9 Flashcards
(34 cards)
1
Q
What is the definition of Tubercolosis?
A
-chronic communicable disease caused by mycobacterium tuberculosis (MTB)
2
Q
Describe TB microscopy
A
- Rapid and cheap test
- 60-70% of culture positive samples are microscopy positive
- need a large number f bacilli for smear to be positive
- if pt. Is smear negative then no need to place in a side room but place in side room if smear positive
- can not differentiate live and dead organisms
- on smears (ex. Sputum smears) stained by Ziegler’s-Nielsen method
- grow slowly on culture (gold standard) (on media such as Lowenstein-Jensen Medium) takes 2-6 weeks to form colonies
See lecture 9.2 Tub slide 28-29
3
Q
How is TB transmitted?
A
- from person to person by infected droplets
- coughing, sneezing, etc
- suspended in air and reach lower airways
- infection dose: 1-10 bacilli
- contagious but NOT EASY to acquire
- prolonged exposure facilitates transmission (at least 8 hours/day for 6 months)
- easy for family member to acquire
See 9.2 lecture tub slide 13-14
4
Q
What is the pathogenesis and pathology of TB?
A
- alveolar macrophages phagocytose MTB in the alveoli but are unable to kill them
- because MTB have cell wall lipids that block the fusion of phagosomes and lysosomes
- macrophages initiate the development of cell mediated immunity which eventually leads to emergence of activated macrophages with enhanced ability to KILL MTB
- takes about 6 weeks to develop
5
Q
How does the formation of tubercles occur?
A
- when macrophages ingest MTB a granulomatous reaction occurs
- spherical granuloma with central caseous necrossis
See lecture 9.2 tub slide 22
6
Q
How does primary TB occur and devleop into latent?
A
- occurs on first exposure of MTB
- tubercles form called PRIMARY FOCuS or GHON’S FOCUS
- may be in ANY lung zone
- TB bacilli drain from primary focus into hilar lymph nodes
- GHON’S focus + hilar nodes = primary complex
- most primary TB will heal with/without calcification of primary complex
- but before healing, TB bacilli enter blood stream and haematogenous spread occurs resulting in seeding of TB bacilli to other parts of lung and other organs
- cell mediated immunity helps infection to be contained
- known as latent TB
- post-primary Tb; reactivating of latent TB which occurs most often in lungs
-BUT if primary complex DOESNT health it will progress to active TB
See lecture 9.2 tub slide 18-19
7
Q
What are the risk factors for reactivation?
A
- infection with HIV
- substance abuse
- prolonged therapy with corticosteroids
- other immunosuppressive therapy
- TNF antagonists
- organ transplant
- haematological malignancy
- severe kidney disease/haemodialysis
- diabetes mellitus
- silicosis
- low body weight
See lecture 9.2 tub slide 20
8
Q
What test can be done to determine latent TB?
A
- characterized by positive QuantiFERON test
- based on ability of MTB antigens to stimulate host production of interferon gamma
- lymphocytes from patient’s blood are cultured wtith these antigens
- if pt. Exposed to TB before, T lymphocytes produce interferon gamma
- or by a positive TB skin test
- TB protein is injected intradermally
- skin reaction within 48-72 hours will indicate previous exposure to TB due to a type IV hypersensitivity reaction to the protein
See lecture 9.2 tub slide 32-35
9
Q
What is post primary pulmonary TB?
A
- most often seen in upper lung zones because higher alveolar pO2
- cavity formation: softening ad liquefaction of caseous material creating cavity
- haemorrhage: results in extension of caseous process into vessels in cavity walls causing haemoptysis
- spread to involve rest of lung: caseous and liquified material spread infection
- pleural effusion: seeding of TB bacilli in the pleura, hypersensitivity
- military TB: rupture of caseous pulmonary focus into a blood vessel may result in miliary TB with formation of multiple miliary seeds
See lecture 9.2 tub slide 21
10
Q
What is extra pulmonary TB?
A
- reactivation of latent TB in areas other than lungs
- results in active TB
- sites involved include lymph nodes, bones, joints, CNS, GI tract, urinary tract, etc.
- lymphadenitis: abscesses and sinuses
- GI: swallowing of tubercles
- peritoneal: ascetic or adhesive
- genitourinary: slow progression to renal disease
- bones and joint: haematogenous spread
- TB meningitis
See lecture 9.2 slide 45-46
11
Q
What are the clinical features of pulmonary TB?
A
- onset is gradual over weeks or months
- tiredness, malaise, weight loss, fever, severe night sweats, cough
- cough may be dry or productive of mucous sputum, and haemoptysis may occur
- potentially no clinical signs even if CXR is abnormal
- crackles may be present
See lecture 9.2 tub slide 25
12
Q
What investigations would you do for pulmonary TB?
A
- CXR
- sputum: 3 early morning samples minimal volume 5mL
- induced sputum
- bronchoscope (patients with dry cough)
See lecture 9.2 slide 26
13
Q
Describe how a chest X-ray would look for pulmonary TB?
A
- shadowing
- may be due to patchy solid lesions, cavitated solid lesions, streaky fibrosis, and flecks of calcification
- healing results in fibrosis
See lecture 9.2 tub slide 27
14
Q
How would you diagnose active TB?
A
- established by identification of tubercle bacillus in the appropriate body fluid by direct smear, culture and other tests when indicated
- NAAT
- must isolate organism by culture and determine its susceptibility to drugs
See lecture 9.2 tub slide 30
15
Q
What is the treatment of TB?
A
- combination of antibiotics over several months
- Main: rifampicin, isoniazid, pyrazinamide, ethambutol
- all 4 drugs used for 2 months followed by rifampicin and isoniazid for extra 4 months (total 6 months)
- to prevent peripheral nerve damage pyridoxine (vit. B6) given along with isoniazid
- 4 drugs used since MTB is resistant due to spontaneous mutations
- so combinations prevents resistance
- prolonged follow up is needed
- must take adherence into account: make sure pt’s taking meds
See lecture 9.2 slide 36-41
16
Q
What is miliary TB?
A
- TB spreading through blood stream
- widespread infection
- often multiple organs involved
See lecture 9.2 slide 43-44
17
Q
How can we control TB?
A
- detection and treatment of cases and contacts
- prevention of transmission: PPE, negative pressure isolation
- reduce susceptible contacts: address risk factors, vaccination
18
Q
What is the BCG vaccine?
A
- live attenuated M.bovis strain
- given to babies in high prevalence communities
- 70-80% effectiveness in childhood TB
- protection wanes
- little evidence in adults
- always consider HIV testing before giving BCG since it is a live vaccine
See lecture 9.2 tub slide 51-52
19
Q
How can we prevent latent TB from becoming active?
A
- latent TB patients are hard to detect
- solution: give CHEMOPROPHYLAXIS (1 drug for 6 months) to get rid of dormant live bacilli in body
- it is only a prevention
See lecture 9.2 tub slide 52
20
Q
When should you suspect TB?
A
- non-UK born/recent migrants: recent arrival or travel
- HIV
- other immunocompromised
- homeless
- drug users, prison inmates
- close contacts of patients with TB
- specific clinical features: unexplained fever, weight loss, malaise, anorexia
21
Q
What is the difference between latent TB vs. TB (in lungs)?
A
- inactive vs. Active
- TST or IFN gamma results positive vs. TST or blood test positive
- CXR normal vs. CXR abnormal
- sputum smears and cultures negative vs. Sputum smears and cultures positive
- asymptomatic vs. Symptomatic
- not infectious vs. Infectious
- not a case of TB vs. A case of TB
See lecture 9.2 tub slide 16-17
22
Q
Describe the structure of MTB
A
- non-motile rod-shaped bacteria
- obligate aerobe
- long-chain fatty (mycolic) acids, complex waxes and glycolipids in call wall (so difficult to kill and stain because of waxy cell wall)
- structural rigidity
- acid alcohol fast: have to use acid and alcohol to stain it
- relatively slow-growing compared to other bacteria
- generation time 15-20hours
- takes ages for culture to grow
- commonly affects right apex of lung
See lecture 9.2 tub slide 11-12
23
Q
Would you have increased or decreased vocal resonance in pneumonia?
A
-increased
24
Q
What is the commonest male cancer?
A
Lung cancer
25
Why is lung cancer more common in less affluent people?
- more of them smoke
- poor diet cant afford healthy food etc
See lecture 9.2 2019 slide 3-12
26
What are the risk factors of lung cancer?
Major: smoking with the risk being proportional to the duration of the habit and the number of cigarettes smoked
-90% in men and 80% in women caused by smoking
Other risk factors
- exposure to asbestos and radon
- genetic and dietary factors
See lecture 9.2 2019 slide 13-14
27
What investigations would you do for lung cancer?
- bronchoscopy and needle biopsy of lung or pleura to obtain tissue
- make histological diagnosis which is essential to confirm lung cancer
- must decide cell TYPE which is important in terms of prognosis and treatment
- USS: neck node, lung wall mass, pleural fluid
- CT biopsy: lung, pleura
- CXR, CT scan, Pet scan, MRI, bone scan
See lecture 9.2 2019 slide 27, 35-36
28
Explain the staging of lung cancer
TNM classification
- t: size, # of nodules, location
- N: where the nodes are (N1 is operable but N2 and N3 are inoperable)
- M: within Chest or out of chest
See lecture 9.2 2019 slide 20-26
29
What are the symptoms of lung cancer?
Primary tumour
-cough, dyspnoea, wheezing, chest/shoulder pain, wight loss, malaise, haemoptysis
Regional metastases
-bloated face, hoarseness, dyspnoea, dysphagia, chest pain
Distant metastases
-bone pain/fractures, CNS symptoms
Metabolic
-thirst, constipation, seizures
SOMETIMES EVEN NO SYMPTOMS
see lecture 9.2 2019 slide 30
30
What are the signs of lung cancer?
- cachexia
- pale conjunctiva
- cervical lymphadenopathy
- horners syndrome
- consolidation
- SVC obstruction
- signs of pleural effusion
- muffled heart sounds
- liver enlargement
- skin metastases
- neurological long tract signs
SOMETIMES NO SIGNS
See lecture 9.2 2019 slide 31
31
What are some paraneoplastic syndromes caused by lung cancer?
Endocrine
- hypercalcaemia
- Cushing’s syndrome
- inappropriate antidiuretic hormone secretion (SIADH)
Haematological
- anaemia
- thrombocytosis
Cutaneous
-dermatomyositis
Skeletal
-finger clubbing
Neurological
- encephalopathy
- peripheral neuropathy
- Easton-lambert syndrome
- pancoast syndrome
See lecture 9.2 2019 slde 32
32
Describe the pathology of lung cancer
-carcinoma
Main types
- Non-small cell lung cancer: squamous cell carcinoma, adenocarcinoma, large cell carcinoma
- small cell carcinoma
- rare tumours
See lecture 9.2 2019 slide 40
33
What are the molecular markers of lung cancer
- EGFR mutations
- ALK mutation
- KRAS mutations
- PD1 mutations
- PDL1 mutations
See lecture 9.2 2019 slide 41
34
How can we treat lung cancer?
- surgery
- chemotherapy
- radiotherapy
- palliative therapy
- often used in combination
- tailors to individual pt. So need a Multi-Disciplinary Team (MDT)
- “cure” rate is shit
- surgery most likely to result in long-term survival
- biological and immunotherapies is a potential “game changer”
- performance/functional status of pt. Is most important part of assessment
See lecture 9.2 2019 slide 43-48**
