Reproductive System Disorders

2. Overview
Male Infertility
Benign Prostatic Hypertrophy
Prostate Cancer
Female Infertility
Endometriosis
Pelvic Inflammatory Disease
Ovarian Cysts
Cancer
Breast
Cervical
Uterine

3. Male Infertility
Can be solely male, solely female, or both
Considered infertile after one year of unprotected
intercourse fails to produce a pregnancy
Male problems include
Changes is sperm or semen
Hormonal abnormalities
 Pituitary disorders or testicular problems
Physical obstruction of sperm passageways
 Congenital or scar tissue from injury
Semen analysis
Assess specific characteristics
 Number, motility, normality

4. Benign Prostatic Hypertrophy (BPH)—
Pathophysiology
Common in older men; varies from mild to severe
Change is actually hyperplasia of prostate
Nodules form around urethra
Result of imbalance between estrogen and testosterone
No connection w/ prostate cancer
Rectal exams reveals enlarged gland
Incomplete emptying of bladder leads to infections
Continued obstruction leads to distended bladder, dilated
ureters, renal damage
If significant, surgery required

8. BPH—Signs and Symptoms
Initial signs
Obstruction of urine flow
 Hesitancy, dribbling, decreased force of urine stream
 Incomplete bladder emptying
 Frequency, nocturia, recurrent UTIs

9. BPH—Treatment
Only small amount require intervention
Surgery when obstruction severe
Drugs (Flomax) used to promote blood flow helpful
when surgery not required

10. Prostate Cancer
Common in men older than 50; ranks high as
cause of cancer death
3rd
leading cause of death from cancer

12. Prostate Cancer—Pathophysiology
Most are adenocarcinomas from tissue near surface of gland
 BPH arises from center of gland
 Many are androgen dependent
Tumors vary in degree of cellular differentiation
 The more undifferentiated, the more aggressive and the faster they grow
and spread
Metastasis to bone occurs early
 Spine, pelvis, ribs, femur
Cancer has typically spread before diagnosis
Staging based on 4 categories:
 A  small, nonpalpable, encapsulated
 B  palpable confined to prostate
 C  extended beyond prostate
 D  presence of distant metastases

13. Prostate Cancer—Etiology
Cause not determined
Genetic, environmental, hormonal factors
Common in North American and northern Europe
Incidence higher in black population than white
Genetic factor?
Testosterone receptors found on cancer cells

14. Prostate Cancer—Signs and Symptoms
Hard nodule in periphery of gland
Detected by rectal exam
No early urethral obstruction
b/c of location
As tumor develops, some obstruction occurs
 Hesitancy, decreased stream, urinary frequency, bladder
infection

15. Prostate Cancer—Diagnostic Tests
2 helpful serum markers
Prostate-specfic Antigen (PSA)
 Useful screening tool for early detection
Prostatic acid phosphatase
 elevated when metastatic cancer present
Ultrasound and biopsy confirms

16. Prostate Cancer—Treatment
Surgery and radiation
Risk of impotence or incontinence
When tumor androgen sensitive:
orchiectomy (removal of testes) or
Antitestosterone drug therapy
5 yr survival rate is 85-90%

17. Female Infertility
Associated w/ hormonal imbalances
Result from altered function of hypothalamus, anterior pituitary,
or ovaries
Typically after long use of birth control pill
Structural abnormalities
Small or bicornuate uterus
Obstruction of fallopian tubes
Scar tissue or endometriosis
Access of viable sperm
Change in vaginal pH
 Due to infection or douches
Excessively thick cervical mucus
Development of antibodies in female to particular sperm
Smoking by male or female

18. Female Infertility
Broad range of tests avail
General health status checked 1st
Pelvic examinations, ultrasound, CT scans check for
structural abnormalities
Tubal insufflation (gas/pressure measurement) or
hysterosalpingogram (X-ray w/ contrast material) used
to check tubes
Blood tests throughout cycle to check hormone levels

20. Normal Laparoscopy

22. Endometriosis
Presence of endometrial tissue outside uterus
(ectopic)
Found on ovaries, ligaments, colon, sometimes lungs
Responds to cyclic hormonal variations
Grows and secretes then degenerates, sheds and bleeds
 What is the problem? (Where does it go?)
Blood irritating to tissues = inflammation and pain
 Recurs w/ e/ cycle w/ eventual fibrous tissue
 Causes adhesions and obstruction
Diagnosis confirmed w/ laparoscopy

23. Endometriosis
Infertility results from
Adhesions pulling uterus out of normal position
Blockage of fallopian tubes
“chocolate cyst” develops on ovary
Fibrous sac containing old brown blood
Primary manifestations
Dysmenorrhea
 More severe e/ month
Painful intercourse if vagina and supporting ligaments
affected by adhesions

24. Endometriosis
Cause not established
Migration of endometrial tissue up thru tubes to
peritoneal cavity during menstruation, development
from embryonic tissue at other sites, spread thru blood
or lymph, transplantation during surgery (C-section) all
possibilities
Treatment
Hormonal suppression of endometrial tissue
Surgical removal of endometrial tissue
Pregnancy and lactation delay further damage
and alleviate symptoms

25. Endometriosis

26. Pelvic Inflammatory Disease (PID)
Common infection of reproductive tract
Particularly fallopian tubes and ovaries
Includes:
Cervicitis (cervix)
Endometritis (uterus)
Salpingitis (fallopian tubes)
Oophoritis (ovaries)
Infection either cute or chronic
Short-term concerns: peritonitis, pelvic abscess
Long-term concerns: infertility, high risk of
ectopic pregnancy

27. PID—Pathophysiology
Usually originates as vaginitis or cervicitis
Often involves several causative bacteria
Uterus  fallopian tube
Edema, fills w/ purulent exudate
 Obstructs tube and restricts drainage into uterus
 Exudate drips out of fimbriae onto ovaries and surrounding
tissue
 Peritoneal membrane attempts to localize but peritonitis may
develop
 Abscesses may form; life-threatening
 Cause septic shock
Adhesions affect tubes and ovaries
Lead to infertility and ectopic pregnancies

29. PID

30. PID—Etiology
Arise from sexually transmitted diseases
Gonorrhea
Chlamydiosis
Prior episodes of vaginitis or cervicitis precedes
development
Infection acute during or after menses
Endometrium more vulnerable
Can also result from IUD or other contaminated
instrument
Can perforate wall and lead to inflammation and
infection

31. PID—Signs and Symptoms
Lower abdominal pain (1st
indication)
Sudden and severe or gradually increasing in intensity
Tenderness during pelvic exams
Purulent discharge at cervix
Dysuria
Fever and leukocytosis can occur
Depends on causative organism

32. PID—Treatment
Aggressive antibiotics
Cefoxitin, doxycycline
Recurrent infections common
Sex partners should be treated as well
Follow-up appt to ensure eradication

33. Benign Tumors: Ovarian Cysts
Variety of types
Follicular and corpus luteal cysts common
 Develop unilaterally in both ruptured and unruptured follicles
Usually multiple fluid-filled sacs under serosa
that covers ovary
May become large enough to cause discomfort,
urinary retention, or menstrual irreg
Bleeding if ruptures
 Cause even more serious inflammation
Risk of torsion of the ovary
Ultrasound and laparoscopy to ID cyst

34. Ovarian Cysts

36. Malignant Tumors: Carcinoma of the Breast
—Pathophysiology
Develop in upper outer quadrant of breast in ½ of
the cases
Central portion of the breast is also common
Most tumors are unilateral
Different types; majority arise from ductal
epithelium
Infiltrates surrounding tissue and adheres to skin
 Causes dimpling
 Tumor becomes fixed when adheres to muscle or fascia of chest
wall

37. Carcinoma of the Breast—Pathophysiology
Malignant cells spread at early state
1st
to close lymph nodes
 Axillary nodes
In most cases, several nodes infected at time of diagnosis
 metastasizes quickly to lungs, brain, bone, liver
Tumor cells graded on basis of degree of differentiation or
anaplasia
Tumor then staged based on size of primary tumor, # lymph
nodes, presence of metastases
Presence of estrogen and progesterone receptors
Major factor in determining how to treat the pt’s cancer

38. Breast Cancer

39. Breast Cancer—Etiology
Major cause of death in women
Incidence continues to increase after age of 20
Strong genetic predisposition
identification of specific genes related to cancer
Hormones also a factor
Specifically exposure to high estrogen levels
 Long period of regular menstrual cycles (early menarche to late
menopause)
 No kids (nulliparily)
 Delay of 1st
pregnancy
Role of exogenous estrogen (birth control pills,
supplements) still controversial

40. Breast Cancer—Signs and Symptoms
Initial sign is single, hard, painless nodule
Mass is freely movable in early stage
 Becomes fixed
Advanced signs
Fixed nodule
Dimpling of skin
Discharge from nipple
Change in breast contour
Biopsy confirms diagnosis of malignancy

41. Breast Cancer—Treatment
Surgery, radiation, chemo
Surgery
Lumpectomy
 Preferred; removal of tumor
Mastectomy
 Sometimes necessary
Some lymph nodes removed as well
 # removed depends on the spread of the tumor cells
 Impairs draining of lymph; swelling and stiffness of arm common
Chemo and radiation
Useful for eradicating undetected micrometastases

42. Breast Cancer—Treatment
If responsive to hormones, removal of hormone
stimulation
Premenopausal women: ovaries removed
Postmenopausal women: hormone-blocking agent
Prognosis
Relatively good if nodes not involved
As # nodes increases, prognosis becomes more negative
May recur years later
 Longer the period w/o recurrence, better the chances
BSE if over 20 yrs.
Mammography routine screening tool
Detect lesions before they become palpable or if they are deep in
the breast tissue

43. Carcinoma of the Cervix
# deaths has decreased due to Pap smear
Screening and early diagnosis while cancer in situ
However, # cases of carcinoma in situ has increased
in the US
Avg age of in situ onset is 35
Invasive carcinoma manifests at 45
Age range dropping to younger women

44. Cervical Cancer—Pathophysiology
Early changes in cervical epithelial tissue consist of
dysplasia
Mild then becomes severe (takes 10 yrs)
Occurs at junction of columnar cells and squamous cells of
external os of cervix
Cervical intraepithelial neoplasia (CIN) graded from I to
III
Based on amount of dysplasia and cell differentiation
Grade III
 Carcinoma in situ
 Many disorganized, undifferentiated, abnormal cells present (severe
dysplasia)
Takes 10 yrs from mild to carcinoma in situ so plenty of chances to
detect

46. Cervical Cancer—Pathophysiology
Carcinoma in situ is noninvasive stage
Leads to invasive stage
Invasive has varying characteristics
Protruding nodular mass or ulceration
Eventually all characteristics present in the lesion
Carcinoma spreads in all directions
Adjacent tissues (uterus and vagina); bladder, rectum, ligaments
Metastases to lymph nodes occur rarely or in late stage
Staging:
0: carcinoma in situ
I: cancer restricted to cervix
II to IV: further spread to surrounding tissues

48. Normal Cervix; Cancerous Cervix

49. Cervical Cancer—Etiology
Strongly linked to STDs
Herpes simplex virus type 2 (HSV-2)
Human papillomavirus (HPV)
Virus exerts direct effects on host cell or may cause
antibody rxn
Increased antibodies have been assoc w/ increasing dysplasia
High risk factors
Multiple sex partners
Promiscuous partners
Sexual intercourse in early teen years
Pt history of STDs
Environmental factors such as smoking can predispose
women

50. Cervical Cancer—Signs and Symptoms
Asymptomatic in early stage
Can be detected by Pap test
Invasive stage indicated by slight bleeding or spotting
Anemia and wt loss can accompany

51. Cervical Cancer—Treatment
Biopsy to confirm diagnosis
Surgery and radiation to treat
5 yr survival rate 100% if carcinoma still in situ
Prognosis for invasive depends on the extent of the
spread of cancer cells

52. Carcinoma of the Uterus (Endometrial
Carcinoma)
Common cancer in women older than 40
Majority 55-65 yrs old
Simple screening not available for this cancer
Early indication is bleeding
Significant sign in postmenopausal women

53. Uterine Cancer—Pathophysiology
Majority are adenocarcinomas
arise from glandular epithelium
Malignant changes develop from endometrial
hyperplasia
Excessive estrogen stimulation major factor for
hyperplasia
Cancer is slow-growing
May infiltrate uterine wall (thickened area) or
may spread out to endometrial cavity
Eventually tumor mass fills interior of uterus
 Expands thru wall into surrounding structures

54. Uterine Cancer—Pathophysiology
Graded from 1-3
1: indicate well-differentiated cells
3: poorly differentiated cells
Staging
Based on degree of localization
I: tumors confined to body of uterus
II: cancer limited to uterus and cervix
III: cancer spread outside of uterus; still in true pelvis
IV: tumor spread to lymph nodes and distant organs

56. Uterine Cancer—Etiology
Higher risk if increased estrogen levels
Assoc w/ exogenous estrogen (postmenopausal women)
 Recommended dosage lowered
Oral contraceptives
Infertility
Obesity, diabetes, hypertension increase risk

57. Uterine Cancer—Signs and Symptoms
Painless vaginal bleeding or spotting is key sign
b/c cancer erodes surface tissues
Pap smear not dependable for detection
Direct aspiration of cells provides best analysis
Late signs of malignancy include palpable mass,
discomfort or pressure in lower abdomen, bleeding
following intercourse

58. Uterine Cancer—Treatment
Surgery and radiation
Prognosis relatively good
5 yr survival rate 90% if cancer well localized at time of
diagnosis