TB clinical cases and therapeutics

Question 1

conversion rate of latent TB to active disease

Answer 1

Conversion:
0.2% average annual risk of active disease

HIV +ve:
8-10% average annual risk c.f. lifetime risk

Question 2

the problem of not treating TB patients

Answer 2

Untreated each index case will infect 10-15 people

Question 3

first line anti-TB drugs

Answer 3

SPIRE

Isoniazid (I)
Rifampicin (R)
Pyrazinamide (P)
Ethambutol (E)
Streptomycin (S)
(Moxifloxacin)

ALL TB – Induction phase
I+R+P+E

Maintenance phase:
CNS TB – I+R 10 months
All other – I+R 4 months

Question 4

second line anti-TB drugs

Answer 4

Amikacin/kanamycin
Cipro/Ofloxacin
PAS
Cycloserine
Prothionamide/Ethionamide
Clarithromycin/Azithromycin

Question 5

potential side effects of isoniazid

Answer 5

Isoniazid:
Hepatotoxicity
Peripheral neuropathy (B6 responsive)
Drug-induced lupus

Question 6

potential side effects of rifampicin

Answer 6

Rifampicin:
Orange discolouration – urine/sweat/tears
CyP450 – induction – OCP/warfarin/anti-epileptics
Hepatotoxicity
Drug-induced interstitial nephritis

Question 7

potential side effects of pyrazinamide

Answer 7

Pyrazinamide:
Hepatotoxicity
Gout
Rash

Question 8

potential side effects of ethambutol

Answer 8

Ethambutol
Occular toxicity – optic neuritis
rash

Question 9

what is ARDS and its mechanism

Answer 9

Clinical syndrome caused by diffuse alveolar capillary damage

Clinically – rapid onset of severe life threatening resp insufficiency that may progress to extra pulmonary multisystem organ failure.

Pathogenesis:

• infectious or non-infectious inflammatory stimuli
• “alveolar capillary membrane” damage
• Release on inflammatory mediators

Resulting in a cascade of cellular events:

• Increased vascular permeability
• Flooding of the alveoli
• Loss of diffusion capacity
• Surfactant abnormalities secondary to type 2 pneumocyte damage

Stimuli
-Shock – sytemic hypoperfusion caused by reduction in cardiac output or in the effective circulating blood volume -> hypotension, impaired tissue perfusion and cellular hypoxia

Question 10

mechanism of bronchiectasis

Answer 10

Obstruction -> collapse of distal lung parencyhma and pooling of secretions distal to obstruction -> inflammation -> necrotising inflammation, fibrosis -> dilatation of the airways.

Question 11

7. What respiratory diseases can be associated with HIV infection?

Answer 11

Pneumocystis jirovecii pneumonia
Invasive aspergillosis/candidiasis
CMV pneumonitis
Bacterial pneumonia
Tuberculosis
Interstitial pneumonitis & fibrosis
Kaposi’s sarcoma 
Non-Hodgkin’s lymphoma

Question 12

11. How would you investigate a pleural effusion and why?

Answer 12

Cytology - malignancy

Biochemistry - type of effusion

Microbiology - bacterial infection

Histology (pleural bx) - malignancy Tb or fungal infection.

Question 13

how are asbestos fibres classified

Answer 13

Size and shape: Crocidolite (blue) / Amosite (brown) / Chrysotile (white)

Question 14

16. What other disease processes are associated with asbestos?

Answer 14

Pleural effusion
Asbestosis
Malignant mesothelioma of pleura/pericardium
Malignant mesothelioma of peritoneum
Paratesticular malignant mesothelioma
Bronchial carcinoma
Laryngeal carcinoma
Caplan’s syndrome