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Pulmonary Week 2 > TB > Flashcards

TB Flashcards

1
Q

How is TB spread?

A

human to human via aerosols from coughing

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2
Q

T or F. Everyone that becomes infected by MTB develops disease

A

F. 90% do not

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3
Q

Describe TB

A

acid-fast bacillus, obligate aerobe that grows VERY slowly (thus, cultures take up to 6-8 weeks)

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4
Q

How does primary TB infection present?

A

most are asymptomatic (only evidence of infection is fibrocalcific nodules at the site of infection)

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5
Q

How does secondary TB infection occur?

A

viable organisms can remain dormant for years and reactivate

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6
Q

Secondary infection usually involves what part of the lungs?

A

apices

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7
Q

How does the mycolic acid of the cell wall of MTB promote infection?

A

Mycolic acids, glycolipids, arabinagalactans, and free lipids make the cell wall impermeable to many host systems

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8
Q

Virulence factors of MTB?

A
  • cord factor

- sulfatides (surface glycolipids that inhibit phagolysosomal fusion once inside macrophages)

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9
Q

What does cord factor do?

A

inhibits macrophage maturation and induces TNF-a release (virulent strains grow in a cord-like pattern)

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10
Q

Where does MTB reside in the body?

A

inside alveolar macrophages (antibodies and complement ineffective)

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11
Q

What polymorphism promotes for bacteremia of MTB?

A

NRAMP1

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12
Q

When do granulomas begin to appear following TB infection?

A

3 weeks

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13
Q

How do granulomas form?

A

after TB enters macrophages, the macrophages produce Il-12 which activate TH1 cells to produce IFN-y, which then further activates them to produce TNF-a and cytokines that cause monocyte recruitment and caseous necrosis and containment of infection

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14
Q

Why are rheumatoid arthritis patients at an increased risk for TB?

A

because they are often treated with TNF-a antagonists, which is critical for granola formation

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15
Q

What are the risk factors for TB?

A
  • crowded conditions
  • malnourished
  • alcoholism, poverty
  • AIDS
  • elderly
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16
Q

What diseases predispose a patient to Tb risk?

A

DM, Hodgkin lymphoma, CKD, immunosuppression

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17
Q

What is Miliary TB?

A

lympho-hematogenous disseminated Tb (BM, liver, spleen, etc.). Can follow primary OR secondary TB

HIV patients at high risk

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18
Q

What is ‘progressive’ primary TB?

A

Tb that produces symptoms (roughly 10%)

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19
Q

How does secondary TB present?

A

insidious onset of malaise, anorexia, low-grade fever weight loss, night sweats, SOB, purulent sputum, blood streaked sputum, and rarely pleuritic pain

20
Q

What happens in progressive primary TB?

A

the initial infected tubercle can erode into a bronchus, spill its contents and infection then spread to other parts of the lung

21
Q

What does progressive primary TB resemble?

A

acute bacterial pneumonia.

22
Q

CXR of primary progressive TB?

A
  • lobar consolidation
  • hilar LAD
  • pleural effusion
23
Q

What is characteristic of military TB upon CXR?

A

millet seeds

24
Q

What are some complications of miliary TB?

A
  • meningitis
  • Pott’s disease
  • N/V, diarrhea
  • hematuria, proteinuria, sterile pyuria
25
Q

What is Pott’s disease?

A

vertebral osteomyelitis

26
Q

Other complications of Miliary TB?

A
  • pancytopenia (fom BM involvement)
  • Adrenal insufficiency
  • Epididymitis
  • prostatitis
27
Q

How is TB diagnosed?

A
  • acid fast sputum stain
  • culture (takes 3-6 weeks)
  • PCR
28
Q

What agar is needed to culture TB?

A

Lowenstein-Jensen agar (will not grow on BAP) OR

culture in liquid media (shows in 2 weeks)

29
Q

When should TB treatment be initiated?

A

When TB is suspected, do not wait for confirmed diagnosis- start treatment

30
Q

Treatment for primary/secondary TB?

A

-Isoniazid, Rifampin, Pyrazinimide, Ethambutol (RIPE)

31
Q

Why is such long treatment regimen needed for TB?

A
  • granuloma blocks ABX

- organism is slow growing

32
Q

What is MDR TB?

A

resistant to INH and RIF (common in AIDs patients)

33
Q

What is XDR TB?

A

resistance to INH, RIF, fluoroquinolone, and at least 1 other drug

34
Q

How does HIV affect TB?

A
  • increased frequency of false negative sputum smears
  • absence of granulomas
  • cavitation/bronchial damage less severe
35
Q

How is latent Tb diagnosed?

A
  • PPD (purified protein derivative)

- IGRA

36
Q

How does a PPD work?

A

I.D. injection of tuberculin material which stimulates a delayed type hypersensitivity mediated by T cells (causes induration within 48-72 hrs)

37
Q

What can cause a false positive PPD?

A

immunization with BCG or infection is a non-TB mycobacteria

38
Q

How does an IGRA (Quantiferon gold Quan-TB, T-spot) work?

A

Patient blood cells are exposed to antigens from MTB and the amount of INF-y released is measured. (no false positive from BCG or NTM infections)

39
Q

Latent Tb tests in HIV patients

A

False negatives can occur in both tests due to lack of immune response, called anergy

40
Q

How is latent Tb treated?

A

INH for 9 months OR

INH and Rifapentine for 3 months

41
Q

What determines a positive PPD?

A

risk factors

42
Q

What is a positive PPD in someone with no known risk factors?

A

15+mm

43
Q

What is a positive PPD in a homeless, IVDU, nursing home resident, recent immigrant, children under 4?

A

10-15mm

44
Q

What is a positive PPD in a HIV, immunosuppressed, organ transplant, prior TB?

A

5-10mm

45
Q

Do you measure the erythema or induration in a PPD?

A

induration!

46
Q

How can TB be prevented?

A
  • screen those with risk factors
  • treat latent converters
  • masks

Pulmonary Week 2 (25 decks)

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