Block 4 - Reproductive Flashcards

Question 1

Q

Compare Visceral Pain, Somatic Pain & Referred Pain:

Definitions
Innervation
Description of pain
Stimulus

Question 2

Q

Give Examples of Visceral (12), Somatic (1) & Referred (1) Lower Abdominal Pain?

Answer

A

Visceral

Appendicitis
Inflammatory Bowel Disease
Pelvic Inflammatory Disease
Ischemic Colitis
Ovarian Cyst Rupture
Ectopic Pregnancy
Bladder Distention
Ovarian Torsion
Testicular Torsion
Muscle Spasm
Labour Pain
Dysmenorrhea

Somatic - Peritonitis (often secondary to abdominal inflammation or infection)

Referred - Renal Colic (Groin Pain)

Question 3

Q

Compare the primary afferent fibres: A-beta, A- and C fibres, in terms of:

Diameter
Myelination
Conduction Velocity
Receptor Activation Thresholds
Sensation on Stimulation

Question 4

Q

Describe the 6 steps in the pathophysiology of nociception?

Where do first-order afferent neurons synapse with second-order afferent neurons in the spinal cord? Where does it go then?
Where do first-order afferent neurons synapse with motor efferent neurons in the spinal cord? What happens next?
The Aδ and C fibres that synapse with second-order neurons release which 3 substances? What do these neurotransmitters bind to?
Where do second and third-order afferent neurons synapse?
Where do third-order neurons send their axons to? (5 examples)

Answer

A

Pathophysiology of Nociception:

Nociceptors detect noxious stimuli (non-mechanical, mechanical, heat and chemical stimuli).
Transmission of sensory signal via Aδ or C fibres (first-order afferent neurons) to dorsal root ganglion (DRG).
Aδ and C fibres can synapse with second-order afferent neurons in the dorsal horn of the spinal cord for signal transmission to the brain, or can synapse with motor neurons in the ventral horn of the spinal cord to instigate the pain withdrawal reflex.
The Aδ and C fibres that synapse with second-order neurons in the dorsal horn of the spinal cord are excitatory neurons and release glutamate as their primary neurotransmitter as well as other components such substance P, calcitonin gene-related peptide (CGRP) and somatostatin. These neurotransmitters bind to NMDA receptors on the post-synaptic neurons.
Second-order afferent neurons decussate (intercept in the shape of an X) at the spinal cord and follow the ascending spinothalamic tract where they then synapse with third-order afferent neurons in the thalamus.
Third-order neurons send their axons into the cerebral cortex to many regions (22 loci) including the somatosensory cortex (localisation of pain), prefrontal cortex and limbic system (emotional and motivational responses to pain), hippocampus (memory of pain) and amygdala (anxiety and fear of pain) - NB: Paleothalamic tract (spino-parabrachial-limbic pathway), the older portion of the spinothalamic tract, is linked to sense of impending doom.

Question 5

Q

List the differential diagnosis of acute lower abdominal pain.

Question 6

Q

What are 7 Normal Host Defence Mechanisms of the Female Genital Tract?

Answer

A

Epithelial Barrier: Vagina composed of stratified squamous epithelium with rapid turnover which prevents colonisation.
Protective Mucus: Traps and eliminates microbes. Acts as a barrier to microbes and contains antimicrobial peptides.
Antimicrobial Peptides Vaginal epithelial cells secrete lactoferrin, lysozyme, defensins and cathelicidin which have antimicrobial activity.
Acidic Environment: Lactobacilli produce high levels of lactic acid which create an acidic (pH 3.8-4.5) antimicrobial environment (prevents overgrowth of bacteria and pathogens).
Proinflammatory Cytokines: Vaginal epithelial cells release proinflammatory cytokines that recruit phagocytic cells to enter the vaginal epithelial layers.
MALT: Small diffuse concentrations of lymphoid tissue found in submucosa, populated by lymphocytes which encounter antigens passing through the mucosal epithelium.
Adaptive Humoral Immunity: IgG (dominant) and IgA for the neutralisation and clearance of microbes.

Question 7

Q

What are 6 Normal Host Defence Mechanisms of the Male Genital Tract?

Answer

A

Epithelial Barrier: Distal urethra composed of stratified squamous epithelium with rapid turnover which prevents colonisation.
Protective Mucus: Traps and eliminates microbes. Acts as a barrier to microbes and contains antimicrobial peptides.
Urine: Allows for frequent flushing of urethra to prevent ascending infection.
Antimicrobial Peptides Urethral epithelium secretes lactoferrin, lysozyme, defensins and cathelicidin which have antimicrobial activity.
MALT: Small diffuse concentrations of lymphoid tissue found in submucosa, populated by lymphocytes which encounter antigens passing through the mucosal epithelium.
Adaptive Humoral Immunity: IgG (dominant) and IgA for the neutralisation and clearance of microbes.

Question 8

Q

List the 8 flora of the female genital tract in health.

Answer

A

Commensal Flora of the Vagina (Uterine Cavity Sterile):

Lactobacilli (Dominant)
Gardnerella vaginalis: A gram-variable staining facultative anaerobic bacteria (clue cells)
Group B Streptococci
Candida albicans
Staphylococcus
Prevotella
Corynebacterium
Peptostreptococcus
NB: Overgrowth or imbalance of normal commensal bacteria of vagina flora can cause disease

Question 9

Q

How does Lactobacilli become part of the normal flora of the female genital tract?

What is the Physiologic Role of Lactobacilli in the vaginal Microenvironment?

Answer

A

Lactobacilli = Gram-positive rods.
Growth occurs at puberty through increased glycogen levels in response to estrogen.
Produce high levels of lactic acid which create an acidic (pH 3.8-4.5) that inhibits the growth of several bacterial and fungal species.
Produce H2O2 which increases the activity of host AMPs (muramidase and lactoferrin) as well as the antibacterial activity of the epithelial cells.
The loss of vaginal Lactobacilli due to antibiotic therapy, douching, sexual activity, pathologies or other factors is associated with increased susceptibility to infection.

High estrogen states (puberty and pregnancy) promote the preservation of a homeostatic (eubiotic) vaginal microenvironment → estrogen stimulates the maturation and proliferation of vaginal epithelial cells and the accumulation of glycogen. A glycogen-rich vaginal milieu is a haven for the proliferation of Lactobacilli facilitated by the production of lactic acid and decreased pH. Lactobacilli and their antimicrobial and anti-inflammatory products along with components of the epithelial mucosal barrier provide an effective first-line defense against invading pathogens.

Question 10

Q

Which commensal flora of the vagina is detected by the presence of clue cells?

Answer

A

Gardnerella vaginalis

Question 11

Q

Construct a clinical approach to a patient with acute abdominal pain.

Answer

A

History
Exam & Vitals
Ixs

Question 12

Q

What are 15 Common Pathogens of the Female Genital Tract?

Which 8 are STIs?

Answer

A

Bacterial Vaginosis
Aerobic Vaginosis
Vaginal Thrush
Trichomonas Vaginalis (STI)
Chlamydia Trachomatis (STI)
Neisseria Gonorrhoeae (STI)
Mycoplasma Genitalium (STI)
Donovanosis (STI)
Herpes Simplex Virus (STI)
Human Papilloma Virus (STI)
Syphilis (STI)
Hepatitis B
HIV
Pubic Lice
Public Scabies

Question 13

Q

What is Bacterial Vaginosis?

How does it present clinically?

Diagnosis?

Answer

A

Bacterial Vaginosis

The presence of mainly anaerobic microorganisms including Gardnerella vaginalis, Prevotella species, and Mycoplasma hominis, Mobiluncus species, with a decrease in Lactobacilli.
Presents with an offensive greyish “fishy” vaginal discharge, raised pH and mild vulval irritation.
Diagnosed by clue cells (vaginal epithelial cells studded with bacteria).

Question 14

Q

What is Aerobic Vaginosis?

Answer

A

Aerobic Vaginosis

The presence of mainly aerobic enteric commensals or pathogens, including Group B Streptococcus (S. agalactiae), Enterococcus faecalis, Escherichia coli, and S. aureus, with a decrease in Lactobacilli.

Question 15

Q

What is vaginal thrush?

How does it present clinically (8)?

Answer

A

Vaginal Thrush: An overgrowth of Candida albicans (yeast).

Presents with white “curd-like” vaginal discharge, normal pH, vulval itch, superficial dyspareunia, external dysuria, erythema, fissures and swelling.

Question 16

Q

What is Trichomonas Vaginalis?

How does it present clinically (5)?

Where is it more commonly found?

Answer

A

Trichomonas Vaginalis (STI)

Infection of a protozoan parasite at the vagina, the urethra and under the foreskin of the penis.
Presents with malodorous vaginal discharge (profuse and frothy), raised pH, “strawberry cervix”, vulval itch and cervicitis.
Rare, common in regional and remote areas.

Question 17

Q

What is Chlamydia Trachomatis?

What kind of pathogen is it?

How does it present clinically (6)?

Which sites can it infect? (3)

Answer

A

Chlamydia Trachomatis (STI)

Infection with Chlamydia trachomatis, a Gram-negative pleomorphic bacteria.
Presents asymptomatically (75%) or with vaginal discharge, normal pH, pelvic pain, intermenstrual bleeding, post-coital bleeding and ano-rectal symptoms.
Infection commonly at cervix in FRT, but can also affect rectum and throat.

Question 18

Q

What is Neisseria Gonorrhoeae?

What type of pathogen is it?

How does it present clinically?

Which sites can it infect? (3)

Answer

A

Neisseria Gonorrhoeae (STI)

Infection with Neisseria gonorrhoeae, a Gram-negative diplococci bacteria.
Presents with vaginal discharge, normal pH, dyspareunia with cervicitis, ano-rectal symptoms such as discharge, irritation, painful defecation and disturbed bowel function and conjunctivitis.
Infection commonly at cervix in FRT, but can also affect rectum and throat.

Question 19

Q

What is Mycoplasma Genitalium?

Which other STI does it have the same disease pattern as?

Which sites can it infect?

Answer

A

Mycoplasma Genitalium (STI)

Infection with Mycoplasma Genitalium.
Same disease pattern as for Chlamydia.
Infection commonly at cervix in FRT, but can also affect rectum and throat.

Question 20

Q

What is Donovanosis?

Which pathogen causes it?

Clinical features?

Where is the disease endemic?

Answer

A

Donovanosis (STI)

Infection with Klebsiella granulomatis which infects the skin around the genitals, groin or anal area and causes ulcers and destruction of the skin.
Rare cause of genital ulceration but should be considered in patients returning from areas where the disease may be endemic such as PNG, Southern Africa, India and parts of South America.

Question 21

Q

What is Herpes Simplex Virus (STI)?

Clinical Presentation?

Answer

A

Herpes Simplex Virus (STI): Infection with Herpes Simplex Virus 1 or 2 can cause genital herpes.

Presents with recurrent ano-genital ulcers or blisters, skin splits, erythema with itching/tingling, cervicitis often with visible ulcers and proctitis.

Question 22

Q

What is Human Papilloma Virus (STI)?

Which 2 strains cause it?

Clinical presentation?

Which strains cause cervical cancer?

Answer

A

Human Papilloma Virus (STI)

Infection with HPV 6 and 11 causes genital warts and presents with warty growths in and around genital skin, cervical lesions, perianal itch and rectal bleeding after passage of stools with anal lesions.
HPV 16 and 18 can cause cervical and other cancers.

Question 23

Q

What is Syphilis?

Which pathogen is responsible? What kind of bacteria is it?

How does it enter the body?

How does primary vs. secondary vs. tertiary syphilis present clinically?

Answer

A

Syphilis (STI)

Infection with Treponema pallidum
Gram-negative spirochete bacteria that enters the body through mucous membranes or abraded (torn or cut) skin.
Primary syphilis can present asymptomatically, or with non-tender genital ulcers, painless chancre and painless inguinal lymphadenopathy.
Secondary syphilis can present with fever, malaise, headache, lymphadenopathy, condylomata lata (warts), skin maculopapular rash of trunk, palms and feet and/or with neurological signs of cranial nerve palsies, ophthalmic signs and meningitis.
Tertiary syphilis can present with general paresis, aortic aneurysm and dilated aortic root (tertiary).

Question 24

Q

What is Hepatitis B?

How does it present clinically?

Answer

A

Hepatitis B: Infection with Hepatitis B virus. Presents asymptomatically, or with acute hepatitis and lethargy, nausea, fever and anorexia for a few days then jaundice, pale stools and dark urine.

Question 25

Q

What is HIV?

How does it present clinically?

What are the signs of subsequent immunodeficiency?

Answer

A

HIV

Infection with human immunodeficiency virus.
Presents with acute fever, rash, lymphadenopathy, pharyngitis, myalgia, diarrhoea two weeks after exposure, and will then be asymptomatic for several years following infection.
Signs of subsequent immunodeficiency include oral thrush, diarrhoea, weight loss, skin infections and herpes zoster.

Question 26

Q

What are Pubic Lice?

Which pathogen is responsible?

Which sites can it infect?

How does it present clinically?

Answer

A

Pubic Lice

Infestation of the small ectoparasite Phthirus pubis (can occur also at eyebrows, beards and armpits).
Presents with pubic or genital itch and/or rash, and debris in underwear.

Question 27

Q

What are the diagnostic criteria for STIs in:

Asymptomatic females?

Answer

A

Diagnostic Criteria for STIs: ASYMPTOMATIC FEMALE

Self-Obtained Low Vaginal Swab (SOLVS) for PCR (CT/NG)
First Void Urine (FVU) for PCR (CT/NG)
Serology (HIV, HBV, Syphilis +/- HCV)
+/- Rectal or throat swabs for PCR (CT/NG)

Question 28

Q

What are the diagnostic criteria for STIs in:

Asymptomatic males?

Answer

A

Diagnostic Criteria for STIs: ASYMPTOMATIC MALES

First Void Urine (FVU) for PCR (CT/NG)
Serology (HIV, HBV, Syphilis +/- HCV)
+/- Rectal or throat swabs for PCR (CT/NG)

Question 29

Q

What are the diagnostic criteria for STIs in:

Symptomatic females?

Answer

A

Diagnostic Criteria for STIs: SYMPTOMATIC FEMALES

Endocervical Swab (ECS) for PCR (CT/NG)
ECS for PCR (MG)
ECS for MC&S (NG)
HVS for MC&S (BV/Candidia/Trichomonas) + pH
Bimanual Pelvic Examination
Serology (HIV, HBV, Syphilis +/- HCV)
+/- Genital Ulcer Multiplex PCR (GUMP) for PCR
+/- Rectal or throat swabs for PCR

Question 30

Q

What are the diagnostic criteria for STIs in:

Symptomatic males?

Answer

A

Diagnostic Criteria SYMPTOMATIC MALES

Urethral Swab for PCR (CT/NG)
Urethral Swab for PCR (MG)
Urethral Swab for MC&S (NG)
Serology (HIV, HBV, Syphilis +/- HCV)
+/- Genital Ulcer Multiplex PCR (GUMP) for PCR
+/- Rectal or throat swabs for PCR

Question 31

Q

What are the diagnostic criteria for Gonorrhoea in females? and in males?

Answer

A

Diagnostic Criteria - Gonorrhoea

Females:

Self-collected lower vaginal swab for PCR and MC&S if not examined
First pass urine for PCR only if ECS or vaginal swab cannot be taken
Endocervical swab for PCR and MC&S if discharge or dysuria present
Pharyngeal swab for PCR and MC&S if patient had oral sex
Ano-rectal swab for PCR and MC&S if patient had anal sex or ano-rectal symptoms

Males:

First pass urine for PCR always
Urethral swab for PCR and MC&S if discharge or local symptoms present
Ano-rectal swab for PCR and MC&S in MSM even if asymptomatic
Pharyngeal swab for PCR and MC&S in MSM even if asymptomatic

Question 32

Q

What are the diagnostic criteria for Chlamydia in females? and in males?

Question 33

Q

What are the diagnostic criteria for herpes in males and females?

Answer

A

Herpes

Swab of base of ulcer or de-roofed vesicle for PCR (requires visible lesions to be present)

Question 34

Q

What are the diagnostic criteria for syphilis?

Answer

A

Diagnostic Criteria - Syphilis

Blood serology via enzyme immunoassay (EIA), Treponema pallidum Particle Agglutination Assay (TPPA), Treponema pallidum Hemaglutination Assay (TPHA) or Rapid plasma reagin (RPR) laboratory tests
Swab of ulcer for PCR to directly detect pathogen
Diagnosis is by a combination of serology, history and clinical assessment
If serology is negative, repeat testing after 2 weeks if clinical suspicion of syphilis

Question 35

Q

What are the diagnostic criteria for HIV?

Answer

A

Diagnostic Criteria - HIV

Blood test for HIV Ag/Ab, Western blot (confirmatory test), HIV p24 antigen (high during primary illness), CD4 lymphocyte (marker of immune function), HIV RNA (viral load, marker of HIV level in serum)
Blood or saliva sample for HIV rapid point of care test (result in 10 – 20 minutes but less sensitive or specific than standard test)

Question 36

Q

What are the 8 high-risk groups for STIs whom opportunistic testing should be considered?

Answer

A

People at the highest risk of STIs include:

Sexually active males and females who are 35 years or younger, and not in a stable, long-term relationship.
Those who are from a high prevalence country or have a sexual partner who is from a high prevalence country.
People who are experiencing homelessness.
People who have recently changed sexual partner.
People who frequently change their sexual partners.
Men who have sex with men (MSM) and women who have sex with MSM.
Aboriginal people
People who use methamphetamine and/ or inject drugs.

Question 37

Q

What is the Pharmacological Treatment for Gonorrhoea?

Answer

A

Pharmacological Treatment for Gonorrhoea

Ceftriaxone 500mg IMI, stat in 2mL 1% lignocaine PLUS
Azithromycin 2g PO, stat

Alternative treatments are not recommended because of high levels of resistance,

EXCEPT for some remote Australian locations and severe allergic reactions

Question 38

Q

What is the Pharmacological Treatment for Chlamydia?

Answer

A

Pharmacological Treatment for Chlamydia

Doxycycline 100mg PO, BD (twice a day) 7 days (21 days if symptomatic ano -rectal infection)
OR
Azithromycin 1g PO, stat (will not clear rectal infection)

Question 39

Q

What is the Pharmacological Treatment of Herpes?

Answer

A

Pharmacological Treatment of Herpes

Valaciclovir 500mg PO, BD for 5 - 10 days (for initial episode), 3 days (for episodic therapy) or 6 months (for suppressive therapy)
Alternative treatment includes Aciclovir 400mg PO, TDS for 5 - 10 days (for initial episode), Famciclovir 1g PO, BD for 1 day (for episodic therapy) or Famciclovir 250mg PO, BD for 6 months (for suppressive therapy)

Question 40

Q

What is the Pharmacological Treatment of Syphilis?

Answer

A

Pharmacological Treatment of Syphilis

Benzathine penicillin 1.8g IMI, stat (for infectious syphilis) or weekly for 3 weeks for non-infectious syphilis
Alternative treatment includes Procaine penicillin 1.5g IMI, for 10 days (for infectious syphilis) or 15 days (for non-infectious syphilis)

Question 41

Q

What is the Pharmacological Treatment of HIV?

Answer

A

Pharmacological Treatment of HIV

First-line initial HIV therapy is currently a combination of two nucleoside/nucleotide reverse transcriptase inhibitors (NRTIs) and an integrase strand transfer inhibitor (INSTI).

Highly active antiretroviral therapy (HAART)
2 x Nucleoside Reverse Transcriptase Inhibitors (emtricitabine and tenofovir)
PLUS
1 x Non-NRTI (efavirenz) OR 1 x Protease Inhibitor (atazanavir plus ritonavir) OR 1 x Integrase Inhibitor (dolutegravir)

Question 42

Q

What are the 9 Principles of Management and Treatment of STIs?

Answer

A

Principles of Management and Treatment of STIs

Antibiotic therapy (treat early on suspicion i.e. ceftriaxone and azithromycin can treat chlamydia and gonorrhoea)
Advise no sexual contact for 7 days after treatment is administered
Advise no sex with partners from the last 6 months until the partners have been tested and treated if necessary
Notify the state health department (notification form)
Contact tracing
Follow up with patient
Provide patient with STI factsheet, education, risks and post-test counselling
Provide patient with education on safe sex and prevention measures
People should have regular STI tests (screening) if they think they might have an STI, they have had unprotected sex, they have had a condom break or it has fallen off during sex, their partner has another sexual partner or has had previous sexual partners, they have shared injecting equipment and they are starting a new sexual relationship

Question 43

Q

Show ability in taking a sexual history.

Question 44

Q

Perform, under supervision, an examination of the female genitalia and pelvic organs including how to undertake cervical sampling.

Question 45

Q

Develop skills in the appropriate collection of microbiological and serological samples in a female sexual health check-up.

Question 46

Q

Develop skills in the appropriate collection of microbiological and serological samples in a male sexual health check-up.

Question 47

Q

Outline an approach to HIV pre-test counselling, including informed consent and confidentiality.

Who Should Be Offered HIV Testing? (7)

Answer

A

Who Should Be Offered HIV Testing

Unprotected sexual contact, particularly contact that took place in a country with a high prevalence of HIV, or with a person who has recently travelled to or migrated from a high prevalence country

Travel within a country with a high prevalence of HIV

Unprotected male to male sex

Presence of a sexually transmitted infection

Sharing injecting equipment or the use of unsterile tattooing or body piercing equipment

Exposure to unscreened blood or blood products through medical procedures

Anyone who is subjected to sexual assault

Question 48

Q

Outline an approach to HIV pre-test counselling, including informed consent and confidentiality.

What Information should be given to the Patients Before an HIV Test? (12)

Answer

A

Information For Patients Before an HIV Test

Talk to patient about patient confidentiality and legal responsibilities, such as the need to notify the Department of Health about any HIV diagnosis
Informed patient consent is always required
Discuss that HIV is a virus that is predominantly transmitted through blood-to-blood contact, or contact with sexual secretions.
Discuss possible transmission routes of HIV, e.g. unprotected sex, sharing of injecting equipment
Explain what an antibody test is and what the test involves
Explain that there is a 3-month window period, and follow up testing may be needed depending on the patient’s circumstances
Ensure your patient is aware of the possibility of a positive result
Explain that positive results are reported to the Department of Health
Explain that for positive results there is a requirement for contact tracing, and explain ways this can be done
Be aware of cultural understandings of sickness and wellbeing, and whether language is a barrier for understanding
Check that the patient knows they have to return to collect the test results in person and organise a follow-up appointment
Discuss that, in the event of a positive result, HIV can be treated with ongoing daily medication, and that although HIV is a chronic condition, people who live with HIV can expect to lead long healthy lives and enjoy healthy family life

Question 49

Q

Outline an approach to HIV pre-test counselling, including informed consent and confidentiality.

How should a Negative HIV Result be conveyed?

Answer

A

Conveying a Negative HIV Result:

Ensure the name, result, date of birth and postcode are correct before seeing patient
Check that patient understands how to minimise risk of acquiring HIV (e.g. safer sex and safer injecting practices)
Review the window period and consider the need to retest

Question 50

Q

Outline an approach to HIV pre-test counselling, including informed consent and confidentiality.

How should a Positive HIV Result be conveyed?

Answer

A

Conveying a Positive HIV Result:

Should always be provided in person except in extenuating circumstances
Ensure the name, result, date of birth and postcode are correct before seeing your patient
Give the test result in person, and in a manner that is sensitive and appropriate to the patient’s gender, culture, behaviour, and language
Organise onwards referral to a HIV specialist, and answer questions about the referral process and indicate in referral that patient has been recently diagnosed with HIV
Confirm that HIV is a condition which can be treated, but not cured and that people living with HIV can live long and healthy lives when on treatment
Assess any immediate known support (family/friend/partner) who may provide any needed emotional support
Organise onwards referral to a support agency, to be accessed at the patient’s discretion
Perform contact tracing and partner notification
Discuss transmission of HIV, and how onwards transmission may be prevented
Discuss legal obligations and considerations, for example using condoms and practising safer sex

Question 51

Q

What is the Clinical Presentation of Acute PID?

Answer

A

Clinical Presentation - Acute PID

Variable presentation!
Many asymptomatic early in disease!
Severe lower abdominal/pelvic pain (usually bilateral and rarely more than two weeks’ duration)
Abnormal vaginal discharge
Abnormal uterine bleeding (intermenstrualbleeding, post-coital bleeding or menorrhagia)
RLQ pain or low back pain
Urinary frequency and dysuria
Fever
Abdominal tenderness
Acute cervical motion, uterine, and adnexal tenderness on bimanual pelvic examination
Purulent endocervical discharge and/or vaginal discharge

Question 52

Q

What is the Clinical Presentation of Chronic PID?

Answer

A

Clinical Presentation - Chronic PID

Abdominal/pelvic pain
Heavy and painful menstrual periods
Dyspareunia
Low-grade fever
Weight loss
Infertility

Question 53

Q

What is the Clinical Presentation of a General STI?

Answer

A

Clinical Presentation - General STI

Can be asymptomatic!
Sores or bumps on the genitals or in the oral or rectal area
Skin itch, rash, erythema, blisters or ulcers
Abnormal vaginal or urethral discharge
Dysuria
Dyspareunia
Abnormal uterine bleeding
Sore, swollen lymph nodes, particularly in the groin
Lower abdominal pain
Fever
Rash over the trunk, hands or feet
Painful defecation

Question 54

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Chlamydia?

Question 55

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Gonorrhoea?

Question 56

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Syphilis?

Question 57

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Anogenital Herpes?

Question 58

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Human Papilloma Virus?

Question 59

Q

What is the:

Causative pathogen
Epidemiology
Clinical Course
Treatment
Complications

of Trichomoniasis?

Question 60

Q

From what embryological tissue does the male reproductive system develop in the trilaminar embryo?

Answer

A

Trilaminar Embryo: Reproductive system develops from mesoderm (and some endoderm)

Question 61

Q

What is the embryological development of the male reproductive system before 6 weeks? What is this stage known as? Which important ridge forms?

Answer

A

Before 6 Weeks (Indifferent Stage): Gonadal ridge formation (why males and females both have nipples)

Question 62

Q

What is the embryological development of the male reproductive system at 6 weeks?

Which important gene is involved

Answer

A

At 6 Weeks: SRY (sex-determining region on the Y chromosome) gene stimulates the development of the primitive sex cords to form testes, giving rise to the male gender.

Absence of SRY gene promotes ovary and female development.

Question 63

Q

What is the embryological development of the male reproductive system at 8 weeks?

Which duct develops?

Which hormone is secreted and which duct degenerates as a result?

Answer

A

At 8 Weeks: Leydig cells begin to produce testosterone which maintains and drives differentiation of Wolffian duct. Sertoli cells begin to produce Mullerian Inhibiting Substance or Anti-Mullerian Hormone which causes the degeneration of the paramesonephric ducts in males (may leave remnant on testes).

Question 64

Q

What is the embryological development of the male reproductive system at 8-10 weeks?

What does the internal male genitalia differentiate from?

Answer

A

8 to 10 Weeks: Mesonephric (Wolffian) duct differentiates into male internal genitalia, by forming the efferent ductules and epididymis, the vas deferens and the ejaculatory duct. The seminal vesicles form as an outgrowth from the ductus deferens, and the prostate gland arises from numerous outgrowths from the urethra.

Answer 51

A

9 to 12 Weeks: Androgens (dihydrotestosterone) from the testes promotes the development of male external genitalia.

The primordial phallus grows to form the penis.
From week 12 gender can be identified, but gender normally identified at 20-week scan to avoid mistakes.

Answer 52

A

7 Weeks to 9 Months (Testes Descent)

The gonads develop retroperitoneally (near kidneys), moving into the abdomen and eventually into the scrotal sacs.
Between the 7th and 12th weeks, the gubernaculum shortens and pulls the testes down to the vicinity of the deep inguinal ring.
The testes remain in the vicinity of the deep ring from the 3rd to about the 7th month.
At around 6 months, testes descend and pass through the abdominal wall and deep inguinal ring into inguinal canal.
At 8 months, testes descend and pass through superficial inguinal ring. During the last month of development, the testes descend into the scrotum.
- Transversalis Fascia becomes Internal Spermatic Fascia
- Internal Obliques become Cremaster muscle
- External Obliques become External Spermatic Fascia

Answer 53

A

Birth to 3 Months: Processus vaginalis (outpouching of parietal peritoneum) closes off and the remaining portion around the testes becomes the tunica vaginalis. Some individuals have a patent processus vaginalis (opening between peritoneum and scrotum).

Answer 54

A

Biological Basis of Gender and Sexual Development:

Sex Chromosomes: Males (XY) and Females (XX)
The SRY Gene: Sex‐determining region of the Y chromosome. SRY gene acts as a transcription activator which binds to DNA and initiates male sex determination and testes development. In females, (absence of Y chromosome and SRY gene), the transcription factor is absent and female development occurs.
Internal Genitalia: The presence of testosterone (Leydig cells) drives maintenance and differentiation of Wolffian duct and Mullerian Inhibiting Substance (Sertoli cells) drives degeneration of the paramesonephric ducts in males, producing the male internal genitalia. The absence of testosterone allows for the development of the Mullerian duct and regression of the Wolffian duct, producing the female internal genitalia.
External Genitalia: The presence of dihydrotestosterone (DHT) drives the development of male external genitalia. The absence of DHT drives the development of female external genitalia.

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Brain: Responsible for sexual/gender identification, orientation, proception, gratification and procreation, under hormonal influence.
Sexuality: Combination of genotype expression, gonadal expression, genital expression and brain expression.

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Penile Erection—Role of the Parasympathetic Nerves.

Erection is caused by parasympathetic impulses that pass from the sacral portion of the spinal cord through the pelvic nerves to the penis. These parasympathetic nerve fibers, in contrast to most other parasympathetic fibers, are believed to release nitric oxide and/or vasoactive intestinal peptide in addition to acetylcholine. Nitric oxide activates the enzyme guanylyl cyclase, causing increased formation of cyclic guanosine monophosphate (GMP). The cyclic GMP especially relaxes the arteries of the penis and the trabecular meshwork of smooth muscle fibers in the erectile tissue of the corpora cavernosa and corpus spongiosum in the shaft of the penis. As the vascular smooth muscles relax, blood flow into the penis increases, causing release of nitric oxide from the vascular endothelial cells and further vasodilation.

The erectile tissue of the penis consists of large cavernous sinusoids, which are normally relatively empty of blood but become dilated tremendously when arterial blood flows rapidly into them under pressure while the venous outflow is partially occluded. Also, the erectile bodies, especially the two corpora cavernosa, are surrounded by strong fibrous coats; therefore, high pressure within the sinusoids causes ballooning of the erectile tissue to such an extent that the penis becomes hard and elongated.

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When the sexual stimulus becomes extremely intense, the reflex centers of the spinal cord begin to emit sympathetic impulses that leave the cord at T-12 to L-2 and pass to the genital organs through the hypogastric and pelvic sympathetic nerve plexuses to initiate emission, the forerunner of ejaculation.

Emission begins with contraction of the vas deferens and the ampulla to cause expulsion of sperm into the internal urethra. Then, contractions of the muscular coat of the prostate gland followed by contraction of the seminal vesicles expel prostatic and seminal fluid also into the urethra, forcing the sperm forward. All these fluids mix in the internal urethra with mucus already secreted by the bulbourethral glands to form the semen. The process to this point is emission.

The filling of the internal urethra with semen elicits sensory signals that are transmitted through the pudendal nerves to the sacral regions of the cord, giving the feeling of sudden fullness in the internal genital organs. Also, these sensory signals further excite rhythmical contraction of the internal genital organs and cause contraction of the ischiocavernosus and bulbocavernosus muscles that compress the bases of the penile erectile tissue. These effects together cause rhythmical, wavelike increases in pressure in both the erectile tissue of the penis and the genital ducts and urethra, which “ejaculate” the semen from the urethra to the exterior. This final process is called ejaculation.

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Somatic Nervous System: Moderates Ejaculation (Pudendal Nerve S2-S4)

Semen in the urethra triggers a spinal reflex through somatic motor neurons. The bulbospongiosus muscles of the penis undergo a rapid series of contractions via the pudendal nerve, propelling semen from the urethra at a speed of up to 500 cm/s. These rhythmic contractions are accompanied by intense pleasure and many systemic changes, such as generalized muscle contraction, rapid heartbeat, and elevated blood pressure.

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Key Hormones:

GnRH: Stimulates release of FSH and LH from anterior pituitary
FSH: Stimulates Sertoli cells to release ABP, thereby stimulating spermatogenesis
LH: Stimulates Leydig cells to secrete testosterone (and some estrogen)
Testosterone: Triggers spermatogenesis, maturation of sex organs, development/maintenance of secondary sexual characteristics and sexual behaviour and libido. When levels are high, has negative feedback on hypothalamus to inhibit the release of GnRH and on the anterior pituitary to inhibit release of gonadotropin (FSH and LH)
ABP: Released by Sertoli cells to allow for high concentration of testosterone in lumen of seminiferous tubules
Inhibin: Released by Sertoli cells when sperm count is high to inhibit the release of FSH from anterior pituitary and GnRH from hypothalamus

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Definition of Erectile Dysfunction: The consistent or recurrent inability to attain and/or maintain a penile erection sufficient for sexual performance

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Causes of Erectile Dysfunction:

Psychological
Vascular
Neurological
Hormonal
Drug-Induced
Anatomic
Trauma

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Causes of Erectile Dysfunction - Drug-Induced

Examples → Antihypertensives, antidepressants, antipsychotics, alcohol, tobacco and street drugs (cocaine, heroin and methadone)

Antihypertensives (β-blockers and Thiazide Diuretics): Diuretics can decrease forceful blood flow to the penis and β-Blockers cause peripheral vasoconstriction.
Antidepressants (SSRIs): Increased serotonin causes anorgism and decreased libido.
Antipsychotics (Dopamine Antagonists): Increases prolactin and decreases GNRH, LH and testosterone causing hypogonadotropic hypogonadism.
* *Alcohol:** CNS depressant and peripheral neuropathy.
Tobacco: Contributes to vascular disease.
Street Drugs: Acts on the CNS, impairing the body’s ability to respond sexually.

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Anatomic causes of Erectile Dysfunction

Examples → Peyronie’s disease and phimosis.

Mechanisms → May cause pain

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Traumatic causes of Erectile Dysfunction

Examples → Pelvic fracture, urethral injury, perineal injury, spinal cord injury, vascular injury, head trauma or genital injury.
Mechanisms → May cause pain and nerve or artery damage.

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Assessment of Patient with Erectile Dysfunction:

History:

International Index of Erectile Function (IIEF): Five-item questionnaire to evaluate male sexual function
Sexual History: Sexual function, erection history, libido, ejaculation, sexual lifestyle or partner issues
General Medical History: Cardiovascular, neurologic, psychiatric, metabolic, trauma, surgery and respiratory (COPD or sleep apnoea) history
Medication History: Antihypertensives, antipsychotics, antidepressants or other drugs with erectile dysfunction side effects
Social History: Stress, job and social position, relationships status and history, economic position, education level, religion, sexual abuse or trauma

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Assessment of Patient with Erectile Dysfunction:

Examinations: Focus on the genitourinary (features of hypogonadism), vascular (abnormal pulses), and neurological (neurogenic dysfunction) exams

Cardiovascular: Pulse and BP, heart, peripheral pulses and peripheral venous status
Secondary Sex Characteristics: Male hair pattern, fat distribution and gynecomastia
Genito-Urinary: Penis for fibrosis, nodules, functional length and hygiene, and testicles for size, symmetry, nodules and tenderness

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Primordial follicle - single layer of flattened follicle cells around ovum
Primary follicle - Follicle cells convert to cuboidal granulosa cells
Early secondary follicle - Multiple granulosa cell layers emerge
Late Secondary/Antral Follicle - Emergence of thecal cell layers, granulosa cells secrete fluid that forms the antrum
Mature/Graafian Follicle - Ovum eccentrically positioned, surrounded by granulosa cell layer (corona radiata).
Follicle rupture & Ovulation
Corpus Luteum - Granulosa cells convert to luteal cells that secrete progesterone and estrogen, prepare endometrium
Corpus Albicans - Produced when corpus luteum undergoes apoptosis after 12 days, hormone production stops, triggers menstruation.

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Definition: the absence of menarche at 15 years of age despite normal development of secondary sexual characteristics, or absence of menses at 13 years of age in female individuals with no secondary sexual characteristics

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Secondary Amenorrhea: The absence of menses for three consecutive cycle in the absence of pregnancy, lactation, cycle suppression with systemic hormonal contraceptive (birth control) pills, or menopause.
Definition: the absence of menses for more than 3 months in individuals with previously regular cycles, or 6 months in individuals with previously irregular cycles.

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Anatomical Causes of Abnormal Uterine Bleeding:
1. Leiomyoma (Fibroids)
2. Endometrial Polyps
3. Adenomyosis
4. Endometrial Hyperplasia
5. Malignancy

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Infectious Causes of Abnormal Uterine Bleeding: Inflammation causing increased vascularisation (vascular dilation and congestion), as well as local cell damage due to host immune reaction, leading to abnormal bleeding (as described above).
1. Endometritis
2. Pelvic Inflammatory Disease
3. Cervicitis

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**Hormonal Changes in Menopause: **
1. Combined ovarian and hypothalamic aging.
2. Desynchronised GnRH release from hypothalamus
3. Decline in ovarian follicles producing anovulatory cycles.
4. Decline in estrogen levels associated with decline in available follicles.
5. Decline in inhibin B levels and AMH with decline in available follicles.
6. FSH and LH levels rise in the absence of negative feedback from ovarian follicles (estrogen, AMH, inhibin B)
7. Anovulatory cycles don’t produce a corpus luteum, decreasing progesterone levels associated with lighter bleeds.

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**Urogenital Symptoms: **Estrogen withdrawal leads to decreased collagen synthesis and subsequent weakening of vaginal walls and urinary structures. It also causes decreased blood flow to vaginal epithelium and subsequent epithelial atrophy and decreased glycogen production, decreased lactobacilli and increased vaginal pH.

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Vasomotor Symptoms: Estrogen withdrawal leads to peripheral vasodilation, blood flow and sweating (estrogen administration abolishes hot flashes) though exact mechanism poorly understood.
Cardiovascular Disease: Estrogens are highly vasoactive, promote vascular remodelling, elasticity, regulating dilation and inflammation. Estrogen withdrawal has indirect effects on cardiovascular risk factors (visceral adiposity, dyslipidaemia, increased TGLs, insulin resistance and increased BP) and direct vasoconstrictive effects on vasculature (activation of RAAS, increased endothelin and decreased NO synthase). Estrogen decline increases risk of atherosclerosis and ischaemic heart disease and stroke.

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Psychological and Cognitive Changes: Mood disorders often occur for the first time during menopause, but not considered to be caused by it. Menopause often occurs concurrently with significant life stressors (children leaving home, caring for elderly parents). Many symptoms of menopause can effect quality of life (sleep disturbance due to hot flushes, changes to sexual function associated with urogenital changes).
Osteoporosis: Estrogens couple bone formation and reabsorption. Estrogen decline leads to excessive resorption (osteoclast activity) and reduced formation of bone (osteoblast activity).

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The focus on sexual history/menstrual history/pregnancy history will depend on the context and presenting complaint. For example a 50 year old woman with irregular bleeding - focus more on menstrual history but it is important to establish brief pregnancy and sexual history.

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The components of pelvic examination are inspection, speculum, Cervical Screening Test, swabs and bimanual examination. Which components are done depends on the patient clinical circumstances.
Inform patient of Cervical Screening Test registry and obtain consent
Discuss how to obtain results

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Squamous Cell Hyperplasia
Previously called hyperplastic dystrophy or lichen simplex chronicus, squamous cell hyperplasia is a nonspecific condi- tion resulting from rubbing or scratching of the skin to relieve pruritus. Clinically it presents as leukoplakia, and histologic examination reveals thickening of the epidermis (acanthosis) and hyperkeratosis (see Fig. 22.5B). Lymphocytic infiltration of the dermis is sometimes present. The hyper- plastic epithelium may show mitotic activity but lacks cellular atypia. While squamous cell hyperplasia is not considered premalignant, it is sometimes present at the margins of vulvar cancers.

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Bartholin Cyst: Cystic dilation of the Bartholin gland that arises due to inflammation and obstruction of gland. Usually occurs in women of reproductive age.
Macroscopic Pathology: Presents as a unilateral, painful cystic lesion (3 to 5cm) at the lower vestibule adjacent to the vaginal canal, which may cause abscess.
Microscopic Pathology: Cysts are lined by transitional or squamous epithelium.

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Lichen sclerosis presents as smooth, white plaques or macules that in time may enlarge and coalesce, producing a surface that resembles porcelain or parchment. When the entire vulva is affected, the labia become atrophic and agglutinated, and the vaginal orifice constricts. Histologically, the lesion is characterized by marked thinning of the epidermis (Fig. 22.5A), degeneration of the basal epithelial cells, excessive keratinization (hyperkeratosis), sclerotic changes of the superficial dermis, and a bandlike lymphocytic infiltrate in the underlying dermis. The disease occurs in all age groups but is most common in postmenopausal women. It may also be encountered elsewhere on the skin. Its pathogenesis is uncertain, but the presence of activated T cells in the subepithelial inflammatory infiltrate and the increased frequency of autoimmune disorders in affected women suggest that an autoimmune reaction is involved. Although lichen sclerosus is not itself a premalignant lesion, women with symptomatic lichen sclerosus have a slightly increased chance of developing squamous cell carcinoma of the vulva.

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Condyloma Acuminatum
Condylomata acuminata are benign genital warts caused by low-risk HPV, mainly types 6 and 11. They may be solitary, but are more frequently multifocal, and they may involve vulvar, perineal, and perianal regions as well as the vagina and, less commonly, the cervix. The lesions are identical to those found on the penis and around the anus in males.

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On histologic examination, they consist of papillary, exophytic, treelike cores of stroma covered by thickened squamous epithelium (Fig. 22.6A). The surface epithelium shows characteristic viral cytopathic changes referred to as koilocytic atypia, which manifest as nuclear enlargement, hyperchromasia, and a cytoplasmic perinuclear halo. Condylomata acuminata are not precan- cerous lesions. HPV vaccines (described later) provide excellent protection against infection by low-risk HPV and genital warts.

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Vulvar Intraepithelial Neoplasia:
Refers to particular changes that can occur in the skin that covers the vulva (in-situ precursor lesions). Can disappear without treatment. Are benign, but if the changes become more severe, risk of cancer increases. Risk factors include HPV, HSV, smoking, immunosuppression, chronic valvular irritation and conditions such as Lichen Sclerosis.
- Macroscopic pathology: Discrete white (hyperkeratotic) or a slightly raised, pigmented lesion.
- Microscopic pathology:
- Classic VIN: Epidermal thickening, nuclear atypia, increased mitoses, and lack of cellular maturation.
- Differentiated VIN: Marked atypia of the basal layer of the squamous epithelium and normal-appearing differentiation of the more superficial layers.

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Approximately 30% of vulvar cancers are caused by infection with high-risk HPVs, principally HPV-16.These cancers develop from an in situ lesion termed classic vulvar intraepithelial neoplasia (classic VIN).
Most vulvar cancers (70%) are not related to HPV and develop in a background of lichen sclerosus or squamous cell hyperplasia from the premalignant lesion called differentiated vulvar intraepithelial neoplasia (differentiated VIN).

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What: Malignant mesenchymal proliferation of immature skeletal muscle (rare). Also known as sarcoma botryoides.
Macroscopic: Bleeding and a grape-like mass protruding from the vagina or penis of a child (usually < 5 years of age).
Microscopic: Rhabdomyoblast, the characteristic cell, exhibits cytoplasmic cross- striations and positive immunohistochemical staining for desmin and myogenin.

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Bartholin Cyst
Inflammatory Dermatoses
Lichen Sclerosus
Squamous Cell Hyperplasia / Lichen Simplex Chronicus
Condyloma Acuminatum
Vulvar Intraepithelial Neoplasia
Squamous Neoplastic Lesions - Basaloid and Warty Carcinoma
Squamous Neoplastic Lesions - Keratinizing Squamous Cell Carcinoma
Glandular Neoplastic Lesions - Papillary Hidradenoma
Glandular Neoplastic Lesions - Extramammary Paget Disease

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Vaginitis
Vaginal Squamous Cell Carcinoma
Embryonal Rhabdomyosarcoma

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Cervicitis
Endocervical Polyps
Cervical Ectropion
Cervical Intraepithelial Neoplasm
Cervical Carcinoma

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Endometritis
Endometriosis
Adenomyosis
Endometrial Polyp
Endometrial Hyperplasia
Endometrial Carcinoma - Type I Endometrial Adenocarcinoma
Endometrial Carcinoma - Type II Endometrial Serous Carcinoma (15% of cases)
Uterine Leiomyoma (Fibroids)
Leiomyosarcoma

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Endometrial carcinoma is the most common malignancy of the female genital tract.
There are two major types of endometrial carcinoma: type I and type II.Type I tumors are low-grade and usually indolent; type II tumors are high-grade aggressive tumors and have a poor prognosis.
Four molecular subtypes of endometrioid and serous carcinoma are currently recognized.
Endometrioid (type I) carcinoma is often preceded by atypical hyperplasia and commonly has mutations that upregulate PI3K/ AKT signaling.
Serous (type II) carcinoma is associated with serous endometrial intraepithelial carcinoma, and the most common mutations are in TP53. TP53 mutations are also found in precursor lesions.
Stage remains the most important factor in outcome; serous tumors are much more likely to present at advanced stage and have a decidedly worse prognosis.
Carcinosarcomas are aggressive tumors that resemble endo- metrial carcinoma genetically and have poor outcomes with current therapies.

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Endometrial stromal tumors include stromal nodules, low-grade stromal sarcoma, and high-grade stromal sarcoma.
Stromal nodules are benign, well-circumscribed tumors.
Low-grade stromal sarcoma resembles stromal nodules but infiltrates into the surrounding myometrium. It is associated with fusion of the JAZF1 gene and various polycomb factor genes, usually SUZ12.
High-grade stromal sarcoma shows marked atypia and is associated with other gene fusions.
Both low- and high-grade stromal sarcoma are prone to late recurrences.
Leiomyomas are very common benign smooth muscle tumors that cause significant morbidity, but are not prone to malignant transformation.
Leiomyosarcoma (a malignant smooth muscle tumor) is an uncommon, highly malignant myometrial tumor that usually arises de novo.