Tuberculosis Flashcards

1
Q

how is TB distributed in the UK?

A

• it is more common in more deprived areas of the world?

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2
Q

What is happening to the TB incidence worldwide?

A

• it is reducing

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3
Q

2/3 of TB cases are found in how many countries?

A

• 8 countries

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4
Q

Where are most of the cases of TB found in the UK?

A

• London (clusters in cities)

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5
Q

What groups are vulnerable to TB?

A

• People from high prevalence countries, HIV positive, Immunocompromised, Elderly, Neonates, Diabetics, Homeless, Alcohol dependency, IV drug use, Mental health problems, prisoners

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6
Q

What is the characteristic of TB?

A

• It is non motile, it is very slowly growing and it is aerobic, uniquely has a very thick fatty cell wall (resistant to acids, alkalis, detergents, neutrophil and macrophage destruction)

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7
Q

How does TB spread?

A

• Airborne, someone with TB bacteria in their lungs coughs, TB bacteria attached to aerosol droplets which can remain suspended in air for many hours, especially if there is poor air circulation, someone breathes this bacteria in, requires prolonged close contact.

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8
Q

How is TB not spread?

A

• Shaking hands, sharing food, touching surfaces, sharing toothbrushes, kissing

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9
Q

What is the primary infection of TB?

A

• no preceding exposure or immunity, Mycobacteria spread via lymphatics to draining hilar lymph nodes. Usually no symptoms, can be fever, malaise

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10
Q

What are the three outcomes of primary infection?

A

• Progressive disease - ineffective immune response from the patient, Contained latent - activates when the patient becomes immunocompromised, Cleared + cured

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11
Q

What happens during progressive disease after primary infection?

A

• Primary infection prgresses to TB bronchopneumonia, primary focus continues to enlarge, enlarged hilar lymph nodes compress bronchi, lobar collapse, enlarged lymph nodes discharged into bronchus, poor prognosis

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12
Q

What happens in post-primary disease?

A

• TB bacteria enetering a dormant stage with low or no replication over prolonged periods of time, Balnced stage of replication and destruction by immune mechanisms

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13
Q

What are the main clinical presentations of TB?

A
  • Cough
  • Fever
  • Sweats
  • Weight loss
  • All three symptoms
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14
Q

How to identify TB?

A
  • Sputum; 3 samples, 8-24hr gap, at least 1 morning sample
  • induced sputum
  • Bronchoscopy with BAL
  • Endobronchial ultrasound with biopsy
  • lumbar puncture in CNS TB
  • Urine in urogenital TB
  • Aspirate/biopsy from tissue (bone, lymph node, joint, brain, abscess)
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15
Q

What are the drugs used for TB?

A

• Isoniazid, Pyrazinamide, Rifampicin, Ethambutol

Immunosupressive drugs

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16
Q

What are the rules for TB treatment?

A
  • multiple drug therapy is essential (single treatment leads to drug resistant organisms within 14 days)
  • Therapy must continue for at least 6 months
  • TB therapy is a job for committed specialists only
  • Legal requirement to notify all cases
  • Test for HIV, Hepatitis A, B and C
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17
Q

What are the main side effects of treatment for TB?

A
  • hepatitis
  • rash
  • Rifampicin - ornage irn bru urine, tears, lenses, induces liver enzymes, all hormonal contraceptive methods ineffective
  • Isoniazid - Peripheral neuropathy
  • Pyrazinamide - Gout
  • Ethambutol - Optic neuropathy
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18
Q

What is the microorganism responsible?

A

Mycobacteria

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19
Q

What are the other mycobacterium that don’t cause tb?

A

Mycobacteria other than tuberculosis (MOTT) (about 30% of UK isolations)

Mycobacterium avium-intracellulare (HIV)

M. kansasii, M. malmoense, M. xenopii

Mycobacterium leprae leprosy

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20
Q

What removes mycobacteria outdoors?

A

UV radiation and infinite dilution

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21
Q

Which type of droplet nuclei impact in the alveoli and slowly proliferate?

A

Small nuclei, Larger droplet nuclei impact on large airways and cleared

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22
Q

How is infection of mycobacterium bovis spread?

A

Consumption of infected cows’ milk

  • deposited in cervical, intestinal lymph nodes
23
Q

What stimulates the macrophages to become activated?

A

Th1 helper cells from the lymph node, these Th1 cells are activated by antigen presenting cells.

These Th1 cells after receiving the signal from the antigen presenting cell then clonially proliferate in the lymph node

24
Q

What are Th1 cells?

A

Type 1 T helper (Th1) cells produce interferon-gamma, interleukin (IL)-2, and tumour necrosis factor (TNF)-beta, which activate macrophages and are responsible for cell-mediated immunity and phagocyte-dependent protective responses.

25
Q

Which specific chemical activates macrophages?

A

Interferon gamma CD40 - which is produced by Th1 cells in the lymph node

26
Q

What is the result of activated macrophages?

A

Damaged epithelioid cells

Langhan’s giant cells

Accumulation of macrophages, epithelioid & Langhan’s cells GRANULOMA

Central caseating necrosis (may later calcify)

27
Q

What disease is caseus necrosis usually indicative of ?

A

TB

28
Q

What is meant by the 2 edged sword of the Th1 cell mediated immunological response?

A

Eliminates / Reduces number of invading mycobacteria

Tissue destruction is a consequence of activation of macrophages

29
Q

What is the pathology for a resistant and susceptible host?

A

Tissue destruction

Organism contained

Disease

30
Q

Who is normally affected by the primary infection?

A

Usually children, 80% Infected focus in alveolus, (lymph nodes, gut)

31
Q

Where do mycobacteria spread to once they are in the alveoli?

A

Spread via lymphatics to draining hilar lymph nodes

Then there is haematogenous seeding of mycobacteria to all organs of the body (lung, bone, genitourinary system)

32
Q

What is the mantoux test?

A

Injection of tuberculin into the transdermal layer of skin. After 48-72 hours amount of induration present can identify possible health problems.

33
Q

What is responsible for the induration in the mantoux test?

A

Intra dermal administration of tuberculoprotein (PPD - Purified protein derivative) results in lymphocytic and macrophage based area of inflammation/induration after 48 hours

34
Q

how does TB affect the CSF and the pleura?

A

Can cause meningeal TB (severe, CSF high protein, lymphocytes)

AND

Tuberculosis pleural effusion

35
Q

What are the sites of post primary disease from TB?

A

Pulmonary disease

Lymph nodes, usually cervical

Bone and joint; spine, hip, etc

Genito-urinary; kidney, ureter, bladder

Males; infertility - vas deferens

Females; infertility - uterus, Fallopian tubes

Pericardium; constrictive pericarditis

Abdomen; ascites, ileal TB ® obstruction

Adrenal ® Addison’s disease

Skin; lupus vulgaris

Just about any other tissue!

36
Q

What are the features of TB usually after 6-12 months?

A

Miliary , meningeal, pleural TB

37
Q

What are the features of TB after 1-5 years?

A

Post primary disease - pulmonary and skeletal

38
Q

What are the features of TB after 10 years?

A

Genitourinary, Cutaneous T

39
Q

What are the symptoms for Post primary TB?

A

Respiratory; cough, sputum, haemoptysis, pleuritic pain or breathlessness

Systemically unwell

malaise, fever, weight loss (“night sweats”) - very characteristic of TB

40
Q

What is characteristic PMH for Post-primary Pulmonary Tuberculosis?

A

Diabetes, Immunosuppressive diseases, Previous TB

41
Q

What is the PSH for post primary pulmonary TB?

A

Alcohol – poor nutrition, immune system is suppressed, IVDA (intravenous drug users? Immnue system suppressed), poor social circumstances, Immigrants from high incidence areas

42
Q

What are the signs for Post-primary Pulmonary Tuberculosis?

A

May be none at all - extensive TB can be present without physical signs!

If more advanced, may be crackles, bronchial breathing.

Finger clubbing is rare unless very chronic infection

43
Q

What are the means of diagosing TB?

A

Sputum analysis

Chest radiograph

CT scan of thorax

Bronchoscopy with alveolar lavage, transbronchial biopsy

Pleural aspiration and biopsy if peural effusion

44
Q

How do we analyse sputum samples for TB?

A

ZN stain - immediate answer if AAFB

Culture

Sputum PCR

45
Q

What features of a chest radiograph confirms presence of TB?

A

Patch shadowing, often in apices/upper zones, or apex or lower lobes

Cavitation

Calcification if chronic or healed TB

46
Q

What happens after the fluid is collected from the pleural aspiration?

A

FLuid cytology (lymphocytes)

Fluid for AAFB and culture

Biopsy histology

1 biopsy sent in Saline for culture

47
Q

What is treatment of tuberculosis?

A

Vitamin D causes macrophages to release Cathelecidin which is a very potent antibiotic.

Surgery - Collapse of the cavity by: Phrenic crush (crushing the phrenic nerve causes the diaphragm on that side to become paralysed and rise up, closing the cavity), artificial pneumotorax (collapses the lung and therefore the cavity), pneumoperitoneum, thoracoplasty (Six to eight ribs were broken and pushed into the thoracic cavity to collapse the lung beneath), lung resection (removal of a segment of lung).

48
Q

How are drugs used against TB?

A

Multiple used to prevent resistant organisms forming,

Therapy at least 6 months, slowly growing organism

ONLY SPECIALISTS TREAT

49
Q

Likelihood of infection with TB depends on?

A

Duration of contact

Intensity of infection

50
Q

How do you screen for TB using tuberculoprotein?

A

If younger than 16 and no BCG there should be no immunity to Tuberculoprotein

51
Q

What other test besides the mantoux test can determine the presence of TB?

A

Heaf test

52
Q

How would you treat a patient who is heaf positive (2-4) exposed to TB?

A

If their X-ray is normal they are at risk of disease (miliary, or meningeal)

Chemoprophylaxis to kill mycobacteria

Rifampicin + Inh (isoniazid) 3 months

Inh 6 months

If their X-ray is abnormal - Treat as primary TB

53
Q

What should you do 6 weeks after a heaf negative result?

A

2nd heaf test

If it is negative - BCG

If it is positive - follow procedures with a chest X-ray and follow up procedure

54
Q

If older than 16 with an abnormal chest X-ray?

A

Investigate for TB and treat if necessary