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Pharmacology > FA Endocrine > Flashcards

FA Endocrine Flashcards

1
Q

Insulin, Rapid Acting

A

Lispro, Aspart, Glulisine

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2
Q

Insulin, Short Acting

A

Regular

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3
Q

Insulin, Intermediate Acting

A

NPH

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4
Q

Insulin, Long Acting

A

Glargine, Detemir

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5
Q

Insulin Mechanism

A

Bind insulin receptor (tyrosine kinase activity).
Liver: ↑ glucose stored as glycogen.
Muscle: ↑ glycogen, protein synthesis; ↑ K+ uptake.
Fat: ↑ TG storage.

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6
Q

Insulin, Rapid Acting Use

A

DM1, DM2, GDM (postprandial glucose control)

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7
Q

Insulin, Short Acting Use

A

DM1, DM2, GDM, DKA (IV), hyperkalemia (+ glucose), stress hyperglycemia.

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8
Q

Insulin, Intermediate Acting Use

A

DM1, DM2, GDM.

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9
Q

Insulin, Long Acting Use

A

DM1, DM2, GDM (basal glucose control).

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10
Q

Insulin Toxicity

A

Hypoglycemia, rare hypersensitivity reactions.

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11
Q

Biguanides

A

Metformin

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12
Q

Metformin Mechanism

A

Exact mechanism unknown. ↓ gluconeogenesis, ↑ glycolysis, ↑ peripheral glucose uptake (insulin sensitivity).

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13
Q

Metformin Use

A

Oral. First-line therapy in type 2 DM. Can be used in patients without islet function.

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14
Q

Metformin Toxicity

A

GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure).

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15
Q

Sulfonylureas

A

First generation: Tolbutamide, Chlorpropamide

Second generation: Glyburide, Glimepiride, Glipizide

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16
Q

Sulfonylurea Mechanism

A

Close K+ channel in β-cell membrane, so cell depolarizes → triggering of insulin release via ↑ Ca2+ influx.

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17
Q

Sulfonylurea Use

A

Stimulate release of endogenous insulin in type 2 DM. Require some islet function, so useless in type 1 DM.

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18
Q

Sulfonylurea Toxicity

A

Risk of hypoglycemia ↑ in renal failure. First generation: disulfiram-like effects. Second generation: hypoglycemia.

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19
Q

Glitazones/thiazolidinediones

A

Pioglitazone, Rosiglitazone

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20
Q

Glitazone Mechanism

A

↑ insulin sensitivity in peripheral tissue. Binds to PPAR-γ nuclear transcription regulator.

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21
Q

Glitazone Use

A

Used as monotherapy in type 2 DM or combined with other agents.

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22
Q

Glitazone Toxicity

A

Weight gain, edema. Hepatotoxicity, heart failure.

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23
Q

α-glucosidase Inhibitors

A

Acarbose, Miglitol

24
Q

α-glucosidase Inhibitor Mechanism

A

Inhibit intestinal brush-border α-glucosidases. Delayed sugar hydrolysis and glucose absorption → ↓ postprandial hyperglycemia.

25
Q

α-glucosidase Inhibitor Use

A

Used as monotherapy in type 2 DM or combined with other agents.

26
Q

α-glucosidase Inhibitor Toxicity

A

GI disturbances

27
Q

Amylin analogs

A

Pramlintide

28
Q

Pramlintide Mechanism

A

↓ gastric emptying, ↓ glucagon.

29
Q

Pramlintide Use

A

Type 1 and 2 DM.

30
Q

Pramlintide Toxicity

A

Hypoglycemia, nausea, diarrhea.

31
Q

GLP-1 Analogs

A

Exenatide, Liraglutide

32
Q

GLP-1 Analog Mechanism

A

↑ insulin, ↓ glucagon release.

33
Q

GLP-1 Analog Use

A

Type 2 DM.

34
Q

GLP-1 Analog Toxicity

A

Nausea, vomiting; pancreatitis.

35
Q

DPP-4 Inhibitors

A

Linagliptin, Saxagliptin, Sitagliptin

36
Q

DPP-4 Inhibitor Mechanism

A

↑ insulin, ↓ glucagon release.

37
Q

DPP-4 Inhibitor Use

A

Type 2 DM.

38
Q

DPP-4 Inhibitor Toxicity

A

Mild urinary or respiratory infections.

39
Q

PTU, Methimazole Mechanism

A

Block thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine → inhibition of thyroid hormone synthesis. PTU also blocks 5’-deiodinase, which ↓ peripheral conversion of T4 to T3.

40
Q

PTU, Methimazole Use

A

Hyperthyroidism. PTU blocks Peripheral conversion, used in Pregnancy.

41
Q

PTU, Methimazole Toxicity

A

Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (PTU). Methimazole is a possible teratogen (can cause aplasia cutis).

42
Q

Levothyroxine, Triiodothyronine Mechanism

A

Thyroxine replacement.

43
Q

Levothyroxine, Triiodothyronine Use

A

Hypothyroidism, myxedema.

44
Q

Levothyroxine, Triiodothyronine Toxicity

A

Tachycardia, heat intolerance, tremors, arrhythmias.

45
Q

GH Use

A

GH deficiency, Turner syndrome

46
Q

Somatostatin (octreotide) Use

A

Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices.

47
Q

Oxytocin Use

A

Stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage.

48
Q

ADH (DDAVP) Use

A

Pituitary (central, not nephrogenic) DI.

49
Q

Demeclocycline Mechanism

A

ADH antagonist (member of tetracycline family).

50
Q

Demeclocycline Use

A

SIADH

51
Q

Demeclocycline Toxicity

A

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth.

52
Q

Glucocorticoids

A

Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone, fludrocortisone (mineralocorticoid and glucocorticoid activity).

53
Q

Glucocorticoid mechanism

A

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid respones elements and inhibition of transcription factors such as NF-κB.

54
Q

Glucocorticoid Use

A

Addison disease, inflammation, immune suppression, asthma

55
Q

Glucocorticoid Toxicity

A

Iatrogenic Cushing syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis (treat with bisphosphonates), adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
Adrenal insufficiency when drug stopped abruptly after chronic use.

Pharmacology (14 decks)

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