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Principles - Kate > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

what is pharmacodynamics?

A

what a drug does to the body (biological effects and mechanism of action)

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2
Q

what is pharmacokinetics?

A

what the body does to the drug (absorption, distribution, metabolism and excretion of drugs and their metabolites)

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3
Q

what is a drug?

A

a synthetic or natural, substance of known structure used in the treatment, prevention or diagnosis of disease

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4
Q

what is medicine?

A

a chemical preparation containing one or more drugs used with the intention of causing therapeutic effect. medicines usually act with a degree of selectivity

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5
Q

what do drugs bind to?

A

regulatory proteins:
enzymes, carrier molecules, ion channels, receptors
rarely does a drug have no specific target

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6
Q

what are receptors?

A

macromolecules on or within cells that mediate the biological actions of hormones, neurotransmitters and other endogenous substances

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7
Q

what is an agonist?

A

a drug that binds to a receptor to produce a cellular response

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8
Q

what is an antagonist?

A

a drug that reduces, or blocks the actions of an agonist by binding to the same receptor

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9
Q

what is affinity?

A

strength of association between ligand and receptor, determined by chemical bonds between a ligand and its receptor

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10
Q

what is efficacy?

A

the ability of an agonist to evoke a cellular response

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11
Q

what are the characteristics of an agonist?

A

bind reversibility to receptors to activate them temporarily, posses affinity and efficacy

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12
Q

what are the characteristics of an antagonist?

A

bind to receptors (usually reversibly), but do not activate them, posses affinity but not efficacy, block receptor activation by agonist

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13
Q

what is the relationship between concentration and response? (linear plot)

A

hyperbolic

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14
Q

what is the relationship between concentration and response? (semi-logarithmic plot)

A

sigmoidal

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15
Q

what is EC50?

A

the concentration of agonist/antagonist that elicits a half maximal response

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16
Q

what is reversible competitive antagonism?

A

binding of agonist and antagonist, both of which are reversible, occur at the same (orthosteric) site and is thus competitive and mutually exclusive. reversible competitive antagonism can be overcome by increasing the concentration of agonist

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17
Q

what is non-competitive antagonism?

A

agonist binds to the orthosteric site and antagonist binds to a separate allosteric site and thus is non-competitive, both may occupy the receptor reversibly and simultaneously, but activation cannot occur when antagonist is bound

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18
Q

what happens to the agonist concentration and response graph with a competitive antagonist?

A

parallel rightward shift of the agonist concentration response curve but the maximum response is unchanged

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19
Q

what happens to the agonist concentration and response graph with a non-competitive inhibitor?

A

depresses the slope and maximum of the concentration response curve, but does not cause a rightwards shift

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20
Q

what are the main types of receptors?

A

ligand-gated ion channels, G-protein-coupled receptors, kinase-linked receptors, nuclear receptors

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21
Q

what is a ligand-gated ion channel?

A

located at the plasma membrane, targeted by hydrophilic signalling molecules, action of a millisecond time scale. consists of separate glycoprotein subunits that form a central, ion conducting channel, allow very rapid change in the permeability of the membrane to certain ions and alter membrane potential

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22
Q

what is a G-coupled receptor?

A

located in the plasma membrane, targeted by hydrophilic signalling molecules, signal on a time scale of seconds. many are linked to a cell-membrane-located effector by intermediary G proteins, ion channel effectors cause changes in membrane electrical properties

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23
Q

what is a kinase-linked receptor?

A

located in the plasma membrane, targeted mainly by hydrophilic protein mediators, work of a time scale of hours

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24
Q

what is a nuclear receptor?

A

located intracellularly in the nucleus (or cytoplasm), targeted mainly by hydrophobic signalling molecules, act to alter gene expression in cells, on an hour/day time scale

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25
what are ion channels?
transmembrane pores formed by glycoproteins that span the membrane to create as ion conduction pathway for selected ions, usually regulated by signals that cause the channel to cycle reversibly between a closed (non-conducting) state and open (conducting conformation
26
what are ion channels gated by?
chemical signals and physical stimuli (including thermal and mechanical energy)
27
how is a ligand gated ion channel activated?
agonist binds causing a rapid conformational change, channel opens permitting a conduction pathway for selected ion, ions flow down their electrochemical gradient
28
what is the basic structure of a G protein? (receptor)
integral membrane protein, single polypeptide with extracellular NH2 and intracellular COOH termini, contains seven transmembrane alpha-helical spans joined by 3 extracellular and 3 intracellular connecting loops
29
what is the basic structure of G protein? (guanine nucleotide binding protein)
peripheral membrane protein, consists of 3 polypeptide subunits (alpha, beta gamma), contains guanine nucleotide binding site on the alpha subunit that and hold GTP or GDP
30
how are G proteins activated?
agonist binds to the GPCR to which they preferentially couple, in the inactive state the guanine nucleotide binding site if the alpha subunit is occupied by GDP, in the active state the guanine nucleotide binding site of the alpha subunit is occupied by GTP and the alpha and beta gamma subunits dissociate from each other
31
how are G protein-coupled receptors activated?
by agonist which causes a conformation change that is transmitted to the G protein alpha subunit which: releases GDP and allows GTP is bind in its place, separated from the receptor and beta gamma- dimer (subunit dissociation) generated a free GTP-bound alpha subunit and beta gamma dimer
32
how do G protein-coupled receptors work?
no signalling - the receptor is unoccupied, G protein alpha unit bind GDP, the effector is not modulated Turing on the signal - agonist activated receptor, G protein couples with receptor, GDP dissociate from, and GTP binds to, the alpha subunit G protein dissociated into separate alpha and beta gamma subunits, G protein alpha subunit combines with and modifies activity of effector turning off the signal - the alpha subunit acts as an enzyme to hydrolyse GTP to GDP and Pi. the signal is turned off, GTP does not dissociate. the G protein alpha subunit recombines with the beta gamma subunit
33
how do nuclear receptors work?
they are ligand-gated transcription factors. steroid hormones are lipophilic molecules - enter cells by diffusion across the plasma membrane, within the cell, they combine with an intracellular receptor producing dissociation of inhibitory HSP proteins. in the case of the steroid receptors, the inactive receptor is located in the cytoplasm. the receptor steroid complex moves to the nucleus, forms a dimer and binds to hormone response elements in DNA . the transcription of specific genes is either switched on or switched off to alter mRNA level and the rate of synthesis of mediator proteins
34
what is elimination?
frug and/or metabolites excreted in urine, faeces or bile
35
what are the principle organs of drug elimination?
kidneys, drug elimination is mostly accomplished by renal filtration of blood plasma, water and most electrolytes are reabsorbed into blood circulation in the renal tubes
36
what is clearance?
elimination - CL is the volume of blood removed of drug per unit of time. helps determine the dosage rate needed to maintain desired plasma
37
what is the equation of CL?
CL= rate of drug elimination / drug plasma
38
what is first order kinetics?
rate of drug elimination increases as plasma drug concentration increases
39
what is V max?
maximal elimination rate
40
what is steady state?
exists when the rate of drug administration = rate of drug elimination
41
what does the elimination half life depend on?
the volume of distribution and clearance
42
what does elimination half life determine?
the time required for drug plasma to achieve drug plasma steady state
43
how many half lives are usually required to reach steady state?
five
44
what happens to the elimination half life if CL increases?
elimination half life decreases
45
what happens to the elimination half life is the volume distribution increases?
the elimination half life increases
46
which is the most important, drug-metabolising organ?
liver
47
where do the two drug metabolism phases occur?
liver
48
how is hepatic drug work?
metabolising enzymes are embedded in the smooth endoplasmic reticulum of the liver hepattocytes
49
which molecules cross the plasma membrane more readily - non-polar or polar?
non-polar
50
what happens in phase I of metabolism?
change in the drug by oxidation, reduction or hydrolysis, oxidation accomplished by cytochrome P450 enzymes, during oxidation the drug molecules incorporate one atom of oxygen to the drug to form a hydroxyl group. cytoplasmic enzymes can metabolise the drug, hydrolytic reaction, usually form chemically reactive metabolites
51
what are cytochrome P459 enzymes?
ahem proteins which comprise of a large super family, P450 activity is genetically determined
52
what does the drug oxidation by the monooxygenase P450 system require?
drug, the P450 enzyme, molecular oxygen, NADPH and flavoprotein
53
what happens in phase II of metabolism?
involves the combination of the drug with one of several polar molecules to form a water-soluble metabolite conjugation usually involve the reactive group produced by phase I, usually determines all biological activity, conjugated produces can be readily excreted via the kidney
54
how do drugs. one around the body?
bulk flow (via the circulatory system) diffusion of drug molecules over short distances, solubility (large drugs move more slowly than small ones)
55
how do small molecules cross cell membranes?
passive diffusion, facilitated diffusion, active transport, endocytosis
56
what is endocytosis?
the drug is encased in as small vesicle then released inside the cell
57
what are the principle sites of carrier mediated drug transport?
both facilitated by diffusion and active transport, blood brain barrier, GI tract, placenta, renal tube, biliary tube
58
what does the proportion of ionisation of a drug depend upon?
the pKa of the drug and the local pH
59
where do weak acids and bases accumulate in drug absorption?
bases - compartments with low pH | acids - compartments with high pH
60
where does most oral route drug absorption occur?
in the small intestine due to the large surface area
61
what is the apparent volume distribution?
describes the extent to which drug partitions between the plasma and tissue compartments
62
what is the most abundant plasma protein?
albumin
63
what does plasma protein binding reduce?
the availability of the drug from diffusion to the drug target organs, may also reduce the transport of the drug to non-vascular compartments
64
what is depolarisation?
the membrane potential becomes less negative or even positive
65
what is hyperpolarisation?
the membrane potential becomes more negative
66
what does influx and efflux mean?
influx - into the cell | efflux - out of the cell
67
which direction does Na+ flow?
inwards because the concentration gradient is inwards and the electrical gradient is inwards, negative equilibrium potential
68
which direction does K+ flow?
outwards because the concentration gradient is outward and has an energy that exceeds that of the inward electrical gradient
69
which ion channel is responsible for the action potential in neutrons ?
voltage gated ion channels Na+ depolarising K+ hyperpolarising
70
what are the propertied of the action potential neutrons?
brief electrical signals in which the polarity of the nerve cell membrane is momentarily reversed, action potentials propagate along nerve cell axons which constant magnitude and velocity allowing signalling over long distances
71
why do Na+ channels initially open?
in response to depolarisation
72
what is required for the channel to enter closed state?
repolarisation, inactivation contributes to the repolarising phase of the action potential and is responsible for the refractory period
73
what do action potentials allow?
electrical signals to be conducted over large distances without decaying
74
what is passive conduction?
a factor in the propagation of the action potential, less leaky the axon the greater the local current spread, increases action potential conduction velocity
75
how do you increase passive current and thus action potential velocity?
increase axon diameter (increase current spread), decrease leak of current across the axon (possible by adding myelin by Schwann or oligodendrocytes) saltatory conduction in the myelinated axons - action potential jumps from one node of ranvier to the next
76
what transmitter of the preganglionic neurones is always used?
acetylcholine acting via excitatory nicotinic cholinoreceptors
77
what opens ligand-gated ion channels in the postganglionic neurone?
ACh causing depolarisation and the initiation of the action potentials that propagate to the presynaptic terminal of the neurone, triggering Ca2+ entry and the release of noradrenaline
78
where does noradrenaline activate G-protein coupled adrenoceptors?
in the effector cell membrane to cause cellular response via ion channels/enzymes
79
what does the motor component comprise of?
cholinergic preganglionic neurones with a sympathetic thoracolumbar origin, or a parasympathetic craniosacral origin
80
what do adrenergic fibres release?
NA as a transmitter that activates adrenoceptors, all of which (alpha and beta) are G-protein-coupled receptors
81
what are examples of co-transmitters and what do they regulate?
ATP, NYP, NO and VIP | they also regulate the activity of target organs
82
what do nicotinic acetylcholine (ACh) receptors consist of?
five glycoprotein subunits that form a central, cation conducting (Na+, K+ and Ca2+) channel
83
how can a blockade be achieved for transmissions at ganglia?
depolarisation block by high concentrations of agonists, competitive antagonism, non-competitive antagonism all ganglionic transmission is blocked by hexamethonium
84
what do presynaptic auto receptors mediate?
negative feedback inhibition of transmitter release. agonists decrease release, antagonists increase release

Principles - Kate (10 decks)

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