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Week 7 TB/ lung cancer Flashcards

1
Q

describe the microbiology of mycobacterium tuberculosis- species, shape, cell wall, staining, growing time

A

TB is caused by bacteria belonging to mycobacterium tuberculosis complex- 7 closely related species
- M tuberculosis- causes most human infections
- M bovis- cause of Tb in cattle most- has been transmitted to man
- M africanum- in pts bringing TB into uk from Africa
non motile rod shaped- obligate aerobes
Cell wall- UNUSUAL - long chain FAs, complex waxes and glycolipids in cell wall- structural rigidity- survive and multiply in macrophage, staining characteristics, acid alcohol fast
- slow growing- takes time for cultures

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2
Q

who is at risk of TB and what should be covered in a history?

A 
non UK born
HIV or immunocompromised
homeless
drug users
prisons
close contact
young adults 
history- ethnicity, travel, contact with TB, BCG vaccination
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3
Q

how does TB cause infections- transmission- how infectious, common settings for spread?

A

spread by respiratory droplets- coughing, sneezing
droplet nuclei- airborne- suspended in air- air remains infectious 30mins- reach lower airway macrophages
-infectious dose 1-10 bacilli
- 3000 infectious nuclei- cough/talking 5 mins
- contagious not easy to catch- need prolong exposure- facilitates transmission- 8hrs/days up to 6 months- common within overcrowded families, schools, prisons
- treatment brings down droplet to non infectious level within 2 weeks

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3
Q

Describe the overall pathogenesis of TB

A

Inhaled aerosol- engulfed by alveolar macrophage when carried into lungs- cannot be killed- multiplies here- carried to local lymph nodes= called primary complex- site on lung and LN (ghons focus and draining LN)
- where ends up depends on immune system- predominant immune system should be cellular response not AB response- as macrophages involved- intracellular- T lymphocytes

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3
Q

what is miliary disseminated TB?

A

spread through blood- widespread infection
during primary infection or during reactivation
lungs are involved by few respiratory symptoms
often multiple organs involved- headaches suggest meningeal involvement, pericardial, pleural effusion small, ascites may be present

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5
Q

What path does active TB (primary) take to develop from primary complex stage?

A
  • in 5%- some primary complex progresses straight away to active disease- PRIMARY TB- immune dysfunction
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6
Q

What path does latent TB take to develop from primary complex disease and what are the possible outcomes?

A
  • 95% - T cells try to keep localised to point of entry= initial containment of infection- bacilli alive but not causing disease- no signs- LATENT TB
    • 95% heal/ self cure- immune system wins
    • 5% POST PRIMARY (SECONDARY) TB- reactivation- multiply and overcome immune response years later
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7
Q

What are the characteristics of latent TB?

A

inactive- contained bacilli in body
TST or IFN gamma test result usually positive
normal CXR
negative sputum and smears
no symptoms
not infectious
not a CASE of TB but may go on the develop TB disease

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7
Q

describe when latent TB develops into post primary TB?

A

reactivation or exogenous re-infection
>5 years after primary infection- shortened if have HIV
5-10% risk per lifetime
clinical presentation- pulmonary or extra pulmonary- bacilli move and cause disease in other organs

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9
Q

What are the risk factors of reactivation in latent TB?

A 
HIV
Substance abuse
Prolonged therapy with corticosteroids or immunosuppressive medication
TNF alpha antagonists- chrons, UC
Organ transplant
Haematological malignancy 
Severe kidney disease- haemodyalysis
DM
Silicosis
Low body weight
Close contact
Travel
Vaccination
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10
Q

What are the characteristics of TB disease?

A 
Active multiplying bacilli in the body
TST or blood test usually positive
abnormal CXR
sputum and smear cultures may be positive
symptoms- cough, fever, weight loss
often infectious before treatment
a CASE of TB
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11
Q

describe the pathology of TB?

A

caseating granulomata develop

  • lung parenchyma (part involved in gas exchange) and mediastinal lymph nodes
  • cells present are lymphocytes, epitheloid cells (active form of multiplying macrophage) and giant cells (aggregates of macrophage)
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12
Q

how does the host respond to TB infections?

A

healthy contact (LTBI)- lymph node- localised extra pulmonary- pulmonary (localised)- pulmonary (widespread)- meningeal- miliary
Less effective immune system- worse diseased state
Better immune system- localised or no disease

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13
Q

what are the typical clinical presentations and radiographic changes in pulmonary TB?

A
  1. Symptoms- fever, night sweats, weight loss and anorexia, tired, cough, breathlessness in pelueral effusion- fluid
    Signs on exam- fever, weight, often no CXR abnormalities- primary TB, maybe crackles in affected area, in extensive disease- signs of cavitation, fibrosis
  2. Radiology- apex involved- obligate aerobes, ill defined patchy consolidation- cavitation develops within consolidation, healing results in fibrosis
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14
Q

what are the different types of NON respiratory TB?

A
  1. Extra pulmonary TB- places other than lungs- larynx, lymph nodes- lymphadenitis, GI- swallowed tubercle, pleura, brain- tb meningitis, kidneys, joints and bones- heamatogenous spread
    - in HIV or immunosuppresed, children
    Miliary TB- carried to all parts of body through blood- rare
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15
Q

how is TB diagnosed?

A

CXR
Sputum sample- 3 early morning samples- min 5ml
Induced sputum
Bronchoscope is cannot get samples- pt with dry cough

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16
Q

what lab test should be performed to diagnose TB?

A

sputum smears- 60% sensitivity- increased with 2nd and 3rd samples
Ziehl nielsen stain
culture is the GOLD STANDARD- solid and liquid culture but take up to 6weeks

17
Q

what does the interferon gamma releasing assay (IGRAs) do- problems?

A

detection of antigen specific IFN gamma production

cannot distinguish latent and active TB

18
Q

how does treatment affect toxicity, and what problems are they with the schedules?

A
  • drugs make pt non infectious
  • need close monitoring of complicance as course is so long- DOT- directly observed therapy, VOT- video observed therapy
    pts may be vitamin D deficient
    may need surgery
19
Q

how is drug resistance developed in TB- molecular mechanisms, causes, risk factors and how is this overcome?

A

naturally drug resistant organisms arising through spontaneous mutations
- acquired drug resistance- occurs due to poor compliance
- primary drug resistance- due to diagnostic delay, overcrowding and inadequate infection control
increased risk in reinfection, HIV- results in a longer duration and more drugs

20
Q

how is TB managed- multi drug therapy (first/second line) and what complications can this cause?

A
  1. 4 first line medications:
    rifampicin- raised transaminases and induces cytochrome p450, orange secretions
    isoniazid- peripheral neuropathy, hepatotoxicity
    pyrazinamide- hepatotoxicity
    ethambutol- visual disturbances
    - take 3/4 for 2 months then rifampicin and isoniazid for 4months, if CNS TB for 18months
    - cure rate 90%
  2. second line medications for pts with drug resistance:
    quinolones- moxifloxacin, injectables
20
Q

what does the tuberculin sensitivity test (TST) do- how is it performed, any problems?

A

measures the CMI- cell mediated immunity - tuberlin injected intradermally- read 48-72 hrs later
false positives or false negatives- immunocompromised
but cheap

20
Q

how can TB prevented- healthcare professionals involvement?

A

all TB suspected or diagnosed must be reported to public health England
prevention of transmission- PPE, negative pressure isolation

21
Q

what is the role of the BCG vaccine?

A

live attenuated M bovis strain- given to babies in high prevalence communities only
70-80% effectiveness in preventing severe childhood TB

22
describe the incidence of lung cancer in different groups and death rates
socioeconomic gradient- poorest communities- higher incidence- smoking more common, education, present later, access to services highest cancer related deaths in world 35000 deaths per year- UK 500 deaths per year- Leicester
23
what are the aetiological factors (causes) involved in lung cancer?
smoking causes 90% of lung cancer deaths in men, 80% in women 20% cases non smokers 35yrs 25cigs per day- 1in7 chance of dying from lung cancer before 75yrs, 1 in 10 risk of dying from coronary disease, 1 in 2 risk of dying prematurely from smoking related diseases - also asbestos 1000 deaths/yr, radon, occupational carcinogens- nickel, genetic factors
24
screening for lung cancer- yes/no - why?
expensive to screen all smokers, time consuming only works if certain conditions met- only successful if disease specific mortality decreased as a result of screening in lung cancer- doesnt decrease deaths -now in high risk individuals might start
25
what are the typical pattern of symptoms, charecteristics reported by pts with lung cancer?
age 55-75years most diagnosis persistent cough 4months working with causative agents- asbestos
26
what are the common clinical symptoms associated with lung cancer and what structural abnormalities underly them?
primary tumour- cough, dyspnoea (SOB), wheeze, haemoptysis, lung infection, weight loss, lethargy commonist symptom-NO SYMPTOM - regional metastases- bloated face (SVC obstruction), hoarseness (L RLN palsy), dyspnoea (anaemia, pericardial effusion), dysphagia (mechanical blockage-oesophageal compression) - distant- bone pain, CNS symps - metabolic- thirst and constipation (hypercalcaemia), seizures (hyponatraemia- low Na)
27
what are some of the common clinical signs of ling cancer that a pt may present with?
``` most commonly no signs finger clubbing cachexia- weakness pale conjunctiva cervical lymphadenopathy signs of pleural effusion muffled heart sounds liver enlargement skin metastasis ```
28
describe staging of lung cancer and how does this relate to treatment options?
TNM system- T-size, location (invading chest wall, bronchi) and number of nodule/s (several in same lobe- T3, different lobe same side-T4, different sides-M1a) N- lymph node- no involvement- N0, same side hilar nodes- N1, mediastinal lymph node- N2, different side- N3, above clavicle on either side- N3 M- in chest- M1a, outside chest- M1b stage determines treat- radical- trying to treat (IA-IIB), or palliative (IIB or IV) - 80% at presentation present with advanced stage so dont have radical treatment option -overall staging is IA, Ib, IIA, IIB, IIIA, IIIB, IV
29
what imaging techniques are used in the diagnosis and staging of lung cancer?
CXR- ALL staging chest CT- slightly lower- kidney, adrenal and liver also captured- common areas of metastasis (standard CT- chest)- MOST - DONT SUBJECT FRAIL OLD PEOPLE- WONT WITHSTAND TREATMENT SOME HAVE: Pet Scan- picks up distant metastasis that staging chest CT wont MRI- as needed ultrasound- as needed bone scan- as needed
30
can you diagnose lung cancer only from imaging?
no need tissue sampling as could be something else
31
what are the common methods used to obtain material for histological diagnosis- tissue sampling?
bronchoscopy- endobronchial ultrasound- can image mediastinal lymph nodes ultrasound- neck nodes, lung chest wall mass, pleural fluid, liver CT guarded biopsies- lung, pleura thorocoscopy- pleural and thoracic cavity surgical - if think lymph node affected- try and biopsy metastasis if suspected- prove both at same time
31
what different biopsies may be taken in the diagnosis of lung cancer?
one or more possible of: bronchoscopy cervical lymph node fine needle aspiration (FNA) pleural fluid aspiration- thorocentesis CT guided lung/ pleural/liver biopsy adrenal, bone, skin, brain, lymph node biopsy
32
describe the histology and classification of common lung tumours
``` carcinoma- malignant epithelial tumour main types are: 1. non-small cell lung cancer: - squamous cell carcinoma ~40% - adenocarcinoma ~30% (commonest in non smokers) - large cell carcinoma ~5% 2. small cell carcinoma ~12% 3. rare tumours eg carcinoid 5% ```
33
how are molecular markers now related to lung cancer treatment?
treatments that target these specific mutations- NEW test pts for these- personalised medicines EGFR mutations, ALK mutations, KRAS mutations, PD1 mutations
34
how does the WHO performance status of lung cancer affect the treatment which is chosen for patients- cut off?
grade 0-5 0- fully active able to carry on all pre disease things without restriction 4- completely disabled- cant carry out any self care 5- dead dont offer treatment for 3 or above- palliative- only treat symptoms
35
what are the different treatments available for lung cancer and how do they affect survival?
1. surgery- mostly for non-small cell 20-25% operable- best chance of cure 2. radiotherapy - radical- curative intent, palliative- symptom control 3. combination chemo - small cell- potentially curative in a minority - non- small cell- modest survival increase, sympt control - neoadjuvant therapy- chemo before surgery- to downstage tumour - adjuvant chemo after surgery- no benefit if after stage 2 4. combination therapy- chemo/radiotherapy- potentially curative 5. biological- targeted therapy- based on mutation analysis 6. palliative care- control symptoms, pt support group
35
where does lung cancer commonly spread to?
draining lymph nodes, liver, adrenal, brain, bone, pericardium, pleura
36
how are MDTs important in pt care of lung cancer?
7 different opinions- start with why referred- use tissue and radiological info- performance status and co-morbidity- discuss other tests- come up with treatment

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