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IB chemistry > D1-D5 > Flashcards

D1-D5 Flashcards

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1
Q

define the lethal dose (LD50)

A

the dose of a drug that causes death in 50% of laboratory animals

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2
Q

define the toxic dose (TD50)

A

the dose of a drug that causes toxicity (an unacceptable adverse effect) in 50% of patients

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3
Q

define the effective dose (ED50)

A

the minimum dose of a drug that produces the desired therapeutic effect in 50% of laboratory animals or human patients

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4
Q

define the therapeutic index in animal studies

A

the lethal dose of a drug for 50% of the population divided by the minimum effective dose for 50% of the population (LD50/ED50)

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5
Q

define the therapeutic index in humans

A

the toxic dose of a drug for 50% of the population divided by the minimum effective dose for 50% of the population (TD50/ED50)

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6
Q

the greater therapeutic index, the —– the drug

A

safer

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7
Q

define the therapeutic window

A

the range of dosages between the minimum amounts of the drug that produce the desired effect and a medically unacceptable adverse effect

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8
Q

where does the therapeutic window typically occur?

A

it usually opens below the ED50 (where some patients can still be provided with minimal beneficial effect) and closes below the TD50 (where only a small percentage of patients might experience significant adverse effects)

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9
Q

why should animal and human tests for drugs be kept to a minimum?

A

for ethical and economic reasons

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10
Q

name the 6 methods of drug administration

A

orally
rectally
parenterally
by inhalation
transdermally

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11
Q

describe when and how drugs would be taken orally

A
  • drugs with any polar groups are generally water soluble and can be administered orally
  • ingested by mouth
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12
Q

describe when and how drugs would be taken rectally

A
  • some chemical compounds are unstable in the highly acidic gastric juice
  • in the form of suppositories or enemas
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13
Q

describe when and how drugs would be taken parenterally, and state the 3 types of administration

A
  • some chemical compounds are unstable in the highly acidic gastric juice
  1. injected under the skin (subcutaneous injection)
  2. injected into muscle tissue (intramuscular injection)
  3. injected into the bloodstream (intravenous injection)
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14
Q

describe when and how drugs would be taken by inhalation

A
  • some volatile or highly dispersed drugs
  • breathed in through the nose and mouth
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15
Q

describe when and how drugs would be taken transdermally

A

non polar compounds can be applied to the skin in the form of patches, ointments, or therapeutic baths

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16
Q

what are 4 considerations of drug administration?

A

dosage, tolerance, addiction and side effects

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17
Q

what is a double blind test?

A

neither the researchers directly observing the patients nor the patients themselves know who is given the real drug and who receives the placebo- this is to reduce the possibility of conscious or subconscious bias in the interpretation of the experimental results

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18
Q

what is a placebo?

A

a biologically inert substance

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19
Q

what is the placebo effect and what is its role in clinical trials?

A

the idea that the body can sometimes be deceived into healing itself without receiving any help in the form of medical drug

this effect must be taken into account during clinical trials, so volunteers are split into 2 groups

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20
Q

describe how drugs can have side effects and what these are

A

pharmaceutical drugs interfere with biological processes so no drug is completely safe or free from non-beneficial effects on the human body.

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21
Q

define drug bioavailability

A

the fraction of the administered dose that is absorbed into the bloodstream

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22
Q

what 4 things affect the bioavailability of drugs (and therefore the effective and toxic doses of a drug)?

A
  • solubility
  • polarity
  • presence of certain functional groups
  • method of administration
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23
Q

give an example of how functional groups affect drug bioavailability

A

polar molecules containing hydroxyl, carboxyl, and amino groups are usually soluble in water and are therefore quickly absorbed from the gastrointestinal tract into the bloodstream. However, such molecules cannot easily pass through hydrophobic cell membranes, which in many cases reduces their biological activity

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24
Q

why is intravenous injection the only route of administration that results in 100% bioavailability?

A

other routes of administration decrease bioavailability due to incomplete absorption, decomposition and other factors such as physiological differences

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25
Q

describe drug tolerance

A
  • regular administration of certain drugs may reduce the body’s response to specific medications or classes of pharmaceutical drugs due to accelerated drug metabolism or changes in cellular functions
  • drug users need progressively higher doses of the drug to obtain the desired therapeutic effect
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26
Q

what effect does drug tolerance have on the therapeutic window for some patients?

A
  • increased doses lead to more pronounced side effects, which may eventually become unacceptable and close the therapeutic window
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27
Q

describe drug addiction

A
  • the compulsive desire of a user to take a drug regardless of the health problems it might cause.
  • this addiction may be purely psychological but it often involves some degree of physiological dependence that leads to withdrawal symptoms when the drug is interrupted
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28
Q

describe how drugs function at the molecular level

A

they interact with the binding sites of enzymes or cellular receptors (proteins composed of 2-amino acids)

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29
Q

describe a drug’s interaction with enzymes

A

by binding to enzymes most drugs act as inhibitors, reducing the activity of enzymes via competitive or non-competitive mechanisms.

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30
Q

describe a drug’s interaction with cellular receptors

A

if a drug binds to a cellular receptor, the cell responds to this chemical message by altering its state or allowing specific molecules to pass through the cell membrane

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31
Q

what does the type and efficiency of drug-receptor interactions depend on?

A

the chemical structures of the drug and the binding site

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32
Q

what type of bonds do drug-receptor interactions involve?

A

they can involve any types of chemical bonds

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33
Q

what are the two requirements for the drug and receptor to form interactions such as dipole-dipole, H, ionic bonds or London forces?

A

ideally, the functional groups of the drug and receptor should be complementary to one another and have correct orientations

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34
Q

how can efficient binding still be achieved if the structures of real drugs and their target receptors/enzymes do not match exactly?

A

by slight conformational changes of both the binding site and the drug molecule (induced fit theory for enzymes)

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35
Q

what can we do to change the nature and strength of binding of drugs?

A

chemical modification of certain functional groups of the drug

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36
Q

what is the first step of a drug development?

A

the identification of a lead compound (also known as a new chemical entity, NCE) that shows any kind of promising activity towards a specific biological target

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37
Q

describe the difference between drug discovery and drug design

A

drug discovery:
the lead compound can be isolated from natural products with known therapeutic effects or synthesised in the lab and screened against cell cultures, bacteria or animals.

drug design:
if the chemical composition and 3D structure of a biological target are known, a small molecule with a complementary structure. can be designed using computer modelling techniques. This is then synthesised, tested and adjusted

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38
Q

what is the second step to drug development?

A

a series of compounds similar to the lead compound are synthesised, characterised and subjected to preclinical trials

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39
Q

what happens during preclinical trials?

A

each compound is rated according to its:
- activity towards the target as well as unrelated biological targets
- chemical stability
- toxicity
- solubility in water and lipids
- preparation cost
- accessibility
- environmental impact

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40
Q

if all preclinical tests are successful, what happens?

A

information about the new drug is submitted to regulatory authorities and, with their approval, the drug is tested on humans in a series of clinical trials

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41
Q

describe phase I of clinical trials

A

SUBJECTS; small no of healthy volunteers
TEST RESULTS; toxicity and safety dosage (TD50), side effects

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42
Q

describe phase II of clinical trials

A

SUBJECTS; small no of patients
TEST RESULTS; effectiveness and effective dosage (ED50), safety and side effects

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43
Q

describe phase III of clinical trials

A

SUBJECTS; large no of patients
TEST RESULTS; comparison with other available drugs, drug compatibility, further data on effectiveness, safety and side effects

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44
Q

describe phase IV of clinical trials

A

post-clinical studies, where the study of effectiveness and safety of the drug continues during the whole period of its commercial use.

long term effects and chronic toxicity of the drug can be identified, including carcinogenic properties and effects on the immune system, fertility and reproductive functions

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45
Q
A
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46
Q

what is aspirin?

A

a mild analgesic

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47
Q

how do mild analgesics function?

A

by intercepting the pain stimulus at the source, often by interfering with the production of substances that cause pain, swelling or fever/

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48
Q

describe why salicylic acid (2-hydrobenzoic acid) cannot be used in its pure form

A

it causes severe digestive problems such as stomach irritation, bleeding and diarrhoea

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49
Q

how was salicylic acid first isolated?

A

it was taken from the bark of willow tree

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50
Q

how can the side effects of salicylic acid be minimised?

A

by using the chemically modified salicylic acid, known as acetylsalicylic acid or aspirin

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51
Q

how is aspirin prepared from salicylic acid?

A

via a condensation reaction

salicylic acid + ethanoic anhydride -> aspirin + ethanoic acid

SA is mixed with excess ethanoic anhydride and several drops of catalyst (conc phosphoric acid). the mixture is heated for a short time, diluted with water and allowed to cool down slowly, producing crystals of aspirin. The obtained product is usually impure so needs to be recrystallised from hot ethanol.

The identity of the product can be confirmed by IR spectroscopy and determining its melting point.

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52
Q

what are mild analgesics also known as ?

A

non-narcotic analgesics

non-steroidal anti-inflammatory drugs (NSAIDs)

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53
Q

how are mild analgesics different to strong analgesics?

A

mild analgesics affect the nervous system by intercepting the pain stimulus at the source.

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54
Q

describe the two main effects that aspirin has on the body

A

aspirin irreversibly binds to the enzyme cyclooxygenase and suppresses the production of prostaglandins, which are responsible for fever, swelling and the transmission of pain impulses from the site of injury to the brain

prostaglandins are also involved in the production of thromboxjnes, which stimulate the aggregation of platelets (thrombocytes) and blood clotting. So aspirin acts as n anticoagulant, reducing the risk of strokes and heart attacks

55
Q

describe the main side effect of aspirin

A

the anticlotting action of aspirin can lead to excessive bleeding and ulceration of the stomach.

56
Q

what is the synergetic side effect of aspirin?

A

the fact that stomach bleeding significantly increases when aspirin is taken with alcohol or other anticoagulants. This is an example of a drug interaction

57
Q

why is aspirin’s bioavailability limited?

A

because it is almost insoluble in water.

58
Q

describe how soluble aspirin can be made

A
  • the carboxyl group can be neutralised with sodium hydroxide, producing the water-soluble sodium salt of the acid
  • in aqueous solution this dissociates into sodium cations and acetylsalicylate ions, which form multiple ion-dipole interactions and hydrogen bonds with water
59
Q

why is the bioavailability of soluble aspirin only slightly higher than that of plain aspirin?

A

the sodium salt is immediately converted back into aspirin by the reaction with hydrochloric acid in the stomach

60
Q

what are penicillins?

A

antibiotics produced by fungi

61
Q

what is a core structure of penicillins?

A

the four-membered beta-lactam ring (refer to textbook) which is responsible for the antibacterial properties of the drugs

62
Q

what are some of the disadvantages of natural medicines?

A
  • low efficiency
  • variable composition
  • instability
  • side effects caused by the presence of many bioinactive substances in the same material

this means scientists have to work to identify, isolate and modify the relevant chemical properties of natural compounds .

63
Q

what makes the amide group in beta lactam rings so reactive?

A

the bond angles of the carbon and nitrogen atoms in this ring are ~90’- such bond angles create significant ring strain, making the group very reactive

64
Q

how does a penicillin antibiotic work (chemically)?

A

once in bacteria the beta-lactam ring opens and irreversibly binds to the enzyme transpeptidase, which is responsible for cross-linking of bacterial cell walls. This weakens the cell walls in multiplying bacteria and makes them more permeable to water. the osmotic pressure causes water to enter the bacteria til they burst open and die.

65
Q

what is a prophylactic medicine?

A

a medication or a treatment designed and used to prevent a disease from occurring.

66
Q

why did antibiotic resistance arise?

A

penicillin was routinely described across the world for treating minor illnesses or even as a prophylactic medicine. As a result, certain Bacteria mutated and developed varying degrees of antibiotic resistance due to increased production of the enzyme penicillinase. Over time bacteria w high levels of penicillinase became dominant

67
Q

how does penicillinase work?

A

this enzyme is able to deactivate benzylpenicillin and prevent it from binding to transpeptidase.

68
Q

how was bacterial resistance fought?

A

new penicillins with modified side chains were developed.

  • These penicillins could not be deactivated by penicillinase and were effective against a wider range of bacteria.
  • Some modified penicillins were stable in the acidic environment of the stomach and thus could be administered orally
69
Q

Why did scientists have to create a new class of antibacterial drugs and what did this cause?

A

new strands of constantly mutating bacteria became resistant to most strands of penicillins.

This led to the development of multi drug resistance (MDR) in bacteria.

70
Q

what does the treatment of infectious diseases caused by MDR bacteria require?

A

the use of a cocktail of different antibiotics and strict patient compliance to medical procedures.

71
Q

what are opiates?

A

natural narcotic analgesics that are derived from the opium poppy

72
Q

what are morphine and codeine used as?

A

strong analgesics

73
Q

how do strong analgesics work?

A

by temporarily binding to opioid receptors in the brain

74
Q

describe the difference of the effects of low and high doses of strong analgesics

A

low/moderate doses: although they act as depressants if the CNS, they do not significantly affect perception, attention or coordination when taken in low to moderate doses.

high doses:
affect all functions of the CNS and can lead to drowsiness, confusion and potentially fatal asphyxia caused by respiratory depression.

75
Q

what are opiates also known as and why?

A

narcotic analgesics because in addition to their painkilling properties, large doses of opiates cause a strong feeling of euphoria, provide relief from all forms of distress and stimulate sociability.

76
Q

describe the primary bioactive ingredient of opium

A

morphine, a natural analgesic that belongs to the group of alkaloids (naturally occurring chemical compounds containing basic nitrogen atoms)

77
Q

what are morphine and its derivatives (opiates) used for in medicine?

A

relieve severe pain caused by injury, surgical procedures, heart attack or chronic diseases such as cancer

78
Q

describe the problems of addiction to opiates

A

non-medical use of opiates quickly leads to psychological dependence and tolerance, forcing the user to take constantly increasing doses of the drug to achieve the desired effect. This affects the metabolic processes in the body and leads to physiological dependence, further increasing the required dose of the drug and the risk of adverse effects

79
Q

what does the physiological activity of opiates strongly depend on?

A

their ability to cross the blood-brain barrier

80
Q

what is the blood brain barrier?

A

a series of lipophilic cell membranes that coat the blood vessels in the brain and prevent polar molecules from entering the CNS

81
Q

what limits morphine’s ability to reach the opioid receptors in the brain?

A

the presence of one amino and two hydroxyl groups- these make morphine sufficiently polar to be soluble in water but reduce its solubility in lipids

82
Q

how can the polarity of morphine be reduced?

A

by chemical modification of one or both hydroxyl groups in its molecule

83
Q

describe how codeine differs from morphine

A

the phenolic -OH group is replaced with the less polar ether group, -OCH3

84
Q

codeine is —- potent than morphine; why?

A

less; it readily crosses the blood-brain barrier but does not bind to the opioid receptor because of the steric effect of the ester group

85
Q

why is codeine the most widely used opiate in the world?

A
  • low activity
  • wide therapeutic window
  • limited potential for abuse
86
Q

describe how diamorphine differs from morphine

A

both hydroxyl groups are substituted with ester groups

87
Q

diamorphine is —- potent than morphine; why?

A

more; diamorphine is soluble in lipids and can easily cross the blood-brain barrier. In the brain diamorphine is quickly metabolised into morphine, which binds to the opioid receptor

88
Q

diamorphine is also known as ——

A

heroin

89
Q

how can diamorphine be prepared from morphine?

A

in the same way as aspiring is prepared from salicylic acid, with ethanoic anhydride

90
Q

how does codeine have similar pharmaceutical properties to morphine?

A

once codeine has crossed the blood-brain barrier, it is slowly metabolised into morphine.

91
Q

what is gastric juice composed of?

A
  • water
  • salts (mostly KCl and NaCl)
  • hydrochloric acid
  • enzymes (pepsins)
92
Q

what are pepsins secreted by and what are they responsible for ?

A

cells in the stomach lining; they are responsible for the breakdown of proteins into peptides and individual amino acids

93
Q

how does the body keep stomach conditions bearable?

A

some cells produce hydrogen carbonate ions (HCO3-) and gastric mucus to buffer the acid and prevent the gastric juice from digesting the stomach tissues

94
Q

what is the role of the hydrochloric acid in the stomach?

A

although the acid itself does not break down food molecules, it:

  • denatures proteins
  • provides an optimum pH for enzymes in the gastric juice
  • acts as a disinfectant, killing harmful microorganisms ingested with the food
95
Q

define an active metabolite

A

the active form of a drug after it has been processed by the body

96
Q

what are antacids used for

A

to reduce the excess stomach acids by reacting with hydrochloric acid increasing the pH of gastric juice

97
Q

give examples of common antacids

A

calcium hydroxide, magnesium hydroxide, aluminium hydroxide, sodium carbonate and sodium bicarbonate

98
Q

how do antacids work?

A

they reduce the concentration of H+ (aq) ions and therefore increase the pH of gastric juice

99
Q

how can the acidity of gastric juice be controlled at the cellular level?

A

by targeting the biochemical mechanisms of acid production

100
Q

what is the secretion of acid in the stomach triggered by?

A

histamine (a derivative of amino acid histidine) that binds to H2-histamine receptors in the cells of the gastric lining

101
Q

what can be used top inhibit stomach acid production?

A

compounds such as ranitidine (Zantac)

102
Q

how does ranitidine (Zantac) function?

A

it blocks H2-histamine receptors and reduces the secretion of stomach acid. This provides short-term relief from symptoms of indigestion

103
Q

how do omeprazole (Prilosec) and esomeprazole (Nexium) work?

A

they reduce the production of stomach acid by inhibiting a specific enzyme, known as the gastric proton pump, which is directly responsible for secreting H+ (aq) ions into the gastric juice.

104
Q

how are proton pump inhibitors different to ranitidine?

A

they reduce the secretion of stomach acid for prolonged periods (up to 3 days)

105
Q

describe the similarity and difference between omeprazole and esomeprazole

A

they have the same molecular formula (C17H19N3O3S) but whereas omeprazole is a racemic mixture of both enantiomers (R-omeprazole and S-omeprazole), esomeprazole is a single enantiomer (S- omeprazole).

106
Q

how do the two enantiomers of omeprazole contrast to many other drugs?

A

show very similar pharmacological activity (refer to textbook for images)

107
Q

describe how omeprazole and esomeprazole work

A
  • in their original form, they are inactive and do not interact with the gastric proton pump directly
  • due to their low polarity they readily cross cell membranes and enter the intracellular compartments containing HCl acid
  • in this acidic environment both enantiomers undergo a series of chemical transformations and produce the same active metabolites, which bind to the proton pump enzymes and inhibit the secretion of stomach acid
108
Q

why is the mechanism of action of omeprazole and esomeprazole beneficial ?

A

it increases the efficiency of both drugs and allows a reduced frequency of administration

109
Q

describe how the pH of gastric juice is different to the pH of other biological fluids

A

whereas the concentration of stomach acid varies by a factor of 100, the pH of other biological fluids remains relatively constant

110
Q

how is the stability of biological fluids achieved?

A

by the action of acid-base buffers, which can neutralise small amounts of strong acids and bases without significantly changing their pH.

111
Q

how do acid base buffers work?

A

they each contain two molecular or ionic species which differ by a single proton (H+)- conjugate acid base pairs

112
Q

in a conjugate acid base pair, the more protonated species is the ——-

A

conjugate acid

113
Q

in a conjugate acid base pair, the less protonated species is the ——-

A

conjugate base

114
Q

describe an acetate buffer

A

consists of ethanoic (acetic) acid, CH3COOH and ethanoate (acetate) anions, CH3COO-

115
Q

in buffer solutions both the conjugate acid and the conjugate base are —– and exist in ——

A

weak, equilibrium

116
Q

state the equilibrium equation for an acetate buffer

A

CH3COOH (aq) <-> CH3COO- (aq) + H+ (aq)

117
Q

what is the primary acid-base buffer system in the human body? give the TWO equilibrium equations for this

A

one that consists of carbon dioxide and hydrogen carbonate ions:

BASE CO2 . H2O <-> ACID HCO3- (aq) + H+ (aq)
pKa1= ~6

at a higher pH
ACID HCO3- (aq) <-> BASE CO32- (aq) + H+ (aq)
pKa2= ~10

118
Q

the ability of acid-base buffers to resist pH changes is —– and depends on ——

A

the concentrations and ratios of the conjugate acid and base in the solution

119
Q

when does an acid-base buffer reach its maximum efficiency and can neutralise the greatest amounts of strong acids or bases

A

pH=pKa

it can be used between pH=pKa±1 as outside this range the concentration of one of the buffer components becomes too low and the buffer loses its ability to maintain a constant pH of the solution

120
Q

what makes viruses so complex

A

they lack a cell structure and so are more difficult to target than bacteria

121
Q

describe the differences between viruses and bacteria

A

while bacteria are living cells that can feed, excrete, grow and multiply, viruses lack cellular structure and do not have their own metabolism.

therefore viruses are not considered to be life forms but rather very complex chemical compounds

122
Q

describe the structure of most viruses

A
  • nucleoproteins containing a nucleic acid surrounded by a capsid (protein coat)
  • this consists of multiple protein units (capsomeres) arranged in helical or polyhedral structures
123
Q

describe how viruses function

A
  1. capsid proteins of viruses bind to receptors on the host cell surface
  2. they either cross the cell membrane or inject their genome into the cell
  3. virus genome is interpreted as a set of instructions for synthesising proteins and nucleic acids, which self-assemble into new copies of the virus
  4. replicated viruses are released from the host cell usually by lysis
124
Q

what has the best defence against specific types of virus been in the past few years?

A

immunisation

125
Q

give the two main ways that antiviral drugs can work

A
  • by preventing the viruses from multiplying by blocking enzymes activity within the host cell (stage 4)
  • by altering the cell’s genetic material so that the virus cannot use it to multiply (stage 3)
126
Q

stage 2 antivirals

A

inhibit the binding of the virus and the injection of its genetic material into the cell (amantadine and rimantadine) but resistance has been developed

127
Q

stage 3 antivirals

A

biosynthesis of viral compounds by the host cell is targeted by antivirals that mimic the structures of nucleotides (eg acyclovir and zidovudine)

these undergo phosphorylation and produce non-standard nucleotides which are mistakenly incorporated into RNA and DNA sequences. the enzymes produced from these altered nucleic acids are inactive and cannot be used for replicating viral components.

128
Q

stage 4 antivirals

A

prevent the release of virus copies from the cell by inhibiting neurominidases (viral enzymes), which trigger the process of budding, which allows viruses to bulge through the outer membrane of the host cell. this inhibition therefore keeps viruses trapped within the cell and prevents spread

eg oseltamivir (Tamiflu) and zanamivir (Relenza)

129
Q

give similarities and differences between oseltamivir (Tamiflu) and zanamivir (Relenza)

A
  • both target same enzymes
  • both contain a six-membered ring with three chiral carbon atoms
  • side chains contain different functional groups (O-COO and Z-COOH)
  • cases of resistance in zanamivir more rare
  • O inactive in original form, Z active
130
Q

why is oseltamivir inactive in its original form and how is this overcome?

A

inactive; due to presence of the ester group.

in the body the ester group is hydrolysed into a carboxyl group, producing an active metabolite with enhanced antiviral activity

131
Q

describe HIV and AIDS

A

human immunodeficiency virus is responsible for acquired immunodeficiency syndrome which is the progressive failure of the immune system and the development of life-threatening opportunistic infections and cancers

132
Q

why is HIV so difficult to tackle?

A
  • fast replication cycle and high mutation rate
  • infects lymphocytes/white blood cells that are responsible for righting viral and bacterial infections
  • HIV is able to incorporate itself into the host DNA where it can remain dormant for many years
133
Q

what are retroviruses? how can they be fought?

A

viruses like HIV that use reverse transcriptase enzymes to produce DNA strands from their RNA genomes.

inhibition of reverse transcriptase, which is not used in normal cells.

IB chemistry (29 decks)

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