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Animal Disease > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Name the 4 cells that compose the Islets of Langerhans

A

alpha
beta
delta
F

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2
Q

alpha cells produce

A

glucagon

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3
Q

What does glucagon do?

A

makes a higher serum glucose level

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4
Q

what do beta cells produce?

A

insulin

amylin

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5
Q

What does insulin do?

A

lowers serum glucose level buy letting glucose be absorbed by tissues

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6
Q

What do delta cells produce?

A

somatostatin

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7
Q

What does somatastatin do?

A

results in extension in the period of time nutrietns are available in the GI tract for digestion and assimilation

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8
Q

What do F cells produce?

A

pancreatic polypeptide

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9
Q

Define diabetes mellitus

A

a condition characterized by a relative or absolute insulin deficiency

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10
Q

2 general ways diabetes can occur

A
  • beta cell destruction/dysfunction

- decreased response of the target tissue to circulating insulin

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11
Q

What can cause beta cell destruction/dysfunction?

A
  • genetic factors
  • immune mediated destruction of islet cells (dog)
  • pancreatic induced destruction of islet cells (dog)
  • amyloid depsostion displacing or effacing islet cells (cat)
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12
Q

What can cause decreased response of the target tissue to circulating insulin?

A
  • presence of insulin antagonizing hormones
  • poor absorption of insulin
  • improper handling or administration of insulin, use of expired insulin, improper dosage/frequency
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13
Q

What does insulin to do help maintain glucose homeostsis?

A

facilitates the entry of glucose into the cells

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14
Q

Why is glucose important to the body?

A

only source of energy for the CNS under normal conditions; CNS must get a constant supply of glucose from systemic circulation

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15
Q

Dow does insulin deficiency effect glucose homeostasis?

A

glucose can’t enter the cells to be metabolized for energy production, meaning glucose stays in the blood creating hyperglycemia

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16
Q

List clinical signs of Diabetes

A 
glucosuria
polyuria
polydipsia
decreased weight 
polyphagia
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17
Q

How does hyperglycemia result in glucosuria

A

BG concentration rises enough to exceed the renal threshold, resulting in a spill over of excess glucose into the urine

18
Q

How does hyperglycemia result in polyuria

A

excess glucose in urine changes the osmotic pressure of urine, stimulating the kidneys to excrete more water

19
Q

How does hyperglycemia result in polydipsia

A

loss of excess water signals CNS that increased water intake is needed to maintain normal hydration status

20
Q

How does hyperglycemia result in decreased weight

A

the excessive amount of glucose in circulation and therefore lack of glucose in tissues makes the body believe that there is an energy deficiency; body attempts to utilize any energy stores it has left resulting in muscle wasting and weight loss

21
Q

How does hyperglycemia result in polyphagia

A

insulin also mediates movement of glucose into cells of hypothalamus in the region of the satiety center; lack of glucose means there is no inhibition of the satiety center so the patient is hungry

22
Q

Describe how diabetes mellitus is classified in vet med

A

Insulin dependent- insulin can be given to manage the Dz

Non insulin dependent- usually seen in obese cats as result of the inability of the target tissues to recognize and react with insulin resulting in hyperglycemia; other Tx such as weight loss, dietary management, and hypoglycemic meds may be needed instead

23
Q

Other than IDDM and NIDDM, be able to describe 2 other types of diabetes mellitus that may occur in vet med

A

a. Transient Diabetes Mellitus
i. Primarily in cats that have subclinical diabetes where destruction of beta cells is gradual and some functional beta cells remain; once the event that pushed the pancreas beyond its ability to produce insulin resolve and the CS are treated with insulin, cat may no longer need insulin
ii. May eventually become permanently diabetic in the future
b. Secondary Diabetes Mellitus
i. Usually occurs with increased progesterone levels, administration of megestrol acetate, or presence of increased cortisol levels (hyperadrenocorticism, corticosteroid meds)
ii. Resolves with resolution or removal of whatever is causing the insulin antagonism

24
Q

What might a PE look like on a diabetic patient?

A
  • Minimal to no changes on PE
  • Possibly weight loss and muscle wasting
  • Unkempt haircoat
  • Other abnormalities dependent on presence or absence of any concurrent disease
25
Q

2 lab alterations that are necessary to document the presence of diabetes mellitus

A

persistent hyperglycemia with concurrent glucosuria

26
Q

List several other alterations that may occur in the serum biochem with diabetes mellitus

A
  • CBS usually normal
  • Serum biochem panel
    - Hyperglycemia
    - Increased hepatic enzymes (result of fat deposition in liver which is common in diabetes or a result of pancreatitis)
    - Hyperlipidemia
    - Hypercholesterolemia
  • UA
    - Glucosuria
27
Q

The common therapeutic goal for either IDDM or NIDDM

A

eliminate CS of polyuria, polydipsia, polyphagia

28
Q

Describe the therapeutic approach to IDDM

A
  • Insulin therapy is mandatory

- Dietary management is highly suggested

29
Q

Describe the therapeutic approach to NIDDM

A
  • Dietary management
  • Weight loss and exercise –> reversing any obesity-induced insulin antagonism
  • Oral hypoglycemic meds –> directed at increasing insulin secretions from whatever beta cells may still be function or at facilitating glucose entry into the target cells; overall goal of this med is to decrease the serum glucose concentration into normal range
30
Q

How should insulin be stored?

A

refrigerate

gently rock or roll bottle to redistribute insulin molecules into soln before giving

31
Q

Serial Blood Glucose Curve

  • what it is
  • uses
  • when to do
A
  • serum BG measured immediately prior to admin of insulin and continuing measurements of serum BG every 2hrs for 8 to 24hrs
  • used to determine changes for… dose, duration of admin, type of insulin
  • done every 3-4 months or if P demo continuing or worsening CS`
32
Q

Fructosamine

  • what it tells you
  • uses
A
  • picture of where serum BG levels have been over past week

- not adequate for determining proper adjustments in insulin dose or type of insulin

33
Q

Fructosamine vs glycosylated hemoglobin

A

glycosylated hemoglobin gives you past month

34
Q

Urine dipstick monitoring

A
  • beneficial in diagnosis but not a helpful monitoring tool b/c presence of glucosuria may vary throughout day depending on feeding schedule
  • O may try and change insulin dose
35
Q

Common diseases diabetic animals make be prone to ot develop

A 
UTIs
cataract formation
diabetic polyneuropathy
diabetic ketoacidosis
insulin-induced hypoglycemia (Somogyi phenomenon)
36
Q

Why do UTIs occur in diabetic pets?

A

-Secondary to persistence of glucosuria
-Diabetic immune system is not completely normal.
-Add that with an excess of glucose in the urine that provides energy for bacteria, and you get a UTI
May no show any CS of UTI

37
Q

Why do cataracts form? Dog or cat?

A

Dog

  • Form as result of excessive glucose diffusing to the lens that results in formation of sorbitol and fructose which can’t diffuse out of the lens and instead attract water
  • Results in swelling of fibers of lens and cataract formation
38
Q

What is diabetic polyneuropathy?

A
  • Rare
  • Cats with dropped hock stance
  • Cause unknown
  • Reversible with proper Tx
39
Q

What is diabetic ketoacidosis?

A

Occurs as result of insufficient insulin availability, persistent hyperglycemia, and subsequent production of ketone bodies that have detrimental effects on many organ systems

40
Q

Describe what happens with insulin induced hypoglycemia

A
  • When excessive insulin is given, a massive entry of glucose into cells results in significant decrease in circulating serum glucose
  • This puts pet into hypoglycemic state, so glucogenic hormones start increasing the serum glucose concentration which results in a surge in serum glucose concentration
  • There is no endogenous insulin present, so rising serum glucose concentration cannot be dampened and serum glucose levels can become significantly high

Animal Disease (54 decks)

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