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Respiratory > Pathology > Flashcards

Pathology Flashcards

1
Q

Obstructive vs restrictive disease

A

Airway pathology - Obstructive

Lung pathology - Restrictive

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2
Q

Obstructive airway syndromes

A

Asthma, COPD, emphysema

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3
Q

What is ACOS

A

Asthma/COPD overlap syndrome, usually in smokers with reversible COPD and eosinophilia who are steroid responsive. Blood eosinophilia > 4%

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4
Q

What is the asthma triad

A

Reversible airflow obstruction, airway inflammation and airway hyperresponsiveness

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5
Q

How does asthma evolve

A

Bronchoconstriction - chronic airway inflammation - airway remodelling

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6
Q

Histological remodelling of basement membrane, submucosa and smooth muscles in asthma

A

Basement membrane - Thickening
Submucosa - Collagen deposit
Smooth muscles - Hypertrophy

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7
Q

Response of airway cells to allergen in asthma

A

Dendritic cells take up antigen and present it to naive T cells in the lymph nodes. This causes maturation to Th2 and B cell. Th2 cells release IL5 which stimulates eosinophils to secrete leukotrienes and cytokines. B cells secrete IgE. Mast cells have IgE receptors and degranulate releasing histamine causing bronchoconstriction. Basophils also bind to IgE and secrete Leukotriene D4 which increases mucus secretion. Mast cells release IL-4 which further causes B cells to release IgE.

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8
Q

How can airway inflammation be measured

A

Bronchoscope and bronchial biopsy

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9
Q

What predisposes patient to airway hyperresponsiveness in asthma

A

Desquamation due to eosinophil influx

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10
Q

What drugs can cause asthma symptoms

A

NSAIDS and B blockers

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11
Q

What happens to FEV1/FVC ratio in asthma

A

< 75% as FEV1 drops by FVC remains normal

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12
Q

Components of COPD

A

Muco-ciliary dysfunction, tissue damage and inflammation

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13
Q

Disease process in COPD

A

Irritants such as cigarette smoke activate macrophages and airway epithelial cells. This causes release of neutrophil chemotactic factors including IL 8 and leukotriene B4. Macrophage and neutrophils release proteases that break down connective tissue in lung (emphysema) and stimulate muscus hypersecretion. These are normally counteracted by antiproteases however in COPD, there’s an imbalance between proteases and antiprotease.

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14
Q

What does protease-antiprotease imbalance lead to

A

Alveolar destruction and emphysema

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15
Q

What are indicators of high risk in COPD

A

Two exacerbations or more within last year (or)

FEV1 < 50% predicted are indicators or high risk

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16
Q

General symptoms in COPD

A

Non-atopic, smoker, daily productive cough, progressive breathlessness, frequent infective exacerbations, chronic bronchitis - wheezing, emphysema causing reduced breath sounds

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17
Q

Non pharmacological management of COPD

A

Smoking caessation, immunisation for influenza/pneumococcal, physical activity oxygen

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18
Q

Smoking caessationg techniques

A

Nicotine replacement therapy, varenicline, bupropion

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19
Q

Main inflammatory cells in asthma vs COPD

A

Asthma - Eosinophils, COPD - Neutrophils

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20
Q

Asthma vs COPD cough

A

Asthma - Non-productive cough whereas COPD is productive

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21
Q

Asthma vs COPD diurnal variation

A

Asthma has diurnal variation whereas COPD doesn’t

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22
Q

Asthma vs COPD gas exchange

A

Normal gas exchange in asthma where it’s impaired in COPD

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23
Q

Thoracic restriction not due to lung causes

A

Skeletal - Kyphoscoliosis, ankylosing spondalitis, multiple rib fracture
Muscle weakness, obesity, ascites

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24
Q

Interstital lung disease are also known as

A

Diffuse parenchymal lung disease (DPLD)

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25
Q

Is CO2 elimination impaired in DPLD

A

No as expiration is determined by diaphragm and intercoastal movement

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26
Q

What can cause fluid in alveolar spaces

A

Cardiac pulmonary oedema - Due to raised pulmonary venous pressure, ex: left ventricular failure
Non-cardiac pulmonary oedema - Leaky pulmonary capillaries due to sepsis or trauma (acute respiratory distress syndrome -ARDS)

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27
Q

Aetiology of DPLD

A

Infective pneumonia, infarction, rheumatoid disease, drugs, cryptogenic, alveolitis, granulomatous-alveolitis, extrinsinc allergic alveolitis, sarcoidosis, drug induced (amiodarone, bleomycin, methotraxate, gold), toxic gas/fumes, pulmonary fibrosis (rheumatoid/idiopathic), autoimmune

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28
Q

What is pneumoconiosis

A

Occupational restrictive lung disease caused by inhalation of dust, often mines and agriculture.

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29
Q

What is commonly used to treat urinary tract infection

A

Nitrofurantoin

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30
Q

Clinical syndrome of DPLD

A

Breathless on exertion, cough, no wheeze, finger clubbing, lung crackles, central cyanosis (if hypoxaemic) and pulmonary fibrosis as end stage to chronic inflammation

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31
Q

Important questions for DPLD history

A

Pets, occupation, drugs, arthritis

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32
Q

Lung volumes in DPLD

A

Reduced FEV1 and FVC however FEV1/FVC > 75%

Reduced gas diffusion (DLCO) as well as reduced oxygen saturation (PaO2 and SaO2)

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33
Q

Transbronchial or thoracoscopic lung biopsy in DPLD

A

Rarely indicated

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34
Q

What is ground glass opactiy

A

Nonspecific finding on CT scan that indicates partial filling of air spaces in the lungs by exudate or transudate, as well as interstitial thickening or partial collapse of lung alveoli

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35
Q

First line treatment for DPLD

A

Oral corticosteroids such as Prednisolone as ICS aren’t effective

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36
Q

Second line treatment of DPLD

A

Azathioprine - Immunosuppression, by inhibiting purine synthesis, less DNA and RNA is produced for synthesis of white blood cells.

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37
Q

Treatment of interstitial pulmonary fibrosis (IPF)

A

Anti-fibrotic agents such as pirfenidone, nintedanib

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38
Q

What is erythema nodosum

A

Swollen patches of fat under the skin causing red bumps and patches. Due to sarcoidosis

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39
Q

What is desquamative interstitial pneumoniae (DIP)

A

Form of idiopathic interstital pneumoniae featuring elevated macrophage levels. It is believed that these macrophages were pneumocytes (alveolar cells) that desquamated. Usually history of smoking

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40
Q

What can be used to treat desquamative interstitial pneumoniae

A

Methylprednisolone - Corticosteroids

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41
Q

Obstruction of airway generally leads to

A

Pneumonia

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42
Q

Ulceration generally leads to

A

Haemoptysis

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43
Q

Common types of lung tumours

A

Adenocarcinoma, squamous carcinoma, small and large cell carcinoma

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44
Q

Serious complication following needle aspiration of metastasis

A

Implantation of malignant cells along needle tract

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45
Q

When is biopsy or needle aspiration of metastasis generally used

A

For specimen collection from mediastinal and supraclavicular lymph nodes

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46
Q

Which lung cancer type is sensitive to chemotherapy

A

Small cell lung carcinoma

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47
Q

What is used to treat non-small cell lung carcinoma (NSCLC)

A

Surgery with chemothereapy used pre and post operatively

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48
Q

Prognosis of different cancer types

A

Worse - Small cell > large cell > squamous > adenocarcinoma

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49
Q

Small cell cancers react to chemotherapy. Why do they have a worse prognosis

A

Small cell lung cancers divide rapidly. Hence, they also die fast. However some of them may become resistant to treatment and bounce back aggresively

50
Q

What drug used to treat adenocarcinoma is contraindicated in squamous cell carcinoma

A

Pemetrexed

51
Q

What immunohistochemistry factors do small cell carcinioma express

A

Antigen p63 and high molecular weight cytokeratins

52
Q

What immunohistochemistry factors do adenocarcinomas express

A

Thyroid transcription factor (TTF) 1

53
Q

Common oncogenes in lung cancer

A

MYC - regulatory gene that codes for a transcription factor that plays a role in cell cycle progression, apoptosis and cellular transformation

54
Q

Common tumour suppressor genes in lung cancer

A

p53 and Rb

55
Q

What epithelial growth factor is mutated in lung epithelium

A

MAPK/ERK pathway. Specific mutations render EGFR gene active in the absence of ligand (epidermal growth factor) binding.

56
Q

What mutation is almost exclusively seen in non-smokers and asian populations with adenocarcinoma of lung

A

EGFR overexpression

57
Q

What do EGFR overexpression tumours response to

A

Tyrosine kinase inhibitors such as erlotinib. Used for treatment of non-small cell lung carcinoma

58
Q

EML4-ALK fusion oncogenic lung cancers are a target for?

A

Crizotinib, anti-cancer drug acting as an ALK and ROS1 inhibitor. Used for treatment of non-small cell lung carcinoma

59
Q

What is atypical adenomatous hyperplasia (AAH)

A

Subtype of pneumocytic hyperplasia in the lung. Involves spread of neoplastic cells along alveolar walls (bronchioalveolar carcinoma) which can eventually become invasive adenocarcinoma

60
Q

What are carcinoids

A

Neuroendocrine tumours arising in cells of neuroendocrine system

61
Q

Where are bronchial gland neoplasms usually seen

A

In salivary glands -

Adenoid cystic carcinoma and Mucoepidermoid carcinoma

62
Q

What are paraneoplastic features

A

Systemic effects from biologically active molecules released from tumour cells

63
Q

Why is incidence of lung cancer high but prevalence low

A

As most patients diagnosed with lung cancer do no live long, 50% pass away within 6 months

64
Q

General symptoms of lung cancer

A

Haemoptysis, recurrent pneumonia, stridor, dyspnoea, hoarse voice, pleural effusion, distended jugular vein

65
Q

Why does lung with tumour tend to shrink as tumour becomes bigger

A

When a lobe is obstructed, all of the air beyond is absorbed and the lung shrinks down to a smaller size.

66
Q

Difference in wheeze in lung cancer vs asthma and COPD

A

Asthma and COPD produce an expiratory wheeze whereas lung cancer can produce a stridor - inspiratory wheeze

67
Q

What can lead to hoarseness of voice

A

Tumour pressing onto the recurrent laryngeal nerve

68
Q

How can metastatic lung cancer affect cardiovascular system

A

Atrial fibrillation followed by pericardial effusion. Patient will have dyspnoea and trouble breathing

69
Q

How can a pancoast tumour cause wasting of hand muscles

A

Pancoast tumour can erode through the ribs and into the lower part of brachial plexus. This can also lead to weakness in the hands

70
Q

How does patient present with pain that is due to cancer eroding the ribs

A

Worse at night and on movement

71
Q

Common metastases sites for lung cancer

A

Liver, brain, bone, adrenal, skin, lung

72
Q

Cerebral metastases vs stroke

A

Stroke is acute and develops within minutes whereas cerebral metastases leaks to stroke like symptoms over days and weeks.

73
Q

Cerebral metastases presents with symptoms that are worse when

A

When patient wakes up in the morning and improves as the day goes by

74
Q

Liver function tests for liver metastases

A

Abnormal, especially alkaline phosphate (ALP)

75
Q

Common presentation of bone metastases

A

Localised pain worse at night or fracture due to trivial mechanical stress

76
Q

Adrenal metastases causes functional problems

A

Yes but very rarely, hormones are generally still produced

77
Q

Common paraneoplastic symptoms

A

Finger clubbing, hypertrophic pulmonary osteoarthropathy, weight loss, thrombophlebitis, hypercalcaemia, hyponatraemia, muscular weakness - eaton lambert syndrome

78
Q

What is hypertrophic pulmonary osteoarthropathy

A

Medical condition combining clubbing and periostitis of the small hand joints

79
Q

What is the eaton lambert syndrome

A

Autoimmune disorder characterized by muscle weakness of limbs

80
Q

Important follow up for pneumonia

A

Chest x-ray 6 week down

81
Q

Why does thrombophlebitis occur in cancer patients

A

Due to increased coagulability of blood

82
Q

Signs and symptoms of hypercalcaemia

A

Stones, bones, abdominal groans, thrones and psychiatric overtones. Also cardiac arrhythmias and left ventricular hypertrophy

83
Q

Treatment of hypercalcaemia

A

Initial treatment if rehydration. If Ca2+ levels are very high then use IV Bisphosphonate. Treat underlying cancer

84
Q

Usual cancer that causes hypercalcaemia

A

Squamous cell carcinoma

85
Q

Syndrome of inappropriate anti diuretic hormone is generally caused by

A

Small cell lung cancer. It results in small cell lung cancer

86
Q

What can be used in the treatment of syndrome of inappropriate anti-diuretic hormone

A

Demeclocycline

87
Q

What can be administered by IV if calcium is very high

A

Bisphosphonate

88
Q

Most smokers cough up clear sputum almost everyday and they think this is normal. Is it?

A

No, this is chronic bronchitis

89
Q

What does stony dull percussion suggest

A

Pleural effusion

90
Q

What does hyper-resonant percussion suggest

A

Pneumothorax

91
Q

What does dull percussion suggest

A

Solid mass such as pulmonary consolidation

92
Q

Why should sputum cytology not be asked for

A

As the end result (positive or negative) for sputum cytology is bronchoscopy and it’s a time consuming process. Ask for bronchoscopy instead

93
Q

What is positron emission tomography (PET)

A

Scan to assess function rather than structure of lung. Tissues with high metabolic activity light up upon uptake of radioactive glucose

94
Q

Can a bronchoscope investigate possible tumours in the periphery of lungs

A

No because you can’t inspect bronchial divisions smaller than the diameter of the bronchoscope

95
Q

Differential diagnosis for smoker, haemoptysis and abnormal chest x-ray

A

Lung cancer, tuberculosis, vasculitis, pulmonary embolism, secondary cancer, lymphoma, brochiectasis

96
Q

Breaking news of cancer to a patient

A

Bring a relative for the patient and an experienced nurse (if needed) to comfort the patient
Ask if the patient has an idea of what it might be
Make sure they understand
Tell their GP and arrange a follow up

97
Q

When is surgery viable for cancer

A

When the cancer is recognised before it spreads beyond its primary site

98
Q

Which has a higher survival rate, small vs non-small cell

A

Non-small cell

99
Q

Treatment options for cancer

A

Surgery, radiotherapy, chemotherapy, palliative care

100
Q

Options for considering surgery

A

Is the disease localised, will patient survive operation, can we cut it out

101
Q

What is staging for surgery important

A

To make sure the cancer hasn’t metastasized and can be completely removed by surgery. Can use -
Bronchoscopy, CT scan of thorax, PET scan, CT scan of brain, mediastinoscopy

102
Q

Role of PET staging

A

To ensure there’s no metastases present before undergoing surgery

103
Q

Surgery options for lung cancer

A

Pneumonectomy or lobectomy, thoracotomy, minimal access video assisted thoracic surgery (VATS)

104
Q

VATS vs pneumonectomy

A

Faster recovery time and less traumatic

105
Q

Is small cell carcinoma suitable for surgery

A

No as it divides rapidly, it may metastasize easily making it hard to pinpoint the exact location of tumour to remove during surgery. Chemotherapy is a better alternative

106
Q

What is the ECOG score used for

A

To assess how the disease impacts the patients daily living abilities

107
Q

Side effects of chemotherapy

A

Targets rapidly diving cells, these types are also present in intestinal epithelium and bone marrow. Can lead to opportunistic infection and anaemia, nausea, vomiting, tiredness, hair loss and pulmonary fibrosis

108
Q

2 uses of radiotherapy

A

Radical - Curative intent

Palliative - Delaying tactic useful for metastases

109
Q

Disadvantages of radiotherapy

A

Collateral damage to spinal cord, oesophagitis and adjacent lung tissue (fibrosis)
It always goes only to where you point it to, not good for subclincal metastases

110
Q

What is SABR

A

Stereotactic Ablation Radiotherapy - Fires more beams than radiotherapy but with less intensity which causes lesser collateral damage. 4D scanning required

111
Q

What determines lung cancer treatment

A

Cell type, extent of disease, co-morbidity and patients wishes

112
Q

Prognosis for lung cancer

A

Half dead within 6 months

1 in 20 survive more than 5 years

113
Q

What is induration

A

Swelling or hardening of normally soft tissue

114
Q

What is lobar pneumonia

A

Confluent consolidation involving a complete lobe. Most often due to Streptococcus pneumoniae

115
Q

Is pneumonia always fatal

A

Usually self-limiting and solves by resolution. Can be fatal in immunocompromised or immune-deficient

116
Q

What is bronchopnemonia

A

Infection starts in bronchi and spreads to adjacent lungs. More often with pre-existing conditions

117
Q

What organism would you expect in a aspiration pneumonia

A

Staphylococcus aureus, coliforms and anaerobes as these are generally found in the gut

118
Q

What can lung abscess be mistaken for

A

Lung cancer

119
Q

When do you generally get lung abscess

A

Aspiration pneumonia

120
Q

Hypersensitivity in tuberculosis

A

Generally type 4 hypersensitivity - Granulomas with necrosis

Respiratory (26 decks)

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