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Y3M - Respiratory > Tuberculosis > Flashcards

Tuberculosis Flashcards

1
Q

Causative organism of TB.

A

Mycobacterium tuberculosis

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2
Q

Where is most of TB cases seen?

A

Africa and Asia

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3
Q

Risk factors of developing TB.

A

Origination from a high-incidence country

Frequent travel to high-incidence areas

Immunodeficiency

Drug/alcohol misuse

Homelessness/Hostels/Overcrowding

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4
Q

Characteristics of Mycobacterium tuberculosis.

A

Aerobic intracellular pathogen.

Relatively impermeable to acid-based dyes leaves it called acid-fast bacilli + red staining on Zeihl-Neelsen staining.

It is an airborne infection spread by coughing via respiratory droplets.

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5
Q

Explain pathogenesis of primary TB.

A

Bacteria reaches alveolar macrophages. The macrophages ingest the bacteria and subsequent inflammatory reaction leads to tissue necrosis and formation of a granuloma.

It is a caseating granuoma surrounded by epithelioid cells and Langhans giant cells.

The caseated area heals, some heal completely, some become calcified.

Some calcified nodules will contain the bacteria. The immune system will prevent it from getting out and it can lay dormant for years.

They lay dormant in the primary/Ghon’s focus.

This can be seen on a CXR.

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6
Q

What is the most common cause of active TB?

A

Reactivation of latent TB.

It is usually not the immediately from the primary infection.

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7
Q

When might newly acquired TB occur?

A

In HIV patients.

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8
Q

Risk factors for reactivation of latent TB.

A

HIV co-infection

Immunosuppressant therapy

DM

End stage CKD

Ageing

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9
Q

Clinical features of TB in general.

A

Cough

Haemoptysis

Fever

Night sweats

Weight loss

Lymphadenopathy

Erythema nodosum

Spinal pain

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10
Q

When suspecting TB, which investigations should be done?

A

Sputum sample (3x)

Gram stain

Biopsy samples

Fluid for microscopy

Smear

Culture

CXR

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11
Q

Symptoms of pulmonary TB.

A

Productive cough

Haemoptysis

Hoarse voice and severe cough if there is laryngeal involvement.

Pleuritic pain if the pleura has been affected.

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12
Q

Findings on CXR of TB.

A

Consolidation with or without cavitation.

Pleural effusion

Thickening or widening of mediastinum by hilar or paratracheal adenopathy.

Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy

Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones

Disseminated Miliary TB give a picture of “millet seeds” uniformly distributed throughout the lung fields

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13
Q

How should sputum samples be collected in TB?

A

Serial sputum sample on at least 3 occassions.

This should be done first thing in the morning.

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14
Q

What does a smear-positive sputum tell you about the TB?

A

The patient is considered to be infectious and should be isolated.

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15
Q

What does a smear-negative and a culture-positive result tell you about the patient?

A

Less infectious and generally do not need to be isolated.

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16
Q

What is the second most commonly affected organ in TB?

A

Lymph nodes.

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17
Q

What lymph nodes are involved?

A

Extrathoracic more commonly than intrathoracic and mediastinal.

It is usually firm, non-tender enlargement of the cervical or supraclavicular lymph nodes.

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18
Q

Clinical features of lymph node TB.

A

Node is necrotic centrally and can liquefy.

Overlying sin is frequently hard and firm (indurated).

There can be sinus tract formation with purulent discharge.

Usually no erythema.

This is called a cold abscess formation.

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19
Q

When are nodes enlarged compared to diagnosis of TB?

A

Can be enlarged for several months prior to the diagnosis.

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20
Q

Investigations of lymph node TB.

A

Fine needle aspiration via ultrasound guidance.

Core biopsy

If necessary removal of the lymph node.

Samples should be sent for AFB smear, culture and cytology to exclude cancer.

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21
Q

What other systems might TB affect?

A

GI tract

Bone and spine

General (miliary)

CNS

Pericardium

Skin

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22
Q

What might TB affect in the GI tract?

A

Intestines and peritoneum

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23
Q

Clinical features of GI TB.

A

Abdo pain

Weight loss

Anaemia

Fever with night sweats

Obstruction

Right iliac fossa pain or palpable mass

Usually it is the ileocaecal area that is affected.

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24
Q

Diagnosis of GI TB.

A

Small bowel follow-through

USS, MRI or CT

Histology and culture of tissue

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25
Q

What might be seen on small bowel follow-through in GI TB?

A

Transverse ulceration

Diffuse narrowing of the bowel

Shortening of the caecal pole

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26
Q

What might be seen on USS, CT or MRI in GI TB?

A

Mesenteric thickening and lymph node enlargement.

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27
Q

What is the second most common form of abdominal TB?

A

Tuberculous peritonitis.

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28
Q

Three sub groups of TB peritonitis.

A

Wet

Dry

Fibrous

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29
Q

What indicates wet TB peritonitis?

A

Protein concentration >20 g/L and tubercle bacilli

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30
Q

What indicates dry TB peritonitis?

A

Subacute intestinal obstruction

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31
Q

What indicates fibrous TB peritonitis?

A

Abdo pain

Distension

Ill-defined, irregular tender abdominal masses.

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32
Q

Treatment of GI TB?

A

Similar to pulmonary TB.

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33
Q

Explain how tuberculous arthritis comes about.

A

M. tuberculosis invades the synovium or intervertebral disc.

Here caseating granulomas develop and casues rapid destruction of cartilage and adjacent bone.

Some people might also develop Poncet’s disease which is a reactive polyarthritis.

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34
Q

How does M. tuberculosis spread to synovium and intervertebral discs?

A

Haematogenously

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35
Q

What does osteoarticular TB most commonly affect?

A

Spine (50%)

Hip (12-15%)

Knee (10%)

Ribs (10%)

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36
Q

Clinical features of TB arthritis.

A

Fever

Night sweats

Anorexia

Weight loss

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37
Q

Investigations of TB arthritis.

A

Culture of fluid and culture and biopsy of the synovium.

CXR

Joint or spinal Xray might be normal at first.

MRI will show developments earlier.

CT guided biopsy might be needed to obtain cultures of an affected disc.

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38
Q

What X-ray features might develop if treatment is delayed?

A

Rapid joint space reduction and bone destruction.

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39
Q

Treatment of TB arthritis.

A

9 months of treatment.

Joint should be rested and spine immobilised in the acute phase.

40
Q

Explain Tuberculous osteomyelitis.

A

Haematogenous spread from a reactivated primary focus in lungs or GI.

Disease starts in intra-articular bone. Spine is commonly involved aka Pott’s disease, where there is damage to the bodies and the two neighbouring vertebrae leading to vertebral collapse and acute angulation of the spine.

Furthermore a cold abscess will form.

The pus can track along the tissue planes and discharge at a point far away from the affected vertebrae.

41
Q

Clinical features of TB osteomyelitis.

A

Local pain and later swelling if pus has collected.

Systemic symptoms of malaise, fever and night sweats.

42
Q

Management of TB osteomyelitis.

A

Tx extended to 9 months, together with initial immobilisation.

43
Q

What miliary TB?

A

When TB spreads to multiple sites via haematogenous spread. This includes CNS in 20% of cases.

44
Q

Clinical features of miliary TB.

A

Similar systemic symptoms that normal TB exhibits.

45
Q

Investigations important to be done in miliary TB.

A

CXR which will usually show multiple nodules like millet seeds.

Liver and splenic microabscesses with deranged liver enzymes, cholestasis and GI symptoms.

All patients should have a brain MRI to look for cerebral disease. This can present as an asymptomatic brain tuberculoma.

46
Q

Clinical features of tuberculous meningitis (TBM).

A

A chronic meningitis that present with a vague headache, lassitude (fatigue), anorexia and vomiting.

Drowsiness, focal signs like diplopia, papilloedema, hemiparesis and seizures may occur as well.

47
Q

Investigations of TB meningitis.

A

MRI showing meningeal enhancement, hydrocephalus and tuberculomas. It may also appear completely normal.

PCR (may come back negative)

Repeated CSF examination often necessary and it will be some weeks before cultures are confirmatory.

48
Q

Management of TB meningitis.

A

Rifampicin, isoniazid and pyrazinamide on a presumptive basis and continue for at least 9 months, some say 12 months.

Some studies include ethambutol as well, some say that ethambutol should be avoided due to its potential eye complications.

Adjuvant corticosteroids such as prednisolone 60 m for 3 weeks should also be given.

49
Q

Clinical features of tuberculous pericarditis.

A

Chronic low grade fever particularly in the evening.

Acute pericarditis

Dyspnoea

Malaise

Night sweats

Weight loss

50
Q

Investigation of TB pericarditis.

A

Pericardial aspiration.

51
Q

Complication of TB pericarditis.

A
52
Q

Management of TB pericarditis.

A

Same as normal TB + prednisolone 60 mg daily for 2-3 weeks.

53
Q

Skin manifestations that might occur in TB.

A

Lupus vulgaris (red-brown nodules of head or neck)

Tuberculosis verrucosa cutis (warty lesions)

Scrofuloderma (discharge from affected lymph node into skin with ulceration and scarring)

The tuberculides (Erythema nodosum and erythema induratum)

54
Q

Types of microbiological diagnosis investigations of TB.

A

Stains

Cultures

Nucleic acid amplification testing (NAAT)

55
Q

Explain what stains are done in TB.

A

Auramine-rhodamine staining (more sensitive)

Ziehl-Neelsen (more specific)

First one requires fluorescence microscopy and highlights bacilli as yellow-orange on a green background.

56
Q

When are TB cultures used?

A

They are more or less always used.

Sputum samples on three occassions first thing in the morning.

Treatment should commence before culture results come back if clinical signs and presentation are consistent with TB.

57
Q

When is NAAT used?

A

Increasingly used for rapid identification of MTb complex and particularly useful in distinguishing between M. tuberculosis and non-tuberculous mycobacteria.

It can also identify TB in smear-negative sputum specimens.

58
Q

How does NAAT work?

A

By using the polymerase chain reaction (PCR) to replicate and then identify mycobacterium DNA.

59
Q

Culture and staining are still necessary and should not be replaced by NAAT.

Why?

A

NAAT is only useful at the initial stage of diagnosis as it frequently remains positive despite treatment as it can detect dead organisms.

60
Q

Why is NAAT useful?

A

Rapid commencement of treatment

Rapid identification of drug resistance.

61
Q

Management of TB.

A

Routine blood tests and a viral hepatitis screen. (people with acute viral hepatitis might develop fatal drug-induced hepatitis as well)

HIV test to be offered.

Treatment should be done for 6 months (RIPE). CNS is done for 12 months, bone TB is done for 9 months.

Pericardial and CNS also have corticosteroids for 2-3 weeks.

Non-CNS TB = RIPE for 2 months, RI for 4 months extra

CNS TB = RIPE for 2 months (sometimes no E) and RI for 10 months extra.

Bone TB sometimes have 9 months (RIPE 2 and RI 7 extra).

62
Q

What is directly observed therapy (DOT) in TB?

A

It is used when there are concerns about adherence to treatment or difficulties in taking it.

63
Q

Criteria for DOT in TB.

A

Serious mental illness

History of non-adherence

Previous TB treatment

Multidrug-resistant TB

Street/shelter/hostel dwelling

Prison history

Substance misuse.

64
Q

Characteristics of CSF indicating TB.

A

Protein that is very high >2-3 g/L

Glucose less than half of blood glucose

CSF lymphocytosis

65
Q

Most common side-effects of quad TB therapy.

A

Nausea

Vomiting

Rash

Itching

Antiemetics or antihistamines might be prescribed for this reason.

66
Q

Why are LFTs commonly checked during TB treatment?

A

Because if they become deranged there is a risk of causing drug-induced hepatitis.

67
Q

What should be done if LFTs becomes deranged in TB treatment?

A

They should all be stopped and then re-introduced one at a time.

68
Q

What specific LFT numbers are needed to stop treatment?

A

Serum bilirubin elevated

or

Transferases more than 3 times elevated.

69
Q

Specific side-effects of isoniazid.

A

Can cause polyneuropathy due to B6 def. as it interactis with pyridoxal phosphate. This means B6 should be given daily.

Can more rarely cause allergic reactions.

Can also cause (< 1%) hepatitis.

70
Q

Side-effects of rifampicin.

A

Induces liver enzymes which can cause them to be transiently elevated in the blood.

Concomitant treatment will be less effective.

Antidepressants, anticoagulants and antiepileptics need to be reviewed.

COCP will not be effective.

Rifampicin also stains body secretions red/pink. Patients should be warned that this might happen.

71
Q

Specific side-effects of pyrazinamide.

A

Hepatic toxicity

Itching

Rash

Arthralgia

Hyperuricaemic gout as it reduces renal excretion of urate.

72
Q

Specific side-effects of ethambutol.

A

Dose-related optic retrobulbar neuritis.

Colour blindness

Reduced visual acuity

73
Q

How does dose-related optic retrobulbar neuritis present?

A

Colour blindness for green, reduction in visual acuity and a central scotoma.

74
Q

What should be done prior to treatment of ethambutol.

A

Visual acuity and colour vision assessment to establish a baseline.

The side-effects are reversible which means it is important to notify the patient that vision changes might occur and they need to report it.

75
Q

Why does mono or multidrug resistance of TB occur?

A

Due to incomplete or incorrect drug treatment. This can be spread from person to person.

76
Q

Prevalence of;

Isoniazid monoresistance

Multidrug resistance (R and I)

A

Mono = 10%

MDR = around 1%

77
Q

When might Mycobacterium bovis infection occur?

A

Consumption of unpasteurized milk

Farmers working with infected cows

Abattoir workers

78
Q

Difference between normal TB and M. bovis.

A

Chest is the same.

Extrapulmonary sites of infection is more common in M. bovis.

79
Q

Treatment of M. bovis.

A

RIE.

Pyrazinamide resistance is common

80
Q

Specific issues with TB and HIV co-infection.

A

Higher incidence of drug interactions and intolerability

Increased risk of treatment toxicity

Higher incidence of drug resistance

81
Q

Two types of Latent TB infection diagnosis.

A

Tuberculin skin test (Mantoux)

Interferon-gamma release assays (IGRAs)

82
Q

Explain the tuberculin test.

A

Hypersensitivity reaction (T4) after 48-72 hours of an intradermal injection.

A positive test shows a raised, indurated lesion.

NICE suggest considering an induration of 5mm or more a positive result. After a positive result they should be assessed for active disease.

83
Q

When might false-negative occur in tuberculin testing?

A

Immunosuppressed patients due to HIV infection with CD4+ < 200/mm3.

Immunosuppressed due to medication

Extremes of ages

Active TB

84
Q

When might false-positive occur in tuberculin test?

A

Cross-reactivity with non-TB mycobacteria

Cross-reactivity with bacille Calmette-Guerin (BCG) vaccination

85
Q

Explain IGRA testing.

A

It detects T-cell secreting IFNgamma following the exposure to M. tuberculosis-specific antigens.

If a patient has been previously infected or is currently infected with TB the activated T cells will secrete IFN gamma in response to re-exposure to TB-specific antigens.

86
Q

Con of IGRA testing.

A

Does not differentiate between active and latent infection.

87
Q

Pros of IGRA testing.

A

Highly specific

Similar or better sensitivity compared to tuberculin test.

Only requires a single patient visit.

No cross-reactivity with BCG vaccine.

This means that tuberculin test will show latent TB or immunity by vaccination, IGRA will only show whether you have latent/active TB or you do not.

It can however not show if it is latent or active TB.

88
Q

In certain groups with latent TB chemoprophylaxis might be given.

When?

A

Household and close workplace contacts of patients with pulmonary and laryngeal TB

Health workers

Recent new migrant entrants from high-risk countries

Immunocompromised

Organ transplants

89
Q

Latent TB treatment.

A

RI for 3 months or isoniazid monotherapy for 6 months.

90
Q

What is the BCG vaccination?

A

M. bovis that has lost its virulence.

Develop antibodies and immunity.

91
Q

Where can you find non-TB mycobacteria?

A

Soil and water

They are usually not pathogenic due to their lack of pathogenic.

They become pathogenic if there is compromise to immune defences.

92
Q

Risk factors of NTM infections.

A

COPD

Bronchiectasis

CF

HIV

93
Q

If diagnosis between pneumonia and TB is not clear.

What should be done?

A

Start antibiotics for pneumonia as per CURB-65.

94
Q

If the patient is critically unwell and there is high likelihood of TB, what should be done?

A

Start anti-TB meds after sputum samples have been sent.

95
Q

When should IGRA testing be done?

A

The IGRA test is used in patients that do not have features of active TB but do have a positive Mantoux test to confirm a diagnosis of latent TB.

96
Q

What other management should be done in TB?

A

Notify Public Health of all suspected cases.

Test for other infectious diseases (HIV, hepatitis B and hepatitis C).

Test contacts for TB.

Patients with active TB should be isolated to prevent spread until they are established on treatment (usually 2 weeks). In hospital negative pressure rooms are used to prevent airborne spread. Negative pressure rooms have ventilation systems that actively remove air to prevent it spreading out on to the ward.

Management and followup should be guided by a specialist MDT.

Treatment is slightly different for extrapulmonary disease and often includes using corticosteroids.

Individualised drug regimes are required for multidrug‑resistant TB.

Y3M - Respiratory (21 decks)

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