IP exam Flashcards

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
Q

At risk groups?

A

Neonate – child
■ Pregnant / Breast feeding
■ Kidney/ liver impairment
■ Hereditary disorders
■ Pre-existing condition(s)

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26
Q

Risks from medications include?

A

■ Drugs with cumulative effects
■ Drugs requiring dose adjustments
■ Polypharmacy
■ ADRs
■ Errors
■ High risk drugs
■ Interactions

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27
Q

What are competency frameworks?

A

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

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28
Q

What does COO management guidelines state about IP?

A

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

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29
Q

What is a clinical management plan?

A

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

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30
Q

What should a clinical management plan include?

A

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

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31
Q

What is an ADR?

A

An adverse drug reaction (ADR) is defined as an unwanted or harmful reaction experienced following the administration of a drug (or combination of drugs)

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32
Q

What are the types of ADR?

A

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

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33
Q

What is a type A drug reaction known as?

A

pharmacological- exaggeration of the normal pharmacological reaction of the drug

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34
Q

What is a type B drug reaction known as?

A

idiosyncratic- uncommon and unrelated to the known action of the drug-

35
Q

Determinants of ADR

A

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
Q

How to work out the TI?

A

Minimum toxic dose (highest)
divided by
Minimum effective dose ( lowest)
TI is larger- Narrow TI means higher risk of ADR.

37
Q

What is pharmacosurvelliance?

A

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
Q

What should be reported? Under yellow card scheme?

A

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
Q

Difference between additional supply, supplementary & IP Optoms?

A

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
Q

What is patient specific direction?

A

EG: Ophthalmologist & IP working together for intravitreal injections, this is PSD, Ophthalmologist trusts IP to administer these.

41
Q

Additional supply Optoms can sell/supply what medications?

A

Topica antihistamines
Mast cell stabilisers
NSAIS- Diclofenac sodium
Atroine
Homatrophine
Pilocarpine
Acetylcysteine- (ILUBE) Dry eye drop

42
Q

What is Fuchs Hetrochromic Iridocyclycltis

A

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
Q

Side effects of AH?

A

Dry mouth, dry eye, constapation, blurred vision

44
Q

What are NSAIDS & Side effects?

A

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
Q

What is Acetazolomide

A

Systemic meds, for emergency of AAG
Inhibits aqueous production
Single 50mg dose
Side effects, dizziness, flushing, thirst.

46
Q

Name some medication which causes Ocular toxicity?

A

Digoxin - Yellow/green tint in vision
Amiodrane- Vortex keratopathy
C&Hcloroquine
Cortciosteroids
Tampoxifen
C-Pill

47
Q

What is Diclofenac sodium used for?

A

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
Q

What are corticosteroids used for?

A

For inflammatory components:
There are.2 main pharmacological actions
1) Antiiflammtory/immunosupressive
2) Metabolic effect

49
Q

Types of prednisolone

A

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
Q

Why prescribe Predisolone acetate over FML

A

Morepotent, crosses ocular barrier

LOtepredonol- v milk, reduced risk of adverse reaction - Less likely to cause increase in IOP

Phosphate & FML- Mild steroids

51
Q

What is the target of AB?

A

x5 different target
Protein synthesis- EG CLPH, Fucidic acid
DNA synthesis - Fluoroquinolones
Cell wall synthesis
Bacterial metabolism
Bacterial cell membrane

52
Q

What are fluoroquinolone?

A

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
Q

How is Glaucoma diagnosed?

A

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
Q

What is traditional glaucoma classification?

A

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
Q

What is mechanism based glaucoma?

A

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
Q

What is initial pathological event based Glaucoma?

A

Another way to diagnose Glaucoma- this is a subtype

Grouped by knowledge of cause leading to Glaucomatous change
EG: Trabecular effect
Uveoscleral outflow

57
Q

What are the types of COAG?

A

POAG
PDS
PXD
NTG

58
Q

What is the cause of ACG?

A

Circumferential apposition of the peripheral Iris against the trabecular meshwork.

Subdivionns of ACG:
Pupillary block
Non pupillary block

59
Q

What are the 3 classification oa primary angle closure?

A

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
Q

Discuss PDS

A

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
Q

Discuss PXF

A

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
Q

What is target IOP?

A

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
Q

COAG first line tx

A

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
Q

Types of Glaucoma drugs/

A

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
Q

What is the mechanism of action of CAI?

A

Reduced aqueous production

66
Q

What is the mechanism of AA?

A

Reduced aqueous production & enhances aqueous outflow by uveoscleral flow

67
Q

What is the mechanism of BB?

A

Reduced aqueous production

68
Q

What is the mechanism of Protoglandin?

A

Enhance aqueous outflow by uevoscleral flow.

69
Q

What is the mechanism of Cholinergic & RHO?

A

Enhances aqueous outflow by increasing outflow through trabecular meshwork.

70
Q

Discuss prostaglandin analogues

A

Works by enhancing aqueous outflow through uveal scleral for

Side effects:
Conj hyperima
Darkening, thinking of eyelashes
Increasing iris pigment

71
Q

Discuss Beta Antagonists

A

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
Q

Discuss Alpha agonists

A

enhances Increase uveal sclera outflow & redcues aqueous production
Brimondine
High ocular & systems sideeffects
Follicular conjunctivitis
Hypotension, dry mouth, nose , headaches, anxiety

73
Q

CAI Discuss

A

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
Q

Chlornergic agents discuss

A

Enhances outflow through trabecular meshwork
Pilocarpine

Side effects:
Misos, myopia, confusion, vomitting

75
Q

Discuss Steroid retailed OH

A

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
Q

COAG TX options

A

SLT
Therapeutics
Mod/Mild- MIGS
Advanced- trabeculotomy-

77
Q

Diff reasons AG occur?

A

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
Q

What are the 3 stages of AC disease

A

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
Q

Management of AG?

A

Iridotomy
IOL surgery
Therapeutic management

80
Q

Management of AAC?

A

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
Q

What to check in FB assessment?

A

VA before & after
Globe perforation
Dilated fundus
A/C activity
Pupil resposes

82
Q

For chemical injuries what do you advise?

A

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
Q

Give examples of Glaucoma drugs

A

PSA: Bimaprost, Latanprost,
BB, Timolol, Beraxlol
AA: Brimonidine, Apraclonidine
CAI: Dorzolomide, Brinzolodmie
CA: Pilocarpine