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ESA 3 Callum's Cards > Respiratory S6 (Done) > Flashcards

Respiratory S6 (Done) Flashcards

1
Q

What is the NICE definition of COPD?

A

COPD is characterised by airflow obstruction that is progressive and not fully reversible

Does not change markedly over several months

Predominant cause is smoking

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2
Q

What are the two processes occuring in COPD?

A

Chronic bronchitis

Emphysema

Patients may have features of either or both

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3
Q

Describe emphysema

A

Loss of alveolar surface and impairement of gas exchange resulting from destruction of terminal bronchioles and distl airspaces

Often progresses to creating larger redundant airspaces in the lung called bullae

Also causes destruction of the supporting tissues surrounding small airways which therefore tend to close during expiration when pressure outside airway rises. This results in Airflow obstruction

Additionally the loss of elastic tissues cause the lungs to hyperinflate as they are unable to resist the tendency of the rib cage to expand

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4
Q

Describe Chronic bronchitis

A

Characterised by an inflammatory process that leads to proliferation of mucus secreting cells in the large airways epithelium

This causes mucus hypersecretion and remodelling of inflammed airways

Excess mucs can lead to chronic productive cough and frequent repiratory infections

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5
Q

What are the causes of COPD?

A

Smoking (most)

Alpha-1-antitrypsin deficiency

Occupational exposure (E.g. Coal dust)

Pollution

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6
Q

What proportion of smokers get COPD?

A

15%

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7
Q

What are the predominant symptoms of COPD?

A

Cough and sputum production often occur first

Patients present when initially become breathless, this is progressive

Exacerbations associated with increase in all three symptoms compared to baseline, may be infective

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8
Q

How is breathlessness graded?

A

MRC dyspnoea score

  1. Breathlessness on strenuous exercise
  2. Breathlessness on slight hill or hurrying
  3. Walks slower than contemporaries on flat ground due to breathlessness or has to stop for breath when walking at normal pace
  4. Stops for breath every 100m or every few minutes on flat ground
  5. Too breathless to leave house or breathless when dressing and undressing
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9
Q

What are the signs of COPD?

A

‘Pursed lip’ sign:

Increases pressure in airways to cause reduction or delay in airway closure

Tachypnoea

Bracing arms to utilise accessory muscles:

Hyperinflation of chest:

Cause of breathlessness as diaphragm and accessory muscles must work harder to ventilate

Wheeze or quiet breath sounds

Cyanosis

CO2 retention

Cor Pulmonale (w/oedema)

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10
Q

How can airflow obstruction be measured and what use is this in COPD patients?

What spirometry measurements indicate obstructive pathology?

A

Spirometry:

Can be used to diagnose and track COPD and severity of airflow obstruction

Measurements:

FEV1/FVC ratio of <70% (FEV1 reduced) = Obstructive

FEV1 of 50-80% predicted = Mild obstruction

FEV1 of 30-49% predicted = Moderate obstruction

FEV1 of <30% predicted = Severe obstruction

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11
Q

How is COPD diagnosed?

A

Combination of suggestive symptoms, signs and airflow obstruction

Common suggestive features:

Smoker or Ex smoker

Older (>40) and late in life onset

Chronic productive cough

Breathlessness (persistent and worsening)

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12
Q

What other investigations might you perform on someone with suspected COPD and why?

A

CXR:

To exclude other Dx

High resolution CT scan:

Detailed assessment of degree of macroscopic alveolar destruction, helpful for considering surgery or if diagnosis is in doubt

ABG:

Assess for resp failure

Alpha-1-antitrypsin blood test:

Common for yound patients

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13
Q

What is involved in stable COPD care?

A

SMOKING CESSATION

Pulm. Rehab

Drugs

Diet - supplements/dietician review

Supportive - E.g. Flu vaccine

Long term O2 therapy if appropriate

Lung volume reduction if appropriate

Education - Inhaler technique

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14
Q

What drugs might be used in COPD?

A

Bronchodilators (E.g. B2 agonists)

Steroids (inhaled)

Anti-muscarinics

Mucolytics

Methylxanthines

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15
Q

What can be the side effects of B2 agonists such as salbutamol?

A

Tachycardia (atrial B2 receptors)

Tremor (Skeleatal B2 receptors)

Anxiety

Palpitations

Hypokalaemia (Intake of K+ in skeletal muscle)

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16
Q

What is the mechanism of action of Anti-muscarinic drugs?

Give an example of such a drug

A

Blocks Muscarinic Ach receptors in airways causing the airways to relax/widen

E.g. Ipratropium Bromide

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17
Q

What are the adverse effects of Anti-muscarinic drugs?

A

Dry mouth and cough

Pharyngitis

URTI

Nausea

Supraventricular tachycardia

Atrial fibrillation

Urinary retention

Constipation

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18
Q

Why are Methylxanthines used in COPD?

What are their side effects?

A

Why:

Bronchodilators

Increase respiratory drive

Increase strength of respiratory muscles

Anti-inflammatory

Side effects:

Tachycardia, SVT, Nausea, Seizures

Hence needs blood level monitoring!

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19
Q

Give the mechanism of action of Methylxanthines and two examples

A

Inhibition of phosphodiesterases:

PDEs break down cAMP, inhibition leads to increase in cAMP leading to bronchodilation etc.

Examples:

Aminophylline

Theophylline

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20
Q

Above what dose of inhaled steroids do side effects start to commonly occur?

Give examples of side effects

A

800mcg/day

Examples:

Thin skin/Bruising

Osteoporosis

Diabetes

Adrenal insufficiency

Mental disturbance

Fluid retention

Proximal myopathy

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21
Q

Give an example of a mucolytic drug

Why are they useful in COPD treatment?

A

Carbocysteine

Useful to reduce sputum thickness, helping reduce airway resistance

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22
Q

What is the concept of ‘deconditioning’ and how does it apply to COPD?

A

Many patients with COPD avoid excersize and strain to avoid breathlessness

This leads to weakening of the muscles and increased breathlessness, which leads to further avoidance

Cyclic process that increases inactivty and social isolation leading to the worsening of symptoms = Deconditioning

23
Q

What is the aim of pulm. rehab?

A

Break the deconditioning cycle through a 6-12 week program of supervised exercise, unsupervised home exercise, nutritional advice and education

24
Q

What are the advantages and disadvantages of long term O2 therapy?

When is it used?

A

Advantages:

Prevention of renal and cardiac damage due to extended periods of hypoxia

Disadvantages:

Loss of activity/independence

Must be 16+ hrs/day for survival benefit

When:

When pO2 consitently below 7.3kPa

Or below 8kPa with Cor Pulmonale

25
Q

What are the surgical options for COPD?

A

Lung volume reduction:

Reduce hyperinflation by reducing lung volume

Lung transplant:

Option for younger patients

26
Q

How might you manage an acute exacerbation of COPD?

A

Aim for Sats 88-92% with O2 therapy

Nubulised bronchodilators

Steroids (Oral or IV)

Antibiotics is infective (Raised CRP/WBCC or purulent sputum)

Consider IV Aminophylline

Repeat ABG, if no change consider Non-invasive ventilation or transfer to ITU for invasive ventilation

27
Q

What is Non-invasive ventilation?

What are the contraindications?

A

Provision of ventilation support through mask or similar device

Contraindications:

Untreated pneumothorax

Impaired conscious level (Glasgow coma scale <8)

Facial injury

Life threatening hypoxia

Vomiting

Agitated

28
Q

Give a brief description fothe organism that causes TB

A

Mycobacterium tuberculosis

Aerobic, acid and alcohol fast bacilli

29
Q

How is TB transmitted?

A

Aerosolised droplets

Coughing, sneezing, talking and other resp manoeuvres create small particles called ‘droplet nuclei’ that disperse in the air

30
Q

What happens in the first 6 weeks from contact and infection of TB occuring?

A

Alveolar macrophages phagocytose bacteria but cannot kill them (cell wall lipids block fusion of phagosomes and lysosomes)

Macrophages initiate development of cell mediated immunity which leads to the emergence of macrophages that can kill MTB bacteria

31
Q

After cell mediated immunity is activated what is the further reaction to MTB bacteria?

Hint: Stop before explaining the active disease, or this would be a very long flashcard

A

A Ghon’s focus is formed

A ghon’s focus is a small, subpleural region of granulomatous inflammation

Appears as normal granuloma (Caseous necrosis surrounded by epitheloid macrophages, lymphocytes and Langerhan’s giant cells)

TB bacilli drain into surrounding (Hilar) lmph nodes

Surrounding nodes + Ghon’s focus are called ‘Ghon’s complex’

Normally heals in most patients, however before healing some TB bacilli enter the bloodstream (most likely via lymph drainage)

If it doesn’t heal primary TB infection results

TB bacteria seed other parts of the lung and other organs (In the case of other organs, can cause Miliary TB)

In this state, TB can remain inactive for years as latent TB to be reactivated as Secondary TB

32
Q

What percentage of those infected with TB will develop active disease?

A

10%

5% Primary

5% Secondary

33
Q

How is Latent TB tested for?

Outline how the test works and what happens if positive

A

Mantoux Tuberculin test

How it works:

Tuberculin (a complex mix of TB antigens extracted from TB) is injected transdermally

If an induration (raised, hardened patch of skin) persists at injection site after 48-72hrs indicates latent TB

34
Q

Who are at greatest risk of developing active disease after latent infection?

A

IV drugs users

HIV cases

Those with Haematological malignancy

Chronic renal failure

Underweight

Immunocompromised

35
Q

Describe the common active disease processes for Respiratory TB

Hint: Don’t go so far as to mention specific process that MAY occur, just the general stuff

A

Proliferation of TB bacteria in caseous centres leads to softening and liquefaction of necrotic tissue which may discharge into a bronchus

This results in a cavity formation, fibrous tissue forms around the periphery, containing it

Haemorrhage and Haemoptysis can result from extension of the caseous process into a blood vessel or Ramussen’s Aneurysm

Caseous material can spread through the bronchial tree to disseminate infection

36
Q

Outline the pleural involvement in active TB

A

Pleural TB may occur

2 mechanisms for pleural involvement:

Hypersensitivity response in primary infection leads to acute pleuritic process (pleural effusion) with fever

Tuberculous Empyema (Pus) from a ruptured cavity spreads into the pleural space (has a tendency to burrow through chest wall)

37
Q

What is meant by Tuberculous pneumonia?

A

Marked inflammatory exudate into alveoli and small airways

Appears similar on CXR to normal bacterial pneumonia

38
Q

What are the symptoms of respiratory tuberculosis?

A

Commonly non specific

Include:

Tiredness and malaise

Weight loss and anorexia

Fever

Cough (most common)

Breathlessness (Pleural effusion)

Haemoptysis

39
Q

What are the signs of respiratory TB?

A

Pallor

Fever

Evidence of weight loss

Often no external chest signs

Localised wheezing

Carvical nodes palpable

40
Q

What is a Ramussen’s Aneurysm?

A

A pulmonary artery aneurysm adjacent or within a tuberculous cavity, It may lead to rupture and haemorrhage.

Haemoptysis results

41
Q

What is lymph node tuberculosis?

A

Spread of TB bacteria to the lymph nodes, most commonly Cervical

Often painless

Results in swelling, can progress to marked inflammation and skin rupture

Swelling of the intra-thoracic nodes may collapse bronchi

42
Q

What is osteo-arthritic TB?

A

A chronic inflammatory disease that affects the joints

Caused by the spread of TB bacteria to the joints

May present as:

Tuberculous spondylitis (most common)

Peripheral arthritis

Osteomyelitis

Poncet’s disease

43
Q

Describe tuberculous spondylitis

A

Result of haematogenous spread of TB to the spinal vertebrae

Spreads to adjacent vertebrae via the vertebral disk space

Most common in upper lumbar and lower thoracic

Insidious onset over months

Paraplegia and quadraplegia result in 25% of cases

Leads to collapse of vertebral disks through caseation

Caseous lesions form on vertebral bodies

Vertebral narrowing and collapse may occur

44
Q

Describe Miliary TB

A

Spread of Tb bacterium haematogenously leads to seeding of bacteria throughout the lungs and body, these can develop into active TB

Active TB process occur as normal but widely disseminated

May cause few rep symptoms

However Pericardial or pleural effusions and ascites may be present

45
Q

What is Chronic ‘Cryptic’ Miliary TB?

A

Usually found in 60+

High mortality miliary TB with insidious onset

Syptoms include weight loss, lethargy and intermittent fever

Common to find at post-mortem

46
Q

What investigations may be performed in a patient with suspected TB?

A

CXR

Sputum culture x3

Bronchoscopy

Gastric lavage

Biopsies

Detailed imaging (CT)

47
Q

What radiological features might be seen on a CXR of a TB patient?

A

Pleural effusions

Multilobar shadowing

Cardiac enlargement (life threatening)

Multiple cavities (Very contagious)

Miliary shadowing (life threatening)

Flecks of calcification

48
Q

How is tuberculosis diagnosed?

A

A combination of radiological and microbiologica findings paired with clinical presentation of the patient

49
Q

Why is a multi-drug approach necessary for TB?

A

About one in a millin TB bacteria are spontaneously drug resistant

as there are 1x10^9 bacteria per typical TB cavitation a multidrug regimen is necessary to prevent the development of resistance

50
Q

Outline a typical drug regimen for TB

Haw is this changed if there is CNS involvement (TB meningitis)?

A

Inital phase (2 months):

Rifampicin

Isoniazid

Pyrazinamide

Ethambutol

Continuation phase (4 months):

Rifamipicin

Isoniazid

Continuation phase is 10 months if there is CNS involvement

51
Q

What is the BCG vaccine?

How is it used?

A

The BCG vaccine consists of live, attenuated TB bacteria with greatly reduced virulence

Exposure to the antigens of the BCG vaccine confer resistance to TB as they are the same antigens

Used to protect high risk groups in the UK

Immunization of all school children was scrapped in 2005

52
Q

Which ethnic group is at highest risk of TB in the UK?

A

The Asian and Asian British populations, commonly originating from India, Pakistan and Bangladesh

53
Q

What is the relationship between HIV and TB?

A

HIV causes immunocompromisation by impairing cellular immunity (Decreasing CD4+ cell counts), this understandably raises the risk of infection.

Those with HIV are estimated 26-31x more likely to contract TB

Of 9 million TB cases worldwide in 2013, 1.1 million were in those with HIV

54
Q

What is DOT (Directly observed therapy) and how and why is it used for TB treatment?

A

What:

Directly observed therapy is where drugs are administered under supervision by a medical professional

How:

Having the out-patient come in 3x per week to recieve treatment

Possible compulsory admission and dentention

Compulsory treatment not possible

Why:

Improves cure rates, TB rates, drug resistance and relapses

Often most useful in homeless, alcoholics, addicts, the seriously mentally ill and those with multi-drug resistances

ESA 3 Callum's Cards (55 decks)

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