Autonomic nervous system Flashcards
What is asthma? What are the signs and symptoms?
Hyper- responsiveness to stimulus such as infections, allergens (dust, polled), cigarette smoke, cold air, exercise ect, causing swelling and constriction of airways and them filling with fluid
Symptoms inc wheeze, tightness of chest, cough, night time cough
What are 3 main methods of treating athsma?
- B2 adrenoreceptor agonists (salbutamol, salmeterol)
- M3 receptor antagonists (not as effective as will only cause bronchiodilation if cause of constriction if cause is parasympathetic stimulation
- Glucocorticosteroids (anti inflammatories) to prevent response
What is hypertension? What 2 processes in the body cause it ?
High blood pressure (>140/90)
- Sympathetic nervous system activation: B1 stimulated to increase HR, a1 and B1 stimulated to constrict blood vessels
- RAAS system activated: Kideneys produce more renin, so more angiotensinogen (from liver) activated, ACE (from lungs) activates the angiotensin to angiotensin 2 which causes vasoconstriction and water retention both incease BP
State 2 ways blood pressure can be reduced by acting on the nervous system
- B1 blockers to reduce heart rate (propanolol)
- a1/ B2 blockers to cause vasodilation (prazosin)
State 4 ways hypertension can be reduced, not using adrenoreceptors
- ACE inhibitors (stop angiotensin 1–>2)
- Diuretics (decrease blood volume)
- Angiotensin inhibitors
- Calcium channel inhibitors so less ca release and less contraction of blood vessels
What is thryoxicosis? What are signs and symptoms?
Increases thyroid hormone levels (T3 & T4) usually due to hyperthyroidism. This also causes upregulation of adrenoreceptors so high HR and BP Sweating Weight loss Tiredness Fast and irregular HR Irritable and mood swings Changes to peroids Tremor Heat intolerance
How can you treat the symptoms of hyperthyroidism?
- Non- selective B antagonists (blockers) to decrease HR and BR, but need to be careful with athsmatics cos cause bronchioconstriction too
- iodine blocks release of T3 and T4 from vesicles and reduces their conversion of T4 to T3
- Thiomides inhibit thyroid hormone synthesis and storage
Give the location, G protein and effector and mode of action for a1 and a2 adrenoreceptors
a1:
- blood vessels
- q protein
- PLC
- IP3 causes ca release from SER, Ca and DAG activate PKA which phosphorylates VOCC so more Ca so blood vessels constrict
a2: - smooth muscle
- i protein
- adenylyl cyclase
- adenylyl cyclase inhibited, less PKA activates, less VOCC phosphylated so less Ca, less contraction
Give the location, G protein and effector and mode of action for B1 and B2 adrenoreceptors
B1: - heart - s type (both) - Adenylyl cyclase (both) - more ATP--> cAMP so more activation of PKA, more activation of VOCC B2: - Lungs - same but causes less Ca release and more uptake at the SER to dilate bronchi
Where can M1, M2 and M3 receptors be found?
m1= sweat glands m2= heart m3= lungs and other smooth muscle (GI, GU tract)
What G proteins do Histamine, U opioid and D1 and D2 receptors have?
H= Q
U- i
D1= s
D2= i
How is noradrenaline synthesised, stored and released and reuptaken at a sympathetic postganglionic neurones of the smooth muscle in the GI tract?
Synthesis: Tyrosine enters cell, converted to DOPA, converted to dopamine, put into vesicle and then converted to noradrenaline by dopamine-b- hydroxylase
Storage: in vesicle
Release: Ca causes release by binding to synaptotagmin and creating fusion pore
Re-uptake: 95% back in through Na dependant high affinity transporter (Uptake1). 5% in through other methods (uptake2). 10% then metabolised and 90% reuptaken into vesicles
Are nicotinic ACh receptors are neuromuscular junctions and at autonomic ganglia (not post ganglia) different enough to allow selectivity of drugs towards them?
Yes- eg trimethaphan causes hypotension in hypertensive emergencies
Are many drugs available that are selective to the different muscarinic ACh receptors?
Nope, some can exhbit tissue selectivity though
How can the actions of endogenously released ACh be enhanced, for example for treatment of myasthenia gravis
Acetyl choline esterase inhibitors
What stages of synaptic transmission are common sites for drug action?
- degradation of transmitter not in a vesicle
- inactivation of transmitter (eg by AChesterase, quite unique to ACh)
- Interaction with post synaptic receptors (eg B2 blockers ect)
- Interaction of neurotransmitter with PRE synaptic membrane
- Re- Uptake of neurotransmitter
What could cause massive discharge of the parasympathetic nervous system(SLUDGE syndrome) ?
Drug overdose
Ingestion of magic muschrooms
Exposure to nerve gases or organophosphorus insecticides which modify and inactivate ACh esterase so ACh levels raise
What does the SLUDGE mneumoic stand for?
How can it be treated?
Salivation Lacrimation - lacrimal glands (tears?) Urination Defection GI upset- inc diarrhoea Emesis- vomiting // Treat with anti- cholinergic agents (atropine)
From what regions do sympathetic nerves originate?
Describe their pre and post ganglionic fibres?
Where are the ganglia of the post ganglia located?
- Originate from thoracic and lumbar regions (middle and lower)
- pre ganglions are short and myelinated
- Post ganglions are long and unmyelinated
- ganglia located along paravertebral chain close to spinal cord
Where do the parasympathetic nerves originate?
Describe the pre and post ganglionic fibres
Medullary and sacral regions (although some now think its only medullary and sacral is sympathetic)
Long myelinated preganglionic fibres
Short unmyelinated postganglion fibres in the innervated tissue
Describe the neurotransmitters and receptors at pre and post ganglia of the sympathetic nervous system
Pre ganglia: usually ACh to nicotinic ACh receptor
Post ganglia: usually noradrenaline to adrenergic receptor
Describe the neurotransmitters and receptors at pre and post ganglia of the parasympathetic nervous system
pre ganglia: ACh released to nicotinic ACh receptor
post ganglia: ACh released to muscarinic ACh receptor
Give two exceptions to the neurochemical anatomy of the sympathetic nervous system
- post ganglion nerves to sweat glands and heart erector muscles use muscarinic Ach receptors and release ACh not NA
- there is only one nerve going to the adrenal medulla , it releases ACh onto nicotinic ACh receptors on chromaffin cells which secrete adrenaline into blood stream
State two neurotransmitters used by Non- Adrenergic, Non- cholinergic receptors
ATP, Nitric Oxide
State consequences of increase sympathetic stimulation
- increased HR (by + intropy in ventricles and tachycarida at SA node)
- Vasoconstriction (both = higher BP)
- bronchioles relax
- bladder sphincer contract
- radial muscle contract (eye)
- increased salivary secretion
- renin release ( increase BP)
