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CMBM exam 3 > Diabetic Cellular Damage > Flashcards

Diabetic Cellular Damage Flashcards

1
Q

In the fasting state blood glucose concentration is determined by the balance between endogenous glucose production is through…

A

Hepatic glycogenolysis and gluconeogenesis and use insulin dependent tissues

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2
Q

What is different about diabetes insipidus when compared the diabetes mellitus?

A

The symptoms of both are similar (inc urination and thirst)

Different b/c urine not concentrated normally, frequent, pale in color, low concentration of solutes

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3
Q

What is type 1 diabetes mellitus?

A

The inability to produce insulin and usually diagnosed in childhood

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4
Q

What is type 2 diabetes mellitus?

A

Combination of insulin resistance and dysfunctional pancreatic beta cells

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5
Q

What types of food and hormones stimulate insulin release?

A

Sugars, amino acids, free fatty acids

Glucagon, GLP-1, GIP and secretin

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6
Q

What is the key feature of diabetes?

A

increase in Insulin resistance

Uncontrolled liver glucose production

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7
Q

Do beta cells still function in type 2 diabetes?

A

Yes but there is not enough insulin being made

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8
Q

What are the macrovascular complications of diabetes?

A

Cardiovascular disease (dyslipipdemia)
Ischemic heart disease
Stroke
Peripheral vascular disease

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9
Q

What are the microvascular complications of diabetes?

A

Retinopathy
Nephropathy
Peipheral neuropathy

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10
Q

<p>Which tissues are damaged in long-term hyperglycemia?</p>

A

<p>Capillary endothelia in retina</p>

Renal mesangial glomerulus cells</p>
Schwann cells in the peripheral nerves</p>

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11
Q

Diabetic complication are indicated to occur…

A

Intracellularly

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12
Q

What does aldose redutase do?

A

Reduces toxic aldehydes to sugar alcohol

ex. reducing galactose to galacticol using electrons from NADPH

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13
Q

If glucose levels are too high in the eye what forms?

A

Sorbitol using NADPH

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14
Q

Why would oxidative stress occur if there is excess glucose?

A

NADPH is wasted converted glucose to sorbitol so there is less to re-reduce glutathione, a critical antioxidant. The build up of sorbitol causes osmotic swelling (in the eye for example) because it is trapped in cells.

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15
Q

What does the gene AKR1B1 do?

A

Encodes aldose reductase
Eliminates some toxic lipid aldehydes
May reduce inflammatory responses

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16
Q

What happens to sorbitol of AKR1B1 (aldose reductase) is inhibited?

A

The sorbitol level is reduced and NADPH is not wasted

17
Q

The process of aldose reductase reducing aldehydes incorrectly in a diabetic state is called…

A

Increased flux through polyol pathway

18
Q

What are Advanced Glycation Endproducts (AGEs)?

A

Low molecular weight products that diffuse out of cells

Large molecules derivatives that have been damaged (or crosslinked)

19
Q

What are the step in intracellular AGE precursor damage?

A
  1. Intracellular proteins damaged (gene regulators)
  2. Modification of extracellular matrix molecules - affects signalling
  3. Modification of circulating proteins in blood (albumin)
20
Q

What is a protein that is irreversibly modified or crosslinked by AGEs?

A

Hemoglobin A modified to Hemoglobin A1c

21
Q

What can A1c be used for in term of diabetic testing?

A

Long term glucose damage

22
Q

What do Receptors for AGEs react to in the blood?

A

Activates inflammatory cytokines and growth factors

23
Q

What causes protein kinase C (PKC) activation in hyperglycemia?

A

Lipid second messenger diacylglycerol (DAG)

24
Q

What happens in the hexosamine pathway?

A

Excess glucose is shunted to the pathway which may cause N-acetyl glucosamine to be added to Ser/Thr instead of phosphorylation

25
Q

What does the hexosamine pathway affect?

A

Endothelial cells and kidney cells

26
Q

In the four types of damage pathways, how did inhibitors hold up?

A

They were ineffective

27
Q

What is the common factor in the four types of damage pathways?

A

Increased production of reactive oxygen species by mitochondrial electron transport

28
Q

If there is too much glucose, too much ____ is made and the ___ gets backed up.

A

NADH, ETC

29
Q

What is the diabetes pathway model of all four pathway damage together?

A

Hyperglycemia to superoxide to ultimately damages glycolytic enzyme glyveraldehyde-3-P-dehydrogenase (GAPDH)

30
Q

What is a possible treatment for the pathway damage model?

A

Transketolase activators

CMBM exam 3 (24 decks)

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