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HLTH 2511 > Module B > Flashcards

Module B Flashcards

1
Q

Provocholine (Methacoline)

A
  • Direct acting cholinergic with greater M3 muscarinic specificity
  • broad systemic effects, but mainly respiratory, decreased heart rate, increased PR, decreased gastric secretions and GI motility
  • used in the Methacholine challenge test (MCT) for asthma. Small doses of methacoline may induce bronchospasm and excessive mucus production in those with reactive airways.
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2
Q

Compare and contrast parasympathetic and sympathetic systems based on anatomy, function and neurotransmitters

A

Parasympathetic
Anatomy:
Funtion:
Neurotransmitters:

Sympathetic
Anatomy:
Funtion:
Neurotransmitters:

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3
Q

Sympathetic nerves have _____ pre-ganglionic neurons and ____ post-ganglionic neurons

A

Short pre- ganglionic
Long post- ganglionic

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4
Q

Parasympathetic nerves have _____ pre-ganglionic neurons and ____ post-ganglionic neurons

A

Long pre-ganglionic
Very short post-ganglionic

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5
Q

Neurotransmitters

A

A substance released by nerve terminals that act as a chemical signal to stimulate the next nerve in the nero-pathway.

Released at the pre ganglionic synapses and neuroeffector site ( also known as target organ site or post-ganglionic synapses)

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6
Q

What neurotransmitters are released by sympathetic and parasympathetic systems?

A

Acetylcholine and norepinephrine

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7
Q

Describe the process of acetylcholine synthesis, storage and release

A
  1. Synthesized from choline and acetate by choline acetyltransferase
  2. Stored in presynaptic vesicles
  3. Action potential triggers vesicles fusion with presynaptic membrane
  4. ACh released across synpase to bind with post-snyaptic receptors
  5. Choline is recycled through presynaptic reuptake
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8
Q

How is the action of acetylcholine terminated?

A

Breakdown of ACh occurs rapidly by hydrolysis by two enzymes
1. Acetylcholinesterase
2. Pseudocholinesterase

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9
Q

Botulinum toxin

A

Blocks the exocytotic release of ACh and decreases neuromuscular transmission

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10
Q

Tensilon (Edrophonium)

A
  • short acting reversible cholinesterase inhibitor (indirect acting cholinergic)
  • rapidly increases ACh concentrations
  • may be used to reverse neuromuscular blockade
  • used to diagnose between myasthenia crisis (not enough ACh) and a cholinergic crisis ( too much ACh) in myasthenia gravis.
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11
Q

____ is similar to acetylcholinesterase but is found in blood plasma and is important in breakdown of cholinergic drugs

A

Pseudocholinesterase

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12
Q

Prostigmin (Neostigmine)

A
  • reversible cholinesterase inhibitor (indirect acting cholinergics)
  • relatively long acting
  • used in long-term treatment of myasthenia gravis and in reversal of NMBA blockade
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13
Q

Cholinergic receptors

A

Respond to ACh and ACh like drugs
Two subdivisions; muscarinic and nicotinic

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14
Q

Muscarinic receptors (describe M2 and M3)

A

G- protein coupled receptors
5 subtypes (M1-M5)

M2: located ok cardiac muscle cells. Slow HR

M3: located on bronchial smooth muscle , exocrine glands. Result in bronchocontrictuon, increases mucus secretion, vasodilation

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15
Q

Nicotinic receptors belong to the receptor class ________

A

Ligand-gated sodium channels

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16
Q

The bronchial effects of muscarinic activation are:

A

Bronchoconstriction, hypersecretion of mucus

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17
Q

nN receptors

A

Neuronal or ganglionic nictontic
- located in the pre-synaptic and autonomic ganglia
- stimulation results in excitement of postganglionic fibres and subsequent release of the neurotransmitter.

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18
Q

mN receptor

A

Muscle nictotinic
- located around the neuromuscular junction (skeletal muscle)
- stimulation of these receptor results in skeletal muscle contraction.

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19
Q

Direct- acting Cholinergics

A

Are drugs similar in chemical shape to acetylcholine or natural plant alkaloids

Not clinically useful - cause contraction of bronchial smooth muscle and decrease heart rate.

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20
Q

The effect of stimulating M3 muscarinic receptors in non-vascular smooth muscle is

A

Increase calcium release and muscle contraction

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21
Q

The effect of stimulating M2 muscarinic receptors is

A

Decrease cAMP production in cardiomyocytes, slowing heart rate and conduction

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22
Q

Indirect- acting cholinergics

A

Two different forms reversible and quasireversible

Short-acting drugs = reversible
Long-acting compounds = quasi reversible

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23
Q

Describe reversible cholinesterase inhibitors

A

Reversible: reverse neuromuscular blockade caused by non-depolarizing neuromuscular blockers. Diagnose and/or treat disease where lack of ACh is the problem. Treat glaucoma

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24
Q

Mestinon (Pyridostigmine)

A
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25
The ocular effects of M3 muscarinic receptor activation are:
Miosis (pupillary constriction) Accommodation (ciliary muscle contraction for near vision) Lacrimation
26
The cardiac effect of muscarinic activation are:
Decreased SA diastolic depolarization (slows heart rate), slow AV nodal conduction (prolonged P-R interval)
27
The vascular effect of muscarinic activation are:
Vasodilation due to nitrous oxide release, simulated by increase in IP3 and DAG levels
28
Muscarinic receptors belong to the receptor class
G-protein coupled receptors (GPCRs)
29
List three uses of reversible cholinesterase inhibitors (indirect acting cholinergics)
1. Reversal of neuromuscular blockade by curariform drugs 2. Diagnose/treated disorders of ACh (example; edrophonium for myasthenia gravis) 3. Treat glaucoma (example: pilocarpine)
30
What are the two type of nicotinic receptors?
Neuronal type (nN) and muscle type (mN)
31
What are the two types of acetylcholine receptors?
Nicotinic and muscarinic
32
Nicotinic receptors are found at:
All autonomic ganglia, neuromuscular junctions and in the CNS
33
The effect of stimulating M3 muscarinic receptors in vascular smooth muscle is
Nitric oxide synthesis and smooth muscle relaxation
34
Muscarinic receptors are found at
Smooth muscle, cardiac tissue and glands innervated by the parasympathetic nervous system. Also found at some sympathies neuroeffector junctions specifically sweat glands and chromaffin cells
35
The effect of stimulating M3 muscarinic receptors in glands is
Increased glandular secretion
36
The purpose of ACh autoreceptor is
To provide negative feedback at cholinergic synapses
37
What are the primary clinical uses of muscarinic receptors antagonists?
1. Relax smooth muscles (vasodilation) 2. Reduce glandular secretion 3. Increase heart rate
38
What is the primary clinical use of nicotinic receptor antagonist?
Relax skeletal muscles during medical Procedures
39
Three examples of belladonna alkaloids and what drug class do they belong to?
Atropine, scopolamine and hyoscyamine Muscarinic receptors antagonist (parasympatholytic)
40
What is NMBA? How many classes and what are they?
Neuromuscular blocking agents 2 classes : non-depolarizing (ND) and depolarizing (D)
41
Curariform drugs
Another name for NMBAs named after their biological source
42
ND NMBAs (curariform drugs) generally function by:
Acting as competitive muscle-type nicotinic acetylcholine receptor antagonists
43
ND NMBAs may potentiate hypotension, bronchocostriction and tachycardia stimulating release of ___ from mast cells
Histamine
44
The advantage of modern curariform drugs over older ones is?
They cause less histamine release and have higher mN nicotinic receptor specificity (lower ganglionic blockade)
45
The only depolarzing neuromuscular blocking agent
Succinylchline
46
Transient muscle contractions during the onset of succinylcholine are called
Fasciculations
47
Describe the general strategies for countering NMBA overdose
- use cholinesterase inhibitors (neostigmine) to increase ACh concentration at neuromuscular junction. Quaternary amine muscarinic antagonists may be given to limit muscarinic side effects of this strategy. Sugammadex directly binds NMBAs for excretion
48
The only type of adrenergic receptor that does not involve the adenylyp cyclase pathway
Alpha-1
49
List and compare the activation effects of the adrenergic receptors
a1: smooth muscle contraction (vasoconstriction), glandular secretion a2: autoreceptor for negative feedback inhibition of catecholamine release B1: increase heart rate, contractility, conduction. Increase renin secretion B2:smooth muscle relaxation (vasodilation, bronchodilation), glycogenolysis, skeletal muscle potassium intake B3: lipolysis, thermogenesis, uterine relaxation
50
Describe the synthesis and release of Norepinephrine at sympathetic neuroeffector junctions
1. Tyrosine is converted to dopamine by tyrosine hydroxylase 2. Dopa is converted to dopamine by dopa decarboxylase 3. Dopamine is converted to norepinephrine by dopamine beta hydroxylase 4. Norepinephrine is stored in presynaptic vesicles and released by calcium mediated exocytosis
51
Describe the effects of cocaine on sympathetic neurotransmission
Cocaine inhibits reuptake of norep into the neuronal cells for MAO metabolism
52
COMT
Catechol-O-methyl transferase Is the major enzyme responsible for terminating the action of norep-like drugs. Found in neuroeffector synapse and in non-neuronal cells
53
MAO
Monoamine oxidase Is capable of inactivating norep-like drugs
54
Describe the roles of MAO, COMT and catecholamine transporter in the reuptake and metabolism of both endogenous and exogenous catecholamines
Norepinephrine (endogenous) is taken back into the sympathetic neuron through the catecholamine transporter through uptake 1 and is metabolized intracellularly by MAO Exogenous catecholamines (dobutamine, epinephrine) are either directly metabolized in the synapses by COMT or are taken into the non-neuronal cell through uptake 2 and metabolized by MAO and COMT. MAO is the major enzyme of exogenous catecholamine metabolism
55
Describe the process of reflex bradycardia and reflex tachycardia as part of the baroreceptor reflex
The baroreceptor reflex arises from stimulation of mechanoreceptors in the aortic arch and carotid arteries which send impulses to the vasomotor Center and influence vagal outflow Drugs or diseases that cause increased BP will cause an increased stretch of the baroreceptors, leading to reflex bradycardia aka a vagal reflex.
56
What are the three classes of adrenergic agonists
Direct-acting (dobutamine), indirect- acting (cocaine) and mixed acting (ephedrine)
57
Why must catecholamines be delivered parenterally?
Because otherwise they will be rapidly degraded by GI COMT and MAO
58
List the 5 common catecholamine vasopressors and describe their receptor specificities
Epinephrine: activates both alpha and beta receptors. Increasing alpha-affinity with higher doses Dopamine: at low doses only D1-affinity, with increasing doses it activates beta and than alpha Norepinephrine: high a1 specificity, little to no beta effect Dobutamine: had only beta affinity with a strong inotropic and almost no chrontropic effect Isoproterenol: has only beta affinity with a strong chrontropic effect
59
Inotropic effect
Increased contractility
60
Chronotropic effect
Increased heart rate
61
Dromotropic effect
Increase cardiac impulse conduction velocity

HLTH 2511 (4 decks)

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