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PHAR222 > L2 ANS > Flashcards

L2 ANS Flashcards

1
Q

Therapeutic Uses of Cholinesterase Inhibitors for the EYE

A

– constriction of the pupil
– decrease intraocular pressure in open-angle glaucoma
– in cycloplegia
* ciliary muscle contracts, lens thickens, pupil constricts
* eye accommodates for near vision

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2
Q

Therapeutic Uses of Cholinesterase Inhibitors for the Skeletal neuromuscular junction

A

– nicotinic receptors
– reversal of paralysis caused by curare-like drugs
– diagnosis and treatment of myasthenia gravis

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3
Q

Therapeutic Uses of Cholinesterase Inhibitors for the Gastrointestinal system

A

– lack of normal smooth muscle tone or stretch
* lower oesophageal and gastric contraction
* paralytic ileus

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4
Q

Therapeutic Uses of Cholinesterase Inhibitors for the Treatment of atropine poisoning

A

– acute toxicity caused by atropine
* muscarinic antagonist will bind to muscarinic receptors to prevent ACh from binding so that there is more ACh

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5
Q

Long-acting, Irreversible Cholinesterase Inhibitor

A
  • Organophosphates
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6
Q

Organophosphates

A
  • Long acting
  • Irreversible
  • – insecticides and nerve gases
  • Spontaneous hydrolysis of phosphorylated acetylcholinesterase very slow
  • Pralidoxime re-activates phosphorylated acetylcholinesterase if administered before bonding within the enzyme ages
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7
Q

Organophosphates: Risks

A
  • Insecticides – parathion
    – agriculture, horticulture, urban gardening
    – accidental deaths due to poisoning
  • Nerve gases
    – sarin
    – assassination, terrorist attacks
    – deadly at extremely low concentrations
    – toxicity due to increase ACh at cholinergic synapses
    – persistent stimulation -> neurotransmission paralysis
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8
Q

Acute Poisoning with Cholinesterase Inhibitors

A
  • Signs and symptoms due to activation of muscarinic and nicotinic receptors
  • Death may result from respiratory failure following neuromuscular junction blockade in respiratory skeletal muscles
    – bronchoconstriction, accumulation of respiratory secretions, weakened or paralysed respiratory muscles, central respiratory paralysis
    – bradycardia
    – sweating, salivation, lacrimation
    – constriction of the pupils
    – increase gastrointestinal activity (all para)
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9
Q

Cholinesterase Inhibitor Poisoning: Treatment

A
  • Stop exposure to cholinesterase inhibitor to prevent further absorption
  • Assist respiration
  • Administer cholinergic antagonist e.g., atropine
  • Administer pralidoxime in the case of organophosphate poisoning
  • Administer anticonvulsant if required
  • Monitor for potential cardiac irregularities
  • Administer diazepam to treat agitation and provide sedation
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10
Q

Muscarinic Antagonists - Atropine

A
  • Typical competitive muscarinic antagonist
  • Highly soluble belladonna alkaloid from Atropa belladonna (deadly nightshade)
  • Cause pupil enlargment
  • Muscarinic antagonists compete with acetylcholine at the muscarinic receptor
  • Atropine inhibits acetylcholine effect
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11
Q

Major Pharmacological Effects of Muscarinic Antagonists (Atropine)

A
  • ↓ sweating, salivation, lacrimation
  • ↓ gastrointestinal motility
  • ↓ gastric acid secretion
  • ↓ production of bronchial mucus in airways
  • Bronchodilatation
  • ↑ heart rate
  • Side effects
    – dry mouth & skin, urinary retention, cycloplegia, glaucoma, depression, hallucinations, ↑ body temperature
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12
Q

Therapeutic Uses of Muscarinic Antagonist

motion sickness

A

for motion of short duration

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13
Q

Therapeutic Uses of Muscarinic Antagonist

ophthalmology

A

mydriasis and cycloplegia to examine the retina

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14
Q

Therapeutic Uses of Muscarinic Antagonist

acute myocardial infarction

A

bradycardia opposed due to excess vagal tone

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15
Q

Therapeutic Uses of Muscarinic Antagonist

asthma

A

airway tone reduced

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16
Q

Therapeutic Uses of Muscarinic Antagonist

peptic ulcers

A

gastric acid secretion reduced

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17
Q

Therapeutic Uses of Muscarinic Antagonist

irritable bowel

A

spasms reduced

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18
Q

Therapeutic Uses of Muscarinic Antagonist

Parkinson’s disease

A

tremor, involuntary movements, rigidity reduced

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19
Q

Therapeutic Uses of Muscarinic Antagonist

premedication

A

airway mucus secretion decreased

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20
Q

Therapeutic Uses of Muscarinic Antagonist

organophosphate poisoning

A

antidote to poison

21
Q

Treatment of Atropine Poisoning

A
  • Gastric lavage
    – prevent further absorption
  • Cholinesterase inhibitor
    – ↑ ACh at cholinergic synapse by competing
  • Body temperature is lowered
    – counter rise in temperature that happens with atropine
    – CNS effects
    – ↓ sweating
  • Anticonvulsant e.g., diazepam
    – counter CNS effects
22
Q

Noradrenergic Neurotransmission: Noradrenaline

A
  • Primary neurotransmitter released from sympathetic autonomic neurones
  • Sympathomimetic catecholamine
  • Synthesised and stored in sympathetic nerves
  • Released upon electrical excitation of the nerve varicosities
23
Q

Catecholamine Synthesis

A

tyrosin (→neurones)
↓
Dihydroxyphenylalanine (cytosol)
↓
Dopamine (cytosol)
↓
Noradrenaline (vesicle)
↓
Adrenaline (adrenal medulla)

24
Q

Adrenal Medulla: Adrenaline

A
  • Inner portion of adrenal gland that sits above each kidney
  • Synthesises and stores adrenaline – similar struc & func to noradrenaline
  • Modified sympathetic ganglion
    – innervated chromaffin cells contain adrenaline
  • Adrenaline is synthesised from noradrenaline by phenylethanolamine N-methyltransferase
  • Adrenaline is stored in vesicles and released upon electrical stimulation of preganglionic nerves innervating the adrenal gland
25
Q

Structures of Catecholamines

Structural modification of noradrenaline to produce synthetic catecholamines

A

– ↑ bulkiness of substituents on the N-atom
* resistance to monoamine oxidase (MAO)
– modification of catechol –OH groups
* resistance to catechol-O-methyl transferase (COMT)

26
Q

Adrenoceptors: Location and Function APLHA

BV, Lung, GI, eye

A
  • Alpha1-receptors (post-synaptic)
    –bloodvessels: vasoconstriction
    –lung: ↓ secretion
    – GI tract: ↓ smooth muscle motility and tone
    – eye: radial muscle contraction (mydriasis, dilation)
27
Q

Beta-adrenoceptors: Location and Function

Heart, BV, GI, lung, eye

A
  • Beta-receptors
    – heart: ↑ rate and force of contraction
    –bloodvessels: vasodilatation
    – GI tract: ↓ smooth muscle motility and tone
    –lung: bronchodilatation, ↑ secretion
    – eye: ciliary muscle relaxation (distant vision)
28
Q

Adrenoceptor agonists types

A

– direct-acting sympathomimetics
– indirect-acting sympathomimetics
– mixed-acting sympathomimetics

29
Q

Type of adrenergic drugs

A
  • Adrenoceptor agonist
  • Adrenoceptor antagonst
  • Monoamin oxidase inhibitors
30
Q

Potencies of various stimulatory catecholamines alpha

A

noradrenaline > adrenaline > isoprenaline

31
Q

Potencies of various stimulatory catecholamines beta

A

isoprenaline > adrenaline > noradrenaline

32
Q

Adrenoceptors are classified into a or b subtypes based on what?

A

– molecular cloning of distinct protein moieties
– functional characteristics
– potencies of various stimulatory catecholamines

33
Q

alpha-1 found where and affect what?

A
  • primarily at postjunctional sites
  • smooth muscle cells, contraction
34
Q

alpha-2 found where and affect what?

A
  • mostly on prejunctional sympathetic nerve endings
  • activation inhibits noradrenaline release
  • negative feedback loop
35
Q

Beta-1 found where and affect what?

A
  • Adrenoceptors in abundance in heart
  • increase in heart rate and force
36
Q

Beta-2 found where and affect what?

A
  • Adrenoceptors in abundance in respiratory tract, blood vessels and liver
  • relaxation of airway and vascular smooth muscle, glycogenolysis/ gluconeogenesis in the liver
37
Q

Beta-3 found where and affect what?

A
  • Adrenoceptors in adipose tissue, bladder, brain,
  • potential treatment for diabetes; overactive bladder; anxiety and depression
38
Q

Direct effects of an adrenoceptor agonist on an effector cell depends on what?

A
  • receptor selectivity of the drug
  • adrenoceptor profile of the cell
  • cellular response to receptor activation
39
Q

Relative potency at a-receptors:

A

NOR > ADR > ISO

40
Q

Relative potency at b-receptors:

A

ISO > ADR > NOR

41
Q

Clinical Uses of Catecholamines: Adrenaline in anaphylatic reactions

A

(b-adrenoceptors)
– first-line treatment for acute anaphylactic reactions caused by bee stings and drugs (e.g., penicillin)
– administered in conjunction with antihistamines and glucocorticoids

42
Q

Clinical Uses of Catecholamines: Adrenaline in cardiac arrest

A

(b1-adrenoceptors)
– helps to restore cardiac rhythm

43
Q

Clinical Uses of Catecholamines: Adrenaline in local anaesthetic solutions

(a1-adrenoceptors)

A

– vasoconstrictor effect
– ↑ duration of action
– ↓ risk of systemic toxicity

44
Q

Amphetamine as an Indirect-Acting Sympathomimetic

A
  • No direct agonist activity at a- or b-receptors
    – release noradrenaline from nerves
    – block noradrenaline uptake
    – Inhibit noradrenaline metabolism
  • noradrenaline activates a- and/or b-receptors
45
Q

Mixed-Acting Sympathomimetics: example

A

Ephedrine

46
Q

Ephedrine as a mixed acting sympathomimetic

A
  • Exert action by a combination
    – direct actions on adrenergic receptors
    – releases noradrenaline from sympathetic nerves
  • First orally active sympathomimetic
  • Not a substrate for COMT or MAO
    – prolonged duration of action
  • Used clinically to relieve nasal congestion
    – vasoconstrictor
    – pseudoephedrine is the stereoisomer l-ephedrine
47
Q

Adrenoceptor Antagonists

A

Prevent endogenous adrenoceptor agonists from binding to and stimulating adrenoceptors
* Clinical used for alpha-1 in hypertension treatment
* Clinical use for beta-1 for treatment in angina, arrhythmia, hypertension, post-myocardial infarction etc.
* Antagonism not useful for alpha or beta -2 and has adverse effects

48
Q

b-Adrenoceptor Antagonists

A

Prevent endogenous adrenoceptor agonists from binding to and activating b-adrenoceptors
* Used to treat cardiovascular diseases
– hypertension, angina, cardiac remodelling, myocardial infarction, heart failure, arrhythmia
Metoprolol
* different spectrum of properties

49
Q

Non-Selective b-Adrenoceptor Antagonists: Adverse Effects

A
  • Most adverse reactions are due to excessive b- adrenoceptor blockade and the greatest danger occurs when the drug is first given
  • Precipitate congestive heart failure (b1-blockade)
  • induce bronchoconstriction in asthmatics (b2-blockade)
  • potentiate hypoglycaemia in diabetics

last point: inhibiting catecholamine-induced mobilisation of glycogen stores (b2-blockade) and masking symptoms of hypoglycaemia such as tachycardia (b1-blockade)

PHAR222 (25 decks)

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