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Repo Path Flashcards

1
Q

GENITAL HERPES (Goodman, pg 328)

A

Caused by herpes simplex-2, a type of herpesvirus
• HSV-2 is primarily the cause of genital herpes but HSV-1 can be transmitted to the
genital area

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2
Q

of Americans have HSV-2, 4/5 have HSV-1?

A

1/5

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3
Q

common method for transmission?

A

Asymptomatic viral shedding is common and is responsible for transmission, usually
just before the onset of sores

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4
Q

Herpes simplex virus produces recurring episodes of

A

small, painful, fluid-filled ulcers
on the glans penis or the skin of the shaft of the penis or the scrotum
• Lesions are often small and grouped with itching or burning
• The vesicles rupture and transform into shallow, painful ulcers that heal without
scarring

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5
Q

Herpes simplex virus Tends to recur, because

A

because the virus remains dormant in the dorsal root ganglia until
reactivated (by physical or emotional stress, another infection or a decreased
immune system)

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6
Q

Herpes simplex virus Diagnosis is

A

symptomatic
• No permanent cure
• Some antiviral drugs provide relief (acyclovir, Valtrex ®)

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7
Q

GENITAL WARTS/VENEREAL WARTS

• Aka verrucae

A
  • Common benign, viral infections of the genital region
  • Caused by the sexually transmitted human papillomaviruses (HPV)
  • Usually affect men on the end of the shaft of the penis and below the foreskin
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8
Q

warts usually appear

A

1-6 months after infection, beginning as tiny, soft, moist, pink or red swellings
• They grow rapidly and may develop stalks
• Multiple warts often grown in the same area, and their rough surfaces give them the appearance of a small cauliflower

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9
Q

HVP Usually diagnosed based on…. Treatment can include….

A

appearance.
laser, cryotherapy, or surgery
• Usually requires repeated treatments

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10
Q

ORCHITIS (Goodman, pg 978)

A
  • Inflammation of the testes
  • Acute or chronic
  • The testis becomes swollen and painful and may be warm; fever; malaise
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11
Q

ORCHITIS May be isolated but more often it is

A

is combined with epididymitis
• Often follows chlamydia infection (Chlamydia trachomatis)
• May also be a complication of a bladder infection, urethritis, gonnorrhea, prostate surgery, mumps or a procedure such as urinary catheterization, pneumonia, scarlet fever, etc.

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12
Q

ORCHITIS risk….
Diagnosis….
Treatment…

A
  • Men with multiple partners are at risk, STIs
  • Diagnosis – palpation of the testes; lab tests, urinalysis
  • Treatment usually consist of antibiotics, bed rest, ice packs, and pain meds
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13
Q

EPIDIDYMITIS (Goodman, pg 979)

• Inflammation of the epididymis (coiled tube at the back of the testicle that stores and carries sperm.)

A
  • Usually a complication of urethritis or prostatitis
  • In young men, it is most often a complication of sexually acquired infections
  • In older patients it is typically a complication of urinary obstruction, catheterization, or prostate surgery
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14
Q

EPIDIDYMITIS
Manifests with…
Diagnosis –
Treatment includes

A

-pain, urinary dysfunction, fever, discharge, scrotal swelling
– clinical manifestation, UA, blood tests
Tx-scrotal elevation and support, NSAIDS, antibiotics, rest

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15
Q

URETHRITIS

A
  • Inflammation (non-bacterial) or infection of the urethra

* If there is a purulent exudate present it is typical of infection with neisseria gonorrhoeae

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16
Q

PROSTATITIS (Goodman, pg 965)

A

 Pain and discomfort of the prostate

 Typically preceded by UTI

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17
Q

PROSTATITIS Classification:

A

o Acute bacterial prostatitis (Category I)
 Chills, fever, pain, frequency, urgency, burning
 UA
 Treatment antibiotics
o Chronic bacterial prostatitis (Category II)
 Defect in the prostate predisposes to bacterial infection
o Chronic prostatitis/chronic pelvic pain syndrome (Category III)
 Most common
 Idiopathic inflammatory or non-inflammatory symptoms which come and go
 No standard treatment
o Asymptomatic inflammatory prostatitis

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18
Q

PROSTATITIS

Incidence and Risk Factors-

A
  • Millions
  • Half of all men have at least one episode in their lifetime
  • M/c over 40
  • UTIs
  • Instrumentation
  • Multiple sex partners
  • Stress emotional factors
  • Alcohol
  • Spicy food
  • Caffeine
  • Diabetes
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19
Q

PROSTATITIS

Etiology and Pathogenesis-

A
  • Multifactorial
  • Idiopathic
  • Poorly understood
  • Inflammatory process
  • Autoimmunity
  • Pelvic floor muscle spasm
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20
Q

PROSTATITIS Bacteria-

A 
 Escherichia coli
 Klebsiella pneumoniae
 Pseudomonas aeruginosa
 Staphylococci
 Streptococci
 Gonococci
 Chlamydiae
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21
Q

PROSTATITIS Clinical Manifestation-

A 
 Variable depending on chronic, acute, bacterial, non-bacterial
 Frequency
 Urgency
 Nocturia
 Dysuria
 Discharge
 Fever
 Chills
 Malaise
 Myalgia
 Arthralgia
 Pain
 Impotence
 Decreased libido
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22
Q

PROSTATITIS
Diagnosis
Treatment

A 
Diagnosis
• Clinical manifestation
• Digital rectal exam
• CT scan
Treatment
 Category I – antibiotics
 Category II – antibiotics
 Category III – antibiotics; antiinflammatories; biofeedback; pelvic floor re-education; alpha-blockers; pain medication; herbal treatment; surgery
 Category IV – no treatment
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23
Q

TESTICULAR TORSION (Goodman, pg 979)

A
  • Abnormal twisting of a testis on its spermatic cord
  • The twisted cord cuts off blood supply to the testis
  • Often associated with congenital abnormalities
  • Usually results from an abnormal development of the spermatic cord or the membrane covering the testis
  • Most often occurs in males between puberty and 25 yoa (however it can occur at any age)
  • May happen spontaneously or after strenuous activity
  • Severe pain and swelling in the scrotum along with nausea and vomiting occur immediately
  • The only hope of saving the testis is surgery to untwist the cord within 3 hours of the onset of symptoms
  • During surgery the other testis is usually better secured to prevent torsion on that side
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24
Q

TESTICULAR CANCER (Goodman, pg 980)

A 
 Cells in testicles become malignant
 Two types: seminoma and nonseminoma
 95% of tumours of germ cell origin
 5% are stromal or sex cord origin
 Secondary tumours are rare
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25
Q

TESTICULAR CANCER Incidence-

A

 Rare – occur during prime of life and potentially affect sexual and reproductive capabilities
 Most common solid organ tumour in young men
 Mainly affects Western populations
 Increasing incidence
 Six times higher in developed world
 Most common cancer in 15-35 y.o. age group
 Whites > blacks (5:1)

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26
Q

TESTICULAR CANCER Etiology and Risk Factors

A 
 Poorly understood
 Hormonal imbalance
 Congenital factors
o Cryptorchidism
o Klinefelter’s syndrome
 Estrogen exposure
 Genetic factors
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27
Q

Pathogenesis of Germ Cell Tumours

A

 Carcinoma in situ becomes invasive carcinoma in approx. 5 years
o Results in:
-Seminoma (m/c – up to 50%) (also known as pure seminoma or classical seminoma) is a germ cell tumor of the testicle or, more rarely, the mediastinum or other extra-gonadal locations. It is a malignant neoplasm and is one of the most treatable and curable cancers, with a survival rate above 95% if discovered in early stages.
 Undifferentiated tumour
 Nonseminomatous tumour

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28
Q

TESTICULAR CANCER Clinical Manifestation-

A 
 Enlargement of testis
 Diffuse pain
 Swelling
 Hardness
 Heaviness
 Back pain
 Abdominal mass
 Hemoptysis
 Metastasis to lymphatics, bone, lung, liver
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29
Q

TESTICULAR CANCER Diagnosis

Treatment

A 
Diagnosis
 UA
 PE
 Transillumination
 Blood test (AFP, hCG)
 CT
 MRI
 Biopsy
Treatment
 Surgery
 Radiation
 Chemotherapy
 Chemotherapeutics
Prognosis
 95% cure with early detection
Prevention
 Self-examination
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30
Q

BENIGN PROSTATIC HYPERPLASIA (Goodman, pg 967)

A

 Age-related non-malignant enlargement of the prostate gland
 Aka benign prostatic hypertrophy (BPH)

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31
Q

BPH Incidence and Risk Factors-

A 
 75% of men over age 50 experience symptoms of BPH
 Rare under 40
 m/c in US and Western Europe
 Uncommon further East
 Higher in blacks than white
 Drinking moderate reduces the risk
 Smoking increases the risk
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32
Q

BPH Pathogenesis

A

 Idiopathic
 Hormone imbalance, androgens and estrogens
 Multiple prostatic nodules develop
 Proliferation of epithelial cells, smooth muscle cells, fibroblasts
 Lumen of urethra becomes progressively narrowed

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33
Q

BPH Clinical Manifestation-

A 
 Related to secondary involvement of the urethra and restriction of urine flow
 Decreased calibre and force 
of stream Difficulty initiation or continuing
 Frequency
 Nocturia
 Fatigue
 Sleep disturbance
 Increased UTIs
 Bladder distension
 Renal failure
 Death
 Dribbling
 Urgency
 Hematuria
 Dysuria
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34
Q

BPH Diagnosis

Treatment

A 
Diagnosis
 History
 Palpation
 Urodynamic tests
 Blood test (PSA)
 UA
 Imaging
Treatment
 Watch and wait
 Medications
 Surgery
 Botox
 Other
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35
Q

BPH
Complications-
Prevention-

A 
Complications
 Chronic UTIs, ED, cancer
Prevention
 Antioxidants – saw palmetto, lycopene, tomatoes
Prognosis
 Variable
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36
Q

PROSTATE CANCER (Goodman, pg 970)

A

 98% adenocarcinoma (a malignant tumor formed from glandular structures in epithelial tissue.)
 2% ductal and transitional cell carcinomas

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37
Q

PROSTATE CANCER Incidence

A 
 Most frequently diagnosed visceral malignancy in American men
 Second most common cause of male death
 1/5 (US)
 Increasing (up 200%)
 Blacks > whites
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38
Q

PROSTATE CANCER Risk Factors

A 
 Age > 50
 Ethnicity
 Geography
 Family history
 Environment
 Diet
 Alcohol
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39
Q

PROSTATE CANCER
Etiology
Pathogenesis

A

Etiology
 Unknown
 Endocrine system dysfunction
 Higher levels of androgens esp. testosterone
 Viral exposure
Pathogenesis
 Small/moderate-sized disorganized glands infiltrated the stroma of the prostate
 Develops initially at the periphery of prostrate
 Invades adjacent local structures
 Spreads to musculoskeletal system (axial skeleton), lungs, lymphatic system

40
Q

PROSTATE CANCER Clinical Manifestation

A 
 Extremely variable
 Asymptomatic
 Urinary obstruction
 Pain
 Fatigue
 Weight loss
41
Q

PROSTATE CANCER Diagnosis

Treatment

A 
Diagnosis
 DRE
 US
 Blood test (PSA)
 Biopsy
Treatment
 Variable
 Watch and wait
 Surgery
 Radiation
 Hormone therapy
 Chemotherapy
Prognosis
 Variable
Complications
 Incontinence
 Rectal cancer
Prevention
 Diet
 Supplements
 Screening – blood test (PSA), DRE (digital rectal exam)
 Physical activity
 Control weight
42
Q

CANDIDIASIS

A

 Aka – yeast infection

 Genital infection with candida albicans

43
Q

CANDIDIASIS
Risk Factors-
Clinical Manifestation-
Treatment-

A 
Risk Factors
 Hot weather
 Clothing
 Diet
 Immunosuppression
 Poor hygiene
 Antibiotics
 IUD
 Pregnancy
Clinical Manifestation
 Itching
 Discharge
Treatment
 Antifungals
 Lifestyle modification
44
Q

GENITAL WARTS

female

A

 Aka venereal warts; condyloma acuminata; anogenital warts
 Benign lesions of the skin or mucous membranes of the genitals
 Caused by human papillomavirus (HPV)
 Some strains cause flat warts in the cervical canal or anus
 Can become cancerous
 80% of women have been affected once by age 50
 Most clear spontaneously within 1-2 years
 Manifestation includes soft, moist, tiny, pink or grey polyps that may become pedunculated
 May be rough or occur in clusters
 Can be asymptomatic or cause itching/burning
 Occur most commonly on the vulva, vaginal wall, cervix, and perineum; the urethra and anal region may be affected
 Prevention includes vaccination

45
Q

PELVIC INFLAMMATORY DISEASE (PID) (Goodman, pg 1010)

A

 Infection and inflammation of the upper female genital tract: the cervix, uterus, fallopian tubes, and ovaries
 Common cause of infertility, chronic pain and ectopic pregnancy
Etiology
 Results from microorganisms ascending from the vagina and cervix into the endometrium and fallopian tubes
 Neisseria gonorrhoeae and Chlamydia trachomatis
 Cervicitis – infection of the cervix; can cause mucopurulent discharge
 Salpingitis – infection of the fallopian tubes; can become red, swollen, pus-filled
 Endometritis – infection of the uterus
 If severe, infection can spread to the ovaries (oophoritis) and then the peritoneum (peritonitis). These infections are called salpingitis even though they involve other structures.
Incidence and Risk Factors
 1 million women affected / year
 Age
 STIs
 PIDs
 Multiple/new sex partners

46
Q

PID Signs and Symptoms/Complications
Diagnosis
Treatment

A 
Signs and Symptoms/Complications
 Widely variable
 Asymptomatic
 Pain
 Discharge
 Irregular bleeding
 Fever, chills
 Nausea
 Vomiting
 Dyspareunia
 Dysuria
 Burning with urination
 Menstrual irregularities
 Ectopic pregnancies
 Infertility
 Chronic pain
 Death
Diagnosis
 History
 Culture
Treatment
 Antibiotics
 Prevention – safer choices; checkups
47
Q

Disorders of the Cervix

EROSION

A

The cervix is the neck or narrow end of the uterus where it meets the vagina. Outside, the cervix is normally covered by squamous cell epithelia, while the tissue inside the canal is glandular tissue. These two different tissues converge at the opening of the cervical canal (os). A cervical erosion occurs when some of the cells on the opening have eroded, exposing the raw surface of the cervix. The effect is similar to a scrape on the skin of the arm or other outer body surface. There may be a red or dark pink spot on the cervix, and sometimes a white discharge is present. Erosions are quite common, and thought to occur in 95 percent of women at some point. Typically, they cause no symptoms, and require no treatment, unless there’s also an infection.

48
Q

Disorders of the Cervix EVERSION

A

This describes red columnar tissue that grows beyond or drops out of its normal place in the cervical canal, onto the cervix. Eversion may happen as a result of infection, which causes swollen tissue to protrude from the cervical opening. Or, women may be born with this condition. Again, treatment is not usually required. With both erosion and eversion it’s wise to do a Pap smear and perhaps a cervical biopsy, just to rule out any suspicion of cancer.

49
Q

CERVICAL POLYPS

A
  • Common benign growths of the cervix or endocervix
  • Occur in about 2 to 5% of women, usually due to chronic inflammation.
  • Most cervical polyps are asymptomatic.
  • Endocervical polyps may bleed between menses or after intercourse or become infected, causing purulent vaginal discharge (leukorrhea).
  • Endocervical polyps are usually reddish pink,
50
Q

CERVICAL CANCER (Goodman, pg 1000)

A 
• 3700 deaths per year
• Mortality declined rapidly since 1930s
• Largely preventable
Etiology
 Human papillomavirus (HPV)
51
Q

CERVICAL CANCER Risk Factors

A
  • Smoking
  • Hormonal contraceptives
  • High parity
  • Low SE
  • Ethnicity
  • Young age of 1st intercourse
  • Multiple sex partners
  • Alcohol and drug use
  • IC
52
Q

CERVICAL CANCER Pathogenesis

Symptoms and Signs

A

Pathogenesis
 HPV inactivates tumour suppressor genes
 Leads to dysplastic changes in epithelium of cervix
Symptoms and Signs
• Asymptomatic
• Abnormal bleeding

53
Q

CERVICAL CANCER
Diagnosis
Tx

A 
Diagnosis
 Pap test
Treatment
 Cryotherapy
 Laser
 Excision
 Chemotherapy, radiation
 Hysterectomy
Prognosis
• Good; slow growing neoplasm; responds well to treatment
• Depends on early detection
• Largely preventable with early screening
• Later stages associated with high mortality
• Early detection  100 % cure
Prevention
 Pap test
 Barrier protection
 Monogamy
54
Q

ENDOMETRIAL HYPERPLASIA

A
  • Benign
  • Overgrowth of the endometrium (endometrial cells)
  • Due to excess estrogen and deficient progesterone
  • Most common symptom is abnormal vaginal bleeding
  • Can lead to endometrial cancer
  • Risk factors include: being around menopausal age, skipping or having no periods, being over-weight, diabetes, polycystic ovarian syndrome, increased levels of unopposed estrogen
  • Diagnosis - pap smear
  • Treatment – hormones; hysterectomy
55
Q

ENDOMETRIOSIS (Goodman, pg 995)

A
  • An estrogen-dependant, non-cancerous disorder in which functioning endometrial tissue is implanted outside the uterine cavity
  • Most common locations include ovaries, fallopian tubes, broad ligaments, bladder, pelvic musculature, perineum, vulva, vagina, intestines
  • Can also occur in abdominal cavity, kidneys, appendix, diaphragm, bone, lungs, brain, nose, joints
  • Common
  • Up to 60% of women
56
Q

ENDOMETRIOSIS
Risk Factors
Pathogenesis

A

Risk Factors
• Incidence of endometriosis is increased in first-degree relatives of women with endometriosis, suggesting that heredity is a factor.
• Incidence is also increased in women who delay childbearing, who have shortened menstrual cycles ( 7 days)
Pathogenesis
• Unclear
• The most widely accepted hypothesis is that endometrial cells are transported from the uterine cavity and subsequently become implanted at ectopic sites.
• Retrograde flow of menstrual tissue through the fallopian tubes could transport endometrial cells intra-abdominally; the lymphatic or circulatory system could transport endometrial cells to distant sites (e.g., the pleural cavity).
• Microscopically, endometriotic implants are identical to intrauterine endometrium. These tissues contain estrogen and progesterone receptors and thus usually grow, differentiate, and bleed in response to changes in hormone levels during the menstrual cycle.
• Bleeding from peritoneal implants is thought to initiate inflammation, followed by fibrin deposition, adhesion formation, and, eventually, scarring, which distorts peritoneal surfaces of organs and pelvic anatomy.
• May also be related to dysregulation of immune system; metaplasia; surgical procedures; abnormal differentiation during embryology

57
Q

ENDOMETRIOSIS
Symptoms and Signs
Diagnosis
Treatment

A 
Symptoms and Signs
 Depends on the location of the implants
 Includes pain, dysmenorrhea, fatigue, mood changes, dyspareunia, pain during defecation, fever, diarrhea, rectal bleeding, alternation of menses, infertility
 Classification: I (minimal); II (mild); III (moderate); IV (severe); V (extensive)
 Some women with extensive endometriosis are asymptomatic; some with minimal disease have incapacitating pain.
Diagnosis
 Biopsy
 Imaging
 History and manifestation
Treatment
• Pregnancy
• NSAIDs and analgesics
• Meds to inhibit ovulation
• Synthetic male hormones
• Birth control pills
• Surgery
• Non-traditional therapies
58
Q

LEIOMYOMA (FIBROIDS) (Goodman, pg 998)

A 
• Benign uterine tumours of smooth muscle origin
• Up to 25% of w.c.a
• Primary reason for hysterectomies
Clinical Manifestation
• Asymptomatic
• Pain
• Heavy bleeding
• Anemia
• Constipation
• Frequency
• Nocturia
• LBP
Treatment
• Medications, surgery, diet
59
Q

UTERINE CANCER (ENDOMETRIAL CARCINOMA) (Goodman, pg 998)

A 
• Cancer of the lining of the uterus
• Most common cancer of the female reproductive organs
Risk Factors
• Age
• White
• Affluent
• Obese
• Low parity
• Post-menopause
• Hypertension
• Diabetes
• PCOS
60
Q 
UTERINE CANCER (ENDOMETRIAL CARCINOMA) 
Pathogenesis
A

• Related to any condition that increases estrogen exposure, unopposed by progesterone
o Cigarette smoking, physical activity, hormonal contraceptives appear to decrease the risk
Metastasis
The cancer may spread:
• from the surface of the uterine cavity to the cervical canal
• through the myometrium to the serosa and into the peritoneal cavity
• via the lumen of the fallopian tube to the ovary, broad ligament, and peritoneal surfaces
• via the bloodstream or the lymphatics
Symptoms and Signs
• Irregular bleeding
Diagnosis
• Symptoms
• Biopsy
• Pap smear
• D&C
Medical Management
• Treatment – radiation, chemotherapy, surgery
• Prognosis - extremely treatable with early detection but can recur
• Prevention – healthy weight, diet, exercise

61
Q

OVARIAN CYSTS (Goodman, pg 1005)

A

• Aka functional cysts or unruptured follicles
• Benign
• Idiopathic
• Generally asymptomatic and resolve spontaneously
Ovarian follicles enlarge during the proliferative stage of the menstrual cycle and transform into graafian follicles. Only one graafian follicle ruptures at ovulation
o Follicles that have not ruptured may remain filled with follicular fluid and may further enlarge into fluid filled follicular cysts
o If the ovulated follicle transforms into a corpus luteum but does not involute and transform into a fibrotic corpus albicans, its cavity could fill in with fluid and a luteal cyst could form

62
Q

POLYCYSTIC OVARIAN SYNDROME (PCOS)

A

• Also known as Stein-Leventhal syndrome
• Systemic metabolic endocrine disorder affecting premenopausal women
• Involves anovulation, androgen excess and multiple cysts
• Unclear etiology but related to inherited insulin resistance
• Common
• Occurring in 20% of women (US)
• One of the most common causes of infertility
Pathogenesis
• Excess circulating androgens converted to estrone in adipose tissue
• Elevated estrogens stimulate release of Gn-RH
• Elevated Gn-RH stimulates pituitary to produce LH
• LH stimulates ovary to secrete more androgens
• Results in abnormal maturation of ovarian follicles, development of multiple cysts and persistent anovulation

63
Q

POLYCYSTIC OVARIAN SYNDROME (PCOS)

Symptoms and Signs

A 
• Variable
• Abdominal pressure
• Pain
• Abdominal bloating
• Discomfort during urination, b.m, or intercourse
• Irregular menstruation
• Infertility
• Obesity
• Hirsuitism
• Acne
• Alopecia
Diagnosis
• History
• Pelvic exam
• Imaging
• Lab tests
Treatment
• Hormones
• Infertility treatment
• Manage weight and/or diabetes
64
Q

NEOPLASMS OF THE OVARIES (Goodman, pg 1007; Damjanov)

Etiology and Risk Factors

A

• A complex group of benign and malignant lesions
• Benign tumours are more common than malignant tumours
• Ovarian cancer is the 2nd most common gynecologic cancer but is ranked 1st for death caused by gynecologic cancer
• Classified according to cell type (histology) and type of secretion
• Diagnosis is difficult and often delayed
Etiology and Risk Factors
• Poorly understood
• Hormonal, genetic, environmental factors
• Family history of breast or ovarian cancer
• Nulliparous

65
Q

NEOPLASMS OF THE OVARIES
Pathogenesis-
Clinical Manifestation-

A 
Pathogenesis
• Correlates with the number of times a woman ovulates during a lifetime
• Pregnancy, breastfeeding, hormonal contraceptives may decrease the risk
Clinical Manifestation
 Asymptomatic
 Really vague
 Abdominal bloating
 Flatulence
 Fatigue
 Malaise
 Gastritis
 Abdominal discomfort
 Abnormal bleeding
 Leg pain
 Pelvic mass
 Low back pain
 Weight loss
 Weakness
 Pleurisy
 Ascites
 Cachexia
 Cerebellar degeneration
66
Q

POLYCYSTIC OVARIAN SYNDROME (PCOS)

BENIGN

A
  1. Mucinous Cystadenoma
    • Surface epithelial tumour
    • Usually unilateral
    • The cavity of these tumours are filled with thick yellowish or white jellylike material
    • If these tumours rupture the entire belly is filled with mucus - “jelly belly”
  2. Serous Cystadenoma
    • Most common type of surface epithelial tumour
    • They often consist of several cysts lumped together within a common outer capsule
    • The cavity of these tumours is filled with clear fluid resembling serum
  3. Benign Teratoma
    • Germ cell tumour
    • Teratoma presents as a cyst lined on the inside with hairy skin
    • Often called dermoid cysts
    • The wall of the tumour contains other tissues, most often teeth and cartilage
    • The skin appendages, such as sebaceous and sweat glands, secret sebum and sweat into the cavity
    • This remains there and decomposes into malodorous, mushy material; when the tumour is resected and the cavity is opened , the contents stink, the same way our skin would stink if it were not washed for a few years
    • Teratomas are benign tumours that nevertheless should be resected
    • If they are left in place, the skin and other tissues on its wall may gradually undergo malignant transformation
    • This usually occurs in older women; although it is rare, and should not occur at all if the women is under appropriate gynecologic supervision
67
Q

POLYCYSTIC OVARIAN SYNDROME (PCOS)

MALIGNANT

A

Primary tumours
 Serous cystadenocarcinoma – filled with clear fluid
 Mucinous cystadenocarcinoma – filled with mucous
 Papillary cystadenocarcinoma - tumour elements are arranged as finger-like processes
 Serous papillary cystadenocarcinoma accounts for 40% of all ovarian cancer and most common malignant tumors.
Secondary tumours
• Metastasize from other malignancies
• Metastases involving the ovaries originate most often from carcinomas of the endometrium and breast
• These tumours often have estrogen receptors, which could explain their predilection for metastasizing to the ovaries
• Tumours of the gastrointestinal tract also metastasize to the ovaries
• Most notable among these is carcinoma of the stomach, which tends to produce bilateral enlargement of the ovaries (Krukenberg tumours)

68
Q

HYPEREMESIS GRAVIDARUM

A

• Severe nausea and uncontrollable vomiting during pregnancy
• Results in dehydration, starvation and ketosis
• Diagnosis is clinical and by measurement of urine ketones, serum electrolytes, and renal function.
• Treatment is with IV fluids, antiemetics, and temporary suspension of oral intake
• Hyperemesis gravidarum is distinguished from morning sickness by weight loss
• Etiology - unknown
• Dehydration can cause dangerous shifts in the electrolyte levels in the blood, and the blood becomes too acidic
• Hyperemesis gravidarum that persists past 18 wks is uncommon but may cause serious liver damage, encephalopathy, esophageal rupture
• Another serious complication is bleeding in the retina of the eye (hemorrhagic retinitis), caused by increased blood pressure during vomiting
Treatment
• IV rehydration and vitamin therapy
• Termination of pregnancy

69
Q

TOXEMIA

A
  • Occurs as a result of an abnormally functioning placenta or abnormal maternoplacental interaction
  • Etiology unknown
  • Two types: preeclampsia and eclampsia, the latter is more severe
  • Preeclampsia is pregnancy-induced hypertension plus proteinuria
  • Eclampsia is unexplained generalized seizures in patients with preeclampsia
  • Preeclampsia and eclampsia develop between 20 wk gestation and the end of the 1st wk postpartum
  • Preeclampsia affects 3 to 7% of pregnant women usually primigravidas and women with pre-existing hypertension or vascular disorders (e.g., renal disorders, diabetic vasculopathy).
  • Other risk factors may include maternal age
70
Q

Preeclampsia

A

pregnancy-induced hypertension plus proteinuria

71
Q

Eclampsia

A

unexplained generalized seizures in patients with preeclampsia

72
Q

TOXEMIA

Clinical Manifestation

A 
• Asymptomatic
• Edema
• Weight gain
• Petechiae
• Increased reflex reactivity, indicating neuromuscular irritability, can progress to seizures (eclampsia)
• Severe preeclampsia may cause organ damage; manifestations may include headache, visual disturbances, confusion, abdominal pain, nausea, vomiting, shortness of breath
Diagnosis
• Clinical picture
• Hypertension
• Proteinuria
Treatment
• Delivery
• Bed rest
• Lying on left side
• Increased fluid intake
• Decreased salt intake
• Untreated eclampsia is usually fatal.
73
Q

ECTOPIC PREGNANCY (Goodman, pg 1004)

A 
• Aka “tubal pregnancy”
• The fetus develops outside the uterus - in the fallopian tubes (m/c), the cervical canal, or the pelvic or abdominal wall
• Medical emergency – one of the primary causes of maternal death in the US
Incidence and Risk Factors
• Increasing incidence
• Increasing maternal age
• PID
• Tubal pregnancy
• Cigarette smoking
• Induced abortion
• STI
• IUD
Etiology and Pathogenesis
Related to:
 Delayed transport of egg
 Decreased fallopian motility
 Distorted anatomy
74
Q

ECTOPIC PREGNANCY

Clinical Manifestation

A 
• Variable
• Pelvic pain
• Cramps
• Irregular bleeding/spotting
• Amenorrhea
• Fainting
• Death
• Fatigue
• Nausea
• Breast tenderness
• Increased urinary frequency
Diagnosis
• Pelvic mass
• Clinical picture
• Blood tests
• Urine tests
• US
Treatment
• Surgery
75
Q

SPONTANEOUS ABORTION (MISCARRIAGE)

A
  • Noninduced embryonic or fetal death or passage of products of conception before the 20th wk of pregnancy.
  • Incidence of spontaneous abortion is about 10 to 15% in confirmed pregnancies.
  • Incidence in all pregnancies is probably higher because some very early abortions are mistaken for a late menstrual period
  • Isolated spontaneous abortions may result from certain viruses—most notably cytomegalovirus, herpesvirus and rubella virus—or from disorders that can cause sporadic or recurrent abortions
  • Symptoms include crampy pelvic pain, bleeding, and eventually expulsion of tissue.
  • If products of conception remain in the uterus after spontaneous abortion infection may also develop, causing fever, pain, and sometimes sepsis.
76
Q

PLACENTA PREVIA

A
  • Implantation of the placenta over or near the cervix, in the lower rather than the upper part of the uterus.
  • The placenta may completely or partially cover the opening of the cervix.
  • Placenta previa occurs in 1 of 200 deliveries, usually in women who have had more than one pregnancy or who have structural abnormalities of the uterus, such as fibroids.
  • Placenta previa can cause painless bleeding from the vagina that suddenly begins late in pregnancy. The blood may be bright red. Bleeding may become profuse, endangering the life of the woman and the fetus.
  • Ultrasonography helps doctors identify placenta previa and distinguish it from a placenta that has detached prematurely (placental abruption).
  • When bleeding is profuse, women may be hospitalized until delivery, especially if the placenta is located over the cervix. Women who bleed profusely may need repeated blood transfusions.
  • When bleeding is slight and delivery is not imminent, doctors typically advise bed rest in the hospital. If the bleeding stops and does not recur, women are usually sent home, provided that they can return to the hospital easily. A cesarean section is almost always performed before labor begins. If women with placenta previa go into labor, the placenta tends to become detached very early, depriving the baby of its oxygen supply. The lack of oxygen may result in brain damage or other problems.
77
Q

ABRUPTIO PLACENTAE

A
  • Placental abruption is the premature detachment of a normally positioned placenta from the wall of the uterus. The placenta may detach incompletely (sometimes just 10 to 20%) or completely. The cause is unknown.
  • Detachment of the placenta occurs in 0.4 to 3.5% of all deliveries. This complication is more common among women who have high blood pressure (including preeclampsia) and among women who use cocaine.
  • The uterus bleeds from the site where the placenta was attached. The blood may pass through the cervix and out the vagina as an external hemorrhage, or it may be trapped behind the placenta as a concealed hemorrhage. Symptoms depend on the degree of detachment and the amount of blood lost (which may be massive).
  • Symptoms may include sudden continuous or crampy abdominal pain, tenderness when the abdomen is pressed, and shock. Premature detachment of the placenta can lead to widespread clotting inside the blood vessels, kidney failure, and bleeding into the walls of the uterus, especially in pregnant women who also have preeclampsia.
  • When the placenta detaches, the supply of oxygen and nutrients to the fetus may be reduced.
  • Doctors suspect premature detachment of the placenta on the basis of symptoms. Ultrasonography can confirm the diagnosis.
  • Women with premature detachment of the placenta are hospitalized. The usual treatment is bed rest. If symptoms lessen, women may be discharged from the hospital. If bleeding continues or worsens (suggesting that the fetus is not getting enough oxygen) or if the pregnancy is near term, an early delivery is often best for the woman and the baby. If vaginal delivery is not possible, a cesarean section is performed.
78
Q

HYDATIDIFORM MOLE

A

• A hydatidiform mole is growth of an abnormal fertilized egg or an overgrowth of tissue from the placenta.
• Most often, a hydatidiform mole develops from an abnormal fertilized egg.
• Complete mole
• Incomplete mole
• Hydatidiform mole can also develop from cells that remain in the uterus after a miscarriage or a full-term pregnancy.
Pathogenesis
• Normally, the fetus and the placenta have 46 chromosomes, half of which have been inherited from the mother (X) and the other half from the father (Y)
• The cells of the complete mole (molar pregnancy) have a 46 XX or 46 YY karyotype; all of which have been inherited from the father.
• During fertilization the maternal chromosomes are lost and the paternal chromosomes (23X or 23Y) reduplicate, bring the number of chromosomes to 46 - this process is known as androgenesis.
• Thus, the hydatidiform mole has the correct number of chromosomes but the incorrect genetic makeup
• The incomplete moles (partial molar pregnancy) evolve from the oocytes fertilized with two spermatozoa; therefore, the cells have 69 chromosomes – one set from the mother and two sets from the father

79
Q

HYDATIDIFORM MOLE
Risk Factors
Symptoms and Diagnosis

A

Risk Factors
• The risk of hydatidiform moles is highest for women who become pregnant before age 17 or in their late 30s or later.
• Hydatidiform moles occur in about 1 of 2,000 pregnancies in the United States and, for unknown reasons, are nearly 10 times more common among Asian women
Symptoms and Diagnosis
• Women who have a hydatidiform mole feel as if they are pregnant. But because hydatidiform moles grow much faster than a fetus, the abdomen becomes larger much faster than it does in a normal pregnancy.
• Severe nausea and vomiting are common, and vaginal bleeding may occur. These symptoms indicate the need for prompt evaluation by a doctor. Hydatidiform moles can cause serious complications, including infections, bleeding, and preeclampsia or eclampsia
• Often, doctors can diagnose a hydatidiform mole shortly after conception. No fetal movement and no fetal heartbeat are detected. As parts of the mole decay, small amounts of tissue that resemble a bunch of grapes may pass through the vagina. After examining this tissue under a microscope, a pathologist can confirm the diagnosis.
• Ultrasonography may be performed to be sure that the growth is a hydatidiform mole.
• Blood tests to measure the level of human chorionic gonadotropin may be performed. If a hydatidiform mole is present, the level is usually very high because the mole produces a large amount of this hormone.
• Treatment is surgery and D&C.

80
Q

INVASIVE MOLE

A
  • About 80% of hydatidiform moles disappear spontaneously.
  • About 15 to 20% invade the surrounding tissue and tend to persist.
  • Of these invasive moles, 2 to 3% become cancerous and spread throughout the body; they are then called choriocarcinomas. Choriocarcinomas can spread quickly through the lymphatic vessels or bloodstream
81
Q

D & C

A

Dilation and curettage (D&C) is a procedure to remove tissue from inside your uterus. Doctors perform dilation and curettage to diagnose and treat certain uterine conditions — such as heavy bleeding — or to clear the uterine lining after a miscarriage or abortion.

82
Q

CHORIOCARCINOMA

A
  • A malignant tumour composed of cytotrophoblastic and syncytiotrophoblastic cells
  • In 50% of cases, choriocarcinoma arises from preexisting complete moles; in 25% it arises from placental cells retained after miscarriage; and another 25% arises from normal placenta after completion of a normal pregnancy
  • Choriocarcinoma cells are highly invasive and secrete hCG
  • hCG is used for estimating the amount of tumour tissue and for monitoring tumour tissue recurrence after chemotherapy
  • Choriocarcinoma forms bulky hemorrhagic nodules in the placental bed
  • It invades through the walls of the uterus and often implants in the vagina
  • By invading the veins, it metastasizes to the lung, liver, and most commonly to the brain
  • Fortunately, this tumour responds well to combination of chemotherapy and medications
  • Cure rates of 80% to 100% have been achieved but only in those patients who do not have brain metastases
83
Q

MASTITIS

A
  • The most important and most common inflammatory disease of the breast
  • Usually affects woman who are lactating (acute)
  • Typically is caused by purulent bacteria, such as staphylococcus or streptococcus
  • The microbes invade the breast through the dilated milk ducts or through skin lacerations or minor injuries acquired during suckling
  • Stagnant milk in breast that has not been fully emptied by suckling provides a good growth medium for the bacteria
  • Acute inflammation may spread through the entire breast or cause a localized abscess to form - in either case, the lesion develops quickly and causes localized or diffuse swelling of the breast
  • The inflamed area appears red, is painful, and is sensitive to palpation
  • The entire area is edematous and, histologically, is infiltrated with numerous acute inflammatory cells, mostly polymorphonuclear leukocytes (PMNs)
  • The excretory ducts may contain pus, and if massive suppuration occurs in conjunction with destruction of tissue, an abscess will develop.
  • However, this does not usually happen if acute mastitis is recognized early and the lesion is properly treated
  • Treatment is with antibiotics and emptying the breast
84
Q

BENIGN BREAST DISEASE AND FIBROADENOMA (Goodman, pg 1015)

A

• Benign breast disease aka mammary dysplasia (formerly fibrocystic breast disease)
• Common, benign breast irregularities
• “Tissue nodularity”
Clinical Manifestation
• Cyclical swelling, discomfort, tenderness, pain
• Bilateral
• Mastalgia
• Nodularity – regular, firm, mobile, rubbery
• Nipple discharge
• Infections and inflammation
• Fluctuations in size

85
Q

BENIGN BREAST DISEASE AND FIBROADENOMA

Etiology and Pathogenesis

A 
• Idiopathic
• Related to estrogen levels (pregnancy, lactation, menopause)
Diagnosis
• Examination
• Palpation
• Mammogram
• Biopsy
Treatment
• Analgesics
• Local heat/cold
• Dietary changes
• Adequate support
86
Q

FAT NECROSIS OF THE BREAST

A
  • Sometimes the normal fat cells in the breast become round, firm lumps made up of damaged fatty tissue. This is called fat necrosis of the breast.
  • The lumps may or may not be painful.
  • This problem is most often seen in obese women who have very large breasts or after an injury to a breast.
  • Fat necrosis can be caused by an injury or blow to the breast. Sometimes the skin around this lump looks red or bruised. Fat necrosis is sometimes seen following a motor vehicle accident in which the seat belt has forcefully squeezed the breast
  • The inadequate blood supply causes some cells to die and release particles of fat. These drain to the surface
87
Q

BREAST CANCER (Goodman, pg 1016)

A

36 Systemic Pathology 300 – The Reproductive System
Epidemiology
 Second leading cause of cancer death among women
 Mortality decreasing due to earlier diagnosis and better treatment
Etiology and Risk Factors
 Age
 Gender
 Personal or family history of breast cancer
 Breast cancer gene
 Radiation exposure
 Age at puberty, first pregnancy, menopause
 Prolonged use of oral contraceptives or estrogen therapy (HRT)
 Ethnicity
 Weight gain/obesity
 Alcohol

88
Q

BREAST CANCER

Classification

A
  • Breast cancer is classified by the kind of tissue in which the cancer starts and by the extent of its spread.
  • Breast cancer that starts in the milk ducts is called ductal carcinoma (80%)
  • Breast cancer that starts in the milk-producing glands (lobules) is called lobular carcinoma (20%)
89
Q

BREAST CANCER

Ductal carcinoma in situ (DCIS) –

A

most common type of in situ cancer; precancerous; highly treatable (30%)

90
Q

BREAST CANCER

Invasive ductal carcinoma (IDC) –

A

most common invasive breast cancer; begins in a duct, breaks through the duct wall; invades fatty tissue with further mets possible through lymphatic vessels

91
Q

BREAST CANCER

Invasive lobular carcinoma –

A

grows through the wall of the lobule and spreads via lymphatics or circulatory system (15%)

92
Q

BREAST CANCER

Medullary, tubular and mucinous carcinoma

A

uncommon ductal carcinomas; invasive but better outcome than other types (

93
Q

BREAST CANCER

Inflammatory breast cancer (IBC) -

A

rare, aggressive, invasive ductal cancer; presents similar to an infection with warmth, redness, lymphatic blockage

94
Q

BREAST CANCER

Paget’s disease of the nipple –

A

rare ductal cancer arising near ducts of nipple; symptoms include itching, flaking, bleeding nipple

95
Q

BREAST CANCER

Clinical Manifestation

A

• Asymmetry
• Lump
• Puckering
• Pain
• Tender lymph nodes
• Bruising
Metastases
• Local extension may involve the chest wall, ribs, pleura, lungs, bronchi, vertebrae
• Can spread via lymph nodes to lungs, liver, bone, adrenals, skin, brain
• Most commonly mets to bone – vertebrae, pelvis, hip, ribs, femur, humerus

96
Q

BREAST CANCER

Early Detection

A 
Early Detection
 Self breast examinations (SBE)
 Clinical breast exam (CBE)
 Mammography
 Genetic testing
Diagnosis
 Palpation
 Mammography
 Biopsy
 X-rayTreatment
 Radiation
 Chemotherapy
 Medications
 Surgery
Prevention
• Physical activity
• Weight control
• Alcohol restriction
• Meds
• Diet and supplements
• Risk reduction mastectomy

Sys Path (3 decks)

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