BSI mod 2 Flashcards
voluntary NS
ach, skeletal, nicotinic M cholinergic, myelinated
curare and gallamine
nicotinic M blocker. comp but non depolarizing,
- ach can be increased by anticholinesterase (phisostigmine)
succinylcholine
nicotininc M blick, irriversible, short lasting, depolarizing non comp, degraded by cholinesterase eventually
- patients must be ventillated
anticholinesterase
neostigmine
- increase ACH everywhere. alzheimers, treat myasthenia gravis, muscle contraction since its agonist. reversible
- could work for xerostomia but increases contraction so not best
novichok
irrversibly binds cholinesterase. increases ach. sludge (musccarinic agonist) increase parasymp and blocks NMJ
* atropine antidote but not for muscccle paralysis
parasymp
long pre gang, short post gang from sacral spine
- ach is pre and post
- nicotininc N and muscarinic
- pupil small (myosis), bronchi, HR, sweat also down
symp
lumbar of spine is short pre gang, long post (many), pre NT is ach, post is NE, E, ACH
- nicotininc N
alzheimers
donepesil anticholinesterase
- glutamate too
atropine
muscarininc antagonist. dries mouth. pupil dialate (mydriasis), decrease sweating since less ach, increase HR, decrease bronchi, increase symp
** doesn’t block skeletal muscle
pilocarpine
muscarininc agonist. increase saliva for xerostomia. miosis, increase sweat and down hr, more poops
benadryl or scopolamine
muscarininc antagonist to stop motion sickness (stomach and ear). pass BBB. lower ACH, increase dopamine! antishistamine
- doesn’t work for opioids since doesn’t block dopa and serotonin too
alpha 1
everything tight on skin and mucous
prazoin (minipres)
block alpha 1 so vasodilate and bp (orthostatic hypotension)
phentolamine (oraverse)
nonselective block for alpha 1 and 2. tachycardia because of alpha 2. speeds up recovery and lip freeze
doxazosin, terazosin
block alpha 1. hypertension treatment (orthostatic problem)
tamsulosin (flomax)
alpha 1 selective. increase pee for prostate
alpha 2
DECREASES bp by stopping NE release
clondine (catapres)
stim alpha 2 so decrease Ne release and lower bp
beta 1
tight again. increase HR AND contraction force
epinephrine
agonist of alpha 2, b1 and 2. NOT in CNS from BBB. mixed with lidocaine. high HR but no hypertension for B2
propanolol (inderal)
block beta 1 and 2. slow HR. treat hypertension but blocks beta 2 so vasoconstriction
metoprolol
selectie beta 1 block so slow HE and contraction force
which 2 receptors are opposive
muscarinic M (para_) and Beta 1 (symp)
beta 2
bronchodilation. vasodilate muscle and organs.
albuterol (proventil)
agonist of beta 2. anti asthma NOT beta 1. no heart stim
atropine –> ipatropium (atrovennt)
also asthma. muscarinic antagonist so dry mouth.
* can’t pass BBB so no CNS or motion sickness blcik
l dopa synthesis
- tyrosine to dopa to dopamine then norepi (add OH) then epi (add methyl)
stop L dopa breakdown
methyl transferase inhibitor
carbidopa
stops dopa conversion OUTSIDE brain (so not for parkinsons)
what locks dopamine reuptake
cocaine
how to treat depression
block MAO, block NE reupta)ke and serotonin (kinda like cocaine)
parkinsons treatment
inhibit L dopa breakdown in brain. block COMT (C for cranial)
- benadryl to stop muscarinic . l dopa to increase dopamine, benztropine to stop muscarinic
- always HIGH muscarinic, low dopamine
nicotine
N and M agonist. increase dopamine
how to decrease BP
- blcok alpha 1 (vasodilate), block beta 1 (HR), stimulate alpha 2 (stop NE release)
ephedrine and pseudoephedrine
- stimulate alpha 1, beta 1, beta 2
- indirectly release NE
- tachyphylaxis possible where nerve terminals desen
- crosses BBB
- can make meth!
meth
- for ADHD. when withdrawal, it causes sleep and low HR
oxymetazoline (afrin)
- nasal decongest
- alpha 1 2 stim to increase BP
- bradychardia (increase HR)
- vasoconstrict
- does the teeth numb thing with tetracaine (NOT for superior alveolar nerve)
norepi
- alpha 1 and beta 1 stimulator (not beta 2)
- no bronchodilate so hypertension
dopamine
stim beta 1
- stim vasodilation! high HR through heart stimulation?? but hypotension. no BBB
isoproterenol (isuprel)
stim beta 1 and 2. anti asthma. BUT beta 1 increases HR and o2 demand
haloperidol (haldol)
schizo treatment. blocks dopamine so cause parkinsons. also block alpha 1 so hypotension
- treat the extrapyramidal effects with benztropine
benztropine
treat parkinsons. lowers ACH, increases dopa. block muscarinic
active AP propagation
charges close together so lower resistance and higher current so faster
ca channels, vescicles and speed
ca channels are close to vesicles so its fast 200 micro sec vs AP is mili sec
- ca rises from 100 nM to 100 micro M (1000x higher)
3 ways to do synaptic drugs
transmitter production, release, clearance
tetrodotoxin synaptic drug
stops synaptic transmission physically
caffeine synaptic drug
alters transmitter release by competing with presyn
cocaine and meth in synapse
- stop reuptake of transmitter
monoamine oxidase in synapse
blocks transmitter degredation
neuropeptide Y and pain
in dental caries
where does atp act in synapse
post synap
spinal chord pain inhibition
works on AbC fibers. has opiods that stimulate presynp enkephalin to crease CA and NT.
medulla and midbrain pain
diffuse control with PAG. nuclei send efferent signals to activate interneurons to mask pain with another thing
descending supra spinal
placebo response. prefrontal cortex stim the anterior cingulate cortex (ACC) via endorphine and then acc signals to midbrain and medulla. also PAG stimulates the spinal chord opiates
sympathetially maintained pain
chronic pain. rewiring of nerves
how does opioid pain work
use GPCR to increase K out, hyperpolarize mem. decrease ca in. stop adenylate cyclase to decrease camp and stop neuro activity
- also recruit b arrestin that internalize opioid receptor
c fibers are how big
0.2 to 1.5 micro m
chronic pain uses
gabapentinoids
ageusia
loss of taste
parosmia
altered perception of smell in bad odor
salty and bitter receptors are calld
KIR2.1 and T2R38
all taste GPCR pathway
activate phospholipase C of B2 (called PLCB2) using beta gamma receptor. membrane breaks off IP3, bind to ER increase Ca, then bind to TRP receptor to let Na in and calmodulin CALHM release atp to brain
pathway of taste signal
mitral cells to olfactory bulb to hypothal then orbitofrontal cortex then hippocampus
hypothal
does viscueral reactions. contains amygdala for memories
piriform cortex and orbitofrontal cortex
where taste and smell converge to get flavor. also conscious perception of food
hippocampus
does memories
taste integration
all goes to nucleus of solitary tract via cranial nerves. does salivation then hypothalamus then to taste cortex via the VPMpc (ventral basal thalamus)
chemesthesis receptors
TRP or transient receptor potential is the ion channel involved in trigger. VR1 is warm and spicy. TRPA is cold and mustard. TRPM8 is menthol and cold
smell is done by
ciliated, bipolar neuron. cn1 sensed by olfactory bulb
taste is done by
epi cells. CN 7,9,10. go to nuc of solitary tract
gymnemic acid
blocks t2 and t3 using riterpenoid saponins
Where is the first place in the brain where the olfaction and gustation systems integrate?
Orbitofrontal cortex
summary slide of how glucose gets into blood
first make na gradient using Na/K pump then use Na to get glucose in by secondary active transport. let glucose flow into blood by facilitated diffusion
cl- ion nenrnst potential
even though its pore positive than inside of cell, cl- flows OUT
how does cell NOT burst
- ions inside that make a electro eq but not concentration eq. na k pump also since we loose +1 ion so water follows it out
metabotropic ion channel pathway
stim g alpha, phospholipase c then IP3 goes to ER to release ca
what marks synapse location on dendrites
psd-95
bafilomycin
PPI of vH-atpase
choloroquine
blocks na/k channel. causes fake long QT syndrome
v1 unit in Vh-ATPAS
hydrolyses atp
name biogenic amines
dopamine, epi, norepi
acetycholine
serotonin and histamine
order of tongue
vagus innervates back of tongue
glossopharangeal does circumvallate and FOLIATE
memorize equations
yes
