Endo

Question 1

Rapid-acting Insulin (Lispro, Aspart, Glulisine)

[MOA, clinical use]

Answer 1

Binds insulin receptor.

For DM 1, 2, GDM – postprandial control

Question 2

Short-acting Insulin (Regular)

Clinical use

Answer 2

DM 1, 2, GDM
DKA, Hyperkalemia (+ glucose)
Stress hyperglycemia

Question 3

Intermediate-acting Insulin

[Name, use]

Answer 3

NPH (Neutral Protamine Hagedorn; Humulin N, Novocain N).

DM 1, 2, GDM.

Question 4

Long-acting Insulin (Detemir, Glargine)

[Clinical use]

Answer 4

DM 1, 2, GDM – basal glucose control.

Question 5

Biguanides (Metformin)

[Clinical use, Toxicity]

Answer 5

Suppresses hepatic gluconeogenesis.
First-line for DM2; can be used for DM1.
>Toxicity: lactic acidosis (lactate produced in intestine is normally converted to glucose in hepatic gluconeogenesis; CI in renal insufficiency).

Question 6

Sulfonylureas

[Names (1st gen, 2nd gen), MOA, use]

Answer 6

> 1st gen: Chlorpropamide, Tolbutamide.
2nd gen: Glimepiride, Glyburide, Glipizide.
Closes K channel in B-islet cells – depol – opens voltage-gated Ca channels – inc. intracellular Ca – release insulin.
For DM2.
*Needs islet cell function – can’t be used in DM1

Question 7

Glitazones/Thiazolidinediones (Pioglitazone, Rosiglitazone)

[MOA, Use, Toxicity]

Answer 7

> Inc. insulin sensitivity in peripheral tissues (adipose, skeletal muscle) – upregulates GLUT4 and adiponectin by binding to PPAR-gamma transcription regulator.
For DM2; monotherapy or combined w/ sulfonylureas, biguanides.
SE: wt. gain, edema; hepatoxicity, HF

Question 8

GLP-1 analogs (Exenatide, Liraglutide)

[MOA, use, SE]

Answer 8

> Inc. insulin, Dec. glucagon.
For DM2.
SE: pancreatitis
*Glucose-like peptide: inc. glucose-dependent insulin secretion.

Question 9

DPP-4 inhibitors (Linagliptin, Saxagliptin, Sitagliptin)

[MOA, use, SE]

Answer 9

> Inc. endogenous GLP-1 – inc. insulin, dec. glucagon.
For DM2.
SE: urinary/respi infections (nasopharyngitis)
*DPP-4 inhibits endogenous GLP-1 secretion

Question 10

Pramlintide (Amylin analog)

[MOA, use]

Answer 10

> Dec. gastric emptying, dec. glucagon.
For DM1, 2
*Amylin: peptide co-secreted w/ insulin from pancreatic beta cells (satiety agent)

Question 11

Canagliflozin (SGLT-2 inhibitor)

[MOA, use, SE]

Answer 11

> Blocks glucose reabsorption in PCT.
For DM2.
SE: glycosuria, vaginal yeast infxn.
*Assess renal impairment

Question 12

alpha-glucosidase inhibitors (Acarbose, Miglitol)

[MOA, use]

Answer 12

> Inhibit intestinal brush border alpha-glucosidases – delayed carb hydrolysis and glucose absorption – dec. postprandial hyperglycemia.
Can be monotherapy or combination for DM2.

Question 13

Propylthiouracil, Methimazole

[MOA, use, toxicity]

Answer 13

> Block thyroid peroxidase – inhibits oxidation and coupling of iodine – inhibits TH synthesis.
PTU also inhibits 5’-deiodinase – no peripheral conversion of T4 into T3.
For Hyperthyroidism.
SE: Agranulocytosis (rare), aplastic anemia; hepatotoxicity (PTU); teratogen (methimazole).

Question 14

Levothyroxine (T4), Triiodothyronine (T3)

[use]

Answer 14

Thyroid hormone replacement.
For hypothyroidism, myxedema.
Off-label weight loss supplements.

Question 15

Conivaptan, Tolvaptan (ADH antagonists)

[use, MOA]

Answer 15

For SIADH

Blocks ADH at V2 receptor

Question 16

Desmopressin acetate

[use]

Answer 16

For central DI

Question 17

Somatostatin (octreotide)

[use]

Answer 17

For acromegaly, carcinoid syndrome, gastronoma, glucagonoma, esophageal varices

Question 18

Demeclocycline (ADH antagonist)

[Use, toxicity]

Answer 18

> Member of tetracycline family.
For SIADH.
Toxicity: nephrogenic DI, abnormalities w/ bone and teeth.

Question 19

Cinacalcet

[MOA, use]

Answer 19

> Sensitizes Ca-sensing receptor in parathyroid gland to circulating Ca – dec. PTH.
For Hypercalcemia (due to hyperparathyroidism).
*Sense the Calcium

Question 20

Glucocorticoids (-one)

Names

Answer 20

Beclomethasone, Dexamethasone, Hydrocortisone, Methylprednisolone, Prednisone, Triamcinolone,
Fludrocortisone (mineralocorticoid and glucocorticoid activity)

Question 21

Glucocorticoids

[MOA, Use]

Answer 21

Metabolic, Catabolic, Anti-inflammatory, immunosuppressive.
>Inhibits phospholipase A2 – no leukotrienes, PGs.
>Inhibits NFkB transcription factor – blocks DNA and cytokine production.
>For Addison dse, inflammation, immunosuppression, asthma.

Question 22

Glucocorticoid

Toxicity

Answer 22

> Iatrogenic Cushing syndrome (HTN, wt. gain, obesity, buffalo hump, striae, hyperglycemia, etc).
Adrenal insufficiency when abruptly stopped after chronic use.
Immunosuppression.

Question 23

Why should you beware of chronic glucocorticoid use?

Answer 23

CRH, ACTH, and cortisol will no longer rise in stressful situations. There will be relative glucocorticoid deficiency even if baseline is maintained w/ therapy. This may lead to hypotension and shock.
>Higher stress dose needed to compensate and prevent adrenal crisis.