Exam 1 Flashcards
1
Q
Hyperprolactinemia hormone changes and organ
A
Increase prolactin
Organ- pituitary gland
2
Q
Acromegaly hormone changes and organ
A
Hormone changes- increase growth hormone
Organ- pituitary gland
3
Q
Cushing’s disease hormone changes and organ
A
Hormone changes- increase glucocorticoids (cortisol)
Organ- adrenal gland
4
Q
Growth hormone deficiency hormone changes and organ
A
Hormone changes- decrease growth hormone
Organ- pituitary gland
5
Q
Addison’s disease hormone changes and organ
A
Hormone changes- decrease glucocorticoids (cortisol), decrease mineralocorticoids (aldosterone)
Organ- addison’s disease
6
Q
Hyperaldosteronism hormone changes and organ
A
Hormone changes- increase mineralocorticoids (aldosterone)
Organ- adrenal gland
7
Q
What is prolactin regulated by?
A
Regulated by inhibitory effects of dopamine
8
Q
Prolactin secretion
A
Secreted in a pulsatile fashion
9
Q
Prolactin promotes what?
A
Lactation, breast development, and reproductive function
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
11
Q
Etiology of hyperprolactinemia
A
Pituitary tumors Drug-induced (dopamine antagonists) CNS lesions Hypothyroidism Idiopathic
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
13
Q
Hyperprolactinemia clinical presentation female
A
menstrual cycle changes: oligomenorrhea or amenorrhea Galactorrhea Infertility Decreased libido Hirsutism Acne
14
Q
Hyperprolactinemia clinical presentation male
A
Decreased libido Erectile dysfunction Infertility Reduced muscle mass Galactorrhea Gynecomastia
15
Q
Clinical sequelae of hyperprolactinemia
A
Osteoporosis, ischemic heart disease
16
Q
Hyperprolactinemia medications
A
Cabergoline
Bromocriptine
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
18
Q
AE of cabergoline
A
GI: Nausea, vomiting, constipation
CNS: headache, dizziness, anxiety, depression
Nasal decongestion
Dose adjust for hepatic failure
19
Q
Bromocriptine
A
MOA: D2 receptor agonist
1.25-2.5mg QD at bedtime
Increase weekly based on prolactin levels
20
Q
Bromocriptine AE
A
CNS: headache, lightheadedness, dizziness, nervousness, fatigue
GI: nausea, abdominal pain, diarrhea (administer WF)
21
Q
Pregnancy with hyperprolactinemia treatment
A
Recommend discontinuing cabergoline or bromocriptine
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
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
24
Q
Growth hormone secretion
A
Secreted by anterior pituitary in pulsatile fashion
25
Acromegaly
Excessive GH production
| Etiology: GH-secreting pituitary tumor
26
Acromegaly clinical presentation
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
27
Acromegaly clinical sequelae
```
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
```
28
Management of acromegaly
```
Transsphenoidal surgery (most patients)
Persistent disease/incomplete surgery-
Medications
-SRL, DA, Pegvisomant
Consider SRT (conventional radiation) if not medication candidate
```
29
Somatostatin analogs
1st line for acromegaly
Octreotide, lancreotide, pasireotide
IM every 28 days
30
Somatostatin analogs AE
```
GI: diarrhea, nausea, abdominal cramp, malabsorption of fat, flatulence- subside within 10-14 days
Arrhythmias
Subclinical hypothyroidism
Biliary tract disorders
Abnormalities in glucose metabolism
```
31
Dopamine agonists
Acromegaly treatment
Bromocriptine and cabergoline
MOA: causes paradoxical decrease in GH
Dosing: similar to hyperprolactinemia, but doses may be higher
32
Pegvisomant
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
33
Pegvisomant AE
GI: nausea, diarrhea
| Reversible LFT elevation (monitor)
34
Growth hormone deficiency
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)
35
Growth hormone deficiency clinical presentation
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
36
Growth hormone deficiency treatment
```
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
```
37
Hormones in adrenal cortex:
| Zona glomerulosa
Makes aldosterone
38
Hormones in adrenal cortex: Zona fasciculata
Makes cortisol
39
Hormones in adrenal cortex: Zona reticularis
Makes testosterone
40
Addison's disease, primary adrenal insufficiency
Primary adrenal insufficiency- deficiencies in cortisol, aldosterone, and androgens
Etiology: Autoimmune destruction of all regions of adrenal cortex, medications
41
Primary adrenal insufficiency, Addisons disease medications causes
Ketoconazole
Phenytoin
Rifampin
Phenobarbital
42
Secondary adrenal insufficiency, Addison's disease
Secondary adrenal insufficiency- decreased glucocorticoid production secondary to decreased ACTH levels
Etiology:
Exogenous steroid use, mirtazapine, progestins (medroxyprogesterone and megestrol)
43
Clinical presentation of addison's disease
Hyperpigmentation
Weight loss
Dehydration
Hyponatremia
Elevated BUN
Secondary- aldosterone secretion is preserved
Abnormal response to corticotropin stimulation test
44
Corticotropin stimulation test
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
45
Addison's disease treatment
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
46
Addisons disease treatment: Patient education
Consequences of missed doses
Drug side effects
Expected outcomes
Treatment complications
Exercise --> additional 5-10mg hydrocortisone
Sick day management --> double daily dose
47
Addison's disease monitoring and follow up
Every 6-8 weeks
Relief of symptoms
Avoid development of Cushing syndrome features
48
Cushing's syndrome
Excessive cortisol production
Etiology:
Exogenous administration
Endogenous:
-ACTH-dependent (pituitary adenomas, ectopic ACTH- secreting tumor)
-ACTH-independent (adrenal adenomas, adrenal carcinomas)
49
Cushing's syndrome: clinical presentation
Central obesity, facial rounding, myopathies, muscular weakness, buffalo hump, HTN, osteoporosis, amenorrhea, hirsutism
50
Hyperaldosteronism clinical presentation
Muscle weakness, fatigue, parethesias, headache, HTN, tetany/paralysis, polydipsia/nocturnal polyuria
51
Hyperaldosteronism treatment
Aldosterone receptor antagonists
Amiloride
Eplerenone
Spironolactone
52
Hyperthyroidism etiology
```
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
```
53
Hyperthyroidism evaluation
Radioactive iodine uptake (RAIU) test
Increased RAIU= overproduction of T3 and T4
Decreased RAIU- excess T3 and T4 not due to overproduction
54
Total T4 normal value
4.8-10.4 mcg/dL
55
Free T4 normal value
0.8-1.4 ng/dL
56
Total T3 normal value
59-156ng/dL
57
TSH normal value
0.45-4.12 mcgIU/mL
58
RAIU at 24 hrs normal value
5-35%
59
Thyroglobulin autoantibodies normal value (Tg-Ab)
<200 IU/mL
60
Thyroid peroxidase autoantibodies (ATPO) normal values
<100 WHO units
61
TSH receptor-stimulating antibody normal value
Negative <140% of baseline
62
Hyperthyroidism clinical presentation
```
Eyelid retraction
Thyroid dermopathy
Thyroid acropachy
Nervousness
Anxiety
Palpitations
Emotional lability
Easy fatiguability
Menstrual disturbances
Heat intolerance
Weight loss with increased appetite
```
63
Hyperthyroidism lab values
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
Hyperthyroidism treatment options
Methimazole
Propylthiouracil
Radioactive iodine
Surgery
65
Methimazole
Hyperthyroidism treatment
MOA- inhibit biosynthesis of thyroid hormone through multiple mechanisms (antithyroid)
30-60mg/day in 2-3 divided doses
66
Propylthiouracil
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
Adverse effects and f/u of methimazole and propylthiouracil
```
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
Iodides
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
AE of iodides
Hypersensitivity, iodism (metallic taste, burning mouth and throat, sore teeth and gums)
Gynecomastia
70
Radioactive iodine
Cytotoxic to thyroid gland
Contraindicated in pregnancy
Can repeat dose in 6 months if still hyperthyroid
71
Beta blockers
Inhibition of beta adrenergic receptors
Used for symptom control (palpitations, anxiety, tremor, heat intolerance) of hyperthyroidism
Propranolol most common.
72
Subclinical hyperthyroid
Low TSH, normal T4 and T3
Increased risk of mortality, Afib, hip fractures
Treat is age >65 with TSH <0.1mIU/L
73
Pregnancy and hyperthyroidism
Surgery or RAI before pregnancy is preferred
PTU preferred in 1st trimester then switch to MMI
Surgery preferred 2nd trimester if needed
74
Neonatal hyperthyroidism
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
Thyroid storm
Life-threatening emergency
Presentation- fever, tachycardia, dehydration, delirium, coma, N/V,D
Precipitating factors- infection, trauma, surgery, RAI tx, withdrawal of ATDs
76
Thyroid storm tx
Suppress thyroid hormone formation and secretion
Antiadrenergic therapy
Corticosteroids
77
Hyperthyroidism monitoring and follow up
Monthly immediately after initiation until euthyroid
Note signs and symptoms of hyperthyroidism
Monitor for hypothyroidism
78
Hypothyroidism
Overt: elevated TSH with decreased free T4
Subclinical: elevated TSH with normal free T4
79
Etiology of hypothyroidism
Iodine insufficiency
Autoimmune thyroid diseases (AITs)- Hashimotos
Iatrogenic
Pituitary or hypothalamic diseases
80
Sources of iodine
```
Fish (cod, tuna)
Seaweed
Shrimp
Dairy product
Iodized salt
```
81
Hypothyroisism clinical presentation
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
Hypothyroidism labs
Total T4, Free T4, Total T3- LOW
TSH- HIGH
RAIU at 24 hours- not indicated
Tg-Ab, ATPO or TPO-Ab- Present
83
Who should be treated for hypothyroidism?
TSH >10mU/L
| TSH > upper limit of lab range <10 mU/L with symptoms, positive antibodies, evidence of CV disease, or HF
84
Levothyroxine
Synthetic T4 prohormone
DOC- stable, predictable potency, inexpensive, accurate
Abs affected by food, oral bioavailability 70%
Well tolerated
85
Levothyroxine dosing
```
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
Liothyronine
Synthetic T3
| Higher incidence of CV AE, higher cost, TID, longer time to achieve euthyroid, difficult to monitor
87
Liotrix
Synthetic T4 and T3 in 4:1 ratio
| High cost
88
Dessicated thyroid
Derived from pig, beef, sheep
Inconsistent potency (up to 15% variation in T4 and 10% in T3)
Allergic rxns
89
BBW for hypothyroidism treatments
Not to be used for weight loss.
In euthyroid patients, thyroid treatment is ineffective for weight loss
Large doses can be life-threatening
90
Hypothyroidism monitoring and follow-up
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
Hypothyroidism in pregnancy
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
Hypothyroidism in pregnancy TSH measurement
1st trimester- 0.2-2.5 mU/L
| 2nd and 3rd- 0.3-3 mU/L
93
Treatment of hypothyroidism in pregnancy
Levothyroxine
| Increase dose of T4 by 30-50% by week 4-6
94
Normal TSH
0.45-4.12 mU/L
95
Myxedema coma
Decompensated hypothyroidism
Clinical features- hypothyroidism, delirium, coma, diastolic HTN, hypoventilation
60-70% mortality rate
96
Myxedema coma precipitating factors
Burns, GI hemorrhage, hypoglycemia, infection, stroke, surgery, trauma
97
What are the most effective contraceptives?
IUDs and progestin only implant
| Oral pills and rings have a 9% efficacy with typical use
98
Rule out pregnancy before contraceptives
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
Combined hormonal contraceptives (CHC) MOA
Progestin- thickens cervical mucus
| Estrogens- Suppress FSH
100
Progestin MOA BC
Thickening of cervical mucus
- Prevent sperm penetration
- Slow tubal motility
- Delay sperm transport
Block LH surge, inhibiting ovulation
101
Estrogens BC MOA
Suppress FSH, blocking LH surge and inhibiting ovulation
| Stabilize endometrial lining and provide cycle control
102
Estrogens used in CHC
Ethinyl estradiol
mestranol (metabolized to ethinyl estradiol)
Estradiol valerate
103
Estrogen in CHC dosing
High >/= 50 mcg
Regular >/= 30-35mcg
Low >/= 10-20mcg
104
1st gen progestins used in CHC
Norethindrone
Ethynodiol diacetate
Norethynodrel
105
2nd gen progestins used in CHC
Levonorgestrel
Norgestrel
MOST androgenic
106
3rd gen progestins used in CHC
Desogestrel
Etonogestrel
Norgestimate
107
4th gen progestins used in CHC
Anti-androgenic, may increase K
Drospirenone, dienogest, segesterone
108
Androgenic AE
```
Weight gain
Acne
Hirsutism
Oily skin
Increased libido
```
109
Which progestin do you switch to if a pt is experiencing androgenic AE?
4th gen- anti-androgenic
| Drospirenone, dienogest, segesterone
110
Which progestin is most likely to cause androgenic AE?
2nd gen
Levonorgestrel
Norgestrel
111
ADR associated with excess estrogen
Nausea, breast tenderness, increased BP, HA, edema/bloating
Management- decrease estrogen amount, consider progestin only options
112
ADR associated with estrogen deficiency
Early to mid-cycle (days 1-9) break through bleeding
Increased spotting
Dry vaginal mucosa
Hypomenorrhea
Management- increase estrogen content
113
ADR associated with excess progestin
Breast tenderness, depression or irritability, fatigue, constipation
Manage by decreasing progestin
114
ADR associated with progestin deficiency
Late cycle BTB
Hypomenorrhea
Amenorrhea
Weight loss
Manage by increasing progestin
115
ADR associated with excess androgen
Increase appetite, increased libido, oily skin/acne, hirsutism, weight gain
116
Serious AE with CHC
```
Abdominal pain
Chest pain
Headaches
Eye problems
Severe leg pain
```
117
Contraindications to CHC
```
<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
Abx reactions with CHC
Rifampin
| Case reports with tetracyclines and penicillin derivatives
119
Anticonvulsant interactions with CHC
Phenobarbital, phenytoin, carbamazepine- induce metabolism of estrogen and progestin
Lamotrigine- decrease lamotrigine efficacy
120
Advantages of CHC
```
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
Disadvantages of CHC
```
AE
Patient adherence
No protection against STDs
Increased BP
May decrease milk production during lactation
```
122
Monophasic CHC
Same amounts of estrogen and progestin for 21 days, then 7 days of placebo
123
Multiphasic CHC
Varying amounts of estrogen and progestin for 21 days then 7 days placebo
124
Extended cycle CHC
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
First day start method of CHC
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
Sunday start method of CHC
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
Quick start method of CHC
First active pill taken day of visit regardless of timing
| Back up method required for 7 days
128
What to do if missed CHC (24-48 hours late)
Take pill ASAP
Continue taking remaining pills at usual time
No additional contraceptive method needed
Emergency contraceptives usually not needed
129
What to do if missed CHC dose (>48 hours)
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
Twirla
30mcg ethinyl estradiol and 120mcg levonorgestrel/day
Transdermal contraceptive patch
Not first line in BMI >30
131
Xulane
150mcg norelgestromin and 35mcg ethinyl estradiol/day
| Not first line in weight >90kg
132
Transdermal patch BBW
Women over 35 years who smoke should not use
133
Transdermal patch counseling points
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
What to do if a transdermal patch was off for <48 hours?
Apply new patch ASAP
Keep same patch change day
No backup method needed
135
What to do if transdermal patch is off >48 h
Apply new patch ASAP
Keep same patch change day
Use back up contraception for 7 days
136
NuvaRing
Delivers 0.12mg etonogestrel and 0.015mg ethinyl estradiol per day
Similar efficacy and ADRs as oral CHCs
Better adherence than oral CHCs
137
NuvaRing counseling points
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
What to do if NuvaRing falls out
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
Annovers
13 mcg ethinyl estradiol and 150mcg segesterone acetate QD
Insert for 3 weeks then remove for one week
Used for 1 year
140
Initiating Annovera
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
Annovera counseling points
If Annovera falls out reinsert within 2 hours. If out for > 2 hours use backup method for 7 days
142
Advantages of progestin only contraceptives
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
Progestin only pills disadvantages
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
Depot-medroxyprogesterone acetate (DMPA)
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
DMPA BBW
Bone mineral density decrease
146
DMPA AE
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
Nexplanon
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
Nexplanon AR
Menstrual irregularities most common- spotting, prolonged bleeding, amenorrhea
Prolonged bleeding (short course NSAIDS, 10-20 days estrogen)
Depression
Breast tenderness
Weight gain
149
IUD contraindications
```
Pregnancy
PID
Current STD
Undiagnosed abnormal vaginal bleeding
Malignancy of genital tract
Uterine abnormalities
Wilsons disease (copper IUD)
```
150
Copper containing IUD
Paragard
Lasts 10 years
Increases menstrual flow
Releases copper ions
151
Levonorgestrel intrauterine systems (LNG-IUS)
Mirena- lasts 7 years
Liletta- 6 years
Skyla- lasts 3 years
Kyleena- 5 years
152
IUD warning signs
```
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
Checking for IUD strings
Check once monthly
| May be missing if strings have moved, pregnancy, uterine perforation, IUD expulsion
154
Emergency contraception
```
Can be given up to 72-120 hours after unprotected intercourse
Methods:
levonorgestrel and ulipristal
Yuzpe method
Copper IUD
```
155
Yuzpe method
2 doses of oral CHC 12 hours apart
100mcg ethinyl estradiol and 0.5-1 levonorgestrel
Most effective within 72 hours
156
Copper IUD
May be placed up to 7 days after intercourse
| Most effective with a failure rate of only 0.09%
