Introduction to Gastric cancer

Introduction

Common throughout the world, gastric cancer affects all races. However, unexplained geographic and cultural differences in incidence occur; for example, mortality is high in Japan, Iceland, Chile, and Austria. In the United States, incidence has decreased 50% during the past 25 years, and the death rate from gastric cancer is one-third that of 30 years ago.
The decrease in gastric cancer incidence in the United States has been attributed, without proof, to the balanced American diet and to refrigeration, which reduces the number of nitrate-producing bacteria in food.
Incidence is highest in men over age 40. The prognosis depends on the stage of the disease at the time of diagnosis; overall, the 5-year survival rate is about 15%.

Etiology
The cause of gastric cancer is unknown. 

This cancer is commonly associated with 

• gastritis, 
• chronic inflammation of the stomach, 
• gastric ulcers, 
• Helicobacter pylori bacteria, and 
• gastric atrophy. 

Predisposing factors include environmental influences, such as smoking and high alcohol intake.

Genetic factors have also been implicated because this disease occurs more frequently among people with type A blood than among those with type O; similarly, it’s more common in people with a family history of such cancer.
Dietary factors include types of food preparation, physical properties of some foods, and certain methods of food preservation (especially smoking, pickling, and salting).

Classification
According to gross appearance, gastric cancer can be classified as 

Brief Summary of Hemorrhoids

Hemorrhoidal varices are part of the normal anatomy. Dilation and enlargement of the superior plexus of the superior hemorrhoidal veins located above the dentate line produce internal hemorrhoids. Enlargement of the plexus of the inferior hemorrhoidal veins located below the dentate line produces external hemorrhoids.External hemorrhoids may protrude from the rectum. Hemorrhoids occur in both sexes. Incidence is generally highest between ages 20 and 50.

Causes
Hemorrhoids result from activities that increase intravenous pressure, resulting in distention and engorgement. 

Predisposing factors include 

• prolonged sitting, 
• straining at defecation,
•  constipation,
• low-fiber diet, 
• pregnancy, and 
• obesity.

Other factors include hepatic disease, such as cirrhosis, amebic abscesses, or hepatitis; alcoholism; and anorectal infections.

Signs and symptoms

Internal hemorrhoids may produce no symptoms. They characteristically cause painless, intermittent bleeding during defecation. Bright red blood appears in stools or on toilet paper because of injury to the fragile mucosa covering the hemorrhoid.
When hemorrhoids prolapse, they’re usually painless and spontaneously return to the anal canal after defecation.

Introduction to Appendicitis

The most common abdominal surgical disease, appendicitis is inflammation of the vermiform appendix due to an obstruction. Although appendicitis may occur at any age and affects both sexes equally, it’s most common between puberty and age 30. Since the advent of antibiotics, the incidence and the death rate of appendicitis have declined. If left untreated, gangrene and perforation develop within 36 hours.

Causes
Appendicitis probably results from an obstruction of the intestinal lumen caused by a fecal mass, stricture, barium ingestion, or viral infection. This obstruction sets off an inflammatory process that can lead to infection, thrombosis, necrosis, and perforation. If the appendix ruptures or perforates, the infected contents spill into the abdominal cavity, causing peritonitis, the most common and most perilous complication of appendicitis.

Signs and symptoms
Appendicitis usually begins with generalized or localized colicky periumbilical or epigastric pain, followed by anorexia, nausea, and a few episodes of vomiting. Pain eventually localizes in the right lower quadrant of the abdomen (McBurney’s point), with abdominal “boardlike” rigidity, retractive respirations, increasing tenderness, increasingly severe abdominal spasms and, almost invariably, rebound tenderness. (Rebound tenderness on the opposite side of the abdomen suggests peritoneal inflammation.)
Later signs and symptoms include constipation (although diarrhea is also possible), slight fever, and tachycardia. Sudden cessation of abdominal pain indicates a perforation or infarction of the appendix. The elderly patient may present with minimal, vague symptoms and mild abdominal tenderness, delaying diagnosis of appendicitis.

Mallory-Weiss syndrome

Mild to massive and usually painless bleeding due to a tear in the mucosa or submucosa of the cardia or lower esophagus characterizes Mallory-Weiss syndrome. Such a tear, usually singular and longitudinal, results from prolonged or forceful vomiting. About 60% of these tears involve the cardia; 15%, the terminal esophagus; and 25%, the region across the esophagogastric junction. Mallory-Weiss syndrome is most common in men older than age 40, especially alcoholics.

Causes
The direct cause of a tear in Mallory-Weiss syndrome is forceful or prolonged vomiting, probably when the upper esophageal sphincter fails to relax during vomiting. This lack of sphincter coordination is more common after excessive intake of alcohol. Other factors and conditions that may also increase intra-abdominal pressure and predispose to esophageal tearing include coughing, straining during bowel movements, trauma, seizures, childbirth, hiatal hernia, esophagitis, gastritis, and atrophic gastric mucosa.

Signs and symptoms
Typically, Mallory-Weiss syndrome begins with the vomiting of blood or the passing of large amounts of blood rectally a few hours to several days after normal vomiting. This bleeding, which may be accompanied by epigastric or back pain, may range from mild to massive but is generally more profuse than in esophageal rupture.
In patients with Mallory-Weiss syndrome, the blood vessels are only partially severed, preventing retraction and closure of the lumen. Massive bleeding—most likely when the tear is on the gastric side, near the cardia—may quickly lead to fatal shock.

Brief Summary of Inguinal Hernia

Introduction

A hernia occurs when all or part of a viscus protrudes from a normal location in the body. Most hernias are protrusions of part of the abdominal viscus through the abdominal wall. Although many kinds of abdominal hernias are possible, inguinal hernias are most common.
With an inguinal hernia, the large or small intestine, omentum, or bladder protrudes into the inguinal canal. Hernias can be reducible, incarcerated, or strangulated.

Pathophysiology
In males, during the 7th month of gestation, the testes normally descend into the scrotum, preceded by the peritoneal sac. If the sac closes improperly, it leaves an opening through which the intestine can slip. In either sex, a hernia can result from weak abdominal muscles or increased intra-abdominal pressure. An inguinal hernia may be indirect or direct.

Indirect inguinal hernia
An indirect inguinal hernia, the more common hernia, results from weakness in the fascial margin of the internal inguinal ring. This type of hernia enters the inguinal canal through the internal inguinal ring and emerges through the external inguinal ring. The hernia extends down the inguinal canal into the scrotum or labia.
An indirect inguinal hernia may develop at any age, is three times more common in males, and is especially prevalent in infants younger than age 1.

Abdominal Trauma - An Overview

Blunt and penetrating abdominal injuries may damage major blood vessels as well as internal organs. Their most immediate life-threatening consequences are hemorrhage and hypovolemic shock; later threats include infection. The prognosis depends on the extent of the injury and on the organs damaged, but it’s generally improved by prompt diagnosis and surgical repair.

Causes
Blunt (nonpenetrating) abdominal injuries usually result from motor vehicle accidents, falls from heights, or athletic injuries; penetrating abdominal injuries, from stab or gunshot wounds.

Signs and symptoms
Depending on the degree of injury and the organs involved, signs and symptoms vary as follows

Penetrating abdominal injuries cause obvious wounds. For example, gunshots commonly produce both entrance and exit wounds, with variable blood loss, pain, and tenderness. These injuries can cause pallor, cyanosis, tachycardia, shortness of breath, and hypotension.

Blunt abdominal injuries can cause severe pain (such pain may radiate beyond the abdomen, for example, to the shoulders), bruises, abrasions, contusions, and distention. They may also result in tenderness, abdominal splinting or rigidity, nausea, vomiting, pallor, cyanosis, tachycardia, and shortness of breath. Rib fractures commonly accompany blunt injuries.

With both penetrating and blunt injuries, massive blood loss may cause hypovolemic shock. Generally, damage to a solid abdominal organ (liver, spleen, pancreas, or kidney) causes hemorrhage, whereas damage to a hollow organ (stomach, intestine, gallbladder, or bladder) causes rupture and release of the affected organ’s contents (including bacteria) into the abdomen, which, in turn, produces inflammation.

Jaw dislocation or fracture

Jaw dislocation is a displacement of the temporomandibular joint. 

Jaw fracture is a break in one or both of the two maxillae (upper jawbones) or the mandible (lower jawbone). Treatment can usually restore jaw alignment and function.

Causes
Simple fractures or dislocations are usually caused by a manual blow along the jawline; more serious compound fractures, from car accidents and penetration injuries.

Signs and symptoms
Malocclusion is the most obvious sign of dislocation or fracture. Other signs and symptoms include mandibular pain, swelling, ecchymosis, loss of function, and asymmetry. In addition, mandibular fractures that damage the alveolar nerve produce paresthesia or anesthesia of the chin and lower lip. Maxillary fractures produce infraorbital paresthesia and commonly accompany fractures of the nasal and orbital complex.

Diagnosis
Abnormal maxillary or mandibular mobility during physical examination and a history of trauma suggest fracture or dislocation. X-rays can confirm diagnosis, but a computed tomography scan is usually necessary for accurate diagnosis and repair.

Brief Summary of Intestinal obstruction

An intestinal obstruction is a partial or complete blockage of the lumen in the small or large bowel. A small-bowel obstruction is more common (90% of patients) and usually more serious. A complete obstruction in any part of the bowel, if untreated, can cause death within hours from shock and vascular collapse. Intestinal obstructions are most likely to occur from adhesions caused by previous abdominal surgery, an external hernia, volvulus, Crohn’s disease, radiation enteritis, an intestinal wall hematoma (after trauma or anticoagulant therapy), or a neoplasm.

Causes
Adhesions and strangulated hernias usually cause small-bowel obstructions; carcinomas usually cause large-bowel obstructions. 

A mechanical intestinal obstruction results from a foreign body (fruit pits, gallstones, or worms) or compression of the bowel wall due to stenosis, intussusception, volvulus of the sigmoid or cecum, tumors, or atresia.

A nonmechanical obstruction results from a physiologic disturbance, such as paralytic ileus (see Paralytic ileus), electrolyte imbalance, toxicity (uremia or generalized infection), a neurogenic abnormality (spinal cord lesions), or thrombosis or embolism of mesenteric vessels.

The three forms of intestinal obstruction are:

1. simple—blockage prevents intestinal contents from passing with no other complications.
2. strangulated—blood supply to part or all of the obstructed section is cut off in addition to blockage of the lumen
3. close looped—both ends of a bowel section are occluded, isolating it from the rest of the intestine.

Pathophysiology

In all three forms, the physiologic effects are similar. When intestinal obstruction occurs, fluid, air, and gas collect near the site. Peristalsis increases temporarily as the bowel tries to force its contents through the obstruction, injuring intestinal mucosa and causing distention at and above the site of the obstruction. This distention blocks the flow of venous blood and halts normal absorptive processes. As a result, the bowel begins to secrete water, sodium, and potassium into the fluid pooled in the lumen. This results in distention and enormous amounts of fluid in the gut.
An obstruction in the upper intestine results in metabolic alkalosis from dehydration and loss of gastric hydrochloric acid; a lower obstruction causes slower dehydration and loss of intestinal alkaline fluids, resulting in metabolic acidosis. Ultimately, an intestinal obstruction may lead to ischemia, necrosis, and death.

Signs and symptoms
Signs and symptoms depend on the location and extent of the obstruction.

Summary of Bladder cancer

Bladder tumors can develop on the surface of the bladder wall (benign or malignant papillomas) or grow within the bladder wall (generally more virulent) and quickly invade underlying muscles. Most bladder tumors (90%) are transitional cell carcinomas, arising from the transitional epithelium of mucous membranes. Less common are adenocarcinomas, epidermoid carcinomas, squamous cell carcinomas, sarcomas, tumors in bladder diverticula, and carcinoma in situ. Bladder tumors are most prevalent in men older than age 50 and are more common in densely populated industrial areas, but women are diagnosed at more advanced stages.

Causes
Certain environmental carcinogens—such as 2-naphthylamine, benzidine, tobacco, and nitrates—predispose people to transitional cell tumors. Thus, workers in certain industries (rubber workers, weavers, leather finishers, aniline dye workers, hairdressers, petroleum workers, and spray painters) are at high risk for such tumors. The period between exposure to the carcinogen and development of symptoms is about 18 years.
Squamous cell carcinoma of the bladder is most common in geographic areas where schistosomiasis is endemic. It’s also associated with chronic bladder irritation and infection (for example, from kidney stones, indwelling urinary catheters, and cystitis caused by cyclophosphamide).

Signs and symptoms
In early stages, about 25% of patients with bladder tumors have no symptoms. Commonly, the first sign is gross, painless, intermittent hematuria (often with clots in the urine). Patients with invasive lesions often have suprapubic pain after voiding. Other symptoms include bladder irritability, urinary frequency, nocturia, and dribbling.

Diagnosis
Only cystoscopy and a biopsy can confirm bladder cancer. Cystoscopy should be performed when hematuria first appears. When it’s performed under anesthesia, a bimanual examination is usually done to determine if the bladder is fixed to the pelvic wall. A thorough history and physical examination may help determine whether the tumor has invaded the prostate or the lymph nodes.

Special Considerations in Patients with Laryngeal cancer

Special considerations

• Psychological support and good preoperative and postoperative care can minimize complications and speed recovery.
• Before partial or total laryngectomy:
• Instruct the patient to maintain good oral hygiene. If appropriate, instruct a male patient to shave off his beard.
• Encourage the patient to express his concerns before surgery. Help him choose a temporary nonspeaking method of communication (such as writing).
• If appropriate, arrange for a laryngectomee to visit him. Explain postoperative procedures (suctioning, nasogastric [NG] tube feeding, and care of laryngectomy tube) and their results (the need to breathe through the neck, altered speech). Also, prepare him for other functional losses: He won’t be able to smell, blow his nose, whistle, gargle, sip, or suck on a straw.

After partial laryngectomy:

• Give I.V. fluids and, usually, tube feedings for the first 2 days postoperatively; then give the patient oral fluids. Keep the tracheostomy tube (inserted during surgery) in place until edema subsides.
• Keep the patient from using his voice until he has medical permission (usually 2 to 3 days postoperatively). Then caution him to whisper until healing is complete.

After total laryngectomy:

• As soon as the patient returns to his bed, place him on his side and elevate his head 30 to 45 degrees. When you move him, remember to support his neck.
• The patient will probably have a laryngectomy tube in place until his stoma heals (7 to 10 days). This tube is shorter and thicker than a tracheostomy tube, but requires the same care.
• Watch for crusting and secretions around the stoma, which can cause skin breakdown. To prevent crust formation, provide adequate room humidification. Remove crusting with petroleum jelly, antimicrobial ointment, and moist gauze.
• Teach the patient stoma care.

Mastitis and Breast Engorgement

Mastitis (parenchymatous inflammation of the mammary glands) and breast engorgement (congestion) are disorders that may affect lactating females.

Mastitis occurs postpartum in about 1% of patients, mainly in primiparas who are breast-feeding. It occurs occasionally in nonlactating females and rarely in males. All breast-feeding mothers develop some degree of engorgement, but it’s especially likely to be severe in primiparas. The prognosis for both disorders is good.

Causes
Mastitis develops when a pathogen that typically originates in the nursing infant’s nose or pharynx invades breast tissue through a fissured or cracked nipple and disrupts normal lactation. The most common pathogen of this type is Staphylococcus aureus; less commonly, it’s Staphylococcus epidermidis or beta-hemolytic streptococci. Rarely, mastitis may result from disseminated tuberculosis or the mumps virus. Predisposing factors include a fissure or abrasion on the nipple; blocked milk ducts; and an incomplete let-down reflex, usually due to emotional trauma. Blocked milk ducts can result from a tight bra or prolonged intervals between breast-feedings.
Causes of breast engorgement include venous and lymphatic stasis and alveolar milk accumulation.

Signs and symptoms
Mastitis may develop anytime during lactation but usually begins 3 to 4 weeks postpartum with fever (101° F [38.3° C] or higher in those with acute mastitis), malaise, and flulike symptoms. The breasts (or, occasionally, one breast) become tender, hard, swollen, and warm. Unless mastitis is treated adequately, it may progress to breast abscess.
Breast engorgement generally starts with onset of lactation (day 2 to day 5 postpartum). The breasts undergo changes similar to those in mastitis, and body temperature may be elevated. Engorgement may be mild, causing only slight discomfort, or severe, causing considerable pain. A severely engorged breast can interfere with the infant’s capacity to feed because of his inability to position his mouth properly on the swollen, rigid breast.

Introduction to Diverticular disease

Diverticular disease is an outpouching of the colon, usually the sigmoid. It develops from the musculature in the colon working against increased intraluminal pressures to move hard stools through. Other typical sites are the duodenum, near the pancreatic border or the ampulla of Vater, and the jejunum. Diverticular disease of the stomach is rare and commonly a precursor of peptic or neoplastic disease. Diverticular disease of the ileum (Meckel’s diverticulum) is the most common congenital anomaly of the GI tract.
Diverticular disease has two clinical forms. In diverticulosis, diverticula are present but usually the patient is asymptomatic or the symptoms (abdominal pain, fluctuating bowel habits, constipation) are questionable because they may be related to underlying irritable bowel syndrome. In diverticulitis, diverticula are inflamed and may cause potentially fatal obstruction, infection, or hemorrhage.

Causes
Diverticular disease is most prevalent in men older than age 40 and is rarely found in cultures whose diets are high in residue. Diverticula probably result from high intraluminal pressure on areas of weakness in the GI wall, where blood vessels enter. Herniation of mucosa occurs through weak areas of the GI tract.
Diet may also be a contributing factor because lack of roughage reduces fecal residue, narrows the bowel lumen, and leads to higher intra-abdominal pressure during defecation. The fact that diverticulosis is most prevalent in Western industrialized nations, where processing removes much of the roughage from foods, supports this theory. Diverticulosis is less common in nations where the diet contains more natural bulk and fiber.
In diverticulitis, retained undigested food mixed with bacteria accumulates in the diverticular sac, forming a hard mass (fecalith). This substance cuts off the blood supply to the thin walls of the sac, making them more susceptible to attack by colonic bacteria.
Inflammation follows, possibly leading to perforation, abscess, peritonitis, obstruction, or hemorrhage. Occasionally, the inflamed colon segment may produce a fistula by adhering to the bladder or other organs.

Signs and symptoms
The two forms of diverticular disease produce different signs and symptoms.

Sprains and Strains

 Definitions: 

Sprain: A sprain is a complete or incomplete tear in the supporting ligaments surrounding a joint that usually follows a sharp twist. 

Strain: A strain is an injury to a muscle or tendinous attachment. 

Both usually heal without surgical repair.

Causes

• Sprains occur when there is trauma to the joint, causing the joint to move in a position it wasn’t intended to move. 
• Strains may be caused by excessive physical effort or activity, improper warming up before an activity, or poor flexibility.

Signs and symptoms
Sprains and strains cause varying signs and symptoms.

Sprains
A sprain causes local pain (especially during joint movement), swelling, loss of mobility (which may not occur until several hours after the injury), and a black-and-blue discoloration from blood extravasating into surrounding tissues. A sprained ankle is the most common joint injury.

Strains
A strain may be acute (an immediate result of vigorous muscle overuse or overstress) or chronic (a result of repeated overuse).
An acute strain causes a sharp, transient pain (the patient may say he heard a snapping noise) and rapid swelling. When severe pain subsides, the muscle is tender; after several days, ecchymoses appear.
A chronic strain causes stiffness, soreness, and generalized tenderness. These conditions appear several hours after the injury.

Special Considerations In Cases With Traumatic Amputation

Traumatic amputation involves the accidental loss of a body part, usually a finger, a toe, an arm, or a leg. In complete amputation, the member is totally severed; in partial amputation, some soft-tissue connection remains.

The prognosis has improved as a result of early improved emergency and critical care management, new surgical techniques, early rehabilitation, prosthesis fitting, and new prosthesis design. New limb reimplantation techniques have been moderately successful, but incomplete nerve regeneration remains a major limiting factor.

Causes
Traumatic amputations usually result directly from accidents at a factory or farm, or from power tools or motor vehicle accidents.

Diagnosis
Any patient with a traumatic amputation requires careful monitoring of vital signs as well as assessment for other traumatic injuries. If amputation involves more than just a finger or a toe, assessment of airway, breathing, and circulation is also required. Because profuse bleeding is likely, watch for signs of hypovolemic shock, and draw blood for hemoglobin level, hematocrit, and typing and crossmatching. If the patient has a partial amputation, check for pulses distal to the amputation.

Testicular cancer

Introduction

Malignant testicular tumors, which rank first in cancer deaths among men ages 20 to 35, primarily affect young to middle-aged men; they are the most common solid tumor in this group. (In children, testicular tumors are rare.) Most testicular tumors originate in gonadal cells. About 40% are seminomas— uniform, undifferentiated cells resembling primitive gonadal cells. The rest are nonseminomas—tumor cells showing various degrees of differentiation.
The prognosis varies with the cell type and disease stage. When treated with surgery and radiation, almost all patients with localized disease survive beyond 5 years.

Causes
The cause of testicular cancer isn’t known, but incidence (which peaks between ages 20 and 40) is higher in men with cryptorchidism (even when surgically corrected) and in men whose mothers used diethylstilbestrol during pregnancy. Exposure to certain chemicals, infection with human immunodeficiency virus, and a family history of testicular cancer increase risk. (Testicular cancer accounts for 1% of all cancers in men.)
Testicular cancer spreads through the lymphatic system to the para-aortic, iliac, and mediastinal lymph nodes and may metastasize to the lungs, liver, viscera, and bone.

Signs and symptoms
The first sign is usually a firm, painless, smooth testicular mass, varying in size and sometimes producing a sense of testicular heaviness. When such a tumor causes chorionic gonadotropin or estrogen production, gynecomastia and nipple tenderness may result.
In advanced stages, signs and symptoms include ureteral obstruction, abdominal mass, cough, hemoptysis, shortness of breath, weight loss, fatigue, pallor, and lethargy.

Benign Prostatic Hyperplasia

Introduction

Although most men older than age 50 have some prostatic enlargement, with benign prostatic hyperplasia (BPH), the prostate gland enlarges sufficiently to compress the urethra and cause some overt urinary obstruction. Depending on the size of the enlarged prostate, the age and health of the patient, and the extent of obstruction, BPH is treated symptomatically or surgically.

Causes
Recent evidence suggests a link between BPH and hormonal activity. As men age, production of androgenic hormones decreases, causing an imbalance in androgen and estrogen levels and high levels of dihydrotestosterone, the main prostatic intracellular androgen. Other causes include neoplasm, arteriosclerosis, inflammation, and metabolic or nutritional disturbances.
Whatever the cause, BPH begins with changes in periurethral glandular tissue. As the prostate enlarges, it may extend into the bladder and obstruct urinary outflow by compressing or distorting the prostatic urethra. BPH may also cause a pouch to form in the bladder that retains urine when the rest of the bladder empties. This retained urine may lead to calculus formation or cystitis.

Signs and symptomsSigns and symptoms of BPH depend on the extent of prostatic enlargement and the lobes affected.

Urinary symptoms
Characteristically, the condition starts with a group of symptoms known as prostatism: reduced urinary stream caliber and force, difficulty starting micturition (straining), feeling of incomplete voiding and, occasionally, urine retention. As obstruction increases, urination becomes more frequent, with nocturia, incontinence and, possibly, hematuria.

Physical examination reveals a visible midline mass (distended bladder) that represents an incompletely emptied bladder; rectal palpation discloses an enlarged prostate. The examination may also detect secondary anemia and, possibly, renal insufficiency secondary to obstruction.

Later effects
As BPH worsens, complete urinary obstruction may follow infection. Complications include infection, renal insufficiency, hemorrhage, and shock.

Necrotizing Enterocolitis

Neonatal necrotizing enterocolitis (NEC) is a clinical condition characterized by an initial mucosal intestinal injury that may progress to transmural bowel necrosis. Although NEC is common, its cause is unknown. NEC is the leading surgical emergency in neonates in North America.
Infectious complications associated with bowel necrosis include bacterial peritonitis, systemic sepsis, and intra-abdominal abscess formation.

Causes
NEC usually occurs in premature neonates (less than 34 weeks’ gestation) and those of low birth weight (less than 5 lb [2.3 kg]). NEC is occurring in more neonates, possibly because of the higher incidence and survival of premature and low-birth-weight neonates.

Possible risk factorsNEC can develop when the infant suffers perinatal hypoxemia due to shunting of blood from the gut to more vital organs. Subsequent mucosal ischemia provides an ideal medium for bacterial growth. Hypertonic formula may increase bacterial activity because—unlike maternal breast milk—it doesn’t provide protective immunity and because it contributes to the production of hydrogen gas. As the bowel swells and its integrity breaks down, gas-forming bacteria invade damaged areas, producing free air in the intestinal wall. This may result in fatal perforation and peritonitis.

Signs And Symptoms

• Any infant who has suffered from perinatal hypoxemia has the potential for developing NEC. 
• A distended (especially tense or rigid) abdomen, with gastric retention, is the earliest and most common sign of oncoming NEC, usually appearing from 1 to 10 days after birth.
• Other signs and symptoms include increasing residual gastric contents (which may contain bile), bilious vomitus, and occult or gross blood in stools. One-fourth of patients have bloody diarrhea. 
• A red or shiny, taut abdomen may indicate peritonitis.
• Nonspecific signs and symptoms include thermal instability, lethargy, metabolic acidosis, jaundice, and disseminated intravascular coagulation (DIC). 
• The major complication is perforation, which requires surgery.
• Recurrence of NEC and mechanical and functional abnormalities of the intestine, especially stricture, are the usual cause of residual intestinal malfunction in any infant who survives acute NEC. They may develop as late as 3 months postoperatively.

Thyroid cancer - A Short Discussion

Thyroid cancer occurs in all age groups, especially in persons who have had radiation treatment to the neck area. 

Papillary and follicular carcinomas are most common and are usually associated with prolonged survival.

Papillary carcinoma accounts for half of all thyroid cancers in adults; it’s most common in young adult females and metastasizes slowly. It’s the least virulent form of thyroid cancer. 

Follicular carcinoma is less common but more likely to recur and metastasize to the regional nodes and through blood vessels into the bones, liver, and lungs.

Medullary carcinoma originates in the parafollicular cells derived from the last branchial pouch and contains amyloid and calcium deposits. It can produce calcitonin, histaminase, corticotropin (producing Cushing’s syndrome), and prostaglandin E2 and F3 (producing diarrhea).
This rare form of thyroid cancer is familial, associated with pheochromocytoma, and completely curable when detected before it causes symptoms. Untreated, it progresses rapidly.
Seldom curable by resection, giant and spindle cell cancer (anaplastic tumor) resists radiation and metastasizes rapidly.

Causes
Predisposing factors include radiation exposure, prolonged thyrotropin stimulation (through radiation or heredity), familial predisposition, or chronic goiter.

Signs and symptoms
The primary signs of thyroid cancer are a painless nodule, a hard nodule in an enlarged thyroid gland, or palpable lymph nodes with thyroid enlargement. Eventually, the pressure of such a nodule or enlargement causes hoarseness, dysphagia, dyspnea, and pain on palpation.
If the tumor is large enough to destroy the gland, hypothyroidism follows, with its typical symptoms of low metabolism (mental apathy and sensitivity to cold). However, if the tumor stimulates excess thyroid hormone production, it induces symptoms of thyrotoxicosis (sensitivity to heat, restlessness, and hyperactivity).
Other clinical features include diarrhea, anorexia, irritability, vocal cord paralysis, and symptoms of distant metastasis.

Abdominal Aneurysm

Abdominal aneurysm, an abnormal dilation in the arterial wall generally occurs in the aorta between the renal arteries and iliac branches. 

Such aneurysms are four times more common in men than in women and are most prevalent in whites ages 50 to 80. More than 50% of all people with untreated abdominal aneurysms die within 2 years of diagnosis, primarily from rupture of the aneurysm; more than 85%, within 5 years.

Causes
About 95% of abdominal aortic aneurysms result from arteriosclerosis; the rest, from cystic medial necrosis, trauma, syphilis, and other infections. These aneurysms develop slowly.
First, a focal weakness in the muscular layer of the aorta (tunica media), due to degenerative changes, allows the inner layer (tunica intima) and outer layer (tunica adventitia) to stretch outward. Blood pressure within the aorta progressively weakens the vessel walls and enlarges the aneurysm.

Signs and symptoms

• Although abdominal aneurysms usually don’t produce symptoms, most are evident (unless the patient is obese) as a pulsating mass in the periumbilical area, accompanied by a systolic bruit over the aorta. Some tenderness may be present on deep palpation. A large aneurysm may produce symptoms that mimic renal calculi, lumbar disk disease, and duodenal compression. Abdominal aneurysms rarely cause diminished peripheral pulses or claudication unless embolization occurs.
• Pain, rupture, and hemorrhage
• Lumbar pain that radiates to the flank and groin from pressure on lumbar nerves may signify enlargement and imminent rupture. If the aneurysm ruptures into the peritoneal cavity, it causes severe, persistent abdominal and back pain, mimicking renal or ureteral colic.
• Signs and symptoms of hemorrhage—such as weakness, sweating, tachycardia, and hypotension—may be subtle because rupture into the retroperitoneal space produces a tamponade effect that prevents continued hemorrhage. Patients with such rupture may remain in stable condition for hours before shock and death occur, although 20% die immediately.

Introduction to Breast cancer

Breast cancer is the most common cancer affecting women and is the number two killer (after lung cancer) of women ages 35 to 54. It occurs in men, though only rarely. (See Breast cancer in men.) The overall breast cancer death rate for American women has fallen. Lymph node involvement is the most valuable prognostic predictor. With adjuvant therapy, 70% to 75% of women with negative nodes will survive 10 years or more, compared with 20% to 25% of women with positive nodes.
Although breast cancer may develop anytime after puberty, it’s most common after age 50.

Causes
The cause of breast cancer is unknown, but its high incidence in women implicates estrogen. Certain predisposing factors are clear; women at high risk include those who:

• have a family history of breast cancer
• have long menses; began menses early or menopause late
• have never been pregnant
• were first pregnant after age 31
• have had unilateral breast cancer
• have had endometrial or ovarian cancer
• have been exposed to low-level ionizing radiation.

Many other predisposing factors have been investigated, including estrogen therapy, antihypertensives, high-fat diet, obesity, and fibrocystic disease of the breasts.

Women at lower risk include those who:

• were pregnant before age 20
• have had multiple pregnancies
• are Indian or Asian.

Pathophysiology
Breast cancer is more common in the left breast than in the right and more common in the upper outer quadrant. Growth rates vary. Theoretically, slow-growing breast cancer may take up to 8 years to become palpable at 1 cm in size. It spreads by way of the lymphatic system and the bloodstream, through the right side of the heart to the lungs and, eventually, to the other breast, the chest wall, liver, bone, and brain.
Many refer to the estimated growth rate of breast cancer as doubling time, or the time it takes the malignant cells to double in number. Survival time for breast cancer is based on tumor size and spread; the number of involved nodes is the single most important factor in predicting survival time.

Classified by histologic appearance and location of the lesion, breast cancer may be:
adenocarcinoma—arising from the epithelium
intraductal—developing within the ducts (includes Paget’s disease)
infiltrating—occurring in parenchymatous tissue of the breast
inflammatory (rare)—reflecting rapid tumor growth, in which the overlying skin becomes edematous, inflamed, and indurated
lobular carcinoma in situ—reflecting tumor growth involving lobes of glandular tissue
medullary or circumscribed—a large tumor with a rapid growth rate.