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Patient > Hormones and reproduction > Flashcards

Hormones and reproduction Flashcards

1
Q

define glaucoma?

A

blanket term for a variety of conditions

common factor is acquired progressive neuropathy if untreated

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2
Q

pathophysiology of glaucoma

A

optic nerve damage
visual field loss
eventual blindness

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3
Q

symptoms of glaucoma?

A

usually asymptomatic

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4
Q

what should happen if you’re over 40 years

A

yearly checks

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5
Q

what is the normal range for interoccular pressure?

A

12-16 mmHg

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6
Q

what is the IOP in people with glaucoma?

A

> 21mmHg

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7
Q

risk factors for glaucoma?

A 
family history 
race- africans 
systemic hypertension 
CVD 
migraine 
previous ocular disease r surgery
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8
Q

what is glaucoma usually caused by?

A

impaired drainage of aq humour

can be primary or secondary- due to something else

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9
Q

closed angle tends to be treated by?

A

surgery

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10
Q

what does open angle refer to?

A

the angle between the iris and outer bit

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11
Q

what is the trabecular meshwork?

how does this allow for aq humour flow

A

at the crook of the angle: with lots of spaces between the cells so the AH can flow through these spaces into the collector tunnel and into the episcleral vein

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12
Q

once the AH has flowed through the spaces in the TM where does it go?

A

into the collector tunnel and into the episcleral vein

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13
Q

where is the AH produced?

A

Cilary muscle, where the outer epithelial cells create the AH from the capillary fluid

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14
Q

why does the AH flow into the episcleral vein?

A

as the pressure in the anterior chamber is higher than the vein
16mmHg compared to 8mmHg

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15
Q

the trabecular network allows ___% of the AH to flow through

A

80

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16
Q

what is another method of AH outflow besides the TM

A

scleral outflow- it can bypass the TM and go through the cells of the sclera and ciliary body into the venous system

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17
Q

why is scleral outflow less than the TM

A

cells are held tighter together so there’s more resistance

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18
Q

what do we look for in antiglaucoma treatment?

A

reduced IOP- as this is what causes neuropathy
<16-20mmHg
drug to have a sufficient duration of action
prevention of vision loss
compatible with other drugs
lack of side effects
no loss of effects over time

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19
Q

why do we want IOP below 16-20 mmHg

A

as below 21 will prevent neuropathy

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20
Q

why dont we want the drugs to lose effects over time

A

as usually life long

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21
Q

what are first line glaucoma treatment?

A

prostaglandins and prostamide analogues

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22
Q

PG__ has a huge impact of AH production

A

E

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23
Q

why cant we use PGE for treatment?

A

as its very unstable so gets broken down quickly

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24
Q

analogues of PG F2a are used as they are?

A

more stable

esters- more stable in formulation

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25
Q

why are prostaglandins a good treatment?

A

unique mechanism of action to decrease IOP

most efficacious

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26
Q

examples of the prostaglandin (F2a) analogues?

A

latanoprost
travoprost
Tafluaprost

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27
Q

what do prostaglandin F2a act on?

A

PGF2a receptor (FP receptor)

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28
Q

what happens to the prostaglandin (F2a) analogues? they’re _______

A

converted back to the acid (from the ester) so they’re prodrugs
only the acid binds to the FP receptor

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29
Q

the FP receptor is a _______

A

GPCR

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30
Q

what happens once the FP receptor is stimulated?

A

Gaq

once stimulated will activate PLC, dag and IP3

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31
Q

where are FP receptors present?

A

Hilary body
ciliary muscle
sclere
iris sphincter- doesn’t have much effect on IOP

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32
Q

where do the prostaglandin (F2a) analogues have little effect on IOP? why?

A

iris sphincter
TM

as there’s few of the receptors present

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33
Q

what are the 3 PG analogues?

A

latanoprost
tafluprost
travoprost

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34
Q

the 3 PG analogue are ______

A

prodrugs

ester converted to acid

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35
Q

the 3 PG analogues have a _____ duration action, hence

A

short

only need to take once at night

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36
Q

PG analogues lower IOP by?

A

35%

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37
Q

how well are PG analogues tolerated?

A

well!

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38
Q

what are protamine analogues?

A

analogues of prostaglandin F2a1

ethanol amide

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39
Q

what do prostamide analogues act on?

A

also FP receptors

prostamide receptors- more expressed in TM

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40
Q

where are prostamide receptors expressed more in comparison to PG

A

TM

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41
Q

effects of prostamide analogues?

A

increased uveoscleral and trabecular outflow

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42
Q

are prostamide analogues a prodrug

A

no

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43
Q

TF: PG analogues are more potent at FP receptors than prostamide analogues?

A

false- just as potent as each other

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44
Q

are the efficacy, tolerability and side effects of prostamide analogues the same as PG analogues? why?

A

yes

as predominant action for both is via the same receptors

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45
Q

example of prostamide analogues?

A

only one

bimatoprost

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46
Q

prostamide analogues mechanism of action?

A

increase uveoscleral outflow

reduced resistance to outflow by remodelling extracellular matrix which is achieved by: Increase matrix metalloproteinases
Degrades collagen and extracellular matrix
Decreases resistance of ciliary muscle and sclera to increase outflow

FPs on ciliary muscles and body and sclera
TB- negabile increase

47
Q

how do protamine analogues cause reduced resistance to outflow?

A

Increase matrix metalloproteinases
Degrades collagen and extracellular matrix
Decreases resistance of ciliary muscle and sclera to increase outflow

48
Q

how do prostamine analogues increase AH flow through the scleral cells?

A

change the cell structure
more enzymes introduced to break down collagen structure of the scleral cells

lose and holey cells like the TM

49
Q

side effects of PG and PA analogues?

A

red eye- vasodilation
increased pigmentation in iris, eyelashes and periocular skin
eyelash growth and darker
sensitivity to light
pregnancy its contraindicated as PGs are needed for cell growth and can induce labour

50
Q

will you always get vasodilation with PGs and PA analogues?

A

no decreases after the first couple of times

51
Q

why does PGs and PA analogues cause pigmentation?

A

FP receptors are onmelanocytes

52
Q

what are rare side effects fo PG and PA analogues?

A

sensitivity to light

precipitate or worsen cymoid macular oedema in aphakic eyes

53
Q

how do beta 2 cells contribute to AH production?

A

GPCR
cAMP production- which regulates ion transport in the ciliary epithelium
greater ion movement into the posterior chamber which = osmotic gradient
more fluid is thus filtered into the chamber

54
Q

which ion channels does cAMP have an effect on in pigmented cells?

A

Na/ K/ 2Cl

55
Q

which ion channels does cAMP have an effect on in non- pigmented cells?

A

Cl- efflux

56
Q

what treatment can target B2 cells for glaucoma?

A

beta blockers to prevent AH production

57
Q

mechanism of action: beta blockers

A

Decreased ion concentration
Decreased fluid along gradient
Decreased volume of aqueous humour
Better balance of production and drainage

58
Q

advantages of beta blocker treatment?

A

well tolerated
rapid
very effective (75%)
compatible with other drugs

59
Q

how effective are beta blockers?

A

work in 75% of patients

60
Q

how much do BBs lower IOP?

A

lower IOP by 20-30%

61
Q

TF: beta blockers are better than PG analogues?

A

false

62
Q

disadvantages of beta blockers?

A

systemic absorption- effects on both eyes

efficacy declines over time

63
Q

administration of BBs?

A

twice daily

od in some preparations

64
Q

CV side effects of BBs?

A

bradycardia
hypotension
peripheral vasoconstriction

65
Q

bronchial side effects of BBs?

A

construction

cant be used in asthma or obstructive airway disease

66
Q

diabetic side effects of BBs?

A

masks hypoglycaemia

67
Q

can you use BBs and PGs in combination?

A

yes- additive effects

68
Q

advantages of using BBs and PGs in combination?

A

decrease cost
avoids washout effect- with 2nd drop
reduced exposure to preservatives
patient compliance

69
Q

what is the third line treatment for glaucoma

A

carbonic anhydrase inhibitors

70
Q

when are CAIs used?

A

if BBs and PGs aren’t tolerated or suitable

71
Q

TF: CAIs are only used locally

A

false- also systemically but only in emergencies

72
Q

so when are CAIs systemically used?

A

only in emergencies

73
Q

where do the CAIs work in the eye?

A

in the ciliary epithelium

74
Q

mechanism of action?

A

inhibits
CO2+H20 H2CO3 H+ HCO3-

bicarbonate formation is required for Aq secretion

75
Q

______ formation is required for aq secretion

A

bicarbonate

76
Q

what does bicarbonate do help aqueous secretion?

A

moves into the posterior chamber and fluid follows along a gradient

77
Q

effects of CAIs?

A 
prevent bicarbonate being moved into posterior chamber
decreased: 
ion concentration 
fluid along gradient 
volume of AH
78
Q

systemic CAIs? why not topical?

A

acetazolamide- not lipophilic so not topically absorbed

79
Q

when is acetazolamide used?

A

OAG

secondary glaucoma and peri-operatively in acute glaucoma

80
Q

how is acetazolamide administered?

A

emergency injection

81
Q

side effects of acetazolamide?

A

increased risk of allergy and blood disorders as it has a sulphonamide group

GI problems 
diuresis 
acid/base disturbances 
drowsiness and depression 
parasthesias
82
Q

acetazolamide is a _______ derivative

A

sulfonamide

83
Q

why is there an increased risk of allergy and blood disorders in acetazolamide?

A

as it has a sulphonamide group

84
Q

how can CAIs be developed to make a better glaucoma treatment

A

better lipid solubility for corneal absorption

decrease side effects
more selective- CA II enzyme

= Dorzolamide and brinzolamide

85
Q

CA __ are mostly expressed in the eye. so…

A

II

so if you can target those it will decrease systemic side effects

86
Q

what drugs are a result of CAI modification?

A

dorzolamide

brinzolamide

87
Q

can CAIs be used with BBs or PGs?

A

yes

88
Q

when is CAIs indicated as sole therapy?

A

when BBs cant be used

89
Q

CAIs produce an approximate reduction in IOP of?

A

20%

90
Q

topical CAIs side effects?

A

transient burning and stinging- acidic
blurred vision
conjunctival hyperaemia (redenning)
taste disturbances, dry mouth and headache

91
Q

why do CAIs (topical) cause burning?

A

acidic

92
Q

pH of brinzolamide drops?

A

7.5

93
Q

pH of dorzolamide drops?

A

5.6-6

94
Q

where are A2 receptors in the eye?

A

ciliary epithelial cells

conjunctival and corneal epithelial cells

95
Q

advantages of A2 adrenoceptor agonists

A

no mydriasis
no vasoconstriction
little effect on CV system- a2 selective

96
Q

why do A2 agonists have little effect on CV system

A

A2 selective

97
Q

A2 agonist mechanism of action?

A

 Decrease secretion of aqueous
Decreases cAMP (Gi coupled; inactivates adenylate cyclase)
Decreases ion transport and ion efflux. Decreased osmotic gradient
Decreases aqueous secretion
Decreases ultrafiltration- less fluid filtered from the capillaries
(reduced blood flow, vasoconstriction)
Increases uveo-scleral outflow
Neuroprotective

98
Q

why are a2 agonists thought to be neuroprotective

A

preserve optic nerve

retinal ganglion cells

99
Q

a2 agonists show tachyphylaxis, what does this mean?

A

rapid, non selectivity to agonists

therefore limited lifetime of action

100
Q

why do a2 agonists have a limited lifetime of action?

A

as they show tachyphylaxis:

rapid, non selectivity to agonists

101
Q

due to the tachyphylaxis, what are a2 agonists used for?

A

NOT chronic management

post surgery and pre surgery to prevent changes in IOP

102
Q

why are a2 agonists used pre and post surgery?

A

to prevent changes in IOP

103
Q

2 a2 agonists used?

A

brimonidine

apraclonidine

104
Q

Brimonidine are ____ selective.

_____ onset

A

a2

rapid- 2 hours

105
Q

apraclonidine are ____ selective for a2 agonists than brimonidine
used _____ term
limited because of its?

A

less
short
side effects

106
Q

local side effects of a2 agonists?

A

allergies
stining
blurred vision
photophobia

107
Q

systemic side effects of a2 agonists?

A 
hypotension 
droziness 
fatigue 
dry mouth 
taste disturbances
108
Q

what is pilocarpine?

A

muscarinic agonist- M3

109
Q

pilocarpine mechanism of action?

A

Contract ciliary muscle M3. Those in the iris doesn’t contribute to the MOA for glaucoma treatment
Ciliary muscle contracts which
Pulls scleral spur (bit that juts into the eye)
Opens trabecular meshwork
Increases trabecular outflow- drainage
Decreases IOP

110
Q

pilocarpine effects last for?

A

6 hours

111
Q

how often do you use pilocarpine?

A

4 times a day

COMPLIANCE!!

112
Q

Pilocarpine has a _____ effect on lowering IOP.

A

Cyclical

113
Q 
Which of the drugs used to treat glaucoma would bring an increased intraocular pressure of 32mmHg back within an acceptable range?
Alpha 2 adrenoceptor agonist
Beta blocker
Carbonic anhydrase inhibitor
Parasympathomimetic
Prostaglandin analogue
A

Prostaglandin analogue- only just into the normal range. At pressures above this you will probably used a fixed dose combination for 2 different mechanism

114
Q 
Which class of drug most effectively reduces ion transport in the ciliary epithelium?
Alpha 2 adrenoceptor agonist- <20%
Beta blocker
Carbonic anhydrase inhibitor- <20%
Parasympathomimetic
Prostaglandin analogue
A

Beta blocker- about 20-30% reduction

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