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Endocrine Pharmacology > WK2 > Flashcards

WK2 Flashcards

1
Q

Ketaconazole does what?

A

Inhibits Side-Chain cleavage and other CYP enzymes (Anti-fungal)

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2
Q

Metyrapone does what?

A

Inhibits 11-b-hydroxylase

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3
Q

Etomidate does what?

A

Inhibits 11-b-hydroxylase

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4
Q

Ketaconazole is used for what in endocrine?

A

Decrease Cortisol in Cushing Disease

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5
Q

Metyrapone and Etomidate are used for what?

A

DecreaseCortisol levels in Cushing Disease

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6
Q

Which drug can be used when waiting for definitive diagnosis of Cushing Disease?

A

Metyrapone

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7
Q

Toxicity of Ketaconazole

A

LIVER TOX

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8
Q

Treatments for Cushing disease that decrease ACTH release?

A 
DA agonist (Cabergoline)
SST analog (Pasireotide)
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9
Q

Mifepristone does what?

A

Anatagonist of Glucocorticoid Receptor

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10
Q

Mifepristone is used for what? (2)

A

Inoperable disease

Ectopic ACTH tumors that have failed other treatments

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11
Q

Mitotane is what?

A

a DDT insecticide with adrenal toxicity

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12
Q

SE of Mitotane?

A

Adrenal Carcinoma

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13
Q

Symptoms of Cushing Syndrome

A 
Truncal Obesity
Moon Facies
HTN
Wt Gain
Hyperglycemia
Glucose intolerance
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14
Q

Symptoms of Addison’s Disease?

A

Hypoglycemia
Metabolic Acidosis
Hyperpigmentation
Hypotension

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15
Q

Symptomatic difference between primary adrenal insufficiency (Addisons) and secondary?

A

Secondary = Decreased ACTH

  • Normal Aldosterone = NO HYPOTENSION
  • Low ACTH = NO HYPOPIGMENTATION
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16
Q

Glucocorticoid toxicity in heart?

A 
Positive ionotrope (Tachycardia)
HTN
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17
Q

Glucocorticoid toxicity in in CNS?

A

Lowered seizure threshold (hypokalemia)

Behavior changes

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18
Q

Glucocorticoid toxicity in GI?

A 
Increased HCl (Peptic Ulcer)
Antagonizes VitDR = decreased Ca and PO4 absorption
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19
Q

Glucocorticoid toxicity in in bones?

A

DIRECT osteoblast inhibition

Decreased Ca –> Increased PTH increased osteoclast action

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20
Q

Glucocorticoid toxicity in muscles?

A

Hypokalemia (cramps, myopathy)

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21
Q

How are specific blood cells affected?

A

Decreased Lymphocytes, Eosinophils and Basophils
Increased RBC and Neutrophils
Leukocyte extravasation inhibited

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22
Q

Anti-inflammatory effects of glucocorticoids (5)?

A 
Decreased AA conc
Reduced COX-2
Decreased peripheral leukocytes
Stabilized lysosomal membranes
Reduction of vasoactive factors
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23
Q

What enzyme activates Prednisone?

A

11-b-hydroxylase-2 (inhibits cortisol)

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24
Q

Hydrocortisone GC, MC, and duration of action?

A

1, 1, 8hrs

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25
Q

Prednisolone GC, MC, and duration of action?

A

4, 0.8, 16-36 hrs

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26
Q

Dexamethasone GC, MC, and duration of action?

A

25-80
0
36-54 hrs

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27
Q

Betamethasone GC, MC, and duration of action?

A

25-30
0
36-54

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28
Q

Fludocortisone GC, MC, and duration of action?

A

15
200
24 hrs

29
Q

Which glucocorticoid agonizes the minerocorticoid receptor the most?

A

Fludocortisone

30
Q

What enzyme does licorice inhibit?

A

11-b-hydroxylase

31
Q

Metformin (Biguanides) acts how?

A

Activates AMPK
Inhibits gluconeogenesis
Increased skeletal and adipocyte glucose uptake

32
Q

Metformin is used for what?

A

Type II DM (Insulin independent)

33
Q

SE of metformin? What isn’t a SE of metformin, but is of other diabetes drugs?

A

GI distress, lactic acidosis

Hypoglycemia

34
Q

Chlorpropramide is what?

A

1st gen sulfonylurea

35
Q

Tolbutamide is what?

A

1st gen sulfonylurea

36
Q

Tolazamide is what?

A

1st gen sulfonylurea

37
Q

Glyburide is what?

A

2nd gen sulfonylurea

38
Q

Glipizide is what?

A

2nd gen sulfonylurea

39
Q

Glimepride is what?

A

2nd gen sulfonylurea

40
Q

Sulfonylurea MOA?

A

Bind ATP dep K channels and close them, increasing intracellular Ca, causing Insulin release

41
Q

SE of sulfonylureas?

A

Hypoglycemia

Wt Gain

42
Q

Sulfonylurea in pregnancy? Why?

A

NOT IN PREG

Cross the placenta and cause hypoglycemia

43
Q

Why are 2nd gen sulfonylureas better than 1st?

A

2nd gen have shorter half life and more potency

44
Q

Lispro onset, max, and duration?

A

15 min - 1 hr - 4 hrs

45
Q

Regular Insulin onset, max, duration?

A

30 mins - 2 hr - 8 hrs

46
Q

NPH Insulin onset, max, duration?

A

2 hrs - 10 hrs - 20 hrs

47
Q

Insulin Glargine inset, max, duration?

A

2 hrs - no peak - 24 hrs

48
Q

Who needs supplemental Insulin?

A

Type I (insulin-dependent)

49
Q

SE of insulin supplementation?

A

Hypoglycemia

Wt gain

50
Q

GLP-1 analog MOA?

A

GLP-1 = glucagon like hormone secreted by intestinal epithelial cells
Stimulates Insulin
Decreased Glucagon
Induces Saiety

51
Q

Exenatide is what?

A

GLP-1 Analog (INJECTED)

52
Q

SE of GLP-1 analog?

A

Wt loss
hypoglycemia
PANCREATITIS

53
Q

Sitagliptin is what?

A

DPP-4 inhibitior

54
Q

Sitagliptin MOA?

A

Inhibits dipeptidyl peptidase-4, which usually metabolizes GLP-1
Increases GLP-1 half-life

55
Q

Meglitinites (Repeglinitide, nateglinitide) are what?

A

Insulin secretagogues

56
Q

Meglitinites MOA?

A

bind different binding site on K channels, increasing Insulin release

57
Q

SE of Sitagliptin?

A

Nausea and vomiting

No hypoglycemia or wt changes

58
Q

SE of Megltinites?

A

Wt gain

Hypoglycemia

59
Q

Acarbose is what?

A

a-glucosidase inhibitor

60
Q

Miglitol is what?

A

a-glucosidase inhibitor

61
Q

Acarbose and Miglitol MOA?

A

Inhibit a-glucosidase in brush border intestinal cells, decreasing glucose intake with meals

62
Q

SE of a-glucosidase inhibitors?

A

Flatulence

Diarrhea

63
Q

Pramlintide is what?

A

Amylin analog

64
Q

Pramlintide MOA?

A

Binds Amylin receptor
Decreases glucagon synthesis
Delays gastric emptying
Increases Saiety

65
Q

Pramlintide SE?

A

GI distress

66
Q

Rosiglitazone, pioglitazone, troglitazone is hwat?

A

Thiazolidinediones

67
Q

Thazolidinediones MOA?

A

Binds PPARy upregulates genes to increase skeletal and adipocyte glucose uptake
decrease insulin resistance

68
Q

SE of thazolidines?

A

Hypoglycemia
Edema (HF?)
Liver Tox

Endocrine Pharmacology (5 decks)

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