ANS Flashcards

1
Q

What does the peripheral nervous system contain?

A

Sensory system and motor system

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2
Q

What is the motor system composed of?

A

Somatic (I control) and Autonomic nervous system (i cant control e.g heart)

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3
Q

What is the autonomic nervous system composed of?

A

Parasympathetic NS, sympathetic NS, Entric NS

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4
Q

What is the basic difference between Somatic NS and Autonomic NS

A

Somatic NS
Takes one motor neuron to reach the effector organ (skeletal muscles) from spinal cord. Ach acetylcholine released on target tissue is a nicotinic M receptor cause contraction of skeletal muscle.

Autonomic NS
Takes two motor neurons to reach the effector organ. The first one coming from the brain stem or spinal cord is called the PRE ganglionic and the second neuron is called the POST ganglionic neuron. Parasympathetic and sympathetic

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5
Q

Where is the sympathetic NS in spinal cord?

A

thoracic lumbar regions

Thoracic Lumbar T1 vertebrate to L2 this is where the preganglionic

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6
Q

Where is the parasympathetic NS in spinal cord?

A

Cranial and sacral regions

Cranial Nerve 3
Superior salvitorial nucleus - cranial nerve 7
Inferior salvitorial nucleus - cranial nerve 9
Vagous - cranial nerve 10
S2, S3 and S4 pelvic
ALL above are from Cranio sacral outflow

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7
Q

How long are the Preganglionic and postganglionic neurons in the sympathetic NS?

A

Preganglionic motor neurons are short
Post ganglionic neurons are long

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8
Q

How long are the Preganglionic and postganglionic neurons in the parasympathetic NS?

A

Preganglionic neurons are long
Post ganglionic neurons are short

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9
Q

What chemicals are released in the sympathetic NS to stimulate the pre and post ganglionic neuron? What are the PRE and POST ganglions special names?

A

Acetylcholine. The preganglionic fibres are called cholinergic fibres because they are releasing actylCHOLINE. The post ganglionic neurons will release norephedrine so they are ADRENERGIC neurons.

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10
Q

What chemicals are released in the parasympathetic NS to stimulate the pre and post ganglionic neuron? What are the PRE and POST ganglions special names?

A

The preganglionic fibres are called cholinergic fibres because they are releasing actylCHOLINE. The post ganglionic neurons will release acetylcholine therefore the parasympathetic post ganglionic neurons are cholinergic.

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11
Q

What is responsible for secretion of adrenaline in fight or flight?

A

Adrenal medulla

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12
Q

What pathway and symptoms occur in fight or flight

A

SYMPATHETIC PATHWAY

Heart rate inc to deliver blood to muscles
contractile force increases - more blood, oxygen nutrience gets delivered to tissues in body
Breathing rate increases
Bronchodilation
peripheral blood vessels constrict (skin) however muscle blood vessels dilate
Pupils dilate - can see more

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13
Q

What pathway and symptoms occur in rest and digest?

A

PARASYMPATHETIC PATHWAY
Heart rate drops
heart contraction decreases
breathing rate decrease
bronchoconstriction
Blood vessels constrict - peripheral dilate, muscles constrict
Pupils constrict

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14
Q

Where does fight and flight occur?

A

Thoracic lumbar regions

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15
Q

Where does rest and digest occur?

A

cranial and sacral regions

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16
Q

what are the neurotransmitters for fight and flight?

A

PREganglionic - Ach (cholinergic)
POSTganglionic- noradrenaline (adrenergic receptors) (alpha and beta)

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17
Q

what are the neurotransmitters for rest and digest?

A

PREganglionic - Ach (cholinergic)
POSTganglionic- Ach (nicotinic)

target effector muscarinic receptors

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18
Q

Why do all symptoms occur not just one for the sympathetic pathway?

A

The adrenal gland (on top of kidney) has no post ganglionic neuron just ONE preganglionic neuron. This releases acetylcholine. The adrenal gland has multiple nicotinic receptors acetylcholine receptors which releases adrenaline to the blood stream. Hormones get released to blood stream and will go to all structures to give a responses eg. heart rate inc, pupils dilate.

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19
Q

What adrenergic receptors are there? Where are they found

A

a1 b1 stimulate
a2 b2 inhibit

a1 - smooth muscle, glands and tissues
b1 - heart, juxaglomelular cells (kidneys)
a2 - presynaptic terminals
b2 - all smooth muscle, glands, tissue

If noradrenaline or adrenaline is thrown at

a1 - the SM will contract or the glands will release

b2 - it will relax or glands will not release

b1 - inc HR, inc contract force,

a2 = inhibits post ganglionic neurons

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20
Q

What are beta blockers? Which ones are better for asthmatics?

A

Specific and non specific

Non specific block B1 and B2 slow your heart rate down and Broncho restriction,

Specific better for asthmatic bc doesnt cause bronchorestriction just reduces blood pressure

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21
Q

How does the neurotransmitter from the preganglionic stimulate the postganglionic neuron?

A

The release of either ACh, or NA, from presynaptic sites is triggered by the arrival of an action potential. This causes membrane depolarization that opens voltage-activated calcium-selective ion channels that allow influx of Ca2+.

The resultant local increase in intracellular
Ca2+ concentration causes vesicles in which the transmitter is stored to fuse with the presynaptic/prejunctional membrane liberating the transmitter to activate postsynaptic receptors. Such release of transmitters from vesicles in response to Ca2+ is known as exocytosis.

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22
Q

What examples are there for selective and non selective M receptor antagonists

A

. Pirenzepine and solifenacin are examples of antagonists with
marginal selectivity for M1 and M3 receptors, respectively, whilst atropine
(above) and ipratropium are non-selective.

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23
Q

What are sympathetic agonists examples?

A

phenylephrine (α1-adrenoceptor
selective)
adrenaline (non-selective)
salbutamol (β2-adrenoceptor
selective)
dobutamine (β1-adrenoceptor
selective)

24
Q

What are para sympathetic agonists examples?

A

bethanechol (muscarinic,
non-selective)
pilocarpine (muscarinic
non-selective)

25
Q

What are sympathetic antagonists?

A

prazosin (α1-adrenceptor selective)
propranolol (β-adrenoceptor
selective)
atenolol (β1-adrenocptor selective)

26
Q

What are parasympathetic antagonists?

A

atropine (muscarinic, nonselective)
ipratropium (muscarinic,
non-selective)

27
Q

What are the effects of parasympathetic drugs?

A

INCREASED SALIVARY/BRONCHIAL SECRETIONS
INCREASED PERISTALSIS
BRONCHCONSTRICTION
BRADYCARDIA AND HYPOTENSION

LARGE DOSES
DEPOLARISING BLOCK (LOSS OF ELECTRICAL EXCITABILITY AT THE ENDPLATE)
BUILD UP OF Ach IN PLASMA AND BODY FLUIDS

28
Q

What is an example of muscarinic receptor agonist?

A

Pilocarpine - Intraocular pressure - effects muscarinic receptors inc systemically risk of systemic effects - get dec heart rate, broncho restriction, potential hypotension (blood pressure) transition from sitting and standing insignificant blood flow from brain - dizzy/ black out. Peripheral vision may occur or fainting.

Bethanechol - Is selective muscarinic cholinergic agonist - it has impact on GI tract and used as a laxative may impact bladder function. Risks are side effects. Hypotension result, slow heart rate, inc gi motility, broncho restriction, inc salvation (sweating)

29
Q

What do muscarinic receptor agonists do to the the cardiovascular system?

A

DECREASED FORCE OF CONTRACTION
GENERALISED VASODILATION
SLOWED HEART BEAT
DECREASED CARDIAC OUTPUT

30
Q

What do muscarinic receptor agonists do to the the smooth muscle?

A

NON-VASCULAR SMOOTH MUSCLE CONTRACTS
GASTROINTESTINAL (BLOCKAGE)
UTERINE
DETRUSOR (
BLOCKAGE)
AIRWAY (*ASTHMA)

31
Q

What do muscarinic receptor agonists do to gland stimulation?

A

SECRETIONS
SALIVARY
SWEAT GLANDS
BRONCHIAL
PANCREATIC
GASTRIC

32
Q

Give an example of short acting anticholinesterases?

A

EDROPHONIUM

USED AS DIAGNOSTIC TOOL (MYASTHENIA GRAVIS)
SHORT ACTING AND ADMINISTERED I.V.
READILY REVERSIBLE AND ACTION IS BRIEF
BINDS TO ANIONIC SITE OF ENZYME

Short term - edrophonium diagnostic tool to see if too much or too less of myasthenia gravis has been used. Myasthenia gravis is an autoimmune disease where you have got gradual loss of nicotinic cholinergic receptors in skeletal muscle - inc muscle weakness. Inc availablity of acetycholine in muscle to maximal stimulate receptors, if there is not enough drug using cholinesterase inhibit identifies if drug dosing is correct.

33
Q

Give an example of medium acting anticholinesterases?

A

NEOSTIGMINE
BINDS TO ANIONIC SITE OF ENZYME
CARBAMYLATES THE ENZYME, WHICH TAKES MINUTES TO HYDROLYSE/REVERSE
SLOW RECOVERY OF CARBAMYLATED ENZYME MEANS THE DRUG ACTION IS PROLONGED
NEOSTIGMINE – THERAPEUTIC EFFECT FOR 4 HOURS

Medium acting
Drug - Neostigmine muscle relaxant - only works in periphery does not cross blood brain barrier so it cant treat neurological conditions such as alzimers. Very Effective inc availably of acetylcholine to outcompete the muscle relaxant - reverse effects of muscle relaxants used in surgical procedures.

34
Q

How do anticholinesterases work?

A

Can stimulate M receptors not by activating directly but increasing availability of acetylcholine this can be done by cholinesterase inhibitors or anticholinesterases these come in three classes, short acting, medium acting and long term irreversible.

35
Q

What drugs enhance cholinergic transmission?

A

DONEPEZIL (~24hr DURATION, SLIGHT SIDE EFFECTS)
RIVASTIGMINE (~8hr DURATION – SIDE EFFECTS SUBSIDE)

ENHANCING CHOLINERGIC TRANSMISSION MAY COMPENSATE FOR DEFICITS
LIMITED USE DUE TO ADVERSE EFFECTS AND SO BENEFIT MUST OUTWEIGH THE SIDE EFFECTS

Donepezil and Rivastigmine cross the blood brain barrier, neostigmine doesn’t cross bbb. They inc availability of acetylcholine in the CNS, helps to contempsate for the loss of cholinergic transition as disease progresses. It also has an impact on the availability of acetylcholine in periphery as a consequence there’s an inc risk of side effects like you would with overstimulation of parasympathetic nerves. GI disturbance loose stools, inc contractility in bladder smooth muscle, hypotensive, reducing heart rate, broncho restriction. Sick signs syndrome irregular it in heart rate proposes you to dysrhythmia. Heart rate slows down more placemaking sites can kick in and develop self-sustaining patterns of activity if they are out pf sync tissue can quiver and not be effective.

36
Q

How do muscarinic receptor antagonists work?

A

Block pathways can have a different effect block M receptors you can get an elevated heart rate, degree of elevation and time is age dependant - young individuals high tone of parasympathetic nerves (vagal nerve) which means we recover from stressful occasions very quickly . Stress situation heart rate goes up and then reduces. Older people heart rate is elevated for longer time. In secretion if you have activates secretion blockage pathways from muscarinic dry mouth. Inhibition of bronchial secretion cant clear mucus in lunch but may be beneficial to people who have mucus problem. In smooth muscle GI motility may result in constipation, bronchodilation preventing que which causes contraction. Urinary tract relaxation bladder wall - means bladder will fill for longer will come a point where the bladder will stretch and is unable to hold urine so you need to pee.

37
Q

Examples of muscarinic antagonist receptors?

A

ATROPINE AND HYOSINE
READILY ABSORBED FROM GUT AND CROSS BLOOD BRAIN BARRIER
NATURALLY OCCURING PLANT COMPOUNDS

ATROPINE METHONITRATE
LIMITED LIPID PERMEABILITY. LESS ABLE TO CROSS BLOOD BRAIN BARRIER (REDUCED CENTRAL SIDE EFFECTS)
ATROPINE DERIVATIVE

PIRENZEPINE
M1 SELECTIVE REDUCE GASTRIC ACID SECRETION

DARIFENACIN
M3 SELECTIVE REDUCE BLADDER CONTRACTION

38
Q

What muscarinic receptor antagonist is for asthma?

A

ASTHMA
SHORT TERM RELIEF OF SYMPTOMS (DILATION)
BETA-2 AGONISTS ARE PREFERED

39
Q

What muscarinic receptor antagonist is for motion sickness?

A

MOTION SICKNESS
PREVENTATIVE (HYOSINE)
TRANSDERMAL PATCH APPLIED HOURS BEFORE TRAVEL
MOST OTHER ANTI-EMETICS ARE INEFFECTIVE

40
Q

What muscarinic receptor antagonist is for parkinsons?

A

PARKINSONS
DOPAMINE DEFICIENCY RESULTS IN CHOLINERGIC EXCESS
USED IN DRUG-INDUCED PARKINSONS (BENZATROPINE)
REDUCE TREMOR AND RIGIDITY
USE HAS DECLINED DUE TO SIDE EFFECTS

41
Q

What is an adrenoreceptor agonist?

A

ADRENALINE

CARDIAC ARREST
I.V. ADMINISTRATION CENTRAL LINE

ANAPHYLACTIC SHOCK
LARENGEAL OEDEMA, BRONCHOSPASM & HYPOTENSION
INTRAMUSCULAR ADMINSTRATION FIRST CHOICE
I.V. ADMINSTRATION IN EMERGENCY

SELF-ADMINISTRATION (EpiPEN)

WITH LOCAL ANAESTHETICS
LOCAL ANAESTHETICS DILATE BLOOD VESSELS
ADMINISTRATING VASOCONSTRICTOR SLOWS RATE OF ABSORPTION = PROLONGED ACTION

DECONGESTANTS

42
Q

example of a1 agonist?

A

α1 AGONISTS
PHENYLEPHRINE
DECONGESTANT

43
Q

example of a2 agonist?

A

CLONIDINE
HYPERTENSION & MIGRAINE
CENTRALLY ACTING HYPERTENSIVE
DECREASES CARDIAC OUTPUT & PERIPHERAL RESISTANCE
CANNOT WITHDRAW TREATMENT SUDDENLY
(HYPERTENSIVE CRISIS)

44
Q

side effects of a1 and a2?

A

SIDE EFFECTS
SEDATION
DEPRESSION
FLUID RETENTION
CONSTIPATION

45
Q

What do beta adrenoreceptors do?

A

STIMULATION OF THESE RECEPTORS RESULTS IN RELAXATION OF MOST TYPES OF SMOOTH MUSCLE (β2)

β2 (β3?) -ADRENOCEPTOR VASODILATION IS MAINLY ENDOTHELIUM DEPENDENT AND MEDIATED BY NITRIC OXIDE

β2-ADRENOCEPTOR RELAXATION MEDIATED NOT ONLY BY cAMP SIGNALLING BUT BY BKCa CHANNEL ACTIVATION.

Β3 MEDIATED SIGNALLING NOT ONLY VIA cAMP BUT BY DELAYED RECTIFIER K+ CHANNELS

46
Q

How do beta receptors effect the heart?

A

β1-ADRENOCEPTOR POWERFUL STIMULANT ACTION ON HEART

HEART RATE AND FORCE OF CONTRACTION INCREASED

INCREASED CARDIAC OUTPUT AND OXYGEN CONSUMPTION

CATECHOLAMINES CAUSE DISTURBANCE OF VENTRICULAR FIBRILLATION. (BUT ALSO USED TO TREAT FIBRILLATION ARREST)

47
Q

What do alpha receptors do?

A

VASCULAR SMOOTH MUSCLE CONSTRICTION
SKIN AND SPLANCHNIC VASCULAR BED CONSTRICTION
LARGE VEINS, ARTERIES AND ARTERIOLES CONSTRICTION

DECREASED VASCULAR COMPLIANCE
INCREASED CENTRAL VENOUS PRESSURE
INCREASED PERIPHERAL RESISTANCE

INCREASED BP INITIATES BARORECEPTOR REFLEX
CEREBRAL/CORONARY/PULMONARY BEDS UNAFFECTED

INCREASED SYSTOLIC & DIASTOLIC ARTERIAL PRESSURE INCREASED CARDIAC WORK**

48
Q

What impact do beta agonists do to metabolism?

A

ENCOURAGE THE CONVERSION OF ENERGY STORES (GLYCOGEN AND FAT) TO FREELY AVAILABLE FUELS
β1/β2-ADRENOCEPTOR -
LIVER AND MUSCLE CARBOHYDRATE METABOLISM
β3-ADRENOCEPTOR - LIPOLYSIS STIMULATION
α2-ADRENOCEPTORS - INSULIN SECRETION - HYPERGLYCAEMIA
ADRENALINE INDUCED HYPERGLYCAEMIA CAN BE BLOCKED BY BLOCKADE OF BOTH RECEPTORS (BUT NOT INDIVIDUALLY)

49
Q

What impact do beta agonists do to skeletal muscle?

A

TWITCH TENSION IS INCREASED BY β2-ADRENOCEPTOR
TREMOR OR SHAKINESS FROM DRUGS/EXCITEMENT/FEAR

50
Q

B1 adrenoreceptors example

A

β1-ADRENOCEPTORS (DOBUTAMINE)
CARDIOGENIC SHOCK (OR SEPTIC SHOCK)
INCREASE CONTRACTILITY (LITTLE EFFECT ON HEART RATE)
I.V. ADMINISTRATION

51
Q

B2 adrenoreceptors?

A

UTERINE SMOOTH MUSCLE DILATED BY THE ACTIVATION OF β2-ADRENOCEPTORS
AGONISTS CAN DELAY PREMATURE LABOUR

BRONCHIAL SMOOTH MUSCLE DILATED BY THE ACTIVATION OF β2-ADRENOCEPTORS
IMPORTANT IN THE TREATMENT OF ASTHMA

52
Q

a1 antagonists selective example and what they do?

A

PRAZOSINE – FIRST SELECTIVE ANTAGONIST
DOXAZOSINE – LONGER HALF-LIFE (ONCE DAILY DOSING)

vasodilation and fall in atrial pressure
inc cradiac output
blockage of a 2 adrenoreceptor inc noradrenaline rlease
relaxation of baldder smooth muscle neck.

53
Q

What does beta antagonists do?

A

ANTIHYPERTENSIVE ACTION

PATIENTS WITH HYPERTENSION (NOT NORMOTENSIVE) HAVE GRADUAL FALL IN ARTERIAL PRESSURE

REDUCTION IN CARDIAC OUTPUT

REDUCTION OF RENIN RELEASE (JUXTAGLOMERULAR CELLS)

CENTRAL ACTION –  SYMPATHETIC ACTIVITY

54
Q

selective b antagonists

A

PROPRANOLOL: POTENT AND PURE ANTAGONIST AT BOTH TYPES

OXPRENOLOL/ALPRENALOL :NON-SELECTIVE/PARTIAL AGONIST
NEBIVILOL: β1-SELECTIVE/ NO AGONIST ACTIVITY
ATENALOL: β1-SELECTIVE

55
Q

Which b antagonists activity depend on cardiac activity?

A

AT REST&raquo_space; PROPRANOLOL DOES NOT AFFECT HEART RATE, CARDIAC OUTPUT OR ARTERIAL PRESSURE
REDUCES EFFECTS OF EXERCISE/EXCITEMENT ON THESE

56
Q

side effects of beta antagonists?

A

bronchoconstriction - problem with asthmatics
cardiac depression - heart failure, depression can occur before benefits
bradycardia- deathly with coronary disease
hypoglaecemia- sympathetic NS warns patient when carbs is needed, blockage can mask this
fatigue - reduced cardiac output and muscle perfusion during exercise
cold extremities - reduced b mediated vasodilation

57
Q

How does adrenaline used in allergic reactions save lives?

A

Adrenaline can be used when allergic reaction occurs
Anaphalatic shock, cause massive histamine release causes bronchconstriction, hypotensive response activating H1 receptors on endothelium which activates Gq signalling so inc calcium. Calcium plus calmodium increase nitric oxide synthase which is a vasodilator and blood pressure drops. Adrenaline helps to stimulate alpha adrenoreceptors present to inc blood pressure, lots of large veins have alpha 1 adrenoreceptors inc central hamous pressure, constrction peripheral blood vessels (micro blood vessels). Help inc peripheral resistance inc blood pressure. It elevates bronchspasm - activation of beta 2 adrenoreceptors and these facilitate relaxation of airways smooth muscle making it easier to breathe.