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Pharmacology > Drug Receptor Interactions II > Flashcards

Drug Receptor Interactions II Flashcards

1
Q

Drug+Receptor= Cellular effect

A

A drug can activate or prevent the activation of a cascade of intracellular processes
*Drug has its particular effects according to which receptors it interacts with and what the receptors do

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2
Q

Receptor mediated actions of drugs

A
  1. Act on ion channels
  2. Receptor with enzymatic activity
  3. Activating protein complex that generate 2a messenger (alters metabolism, change expression of proteins, cell division, etc)
  4. Receptor with intracellular enzyme component (tyrosine kinase activity)
  5. Receptor drug complex goes to Nucleus–> directly stimulate DNA transcription/translation
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3
Q

Drugs that act at ion channels

A

Benzodiazepines

Local anesthetics

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4
Q

Drugs that act at tyrosine kinases

A

Insulin

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5
Q

Drugs that act by blocking enzymes

A

Acetylcholinesterase inhibitors

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6
Q

Drugs that bind intracellular receptors

A

Steroids

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7
Q

Drugs that act at G protein receptors

A 
Muscarinics
Adrenergics
Histaminergics
Serotonergics
Angiotensin II inhibitors
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8
Q

G-protein receptors

A

General set of receptors w/three subunits that initiate production of intracellular substances

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9
Q

Intracellular substances

A

Secondary messengers

  1. Agonist binds to Alpha subunit of G (which binds GDP)
  2. GDP exchanged for GTP (alpha subunit breaks off from beta and gamma subunits)
  3. Alpha subunit activates enzyme system to create 2a messenger (or have a direct effect)
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10
Q

Gq Protein

A

Gq stimulates phospholipase C==> DAG and IP3
These open internal calcium stores, activate protein kinase C (can turn off or on 50 other proteins) resulting in smooth mm contraction, hormone production or inflammation

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11
Q

Gs Proteins

A

Stimulate adenylyl cyclase==> cAMP

This activates cellular energy production by phosphorylation of enzymes and K+ channel opening

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12
Q

Gi proteins

A

Inhibit adenylyl cyclase

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13
Q

Major secondary effectors (review)

A 
DAG
IP3
cAMP
cGMP
Calcium
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14
Q

Some drugs work by directly altering concentration of 2a messengers

A

Caffeine

Sildenafil (Viagra)

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15
Q

Steps three and four

A

Cellular actions combine to have a physiological effect

Collection of activated cells will have a tissue effect which= a physiological effect

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16
Q

Cellular actions and physiological effects of agonist on skeletal mm channel

A

Opening up sk mm Na channels will cause contraction (myasthenia gravis meds)

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17
Q

Cellular actions and physiological effects of antagonists

A

Prevents sk mm from contracting (neuromuscular paralysis for surgery)

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18
Q

Physiological effects of epinephrine

A

Will increase HR, BP, etc: useful for anaphylactic shock

Antagonist of this given to pt with high BP (prevents action of endogenous epi)

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19
Q

Drugs do not act unilaterally

A

Body reacts

Compensatory mechanisms kick in to readjust heart rate and BP (in the case of epinephrine or antagonist)

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20
Q

Physiological effect of Histamine in:

Veins
Mast Cells
Skin

**Block histamine and you block these effects (anti-histamines)

A

It binds histamine receptors, these receptors in the veins cause vasodilation which causes:

  1. A significant drop in BP.
  2. Increased capillary permeability.
  3. Body reacts to drop in BP by increasing HR.

Histamine from mast cells (nasal membranes, eyes, mouth, bronchioles) cause:

  1. Tissue swelling and fluid leakage
  2. Runny nose, difficulty breathing

Histamine in dermis promotes itching

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21
Q

Direct and indirect effectors of ACh action

A
  1. Cholinergics (compounds that mimic ACh): muscarinics and nicotics, have an effect of intracellular actions
  2. Acetylcholinesterase inhibitors are used to enhance ACh action at neuromuscular junctions and in CNS (by preventing breakdown of ACh)
  3. Anticholinergics (block ACh by binding its receptors at the neuromuscular junction): Antimuscarinics, neuromuscular blockers, ganglionic blockers
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22
Q

ACh effect on pupillary constriction

A

Causes dilation

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23
Q

Effect of epinephrine during anaphylaxis:
Histamine has flooded the system causing vasodilation (BP drops), bronchoconstriction, bronchospasm, and swelling of mucous tissue

A

Epinephrine: Vasoconstricts (reverses drop in BP), reduces swelling around pharynx and larynx, open up bronchioles, stimulates heart.
***Doesn’t block histamine, but acts as an agonist at same tissues to reverse effects of histamine.
Glucocorticoids and Antihistamines are given for maintenance.

24
Q

Effect of local concentration of a drug:

follows the law of mass action

A

More drug=more effect

Basically, how many receptors it triggers/blocks is dependent on local concentration of the drug

25
Q

Law of mass action

A

E=Emax* C/C + ED50 meaning:
Need some drug to get effect
For a little while, more drug=linear effect (increasing effect)
Then reach near max effect, and you can add more and more drug but it will only give you a small effect
(law of diminishing return, like more and more caffeine when you’re already tired)

26
Q

Log drug concentration vs receptor occupied

A

Again, more drug more receptors
X axis is the log of drug concentration
Y is % of receptors occupied

27
Q

Log dose response curve (LDR):

A

Measures degree of response
X axis still log of drug concentration
Y axis is the %max effect of drug (Emax)

28
Q

Spare receptors

A

Non-active receptors on outside of cell (ACh in smooth mm)
Meaning that the receptor occupied curve won’t match drug response
***An agonist can have its action with few receptors activated

29
Q

How is drug efficacy measured?

A

By how great an effect it can produce (Emax)
Drug w/higher Emax is more effective
**Efficacy is very important

30
Q

What is a partial agonist?

A

A drug that achieves an effect less than Emax

31
Q

How does a partial agonist bind to same receptors as a full agonist but still produce less of an effect?

A

Receptors exist in equilibrium of two forms: active and inactive.

  1. Full agonists bind tightly to active form.
  2. The inactive form is recruited to become an active form=restores equilibrium=increase active receptors=increasing max effect.
  3. Partial agonists bind inactive form, preventing it from becoming active=total number of possible active receptors are fewer.
32
Q

Intrinsic activity as a measure of the effect of an agonist:

A

Is measured by the ability/effect of an agonist by activating a receptor

  1. A full agonist has intrinsic activity of 1
  2. Partial agonist w/half the effect of a full agonist has an intrinsic activity of 0.5
  3. Antagonists have intrinsic activity of 0
33
Q

ED50

A

Drug concentration in blood that delivers 50% of max effect

Eg. If the max effect of lower MBP is 40mmHg then Emax is a drug that lowers it 20mmHg

34
Q

ED90

A

Drug concentration in blood that delivers 90% max effect.

Using the MBP Emax example (40mmHg), the ED90 lowers MBP by 36mmHG

35
Q

Drug Potency: drug that is effective at a lower concentration is more potent

A

How strongly a drug binds to its receptor can be measured by its affinity constant or dissociation constant.
**Defined by what concentration half of receptors are bound.
Drug with high affinity is highly potent.

36
Q

Graphs comparing drug potencies: Which line would indicate the most potent drug?

A

The line that is furthest to the left is more potent b/c lesser ED50 means that its effect happens requiring less concentration of the drug than the other drug.

37
Q

Efficacy vs. potency: graphs

A

The more efficacious drug will usually have a higher flat line, whereas the most potent drug will be the line that is further to the left

38
Q

Definition of down-regulation

A

When a receptor is regularly activated a cell may produce less of these receptors.
***Causes tolerance

39
Q

Tolerance

A

When more drug is required to achieve the same effect

40
Q

Desensitization

A

Number or receptors stay the same, but the cell deactivates them.
Reduced action.

41
Q

Tachyphylaxis

A

Same as desensitization.

Reduced action of receptors.

42
Q

Downregulation and desensitization in terms of potency and efficacy:

A

Can reduce potency and maximal efficacy of drug.
Ex:Oxymetaazoline (decongestant, afrin); after a few days, receptors downregulate, drug is less effective and pt experiences a rebound.

43
Q

Other causes of tachyphylaxis

A

Reduced production of neurotransmitters or through other pathways

44
Q

Tachyphylaxis and morphine:

Morphine’s 3 effects are analgesia, respiratory depression and constipation

A

Prolonged use of morphine causes less pain-relief over time, so you up the dosage and pain relief returns to original level but increased constipation and respi depression.
**B/c CNS opioid receptors downregulate but not the GI or respi receptors

45
Q

Tolerance in graphs

A

Emax lowers, looks like a partial agonist.

Basically, tolerance to a drug is akin to converting it to a partial agonist.

46
Q

Up regulation

A

When a receptor is regularly blocked by an antagonist, cell increases the number of receptors.
Can cause SUPERsensitivity

47
Q

Supersensitivity example

A

Chronically blocking Beta adrenergic receptors increase their numbers. Stop taking med, pt become super-responsive (sensitive) to a B-adrenergic agonist (or own production of epinephrine)

48
Q

Constant exposure to an antagonist increases number of working receptors:

A

Emax is elevated in a graph (flat line higher)

Upregulation or supersensitivity

49
Q

Reversible antagonists:

A

Competitive antagonists

Only blocks the receptor while the drug is present.

50
Q

Irreversible antagonists:

A

modifies the receptor to irreversibly shut it off.
non-competitive antagonist
As if a key breaks off in a lock

51
Q

Physiological antagonist

A

A drug that counteracts the effect of another drug but through different mechanisms or receptors
Rise in HR caused by a stimulant (epi) can be countered by a CNS depressant (benzo)

52
Q

Competitive antagonists (Reversible) on the LDR

A

Blocks agonists action, but can be overwhelmed by more agonist.
Makes the agonist less potent.
**Drug curve shifts to the RIGHT

53
Q

Non-competitive/irreversible antagonists effect on LDR

A

Alters and deactivates the receptor.
Turns a full agonist into a partial one, lowering flat line of the drug curve.
**Recovery depends on the production of new receptors.

54
Q

Real life irreversible antagonists:

A

aspirin, omeprazole
More powerful than reversible inhibitors.
May have an effect for days after the drug is discontinued.

55
Q

Quantal dose-response curve

A

Measured by % of people for whom the drug worked. All or nothing.
Ed50 is concentration where 50% of ppl are cured/affected; ED90 is where 90% are affected.

56
Q

Quantal LDR and drug effectiveness

A

Y axis is % of patients showing desired effect.

X axis is the log drug concentration

Pharmacology (14 decks)

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