Exam 1 Flashcards
Hyperprolactinemia hormone changes and organ
Increase prolactin
Organ- pituitary gland
Acromegaly hormone changes and organ
Hormone changes- increase growth hormone
Organ- pituitary gland
Cushing’s disease hormone changes and organ
Hormone changes- increase glucocorticoids (cortisol)
Organ- adrenal gland
Growth hormone deficiency hormone changes and organ
Hormone changes- decrease growth hormone
Organ- pituitary gland
Addison’s disease hormone changes and organ
Hormone changes- decrease glucocorticoids (cortisol), decrease mineralocorticoids (aldosterone)
Organ- addison’s disease
Hyperaldosteronism hormone changes and organ
Hormone changes- increase mineralocorticoids (aldosterone)
Organ- adrenal gland
What is prolactin regulated by?
Regulated by inhibitory effects of dopamine
Prolactin secretion
Secreted in a pulsatile fashion
Prolactin promotes what?
Lactation, breast development, and reproductive function
Hyperprolactinemia
Persistent prolactin concentrations >25 mcg/L
Most commonly affects women ages 24-35 with about 24 cases per 1,000 person years
Etiology of hyperprolactinemia
Pituitary tumors Drug-induced (dopamine antagonists) CNS lesions Hypothyroidism Idiopathic
Drug induced hyperprolactinemia
Dopamine antagonists- antipsychotics, metoclopramide
Prolactin stimulators- estrogens, progestins, SSRIs, 5HT1 receptor agonists, Benzos, MAO inhibitors, TCAs, opioids, H2 receptors antagonists
Other- verapamil
Hyperprolactinemia clinical presentation female
menstrual cycle changes: oligomenorrhea or amenorrhea Galactorrhea Infertility Decreased libido Hirsutism Acne
Hyperprolactinemia clinical presentation male
Decreased libido Erectile dysfunction Infertility Reduced muscle mass Galactorrhea Gynecomastia
Clinical sequelae of hyperprolactinemia
Osteoporosis, ischemic heart disease
Hyperprolactinemia medications
Cabergoline
Bromocriptine
Cabergoline
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
AE of cabergoline
GI: Nausea, vomiting, constipation
CNS: headache, dizziness, anxiety, depression
Nasal decongestion
Dose adjust for hepatic failure
Bromocriptine
MOA: D2 receptor agonist
1.25-2.5mg QD at bedtime
Increase weekly based on prolactin levels
Bromocriptine AE
CNS: headache, lightheadedness, dizziness, nervousness, fatigue
GI: nausea, abdominal pain, diarrhea (administer WF)
Pregnancy with hyperprolactinemia treatment
Recommend discontinuing cabergoline or bromocriptine
Hyperprolactinemia monitoring and follow-up
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
Growth hormone
GH has direct anti-insulin effects
Growth-promoting effects mediated by insulin-like growth factors (ICF’s), which directly stimulate cell proliferation and growth
Growth hormone secretion
Secreted by anterior pituitary in pulsatile fashion
Acromegaly
Excessive GH production
Etiology: GH-secreting pituitary tumor
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
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
Management of acromegaly
Transsphenoidal surgery (most patients) Persistent disease/incomplete surgery- Medications -SRL, DA, Pegvisomant Consider SRT (conventional radiation) if not medication candidate
Somatostatin analogs
1st line for acromegaly
Octreotide, lancreotide, pasireotide
IM every 28 days
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
Dopamine agonists
Acromegaly treatment
Bromocriptine and cabergoline
MOA: causes paradoxical decrease in GH
Dosing: similar to hyperprolactinemia, but doses may be higher
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
Pegvisomant AE
GI: nausea, diarrhea
Reversible LFT elevation (monitor)
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)
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
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
Hormones in adrenal cortex:
Zona glomerulosa
Makes aldosterone
Hormones in adrenal cortex: Zona fasciculata
Makes cortisol
Hormones in adrenal cortex: Zona reticularis
Makes testosterone
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
Primary adrenal insufficiency, Addisons disease medications causes
Ketoconazole
Phenytoin
Rifampin
Phenobarbital
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)
Clinical presentation of addison’s disease
Hyperpigmentation
Weight loss
Dehydration
Hyponatremia
Elevated BUN
Secondary- aldosterone secretion is preserved
Abnormal response to corticotropin stimulation test
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
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
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
Addison’s disease monitoring and follow up
Every 6-8 weeks
Relief of symptoms
Avoid development of Cushing syndrome features
Cushing’s syndrome
Excessive cortisol production
Etiology:
Exogenous administration
Endogenous:
-ACTH-dependent (pituitary adenomas, ectopic ACTH- secreting tumor)
-ACTH-independent (adrenal adenomas, adrenal carcinomas)
Cushing’s syndrome: clinical presentation
Central obesity, facial rounding, myopathies, muscular weakness, buffalo hump, HTN, osteoporosis, amenorrhea, hirsutism
Hyperaldosteronism clinical presentation
Muscle weakness, fatigue, parethesias, headache, HTN, tetany/paralysis, polydipsia/nocturnal polyuria
Hyperaldosteronism treatment
Aldosterone receptor antagonists
Amiloride
Eplerenone
Spironolactone
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
Hyperthyroidism evaluation
Radioactive iodine uptake (RAIU) test
Increased RAIU= overproduction of T3 and T4
Decreased RAIU- excess T3 and T4 not due to overproduction
Total T4 normal value
4.8-10.4 mcg/dL
Free T4 normal value
0.8-1.4 ng/dL
Total T3 normal value
59-156ng/dL
TSH normal value
0.45-4.12 mcgIU/mL
RAIU at 24 hrs normal value
5-35%
Thyroglobulin autoantibodies normal value (Tg-Ab)
<200 IU/mL
Thyroid peroxidase autoantibodies (ATPO) normal values
<100 WHO units
TSH receptor-stimulating antibody normal value
Negative <140% of baseline
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
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
Hyperthyroidism treatment options
Methimazole
Propylthiouracil
Radioactive iodine
Surgery
Methimazole
Hyperthyroidism treatment
MOA- inhibit biosynthesis of thyroid hormone through multiple mechanisms (antithyroid)
30-60mg/day in 2-3 divided doses
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
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
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
AE of iodides
Hypersensitivity, iodism (metallic taste, burning mouth and throat, sore teeth and gums)
Gynecomastia
Radioactive iodine
Cytotoxic to thyroid gland
Contraindicated in pregnancy
Can repeat dose in 6 months if still hyperthyroid
Beta blockers
Inhibition of beta adrenergic receptors
Used for symptom control (palpitations, anxiety, tremor, heat intolerance) of hyperthyroidism
Propranolol most common.
Subclinical hyperthyroid
Low TSH, normal T4 and T3
Increased risk of mortality, Afib, hip fractures
Treat is age >65 with TSH <0.1mIU/L
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
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
Thyroid storm
Life-threatening emergency
Presentation- fever, tachycardia, dehydration, delirium, coma, N/V,D
Precipitating factors- infection, trauma, surgery, RAI tx, withdrawal of ATDs
Thyroid storm tx
Suppress thyroid hormone formation and secretion
Antiadrenergic therapy
Corticosteroids
Hyperthyroidism monitoring and follow up
Monthly immediately after initiation until euthyroid
Note signs and symptoms of hyperthyroidism
Monitor for hypothyroidism
Hypothyroidism
Overt: elevated TSH with decreased free T4
Subclinical: elevated TSH with normal free T4
Etiology of hypothyroidism
Iodine insufficiency
Autoimmune thyroid diseases (AITs)- Hashimotos
Iatrogenic
Pituitary or hypothalamic diseases
Sources of iodine
Fish (cod, tuna) Seaweed Shrimp Dairy product Iodized salt
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
Hypothyroidism labs
Total T4, Free T4, Total T3- LOW
TSH- HIGH
RAIU at 24 hours- not indicated
Tg-Ab, ATPO or TPO-Ab- Present
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
Levothyroxine
Synthetic T4 prohormone
DOC- stable, predictable potency, inexpensive, accurate
Abs affected by food, oral bioavailability 70%
Well tolerated
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
Liothyronine
Synthetic T3
Higher incidence of CV AE, higher cost, TID, longer time to achieve euthyroid, difficult to monitor
Liotrix
Synthetic T4 and T3 in 4:1 ratio
High cost
Dessicated thyroid
Derived from pig, beef, sheep
Inconsistent potency (up to 15% variation in T4 and 10% in T3)
Allergic rxns
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
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.
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
Hypothyroidism in pregnancy TSH measurement
1st trimester- 0.2-2.5 mU/L
2nd and 3rd- 0.3-3 mU/L
Treatment of hypothyroidism in pregnancy
Levothyroxine
Increase dose of T4 by 30-50% by week 4-6
Normal TSH
0.45-4.12 mU/L
Myxedema coma
Decompensated hypothyroidism
Clinical features- hypothyroidism, delirium, coma, diastolic HTN, hypoventilation
60-70% mortality rate
Myxedema coma precipitating factors
Burns, GI hemorrhage, hypoglycemia, infection, stroke, surgery, trauma
What are the most effective contraceptives?
IUDs and progestin only implant
Oral pills and rings have a 9% efficacy with typical use
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
Combined hormonal contraceptives (CHC) MOA
Progestin- thickens cervical mucus
Estrogens- Suppress FSH
Progestin MOA BC
Thickening of cervical mucus
- Prevent sperm penetration
- Slow tubal motility
- Delay sperm transport
Block LH surge, inhibiting ovulation
Estrogens BC MOA
Suppress FSH, blocking LH surge and inhibiting ovulation
Stabilize endometrial lining and provide cycle control
Estrogens used in CHC
Ethinyl estradiol
mestranol (metabolized to ethinyl estradiol)
Estradiol valerate
Estrogen in CHC dosing
High >/= 50 mcg
Regular >/= 30-35mcg
Low >/= 10-20mcg
1st gen progestins used in CHC
Norethindrone
Ethynodiol diacetate
Norethynodrel
2nd gen progestins used in CHC
Levonorgestrel
Norgestrel
MOST androgenic
3rd gen progestins used in CHC
Desogestrel
Etonogestrel
Norgestimate
4th gen progestins used in CHC
Anti-androgenic, may increase K
Drospirenone, dienogest, segesterone
Androgenic AE
Weight gain Acne Hirsutism Oily skin Increased libido
Which progestin do you switch to if a pt is experiencing androgenic AE?
4th gen- anti-androgenic
Drospirenone, dienogest, segesterone
Which progestin is most likely to cause androgenic AE?
2nd gen
Levonorgestrel
Norgestrel
ADR associated with excess estrogen
Nausea, breast tenderness, increased BP, HA, edema/bloating
Management- decrease estrogen amount, consider progestin only options
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
ADR associated with excess progestin
Breast tenderness, depression or irritability, fatigue, constipation
Manage by decreasing progestin
ADR associated with progestin deficiency
Late cycle BTB
Hypomenorrhea
Amenorrhea
Weight loss
Manage by increasing progestin
ADR associated with excess androgen
Increase appetite, increased libido, oily skin/acne, hirsutism, weight gain
Serious AE with CHC
Abdominal pain Chest pain Headaches Eye problems Severe leg pain
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
Abx reactions with CHC
Rifampin
Case reports with tetracyclines and penicillin derivatives
Anticonvulsant interactions with CHC
Phenobarbital, phenytoin, carbamazepine- induce metabolism of estrogen and progestin
Lamotrigine- decrease lamotrigine efficacy
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
Disadvantages of CHC
AE Patient adherence No protection against STDs Increased BP May decrease milk production during lactation
Monophasic CHC
Same amounts of estrogen and progestin for 21 days, then 7 days of placebo
Multiphasic CHC
Varying amounts of estrogen and progestin for 21 days then 7 days placebo
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
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.
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
Quick start method of CHC
First active pill taken day of visit regardless of timing
Back up method required for 7 days
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
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
Twirla
30mcg ethinyl estradiol and 120mcg levonorgestrel/day
Transdermal contraceptive patch
Not first line in BMI >30
Xulane
150mcg norelgestromin and 35mcg ethinyl estradiol/day
Not first line in weight >90kg
Transdermal patch BBW
Women over 35 years who smoke should not use
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
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
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
NuvaRing
Delivers 0.12mg etonogestrel and 0.015mg ethinyl estradiol per day
Similar efficacy and ADRs as oral CHCs
Better adherence than oral CHCs
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
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
Annovers
13 mcg ethinyl estradiol and 150mcg segesterone acetate QD
Insert for 3 weeks then remove for one week
Used for 1 year
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
Annovera counseling points
If Annovera falls out reinsert within 2 hours. If out for > 2 hours use backup method for 7 days
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
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
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
DMPA BBW
Bone mineral density decrease
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
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
Nexplanon AR
Menstrual irregularities most common- spotting, prolonged bleeding, amenorrhea
Prolonged bleeding (short course NSAIDS, 10-20 days estrogen)
Depression
Breast tenderness
Weight gain
IUD contraindications
Pregnancy PID Current STD Undiagnosed abnormal vaginal bleeding Malignancy of genital tract Uterine abnormalities Wilsons disease (copper IUD)
Copper containing IUD
Paragard
Lasts 10 years
Increases menstrual flow
Releases copper ions
Levonorgestrel intrauterine systems (LNG-IUS)
Mirena- lasts 7 years
Liletta- 6 years
Skyla- lasts 3 years
Kyleena- 5 years
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
Checking for IUD strings
Check once monthly
May be missing if strings have moved, pregnancy, uterine perforation, IUD expulsion
Emergency contraception
Can be given up to 72-120 hours after unprotected intercourse Methods: levonorgestrel and ulipristal Yuzpe method Copper IUD
Yuzpe method
2 doses of oral CHC 12 hours apart
100mcg ethinyl estradiol and 0.5-1 levonorgestrel
Most effective within 72 hours
Copper IUD
May be placed up to 7 days after intercourse
Most effective with a failure rate of only 0.09%
