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IP exam Flashcards

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1
Q

What are the types of Trauma?

A

Chemical - Nail polish, acid
Physical - Blunt, sharp, perforating
Electrical - Shock, burn
Thermal- Heat, Cold
Radiation - Ionizin, UV, laser

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2
Q

Mechanisms of ocular trauma

A

Self inflicted
Accidental
Environmental
Occupational

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3
Q

How do you classify eye trauma?

A

Using the Birmingham eye trauma terminology system.
Which classifies into
Closed glove or Open globe.

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4
Q

What is the Glasgow coma scale?

A

This checks the eye responses: From NT– Not testable to +4 Spontaneously.(Normal)

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5
Q

What to check for visual function with Ocular Trauma?

A

VA
RAPD
Colour vision
Confrontation
Motility
IOP

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6
Q

Investigation for Ocular trauma?

A

Blood work- to check tents status & immunisation
BScan
CT scan
MRI
Facial X rays

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7
Q

Systemic drugs- IP

A

AH
AB
NSAIDS
CAI- Azetozolamide

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8
Q

What is pharmacodynamic?

A

Describes what the drug does to the body, . It refers to the relationship between the drug concentration at the site of action and the resulting effect, including the time course and intensity of therapeutic and adverse effects.

Biochemical & physiological effects
Receptors
Dose response

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9
Q

What is pharmacokinetics?

A

Describes what the body does to the drug
Absorption
Distribution
Biotransformation (Metabolism)
Excretion

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10
Q

Why is pharmacokinetics important to understand?

A

To ensure the appropriate drug is being administered, pharmacokinetics factors takes into account inter individual variability in therapeutic response meaning the way the drugs metabolised & is excreted.

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11
Q

How do drugs work?

A

Drugs are chemical which altering cell functions specific ways

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12
Q

How do drugs achieve there effects?

A

By binding to specific target protein molecules, targets include
Receptors
Enzymes
Transporters
ION channels

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13
Q

Discuss the different drug targets.

A

Drug achieve there effects by binding to specific target including,

Enzymes- CAI, NSAIDS
ION channels- TA
Receptors- BB, AA, Histamines
Transporters

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14
Q

What are antagonist?

A

Drugs that bind to receptors WITHOUT stimulating them. They block receptors preventing natural binding ligand.
They can be competitive meaning bind to same site as the natural agonise OR
Non competitive bind to alternative site and affect binding of agonist indirectly.

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15
Q

What are agonist?

A

Drugs that STIMULATE receptors, agonists perform the same function as naturally occurring receptors, they can produce partial or maximal response.

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16
Q

What is drug specificity?

A

Ideally a drug should have a high specificity meaning only able to bind to one site, but this is rare& drugs can bind to multiple sites. Increasing drug dosage can lead to affect on other target sites meaning increased side effects.

The lower the drug potency= higher dose needed & greater likelihood of wanted effects.

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17
Q

What is TI?

A

The ratio between the toxic dose and the therapeutic dose of a drug, used as a measure of the relative safety of the drug for a particular treatment. Drugs with a narrow TI= high side effects eg: Digoxin, Warfarin

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18
Q

What are the 4 parts of Pharmacokinetics

A

1) Absorption
2) Distribution
3) Biotransformation & Excretion

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19
Q

Describe the absorption of a drug?

A

This is pharmokinetics- What the body does to the drug
Absorption: Administered through site of entry eg, intravenous, topical, oral.
The degree of absorption is dependent on the degree of Ionisation.
High polar molecules are poorly absorbed where is non polar meaning unionised readily penetrate cell membranes.

The absorption of drugs is determined by the surrounding PH, this determines degree of ionisation of a drug,
Low ph: Absorbed across stomach
High ph Absorbed across Small intestine

Factors affecting absorption
Gut mobility
Blood flow
Drug formulation- drugs can be formulated for slow release, eg resistant coating

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20
Q

discuss the distribution of a a drug

A

This is pharmokinetics- What the body does to the drug
After absorption, drug taken into blood stream is distributed to the site of action, distribution is affected by a number of factors including,
1) plasma proteins
2) melanin/fat of tissue
3) Physiochemical properties of the drug
4) Bloodflow between tissues
5) Degree of leakiness of BV

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21
Q

What is excretion in pharm-kinetics?

A

This is pharmokinetics- What the body does to the drug , after absorption & distribution there is elimination.

This occurs by metabolism (biotransformation) & excretion- Most drugs eliminated by the kidney.
Some by the liver.

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22
Q

When monitoring AS diseases what factors to think about?

A

Assess the risks and benefits

Select the most appropriate drug, dose & formulation

Monitor effectiveness of treatment & side effects

Modify the treatment plan

Identify endpoint of treatment

Repeat prescribing

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23
Q

What is supplementary prescribing?

A

‘A voluntary partnership between the responsible prescriber
and a supplementary prescriber, to implement an agreed
patient-specific clinical management plan with the patient’s
agreement, particularly but not only in relation to prescribing
for a specific non-acute medical condition or health need
affecting the patient.’

3-way partnership between a medical practitioner (independent prescriber) who establishes the diagnosis and initiates treatment an optometrist (supplementary prescriber) who monitors the patient and prescribes further supplies of medication and the patient who agrees to the supplementary prescribing arrangement

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24
Q

What is good prescribing practice?

A

Prescription writing
Record keeping
Review practice- audit, identify errors
CPDS- develop

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25
At risk groups?
Neonate – child ■ Pregnant / Breast feeding ■ Kidney/ liver impairment ■ Hereditary disorders ■ Pre-existing condition(s)
26
Risks from medications include?
■ Drugs with cumulative effects ■ Drugs requiring dose adjustments ■ Polypharmacy ■ ADRs ■ Errors ■ High risk drugs ■ Interactions
27
What are competency frameworks?
A competency framework is a collection of competencies thought to be central to effective performance. There is something called Optometrists Competency Framework published jointly by the National Prescribing Centre (NPC) and General Optical Council in 2004. The competencies within the framework 2 domains, consultation & prescribing governance. There are 10 diff competencies between these 2. Competency frameworks can be used to: Inform development of curricula for basic or specialist training Provide a framework for assessment Support continuing professional development (CPD
28
What does COO management guidelines state about IP?
CHM’s recommendation was that suitably qualified optometrists should be able to prescribe any licensed medicines (except for controlled drugs or medicines for parenteral (injected) administration) for ocular conditions affecting the eye, and the tissues surrounding the eye, within their recognised area of expertise and competence
29
What is a clinical management plan?
A clinical management plan is a plan of care that relates to a named patient and the specific condition(s) to be managed by the SP made by the IP
30
What should a clinical management plan include?
1) Name of px; 2) The illness or conditions which may be treated by the supplementary prescriber 3) The date on which the plan is to take effect, and when it is to be reviewed by the doctor (independent prescriber) who is party to the plan 4)Reference to the class or description of medicines which may be prescribed or administered under the plan 5) Any restrictions or limitations as to the strength or dose of any medicine 6) Relevant warnings about known sensitivities of the patient to 7) Relevant suspected or known adverse reactions to any other medicine 8) The circumstances in which the SP should refer to, or seek the advice of, the doctor (independent prescriber) who is party to the plan
31
What is an ADR?
An adverse drug reaction (ADR) is defined as an unwanted or harmful reaction experienced following the administration of a drug (or combination of drugs)
32
What are the types of ADR?
ADRs can be classified as Type A (pharmacological) or Type B (idiosyncratic) Type A reactions represent an exaggeration of the normal pharmacological reaction of the drug Type B reactions are uncommon and unrelated to the known action of the drug
33
What is a type A drug reaction known as?
pharmacological- exaggeration of the normal pharmacological reaction of the drug
34
What is a type B drug reaction known as?
idiosyncratic- uncommon and unrelated to the known action of the drug-
35
Determinants of ADR
There is px variables & Pharmacological variable Patient variable: Age Gender Renal and hepatic function History of drug allergy General health Pharmacological variables" Dose Therapeutic index Formulation Route of delivery Duration Multiple drug therapy
36
How to work out the TI?
Minimum toxic dose (highest) divided by Minimum effective dose ( lowest) TI is larger- Narrow TI means higher risk of ADR.
37
What is pharmacosurvelliance?
Process meds need to go through for licensing? Including drug trials Post marketing- ADRS there is no formal process done through yellow card adverse reactions scheme. If a drug is newly licences ALL ADR need to be reported these are known as BLACK TRIANGLE DRUGS. Can be found on MRNA website.
38
What should be reported? Under yellow card scheme?
Optometrists should not report well recognised OARs unless they are severe Serious suspected adverse reactions should be reported e.g. Any change in acuity Any change in IOP Any change in ocular structures Report all adverse reactions to new new therapeutic agents (Black Triangle Drugs) Report all adverse reactions in children
39
Difference between additional supply, supplementary & IP Optoms?
Additional supply do not have the whole range, supplementary can manage and prescribe under the clinical management plan set up of IP, Optom, Pharmacist known as PSD!
40
What is patient specific direction?
EG: Ophthalmologist & IP working together for intravitreal injections, this is PSD, Ophthalmologist trusts IP to administer these.
41
Additional supply Optoms can sell/supply what medications?
Topica antihistamines Mast cell stabilisers NSAIS- Diclofenac sodium Atroine Homatrophine Pilocarpine Acetylcysteine- (ILUBE) Dry eye drop
42
What is Fuchs Hetrochromic Iridocyclycltis
AU- but low grade No steroids needed Star shaped KP in Cornea, over posterior surface No posterior synechia Change in Iris colour PSC& Seconday glaucoma.
43
Side effects of AH?
Dry mouth, dry eye, constapation, blurred vision
44
What are NSAIDS & Side effects?
Both anti-inflammatory & analgesic properties They inhibit COX and redcue production of inflammatory mediators & raise thereshold of pain receptors/ Caution in asthma can cause bronchospasm GI uses
45
What is Acetazolomide
Systemic meds, for emergency of AAG Inhibits aqueous production Single 50mg dose Side effects, dizziness, flushing, thirst.
46
Name some medication which causes Ocular toxicity?
Digoxin - Yellow/green tint in vision Amiodrane- Vortex keratopathy C&Hcloroquine Cortciosteroids Tampoxifen C-Pill
47
What is Diclofenac sodium used for?
NSAIDS- Used for pre&post Operation, helps reducing mitosis during surgery. Allergic conj (Seasonal) + Episcleritis One main side effect: Corneal melting. Other NSAIDS: Fluriprofen
48
What are corticosteroids used for?
For inflammatory components: There are.2 main pharmacological actions 1) Antiiflammtory/immunosupressive 2) Metabolic effect
49
Types of prednisolone
Acetate - Better penetrate through ocular surface- Stronge Sodium phosphate- Less effective, as less able to penetrate through ocular surface. More hyporphillic. Predisolone acetate & dexmatheosne -Potent
50
Why prescribe Predisolone acetate over FML
Morepotent, crosses ocular barrier LOtepredonol- v milk, reduced risk of adverse reaction - Less likely to cause increase in IOP Phosphate & FML- Mild steroids
51
What is the target of AB?
x5 different target Protein synthesis- EG CLPH, Fucidic acid DNA synthesis - Fluoroquinolones Cell wall synthesis Bacterial metabolism Bacterial cell membrane
52
What are fluoroquinolone?
This is an AB which affects bacterial DNA synthesis Works against gram+ & Gram -inluding psuedonomas Moxoflaxcin- not active against pseudomonas. Levoflaxcin- better corneal penetration therefore preffered in bacterial keratitis.
53
How is Glaucoma diagnosed?
This is a disease of the ONH- which forms progressive optic neuropathy. Glaucoma is diagnosed by looking at subtypes CAUSE & MECHANISM x3 main classifications 1) Traditional- Caused based 2) mechanism based 3) Initial pathological event based
54
What is traditional glaucoma classification?
This is caused based- meaning, What's the cause of the IOP elevation? Is this a primary/secondary case 1 major disadvantage is what about Glaucoma with normal IOPS?
55
What is mechanism based glaucoma?
Another way to diagnose Glaucoma- this is a subtype- This looks at how aqueous outflow reduction leads to raised IOP, so what mechanism is causing the IOP to raise? Disadvantages of this is ignores underlying cause, what about IOP independent. causality.
56
What is initial pathological event based Glaucoma?
Another way to diagnose Glaucoma- this is a subtype Grouped by knowledge of cause leading to Glaucomatous change EG: Trabecular effect Uveoscleral outflow
57
What are the types of COAG?
POAG PDS PXD NTG
58
What is the cause of ACG?
Circumferential apposition of the peripheral Iris against the trabecular meshwork. Subdivionns of ACG: Pupillary block Non pupillary block
59
What are the 3 classification oa primary angle closure?
1) PAC SUSPECT Normal IOPS/Field/ Disc-Narrow angle no PAS 2)PAC- Occluded angle, High IOP/PAS Normal ONH & Fields 3) PACG All sigs
60
Discuss PDS
This is a type of COAG, Pigment dispersion syndrome, this causes secondary Glaucoma- Usually to do with the bowing of the It is, which Iris rubs against CB & releases pigment- can spike IOP. Causes Krunkenberg Spindle Same tx as POAG
61
Discuss PXF
This is a type of COAG- Psedoexfoliation, This is a secondary Glaucoma. Usually occurs due to a systemic disorder, there is an accumulation of granular material which leads to psuedopxfolicative material depositing over the lens + zones of the CB + Deposits in the A/C chamber- spiking IOP. Same management as COAG. Risk factors: Scandinavia Symptoms: Misty vision & coloured haloes Signs: High IOP PXF on border of lens surface- Granular deposition Iris changes- Atrophy/ poor dilation Pigment in A/C Angle
62
What is target IOP?
Target IOP should be reached with the lowest risk intervention, fewest side effects& least amount of medication in order to minimise tx effects vision, general health & quality of life. Target IOP represents a clinical estimation of IOP required to minimise to arrest disease progression & achieve management goal. Target IOP is calculated from severity of disease, presentation IOP, life expectancy. At least 20% below presentation pressure. <18mmhg in advances Glaucoma.
63
COAG first line tx
SLT but not in PDS, can be used in OHT if 24mmHGS & at risk of visual impairment. then therapeutic management mono tx. Usually check IOP after 2-4 months.
64
Types of Glaucoma drugs/
Prostaglandin analogues BB Alpha 2 CAI Chloroogenic agonists There is also RGOKinase inhibitors- which is a dual tx- prostaglandin analogues & ROCK called Netarsudil- works by enhancing aqueous flow through trabecular meshwork Meant to help rescue IOP by 20-35%- Approx 5-7mmHg
65
What is the mechanism of action of CAI?
Reduced aqueous production
66
What is the mechanism of AA?
Reduced aqueous production & enhances aqueous outflow by uveoscleral flow
67
What is the mechanism of BB?
Reduced aqueous production
68
What is the mechanism of Protoglandin?
Enhance aqueous outflow by uevoscleral flow.
69
What is the mechanism of Cholinergic & RHO?
Enhances aqueous outflow by increasing outflow through trabecular meshwork.
70
Discuss prostaglandin analogues
Works by enhancing aqueous outflow through uveal scleral for Side effects: Conj hyperima Darkening, thinking of eyelashes Increasing iris pigment
71
Discuss Beta Antagonists
Works by reducing aqueous production EG: Timolo, betaxlol- Also fixed combinations of BB+ PGA Side effects: Risk factors of respiratory patients. Studies show even if px not diagnosed yet BB can cause shortness of breath If prescribing: Check peak flow before & after 1 month
72
Discuss Alpha agonists
enhances Increase uveal sclera outflow & redcues aqueous production Brimondine High ocular & systems sideeffects Follicular conjunctivitis Hypotension, dry mouth, nose , headaches, anxiety
73
CAI Discuss
Reduces aqueous production Brizolomide- use in combination with timolol Acatazolomide- Dimox for AAC Side effects: Metallic tast, rashes, irritation, blurred vision Oral: Allergy, kidney stones, depression
74
Chlornergic agents discuss
Enhances outflow through trabecular meshwork Pilocarpine Side effects: Misos, myopia, confusion, vomitting
75
Discuss Steroid retailed OH
Steroid response usually happens after 3 week due to increase in aqueous outflow resistance- causing high IOP due to changes in trabecular meshwork Steroidresponse can eb divided into 3 caterogies High, medium, non- responders. Non responders have the highest amount of IOP spike >5mmhg. Usually self resolves in 1-4 weeks Given topical antiglcuaoma drugs after 18 months- permanent IOP.
76
COAG TX options
SLT Therapeutics Mod/Mild- MIGS Advanced- trabeculotomy-
77
Diff reasons AG occur?
Pupillary block- Aqueous is impeded on its passage between lens & posterior surface of the iris. Aqueous blocked. Non pupillary block- Iris & lens induced angle closure
78
What are the 3 stages of AC disease
PACS PAC PACG difference between all three is ITC >180 degrees meaning the iridotrabecular contact is touching In Angle closure- there is also elevated IOP & PAS in PACG- there is optic neuropathy.
79
Management of AG?
Iridotomy IOL surgery Therapeutic management
80
Management of AAC?
Pilocarpine 2% blue eyes 4% brown eyes Ineffective if IOP >40mmHG Beneficial in pupil block but if lens induced (non pupil AC) can be harmful. Analgesia Acetazolamide- Diamox- 500mg x1 Non pupillary block; Cyclopentolate instead of pilocarpine.
81
What to check in FB assessment?
VA before & after Globe perforation Dilated fundus A/C activity Pupil resposes
82
For chemical injuries what do you advise?
Irrigate- longer you leave poorer prognosis 1L of saline or tap water 1530mins irrigation w topical aesthetic if needed Until PH is 7-8.
83
Give examples of Glaucoma drugs
PSA: Bimaprost, Latanprost, BB, Timolol, Beraxlol AA: Brimonidine, Apraclonidine CAI: Dorzolomide, Brinzolodmie CA: Pilocarpine

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