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AAI: Pharmacology + Biology > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

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1
Q

What is Asthma?

A

Reversible airflow obstruction increases in airway resistance involving bronchoconstriction + inflammation

Decreases in FEV1 (forced expiration volume in first second)

Value of < 70% means increased airway resistance

If asthma, then reversed using Beta2-agonist

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2
Q

What is COPD?

A

Airflow limitation that is not fully reversible

Both chronic bronchitis + emphysema

Loss of lung function

80-90% deaths related smoking

Diseases of late onset in life (elderly)

High energy demand + difficulty eating, e.g. use inhaler before meal, leading to weight loss

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3
Q

Describe the phases of asthmatic attack

A
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4
Q

What are the two categories for asthma therapy?

A

1) relief of symptoms (bronchodilators) - block early phase if asthma attack caused by bronchoconstriction
2) prevention of attack (anti-inflammatory agents) - prevents late phase caused by release of cytokines

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5
Q

What are bronchodilators?

A

Reverse bronchospasm + rapid relief

Beta2 adrenoceptor agonists e.g. salbutamol

  • 1st choice
  • Increase FEV1
  • Given by inhalation

Longer acting agents (salmeterol) given for long-term prevention

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6
Q

Where are Beta2-adrenoceptors + function?

A

On smooth muscle and mast cell

Increase in cAMP prevents release of histamine

Affects on mucus secretion

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7
Q

What is Desensitisation?

A

Caused by long-term use of Beta-adrenoceptor agonists which leads to tolerance/desensitisation

Due to internalisation of the receptor

Prevented by steroids

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8
Q

Examples of Long-acting beta-adrenoceptor agonist

A

Salmetorol

Formoterol

Indacaterol

Dont know why they are long acting

Current theory = absorbed into lipid bilayer of cells - slowly released over time to activate

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9
Q

Adverse effects of beta2-adrenoceptor agonists

A

Tremor

Palpitations

Hypokalaemia

Due to high doses of drugs e.g. nebulisers

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10
Q

Example of Phosphodiesterase inhibitor

A

Roflumilast (PDE4) inhibitor (DAXAS)

For COPD

Reduces inflammation

Can enhance Beta-adrenoceptor effects

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11
Q

Function of Muscarinic M-receptor antagonist

A

Block parasympathetic bronchoconstriction

e.g. ipratropium (non-selective antagonist)

Inhaled (fewer systemic effects)

Inhibits mucous secretion

Tiotropium = long-acting, due to slow dissociation from receptor

Aclidinium = long-acting but newer

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12
Q

What are the side effects of Muscarininc M-receptor?

A

They are non-selective so they block muscarinic receptors all over body

Dry mouth

Nausea/headache

Constipation

Urinary retention

Blurred vision

Atrial fibrillation + Tachycardia + Palpitation

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13
Q

What are Xanthines + example?

A

Bronchodilators (not as good as b2-adrenoceptor agonist)

E.g. theophylline

2nd line use

Orally inhaled (or IV aminophylline in emergencies)

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14
Q

What is Aminophylline?

A

Mix of theophylline + ethylenediamine (2:1 ratio)

Improves solubility

Measure plasma theophylline 4-6 hrs after infusion (iv)

Monitor plasma levels - toxicity

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15
Q

What are the side effects of Theophylline?

A

Tremor

Palpitations

Nausea

CNS stimulations

Drug interactions:

  • inhibit of metabolism increases toxicity (cimetidine)
  • induce metabolism reduces plasma levels
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16
Q

What are anti-inflammatory agents?

A

Preventative - do not reverse an attack

Target late phase of asthma response

e.g. Corticosteroids

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17
Q

What receptors do steroids act on?

A

Act at intracellular or glucocorticoid receptor

18
Q

Examples of Inhaled steroids

A

Beclometasone

Bidesonide

Ciclesonide

Fluticasone

Mometasone

19
Q

Example of an oral steroid

A

Prednisolone

e.g. acute asthma attack

20
Q

Example of an IV steroid

A

Hydrocortisone

e.g. life threatening asthma

21
Q

What genes are switched on/activated by glucocorticoids when steroid has bounded?

A

Annexin A1

Beta2-adrenoceptors

IkB (Inhibitor of NF-kB)

MKP1 (inhibits MAP kinase)

Anti-inflammatory cytokines e.g. IL-10, 1L-12

22
Q

What genes are switched off/repressed by glucocorticoids when crosslinked with steroid?

A

Inflammatory cytokines - e.g. IL-2, IL-3, IL-6, TNFα

Chemokines

Inflammatory enzymes - e.g. iNOS, COX-2

Inflammatory peptides - e.g. endothelin-1

23
Q

How can genes be repressed when steroid binds to glucocorticoid receptor?

A
24
Q

What is Annexin A1?

A

Involved in the up-regulation of anti-inflammatory genes

Act through formyl peptide receptors (FPR)

  • inhibits histamine release from mast cells
  • inhibits cPLA2 - PGs
25
Q

How do steroids affect Beta2-adrenoceptor?

A

Increase transcription of B2-AR

Protect against downregulation of B2-ADR after long term use (desensitisation)

Benefits of co-administration

26
Q

What are the side effects of corticosteroids?

A

Throat infections/oral candidiasis with inhaled steroids

Osteoporosis

Adrenal suppression in children

  • use lowest effect dose of steroid
  • monitor height

Indigestion

Chicken pox severe (avoid contact) - immune response

Withdrawal effect (reduce oral steroids gradually if more than 3 weeks)

27
Q

Patients with severe asthma + COPD have poor response to steroids (Steroid resistance)

What are the reasons for the resistance?

A

Genetics

GR receptor modification

Decreased nuclear translocation of GR

Increases efflux of steroids

28
Q

How are leukotrienes made?

A
29
Q

Function of Leukotriene mediator

A

They have a role in inflammation + asthma

Stimulate mucus secretion

Cause bronchoconstriction

Role in airway remodelling

Linked to hyperresponsiveness

Link with exercise-induced asthma

30
Q

Function of Cysteinylleukotriene receptor antagonist

A

Block LT receptors - block inflammatory actions of cystLTs

e.g. montelukast

Leukotriene receptor antagonist block production of leukotrienes + LTB4

Antagonist block bronchoconstriction

Zileuton = Suppressor of leukotriene synthesis + LTB4

31
Q

What are the side effects of CystLT receptor antagonist?

A

Headache

Rash

Nausea

Jaundice

Mood disorders/suicidal thoughts (from montelukast)

32
Q

What is Omalizumab?

A

Used for severe allergic asthma that cannot be controlled by steroids

It’s a monoclonal antibody against free IgE - Prevents IgE from binding to immune cells preventing allergen-induced mediator release (e.g. histamine)

S.C. Injection every 2-4 weeks

33
Q

How can drug-induced asthma occur?

A

Affects 15% of asthmatics

Drugs involved are NSAIDS, Beta-AR + drug allergies

NSAIDS inhibit COX

  • more arachidonic acid leukotriene production
  • leads to inflammation/spasm + bronchoconstriction

B-adrenoceptor antagonist

  • non-selective (propranolol)
  • selective (atenolol)

Drug allergy (e.g. penicillins, cephalosporins, dipyridamole, tramadol)

34
Q

Example of a cromone

A

e.g. sodium cromoglicate

Preventative (mast cell stabilisers)

  • Prevent + relieve swelling of the airways
  • buildup of mucus + asthma

Benefit in exercise-induced asthma

Given by Inhalation

35
Q

Function of mucolytics

A

Break up thick mucus

e.g. carbocysteine, erdosteine, mecysteine, dornase alfa

Act as an antioxidants

Used in COPD

Dornase alfa (recombinant deoxyribonuclease) breaks down extracellular DNA from dying neutrophils

  • used in CF to reduce mucus viscosity
36
Q

What is a Cough?

A
37
Q

What are Anti-tussive agents?

A

Stops coughing

e.g. Codeine (opioid) + dextromethorphan (non-opioid)

  • act in cough centre
  • little bit better than placebo
  • codeine is avoided in children under 18 years
  • dextromethorphan avoided in children under 6 years

e.g. Levodropropizine

  • inhibit release of sensory neuropeptides
  • compared to Codeine + dextromethorphan
38
Q

What is Cystic Fibrosis?

A

Inherited disorder of ion transport in epithelial cells

Affects respiratory, hepatobiliary, gastrointestinal, reproductive tracts, pancreas

Defect in chloride transporter leading to reduced Na+ and H20 transport

  • Thicker secretions w/obstruction + destruction of exocrine glandular ducts
  • recurrent infections
39
Q

Discuss the disease characteristics of CF

A

Pancreatic exocrine insufficiency

  • reduced/absent secretions

Patients living longer - but developing other complications:

  • diabetes
  • liver disease
  • osteoporosis
40
Q

How can we manage CF?

A

Aim is to clear viscous mucus from airways to treat respiratory infections, improving respiratory function

Physiotherapy

Antibiotics

Corticosteroids

Bronchodilators

Dornase Alfa administered using Nebuliser

  • synthetic version of enzyme which cleaves extracellular DNA
  • ‘Digests’ extracellular DNA released from dying neutrophils in the airway which contributes to increased mucus viscosity

AAI: Pharmacology + Biology (11 decks)

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