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pharmacology Flashcards

1
Q

Define pharmacodynamics

A

What a drug does to the body

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2
Q

Define pharmacokinetics

A

what the body does to a drug

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3
Q

What is a receptor?

A

Protein macromolecules

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4
Q

What is an agonist?

A

drug that binds to a receptor to produce a cellular response

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5
Q

define affinity

A

strength of association between ligand and receptor

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6
Q

Define efficacy

A

ability of an agonist to evoke a cellular response

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7
Q

What is an antagonist?

A

drug that blocks the effects of an agonist - has affinity but no efficacy

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8
Q

What is competitive antagonism?

A

binding of an agonist and antagonist occur at same (orthosteric) site and is thus competitive

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9
Q

What does competitive antagonism do to the potency and efficacy graph?

A

parallel rightward shift of agonist concentration response curve with no depression in maximal response(efficacy)

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10
Q

What is non competitive antagonism?

A

agonist binds to normal site but antagonist binds to a separate (allosteric site)

can occur simultaneously but cant be activated if antagonist is bound

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11
Q

How does a non competitive antagonist effect the graph?

A

depress slope and maximum curve response, does not cause rightward shift

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12
Q

Potency

A

the amount of drug required to permit a cellular response

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13
Q

Define absorption

A

process by which a drug enters the body from its site of administration

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14
Q

distribution

A

process by which drug leaves circulation and enters the tissues perfused by blood

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15
Q

How is a drug more readily excreted by the body?

A

tissue enzymes catalyse chemical conversion of a drug to a more polar form that is more readily excreted by the body

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16
Q

What are some factors that control drug absorption?

A

solubility - must dissolve
chemical stability - some drugs are destroyed by acid
lipid to water partition coefficient - rate of diffusion of drug increases with lipid solubility
degree of ionisation - only unionised forms can diffuse across lipid bilayer

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17
Q

What does the degree of ionisation depend on?

A

pKa of the drug and local pH

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18
Q

What is the pKa?

A

pH at which 50% of the drug is ionised and 50% isnt

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19
Q

What equation is used to determine how active a drug will be in the body?

What happens when Ka is large?

A

henderson-hasselbalch (pH - pKa = log(A-/AH) = acid

is Ka is large then it is a strong acid

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20
Q

What are some routes of administration?

A

Enteral - oral, sublingual and rectal

paraenteral - IV, intramuscular etc

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21
Q

What is the volume of distribution?

A

Apparent volume in which a drug is dissolved

IV - Vd = dose/ plasma

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22
Q

What does MEC stand for

A

Minimum effective concentration

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23
Q

What does MTC stand for?

A

maximum tolerated concentration

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24
Q

What is the therapeutic ratio

A

MTC/MEC - the higher the TR the safer the drug

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25
Q

What is first order kinetics?

A

Rate of elimination is directly proportional to drug concentration
plasma concentration falls exponentially
half-life is inversely proportional to elimination rate constant

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26
Q

What is clearance?

A

The volume of plasma cleared of drug in unit time

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27
Q

What does the rate of elimination equal?

A

clearance x plasma concentration

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28
Q

What does a constant plasma steady state equal?

A

maintenance dose rate/ clearance

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29
Q

when is a constant steady state reached?

A

after approximately five half lives

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30
Q

What is volume of distribution?

A

volume into which a drug appears to be distributed with a concentration equal to that of plasma

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31
Q

What is loading dose?

A

initial higher dose of drug before stepping down to maintenance dose

employed to decrease time to steady state for drugs with long half-life

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32
Q

what is half life?

A

time for concentration of drug in plasma to half

dependant upon Vd and Cl

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33
Q

What is zero order kinetics?

A

initially eliminated at a constant rate, then return to first first order kinetics

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34
Q

What affects drug distribution?

A

ADME - absorption, distribution, metabolism, excretion

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35
Q

What are the two phases of drug metabolism?

A

1st phase - RHS of the liver - oxidation, reduction and hydrolysis
makes drugs more polar, adds a chemically reactive group permitting conjugation

2nd phase - LHS of liver
conjugation, adds an endogenous compound increasing polarity

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36
Q

What are drugs converted to to facilitate excretion

A

more polar metabolites that are not readily absorbed iin renal tubules

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37
Q

WHat are the three basic processes of reanl excretion fo drugs?

A

glomerular filtration
active tubular secretion
passive reabsorption across tubular epithelium

38
Q

Define depolarization

A

the membrane potential becomes less negative (positive)

39
Q

Define hyperpolarization

A

membrane potential becomes more negative

40
Q

What are some characteristics of sodium channels?

A

Na flows inwardly
140mM outside of cell
negative driving force = inward movement of sodium

41
Q

Potassium channels?

A

K moves outwardly

when positive - outward movement of potassium

42
Q

What are some characteristics of ion channels?

A

Protein complexes spanning lipid bilayer, central pathway to allow rapid flow of selected ions

43
Q

How are voltage activated Na and K channels activated?

A

membrane depolarisation - sodium channels rapidly but potassium channels with a slight delay

opening of a few sodium channels causes causes further depolarisation ( positive feedback - upstroke of graph)

44
Q

How do potassium channels work?

A

Self-limiting, outward movement of K causes repolarisation which turns off the stimulus ( negative feedback)

45
Q

Where is there an undershoot on the graph when (potassium channels)

A

Delayed closure of potassium channels

46
Q

What are some characteristics of closed state channels? (depolarisation to open)

Open state (maintained depolarisation to closed)?

Inactivated state? (repolarized to closed)

A

Activation gate close, inactivation gate open - non(conducting)

Activation gate open, inactivation gate open
CONDUCTING

Activation gate open, inactivation gate closed
non-conducting

47
Q

What is absolute refractory period?

A

no stimulus can elicit a second action potential

all Na channels are closed

48
Q

What is relative refractory period?

A

Stronger than normal stimulus may elicit a second action potential

possive conduction is a factor in the propagation of the action potential - longer the length constant - greater the local spread (increases AP velocity)

49
Q

What are oligodendrocytes?q

A

Produce myelinated cells in CNS (Schwann cells do it in PNS)

50
Q

Astrocytes?

A

star shaped - support homeostasis and maintain BBB

51
Q

Microglia?

A

Immune surveillance - macrophage of the CNS

52
Q

What are the functions of the ANS

A
  • Carries output from the CNS to the whole of the body other than skeletal muscle
  • Regulates visceral functions that are largely involuntary
  • Subdivided into sympathetic and parasympathetic divisions
53
Q

What do sympathetic nerves do?

A
  • Coordinates the body’s response to stress, associated with fight, flight and fright reactions
  • Preganglionic neurones always ACh
  • Post ganglionic neurone usually noradrenaline
  • Thoraco-Lumbar outflow (T1-L2)
  • Increases HR and force of contraction
  • Relaxes bronchi, decreases mucus production
  • Reduces GI motility and constricts sphincters
  • Vasoconstriction but relaxation in skeletal muscle
  • Release of adrenaline from adrenal gland
  • Ejaculation
54
Q

What do parasymapthetic nerves do?

A
  • Coordinates the body’s basic homeostatic functions
  • Preganglionic and post ganglionic neurones ACh
  • Cranial Nerves 3/7/9/10
  • Decreases HR
  • Bronchoconstriction, stimulates mucus production
  • Increases GI motility and relaxes sphincters
  • No effect on blood vessels or adrenal glands
  • Erection
55
Q

How are neurochemicals transported in the body?

A
  • Precursor taken up
  • Transmitter synthesised and stored
  • Action potential depolarises
  • Calcium influx through voltage-activated channels
  • Calcium induced release of transmitter
  • Receptor activation
  • Enzyme-mediated inactivation of transmitter or reuptake of transmitter
56
Q

How are sympathetic chemicals transmitted in the body?

A
  • Sympathetic
    o Action potential from CNS
    o Travels to presynaptic terminal of preganglionic neurone triggering Calcium entry and release ACh
    o ACh opens ligand-gated ion channels in the postganglionic neurone
     Causes depolarisation and generation of action potentials that travel to presynaptic terminal of the neurone, triggering calcium entry and release, usually of noradrenaline
    o Noradrenaline activates G protein coupled receptors - adrenoceptors
57
Q

How are parasympathetic signals transferred?

A
  • Parasympathetic
    o Pretty much the same as sympathetic BUT
    o ACh always the transmitter used by postganglionic neurones
    o ACh activates G protein coupled muscarinic acetylcholine receptors in target cell membrane
58
Q

Ligand gates ion channels ?

A
  • Consist of separate glycoprotein subunits forming a central, ion conducting channel
  • Allow rapid changes in the permeability of membrane to certain ions
  • Rapidly alter membrane potential
59
Q

G-protein Coupled Receptors – Muscarinic ACh receptors ?

A
  • Receptor, G-protein and effector are separate proteins
  • G protein couples receptor activation to effector modulation
  • Signalling slow in comparison to transmitter-gated ion channels
60
Q

Structure of G protein Coupled Receptors ?

A
  • Receptor
    o Integral membrane protein
    o 7 transmembrane spans joined by 3 extra cellular and 3 intracellular connecting loops
  • G-protein
    o Peripheral membrane protein
    o 3 polypeptide subunits (alpha = binding site)
    o Contains guanine nucleotide binding site which can hold GTP
61
Q

How do G-protein coupled receptors work? (no signalling, turning on signal and turning off signalling)

A
  • No signalling
    o Receptor unoccupied
    o G protein binds GDP
    o Effector not modulated
  • Turning on the signal
    o Agonist activates receptor
    o G protein couples with receptor
    o GDP dissociates from and GTP binds to alpha subunit
    o G protein dissociates
    o Alpha subunit combines with and modifies activity of effector
    o Agonist may dissociate from the receptor, but signalling persists
  • Turning off the signal
    o Alpha subunit acts as an enzyme to hydrolyse GTP  GDP
    o G protein alpha subunit recombines with the By subunit completing G protein cycle
62
Q

Nicotinic Acetlycholine Receptors (Ligand-gated)?

A
  • Consist of 5 glycoprotein subunits forming a central, cation conducting, channel
  • Diverse range of subunits
  • Alpha 1-10, beta 1-4, gamma, delta, epsilon
  • Binding of transmitter opens gate
63
Q

Cholinergic Transmission

A
  • Uptake of choline
  • Synthesis of ACh
  • Storage of ACh
  • Depolarisation by action potential
  • Calcium influx through voltage-activated calcium channels
  • Calcium induced release of ACh – exocytosis
  • Activation of ACh receptors causing cellular response
  • Degradation of ACh to choline and acetate by AChE which terminates transmissions
  • Reuptake and reuse of choline
  • Nicotine acts as an agonist – mimics the action of ACh
64
Q

Cholinergic Transmission at Parasympathetic Neuroeffector Junctions

A
  • Synthesis and storage of ACh
  • Depolarisation by action potential
  • Calcium influx through voltage-activated calcium channels
  • Calcium induced release of ACh
  • Activation of muscarinic ACh receptor subtypes (M1-M3) causing cellular response
  • Degradation of ACh to choline and acetate by AChE – terminates transmission
  • Reuptake and reuse of choline
65
Q

What is the process of M1 receptors?

A

Gq – stimulates phospholipase C – increased stomach acid secretion

66
Q

M2 receptors?

A

Gi – inhibition of adenylyl cyclase, opening of K+ channels – deacreased HR

67
Q

M3 receptos?

A

Gq – stimulates phospholipase C – increased saliva secretion and bronchoconstriction

68
Q

Noradrenergic Transmission at Sympathetic Neuroeffector Junctions

A
  • NA synthesis and storage
  • Depolarisation by action potential
  • Calcium influx through voltage activated calcium channels
  • Calcium induced release of NA
  • Activation of adrenoceptor subtypes causing cellular response
  • Reuptake of NA by transporters U1/U2
  • Metabolism of NA by MAO and COMT
69
Q

What do Beta 1 receptors do?

A
  • B1 – Gs – stimulation of adenylyl cyclase – Increased HR and force
70
Q

What do beta 2 receptors do

A
  • B2 – Gs – stimulation of adenylyl cyclase – Relaxation of bronchial and vascular smooth muscle
71
Q

What do alpha 1 receptors do

A
  • A1 – Gq – stimulation of phospholipase C – contraction of vascular smooth muscle
72
Q

What do alpha 2 receptors do?

A
  • A2 – Gi – inhibition of adenylyl cyclase – inhibition of NA release
73
Q

Amphetamine?

A
  • U1 substrate
  • Inhibits MAO
  • Displaces NA into cytoplasm
  • NA accumulates in synaptic cleft causing increased adrenoceptor stimulation
74
Q

Prazosin?

A
  • Selective, competitive antagonist of a1

- Vasodilator used as anti-hypertensive

75
Q

Atenolol

A
  • Selective, competitive antagonist of B1

- Used as an anti-anginal and anti-hypertensive agent

76
Q

Atropine?

A
  • Competitive antagonist of Muscarinic ACh receptors, does not block nicotinic ACh receptors
  • Blocks parasympathetic division of ANS
  • Used to reverse bradycardia post MI and in AChE poisoning
77
Q

Which neurotransmitter acts on muscarinic receptors and what is its action in
the airways?

A

Acetylcholine, constriction of the airways

Muscarinic receptors in airway smooth muscle
cause constriction when activated.

78
Q

In gastric parietal cells, which secretagogue acts on the M3 receptor?

A

Acetylcholine acts on M3 muscarinic receptors.

79
Q

What does gastrin bind to?

A

Gastrin binds to G/CCK2 receptors,

80
Q

What does histamine bind to?

A

histamine acts via H2 receptors

81
Q

What is ghrelin?

A

is the “hunger hormone”

82
Q

How does a steroid hormone work?

A

Binding to an intracellular receptor that then activates gene expression in the nucleus

83
Q

What substance directly stimulates protein kinase A?

A

Cyclic AMP

84
Q

What is the primary target of a statin?

A

liver cells - hepatocytes

85
Q

What do ligand gated ion channels conduct more quickly ?

A

Conduct ions more quickly compared to carrier molecules

86
Q

How is signalling terminated in the G protein cycle?

A

hydrolysis of GTP to GDP at the alpha subunit

87
Q

What is the mechanism of action of glyceryl trinitrate?

A

Arginine is converted into a neurotransmitter that activates guanylate cyclase

88
Q

How does hypotension in sepsis occur?

A

vasoactive mediators that are released to maintain tissue oxygenation - nitric oxide released by activated endothelium is one of the central mediators

89
Q

What oncogene is tested for in breast cancer?

A

HER2

90
Q

What is obesity a risk factor for?

A

Cancer

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