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USMLE Step 1 > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

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USMLE® Step 1 flashcards
0
Q

Treatment strategy for type 2 DM

A

Dietary modification and exercise for weight loss; oral hypoglycemics and insulin replacement

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1
Q

Treatment strategy for type 1 DM

A

Low sugar diet, insulin replacement

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2
Q

Rapid Acting Insulin

A

Lispro, Aspart, Glulisine

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3
Q

Short acting insulin

A

Regular insulin

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4
Q

Intermediate Insulin

A

NPH

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5
Q

Long acting insulin

A

Glargine, Detemir

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6
Q

Insulin: Action

A

Bind insulin receptor (tyrosine kinase activity)
Liver: increase glucose stored as glycogen
Muscle: increase glycogen and protein synthesis
Fat: aids TG storage

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7
Q

Insulin: Clinical Use

A

Type 1 DM, type 2 DM
Gestational Diabetes
Life-threatening hyperkalemia
Stress-induced hyperglycemia

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8
Q

Insulin : Toxicity

A 
Hypoglycemia
Hypersensitivity Reactions (very rarely)
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9
Q

Biguanides

A

Metformin

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10
Q

Metformin: Action

A

Exact mechanism is unknown

  • decrease* gluconeogenesis
  • increase* glycolysis, peripheral glucose uptake (insulin sensitivity)
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11
Q

Metformin: Clinical Use

A

Oral: 1st line therapy in type 2 DM

Can be used in patients without islet function

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12
Q

Metformin: Toxicity

A

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

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13
Q

1st generation: Sulfonylureas

A

Tolbutamide

Chlorpropramide

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14
Q

2nd generation: Sulfonylureas

A

Glyburide
Glimepiride
Glipizide

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15
Q

Sulfonylureas

A

Close K+ channel in B-cell membrane, so cell depolarizes –> triggering of insulin release via increase of Ca+ influx
(JUST LIKE INSULIN)

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16
Q

Sulfonylureas: Clinical 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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17
Q

Sulfonylureas: Toxicity

A

1st generation: disulfiram-like effect.

2nd generation: hypoglycemia (avoid use with EtOH)

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18
Q

Glitazones/ thiazolidinediones

A

Pioglitazone

Rosiglitazone

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19
Q

Glitazones/thiazolidinediones (Pioglitazone, Riosiglitazone): Action

A

Increase insulin sensitivity in peripheral tissue. Binds to PPAR-gamma nuclear transcription regulator.

*PPAR-gamma regulate FA storage and glucose metabolism. Activation of PPAR-gamma increases insulin sensitivity and levels of adiponectin.

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20
Q

Glitazones/ Thiazolidinediones: Clinical Use

A

Used as monotherapy in type 2 DM or combined with above agents

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21
Q

Glitazones/ Thiazolidinediones: Toxicity

A

Weight gain, edema, hepatotoxicity, heart failure

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22
Q

Alpha Glucosidase inhibitors

A

Acarbose

Miglitol

23
Q

Alpha-Glucosidase Inhibitors: Action

A

Inhibit intestional brush border alpha glucosidases

Delayed sugar hydrolysis and glucose absorption –> DECREASED postprandial hyperglycemia

24
Q

Alpha-glucosidase inhibitors: Clinical Use

A

Used as monotherapy or in combination with other diabetic drugs

25
Q

Alpha-glucosidase: Toxicity

A

GI disturbances

26
Q

Amylin analogs

A

Pramlintide

27
Q

Pramlintide: Action

A

Decrease glucagon

28
Q

Pramlintide: Clinical Use

A

Type 1 and type 2 DM

29
Q

Pramlintide: Toxicity

A

Hypoglycemia, Nausea, Diarrhea

30
Q

GLP-1 analogs:

A

Exenatide

Liraglutide

31
Q

GLP-1: Action:

A

Increase insulin

Decrease glucagon release

32
Q

GLP-1 analog (Exenatide, Liraglutide): Clinical Use

A

Type 2 DM

33
Q

GLP-1 analog (Exenatide, Liraglutide): Toxicity

A

Nausea, vomiting, pancreatitis

34
Q

DPP-4 inhibitors:

A

Linagliptin, Saxagliptin, Sitagliptin

35
Q

DPP-4 inhibitors: Linagliptin, Saxagliptin, Sitagliptin: Mechanism

A

Increase insulin, Decrease Glucagon release

36
Q

DPP-4 inhibitors (Litaglipton, Saxagliptin, Sitagliptin): Clinical Use

A

Type 2 DM

37
Q

DPP-4 inhibitors (Litagliptin, Saxagliptin, Sitagliptin): Toxicity

A

Mild urinary or respiratory infections

38
Q

Thioamides

A

Propylthiouracil, Methimazole

39
Q

Thioamides (Propylthiouracil, Methimazole): Mechanism

A

Block peroxidase, thereby inhibiting organification of iodine and coupling of thyroid hormone synthesis.

*Propylthiouracil also blocks 5’-deiodinase which decrease peripheral converseion of T4 to T3.

40
Q

Thioamides (Propylthiouracil, Methimazole): Clinical Use

A

Hyperthyroidism

41
Q

Thioamies (Propylthiouracil, Methimazole): Toxicity

A

Skin rash, agranulocytosis (rare), aplastic anemia
Propylthiouracil: hepatotoxicity, safer during pregnancy
Methimazole: possible teratogen

42
Q

Levothyroxine, Triiodothyronine: Mechanism

A

Thyroxine replacement

43
Q

Levothyrozine, Triiodothyronine: Clinical Use

A

Hypothyroidism, Myxedema

44
Q

Levothyroxine, Triiodothyronine: Toxicity

A

Tachycardia, Heat intolerance, Tremors, Arrhythmias (signs of hyperthyroidism)

45
Q

Growth Hormone: Clinical Use

A

GH deficiency, Turner Syndrome

46
Q

Somatostatin (Octeotride): Clinical Use

A

Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

47
Q

Oxytocin: Clinical use

A

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

48
Q

ADH (desmopressin): Clinical Use

A

Pituitary (central NOT nephrogenic) DI

49
Q

Demeclocycline: Mechanism

A

ADH antagonist (member of tetracycline family)

50
Q

Demeclocycline: Clinical Use

A

SIADH

51
Q

Demeclocycline: Toxicity

A

Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

52
Q

Glucocorticoids

A

Hydrocortisone, Prednisone, Triamcinolone, Dexamethasone, Beclamethasone

53
Q

Glucocorticoids (-asone/ - isone): Mechanism

A

Decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2

54
Q

Glucocorticoids: Clinical Use

A

Addison’s disease, inflammation, immune suppression, asthma

55
Q

Glucocorticoids (-asone/-isone: Toxicity

A

Iatrogenic Cushing’s syndrome - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic)

56
Q

Risk of stopping glucocorticoids abruptly

A

Adrenal insufficiency – must taper the glucocorticoids to prevent this.

USMLE Step 1 (34 decks)

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