Pelvic inflammatory disease (PID) is an inflammatory condition of the pelvic cavity that is usually caused by bacteria, viruses, or other microbes. It commonly affects sexually active young women and can cause long-term complications like infertility or ectopic pregnancy if left untreated. Symptoms include lower abdominal pain and vaginal discharge. Treatment involves antibiotics, bed rest, and care of any sexual partners. Nursing care focuses on monitoring, education, and supporting patients through treatment.

2. DEFINITION--
 Pelvic inflammatory disease(PID) is an inflammatory
condition of the pelvic cavity that may involve the
uterus ,fallopian tubes, ovaries, pelvic peritoneum, or
pelvis vascular system.
 Infecetion which may be acute , subacute,
recurrent,or chronic and localized or widespread, is
usually caused by—
 Bacteria.
 Virus.
 fungus or parasites.

3. Contd....
 Organism most commonly associated are..
1. GONORRHEAL.
2. CHLAMYDIAL.
3. MYCOPLASMA.

4. INCIDENCE RATE--
 About 1 million women are diagnosed with PID each
year in U.S.
 Most are younger than 25 years of age.
 One fourth of them have serious sequelae
e.g..infertility, ectopic pregnancy.
 Rupture of tubo ovarian abscess has a 5% to 10%
mortality rate.
 Many of them need a total hystrectomy.

5. CAUSE’S
 The exact cause is not determined.
I. It is presumed that organisms usually enter the body
through the vagina, and move upword through the
cervical canal, colonize the endocervix, and move
upward into uterus.
 This all usually occurs after-
I. Childbirth.
II. Abortion.
III. Surgical procedures.
IV. Sexually transmitted.
V. IUD insertion.
VI. Endometrial biopsy.

6. RISK FACTOR’S--
 Early age at first intercourse.
 Multiple sexual partner’s.
 Frequent intercourse.
 Sex with a partner with an STD.
 History of STD and previous pelvic infection.

7. Pathophysiology-
 In PID organisms usually ascends from lower tract to
upper side , this commonly occurs during pregnancy,
becuse there is increased blood supply to the organs.
 These post partum and post abortion infectiontend to
be unilateral.
 Infection can cause perihepatic inflammation when
the organisms invades the peritoneum.
 In gonorrheal infection, the gonococci pass through
the cervical canal into the uterus especially during
menstruation, when the environment is favourable.

8. Cont..
 In rare cases the infection spread through the blood
stream from the lungs.

9. Clinical manifestation-
 Vaginal discharge.
 Lower abdominal, pelvic pain and tenderness that
occurs after menses.
 Pain usually increase during voiding or defecation.
 Others are –fever, general malaise, anorexia.
 Nausea , headache, possibly vomiting.
 Symptoms may be actue or severe.

10. DIAGNOSIS-
 History taking.
 Physical examination of gyanecological importance(it
reveals tenderness on palpation and movement of
cervix and uterus)
 Blood culture.
 Sonography.

11. MANAGEMENT-
 Patient’s with mild infection are treated in out patient
department but hospitalization may be necessary in
some cases.
 Bed rest.
 Intravenous fluids.
 Broad spectrum iv antibiotic are started.
 If patient has abdominal distension than nasogastric
intubation and suction are intiated.
 Treatment of sexual partner is also needed.

12. NURSING MANAGEMENT-
 Monitoring vital signs.
 Maintaing bed rest and fowler’s position during
hospital stay.
 Note amount and characterstics of vaginal discharge.
 Health education regarding safe sex and on personal
hygiene.

14. OVARIAN CYST
 The ovary is a common site for cysts, which may be
simple, enlargementof normal ovarian constituents,
the graffine follicle, or corpuse lutem, or they may
arise from abnormal growth of the ovarian
epithelium.
 Cysts are usually soft, surrounded by thin capsule, and
are seen mainly duringthe reproductive age.

15. TYPES OF OVARIAN CYSTS:-
 Follicular ovarian cysts.
 Corpus luteum cysts.
 Dermoid cysts.
 Serous tumours.
 Endometrial tumours.

16.  Corpus luteum cyst.:--
 Less common variety.
 Associated with normal ovarian fx.or elevated progesterone.
 Avg. Diameter 4cm.
 May appear purplish red due to bleeding within corpus luteum.
 Mennorrhagia is common.
 Follicular ovarian cysts:--
 These are most common form of cyst.
 Frequently multiple, range in size from a few mm to as large as
15cm in diameter.
 Depend on gonadotropine for growth.

17. Dermoid cysts:--
 These are tumors that are thought to arise from parts
of the ovum that normally disappear with ripening.
 Their origin is unidentified, and they consists of
undifferentiated embryonal cells.
 They grow slowly and found during surgery to contain
a thick yellow sebaceous material arising from skin
material.
 Hair ,teeth, bone may found inside the cysts.

19.  Endometroid tumors:--
 Small lesion , purplish blue in color.
 Large tumors are called CHOCOLATE CYSTS, because they
contain chocolate color clots.
 Very loe malignancy potential.

20. CAUSES:--

21. CLINICAL MANIFESTATION
 Ovarian cysts are often asymptomatic until they are
large enough to cause pressure in the pelvis,
constipation, menstrual irregularities, urinary
frequency.
 A feeling of fullness in the abdomen.
 Anorexia and peripheral edema.
 Pelvic pain.
 More severe in twisted ovarian cysts.

22. DIAGNOSIS:--
 History of chronic pelvic pain .
 Other causes are excluded.
 Palpation of pelvic organs during examination reveals
the presence of any mass or enlargement of ovary.
 Increase in abdominal girth in case of large tumour.
 Ultrasonography.
 CT SCAN.

23. MANAGEMENT:--
 Many ovarian cysts resolve spontaneously .
 If the cyst does not decrease in size oral contraceptive
are prescribed to shrink the cysts.
SURGICAL MANAGEMENT:--
 Surgery is recommended only when the cysts are
larger than 8cm.
 A cystectomy rather than oopherectomy is performed.

24. NNURSING MANAGEMENT
 Assurance.
 Education regarding disease process.
 All routine post operative care.
 Advise to use abdominal binder after surgery.
 Follow up care.

25. OVARIAN CANCER

26. OVARIAN CANCER
 Ovarian cancer is very distressing disease to patients
and health care provider because of its silent feature it
came in diagnosis usually in later stages.
 It causes more death then any other cancer of female
reproductive system disorder.About 75% cases
detected in later stage.
 Malignant neoplasma of ovary can occur at any age,
including infancy and childhood.
 Most frequent in women between 55 to 65 years of age.
 Higher incidence in industrialised countries excepts
JAPAN.

27. Cusative factors:--
 Exact etiology is not know but several risk factors are
there to dispose women to ovarian cancer these are
following:--
 Hereditary
 Endocrine
 Industrialized exposure
 Women having BRCA-1 GENE mutation have higher chances.
 Exposure to talk , asbestos, diet high in meat and animal fats
and high milk consumption all these linked to ovarian cancer.
 Nulliparity,infertility, anovulation.

28. FAVOURABLE FACTORS:--
 Breast feeding.
 Multiple pregnancies.
 Oral contraceptive use.
 Early age at first birth.

29.  Women with ovarian cancer has a three fold to four
fold increase in risk for breast cancer or vice versa.
 No early screening mechanism pressent till now.


30. PATHOPHYSIOLOGY:--
 The four main type of ovarian cancer are:--
I. Epithelium; serous, mucinous.
II. Germ cell:
III. Gonadal stroma
IV. Mesenchyma.
They are having two pattern of metastasis; lymphatic and direct.
Primary lymphatic drainage of the ovary is thought the
retroperitoneal nodes surroundin the renalilium. Secondry
drainage is through the inguinal lymphatics.ovarian cancer
directly metastasizes to the abdominal cavity.

31. STAGES:--
STAGE 1 Limited to ovaries.
STAGE 2 Involving one or both ovary with pelvic extension.
STAGE 3 Involving one or both ovary with intraperitoneal metastasis outside
pelvis or positive lymph nodes.
STAGE 4 Involving one or both ovaries with distinct metastasis to liver or
lungs.

34. CLINICAL MANIFESTATION
Usually it is asymptomatics.
 In later stage
 Pelvic discomfort, lower back pain, breast tenderness
 Weight change , abdominal pain, gastroesophageal
reflux.
 Nausea vomiting, constipation and urinary frequency.
 Increase in abdominal girth.
 Bowel and bladder dysfunction, dysparenuia
 Menstrual irregularties.
 Ascites , abnormal uterine bleeding.

35. Diagnosis:--
 Clinical history.
 Physical examination.
 USG & TVS.
 MRI.
 CT SCAN.
 Laparotomy
 Tumor marker.
 CA 125.
 Screeing for BRCA 1,2

37. TREATMENT:--
SURGERY;-- surgery is the primary therapeutic approach and
usually involves TAH BSO.Ascites fluids or washing are
submitted for cytology.
 All the tissue of pelvis are carefully observed and sent for cytology.
ADJUVANT THERAPY:--
 STAGE 1ST :--CHEMOTHERAPHY.
 STAGE 2ND :--INSTILLATION OF RADIOACTIVE PHOSPHORUS
into the peritoneal cavity or combined chemotheraphy.
 STAGE 3RD :--SURGICAL REMOVAL OF TUMOR.

38. PHARAMOCOLIGICAL MX.
 CHEMOTHERAPHY:--
 cyclophosphomide
 cisplatin
 carbop lastin
 PACLITAXEL

39. NURSING AMNAGEMENT--
 Emotional support to the patient.
 Comfort measures.
 Imaprting information.
 Pre operative management—
 Bowel preparation.
 Interavenous fluid support.
 Pre operative medicines.