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MPharm 2 - PH2113 > PH2113 - Pulmonary > Flashcards

PH2113 - Pulmonary Flashcards

1
Q

Why do you need to use a preventer and a reliever for the treatment of asthma instead of one?

A

Preventors only stop inflammation they do not affect smooth muscle contraction.

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2
Q

What is the equation for airflow in lungs?

How does the body increase airflow to help symptoms of airflow resistance during an asthma attack?

A

Airflow = pressure gradient/resistance.

Increase and external intercostal muscle- greater pressure difference to overcome increased resistence.

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3
Q

How does an asthma attack affect the lungs- symptomology of asthma?

A

Bronchoconstriction from contraction of smooth muscle.

Release of inflammatory response and mucus production.

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4
Q

Explain how sensitisations causes asthma?

A
  1. Allergen recognised by foreign protein by dentritic cell.
  2. Dentritic cell migrate to lymph nodes where allergen is displayed on T-cell.
  3. T-cell differentiate to Th2 lymphocyte.
  4. Activation of B-cells generate IgE and binds to allergen.
  5. Fc region of IgE binds to high affinity receptors on mast cells causing inflammation.
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5
Q

What are the different phenotypes in asthma- give examples.

A

Intrinsic/allergen: pollen, mould.

Extrinsic/non-allergen based: weather, aspirin and exercise.

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6
Q

Explain the early phase of asthma.
What mediators cause 1. bronchoconstriction & eosinophil release.
2. prostaglandin release?

A
  1. Activation of degranulation of mast cell by allergen-induced cross linking IgE.
  2. Mast cells release humoral inflammatory mediated- histamine causing bronchoconstriction.
  3. Activation of phospholipase A2 triggers Arachidonic acid cascade for inflam mediators. eg. CysLT1 and cyclo-oxygenase COX1 &2.
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7
Q

How does affects of asthma cause late response?

A

Eosinophils continue to cause inflammation in late phase- increase vascular permeability leading to oedema causing further narrowing. Build up of mucus.

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8
Q

What happens structural in lungs during airway remodelling? x4

A

Thicker airway reducing blood flow.
Muscus occlusion of airway.
Increased expsoure of underlying sensory nerves.
Hypertropy and hyperplasia.

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9
Q

How do relievers generally work?

A

Reduce cytosolic Calcium for smooth muscle contraction- activation of cAMP and activate beta-2-adrenoceptors.

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10
Q

What is the treatment for acute COPD exabations?

A

SABA, Corticosteriods, Doxapram.

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11
Q

What are the 2 lung function parameters: which is for obstructive and restrictive?

A

Lung capacity- how much air the lungs can hold. Airflow- how quickly air can be removed from the lungs.

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12
Q

What is the mechanism of action for beta-2 adrenoceptors?

A
  1. Binds to Gs.
  2. Gs activated adenyl cyclase to generate cAMP.
  3. cAMP activated protein kinase to reduce cytosolic Ca2+.
  4. PKA reduces IP3 preventing release of Ca2+store. Limited contraction from myosin filaments.
  5. Na/K increases K for the cell to be hypopolarised.
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13
Q

What is the MOA for xanthines?

A

Inhibit phosphodiesterase to increase cAMP which decreases ATP to limit inflammation.

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14
Q

What is the MOA of Muscarinic receptor antagonists?

A

Inhibit M3 receptors for bronchoconstriction to be released by ACh from parasympathetic nerves causing bronchodilation.

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15
Q

Why are Muscarinic receptor antagonists used for COPD more?

A

Parasynthetic tone needed for action.

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16
Q

Why is muscarinic receptor antagonist limited when increasing dose?

A

Limit receptor sensitivity.

17
Q

How do corticosteriods work?

Why do they take time to work?

A
  1. Drug diffused and binds to cortisol receptors.
  2. translocate in nucleus causing transcription of anti-inflammatory gene IL-10.
  3. Reduce transcription of pro-inflamm genes eg. cyclo-oxygenase and nitric oxide synthase.
18
Q

What are the factors that affect glucocorticoid potency?

A

Affinity- higher binding affinity = lower dose needed.

Lipophilicity- access inside of cell- increased lipohilicty increases potency.

19
Q

What is the MOA for leuktriene receptor antagonists?

A

Block cysteinyl leukotriene receptor 1- needed for contraction of C4 and D4 for inflammation.

20
Q

What is the MOA of chromones?

A

Inhibit mast cells reducing inflammation.

21
Q

What is the MOA for biologics in asthma?
IL-5?
Omalizumab?

A

use of anti-bodies: IL-5: reduce recruitment and activation limits remodelling and asthma attacks.
Omalizimab: Target IgE b;acl Fc receptor to prevent cross-linking.

22
Q

What are differences in symptoms between asthma and COPD?

A

COPD: persistent, increased breathlessness, chesty cough where symptoms get progressively worse. No genetic link.
Asthma: Episodic breathlessness, episodes of wheezing, genetic link.

23
Q

What is the first line treatment for COPD?

A

SAMA or SABA.

24
Q

What is the typical treatment for COPD and Asthma?

A

LABA and ICS.

25
Q

What are typical treatments for COPD exabations?

A

Bacterial infection- antibiotics.
oral corticosteriods- viral.
Oxygen therapy, physio and IV theophylline.

26
Q

Why is lung function restricted in COPD?

Why is airflow obstructed in COPD and asthma?

A

Lungs become complient and stretchy- unable to expand and hold more air.
Diameter of radius reduces increasing resistance to airflow.

27
Q

What does FEV1 mean?
What does FVC mean?
What is the FEV1/FVC mean?
How are these altered for restrictive diseases?

A

FEV1: forces exhaled volume in 1 second.
FVC: Force vital capacity (amount of air exhaled).
FEV1/FVC ratio: % of lung capcity that can be exhaled forcefully in 1 second.

28
Q

What is the mechanism of a MDI?

A

Pressurised canister needed a slow deep breath.

29
Q

What is the mechanism of DPI?

A

Force of inspiration needed to initiate the drug and release it from carrier molecule.

30
Q

What leads to permanent damage to lung elastricity?

A

Damage of aveolar extracellular

31
Q

What is the pathology that causes the symptoms in COPD?

A

Neutrophils release cause thickening of airways and hypertrophy and hyperplasia of smooth muscle.
Hyper-secretion of mucus.
Bronchoconstriction- high parasympathetic tone.
Oedema- increased vascular permeability.
Damage to aveolar extracellular matrix leading to irreversible lung elasticity and restriction of air-space.

32
Q

What is pulmonary rehabilitation?

A

Disease education, Exercise, dietry advice and psychological care.

33
Q

What negative impact can O2 treatment for COPD have?

A

Can cause respiratory depression.

MPharm 2 - PH2113 (50 decks)

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