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Phase 2A Tom > ICS pharmacology > Flashcards

ICS pharmacology Flashcards

1
Q

What is pharmacology?

A

The study of the effects of drugs

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2
Q

What is pharmokinetics?

A
  • How the body affects the drug:
  • Absorbtion,
  • Distribution,
  • Metabolism
  • Excretion

ADME

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3
Q

What is pharmacodynamics?

A

How the drug affects the body

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4
Q

What is the main target for drugs?

A

Receptors

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5
Q

What are 3 things that naturally target receptors?

A
  • Neurotransmitters e.g., acetylcholine, serotonin
  • Autoacids (local hormones) e.g., cytokines, histamine
  • Hormones e.g., testosterone hydrocortisone
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6
Q

What are the different types of receptors?

A
  • Ligand-gated ion channels
  • G protein coupled receptors (most common)
  • Kinase-linked receptors
  • Cytosolic/nuclear receptors
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7
Q

Name some drug targets that aren’t receptors?

A
  • Enzymes
  • Transporters
  • Ion channels
    Most drug targets are proteins
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8
Q

What receptors do ligand-gated ion channels have?

A

Nicotinic ACh receptors

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9
Q

What receptors do G protein coupled receptors have?

A
  • M3R (muscarinic receptor)
  • Beta-2-adrenorecepto. Produces second messenger cyclic-AMP
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10
Q

What are kinase-linked receptors targets for?

A

Growth factors

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11
Q

What are cytosolic receptors targets for?

A

Steroids

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12
Q

What disease is the loss of nicotinic ACh receptors implicated in?

A

Myasthenia gravis

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13
Q

Define potency?

A

Measure of how well a drug works

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14
Q

What is a drug agonist?

A

A compound that binds to a receptor and ACTIVATES IT

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15
Q

What is intrinsic activity?

A
  • Emax of partial agonist/Emax of full agonist
  • Basically, how well a drug works against something that fully works
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16
Q

What is the difference between potency and efficacy?

A
  • Potency is which drug is more effective at the same concentration
  • Efficacy is with unlimited concentration which drug will be more effective
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17
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist

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18
Q

How do competitive antagonism work?

A
  • The reverse the effects of agonists by competing with them to bind with receptors.
  • This therefore prevents agonists from having as strong of an effect
  • They shift the curve to the right meaning more agonist is required for the same response
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19
Q

How does non-competitive antagonism work?

A
  • It binds to a receptor and prevents activation of the receptor. The same amount of agonist can still bind it will just be less effective
  • It shifts the curve right and down meaning even more agonist is required to illicit the same response
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20
Q

What is affinity?

A

How well a ligand/drug binds to the receptor
- Property shown by both agonists and antagonists

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21
Q

What is efficacy?

A

Describes how well a ligand/drug activates the receptor
- Only agonists show efficacy

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22
Q

What is allosteric modulation?

A
  • Binding of an allosteric ligand to a receptor can affect an agonists effect
  • Can change affinity and efficacy
  • Can be positive or negative
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23
Q

What is tolerance?

A
  • The reduction in drug effect over time
  • Seen with continuous, repeated high concentration of drug over time
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24
Q

How does tolerance occur?

A
  • Receptor can’t interact with G-protein
  • Receptor becomes internalised in vesicle of the cell
  • Receptor becomes degraded
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25
Q

Why is selectivity used to describe drug targeting than specificity?

A

Because no compound is truly specific

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26
Q

Give an example of a drug that is highly selective and one that is not?

A
  • Isoprenaline is a non-selective B-adrenoreceptor agonist it activates both heart (B1) and lung (B2) receptors
  • Salbutamol is a selective B”-adrenoreceptor and only activates lung (B2) receptors
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27
Q

Name a drug that targets enzymes?

A

NSAIDs

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28
Q

What are the actions of NSAIDs?

A
  • Analgesic
  • Anti-pyretic (reduces fever)
  • Anti-inflammatory
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29
Q

What is the action of NSAIDs?

A
  • They inhibit the COX enzyme
  • COX is responsible for the breakdown of arachidonic acid to prostaglandin H2 (PGH2)
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30
Q

How do NSAIDs inhibit COX?

A
  • They prevent arachidonic acid from reaching the active site of COX
  • They are antagonists, so they bind to the active site of COX
  • NSAIDs are competitive inhibitors
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31
Q

How is Aspirin different to other NSAIDs?

A

It irreversibly blocks the active site of COX resulting in irreversible inactivation

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32
Q

What are the two COX isomers and what do they do?

A
  • COX-1 found normally and widely around the body
  • COX-2 induced and found mainly in inflammation
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33
Q

Give an example of a selective and non-selective NSAID?

A
  • Aspirin is non-selective inhibits COX-1,2.
  • Celecoxib is COX-2 selective
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34
Q

What are ACE inhibitors?

A
  • They are angiotensin-converting-enzyme inhibitors
  • They are anti-hypertensive
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35
Q

How do ACE inhibitors work?

A
  • They prevent the conversion of angiotensin I to angiotensin I
  • This means there is less angiotensin II so less bind to angiotensin receptors (AT1)
  • This results in reduced vasoconstriction and thus
    hypertension as well as less aldosterone release further reducing
    hypertension
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36
Q

Name two ACE inhibitors?

A
  • Captopril
  • Enalapril
  • Both are competitive inhibitors and bind to ACE active site to prevent angiotensin I from binding
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37
Q

Give some examples of B-lactam antibiotics?

A

Penicillins, amoxicillin & cephalosporins

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38
Q

How do B-lactam antibiotics work?

A
  • They inhibit the biosynthesis of peptidoglycan bacterial cell walls
  • This is achieved by inhibiting the activity of certain enzymes
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39
Q

How are drugs inactivated?

A

-Most drugs are excreted by the kidneys
- Lipophilic drugs are not effectively removed
- Lipophilic drugs require Cytochrome P450 (addition of OH group) to make them soluble so they can be excreted by the kidneys
- Some drugs induce or inhibit cytochrome P450 to either be removed quickly or stay in the system for longer

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40
Q

What is summation?

A

When 2 drugs used at the same time both have the expected effect

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41
Q

What is synergism?

A
  • When using two drugs together makes both of the drugs more effective
  • For example, paracetamol and morphine
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42
Q

What is blockage

A
  • When one drug blocks the action of another
  • For example, salbutamol and non-selective beta blockers
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43
Q

What is potentiation?

A

When one drug makes the other more potent, but its potency stays the same

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44
Q

What is bioavailability?

A

How much of a drug taken is used. IV is always 100% but orally, this figure can change

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45
Q

Name some proton pump inhibitors (PPI)

A
  • Omeprazole
  • Lansoprazole
  • Pantoprazole
  • Rabeprazole
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46
Q

How do PPIs work?

A
  • Activated in acidic conditions
  • Inhibit acid secretion
  • PPIs act to irreversibly inactivate the proton pump (H+/K+ ATPase)
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47
Q

Name a loop diuretic?

A

Furosemide

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48
Q

How does Furosemide work?

A
  • It inhibits symporters
  • It inhibits the NKCC2 pump on the thick ascending part of the loop of Henle
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49
Q

How do you treat a paracetamol overdose?

A
  • If it has been less than 1 hour since OD give activated charcoal
  • If longer than this give intravenous N-acetylcysteine
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50
Q

Name some calcium channel blockers

A
  • Amlodipine
  • Verapamil
  • Diltiazem
    All used in the treatment of hypertension
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51
Q

How does Amlodipine work?

A
  • It blocks voltage dependant calcium channels found in cardiac muscle and vascular smooth muscle
  • This means there is less vasoconstriction useful for hypertension
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52
Q

Name some local anaesthetics

A
  • Lidocaine
  • Procaine
    They interrupt axonal neurotransmission.
53
Q

How do local anaesthetics work?

A
  • They block voltage dependant sodium channels thus preventing the neurons from depolarising.
  • Therefore, there is no action potential, so no pain signal is sent to the brain
54
Q

What is an adrenergic receptor?

A

Receptors that react to noradrenaline and adrenaline (sympathetic nervous system)

55
Q

What is a cholinergic receptor?

A

Receptors that react to acetylcholine (parasympathetic nervous system)

56
Q

Name 3 things that define the somatic nervous system

A
  1. Single neuron between CNS and skeletal muscle
  2. Innervates skeletal muscle
  3. Leads to muscle excitation (not inhibition)
57
Q

Name 3 things that define the autonomic nervous system

A
  1. Two-neuron chain
  2. Smooth muscle, cardiac muscle, glands, (GI neurons)
  3. Leads to excitation or inhibiton
58
Q

Is the postganglionic neuron closer to the effector organ in the sympathetic or parasympathetic nervous system

A

Parasympathetic

59
Q

How are the sympathetic and parasympathetic nervous systems similar (in terms of neurotransmitters and receptors used)?

A

Acetylcholine acts on nicotinic receptors in preganglionic neurons

60
Q

What receptors are acted on in postganglionic neurons in the parasympathetic system?

A

Acetylcholine acts on muscarinic receptors

61
Q

What receptors are acted on in postganglionic neurons in the sympathetic system?

A

Noradrenaline acts on alpha and beta receptors

62
Q

What are some exceptions to the usual receptors used in the parasympathetic and sympathetic systems

A
  • Acetylcholine is released at sympathetic postganglionic termini (sweat glands)
  • Nitric oxide is released from parasympathetic postganglionic termini in blood vessels
63
Q

What are the 5 types of muscarinic receptors?

A

M1- Brain
M2 - Heart
M3- all organs with parasympathetic innervation
M4- mainly CNS
M5- mainly CNS
All are found outside the cell and activate intracellular processes through G-proteins

64
Q

What do M3 receptors do when stimulated in the respiratory system?

A
  • Produce mucus
  • Induces smooth muscle contraction
65
Q

What do M3 receptors do when stimulated in the GI tract?

A
  • Increase saliva production
  • Increase gut motility
  • Stimulates biliary secretion
66
Q

What do M3 receptors do when stimulated in the skin?

A
  • Only place where sympathetic system releases ACh
  • Stimulation causes sweating
67
Q

What do M3 receptors do when stimulated in the urinary system?

A
  • Contracts detrusor muscle
  • Relaxation of internal urethral sphincter
68
Q

What do M3 receptors do when stimulated in the eye?

A
  • Causes myosis
  • Increases drainage of aqueous humour
  • Secretion of tears
69
Q

What do pilocarpine drops do?

A
  • M3 agonists in the eye
  • Increases drainage of aqueous humour
  • Reduces ocular pressure
70
Q

What is atropine used for?

A
  • Is a muscarinic antagonist
  • used to increase heart rate, treat bradyarrhythmias and AV node block
71
Q

What are some direct-acting Cholinergic agonists, and how do they work?

A
  • Carbachol (pupil constriction)
  • Bethanechol (increases smooth muscle tone in the GI tract)
  • Pilocarpine (stimulates saliva secretion)
    Work by mimicking ACh and bind to receptors
72
Q

What are some indirect-acting Cholinergic agonists, and how do they work?

A
  • Neostigmine ( reverse anaesthesia, myasthenia gravis)
  • Donepezil, Rivastigmine (Alzhimers)
    They inhibit acetylcholine esterase, so it stays in the synapse for longer
73
Q

Name some Muscarinic antagonists and how do they work?

A
  • Atropine, Scopolamine, Belladonna alkaloids (treat bradycardia, diarrhoea, bladder spasms; dilate bronchi, reduce secretions, dilate pupils; as sedatives, respectively)
  • Compete with ACh for binding to the muscarinic receptor
74
Q

Name some Nicotinic antagonists and how they work

A
  • Curare, Pancuronium (relax skeletal muscles during surgery)
  • Compete with ACh for binding to the nicotinic receptor
75
Q

What happens in Myasthenia Gravis?

A
  • Antibody is produced that binds to ACh receptors
  • Prevents ACh from binding at skeletal muscle
  • Results in muscle weakness
  • Treatment is anti-cholinesterase
76
Q

What is the pathway from L-dopa to adrenaline?

A

L-dopa> Dopamine > Noradrenaline> Adrenaline

77
Q

What do Alpha 1 adrenergic receptors do?

A
  • Vasoconstriction
  • Increase in peripheral resistance
  • Increased blood pressure
  • Increased closure of internal sphincter of the bladder
78
Q

What do Alpha 2 adrenergic receptors do?

A
  • Mixed effects on smooth muscle
  • Inhibition of noradrenaline release
  • Inhibition of ACh release
  • Inhibition of insulin release
79
Q

What do Beta 1 receptors do?

A
  • Positively chronotropic (heart rate)
  • Positively Ionotropic (force of contraction)
  • Increased release of renin
  • Increased lipolysis
80
Q

What do Beta 2 receptors do?

A
  • Vasodilation
  • Decreased peripheral resistance
  • Bronchodialtion
  • Increased glycogenolysis in the liver and muscle
  • Increased glucagon release
  • Relaxation of uterine smooth muscle
81
Q

When would Alpha 1 agonists be used?

A
  • Noradrenaline is given IV for shock
  • Also used to overcome anaesthetic agents
  • Adrenaline can be used to overcome anaphylaxis
  • Xylometazoline can be used as a nasal decongestion
82
Q

Name an Alpha 2 agonist.

A
  • Clonidine can be used in ADHD to help concentration`
83
Q

Name some Alpha 1 antagonists.

A
  • Doxazosin used to lower blood pressure (not commonly used)
  • Phenoxybenzamine used to treat pheochromocytoma ( catecholamine secreting tumour)
84
Q

What do Beta 1 agonists do?

A
  • Tachycardia
  • Increase in stroke volume
  • Renin release
  • Lipolysis and hyperglycemia
85
Q

What do Beta 1 antagonists (Beta-blockers) do?

A
  • Reduce heart rate
  • Reduce stroke volume
    E.g., Carvedilol, Bisoprolol, Atenolol
    Caution in asthma if non-selective beta blocker
86
Q

How can glucagon be useful in beta-blocker poisoning?

A
  • It bypasses the beta-adrenergic receptor site and increases heart rate and myocardial contractility
87
Q

What does Beta 2 agonism do in the bronchi?

A

Bronchodilation

88
Q

What does Beta 2 agonism do in the bladder wall?

A

Inhibits micturtion

89
Q

What does Beta 2 agonism do in the uterus?

A

Inhibits labour

90
Q

What does Beta 2 agonism do in smooth muscle?

A

increases contraction speed

91
Q

What does Beta 2 agonism do in the pancreas?

A

Insulin and glucagon secretion

92
Q

When is a beta 2 agonist useful?

A
  • Asthma/COPD (side effect hyperglycemia and tachyarrhythmia)
  • Can be used to delay labour
    Salbutamol is an example
93
Q

What is the bioavailability of morphine taken orally?

94
Q

10mg of morphine is taken orally. What is the equivalent dose if given parenterally?

95
Q

Give 5 side effects of opioid use

A
  1. Respiratory depression.
  2. Sedation.
  3. Nausea.
  4. Vomiting.
  5. Constipation
96
Q

Describe the dose-response curve for morphine

A

As dose increases response increases. This association is initially rapidly and then the graph plateaus. It is not sigmoidal

97
Q

What it do you give to reverse a morphine overdose

A

Naloxone - its an antagonist to morphine

98
Q

What it do you give to reverse a morphine overdose

A

Naloxone - it’s an antagonist to morphine

99
Q

Briefly outline how opioids work.

A

They Inhibit the release of apin transmitters at the spinal cord and midbrain

They modulate the pain perception at higher centres, to create euphoria

100
Q

What is the main opioid receptor, that all the drugs we currently use act on?

A

μ (Kappa) receptors
(MOP)

101
Q

Name other receptors that morphine been found to bind to. Agonism of what receptor has been known to cause mental depression instead of euphoria?

A

after delta (DOP) and kappa (KOP) receptors.

Kappa agonists cause mental depression instead of euphoria

102
Q

Where may you find kappa μ receptors (MOP) in the body?

A
  • Midbrain
  • Spine
  • GI tract - can get constipated with opioid use
  • Breathing centre - it communicates using opioid receptors, opioid use can cause respiratory depression
103
Q

Why can giving Buprenorophine be safer?

A

Because it is only a partial agonist, so only reaches up to 50% response.

104
Q

Outline the potentsies of Diamorphine and pethidine, relative to morphine.

A

Relative potencies:
- Diamorphine (Heroin)- 5mg (twice as potent as morphine)
- Morphine - 10mg
- Pethidine - 100mg (10 times weaker than morphine)

Diamorphine - Heroin:
- More potent and faster acting (crosses blood-brain barrier quickly)

105
Q

Name some statistics regarding adverse drug reactions

A
  • Account for 6-7% of hospital admissions
  • 2% admitted will die
  • 5th most common cause of hospital death
  • 60% preventable
106
Q

What are the 5 types of adverse drug reactions?

A
  • Augmented
  • Bizarre
  • Chronic
  • Delayed
  • End of use

ABCDE (Rawlins-Thompson)

107
Q

What is an augmented drug reaction?

A
  • Most common
  • An extension of the clinical effect
  • Dose related
  • Those with renal or hepatic impairment more at risk due to elimination difficulties
    E.g., diuretic causing dehydration, anticoagulant causing bleeding
108
Q

What is a bizarre drug reaction?

A
  • Unexpected
  • Not dose related and not from known pharmacological action
  • Mostly immunological mechanisms
  • Those with history of allergy’s more at risk
    E.g., Heparin causing hair loss
109
Q

What is a chronic drug reaction?

A
  • Occurs after long term therapy
  • May not be immediately obvious with new medicines
    E.g., Steroids predispose to hyperglycaemia may result in diabetes
110
Q

What is a delayed drug reaction?

A
  • Occurs a long time after the treatment (many years, common to be 20-30 years)
    E.g., Neoplasia, Teratogenesis (congenital malformation in foetus) after taking thalidomide
111
Q

What is an end of use drug reaction?

A
  • Relatively long-term use (days/weeks)
  • Withdrawal reactions
112
Q

What are some important questions to ask when trying to identify what type of drug reaction has occured?

A
  • Is it predictable? Does it seem dose related? (augmented)
  • Is there a history of allergy in family or patient (bizarre)
  • Has the patient been using the medication for a long time (chronic)
  • What drugs has the patient taken in the past (delayed)
  • Is the patient withdrawing from a medicine (end of use)
113
Q

What are patient risk factors for an adverse drug reaction?

A
  • Gender (women more at risk)
  • Elderly
  • Neonates
  • Polypharmacy
  • Genetic predisposition
  • Allergies
  • Hepatic/renal impairment
  • Adherence problems
114
Q

What are drug risk factors for an ADR?

A
  • Steep-dose curve
  • Low therapeutic index
115
Q

What are the most common drugs to have ADR’s?

A
  • Antibiotics
  • Anti-neoplastics
  • Cardiovascular drugs
  • Hypoglycaemics
  • NSAIDS
  • CNS drugs
116
Q

What are the most common systems to be affetcetd?

A
  • GI
  • Renal
  • Haemorrhagic
  • Metabolic
  • Endocrine
  • Dermatologic
117
Q

What is the yellow card scheme?

A
  • Was introduced in 1964
  • Collects spontaneous reports
  • Collects suspected adverse reactions
118
Q

When would you fill out a yellow card?

A
  • All suspected reactions for, herbal medicine and black triangle drugs
  • All serious suspected reactions for, established drugs, vaccines and drug interactions
119
Q

What does a black triangle drug mean?

A
  • A drug that contains a new active substance
  • Is a biological medicine- a vaccine or medicine derived from plasma
  • Has been given conditional approval

This means the company markets the medicine is required to carry out additional tests

120
Q

What are the 4 pieces of information to include on a yellow card?

A
  1. Suspected drugs/drugs
  2. Suspected reaction
  3. Patient details
  4. Reporter details
121
Q

Give an example of a proton pump inhibitor.

A

Omeprazole, lansoprazole

122
Q

Give an example of a statin.

A

Simvastatin.

123
Q

Give an example of an ACE inhibitor.

A

Enalapril.

124
Q

Give an example of a COX inhibitor.

A

Aspirin and paracetamol

125
Q

Give an example of a β2 adrenoceptor agonist.

A

Salbutamol.

126
Q

Give an example of a β1 adrenoceptor blocker.

127
Q

Give an example of a Ca2+ channel blocker.

A

Amlodipine.

128
Q

Give an example of a broad spectrum antibiotic.

A

Amoxicillin.

129
Q

Give an example of an opiate analgesic.

Phase 2A Tom (15 decks)

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