EENT MOA of drugs

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  • Created by: Rscottqub
  • Created on: 07-01-20 15:13
ophthalmology
study of the eye
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otolaryngology
study of ear nose and throat
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aim of glaucoma treatment
reduce intra occular pressure (IOP) which is a main cause of glaucoma
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glaucoma 1st line treatment
prostaglandin analogues or bitmatoprost
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what are prostaglandins
key mediators in inflammation. powerful vasodilators
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where are they produced
often at site of action, usually in response to trauma, injury, infection etc
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how are they produced
they are a metabolite of arachidonic acid
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anti inflammatory drugs target
prostaglandin synthesis
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arachidonic acid is converted to prostaglandin by
COX enzymes
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examples of prostaglandin analogues
latanoprost, travoprost
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prostaglandin analogues are
agonists of prostaglandin F2 receptor - which is widely expressed in the eye
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how do prostaglandin analogues work
usually a prodrug so can absorb across eye- once in eye converted into active drug. they increase permeability to sclera - promote drainage of aq fluid.
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glaucoma drugs either
promote drainage of aq. humour or reduce production of aq. to reduce IOP
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detailed process
analogue triggers matrix metalloprotease (MMPs) they then digest parts of extracellular matric (ECM) this increases the outflow of aq.hum therfore decreasing the IOP
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2nd line/other treatments
B blockers
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Histamine is a
inflammatory mediator
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what causes they symptoms in allergies
histamine (sneezing,runny nose, streaming eyes)
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Histamine is an
endogenous substance
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where is it synthesised stored and released from
mast cells, basophils
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Sythesis of histamine
L histadine (AA from diet) converted to histamine by decarboxylation
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mechanism of histamine
interacts with histamine receptors, GPCRs and 7 transmembrane domains
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4 main histamine receptors
H1, H2. H3 . H4
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Histamine in allergies causes
mild allergic reaction . anaphalactic shock
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H1
smooth muscle , brain
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H2
GIT, brain , cardiac muscle
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H3
brain, neurons
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H4
WBCS
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how does H1 act on body
constrict airways, dilate vessels,--> blocked nose , iriritates nerve endings - itch
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how does H2 act on body
found in GIT - onvolved in gastric secretions
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Type 1 hypersensitivity reactions
allergen presents self to CD4+Tcells --> B cell produces ABs
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a normal immune response produces which ABs
IgA, IgG, IgM
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type 1 hypersen produces
IgE antibods
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IgE will
bind to surface of basophils or mast cells, then on re-exposure to allergen - allergen will bind to IgE on surface -- cross link IgE ABs- this triggers degranulation
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degranulation
mast cells and basophils have histamine rich granules which are released
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release of histamine
dilation of blood vessels , swelling and recruitment of inflam. cells . cause iritation at nerve ending -> itch
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types of drugs which target histamine
1. antagonists 2. inhibitors 3. receptor antagonists
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antagonists
oppose effect by binding to DIFFERENT receptor - example epipen and adrenaline --> vasconstriction
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inhibitors
reduce release of histamines from mast cells /basophils
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these types of drugs
take a while to build up and need to be used from the start of hayfever season
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receptor antagonists
target H1 and H2
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antihistamines really only target
H1 receptors
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generations of antihistamines
1st and 2nd
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1st generation, chlorphenamine
can cross BBB, drowsy/more sedating . less H1 selective - more side effects . shorter lasting action- need multiple doses throughout the day
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2nd generation , cetirizine, loratidine , fexofenandine
less sedating, more H1 selective- less side effects . longer lasting action- one dose daily
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Card 2

Front

otolaryngology

Back

study of ear nose and throat

Card 3

Front

aim of glaucoma treatment

Back

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Card 4

Front

glaucoma 1st line treatment

Back

Preview of the front of card 4

Card 5

Front

what are prostaglandins

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