Pharmacology Flashcards

(68 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

its solubility

must not be bound to protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are some methods of drugs crossing the membrane

A

passive diffusion
transporters
membrane pores
vesicle mediated transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is pinocytosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do PPI’s effect transport

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

must be uncharged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the difference between acids and bases

A

acids can dissociate to donate one or more protons

bases are proton receivers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do you determine concentration of drugs at site of action

A

using modified dose forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the ten routes of transmission

A
oral 
intramuscular 
subcutaneous 
intravenous 
buccal 
transdermal 
inhalation 
intrathecal 
epidural 
topical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what is distribution
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
26
what factors influence distribution of drugs from plasma
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
27
what is the volume of distribution
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
28
what is drug protein binding
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
how do drug displacement occur
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
when do changes in plasma protein binding become significant
drugs that are greater than 90% bound to plasma proteins
31
what is the rule with albumin bound drugs
need to be routinely checked for dose adjustments - secondary drug administered has higher affinity to protein
32
what are some albumin bound vs glycoprotein bound drugs
albumin: fureosimde - ibuprofen - thiazides - warfarin glycoprotein - propronaolol - tricyclic antidepressants - lidocaine
33
what is metabolism
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
what is first pass metabolism
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
what is the differences between phase 1 and 2 reactions
phase 1 - oxidation reduction hydrolysis usually forms more reactive products sometimes toxic phase 2 - conjugation usually forms inactive form and readily excreted products
36
what is the process of excretion from the liver
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
what is the process of excretion from the kidney
depends on blood flow to kidney, glomerular (capillary) filtration fate, active secretion of drugs unto kidney tubule, passive reabsorption back into tubule
38
what is creatinine clearance
- 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
what is the cockcroft Gault equation
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
what is the estimated glomerular filtration rate
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
describe the mechanism of drugs binding to receptors
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
give examples of drug enzyme interactions
- 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
what are the different types of drug receptor
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
what are the dose differences between high potency and low potency drugs
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
what will the difference in effects be of an agonist with a competitive antagonists vs irreversible antagonist
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
what are the uses of the log concentration-response curve for drugs
- 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
what is Kd
rate of chemical reaction is directly proportional to the product of the activities or concentrations of the reactants
48
what is EC50
conc. of drug that produces 50% of max. response
49
what is TD50
conc. of drug when becomes toxic
50
how would you use an full agonist and partial agonist together
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
what is the therapeutic index
the ratio of dose that causes toxicity compared to the dose that produces desired effect
52
what is drug monitoring and give examples
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
what does salbutamol, propronaolol and atenolol do
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
what is a bioavailability and how does it change
Bioavailability, proportion of dose that actually gets into systemic circulation Same drug but 3 different formulations could have same bioavailability
55
what affects the bioavailability of a drug
preparation, physiochemical interaction, patient factors, pharmacokinetic reactions and first pass metabolism
56
what is bioequivalence
two or more chemically or pharmaceutically equivalent products produce comparable bioavailability - can replace one drug with another without causing clinical problems
57
what is clearance
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
what is the half life
time taken for conc to reduce by half - assume point of ingestion there is 100% availability regardless of method of administration
59
how is the half life affected
half life increased by diminished renal plasma flow | addition of second drug that displaces first from albumin
60
what causes decreased extraction and metabolism
renal disease | liver disease
61
what are the uses of volume of distribution
determines the loading dose necessary for a desired blood conc. of a drug, and for estimating a blood conc. in treatment of overdose
62
How do NSAIDS work and give two examples
Block COX1 and 2, non-selective prevent inflammatory response, pain receptors and blood clotting eg aspirin and ibuprofen
63
how to ACE inhibitors work
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
what are ARBS
angiotensin 2 receptor blockers - cannot be used at the same time as ACE's
65
what is the structure of local anaesthetics and what are the two types of bond they form
have lipid soluble hydrophobic aromatic group and charged - hydrophilic amine group amide or ester
66
how are local anaesthetics administrated
topically or via injection - weak bases and can cross the cell membrane
67
what is the difference between amide and ester bonding in local anaesthetics
- 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
what is the mechanism of action of local anaesthetics
- 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