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Unit 14 week 4 > Eye pharmacology > Flashcards

Eye pharmacology Flashcards

1
Q

Opsin receptors in rod and cone cells

A

Opsin receptors:

Rods-

Rod cells are stimulated by light over a wide range of intensities and are responsible for perceiving the size, shape, and brightness of visual images. They do not perceive colour and fine detail, tasks performed by the other major type of light-sensitive cell, the cone.

  • Rhodopsin- A biological pigment containing protein that sits in organelle membranes called discs.

Made up of a protein called an opsin and a photosensitive chemical called a chromophore derived from vitamin A- 11-cis-retinaldehyde.

Cones- come in different types reflecting the varying quantities of long, medium or short-wave sensitive opsins.

Long wave sensitive opsin 1- red cones

Medium wave sensitive opsin - green cones

Short wave sensitive opsin 1- blue cones

  • Rhodopsin= apoprotein* (AKA opsin) + *chromophore (11 cis-retinal)
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2
Q

11-cis-retinal response to light with and without apoprotein opsin present

A

without opsin- In solution, 1 photon can induce isomerisation of 11-cis-transretinal to all-trans-retinal (structural change ) with an efficiency of 1/3.

In rhodopsin***, 1 photon can induce the same change with an ***efficiency of 2/3.

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3
Q

Signalling involved in light transduction

A

Transducin (Gt) is comprised of 3 subunits:

  • a-GTPase

binds GDP in inactive state

Binds GTP in active state

Linked to membrane

C-terminal interacts with rhodopsin

B and y G subunits form a single regulatory functional unit

Rhodopsin activates transducin

Light activation results in release of GDP* and *binding of GTP to Gta

GTP bound Gta* is then f_ree to activates downstream signalling methods_* cGMP phosphodiesterase

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4
Q

Ga subunits and their effects

Gas

Ga1/0

Gaq/11

which one does transudcin have?

A

Gas- increases adenylate cylase –> increase cAMP –> incresae PKA

Ga1/0- decreases adenylate cyclase “”””

Gaq/11- increases phospholipase CB causing cGMP phosphodiesterase and decreased cGMP

Tansducin has a Ga subunit causing increased cGMP phosphodiesterase and decreased cGMP causing increased visual perception.

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5
Q

Term for large pupils?

term for constricted pupils?

A

mydriasis

miosis

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6
Q

Radial muscle

innervation

neurotransmitter

receptor

signalling proteins

function

A
  • innervation- sympathetic
  • neurotransmitter- Noradrenaline
  • receptor- a1 receptor
  • signalling proteins- Gq –> increase PLCB –> increase IP3–> increase Ca2+i
  • function- contraction
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7
Q

Circular muscle

A

innervation- parasympathetic

neurotransmitter- acetylcholine

receptor- M3

signalling proteins- Gq –> increase PLCB–> increase IP3 –> increase Ca2+i

function- contraction- constriction of eye

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8
Q

Atropine

A

CLASS- antimuscarininc/ parasympatholytic

CHEM- natural

PHARM- target: muscarininc GPCR receptors effect: non-selective competitive antagonist

PHYS- mydriasis, cycloplegia

CLIN- lazy ey, anterior uveitits

symp> para –> blocks this:

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9
Q

Cyclopentolate

A

CLASS: antimuscarinic/ parasympatholytic

CHEM: synthetic

PHARM: target: muscarinic receptors (GPCR)

Action: non-selective, competitive antagonist

PHYS: multiple effects; myadriasis, cycloplegia (paralysis of ciliary body- can’t convex lens)

CLIN: used in eye examination

BLOCKS THIS

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10
Q

Tropicamide

A

CLASS: antimuscarinic/ parasympatholytic

CHEM: synthetic

PHARM: target: muscarinic receptors (GPCR)

Action: non-selective, competitive antagonist

PHYS: mydriasis, cycloplegia

CLIN: eye examination

blocks this vvvvvv

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11
Q

Phenylephrine

A

CLASS: sympathomimetic

CHEM: synthetic, adrenaline derivative

PHARM: target- a1 receptors

Action: full agonist

PHYS: mydriasis, vasoconstriction

CLIN: eye examination and surgery

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12
Q

oTHER drugs that can cause mydriasis

A

Hyoscine butylbromide— anticholinergic

L-dopa- precursor of adrenaline

Mydriasis reduced by carbidopa

Cocaine- sympathomimetic, drug abuse

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13
Q

opiates- diamorphine

A

CLASS: opiate

CHEM: semi-synthetic, morphine derivative

PHARM: target: u receptors (GPCR)

Action: full agonist

PHYS: stimulates oculomotor nerve  miosis (constriction) among other things

CLIN: analgesic…

Para on

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14
Q

Pyridostigmine

A

CLASS: cholinesterase inhibitor

CHEM: synthetic

PHARM: target: acetylcholinesterase (enzyme)

Action: competitive reversible inhibitor

PHYS: increase [Ach] at cholinergic synapses  increase niconitic activity at NMJ (myasthesia gravis) in overdose

 increases muscarinic activity

CLIN: myasthesia gravis

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15
Q
A
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16
Q

Ciliary muscles are caused to contract by what innervation?

receptors?

signalling?

A

parasympathetic

M3- acetylcholine contraction . B2- adrenaline relax

M3 in iris- Gq- increased Ca2+i

B2 Gs–> increased AC– increased cAMP

17
Q

Gq Smooth muscle contraction pathway of signalling

A

Gq is the key pathway that can be coupled to multiple kinds of receptors (M3, a1, H1).

Gaq can be activated by things like opsins,,,,,,,,,

Calmodulin binds to elevated levels of calcium.

This complex activates MLC kinase, which in turn ohosphorylates MLC, which then triggers muscle contraction

18
Q

Gas activation to cause smooth muscle relaxation

A

19
Q

Glaucoma

A

Visual impairment

Progressive optic neuropathy, optic nerve cupping

Classification:

Primary/ secondary, acute/ chornic, open angle/ closed

IOP increased

IOP regulated by production and drainage of aqueous humor

impaired drainage through the trabecular meshwork (canal of Schlemm)

20
Q

production of aqueous humor

A

Ciliary body synthesises aqeous humour

Flow path:

INFLOW: ciliary body –> posterior chamber –> pupil –> anterior chamber 

OUTFLOW: 90% trabecular meshwork –> Schlemm’s canal –> scleral and episcleral veins. (pressure sensitive)

UVEOSCLERAL ROUTE (PRESSURE insensitive)

21
Q

production of aqueous humor by 3 methods

A
  1. Passive diffusion of solutes down pressure gradient
  2. Filtration of fluid from fenestrated capillaries into interstitium of ciliary stroma (passive)
  3. Active secretion of solutes against gradient 80-90%)

2 important biochemical mechanisms

sodium potassium ATPase pump

Carbonic anhydrase

22
Q

Drugs for galucoma work by:

increasing aqueous drainage:

x

x

x

reducing aqueous production:

xxx

A

increasing drainage

  • Fc receptor agonists (-prost) –> via uveoscleral route
  • cholimemtics –> via trabecular/ schlemm route

reducing aqueous production

  • B blockers -olol
  • carbonic anhydrase inhinbitors -zolamide
  • A2 adrenergic agonists -onidine
    *
23
Q
A
24
Q

Prostaglandin

A

CHEM- all prodrug analogues of PGF2a

Free acid forms are most active (esters and amide)

PHARM- target- FP receptor (GPCR)

Action- agonist

1* signalling- Gq/11

PHYS-

Increase permeability of sclera

Increase aqueous outflow via the uveoscleral route

No effect on aqueous production

CLIN- 1st line treatment for glaucoma in many cases

Topical application

25
Q

trepostinil

A

Synthetic analogue of PGI2

IP receptor agonist

Vasodilation

Pulmonary art hypertension

26
Q

B blockers

A

CLASS: B blockers (-olol)

CHEM: all small molecules

PHARM: all competitive antagonists

PHYS: decrease sympathetic tone of ciliary body

Decrease aqueous humour formation (decrease inflow)

CLIN: chronic open-angle glaucoma, ocular hypertension

27
Q

apraclinidine

A

CLASS: sympathomimetic

CHEM: synthetic

PHARM: target- a2-adrenergic receptor GPCR

Action- full agonist

1* signalling- Gi/o

PHYS:

Decreased sympathetic tone (pre-synaptic)  decreased aqeous formation

Increased uveoscleral drainage causing increased outflow

Also: mydriasis, disruption of accommodation

CLIN: glaucoma

28
Q

clonidine

A

CLASS: sympathomimetic

CHEM: synthetic

PHARM:

Target- a2-adrenergic receptor (GPCR)

Action- partial agonist

1* signalling: Gi/o

PHYS:

Can enter CNS

Direct action on ventral medulla

Pre-synaptically  decreases cAMP  decreases Ca2+ influx and NA release

Decreases sympathetic tone

CLIN:Hypertension

29
Q

adrenoreceptor classification and signalling

A
30
Q

acetolazamide

A
31
Q

carbonic anhydrase in ciliary processes

A

Carbonic anhydrase in ciliary processes

Ca –> increases [HCO3-]I –> more Na+ transport

Formation of intracellular HCO3- by CA contributes to the movement of Na+ into the cell, ensuring Na+i is sufficiently high to supply sodium pump with substrate.

HCO3- also enters via the co-transporter with Na+. CA facilitates rapid transport/ diffusion of HCO3- as CO2 between epithelial layers. HCO3- passes into aqueous.

32
Q

dorzolamide

A

CLASS: carbonic anhydrase inhinbitor

CHEM: synthetic

PHARM: target- carbonic anhydrases

Action- competitive inhibitor

PHYS:

Decreases [HCO3-] in ciliary epithelia

Decreased HCO3  decreased Na+  substrate for NA+/K+-ATPase

“ decreases pH  decreases action of NA+/K+-ATPase

“ decreases co-transport into aqueous with Na+  decreased aqueous formation

CLIN: open-angle glaucoma

33
Q

pilocarpine

A

CLASS: parasympathomimetic

CHEM: natural small molceule

PHARM:

Target- muscarinic receptors (GPCR)

Action- non-selective, partial agonist

1* signalling: M1, 3, 5

PHYS:

M3 on ciliary muscle  contraction of LCM  opening of trabecular meshwork/Schlemm’s canal decreases outflow resistance  increases ocular aqueous outflow

Miosis, disruption of accommodation, headache

CLIN: acute closed angle glaucoma

34
Q

Age related macular degneration

A

Progressive degeneration of central retinal cells –> vision loss

Classification

Dry (non-neovascular): degeneration without formation of new blood vessels

Wet (neovascular): new vessels form and damage retina

Active- may benefit from treatment

Inactive- changes probably irreversible- unlikely to benefit from treatment

Available drugs all target VEGF pathway

35
Q

VEGF-A – vascaulr endothelial growth factor

A

CHEM: homodimer

PHARM: binds to VEGF receptors- receptor tyrosine kinase

PHYS:

Endothelial cell proliferation

Promotes cell migration

Inhibits cell migration

Inhinits apoptosis

Induces permeabilization of blood vessels

CLIN: ANTI-VEGF used in tumours, AMD and diabetic eye disease

36
Q

Bevacizumab

A

CLASS: angiogenesis inhibitor

CHEM: IgG

PHARM: target- VEGF-A

Action- blocking

PHYS:

VEGF promotes angiogenesis

Decreased blood vessel formation slows degeneration of retina

CLIN:

Wet-type age related macular degeneration

37
Q

Ranibizumab

A

CLASS: angiogenesis inhibitor

CHEM: fab fragment of bevacizumab

PHARM: target- VEGF-A

Action- binding/ blocking

PHYS: VEGF promotes angiogenesis

Decreased blood vessel formation slows degeneration of retina

CLIN: Wet-type age related macular degeneration

38
Q

Aflibercept

A

CLASS: angiogenesis inhibitor

CHEM: fusion protein of human IgG Fc and ligand binding domain of VEGRF-1 and VEGRF-2 receptors

PHARM:

Target- VEGF-A and B growth factors

Action- binding/ blocking

PHYS:

VEGF promotes angiogenesis

Decreased blood vessel formation slows degeneration of retina

CLIN: Wet-type age related macular degeneration

Unit 14 week 4 (5 decks)

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