Exam 6 (Renal and GU) Flashcards
1
Q
Where is right kidney
A
Under liver.
L1-L4
2
Q
Where is left kidney
A
T12-L3
3
Q
Hilum
A
Central region where ureter, renal artery, and renal vein attach to kidneys
4
Q
Ureter
A
Connects kidney to bladder constantly draining urine into bladder.
Exits kidney at ureteropelvic junction
5
Q
Kidney cortex
A
Outer region.
URINARY GENERATION
Holds renal capsule, PCT, DCT, glomeruli
6
Q
Kidney Medulla
A
Middle layer
URINARY GENERATION AND DRAINAGE
Consists of medullary pyramids, renal columns, loop. of henle, collecting ducts
7
Q
Pelvis of Kidney
A
Inner central cavity
URINARY DRAINAGE
Empties into ureter
8
Q
Blood flow through kidney
A
Bowman’s capsule –> Proximal tubule -> Descending loop of Henle –> Ascending loop of Henle –> Distal tubule
9
Q
Nephron
A
Functional unit of kidney
Millions in each kidney.
Mostly in cortex
Bowman’s capsule
PCT
Loop of Henle
DCT
Collecting duct
10
Q
Cortical Nephrons
A
85% of nephrons
In outer cortex
Loop of Henle short
Filter toxins and regulate Electrolytes
Less strict in filtration
11
Q
Juxtamendullary Nephrons
A
15% of nephrons
Deep in cortex
Loop of Henle long so project into medulla
Reabsorb higher higher proprtion of glomerular FILTRATION rate.
Stimulate Na retention in states of low perfusion
12
Q
Glomerulus
A
Filter
Primary site of urine formation
In Bowman’s Capsule
13
Q
Bowman’s Capsule
A
Double walled funnel
Reservoirs for glomerular filtrate
14
Q
PCT
A
Proximal convoluted tubule
High water permeability
2/3 glomelular filtrate reabsorbed
Reabsorbs NaHCO3, NaCL, K, glucose, AA, water
Adjusts pH
15
Q
Loop of Henle
A
Allows water to pass from filtrate to interstitial fluid.
Ascending limb is water impermeable.
Descending limb is water permeable
16
Q
Distal tubule
A
Selectively secretes and absorbs ions to maintain blood pH and electrolytes
17
Q
Collecting ducts
A
Rabsorbs solutes and water from filtrate
18
Q
Glomerular filtration barrier layers
A
- Fenestrated endothelium
- Glomerular basement membrane
- Podocyte slit diaphragm
19
Q
Podocytes
A
Form slit diaphragm of glomerullus
20
Q
Steps of Urine formation
A
- Glomerular Filtration
- Tubular reabsorption
- Tubular secretion
21
Q
Why does the kidney excrete electrolytes
A
AWETBED
Acid-base balance
Water balance
Electrolyte balance
Removal of toxins
BP control
Erythropoietin production
D vitamin metabolism
22
Q
ADH effect on kidney
A
Permeability of collecting tubules
Fluid regulation
Increases water reabsorption
Affects specific gravity
23
Q
Aldosterone
A
Increases water and Na absorption by DCT.
Decreases potassium by increasing excretion.
Made and released by adrenal cortex
24
Q
Calcitriol
A
Converted from calcidiol into calcitriol (active form of vitamin D) by kidney
25
Erythropoietin
Stimulates red blood cell production in bone marrow.
Released from kidneys when O2 is low.
26
Renalase
Metabolizes catecholamines, affects HR and BP
27
Renin
BP regulation via angiotensin
Released from kidneys when BP low to start RAAS pathway
28
Kidney role in glucose regulation
Catabolism of peptide hormones like insulin.
Can perform gluconeogenesis during times of fasting
29
How much cardiac output goes to kidneys
20-25%
30
Decreased perfusion to kidney
Stimulates RAAS system to increases blood pressure
31
Prerenal failure
Most common
Caused by decreased perfusion
32
Intrarenal failure
Direct damage to renal parnchyma
33
Postrenal failure
Obstruction
34
Types of acute renal failure
Prerenal
Intrarenal
Postrenal
35
Chronic Renal failure
Lasts longer than 3 months
36
Three phases of acute kidney injury
Oliguric - decreased output
Diuretic - increased output
Recovery - GFR normalizes
37
First phase of acute kidney injury
Oliguric
Decreased urine output
Edema
Decreased Na and water absorption
Hypervolemic
Weight gain
HTN
BUN and creatinine levels rise
38
Second phase of acute kidney disease
Diuretic
Increased urine output
Improved Na and water absorption.
Hypokalemia and hyponatremia can occur.
Hypovolemic
Weight loss
Dehydration
BUN and creatinin levels rise
39
Third phase of kidney disease
Recovery
Normal urine output
Recovery of GFR
40
Renal failure symptoms
Hyper/hypotension depending on phase
Dy mucous membrane
Poor skin turgor
Decrease/increase urine output depending on phase.
Mental status changes
Muscle aches
Nausea
41
First thing to look at to check for renal failure
Look at urine output and concentration of the urine (color)
42
First sign of kidney failure in lab
Albumin in the urine
43
First sign of kidney failure
Decreased urine output
44
Most accurate measure of GFR
Creatinine clearance because creatinine is filtered by glomeruli but not reabsorbed by tubules
45
Cast formation
Occurs in DCT and collecting ducts when Tamm-Horsfall protein is secreted by epithelial tube cells.
46
Tam Horsfall protein
Attracts adhesion of other tubular particles (cells, bile, hemoglobin, albumin, immunoglobulins).
Forms casts
47
Five main sections of nephrons
Glomerulus
PCT
Thin descending and thick ascending loop of Henle
DCT
Collecting duct
48
Diuretics that work in PCT
Carbonic anhydrase inhibitors
Osmotic diuretics
49
Diuretics that work in loop of henle
Loop diuretics
50
Diuretics that work in DCT
Thiazides
51
Diuretics that work in collecting duct
Potassium sparing diuretics
(Aldosterone inhibitors
Epithelial sodium channel antagonists)
52
What regulates bicarbonate reabsorption in PCT
Carbonic anhydrase
53
PCT drug targets
Carbonic anhidrase
SGLT2
Osmolality (Mannitol)
54
Thick ascending limb of Loop of Henle
High in NaCl reabsorption via Na/K/Cl cotransporter (NKCC2).
Diluted in lumen.
Impermeable
K transported through NKCC2
55
Loop of Henle drug target
N/K/CL cotransporter type 2 (NKCC2)
56
DCT
Distal convoluted tubule
NaCl reabsorption via Na/Cl cotransporter (NCC)
Dilutes tubular fluid
Results impermeability to water
57
DCT drug target
Na/Cl cotransporter
Thiazide diuretics
58
Collecting duct system
Final site of NaCl reabsorption
Determines Na concentration
Most important site of K secretion
59
Principal cells
In Collecting duct
Na reabsorption
K excretion
Water transport
No apical cotransporters
Regulated by aldosterone
60
Intercalated cells
In collecting duct.
Alpha does H secretion
Beta does bicarbonate secretion
61
Na and K relationship
Na transported back to blood via Na/K pump.
Na reabsorption happens more often than K secretion resulting in negative lumen.
Drives Cl back into blood.
Draws K into lumen from cell
62
Principal cells drug targets
Potassium sparing diuretics
Aldosterone receptor for potassium aldosterone antagonists
Epithelial Na channel for and epithelial Na channel antagonists
63
Acetazolamide
Carbonic anhydrase inhibitor
Decreases NaHCO3 rabsorpton
Attack at PCT
64
Carbonic anhydrase inhibitor mechanism
Acetazolamide
Blocks carbonic anhydrase thus inhbiting formation of carbonic acid.
Carbonic acid doesn't dissociate into HCO3 and H.
No driving force for Na to be reabsorbed
Increased Na excretion in PCT
65
Acetazolamide uses
Carbonic anhydrase inhibitor
NOT used as diuretic
Glaucoma
Urinary alkalinization
Metabolic alkalosis
Acute altitude sickness
66
Acetazolamide adverse effects
Drowziness
Metabolic acidosis
Renal stones
K wasting
Neurotoxicity if renal failure
67
Mannitol
Osmotic diuretic
Solute that draws water out of cells.
Decreases intracranial pressure
Not really used as diuretic
68
Loop diuretics
Most effective (potent) diuretic against highest reabsorption of NaCl in thick ascending limb of Henle's loop
69
Loop diuretics mechanism
Inhibits NKCC2 in thick ascending limb.
Decreases reabsorption of Na K Cl
Diminish lumen positive potential increasing secretion of K Mg and Ca.
70
Loop diuretics uses
Acute pulmonary edema.
Hyperkalemia
Hypercalcemia
71
Loop diuretic adverse effects
Acute hypovalemia (hypotension)
Hypokalemia
Hypomagnesemia
Ototoxicity
Hyperuricemia
72
Thiazides mechanism
Block Na Cl cotransporter in DCT decreasing Na and Cl reabsorption.
Low ceiling - at certain dose we don't see increased effect
73
Thiazide uses
HTN
Heart failure
Prevention of Ca containing kidney stones caused by hypercalciuria
74
Thiazide adverse effects
Hypercalcemia
Hyperuricemia
Hyperglycemia
Hyperlipidemia
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypovolemia
75
Potassium sparing diuretics
Antagonize effects of aldosterone by inhibiting Na reabsorption and inhibiting K excretion.
Aldosterone antagonists
Epithelial Na channel antagonists
76
Aldosterone antagonists method of action
Potassium sparing
Inhibit aldosterone receptor.
Decreases reabsorption of Na.
Decreases secretion of K
77
Spironolactone
Aldosterone antagonist
Potent inhibitor of aldosterone receptor
Used in acne and hirsutism.
Active at progesterone receptors
78
Eplerenone
Aldosterone antagonist
Less active on androgen and progesterone receptors
79
ENaC Antagonist mechanism
Potassium sparing diuretic.
Directly inhibits ENaC leading to decrease of Na reabsorption and decrease of K secretion.
80
ENaC antagonist
Potassium sparing diuretic
Mostly ued for K sparing effects, not diuretic effects
Ex. amiloride triametrene
81
Amiloride
ENaC that is not metabolized
82
Triametrene
ENaC that is metabolized.
Has very short half life
83
Potassium sparing diuretic uses
Edema
Hypokalemia
Heart failure
Resistant hypertension
Polycystic ovary syndrome
84
Potassium sparing diuretics adverse effects
Hyperkalemia
Spironolactone-gynecomastia
Triamterene (kidney stones)
85
Wolffian ducts
Become male reproductive organs
AKA mesonephric
86
Mullerian ducts
What become female reproductive organs
87
Reproductive embriology order in males
Primordial germ cells--> Spermatagonia + Sertoli cells--> Male gametes
88
Leydig cells
Produce testosterone
89
What causes differentiation in whether something ends up male or female
Presence of testosterone.
Decided at fertilization though
XY vs XX
90
Primordial germ cells
What males and females both start out as
91
Reproductive embryology order in females
Primordial germ cells --> oogonia --> granulosa and thecal cells --> estrogen and progestin in mature females
NO testosterone during this point so Wolffian duct degenerates
92
Complete Androgen Insensitivity Syndrome
46 XY DSD
Genotypically male but phenotypically female
No androgen receptors so testosterone can't do its job.
Diagnosed by failure of menstrual cycle
93
Deficiency of 5 alpha-reductase
46 XY DSD
Genotypically male but phenotypically female
No 5 alpha reductase to convert testosterone into DHT (usable form)
94
Congenital Adrenal Hyperplasia
46 XX DSD
Genotypically female but phenotypically male
Impaired cortisol synthesis.
Virilization of female fetus
Excessive/deficient production of androgens/hormones
95
When do testes begin to enlarge
9-14
96
Male puberty
Testes inlarge
Spermatogenesis in seminiferous tubules
Scrotum and penis enlarge
INcreased testosterone leads to thicker hair, deeper voise, increased muscle strength
97
When does breast enlargement start
8-10
98
Female puberty
Breast enlargement
Ovarian cycle starts
ENlargement of uterus, labia majora, and labia minora
Widening of pelvis
99
Menarche
First period
100
Adrenarche
Surge of hormones and androgens leading to pubic and axillary hair before puberty
101
Precocious puberty
Early puberty
102
Gynecomastia
Enlargement of male breast
Occurs when estrogen levels are elevated in neonatal period or before normal male puberty.
Also can happen in elderly men
103
Testicle function
Secreting testosterone and make sperm
104
Epidymitis function
Store sperm
105
Vas deferens function
Expel sperm to urethra during ejaculation
106
Semeinal vesicles function
Produce fluid for nourishment for ejaculated sperm
107
Prostate gland function
Secretes acid phosphatase, contracts to deliver secretions into urethra, and liquifies semen until it gets to female reproductive tract.
Makes prostate specific antigen
108
Penis function
Urination and intercourse
109
Three phases of spermatogenesis
1. Proliferation of spermatogonia
2.Generation of genetic diversity via miosis
3. Maturation of sperm
110
LH job in males
Stimulate Leydig cells to PRODUCE testosterone
111
FSH job in males
Stimulates Sertoli cells to secrete androgen binding protein that INCREASES testosterone.
Inhibin also secreted from sertoli cells that works in negative feedback against FSH
112
Phases of ejaculation
1. Erection
2. Emission
3. Ejaculation
113
Erection
Sinusoidal spaces fill with blood
114
Emission
Spermatozoa and seminal plasma move into urethra
115
Ejaculation
Semen ejected from urethra
116
Stages of sexual response
1. Excitement
2. Plateau
3. Orgasm
4. Resolution
117
Excitement phase of sex
Penile erection
Vaginal lubrication
118
Plateau phase of sex
Vascular congestion
Engorgement of scrotum and labia
119
Orgasm phase of sex
Ejaculation in males
Pleasure
Rhythmic contractions of perineum
120
Resolution phase of sex
Penile falccidity
Vaginal relaxation
Refractory period in males
121
Ovaries
Where oogenesis occurs and eggs formed
Major source of sex steroids and hormones
122
Fallopian tubes
Transport ovum and sperm to fertillization
Transports zygote to uterus for implantatoin
123
Where does fertilization happen
Ampulla of Fallopian tube
124
Uterus
Supports growing fetus during preg.
Undergoes dramatic changes during menstrual cycle.
Growth through hyperplasia in preg.
Fundus
Corpus
Cervix
125
Vagina
Receive penis in intercourse
Temporarily retain sperm
Tube extending from cervix to vaginal opening.
Many mucus secreting glands for lubrication
126
Pelvic inflammatory disease
Caused by STD.
Usually chlamydia and gonorrhea
127
What increases risk of ectopic pregnancy
SCarred fallopian tubes.
Most common site of implantation in ectopic preg is ampulla
128
Fundus
In Uterus.
Area above opening to fallopian tubes
129
Corpus
Main body of uterus
130
Cervix
lower portion of uerus that extends and protrudes into vagina
131
Vulva
Collective name for female external genitalia Includes Lower 1/3 of vagina, labia, clitorus
132
Where does Oogenesis occur
Ovaries
133
Oogenesis
Forming of eggs
OOgonium --> 1º Oocyte --> 2º Oocyte --> Ovum
134
Graafian Follicle
Dominant Follicle
Emerges and LH surge makes it a secondary Oocyte.
Bursts and ruptures during period
135
When is Oogenesis complete
Fertilization
Becomes Ovum
136
Menstrual cycle phases
1. Follicular- 1-14
2. Ovulatory - 13-15
3. Luteal - 15-28
137
Follicular phase
Days 1-14
Day 1 is first day of bleeding
Primary follicles develop
Dominant follicle emerges
138
Ovulatory phase
Days 13-15
LH surge and increased estrogen
Ptimary oocyte completed meiosis I
Dominant follicle rupture causing ovulation.
Oocyte released
139
Best time to get pregnant
Days 12-14
140
When is ovulaton
Day 14
141
Luteal Phase
Days 15-28
Corpus luteum formed
If no preg corpus luteum degenerates.
If preg continued progesterone secretion essential.
142
Hydatidiform mole
Benign molar pregnancy
Incompatible with life.
Looks like cluster of grapes
143
Implantation
Fertilized egg develops 6-7 days prior to implantation.
Now a blastocyst
Endometrium develops
144
3 stages of implantation
1.Apposition - formation of loose connection in endometrium
2.Adhesion - microvilli extend from cell
3. Invasion - Embryo becomes completely embedded in endometrium of uterus
145
Placenta function
Transport glucose, LDL, AA, large molecules to fetus between maternal and fetal circulations.
Secretion of hormones to maintain function
146
Placenta hormone secretion
Estrogen for growth of uterus starts 12 weeks in.
Progesterone starts at 9 weeks in
Progesterones for maintaining endometrium and reducing uterine contractions to prevent premature birth.
Progesterone drops at the end of preg to let birth happen
Estrogen drops at end to allow milk let down
147
Placental peptides examples
Human chorionic gonadotropin (hCG)
Human chorionic somatomammotropin hormone (hCS)
Start off high at begining of preg. Drop off at the end
148
hCG
Human chorionic gonadotropin
Placental peptides
Keeps corpus luteum from degenerating.
Allows ocntinued progesterone to be secreted for early preganncy until placenta can take over making and secreting progesterone
149
hCS
Human chorionic somatomammotropin hormone
Plancental hormone
Stimulates production of fatty acid and ketones for energy for fetus and placenta
Promotes mammary gland development
Creates state of insulin resistance in mother to promote availability of glucose for fetus
150
What keeps labor going (parturition)
Prostaglandin and oxytocin
151
Phase 0 of parturition uterine activity
Majority of pregnancy with uterus inactive/relaxed
152
Phase 1 of parturition uterine activity
Cervix dilates and amniotic fluid ruptures (water breaks).
False contractions
153
Phase 2 of parturition uterine activity
Fetus is expelled from uterus
154
Phase 3 of parturition uterine activity
Placenta is birthed
155
What is breast milk made of
Lactose
Triglycerides
Protein
156
Colostrum
Liquid gold.
Very nutritious breast milk made after first few days of parturition
157
What hormone does breast milk production
Prolactin
158
What stimulates milk let down
Oxytocin. Works in positive feedback loop.
159
When does milk production start
about 2 days after parturition because estrogen and progesterone were just very high
160
Suckling reflexes
Prolactin and oxytocin stimulated by baby sucking on breast. Positive feedback
161
What happens to other organ systems during preg
Blood volume and coagulabibity increases\
Alveolar ventilation increases
GFR increases
Nutritional demands increase
Suppression of immunity
162
Overactive bladder meds
Antimuscarinics
beta-3 adrenergic agonists (-begron)
163
Benign prostatic hyperplazsia drugs
alpha-1 adrenergic agonist (-osin)
5-alpha reductase inhibitors (-asteride)
164
Overactive bladder
Frequent strong urge to urinate even when not really necessary
165
Goals of overactiv bladder meds
Decrease urge frequency
Increase voided volume
166
Antimuscarinic meds mechanism
Block M3 receptors on bladder.
Decreases freq of bladder contractions and increases capacity
167
Most selective antimuscarinics
DariFENACIN
SoliFENACIN
Fewer adverse effects
168
Trospium
Antimuscarinic
Doesn't undergo CYP450 metabolism.
So good option for someone in liver failure
Does not cross BBB so fewer CNS effects
169
Antimuscarinic adverse effects
Dry mouth
Constipation
Blurred vision
CNS impairments
170
Ocybutyynin
Antimuscarinic
OTC patch
Gel
171
Beta-3 adrenergic agonist mechanism
Bind and activate B3 adrenergic receptors.
Increases cAMP
Relaxes detrusor muscle increasing bladder capacity
172
Beta-3 adrenergic agonist adverse effects
Urinary retention
UTI
Mirabegron increases BP inhibits CYP2D6, and causes angiodema
173
Benign prostatic hyperplasia (BPH)
Non-malignant enlargement of prostate
Common in men over 60
Increase in size (static) and/or tone (dynamic)
174
alpha-1 adrenergic antagonist
-osin
address tone of prostate
175
alpha-1 adrenergic receptors subtypes locations
A - prostate
B - prostate and vasculature
D - vasculature
176
alpha-1 adrenergic antagonist mechanism
Block prostatic alpha-1A and alpha1-B this is in prostate and blood vessels
177
Adrenergic antagonis selective for alpha 1A
Silodosin
Tamsulosin
no Z in name
178
alpha-1 adrenergic receptor antagonist adverse effects
Dizziness
Orthostatic hypotension
Tachycardia
Drowsiness
Inhibition of ejaculation
Retrograde ejaculation (shooting blanks)
179
5-alpha reductase inhibitors
-asteride (five asteroids coming to blow up prostate to reduce size)
Address size of prostate
180
5-alpha reductase inhibitor mechanism
Irriversibly inhibits alpha-5 reductase.
Testosterone not turned into usable form DHT.
Decreased growth signaling
Improved urine flow
181
5-alpha reductase inhibitor Adverse Effects
Risk of prostate cancer.
Decreased ejaculate and libido
Erectile disfunction
Oligospermia
Teratogenic
182
Day 2-7
FSH increase
183
Day 7
Estrogen increase
184
Day 14
LH FSH surge in response to estrogen causing ovulation
185
Day 15
Ovulation.
Progesterone increases
186
Day 21-28
Estrogen and progesterone drop if no fertilization
187
Day 28
Wthdrawal of estrogen and progesterone
188
Estrogen use as contraceptive
Blocks GnRH production from hypothalamus and FSH production from ant pit.
Prevents follicle development
189
Progestin use as contraceptive
Blocks GnRH production from hypothalamus and LH production from ant pit.
No LH surge preventing ovulation half the time
Thickens cervical mucus to inhibit sperm migration.
Thins endometrium
190
What are the type of hormonal contraceptive
Estrogen and progestin
Or just progestin
191
Most common estrogen component in oral contraceptiv
Ethinyl estradiol
192
What is the design of taking birth control pills
21 active tablets
7 placebo tablets
mimic the natural process
193
Is combined pill or progestin only pill more effective
They are the same.
194
What is the main mechanism of progestin contraceptive
Thinning of endometrium
Thickening of cervical mucus
195
What is the main mechanism of combined (estrogen and progestin) contraceptive
Preventing ovulation (does it every time)
196
Combined oral contraceptives
Estrogen + Progestin
Mono bi or triphasic
Cyclic
197
Cyclic combined contraceptives
Traditional
Take active pills for 21-24 days.
Placebo for 7-4 days
24/4 recomended over 21/7 because can use lower estrogen content
198
Extended cycle combined contraceptive
Active pill for 84 days.
7 days of placebo.
Withdrawal bleeding every three months
199
Continuous cycle combine contraceptive
Actie pills taken every day
No withdrawal bleeding
No medical need for menstruation with oral contraception
Write "for continuous use" on Rx
200
Is natural or synthetic progesterone better on gettig past first past metabolism
Synthetic
201
What progestins have high affinity for androgen receptors
Levonorgestrel
Norgestrel
202
What progestins have low affinity for androgen receptors
Drospirenone
203
What progestins have high affinity for progesterone receptors
All of them
204
Estrogen negative feedback
INhibits GnRH LH and FSH.
Causing no ovulation.
Most important mechanism in combined contraceptives
205
What stimulates menstrual bleeding
Withdrawal of progestin
206
Non-contraceptive benefits of oral contraceptives
Reduction of dysmenorrhea
Reduction in pelvic pain from endometriosis
Reduction in premenstrual syndrome
Reduction in endometrial cancer
Reduction of acne
Reduction of hirsutism
207
Venous thromboembolism
Blood clots
Caused by estrogen effect on clotting cascade
Caused by combined oral contraceptives
208
Who should not be prescribed combined with oral contraceptive
35 yo smoker
CV disease
Hx of breast cancer
Migraine with aura
You CAN give these people progestin-only pill instead
209
Progestin-only pill
Supppresses GnRH and LH
210
Norethindrone
Older Progestin-only pill
Must be taken same time each day.
All tablets are active
Short duration of action
211
Drosperinone
Newer Progestin-only pill
Should be taken same time each day but more forgiving because have a longer half-life.
4 placebo pills
212
Drosperinone adverse affects
Hyperkalemia
Hyperglycemia in diabetics
Don't give to pts with adrenal or renal problems.
Don't give to pt with hx of cervical cancer
213
Norgestrel
Progestin-only pill
No rx required (OTC)
214
Benefits of progestin only pill
No weight gain
No increase in headache
Safe for CVD HTN who can't take combined pill
215
Progestin only pill adverse effects
Unscheduled bleeding
Increased prevalence of follicular ovarian cysts.
Drosperinone can cause hyperkalemia
216
IUDs as emergency contraception
Copper inserted within 120 hours
Hormonal inserted within 5 days
217
Plan B
Emergency contraceptive
Singl high does of levonorgestrel
Progestin
Must be taken within 72 hours
Less efective in women >165 lbs
218
Ulipristal
Prescribed emergency contraception.
Binds to progesterone receptor inhibiting or delaying ovulation.
Must be taken within 5 days.
Less effective in women >195 lbs
