Endocrine

Question 1

Lispro

Answer 1

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

Question 2

Aspart

Answer 2

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

Question 3

Glulisine

Answer 3

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Rapid-acting

Question 4

Regular

Answer 4

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Short-acting

Question 5

NPH

Answer 5

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Intermediate

Question 6

Glargine

Answer 6

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting

Question 7

Detemir

Answer 7

1) Type I DM, Type II DM, gestational DM, life-threatening hyperkalemia, stress-induced hyperglycemia
2) Insulin/Bind insulin receptor (tyrosine kinase activity)
- Liver: increase glucose stored as glycogen
- Muscle: increase glycogen and protien synthesis and K+ uptake
- Fat: aids in TG storage
3) Hypoglycemia, very rarely hypersensitivy rxns
4) Long-acting

Question 8

Metformin

Answer 8

1) First-line therapy in Type II DM, can be used in pts w/o islet function
2) Biguanide/ Exact MOA unknown –> decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity)
3) GI upset, lactic acidosis (most serious)
4) Contraindicated in renal failure

Question 9

Tolbutamide

Answer 9

1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function

Question 10

Chlorpropamide

Answer 10

1) Type II DM –stimulate endogenous insulin release
2) Sulfonylureas (1st generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Disulfiram-like effects
4) Useless in Type I DM b/c requires some islet cell function

Question 11

Glyburide

Answer 11

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

Question 12

Glimepiride

Answer 12

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

Question 13

Glipizide

Answer 13

1) Type II DM – stimulates endogenous insulin release
2) Sulfonylureas (2nd generation)/Close K+ channel in beta cell membrane so cell depolarizes –> triggers insulin release via Ca2+ influx
3) Hypoglycemia
4) Useless in Type I DM b/c requires some islet cell funciton

Question 14

Pioglitazone

Answer 14

1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure

Question 15

Rosiglitazone

Answer 15

1) Monotherapy in Type II DM or in combination therapy
2) Glitazone/Thiazolidinedione: Incraeses insulin sensitivity in peripheral tissue;, binds PPAR-gamma nuclear transcription regulator
3) Weight gain, edema, hepatoxicity, heart failure

Question 16

Acarbose

Answer 16

1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances

Question 17

Miglitol

Answer 17

1) Monotherapy in Type II DM, or in combination therapy
2) Alpha-glucosidase Inhibitor/ Inhibits intestinal brush-border alpha-glucosidases –> get delayed sugar hydrolysis and glucose absorption
- decreases postprandial hyperglycemia
3) GI disturbances

Question 18

Pramlinitide

Answer 18

1) Type I and II DM
2) Amylin Analog/ Decreases glucagon
3) Hypoglycemia, nausea, diarrhea

Question 19

Exenatide

Answer 19

1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis

Question 20

Liraglutide

Answer 20

1) Type II DM
2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis

Question 21

Linagliptin

Answer 21

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

Question 22

Saxagliptin

Answer 22

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

Question 23

Sitagliptin

Answer 23

1) Type II DM
2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections

Question 24

Propylthiouracil

Answer 24

1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide anda coupling of thyroid hormone synthesis
- also blocks 5’-deiodinase –> decreases peripheral conversion of T4 to T5
3) Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity

Question 25

Methimazole

Answer 25

1) Hyperthyroidism
2) Block peroxidase inhibiting organificatoin of iodide anda coupling of thyroid hormone synthesis
3) Skin rash, agranulocytosis (rare), aplastic anemia
4) Possible teratogen

Question 26

Levothyroxine

Answer 26

1) Hypothyroidism, myxedema
2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias

Question 27

Triiodothyronine

Answer 27

1) Hypothyroidism, myxedema
2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias

Question 28

GH

Answer 28

1)GH deficiency, Turner’s Syndrome

Question 29

Somatostatin (octretodie)

Answer 29

1)Acromegaly, carcinoid, gastrinoma, glucagonoma, espohageal varices

Question 30

Oxytocin

Answer 30

1)Stimulate labor, uterine contractions, milk let-down, controls uterine hemorrhage

Question 31

ADH (Desmopressin)

Answer 31

1)Central DI

Question 32

Demeclocycline

Answer 32

1) SIADH
2) Tetracycline/ ADH antagonist
3) Nephrogenic DI, photosensitivity, abnormalities of bone and teeth

Question 33

Hydrocortisone

Answer 33

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

Question 34

Prednisone

Answer 34

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

Question 35

Triamcinolone

Answer 35

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

Question 36

Dexamethasone

Answer 36

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use

Question 37

Beclomethasone

Answer 37

1) Addison’s Disease, inflammation, immune suppression, asthma
2) Glucocorticoid/Decrease production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and COX-2 expression
3) Iatrogenic Cushing’s –> buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, bruise easily, osteoporosis, adrenocortical atrophy, peptic ulcers, DM (if chronic)
4) Can see adrenal insufficiency when drug is stopped abruptly after chronic use