systemic drugs and ocular adverse reactions Flashcards

1
Q

what are the non-modifiable risks of cardiovascular disease?

what are the modifiable risks of cardiovascular disease?

A

Non-modifiable risks: Can’t change some risk (age and ethnicity)

Modifiable risks (50%): smoking, hypertension, hyperlipidaemia, weight, diet (reduce salt, saturated fat), alcohol consumption

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2
Q

what is hypertension a risk factor for?

A

stroke, myocardial infarction, heart failure, chronic kidney disease, cognitive decline (vascular dementia) and premature death

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3
Q

how is hypertension diagnosed?

A

if blood pressure is above 140/90 mmHg, ambulatory blood pressure monitoring is offered or home blood pressure monitoring to confirm hypertension

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4
Q

what shouldn’t be used in black ethnicity to treat blood pressure?

A

ACE inhibitors

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5
Q

how to ACE inhibitors lower blood pressure?

how is angiotensin II produced ?

A

they inhibit enzyme ACE so angiotensin II isn’t produced.

kidney produces an enzyme called renin which catalyses conversion of angiontension I to angiotensin II.

angiontension I becomes substrate for ACE which converts it into asngiontension II.
angiotensin II is a potent vasoconstrictor.
constricts blood vessels which increases peripheral resistance and increased blood volume.

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6
Q

what are the side effects of ACE inhibitors?

A

15% of px develop a cough

Taste disturbance

Angioedema-swelling of lower extremities

First dose hypotension

Hyperkalaemia-raised potassium levels in blood

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7
Q

what types of drugs are used to treat hypertension?

A

ACE inhibitors
angiotensin II receptor antagonists
calcium channel blockers
diuretics
beta blockers

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8
Q

Name ACE inhibitors

A

end in PRIL
captopril
enalapril
lisinopril
ramipril

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9
Q

what do angiotensin II receptor antagonists do?

Name them

why are they better than ACE inhibitors?

A

block angiotensin II receptor

ends in ARTAN
candesartan, losartan, valsartan

fewer side effects

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10
Q

how do calcium channel blockers reduce blood pressure?

what are they used to treat?

name them

A

Inhibit inwards movement of calcium ions through the slow L-type calcium channels in active membranes:
-cells of the myocardium
-cells within the His-purkinje system of the heart
-cells of vascular smooth muscle

*Work by reducing contractability of smooth muscle cells around blood vessels
*Regulates blood pressure by changing contractibility of the heart or causing vasodilation and reducing peripheral resistance.Also reduces cardiac output.

hypertension, angina

nifedipine
amlodipine
verapamil
diltiazem

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11
Q

How do diuretics reduce blood pressure?

what are the different types?

A

promote excretion of salt and water by increasing urine production and increasing salt composition
prevent re-uptake of salt in kidney to reduce blood volume

thiazides
loop diuretics
potassium sparring

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12
Q

how do thiazides work?
what is the side effect?
name them

A

Inhibit re-absorption of sodium into distal tubule

Reduce BP by vasodilation and reduction in blood volume

Can lead to potassium deficiency

bendrofluazide
hydrochlorothiazide
indapamide

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13
Q

how do loop diuretics work?
what is the benefit of using them?
what are they used to treat?
name them

A

Inhibit reabsorption of sodium and potassium in the thick ascending limb (TAL) of Henle

fast acting

renal failure, heart failure

furosemide
bumetanide

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14
Q

how do potassium sparring diuretics work?
name them

A

Act at DCT (distal convoluted tubule)
Retain potassium

amiloride
spironolactone

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15
Q

how do beta blockers reduce blood pressure?
what are they used to treat?

Name them

A

Reduce heart rate and force of contraction
Reduce peripheral resistance
Inhibition of renal release

angina, people who have had a heart attack

atenolol
metoprolol

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16
Q

name less commonly used anti-hypertensive agents

A
  • Alpha-adrenoceptor antagonists
  • Doxazosin
  • Centrally acting agents
  • Methyldopa
  • Moxonidine
  • Vasodilators
  • Hydralazine
  • Minoxidil
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17
Q

what is angina pectoris?

how can it be treated pharmacologically?

A

insufficient oxygen supplied to cardiac muscles due to narrowing of coronary arteries (thrombi in them)

Single acute attack: glyceryl trinitrate potent vasodilator

Prophylaxis: sublingual GTN, aspirin, beta blockers, calcium channel blockers.

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18
Q

how can you pharmacologically treat a myocardial infarction?

A

Analgesia for pain relief
IV infusion to try and dissolve clot aspirin (blood thinner)

Prophylaxis: beta blockers, ACE inhibitors, aspirin, lipid lowering therapy

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19
Q

what is the treatment for heart failure?

A
  • Diuretics
  • ACE inhibitors
  • Nitrates
  • Beta blockers
  • Ionotropic drugs e.g., Digoxin
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20
Q

what are the different cardiac arrhythmias and what drugs are used?

A

Supraventricular tachycardia e.g., Adenosine, Verapamil

Arrhythmias caused by Wolf-Parkinson-White Syndrome e.g., Amiodarone, Disopyramide, Flecainide

Atrial fibrillation (atria not fully contracting) e.g., Digoxin, Disopyramide, Amiodarone

Ventricular tachycardia e.g., Lidocaine, Amiodarone

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21
Q

what are the types of cholesterol?

A
  • Low density lipoprotein (LDL)
  • High density lipoprotein (HDL)

LDL cholesterol (bad cholesterol) is particularly associated with atheroma and cardiovascular disease
HDL is good cholesterol

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22
Q

how do statins work?

A

Liver cells synthesis cholesterol.
Sometimes people are producing excessive levels of cholesterol.
Statins target key enzyme in synthetic pathway to cholesterol. Enzyme is called HMG-CoA.
Cholesterol production is blocked.
Cell wants to absorb more cholesterol so increases number of receptors on its surface and cell just takes all the LDL out of the system which is normally circulating in the blood.

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23
Q

what is recommended for px with mild depression?

A

watchful waiting-may recover with no intervention

CBT: individual guided self-help base on principles of cognitive behavioural therapy

CCBT: computerised cognitive behavioural therapy

Structured group physical activity programme

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24
Q

who should antidepressants be considered for?

A

*a history of moderate or severe depression

*subthreshold depressive symptoms present for a long time

*subthreshold depressive symptoms or mild depression that persist(s) after other interventions.

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25
Q

what is first line therapy for depression and why?

A

SSRIs: selective serotonin reuptake inhibitors. Suitable as first line therapy.

SSRIs are as effective as tricyclic antidepressants but much safer in overdose

26
Q

what causes depression?

A

reduced levels of the following monamine neurotransmitters in the brain:

-serotonin
-noradrenaline
-dopamine

27
Q

What types of drugs are used to treat depression?

A

SSRIs

tricyclic antidepressants

serotonin and noradrenaline reuptake inhibtors

monamine oxidase inhibitors (MAOIs)

28
Q

how do selective serotonin re-uptake inhibitors work?

A

*Monoamines are stored in pre-synaptic terminal
*They are released across the synaptic cleft and bind to a receptor on the post synaptic membrane. This receptor is called a 5-hydroxytrytamine (5-HT)
*Drug blocks 5-HT re-uptake transporter to prevent re-uptake of monamines which maintains level of 5-HT.
*This increases likelihood of binding to the target.

29
Q

name all the SSRIs

A

*Citalopram
*Escitalopram
*Fluoxetine
*Paroxetine

30
Q

how do tricyclic antidepressants work?

A

TCAs bind to 5-HT AND noradrenaline re-uptake transporters prevents the re-uptake of these monoamines from the synaptic cleft and their subsequent degradation.

Leads to the accumulation of 5-HT and noradrenaline in the synaptic cleft and the concentration returns to within the normal range

31
Q

why are TCAs not first line therapy in depression anymore?

what is one benefit of using TCAs over SSRIs?

A

High rate of side effects that may lead to lower compliance.

Longer half-live than SSRI – single dose regime, helps people sleep during the night

32
Q

name all the tricyclic antidepressants

A

Amitriptyline
Clomipramine
Imipramine
Lofepramine

33
Q

how do serotonin noradrenaline re-uptake inhibitors work?

name them

A

Serotonin-Noradrenaline Re-uptake Inhibitors- block re-uptakes of these neurotransmitters thereby increasing the concentration of these neurotransmitters at the synaptic cleft

Difference is chemical structure

venlafaxine
duloxetine

34
Q

how do monamine oxidase inhibitors work?

why is their use limited?

A

Monoamine oxidase is an enzyme that breakdowns monoamines into carboxylic acid in the presynaptic terminal so they can’t be released
MAOI inhibits monoamine degradation and results in greater stores available for release

due to the dietary restrictions (foods containing tyramine). Couldn’t eat cheese or anything fermented. Had to regulate their diet.

Can’t use antimuscarinic mydriatics on people on this drug

35
Q

name all MAOIs

A

Phenelzine
-Isocarboxazid
Moclobemide

36
Q

what are hypnotics used for?

what are anxiolytics used for?

A

short-term management of insomnia

short-term relief (two to four weeks) of anxiety that is severe, disabling or causing unacceptable distress to the patient

37
Q

what should be used if chronic anxiety is lasting more than 4 weeks?

A

antidepressant

38
Q

give examples of anxiolytics

A

Benzodiazepines (anxiety): Short half-life
Nitrazepam
Flurazepam

Benzodiazepines: Long half-life
Diazepam
Lorazepam
Oxazepam

39
Q

give examples of hypnotics

A

Non-benzodiazepine: hypnotics
Zopiclone

40
Q

how do benzodiazepines work?

what else can they be used for?

A

GABA is an inhibitory neurotransmitter
Bind to a binding site on GABA receptors. Enhances the effectiveness of GABA to reduce excitability at post synaptic membranes

relax muscle spasms so may be used for musculoskeletal problems

41
Q

what are antiphyschotic drugs used to treat?

what type of drug are they?

what are they divided into?

A

schizophrenia, bipolar disorder (mania), psychotic depression

synthetic drugs

atypical
typical

42
Q

what are typical antipsychotic drugs?

what are the side effects?

name them

A

Called conventional
Act primary at dopamine receptors

Parkinson’s disease: sedation, extrapyramidal effects, restlessness, dystonia, anti-cholinergic effects

Phenothiazines e.g., chlorpromazine. Effects accommodation and can see pigment/lesions in fundus.
*Thioxanthenes e.g., flupentixol
*Butyrophenones e.g., haloperidol

43
Q

how to atypical antipsychotics work?

why are they better than typical ones?

name them

A

Atypical antipsychotics act on other receptors as well as dopamine and are less likely than typical antipsychotics to cause movement disorders

less likely to cause side effects

  • Amisulpride
  • Clozapine
  • Olanzapine
  • Quetiapine
  • Risperidone
44
Q

what causes psychosis?

what do most antipsychotic drugs do?

A

is induced by increased levels of dopamine activity

Most antipsychotic drugs block postsynaptic dopamine receptors (D2 in particular)
May also affect cholinergic, histaminergic, serotoninergic receptors

45
Q

what is used to treat schizophrenia?

what are adverse effects of drug treatment?

A

atypical antipsychotics are better tolerated than typical antipsychotics

adverse effects: such as weight gain, hyperglycaemia, and occasional diabetes

46
Q

what drugs are used in bipolar disorder?

A

Acute attack :Benzodiazepines, Antipsychotics

Prophylaxis: Lithium

47
Q

what is an epileptiform event?

what do antiepileptics do?

how do anti epileptics prevent depolarisation of neurones?

A

a sudden, excessive depolarisation of cerebral neurones which may remain localised (focal epilepsy) or spread (generalised epilepsy)
Spontaneously or after brain trauma/stroke

prevent the recurrence of epileptiform events (seizures)

inhibition of excitatory neurotransmitters
direct membrane stabilisation
stimulation of inhibitory neurotransmitters

48
Q

what are common anti epileptics?

what anti epileptics with significant ocular adverse reactions?

A

Common antiepileptics:
Carbamazepine
Lamotrigine
Sodium Valproate

Antiepileptics with significant ocular adverse reactions:
Vigabatrin
Topiramate

49
Q

what is an adverse reaction?

what are the 2 types of adverse reactions?

A

Unwanted/harmful effect that happens following the use of a drug at its normal therapeutic concentration

type A: exaggeration of normal pharmacological reaction to a drug

type B: uncommon and unrelated to the known action of the drug

50
Q

what pharmacological variables mean the px is more at risk of getting an adverse reaction?

A
  • Dose-higher dose more risk
  • Duration- using for longer more risk
  • Formulation- can formulate to minimise risk
  • Route of delivery
  • Multiple drug therapy
  • narrow Therapeutic index
51
Q

what is digoxin derived from?
what does it treat?
how common are ocular ADRs?
how does it work?
what are the common ocular ADRs?
what are the other ADRs?

A

Purple foxglove.

Used to treat cardiac arrhythmias and heart failure

occur in 11-25% taking this drug

It’s a cardiac glycoside. Inhibits an important transporter found in heart and cornea and elsewhere: ATPase.

The most common ocular ADRs are disturbances of colour vision and various entopic phenomena
Xanthopsia (px seeing yellow or green tinge to objects).

Acts as diuretic (excessive urination), bradycardia (slow pulse)

52
Q

what is the yellow card scheme?

A

The Yellow Card Scheme was introduced at the wake of the Thalidomide disaster in 1964 to monitor the safety of UK medicines and act as an early warning system to identify potential side-effects and adverse reaction.

Administered jointly by the Medicines and Healthcare Products Regulatory Agency (MHRA) and the Commission on Human Medicines

The scheme relies on the voluntary reporting of adverse drug reactions (ADRs) by health professionals and patients

53
Q

what information does the yellow card scheme collect?

A

*adverse drug reactions
*medical device adverse incidents
*defective medicines (those that are not of an acceptable quality)
*counterfeit or fake medicines or medical devices
*safety concerns for e-cigarettes or their refill containers (e-liquids)

54
Q

as an optometrist what should we report to yellow card scheme?

A

*Any change in acuity
*Any change in IOP
*Any change in ocular structures
*Report all adverse reactions to new therapeutic agents (Black Triangle Drugs)
*Report all adverse reactions in children

55
Q

how are newly licensed drugs identified?

A

inverted black triangle

56
Q

what is amiodarone used to treat?

what ocular adverse reactions can you get?

A

treats cardiac arrhythmias

vortex keratopathy- occurs in 70-100% of px. reversible, takes 3 months to clear, VA not effected. looks like an octopus, starts as a horizontal line. px can experience halos around lights, blurred vision and glare

punctate lens deposits

optic neuropathy

57
Q

what is chloroquine used to treat?
what is hydroxychloroquine used to treat?

in which drug is an ocular adverse reaction more likely?

what ocular adverse reactions can you get?

are people on this drug monitored?

A

May be used in treatment of rheumatoid arthritis if other drugs have failed and to treat some forms of malaria

Not used commonly for malaria prophylaxis. Used very commonly in rheumatology
Used to treat rheumatoid arteritis and systemic lupus erythematosus (SLE)

chloroquine

the drug binds to melanin
retina toxicity in 2-3% of px on chloroquine chloroquine retinopathy is fine pigment mottling within the macula progressing to the classic “Bulls-eye maculopathy”
Chloroquine keratopathy is also commonly observed (~30%)
can lead to irreversible vision loss

*Every px put on the drug (will be on it for more than 5 years) are referred to an ophthalmologist who takes fundus photo and OCT as baseline. Also do a Humphrey 10-2.
*These tests are repeated periodically during the lifetime of px.

58
Q

what is chlorpromazine used to treat?
what ocular adverse reactions is it associated with?
what symptoms can px report?

A

Antipsychotic drug used in treatment of schizophrenia
Given systemically so reaches eye through circulation or aqueous humour.

Associated with pigmentary deposition in the eyelids, conjunctiva, cornea, lens, and retina
Corneal and lenticular changes are dose dependant
Lenticular changes initially observed as fine deposits under the anterior capsule
progressing to a stellate opacity (looks like a snowflake)

Patients may occasionally report glare, halos around lights and hazy vision
Asymptomatic

59
Q

what are the ocular adverse reactions associated with corticosteroids?

A

Risk of raised IOP (fluoromethalone/loteprednol less likely to raise IOP as don’t penetrate that much)
Posterior subcapsular cataract

60
Q

what is tamoxifen used for?

what ocular adverse reactions can occur?

is there monitoring?

A

Anti-estrogen drug used in the treatment of breast cancer at a dose of 20 mg daily
Reduces risk of reoccurrence of breast cancer

Retinopathy is rare (3%) but potentially serious

Macular oedema and yellow white refractile opacities within retina which may be associated with pigmentary changes and haemorrhage

Once VA reduced the effects are irreversible

Keratopathy (4%) can also occur (similar to that seen with amiodarone)

Can deposit in the lens

Possible dry eye problems

*baseline screening before therapy is recommended (VAs, Amsler, central visual fields and fundus photography)
*then annual monitoring

61
Q

what ocular adverse reactions can you get from contraceptive pill?

A

Decreased tolerance to contact lens wear (mediated through change in the tear film)

retinal vascular abnormalities (hemorrhage, thrombosis etc.)