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Principles of Drug Action > Diabetic Retinopathy > Flashcards

Diabetic Retinopathy Flashcards

1
Q

Pathophysiology of Diabetic retinopathy

A
  • Prog. damage to retina due to complications of diabetes mellitus
  • can cause blindness
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2
Q

The retina is composed of the ____ and the _____.

A
  • Macula

- Fovea

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3
Q

What is the macula?

A
  • Retinal area about 5 mm diameter; directly behind pupil

- high conc. of cones for crisp central vision

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4
Q

What is the fovea?

A
  • Found at center of macula
  • highest density of cones in retina
  • important for central vision (color res., driving, reading)
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5
Q

What are the 3 classifications of diabetic retinopathy?

A
  • Nonproliferative DR (inital stage of disease)
  • Proliferative DR (advanced stage)
  • Diabetic macular edema (can occur at any stage of disease)
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6
Q

What initiates the cascade of biochemical processes that drive DR disease progression?

A

Chronic intracellular hyperglycemia

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7
Q

Which processes are compromised in the cascade?

A
  • Aldose reductase(Sorbitol) and protein kinase pathways(PKC)
  • Renin-angiotensin system (RAS)
  • Oxidative stress
  • Accumulation of advanced glycation end products (AGE)
  • Release of inflamm. mediators and VEGF which damage ophthalmic vascular endothelial cells
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8
Q

non-proliferative DR can be classified as mild, ____, and ______.

A

moderate and severe

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9
Q

Mild NPDR

A

-tiny swellings (microaneurysms) in retinal capillary walls

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10
Q

Moderate NPDR

A
  • has exudates (lipid-rich deposits from leaky damaged capillaries)
  • edema and retinal hemorrhages
  • capillary occlusions (body trying to repair vessel damage—>ischemic retina)
  • cotton wool spots (formed by oxygen-deficit distal to capillary occlusion)
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11
Q

Severe NPDR

A

-severe hemorrhages, microaneurysms, and exudate formation

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12
Q

Describe the clinical findings of diabetic macular edema (DME)

A
  • retinopathy (thickening and edema) within macula area
  • most common cause of vision loss in DR
  • peripheral vision is sustained
  • can occur at any stage of DR
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13
Q

Clinical findings: Pathophysiology of Proliferative DR

A
  • Occlusion of blood vessels with ischemia –>upregulation of growth factors
  • ->stimulate formation of new blood vessels
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14
Q

What are the complications of proliferative DR?

A
  • New blood vessels are abnormal and thin
  • easily ruptured; bleed into retina and vitreous
  • scar tissue may form on blood vessels
  • damaged tissue may pull on retina (retinal detachment)–>spotty vision, light flashes, vision loss
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15
Q

How does proliferative DR’s vision loss differ from nonproliferative DR?

A

Proliferative DR causes more severe vision loss, and it can affect both central and peripheral vision.

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16
Q

Why is VEGF important in Proliferative DR?

A
  • major factor in new blood vessel formation
  • increased levels reported in patients with disorder
  • activates two kinase receptors (VEGFR-1 and VEGFR-2)–>regulate pathophysiological angiogenesis
  • proliferation, migration, survival, and angiogenesis of endothelial cells
17
Q

VEGF also increases retinal vascular permeability and causes breakdown of ____ leading to ______.

A
  • blood-retinal barrier

- retinal edema

18
Q

What is the strategy of pharmacological intervention in DR?

A

prevent, slow, or reverse vision loss in order to maintain or improve vision-related quality of life

19
Q

Which drug classes are used in the treatment of DR?

A
  • Corticosteroids

- VEGF inhibitors

20
Q

Which corticosteroids are used?

A
  • Dexamethasone

- Fluocinolone

21
Q

Corticosteroid MOA

A

produce anti inflamm actions by:

  • decrease release of vasoactive/chemo-active factors at sites
  • decreased secretion of lipolytic and proteolytic enzymes
  • decrease leukocyte migration
  • increase tight junctions b/t capillary endothelial cells
22
Q

What is Dexamethasone used to treat? How is it administered?

A

-intravitreally active
-Treats macular edema following branch or central retinal vein occlusion
-Treats diabetic macular edema
-Treats non-infectious uveitis affecting
posterior segment of eye

23
Q

What is Fluocinolone used to treat? How is it administered?

A
  • Active intravitreally (as an implant)

- Treats diabetic macular edema in pats previously treated with corticosteroids without significant rise in IOP

24
Q

What is the MOA of VEGF inhibitors?

A

inhibit VEGF production and preventing retinal neovascularization

25
Q

How is Ranibizumab used for DR?

A
  • recombinant humanized antibody fragment; active against all VEGF-A isoforms
  • active intravitreally
  • Treats DR, diabetic macular edema, neovascular (wet) age-related macular degeneration*
  • macular edema following retinal occlusion
  • myopic choroidal neovascularization*
26
Q

How is Aflibercept used?

A
  • recombinant fusion protein
  • binds VEGF-A w/ higher aff than ranibizumab
  • binds VEGF-B and placental growth factor
  • active intravitreally
  • Treats DR, diabetic macular edema, neovascular (wet) age-related macular degeneration*
  • macular edema following retinal vein occlusion

Principles of Drug Action (4 decks)

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