Exam 8: L. 8: Glucose! Flashcards Preview

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Flashcards in Exam 8: L. 8: Glucose! Deck (30):
1

Normal blood glucose

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

2

Glycogenolysis

Hepatic glycogen stores exhausted after 2-3 days of fasting
-glycogen stores depleted = = >gluconeogenesis

3

Where does gluconeogenesis occur?

1) liver*
2) kidney

4

Insulin

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

5

Normal response to hypoglycemia

1) blood glucose falls below 70 mg/dl:
-stimulates release of hormones: cortisol, catecholamines, growth hormone, glucagon (DIABETOGENIC HORMONES)

6

Normal response to hypoglycemia

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

RESULT: normalize blood glucose

7

Etiologies of hypoglycemia

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)

8

More etiologies of hypoglycemia

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

9

Clinical effects of hypoglycemia

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

10

Neurologic sequela

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)

11

Clinical signs: neuroglycopenia

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

12

Clinical signs: sympathoadrenal

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

13

Clinical signs of hypoglycemia

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

14

Clinical approach

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

15

Insulinoma

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

16

Insulinoma

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)

17

Emergency therapy for hypoglycemia

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*

18

Use caution…

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)

19

Hyperglycemia

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

20

Too much hormone

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)

21

Stress hyperglycemia

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)

22

Not enough hormone to decrease glucose

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

23

DM pathophysiology-step 1

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 in*hyperglycemia*

24

DM pathophysiology-step 2

Hyperglycemia
1) exceeds renal tubular resorption abilities
2) eventual*glucosuria*
3) causes and osmotic diuresis
4) results in*polyuria*
5) results in compensatory*polydipsia*to prevent dehydration

25

DM pathophysiology-step 3

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 in*polyphagia*in face of hyperglycemia

26

Classic signs of diabetes mellitus

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

27

Diabetes mellitus

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

28

DM signalment's

Dog = 7-10 years, females >males
= most >6 years, neutered males

29

Types of DM

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

30

Diagnosis of DM

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