UNIT 11

DIABETES MELLITUS
DKA/HHS
Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body
produces high levels of blood acids called ketones. The condition develops when your body can't
produce enough insulin.
DIA/SIADH
HYPERTHYROIDISM
-Hyperthyroidism, a common endocrine disorder, it is a form of thyrotoxicosis resulting from an
excessive synthesis and secretion of endogenous or exogenous of thyroid hormones by the
thyroid gland.
-if you have an increase thyroid hormones you will have everything in acceleration, like super
fast heart rate, super high BP and etc.
Pathophysiology
-Hypothalamus and pituitary gland are also involved because hypothalamus would release a
thyroid regulating hormone and
-your anterior pituitary gland would receive so that it would release also the thyroid stimulating
hormone and
-this TSH it would stimulate your thyroid gland to release the T3, T4 and your calcitonin.
 Calcitonin main function is to transport calcium from the blood into the bone
 T3 and T4 main function is the metabolism regulation, they would regulate now your
metabolism, the conversions of your calories or the food intake into energy, regulation of
the heart rate, regulate the energy levels inside the body, regulate the temperature inside
the body and also for the growth development such as with your nails, hair, and skin.
CAUSES
-So, if we have an issue with the thyroid gland itself, so that would be primary hyperthyroidism.
-The most common cause is Graves’ disease which is an autoimmune issue, but we can also have
some kind of thyroid nodule.
-Due to the one of these causes, we have hypersecretion of T3 and T4, so that's primary
hyperthyroidism.
-With secondary hyperthyroidism, this is where we have some kind of pituitary disorder such as
a tumor, which is causing excess secretion of TSH. So, with all this extra TSH, the thyroid gland
is getting the message to produce more and more thyroid gland hormones even though it doesn't
really need to, but that's the order it's getting from the pituitary gland.
-And then with tertiary hyperthyroidism, that means we have an issue in the hypothalamus. So
due to some kind of hypothalamus dysfunction, the hypothalamus is producing too much TRH,
which is causing the production of too much TSH, which is causing the thyroid gland to go into
overdrive, producing all that T3 and T4 even though it really isn't supposed to.
Signs and symptoms
 Warm – it means that you have increasing metabolism, increase heat metabolism means
you will develop heat intolerance it means that your body would become very sensitive to
heat and if the surrounding is hot your body is also hot.
 Wet – you will become sweaty it’s not just a regular sweating but rather a diaphoresis
 Wild – you will develop increase palpitations (tachycardia) and also they will develop
diarrhea it’s because of fast metabolism.
 Moist skin
 Shiny hair
Complication
 Heart Problem
 Thyrotoxicosis
 Thyroid storm
Management
 Monitor vital signs, especially heart rate and blood pressure (both are increased in
hyperthyroidism)
 Provide a cool environment
Surgical Management:
 Thyroidectomy
Pharmacologic:
-Administering radio isotope
-antithyroid medications

HYPOTHYROIDISM
-Hypothyroidism also known as underactive thyroid disease, it is a condition in which the
thyroid gland is not able to produce enough thyroid hormones or low production of thyroid
hormones
-in contrast to your hyperthyroidism in hypothyroidism you will have everything in deceleration
Pathophysiology
There are three types of hypothyroidism
 Primary hypothyroidism - In primary hypothyroidism, there is a problem with the
thyroid gland itself. If the thyroid gland is damaged, it cannot produce the T3 and T4
that it should. The leading cause of primary hypothyroidism is Hashimoto’s disease.
Hashimoto’s disease, also called chronic lymphocytic thyroiditis, is an autoimmune
disorder that causes antibodies to attack and destroy the thyroid tissue.
 Secondary hypothyroidism - Secondary causes of hypothyroidism occur when
there is an issue with the pituitary gland, like a pituitary tumor. In this case, the
pituitary gland is not functioning properly and therefore not producing enough TSH.
Remember TSH is thyroid-stimulating hormone, so without the right stimulation, the
thyroid gland is not prompted to make the correct amount of T3/T4.
 Tertiary hypothyroidism - Tertiary hypothyroidism occurs when there is a
dysfunction of the hypothalamus. It creates a domino effect along the hormone
pathway. If there is a problem with the hypothalamus, then it’s not producing enough
TRH, so the pituitary gland is not being prompted to make enough TSH, so the
thyroid gland doesn’t get the message to produce adequate T3/T4.
The hypothyroidism also causes:
 Iodine deficiency: not consuming enough foods with iodine. Thyroid cannot make
thyroid hormones without iodine which comes from foods. If you don’t have enough
iodine in your diet. Low T3 and T4 this leads to hypothyroidism.

Signs and symptoms

 Slow heart rate
 Weight gain
 Anorexia
 Apathetic face
 Dry skin
  Brittle hair
 Amenorrhea
COMPLICATIONS
 Myxedema coma – present in adult, complication of excessive hypothyroidism
 Cretinism – be present in children, due to the problem such as anorexia or congenital
hypothyroidism
Diagnostic Procedure
 Check T3 and T4
 Biopsy
 Radioactive iodine 1, 2, 3
Management
 Provide iodine
 Drug of choice is Synthroid or Levothyroxine, Liothyronine and Cytomel

GRAVES DISEASE
-it is the most common cause of hyperthyroidism
-In grave’s disease there are auto-antibodies that are being produced (the antibodies against
ourselves)
-These auto antibodies mimic the TSH function
-it will now stimulate the thyroid glands to produce Thyroid hormones (T3 and T4)
-resulting into increased thyroid hormones
-the increased of TH will cause negative feedback to hypothalamus and tell it to stop making
TRH and TSH because there are already enough T3 and T4 or TH.
-now, regardless the decrease in TSH, the TSH receptor autoantibodies will still exist and so it
will keep telling the thyroid gland to produce more hormones
-causing a lot of hormones in the circulation
-overactivity of thyroid hormones causing hyperthyroidism.
-Graves’ disease also related into your exophthalmos it’s because your graves’ disease is an
autoimmune antibody means they have the capacity to create inflammation or irritation on the
muscle or tissue inside the body. Specifically, on the tissue of the eyes if they’re would be
possible irritation on the tissue the tendency it would later lead on to bulging of the eyes
Signs and symptoms
 Enlargement of thyroid gland (goiter)
 Bulging eyes (Graves’ ophthalmology)
 Conjunctivitis
 Corneal irritation
Diagnostic Procedure
 Check the T3 and T4
 Circulating hormone
 Biopsy
  Radioactive iodine 1, 2, 3
Management
 Common medications are PTU and Metamazole its main function is to block the
conversion of the T4 into T3 to become stable
 Advise eye drops, eye patch, and sun glasses

MYXEDEMA COMA
-it is a severe hypothyroidism resulting in decompensated metabolic state and mental status
change
-it is a life-threatening condition that occurs in patient with hypothyroidism (present with
severely low thyroid hormones)
- Patients with hypothyroidism often suffer from physiological alterations as a result of the body
trying to compensate for the lack of thyroid hormone.
-Most patients with myxedema coma have a history of hypothyroidism, thyroid surgery, or
radioactive iodine treatment for thyroid disease.
-Very rarely, the problem is not caused by the inability of the thyroid gland to make thyroid
hormone; but rather it is caused by the failure of the pituitary gland or the hypothalamus to
correctly signal the thyroid gland to perform its normal functions.
-In this situation, the thyroid gland is normal, but it is not receiving the signals from the pituitary
gland or hypothalamus to make the thyroid hormone where it is capable of producing.
-also, your thyroid cannot produce thyroid hormones without iodine so we get iodine through our
food. So if we’re not taking enough iodine we can enter into hypothyroidism which could
eventually lead to myxedema
Signs and symptoms
 Hypothermia
 Hypotension
 Hyponatremia
 Same as the signs and symptoms of Hypothyroidism but this time symptoms are severe to
the point where it could lead to death.
Management
 Increase fluid intake
 Airway management
 Thyroid home replacement
Nursing Care
 monitor heart rate, BP, temperature and respiratory status
 administer IV solution as prescribed
LIVER DISORDER
FUNCTIONS
Glucose Metabolism
-The liver plays a major role in the metabolism of glucose and the regulation of blood glucose
concentration.
-After a meal, glucose is taken up from the portal venous blood by the liver and converted into
glycogen, which is stored in the hepatocytes.
-The glycogen is converted back to glucose (glycogenolysis) and released into the bloodstream
to maintain normal levels of blood glucose.
-However, this process provides a limited amount of glucose.
-Additional glucose can be synthesized by the liver through a process called gluconeogenesis.
For this process, the liver uses amino acids from protein breakdown or lactate produced by
exercising muscles. This process occurs in response to hypoglycemia

Ammonia Conversion
-The use of amino acids from protein for gluconeogenesis results in the formation of ammonia as
a by-product.
-The liver converts this metabolically generated ammonia into urea.
-Ammonia produced by bacteria in the intestines is also removed from portal blood for urea
synthesis.
-In this way, the liver converts ammonia, a potential toxin, into urea, a compound that is excreted
in the urine.
(Ammonia is a by-product from digestive system or from protein breakdown.)
Protein Metabolism
-It synthesizes almost all of the plasma proteins (except gamma-globulin), including albumin,
alpha-globulins and beta-globulins, blood clotting factors, specific transport proteins, and most
of the plasma lipoproteins.
-Amino acids are used by the liver for protein synthesis
Fat Metabolism
-Fatty acids can be broken down for the production of energy and ketone bodies.
-Ketone bodies are small compounds that can enter the bloodstream and provide a source of
energy for muscles and other tissues.
-Breakdown of fatty acids into ketone bodies occurs primarily when the availability of glucose
for metabolism is limited, as in starvation or in uncontrolled diabetes.
-Fatty acids and their metabolic products are also used for the synthesis of cholesterol, lecithin,
lipoproteins, and other complex lipids.
Vitamin and Iron Storage
-Vitamins A, B, and D and several of the B-complex vitamins are stored in large amounts in the
liver.
-Certain substances, such as iron and copper, are also stored in the liver.
Bile Formation
-Bile is continuously formed by the hepatocytes and collected in the canaliculi and bile ducts.
-It is composed mainly of water and electrolytes such as sodium, potassium, calcium, chloride,
and bicarbonate, and it also contains significant amounts of lecithin, fatty acids, cholesterol,
bilirubin, and bile salts.
Bilirubin Excretion
-Excreted through kidneys.
-Bilirubin comes from RBC, RBC could be breakdown to Heme and Globin.
-The Heme when breakdown will be now unconjugated bilirubin (also known as in directed type
of bilirubin) it cannot be excreted by the kidney (there’s a discoloration of skin if stayed in the
bloodstream)
-the liver will convert the unconjugated bilirubin into conjugated bilirubin or direct type.
-Once converted it will be now easily being excreted by the kidney due to help of the water
solution. (water soluble) mixed with urine and fecal (mao color yellow).
-If liver is damaged, the conjugated type bilirubin could no longer be excreted by the kidneys
because it is not affected by the aqueous solution. (and could stay in the bloodstream, maonaay
jaundice discoloration of skin and sclera, clay colored stool and the tea colored urine)
Drug Metabolism
-The liver help in breaking down, in order to absorb drug and excrete the things that we don’t
need.
-The liver metabolizes many medications, such as barbiturates, opioids, sedatives, anesthetics,
and amphetamines.
-Metabolism generally results in drug inactivation, although activation may also occur.
-One of the important pathways for medication metabolism involves conjugation (binding) of the
medication with a variety of compounds, such as glucuronic acid or acetic acid, to form more
soluble substances.
-These substances may be excreted in the feces or urine, similar to bilirubin excretion.
Bioavailability is the fraction of the given medication that actually reaches the systemic
circulation.
-The bioavailability of an oral medication (absorbed from the GI tract) can be decreased if the
medication is metabolized to a great extent by the liver before it reaches the systemic circulation;
this is known as first-pass effect.
-Some medications have such a large first-pass effect that their use is essentially limited to the
parenteral route, or oral doses must be substantially larger than parenteral doses to achieve the
same effect.)

PORTAL HYPERTENSION
ESOPHAGEAL VARICES
HEPATIC ENCEPALOPHATY
ASCITES
 UNIT 13
SYPHILIS
TRICHOMONIASIS
BACTERIAL VAGINOSIS
HERPES SIMPLEX 1 AND 2
GENITAL WARTS

-Genital warts are contagious soft growths that appear in the genital or it could also be in anal
area.

-Genital warts are one of the most common types of sexually transmitted infection, they are
generally being flesh colored and project out from the surface of the skin.
-If several genital warts cluster together, they may resemble a cauli flower. In many cases, the
warts are too small to be visible.

-Genital warts affect both men and women but women are more vulnerable to complications, for
woman they can appear on or near the vulva cervix inside of the vagina or anus or outside of the
vagina or anus while for a man they can appear near or on the penis scrotum groin, thigh, and
anus.

-Genital warts are more dangerous for women because they can cause problems during
pregnancy. Warts on the vaginal walls may reduce the ability of the vaginal tissue to stretch
during childbirth

-Genital warts are caused by the human papilloma virus or HPV, there are thirty to forty different
strains of HPV that affect the genitals but just few of these strains cause genital warts the most
common strain that causes HPV is highly transmissible.

Transmission
-Genital warts are spread through a sexual contact
-it is spread through skin-to-skin contact usually during anal, oral or genital sex with an infected
partner.
-Genital warts may appear on the lips, tongue, mouth or throat of a person who has had oral
sexual contact with an infected partner.

Risk factors
Having unprotected sex with multiple partners, oral sex, a previous case of another STI, and
starting sexual relation at a young age.

Signs and Symptoms

 Several warts that cluster together (cauliflower)
 Small, flesh colored swelling in the genitals
 Pain and itching in the genital area
 Bleeding during intercourse
 Redness in the genital areas

Complication
If uncontrolled, complications may include:
 Cancer
 Laryngeal papillomatosis can occur
 Hormonal changes during pregnancy may also cause genital warts to grow, bleed, or
multiply

Diagnosis
 Pap test
 HPV test

Management
Genital wart treatments that can be applied directly to your skin include: ointment, resin or
solution.

 Imiquimod (Aldara, Zyclara)

 Podophyllin and podofilox (Condylox)
 Trichloroacetic acid
 Sinecatechins (Veregen)
 Surgeries for larger warts (laser treatments)

GRANULOMA INGUINALE
Granuloma inguinale is a sexually transmitted infection (STI) caused by the bacteria previously
classified as Calymmatobacterium granulomatosis and now reclassified as Klebsiella
granulomatis. It is also called donovanosis after ‘Donovan bodies’, which
are cellular components that are seen when scrapings from the genital skin lesions are viewed
under a microscope.
Clinically, the disease is commonly characterized as painless, it is slowly progressive ulcerative
lesions on the genitals or perineum without regional lymphadenopathy and subcutaneous
granulomas (pseudobuboes) also might occur. The lesions are highly vascular (that is beefy red
appearance) and bleed. The extra genital infection can occur with extension of infection to the
pelvis, or it can disseminate to intra-abdominal organs, bones, or the mouth. The lesions also can
develop secondary bacterial infection and can coexist with other sexually transmitted pathogens.

Granuloma Inguinale is generally considered to be transmitted via sexual contact but not always
and it could be transmitted by close personal contact or fecal contamination. Infections that cause
ulcers and sores around the genitals may increase the risk of HIV transmission. Other causes of
ulcers or sores need to be considered, before a diagnosis is made.

The skin lesion progresses through three stages:

 Stage One - In the first stage, the small pimple will begin to spread in the surrounding
tissue. As the tissue begins to wear away, it turns pink or a faint red. The bumps then turn
into raised red nodules with a velvety texture. This happens around the anus and genitals.
Although the bumps are painless, they can bleed if they are injured.
 Stage Two - In the second stage of the disease, bacteria begin to erode the skin. Once this
occurs, you will develop shallow ulcers that will spread from the genitals and anus to the
thighs and lower abdomen, or inguinal area. You will notice that the perimeters of the
ulcers are lined with granulated tissue. A foul smell may accompany the ulcers.
 Stage Three - When granuloma inguinale advances to the third stage, the ulcers become
deep and morph into scar tissue.
Signs and Symptoms
 Sores in the anal area in about half of the cases.
 Small, beefy-red bumps appear on the genitals or around the anus.
 The skin gradually wears away, and the bumps turn into raised, beefy-red, velvety
nodules called granulation tissue. They are often painless, but they bleed easily if injured.
 The disease slowly spreads and destroys genital tissue.
 Tissue damage may spread to the groin.
 The genitals and the skin around them lose skin color.
Complications
 Genital damage and scarring
 Loss of skin color in genital area
 Permanent genital swelling due to scarring
Diagnostic Procedure
 Microscopic examination
 Biopsy
Management
 Azithromycin, 1g orally per week for at least 3 weeks, or until healing is complete
 Azithromycin, 1g initially, then 500mg daily until healing is complete
 Docycycline, 100 mg twice daily for at least 3 weeks, or until lesions have healed
  Ciprofloxacin 750mg daily for at least 3 weeks, or until healing is complete
 Trimethoprim-sulfamethoxazole (160mg/800mg), twice daily for at least 3 weeks, or until
healing is complete
 Erythromycin base, 500mg four times a day for at least 3 weeks, and until all lesions have
healed

CANDIDIASIS
-It is a fungal infection caused by yeast called candida albicans.
-It usually occurs due to excessive taking of drugs that can alter the good bacteria/flora in our
body.
-typically, C, albicans live as harmless commensals in the gastrointestinal and genitourinary tract
and are found in over 70% of the population. Overgrowth of these organisms, however, will lead
to the disease.
-It can only cause infections if it grows out of control or if it enters deep into the body, like in the
bloodstream or internal organs such as kidneys, heart or brain).

Pathophysiology
- candidiasis is caused by the abnormal growth in C. albicans, which is usually due to an
imbalance in the environment.
- usually, this imbalance occurs in a woman’s vagina this infection less likely to occur for men.
- several events can spark an imbalance. For example, antibiotic use can decrease the amount of
lactobacillus bacteria, which decreases the amount of acidic products and the Ph of the vagina.
- other events are pregnancy, uncontrolled diabetes impaired immune system, and irritation of
the vagina.
- C. albicans are able to take advantage of the conditions and outcompete the normal microflora,
resulting in candidiasis or a yeast infection

Sx:
- Vaginal itching/soreness
- Abnormal vaginal discharge
- Mouth sores
- Onychomycosis
Rf:
- Pregnant
- Use of hormonal contraceptives
- Diabetic patient
Complications:
- Skin infections
Test:
- Culture and sensitivity
Treatment:
- Single dose of fluconazole (oral)
- Nystatin (take it 4wks straight)

ONCOLOGY

DISSEMINATED INTRAVASCULAR COAGULATION

-a rare but serious condition that causes abnormal blood clotting throughout the body’s blood
vessels.
-DIC happens when there is an activation of coagulation both in bleeding and thrombosis.
-There is a presence both of the thrombin and the plasmin the one that would make a clot
(thrombin) and the one that would destroy the clot (plasmin).
-The common factors that lead to DIC are infections, sepsis, and trauma.
Pathophysiology
-normally, when there’s damage in the endothelium there is an immediate vasoconstriction that
limits blood flow, platelets then form a plug (what we call the primary hemostasis).
- When there’s a pathway response there will be activation of thrombin. The activation of
thrombin would lead to activation of your fibrinogen and it would deposit now throughout the
micro-circulation. The triggering factor of fibrin to be increase is due to the activation of
thrombin
-so, final step is activation of fibrinogen to fibrin which deposits into platelets (secondary
hemostasis) resulting into HARD CLOT.
-As soon as that happen our body now would initiate fibrinolysis (breakdown of clots)
-normally, formation of new clots and fibrinolysis are balance
-but in serious medical condition like sepsis, malignancy trauma, intravascular hemolysis
-they causes release of procoagulants or the excessive Thrombin (the one that forms the clots)
-formations of new clots now happens result into widespread clot formation.
- If it’s clumping it means, there is too much clotting or fibrin clots and also known the micro-
thrombi.
- In short, if there’s micro thrombi already that thrombus itself, it means that there is occlusion
happen.
-The common problem of occlusion is micro-infarction that would cause to CVA, coronary heart
attack, MI, angina pectoris it’s because it would block now the coronary artery, the carotid artery
with those called micro thrombi itself
-smaller number of platelets and clotting factors
-because of fibrinolysis, it will now lead to fibrin degradation products in circulation which
interfere with clot formation making hemostasis even more difficult.
-our body will produce plasmin (destroy the clots) to prevent further occlusion of the system.
- There is now thrombocytopenia the breakdown of your platelet, the depletion of the different
clotting factors. When there is depletion of the different clotting factors it loses the ability to clot
that’s why there is bleeding.

S/Sx
 Bleeding from different parts of the body such as the mouth and nose
 Blood clots
 Decreased Blood pressure
 Getting bruised easily
 Vaginal or rectal Bleeding

 Petechiae (pinpoint, round spots that appear on the skin as a result of bleeding)

Complication
  Lack of oxygen in limbs and organs-caused by blood clots
 Stroke
 Death due to excessive bleeding
Diagnostic Procedure
 Fibrin degradation product test:
 Complete blood count (CBC):
 Clotting factor tests:
 Partial thromboplastin time:
 Serum fibrinogen:
 D-dimer test:
 Prothrombin time[PT] test:

Management
 Anticoagulants:
 Plasma transfusion:
 Focus on the underlying cause

MULTIPLE MYELOMA
-Malignant disease of plasma cells (the type of cells that produce antibodies) in the bone marrow.
-it the second most common haematological cancer
-generally it affects more common in older people
4 MECHANISMS
-monoclonal (forming a clone) production of Immunoglobulin (an antibodies) leads to renal
failure
It is caused by deposits of the protein immunoglobulin A (IgA) inside the filters (glomeruli) in
the kidney. These glomeruli normally filter waste and excess water from the blood and send
them to the bladder as urine.
-increase bone turnover leads to lytic bone lesions and increase the risk of fractures
-Crowding in the bone marrow leads to anemia (low level of RBC) or thrombocytopenia (low
level of platelets)
-decrease production of Immunoglobulin leads to increase risk of infection.

Pathophysiology
-The myeloma cells produce monoclonal (forming a clone) production of Immunoglobulin
antibodies that our body cannot use
-it usually begins with one plasma cell in the bone marrow
-it will now multiply rapidly, which they will now accumulate, overwhelming the production of
healthy cells
-literally, crowding out the healthy blood cells, causing fatigue and inability to fight infections.
-myeloma cells continue to produce antibodies that cannot be used by our body
-causing problems.
S/Sx
 Decreased Immunity/ Increased Infections
  Anemia/Pancytopenia
 Bone Pain/Lytic Lesions
 Impaired Kidney Function
 Hypercalcemia

Complication
 Bone damage
 Frequent infections
 Renal insufficiency
 Hematologic complications like anemia, bone marrow failure and, bleeding disorders

Diagnostic Procedure:
 Blood test:
 X-ray:
 CT scan:
 Magnetic resonance imaging (MRI):
 Positron emission tomography (PET)
 Bone marrow biopsy
Management
 Chemotherapy: To kill rapidly multiplying cells; is non-specific and can also kill healthy
fast-growing cells.
 Targeted therapy: Destroys cancer cells only.
 Corticosteroids: To control inflammation in the body.
 Bone marrow transplantation: To replace the bone marrow with a healthy one.

BRAIN TUMOR
Brain tumor is an abnormal growth of cells that occurs in the brain. Many different types of brain
tumors exist. Some brain tumors are noncancerous (benign), and some brain tumors are
cancerous (malignant). Brain tumors can begin in your brain (primary brain tumors), or cancer
can begin in other parts of your body and spread to your brain as secondary (metastatic) brain
tumors. 
Pathophysiology
-Brain tumors occur when cells in the brain begin to grow out of control and start to displace or
invade nearby tissues. Some brain tumors can spread throughout the body.
-Tumors that can spread to other parts of the brain or body are called malignant. When tumors
start in the brain, they are called primary brain tumors. Secondary brain tumors, or brain
metastases, are cancers that start elsewhere in the body and metastasize (spread) to the brain.
- Metastatic tumors reach the brain via hematogenous dissemination through the arterial system.
Lung cancer—especially small cell lung cancer—is by far the most common solid tumor
disseminating to the brain, followed by breast cancer, melanoma, and colon cancer. Less
common sources of metastasis are testicular cancer and renal cell cancer. Prostate, uterine, and
ovarian cancers are unlikely sources of brain metastasis.

-Brain metastases are more common than primary brain tumors.

-Brain tumors are classified by both the cell of the brain that makes them up, and how the tumor
looks under a microscope.
-Primary brain tumors can arise from any of the cells in the brain. They can come from the
neurons, the glial cells, the lining of the brain, or from specific structures in the brain.
-Tumors that arise from these cells are known as glial tumors.
-The membrane that surrounds the brain can also develop tumors these are known as
meningiomas.
-About 80% of malignant primary brain tumors arise from the glial cells of the brain and are
called gliomas.
-A majority of these tumors are the most aggressive type, called glioblastoma multiforme (or
GBM).
-Astrocytic tumors are another type of glioma, which arise from star-shaped cells called
astrocytes. 
-Brain tumors are not really thought of as a single disease, but rather as a collection of several
diseases that are characterized by cell type, clinical behavior, and type of therapy.
-One of the special characteristics of brain tumors is that sometimes benign tumors can be as
challenging to treat as a malignant tumor, depending on their size and location within the brain.
This is because the brain is locked into place by the skull and can't move out of the way if a
tumor is growing near it (The Monro-Kellie doctrine or hypothesis states that the sum of
volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood is constant.
-An increase in one should cause a reciprocal decrease in either one or both of the remaining
two). Even a benign tumor can cause pressure on the brain. This pressure can cause symptoms
and be life-threatening.
Types of Primary Brain Tumors
 Intracerebral Tumors
 Tumors Arising from Supporting Structures
 Developmental Tumors
 Metastatic Lesion
Signs and Symptoms
 Increased ICP (monro-killie hypothesis)
 Headache/ Seizures
 Vomiting/Fatigue / Nausea
 Changes in speech, hearing, or vision
 Problems of balancing or walking
 Changes in mood, personality, or ability to concentrate
Complications
 Seizures
 Mental function
 Brain herniation can cause anything from speech issues
Diagnostic Procedure
 Computed tomography (CT) scans
 A magnetic resonance imaging (MRI) scan
 Computer-assisted stereotactic (three-dimensional) biopsy
 Positron emission tomography (PET)
Management
 Craniotomy
 Radiation Therapy/Chemotherapy
 Corticosteroids such as dexamethasone (Decadron)
 Anticonvulsant medications
 Manage pain with upright positioning and pain medications
 Performs neurologic checks; monitors vital signs and maintain a neurologic observation
record.

HEAD AND NECK CANCER

Head and neck cancer develops from tissues in the lip and oral cavity (mouth), larynx (throat),
salivary glands, nose, sinuses or the skin of the face. Its names depend on the location of the
particular cancer for example the laryngeal cancer, pharyngeal cancer. The most common types
of head and neck cancers occur in the lip, mouth, and larynx.

Pathophysiology

-Cancers that are known collectively as head and neck cancers usually begin in the squamous
cells, that line the mucosal surfaces of the head and neck (for example, those inside the mouth,
throat, and larynx).

-These cancers are referred to as squamous cell carcinomas of the head and neck.

-Head and neck cancers can also begin in the salivary glands, sinuses, or muscles or nerves in the
head and neck, but these types of cancer are much less common than squamous cell carcinomas.

-If a squamous cell carcinoma of the head and neck is going to spread, it almost always does so
locally and/or to the lymph nodes in the neck that is why Sometimes, cancerous squamous cells
can be found in the lymph nodes of the upper neck when there is no evidence of cancer in other
parts of the head and neck, possibly because the original primary tumor is too small. When this
happens, the cancer is called metastatic squamous cell carcinoma with unknown (occult)
primary.

-If a head and neck cancer starts in the salivary glands, the tumor will usually be classified as an
adenocarcinoma, adenoid cystic carcinoma, or mucoepidermoid carcinoma.

Types of head and neck cancer

 Laryngeal and hypopharyngeal cancer

 Nasal cavity and paranasal sinus cancer

 Nasopharyngeal cancer

 Oral and oropharyngeal cancer

 Salivary gland cancer

Signs and Symptoms

 Swelling or a sore that does not heal; this is the most common symptom

 Red or white patch in the mouth

  Lump, bump, or mass in the head or neck area, with or without pain

 Persistent sore throat

 Foul mouth odor not explained by hygiene

 Hoarseness or change in voice

 Nasal obstruction or persistent nasal congestion

 Frequent nose bleeds and/or unusual nasal discharge

Complication

 Airway obstruction
 Loss of voice and ability to speak
 Disfigurement of the neck or face
 Hardening of the skin on neck

Diagnostic Findings

 Physical examination/blood and urine tests

 Endoscopy/ Biopsy
 Biomarker testing of the tumor
 X-ray/barium swallow
 Panoramic radiograph
 Ultrasound
 CT scan/MRI/PET scan/Bone scan
Management
 Laser technology
 Excision
 Lymph node dissection or neck dissection
 Chemotherapy/Targeted therapy/Immunotherapy
 Wound management
 Drain assessment and care
 Oral care
 Wound complication
RETINOBLASTOMA
NEPHROBLASTOMA
-A malignant renal tumor
-Wilms’ tumor, or Nephroblastoma, is a type of kidney tumor composed of metanephric
blastemal cells, (cells involved in kidney development) and is the most common malignant
kidney tumor in children; only rarely is it seen in adults.
-this is the only cancer that is encapsulated in the renal system which make it different from
other cancer
-Most Wilms tumors are unilateral, which means they affect only one kidney. Most often there is
only one tumor, but a small number of children with Wilms tumors have more than one tumor in
the same kidney. About 5% to 10% of children with Wilms tumors have bilateral disease (tumors
in both kidneys).
Types of Nephroblastoma
Wilms tumors are grouped into 2 major types based on how they look under a microscope (their
histology):
 Favorable histology: The cancer cells in these tumors don’t look quite normal, but there
is no anaplasia (the cells in these tumors are just the same with normal cells)
 Unfavorable or Anaplastic histology: In these tumors, the look of the cancer cells varies
widely, and the cells’ nuclei (the central parts that contain the DNA) tend to be very large
and distorted. This is called anaplasia. (the cancer cells in these tumors divide rapidly and
have little or no resemblance to normal cells.)

Pathophysiology

-Wilms’ tumor is thought to be caused by mutations in genes responsible for normal

genitourinary (refers to the urinary and genital organs) development, which includes the kidneys
as well as the gonads, typically the genes are located around chromosome 11.

-One gene critical for normal kidney and gonad development is WT1 (or Wilms’ Tumor 1),
which a tumor suppressor gene.

-Mutations (change in DNA sequence) that result in a “loss of function” of WT1, like deletions,
for example, the development of tumor cells seen with Wilms’ tumor.

-Wilms’ tumors which is result of WT1 mutations are sometimes part of a developmental
syndrome, meaning other abnormalities are present as well, because of deletion or there is a
mutation of other genes in addition to WT1.

-For example, in WAGR syndrome, a mutation in the chromosomes 11 region causes deletion of
both WT1 and the PAX6 genes (role in the formation of tissues and organs during embryonic
development), which leads to Wilms’ tumor and Genitourinary malformations as a result of WT1
deletion, as well as Aniridia (which is absence of iris) and intellectual disability (which is
formerly referred to as mental Retardation), as a result of PAX6 deletion.

-Another syndrome associated with WT1 mutations is Denys-Drash syndrome, which is

characterized by Wilms tumor, its early-onset are nephrotic syndrome (kidney disorder) and
male pseudohermaphroditism (a person whose gonads are consistent with the chromosomal sex
but who has external genitalia of the opposite sex.)

-Another gene is WT2 which is also located on chromosome 11, seems to also be involved with
other Wilms’ tumor-containing syndromes, like Beckwith-Wiedemann syndrome where internal
organs and limbs of children are enlarged

-All that being said, Wilm’s tumor, in the majority of cases, happens in otherwise healthy
children, and doesn’t seem to be associated with WT1 and WT2, or any developmental syndrome
of any kind.

Signs and Symptoms

The hallmark symptom is the non-tender mass on the abdominal area usually midline near the
liver
  high blood pressure, which may cause chest pain, shortness of breath, and headaches
 abdominal pain, swelling, or discomfort
 nausea and vomiting
 weakness and fatigue
 loss of appetite
 fever
 blood in their urine or discoloration of their urine (painless)
 increased and uneven growth of one side of their body
PRECAUTIONARY MEASURES:
-do not palpate the abdominal mass
Complications
 Cancer could spread to other parts(metastasize)
 kidney damage

Diagnosis
 blood or urine tests
 complete blood count (CBC)
 abdominal X-ray or ultrasound
 CT scan or MRI
Management
 Chemotherapy:
 Nephrectomy:
 Radiation therapy
 Radical nephrectomy
 Partial nephrectomy (nephron-sparing surgery)
 Prevent transfer of microorganism
 Prevent oral trauma
 Prevent anxiety
 Prevent injury

BREAST CANCER
-Breast cancer is a type of cancer that starts in the breast.
-Cancer starts when the cells begin to grow out of control.
-Breast cancer cells usually form a tumor that can often be seen on an x-ray or felt as a lump.
-Breast cancer occurs almost entirely in women, but men can also get breast cancer.
-however, it is important to understand that most breast lumps are benign and not cancer
(malignant). 
-Non-cancerous breast tumors are abnormal growths, but they do not spread outside of the breast.
They are not life threatening, but some types of benign breast lumps can increase a woman's risk
of getting breast cancer.
-Any breast lump or change in our breast needs to be checked by a health care professional to
determine if it is benign or malignant (cancer) and if it might affect your future cancer risk.

Breast cancers can start from different parts of the breast

 Most breast cancers begin in the ducts that carry milk to the nipple (ductal cancers)
 Some start in the glands that make breast milk (lobular cancers)
 There are also other types of breast cancer that are less common like phyllodes tumor
and angiosarcoma
-A small number of cancers start in other tissues in the breast. These cancers are called sarcomas
and lymphomas and are not really thought of as breast cancers.
-Although many types of breast cancer can cause a lump in the breast, not all do.
-Many breast cancers are also found on screening mammograms, which can detect cancers at an
earlier stage, often before they can be felt, and before symptoms even develop

Pathophysiology

- Breast cancer is a malignant tumor that starts in the cells of the breast. Like other cancers, there
are several factors that can raise the risk of getting breast cancer for example and the most
common is the Damage to the DNA and genetic mutations can lead to breast cancer that have
been experimentally linked to estrogen exposure (estrogen is a female hormone that
stimulates normal breast cells. A higher lifetime exposure to estrogen may increase breast cancer
risk).

-Some individuals inherit defects in the DNA and genes like the BRCA1, BRCA2 (breast cancer
gene 1 and breast cancer gene 2 they are genes that produce proteins that help repair damaged
DNA. Everyone has two copies of each of these genes—one copy inherited from each
parent.)And P53 gene (acts to control cell division and cell death).

-Those with a family history of ovarian or breast cancer thus are at an increased risk of breast
cancer.

-because basically, when an individual inherit defects of these genes or genetic mutations of the
BRCA1 and BRCA2 or the P53 gene, they are most likely to get breast cancer.

-The immune system normally seeks out cancer cells and cells with damaged DNA and destroys
them.

-Breast cancer may also be a result of failure of such an effective immune defence and
surveillance.

-These are several signalling systems of growth factors and other mediators that interact between
stromal cells and epithelial cells. Disrupting these may lead to breast cancer as well.

-Cancer begins when healthy cells in the breast change and grow out of control, forming a mass
or sheet of cells called a tumor.

-A tumor can be cancerous or benign. A cancerous tumor is malignant, meaning it can grow and
spread to other parts of the body. A benign tumor means the tumor can grow but will not spread.

-Breast cancer spreads when the cancer grows into adjacent organs or other parts of the body or
when breast cancer cells move to other parts of the body through the blood vessels and/or lymph
vessels. This is called a metastasis.
 -This guide covers both non-invasive (stage 0) as well as early-stage and locally advanced
invasive breast cancer, which includes stages I, II, and III. The stage of breast cancer describes
how much the cancer has grown, and if or where it has spread.

-Although breast cancer most commonly spreads to nearby lymph nodes, it can also spread
further through the body to areas such as the bones, lungs, liver, and brain. This is called
metastatic or stage IV breast cancer and is the most advanced type of breast cancer.

-However, the involvement of lymph nodes alone is generally not stage IV breast cancer. If
breast cancer comes back after initial treatment, it can recur locally, meaning in the same breast
and/or regional lymph nodes. It can also recur elsewhere in the body, called a distant recurrence
or metastatic recurrence.

Signs and Symptoms

 New lump in the breast on the upper outer quadrantsof the axillary
 Orange pale skin
 Thickening or swelling of part of the breast.
 Dimpling of breast skin (cancer retracted on the lower parts)
 Venous prominence
 Redness or flaky skin in the nipple area or the breast.
 Pulling in of the nipple or pain in the nipple area.
 Nipple discharge other than breast milk, including blood.
 Any change in the size or the shape of the breast.
 Pain in any area of the breast.
Risk Factors
 Early Menarche
 Nulliparity
 Hormone replacement therapy (HRT)
 Benign breast disease Especially in fibro adenoma

Complication
 Spread of cancer to other organs or bones and resulting symptoms are the complications
associated with advanced stages of breast cancer.
 Cancer treatment is associated with complications such as lymphedema, pain, and
sickness.

Diagnostic Procedures
 Staging
 Mammogram
 Chest x-rays
 Computed tomography (CT) scan
 MRI scan
 Positron Emission tomography (PET) scan
 Bone scan
Early prevention:
-Breast self –examination
Medical management
Chemo prevention drugs: Tamoxifen (nolvadex) treatment for breast tumor could be given with
Raloxifene (Evista) to prevent endometrial cancer\
Chemotherapy
-brachial therapy
Surgical Management
 Lumpectomy
 Prophylactic Mastectomy (health education and explanation of body image disturbances)
 Breast reconstruction
 Radiation therapy
 Chemotherapy
 Hormone therapy
 Lifestyle changes (decrease intake of fats)
 Health maintenance activities (mammography, PET, MRI, breast self-examination)
 Monitor for adverse effects of chemotherapy; bone marrow suppression, nausea and
vomiting, alopecia, weight gain or loss, fatigue, stomatitis, anxiety, and depression.
 Administer antiemetics prophylactically, as directed, for patients receiving
chemotherapy.
 Administer I.V. fluids and hyperalimentation as indicated.

LUNG CANCER
LIVER CANCER
COLORECTAL CANCER/COLON CANCER
-Colon cancer is a type of cancer that begins in the large intestine (colon).

-The colon is the final part of the digestive tract. Colon cancer typically affects older adults,
though it can happen at any age.

Pathophysiology

-Colon cancer usually starts from a small growth called a polyp (tissue growth).
-Polyps are very common, but most polyps do not become cancers.
-Polyps can be of various types, some of which are more likely to develop into malignant tumors
than others.
 Early-stage colon cancer generally produces no symptoms. Advanced-stage symptoms
vary depending on the location of the tumor, and may include: changes in bowel habits
that persist for weeks; blood in stool; abdominal pain and discomfort; constant feeling
that the bowel doesn’t empty completely; fatigue; and unexplained weight loss.
 Early detection is the key to prevent colon cancer. Because a pre-cancerous polyp usually
takes years to develop into a malignant tumor, colon cancer can be effectively prevented
with regular screening.
Colorectal cancers are caused by mutations that increase the rate of cellular division. Some of
these mutations can be inherited from parents. Examples of inherited colorectal cancers include:
 Familial  adenomatous polyposis, or FAP: a condition caused by mutations in
the APC gene.
 The APC protein acts as a tumor suppressor, keeping cells from growing and dividing too
fast. Mutations in APC result in uncontrolled cell division, causing hundreds of polyps to
grow in the colon. FAP patients usually develop colon cancer by the age of 40.
 Lynch syndrome: another inherited condition caused by changes in genes that normally
help repair DNA damages. A faulty DNA repair results in increased rate of mutations.
Patients are at high risks of colorectal cancer as well as other types of cancers.
In most cases, however, the mutations that lead to cancer are acquired during a person’s life
rather than being inherited. The early event is usually a mutation in the same APC gene that is
responsible for FAP. While FAP is a rare condition, APC mutations are very common in
sporadic colorectal cancers.
Signs and Symptoms
 Diarrhea
 Constipation
 Blood in stool
 Fatigue
 Unexplained weight loss
 Abdominal pain
 Bloating
Complications
 Partial or complete bowel obstruction
 Perforation
 Hemorrhage
Diagnostic Procedure
 Stool-based tests: stool samples
 Colonoscopy
 Flexible sigmoidoscopy
 CT colonography (virtual colonoscopy):
 Carcinoembryonic antigen
Management
 Antigen test
 Liver function tests:
 CEA test
 Endoscopic ultrasound
 Attainment of optimal level of nutrition
  Prevention of infection
 Maintenance of fluid balance

CANCER OF THE STOMACH (GASTRIC CANCER)

-Stomach cancer (also known as gastric cancer) is a disease in which the cells forming the inner
lining of the stomach become abnormal and start to divide uncontrollably, forming a mass called
a tumor.

Types
 Adenocarcinomas - Adenocarcinomas of the stomach develop in the cells of the
innermost lining.
 Lymphomas - Are cancers of the immune system tissue that may start anywhere lymph
tissues are found, including in the stomach.
 Gastrointestinal stromal tumors, or GISTs - Are a rare type of stomach cancer that forms
in a special cell found in the lining of the stomach called interstitial cells of Cajal (ICCs).
 Hereditary (familial) diffuse gastric cancer - This type of stomach cancer, which is
caused by a genetic condition passed down from parents to children, tends to grow in
multiple parts of the stomach and quickly spread to other areas of the body.
 Carcinoid tumors - Typically start in the hormone-producing cells of the stomach. These
tumors usually don’t spread to different organs and account for about 3 percent of
stomach cancer incidence.

Pathophysiology
-The exact cause of what causes stomach cancer is not known.
-However, doctors believe that stomach cancer, as any other causes begins when there are
changes in the DNA of the cells.
-The DNA contains information that tells the cells what to do. These changes in the DNA tell the
cells to grow rapidly.
-The abnormal cells do not die and keep growing to form a tumor that invades and destroys
healthy cells.

-Other factors that may contribute to the cause of gastric cancer are bacteria present inside the
stomach, known as H. pylori. These bacteria causes stomach ulcers that may transform into
cancer.
-also, Certain growths in your stomach called polyps, a type of long-lasting anemia called
pernicious anemia, or an inflammation in the gut called gastritis are suspected of causing gastric
cancer.
-Most stomach cancers are a type called adenocarcinoma this means that the cancer started in the
glandular tissue that lines the inside of the stomach.
-Other types of cancerous tumors that form in the stomach include lymphoma, gastric sarcoma,
and neuroendocrine tumors, but these are rare.

Sign and Symptoms

 Fatigue
 Stomach pain, which worsens after eating
 Bloating of stomach, especially after eating
 Feeling of stomach fullness, even after eating very little
  Severe and persistent heartburn
 Severe and persistent indigestion
 Persistent nausea and vomiting
 Loss of appetite
 Unintentional weight Loss
Complications
 Obstruction of the gastroesophageal junction and stomach outlet
 Bleeding in the stomach
 Jaundice
 Starvation
Diagnostic Procedures
 Blood test
 Endoscopy
 Barium swallow
 Biopsy
 Laparoscopy
Management
 Chemotherapy
 Immunotherapy
 Esophagectomy:
 Endoscopic mucosal resection
 Subtotal gastrectomy
 Total gastrectomy
 Radiation therapy

COLOSTOMY
-A colostomy is a surgery that makes a temporary or permanent opening called a stoma.
-A stoma is a path that goes from the large intestine to the outside of your abdomen.
-This helps solid waste and gas exit the body without passing through the rectum. The waste is
collected in a pouch worn on the outside of your body.
Types of colostomies
Sigmoid colostomy - This is the most common type. It is located in the bottom part of the large
intestine. The sigmoid colon moves waste to the rectum. Sigmoid colostomies produce stool that
is more solid and regular than other colostomies.
Transverse colostomy - The transverse colon crosses the top of the abdomen. Stool in this area
is usually soft. This is because only a small portion of the colon has absorbed water from the
indigestible material. This common type of colostomy has 3 versions:
 A loop colostomy
o This colostomy creates a stoma through which stool exits. In this type, the colon
stays connected to the rectum. As a result, people will sometimes pass stool or gas
through the rectum.
 A single-barrel colostomy
o This surgery removes the colon below the colostomy, including the rectum and
anal opening. This type of colostomy is permanent.
 A double-barrel colostomy
 o This divides the colon into 2 ends that form separate stomas. Stool exits from 1 of
the stomas. Mucus made by the colon exits from the other. This type of transverse
colostomy is the least common.
Descending colostomy - The descending colon takes waste down the left side of the abdomen.
The stool there is usually firm because it has moved through the working parts of the colon.
Ascending colostomy
The ascending colon runs from the beginning of the large intestine to the right side of the
abdomen. In this procedure, only part of the colon still works. As a result, little water is absorbed
from the waste. This means the stool is usually liquid. This type of colostomy is rare. An
ileostomy is more appropriate for this portion of the colon.
Management
Pre-operative Nursing Care
 Psychological preparation
 Nutrition
 Care of the Bowel
Post-operative Nursing Care
 Skin Care
 Psychosocial Adaptation
 Nutrition
 Patient Education
 Medications
 Control of Odor
 Applying an ostomy appliance
Protecting the skin around the stoma
 Use the right size pouch and skin barrier opening
 Change the pouching system regularly to avoid leaks and skin irritation
 Be careful when pulling the pouching system away from the skin and don't remove it
more than once a day unless there’s a problem
 Clean the skin around the stoma with water
 Watch for sensitivities and allergies to the adhesive, skin barrier, paste, tape, or pouch
material.
BLADDER CANCER
PROSTATE CANCER
-Prostate cancer is a cancer of the prostate gland, a part of the male reproductive system.
-it is the most common cancer in men other than non-melanoma skin cancer. It is the second
most common cause of cancer death in American men, exceeded only by lung cancer, and is
responsible for 10% of cancer-related deaths in men.
Types of Prostate Cancer
 Acinar adenocarcinoma
 o Adenocarcinomas are cancers that develop in the gland cells that line the prostate
gland. They are the most common type of prostate cancer. Nearly everyone with
prostate cancer has this type.
 Ductal adenocarcinoma
o Ductal adenocarcinoma starts in the cells that line the ducts (tubes) of the prostate
gland. It tends to grow and spread more quickly than acinar adenocarcinoma.
 Transitional cell (or urothelial) cancer
o Transitional cell cancer of the prostate starts in the cells that line the tube carrying
urine to the outside of the body (the urethra). This type of cancer usually starts in
the bladder and spreads into the prostate. But rarely it can start in the prostate and
may spread into the bladder entrance and nearby tissues.
 Squamous cell cancer
o These cancers develop from flat cells that cover the prostate. They tend to grow
and spread more quickly than adenocarcinoma of the prostate.
 Small cell prostate cancer
o Small cell prostate cancer is made up of small round cells. It’s a type of
neuroendocrine cancer.
Pathophysiology
-Male hormone such as testosterone cause prostate cancer to grow and survive.

-Early treatment for prostate cancer attempt to lower levels of testosterone in the body
this is known as hormone therapy.

-However, prostate cancer tumor may eventually begin to grow again even a level of
testosterone in the body are low at this point the cancer is considering to be advance.
-One possible reason that tumor continue to grow is that they become extremely sensitive
to the low level of testosterone that surround them.
-In this way tumors can grow even though there are extreme low levels of testosterone in
the bloodstream.
-Additionally, tumor may begin to produce its own supply of testosterone this means that
tumors capable of filling of its growth. In other words, in advance prostate cancer there is
evidence that suggest that the tumor may be providing of its own testosterone so that they
can grow without depending on other sources of testosterone production.
Signs and Symptoms
 Trouble urinating
 Frequent urination
 Decreased force of urination
 Difficulty starting or stopping urine stream
 Blood in semen
 Pain or discomfort in the pelvic area
 Bone pain
Complications
 Hemorrhage
 Infection
 Venous Thromboembolism
 Potential Catheter Problems
 Urinary Incontinence
 Sexual Dysfunction
Diagnostic Procedure
 Digital Rectal Examination
 Protein-Specific Antigen Test
 Ultrasound guided (Transrectal ultrasonography with biopsy)
Management
 Hormone therapy - Luteinizing hormone-releasing hormone (LH-RH) agonists
 Anti-androgens
 Chemotherapy
 Radical prostatectomy
 Orchiectomy
 Cryoablation
 Radiation therapy

TESTICULAR CANCER
-Testicular cancer is a Cancer that develops in the testicles, a male organ that produce sex
hormones and sperm for reproduction.
-It is the most common cancer in men aged 15 to 35 years and the second most common cancer
in men aged 35 to 39 years.
-Some testicular tumors tend to metastasize early, spreading from the testis to the lymph nodes in
the retroperitoneum and to the lungs.
Types of Testicular Cancer
 Germinal tumors make up approximately 90% of all cancers of the testis and may be
further classified as
o Seminomas (slow-growing, remain localized) and
o Fast growing non seminomas
 Nongerminal tumors accounts for less than 10% of the testicular cancers.
o may develop in the supportive and hormone-producing tissues, or stroma, of the
testicles.
 Leydig cell tumors
 Sertoli cell tumors
 Secondary testicular tumors (lymphoma) metastasize from other organs.
Pathophysiology
-Testicles are a pair egg-shaped glands enclosed in your scrotum which is a pouch that hangs
behind your penis.
-normally, your testicles produce sperm cells and make the hormone testosterone.
-Inside testicle are coiled tubes called seminiferous tubules where your body creates immature
sperm cells also known germ cells or spermatogonia through a series of stages called
spermatogenesis.
-Spermatogonia develop into mature sperm.
-Testicular cancer is a disease of abnormal cell growth in one or both of your testicles.
-It usually begins in your germ cells where genetic damage or changes called mutations cause the
cells to grow uncontrollably. The cancerous germ cells clump together to form a tumor which
continue to grow.
-In most cases, these mutations occur in your germ cells and are called germ cell tumors.
-Germ cell tumors classified as non-seminoma or seminoma or based on the appearance of the
cells under a microscope.
-Non seminoma tests tumors are usually more aggressive and spread quickly while seminoma
test tumor tends to progress at slower rate.
Signs and Symptoms
 Lump in the testes which may be painful
 Sudden shrinking of a testicle
 Gynecomastia (enlargement of the breast)
 Swelling and collection of fluid in the scrotum
 Dull ache in the lower abdomen
 Shortness of breath and chest pain due to pulmonary embolism
 Lump in the neck due to metastasis to the lymph nodes
Complications
 Pulmonary embolism- During the later stages of testicular cancer, blood can clot in an
artery in the lungs leading to shortness of breath
 Metastasis to other organs and lymph nodes
 Infertility due to impaired production of sperms because of malignancy
 Hypogonadism due to decreased testosterone production by the testes
Diagnostic Procedure
 Physical examination
 Ultrasound
 CT scan
 Positron emission tomography (PET)
 Tumor marker test
Management
 Chemotherapy
 Inguinal orchiectomy
 Retroperitoneal lymph node dissection
 Hormone therapy
 Radiation therapy
 Assess the patient’s physical and psychological status, and monitor for response to and
possible effects of surgery, chemotherapy, and radiation therapy

CERVICAL CANCER
-Cervical cancer is a cancer that's found anywhere in the cervix.
-The cervix is the opening between the vagina and the womb (uterus).It is part of the
reproductive system and is sometimes called the neck of the womb.
-Nearly all cervical cancers are caused by an infection from certain types of human
papillomavirus (HPV).It can often be prevented by attending cervical screening, which aims to
find and treat abnormalities before they turn into cancer.
-Cervical cancer usually grows very slowly and how serious it is depending on how big it is, if it
has spread and your general health.
Types of Cervical Cancer
  Squamous cell carcinoma- this form in the lining of your cervix. It’s found in up to 90%
of cases
 Adenocarcinoma - this form in the cells that produce mucus
 Mixed carcinoma - this has features of the two other types
Pathophysiology
-Cervical cancer is cancer of the cervix, the lower part of the uterus that opens into the birth
canal. It is one of the most common types of cancer in women worldwide, but also one of the
most preventable, thanks to early detection with pap tests.
-The cervix has 2 major cell types: flat squamous cells lining the outer part, and column-shaped
glandular cells covering the inside of the cervical canal.
-Both types can become cancerous but squamous cell carcinomas are much more common.
-Cancer usually starts in the zone where the two cell types meet, known as the transformation
zone.
-Virtually all cervical cancers are caused by human papillomaviruses, or HPVs.
-There are over a hundred different types of HPV, some of which pose higher risks than others.
About 70% of all cases are caused by just two types: hpv-16 and hpv-18.
-Two proteins produced by HPV, known as e6 and e7 proteins, it interfere with cell functions
that normally prevent excessive cell division which causes the cells to grow in an uncontrolled
manner.
-HPV is sexually transmitted and is very common, but in most women, HPV infections resolve
on their own and do not cause cancers.
-Factors that may increase the risk of persistent HPV infections include weakened immune
system, other sexually transmitted diseases and smoking. Chances of developing cervical cancer
also increase with having many children and long-term use of birth control pills.
Signs and Symptoms
-Early-stage cervical cancer generally produces no symptoms.
-Advanced-stage disease may cause abnormal or irregular vaginal bleeding, pelvic pain, or
unusual vaginal discharge or painful sexual intercourse

Complications
Surgery Complications (Hysterectomy and lymphadectomy)
 Bleeding
 Bladder instability
 Lymphoedema
 Lymphocysts
 Ureteric fistula
Radiotherapy complications
 Vaginal stenosis/atrophy
 Bowel or bladder Fistulae
 Sexual dysfunction following treatment
 Chemotherapy associated toxicity
 Pulmonary embolism (PE)
Diagnostic Procedure
 Pap smear
 X-ray
 CT scan
 Cone biopsy
 Punch biopsy
 Endocervical curettage
 Magnetic resonance imaging (MRI)
Management
 Chemotherapy
 Simple hysterectomy
 Radical hysterectomy
 Radiation therapy

UTERINE CANCER/ENDOMETRIOSIS
-Cancer of the uterine endometrium (fundus or corpus) is thefourth most common cancer in
women.
-Most uterine cancers are endometriosis (ie, originating in the lining of the uterus).
-Uterine cancer definition states that when normally, healthy cells in the uterus lining are
mutated into abnormal cells which become cancerous, it leads to the growth of tumors in the
uterus which is known as endometrial cancer.
-Endometrial cancer occurs when the cells of the endometrium start to grow too rapidly.
-The lining of the uterus may thicken in certain places. These areas of thickness may form a mass
of tissue called a tumor. Cancer cells also can spread (metastasize) to other areas of the body.
Types of Uterine Cancer:

There are mainly two uterine cancer types found in patients:

 Endometrial Carcinomas – Cancerous cells build in the inner lining of the uterus (the
endometrium), and endometrial carcinomas are commonly referred to as ‘uterine cancer
or adenocarcinoma.
 Uterine sarcomas – Starts in the supportive connective tissues or the muscle layer
(myometrium) of the uterus. 2% to 4% of uterine cancer cases fall into this type and
treatment is different in most cases.

Pathophysiology
-Endometrial carcinoma, or endometrial cancer, is when malignant or cancer cells arise in the
glands of the endometrium, the lining of the uterus.
-The wall of the uterus has three layers: the perimetrium, which is a layer continuous with the
lining of the peritoneal cavity, the myometrium, which is made of smooth muscle that contracts
during childbirth to help push the baby out, and the endometrium, a mucosal layer, that
undergoes monthly cyclic changes.
-Endometrial carcinoma involves the abnormal growth of the epithelial cells that make up
endometrial glands, and there are two main types.
-The most common is Type 1 endometrial carcinoma, which is also called endometrioid
carcinoma because the tumors grow in a way that looks like normal endometrial glands.
-It usually involves several genetic mutations in endometrial cells, including of PTEN, a tumor
suppressor gene; PIK3CA, an oncogene; and ARID1A, a gene regulating chromatin structure.
-All of these mutations increase signaling in the PI3K/AKT pathway, which promotes growth
and replication of endometrial cells.
-More signaling in the PI3K/AKT pathway also enhances the expression of genes which are
linked to estrogen receptors.
-So having high levels of estrogen will cause the endometrium undergoes hyperplasia, leading to
increased risk of developing type 1 endometrial carcinoma.
-Now, excessive estrogen can come from obesity, because fat cells convert adrenal precursors
into sex hormones; taking tamoxifen, a breast cancer medication that blocks estrogen receptor in
the breasts, but stimulates them in the uterus; and postmenopausal estrogen therapy given
without a progestin to “balance” it out.
-Now, type 2 endometrial carcinoma is rarer, and it has a number of subtypes.
-The most common subtype is serous carcinoma. The genetic mutations found most often in
serious carcinoma involve TP53 gene, another tumor suppressor, and aneuploidy, or an abnormal
number of chromosomes after cell division.
-Type 2 carcinomas don’t appear to be linked with estrogen levels. These cancers typically affect
women who have endometrial atrophy (Thinning of the uterine lining) and who have lower body
weight.
Signs and Symptoms
 Abnormal vaginal bleeding (most common symptom)
 Vaginal discharge
 Pain with urination and/or sex
 Pelvic pains
Complications
 Bladder instability following surgery
 Radiotherapy induced vaginal stenosis/atrophy
 Radiotherapy induced bowel or bladder distulae
 Sexual dysfunction following treatment
 Metastatic disease
 Lymphoedema
 Chemotherapy associated toxicity
Diagnostic Procedure
 Ultrasound
 Hysteroscopy
 Pelvic examination
 Endometrial biopsy
Management
 Chemotherapy
 Hysterectomy
 Oophorectomy
 Cervicectomy
 Lymphadenectomy
 Salpingectomy
 Hormone therapy
 Radiation therapy
ENDOMETRIOSIS
Endo- means internal and -metrium means womb, so endometrium is the innermost layer
of the womb, and endometriosis is where these endometrial cells grow outside of the
womb.Endometriosis is a common, benign, and chronic disease that containendometrial tissue
(similar to thatlining the uterus) found in the pelvic cavity outside the uterus.

Types
 Pelvic
 Ovarian
 Deeply infiltrating endometriosis
Pathophysiology
-Endometriosis is a condition where tissue, similar to the lining in your uterus, grows in other
areas of your body.
-If you are a woman, your reproductive system includes the vagina, uterus, fallopian tubes, and
ovaries.
-During a normal menstrual cycle, your ovaries make chemicals called hormones, which signal
the lining of your uterus to thicken.
-The lining, called the endometrium, builds up to prepare to receive a fertilized egg.
-If the egg isn't fertilized, the uterus sheds the lining through your vagina.
-This monthly bleeding is called your menstrual period.
-If you have endometriosis, the lining type tissue grows outside your uterus for reasons that
aren't clear.
-The misplaced tissue response to the hormones just like it would if it were inside your uterus.
The tissue continues to thicken, then sheds, and bleeds with every menstrual cycle.
-However, the blood and tissue that are shed outside the uterus have no way to leave your body.
-The trapped endometrial flow can irritate the surrounding area causing inflammation and pain.
-Bands of scar tissue, called adhesions, may form, sticking one organ to another or causing your
fallopian tubes to close.
-This can affect your fertility, which is the ability to become pregnant.
-Endometriosis can form endometriomas, also known as chocolate cysts. These cysts are fluid
filled sacs on your ovaries that can affect fertility. Endometriosis may also result in abnormal
bleeding.
Signs and symptoms
 Painful menstrual periods
 Chronic pain in the lower back and pelvis
 Pain during or after sex
 Painful bowel movements or pain when urinating during menstrual periods
 Infertility
 Might experience diarrhea, constipation, bloating, or nausea, especially during menstrual
periods
Complications
  Fertility problems
 Long-term pelvic pain that interferes with social and work activities
 Large cysts in the pelvis that may break open (rupture)
 in rare cases, endometriosis tissue may block the intestines or urinary tract
 Very rarely, cancer may develop in the areas of tissue growth after menopause
Diagnostic Procedure
 Full blood count
 Bimanual pelvic examination
 Laparoscopic examination
 Abdominal and transvaginal ultrasound
 Magnetic resonance imaging (MRI) and CT scans
Management
 Analgesics
 Laparoscopy
 Hysterectomy
 Hormone therapy

LEUKEMIA

-cancer of the blood because its origin is into the hemopoetic site directly.
-the term leukocytosis refers to an increased level of leukocytes (WBC) in the circulation
typically, only one specific cell type is increased, because the proportion of the several types of
leukocytes examples eosinophils, basophils, and monocytes are small, an increase in other types
can be great enough to elevate total leukocyte count.
-although the elevation of leukocytes is normal for example in infection, however it should
decrease as the physiologic need decreases.
-The common feature of the LEUKEMIAS is an unregulated proliferation of leukocytes in the
bone marrow.
-in acute or chronic forms the proliferation of leukemic cells leaves little room for normal cell
production.
-there can be also proliferation of cells in the liver or spleen (extra medullary hematopoiesis).
-in acute forms there can be also infiltration of leukemic cells in other organs, such as meninges,
lymph nodes, gum, and skin.

Risk Factors:
-the cause of leukemia is not fully known, but exposure to radiation or chemicals
-certain genetic disorders
-and viral infections are known to be risk factors for certain types of leukemia
-also, bone marrow damage from pelvic radiation or certain types of chemotherapy drugs can
cause acute leukemia.

TYPES OF LEUKEMIA

-the leukemias are commonly classified according to the stem cell line involved, either lymphoid
(the stem cells that produce lymphocytes) or myeloid (stem cells that produce nonlymphoid
blood cells)
-they are also classified as either acute or chronic, based on the time it takes for symptoms to
evolve and the phase of cell development.
-in acute leukemia, the onset of symptoms is abrupt, often occurring within a few weeks.
-in chronic leukemia symptoms evolve over a period of months to years.
Acute Myeloid Leukemia
-it is the most common non-lymphocytic leukemia that results from a defect in the hematopoietic
stem cell that differentiates into all myeloid cells.
-any age group can be affected although it infrequently occurs before age 45.
-signs and symtoms can involve fever and infection, weakness and fatigue, dyspnea on exertion,
pallor from anemia, petechiae, and ecchymoses
-assessment can involve CBC
-Complication: Bleeding and infection

Chronic Myeloid Leukemia

-it arises from the mutation in the myeloid stem cell
-here is, normal myeloid cells continue to be produced
-but there is a pathologic increased in the production of forms of blast cells (precursor of the
mature cells)
- therefore, wide spectrum of cell types exist in the blood, from blast forms to mature
neutrophils.
-because of uncontrolled proliferation of cells, the bone marrow expands into cavities of long
bones, such as the femur, and cells are also formed in the liver and spleen.
-resulting into enlargement of these organs
-signs and symptoms: shortness of breath or slightly confused, enlarged and tender spleen and
liver, malaise, anorexia and weight loss.

Acute Lymphocytic Leukemia

-results from acute proliferation of mature cells (lymphoblast) derived from lymphoid stem cell.
-most common in young children.
-pain from enlarged liver or spleen, bone pain, since the CNS is frequently a site for leukemic
cells patient may exhibit cranial nerve palsies, or headache and vomiting.

Chronic Lymphocytic Leukemia

-common malignancy of older adults
-unlike other leukemias a strong familial predisposition exist in CLL
-CLL is typically derived from malignant clone of B lymphocytes
-most leukemia cells in CLL are fully mature
-One possible mechanism that explains the
oncogenesis is that this cells can escape apoptosis (programmed cell death)
-resulting in excessive accumulation of the cells in the marrow and circulation.
-because lymphocytes are small they can easily travel through the small capillaries within the
circulation.
-these cells often accumulate within the lymph nodes and spleen.

Diagnostic Procedure
 Bone marrow biopsy – common one and confirmatory test for leukemia
 Check for CBC – especially if your WBC would be very increase or very decrease but
it’s not a confirmatory test
Normal WBC – 6 to 1 0k
Normal RBC – 4 to 5k
Treatments
 Chemotherapy
 Targeted type of therapy
 Bone marrow transplant
 Blood transfusion
 Leukapheresis – prevent TLS, extract WBC to prevent the crisis
Management
Specifically, on bleeding
 Avoid IM
 Avoid no tourniquet test – due to petechial or hemorrhage
  In WBC if there’s infection do handwashing, isolate your patients, you would have
reverse isolation, aseptic techniques, avoid crowded areas and no fresh fruits and
vegetables.
 They are contraindicated for vaccination also it’s because they would now acquire the
specific disease that you have been vaccine.

HODGKIN AND NON-HODGKIN DISEASE

PRIMARY LYMPHOID TUMOR

-it means that it originates most likely in your thymus and bone marrow
SECONDARY LYMPHOID TUMOR
-It involves in the tissue itself, specifically it’s in your lymph nodes, spleen, tonsils, intestinal
lymphoid tissues (non-hodgkin’s disease)

-the most common type of Lymphoma is the secondary

-Major subdivision of this Lymphoma is the Non-hodgkin and Hodgkin disease

-Non-hodgkin and Hodgkin disease have the same clinical manifestations

HODGKIN AND NON-HODGKIN LYMPHOMA

-it is the neoplasms of cells of lymphoid origin
-these tumors usually start in lymph nodes but it can also involve lymphoid tissue in the spleen,
GI tract (example wall of the stomach), liver or bone marrow
-Lymphomas are classified broadly into two categories: HODGKIN LYMPHOMA and NON-
HODGKIN LYMPHOMA
-first we are going to talk about the HODGKIN LYMPHOMA
HODGKIN LYMPHOMA
-unlike other lymphomas, Hodgkin lymphoma is unicentric (localized) it means it initiates in a
single node, also it spreads orderly.
-is a nodal type it means that its more on that its spread is more on the lymphatic system
-usually found in cervical area, axillary area and mediastinal areas are common areas.

-which means that the disease spreads by contiguous extension along the lymphatic system.
-the malignant cell of Hodgkin is the Reed-sternberg cell (a gigantic tumor cell that is
morphologically unique and thought to be of immature lymphoid origin.
-it is one of the pathologic hallmark
-the tumor is very heterogenous (which means it is outside) which they contain few reed-
steernberg cells.
-the remaining tumor volume is composed of benign, reactive, inflammatory cells that support
the growth and survival of the reed-steernberg cells.
-although the cause of Hodgkin is not fully known, but a viral etiology is suspected
-because fragments of the Epstein barr viruss have been found in some of the reed-steernberg
cells, however the exact role of this virus in the development of Hodgkin is unknown.
SYMPTOMS
- enlargement of one or more lymph nodes (nodes are painless and firm but not hard most
common in the cervical, supraclavicular, and mediastinal nodes)
-dyspnea (if trachea is compressed by the mass)
-pruritus
-jaundice (fromhepatic involvement)
-abdominal pain
-or bone pain
-fever without chills
-unintentional weight loss
-drenching sweats specially at nights
symptoms are most commonly found in the hodgkin’s diease, but in non-hodgkin disease it is
rarely found.

NON-HODGKINS
-non-hodgkin means an absence of key cell that is seen in Hodgkin which is the reed-steernberg
cells.
-it is a tumor derived from Lymphocytes specifically the B-cell and T-cell which mainly lives
in the lymph nodes and moves through the blood and lymphatic system
- it’s extranodal it involves not just only one node but rather other nodes and other part of the
lymphoid system or it has the capacity to spread through blood vessels which is why it can be
found in other parts -
-it is a multiple type of peripheral node, it has random spread because of blood vessels
involvement
- it’s commonly found in the mesenteric (stomach areas) and it can also be found in the groin in
the lower portion of the body.

PATHOPHYSIOLOGY
-B-cell development start in the bone marrow which is the primary lymphoid organ, it is
where a young b-cells mature.
-it then leave the bone marrow and circulate in the blood and eventually settle down in the
lymph nodes
-now, t-cell development starts in the thymus, in the thymus these precursor T-cells mature
-mature t-cells circulate in the blood and are found in the paracortex of the lymph nodes
- in non-hodgkin there is usually a genetic mutation in the lymphocyte either the b-cell or the t-
cell
-when something like that happens cells are supposed to undergo apoptosis- or programmed cell
death
-but instead the lymphocytes starts to divide uncontrollably- becoming neoplastic cell.
-usually lymphomas develop in lymph nodes and they are called nodal lymphomas
-however, it can happen anywhere in the body and when they develop in other tissues or organs
this is where they are called EXTRANODAL LYMPHOMAS
-since this type of lymphoma can spread into the blood
-like, if they go to the gastrointestinal tract it will cause bowel obstruction
-if in to the bone marrow it will crowd out normal cells and decreased RBC, WBC, and platelets
-if in the spinal cord they can cause spinal cord compression.

STAGING
 stage I: one nodal group or lymphoid organ (e.g. spleen or thymus)
o stage IE: one extranodal site
 stage II: two or more nodal groups, same side of the diaphragm
o stage IIE: localized extranodal site with stage II criteria, both on the same side of
the diaphragm
 stage III: nodal groups on both sides of the diaphragm
o stage IIIS (1): with splenic involvement
o stage IIIE (2): with localized extranodal site
o stage IIISE: both
 stage IV: disseminated involvement of one or more extralymphatic organ (e.g. lung,
bone) with or without any nodal involvement

Diagnostic Procedure
-lymph node biopsy

BONE MARROW TRANSPLANT

It is a procedure that infuses healthy blood-forming stem cells into your body to replace
your damaged bone marrow.
Types
 Allogeneic stem cell transplant- it means the donor is other person, as long as it matches
 Autologous stem cell transplant- means own bone marrow that they preserve before the
chemotherapy

Why it’s done?

 Replacing the bone marrow damaged by treatment
 Provide new stem cells which can help kill cancer cells directly

Complications
 Organ damage
 Infections
  Infertility
 New cancers
 Death

Management
 Limit salt intake
 Restrict alcohol
 Avoid grapefruit
 Provide emotional support to patient.

GRAFT VERSUS HOST DISEASE (GVHD) (ACUTE/CHRONIC)

In GVHD, the donated bone marrow/peripheral blood stem cells view the recipient’s
body as foreign, and the donated cells/bone marrow attack the body.
-2 or 3 mismatched in human leukocyte antigen (HLA) is a risk for rejection
-older patient more than 30-year-old
-age gap between the donor and the recipient is high
-sex difference
Types
 Acute GVHD
 Chronic GVHD

Acute GVHD might occur once the donor’s cells have engrafted in the transplant
recipient. It might develop in your skin, liver/GI tract, and symptoms might appear within weeks
after the transplant.

Risk Factors
 Recipients who have received peripheral blood stem cells
 A female donor who has been pregnant in the past
 Advanced age of either the donor or recipient

Signs and Symptoms

 Skin rash
 Jaundice
 Nausea and vomiting

Treatment
 Increasing the immunosuppression in the form of oral
 Steroids

Chronic GVHD can appear at any time after allogenic transplant. It might occur in skin,
liver, mouth, lungs, GI tract, neuromuscular system, or genitourinary tract.
Risk Factors
 Who received bone marrow from a human leukocyte antigen
 Who have experienced acute GVHD
 Older transplant recipients

Signs and symptoms

 Skin rash
  Abdominal swelling
 Vision changes
 Shortness of breath

Treatment
 Long-term immunosuppressive drugs

STAGES

4 types of delayed reactions

-anaphylactic (immediate reactions)
-cytotoxic
-immune complex hypersensitivity
-cell mediated late phase

THERAPY (ALL 4 MODALITIES)

CHEMOTHERAPY, BIOTHERAPY/IMMUNOTHERAPY, RADIATION THERAPY,
SURGERY

1. Surgery- primary treatment for cancer where you would incise the tumor, you would
remove it.
2. Radiation therapy- it is a controlled type of radiation; the common one is internal
radiation and the external radiation, it will kill the tumor through reducing the size.
  Internal Radiation- we have the sealed (common is the brachytherapy where they
would implant on your hand or directly on the specific parts of the body the radio
isotopes, or any parts of the body that has cancer but once removed automatically
the patient is no longer radioactive) and the unsealed(most likely it is oral they
would like drink our radiation therapy drugs or could also be through IV, but the
bad thing is your patient is still radioactive even after few days and it is bad for
the significant others or nurses because there are chancer that you will be expose).
We have the STD (shield; Time you limit the time exposure to the patient most
likely 30 minutes only per shift and 10-15 minutes only for the visitors; Distance
6 feet). For unsealed the secretions of the patients are all radioactive.
 External Radiation- we have here the targeted type it means that you would put a
laser beams directly on the area where the tumors or malignant cells are located
then you would provide the therapy to kill the cancer cells and reduce the size of
the tumors.

-here we should not remove the marking, avoid constrictive clothing, and avoid
medications or creams directly on the area.

3. Chemotherapeutic Drugs- in this treatment they would have kill all cells that are fast
growing cells, here in chemotherapeutic drugs they won’t choose whether the cells are bad or
good as long as they are fast growing cells they would kill it.

Types of chemotherapeutic drugs

Specific Cells or the CCS (cell cycle specific drugs)- it means that it inhibits on the specific
area of the development of the cancer cells either on the meiosis or mitosis and the stages of
the cancer

Cell Cycle non-specific drugs (CCNS)- it means that it is applicable on every area in all
areas of your cancer development.

Common Side effects of Chemotherapy

1. bone marrow suppression and Hematologic Problems

 RBC in RBC you will have anemia problems so most likely you have to advice your
patient to rest.
 WBC drop it means that immunosuppression and leukopenia would most likely occur
in your patient and they are prone to infections that’s why advice your patient to
isolate
 Platelets it will cause thrombocytopenia or drop of the platelets patient is prone for
bleeding that is why advice patient to avoid injury and anything that would cause it.
Your patient also may develop nosebleeds.

2. G.I tract
 patients are anorexic, symptoms of nausea and vomiting. That is why you will give
antiemetic drugs before chemotherapy started also advice patient to have bland diet.
 Patient also can develop diarrhea advice patient to have clear liquid therapy as
tolerated
 Monitor also the patient’s potassium and sodium
 Maintain electrolytes balance

3. Integumentary
 Patients will develop body image disturbance due to alopecia
 Stomatitis also you advice patient for good oral hygiene

4. Renal System
  Most likely patient will develop increased uric acid
 You will give fluids and uric acid medications

5. Reproductive System- patient becomes infertile or sterile during chemo.

4. Biotherapy- it means that its mean purpose is to give medications or vitamins for your
patients to boost their immune system, so its mean purpose here Is to increase the immune
system of your patients so that the immune system will be the one to kill directly the outgrowth
or the growth of cancer cells inside the body.
-this type of therapy won’t destroy the cells rather it will boost the immune system.
-

STAGES ON THE TREATMENT OF CANCER

 Induction- initial phase in which they would provide high rates of chemotherapeutic
drugs or high frequency of radiation therapy. The main purpose is to really remove a bulk
of tumor or to shrink it as much as possible. That is why in this stage they will give a
very high doses of medication.
 Consolidation- it means that what are the cells that has been remained in the
introduction, in this stage they will kill the remaining cancer cells that has been left
during the introduction phase. On this stage some patient will not survive.
 Maintenance- the main goal is to make your patient cancer free to become on the state of
remission, or it is a state of remission. Continuous chemotherapeutic medication but on
the lesser type of doses.
 Observation- most likely your patient will no longer take medications but rather they
would always be checked for reoccurrence of cancer because there is chancer that cancer
will reoccur.

4 STAGES OF TRANSFORMATION OF NORMAL CELL INTO CANCER CELLS

(CARCINOGENESIS)

1. Initiation Phase (Initial phase)- changes in the structure of DNA due to the initial
exposure of the different factors (e.g., exposure to radiation, chemicals, environmental,
occupational) could lead to slight changes in your DNA structures or genetic mutations
but at this stage it is still reversible.
2. Promotion Phase- it promotes further assault on the normal cells, it further cause assault
on the normal cells, so there’s continuous exposure (like you’re still exposing yourself to
the factors) and causes further genetic mutations of the cells.
3. Malignant Conversion- it means that it’s no longer mutation in your cells but rather it
becomes now irreversible genetic mutations due to continuous assault. In this phase
your cells become a cancerous type.
4. Progression- it means cells are increasingly malignant and it develops now to an
invasive cancer types which lead to metastasis to other distant body (Last stage).

DIFFERENT STAGES OR GRADES FOR CANCER PATIENTS

A deciding factors to appropriate treatment

 Stage 1 and Stage 2- it is well differentiated; it deviates only minimally from normal
cells. They have high chances of survival. Stage 1: it spreads only to nearby tissues and
 most likely it’s 2 centimeter below; Stage 2: a tumor with lymph nodes involvement, it is
2-5 centimeters.
 Stage 3- poorly differentiated, it is a big tumor with increase number of lymph nodes
involvement, and it is more than 5 centimeters
 Stage 4- presence of metastasis, means your cells here are no longer in the specific
organs but rather it spread now to other parts of the body.