Pathophysiology(Cervical Cancer) Case Study

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

have been described,

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)

   

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

PRECIPITATING FACTORS Sexual partner who had multiple sexual  partner (HPV exposure) Low economic status Diet and lifestyle Multiple Pregnancies (7 and above delivered)

Tumor cells engulf  lymphocytes

Through sexual intercourse: HPV  penetrates squamous columnar epithelial cervix cells

Altered production of normal cells

Hematology Lab Result: Increased WBC  –  11.2

Virus transcripts stroma

Activation of oncogenic cell growth factor 

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

S/Sx: Infection Fatigue Pallor  Increased RR: 25c m

Host cells put up tissue barrier 

Tumor cells attach in the cervix cells Treatment: ampicillin

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

Gain access to pelvic lymph nodes

 Necrosis and infection of  the tumor 

Treatment: tranexamic acid

Fundus

S/Sx: Vaginal Bleeding Dark and Foul Odor 

Irritation of nerve endings

Increased tumor growth

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

Hypermetabolic activity

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

Treatment: analgesic

Pressure on the surrounding tissue

PROGNOSIS

With Medical Management: Hysterectomy  Chemotherapy  Radiation Therapy 

Good Prognosis

 

S/Sx: Excruciating pain in back and legs

IVF Replacement Follow prescribed medication by the  physician



Without Medical Management: Tumor Metastsis may occur 

Poor Prognosis

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

MANIFESTATIONS

MANAGEMENT/DIAGNOSTIC TEST

LABORATORY TEST/RESULT