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Pharmacology III > Adrenal/Pituitary > Flashcards

Adrenal/Pituitary Flashcards

1
Q

What conditions results from hyperfunction of the adrenal glands?

A

Cushings syndrome

Hyeraldosteronism

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2
Q

What conditions result from hypofunction of the adrenal glands?

A

Primary adrenal insufficiency- addisons disease

Secondary adrenal insufficiency

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3
Q

What is the adrenal gland regulation and function?

A
  • Hypothalamus releases corticotropin releasing hormone (CRH)
  • Stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary
  • ACTH stimulates the adrenal gland to release cortisol (also releases aldosterone and androgens)
  • As cortisol levels rise it inhibits further release of CRH and ACTH through negative feedback
  • Renin is released from the kidney (In response to ↓ blood pressure, salt depletion, CNS excitation)
  • Conversion of angiotensinogen to angiotensin I then II stimulates aldosterone synthesis (Renal sodium and water retention and increased BP occur as a result of aldosterone secretion)
  • Negative feedback to turn off renin release
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4
Q

What is involved with cushings syndrome?

A

↑adrenal function =↑cortisol production

Excess of cortisol in the plasma- hypercortisolism

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5
Q

What is the cause of Cushing’s Syndrome?

A

ACTH-dependent:
Pituitary tumor: excess ACTH secretion
Stimulates adrenal glands to secrete excess cortisol
Ectopic disease: ACTH secretion from another tumor

ACTH-independent: abnormal adrenocortical tissues (ACTH is functioning fine but you are still releasing too much cortisol)
Adrenal adenoma: benign
Adrenal carcinoma
Exogenous Steroids

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6
Q

What is the clinical presentation of Cushing’s Syndrome?

A
  • Altered Fat Distribution- Central obesity
  • Purple striae along the lower abdomen
  • Facial rounding- “moon face”
  • Supraclavicular fat pads
  • Fat accumulation in the dorsocervical area- “buffalo hump”-Fat accumulation over chest & abdomen
  • Hypertension
  • Glucose intolerance
  • Muscle weakeness
  • Osteoporosis
  • Psychiatric changes
  • Gonadal dysfunction- Amenorrhea
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7
Q

How is Cushing’s syndrome diagnosed (confirmation)?

A
  1. Elevated urinary free cortisol- confirms hypercortisolism
  2. Plasma ACTH concentrations determine the etiology
    Pituitary dependent
    Ectopic ACTH
    Adrenal Adenoma
    Adrenal Carcinoma
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8
Q

What is the treatment of choice for Cushing’s syndrome?

A

Dependent on the etiology
Surgery is the treatment of choice
Transphenoidal removal of the pituitary tumor
Removal of the adrenal glands
Patient will require life-long treatment with glucocorticoids and mineralcorticoids

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9
Q

Steroidogenic inhibitors (Metyrapone (Metopirone®))- indications

A

Used for non-surgical candidates with cushings disease

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10
Q

Steroidogenic inhibitors (Metyrapone (Metopirone®)) - MOA

A

Steroidogenic inhibitors: inhibit synthesis and secretion of cortisol from the adrenal gland

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11
Q

Metyrapone (Metopirone®)- MOA

A

inhibits 11-hydroxylase activity in the adrenal cortex
Sudden drop in cortisol levels can result in an increase in plasma ACTH levels → increased androgenic and mineralcorticoid levels

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12
Q

Metyrapone (Metopirone®) (steroidogenic inhibitor)- indications

A

Used for Ectopic ACTH (something is causing the release of ACTH and it cant be reverse and these people are not candidates for surgery)

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13
Q

Metyrapone (Metopirone®) (steroidogenic inhibitor)- adverse effects

A

N/V
Hypertension
Alopecia
Hirsutism

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14
Q

Aminoglutethimide (Cytadren®) (steroidogenic inhibitor)- MOA

A

inhibits conversion of cholesterol to pregnenolone in adrenal glands
Blocks conversion of androstenedione to estrone and estradiol in the peripheral tissues
↓ production of cortisol, aldosterone, and estrogens

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15
Q

Aminoglutethimide (Cytadren®) (steroidogenic inhibitor)- Indications

A

Used for ectopic ACTH syndrome

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16
Q

Aminoglutethimide (Cytadren®) (steroidogenic inhibitor)- Adverse effects

A

N/V
Sedation
Hypothryoidism- blocks synthesis of thyroxine
Can cause problems with amenorrhea and fertility due to estrogen suppression

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17
Q

Ketoconazole (Nizoral) (Steroidogenic inhibitors)- MOA

A

imidazole antifungal agent

Also inhibits androstenedione synthesis

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18
Q

Ketoconazole (Nizoral) (Steroidogenic inhibitors)- Indications

A

Used for adrenal adenoma

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19
Q

Ketoconazole (Nizoral) (Steroidogenic inhibitors)- Adverse effects

A

Hepatotoxicity (need to monitor LFTs)
Gynecomastia (due to decreased testosterone levels)
Nausea

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20
Q

Ketoconazole (Nizoral) (Steroidogenic inhibitors)- drug interations

A

Inhibits CYP3A4, 1A2, 2C9, 2D6, 2A6

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21
Q

Ketoconazole (Nizoral) (Steroidogenic inhibitors)- absorption

A

Absorption requires an acidic pH

Administer 2 hours before antacids to reduce chance of decreased absorption

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22
Q

What are the adrenolytic agents?

A

Mitotane (Lysodren®)

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23
Q

Mitotane (Lysodren®) (adrenolytic agents)- MOA

A

cytotoxic drug that results in atrophy of the adrenal cells

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24
Q

Mitotane (Lysodren®) (adrenolytic agents)- indications

A

Used for adrenal carcinoma

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25
Q

Mitotane (Lysodren®) (adrenolytic agents)- adverse effects

A

Severely suppresses adrenal function (need to monitor urinary free cortisol)
N/V- administer w/ food
Lethargy and somnolence
Hypercholesterolemia

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26
Q

What causes primary hyperaldosteronism?

A

Abnormality is within the adrenal cortex
Aldosterone producing adenoma
Bilateral adrenal hyperplasia (BAH)

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27
Q

What do you screen with to detect primary hyperaldosteronism?

A

Screen with plasma aldosterone to plasma-renin activity ratio.

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28
Q

What causes secondary hyperaldosteronism?

A 
Stimulation of the zona glomerulosa by an extraadrenal factor
Usually the RAAS 
Other causes
Excessive potassium intake
Pregnancy
CHF
Cirrhosis
Renal artery stenosis
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29
Q

What are the signs and sx of hyperaldosteronism?

A 
Hypertension
Hypervolemia
Hypokalemia
Hypernatremia- Leads to fluid retention
Muscle weakness
Fatigue
Headache
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30
Q

What is the treatment for hyperaldosteronism?

A

Surgery if the cause is an adenoma
Spironolactone is the drug of choice : Aldosterone antagonist
Interferes with testosterone biosynthesis

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31
Q

What are the monitoring parameters with spirolactone?

A

Blood Pressure
Sodium and potassium
SCr

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32
Q

What are the adverse effects of spirolactone?

A

Hyperkalemia

Gynecomastia

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33
Q

Eplerenone (Inspra)

A

Hyperaldosteronism treatment
aldosterone antagonist
Less affinity for other steroid receptors
Use as an alternative for patients who can’t tolerate the anti-androgenic side effects of spironolactone
Monitor: Na, K, blood pressure, and renal function

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34
Q

Amiloride

A

Hyperaldosteronism treatment
potassium sparing diuretic
Not as effective as the aldosterone antagonists
Monitor: Na, K, blood pressure, and renal function
Typically need another agent for additional blood pressure control

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35
Q

What is Primary hypofunction of the adrenal gland (adrenal insufficiency) (addison’s disease) due to?

A

Destruction of the adrenal cortex

Deficiency in cortisol, aldosterone and androgens

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36
Q

What is secondary hypofunction of the adrenal gland (adrenal insufficiency) due to?

A

Suppression of the HPA axis from exogenous steroid use
ACTH deficiency
Deficiency in cortisol and androgens
Not mineralcorticoids

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37
Q

Which pathways does primary adrenal insufficiency block?

A

The glucocorticoids (cortisol) and mineralcorticoid (aldosterone)

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38
Q

What are the signs and sx of adrenal insufficiency?

A
  • Weakness/fatigue
  • Anorexia- Weight loss
  • N/V, abdominal pain
  • Can lead to adrenal crisis
  • Hypotension- Postural dizziness
  • Salt craving
  • Hyperpigmentation
  • Muscle/Joint symptoms
  • Sexual dysfunction
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39
Q

What are the laboratory findings of chronic primary adrenal insufficiency?

A

Hyponatremia
Hyperkalemia
Hypercalcemia
Azotemia

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40
Q

How is adrenal insufficiency usually diagnosed?

A

COSYNTROPIN STIMULATION TEST FOR DIAGNOSIS
Cosyntropin is synthetic ACTH
In normal adrenal function you would expect plasma cortisol levels to rise after stimulation by ACTH
Administer 250 mcg cosyntropin IV or IM, draw serum cortisol levels at baseline and then at 30-60 minutes post dose
An increase in serum cortisol level ≥ 18 mcg/dL rules out adrenal insufficiency

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41
Q

What is another test that can be done for adrenal insufficiency diagnosis but is more specific and sensitive?

A

Low dose cosyntropin test
1 mcg cosyntropin IV with a baseline serum cortisol and a 30 minute post dose serum cortisol
Requires a more carefully timed sample
Administered IV
More sensitive than the 250 mcg dose test

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42
Q

Which side of the pathway needs replaced in primary adrenal insufficiency?

A

Both

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43
Q

What is the goal of treament with adrenal insufficiency?

A

Goal is to mimic endogenous cortisol production

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44
Q

What is diurnal variation?

A

More cortisol is produced in the early morning than in the evening (very little cortisol is produced from 6pm-3am)

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45
Q

What is the treatment for adrenal insufficiency?

A

Glucocorticoid replacement is needed in primary and secondary adrenal insufficiency
Endogenous secretion is ~5-10 mg/m2 of cortisol
Equivalent to 5 mg prednisone or 20 mg hydrocortisone
Short-acting glucocorticoid regimens:
Hydrocortisone
15-30 mg/day divided BID
Give ~ 2/3 of the total daily dose in the morning and 1/3 in the afternoon

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46
Q

What are the alternative glucocorticoid regimens?

A

Cortisone 25 mg in the am 12.5 in the pm
Prednisone 5 mg in the am 2.5 mg in the pm
Dexamethasone 0.5 mg in the am 0.25 mg in the pm
Prednisone and dexamethasone have longer half-lives

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47
Q

When should glucocorticoids be given?

A

In the morning.

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48
Q

Glucocorticoids- Dose adjustment

A

-Use lowest dose possible and titrate up
-Monitor symptoms every 6 to 8 weeks
-Signs of glucocorticoid excess: reduce the dose
Body fat redistribution
Mood changes/sleeping difficulty
Glucose intolerance
Muscle weakness
-If presenting signs and symptoms of adrenal insufficiency don’t resolve: increase the dose
-If patient feels symptoms at a certain time of day, can adjust dosing intervals

49
Q

What is a mineralcorticoid replacement drug?

A

Fludrocortisone (Florinef)

50
Q

Fludrocortisone (Florinef)- Indication

A

Only necessary in PRIMARY insufficiency (Addison’s disease)

Goal: prevent hyponatremia, hyperkalemia, intravascular volume depletion

51
Q

What are the signs of an insufficient mineralcorticoid dose (Fludrocortisone (Florinef))?

A

Hypotension
Hyponatremia
Hyperkalemia

52
Q

What are the signs of excess mineralcorticoid dose (Fludrocortisone (Florinef))?

A

Hypertension
Edema
Hypokalemia

53
Q

What is suppressed with long term use of high dose glucocorticoids?

A

The hypothalamus pituitary axis

54
Q

What needs to be replaced in secondary adrenal gland insufficiency?

A

Glucocorticoids (Cortisol)

55
Q

What occurs in secondary adrenal insufficiency?

A

Suppression of the hypothalamic-pituitary-adrenal (HPA) axis
One way of doing this Is by administering high doses of glucocorricoids for a long time like in those with cancer.
Long-term suprapysiologic doses of glucocorticoids
After treatment is stopped the adrenal glands can’t generate enough cortisol on their own (HPA axis has been suppressed by the steroids they were receiving and doesn’t realize it needs to make its own hormones?)
Risk for HPA axis suppression
↑ potency = ↑ risk of suppression
Dexamethasone>prednisone>hydrocortisone
Supraphysiologic doses

56
Q

What are the signs and sx after glucocorticoid withdrawl?

A

Malaise, myalgias, weakness, fatigue, anorexia

57
Q

What is the risk factor associated with glucorticoid use in secondary adrenal insufficiency?

A

Duration of therapy is a risk factor

Low risk when therapy is < 1 week (Even if high dose steroids)

58
Q

How are glucocorticoids tapered?

A

Glucocorticoid tapering – no evidence based guidelines
↓ prednisone (or equivalent) by 2.5-5 mg q 3-7 days until you reach 5-10 mg/day
Switch to am hydrocortisone or alternate day dosing
Either use morning cortisol levels to determine adrenal suppression or a very gradual

59
Q

When is it okay to stop the use of glucocorticoids and when do you still need to continue tapering?

A
  • If am cortisol >20 mcg/dL the HPA axis has recovered (means you can discontibue the exogenous steroids)
  • If am cortisol < 3 mcg/dL the HPA axis is still suppressed
  • If am cortisol 3-20 mcg/dL use another test: cosyntropin stim test
60
Q

What is the adverse effects of withdrawl of glucocorticoids?

A

Flare-up of underlying disease

Acute adrenal insufficiency- symptoms of withdrawl=symptoms of adrenal insufficiency

61
Q

What are the general adverse effects of chronic glucocorticoids use?

A
  • Weight gain

- Increased appetite

62
Q

What are the CNS adverse effects of chronic glucocorticoids use?

A
  • Mood changes- euphoria -> depression

- Psychosis (rare)

63
Q

What are the opthamology adverse effects of chronic glucocorticoids use?

A
  • Cataracts: later in life (children would show up with them later in life, but more risky for the elderly)
  • Glaucoma due to increased intraocular pressure
64
Q

What are the CV adverse effects of chronic glucocorticoids use?

A
  • HTN

- Dyslipidemia (Increased TC, LDL, TG)

65
Q

What are the heme adverse effects of chronic glucocorticoids use?

A
  • Immunosuppression
  • Infection
  • Impaired wound healing
66
Q

What are the GI adverse effects of chronic glucocorticoids use?

A
  • Peptic ulcer disease
  • Controversial, may occur more w/ NSAID use
  • Suppression of response to H. Pylori
67
Q

What are the bone adverse effects of chronic glucocorticoids use?

A
  • Osteoporosis: inhibition of bone formation (DEXA scan to assess bone mineral density) (>5mg/day of prednisone equivalent for >3mo tx needs preventative bisphosphonate therapy plus 1500mg elemental calcium & 800-1200 units vit. D/Day)
  • Aseptic Necrosis Hip
  • Growth suppression (PO steroids in asthma and kids w/ cancer)
  • Myopathy
68
Q

What are the endocrine adverse effects of chronic glucocorticoids?

A

-Cushing’s syndrome
-Adrenal suppression (not seen until steroid is taken away)
-Glucose Intolerance/Diabetes mellitus (DM)/Exacerbation of DM (↓ insulin sensitivity
↑ gluconeogenesis)
- Mineralcorticoid ADR- kidney and RAA system

69
Q

What are the skin adverse effects of chronic glucocorticoids use?

A
  • Acne
  • Easy bruising (loss if collagen support for blood vessels)
  • Thin skin (atrophy of epidermal and dermal skin layers)
  • Striae (atrophy of the subcutaneous tissue)
70
Q

What should you counsel patients on that are taking glucocorticoids?

A
  • TAKE THEM WITH FOOD
  • NEVER STOP STEROID THERAPY ABRUPTLY
  • Carry or wear a medical ID (patients on chronic glucocorticoids or those with adrenal insufficiency)
  • Ensure daily calcium intake is adequate
  • Adverse reactions
71
Q

How long does a patient have to be taking a steroid for them to have to taper before stoping?

A

Anyone taking a steroid for longer than a week cannot stop the steroid abruptly and needs to taper

72
Q

What causes acute adrenal insufficiency (adrenal crisis)?

A

Trauma, surgery, illness or stress activate the HPA axis

Increased CRH → ACTH →cortisol production

73
Q

What are the signs and sx of acute adrenal insufficiency (adrenal crisis)?

A

SHOCK
Coma
N/V, weakness, lethargy
Patients with adrenal insufficiency require stress doses of glucocorticoids in the above situations

74
Q

What is the inpatient tx for acute adrenal insufficiency (Adrenal crisis)?

A

Hydrocortisone 100mg IV push followed by continuous infusion or 100mg Q6-8° x 48 hrs, then taper
IV fluids (D5NS)
BP support
Fludrocortisone (kinda like aldosterone it’s a mineral corticoid) if needed to decrease potassium levels

75
Q

What should you educate patients about for adrenal crisis?

A

Emergency situations- can precipitate an adrenal crisis
Injury with substantial blood loss or a fracture
N/V and inability take PO medications
Unresponsive patient

Patients with primary adrenal insufficiency should wear a medical alert bracelet

Patients should carry an injectable glucocorticoid (100 mg hydrocortisone or 4 mg dexamethasone)

76
Q

What hormones is the anterior pituitary responsible for?

A
  • Growth hormone (GH or somatropin)
  • Prolactin
  • Adrenocorticotropic hormone (ACTH)
  • Thyroid stimulating hormone (TSH)
  • Luteinizing hormone (LH)
  • Follicle-stimulating hormone (FSH)
77
Q

What hormones is the posterior pituitary responsible for?

A
  • Oxytocin

- Vasopresin (antidiuretic hormone)

78
Q

What is an excess production of GH typically due to a GH-secreting pituitary adenoma?

A 
Growth hormone (GH) excess
Acromegaly
79
Q

What are the sx of acromegaly?

A 
Slow onset of symptoms- overtime
Soft tissue overgrowth
High mortality risk
Cardiovascular
Respiratory
Neoplastic disease
80
Q

How is GH excess (acromegaly) diagnosed?

A

Oral glucose tolerance test followed by a GH level
GH level >1 mcg/L
Elevated IGF-1 levels

81
Q

Why should you start with an oral glucose tolerance test followed by a GH level?

A

Give oral glucose tolerance test first to distinguish if the elevated growth hormone level is related to patient not having sugars right now. GH takes up sugars so you need to double to take it up so if glucose is too low then you might have a higher GH so you need to do that

*Tried typing this in class while she was talking doesn’t make much sense now but i feel like its important ahhah

82
Q

What is the treatment for GH excess (acromegaly)?

A

Surgery (First line treatment)
Pharmacologic treatment (Done only while patient is waiting for surgery or if there are contraindications)
Somatostatin analogs
More potent GH secretion inhibitors than endogenous somatostatin
Dopamine agonists
Decrease GH production
GH receptor antagonist
Blocks the effects of GH on target tissue

83
Q

Octreotide (Sandostatin®, Sandostatin LAR®)- Indication

A

Somatostatin Analog

FIRST LINE THERAPY FOR GH EXCESS (ACROMEGALY)

84
Q

Octreotide (Sandostatin®, Sandostatin LAR®)- Adverse effects

A 
Nausea, diarrhea
Hyperglycemia
Arrhythmias
Hypothyroidism
Cholelithiasis
85
Q

Bromocriptine (Parlodel®) & Ergot alkaloid- Indications

A

Dopamine agonists

Used in treatment of growth hormone excess (acromegaly)

86
Q

Bromocriptine (Parlodel®) & Ergot alkaloid- clinical response

A

Clinical response seen after 4-8 weeks of therapy (clinical effect)
Reduces GH levels within 1-2 hours (clad effect)

87
Q

Bromocriptine (Parlodel®) & Ergot alkaloid- Adverse effects

A

N/V- most common
Headache
Dizziness
Hypotension

88
Q

Pegvisomant (Somavert®) - MOA

A

GH receptor antagonist

Binds to GH receptors on the cell surface

89
Q

Pegvisomant (Somavert®) - indications

A

FDA approved for acromegaly as 2nd line therapy. (Only used after starting other meds and they aren’t working very successfully)

90
Q

Pegvisomant (Somavert®) - response

A

Response is seen in 2 weeks

91
Q

Pegvisomant (Somavert®) - adverse effects

A

Nausea, diarrhea
AST, ALT elevations
Monitor liver function tests during treatment

92
Q

What is the post common presentation of GH deficiency?

A

Short stature

93
Q

What is involved with short stature?

A

> 2 SD below the population mean and lower than the third percentile for height in a specific age group
Prominence of the forehead
Immaturity of the face
Central obesity
Can also occur with other conditions not associated with GH deficiency

94
Q

What is GH deficient (GHD) short stature?

A

True lack of GH (children are usually born with an average birth weight)

95
Q

Is GH insufficiency a congenital or acquired disorder?

A

Acquired

96
Q

Recombinant GH- Indications

A
  • First line for children with GHD short stature
  • Improves growth velocity in the first year of treatment

Other FDA Indications

  • Turner’s syndrome
  • Prader-Willi’s syndrome
  • Children with chronic renal insufficiency
  • Idiopathic short stature
  • Adult GH deficiency
  • Short-bowel syndrome
  • AIDS wasting syndrome
97
Q

What do all recombinant GH products contain?

A

Somatropin

98
Q

What are the 11 products available for recombinant GH?

A 
Genotropin
Humatrope
Norditropin
Nutropin
Nutropin AQ
Nutropin Depot- once or twice montly injection
Omnitrope
Saizen
Serostim
Tev-Tropin
Zorbtive

*Don’t have to memorize in test she will indicate that it is a GH recombinant

99
Q

Recombinant GH- Route

A

All given IM or SC

Continue therapy until growth velocity decreases to <2.5 cm/year after puberty

100
Q

Recombinant GH- Adverse effects

A
  • Well tolerated
  • Slipped capital femoral epiphysis
  • Idiopathic intracranial hypertension
101
Q

What are the recombinant insulin-;like-growth factor-1 (IGF-1) drugs?

A 
Mescasermin (Increlex®)
Mescasermin rinfabate (Iplex®)
102
Q

Mescasermin (Increlex®), Mescasermin rinfabate (Iplex®) (recombinant insulin-;like-growth factor-1 (IGF-1))- Indications

A

Approved for children with short stature due to primary IGF-1 deficiency

103
Q

Mescasermin (Increlex®), Mescasermin rinfabate (Iplex®) (recombinant insulin-;like-growth factor-1 (IGF-1))- adverse effects

A

HYPOGLYCEMIA- INSULIN LIKE EFFECTS
Dizziness
Arthralgias

104
Q

What is hyperprolactinemia?

A

Persistent prolactin levels > 20 mcg/L
Affects women of reproductive age
Incidence < 1%

105
Q

What is the etiology for hyperprolactinemia?

A

Prolactinomas

Drug-induced

106
Q

What does 10x ↑Prolactin levels inhibit?

A

10x ↑Prolactin levels inhibit gonadotropin secretion and sex-steroid synthesis
Increased risk of osteoporosis
Make sure to tx this

107
Q

What are the DA antagonists that cause drug induced hyperprolactinemia?

A

Antipsychotics
Phenothiazines (promeclizine aka phenergen)
Metoclopramide

108
Q

What is the other drug that causes drug induced hyperprolactinemia?

A

Verapamil

109
Q

What are the prolactin stimulators that cause drug induced hyperprolactinemia?

A 
Methyldopa
Reserpine
SSRIs
Estrogens/Progestins
Protease inhibitors
Benzodiazepines
TCAs
MAO-I
H2-receptor antagonists
Opioids
110
Q

What are the signs and sx of hyperprolactinemia in females?

A 
Anovulation
Oligomenorrhea or ameorrhea
Infertility
Galactorrhea
Decreased libido
Hirsutism
Acne
111
Q

What are the signs and sx of hyperprolactinemia in males?

A 
Erectile dysfunction
Infertility
Decreased muscle mass
Galactorrhea
Gynecomastia
112
Q

Bromocriptine (Parlodel®)- MOA

A

Stimulates hypothalamic dopamine receptors

113
Q

Bromocriptine (Parlodel®)- indications

A

Hyperprolactinemia tx
Treatment of infertility due to hyperprolactinemia
Use barrier contraceptive method until prolactin levels are normalized
Reduce dose to minimum therapeutic dose before attempting to become pregnant

114
Q

Bromocriptine (Parlodel®)- ADRs

A

N/V- most common
Headache
Dizziness
Hypotension

115
Q

Cabergoline (Dostinex®)- MOA

A

long-acting dopamine agonist

116
Q

Cabergoline (Dostinex®)- Indications

A

First line for prolactinomas
Better efficacy than bromocriptine

Treatment of infertility
Little data on use in pregnancy
Few observational studies have not shown detrimental effects on the pregnancy or fetus

117
Q

Cabergoline (Dostinex®)- ADRs

A

Adverse effects – similar to bromocriptine
Possibly a lower incidence
Reports of valvular heart disease when used in high doses (2 mg/day) for long-term therapy

118
Q

What are the monitoring parameters for those receiving hyperprolactinemia treatment?

A
  • Serum prolactin concentrations q 3-4 weeks after the initiation of drug therapy
  • Evaluate clinical signs and symptoms
  • Once serum levels are normalized, monitor every 6-12 months

Pharmacology III (19 decks)

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