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1ST YEAR SYSTEMS: Respiratory > Tuberculosis COPY (Graeme M) > Flashcards

Tuberculosis COPY (Graeme M) Flashcards

1
Q

How many of the 2 billion infected people with tuberculosis have HIV?

A

1.1 million

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2
Q

How likely is TB to cause death?

A

Second leading cause of death from an infectious disease worldwide

  1. 3 million deaths annually
  2. 3 million HIV positive

74 000 children

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3
Q

Describe the trend in incidence of TB before and after 1980?

A

Until mid-1980s TB in the UK was declining and considered to be under control

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4
Q

Where are 39% of TB cases in the UK?

A

London

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5
Q

What is the microrganism responsible?

A

Mycobacteria

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6
Q

What are the specific names for the organisms responsible for TB?

A

Mycobacterium tuberculosis

M. bovis (“bovine TB”)

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7
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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8
Q

Describe the type of bacterium that Mycobacterium tb is?

A

Non-motile bacillus

Very slowly growing

Aerobic - predilection for apices of lungs (ventilated but not perfused)

Very thick cell wall lipids, peptidoglycans, arabinomannans

Resistant to acids, alkalis and detergents

Resistant to neutrophil and macrophage destruction

Aniline based dyes such as carbol fuschin complex with cell wall

Unable to remove dye from cell wall

Acid - and alcohol - fast bacilli (AAFB) (Ziehl Neilson stain)

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9
Q

What is the source of TB?

A

‘Open’ pulmonary TB = coughing and sneezing releases respiratory droplets which evaporate. These droplet nuclei remain airborne for very long periods.

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10
Q

What removes mycobacteria in outdoors?

A

UV radiation and infinite dilution

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11
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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12
Q

How is infection of mycobacterium bovis spread?

A

Consumption of infected cows’ milk

  • deposited in cervical, intestinal lymph nodes
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13
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

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14
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.

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15
Q

Which specific chemical activates Macrophages?

A

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

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16
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)

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17
Q

What disease is caseus necrosis usually indicative of ?

A

TB

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18
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

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19
Q

What are the factors affecting susceptibility?

A

Genetics

Race

Nutrition

Age

Immunosuppression

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20
Q

What is the pathology for a susceptible host?

A

Tissue destruction

Proliferation of organism

Progressive disease

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21
Q

What is the pathology for a resistant host?

A

Tissue destruction

Organism contained

Disease

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22
Q

Who is normally affected by the primary infection?

A

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

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23
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)

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24
Q

What are the symptoms of TB?

A

Usually no symptoms, can be fever, malaise, Erythema nodosum (sarcoidosis also causes this), rarely chest signs

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25
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.

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26
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

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27
Q

What are the three outcomes of a primary infeection?

A

Progressive disease - ineffective immune response from the patient

Contained latent - activates when the patient becomes immunosuppressed (old)

Cleared and cured

28
Q

How common is a primary infection of TB?

A

Small percentage (1%)

29
Q

How does a primary infection of TB progress?

A

Primary focus continues to enlarge - cavitation

Hilar lymph nodes become enlarged to the point they compress bronchi causing lobar collapse

Lymph node discharges into bronchus (tuberculosis bronchopneumonia)

30
Q

Describe the incidence and findings in miliary TB?

A

Small percentage (1%)

6-12 months after infection

Fine mottling on the X-ray, widespread small granulomata - looks like millet seed in the lung - very serious

31
Q

How can TB affect the CSF and the pleura?

A

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

AND

Tuberculosis pleural effusion

32
Q

What is menat by post primary disease?

A

Reactivation of mycobacterium from latent primary infection disseminated by the blood stream around the body.

New re-infection from outside source

33
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!

34
Q

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

A

Miliary , meningeal, pleural TB

35
Q

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

A

Post primary disease - pulmonary and skeletal

36
Q

What are the features of TB after 10 years?

A

Genitourinary, Cutaneous TB

37
Q

How would you decribe the progression of Post-primary TB?

A

Slow, may be no symptoms for many months

38
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

39
Q

What is characteristic PMH for Post-primary Pulmonary Tuberculosis?

A

Diabetes, Immunosuppressive diseases, Previous TB

40
Q

What are common drugs included in Drug history for Post-primary Pulmonary Tuberculosis?

A

Immunosuppressive drugs

41
Q

What is the past social history for Post-primary Pulmonary Tuberculosis?

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

When is there going to be a high index of suspicion?

A

Immunosuppressed - HIV, corticosteroid therapy, etc.

In Africa 70% of TB patients are HIV+

Malnutrition, alcoholism, vagrants,previous gastric surgery, malignancy

Diabetes mellitus

Adolescence, elderly

Recent immigrants from high prevalence countries

44
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

45
Q

How do we analyse sputum samples for TB?

A

ZN stain - immediate answer if AAFB

Culture

Sputum PCR

46
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

47
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

48
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).

49
Q

What is prognosis of cavitating disease?

A

5 year survival of 25%

50
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

51
Q

What are the legal requirements behind treating TB?

A

Legal requirement to notify all cases

(low threshold for HIV testing, AIDS defining condition)

52
Q

What are the current TB regimens?

A

Isoniazid

Ethambutol

Pyrazinamide

Rifampicin

53
Q

What are the side effects of Rifampicin?

A

Orange urine, tears, induces liver enzymes,prednisolone, anticonvulsants, oral contraceptive pill is ineffective. Hepatitis

54
Q

What are the side effects of Isoniazid?

A

Hepatitis, peripheral neuropathy

55
Q

What are the side efects of ethambutol?

A

Optic neuropathy

56
Q

What are the side effects of pyrazinamide?

A

Gout

57
Q

What is the point of TB contact tracing?

A

Find out where the patient has caught it and who they might have spread it to

58
Q

Likelihood of infection with TB depends on?

A

Duration of contact

Intensity of infection

59
Q

What is the general guidance for TB contact tracing?

A

First screen close household contacts

5-14% become infected (1 in 6 develop disease)

If close contacts have been infected, virulent organism/high transmission

screen casual contacts

‘stone in pond principal’

60
Q

How do you screen for TB using tuberculoprotein?

A

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

61
Q

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

A

Heaf test

62
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

63
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 procedures

64
Q

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

A

Investigate for TB and treat if necessary

65
Q

What is the drug combination pattern?

A

Treat with 4 drugs 2 months, 2 drugs 4 months

1ST YEAR SYSTEMS: Respiratory (38 decks)

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