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Clin Phys > 3. Respiratory diseases > Flashcards

3. Respiratory diseases Flashcards

1
Q

Inhalation

A

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

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2
Q

exhalation

A

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

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3
Q

perfusion matching

A

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

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

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4
Q

atopy

A

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.

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5
Q

asthma definition

A

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

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6
Q

asthma risk factors

A

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

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7
Q

extrinsic or atopic asthma

A

known external cause
airway inflammation due to allergen exposure

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8
Q

rhinitis

A

nasal blocking

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9
Q

intrinsic or non atopic asthma

A

no cause identified
not due to allergen exposure

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10
Q

difference in pathophysiology of asthma for asthmatic airway

A

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)

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11
Q

pathophysiology of asthma (role of IGE)

A

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

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12
Q

asthma is characterised by 3 main features… (pathophysiology)

A

airflow limitation: usually reversible

airway hyper-responsiveness: to an inhaled antigen or other

airway inflammation: infiltration of airways by immune cells

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13
Q

intrinsic asthma triggers

A

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

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

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14
Q

diagnosing airway obstruction

A

wheeze, breathlessness, chest tightness

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15
Q

spirometry

A

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

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16
Q

spirometry key measures

A

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

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17
Q

corticosteroids

A

(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

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18
Q

leukotriene receptor antagonists

A

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

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19
Q

monoclonal antibody therapies

A

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

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20
Q

beta-2-agonists

A

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

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21
Q

muscarinic antagonists

A

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

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22
Q

theophyllines

A

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

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23
Q

COPD chronic obstructive pulmonary disease definition

A

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

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24
Q

chronic bronchitis

A

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

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25
Q

emphysema

A

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

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26
Q

risk factors of COPD

A

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

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27
Q

pathophysiology of COPD 1 (cilia)

A

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)

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28
Q

pathophysiology of COPD 2 (alveoli)

A

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

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29
Q

COPD effect on V/Q

A

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

30
Q

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

A

air trapping ie. anatomical dead space (trapped air in alveoli) abnormal V/Q

breathlessness, hyperinflation ie. barrel chest

muscle wasting

31
Q

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

A

airway obstruction

wheeze, productive cough and chest tightness

32
Q

spirometry for copd

A

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

33
Q

pharmacological management in copd:
airway obstruction

A

beta agonists
muscarinic antagonists
theophyllines

34
Q

pharmacological management in copd: airway inflammation

A

corticosteroids

35
Q

CAT measurement

A

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

36
Q

non pharmacological management in copd

A

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

37
Q

Cor Pulmonale and pulmonary hypertension

A

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

38
Q

pathophysiology of cor pulmonale

A

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

39
Q

diagnosis of cor pulmonale

A

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)

40
Q

managing cor pulmonale

A

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

41
Q

differences between asthma and copd

A

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

42
Q

pneumonia

A

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

43
Q

risk factors for pneumonia

A

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

44
Q

community acquired pneumonia ‘CAP’

A

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

45
Q

hospital acquired pneumonia

A

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

46
Q

aspiration pneumonia

A

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

47
Q

pathophysiology of bacterial pneumonia

A

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

48
Q

pathophysiology of viral pneumonia

A

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

49
Q

diagnosing pneumonia: alveolar congestion w inflammatory exudate/pus:

A

chest pain, productive cough, breathlessness

reduced air entry
bronchial breathing
dull to percussion
coarse crackles (mucus at bottom of lungs)

50
Q

diagnosing pneumonia: cytokines entering systemic circulation

A

fever/rigors, fatigue/malaise, confusion

hypotension
tachypnoea
altered mental state

51
Q

diagnosing pneumonia: airway inflammation

A

wheeze, breathlessness, chest pain

respiratory distress
hypoxia

52
Q

investigating suspected pneumonia

A

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

53
Q

Pneumonia: CURB-65 scoring system

A

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

3 or more is high severity

54
Q

treating pneumonia

A

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

55
Q

analgesics

A

painkillers

56
Q

Covid-19

A

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

57
Q

diagnosing covid-19

A

release of inflammatory cytokines: dry cough, fever, fatigue/myalgia

interstitial oedema and alveolar oedema: breathlessness, hypoxia, tachycardia

alveolar collapse: breathlessness, hypoxia

58
Q

myalgia

A

muscles pains and aches

59
Q

investigating covid-19

A

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

60
Q

management of covid-19

A

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

61
Q

pulmonary embolism

A

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

62
Q

risk factors for pulmonary embolism

A

previous PE, malignancy, recent surgery, immobility, pregnancy, increasing age, smoking, obesity, clotting problems, oral contraceptive pill

30-50% of cases are unprovoked

63
Q

thrombus formation Virchow’s triad

A

stasis
vessel wall injury
hypercoagulability

64
Q

thrombus formation: stasis

A

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

65
Q

thrombosis: vessel wall injury

A

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

66
Q

thrombosis: hypercoagulability

A

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

67
Q

pathophysiology of pulmonary embolism

A

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

68
Q

diagnosing pulmonary embolism

A

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

69
Q

pulmonary embolism Wells score

A

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

70
Q

investigating pulmonary embolism

A

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

71
Q

managing pulmonary embolism

A

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

Clin Phys (14 decks)

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