Pharmacology 1A Flashcards
1
Q
pharmacodynamics
A
what the drug does to the body
2
Q
pharmacokinetics
A
what the body does to the drug
3
Q
drug
A
substance with a known chemical structure that produces a biological effect when administered to a living organism
4
Q
drug product
A
substance or combination of substances with added ingredients which is intended to treat, prevent, diagnose or relieve symptoms of disease or abnormal conditions
5
Q
drug target
A
molecule in the body which is intrinsically associated with a particular disease process that can be targeted by a drug to reach a therapeutic effect
6
Q
post translational modification: phosphorylation
A
adds phosphate to serine, threonine or tyrosine
7
Q
post translational modification: lipidation
A
adds a lipid to a protein chain
8
Q
post translational modification: ubiquitination
A
adds ubiquitin to a lysine residue of a target protein marking it for destruction
9
Q
post translational modification: disulfide bond
A
covalently links two S atoms of two cytosine residues
10
Q
post translational modification: acetylation
A
adds acetyl group to N terminus of a protein to increase stability
11
Q
post translational modification: glycosylation
A
attaches sugar to N or O atom in aa side chain
12
Q
protein traffic process
A
protein synthesis by RER
folding by chaperone proteins
progression and modification along golgi
transported
13
Q
drug targets: receptor
A
membrane
activates target protein causing bioligical response
14
Q
drug targets: ion channels
A
membrane
changes channel conformation
changes ion conductance
15
Q
drug targets: enzymes
A
cytosol
blocks substrate
16
Q
drug targets: transport proteins
A
membrane
changes transport
17
Q
process of intracellular singalling
A
ligan binds to receptor
intracellular protein activated
activates effector proteind
18
Q
protein kinases function
A
phosphorylate proteins
19
Q
intracellular signalling: contact dependent
A
membrane boiund signal molecule binds to receptor on target cell
short range
20
Q
intracellular signalling: paracrine
A
signalling cell releases local mediators which bind to target cells
short range
21
Q
intracellular signalling: synaptic
A
neurotransmitter released from synapse
long range
22
Q
intracellular signalling: endocrine
A
releases hormone into bloodstream which binds to receptors on target cells
long range
23
Q
GPCRs function
A
ligand binds
activated G protein
activates effectors
24
Q
Gs alpha
A
activates adenylyl cyclase
25
Gi alpha
inhibits adenylyl cyclase
26
Gq alpha
activates phospholipase C
27
Gi beta gamma
opens K+ ion channels
28
mechanism of propanolol
blocks Gs coupled beta adrenergic receptor stopping effect of adrenaline on heart
reduces blood pressure
29
mechanism of salbutamol
Gs beta 2 adrenergic receptor mimics action of adrenaline on lungs
30
mechanism of atropine
blocks muscarinic coupled Ach receptor blocking effect of Ach on heart
31
mechanism of cimetidine
competitive antagonist of Gs coupled H2 receptors
blocks stomach acid secretion
32
kinase linked receptors
inactive until signal molecule binds
monomers which can become dimers
allow intracellular signalling proteins to interact
33
mechanism of receptor tyrosine kinases
signal binds
RTK phosphorylated
inactive intracellular proteins bind
34
mechanism of nuclear receptors
signal enters cell
interacts with intracellular nuclear receptor in cytosol or nucleus
signal enters nucleus
signal interacts with DNA to alter transcription
altered protein synthesis
35
examples of nuclear receptors
GR receptor - immune disorders
ER receptor - breast cancer
36
competitive enzyme drugs
mimics substrate but not catalysed
37
false substrate enzyme drugs
mimics substrate and is catalysed
38
non-competitive enzyme drugs
binds to allosteric site
39
reversible enzyme drugs
high levels of substrate overcomes inhibition
40
irreversible enzyme drugs
binds very tightly/ covalently modifying the enzyme
41
irreversible inactivation by aspirin
inactivation of COX-1 and 2 by enzyme acetylation
anti-inflammatory: reduces synthesis of prostanoids
anti-thrombotic: reduces platelet function
42
pro drug
enzyme converts inactive drug to active drug
43
multipass transmembrane protein
cross membrane many times
change conformation many times to transfer molecule
active or passive
44
uniport
one molecule down its conc gradient
45
symport
1 molecule down conc, one molecular against conc in same direction
46
antiport
1 molecules in opposite directions
47
mechanism or digoxin
blocks Na+/K+ ATPase
decreases electrochemical gradient
increased Ca2+ in cell
increased contraction
48
mechanism of tubocurarine
blocks ACh receptor
reduced contractions
49
causes of side effects and toxicity
insufficiently selective
too selective
permanent changes after long term use
lack of knowledge of disease process
patient variability
drug interactions
50
agonistt
evokes response
51
antagonist
blocks another effector molecule
52
what determines the selectivity of a drug
mutual affinity of drug and receptor
53
law of mass action
rate of chemical reaction is proportional to the product concentration of the reactant
54
k+1
rate of association
55
k-1
rate of dissociation
56
KD
affinity
[D] which occupies 50% of R at equilibrium
57
high KD
low affinity for receptor
58
low KD
high affinity for receptor
59
receptor occupany equation
P = [D]/[D]+KD
60
when is the receptor occupancy equation valid
equilibrium
[D] at receptors = [D] applied
1 drug binds to 1 receptor
negligible amount of drug added binds
binding of one drug does not affect binding of another
61
asymptote on binding curve
RT
62
efficacy
amount of time complex spends in DR*
63
the pharmacological response
binding of drug to receptor
activation of receptors and production of response
64
affinity and efficacy equation
D+RDRDR*
65
what does a large beta in efficacy show
high efficacy
66
what does a large alpha in efficacy show
low efficacy
67
EC50
concentration of drug that gives 50% of maximum response
68
what does greater efficacy mean on a concentration response curve
greater separation of functional response curve from the binding curve
69
binding curve
always to the right of the functional response curve
70
calculating receptor reserve
KD/EC50
71
relationship of EC50 to KD for weak agonists
EC50 close to KD
72
effect of reducing receptor number on CRC
shifts right
73
potency
relative concentration of drug required to produce a particular response
74
testing different agonists on same preparation
relative position of curve dependent on affinity and efficacy of each agonist
75
testing same agonist on different preparations
relative position of curve dependent on receptor number
76
full agonists
evoke maximum response by tissue
high efficacy
77
partial agonists
efficacy so low that maximum response is less than full response
no spare receptors
78
receptor desensitisation
receptor function is downgraded if they are activated continuously for too long or too frequently
changes to receptors
79
antagonism
inhibition of an agonist
80
competitive antagonism
binds at agonist recognition site preventing access of normal logand
81
non-competitive antagonism
does not bind at agonist site but inhibits another way
82
uncompetitive antagonism
binding occurs to an active form of the receptors
83
physiological antagonism
effect of hormone/ neurotransmitter is countered by action of anothet
84
effect of antagonist on CRC
depression of maximum response
curve shifts right
shows decrease in sensitivity to the agonist
85
effect of competitive antagonism on CRC
CRC shifts right with increase antagonist conc
calculate KB of antagonist
86
concentration ratio
[agonist] w/antagonist: [agonist] wo/antagonist which produces the same response
87
schild plot
slope = 1, antagonist is competitive
x-intercept = -logKB
88
experimental conditions required to draw a schild plot
parallel shift in CRC to right
no reduction in maximum response
89
gaddum-schild method
crc wo and w antagonist
find conc ratio
apply gaddum schild equation
90
gaddum-schild equation
[D1]/[D1]^1 = 1 + ([B]/KB)
91
advantages of using the Gaddum Schild equation
quick
only 2 CRC required
92
disadvantages of using gaddum schild equation
produces only one shift by the antagonist, may not be sufficient to ensure it would produce parallel shifts
variability of any CRC along conc. axis reduced when multiple curves used
93
haloperidol
dopamine receptor antagonist
antipsychotic
94
irreversible competitive antagonism on CRC
reduces receptor reserve sp maximum response decreases
95
allosteric modulator
binds and changes binding of agonist to its site
rightward shift of curve
96
what can radioligand binding be used to study
cell membrane fragments
whole cell
intact tissue
97
components of a radioligand binding assay
radioligand
cell membranes
buffer
98
non-specific binding
radioligand binds to non-receptor sites
99
accounting for non-specific binding
use high concentration of non-radioactive drug
competing ligand blocks all specific binding but non--specific binding
specific binding of ligand to receptor
non-specific binding involves ligand charge and hydrophobicity
100
ligand binding kinetics equations
KD = k off/ k on
101
ligand binding kinetics graph exponential
k on
102
ligand binding kinetics plateau into curve down
k off
103
rate constant equations
Ct = C0*e^-kt
t1/2 = 0.693/k
104
determining k on equation
t1/2 = 0.693/k obs
k obs = k on * [L] + k off
105
determining k off equation
t1/2 = 0.693/k off
k off = 0.693/t1/2
106
why is maximum binding of a radioligand lower than Bmax in a competition assay
[R] is usually around the KD of the radioligand
107
IC50
concentration of displacing ligand that displaces 50% of specific radioligand binding
108
why is IC50 not equal to KDD
IC50 is not constant
depends on concentration of R used in assay
KD is constant
109
calculate KD from IC50
Ki/KD = IC50/ 1+([L]/KD)
110
Ki
KD of nonradioactive ligands
111
recombinant therapeautic proteins
gene extracted, amplified and modified
added to vector then to bacterium
bacterium suynthesises new protein
112
characteristics of biologics
produced by living cells
structure depends on cell used
not available orally
long half life
highly specific extracellular targets
too large to cross cell membrane
113
therapeutic uses of biologics
replace deficient or abnormal proteins
enhancing or inhibiting bioligcal processes
provides novel function or activity
114
monoclonal antibodies: ligand blockade
binds to endogenous ligand so cannot bind to receptor
binds to receptor so ligand cannot bind
115
monoclonal antibodies: receptor downregulation
antibody binds to receptor on active immune cell
receptor internalised
immune cell deactivated
116
monoclonal antibodies: signalling induction
antibody binds to receptor
apoptosis
117
monoclonal antibodies: complement dependent cytotoxicity
antibodies bind
further molecule binds
apoptosis
118
monoclonal antibodies: antibody dependent cell mediated cytotoxicity
antibody binds to tumour cell
natural killer cell binds to antibody
tumour cell apoptosis
119
monoclonal antibodies: antibody dependent cellular phagocytosis
antibodies bind to cell
macrophage binds to antibodies
phagocytosis
120
monoclonal antibodies: payload delivery
payload/ drug attached to antibody
antibody binds
effect
121
treatments using monoclonal antibodies
autoimmune diseases
cancer
inflammatory diseases
122
mechanism of treating rheumatoid arthritis
TNF alpha converted to soluble form by enzyme
TNF binds to receptor causing effect
use ligand blockade to treat
123
recombinant proteins as biologics
fast acting insulin analogues
long acting insulin analogues
124
fast acting insulin analogues
meal control
quick absorption
produced in yeast and bacteria
125
long acting insulin analogues
basal control
safer
flexible dosing
126
why are vectors required for DNA insertion
DNA is negative so cannot cross cell membrane
127
process of vector delivery
uptake, uncoating and transport
genome persistence
transcriptional activity
immune response
128
in vivo gene delivery
vector created
injected into patient
reaches target organ
129
ex vivo gene delivery
cells extracted, isolated and grown
therapeautic gene added to vector then to cell
modified cells introduced to patient
reaches target organ
130
properties for an ideal vector for monogenic diseases
high conc
amenable to larger scale
stable
site specific
tuneable expression
selective
non-immunogen
131
AAV transfection
vector englufed into endosome
vector escapes or doesn't escape endosome
enters nucleus
132
why can vectors escape the endosome
endosome has relatively low pH so enzymes on virus can escape
133
retroviral vectors
integrate into host DNA
use reverse transcriptase
134
disadvantages of vectors
cells which vector enters could be destroyed by immune system
little control over where in genome new gene is added
retroviral vectors less common as cut genes in wrong place
135
autologous and allogenic cells as bioloigics
blood and blood products
embryonic stem cells
induced pluripotent stem cells
genetically modified cells
136
antisense oligonucleotides as biologics
short DNA/RNA molecules
complementary to target gene
suppress expression of harmful gene
enzyme resistant
do not reach CNS
137
why is ADME important
know if drug will be absorbed if given by particular route
estimate accurate Cp of a drug as a function of time
to know where the drug goes once in the body
if drug metabolites are safe
138
why must you not give the second dose of a drug too soon
will exceed safe Cp
139
why must you not give the second dose of a drug too late
Cp spends too long below minimum effective dose
140
enteral
via GI tract
oral administration
141
advantages of oral administration
easy
142
disadvantages of oral administratipn
issue of compliance
vomitting/ unconsciousness
143
parentral
not via GI tract
IV, IM or SC
144
advantages of IV administration
no absorption phase
rapid
145
advantages of IM administration
no issue of compliance
146
advantages of SC administration
relatively easy to self-administer
147
oral bioavailability
F
fraction of drug that reaches systemic circulation
148
oral bioavailability equation
F = AUC oral / AUC IV
149
factors affecting oral bioavailability
poor absorption in GI tract
breakdown of drug in GI tract
first pass effect
lipid solubility
150
henderson-hasselbalch for weak acids
pH = pKa + log([A-]/[HA])
151
henderson-hasselbalch for weak bases
pH = pKa + log([HA]/[A-])
152
what does the degree of drug distribution depend on
lipid solubility
plasma protein binding
153
what does rate of distribution depend on
rate of blood flow
154
apparent volume of distribution
Vd
volume of water which a drug would have to be distributed to give its Cp
155
Vd equarion
Vd = amount of drug in body / Cp
156
plasma half life
how long drug stays in body
157
excretion
movement of drug from inside body to outside of body
158
metabolism
chemical change in drug structure
159
elimination
overall removal of drug from body
160
locations of metabolism
kidneys
plasma
lungs
liver
161
methods of excretion
bile
milk
faeces
vomit
urine
162
calculating rate of elimination
Cl * Cp
163
calulcating Cl
rate of elimination / Cp
164
clearance
Cl
amount of plasma which is cleared of drug content per unit time
usually constant
165
when does Cl change
renal/ hepatic disease
166
1st order drug elmination
Cl is constant but rate of elimination depends on how much drug is present
faster rate at higher Cp
167
0 order drug elimination
rate independent of drug concentration
168
pseudo-0 order drug elimination
0 order at high Cp
1st order at lower Cp
169
describing first order elimination
exponential equation
Ct = C0*e^-kt
t1/2 = 0.693*Vd/Cl
170
what happens to Cp as rate of absorption decreases
peak Cp decreases
time to reach peak Cp increases
longer the drug persists in the body
171
what does the plateau of an IV Cp-t graph show
steady state concentration
(Css)
172
calculating rate of elimination
Css*Cl
173
how many half lives does it take to reach Css
5
174
what is constant about Css
time to reach Css
175
calculating Css of oral infusion
Css = D*F/T*Cl
D = dose
T = time between doses
176
when are drugs excreted via the kidney
non lipid soluble drugs
non lipid soluble metabolites
177
3 ways of renal drug excretion
glomerulus filtration
active secretion
passive reasborption
178
changes in urinary pH due to weak acid drug
make urine more alkaline
179
changes in urinary pH due to weak base drug
make urine more acidic
180
forced alkaline diruesis
bicarbonate + diuretic
181
drug metabolites
drug to inactive metabolite
drug to active metabolite
drug to toxic metabolite
inactive drug to active drug
182
hepatic drug metabolism process
drug (lipid soluble)
phase 1 metabolism
derivative
phase 2 metabolism
conjugate (less lipid soluble)
183
phase 1 drug metabolism
dug oxidises, reduced or hydrolysed
introduces active site/ exposes reactive site on drug
184
example of oxidation in phase 1 metabolism
aromatic hydroxylation - propanolol
185
example of reduction in phase 1 metabolism
nitro reduction - chloramphenicol
186
example of hydrolysis in phase 1 metabolism
ester hydrolysis - procaine
187
phase 2 metabolism
conjugation of phase 1 to polar molecules
easier to excrete in urine as is less lipid soluble
188
example of phase 2 metabolism
glycine conjugation - salicylic acid
189
which enzymes carry out phase 1 metabolism
microsomal enzymes in the ER of the liver
cytochrome P450 enzymes
190
where does phase 2 metabolism generally occur
cytosol of liver cells
191
full metabolism of aspirin
aspirin
phase 1 hydrolysis to salicylatye
phase 2 glucoronidation, glycine conjugation and oxidation
192
factors affecting drug metabolism: enzyme induction
drugs and environmental pollution induce increased cytochrome P450 production
leads to some drugs unable to produce significant effect
193
factors affecting drug metabolism: enzyme inhbition
some drugs inhbit cytochrome P450 enzymes
increases chance of side effects
194
factors affecting drug metabolism: genetic polymorphisms
poor ability to metabolise drugs in some people
195
isoniazid experiment
some people fast acetylators, some slow
shows genetic polymorphisms
196
factors affecting drug metabolism: disease
liver disease, drug not metabolised
renal disease, excreted unchanged
thyroid disease, decreased drug metabolism
cardiovascular disease, slower rate of delivery to livery and kidneys
197
factors affecting drug metabolism: age
very young and very old worse at metabolism
198
absorption of biologics
parenteral administration
long time to peak Cp
199
distribution of biologics
small Vd
via lymph
200
elimination of biologics
long half life
via proteolysis
201
GABAergic neurone
releases GABA
synthesised by glutamate decarboxylase
202
noradrenergic modulatory neurone
releases catecholamines
synthesised by tyrosine hydroxylase and dopamine beta hydroxylase
203
mechanisms of fast post synaptic responses
isonotropic actions
ion channels
204
neurotransmitters involved in fast post synaptic responses
glutamate
GABA
acetylcholine
205
mechanisms of slow post synaptic responses
metabotropic actions
GPCRs
206
neurotransmitters in fast post synaptic responses
glutamate
GABA
acetylcholine
monoamines
207
voltage gated sodium ion channels as drug targets
blockers stop electrical transmissiomn
208
examples of sodium ion channel blockers
lignocaine - anaesthetic
phenytoin - epilepsy
209
voltage gated calcium ion channels as drug targets
blockers inhibit neurotransmitter release
210
examples of calcium ion channel blockers
ziconotide - neuropathic pain
211
exocytosis as a drug target
precursor of transmission stimulating production of neurotransmitter
212
examples of exocytosis drugs
carbidopa - parkinsons
213
vesicular storage as a drug target
blockers lead to empty vesicles
214
examples of vesicular storage blockers
ampethamine - stimulant
215
presynaptic transmitter uptake as a drug target
blockers prolong transmitter action
216
examples of presynaptic transmitter blockers
fluoxetine - depression
217
transmitter breakdown as a drug target
blockers prolong transmitter actions
218
examples of transmitter breakdown blockers
neostigmine - myasthenia gravis
219
post synaptic isonotropic receptors as drug targets
blockers inhibit transmitter effects
allosteric modulators enhance effects
220
examples of post synaptic isonotropic receptor blockers
tubocurarine - muscle relaxation
221
examples of post synaptic isonotropic receptor allosteric modulators
diazepam - anxiety
222
fight or flight: cardiovascular
increased blood supply to brain and muscles
223
fight or flight: airways
facilitated breathing
224
fight or flight: energy metabolism
provision of glucose for respiration
225
fight or flight: eyes
adjust to widefield
more but less clear
226
fight or flight: sweat glands
cooling during sustained exertion
227
fight or flight: digestion
suppressed
228
rest and digest: digestion
stimulated
229
rest and digest: cardiovascular
slows down, blood pressure drops
230
rest and digest: airways
breathing efficiency decreased to clear muccus from airways
231
rest and digest: eyes
adjusted to near vision
232
neuronal organisation of the parasympathetic nervous system
long preganglionic axon
short postganglionic axon
233
neuronal organisation of the sympathetic nervous system
short preganglionic axon
long postganglionic axon
234
parasympathetic control of vital organs
vagus nerve
medulla oblongata
235
sympathetic control of vital organs
chain of sympathetic ganglia
236
why is drug treatment for the ANS important
and examples
major physiological role in homeostasis
angina, asthma, urinary problems
237
enzyme that synthesises ACh
choline acetyl transferase
CAT
238
enzyme that hydrolyses ACh
acetylcholine esterase
AChE
239
termination of ACh signal by AChE
acetyl binds to esteratic region
choline binds to anionic region
240
muscarinic ACh receptor mechanism
2 ACh binding sites
ligand gated ion channels
allow depolarisation of post ganglionic neurone
241
M2 receptor
heart
Gi/oPCR
decreases cAMP and Ca2+ signalling
decreases electrical excitability
242
M3 and M1 receptor
GI, airways, bladder, eyes
GqPCRs
increase Ca2+ signalling
increase smooth muscle contraction
stimulate glandular secretion
243
parasympathetic control of secretion
signalled by vagus nerve
increases secretion
244
parasympathetic contraction of smooth muscle process
ACh to M3
Gq > PLC > IP3
Ca2+ enters cytosol and binds to calmodulin
CaM phosphorylates MLCK
contracts
245
noradrenergic nerve terminal process
Ca2+ move in during depolarisation
NA released into synapse
binds to alpha and beta receptors
reuptake by NA transporter
broken down by MAO or COMT
246
tyrosine to adrenaline
tyrosine to DOPA by tyrosine hydroxylase
DOPA to dopamine by DOPA decarboxylase
dopamine to noradrenaline by dopamine beta hydroxylase
noradrenaline to adrenaline by PNMT
247
adrenergic receptors on ANS effector organs: alpha 1
blood vessels, eyes
GqPCRs
increase Ca2+ signalling
smooth muscle contracts
248
adrenergic receptors on ANS effector organs: beta 1
heart
GsPCR
increase cAMP signalling
increase electrical excitability and muscle contraction
249
adrenergic receptors on ANS effector organs: beta 2
bronchi, uterus, GI, vascular, liver, adipose, bladder, eyes
GsPCR
increase cAMP signalling
relax smooth muscle
increase glucose conc
250
parasympathomimetics
activate PSNS
251
sympathomimetics
activate SNS
252
parasympatholytic
inhibits PSNS relative to SNS
253
sympatholytic
inhibits SNS relative to PSNS
254
parasympathetic activation of the heart
ACh activates M2 receptors in atria
decreases heart rate
255
clinical application of parasympathetic activation of the hjeart
atropine to treat brachycardia
256
sympathetic activation of the heart
noradrenaline activates beta 1
increase HR, conductivity and force of contraction
257
clinical applications of sympathetic activation of the heart
adrenaline during cardoiac arrest
isoprenaline during shock
258
parasympathetic activation of blood vessels
ACh activates M3 on endothelium
stimulates NO production in cells
relaxes smooth muscles
decreases BP
259
clinical application of parasympathetic activation of blood vessel
glyceryl trinitate - donates NO lowering BP for anginas
260
sympathetic activation of blood vessels
noradrenaline and adrenaline
alpha 1 receptors causing contraction
beta 2 receptors causing relaxation
261
clinical application of sympathetic activation of blood vessels
adrenaline - anaphylaxis
phenylephrine - hypotension
262
parasympathetic activation of airways
ACh actiavtes M3
bronchoconstriction
stimulates secretion from airway glands
recuperate airway apithelia
263
clinical applications of parasympathetic activation of airways
ipratropium - muscle relaxation in esthma
264
sympathetic activation of of airways
NA activates beta 2 in trachea and bronchi
relaxation
increases airflow
increases blood O2
265
clinical application of sympathetic activation of airwayts
salbutamol - asthm,a
266
parasympthetic activation of digestion
ACh activates M3 in smooth muscle, increased peristalsis
ACh activates M1 and M3 in glands, icreased saliva and acid
267
clinical application of parasympathetic activation of digestiuon
pilocarpine - M3 agonist increases saliva
bethanechol - M3 agonist stimulates GI motility
268
sympathetic activation of digestion and metabolisation
NA and A activate alpha and beta in liver and adipose
glycogenolysis, gluconeogenesis, lipolysis
NA activates beta 2 in GI
decreases peristalsis
increases blood glucose
269
clinical application of increased sympathetic activation of digestiob and metabolisation
clenbuterol - weight loss and body building
270
parasympathetic activation of the bladder
ACh activates M3 in detrusor musckle
detrusor contracts to empty bladder
271
clinical application of parasympathetic activation of the bladder
bethanecol - M3 agonist, bladder emptying
272
sympathetic activation of the bladder
NA activates B2 receptors on detrusor muscle - relaxes
NA activates a1 receptors on sphincter - constricts
273
clinical application of sympathetic activation of the bladder
prazosin - a1 antagonist, bladder emptying
274
sympathetic activation of the pupil
NA activates a in radial dilator
contracts
widens pupil
increases field of view and light sensitivity
275
clinical applications of sympathetic activation of the pupil
atropine - M3 antagonist, mydriasis
276
parasympathetic activation of the pupil
ACh activates M3 in circular iris muscle
constricts
miosis
277
parasympathetic activation of the lens
ACh activates M3 in ciliary muscles
decrease focal length
near vision
278
sympathethic activation of intraocular fluid
NA activates b receptors in epithelium of ciliary
fluid secretion
NA activates a receptors on iris radial muscle
hinders fluid drainage
increase IO pressure
279
parasympathetic activation of intraocular fluid
fluid drained from canal of schlemm
activation of circular pupil muscle helps fluid drainage
decreases IO pressure
280
clinical application of parasympathetic activation of intraocular fluid
dilocarpine - glaucoma
281
sympathetic activation of sweat glands
keep body cool
282
clinical application of sympathetic activation of sweat glands
glycopyrronium - reduce excessive perspiration
283
indirectly acting drugs
dont act directly on the ANS receptors but affect the concentration of ANS transmitters in extracellular space
284
indirectly acting on cholinergic transmission
parasympaths
285
indirectly acting on adrenergic transmission
sympaths
286
activation/ inhibition of ganglionic nicotinic ACh receptors
no distinction between symp and parasymp ganglia
combination of effects
287
clinical application of activation/ inhibition of ganglionic nicotinic ACh receptors
carbachol - nictotine addiction
288
mechanism of autonomic relfexes in brain stem
detect change
afferents]
processing
efferents
effector
289
eexample of autonomic relfexes in brain stem
baroreceptor reflex
290
mechanism of autonomic reflexes in the spinal chord
detects
afferents
291
what triggers ANS responses
visceral and somatic effects
292
clinical applications of autonomic reflexes in the spinal chord
noxious or non-noxious stimuli in autonomic dysreflexia
293
AChE inhbitors
reversible medium term action - neostigmine
irreversible long term action - insecticides and nerve gases
294
indirect sympahomimeticas
longer ACh signals at cholinergic syunapses
295
indirect parasympatholytics
affect ACh synthetsisn storage and release
296
clinical application of parasympatholytics
botox
297
indirectly acting symopatholytics
displace NA from vesicles
298
sympaethetic inhibition of transmitter release
NA activates a2 receptors on presynaptic terminals
inhibits PSNS terminal via heteroreceptors
299
parasympathetic inhbition of transmitter release
activation M2 on nAChRs on presynaptic terminals
inhbition of noradrenergic terminals
300
indirectly acting sympatholytics
affect NA storagr and release
301
stereoisomer
same sequence of atoms and bonds bit different 3D arrangement
302
enantiomers
non-superimposable mirror images
303
diastereoisomers
not mirror images of each other
304
entomer
useful isomer
305
distomer
not useful isomer
306
eudismic ratio
eutomer:distomer ratio
307
alkylating agents
covalently bond to DNA base pairs triggering apoptosi
308
doxorubicin
planar structure allows is tot slide between parallel base pairs
prevents DNA replication in cancer cells
309
DNA groove binding drugs
specific to certain sequences
