FORM & FUNCTION (DM Complications)

Question 1

Glucotoxicity and cataracts definition:

Answer 1

-opacity of lens (due to precipitates) leading to light scattering (blind)
>can’t focus light on retina
*once occurred, changes are irreversible (will need surgery)

Question 2

Cataracts prevalence dogs:

Answer 2

-50% develop it within 6 months of diabetes diagnosis
-more than 80% develop it by 16 months after diagnosis
*rare in cats

Question 3

Cataract formation:

Answer 3

-glucose is converted to sorbitol by aldose reductase
-when glucose is increase=more converted to sorbitol
>accumulation of sorbitol in lens

Question 4

Aldose reductase activity:

Answer 4

-normal: 5% glucose converted
-hyperglycemia: 10-33% converted

Question 5

Accumulation of sorbitol:

Answer 5

-hyperosmolarity sets in (increase solute concentration)
1. Proteins aggregation (insoluble, clouding)
2. Influx of water into lens fiber (swelling)
*leads to cataract formation

Question 6

Feline vs. canine lenses:

Answer 6

-aldose reductase activity is lower in feline lenses vs. canine lenses (older animals, over 4 years old)

Question 7

DM glucose toxicity:

Answer 7

-glucose spontaneously react with amino groups of protein, DNA and lipids to form Amadori products = GLYCATION

Question 8

Glycated proteins: hyperglycemia

Answer 8

-increased leading to altered function
*fructosamine

Question 9

Fructosamine:

Answer 9

-glycated serum albumin
-used as a diagnostic tool for DM
-half life around 20 days: 2-3 weeks of glucose range =more accurate than single blood draw

Question 10

HbA1c: humans

Answer 10

-gold standard in humans as it’s more stable (2-3months glucose range)
-increasing for vet med, but clinical efficacy still TBD

Question 11

DM lipid toxicity: insulin deficiency/resistance affects

Answer 11

-reduced VLDL synthesis
-reduced LPL activity
-uninhibited HSL activity
*leads to hyperlipidemia and then hepatomegaly (fatty liver cirrhosis)=LIVER FAILURE

Question 12

Liver failure leads to loss of:

Answer 12

-protein synthesis (ex. serum albumin)
-glucose and glycogen regulation
-lipid biosynthesis, uptake and export

Question 13

DM pancreatitis:

Answer 13

-hyperlipidemia (diabetes, obesity) increases the risk factor of pancreatic inflammation
-high levels of circulator fat associated with immune cells=trigger inflammation events at pancreas=necrosis and cell death

Question 14

Pancreas vital functions:

Answer 14

-endocrine system: produce insulin and glucagon
-digestive system: secretion of digestive enzymes into small intestine

Question 15

DM ketoacidosis:

Answer 15

-high rates of ketogenesis=reduction of bicarbonate=metabolic acidosis (diabetic ketoacidosis)

Question 16

Adverse effects of metabolic acidosis:

Answer 16

-majority of enzymes for energy metabolism are pH dependent
-low pH=protein denaturation=loss of protein function=impaired energy production

Question 17

DM fluid/electrolyte imbalance steps:

Answer 17

1. Enter the kidney tubercule (concentration exceeds the renal threshold) (glucose and ketone)
2. Increase tubule osmotic concentration of fluids inside the nephron
3. Decrease water reabsorption
4. Increase polyuria and polydipsia

Question 18

Renal threshold:

Answer 18

-concentration of a substance dissolved in blood which leads to kidney removing the substance from blood into urine

Question 19

Polyuria

Answer 19

-increase urination

Question 20

Polydipsia:

Answer 20

-increase thirst

Question 21

Consequences of increase polyuria and polydipsia:

Answer 21

-decrease in blood volume (hypovolemia)=circulatory shock=organ failure leading to death
*acute and life-threatening condition:
*requires fluid therapy

Question 22

Renal function: water normally

Answer 22

-usually reabsorbed due to higher osmotic concentration of the interstitial fluid