CPC 2 - Haemoptysis Flashcards

1
Q

What is the commonest bacterial cause of CAP?

A

Strep pneumoniae

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2
Q

What are the risk factors for CAP?

A

Extremes of age
Impaired gag reflex/mucociliary escalator
Non-functioning or no spleen
Impaired immunity
Chronic medical conditions of liver, heart, lung
Smoking or alcoholism

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3
Q

What are the treatments of choice for CAP?

A

Beta-lactam antibiotic +/- macrolide

eg. Amoxicillin or co-amoxiclav +/- clarithromycin

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4
Q

What are some things one must consider before beginning treatment for CAP?

A

CURB-65 severity score to guide treatment (>/= 2 requires admission to hospital/ IV antibiotics)

Antibiotic allergies

Local antibiotic susceptibility patterns

Avoid cephalosporins to prevent C. difficile associated diarrhoea

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5
Q

Which organisms can be associated with cavitation and haemoptysis?

A

Aspergillus fumigatus
Klebsiella penumoniae
Mycobacterium tuberculosis
Staph aureus

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6
Q

What is Aspergillus lung infection and what types are there?

A

A fungal infection

Three types:
Allergic pulmonary aspergillosis (associated with asthma)
Aspergilloma (fungal balls in patients with pre-existing lung cavities eg. following TB)
Invasive pulmonary aspergillosis (immunosuppression with impaired neutrophil function; high mortality)

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7
Q

What is community-acquired Klebsiella Pneumonia?

A

Gram-ve bacilli
Affects debilitated older patients with alcoholism
Production of sputum described as “red currant jelly”
Causes acute necrotizing pneumoonia
Affects upper lobes
High mortality rate (50%) even with antimicrobial therapy

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8
Q

Which organisms would not be treated with a beta lactam?

A

The following two are examples of organisms with no cell wall, hence not susceptible to beta lactams:

Chlamydophyla pneumoniae
Mycoplasma pneumoniae

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9
Q

What is S. aureus Pneumonia?

A

Primary pneumonia associated with Panton Valentine leucocidin (PVL)
Secondary post-viral pneumonia
Causes necrotising pneumonia with cavitating lesions and lung abscesses

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10
Q

How is TB transmitted?

A

Person to person spread
Inhalation of respiratory droplets
Prolonged close contact
Increased risk of transmission with highly infectious host or highly susceptible contact

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11
Q

What are some host factors for TB?

A
Previous exposure - BCG
Extremes of age
Nutritional status
Living conditions
Other medical conditions (DM, damaged lungs (eg. silicosis))
Immunosuppression (steroids, HIV)
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12
Q

What are some environmental factors for TB?

A

Endemic infection
Homeless
Drug and alcohol misuse
Imprisonment

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13
Q

What is the pathogenesis of TB?

A

Primary infection (ineffective immune response):
The bacilli are taken up and multiply in the alveolar macrophages
Macrophages are transported to local (hilar) lymph nodes
T cells are sensitised
Type 1 cytokines (IL-2, Interferon Gamma, TNF alpha) cause accumulation of macrophages/histiocytes

Granuloma formation in lung and lymph node:
Granuloma undergoes necrosis and some bacilli die

Reactivation or re-infection:
Extensive tissue necrosis - apex of lung
Cavitation
Spread to other sites

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14
Q

How can a lower respiratory tract infection be diagnosed?

A

Sterile site sample microscopy, culture, sensitivity (MCS) - blood, pleural fluid, biopsy

Non-sterile sample MCS (sputum; non-bronchoscopic blind sampling of lower airway; bronchoscopic methods eg. broncho-alveolar lavage)

Lung biopsy

Antigen detection using immunoassays, latex agglutination and molecular tests (eg. PCR)

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15
Q

How can TB be diagnosed?

A
Microscopy:
Ziehl Neelsen (ZN) stain
Auramine phenol (AP) stain with fluorescent microscope

Culture:
Solid media eg. Lowenstein-Jensen
Liquid media eg. Kirschner’s medium
Automated systems

Molecular methods:
PCR
DNA probes
Allows identification, resistance detection, and typing

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16
Q

What options for treatment of TB are available?

A

Isoniazid and rifampicin for 6 months

Pyrazinamide and ethambutol for 2 months

17
Q

Why is TB treatment so prolonged?

A

Extremely slow growing
Waxy outer cell wall
IC organism

18
Q

Why might TB treatment fail?

A

Drug resistance

Non-adherence

19
Q

What are the mechanism of action and main side-effects of Rifampicin?

A

Mech:
Binds RNA polymerase and inhibits the synthesis of mRNA

SEs:
Hepatitis
Rash
GI upset

20
Q

What are the mechanism of action and main side-effects of Isoniazid?

A

Mech:
Inhibits mycolic acid synthesis

SE:
Hypersensitivity
Peripheral neuropathy (prevented by pyridoxine)
Hepatitis

21
Q

What are the mechanism of action and main side-effects of Pyrazinamide?

A

Mech:
Inhibits mycolic acid synthesis

SE:
Hepatotoxicity

22
Q

What are the mechanism of action and main side-effects of Ethambutol?

A

Mech:
Inhibits polymerisation of arabinoglycan

SE:
Optic neuritis

23
Q

How do you treat Multi-Drug Resistant TB?

A

Four drugs, 8-months intensive phase
20 months recommended

Infection control:
Isolation in single rooms with negative pressure ventilation
Respiratory protection with particulate masks

24
Q

What is the definition of multidrug resistant TB?

A

TB resistant to treatment by at least two or more first line agents

25
Q

What are some markers for MDRTB?

A

Rifampicin resistance
Not responding to treatment
Have had contact with are are from high incidence areas for MDRTB

26
Q

What is vasculitis?

A

A disease that results in inflammation of the blood vessels

The diseases differ according to:
The blood vessels involved,
The organs involved,
The underlying cause if known

Can be infectious (eg. bacteria and fungi) or non infectious (immune complex-associated vasculitis; antineutrophil cytoplasmic antibodies (ANCA); anti-endothelial cell antibodies)

27
Q

What are the classifications of systemic vasculitides according to the Chapel Hill Classification?

A

Large-vessel vasculitis
Medium-vessel vasculitis
Small-vessel vasculitis

28
Q

What are some examples of large-vessel vasculitis?

A

Giant-cell arteritis

Takayasu arteritis

29
Q

What are some examples of medium-vessel vasculitis?

A

Polyarteritis nodosa

Kawasaki disease

30
Q

What are some examples of small-vessel vasculitis?

A

Wegener’s granulomatosis
Churg-Strauss syndrome
Microscopic polyangitis

31
Q

What is anti-neutrophil cytoplasmic antibodies (ANCA)?

A

ANCA are autoantibodies against antigens in the cytoplasm of neutrophils.
ANCA formation may be induced by cross-reactive microbial antigens, drugs or neutrophil surface expression of MPO and PR3.
ANCA activate neutrophils

32
Q

Pathogenesis of ANCA?

A

ANCA activate neutrophils;
Activated neutrophils are then primed by cytokines to show MPO and PR3 on their surfaces.
Neutrophils then adhere to the endothelium and release oxygen radicals and enzymes that damage the tissue.

33
Q

Treatment of vasculitis?

A

It is important to distinguish between infectious and immunological mechanisms!!