Lecture 8: TB Flashcards

1
Q

What shape is TB? What stain? Intra/extracellular?

A

Aerobic, rod-shaped; acid-fast; intracellular

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2
Q

Describe primary TB infection

A

Mycobacteria in alvoeli –> Gohn lesion (small focus) –> spread (hilar lymph nodes) to distant organs or lung apex

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3
Q

Generally, what happens after primary infection?

A

Body’s defense control it and leaves only scarring

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4
Q

In 5% of patients, you can get (during the primary infection)…

A

Progressive primary TB (due to immunosupression, alcoholism…)

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5
Q

What causes the development of granulomas?

A

Cell-mediated hypersensitivity

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6
Q

Describe the process of healing granulomas

A

Fibrosis often with deposition of calcium

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7
Q

What surrounds caseous center of a granuloma?

A

Macrophages that have become epithelioid histiocytes, surrounded by lymphocytes and fibroblasts

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8
Q

Which cell begins the process of granuloma formation? What happens?

A

Alveolar macrophages: come in contact with TB, secrete cytokines, interact w/ lymphocytes

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9
Q

Describe latent TB

A

TB not totally cleared creating balance b/t TB and immune system, but majority of patients will never have further difficulty

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10
Q

Describe reactivation TB (%)

A

Immune system weakens; 10% will reactivate (50% within 2 years, 50% for rest of life)

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11
Q

What is injected in PPD? Does it distinguish b/t active TB or previous infection? Why might you get a false negative? False positive?

A

Small amount of purified TB protein; nope; impaired cell-mediated immunity; if you’ve had infection w/ other mycobacterium

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12
Q

What’s an alternative to PPD? Why is this test better?

A

Interferon-gamma release assay; antigens used are specific to TB

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13
Q

Does IGRA solve the immuno compromised problem?

A

Nope! Still must develop cellular immunity

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14
Q

During primary spread, organism spreads through the…

A

Bloodstream (to other organs and lung)

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15
Q

Characteristic location of reactivation TB

A

Higher lobes of lungs: high pO2 and less perfusion (likes aerobic bacilli, dislikes immune cells in the blood)

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16
Q

Why is TB called consumption?

A

Patient looks consumed: weight loss, wasting, loss of appetite

17
Q

How does TB affect lung function and V/Q matching?

A

Respiratory function preserved because the disease is in upper lungs; no V/Q mismatch because ventilation and perfusion destroyed simultaneously

18
Q

TB systemic symptoms (4)

A

Weight loss, fatigue, night sweats, low-grade fever

19
Q

TB pulmonary symptoms (3)

A

Cough, sputum, hemoptysis

20
Q

Chest radiograph (primary, healed primary, reactive, miliary)

A

Primary: non-specific infiltrate in lower lobes (+/-) lymph enlargement, effusion; Healed primary: small calcified lesions; Reactivation: apical lobes with infiltrates, cavities, nodules, scarring, contraction; Miliary: dots all over lungs

21
Q

Describe miliary TB

A

Progressive, disseminated hematogenous spread of TB (primary or secondary) that looks like millet seeds

22
Q

Diagnose TB methods

A
  1. Stained smears looking for acid fast bacilli via sputum sample; 2. Nucleic acid amplification (requires fewer organisms, more specific); 3. Culture (required for drug susceptibility)
23
Q

TB Treatment

A

Active: multiple agents for 6 months – isoniazid, rifampin, pyranzinamide, ethambutol

24
Q

Who do you treat if they have latent TB?

A

People who are exposed to those with active infection or the immunocompromised

25
Q

Describe non-TB mycobacteria: most common organism, those at risk

A

There are many and they are potential pulmonary pathogens, most common is MAC (mycobacterium avium complex); ppl with lung disease or immunocompromised

26
Q

BCG vaccine: living? greatest benefit? who do you give it to?

A

Live strain of another mycobacterium; diminishes risk of TB meningitis and disseminated disease in children; neonates in countries with high prevalence