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

(48 cards)

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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

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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

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

AFFINITY *

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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) *

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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 *

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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
ANTAGONISTS * > how it works?
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
COMPETITIVE ANTAGONISM
- competing for a particular receptor type | - the agent with the HIGHEST CONCENTRATION will occupy the receptor
27
Give an example of COMPETITIVE ANTAGONISM
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
PARTIAL AGONIST +
- 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
Example or a PARTIAL AGONIST +
BUPRENORPHINE - used in opioid analgesic and in opioid dependence - difficult to overdose due to ceiling effect
30
INVERSE AGONISTS +
- 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
Example of an INVERSE AGONISTS
Several anti-histamines | e.g. Loratadine
32
Outline DOSE-RESPONSE CURVES
- 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
What is a LOG SCALE?
- each unit on x-axis represents a ten-fold increase in dose
34
Outline LOG DOSE-RESPONSE CURVES
- 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
Minimal dose (Emin)
- 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
Maximal dose (Emax)
- 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
TACHYPHYLAXIS
pharmacological term to describe... | some receptors lose responsiveness after repeated exposure to the same concentration (dose) of a particular drug
38
DESENSITISATION
- a decrease in the response of RECEPTOR-SECOND MESSENGER systems - associated with chronic exposure to a particular drug
39
TOLERANCE | e.g. demonstrating how to prevent this
- 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
RECEPTOR UP-REGULATION
The number of receptors can be INCREASED in response to strong signals at these receptors. > generally caused by antagonists
41
RECEPTOR DOWN-REGULATION
The number of receptors can be DECREASED in response to strong signals at these receptors > generally caused by agonists
42
Explain how a drug causes RECEPTOR DOWN-REGULATION using an example
down-regulation of opioid receptors occurs following chronic exposure to OPIOID AGONIST drugs (morphine, codeine)
43
DEPENDENCE
withdrawal symptoms when drug removed
44
Explain how drugs can cause RECEPTOR UP-REGULATION | e.g.
chronic use of BETA-ANTAGONIST drugs (beta-blockers e.g. atenolol, bisoprolol, metoprolol) leads to an increased expression of beta-adrenoreceptors
45
* Give an example of ENZYMATIC DEGRADATION of drug or ligand.
Acetylcholine broken down by cholinesterase into choline + acetate
46
* Give an example in which REUPTAKE BACK INTO CELLS FROM WHICH RELEASED occurs
noradrenaline, serotonin
47
Give an example of ENDOGENOUS RECEPTOR DOWN-REGULATION
- 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
Outline why beta-antagonists should not be stopped suddenly?
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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