Session 6 Flashcards

1
Q

Describe the age distribution of TB infections in the UK.

A

Very few infections in the very young or very old, peak in middle aged people in late 20s/early 30s.

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2
Q

What causes TB?

A

Bactria belonging to the Mycobacterium tuberculosis complex: 7 species such as M. tuberculosis, M. bovis, M. africanum.

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3
Q

Describe the properties of Mycobacterium tuberculosis.

A

Non-motile; rod-shaped; obligate aerobe; mycolic acids, complex waxes and glycolipids make cell wall very thick, rigid and resistant to staining; slow-growing.

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4
Q

What staining is done when looking for TB causative organisms?

A

Acid alcohol fast staining as gram staining is ineffective because of the bacterias thick cell wall.

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5
Q

How is TB spread?

A

Via droplets produced in sneezing, coughing, etc.

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6
Q

How long must someone typically be exposed to TB before they will acquire it?

A

Prolonged exposure of typically 8 hours/a day to 6 months.

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7
Q

Describe the pathogenesis of a primary TB infection.

A

Pathogen is inhaled and engulfed by alveolar macrophages; can multiply within macrophages and resist destruction; macrophages move to local lymph nodes; primary complex is formed of Ghon’s focus and a draining lymph node and the TB infection begins.

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8
Q

How may latent TB develop?

A

If a primary TB infection is contained in the lungs it may remain there inactively and cause post-primary TB if the bacteria overcome the body’s immune defences later on.

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9
Q

Describe the features of latent TB on examination.

A

Bacterial contained so CXR usually normal, negative sputum cultures, no symptoms, not infectious, TST or IFN gamma test results are usually positive.

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10
Q

Describe the main features of TB disease on examination.

A

Abnormal CXR, positive sputum cultures, cough, fever, weight loss, often infectious, positive TST or blood tests.

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11
Q

What are the risk factors of reactivation of TB?

A

HIV, substance abuse, long-term corticosteroid use, immunosuppressive therapy, TNF-alpha antagonists, organ transplant, haematological malignancy, kidney disease/dialysis, DM, silicosis, low weight.

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12
Q

What is a caseating granulomata?

A

A mass of dead/dying inflammatory cells in the lung parenchyma or mediastinal lymph nodes, usually due to TB infection.

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13
Q

Where is extrapulmonary TB likely to affect?

A

Larynx, lymph nodes, pleura, brain, kidneys, bones, joints.

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14
Q

In whom is extrapulmonary TB typically found?

A

Hiv-infected/immunocompromised people, young children.

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15
Q

What is miliary TB?

A

Rare and severe TB infection where the infection is carried to all parts of the body via the bloodstream.

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16
Q

What are the risk factors in contracting TB?

A

Travel history (mainly south Asia and sub-saharan Africa), HIV, immunocompromisation, homeless, drug users, prisoners, people in close contact with sufferers, young adults.

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17
Q

What causes the symptoms of TB?

A

Macrophages releasing cytokines.

18
Q

How is TB investigated?

A

CXR, sputum early morning samples, induced sputum, bronchoscopy.

19
Q

What laboratory tests are performed in ?TB?

A

Sputum smears, Ziehl Nielsen/auramine staining, gastric aspirates in children, cultures (gold standard).

20
Q

What is TST testing?

A

Tuberculin sensitivity testing to assess immune response in order to test for latent TB.

21
Q

What are IGRAs in TB testing?

A

Interferon gamma releasing assays used to detect TB infection, but cannot distinguish between latent and active TB infections.

22
Q

What drugs are given to treat TB?

A

First line: rifampicin, isoniazid, pyrazinamide, ethambutol. Second line: quinolones, ethionamide, cycloserine, etc.

23
Q

How is TB treated?

A

Combination therapy with anti TB drugs and vit D, close monitoring and compliance. May consider surgery

24
Q

Why is combination therapy used in TB?

A

The causative bacteria are quick to mutate and can confer increased resistance so the infection is more difficult to treat.

25
Q

How is TB treatment adherence ensured?

A

Via directly observed therapy or video observed therapy so it is ensured that patients are definitely taking medications properly.

26
Q

What is MDR TB resistant to?

A

Rifampicin and isoniazid.

27
Q

What is XDR YB resistant to?

A

Fluoroquinolones and at least one injectable.

28
Q

How is resistant TB treated?

A

4/5 drug regime over a longer duration using quinolones, aminoglycosides, PAS, cycloserine, ethionamide, etc.

29
Q

How is TB prevented?

A

Disease is notifiable by law to Public Health England to monitor spread and trigger tracing procedures; PPI and negative pressure isolation used in treatment; susceptibility of sufferer’s contacts is reduced via addressing risk factors and vaccination; BCG given to at risk groups.

30
Q

Define asthma.

A

Chronic inflammatory disorder of the airways resulting in reversible airway obstruction, inflammation, bronchoconstriction and increased mucus production.

31
Q

Describe the pathogenesis of asthma.

A

Allergen binding to IgE on mast cells causes activation of the Th-1 and Th-2 responses via IL-12, this causes cytokine release which produces the symptoms of asthma (type 1 hypersensitivity reaction).

32
Q

What do repeated asthma attacks lead to/

A

Remodelling causing damaged epithelium which leads to increased smooth muscle thickness.

33
Q

What is the effect of asthma on the FEV1.0/FVC ratio?

A

Decreases it as air takes longer to enter the lungs due to the obstructive pathology.

34
Q

How does asthma usually present?

A

Tight chested, persistent cough (often worse at night, exercise-induced or dry), attacks where can’t breathe, wheeze, breathlessness.

35
Q

Define a respiratory wheeze.

A

High pitched, expiratory musical sound due to narrowed airways.

36
Q

Define stridor.

A

High pitched, inspiratory musical sound.

37
Q

What is useful in taking a history for asthma?

A

Full symptom history, PMH for other allergies, family history, social history for allergens, drug history for exacerbating medications (ACE-I, beta-blockers).

38
Q

How is asthma managed?

A

Educate patients on how to use inhalers, prevent exacerbations by reducing allergens

39
Q

How is asthma treated initially?

A

Give bronchodilators for a moth then review to see if improvement, if improved then continue to treat as asthma.

40
Q

What treatment options can be given for more severe asthma?

A

Short acting beta agonist inhalers, steroid inhalers, long acting beta agonist inhalers, steroid tablets.

41
Q

What treatment should be given for a severe asthma attack?

A

Salbutamol nebs and oxygen or IV salbutamol if very severe, if life-threatening then consider intubation and ITU.