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Infectious diseases > TB > Flashcards

TB Flashcards

1
Q

Where is TB most prevalent?

A

Africa
SE Asia
Western pacific

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2
Q

What is the cause of TB

A

Mycobacterium tuberculosis

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3
Q

What is primary TB?

A

infection in the lungs

Ghon focus develops

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4
Q

What is a ghon focus?

A

granulomata forming to wall of bacteria where caseous necrosis occurs

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5
Q

What is a Ghon complex?

A

focus + LN

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6
Q

Where do Ghon complexes tend to form?

A

sub pleural in lower lobes of lungs

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7
Q

What two things can happen to Ghon complex?

A

either heals by fibrosis and can be seen as a Ranke complex on CXR
or
leads to disseminated disease (miliary TB)

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8
Q

How is TB spread?

A

inhalation of aerosol droplets containing bacterium

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9
Q

What is latent TB? How does it present? Is the pt infectious?

A

Infection w/o disease due to persistent immune system containment
Asymptomatic w normal sputum/CXR
NOT infectious

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10
Q

What are the causes of active infection?

A
  1. arise from primary inf

2. reactivation of latent disease

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11
Q

What are the causes of reactivation of latent diseasE?

A 
IMMUNOCOMPROMISE:
new infection
HIV
organ transplantation 
Immunosuppression (CS)
Malnutrtion 
illicit drug use
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12
Q

Where does reactivation of TB usually occur?

A

apex of the lungs, may spread locally or to more distant sites

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13
Q

What is the most common site for secondary TB?

A

lungs

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14
Q

Where can extra-pulmonary infection occur?

A 
CNS - tuberculous meningitis
Vertebral bodies - Pott's diseas
Cervical LN - scrofuloderma
Adrenals - Addisons
Kidneys - sterile pyuria 
GI tract 
anywhere rlly
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15
Q

What are systemic features of TB?

A 
Low grade fever
anorexia
WL
malaise
night sweats 
clubbing (bronchiectasis)
erythema nodosum
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16
Q

What are the pulmonary sx

A

Cough (>2-3w) dry then productive
SOB
Haemoptysis (uncommon but seen in bronchiectasis so not always active disease)

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17
Q

What are lymphatic sx of TB

A

Tuberculous lymphadenitis:

painless enlargement of cervical or supraclavicular LN

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18
Q

What are GI sx of TB? which part of the tract is most commonly affected?

A

Colicky abdo pain and vomiting
Bowel obstruction - wall thickening, stricture formation or inflammatory adhesions
Most commonly - ileocaecal

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19
Q

How does spinal TB present?

A

local pain and bony tenderness for weeks to months

slow insidious progression

20
Q

What is miliary TB and how does it present?

A

widespread dissemination of TB via haematogeneous spread

seeding of TB bacilli in the lung seen on CXR

21
Q

How does CNS TB present?

A 
headache 
meningism
confusion]
seizures 
focal neuro déficit
22
Q

How does GU TB present?

A 
dysuria
frequency 
loin pain 
haematuria 
sterile pyuria
23
Q

How does cardiac TB usually present?

A

pericardis
pericardial effusion
constrictive pericarditis

24
Q

What is lupus vulgaris?

A

persistent progressive cutaneous TB: red brown ‘apple-jelly’ nodules

25
Q

What are scrofuloderma?

A

Skin lesions result from direct extension of underlying TB infection of lymph nodes, bone or joints

26
Q

Who should be offered testing for latent TB?

A
  • Close contacts or those w pulm/laryngeal TB
  • Immune dysfunction
  • healthcare workers
  • high risk popn (prison, homeless, vulnerable migrants)
27
Q

How can latent TB be tested for?

A
  1. Mantoux test

2. Interferon-gamma release assays (IGRAS)

28
Q

What does the mantoux test involve? How do you interpret the results?

A

Intradermal injection of purified protein derivative (PPD) tuberculin, rust read 2-3days later
Greater induration shows greater sensitivity to tuberculin (greater sensitivity if latent or active TB)
+ve result implies prev exposure to tuberculin protein
>6mm = -ve
6-15mm = +ve due to prev TB inf or BCG
>15mm - strongly +ve - suggests TB infection

29
Q

What doesn’t the Mantoux test not distinguish between?

A

TB infection or prev BCG exposure

30
Q

What can cause false -ve in the Mantoux test?

A 
miliary TB
sarcoidosis
HIV
lymphoma
<6m age
31
Q

What is the IGRA test?

A

diagnoses exposure to TB

measures release of IG from T cells reacting to TB antigen

32
Q

What can be seen on CXR in active pulmonary TB?

A 
fibronodular/linear opacity sin upper lobe (typical)
calcification 
cavitation 
miliary disease
effusion
33
Q

What are the diagnostic tests for active pulmonary TB?

A
  1. CXR
  2. Sputum smear + culture
  3. Nucleic acid amplification test (NAAT)
34
Q

How are sputum samples tested?

A

STAIN 3 specimens are stained w auramine-phenol for presence of acid-fast bacilli (TB)
CULTURE - 1-3 weeks (liquid media) or 4-8weeks (solid media)

35
Q

What test allows for rapid detection of TB? How quickly? What can this test also be useful for?

A

NAAT
in sputum by DNA or RNA amplification <8hrs
can also detect rifampicin sensitivity

36
Q

What is the treatment of TB

A 
RIPE 
Rifampicin (R)
Isoniazid (H)
Pyrazinamide (Z) 
Ethambutol (E)
Give H + R for 6 months and Z + E for first 2 months
37
Q

How is TB treatment given?

A

Daily tablets

38
Q

What is the treatment of TB meningitis + CNS TB?

A

12 months RIPE + initial steroids

39
Q

What is the treatment of multi-drug resistant TB?

A

18-22m of RIPE

40
Q

What are the SE of rifampicin?

A

Hepatitis
Orange secretions
Potent liver enzyme inducer

41
Q

What drugs should you take caution with when giving rifampicin?

A

warfarin
calcineruin inhibitors
oestrogen
pheytoin

42
Q

What are the SE of isoniazid? What increases the risk of these SE? what should be done to reduce this risk?

A

Peripheral neuropathy
Increased risk w DM, CKD, HIV, malnutrition
Prevent w prophylactic pyridoxine (vit B6)

43
Q

What are the SE of pyrazinamide?

A

Hepatoxicity
Arthralgia
Hyperuricaemia - gout

44
Q

What are the SE of ethambutol? how can u reduce the risk of SE?

A

optic neuritis

check visual acuity at start of treatment, monitor for sx and monthly visual checks if treatment >2m

45
Q

What should be done if transaminases are raised to x5 above upper limit?

A

Withdraw rx until normal

Reintroduce w graded doses w regular LFTs

Infectious diseases (8 decks)

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