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Flashcards in deck_850315 Deck (32):
1

Describe some characteristics of the parasympathetic nervous system

Long, myelinated pre-ganglionic neuronesShort unmyelinated post-ganglionic neuronesOppose sympathetic actionsOriginate in medulla and sacral regionsGanglia located in tissue innervated by para. fibres

2

Describe some characteristics of the sympathetic nervous system

Short, myelinated pre-ganglionic neuronesLong, unmyelinated post ganglionic neuronesGanglia located close to spinal cord in paravertebral cordFight or flight responseOriginate from lumbar and thoracic vertebrae

3

What type of neurones are pre-ganglionic neurones?

Cholinergic-- ACh

4

What type of neurones are parasympathetic post-ganglionic neurones?

Cholinergic with muscarinic AChRG protein coupled

5

What type of neurones are sympathetic post-ganglionic neurones?

Noradrenergic with alpha 1 and beta 1 adrenoceptorsG protein coupled

6

Which receptors are G protein coupled?

M1, M2, M3, alpha1, alpha2, beta1, beta2, eta3

7

What type of transmitters are used for sweat gland and follicle innervation?

Non-adrenergic, non-cholinergic transmitters (NANC) transmitterse.g. nitric oxide, ATP, 5-hydroxytryptamine (seratonin)-- Usually co-released with NA or ACh

8

Describe the sympathetic innervation in adrenal glands

Have chromaffin cells "postganglioninc sympathetic neurons that do not project to a target tissue"Stimulated by nAChR which causes the release of adrenaline in to the bloodstream

9

What is familial dysautonomia?

Autosomal, recessive disorder affecting the development and survival ofsensory, sympathetic and (some) parasympathetic neurones

10

Symptoms of familial dysautonomia?

Dysautonomic crises - response to physical or emotional stress included vomiting, increased HR and BP, sweating and droolingSpinal curvaturePoor growthCardiovascular and respiratory dysfunctionAltered sensory perception

11

Why are cholinergic therapeutic interventions not commonly used?

The drugs are not very selective for their target receptors, so multiple side effects ail arise.

12

What do acetylecholinesterase inhibitor do?

Enhance the effects of acetylcholinee.g. pyridostigmine in myasthenia gravisdonepezil in Alzheimers

13

What are some possible side effects for cholinergic drugs?

Bradycardia and decreased cardiac outputIncreased bronchoconstriction in smooth muscleIncreased peristalsisIncreased sweating and salivation

14

How are some cholinergic drugs used clinically?

Are administered locally in order to limit side effects and increase effectivity

15

Describe some mAChR agonists

Pilocarpin and bethanechol for glaucoma and to stimulate bladder emptying

16

Describe some mAChR antagonists

Ipratropium and tiotropium for asthma and COPDTolterodine for overactive bladder

17

What type of receptors do you usually find in post-ganglioninc sympathetic neurones?

Noradrenergic

18

What is a particular characteristic of innervation around smooth muscle?

A highly branched axonal network with variscosities (beads along axons) overlies the entirety of smooth muscle. These are specialised for Ca2+ dependent noradrenaline release

19

How is noradrenaline synthesised?

Tyrosine to DOPA (tyrosine hydroxylase)DOPA to dopamine (DOPA carbosylase)Dopamine to noradrenaline (dopamine beta-hydroxylase)

20

Where does noradrenaline synthesis take place?

Takes place in variscosities over smooth muscle cells. Tyrosine to dopamine stage takes place in cell cytosol whilst dopemine conversion to noradrenaline takes place in vesicles

21

How is noradrenaline removed from post-synaptic adrenoceptors?

Noradrenaline transporter proteins

22

What are the two methods of re-uptake of noradrenaline?

Uptake One-- uses Na+ dependent, high affinity transports to take NA back into presynaptic cells (takes place for majority of noradrenaline)Uptake Two -- uses a lower affinity, non-neuronal mechanism for NA not taken up by uptake one, into the post-synaptic cells

23

Describe NA metabolism

Some NA which has been brought back into the cell is taken up by vesicles. The NA which has not been taken up by vesicles is metabolised by:Monoamine oxidase (MAO)Catechol-O-methyltransferase (COMT)

24

What regulates the release of noradrenaline?

Inhibition and activation of Ca2+ dependent exocytosis-- inhibit VOCCsless Ca2+ in the cell leads to less neurotransmitter release

25

What are the classes of drugs that have an effect on adrenergic receptors?

Indirectly acting sympathomimetic agentsandUptake One inhibitors

26

Describe "indirectly acting sympathomimetic agents"

The drug is taken up into the synaptic vesicles and cause NA to leak from those vesicles. NA then leaks into the synaptic cleft without being exocytosed.-- They mimic the actions of sympathetic transmitters (allows them to be taken up into vesicles)E.g. Tyramine, amphetamine (rapidly penetrates blood-brain barrier -- drug of abuse), ephedrine

27

Describe "uptake one inhibitors"

Inhibit the re-uptake of noradrenaline into the pre-synaptic cells eg. Tricyclic antidepressants and selective noradrenaline re-uptake inhibitors

28

Where do uptake one inhibitors have their main effect and what side effects can they causes?How can these side-effects be limited?

Mostly effect the CNSCan cause tachycardia and cardiac dysarrythmias -- minimised by the specific drug used and the therapeutic dose of the drug

29

Name two beta2 selective agonists and describe what they do

Salbumatol and salbumetrolActivate bronchodilation in the lungs by opposing bronchoconstriction

30

What is the advantage of selectivity of drug for certain receptors?

Specificity of drug action to limit side effects in other parts of the body

31

What is the purpose of alpha 1 selective and beta 1 selective antagonist?

Treat CVS disorders such as hypertensionAlpha one -- doxazosinBeta one -- atenolol

32

What drugs are usually combined to treat congestive heart failure?

Diuretic (lower blood volume & BP)ACE inhibitor (reduce fluid retention)Beta blocker (reduces force of contracion and cardiac output)