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IMS > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is the difference between pharmacodynamics and pharmacokinetics

A

dyn - interaction with cellular component, concentration - effect relationship - modification of dais progression
kin - absorption from site of administration, time of onset of effect and elimination from the body

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2
Q

what is the factors for passive diffusion of a drug across a membrane

A

its solubility

must not be bound to protein

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3
Q

what must be the structural case of a drug to be able to pass through a membrane from the blood

A

it must not be bound to a protein

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4
Q

what are some methods of drugs crossing the membrane

A

passive diffusion
transporters
membrane pores
vesicle mediated transport

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5
Q

what is pinocytosis

A

molecules engulfed by cell membranes forming vesicle which is moved inside the cell and released within the cell

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6
Q

how do PPI’s effect transport

A

they stop H+ secretion into the stomach with increases the pH

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7
Q

how to Ca channel blockers effect cellular transport

A

bind to ca channels on smooth muscles blocking influx of Ca causing smooth muscle relaxation and decreased heart rate

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8
Q

drugs can be acids or bases but what must occur for an acid to cross the cell membrane

A

must be uncharged

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9
Q

what is the difference between acids and bases

A

acids can dissociate to donate one or more protons

bases are proton receivers

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10
Q

how do the environment effect degree of ionisation of acids and bases

A

in water - strong acids and bases are 100% dissociated
with increasing pH acids become increasingly ionised and bases become increasingly unionised
in stomach very acidic so basic drugs will cross membrane more readily than acidic ones which can cross more easily in the small intestine

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11
Q

how do you determine concentration of drugs at site of action

A

using modified dose forms

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12
Q

what are benefits of modified dose forms

A
  • Improved patient adherence, reduction in incidence and severity of GIT effects, improved control over therapeutic plasma concentrations, improved treatment of chronic conditions which steady plasma concentration required, maintenance of therapeutic action overnight, minimise adverse effects associated with high plasma concentrations
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13
Q

what are the disadvantages of modified does forms

A
  • Cost more per unit dose than conventional forms, possibility of unsafe over dosage if used incorrectly or if failure of MR tablet, rate of transit through GIT limits maximum period for which a therapeutic response can be maintained, variability in physiological factors e.g. GIT pH, enzymes, food etc. influence drug bioavailability
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14
Q

what are the ten routes of transmission

A 
oral 
intramuscular 
subcutaneous 
intravenous 
buccal 
transdermal 
inhalation 
intrathecal 
epidural 
topical
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15
Q

what is an advantage and disadvantage of oral

A

convenient, safe, economical

cannot be used for drugs that are inactivated by 1st pass metabolism or that irritate the gut

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16
Q

what is an advantage and disadvantage of intramuscular

A

Suitable for suspensions and oily vehicle
Rapid absorption from solutions
Slow and sustained absorption from suspensions

May be painful
May cause bleeding at site of injection

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17
Q

what is an advantage and disadvantage of subcutaneous

A

through fatty layer - need to be fat soluble
Suitable for suspensions and pellets

Cannot be used to deliver large volumes of fluid
Cannot be used for drugs that irritate cutaneous tissue

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18
Q

what is an advantage and disadvantage of intravenous

A

can provide very large doses
Bypasses absorption yielding immediate effect
100% immediate bioavailability

but poses more risk to toxicity

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19
Q

what is an advantage and disadvantage of buccal

A

through cheek or mouth - rapidly absorbed, avoids 1st pass metabolism

only effective for low doses - drugs must be water and lipid soluble

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20
Q

what is an advantage and disadvantage of transdermal

A

patch placed on skin straight through skin to blood stream - avoids 1st pass metabolism

effective only for low doses that must be highly lipid soluble

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21
Q

what is an advantage and disadvantage of epidural

A

injection into spaces in spinal cord - provides a targeted effect

can cause paralysis, risk of failure and infection

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22
Q

what is an advantage and disadvantage of topical

A

creams etc - non invasive and easy to administer

poorly lipid soluble and not absorbed via skin or mucous membrane - very slow absorption

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23
Q

describe route of oral absorption

A

approx 75% of drug given orally will be absorbed in 1-3 hours - drug is wanted to reach small intestine so bulking agents incorporated to help protect until reaches there

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24
Q

what factors effect oral absorption

A

particle size and formation, GIT enzymes/acid, GIT motility, helps drug travel along, gut muscles move more quickly, but when have stomach upset moved along too quickly, not enough time for absorption, physiochemical factors, food, some fatty foods allow easier absorption, some drugs taken with food, some without as can block cell membranes

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25
Q

what is distribution

A

the process by which a drug is transferred reversibly
from the general circulation into the tissues as concentrations in blood increase
from the tissues into blood as blood concentrations decrease

Passive diffusion of un-ionised form across cell membrane
After IV injection, high plasma conc. and drug rapidly equilibrates with well-perfused tissue giving relatively high conc. in these tissues

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26
Q

what factors influence distribution of drugs from plasma

A

Plasma protein binding, proteins act as carriers until reach site of action
Specific drug receptor sites in tissues
Regional blood flow, if low blood flow to area not a lot of drug distribution
Lipid solubility, biggest feature of allowing crossing of membrane
Disease
Skin, skeletal muscle and fat poorly perfused organs, drug needs to be given more often or for longer period of time to have effect here

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27
Q

what is the volume of distribution

A

volume of plasma that accounts for total amount of drug

used to determine the loading dose necessary for a desired blood concentration of a drug

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28
Q

what is drug protein binding

A

forms a drug protein complex
binding of drugs to albumin and glycoproteins. it is a reversible structure where the drug dissociates form the protein at the receptor site

29
Q

how do drug displacement occur

A

when a drug that becomes highly bound to a protein interacts with a drug that is more favourable to bind to then displacement of the first drug will occur which produces increased unbound conc of drug and more biological activity

30
Q

when do changes in plasma protein binding become significant

A

drugs that are greater than 90% bound to plasma proteins

31
Q

what is the rule with albumin bound drugs

A

need to be routinely checked for dose adjustments - secondary drug administered has higher affinity to protein

32
Q

what are some albumin bound vs glycoprotein bound drugs

A

albumin: fureosimde - ibuprofen - thiazides - warfarin

glycoprotein - propronaolol - tricyclic antidepressants - lidocaine

33
Q

what is metabolism

A

drug either excreted and unchanged or metabolised and then excreted
it is the activation of inactive drug - production fo active drug with increased activity form or inactivation of active drug or change in nature of activity

34
Q

what is first pass metabolism

A

drugs have 4 main barriers before they reach blood circulation
intestinal lumen - digestuve enzymes secreted by mucosal cells and pancreas
intestinal wall - rich in enzymes that further metabolise drugs
liver - major site of drug metabolism
lungs - high affinity for many drugs site of metabolism for local hormones too

35
Q

what is the differences between phase 1 and 2 reactions

A

phase 1 - oxidation reduction hydrolysis usually forms more reactive products sometimes toxic
phase 2 - conjugation usually forms inactive form and readily excreted products

36
Q

what is the process of excretion from the liver

A

depends on blood flow to liver and activity of enzymes in liver, liver enzymes chemically alter drug to form metabolites which are inactive or equally/more active than the parent drug, metabolites eventually eliminated via kidney as become more water soluble, may be reduced due to elderly (poor blood flow), neonates (low liver enzyme activity), drugs reducing enzyme activity, extensive liver damage

37
Q

what is the process of excretion from the kidney

A

depends on blood flow to kidney, glomerular (capillary) filtration fate, active secretion of drugs unto kidney tubule, passive reabsorption back into tubule

38
Q

what is creatinine clearance

A
  • substance produced in skeletal muscle excreted through kidneys, neither passively reabsorbed or actively secreted, estimation of creatinine clearance estimates clearance of drugs filtered at glomerulus
39
Q

what is the cockcroft Gault equation

A

estimated creatine clearance in mL/min = (140-age) x weight x constant
/ serum creatinine
age in years, weight in kg, serum in micromole/litre
constant 1.23 in men and 1.04 in women
gives good indication of liver function

40
Q

what is the estimated glomerular filtration rate

A

uses serum creatinine, age, sex, race
normalised to body surface area of 1.73m^2 and derived from formula
absolute GFR = eGFR x individuals body surface area / 1.73
in relation to muscle mass not actual weight
not a good indicator but can show renal impairment

41
Q

describe the mechanism of drugs binding to receptors

A

receptor must be specific to the drug - drug receptor interaction follows mass-action relationship ie one drug molecule occupies each receptor and binding is reversible
the magnitude of response is proportional to the fraction of total receptor site occupied by drug molecules
binding to receptor causes event which leads to response

42
Q

give examples of drug enzyme interactions

A
  • Neurotransmitters and synapses
  • Nerve impulses transmitted along neurone, impulses conducted across space by neurotransmitters, neurones conduct to the synapse are presynaptic neurones, conduct the impulse away from the synapse are synaptic neurones
  • Enzyme action, usually proteins that act on specific molecules called substrates, lock and key concept, enzyme and substrate bind temporarily to form enzyme-substrate complex
43
Q

what are the different types of drug receptor

A

Cell-surface receptors – ligand must be lipid soluble
Ligand-gated ion channels
G-protein coupled receptors
Enzyme-linked transmembrane receptors – two kinases join and form dimer

44
Q

what are the dose differences between high potency and low potency drugs

A

high potency are given in low doses or less frequently

low potency - doses given to rely effect of drug or if want a smaller effect

45
Q

what will the difference in effects be of an agonist with a competitive antagonists vs irreversible antagonist

A

still full effect of agonist as can bind when antagonist has moved on - antagonist can be competed out
minimised effect of of agonist as antagonist binds irreversibly so agonist cannot bind

46
Q

what are the uses of the log concentration-response curve for drugs

A
  • Scale allows us to compare more than one drug, use log scale instead of conc. scale as drugs may have different conc. scales
  • As drug conc. increases get bigger response, plateaus because all receptors saturated
47
Q

what is Kd

A

rate of chemical reaction is directly proportional to the product of the activities or concentrations of the reactants

48
Q

what is EC50

A

conc. of drug that produces 50% of max. response

49
Q

what is TD50

A

conc. of drug when becomes toxic

50
Q

how would you use an full agonist and partial agonist together

A

Full agonist elicits bigger response at same drug conc. than a partial agonist, may use partial agonist as want drug to have effect but minimise side effects

51
Q

what is the therapeutic index

A

the ratio of dose that causes toxicity compared to the dose that produces desired effect

52
Q

what is drug monitoring and give examples

A

Drug monitoring performed by monitoring clinical effects e.g. blood pressure, reduction in pain, monitoring biological effects e.g. prothrombin time and glucose, plasma concentrations, variable if plasma conc. is related to biological effect of drug

53
Q

what does salbutamol, propronaolol and atenolol do

A

sal - selective B2 adrenergic agonist - treatment of asthma and COPD
prop - non-selective beta blocker - reduces heart work load ie angina, treat high blood pressure - adrenergic antagonist
atenolol - another beta blocker selective for B 1 - antagonist for arteries and blood pressure etc

54
Q

what is a bioavailability and how does it change

A

Bioavailability, proportion of dose that actually gets into systemic circulation
Same drug but 3 different formulations could have same bioavailability

55
Q

what affects the bioavailability of a drug

A

preparation, physiochemical interaction, patient factors, pharmacokinetic reactions and first pass metabolism

56
Q

what is bioequivalence

A

two or more chemically or pharmaceutically equivalent products produce comparable bioavailability - can replace one drug with another without causing clinical problems

57
Q

what is clearance

A

measure of removal of a drug from myth body or volume of plasma completely emptied of drug per unit of time
include metabolic and renal/biliary clearance

58
Q

what is the half life

A

time taken for conc to reduce by half - assume point of ingestion there is 100% availability regardless of method of administration

59
Q

how is the half life affected

A

half life increased by diminished renal plasma flow

addition of second drug that displaces first from albumin

60
Q

what causes decreased extraction and metabolism

A

renal disease

liver disease

61
Q

what are the uses of volume of distribution

A

determines the loading dose necessary for a desired blood conc. of a drug, and for estimating a blood conc. in treatment of overdose

62
Q

How do NSAIDS work and give two examples

A

Block COX1 and 2, non-selective
prevent inflammatory response, pain receptors and blood clotting
eg aspirin and ibuprofen

63
Q

how to ACE inhibitors work

A

stops pathway before angiotensin 2 production
can cause dry cough as prevents breakdown of bradykinin which accumulates
prevents vasoconstriction stops in crease in blood pressure and stops water reabsorption

64
Q

what are ARBS

A

angiotensin 2 receptor blockers - cannot be used at the same time as ACE’s

65
Q

what is the structure of local anaesthetics and what are the two types of bond they form

A

have lipid soluble hydrophobic aromatic group and charged - hydrophilic amine group
amide or ester

66
Q

how are local anaesthetics administrated

A

topically or via injection - weak bases and can cross the cell membrane

67
Q

what is the difference between amide and ester bonding in local anaesthetics

A
  • Amides relatively stable and hypersensitivity reactions rare, esters rapidly hydrolysed and breakdown product is associated with allergic and hypersensitive reactions
  • Ester linkage more easily broken so less stable in solution and can’t be stored as long, amide’s more common than esters
68
Q

what is the mechanism of action of local anaesthetics

A
  • Disrupt ion channel function within neurone cell membrane, preventing transmission of neuronal action potential
  • Occur via specific binding of local anaesthetic molecules in ionised form to sodium channels, holding them in inactive state so no further depolarisation can occur
  • Ionisation happens as inside of neuron is weakly acidic, once local anaesthetic enters weak environment become ionised
  • Blocked Na+ channels stop pain sensation feedback to brain

IMS (20 decks)

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