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Applied Health Science > Introduction of pharmacology > Flashcards

Introduction of pharmacology Flashcards

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1
Q

What is pharmacokinetics?

A

What the body does to the drug
Metabolism and absorption

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2
Q

What is pharmacodynamics?

A

What the drug does to the body
Binding, drug-receptor interaction
How drug works as therapeutic agen

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3
Q

define - drug

A

a chemical substance of known structure, which when administered to a living organism produces a biological effect
Can be used as part or wholly as a medicine

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4
Q

define - medicine

A

‘usually, but not necessarily, contains one or more drugs which is administered with the intention of producing a therapeutic effect.
• any substance or combination of substances presented as having properties of preventing or treating disease in human beings
• any substance or combination of substances that may be used by or administered to human beings with a view to restoring, correcting or modifying a physiological function by exerting a pharmacological, immunological or metabolic action, or making a medical diagnosis’

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5
Q

Define - therapeutics

A

use of drugs to diagnose, prevent and treat illness (and/or pregnancy) i.e., the medical use of drug

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6
Q

define - formulations

A

how the drug is ‘packaged’ e.g., different chemical substances, including the active drug, are combined to produce a medicine

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7
Q

define - excipients

A

Substances formulated along side drug

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8
Q

State the three different names of drugs

A
  • chemical name (chemical structure described)
  • Generic name (which molecule class of drug belongs)
    Proprietary name (manufacturers came for drug – trade name)
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9
Q

What is a ligand?

A

Molecule that binds to receptor

Can be – drug, neurotransmitter or hormone
Act on different receptors
Synthetic vs natural
Exogenous (outside body) vs endogenous (within body)

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10
Q

What is a receptor?

A

molecular target for a drug

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11
Q

what is an agonist?

A

molecule that activated a receptor

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12
Q

what is an antagonist?

A

blocks or reduces agonist medicated responses

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13
Q

what an ideal drug would do?

A
  • Describe pharmacological action
  • Acceptable side effects or none
  • Reach target in right concentration at the right time
  • Remain at site of action for sufficient time in sufficient concentration
  • Rapidly and completely removed from body when no longer needed
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14
Q

define affinity

A
  • How well the ligand binds to receptor
    Strong or weak?
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15
Q

What are the aspects of drug binding?

A
  • Drugs usually interact in structurally specific way it targets
  • Steric interaction – based on spatial 3D relationship
  • Lock and key model
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16
Q

what properties affect drug receptor binding?

A

1.physico-chemical properties (electrostatic charges)
2/ steric properties (physical shape)

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17
Q

what are physical-chemical properties?

A

electrostatic charges

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18
Q

what are steric properties?

A

physical shape of binding

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19
Q

what is pharmacogenomics?

A

The way an individuals genetics attributes affect response to therapeutic drugs

Genetic variation can lead to differences in the way people respond to any given drug – most drugs are proteins so encodes in genome and have specific shape and receptor site

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20
Q

State the targets for drug action

A

RICE

  1. Receptors
  2. Ion channels
  3. Carrier molecules
  4. Enzymes
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21
Q

what are receptors?

A

Biological relevant molcular site with which a drug binds to produce a response
- Endogenous ligand activates exogenous agonist activated – antagonist (receptor)

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22
Q

how are G-protein linked trans-membrane receptors ?

A

-Ligand binds and alters rejector confomation and activation of intracellular second meddagers cascade (knock on effect)
- Diverse intracellular effects – cellular excitability
- modulation of other ion channels
- calcium ion channels -c ell excitability
- down regulation of G-protein linked receptors

23
Q

what are ion channels?

A

Movement of ion across membranes (down electrochemical gradient)
- Complex membrane protein (actual physical pore)
- Molecular selectivity filter – specific substrates

24
Q

what are carrier proteins?

A

-Facilitators for transport
Activ e transport or facilitated diffusion
- Circa. 400 characterised and uncharacterised transporter proteins
Inhibitor or false substrates are common drug types

25
Q

WHat are enzymes?

A

-Normal reaction inhibited and blocked by drug (substrate analogues)
- enzyme inhibitor
- false substrate – abnormal metabolite produced
- Pro-drug – active drug produced
Eg. Aspirin – pain, inflammation and clotting – blocks pain signals

26
Q

What are the families of drugs that interact with enzymes?

A
  1. Enzyme inhibitors
  2. False substrates
  3. Prodrugs
27
Q

what is drug specificity?

A

Binding site specificity (no drug acts with complete specificity)
- More likelihood of non-specific interactions becoming significant with larger doses
- Side effects often related to non-specific interaction (less potent effect than drug

28
Q

Pharmacokinetics – ADME

4 processes determine time and onset and duration of drug action in the body

A
  1. Absorption
  2. Distribution
  3. Metabolism
    Excretion
29
Q

WHat is absoprtion?

A

Th eprocess by which drug reaches the systemic circulation

Effected by – route of administration – and permeation (the absorption process)

30
Q

WHat are the two types of routes of administration?

A

Enteral administration – via gut – oral, buccaneers and rectal
Parenteral administration – not via gut – injection and topical

31
Q

What are the Pros and cons of enteral routes of administration ?

A

pros
- Oral ingestion – gut absorption
- Low infection risk
- Very simple for self administration
cons
- Harsh environment – stomach/duodenum
- First pass metabolism

32
Q

What is first pass metabolism?

A

Reduced bioavailability of drug due to loss by metabolism or excretion
- Intestinal lumen
- Intestinal wall
- Liver (main organ)
- Lungs (main organ)
Avoided by drug into a region of gut that does not drain into hepatic portal vein.

33
Q

What are the Pros and cons of topical

Parenteral administration

A

Pros – local effects, low systemic effects

  • Limited first pass metabolism
  • Low infection risk
  • Suited to low continuous – long period administration
  • Risk of systemic absorption – direct absorption to blood
  • Process of lipid permeation (drug must be lipid soluble, small molcular size and use a carrier molecule)
34
Q

What are teh types of injection?

A

-Intravascular (IV, IA) – drugs enters directly into blood stream
- INtramuscual r(IM) drug injected into skeletal muscle
- subcutaneous (SC) – drug absorbed from subcutaneoyse tissue
- dermal (ID) – dermal vascular layer
- depot injection (slow release formulations)

35
Q

What are the Pros and cons injections

Parenteral administration

A

Cons – high infection rapid, targeting risks

Pros – rapid bioavailability for IV and IA and avoids first pass metabolism

36
Q

What is bioavailability?

A

Proportion of active drug that reaches the systemic circulation and is free to bind to its target

Over time the plasma conc. Reduces as used up

37
Q

What effects bioavailability?

A
  • Route of administration
  • Formulation – enteric coating
  • Bioavailability is not a measure of how effective a drug is

IV – rapid but short term -slow release – less absorbed but over long term

38
Q

What factors that effect distribution of drugs?

A

1.Protein binding
2. blood flow
3. membrane permeation/ tissue solubility

39
Q

How is distribution effected by protein binding?

A

• Dynamic equilibrium for most drugs
• Partly bound to plasma protein and partly in plasma water
• Binding is reversible
Only the UNBOUND fraction can cross membranes or bind to receptor
Bound drug is locked in the plasma

40
Q

What can unbound or free drugs do – compared to bound drugs?

A

-Diffuse through capillary walls
- produce pharmacological effect
- metabolised and excreted
- subtle changes in binding have profound effects
- particular problem in elderly amlnourished patients

Bound drugs – are locked in the plasma

41
Q

How does blood flow effect distribution?

A

-primariy through ciculatory system
- tissue perfusion rate per tissue is important

42
Q

What is lipophilicity?

A

-Charged molecules, ions, ionised molecule diffuse less efficiently
- uncharged, non-ionised drugs have better access to membrane bound compartments

43
Q

What are the two phases of metabolism?

A

-Phase 1 – produces toxic metabolites
- Phase 2 – converts toxins to soluble metabolites for excretion

Normal occur sequentially but phase 2 can precede phase 1 and can occur with the absence of phase 1

44
Q

What is phase 1 of metabolism?

A

-Involves oxidisation, reduction and hydrolysis reactions
- Chemical reactions change polarisation of substance, increase water solubility, reduce pharmacological activity and may activate prodrugs

45
Q

What is phase 2 of metabolism?

A

Conjugation -a ding of endogenous substance
1.make water soluble and 2. biologically inactive

Convert drug/toxin by covalently joining them to other molecules

46
Q

What is excretion?

A

mainly kidney and renal

-Filtrtatoin
- only unbound drugs, metabolites can be processed via glomerular filtration
- proximal convoluted tubule cells actively secrete into nephron
- reaborption of lipophilic drugs – unionised at urine pH
- other routes – biliary, saliva, breat milk, sweat and tears

47
Q

What is biliary excretion?

A

Enteropheptic circulation
-principle route of excretion – kepatocyte uptake -> bile -> duodenum -> excretion in faeces

But – gut can convert drug to original form – can be resabsorded across intestinal wall – re-circulate in blood and be metabolised in liver again and re-secreted into bile

48
Q

What is a drug elimination half-life?

A

Half life – t ½

Time taken to decrease plasma concentration to 50%

49
Q

What is enterohepatic circulation?

A

the movement of bile acid molecules from the liver to the small intestine and back to the liver

50
Q

What is potency?

A

Concentration of a drug necessary to produce a given response

Eg. Two drugs that bind to the same receptor may not activate it to an equal extent, one may be more potent.

51
Q

What is affinity for a receptor?

A

Strength of the ligand – receptor interaction at molecular level

Strong or weak binding

52
Q

What is efficacy?

A

Drug ability to produce maximum possible effect when it binds to a receptor.

Some drugs fully activate the receptor once they reach a suitable concentration.

Full agonist – trigger max response once reach a sufficient concentration

53
Q

What is a full agonist?

A

trigger max response once reach a sufficient concentration

Applied Health Science (11 decks)

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