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TUBERCULOSIS > Tuberculosis > Flashcards

Tuberculosis Flashcards

1
Q

How many percentage of the world’s population have TB?

A

30%

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2
Q

How many people develop TB annually

A

About 8 to 10 million

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3
Q

How many children U15 develop TB and what percentage?

A

1 million (11%)

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4
Q

How many people die from TB annually? How many children are included in this number?

A

About 3 million people die from TB annually including 250,000 children

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5
Q

Majority of children with TB infection develop clinical symptomatology - True/False

A

False - Majority of children with TB infection develop NO clinical symptomatology

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6
Q

What is the lifetime risk of progression of TB in older children

A

5 to 10%

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7
Q

What is the difference between smear negative and smear positive TB and what is the significance of this difference?

A

Patients with sputum smear–negative TB are less infectious than patients with sputum smear–positive TB

Nevertheless, patients with smear-negative, culture-positive pulmonary TB are capable of transmitting M. tuberculosis

In a case where only smear positive cases are reported, it leads to underestimation of the burden of TB in children.

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8
Q

What is the percentage of smear negative cases of TB in U12 children

A

95%

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9
Q

There is decreased risk of progression and development of extra pulmonary disease in the first 2 years of life - True/False

A

False - There is INCREASED risk of progression and development of extra pulmonary disease in the first 2 years of life

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10
Q

What are the factors responsible for the resurgence in the incidence of TB globally?

A

Worsening economic situations

Multidrug resistance

HIV pandemic

Large number of displaced persons living in poor conditions as a result of conflicts and wars

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11
Q

What are the pathogens that can cause TB

A

M. TB
M. bovis
M. africanum
M. microti
M. canetti

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12
Q

How can M. bovis infection be acquired?

A

Drinking unpasteurized milk

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13
Q

What type of TB does M. bovis cause?

A

Abdominal TB

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14
Q

Why is M. TB referred to as an acid fast bacilli?

A

They have a waxy outer capsule so they do not take up the usual stains for bacteria but absorb carbol fushcin stain when heated and resist decolourization by acid and alcohol – “acid fast bacilli”

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15
Q

What are the predisposing factors for developing TB?

A

Very young and very old, adolescents and pregnant women

Malnutrition

Over crowding

Immunosupression from drugs or disease e.g HIV, diabetes, malnutrition, steroid use.

Measles, pertussis, kwashiorkor

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16
Q

How is M. TB acquired?

A

Inhalation of infected droplets
Drinking infected milk
Abrasions on the skin
Conjunctival sac and genitalia
Congenital via placenta transmission

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17
Q

What happens when the tubercle bacilli enter the alveolar spaces of the lungs?

A

The tubercule bacilli are engulfed by macrophages.

The macrophages destroy some of these tubercules while some multiply in the macrophages, causing their death.

The organisms are then released and they attract more macrophages as well as lymphocytes from the blood stream, forming a small focus of granulomatous infiltration called a tubercule

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18
Q

What is the primary complex?

A

The primary focus + regional lymph glands

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19
Q

What is the fate of the primary complex?

A

It usually heals with or without calcification

It may become dormant with possible later reactivation

It may be complicated by acute dissemination (especially in infants) and give rise to miliary TB or TB meningitis

The local lesion may heal but organisms disseminated to other sites e.g the bones, joints, liver, kidney etc may cause disease at a later date

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20
Q

Signs of early manifestation of TB

A

Evidence of primary lesion

Erythema nodosum

Phlycternular conjunctivitis

Poncet’s arthritis

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21
Q

Signs of TB within 3 months

A

Military TB
TB meningitis

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22
Q

Signs of TB within 1 year

A

Pleural effusion

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23
Q

Signs of TB within 3 years

A

Bone and joint lesions

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24
Q

Signs of TB within 5 years

A

Progressive pulmonary disease

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25
Q

Signs of TB after 5 years

A

Renal TB

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26
Q

What is the basis of the tuberculin skin sensitivity test?

A

Infection with mycobacterium TB or mycobacterium bovis leads to development of delayed hypersensitivity to the tubercular protein which forms the basis of the tuberculin skin sensitivity test

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27
Q

When does the tuberculin skin test become positive?

A

Within 4 to 8 weeks after exposure, either due to a natural infection or after BCG vaccination. The skin response is more after a natural infection.

28
Q

What are the types of the tuberculin skin test

A

Mantoux test
Head
Tine
BCG vaccination

29
Q

Describe the mantoux test

A

Mantoux test
0.1ml of diluted tuberculin at a dose of 5 tuberculin units (TU) of purified protein derivative (PPD) is given intradermally into the volar aspect of the forearm and the reaction is read after 48 – 72hrs. The reading is based on the size of the transverse induration.
Positive - ≥10mm
6 – 9mm - equivocal
≤ 5mm – negative
≥ 15mm or presence of any vessiculation should be regarded as due to TB infection

30
Q

Describe the response of a patient that has naturally been exposed to TB to BCG vaccine

A

Children with natural TB infection will respond to BCG vaccination with an accelerated reaction i.e. induration within 48hrs, a pustule on the 3rd day and a scab by 5-6 days leading to scar formation within about 2 weeks.

31
Q

What are the clinical features of primary TB

A

There may be no apparent illness

Conversion of tuberculin test from negative to positive

General symptoms: weight loss and failure to thrive, unexplained pyrexia, loss of appetite, lack of energy, sweating, abdominal pain.

Other symptoms: erythema nodosum, phlyctenular conjunctivitis, Poncet’s arthritis.

32
Q

What are the types of TB

A

Pulmonary TB
Extra pulmonary TB

33
Q

List the types of extra pulmonary TB

A

TB lymphadenitis
Abdominal TB
TB meningitis
Bone and joint TB
TB of the spine
Renal TB
TB epididymo-orchitis
Female genital tuberculosis
TB of the skin
TB of the larynx
TB of the nose and palate

34
Q

Describe the clinical presents of pulmonary TB

A

Enlarged hilar glands causing obstructive emphysema, lung collapse, bronchiectasis, or endobronchial TB.

Tuberculous bronchopneumonia

Pericardial effusion or constrictive pericarditis

Pleural effusion

Pneumothorax

Miliary TB

Tracheal compression from enlarged mediastinal or paratracheal glands causing stridor.

35
Q

How would you make a diagnosis of pulmonary TB

A

History of contact
Positive tuberculin test
Chest x-ray
Detection of M.TB in pulmonary secretions i.e. sputum or gastric aspiration
Therapeutic trial of anti-TB drugs

36
Q

Describe TB lymphadenitis

A

Most commonly affected site is the neck

Glands are initially discrete, rubbery in consistency and slightly tender but soon become matted together and may break down to form discharging ulcers or sinuses.

37
Q

How would you make a diagnosis of TB lymphadenitis?

A

Detection of organisms from exudates from ulcers or sinuses

Biopsy of the lymph nodes for microbiology and histology

Therapeutic trial of anti-TB drugs

38
Q

Abdominal TB only occurs with M. bovis infection - True or False

A

False - May occur as a secondary disease from infection with M.TB or as a primary disease from infection with M. bovis.

39
Q

What organs are affected in abdominal TB

A

Organs affected: mesenteric and retroperitoneal lymph nodes, peritoneum, omentum and gut

40
Q

Describe the pathology of abdominal TB

A

Lymph nodes may become massively enlarged and present as abdominal tumors

There may be ascites

Intestinal obstruction may occur

Involvement of the bowel may result in chronic malabsorption or TB enteritis

41
Q

What are the clinical features of abdominal TB

A

Insidious onset with malaise, low grade fever, weight loss, diarrhoea, constipation

Abdominal distension

Symptoms of intestinal obstruction like colicky pain, vomiting and constipation

Occasionally, chronic diarrhoea, weight loss, abdominal distension and other signs suggestive of malabsorption.

Signs: vague sense of fullness and increased resistance to palpation described as “doughy abdomen”

42
Q

How would you diagnose abdominal TB

A

Tuberculin skin test is usually positive
Evidence of PTB on chest x-ray is supportive
Plain abdominal x-ray may reveal calcification of lymph nodes
Aspiration of the ascitic fluid shows that it is an exudate
Demonstration of the organism in ascitic fluid
Therapeutic trial of anti-TB drugs

43
Q

What is the most common cause of death in very young children with TB

A

TB meningitis

44
Q

When is the greatest incidence and most severe manifestations of TB meningitis

A

first 2-3 years of life

45
Q

Describe the pathogenesis of TB meningitis

A

May occur as part of a miliary TB but more often arises in the absence of miliary TB

Results from hematogenous seeding of the brain or spinal cord by tubercule bacilli during primary infection

There is an inflammatory process in the meninges which tends to occur at the base of the brain involving the cranial nerves, obstructing CSF circulation with peri-arteritis and end-arteritis of the cerebral blood vessels which may impair blood supply to areas

46
Q

Describe the clinical presentation of TB meningitis

A

Three phases

General symptoms and signs: malaise, fever, poor appetite, apathy, irritability, headache, vomiting

Signs of neurologic involvement: convulsion, signs of meningeal irritation, cranial nerve palsies, pyramidal signs, significant behavioural modification

Coma
Examination of the fundi occuli may show papilloedema and/or choroidal tubercules

47
Q

How would you diagnose TB meningitis

A

Tuberculin skin test may be positive

Chest x-ray may show evidence of PTB

Sputum or gastric lavage may reveal mycobacteria

FBC: marked lymphocytosis

CSF studies: raised CSF pressure, or there may be a block, CSF may be xanthochromic

CSF may be xanthochromic or turbid. A delicate “spider web” clot will form in the CSF left undisturbed for some hours. The organisms may be identified from a smear of this clot.

CSF microscopy: in early disease, there is a mixture of polymorphs and lymphocytes, with polymorphs predominating but later, lymphocytes predominate.

CSF protein is usually raised

CSF glucose is usually low

48
Q

How does brain tuberculoma present

A

As space occupying lesion

49
Q

Describe bone and joint TB

A

Lesions are characterized by bone destruction without evidence of new bone formation
Most common site is the spine
Most common joints affected are the knees and hips

50
Q

Describe TB of the spine

A

Usually originates in the body of the vertebrae leading to bone destruction

The spinal processes and vertebral arches are usually spared

The intervertebral disc spaces are usually involved with erosion and narrowing of the disc spaces

51
Q

What are the clinical features of TB spine

A

Pain in the spine, exacerbated by impact on walking, running, jumping and bending

With disease progression, the affected vertebral bodies collapse, causing angulation of the spinal column “gibbus”

There may be spinal cord compression leading to increased muscle tone, exaggerated tendon reflexes and positive ankle clonus

52
Q

How would you diagnose TB spine

A

Clinical evidence of spinal involvement
X-ray of the spine: bone destruction without new bone formation with involvement of the disc spaces

Positive tuberculin test

Evidence of TB at other sites e.g. PTB

There may be para-spinal abscess

53
Q

How would you treat TB spine

A

Prolonged immobilization e.g. with the use of a spinal jacket + TB chemotherapy

54
Q

Why type of TB is seen in PLWHIV

A

In addition to pulmonary lesions, there may be extra-pulmonary TB in 40-75% of cases. TB is usually atypical

55
Q

What are the principles of drug treatment in chemotherapy of TB

A

Drugs must never be given singly
Treatment must be continuous and long enough to kill off the bacilli i.e about 6-18 months
At the onset, at least 3 drugs should be given
Once a drug regimen has been started, it should not be altered unless there is toxicity

56
Q

What are the first line TB drugs

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol
Streptomycin
Thiacetazone

57
Q

What are the second line anti TB drugs

A

ethionamide
para-aminosalicylic acid
Ofloxacin/levofloxacin/moxifloxacin, Cycloserine/terizidone, Kanamycin/amikacin, Capreomycin

58
Q

What are the bacterocidal TB drugs

A

Rifampicin
Isoniazid
Pyrazinamide
Streptomycin

59
Q

What are the bacterostatic TB drugs

A

Thiacetazone
Ethambutol
Ethionamide

60
Q

What are the doses of the first line TB drugs

A

Rifampicin 15mg/kg
Isoniazid 10
Pyrazinamide 35
Ethambutol 20
Streptomycin 15

61
Q

What is the treatment for TB in Nigeria

A

2RHZE/4RH for TB and TB lymphadenitis

2RHZE/10RH for severe forms of TB

62
Q

List the adverse effects of the first line TB drugs

A

Isoniazid
Skin rash, hepatotoxic, peripheral neuritis, psychosis

Rifampicin
Hepatoxic, red urine, anorexia, nausea, abdominal pain, thrombocytopenia, drug interactions

Pyrazinamide
Hepatotoxic, arthralgia

Ethambutol
Optic neuritis

Streptomycin
Rash, anaphylaxis, oto-and nephrotoxic

63
Q

What are the indications for corticosteroids in TB treatment

A

Compression of airway by enlarged glands
TB meningitis
TB pericarditis
Miliary TB
Endobronchial TB
Large pleural effusion

64
Q

What is the supportive therapy for TB treatment

A

Improved Nutrition
Screening of immediate family members
Surgical intervention where necessary

65
Q

Define the various drug resistance in TB

A

Mono-drug resistance: Resistance to single drug

Poly-drug resistance: Resistance to 2 or more drugs, but not to both INH and RMP

MDR TB: Resistance to INH & RMP +/- other drugs

XDR (extensively drug resistant)TB: MDR & 2nd-line injectable & quinolone

Primary resistance: No previous anti-TB Rx or less than 1 month

Acquired resistance: Previous anti-TB Rx >1 month

66
Q

What are the causes of drug resistant TB

A

Poor management of drug-susceptible or mono-resistant TB cases, e.g. incorrect regimens, interrupting treatment (drug supplies, poor bio-availibility), poor adherence by patients

Poor management of MDR-TB cases leads to transmission of MDR-TB strains, e.g. late diagnosis, not doing drug susceptibility in relapse/retreatment cases, poor infection control measures especially in high prevalence HIV settings

67
Q

How would you prevent TB in a community

A

Case-finding and effective treatment.
Contact tracing and INH chemoprophylaxis.
BCG vaccination.
Improvement in the general standard of living.

TUBERCULOSIS (1 decks)

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