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OD1 Semester 2 - Integrated Ophthalmic Sciences and Preclinical Optometry > Metabolic Disease - Week 4 > Flashcards

Metabolic Disease - Week 4 Flashcards

1
Q

From which process does the majority of retinal ATP production come from?

A

Oxidative metabolism

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2
Q

What systems have ATP usage the highest?

A

Any system for:

  • dark current
  • neurotransmission
  • ionic transport
  • cGMP, GTP production

remember by *dinc

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3
Q

What happens when blood glucose homeostasis is impaired?

A

Biochemical abnormalities in cells and tissues

Also diabetes

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4
Q

How does having diabetes affect risk of blindness?

A

25 times increased risk of blindness

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5
Q

What are three types of diabetes and their usual time of onset?

A

Type 1: little or no insulin. Less than 18 years old (unless you are Sean)

Type 2: resistance to insulin. Over 40 years old.

Gestational DM: during pregnancy

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6
Q

List ophthalmic complications of diabetic retinopathy [5]

A
  • corneal abnormalities
  • glaucoma
  • iris neovascularisation
  • cataracts
  • neuropathies
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7
Q

Which disease is the leading cause of new blindness?

A

Diabetic retinopathy

DR, because you’ll need a doctor to fix your blind eyes … I dunno

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8
Q

Prevalence of diabetic retinopathy?

A

28.5% among those with diabetes aged 40 years and older

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9
Q

Biochemical effect of hyperglycaemia?

A

Stimulates insulin secretion, promoting uptake of glucose by muscle and adipose tissue

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10
Q

Biochem effect of hypoglycaemia?

A

Elicits secretion of glucagon, epinephrine, cortisol, growth hormone, and counter-regulatory hormones that antagonise insulin action

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11
Q

Which mechanisms in the body are more efficient: glucose clearance or accumulation?

A

Clearance

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12
Q

How high is the glycemic index for foods that raise glucose levels gradually?

A

Low

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13
Q

Which glycaemic index level is associated with increased risk certain diseases? And what are they?

A

High

Diabetes, CVD, and AMD

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14
Q

In type 1 diabetes, what does intensive blood glucose control reduce the risk of and by how much?

A

Eye disease - by 76%

Kidney disease - by 50%

Nerve disease - by 60%

CVD - by 42%

Non-fatal heart disease, stroke or death from cardiovascular causes - by 57%

Ekncn - ekans n

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15
Q

What does DME stand for? And what does it mean?

A

Diabetic Macular Edema

- leakage into the retina. causes swelling of the retina and vision loss

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16
Q

What happens to the retina in proliferative Diabetic Retinopathy?

A

The retina is pulled away from its source of nutrition due to the growth of new blood vessels
- retina will die

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17
Q

What is the likelihood of the development of new blood vessels in severe non-proliferative Diabetic Retinopathy? What does this lead to?

A

Very high. Results in Proliferative diabetic retinopathy

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18
Q

What is the biochemical effect of hyperglycemia?

A

hyperglycemia stimulates insulin secretion, promoting uptake of glucose by muscle and adipose tisue

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19
Q

What is the biochemical effect of hypoglycemia? What is secreted?

A

Hypoglycemia causes secretion of:

  • glucagon
  • epinephrine
  • cortisol
  • growth hormone
  • counter-regulatory hormones

All these will antagonize insulin action

*GG C? EC! (it’s like you win a game and say gg, and you’re like ‘see?’ it’s ‘easy’)

20
Q

When testing for hyperglycemia (and diabetes) What percentage of glycosylated haemoglobin do you want to see for a patient to NOT have hyperglycemia?

A

A low percentage of glycosylated haemoglobin

21
Q

How does the percentage of glycosylated haemoglobin (i.e. HbA1c) affect the probability of Diabetic Retinopathy?

A

As percentage of HbA1c increases, so too does the probability of DR

22
Q

What are the aims in Type 2 Diabetic therapy?

A
  1. HbA1c less than 7%
  2. Blood pressure of 144/82 mmHg
  • also need to keep their lipids down
23
Q

How does reducing the percentage amount of HbA1c influence the risk of complications in type 2 diabetes?

A

For every 1% decrease in HbA1c: you get a 35% reduction in the risk of complications

24
Q

How does hyperglycemia and diabetic retinopathy affect the capillary basement membranes?

A

They get THICCer

25
Q

Consequences of a thick capillary basement membrane?

A
  • higher pressure in vessel
  • less elasticity/flexibility
  • smaller lumen (less blood volume)
  • more difficult perfusion/diffusion/active transport (it’s harder for oxygen to get through)
26
Q

Can diabetic retinopathy cause vessel and capillary death?

A

Yes

27
Q

Define pericytes

A

contractile cells that wrap around endothelial cells that line the capillaries and venules throughout the body

28
Q

Pathological effects of Diabetic Retinopathy?

A
  • pericyte loss
  • retinal capillary cell death
  • increased vascular permeability
  • progressive vascular occlusion
29
Q

How is glucose normally metabolised?

A

Through:

  • Glycolysis
  • TCA cycle
  • Electron Transport Chain (ETC)
30
Q

What pathways does Hyperglycemia influence that increase oxidative stress?

A
  • polyol pathway

- hexosamine pathway

31
Q

How does hyperglycemia affect the production of advanced glycation end products?

A

Increases it

32
Q

How does hyperglycemia affect protein kinase C activation?

A

activates it

33
Q

What are the pathway steps influenced by Hperglycemia? (pathways relating to glucose?)

A
  1. Increased glucose flux through polyol pathway
  2. Advanced glycation end-product formation
  3. Activation of PKC
  4. Increased activity through hexosamine pathway
34
Q

How does treatment with an aldose reductase inhibitor affect sorbitol levels (from the polyol pathway)?

A

Reduces sorbitol levels

35
Q

How does treatment with an aldose reductase inhibitor affect nerve fibre density?

A

Increases it

36
Q

Effect of increased sorbitol?

A
  • glycates nitrogen on proteins

- contributes to increased advanced glycation end products

37
Q

Ho do AGE precursors damage cells?

A

Several ways:

  • modification of intracellular proteins
  • diffuse out of cell and modify ECM molecules
  • diffuse out of cell and modify circulating proteins (such as albumin)
38
Q

How can you reduce accumulation of AGE in hyperglycemia?

A

Treatment with Aminoguanidine

39
Q

How did Aminoguanidine effect the histopathology seen in hyperglycemia?

A

reduced:

  • abnormal endothelial cells
  • pericyte dropout
  • acellular capillaries
40
Q

Explain the effect of PKC activation

A

PKC activation modifies gene expression, resulting in:

  • increased vascular permeability
  • fibrosis and increased risk of vascular occlusion
  • blood flow abnormalities
  • increased pro-inflammatory genes
41
Q

How does hyperglycemia lead to PKC activation?

A

Hyperglycemia increases the synthesis of DAG (Diacylglycerol), which then activates PKC beta, omega, and alpha

Hyperglycemia – DAG – PKC

42
Q

What does Streptozotocin do?

A

Kills insulin producing pancreatic beta-cells i.e. causing diabetes

43
Q

How was the action of PKC in diabetes examined in rats?

A

Mice made diabetic with streptozoticin and fluoroscein staining revealed blood vessel leakage.

PKC was then silenced with an interfering RNA, which stopped the leakage.

44
Q

What type of pathway is the Hexosamine pathway?

A

It is a glucose metabolic pathway

45
Q

Explain the hexosamine biosynthesis pathway

A
  1. F-6-P is converted to GA-6-P with GFAT
  2. The G.A-6-P is N-acetylated to form GluNac-6-phosphate
  3. This is dephosphorylated and linked to UDP to create UDP-GluNAc
  4. UDP-GluNAc is then used for protein glycosylation

*F6P = Fructose-6-phosphate, GA6P = glucosamine-6-phosphate, GluNAc = N-acetylgucosoamine

46
Q

What is GFAT (or GFA)?

A

Glutamine fructose-6-phosphate-aminotransferase. Is the rate limiting enzyme in the hexosamine pathway

47
Q

Define glycosylation

A

the controlled enzymatic modification of a molecule, especially a protein, by adding a sugar molecule

OD1 Semester 2 - Integrated Ophthalmic Sciences and Preclinical Optometry (49 decks)

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