Endo/Repro

Question 1

<p>Lispro</p>

Answer 1

<p>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</p>

Question 2

<p>Aspart</p>

Answer 2

<p>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</p>

Question 3

<p>Glulisine</p>

Answer 3

<p>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</p>

Question 4

<p>Regular</p>

Answer 4

<p>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</p>

Question 5

<p>NPH</p>

Answer 5

<p>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</p>

Question 6

<p>Glargine</p>

Answer 6

<p>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</p>

Question 6

Sprionolactone

Answer 6

1) Use: Polycytic ovarian syndrome prevent hirsuitsm
2) Class/MOA: Antiandrogen/inhibits steroid binding
3) Side effects/ADEs: Gynecomastia and amenorrhea

Question 7

<p>Detemir</p>

Answer 7

<p>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
</p>

Question 8

<p>Metformin</p>

Answer 8

<p>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</p>

Question 9

<p>Tolbutamide</p>

Answer 9

<p>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</p>

Question 10

<p>Chlorpropamide</p>

Answer 10

<p>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</p>

Question 11

<p>Glyburide</p>

Answer 11

<p>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</p>

Question 12

<p>Glimepiride</p>

Answer 12

<p>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</p>

Question 13

<p>Glipizide</p>

Answer 13

<p>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</p>

Question 13

Progestins

Answer 13

1) Use: OCP, Mirena IUD, treatment of endometrial cancer and abnormal uterine bleeding
2) Class/MOA: Binds progesterone receptors, reduce growth and increase vascularizaiton of endometrium
4) For OCP have to take at same time everyday so not as effective contraceptive

Question 14

<p>Pioglitazone</p>

Answer 14

<p>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</p>

Question 15

<p>Rosiglitazone</p>

Answer 15

<p>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</p>

Question 16

<p>Acarbose</p>

Answer 16

<p>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</p>

Question 16

Terbutaline

Answer 16

1) Use: Reduces premature uterine contraction

2) Class/MOA: B2 agonist that relaxes the uterus

Question 17

<p>Miglitol</p>

Answer 17

<p>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</p>

Question 18

<p>Pramlinitide</p>

Answer 18

<p>1)Type I and II DM

2) Amylin Analog/ Decreases glucagon
3) Hypoglycemia, nausea, diarrhea</p>

Question 18

Sildenafil, vardenafil

Answer 18

1) Use: Erectile dysfunction
2) Class/MOA: Inhibits phosphodiesterase 5, increase cGMP, smooth muscle relaxaiton in corpus cavernosum, increase blood flow and penile erection
3) Side effects/ADEs: Headache, flushing, dyspepsia, impaired blue green color vision, risk of life threatening hypotension in patients taking nitrates “Hot and sweath” but then Headace, Heartburn, Hypotension
4) Fun Facts: DON’T USE WITH NITRATES

Question 19

<p>Exenatide</p>

Answer 19

<p>1)Type II DM

2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis</p>

Question 20

<p>Liraglutide</p>

Answer 20

<p>1)Type II DM

2) GLP-1 Analog/ Increase insulin and decrease glucagon release
3) Nausea, vomiting, pancreatitis</p>

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

Question 38

Leuprolide

Answer 38

1) Use: Infertility (Pulsatile), Prostate Cancer (continuous + flutamide), uterine fibroids (continuous), precocious puberty (continuous) 2) Class/MOA: GnRH analog, pulsatile use=agonist properties, continous use=antagonist properites because downregulates GnRH receptor in pituitary causing decrease FSH/LH 3) Side effects/ADEs: Antiandrogen, N/V 4) Fun Facts Leuprolide can be used in lieu of GnRH

Question 39

Testosterone, methyltestosterone

Answer 39

1) Use: Hypogonadism, development secondary sex characteristics, stimulates anabolism to promote recovery after burn or injury 2) Class/MOA: Agonist at androgen receptor 3) Side effects/ADEs: Masculinization in females, reduces intratesticular testoerone b/c inhibit relase of LH causing gonadal atropy, premature closing epiphyseal plate, increase LDH, decrease HDL

Question 40

Finasteride

Answer 40

1) Use: BPH, hair growth male pattern baldness 2) Class/MOA: Antiandrogen/5alpha reductase inhibitor (decrease conversion of testosterone to DHT) 3) Side effects/ADEs: Female breast growth

Question 41

Flutamide

Answer 41

1) Use: Prostate carcinoma | 2) Class/MOA: Antiandrogen/ nonsteroidal competitive inhibitor of androgesn at testosterone receptor

Question 42

Ketoconazole

Answer 42

1) Use: Polycystic ovarian syndrome to prevent hirsutism 2) Class/MOA: Antiandrogen/ inhibits 17,20 desmolase and inhibits steroid synthesis 3) Side effects/ADEs: Gynecomastia and amenorrhea

Question 44

Estrogens (ethinyl estradiol, DES, mestranol)

Answer 44

1) Use: Hypogonadism, ovarian failure, menstural abnormalities, HRT postmenopausal, men with androgen dependent prostate cancer 2) Class/MOA: Binds estrogen receptors 3) Side effects/ADEs: Increase risk endometrial cancer, bleed postmenopausal, vaginal clear cell adenocarcinoma if exposed to DES in utero, increase risk thormbi 4) Fun Facts: contraindicated if ER positive breast cancer or history of DVTs

Question 45

Clomiphene

Answer 45

1) Use: Infertility and PCOS 2) Class/MOA: Selective estrogen receptor modulator (SERMs)/ partial agonist at estrogen receptors in hypothalamus, prevents normal feedback inhibition and increases relase of LH and FSH from pituitary and stimulates ovulaiton 3) Side effects/ADEs: Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances 4) Fun Facts: Remember, infertile, take clomiphene have twins, seeing double

Question 46

Tamoxifen

Answer 46

1) Use: Treat and prevent recurrence ER positive breast cancer 2) Class/MOA: SERM/Antagonist on breast tissue

Question 47

Raloxifene

Answer 47

1) Use: Osteoporosis | 2) Class/MOA: SERM/Agonist on bone, reduces resorption of bone

Question 48

Hormone Replacement Therapy

Answer 48

1) Use: Relief/prevent menopausal symptoms (hot flashes, vaginal atrophy) and osteoporosis 2) Class/MOA: 3) Side effects/ADEs: Unopossed estrogen replacement therapy (ERT) causes increase endometrial cancer so add progesterone, possible increase in CV risk

Question 49

Anastrozole/ exemestane

Answer 49

1) Use: Postmenopausal women with breast cancer | 2) Class/MOA: Aromatase inhibitor

Question 51

Mifepristone (RU 486)

Answer 51

1) Use: Terminiation of pregnancy +misoprostol (PGE1) 2) Class/MOA: Competitive inhibitor of progestins at progesterone receptors 3) Side effects/ADEs: Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain

Question 52

Oral contraception (synthetic progestins, estrogen)

Answer 52

1) Use: Prevent pregnancy 2) Class/MOA: Estrogen and progestins inhibit LH/FSH and prevent estrogen surges so no LH surge and no ovulaiton. Progestins cause thickenign of cervical mucus, limiting access of sperm to uterus. Also inhibits endometrial proliferation, making endometirum less suitable for implanation of embryo 3) Side effects/ADEs: Contraindicated in smokers >35 yo becuase increase risk of DVT and CV events, patients with history of thormoembolism and storke or estrogen dependent tumor

Question 54

Tamsulosin

Answer 54

1) Use: BPH 2) Class/MOA: Alpha 1 antagonist, inhibits smooth muscle contraction. Selective for alpha 1 A,D receptors on prostate (not vascular alpha 1B receptor)

Question 56

Danazol

Answer 56

1) Use: Endometriosis and hereditary angioedema 2) Class/MOA: Synthetic androgen acts as partial agonist at andorgen recpetors 3) Side effects/ADEs: Weight gain, edema, acne, hirsutism, masculinizaiton, decrease HDL levels, hepatotoxicity