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DAQ 1 revision Case 1-4 > TB/Pneumonia > Flashcards

TB/Pneumonia Flashcards

1
Q

What are some differentials for cough, fever +/- chest pain?

A
  • Pneumonia
    green sputum, recent hospital admissions, acute URTI…
  • COPD exacerbation
    smoking history, diagnosed COPD, wheezing
  • TB
    occupational, social exposures (travelling, social workers), immunocompromised (HIV, steroids, IV drug, substance use)
    constitutional symptoms –> chronic development
  • Lung cancer
    smoking, FHx, hemoptysis, constitutional symptoms
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2
Q

Risk factors for TB

A
  • Social and environmental factors
    Travel or birth in a country with high TB prevalence (Asia, Latin America, sub-Sharan Africa, Eastern Europe)
    Person/occupation contacts, homeless, prison, refugee camp, crowded living
  • Host factors
    Immunocompromised (HIV, age, pregnancy, steroid use)
    IV drug use
    Systemic disease: end-stage renal disease, COPD, diabetes
    Chemotherapy
    Substance use (drug, alcohol, smoking can suppress cough reflex)
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3
Q

What is the organism cause TB?

A

mycobacterium tuberculosis
aerobe
duration of contact: 8 hours, lower for immunocompromised

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4
Q

Can latent TB pass to people?

A

NO

confined within Ranke complex

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5
Q

What factors can precipitate reactivation of latent TB?

A

Immunocompromised state, corticosteroids, malnutrition, elderly, HIV, diabetes, smoking, alcohol, drug, chemotherapy, transplant, pregnancy

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6
Q

How does TB escape macrophage killing?

A
  • Cord factor: surface glycolipid prevents fusion b/w phagocytes containing TB and lysosomes
  • Heat-shock protein
  • Mycolic acid inhibits macrophage expression of IL12, TNF and other cytokines
  • Resistance to ROS
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7
Q

Mech for active TB?

A

droplet inhalation –> alveolar macrophages are recruited to engulf TB –> intracellular destruction inside macrophages –> infected macrophages are activated and release inflammatory cytokines –> more immune cells are recruited (neutrophils) –> immune cells form a GRANULOMA to isolated TB within the region of the lung –> TB antigen are present to T cells by dendritic cells –> T cell response is delayed in immunocompromised hosts –> centre of granuloma necroses & liquifies –> TB escape from granuloma back to airway –> ACTIVE TB

  • -> accumulation of cytokines + necrotic tissue in lung –> airway irritation –> chronic cough
  • -> accumulation of cytokines –> systemic inflammation within the body –> inc basal metabolic rate –> fever, night sweats, weight loss
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8
Q

Mech for Ranke complex/ghon focus/granuloma formation

A

droplet inhalation –> alveolar macrophages are recruited to engulf TB –> intracellular destruction inside macrophages –> infected macrophages are activated and release inflammatory cytokines –> more immune cells are recruited (neutrophils) –> tissue inside granuloma undergo necrosis –> GHON FOCUS –> ghon focus (undergo calcification & fibrosis) + hilar lymphadenopathy –> RANKE COMPLEX

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9
Q

Mech for latent TB?

A

droplet inhalation –> alveolar macrophages are recruited to engulf TB –> intracellular destruction inside macrophages –> infected macrophages are activated and release inflammatory cytokines –> more immune cells are recruited (neutrophils) –> immune cells form a GRANULOMA to isolated TB within the region of the lung –> TB antigen are present to T cells by dendritic cells –> CD4 T cells release IFN gamma –> activate infected macrophages within granuloma to release enzymes –> resilient TB within granuloma survives and become dormant –> LATENT TB
when immunocompromised –> ranke complex reactivation –> memory T cells release cytokines –> more lung damage

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10
Q

Mech for extra-pulmonary TB?

A

droplet inhalation –> alveolar macrophages are recruited to engulf TB –> intracellular destruction inside macrophages –> infected macrophages are activated and release inflammatory cytokines –> more immune cells are recruited (neutrophils) –> infected macrophages travel to thoracic lymph nodes –> TB activate macrophage death –> release into lymph & circulatory system

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11
Q

What does RANKE COMPLEX do?

A

prevents spread of primary infection to other organs in infected individual –> scar tissue

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12
Q

What are some symptoms of TB?

A

SCREEN FOR RF
primary TB: asymptomatic, chronic cough, constitutional symptoms, haemoptysis

secondary TB: constitutional symptoms, haemoptysis + ORGAN DEPENDENT symptoms

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13
Q

physical exams of TB?

A
  • Clubbing
  • Lymphadenopathy: supraclavicular/Cervical lymph nodes enlargement
    Occur in an organ
  • Hepatitis: hepatomegaly, abdo tenderness
  • Meningitis: neck stiffness
  • Long bones: osteomyelitis
  • Spine: pott disease
  • Adrenal (Addison’s disease)
  • Kidney: sterile pyuria (inc WBC in urine)
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14
Q

investigations of latent TB/asymptomatic patients?

A

Purified protein derivative (PPD)

  • Inject tuberculin –> if previously exposed, immune reaction on skin occur within 48-72 hrs –> large area of infection confirms the result
  • Positive: patients have been exposed at some point, but DOES NOT differentiate active/latent/resolved
  • False positive from TB vaccinations

IFN gamma release assay (IGRA)

  • Measure the amount of interferon gamma released by T cells when exposed to TB antigens
  • Fewer false positives as it does not detect antigens in vaccines or non-TB mycobacteria

If any of the two screening tests are positive + symptoms –> chest -ray for active TB

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15
Q

investigations of active pulmonary TB patients?

A

Chest X-ray

  • Ghon focus with calcification (nodules around hilum of the lungs)
  • hilar lymphadenopathy
  • inactive TB: scarring in upper lobes (aerobes)

If positive –> sputum microscopy/culture

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16
Q

Whats the approach of diagnosing TB?

A

No symptoms –> latent screening tests (IGRA, PPD)

Symptoms –> chest x ray –> 3 sputum sample specimen for acid fast bacilli –> culture (gold standard) –> nucleic acid amplification test (NAAT)/PCR –> drug susceptibility test –> contact tracing

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17
Q

What happens in sputum acid fast bacilli?

A

3 specimens can be collected on the same day (at least one early morning), a minimum of 8 hour apart
Fast & inexpensive, but cannot differentiate TB bacilli and non-TB
Smear positive patients are FAR more contagious
appear red and pink

18
Q

What is the gold standard investigation of diagnosing TB?

A

Cell culture
Identification takes 10-21 days
Paired with a fluorescence-based oxygen sensor –> when bacteria use up all oxygen, the sensor goes fluorescent, and it’s sensed by UV light –> positive vial

19
Q

What happens in NAAT/PCR?

A

Gene Xpert assay: detect mycobacterium TB complex

Rapid diagnosis (24-48 hrs) by amplifying specific target region of DNA –> identify the organism

20
Q

What happens in drug susceptibility test?

A

might take 15-30 days
Perform upon the culture/try DNA sequencing as it takes very long
where there is resistance to rifampicin, second line agents should be tested (MDR-TB)

21
Q

What is the management of active TB?

A

RIPE for 2 months (intense phase)
RI for remaining 4 months (maintenance)

Rifampicin (6 months)
Isoniazid (6 months)
Pyrazinamide (2 months)
Ethambutol (2 months)

monitor with LFT

22
Q

What is the prevention of TB?

A

BCG vaccine (live-attenuated), give to infants (10-15 years) but give adults immunity drops within 3 months (not economically viable to vaccinate the whole Australian population)

23
Q

What is the discharging criteria of TB?

A
  • Absence of cough with/without other symptoms
  • 3 Cultures negative
  • Assured treatment (RIPE is working)
24
Q

MOA and side effects of RIPE

A

Rifampicin: inhibit bacterial RNA polyerase, red body fluids

Isoniazid: inhibit synthesis of cell wall, VIT B6 DEFICIENCY + PYRIDOXINE (peripheral neuropathy), rash, hepatotoxicity

Pyrazinamide: against TB within macrophages, most hepatotoxicity

Ethambutol: inhibit synthesis of cell wall, optic neuritis –> reversible

25
Q

What are some common organisms causing community-acquired pneumonia?

A

Streptococcus pneumoniae G+
G-
- H influenzae (COPD)
- Moraxella catarrhalis

26
Q

What are some common organisms causing atypical pneumonia?

A

legionella pneumoniae

viruses (influenza A and B)

27
Q

What are some common organisms causing hospital pneumonia?

A

G+: staphylococcus aureus /MRSA

G-: E.coli

28
Q

Risk factors of pneumonia?

A
  • Age > 65 yo
  • Residence in healthcare setting
  • COPD, exposure to smoking, smoking
  • Poor oral hygiene
  • Acute UTRI (viral)
  • CF
  • Alcohol abuse
  • Obstruction by foreign body/tumour
  • Diabetes
29
Q

Reasons for admission CAP

A 
RR > 30
altered mental state
systolic BP < 90
O2 sat < 92%
HR > 100
multilobar involvement
30
Q

Physical exam findings of CAP

A

Abnormal auscultatory findings

  • Pleural rubs, localised crackles
  • dec breath sounds
  • Dullness to percussion consolidation/pleural effusion
31
Q

Investigations for CAP

A

CXR
- lobes that are affected: consolidation, effusion
PCR from nose/throat swaps
- identify pathogen
sputum culture/gram straining
(hospitalised pts)
drug susceptibility test
CBE: neutrophil dominance –> bacterial infection
ABG: severity of pneumonia, resp acidosis

32
Q

Complications of CAP

A

Septic shock
Acute resp distress syndrome
Heart failure
Pleural effusion, lung abscess

33
Q

Management of CAP

details see in prescribing antibiotics

A

Safe to prescribe penicillin/cephalosporins

Avoid penicillin but safe cephalosporins

Avoid both: doxycycline, moxifloxacin/quinolone

If severe, start with IV antibiotics
after 48 hrs, clinical improvements and afebrile –> safe to switch to oral

34
Q

Mech for cough, fever in CAP

A

exposure to pathogens (along with RF) –> pathogens overcome resp defence mechanisms –> proliferation in lower airways –> inflammatory response due to immune cells –> fever

inflammatory response –> accumulation of neutrophils and exudate in alveoli –> irritation triggers clearance –> productive cough

35
Q

COPD revision

symptoms + signs

A 
symptoms 
- smoking hx
- smokers cough, white stringy, worse in the morning
- wheezing
signs
- wheezing
- use of accessory muscles
- dec chest expansion
- chest deformities (barrel)
- hyper resonant percussion notes
- reduced vocal resonance
36
Q

What are some triggers of COPD exacerbation?

A
  • 24-48 hrs, worse SOB, cough, more sputum…
  • bacterial/viral infection
  • LV failure
  • urban pollutions
37
Q

COPD mech simple

A

chronic exposure to cigarrettes/irritants –> deposit in the lungs –> recruitment of neutrophils and macrophages –> release enzymes –> break down elastin –> alveoli breakdown –> dec gas exchange + loss of elastic recoil –> inc CO2 retention –> hyperventilation –> SOB

38
Q

Antibiotics for low severity CAP

A

safe to administer beta lactams

  • amoxicillin
  • doxycycline

Not safe
- doxycycline

39
Q

Antibiotics for moderate severity CAP

A

safe to administer beta lactams

  • benzylpenicillin
  • azithromycin

Not safe
- moxifloxacin

40
Q

Antibiotics for high severity CAP

A

Safe to administer beta lactams

  • ceftriaxone
  • azithromycin

Not safe
- moxifloxacin IV

DAQ 1 revision Case 1-4 (5 decks)

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