Professional Documents
Culture Documents
70-80%
Amount of air forcibly expelled at the end of normal expiration
TLC decreased, RV decreased, FEV1 decreased, FVC decreased,
FEV1/FVC normal to increased, PaO2 decreased, A-a gradient
increased (if disease of lungs, not just restriction of chest wall
TLC increased, RV increased, FEV1 decreased, FVC decreased,
FEV1/FVC decreased, PaO2 decreased, A-a gradient increased
Difficulty breathing. Can be due to stimulation of J receptors
causing decrease in full inspiration. Also decreased compliance,
e.g. interstitial fibrosis; increased airway resistance, e.g. chronic
bronchiti; chest bellows disease, e.g. obesity; kyphoscoliosis,
interstitial inflammation or fluid accumulation, e.g. left sided heart
failure.
They're at the bifurcation of airways, larynx and distal esophagus
Postnasal discharge
GERD from acid refluxing into the bronchial tree at night. Bronchial
asthma due to airway constriction
Chronic bronchitis, usually associated with smoking cigarettes.
Typical
bacterial pneumonia.
Bronchiectasis
ACE inhibitors-inhibit
degradation
of bradykinin which causes
Normal breath sounds come from the trachea and are caused by
air velocity and turbulence inducing vibrations in airway walls
Terminal bronchioles where the increased surface area converts
turbulent
laminar
flow
Sound liketoair
blowing
through a tube-this is normal over the
What is a Nasopharyngeal
Carcinoma?
What is Atelectasis?
What is resorption
atelectasis?
What is compression
atelectasis?
Describe Primary TB
Infection.
Describe Secondary TB
Infection.
Respiratory Syncitial Virus. Occurs in late fall and winter. Can give
Palivizumab to high risk kids (passive immunity)
Right side because the bronchi going to the right lobes are more
direct (straight) so it's easier to aspirate crap into there. Usually in
the upper portion of the right lower lobe, but it depends on the
position of the person when they aspirated.
Spiking fever with productive cough and foul smelling sputum.
CXR shows cavitation with an air/fluid level.
Venous clot, most commonly from the femoral vein. Risk factors
are Virchow's triad-stasis of blood flow, hypercoagulable states and
trauma to the vessel. Clot breaks off and goes to the lung-size of
the embolus determines what it will block. Large embolus blocks
major vessels (saddle embolus) while small emboli occlude
medium
small vessels.
Increase and
in pulmonary
artery pressure, decreased flow to
What is Goodpasture's
Syndrome?
What is silicosis?
Fibers are coated in iron and protein (ferruginous bodies) which are
then pahgocytosed, coated with ferritin and look golden and
beaded in sputum or distal small airways. Causes calcified pleural
plaques which don't predispose to mesothelioma, diffuse interstitial
fibrosis, primary bronchogenic carcinoma (esp if smoker),
malignant mesothelioma of the pleura arising from serosal cells of
the pleura. Can cause cor pulmonale or Caplan syndrome.
What is Sarcoidosis?
What is Berylliosis?
What is Byssinosis?
What drugs are associated
with interstitial fibrosis?
What is obstructive lung
disease?
What is Emphysema?
What is Bronchiectasis?
Smoking, Radon gas (uranium mining), asbestos, metal exposurechromium, cadmium, beryllium, arsenic- secondhand smoke,
ionizing radiation, air pollution, prior TB
What
Pancoast tumor?
What is
area some
paraneoplastic changes
associated with lung
cancers?
Ratio of pleural fluid protein and LDH to serum protein and LDH.
PF protein/serum protein <0.5 is transudate, >0.5 is exudate. PF
LDH/serum LDH <0.6 is transudate, >0.6 is exudate. PF LDH
<200 U/L is transudate, >200 U/L is exudate
Commonly seen in tall, thin young men, 20-40 yrs old, increased
risk with smoking. Can be caused by rupture of apical subpleural
blebs (secondary to high negative intrapleural pressure), COPD,
Marfan syndrome, scuba diving, insertion of a subclavian catheter.
Loss of negative intrapleural pressure causes collapse of lung.
Sudden onset of dyspnea with pleuritic chest pain.
Penetrating trauma to the lungs, rupture of tension pneumocytes.
Flap like tear in pleura allows air into pleural cavity but prevents its
release resulting in increasing positive intrapleural pressure. This
results in compression atelectasis. Sudden onset of severe
dyspnea and plueritic chest pain, can cause trachea and
mediastinal structures to deviate to contralateral side. Can cause
compromised venous return to the heart.
Reproductive
What vein drains the ovaries/testes?
What is the lymphatic drainage of the
Ovaries/Testes?
Where does lymph from the
vagina/vulva/scrotum drain to?
What does the suspensory ligament of
the ovaries connect?
What does the Cardinal ligament
connect?
What does the Round ligament of the
uterus connect?
What is the round ligament of the
uterus derive from?
What does the Broad Ligament
connects?
What does the Ligament of the ovary
connect?
What does the Genital Tubercle
become?
What does the Urogenital Fold
become?
What does the labioscrotal swelling
become?
What is the pathway of sperm during
ejaculation?
What is the autonomic innervation
causing an erection?
What is the autonomic innervation
causing Sperm Emission?
What is the autonomic innervation
causing Ejaculation?
What are the different parts of the
sperm?
Where do the different parts of the
spermiscome
from? of
What
the function
spermatogonia?
Left Gonadal vein to the left renal vein to the IVC. Right ovary/testis drains to right gonadal vein straight to
the IVC.
Ovary/Testis drains to the para-aortic lymph nodes.
Distal 1/3 of the vagina/vulva/scrotum drains to the superficial lymph nodes. Proximal 2/3 of vagina/uterus
drains to the obturator, external iliac and hypogastric lymph nodes
Connects ovaries to the lateral pelvic wall and contains the ovarian vessels.
Connects the cervix to the side wall of the pelvis and contains the uterine vessels.
Contains the Uterine fundus to the labia majora but carries no structures.
Derivative of the Gubernaculum. Travels through the round inguinal canal.
Connects the uterus, fallopian tubes, and ovaries to the pelvic side wall. Contains the ovaries, fallopian
tubes, and round ligaments of the uterus.
Connects the ovary to the uterus and does not contain any structures.
Becomes the Glans Penis or Clitoris
Becomes the shaft of the penis or the labia minora
Scrotum and Labia majora
(SEVEN UP) Seminiferous tubules to epididymis to vas deferens to ejaculatory ducts (nothing) to urethra to
the penis
Erection-Parasympathetic nervous system (pelvic nerve). Nitric oxide increases cGMP which causes smooth
muscle relaxation which causes vasodilation and is proerectile. Also Norepinephrine causes an increase in
Calcium which causes smooth muscle contraction which causes vasoconstriction and is antierectile.
Sympathetic nervous system via the hypogastric nerve
Visceral and somatic via the pudendal nerve
Acrosome, head, nucleus, neck, middle piece, tail
Acrosome-Golgi apparatus, Flagellum/Tail-Centrioles, Middle Piece-contains the mitochondria, Head and
nucleus come from the nucleus.
Maintaininhibin
the germ
pool
and produce
primary
spermatocytes
Secrete
which
inhibits
FSH. Secrete
Androgen
Binding Protein to maintain the level of testosterone.
Form tight junctions between adjacent Sertoli Cells to form the blood-testis barrier, isolating gametes from
immune attack. Support and nourish spermatozoa. Regulate spermatogenesis. Produce Anti-Mullerian
hormone.
Secrete testosterone
Seminal Vesicle Products(fructose, ascorbic acid, prostaglandins, phosphorylcholine, flavins), Prostate
Products (Zinc, citrate acid, phospholipids, acid phosphatase, fibrinolysin), Sperm
Spermatogenesis begins at puberty with spermatogonia. Full development takes 2 months. Occurs in
seminiferous
that undergo
spermiogenesis
to form
mature
spermatozoa
Maturation of tubules.
sperm asProduces
they losespermatids
their cytoplasmic
contents,
gain an acrosomal
cap
and become
mature
spermatozoa
Spermatogonium (diploid 2N) copies genome to make Primary spermatid (Diploid 4N). Primary spermatocyte
divides into 2 secondary spermatocytes (Haploid 2N). The Secondary spermatids divide again to produce 4
spermatids (Haploid, 1N). These undergo spermiogenesis to form mature spermatozoa
Hypothalamus releases GnRH which causes FSH and LH release from the anterior pituitary. LH stimulates
testosterone release from Leydig cells which release testosterone into the seminiferous tubules and the blood.
FSH stimulates Sertoli cells to produce Androgen Binding Protein and Inhibin. Testosterone from the Leydig
cells stimulates spermatogenesis and stimulates the Sertoli Cells to nurse the Spermatozoa. Inhibin from the
Sertoli cells feeds back and downregulates FSH release. Testosterone from Leydig cells feeds back and
downregulates LH production and GnRH release.
Testosterone (Testes), Dihydrotestosterone (Converted peripherally) and Androstendione (Adrenal)
Differentiation of the Epididymis, Vas deferens and seminal vesicles. Growth spurt of the penis, the seminal
vesicles, sperm, muscle, and red blood cell growth. Deepening of voice, closing of epiphyseal plates (via
estrogen converted from testosterone) and Libido.
In early differentiation it causes development of the penis, scrotum and prostate. In later/pubertal
development it causes prostate growth and sebaceous gland activity.
5 Alpha reductase converts Testosterone to DHT.
Ovary makes 17 Beta estradiol, Placenta makes estriol and blood/peripheral tissues can aromatize androgens
to estrogen.
Development of genitalia (external) and breast, and female fat distribution.
Growth of the follicle, endometrial proliferation, increased myometrial excitability. Upregulates LH, FSH and
estrogen receptors and thus upregulates itself. Feedback inhibition of LH and FSH and then the LH surge.
Stimulates prolactin secretion but blocks its action at the breast. Increases transport of proteins, Steroid
hormone binding globulin synthesis, increases HDL and decreases LDL.
50 fold increase in estradiol and estrone. 1000 fold increase in estriol indicates fetal well being.
Pulsatile GnRH from the Hypothalamus causes release of FSH and LH from the anterior pituitary. FSH
stimulates the granulosa cells of the ovaries to increase Aromatase which can then convert androstendione to
estrogen. LH acts on the Theca cells to upregulate Desmolase which convert cholesterol to androstendione.
The androstendione goes to the granulosa cells to be converted to estrogen.
Corpus Luteum, placenta, adrenal cortex and testes (in men obviously)
Ovulation!!!
Stimulation of endometrial glandular secretions and spiral artery development. Maintains pregnancy.
Decreases myometrial excitability. Increases production of thick cervical mucous, which inhibits sperm entry
into the uterus. Increases body temperature (hence why you take your temp), inhibits gonadotropins (LH
and FSH), relaxes uterine smooth muscle (prevents contraction) and decreases estrogen receptor
expressivity.
Granulosa cells respond to FSH and stimulate growth of 10-20 follicles. LH responsive Theca cells stimulate
growth of the corpus luteum and produce androgens which are converted to estrogen by granulosa cells (to
stimulate the developing follicle). Estrogen encourages growth of the endometrium and provides positive
feedback to the anterior pituitary to stimulate release of more FSH/LH leading to the midcycle gonadotropin
surge. About 1 week before ovulation, one follicle becomes dominant meaning that it becomes more
responsive to FSH. The follicle secretes lots of inhibin which downregulates FSH and causes atresia of the
other follicles.
2nd week of the proliferative phase.
Estrogen
Progesterone
Cycle greater than 35 days
Cycle less than 21 days
Frequent but irregular menstruation
Heavy, irregular menstruation
During the follicular phase, both estrogen and progesterone are low. FSH is fairly low as is LH initially. LH
spikes about halfway through the follicular phase which increases estrogen above its threshold. Estrogen
feeds back onto LH which causes it to spike along with an estrogen spike. FSH is also increased and has a
small spike along with the LH spike. This causes ovulation and begins the secretory/luteal phase. LH and
FSH then drop. Estrogen increases again but Progesterone increases a lot throughout the whole phase thus
maintaining the lining of the endometrium. Everything drops when entering the menstrual phase which
allows the endometrial llining to shed.
A primordial follicle consists of an oocyte surrounded by a single layer of squamuos granulosa cells. The
granulosa cells enlarge and become cuboidal turning the follicle into a primary follicle. The primary follicle
then enlarges and the granulosa cells form more than one layer. The Zona Pellucida then forms around the
oocyte. The structure becomes a secondary follicle when fluid filled vesicles develop among the granulosa
cells and a well developed capsule, Theca layer, becomes apparent around the granulosa cells. The Theca
has both internal and external layers. It becomes a mature follicle when the vesicles form a single antrum.
At full maturity, the oocyte is located in the cumulus mass.
During ovulation, the oocyte is released with some granulosa cells called the corona radiata. The remaining
granulosa cells divide rapidly and enlarge to form the corpus luteum which makes progesterone for the
remainder of the cycle or the beginning of pregnancy. The corpus luteum then degenerates to form the
corpus albicans and eventually becomes fibrotic.
Increased estrogen, increased GnRH and increased GnRH receptors on anterior pituitary, estrogen surge
precedes LH surge. Increased temperature from increased progesterone.
Blood from ruptured follicles which can cause peritoneal irritation that mimics appendicitis.
Primary oocytes begin Meiosis I during fetal life but don't complete Meiosis I until just before ovulation. Thus
Meiosis I is arrested in Prophase for years until ovulation. Meiosis II arrests in metaphase until fertilization.
If there is no fertilization, the secondary oocyte degenerates.
Begins with a diploid Oogonium (2N) which replicates (interphase) to become a diploid primary oocyte (4N).
The Primary oocyte then arrests in Prophase I until ovulation. During ovulation it divides to become a
secondary haploid oocyte (2N) and a polar body which degenerates. It arrests in Metaphase II here until
fertilization. The secondary Oocyte divides again to become a Haploid Ovum (1N) and another polar body
that degenerates.
Most commonly happens in the upper end of the Fallopian tube (the ampulla). Typically within a day after
ovulation.
6 days after fertilization. The trophoblast secretes Beta-HCG which is detectable in the blood 1 week after
conception and in urine (home test) 2 weeks after conception.
The decrease in maternal steroids induces lactation.
Suckling increases nerve stimulation which increases oxytocin and prolactin production thus maintaining milk
production.
PRL induces and maintains lactation and decreases reproductive function.
Helps with milk letdown and may be involved with uterine contractions.
Syncytiotrophoblast of the placenta.
Maintains corpus luteum (thus progesterone) for the first trimester by acting LH. The Placenta synthesizes its
own estriol and progesterone during the 2nd and 3rd trimester and the corpus luteum degenerates.
hCG is used to detect pregnancy because it appears early in the urine.
hCG is elevated in Hydatidiform moles, Choriocarcinoma, Gestational trophoblastic tumors (and other tumors
IDecreased
think)
Estrogen production due to age linked decline in follicles. Significantly increased FSH, increased
LH, increased GnRH. Average age of onset is 51, earlier in smokers. Usually preceded by a few years of
irregular periods.
Estrone from peripheral conversion of androgens. Increased androgens can cause hirsutism (that's why your
grandma has a mustache)
HHAVOC-Hirsutism, Hot flashes, Atrophy of the Vagina, Osteoporosis, Coronary artery disease
47 (XXY). Causes testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair
distribution. May cause developmental delay. Usually a Barr body is present (inactive X chromosome)
Dysgenesis of seminiferous tubules causes decreased inhibin which leads to increased FSH. Abnormal Leydig
cell
function
causes
decreased
and increased
and estrogen.
45 (XO).
Causes
short
stature,testosterone
ovarian dysgenesis
(streakLH
ovaries),
shield chest, bicuspid aortic valve,
webbing of the neck from cystic hygroma, preductal coarctation of the aorta, no Barr body and primary
amenorrhea.
47 (XYY). Phenotypically normal, very tall, severe acne, antisocial behavior in 1-2%, normal fertility.
Increased testosterone and increased LH (female phenotype I think)
Decreased testosterone and increased LH from gonadal failure and lack of feedback.
Decreased testosterone and decreased LH from pituitary failure not stimulating the gonads.
Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex.
46 (XX). Ovaries are present but the external genitalia are virilized or ambiguous. It's due to excessive or
inappropriate androgen exposure during early gestation. Usually congenital adrenal hyperpasia or exogenous
androgen administration.
46 (XY). Testes are present but external genitalia are female or ambiguous. The most common reason is
androgen insensitivity syndrome aka testicular feminization.
(46, XX or 47, XXY). Both ovaries and testicular tissue present. Ambiguous genitalia. Very rare.
Defect in androgen receptors resulting in normal-appearing female. Female external genitalia with a
rudimentary vagina. Uterus, uterine tubes are generally absent. No sexual hair. Testes are often found in
the labia majora and must be surgically removed to prevent malignancy. Increased testosterone (although
no response), increased estrogen and LH
Inability to convert testosterone to DHT. Ambiguous genitalia until puberty when the massive testosterone
increase causes masculinization and increased growth of the external genitalia. Testosterone/estrogen levels
are
normal;
LH of
is normal
or villi
increased.
Internal genitalia
are epithelium
normal. (trophoblast) that presents with
Cystic
Swelling
chorionic
and proliferation
of chorionic
What is a female
pseudohermaphrodite?
abnormal vaginal bleeding. Most common cause of Choriocarcinoma. See increased Beta-hCG, a
honeycombed uterus, looks like a cluster of grapes (if a cluster of grapes is totally disgusting looking). See
an
abnormally
uterus.
2 sperm
with aenlarged
completely
empty egg. Classically have a snowstorm appearance with no fetus during first
sonogram. Moles can lead to uterine rupture. Treat with dilitation and curettage and methotrexate. Monitor
Beta-hCG.
Karyotype is 46,XX or 46, XY. Massively increased hCG, increased uterine size, 2% convert to
adenocarcinoma, no fetal parts, 2 sperm +empty egg, 15-20% form malignant trophoblastic disease.
Karyotype is 69,XXY, slightly increased hCG, no change in uterine size, rare for it to convert to
choriocarcinoma, 2 sperm+1 egg, risk of malignancy is less than 5%
during the 1st weeks- low progesterone levels (no response to Beta-hCG, 1st trimester-chromosomal
abnormalities, 2nd trimester-bicornate uterus
Combination of hypertension, proteinuria and edema.
Pre-eclampsia + Seizures
Pre-existing hypertension, diabetes, chronic renal disease and autoimmune disorders.
Caused by placental ischemia due to impaired vasodilation or spiral arteries, resulting in increased vascular
tone. May be an issue with implantation.
Hemolysis, Elevated LFT's, Low Platelets from Pre-eclampsia
Headache, blurred vision, abdominal pain, edema of the face and extremities, altered mentation,
hyperreflexia. Lab findings include thrombocytopenia and hyperuricemia.
Delivery of the fetus as soon as it's viable. Otherwise bed rest, salt restriction, and monitoring/treatment of
hypertension. Treatment is IV magnesium sulfate and diazepam to prevent seizures of eclampsia.
What is Endometriosis?
How does Endometriosis manifest
clinically?
What are possible complications of
Endometriosis?
What is Adenomyosis?
Premature detachment of the the placenta from the implantation site. Fetal death and DIC may occur.
Increase in risk with smoking, hypertension and cocaine use.
Defective decidual layer allows the placenta to attach to the myometrium. No separation of the placenta after
birth. May cause massive bleeding after delivery. Associated with prior C-Section. Acreta does not penetrate
the entirety of the myometrium.
Just like Placenta Acreta but extends further into the myometrium.
The worst form of Placenta Acreta which involves the placenta extending all the way through the myometrium
to the serosa. The placenta may then attach to other organs like the bladder or rectum.
Attachment of the placenta to the lower uterine segment. May then occlude the internal os (so baby can't get
out). Associated with multiparity and prior C-Section.
Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
May cause postpartum hemorrhage.
History of infertility, Salpingitis/PID, ruptured appendix (at any point), prior tubal surgery or any lower
abdominal surgery, endometriosis.
Greater than 1.5-2 Liters of amniotic fluid. Associated with esophageal and duodenal atresia, causing
inability to swallow amniotic fluid. Also associated with anencephaly.
Less than 0.5 Liters of amniotic fluid. Associated with placental insufficiency, bilateral renal agenesis or
posterior urethral valves (in men) and thus an inability to excrete urine. Can cause Potter's syndrome.
Atypical appearance of the fetus in the womb as a result of oligohydramnios. Causes clubbed feet,
pulmonary hypoplasia and cranial anomalies.
Disordered epithelial growth. Begins at the basal layer of the squamo-columnar junction and extends
outward. Classified as CIN I, CIN II or CIN III (Carcinoma in Situ), depending on the extent of the dysplasia.
HPV 16 and 18
Multiple
sexual
smoking,
early
sexual
intercourse,
HIV infection
Pretty
much
thepartners,
cervical cancer
gone
really
nasty.
Often squamous
cell carcinoma. Papsmear can catch
cervical dysplasia (koilocytes) before it becomes invasive carcinoma. Lateral invasion can block ureters
causinf renal failure.
Cervical cell infected with HPV that is undergoing dysplasia. See large nuclei and large ring of cytoplasm.
See Attachment 3 for some pics.
Non-neoplastic endometrial glands/stroma in an abnormal location outside the uterus. Characterized by
cyclic bleeding from the ectopic endometrial tissue resulting in blood filled "chocolate cysts." Does anyone
else want to puke right now? Often in the ovary or on the peritoneum.
Severe menstrual-related pain.
Often causes infertility, possibly due to retrograde mentrual flow or ascending infection.
Endometrium within the myometrium
Abnormal endometrial gland proliferaton usually caused by excess estrogen stimulation. Associated with
increased risk for endometrial carcinoma.
Postmenopausal vaginal bleeding. Risk factors are anovulatory cycles, hormone replacement therapy,
polycystic ovarian syndrome and granulosa cell tumors.
Most common gynecologic malignancy, usually between 55 and 65 years of age. Usually a progression of
endometrial hyperplasia so presents with vaginal bleeding after menopause. Risk factors are prolonged
estrogen exposure without progesterone, obesity, diabetes, hypertension, nulliparity and late menopause.
The more it's invaded the myometrium, the worse the prognosis.
Describe a Leiomyoma?
Most common cause of all tumors in females. Essentially a Fibroid. Often causes multiple tumors with well
demarcated borders. This is a benign smooth muscle tumor and malignant transformation is very rare.
Mostly occurs between 20-40 years old and is often asymptomatic. may cause abnormal uterine bleeding or
result in miscarriage. If bleeding is severe it may cause Iron deficiency anemia. See a whorled pattern of
smooth muscle bundles (doesn't become Leiomyosarcoma). See attachment 4 for a picture.
What is a Leiomyosarcoma?
What is the epidemiology of
gynecologic tumors?
What is premature Ovarian failure?
what are the most common causes of
anovulation?
What is a Choriocarcinoma?
Bulky, irregularly shaped tumor with areas of necrosis and hemorrhage. Nasty tumor. Typically arises de
novo, not from a Leiomyoma. Highly aggressive tumor with a tendency to recur. May protrude out of the
cervix and bleed (yuck!). More common in middle aged women and African American women.
Incidence- Endometrial>Ovarian>Cervical. Worst Prognosis- Ovarian>Cervical>Endometrial
Premature atresia of ovarian follicles in women of reproductive age. Presents with signs of menopause after
puberty
but
beforesyndrome,
age 40. See
decreased
estrogen
but increased
LH and HPO
FSH axis
b/c no
feedback. premature
Polycystic
ovarian
obesity,
Asherman's
Syndrome
(adhesions),
abnormalities,
ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, Cushing Syndrome and adrenal
insufficiency
Increased LH production leading to anovulation, hyperandrogenism due to deranged steroid synthesis by
theca cells. Enlarged bilateral cystic ovaries manifest clinically with amenorrhea, infertility, obesity and
hirsutism. Associated with insulin resistance, increased risk of endometrial cancer. Treatment is weight loss,
OCP, gonadotropin analogs, clomiphene or surgery.
Increased LH and FSH and increased Testosterone.
Distention of a ruptured Grafian Follicle. May be associated with hyperestrinism and endometrial hyperplasia.
Hemorrhage
into persistent
corpus
luteum.
regresses
spontaneously.
Commonly bilateral
or multiple
cysts.
Due toCommonly
gonadotropin
stimulation.
Associated with choriocarcinoma and
moles.
Blood-containing cyst from ovarian endometriosis. Varies with the menstrual cycle.
Most common
in adolescents
Malignant,
equivalent
to a male seminoma, but rarer (1% vs 30%). Sheets of uniform cells with hCG and
LDH.
Rare but malignant. Can develop during pregnancy in mother or the baby. Large, hyperchromatic
syncitiotrophoblastic cells. Increased frequency of theca-lutein cysts. Along with moles, comprise spectrum
of gestational trophoblastic neoplasia. hCG is the tumor marker.
What is a teratoma?
What is a serous cystadenoma?
What is a serous cystadenocarcinoma?
What is a Mucinous Cystadenoma?
What is a Mucinous
Cystadenocarcinoma?
What is a Brenner tumor?
What is a Fibroma?
What is Meigs' Syndrome?
What is a Granulosa Cell Tumor?
What is a Krukenberg tumor?
What causes squamous cell carcinoma
of the vagina?
What predisposes to Clear Cell
Adenocarcinoma?
Who is affected by Sarcoma
Botryoides (variant of
Rhabdomyosarcoma)
How do Bartholin's gland cyst
present?
Aggressive malignancy in the ovaries (testes in boys) and sacrococcygeal area of young children. These are
yellow, friable, solid masses. 50% have Schiller Duval bodies that resemble glomeruli. Alpha fetoprotein is
the tumor marker.
90% of ovarian germ cell tumors. Contain cells from 2-3 germ layers. Mature teratomas/Dermoid cysts are
the most frequent benign ovarian tumors/teratomas. Immature teratomas are aggressively malignant.
Struma
Ovarii
contain
functional
thyroid tissue.
Can bilateral,
present as
hyperthyroidism.
Makes up
about
20% of
ovarian tumors.
Frequently
lined
with Fallopian tube-like epithelium.
Benign.
Makes up about 50% of ovarian tumors, malignant and frequently bilateral.
Multilobular cyst lined by mucus-secreting epithelium. Benign. Intestine-like tissue.
Malignant! Pseudomyxoma peritonei- intraperitoneal accumulation of mucinous material from ovarian or
appendiceal tumor.
Benign tumor that looks like the bladder.
Bundles of spindle
shaped fibroblasts.
Associated
with Fibromas.
Triad of ovarian fibroma, ascites and hydrothorax. Causes pulling sensation in the
groin.
Secretes estrogen-causes precocious puberty. Can cause endometrial hyperplasia or carcinoma in adults.
See Call-Exner bodies-small follicles filled with eosinophilic secretions. Abnormal uterine bleeding.
GI Malignancy that metastasizes to the ovaries, causing a mucin-secreting signet cell adenocarcinoma.
Secondary to squamous cell carcinoma of the cervix.
Affects women who had exposure to DES in utero.
Affects girls < 4 years of age. Spindle shaped tumor cells that are desmin positive.
Rare. Present with pain in the labia majora. Can result from previous infection.
Small, mobile, firm mass with sharp edges. Most common tumor in those <25 years. See increasing siza
and tenderness with increasing estrogen such as during menstruation. Not a precursor to breast cancer.
Small tumor that grows in lactiferous ducts. Typically beneath areola. See serous or bloody nipple
discharge. Slight (1.5-2X) increased risk for breast carcinoma.
Large bulky mass of connective tissue and cysts with "Leaf like projections." Most common in the 6th
decade. Some may become malignant.
Common postmenopause. Arise from mammary duct epithelium or lobular glands. Overexpression of
estrogen/progesterone receptors on erb-B2 (HER-2 and EGF Receptor) is common. Affects therapy and
prognosis. Axillary lymph node involvement is the single most important prognostic factor.
Risk factors are increased estrogen exposure. Increased total number of menstrual cycles, older age at 1st
live birth, obesity (adipose tissue serves as a major source of estrogen in post-menopausal women by
converting androstenedione to estrone).
Malignant tumor of the breast that fills the ductal lumen. Arises from ductal hyperplasia. Early malignancy
without basement membrane penetration.
Worst and most invasive ductal carcinoma but also most common. Forms firm, fibrous, rock hard masses
with sharp margins and small, glandular duct like cells.
Malignant breast tumor, often multiple and often bilateral. See an orderly row of cells.
Malignant tumor with a good prognosis. See fleshy, cellular, lymphatic infiltrate.
Subtype of DCIS. See ductal caseous necrosis.
Nasty, malignant tumor with a 50% 5 year survival. See dermal lymphatic invasion by breast carcinoma.
See Peau d'orange-breast skin looks like orange peel.
Eczematous patches on nipples. Paget cells are large cells in the epidermis with clear halo around them.
May
be seen
on the
vulva.lumps
Suggests
underlying
carcinoma.
Mostalso
common
cause
of breast
after an
age
25. Presents
with premenstrual breast pain and multiple
lesions, often bilaterally. See a fluctuation in size of the mass. Usually does not indicate increased risk of
carcinomas.
Fibrosis-hyperplasia of breast stroma. Cystic-fluid filled, blue dome. Ductal dilation. Sclerosing adenosisincreases acini and intralobular fibrosis. Associated with calcifications. Epithelial hyperplasia-increase in
number of epithelial cell layers in terminal duct lobule. Increases risk of carcinoma with atypical cells.
Occurs in women >30 years of age.
Breast abscess. During breast feeding. Increases risk of bacterial infection through cracks in the nipple.
Staph
Aureus
is thelump.
most common
A
benign,
painless
Forms as pathogen.
a result of injury to breast tissue. Up to 50% of patients may not report
trauma.
Results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelter's syndrome or drugs
(estrogen, marijuana, heroin, psychoactive drugs, Spironolactone, Digitalis, Cimetidine, Alcohol,
Ketoconazole).
Nipple, Lactiferous sinus, major duct, terminal duct, lobules. All surrounded by stroma
Nipple-Paget's disease, breast abscesses. Lactiferous sinus-Intraductal papilloma, breast abscess, mastitis.
Major duct-Fibrocystic change, ductal cancer. Terminal ducts-Tubular carcinoma. Lobules-lobular carcinoma,
sclerosing adenitis. Stroma-Fibroadenoma, phyllodes tumor.
Dysuria, frequency, urgency, low back pain.
Usually bacterial, especially E. Coli
May be bacterial or abacterial.
Hyperplasia (not hypertrophy) of the prostate gland. May be due to an age related increase in estradiol with
possible sensitization of the prostate to the growth-promoting effects of DHT. Characterized by a nodular
enlargement of the periurethral (lateral and middle) lobes, which compress the urethra into a vertical slit.
Often present with increased frequency of urination, nocturia, difficulaty starting and stopping the stream of
urine and dysuria. May lead to distention and hypertrophy of the bladder, hydronephrosis and UTI's. Not
considered premalignant. Do see increased free PSA but not rapidly increasing like in cancer.
Use
alphainantagonists
Terazosin,
tamulosin,
which
relaxation
smooth
muscle.
Common
men >50. like
Arises
most frequently
from
thecause
posterior
lobe of of
the
prostate(peripheral
zone) and is
most commonly diagnosed by digital rectal exam and prostate biopsy. Prostatic acid phosphatase and PSA
are the most useful tmor markers. See increased total PSA with decreased fraction of free PSA. Osteoblastic
metastases in bone may develop in later stages and appears as lower back pain and an increase in serum
alkaline phosphatase and PSA.
Undescended testis. Lack of spermatogenesis due to increased body temperature. Also associated with
increased risk of germ cell tumors. Prematurity increases the risk of cryptorchidism.
95% of all testicular tumors. May present as a mixed germ cell tumor.
What is a Seminoma?
What is an embryonal carcinoma?
What is a yolk sac (endodermal sinus)
tumor in a man?
What is a Choriocarcinoma in a man?
What is a teratoma in a man?
How common are testicular non-germ
cell tumors?
What
What
What
What
What
What
What
is
is
is
is
is
is
is
Malignant, painless, homogenous testicular enlargement. Most common testicular tumor, mostly affecting
males age 15-35. See large cells in lobules with watery cytoplasm and a fried egg appearance. These are
radiosensitive, only metastasize late and have a great prognosis.
Malignant, painful tumor with a worse prognosis than a seminoma. Often glandular or papillary morphology.
Can differentiate and become other tumors and is associated with increased AFP and hCG.
Yellow, mucinous tumor analagous to an ovarian yolk sac tumor. See Schiller Duval bodies which resemble
primitive glomeruli.
Malignant, hCG secreting tumor. Has distinct syncytiotrophoblastic and cytotrophoblastic elements. Causes
hematogenous metastases.
Similar to females except that mature teratomas in men are usually malignant.
5% of all testicular tumors, most of which are benign.
Androgen producing tumor which causes gynecomastia in men, precocious puberty in boys. Contains Reinke
crystals and is golden brown in color.
Androblastoma from the sex cord stroma.
Most common testicular cancer in older men. It's pretty much lymphoma in the testicles.
A lesion in the serous covering of the testis. Presents as testicular masses that can be transilluminated.
Dilated vein in pampinoform plexus which can result in infertility. Looks like a bag of worms.
Increased fluid secondary to incomplete fusion of the processus vaginalis
Dilated epididymal duct
Gray, solitary, crusty plaque, usually on the shaft of the penis or on the scrotum. Peak incidence is in the 5th
decade of life. Progresses to invasive squamous cell carcinoma in <10% of cases.
Red, velvety plaques, usually involving the glans penis. Otherwise similar to Bowen's disease.
Multiple papular lesions. Affects younger men but isn't usually invasive
Essentially like any other SCC, just on the penis. Commonly associated with HPV and lack of circumcision.
More common in Asia, Africa and South America.
Bent penis due to acquired fibrous tissue formation.
Glycogen and lipid accumulation, extra-cellular matrix changes, prolactin and IGF binding proteins increased,
COX-2 increase which increases PGE2, and influx od dedidual NK cells.
When the blastocyst enters the endometrial cavity, about 5 days after fertilization.
Non-cellular, porous layer of glycoproteins around the oocyte.
Early pregnancy factor, Platelet activating factor, human Chorionic Gonadotropin, Matrix Metalloproteinases
and Inhibitors of Matrix Metalloproteinases, Heparin binding-EGF like growth factor receptors
Apposition, Adhesion and Invasion
Decidua that forms underneath the embryo
Capsule of decidua over the embryo
Other decidua lining the uterine cavity
Both are increased but plasma is increased more than RBC. This results in a dilutional effect in hematocrit.
Creatinine clearance is increased. GFR increases fairly significantly. Increased clearance of creatinine and
urea results in serum creatinine and urea that are really low. Thus normal creatinine and urea are
problematic.
Estrogen
and progesterone both stimulate the respiratory center. Greater tidal volume and increased
respiration rate also cause increased minute ventilation, thus more CO2 is blown off. Thus respiratory
alkalosis from decreased PaCO2
May be due to decreased CO2 stimulating the respiratory center and causing subjective shortness of breath.
hCG simulates TSH since they share the same alpha subunit. Thus it stimulates T4 secretion during the first
10 weeks. Estrogen promotes growth of the pituitary and the thyroid and synthesis of thyroid binding
globulin. Thus T4 and cortisol are increased but free T4 and cortisol are the same.
No menses
one year
after age
40. from decreased ovarian function. Depletion of granulosa and thecal
Waxing
and for
waning
of estrogen
levels
cells. Lack of response to gonadotropins. Increased LH stimulates androgen production in stromal cells (thus
hirsutism)
Surgical removal or radiation of ovaries. Turner syndrome. Family history of early menopause and left
handedness (seriously???)
Average age is 51. The age at which it's determined is genetically determined, but smokers reach
menopause early and peri-menopause is mid-to late 40's.
Secondary amenorrhea, hot flushes, night sweats, atrophic vaginitis with pruritis, burning, bleeding and
dyspareunia. Also see mood swings, anxiety, depression, insomnia, decreased libido, urinary incontinence,
headaches, tiredness, lethargy, and osteoporosis with increased risk of Colle's and vertebral fractures.
Increase in LH and FSH from a drop in estrogen (LH) and progesterone (FSH)
Estrogen replacement, progestins added if the uterus is still present to prevent endometrial adenocarcinoma.
Thromboembolism, Coronary heart disease, stroke, slightly increased risk for breast cancer, increased risk for
dementia in women over 65.
Excess hair in normal hair-bearing areas.
Hirsutism plus male secondary sex characteristics
Polycystic ovary syndrome, idiopathic causes, adrenogenital syndrome, insuline resistance, drugs like
androgenic progestins, phenytoin, cyclosporin, minoxidil. Can also be from ovarian tumors like a leydig or
sertoli-leydig cell tumor, adrenal tumors producing Cushing syndrome, decreased steroid hormone binding
globulin from obesity and hypothyroidism.
What is Dysmenorrhea?
What is the treatment for Primary
Dysmenorrhea?
What is the treatment for secondart
Dysmenorrhea?
What is dysfunctional uterine
bleeding?
What are some types of dysfunctional
uterine bleeding?
What is most common cause of
irregular bleeding?
What causes anovulatory
dysfunctional uterine bleeding?
What causes ovulatory dysfunctional
uterine bleeding?
How do you treat ovulatory
dysfunctional uterine bleeding?
What is Primary Amenorrhea?
What is Secondary Amenorrhea?
What are some causes of
amenorrhea?
What are causes of abnormal vaginal
bleeding in a pre-pubertal girl?
What are some causes of abnormal
vaginal bleeding between menarche
and 20 years?
Syndrome that occurs around menarche. See increased synthesis of LH and decreased synthesis of FSH.
Increased LH increases androgen synthesis resulting most often in hirsutism. Androgens are then aromatized
to estrogen in adipose cells increasing the risk of endometrial carcinoma. The increased estrogen feeds back
positively on LH and negatively on FSH. Suppression of FSH causes follicle degeneration resulting in fluid
accumulating and producing subcortical cysts that then enlarge the ovaries.
Menstrual irregularities, mostly oligomenorrhea and often hirsutism, infertility or obesity.
LH:FSH ratio >2. Increased serum testosterone and androstendione. Increased serum estrogen.
Weight reduction in obese women. Low dose OCP's or medroxyprogesterone to suppress steroidogenesis and
LH. Can use Spironolactone if OCP's are unacceptable to block androgen receptors on the hair follicle. LHreleasing hormone analogs inhibit ovarian androgen production.
Loss of blood >80 mL per period. It's likely if sheets are stained despite heavy protection. Excessive
passage of clots indicates that plasmin does not have enough time to dissolve clot.
Painful menses, occuring in approximately 50% of women. Primary type occurs in ovulatory cycles due to
increased prostaglandin PGF-2alpha. See increased uterine contractions from increased prostaglandins. The
secondary type is from endometriosis, adenomyosis, leiomyomas, or cervical stenosis.
NSAID's, OCP, nifedipine, magnesium sulfate
Essentially deal with the underlying disease.
Abnormal uterine bleeding that is unrelated to an anatomic cause. Note that this is a diagnosis of exclusion.
Menorrhagia, Hypomenorrhea, Metrorrhagia, Menometrorrhagia, Oligomenorrhea, Polymenorrhea
Anovulatory cycle in 90% of cases but less than 10% due to anovulation during reproductive years.
Excessive estrogen stimulation relative to progesterone resulting in an absent secretory phase. It produces
excessive endometrial
hyperplasia
and
excessivematuration
bleeding. of the corpus luteum. This causes inadequate
Inadequate
luteal phase
resulting in
inadequate
synthesis of progesterone and delay in the development of the secretory phase. May see decreased 17-OH
progesterone .
If the follicle size is normal, supplement progesterone. If the follicle size is inadequate, give clomiphene
sulfate.
Absence of menses by age 16. Most cases are due to constitutional delay with a family history of delayed
menses.
Absence of menses for 3 months, most commonly due t pregnancy.
Hypothalamic or pituitary dysfunction resulting in decreased LH and FSH which results in decreased estrogen
and progesterone. Ovarian disorders cause problems in synthesis of estrogen or progesterone.
Vulvovaginitis, poor hygeine, infection, gonrrhea, sexual abuse, foreign bodies, embryonal
rhabdomyosarcoma
Pregnancy and related complications, ovulatory dysfunctional uterine bleeding, PID, hypothyroidism,
submucosal leiomyomas, adenomyosis, endometrial polyp, endometriosis
Anovulatory dysfunctional uterine bleeding, endometrial hyperplasia, cancer.
Entirely covered by the chorionic plate. The chorionic villi vessels converge with the umbillical cord.
Chorion is covered with amnion
Contains cotyledons covered by decidua basalis.
Into the intervillous
space oxygen and nutrients and spiral arteries from the uterus that empty into the
Maternal
blood that delivers
space
Trophoblastic tissue
Syncytiotrophoblast.
Synthesizes hCG, and HPL which directly correlates with placental mass and has anti-insulin activity.
Cytotrophoblastic tissue
One umbillical vein and two umbillical arteries. The vein carries the oxygenated blood in this case
Increased incidence of congenital anomalies, defects including cardiovascular defects, trisomy 18 and
esophageal atresia.
Ascending infections, often from premature rupture of membranes
Treat prophylactically with IV Ampicillin+Erythromycin followed by PO amoxicillin and erythromycin. If
culture positive you can give IV penicillin or ampicillin
Infection of the umbillical cord
Infection of the placenta
Infection of the fetal membranes
Neonatal sepsis and meningitis. Treat with Cefoxitin or Ticaricillin-Clavulanate
Implantation over cervical os. Previous C Section is major risk factor
Painless vaginal bleeding, usually second or third trimester. The uterus is soft and non-tender and fetal
distress is usually not present.
Do not do a pelvic exam. Transabdominal ultrasound localizes the placenta and transvaginal ultrasound
confirms placenta previa.
Premature separation of the placenta due to formation of a retroplacental clot. This separates the placenta
from the implantation site. This is most common cause of late pregnancy bleeding
Hypertension, smoking, cocaine, advanced maternal age, trauma, chorioamnionitis, premature membrane
rupture, previous abruptio placentae.
Painful uterine bleeding, forceful uterine contractions or signs of preterm labor, usually see evidence of fetal
distress
Direct implantation into muscle without intervening decidua. Causes great risk for hemorrhage during
delivery, commonly requiring surgery to control bleeding. Often requires hysterectomy.
Umbilical cord inserts away from the placental edge-the vessels pass to the placenta through the membranes
between the amnion and chorion. Causes increased risk for hemorrhage if the vessels are torn. Deliver by C
Section to avoid vessel tear.
Increased risk of hemorrhage if they are detached.
Diabetes mellitus, Rh hemolytic disease of the newborn, congenital syphilis
Monochorionic and monoamniotic although they can have dichorionic placentas
Twin Twin Transfusion syndrome.
Toxemia of pregnancy
First pregnancy, more common in women <20 years and >35 years, history of previous preeclampsia,
positive family history, multiple gestations, african american, thrombocytosis, obesity
Abnormal placentation causing mechanical or functional obstruction of the spiral arteries. The abnormal
trophoblastic tissue invades the spiral arteries. Imbalance favors vasoconstriction over vasodilation
(decreased PGE2 and NO, increased TXA2, Ang II and increased sensitivity to Ang II)
Premature
aging
of the placenta,
multiple
placental
infarctions,
spiral arteries
show atherosclerosis
Hypertension,
proteinuria
from leaky
capillaries
(increased
inflammation),
dependent
pitting edema from loss
of albumin, weight gain, seizures in eclampsia, swollen endothelial cells in glomerular capillaries producing
oliguria.
Right upper quadrant pain and hepatomegaly, periportal necrosis with increased transaminases, HELLP
syndrome
Benign tumor of the chorionic villus from an empty egg and 2 sperm or an egg and 2 sperm.
The entire placenta is neoplastic. Dilated swollen villi without fetal blood vessels. No embryo is present.
Ovum 46, XX, lacking maternal chromosomes. The chromosomesare derived from the father, either 2 sperm
or duplicated 23X sperm in the ovum
Complete mole. Presents with painless vaginal bleeding in fourth, fifth month of pregnancy. Causes severe
vomiting, pre-eclampsia, uterus that is too large for gestational age, increased hCG for gestational age, and
snowstorm
appearance
onorultrasound.
Not all villi are
neoplastic
dilated? Embryo is present but this is triploid. Egg with 23X is fertilized by 23X
and 23Y sperm. (Not that if the embryo is doubled, it's not considered a mole). This has a low risk of
choriocarcinoma.
malignant tumor composed of syncytiotrophoblast and cytotrophoblast without chorionic villi. Risks are
complete mole, spontaneous abortion and normal pregnancy
Lungs and vagina-hemorrhagic lesions
Predominantly fetal urine, initially plasma ultra-filtrate from mom. High salt content causes ferning when
dried on a slide-good sign of premature rupture of amniotic sac.
Most common painful breast mass in women <50 years old. Causes distortion of normal cyclic breast
changes. Some cysts have hemorrhage into the cyst fluid-called blue-domed cysts. Vary in size with the
menstrual cycle but have no malignant potential
Proliferation of small ductules/acini in the lobule-pattern is often confused with infiltrating ductal cancer.
Often contains microcalcifications.
Ducts are estrogen sensitive. See papillary proliferation called papillomatosis, apocrine metaplasia (change
to sweat producing glands), and atypical ductal hyperplasia (increased risk for carcinoma)
Main ducts fill up with debris causing dilation, rupture and inflammation. Results in greenish-brown nipple
discharge. May result in skin and nipple retraction stiulating cancer but no increased risk for breast cancer.
Trauma to breast tissue. Microscopic findings are lipid-laden macrophages with foreign body giant cells,
fibrosis and dystrophic calcification. See a painless indurated mass which is painful in the acute stage and
may
retraction
stimulating
cancer.
Most produce
commonskin
breast
tumor in
women <35
years. Discrete movable, painless or painful mass. It's a benign
tumor derived from the stroma which proliferates and compresses the ducts. The duct epithelium is not
neoplastic. Estrogen sensitive so increases in size during pregnancy. May spontaneously involute during
menopause.
Bulky tumor derived from stromal cells. Most commonly benign but can be malignant in some cases-see
hypercellular stroma with signs of mitoses in malignancy. Lobulated tumor with cystic spaces containing leaflike extensions.
Most common cause of bloody nipple discharge in women <50. Develops in the lactiferous ducts or sinuses.
No increased risk for cancer.
Prolonged estrogen stimulation, genetic susceptibility, especially if first generation relatives. Prolonged
estrogen stimulation from either early menarche or late menopause or nulliparity.
BRCA 1 and BRCA 2, Li-Fraumeni, RAS oncogene, ERBB2, RB suppressor gene
Breast feeding, moderate or vigorous physical training, healthy body weight.
Painless mass in the breast, usually the upper outer quadrant. Skin or nipple retraction, painless axillary
lymphadenopathy, hepatomegaly and bone pain if there are metastases.
Mammography-detects 80-90% of non-palpable breast masses. Does not distinguish benign from malignant
lesions. Can identify microcalcifications and spiculated masses with or without microcalcification.
Ductal carcinoma in situ, and sclerosing adenosis. Five or more microcalcifications that are punctate,
microlinear or branching all suggest malignancy
ER/PR expression generally confers a good prognosis whereas ERB2/NEU has a poor prognosis if amplified.
Nonpalpable mass. Forms a cribiform pattern (seive like) or comodo like pattern (necrotic center).
Commonly contains microcalcifications which allow it to be detected on mammogram.
Nonpalpable mass. Virtually always an incidental finding on breast biopsy for something else. Not
identifiable on mammography. Lobules are distended with bland neoplastic cells. Usually ER/PR positive.
Increased incidence of cancer in the opposite breast, that isn't LCIS.
Malignant, invasive breast tumor. Has a stellate morphology. Indurated, gray-white tumor. 1/3 have ERB2
amplification conferring poor prognosis. These look gritty on cut section and have reactive desmoplasia
causing induration.
Extension of DCIS into the lactiferrous ducts and skin of the nipple producing a rash with or without nipple
retraction. Palpable mass often present, see Paget's cells as well.
Invasive tumor associated with BRCA1 mutations. Bluky, soft tumor with large cells and a lymphoid infiltrate.
Most are ER/PR negative.
Invasive tumor that presents with erythematous breast with dimpling of the skin like an orange peel from
fixed opening of the sweat glands. Plugs of tumor block the lumen of dermal lymphatics causing localized
lymphedema. Has a very poor prognosis.
Invasive mass of neoplastic cells arranged in a linear fashion or in concentric circles.
Invasive mass that develops in terminal ductules. Increased incidence of cancer in the opposite breast.
Invasiveglandular
mass that
usually occurs
in male
older breast
women.
cells
surrounded
extracellular
mucin.
Benign
proliferation
in the
dueNeoplastic
to estrogen
from
increasedby
enstrogens,
decreased
androgens or a defect in androgen receptors. Most often unilateral. Normal in newborns, puberty or the
elderly.
Cirrhosis causes an inability to metabolize estrogen or to metabolize 17-ketosteroids which are then
aromatized to estrone. Genetic diseases like Klinefelter's and testicular feminization cuase gynecomastia.
Drugs that displace estrogen from SHBG, such as spironolactone or ketoconazole or drugs with estrogen
activity like DES or digoxin, or androgen blocking drugs like spironolactone or flutamide or that decrease
androgen production like leuprolide. These all increase estrogen.
Infection with Neisseria Gonorrhea
Thinning of the epidermis with parchment appearing skin. Most commonly in post-menopausal women.
White plaque like skin lesion (leukoplakia) due to squamous cell hyperplasia. Small risk for developing
Squamous Cell Carcinoma.
Benign tumor of the apocrine sweat gland. Causes painful nodule on the labia majora.
Dysplasia of the vulva, ranging from mild to carcinoma in situ. Strong association with HPV 16 and high risk
of developing squamous cell carcinoma
HPV 16, smoking, immunodeficiency.
Red, crusted vulvar lesion. Intraepithelial adenocarcinoma derived from primitive epithelial progenitor cells.
Malignant Paget cells contain mucin which is Periodic Acid Schiff positive. Spreads along the epithelium but
rarely invades the dermis.
Melanoma cells, histologically similar to Paget cells except these are PAS negative.
Gram negative coccobacilli that causes granuloma inguinale. It's phagocytosed by macrophages forming
Donovan bodies and results in creeping, raised sores that heal by scarring. Treat with bactrim or doxy.
Yeast and pseudohyphae which should be part of the normal vaginal flora. Causes vaginitis, pruritic vaginitis
with
a white discharge
and fiery
red mucosa.
Risk factors
and OCP's
STD-commonly
coinfecting
with Neisseria
Gonorrhea.
See are
red diabetes,
inclusionsantibiotics,
(reticulate pregnancy
bodies) in squamous
cells which then divide and form elementary bodies which can reinfect other cells. Causes sterile pyuria,
epididdmitis, proctitis (in males obviously) and urethritis, cervicitis, PID, perihepatitis (Fitz-Hugh Curtis),
proctitis and bartholin gland abscesses (in females obviously). Can also cause conjunctivitis and pneumonia
in a newborn.
Types 6 and 11 associated with Condyloma Acuminata (warts)-fernlike or flat lesions in the genital area.
Types 16 and 18 associated with dysplasia and squamous cell carcinoma. See koilocytes in squamous
epithelium. Cells have wrinkled, pyknotic nuclei surrounded by a clear halo.
Vaccine! Topical podophyllin, alpha-IFN injections and imiquimod cream
Gram negative diplococcus that infects glandular transitional epithelium in sites similar to Chalmydia. Causes
prululent lesions and urethritis. Can cause ectopic pregnancy, male sterility, disseminated gonococcemia,
septic arthritis, and Fitz Hugh Curtis.
Septic arthritis in the knee, tenosynovitis of the hands and feet, pustules on the hands and feet
Gram negative spirochete that causes syphillis. Primary syphillis presents with a solitary, painless, indurated
chancre on the penis, labia or mouth. Secondary presents with a maculopapular rash on the trunk, palms
and soles along with generalized lymphadenopathy, condylomata lata (flat lesions) and alopecia. Tertiary
syphillis presents with neurosyphillis, aortitis and gummas.
RPR or VDRL. Titers should decrease after treatment.
FTA-ABS which is positive with or without treatment
Intensification of rash in primary or secondary syphillis after proteins are released from the dead organisms
following penicillin treatment
Flagellated protozoan with jerky motility which produces vaginitis, cervicitis and urethritis. Causes a
strawberry colored cervix and fiery red vaginal mucosa with greenish, frothy discahrge.
Absence of the upper vagina and uterus resulting in primary amenorrhea
Remnant of the Wolffian/mesonephric duct which presents as a cyst on the lateral wall of the vagina.
Benign tumor of skeletal muscle in the vagina (can also be on the tongue or heart)
What is an Embryonal
Rhabdomyosarcoma?
What is clear cell adenocarcinoma of
the vagina?
What is Vaginal Adenosis?
What are some other DES related
abnormalities?
What is vaginal squamous cell
carcinoma?
What
does the cervix actually consist
of?
What lines the exocervix?
What lines endocervical glands?
How does the endocervical epithelium
transform into the exocervical
epithelium?
What is the pathogenesis of a
Nabothian cyst?
What is acute cervicitis?
What are clinical findings in acute
cervicitis?
What causes chronic cervicitis?
What is follicular cervicitis?
What is the purpose of a Cervical Pap
test?
What do superficial squamous cells
indicate on Pap?
What do intermediate squamous cells
on
Papdoindicate?
What
parabasal cells on Pap
indicate?
What types of cells are seen on Pap
from a non-pregnant and pregnant
woman?
What is a Cervical Polyp?
Describe Cervical Intraepithelial
Neoplasia, CIN
What is CIN I?
What is CIN II?
What is CIN III?
Necrotic, grape like mass protruding from the vagina, most often in girls <5 years
Adenocarcinoma of the vaginal wall (pretty self explanatory). Occurs in women with DES exposure since DES
inhibits mullerian
differentiation-tubes,
uterus, Produces
cervix andred,
upper
third of ulcerations
the vagina in the upper portion of
Precursor
lesion for
squamous cell carcinoma.
superficial
the vagina
Abnormally shaped uterus that thwarts implantation (T shape). Cervical incompetence which can cause
recurrent miscarriage.
It's what it sounds like. That said, primary SCC is associated with HPV 16. Most of these are actually
extensions of cervical SCC into the vagina.
Endocervix and exocervix. The exocervix begins at the cervical os
squamous epithelium
Mucus secreting columnar cells
Endocervical epithelium migrates down to the exocervix where exposure to the acid pH of the vagina causes
squamous metaplasia. This area is called the transformation zone and is the most likely location for
squamous dysplasia and cancer.
Metaplastic squamous cells block endocervical gland orifices resulting in obstruction to outflow of mucus.
This is a normal finding however.
Acute inflammation is often present in the transformation zone, however pathologic acute inflammation may
be due to infection-Chlamydia, Neisseria, Trichomonas, Candida, HSV, HPV.
Vaginal discharge, pelvic pain, dyspareunia, pain on palpation (chandelier sign), easy bleeding and
erythematous or exudative cervical os.
Essentially persistence of acute cervicitis
Pronounced lymphoid infiltrate with germinal centers caused by Chlamydia Trachomatis.
Screening test for squamous dysplasia and cancer. Evaluate the hormone status of the patient.
Adequate estrogen
Adequate progesterone
Lack of estrogen and progesterone.
Non-pregnant: 70% superficial, 30% intermediate squamous cells. Pregnant: 100% intermediate squamous
cells from progesterone effect.
Non-neoplastic polyp that protrudes from the cervical os. Arises from the endocervix, most commonly in
perimenopausal or multigravida women.
Most cases associated with HPV which produces koilocytes in squamous cells. Associated with early age of
sexual intercourse, multipe high-risk partners, high risk HPV types, smoking, OCP's and immunodeficiency.
Mild dysplasia involving the lower third of the epithelium
Moderate dysplasia involving the lower 2/3 of the epithelium
Severe dysplasia to carcinoma in situ involving the full thickness of the epithelium
Least common GYN cancer with higher incidence in developing countries. Most are squamous cell carcinomas
with the same risk factors as CIN
Abnormal vaginal bleeding, often post coital, malodorous discharge
Cancer often extends down into the vagna and out into the lateral wall of the cervix and vagina. May
infiltrate the bladder wall and obstruct the uterus causing postrenal azotemia and possibly death. May
metastasize distantly, e.g. to the lungs.
Breast budding (Thelarche), growth spurt, pubic hair, axillary hair, menarche (mean age is 12.8 years).
Between days 14 and 16
Progesterone
Fertilization usually occurs in the ampullary portion of the Fallopian tube. The fertilized egg spends 3 days
there, 2 days in the uterine cavity and then implants in the endometrial mucosa on day 21. There is an
exaggerated secretory phase in pregnancy called the Arias-Stella phenomenon.
Drop-off in serum estrogen and progesterone signalling endometrial cells to undergo apoptosis.
Prepares the follicle of the month, increases aromatase synthesis in the granulosa cells, increased synthesis
of LH receptors.
Increases synthesis of 17-ketosteroids in the theca interna (DHEA and androstenedione). Convert DHEA to
androstenedione and androstenedione to testosterone. Increase aromatization of testosterone. (Obviously
LH isn't doing these things directly but it uprgulates necessary enzymes)
Human chorionic gonadotropin-synthesized in the syncytiotrophoblast lining the chorionic villus. hCG acts as
an LH analog and maintains the corpus luteum to produce progesterone.
Mixture of estrogens and progestins which then prevent the midcycle LH surge and ovulation. Progestin
arrests the proliferative phase and cause gland atrophy and also inhibit LH directly. OCP's also render the
cervical mucus hostile to sperm and alter Fallopian tube motility.
Aromatized testosterone in granulosa cells. Primary estrogen in non-pregnant women.
Weak estrogen produced during menopause from adipose cell aromatization of androstendione
End product of estradiol metabolism. Primary estrogen of pregnancy derived from fetal adrenal, placenta and
maternal liver.
Equal derivation from ovaries and adrenal cortex
Almost exclusively from the adrenal cortex
derived from conversion of androstenedione to testosterone in the ovaries and adrenal glands. Can be
converted to DHT peripherally.
Binding protein for both estrogen and testosterone, mostly synthesized in the liver. Androgens, obesity and
hypothyroidism all decrease SHBG
SHBG preferentially binds testosterone over estrogen thus lack of SHBG can cause hirsutism in women.
What is Endometriosis?
What are clinical findings in
Endometriosis?
What is an endometrial polyp?
What are clinical findings of an
endometrial polyp?
What is a Hyatid Cyst of Morgagni?
Acute inflammation of the endometrium, most commonly as a result of bacterial infection following delivery
or miscarriage. Group B strep, staph a, bacteroides, C. trachomatis, N. Gonorrhoeae, E Coli.
Fever, uterine tenderness, prululent or foul vaginal discharge and abdominal pain.
Retained placenta, gonorrhea, IUD (with infection)
Like all chronic inflammatory conditions, you see plasma cells
Invagination of the stratum basalis into the myometrium. See glands and stroma thickening in the
myometrium and general enlargement of the uterus.
Menorrhagia,
dysmenorrhea
or pelvic
pain located outside the uterus causing cyclic bleeding of gland and
Functioning endometrial
glands
and stroma
stromal implants. Essentially reverse menses through the Fallopian tube allows inplantation of viable
endometrial cells. Can also be from vascular spread. Most common sites are ovaries, rectal pouch, Fallopian
tubes and intestines.
Dysmenorrhea, abnormal bleeding, painful stooling during menses, intestinal obstruction and bleeding during
menses, increased risk for ectopic pregnancy and enlargement of the ovaries with blood filled cysts
Benign polyp on the endometrium that enlarges with estrogen stimulation. Does not progress to endometrial
carcinoma but it can protrude through the cervix into the vagina.
Common cause of menorrhagia, spotting in between periods or after menopause
Cystic mullerian remnant most often in the fibriated end of the tube. May undergo torsion causing pain.
Inflammation in the pelvis, often due to N. Gonorrhoeae or C. Trachomatis. See Fallopian tubes that are filled
with pus or see hydrosalpinx (clear fluid in Fallopian tube). Causes fever, lower abdominal pain, cervical
motion tenderness, abnormal uterine bleeding, vaginal discharge, mucopurulent discharge in the cervical os,
and right upper quadrant pain (FHC Syndrome)
Multiple sex partners, vaginal douching, prior PID, unprotected sex
Invagination of the mucosa of the tube into muscle (tubal diverticulosis). Produces nodules in the tube that
narrow the lumen. Most likely a result of infection and can result in infertility and ectopic pregnancy.
Pregnancy that isn't in the uterus. Most often in the Fallopian tubes. Suspect with increased hCG and
sudden lower abdominal pain. Confirm with ultrasound. May be clinically mistaken for appendicitis.
Scarring from previous PID, Endometriosis, Altered tubal motility (SIN), progestin only pill, previous tubal
ligation, prior abdominal surgery.
Most occur in the broad ampullary region below the fimbriae.
Sudden onset of lower abdominal pain and tenderness, usually about 6 weeks after LMP, adnexal tenderness,
peritoneal signs, abnormal uterine bleeding, hypovolemic shock as a result of intraperitoneal hemorrhage.
Beta hCG is a good screening test but a positive hCG doesn't mean that there is an ectopic pregnancy.
Vaginal ultrasound showing an amniotic sac is confirmatory.
Inflammation of the ovary, possible as a result of mumps or PID.
Bilateral ovarian enlargement from hypercellular ovarian stroma. Stroma have vacuolated (leutenized)
stromal hilar cells which synthesize excess androgens. May cause hirsutism or virilization. Associated with
obesity, acanthosis nigracans, insulin resistance, and hypertension.
Nulliparity-increased number of ovulatory cycles increases risk, also causes increased risk for surface-derived
ovarian tumors. Genetic factors are BRCA1 and BRCA2 suppressor gene mutations, Lynch syndrome, Turner
syndrome (dysgerminoma), Peutz-Jeghers syndrome (sex cord tumors with annular tubules), history of
breast cancer, postmenopausal estrogen replacement, obesity
cancers are similar to those seen in the testicle, not many are malignant. Sex cord stromal tumors-derive
from stromal cells, may be hormone producing, most are benign. Metastases-most commonly from breast,
and stomach (Krukenberg tumors)
is
is
is
is
a
a
a
a
cystic teratoma?
Thecoma-Fibroma?
Granulosa-Theca cell tumor?
Sertoli-Leydig cell tumor?
What is a Gonadoblastoma?
What is a Krukenberg tumor?
Abdominal enlargement from fluid. Malignant ascites may cause induration in the rectal pouch on digital
rectal exam and intestinal obstruction with colicky pain. Palpable ovarian mass in postmenopausal woman,
malignant pleural effusion, torsion and infarction (cystic teratomas), signs of hyperestrinism in estrogen
secreting tumors or virilization in androgen secreting tumors.
Increased CA-125- only in surface derived tumors
Most common group of primary benign and malignant tumors, many are bilateral. Cysts are lined by ciliated
cells (like Fallopian tubes). A Serous Cystadenoma is benign. A Serous Cystadenocarcinoma is malignant
and has psammoma bodies and dystrophic calcification.
Cysts lined by mucus-secreting cells (like endocervical cells). Cause large multi-nucleated tumors. Seeding
of tumor produces pseudomyxoma peritonei. A mucinous cystadenoma is benign and may be associated with
Brenner tumors. A mucinous cystadenocarcinoma is malignant.
Malignant tumor associated with endometrial carcinoma. Commonly bilateral
Usually
a benign
tumor
thatcell
contains
rests (traditional-like
epithelium)
Most
common
benign
germ
tumor.Walthard's
See ectodermal
differentiation (hair,
sebaceous glands, teeth) mostly
found in a nipple like structure called Rokitansky Tubercle. A Struma Ovarii subtype has functioning thyroid
tissue
Benign tumor associated with Meigs' syndrome (ascited, right sided pleural effusions). Commonly calcify.
Low grade malignant tumor which produces estrogen and contains Call-Exner bodies
Benign tumor that produces androgens. Pure leydig cell tumors contain cells with crystals of Reinke.
Malignant tumor with a mixture of germ cells (dysgerminoma) and sex-cord stromal cells. Associated with
abnormal sexual development. May calcify
Metastasis to the ovary. Contains signet ring cells from hematogenous spread of gastric cancer.
Renal
What does the urinary system
derive from?
How many sets of kidneys are
there?
What is the pronephros?
Water goes under the bridge. Pass across the bifurcation of the
common iliac and pass under the uterine arteries or vas
deferens and then join the bladder on the posteroinferior side.
the
the
the
the
Lined by columnar epithelium
is Renal
Clearance?
What does
is mean
if
Cx<GFR?
What does it mean if Cx>GFR?
What does it mean if Cx=GFR?
How is Inulin used to calculate
GFR?
Describe autoregulation of
blood flow in the kidneys
What is Filtration Fraction?
What is Filtered Load?
Define
Nephron.
How
dothe
tubules
of the nephron
maintain low intracellular Na
and the Na gradient across the
tube?
How is bicarb
regulated/excreted in the
Proximal tubule?
CO2 and H2O cross the membrane and are made into bicarb by
carbonic anhydrase. That is excreted and then made into CO2
and H2O again.
Principle cells reabsorb Na and H2O and secrete K via the Na/K
ATPase. Intercalated cells secrete H and reabsorb K and HCO3.
Inserts more Na channels on the luminal side increasing Na
reabsorption.
normally accompany pressors. Constricts efferent arteriolesincreased FF to maintain GFR in low volume states. Increases
proximal tubule Na/H activity and can stimulate thirst in the
hypothalamus.
What is Erythropoietin?
What do prostaglandins do in
the kidney?
What is Renin?
What
What
What
What
Whatmuch
is Winter's
How
shouldFormula?
PCO2
increase when bicarb
increases?
What is respiratory acidosis?
What is respiratory alkalosis?
What are some causes of
Respiratory Acidosis?
What are some causes of
Anion Gap Metabolic Acidosis?
What are some causes of nonAnion Gap Metabolic Acidosis?
What are some causes of
Respiratory Alkalosis?
What are some causes of
Metabolic Alkalosis?
What is Type 1 (Distal) Renal
Tubular Acidosis?
What is Type 2 (proximal)
Renal Tubular Acidosis?
Blood in the urine. Causes fro, the upper urinary tract- renal
stone, glomerulonephritis (dysmorphic RBC's), Renal cell
carcinoma. Causes from the lower urinary tract- Infection,
transitional cell carcinoma, benign prostatic hyperplasia. Drug
related causes-anticoagulants, cyclophosphamide (hemorrhagic
cystitis and risk for transitional cell carcinoma)
Protein >150 mg/24 hours or >30 mg/dL via dipstick.
What is Orthostatic
Proteinuria?
often have alkaline pH, meat eaters have acidic pH. An alkaline
pH plus strong ammonia smell indicates a urease producing
pathogen.
is
is
is
is
a
a
a
a
WBC cast?
renal tubular cast?
fatty cast?
Waxy/Broad cast?
Heparan Sulfate
What is Post-Streptococcal
Glomerulonephritis?
What is Tubulointerstitial
Nephritis?
Hematogenous
spread
of the infection
to the
kidneys.
Grayish white areas
of abscess
formation
in the
cortex and
medulla. Microabscesses form in the tubular lumens and
interstitium.
Clinical-spiking fever, flank pain, frequency and dysuria. LabWBC casts, pyuria, bacteruria, hematuria
Chronic Pyelonephritis, Perinephric Abscess, Renal Papillary
necrosis, septicemia with endotoxic shock
U shaped cortical scars overlying a blunt calyx, visible on IV
pyelogram.
Hypertension
Penicillin esp. methicillin. Rifampin, sulfonamides, NSAIDs,
diuretics
Combination of Type I and IV hypersensitivity. Abrupt onset of
fever, oliguria and rash that resolves with withdrawal of the
drug. Causes tubular disease with a BUN:Cr <15, eosinophilia
and eosinophiluria
What is Renal
Osteodystrophy?
What is benign
nephrosclerosis?
Reduce
proteinuria
and in
treat
hypertension.
Common
renal disease
essential
hypertension caused by
hyaline arteriolosclerosis of arterioles in the renal cortex.
Results in tubular atrophy, interstitial fibrosis and glomerular
sclerosis. See small kidneys with a finely granular cortical
surface.
Sudden onset of accelerated hypertension with end organ
What is Malignany
Hypertension?
What is an Angiomyolipoma?