Predisposing Factors Age Gender Environment Stress INITIATION STAGE Cellular aberration or change in genome of epithelial cells specifically

in the pituitary gland.

Precipitating Factors Immunosupression Hereditary Medications Diet Parental Occupation

Activation of growth promoting gene.

Inactivation of growth inhibiting gene. PROMOTION STAGE Expression of altered gene productions & loss of regulatory gene productions PITUITARY ADENOMA Osmotic gradient absorbs the fluid does promoting tumor growth. PITUITARY MACROADENOMA

Compression of adjacent brain structures. Compressio n of optic chiasm Bitempora l hermiano psia

Venous Compressi on Decreased oxygen supply.

Increased intracranial pressure. Breakdown of blood brain barrier.

Vomiting Headach e Papillede ma Altered LOC Obstruction of cerebrospinal flow HYDROCEPHAL US

Compression Necrosis of brain in the tissue hypothalamu Polydipsia Anterior s Loss of pituitary Abnormal appetite gland secretion of Irregular hormones thermoregulat ion Disturbs Thyroid control of Growth stimulating wakefulness hormo hormone ne DWARFIS M Goite r HYPOTHYROIDI SM Production of thyroid hormone

Abnormal secretion of hormones in the pituitary gland. Posterior pituitary gland Deficiency of anti-diuretic hormone. DIABETES INSIPIDUS Polyuria Polydipsia creatinine level Dehydration

Decreas edcereb ral blood flow Cereb ral hypox Confusio ia n Lethargy Clumsy moveme nts Appetite

Accumulat basal Reduc Reduced ion metabolic Heat ed blood flow of rate & producti perista & hyaluronic reduced on ltic glomerula acid which oxygen activit r filtration Decreas binds to requirement Cool y rate ed water s. skin Normocyti absorpti renal Myxede c or on of excreti ma normochro nutrient on of or mic s water edema anemia Retarde iron total d absorpti protein body skeletal on metaboli water & soft sm capillary tissue Iron permeab growth. deficiency ility DWARFIS Anemia M High concentrations of constipa exchangeable albumin in tion the extravascular space.

ETIOLOGY Predisposing factor Age Primary brain tumors have a bimodal distribution, with a small peak in the pediatric population and a steady increase in incidence with age, beginning at age 20 years and reaching a maximum of 20 cases per 100,000 population between the ages of 75 and 84 Gender years. Males have a 24% higher incidence of invasive brain certain tumors than females. tumors, and Compared to females, there is a male preponderance for brain especially The medulloblastomas ependymomas. Actual Rationale

reasons are unknown. The predominance of males over females persists among both white Environment and black children. It has been proposed that a small part of the apparent increase in incidence of brain tumors may be due One to environmental of these neurocarcinogens. category

environmental exposures, also called chemical neurocarcinogens, has attracted considerable interest, tobacco, especially cosmetics, N-nitroso lotions, compounds. These compounds are found in diet, in alcohol, antihistamines, diuretics, and rubber baby bottle and pacifier nipples (Gurney et al, 2001). In addition, the ingredients in pesticides can react with nitrite in the stomach and cause the formation of N-

nitroso compounds (Inskip et al, 1995). Studies have been largely inconsistent in showing the linkage between N-nitroso compounds and brain tumors in humans. Many studies have tried to evaluate parents exposures to these substances before, during and after pregnancy, without conclusive results (Little, 1999). However, a number of chemical compounds, including N-nitroso compounds, have been shown to cause CNS tumors in experimental animals. These animal studies have shown that susceptibility to these compounds is greatest during the in utero or early postnatal period of life in animals (NCI, 1996). Additional studies need to be done to examine the potential role of chemical neurocarcinogens in the etiology of childhood brain tumors. Precipitating factor Immunosupressio n Actua l Rationale The patient is immunosupressed because she is already malnourished and has a previous hospitalization last month and has undergone craniotomy which is a major procedure. She is Hereditary still in her recovery stage. Other evidence for the role of genetics in the origins of childhood brain cancer comes from studies of family history. When a sibling or parent has brain tumor, there is an increased risk for brain tumors of 3 to 9 fold (Gurney et al, 2001). Some studies show an elevated risk of brain tumors in children when a sibling or

parent has certain types of seizure disorders. Similarly, a positive family history of epilepsy and mental retardation has been associated with brain tumors in some studies. In addition, there have been several studies evaluating anticonvulsant use in mothers during pregnancy with inconclusive results to date Lifestyle (Little, 1999). Passive cigarette smoke exposure, electric blanket use and ultrasound testing during pregnancy have been studied and have not been linked to development of CNS head Diet injuries in patients with brain tumors. Frequent maternal consumption during pregnancy of cured meat, which contains Nnitroso compounds or precursors, has been consistently associated with a small (1.5 to 2 fold) increased risk of developing a brain tumor. It is unclear whether uncured meats alone or in combination with other dietary factors are responsible. Several studies have looked at the role of nutritional habits during gestation and childhood and brain tumor development. One study showed that increased consumption of vegetable fat in children and maternal potassium intake during gestation were associated with an increased risk of brain tumors (Lubin et al, 2000). But this same study did not find evidence to support the recent hypothesis for the role of nitrates, nitrites and vitamin C during gestation and early childhood

as being associated with pediatric brain tumors. In summary it seems that specific nutritional etiologies need to be further Parental Occupation evaluated. Parents work in certain industries with a variety of chemical exposures has been linked to CNS tumors in their children in some studies. Specifically, aircraft, work in industries petroleum, found a involving painting, two-fold agriculture, One

printing and chemical solvents have been implicated. fathers study in the elevated risk for brain tumors in children whose worked chemical-petroleum industry or as electrical workers (McKeanCowdin et al, 1998). Some researchers have linked brain tumors in adults with exposure to farm animals. This suggests that viruses may be involved, but this hypothesis needs further evaluation.

NARRATIVE Pituitary adenoma starts in initiation stage of tumor development wherein cellular aberration or change in genome of epithelial cells specifically in the pituitary gland. Then, there will be an activation of growth promoting gene and inactivation of growth inhibiting gene leading to promotion stage of tumor development wherein expression of altered gene productions and loss of regulatory gene productions which leads o pituitary adenoma. Then, osmotic gradient absorbs the fluids that promote tumor growth that leads to pituitary macro adenoma. With the chief complain of the patient which is vomiting, there are two ways vomiting will occur. First, the pituitary macro adenoma will compress adjacent brain structures leading to venous compression, and then there will be a breakdown of blood brain barrier leading to increase intracranial pressure. Second, pituitary macro adenoma directly increases intracranial pressure and obstructs cerebrospinal flow leading to hydrocephalus and then again to increase intracranial pressure. The increase in intracranial pressure leads to vomiting, headache, and altered level of consciousness. Vomiting leads to dehydration. Our patient is experiencing mild dehydration with signs and symptoms of cool skin, polydipsia, weakness, dry mucous membranes, restlessness or irritability, slightly sunken eyes, skin pinch goes back slowly, decreased tears, and decreased urine output that may appear dark yellow. If treated with antibiotics or anti-infectives, rehydration therapy, oral rehydration solutions, intravenous solutions, proper nutrition, and vitamin supplements there will be a good prognosis. If not treated it may lead to hypovolemic shock, seizures, septicemia, meningitis, ande death which leads to poor prognosis

SYMPTOMATOLOGY Symptoms Actual Rationale

Vomiting

Vomiting results from increase intracranial pressure and is the main chief complaint of the patient. This signs and symptoms are manifested by

Cool Skin Weakness Dry mucous membranes Restless irritable Slightly of

the patient due to dehydration. The main chief complaint of the patient is vomiting which is one of the factors that lead to dehydration. In vomiting, the gastric contents backflows from

sunken goes

the small intestine, stomach, esophagus to the mouth. Nutrients, fluids, and electrolytes are not properly absorbed by the body so dehydration occurs.

eyes Skin pinch

back slowly Decreased tears Decrease urine output appears dark yellow

Chief Complaint: Vomiting Dehydratio n Mild dehydration: Cool skin Polydipsia Weakness Dry mucous membranes Restless or irritable Slightly sunken eyes Skin pinch goes back slowly Decreased tears urine output appears dark yellow If treated with: Antibiotics / antiinfectives Rehydration Therapy Oral Rehydration solutions Intravenous solutions Proper Nutrition Vitamin Supplements If not treated: Hypovolemic shock Seizures Septicemia Meningitis Death

GOOD PROGNOSIS

POOR PROGNOSIS