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Laguna State Polytechnic University

Sta. Cruz Campus


Sta. Cruz, Laguna

In Partial Fulfillment
Of the Course Requirement
In NCM 104

An Interview with a Client with Cancer

Submitted By:
Mario Mandilag
Patricia Xyrille Cariño
Nysell delos Reyes
Dianne Criselle Nuñez
Rachelle Anne Villafranca
BSN IV A
Group IV

Submitted to:
Mrs. May Mesina-Veridiano RN, MAN
Clinical Instructor/Dean of the College of Nursing
Anatomy
Nasopharynx

The nasopharynx is defined anteriorly by the posterior choanae, posteriorly by the


clivus and the first 2 cervical vertebrae, superiorly by the floor of the sphenoid, and
inferiorly by the level of the free border of the soft palate. The nasopharynx is divided
into 3 subsites: the posterosuperior wall, the lateral walls, and the posterosuperior surface
of the soft palate. The torus tubarius is the opening of the eustachian tube into the lateral
nasopharyngeal wall. The fossa of Rosenmüller is the groove or recess posterior to the
torus at the junction between the lateral and posterior walls. Nasopharyngeal carcinoma
(NPC) most commonly occurs in this location.
The posterior and lateral nasopharyngeal walls are composed of 3 layers of tissue.
The mucosal epithelium of the nasopharynx is complex, consisting mainly of
pseudostratified columnar ciliated epithelium near the choanae and the adjacent part of
the roof of the nasopharynx, a transitional epithelium in the roof and the lateral walls, and
stratified squamous epithelium along the posterior and inferior portions of the
nasopharynx. The superior constrictor muscle and the buccopharyngeal fascia surround
the mucosa. Superiorly, the buccopharyngeal fascia unites with the pharyngobasilar
fascia, which is attached to the skull base.

The buccopharyngeal fascia extends posterolaterally from the free edge of the
medial pterygoid plate to the lateral border of the carotid artery. This fascia separates the
nasopharynx from the parapharyngeal (paranasopharyngeal) space. A line joining the free
edge of the medial pterygoid plate posterolaterally to the styloid process divides the
paranasopharyngeal space into the prestyloid space anteriorly and the retrostyloid space
(containing the carotid sheath and the cranial nerves) posteriorly.

The paranasopharyngeal space is bound anteriorly by the pterygomandibular


raphe, which joins the lateral pterygoid plate to the mandible. The retropharyngeal space
contains the retropharyngeal lymph nodes and the node of Rouviere. This space is located
posterior to the buccopharyngeal fascia and anterior to the prevertebral fascia; therefore,
lesions that extend beyond the buccopharyngeal fascia posteriorly involve the
retropharyngeal space, while lesions extending laterally beyond this fascia reach the
parapharyngeal space.

The nasopharynx is an anatomically difficult area to expose surgically. This area


is in close proximity to several foramina and associated vital neurovascular structures.
These include the foramen ovale, the foramen spinosum, the foramen lacerum, the carotid
canal, and the jugular foramen.

Neck
The supraclavicular fossa described as a triangular region defined by 3 points: the
sternal end of the clavicle, the lateral end of the clavicle, and the point where the neck
meets the shoulder. This area is clinically significant in that any nodal involvement within
this triangle is, by definition, an N3 lesion and, therefore, stage IV cancer.
Nasopharyngeal carcinoma

Nasopharyngeal carcinoma
Classification and external resources

Metastatic nasopharyngeal carcinoma in a lymph node

Nasopharyngeal carcinoma (NPC) is a cancer originating in the nasopharynx, the


uppermost region of the pharynx or "throat", where the nasal passages and auditory tubes
join the remainder of the upper respiratory tract. NPC differs significantly from other
cancers of the head and neck in its occurrence, causes, clinical behavior, and treatment. It
is vastly more common in certain regions of East Asia and Africa than elsewhere, with
viral, dietary and genetic factors implicated in its causation. . It accounts for fewer than
1% of cases of childhood malignancy. Whereas almost all adult nasopharyngeal cancers
are carcinomas, only 20-35% of nasopharyngeal malignancies are carcinomas in children.
In the pediatric population, most nasopharyngeal malignancies are rhabdomyosarcomas
or lymphomas.

Causes

Viral DNA in nasopharyngeal carcinoma has revealed that Epstein-Barr virus (EBV) can
infect epithelial cells and is associated with their transformation to cancer.

Risk factors:
Sex

A male preponderance is observed. The male-to-female ratio is approximately 2:1.


Age

Nasopharyngeal carcinoma has a bimodal age distribution. A small peak is observed in


late childhood, and a second peak occurs in people aged 50-60 years. Childhood
nasopharyngeal carcinoma is usually a disease of adolescence.3

Classification
Nasopharyngeal carcinoma, commonly known as nasopharyngeal cancer, is classified as:

• a malignant neoplasm
• cancer

Arise from the mucosal epithelium of the nasopharynx, most often within the lateral
nasopharyngeal recess or fossa of Rosenmüller.

There are three microscopic subtypes of NPC:

• well-differentiated keratinizing type


• moderately-differentiated nonkeratinizing type
• undifferentiated type, which typically contains large numbers of non-cancerous
lymphocytes (chronic inflammatory cells), thus giving rise to the name
lymphoepithelioma. The undifferentiated form is most common, and is most
strongly associated with Epstein-Barr virus infection of the cancerous cells.

Undifferentiated Undifferentiated Undifferentiated


nasopharyngeal carcinoma - nasopharyngeal carcinoma - nasopharyngeal carcinoma -
low power med. power high power
Physical findings

• The most common physical finding is a neck mass, which is observed in 80% of
patients. Painless firm lymph node enlargement is present.
• Neck involvement is often bilateral; the most common nodes involved are the
jugulodigastric and upper and middle jugular nodes in the anterior cervical chain.
• Cranial nerve palsy at initial presentation is observed in 25% of patients.
• On nasopharyngoscopy, a mass arising in the nasopharynx is often visible. The
most frequent site is the fossa of Rosenmüller.
• A paraneoplastic osteoarthropathy has been described in patients with widespread
or recurrent disease.

Laboratory Studies

• Perform routine blood work, including a CBC count and chemistry profile. Liver
function test results may be abnormal in those rare cases with hepatic metastases.
• Epstein-Barr virus (EBV) titers, including immunoglobulin A (IgA) and
immunoglobulin G (IgG) antibodies to the viral capsid antigen, should be
performed. These titers correlate with tumor burden and decrease with
treatment.5,6
• If invasion through the base of the skull has occurred, a cerebrospinal fluid
examination is performed to detect tumor seeding.

Imaging Studies

• CT scanning
o CT scanning of the head and neck is used to determine tumor extent, base
of skull erosion, and cervical lymphadenopathy.
o CT scanning of the chest and bone imaging are used to search for distant
metastases.
• When intracranial extension is suspected, MRI may reveal the extent of the tumor.
• Positron emission tomography (PET) imaging has been used to assess
questionable neck nodes.

Other Tests

• A baseline audiogram is helpful prior to radiotherapy, especially in children who


receive cisplatin.

Procedures

• A biopsy of the primary lesion or neck node is obtained for diagnosis.


Histologic Findings

• The World Health Organization (WHO) has classified nasopharyngeal carcinoma


into 3 categories.
o WHO-1 is defined as well–to–moderately differentiated squamous or
transitional cell carcinoma with keratin production.
o WHO-2 is nonkeratinizing carcinoma.
o WHO-3 is undifferentiated carcinoma, including lymphoepithelioma. This
entity consists of malignant epithelial cells with lymphocytic infiltration.
• The vast majority of children are found to have WHO-3 disease.7,8

Staging

• Various staging schema have been proposed for nasopharyngeal carcinoma in


children.9 No single system has proven satisfactory in correlating disease extent to
prognosis.
• The TNM system, widely used in adult head and neck cancers, places most
childhood disease in the advanced-stage category and does not recognize the
relatively good prognosis of many children in these stages. Modification of the
TNM system that further divides patients into various groups based on prognosis
has been proposed. The T stage alone has been shown to have limited predictive
value.

Treatment
Medical Care

Radiation therapy is the mainstay of treatment, with chemotherapy used in advanced


cases. Concurrent cisplatin, 5-fluorouracil, and radiotherapy have been shown to improve
survival.10,11,12 Many pediatric studies have used neoadjuvant chemotherapy followed by
radiation therapy with improvement in local control or progression-free survival rates
over radiotherapy alone.13,14,15

• Radiotherapy is administered to the primary tumor and level II-V neck nodes.
Care should be taken to include the skull base in the initial field because
nasopharyngeal cancer can travel via the foramen lacerum. Traditionally, the
initial radiotherapy fields are often treated with 2 parallel opposed lateral fields
that encompass the nasopharynx and upper cervical nodes. The lower cervical
nodes are treated with an anterior field, which abuts the upper lateral fields
superiorly. These patients are now commonly treated with 3-dimensional
treatment, conformal radiotherapy, or intensity modulated radiation therapy
(IMRT).
• Avoid overdose to the spinal cord at this junction by using a spinal cord block at
the upper lateral fields or lower anterior supraclavicular field. Treatments are
administered at 1.8-2 Gy/d for 5 days a week until a dose of 40-44 Gy has been
administered. Thereafter, additional radiation is administered to the posterior neck
nodes using electron beam to avoid radiation myelitis. A dose of 50 Gy to the
neck is desirable; bulky neck masses may need higher doses of 66-70 Gy.
• Nasopharyngeal tumors and anterior neck tumors continue to be treated with
parallel opposed fields to a dose of at least 50 Gy. The primary site then receives
a boost, delivering a dose of 50-70 Gy. Three-dimensional (conformal)
radiotherapy may be used to spare more critical structures next to the
nasopharynx, such as the brain, pituitary gland, optic chiasm, optic nerve, and
spinal cord. Data show that lower doses of radiotherapy may suffice when the
response to neoadjuvant chemotherapy is excellent.16 However, a multi-
institutional study showed that doses of at least 66 Gy are needed for optimal
local control.17
• Parotid sparing techniques are also available in some centers with 3-dimensional
treatment capability or IMRT.18 Data using IMRT reveal equivalent or better
locoregional control compared with conventional radiotherapy and sparing of the
parotid glands from high doses of radiation therapy.19
• During the course of radiotherapy, several immediate effects may occur, usually
after the first 2 weeks of treatment. Confluent mucositis usually occurs, especially
in children receiving both radiotherapy and 5-fluorouracil. Dry mouth and thick
saliva are also likely secondary to irradiation of the salivary glands. Redness,
itching, and peeling of the treated skin can occur towards the end of radiotherapy
and may need to be treated with topical antibiotics and Silvadene. Because of this
oropharyngeal mucositis, consideration of placement of a gastrostomy tube prior
to initiation of radiotherapy. If a gastrostomy tube is not placed, poor nutrition
and dehydration are quite common, and intravenous fluids may need to be
administered.
• Some centers use amifostine, a radioprotective agent, to help reduce radiation-
related xerostomia. Possible side effects of amifostine such as flulike symptoms,
nausea and hypotension have limit its widespread use in the oncologic
community.

Surgical Care

Surgical therapy for these patients is often limited to a biopsy for tissue diagnosis. Nearly
all tumors are unresectable at diagnosis because of tumor location.

Consultations

Consultation with an otolaryngologist is often required in the initial management to


obtain tissue diagnosis and in follow-up endoscopic examinations to rule out recurrence.
An otolaryngologist may also be involved if the child develops sensorineural hearing loss
from cisplatin and radiotherapy.

Consultation with an endocrinologist may be required in the future if the child shows
signs of growth retardation or hypothyroidism secondary to radiotherapy. Occasionally,
children develop panhypopituitarism.
Consultation with a dentist familiar with radiation effects should be performed prior to
initiation of radiotherapy to minimize risk of osteoradionecrosis. Patients also need to be
followed after treatment as xerostomia and change in salivary consistency may
predispose the patient to dental caries.

Diet

Many patients experience severe mucositis during radiotherapy. Certain foods may
irritate irradiated mucosa, causing pain or difficulty swallowing or chewing. Soft foods
such as milkshakes, mashed potatoes, and pureed meats are advisable during the course
of radiotherapy. Citrus fruits, spicy foods, salty foods, and coarse foods can make the
irritated mucosa worse. Gastrostomy tube placement allows adequate hydration and
calorie intake during radiotherapy.

Activity

Activity depends on the child's condition. During periods of chemotherapy-induced


thrombocytopenia, some limitation of strenuous activity and avoidance of contact sports
is necessary. Infectious contacts should be avoided where possible, especially during
periods of neutropenia.

Medication
Medical therapy consists of radiation therapy and chemotherapy. Concurrent treatment
with cisplatin, 5-fluorouracil, and radiotherapy has been shown to improve survival rates.
Other studies have used neoadjuvant chemotherapy followed by radiation therapy with
improvement in local control or progression-free survival rates.

Anesthetic lozenges and sprays may be helpful during the course of radiotherapy to
minimize oral or throat pain.

Antineoplastic agents

Chemotherapy is used to decrease the bulk of disease and to limit the risk of recurrence.
Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs
affect this growth. After cells divide, they enter a period of growth (ie, phase G1),
followed by DNA synthesis (ie, phase S). The next phase is a premitotic phase (ie, G2);
then, finally a mitotic cell division (ie, phase M) occurs.

Cell division rate varies for different tumors. Most common cancers increase very slowly
in size compared to normal tissues, and the rate may decrease further in large tumors.
This difference allows normal cells to recover more quickly than malignant ones from
chemotherapy and is the rationale behind current cyclic dosage schedules. Dosage cycles
are determined by cancer stage and tolerance of adverse effects.
Antineoplastic agents interfere with cell reproduction. Some agents are cell cycle
specific, whereas others (eg, alkylating agents, anthracyclines, cisplatin) are not. Cellular
apoptosis (ie, programmed cell death) is also a potential mechanism of many
antineoplastic agents.

Cisplatin (Platinol)

Inhibits DNA synthesis and, thus, cell proliferation by causing DNA crosslinks and
denaturation of double helix.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

Pediatric

80-100 mg/m2 per cycle IV on day 1 of cycle; alternatively 200 mg/m2 per cycle IV
divided over 5 d (ie, 40 mg/m2/d for 5 d)

• Dosing
• Interactions
• Contraindications
• Precautions

Increases toxicity of bleomycin and ethacrynic acid; cisplatin-related nephrotoxicity is


increased when concurrently used with other nephrotoxic drugs (eg, aminoglycosides,
amphotericin B, cyclosporine); bleomycin, cytarabine, methotrexate, and ifosfamide may
accumulate when used with cisplatin because of decreased renal excretion; may enhance
cytotoxicity of etoposide; coadministration of mesna and sodium thiosulfate directly
inactivate cisplatin; dipyridamole increases cytotoxicity by enhancing cellular uptake;
paclitaxel-related peripheral neuropathy may be increased in patients previously treated
with cisplatin

• Dosing
• Interactions
• Contraindications
• Precautions

Documented hypersensitivity; preexisting renal insufficiency; myelosuppression;


significant hearing impairment (especially speech-range hearing loss)

• Dosing
• Interactions
• Contraindications
• Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Administer adequate hydration before and 24 h after dosing to reduce risk of


nephrotoxicity; adverse effects include bone marrow suppression, nausea, vomiting,
mucositis, and high-frequency hearing loss; major dose-limiting toxicity is peripheral
neuropathy; can cause acute or chronic renal failure in as many as one third of patients
treated, but renal failure can usually be prevented by vigorous hydration and saline
diuresis; renal tubular wasting of potassium and magnesium are common (monitor
closely and supplement as needed); cellulitis and fibrosis rarely have occurred after
extravasation; avoid aluminum needles

5-Fluorouracil (5-FU, Adrucil)

Fluorinated pyrimidine antimetabolite that inhibits thymidylate synthase and also


interferes with RNA synthesis and function. Has some effect on DNA. Useful in
symptom palliation for patients with progressive disease.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

Pediatric

15 mg/kg/d IV continuous infusion (over 24 h) for 5 consecutive d, often in combination


with cisplatin

• Dosing
• Interactions
• Contraindications
• Precautions

Increased risk of bleeding with anticoagulants, NSAIDs, platelet inhibitors, and


thrombolytic agents; enhanced bone marrow toxicity with other immunosuppressive
agents

• Dosing
• Interactions
• Contraindications
• Precautions

Documented hypersensitivity; bone marrow suppression; serious infection

• Dosing
• Interactions
• Contraindications
• Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Nausea, oral and GI ulcers, depression of immune system, and hemopoiesis failure (bone
marrow suppression) may occur; adjust dosage in renal impairment

Antiemetic agents

Prevention and treatment of chemotherapy-induced nausea and vomiting. Prevention is


essential for highly emetogenic drugs (eg, cisplatin-based chemotherapy).

Antineoplastic-induced vomiting is stimulated through the chemoreceptor trigger zone


(CTZ), which then stimulates the vomiting center (VC) in the brain. Increased activity of
central neurotransmitters, dopamine in CTZ, or acetylcholine in VC appears to be a major
mediator for inducing vomiting. Following administration of antineoplastic agents,
serotonin (5-HT) is released from enterochromaffin cells in the GI tract. With serotonin
release and subsequent binding to 5-HT3-receptors, vagal neurons are stimulated and
transmit signals to the VC, resulting in nausea and vomiting.

Antineoplastic agents may cause nausea and vomiting so intolerable that patients may
refuse further treatment. Some antineoplastic agents are more emetogenic than others.
Prophylaxis with antiemetic agents prior to and following cancer treatment is often
essential to ensure administration of the entire chemotherapy regimen.

Ondansetron (Zofran)

Selective 5-HT3-receptor antagonist that blocks serotonin both peripherally and centrally.
Prevents nausea and vomiting associated with emetogenic cancer chemotherapy (eg,
high-dose cisplatin) and complete body radiotherapy.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

Pediatric

Oral:
4-12 years: 4 mg PO 30 min prior to chemotherapy, repeat q4h for 2 doses, then q8h for
1-2 d
>12 years: 8 mg PO 30 min prior to chemotherapy, repeat once in 8 h, then q12h for 1-2
d
Intravenous: O.45 mg/kg/d IV divided q8h or administered as a single daily dose

• Dosing
• Interactions
• Contraindications
• Precautions

Although potential for cytochrome P-450 inducers (eg, barbiturates, rifampin,


carbamazepine, phenytoin) to change half-life and clearance of ondansetron exists,
dosage adjustment is not usually required

• Dosing
• Interactions
• Contraindications
• Precautions

Documented hypersensitivity

• Dosing
• Interactions
• Contraindications
• Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus

Precautions

More effective when administered for prevention of nausea and vomiting than as rescue;
may cause headache

Colony-stimulating factors
These agents act as a hematopoietic growth factor that stimulates the development of
granulocytes. They are used to treat or prevent neutropenia in patients receiving
myelosuppressive cancer chemotherapy and to reduce the period of neutropenia
associated with bone marrow transplantation. They are also used to mobilize autologous
peripheral blood progenitor cells for bone marrow transplantation and in the management
of chronic neutropenia.

Filgrastim (G-CSF, Neupogen)

Granulocyte colony-stimulating factor that activates and stimulates production,


maturation, migration, and cytotoxicity of neutrophils. Is most often administered to
prevent neutropenia, starting 1 d after completion of highly myelosuppressive
chemotherapy. Can also be used to treat neutropenia in the setting of significant infection.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

Pediatric

5 mcg/kg/d SC until ANC has recovered (ie, >2,000-10,000/mcL)

Complications

• Late toxicity of radiotherapy may include xerostomia, hypothyroidism, fibrosis of


the neck with complete loss of range of motion, trismus, dental abnormalities, and
hypoplasia of irradiated muscular and bony structures. Because of the high doses
of radiotherapy used in this disease, these late toxicities can be significant,
especially in younger children.
• Growth retardation can occur secondary to radiotherapy to the pituitary gland.
Panhypopituitarism can occur in some instances.
• Sensorineural hearing loss may occur with the use of cisplatin and radiotherapy.21
• Renal toxicity can occur in patients receiving cisplatin. Those who receive
bleomycin are at risk for developing pulmonary fibrosis.
• Caries and poor dental hygiene are associated complications. Osteonecrosis of the
mandible is a rare complication of radiotherapy and is often avoided with proper
dental care.
• Second malignancy may occur in a child who has received previous radiotherapy.
This risk is small but continues throughout life.
• With proper radiotherapy techniques, the chance for development of radiation
myelitis should be less than 1%.
Patient Education

• Patients and parents should be educated regarding the importance of follow-up


after completion of all therapy. A detailed discussion of the risks of
chemotherapy, especially the risk of febrile neutropenia, is necessary. Families
should also be well informed of the issues of late effects.
• For excellent patient education resources, visit eMedicine's Cancer and Tumors
Center. Also, see eMedicine's patient education article Cancer of the Mouth and
Throat.

Q and A

1. What is your usual eating pattern before you were diagnosed of


Nasopharyngeal Carcinoma?

Madalas gulay at isda, minsan lang ako kumain ng karne mga isang beses lang sa isang
buwan.

2. What is your occupation before?

Noong 2006 hanggang 2009, nagtrabaho ako sa pabrika ng tela sa Calamba. Kapag
wala ang aking amo, tinatanggal ko ang mask ko kasi hindi ako makahinga. Yung mga
tela na yun ay galing sa abroad ay matapang ang amoy kaya tinitiis ko na lang kaysa
hindi ako makahinga ng maayos. Tapos mayroon kaming babuyan, ako ang naglilininis
at nagapapakain ng mga baboy.

3. Did you exposed in any form of radiation? How often?

Oo, mula nung una akong nagpatingin, dalawang beses sa isang taon ako ngpapa X-ray.

4. Did you have any relatives that were also diagnosed of having cancer?

Oo, yung panganay kong kapatid ay may leukemia.

5. When the tumor mass was seen?

2008 ko naramdaman yung maliit na bukol sa may kaliwa kong leeg. Hindi ko pinansin
kasi hindi naman sya masakit.

6. What manifestations did you experience hat made you decide to consult to
the specialist?

Madalas sumasakit ang ulo ko akala ko migraine lang. Tatlong beses sa isang araw
dumudugo ang ilong ko, hindi ko masukat kung gaano karami sinisinga ko din dahil may
buo buong dugo.
7. Did you consult for second opinion?

Hindi na kasi sa PGH walong doctor na yung tumingin sa akin.

8. What are the procedures that were done when you were diagnose that
disease?

X-ray, ok naman daw wala naman daw problema. Kasi minsan yung dugo sa bibig ko na
lumalabas.

Biopsy, kumuha sila ng tissue sa tumor sa leeg ko. Noong una ayaw pang sabihin ng
doctor sa akin ang resulta dahil mag-isa lang ako baka hindi ko daw kayanin. Pero
pinilit ko sila na sabihin na sa akin.

CT Scan, nahilo nga ako eh, kasi 12 hours ako hindi kumain bago yung procedure.

Nasal endoscopy, ditto nakita na sa ilong sya nagsimula nagddraine daw sa may leeg.
Kaya daw lumalaki yung sa leeg ko.

9. What medications your doctor prescribed for the disease? Did you comply
with this medication?

Co-amoxiclav at celecoxib, yan lang yung iniinom ko para sa kirot.

10. Did you take any medications aside for the prescribed medication given by
your doctor?

Herbal, yung malunggay at luyang dilaw. Lactulose, kapag dalawang araw na hindi pa
ako nakakadumi.

11. What did you so to cope with the disease?

Inisip ko na lang na maging positive, dahil kapag daw puro negative ay lalong lalala
yung sakit ko,

12. What is the effect of this disease to your family?

Mas natakot sila sa kondisyon ko, pero ako tanggap ko na kasi kung hanggang saan na
lang ako. Pero ramdam ko na magtatagal pa ako kasi malakas pa ako. Yung mga anak
ko lagi silang nagdadasal na pagalingin na ako.

13. What is the effect of this disease to your relationship with God?

Mas tumibay ang pananalig ko sa kanya, sya na lang kasi ang pinanghahawakan ko.

14. What is the difference now with your lifestyle?


Wala naman, pero tumigil na ako sa pag-aalaga ng baboy. Pinagbawalan din akong
kumain ng alamang, manok at iba pang malalansang pagkain.

15. Did the doctor told you how long you will live from the time you were
diagnosed of this disease?

Hindi ako binigyan ng taning, pero kung sakaling bibigyan ako hindi rin ako maniniwala
kasi Diyos lang naman ang magsasabi kung hanggang saan ako.