Exam 8: L. 8: Glucose!

Question 1

Normal blood glucose

Answer 1

1) sole source of energy for the brain (to a limited extent in extreme cases the brain may use ketone bodies)
- blood glucose kept tightly regulated
- normal blood glucose: 70-120 mg/dl

Question 2

Glycogenolysis

Answer 2

Hepatic glycogen stores exhausted after 2-3 days of fasting

-glycogen stores depleted = = >gluconeogenesis

Question 3

Where does gluconeogenesis occur?

Answer 3

1) liver*

2) kidney

Question 4

Insulin

Answer 4

1) promote cellular uptake of:
- glucose*
- also amino acids, fatty acids, and electrolytes
2) promote storage of glucose as glycogen
3) inhibits lipolysis and subsequent release of FFA into circulation
4) inhibits gluconeogenesis and glycogenolysis

Question 5

Normal response to hypoglycemia

Answer 5

1) blood glucose falls below 70 mg/dl:

- stimulates release of hormones: cortisol, catecholamines, growth hormone, glucagon (DIABETOGENIC HORMONES)

Question 6

Normal response to hypoglycemia

Answer 6

1) net effect of the diabetogenic hormones:-promotes gluconeogenesis
- promotes glycogenolysis
- decreased peripheral glucose use
- shutdown insulin secretion

RESULT: normalize blood glucose

Question 7

Etiologies of hypoglycemia

Answer 7

1) lack of intestinal absorption
- severe malnutrition/starvation
- severe intestinal disease
2) lack of hepatic production
- portosystemic shunts*
- hepatic failure*(acute or chronic)
- glycogen storage diseases (usually genetic disorders)
3) endocrine disorders
- lack of diabetogenic hormones (Addison’s disease)
4) increased glucose utilization
- sepsis!
- Polycythemia (excess red blood cells use of glucose)
- extreme exertion
- too much insulin (insulinoma)

Question 8

More etiologies of hypoglycemia

Answer 8

1) xylitol toxicity
- induces insulin release!!
2) paraneoplastic
3) artifact-if blood sits out longer than it should it may appear falsely hypoglycemic

Question 9

Clinical effects of hypoglycemia

Answer 9

1) CNS carbohydrate reserves are limited-dependent on a continuous supply from outside CNS
2) cerebral cortex is the 1st area affected by hypoglycemia
3) glucose entrance into CNS is NOT insulin-dependent

Question 10

Neurologic sequela

Answer 10

1) brain is 1st organ affected by hypoglycemia
2) clinical signs result from:
- Neuroglycopenia (lack of glucose to brain)
- sympathoadrenal stimulation (diabetogenic hormones: epinephrine-anxiety, tremors)

Question 11

Clinical signs: neuroglycopenia

Answer 11

1) weakness
2) lethargy
3) ataxia
4) behavioral change
5) seizures
6) coma

Question 12

Clinical signs: sympathoadrenal

Answer 12

1) muscle tremors
2) nervousness
3) restlessness
4) hunger

Question 13

Clinical signs of hypoglycemia

Answer 13

1) depend on duration and severity of hypoglycemia
2) rapid*onset of hypoglycemia = more severe signs
- i.e.: insulin overdose, sepsis
3) chronic onset = animal may be relatively asymptomatic with significant hypoglycemia
- i.e.: insulinoma

Question 14

Clinical approach

Answer 14

1) consider list of differentials and decide which is most likely
2) hypoglycemia mild (>45 mg/dl) -Addison’s disease, hepatic disease
3) hypoglycemia severe (<40 mg/dl)-sepsis, neoplasia, juvenile

Question 15

Insulinoma

Answer 15

1) tumor of pancreatic beta cells
- autonomously secretes insulin = hypoglycemia
- majority are malignant and have gross/microscopic metastasis at time of diagnosis
2) common in ferrets, uncommon in dogs (large breeds overrepresented, 9-10 years), rare in cats

Question 16

Insulinoma

Answer 16

1) Chronic, insidious onset
- may have severe hypoglycemia with relatively mild clinical signs
2) demonstrate (inappropriately) high insulin with concurrent low*glucose
- MUST measure insulin when blood glucose is low (ideally <50 mg/dl)

Question 17

Emergency therapy for hypoglycemia

Answer 17

1) IV catheter
2) 50% dextrose
3) administer 1-5 ml/kg slowly over 10 minutes
4) hyperosmolar, therefore dilute 1:4
5) total infusion amount 4-20 ml solution
* treat to resolution of clinical signs

Question 18

Use caution…

Answer 18

1) insulinoma may respond poorly to dextrose administration
- increase in blood glucose promotes insulin secretion
- ultimate worsening of hypoglycemia!

2) treat the ANIMAL not the BG
- alternative option: glucagon (if patient doesn’t respond well to glucose)

Question 19

Hyperglycemia

Answer 19

Normal finding postprandial

• 2-4 hours after eating (mild)
  2) hyperglycemia etiologies:
• too much of one or more hormones that raise BG
• deficient in hormone that decreases BG (insulin-diabetes)
• various drugs

Question 20

Too much hormone

Answer 20

1) hypoglycemia not sold clinical presentation
2) successful treatment of underlying etiology should lead to resolution of hyperglycemia
3) therapy for hyperglycemia (insulin) usually*only indicated for acromegaly (potentially it may cause diabetes)

Question 21

Stress hyperglycemia

Answer 21

1) sources
-catecholamine release
glucocorticoids (endogenous or exogenous)
2) blood glucose can exceed renal threshold in stress
-hyperglycemia and glucosuria
-dogs (180 mg/dl), (280 mg/dl)

Question 22

Not enough hormone to decrease glucose

Answer 22

1) insulin: beta cells of endocrine pancreas
2) insulin deficiency = diabetes mellitus
- anything destroying beta cells of pancreas or interfering with insulin action = diabetes

Question 23

DM pathophysiology-step 1

Answer 23

Insulin deficiency (relative or absolute)

1) decreased tissue utilization
2) increased hepatic glycogenolysis and gluconeogenesis
3) glucose from liver and diet accumulates in circulation
4) results inhyperglycemia

Question 24

DM pathophysiology-step 2

Answer 24

Hyperglycemia

1) exceeds renal tubular resorption abilities
2) eventualglucosuria
3) causes and osmotic diuresis
4) results inpolyuria
5) results in compensatorypolydipsiato prevent dehydration

Question 25

DM pathophysiology-step 3

Answer 25

1) satiety center in the brain normally inhibits the feeding center after a meal
2) satiety center requires insulin for glucose transport
3) insulin deficiency = glucose does not enter satiety center = failure to inhibit feeding center
4) results inpolyphagiain face of hyperglycemia

Question 26

Classic signs of diabetes mellitus

Answer 26

1) polyuria
2) polydipsia
3) polyphagia
4) weight loss (cells aren’t taking up energy!)

Question 27

Diabetes mellitus

Answer 27

1) most common endocrine disease in dogs and cats
2) hyperthyroidism probably most common endocrine disease of older cats (>8 years)
3) many similarities and many differences between dogs and cats with DM

Question 28

DM signalment’s

Answer 28

Dog = 7-10 years, females >males

= most >6 years, neutered males

Question 29

Types of DM

Answer 29

1) Type 1 = “insulin-dependent”
- most common type in DOGS-absolute and permanent insulin deficiency
- genetic predispositions, support for auto-immune component
2) Type 2 = “non-insulin-dependent”
- most common type in CATS
- relative/possible reversible insulin deficiency
- defective pancreatic beta cells
- one or more sources of insulin resistant

BOTH are treated with insulin

Question 30

Diagnosis of DM

Answer 30

Resting hyperglycemia with glucosuria in animals with clinical signs (the 3 P’s with weight loss!!)