Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

213- pharmacology > block A - intro > Flashcards

block A - intro Flashcards

learn the intro to pharmacology

1
Q

what is pharmacology?

A

it deals with the mechanisms of action, uses and unwanted effects if drugs on living tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is a drug?

A

its a substance that modifies the activity of living tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is physiology?

A

its the science of how living tissues function
they interfere with either normal or abnormal phisiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

can drugs modify activity positively or negatively?

A

both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is abnormal physiology also referred to as?

A

pathophysiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is therapeutics?

A

its the study of the use of pharmacological agents in disease states
its also the attempted remediation of a health problem, usually following a medical diagnosis
therapies usually have inidcations and contradictions
there are many different types of therapies and many can produce unwanted adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is pathology?

A

its the study of how the body goes wrong in disease
it also refers to the study of disease in general
this incorperates a huge breadth of biology research areas and medical practices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

whats an agonist?

A

it activates the receptor i.e. it elicits a response
its affinity is to the binding of the agonist (or any drugs) to its receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how do you quantify the response of an agonist

A

you create a measurable response to be quantified, as you increase the concentrations, you can see that the response gets greater
a sigmoidal-response curve can be generated on a semi-log scale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the Ec50 value?

A

its the concentration of the drug on a semi-log scale
the Ec50 value is the concentration of the drug at 50% max effective concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does an agonist’s efficacy mean?

A

its the ability of the agonist (or any drug) to activate the receptor i.e. elicit a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the affinity of a drug? [agonist]

A

its the binding of the drug to its receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what type of graph can be created when a measurable response is created and the response is quantified?

A

a sigmoidal dose-response curve can be generatef on a semi-log scale
the name of the graph is a concentration-response curve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what agonist concentration do you always try and get Ec50 under?

A

10*-9 / under micromolar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does the lower the Ec50 value mean?

A

the lower the value, the more potent the drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the affinity of an antagonist?

A

its the binding of the antagonist (or any drug) to its receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the efficacy of the antagonist?

A

there is none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is pharmacological antagonism?

A

its when drugs counteract each other by acting on the same receptor type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what id chemical antagonism?

A

its when one drug antagonises the action of another by chemically combining with it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is physiological antagonism?

A

its when two drugs counteract each other by producing opposing effects on different receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what often has a higher affinity for the receptor, the agonist or antagonist?

A

the antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what will increasing agonist concentration do?

A

it will restore the response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what does a rightward parallel shift do on a response curve?

A

it shows competitive antagonism as the agoinst and antagonist are competing for the same site on the recpetor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

if the sigmoidal curves aren’t parallel on the response curve, what does that show?

A

its not a competitive antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does a control curve parallel shifted to the rigt by increasing concentrations of the antagonist show?

A

competitive antagonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is irreversible-competitive antagonism?

A

this is when the bond between the antagonist and the receptor is so strong that even increasing concentrations of agonists cant displace the antagonist
its often due to covalent bonding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is non-competitive antagonism?

A

antagonists that act as sites other than the agonist binding site are classified as non-competitive antagonists
the antagonist binds to a different receptor from the agonist so theres no competition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

antagonists and agonists can have the same physiological effect, but what does it depend on?

A

receptor location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what is toxicology?

A

its the toxic effects of drugs and environmental hazards

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ideally, how big do you want the theraputic window to be?

A

as big as possible so that if theres a slight error in dosing, theres no adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

give an example of something that is very toxic but is still used as a theraputic compound?

A

botulinum toxin
its caused by clostridium botulinum and is one of the most deadly poisons in the world, just a tsp could kill millions of people
DOSE MATTERS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the therapeutic use of botulinum toxin?

A

Temporary removal of facial wrinkles
Severe underarm sweating
Cervical dystonia - a neurological disorder that causes severe neck and shoulder muscle contractions
Blepharospasm - uncontrollable blinking
Strabismus - misaligned eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what does iatrogenicity mean?

A

its the capacity to produce disease from the side effects or innapropriate prescribing of drugs i.e. anti-malairial drugs mefloquine (lariam) associtaed with neuropsychiatric side effects
it could cause suicidal thoughts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what does teratogenicity mean?

A

its the capacity to produce abnormalities of the unbirn child or foetus e.g. thalidomide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what does thalidomide being a racemic mixture mean?

A

it means its got an R form (sedative) and S form (teratogenic)
the r form helps with nausea but the s form can bind to enzymes involved in the development of limbs in the unborn foetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

why cant just the R form of thalidomide be created?

A

becuase it can just be converted to the S-form in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what is high-throughput screening?

A

this is the method of choice for most drug companies
thousands of compounds are screened every day (first pass)
cell lines can be used (sometimes theyre genetically modified) to screen drugs and characterise pharmacological properties
then ex-vivo tissues are used , if the properties are good, the drug could be taken to in vivo testing in animals
testing on tissue is much more reliable than testing on just cells or on just enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are types of drug targets?

A

ion channels - either open or closed (Ca2+ channel blocker= verapamil)
enzymes - inhibitors (ibeprofern = cyclo-oxegenase inhibitor)
transporters/ carriers - (prosac = 5-HT uptake inhibitor)
receptors - agonists (salbutamol for asthma)
antagoniusts (cimetidine - for peptic acid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

receptors as drug targets

A

they’re chemical structures made up of protein
they have recognition molecules to receive and transduce signals that might be integrated into biological systems
the concept of receptors are central to pharmacology to recognise and respond
soluble physiological mediators can produce their effects (hormones, neurotransmitters and inflammatory mediators)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

why do we need receptors in physiology?

A

they act as a central switchboard of chemical communication in the body
they coordinate the activities of their cells and organs
ligands- agonist, soluble mediator - released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what condition would an agonist be useful in treating?

A

asthma- it would be useful in opening the airways- the drug is called salbutamol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what natural hormone is salbutamol similar to?

A

adrenaline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what is the mechanism of action of salbutamol?

A

it works on a receptor of the smooth muscle of the airways of the bronchiole
beta-2-receptor is the receptor and it is a GCPR and interacts with G proteins
the receptor is activated by the agonist and causes the inhibition of Ca - it promotes relaxation of the airways to open them up to allow more air into the lungs

44
Q

what else do you need to consider when developing a drug?

A

the way to take the drug
asthma drugs wouldnt be needed in the gut, so you take it in an inhaler so the drug goes straight into the lungs

45
Q

what is an example of an antagonist?

A

anti-histamines

46
Q

what happens during hay fever and what can be used to treat it?

A

its a hyperresponsiveness to pollen
too much IgE is produced and the pollen binds to the IgE then it binds to its receptor and then promotes the release of histamine in granules in the mast cells
this causes the lining of the cells to become irritated

47
Q

what happens in your nose when histamine activate the histamine H1 receptor?

A

histamine H1 receptors - this causes a widening of the blood vessels, the space between the endothelial cells becomes wider
white blood cells come to the area, causign swelling an inflammation, the inflammation is mediated by the histamine receptors

48
Q

what is the mechanism of mepyramine? [H1 blockers]

A

these block the histamine receptor with a hitamine antagonist = H1 blocker
the receptor is a GCPR and it has 7 transmembrane spanning domains

49
Q

name some drugs directed towards GCPR receptors and what they treat?

A

beta blockers for heart arrythmias
antagonists of histamine H2 receptors for stomach ulcers
antagonists of angiotensin II receptor - to lower blood pressure
antagonist of puirenic receptor on platelets - heart attacks (this inhibits platelet aggregation)

50
Q

what type of drug is the contraceptive pill?

A

its a steroid hormone drug - the contraceptive pill - oestrogen and progesterone analogues (agonists)
these act on nuclear receptors

51
Q

what are enzymes?

A

theyre drugs which drive chemical reactions inside the cell
theyre essential for cell function

52
Q

what makes aspirin a blockbuster drug?

A

it made a lot of money and was one of the biggest drugs of the 20th century

53
Q

what is the chemical makeup of aspirin? [the chemical name for it]

A

acetyl aalasilic acid

54
Q

how does aspirin work?

A

its a cyclo-oxygenase inhibitor (COX) inhibitor
the COX oxygenase arachidonic acid and takes it into the catalytic sire and makes it into prostaglandin H2 (PGH2), then enzymes turn it into prostaglandin E2
it then acylates the seine residue with the cyclooxylase enzyme

55
Q

what 2 types of COX enzyme does aspirin inhibit?

A

COX-1
COX-2- this is relates to inflammation so the aspirin works as an anti-inflammatory

56
Q

what is PGE?

A

its a prostaglandin and is involved in inflammation - mediated by COX-2

57
Q

what is TXA2 (thromboxane A2)?

A

this is another prostoglandin like product and is involved in platelet aggragation during clotting - this is mediated by COX-1

58
Q

what is a drug which inhibits COX-2 in inflammation treat? (this is what aspirin does)?

A

Good for arthritus, sports injuries, headaches and period pain

59
Q

what else is aspirin good for (in small quantities)?

A

its good for inhibiting COX-1 in platelets - low does aspirin is used for the prevention of secondary heart attacks (in combination with other drugs)
this is only useful for patients who have already had heart attacks as it stops them having another
this dose is only 75mg compared to 300mg for pain
the pills are coated in icnteric coating beciase theyre taken continuously so theres no urgenvy to how quickly they have to be absorbed

60
Q

what are ACE inhibitors? [theyre long name is angiotensin converting enzyme inhibitors]

A

it converts angiotensin I to II, this is a peptide
ACE inbteracts with GCPR receptors
Ang I increases blood pressure as it increases salt and water concentrations so theres a bigger volume of blood

61
Q

what did scientists find out that the venom of the brazillian pit viper do?

A

it reduced peoples blood pressure because of the peptides blocking the enzyme so it could lower the victim’s blood pressure

62
Q

what did scientists make when they found out that the snake venome peptides can lower blood pressure?

A

they made non-pepide analogues of the venom

63
Q

what do ACE inhibitors do?

A

they stop the production of angiotensin 2

64
Q

how are ACE inhibitors good blood pressue mediacation?

A

they reduce the salt and water content in the blood

65
Q

what do statins do?

A

they lower cholesterol and prevent heart attacks

66
Q

what does sildenafil (viagra) do?

A

it inhibits the enzyme that breaks down cGMP
this helps with erectile dysfunction
PDE5 enzyme inhibitor

67
Q

what does nevirapine do?

A

its a non-nucleoside reverse transcriptase inhibitor (NNRTI) of HIV-1
its used to treat patients with HIV and AIDs

68
Q

what type of drug is penicilin?

A

its an enzyme inhibitor

69
Q

how does penicilin work?

A

it kills bacteria through the binding of the beta-lactam ring to DD-transpeptidase, it inhibits its cross-linking activity and preventing new cell wall formation
without a cell wall, the bacterial cell of vulnerable to outside water and molecular pressures, which causes the cell to die

70
Q

who discovered penicilin?

A

alexander flemming

71
Q

what is a transporter?

A

its a protein which helps move molecules accross the membrane in/ out of the cell

72
Q

what are examples of transporters?

A

glucose transporters, these move glucose in the liver and skeletal muscle
amino acid transporters, theyre in the intestine and take up amino acids into the body

73
Q

what is an example of a condition where blocking the receptors would be a good thing?

A

depression

74
Q

what is a drug for depression and what does its focus on?

A

prosac
it focuses on neurotransmitters in the brain and it regulates mood, anxiety and depression
it focuses on the seratonin part of the disorder

75
Q

what is serotonin? And how does it work?

A

its a neurotransmitter called 5-hydroxytryptamine (5-HT)
its released from nerve cells in the brain and affects other target nerve cells increasing activity
it interacts with a 5-HT receptor on the target cells
its known as an excitatory neurotransmitter so it increases brain activity

76
Q

what is the definition of a neurotransmitter?

A

its an agent that works in the brain

77
Q

does a lack or seratonin cause depression?

A

enough seratonin activates the next neuron in the chain, if theres not enough then its ability to stimulate the receptors on the next neuron decreases
with treatment, it can help to activate the next neuron

78
Q

what receptor does prozac block?

A

the 5HT reuptake transporter
its an SSI (selective seratonin re-uptake inhibitor)

79
Q

how do serotonin re-uptake inhibitors work?

A

nerve stimulation releases vesicles and activates the next neuron, you only ant neurotransmitters to be active only when you need them

80
Q

what would happen if your neurotransmitters were always active?

A

you would be hyperactive

81
Q

how are neurotransmitters removed?

A

theyre removed by a transporter protein throgh 5HT reuptake transporter protein

82
Q

how does prozac block the transporter

A

it blocks the reuptake transporter so it doesnt get taken up by the transporter and it activates its receptors more, increasing the mood by regaining the stimulation levels of the receptors- this is how it works to wnhanse the 5HT in the space

83
Q

what does more 5-HT hanging around in the space between the 2 neurotransmitters cause?

A

thyere more likely to stimulate the 5-HT receptor on the target neuron, more activity means better mood

84
Q

what does a proton pump transport?

A

H+ ions

85
Q

what are the medical uses of proton pump inhibitors?

A

peptic ulsers - too much acid damages the lining
GERD- gastorintestinal reflux disease (this means that the sphincter doesnt shut properly which leads to acid in the oesophaagus)
gastrin producing tumour- pancretic tumour which produces too much gastrin - this stumulatess pariteal cells to release acid

86
Q

what are the 3 side effects of excess stomach acid?

A

peptic ulsers
gastrointestinal reflux disease
zollinger-ellinson syndrome

87
Q

what are ion channels?

A

theyre pores in the membrane made up of proteins?

88
Q

what are the different types of ion channels?

A

lugand-gates
mechanically-gated
always open
voltage-gated

89
Q

what are ion channels made up of?

A

they’re made up if protein subunits - many different types of channel and variations due to the subunit composition

90
Q

what do ion channels allow into and out of the cell?

A

ions, duh

91
Q

what types of cells usually have lots of ion channels?

A

cells which are excitable becuse they have to respond quiickly such as nerve cells, skeletal cmuscle cells and heart cells

92
Q

how quickly do ion channels open in?

A

milliseconds

93
Q

what is the action poteintial?

A

its a change in the membrane potential

94
Q

what is the membrane potential of the threshold of exitation?

A

-70mV

95
Q

what causes a massive depolariastion in the plasma membrane?

A

a massive influx of Na ions into the cell

96
Q

what does depolariasation of the membrane cause?

A

it sets off K+ channels to be opened to allow K+ out of the cell and the Na channels start to shut off

97
Q

what starts the repolarisation of the cell?

A

the Na channels start to shut off

98
Q

how does the signal get to the end of the nerve?

A

the action potental relays down the nerve, until it gets to the end organ where the transmitter release happens, this is the point of the action potential is to spread electrical activity from one cell to antoher to the end point to cause something to happen

99
Q

what other cells, apart form nerve cells, have action potentials?

A

cardiac cells
the Ca rushes through the Ca channels, this is significant because muscle cells have to contract and they need Ca to do this

100
Q

what are the different classes of sodium channel blockers?

A

the different classes are weak, moderate and strong
these are used for different conditions
class IA
class IB
class IC

101
Q

what is lidocane?

A

its a soduim channel inhibitir
it blocks the channel from the inside of the cell

102
Q

what is lidocane used for?

A

its used for pain as it blocks action potentials

103
Q

what are Ca2+ channels used for?

A

theyre used in the vascular smooth muscle
it mediates contriaction and controls blood pressure

104
Q

what do calcium channel blockers block?
and what is this good for?

A

the site of action
theyre good for treating anti-arrhythmic conditions or high blood pressure

105
Q

what are Ca channel blockers good for?

A

cardiac arrhythmias
angia petrous
high blood pressure

213- pharmacology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions