Respiratory Flashcards

1
Q

Classify asthma into early and late onset and discuss the likely presenting characteristics of each

A
Early onset:
Usually extrinsic (allergic)
Younger patients
Elevated IgE 
Eczema and rhinitis
Late onset:
May be intrinsic
>30yo
No history of atopy
May be caused by stress cold etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline common precipitants of an asthma attack. 12

A
Allergens
Stress
Emotions
Cold
Exercise
Smoking
URTI
Drugs (B-blocker, NSAIDs)
Work (paint sprayers)
GORD
Food/drink
Pollution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the clinical features of an acute asthma attack 5

A
Reduced air entry
Polyphonic wheeze
Hyperresonance
Hyperinflated chest
Tachypnoea

Severe:
High pulse and resp rate
confused

Life threatening:
Silent chest
Bradycardia
Cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the blood gas abnormalities associated with severe asthma and highlight other clinical indices of severity

A

In mild attacks pCO2 may be low
A normal pCO2 indicates deterioration
In life threatening conditions an high pCO2, severe hypoxia and a low pH.
Predicted PEF<50% indicates severe, and <33% life-threat.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe how to use inhaler devices and other aids appropriately

A

Shake the inhaler, take a normal breath out, place the inhaler in your mouth and simultaneously breathe in and press the button to release the aerosol. Hold the breath in for 10 seconds if possible. Important not to just spray the inhaler into the mouth! With the steroid inhaler, the patient should be counselled to rinse the mouth out after use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the morphology and pathological consequences of asthma

A

Type 1 hypersensitivity reaction: Th2 cells activate plasma cells to produce antibodies.
These cross-link antigens and stimulate mast cells to produce inflammatory mediators.
Eosinophils also produce inflammatory mediators.
Type 4 hypersensitivity may also occur where the smooth muscle becomes hypertrophied.
Smooth muscle constricts the bronchioles (may cause a chronic thickening of bronchiole walls) and a mucus plug may also form.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the principles and elements of spirometry including measurements of FEV1 and FVC and the difference between obstructive and restrictive abnormalities

A

FEV1 is the maximum amount of air that can be expired in 1 second.
FVC is the difference between the maximum inspiratory volume and the minimum inspiratory volume.

In obstructive lung disease eg asthma FEV1/FVC can be <0.7
In restrictive both FEV and FVC may be reduced but ratio may be normal or slight increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define chronic obstructive pulmonary disease (COPD).

A

A chronic disease state causing a reduced airflow which is not fully reversible.
It is progressive and involves an inappropriate inflammatory response in the lungs to noxious substances and gases.
Encompasses bronchitis and emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the typical history of a patient with COPD 5 and 4 systemic effects

A
SOB
Wheeze
Clear/white sputum
Cough
Frequent chest infections
Systemic effects:
Hypertension
depression, 
decrease in muscle mass
osteoporosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the pathology features and complications of chronic bronchitis.

A

Caused by inflammation of bronchioles due to cigarette smoke.
Causes an increase in goblet cells, resulting in increased cough and sputum production.
This may result in airway narrowing du to scarring and thickening of walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the pathology features and complications of emphysema

A

Caused by the destruction of alveoli in the lung.
Smoke inactivates alpha-1 antitrypsin which protects lungs against the actions of proteases such as neutrophil elastase, breaking down alveolar walls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List recognised risk factors for the condition 4

A

Smoking (largest)
Pollution
Alpha-1 antitrypsin deficiency
Occupation (mining)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the signs of COPD? 7

A
Use of accessory muscles to breathe
Pursed lips
May have barrel chest
May be tachypnoeic
Flapping tremor
Bounding pulse
Reduced chest expansion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe features which are consistent with a pink puffer. 2

A

Increased respiratory rate

Weight loss and muscle wasting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe features which are consistent with a blue bloater. 6

A
Increased lung volume 
Polycythemia
Cyanosis
Regular/reduced resp rate
Hypercapnia
hypoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline the investigation of a patient with suspected COPD.

A
Spirometry - reduced FEV/FVC ratio.
Raised haematocrit, Hb, CRP
CT may show bullae
Echo/ECG if suspected heart involvement
Alpha - 1 antitrypsin testing if non smoker and/or young
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Interpret a CXR showing features of COPD/emphysema

A

Bullae may be present

Hyperexpansion of lungs may present via narrow heart shape and a flat diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the typical history of a patient with bronchiectasis and differentiate it from COPD.

A

Cough
Purulent sputum production (often worse in the morning)
Haemoptosis
Halitosis
Systemic effects: Fever, malaise, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline the morphology and pathological consequences of Bronchiectasis.

A

Bronchioles become thickened, inflammed and dilated.
Mucus transport mechanisms fail, leading to mucostasis and recurrent infections.
Squamous metaplasia and loss of cilia also occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List recognised risk factors for bronchiectasis 5

A
Congenital
Post infection (TB, pneumonia)
Mechanical obstruction (bronchial carcinoma)
Mucocilliary defects - CF
Immunocompromised patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the physical signs of bronchiectasis?

A

Clubbing
Halitosis
Course inspiratory crackles over affected area
Production of thick khaki coloured sputum
Patient may be febrile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Outline the investigations of a patient with suspected bronchiectasis

A

CXR may be clear or show bronchiole dilation
CT may show bronchiole wall thickening with cyst formation at the terminal end.
Sputum culture may show organisms responsible for infection if present.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How would one differentiate bronchiectasis from COPD?

A

Clubbing is common, unlike in COPD.
Sputum in COPD is not of the same quantity.
Unlike in COPD, there is no wheeze.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the typical presentation of a patient with a community acquired pneumonia.

A

Often preceded by a viral infection.
Patient becomes more ill, develops a temperature.
Dry cough at first with pleuritic CP.
Then cough starts to produce rusty sputum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the CURB 65 scoring system.

A
Confusion
Urea >7
Respiratory rate >30
Blood pressure <90/60
>65 years of age
26
Q

List the common pathogens causing community acquired 5 and hospital acquired pneumonia 4

A

CAP: Strep pneumonie, myco pneumonie, chlamydia pneumo, Hib, legionella.
HAP: Gram -ve (E.Coli, klebsiella, pseudomonas), staph aureas.

27
Q

Outline factors that predispose to pneumonia 9

A
Post viral infection
Smokers
Bronchiectasis
Bronchial obstruction
IVDU
GORD
Alcoholics
Hopitalised and ill
Immunosuppressed
28
Q

Describe the pathology of acute lobar pneumonia and bronchopneumonia

A

Bronchopneumonia is caused by bronchial inflammation which spreads downwards into alveoli causing inflammation in the alveoli and may result in scarring
Cilia are destroyed and vessels congested

Acute lobar pneumonia affects a whole lobe of the affected lung and preogresses through 4 distinct phases.
Phase 1: Congestion
Phase 2: Red hepatisation
Phase 3: Grey hepatisation
Phase 4: Resolution
29
Q

Outline the investigation of a patient presenting with a community-acquired pneumonia

A

CXR - may show consolidation but lags behind clinical diagnosis.
CRP, ESR, WBC may be elevated
Sputum culture may allow confirmation of the offending microorganism.
Blood cultures should be taken before starting antibiotics
U+Es for CURB 65

30
Q

Discuss general aspects of treatment of pneumonia

A

Suggest counseling on stopping smoking.
Appropriate physiotherapy to clear mucus should be given.
Analgesia should be administered to relieve pain
Appropriate antibiotic therapy, in keeping with local guidelines should be administered.

31
Q

Describe the complications of pneumonia

A

Septicaemia
Lung abscess - Localised suppuration associated with a cavity and fluid level.
Empyema - Fluid in the pleural cavity formed by bacterial spread

32
Q

What are the classic features of consolidation on examination? 3

A

Increased vocal fremitus
Bronchial breathing
Dull to percussion

33
Q

Recognise the radiological features of consolidation on CXR.

A

Greyness/opacity: Patchy in bronchopneumonia and homogenous in acute lobar
Middle lobe: Loss of the heart border
Lower lobe: Diaphragm obscured and blunting of costophrenic angle.

34
Q

Describe the process of tuberculous infection and its dissemination.

A

TB micro-organisms are inhaled
Bacilli are engulfed by macrophages and may be transported to lymph nodes to form the Ghon focus.
Bacilli may then desseminate via bronchial/haematogenous/local spread.
Bacilli may then lie dormant in distant foci.
In 5% of patients, they will develop clinical disease, mostly within a year if infection.

35
Q

Discuss the presentation of reactivation infection of TB, compared to post-primary TB 6

A

B symptoms - Fever, night sweats, weight loss
Productive cough
Haemoptosis
Plueral rub if associated with effusion

36
Q

Outline common predisposing factors for TB infection

A

Social deprivation
Overcrowding and houses with poor ventilation
Non-white
Return trips to countries with higher prevalence
Age
HIV infection or other immunosuppression
Alcoholic dependence

37
Q

Outline the investigation of a patient with suspected TB

A
CXR which may show:
Cavitation
Consolidation/collapse
Effusion
Miliary shodowing

Mantoux test and culture with ZN stain are also recommended

38
Q

List the common sites and outline the pathological features of non-pulmonary TB infection

A

Lymphadenopathy - TB spreads to LN and stays there
Pericardium - TB infiltrates pericardial sac and may cause contrictive pericardium
Bones/joints - May cause joint pain and back ache if it affects the spine (Potts disease). Psoas spasm
Skin -Scrofulderma
Adrenal gland - Important cause of hypoadrenalism - may be mistaken for Addison’s
CNS - May cause meningism
Abdominal - May cause lymphocytic ascites and/or obstruction
UG - Very important cause of sterile pyuria

39
Q

Describe the typical clinical presentation of pneumothorax

A

Sudden onset unilateral pleuretic CP and/or SOB

If it enlarges, SOB may become more severe and patient may become tachycardic and develop pallor.

40
Q

Describe risk factors for pneumothorax development

A

Tall thin young males often affected. 6:1 sex ratio
In older patients, cause is usually underlying COPD
Rarer cause may be asthma, abscess, carcinoma or fibrosis.

41
Q

Distinguish between pneumothorax and ‘tension’ pneumothorax

A

A tension pneumothorax occurs via a valvular mechanism.
Air moves into the pleural space but is not expelled during expiration.
This leads to a progressive build up of air in the pleural space.

42
Q

What are the clinical features indicative of a tension pneumothorax? 9

A
Tracheal deviation away from affected side
Tachypnoea
Tachycardia
Hypotension
Raised JVP
Decreased vocal resonance
Decreased expansion on the effected side
Hyperresonance
Absent breath sounds on affected side
43
Q

Outline the underlying pathology of pneumothorax

A

A rupture of pleural blebb/bulla causes air entry into pleural space which usually has a negative pressure.
Lung collapses by intrinsic recoil

44
Q

Outline the investigation of a patient with a suspected pneumothorax

A

CXR - Will show a line with absence of lung markings outside it. It may also show tracheal deviation and mediastinal shift away from affected lung.

45
Q

Outline the emergency treatment of a tension pneumothorax

A

Wide bore cannula 2nd ICS MCL

46
Q

Outline the major pathological classification of lung cancers and their prognosis 4

A

Small cell
Large cell
Adenocarcinoma
Squamous cell

5 year survival if caught early is 55-67% but reduces to 1-3% if not caught earlier

47
Q

Describe risk factors that increase the risk of lung cancer

A

Smoking
fibrosis
Occupational hazards - asbestos, petrolium, radiation, coal tar

48
Q

Outline the epidemiology of lung cancer in developed countries

A
  1. 6% of cancer in the UK, but accounts for 22% of mortalities
    male: female ratio is 3:1
49
Q

Describe the common clinical presentation of lung cancer. 5

A
Most commonly:
Cough
Chest pain
Haemoptosis 
Clubbing
enlarged lymph nodes
Less common:
Hoarseness of voice
SOB
Weight loss
Symptoms of metastasis may present first or endocrine symptoms if small cell
50
Q

Outline local manifestations of lung cancer.

A

If in apex (Pancoasts tumour) may erode ribs and cause compression of brachial plexus
If involves pleura may cause haemorrhagic effusion.
If involves sympathetic chain = horners syndrome (miosis, ptosis and anhidrosis)
If recurrent laryngeal nerve compressed hoarseness of voice
If oesophagus compressed = dysphagia
If phrenic nerve compressed may cause unilateral ipsilateral diaphragmatic paralysis.
If SVC compressed = Early morning headache, facial congestion, upper limb oedema and raised JVP

51
Q

Discuss relevant investigations

A

CXR - Adenocarcinomas more peripheral, the rest central
CT - Identify mass and check for mets whilst visualising hilar lymph nodes
Bronchoscopy - detect bronchial carcinoma and take biopsy.
Sputum cytology - detect bronchial carcinoma

52
Q

Classify causes of a pleural effusion.

A
Transudate = 
Heart failure 
Hypoproteinaemia (kidney, liver intestinal failure)
Hypothyroidism
Ovarian tumours
Constrictive pericarditis

Exudate = High protein content >30g/L
Pneumonia
Carcinoma
TB

53
Q

Describe the clinical features of a pleural effusion.

A

Chest wall movement decreased on affected side
Dull percussion note
Decreased vocal fremitus and breath sounds
Mediastinum deviates away from affected side

54
Q

Describe the aetiology and clinical features 5 of an empyema.

A
Pus in the pleural space
May be caused by bacterial infections or TB
Symptoms include:
SOB
fever
rigors
pleuritic CP
Malaise
55
Q

Discuss the investigation of a unilateral pleural effusion

A

CXR may reveal an unilateral white out with tracheal deviation away from the affected side. Further more, blunting of costophrenic angles may occur as well as the presence of a meniscus.
CT may be used to detect metastasis.
Pleural tap is used in all but the smallest of effusions.
Ultrasound is used to guide a needle with is used to draw out fluid from the pleural space.
This fluid may be used for cytology to detect cause eg TB/carcinoma.

56
Q

Describe the main conditions associated with asbestos inhalation 2

A

Asbestososis - Fibrosis caused by asbestos

Mesothelioma - Tumour of the pleura

57
Q

Describe the pathology of simple and complicated coal workers pneumoconiosis

A

Caused by the accumulation of coal dust in the lungs
Produces fine micronodular shadowing on CXR
May progress to Progressive Massive fibrosis (PMF) where large black fibrotic masses develop in the apices of the lungs.

58
Q

Describe the nature of restrictive lung disease and contrast this with features of obstructive lung disease

A

A decrease in the patient’s total lung capacity due to the apoptosis of endothelial cells.
This is replaced with fibrotic collagenous matter which lacks elasticity.

59
Q

Outline the main groups of disease leading to pulmonary fibrosis and clinical restrictive lung disease and relate this to an occupational history.

A

Localised fibrosis - Sarcoidosis, tuberculosis, sclerosis, asbestosis, beryllosis
Generalised - IPF, rheumatoid lung, tuberous sclerosis, neurofibromatosis

60
Q

Distinguish type-2 (ventilatory) from type-1 (respiratory) failure and understand the implications of having a high arterial pCO2

A

Type 1: PO2 is low <8 but pCO2 is normal or low
Type 2: PO2 is low <8 and CO2 is high >7

Hypercapnia may lead to unconciousness and death.

61
Q

Distinguish between acute and chronic type II respiratory failure and respiratory and metabolic causes of acidosis

A

Chronic failure is mostly caused by COPD and will have metabolic compensation.
Acute failure will not have compensation and may be caused by morphine overdose, airway collapse and foreign body.
Respiratory acidosis is caused by a high PCO2 whereas metabolic acidosis is caused by a negative base excess.

62
Q

Describe the causes of ventilatory failure

A

COPD
Respiratory muscle weakness (Guillan Barre syndrome)
Chest wall deformities (Kyphoscoliosis) - Limits ability of chest to expand
Depression of the respiratory centre (morphine overdose)