3. Respiratory diseases

Question 1

Inhalation

Answer 1

diaphragm contracts (moves down)
rib cage expands as rib muscles contract

Question 2

exhalation

Answer 2

diaphragm relaxes (moves up)
rib cage gets smaller as rib muscles relax

Question 3

perfusion matching

Answer 3

Ventilation rate V/perfusion Q
V/Q = 1 for ideal

to ensure continuous delivery of oxygen and removal of carbon dioxide from the body

Question 4

atopy

Answer 4

Atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema). Atopy is typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.

Question 5

asthma definition

Answer 5

chronic inflammatory disorder of the airways characterised by bronchial wall hyper-reactivity and airway obstruction which is reversible

Question 6

asthma risk factors

Answer 6

family history, prematurity, tobacco smoke exposure, obesity, exposure to allergens

Question 7

extrinsic or atopic asthma

Answer 7

known external cause
airway inflammation due to allergen exposure

Question 8

rhinitis

Answer 8

nasal blocking

Question 9

intrinsic or non atopic asthma

Answer 9

no cause identified
not due to allergen exposure

Question 10

difference in pathophysiology of asthma for asthmatic airway

Answer 10

more goblet cells
more mast cells, which release histomines
more immune cells… neutrophils, CD4 T helper cells
eosinophils (promote airway inflammation)
thicker bronchial wall (narrower airways)

Question 11

pathophysiology of asthma (role of IGE)

Answer 11

plasma cells release IGE (marker for atropy)
IGE binds to mast cells (IGE primed mast cells)
mast cells degranulate to release histamines, cytokines …
airway inflammation
bronchoconstriction

Question 12

asthma is characterised by 3 main features… (pathophysiology)

Answer 12

airflow limitation: usually reversible

airway hyper-responsiveness: to an inhaled antigen or other

airway inflammation: infiltration of airways by immune cells

Question 13

intrinsic asthma triggers

Answer 13

emotion, viral infections, atmospheric pollution and irritants, smoking, drugs

avoid beta blockers, NSAIDS (aspirin) - these trigger asthma

Question 14

diagnosing airway obstruction

Answer 14

wheeze, breathlessness, chest tightness

Question 15

spirometry

Answer 15

gold standard test
assesses lung function by measuring the volume of air that the patient is able to expel from the lungs after maximal inspiration
differentiates between obstructive airways disorders and restrictive diseases
monitors severity

Question 16

spirometry key measures

Answer 16

FEV1: volume of air forcibly exhaled after deep inspiration in 1 s
FVC: total vol of air forcibly exhaled in 1 breath
FEV1 and FVC based on age, gender, height
normal ranges FEV1: >80% predicted
FVC: >80% predicted
FEV1/FVC ratio: >0.7

Question 17

corticosteroids

Answer 17

(eg inhaler)
bind to intracellular glucocorticoid receptors within bronchial smooth muscle cells to form receptor complexes. these complexes interfere in gene transcription, inhibiting formation of PLA2, resulting in decreased prostaglandin and leukotriene formation -> decreased inflammation

side effects: osteoporosis, dysphonia (voice disorder), oral candida, hyperglycaemia
eg. beclometasone, budenoside, fluicasone, prednisolone

Question 18

leukotriene receptor antagonists

Answer 18

bind to leukotriene receptors on mast cells, eosinophils and alveolar macrophages, preventing leukotrienes from binding, resulting in reduced bronchoconstriction, reduced cytokine release, and overall reduced airway oedema.
side effects: headaches, GI disturbance
eg. montelukast

Question 19

monoclonal antibody therapies

Answer 19

bind to IL-5, preventing this from binding to eosinophils, reducing inflammation and subsequent cytokine release
side effects: abdominal pain, fever, headache, hypersensitivity
eg. mepolizumab, benralizumab

Question 20

beta-2-agonists

Answer 20

bind to beta-2-receptors on bronchial smooth muscle, resulting in activation of adenylyl cyclase and generation of cAMP. This activates PKA leading to bronchial smooth muscle relaxation via potentiation of the SNS.
side effects: fine tremor, palpitations, arrhythmia, hypokalaemia
eg. salbutamol, formoterol, tertubuline

Question 21

muscarinic antagonists

Answer 21

bind to M2 receptors on bronchial smooth muscle, preventing Ach from binding. this minimises activation of the PNS, resulting in reduced bronchoconstriction.
side effects: dry mouth/eyes
eg. ipratropium bromide, tiotropium bromide

Question 22

theophyllines

Answer 22

inhibit phosphodiesterase enzyme which normally breaks cAMP to AMP. this means more cAMP remains within bronchial smooth muscle and can go on to activate PKA and induce bronchial smooth muscle relaxation (potentiating SNS)
side effects: arrhythmia, GI disturbances, seizures, hypokalaemia
eg. aminophylline, theophylline

Question 23

COPD chronic obstructive pulmonary disease definition

Answer 23

an obstructive airway disease
commonly the result of chronic bronchitis and emphysema
characterised by airflow limitation

Question 24

chronic bronchitis

Answer 24

productive cough for more than 3 months each year for 2 or more consecutive years

Question 25

emphysema

Answer 25

(lung condition causing shortness of breath) destruction of the alveolar wall with dilation of the airspaces

Question 26

risk factors of COPD

Answer 26

cigarette smoking, chemical dusts (eg. coal dusts), exposure to atmospheric pollution including biofuels, low birth weight and genetic causes including alpha-1-antitrypsin deficiency

Question 27

pathophysiology of COPD 1 (cilia)

Answer 27

damaged cilia increased mucus extra goblet cells inhaled toxins, repeated exposure leads to airway inflammation goblet cell hypertrophy increased mucus overwhelms cilia damaged cilia airway wall fibrosis (walls permanently scarred, irreversible)

Question 28

pathophysiology of COPD 2 (alveoli)

Answer 28

antiproteases protect elastic fibres neutrophils predominant -> secretes proteases alveolar macrophages -> secretes proteases the increase in proteases breaks elastic fibres alveoli destroyed further recruitment of immune cells

Question 29

COPD effect on V/Q

Answer 29

abnormal V/Q resulting in a respiratory acidosis ( a condition that occurs when your lungs can't remove all of the carbon dioxide produced by your body. This causes the blood and other body fluids to become too acidic. ) ie. low O2 and high CO2

Question 30

diagnosing copd: emphysema & destruction of alveolar walls and elastic fibres

Answer 30

air trapping ie. anatomical dead space (trapped air in alveoli) abnormal V/Q breathlessness, hyperinflation ie. barrel chest muscle wasting

Question 31

diagnosing copd: chronic bronchitis & airway wall inflammation and mucus hypersecretion

Answer 31

airway obstruction wheeze, productive cough and chest tightness

Question 32

spirometry for copd

Answer 32

in copd we see an obstructive pattern of lung disease with no clinically significant degree of reversibility ie. improvement FEV1/FVC ratio spirometry by <15% after administration of bronchodilators

Question 33

pharmacological management in copd: airway obstruction

Answer 33

beta agonists muscarinic antagonists theophyllines

Question 34

pharmacological management in copd: airway inflammation

Answer 34

corticosteroids

Question 35

CAT measurement

Answer 35

CAT symptom score a COPD assessment test higher score is worse >10

Question 36

non pharmacological management in copd

Answer 36

smoking cessation and nicotine replacement therapy pulmonary rehabilitation long term oxygen therapy non-invasive ventilation occasionally lung surgery

Question 37

Cor Pulmonale and pulmonary hypertension

Answer 37

complications of copd structural alteration and dysfunction of the right ventricle due to lung disease can be acute/chronic occurs due to increased right ventricular filling pressures from longterm pulmonary hypertension ie a pulmonary arterial pressure of >20mmHg

Question 38

pathophysiology of cor pulmonale

Answer 38

copd and other lung diseases damages lungs low oxygen or hypoxia leads to hypoxic pulmonary vasoconstriction, which limits blood flow to hypoxic alveoli vascular remodelling: neomuscularisation of arterioles, intimal thickening and medial hypertrophy increased pulmonary arterial pressure (mean above 20mmHg) increased right ventricular afterload leading to RV dysfunction and failure

Question 39

diagnosis of cor pulmonale

Answer 39

based on ECHO (RV enlargement w triscuspid valve regurgitation) CXR (chest xray) (cardiomegaly = enlarged heart), sign consistent with copd, chunky pulmonary vessels) V/Q scan (to rule out other causes of pulmonary hypertension) Right heart catheterisation findings (pulmonary artery pressure of >20mmHg)

Question 40

managing cor pulmonale

Answer 40

optimising copd treatment and long term oxygen therapy heart-lung transplants considered in certain cases

Question 41

differences between asthma and copd

Answer 41

asthma young, copd old age >35 asthma dry cough, copd productive cough asthma reversibility of airway obstruction copd typically in smokers

Question 42

pneumonia

Answer 42

a type of lower respiratory tract infection, characterised by inflammation of lung tissue due to bacterial, viral, fungal lung infection most affected are >75y/o 16% pneumonia patients die in hospital or within 30 days of discharge once discharged, 1 in 3 will be back in hospital within 30 days

Question 43

risk factors for pneumonia

Answer 43

smoking, underlying lung disease, being immunocompromised, being malnourished and other underlying cardiovascular disease

Question 44

community acquired pneumonia 'CAP'

Answer 44

pneunomia acquired outside the hospital or healthcare facilities typically caused by bacteria or biruses eg. streptococcus penumoniae, haemophilus influenza eg. influenza or RSV fungal rare pneumocystis carinii and aspergillosis

Question 45

hospital acquired pneumonia

Answer 45

pneumonia that occurs 48h or more after hospital admission typically bacteria streptococcus pneumoniae, MRSA

Question 46

aspiration pneumonia

Answer 46

due to aspiration of gut anaerobes/GI contents into lower respiratory tract risk factors: anything that might impair a safe swallow alcohol/drug intoxication, general anaesthesia, loss of consciousness, swallowing disorders, structural abnormalities of pharynx and oesophagus

Question 47

pathophysiology of bacterial pneumonia

Answer 47

inhaled bacteria uncontrollably replicate colonises alveoli initiates immune response vasodilation of pulmonary capillaries increased vascular permeability leaky recruits neutrophils neutrophils in alveoli through leaky wall backflow into other alveoli

Question 48

pathophysiology of viral pneumonia

Answer 48

inhaled virus enters alveolar epithelial cells replicates same as bacteria but lymphocytes not neutrophils

Question 49

diagnosing pneumonia: alveolar congestion w inflammatory exudate/pus:

Answer 49

chest pain, productive cough, breathlessness reduced air entry bronchial breathing dull to percussion coarse crackles (mucus at bottom of lungs)

Question 50

diagnosing pneumonia: cytokines entering systemic circulation

Answer 50

fever/rigors, fatigue/malaise, confusion hypotension tachypnoea altered mental state

Question 51

diagnosing pneumonia: airway inflammation

Answer 51

wheeze, breathlessness, chest pain respiratory distress hypoxia

Question 52

investigating suspected pneumonia

Answer 52

blood tests and cultures sputum culture urine test for s. pneumoniae and legionella spp imaging, chest xray PCR

Question 53

Pneumonia: CURB-65 scoring system

Answer 53

1 point for each feature: confusion, respiratory rate >30bpm blood pressure <90mmHg / <60 age >65 y/o 3 or more is high severity

Question 54

treating pneumonia

Answer 54

antibiotic therapy: CURB-65 score 0/1: amoxicillin 500mg TDS PO for 5 days score 2: amoxicillin 1g TDS PO + consider doxycycline PO score >3: Co-amoxiclav 1.2g TDS IV + Clarithromycin 5--mg BD PO supplementary oxygen if needed fluids for dehydration analgesics for pleuritic pain and fever chest physiotherapy in certain cases

Question 55

analgesics

Answer 55

painkillers

Question 56

Covid-19

Answer 56

coronavirus severe acute respiratory syndrome coronavirus 2 diff variants: alpha, beta, gamma, delta, omicron transmission occurs via droplet infection through close range contacts, also airborne transmission lower risk through contaminated surfaces

Question 57

diagnosing covid-19

Answer 57

release of inflammatory cytokines: dry cough, fever, fatigue/myalgia interstitial oedema and alveolar oedema: breathlessness, hypoxia, tachycardia alveolar collapse: breathlessness, hypoxia

Question 58

myalgia

Answer 58

muscles pains and aches

Question 59

investigating covid-19

Answer 59

COVID antigen nasopharyngeal swab blood tests inc cell count sputum culture troponin and ECG ECHO if abnormal troponin chest xray CT pulmonary angiogram if concerned about pulmonary embolism

Question 60

management of covid-19

Answer 60

dexamethasone remdesivir monoclonal antibodies antibiotics supportive management: IV fluid, physiotherapy... controlled oxygen therapy

Question 61

pulmonary embolism

Answer 61

complication of covid-19 the obstruction of the pulmonary artery or one of its branches by material- usually a thrombus typically originates in a deep vein elsewhere and then travels in the blood stream through the right side of the heart, then through pulmonary trunk and becomes lodged within the pulmonary artery acute/sub-acute or chronic more common in men 3rd most common cardiovascular disease in uk

Question 62

risk factors for pulmonary embolism

Answer 62

previous PE, malignancy, recent surgery, immobility, pregnancy, increasing age, smoking, obesity, clotting problems, oral contraceptive pill 30-50% of cases are unprovoked

Question 63

thrombus formation Virchow's triad

Answer 63

stasis vessel wall injury hypercoagulability

Question 64

thrombus formation: stasis

Answer 64

venous obstruction due to obesity, pregnancy, tumour immobility varicose veins heart failure and atrial fibrillation

Question 65

thrombosis: vessel wall injury

Answer 65

trauma/surgery atherosclerosis foreign bodies inc artificial heart valves, catheters...

Question 66

thrombosis: hypercoagulability

Answer 66

malignancy pregnancy/oestrogen infection/inflammation surgery or trauma coagulation disorders smoking

Question 67

pathophysiology of pulmonary embolism

Answer 67

thrombus lodges in pulmonary artery increase in pulmonary vascular pressure increase in right ventricular pressure right heart failure reduced cardiac output and hypotension stimulation of sympathetic nervous system' tachycardiac and vasoconstriction persistent hypotension thrombus lodges reduced blood flow to area of lung supplied by PA V/Q mismatch and inflammation hypoxia, resultant compensatory hyperventilation, persistent hypoxia&hypocapnia, respiratory alkalosis lung infarction, alveolar collapse respiratory failure

Question 68

diagnosing pulmonary embolism

Answer 68

right ventricular failure and decreased cardiac output: hypotension, syncope, dizziness, breathlessness V/Q mismatch: breathlessness, palpitations, hypoxia and hypocapnia lung infarction: chest pain and haemoptysis (blood loss) bronchorestriction: chest pain, wheeze, cough evidence of original thrombus: calf pain/swelling/redness

Question 69

pulmonary embolism Wells score

Answer 69

PE likely is >4 points criteria involving tachycardia, hemoptysis, immobilisation/previous surgery, clinical symptoms...

Question 70

investigating pulmonary embolism

Answer 70

wells score <4: D-Dimer blood test wells score>4: definitive diagnostic imaging, CT pulmonary angiogram, V/Q nuclear medicine scan other: blood tests: troponin arterial bloos gas ECG chest xray bedside ECHO

Question 71

managing pulmonary embolism

Answer 71

if haemodynamically stable: anticoagulation treatment and discharged if not: urgent life-saving treatment inc. systemic thrombolysis, catheter directed thrombolysis or surgery