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FOUNDATIONS > PHARMACOLOGY > Flashcards

PHARMACOLOGY Flashcards

1
Q

Pharmcodynamics vs pharmakinetics

A

what drugs do to the body
what the body does to the drug

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2
Q

describe ion channel receptors

A

these are “gateways” into the cell membrane
they allow the selective passage of particular ions (think sodium, potassium, calcium etc)
they are fast and short acting
distributed widely
examples: nicotinic acetylcholine receptor, GABA A receptor

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3
Q

Ligand gated vs voltage gated receptors

A

Ligand gated –> responds to a particular ligand
voltage gated–> activated or deactivated by membrane potential changes

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4
Q

G coupled protein receptors

A

located on the cell membrane
need to be activated
once activated they transduce extracellular stimuli to intracellular stimuli
use ion channels or enzymes
most are olfactory
examples are muscarinic acetylcholine or adrenoreceptors

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5
Q

Kinase linked receptors

A

located on the cell membrane
transduce signals that regulate cell growth, differentiation, surival and migration
there are 3 subtypes
effects are very slow –> hours
example: insulin, growth factors, cytokine receptors

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6
Q

Nuclear receptors

A

they regulate gene expression
couples via DNA
very slow response
binds with a ligand and then goes under conformational change which recruits other proteins into a complex
example : corticosteroid (effect is slow as it promotes inflammation)

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7
Q

Define specificity

A

drugs with specific action, act directly on their receptor, one receptor one physiological response
no one drug currently available acts with complete specificity

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8
Q

Define selectivity

A

acts at one target and one target alone to produce a response

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9
Q

define affinity

A

extent to which a drug binds to receptors
drug with high affinity generally is associated with a low dose requirement

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10
Q

efficacy

A

ability of a ligand to bind to a receptor and produce a response
depends on the potency and interaction of the drug and the body

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11
Q

potency

A

describes the relationship between drug dose and magnitude of effect

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12
Q

full agonist

A
  • Creates change at the site of action that mimics a physiological ligand
  • Potency is determine by affinity and efficacy
  • A full agonist has high efficacy
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13
Q

partial agonist

A
  • Has both agonist and antagonist action
  • Submaximal effect (low efficacy)
  • Not able to produce a maximal physiological effect even if it binds to ALL of the receptors
  • They can compete with full agonists for receptor occupancy and decrease the overall physiological response
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14
Q

inverse agonist

A

produces the oppposite biological response of the endogenous ligand

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15
Q

antagonist

A
  • A drug which reduces the physiological response of another drug (decreases the efficacy of another ligand)
  • The effect of one drug is diminished or completely abolished in the presence of another
  • Binds at the site of action but does not produce the conformation change required to produce a response
  • It also blocks an agonist from binding
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16
Q

competitive antagonism

A
  • Some can be reversed or displaced by increasing the dose of the agonist (this is known as surmountable antagonism) ie it can be overcome
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17
Q

competitive irreversible antagonism

A
  • Usually bind to the same site as the agonist however is not as readily displaced from the binding site like a competitive antagonist
  • Compete for the same receptor site
  • Modifies the receptor and prevents the release of the antagonist and binding of agonist
  • Can be months or weeks
  • This is due to a covalent bond that is formed between the antagonist and receptor which in essence reduces the amount of receptors that any circulating agonist can bind to
  • Any agonist present is going to exert a lower maximum response
  • Adding more agonist is not going to be able to produce maximal response
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18
Q

competitive reversible

A
  • Competes at the same site as the agonist
  • Example is naloxone, ipratropium bromide
  • Adding more agonist can displace the antagonist and produce the maximal response
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19
Q

non competitive antagonism

A
  • Antagonist targets a site that is different to the primary ligand binding site
  • There are primary AND alternative sites on receptors
  • So the focus is on the alternate site
  • Doesn’t stop the agonist from binding
  • But interferes with secondary chemical messengers within the cell that the agonist depends on to generate a response
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20
Q

physiological antagonism

A
  • Binding of two ligands causing opposing physiological effects
  • Results when medications that do not bind to the same receptor as the endogenous agonist produce an effect that is opposite to the agonist effect
    eg –> histamine in anaphylaxis and adrenaline
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21
Q

pharmacokinetic antagonism

A
  • Increase or decreases the activity of another ligand or drug
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22
Q

chemical antagonism

A
  • Results when drugs do not interact at the agonist receptor, rather reduce the concentration of an agonist by forming a chemical complex (chelating agents)
  • Crushing medications separately so they don’t bind together and alters their structures and effects
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23
Q

desensitisation / tachyphylaxis

A

the effect of the drug gradually diminishes when it is given repeatedly or continuously
usually develops over a few minutes
can result in increasing doses of a drug required to achieve the same biological effect, which in turn can lead to greater desensitisation

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24
Q

tolerance

A

gradual decrease in responsiveness to a drug
takes hours days or weeks to develop
happens after repeated doses

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25
Q

mechanisms for desensitisation and tolerance

A
  • Chronic exposure to agonist = decrease number of receptors
  • Downregulation  reduced synthesis of new receptors
  • Sequestration or internalisation  degradation of pre existing receptors through endocytosis
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26
Q

refractoriness and resistance

A
  • Used to describe a lack of therapeutic responsiveness to a drug
  • Describes the loss of effectiveness of antimicrobial or antitumor cells
  • Resistant bacterial cells adopt different survival mechanisms such as target changing through mutation
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27
Q

persistance

A
  • Defined as dormant cells that form spontaneously and are resistant to antibiotics
  • Antimicrobial agents are only effective when a cell is active and not in a dormant state
  • Some bacteria exist in a stationary growth phase; most antimicrobial agents have no effect on cells that are not actively growing and dividing
  • These bacteria are referred to a persistent cells and are therefore drug persistent
28
Q

mutagenesis

A

modification of cellular DNA
common cause of carcinogenesis

29
Q

teratongenesis

A

formation of gross structural formations during fetal development

30
Q

Immunologic reactions type 2

A
  • Also known as cytotoxic reactions
  • IgG and igM mediated
  • Activate the complement system and cause phagocytosis
  • Attacks bodies own blood cells including erythrocytes and platelets
31
Q

immunologic reactions type 3

A
  • Immunocomplex reactions
  • Occurs in joints, skin, blood vessels or glomeruli and trigger the activation of inflammatory cells (monocytes and neutrophils)
  • Release of enzymes causing tissue damage
32
Q

immunologic reactions type 4

A
  • Cell or antibody mediated reactions
  • Skin rashes are common
  • Ranging from mild to fatal
    t cell mediated
33
Q

therapeutic index vs therapeutic window

A

TI- is the range of doses at which a medication is effective without unacceptable side effects
TW- the dosage range between a minimum effective therapeutic concentration, and the minimum toxic concentration

34
Q

what is spare receptor theory

A
  • Not all of the receptors associated with a particular physiological response need to be occupied for a maximal response to be produced
  • Maximal response can be achieved with less than 1% occupancy
35
Q

drug liberation

A

the process of the active ingredient of a drug separating from its pharmaceutical formulation
helps us understand bioavailbulity
purpose is to enhance therapeutic effect or enhance solubility

36
Q

absorption

A

the transportation of unmetabolised drug to the administration site
the composition and route of drug administration work togethet to determine rate and extent of absorption

37
Q

the rate and extent to which a drug is absorbed is influenced by ….

A
  • The nature of the absorbing surface (number of cells and surface area, think about size of small intestine)
  • Blood flow (think cardiac arrest)
  • Solubility of the drug (more soluble the faster its absorbed)
  • Ionisation (hydrophilic dissolves in H2O, lipophilic can easily cross membranes)
  • Formulation (manipulated for slow release)
38
Q

what type of molecules can pass through the phospholipid bilayer

A

allows hydrophobic and small uncharged molecules (oxygen and co2) to pass through

39
Q

Oral admin

A

75% are absorbed within 1-3 hours
small intestine is the major site

40
Q

what are things that effect GI absorption

A

presence of absence of food in the gut,
GI motility(migraines and diabetic neuropathy cause gastric stasis), splanchnic blood flow(increased flow = increased absorption), particle size and formation, physiochemical factors (solubility, lipophilicity),
other ingested drugs

41
Q

bioavailbility

A

= the fraction of administered drug that reaches systemic circulation
* Depends on absorption and first pass metabolism

42
Q

first pass metabolism

A
  • Oral drugs have lower bioavailability as they must pass through the intestinal mucosa which contain enzymes.
  • The liver also contains these enzymes which the drug must pass through before reaching systemic circulation.
43
Q

bioequivalence

A
  • Is the biochemical similarity of two (or more) drugs that share the same active ingredients
  • Refers to the extent and rate of which the active drug is absorbed and becomes available at the site of drug action
  • This is important when the manufacturer wants to change the form of medication, ie from an oral tablet to oral liquid
  • Example is warfarin, you cannot substitute different brands as they have different bioequivalence = more public health safety education
44
Q

IM route absorption

A
  • Slower absorption = safer plasma concentration profile compared to IV
  • Rate of absorption depends significantly on local blood flow to the site of administration
45
Q

topical absorption

A
  • Only lipid soluble compounds are absorbed readily through the skin
  • Transdermal patches produce a steady state of drug delivery that can be left for significant periods of time
46
Q

Distribution

A
  • Refers to the reversible transfer of a drug from one location to another in the body
  • Once administered and absorbed the drug is distributed between the body fluid compartments
  • Ie plasma water, interstitial water, intracellular water and transcellular water (pleural, synovial, cerebrospinal, in ocular, peritoneal fluids, digestive secretions and fetus in pregnant women)
47
Q

what compartment do lipid soluble drugs have high affinity for ?

A

adipose tissue - they are usually stored here

48
Q

what is plasma protein binding

A
  • Refers to the degree to which medications attach to blood protein within blood plasma
  • This can impact efficacy
  • Common blood proteins include: albumin, lipoprotein, glycoprotein
  • Protein binding can affect a bloods half life because the bound protein portion may act as a reservoir from which the medication is slowly released, prolonging the effects of the medication
49
Q

VOD

A
  • Represents an individuals medications propensity to either remain in the plasma or redistribute to other tissue compartments (e.g. adipose tissue)
  • The distribution of drugs throughout the body is not even, resulting in accumulation in tissues at a much higher concentration than in the blood
  • The extent of tissue concentration is measured as VOD
50
Q

Low VOD vs High VOD

A

a medication with a HIGH VOD has a propensity to leave the plasma and enter the extravascular compartments. Conversely, a medication with a LOW VOD have the propensity to remain in the plasma . Drugs with a higher VOD require higher dosing to achieve a required plasma concentration

51
Q

factors that influence VOD

A

body composition, obesity, plasma protein concentration

52
Q

Elimination

A

The irreversible loss of a drug from the body through the processes of metabolism and excretion
* The amount of drug removed will affect the time that the concentration is above the therapeutic level and the steady state concentration
* Determines the rate of termination of the physiological response

53
Q

half life

A
  • Is the time taken for the drug plasma concentration to fall by one half
  • It is directly influence by the VOD and clearance rate
  • This is important for dosing frequency to avoid large fluctuations in plasma concentration
54
Q

Metabolism / biotransformation

A
  • = chemical modification of an administered drug
  • Can covert a drug into an active substance or degrade a drug into its metabolites
  • Not all drugs undergo metabolism, some are excreted
  • Primary purpose of metabolism is to decrease lipid solubility to aid renal excretion of drug in the urine
55
Q

phase 1 vs phase 2 metabolism

A

Phase one reactions (functionalisation)
* Catabolic = breakdown substances via enzymes
* Involves, oxidisation, reduction or hydrolysis
* They yield polar, water soluble drug metabolite that may still be active
* Many phase 1 products become substrates for phase 2 reactions
* Oxidisation is the most common biochemical phase 1 reaction

Phase two (conjugation)
* Anabolic = conjugation, attachment of a substance by enzymes
* Yield a large polar metabolite by adding hydrophilic groups to form water soluble inactive compounds which are readily excretable by the kidneys
* Usually have decreased pharmacological activity

56
Q

what is the most clincally significant enzyme involved in metabolism?

A
  • The cytochrome P450 (CYP) are of the greatest significance in drug and chemical metabolism (enzyme)
  • Due to is specificity there are several CYP isoforms which differ in the drugs they metabolise
57
Q

What is enzyme induction and inhibition

A
  • Induction is the process in which a molecule/medication induces/initiates/enhances the expression of an enzymes
  • Whereas inhibition refers to the inhibition of the expression of the enzyme by a molecule
58
Q

excretion

A
  • Removal of unchanged drug or metabolite
  • Urine, bile, sweat, breast milk, saliva, tears and faeces
  • Most important are liver and kidneys
59
Q

first order kinetics vs zero order

A

first order = speed of which the drug is eliminated slows down as the plasma concentration decreases, half life is constant. or the more drug that is in the plasma the greater the unit elimination of time

ZERO ORDER
constant amount eliminated per unit of time. rate of excretion is independent of concentration of drug in the plasma. more susceptible to overdose here.
**Once the enzyme is no longer saturated the pattern will follow first order

60
Q

Kidneys role in excretion

A
  • Glomerular filtration = passive, removes molecules smaller than albumin
  • Tubular secretion = active
  • Therefore, drugs that are highly protein bound are not filtered and small molecule drugs that are not protein bound are cleared rapidly
61
Q

liver role in excretion

A
  • Secretes some drugs into bile which is then excreted into the digestive tract
  • The drug is then eliminated via the digestive tract via faeces or is reabsorbed as part of the enterohepatic circulation
  • Drugs that go through this include = opioids, NSAIDS, digoxin and warfarin
  • Enterohepatic circulation results in a drug ‘reservoir’ of recirculating drug that can amount to 20% of the drug in the body, prolonging duration of action
62
Q

what type of drugs are subcut injections used for

A

peptide and protein based

63
Q

subcut drugs and bioavailbility

A
  • Used for when delayed or prolonged absorption is necessary
  • Bioavailability is variable and often incomplete, ranging from 50-80% of the administered drug becoming available in the systemic circulation
  • Usually rapid onset of action, but can vary based on systemic and local injection site factors
64
Q

cmax vs tmax

A

cmax= maxium blood concentration
tmax = the time to reach maximum concentration
these affect bioavailbility

65
Q

gastric pH required for absorption

A

2.5-3

66
Q

pharmacogenomics

A

the right drug for the right person based on their genetics
* It aims to rationalise and optimise drug therapy to ensure maximum efficacy with minimal adverse effects (a form of personalised medicine)

67
Q
A

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