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Pharmacology > Endocrine drugs > Flashcards

Endocrine drugs Flashcards

1
Q

Treatment strategy for Type 1 DM

A

low-carb diet, insulin replacement

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2
Q

Treatment strategy for Type 2 DM

A

diet and exercise; oral agents, non-insulin injectables, insulin replacement

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3
Q

Treatment strategy for gestational DM

A

dietary and exercise modifications, insulin replacement if that fails

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4
Q

Insulin, rapid acting

A

Aspart, Glulisine, Lispro

Mechanism: Binds insulin receptor

  • liver: increased glucose stored as glycogen
  • muscle: increased glycogen, protein synthesis; increased K+ uptake
  • fat: increased TG storage

Use: Type 1 and 2 DM, Gestational DM (postprandial glucose control)

Toxicity: Hypoglycemia, rare hypersensitivity rxn

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5
Q

Insulin, short acting

A

insulin

Uses: Type 1 and 2 DM, Gestational DM, *DKA (IV), hyperkalemia (+glucose), stress hyperglycemia

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6
Q

Insulin, intermediate acting

A

NPH

Use: Type 1 and 2 DM, GDM

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7
Q

Insulin, long acting

A

Detemir, Glargine

Use: Type 1 and 2 DM, GDM (basal glucose control)

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8
Q

Metformin

A

Drug class: Biguanides

Action: exact mech unknown, decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (increased insulin sensitivity)

Use: Oral. 1st line in T2DM, causes modest weight loss. Can be used in patients w/out islet fxn

Toxicity:
GI upset (can cause decreased B12 and folate absorption)
Lactic acidosis (most serious side effect) -> contraindicated in: renal insufficiency, CHF, liver dysfunction, sepsis, EtOH abuse
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9
Q

Sulfonylureas

A

1st gen: Chlorpropamide, Tolbutamide
2nd gen: Glimepiride, Glipizide, Glyburide

Mechanism: Closes K+ channel in beta-cell membrane -> cell depolarizes -> increases insulin release via increased calcium influx

Use: T2DM; requires some islet fxn so useless in T1DM

Toxicity:
Weight gain
Cardiac effects (sulfonylurea channels in heart too)
Hypoglycemia risk increase in renal failure
1st gen: disulfiram-effects
2nd gen: hypoglycemia

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10
Q

Glitazones/ Thiazolidinediones

A

Pioglitazone, Rosiglitazone

Mechanism: Binds to PPAR-gamma nuclear transcription regulator -> increases insulin sensitivity in peripheral tissue; PPAR-gamma regulates fatty acid storage and glucose metabolism –> activation will increase insulin sensitivity and adiponectin levels

Clinical use: Used as monotherapy in T2DM or combined with other oral hypoglycemic drugs

Toxicity: Weight gain, edema
Hepatotoxicity, HF, increased risk of fractures
Increased LDL, HDL

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11
Q

Meglitinides (repaglinide)

A

Mechanism: Similar to sulfonylureas without sulfa; Close ATP dependent K+ channels -> increase insulin release. Short half life, metabolized by CYPs to glucuronic acid

Clinical use: T2DM with sulfa allergy

Toxicity:

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12
Q

GLP-1 analogs

A

Exenatide, Liraglutide

Mechanism: GLP-1= glucagon like peptide, incretin released by stomach when food is present. Increase insulin, decrease glucagon release.

Clinical use: Type 2 DM

Toxicity: Nausea, vomiting, pancreatitis

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13
Q

DDP-4 Inhibitors

A

Linagliptin, Saxagliptin, Sitagliptin

Mechanism: Increases insulin, decreases glucagon

Clinical use: T2DM

Toxicity: Mild urinary or respiratory infections

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14
Q

Amylin analogs

A

Pramlintide

Mechanism: Decreases gastric emptying, decreases glucagon

Clinical use: T1DM and T2DM

Toxicity: Hypoglycemia, nausea, diarrhea

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15
Q

SGLT-2 inhibitors

A

Canagliflozin

Mechanism: Block reabsorption of glucose in PCT

Clinical use: T2DM

Toxicity: Glucosuria, UTIs, vaginal yeast infections

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16
Q

alpha-glucosidase inhibitors

A

Acarbose, Miglitol

Mechanism: Inhibit brush-border alpha-glucosidases. Delayed carbo hydrolysis and glucose absorption -> decreases postprandial hyperglycemia (given w/ meals)

Clinical use: Can be monotherapy in T2DM or combo

Toxicity: GI disturbances- malabsorption diarrhea, can lower absorption of other drugs

17
Q

Propylthiouracil (PTU), methimazole

A

Mechanism: Block thyroid peroxidase, inhibiting the oxidation of iodide, and organification of iodine -> inhibits thyroid hormone synthesis

PTU also inhibits 5’-deiodinase which decreases peripheral conversion of T4->T3

Clinical use: Hyperthyroidism; PTU blocks peripheral conversion, used in pregnancy

Toxicity: Skin rash, agranulocytosis (rare), aplastic anemia,
hepatotoxicity (PTU)
Methimazole is possible teratogen (aplasia cutis)

18
Q

Levothyroxine (T4), Triiodothyronine (T3)

A

Mechanism: Thyroid hormone replacement

Clinical use: Hypothyroidism, myxedema; used off-label as weight loss supplements

Toxicity: Tachycardia, heat intolerance, tremors, arrhythmias

19
Q

Demeclocycline

A

Mechanism: ADH antagonist (tetracycline family)

Clinical use: SIADH

Toxicity: nephrogenic DI, photosensitivity, abnormalities of bone and teeth

20
Q

Glucocorticoids

A

Beclomethazone, dexamethasone, fludrocortisone (mineralo- and glucocorticoid activity), hydrocortisone, methylprednisolone, prednisone, triamcinolone

Mechanism: Interacts with glucocorticoid response elements, inhibits phospholipase A2 and inhibits TFs like NF-kB. Metabolic, catabolic, anti-inflammatory and immunosuppressive effects

Clinical use: Adison disease, inflammation, immunosuppression, asthma

Toxicity:

  • Cushing syndrome (HTN, weight gain, moon facies, truncal obesity, buffalo hump, thinning skin, striae, osteoporosis, hyperglycemia, amenorrhea, immunosuppression)
  • Adrenocortical atrophy
  • Peptic ulcers
  • Steroid diabetes
  • Steroid psychosis
  • Adrenal insufficiency when stopped abruptly
21
Q

Cinacalcet

A

Mechanism: Sensitizes calcium sensing receptor (CaSR) in parathyroid gland to circulating calcium -> decreases PTH

Clinical use: hypercalcemia due to primary or secondary hyperparathyroidism

Toxicity: hypocalcemia

22
Q

ADH antagonists

A

conivaptan, tolvaptan

Mech: Block action of ADH at V2 receptor

Clinical use: SIADH

23
Q

Desmopressin acetate

A

Use: central (NOT nephrogenic) DI

Also used in von Willlebrand disease -> induces procoagulation factors including vWF

24
Q

GH

A

GH deficiency, Turner Syndrome

25
Q

Oxytocin

A

stimulates labor, uterine contractions, milk let-down; controls uterine hemorrhage

26
Q

Somatostatin (octreotide)

A

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices

27
Q

What drugs can exacerbate and mask the signs of hypoglycemia?

A

Non-selective beta blockers –> do not use in patients with diabetes milletus

Pharmacology (19 decks)

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