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Therapeutics 5 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Hyperprolactinemia hormone changes and organ

A

Increase prolactin

Organ- pituitary gland

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2
Q

Acromegaly hormone changes and organ

A

Hormone changes- increase growth hormone

Organ- pituitary gland

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3
Q

Cushing’s disease hormone changes and organ

A

Hormone changes- increase glucocorticoids (cortisol)

Organ- adrenal gland

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4
Q

Growth hormone deficiency hormone changes and organ

A

Hormone changes- decrease growth hormone

Organ- pituitary gland

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5
Q

Addison’s disease hormone changes and organ

A

Hormone changes- decrease glucocorticoids (cortisol), decrease mineralocorticoids (aldosterone)
Organ- addison’s disease

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6
Q

Hyperaldosteronism hormone changes and organ

A

Hormone changes- increase mineralocorticoids (aldosterone)

Organ- adrenal gland

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7
Q

What is prolactin regulated by?

A

Regulated by inhibitory effects of dopamine

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8
Q

Prolactin secretion

A

Secreted in a pulsatile fashion

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9
Q

Prolactin promotes what?

A

Lactation, breast development, and reproductive function

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10
Q

Hyperprolactinemia

A

Persistent prolactin concentrations >25 mcg/L

Most commonly affects women ages 24-35 with about 24 cases per 1,000 person years

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11
Q

Etiology of hyperprolactinemia

A 
Pituitary tumors
Drug-induced (dopamine antagonists)
CNS lesions
Hypothyroidism
Idiopathic
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12
Q

Drug induced hyperprolactinemia

A

Dopamine antagonists- antipsychotics, metoclopramide
Prolactin stimulators- estrogens, progestins, SSRIs, 5HT1 receptor agonists, Benzos, MAO inhibitors, TCAs, opioids, H2 receptors antagonists
Other- verapamil

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13
Q

Hyperprolactinemia clinical presentation female

A 
menstrual cycle changes: oligomenorrhea or amenorrhea
Galactorrhea
Infertility
Decreased libido
Hirsutism
Acne
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14
Q

Hyperprolactinemia clinical presentation male

A 
Decreased libido
Erectile dysfunction
Infertility
Reduced muscle mass
Galactorrhea
Gynecomastia
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15
Q

Clinical sequelae of hyperprolactinemia

A

Osteoporosis, ischemic heart disease

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16
Q

Hyperprolactinemia medications

A

Cabergoline

Bromocriptine

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17
Q

Cabergoline

A

MOA: long acting D2 receptor agonist
First line- shown to be more effective than bromocriptine
0.25-0.5 mg WEEKLY or twice weekly
Increase at 4 week intervals based on prolactin levels

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18
Q

AE of cabergoline

A

GI: Nausea, vomiting, constipation
CNS: headache, dizziness, anxiety, depression
Nasal decongestion
Dose adjust for hepatic failure

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19
Q

Bromocriptine

A

MOA: D2 receptor agonist
1.25-2.5mg QD at bedtime
Increase weekly based on prolactin levels

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20
Q

Bromocriptine AE

A

CNS: headache, lightheadedness, dizziness, nervousness, fatigue
GI: nausea, abdominal pain, diarrhea (administer WF)

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21
Q

Pregnancy with hyperprolactinemia treatment

A

Recommend discontinuing cabergoline or bromocriptine

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22
Q

Hyperprolactinemia monitoring and follow-up

A

Prolactin levels every 3-4 weeks until stable then every 6-12 months
Assess symptoms
After 2 years of treatment may be tapered or discontinued in the absence of visible tumor

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23
Q

Growth hormone

A

GH has direct anti-insulin effects
Growth-promoting effects mediated by insulin-like growth factors (ICF’s), which directly stimulate cell proliferation and growth

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24
Q

Growth hormone secretion

A

Secreted by anterior pituitary in pulsatile fashion

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25
Q

Acromegaly

A

Excessive GH production

Etiology: GH-secreting pituitary tumor

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26
Q

Acromegaly clinical presentation

A

Slow developing soft-tissue overgrowth
Often not diagnosed until 7-10 years after GH secretion is thought to have started
Symptoms:
local effects from tumor- HA, visual disturbances
Excessive sweating, neuropathies, joint pain, paresthesias
Increased hand volumes, increased ring or shoe size, coarsening of facial features
GH concentrations >1mcg/L following oral glucose tolerance test
IGF-1 elevation

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27
Q

Acromegaly clinical sequelae

A 
CV disease- HTN, CAD, cardiomyopathy, left ventricular hypertrophy
Osteoarthritis and joint damage
Respiratory disorders and sleep apnea
Type 2 diabetes
Esophageal, colon, and stomach cancers
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28
Q

Management of acromegaly

A 
Transsphenoidal surgery (most patients)
Persistent disease/incomplete surgery-
Medications
-SRL, DA, Pegvisomant 
Consider SRT (conventional radiation) if not medication candidate
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29
Q

Somatostatin analogs

A

1st line for acromegaly
Octreotide, lancreotide, pasireotide
IM every 28 days

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30
Q

Somatostatin analogs AE

A 
GI: diarrhea, nausea, abdominal cramp, malabsorption of fat, flatulence- subside within 10-14 days
Arrhythmias
Subclinical hypothyroidism
Biliary tract disorders
Abnormalities in glucose metabolism
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31
Q

Dopamine agonists

A

Acromegaly treatment
Bromocriptine and cabergoline
MOA: causes paradoxical decrease in GH
Dosing: similar to hyperprolactinemia, but doses may be higher

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32
Q

Pegvisomant

A

Acromegaly treatment
MOA: genetically engineered GH derivative that binds to, but does not activate GH receptors and inhibits IGF-1 production
Only affects IGF-1 levels not GH

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33
Q

Pegvisomant AE

A

GI: nausea, diarrhea

Reversible LFT elevation (monitor)

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34
Q

Growth hormone deficiency

A

Also known as growth hormone deficiency short stature
Etiology:
Absolute deficiency- congenital from various genetic abnormalities
GH insufficiency- hypothalamic or pituitary tumors, cranial irradiation, head trauma, pituitary infarction, CNS infections, hypothyroidism, poorly controlled diabetes, medications (glucocorticoids, methylphenidate, and dextroamphetamine)

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35
Q

Growth hormone deficiency clinical presentation

A

Physical height greater than two standard deviations below the population mean
Delayed skeletal maturation, central obesity, immaturity of the face
Peak GH concentration <10mcg/L

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36
Q

Growth hormone deficiency treatment

A 
Recombinant GH (rhGH) or somatropin
Dosing 0.1-0.2 mg/day and titrate based on IGF-1 levels every 1-2 months
F/U 6-12 months for maintenance
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37
Q

Hormones in adrenal cortex:

Zona glomerulosa

A

Makes aldosterone

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38
Q

Hormones in adrenal cortex: Zona fasciculata

A

Makes cortisol

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39
Q

Hormones in adrenal cortex: Zona reticularis

A

Makes testosterone

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40
Q

Addison’s disease, primary adrenal insufficiency

A

Primary adrenal insufficiency- deficiencies in cortisol, aldosterone, and androgens
Etiology: Autoimmune destruction of all regions of adrenal cortex, medications

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41
Q

Primary adrenal insufficiency, Addisons disease medications causes

A

Ketoconazole
Phenytoin
Rifampin
Phenobarbital

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42
Q

Secondary adrenal insufficiency, Addison’s disease

A

Secondary adrenal insufficiency- decreased glucocorticoid production secondary to decreased ACTH levels
Etiology:
Exogenous steroid use, mirtazapine, progestins (medroxyprogesterone and megestrol)

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43
Q

Clinical presentation of addison’s disease

A

Hyperpigmentation
Weight loss
Dehydration
Hyponatremia
Elevated BUN
Secondary- aldosterone secretion is preserved
Abnormal response to corticotropin stimulation test

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44
Q

Corticotropin stimulation test

A

250mcg of ACTH (corticotropin or cosyntropin) IV or IM
Serum cortisol measured at baseline and 30-60 minutes after injection
Cortisol levels >18 mcg/dL rules OUT adrenal insufficiency
CANNOT use for critically ill patients

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45
Q

Addison’s disease treatment

A

Glucocorticoid replacement
-Hydrocortisone, cortisone, prednisone
15-25mg hydrocortisone 67% in AM and 33% 6-8 hours later
Adjust every 6-8 weeks based on symptoms
Fludrocortisone 0.05-2 mg daily in primary insufficiency

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46
Q

Addisons disease treatment: Patient education

A

Consequences of missed doses
Drug side effects
Expected outcomes
Treatment complications
Exercise –> additional 5-10mg hydrocortisone
Sick day management –> double daily dose

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47
Q

Addison’s disease monitoring and follow up

A

Every 6-8 weeks
Relief of symptoms
Avoid development of Cushing syndrome features

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48
Q

Cushing’s syndrome

A

Excessive cortisol production
Etiology:
Exogenous administration
Endogenous:
-ACTH-dependent (pituitary adenomas, ectopic ACTH- secreting tumor)
-ACTH-independent (adrenal adenomas, adrenal carcinomas)

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49
Q

Cushing’s syndrome: clinical presentation

A

Central obesity, facial rounding, myopathies, muscular weakness, buffalo hump, HTN, osteoporosis, amenorrhea, hirsutism

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50
Q

Hyperaldosteronism clinical presentation

A

Muscle weakness, fatigue, parethesias, headache, HTN, tetany/paralysis, polydipsia/nocturnal polyuria

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51
Q

Hyperaldosteronism treatment

A

Aldosterone receptor antagonists
Amiloride
Eplerenone
Spironolactone

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52
Q

Hyperthyroidism etiology

A 
Overproduction of T3 and T4 by thyroid gland
Women > Men
Most common in ages 20-39
Etiology:
Graves disease- most common
TSH induced
TSH secreting pituitary adenomas
Pituitary resistance to thyroid hormone
Trophoblastic diseases
Toxic adenoma
Multinodular goiters
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53
Q

Hyperthyroidism evaluation

A

Radioactive iodine uptake (RAIU) test
Increased RAIU= overproduction of T3 and T4
Decreased RAIU- excess T3 and T4 not due to overproduction

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54
Q

Total T4 normal value

A

4.8-10.4 mcg/dL

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55
Q

Free T4 normal value

A

0.8-1.4 ng/dL

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56
Q

Total T3 normal value

A

59-156ng/dL

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57
Q

TSH normal value

A

0.45-4.12 mcgIU/mL

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58
Q

RAIU at 24 hrs normal value

A

5-35%

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59
Q

Thyroglobulin autoantibodies normal value (Tg-Ab)

A

<200 IU/mL

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60
Q

Thyroid peroxidase autoantibodies (ATPO) normal values

A

<100 WHO units

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61
Q

TSH receptor-stimulating antibody normal value

A

Negative <140% of baseline

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62
Q

Hyperthyroidism clinical presentation

A 
Eyelid retraction
Thyroid dermopathy
Thyroid acropachy
Nervousness
Anxiety
Palpitations
Emotional lability
Easy fatiguability
Menstrual disturbances
Heat intolerance
Weight loss with increased appetite
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63
Q

Hyperthyroidism lab values

A

Total T4, free T4, total T3, RAIU at 24 hours all high
Tg-AB and ATPO usually present
TSH low
TSH-receptor stimulating antibody elevated in Graves disease

64
Q

Hyperthyroidism treatment options

A

Methimazole
Propylthiouracil
Radioactive iodine
Surgery

65
Q

Methimazole

A

Hyperthyroidism treatment
MOA- inhibit biosynthesis of thyroid hormone through multiple mechanisms (antithyroid)
30-60mg/day in 2-3 divided doses

66
Q

Propylthiouracil

A

Hypothyroidism treatment
MOA- inhibits biosynthesis of thyroid hormones through multiple mechanisms (antithyroid)
Inhibits peripheral conversion of T4 to T3
Dose 300-600 mg/day in 3-4 divided doses

67
Q

Adverse effects and f/u of methimazole and propylthiouracil

A 
Maculopapular rashes
Arthralgias
Fever
Benign transient leukopenia
Agranulocytosis
Hepatotoxicity
Lupus-like syndrome

40-50% of people go to remission after 12-24 months.
F/U 6-12 months after remission
If relapse, radioactive iodine is preferred

68
Q

Iodides

A

Hyperthyroidism treatment
MOA- acutely block thyroid hormone release. Wolff-Chaikoff effect
Quick onset, but inhibition is overcome within 1-2 weeks
Products: potassium iodide, saturated solution (SSKI), Lugols solution

69
Q

AE of iodides

A

Hypersensitivity, iodism (metallic taste, burning mouth and throat, sore teeth and gums)
Gynecomastia

70
Q

Radioactive iodine

A

Cytotoxic to thyroid gland
Contraindicated in pregnancy
Can repeat dose in 6 months if still hyperthyroid

71
Q

Beta blockers

A

Inhibition of beta adrenergic receptors
Used for symptom control (palpitations, anxiety, tremor, heat intolerance) of hyperthyroidism
Propranolol most common.

72
Q

Subclinical hyperthyroid

A

Low TSH, normal T4 and T3
Increased risk of mortality, Afib, hip fractures
Treat is age >65 with TSH <0.1mIU/L

73
Q

Pregnancy and hyperthyroidism

A

Surgery or RAI before pregnancy is preferred
PTU preferred in 1st trimester then switch to MMI
Surgery preferred 2nd trimester if needed

74
Q

Neonatal hyperthyroidism

A

Placental transfer of TSAbs- stimulates thyroid hormone production in utero and postpartum
7-10 days postpartum
Treatment: ATDs for 8-12 weeks until antibodies clear
Iodides can be used the first few days

75
Q

Thyroid storm

A

Life-threatening emergency
Presentation- fever, tachycardia, dehydration, delirium, coma, N/V,D
Precipitating factors- infection, trauma, surgery, RAI tx, withdrawal of ATDs

76
Q

Thyroid storm tx

A

Suppress thyroid hormone formation and secretion
Antiadrenergic therapy
Corticosteroids

77
Q

Hyperthyroidism monitoring and follow up

A

Monthly immediately after initiation until euthyroid
Note signs and symptoms of hyperthyroidism
Monitor for hypothyroidism

78
Q

Hypothyroidism

A

Overt: elevated TSH with decreased free T4
Subclinical: elevated TSH with normal free T4

79
Q

Etiology of hypothyroidism

A

Iodine insufficiency
Autoimmune thyroid diseases (AITs)- Hashimotos
Iatrogenic
Pituitary or hypothalamic diseases

80
Q

Sources of iodine

A 
Fish (cod, tuna)
Seaweed
Shrimp
Dairy product
Iodized salt
81
Q

Hypothyroisism clinical presentation

A

Dry skin, cold sensitivity, fatigue, muscle cramps, voice changes, constipation, menorrhagia
Weakness, relaxation of deep tendon reflexes, coarse skin and hair, cold or dry skin, bradycardia, slowed speech and hoarse voice, carpal tunnel syndrome, polyneuropathy

82
Q

Hypothyroidism labs

A

Total T4, Free T4, Total T3- LOW
TSH- HIGH
RAIU at 24 hours- not indicated
Tg-Ab, ATPO or TPO-Ab- Present

83
Q

Who should be treated for hypothyroidism?

A

TSH >10mU/L

TSH > upper limit of lab range <10 mU/L with symptoms, positive antibodies, evidence of CV disease, or HF

84
Q

Levothyroxine

A

Synthetic T4 prohormone
DOC- stable, predictable potency, inexpensive, accurate
Abs affected by food, oral bioavailability 70%
Well tolerated

85
Q

Levothyroxine dosing

A 
Overt: 1.6mcg/kg IBW
Subclinical: 25-75mcg QD
Elderly: Start at 50mcg
CV disease: Initial dose 12.5-25mcg
Take 30-60 minutes before breakfast with water OR 4 hours after last meal
86
Q

Liothyronine

A

Synthetic T3

Higher incidence of CV AE, higher cost, TID, longer time to achieve euthyroid, difficult to monitor

87
Q

Liotrix

A

Synthetic T4 and T3 in 4:1 ratio

High cost

88
Q

Dessicated thyroid

A

Derived from pig, beef, sheep
Inconsistent potency (up to 15% variation in T4 and 10% in T3)
Allergic rxns

89
Q

BBW for hypothyroidism treatments

A

Not to be used for weight loss.
In euthyroid patients, thyroid treatment is ineffective for weight loss
Large doses can be life-threatening

90
Q

Hypothyroidism monitoring and follow-up

A

TSH levels at 4-8 weeks and then every 6-12 months
Dose changes 12.5-25mcg/day
Some symptoms take several months to resolve.

91
Q

Hypothyroidism in pregnancy

A

Estrogen-induced total T4 elevation by increasing T4 binding globulin
Adverse outcomes- spontaneous miscarriage, preterm delivery, preeclampsia, maternal HTN, postpartum hemorrhage, low birth weight, stillbirth

92
Q

Hypothyroidism in pregnancy TSH measurement

A

1st trimester- 0.2-2.5 mU/L

2nd and 3rd- 0.3-3 mU/L

93
Q

Treatment of hypothyroidism in pregnancy

A

Levothyroxine

Increase dose of T4 by 30-50% by week 4-6

94
Q

Normal TSH

A

0.45-4.12 mU/L

95
Q

Myxedema coma

A

Decompensated hypothyroidism
Clinical features- hypothyroidism, delirium, coma, diastolic HTN, hypoventilation
60-70% mortality rate

96
Q

Myxedema coma precipitating factors

A

Burns, GI hemorrhage, hypoglycemia, infection, stroke, surgery, trauma

97
Q

What are the most effective contraceptives?

A

IUDs and progestin only implant

Oral pills and rings have a 9% efficacy with typical use

98
Q

Rule out pregnancy before contraceptives

A

7 or fewer days from onset of menses, spontaneous abortion, or elective abortion
No intercourse since onset of latest menses or last pregnancy test
Correctly and consistently using contraception
Breastfeeding at least 85% of the time, still experiencing amenorrhea, and is fewer than 6 months postpartum
Within 4 weeks postpartum

99
Q

Combined hormonal contraceptives (CHC) MOA

A

Progestin- thickens cervical mucus

Estrogens- Suppress FSH

100
Q

Progestin MOA BC

A

Thickening of cervical mucus

  • Prevent sperm penetration
  • Slow tubal motility
  • Delay sperm transport

Block LH surge, inhibiting ovulation

101
Q

Estrogens BC MOA

A

Suppress FSH, blocking LH surge and inhibiting ovulation

Stabilize endometrial lining and provide cycle control

102
Q

Estrogens used in CHC

A

Ethinyl estradiol
mestranol (metabolized to ethinyl estradiol)
Estradiol valerate

103
Q

Estrogen in CHC dosing

A

High >/= 50 mcg
Regular >/= 30-35mcg
Low >/= 10-20mcg

104
Q

1st gen progestins used in CHC

A

Norethindrone
Ethynodiol diacetate
Norethynodrel

105
Q

2nd gen progestins used in CHC

A

Levonorgestrel
Norgestrel

MOST androgenic

106
Q

3rd gen progestins used in CHC

A

Desogestrel
Etonogestrel
Norgestimate

107
Q

4th gen progestins used in CHC

A

Anti-androgenic, may increase K

Drospirenone, dienogest, segesterone

108
Q

Androgenic AE

A 
Weight gain
Acne
Hirsutism
Oily skin
Increased libido
109
Q

Which progestin do you switch to if a pt is experiencing androgenic AE?

A

4th gen- anti-androgenic

Drospirenone, dienogest, segesterone

110
Q

Which progestin is most likely to cause androgenic AE?

A

2nd gen
Levonorgestrel
Norgestrel

111
Q

ADR associated with excess estrogen

A

Nausea, breast tenderness, increased BP, HA, edema/bloating

Management- decrease estrogen amount, consider progestin only options

112
Q

ADR associated with estrogen deficiency

A

Early to mid-cycle (days 1-9) break through bleeding
Increased spotting
Dry vaginal mucosa
Hypomenorrhea

Management- increase estrogen content

113
Q

ADR associated with excess progestin

A

Breast tenderness, depression or irritability, fatigue, constipation

Manage by decreasing progestin

114
Q

ADR associated with progestin deficiency

A

Late cycle BTB
Hypomenorrhea
Amenorrhea
Weight loss

Manage by increasing progestin

115
Q

ADR associated with excess androgen

A

Increase appetite, increased libido, oily skin/acne, hirsutism, weight gain

116
Q

Serious AE with CHC

A 
Abdominal pain
Chest pain
Headaches
Eye problems
Severe leg pain
117
Q

Contraindications to CHC

A 
<21 days postpartum 
Acute DVT/PE
Migraine with aura
Age >/= 35 and smokes >/= 15 cigarettes/day
BP >160/100
Higher risk for recurrent DVT/PE
Surgery with prolonged immobilization
Thrombotic mutations
H/O ischemic disease, stroke, valvular heart disease
Current breast cancer
Decompensated cirrhosis 
Liver tumors
118
Q

Abx reactions with CHC

A

Rifampin

Case reports with tetracyclines and penicillin derivatives

119
Q

Anticonvulsant interactions with CHC

A

Phenobarbital, phenytoin, carbamazepine- induce metabolism of estrogen and progestin
Lamotrigine- decrease lamotrigine efficacy

120
Q

Advantages of CHC

A 
Decreased menstrual cramps, decreased blood loss, improvement in menstrual regularity, decreased iron deficiency anemia
Reduced risk of endometrial cancer
Quick return to fertility
Decreased risk of ovarian cysts
May decrease acne
121
Q

Disadvantages of CHC

A 
AE
Patient adherence
No protection against STDs
Increased BP
May decrease milk production during lactation
122
Q

Monophasic CHC

A

Same amounts of estrogen and progestin for 21 days, then 7 days of placebo

123
Q

Multiphasic CHC

A

Varying amounts of estrogen and progestin for 21 days then 7 days placebo

124
Q

Extended cycle CHC

A

Active pills for 84-364 days then 7 days placebo
First 3-6 months may have intermenstrual bleeding and spotting
Can achieve with monophasic CHCs or ethinyl estradiol/etonogestrel vaginal ring

125
Q

First day start method of CHC

A

First active pill taken the first day of menses.

  • Offers immediate protection and less breakthrough bleeding.
  • People with irregular cycles may have to wait to start.
126
Q

Sunday start method of CHC

A

First active pill taken the sunday after the start of menstruation

  • Most packs set up for sunday start, weekend free from menstruation
  • Back up protection required for 7 days
127
Q

Quick start method of CHC

A

First active pill taken day of visit regardless of timing

Back up method required for 7 days

128
Q

What to do if missed CHC (24-48 hours late)

A

Take pill ASAP
Continue taking remaining pills at usual time
No additional contraceptive method needed
Emergency contraceptives usually not needed

129
Q

What to do if missed CHC dose (>48 hours)

A

Take most recent pill ASAP, discard any other missed pills.
Continue taking the rest as normal.
Use back up method for 7 days
If pills were missed in the last week of hormonal pills, omit hormone-free interval and start new pack the next day
Emergency contraception may be considered

130
Q

Twirla

A

30mcg ethinyl estradiol and 120mcg levonorgestrel/day
Transdermal contraceptive patch

Not first line in BMI >30

131
Q

Xulane

A

150mcg norelgestromin and 35mcg ethinyl estradiol/day

Not first line in weight >90kg

132
Q

Transdermal patch BBW

A

Women over 35 years who smoke should not use

133
Q

Transdermal patch counseling points

A

Apply patch during first 24 hours of starting period= “patch change day”
Check patch daily
Avoid creams/lotions
Rotate patch site- butt, upper arm, upper thigh, upper back

134
Q

What to do if a transdermal patch was off for <48 hours?

A

Apply new patch ASAP
Keep same patch change day
No backup method needed

135
Q

What to do if transdermal patch is off >48 h

A

Apply new patch ASAP
Keep same patch change day
Use back up contraception for 7 days

136
Q

NuvaRing

A

Delivers 0.12mg etonogestrel and 0.015mg ethinyl estradiol per day
Similar efficacy and ADRs as oral CHCs
Better adherence than oral CHCs

137
Q

NuvaRing counseling points

A

Insert and leave in for 3 weeks then remove for one week
Initiate on first day of menstrual period
Use each ring only once

138
Q

What to do if NuvaRing falls out

A

WIthin 3 hours- rinse and re-insert
After 3 hours-
weeks 1-2- reinsert ASAP and use backup for 7 days
week 3- insert new ring and start a new cycle OR insert within 7 days and use backup for 7 days

139
Q

Annovers

A

13 mcg ethinyl estradiol and 150mcg segesterone acetate QD
Insert for 3 weeks then remove for one week
Used for 1 year

140
Q

Initiating Annovera

A

No hormonal contraceptive in preceding cycle:

  • Insert between days 2 and 5 of bleeding, no backup
  • If menstrual cycles are irregular or 5+ days from menstrual bleeding, use backup for 7 days

Using CHC- start anytime in cycle without backup

Progestin-only contraceptive
-Pills: at time of next pill
-Injection: At time of next injection
Implant of IUD: At time of removal
Backup for 7 days
141
Q

Annovera counseling points

A

If Annovera falls out reinsert within 2 hours. If out for > 2 hours use backup method for 7 days

142
Q

Advantages of progestin only contraceptives

A

Can be used if estrogen is contraindicated
No estrogenic AE
Decreased risk for MI and stroke in those >35
Safe for breastfeeding moms
Quick return to fertility

143
Q

Progestin only pills disadvantages

A

Not as effective
Requires strict compliance (if dose is 3+ hours late, backup method needed)
No hormone free interval
Androgenic AE
More breakthrough bleeding, less cramping

144
Q

Depot-medroxyprogesterone acetate (DMPA)

A

Administer once every 3 months
Deep IM in gluteal or deltoid muscle OR SC in abdomen or thigh
w/in 5 days of onset of bleeding

No interactions with seizure meds, decreased pain crises in sickle cell pts

145
Q

DMPA BBW

A

Bone mineral density decrease

146
Q

DMPA AE

A

Menstrual irregularities most common- spotting, prolonged bleeding, amenorrhea
Prolonged bleeding- short course (5-7 days) of NSAIDs, 10-20 days of estrogen
Breast tenderness
Depression
Weight gain

147
Q

Nexplanon

A

Long acting reversible contraceptives (LARC)
4 cm implant containing 68 mg etonogestrel
Releases 60mcg daily for first month then 30mcg daily for 3 years
Suppresses ovulation
Insert between days 1 and 5 of menstrual cycle OR use backup for 7 days

148
Q

Nexplanon AR

A

Menstrual irregularities most common- spotting, prolonged bleeding, amenorrhea
Prolonged bleeding (short course NSAIDS, 10-20 days estrogen)
Depression
Breast tenderness
Weight gain

149
Q

IUD contraindications

A 
Pregnancy
PID
Current STD
Undiagnosed abnormal vaginal bleeding
Malignancy of genital tract
Uterine abnormalities
Wilsons disease (copper IUD)
150
Q

Copper containing IUD

A

Paragard
Lasts 10 years
Increases menstrual flow
Releases copper ions

151
Q

Levonorgestrel intrauterine systems (LNG-IUS)

A

Mirena- lasts 7 years
Liletta- 6 years
Skyla- lasts 3 years
Kyleena- 5 years

152
Q

IUD warning signs

A 
Period-late, abnormal spotting or bleeding
Abdominal pain, pain with intercourse
Infection, abnormal vaginal discharge
Not feeling well, fever, chills
String missing, shorter or longer
153
Q

Checking for IUD strings

A

Check once monthly

May be missing if strings have moved, pregnancy, uterine perforation, IUD expulsion

154
Q

Emergency contraception

A 
Can be given up to 72-120 hours after unprotected intercourse
Methods: 
levonorgestrel and ulipristal
Yuzpe method
Copper IUD
155
Q

Yuzpe method

A

2 doses of oral CHC 12 hours apart
100mcg ethinyl estradiol and 0.5-1 levonorgestrel
Most effective within 72 hours

156
Q

Copper IUD

A

May be placed up to 7 days after intercourse

Most effective with a failure rate of only 0.09%

Therapeutics 5 (6 decks)

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