TB (MED 1 ILOs) Flashcards
LOs
explain the difference between pulmonary and extra-pulmonary TB
explain the principal apporaches to managing TB
describe the clinical tests used to identify a TB infection
understand how HIV can influence the progression of TB and vice versa
understanf the interaction and potnetial adverse effects of drugs used in the treatment of HIV/tuberculosis co-infection
Mycobacterium tuberculosis
- aerobic- have a predilection for lung apices
- high lipid content in cell wall
likely the reason for virulence and resistance
“acid fast bacillus” staining not decolourised by alcohol
unable to gram stain
use ZN staining instead
- Slow growing (resistant to being killed) and long living
- group of genetically related mycobacteria (mycobacterium TB ciomplex)
TB infection and spread
airborne droplet nuclei- coughing singing
can remain suspended in air for hours
overcrowded living, prisons
oropharyngeal/ intestinal deposition
what can happen to a granuloma over time
calcify then
a) resolution of infection
b) latent TB to active
Symptoms of TB
- pulmonary-cough, wheeze, haemoptysis, breathlessness
- extrapulmonary- CNS, bones, GI etc.
- Constitutional- fever, cachexia, night sweats
primary tB
Symptoms of tb but may be asymptomatic or mild
look for people who have had close contact over 2-5 years
usually only a clinical disease in children/ immunosuppressed
radiological signs of primary TB
Mediastinal lymphadenopathy
Pleural effusion
Lobal collapse/ consolidation
Miliary shadowing
Classically, pneumonia with enlarged hilar (root of lung) lymph nodes
CXR appearance of post primary TB
- look at apices
- soft, “fluffy” or nodular in upper zones
- cavitation
- consolidation
- lymphadenopathy
miliary TB
haematogenous spread
often suggets immunodeficiency
in the lung: widespread fine nodules of uniform distribution
patients are very unwell
extrapulmonary TB
most commonly affects lymph glands, pleura, bone and joints, GU and CNS
TB lymphadenitis
Used to be called scrofula
Commonest presentation
Cervical nodes most affected
Slowly progressing swelling
Fever
Diagnosis fine needle aspiration
Treatment standard treatment for TB
CNS TB
TB meningitis
Meningeal symptoms
Cranial nerve palsies
Diagnosis through CNS examination
diagnosis of TB
microbiology- sputum sample, ZN staining to show acid fast bacilli, 10-100 microorganisms needed to be diagnostic
bronchoscopy
othrt tissue samples if extrapulmonary (morning urine for renal)
molecular techniques- PCR, whole genome sequencing
PCR for diagnosis of TB
rapid confirmation of mTB complex
can identify rifampcin resistance
whole genome sequencing for TB diagnosis
- Identifies species, drug resistance and can identify transmission cluster
- Important in controlling endemics
- Increasingly quick and affordable
rifampcin
Bactericidal
Kills both active and semi-dormant bacteria
Potent inducer cytochrome P450
High drug interactions
Anti-retrovirals
Side effects: orange urine, tears, stain contact lenses
Rash, skin reactions itch
Abnormal liver function usually transient
Influenza like reaction
Haemolysis rare
Thrombocytopaenia
Renal failure
Shock
isoniazid
Only active against MTB
Kills actively dividing cells
Metabolised by acetylation
Hepatoxicity (small AST increase) this increases with age
Histamine food reactions
Nausea and vomiting
Aplastic anaemia
Cutaneous hypersensitivity
Neurotoxicity
ethambutol
bacteriostatic
Inhibits arabinosyl transferase
principles of treatment
start with all 4 drugs and do not reduce until you’ve had 2 months of treatment
consider changing to more sensitive drugs after 4 months
side effects of treatment: advice to patients
Nausea/ abdominal pain
Persistent vomiting/ jaundice-stop drugs and seek attention heaptic damage
Red urine and contact lenses
Visual disturbances
Drug interactions
Isoniazid induced peripheral neuropathy
IRIS- immune reconstitution inflammatory syndrome
Paradoxical worsening of symptoms
Absence of alternative diagnosis
Usually starts 2 weeks after starting antiretrovirals, but can be up to 2 months
Associated with more advanced HIV, lower CD4 count
Significant morbidity requiring hospital admission
Treat with prednisolone
how important is contact tracing in TB
vital
aidentificatio of latent tB
identify with skin test or IGRA
risk of developing TB is increased by:
Recent contact (<2 years) with infectious (smear positive) individual
HIV coinfection/ immunosuppressed
Chronic alcohol excess
Diabetes
Anti-TNF drug therapy/ immunosuppressive therapy
Partial gastrectomy
how to support the patient to be compliant with TB treatment
Monitoring the patient at home
Ensuring patient is taking medication as prescribed
Maintaining adequate medication
Monitoring side effects of Abx
Supporting patient attendance with hospital appointments
