OptoP: Ocular Analgesics - Week 10 Flashcards
How many Drug schedules are there? Describe 3 of them
9 in total.
Schedule 2: therapeutic use available for supply by pharmacists or appropriately licensed persons
Schedule 3: therapeutic use but are dangerous or liable to abuse so as to restrict supply by pharmacists etc.
Schedule 4: prescription only substances intended for therapeutic use but the safety or efficacy requires further evaluation
For currently listed S2 drugs for optometrists:
- name 2 anti-infectives
- dibromopropamidine
- propamidine
For currently listed S2 drugs for optometrists:
- name 2 anti-inflammatories
- antazoline
- azelastine
- ketotifen
- levocabastine
For currently listed S2 drugs for optometrists:
- name 2 decongestants/analgesics
- lodoxamide
- naphazoline
- pheniramine
- sodium cromoglycate
For currently listed S2 drugs for optometrists:
- name 1 drug for miotic, mydriatic or cycloplegia
- what schedule of drug do other drugs that have this effect typically fall under?
phenylephrine
other drugs fall under S4 generally (prescription only)
What class and schedule of drug does chloramphenicol fall under?
S3 drug and is an anti-infective
What schedule of drug for optometry use is the most common for the following?
- anti-infectives, anti-inflammatories, anti-glaucoma, miotic, mydriatic, cycloplegic, local anaesthetics
S4
In fact, anti-glaucoma and local anaesthetics for optometrists are all S4 (and have no drugs in S2 or 3)
Name 3 characteristics of a not so serious red eye
- tired, drinking
- vasodilation of blood vessels
- usually associated soreness
Name 1 characteristic of a more serious red eye
- persistent red-eye
What actions should you take when you see a more serious red eye (2)
- identify cause
- decide on best option (understand mediators involved)
What type of drug is usually adequate to treat a not so serious red eye?
S2 vasoconstrictors (alpha-adrenoceptor agonists) usually adequate
What 2 drug classes might be used to treat a more serious red eye?
- Anti-inflammatory: if irritation due to foreign particles or allergic conditions
- Anti-infective: if bacterial, viral, or fungal cause
What is the vascular response and cellular response to inflammation? What is the primary defence mechanism in inflammation?
Vascular: vasodilation
Cellular: cell migration (WBCs, mast cells)
Primary defence mechanism = pain
Name the 5 mediators of inflammation and rate how much they contribute to the following:
A: dilatation
B: vascular permeability
C: chemotaxis
D: pain
A B C D
Histamine ++ +++ - -
Serotonin +/- + - -
Bradykinin +++ + - +++
Prostanoids +++ + +++ +
Leukotrienes - +++ +++ -
Which mediators of inflammation have the largest effect on dilatation? (2)
Bradykinin and Prostanoids (closely followed by histamines)
Which mediators of inflammation have the largest effect on vascular permeability? (2)
Histamine and Leukotrienes
Which mediators of inflammation have the largest effect on chemotaxis? (2)
Prostanoids and Leukotrienes
Which mediator of inflammation has the largest effect on pain? (1) Are there any other mediators that cause pain?
Bradykinin. (prostanoids cause slight pain)
How does pain intensity and duration correlate with the use of the following:
A: Prostaglandin (PGE2)
B: Bradykinin
C: PGE2 + Bradykinin
A: slight pain
B: slightly more pain
C: a lot more pain
How can we reduce the pain intensity of PGE2 + Bradykinin?
By blocking the action of one of this synergistic pair - this may be sufficient to inhibit the overall pain response
e.g. prostaglandin synthesis inhibitors
Describe the Arachidonic Acid (AA) pathway and how it branches out in 2 steps
- Lipid Membrane produces A.A via phospholipase
- A.A differentiates into either prostanoids (via cyclooxygenase) or Leukotrienes (via lipoxygenase)
Name 2 types of prostanoids and describe their effects (4 effects for 1 type and 1 effect for the other)
- Prostaglandins:
- hyperalgesia, vasodilation, vasc. permeability (leukocyte trapping) - Thromboxane A2:
- aggregation of platelets
Name 2 prostaglandins
Prostaglandins:
- PGE2
- PGI2
Name 1 leukotriene and describe its effects (2)
LTB4:
- chemoattraction
- neutrophil function (phagocytosis)
What class of molecule are prostanoids and leukotrienes?
Eicosanoids
In regards to NSAIDS, describe the following:
A: What pathways do they inhibit?
B: What treatment are they accepted as an alternative for?
A: Inhibits prostanoid pathway only (by reducing amplification of inflammatory signals)
B: Accepted alternative/adjucent to steroid treatment
How safe are NSAIDs? List Contraindications (2)
Generally considered Safe.
Contraindications:
- aspirin/NSAID anaphylactic reaction
- bisulphate sensitivity (for Indomethacin only)
List 4 potential adverse effects of NSAIDs
- burning, stinging or mild discomfort on application
- ocular irritation, itching and redness
- delayed epithelial growth and wound healing (Diclofenac only)
- Potential bleeding risk (local + systemic)
Describe the action of the following classes of drugs on the AA pathway:
A: Steroids
B: NSAIDS
A: steroids inhibit phospholipase and cyclooxygenase
B: NSAIDs inhibit cyclooxygenase
Describe the mechanism of action of ‘transactivation’ with glucocorticoids (a steroid) (5)
- Glucocorticoids travel through the membrane and bind to the cytosolic GR (glucocorticoid receptor)
- The newly formed complex then translocates itself into the cell nucleus,
- where it binds GREs (glucocorticoid response elements) in the promoter region of the target genes
- resulting in the regulation of gene expression (transactivation) (“these genes turn ON”)
- result in increase in Lipocortin-1
What is the function of Lipocortin-1?
it is a phosphoprotein that inhibits PLA-2
Describe the mechanism of action of ‘transrepression’ with glucocorticoids (a steroid) (3)
- the activated GR binds to DNA in the same site where the transcription factor would bind (GR binds nGREs)
- this prevents the transcription of genes that are transcribed via the activity of that factor “these genes turn OFF”
- results in reduction of cytokines, COX-2 and PLA2
What does nGRE stand for?
Negative Glucocorticoid Response Element
List 12 systemic side effects of steroids (don’t really have to know all of these)
- osteoporosis
- immunosuppression/risk of infection
- hypertension
- fat deposition, abdominal, face, neck
- thinning skin, arms, legs
- muscle wasting
- behavioural disturbances
- peptic ulceration
- growth inhibition
- delay/poor wound healing
- cataracts
List 3 advantages of topical steroids
- minimise systemic effects
- can place where needed
- can treat uniocular disease
List 1 disadvantage and 2 sub-disadvantages of topical steroids
- specific local reactions: - may leave white residue, may affect vision
list 4 common ocular side-effects of topical steroids
- ocular hypertension
- reduced corneal healing
- rebound inflammation
- cataract formation
List 6 rare ocular side-effects of topical steroids
- corneal melt
- refractive changes
- ptosis
- lid swelling
- exophthalmus
- adrenal insufficiency
Name 2 indications for the use of topical steroids
- allergic and selected inflammatory conditions of lids, conjunctiva, cornea, iris and cil. body
- post-operative inflammation
Name 1 contra-indication for the use of topical steroids
ocular infection
Name 2 specific considerations for the use of topical steroids
- aggravation of glaucoma
- increase risk of ocular hypertension and cataract
Name 5 topical steroids and rate the following features:
A: potency
B: penetration
C: IOP rise
A B C
Dexamethasone 4+ 2+ 4+
Fluorometholone 3+ + 3+
Hydrocortisone + + 2+
Medrysone + - +
Prednisolone 3+ 3+ 3+
How long should you prescribe topical steroids for? Any exceptions?
No longer than 2 weeks unless you are able to monitor corneal epithelium and measure IOP
In regards to topical cyclosporin, describe the following:
A: State it’s effect on the immune system
B: What does it inhibit or activate? (2)
Cyclosporin is an immunosuppressant that specifically inhibits T-lymphocyte activation and cytokine production
List 5 indications for the use of topical cyclosporin
- dry eye
- vernal keratoconjunctivitis
- eczema
- atopic keratoconjunctivitis
- allergic conjunctivitis
Name 3 systemic side effects that are lessened/absent as a consequence of the topical administration of cyclosporin
- IOP increase
- delay in wound healing
- cataract formation
List 2 contraindications for the use of topical cyclosporin
- known hypersensitivity
- active ocular infections
Name 2 Histamine H1 antagonists and briefly describe them
- Levocabastine - used for seasonal allergic conjunctivitis; full adverse profile not known
- Oloptadine - histamine receptor antagonist and mast cell stabiliser
In 2 steps, describe what you should do before removing a foreign particle from the eye
- ensure no infection
- use local anaesthetic
Name drugs that can target the following:
A: mediator release (2)
B: cell migration (2)
C: vascular response (1)
A: NSAIDs (to inhibit prostaglandin formation) and Oloptadine (to inhibit histamine receptor)
B: suppress WBCs and mast cells with Steroids, Cyclosporin
C: alpha-adrenoceptor agonists
List 3 factors to consider when thinking about the quality use of medicine
- selecting management options wisely
- choosing suitable medications
- using medicines safely and effectively
List 2 factors to consider when thinking about considerations of the patient
- presentation of signs and symptoms
- medical history: other medications, known drug allergies
List 6 factors to consider when thinking about the pharmacology of drug use
- indications/contraindications
- normal clinical response expected
- suitable dosing regimes
- potential side effects (topical and systemic)
- interactions with other drugs
- how such complications can be managed/avoided
Name 4 topical NSAIDs
- Diclofenac
- Flurbiprofen
- Indomethacin
- Ketorolac
