Pulmonary tuberculosis Flashcards

1
Q

what is the definition of TB?

A

Pulmonary tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. In many patients, M tuberculosis becomes dormant before it progresses to active TB. TB most commonly involves the lungs and is communicable in this form, but may affect almost any organ system including the lymph nodes, central nervous system, liver, bones, genitourinary tract, and gastrointestinal tract.

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2
Q

what is the epidemiology of TB?

A

More devastating in area with a high prevalence of HIV

More common in africa and southeast asia

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3
Q

what is the aetiology of TB?

A

The development of TB requires infection by Mycobacterium tuberculosis and inadequate containment by the immune system. Patients infected with M tuberculosis who have no clinical, bacteriological, or radiographic evidence of active TB are said to have latent TB infection. Active TB may occur from re-activation of previously latent infection or from progression of primary infection.
Transmission of TB occurs from individuals infected with pulmonary (and rarely laryngeal) disease. Infection results from the inhalation of aerosolized droplets containing the bacterium.

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4
Q

what are the risk factors for TB?

A
Exposure to infection 
Birth in an endemic country 
HIV
Immunosuppression 
Silicosis 
apical  fibrosis
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5
Q

what is the pathophysiology of TB?

A

Infection with TB requires inhalation of droplet nuclei. Following deposition in the alveoli, Mycobacterium tuberculosis is engulfed by alveolar macrophages, but survives and multiplies within the macrophages. Proliferating bacilli kill macrophages and are released; this event produces a response from the immune system. Exposure may lead to clearance of M tuberculosis, persistent latent infection, or progression to primary disease.
Successful containment of TB is dependent on the cellular immune system, mediated primarily through T-helper cells (TH1 response). T cells and macrophages form a granuloma with a centre that contains necrotic material (caseous centre), M tuberculosis, and peripheral granulation tissue consisting primarily of macrophages and lymphocytes; the granuloma serves to prevent further growth and spread of M tuberculosis. These individuals are non-infectious and have latent TB infection; the majority of these patients will have a normal chest x-ray and be tuberculin skin test-positive.
Active TB typically occurs through a process of re-activation. Approximately 10% of individuals with latent infection will progress to active disease over their lifetime. The risk is greatest within the 2 years following initial acquisition of M tuberculosis. A number of conditions can alter this risk, particularly HIV infection, in which the annual risk of developing active TB is 8% to 10%. Immunocompromised conditions and treatment with immunosuppressive medicines, including systemic corticosteroids and tumour necrosis factor-alpha antagonists, also contribute to re-activation.

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6
Q

what are the key presentations of TB?

A
Risk factors 
Cough 
Fever
Anorexia
Weight loss
Malaise
Night sweats 
Chest pain
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7
Q

what are the first line and gold standard investigations for TB?

A

Chest x-ray - abnormal typical for TB; abnormal atypical for TB; or normal, ghon complex
Sputum acid-fast bacilli smear - positive for AFB
Sputum culture - positive; no growth; or other mycobacteria
FBC - raised WBC; low Hb
Nucleic acid amplification test - positive for M tuberculosis
IGRAs - interferon gamma release assay

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8
Q

what is the differential diagnoses for TB?

A

COVID 19
Community acquired pneumonia
Lung cancer

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9
Q

how is TB managed?

A

Active TB non-pregnant:
isoniazid: 5 mg/kg orally once daily, maximum 300 mg/dose; or 15 mg/kg orally twice weekly, maximum 900 mg/dose; or 15 mg/kg orally three times weekly, maximum 900 mg/dose and pyridoxine: 25-50 mg orally once daily; or 50 mg orally twice or three times weekly and rifampicin: 10 mg/kg orally once daily, maximum 600 mg/dose; or 10 mg/kg orally twice weekly, maximum 600 mg/dose; or 10 mg/kg orally three times weekly, maximum 600 mg/dose and pyrazinamide: dose is based on lean body weight and tablet formulation available; consult specialist, guidelines, or local protocols for guidance on dose and ethambutol: dose is based on lean body weight and tablet formulation available; consult specialist, guidelines, or local protocols for guidance on dose
Acute TB pregnant or drug induced hepatic dysfunction:
Specialist consultation

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10
Q

how is TB monitored?

A

Liver function (aminotransferases, bilirubin, alkaline phosphatase) should be checked at baseline prior to starting therapy. Monthly liver function tests should be obtained in patients

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11
Q

what are the complications of TB?

A
Transmission of TB 
IRIS
ARDS
constrictive pericarditis 
side effects of medication - hepatotoxicity
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12
Q

what is the prognosis of TB?

A

Without treatment the mortality rate of TB exceeds 50%; however, TB is a treatable disease.

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13
Q

what stain does Mycobacterium tuberculosis stain with?

A

ziehl-neelsen stain

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14
Q

what type of hypersensitivity reaction is TB?

A

4

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15
Q

what culture agar should be used to identify mycobacterium tuberculosis?

A

lowenstein-jensen

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16
Q

which drug used to treat TB causes optic neuritis?

A

ethambutol

17
Q

which drug used to treat TB causes orange tears and urine?

A

rifampicin

18
Q

what would been see histologically from lung biopsy of a patient with granulomas resulting from a TB infection?

A

epithelioid histiocytes

19
Q

where in the lung does TB most commonly reactivate?

A

apex of the lung

20
Q

what are the adverse effects of rifampicin?

A

mechanism of action: inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

21
Q

what are the adverse effects of isoniazid?

A

mechanism of action: inhibits mycolic acid synthesis
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

22
Q

what are the adverse effects of pyrazinamide?

A

mechanism of action: converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

23
Q

what are the adverse effects of ethambutol?

A

mechanism of action: inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
optic neuritis: check visual acuity before and during treatment
dose needs adjusting in patients with renal impairment