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pharmacology > adrenergic pharmacology > Flashcards

adrenergic pharmacology Flashcards

adrenoreceptors and the effects they mediate

1
Q

what neurotransmitter does post ganglionic sympathetic neurones release to sweat glands and what receptors do these neurotransmitters bind to

A
  • release acetylcholine
  • bind to muscarinic cholinergic receptors
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2
Q

what is the common neurotransmitter released by post ganglionic neurone of the parasympathetic nervous system

A
  • noradrenaline which binds to adrenergic receptors
  • sometimes release ATP as a co-transmitter along side with NA
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3
Q

what is unique about the adrenal medulla in sympathetic nervous system

A
  • there’s no post ganglionic neurone
  • pre ganglionic neurone directly innervates adrenal medulla
  • releases Ach and binds to nicotinic cholinergic receptors
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4
Q

what is the synthetic pathway of catecholamines

A
  • tyrosine
  • L-DOPA
  • dopamine
  • noradrenaline
  • adrenaline
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5
Q

what are the different groups of adrenoreceptors

A
  • alpha (alpha 1,2)
  • beta (beta 1,2,3)
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6
Q

what adrenoreceptors does adrenaline bind to

A
  • alpha 1,2 and beta 1,2
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7
Q

what adrenoreceptors does noradrenaline bind to

A
  • alpha 1,2 and beta 1,3
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8
Q

what adrenoreceptors does isoprenaline

A
  • beta 1,2,3
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9
Q

what type of G protein is alpha 1 adrenoreceptor

A
  • Gq/11- so activates phospholipase c which increases synthesis of IP3 and DAG
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10
Q

What type of G protein is alpha 2 adrenoreceptor

A
  • Gi/o- inhibits activation of adenylate cyclase meaning decreased synthesis of cAMP
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11
Q

what type of G protein is beta 1,2 adrenergic receptor

A

Gs- activates adenylate cyclase increasing synthesis of cAMP

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12
Q

what type of G protein is beta 3 receptor

A
  • can either be Gs or Gi/o
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13
Q

where is alpha 1 adrenergic receptors found and what is their roles

A
  • alpha 1 adrenergic receptors found on smooth muscle of blood vessels
  • activates phospholipase c which increases synthesis of IP3 and DAG
  • IP3 binds IP3 receptors which causes influx of calcium ions leading to smooth muscle contraction leading to vasoconstriction and therefore increasing in blood pressure
  • Noradrenaline is released by the presynaptic neurone and binds to the receptor
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14
Q

where is alpha 2 adrenergic receptors found and what is its role

A
  • can be auto receptors or hetero receptors
  • can be found on presynaptic neurone and binding of noradrenaline can inhibit release of further neurotransmitter
  • can be also found post junction on smooth muscle leading to vasoconstriction, on platelets leading to platelet aggregation and on beta pancreatic cells leading to inhibition of the release of insulin
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15
Q

where is beta 1 adrenergic receptors found and what can it cause

A
  • mainly found In heart and kidneys
  • binding of noradrenaline in heart can cause positive chronotropic (increased heart rate) and positive inotropic (increased contractility)
  • can also be found on juxtaglomerular cells in kidneys causing releases of renin (enzyme used in blood pressure maintenance)
  • can be found in white adipose tissue which leads to lipolysis
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16
Q

where are beta 2 adrenergic receptors found and their role

A
  • found in lungs cause dilation of muscle and relieve bronchospasm
  • skeletal muscle vasculature which can cause vasodilation
  • white adipose tissue- lipolysis
  • glycogenolysis of glycogen stores in liver and skeletal muscle
  • increase release of insulin from pancreas
  • uterine smooth muscle relaxation
17
Q

where are beta 3 adrenergic receptors found and their roles

A
  • found in brown adipose tissue for lipolysis and thermogenesis
  • endothelial cells of blood vessels triggering release of NO which diffuses in muscle cells and cause vasodilation
  • relaxation of smooth muscle of bladder- for over active bladder
18
Q

what is a non selective drug that binds to adrenoreceptors

A
  • adrenaline binds to adrenergic receptors
  • effects include bp maintenance, bronchodilation, skeletal muscle tremor, mast cell stabilisation
  • bp- low levels cause vasodilation high levels cause vasoconstriction
  • mast cell stabilisation= inhibit mast cell degranulation due to increases in cAMP which reduce calcium ion mobilisation which reduce release of prostaglandins, leukotrienes, histamines and cytokines
  • clinical uses include anaphylactic shock, cardiac arrest and prolonging anaesthesia
19
Q

how is adrenaline used for anaphylactic reaction

A
  • histamines and other mediators make blood vessels permeable causing fluid to build up leading to hypotension, larygeal oedema
  • bronchodilation by binding to beta 2 receptors
  • binding to alpha 1,2 receptors clause vasoconstriction and decreased permeability of vessels
20
Q

what are some selective alpha 1 agonsists

A
  • noradrenaline- used for circulatory shock- causes vasoconstriction, decreased permability
  • methoxamine, phenylephrine used for nasal decongestion by causing vasoconstriction of blood vessels going to the nasal mucousa this reduces blood flow and therefore swelling and inflammation which causes congestion
21
Q

what are some alpha 2 agonists

A
  • brimonidine- for glaucoma
  • dexmedetomidine- sedation and anaesthesia
  • clonidine- anti hypertension (noradrenaline binds to presynaptic alpha 2 receptors which inhibit release of noradrenaline so less vasoconstriction)
22
Q

what is the mechanisms of brimonidine

A
  • used to treat glaucoma
  • a eye conditions caused by reduced flow of aqueous humour leading to increased intraocular pressure resulting in damage to optic nerve
  • brimodine binds to presynaptic alpha 2 receptors inhibitig release of noradrenaline, results in decreased production of aqueous humour, less intraocular pressure
23
Q

what is the mechanism for dexmedetomidine

A
  • used for sedation and analgesia
  • binds to presynaptic alpha 2 receptor inhibiting release of NA
  • also binds to alpha 2 receptors found on other neurone which causes hyperpolarisation of neurone and reduced excitatory effect
24
Q

what are ergot alkaloids, where are they derived and what do they target

A
  • derived from fungus, naturally occurring
  • can be partial agonists (at low doses) or antagonists at high doses
  • can bind to adrenergic receptors, dopamine receptors, serotonin receptors
  • historically used but not as widely used clinically now
25
Q

what are examples of ergot alkaloids which act as alpha 1 agonists

A
  • ergometrine- used for postpartum haemorrahage causes uterus muscle contraction
  • ergotamine for migraines (causes vasoconstriction of blood vessels)
  • dihydroergotamine has a higher efficacy but less vasoconstriction
26
Q

what is an example of a beta 1 agonist

A
  • dobutamine- cardiac inotrope (increase contractility of heart)
27
Q

what is an example of beta 2 agonist

A
  • salbutamol- bronchodilation for asthma
28
Q

what is an example of beta 3 agonist

A
  • linabegron - for overactive bladder and anti-obesity
29
Q

how can adrenergic receptors affect potassium levels in blood

A
  • activation of beta 2 adrenoreceptors cause increased pottasium uptake and decreased potassium levels in blood resulting in hypokalaemia
  • activation of alpha 1 adrenoreceptors cause increasing potassium levels in blood causing hyperkalaemia
30
Q

what is the effect of adrenaline of potassium levels in blood

A
  • initial acute hyperakalemia followed by sustained hypokalaemia
31
Q

what is the effect of salbutamol on potassium levels in blood

A
  • high doses can cause hypokalaemia
32
Q

how can we increase transmitter release by inhibition of..

A
  • pre synaptic reuptake
  • noradrenaline metabolism
33
Q

what are examples of uptake blockers

A
  • cocaine- uptake inhibitor for dopamine, noradrenaline and serotonine
  • tricyclic antidepressants- serotonine and noradrenaline
  • reboxetine- noradrenaline
34
Q

what are MOA inbitors and how are the classified

A
  • monoamine oxidase inhibitors inhibit enzyme monoamine oxidase which is an enzyme used to breakdown monoamines
  • can be divided into MOA-A inhibit break down of NA, DA, 5HT3, tyramine
  • MOA-B inhibit breakdown of DA, tyramine
35
Q

what is an example of an irreversible non selective monamine inhibitor

A
  • phenelzine- causes the cheese reaction as it means the tyramine we obtain from food (cheese) is not broken down in the gi tract this causes tyramine to enter the blood leading to more noradrenaline being produced resulting in hypertension
36
Q

what is an example of a reversible MOA-A inhibitor which reduce the ‘cheese reaction’

A

moclobemide

37
Q

what are some examples of indirectly acting sympathomimetic amines which don’t bind to adrenergic receptors but enhance the action of sympathetic nervous system

A
  • tyramine
  • amphetamine
  • ephedrine

pharmacology (4 decks)

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