drugs

Question 1

can receptors be present where innervation is not? 2 examples?

Answer 1

yes.

• receptor and nerve for bronchioles in parasympathetic ns (restriction) but only receptors in sympathetic
• receptor and nerve in blood vessels for sympathetic (restriction), but not parasymp

Question 2

increased heart rate is aka

decreased heart rate is

Answer 2

tachycardia

bradycardia

Question 3

what’s special about the heart, in terms of exception?

Answer 3

usually, alpha NA receptors cause excitation, beta cause inhibition. here,

• alpha causes decreased herat rate
• beta causes increased heart rate

Question 4

what’s special about sweating?

Answer 4

its a sympathetic response, but nt involved is ACh not NA. therefore, these nerves are called sympathetic cholinergic nerves

Question 5

can ACh and NA receptors coexist

Answer 5

yes

Question 6

whawt are the two types of ACh receptors and where are they found?

Answer 6

nicotinic - skeletal muscle, adrenal medulla, in ganglion

muscarinic: postganglionic neuron - target junction

Question 7

adrenoreceptors are organised into types based on the relative strength of isoprenaline, noradrenaline and adrenaline at the receptors. what are the relative strengths for alpha and beta?

Answer 7

alpha –> excitatory –> N>A>I

beta –> inhibitory –> I>A>N

Question 8

what drug targets ACh release

Answer 8

botulinium neurotoxin

Question 9

how does botulinium neurotoxin work, and its effects?

Answer 9

cleaves snare proteins, preventing ACh vesicle release
effects
-reduced skeletal muscle activation: drooping, difficulty swallowing, slurred speech
-increased sympaethic effects

Question 10

uses of botulinium neurotoxin?

Answer 10

• as botox

- treating diseases with spasms: eg. cerebral palsy (unregulated) and blepharospasm (eye spasm)

Question 11

effects of muscarinic agonists (parasympathomimetics)

Answer 11

increased parasympaethic activation

Question 12

effects of muscarinic antagonists? (parasympatholytics)

Answer 12

increased sympathetic activity

Question 13

describe how anti-acetylcholinesterases work

Answer 13

inhibit ACh-esterases

results in more ACh present, also more parasympathetic effects

Question 14

therapeutic effects of anti ACHases

Answer 14

treat diseases where ACh reduction is implicated

• alzheimers
• myasthenia gravis: autoimmune disease targetting nicotinic receptors

Question 15

ACHase side effects

Answer 15

increased parasympathetic activation, ultimately cholinergic crisis

Question 16

can NA be used itself?

Answer 16

yes - eg in epipen

Question 17

describe how NA synthesis can be taken advantage of to use dopamine

Answer 17

tyrosine –> dopamine –> DOPA –> NA –> A
DOPA can cross BBB and treat parkinson’s
medication has DOPA decarboxylase inhibitors to prevent it from turning to NA.

Question 18

effects of drugs blocking NA release?

Answer 18

increased parasympathetic arousal

Question 19

how do drugs facilitating NA release work? effects? examples?

Answer 19

drugs go into A.T. cause NT’s to be relased from vesicles and come out through an alternative pathway. increasing sympathetic activity
eg. amphetamine (also implicated in dopamine production, hence additction)

Question 20

Uptake I and II inhibitors for NA?

effects

Answer 20

• cocaine for I
• corticosteroids for II
• -> increased sympaethic arousal

Question 21

drugs affecting NA metabolism

Answer 21

MAO - inhibitors

MAO removes NA in the AT. therefore, MAO-I causes increase in NA, hence sympathetic effecs