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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
Q

What can drugs bind to

A

receptors
enzymes
transporters
ion channels

26
Q

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?

A

the three subunits that make up a heterotrimeric G protein are:
alpha, beta, gamma (Y)

subunit alpha binds to GDP

27
Q

What are the main features of a kinase-linked receptor?

A

Single transmembrane protein activated by a range of protein mediators
usually involved with growth

28
Q

What is the typical pathway for a kinase-linked receptor

A

Agonists binds to 2 receptors - two receptors dimerise - phosphorylation - effect

29
Q

What hormones are associated with nuclear receptors

A

steroid hormones

30
Q

What is the typical pathway of a nuclear receptor

A

agonist binds to receptor - receptor binds to another agonist-bound receptor - dimerises - dimer translocates - binds to DNA - transcription - effect

31
Q

in phase 1 metabolism, induction and inhibition effect cytochrome P450 activity. explain both of these factors

A

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
Q

What are the two phases of metabolism? What do they aim to do?

A

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
Q

What are the aims of metabolism

A

to increase the rate of excretion
reduce toxicity

34
Q

Why do drugs accumulate in adipose (fat) tissue?

A

site of accumulation since its very lipophilic
can act as a reservoir for slow release

35
Q

What is needed from a drug to be able to cross the blood brain barrier?

A
  1. small mw
  2. very lipohilic
  3. must be a substrate for specific transporters
  4. not substrates for MDRs
36
Q

what is ion trapping

A

acid drugs accumulate in basic areas

basic drugs accumulate in acidic areas

37
Q

Name three body fluid compartments and what they are made of

A

body comprtments dictate volume of distribution

plasma compartment - large drugs

extracellular compartment - plasma and interstitial

total body water - plasma, interstitial, intracellular

38
Q

Why is plasma-protein binding important?

A
  1. acts as a reservoir
  2. change in plasma proteins
  3. change in blood volume
  4. species dependence
39
Q

What is the rate of diffusion into the blood affected by

A

blood flow/tissue volume
Drug characteristics
PLasma/tissue barriers

40
Q

What is the equation that represents distribution?

A

k1 x C plasma = k2 x C tissue

remember c - concentration of unbound/ free drug

41
Q

what is atropine used to treat

A

asthma

42
Q

what are five important things to remember when it comes to plasma-protein binding

A
  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
Q

give an example of a ligand gated ion channel

A

nicotinic acetylcholine receptors

44
Q

how do amphetamines work

A

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
Q

What are the effects of nicotine?

A

can activate parasympathetic and sympathetic pathways

MTWThF

Mydriasis
Tachycardia
Weakness
hypoTHermia
Fasciculation - muscle twitches

46
Q

What adrenergic receptor regulates feedback

A

alpha 2

47
Q

Give an example of a ganglionic blocker. what are the effects?

A

Trimethapan

it increases constipation and heart rate, it decreases blood pressure and vasodilation

48
Q

Name two muscarinic antagonists

A

atropine and scopolomine

49
Q

What are the effects of sympathetic innervation

A

Dry mouth
Mydriasis
Urinary retention
Constipation
Increased breathing
Hypertension

50
Q

What are beta-blockers and what are they used to treat?

A

beta-blockers are adrenergic antagonists that treat disrhythmia and hypertension

51
Q

what does botox do

A

inhibits released of Ach via exocytosis and causes flaccid paralysis in muscles

52
Q

what is constitutive receptor activation

A

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
Q

what are the three lasting effects of drug use on receptors? what are the time frames of these effects?

A

desensitisation - reduced response - few minutes

tolerance - reduced response - prolonged use

resistance - loss of effectiveness - chemotherapeutic drug

54
Q
A

BIOM2402 (9 decks)

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