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NSG 785 - Clinical Reasoning in Pharmacotherapeutics > L1. Pharmacodynamics 1 - Basic Principles of Pharmacology & Intro to Pharmacodynamics > Flashcards

L1. Pharmacodynamics 1 - Basic Principles of Pharmacology & Intro to Pharmacodynamics Flashcards

1
Q

RISK versus BENEFIT assessment - purpose?

A

knowing HOW a drug achieves its action allows us to predict it’s BENEFICIAL and UNWANTED/HARMFUL effects

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2
Q

Examples of SIGNALING MOLECULES

A
  • NEUROTRANSMITTERS
  • AUTOCOIDS
  • CYTOKINES
  • HORMONES
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3
Q

Key steps in INTERCELLULAR SIGNALLING

e.g.

A
  1. specific PROTEINS in cell membranes (MEMBRANE RECEPTORS) recognise specific ligands
  2. ligand binds REVERSIBLY with receptor
  3. ligand-receptor binding causes further signaling WITHIN the cell (second messenger systems) and alteration in cell function
    e. g. myocardial cell contracts
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4
Q

Key features of MOLECULAR DRUG TARGETS

A
  • most molecular drug targets are PROTEINS

- have a specific CHEMICAL CONFIGURATION or shape that is recognised by the appropriate ligand or drug

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5
Q

State the x5 main locations of MOLECULAR DRUG TARGETS.

A
  • cell membrane receptors (major site)
  • cell nucleus receptors
  • ion channels
  • enzymes
  • carrier molecules (transporters)
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6
Q

Outline Drug-receptor activation

e.g.

A

Membrane receptor

  • attachment of drugs (ligands) to receptors
  • REVERSIBLE interaction in most cases
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7
Q

Outline the key steps in Second-messenger or signalling systems with example

A
  • receptor is activated
  • it sets off a train of events or ‘signals’ that change the FUNCTION of the cell in some way
    e. g. smooth muscle cells contract
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8
Q

CESSATION OF LIGAND EFFECTS

key point

A
  • the drug-receptor interaction is REVERSIBLE

- only a few exceptions

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9
Q
  • State the two main mechanisms for CESSATION OF LIGAND EFFECTS
A
  1. ENZYMATIC DEGRADATION of drug or ligand
    e. g. acetylcholine broken down by cholinesterase into choline + acetate
  2. REUPTAKE BACK INTO CELLS FROM WHICH RELEASED
    e. g. noradrenaline, serotonin
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10
Q

Serotonin is also known as …

A

5-HT = 5-hydroxytryptamine

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11
Q

Give an example of how a drug can influence ENZYMATIC DEGRADATION, describe what occurs
e.g.

A

when acetylcholinesterase is INHIBITED / BLOCKED, then the effects of acetylcholine will be INCREASED / PROLONGED
e.g. muscle contraction

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12
Q

Example of REVERSIBLE acetylcholinesterases

A

NEOSTIGMINE = cholinesterase inhibitor.
Used to treat conditions such as glaucoma, myasthenia gravis, dementia in Alzheimer’s disease (limited success) e.g. DONEPEZIL

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13
Q

Examples of IRREVERSIBLE acetylcholinesterases

A

Found in …

  • many insecticides (organophosphates)
  • nerve agents e.g. sarin, novichok
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14
Q

Give an example of how a drug can affect the REUPTAKE MECHANISM
e.g.

A

if reuptake transporter is inhibited / blocked, then the neurotransmitter effects will be increased / blocked

e.g. SSRIs & SNRIs act as ANTIDEPRESSANTS by increasing the levels of serotonin & noradrenaline at receptors in certain areas of the brain

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15
Q

Examples of RECEPTOR TYPES & SUBTYPES for different ligands

A 
- HISTAMINE 
 >  x2 main subtypes - H1, H2
- ADRENERGIC - Noradrenaline/adrenaline
 > x2 main subtypes alpha & beta (with subfamilies)
- DOPAMINE
 > x5 subtypes - D1, D2, D3, D4, D5
- SEROTONIN (5-HT)
 > x7 subtypes - 5-HT1 to 5-HT2 (with subfamilies)
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16
Q

H1 receptors are located in …

H1 receptor antagonists - e.g.

A

skin, blood vessels, CNS, bronchi
- stimulation –>
itching, vasodilation, nausea, bronchoconstriction

promethazine, cetrizine
- to reverse or prevent itching, vasodilation, nausea & bronchoconstriction

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17
Q

H2 receptors are located in …

H2 receptors antagonist e.g.

A

parietal cells of stomach
- stimulation –> produce gastric acid

ranitidine
- to reduce gastric acid secretion in treatment of peptic ulcer etc.

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18
Q

5-HT1B & 5-HT1D are located in …

5-HT1B & 5-HT1D receptor agonists

A

cerebral blood vessels
- stimulation –> produce constriction of blood vessels

sumatriptan
- to prevent dilation of cerebral blood vessels in treatment or prevention of migraine

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19
Q

5-HT3 receptors are located in …

5-HT3 receptors antagonist

A

stomach & chemoreceptor trigger zone
- stimulation –> produce emesis (vomiting)

ondansetron
- to treat or prevent nausea/emesis during chemotherapy

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20
Q

Selectivity / specificity of drug action

A
  • aim to TARGET a specific sub-type of receptor
  • very few drugs are ABSOLUTELY SPECIFIC to one receptor subtypes, therefore explains a lot the unwanted side effects of a drug
  • at best they are SELECTIVE
21
Q

Structure-activity relationships

A
  • even small changes in CHEMICAL STRUCTURE can change receptor selectivity markedly
22
Q

AFFINITY *

A

a measure of the STRENGTH OF INTERACTION between the ligand (drug) and receptor
e.g. how easily or readily they BIND TOGETHER

23
Q

INTRINSIC ACTIVITY (EFFICACY) *

A

a measure of the ability of the ligand (drug)-receptor interaction to cause a CHANGE IN FUNCTION
e.g. TO PRODUCE AN EFFECT

24
Q

AGONISTS *

A

agents with:

  • good affinity for the receptor AND
  • INTRINSIC ACTIVITY
    e. g. the drug-receptor interaction results in a CHANGE IN FUNCTION (muscle cell contracts)
25
Q

ANTAGONISTS *

> how it works?

A

agents with:

  • good affinity for the receptor
  • NO / VERY LITTLE INTRINSIC ACTIVITY

> PREVENTING ACCESS TO THE RECEPTORS for endogenous ligands e.g. block the effect of naturally occuring transmitters or autocoids

26
Q

COMPETITIVE ANTAGONISM

A
  • competing for a particular receptor type

- the agent with the HIGHEST CONCENTRATION will occupy the receptor

27
Q

Give an example of COMPETITIVE ANTAGONISM

A

Naloxone

  • an OPIOID ANTAGONIST
  • if administered to a patient that has overdosed on an OPIOID AGONIST (morphine, heroin) the naloxone will DISPLACE the opioid by COMPETITIVE ANTAGONISM
  • this reverses the respiratory depression
28
Q

PARTIAL AGONIST +

A
  • a few drugs are partial agonists
  • in SMALL CONCENTRATIONS these drugs act as AGONISTS (trigger a response) but their intrinsic activity (efficacy) is less than a full agonist
  • there is a CEILING EFFECT
  • in HIGHER CONCENTRATIONS they can act as ANTAGONISTS blocking further access to receptors for other agonists or endogenous substances
29
Q

Example or a PARTIAL AGONIST +

A

BUPRENORPHINE

  • used in opioid analgesic and in opioid dependence
  • difficult to overdose due to ceiling effect
30
Q

INVERSE AGONISTS +

A
  • relatively few drugs are classified as inverse agonists

- binds to the same receptor as an endogenous agonist BUT induces a pharmacological response OPPOSITE to that agonist

31
Q

Example of an INVERSE AGONISTS

A

Several anti-histamines

e.g. Loratadine

32
Q

Outline DOSE-RESPONSE CURVES

A
  • the relationship between the AMOUNT OF DRUG a tissue is exposed to (e.g. its CONCENTRATION AT THE RECEPTOR) and the LEVEL OF RESPONSE that occurs at these receptors
  • the response increased as the concentration increases
  • there is a PLATEAU EFFECT once we reach a certain concentration
33
Q

What is a LOG SCALE?

A
  • each unit on x-axis represents a ten-fold increase in dose
34
Q

Outline LOG DOSE-RESPONSE CURVES

A
  • when the dose (concentration) is put onto a log scale on x-axis there is a definite ‘S-shaped’ curve & a LINEAR RELATIONSHIP between dose & response
35
Q

Minimal dose (Emin)

A
  • a certain MINIMUM NUMBER OF RECEPTOR SITES must be activated BEFORE a response can occur
  • on the ‘S-shaped’ curve as dose (concentration) increases, more receptor sites are activated & a bigger response occurs
    > there is no point in under-dosing
36
Q

Maximal dose (Emax)

A
  • the point when ALL AVAILABLE RECEPTOR SITES HAVE BEEN ACTIVATED
  • at this point response is ‘maximal’ - no matter how much the dose increases you cannot get a bigger response
    > there is no point in overdosing
37
Q

TACHYPHYLAXIS

A

pharmacological term to describe…

some receptors lose responsiveness after repeated exposure to the same concentration (dose) of a particular drug

38
Q

DESENSITISATION

A
  • a decrease in the response of RECEPTOR-SECOND MESSENGER systems
  • associated with chronic exposure to a particular drug
39
Q

TOLERANCE

e.g. demonstrating how to prevent this

A
  • DESENSITISATION & TACHYPHYLAXIS (together or separately) can contribute to development of tolerance
  • need increasing doses of drug to get the same effect

e.g. it is recommended that GTN transdermal patch, used in the prophylaxis of angina, is removed at night

40
Q

RECEPTOR UP-REGULATION

A

The number of receptors can be INCREASED in response to strong signals at these receptors.
> generally caused by antagonists

41
Q

RECEPTOR DOWN-REGULATION

A

The number of receptors can be DECREASED in response to strong signals at these receptors
> generally caused by agonists

42
Q

Explain how a drug causes RECEPTOR DOWN-REGULATION using an example

A

down-regulation of opioid receptors occurs following chronic exposure to OPIOID AGONIST drugs (morphine, codeine)

43
Q

DEPENDENCE

A

withdrawal symptoms when drug removed

44
Q

Explain how drugs can cause RECEPTOR UP-REGULATION

e.g.

A

chronic use of BETA-ANTAGONIST drugs (beta-blockers e.g. atenolol, bisoprolol, metoprolol) leads to an increased expression of beta-adrenoreceptors

45
Q
  • Give an example of ENZYMATIC DEGRADATION of drug or ligand.
A

Acetylcholine broken down by cholinesterase into choline + acetate

46
Q
  • Give an example in which REUPTAKE BACK INTO CELLS FROM WHICH RELEASED occurs
A

noradrenaline, serotonin

47
Q

Give an example of ENDOGENOUS RECEPTOR DOWN-REGULATION

A
  • when INSULIN levels are continually high in response to high blood glucose levels (T2DM)
  • high insulin levels lead to insulin receptors being endocytosed & broken down leading to FAR FEWER RECEPTORS & INSULIN-RESISTANCE (reduced sensitivity to insulin)
48
Q

Outline why beta-antagonists should not be stopped suddenly?

A

these drugs should be WITHDRAWN GRADUALLY as abrupt cessation can lead to severe rebound hypertension

NSG 785 - Clinical Reasoning in Pharmacotherapeutics (4 decks)

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