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
Side effects of the 2nd gen sulfonylureas
hypoglycemia ***metformin does not decrease blood sugar a lot, so it does not risk hypoglycemia!
26
Describe the mechanism of action of meglitinides (glinides) and the difference with sulfonylureas
Stimulate pancreas to secrete more insulin & has a risk of hypoglycemia Difference: short acting than sulfonylureas
27
List 2 examples of glinides
Nateglinides Repagiinides
28
Specify the precautions to take while taking meglitinides
Patients need to eat within 30 min of taking glinides
29
The interaction between glinides & gemfibrozil will result in...?
Gemfibrozil (cholesterol medication) slows down the removal of other meds from body --> when taken with glinides, it causes the increased risk of toxicity!
30
List 2 examples of thiazolidinediones (glitazones; TZD)
- pioglitazone - rosiglitazone
31
Describe the MOA of TZD
Glitazones decreases insulin resistance (help body use insulin that's there more effectively)
32
What is the most significant side effect of TZD
If a patient has congestive heart failure (CHF), TZD will cause more fluid retention
33
Head to toe, what are other side effects of TZD
Headache Sinusitis Upper respiratory infection hepatotoxicity Women: risk of fracture & ovulation in premenopausal women
34
Describe the MOA of alpha-glucosidase inhibitors (not used much in the US!)
Alpha-glucosidase is an enzyme that breaks down carbs into monosaccharides --> AGIs work in the intestine to delay dietary carbohydrate absorption
35
List 2 examples of alpha-glucosidase inhibitors
Acarbose Miglitol
36
Specify the side effects of alpha-glucosidase inhibitors
borborygmus (weird stomach noises)
37
List 2 examples of DPP-4 inhibitors
suffix: -gliptin sitagliptin sexagliptin linagliptin
38
Specify the functions of glucagon, incretin, and DPP-4
glucagon: hormone that increases glucose production in the liver incretin: hormones that stimulate the release of insulin DPP-4: hormone that inactivates incretin
39
Describe MOA of gliptin
DPP-4 inhibitors block the breakdown of incretin and increase the insulin release from pancreas
40
What is a rare but serious side effect of DDP-4 inhibiotr
pancreatits
41
Describe the mechanism of action of dopamine agonists and name 1 example of a dopamine agonist
MOA: unknown! (may alter glycemic control in hypothalamus?) bromocriptine
42
Identify 3 side effects of dopamine agonists
drowsiness exacerbate psychosis orthostatic hypotension
43
Describe the MOA of SGLT-2 inhibitors
SGLT-2 inhibitors block SGLT-2 in the renal tubules and increase glucose excretion in urine
44
Name 2 SGLT-2 inhibitors
canagliflozin (INVOKANA) dapagliflozin (farxiga) J **Jardiance, too!
45
List 3 side effects of SGLT-2 inhibitors
Orthostatic hypotension female mycotic infections (fungal infection) UTI and polyuria
46
List 2 non-insulin injectable drugs along with their respective indications
1. incretin mimetic: type 2 only 2. Amylin mimetics: type 1 & 2
47
Name 2 examples of incretin mimetics
Exenatide Exenatide extended release
48
Describe 4 MOA of incretin mimetics
incretin mimetics are also known as GLP-1 receptor 1. slows gastric emptying 2. stimulates insulin release 3. inhibits glucagon 4. suppresses appetite
49
Describe 3 mechanisms of action of amylin mimetics
Amylin is a peptide hormone that also has the same effects as incretin
50
Example of amylin mimetics
pramlintide