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Reproductive Flashcards

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1
Q

Sonic Hedgehog gene?

A

Produced at the base of the limbs
Involved in patterning (anteriorposterior)
Mutation will cause holoprosencphalu

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2
Q

Wnt-7 gene?

A

Produced at ectodermal ridge

Necessary for proper organization along dorsal/ventral axis

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3
Q

FGF gene?

A

Provides lengthening of the limbs

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4
Q

Homeobox genes?

A

Hox mutations lead to appendages

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5
Q

Milestones in fetal developpment?

A

Week 1: blastocyte sticks at day 6
week 2: 2 layers
Week 3: three layers (cells from epiblast invginate—> primitive streak—> endoderm, mesoderm, ectoderm

Notochord arises from midline mesoderm

week 3-8: embryonic period (neuroectoderm and closes by week 4)
Organogenesis

Week 4: Heart begins to beat (has 4 limbs and 4 heart chambers)

week 6: Fetal cardiac activity is visible

week 8: fetal movements start

week 10: genitila have male and female characteristics

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6
Q

Parts formed by surface ectoderm?

A 
lens of the eyes
epithelial linings of the oral cavity 
sensory organs of the ear
olfactory epithelium
epidermis 
Sweat 
Mammary glands
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7
Q

Formed by neuroectoderm?

A 
Brain
CNS neurons
Autonomic ganglia
Melanocytes
Chromaffin cells of adrenal medulla
aortopulmonary septum
endocardial cushions
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8
Q

Formed by mesoderm?

A 
Muscle
Bone
Linings
Vagina
Kidneys
adrenal cortex
Dermis
Testes
Ovaries
Mesoderm defects
Vertebra defects
Anal atresia
Cardiac defects
Tracheo-esophageal fistula
Renal defects
Limb defects
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9
Q

what does endoderm form?

A

Gut tube epithilium (including anal canal above the pectinate line)

Urethra
Lower vagina 
lungs
liver
gallbladder
pancreas
eustachian tube
thymus
parathryroud
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10
Q

What is agenesis?

A

Absent organ due to absent premordial tissue

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11
Q

Aplasia?

A

Absent organ even in the presence of primordial tissue

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12
Q

Hypoplasia?

A

Incomplete organ developpement (premordial tissue present)

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13
Q

Disruption?

A

Secondary breakdown of of normal tissue or disruption

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14
Q

Deformation?

A

extrinsic disruption (occurs during embryonic period 3-8)

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15
Q

Malformation?

A

Intrinsic disruption (during embryonic period 3-8 days)

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16
Q

Sequence?

A

Abnormalities result from single 1 embryologic event

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17
Q

When are babies most suscpetible to teratogens?

A

From the 3rd to the 8th week
(organogenesis

Before week 3 (all or none effect) and after the 8th week (growth and function are affected)

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18
Q

List common medications that are teratogens ( and the effect)

A

ACE : renal damage
Alkylating agent: absence of digits
Aminoglycosydes: ototoxicity
Anti-epileptice: neural tube, cardiac, cleft palate, skeletal abnormalities, phalanx/nail hypoplasia, facial dysmorphism

Diethylstilbestrol: vaginal clear cell adenocarcinoma
Congenital mullerin anomalies

Folate antagonists: neural tube defects

Isotretinoin: multiple birth defects

Lithium: Ebstein anomaly

Methimazole: aplasia cutis congenita

Tetracyclines: discolored teeth

Talidomaide: limb defect, phocomelia, micromelia, flipper limbs

Warfarin: bone deformities, fetal hemorrhage, abortion, oprthalmologic abnormalities

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19
Q

effects of alcohol?

A

Itellectual disability

Fetal alchol syndrome

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20
Q

Effects of cocaine?

A

Low birth weight
Preterm birth
IUGR
placental abruption

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21
Q

Effects of smoking?

A 
Low birth weight 
Preterm labor
SIDS
IUGR
placental problems

Nicotine causes vasoconstrcition (CO impairs O2 delivery)

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22
Q

Lack or excess Iodine?

A

Congenital goiter or hypothyroidism

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23
Q

Maternal diabetes?

A

Caudal regression syndrome

Congenital heart defects

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24
Q

Methyl mercury?

A

Neurotoxicity (swordfish, shark, tilefish, lin

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25
Q

Vitamin A excess

A

High risk for spontaneous abortions

And birth defects

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26
Q

X-rays?

A

Microcephaly
Intellectual disability
Minimized by lead shielding

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27
Q

Symptoms of fetal alcohol syndrome?

A 
Mental retardation
Microcephaly
Facial abnormalities
Smooth philtrum
Thin vermillion brder
Small palpebral fissures
Limb dislocaton
Heart defects
Heart-lung fistulas
Holoprosencephaly
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28
Q

Dizygotic twins?

A

Faternal twins
2 eggs that are seperately fertilized by 2 different sperm
2 seperate amniotic sacs
2 zygots

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29
Q

Monozygotic twins?

A

1 fertilized egg (1 egg and 1 sperm) that splits early in pregnenacy
The timing of clevage determines the chorionicity and amnionicty

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30
Q

what is the most common type of monzygotic twins development?

A

Monochorionic (diamniotic) 75%

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31
Q

What are the fetal components of the placenta?

A

Cytotrophblast: inner layer of chorionic villi
Cytotophhoblast makes cells

Synctiotrophoblast: outer layer of chorionic villi
Synthesizes and secretes hormones hCG (structurally similar to LH) stimulates corpis luteum to secrete progesterone during first trimester

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32
Q

what are the maternal components of the placenta?

A 
Decidua basalis (derived from the endometriym) 
Maternl blood in lacuna
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33
Q

How does the fetal exchange work?

A

Fetal circulation (CO 2 and H20, urea, waste products and hormones are out of the cell

Maternal circulation
Sends O2
H2O electrotlytes
Nutrients
Hormones
IgG
Drugs
Virus.
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34
Q

How does the umbilical cord work?

A

Two umbilical arteries return deoxygenated blood from fetal internal iliac arteries to the placenta

Ombilical vein supplies oxygenated blood from placenta to fetus

Drains into the IVC via ductus venosus

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35
Q

What is urachus?

A

Yolk sac forms in the allantois (extends into the urogenital sinus)

Allantois becomes urachus a duct between the fetal bladder and the umbilicus

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36
Q

What is a patent urachus?

A

Failure of the urachus to obliterate and urine is discharged from the umbilicus

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37
Q

what is a urachel cyst?

A

Partial failure of the urachus to obliterate
Fluid filled cavity lined with uroepithilium (between the umbbilicus and bladder)

Can lead to infection
Can lead to adenocarcinoma

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38
Q

Characteristics of vesicourachel diverticulum?

A

Slight failure of the urachus to obliterate (outpouching of the bladder)

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39
Q

What is the vitelline duct?

A

Obliteration of the vitelline duct (connecys the yolk sac to the midgut lumen)

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40
Q

What is a vitelline fistula?

A

Vitelline duct fails to close with meconium discharge from the umbilicus

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41
Q

What is Meckel diverticulum?

A

Partial closure of the vitelline duct
Patent portion attached to the ileum (true diverticulum)
May have gastric or pancreatic tissue
Can result in melena, hematochezia, abdominal pain

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42
Q

what are the aortic arch derivatives?

A

1st: maxillary artery, branch of the external carotid
2nd: stapedial artery and hyoid artery
3rd: Common carotid artery and proximal part of the internal carotid
4th: proximal part of right subclavian artery
6th: Proximal part of pulmonary arteries and ductus

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43
Q

what is Di Geororge’s syndrome?

A

Chromosome 22q11 deletion
Thymic aplasia
Hypocalcemia
Cardiac defects

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44
Q

Cleft lip and cleft lip palare

A

Cleft lip: failure of fusion of the maxillary and medial nasal processes

Cleft palate: failure of fusion of the two lateral palentine shelves

Both usually occur together

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45
Q

what is the mullerian duct?

A

Develops into female internal structures
Fallopian tubes, uterus, upper portion of the vagina
Male remnant is appendix testes

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46
Q

what is the mesonephric (wolfmann duct)

A 
Develops into the internal structures of the male
Seminal vesicls
Epididymis
Ejaculatory duct
Ductus deferens
In females, remnant mesonephric duct
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47
Q

what does the SRY gene on Y chromosome do?

A

Produces testis determining factor (and testes developpement)

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48
Q

what do sertoli cells secrete?

A

Mullerian inhibitary factor (MIF)

suppresses developpement of parameonephric ducts

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49
Q

What do Leydig cells do?

A

Secrete androgens that stimulate the developpement of paramesonephric ducts

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50
Q

What happens if have no sertoli cells or lack Mullerian inhibitaory factor?

A

Will develop male and female internal genitilia

BUT male external genitilia

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51
Q

What if have 5 reductase deficiency?

A

Inability to convert testosterone into DHT
Male internal genitilia
Ambigous external genitilia until hits puberty, and then the increase in testosterone will cause masculinization

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52
Q

Characteristics of septate uterus?

A

Common anomly vs normal
Incomplete resorption of the septum
Decrease in fertility
Treat with septoplasty

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53
Q

Bicornate uterus?

A

Incomplete fusion of theMullerian ducts

Increase risk of complicated pregnaney

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54
Q

Uterus didelphys?

A

Complete failure of fusion
Double uterus, vagina and cervix
Pregnancy is possible

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55
Q

What is hypospadias?

A

Abnoraml opening of penile urethra on ventral surface of the penis due to failure of the urethral folds to fuse

Hypospadias is more common then epispadias
Associated with inguinal hernia

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56
Q

what is epispadias?

A

Abnormal opening of the penile urethra on the dorsal surface of the penis

Due to faulty positioning of the tubercle

Extrophy of the bladder is asscoated with epispadias

(Goes up the pee)

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57
Q

what parts of the body anchor the testes?

A

Gubernaculum (band of fibrous tissue)

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58
Q

What does the processus vaginalis do?

A

forms turnica vaginalis

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59
Q

what is the female remnant of the guernaculum ?

A

rian ligament with round ligament of uterus

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60
Q

How does the venous drainage of the left ovary/testes?

A

Left gonadal vein to the left renal vein to the IVC

right ovary/testes to the right gonadal vein to the IVC

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61
Q

How does lymphatic drainage occur?

A

Ovaries and testes drain to para aortic lymph nodes
Body of the uterus/cervix/superior bladder to the external iliac nodes

Prostate/cervox/corpus cavernosum/proximal vagina drains into the internal iliax nodes

Glans penis : drains in deep inguinal nodes

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62
Q

What does the infundibulopelvic ligament do?

A

Connects overies to the lateral pelvic wall

They are ligated during oophprectomy to avoid bleeding

Ureter courses retroperitoneally close to the gonad vessels

At risk during ligation of the ovarian vessels

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63
Q

What does the cardinal ligament do?

A

Cervix to the side wall of the pelvis
Contains uterine vessels
Ureter at risk during ligation of the uterine vessels in hysterectomy

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64
Q

What does round ligament of the uterus do?

A

Uterine fundus to the labia majora
Can be an issue in derivative of gubernaculum
Travels through round inguinal canal
Above the artery of Sampson

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65
Q

What does broad ligament do?

A

Connects the uterus, fallopian tubes and ovaries to the pelvic wall

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66
Q

what does Ovarian ligament do?

A

Median pole of the ovary to lateral uterus

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67
Q

Type of cell in the vagina?

A

stratefied squamous epithelium , non keratin

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68
Q

Type of cell in ectocervix?

A

Stratefied squamous epithelium, non keratin

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69
Q

Transformation zone?

A

squamocolumnar junction (most commone area for cervical cancer)

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70
Q

Uterus?

A

Columnar epithilium with long tubular glands in proliferative phase

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71
Q

Fallopian tubes>

A

Simple columnar epithilium (ciliated)

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72
Q

Ovary (outer surface)

A

Cuboidal epithelium

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73
Q

What is the pathway of semen ejaculation?

A 
Seminiferous tubules
epipidymis 
Vas deferens
ejaculatory ducts
Ureathra
Penis
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74
Q

Characteristics of urethral injury?

A 
Suspect if there is blood seen on the urethral meatus
Prosterior urethra (membraneous urethra prone to injury from pelvic injury
Can cause urine to leak into the retropubic space

Anterior urethra at risk of damage due to perineal saddle injury

Can cause the urine to leak beneath the fascia of Bcuk

If fascia is torn, urine escapes into superficial perineal space

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75
Q

what is autonomic innervation of male sexual response?

A

Erection is parasympathetic nervous system

NO —–> cGMP—->Smooth muscle relaxation—-> vasodilation —> proerectile

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76
Q

What is the anti-erectile response?

A

Norephineprine—> to Ca —-> smooth muscle constriction —-> anti-erectile

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77
Q

what is responsible for emission of the semen?

A

Sympathetic nervous system (hypogasrtic nerve)

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78
Q

What is responsible for the ejaculation of semen?

A

Visceral and somatic nerves

Pudendal nerve

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79
Q

How does sildenafil work?

A

PDE-5 inhibitors decrease cGMP breakdown

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80
Q

Function of speratogonia (germ cells)

A

Maintain germ pool and produce 1 spermatocytes

Line semingerous tubules

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81
Q

Function of sertoli cells (non-germ cells)

A

Secrete inhibitn B -inhibit FSH
Secrete androgen-binding protein (maintain local levels of testosterone)
Produce MIF
Tight junctions between sertoli cells form barrier and protect against autoimmune attack

Supports and noursihes developping spermatozoa

Temperature sensative: decrease sperm production and inhibin B with increase in temperature

Hormone functions: Lines seminiferous tubules
Convert testosterone and androstenedione to estrogen via aromatase

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82
Q

Functions of Leydig cells?

A 
Secrete testosterone in the presence of LH
These cells (unlike sertoli cells) are unafected by the temperature

Found in the interstitium
Homolog of female theca interna cells

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83
Q

Source of estrogen?

Potency of types of estrogen?

A

Estradiol > estrone > estriol

Produced by the ovary, placenta, adipose tisse

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84
Q

What is the function of estrogen?

A

Developpement of genitilia and breast
Female fat distribution
Growth of follicle, endometrial proliferation, increase of myometrial excitability

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85
Q

Levels of estrogen in pregnancy?

A

50 fold increase in estradiol and estrone

1000 fold in estriol (indicator of fetal well being)

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86
Q

what causes upregulation of estrogen?

A

Upregulation of estrogen, LH, and progesterone receptors

Estrogen causes feedback inhibition of FH and FSH

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87
Q

What does LH surge cause?

A

Stimulation of prolactin secretion

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88
Q

What is the source of progesterone?

A

Corpus luteum, placenta, adrenal cortex, testes

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89
Q

What happens to progesterone after delivery?

A

Decrease in progesterone which disihnits prolactin and causes lactation

An increase in progesterone is indicative of ovulation

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90
Q

what are the functions of progesterone?

A

Stimulation of endometrial glandular secretions and spiral artery developpement

Maintains pregnancy

Decrease in myometrial excitability

Production of thick cervical mucis which inhibits sperm entry into uterus

Increases body temperature

Inhibition of gonadotropins (LH and FSH)

Uterine smooth muscle relaxation (prevent contractions)

Decrease estrogen receptor expression

Prevents endometrial hyperplasia

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91
Q

The steps of oogenesis?

A

1 (primary) oocytes begin meiosis during fetal life and complete it just prior to ovulation

Meiosis 1 stops for years in prophase until ovulation

Meiosis 2: arrested in metaphase until fetlizatio (where they become 2 oocytes)

If fertilization doesnt occur within 1 day, the 2 secondary oocyte degnerates

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92
Q

How do hormones cause ovulation?

A

Increase in estrogen
Increase i GnRH receptos on the anterior pituary
Estrogen surge stimulates LH release
Leads to ovulation (rupture of the follicle)
Increase in temperature (due to progesterone)

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93
Q

What is mittelschemerz ?

A 
Transient mid cycle ovulation pain 
Due to peritoneal irritation 
Due to follicular swelling/rupture
Fallopian tube contraction 
Can mimic appendicitis
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94
Q

Roughly describe the mentrual cycle?

A

Follicular phase can vary in length
Luteal phase is 14 days
Ovulation + 14 days = mentruation

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95
Q

When is follicular growth the fastest?

A

During the second week of the follicular phase

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96
Q

Role of estrogen in menstrual cycle?

A

Stimulates endometrial proliferation

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97
Q

Role of progesterone in the menstrual cycle?

A

Progesterone maintains the endometrium to support implantation

Decrease in progesterone leads to decrease in fertility

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98
Q

What is dysmenorrhea?

A

Pain with menses, often associated with endometriosis

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99
Q

What is oligomenorrhea?

A

> 35 days in a cycle

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100
Q

What is metorrhagia?

A

Frequent or irregular menstruation

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101
Q

What is menorrhagia?

A

Heavy mentrual bleeding (more 80 ml, or blood loss that is more then 7 days of menses)

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102
Q

What is menometrorrhagia?

A

Heavy, irregular menstruation

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103
Q

Where does fertilization occur?

A

In upper end of the Fallopian Tube (the ampulla)

Occurs within 1 day of ovulation

104
Q

When does implantation occur?

A

Wall of the uterus within 6 days of fertilization

105
Q

When does HCG surge occur?

A

Detectable 1 week after conception

At home urine test 2 weeks after conception

106
Q

What is the gestational age?

A

From date of the last menstrual period

107
Q

What is embryonic age?

A

Calculated from the date of conception (gestational age minus 2 weeks)

108
Q

Physiologic adaptations in pregnancy?

A

Increase cardiac output
Increase preload, and decrease afterload
Increase HR (increase plasma, increase RBC, decrease viscosity)

Hypercoagulability (decrease blood loss at delivery)
Hyperventilation (eliminate fetal CO2)

109
Q

What is the source of HCG?

Function of HCG?

A

Placenta
Function:
Maintains corpus luteum for 8-10 weeks of pregnancy acting like LH

After 8 weeks, placenta synthesizes it’s own estriol and progesterone as the corpus luteum degenerates

Used to detect pregnancy in the urine

110
Q

What happens to HCG in pathological states?

A

HCG increased in multiple gestation
Hydatiform moles
Choriocarcinomas
Down’s syndrome

B-HcG decreases in ectopic or failing pregnancy
Edward syndrome
Patau sundrome

111
Q

What is the Apgar score?

A

Appearance (2 pink, 1 extremities blue, 0 pale or blue)
Pulse (2 > 100 npm, < 100 bmp 1, no pulse 0)
Grimace (Cries and pulls away 2, weak cry 1, no response 0)
Activity (2, active movement, 1 arms and legs flexed, 0 no movement)
Respiration (strong cry 2, slow and irregular 1, no breathing 0)

112
Q

what is low birthweight?

Causes?

A

Defined as less then 2500 grams
Caused by prematurity or IUGR
Associated with increase rsik of SIDS and with mortality

113
Q

Problems associated with low birthweight?

A 
Imparied thermoregulation
Compormised immune function 
Hypoglycemia
Polycythemia
Impaired neuorcognitive/emotional developpement
114
Q

What are complications of low birth weight?

A 
Infections
Respiratory distress
Necrotizing enterocolitis
Intraventricular hemmorrhage
Persistent fetal circulation
115
Q

How do hormones begin lactation?

A

After labor have decrease in progesterone and estrogen dishinbits lacations

Suckling causes nerve stimulation with release of oxytocin and prolactin

116
Q

what does prolactin do?

A

Induces and maintains lactation and decreases reproductive function

117
Q

What does oxytocin do?

A

assists in milk being let down

Promotes uterine contractions

118
Q

Why is breast milk best for the baby?

A 
Ideal for infants < 6 months
Contains maternal immunoglobulins
Passive immunity mostly IgA 
Breast milk reduces infections
Decreases change of asthma, allergies, DM, and Obesity

If have exclusively breastfed infant, will require vitamin D supplementation

119
Q

What are the benefits of breastfeeding?

A

Decrease maternal risk of breast and ovaria cancer

Facilitates mother and child bonding

120
Q

What is menopause?

Hormone response?

A

Amenorrhea for 12 months
Decrease in estrogen due to age linked decline i umber of ovarian follicles
Average onset is 51 years old (earlier if smojer)

Usually have 4-5 years of abnormal mesntrual cycle

Source of estrogen (estrone) after menopuase becomes peripheral conversion of androgens

FSH increases for menopase (due to negative feedback of FSH due to decrease om estrogen)

121
Q

What are symptoms of menopause?

A 
Hot flashes
Atrophy of the Vagina
Osteoporosis
CAD
Sleep disturbances 
Menopause before 40 suggests primary ovarian insufficency
122
Q

What are the different types of androgens?

A

Testosterone
Dihydrotrestosterone
Androstenedione

123
Q

what is the source of androgens?

A

DHT and testosterone

Androstenedione (adrenal)

124
Q

what are the relative potency of testosterone?

A

DHT > testosterone > androstenedione

125
Q

What is the function of testosterone?

A

Differention of epididymyus
Vas deferens
Seminal vesicles
Growth spurt (penis and seminal vesicales) sperm, muscles, RBC
Voice is deeper
Closing of epiphyseal plates (via estrogen that is converted to testosterone)
Libido

126
Q

What is the function of DHT?

A

Differentiation of penis, scrotum and prostate

Late: prostate growth
Balding
Sebaceous gland activity

127
Q

How is testosterone converted to DHT?

A

5 alpha reductase (this is inhibited by finasteride)

Androgens converted to estrogen by cytochrome p450 (in males) in adipose tissue and testis

Aromatase is key in conversion of androgens to estrogen

128
Q

What happens after exogenous testosterone is given?

A

Inhibition of the hypothalamus-pituaitry-gonadal axis
Decrease intratesticular testosterone
Decrease in testicular size
Azzospermia

129
Q

When does spermatogenesis occur?

A

Begins at puberty with spermatogonia
Full developpemt takes 2 months
Occurs in the seminferous tubules
Produces spermatids that undergo speriogenesis (loss of cytoplasmic contents, gain of acrosomal cap) to form mature spermatozoon.

130
Q

What are the Tanner stages of developement?

A

Stage 1:No sexual hair (flat appearing chest with raised hair)

Stage 2: Pubic hair appears at the pubarche
Testicular enlargement
Breast bud forms (thelarche)

Stage 3:
Coasing of pubic hair
Penis size increases in size (length)
Breast enlarge and mound forms

Stage 4:
Coarse hair accross the pubis
Sparing thigh (penis size increases in width and glans increase)
Breast enlarge with raised areola

Stage 5:
Coarse hair accross the pubis and the medial thigh
Penis and testes enlarge to adult size
Adult breast contou, areola flattens

131
Q

Characteristics of Klinefelter syndrome?

A 
47, XXY 
Testicyle atrophy
Enuchoid body shape
Tall and long extremeties
Gynecomastia 
Female hair distribution 
Presence of inactivated X chromosome
Common cause of hypogonadism seen in infertility 
Dysgenesis of the seminferous tubules
Decrease inhibit B
Increase of FSH 
Abnormal Leydig cell function 
Decrease in testosterone
Increase LH
Increase in estrogen
132
Q

Characteristics of Turner’s syndrome?

A 
Short stature (if untreated)
Ovarian dysgenesis
Sheilf chest
Bicuspid aortic valve 
conarctation (femoral < brachial pulse) 
Lymphatic defects (webbed neck or cystic hygroma, lyphedema in feet and hands, horseshoe kidney

Most common cause of amenorrhea

Menopause before menarche

Decrease in estrogen leads to increase in LH and FSH

Sometimes due to mitotic error (mosaicism)

45 XO, XO
Pregnancy is possible (IVF) exogenous estradiol 17B and progesterone

133
Q

What are double Y males?

A

XYY

Phenotypically normal
Normal fertility
Severe acne
Learning disability
Autism spectrum disorders
134
Q

Ovotesticular disorder of sex developpement?

A

46 XX > 46 XY
Both ovarian and testicular tissue present (ovotestis)
Ambiguous genitilia
Previously called true hemaphrodisme

135
Q

Testosterone is high, LH is high, disorder?

A

Defective androgen receptor

136
Q

Testosterone is high, LH is low?

A

Testosterone secreting tumor or exogenous steroids

137
Q

Testosterone is low, and LH is high?

A

Primary hypogonadism

138
Q

Testosterone low, and LH low?

A

Hypogonadotropic hypogonadism

139
Q

Disease with 46 XX, DSD

A

Ovaries present
External genitilia are virulized or ambiguous
Due to excessive and inapprpriate exposure to androgenic steroids during early gestation

140
Q

Disease with 46 XY, DSD?

A

Testes are present
external genitlia are female or ambiguous
Most common form is androgen insensitivty syndrome

141
Q

Placenta aromatase deficiency?

A

Inability to synthesize estrogen from androgens
Musculinization of female (46 XX)
Infants with ambigious genitilia
Increase in serum testosterone and androstenedione
Can present with maternal virilization during pregnancy (the fetal androgens cross the placenta)

142
Q

Androgen insensitivity syndrome? (46 XY)

A

Defect in androgen receptor leading to normal appearing female
Female external genitlia, scant sexual hair
Rudimentary vagina
Uterus and fallopian tubes absent

Patients develop normal functioning testes
Often found in the labia majora (removed to prevent Cancer)

Increase in testosterone, estrogen, and LH

143
Q

5 alpha reductase deficiency?

A 
Autosomal recessive
Sex linked to genetic males (46 XY)
Inability to convert testosterone to DHT
Ambiguous genitilia until puberty
When testosterone causes masculinization and increase in growth of genitilia

Testoterone/estrogen levels are normal
Internal genitilia are normal

144
Q

Kallmann syndrome?

A 
Failure to complete puberty
A form of hypogonadotropic hypogonadism
Defective migration of GnRH cells
Formation of olfactory bulb
Decrease in synthesis of GnRh in the hypothalamus
Anosmia
Decrease in GnRH, FSH, LH, testosterone
Infertility (low sperm count in males, and amenorrhea in females).
145
Q

General characteristics of hydatidform mole?

A

Cystic swelling of chorionic villi and proliferation of chorionic epithelim

Presents with vaginal bleeding, uterine enlargement and pelvic pressure/ pain

Associated with hCG mediated sequelae
early preclampsia (before 20 weeks)
Theca lutein cysts
Hyperemesis gravidarum 
hyperthyroidism

Treatement: dilatation and curettage
with methotrexate
Monitor with B HCG

146
Q

Charactersitics of the complete mole?

A

Karyotype: 46 XX or 46 XY
Componets: enucleated egg and single sperm

Duplicated paternal DNA

No fetal parts

Uterine size is increased

HCG is very increased

Imaging: Honeycombed uterus with clusters of grapes or snowstorm on the US

Risk of malignancy is 15-20%

Risk of choriocarcinoma is 2%

147
Q

Characteristics of partial mole?

A 
Karyotype: 69 XXX or 69XXY, 69 XYY
Components: 2 sperm and 1 egg
Fetal parts: yes
No change in uterine size
HCG mildly increased 
Risk of malignancy is less then 5%
Risk of choriocarcinoma: RARE
148
Q

What is choriocarcinoma?

A

Rare
Develops during or after pregnancy in mother or the baby
Malignancy of the trophoblastic tissue
No chorionic villi present
Increase frequency of bilateral multiple theca-lutein cysts
Presents with abnormal increase in B-Hcg
Shortness of breath, hemoptysis
Can have hematogenous spread to the lungs.

149
Q

Placenta abruption?

A

Premature seperation of the placenta from the uterine wall before delivery

Risk factors:
Trauma
Smoking
HT
Preeclampia
Cocaine abuse
Presentation: 
Abrupt, painful bleeding in third trimester
Possible DIC
maternal shock 
Fetal distress

Life threatening for the mother and fetus

150
Q

Placenta accreta/increta/percreta?

A

Defective decidual layer (abnormal attachement and seperation)

Risk factors:
Previous C section
Inflammation
Placenta Previa

151
Q

Placenta accreta?

A

placenta attaches to the myometrium without penetrating it. This is the most common type

152
Q

Placenta increta?

A

Placenta penetrates into the myometrium

153
Q

Placenta percreta?

A

Placenta perforates through the myometrium and into the uterine serosa

The placenta can attach to the rectum or the bladder

Presentation: often by ultrasound
No seperaton of placenta after the delivery
Can cause post partum bleeding with Sheehan syndrome

154
Q

Placenta previa?

A

Attachement of placenta to lower uterine segment over internal os (or less then 2 cm away)

Risk factors:
multiparity
prior C-section
Associated with painless third semester bleeding

155
Q

Vas previa?

A 
Fetal vessels run near the cervical os
Can result in rupture and extrangination 
Painless vaginal bleeding
Fetal bradycardia (< 110 per minute)
Emergency C-section

Associated with velamentous unmbilcial cord (insertion of chord in choroamniotic membrane rather then placenta) so unprotected by Wharton Jelly.

156
Q

What are causes of postpartum hemorrhage?

A

Tone (uterine atony)
Trauma (lacerations, incisions, uterine rupture)
Thrombin (coagulopathy)
Tissue (retained products of conception)

157
Q

Characteristics of ectopic pregnancy?

A

Most often in ampulla of fallopian tubes

Shows 10 mm embryo in oviduct at 7 weeks of gestation

158
Q

When to suspect history of amenorreha?

A

Lower then expected HCG (based on dates)
Sudden lower abdominal pain
Confirmed with US
Often clinically mistaken for appendicitis

159
Q

What are risk factors for ectopic pregnancy?

A 
Prior ectopic
History of infertility
Salpingitis
Ruptured appendix
Prior tubal surgery
160
Q

Two types of amniotic fluid abnormalities?

A 
Polyhyraminos: too much amniotic fluid
Associated with fetal malformations 
Maternal diabetes
Fetal anemia 
multiple gestations

Can result in esophageal/duodenal atresia
Anencephaly
Both result in inability to swallow animotic fluid

Oligohydraminos: too little amniotic fluid
Assocayed with placental insufficnecy
bilateral renal agenesis
Posterior urethral valves
Inability to excrete urine
Profound oligohydraminos can cause Potter sequence.

161
Q

What are the types of HTN in pregnancy?

A

Gestational HTN
Preeclampsia
Eclampsia
HELLP syndrome

162
Q

Gestational HTN?

A

BP > 140/90 after 20th week of gestation
No preexisting HTN
No proteinuria
No end organ damage

Treatment: hydralazine, methyldopa, labetalol, Nifedipine

Deliver at 37-39 weeks

163
Q

Preeclampsia?

A

New onset HTN
Has protinuria
End organ dysfunction after 20th week of gestation
May proceed to preeclampsia (which is siezures)
HELLP syndrome

Caused by abnormal placental spiral arteries that cause endothelial dysfunction and vasoconstriction

Risk factors include:
HTN
DM 
Chronic renal disease 
Autoimmune
164
Q

What are complications of preeclampsia?

A 
Placental abruption 
Coagulopathy
Renal failure
uteroplacental insufficiency 
Eclampsia
165
Q

Characteristics of Ecclampsia?

Treatement?

A

Need to have preeclampisa AND maternal seizures
Can have death due to stroke, intracranial hemorrage or ARDS

Treatment: IV Magnesium sulfate
Antihypertensives
Immediate delivery

166
Q

Characteristics of the HELPP syndrome?

A 
Hemolysis
Elevated liver enzymes
Low platelets
Blood smear will show schistocytes
Can lead to hepatic subcapsular hematomas (rupture and severe hypotension)
167
Q

What are characteristics of gynecological tumors?

A

Incidence of tumors in the US
endometrial > ovarian> cervical

(Cervical cancer is more common in the other parts of the world due to lack of screening and lack of HPV vaccination)

168
Q

What are the type of vaginal tumors?

A

Usually secondary to squamous cell carcinoma, because primary vaginal carcinoma is rare

Clear cell adenocarcinoma: Affects women who have exposure to DES in utero

Sarcoma botryoides (embyronal rhabdomyosacoma variant)  Affects girls less the 4 years old. Spindle shaped cells.
Presents as clear, grape-like polypoid mass emerging from the vagina
169
Q

What are the characteristics of cervical pathology?

A

Dyplasia and carcinoma in situ: disordered epithelial growth, usually begins ar the basal layer of squamocoloumnar junction (transformation zone)

Associated with HPV 16 or HPV 18

May progress to invasive carcinom if left untreated

Typically is assymptomatic

Risk factors include: multiple sexual partners

170
Q

Characteristics of invasive carcinoma in-situ?

A

Usually squamous cell carcinoma in situ
Pap smear can catch cervical dysplasia before it progresses
Diagnosis is with colposcopy and biospy
Lateral invasion can block the ureters

171
Q

What is premature ovarian failure?

A

Premature atresia of ovarian folliciles in women of reproductive age

Patients present with signs of menopause before the age of 40

Have decrease in estrogen, increase in LH and increase in FSH

172
Q

What are most common cause of anovulation?

A 
Pregnancy
Polycystic ovarian syndrome
Obesity 
HPO axis abnormality 
Premature ovarian failure 
Hyperprolactinemia 
thyroid disorder
Eating disorder 
Competitive athletics
Cushing syndrome
Adrenal insufficiency
173
Q

Charcteristics of polycystic ovarian syndrome?

A

Hyperinsulinemia
Insulin resistence
Will alter the hypothalamic hormonal feedback response (increase in LH: FSH) from internal theca cells

Decrease the rate of follicular maturation

Unrupturedfollicles (cysts) + anovulution
Common cause of subfertility in women

Enlarged bilateral cystic ovaries 
Presentes with amenorrhea/oligomenorrhea
hirutism 
acne 
decrease in fertility 
obesity 
Increased risk of endometrial cancer due to unopposed estrogen from repeated anovulatory cycle 
Treatment:
Weight reduction
Oral contraceptive pills
Clomiphene citrate
Ketaconazole 
Spironolactone
174
Q

Types of Ovarian cysts and characteristics?

A

Follicular cyst: distention of unruptured graafian follicle
Associated with hyperestogenism
Endometrial hyperplasia
Most common ovarian mass in young women

Theca-lutein cyst: bilateral/multiple
Due to gonadotropin stimulation
Associated with choriocarcinoma and hydatidiform moles

Ovarian neoplams: most common adrenxal mass in women > 55 years old

Can be benign or malignant

Arise from surface epithelium, germ cells, or sex cord tissue

Majority of malignant tumors are epithelial 
Risk increased with ade
infertility
endometriosis 
PCOS
BRACA 1 and BRACA 2
Lynch syndrome
Family history

Risk will decrease with previous pregnancy, history of breastfeeding, oral contraception, tubal ligation

Presents with adnexal mass
Abdominal distention
Bowel obstruction
Pleural effusion

Monitor relapse and therapy by measuring CA 125 levels (not good for screening)

175
Q

Serous cystadenoma?

A

Most common ovarian neoplams (lined with fallopian tube like epithelium, often bilateral

176
Q

Mucinous cystadenoma?

A

Multiloculated, large, lined by mucos-secreting epithelium

177
Q

Endomerioma?

A

Endometriosis (ectopic endometrial tissue) within the ovary with cyst formation

Presents with pelvic pain

Dysmenorrhea
Dyspareunia

Symptoms may vary with menstrual cycle

Chocolate cyst endometrioma filled with dark, reddish brown blood

Complex mass on ultrasound

178
Q

Mature, cystic teratoma (dermoid cyst)

A

Germ cell tumor
Most common in females 10-30 years old
Cystic mass containing elements from all 3 germ layers (teeth, hair, sebum)
Can present secondary to ovarian torsion or enlargement

A monodermal form with thyroid tissue (stuma ovarii) can sometimes present as hypothyroid

179
Q

Brenner tumor?

A

Looks like a bladder
Solid tumor that is pale yellow-tan and appears encapsulated
Coffee bean nuclei on H & E stain

180
Q

Fibromas?

A

Bundles of spindle shaped fibroblasts
Meigs syndrome: triad of ovarian fibromas, ascites, hydrothorax

Pulling sensation in the groin

181
Q

Thecoma?

A

Simular to granulosa cell tumor
May produce estrogen
Usually presents as abnormal uterine bleeding in a post menopausal women

182
Q

Granulosa cell tumor?

A

Most common malignant stromal tumor
Predominantly women in the 50’s
Often produces estrogen and progesterone
Presents with postmenopausal bleeding, sexual precocity (in pre-adolescents)
Breast tenderness
Histology shows Call-Exner bodies
Granulosa cells arrange haphazardly around collection of eosinophilc fluid (resembles primordial follicles)

183
Q

Serous cystadenocarcinoma?

A

Most common malignamnt ovarian neoplasm (frequenlt bilateral) Psammona bodirs

184
Q

Mucinos cystadenocarcinoma>

A

Pseudomyxoma perionei0intraperitoneal accumulation of mucinous material from ovaian appendiceal tumor

185
Q

Immature teratoma?

A 
Aggressive.
Contains fetal tissue
Neuroectoderma
Commonly diagnosed after menopaise 
Typically represented by immature/embryonic like neural tissue
186
Q

Dysgerminoma?

A 
Most common in adolescents
Equivalent to male semnoma but rarer
1% of all ovarian tumors
30% of germ cell tumors
Sheets of uniform *fried egg cells*
HCG, LDH (tumor markers)
187
Q

Yolk sac (endodermal sinus) tumor?

A

Aggressive in ovaries or testes and sacrococygea area in young children
Most common umore in male infants
Yellow
Friable
Solid mass
50% have Schiller-Duval bodies (resemble glomeuli)
AFP = tumor markers

188
Q

What is Krukenberg tumor?

A

GI malignancy that has metastasize to the ovaries

Mucin-secreting signet cell adenocarcinoma

189
Q

Endometiral polyp?

A

Collection of endometrial tissue within uterine wall
May contain smooth muscle cells
Can extend into the endometrial cavity in the form of polyp
May be assymptomatic or present with painless abdominal uterine bleeding

190
Q

Adenomyosis?

A

Extension of endometiral tissue (glandular( into the uterine myometrium

Caused by hyperplasia of basal layer of endometrium
Presents with dysmenorrhea, menorrhagia
Uniformly enlarged, soft, flobular uterus

Treatment with GnRh agonists, hysterectomy

191
Q

Leiomyoma (Fibroid)

A

Most common tumor in females
Presents with multiple, discrete tumors
Increase incidence in African American
Benign smooth muscle tumor
Malignant transformation to leiomyosarcoma is rare
Estrogen sensitive (tumor size increases with pregnancy and decreases with menopause)

Peak occurrence is 20-40 years old
May be asymptomatic, cause abnormal uterine bleeding or result in miscarriage

Severe bleeding may lead to iron deficinecy anemia
Whorled pattern of smooth muscle bundles with well demarcated borders

192
Q

Endometrial hyperplasia?

A

Abdnormal endometrial gland proliferation
Caused by excess estrogen stimulation
Increase risk for endometrial carcinoma
Nuclear atypia is greater risk factor then complex architecture
Presents as postmenopausal vaginal bleeding
Risk factors include anovuloatroy cyctes
Hormone replacement therapy
Polycystic ovarian syndrome
Granulosa cell tumor

193
Q

Endometrial carcinoma?

A 
Most common gynecological malignancy 
Peak occurence at 55-65 years old 
Presents with vaginal bleeding 
Preceeded by endometrial hyperplasia 
Risk factors include prolonged use of estrogen withour progestins, obesity, diabetes, HTN, nulliparity, late menopause, Lynch syndrome
194
Q

Endometritis?

A

Inflammation of the endometrium
Associated with retained products of conception after delivery, miscarriage, abortion, or foreign body (IUD)
Retained material in the uterus promotes infection by bacterial flora from vagina or intestinal tract

Treatment: gentamicin and clindamycin
+/- ampicillin

195
Q

Endometriosis?

A

Non-neoplastic endometrial glands/stome outside of the endometrial cavity

Can be found anywhere
The most common sites are the ovary (frequently bilateral, pelvis, peritoneum)

In ovary appears as endometroma (blood filled-chcholate cyst)

Can have metastatic transformation of multipotent cells

Endometirosis occurs because the cells are transported via lymphatic system

Characterised by cyclic pelvic pain, bleeding,dysmenorreha, dyspareeunia, dychezia *pain with defecation), infertility and normal sized uterus

Treatment: NSAIDS, OCPS, progestins, GnRH agonists, danazol, laproscopic removal

196
Q

what are parts of the breast pathology?

A

(from the nipple into the breast)

Nipple then lactiferous sinus—-> major duct—>terminal lobular duct —–>stoma)

The terminal duct (lobular unit), is where you get fibrocystic change, DCIS, LCIS, Ductal carcinoma, lobular carcinoma

197
Q

Fiboradenoma?

A

Common in women under 35 years old
Small, well defined mobile mass
Increase in size and tenderness with estrogen (pregnancy or prior to mensturation)

Risk of cancer is not increased

198
Q

Fibrocystic changes?

A

Extensio of endometrial tissue (glandular) into uterine myometrium
Hyperplasia of the basal layer
Presentes with dysmenorrhea, menorrhagia
Uniformly enlarged, soft, globular uterus
Treatment with GnRH agonisr, hysterectomy

199
Q

Sclerosing adenosis?

A

Increase in acinii
Increase in stromal fiboris
Associated with calcifications
Slight 1.5 to 2X risk for cancer

200
Q

Intraductal papilloma?

A

Small papillary tumor with lactiferous ducts
Typically right below the areola
Common cause of nipple discharge
Increase of 1.5-2X the risk of cancer

201
Q

epithilial hyperplasia?

A

Increase cells in terminal duct or lobular epitheliem

Increase risk of carcinoma with atypical cells

202
Q

Phyllodes tumor?

A

large mass of connective tissue with cysts and leaf-lke lobulations
Most common in the 5th decade
Some may become malignant

203
Q

Fat necrosis of the breast?

A

Benign
Usually painless lump due to injury to the beast tissue
Calcified oil cyst on the mammography
Necrotic fat and giant cells on biposy
Up to 50% of patients may not report the trauma

204
Q

Lactational mastitis?

A

Occurs during breast feeding
Increased risk of infection through cracks in the nipple
Staph aureus is the most common pathogen
Treat with antibiotics and continue breast feeding

205
Q

Gynecomastia?

A

Breast enlargement in males due to increase estrogen compared with androgen activity

Physiologic in newborns, pubertal, and elderly males

May presist after puberty

Other causes incloude cirrhosis, hypogonadism (Klinefleter syndrome)

Testicular tumors and drugs

Include: spironolactone, hormones, cimentidine, ketaconazole

206
Q

Characteristics of malignant tumors?

A

Usually post menopause
From terminal duct lobular unit
Overexpression of estrogen/progesterone receptor or c-erbB2, Her02 an ECF receptor

Commonly triple negative ER-, PR- Her2/Neu-

More aggressive

Axillary node involvement usually means metastasis (important prognostic factor in early stage disease)

Most often uppper quadrant of the breast

207
Q

what are risk factors for malignant breast tumors?

A

Increase estrogen exposure
Increase in total number of mentrual cycle
Older age at first live birth
Increase estrogen exposure in the adipose tissue
BRCA 1 and BRCA 2 gene mutations
African American ancestry (increase risk of triple negative breast cancer)

208
Q

Ductal carcinoma in situ?

A

fills ductal lumen
Arises from ductal atypia
Often seen as cacifications on the x-ray

209
Q

Comedocarcinoma?

A

Ductal central necrosis

Subtype of DCIS

210
Q

Paget disease?

A

Results from underlying DCIS or ivasive breast cancer
Ecsematous patches on the nipple
Paget cells = intraepithiliak adenocarcinoma

211
Q

Invasive ductal carcinoma?

A

Firm, fibrous, and rock hard mass with small, glandular duct like cells

Will see stellate infiltration

212
Q

Invasive lobular carcinoma?

A

Orderly row of cells (indian file)
Due to E-cadherin expression

Often bilateral with multile lesions in the same location

213
Q

Medullary carcinoma?

A

Fleshy cellular, lymphocytic infiltrate

Good prognosis

214
Q

Inflammatory breast cancer?

A

Dermal lymphatic invasion by breast carcinoma
Peau d’orhange (breast cancer resembles orange peel)
Neoplastic cells block lympathic drainage

Poor prognosis: 50% survival at 5 years
Often mistaken for mastitis of Paget’s disease

215
Q

Peyronie disease?

A

Abnormal curvature of the penis due to fibrous plaque within the tunica albuginea
Associated with erectile dysfunction
Can cause pain, anxiety
surgical repair once curvature stabilizes
Distinct from penile fracture

216
Q

Ischemic priapism?

A 
Painful erection lasting more then 4 hours
Associated with sickle cell disease
Medications (sildenafil)
Trazadone
Treat with corperal aspiration 
intracavernosal pheyephrine
Surgical decompression
217
Q

Squamous cell carcinoma of the penis?

A

Most common in Asia, Africa, South America
There are usually precursor lesions such as Bowen disease (in penile shaft, presents as leukoplakia), erythroplasia of Querat (cancer of glans, presents as erythroplakia)

Bowenoid papulosis (carcinoma in situ of unclear malignant potential presenting as reddish papules

Associated with HPV and lack of circumcision

218
Q

Cryto-orchidism?

A

Undescended Testis (one or both)
Impaired spermatogenesis
Sperm develope at < 37 degrees
Can have normal testosterone levels (Leydig cells are unaffected by temperature)
Associated with increase in germ cell tumors
Prematurity is a risk of crytopochidims
Decrease in inhibin B
Increase in FSH
Increase in LH
Testosteron is decreased in cryptoorchidimsm
Normal in unilateral

219
Q

Varicocele?

A

Dilated veins in pampiniform plexus due to increase in venous pressure
Most common cause of scotal enlargement within males

Most often on the left side because increase in resistance of the gonadal vein draining into the left renal vein

Diagnosed by clinical exam (distention on inspection and bag of worms)

Distention on inspection (bag of worms) or on ultrasound

Treatment: vriocelectomy or embolzation

220
Q

Scrotal mass?

A

Benign scrotal leisions
Present as testicular masses
Can be translluminated (vs solid testicular tumors)

221
Q

Congenital hydrocele?

A

Common cause of scrotal swelling within infants due to incomplete oblieration of processus vaginalis

222
Q

Acquired hydrocele?

A

Scrotal fluid collection secondary to infection
Trauma
Tumore
If bloody hematocele

223
Q

Spermatocele?

A

Cyst due to dilated epipidiymal ducte or rete testes

Will have paratesticular fluctuant nodule

224
Q

Seminoma?

A

Malignant, painless, homogenous testicular enlargement
Most common testicular tumor
Does not occur in infacny
large cells with watery cytoplasm and fried egg appearence
increase placantal ALP
Radiosensitive
Late mets, excellent prognosis

225
Q

Yolk sac (endodermal sinus tumor)

A 
Yellow, mucinous
Aggressive malignance of the testes
Analogous to Ovarian yolk sac tumor 
AFP is highly characteristic
Most common testicular tumor in boys is < 3 years old
226
Q

Choriocarcinoma?

A

Malignant
Increase in BHCG
Disordered synctiotrophoblasts and cytotrophoblastic elements

Hematogenous mets to the lungs and the brain
May produce gynecomastia, symptoms of hypothyroidism

227
Q

Teratoma?

A

Unlike females, mature teratoma in adult males may be malignant

Usually benign in children

228
Q

Embyonal carcinoma?

A

Malignant, hemoragic mass with necrosis, painful
Worst prognosis than seminoma
Often glandular/papillary morphology
Pure embyonal carcinoma is rare
Most commonly mixed with other tumor types

229
Q

Leydig cell?

A

Goldne brown color
Contains Rinke crystals (esinophilc cytoplasmic inclusions)
Produce androgen/estrogen and cause gynecomastic in men
Precococious puberty in boys

230
Q

Sertoli cells?

A

Androblastoma from sex cord stroma

231
Q

Testicular lymphoma?

A

Most common testicular cancer in older men

Arises from mestastic lymphoma to testes, it is aggressive

232
Q

Benign protatic hyperplasia?

A

Common in men > 50 years old
Characterized by smooth, elastic, firm nodule enlargement (hyperplasia and firm nodular enlargement)

Lobes can compress the periurethral (lateral and middle lobes)

These compress the urethra into a vertical slit

Can often present with increase in frequency of urination, nocturia, difficulty in starting and stopping urine stream or dysuria

May lead to distention or hypertrophy of the bladder

Hydronephorsis
UTI
Increase in free prostate specific antigen

Treatment (terzosin, tamsulosin)

Relaxation of smooth muscle
Tadalafil

233
Q

Prostatitis?

A 
Dysuria
Frequency 
Urgency
Low back pain
Warm, tender, enlaged prostate

Acute: bacterial, chronic bacterial or abacterial

234
Q

Prostatic adenocarcinoma?

A

Common in men > 50 years old
Arises within the posterior lobe of prostate gland
Usually diagnosed by increase in PSA and subsequenct needle core biopsies
Prostatic acid phophatease (PAP) and PSA are useful markers

LOOK at total PSA with decrease in fraction of free PSA

Osteoblastic mets in bone may develop in the late stages as indicated by lower back pain, and increase in serum ALP and PSA

235
Q

The path of reproductive hormones (control)?

A

Hypothalums—–> GnRH—–>anterior pituitary—-> LH/FSH (ovary)—–>androstenedione and testsoterone—–>aromatase converts to estriol—>estrone—->estradiol

Men:
Hypothalaum—->GnrH—–> anterior pituitaty—->LH (testes)—->testosterone—->dihydrotestosterone—->androgen receptor complex—–> gene expression in androgen responsive cells

236
Q

What is leuprolide used for?

A

GnRh analog with agonist properties when used in pulsatile fashion

When used in continuous fashion can be used to downregulate GnRh receptors in pituitary (decreased FSH/LH)

Clinical uses:
Uterine fibroids
Endometriosis
Precocious puberty
Prostate Cancer
Infertility
237
Q

When to use estrogens?

A

Bind estrogen receptors
Clinical uses:
Hypogonadism or ovarian failure
Menstrual abnormalities
Hormone replacement therapy in postmenopausal women
Used in men with androgen-dependent prostate cancer

Adverse effects: Increase risk of endometrial cancer
Bleeding in postmenopausal women
Clear cell adenocarcinoma in vagina of women exposed to DES in utero
Increase risk of thrombi

Contraindications to estrogen therapy
estrogen receptor postive cancer
History of DVT

238
Q

What are selective estrogen receptor modulators?

A

Clomiphene: Antagonist estrogen receptors in hypothalamus
Prevents normal feedback inhibition and release of LH and FSH from pituitary which stimulates ovulation

Causes hot flashes, ovarian enlargement
Multiple simultaneous pregnancies
Visual disturbances

239
Q

Use of Tamoxifen?

A

Antagonis at estrogen receptors in the hypothalamus
Prevents normal feeback inhibition (increase release of LH and FSH from pituitay) which stimulates ovulation

Used to treat infertility due to anovaultion (PCOS)

May cause hot flashes, ovarian enlargement, multiple simultaneous pregnencies and endometrial cacer

Used to treat ER/PR + breast Cancer

240
Q

Use of Raloxifene?

A

Antagonist at breast, uterus, agonist at bone
Increases risk of thromboembolic events BUT no increase in the risk of endometrial cancer
Used to primarily treat ostroporosis

241
Q

Use of aromatase inhibitors?

A

Names: anastrozole, letrozole, exemestane

Mechanism: inhibit peripheral conversion of androgens to estrogen

Clinical use: ER+ breast cancer in postmenopausal women

242
Q

Hormone replacement therapy?

A

Use for prevention of menopausal symptoms (hot flashes, vaginal atrophy)

Will cause osteoporosis due to increase in estrogen and decrease in osteoclast activity

Unopposed estrogen replacement therapy will increase the risk of endometrial cancer, so progesterone is added

Possible increase risk of cardiovascular

243
Q

Use of Progestins?

A

Levonogestrel, medoxyprogesterone, etonogestrel, norethindrone and many otheres

Mechanism: binds progesterone receptors, decreases growth, increase vascularisation of endometrium, and will thicken the cervical mucos

Clinical use: contraception (pill, intrauterine device, implant, depot injection)

Effects: abnormal uterine bleeding and endometrial bleeding

244
Q

What is the progestin challenge?

A

Asherman syndrome

Chronic anovulation without estrogen

245
Q

Anti-progestins?

A

Mifepristone, ulipristal

Mechanism: competitive inhibitors of progestins at progesterone receptors

Clinical use: termination of pregnancy (misoprostol) and emergency contraception (ulipristal)

246
Q

Use of combined contraception?

A

Progestins and ethinyl estradiol include the pill, patch and vaginal ring

Estrogen and progestins inhibit LH/FSH and prevent estrogen surge

No estrogen surge—> no LH surge—> no ovulation

Progestins: cause thickening of the mucus, limiting access of sperm to the uterus

Progestins inhibit endometrial proliferation, and it is less suitable to implantation of an embryo

247
Q

What are contraindications to combined contraception?

A

Smokers more then 35 years old

Patients with cardiovascular disease (include history of DVT, CAD, stroke, migraine) and breast CA

248
Q

How does the IUD work?

A

Produces local inflammatory reaction to toxic sperm and ova preventing fertilizaion and implantation (hormone free)

Clincial: long term reversible contraception
Most effective emergency contraceptopn

Adverse effects: loger menses, dysmenorrhea, risk of PID with insertion

249
Q

Use of terbutaline, ritodrine?

A

B2 agonsit that relaxes the uterus

Used to decrease contraction frequency in women during labor

250
Q

Danazol use?

A

Mechanism: synthetic androgen that acts as agonist at individual androgen receptors

Clinical use:endometrioisis, hereditary angioedema

Adverse effects: 
weight gain
edema
Acne
Hirutisme
Masculinization
Decrease HDL levels
Heptatotoxicity
251
Q

Uses of testosterone, methytestosterone?

A

Agonist at androgen receptors
Clincial: treat hypogonadism and promote development of secondary characteristics

When give to females:
Masculinization
Decrease in intratesticular testosterone in males
Stimulates anabolism 
Gonadla atrphy
Premature closure of epiphysiseal plates
Increase in LDL and decrease in HDL
252
Q

Uses, and examples of antiandrogens??

A

Testosterone (5 alpha reductase) to DHT (more potent)
Finasteride: 5 alpha reductase inhibitos (decrease conversion of testosterone to DHT)

Used for BPH and male pattern baldness

253
Q

Use of ketocanazole (form antiandrogen)

A

Inhibits steroid synthesis (inhibits 17, 20 desmolase)

254
Q

Use of spironolactone?

A

Inhibits steroid binding (17 alpha hydroxylase and 17, 20 desmolase)

Used for polycystic ovarian syndrome to reduce androgenic symptoms

Both have side effects of gynecomastia and amenorrhea

255
Q

Use of tamsulosin?

A

Alpha agonist used to treat BPH by inhibiting smooth muscle contraction

Selective for alpha 1A, D receptors (found in the prostate)

256
Q

Use of phosphodiesterase type 5 inhibitors?

A

Sildenafil, vardenafil, tadlafil

Mechanism: inhibits PDE05 and increases cGMP and causes prolonged smooth muscle relaxation in response to NO

Increase flow in corpus cavernosum of the penis

Decrease in pulmonary vascular reistance

Clinical use: erectile dysfunction, pulmonary hypertension and BP (tadafil only)

Adverse effects: headache, flushing, dyspepsia, cyanopia (blue tinted vision) risk of life-threatening hypotension if taking nitrates

257
Q

Use of minoxidil?

A

Direct arteriolar vasodilator

Clinical use: androgenetic alopecia, and severe refractory hypertension

US (17 decks)

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