are typically seen scattered throughout the lungs
1.3.3.2. resembling millet seeds
2. TB complication & prognosis
2.1. complications of TB
2.1.1. complications of TB
2.1.1.1. Pulmonary complications of TB:
2.1.1.1.1. Hemoptysis
2.1.1.1.2. Pneumothorax
2.1.1.1.3. Bronchiectasis
2.1.1.1.4. Extensive pulmonary destruction
2.1.1.1.5. Malignancy
2.1.1.1.6. Venous thromboembolism
2.1.1.1.7. Chronic pulmonary aspergillosis
2.1.1.2. Extrapulmonary TB include:
2.1.1.2.1. Miliary tuberculosis
2.2. Prognosis of TB
2.2.1. predictors of a poorer prognosis include
2.2.1.1. Extreme ages
2.2.1.2. Chronic comorbidities
2.2.1.3. Coexistent HIV/ADIS
2.2.1.4. Being on immunocompromising drugs, Smoking, alcoholism
3. Pharmacology of Anti-tuberculosis drugs
3.1. First-line drug for TB
3.1.1. Isoniazid
3.1.1.1. • Converted into its active form by a mycobacterial catalase–peroxidase (KatG)
3.1.1.2. • Disruption of bacterial cell wall.
3.1.1.3. PK: • Orally. • Distributes into all body fluids
3.1.2. Rifamycins
3.1.2.1. e.g. Rifampin, Rifabutin and Rifapentine
3.1.2.2. Interfere with β subunit of mycobacterial DNA-dependent RNA polymerase then blocks RNA synthesis
3.1.3. Pyrazinamide
3.1.3.1. • Oral • Most clinical benefits in early treatment; discontinued after the first 2 months
3.1.4. Ethambutol
3.1.4.1. Bacteriostatic
3.1.4.1.1. Disruption of mycobacterial cell wall
3.1.4.2. Adverse effects: Optic neuritis, red-green color blindness
3.2. Second-line drug for TB
3.2.1. Less effective, more toxic, less extensively
3.2.2. Para-aminosalicylic acid (PAS)
3.2.2.1. Bacteriostatic
3.2.2.1.1. interferes with the folate biosynthetic pathway
3.2.3. Capreomycin
3.2.3.1. Inhibits protein synthesis
3.2.3.2. parenterally
3.2.4. Ethionamide
3.2.4.1. Inhibits the activity of the InhA gene
3.2.4.1.1. impairment of cell wall synthesis
3.2.5. Bedaquiline
3.2.5.1. Inhibits ATP synthase
3.2.6. Pretomanid and Delamanid
3.2.6.1. prodrugs
3.2.6.1.1. require activation by bacterial enzyme
3.2.6.2. Used in treatment (XDR) & (MDR)
3.2.7. Clofazimine
3.2.7.1. Orally absorbed; accumulates in tissues
3.2.7.1.1. Gastrointestinal problems, discoloration of body secretions/eye/skin
3.3. Directly Observed Treatment Short-Course (DOTS)
3.3.1. is a component of case management that helps ensure patients adhere to therapy.
3.3.2. A strategy where trained health-care worker or another trained designated person watches a patient swallow each dose of anti-TB drugs and documents it.
3.3.3. It’s the recommended international strategy for controlling TB.
4. Pleural Effusion
4.1. Fluid accumulation
4.1.1. Chyle ( Chylothorax )
4.1.1.1. lymphatic fluid leakage
4.1.2. bood ( Hemothorax )
4.1.3. Serous fluid
4.1.4. Pus ( Pyothorax )
4.2. Types of effusion
4.2.1. Transudative effusion
4.2.2. Exudative effusion
4.3. Clinical manifestation
4.3.1. Pleuritic chest pain
4.3.2. Fever
4.3.3. Non- Productive cough
4.3.4. Dyspnea
5. Medical errors
5.1. preventable event that may cause or lead to inappropriate medication use or patient harm
5.1.1. choosing medicine
5.1.1.1. knowledge-based error
5.1.1.1.1. contraindications
5.1.1.1.2. allergies
5.1.2. Prescription writing
5.1.2.1. bad handwriting
5.1.2.2. units
5.1.2.3. Abbreviations
5.1.3. Dispensing
5.1.4. Administering
5.1.5. Monitoring
5.1.6. Monitoring
6. Chest physical examination
6.1. Inspection
6.1.1. Hands :
6.1.1.1. Cyanosis
6.1.1.2. Clubbing
6.1.1.3. Wasting of small muscles
6.1.2. FACE
6.1.2.1. Pink puffers
6.1.2.2. Blue bloaters
6.1.2.3. Congested neck veins
6.1.2.4. Rashes
6.1.2.5. Edema
6.1.3. Neck
6.1.3.1. Lymph nodes
6.1.4. Chest
6.1.4.1. Shape
6.1.4.1.1. Pectus excavatum
6.1.4.1.2. Pectus carinatum
6.1.4.2. Dilated veins
6.2. Palpation
6.2.1. Temperature
6.2.2. Heart rate
6.2.3. Trachea deviation
6.2.4. Palpate the Apex beat
6.2.5. Assess chest expansion
6.3. Percussion
6.3.1. Supraclavicular region
6.3.2. Infraclavicular region
6.3.3. Chest wall
6.3.4. Axilla
6.3.5. Types
6.3.5.1. Resonant
6.3.5.1.1. Normal
6.3.5.2. Dullness
6.3.5.2.1. Increased tissue density
6.3.5.3. Stony dullness
6.3.5.3.1. Pleural effusion.
6.3.5.4. Hyper-resonance
6.3.5.4.1. The opposite of dullness
6.4. Auscultation
6.4.1. Vesicular
6.4.1.1. Insp. twice that of expiration
6.4.1.1.1. Normal
6.4.2. Bronchial
6.4.2.1. Inspiration is shorter than expiration
6.4.2.2. Gap between insp. and exp
7. Prevention
7.1. Primordial
7.1.1. Changing environmental and societal determinants in a population that does not have the disease
7.2. Primary
7.2.1. changing risk factors in a susceptible population
7.3. Secondary
7.3.1. tackling the disease in the pre-clinical asymptomatic phase to prevent progression
7.4. Tertiary
7.4.1. tackling the disease in the clinical phase to prevent progression and disability
8. Coughing
8.1. Is a forceful expulsion of air from the lungs that helps to clear secretions, foreign bodies and irritants from the airway
8.2. Classification
8.2.1. Durations
8.2.1.1. Acute
8.2.1.1.1. <3 weeks
8.2.1.1.2. URI
8.2.1.1.3. Acute bronchitis
8.2.1.2. Chronic
8.2.2. Quality
8.2.2.1. Productive
8.2.2.2. Dry
8.2.3. Timing
8.2.3.1. Nocturnal
8.2.3.2. Seasonal