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BIOM2402 > cards i couldn't learn from anki > Flashcards

cards i couldn't learn from anki Flashcards

1
Q

What do opioids induce

A

segmental contractions

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2
Q

what does seratonin do to gut motility?

A

increases motility

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3
Q

what do D2 blockers do?

A

promote motility and stop vomiting

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4
Q

what are the three main modulators that regulate gut motility

A

opioids
dopamine
seratonin

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5
Q

What are the main factors of noradrenergic transmission

A

VMOA (vesicular monoamine transporter) = NA into synaptic vesicles
MOA (monoamine oxidase) breaks down NA and inibits Ca2+
NAT = noradrenaline transporter = reuptakes NA

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6
Q

what are the two ways adrenaline can be used as a drug

A
  1. treatment of anaphylaxis
  2. local anaesthetic - limits diffusion of local anaesthetic
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7
Q

How do drugs indirectly cause innervation?

A

indirect innervation is caused when a drug inhibits uptake/ breaks down enzymes that are responsible for the removal of neurotransmitters

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8
Q

What is a drug that induces indirect sympathetic innervation>

A

amphetamines

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9
Q

Whats the difference between adrenaline and noradrenaline

A

adrenaline is a hormone, noradrenaline is the neurotransmitter

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10
Q

name an adrenergic agonist

A

noradrenaline

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11
Q

name the four main types of adrenergic receptors and what they do. where are beta 3 receptors usually found?

A

The four main types of adrenergic receptors are :
alpha 1 - smooth muscle contraction
alpha 2 - mainly presynaptic
beta 1 - heart frequency and cardiac contractility
beta 2 - smooth muscle relaxation

beta 3 receptors are predominantly found in adipose tissue

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12
Q

explain the difference in nicotinic antagonist effects in the somatic system and in the ANS

A

nicotinic antagonist in the somatic system are muscle relaxers, as blocking the binding of Ach prevents muscles from contracting. Nicotinic antagonists in the ANS are called ganglionic blockers, due to them blocking Ach binding onto the nAchR receptors on the ganglion

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13
Q

name a nicotinic agonist

A

nicotine

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14
Q

what do ACHE-inhibitors de at the neuromuscular junction

A

ACHE-inhibitors cause agonistic effects at the neuromuscular junction

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15
Q

What is ACHE (acetylcholinersterase)

A

an enzyme that breaks down acetylcholine that is left in the synaptic cleft

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16
Q

name two muscarinic agonists

A

carbachol, pilocarpine

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17
Q

what type of receptor are muscarinic receptors?

A

G-protein coupled

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18
Q

name all five muscarinic receptors and what they do

A

M1, M3, M5 = increase IP 3
M2, M4 = decrease cAMP

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19
Q

What are the effects of the parasympathetic innervation?

A

DUMBBBELS

Defecation
Urination
Miosis
Bronchorrea - excess pulminory fluid
Bronchospasm - difficulty breathing
Bradycardia - slowed heart rate
Emesis
Lacrimation
Salivation

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20
Q

What is the adrenergic (sympathetic) pathway starting from the spinal chord?

A
  1. Preganglionic neuron released Ach
  2. Ganglionic nAchr binds to Ach
  3. post ganglionic neuron releases noradrenaline
  4. adrenergic receptors bind NA
  5. effect
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21
Q

What is the muscarinic (parasympathetic) pathway starting from the spinal cord?

A
  1. Preganglionic neuron released Ach
  2. Ganglionic nAchr binds to Ach
  3. post ganglionic neuron releases Ach
  4. mAchR binds Ach
  5. effect
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22
Q

What do normal and non-normal distribution curves mean for genetic variability?

A

normal - gene is NOT SUSCEPTIBLE to polymorphisms

non-normal - gene is SUSCEPTIBLE to polymorphisms

23
Q

what factors affect renal excretion

A
  • drug size
  • amount of free drug
  • competition for active secretory pathway
  • passive absorption
  • renal failure
24
Q

What is an inverse agonist

A

inverse agonists promote an opposite response to an agonist

25
What can drugs bind to
receptors enzymes transporters ion channels
26
what are the three main subunits that make up a g-protein? what type of energy does it use and what subunits bind to GDP?
the three subunits that make up a heterotrimeric G protein are: alpha, beta, gamma (Y) subunit alpha binds to GDP
27
What are the main features of a kinase-linked receptor?
Single transmembrane protein activated by a range of protein mediators usually involved with growth
28
What is the typical pathway for a kinase-linked receptor
Agonists binds to 2 receptors - two receptors dimerise - phosphorylation - effect
29
What hormones are associated with nuclear receptors
steroid hormones
30
What is the typical pathway of a nuclear receptor
agonist binds to receptor - receptor binds to another agonist-bound receptor - dimerises - dimer translocates - binds to DNA - transcription - effect
31
in phase 1 metabolism, induction and inhibition effect cytochrome P450 activity. explain both of these factors
induction = several drugs/carcinogens increase p450 activity. Results in more rapid metabolism of substrates and lower plasma drug levels = decrease in drug effect E.g. tobacco inhibition = occurs when two drugs are metabolised by same p450 enzyme. Consequence can be toxicity of the drug with less metabolism E.g. caffeine
32
What are the two phases of metabolism? What do they aim to do?
Phase 1 - functionalisation liver catabolic reaction e.g. oxidation, reduction, hydrolysis Phase 2 - conjugation liver, lungs, kidneys anabolic reaction Adds water soluble parts to the drug
33
What are the aims of metabolism
to increase the rate of excretion reduce toxicity
34
Why do drugs accumulate in adipose (fat) tissue?
site of accumulation since its very lipophilic can act as a reservoir for slow release
35
What is needed from a drug to be able to cross the blood brain barrier?
1. small mw 2. very lipohilic 3. must be a substrate for specific transporters 4. not substrates for MDRs
36
what is ion trapping
acid drugs accumulate in basic areas basic drugs accumulate in acidic areas
37
Name three body fluid compartments and what they are made of
body comprtments dictate volume of distribution plasma compartment - large drugs extracellular compartment - plasma and interstitial total body water - plasma, interstitial, intracellular
38
Why is plasma-protein binding important?
1. acts as a reservoir 2. change in plasma proteins 3. change in blood volume 4. species dependence
39
What is the rate of diffusion into the blood affected by
blood flow/tissue volume Drug characteristics PLasma/tissue barriers
40
What is the equation that represents distribution?
k1 x C plasma = k2 x C tissue remember c - concentration of unbound/ free drug
41
what is atropine used to treat
asthma
42
what are five important things to remember when it comes to plasma-protein binding
1. only unbound drugs can diffuse into peripheral tissue 2. albumin is the most important and most abundant protein for drug binding 3. albumin mostly binds to acidic drugs 4. plasma-protein binding can be saturable for some drugs 5. drugs can compete for plasma protein binding
43
give an example of a ligand gated ion channel
nicotinic acetylcholine receptors
44
how do amphetamines work
by being uptaken into the presynaptic terminal by NAT - they then inhibit MOA by inhibiting Ca2+ channels, uptake of VMAT, displacement of NA, Na leaks out
45
What are the effects of nicotine?
can activate parasympathetic and sympathetic pathways MTWThF Mydriasis Tachycardia Weakness hypoTHermia Fasciculation - muscle twitches
46
What adrenergic receptor regulates feedback
alpha 2
47
Give an example of a ganglionic blocker. what are the effects?
Trimethapan it increases constipation and heart rate, it decreases blood pressure and vasodilation
48
Name two muscarinic antagonists
atropine and scopolomine
49
What are the effects of sympathetic innervation
Dry mouth Mydriasis Urinary retention Constipation Increased breathing Hypertension
50
What are beta-blockers and what are they used to treat?
beta-blockers are adrenergic antagonists that treat disrhythmia and hypertension
51
what does botox do
inhibits released of Ach via exocytosis and causes flaccid paralysis in muscles
52
what is constitutive receptor activation
the phenomenon which describes how some receptors are in an equilibrium state of activity and inactivity. according to what binds to these receptors, this equilibrium can be shifted.
53
what are the three lasting effects of drug use on receptors? what are the time frames of these effects?
desensitisation - reduced response - few minutes tolerance - reduced response - prolonged use resistance - loss of effectiveness - chemotherapeutic drug
54

BIOM2402 (9 decks)

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