Polycystic Ovarian Syndrome (PCOS), Sexually Transmitted Infections (STIs), Ectopic Pregnancy,

Miscarriage, Post-natal Depression, Breast Cancer

Epidemiology, Etiology &
Risk Factors
Polycystic Ovarian Syndrome (PCOS)
 Worldwide Incidence: 1 in 10  PCOS is a polygenic condition characterized by  Diagnosis: ASRM Rotterdam Criteria
women; most common
endocrine disorder & cause
of infertility in women
 Australian Incidence: 12-21%
women of reproductive age
 Etiology: Unknown
 Risk Factor: Insulin-resistant
hyperinsulinemia, obesity
Diagnostic Criteria, Investigations & Health Complications, Treatment
Pathophysiology & Pathogenesis
Physical Exam/Clinical Features and Management
 Health Complications: Type II DM,
elevated androgen levels, menstrual irregularities,  Hyperandrogenism gestational DM, NAFLD, metabolic
and/or small cysts in one or both the ovaries.  Oligo-menorrhea/Oligo-ovulation/ syndrome, cardiovascular disease,
 Androgen Abnormalities: 60-80% of women with anovulation endometrial cancer, and pregnancy
PCOS have high circulating levels of testosterone;  Polycystic Ovaries on USG (>20 complications (preterm labor, DVT,
whereas 25% have high [dehydroepiandrosterone follicles of 2-9 mm) pre-eclampsia).
sulfate] or [DHEAS].  Diagnosis: AES Criteria  Pharmacological Therapy:
 Polycystic ovaries are characterized by a  Hyperandrogenism  Clomiphene: e.g. clomiphene
thick thecal layer, and thecal cells from these  Oligo-menorrhea/Oligo-ovulation/ citrate
ovaries secrete excess amount of androgens anovulation  Induces ovulation
under basal condition or in response to  Polycystic Ovaries on USG  Biguanide: e.g. metformin
stimulation by LH.  Exclusion of other related disorders  Improves fertility, decreases
 Abnormalities of Folliculogenesis:  Diagnosis: NICHD/NIH Criteria insulin resistance, and
 In anovulatory or oligo-ovulatory women with  Hyperandrogenism reduces circulating levels of
PCOS, antral follicle growth stops when the  Oligo-menorrhea/Oligo-ovulation/ testosterone
follicle is <10 mm in diameter. anovulation  Gonadotropins: e.g. FSH and
 Follicular arrest results from excessive  Exclusion of other related disorders HMG (Human menopausal
stimulation of follicular cells by insulin, LH, or  Clinical Features and Physical Exam: gonadotropin)
both.  Clinical Features: Hirsutism, infertility,  Used to induce ovulation, if
 Insulin enhances the response of granulosa menstrual irregularity, androgenic clomiphene/metformin
cells to LH, inducing premature luteinization alopecia (hair loss), acne, acanthosis therapy fails
of arrested follicles. nigricans (dark discoloration of body).  Aromatase Inhibitor: e.g.
  Further, granulosa cells from women with  Metabolic Features: Obesity, insulin Letrozole and Anastrozole
PCOS exhibit insulin resistance, impairing resistance, hyperlipidemia, and  Induces ovulation and
insulin-mediated glucose metabolism. hyperandrogenism. reduces circulating level of
 Thus, deficient energy mobilization within the  Psychological Features: Low self- testosterone (TST)
follicle contributes to anovulation or oligo- esteem, depression, anxiety, and  Statins: e.g. Simvastatin
ovulation. reduced quality of life.  Reduces TST synthesis, by
 Insulin Action Abnormalities:  Investigations and Assessments: inhibiting biosynthesis of
 Women with PCOS are also characterized by  Hyperandrogenism: Serum total cholesterol
peripheral insulin resistance, identical to that testosterone and sex hormone  Oral Contraceptives: e.g. ethinyl
of type II diabetes mellitus, leading to a 35- binding globulin (SHBG) estradiol + progestin
40% decrease in insulin-mediated glucose  Anovulation: Serum progesterone of  Decreases serum LH levels,
uptake. luteal phase decreasing ovarian
 Insulin resistance contribute to gonadotropin  Polycystic Ovary: Ultrasonography & synthesis of androgen and
abnormalities and hyperandrogenism via: serum anti-Mullerian hormone (AMH) SHBG; inhibits 5-
 High serum [insulin] reduce circulating  Cardiometabolic: Fasting serum lipids reductase
levels of SHBG, increasing bioavailability (total cholesterol, LDL, HDL, VLDL,  Antiandrogen Agents: e.g.
of testosterone TG), glucose, HbA1c; oral glucose Spironolactone, and Finasteride
 Acts directly on the anterior pituitary, tolerance test (OGTT); BMI; and BP.  Suppresses testosterone
hypothalamus, or both to induce GnRH  Renal: Serum creatinine, electrolytes; level
release. and GFR  Non-Pharmacological Therapy:
 Insulin resistance leads to impaired insulin  Nutritional Supplement: e.g.
response in target tissues (skeletal muscles, pyridoxine (B6), folate (B9), iron,
adipose tissues, liver) vitamin D3, omega 3
 Role of Gut Dysbiosis in PCOS:  Lifestyle Modification: Smoking
 Dysbiosis activates zonulin pathway, leading cessation, alcohol cessation,
to increased intestinal permeability due to: (i.) recreational drugs cessation,
disassembly of intestinal tight junctions; and increase in physical activity, and
(ii.) disruption of protective mucous layer. adequate sleep

Endometriosis
 Worldwide Incidence: 10% of  It is an estrogen-dependent, inflammatory, and  Clinical Symptoms: Patients commonly  Health Complications: Chronic pelvic
reproductive aged woman
 Risk Factors:
 Early menarche; >11-13
years
 Late menopause
 Short menstrual cycles;
<27 days
 Menorrhagia; i.e. heavy
menstrual bleeding
 Mullerian anomalies
 Nulliparity
 Low BMI
 Etiology: Retrograde Theory
Ectopic Pregnancy
 Incidence: 1-2% of the  Ectopic pregnancy refers to the implantation of  Clinical Features: Ranges from no  Surgical Management:
 Activates TLRs on immune cells, triggering
systemic inflammation.
 Systemic inflammation, combined with a high
fat and hyperglycemic diet, leads to insulin
resistance, observed phenotypic features of
PCOS, hyperandrogenism, hyperinsulinemia.
 Role of Lifestyle Factors in PCOS:
 Includes poor quality diet, inactivity, obesity,
stress, and sleep disturbance.
gynecologic disease characterized by
implantation of normal endometrial tissue outside
of the uterine cavity.
 Retrograde Theory: Endometriosis results from
retrograde movement of endometrial tissue into
the peritoneal cavity/pelvis through the fallopian
tubes.
 Leads to ectopic endometrial tissue which
undergo cyclical hormonal changes identical to
intrauterine endometrium.
 Becomes proliferative, secretory, and sheds-
off into the peritoneal cavity; which triggers
release of cytokines and prostaglandins.
 Cytokines (IL-1, IL-6, TNF-) and prostaglandins
trigger chronic inflammation; leading to deposition
of fibrous tissue.
present with pelvic pain, heavy menses,
painful menses, painful sex (dyspareunia),
painful defecation (dyschezia), painful  Pharmacological Therapy:
urination (dysuria), nausea/vomiting, and
bloating.
 Physical Examination: Generalized pelvic
tenderness, fixed/retroverted uterus  Surgical
 Investigations and Assessments:
 Laboratory Investigations: Complete
blood count (CBC); screening for
cancer antigen (CA-125), leukocyte
marker (CCR1) and STIs.
 Imaging: Transvaginal ultrasound, CT
scan, MRI
 Laparoscopy: “Gold Standard” for
diagnosis, and also has therapeutic
value.
 Dietary Modification: Low fat &
carbohydrate intake; increased
intake of fibers, unsaturated FAs,
vitamins, polyphenols
pain, infertility, dyschezia,
dyspareunia, and dysmenorrhea.
 Oral Contraceptive Pills: e.g.
progestin
 GnRH Agonists: e.g. leuprolide
Therapy: Involves
destruction of endometrial lesion,
drainage of the lesion, and removal of
cystic capsule
 general population the embryo outside of the uterine cavity, most symptoms to pelvic pain, abdominal  Salpingectomy: Involves removal
 Risk Factors: Tubal ligation, commonly in the fallopian tube (95%). discomfort, nausea/vomiting, syncope, of the fallopian tube partially or in
STIs, advanced maternal  Can also occur in the cervix, uterine cornea, and vaginal bleeding. full
age, smoking, prior history of ovaries, myometrium, and/or abdominal cavity.  Physical Examination: For determination  Salpingotomy: Involves removal
ectopic pregnancy, etc.  Damage to the fallopian tube, due to of hemodynamic stability, location of of the ectopic pregnancy via
inflammation, induces tubal dysfunction which tenderness; bimanual pelvic exam (for tubal incision while leaving the
results in impaired smooth muscle contraction and palpation of bilateral adnexa for abnormal fallopian tube in-situ
ciliary beating, leading to the implantation of the masses/structures, if any)  Intramuscular (IM) Methotrexate:
embryo within the fallopian tube.  Investigations & Assessments: Administered in patients with low
 Transvaginal USG + Serum hCG: For hCG levels
diagnosing suspected ectopic
pregnancy, and its confirmation with
hCG
 USG: Identification of fetal heartbeat,
gestational sac outside of the uterine
cavity
 Direct Laparoscopy: Performed when
imaging fails
Miscarriage/Spontaneous Abortion
 Incidence: ~26% of all  Miscarriage refers to expulsion from its mother  Clinical Features Depends on Type:  Threatened: USG should be
pregnancies end in embryo or fetus weighing ≤500 grams before 20  Missed: Mostly asymptomatic performed to assure the viability of
miscarriage weeks of gestation.  Threatened/Inevitable/Incomplete/ the fetus
 Etiology:  Clinical Classification: Complete: Characterized by vaginal  Incomplete/Missed/Anembryonic/
 Fetal chromosomal  Threatened Miscarriage; vaginal bleeding bleeding and abdominopelvic cramps Septic: Evacuation of retained
abnormality: trisomy of occurs but pregnancy continues  Septic: Characterized by vaginal products of conception (ERPOC)
autosomal recessive  Inevitable Miscarriage; cervix begins to dilate bleeding, abdominopelvic cramps, from the uterus under general
chromosome (50%); 45,  Incomplete Miscarriage; some, but not all, purulent cervical/vaginal discharge, anesthetic alongwith medical therapy
XO monosomy (20%); products of conception are expelled from the fever, tachycardia, and hypotension. with either mifepristone or
polyploidy (20%); and uterus  Investigations & Assessments: misoprostol
 others (10%)
 Risk Factors:
 Advanced maternal age:
~80% for women >40
 Prior miscarriage: 1 expelled
(~20%), 2 consecutive
(~28%), ≥3 consecutive
(~43%)
 Underlying Pathologies:
Thrombophilia, extreme
maternal weight, HTN,
antiphospholipid
antibody syndrome, &
PCOS.
 Lifestyle: Smoking, large
caffeine intake, trauma,
& malnutrition.
Hyperemesis Gravidarum
 Etiology: Unknown  It is characterized by inability of pregnant women
Epidemiology & Etiology
 Complete Miscarriage; all products of  Beta-hCG Levels  Septic: Involves treatment of infection
conception are expelled from the uterus  Transvaginal & Pelvic USG
 Missed/Silent Miscarriage; fetus died in-utero
prior to 20 weeks of gestation, but not
 Septic Miscarriage; intrauterine infection
results from an incomplete miscarriage
 Recurrent Miscarriage; ≥3 miscarriage have
occurred consecutively
 Anembryonic Miscarriage; embryonic
development ceases at early stage during
pregnancy, but the embryonic sac continues
to develop without fetal parts being evident
on an USG
 Clinical Features: Nausea and vomiting  IV Fluids Administration
to retain fluids or solids; leading to weight loss,  Investigations & Assessments:  Anti-emetics: e.g. metoclopramide
dehydration, and electrolyte imbalance.  Beta-hCG Levels
Pathophysiology & Pathogenesis Clinical Features & Diagnosis Complications & Treatment
 Sexually Transmitted Infections (STIs)
 STIs affecting the urogenital tract commonly manifest as anogenital discharge or changes to the anogenital skin (ulceration or lumps & bumps).
 Infections causing Genital Discharge:
 STIs: Chlamydia trachomatis, Neisseria gonorrhea, Trichomonas vaginalis, Mycoplasma genitalium
 Non-STIs: Bacterial Vaginosis, Candidiasis
 Infections causing Anogenital Skin Changes:
 Ulceration: Syphilis, Herpes Simplex Virus (HSV), Tropical Genital Ulcer Disease
 Lumps & Bumps: Human Papilloma Virus (HPV), Scabies, Pubic Lice, Molluscum Contagiosum
Chlamydial Infection
 Etiology: Chlamydia trachomatis  C. trachomatis is an opportunistic, gram negative,  Diagnosis: Nucleic Acid  Female: Tubal infertility
 Epidemiology: Most common intracellular, obligate bacteria. Amplification Tests (NAATs), PCR  LGV Complications: Pneumonitis,
bacterial STI in Australia,  Mode of Transmission: Via sexual contact  Male: Often symptomatic infection; Proctitis, Meningoencephalitis, and
particularly in 15-19 year old  Identical to virus, it can reproduce within the host characterized by urethral discharge Hepatitis.
females cell only following infection.  Female: Often asymptomatic.  Antibiotics: Azithromycin and/or
 Its growth cycle consists of two phase:  Symptomatic infection presents doxycycline (if complex)
 In the first phase; a small, metabolically with mucopurulent cervicitis,
inactive, resilient elementary body, which is which can progress to pelvic
capable of surviving extracellularly, attaches to inflammatory disease over days
the host cell followed by internalization through with a range of symptoms from
parasite-induced endocytosis. mild to severe (e.g. postcoital
 In the second phase; organism becomes bleeding, dyspareunia, fever,
metabolically active reticular body, multiplying pelvic & abdominal pain).
within the cell to produce upto 1000 new
elementary bodies within 20 hours, leaving the
host cell destroyed.
 Uses squamocolumnar and columnar epithelial cells
as their host in the endocervix and urethra initially,
but gradually spreads throughout the male & female
(fallopian tube, called acute salpingitis) genital tract.

Gonorrhea
 Etiology: Neisseria gonorrhea
 Epidemiology: Most common in
males having sex with men
 Following infection, an inflammatory cascade is
triggered characterized by neutrophil invasion.
 Infection could be either self-limiting or may
progress to a chronic infection (low grade, persistent
infection with inflammatory response).
 Chronic chlamydial infection is caused by
Lymphogranuloma venereum (LGV) serotype of
C. trachomatis, which invasibly penetrates the
skin and mucous membranes through tiny
abrasions.
 Triggers severe inflammation, necrosis, and
abscess of the inguinal lymph nodes once in
the lymphatic tissue, with spreading infection to
the surrounding tissue.
 N. gonorrhea is an aerobic, gram negative,  Diagnosis: Nucleic Acid  Female: Infection during pregnancy
diplococci bacteria having a short intubation period Amplification Tests (NAATs), can lead to miscarriage or preterm
(2-5 days). Culture delivery
 Mode of Transmission: Via sexual contact  Male: Often symptomatic infection;  Male: Urethral stricture & infertility,
 It uses hairlike filaments, called pili, for attachment characterized by profuse, purulent, but rarely
to epithelial cells (columnar, transitional, and urethral discharge  Antibiotics: Ceftriaxone with
stratified squamous) of the mucous membrane.  Female: Often asymptomatic. Azithromycin
 Following mucosal invasion, it triggers a rapid
inflammatory cascade alongwith exudation at the
site of infection.
 Females: Common site of infection is the urethra,
endocervical canal, and Skene’s or Bartholin glands.
 Males: Common site of infection is the urethra
 Concurrent oropharyngeal and anorectal infection

Non-gonococcal Urethritis
 Etiology: C. trachomatis, T.
vaginalis, M. genitalium,
Ureaplasma urealyticum, and
Bacteroides spp.
 Epidemiology: ~50% of all cases
of urethritis
Bacterial Vaginosis
 Etiology: Gardnerella vaginalis,
Mycoplasma hominis, Mobiluncus
spp., and Bacteroides spp.
 Epidemiology: Sexually active
women of reproductive age
Trichomoniasis
 Etiology: Trichomonas vaginalis
Candidiasis (Thrush)
 Etiology: Candida albicans
Syphilis
 Etiology: Treponema pallidum
 Epidemiology: Common in urban
men having sex with man; and in  Mode of Transmission: Via sexual contact from an
remote aboriginal populations
may be found in both males and females, in case of
oral or anal sexual contact.
 Occurs when there is dysbiosis of normal vaginal
flora (Lactobacilli spp.), leading to the adherent of
causal organism to the vaginal epithelium followed
by their overgrowth
 Triggers non-inflammatory response
 Infection characterized by “fishy odor” due to raised
vaginal pH, resulting from catabolic degradation of
proteins to amines.
 T. vaginalis is an anaerobic, unicellular, flagellated,
parasitic protozoan.
 C. albicans is a non-invasive, sugar fermenting
yeast (fungus).
 Infects vulvovaginal region in females; whereas
glans penis in males.
 T. pallidum is an anaerobic, spirochete bacterium.
 Capable of infecting any tissue or organ of the body.
infected partner (called horizontal transmission), and
 Male: Characterized by clear, white,
urethral discharge; dysuria; and
varying levels of penile discomfort or
itching.
 Female: ~50% cases asymptomatic;
while symptomatic cases involve
offensive vaginal discharge.
 Urethritis, in both sexes
 Female: Irritant vaginitis with “curdy”
or “cheesy” discharge
 Males: Balanitis (inflammation of the
gland penis)
 Diagnosis: Serology, PCR, ELISA,  CNS Complications: Neurosyphilis
FTA, TPPA, RPR  Cardiovascular Complications:
 Primary Syphilis (2-10 weeks to 1-3 Aneurysms, valve insufficiency (aortic
months): Chancre, Enlarged inguinal incompetence), heart failure
 via transplacental infection to the fetus (called lymph nodes  Co-factor in HIV transmission
vertical transmission).  Secondary Syphilis (2-6 weeks):  Antibiotics: Penicillin
 Organism enters the body through minute abrasions Flu-like illness, malaise, headache,
on the skin and mucous membrane, which occur fever, mucocutaneous rash
during intercourse.  Latent Syphilis (3-30 years): No
 Infection with T. pallidum is divided into four stages: symptoms
 Primary Syphilis: Begins at the site of invasion,  Tertiary Syphilis: Gummas
where the organism multiplies in the epithelium,
producing a granulomatous tissue reaction
called chancre. Chancre is a painless ulcer
most commonly present on the glans penis,
penile shaft, vagina, vulva, anus, or mouth.
Also, some organism drains into the nearby
lymph node, thereby stimulating an immune
response.
 Secondary Syphilis: During this stage, the
bacteria spreads to all major organ systems
through blood.
 Latent Syphilis: This phase involves
suppression of the infection by immune
responses mediated against the bacteria,
resulting in no clinical manifestation of the
disease. In early latent infection, transmission is
still possible; whereas in late latent infection,
patient can still develop clinical manifestation of
the disease but the infection is no longer
transmissible to partners.
 Tertiary Syphilis: Refers to lesions in the soft
 tissue, skin, and bones, called gummas.
Genital Herpes
 Etiology: Herpex Simplex Virus  Mode of Transmission: Via intimate contact from a  Diagnosis: Nucleic Acid  In-utero transmission can cause
(HSV-1 or HSV-2) person shedding virus either through his/her Amplification Tests (NAATs), spontaneous abortion or premature
 HSV-1: Causes primary secretion, peripheral lesion, or mucosal surface serology, ELISA delivery
infection  Susceptible mucosal surfaces include genital tract,  Causes blisters
 HSV-2: Causes either rectum, mouth, or oropharynx.
primary or recurrent  Following entry through the skin or mucocutaneous
infection layer, the virus undergoes replication in the dermis
and epidermis, leading to cell destruction.
 Virus spread to adjacent cells and eventually
localize within the sensory nerves of the dorsal root
ganglion, and remains in latent state until re-
activation.
 During latent state, viral genome is maintained in
the host cell nucleus without causing cell death.
Genital Warts
 Etiology: Human papilloma virus  HPV is a double stranded DNA virus devoid of an  Diagnosis: Hybrid Capture 2 DNA  Cancer
(HPV) envelope. Test  Laryngeal Papilloma: Occur in infant
 Trauma to the urogenital epithelium, which may  Causes dyspareunia whose mother had genital warts at
occur during intercourse, allows the virus to be the time of delivery; causing stridor,
transmitted to the basal cells of the epithelium. cough, hoarseness, abnormal cry,
 Infected epithelial cells undergo transformation and and respiratory distress.
proliferation.
 Low Risk Serotypes (PHV 6 & 11): Causes benign
lesions, called genital warts or condylomata.
 High Risk HPV Serotypes (PHV 16 & 18): Causes
anogenital intraepithelial neoplasia and cancer
(cervical, vaginal, vulval, anal).
 Gardasil, HPV vaccine in Australia, is administered

Scabies
 Etiology: Sarcoptes scabei
Pediculosis Pubis
 Etiology: Phthirus pubis
in Year 7 which protects against the HPV serotypes
6, 11, 16, and 18.
 Condylomata Acuminata: Refers to discrete warty
growths which are soft, skin-colored, whitish pink to
reddish brown.
 Mode of Transmission: Via skin-to-skin or sexual  Females: Lesions on the nipples,  Secondary infections
contact and buttocks  Hypersensitivity reactions
 Once the parasite is deposited on the skin, female  Males: Pruritic papules on the shaft  Treatment: Topical permethrin
parasite burrows through the stratum corneum, & glans of the penis, scrotum, and
followed by laying of eggs which matures into adult buttocks
mite in ~10 days.  Characterized by intense itching of
 Major site of burrowing: B/w the fingers, flexor the lesion, especially at night
surface of the wrist, & extensor surface of the elbow.
 Mode of Transmission: Via sexual contact, infected  Itching (pruritis)  Secondary infections
linen or clothing  Treatment: Topical permethrin
 Usually infects the pubic area, but also found in the
perineal and axillary hair