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Respiratory > Week 7 - TB > Flashcards

Week 7 - TB Flashcards

1
Q

What cell does mycobacterium tuberculosis infect?

A

-Alveolar macrophages (type 2 pneuomocytes)

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2
Q

How is TB transmitted?

A
  • Respiratory droplets when coughing/sneezing get suspended in the air which remains infectious for 30 mins
  • Requires prolonged exposure as not very contagious
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3
Q

Describe the pathogenesis of TB

A

1)Inhaled aerosols are engulfed by alveolar macrophages and deposit in a section of the lung forming primary focus
2)TB bacilli spread to draining lymph nodes resulting in the primary complex of the primary focus and its draining LN
Then there are two pathways which can be followed either:
-Progression of primary complex to primary infection resulting in host response damage
or
-Initial containment of primary complex progressing to latent infection resulting in either self-cure or post primary TB

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4
Q

What determines the fate of the primary complex?

A

-Host response and pathogen virulence

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5
Q

What prevents the primary complex always developing to primary infection?

A

-T lymphoctes are capable of containing the bacilli at the site of infection and prevent it developing

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6
Q

Why is it that the alveolar macrophages cannot kill the myco.TB?

A

-cell wall

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7
Q

What is the primary cause of damage in TB?

A

-Host reponse

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8
Q

Does latent TB have any symptoms?

A

-No it is only when post-primary TB develops that symptoms occur

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9
Q

Name some risk factors for reactivation of latent infection

A
  • HIV
  • Substance abuse
  • Prolonged corticosteroid use
  • Malignancy
  • DM
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10
Q

Which type of adaptive immunity mainly takes place in TB?

A

-Cell mediated

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11
Q

How long after infection does post primary TB reactivate?

A

->5years

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12
Q

Describe the host immune response to TB

A
  • Intracellular microbial peptide displayed on MHC1
  • CD8+ cell binds and recognises as non-self
  • Cytotoxic T cell begins to kill infected cell as well as secrete cytokines which trigger inflammatory processes
  • Damage to the tissue is via host response
  • If response is adequate then the infection is contained
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13
Q

What are the types of TB?

A
  • Localised pulmonary TB
  • Widespread pulmonary TB
  • Localised extra-pulmonary TB
  • Meningeal TB
  • Miliary TB
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14
Q

What is microscopically characterisitic of TB? Describe this finding

A
  • Caseating granulomas
  • Epithleoid histiocytes, langhan giant cells and T lymphocytes wall off the infected area and form a granuloma with a caseating centre
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15
Q

Where does TB commonly occur within the lung and why?

A

-Upper lobes as they are obligate anaerobes

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16
Q

How does a CXR typically look of TB?

A

-Consolidation with cavitation

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17
Q

In whom does extra-pulmonary TB commonly occur?

A
  • Immunosuppressed

- Young children

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18
Q

List some risk factors for TB

A
  • Ethnicity -> south asian/sub-saharan
  • HIV or other immunocompromised
  • Homeless
  • Drug users
  • children/elderly
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19
Q

Describe some signs and symptoms of pulmonary TB

A
  • Cought, haemoptysis, SoB, pulmonary crackles

- Fever, night sweats, weight loss and anorexia, tiredness and malaise

20
Q

What investigations are carried out to diagnose TB?

A
  • CXR
  • Sputum -> 3 early morning samples
  • Culture
  • Molecular tests
  • TST
  • IGRAs
21
Q

What would a CXR of TB look like?

A
  • Apex often involved

- Ill defined patchy consolidation with cavitation

22
Q

What stain is used in sputum sample?

A

-Acid fast such as ziehl nielson

23
Q

Why is culture not always appropriate for TB?

A

-Can take upto 6 weeks

24
Q

What is tuberculin skin testing?

A
  • Diagnostic test and screening tool for TB

- If induration of reaction is significant then indicates TB exposure

25
Q

Describe the advantages and disadvantages of TST

A

Advantages -> cheap

Disadvantages ->generates false positives

26
Q

What are IGRAs?

A

-Interferon Gamma Releasing Assays which detect antigen specific IFN-g production in a blood sample

27
Q

What is a disadvantage of IFN-g assays for TB?

A

-Cannot distinguish between latent and active TB

28
Q

What is the first line treatment for TB?

A

-Multi-drug therapy for 6 months = RIPE ->Rifampicin, Isoniazid, Pyrazinamide, Ethambutol

29
Q

What drug is given in MDR TB?

A

-Quinolones

30
Q

What is miliary TB?

A

-Widespread infection in the bloodstream

31
Q

Describe the molecular tests used in TB diagnosis

A

-NAAT -> detection of nucleic acids specific for TB in 1-2 days

32
Q

Why is compliance an issue in TB?

A

-Becuase the treatment regime is prolonged with a high amount of drugs

33
Q

When is the likelihood of MDR TB increased?

A
  • Previous TB Rx
  • HIV+
  • Known contact of MDR TB
34
Q

Describe the BCG vaccination

A
  • Live attenuated M Bovis strain which produces Ab protection to TB
  • Protection diminishes over time and is now only given to babies in high risk areas
35
Q

How does Lymph TB often present?

A

-Lynphadenitis -> Cervical LNs most common

36
Q

How does TB develop in bones and joints?

A

-Haematogenous spread

37
Q

What is Potts disease?

A

-TB in the vertebrae

38
Q

How does meningeal TB present?

A
  • Chronic headache, fevers

- Proteins and lymphocytosis in CSF

39
Q

What is meant by TB been a notifiable disease?

A

-The doctor is leagally responsible for notifying public health

40
Q

What happens once public health are notified of TB?

A
  • Contact tracing procedures

- Surveillence to detect outbreaks

41
Q

How is TB prevented?

A
  • Notifiable disease
  • PPE and negative pressure isolation room
  • Vaccination of susceptible contacts
42
Q

Describe mycobacterium tuberculosis, including its cell wall and he advantages it confers

A
  • Non-motile rod-shaped bacteria which is a obligate anaerobe
  • Cell wall is made up of FA, complex waxes and glycolipids which provide structural rigidity, acid alcohol fast and evasion of the immune system
43
Q

After how long on treatment is a person with TB no lomger contagious?

A

-2 weeks

44
Q

How does the TB infection spread from its primary complex?

A

1) Proliferation of TB bacilli in the caseous centre is followed by softening and liquefaction of caseous material
2) Fibrous tissue cannot contain the growing complex
3) Spread of caseous and liquefied material through bronchial tree may disseminate the infection to other lung zones

45
Q

What is tuberculous pneumonnia?

A

-When marked inflammatory exudate fills the alveoli causing consolidation

46
Q

Why can pleural effusion result from pulmonary TB?

A

-Seeding of TB in the pleura or hypersensitivity rxn

Respiratory (17 decks)

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