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Drugs > Endo/Repro > Flashcards

Endo/Repro Flashcards

1
Q

<p>Lispro</p>

A

<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>

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2
Q

<p>Aspart</p>

A

<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>

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3
Q

<p>Glulisine</p>

A

<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>

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4
Q

<p>Regular</p>

A

<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>

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5
Q

<p>NPH</p>

A

<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>

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6
Q

<p>Glargine</p>

A

<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>

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6
Q

Sprionolactone

A

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

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7
Q

<p>Detemir</p>

A

<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>

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8
Q

<p>Metformin</p>

A

<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>

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9
Q

<p>Tolbutamide</p>

A

<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>

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10
Q

<p>Chlorpropamide</p>

A

<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>

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11
Q

<p>Glyburide</p>

A

<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>

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12
Q

<p>Glimepiride</p>

A

<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>

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13
Q

<p>Glipizide</p>

A

<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>

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13
Q

Progestins

A

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

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14
Q

<p>Pioglitazone</p>

A

<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>

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15
Q

<p>Rosiglitazone</p>

A

<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>

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16
Q

<p>Acarbose</p>

A

<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>

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16
Q

Terbutaline

A

1) Use: Reduces premature uterine contraction

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

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17
Q

<p>Miglitol</p>

A

<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>

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18
Q

<p>Pramlinitide</p>

A

<p>1)Type I and II DM

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

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18
Q

Sildenafil, vardenafil

A

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

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19
Q

<p>Exenatide</p>

A

<p>1)Type II DM

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

20
Q

<p>Liraglutide</p>

A

<p>1)Type II DM

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

21
Q

<p>Linagliptin</p>

A

<p>1)Type II DM

2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections</p>

22
Q

<p>Saxagliptin</p>

A

<p>1)Type II DM

2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections</p>

23
Q

<p>Sitagliptin</p>

A

<p>1)Type II DM

2) DPP-4 Inhibitors/ Increase insulin and decrease glucagon release
3) Mild urinary or respiratory infections</p>

24
Q

<p>Propylthiouracil</p>

A

<p>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</p>

25
Q

<p>Methimazole</p>

A

<p>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</p>

26
Q

<p>Levothyroxine</p>

A

<p>1)Hypothyroidism, myxedema

2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias</p>

27
Q

<p>Triiodothyronine</p>

A

<p>1)Hypothyroidism, myxedema

2) THyroxine replacement
3) Tachycardia, heat intolerance, tremors, arrhythmias</p>

28
Q

<p>GH</p>

A

<p>1)GH deficiency, Turner's Syndrome</p>

29
Q

<p>Somatostatin (octretodie)</p>

A

<p>1)Acromegaly, carcinoid, gastrinoma, glucagonoma, espohageal varices</p>

30
Q

<p>Oxytocin</p>

A

<p>1)Stimulate labor, uterine contractions, milk let-down, controls uterine hemorrhage</p>

31
Q

<p>ADH (Desmopressin)</p>

A

<p>1)Central DI</p>

32
Q

<p>Demeclocycline</p>

A

<p>1)SIADH

2) Tetracycline/ ADH antagonist
3) Nephrogenic DI, photosensitivity, abnormalities of bone and teeth</p>

33
Q

<p>Hydrocortisone</p>

A

<p>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</p>

34
Q

<p>Prednisone</p>

A

<p>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</p>

35
Q

<p>Triamcinolone</p>

A

<p>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</p>

36
Q

<p>Dexamethasone</p>

A

<p>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</p>

37
Q

<p>Beclomethasone</p>

A

<p>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</p>

38
Q

Leuprolide

A

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

39
Q

Testosterone, methyltestosterone

A

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

40
Q

Finasteride

A

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

41
Q

Flutamide

A

1) Use: Prostate carcinoma

2) Class/MOA: Antiandrogen/ nonsteroidal competitive inhibitor of androgesn at testosterone receptor

42
Q

Ketoconazole

A

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

44
Q

Estrogens (ethinyl estradiol, DES, mestranol)

A

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

45
Q

Clomiphene

A

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

46
Q

Tamoxifen

A

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

47
Q

Raloxifene

A

1) Use: Osteoporosis

2) Class/MOA: SERM/Agonist on bone, reduces resorption of bone

48
Q

Hormone Replacement Therapy

A

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

49
Q

Anastrozole/ exemestane

A

1) Use: Postmenopausal women with breast cancer

2) Class/MOA: Aromatase inhibitor

51
Q

Mifepristone (RU 486)

A

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

52
Q

Oral contraception (synthetic progestins, estrogen)

A

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

54
Q

Tamsulosin

A

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)

56
Q

Danazol

A

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

Drugs (11 decks)

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