TB Flashcards

1
Q

what is the aetiology of tuberculosis

A

myobacterium tuberculosis complex
5
m microti

bovis - transmitted by unpasteured milk

tuberculosis - important agent for human- transmitted by droplet nuclei

carnetti

bacterial spread through air , blood , lymphatic , gastrointestinal

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2
Q

diagnosis of tuberculosis

A

chest x ray - upper lobe classic infiltration and cavity
fibrocavernous

high index suspicion - high risk patient 
homeless 
diabetes 
alcohol 
chronic renal failure

sputum cytology - collect sputum early in the morning and 3 specimens

ziehl neelson staining - appears red
lowenstein- jensen medium culture 4-8 weeks - green with yellow dots in the middle

bactec machiene - 21days
PCR - detecting specifc segments of dna

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3
Q

how do you know if you have meningitis from tb?

A

basal meningitis

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4
Q

if person has remission of tb how do you diagnose them ?

A

x ray - ghon foccus

you do tuberculum mantoux skin test - sensitized cd4 lymphocytes - proliferate and produce cytokines

5 doses of dead tb intradermal
after 3 days see the diameter of the area of reaction
5mm or more - positive in HIV people only
10mm more - positive in drug users , children less than 4
high risk population - homeless , alcohol, diabetes , lab personal
15mm or more - no risk for tb

false positive - bcg vaccine Bacillus Calmette–Guérin
do not have the active disease

false negative - hodgkin disease sarcodosis
immunosuppressed

tuberculosis gold test - quantiferon
gamma interferon in the blood

t spot tb - number of effector t cell that produces the gamma interferon

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5
Q

clinical manifestations of primary tb ?

A

prodromal period - non specific symptoms - fever , night swats
initally non productive cough
blood streaking sputum
then massive hemoptysis

mild anemia , leukocytosis in blood test

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6
Q

pleural effusion marker in tb ?

A

adenosine d aminase

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7
Q

extrapulmonary metastasis of tb goes where tb ?

A

most commonly seen in HIV

peritoneum 
pleural 
liver 
meninges
genitourenal tract
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8
Q

what is the treatment of tb ?

A

distinguishing the 4 pop of tuberculosis

actively multiplying 
slowly '            '
sporadically multiplying 
dormant - no effect for ant tb drugs 
----------
initial phase -2 months:
first line rapidly dividing - isoniaside - 5mg/kg daily
hepatotoxicity and
 peripheral neurotoxicity 

rifampcin - rapidly divinding
hepatoxicity
10mg/kg
(rifabutin - substitue - battles all forms of tb)

pirazinamid(dormant) -
20mg/kg
hepatotoxcity, non gouty polyarthralgia

3x combo until culture negative and no radiological findings

ethambutol (treatment against all forms)
20mg/kg
retrobulbaretinitis

high risk patients - resistance , immunosuppression

4x combo - exceeding 20 months

streptomycin reserve for very high risk

second line - fluroquinilones - levofloxasin
moxifloxacin

amikacin

antituberculosis treatment divided into 2 phases ?
intensive phase
continuation phase

initial phase 2 months - RIF , izoniside , pirazinamide -IMPORTANT - not included then cavitation , and positive tb after 2 months
continuation phase 2 months - RIF and INH

suprvised therapy - DOT (direct observation therapy watching the patient taking the drug is the preferred core management

3 sputum specimens take 24 hours apart

relapse -inh , rif pza plus additional three agents

SINGLE NEW DRUG NEVER SHOULD BE ADDED TO FAILING REGIMEN

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9
Q

pathophysiology of tuberculosis ?

A

diseases that favour the development of active tb - HIV , silicosis , lymphoma

split into primary and secondary infection

primary - previusly unexposed

inhalation of the droplet nuclei from infectious patients - fewer than 10 percent bacilli reach alveoli
alvolar macrophages ingest the bacilli
prodromal phase

cell mediated immunity :
giving rise to two outcomes - bacillary multiplication - killing macrophage and lyses
monocyts ingest the bacilli and becoming antigen representing cells inducing lymphocytes arrive to give Th1 - INF-Y IL-2
and Th2 - IL-4 , IL-5 - IgE production
formation of granulamtous inflammation and
caseous necrosis in the middle - inhibition of bacterial growth within necrotic environment
viable bacilli remain dormant within macrophages for years if needed

cavities formed - liquefied caseous material containing large number of bacilli drain to lymph nodes - to cause caseating necrosis there to - and dissemination

latent tb - scaring and calcification

immunocomprimised - primary progressive tb - millary tb hematogenous spread

secondary tb - fibrotic granulome reactivated
bronchigenous dissemination

granuloma in tb - ghon focus

granuloma affects the lung and the lymph nod - hon complex

calcification and fibrosis of the granuloma - ranke complex

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10
Q

what are the physical findings in tuberculosis ?

A

PHYSICAL FINDINGS LIMITED USE
rales - esp after coughing found
occasional rhonchi , amphoric breath sounds - within areas which have large cavity

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11
Q

what are the characteristics of a primary tuberculosis ?

A

occurs in children

peripheral lesion accompanied by hilar or paratracheal lymphadenopathy

lesion heals spontaneouslu - and later evident as small calcified nodule - GHON lesion

progression by - pleural effusion and empyema
cavitation
hilar or mediastinal lymphadenopathy
hematogenous dissemniation

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12
Q

what are the characteristics of secondary tuberculosis ?

A

called adult type

results from endogenous activation of latent infection or reinfection

localised in the APCIAL and posterior segments of the upper lobes as well as superior segments of the lower lobes - high oxygen conc

can have necrotic satellite lesions - parenchymal involvement varies

tuberculous pneumonia

proceed to chronic porgressive debilitaing course - becoming formic and can calcify

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13
Q

what are the characteristics for hiv associated tuberculosis ?

A

upper lobe infiltration and cavitation
late stage of HIV - diffuse interstitial , millary infiltrate
less freq positive sputum smears
MOST COMMON EXTRAPULMONARY Tb

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14
Q

what are some differential diagnosis for TB

A

influenza
pneumonia
bronchail cancer

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