obstructive diseases 1

Question 1

consolidation

Answer 1

fluid or cells in alveoli
lung is more solid
lungs are more white in X-ray
transmit sound and vibration easily

Question 2

major respiratory tract causes of morbidity and mortality

Answer 2

respiratory tract infections
lung cancer
chronic airway diseases
asthma

Question 3

smoking

Answer 3

1 in 5 deaths 
atherosclerotic cardiovascular disease 
COPD
increases the risk of tuberculosis 
worsens asthma 
low birth weight babies 
lung cancer 
mesothelioma

Question 4

lung cancer

Answer 4

the most common cancer
mortality decreasing
incidence increasing

Question 5

if lung tissue becomes stiffer

Answer 5

loss of compliance

inflating and deflating becomes harder

Question 6

If thorax is opened

Answer 6

pneumothorax - negative pressure space equalises with the atmosphere

Question 7

if bronchial tree is narrowed/damaged

Answer 7

it is harder to get air in and out

Question 8

hyperinflation

Answer 8

air that doesn’t get out

Question 9

obstructive diseases

Answer 9

airway diseases

increase to resistance to airflow due to partial or complete obstruction

Question 10

restrictive diseases

Answer 10

parenchymal diseases

reduced expansion of lung parenchyma, often loss of gas transfer surface area, decreased total lung capacity

Question 11

obstructive analogy

Answer 11

pinch the neck of the balloon

Question 12

restrictive analogy

Answer 12

grip the sides of the balloon

Question 13

obstructive effects

Answer 13

v decreased FEV1
decreased/normal FVC
decreased FEV1/FVC
increased TLC
increased residual volume

Question 14

restrictive effects

Answer 14

increased FEV1
decreased FVC
increased FEV1/FVC
decreased TLC 
decreased residual volume

Question 15

dyspnoea

Answer 15

difficult or laboured breathing
shortness of breath
symptom not a sign

Question 16

wheeze

Answer 16

high pitched, polyphonic sound produced predominantly in expiration by airways of any size

Question 17

stridor

Answer 17

single high pitch

upper airway, inspiratory, usually laryngeal

Question 18

stertor

Answer 18

low pitch, upper airway, nasal back of throat

eg. snoring

Question 19

chronic bronchitis

Answer 19

mucous gland hypertrophy and hyperplasia, hypersection
caused by tobacco smoke and air pollutants
causes cough and sputum production

Question 20

bronchiectasis

Answer 20

airway dilation and scarring
caused by persistent and severe infections
causes cough, purulent sputum, fever

Question 21

asthma

Answer 21

smooth muscle hypertrophy and hyperplasia, excessive mucous and inflammation
immunologic or undefined causes, often triggered by air pollutants
causes episodic wheezing, cough and dyspnoea

Question 22

three clinical entities in the bronchus

Answer 22

asthma
chronic bronchitis
bronchiectasis

Question 23

emphysema

Answer 23

in the acinus/alveoli
air space enlargement and wall destruction
caused by tobacco smoke
causes dyspnoea

Question 24

bronchiolitis - small airway disease

Answer 24

in the bronchioles
inflammatory scarring, partial obliteration of bronchioles
caused by tobacco smoke, air pollutants
causes cough and dyspnoea

Question 25

COPD

Answer 25

chronic obstructive pulmonary disease
spectrum between chronic bronchitis and emphysema
mixed features of both
isolated emphysema and pure chronic bronchitis are both relatively uncommon - most patients have a combination of both

Question 26

2 groups of asthma

Answer 26

extrinsic and intrinsic

Question 27

four subtypes of asthma

Answer 27

atopic
drug induced
occupational
non atopic

Question 28

atopic asthma

Answer 28

type 1 IgE mediated hypersensitivity reaction
childhood, string family history, associated with allergic rhinitis
triggered by allergens
positive skin tests

Question 29

drug induced asthma

Answer 29

aspirin and other drugs

Question 30

occupational asthma

Answer 30

fumes - plastics, epoxy resins
organic and chemical dusts
gases and other chemicals
usually requires repeatd exposure

Question 31

intrinsic asthma

Answer 31

non atopic
no evidence of allergen sensitisation
negative skin test
don’t always have family history

Question 32

asthma clinical presentation

Answer 32

dyspnoea with wheezing
lasts for several hours or more
subsides naturally with response to bronchodilators

Question 33

status asthmaticus

Answer 33

failure to subside for days to weeks

possibly caused respiratory failure or death

Question 34

pathogenesis of asthma

Answer 34

atopic

excesive type 2 helper T cells

Question 35

cytokine production of type 2 helper T cells

Answer 35

produce cytokines

• IL-5 activates eosinophils
• IL-13 stimulates mucus production
• IL-4 and IL-3 stimulate IgE production which causes mast cells to degranulate

Question 36

asthma reaction

Answer 36

early phase - bronchoconstriction, histamine, prostaglandin D2 and leukotrienes, increased mucus, vasodilation
late phase reaction - inflammatory mediators stimulate epithelial cells to produce chemokine, recruit Th2 cells and eosinophils which amplifies the inflammatory response

Question 37

repeated bouts of asthma lead to

Answer 37

airway remodelling
smooth muscle hypertrophy, mucus gland hypertrophy and increased collagen deposition
often occurs before the patient presents with symptoms
re exposure to pre sensitised antigen is the trigger

Question 38

asthma histologically

Answer 38

mucus plugging of bronchi
focal necrosis of epithelium with eosinophilic inflammation and oedema of bronchial walls - triggered by excessive inflammation
thickening of epithelial basement membrane
hypertrophy of bronchial mucous glands
hypertrophy of smooth musclee of the bronchial wall

Question 39

emphysema description

Answer 39

abnormal parmanent enlargement of the airspaces distal to terminal bronchiole
destruction of walls, without interstitial firbrosis
trapping of air in dilated airspaces and loss of elastic recoil due to damage of parenchyma