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Respiratory SB > Pharmacology > Flashcards

Pharmacology Flashcards

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

A

false

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

25
Q

what are LABA’s useful for

A

nocturnal asthma

26
Q

what do CysLT1 receptor antagonist do

A

block cysLTs which are derived from mast cells and cause smooth muscle contraction, mucus secretion and oedema

27
Q

what is the mechanisms of action for CysLT1 receptor antagonist drugs

A

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
Q

what are CysLt1 receptor antagonist used for in the treatment of asthma

A

add on therapy in mild persistent asthma

effective against antigen-induced and exercise-induced bronchospasm

29
Q

what are the two actions xanthines combines

A

bronchodilator and anti-inflammatory

30
Q

when are xanthines used in the treatment of asthma

A

second line drugs used in combination with β2-adrenoceptor agonists and glucocorticoids

31
Q

why do we give glucocorticoids

A

prophylaxis of asthma

32
Q

what is the mechanism of action of glucocorticoids

A

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
Q

how does glucocorticoids prevent transcription

A

they recruit histone deactylases to activated genes and switch off gene transcription

34
Q

what do glucocorticoids do in an allergic response

A

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
Q

how does glucocrticoids impact the inflammatory aspect of asthma

A

1 - prevent inflammation

2 - resolve established inflammation

36
Q

what is the mechanism of Monoclonal antibodies directed against IgE

A

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
Q

example of Monoclonal antibodies directed against IgE

A

Omalizumab

38
Q

what are the 5 steps to COPD

A

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
Q

what step leads specifically to COPD

A

Step 5

Release of matrix meralloproteinases (e.g. elastase), free radicals.

40
Q

what is the molecular mechanism of airway smooth muscle contraction in Muscarinic Acetylcholine Receptor Antagonists

A

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
Q

what are the actions of Muscarinic ACh Receptor Antagonists

A

Relax bronchospasm
Basal block ACh-mediated basal tone
Decrease mucus secretion

42
Q

what are the 3 types of rhinitis

A

1 - allergic
2 - non allergic
3 - mixed

43
Q

what is the mechanism of allergic rhinitis

A

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
Q

what do both rhinitis and rhinorrhoea involve and what do these things cause

A

increased mucosal blood flow
increased blood vessel permeability
increase the volume of the nasal mucosa and cause difficulty breathing in

45
Q

how do glucocorticoids reduce rhinitis

A

Reduce vascular permeability, recruitment and activity of inflammatory cells and the release of cytokines and mediators

46
Q

what is the most common route of administration for glucocorticoids in the treatment of rhinitis

A

nasal spray

47
Q

how do anti-cholinergic/muscarinic antagonist drugs reduce rhinitis

A

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
Q

what do anti-cholinergic/muscarinic antagonist do in rhinitis

A

reduce rhinorrhoea

NO effect on itching, sneezing and congestion

49
Q

what route are anti-cholinergic/muscarinic antagonist drugs in rhinitis administered

A

nasal route

50
Q

what is the sole anti-cholinergic/muscarinic antagonist drug in rhinitis

A

ipatropium

51
Q

what CysLT1 receptor antagonist drug is used in rhinitis

A

monetlukast

52
Q

why is using a spacer device useful

A
  • avoids coordination problems
  • reduces oropharyngeal and laryngeal side effects
  • reduces systemic absorption from swallowed fraction
  • reduced particle size and velocity
  • improved lung deposition
53
Q

what are cromones

A

e.g. cromoglycate
only used in asthma
mast cell stabiliser
inhaled route only

54
Q

what are SMART inhalers

A

combined inhaler
i.e flucticasone/salmeterol
preventative and controller
beta agonist and steroid in one go

55
Q

what is used for COPD treatment only

A

Long acting Muscarinic and beta antagonist

56
Q

what are SABA side effects

A

hypokalaemia, tremor, tachycardia

57
Q

what are Anticholinergics side effects

A

dry mouth, tachycardia, constipation

58
Q

side effects of Methylxanthines

A

hypokalaemia

59
Q

side effects of Corticosteroids

A 
Cushing Syndrome
Hyperglycaemia
Growth retardation
Osteoporosis
Hypokalaemia
Peptic ulceration

Respiratory SB (14 decks)

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