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PATHOPHYSIOLOGY (NARRATIVE FORM) Cancer of the cervix typically originates from a dysplastic or premalignant lesion previously present at the

active squamous columnar junction. The transformation from mild dysplastic to invasive carcinoma generally occurs slowly within several years, although the rate of this process varies widely. Carcinoma in situ is particularly known to precede invasive cervical cancer in most cases. In different reported series of patients with untreated carcinoma in situ who were followed up for many years, invasive carcinoma developed in about 30% of patients at 10 years and in about 80% of patients at 30 years. However, the carcinoma-in-situ lesion may regress after the initial diagnosis; such an occurrence was reported in 17 (25%) of 67 patients who were followed up for at least 3 years. Progression to invasive carcinoma becomes established and is considered irreversible once the malignant process extends through the basement membrane and invasion of the cervical stroma occurs. Multiple local growth patterns of invasive cervical cancer have been described, with combination growth patterns being common. The patterns include the following: exophytic, nodular, infiltrative, and ulcerative. The exophytic variety is the most common growth pattern. It usually arises from the exocervix and is often polypoid or papillary in form. Exophytic cervical cancer may result in a large, friable, bulky mass that involves only the superficial aspect of the cervix and has the tendency for excessive bleeding. The nodular variety typically arises in the endocervix and grows through the cervical stroma into confluent, firm masses that cause the cervix and isthmus to expand. Large, nodular-type tumors that circumferentially involve the endocervical region and large, exophytic-type tumors that originate from the endocervix and

extend into the endocervical canal result in what has been referred to as a barrelshaped cervix. The infiltrative growth pattern leads to a stone-hard cervix that may be predicated to have minimal visible ulcerations or an exophytic mass. Infiltrative exocervical lesions tend to invade the vaginal fornices and the upper part of the vagina. On the other hand, infiltrative endocervical lesions tend to extend into the corpus and the lateral parametrium.

PATHOPHYSIOLOGY (SCHEMATIC DIAGRAM)


PREDISPOSING FACTORS Age (64 years old) Sex (exclusively for female) Heredity (history of cervical CA) PRECIPITATING FACTORS Sexual partner who had multiple sexual partner (HPV exposure) Low economic status Diet and lifestyle Multiple Pregnancies (7 and above delivered) Somatic Mutation in DNA or Gene Altered genetic structure and autoimmune response Activated oncogene or deactivate cell tumor suppressor gene

Malignant transformation of lymphoid stem cells

Formation of clones or uncontrolled proliferation lymphocytes Cervix cells dysplasia after lymphoblastic cell event

Acquisition of invasive characteristics

Tumor cells engulf lymphocytes

Through sexual intercourse: HPV penetrates squamous columnar epithelial cervix cells Virus transcripts stroma

Altered production of normal cells

Hematology Lab Result: Increased WBC 11.2

Hematology Lab Result: Decreased RBC 2.43 10^12/L

Activation of oncogenic cell growth factor

Host cells put up tissue barrier Tumor cells attach in the cervix cells Treatment: ampicillin

S/Sx: Infection Fatigue Pallor Increased RR: 25cpm

Spread and invades distant tissues (vagina)

Autoimmune inhibition progression (malignant)

Asymptomatic tumor growth Cervical Cancer Affection of the surrounding tissues of the cervix along the vagina Diagnostic Test: Cervical Biopsy

Necrosis and infection of the tumor

Gain access to pelvic lymph nodes Fundus


S/Sx: Excruciating pain in back and legs

Treatment: tranexamic acid

S/Sx: Vaginal Bleeding Dark and Foul Odor

Increased tumor growth Hypermetabolic activity

Irritation of nerve endings

Hematology Lab Result: Decreased HGB 2.78 10^12/L

Weight loss: 45 40 kl. of the pt. weight.

Pressure on the surrounding tissue

Treatment: analgesic

PROGNOSIS

With Medical Management: Hysterectomy Chemotherapy Radiation Therapy

Without Medical Management: Tumor Metastsis may occur

Good Prognosis

Poor Prognosis

IVF Replacement Follow prescribed medication by the physician

Multi-organ failure or complication and Sepsis

Possible for recovery

Coma

35 40% Rate of Survival; about 5 yrs. in Cervical CA Stage III

Death

LEGENDS: RISK FACTORS PATHOLOGY MANAGEMENT/DIAGNOSTIC TEST

MANIFESTATIONS

LABORATORY TEST/RESULT

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