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Respiratory SB > Pharmacology > Flashcards

Pharmacology Flashcards

(59 cards)

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1
Q

what type of fibres does the vagus nerve carry

A

preganglionic fibres

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2
Q

what mediated bronchial smooth muscle contraction

A

ACh acting on M3 muscarinic ACh receptors

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3
Q

what mediates increased mucus secretion

A

ACh acting on M3 muscarinic ACh receptors

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4
Q

what do bronchial contraction and increased mucus secretion cause

A

increased airway resistance

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5
Q

through what receptor does the sympathetic division relax smooth muscles

A

β2-adrenoceptors activated by adrenaline released from the adrenal gland

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6
Q

what does β2-adrenoceptors mediate

A

decreased mucus secretion
increased mucociliary
reduce air way resistance

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7
Q

how does asthma cause airway narrowing

A

inflammation
bronchoconstriction
decrease FEV1 and PEFR

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8
Q

what are the two components of neurogenic inflammation

A

hypersensitivity and hyperreactivity

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9
Q

what is the first stage of development of allergic asthma

A

initial presentation of an antigen (e.g. dust mite or pollen) initiates an adaptive immune response

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10
Q

what are the steps of the induction phase

A

1 - aeroallergen breaches airway epitheliumt
2 - allergen processed by CD4+
T cell
3 - becomes Th0 cell
4 - Th0 cell preferentially mature to Th2 cells that produce a cytokine environment
5 - Th2 cells activate B cells by binding to them and by IL-4 production
6 - B cells mature to IgE secreting P cells

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11
Q

What are the two parts of the induction phase

A

Antigen presentation

Clonal expansion and maturation

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12
Q

what is the second stage of development of allergic asthma

A

effector phase

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13
Q

what are the stages of the effector phase

A

1 - Eosinophils differentiate and activate in response to IL-5 released from Th2 cells
2 - Mast cells in airway tissue express IgE receptors in response to IL-4 and IL-13 released from Th2 cells

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14
Q

what is the third stage of development of allergic asthma

A

subsequent presentation of antigen

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15
Q

what do cross linked IgE receptors stimulate

A
  • calcium entry into mast cells

- release of Ca2+ from intracellular stores

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16
Q

what does the release of calcium from intracellular stores cause

A
  • release of secretory granules containing histamine and the production and release of other agents that cause airway smooth muscle contraction
  • release of substances that attract cells causing inflammation into the area
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17
Q

what happens in the immediate phase of asthma

A
  • stimulus
  • mast cell degranulation
  • bronchospasm caused by spasmogens-chemical e.g. histamine
  • chemotaxins attract inflammatory cells (Th2) cells into the area
  • chemokines activate cells
  • leads to late phase
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18
Q

what happens in the late phase of asthma

A
  • infiltration of releasing TH2 cells and monocytes
  • activation of inflammatory cells e.g. eosinophils
  • Eosinophils release proteins damaging to airway structure
  • Proteins cause shedding of airway i.e. epithelial damage
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19
Q

what is the mechanism of action of beta2 adrenoreceptor agonists

A 
1 - Drug attaches to receptor
2 - Increased Gs secretion
3 - Increased Adenylyl cyclase release
4 - AC reacts with ATP to form cAMP 
5 - cAMP inhibits release of PDE
6 - cAMP stimulates release of PKA
7 - PKA phosphorylates MLCK 
8 - Relaxation
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20
Q

what does persistent activation of beta2 adrenoceptors cause

A

receptor desensitisation
endocytosis
results in loss of function

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21
Q

what are the two kinase involved in beta2 adrenoceptors agonist drug mechanisms

A

protein kinase A (PKA) and G protein receptor kinases (GRKs)

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22
Q

stages of phosphorylation and endocytosis by GRK

A 
1 - Agonist binds
2- Phosphorylation by GRK
3 - G-protein coupling stops
4 - Binding of B-arrestin
5 - Pit is formed 
6 - Pit buds off and comes vesicle
7 - B-arrestin unbinds from vesicle 
EITHER
8 - vesicle is targeted for degradation by lysosomes
OR
9 - recycling vesicle
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23
Q

what do beta2 adrenoceptor agonists do

A

increase mucous clearance

decrease mediator release from mast cells and neutrophils

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24
Q

beta2 adreoceptor are selective - true or false

Study These Flashcards
A

false

non-selective - will also activate B1 receptor causing heart to act more forcefully

25
what are LABA's useful for
nocturnal asthma
26
what do CysLT1 receptor antagonist do
block cysLTs which are derived from mast cells and cause smooth muscle contraction, mucus secretion and oedema
27
what is the mechanisms of action for CysLT1 receptor antagonist drugs
1 - Mast cell activation 2 - intracellular release of arachidonic acid by phospholipase A2 3 - stimulation of mast cell 5-lipoxygenase by FLAP 4 - infiltration of inflammatory cells releasing cysLTs 5 - CysLT1 receptor activation 6 - bronchoconstriction and inflammation
28
what are CysLt1 receptor antagonist used for in the treatment of asthma
add on therapy in mild persistent asthma | effective against antigen-induced and exercise-induced bronchospasm
29
what are the two actions xanthines combines
bronchodilator and anti-inflammatory
30
when are xanthines used in the treatment of asthma
second line drugs used in combination with β2-adrenoceptor agonists and glucocorticoids
31
why do we give glucocorticoids
prophylaxis of asthma
32
what is the mechanism of action of glucocorticoids
1 - glucocorticoids enter the cell by diffusion 2 - they combine with GRalpha producing a dissociation of inhibitory heat shock proteins 3 - activated receptors move to nucleus 4 - monomers assemble into homodimers 5 - these bind to glucocorticoid response elements 6 - transcription of specific genes is either "switched on" (transactivated) or "switched off" (transrepressed) to alter mRNA levels 7 - alter rate of synthesis of mediator proteins
33
how does glucocorticoids prevent transcription
they recruit histone deactylases to activated genes and switch off gene transcription
34
what do glucocorticoids do in an allergic response
1 - decrease formation of Th2 cytokines and cause apoptosis 2 - prevent IgE production 3 - prevent allergen-induced influx into lung and cause apoptosis 4 - reduce number of cells and decrease FcE expression
35
how does glucocrticoids impact the inflammatory aspect of asthma
1 - prevent inflammation | 2 - resolve established inflammation
36
what is the mechanism of Monoclonal antibodies directed against IgE
Binds IgE via Fc to prevent attachment to Fcε receptors – suppresses mast cell response to allergens Reduces the expression of Fcε receptors on inflammatory cells
37
example of Monoclonal antibodies directed against IgE
Omalizumab
38
what are the 5 steps to COPD
1 - smoking 2 - Stimulation of Resident Alveolar Macrophages 3 - cytokine production 4 - activation of neutrophils, CD8 T cells, increased macrophage numbers 5 - Release of matrix meralloproteinases free radicals
39
what step leads specifically to COPD
Step 5 | Release of matrix meralloproteinases (e.g. elastase), free radicals.
40
what is the molecular mechanism of airway smooth muscle contraction in Muscarinic Acetylcholine Receptor Antagonists
1 - Activation of M3 muscarinic receptor by ACh is blocked 2 - increase Gq/11 3 - increased phospholipase C 4 - PLC binds with phosphatidylinositol bisphosphate 5 - produces inositol trisphosphate 6 - causes Calcium ion release from Sacroplasmic reticulum 7 - contraction
41
what are the actions of Muscarinic ACh Receptor Antagonists
Relax bronchospasm Basal block ACh-mediated basal tone Decrease mucus secretion
42
what are the 3 types of rhinitis
1 - allergic 2 - non allergic 3 - mixed
43
what is the mechanism of allergic rhinitis
1 - Inhalation of allergen increases specific IgE level 2 - IgE binds to receptors on mast cells and basophils 3 - Re-exposure allergen causes mast cell and basophil degranulation 4 - Released of mediators causing acute rhinitis 5 - delayed response caused by recruitment of lymphocytes and eosinophils to nasal muscosa contributes to congestion and obstruction.
44
what do both rhinitis and rhinorrhoea involve and what do these things cause
increased mucosal blood flow increased blood vessel permeability increase the volume of the nasal mucosa and cause difficulty breathing in
45
how do glucocorticoids reduce rhinitis
Reduce vascular permeability, recruitment and activity of inflammatory cells and the release of cytokines and mediators
46
what is the most common route of administration for glucocorticoids in the treatment of rhinitis
nasal spray
47
how do anti-cholinergic/muscarinic antagonist drugs reduce rhinitis
ACh released from post-ganglionic parasympathetic fibres activates muscarinic receptors on nasal glands causing a watery secretion that contributes to rhinorrhoea – blocked by muscarinic antagonist
48
what do anti-cholinergic/muscarinic antagonist do in rhinitis
reduce rhinorrhoea | NO effect on itching, sneezing and congestion
49
what route are anti-cholinergic/muscarinic antagonist drugs in rhinitis administered
nasal route
50
what is the sole anti-cholinergic/muscarinic antagonist drug in rhinitis
ipatropium
51
what CysLT1 receptor antagonist drug is used in rhinitis
monetlukast
52
why is using a spacer device useful
- avoids coordination problems - reduces oropharyngeal and laryngeal side effects - reduces systemic absorption from swallowed fraction - reduced particle size and velocity - improved lung deposition
53
what are cromones
e.g. cromoglycate only used in asthma mast cell stabiliser inhaled route only
54
what are SMART inhalers
combined inhaler i.e flucticasone/salmeterol preventative and controller beta agonist and steroid in one go
55
what is used for COPD treatment only
Long acting Muscarinic and beta antagonist
56
what are SABA side effects
hypokalaemia, tremor, tachycardia
57
what are Anticholinergics side effects
dry mouth, tachycardia, constipation
58
side effects of Methylxanthines
hypokalaemia
59
side effects of Corticosteroids
``` Cushing Syndrome Hyperglycaemia Growth retardation Osteoporosis Hypokalaemia Peptic ulceration ```

Respiratory SB (14 decks)

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