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270 S1 > 2.1 > Flashcards

2.1 Flashcards

1
Q

What is a receptor?

A

Specialized target macromolecule that binds drug or ligand and mediates its pharmacologic action

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2
Q

What is drug specificity? How are receptors specific?

A

Have structural features that permit drug specificity
Specificity  selectivity of response
Must have both a drug-binding domain and an effector (active) domain

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3
Q

What are some examples of drugs that don’t have to bind to a receptor?

A 
Antacids
Osmotic Diuretics 
manitol	
Heavy Metal Chelating Agents 
EDTA(Ethylenediaminetetraacetate) – lead poisoning	
Barrier Ointments and Cream
A&D ointment, Zinc oxide ointment
Disinfectants
Chlorhexidine (hibiclens)
Alkylating anticancer agents
Cyclophosphamide
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4
Q

What are soluble receptors?

A

Lipid soluble ligand  crosses cell membrane  act on intracellular receptor  in nucleus for transcription/translation

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5
Q

What are examples of lipid-soluble receptors?

A

Ex: steroids, vitamin D, and thyroid hormone  stimulate the transcription of genes
Consequences:

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6
Q

What are the consequences of lipid-soluble receptors?

A 
Take time (at least 30min) 
Transcribe genes and synthesize new proteins  Not immediately relieve sx
The effects can persist for hours or days after the drug has long been eliminated (need to wait for the proteins these drugs encode for to be used)
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7
Q

What are transmembrane receptors? How do they work? Example?

A

Drug binds to a receptor on a protein that spans the cellular membrane which starts a cascade of effects within the cell. Ex: tyrosine kinase

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8
Q

How does tyrosine kinase work? Broadly? With a specific example?

A

Broadly- add a phosphate group to tyrosine

More specifically: EGF(epidermal growth factor) binds to receptor  convert from monomeric to dimeric state initiates phosphorylation of tyrosine  promote cell growth

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9
Q

What are the consequences of using tyrosine kinase?

A

Target site for drug therapy
Ex: gefitinib (Iressa), erlotinib (Tarceva) – NSCLC
Inhibit receptor’s kinase activity in the cytoplasm
Inhibit cell growth

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10
Q

How do ligand-gates transmembrane channels function? Common example?

A

Channel that opens when a messenger (ligand) binds to it.

Nicotinic acetylcholine (Ach) receptor
	Ach binds to the receptor 
Open Na+ channel  Na+ to rush into cell  skeletal muscle contraction
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11
Q

What are the consequences of ligand-gated channels?

A

Time to response is fast; can be in milliseconds
Create important drug target (i.e. Verapamil inhibits voltage-gated calcium channels in heart and smooth muscle  antiarrhythmic effects and reducing BP

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12
Q

How does a G-membrane channel work?

A

Transmembrane receptor stimulates GTP-binding signal transducer G protein  increase intracellular second messenger  signal amplified

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13
Q

What is an example of a g-membane receptor?

A

Norepi  stimulates receptor  stimulates production of GTP  amplify the original signal  produce effects

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14
Q

Which classes of receptors require gene transcription?

A

Tyrosine Kinase

Transmembrane diffusing nuclear receptors

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15
Q

What are full and partial agonists?

A

Full Agonist – trigger a full response

Partial Agonist – trigger a “partial” response (i.e. not as pronounce as the full agonist regardless of concentration)

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16
Q

What is an allosteric agonist?

A

Uses a separate active site to magnify response of agonist

17
Q

What is an inverse agonist? What needs to be present for this response to occur?

A

Receptor needs basal activity; that is, without a ligand bound it does something, so when the inverse agonist binds the signal is suppressed and theres an opposite effect

18
Q

What is a non-competitive antagonist?

A

bind to receptor equally well whether or not receptors already bound the substrate
Binding to same active site

19
Q

What is an allosteric non-competetive antagonist?

A

binding to a separate site

antagonist that doesn’t need to compete. Just turns off fxn.

20
Q

What is an un-competetive antagonist?

A

ligand binds to a receptor, THEN a new site opens up, that allows an antagonist to bind

21
Q

What is a neutral antagonist?

A

blocks the docking of the agonist but does not trigger an effect
Like a hat- blocks the receptor but doesn’t do anything

22
Q

What is efficacy?

A

Percent of maximum effect that can be achieved?

23
Q

What is potency?

A

How much is needed to trigger a given effect

24
Q

What is EC50? Why is it used?

A

The concentration of drug that produce 50% of response – use to compare potency

25
Q

What is affinity? What influences it?

A

The tendency of a drug to bind to a receptor
Directly proportional to efficacy and potency
Mostly influenced by the rate of dissociation (KD)
i.e. the lower KD, the higher affinity
Allow us to measure the fraction of receptors occupied to reach a full biological response

26
Q

What is a graded response curve?

A

Continuous data points needed

27
Q

What is a quantal response curve?

A

Response is discrete: yes/no; impossible to make a graded curve; eg with toxicity alive or dead

28
Q

What is ED50?

A

50% Effective Dose

The dose at which 50% of maximum effect is achieved.

29
Q

What is LD50?

A

50% Lethal Dose

the dose at which 50% of the animals die.

30
Q

What is TD50?

A

50% Toxic Dose

the dose at which 50% of the humans developed toxicity.

31
Q

What is the therapeutic index? How is it measured?

A

A measure of drug safety
Therapeutic index = LD50 / ED50 (animal)

Therapeutic index = TD50 / ED50 (human)

32
Q

What is tachyphylaxis?

A

Responsiveness drop rapidly after administration of a drug (i.e. tolerance)
Diminished response with subsequent doses

33
Q

What affects tachyphylaxis in pts?

A

Age, gender, body size
Dz state, genetics
Co-administration with other drugs

34
Q

At a cellular level, why does tachyphylaxis occur?

A

Drug conc. change at receptors site
Soluble receptor conc. Change
Change in number or function of transmembrane receptors
When agonist induces decrease # of receptors  down regulation of receptors or desensitization
Change in components different from receptor (i.e. disease compensatory mechanism)

35
Q

What are the 2 types of desensitization?

A

Homologous desensitization

Heterologous desensitization

36
Q

What is homologous desensitization?

A

Decreased response at a single type of receptor (i.e. only the activated receptors are “turn off”)
Loss of response to one single subtype of receptor
agonist-dependent
Rapid (seconds~minutes)
receptor stays in the plasma membrane (usually)
Ex: Continuous administration of Nitrates reduce in drug response  must allow nitrate free period

37
Q

What is heterologous desensitization?

A

Decreased response at two or more types of receptor (i.e. activation of one receptor resulted in the inhibition of another)
= “Cross desensitization” – unresponsiveness to a variety of other agonists after prolonged stimulation by one agonist
agonist-independent
Slow (min~hrs)
receptor is internalized (usually)
Ex: Morphine inducing desensitization of opioid-receptors leading to desensitization to other opioid agonists

38
Q

What is drug inactivation?

A

The loss of ability of a receptor to respond to stimulation by a drug or ligand.

Complete turning off the receptor may result from phosphorylation of the receptor  completely block the signaling activity  lead to the removal of the receptor from the cell surface.

39
Q

What is the refractory period/

A

The time lapse between the first and the next interaction of a drug that can produce an effect on a receptor

Voltage-gated Sodium channel mediate firing of the neuronal action potentials are subject to refractory periods.

270 S1 (19 decks)

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