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Principles > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Define pharmacodynamics?

A
  • what the drug does to the body
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2
Q

Define pharmacokinetics?

A
  • what the body dooes to the drug
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3
Q

What is a drug?

A
  • any substance that can be used in the treatment, diagnosis and prevention of disease
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4
Q

What does selectivity mean?

A
  • the ability of a drug to distinguish between different molecular targets
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5
Q

What are receptors?

A
  • protein macromolecules
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6
Q

What is an agonist?

A
  • binds to a receptor to produce a cellular response
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7
Q

What is an antagonist?

A
  • binds to a receptor to block the effect of an agonist
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8
Q

Define affinity?

A
  • the strength of association between a ligand and its receptor
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9
Q

Define efficacy?

A
  • the ability of an agonist to evoke a cellular response
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10
Q

Antagonists ____ affinity and _____efficacy

A
  • possess

- lack

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11
Q

Agonists _____ affinity and _____ efficacy

A
  • possess

- possess

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12
Q

What is EC50?

A
  • the concentration of agonist required to produce a half maximal effect
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13
Q

What relationship is the graph between agonist concentration and effect when agonist conc is in log?

A
  • sigmoidal relationship
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14
Q

How can competitive antagonism be overcome?

A
  • increasing the concentration of agonist
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15
Q

What effect does competitive antagonism have on the graph?

A
  • parallel shift to the right
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16
Q

What effect does non-competitve antagonism have on the graph?

A
  • depression in the slope

- no parallel shift

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17
Q

What are receptors?

A
  • protein macromolecules

- sensing elements

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18
Q

What are autocrine signals?

A
  • the same cell that produces a signal responds to its own signal
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19
Q

What are paracrine signals?

A
  • signalling over a short distance, doesnt require the signalling molecule to enter the circulatory system
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20
Q

What are endocrine signals?

A
  • signalling over a larger distance, requires the signalling molecule to enter the blood stream
  • much slower
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21
Q

Where are ligand gated ion channels located? what signalling molecule binds to them? and are they fast or slow?

A
  • located in plasma membrane
  • hydrophillic signals
  • fast signalling
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22
Q

Where are GPCRs located? what signalling molceule binds? are they fast or slow?

A
  • located in plasma membrane
  • hydrophillic signals
  • slow signaling
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23
Q

Where are kinase linked receptors located? what signalling molecule binds? are they fast or slow?

A
  • plasma membrane
  • hydrophillic
  • work on a hours time scale
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24
Q

where are nuclear recpetors located? what signalling molecule binds to them? are they fast or slow?

A
  • cytoplasm or nucleus
  • hydrophobic
  • very slow
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25
Q

How might ion channels be gated?

A
  • ligand gated
  • voltage gated
  • physical stimuli gated
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26
Q

Example of a ligand gated ion channel?

A
  • nicotinic acetylcholine receptor
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27
Q

Explain how a GPCR works?

A
  • GPCR on plasma membrane, agonist binds, causes a confirmational change
  • G protein bound to GDP –> GDP dissociates to GTP and beta and gamma subunit dissociate
  • a bound to GTP can act as an modulator
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28
Q

How is the G protein made inactive?

A
  • a subunit bound to GTP acts as an enzyme to hydrolyse GTP–> GDP + Pi
  • this then makes it go to inactive form
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29
Q

Example of a kinase receptor?

A
  • insulin
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30
Q

How do kinase receptors work?

A
  • autophosphorylation
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31
Q

What are nuclear receptors?

A
  • transcription factors

- responsible for sensing steroid and thyroid hormones

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32
Q

3 Main ways of drug movement?

A
  • bulk flow
  • diffusion
  • soubility
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33
Q

Explain passive diffusion

A
  • no transporter needed, drug simply passes through lipid membrane
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34
Q

Explain facilitated diffusion

A
  • transporter needed
  • no energy required
  • down concentration gradient
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35
Q

Explain active transport

A
  • transporter needed
  • energy required
  • against concentration gradient
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36
Q

Explain endocytosis

A
  • invagination of drug, and released into a cell
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37
Q

Definition of pKa

A
  • pH at which 50% of drug is ionised and 50% unionised
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38
Q

How do u calculate pKa for an acid?

A

pKa= pH + log (AH/A-)

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39
Q

Weak acids accumulate in areas of ____ pH

A
  • high
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40
Q

Weak bases accumulate in areas of _____ pH

A
  • low
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41
Q

Weak acids are absorbed in areas of _____ pH

A
  • low
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42
Q

Weak bases are absorbed in areas of ___ pH

A
  • high
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43
Q

What is the apparent volume of distribution?

A
  • the extent to which a drug partions between the plasma and the tissue
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44
Q

How do you calculate apparent volume of distribution?

A

Vd= Dose/ [Drug] plasma

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45
Q

Low Vd suggests_____

A

high drug plasma concentration

high plasma protein

46
Q

High Vd suggests____

A

low drug plasma concentration

low plasma protein binding

47
Q

Main protein associated with plasma protein binding?

A
  • albumin
48
Q

Define drug metabolism

A
  • enzymatic conversion of the drug to another chemical enitity
49
Q

What organ is the main organ involved in the metabolism of drugs?

A

-liver

50
Q

hepatic drug metabolising enzymes are located in the _____________ of the liver hepatocytes

A

smooth endoplasmic reticulum

51
Q

non-polar drugs pass through the plasma membrane more easily to be metabolised.
true/false

A

true

52
Q

Explain what occurs during phase 1 metabolsim

A
  • oxidation, hydrolysis or reduction
  • oxidation - cytochrome p450
  • addition of a hydroxyl group
  • makes the drug more polar
  • RHS of liver
53
Q

What is cytochrome p450?

A
  • envymes that are haem proteins

- oxidises drugs during phase 1 metabolism

54
Q

Explain what occurs during phase 2 metabolism?

A
  • conjugation
  • combination of the drug with polar molecules to form a water soluble metabolite
  • terminates all biological activity
  • LHS of liver
  • can therefore be excreted in the kidneys
55
Q

Define excretion

A
  • dug/drug metabolites excreted in urine, faces or bile
56
Q

What is the principal organ involved in excretion?

A
  • kidneys
57
Q

What occurs at the kidney tubules?

A
  • water and most electrolytes reabsorbed into the blood stream
  • drug metabolised rendered polar by phase II metabolism aren’t re absorbed and are excreted in the urine
58
Q

What does Cmax mean?

A
  • maximum drug plasma concentration
59
Q

What does Tmax mean?

A
  • the time at which Cmax occurs

Cmax = the maximum drug plasma conc

60
Q

clearance is a ______ parameter

A
  • flow parameter
61
Q

What is the equation for drug clearance (CL)

A

CL = rate of elimination/[drug] plasma

62
Q

Explain Vmax on a elimination drug graph

A
  • saturation of elimination mechanisms

- maximum drug elminimation

63
Q

what does first order kinetics refer to in drug elimination

A
  • drug elimination increases as drug plasma conc increases
64
Q

What does Km mean?

A
  • drug plasma conc at which it is 1/2 Vmax
65
Q

Equaion for elimination half-life

A

t1/2 = 0.693 x vd / cl

66
Q

factors that effect Vd

A
  • ageing
  • obesity
  • pathological fluid
67
Q

factors that effect Cl

A
  • cytochrome p450
  • renal failure
  • cardiac failure
68
Q

MEC meaning?

A
  • minimum effective concentration
69
Q

MTC meaning?

A
  • maximum therapeutic cncentration
70
Q

Therapeutic ration?

A

TR = MTC/MEC

71
Q

The higher the therapeutic ratio the _______ the drug

A
  • safer
72
Q

Rate of elimination =

wash out

A

= clearance x plasma conc

73
Q

How many half-lifes are normally required in a wash out of infusions?

A
  • 5 half lifes
74
Q

Why would u give a leading dose?

A
  • starting with a higher dosage and then decreasing

- employed to decrease the time taken to reach a steady state

75
Q

Define depolarisation

A

membrane potential becomes less negative

76
Q

Define hyperpolarisation

A

membrane potential becomes more negative

77
Q

Na+ naturaly flows __________

A

inwardly

78
Q

Ena is around_______mV

A

+60mV

79
Q

K+ naturally flows_________

A

outwardly

80
Q

Ek is around _________mV

A

-100mV

81
Q

When ion channels are closed what happens?

A
  • no influx or outflux of ions
82
Q

what is resposible for the upstroke on a neuron action potenital?

A
  • opening on Na+ channels
83
Q

What is responsible for the downstroke on a neuron action potential?

A
  • opening of K+ channels
84
Q

What causes the upstroke of a neuron action potential?

A
  • delayed closure of K+ channels
85
Q

Na+ responds______

radiply/slowly?

A
  • rapidly
86
Q

Na+ is a self_________ channel

A

self-reinforcing

+ve feedback

87
Q

K+ is a self__________channel

A

self-limiting

-ve feedback

88
Q

Name the 3 states of Na+ channels and how the get to each state

A
  • closed state
  • (depolarisation) open state
  • (maintained depolarisation) inactive state
  • recquires repolarisation to closed state again
89
Q

The inactive state of a Na+ channel is responsible for what?

A
  • the refractory peroid
90
Q

Define absolute refractory peroid?

A
  • no stimulus no matter how strong will not elicit a 2nd action potential
91
Q

Define relative refractory peroid?

A
  • a stronger than normal stimulus may elicit a 2nd action potenital
92
Q

Nerve cells may be described as ______ which means the action potenital will ________ far from origin

A
  • leaky

- wont spread far

93
Q

How might the spread of an action poteintial in a nerve cell be improved?

A
  • increase diameter of axon

- insulate (myelin)

94
Q

How do myelinated axons spread action potentials?

A
  • saltatory conduction

- “jump” from raniver

95
Q

ANS is made up of ________ neurons

efferent or afferent?

A
  • efferont neurons
96
Q

What does the ANS regulate?

A
  • regulates functions that do not require conscious effort
97
Q

Explain the length of axons in sympathetic and parasympathetic neurons

A
  • sympathetic (short, long)

- parasympathetic (long, short)

98
Q

Explain how action poteintials are spread

A
  • action potential arrives
  • increase in Ca2+ into cell
  • causes release of Ach
  • Ach binds to postganglionic receptors
  • causes increase in Ca2+
  • increase in Ach (parasympathetic) or NA (sympathetic)
99
Q

In sympathetic neurons NA binds to what type of GPCR?

A
  • Adrenoceptor
100
Q

In parasympathetic neurons Ach binds to what type of GPC?

A
  • Muscarinic
101
Q

What is a nicotinic receptor

A
  • 5 glycoprotein subunits

- central channel (Na+, K-, Ca2+)

102
Q

What can reverisbly block a nicotinic receptor?

A
  • hexamethonium
103
Q

Parasympathetic effects what muscarinics?

A
  • M1 –> Gq
  • M2 –> Gi
  • M3 –> Gq
104
Q

M1 –> Gq causes?

A
  • increased acid secretion
105
Q

M2 –> Gi causes?

A
  • decreased heart rated
106
Q

M3 –> Gq causes?

A
  • increased secretion

- resp constriction of smooth muscle

107
Q

Sympathetic effects what receptors?

A
  • a1 –> Gq
  • a2 –> Gi
  • b 1 –> Gs
  • b2 –> Gs
108
Q

a1 –> Gq causes?

A
  • increased vascular contracility
109
Q

a2 –> Gi causes?

A
  • inhibition of NA release
110
Q

b1 –> Gs causes?

A
  • increased Heart rate
111
Q

b2 –> Gs causes?

A
  • resp relaxation of smooth muscle

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