Umc Pharm Test 6

Front 1

Specifically cytotoxic to the adrenal cortex.
Generally restricted to use in adrenal carcinoma
Selective for mets

Back 1

Mitotane

Front 2

This enzyme inhibitor shuts down 11-beta hydroxylase.
Has some function to diagnose primary and secondary adrenal dysfunction

Back 2

Metyrapone-adrenal enzyme inhibitor

Front 3

This enzyme inhibitor blocks cholesterol side chain cleavage--the rate limiting step in the synthesis of ALL steroid hormones
Not selective for adrenal gland
Has been used as an adjunct in the treatment of breast cancer

Back 3

Aminoglutethimide

Front 4

Nonspecific inhibition of all steroidogenic CYP450s--as well as hepatic 450s.

Back 4

Ketoconazole

Front 5

Inhibits 11-beta hydroxlase and aldosterone synthase at high doses

Back 5

Spironolactone

Front 6

This corticosteroid receptor antagonist may have utility in the management of neoplasms that are glucocorticoid receptor positive.
Good for glucocorticoid-excessive situations
Can block progestrone receptor at much lower concentrations

Back 6

RU 486 (Mifepristone)

Front 7

Aldosterone receptor antagonist that can also be used as a potassium sparring diuretic

At high doses, can block the androgen receptor

Back 7

Spironolactone
Eplerenone

Front 8

Testosterone propionate

Back 8

Androgenic ester

Front 9

Testosterone cypionate

Back 9

Androgenic ester

Front 10

testosterone enanthate

Back 10

androgenic ester

Front 11

fluoxymesterone

Back 11

androgenic alkyl

Front 12

methyltestosterone

Back 12

androgenic alkyl

Front 13

oxymetholon

Back 13

anabolic steroid

Front 14

oxandrolone

Back 14

anabolic steroid

Front 15

nadrolone

Back 15

anabolic steroid

Front 16

stanozolol

Back 16

anabolic steroid

Front 17

calusterone

Back 17

anabolic steroid

Front 18

Testosterone converted into..

Back 18

17 Beta-estradiol

Front 19

Androstenedione converted into...

Back 19

estrone

Front 20

Nine Therapeutic Applications of Androgens/anabolic steroids

Back 20

1) hypogonadism
2) infertility
3) osteoporosis
4) mild anemia
5) breast carcinoma in women
6) anabolic disorders/debilitating disorders
7) promotion of athletic performance
8) treatment of short stature
9) heriditary angioedema

Front 21

Adverse effects of special consideration in HRT in older men (6)

Back 21

1) fluid retention
2) gynecomastia
3) sleep apnea
4) increased erythropoiesis
5) C/V disease
6) prostate

Front 22

Aminoglutethimide actions

Back 22

inhibits testosterone synthesis
nonselective
works thru cholesterol side chain cleavage

Front 23

Cyanoketone

Back 23

inhibitor of testosterone synthesis

Front 24

Trilostane

Back 24

inhibitor of testosterone synthesis

Front 25

Ketoconazole

Back 25

non-selective inhibitor of cytochrome P450

Front 26

Finasteride actions and mechs

Back 26

-inhibitor of activation
-androgen antagonist
-5-alpha reductase inhibitor
-offers the selectivity of treating DHT dependent abnormalities such as prostatic carcinoma, acne, hirsutism, baldness, without affecting testosterone driven functions (sex differntiation, sex drive, skeletal muscle growth)

Front 27

Name the two Androgen Receptor Antagonist

Back 27

1. flutamide
2. bicalutamide

Front 28

Flutamide actions and mechs

Back 28

-non steroidal
-devoid of any intrinsic androgenic activity
-limited usefulness in men due to compensatory increases in LH and testosterone
-useful in inhibiting adrenal androgens in men on GnRH therapy (prostate cancer), women, and castrate men.
-Blocks initial disease flare.

Front 29

Bicalutamide

Back 29

-non steroidal
-devoid of any intrinsic androgenic activity
-limited usefulness in men due to compensatory increases in LH and testosterone
-useful in inhibiting adrenal androgens in men on GnRH therapy (prostate cancer), women, and castrate men.
-Blocks initial disease flare.

Front 30

Cyproterone acetate

Back 30

-Androgen receptor antagonist
-actually a progestin that inhibits gonadotropin secretion
-a MALE CONTRACEPTIVE holy shit
-limited clinical use to sex offenders
-orphan drug status for hirsutism that is really, really nasty

Front 31

Name the "mixed inhibitor" of androgen antagonism

Back 31

spironolactone. It inhibits steroidogenic P450, and it is a weak androgen receptor antagonist

Front 32

When do you give glucocorticoids?

Back 32

1) hypercalcemia of sarcoidosis
2) To increase renal calcium excretion
3) To decrease the expression of renal vitamin D 1-alpha hydroxylase

Front 33

When do you NOT give glucocorticoids?

Back 33

1) primary hypercalcemia/hyperparathyroidism

Front 34

Ergocalciferol

Back 34

Pure vitamin D2.

give when PTH and 1-a-hydroxylase are intact

Front 35

Cholecalciferol

Back 35

Pure Vitamin D3
Calderol

Give when PTH and 1-a-hydroxylase are intact

Front 36

Calcitrol

Back 36

pure 1, 25 dihydroxyvitamin D3.

Use if patient has 1a-hydroxylase deficiency OR rapid fluctuations

Front 37

Dihydrotachysterol

Back 37

Reduced Vitamin D2.

Use if 1a-hydroxylase deficient

Only needs -OH added at C25 for activation

Front 38

Doxercalciferol

Back 38

1a-hydroxyvitamin D2.

Use if 1a-hydroxylase deficient

Only needs -OH added at C25 to be active

Front 39

Name the analogs of Vit D that suppress PTH (2)

Back 39

1) 22-oxacalcitriol
2) paricalcitol

Front 40

22-oxacalcitriol

Back 40

1, 25 dihydroxy-22-O-Vit D3.

Reduces PTH levels while having little activity in the GI tract and bone

No hypercalcemia, no hyperphosphatemia

For use in Primary Hyperparathyroidism ( cancer)
and Secondary Hyperparathyroidism associated with chronic renal failure

Front 41

Paricalcitol

Back 41

19-nor dihydroxyvitamin D2

Reduces PTH levels while having little activity in the GI tract and bone

No hypercalcemia, no hyperphosphatemia

For use in Primary Hyperparathyroidism ( cancer)
and Secondary Hyperparathyroidism associated with chronic renal failure

Front 42

Cinacalcet

Back 42

Calcium sensor mimetic

Front 43

Cinacalcet uses

Back 43

1) hypercalcemia of parathyroid cancer
2) hyperparathyroidism of renal failure

does not effect bone density
more effective in primary than secondary HPT.

start low and titrate upwards to lower risk of hypocalcemia

Front 44

Bisphosphonates all end with...

Back 44

-dronate

Front 45

Bisphosphonates mech and actions

Back 45

1)Potency AND selectivity for osteoclasts increase
2) bone toxicity decreases, for each consecutive generation
3) increases bone density correlated to decreased risk of atraumatic fractures only with 2nd and 3rd generations
4) decreases the recruitment of osteoclasts

Front 46

Hypocalcemic agents and calcitonin are used in combination with what else?

Back 46

1. dietary restriction of calcium
2. volume expansion
3. + or - diuretic

Front 47

Most likely cause of hypophosphatemia?

Back 47

Aluminum or carbonate containing antiacid

Front 48

Hyperphospatemia treatment?

Back 48

sevelamer--a phosphate binding polymer gel

Front 49

Antiresorptive agents in Post-Menopausal Osteoporosis (7)

Back 49

1. calcium
2. thiazide
3. estrogen
4. SERM (raloxifene)
5. Vit D
6. Calcitonin
7. Biphosphonate

Front 50

Bone-Forming Agents (6)

Back 50

1. fluoride
2. androgens
3. PTH cyclic administration
4. Statins
5. GH
6 IGF-1

Front 51

Thyroid Peroxidase functions

Back 51

1. activates Iodide
2. Catalyzes iodination of tyrosyl residues of thyroglobulin
3. Condensation of monoiodinated and diiodinated tyrosine to T3 and T4.

Front 52

T4 is activated by what enzyme and where?

Back 52

Type 1 iodothyronine 5' deiodinase ( 5'D-I) in liver

Front 53

Sodium levothyroxine preparation

Back 53

synthetic T4

Relative dosage: 4 (100 micrograms)

Front 54

Sodium liothyronine

Back 54

synthetic T3.
Faster onset
shorter duration of action
Relative dose: 1 (25 micrograms)
Used when faster onset is required, ie myxedema coma.

Front 55

Thyroid drug with increased risk of cardiotoxicity?

Back 55

Liothyronine

Front 56

Liotrix

Back 56

4:1 mix of T4:T3.

Front 57

Antithyroid drugs (2)

Back 57

Methimazole
PTU (prototype)

Front 58

Can cause fatal aplastic anemia

Back 58

Perchlorate

Front 59

Lithium mechanism

Back 59

inhibits thyroid secretion, but thyroid generally escapes.
Risk of interfering with calcium metabolism

Front 60

Primary action of iodide

Back 60

Inhibits T4 and T3 release.
simple dose causes an acute, transient inhibition of hormone secretion.

Front 61

Indications for iodide

Back 61

1. preop for thyroidectomy
2. In conjunction with PTU or methimazole

Front 62

Untoward rxns of iodide

Back 62

1. hypersensitivity
2. iodism

Front 63

131 I (radioactive iodide)

Back 63

emits beta and gamma rays. Provides definitive treatment. Beta particles are absorbed, leading to necrosis.

Front 64

123 I (radioactive iodide)

Back 64

used for thyroid scans

Front 65

CI of radioactive iodide

Back 65

1. pregnancy
2. less than 25 of 30 y/o due to risk of inducing cancer
3. coexisting, severe opthalmopathy

Front 66

High doses of this drug can inhibit hepatic 5'-D I

Back 66

Propranolol

Front 67

Glucocorticoid effects on hyperthyroidism.

Back 67

Decrease peripheral conversion of T4 to T3.
Increase conversion of T4 to rT3.
Inhibits TSH secretion
Inhibits iodide uptake and T4/T3 release.

Front 68

Cholestyramine

Back 68

Bile acid resin that will bind thyroid hormone conjugates secreted in bile and prevent their enterohepatic recycling

Front 69

Uses of iodinated radiocontrast media

Back 69

1. reduction of T4
2. Inhibits 5'-DI, thus limiting peripheral conversion of T4 to T3.

Front 70

PTU mechanism of action

Back 70

accumlates in the thyroid gland and IRREVERSIBLY inhibits the peroxidase enzyme.

Can cross the placenta

inhibits the peripheral conversion of T4 to T3.

Front 71

Methimazole mechanism of action

Back 71

accumlates in the thyroid gland and IRREVERSIBLY inhibits the peroxidase enzyme.

works faster than PTU

Can cross the placenta, this one more so than PTU

Front 72

Side effects of PTU and Methimazole

Back 72

1. Mild rash
2. Nausea, headache, pain/stiffness in joints
3. mild, transient leukopenia is common in children
4. agranulocytosis/leukopenia

Front 73

Name the Rapid Acting Insulins (3)

Back 73

1. Lispro
2. Aspart
3. Glulisine

LAG

Front 74

Name the short-acting insulin

Back 74

Regular Insulin (Zinc)

Front 75

Name the intermediate acting Insulin

Back 75

Isophane Insulin (NPH)

Front 76

Name the 2 long acting insulins

Back 76

1. insulin Glargine
2. Insulin Detemir

Front 77

Other forms of insulin

Back 77

Inhaled insulin

Front 78

Rapid acting insulin characteristics

Back 78

1. rapid onset, short duration
2. used to control prandial glucose
3. taken immediately before mealtime
4. Risk of hypoglycemia
5. Requires a prescription

Front 79

Short acting insulin (regular zinc) characteristics.

Back 79

1. complex, concentration dependent injection kinetics
2. taken 30-45 minutes before meal

Front 80

Intermediate acting insulins (Isophane/NPH) characteristics

Back 80

1. protamine causes delayed absorption
2. 6 insulin molecules, 1 protamine

Front 81

Long acting insulins- Insulin glargine characterisitcs

Back 81

1. Two Arg residues makes this insoluable at neutral pH.

Front 82

Long acting insulins-Insulin detemir

Back 82

1. myrisitic acid moiety increases self-aggregation and binding to albumin

Front 83

Inhaled Insulin (exubera) characteristics

Back 83

Not used for background coverage
can cause pulmonary fibrosis

Front 84

Name the insulin secretagogues, First Generation, sulfonylureas

Back 84

1. Tolbutamide
2. Cholorproamide
3. Tolazamide

Front 85

Name the insulin secretagogues, Second Gen, Sulfonyureas

Back 85

1. Glyburide
2. Glipizide
3. Glimperidide

Front 86

Name the insulin secretagogues, Meglitinides

Back 86

1. Repaglinide
2. nateglinide

Front 87

Mechanism of sulfonyureas

Back 87

Increase insulin release from the pancreas by binding to a high affinity receptor on B-cells that is associated wtih an ATP-sensitive K+ channel. Inhibits K+ efflux leading to depolarization. Ca++ influx occurs and insulin is released

Front 88

Tolbutamide

Back 88

1st gen sulfonyureas. Inhibits K+ efflux, leading to Ca++ influx and insulin release

-well absorbed, short mech of action, rapidly metabolized by liver

Treats DMII

Front 89

Chlorpropamide

Back 89

1st gen sulfonyureas. Inhibits K+ efflux, leading to Ca++ influx and insulin release

-long half-life, slow metabolism

Front 90

Tolazamide

Back 90

1st gen sulfonyureas. Inhibits K+ efflux, leading to Ca++ influx and insulin release

Front 91

Glimepiride

Back 91

2nd gen sulfonyureas. Much better at reducing glucose than first gen, but cause problems with hypoglycemia.
Not recommended in the elderly, those with hepatic or C/V disease

Most potent and longest duration of action

Front 92

Glyburide

Back 92

2nd gen sulfonyureas. Much better at reducing glucose than first gen, but cause problems with hypoglycemia.
Not recommended in the elderly, those with hepatic or C/V disease

Less potent with fewer side effects

Front 93

Glipizide

Back 93

2nd gen sulfonyureas. Much better at reducing glucose than first gen, but cause problems with hypoglycemia.
Not recommended in the elderly, those with hepatic or C/V disease

Short half life, more potent

Front 94

Repaglinide

Back 94

2nd gen sulfonyurea.

Fast onset of action

Front 95

Nateglinide

Back 95

2nd gen sulfonyurea
D-phenylalanine derivative

Amplifies insulin secretion in response to glucose but has little effect in the prescence of normal glycemic levels.

Lowest incidence of hypoglycemia.

Safe in individuals with renal dysfunction.

Front 96

Metformin (biguanide)

Back 96

Euglycemic agent
Works for Type 1 and Type 2 DM
No hypoglycemia
Insulin-sensitizer
No weight gain
May prevent onset of DMII

Front 97

4 mechanisms of action of Metformin

Back 97

1. Reduces hepatic gluconeogenesis
2. Slows glucose absorption from GI
3. Stimulates glycolysis in tissues
4. Reduces plasma glucagon levels

Front 98

Adverse effects of metformin

Back 98

1. GI
2. Inhibits Vit B12 absorption

Front 99

Thiazolidinediones (2)

Back 99

Pioglitazone
Rosiglitazone

Front 100

Thiazolidinedione mech of action

Back 100

1. Decrease insulin resistance by altering genes controlling glucose and lipid metabolism and adipocyte differentiation.
2. Ligands of PPAR gamma

Front 101

Pioglitazone

Back 101

PPAR alpha and PPAR-gamma.
Greater trigylceride lowering capacity than its counterpart
can alter other drugs metabolism

Front 102

Rosiglitazone

Back 102

Does not alter metabolism of other drugs.

Increased risk of C/V disease

Front 103

Alpha-Glucosidase Inhibitors (2)

Back 103

Acarbose

Miglitol

Front 104

Alph-Glucosidas Inhbitors mechanisms

Back 104

Disrupt transport of monosaccharides out of the intestine by competitively inhibiting the breakdown of starches, oligosaccharides, and disaccharides in the intestine.