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Blood and Drugs > D6 & D7 - ANS > Flashcards

D6 & D7 - ANS Flashcards

1
Q

Parasympathetic nervous system

A
  • connects to the CNS via 2 cholinergic nerves - meaning they synthesise, store and release acetyl choline
  • pre ganglionic nerve in the CNS from cranial or sacral nerves
  • post ganglionic nerve - in the autonomic ganglion
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2
Q

Sympathetic nervous system

A
  • pre ganglionic nerve is a cholinergic nerve
  • post ganglionic nerves: most are adrenergic and some are cholinergic
  • some nerves pass directly through the paravertebral ganglia without synapsing, and do directly to the adrenal medulla - which is stimulated to release adrenaline and noradrenaline into the blood stream which binds to adrenoceptors on cardiac, smooth muscle or exocrine glandular cells
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3
Q

Adrenergic nerves

A

release noradrenaline

- most sympathetic post ganglionic nerves

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4
Q

Cholinergic nerves

A
  • release acetyl choline
  • some sympathetic post ganglionic nerves
  • all parasympathetic post ganglionic nerves
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5
Q

Cholinoceptors

A

2 types

  • nicotinic - ion channel
  • muscarinic - g protein linked coupled receptor
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6
Q

Muscarinic receptors

A
  • 5 subtypes
  • M2 - expressed mainly on cardiac cells, causes decrease in heart rate when activated by acetyl choline
  • M3 - smooth muscle and glandular cells, smooth muscle contraction and glandular secretion
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7
Q

Mascarinic receptors are stimulated by

A

Acetyl choline

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8
Q

Nicotinic receptors are stimulated by

A

Acetyl choline

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9
Q

adrenergic nerves

A
  • release noradrenaline which bind to adrenoceptors

- exist alpha and beta

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10
Q

alpha adrenoceptors

A 
- Alpha
		○ A1
			§ Vascular smooth muscle cells 
			§ Noradrenaline and adrenaline will target to promote contraction 
			§ Vasoconstriction
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11
Q

beta adrenoceptors

A 
- Beta 
		○ B1
			§ Expressed on heart 
			§ Increase in heart rate 
			§ Increases force of contraction 
		○ B2
			§ Present on smooth muscle cells 
			§ Vascular smooth muscle cell relaxation - also in airways and uterus
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12
Q

Modulating activity of end effect

A
  1. Increase/decrease levels of neurotransmitters
    1. Mimic the actions of neurotransmitter - use drugs that activate receptors
    2. Inhibit the actions of neurotransmitter - use drugs that inhibit receptors
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13
Q

Adrenoceptor Agonists

A
  • Bind to and activate adrenoceptors
    • Endogenous compounds eg. adrenaline and noradrenaline - adrenoceptor agonists
    • Drugs can also do this
      ○ Phenylephrine
      ○ Salbutamol
    • Also called Sympathomimetics/adrenomimetics - adrenoceptor agonists
    • Target one or more of 5b subtypes of adrenoceptor
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14
Q

2 adrenoceptor agonists

A

adrenaline, noradrenaline

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15
Q

Adrenaline

A

○ Hormone and drug
○ Stimulate all of the adrenoceptor subtypes
○ Limitation
§ Inactive orally
□ Extensively metabolised in gut and liver by enzymes
□ Inactivate the compound - can no longer bind to and activate adrenoceptors
§ Typically given by injection in settings where blood pressure and ECG can be monitored

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16
Q

adrenaline local infection

A

§ Dose dependant
□ At low doses, adrenaline binds to high affinity B2 on vascular smooth muscle - relaxation - mostly vasodilator effect
□ Increase concentration - binds to low affinity A1 - mostly vasoconstrictive effect
□ Because it has a higher affinity for B2 than A1
§ Net effect - at high concentrations, predominantly vasoconstrictive, but at low doses - vasodilatory effect
§ No adrenaline - status quo maintained
§ Local injection
□ Delivering initially high concentration locally
® Vasoconstriction
□ As it is metabolised
® Dose decreased
® Vasodilation

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17
Q

adrenaline instravascular injection

A

§ Effects on cardiovascular system
□ When adrenaline is injected, the net effect is dependant upon
® Dose
® Rate of administration
□ Intravenous infusion
® Delivering adrenaline at a constant rate into the blood stream
® Starting
◊ Increase in heart rate
} Adrenaline will activate B1 - cause heart rate increase
◊ Associated with an increase in systolic blood pressure - also stimulated B1 receptors that cause heart muscle to constrict more strongly
◊ No change in mean arterial blood pressure
} Increase in systolic blood pressure is counteracted by a decrease in diastolic pressure
– Decrease in diastolic is because when given as IV infusion - decreases total peripheral resistance
– Because adrenaline is activating B2 receptors causing vasodilation in skeletal muscle - will override
– constriction effect in other parts of the body

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18
Q

adrenaline slow bolus injection

A

§ Large amount of adrenaline directly into blood vessels
§ Dose will decrease with time as adrenaline is metabolised and redistributed
§ Effects on heart rate and blood pressure and total peripheral resistance are more complex
§ Delivering high concentration
§ Predominant effect is alpha adrenoceptor mediated vasoconstriction
§ Associated with an increase in total peripheral resistance
□ Will cause an Increase is diastolic blood pressure
§ Increase in mean arterial blood pressure because the systolic blood pressure is also increased - because adrenaline is stimulating cells in the heart to constrict more strongly
§ Heart does not beat more quickly
□ Because Increase in mean arterial blood pressure causes reflex release of acetyl choline to decrease heart rate to counteract increase in mean arterial blood pressure
§ Lower concentrations of adrenaline over time
□ Vasodilator effect - by B2 adrenoceptors
® Decrease in TPR
® Decrease in diastolic blood pressure
® Return mean arterial blood pressure to normal
□ Direct effects of adrenaline on heart rate
® Increase

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19
Q

clinical uses of adrenaline

A

○ Related to effects on blood vessels, heart, other smooth muscle
○ Adrenaline added to local anaesthetic
§ prolong action and delay systemic absorption of local anaesthetics
§ Especially in dentistry
§ Causes constriction to localise the anaesthetic in the region
○ Used in cardiac arrest
§ Helps to restore cardiac rhythm
§ Increase TPR during resuscitation
§ In the community
□ Better to use deregulator and CPR
□ Adrenaline can only be given in a hospital situation
○ Treatment of Acute anaphylactic reaction
§ Massive release of histamine
□ Causes constriction of the airways
§ Adrenaline relaxes airways by targeting B2 receptors on smooth muscle
§ Inhibits mast cell degranulation

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20
Q

○ Adrenaline added to local anaesthetic

A

§ prolong action and delay systemic absorption of local anaesthetics
§ Especially in dentistry
§ Causes constriction to localise the anaesthetic in the region

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21
Q

○ Used in cardiac arrest

A 
§ Helps to restore cardiac rhythm 
			§ Increase TPR during resuscitation
			§ In the community 
				□ Better to use deregulator and CPR 
				□ Adrenaline can only be given in a hospital situation
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22
Q

○ Treatment of Acute anaphylactic reaction

A

§ Massive release of histamine
□ Causes constriction of the airways
§ Adrenaline relaxes airways by targeting B2 receptors on smooth muscle
§ Inhibits mast cell degranulation

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23
Q

Noradrenaline

A

○ Not the same as adrenaline
○ Nor is also not active orally due to extensive metabolism in the gut and liver
○ Adrenaline activates all 5 adrenoceptor subtypes
○ Nor can do most of them but not B2 adrenoceptor
○ Nor does not cause vasodilatation in (esp. in skeletal muscle vascular beds)

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24
Q

Slow IV infusion Noradrenaline

A

§ Mainly - increase in TPR
□ Activate A1 adrenoceptor and cause them to constrict and increase TPR
□ No B2 mediated vasodilator effect
§ Increase in diastolic and systolic blood pressure
§ Increase in mean arterial blood pressure
§ slowing of heart rate (again due to mediated reflexes)
§ Noradrenaline increases mean arterial blood pressure
□ Used to correct acute hypotension in septic shock where there is significant hypotension
□ Infusion of nor
§

25
Q

Selective Adrenoceptor Agonists

A
  • Fewer side effects
    • Developed to be effective orally - don’t undergo metabolism in the gut and liver
    • Phenylephrine - binds to and activates A1 adrenoceptor
    • Salbutamol - activates B2 adrenoceptor
26
Q

2 selective adrenoceptor agonists

A

phenylephrine, salbutamol

27
Q

Phenylephrine

A

○ Selective alpha 1 adrenoceptor agonists
○ Only difference from adrenaline is it lacks a hydroxyl group at the 4 position
○ Binds selectively to A1 - not to other adrenoceptors
○ Predominantly on vascular smooth muscle cells
○ Primarily produces vasoconstriction
○ Used clinically for relief of nasal congestion associated with acute and chronic rhinitis
§ Eg. Sudafed
§ Given orally or topically drops/spray

28
Q

Salbutamol

A

○ Only binds effectively to B2
§ Has a bulky butyl group - creates steric hindrance - it doesn’t fit in the other receptors
○ Selectively
○ B2 on smooth muscle - airway, uterine, vascular
○ Relaxation of smooth muscle
○ Clinically to relieve bronchoconstriction and asthma
§ Ventolin inhalers
○ Topical - aerosol to site of action
○ Given topically directly to site of action because
§ rapid response
§ low overall dose needed
○ Safe
○ Only side effect is skeletal muscle tremor - goes away with continued use

29
Q

Adrenoceptors Antagonists

A

• Antagonists
• Prevent adrenaline or noradrenaline from binding to and activating their adrenoceptors
• Antagonists occupies receptors without activating it which causes reduced binding/activation
• Antagonism of A1 and B1 may be clinically useful
• A2 and B2 is not clinically useful
○ Associated with adverse side effects
• A1 - hypertension
• B1 - many cardiovascular diseases

30
Q

3 adrenoceptor antagonists

A

prazocin, propanolol, metoprolol

31
Q

Prazosin

A

○ Inhibits A1 receptor
○ 5000x higher affinity for this receptor than the A2 - very selective
○ Doesn’t block A2 adrenoceptor
○ Vascular smooth muscle cells
○ Reverse alpha adrenoceptor mediated contraction of vascular smooth muscle
§ Vasodilator effect
§ Lowers blood pressure
○ Anti hypertension
§ No longer a first line treatment for hypertension
□ Exist Better drugs with fewer side effects
□ Causes dizziness when first administered
□ On standing
□ Postural hypotension
□ Most evident when initially used and In the elderly
□ Solutions
® Make initial dose lower
® Administer drugs when postural hypotension is less of an issue
◊ Before going to bed
○ Also used to reverse alpha adrenoceptor mediated contraction of prostatic smooth muscle
§ Alpha adrenoceptors on the prostate are a slightly different sub type
§ This sub type is better targeted with Tamsulocin than Prazocin
§ By blocking prostatic smooth muscle contraction - improved urine flow in men with benign prostatic hypertrophy

32
Q

Propranolol

A

○ First
○ Treats angina and arrythmias
○ Also reduces blood pressure and increase survival in those who have had a myocardial infarction
○ Non selective b adrenoceptor antagonist
○ Binds beta 1 and 2
○ Cant tell the difference between B1 and B2
○ By inhibiting B1
§ Decrease heart rate and contractility
§ Decrease blood pressure
§ Management of angina, arrythmias, hypertension, post-myocardial infarction
○ By inhibiting B2
§ May exacerbate bronchoconstriction on patients with asthma
□ Because B2 mediates bronchodilatation
§ Impair circulation in peripheral arterial disease
§ Worsen glycaemic control in diabetes
○ Adverse side effects for patients with co morbidities

33
Q

propanolol inhibiting B1

A

○ By inhibiting B1
§ Decrease heart rate and contractility
§ Decrease blood pressure
§ Management of angina, arrythmias, hypertension, post-myocardial infarction

34
Q

propanolol inhibiting B2

A

○ By inhibiting B2
§ May exacerbate bronchoconstriction on patients with asthma
□ Because B2 mediates bronchodilatation
§ Impair circulation in peripheral arterial disease
§ Worsen glycaemic control in diabetes
○ Adverse side effects for patients with co morbidities

35
Q

metprolol

A

○ Selectively binds B1
○ Higher affinity for B1
○ Reverse B1 mediated increases in heart rate and contractility
§ Reduce cardiac output and lower blood pressure
○ Useful in management of cardiovascular diseases
○ Doesn’t block B2 at safe doses - lower affinity
○ Doesn’t harm patients with co morbidities - asthma, diabetes, peripheral vascular disease
○ Selectivity for B1 is not absolute - increasing dose will cause binding to B2
○ Should be used with caution in patients that cant have B2 blockage

36
Q

Beta Blockers

A

○ Decrease heart rate and contractility - binding to B1
○ Many beta blockers have other desirable pharmacodynamic actions
○ Some have vasodilatory activity - useful for hypertension
§ Labetalol
□ Beta blocker that also blocks alpha receptors
□ Causes vasodilation
§ Celiprolol
□ Blocks B1 but partial agonist for B2 - vasodilation
§ Nebivolol
□ Blocks B1
□ Releases NO which is a vasodilator

37
Q

Cholinoceptor Agonists

A
  • Mostly those targeting M3 subtype
    ○ Muscle contraction and glandular secretion
    • Available drugs lack selectivity
      ○ Will also bind to M1 and M2 receptors and have adverse effects
      ○ Some may also activate nicotinic receptors - widespread effects
    • Limited number of drugs used clinically to
      ○ Activate muscarinic cholinoceptors
      § Pilocarpine
      ○ Block muscarinic cholinoceptors
      § Atropine, tiotropium, solifenacin
38
Q

cholinoceptor agonists - low selectivity

A

○ Very few agonists used clinically due to low selectivity
§ Activate multiple subtypes of nicotinic and muscarinic receptors
§ Also activate nicotinic receptors - widespread effects
○ Limit side effects by
§ administering topically to site of action - to only activate receptors in the vicinity of the drug

39
Q

1 cholinoceptor agonist

A

pilocarpine

40
Q

Pilocarpine

A

○ Muscarinic cholinoceptor agonist
○ Given topically to the eye in the form of eye drops
○ Less systemic actions
○ Activate M3 receptors on constrictor pupillae muscle
§ Constrict pupil
§ Promotes drainage of aqueous humour from the eye
§ Reduced intraocular pressure
○ Used clinically to treat glaucoma
§ A condition of the eye associated with increase intraocular pressure
○ There now exist better drugs
§ No longer first or second line treatment
§ Beta adrenoceptor antagonist and prostaglandin analogues

41
Q

4 Cholinoceptor Antagonists

A

atropine, tiotropium, tropicamide, solifenacin

42
Q

Atropine

A

○ Non-selective beta adrenoceptor antagonist
○ Naturally occurring substance discovered in a plant
§ Atropa belladonna
§ Has black berries that contain atropine
○ Block all muscarinic cholinoceptor subtypes
§ Dries up secretions - saliva, sweat, tears, gut and lung
§ Inhibits smooth muscle contraction (gut, lungs, eye)
§ Increases heart rate (M2)
○ Crosses into CNS to block muscarinic receptors producing excitatory effects
§ Hyperactivity and body temp
§ Restlessness
§ Difficult to have organ selectivity, causes side effects which limits clinical uses
§ Crosses blood brain barrier
○ Used to treat poisoning with anticholinesterase agents (pesticides, war gases)

43
Q

Tiotropium

A

○ Better selectivity and side effect profile than atropine
○ Used for chronic obstructive pulmonary disease COPD
○ Used in asthma
○ Dilates airway smooth muscle
○ Reduce mucous secretion
○ Given by aerosol - delivers drug directly to the site of action
§ Cant affect the CNS because it has positively charged nitrogen so it cant cross the blood brain barrier (unlike atropine - no CNS effects)
○ Some selectivity for M3
§ Less cardiovascular effects
○ Good side effect profile - better selectivity
○ Long duration of action
§ Used for maintenance therapy - given just once daily
§ Doesn’t produce rapid reversal of bronchoconstriction - not a reliever medication in an asthma attack

44
Q

Tropicamide

A

○ Quick acting muscarinic cholinoceptor antagonist
○ Used for retinal examination
○ Relaxes ciliary muscle and iris sphincter
○ Given as drops, short duration of action

45
Q

Solifenacin

A

○ Relaxes smooth muscle of bladder to increase bladder capacity - reduces sense of urgency
○ Used for urinary incontinence
○ Administered orally
○ Selectivity for M3, less CNS side effects

46
Q

Drugs that act indirectly by altering levels of neurotransmission

A
  • Some drugs can block the metabolism/removal or neurotransmitters from synaptic region eg. Amphetamine blocks removal of noradrenaline, neostigmine blocks metabolism of acetylcholine
    • Increases synaptic levels of neurotransmitter
    • More activation of receptors and increased response
    Don’t bind to and activate receptors themselves
    ○ Alters level of neurotransmitter
    ○ Act indirectlyMay also increase neurotransmitter levels in other cholinergic or adrenergic synapses
    ○ Cholinergic and adrenergic are not just in the autonomic nervous system
    § Cholinergic nerves innovate skeletal muscle cells in CNS
    § Adrenergic synapses in the CNS
    § Primary use of these drugs relate to Effects somatic and CNS
    § Primary clinical uses relate to effects on the somatic and central nervous systems, effects on the ANS are considered side effects
47
Q

Adrenergic nerves

○ Synthesise store and release noradrenaline

A

○ Synthesise store and release noradrenaline
○ Initial substrate in synthesis is the amino acid tyrosine
§ Taken up by a transporter, decarboxylated and hydroxylated to form dopamine
§ Stored in synaptic vesicles and converted into noradrenaline
§ When nerve is stimulated, noradrenaline is released which binds to and activates adrenoceptors on the post synaptic membrane
§ Has a short half life in synaptic region
□ Taken up by noradrenaline transporter (NAT) which pumps it back up into the cell
□ Some of it will be repackaged, some will undergo metabolism by monoamine oxidase on the surface of mitochondria
§ Rapid uptake is a regulatory process by the CNS to control activity of post synaptic nerve

48
Q

Amphetamine - adrenergic nerves

A

§ Noradrenaline is taken back up by noradrenaline transporter (NAT)
§ Amphetamine also uses this transporter
□ Some amphetamine gets pumped into the vesicles through VMAT (vesicular monoamine transporter) and displaces noradrenaline in the vesicles
□ Breaks down monoaminoxidase MAO
□ Induces elevated levels or noradrenaline
□ Induces reverse operation of noradrenaline transporter NAT - pumps noradrenaline into the synapse instead of back into the nerve
§ Causes vasoconstriction, increase in heart rate and contraction - not used clinically for these effects on ANS
§ Used for effects on CNS in children in ADHD

49
Q

Pseudoephedrine - adrenergic nerves

A

§ Causes noradrenaline increase release from adrenergic nerves
§ Use is constricted - can be converted into methamphetamine
§ Nasal decongestant

50
Q

Cholinergic nerves

A

○ Use acetyl choline
○ Formed by conjugation of acetyl CoA and choline through the action of choline acetyl transferase
○ Acetyl choline is stored in vesicles and released during action potential
○ Acetyl choline in the synapse is hydrolysed by acetyl choline esterase
○ Acetylcholine esterase
§ hydrolyses acetyl choline into choline and acetate which are inactive
§ Rapid inactivation of Ach is the process by which the CNS controls the activity of postsynaptic cells
○ Some drugs inhibit acetylcholine esterase - anticholinesterases
§ Increase levels of acetyl choline in the synapse
§ Accumulates in the synapse and causes increased activation of receptors and larger response

51
Q

Anticholinesterase effects on ANS

A

§ Mimic stimulation of parasympathetic nervous system
□ More glandular secretion, smooth muscle contraction, slowing of heart rate
§ Also inactivates acetyl choline in somatic and central nervous system
□ Effects of drug are widespread and complex

	Anticholinesterase
	3 major groups 
		§ Distinguished on the basis of duration of action
52
Q

i. Long acting

A

□ Days
□ Organophosphate pesticides (dimethoate) and organophosphate war gasses (sarin)
□ Long duration of action - irreversible covalent bond with active side on the enzyme
□ Toxicological relevance
□ Poisoning - people that are exposed typically have
® DUMBBELSS
® Diarrhoea, urination, miosis, bronchorrhea, bronchoconstriction, bradycardia, emesis, lacrimation, salivation/sweating, seizures
□ Killer Bs
® Bronchorrhea, bronchoconstriction, bradycardia
® Producing too much mucous and bronchoconstriction
® Deadly
□ Atropine
® Frontline therapy
® Blocks symptoms mediated my muscarinic cholinoceptors
® Crosses blood brain barrier
® Reduces CNS nervous symptoms

53
Q

Medium and short acting agents

A

Medium and short acting agents
□ Form reversible ionic bonds
□ Clinically useful

			1) Medium acting
			□ neostigmine

			1) Short acting
			□ Edrophonium
54
Q

□ Killer Bs

A

® Bronchorrhea, bronchoconstriction, bradycardia
® Producing too much mucous and bronchoconstriction
® Deadly

55
Q

DUMBBELSS

A

® Diarrhoea, urination, miosis, bronchorrhea, bronchoconstriction, bradycardia, emesis, lacrimation, salivation/sweating, seizures

56
Q

Clinical uses of anticholinesterases

A

Myasthenia gravis
□ Used for action on neuromuscular junction
□ Skeletal muscle weakness - autoimmune disease targeting nicotinic receptors on muscle, causing a reduction in the number of receptors
□ Reduced sensitivity to acetyl choline
□ Overcome by agents increasing acetyl choline in the junction
□ Short acting - edrophonium for diagnosing
® If you give it to them and they get better (increased muscle strength) - diagnose
® Doesn’t cause increase in muscle strength with people who don’t have it
□ Medium -
® neostigmine
◊ Needs injection
◊ Variable/low oral bioavailability
® Pyridostigmine
◊ Orally active
◊ Chronic treatment
◊ Used as a medium acting anti cholinesterase
Other uses of anticholinesterase
□ routinely used to reverse neuromuscular blockage caused by non-depolarising neuromuscular blockers
□ Eg. pancuronium
® Used during general anaesthesia - there will also be a muscle relaxant used
® At the end of the procedure this must be reversed - neostigmine given by IV which outcompetes pancuronium
® Effects of neuromuscular blockers are overcome
Effects on autonomic and CNS from anticholinesterases are unwanted side effects

57
Q

Myasthenia gravis

A

□ Used for action on neuromuscular junction
□ Skeletal muscle weakness - autoimmune disease targeting nicotinic receptors on muscle, causing a reduction in the number of receptors
□ Reduced sensitivity to acetyl choline
□ Overcome by agents increasing acetyl choline in the junction
□ Short acting - edrophonium for diagnosing
® If you give it to them and they get better (increased muscle strength) - diagnose
® Doesn’t cause increase in muscle strength with people who don’t have it
□ Medium -
® neostigmine
◊ Needs injection
◊ Variable/low oral bioavailability
® Pyridostigmine
◊ Orally active
◊ Chronic treatment
◊ Used as a medium acting anti cholinesterase

58
Q

Other uses of anticholinesterase

A

□ routinely used to reverse neuromuscular blockage caused by non-depolarising neuromuscular blockers
□ Eg. pancuronium
® Used during general anaesthesia - there will also be a muscle relaxant used
® At the end of the procedure this must be reversed - neostigmine given by IV which outcompetes pancuronium
® Effects of neuromuscular blockers are overcome
Effects on autonomic and CNS from anticholinesterases are unwanted side effects

Blood and Drugs (29 decks)

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