Endocrine

Question 1

Lispro

Answer 1

Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions

Question 2

Aspart

Answer 2

Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions

Question 3

Glulisine

Answer 3

Rapid acting insulin
Binds insulin receptor (tyrosine kinase activity).
Liver: Increases glucose stored as glycogen
Fat: Increases TG storage
Muscle: Increases glycogen and protein synthesis, increases K uptake
Post-prandial glucose control in DM1, DM2, GDM
Hypoglycemia, rare hypersensitivity reactions

Question 4

Insulin

Answer 4

Short acting insulin

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

Question 5

NPH

Answer 5

Intermediate acting insulin

DM1, DM2, GDM

Question 6

Glargine

Answer 6

Long acting insulin

Basal glucose control in DM1, DM2, GDM

Question 7

Detemir

Answer 7

Long acting insulin

Basal glucose control in DM1, DM2, GDM

Question 8

Metformin

Answer 8

Biguanide
Unknown mechanism. Decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity), decreases glucose absorption. Primary effects in liver.
Oral. First line therapy in DM2. Can be used patients without islet function.
GI upset, lactic acidosis (contraindicated in renal failure)

Question 9

Tolbutamide

Answer 9

First generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Risk of hypoglycemia increased in renal failure. Disulfiram-like (nausea, flushing, tachycardia, hyperventilation) effects.

Question 10

Chlorpropamide

Answer 10

First generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Risk of hypoglycemia increased in renal failure. Disulfiram-like (nausea, flushing, tachycardia, hyperventilation) effects.

Question 11

Glyburide

Answer 11

Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.

Question 12

Glimepiride

Answer 12

Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.

Question 13

Glipizide

Answer 13

Second generation sulfonylurea
Closes K channel in β cell membrane, leading to depolarization and insulin release via increased Ca influx.
Stimulates endogenous insulin release in DM2. Not useful in DM1, requires islet cell function.
Hypoglycemia. Risk of hypoglycemia increased in renal failure.

Question 14

Pioglitazone

Answer 14

Glitazones/thiazolidinedione
Increases insulin sensitivity in peripheral tissue. Bind to peroxisome proliferator activated receptor (PPAR-γ), a nuclear transcription regulator.
Mono therapy in DM2 or combined with other agents.
Weight gain, edema, hepatotoxicity, heart failure.

Question 15

Rosiglitazone

Answer 15

Glitazones/thiazolidinedione
Increases insulin sensitivity in peripheral tissue. Bind to peroxisome proliferator activated receptor (PPAR-γ), a nuclear transcription regulator.
Mono therapy in DM2 or combined with other agents.
Weight gain, edema, hepatotoxicity, heart failure.

Question 16

Acarbose

Answer 16

α-glucosidease inhibitor
Inhibits intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption, leading to decreases in postprandial hyperglycemia.
Monotherapy in DM2 or in combination with other agents.
Diarrhea, flatulence, bloating, increased liver enzymes. Contraindicated in cirrhosis.

Question 17

Miglitol

Answer 17

α-glucosidease inhibitor
Inhibits intestinal brush border α-glucosidases. Delayed sugar hydrolysis and glucose absorption, leading to decreases in postprandial hyperglycemia.
Monotherapy in DM2 or in combination with other agents.
Diarrhea, flatulence, bloating, increased liver enzymes. Contraindicated in cirrhosis.

Question 18

Pramlintide

Answer 18

Amylin analog
Decreases gastric emptying, decreases glucagon
DM1 and DM2
Hypoglycemia, nausea, diarrhea

Question 19

Exenatide

Answer 19

GLP-1 analog
Increases insulin, decreases glucagon release
DM2
Nausea, vomiting, pancreatitis

Question 20

Liraglutide

Answer 20

GLP-1 analog
Increases insulin, decreases glucagon release
DM2
Nausea, vomiting, pancreatitis

Question 21

Linagliptin

Answer 21

DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections

Question 22

Saxagliptin

Answer 22

DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections

Question 23

Sitagliptin

Answer 23

DPP-4 inhibitor
Increases insulin, decreases glucagon release
DM2
Mild urinary or respiratory infections

Question 24

Propylthiouracil

Answer 24

Blocks thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine, leading to inhibition of thyroid hormone synthesis. Also blocks 5’-deiodinase, which decreases peripheral conversion of T4 to T3.
Hyperthyroidism. Safe in pregnancy.
Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity.

Question 25

Methimazole

Answer 25

Blocks thyroid peroxidase, inhibiting oxidation of iodide and organification (coupling) of iodine, leading to inhibition of thyroid hormone synthesis. Hyperthyroidism. Skin rash, agranulocytosis (rare), aplastic anemia, teratogen (aplasia cutis).

Question 26

Levothyroxine

Answer 26

Thyroxine replacement Hypothyroidism, myxedema Tachycardia, heat intolerance, tremors, arrhythmias

Question 27

Triiodothyronine

Answer 27

Thyroxine replacement Hypothyroidism, myxedema Tachycardia, heat intolerance, tremors, arrhythmias

Question 28

GH

Answer 28

GH deficiency, Turner Syndrome

Question 29

Octreotide

Answer 29

Somatostatin | Acromegaly, carcinoid, gastrinoma, glucagonoma, esophageal varices

Question 30

Oxytocin

Answer 30

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

Question 31

Demeclocycline

Answer 31

Tetracycline. ADH antagonist. SIADH Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

Question 32

Hydrocortisone

Answer 32

Glucocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.

Question 33

Prednisone

Answer 33

Glucocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.

Question 34

Triamcinolone

Answer 34

Glucocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.

Question 35

Dexamethasone

Answer 35

Glucocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.

Question 36

Beclomethasone

Answer 36

Glucocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.

Question 37

Fludrocortisone

Answer 37

Glucocorticoid and mineralocorticoid Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors such as NF-κB Addison disease, inflammation, immune suppression, asthma Iatrogenic Cushing syndrome, adrenocortical atrophy, peptic ulcers, diabetes (if chronic), adrenal insufficiency when drugs are stopped abruptly after chronic use.