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Pharm. II > Exam II Endocrine Pharm > Flashcards

Exam II Endocrine Pharm Flashcards

1
Q

Thyroxin (T4) and triiodothyronine (T3) is synthesized from __________.
Control of these hormones are determined by _________________

A
  • Iodine

- Negative feedback loop

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2
Q

Lack of iodine in the diet causes what?

A

Excessive secretion of TSH, resulting in thyroid hypertrophy–> Goiter

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3
Q

Primary hypo/hyperthyroidism =

A

Disease of thyroid gland

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4
Q

Secondary hypo/hyperthyroidism =

A

Disease of pituitary or hypothalamus gland

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5
Q

What is the precursor to making thyroid hormones T4 and T3?

A

L-tyrosine

-T4 and T3 are iodinated derivates of tyrosine.

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6
Q

Iodine is required for the synthesis of _____________. With out iodine, buildup of TH precursor, resulting in _________.
Americans obtain iodine from __________

A
  • Thyroid hormones
  • Goiter
  • Iodized salt
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7
Q

Thyroglobulin is NEVER _____________

A

secreted into the bloodstream

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8
Q

How is TH synthesized within the thyroid gland ?

A

1) It is taken up by the thyroid cuboidal epi cells at the basement membrane.
2) Synthesis of polypeptide chain within the ER and completed in the golgi.
3) Newly synthesized thyroglobulin is transported to cell surface in vesicles.

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9
Q

Coupling of todotyrosyl precursors (diiodotyrosine and moneydotyrosine) result in ___________________.
Subsequent storage of iodinized thyroglobulin is in the _______.
Thyroglobulin is retrieved via ___________into small vesicles.

A
  • iodination of thereglobulin
  • lumen
  • micropinocytosis
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10
Q

Lysosomes fuse with vesicles resulting in what?

A

Proteolysis of thyroglobulin and release of iodinated amino acids (T3) and (T4)

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11
Q

T4 and T3 exit the thyroid gland and into the _______.

Diiodotyrosine and moniodotyrosine undergo ________________, allowing for _________________

A

-blood
deiodination
-recirculation of iodine

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12
Q

What are the 2 synthetic thyroid preparations made by industry?

A

1) Sodium levothyroxine
T4= Synthroid, Levoxyl

2) Sodium liothyronine (T3 = Cytomel)

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13
Q

Sodium levothyroxine is the __________ for most cases of hypothyroidism.
_______ dose concentrations available.
__________ is the most widely sold brand name.

A
  • Preferred
  • 11
  • Synthroid
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14
Q

Sodium liothyronine, oral absorption is more _____________

A

erratic (why this agent is not the preferred drug)

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15
Q 
Sodium levothyroxine (T4) is used for what?
What is the adult dose?
A

Use: replacement or supplement therapy in hypothyroidism

The adult dose: 100 to 200 micrograms daily (usually taken in the morning on empty stomach)

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16
Q

What is the mechanism of Sodium levothyroxine (T4) ?

A

1) Affects DNA transcription and stimulates protein synthesis
2) Promotes gluconeogenesis
3) Mobilizes glycogen stores
4) Increases basal metabolic rate

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17
Q

What are important adverse effects of Sodium levothyroxine (T4) ?

A

(indicases overdose= hyperthyroidism)

1) Palpitations, tachycardia
2) Nervousness, sweating
3) Increased appetite
4) Weight loss

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18
Q

What are the drugs used to TX Hyperthyroidism (anti-thyroid drugs?)

A

1) Propylthiouracil
2) Iodides
3) Methimazole (Tapazole)
4) Radioactive Iodide I 131

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19
Q

Propylthiouracil:
is a __________ drug. Nicknamed___________.
Used for _____________ treatment of hyperthyroidism in ______________ or _____________ therapy; management of _____________

A
  • Canadian
  • PTU
  • Palliative
  • preparation for surgery
  • radioactive iodine
  • thyrotoxic
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20
Q

What is the mechanism for Propylthiouracil?

A

Blocks iodination reaction (blocks oxidation of iodine) in thyroid gland; blocks synthesis of T4 and T3.

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21
Q

What is the side effects for Propylthiouracil?

A

1) Skin rash
2) nausea
3) agranulocytosis

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22
Q

Iodides are saturated solution of ____________.
Mechanism of action is ____________
Used in conjunction with ______________ to prepare patients for surgery.

A
  • Potassium iodide
  • Not clear: probably reduces secretion of thyroid hormone.
  • propylthiouracil
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23
Q

What is the use of Methimazole (Tapazole)?

A

1) Palliative treatment of hyperthyroidism, return the patient to a normal metabolic state prior to thyroidectom.
2) control thyrotoxic crisis that may accompany thyroidectomy.

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24
Q

What is the mechanism of Methimazole (Tapazole)?

A

1) Blocks iodination reaction (blocks oxidation of iodine) in thyroid gland
2) blocks iodine’s ability to combine with tyrosine to form T3 and T4.

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25
Q

Why is Methimazole (Tapazole) considered an undesirable drug?

A

1) Expensive
2) Inconvenient (requires monitoring; compliance)
3) Adverse effects (hematologic disorders, fever, rash, vasculitis, arthralgia)
4) Oral side effects: taste alteration, salivary gland swelling.

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26
Q

Radioactive Iodide I 131:
Beta ray emission (15-30 millicuries) _________ thyroid tissue.
Diagnostic dose - about 30 microcuries emit _______________ rays.
This is useful in estimating __________ of the gland.

A
  • Destory
  • gamma
  • activity
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27
Q

Describe dental considerations in hypothyroid disease?

A

1) Easier from management perspective
2) Cold, tired/fatigued
3) More sensitive to CNS depressants
- Need to lower dose = sedatives, opiods

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28
Q

Describe dental considerations in hyperthyroid disease?

A

1) Nervous; may have increased blood pressure
2) May be sensitive to epinephrine
(vasoconstrictor in local anesthetics)= if ACTIVE disease = absolute contradiction to epinephrine
3) Palpitations and tachycardia
4) May perceive more pain
5) Less sensitive to CNS depressants: may require higher dose of pain medications and sedatives
-May be mislabeled as having “drug-seeking” behaviors

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29
Q

What is the most important intervention for diabetes?

A

Test blood sugar regularly

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30
Q

When does diabetes occur?

A

1) When circulating insulin concentrations decline

2) when target cells in tissues become resistant to the hormone.

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31
Q

Beta cells are not producing _______correctly (Type 1).

Insulin receptors become ___________ (Type 2)

A
  • insulin

- blocked/insensitive

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32
Q

Type 1 diabetes results from the _____________ destruction of pancreatic _______cells.
10% of diabetics are Type ________; significantly decreases life expectancy.

____________ is the ONLY EFFECTIVE DRUG in TREATING TYPE _________

A
  • Autoimmune
  • Beta
  • 1
  • Insulin
  • 1
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33
Q

How was insulin prepared?

A

1) Previously from animals - cattle (bovine) and pork (porcine) insulin
2) Now available as human-type insulin (recombinant technology)

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34
Q

Describe how various preparations of insulin are characterized

A

1) Onset
2) Peak
3) Duration of action

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35
Q

Describe the a) short-acting

and b) rapid acting insulin preparations?

A 
a) short-acting: 
insulin Regular (HumuLIN R) *

b) rapid-acting:
* insulin Aspart (NovoLOG)
* insulin Glulisine (Apidra, Apidra Solostar)
* insulin Lispro (HumaLOG) **(common)

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36
Q

Describe

a) intermediate acting
b) intermediate to long acting and
c) long-acting insulin preparations?

A 
a) intermediate-acting:
insulin NPH (HumuLIN, NovoLIN N)
b) intermediate to long-acting:
insulin Detemir (Levemir)

c) insulin Glargine (Lantus, Lantus Solostar)

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37
Q

Regarding Lantus Solostar:

1) generic name?
2) Therapeutic category?
3) Use?
4) Oral complications?

A

1) Insulin glardine
2) Insulin, long-acting
3) *Used for Type I and Type II
4) *Oral complication - numbness of mouth

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38
Q

Type 2 diabetes developed after ________ years of age (now occurring at younger ages)

A

35

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39
Q

In Type 2 diabetes, target cells become ________ to insulin.
More insulin is needed to elicit response in ___________cells.
Outcome:

A
  • insensitive
  • resistant
  • Glucose remains in blood (hyperglycemia)
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40
Q

What is the drug treatment used to treat Type II diabetes?

A

1) Oral drugs
2) Non-Pharmacologic methods are still emphasized (Weight reduction, exercise, diet modification)
3) Insulin injections are oftentimes used as supplementation with oral medications especially if patient is poorly controlled

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41
Q

Goals of oral drug therapy for Type 2 diabetes:

A

1) INCREASE insulin secretion in glucose-dependent manner
2) SUPPRESS hepatic gluconeogenesis
3) IMPROVE insulin sensitivity

Risk: hypoglycemia

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42
Q

What are the 4 classes of Type 2 diabetes oral drugs?

A

1) Sulfonylureas (“Traditional” oral hypoglycemics)
2) Biguanides (metformin)
3) Alpha-glucosidase inhibitors
4) Incretins- GLP-1 agonists, DDP-4 inhibitors

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43
Q

Describe the MOA Sulfonylureas (“traditional” oral hypoglycemics)?

A

1) promote insulin release from pancreatic beta cells
2) may also increase insulin release in pancreas
3) Enhance effect of insulin to stimulate glucose uptake in muscle and fat cells

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44
Q

Describe the newer drugs used for Sulfonylureas?

A

2nd gen. (drugs ALL end in “ide”)

1) glipizide (glucotrol)***COMMON
2) glyburide (Diabeta, Glynase, PresTab, Micronase)
3) 10-100 times more potent (but not more effective) than 1st generation
4) POTENCY is major distinction between 1st and 2nd generations, NOT MORE EFFECTIVE.

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45
Q

What are the 1st generation Sulfonylureas?

A

1) tolbutamide (Orinase)
* OLDEST DRUGS
2) tolazamide (Tolinase)
3) acetohexamide (Dymelor)
4) chlorpropramide (Diabinese

Drugs all end in “amide”

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46
Q

What are the warnings with Sulfonylureas?

A

1) INCREASED cardiovascular mortality
2) Sulfonamide allergy -contraindicated in patients who are ALLERGIC
3) chemical similarities w/ sulfonamides, sulfonylureas & diuretics (thiazide, loop & carbonic anhydrase inhibitors)
4) Caution w/ use if severe HEPATIC disease

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47
Q

What is the serious drug interaction with Sulfonylureas?

A

1) Simultaneous administration of ASPIRIN and SULFONYLUREAS may ENHANCE the hypoglycemic response.
2) ASPIRIN appears to displace SULFONYLUREA from plasma proteins causing increased blood levels of the drug.
3) RESULTS in HYPOGLYCEMIA

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48
Q

What is another mechanism for this interaction with Sulfonylureas?

A

1) Salicylate inhibition of prostaglandin E synthesis
2) PGE inhibits glucose induced insulin secretion
3) Inhibition if PGE by salicylate increases include response and enhances response to sulfonylureas= hypoglycemia

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49
Q

How do Biguanides affect the liver?

A

Stop the liver form making extra sugar when its not needed.

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50
Q

What is the most popular oral drug for Type 2 diabetes?

A

Metformin (Glucophage)

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51
Q

Biguanides:

Describe the “MOA” metformin (Glucophage)

A

1) inhibits absorption of glucose from gut
2) decrease hepatic glucose production
3) increases insulin sensitivity at receptor sites
4) increase peripheral glucose uptake and utilization
5) Reduces LDL cholesterol & triglycerides

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52
Q

What are the benefits from metformin (Glucophage) ?

A

1) MORE effective than other agents for reducing glycemic level
2) fewer episodes of hypoglycemia
3) NO weight gain (decreases weight)
4) reduces LDL cholesterol and triglycerides

5) Patients have regular diet
6) REDUCES all-cause and cardiovascular mortality

7) Helps reduce rates of cancer in patients w/ Type II diabetes

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53
Q

What are the RISKS from metformin (Glucophage) ?

A

1) Lactic acidosis if renal impairment
2) Risk increases with:
3) Excessive alcohol intake; avoid alcohol
4) Hepatic impairment
5) Acute CHF
6) GI side effects

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54
Q

Describe the “MOA” Alpha-glucosidase inhibitors?

A

1) acarbose (Precose); miglitol (Glyset)
2) Inhibits alpha-glucosidase in GUT
3) No monosaccharides are made available for absorption after a meal
4) There is DELAY in BLOOD GLUCOSE CONCENTRATIONS AFTER a MEAL when taking drugs

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55
Q

Describe the “MOA” Thiazolidinediones (TZDs) (drugs end in “zone”)?

A

1) REDUCES insulin resistance by ‘resetting’ receptor when insulin is present
2) ACTIVITY depends on the presence of insulin for activity
3) Decreases hepatic glucose output
4) Increases insulin-stimulated glucose uptake in skeletal muscle
5) Decreases lipolysis in adipocytes

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56
Q

What are the preparations for Thiazolidinediones (TZDs) (drugs end in “zone”)?

A

1) pioglitazone (Actos)

2) rosiglitazone (Avandia)
● associated with LIVER failure
● Increased risk of HEART FAILURE
● contraindicated in patients with serious heart failure

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57
Q

Describe the “MOA” Incretins Mimetics= “Incretins”

A

1) Mimic hormones produces by body to stimulate release of insulin

2) GLP-1 agonists (glucanlike peptide-1)
■ Boost insulin production of pancreas
■injectible drugs that are slow absorption of food

3) DDP-4 inhibitors
■ Blocks DDP-4, which breaks down GLP-1 in gut
■ Drug ends in “liptin”

4) New concerns: these drugs cause inflammation & possible pre-cancerous changes in pancreas

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58
Q

How is the A1C test used to assess glycemic control in patients with diabetes.

A

1) Glycated hemoglobin (HbA1c) is the gold standard for measuring diabetes.
2) Measures the amount of hemoglobin that is glycated over the lifespan of the RBC.

3) For measuring glycemic control from 6-12 weeks (~90 days).
■ Normal value: less than 6%
■ Diabetes diagnosis: greater than or equal to 6.5%
■ Diabetics goal: under 7%

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59
Q

The higher the % bound to Hb the more likely someone is _______

A

diabetic

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60
Q

What are the ACP practice guidelines for Diabetes?

A

1) Add drug therapy when lifestyle modifications have failed to improve hyperglycemia
2) Initial monotherapy with METFORMIN (DRUG of CHOICE)
3) Add second drug if hyperglycemia persists after lifestyle change and metformin fault to control hyperglycemia

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61
Q

What is the AACE 2013 Algorithm?

A

1) Evidence based document guiding
■ Obesity management (primary)
■Cardiovascular risk factor modification (Glycemic control goals)

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62
Q

Discuss common cardiovascular risks that occur in patients with diabetes.

A

1) High blood pressure (hypertension)
High blood pressure a major risk factor for cardio disease–> insulin resistance. When patients have both hypertension and diabetes= risk for cardiovascular disease doubles.

2) Abnormal cholesterol and high triglycerides
(high LDL (“bad”) cholesterol, low HDL (“good”) cholesterol, and high triglycerides. It is also characteristic of a lipid disorder associated with insulin resistance called atherogenic dyslipidemia, or diabetic dyslipidemia in those patients with diabetes.

3) Poorly controlled blood sugars (too high) or out of normal range
4) Obesity
5) Lack of physical activity/smoking

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63
Q

Natural estrogen:
A steroid _____.
Produced and secreted by the ____________.
Physiological effects:
Promotes growth of ___________ and _________
cornification of the _______
_______ female sex characteristics

A
  • estradiol
  • ovary
  • endometrium
  • mammary ducts
  • vagina
  • secondary
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64
Q

Estrogen Replacement Therapy:

Estradiol rapidly inactivated in the ______ and _____.
By placing an ethinyl group (C= CH) at C17, the derivative is _____
This is called ______________.
Found in __________ and ______

A
  • liver
  • GI tract
  • active
  • Ethinyl estradiol
  • oral contraceptives
  • female hormone products
65
Q

What are 3 examples of Estrogen Replacement Drugs (HRT) ?

A

1) Conjugated equine estrogens (Premarin) “horse”
2) Esterified estrogens (Estratab, Menest)
3) Estradiol preps

66
Q

Conjugated equine estrogens (Premarin) is used for Tx of?

A

1) Effective in treatment of vasomotor symptoms of menopause

2) May also be beneficial to PREVENT bone loss with osteoporosis
■ Benefit lasts only while on drug
■ A common dose is 0.625 mg
■ Available in many strengths
■ Now used in lower doses due to adverse cardiovascular and breast CA risks

67
Q

Conjugated equine estrogens (Premarin) Side effects?

A

1) Peripheral edema
2) breast tenderness
3) bloating
4) headache
5) Increased risk for endometrial (UTERINE) cancer (noted in women with an INTACT UTERUS)

68
Q

Taking estrogen (such as Premarin) after menopause may increase risk for what?

A

Breast cancer

69
Q

Describe the forms of estrogen (Esterified estrogens (Estratab, Menest) used by postmenopausal women for hormone replacement ?

A

1) Effective in treatment of vasomotor symptoms of menopause

2) Used to prevent osteoporosis
■ 0.3 mg daily effectively prevents postmenopausal bone loss without endometrial effects
■ This is one-half the dose of Premarin
■ Study tip: same effects as Premarin at half of the dose

70
Q

Describe the forms of estrogen (Estradiol preps) used by postmenopausal women for hormone replacement ?

A

1) Estraderm transdermal patch 2) Estraderm cream
3) Climara transdermal patch
4) Estrace cream

71
Q

Describe the rationale for use of Prempro?

A

1) Combination HRT drug, estrogen with progesterone
2) ADDING progesterone to the preparation reduces risk for endometrial cancer
3) Use: Relieve symptoms of menopause and prevention of osteoporosis

4) Prempro
■ 0.625 mg conjugated estrogen (Premarin) with 2.5 mg medroxyprogesterone (Provera)

72
Q

What is the HRT current thinking studies show?

A

HERS study–> Women saw cholesterol levels go down but suffered INCREASED BLOOD CLOTS and no reduction of heart disease.

73
Q

What id the NURSES HEALTH STUDY show?

A

1) Estrogen in combination w/ progestin may INCREASE RISK of STROKE
2) Outweighs long term use to prevent osteoporosis

74
Q

What did the NIH Prempro Study 2002 show?
Increased risks?
Beneficial effects?

A

Results showed that Prempro increased risk of:

1) heart disease
2) stroke, pulmonary embolism
3) invasive breast cancer.

Beneficial effects:

1) reduced bone fractures
2) reduced incidence of colorectal cancer → These benefits were not enough to outweigh the risks

75
Q

What is the use of HRT today?

A

1) Short term use ONLY (less than 5 years)

2) used to TREAT symptoms of menopause

76
Q

Natural progesterone is a ___________ and produced and secreted by ____________.
Physiologically it induces a ____________
Affects ____________ mobility and ___________mucous.

A
  • Steroid
  • corpus luteum
  • secretory endometrium
  • uterine
  • cervical
77
Q

What are progesterone replacement drugs used for?

A

1) Treatment of menstrual disorders
2) Prevention of habitual abortion
3) Treatment of endometriosis
4) Contraception

78
Q

Oral progesterone is almost completely inactivated in the _______

A

-liver

79
Q

What are 2 Synthetic modification is necessary to produce the orally active forms of progesterone?

A

1) Norethindrone
2) Medroxyprogesterone (Provera)
■ TX: of abnormal uterine bleeding, secondary amenorrhea, endometrial cancer

80
Q

Testosterone is responsible for ____________ characteristics.
Testosterone has ______ effect (muscular bulk)

A
  • Secondary male (androgenic effects)

- Muscular bulk

81
Q

After oral administration of testosterone, liver metabolizes to ___________.
The methylated derivative (methyl testosterone) is not rapidly _______________.

A
  • inactive compound

- metabolized

82
Q

Testosterone is used for the TX of what 4 things?

A

1) Delayed puberty
2) Hypogonadism
3) inoperable female breast cancer
4) Loss of libido in postmenopausal women

83
Q

Regarding Male climacteric: Slow ___________ in sexual function beginning in ________ or ______ decades= relates to drop in _____________

A
  • decrease
  • 4th
  • 5th
  • testosterone
84
Q

What are normal levels of testosterone?

A

Men = 250-800 ng/dl
Women 15-40 ng/dl
Postmenopausal women = 0-20 ng/dl

85
Q

What alters T levels?

A

1) Result of aging
2) Obesity
3) Type 2 DM
4) Pain
5) depression
Other:
6) Metabolic syndrome
7) COPD
8) Osteoporosis
9) Coronary heart disease
10) Inflammatory conditions
11) Cardiac, renal and liver failure

86
Q

What is the prevalence of Low T?

A

1) Unknown
2) Lack of consensus about how to define T insufficiency
3) Clinical guidelines differ about cutoff values
4) Differences in assay techniques
5) Hypogonadism
■Clinical syndrome which comprises both symptoms and biochemical evidence of T deficiency

87
Q

Is T deficiency a biomarker for ill health or is it ____________, causing an adverse effect on underlying disease progression ?
What are examples?

A

-bidirectional

  • Reduced insulin sensitivity
  • central obesity
  • dyslipidemia
  • hypertension
  • osteoporosis
  • muscle weakness and frailty
  • cognitive impairment
  • lethargy and fatigue
  • sexual dysfunction
88
Q

Evidence suggests that testosterone status is linked to ___________________.
Biomarker for presence of occult disease: __________, __________ and ____________

A
  • General health of male
  • atherosclerosis
  • cancer
  • early death
89
Q

List the Testosterone preparations?

A

1) Androderm
2) AndroGel; Andro Gel Pump
3) Aveed
4) Axiron
5) Depo-testosterone
6) First-Testosterone; First Testosterone MC
7) Fortesta
8) Striant
9) Testim
10) Testopel

90
Q

What are the benefits of testosterone therapy?

A

1) Decreases FAT mass
2) Increases muscle power
3) Improves: Insulin resistance,, Hemoglobin A1C, lipid profiles and Libido

91
Q

What are the risks of T Therapy?

A

1) increased prostate size
2) cardiovascular risks
3) water retention
4) problems with fertility
5) Sleep apnea worsens
6) Polycythemia (INCREASED risk for blood clots)
7) Impaired ability to generate endogenous testosterone

92
Q

What are the routes of administration for T?

A

1) Buccal (Bitter taste, gingival edema, or mouth irritation and tenderness, dysgeusia)
2) IM
3) SubQ
4) Topical
5) Transdermal

93
Q

T Therapy for women show no evidence to _________ use in women with low levels of these hormones.
No benefits in women with ________.
Exception: ?

A
  • support
  • adrenal insufficiency

-Exception: Postmenopausal women with hypoacitve sexual desire disorder

94
Q

For women… No ______ approved products for women.

A

FDA

95
Q

Estrogen (esterified) and methyl testosterone is indicated for what symptoms?

A

For moderate to severe vasomotor symptoms associated with menopause not improved by estrogen alone.

96
Q

Anabolic steroids:
Exhibit more ________ effects no _________ effects.
Schedule ________ controlled substance

A
  • Anabolic
  • Androgenic
  • III
97
Q

Why does anabolic steroids enhance athletic performance?

Abuse can lead to what?

A

1) increases muscle mass= can increase mass by 30%
2) Used by athletes to increase muscle mass and physical performance

3) Abuse can lead to
○ mental depression
○ sodium retention
○ cholestatic jaundice
○ temporary impotence 
○ impotence
98
Q

Names of popular Anabolics?

A

1) Nandrolone phenpropionate (Durabolin)
2) Methandrostenolone (Dianabol)
3) Oxandrolone (Anavar)
4) Stanozolol (Winstrol)

99
Q

What are the types of Preparations for BC?

A

1) combination
2) sequential
3) single entity type
4) long acting progestins
5) patch (ortho evra)

100
Q

Describe combination BC’s

A

1) Contain both estrogen and progestin
2) 99% effective
3) taken on days 5 though 25 of cycle (21 days)
4) 7 days of placebo (sugar pill) during menstruation

101
Q

Describe sequential BC’s

A

1) Differnent arts of progestin w. same ant of estrogen
2) 2 dose
3) 3 dose (777’s)
4) 3 dose (7 days + 9 days + 5 days)

102
Q

Describe Single Entity Type BC’s?

A

1) Progestin ONLY (“mini pill)
2) Estrogen alone (post coital or “morning after” = Plan B, ella
3) DES for rape or incest
4) RU - 486 (progesterone antgonist)
- mifepristone (Mifeprex)
- Medical termination of intrauterine pregnancy; off-label for TX of certain cancers

103
Q

Describe long-acting progestins

IM (Depo-Provera)

A
  • Abolishes menstrual cycle as long as it’s given leading to ovarian and endometrial atrophy
  • Hormone injection given in doses for 3 to 6 months
104
Q

Describe the patch form of BC

A

1) Significant higher risk of adverse clotting events/stroke

2) Drugs delivered by patch therapy = more concentrated dose

105
Q

What is the mechanism of action of estrogen and progesterone as ovulatory inhibitors.
(MOA of OC?)

A

1) Inhibition of ovulation
○Estrogen inhibits FSH secretion and thus ovulatory stimulation is inhibited
○Progesterone alters endometrium development

2) endometrium must be in right stage of development under influence of estrogen and progesterone for nidation to occur
3) Progesterone alters endometrial development
4) Abundant water secretion of cervix at time of ovulation has always been regarded as essential to well-being of sperm
5) Thick, tenacious mucus secreted under influence of progesterone is a hostile environment

106
Q

List the adverse effects associated with oral contraceptive use.

A

1) Increased risk for MI and Stroke
2) Stroke risk increases if smoker over age of 35 yrs
3) Nausea/vomiting
4) headache
5) breast pain
6) weight gain
7) breakthrough menstrual bleeding
8) mental depression
9) fatigue
10) lack of initiative
11) ocular considerations
○ corneal sensitivity
○ retinal thrombosis
12) Optic Neuritis
○ diplopia

107
Q

Describe the dental considerations associated with oral contraceptive use.

A

1) Mimic effect of pregnancy on gin-giva
2) Mild inflammation, hyperemia, spontaneous gingival bleeding
3) LOSS of tissue tone
4) tenderness and ulceration
5) DECREASE defense to plaque bacteria resulting in irritation or progression of perio disease
6) Case reports of antimicrobial-induced OC failure represent normal 1% to 3% rate of pregnancy which occurs w/ typical OC use = VERY Rare
7) SHORT-TERM use of antimicrobials = consider additional non-hormonal contraception at initiation and for duration of antimicrobial therapy (or for 14 days, whichever is longer), + 7 more days after completion of antimicrobial therapy

108
Q

Explain the primary mechanism of action of the drug interaction associated w/ oral contraceptives and antibiotics.

A

1) Antibiotics alter normal bacterial flora in small intestine (why you get diarrheas)

2) Oral contraceptives are inactive (prodrugs or zymogens)
○ when drug enters SI normal flora “activate” drug.

3) Active drug is secreted across wall of small intestine into bloodstream

109
Q

ADA recommends what when considering OC and ABX?

A

ADA recommends an alternate form of contraceptives until start of next cycle

110
Q

What happens when there is not enough flora in SI to “activate” the hormones?

A

Risk for ovulation and pregnancy

111
Q

Which ABX do NOT affect OC steroid levels in women taking combination OC?

A

1) tetracycline
2) doxycycline
3) ampicillin
4) metronidazole
5) fluconazole
6) fluoroquinolones

112
Q

If using Rifampin (TB) or griseofulvin what precautions must be taken with OCs?

A

Add second form of contraception

113
Q

What are SERMS?

A

1) Selective estrogen receptor modulators (designer estrogens)
2) Bind to bone and leave breast alone (Result: prevent breast cancer)

114
Q

What are 2 examples of bone drugs?

A

1) SERMS (raloxifene [Evista]
2) Bisphosphonates
(oral: Fosamax, Actonel, and Boniva)

115
Q

SERMS- raloxifene [Evista] :

Activates __________ in bone and is FDA approved for prevention of _____________ in postmenopausal women.

A
  • estrogen receptors

- osteoporosis

116
Q

SERMS- raloxifene [Evista] :

Typically used by women that have what?

A

Osteoporosis risk and also have risk for breast cancer (therefore, they’re unable/unwilling to take estrogen)

117
Q

____________ is the only medicine proven to reduce both the risk of spinal fractures die to osteoporosis and the risk of invasive breast cancer in postmenopausal women with osteoporosis.

A

EVISTA

118
Q

EVISTA does not treat ___________, prevent it from returning. or reduce the ______ of all forms of breast cancer.

A
  • breast cancer

- risk

119
Q

What are the effects of EVISTA?

A

1) Antiresorptive action on bone
2) absence of vaginal bleeding
3) absence of endometrial and breast stimulation.
4) Most common side effects: hot flashes, leg cramps

120
Q

Bisphosphonates are approved to treat ________________.

Known as the BEST available _____________ drug.

A
  • osteoporosis in postmenopausal women

- bone building

121
Q

Bisphosphonates inhibtis ______________activity and Increase bone ____________.
Inhibits formation, growth, and dissolution of bone _______________

A
  • osteoclastic
  • mineral density
  • hydroxyapatite crystals
122
Q

List the Oral drugs for prevention and treatment of osteoporosis.

A

1) alendronate (Fosamax)
2) risedronate (Actonel)
3) ibandronate (Boniva)

123
Q

List the IV drugs - treatment of bone pathologies (chemo)

A

1) etidronate disodium (Didronel)
2) pamidronate (Aredia)
3) zoledronic acid (Zometa)
4) tiludronate (Skelid)

124
Q

List the IV drugs - for osteoporosis prevention

LOWER dose TX for osteoporosis

A

1) zoledronic acid (Reclast)
2) Pamidronate (Aredia)
3) tiludronate (skelid) = paget’s disease

125
Q

What precautions should be taken since Bisphosphonates has POOR oral bio-availability?

A

1) Take on empty stomach
2) Water only (other things decrease absorption by > 60%)
3) remain upright for ~ 30 min
4) No eating for ~ 30 min

126
Q

What are the common side effects of Bisphosphonates?

A

Side effects:

1) Erosive esophagitis
2) Headache
3) GI distress

127
Q

What are oral complications of Bisphosphonates?

A

Oral complications:

1) Osteonecrosis of the jaw
2) Most cases w/ IV Bisphosphonates given at higher dosages for chemotherapy for cancers that have metastasized to the bone

128
Q

Most cases of jaw osteonecrosis are in patients undergoing _______________ with these drugs who also received _________; possible other risk factors.

A
  • chemotherapy

- steroids

129
Q

What are the 4 therapeutic uses of hormones?

A

1) Replace
2) Diagnose
3) Stimulate
4) Inhibit

130
Q

Which hypothalamic releasing hormone is used as a drug?

A

Gonadotropin-releasing hormone (GnRH)

131
Q

__________ is an analog used as ovulatory stimulant

A

Clomiphene (Clomid)

132
Q

Hypothalamic releasing hormones are used for ____________ induction in women with primary hypothalamic amenorrhea.

A

ovulation

133
Q

GnRH stimulates the release of what hormones?

A

LH and FSH

134
Q

What is GnRH used for in men ?

A

1) treatment of idiopathic hypogonadotropic hypogonadism
■ condition of faulty GnRH secretion

2) GnRH replacement therapy results in achieving mature spermatogenesis

135
Q

What is ACTH used for?

A

11) Used as a diagnostic tool
2) used to diagnose apparent adrenal dysfunction
3) Alternative to corticosteroids in inflammatory conditions
4) stimulate release of glucocorticoids from adrenal gland
5) cortisone feedback to shut down ACTH output form pituitary

136
Q

Growth Hormone:

Also known as _____________ and _______________.
Most ___________ hormone in anterior pituitary.
Stimulates growth of ____________ and all _______ in organs and tissues.
Now made from ___________ DNA techniques.

A
  • human growth hormone
  • somatotropin
  • epiphysis
  • cells
  • recombinant
137
Q

GH is used to treat ___________.
Subject to wide ___________.
Athletes and people claim that it halts the __________ process

A
  • pituitary dwarfism
  • abuse
  • aging
138
Q

What are the typical effects of GH?

A

-Duration: supra physiologic levels maintained for 18-20 hours

  • Administer drug SC 3 times per week
  • 17 yr old at 4’2 (pituitary dwarf)
  • 3 years of injections given
  • at 20 years of age 4’9”
  • at 24 5’4”
139
Q

TSH stimulates what?

What is it used for?

A
  • production of thyroid hormone

- Used a diagnostic tool to differentiate between pituitary and primary hypothyroidism

140
Q

What is the preparation of TSH?

A

glycoprotein from bovine pituitaries

141
Q

Describe the FSH hormone

A

1) promotes development of ovarian follicles and maintains spermatogenesis
2) deficiency in males causes sterility; in females, cause menstrual abnormalities
3) A glycoprotein
4) effective only if given IM

142
Q

Describe the LH hormone

A

1) induces ovulation and regulates progesterone secretion in women, testosterone secretion in men
2) a glycoprotein
3) Effective only if given IM

143
Q

What are the 2 non-pituitary gonadotropins ?

A

1) Human menopausal gonadotropin (HMG) = menotropins

2) Human chorionic gonadotropin (HCG)

144
Q

Human menopausal gonadotropin (HMG) induces ovulation in ________ of women.
More than 1 _______ may develop and ovulate.

A
  • 90%

- follicle

145
Q

Human chorionic gonadotropin (HCG):
Secreted by ________ as day 7.
Detected in ________ test (diagnostic).
Used to induce ____________ also stimulate interstitial cells of tests to secrete __________; cryptorchidism (Given by IM)

A
  • fetal placenta
  • pregnancy test
  • pregnancy and ovulation
  • androgen
146
Q

Describe the posterior pituitary hormones vasopressin and their clinical applications in medicine

A

● Vasopressin (ADH; arginine vasopressin: AVP)

○Vasoconstrictor and antidiuretic hormone; used for replacement in diabetes insipidus

147
Q

Describe the posterior pituitary hormones oxytocin and their clinical applications in medicine.

A

●Oxytocin (Pitocin)
○ contracts uterine smooth muscle at term
○ induction of labor
○ control postpartum bleeding or hemorrhage

148
Q

How are these chemicals (ADH and oxytocin) similar to each other?

A

1) oxytocin slight antidiuretic function

2) high levels of vasopressin can trigger uterine contractions

149
Q

Describe PTH

A

1) Increase plasma calcium and maintains at 10 mg%
2) Increases Ca+ mobilization from bone to plasma
3) Increases Ca+ reabsorption in renal tubules

150
Q

Describe Calcitirol

A

1) hormonal form of Vit D
2) produced by kidneys
3) Increases calcium absorption from the intestine
4) limits calcium excretion when blood calcium level are low

151
Q

Describe thyrocalcitonin (calcitonin):

A

1) Synthesized in thyroid gland
2) Reverses action of PTH
3) Increases in blood calcium by inhibiting bone resorption
4) Decreases plasma calcium and phosphate levels
5) Blocks removal of calcium from bone
6) Used in medicine to treat hypercalcemia
7) Minor regulator of blood calcium compared to the actions of PTH and calcitriol

152
Q

How is Vitamin D3 (cholecalciferol) formed and what is its primary action?

A

1) formed in the skin when a cholesterol precursor
2) Primary action of 1,25 - (OH) 2 D3 = Promote gut absorption of calcium by stimulating formation of ca+-binding protein w/ in intestinal epithelial cells
3) In bone, synergistic role w/ PTH = Stimulates osteoclast proliferation and bone resorption

153
Q

How does Vitamin D compare to PTH?

A

exerts a much slower regulatory effect on calcium balance

154
Q

What are the effects of Vitamin D?

A

1) Increases bone mass
2) Decreases fracture rates

3) decreases PTH which
decreases resorption

4) potentially increases bone formation
5) Preparation: ergocalciferol (Vitamin D2; calciferol)

155
Q

How is D deficiency possible?

A

1) sun-blocking pollution
2) Sunscreen; avoiding sun exposure
3) geographic differences

156
Q

How does Vit D lead to systemic diseases?

A

1) Increase Vit D, decrease colon cancer risk
2) Decrease Vit D, increase risk for prostate, breast, and ovarian cancer
3) Low sun exposure = increased Type I diabetes
4) Hypertension increases with distance away from equator
5) calcitriol (pre-vit D) = protective

157
Q

What are the recommended guidelines for Vitamin D?

A

1) Experts recommend annual blood test to screen levels
2) Supplements may be required
3) avoid need for supplements = go outside
4) Dosage for supplements = 200 IU/day–> less than 50 yrs
400 IU/day–> 51-69 yrs
600IU/day more than 70+ yrs

158
Q

In absence of sunlight =

A

800-1000 IU/day (do not exceed 2000 IU)

Pharm. II (13 decks)

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