E1. Drugs acting on glucose metabolism

Question 1

Look at slides 3 – 10 review of glucose metabolism.

Answer 1

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Question 2

What cells are involved in the making of insulin?
A. Alpha cells
B. Beta cells 
C. F cells 
D. Delta cells

Answer 2

B. Beta cells

Question 3

What cells are involved in the making of glucagon?
A. Alpha cells
B. Beta cells 
C. F cells 
D. Delta cells

Answer 3

A. Alpha cells

Question 4

What cells are responsible for somatostatin?
A. Alpha cells
B. Beta cells 
C. F cells 
D. Delta cells

Answer 4

D. Delta cells

Question 5

What cells are responsible for pancreatic polypeptide?
A. Alpha cells
B. Beta cells 
C. F cells 
D. Delta cells

Answer 5

C. F cells

Question 6

What can cause the stimulation of insulin secretion?

Answer 6

– Rise in blood glucose concentration
– G.I. hormones:
– – gastric, CCK, secretin, gastric inhibitory polypeptide, glucagon
– amino acids and fatty acids in the GIT
– vagal stimulation (M receptors)
– – catcholamines  (beta-2 receptors)

Question 7

Whatcauses the inhibition of insulin secretion?

Answer 7

– decrease in blood glucose concentration
– somatostatin
– catecholamines (a2 or I3 receptors)

Question 8

What happens if you have too much insulin?

Too little insulin?

Answer 8

Too much: hypoglycemia

too little: hyperglycemia

Question 9

What are the differentials for hypoglycemia? (5 main, 4 of which have subs)

Answer 9

1. artifact
2. Unable to make glucose
   – liver failure/cirrhosis
   – Portosystemic shunt
   – severe malnutrition (neonates/toy breeds)
   – hyperadrenocorticism (pituitary/GH deficiency)
   – glycogen storage diseases
3. Excessive consumption
   – sepsis
   – extreme exertion
4. Exogenous hypoglycemic agents
   – insulin overdose
   – overdose of other hypoglycemic agents (e.g.. glipizide)
5. Endogenous hypoglycemic agents
   – xylitol toxicity (dogs)
   – insulin secreting islet cells neoplasia (insulinoma)
   – extrapancreatic neoplasia
   – islet cell hyperplasia

Question 10

What are the two main therapeutic considerations for hypoglycemia? (Gen.)

Answer 10

Not involving insulin, and involving insulin.

*Look at slide 13 for subcategories

Question 11

What are the three main pharmacologic therapy for hypoglycemia?

Answer 11

– Replacement
– diet
–Anti-hypoglycemic agents
*look at slide 14 subcategories

Question 12

Is glucagon commonly used to treat hypoglycemia? What’s the initial dilution you should start off with?

Answer 12

Not commonly used. Initial dose should be 50 ng/kg followed by 10 – 15 ng/kg/minute.
*adjust based on blood glucose measurement

Question 13

What is the proper dose if using dextrose for an acute case or maintenance?

Answer 13

Acute: 1 mL/kg of 50% dextrose diluted (1:4)

maintenance:
- 2.5-5% dextrose IV
- Adjust based on blood glucose levels

*don’t want to use greater than 5% dextrose because greater than that will cause phlebitis.

Question 14

What are some considerations you should take into account when using dextrose to treat hypoglycemia? (2)

Answer 14

– Hyperosmolality/irritation

– rising glucose stimulates insulin secretion

Question 15

You use dietary management to treat acute and chronic hypoglycemia?

Answer 15

Acute: Karo syrup/corn syrup (mostly used outside of clinic, as good as dextrose in an emergency situation)

chronic:
– frequent, small meals
– complex carbs  (symbol carbs may stimulate insulin secretion)
– easily digestible
– moderate fat and protein

Question 16

How can use pharmacologic therapy to treat hypoglycemia?

What is the goal of this therapy?

Answer 16

– glucocorticoids
– Diazoxide
– Streptozotocin
– somatostatin

Goal is to eliminate/minimize clinical signs associated with hypoglycemia (this may not be maintaining a “normal” blood glucose!)

Question 17

What is the DOC/ reached for first drug to treat hypoglycemia?

Answer 17

Glucocorticoids (prednisone, prednisolone)

Question 18

What do glucocorticoids do to the gluconeogenesis, glucose uptake (in tissue), and glucagon secretion?

Answer 18

Increase gluconeogenesis, decreased glucose uptake into tissue, stimulate glucagon secretion

Question 19

What is the bioavailability of glucocorticoids is taken orally?

Answer 19

Good oral bioavailability

Question 20

Where does prednisone and prednisolone need to go to be activated? (Organ)

Answer 20

The liver/hepatic metabolism is required

Question 21

What dose should you start off with when using prednisone or prednisolone?S

Answer 21

.5 mg/kg/day, increase as needed

Question 22

What are the side effects of using prednisone or prednisolone?

Answer 22

Generally mild at low doses (PU/PD, panting) and get progressively more severe as this is increased (immunosuppression, etc.).

Question 23

What are the drugs that can be used to treat hypoglycemia?

Answer 23

Diazoxide, somatostatin, octreotide (somatostatin analog), streptozotocin

Question 24

How do you give Diazoxide?
When should you give this?
What are its side effects?

Answer 24

– Oral
– when glucocorticoids and diet longer work
– side effects:
paper celebration, anorexia/vomiting/diarrhea, less commonly (tachycardia, hematologic changes, diabetes, fluid retention)
look at slide 19 and 20 for more information. Slide 20 gives the mode of action.

Question 25

What does somatostatin do?

Answer 25

Inhibits release of insulin, glucagon, growth hormone, CCK, secretin, gastrin, VIP

Question 26

What is octreotide sometimes used to treat? (Dogs, ferrets, cats)

Question 27

Look at slide 22 for information on streptozotocin.

Answer 27

.

Question 28

What are the differential for hyperglycemia? (7)

Answer 28

Physiologic hyperglycemia(Stress, postprandial, Diestrus), diabetes mellitus, hypersdrenocorticism, Pheochromocytoma, Pancreatitis/Exocrine Pancreatic Neoplasia, Some Drugs/Toxins, Head Trauma

Question 29

What are the two types of diabetes mellitus?

Answer 29

Type I: insulin-dependent (IDDM) (insulin deficiency)
Type II: non-insulin-dependent (NIDDM)(insulin resistance
*type II seen in cats

*Look at slide 25 for a bit more info. Two

Question 30

Look at the slides 26-28.

Answer 30

.

Question 31

What is the goal of therapy referring to hyperglycemia?

Answer 31

– Reduce hyperglycemia
– reverse catabolic effects
– reverse ketosis
– control clinical signs

*look at slide 29 for more info

Question 32

What are the three general treatments for diabetes mellitus? (All three have subcategories)

Answer 32

– General management

Question 33

How does acarbose (Precose) work?

Answer 33

It is not a hypoglycemic agents. It inhibits alpha amylase and brush border oligo/disaccharides.

*look at slide 31

Question 34

What are the three types of oral hypoglycemics?

Answer 34

Sulfonylureas, Biguanides,

Question 35

Name the drugs that are Sulfonylureas? (only first 2 really matter)

Question 36

What is the main thing that Glipizide does?

Answer 36

Increased release of insulin

*look at slide 34

Question 37

What is the drug that is considered a Biguanides?

What are the two biggest things you need to know about that drug?

Answer 37

Metformin

recognizes as an anti-hyperglycemic that doesn’t affect insulin secretion

*look at slide 35

Question 38

Look at slide 36-39.

Answer 38

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Question 39

What are the two types of insulin that can be given to animals? What is the concentration? T

Question 40

How should you properly store and handle insulin?

Question 41

What are the types of insulin? (Duration/acting period)

Answer 41

Short, intermediate and long

look at slide 42

Question 42

How can short acting insulin be given?

When is this most commonly used

Answer 42

IV, IM, SC

most commonly used for DKA management

look at slide 43

Question 43

Look at slide 44-51.

Answer 43

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