CR4 Flashcards

1
Q
  1. What is the difference between community-acquired pneumonia and hospital-acquired pneumonia? (2 mark)
A

Community-acquired pneumonia is contracted outside of hospital (1 mark)
Hospital-acquired pneumonia occurs 48 h or more after hospital admission (1 mark)

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2
Q
  1. Define the acronyms CB65 in the diagnostic algorithm CRB65? (3 marks)
A

C: Confusion (1 mark); 65: 65 years of age or older (1 mark);
B: Blood pressure (1/2 mark): SBP< 90 mm Hg OR DBP greater than 60mmHg (1/2 mark, need to include correct units)v

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3
Q
  1. List two clinical investigations carried out in hospital for a patient suspected with community-acquired pneumonia? (2 marks)
A

X-ray
Blood culture
Sputum culture
Full blood count
Liver function tests (1 mark for each)

Urea and electrolytes to inform severity assessment
C-reactive protein to aid diagnosis and as a baseline measure (1/2 mark for each)

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4
Q
  1. What is the minimum number of days a patient with pneumonia may receive antibiotics? (1 mark)
A

Minimum duration of 5 days (1 mark)

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5
Q
  1. Why was Mrs Sinclair prescribed controlled oxygen therapy and what range of SpO2 should be maintained in a patient with asthma on controlled oxygen therapy? (2 marks)
A

To treat her hypoxaemia (i.e. low blood oxygen saturation levels, spO2 below 94%) (1 mark)
Maintain SpO2 between 94–98% (1 mark; 1/2 mark if range not cited)

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6
Q

Asthma is a common chronic inflammatory condition of the lung airways whose cause
is incompletely understood. It has which three characteristics? [3]

A

a) airflow limitation
b) airway hyper-responsiveness
c) inflammation of the bronchi with eosinophils, T-lymphocytes and mast cells

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7
Q

Describe the pathophsyiology of asthma [4]

A

i. Allergen picked up by dendritic cells and presented by MHC Class II molecules
ii. CD4 cells activate the TH-2 lymphocytes through the release of IL4, IL5, IL13.
iII. IL 4 leads to the production of IgE antibodies: coat mast cells and stimulate degranulation and the release histamines, leukotrienes and prostaglandins
iv. IL-5 activates eosinophils: causes more cytokine & leukotrienes release
v IL-9 = mast cell proliferation

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8
Q

Describe the difference in IL-5 and IL-9 in asthma pathophysiology [2]

A
  1. IL-5 = Eosinophil activation
  2. IL-9 = mast cell proliferation
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9
Q

Describe the acute effects of an asthma attack [3]

A
  1. smooth muscle around bronchiole to spasm: bronchoconstriction
  2. increased mucus production
  3. increase in vascular permeability
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10
Q

Describe the chronic effects of asthma [4]

A

Chronic effects: causes airway remodelling
1. Oedema
2. Fibrosis of airways
3. Thickening of epithelial basement membrane
4. mucous gland hyperplasia and hypersecretion

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11
Q

Describe the symptoms of asthma [5]

A

Episodic symptoms:

ii. Diurnal variability. Typically worse at night.
iii. Dry cough with wheeze and shortness of breath
iv. A history of other atopic conditions such as eczema, hayfever and food allergies
vi. Bilateral widespread “polyphonic” wheeze heard by a healthcare professional. BUT: neither sensitive nor specific for asthma
vii. Prolonged expiratory phase (respiratory and expiratory phases should be equal)

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12
Q

Describe lung function test results in asthmatic patients:

FVC [1]
FEV1 [1]
FEV1/FVC [1]
PEF (with treatment) [1]

A

FVC: may be normal in Asthma Ptx
FEV1: reduced
Bronchodilator reversibility test: FEV1 improvement >12% / 200ml is a positive test in adults & > 12% in children
FEV1/FVC: <70%
Peak expiratory flow: Treatment brings a reduction in variability of airflow

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13
Q

Describe asthma treatment pathway

A

Reliever medication: Short acting beta 2 agonists (SABAs)
1. Adrenalin acts on the smooth muscles of the airways to cause relaxation.
2. This results in dilatation of the bronchioles and improves the bronchoconstriction present in asthma

First line therapy:
* Low dose inhaled ICS (if need, may required higher doses)

Add on therapy:
* ICS + inhaled long acting beta 2 agonists (LABA) or long acting anti muscarinic (LAMA)

Add on therapy:
ICS + LAMA / LABA + specialist therapies

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14
Q

What is MART / SMART therapies? [1]

A

is a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.

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15
Q

ICS causes a reduction in why three pro-inflammatory mediators in asthma? [3]

A

IL-6, TNF-a & CXCL8

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16
Q

British thoracic society Guidelines state that Life threatening asthma is
present in a patient with any of which factors?

A
17
Q

Two leading causes of pneumonia? [2]

A
  1. Streptococcus pneumoniae (50%)
  2. Haemophilus influenzae (20%)
18
Q

Why can pneumonia lead to sepsis? [1]

A
  1. Loss of barrier function between alveoli and capillaries may lead to spread of infection (sepsis)
19
Q

Describe the management for mild, moderate and severe pneumonia [3]

A

i. Mild CAP: 5 day course of oral antibiotics: amoxicillin or a macrolide (azithromycin)
ii. Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin AND macrolide (azithromycin)
iII Severe Benzylpenicillin if blood culture tells you something different

20
Q

g. Patient should be reviewed 24 hrs before discharge
i. Should not have two more of those
1. Temp above []
2. HR > [] bpm
3. RR > [] per min

A
  1. Temp above 37.8
  2. HR > 100 bpm
  3. RR > 24 per min
21
Q

What is ‘silent chest’ in life threatening asthma? [1]

A
  • No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
22
Q

What are the PEFRs for:

Moderate
Severe
Life-threatening asthma

A

Moderate: 50-75% predicted

Severe: 33-50% predicted

Life-threatening asthma: < 33%

23
Q

Acute asthma management? [5]

A

O! SHIT!

Oxygen
Salbutamol - (? in cardiac patients with presenting tachy, monitor potassium!)

Hydrocortisone - (or any steroid)

Ipratropium Bromide - (acetylcholine antagonist via blockade of muscarinic cholinergic receptors)

Tube (intubation) - (only if VVV severe)

Magnesium (calcium channel blockade)

24
Q

First line investigations for asthma diagnosis? [2]

Second line? [2]

A

First line
* Fractional exhaled nitric oxide
* Spirometry with bronchodilator reversibility

Second line
* Peak flow variability measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
* Direct bronchial challenge test with histamine or methacholine

25
Q

Characteristic chest signs of pneumonia? [3]

A

Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by
consolidation of the lung tissue around the airway.

Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.

Dullness to percussion due to lung tissue collapse and/or consolidation.

26
Q

Describe the MoA of amoxicillin [1]

A

Amoxicillin competitively inhibit penicillin binding proteins, leading to up-regulation of autolytic enzymes and inhibition of cell wall synthesis.

27
Q

Describe the MoA of Macrolides [2]

A

Macrolides inhibit bacterial protein synthesis.

The mechanism of action of macrolides revolves around their ability to bind the bacterial 50S ribosomal subunit causing the cessation of bacterial protein synthesis.

28
Q

Name an ICS used to treat asthma [1]

A

Beclomethasone