drugs Flashcards
can receptors be present where innervation is not? 2 examples?
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
increased heart rate is aka
decreased heart rate is
tachycardia
bradycardia
what’s special about the heart, in terms of exception?
usually, alpha NA receptors cause excitation, beta cause inhibition. here,
- alpha causes decreased herat rate
- beta causes increased heart rate
what’s special about sweating?
its a sympathetic response, but nt involved is ACh not NA. therefore, these nerves are called sympathetic cholinergic nerves
can ACh and NA receptors coexist
yes
whawt are the two types of ACh receptors and where are they found?
nicotinic - skeletal muscle, adrenal medulla, in ganglion
muscarinic: postganglionic neuron - target junction
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?
alpha –> excitatory –> N>A>I
beta –> inhibitory –> I>A>N
what drug targets ACh release
botulinium neurotoxin
how does botulinium neurotoxin work, and its effects?
cleaves snare proteins, preventing ACh vesicle release
effects
-reduced skeletal muscle activation: drooping, difficulty swallowing, slurred speech
-increased sympaethic effects
uses of botulinium neurotoxin?
- as botox
- treating diseases with spasms: eg. cerebral palsy (unregulated) and blepharospasm (eye spasm)
effects of muscarinic agonists (parasympathomimetics)
increased parasympaethic activation
effects of muscarinic antagonists? (parasympatholytics)
increased sympathetic activity
describe how anti-acetylcholinesterases work
inhibit ACh-esterases
results in more ACh present, also more parasympathetic effects
therapeutic effects of anti ACHases
treat diseases where ACh reduction is implicated
- alzheimers
- myasthenia gravis: autoimmune disease targetting nicotinic receptors
ACHase side effects
increased parasympathetic activation, ultimately cholinergic crisis
can NA be used itself?
yes - eg in epipen
describe how NA synthesis can be taken advantage of to use dopamine
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.
effects of drugs blocking NA release?
increased parasympathetic arousal
how do drugs facilitating NA release work? effects? examples?
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)
Uptake I and II inhibitors for NA?
effects
- cocaine for I
- corticosteroids for II
- -> increased sympaethic arousal
drugs affecting NA metabolism
MAO - inhibitors
MAO removes NA in the AT. therefore, MAO-I causes increase in NA, hence sympathetic effecs