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PHAR222 > L2 ANS > Flashcards

L2 ANS Flashcards

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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

Study These Flashcards
A

antidote to poison

21
Q

Treatment of Atropine Poisoning

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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

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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

Study These Flashcards
A

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

24
Q

Adrenal Medulla: Adrenaline

Study These Flashcards
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
# Structures of Catecholamines Structural modification of noradrenaline to produce synthetic catecholamines
– ↑ 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
Adrenoceptors: Location and Function APLHA | BV, Lung, GI, eye
* Alpha1-receptors (post-synaptic) –bloodvessels: vasoconstriction –lung: ↓ secretion – GI tract: ↓ smooth muscle motility and tone – eye: radial muscle contraction (mydriasis, dilation)
27
Beta-adrenoceptors: Location and Function | Heart, BV, GI, lung, eye
* 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
Adrenoceptor agonists types
– direct-acting sympathomimetics – indirect-acting sympathomimetics – mixed-acting sympathomimetics
29
Type of adrenergic drugs
* Adrenoceptor agonist * Adrenoceptor antagonst * Monoamin oxidase inhibitors
30
Potencies of various stimulatory catecholamines **alpha**
noradrenaline > adrenaline > isoprenaline
31
Potencies of various stimulatory catecholamines **beta**
isoprenaline > adrenaline > noradrenaline
32
Adrenoceptors are classified into a or b subtypes based on what?
– molecular cloning of distinct protein moieties – functional characteristics – potencies of various stimulatory catecholamines
33
alpha-1 found where and affect what?
* primarily at postjunctional sites * smooth muscle cells, contraction
34
alpha-2 found where and affect what?
* mostly on prejunctional sympathetic nerve endings * activation inhibits noradrenaline release * negative feedback loop
35
Beta-1 found where and affect what?
* Adrenoceptors in abundance in heart * increase in heart rate and force
36
Beta-2 found where and affect what?
* Adrenoceptors in abundance in respiratory tract, blood vessels and liver * relaxation of airway and vascular smooth muscle, glycogenolysis/ gluconeogenesis in the liver
37
Beta-3 found where and affect what?
* Adrenoceptors in adipose tissue, bladder, brain, * potential treatment for diabetes; overactive bladder; anxiety and depression
38
Direct effects of an adrenoceptor agonist on an effector cell depends on what?
* receptor selectivity of the drug * adrenoceptor profile of the cell * cellular response to receptor activation
39
Relative potency at a-receptors:
NOR > ADR > ISO
40
Relative potency at b-receptors:
ISO > ADR > NOR
41
Clinical Uses of Catecholamines: Adrenaline in anaphylatic reactions
(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
Clinical Uses of Catecholamines: Adrenaline in cardiac arrest
(b1-adrenoceptors) – helps to restore cardiac rhythm
43
Clinical Uses of Catecholamines: Adrenaline in local anaesthetic solutions | (a1-adrenoceptors)
– vasoconstrictor effect – ↑ duration of action – ↓ risk of systemic toxicity
44
Amphetamine as an Indirect-Acting Sympathomimetic
* 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
Mixed-Acting Sympathomimetics: example
Ephedrine
46
Ephedrine as a mixed acting sympathomimetic
* 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
Adrenoceptor Antagonists
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
b-Adrenoceptor Antagonists
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
Non-Selective b-Adrenoceptor Antagonists: Adverse Effects
* 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 ## Footnote last point: inhibiting catecholamine-induced mobilisation of glycogen stores (b2-blockade) and masking symptoms of hypoglycaemia such as tachycardia (b1-blockade)

PHAR222 (26 decks)

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