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USMLE Step 1 > Endocrine Drugs > Flashcards

Endocrine Drugs Flashcards

(57 cards)

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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

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A

Acarbose

Miglitol

23
Q

Alpha-Glucosidase Inhibitors: Action

Study These Flashcards
A

Inhibit intestional brush border alpha glucosidases

Delayed sugar hydrolysis and glucose absorption –> DECREASED postprandial hyperglycemia

24
Alpha-glucosidase inhibitors: Clinical Use
Used as monotherapy or in combination with other diabetic drugs
25
Alpha-glucosidase: Toxicity
GI disturbances
26
Amylin analogs
Pramlintide
27
Pramlintide: Action
Decrease glucagon
28
Pramlintide: Clinical Use
Type 1 and type 2 DM
29
Pramlintide: Toxicity
Hypoglycemia, Nausea, Diarrhea
30
GLP-1 analogs:
Exenatide | Liraglutide
31
GLP-1: Action:
Increase insulin | Decrease glucagon release
32
GLP-1 analog (Exenatide, Liraglutide): Clinical Use
Type 2 DM
33
GLP-1 analog (Exenatide, Liraglutide): Toxicity
Nausea, vomiting, pancreatitis
34
DPP-4 inhibitors:
Linagliptin, Saxagliptin, Sitagliptin
35
DPP-4 inhibitors: Linagliptin, Saxagliptin, Sitagliptin: Mechanism
Increase insulin, Decrease Glucagon release
36
DPP-4 inhibitors (Litaglipton, Saxagliptin, Sitagliptin): Clinical Use
Type 2 DM
37
DPP-4 inhibitors (Litagliptin, Saxagliptin, Sitagliptin): Toxicity
Mild urinary or respiratory infections
38
Thioamides
Propylthiouracil, Methimazole
39
Thioamides (Propylthiouracil, Methimazole): Mechanism
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
Thioamides (Propylthiouracil, Methimazole): Clinical Use
Hyperthyroidism
41
Thioamies (Propylthiouracil, Methimazole): Toxicity
Skin rash, agranulocytosis (rare), aplastic anemia Propylthiouracil: hepatotoxicity, safer during pregnancy Methimazole: possible teratogen
42
Levothyroxine, Triiodothyronine: Mechanism
Thyroxine replacement
43
Levothyrozine, Triiodothyronine: Clinical Use
Hypothyroidism, Myxedema
44
Levothyroxine, Triiodothyronine: Toxicity
Tachycardia, Heat intolerance, Tremors, Arrhythmias (signs of hyperthyroidism)
45
Growth Hormone: Clinical Use
GH deficiency, Turner Syndrome
46
Somatostatin (Octeotride): Clinical Use
Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices
47
Oxytocin: Clinical use
Stimulates labor, uterine contractions, milk-let down, controls uterine hemorrhage
48
ADH (desmopressin): Clinical Use
Pituitary (central NOT nephrogenic) DI
49
Demeclocycline: Mechanism
ADH antagonist (member of tetracycline family)
50
Demeclocycline: Clinical Use
SIADH
51
Demeclocycline: Toxicity
Nephrogenic DI, photosensitivity, abnormalities of bone and teeth
52
Glucocorticoids
Hydrocortisone, Prednisone, Triamcinolone, Dexamethasone, Beclamethasone
53
Glucocorticoids (-asone/ - isone): Mechanism
Decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX2
54
Glucocorticoids: Clinical Use
Addison's disease, inflammation, immune suppression, asthma
55
Glucocorticoids (-asone/-isone: Toxicity
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
Risk of stopping glucocorticoids abruptly
Adrenal insufficiency -- must taper the glucocorticoids to prevent this.

USMLE Step 1 (34 decks)

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