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Physiology and Pharmacology I > Adrenoceptors > Flashcards

Adrenoceptors Flashcards

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1
Q

What are adrenoceptors?

A

Receptors that mediate actions of adrenaline (epinephtine)/noradrenaline (norepinephrine).

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2
Q

How are adrenoceptors useful therapeutically?

A

Treatment of hypertension and cardiovascular diseases
Treatment of asthma and respiratory diseases
Treatment of depression and phychiatric/neurological disorders
Treatment of ADHD

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3
Q

How do adrenergic agents vary?

A

Different ranges of specificity and durations of action.

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4
Q

What is adrenaline and where is it produced?

A

A hormone released from the chromaffin cells of adrenal medulla of adrenal glands.

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5
Q

What is noradrenaline and where is it produced?

A

A neurotransmitter released by noradrenergic in CNS and ANS.

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6
Q

What is the regulatory function of noradrenaline?

A 
Regulation of:
Attention
Perception
Learning/memory
Arousal
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7
Q

What is the locus ceruleus?

A

The site of origin of most of the noradrenergic projections

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8
Q

What does the locus ceruleus innervate?

A 
Cortex
Amygdyla
Hippocampus
Hypothalamus
Brainstem nuclei
Spinal cord
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9
Q

What is another name for isoprenaline?

A

Isopronetol

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10
Q

What is another name for salbutamol?

A

Albuterol

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11
Q

How does the adrenergic system contribute to the fight or flight response?

A

Adrenaline boosts the response. Sympathetic nervous system innervates the adrenal medulla to prompt adrenaline release. A hormonal response supplements the neuronal activity.

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12
Q

What are varicosities?

A

Neuro-effector junctions connecting efferent axons with tissues.

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13
Q

What is released from varicosities?

A

Noradrenaline

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14
Q

Describe the pathway of noradrenaline synthesis.

A

Tyrosine is converted to DOPA by tyrosine hydroxylase.
DOPA converted to Dopamine by DOPA decarboxylase.
Dopamine converted to Noradrenaline by Dopamine beta-hydroxylase.

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15
Q

Where within the axon is noradrenaline synthesised?

A

In a noradrenergic vesicle, tyrosine enters the vesicle and is synthesised to NA.

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16
Q

How is adrenaline synthesised from noradrenaline?

A

NA is transported out of the vesicle for this step. NA released from varicosities into the adrenal medulla. Chromaffin cells express Phenylethanolamine N-methyltransferase. NA converted to adrenaline in the cell.

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17
Q

What is the rate determining step in the synthesis of noradrenaline?

A

Conversion of tyrosine. Rate of tyrosine hydroxylase is limiting.

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18
Q

What triggers NA release?

A

Depolarisation at the nerve terminal.

Calcium influx and vesicle migration to the presynaptic membrane.

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19
Q

How is the noradrenergic signal transmitted?

A

NA release from presynaptic axon. NA binds to pre and postsynaptic receptors.

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20
Q

How is the noradrenergic signal terminated?

A

High affinity uptake 1 rapidly removes NA from the cleft. Any leftover NA is taken up by the low affinity uptake 2

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21
Q

What is NA metabolised by?

A

MAO - Monoamine oxidases

COMT - Catechol O-methyltransferase

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22
Q

How can synthesis of NA in the CNS be interrupted?

A

Application of alpha-methyltyrosine. Competitive inhibitor of Tyrosine hydroxylase.

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23
Q

Other than alpha-methyltyrosine, what else can be used to inhibit NA synthesis in peripheral neurones?

A

Carbidopa. DOPA decarboxylase inhibitor.

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24
Q

Why can’t Carbidopa be used to inhibit NA synthesis in CNS?

A

Can’t cross the blood-brain barrier.

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25
What effect does alpha-methyldopa have on noradrenergic signalling?
Acts as a false substrate. Poor metabolisation lets it linger longer and accumulate. Acts as a false transmitter. Occupies presynaptic alpha2-adrenergic receptors which reduces neurotransmitter release.
26
What effect does 6-hydroxydopamine have on noradrenergic signalling?
Destroys adrenergic terminals.
27
What effect does reserpine have on noradrenergic signalling?
Blocks NA uptake into vesicles. Causes NA depletion in neurons.
28
What are adrenergic blocking drugs used for? Give an example.
Local anaesthesia. Guanethidine.
29
How does guanethidine cause local anaesthesia?
Partially block reuptake of NA causing depletion of NA from vesicles.
30
Name 3 sympathomimetic agents that act indirectly on neuro-effector junctions.
Tyramine Amphetamine Ephedrine
31
How do sympathomimetic agents perform their function?
Taken up into synaptic vesicles. Cause leaking of NA. NA leaks into cleft without electrical stimulation.
32
Give 2 examples of uptake 1 inhibitors.
Amitriptyline | Imipramine
33
What is the site of action of uptake 1 inhibitors?
CNS.
34
What is the function of presynaptic receptors?
Inhibitory autoreception. Decrease NA release from the terminal
35
What type of receptor is the presynaptic NA receptor?
Alpha2-adrenoceptir. A Gi/o-protein coupled receptor.
36
How do alpha2-adrenoceptors decrease NA release?
The GPCR decreases adenylyl cyclase activity. Decrease calcium VGC opening.
37
What is the basis of adrenoceptor classification?
Agonist potency ranking.
38
What is the agonist potency order of alpha-adrenoceptors?
Adrenaline>Noradrenaline>Isoprenaline
39
What is the agonist potency order of beta-adrenoceptors?
Isoprenaline>Adrenaline>Noradrenaline
40
What effect does activation of alpha-adrenoceptors have?
Arterial vasoconstriction.
41
What effect does activation of beta-adrenoceptors have?
Atrial contraction.
42
Name a selective antagonist for alpha adrenoceptors.
Phentolamine
43
Name a selective antagonist of beta-adrenoceptors.
Propanolol
44
What are the subclasses of Alpha1 adrenoceptors?
Alpha1A Alpha1B Alpha1D
45
What is the specific function of Alpha 1 adrenoceptors?
Vasoconstriction of non-essential blood vessels.
46
How do Alpha1 adrenoreceptors perform their function?
Couple positively with PLC via a Gq/11-proteins.
47
What are the subclasses of Alpha2 adrenoceptors?
Alpha2A Alpha2B Alpha2C
48
How do Alpha2 adrenoceptors perform their function?
Couple negatively with adenylyl cyclase via Gi/o-proteins.
49
What are the subtypes of beta adrenoceptors?
Beta1 Beta2 Beta3
50
What is the function of Beta1 adrenoceptors?
Cardiac contraction | Lipolysis (together with Beta3)
51
What are the chronotropic effects of Beta1 receptors?
Regulation of rate of contraction/dilation of cardiac muscles.
52
What are the ionotropic effects of Beta1 receptors?
Regulation of force of contraction/dilation of cardiac muscles.
53
How can the effects of Beta1 adrenoceptors be strengthened?
Sympathetically released blood-borne adrenaline.
54
Name a selective agonist for Beta1 adrenoceptors.
Dobutamine.
55
What are the Beta2-adrenoceptors responsible for?
Bronchodilation | Dilation of blood vessels in exercising muscles and airways
56
What type of cell surface receptor are Beta-adrenoceptors?
GsPCR
57
Describe the structure of adrenoceptors.
7TM terminals Ligand binding pocket between domains GPCRs
58
Which adrenoceptor agonists are used for treatment of cardiovascular diseases?
Isoprenaline Adrenaline Dobutamine
59
Which cardiovascular diseases can be treated using adrenoceptor agonists?
Heart failure Cardiac arrest Heart block
60
Which adrenoceptor agonists are used for theatment of respiratory diseases?
Salbutamol | Terbutaline
61
Which respiratory diseases can be treated using adrenoceptor agonists?
Bronchoconstriction/asthma
62
Which anaphylactic reactions can be treated with adrenoceptor agonists?
Type 1 Hypersensitivity
63
Which adrenoceptor agonists can be used to treat anaphylactic reactions?
Adrenaline
64
Which Alpha1-adrenoceptor antagonists can be used to treat cardiovascular hypertension?
Prazosin | Doxazosin
65
Which Beta-adrenoceptor antagonists can be used to treat cardiovascular diseases?
Propanolol | Atenolol
66
Which cardiovascular disorders can be treated with beta-adrenoceptor antagonists?
Hypertension Angina Pectoris Cardiac disrhythmia
67
Which Beta-blockers are used to treat glaucoma?
Timolol
68
What are beta-blockers?
beta-adrenoceptor antagonists.
69
Which Beta-blockers are used for treatment of benign essential tremors?
Alaprenolol | Oxprenolol
70
Give examples of the common respiratory diseases.
Bronchitis Chronic obstructive pulmonary disease Adult respiratory distress syndrome Bronchial asthma
71
What are the common stimuli that trigger asthma?
Cold air Exercise Pollen House dust
72
What is the physiological cause of asthma?
Chronic smooth muscle hyper-responsiveness. Inflammation causes the muscle to be more sensitive to stimuli.
73
What are the permanent effects that may be caused by asthma?
Hypertrophy - increase in muscle tissue volume. | Hyperplasia (increase in number of cells) of smooth muscle
74
Describe the events that occur during an asthma attack's immediate phase.
Stimulus acts on Immunoglobin E (IgE) mast cells to release spasmogens and chemotaxins. Spasmogens cause a bronchospasm leading to an asthma attack.
75
What are the mediators released in immediate phase of an asthma attack?
``` Spasmogens: cysLTB4 - Cysteine Leukotriene B4 Hydrogen PGD2 - Prostaglandin 2 Other: Interleukine-4 Interleukine-5 Interleukine-13 Macrophage inflammatory protein 1alpha Tumour necrosis factor alpha ```
76
What reverses the bronchospasm?
Beta2-adrenoceptor antagonists cysLT receptor antagonists Theophyline
77
What chemicals is bronchospasm initiated by?
ACh Histamine Leukotrienes
78
What is the role of chemotaxins/chemokines during an asthma attack?
Attracting leukocytes into the affected area. Prompting Th2 cells to release cytokines. Activation of eosinophils. Setting the stage for late phase of the attack.
79
What are eosinophils?
Inflammatory cells.
80
What is chemotaxin release inhibited by?
Glucocorticoids
81
Describe the events of the late phase of an asthma attack.
A continuation of the early phase. Th2 cells are infiltrated by chemokines and cytokines. Th2 cells release cytokines. Activation of eosinophils by chemokines/cytokines causing release of cysLTs, interleukins and toxic proteins. Release of the mediators causes airway inflammation and hyper-activity. Leads to bronchospasm, wheezing and coughing.
82
Which interleukins are released during late phase of asthma attack?
IL-3 IL-5 IL-8
83
Name the toxic proteins released from eosinophils during the late stage of asthma attack.
Eosinophil cationic protein (ECP) Eosinophil major basic protein (EMBP) Eosinophil-derived neurotoxin
84
What is the effect of toxic proteins released during late phase asthma attack?
Epithelial damage.
85
What inhibits the late phase of asthma attack?
Glucocorticoids
86
Why is asthma treated prophylactically?
To prevent/reduce inflammation
87
What therapeutics are used in prophylactic treatment of asthma? Give examples.
``` Corticosteroids: Beclomethasone (Asmabec) Fluticasone (Flixotide) Non steroidal: Cromoglycate Nedocromil ```
88
What are the consequences of corticosteroid overdose?
Cushing's syndrome.
89
Describe the symptoms of Cushing's syndrome.
``` Thin skin Oedema Poor wound healing Obesity due to increased apetite Osteoporosis ```
90
How has the risk of developing Cushing's syndrome been reduced?
Invention of fluticasone. Poor systemic absorbance means it is less likely to enter bloodstream First pass metabolism. If fluticasone does enter blood, it will be renally excreted after a single kidney filtration.
91
How do non-steroidal drugs prevent asthma attacks?
Prevent release of chemicals from mast cells.
92
Which pharmaceuticals are used for symptomatic relief of asthma?
Salbutamol (Ventolin) Terbutaline (Bricanyl) Salmeterol (Serevent)
93
How is symptomatic relief from asthma achieved?
Reversing bronchoconstriction with Beta2-adrenoceptor agonists (cause bronchodilation)
94
What is FEV1?
Forced Expiratory Volume in 1 second
95
How is FEV1 affected during an asthma attack?
Reduced within minutes
96
Why are Beta2-adrenoceptor antagonists effective in treating the symptoms of asthma?
Relax bronchoconstriction irrespective of cause. Inhibit mucous secretion to free up airways further Stimulat mucous clearance Decrease swelling (oedema) May have an anti-inflammatory effect
97
Could Beta2-adrenoceptors be used as anti-inflammatory drugs?
No, they may have such function but there are therapeutics devoted to anti-inflammatory action
98
How do ACh/Histamine/LTs elicit muscle contraction?
Interact with GPCRs of smooth muscle. Cause calcium influx (GqPCR?). Leads to Calcium/calmodulin dependent activation of Myosin Light Chain Kinase (MLCK) Causes myosin phosphorylation which induces muscle contraction.
99
How do Beta2-adrenoceptor agonists cause bronchodilation?
Via GPCR activation. Leads to activation of adenylyl cyclase hence increased cAMP production (GsPCR?) Leads to decrease in intracellular calcium via activation of efflux and inhibition of influx. Inhibition of myosin phosphorylation via MLCK. Promotion of myosin dephosphorylation. Leads to relaxation of muscle.
100
Which Beta2-adrenergic agonists give a longer-lasting prophylactic action against bronchospasm?
Salmeterol | Formoterol
101
In what instance may Salbutamol be used over Salmeterol to treat asthma?
During an acute attack. Salbutamol is fast acting.
102
In what instance may Salmeterol be used over Salbutamol to treat asthma?
In prophylaxis. Salmeterol is active for 12-18h (2x to 6x longer)
103
What is a LABA? Give examples.
Salmeterol | Formoterol
104
What physical property of LABAs give them a longer lasting action?
Long hydrophilic tail acts as a leash to stay close to the Beta2-adrenoceptor.
105
What are the common therapies used to treat asthma? Give examples.
``` Inhalation of Beta-adrenoceptor agonists e.g.:Formoterol, Terbulatine Inhalation of corticosteroids e.g.:Budesonide, Beclometasone Inhalation of LABA+Corticosteroid e.g.:Salmeterol+Fluticasone (Seretide) ```
106
What are the less common approaches of treating asthma? Give examples.
``` Muscarinic receptor antagonists e.g.:Ipratropium, Tiotropium Leukotriene receptor antagonists e.g.: Zafirlukast Anti-IgE antibody e.g.:Omalizumab ```
107
What are the 5 possible outcomes of drug use?
``` Cure Cessation Reduction Symptomatic relief Aggravation ```
108
What are the properties of a good drug target?
Association with the disease Expression of proteins specific to the site/organ Drugability
109
What are common drug targets? Give examples.
``` Proteins with an active site DNA Adhesion molecules GPCRs Ion channels Enzymes ```
110
Which drug targets are used as a last resort and why?
Antibodies - Used when protein can't be modulated by smaller molecules siRNA - Reduce expression of the prefered drug target.

Physiology and Pharmacology I (5 decks)

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