Lung Pathology Flashcards

1
Q

WHAT ARE THE DIFFERENT MODES FOR OLD TO GET?

A

Vapour.

Gases.

Dusts.

Fume.

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

What is vapour or gases?

A

Liquid or solid substance suspended in air.

Including mists.

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

What is dust?

A

Aerosolised solid particles. Size from 1 to less than 100 nanometers.

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

What is a fume?

A

Normally vapour or gas.

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

When do most occupational lung disorders occur?

A

After a period of latent (asymptomatic) exposure.

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

What improves prognosis in OLDs? What do you need to weigh up though?

A

Earlier recognition

Identify and cease exposure

Health versus income

Loss of employment

Eg allergic OA

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

What is the problem with historical exposure factors for OLD? What effect does this have on prognosis?

A

Recognised years later

Not normally exposed

Supportive measures

Little/no impact on prognosis

Benefits advice

Eg asbestosis

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

What factors do you have to think about when looking at OLDs?

A

Susceptibility
Genetic/individual vs population

Severity
No sx vs disability/death

Reversibility
Reversible vs irreversible

Employment
Working vs employed

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

What are the most common OLDs?

A

Asthma.

Allergic alveoli’s.

Bronchitis/empyhsema.

Non-malignant pleural disease.

Mesothelioma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can occupational asthma be caused?

A

90% Asthma induced by sensitisation (allergy) to an agent inhaled at work.

10% Asthma induced by massive accidental irritant exposure at work (direct airway injury).

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

How much of adult onset asthma does occupational asthma take up?

A

9-15%.

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

What happens with occupational asthma prolonged exposure?

A

Ongoing exposure worse prognosis

Early identification important

Treat or even cure

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

What would some tests of occupational asthma show?

A

Normal spirometry.

Work-effect confirmed by seal PEF.

Positive IgE to wheat flour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is an example of allergic sensitisation?

A

Extrinsic allergic alveolitis

Note, Asthma is also one

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

Where was extrinsic allergic alveolitis first recognised?

A

Farmers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How can extrinsic allergic alveolitis be caused?

A

Occupational or environmental.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is extrinsic allergic alveolitis?

A

An interstital lung disease

Upper lobe predominant, gas trapping, ground glass, progresses to fibrosis.

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

How is extrinsic allergic alveolitis classed?

A

Duration

Acute (may be self-limiting).

Subacute.

Chronic (scarring).

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

What are the different occupational hazards for extrinsic allergic alveolitis?

A

Microorganisms.

Animals.

Vegetation.

Chemcials.

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

What are the different microorganisms causing for EAA?

A

FARMERS!

wood pulp workers, sewage workers, maple bark strippers, cheese washers, metalworking engineers, mushroom workers, suberosis, bagassosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What animals, vegetation and chemicals can cause EAA?

A

Animals
Birds, wheat weevil, fish meal, rodent handlers

Vegetation
Coffee, wood

Chemicals
Vineyard sprayers, insecticide, isocyanates, anhydrides, plastics

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

What does prognosis of EEA depend on?

A

Early recognition and avoiding exposure.

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

What is an example of Chronic inflammation?

A

COPD.

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

What percentage of COPD happens within occupational exposure?

A

10-15%.

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

What historic VGDF substances cause COPD?

A

Coal, silica, grain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is an occupational hazard that can cause COPD?

A

Dust exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What deficiency makes a person more likely to develop COPD?

A

Alpha-1 antitrypsin deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are some asbestos-related lung diseases?

A

Pleural plaques

Diffuse pleural thickening.

Asbestosis.

Lung cancer.

Mesothelioma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is asbestos?

A

Naturally occurring mineral fibre

Used for millenia
Insulating, fire-retardant, tensile strengh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are pleural plaques and why are they important in asbestos-related lung diseases?

A

Pleural collagen, often calcified.

Marker of exposure.

Not pre-malignant.

Aetiology unclear.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is diffuse pleural thickening and what can it cause in asbestos-related lung disease?

A

Follows benign effusion

Obliteration of costophrenicangle

Can cause
Restriction due to thickened pleura
SOB, respiratory failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Is there any treatment for diffuse pleural thickening?

A

No effective treatment.

May progress slowly (without further treatment).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is asbestosis and what does it show in asbestos-related lung disease?

A

Pulmonary fibrosis
Subpleural, basal, UIP pattern.

With/without plaques.

History of heavy exposure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Is there any treatment for asbestosis?

A

No effective treatment.

May progress (without further exposure).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is mesothelioma in asbestos-related lung disease?

A

Rapidly progressive and usually incurable pleural cancer

Lung encased by tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How does mesothelioma present in asbestos-related lung disease?

A

Often presents as an unexplained pleural effusion

Progressive breathlessness, chest pain, weight loss

Average survival 8-14 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How can you prevent OLDs?

A

Requirement under COSHH.

Focus on exposure prevention or minimisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What procedures can you do to help prevent OLDs?

A

Elimination (eg asbestos)

Substitution (eg latex to nitrile gloves)

Engineering controls (eg exhaust ventilation)

Worker education

RPE (masks and respirators)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What can you do if there is an individual risk to a patient?

A

Yearly questionnaire/spirometry/CXR

Identify ill health early

Prevent further harm by reducing/preventing exposure

Review control measures to protect other workers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are some chronic obstructive diseases?

A

Chronic bronchitis and/or emphysema

Asthma

Bronchiectasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

WHAT IS COPD?

A

Collection of lung diseases that cause IRREVERSIBLE obstruction to airflow out of the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the causes of COPD?

A

Smoking

A1AT

IV drug use

Industrial exposure to chemicals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

WHAT IS CHRONIC BRONCHITIS?

https://www.youtube.com/watch?v=Y29bTzKK_P8

A

Bronchial tubes inflammation

IRREVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is chronic bronchitis defined as?

A

Cough, sputum production on most days for 3 months of 2 successive yrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the different layers of the airways?

A

Mucosa
Epithelial cells

Goblet cells

Lamina propria
Basement membrane
Loose connective tissue

Submucosa
Smooth muscle
Connective tissue

Cartilage (bronchi)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What does smoking cause?

What does this cause?

In chronic bronchitis

A

Hypertrophy and hyperplasia of the mucinus glands (bornchi)
Hypertrophy and hyperplasia of goblet cells (bronchioles)
Increase in mucus

Cilia also become short and less motile
Harder to move mucus

Air trapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How can pulmonary hypertension happen in chronic bronchitis?

A

Decreased gas exchange causign vasocontriction

Large proportion

Increases pulminary vascular resistance

Develops pulmonary hypertension

Right side of heart enlarges

Cor pulmonale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How can a person become cyanosed in chronic bronchitis?

A

CO2 trapped in alveoli takes up more space

O2 unable to fill alveoli

Less goes into the blood

More CO2 in alveoli means less CO2 can come out the blood

More CO2 in blood less O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the reid index?

A

Size of the mucinus glands relative to the rest of the layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Who does chronic bronchitis affect?

A

Affects middle aged heavy smokers

Some following pollution chronically

Recurrent low grade bronchial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are the symptoms of chronic bronchitis?

A

Wheeze

Crackles

Cough

Production of mucus (sputum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the signs of chronic bronchitis?

A

Hypoxemia
Hypercapnia
These cause cyanosis

Pulmonary hypertension
Result of low O2
Causing cor pulmonale

Tachypnoea

Use of accessory muscles

Hyperinflation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the differential diagnosis for chonic bronchitis?

A

Alpha1-Antitrypsin Deficiency

Asthma

Bronchiectasis

Chronic Obstructive Pulmonary Disease (COPD)

Chronic Sinusitis

Gastroesophageal Reflux Disease

Influenza

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the investigations for chronic bronchitis?

A

Chest X-ray
Rule out other lung conditions, such as pneumonia.

ECG

Right venticle and atria enlargment (cor pulmonale)

Sputum (bacteria).

A pulmonary function test

CT scan

ABG: PaO2 decrease ± hypercapnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the management options for chronic bronchitis?

A

Reduce risk factors.

Medications
A bronchodilator.
Theophylline is an oral medication that relaxes the muscles in your airways.

General
Short-acting antimuscarinic (ipratropium) or salbutamol
Mild/Moderate
Long-acting antimuscarinic (tiotropium) or salmeterol
Corticosteroids if severe plus long acting
Beclamethosone
Antibiotics

Pulmonary rehabilitation. It often consists of exercise, nutritional counseling, and breathing strategies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

WHAT IS EMPHYSEMA?

What are the different types?

https://www.youtube.com/watch?v=TEuSV_7gWA8

A

Enlargement of alveolar airspaces with destruction of elastin in walls.

Centri-acinar
(proximal part of acinus due to smoking)
(top of lungs)

Pan-acinar
(All acinar affected)
(Genetic condition alpha1-antitrypsin)
(Bottom of lungs)

Paraseptal acinar
(Distal acinus)
(Periphery of lungs)
(Pneuthorax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What are the causes of emphysema?

A

Cigarette smoking. (MAINLY)

Alpha-1-antitrypsin deficiency

Coal dust exposure

Cadmium toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What happens when the alveoli becomes irritated by smoke?

What does this do?

What happens when exhaling?

A

Triggers an inflammatory response, immune cells come in

Releasing inflammatory mediators
(Proteases, Collangenases)
Breaks down the collagen and elastin in the alveoli wall

Bernoulli principle

Exhalation of air has a lower pressure and pulls the airway inwards, ormal airways can withstand this
Emphysema airways have less elastin and collagen therefore collapse

Leads to air trapping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What happens when air comes into emphysema lungs?

A

Lungs are more compliant

Lungs overinflate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What happens in alpha-1 antitrypsin deficiency?

A

Macrophages produce proteases
Helps clear debris
Can damage tissue

Alpha-1 antitrypsin is a protease inhibitor

Protects against damage

Deficiency means proteases can damage lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the oxygen and carbon dioxide levels in emphysema?

A

‘pure’ emphysema appears with reduced PaCO2 and normal PaO2 at rest due to overventillation (‘pink puffers’)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the symptoms of emphysema?

A

Dyspnea - shortness of breath

Exhaling through pursed lips to keep lungs inflated

Cough - sputum

Weight loss due to metabolic demands

1/3 of lung capacity is destroyed before symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the signs of emphysema?

A

Barrel chest - overinflated chest on x-ray

Flattened diaphragm

Pulmonary hypertension

Right heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What are the differential diagnosis of emphysema?

A

Bronchiectasis

Bronchitis

Lymphangioleiomyomatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the investigations for emphysema?

A

Blood tests
Hb level increase secondary polycythaemia.

Chest x-ray
This helps to show hyperexpansion of the lungs.

ECG or Echocardiogram
Right heart failure (a complication of emphysema and COPD).

Pulmonary/Lung Function tests
Spirometry is the best test to detect airflow limitation and obstruction.

Blood gases
Normal, later stages of disease, low oxygen and high carbon dioxide levels.

High resolution CT
Best test for detecting emphysema and bullae (big dilated air spaces).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the treatment for emphysema?

A

Stop smoking

General
Idotropium or salbutamol

Mild/intermediate
Tiotropium (antimuscarinic)) and salmeterol

Severe
corticosteroids (beclemethosone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the complications of COPD?

A

Pneumothorax

Cor pulmoale

Acute exaccerbations

Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

WHAT IS BRONCHIECTASIS?

https://www.youtube.com/watch?v=rTcVPHszU5E

A

Irreversible dilation of the bronchioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the causes of bronchiectasis?

A
**_Congenital_** 
Cystic fibrosis (CF);

Post-infection
TB
HIV

**_Other_**
Bronchial obstruction (tumour, foreign body)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the pathology of bronchiectasis?

A

Infection and imparied drainage

Activates neutrophilic proteases and cytokines causing inflammation

Increaed mucus and increased stagnent bacteria

Cycle starts again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the signs and symptoms of bronchiectasis?

A

Chronic cough - foul smelling sputum

Flecked with blood sometimes.

Finger clubbing

Coarse inspiratory crepitations.

Wheeze

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the differential diagnosis for bronchectasis?

A

Alpha1-Antitrypsin Deficiency

Aspiration Pneumonitis and Pneumonia

Asthma

Bronchitis

Chronic Obstructive Pulmonary Disease (COPD)

Cystic Fibrosis

Emphysema

Gastroesophageal Reflux Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the tests for bronchiectasis?

A

Sputum culture

HRCT chest
To assess extent and distribution of disease.

Spirometry
Obstructive.

Chest X-Ray
Cystic shadows, thickened bronchial walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the management for bronchiectasis?

A

Stop smoking

Airway clearance exercises

Bronchodilators

Corticosteroids

Antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the complications with bronchiectasis?

A

Pneumonia

Emphysema

Septicaemia

Amyloid formation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

WHAT IS ALPHA-1 ANTITRYPSIN DEFICIENCY?

A

A deficiency in alpha-1 antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What does alpha-1 antitryspin do?

What is the gene that codes for it?

What chromosome is it on?

A

Inactivates elastase (a protease)

SERPINA1

Long arm of chromosome 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What happens when there is infection or inflammation in the lungs?

What does A1AT do?

What happens if there is no A1AT?

A

Neutrophils

Neutrophils make neutrophil elastase

Break down bacteria but also elastin in the walls

Liver makes alpha-1 antitrypsin which travels to lungs and inhibits this

Neutrophil elastase breaks down alveoli wall

Alveoli lose elasticity and structural intengrity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When would you favour alpha 1-antitryspin deficiency as a dignosis?

A

Never smoked

Young

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the symptoms of alpha-1 antitrypsin deficiency?

A

Shortness of breath

Wheezing

Mucus production

Chronic cough

Cirrhosis
Inability to make coagulation factors
Build up of toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What investigations are done for alpha-1 antitrypsin deficiency?

A

Bloods
A1AT low

Biopsy
Liver - Periodic-acid shiff stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the treatment of alpha-1 antitrypsin deficiency?

A

Augmentation therapy
IV infusion of normal protein
Slow of halts progression

Inhlaers

Oxygen

Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

WHAT ARE INTERSTITIAL LUNG DISEASES?

A

Disease of the alveoli primarily

Scarring

Fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What are the symptoms of interstitial lung diseases?

A

Dry cough

Digital clubing

Diffuse inspiratory crackles

Dysponea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What can acute interstitial lung diseases cause?

A

Acute respiratory distress syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What are the causes of acute respiratory distress syndrome?

A

Shock

Trauma

Infections

Gas inhalation

Narcotic abuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the symptoms of acute respiratory distress syndrome?

A

Tachypnoea

Dyspnoea

Pulmonary oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What are some Chronic interstitial diseases? (Differential diagnosis of eachother)

A

Idiopathic

Pneumoconiosis

Extrinsic Allergic Alveolitis/ Hypersensitivity pneumonitis

Sarcoidosis, connective tissue disease etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is pneumoconiosis?

A

Lung disease caused by inhaled dust Organic or inorganic dust (mineral)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What happens in coal workers’ pneumoconiosis?

A

Coal is ingested by alveolar macrophages (dust cells)

They aggregate around bronchioles

The consequences vary from trivial to lethal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is Caplan’s syndrome?

A

The association between rheumatoid arthritis, pneumoconiosis, and pulmonary rheumatoid nodules.

92
Q

How do you treat pneumoconiosis?

A

Avoid exposure to coal dust

Treat co-existing chronic bronchitis

93
Q

What happens in silicosis?

A

Inorganic minerals abundant in stone and sand

Toxic to macrophages, leading to their death with release of proteolytic enzymes.

Tissue destruction and fibrosis

Nodules are formed after many years of exposure.

94
Q

How do you treat silicosis?

A

Avoid exposure and claim compensation.

95
Q

What is asbestosis caused by?

A

Inhaltion of asbestos.

96
Q

What are the features of asbestosis?

A

Similar to other fibrotic lung diseases with progressive dyspnoea, clubbing, and fine end-inspiratory crackles.

Also causes pleural plaques, increased risk of bronchial adenocarcinoma and mesothelioma.

97
Q

What is the management of asbestosis?

A

Symptomatic.

Patients are often eligible for compensation through the UK Industrial Injuries Act.

98
Q

WHAT IS EXTRINSIC ALLERGIC ALVEOLITIS?

https://www.youtube.com/watch?v=PIuj6XiMlps

A

Inflammation of the alveoli due to an extrinsic allergen of known type

99
Q

What are two types of extrinsic allergic alveolitis?

A

Bird fancier’s lung
Avian proteins in droppings
Antigens

Farmer’s lung
Caused by fungus (poorly stored / mouldy hay)

100
Q

What is the pathology of EAA?

What type of sensitivity is it?

A

Allergens comes in

Irritates alveoli and activates neutrophils

Releases inflammatory cytokines

Cascade leads to B cell antibody prodction

Complexes form

TYPE 3

101
Q

What are the two types of EEA?

A

Acute (few hours after only inflammation)

Chronic (fibrosis)

102
Q

What is seen in chronic that is not seen in acute EAA?

A

Granulomas

Non-caseating

Macrophages fuse with eachother making granulomas

103
Q

What are the symptoms of extrinsic allergic alveolitis?

A

Acute
Fever
Rigors
Myalgia
Dyspnoea
Crackles (no wheeze).

Chronic
Increasing dyspnoea
Weight decrease
Exertional dyspnoea
Type I respiratory failure
Cor pulmonale.

104
Q

What are the tests for extrinsic allergic alveolitis?

A

CXR
Upper-zone mottling/consolidation

Honeycombing sometimes

Blood
FBC (neutrophilia); ESR increase; ABGS; positive serum precipitins (indicate exposure only).

Lung function tests
Restrictive defect; reduced gas transfer during acute attacks.

105
Q

What are the management options for extrinsic alergic alveolitis?

A

Remove allergen

O2

Oral prednisolone

106
Q

What is the difference between asthma and EAA?

A

Asthma
Obstructive
Larger airways
Type 1 allergic

EAA
Restrictive
Smaller airways
Type 3 and 4 allergic

107
Q

WHAT IS SARCOIDOSIS?

https://www.youtube.com/watch?v=D-ahTqbqnqE

A

Granulomatous disease affecting mainly the lungs, but also lymph nodes in a greater frequency.

108
Q

What type of granuloma is sarcoidosis?

A

Non-ceasiating granulomatous disease

109
Q

What is the epidemology of sarcoidosis?

A

African-americans

Women more than men

Under 40 years of age

Non smokers

110
Q

What is the cause of sarcoidsis?

What cells are disregulated?

A

Unknown

Disregulation of CD4 cells

111
Q

What happens when an uknown antigen comes into the body in sarcoidosis?

A

Unknown cell comes in

Picked up by macrophages

Takes to lymph node

CD4 cell gets antigen preseted

Proliferation of CD4 cells occur

Macrophages get activated and clump together

112
Q

What are the pulmonary symptoms of sarcoidosis?

A

4 D’s!

113
Q

What are the non-pulmonary symptoms of sarcoidosis?

A

Skin – erythema nodosum

Arthritis - esp. of feet, hands

Respiratory - pulmonary infiltrates

Cardiac– heart block, VT, heart failure

Ocular– anterior uveitis, can lead to blindness

Intracranial (brain) – chronic meningitis, seizures, neuropathy

Derangement of liver and renal function – hepatic granuloma (70% patients), hypercalcaemia(

114
Q

What are the tests for sarcoidosis?

A

Tissue biopsy
Diagnostic non-caseating granulomatas

X-ray
Enlarged lymph nodes

24h urine
Ca2+ increase.

Blood
Increased ESR, lymphopenia, LFT incerease,
Serum ACE increase
Increased Ca2+

115
Q

What is the management of sarcoidosis?

A

Nothing usually

Corticosteroids
Prednisolone PO

116
Q

WHAT IS IDIOPATHIC PULMONARY FIBROSIS?

A

Uknown excess amount of collagen in the lungs connective tissue and interstitial tissue after damage

117
Q

What is the cause of IPF?

A

Uknown

118
Q

What are the risk factors for IPF?

A

Old age

Smoking

Male

119
Q

What are the different alveolar epithelial cells?

A

Type 1 and type 2 pneumocytes.

120
Q

What happens when the alveoli lining is damaged in IPF?

A

Causes them to release transforming growth factor beta 1

Type 2 pneumocytes stimualte fibroblasts to turn into myofibroblasts

Myofibroblasts secrete reticular fibres and elastin fibres

Type of collagen with structural stregnth
Provide elasticity to lungs

Myofibroblasts then apoptose

121
Q

What is the pathology of IPF?

A

Type 2 pneumocytes overproliferate

Too many myofibroblasts and too much collagen

No apoptosis

Even more collagen

Collagen accumulation

Thicker interstital

Problems with ventilation and oxygenation

122
Q

What type of lung disease is IPF?

A

Restrictive

Interstitial lung disease

123
Q

What happens with fluid in IPF?

A

Loss of alveoli and start pooling fluid

Seen as honeycombing

124
Q

What are the symptoms of IPF?

A

4 D’s!

Dry cough

Digital clubbing

Dyspnoea

Diffuse inspiatory crackles

125
Q

What are the tests for IPF?

A

CXR
Thickening of alveoli walls
Honeycomb lung

_Spirometry
_Restrictive; decrease transfer factor.

Blood
ABG decrease in oxygen, increase in CO2
CRP increase; immunoglobulins increase;
ANA (30% +ve), rheumatoid factor (10% +ve).

BAL (Bronchoalveolar lavage)

126
Q

What are the management options for idiopathic pulmonary fibrosis?

A

Supportive care
Oxygen, pulmonary rehabilitation, opiates, palliative care input

Antifibrotic medications
Pirfenidone and nintedanib

Lung transplant

127
Q

WHAT ARE THE TWO TYPES OF LUNG TUMOUR?

A

Bronchial.

Pleural.

128
Q

What are the different types of bronchial cancers?

A

Malignant (95%) = lung cancer
non small cell cancer
small cell cancer

Benign
hamartoma
carcinoid
lipoma

129
Q

What are the causes of lung cancer?

A

Smoking

Asbestos

Chromium

Arsenic

130
Q

What are the cell types of lung cancer?

A

Small cell lung cancer 15%

Non small cell lung cancer 85%
Squamous
Adenocarcinoma (adenocarcinoma-in situe)
Large cell 5%
NOS

131
Q

What are the symptoms of local lung cancer?

A

Cough (40%)

Chest pain (20%)

Haemoptysis (7%)

132
Q

What are the signs of lung cancer?

A

Weight loss

Anaemia

Clubbing

Supraclavicular or axillary nodes

133
Q

What are the investigations for lung cancer?

A

CXR

Chest CT

Bronchoscopy

Needle or surgical biopsy

134
Q

What are the sites of metastatic disease from lung cancer?

BBALL

A

Bone

Brain

Adrenal glands

Lymph glands

Liver

135
Q

What is the treatment of lung cancers?

A

Stage I/II
surgical excision and radical deep x-ray therapy

Stage III/IV
Palliative chemotherapy, chemotherapy and radiotherapy, palliative care

136
Q

WHAT IS MESOTHELIOMA?

https://www.youtube.com/watch?v=MMmjTbywMSI

A

Tumour of mesothelial cells in the pleura

137
Q

What is the pathology of mesothelioma?

A

Epithelioid (Activated macrophages resembling epithelial cells)

Sarcomatoid (Sarcomatous, spindled or diffuse malignant fibrous mesothelioma)

Inflammation

DNA damage

138
Q

What are the symptoms of mesothelioma?

A

FEVER

WEIGHT LOSS

FATIGUE

SOB

Persistent cough

Clubbed fingers

139
Q

What are the tests for mesotheiomas?

A

CXR
Pleural thickening/effusion. Bloody pleural fluid

CT scan

Pleural aspiration

Biopsy

140
Q

What is the treatment for mesotheliomas?

A

Symptom control

Palliative chemotherapy (Pemetrexed + cisplatin)

Radical surgery/debulking surgery

Palliative radiotherapy

141
Q

What is type 1 respiratory failure? What is the cause?

A

Type 1: Low PaO2, normal (or low) paCO2, normal or high A-a gradient.

Limited of ventilation, perfusion or diffusion.

142
Q

What is type 2 respiratory failure? What is the cause?

A

Type 2: low paO2, high CO2, usually normal A-a gradient (acute or chronic).

Alveolar hypoventilation.
CO2 enters alveoli, but not removed.

143
Q

WHAT IS PNEUMONIA?

A

An infection in the lungs by microbes

Brings water into lung making it harder to breath

144
Q

Who are the people at risk of pneumonia?

A

Infants and the elderly.

COPD and certain other chronic lung diseases.

Immunocompromised.

Nursing home residents.

Diabetes.

Alcoholics and intravenous drug users.

145
Q

How can pneumonia be classified?

A

Bronchopneumonia
Throughout lung

Atypical
Interstatium

Lobar

146
Q

What are the common microbes that cause pneumonia?

A

Viruses
Influenza

Bacteria
Strep pneumoniae

Staph aureus

Legionella’s (hot country, air conditioning)

Jirovecci (HIV patients)

147
Q

What is the pathogenesis of pneumonia?

A

Bacteria multiplies in the lungs, causes the lungs to become inflamed

Body releases chemicals to try and destroy the bacteria that cause inflammation

148
Q

What are the symptoms of pneumonia?

A

Fever

Rigors

Fatigue

Pleuritic chest pain

SOB

Headache

Cough with sputum (rusty green)

149
Q

What are the signs of pneumonia?

A

Pyrexia

Cyanosis

Tachypnoea

Drop in BP

SPUTUM

Confusion(esp. elderly)

150
Q

How can you investigate if somebody has suspected pneumonia?

A

Listen to the chest

Gold standard
CXR
Consolidation.

Determine the causative organism

Sputum sample and blood culture

Urinary antigen test –Legionellas

Thoracentesis

151
Q

How do you manage pneumonia?

A

Antibiotics for CAP:

Mild: oral amoxicillin

Moderate: oral amxoicillinand clarithromycin

Severe: IV co-amoxiclavand clarithromycin

Antibiotics for Legionellas:

Fluoroquinolone (ciprofloxacin) + clarithromycin

152
Q

What is CURB-65?

A

Confused

Urea >7

Resp rate >30

Blood pressure 90/60

Over 65

153
Q

WHAT IS ASTHMA?

A

REVERSIBLE chronic obstructive airway disease

154
Q

What are the two main types of asthma?

A

Eosinophilic.
Associated with allergy.
Also non-allergic variant.

Non-eosinophilic.

155
Q

What is asthma if not eosinophilic?

A

Overlaps with smoking and obesity.

156
Q

What is often the cause of asthma?

A

Allergic
Genetics, environmental stimuli, hygiene hypothesis

Non-allergic
Intrinsic e.g. stress, cold air, infection

157
Q

What is atopy?

A

Asthma

Hayever

Eczema

158
Q

What happens when allergens from environment come into the body in asthma?

A

Dendritic cells present them to TH2 cells

Produce cytokines

IL4 (production of IGE, coat mast cells and release histamine)

and 5 (Eosinophils, Release more cytokines and leukotrienes)

159
Q

What type of hypersensitivity is asthma?

A

Type 1 as it involves IgE

160
Q

What happens in the airways of asthma?

A

Smooth muscle spasm

Increased mucus secretion

Airway inflammation

161
Q

What are the symptoms of asthma?

A

Chest tightness

Coughing

Wheezing

Dyspnea

Sputum

162
Q

What are the tests for asthma?

A

Spirometry
FEV1/FVC<70% + Reversibility testing

Peak flow
(keep a diary –diurnal variation)

163
Q

What are the differential diagnosis for asthma?

A

Bronchiectasis

CF

PE

Bronchial obstruction - foreign body, tumour, etc

Aspiration

COPD

164
Q

What are the steps of treatment for chronic asthma?

A

Step 1
SABA (salbutamol)
Step 2
Beclametasone
Step 3
LABA (salmeterol) + Beclometasone
Step 4
Prednisolone

165
Q

What is the treatment for an acute asthmatic?

A

Oxygen with nebulised SABA (salbutamol)

100mg hydrocortisone IV or 40-50mg prednisolone PO

166
Q

WHAT IS TUBERCULOSIS CAUSED BY?

What is this bacteria?

A

Mycobacterium Tuberculosis

Which is an AEROBIC, NON-MOTILE SLIGHTLY CURVED ROD

167
Q

What are the risk factors for TB?

A

Born in high prevalence area

IVDU Homeless

Alcoholic

Prisons

HIV+.

168
Q

How is TB spread?

A

AIRBORNE DROPLETS

169
Q

What are the different types of TB?

A

Healthy
Person has never been infected with TB

Active TB
This is when the bacterium are multiplying in the lungs and people have symptoms

Latent
The TB bacteria are NOT dividing in the lungs. Individual asymptomatic.

170
Q

Where do the bacteria normally colonise in the lung?

A

Apex

171
Q

What are the symptoms of TB?

A

Fever

Night sweats

Chills

Chest pain

172
Q

What are the signs of TB?

A

Coughing up BLOOD

Individual will look unwell

173
Q

How can you diagnose TB?

A

Sputum test (3x)
Used to detect acid fast organisms

Mantoux skin test
Latent TB

CXR
Enlarged lymph nodes
GOHN COMPLEX

CT scan

Ziehl–Neelsen stain

174
Q

What is the treatment for active TB?

A

Rifampicin. 6 months

Isoniazid. 6 months

Pyrazinamide 2 months

Ethambutol. 2 months

175
Q

What are some side effects of RIPE?

A

Rifampicin
Red urine, hepatitis, drug interactions.

Isoniazid
Hepatitis, neuropathy

Pyranzidimide
Hepatitis, arthralgia / gout, rash.

Ethanbutol
Optic neuritis

176
Q

WHAT IS PNEUMOTHORAX?

A

Build up of AIR in the pleural space

Sudden onset, sharp, one sided pleuritic chest pain and SOB

177
Q

What are the causes of a pneumothorax?

A

Primary
No underlying lung disease, but risk factors include
MALE, SMOKING, FAMILY HISTORY, CONNECTIVE TISSUE DISEASE (Marfans, Ehlers Danlos).

Secondary
Underlying lung pathology that has caused it.

E.g. Trauma, fractured ribs, stab wound, gunshot, catheter, biopsy

178
Q

What are the symptoms of a pneumothorax?

A

SOB

Sharp

ONE SIDED chest pain

Altered consciousness

179
Q

What are the signs of a pneumothorax?

A

Low blood pressure

Low oxygen levels

Diminished breath sounds on the affected side

180
Q

What are the tests for a pneumothorax?

A

CXR
BLACK

181
Q

What are the management options for a pneumothorax?

A

Heal spontaneously

Treat the underlying cause, e.g. close the hole if there is an open wound causing it

Chest drain

Surgery

182
Q

What is the emergency pneumothroax?

A

Tension pneumothorax

Thrachea deviation

183
Q

How do you treat a tension pneumothorax?

A

Chest drain 2nd intercostal space

184
Q

WHAT IS A PLEURAL EFFUSION?

What type of fluid can be there?

A

Fluid in the pleural space

Chyle, blood, serous, pus.

185
Q

How can pleural effusions be divided?

A

Transudates
Excessive production of pleural fluid or resorption is reduced. E.g. heart failure, cirrhosis, nephrotic syndrome

Exudates
Result from damaged pleura. E.g. PE, bacterial pneumonia, cancer, viral infection, pancreatitis

186
Q

What are the different names for blood in pleural splace etc?

A

Blood in the pleural space is a haemothorax, pus in the pleural space is an empyema, and chyle (lymph with fat) is a chylothorax.

Both blood and air in the pleural space is called a haemopneumothorax.

187
Q

What are the symptoms of a pleural effusion?

A

SOB

Cough

Chest pain

188
Q

What are the signs of a pleural effusion?

A

Decreased chest movement

Reduced breath sounds

Dull to percussion

189
Q

What are the tests for a pleural effusion?

A

CXR
white (fluid),

Listen to the chest
Dull to percussion
Reduced breath sounds

Thoracocentesis

190
Q

What are the management options for a pleural effusion?

A

Aspirate / chest drain

Pleurodesis

191
Q

WHAT IS A PULMONARY EMBOLISM?

Where is it most commonly from?

A

Clot inside a pulmonary vessel

a DVT

192
Q

What are the risk factors for a pulmonary embolism?

A

Immobility - >3 days, surgery within last 4 weeks

Previous DVT/ PE

Pregnancy

Thrombophilic syndromes

Malignancy

Hormone Therapy

193
Q

What are the symptoms of a pulmonary embolism?

A

Sudden onset dyspnoea

Chest pain

Red, swollen leg ?

Haemoptysis

Pre-syncope, syncope

Tachycardia

194
Q

What are the signs of a pulmonary embolism?

A

Pyrecia

Cyanosis

Tachycardia

Tachypnoea

Hypertension

Raised jvp

195
Q

What is Well’s score?

What do the results show?

A

Clinical signs of PE/ DVT– 3

PE most likely diagnosis – 3

Tachycardic>100 – 1.5

Immobility (>3/7, surgery in last 4/52) – 1.5

Previous PE/ DVT– 1.5

Haemoptysis – 1

Malignancy +/- treated in last 6 months – 1

<2 – PE unlikely

2-6 – moderate possiblity– do a D-Dimer

6+ - CTPA

196
Q

What are the tests for a PE?

A

D-dimer – negative excludes PE but positive doe not prove it

If positive, need to do CT

197
Q

What is the management of a PE?

A

Oxygen

Analgesia

Anticoagulation – LMWH, Fondoparinux

Start Warfarin – long term anticoagulation (Rivaroxaban is a suitable alternative)

Embelecetomy if large PE

198
Q

WHAT IS GOODPASTURE’S SYNDROME?

A

Acute glomerulonephritis (blood in urine)

+ lung symptoms (haemoptysis/diffuse pulmonary haemorrhage)

199
Q

What is goodpasture’s syndrome caused by?

A

Antibodies form against type IV collagen

200
Q

What type of sensitivty reaction is goodpastures syndrome?

A

Type 2

201
Q

What are the environmental risk factors for goodpatures syndrome?

A

Smoking

Infection

Oxidative stress

202
Q

What are the symptoms for goodpasture’s syndrome?

A

Haemoptysis
SOB, chest pain, cough,

Haematuria
Proteinuria, oedema, uraemia, high bp

203
Q

What are the tests for goodpasture’s syndrome?

A

CXR
Infiltrates due to pulmonary haemorrhage, often in lower zones.

Kidney biopsy
Crescentic glomerulonephritis.

204
Q

What are the treatment options for goodpasture’s syndrome?

A

Treat shock

Immunosuppressive
Cyclophosphamide, prednisolone, rituximab

Plasmapheresis

205
Q

WHAT IS WEGENER’S GRANULOMATOSIS?

https://www.youtube.com/watch?v=Ax98k35h_jk

A

Small vessel vasculitis with caseating granulomas

206
Q

What type of sensitivity is wegners?

A

Type 4

207
Q

What parts of the body are affected in wegners?

A

Nasal passage

Respiratory tract

Kidneys

208
Q

What are the features of wegener’s granulomatosis?

A

Kidneys
RPGN with crescent cells

Lung
Migrating cavitatingcoin nodules, haemoptysis, pulmonary infiltrates

URT
Saddle nose deformity, epistaxis

Eyes
Iritis, scleritis, episcleritis

Arthritis

Elbow nodules

209
Q

What antibodies are involved in wegners?

A

cANCAs

210
Q

What are the tests for Wegener’s granulomatosis?

A

cANCA
Raised

Urinalysis
Proteinuria or haematuria.

Biopsy of kidneys
Granulomas

CXR
Nodules ± fluffy infiltrates of pulmonary haemorrhage.

Increased ESR/CRP.

211
Q

What is the treatment for wegener’s granulomatosis?

A

Corticosteroids

Cyclophosphamide
Inhibit immune system

212
Q

WHAT IS PULMONARY HYPERTENSION?

https://www.youtube.com/watch?v=Dx4QgdN_hI4

A

Mean arterial blood pressure greater than 25 mmhg

213
Q

What are the causes of pulmonary hypertension?

A

Pre-capillary
Multiple small PEs cause obliteration of vascular bed
Left-to-right shunts cause increased pulmonary blood flow and pressure

Capillary
Disease of pulmonary vascular bed
Eg emphysema, COPD

Post-capillary
Backlog of blood causes secondary pulmonary hypertension
LV failure

Chronic hypoxaemia
Living at high altitude
COPD

214
Q

What are the symptoms of pulmonary hypertension?

A

Fatigue, pre-syncope

Tachycardia

Raised JVP

Altered heart sounds (louder S2)

Peripheral oedema – sacral, ankle

215
Q

What is the diagnosis of pulmonary hypertension?

A

ECG
Increase pressure in pulmonary articles and right venticle

Spirometry
Chronic lung disease sometimes

216
Q

What is the treatment for pulmonary hypertension?

A

Oxygen

Cardiogenic
Increase heart performance or decreease blood pressure

Phosphodiesterase-5 inhibitor
Viagra (sildeafil)

Prostacyclin analogue
Apoprostenol

217
Q

WHAT IS CYSTIC FIBROSIS?

https://www.youtube.com/watch?v=BhFpFiZumS0

A

Excessive mucus build up in lungs and pancreas

218
Q

What causes cystic fibrosis?

A

Autosomal recessive

CF transmembrane conductance regulator (CFTR) gene

Chromosome 7

DeltaF508

219
Q

What is the pathophysiology of cystic fibrosis?

A

Defect in chlorine channel

Chlorine can therefore not be transported into the lumen.

Water does not move out by osmosis, making the mucus thick and sticky, clogging up the lumen.

Na+ also moves into the cells via an electrochemical gradient (Cl- is negative, Na+ is positive), which also draws water in with it and makes the mucus even more thick and sticky.

220
Q

What can happen in newborns for cystic fibrosis?

A

Meconium - first stool

Can get stuck in intestine

Meconium ileus

221
Q

How is pancreatic insufficiency caused in cystic fibrosis?

A

Thick secretions block the duct

No enzymes into intestine

Protein and fat not absorbed

Failure to thrive

Steatorrhoea

Pancreas damaged due to backup of enzymes

Localised inflammation - pancreastitis

222
Q

What are the symptoms for cystic fibrosis?

A

Heavy mucus production, cough

223
Q

What are the signs for cystic fibrosis?

A

Steatorrhea

Children with a failure to thrive

Finger clubbing

Rectal prolapse

224
Q

What tests are done for cystic fibrosis?

A

90% diagnosed before the age of 8.

FAECAL ELASTASE

Sweat (NaCl) test
Parents taste salt when kissing baby

Genetics testing
DeltaF508

225
Q

What are the management options for cystic fibrosis?

A

NO CURE, therefore symptom management

Non-pharmalogical
Physio for airway clearance

Pharmalogical
Antibiotics, anti-mucinolytics, bronchodilators, enzymes, insulin, bisphosphonates

Surgery
Lung transplant

226
Q

What are the complications of CF?

A

INFERTILITY

Pancreatitis

RESP TRACT INFECTIONS

Bronchiectasis