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Pharma A > Autonomic Nervous system + pharmacokinetics > Flashcards

Autonomic Nervous system + pharmacokinetics Flashcards

1
Q

What divisions can the peripheral nervous system be broken into?

A

Afferent division
Efferent division

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2
Q

In which direction does info flow in afferent and efferent divisions?

A

Afferent = from periphery to CNS
Efferent = from CNS to organs, muscles, tissues

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3
Q

What divisions does ANS have?

A

Sympathetic NS - fight or flight
Parasympathetic NS - Rest and digest
Enteric NS - Nerve fibres that control gastrointestinal tract

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3
Q

What divisions can efferent division be divided into?

A

Somatic system (Motor system)
Autonomic system (Involuntary - Reflexes)

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4
Q

Where does the nerves of symapthetic NS arise from?

A

Thoracic and lumbar regions of spinal cord

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5
Q

Where does the nerves of parasympathetic NS arise from?

A

Cranial and sacral regions of spinal cord

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6
Q

Name the parts of a nerve

A
  1. Dendrites
  2. Cell body
  3. Nucleus
  4. Axon
  5. Schwann cell
  6. Myelin sheath
  7. nodes of ranvier
  8. axon terminal
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7
Q

Name difference between sympathetic and parasympathetic nervous system structure of preganglionic and postganglionic fibres

A

In sympathetic NS, ganglion is close to the spinal cord, so short preganglionic fibre and longer postganglionc fibre.

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8
Q

What is the ANS effect on Iris dilator pupillae?

A

Sympathetic NS = Contraction (Mydriasis)

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9
Q

What is the ANS effect on Iris sphincter pupillae?

A

Parasympathetic NS = Contraction (Miosis)

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10
Q

What is the ANS effect on Ciliary muscle?

A

Sympathetic NS = possible relaxation for far vision

Parasympathetic NS = Contraction for near vision (accommodation)

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11
Q

What is the ANS effect on Ciliary epithelium?

A

Sympathetic NS = production of aqueous humour

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12
Q

What is the ANS effect on Conjuctival blood vessels?

A

Sympathetic NS = Contraction - Vasoconstriction

Parasympathetic NS = Relaxation - Vasodilation

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13
Q

What is the ANS effect on Lachrymal gland?

A

Parasympathetic NS = Tear production

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14
Q

How is a resting potential established?

A

Higher conc of Na+ outside and higher conc of K+ inside neurone.
The difference is maintained by sodium potassium pump that moves 3 Na+ out of cell and 2 K+ into cell.

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15
Q

What is resting potential?

A

There is no nerve impulse so there is a potential difference of -70mV across axon.
Membrane is polarised to maintain the potential difference

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16
Q

What is depolarisation?

A

Membrane becomes more permeable to Na+ ions.
If membrane potential reaches threshold then Na+ channels open.
Na+ diffuses into cell.
Inside becomes more positive compared to outside cell so goes from -70mV to +40mV. This is depolarisation.
K+ channels will remain closed.

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17
Q

What is action potential?

A

High concentration of positive ions inside the cell.

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18
Q

What is repolarisation?

A

Once potential difference reaches +40mV, the Na+ channels will close and K+ channels will open. K+ ions diffuse out of the cell down a concentration gradient.

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19
Q

What is hyperpolarisation?

A

The K+ channels remain open longer than needed so becomes hyperpolarised to -90mV.
The sodium potassium pump brings it back to -70mV.

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20
Q

What is a neurotransmitter?

A

Chemical mediators released from presynaptic cell. Carries info across synapse to postsynaptic cell.

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21
Q

What is important for efficient neurotransmission?

A

That the neurotransmitters are removed and elimanated from the synapse once the messages have been transmitted.
This is to prevent constant stimulation of the post synaptic cell.
So the neurotransmitter can either be broken down or recycled.

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22
Q

How does the synapse work?

A
  1. Action potential arrives at pre synapse and Ca2+ channels open
  2. Calcium ions diffuse into synaptic cleft
  3. Ca2+ activate enzymes which cause the synaptic vesicles to move towards the pre synaptic membrane
  4. The vesicles fuse with pre synpatic membrane causing acetylcholine to be released.
  5. Acetylcholine diffuses and binds to post synaptic membrane.
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23
Q

How does our body know how much neurotransmitter should be released?

A

Dependent on how frequently the action potential is fired.

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24
How is acetylcholine synthesised?
1. In pre synaptic neurone 2. Choline acetyltransferase (ChAT) enzyme combines acetyle coenzyme A and choline to form acetylcholine.
25
What are the types of acetylcholine receptors?
1. Nicotinic 2. Muscarinic
26
Describe characteristics of Nicotinic receptors
1. Ligand gated ion channels- faster transmission 2. located in ganglia in ANS 3. subtypes = neuronal and muscle 4. Also at skeletal neuromuscular junction and brain
27
Describe characterisitics of Muscarinic receptors
1. GPCRs - slower transmission 2. Located in the target organ in ANS 3. Subtypes = M1- M5. 4. Also in brain
28
What is the function of M1, M3, M5 receptor subtypes?
Upon acetylcholine binding these receptors couple to Gq which activates the signaling cascades leading to an increase in the calcium released. Stimulatory effect.
29
What is the function of M2 and M4 receptor subtypes?
Couple to Gi which inhibits the production of cAMP
30
Where is acetylcholine found in the ANS?
At preganglionic nerve fibers in both sympathetic NS and parasympathetic NS.
31
Which of the muscarinic subtype receptors is mostly found in the eye?
M3
32
How is acetylcholine removed from the synapse?
Acetylecholinesterase hydrolyses acetylecholine to choline and acetate. Choline is taken back up into the neuron and recyled.
33
How is noradrenaline synthesised?
Tyrosine goes through enzymatic reactions to form noradrenaline.
34
What are the receptors for noradrenaline called?
Adrenoreceptors = two types 1. Alpha receptors 2. Beta receptors
35
What are the subtypes of alpha receptors?
alpha 1 and alpha 2
36
What are the subtypes for beta receptors?
Beta 1, Beta 2 and Beta 3
37
Where are alpha subtype receptors located?
Alpha 1 = post synaptic Alpha 2 = presynaptic Could be on postsynaptic for some tissues
38
Where are Beta subtype receptors located?
Beta 1 = Postsynaptic Beta 2 = Postsynaptic, could be presynaptic for some tissues Beta 3 = Not in eye. In adipose and bladder.
39
What is the function of alpha 1 receptors?
Alpha 1 = couple to Gq, releasing Ca2+
40
What is the function of alpha 2 receptors?
Alpha 2 = couple to Gi, inhibiting cAMP production
41
What is the function of Beta receptors?
All subtypes = couple to Gs, increased cAMP production
42
Where is noradrenaline found in the ANS?
At post ganglionic nerve fibres in sympathetic NS
43
Which adrenoreceptors stimulate iris dilator pupillae?
Alpha 1
44
Which adrenoreceptors stimulate ciliary muscle?
beta receptors
45
Which adrenoreceptors stimulate Ciliary epithelium?
beta receptors
46
Which adrenoreceptors stimulate conjunctival blood vessels?
Alpha 1
47
How is noradrenaline removed from the synapse?
Reuptake into presynaptic neuron. Approx. 75% of noradrenaline is recaptured and repackaged into synaptic vesicles. The remaining amounts of noradrenaline is broken down by COMT, or diffuses and escapes synapse.
48
Drugs that mimic the activation of sympathetic NS are called...
sympathomimetic drugs
49
Drugs that mimic the activation of parasympathetic NS are called...
parasympathomimetic drugs
50
Anticholinesterase drugs prevent acetylcholine breakdown. Describe its uses
1. Includes some of the most toxic nerve gases 2. A related drug, echothiophate was formerly used for glaucome and may rarely been used for accommodative esotropia 3. Reversible inhibitors such as Neostigmine and Pyridostigmine boot cholinergic transmission. No ocular uses 4. Some drugs such as galantamine, rivastigmine and donepezil used to manage Alzheimer's disease.
51
Why is targeting receptors the best approach?
1. Allows more specificity than other approaches 2. Neurotransmission can either be stimulated or blocked as agonists and antagonists are available. 3. Selective drugs for muscarinic, alpha and beta adrenoreceptors to avoid unwanted effects. 4. If drugs don't cross the blood brain barrier then won't reach the acetylcholine receptors in the CNS, reducing unwanted effects.
52
Why is targeting nicotinic receptors in ANS not good?
1. Sympathetic and parasympathetic NS would both be affected. 2. Neuromuscular junction at skeletal muscle also affected. 3. Nicotinc receptors in CNS would also be affected. Side effects outweigh the beneficial actions
53
Why is targeting muscarinic receptors in ANS good?
1. Can use agonists and antagonists 2. Different muscarinic receptor subtypes have different signalling mechanisms and different locations which limits unwanted effects.
54
How is muscarinic agonists used in the eye?
Drug Pilocarpine is used in treatment for open angle and closed angle glaucoma. Eye drops in 1%, 2%, 4% Gel Oral tablets Oral drops
55
How is muscarinic antagonists used in the eye?
Competitive antagonists block the effecs of agonist. Antagonists are preferred as effects can be reversed. Drugs used: Cyclopentolate, Tropicamide, Atropine.
56
What is cylcopentolate (Antagonist drug) used for?
1. Cycloplegic refraction 2. Dilation in iritis to reduce pain and remove adhesions between lens and inflamed iris. Eye drops - minims - 0.5%, 1%
57
What is the use of Tropicamide (Antagonist drug) ?
1. Dilation for ophthalmoscopy. 2. Cycloplegic refraction 3. Dilation in iritis to reduce pain and remove adhesions between lens and inflamed iris. Eye drops - multi dose - 0.5%, 1% Minims - 0.5%,1%
58
What is Atropine (Antagonist drug) used for?
1. Cyclopegic refraction 2. penalisation in orthoptics 3. Dilation in iritis Eye drops - multi dose - 1% minims - 1%
59
What are some possible unwanted systemic effects of Antagonist drugs?
1. Tachycardia (heart) 2. prevention of salivation (Salivary glands) 3. Relaxation of smooth muscle (gut, bladder) 4. prevention of sweating (sweat glands) 5. confustion (CNS effects) Use of eyedrops minimise these systemic effects.
60
What are some possible unwanted effects of Antagonist drugs?
1. ocular side effects such as blurred vision and dry eye 2. patients may be on anti muscarinic drugs for other medical conditions. Used clinically for motion sickness, overactive bladder, asthma, antispasmodics 3. Some antidepressants and antihistamines have unwanted anti muscarinic effects
61
Why is targeting adrenoreceptor receptors in ANS good?
1. Different signallling mechanisms 2. Different locations so fewer unwanted effects
62
What is alpha 1 agonist adrenoreceptor used for?
Promote contraction of: 1. Iris dilator pupillae (dilates pupil) 2. Muller's muscle (lid elevation) 3. Conjuctival blood vessels (vasoconstriction)
63
What is the alpha 1 agonist drug?
Phenylephrine used for dilation of pupil for ophthalmoscopy. Eye drops- minims - 2.5%, 10%
64
What is alpha 2 agonist adrenoreceptor used for?
1. Reduces the amount of noradrenaline released by sympathetic neurone. 2. Promote constriction of some blood vessels 3. increases uveo scleral outflow 4. used for treatment of open angle glaucoma
65
What are the alpha 2 agonist drugs?
Apraclonidine eye drops - 0.5%, 1% Brimonidine eye drops - 0.2%
66
What is Beta antagonism drugs used for?
1. Reduces production of aqueous humour by ciliary epithelium. 2. Decreases IOP so useful for open angle glaucoma
67
What are the beta antagonist drugs?
Beta 1 selective = Betaxolol Eye drops - multidose - 0.25%, 0.5% Beta 1 and 2 non selective = Carteolol (weak partial agonist) and Timolol (inverse agonist) Timolol - eye drops - multidose - 0.25%, 0.5% Eye gel - 0.25%, 0.5%
68
What is the bioavailability for oral route of administration and whats the reason for this value?
Bioavailability = 0.05 to <1 1. The drug is inactivated within the gut lumen by gastric acid, digestive enzymes or bacteria 2. Absorption is incomplete in intestines 3. Metabolism occurs both in gut wall and liver
69
What is the bioavailability for injection route of administration and whats the reason for this value?
Bioavailability = 1 Directly injected into the vein so 100% of the drug is in systemic circulation
70
How is topical drug absorbed? Which route is more desirable and why?
1. From tear film through the cornea. The cornea is permeable to the drug. This route is more desirable because the receptors are located beneath it 2. Across the conjuctiva and sclera into the anterior uvea
71
Why can some pxs tast the eye drops after they are adminsitered? And how to avoid this?
Due to nasolacrimal drainage. To avoid this tell them to put pressure onto their puncta to avoid the drug going to the nose and to the mouth taste receptors.
72
How to treat anterior segment?
Topical drugs absorbed through cornea then transferred to anterior chamber. The dose is carried by aqueous flow and by diffusion into the blood circulation through anterior uvea. Once the drug reaches the aqueous humour it can easily be distributed to the iris and ciliary body.
73
How can the bioavailabilty be affected by iris colour?
Drug molecules bind to melanin and creates a reservoir, meaning it takes longer to be released and drug activity would last longer.
74
How does drug activity decrease in anterior segment?
1. Metabolism from enzymes like esterases, peptidases and cytochrom P450 2. Elimination from anterior segment through aqueous humour by : a) chamber angle and sclemm's canal b) blood flow in anterior uvea
75
What are the advantages of topical drugs?
1. easy application 2. non invasive 3. convenient for Px 4. drug localisation (minimising exposure to other tissues/organs) 5. adequate efficacy 6. low cost
76
What are the disadvantages of topical drugs?
1. low ocular bioavailability 2. nasolacrimal drainage 3. epithelial barriers 4. Not yet effective for posterior segment
77
What are the advantages of intravitreal route of administration?
1. Bioavailability of 1 2. Effective retinal delivery 3. sustained delivery up to 3 years (Sustained drug) 4. bypasses multiple ocular barrier
78
What are the disadvantages of intravitreal route of administration?
1. invasive - risks haemorrhage, retinal detachment 2. inconvenient for Px
79
What is the difference between pharmacokinetics and pharmacodynamics?
Pharmacokinetics = how the body absorbs, distributes, metabolizes, and excretes a drug. It explains what the body does to the drug over time. Pharmacodynamics = the study of the biological and physiological effects of a drug on the body and its mechanism of action. It explains what the drug does to the body.
80
What is the first pass effect?
the process by which a drug's concentration is significantly reduced before it reaches the systemic circulation.
81
What is periocular/suprachoroidal route of administration?
Delivery of drug to tissues around the eye. Drugs reach ocular tissue by diffusion or absorption
82
What are the advantages of periocular/suprachoroidal route of administration?
1. Delivery to both anterior and posterior segments 2. less invasive compared to intravitreal
83
What are the disadvantages of periocular/suprachoroidal route of administration?
1. Invasive 2. Inconvenient to Px 3. Could get cleared by circulation 4. retinal pigment epthelial barrier blocks delivery to retina
84
What are the advantages of subconjunctival route of administration?
1. higher concentration of drug to anterior segment
85
What are the disadvantages of subconjunctival route of administration?
1. scleral thinning (scleral tissue becoming thinner) 2. scleral melt (loss of scleral tissue)
86
What are the advantages of oral and parenteral route of administration?
Systemic administration might be useful in treating posterior segment.
87
What are the disadvantages of oral and parenteral route of administration?
1. liver metabolism 2. kidney clearance 3. blood ocular barriers restrict drug permeability 4. dilution of drug in blood 5. systemic side effects 6. only a small amount of the drug reaches vitreous humour.

Pharma A (6 decks)

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