Reproductive System Disorders

ITS HELPS THE PARAMEDICS & NURSING PERSONNEL TO ENHANCE THEIR KNOWLEDGE REGARDING REPRODUCTIVE SYSTEM DISORDERS & ALSO HELP THE EDUCATOR TO TEACH STUDENTS REGARDING REPRODUCTIVE DISORDERS.

1. Reproductive Reproductive
System System
DisordersDisorders

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
•3
rd
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. Stages

15. 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

16. 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

17. 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

18. 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%

19. 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

20. Female Infertility
•Broad range of tests avail
–General health status checked 1
st
–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

22. Normal Laparoscopy

24. 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

25. 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

26. 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

29. Endometriosis

30. 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

31. 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

33. PID

34. 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

35. PID—Signs and Symptoms
•Lower abdominal pain (1
st
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

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

37. 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

38. Ovarian Cysts

40. 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

41. Carcinoma of the Breast—
Pathophysiology
•Malignant cells spread at early state
–1
st
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

42. Breast Cancer

43. 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 1
st
pregnancy
–Role of exogenous estrogen (birth control pills,
supplements) still controversial

44. 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

45. 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

46. 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

47. 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

48. 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

50. 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

52. Normal Cervix; Cancerous Cervix

53. 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

54. 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

55. 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

56. 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

57. 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

58. 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

60. 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

61. 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

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

63. Thanks