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My Cards- Resipratory > Week 7 TB/ lung cancer > Flashcards

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
Q

describe the incidence of lung cancer in different groups and death rates

A

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
Q

what are the aetiological factors (causes) involved in lung cancer?

A

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
Q

screening for lung cancer- yes/no - why?

A

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
Q

what are the typical pattern of symptoms, charecteristics reported by pts with lung cancer?

A

age 55-75years most diagnosis
persistent cough 4months
working with causative agents- asbestos

26
Q

what are the common clinical symptoms associated with lung cancer and what structural abnormalities underly them?

A

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
Q

what are some of the common clinical signs of ling cancer that a pt may present with?

A 
most commonly no signs 
finger clubbing
cachexia- weakness
pale conjunctiva
cervical lymphadenopathy
signs of pleural effusion
muffled heart sounds
liver enlargement
skin metastasis
28
Q

describe staging of lung cancer and how does this relate to treatment options?

A

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
Q

what imaging techniques are used in the diagnosis and staging of lung cancer?

A

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
Q

can you diagnose lung cancer only from imaging?

A

no need tissue sampling as could be something else

31
Q

what are the common methods used to obtain material for histological diagnosis- tissue sampling?

A

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
Q

what different biopsies may be taken in the diagnosis of lung cancer?

A

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
Q

describe the histology and classification of common lung tumours

A 
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
Q

how are molecular markers now related to lung cancer treatment?

A

treatments that target these specific mutations- NEW
test pts for these- personalised medicines
EGFR mutations, ALK mutations, KRAS mutations, PD1 mutations

34
Q

how does the WHO performance status of lung cancer affect the treatment which is chosen for patients- cut off?

A

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
Q

what are the different treatments available for lung cancer and how do they affect survival?

A
  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
Q

where does lung cancer commonly spread to?

A

draining lymph nodes, liver, adrenal, brain, bone, pericardium, pleura

36
Q

how are MDTs important in pt care of lung cancer?

A

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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