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phar24 > week 10 > Flashcards

week 10 Flashcards

1
Q

5 signs of inflammation

A

heat, redness, swelling, pain, loss of function

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2
Q

what are two key pro-inflammatory mediators

A

prostaglandins & leukotrienes = produce inflammation

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3
Q

list the five major groups of anti-flammatory drugs

A
  1. cyclo-oxygenase inhibitors (NSAIDs)
  2. glucocorticoids
  3. antirheumatic drugs (DMARDs) - arthritis
  4. cytokines modulators & other biological agents (bDMARDs)
  5. others that do not fit in the above groups (antihistamines & other drugs used to control gout)
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4
Q

why inflammatory drugs used so extensively

A

because inflammation is involved in almost all diseases and in some cases can be the cause

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5
Q

steroidal define and examples

A
  • relates to steroidal hormones and their effects
  • steroidal hormones comes from cholesterol
  • sex hormones, glucocorticoids, mineralocorticoid
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6
Q

are cyclo-oxygenase (COX) inhibitors steroidal?

A

no they are non-sterodial anti-inflammatory drugs (NSAIDS)

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7
Q

what are NSAIDs used to treat & are they chemically related

A

minor aches & pains

they are chemically unrelated

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8
Q

what 3 properties do NSAIDs carry

A

analgesic (decrease pain), antipyretic (decrease fever) & anti-inflammatory properties

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9
Q

examples of NSAIDs

A

e.g., diclofenac (voltaren) & naproxen & ibuprofen & celecoxiib & melocicam, aspirin (irreversible)

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10
Q

what is the NSAIDs target

A

an enzyme COX1 = homodimer (two together)

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11
Q

the usual product of COX1 & the action it leads to

= this is without the drug interference so normal bodily functions

A

arachidonic is the endogenous substrate

prostaglandin (product) –> toboxon A2 –> platelet activation/aggregation = blood clot/thickening (inflammation)

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12
Q

endogenous substrate of COX1 enzyme

A

arachidonic acid

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13
Q

affect of the NSAIDs drug e.g., aspirin

A
  • aspirin causes irreversible inhibition = cause a covalent bond in the enzyme COX1 preventing the production of prostaglandins = decrease platelet aggregation = thins the blood
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14
Q

difference between COX-1 & COX-2

A
  • both produce prostaglandins from arachidonic acid

- COX-2 has a side pocket = were able to make drugs cox-2 selective = those drugs have an ending ‘coxib’ & are bulkier

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15
Q

mechanism of action of NSAIDs

A

= inhibit synthesis of prostaglandins by inhibiting COX enzymes

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16
Q

what is the target of prostaglandins & what specific superfamily

A

G protein-coupled receptors = then the second messengers etc

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17
Q

the analgesic effect of NSAIDs

A

= decreased production of prostaglandin: less sensitisation of nocieceptive nerve ending to inflammatory mediators such as bradykinin & 5-hydroxytryptamine (5-HT, serotonin)

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18
Q

the anti-inflammatory action due to NSAIDs

A

reduces vasodilation and, indirectly, oedema by decreasing prostaglandin E2 and prostacyclin synthesis

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19
Q

the antipyretic effect due to NSAIDs

A

NSAIDs prevents the release of prostaglandins by interleukin-1 in the CNS, where prostaglandins elevate the hypothalamic set point for temperature control. therefore preventing fever

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20
Q

difference between COX-1 & COX-2 inhibition in terms of effect

A

1 - impaired gastric protection, antiplatelet effects = gastrointestinal tract

2- more anti-inflammatory action, analgesic action = reduce the risk of gastrointestinal ulceration & upper gastrointestinal bleeding

both - reduction in glomerular filtration & reduction in renal flow

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21
Q

route of administration of NSAIDs

A

topical (cream), enteral (via gastrointestinal tract through tube) & parenteral (injection)

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22
Q

site of absorption of NSAIDs

A

stomach & small intestine (presence of food & antacids (neutralises stomach acid) delays absorption)

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23
Q

distribution of NSAIDs

A

highly bound to plasma protein. wide spread including breast milk & cross placenta

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24
Q

metabolism

A

liver

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25
Q

distribution of NSAIDs

A

highly bound to plasma protein (doesn’t necessarily mean low VD) . wide spread including breast milk & cross placenta

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26
Q

metabolism of NSAIDs

A

liver

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27
Q

excretion NSAIDs

A

kidney

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28
Q

define topical route

A

application of medication to the surface of the skin or mucous membrane of the eye, ear, nose, mouth, vagina, etc

e.g., gels, lotions

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29
Q

define enteral route

A

administration involves the GIT. methods of administration include oral, sublingual (dissolving the drug under the tongue) & rectal

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30
Q

define parenteral administration

A

introduce drugs to the body by a different route from enteral (GIT). the most frequently used parenteral routes are intravenous route (IV), intramuscular route (IM), and subcutaneous route

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31
Q

is body concentration the same as plasma concentration

A

no

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32
Q

what are the two steroid hormones

A

glucocorticoids & mineralocorticoids

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33
Q

what are glucocorticoids synthesised from

A

cholesterol

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34
Q

main effects of glucocorticoids

A
  • resistance to stress
  • metabolic effects
  • anti-inflammatory
  • immunosuppressant
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35
Q

where are glucocorticoids made

A

zona fasciculate in the adrenal gland

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36
Q

what controls the release of glucocorticoids

A

hypothalamic and pituitary control = negative feedback

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37
Q

the two rhythms influence glucocorticoid release

A
  • circadian rhythm (dark-light sleep)

- ultradian rhythm (CRH & ACTH)

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38
Q

what are the effects of glucocorticoids

A

anti-inflammatory, immunosuppressant & metabolic effects

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39
Q

glucocorticoids effect in inflammation

A

they are highly effective in controlling inflammation, but largely limited by their adverse effects

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40
Q

examples of glucocorticoids

A 
hydrocortisone (cortisol)
dexamethasone 
betamethasone 
triamcinolone 
fludrocortisone
  1. short-acting
  2. intermediate acting
  3. long acting

= eliminated quite quickly for the most time

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41
Q

mechanism of action of glucocorticoids

A

nuclear effect: they make our bodies synthese more of the protein annexin-1 = inhibits phospholipaseA2 = inhibits the cascade from the top and the arachidonic acid is not synthesised

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42
Q

in what ways does glucocorticoids modulate gene transcription

A

gene active hormones:

  • promotes or inhibits synthesis of specific mRNA
  • initiation of new protein synthesis (transactivation)
  • blocking of protein production (transrepression)

= alters the required time to produce an effect

non genomic rapid actions = vasorelaxation & maybe PGE2 release inhibition

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43
Q

what is the target for glucocorticoids

A

nuclear receptors

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44
Q

some examples of NSAIDs adverse effects & understanding why (off or on target??)

A 
- nausea, diarrhoea, headache 
REMEMBER THIS ONE 
- dyspepsia, GI ulceration & bleeding (inhibit COX1, e.g., inhibit platlete aggregation)
- raised liver enzymes (Diclofenac) 
- salt & fluid retention 
- hypertension
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45
Q

some examples of corticosteroids adverse effects & understanding why (off or on target??)

A
  • adrenal suppression (if the drug is removed at once so forgets how to signal cortisol it self) = low blood pressure etc
  • dyspepsia (indigestion)
  • hypokalaemia, hyperglycemia (effects processing of carbs)
  • myopathy, msucle weakness & wasting (protein synthesis)
  • sodium & water retention, oedema
  • hypertension
  • fat distribution
  • skin atrophy, bruising (due to increase bleed), acne, hirsutism
  • diabetes, osteoporosis, fractures
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46
Q

what two agonists decrease acid secretion

A

Prostaglandins E2 and I2 & somatostatin

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47
Q

absolute compared to relative conditions

A

absolute condition is where if u have that condition you should no take the drug, relative is where the doctor is to balance out the risks and benefits

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48
Q

what properties does paracetamol have

A

analgesic & antipyretic properties & very weak anti-inflammatory effects = not suitable substitute for NSAIDs in chronic inflammatory conditions such as rheumatoid arthritis

49
Q

paracetamol mechanism of action

A

proposed inhibition of COX isoform mainly available at the CNS, however, alternative explanations have been proposed

50
Q

what can acute overdose of paracetamol cause

A

severe hepatic damage

51
Q

GI adverse effects from paracetamol

A

low incidence of GI adverse affects

52
Q

what is the autonomic nervous system a division of

A

PNS

53
Q

what are the two divisions of the Autonomic Nervous System

A
  1. Sympathetic

2. Parasympathetic

54
Q

what does the ANS link

A

link between the CNS & peripheral organs

55
Q

what does the ANS regulate

A
  • contraction & relaxation of vascular & visceral smooth muscle
  • all exocrine & certain endocrine secretions
  • the heartbeat
  • energy metabolism (especially in the liver & skeletal muscle)
56
Q

when is sympathetic action

A
  • fight or flight
  • energy expenditure
  • both acetylcholine (ACh) & nonadrenaline (NA)
57
Q

when is parasympathetic in action

A
  • rest & digests
  • active in resting phase
  • conserves energy
  • Acetylcholine (ACh) only = transmitter
58
Q

what are the preganglionic nerve fibers & what do they release

A

They are the fibers they take the message from the CNS. They are myelinated & release ACh from the nerve terminals which is then transfered to the next nerve

59
Q

what does ACh produce

A

produces an excitatory postynaptic potential (EPSP) in the postganglionic neurons

60
Q

what does the ACh activate to produce the EPSP

A

by activating nicotinic receptors

61
Q

what does sympathetic postganglionic release

A

mainly noradrenaline (vasoconstriction = increase blood pressure)

62
Q

what does parasympathetic postganglionic release

A

acetylcholine

63
Q

sympathetic fibre lenghts

A

1st is very short & second is long

64
Q

parasympathetic fibre lengths

A

1st long & second shorter

65
Q

what are the ganglions next to in sympathetic nervous system

A

the spinal cord

66
Q

what are the ganglions closer to in the parasympathetic nervous system

A

the effector organ (e.g. heart & lungs)

67
Q

what is released by presynaptic neurons

A

acetylcholine

68
Q

what does acetylcholine crossing the synaptic cleft activate

A

ligand gated ion channel known as nicotinic receptors

69
Q

what does activation of adrenoceptors do

A

lead to an action potential

70
Q

what does the action potential do

A

takes the message to the effector organ

71
Q

in the parasympathetic system what does the release of acetylcholine do in the postsynaptic neurons

A

activates muscarinic receptors

72
Q

what type of receptor are muscarinic

A

GPCR

73
Q

in the sympathetic system what does the release of acetylcholine do in the postsynaptic neurons

A

noradrenaline is released

74
Q

what is receptor is activated by the release of noradrenaline

A

adrenoceptor

75
Q

whats the difference between a ligand-gated ion channel or voltage ion channel

A

the receptor ion channel will have an endogenous agonist

76
Q

how many units is the nicotinic acetylcholine receptor/structure

A

it has 5 units that come together and form a core

77
Q

how is the nicotinic acetylcholine receptor opened

A

two acetylcholine ligands bind to the receptor

78
Q

location of nicotinic acetylcholine receptor muscle & ganglion examples

A

skeletal neuromuscular junction & autonomic glanglia: mainly postsynaptic

79
Q

response of nicotinic acetylcholine receptor opening

A

excitatory: increased cation permeability (mainly sodium & potassium)

80
Q

example of a cholinergic receptors & there systems

A
  1. nicotinic receptor = both

2. muscarinic receptors (5 subtypes) = mostly parasympathetic

81
Q

what are the main three subtypes of muscarinic receptors

A

M1: CNS & gastric parietal cells
M2: heart
M3: smooth muscle & glands

= not very selective

82
Q

what type of receptor is muscarinic receptor

A

metabotropic receptor = GPCR

83
Q

what is ScfV16

A

added to the structure to help stabilise tertiary complexes

84
Q

what are cholingeric receptors associated with

A

acetylcholine

85
Q

what are adrenoceptors associated with

A

sympathetic nervous system binds to adrenaline or nonadrenilie endonouse

86
Q

main areas of adrenoceptors x5

A 
α1 (postsynaptic): vascular smooth
muscles
• α2 (presynaptic): vascular smooth
muscles and CNS
• β1: heart, intestinal smooth muscle
• β2: bronchial, vascular and uterine
smooth muscles
• β3: plasma membrane of adipocytes
87
Q

adrenoreceptor: what does alpha 1 couple with

A

Gq

- more selective to NA (more potent)

88
Q

adrenoreceptor: what does alpha 2 couple with

A

Gi

- a lot more selective to NA

89
Q

adrenoreceptor: what does beta 1 couple with

A

Gs

- more selective to NA

90
Q

adrenoreceptor: what does beta 2 couple with

A

Gs

- more selective to A

91
Q

adrenoceptor: what does beta 3 couple with

A

Gs

- the same selectivity between NA & A

92
Q

how to know if it is a target on the diagram

A

it will have a T on the end standing for transferase and also will cause a change in ligand

93
Q

when is acetycholine in vesicles released in the synapse

A

when intracellular calcium decreases

94
Q

what are the 3 possibilities when acetycholine crosses the synapse

A
  1. binds to postsynaptic receptors
    - muscarinic
    - nicotinic
  2. bind to pre-synaptic receptors = most cause neg feedback which decreases acetycholine
  3. degraded by enzyme acetylcholinsterase
95
Q

what do cholinomimetirc activate (aka muscarinic agonist)

A

directly activates muscarinic receptors, usually producing excitatory effects

96
Q

explain main affect of M1 receptor

A

CNS excitation (improve cognition?), gastric secretion

“neural”

  • Gq
97
Q

explain main affect of M2 receptor

A

cardiac inhibition, neural inhibition, central muscarinic effect (e.g., tremor hypothermia)

“cardiac”

Gi - in heart decreases rate & force of atrial contraction

98
Q

explain main affect of M3 receptor

A

gastric & salivary secretion, GI smooth muscle contraction, ocular accommodation, & vasodilation

“glandular/smooth muscle”

Gq

99
Q

how does the indirect affect work aka use of Anticholinesterases

A

in increase affect by increasing aachetylcholine in the synapse - done by inhibiting the enzyme that breaks it down

100
Q

example of irreversible indirectly acting cholinomimetics

A

• Toxic – Topic malathion (head lice) • Organophosphate insecticides and
warfare agents

101
Q

example of reversible indirectly acting cholinomimetics

A 
Indications: Myasthenia gravis and
Alzheimer's
• Similar effects to muscarinic agonists
in addition to a potentiation of the
transmission in the neuromuscular
junction
102
Q

why irreversible toxic

A

continuously activating the parasympathetic system = strong imbalance

103
Q

what are anticholinergics / antimuscarinics

A

cholinergic receptors antagonist = decreasing response cause not blocking all

104
Q

two types of anticholinergics / antimuscarinics

A
  1. n (nicotinic) ACh = not clinically useful for ANS because they block both systems
  • muscle relaxants act on the neuromuscular junction
    e. g., pancuronium
  1. m (muscarinic) ACh receptors antagonists = they complete & block the action of ACh at the muscarinic receptors = decrease contraction/movement = decrease cramps
    - e.g., hyoscine (scopolamine) butylbromide (buscopan) or hydrobromide (travacalm), atropine & tiotropium (spiriva - COPD)
105
Q

what targets are involved in acetylcholine synthesis

A

ChAT = enzyme or transporter

106
Q

what synthesises noradrenaline in the vesicle & what is released with it

A

dopamine & released with increasing calcium levels

107
Q

what are the three paths of noradrenaline & in path 2 what is the difference between Alpha-2 & Beta-2

A
  1. cross the synaptic cleft & activate post-synaptic alpha/beta adrenergic receptors (GPCR)
  2. bind to pre-synaptic receptors which modulate noradrenaline release.

Alpha-2 = provides negative feedback decreasing noradrenaline release

Beta- 2 = does the opposite

  1. return to the inside of the pre-synaptic neuron by using transporters called NET (noradrenaline transporter). in the cytoplasm, it may return to the besicle or be defraded by monoamine oxidase (MAO) enzymes
108
Q

what is the name of the adrenoreceptor agonists

A

symoathomimetics

109
Q

what does symoathomimetics do

A

= Partially or completely mimics the
actions of noradrenaline (NA) and
adrenaline (A)

110
Q

explain the two types of symoathomimetics - indirect & directly

A

directly - agonist binds to alpha &/or beta receptors

indirectly (act on transporter or enzymes) - Facilitate the release of NA, block
NA reuptake or inhibit metabolism by
MAO or COMT

111
Q

the four type of direct receptors for sympathomimetics

A

alpha 1 (Gq) - vasoconstriction = relaxation of Gi smooth muscle, salivary secretion & hepatic glycogenolysis

alpha 2 (Gi) - inhibition of transmitter release = vascular smooth muscle contraction & inhibition of insulin release

beta 1 (Gs) - increased cardiac rate & force

beta 2 (Gs) - bronchodilation = vasodilation, relaxation of visceral smooth muscle, hepatic glycogenolysis, muscle tremor

beta 3 (Gs) - lypolisis & thermogenesis, & bladder detrusor muscle relaxation (relax bladder wall allowing urine storage)

112
Q

example of 𝛼/β-adrenoceptor agonist

A

Anaphylactic shock, cardiac arrest - adrenaline epipen

113
Q

example of β2-adrenoceptor agonist

A

• Asthma relievers

- Salbutamol

114
Q

example of Selective 𝛼1-adrenoceptor agonist

A

• Decongestants

  • Phenylephrine
  • Oxymetazoline
115
Q

example of Selective 𝛼2-adrenoceptor agonist

A

• Antihypertensive
- Clonidine

  • causes increase which signals it to stop = negative feedback
116
Q

the three type of indirect receptors for sympathomimetics

A
  1. Inhibits the reuptake of noradrenaline
    (Block NET)
    • Stimulants
    - Cocaine
    - Tricyclic antidepressants (e.g. imipramine)
  2. Increase noradrenaline release
    • Stimulants
    - Amphetamines (used in ADHD) – also affect
    serotonin and dopamine release

3.Monoamine Oxidase (MAO) inhibitors

117
Q

role of adrenoceptor antagonists

A

Block the effects of noradrenaline and
adrenaline. Most are selective to 𝛼𝛼 or
β receptors (even subtype selective).

118
Q

examples of role of adrenoceptor antagonists

A

Selective 𝛼𝛼1 antagonists
• Antihypertensive
- Prazosin

Selective 𝛼𝛼1A antagonists
• Treat benign prostatic hypertrophy
- Tamsulosin

Non-Selective β-blockers (blocks β1 and β2)
• Treat hypertension, angina,
tachyarrhythmias, myocardial infarction,
migraine prophylaxis, essential tremor, etc
- Propranolol

Selective β1-
blocker (cardioselective)
• Treat cardiovascular conditions as above
- Atenolol, metoprolol

Non-Selective β-blockers (blocks 𝛼𝛼 and β)
• Treat hypertension and heart failure
- Caverdilol

phar24 (12 decks)

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