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Year 2: LCRS > Pharmacology & Therapeutics 1 > Flashcards

Pharmacology & Therapeutics 1 Flashcards

1
Q

What are the 3 principle efferent outputs from the CNS?

A

Autonomic: responsible for involuntary control, accounts for the innervation of the exocrine glands, smooth muscle, cardiac muscle and is involved in metabolism and host defenceSomatic: it is the innervation of the muscle, including the diaphragm and respiratory musclesNeuroendocrine: this system is responsible for growth metabolism, reproduction, development , salt & water balance and host defence

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2
Q

What are the basic branches of the ANS?

A

Sympathetic: fight and flight Parasympathetic: rest and digest

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3
Q

How does the ANS target the eye?

A

Sympathetic: Dilation of the pupil Parasympathetic: Constriction of the pupil Contraction of the ciliary muscle

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4
Q

How does the ANS target the salivary glands?

A

Sympathetic: Thick, viscous secretion Parasympathetic: Copious, watery secretion

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5
Q

How does the ANS target the trachea and bronchioles?

A

Sympathetic: Dilates Parasympathetic: Constriction

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6
Q

How does the ANS target the skin?

A

Sympathetic: Piloerection Sympathetic cholinergic: Increased sweating

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7
Q

How does the ANS target the liver?

A

Sympathetic: Glycogenolysis and gluconeogenesis

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8
Q

How does the ANS target the heart?

A

Sympathetic: Increase in rate and contractility Parasympathetic: Decrease in rate and contractility

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9
Q

How does the ANS target adipose tissue?

A

Sympathetic: Lipolysis

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10
Q

How does the ANS target the gastrointestinal system?

A

Sympathetic: Decrease in motility and tone Sphincter contraction Parasympathetic: Increase in motility and tone Increase in secretions

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11
Q

How does the ANS target to kidney?

A

Sympathetic: Increased renin secretion

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12
Q

How does the ANS target the ureters and bladder?

A

Sympathetic: Relaxes detrusor; constriction of trigone and sphincter Parasympathetic: Contraction of detrusor Relaxation of trigone and sphincter

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13
Q

How does the ANS target the blood vessels?

A

Sympathetic: (skeletal muscle)Dilation (skin, mucous membranes, splanchnic area) constriction

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14
Q

What are the characteristics of the parasympathetic nervous system?

A
  • Cranial sacral outflow - Long pre-ganglionic fibre - Short post-ganglionic fibre - Ganglia tend to lie within the innervated tissue - Only neurotransmitter involved is Ach, therefore all cholinergic synapses
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15
Q

What are the characteristics of the sympathetic nervous system?

A
  • Thoracolumbar outflow - Short pre-ganglionic fibre - Long post-ganglionic fibre - Ganglia form just outside spinal cord in the paravertebral chains
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16
Q

What do postganglionic fibres of the SNS to effector organs release?

A

Noradrenaline

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17
Q

What to postganglionic fibres of the SNS which innervate sweat glands release?

A

Ach

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18
Q

What do preganglionic fibres of the sympathetic nervous system release?

A

Ach

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19
Q

In which cases do preganglionic fibres of the SNS release noradrenaline?

A

Some preganglionic fibres innervate the adrenal medulla

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20
Q

What is the enteric nervous system?

A

The local nervous system of the digestive tract which consists of the submucosal and myenteric plexus

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21
Q

What is the somatic nervous system?

A

Consists of one long motor neurone, with Ach release to the skeletal muscle

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22
Q

What are the types of Ach receptors?

A

Nicotinic and muscaranic receptors

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23
Q

What are the characteristics of nicotinic receptors?

A
  • Membrane bound receptors that are present at autonomic ganglia - Type 1 ionotrophic receptors therefore they produce rapid responses via iron channel opening - Stimulated by nicotine and acetylcholine - Blocked by hexamethonium
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24
Q

What are the characteristics of muscarinic receptors?

A
  • Tend to be found in the effectors organs which are innervated by post-ganglionic parasympahetic fibres which mediate effector responses - Type 2 G-protein coupled receptors therefore require generation of 2nd messenger molecules. This means the responses are slower. - Stimulated by muscarine and acetylcholine - Blocked by atropine
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25
Q

What are the subtypes of muscarinic cholinoreceptors?

A

M1- founds in neural tissues M2- found in cardiac tissues M3- found in exocrine and smooth muscle

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26
Q

What are the subtypes of adrenoreceptors?

A

Alpha 1 Alpha 2 Beta 1 Beta 2

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27
Q

What is the process of amine transmitter synthesis?

A

1) The precursor is taken up into the pre-synaptic nerve terminal 2) The precursor is enzymatically converted into the active transmitter and then packaged into vesicles 3) Follow pre-synaptic nerve terminal depolarisation, the vesicles fuse and release the transmitter into the synapse 4) The transmitter then binds with the receptor on the effector cel; where it is broken down and the degradation products are taken back up into the nerve terminal

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28
Q

What is the precursor for acetyl choline synthesis?

A

Acetyl CoA & choline

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29
Q

Which enzyme is responsible for the conversion during acetyl choline synthesis?

A

Choline acetyl transferase

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30
Q

Which enzyme is responsible for enzymatic degradation during acetyl choline degradation?

A

Acetylcholine esterase

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31
Q

What is the process of noradrenaline synthesis?

A
  • The precursor is tyrosine - Tyrosine is then hydroxylased into DOPA by tyrosine hydroxylase - DOPA is then decarboxylated to form dopamine which is then packaged into vesicles - In the vesicle, dopamine is hydroxylased to form noradrenaline by dopamine beta hydroxylase - NA is released from the vesicle
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32
Q

What are the two uptake systems for noradenaline?

A

1) Neural reuptake & degradation by MAO-A to form secondary metabolites 2) Extraneural uptake and degradation via COMT

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33
Q

What is pharmacology?

A

The science of the properties of drugs and their side effects on the body

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34
Q

What is pharmacokinetics?

A

The study of how drugs are handled within the body, including their absorption, distribution, metabolisation and excretion This concerns: - How drug concentration changes with time - How drugs pass across cell membranes - How often drugs should be given - What the effect of long-term administration may be - How drugs interact with each other

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35
Q

What is pharmacodynamics?

A

The interactions of drugs with cells and their mechanism of action on the body. It involves - How drugs bind to cells - Uptake of drugs into cells - Intracellular metabolism of drugs

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36
Q

What is a drug?

A

A chemical that affects the physiological function in a specific way

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37
Q

What are drug target sites?

A

Protein complexes key to drug mechanism of action

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38
Q

When a drug is administered, what are the target sites that it must interact with?

A

1) Cell receptors 2) Ion channels 3) Transport systems 4) Enzymes

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39
Q

What are cell receptors?

A

Proteins which usually sit within cell membranes thus exposing an active site waiting to be activating by neurotransmitters or hormones

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40
Q

How are the different families of cell receptors differentiated between?

A

On the basis of protein structure of the receptors and the biochemical/transduction system the receptor interacts with with in the cell

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41
Q

What are the different types of cell receptors?

A

Type 1: Ionotrophic (ligand-gates channels) Type 2: Metabotrophic (G-protein couples Type 3: Kinase-linked Type 3: Intracellular steroid type

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42
Q

What are the characteristics of ionotrophic cell receptors?

A

Location: Membrane Effector: Channel Coupling: Direct Speed: Millisecond Example: Nicotinic Ach receptor

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43
Q

What are the characteristics of metabotrophic cell receptors?

A

Location: Membrane Effector: Enzyme or channel Coupling: G-protein Speed: Seconds Example: Muscarinic Ach receptor

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44
Q

What are the characteristics of kinase-linked cell receptors?

A

Location: Membrane Effector: Enzyme Coupling: Direct or indirect Speed: Minutes Example: Insulin receptor

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45
Q

What are the characteristics of intracellular steroid type cell receptors?

A

Location: Intracellular Effector: Gene transcription Coupling: Via DNA Speed: Hours Examples: Steroid/thyroid receptors

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46
Q

What is an agonist?

A

A drug or other substance that acts on the cell receptor to activate it, initiating a response. E.g. Acetylcholine (at acetylcholine receptors) and nicotine

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47
Q

What are antagonists?

A

A drug or other substance that binds to the cell receptor without activating it. It blocks the receptor active site and therefore inhibits the normal response

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48
Q

What are the shapes of a normal dose-resposne curve and a log dose-response curve?

A

Normal: hyperbolic Log: sigmoidal

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49
Q

What are the different types of ion channels?

A

Voltage sensitive: the channel opens in response to a change in membrane potential e.g. Ca2+ channels (VSCC) Receptor linked: channel opens in response to the activation of a receptors. e.g. choline activates NAChR, which in turns opens an ion channel

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50
Q

Which types of drugs might interact with on or both types of ion channels?

A
  • Local anaesthetics: they interact with or block sensitive Na+ channels on pain conduction neurones in order to reduce the perception of pain - Calcium channel blockers- e.g. Nitradipine; very useful in the treatment of CV disorders for example as anti-hypersentives and anti-angine drugs
51
Q

What are transport systems?

A

Specific carrier molecules that transport substances against their concentration gradients. They are energy dependent.

52
Q

What are examples of transport systems?

A
  • Glucose transporter in hepatocutes - Neurotransmitter transport e.g. active reuptake of noradrenaline into nerve terminals in the sympathetic nervous systems - Na+/K+ ATPase
53
Q

How do tricyclic anti-depressants interact with transport system?

A
  • Used in clinical depression the Na5HT transporter in the brain is not fully functional - Tricyclic anti-depressants slow down the postsynaptic reuptake of NA into the nerve terminals which prolongs the effect of NA
54
Q

How do cardiac glycosides interact with transport systems?

A
  • Acts to slow down the NA/K ATPase which leads to an increase in intracellular Na+. - Useful in cardiac failure, as the increase in intracellular Na+ results in an increased force of contraction e.g. Digoxin
55
Q

How do drugs interact with enzymes?

A

Enzyme inhibitors: act to slow enzyme function False substrate: act to subvert normal pathways by introducing a new substrate Prodrugs: drugs which interact with an enzyme component which then has an effect of the body

56
Q

Give an example of an enzyme inhibitor

A

Neostigmine- an anticholinesterase which slows down the rate of degradation of acetylcholine which enhamces its action

57
Q

Give an example of a false substrate

A

Methyldopa- an antihypertensive drug which subverts the normal noradrenaline synthesis pathways by introducing a different precursor leading to local vasodilation

58
Q

Give an example of a prodrug

A

Chloral hydrate is converted to the active trichloroethanol

59
Q

What mediates the unwanted effects of paracetamol?

A

Enzymes

60
Q

What are examples of non-specific drug action, in which drug action is mediated solely by their own physiochemical properties and not the 4 main drug target sites?

A
  • General anaesthetics: interact with synaptic transmission in the brain - Antacids: used in the treatment of indigestion, dyspepsia and symptoms of ulceration - Osmotic purgatives/ laxatives- actis to draw water into the large intestine causing softening/expansion of faeces and promotion of excretion
61
Q

Give an example of a plasma protein binding site

A

Albumin- acts to allow the storage of drugs in the body in a protein bound form. It allows the transport of the drug but does not mediate any action of the drug

62
Q

What is affinity?

A

The strength of the drug binding to the receptor

63
Q

What is efficacy?

A

The ability of the drug to induce a response in the receptor post-binding

64
Q

What is potency?

A

The powerfulness of a drug, depending on its affinity and efficacy

65
Q

What is a full agonist?

A

An agonist which has the ability to induce a max response in tissue post-binding

66
Q

What is a partial agonist?

A

An agonist which can only produce a partial response in tissue, and in conjunction with a full agonist may act with antagonist activity

67
Q

What is selectivity?

A

The preference of a drug for a receptor

68
Q

What is the structure-activity relationship?

A

Refers to the fact that the activity of a drug is related to the structure of the drug which means small changes in the structure may produce large effects on its action

69
Q

What is receptor reserve?

A

The fact that in many tissues, not all receptors need to be occupied in order to achieve the maximal tissue response

70
Q

What are competitive antagonists?

A

They bind to the same site as the agonist which reduced the number of agonist molecules which can bind to the receptor leading to a reduced normal agonist response They are surmountable- increasing the concentration of the agonist, a competitive antagonist block can be overcome

71
Q

What are irreversible antagonists?

A

They bind tightly either to the same site as the agonist or at a different site to the agonist. They are insurmountable, meaning maximal normal response cannot be achieved regardless of whether the concentration of the agonist is increased further

72
Q

What are the 4 main types of drug antagonists?

A

1) Receptors blockade 2) Physiological antagonism 3) Chemical antagonism 4) Pharmacokinetic antagonism

73
Q

What is physiological antagonism?

A

Drugs may act on different receptors in the same tissue to induce the opposite effect. E.g. noradrenaline acts to induce vascular constriction. Blood pressure increases. Whereas, histamine acts on different receptors to induce vascular dilation and bloop pressure reduction.

74
Q

What is chemical antagonism?

A

Where two drugs interact in solution E.g. chelating agents, dimercaprol, useful in treatment for heavy metal poisoning

75
Q

What is pharmacokinetic antagonism?

A

Antagonists act to reduce the concentration of the active drug at the site of action. Pharmacokinetic antagonism occurs in different ways: - Decrease absorption - Increase metabolism - Increase excretion

76
Q

Give an example of pharmacokinetic antagonism

A

Barbiturate interaction with warfarin - Barbiturates are good enzyme inducers so if they are administered repeatedly, the metabolising system within the liver increases - This can pose a problem with co-administrering another drug which is metabolised b the same enzymes. This leads to this enzymes activity being reduced.

77
Q

What is drug tolerance?

A

The gradual reduction in responsiveness to a particular drug, following repeated administration

78
Q

Which factors can influence drug tolerance ?

A

1) Pharmacokinetic factors - increase the rate of metabolism of the drug i.e. enzyme inducing e.g. barbiturates and alcohol 2) Loss of receptors- by membrane endocytosis which leads to receptor ‘down-regulation’ e.g. beta- adrenoreceptors 3) Receptor desensitisation- the receptor remains on the cell surface but undergoes a conformational change meaning that it can no longer bind with an effective response e.g. nitotinic acetyl CoA receptr at the neuromuscular junction 4) Exhaustion of mediator stores- with repeated stimulation of a system, any required mediator stores may be exhausting meaning tissue response is reduced e.g. amphetamines 5) Physiological adaption- a homeostatic response to the effect of a drug in which the body tries to keep effects within a set range.

79
Q

What is the journey of a drug through the body?

A

Formulate Administration Distribution Metabolism Excretion

80
Q

How can administration routes be categorised?

A

Enteral: routes include sublingal, buccal, oral and rectal - these routes are considered to easier and patients can self-administer these drugs Parenteral: routes include intravenous, intramuscular, subcutaneous, percutaneous and inhalation - these are more invasive routes and are usually administered by a medical professional (exceptions would be asthmatics and diabetics)

81
Q

What are the advantages and disadvantages of the oral route of administration?

A

Advantages: Permits self medication Does not require very sterile preparations Lower incidence of anaphylactic shock Capacity to prevent complete absorption (vomiting) Disadvantages: Inappropriate for drugs which - are easily altered in stomach acid - undergo extensive ‘first pass’ metabolism Requires patient compliance

82
Q

What are the advantages and disadvantages of the intravenous route of administration?

A

Advantages: Rapid onset of action Avoids poor absorption/ destruction of the GI tract Permits care control of blood levels Disadvantages: Slow injection necessary Higher incidence of anaphylactic shock Possible complications include embolism, phlebitis and pain

83
Q

What are the advantages and disadvantages of inhalation for administering drugs?

A

Advantages: Is ideal for particles, gases, volatile liquids and aerosols There is an large surface area available due to alveolar membranes Simple diffusion mechanism and phagocytosis Disadvantages: Possible localised effect within the lungs

84
Q

What are the advantages and disadvantages of the intramuscular route of administration?

A

Advantages: Relatively high blood flow which increases during exercise Enable the depot theory Disadvantages: Possible infection and nerve damage (more common in the gluteal region)

85
Q

What are the advantages and disadvantages of the subcutaneous route of administration?

A

Advantages: Local administration so dissemination can be minimised Enable depot theory Disadvantages: Pain Abscess Tissue Necrosis

86
Q

What are the advantages of the percutaneous route of administration?

A

Advantages: Local application and action Lipid soluble compounds diffuse readily Disadvantages: Local irritation and skin reactions Alteration of skin structure (e.g. steroids)

87
Q

How do drugs cross different barriers (membranes)?

A

1) Passive diffusion 2) Facilitated diffusion 3) Active transport 4) Pinocytosis 5) Filtration 6) Paracellular transport

88
Q

Via which two ways do drug molecules move around the body?

A

Bulk flow transfer- in the bloodstream Diffusional transfer- molecule by molecule over short distances

89
Q

Why do drugs exist in ionised (polar) and non-ionised (non-polar) forms?

A

Most drugs are either weak acids or weak bases

90
Q

What is the PH partition hypothesis?

A

Drugs are absorbed when they are in their unionised state, therefore the rate of absorption is dependent on the amount of drug that is present in an unionised form

91
Q

What factors influence drug distribution?

A
  • Regional blood flow - Extracellular binding (plasma-protein binding) - Capillary permeability (tissue alterations- renal, hepatic, brain/CNS), placental) - Localisation in tissues
92
Q

How are drugs excreted in the kidneys?

A

Responsible for the elimination of most drugs 1) Glomerulus: drug-protein complexes are not filtered 2) Proximal tubule: active secretion of acids and bases 3) Proximal and distal tubules: lipid soluble drugs are reabsorbed

93
Q

Why might treatment with intravenous sodium bicarbonate increase aspirin excretion?

A

I.V sodium bicarbonate will increase the pH of urine. Increased urine pH ionises the aspirin which makes it less lipid soluble and therefore less reabsorbed from the tubule. Its rate of excretion is therefore increased

94
Q

What is enterohepatic cycling?

A

Where the drug/metabolite is excreted into the gut (via the bile) but is then reabsorbed and taken back to the liver to be excreted again

95
Q

What can enterohepatic cycling lead to?

A

Drug persistence

96
Q

Aside from the major 2 routes (kidney and liver) of drug excretion, what other routes exist?

A

Lungs Skin Gastrointestinal secretions Saliva Sweat Milk Genital Secretions

97
Q

What is bioavailability?

A

The proportion of the administered drug that is available within the body to exert its pharmacological effect

98
Q

What is the apparent volume of distribution?

A

The volume in which a drug appears to be when it is distributed - it is an indicator of the pattern of distribution

99
Q

What is biological half-life?

A

The time taken for the concentration of a drug (in blood/plasma) to fall to half its original value

100
Q

What is clearance?

A

Blood plasma clearance is the volume of blood plasma that has been cleared of a drug in a unit time

101
Q

What type of molecule are usually xenobiotics?

A

Lipophilic

102
Q

What is the purpose of metabolism?

A

It tends to reduce or eliminate pharmacological/toxicological activity. Metabolism converts lipophilic chemical to polar derivatives

103
Q

What is the major organ of drug metabolism?

A

The liver. Hepatic ‘first pass’ metabolism can be extensive

104
Q

What are the 3 types of metabolic changes?

A

Phase 1 Phase 2 Excretion

105
Q

What occurs during Phase I reactions of metabolism?

A
  • Oxidation/reduction creates new functional groups and hydrolysis unmasks them. - Functional groups serve as a point of attachment for Phase II reactions. - Phase 1 reactions often inactivate chemicals. - The reactions can activate chemicals such as in the cases involving prodrugs -There is little change in the polarity of the drug after phase I metabolism - Can produce toxic metabolites - Often generate a biologically inactive product
106
Q

Where is the cytochrome P450 enzyme predominantly found?

A

Liver

107
Q

What is an important role of cytochrome P450?

A

Important enzyme in Phase I oxidising reactions

108
Q

How do oxidation reactions in Phase I metabolism usually begin?

A

With a hydroxylation step catalysed by the P450 system

109
Q

What are the reactions and their enzymes that are involves in Phase II metabolism?

A

Glucuronidation (glucuronyl transferase) Methylation (methyl transferase) Sulphation (sulphotransferase) Acetylation (acetyl transferase) Glutathione (glutathione-s-tranferase) Aminoacid conjugation (acyl transferase)

110
Q

What are the characteristics of Phase II metabolism reactions?

A
  • The conjugate is almost always pharmacologically inactive - Less lipid soluble - Easier to excrete
111
Q

What is the conjugating agent and target functional groups in glucuronidation?

A

Conjugating agent: UDP- glucuronic acid Target functional groups: -OH, -COOH, -NH2, -SH

112
Q

What is the conjugating agent and target functional groups in acetylation?

A

Conjugating agent: Acetyl CoA Target functional groups: -OH, -NH2

113
Q

What are the conjugating agents and target functional groups in amino acid conjugation?

A

Conjugating agents: Glycine, Glutamine, Taurine Target functional groups: -COOH

114
Q

What is the conjugating agent and target functional groups in methylation?

A

Conjugating agent: S-adenosyl-methionine Target functional group: -OH, -NH2

115
Q

What is the conjugating agent and target functional groups in suplhation?

A

Conjugating agent: 3’-phosphoadenosine-5’-phosphosulphate Target functional group: -OH, -NH2

116
Q

What is the conjugating agent and target functional groups in Glutathione conjugation?

A

Conjugating agent: Glutathione Target function group: electrophiles

117
Q

What is the high energy intermediate forms in glucuronidation?

A

UDP-glucoronate

118
Q

What acts as an energy rich donor in sulfation?

A

PAPS

119
Q

Why is drug metabolism important?

A
  • The biological half-life of a chemical is decreased - The duration of exposure is reduce - The accumulation of the compound in the body is avoided - The potency/duration of the biological activity of the chemical can be altered - The pharmacology/toxicology of the drug can be governed by its metabolism
120
Q

What are cholinomimetric drugs?

A

They mimic activation of the parasympathetic nervous system?

121
Q

What are muscarinic effects

A
  • Effects that can be replicated by muscarine and can be abolished by low doses of the antagonist atropine - Muscarinic actions correspond to those of parasympathetic stimulation
122
Q

What can happen with larger doses of acetylcholine after an atropine blockade of muscarinic actions?

A

Acetylcholine can induce effects similar to those caused by nicotine

123
Q

What are the subtypes of muscarinic receptors?

A

3 main subtypes:- M1: salivary glands, stomach, CNS M2: heart M3: salivary glands, bronchial/visceral smooth muscle, sweat glands, eye M4/M5: CNS

124
Q
A

Year 2: LCRS (8 decks)

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