MSPC 333 Systemic Pathology > Tuberculosis > Flashcards

Tuberculosis Flashcards

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1
Q

What microorganism causes tuberculosis (TB)?

A

Mycobacterium tuberculosis, a slow‑growing, acid‑fast bacillus with a lipid‑rich cell wall containing mycolic acids.

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2
Q

Is Mycobacterium tuberculosis Gram‑positive or Gram‑negative by standard staining?

A

It does not Gram‑stain well due to its lipid‑rich wall; it is identified by acid‑fast staining (Ziehl–Neelsen/Kinyoun).

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3
Q

Which stain is classically used to visualize Mycobacterium tuberculosis in sputum?

A

Ziehl–Neelsen acid‑fast stain (or Kinyoun method); auramine–rhodamine fluorescence can also be used.

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4
Q

What is the primary human reservoir and route of TB transmission?

A

Humans are the reservoir; transmission is via inhalation of airborne droplet nuclei from someone with active pulmonary TB.

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5
Q

What factors increase the risk of TB transmission in a community setting?

A

Prolonged close contact, poor ventilation/crowding, high bacillary load in the source, and absence of respiratory protection.

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6
Q

Where in the lung does the primary (initial) TB infection typically implant?

A

Lower part of the upper lobe or upper part of the lower lobe (middle zones), subpleural—forming the Ghon focus.

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7
Q

What is a Ghon focus?

A

The primary subpleural lesion (often caseating granuloma) formed at the initial site of Mycobacterium tuberculosis implantation.

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8
Q

What constitutes the Ghon complex?

A

A Ghon focus plus involvement of the draining (hilar) lymph nodes.

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9
Q

What is a Ranke complex?

A

Healed, calcified Ghon complex (calcified parenchymal focus and lymph nodes).

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10
Q

Which arm of the immune response is critical to controlling primary TB?

A

Th1‑mediated cellular immunity with IFN‑γ activation of macrophages.

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11
Q

Which cytokine is essential for macrophage activation and granuloma maintenance in TB?

A

Interferon‑gamma (IFN‑γ); TNF‑α is also crucial for granuloma integrity.

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12
Q

What histologic structure is characteristic of TB lesions?

A

Caseating (cheese‑like) granulomas with epithelioid histiocytes and Langhans giant cells, surrounded by lymphocytes and fibrosis.

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13
Q

What is the role of TNF‑α in TB pathogenesis?

A

It helps form and maintain granulomas; blocking TNF‑α (e.g., anti‑TNF therapy) can lead to TB reactivation.

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14
Q

Which lung regions are typically involved in secondary (reactivation) TB?

A

Apical/posterior segments of the upper lobes.

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15
Q

List three reasons secondary TB favors the lung apices.

A

Higher oxygen tension (M. tb is aerobic), relatively poorer lymphatic drainage, and lower perfusion (reduced immune surveillance).

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16
Q

Name additional factors that support apical reactivation of TB.

A

Relative mechanical under‑expansion with tidal breathing and a niche for dormant bacilli.

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17
Q

What clinical circumstances commonly trigger reactivation of latent TB?

A

Immunosuppression (HIV, steroids, anti‑TNF), malnutrition, diabetes, chronic kidney disease, silicosis, and aging.

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18
Q

What are the cardinal symptoms of pulmonary TB?

A

Chronic cough (often productive), hemoptysis, fever, night sweats, weight loss, fatigue.

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19
Q

When should TB be suspected in a persistent cough illness?

A

Cough ≥2–3 weeks plus systemic symptoms (fever, weight loss), risk factors, or hemoptysis.

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20
Q

What physical exam findings may be seen in advanced pulmonary TB?

A

Rales over apices, cachexia, fever; may have signs of pleural effusion or consolidation.

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21
Q

Define miliary TB.

A

Hematogenous dissemination causing numerous tiny millet‑seed lesions across multiple organs (lungs, liver, spleen, marrow).

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22
Q

What are two serious CNS manifestations of TB?

A

Tuberculous meningitis and intracranial tuberculomas.

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23
Q

What spinal disease is caused by TB and what are its complications?

A

Pott disease (TB spondylitis) causing vertebral body destruction, gibbus deformity, and potential cord compression.

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24
Q

Name two common non‑pulmonary sites of TB involvement besides CNS and spine.

A

Lymph nodes (scrofula) and genitourinary tract (sterile pyuria).

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25
What is 'sterile pyuria' and how does it relate to TB?
Pyuria with negative routine bacterial cultures; suggests genitourinary TB.
26
What component of M. tuberculosis cell wall is responsible for acid‑fastness?
Mycolic acids (long‑chain fatty acids) in the cell wall.
27
What is the function of 'cord factor' in M. tuberculosis?
Trehalose dimycolate; inhibits macrophage maturation, induces TNF‑α, promotes granuloma formation and serpentine cord growth.
28
What is the role of sulfatides in TB virulence?
They inhibit phagosome‑lysosome fusion, allowing intracellular survival in macrophages.
29
What chest X‑ray pattern is typical of reactivation TB?
Cavitary lesions in the apical/posterior upper lobes, with surrounding infiltrates.
30
What radiographic sequelae may follow healed TB?
Fibrosis, calcified nodules or lymph nodes (Ranke complex), bronchiectasis, and volume loss.
31
What causes cavitation in TB lesions?
Caseous necrosis eroding into airways, allowing drainage and formation of air‑filled cavities.
32
What are the first‑line microbiologic tests for suspected pulmonary TB on sputum?
AFB smear microscopy and nucleic acid amplification test (e.g., Xpert MTB/RIF) for rapid detection and rifampicin resistance.
33
What is the gold standard for definitive TB diagnosis?
Mycobacterial culture with species identification and drug susceptibility testing (e.g., on Löwenstein–Jensen or liquid MGIT).
34
Why are multiple sputum specimens collected for TB testing?
Intermittent bacillary shedding; multiple samples increase sensitivity of smear/culture/NAAT.
35
What biosafety measures are required when handling TB specimens in the lab?
BSL‑3 practices for culture/aerosol‑generating procedures; appropriate biosafety cabinets and PPE.
36
What is the standard initial (intensive) regimen for drug‑susceptible TB?
RIPE: Rifampin (R), Isoniazid (H), Pyrazinamide (Z), Ethambutol (E) for 2 months.
37
What is the continuation phase for drug‑susceptible pulmonary TB after RIPE?
Typically 4 months of Rifampin + Isoniazid (total 6 months), adjusted per guidelines and site of disease.
38
Why is TB treated with multiple drugs simultaneously?
To prevent emergence of resistance and to target bacilli in different metabolic states/compartments.
39
What is directly observed therapy (DOT) and why is it used in TB?
A strategy where medications are observed being taken to improve adherence and reduce resistance/relapse.
40
What is the mechanism of action of isoniazid (INH)?
Inhibits mycolic acid synthesis after activation by KatG; bactericidal to rapidly dividing TB.
41
What vitamin deficiency can INH cause and what is given to prevent it?
Pyridoxine (vitamin B6) deficiency leading to neuropathy; give pyridoxine supplementation.
42
What are two major toxicities of isoniazid?
Hepatotoxicity and peripheral neuropathy (risk increased in slow acetylators).
43
What is the mechanism of rifampin?
Inhibits DNA‑dependent RNA polymerase (β‑subunit), blocking RNA synthesis.
44
Name two important adverse effects or interactions of rifampin.
Hepatotoxicity and potent CYP450 induction causing many drug interactions; orange discoloration of body fluids.
45
What is the mechanism of pyrazinamide?
Converted to pyrazinoic acid; active in acidic intracellular environments; exact mechanism not fully defined.
46
What are the key adverse effects of pyrazinamide?
Hepatotoxicity and hyperuricemia (may precipitate gout).
47
What toxicity is classically associated with ethambutol?
Optic neuritis (red‑green color blindness and decreased visual acuity).
48
Which TB drug should be stopped first if optic neuritis develops?
Ethambutol.
49
Which TB drug has the highest risk of CYP450 interactions?
Rifampin.
50
What baseline tests are recommended before initiating RIPE therapy?
Baseline liver function tests (LFTs), visual acuity and color vision (for ethambutol), and review of concomitant medications.
51
Define multidrug‑resistant TB (MDR‑TB).
TB resistant to at least isoniazid and rifampin.
52
Define extensively drug‑resistant TB (XDR‑TB).
TB resistant to isoniazid and rifampin, plus any fluoroquinolone, and at least one of the second‑line injectable drugs (or per updated WHO definitions including newer agents).
53
Name two risk factors for developing drug‑resistant TB.
Prior inadequate/incomplete therapy and poor adherence; also exposure to a known resistant case.
54
What is the general approach to treating MDR‑TB?
Use of at least 4–5 effective drugs guided by susceptibility (e.g., bedaquiline, linezolid, levo/moxifloxacin, clofazimine) for longer durations with close monitoring.
55
Which T‑helper subset drives protective immunity against TB and via which cytokine?
Th1 subset via IFN‑γ.
56
What happens to TB risk in patients receiving anti‑TNF biologics?
Risk of reactivation increases because TNF‑α maintains granuloma integrity.
57
What is the histologic appearance of a Langhans giant cell?
A multinucleated giant cell with nuclei arranged peripherally in a horseshoe pattern.
58
What is caseous necrosis and why is it important in TB?
Cheese‑like acellular necrosis from immune‑mediated destruction; central feature of TB granulomas and cavitation.
59
What vascular complication can cause sudden massive hemoptysis in TB?
Rupture or erosion of a Rasmussen aneurysm (pulmonary artery pseudoaneurysm adjacent to a cavity).
60
How can TB lead to aspergilloma formation?
Old TB cavities can become colonized by Aspergillus, forming a fungus ball that may cause hemoptysis.
61
How does TB cause bronchiectasis?
Chronic inflammation and destruction of airway walls lead to irreversible bronchial dilation.
62
What are common long‑term pulmonary sequelae after healed TB?
Fibrosis, restrictive defect, bronchiectasis, recurrent infections, and chronic hemoptysis.
63
What type of isolation is required for patients with suspected or confirmed pulmonary TB in hospitals?
Airborne precautions in a negative‑pressure room; N95 respirators for staff.
64
When can airborne isolation typically be discontinued in pulmonary TB?
After clinical improvement, effective therapy, and typically three consecutive negative AFB smears on separate days (per local policy).
65
Why are children with TB often paucibacillary?
They mount less cavitary disease and have lower bacillary loads, making bacteriologic confirmation harder.
66
What is a common manifestation of TB in young children compared with adults?
Intrathoracic lymph node disease and primary complex; disseminated/miliary forms are more common in infants.
67
How does pregnancy affect TB management?
Most first‑line drugs (INH, RIF, EMB) are used with caution; avoid streptomycin (ototoxicity). Treat active disease promptly to protect mother and fetus.
68
What causes TB pleural effusion pathophysiologically?
Hypersensitivity reaction to mycobacterial antigens in the pleural space leading to exudative, lymphocyte‑predominant effusion.
69
What are features of tuberculous lymphadenitis (scrofula)?
Painless, matted cervical nodes that may suppurate and form sinus tracts; caseating granulomas on histology.
70
What are epithelioid histiocytes?
Activated macrophages with abundant pink cytoplasm found in granulomas.
71
How does M. tuberculosis survive inside macrophages?
Prevents phagolysosome fusion (via sulfatides), resists reactive oxygen/nitrogen species, and exploits host lipids.
72
Why can TB lesions persist despite immune activation?
Intracellular persistence, hypoxic/necrotic niches, and phenotypic tolerance of bacilli in caseous centers.
73
What is the rationale for using combination therapy and ensuring adherence from a public health perspective?
To reduce transmission by rapidly lowering bacillary load and to prevent emergence/spread of drug‑resistant strains.
74
In a household exposure to smear‑positive TB, which contacts are at highest risk of progression if infected?
Young children (<5 years), HIV‑infected or otherwise immunosuppressed individuals.
75
Name two diseases that can mimic cavitary pulmonary TB on imaging.
Chronic pulmonary aspergillosis and cavitary lung cancer (especially squamous cell carcinoma); also necrotizing bacterial pneumonia.
76
How do nontuberculous mycobacteria (NTM) differ clinically from TB?
NTM (e.g., M. avium complex) are environmental; disease often in underlying lung pathology or immunosuppression and are not usually transmitted person‑to‑person.
77
Why does apical cavitary TB facilitate transmission more than non‑cavitary disease?
Cavities communicate with airways and contain high bacillary loads, increasing aerosolization and infectivity.
78
Which host genetic or acquired factors predispose to severe TB disease?
IL‑12/IFN‑γ axis defects, HIV infection (low CD4), malnutrition, and diabetes mellitus.
79
Why does silicosis increase TB risk?
Silica impairs macrophage function and promotes a milieu favoring mycobacterial survival and reactivation.
80
Which TB medications are most hepatotoxic and require LFT monitoring?
Isoniazid, rifampin, and pyrazinamide.
81
What symptoms should prompt urgent evaluation for TB drug‑induced hepatitis?
Jaundice, right upper quadrant pain, dark urine, marked fatigue/anorexia, or significant LFT elevations.
82
What is the incubation/latent period concept in TB?
After initial infection, bacilli may persist in a latent state for years, with disease developing upon later immunologic failure.
83
Why do patients with advanced HIV have atypical chest X‑rays for TB?
Impaired Th1 response reduces cavitation; lower lobe or diffuse infiltrates and intrathoracic adenopathy are more common.
84
What two antimicrobial classes (besides RIPE) are commonly used in resistant TB regimens?
Fluoroquinolones (levofloxacin/moxifloxacin) and oxazolidinones (linezolid).
85
What skin condition can occur at BCG vaccination sites in disseminated TB of immunocompromised hosts?
Ulceration or local reactivation (BCGitis) in severe immunodeficiency.
86
Summarize why granulomas form in TB.
To contain infection: Th1 cells produce IFN‑γ → activate macrophages → epithelioid cells and giant cells surround bacilli, with caseous necrosis centrally and fibrosis peripherally.
87
Why is prolonged therapy required for TB compared to many bacteria?
Slow growth rate of M. tb, intracellular location, and subpopulations with phenotypic drug tolerance require extended multi‑drug therapy.
MSPC 333 Systemic Pathology
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