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Medicine year 1 semester 2 > Case 6- illness > Flashcards

Case 6- illness Flashcards

1
Q

Pneumothorax

A

Air in pleural cavity, can result in a collapsed lung

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2
Q

Pleural effusion

A

Fluid in pleural cavity

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3
Q

Haemothorax

A

Blood in pleural cavity

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4
Q

Chylothorax

A

Lymph in pleural cavity

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5
Q

What causes a collapsed lung

A

Pneumothorax, pleural effusion, Haemothorax and Chylothorax. These all cause a collapsed lung which is unable to expand

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6
Q

How many cases of lung cancer are caused by smoking

A

90%

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7
Q

Lung cancer- when to refer for chest x-ray?

A

Findings are suggestive of cancer or they are over 40 with unexplained haemoptysis

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8
Q

Lung cancer- when to offer an urgent chest x-ray

A

In people over 40 with 2 or more of the following symptoms. The same is true if they have ever smoked and have one or more of the following unexplained symptoms: cough, fatigue, chest pain, weight loss, shortness of breath and appetite loss.

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9
Q

Lung cancer- what can happen to the tumours

A

Tumours may obstruct airways causing: persistent cough, shortness of breath and chest pain.
Tumours may also invade arteries causing bleeding: Haemoptysis (coughing up blood)
Tumours may compress mediastinal structures: Phrenic nerve compression (difficulty breathing), recurrent laryngeal nerve compression (hoarseness) and compression of the oesophagus (dysphagia).

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10
Q

Other side effects of lung cancer

A

Anaemia, bone pain, finger clubbing, fatigue, loss of appetite and weight loss

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11
Q

Paraneoplastic

A

Where seemingly false signs and symptoms are seen. The tumour may secrete hormones, antibodies and enzymes that affect sites far away from the tumour.

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12
Q

Symptoms of lung cancer associated Paraneoplastic syndrome

A

Neurologic, endocrine, dermatologic, rheumatologic, hematologic, and ophthalmological, nephrotic/glomerular symptoms.

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13
Q

Pancoast tumours

A

Tumour growths in the apical region of the lungs, typically squamous carcinoma. It presents with shoulder pain and Horner’s syndrome causing unilateral: ptosis (dropping of one eyelid), Miosis (pupil constricted in one eye) and Anhidrosis (loss of ability to sweat)

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14
Q

Small lung carcinomas

A

20% of lung cancers. An aggressive tumour with poor prognosis as it grows rapidly and metastases early. It develops centrally near the main bronchus. Neuroendocrine cells of the lung appear to have scant cytoplasm, the nuclei looks bigger by comparison. The cells appear indistinct. Associated with paraneoplastic syndrome.

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15
Q

Types of non-small cell lung carcinomas (80%)

A

1) Squamous cell carcinoma
2) Adenocarcinoma
3) Large-cell carcinoma

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16
Q

Squamous cell carcinoma

A

25% of lung cancers. Develops centrally near the main bronchus. Histological features include a change from columnar epithelium to squamous epithelial cells, deposition of keratin ‘pearls’. And it is surrounded by concentric circles of squamous epithelial cells.

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17
Q

Adenocarcinomas

A

35% of lung cancers. It develops peripherally. Histological features include mucoid glands. It is more common in woman and is the most common lung cancer in non-smokers.

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18
Q

Large cell carcinoma’s

A

10-15% of lung cancers. Epithelial tumours that lack the cytological features of small cell carcinoma and have no glandular or squamous differentiation

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19
Q

Symptoms of pleural effusion

A

Symptoms include chest pain, dyspnoea, cough, finger clubbing and symptoms of the underlying disease like weight loss. There must be a large effusion before it causes symptoms- 200ml for diagnosis (x-ray) and 500ml for it to be clinically evident.

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20
Q

How does pleural effusion present in examination

A

Inspect their hands for clubbing, you should also examine their breathing. During palpations you will see that chest expansion is reduced on the side of the effusion. During auscultation, the breath sound will be lower or absent and the vocal resonance will be lower or absent.

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21
Q

What can you see in an x-ray of pleural effusion

A

It will apear white, as it progresses the costophrenic angle disappears. As the fluid fills the lungs a meniscus will appear (curved upper surface of a liquid in a tube).

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22
Q

Pleural effusion- thoracentesis

A

Aspiration of fluid (removing) can be done to identify cause. This is done under the guidance of ultrasound and you insert the needle between the 7th and 8th rib. You then measure the protein to identify the type of effusion

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23
Q

Pleural effusion- Transudate

A

Pleural effusion caused by an increase in hydrostatic pressure due to venous outflow obstruction. This is caused by congestive heart failure. There will also be a drop in colloid osmotic (oncotic) pressure as not enough protein is made or too much is being lost. This causes the fluid to leak across but the proteins don’t. Most common causes include Heart failure, Hypoalbuminemia, Cirrhosis and Nephrotic syndrome. Less oncotic

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24
Q

How to identify pleural effusion caused by Transudate

A

Light criteria: pleural effusion to serum protein ratio should be <0.5

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25
Q

Pleural effusion- Exudate

A

Inflammation leads to increased permeability and protein and fluid leakage. Most common cause is Pneumonia and malignancy (breast and lung cancer). Large unilateral pleural effusions are probably due to malignancy. More oncotic then transudate

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26
Q

How to identify pleural effusion caused by Exudate

A

Pleural fluid protein vs. serum protein ratio >0.5

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27
Q

Types of Pneumothorax

A
  • Primary spontaneous- occurs in health people (typically tall thin men).
  • Secondary spontaneous- underlying condition (e.g. rupture of bulla in COPD).
  • Traumatic- penetrating chest trauma (e.g. stab wound).
  • Latrogneic- follows a procedure (e.g. mechanical ventilation.
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28
Q

How does Pneumothorax present

A

Unilateral pleuritic chest pain with breathlessness and possible cyanosis

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29
Q

Examination findings in Pneumothorax

A

In examination of the affected side there will be reduced chest expansion, decreased or absent breath sounds and hyper-resonance on percussion.

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30
Q

Chest x-ray of pneumorothorax

A

In a chest x-ray the collapse of lung tissue will be visible as the lung recoils and peels away from the chest wall.

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31
Q

Treatment of pneumorothorax

A

It is treated using a chest drain which when inserted into the pleural space can drain the air and fluid.

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32
Q

Features of tension pneumothorax

A

1) Tracheal deviation away from the site.
2) Tachycardia is >135bpm.
3) You get a pulsus paradoxus when there is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The drop in blood pressure is more than 10mmHg.
4) Hypotension and a raised JVP.
5) It is a life threatening condition that requires instant action such as urgent decompression in the 2nd intercostal space. There is a mediastinal shift and signs of respiratory disease.

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33
Q

Haemothorax

A

Presence of frank blood in the pleural space. It can be caused by chest trauma, cancer or a pulmonary embolism.

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34
Q

Chylothorax

A

Presence of lymphatic fluid in the pleural space

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35
Q

Empyema

A

Presence of pus in the pleural space. Secondary to infection, usually pneumonia. Causes prominent systemic features and severe chest pain

36
Q

Pleural Mesothelioma

A

Malignant mesothelioma affects the mesothelial lining but can also affect the pleura. This tumour rarely metastasises to distant sites and most patients present with locally advanced disease. It has a poor prognosis of approx. 1 year.

37
Q

Signs and symptoms of pleural Mesothelioma

A
  • Breathlessness.
  • Pleural effusion or pleural thickening
  • Chest pain is typically dull, diffuse, progressive.
  • Palpable chest wall
  • Weight loss, fatigue and fever.
  • Finger clubbing (related to asbestosis).
38
Q

What causes pleural Mesothelioma

A

Associated with asbestos in 70-80% of patients, may be many years after exposure of from another family members exposure

39
Q

Pulmonary embolism

A

When one or more emboli (normally a blood clot) are lodged in and obstruct the pulmonary artery system

40
Q

Risk factors for PE

A

Significant immobility and surgery

41
Q

Causes of PE

A
  • Emboli originating in the abdominal or axillary veins, or from the right ventricle.
  • The most common type of emboli is DVT in the lower limbs (80%).
  • Tumours.
  • Fat emboli from long bone fractures.
  • Amniotic fluid-pregnant woman
  • Sepsis- i.e. infected catheters
  • Foreign bodies, during IV drug use.
  • Air- admitted during surgery.
42
Q

Small and medium PE

A

Small and medium PE may not have any specific signs and symptoms. They may have dyspnoea, tachypnoea (abnormally rapid breathing), pleuritic chest pain or features of DVT. These features are present in most people with a PE even if they don’t have a DVT.

43
Q

Signs and symptoms of PE

A

Dyspnoea, tachypnoea (rapid breathing), pleuritic chest pain, tachycardia, haemoptysis, syncope, hypotension (systolic BP less than 90 mmHg), crepitations (crackling sound), cough or fever.

44
Q

Treatment for PE

A

Heparin and anticoagulants

45
Q

PE

A

If untreated the risk of death is 23-87%, for clinically massive PE the risk of death is 50%. PE is the leading cause of maternal death in the UK

46
Q

In PE when should the patient be admitted to hospital

A
  • The patient is pregnant or given birth within the past 6 weeks.
  • They have an altered level of consciousness.
  • Systolic BP of less than 90 mmHg.
  • Heart rate of more than 130 beats per minute.
  • Respiratory rate of more than 25 breaths per minute.
  • Oxygen saturation of less than 91%
  • Temperature of less than 35 degrees
47
Q

How does lung compliance change in emphysema

A

Compliance is higher because a lower pressure can cause a higher volume. There is less recoil due to the loss of elastic tissue

48
Q

How does lung compliance change in alveolar fibrosis

A

The lungs are stiffer and have less compliance as the lung tissue gets replaced by fibrous tissue. A higher pressure causes a lower volume (right shift)

49
Q

Pathway of care- lung cancer

A

GP -detection
Radiologist- diagnosing through investigations (CT scans, biopsy)
Multi-disciplinary team (including lung cancer specialist)- discussion of treatment plan
Surgeon- surgery to remove cancer
Oncologist- chemotherapy
May have to refer to palliative care

50
Q

Airway resistance in COPD and asthma

A

It increases in asthma and COPD, the higher the resistance the harder it is to breathe. In asthma the resistance is reversible, in COPD the resistance is irreversible. In COPD small bronchioles offer the most resistance even though normally they offer the least.

51
Q

Volume/Pressure graph in COPD

A

In inspiration a higher pressure is needed to increase the volume of the lungs. In expiration there is little reduction in volume as the airways collapse. At low pressure the airways do empty

52
Q

COPD

A

Persistent respiratory symptoms due to airway obstruction which is not fully reversible. Includes bronchitis and emphysema

53
Q

Emphysema

A

You get inflammation. There is an increase in elastase and metalloproteinase. Protein and elastin gets broken down and there is damage to tissues and capillaries. Less blood will move into the diffusion barrier. Less gases are able to diffuse across the alveolar membrane. As more tissue gets broken down elastic recoil decreases. You get enlarged alveolar which causes air trapping. There is lung hyperinflation. Air becomes trapped in the lungs as the alveolar membrane breaks down.

54
Q

Risk factors for emphysema

A

Smoking, toxins, pollutants, Genetics ( a mutation in Alpha1- antitrypsin, which causes its deficiency)

55
Q

Morphology of bronchiectasis

A

Permanent dilation of bronchi and bronchioles due to inflammation and scarring, usually the lower lobe

56
Q

Symptoms of bronchiectasis

A

Persistent or recurrent cough and foul-smelling purulent sputum production. Recurrent respiratory infection and Haemoptysis

57
Q

What is bronchiectasis associated with

A

It is associated with respiratory infection. This causes sustained epithelial injury and hypersecretion of mucus. If you have epithelial injury you are more likely to get chronic Bronchial infection. The lungs then become inflamed. There is a decrease in mucocilliary clearance. There is now permanent airway damage. Often associated with COPD.

58
Q

Respiratory infections which can cause bronchiectasis

A

Congenital (diffuse)- Cystic fibrosis and Ciliary dysfunction.
Acquired (localised)- Pneumonia, TB and Bronchial tumours.

59
Q

How is bronchitis diagnosed

A

A persistent productive cough for at least three consecutive months in at least two consecutive years

60
Q

Morphology of chronic bronchitis

A

1) Cilia gets damaged so less mucus is removed.
2) Lumen blockage due to mucus hypersecretion.
3) There is an increase in goblet cells and an increase in mucus gland size and activity.
4) Increase in smooth muscle and bronchospasm

61
Q

Where do you tend to get emphysema

A

In the upper two thirds of the lungs

62
Q

Hyperinflation of lungs

A

Associated with air trapping as there is a bigger lung volume

63
Q

Signs of emphysema

A

Barrel chest and progressive dyspnoea

64
Q

Why do we see the signs and symptoms of chronic bronchitis

A

1) Mucus hypersecretion- productive cough
2) Bronchoconstriction- wheezing
3) Decrease in pO2- cyanosis
4) Alveolar hypoxia- pulmonary hypertension
5) Right sided heart failure- Cr pulmonale
Unlikely to have a fever or dullness to percusion.

65
Q

Chronic bronchitis- bronchial spasm

A

There will be a degree of Bronchiolitis as there is inflammation of the Bronchioles. This causes bronchiole spasm which reduced the area of the lumen.

66
Q

Interstitial lung disease (parenchymal lung disease)

A

A heterogeneous group of restrictive lung disease. An initial injury to the epithelium or endothelium leads to diffuse chronic inflammation and fibrosis with end stage honeycomb appearance. Lung volume and compliance decreases. In pulmonary fibrosis a trigger causes repeated inflammation. This causes the release of cytokines which promote fibrogenesis. Eventually this cycle leads to the dilation of airways.

67
Q

Interstitial lung disease- fibroblasts

A

Pulmonary fibrosis is a pathological feature of interstitial lung disease. The fibroblasts lay down fibrous tissue, this makes the tissue stiffer reducing compliance.

68
Q

Pulmonary fibrosis- Pathogenesis

A

1) Inflammation causes leukocyte induced cytokine release i.e. from inhalation of dust, drugs or idiopathic conditions.
2) Stimulation of fibrosis via increased fibroblasts
3) Alveolar epithelial cell damage.
4) Decreased surface area for gas transfusion.
5) Increased stiffness and decreased compliance

69
Q

Types of interstitial lung disease

A

Huge range of conditions linked by pulmonary fibrosis

70
Q

What can cause interstitial lung disease

A

1) Occupation/Environment- asbestosis, Coal miners pneumconiosis.
2) Hobbies- wine making, glass blowing.
3) Pets- pigeon fancier’s lung
4) Past medical history- connective tissue diseases, lupus, sarcoidosis, rheumatoid arthiritis.
5) Drugs- Amiodarone (heart medication), Nitrofurantoin (antibiotic), Methotrexate.

71
Q

Idiopathic pulmonary fibrosis

A

Accounts for 15-25% of chronic interstitial lung disease where the cause of inflammation is unknown

72
Q

Types of restrictive lung disease

A

Interstitial lung disease

73
Q

Types of obstructive lung disease

A

COPD, asthma and bronchiectasis

74
Q

Obstructive lung disease

A 
Limitation of airflow due to obstruction
Total lung capacity- Normal
Forced vital capacity (FVC)- Normal
Expiratory flow (FEV1)- decreased
FEV1:FVC ratio- decreased
75
Q

Restrictive lung disease

A 
Fibrosis reduces ability of parenchyma to expand
Total lung capacity- decreased
Forced vital capacity (FVC)- decreased
Expiratory flow (FEV1)- decreased
FEV1:FVC ratio- normal
76
Q

Vital capacity (VC)

A

The greatest volume you can expire starting from a position of maximal inspiration = IRV + VT + ERV = 4600 ml. The vital capacity is affected by posture, is proportional to height, decreases with age and is generally higher in males than females.

77
Q

Tidal volume (VT)

A

The volume breathed in or out at rest (500ml)

78
Q

Inspiratory Reserve Volume (IRV)

A

The volume of air that can be inspired in addition to normal resting (tidal) inspiration = 3000 ml.

79
Q

Expiratory Reserve Volume (ERV)

A

The volume of air that can be expired following a normal (tidal) expiration = 1100 ml.

80
Q

Residual volume (RV)

A

The volume of air remaining in the lungs at the end of a maximal expiration (i.e. it is the air that cannot be expired) = 1200 ml.

81
Q

Functional residual capacity (FRC)

A

The volume of air remaining in the lungs at the end of a normal resting expiration = ERV + RV = 2300 ml.

82
Q

Forced Expiratory Volume in one second (FEV1)

A

The greatest volume of air which the subject can expire in the first second starting from the position of maximal inspiration and expiring as hard and fast as possible.

83
Q

Forced vital capacity (FVC)

A

The greatest volume of air the subject can expire starting from a position of maximal inspiration and expiring as hard and fast as possible

84
Q

Peak expiratory flow (PEF)

A

The maximum flow rate during forced expiration

85
Q

FVC and FEV1 in restrictive

A

FEV1 - <80% predicted
FVC- <80% predicted
FEV1/FVC ratio- >0.7

86
Q

FVC and FEV1 in obstructive disease

A

FEV1- <80% predicted
FVC- unchanged, drops in severe disease
FEV1/FVC ratio- <0.7

87
Q

Classification gained from FEV1 % predicted value:

A
  • FEV1 80% or above of predicted: Mild disease
  • FEV1 50-79 % of predicted: Moderate disease
  • FEV1 30-49% of predicted: Severe disease
  • FEV1< 30% of predicted: V. severe disease

Medicine year 1 semester 2 (61 decks)

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