3. PHARMACOLOGY Flashcards
1
Q
what r the two main routes of administration
A
enteral and parenteral
2
Q
define enteral administration
A
through gastro-intestinal tract
3
Q
define parenteral administration
A
not through GI tract
4
Q
two examples of enteral administrations
A
oral and rectal suppositary
5
Q
5 examples of parenteral administration
A
subcutaneous, intramuscularr, intravenous, sublingual, inhalers
6
Q
what routes of administration have a systemic effect
A
enteral and parenteral
7
Q
what two administrations have a local effect
A
transdermal (patches) and topical creams
8
Q
define agonist using the terms affinity, efficacy and what does it do to the receptor
A
full affinity
full efficacy
ligand that increases activation of the receptor
9
Q
define antagonist using the terms affinity, efficacy and what does it do to the receptor
A
full affinity
zero efficacy
ligand that decreases activation of the receptor
10
Q
define inverse agonist and compare it to an antagonist
A
binds to receptor and always has an opposite response to agonist
antagonist= can have a neutral response (not necessarily opposite)
11
Q
define affinity
A
how well a ligand binds to a receptor
12
Q
define efficacy (in terms of ligand and receptor and in terms of drug)
A
how successful a ligand ACTIVATES its receptor
maximum effect a drug can have on the body
13
Q
compare graph shape for log conc and conc
A
log conc= sigmoidal, conc= linear
14
Q
what is EC50
A
value of 50% response on log conc graph
15
Q
what is Emax
A
maximal efficacy
16
Q
define potency
A
relative strength of the drug
17
Q
if a drug is more potent what happens to its dose
A
more potent drugs require lower doses for a response
18
Q
define selectivity and give an example
A
acts on a subtype of a target
selective beta blocker bisoprolol only acts on B1 heart receptors (not B2 in lungs)
19
Q
define specificity and what does low specificity cause
A
receptors ability to response to a single ligand
low= side effects
20
Q
what 4 things can affect drug response
A
efficacy, affinity, number of receptors, signal amplification
21
Q
where do competitive inhibitors bind and how do they affect affinity and efficacy
A
binds at the active site
decreases efficacy reversibly
affinity is unchanged
22
Q
where do non-competitive inhibitors bind and how do they affect affinity and efficacy
A
binds away from the active site which changes its shape
decreases efficacy irreversible
affinity is reduced
23
Q
explain the Dose/response curve for competitive inhibitors (shift direction and use affinity, potency and efficacy to describe the changes)
A
curve shifts right
drug has less affinity and less potency and less efficacy
24
Q
explain the Dose/response curve for non-competitive inhibitors (shift direction and use affinity, potency and efficacy to describe the changes)
A
curve shifts right and down
drug has less affinity, less potency and less efficacy
25
what is bioavailability and what route has 100% of this
how much drug is uptake systemically for effect
IV
26
what is therapeutic range and what does a narrow range mean
upper and lower bounds of safe doses of a drug
the narrower the range, the more care is required in dispensing the drug (more likely to over or underdose)
27
what are the 2 names type of receptors in cholinergic pharmacology and what type of receptors r they
nicotinic= ion channel
muscarinic= G-protein couples
28
what r the 4 drug targets
receptors
enzymes
ion channels
transporters
29
give an example of a G-protein coupled receptor and how it works
beta adrenoreceptor
muscarinic receptors within proteins produce 2nd messenger cAMP which produce further reactions
30
what can an imbalance of NTM/ receptors lead to and give an example
pathology
decreased dopamine causes Parkinson's
31
give an example of a ligand gated receptor and how it works
nicotinic ACh
binding opens pores to allow cations to move into cells
32
give an example of a drug that targets receptors (2)
beta blockers, angiotensin receptor blockers
33
explain the selectivity of aspirin and celecoxib
non selective as it acts on COX 1 and 2, celecoxib is more selective as it only acts on COX 2
34
what is another example of a drug that targets enzymes
ACE inhibitor
35
give two examples of NSAIDs
explain how NSAIDs work (ending with what 3 symptoms it reduces) and what type of inhibition is this
NSAIDs eg aspirin/ ibuprofen: inhibit COX 1 to inhibit breakdown of arachnoid acid to prostaglandin H2 which acts as a painkiller and reduces fever/ inflammation
NSAIDs= competitive inhibition
36
give an example of a drug that targets ion channels
calcium channel blocker
37
how does lidocaine target ion channel
local anaesthesia eg lidocaine
blocks Na+ channels so no action potential is generated for pain transmission
38
how do calcium channel blockers target ion channels, give an example and what it is prescribed for what is their overall effect
calcium channel blocker eg amlodipine for HPT
blocks voltage Ca2+ channels in muscle to prevent influx of calcium ions and an action potential, stopping muscle vasoconstriction
39
what drug targets transporters, give an example and how does it work
proton pump inhibitors eg lansoprazole
inhibit parietal cells H+/K+ATPase pump to decrease stomach acid
40
define pharmacodynamics
the effect of the drug on the body
41
define pharmacokinetics
the effect of the body on the drug
42
what r the three aspects of Pharmacodynamics
affinity, potency and efficacy
43
explain ADME in brief detail
absorption: route of entry, bioavailability of drug
distribution: based on chemical properties eg hydrophilicity can it cross barriers eg BBB
metabolism: via kidney or phase 1&2 in liver
excretion: as urine/ faeces
44
what r the 4 aspects of pharmacokinetics
absorption, distribution, metabolism, excretion (ADME)
45
name 4 factors that affect distribution in pharmacokinetics
affected by blood flow, molecular weight, how lipophillic/phobic a drug is, natural barriers in body eg BBB
46
what r the 3 locations of metabolism
GI tract, hepatic or renal
47
what is metabolised in the GI tract and how
food
mechanical and physical digestion
48
what is metabolised in renal metabolism
simple, already soluble molecules which r easily to pee out directly
49
what is metabolised in hepatic metabolism and how
complex, hydrophobic molecules
undergo phase 1 and/or phase 2 reactions
50
what type of reaction is phase 1 metabolism, what is its aim and what enzyme foes it involve
non-conjugation
aims to slightly increase hydrophilicity
requires microsomal enzymes eg CYP 450
51
what type of reaction is phase 2 metabolism and what is its aim
conjugation
adds functional groups eg glucuronidation to massively increase hydrophilicity
52
what r the three types pf neurotransmission systems
parasympathetic, sympathetic and motor
53
is parasymp autonomic or somatic, name the neurotransmitter at post and pre synaptic neurone, name the final receptor
autonomic (self-governing)
presynaptic acetylcholine
postsynaptic acetylcholine
muscarinic Ach receptor
54
is symp autonomic or somatic, name the neurotransmitter at post and pre synaptic neurone, name the final receptor
autonomic (self-governing)
presynaptic acetylcholine
postsynaptic noradrenaline
Noradrenaline receptor
55
give an example of motor NS, is it somatic or voluntary, what neurotransmitter is involved and name the final receptor
skeletal msucle
somatic
Ach post and presynaptic
nicotinic ACh receptor
56
what are the two main receptors in cholinergic pharmacology and where r these usually found
nicotinic- usually presynaptic
muscarinic-usually postsynaptic
57
location of M1, M2, M3 receptors and what pharmacology is this
M1= brain
M2= heart
M3= lungs
cholinergic
58
name the 5 steps in the cycle of the ACh neurotransmitter lifecycle
synthesis of neurotransmitter
storage in vesicles
release into synapse
breakdown
reuptake
59
what 3 drugs can act at the NMJ
curare, botulinum toxin, ACh-ase inhibitor
60
what is curare's action at the NMJ
curare: antagonist to nicotinic ACh receptor and prevents ACh from binding so it relaxes muslces
61
what is botulinum toxin's action at the NMJ
binds to presynpatic vesicles and inhibits ACh release= paralysis
62
what is ACh-ase inhibitors action at NMJ and what is this used for
causes less breakdown of ACh so increased ACh concentration at NMJ
used in dementia medication
63
what can excessive ACh stimulation cause and what r the symptoms of this
cholinergic crisis
salivation, lacrimation, urination, defecation, GI distress, emesis (vomiting)- SLUDGE
64
what is the issue in myasthenia gravis and how does the treatment work
disrupted Ach transmission at NMJ
Tx: acetylcholinase inhibitors eg rivastigmine (stops breakdown of acetylcholine)
65
what 4 receptors r involved in adrenergic pharmacology
alpha 1&2 receptors and beta 1&2 receptors
66
what do alpha 1 receptors do
on vessel sphincters for vasoconstriction
cause bladder constriction
cause pupil dilation
67
what is an example of a alpha 1 blocker, what is it first line med for and what is its mechanism of action
alpha 1 blocker= tamsulosin= 1st line medication for benign prostatic hyperplasia
mechanism of action: relaxes bladder neck, allowing easier urine flow
68
where r alpha 2 receptors found and what do they do
receptors in brainstem and periphery
inhibit sympathetic activity so they reduce BP
69
where r beta 1 receptors found
heart
70
what is the effect of beta 1 receptors agonists and give an example
increase inotropy and chronotropy of cardiac contraction
eg dobutamine
71
what is the effect of beta 1 receptors antagonists and give an example
decrease inotropy and chronotropy
eg bisoprolol (beta blocker)
72
when r beta blockeres contraindicated
asthma
73
where r beta 2 receptors found
lungs
74
what do beta 2 receptor agonists cause and give 2 examples
bronchodilation of airways
eg SABAs (salbutamol) prescribed for COPD and asthma
eg LABA in asthma
75
give an example of a cardioselective drugs and define this
beta blocker drugs that only act on cardiac tissue
76
what types pf hypersensitivity r immediate and delayed
1,2,3 r all immediate
4 is delayed
77
explain the ABCDE of adverse drug reactions
A- augmented (common/ expected eg ACE-I cough)
B- bizzarre
C- chronic use
D- delayed (type 4 hypersensitivity)
E- end of use (eg opioid withdrawal)
78
what should be done if a patient has an adverse drug reaction
report to MHRA using the Yellow Card Scheme
79
differentiate between tolerance and dependance
tolerance is physiological craving (body wants it because its receptors have been desensitised to it so thee need a higher dose)
dependance is psychological craving (craving euphoria)
80
examples of opiates (4)
morphine, diamorphine (heroin), codeine, pethidine
81
where r opioid receptors found (4)
spinal cord, midbrain, GI tract, breathing centre
82
how do opiates work (3)
1. binds to opiate receptors in spinal cord and midbrain
2. this inhibits release of pain neurotransmitters
3. this blocks the descending pain transmission
83
when r opiates used (2) and give an example
used in chronic sever pain relief eg cancer pain
84
3 main side effects of opiates
respiratory depression, constipation and vomiting
85
what is the oral bioavailability of morphine and how does this relate to IV vs oral doses
morphine has 50% oral bioavailability (oral dose is twice as much as an IV dose)
86
list potency of three opiates in regard to one another and their dose
potency: 5mg diamorphine= 10mg morphine= 100mg pethidine
87
what can opiate overdose cause and what is treatment for this and how is this administered
respiratory DEPRESSION
treatment: naloxone by IV
88
what is typically prescribed for severe pain
opioid analgesia eg morphine and diamorphine
89
what is typically prescribed for moderate pain
tramadol or moderate opiates eg codeine
90
what is typically prescribed for mild pain
weak analgesics eg paracetamol NSAIDs (ibuprofen/ naproxen)
91
what are the 4 types of pain
acute (nociceptive)
cancer
neuropathic (nerve pain)
chronic non cancer (pain 3+ months eg fibromyalgia)
92
what r the 2 main complications with paracetamol overdose
rapidly acute liver failure
shutdown of basic physiological systems eg shock which can lead to death
93
What is the acute ascending pain pathway
1. nociceptors detect pain
2. impulse through C or A delta fibres to dorsal root ganglion in spinal cord
3. second order neurone to thalamus via ascending lateral spinothalamic tract
94
what is the acute descending pain pathway
1. cortex to thalamus
to periaqueductal grey in midbrain
3. to rostral ventral medulla
4. signal to spinal cord and activation of the opiate system to suppress pain
95
what are the 4 physiological processes regarding pain
transduction
transmission
modulation (excitation or inhibition of pain)
perception
96
explain paracetamol metabolism and what is significant about the 5%
undergoes phase 2 hepatic metabolism 95%, phase 1 for 5%
the 5% that undergoes CYP450 metabolism in phase 1 reaction is still hepatotoxic
97
explain paracetamol metabolism in an overdose
in cases of overdose, phase 2 is too saturated so paracetamol is shunted down the phase 1 pathway= build up of NAPQI (product of phase 1 metabolism of paracetamol)
this leads to hepatotoxicity and can cause liver failure
98
what are the indications for anticoagulant drugs (5)
DVT/ PE (deep vein thrombosis/ pulmonary embolism)
atrial fibrillation
prosthetic valves
bleeding disorders
ischaemic stroke/ MI
99
mechanism of DOACs, 2 examples and what do they stand for
Direct acting oral anticoagulants
inhibit factor 10a
eg apixiban, rivaroxaban
100
mechanism of warfarin
inhibit 10, 9, 7, 2 (vitamin K dependant factors)
101
mechanism of alteplase
fibrinolytic, activates plasmin to digest the fibrin mesh
102
mechanism of antiplatelets and 2 examples
inhibits P2Y12 which affects the primary platelet plug
eg clopidogrel and ticagrelor
103
mechanism of LMWPs and what do they stand for
inhibit factor 10 and thrombin
Low molecular weight heparins
104
NAID 2 examples
eg ibuprofen, naproxen
105
what r NSAIDs prescribed for generally
weak analgesics for mild pain
106
mechanism of NSAIDs
inhibits arachidonic acid pathway COX1 and COX 2
107
what is COX 1 pathway involved in and what is a side effect of inhibiting COX 1
involved in prostaglandin synthesis
side effect is peptic ulcer disease (gastric ulcers) because prostaglandin protects the gastric mucosa
108
what is COX 2 pathway involved in and give an example of a specific COX 2 drug
pathway causes inflammation when activated
eg celeoxib
109
how do diuretics work
reduce the volume of water reabsorbed in the kidneys
110
what r the three types of diuretic drugs
loop diuretic, aldosterone antagonist and thiazide diuretic (LooT AlAn)
111
where do loop diuretics act, what does it inhibit and give an example
acts on ascending loop of Henle
inhibits Na-K-Cl co transporter= prevents their uptake= water doesn’t move with them
eg furosemide
112
what r aldosterone antagonists also known as
K+ sparing diuretic
113
where do aldosterone antagonist diuretics act, what does it cause and give an example
acts on aldosterone receptors of the collecting duct
inhibits reabsorption of sodium and water in distal convoluted tubules which increases sodium excretion and retains potassium
eg spironolactone
114
side effect of spironalactone
can cause hyperkalamia
115
where do thiazide diuretics act, what does it do and give two examples
acts on distal convoluted tubules
inhibits Na-Cl cotransporter causes less sodium to be absorbed which absorbs less water
eg bendroflumethiazide and indapamide
116
name two side effect of ACE inhibitors and why they occur
main side effect= dry cough due to bradykinin accumulation
other side effect= worsens kidney function because it dilates afferent glomerular arteriole
117
action of ACE inhibitor, mechanism of action and 1 example
anti-hypertensive by blocking conversion of angiotensin 1 to 2 which prevents aldosterone production eg ramipril
118
action of calcium channel blockers, 2 examples and side effect
anti-hypertensive eg amlodipine, verapamil
side effect= ankle swelling (can be mistaken for heart failure)
119
action of proton pump inhibitor and example
reduces acidity of GI lumen by reducing acids secretion by irreversibly inhibiting H+/K+ ATPase pump in gastric parietal cells eg lansoprazole
120
side effect of antihistamines and beneficial side effect of antihistamines
side effects: older ones can cross the BB and cause sedation
many H1 receipts in the vomitign centres so they can acts as anti-emetics
121
action of antihistamines
H1 receptors antagonist
prevent release of histamine from storage granules in mast cells
122
side effect of long term PPI use
increase risk of fractures in the elderly
123
Effect of sympathetic NS (7) (think heart, lungs, GI, mouth, bladder, skin, arteries)
increased heart rate and cardiac output
vasoconstriction
bronchodilation
reduce GI motility and reduced GI secretions
reduced bladder detrusor activity
increased sweating
reduced salivation
124
Effect of parasympathetic NS (5) (think heart, arteries, lungs, GI, bladder)
decreased heart rate and cardiac output
vasodilation
bronchoconstriction
increased digestion
increased bladder detrusor
