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Pharmacology 2 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Short-Acting Insulin

A

Lispro (humalog), Aspart (Novolog), Glulisine ( Apidra)

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2
Q

Rapid-Acting Insulin

A

Standard (Regular Iletin, Humulin-R), Purified

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3
Q

Intermediate-Acting Insulin

A

Novolin-N, Humulin-N

NPH

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4
Q

Long-Acting Insulin

A

Detemir, Glargine

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5
Q

Biguanide (drug and broad MOA)

A

Metformin, Insulin Sensitizer

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6
Q

Sulfonylureas (drug and broad MOA)

A

Glipizide, increases insulin release from beta cells

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7
Q

Non-sulfonylurea Secretagogues (drug and broad MOA)

A

Repaglinide, KATP channel modulator and increases insulin release from beta cells

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8
Q

Thiazolidinediones (TZDs) (drug and broad MOA)

A

Pioglitazone, insulin sensitizer in target tissues

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9
Q

GLP-1 Receptor Agonists (drug and broad MOA)

A

Exenatide, increases cAMP therefore increases glucose-dependent insulin secretion

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10
Q

Dipeptidyl Peptidase-4 (DPP-4) Inhibitors (drug and broad MOA)

A

Sitagliptin, prolong endogenous GLP-1 activity to increase glucose-dependent insulin secretion

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11
Q

Alpha-Glucosidase Inhibitors (drug and broad MOA)

A

Acarbose, slows digestion of CHO leading to decreased GI glucose absorption

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12
Q

Renal SGLT-2 Inhibitors (drug and broad MOA)

A

Canagliflozin, inhibit SGLT-2 a sodium-dependent glucose co-transporter in the kidney

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13
Q

Primary tx for Type 1 Diabetes

A

Insulin Replacement

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14
Q

Major AE of insulin replacement

A

Hypoglycemia (<70 mg/dl)

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15
Q

Define Dawn Effect

A

Increased morning glucose (adjust overnight dose)

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16
Q

T/F: Insulin is a first line tx for Type 2 DM

A

False; Exercise and Weight control are 1st line Type 2 DM

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17
Q

pharmacokinetic difference between physiological insulin and insulin replacement

A

Physiological insulin goes to the LIVER first, replacement is given Subq and therefore doesn’t hit liver 1st

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18
Q

Pathophysiology of Type 2 DM

A

Dysregulated glucose homeostasis a/w impaired insulin secretion and action

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19
Q

CI to Metformin

A

Renal dysfunction and severe liver dz

@ risk for lactic acidosis w/ renal impairment

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20
Q

1st line drug for Type 2 DM

A

Metformin

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21
Q

3 Pros to Metformin

A
  1. does NOT induce Hypoglycemia
  2. NO weight gain
  3. inhibits Microvascular complications
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22
Q

MOA of Metformin

A

Activates AMPK–> increase FA oxidation and glucose uptake, decrease gluconeogenesis and lipogenesis

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23
Q

CI to Glipizide

A

hepatic and renal dz

+ caution in elderly/cardiac pts

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24
Q

Major AE with glipizide

A

Hypoglycemia****

Others: weight gain

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25
Q

MOA of Glipizide

A

Increase insulin release from beta cells
Bind to and Inhibit ATP-sensitive K channel beta cell (SUR1 binding site)
**requires functional beta cells

26
Q

Long term MOA of Glipizide

A

Decrease serum glucagon

27
Q

AE of Repaglinide

A 
Hypoglycemia (not as severe as glipizide), 
Weight gain (not as severe as glipizide)
28
Q

Rx-Rx interaction with Repaglinide

A

Gemfibrozil, trimethoprim, simvastatin, clarithromycin–> all interfere with metabolism

29
Q

MOA of Repaglinide

A

Increase insulin release from beta cells
Bind to SUR on ATP-sensitive beta cell K channel
**Requires functional beta cells

30
Q

Pioglitazone Metabolism

A

CYP2C/CYP3A4 hepatic metab

31
Q

AEs of Pioglitazone

A

***Fluid Retention, weight gain, decreased bone density, liver failure, increased risk of HF and bladder CA

32
Q

Pioglitazone MOA

A
  1. Blocks FFA release from adipose and
  2. Promotes glucose uptake/utilization in muscle leading to increase insulin sensitivity
  3. decrease hepatic glucose output from liver
33
Q

Exenatide MOA

A

GLP-1 receptor agonist

  1. Increase glucose-dependent insulin secretion
  2. slows gastric emptying/increase satiety to facilitate weight loss
  3. decrease post-prandial glucagon release
  4. decrease hepatic fat accumulation
  5. increase beta cell mass
34
Q

3 major AEs of Exenatide

A
  1. N/V/D
  2. Increased risk of hypoglycemia when given w/ insulin secretagogues
  3. Acute Pancreatitis
35
Q

CI to exenatide

A

Gastroparesis

36
Q

MOA of Sitagliptin

A

Prolong endogenous GLP-1 activity
Increase glucose-mediated insulin
Decrease postprandial glucagon release

37
Q

6 AEs of Sitagliptin

A
  1. **increase risk of hypoglycemia when combo w/ insulin secretagogues
  2. Cleavage not specific to incretins
  3. Acute pancreatitis
  4. Hepatic failure
  5. Hypersensitivity
  6. Long term safety unknown
38
Q

CI to Acarbose

A

Chronic intestinal dz

39
Q

T/F Acarbose is absorbed in the gut

A

False

40
Q

MOA of Acarbose

A

stays in intestine and slows digestion of CHO–> decrease GI glucose absorption

Decrease postprandial glycemia

41
Q

T/F Acarbose is best taken with food

A

True

42
Q

Major AE of Acarbose and its tx

A

Abd. pain, diarrhea, flatulence–> alleviate w/ dose titration/continued use

43
Q

4 major AE to Canagliflozin

A
  1. Genital mycotic infections
  2. Recurrent UTIs
  3. Hyperkalemia, hypermagnesemia, hyperphosphatemia
  4. Long term safety unknown (may lead to ketoacidosis, bone fractures)
44
Q

T/F The pituitary responds to protein bound thyroid hormone.

A

FALSE; pituitary responds to and regulates FREE hormone

45
Q

D1 vs. D2 vs. D3

A

D1: converts T4 to T3 in liver, kidney and thyroid
D2: converts T4 to T4 in brain, pituitary, heart, skeletal muscle
D3: converts T4 into reverse T3 in placenta, skin, brain

46
Q

Which has a longer half-life: T3 or T4?

A

T4 1/2 life is 7 days vs. T3 is 1 day

47
Q

MC form of Hyperthyroidism

A

Grave’s disease–> IgG antibodies bind/activate TSH receptor and stimulate thyroid

48
Q

Wolff-Chaikoff Effect

A

High dose iodide w/ high intrathyroidal iodide uptake leading to suppression of thyroglobulin synthesis and release

49
Q

Iodide CI

A

Pregnancy–> fetal goiter

50
Q

Thioamides Major use

A

Thyrytoxicosis

51
Q

Thioamide use in Pregnancy

A

CI if possible BUT if you must use–> PTU in 1st trimester then MMI

52
Q

Birth defects are more common in MMI or PUT?

A

MMI

53
Q

Major AE of Thioamides

A
  1. Agranulocytosis

2. Hepatotoxicity (worse w/ PTU)

54
Q

Major AE of Anion Inhibitors

A

Aplastic Anemia–> therefore not used often

55
Q

CI of Iodides

A

Children and Pregnancy

56
Q

DoC for replacement therapy in hypothyroidism

A

Levothyroxine (T4, levothyroid sodium)

57
Q

AE of Liothyronine sodium (L-triiodothyronine, T3)

A

greater risk of cardiotoxicity –> avoid in pts with heart dz

58
Q

AE of Levothyroid sodium (L-thyroxin, T4)

A

Cardiac Sxs–> angina, palpitations, use w/ care

59
Q

T4 is absorbed best from _______

A

Duodenum and ileum

60
Q

All naturally occurring thyroid isomers are _______.

A

L-isomers

61
Q

Which is more potent: T3 or T4?

A

T3>T4

62
Q

Which has greater affinity for receptors: T3 or T4?

A

T3 >T4

Pharmacology 2 (2 decks)

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