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Physiology 1 > Pathophysiology Of Respiratory Diseases > Flashcards

Pathophysiology Of Respiratory Diseases Flashcards

1
Q

What is asthma?

A

Chronic, inflammatory and obstructive airway disease

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2
Q

What is the asthma pathway?

A

Allergen inhalation or exercise -> immune system response-> airway inflammation -> impaired airway function -> symptoms

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3
Q

What are the symptoms of asthma?

A

Wheeze
Cough
Dyspnoea
Decreased FEV1/FVC

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4
Q

How does airway inflammation increase airway resistance and decrease airflow?

A

Smooth muscle contracts
Excess mucus secretion
Oedema/swelling
Irritation of sensory neurones (cough)

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5
Q

What is the overall effect of airway inflammation on the airway?

A

Decreased luminal area, increased airway resistance, decreased airflow

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6
Q

What is the main reason for reduced luminal area in asthma?

A

Contraction of airway smooth muscle

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7
Q

Why does the alveolar smooth muscle contract?

A

Allergen induced degranulation

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8
Q

How are the contracted alveolar smooth muscle relaxed again?

A

Beta 2 agonist reducing the airway obstruction by causing the alveolar smooth muscle to relax

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9
Q

Give an example of an airway relaxant

A

Salbutamol

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10
Q

What is the process for inflammatory mediators inducing alveolar smooth muscle contraction?

A

Contractile mediators attach to a GPCR-> intracellular signalling pathways cause Ca2+ to be released from the sarcoplasmic reticulum -> muscle contraction

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11
Q

How does allergen sensitisation work?

A

Allergen exposure -> allergen encountered and processed by the adaptive immune system-> antibodies generated and the immune system ‘primed’

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12
Q

How does the allergic response work?

A

Subsequent allergen exposure -> allergen binds to antibodies -> immune response triggered -> symptoms

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13
Q

Give the details of the immune response in asthma

A

Allergen binds to IgE on mast cells, inducing degranulation -> attracts more granulocytes (like eosinophils) -> more inflammatory mediators are released

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14
Q

What causes the late asthmatic response?

A

Allergen activates Thelper2 cell -> secretes IL4,5,13 -> attract more immune cells -> degranulation

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15
Q

How do corticosteroid drugs reduce asthmatic inflammation?

A

Modulating the function of multiple immune and structural cells

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16
Q

What effect do glucocorticoids have on cells?

A

Inhibits mucus secretion
reduces number of mast cells and dendritic cells
decreases release of cytokines from macrophages and T-lymphocytes
Cause apoptosis in eosinophils
Increased B2 receptors in airway smooth muscle
Decreased leak in endothelial cells
Decreased cytokine mediators in epithelial cells

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17
Q

What is the corticosteroid mechanism of action?

A

Diffuses through the membrane -> binds to intracellular glucocorticoid receptor -> drug receptor complex translocates to the nucleus and binds to the DNA where it affects transcription -> altered transcription of the gene -> translation of gene into protein

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18
Q

How do corticosteroids work?

A

Either increase or decrease expression of a gene dependant on what it does

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19
Q

What are the four endotypes of asthma?

A
  • Aspirin associated respiratory disease
  • cold air/exercise induced asthma
  • allergic broncho-pulmonary mycosis
  • allergic asthma
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20
Q

What is COPD?

A

Umbrella term used for a mixture of chronic bronchitis and emphysema, and encompasses a long-term, progressive and accelerated decline in respiratory function

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21
Q

What % of COPD is associated with long term tobacco smoke exposure?

A

90

22
Q

What % of long-term smokers develop COPD?

A

30

23
Q

What are other risk factors for COPD (not smoking)?

A

Genetic (alpha 1 antitrypsin deficiency) and environmental hazards (pollution)

24
Q

How does tobacco smoke cause tissue damage?

A

Inhalation of toxic chemicals and reactive oxygen species -> tissue damage -> inflammatory response -> macrophage and neutrophil activation -> increased protease burden -> tissue damage

25
Q

Why do anti proteases not help with the excess protease created in smoking?

A

Some chemicals in tobacco smoke inactivate the anti proteases

26
Q

What happens in prolonged smoking/ tissue damage?

A

Tissue remodelling -> impaired mucocillary clearance and increased respiratory infections

27
Q

What are the pathophysiological features of chronic bronchitis?

A
  • damage to cillia
  • mucus hypersecretion (increase in goblet cells and increased mucosal gland secretion)
  • inflamed, swollen airway tissue and oedema
  • weakened airway structure and loss of patency
28
Q

What weakens the airway structure in chronic bronchitis?

A

Loss of elastin

29
Q

What causes the loss of patency in chronic bronchitis?

A

Airway collapse

30
Q

What are the symptoms of chronic bronchitis?

A

Recurrent infection
Cough
Increased airway resistance and airway obstruction

31
Q

Why do you get recurrent infections with chronic bronchitis?

A

Impaired mucocilliary clearance -> increased risk of infection

32
Q

Why do you get a cough with chronic bronchitis?

A

Irritation of sensory neurones

33
Q

Why do you get increased airway resistance and airway obstruction with chronic bronchitis?

A

Decreased luminal area

34
Q

What is emphysema?

A

Airspace enlargement

35
Q

How does emphysema happen?

A

Tissue damage -> alveolar merging

36
Q

What are the effects of emphysema?

A

Decreased SA and perfusion = Decreased gas exchange

Loss of elastin = increased compliance and decreased recoil

37
Q

What are the biological effects of chronic alveolar hypoxia on the body?

A

Hypoxaemia
Hypercapnia
Acidemia
Right heart failure

38
Q

What are the steps that go from chronic alveolar hypoxia to right heart failure?

A

Hypoxic vasoconstriction = increased pulmonary vascular resistance

  • > pulmonary hypertension
  • > increased right ventricular afterload -> RV hypertrophy
39
Q

What are the symptoms of chronic alveolar hypoxia?

A

Decreased exercise tolerance
Increased fatigue
Decreased quality of life

40
Q

What are the the biological effects of cor pulmonale?

A

Distended jugular veins
Dependent edema
Enlarged liver and spleen
Increased peripheral venous pressure

41
Q

What is another word for cor pulmonale?

A

Right sided heart failure

42
Q

What are the symptoms of cor pulmonale?

A

Anorexia and GI distress
Weight gain
Fatigue
Ascites

43
Q

What is ascites?

A

Swollen tummy

44
Q

What is pneumonia?

A

Infection of the lung parenchyma, resulting in inflammation and oedema

45
Q

What are the two classifications of pneumonia can you get?

A

Tissue area and infectious agent

46
Q

What are the types of infectious agent that can cause pneumonia?

A

Bacterial, fungal and viral

47
Q

What are the areas of tissue that can get pneumonia?

A

Lobar, interstitial etc

48
Q

What is the pathophysiology of pneumonia?

A

Host defence is weakened -> colonisation of alveoli by pathogens -> activation of macrophages and cytokines release -> recruitment of neutrophils into the alveolar space -> release of proteases and ROS -> injury to alveolus and surrounding structures

49
Q

How can a hosts defence be weakened?

A

Viral infection, damage to the epithelium or immune suppression

50
Q

What cytokines are released in pneumonia?

A

IL6, IL5 TNF alpha

51
Q

How does alveolar injury lead to impaired gas exchange?

A

Either: dead cells and proteins in the alveolar wall are deposited
Or: the endothelium and basement membrane is disrupted, which means fluid accumulates in the alveoli and/ or interstitum

Physiology 1 (65 decks)

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