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
What are scrofuloderma?
Skin lesions result from direct extension of underlying TB infection of lymph nodes, bone or joints
26
Who should be offered testing for latent TB?
- Close contacts or those w pulm/laryngeal TB - Immune dysfunction - healthcare workers - high risk popn (prison, homeless, vulnerable migrants)
27
How can latent TB be tested for?
1. Mantoux test | 2. Interferon-gamma release assays (IGRAS)
28
What does the mantoux test involve? How do you interpret the results?
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
What doesn't the Mantoux test not distinguish between?
TB infection or prev BCG exposure
30
What can cause false -ve in the Mantoux test?
``` miliary TB sarcoidosis HIV lymphoma <6m age ```
31
What is the IGRA test?
diagnoses exposure to TB | measures release of IG from T cells reacting to TB antigen
32
What can be seen on CXR in active pulmonary TB?
``` fibronodular/linear opacity sin upper lobe (typical) calcification cavitation miliary disease effusion ```
33
What are the diagnostic tests for active pulmonary TB?
1. CXR 2. Sputum smear + culture 3. Nucleic acid amplification test (NAAT)
34
How are sputum samples tested?
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
What test allows for rapid detection of TB? How quickly? What can this test also be useful for?
NAAT in sputum by DNA or RNA amplification <8hrs can also detect rifampicin sensitivity
36
What is the treatment of TB
``` RIPE Rifampicin (R) Isoniazid (H) Pyrazinamide (Z) Ethambutol (E) Give H + R for 6 months and Z + E for first 2 months ```
37
How is TB treatment given?
Daily tablets
38
What is the treatment of TB meningitis + CNS TB?
12 months RIPE + initial steroids
39
What is the treatment of multi-drug resistant TB?
18-22m of RIPE
40
What are the SE of rifampicin?
Hepatitis Orange secretions Potent liver enzyme inducer
41
What drugs should you take caution with when giving rifampicin?
warfarin calcineruin inhibitors oestrogen pheytoin
42
What are the SE of isoniazid? What increases the risk of these SE? what should be done to reduce this risk?
Peripheral neuropathy Increased risk w DM, CKD, HIV, malnutrition Prevent w prophylactic pyridoxine (vit B6)
43
What are the SE of pyrazinamide?
Hepatoxicity Arthralgia Hyperuricaemia - gout
44
What are the SE of ethambutol? how can u reduce the risk of SE?
optic neuritis | check visual acuity at start of treatment, monitor for sx and monthly visual checks if treatment >2m
45
What should be done if transaminases are raised to x5 above upper limit?
Withdraw rx until normal | Reintroduce w graded doses w regular LFTs