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Pharmacology > Endocrine Meds: diabetes > Flashcards

Endocrine Meds: diabetes Flashcards

1
Q

Explain how insulin resistance can be detected

A

When the insulin resistance happens, the serum insulin level becomes elevated.

But cells can’t use insulin to absorb glucose, so blood sugar rises and rises.

***high plasma glucose will damage your microvascular circulation

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2
Q

Identify the duct that connects the liver, gallbladder, and pancreas

A

Common bile duct

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3
Q

Recall the exocrine function of the pancreas

A

Secretion of pancreatic juices (digestive enzymes & bicarbonate) into common bile duct

**Review
CCK –> acinar cells –> enzymes
secretin –> duct cells –> bicarbonate

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4
Q

List the digestive enzymes produced by the pancreas for digestion

A

Pancreatic lipase (tri –> mono & 2 FA)
Pancreatic amylase

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5
Q

Recall the endocrine function of the pancreas

A

Secrete hormones right into the BLOODSTREAM

** islets of Langerhans: alpha cells and beta cells

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6
Q

Recall the endocrine hormones produced by the pancreas

A

Glucagon
Insulin

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7
Q

Differentiate between type 1 and type 2 diabetes

A

Type 1 has NO INSULINE –> insulin replacement is necessary (no oral medications, only sub Q)

Type 2 has insulin resistance

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8
Q

Discuss the differences in the monitoring and management of type 1 versus type 2 diabetes

A

Type 1: always requires frequent blood sugar monitoring and insulin titration

Type 2: patients start off by taking oral meds + when panaceas tire out, they start insulin therapy

Treatment depends on the progression of disease

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9
Q

Name the biggest risk for diabetic patients who receives insulin therapy

A

Hypoglycemia

Brain & rest of the body loses the source of fuel!

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10
Q

List the signs and symptoms of hypoglycemia

A

CNS: headache, confusion, seizures, coma
Cardiovascular: palpitations (due to increased SNS activity)
GI: nausea
Others: sweating and tremor

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11
Q

What would happen if a patient is on beta blocker & receives too much insulin?

A

You will not see a fast heart rate. When plasma glucose is <50, the patient may show confusion and neuro changes

–> remind them to watch their blood sugar closely!!!

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12
Q

Determine how to treat mild-to-moderate hypoglycemia

A

Give carbohydrate-rich food if patient is able to swallow

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13
Q

Determine how to treat severe hypoglycemia

A

Administer IV glucose (hospital)
Give subQ glucagon (at home, facilitate glycogen breakdown in the liver, may take 20 min to kick in)

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14
Q

List 3 factors/drugs that exacerbate hypoglycemia

A
  1. Beta blockers (BB blocks SNS response, inhibits hepatic glu production)
  2. Sulfonylureas & meglitinides (anti-diabetic meds that insulin release from pancreas)
  3. alcohol (consumption stimulates insulin release)
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15
Q

What 3 factors/drugs will put a patient on the risk of elevated sugar

A
  1. Thiazide diuretics
  2. Glucocorticoids
  3. Sympathomimetics (epinephrine, norepinephrine, etc.)
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16
Q

Identify 2 major routes for anti-diabetic medications

A
  1. oral drugs
  2. non-insulin injectable drugs
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17
Q

**Overview: list the first 4 groups oral anti-diabetic medications

A
  1. Biguanides: metformin
  2. 2nd-gen sulfonylureas: glipizide, glyburide
  3. Meglitinides (Glinides): nateglinide, repaglinide
  4. Thiazolidinediones (Glitazones): pioglitazone, rosiglitazone
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18
Q

**Overview: list the next 3 groups of oral antidiabetic medications

A
  1. Alpha-Glucosidase inhibitors: acarbose, miglitol
  2. DPP-4 inhibitors (Gliptins): Linagliptin, saxagliptin
  3. Dopamine agonist: bromocriptine
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19
Q

Describe the mechanism of action of metformin (guanides)

A

Increase glucose uptake by muscles & decrease glucose production by liver
–> lower blood sugar!

prescribed as the first step of treatment
lifestyle modifications + metformin

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20
Q

Two common side effects of metformin

A
  • GI distress
  • rare metabolic acidosis
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21
Q

List 3 drugs that can cause lactic acidosis with metformin

A
  • cimetidine (other H2 antagonists are fine!)
  • alcohol
  • iodine based radiocontrast dye (discontinue metformin 1-2 days before the test)

–> combined with metformin, it knocks down kidney and causes metabolic acidosis!

22
Q

Identify 3 early signs of lactic acidosis

A
  1. unusual drowsiness
  2. hyperventilation (breathing faster to breath CO2 out)
  3. myalgia
23
Q

Describe the mechanism of action of the 2nd gen sulfonylureas

A

Sulfonylureas increase insulin release from the pancreas

24
Q

List 2 examples of the 2nd-generation sulfonylureas

A

glipizide
glyburide

25
Q

Side effects of the 2nd gen sulfonylureas

A

hypoglycemia

***metformin does not decrease blood sugar a lot, so it does not risk hypoglycemia!

26
Q

Describe the mechanism of action of meglitinides (glinides) and the difference with sulfonylureas

A

Stimulate pancreas to secrete more insulin & has a risk of hypoglycemia

Difference: short acting than sulfonylureas

27
Q

List 2 examples of glinides

A

Nateglinides
Repagiinides

28
Q

Specify the precautions to take while taking meglitinides

A

Patients need to eat within 30 min of taking glinides

29
Q

The interaction between glinides & gemfibrozil will result in…?

A

Gemfibrozil (cholesterol medication) slows down the removal of other meds from body
–> when taken with glinides, it causes the increased risk of toxicity!

30
Q

List 2 examples of thiazolidinediones (glitazones; TZD)

A
  • pioglitazone
  • rosiglitazone
31
Q

Describe the MOA of TZD

A

Glitazones decreases insulin resistance (help body use insulin that’s there more effectively)

32
Q

What is the most significant side effect of TZD

A

If a patient has congestive heart failure (CHF), TZD will cause more fluid retention

33
Q

Head to toe, what are other side effects of TZD

A

Headache
Sinusitis
Upper respiratory infection
hepatotoxicity

Women: risk of fracture & ovulation in premenopausal women

34
Q

Describe the MOA of alpha-glucosidase inhibitors (not used much in the US!)

A

Alpha-glucosidase is an enzyme that breaks down carbs into monosaccharides

–> AGIs work in the intestine to delay dietary carbohydrate absorption

35
Q

List 2 examples of alpha-glucosidase inhibitors

A

Acarbose
Miglitol

36
Q

Specify the side effects of alpha-glucosidase inhibitors

A

borborygmus (weird stomach noises)

37
Q

List 2 examples of DPP-4 inhibitors

A

suffix: -gliptin

sitagliptin
sexagliptin
linagliptin

38
Q

Specify the functions of glucagon, incretin, and DPP-4

A

glucagon: hormone that increases glucose production in the liver

incretin: hormones that stimulate the release of insulin

DPP-4: hormone that inactivates incretin

39
Q

Describe MOA of gliptin

A

DPP-4 inhibitors block the breakdown of incretin and increase the insulin release from pancreas

40
Q

What is a rare but serious side effect of DDP-4 inhibiotr

A

pancreatits

41
Q

Describe the mechanism of action of dopamine agonists and name 1 example of a dopamine agonist

A

MOA: unknown! (may alter glycemic control in hypothalamus?)

bromocriptine

42
Q

Identify 3 side effects of dopamine agonists

A

drowsiness
exacerbate psychosis
orthostatic hypotension

43
Q

Describe the MOA of SGLT-2 inhibitors

A

SGLT-2 inhibitors block SGLT-2 in the renal tubules and increase glucose excretion in urine

44
Q

Name 2 SGLT-2 inhibitors

A

canagliflozin (INVOKANA)
dapagliflozin (farxiga)
J
**Jardiance, too!

45
Q

List 3 side effects of SGLT-2 inhibitors

A

Orthostatic hypotension
female mycotic infections (fungal infection)
UTI and polyuria

46
Q

List 2 non-insulin injectable drugs along with their respective indications

A
  1. incretin mimetic: type 2 only
  2. Amylin mimetics: type 1 & 2
47
Q

Name 2 examples of incretin mimetics

A

Exenatide
Exenatide extended release

48
Q

Describe 4 MOA of incretin mimetics

A

incretin mimetics are also known as GLP-1 receptor

  1. slows gastric emptying
  2. stimulates insulin release
  3. inhibits glucagon
  4. suppresses appetite
49
Q

Describe 3 mechanisms of action of amylin mimetics

A

Amylin is a peptide hormone that also has the same effects as incretin

50
Q

Example of amylin mimetics

A

pramlintide

Pharmacology (20 decks)

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