27.28. Tuberculosis and other pulmonary infections Flashcards

1
Q

What is tuberculosis?

A

It is an infectious disease caused by Mycobacterium tuberculosis, a slow-growing bacteria.

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2
Q

What is the mechanism of infection of tuberculosis?

A

It is usually by inhalation of aerosols containing TB, through close contact with patients with active TB infection.

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3
Q

What is latent TB infection?

A

It is a dormant M. tuberculosis infection, typically due to intact innate and cellular immune responses.

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4
Q

What are the other strains of the tuberculosis complex?

A

They are M. bovis, M. africanum

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5
Q

What are the high-risk groups for TB?

A
  • HIV patients,
  • close contacts,
  • patients with old healed apical fibronodular lesions,
  • IV drug users,
  • immigrants from high prevalence countries,
  • those in correctional institutions, nursing homes, and mental institutions.
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6
Q

How does prolonged exposure to TB increase the risk of infection?

A

It increases the risk of infection by 30-50% in people living in the same household.

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7
Q

What are the other routes of TB infection?

A

Intestines (unpasteurized milk) and skin (open wound, tuberculosis verrucosa cutis – butchers, pathologists).

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8
Q

What is the pathomechanism of TB infection?

A
  • Granulomatous inflammation
  • TB antigens activate lymphocytes and NK cells which produce IFN-gamma
  • Macrophages differenciate into epitheloid cells and multinucleated giant cells : enclose the bacteria like a wall
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9
Q

What is the pathophysiology of primary TB?

A

New TB infection → entry of M. tuberculosis into macrophages → survives because of the inhibition of both phagosome maturation and phagolysosome fusion.

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10
Q

What happens following replication of M. Tuberculosis in the alveolar macrophages in primary TB?

A

The released bacteria attacks uninfected macrophages to spread infection.

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11
Q

What causes central caseous necrosis and tissue damage in primary TB?

A

Destruction of M. tuberculosis-infected macrophages causes central caseous necrosis and tissue damage → granuloma limits the spread of infection.

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12
Q

What is a Ghon focus?

A

A granuloma typically located in the middle and lower lobes

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13
Q

What is a Ghon complex?

A
  • A Ghon focus + enlarged lymph nodes + lymphatic vessels connecting the two, which means that the lymph nodes become infected as well.
  • It can be seen on a CXR as a more extensive area of inflammation than the Ghon focus alone.
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14
Q

What is the disease progression of TB with a sufficient immune response?

A

The granulomas in the Ghon complex undergo fibrosis and calcification to form the Ranke complex, which is radiologically detectable.

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15
Q

What is the disease progression of TB with a deficient immune response?

A

Progressive primary TB causing progressive lung disease, bacteremia, and miliary TB (disseminated TB).

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16
Q

What is post-primary (secondary) TB?

A

It is the reactivation of TB due to weakening of the immune response (e.g. HIV).

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17
Q

What are the clinical features of TB?

A
  • Cough, initially dry, later productive (cheesy),
  • fever,
  • night sweats,
  • weight loss
  • hemoptysis.
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18
Q

What is the difference between primary and post-primary TB?

A

Primary TB is the initial infection, while post-primary TB is the reactivation of TB due to weakening of the immune response.

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19
Q

What are the diagnostic follow-ups in suspected tuberculosis?

A
  • History (try to find exposure to TB),
  • chest X-ray,
  • general lab tests,
  • bacteriology.
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20
Q

What are the lab signs of tuberculosis?

A

ESR, CRP, neutrophilia, lymphopenia, hypoalbuminemia, anemia, impaired liver function, hyponatremia, low iron, and increased ferritin.

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21
Q

What are the auscultation findings in tuberculosis?

A
  • Rales
  • Lung consolidation (very clear sounds)
  • wheezing as peribronchial and endobronchial airway obstruction develops
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22
Q

What is the main rule for tuberculosis on chest X-ray?

A

TB can induce any pattern of X-ray shadowing, including upper lung zone fibronodular pattern and upper lung zone fluffy coalescence.

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23
Q

What percentage of TB patients have lower zone involvement?

A

Less than 15%.

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24
Q

Are pleural effusions common in reactivation-type pulmonary TB?

A

No, they are uncommon.

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25
Q

What is the significance of morning sputum in TB diagnosis?

A

It is used to detect the presence of TB bacteria in the patient’s respiratory secretions, after testing with Ziehl Neelsen stain.

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26
Q

How many consecutive days should morning sputum be taken for TB diagnosis?

A

Three.

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27
Q

What is the preferred method of obtaining respiratory secretions if the patient cannot provide morning sputum?

A

Gastric lavage.

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28
Q

Will TB bacteria be destroyed by gastric acid?

A

No.

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29
Q

What are the more invasive measurements that can be done if morning sputum or gastric lavage is not available?

A

Bronchial wash and bronchoalveolar lavage.

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30
Q

What is a special requirement for blood samples taken for TB diagnosis?

A

A special hemoculture container is needed.

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31
Q

What is the gold standard for diagnosing latent TB?

A

Lewenstein-Jensen (solid medium).

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32
Q

What are the pros and cons of Lowenstein Jensen?

A
  • More sensitive
  • But takes 8 weeks
33
Q

How long does it take for liquid medium to diagnose latent TB?

A

2-3 weeks.

34
Q

What does a positive culture and negative sputum sample indicate in TB diagnosis?

A

Latent TB.

35
Q

What skin test can be used for TB?

A

Tuberculin skin test (Mantoux).

36
Q

What is the hypersensitive response to the tuberculin skin test?

A

Edema >10mm.

37
Q

What does anergic response to the tuberculin skin test indicate?

A

Susceptibility to TB or immunocompromised.

38
Q

What factors affect the interpretation of the tuberculin skin test?

A

BCG vaccination, prior infection, immune system

39
Q

What is the Quantiferon TB test?

A

It is a test that isolates mononuclear cells from a patient’s blood sample and checks if they produce IFN-gamma in the presence of MTBC antigens, indicating sensitization to TB.

40
Q

What are the advantages of the Quantiferon TB test over the tuberculin skin test?

A

It is more sensitive and specific than the tuberculin skin test and is not positive in non-TB cases.

41
Q

What is the first-line treatment for TB?

A

The first-line treatment for TB includes Rifampicin, Isoniazid, Pyrazinamide and Ethambutol. (RIPE)

42
Q

What are the side effects of Rifampicin?

A
  • Hepatotoxicity,
  • exanthemas,
  • hemolytic anemia,
  • renal insufficiency,
  • secretion of orange-colored fluids.
43
Q

What are the side effects of Isoniazid?

A

The side effects of Isoniazid include hepatotoxicity, neurotoxicity, and MAO inhibition.

44
Q

What are the side effects of Pyrazinamide?

A
  • Hepatotoxicity,
  • hyperuricemia (jaundice),
  • photosensitive dermatitis
  • polyarthralgia.
45
Q

Should Pyrazinamide be avoided in pregnancy?

A

Yes.

46
Q

How often should Pyrazinamide be administered in renal failure?

A

Every other day.

47
Q

What are the side effects of Ethambutol?

A

Optic neuritis (vision problems), peripheral neuritis.

48
Q

Can Ethambutol be given in pregnancy?

A

Yes.

49
Q

What is the usual 6-month treatment plan for TB?

A

2 months of 4 drugs (intensive phase), followed by 4 months of isoniazid and rifampicin (continuation phase).

50
Q

What is the duration of treatment if the therapeutic response is not adequate?

A

It can be prolonged to 12 months.

51
Q

What are the second-line treatments for TB?

A

Streptomycin, kanamycin, amikacin, cycloserine, ethionamide, PAS, and levofloxacin.

PAS : para-aminosalicylic acid

52
Q

What are the side effects of Levofloxacin?

A

GI symptoms, QT prolongation, photosensitivity.

53
Q

Can Levofloxacin be given in pregnancy and renal failure?

A

Yes.

54
Q

What are the side effects of Ethionamide at a dose of 1g/day?

A

Nausea and hepatotoxicity.

55
Q

What are the side effects of PAS at a dose of 12-15g/day?

A

GI symptoms, hepatotoxicity, coagulopathy, and hypothyroidism.

56
Q

What is the recommended dose range for Levofloxacin or Moxifloxacin in TB treatment?

A

500-1000mg/day.

57
Q

What is drug-resistant TB?

A

TB that is resistant to one first-line agent.

58
Q

What is multidrug-resistant (MDR) TB?

A

TB that is resistant to isoniazid and rifampicin.

59
Q

What is extensively drug-resistant (XDR) TB?

A

MDR TB plus resistance against fluoroquinolones and on second-line IV drug (amikacin, kanamycin).

60
Q

When can we presume resistance in MDR-(XDR) TB treatment?

A

If there is no clinical improvement after 1-2 months of treatment, we can presume resistance even before the culture results.

61
Q

What is the recommended duration of treatment for MDR-(XDR) TB?

A

At least 18-24 months with 4 effective drugs, preferably with DOT (directly observed therapy).

62
Q

What is the recommended drug regimen for MDR-(XDR) TB treatment?

A

Effective first-line drug plus fluoroquinolones plus daily administered IV drug plus effective second-line agent.

63
Q

What is Pneumocystis jirovecii pneumonia (PCP)?

A

It is an opportunistic fungal lung infection that occurs in almost exclusively immunocompromised individuals.

64
Q

What are the risk factors for PCP?

A
  • HIV infection,
  • primary immunodeficiency disorder,
  • immunosuppressive treatment.
65
Q

What are the clinical features of PCP?

A
  • Fever,
  • dyspnea,
  • nonproductive cough,
  • fatigue,
  • weight loss,
  • chills,
  • may progress to respiratory failure.
66
Q

What are the diagnostic tests for PCP?

A
  • Lab test -> beta-glucan (occurs in cell wall of most fungi), CD4 count (HIV),
  • Imaging -> CXR: diffuse, bilateral, symmetrical interstitial infiltrates extending from the perihilar region (butterfly pattern),
  • Histopathology: (confirmatory test) -> Induced sputum and bronchoalveolar lavage.
67
Q

What is the treatment for mild to moderate PCP?

A

Oral TMP/SMX.

68
Q

What is the treatment for moderate to severe PCP?

A

IV TMP/SMX.

69
Q

What is the prophylaxis for patients with HIV infection with low CD4 cell count?

for asp. and pcp prevention

A

Low dose TMP/SMX.

70
Q

What is Aspergillosis?

A

It is the collective term for diseases caused by the mold species in the genus Aspergillus (opportunistic pathogen).

71
Q

What is the etiology of Aspergillosis?

A

Most common : Aspergillus fumigatus + Aspergillus flavus.

72
Q

What is aspergillosis?

A

Aspergillosis is the collective term for diseases caused by the mold species in the genus Aspergillus.

73
Q

How is aspergillosis transmitted?

A

Aspergillosis is transmitted through airborne exposure to mold spores that settle on a source of nutrition, dust, or plants.

74
Q

What are the risk factors for aspergillosis?

A

The risk factors for aspergillosis include severe immunosuppression or neutropenia, as well as preexisting bronchopulmonary conditions such as asthma or CF.

neutropenia : low blood count of neutrophils

75
Q

What is Aspergillus bronchopulmonary aspergillosis (ABPA)?

A
  • Aspergillus bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction caused by exposure to Aspergillus that occurs in patients with CF or asthma
  • It is characterized by asthmatic symptoms and productive cough with brown bronchial mucous casts.
76
Q

What is chronic pulmonary aspergillosis?

A
  • Chronic pulmonary aspergillosis is a long-term Aspergillus infection which can manifest as an aspergilloma, a opportunistic infection of a preexisting cavitary lesion,
  • It is characterized by hemoptysis and dyspnea.
77
Q

What is invasive aspergillosis?

A

Invasive aspergillosis is a severe form of aspergillosis which manifests with severe pneumonia and septicemia with potential involvement of other organs, and is characterized by dry cough, hemoptysis, pleuritic chest pain, and tachypnea.

78
Q

What are the diagnostic methods for aspergillosis?

A
  • chest X-ray, CT scan,
  • culture of Aspergillus in sputum or bronchoalveolar lavage,
  • skin test for Aspergillus antigen,
  • elevated IgE levels in ABPA,
  • elevated galactomannan antigen test in invasive aspergillosis.