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Pharmacology Flashcards

1
Q

What is pharmacodynamics?

A

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

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2
Q

What is pharmacokinetics?

A

what the body does to a drug so the absorption, distribution, metabolism and excretion

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3
Q

What is an agonist?

A

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

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4
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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5
Q

What is affinity?

A

the strength of the association between a ligand and a receptor which is covered by binding and unbinding rate (latter is more significant) and chemical bonds between the ligand and receptor

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6
Q

What is efficacy?

A

the ability of an agonist to evoke a cellular response

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7
Q

Do antagonists have affinity or efficacy?

A

affinity but not efficacy as they don’t activate receptors

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8
Q

What is the relationship between receptor occupancy and agonist concentration?

A

hyperbolic

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9
Q

What is EC50 equal to?

A

the concentration of agonist that elicits a half maximal response

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10
Q

What happens to the receptor occupancy against agonist concentration graph if you make it semi-logarithmic?

A

it will be sigmoidal shape which is easier to use to calculate EC50

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11
Q

What does a lower or higher EC50 say about the potency of an agonist?

A

lower EC50 is more potent

higher EC50 is less potent

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12
Q

What does a higher maximal response say about the efficacy of an agonist?

A
  • higher percentage maximum response is more efficacy so a full agonist
  • lower percentage maximum response is lead efficacy so a partial agonist
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13
Q

What does equipotent mean?

A

the two drugs have equal potency but not necessarily efficacy so same horizontal reach along the graph

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14
Q

What is reversible competitive antagonism and what is it overcome by?

A

competition for the same arthosteric site and can be overcome by increasing agonist concentration

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15
Q

What is non-competitive antagonism?

A

binds to allosteric site and activation can’t occur when antagonist is bound

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16
Q

What does a competitive antagonist do to the sigmoidal graph?

A

rightward shift but no change in the maximum reached

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17
Q

What does a non-competitive antagonist do to the sigmoidal graph?

A

causes a depression of the slope but no sideways shift

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18
Q

What does an increasing concentration of antagonist do to the change in the graph?

A
  • increased concentration of competitive gives a greater rightward shift
  • increased concentration of non-competitive gives a greater depression
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19
Q

What are receptors the targets of?

A

neurotransmitters
hormones
other mediators and therapeutic agents

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20
Q

What do autocrine, paracrine and endocrine cells signal to?

A
  • autocrine signal to itself
  • paracrine signal to close neighbours
  • endocrine signal over long distances using the blood
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21
Q

What are the four types of receptors?

A
  • Type 1: ligand-gated ion channels/ inotropic
  • Type 2: G protein-coupled receptors/ metabotropic
  • Type 3: kinase-linked receptors/ enzyme-linked
  • Type 4: nuclear receptors
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22
Q

What are the features of type 1 receptors?

A
  • ligand-gated
  • ionotropic
  • on plasma membrane
  • react quickly to hydrophilic signalling molecules
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23
Q

What are the features of type 2 receptors?

A
  • G protein-coupled receptors
  • metabotopic
  • on plasma membrane
  • react slowish to hydrophilic signalling molecules
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24
Q

What are the features of type 3 receptors?

A
  • kinase-linked receptors
  • enzyme-linked
  • on plasma membrane
  • slow reactions to hydrophilic protein mediators
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25
Q

What are the features of type 4 receptors?

A
  • nuclear receptors
  • intracellular
  • targeted by hydrophobic signalling molecules
  • very slow reactions
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26
Q

What are ion channels regulated by?

A

signals that cause channel to alternate between conducting and non-conducting states

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27
Q

What can ion channels be gated by?

A
  • chemical signals
  • transmembrane voltage
  • physical stimuli
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28
Q

What is the main example of a ligand-gated ion channel?

A
  • ACh receptor
  • five subunits making a channel and rapid changes
  • agonist binds, channel opens and ions flow down a gradient
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29
Q

How does signalling via a second messenger work?

A

eg GPCRs

  • enzyme effectors increase or decrease the rate of synthesis of second messenger
  • ion channel effectors cause changes in membrane electrical properties
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30
Q

What are GPCRs made up of?

A
  • Receptor: integral membrane protein, 7 transmembrane spans, two together make a dimer
  • G-protein: peripheral membrane protein, 3 polypeptide subunits, binding site holds GTP or GDP
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31
Q

How does GPCR activation occur?

A
  • GDP is in binding site of alpha subunit in the inactive state
  • activated by agonist binding to GPCR to which they couple
  • alpha and gamma are covalently bound by lipid and beta is paired to gamma
  • alpha contains GTPase with Raw and AH (to clamp nucleotide) domains
  • activation by agonist causes conformational change so GDP released and GTP binds
  • alpha and betagamma separate to give GTP-bound alpha subunit and betagamma dimer
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32
Q

What are the states that a GPCR can be in?

A
  • no signal: receptor unoccupied, G protein alpha subunit binds GDP
  • signal on: GDP off, GTP on, alpha and betagamma separation, alpha combines with effector
  • signal off: alpha acts as enzyme to hydrolyse GTP to GDP, alpha recombines with betagamma
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33
Q

How does the process of heart rate change with Gi and Gs occur?

A
  • M2 ACh activates Gi which stops ATP to cAMP by adenyl cyclase so decreased HR and force of atria
  • beta 1 adrenoceptor activated Gs which activates ATP to cAMP by adenylyl cyclase, cAMP then activated protein kinase A so increased HR and force of atria and ventricles
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34
Q

How does Gq cause muscle contraction?

A
  • alpha 1 adrenoceptor activates Gq which activates PLC making DAG
  • activates PKC
  • PLC converts PIP2 to IP3 so Ca2+ released from ER
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35
Q

What is an example of signalling by receptor kinase?

A

insulin binding causes autophosphorylation of intracellular tyrosine

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36
Q

What does signalling via nuclear receptors do?

A

switch on or off genes to change mRNA levels and rate of synthesis

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37
Q

What are the four mechanisms of drug disposition?

A

absorption
distribution
metabolism
excretion

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38
Q

Whats involved in the process of absorption?

A

process of a drug entering the body from its site of administration

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39
Q

What is involved in the process of distribution?

A

process of a drug entering the blood, tissues and then distribution within the tissues

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40
Q

What is involved in the process of metabolism?

A

tissue enzymes catalyse the conversion of drug to a less active and more polar form that can be readily excreted

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41
Q

What is excretion?

A

removing a drug by kidneys or another route

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42
Q

What do metabolism and excretion come together to form?

A

elimination

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43
Q

What are the factors influencing drug absorption?

A
  • solubility: drug must first dissolve before absorption
  • chemical stability: some drugs are destroyed by acid in the stomach or by enzymes in the GI tract
  • lipid to water partition coefficient: rate of diffusion increases with lipid solubility of the drug
  • degree of ionisation: only the unionised form of a drug readily diffuses across the bilayer, depends on pKa of drug and local pH
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44
Q

What conditions ionise acidic or basic drugs more?

A

acidic drugs are less ionised in acid and basic drugs are less ionised in base

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45
Q

What are the factors affecting GI absorption?

A
  • GI motility
  • pH at absorption site
  • blood flow to stomach
  • way that tablet is manufactured
  • physciochemical interactions
  • presence of transporters
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46
Q

What is oral availability?

A

the fraction of the drug that reaches the systemic circulation after oral ingestion

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47
Q

What is systemic availability?

A

the fraction of the drug that reaches that systemic circulation after absorption

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48
Q

What are the main routes of administration?

A 
- Enteral: 
Oral
Sublingual 
Rectal
 - Parenteral:
IV
IM
SC
Inhaled
Transdermal
Topical
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49
Q

What are the four main compartments for body water?

A

plasma
interstitial
intra-cellular
transcellular

50
Q

What drugs move readily in the body?

A
  • ionised and unionised drugs that aren’t bound to plasma proteins
  • unionised in any form
51
Q

What is the volume of distribution?

A

apparent volume in which a drug is dissolved

52
Q

What does a Vd<10 mean?

A

the drug is in a vascular part and is too large to cross capillary walls or too bound to plasma proteins

53
Q

What does a Vd 10-30 mean?

A

the drug is in the extracellular space so drugs with low lipid solubility

54
Q

What does a Vd>30 mean?

A

there is distribution throughout total body water, for highly lipid soluble drugs or those that are very bound to tissue proteins

55
Q

How do drugs leave the body?

A

in the urine

rendered more polar bu metabolism or unchanged

56
Q

What does drug metabolism do?

A

changes drugs to more polar metabolites or less active compounds

57
Q

What is the main organ of drug metabolism in the body?

A

liver

58
Q

What is phase 1 of drug metabolism?

A

oxidation, reduction, hydrolysis which makes the drug more polar and adds a chemically reaction group permitting conjugation

59
Q

What is phase 2 of drug metabolism?

A

conjugation which adds an endogenous compound to increase polarity

60
Q

What are the steps in drug metabolism?

A

Drug –phase1–> Derivative –phase2–> Conjugate

61
Q

What type of reaction is phase 1 and why is this important?

A

phase 1 are catabolic and introduce a part that can be attacked in phase 2

62
Q

Where do the two phases take place?

A

liver

63
Q

What is the CYP450 monooxygenase cycle?

A

drug enter
molecular oxygen provides two O atoms
one O added to the drug
other O makes water

64
Q

Why does CYP450 change in different people?

A

individual variation and environmental factors

65
Q

What are the features of phase 2 reactions?

A

result in inactive products
happen in the liver
glucuronidation occurs frequently

66
Q

What are the processes in excretion?

A

glomerular filtration
active tubular secretion
passive reabsorption by diffusion

67
Q

What do molecules have to be to enter the filtrate?

A

must be unbound to enter filtrate via glomerular filtration

68
Q

What are the transporters that secrete drugs into the lumen of the nephron?

A
  • Organic anion transporter

- Organic cation transporter

69
Q

What so OAT and OCT transporters do?

A
  • move drugs against electrochemical gradient
  • each has a transport maximum
  • can secrete highly-bound drugs
  • some drugs compete for the sam etransporter
70
Q

What are the factors influencing reabsorption of drugs?

A

lipid solubility
polarity
urinary flow rate
urinary pH

71
Q

What does an alkaline or acidic pH do the the excretion of fluids?

A

alkaline pH increases exertion of acids

acidic pH increases excretion of bases

72
Q

What is the therapeutic window?

A

sits in between the maximum tolerates concentration and the minimum effective concentration

73
Q

What does a high or low therapeutic ratio mean?

A 
high = safe
low = unsafe
74
Q

What is Ke?

A

the fraction of the amount of drug eliminated per unit time

75
Q

What is first order kinetics?

A

the rate of elimination is directly proportional to the drug concentration so the graph will curve down

76
Q

What changes the concentration in first order kinetics?

A

does administered changes it but not the time or how fast the elimination occurs

77
Q

What is clearance?

A

the volume of plasma cleared of drug in unit time

78
Q

What does clearance determine?

A

the dose rate

79
Q

What happens at steady state?

A

the rate of drug administration = the rate of drug elimination

80
Q

What is time to reach steady state determined by?

A

half-life not infusion rate

81
Q

What is oral availability?

A

fraction of the administered dose that reaches the systemic circulation

82
Q

What is the volume of distribution?

A

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

83
Q

How is loading dose estimated?

A

from the Vd of the drug

84
Q

What is zero order kinetics?

A

drug is eliminated at a constant rate so the graph goes straight diagonally down

85
Q

What order is elimination?

A

zero order then changes to first order at a lower concentration

86
Q

What is plasma steady-state concentration not related to?

A

not linearly related to dose rate

87
Q

What is depolarisation?

A

the membrane becoming less negative

88
Q

What is hyper polarisation?

A

the membrane potential becoming more negative

89
Q

Which way does Na+ move?

A

in because concentration gradient and electrical gradient are both inward

90
Q

Which way does K+ move?

A

out because outward concretion gradient is larger than inward electrical gradient

91
Q

What happens when Na+ or K+ channels are opened?

A

the gradient shifts toward Ena or Ek respectively

92
Q

What are action potentials?

A

electrical signals where nerve cell membrane polarity is reversed momentarily

93
Q

What are the features of Na+ channel activation?

A

it is self-reinforcing with positive feedback

94
Q

What are the features of K+ channel activation?

A

it is self-limiting with negative feedback

95
Q

What happens to Na+ channel after they have been activated?

A

they become inactive and go into refractory period so they can be closed and ready to open again

96
Q

What is the absolute refractory period?

A

no stimulus can make an AP

97
Q

What is the relative refractory period?

A

a very strong stimulus can make an AP as there is some inactivated and some closed and the membrane is hyperpolarised

98
Q

What characteristics does a less leaky axon have?

A

greater the local current spread so increased AP conduction velocity

99
Q

What increases passive current spread?

A

increased axon diameter

decreased leak by adding Schwaan in PNS or oligodendrocyte in CNS

100
Q

How is conduction spread in unmyelinated or myelinated axons?

A

unmyelinated is by passive spread of current

myelinated is by saltatory conduction

101
Q

What does the ANS do?

A 
contraction and relaxation of smooth muscle
heart rate and force
secretions
metabolism
immune system regulation
102
Q

What is the structure of the motor ANS?

A

synapse in the autonomic ganglion

103
Q

What neurotransmitter is used in the sympathetic conduction?

A

preganglionic is ACh

postganglionic is NA

104
Q

What neurotransmitter is used in the parasympathetic conduction?

A

both preganglionic and postganglionic are ACh

105
Q

What is the structure of the sympathetic nerve chain?

A

short preganglionic which synapse at paravertebral or prevertebral ganglia
postganglionic are long

106
Q

What is the structure of the parasympathetic nerve chain?

A

long preganglionic that are in the walls of the organ

postganglionic are short

107
Q

What is sympathetic outflow?

A

thoracolumbar to the sympathetic chain

108
Q

What is parasympathetic outflow?

A

craniosacral (CN3,7,9,10 and S2-4)

109
Q

What is chemical transmission in ANS sympathetic?

A
  • AP makes Ca2+ move in and ACh out by exocytosis
  • ACh opens LGIC so depolarisation and Ca2+ entry and NA release
  • NA activates GPCR so cellular response
110
Q

What is chemical transmission in ANS parasympathetic?

A
  • ACh is always neurotransmitter

- ACh activates GPCR (muscarinic ACh) to cause cellular response

111
Q

What is NANC?

A

non-adrenergic non-cholinergic transmission

112
Q

What are the neurotransmitters used in sympathetic NANC?

A

sympathetic:
ATP rapid
NA intermediate
NPY slow

113
Q

What are the neurotransmitters used in parasympathetic NANC?

A

parasympathetic:
ACh rapid
NO intermediate
VIP slow

114
Q

What are the two types of ACh cholinceptors?

A
  • nicotinic = LGICs

- muscarinic = GPCRs, M1-5

115
Q

What are NA or A receptors?

A

GPCRs

116
Q

What does the sympathetic ANS do?

A
  • increase HR and force in atria and ventricles
  • relaxes bronchi and decreases mucus
  • decreases intestinal motility and constricts sphincters
  • increases release of adrenaline
  • relaxes bladder
  • ejaculation
117
Q

What does the parasympathetic ANS do?

A
  • decreases HR and force in atria
  • constricts bronchi and increases mucus
  • increases intestinal motility and relaxes sphincters
  • contracts bladder
  • erection
118
Q

What are nicotinic ACh receptors made up of?

A

subunits

119
Q

How can cholinergic transmission be blocked?

A
  • competitive antagonism
  • non-competitive antagonism
  • depolarisation blocking
120
Q

What is ganglionic transmission blocked by?

A

hexamethonium which does open channel block which in non-competitive

121
Q

What are the types of M receptor for parasympathetic and their role?

A

M1- Gq- phospholipase C stimulation- increased acid secretion

M2- Gi- inhibition of adenylyl cyclase, opening of K+- decreased rate of heart

M3- Gq- phospholipase C stimulation- increased secretion in mouth and contraction of visceral smooth muscle in lungs

122
Q

What are the types of M receptor for sympathetic and their role?

A

beta 1- Gs- stimulation of adenylyl cyclase- increase rate and force of heart

beta 2- Gs- stimulation of adenylyl cyclase- relaxation of bronchial and vascular smooth muscle

alpha 1- Gq- phospholipase C stimulation- contraction of vascular smooth muscle

alpha 2- Gi- inhibition of adenylyl cyclase- inhibition of NA release

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