Patho Flashcards

(86 cards)

1
Q

Gastrointestinal system consumes, digests, & eliminates food

A

Includes
Upper division: oral cavity, pharynx, esophagus, and stomach

Lower division: small intestine, large intestine, and anus

Hepatobiliary system: liver, gallbladder, and pancreas

Four layers: mucosa, submucosa, muscle, and serosa
Mucus facilitates movement of contents and protects tissue from low pH

Peritoneum: large serous membrane that lines the abdominal cavity

Parietal peritoneum: outer layer

Visceral peritoneum: inner layer

Peritoneal cavity: space between the two layers

Mesentery: double-layer peritoneum with blood vessels/nerves supplying intestinal wall

Peristalsis: wavelike contractions that push food through GI tract

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2
Q

Food enters through the mouth to begin chemical and mechanical digestion (mastication)

A

Swallowing coordinated by swallowing center in medulla and cranial nerves (V, IX, X, XII)
Aspiration: when food enters the trachea and lungs through the esophagus
Esophagus: a tube of muscular rings to peristaltically guide food to the stomach
Lower esophageal sphincter (LES): opens to allow food into stomach, closing prevents reflux
Stomach: expandable food and liquid reservoir
Rugae: wrinkles formed in the empty stomach wall
Chyme: highly acidic mix of food and gastric juices
Pyloric sphincter: where chyme exits the stomach into the intestines

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3
Q

LIVER

A

Main functions
Metabolize carbohydrates, protein, and fats

Synthesize glucose, protein, cholesterol, triglycerides, and clotting factors

Store glucose, fats, and micronutrients and release when needed

Detoxify blood of potentially harmful chemicals

Maintain intravascular fluid volume

Produce bile

Inactivate and prepare hormones for excretion

Remove damaged or old erythrocytes to recycle iron and protein

Serve as a blood reservoir

Convert fatty acids to ketones

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4
Q

Gallbladder

A

stores bile produced by the liver

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5
Q

Portal vein

A

carries partially deoxygenated blood from GI tract to liver

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6
Q

Hepatic artery

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carries oxygenated blood to liver

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7
Q

Endocrine function

A

produces hormones to help regulate blood glucose

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8
Q

Exocrine functions

A

produces enzymes, electrolytes, and water necessary for digestion

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9
Q

Lower GI Tract

A

Continues digestion
Absorbs nutrients and water

Small intestine: longest section of GI tract for nutrient absorption

Cecum: small pouch ending the small intestine

Appendix: vestigial organ attached to cecum

Large intestine: deep crypts

Colon: absorbs water and electrolytes

Feces: waste with undigested or unabsorbed remnants and

bacteria

Rectum: reservoir to store feces

Defecation: reflex elicited through spinal cord to eliminate waste

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10
Q

GI Changes Associated with Aging

A

Atrophic gastritis

Achlorhydria

Vitamin B12 deficiency

Decreased digestion

Decreased peristalsis

Changes in lactose, calcium, and iron metabolism and absorption

Liver experiences reduced blood flow, delayed drug clearance, and diminished regeneration capacity.

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11
Q

Altered nutrition

A

These conditions include issues consuming, digesting, and absorbing food.
Affected individuals are often underweight and vitamin deficient.

Disorders of the liver: hepatitis, cirrhosis
Disorders of the pancreas: pancreatitis

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12
Q

Impaired elimination

A

These conditions may be symptoms of another secondary condition, or the primary one.
alter nutrition as well as impair elimination

Disorders of the lower GI tract: diarrhea, constipation, intestinal obstruction, appendicitis, peritonitis, celiac disease, inflammatory bowel disease, irritable bowel syndrome, diverticular disease

Cancers: oral cancer, esophageal cancer, gastric cancer, liver cancer, pancreatic cancer, colorectal cancer

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13
Q

Cleft Lip and Cleft Palate

A

Common multifactorial congenital defects of the mouth and face that are apparent at birth and vary in severity; usually develop at 4–9 weeks’ gestation

Associated with genetic mutations, drugs, toxins, viruses, vitamin deficiencies, and cigarette smoking

Most frequent in American Indians, Hispanics, and Asians; African Americans are least likely to develop cleft palate

Males twice as likely to have a cleft lip; females twice as likely to have a cleft palate

Can affect one’s appearance and may lead to feeding issues, speech problems, ear infections, and hearing problems

Cleft lip results from failure of the maxillary processes and nasal elevations or upper lip to fuse during development

Cleft palate results from failure of the hard and soft palate to fuse in development, creating an opening between the oral and nasal cavity

May occur separately or together, unilaterally or bilaterally

Teeth and nose malformations may also be present

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14
Q

Esophageal atresia

A

Incomplete formation of the esophagus
The exact cause is unknown, but associated with

VACTERL (vertebral anomalies, anal atresia, cardiac malformations, tracheoesophageal fistula, esophageal atresia, renal anomalies and radial aplasia, and limb anomalies) and

CHARGE (coloboma, heart defects, atresia of the choanae, retardation of mental and/or physical development, genital hypoplasia, and ear abnormalities)

Risk factors: increased paternal age and maternal use of assisted reproduction

Clinical Manifestations: excessive secretions, coughing, vomiting, and cyanosis after feeding

Possible Complication: aspiration pneumonia

Diagnosis: rarely in utero, commonly after birth; based on history, exam, prenatal ultrasound, postnatal nasogastric or orogastric tube placement

Treatment: surgical repair is the primary treatment

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15
Q

Pyloric stenosis (infantile hypertrophic pyloric stenosis)

A

Narrowing and obstruction of the pyloric sphincter

pyloric sphincter become thick and stiff, making it difficult for the stomach to empty food into the small intestine

May be present at birth or develop later in life

Most cases present at approximately 3 weeks of life

The exact cause of pyloric stenosis is unknown, but it is thought to be multifactorial

Exposure to macrolides (category of antibiotics) in early infancy leads to increased pyloric stenosis risk

Most common in Caucasians and males

Manifestations appear within several weeks after birth and include a hard mass in the abdomen, regurgitation, projectile vomiting, wavelike stomach contractions, small and infrequent stools, failure to gain weight, dehydration, and irritability

Diagnosis: history, physical examination, abdominal ultrasound, barium X-ray, endoscopy, arterial blood gases, and blood chemistry

Treatment: surgical repair called pyloromyotomy or balloon dilation

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16
Q

Dysphagia

A

Difficulty swallowing

Causes: congenital atresia, esophageal stenosis or stricture, esophageal diverticula, tumors, stroke, cerebral damage, achalasia, Parkinson’s disease, Alzheimer’s disease, muscular dystrophy, Huntington’s disease, cerebral palsy, multiple sclerosis, amyotrophic lateral sclerosis, and Guillain-Barré syndrome

Manifestations: a sensation of food being stuck in the throat, choking, coughing, “pocketing” food in the cheeks, difficulty forming a food bolus, delayed swallowing, and odynophagia

Diagnosis: history, physical examination, barium swallow, chest and neck X-ray, esophageal pH measurement, esophageal manometry, and esophagogastroduodenoscopy

Treatment: specific for the causative condition but usually includes speech therapy

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17
Q

Vomiting (emesis):

A

involuntary or voluntary forceful ejection of chyme from the stomach up through the esophagus and out the mouth

Causes: protection (infection), reverse peristalsis, increased intracranial pressure, and severe pain
Coordinated by the medulla:
Deep breath is taken
Glottis closes and soft palate rises
Respirations cease to minimize aspiration risk
Gastroesophageal sphincter relaxes
Abdominal muscles contract, squeezing stomach against diagram to force chyme upwards
Reverse peristaltic waves eject chyme from the mouth
May be preceded by nausea
Recurrent vomiting can lead to fluid, electrolyte, and pH imbalances

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18
Q

Vomiting

A

Aspiration can cause serious damage and inflammation and can occur when supine, unconscious, or the vomiting or cough reflex is suppressed

Hematemesis: blood in the vomitus

Has a characteristic “coffee grounds” appearance resulting from protein in the blood being partially digested

Blood is irritating to the gastric mucosa

Can occur from any conditions that cause upper GI bleeding

Yellow or green vomitus usually indicates the presence of bile

Can occur as a result of a GI tract obstruction

A deep brown vomitus may indicate content from the lower intestine

Frequently results from intestinal obstruction

Undigested food vomitus is caused by conditions that impair gastric emptying

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19
Q

Disorders of the Upper GI Tract: Vomiting (Diagnosis & Treatment)

A

Disorders of the Upper GI Tract: Vomiting (Diagnosis & Treatment)

BRAT diet
bananas, rice, apple sauce, toast

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20
Q

Hiatal Hernia

A

A stomach section protrudes upward through an opening in the diaphragm toward the lung

Causes: weakening of the diaphragm muscle, frequently resulting from increased intrathoracic pressure or increased intra-abdominal pressure; trauma; congenital defects

Risk factors: advanced age and smoking

Manifestations include indigestion, heartburn, frequent belching, nausea, chest pain, strictures, dysphagia, and soft upper abdominal mass (protruding stomach pouch)
Worsen with recumbent positioning, eating (especially after large meals), bending over, coughing

Diagnosis: history, physical examination, barium swallow, upper GI tract X-rays, manometry, and esophagogastroduodenoscopy

Treatment: small frequent meals (six small meals a day), avoiding alcohol, assuming a high Fowler’s position after meals, sleeping with head of bed elevated 6 inches, ceasing smoking, reducing stress (stress increases gastrointestinal ischemia), antacids, acid-reducing agents, mucosal barrier agents, and surgical repair

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21
Q

Gastroesophageal reflux disease (GERD):

A

chyme or bile periodically backs up from the stomach into the esophagus, irritating the esophageal mucosa

Causes: certain foods (e.g., chocolate, caffeine, carbonated beverages, citrus fruit, tomatoes, spicy or fatty foods, and peppermint), alcohol consumption, nicotine, hiatal hernia, obesity, pregnancy, certain medications (e.g., corticosteroids, beta blockers, calcium-channel blockers, and anticholinergics), nasogastric intubation, and delayed gastric emptying

Manifestations: heartburn, epigastric pain (usually after a meal or when recombinant), dysphagia, dry cough, laryngitis, pharyngitis, regurgitation of food, and sensation of a lump in the throat
Often confused with angina and may warrant ruling out cardiac disease

Complications: esophagitis, strictures, ulcerations, esophageal cancer, and chronic pulmonary disease

Diagnosis: history, physical examination, barium swallow, esophagogastroduodenoscopy, esophageal pH monitoring, and esophagus manometry

Treatment: avoid triggers, avoid clothing that is restrictive around the waist, eat small frequent meals, high Fowler’s positioning 2–3 hours after meals, weight loss, stress reduction, elevate the head of the bed approximately 6 inches, antacids, acid-reducing agents, mucosal barrier agents, herbal therapies (e.g., licorice, slippery elm, and chamomile), and surgery

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22
Q

Peptic ulcer disease (PUD)

A

lesions affecting stomach lining or duodenum

Risk factors: being male, advancing age, nonsteroidal anti-inflammatory drug use, H. pylori infections, certain gastric tumors, and those for GERD (e.g., smoking and alcohol use)

Vary in severity from superficial erosions to complete penetration; develops from an imbalance between destructive forces and protective mechanisms

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23
Q

Stress Ulcers

A

Develop because of a major physiological stressor on the body due to local tissue ischemia, tissue acidosis, bile salts entering the stomach, and decreased GI motility

Curling’s ulcers: stress ulcers associated with burns

Cushing’s ulcers: stress ulcers associated with head injuries

Most frequently develop in the stomach; ulcers can form within hours of an event; often hemorrhage is first indicator as ulcer develops rapidly and is masked by primary problem

Complications: GI hemorrhage, obstruction, perforation, and peritonitis

Manifestations: epigastric or abdominal pain, abdominal cramping, heartburn, indigestion, nausea, and vomiting

Diagnosis: history, physical examination, upper GI tract X-ray, esophagogastroduodenoscopy, serum H. pylori antibody levels, H. pylori breath test, and stool analysis (H. pylori and occult blood)

Treatment resembles gastritis treatment, surgical repair, and prophylactic meds

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24
Q

Cholelithiasis (gallstones)

A

a common condition that varies in severity based on size of stone

Cholecystitis: inflammation or infection in the biliary system caused by calculi

Risk factors: advancing age, obesity, diet, rapid weight loss, pregnancy, hormone replacement, and long-term parenteral nutrition. May obstruct bile flow and cause gallbladder rupture, fistula formation, gangrene, hepatitis, pancreatitis, and carcinoma

Manifestations: biliary colic, abdominal distension, nausea, vomiting, jaundice, fever, and leukocytosis

Diagnosis: history, physical examination, abdominal X-ray, gallbladder ultrasound, and laparoscopy

Treatment: low-fat diet, medications to dissolve the calculi (e.g., bile acids), antibiotic therapy, nasogastric tube with intermittent suction, lithotripsy, choledochostomy (surgery to create an opening for drainage), and laparoscopic removal of calculi or gallbladder

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25
Hepatitis
Inflammation of the liver Causes: infections (usually viral), alcohol, medications (e.g., acetaminophen [Tylenol], antiseizure agents, and antibiotics), or autoimmune disease Nonviral hepatitis is non contagious and most will recover May develop liver failure, liver cancer, or cirrhosis Viral hepatitis is contagious but most will recover with sufficient time Advancing age and comorbidity increase the likelihood that liver failure, liver cancer, or cirrhosis will develop Can result in hepatic cell destruction, necrosis, autolysis, hyperplasia, and scarring Diagnosis: history, physical examination, serum hepatitis profile, liver enzyme panel, clotting studies, liver biopsy, and abdominal ultrasound Treatment: vaccinations, limiting exposure, and other preventatives; some may be treated with interferon and antivirals, others with rest and nutrition
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Fulminant hepatitis
Uncommon, rapidly progressing form that can lead to liver failure, hepatic encephalopathy, or death within 3 weeks
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Cirrhosis
Chronic, progressive, irreversible, diffuse damage to the liver resulting in decreased liver function; may develop over 40 years even if underlying cause is addressed Leads to fibrosis, nodule formation, impaired blood flow, and bile obstruction that can result in liver failure Causes: hepatitis and all those factors that can lead to hepatitis Hepatitis C infection and chronic alcohol abuse are the most frequent causes of cirrhosis in the United States Manifestations: portal hypertension, ascites, jaundice, varicosities, enlarged organs, slow or severe bleeding, clotting changes, muscle wasting, hyperlipidemia, hyper- or hypoglycemia, toxin and bile accumulation, clay-colored stools and dark urine, intense itchiness Diagnosis: history, physical examination, liver biopsy, abdominal X-ray, liver enzyme panel, esophagogastroduodenoscopy, clotting studies, and stools examination (for occult blood) Treatment complex and varies depending on the underlying cause Hepatitis-related cirrhosis will be treated with antiviral agents and interferon Avoid alcohol, drugs, and hepatotoxic medication
28
Cirrhosis
``` Nutritional imbalances (usually treated with total parenteral nutrition [TPN]) and metabolic dysfunction are corrected Bile acid–binding agents can aid bile excretion; antacids or acid-reducing agents Fluid restriction, low-sodium diet, diuretics, paracentesis, and shunts treat ascites ``` Portal hypertension is treated with a surgically implanted shunt Esophageal varices are treated with endoscopic bands, shunts, or sclerotherapy Encephalopathy is treated by eliminating the source of protein breakdown Lactulose can promote ammonia excretion in the stools; antibiotics can be given to suppress intestinal flora and decrease endogenous ammonia production
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Disorders of the Pancreas: Pancreatitis
Inflammation of the pancreas, acute or chronic Causes: cholelithiasis, alcohol abuse, biliary dysfunction, hepatotoxic drugs, metabolic disorders, trauma, renal failure, endocrine disorders, pancreatic tumors, and penetrating peptic ulcer Pancreatic injury causes pancreatic enzymes to leak into the pancreatic tissue and initiate autodigestion, resulting in edema, vascular damage, hemorrhage, and necrosis Pancreatic tissue is replaced by fibrosis, which causes exocrine and endocrine changes and dysfunction of the islets of Langerhans Acute pancreatitis is considered a medical emergency Mortality increases with advancing age and comorbidity Complications: acute respiratory distress syndrome, diabetes mellitus, infection, shock, disseminated intravascular coagulation, renal failure, malnutrition, pancreatic cancer, pseudocyst, and abscess Clinical manifestations of acute pancreatitis are usually sudden and severe Upper abdominal pain that radiates to the back, worsens after eating, and is somewhat relieved by leaning forward or pulling the knees toward the chest Nausea and vomiting Mild jaundice Low-grade fever Blood pressure and pulse changes ``` Manifestations of chronic pancreatitis tend to be insidious: Upper abdominal pain Indigestion Losing weight without trying Steatorrhea Constipation Flatulence ``` Diagnosis: history, physical examination, serum amylase and lipase levels, serum calcium levels, complete blood count, liver enzymes panel, serum bilirubin level, arterial blood gases, stool analysis (lipid and trypsin levels), abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, abdominal ultrasound, and endoscopic retrograde cholangiopancreatography Treatment includes close monitoring and aggressive management Resting the pancreas by fasting, administering intravenous nutrition, and gradually advancing diet from clear liquids as tolerated to low fat Pancreatic enzyme supplements when diet is resumed; antacids and acid-reducing agents Maintaining hydration status with intravenous fluids Nasogastric tube with intermittent suction plus antiemetic agents Pain management, anticholinergic agents, antibiotic therapy, insulin Identifying and treating complications early  
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Diarrhea
Change in bowel pattern characterized by an increased frequency, amount, and water content of the stool Results because of increased fluid secretion, decreased fluid absorption, or an alteration in GI peristalsis Acute diarrhea is often self-limiting (depending on cause) Often caused by viral or bacterial infections or certain medications (e.g., antibiotics, antacids, and laxatives) Chronic diarrhea lasts longer than 4 weeks /Causes: inflammatory bowel diseases, malabsorption syndromes, endocrine disorders, chemotherapy, and radiation Originating in the small intestine Stools are large, loose, and provoked by eating Usually accompanied by pain in the right lower quadrant Originating in the large intestine Stools are small and frequent Frequently accompanied by pain and cramping in the left lower quadrant Acute diarrhea is generally infectious and accompanied by cramping, fever, chills, nausea, and vomiting; bowel sounds may be hyperactive and fluids imbalanced Blood (may be frank, occult, or melena), pus, or mucus may be present Diagnosis: history (including usual bowel pattern and completion of the Bristol Stool chart), physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, arterial blood gases, and abdominal ultrasound Treatments: fasting, antidiarrheals, antibiotics, anticholinergics, antispasmodics, diet Dietary fiber helps manage chronic diarrhea, as well as maintaining hydration status and correcting electrolyte and pH imbalances Meticulous skin care in cases of bowel incontinence
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Constipation
Change in bowel pattern characterized by infrequent passage of stool in reference to the individual’s typical bowel pattern Stool remains in the large intestine longer than usual, increasing the amount of water removed Causes: low-fiber diet, inadequate physical activity, insufficient fluid intake, delaying the urge to defecate, laxative abuse, stress, travel, bowel diseases, certain medications, mental health problems, neurologic diseases, and colon cancer Manifestations: pain during bowel movement, inability to pass stool, hypoactive bowel sound Complications: anal bleeding, anal fissure, pH disturbances, hemorrhoids, diverticulitis, impaction, intestinal obstruction, and fistulas Diagnosis: history, examination (may include a digital examination), imaging Treatment: increasing dietary fiber and hydration, increasing physical activity, defecating when urge is sensed, stool softeners, laxatives and enemas, and digital removal
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Intestinal Obstruction
Sudden or gradual, partial or complete blockage of intestinal contents in intestines Causes: Mechanical obstructions: foreign bodies, tumors, adhesions, hernias, intussusception, volvulus, strictures, Crohn’s disease, diverticulitis, Hirschsprung’s disease, and fecal impaction Functional obstructions (also called paralytic ileuses): neurologic impairment; intra-abdominal surgery complications; chemical, electrolyte, and mineral disturbances; infections; abdominal blood supply impairment; renal and lung disease; and medications (e.g., narcotics) Chyme and gas accumulate at the site of the blockage; saliva, gastric juices, bile, and pancreatic secretions begin to collect as the blockage lingers Serum electrolytes and protein increase, causing abdominal distension and pain Intestinal blood flow impairment: strangulation, necrosis, contents seep into abdomen Complications: perforation, pH imbalances, fluid disturbances, shock, and death Manifestations: abdominal distension, abdominal cramping, colicky pain, nausea, vomiting, constipation, diarrhea, borborygmi, intestinal rushes, decreased or absent bowel sounds, restlessness, diaphoresis, tachycardia progressing to weakness, confusion, and shock Diagnosis: history (including usual bowel pattern), physical examination, blood chemistry, arterial blood gases, complete blood gases, abdominal computed tomography, abdominal X-ray, abdominal ultrasound, sigmoidoscopy, and colonoscopy Treatment strategies depend on the underlying causes: Correcting fluid, electrolyte, and pH imbalances, Nasogastric tube with intermittent suctioning , Fasting and total parenteral nutrition until bowel function is restored, Ambulation, Laxatives should be avoided in most cases until the obstruction is resolved, Surgery
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Appendicitis
Inflammation of the vermiform appendix, most often caused by an infection Triggers local tissue edema, which obstructs the small structure As fluid builds inside the appendix, microorganisms proliferate Appendix fills with purulent exudate and area blood vessels become compressed Ischemia and necrosis develop; pressure inside the appendix escalates, forcing bacteria and toxins out to surrounding structures Complications: abscesses, peritonitis, gangrene, and death Manifestations vary from asymptomatic to sudden and severe Sharp abdominal pain develops, gradually intensifies (over about 12–24 hours), and becomes localized to the lower right quadrant of the abdomen (McBurney point) Pain may occur anywhere in abdomen; will temporarily subside if the appendix ruptures, and then the pain will return and escalate Manifestations Nausea, vomiting, abdominal distension, and bowel pattern changes Indications of inflammation and infection (e.g., fever, chills, and leukocytosis) Indications of peritonitis (e.g., abdominal rigidity, tachycardia, and hypotension) Urgent diagnosis and treatment are crucial Diagnosis: history, physical examination, complete blood count, abdominal ultrasound, abdominal X-ray, abdominal computed tomography, and laparoscopy Treatment Surgery, either laparoscopic or open, and may include extensive irrigation Drainage tubes Long-term antibiotic therapy Analgesics Avoid activities that increase intra-abdominal pressure (e.g., straining and coughing
34
Peritonitis
Inflammation of the peritoneum activates several protective mechanisms A thick, sticky exudate that bonds nearby structures and temporarily seals them off Abscesses may form in an attempt to wall off the infections Peristalsis may slow down in a response to the inflammation, decreasing spread of toxins/bacteria Causes: chemical irritation (e.g., ruptured gallbladder or spleen) or direct organism invasion (e.g., appendicitis and peritoneal dialysis) Manifestations usually sudden and severe; classical manifestation is abdominal rigidity Abdominal tenderness and pain, decreased peristalsis, intestinal obstruction, nausea/vomiting Large volumes of fluid leak into the peritoneal cavity Indicators of infection, sepsis, or shock Diagnosis: history, exam, CBC, imaging, paracentesis with fluid analysis, laparotomy Treatment: surgical repair, long-term antibiotic therapy, correcting fluid and electrolyte imbalances, nasogastric tube insertion with intermittent suction, and total parenteral nutrition
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Disorders of the Lower GI Tract: IBD (Inflammatory Bowel Disease)
Term for two conditions (Crohn's disease and ulcerative colitis) that are characterized by chronic inflammation of the GI Tract Chiefly seen in women, Caucasians, persons of Jewish descent, and smokers Characterized by periods of exacerbations and remissions Thought to be caused by a genetically associated autoimmune state that has been activated by an infection Immune cells located in the intestinal mucosa are stimulated to release inflammatory mediators that alter the function and neural activity of the secretory and smooth muscle cells Fluid, electrolyte, and pH imbalances develop Can be painful, debilitating, and life-threatening
36
Crohns Disease
Crohn’s disease Insidious, slow-developing, progressive condition often develops in adolescence Characterized by patchy areas of inflammation involving the full thickness of the intestinal wall and ulcerations (skip lesions); wall is thick/rigid and lumen is narrowed Form fissures divided by nodules, giving the intestinal wall a cobblestone appearance Granulomas develop on the intestinal wall and nearby lymph nodes The damaged intestinal wall loses the ability to digest and absorb The inflammation also stimulates intestinal motility, decreasing digestion and absorption Complications: malnutrition; anemia (especially iron deficiency); fistulas; adhesions; abscesses; intestinal obstruction; perforation; anal fissure; delayed growth and development; and fluid, electrolyte, and pH imbalances Manifestations: abdominal cramping and pain (typically in the right lower quadrant), diarrhea, steatorrhea, constipation, palpable abdominal mass, melena, anorexia, weight loss, and indications of inflammation (e.g., fever, fatigue, arthralgia, and malaise) Diagnosis: history, physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium studies (swallow and enema), sigmoidoscopy, colonoscopy, and biopsy Treatment: low-residue, high-calorie, high-protein diet; oral nutritional supplements; multivitamin supplements; total parenteral nutrition; antidiarrheal agents; aminosalicylates (5-ASAs); glucocorticoids; immune modulators; biologic agents; analgesics; antibiotics; surgical intestine resection; stress management; and support
37
Ulcerative colitis
Progressive condition of the rectum and colon mucosa usually develops in 20s–30s Inflammation triggered by T-cell accumulation in the colon mucosa causes epithelium loss, surface erosion, and ulceration that begins in the rectum and extends to the entire colon Rarely affects the small intestine The mucosa becomes inflamed, edematous, and frail Necrosis of the epithelial tissue can result in abscesses; granulation tissue formed is fragile Ulcers merge into areas of stripped mucosa with inadequate surface area for absorption Complications: malnutrition; anemia; hemorrhage; perforation; strictures; fistulas; pseudopolyps; toxic megacolon; colorectal carcinoma; liver disease; and fluid, electrolyte, and pH imbalances Manifestations: diarrhea (usually frequent [as many as 20x daily], watery stools with blood and mucus), tenesmus, proctitis, abdominal cramping, nausea, vomiting, weight loss, and indications of inflammation (e.g., fever, fatigue, arthralgia, and malaise) Diagnosis: history, physical examination, stool analysis (including cultures and occult blood), complete blood count, blood chemistry, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance imaging, barium enema, colonoscopy, and biopsy Treatment: high-fiber, high-calorie, high-protein diet; oral nutritional supplements; multivitamin supplements; total parenteral nutrition; antidiarrheal agents; antispasmodics; anticholinergics; aminosalicylates (5-ASAs); glucocorticoids; immune modulators; biologic agents; analgesics; antibiotics; surgical intervention (e.g., ileostomy or colostomy); stress management; and support
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Disorders of the Lower GI Tract: IBS (Irritable Bowel Syndrome)
Chronic, noninflammatory, GI condition characterized by exacerbations associated with stress Includes alterations in bowel pattern and abdominal pain not explained by structural or biochemical abnormalities Less serious than IBD, is noninflammatory, and does not cause permanent intestinal damage; more common in women than men Three theories of its etiology: altered GI motility, visceral hyperalgesia, and psychopathology Intensified response to stimuli with increased intestinal motility and contractions—low tolerance for stretching and pain in the intestinal smooth muscle Complications: hemorrhoids, nutritional deficits, social issues, and sexual discomfort Manifestations Stress, mood disorders, food, and hormone changes often worsen symptoms Abdominal distension, fullness, flatus, and bloating Intermittent abdominal pain exacerbated by eating and relieved by defecation Diagnosis: history (including bowel pattern and Rome III criteria), stool analysis (including cultures and occult blood), celiac blood panel, abdominal X-ray, abdominal computed tomography, abdominal magnetic resonance, barium studies (swallow and enema), sigmoidoscopy, colonoscopy, and biopsy Treatment: antidiarrheal agents, laxatives, antispasmodics, antidepressants, avoid triggers, maintain adequate fiber intake, stress management, and support  
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Celiac Disease
Celiac sprue or gluten-sensitive enteropathy”: inherited, autoimmune, malabsorption disorder Results from a combination of the immune response to an environmental factor (gliadin) and genetic predisposition Most common in Caucasians and females; a childhood disease, but can develop at any age Tropical sprue is a related disorder that occurs in tropical regions and is thought to be caused by a bacterial, viral, parasitic, or amoebic infection Can be resolved with antibiotic therapy Results from a defect in the intestinal enzymes that prevents further digestion of gliadin (a product of gluten digestion) Intestinal villi atrophy and flatten, resulting in decreased enzyme production and making less surface area available for nutrient absorption Complications: anemia, arthralgia, myalgia, bone disease, dental enamel defects and discoloration, intestinal cancers, depression, growth and development delays in children, hair loss, hypoglycemia, mouth ulcers, increased bleeding tendencies, neurologic disorders, skin disorders, vitamin or mineral deficiency, and endocrine disorders Manifestations In infants, generally, appear as cereals are added to their diet (usually around 4–6 months of age) Include abdominal pain or distension, bloating, gas, indigestion, constipation, diarrhea, lactose intolerance, nausea, steatorrhea, weight loss, irritability, lethargy, malaise, behavioral changes Diagnosis: history, examine, duodenal biopsy, and celiac blood panel (includes immunoglobulin A antibody–endomysium antibodies, immunoglobulin A antigliadin antibodies, deamidated gliadin peptide antibody, immunoglobulin A anti-tissue transglutaminase, lactose tolerance test, and D-xylose test) Treatment: gluten-free diet, monitoring for cancer development, and long-term support
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Diverticular Disease
Conditions related to the development of diverticula, outwardly bulging pouches of the intestinal wall that occur when mucosa sections or large intestine submucosa layers herniate through a weakened muscular layer May be congenital or acquired Thought to be caused by a low-fiber diet and poor bowel habits that result in chronic constipation The muscular wall can become weakened from the prolonged effort of moving hard stools More common in developed countries where processed foods and low-fiber diets are typical Diverticulosis: asymptomatic diverticular disease, multiple diverticula present
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Oral Cancer
Most cases involve squamous cell carcinomas of the tongue and mouth floor Most common and most deadly in men, especially African Americans Very treatable if caught early, but most cases are advanced upon diagnosis Usually appears initially as one or more painless, whitish thickenings that develop into a nodule or an ulcerative lesion that persists, does not heal, and bleeds easily Additional manifestations: a lump, thickening, or soreness in the mouth, throat, or tongue as well as difficulty chewing or swallowing Risk factors: smoked and smokeless tobacco, alcohol consumption, viral infections (especially human papillomavirus), immunodeficiencies, inadequate nutrition, poor dental hygiene, chronic irritation, and exposure to ultraviolet light Often metastasizes to neck lymph nodes and esophagus Treatment: surgery, radiation, and speech therapy
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Esophageal Cancer
Usually a squamous cell carcinoma in the distal esophagus Most common in men Associated with chronic irritation Tumors grow the circumference of the esophagus, creating a stricture, or they can grow out into the lumen of the esophagus, creating an obstruction Complications: esophageal obstruction, respiratory compromise, and esophageal bleeding Usually asymptomatic early, delaying treatment Manifestations: dysphagia, chest pain, weight loss, and hematemesis Treatment: surgery, chemotherapy, radiation, and speech therapy
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Gastric Cancer
Occurs in several forms, but adenocarcinoma (an ulcerative lesion) is the most frequent type; asymptomatic early stages delay diagnosis and treatment Incidence and mortality rates have declined in the U.S., but remains extremely prevalent worldwide, especially in Japan Strongly associated with increased intake of salted, cured, pickled, preserved, and smoked foods Other risk factors: low-fiber diet, constipation, family history, H. pylori infections, smoking, pernicious anemia, chronic atrophic gastritis, and gastric polyps Manifestations: abdominal pain/fullness, epigastric discomfort, palpable abdominal mass, melena, dysphagia that worsens over time, excessive belching, anorexia, nausea, vomiting, hematemesis, premature abdominal fullness after meals, unintentional weight loss, weakness, and fatigue Treatment: gastrectomy, chemotherapy, radiation, and nutritional support
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Liver Cancer
Most commonly occurs as a secondary tumor that has metastasized from the breast, lung, or other GI structures Causes of primary tumors: chronic cirrhosis and hepatitis Manifestations similar to those of other liver diseases Include anorexia, fever, jaundice, nausea, vomiting, abdominal pain (usually in the upper right quadrant), hepatomegaly, splenomegaly, portal hypertension, edema, third spacing, ascites, paraneoplastic syndrome, diaphoresis, and weight loss Treatment varies depending on the primary site and progression of the cancer Chemotherapy, surgical removal, cryoablation, radiofrequency ablation Liver transplant Pure alcohol injected into the tumor
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Pancreatic Cancer
Aggressive malignancy that quickly metastasizes, usually adenocarcinoma Most frequent in men and African Americans Often asymptomatic until well advanced and has metastasized Risk factors: family history, obesity, chronic pancreatitis, long-standing diabetes mellitus, cirrhosis, alcohol abuse, and tobacco use Manifestations: progressive upper abdominal pain that may radiate to the back, jaundice, dark urine, clay-colored stools, indigestion, anorexia, weight loss, depression, malnutrition, hyperglycemia, and increased clotting tendencies Treatment: surgical tumor removal, chemotherapy, radiation, and surgery or endoscopy repair of any biliary blockages
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Colorectal Cancer
Very common and fatal in the U.S. and worldwide; often asymptomatic until advanced . Associated with fatty, caloric, low-fiber diets with red meat, processed meat, and alcohol Other risk factors: male gender, African American heritage, family history, advancing age, obesity, tobacco use, physical inactivity, and inflammatory bowel disease Manifestations: lower abdominal pain and tenderness, blood in the stool (occult or frank), diarrhea, constipation, intestinal obstruction, narrow stools, unexplained anemia (usually iron deficiency), and unintentional weight loss Routine screening can improve prognosis, including: High-sensitivity fecal occult blood test every year plus fecal immunochemical tests Flexible sigmoidoscopy every 5 years. Colonoscopy every 10 years Treatment: removal during colonoscopy, chemotherapy, surgical resection, colostomy, lifestyle changes (e.g., diet and physical activity), and follow-up screenings
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A&P
``` Urinary system regulates: Fluid volume Blood pressure Metabolic waste and drug excretion Vitamin D conversion Acid–base balance Hormone synthesis ``` Kidneys: located on either side of the vertebrae in retroperitoneal space Renal capsule: connective tissue surrounding the kidney Renal cortex: area immediately beneath the capsule, which contains the nephrons Renal artery: supplies each kidney with blood Renal hilum: opening in the kidney; renal artery and nerves enter, renal vein and ureter exit Renal sinus: cavity forms the renal pelvis Calyces: tubes through which urine drains into the renal pelvis Ureters: transport urine from calyces to bladder Bladder: muscular structure that serves as a reservoir for urine until it can be excreted Urethra: transports urine from bladder to urinary meatus Approximately 1.5 inches long in women and 6–8 inches long in men Shorter urethras in women, in combination with sitting for urination, increase women’s risk for developing urinary tract infections Urination (micturition) is a voluntary activity As urine volume in the bladder increases, the urine exerts pressure on the two bladder sphincters (internal and external) and stretch receptors in the bladder A pressure of 200 to 300 mL on the sphincters and receptors sends nerve impulses to the brain, triggering the urge to urinate The bladder contracts and the external sphincter relaxes, forcing urine out through the urethra Normal daily urine output is 1,500 mL Each kidney contains 1–2 million nephrons Each nephron contains multiple sections responsible for filtering specific substances Bowman’s capsule: double membrane that surrounds the glomerulus Glomerulus: a cluster of capillaries Blood enters the glomerulus through an afferent arteriole, leaves it through efferent Glomerular filtration rate: rate of blood flow through the glomerulus Best indicator of renal function, where normal is 125 mL/min Renin-angiotensin-aldosterone system regulates blood pressure, aided by water and electrolyte regulation in the kidneys Other hormonal influences include: Antidiuretic hormone Aldosterone Waste products: Ammonia is the product of deamination, which strips amino group from amino acid Urea and uric acid ``` Kidneys also: Convert vitamin D to its active form Secrete bicarbonate Excrete or retain hydrogen Synthesize atrial natriuretic peptide, erythropoietin, and renin ``` With age, kidneys function less efficiently Exacerbated by the presence of chronic conditions Increased risk for waste accumulation and loss of homeostatic regulation Other renal-related complications include anemia, hypertension, and osteoporosis Also at increased risk for drug toxicity 
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Altered Urinary Elimination: Incontinence
Urinary incontinence is loss of urinary control Enuresis: Involuntary urination by a child after 4–5 years of age Nocturnal enuresis: bed-wetting Causes may be psychological and structural, but usually resolves with or without treatment
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Stress incontinence
Loss of urine from pressure exerted on the bladder by coughing, sneezing, laughing, exercising, or lifting something heavy Occurs when the sphincter muscle of the bladder is weakened Contributing factors: pregnancy, childbirth, menopause, cystocele, prostate removal, obesity, and chronic coughing
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Overactive bladder (urge incontinence)
Sudden, intense urge to urinate, followed by an involuntary loss of urine Causes: urinary tract infections, bladder irritants, bowel conditions, smoking, Parkinson’s disease, Alzheimer’s disease, stroke, injury, and nervous system damage Overactive bladder: urge incontinence with no known cause
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Gastritis
Inflammation of the stomach’s mucosal lining (may involve the entire stomach or a region) Other causes: organisms transmitted through food and water contamination, long-term use of nonsteroidal anti-inflammatory drugs, excessive alcohol use, severe stress, autoimmune conditions, and other chronic diseases Manifestations include indigestion, heartburn, epigastric pain, abdominal cramping, nausea, vomiting, anorexia, fever, and malaise Hematemesis and dark, tarry stools can indicate ulceration and bleeding
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Reflex incontinence
Urinary incontinence caused by trauma or damage to the nervous system Detrusor hyperreflexia: increased detrusor muscle contractility that occurs even though there is no sensation to void Urgency is generally absent
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Mixed incontinence
Occurs when symptoms of more than one type of urinary incontinence are experienced
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Overflow incontinence
Inability to empty the bladder, or retention Other indications include dribbling urine and a weak urine stream. Causes: bladder damage, urethral blockage, nerve damage, and prostate conditions Chronic overdistension occurs because of a perceived inability to interrupt work to void that results in detrusor muscle areflexia and overflow incontinence
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Transient incontinence
Urinary incontinence resulting from a temporary condition Causes: delirium, infection, atrophic vaginitis, use of certain medications (e.g., diuretics and sedatives), psychological factors, high urine output, restricted mobility, fecal impaction, alcohol, and caffeine
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Gross total incontinence
Continuous leaking of urine, day and night, or the periodic uncontrollable leaking of large volumes of urine The bladder has no storage capacity Causes: anatomic defects; spinal cord or urinary system injuries; and fistulas between the bladder and an adjacent structure, such as the vagina. Risk factors: female gender, advancing age, being overweight, smoking, other diseases Complications: skin breakdown, recurrent urinary tract infections, negative psychological consequences, interruption of usual activities Diagnosis: history, physical examination, bladder diary, urinalysis, urine cultures, cystourethrogram, cystoscopy, pelvic ultrasound, postvoid residual measurement, and urodynamic testing Treatments: Bladder training, scheduled toileting, or fluid and diet management Pelvic floor muscle exercises, electric or sacral nerve stimulation, urethral inserts, pessaries Medications, botulinum toxin A or bulking material injections Radiofrequency therapy, acupuncture, hypnotherapy, or herbal remedies Artificial urinary sphincter, sling, or bladder neck suspension procedures Absorbent pads and protective garments/barrier creams Urinary catheter Good perineal hygiene Safety measures Coping strategies and support
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Altered Urinary Elimination: Neurogenic Bladder
Bladder dysfunction is caused by an interruption of normal bladder nerve innervation Causes: brain or spinal cord injury, nervous system tumors, brain or spinal cord infections, dementia, Parkinson’s disease, spina bifida, diabetes mellitus, stroke, medications, vaginal childbirth, multiple sclerosis, chronic alcoholism, systemic lupus erythematosus, heavy metal poisoning, and herpes zoster Manifestations: symptoms of an overactive and underactive bladder Diagnosis: history, physical examination, bladder diary, urinalysis, urine cultures, cystourethrogram, cystoscopy, pelvic ultrasound, postvoid residual measurement, and urodynamic testing Treatment depends on etiology and includes those for incontinence
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Cystitis/Bladder Pain Syndrome
Chronic bladder condition, more common in women and aging individuals, that causes pain and pressure in the suprapubic, pelvic, and abdominal area Nonulcerative IC/BPS constitutes 90% of all cases: Pinpoint hemorrhages in the bladder wall due to inflammation Ulcerative is 5–10% of all cases: Hunner ulcers/patches: red, bleeding areas on the bladder wall 5% experience symptoms for 2+ years, and 5% develop end-stage disease where bladder hardens, capacity is low, and pain worsens Manifestation: pain in urinary tract (often worse with pressure), frequency and nocturia, urgency (often constant, worsened by stress), sexual dysfunction Diagnosis: history, exam, voiding tests, urodynamic testing, cystoscopy Curing the condition is rare, but individualized treatment is effective
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Functional incontinence
Occurs in many older adults, especially people in nursing home, who have a physical or mental impairment that prevents toileting in time
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Urinary Tract Infections (Cystitis)
Inflammation of the bladder The bladder and urethra walls become red and swollen Causes: infection and irritants Manifestations: UTI symptoms, abdominal pain, and pelvic pressure Diagnosis and treatment follow those usually seen for UTIs
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Pyelonephritis
Acute or chronic infection that has reached one or both kidneys Kidneys become grossly edematous and fill with exudate, compressing renal artery and potentially developing abscesses or necrosis Complications: renal failure, recurrent UTIs, and sepsis Manifestations: severe UTI symptoms, flank pain, and increased blood pressure Diagnosis: history, physical examination, urinalysis, urine and blood cultures, complete blood count, cystoscopy, intravenous pyelogram, computed tomography, renal ultrasound, biopsy, and cystourethrogram Treatment: usual UTI treatments, but long-term antibiotics (4–6 weeks) are usually required
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Nephrolithiasis
Presence of renal calculi, hard crystals composed of minerals that the kidneys normally excrete, in renal pelvis, ureters, or bladder More common in men and Caucasians The most frequent type of calculi contain calcium in combination with either oxalate or phosphate Other types include struvite or infection stones, uric acid stones, and cystine stones Risk factors: pH changes, excessive concentration of insoluble salts in the urine, urinary stasis, family history, obesity, hypertension, and diet
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Congenital Disorders
Kidney development begins about the fifth week of gestation Urine is the main component of amniotic fluid Decreased amniotic fluid can result in serious fetal abnormalities
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Hydronephrosis
Abnormal dilation of the renal pelvis and the calyces of one or both kidneys Unilateral renal involvement indicates an obstruction in one of the ureters Bilateral renal involvement indicates an obstruction in the urethra Causes: urolithiasis, tumors, benign prostatic hyperplasia, strictures, stenosis, and congenital urologic defects Complications: atrophy, necrosis, and glomerular filtration cessation Manifestations: colicky, flank pain or pressure; bloody, cloudy, or foul-smelling urine; dysuria; decreased urine output; frequency; urgency; nausea; vomiting; abdominal distension; and UTIs Diagnosis: history, physical examination, urinalysis, renal ultrasound, computed tomography, intravenous pyelogram, and magnetic resonance imaging Treatment: ureteral stents, nephrostomy tubes, and antibiotics
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Renal Cysts
Typically simple cysts with thin wall and waterlike fluid inside, though some may have a thicker wall or contain solid material Relatively common with age Typically asymptomatic and harmless Complications: infection, bleeding, and enlargement Manifestations: if present, associated with complications; pain or tenderness, changes in urinary patterns, hematuria Diagnosis: during (often unrelated) imaging Treatment: depends on their complexity, but most will not require treatment
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Wilms Tumor
Also known as nephroblastoma, a rare cancer that primarily affects children The exact cause is unknown; may arise in utero when cells that normally form the kidneys fail to develop properly Usually occurs in one kidney, but it can affect both Usually grows as a solitary mass that can become quite large Associated with aniridia, hemihypertrophy, and urinary tract abnormalities Risks include: family history, female gender, African American heritage Long-term survival rate is excellent with early detection and treatment Manifestations: asymptomatic abdominal mass, high blood pressure, hematuria, urinary tract infections, abdominal pain, nausea, vomiting, anorexia, bowel pattern changes, weight loss, and fatigue Diagnosis: history, physical examination, renal ultrasound, and biopsy Staging system guides treatment Treatment: surgery, chemotherapy, and radiation therapy
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Renal Cell Carcinoma
Most frequently occurring kidney cancer in adults Risk factors: being male and smoking Metastasis to the liver, lungs, bone, or nervous system is common Manifestations: asymptomatic, painless hematuria, abnormal urine color, dull and achy flank pain, urinary retention, palpable mass over the affected kidney, unexplained weight loss, anemia, polycythemia, hypertension, paraneoplastic syndromes, and fever Diagnosis: history, physical examination, urinalysis, computed tomography, magnetic resonance imaging, positron emission tomography scan, bone scan, chest X-ray, intravenous pyelogram, cystoscopy, renal arteriogram, biopsy, liver function panel, complete blood count, and blood chemistry Treatment: surgical removal, newer chemotherapies, hormone, and immunotherapy
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Nephrolithiasis
Manifestations: colicky pain in the flank area that radiates to the lower abdomen and groin; bloody, cloudy, or foul-smelling urine; dysuria; frequency; genital discharge; nausea; vomiting; fever; and chills Diagnosis: history, physical examination, urine examination, kidney–ureter–bladder X-ray, computed tomography, ultrasound, intravenous pyelogram, calculi analysis, and serum studies   Treatment: strain all urine, increase fluid intake to 2.5–3.5 L, extracorporeal shock wave lithotripsy, percutaneous nephrolithotomy, ureteroscopy, surgery, pain management, dietary changes, and physical activity
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Prostatic Hyperplasia
A common, nonmalignant enlargement of the prostate gland that occurs as men age; the exact cause is unknown but it may result in urinary stasis and UTIs Declining testosterone and increasing estrogen levels are thought to cause prostatic stromal cell proliferation, enlarging the prostate Or stem cells in the prostate do not mature and die as programmed, enlarging the prostate As the prostate expands, it presses against the urethra and obstructs urine flow Manifestations: frequency, urgency, retention, difficulty initiating urination, weak urinary stream, dribbling urine, nocturia, bladder distension, overflow incontinence, and erectile dysfunction Diagnosis: history, physical examination, urine flow measures, urinalysis, prostate-specific antigen, rectal ultrasound, biopsy, and cystoscopy Treatment: alpha-blockers and alpha5-reductase inhibitors, saw palmetto, partial or complete surgical removal of the prostate, and avoiding alcohol
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Polycystic Kidney Disease
Inherited disorder characterized by numerous grape-like clusters of fluid-filled cysts in both kidneys; cysts enlarge the kidneys while compressing and eventually replacing the functional kidney tissue The exact trigger is unknown Prognosis and progression vary widely depending on the type Autosomal dominant PKD: mutation on the short arm of chromosomes 4 and 16 Occurs in both children and adults, but is much more common in adults Symptoms often do not show up until middle age Autosomal recessive PKD: less common and more serious Appears in infancy or childhood Progresses rapidly, resulting in end-stage kidney failure and generally causing death in infancy or childhood  Symptoms of both forms of PKD: Hematuria and nocturia Drowsiness Grossly enlarged, palpable kidneys ``` In neonates: Potter facies Large, symmetrical masses on flank Respiratory distress Uremia ``` In adults: Hypertension Abdominal girth, swelling, and tenderness/lumbar pain Complications: pyelonephritis, cyst rupture, retroperitoneal bleeding, renal failure, anemia, hypertension, and renal calculi Diagnosis: history, physical examination, urinalysis, blood chemistry, urography, abdominal ultrasound, computed tomography, magnetic resonance imaging, and intravenous pyelogram   Treatment: antibiotics, analgesics, antihypertensive agents, diuretics, adequate hydration, low-salt diet, surgically draining cystic abscesses or retroperitoneal bleeding, dialysis, and kidney transplant
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Glomerulonephritis
Acute or chronic bilateral inflammatory disorder of the glomeruli that typically follows a streptococcal infection; leading cause of renal failure Affects men more than women Inflammatory changes impair the kidneys’ ability to excrete waste and excess fluid Nephrotic and nephritic syndromes are the most prevalent forms Diagnosis: history, physical examination, urinalysis, blood chemistry, serum antibody levels, computed tomography, and renal biopsy   Treatment: antibiotic therapy, corticosteroids, blood pressure management, and temporary dialysis
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Nephrotic Syndrome
Results from antibody–antigen complexes lodging in the glomerular membrane, triggering activation of the complement system Causes: systemic diseases, gold therapy, and idiopathic Results in increased glomerular capillary permeability, leading to marked proteinuria, lipiduria, hypoalbuminemia, and anasarca Other manifestations: hypoalbuminemia, dark and cloudy urine, immunoglobulins in the urine Complications: risk for infection and atherosclerosis
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Bladder Cancer
Types: transitional cell carcinoma, squamous cell carcinoma, and adenocarcinoma Metastasis is common to the pelvic lymph nodes, liver, and bone Risk factors: advancing age, men, Caucasians, working with chemicals, smoking, excessive use of analgesics, experiencing recurrent UTIs, long-term catheter placement, chemotherapy, and radiation Manifestations: painless hematuria, abnormal urine color, frequency, dysuria, UTIs, and back or abdominal pain Diagnosis: history, physical examination, urinalysis, computed tomography, magnetic resonance imaging, positron emission tomography scan, bone scan, chest X-ray, intravenous pyelogram, cystoscopy, biopsy, and liver function panel Treatment: surgical removal, radiation, chemotherapy, and immunologic agents
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Nephritic Syndrome
Inflammatory injury to the glomeruli that can occur because of antibodies interacting with normally occurring antigens in the glomeruli Causes: diseases that initiate the inflammatory response Manifestations: gross hematuria, urinary casts and leukocytes, low GFR, azotemia, oliguria, and high blood pressure Complications: impaired renal function
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Acute Kidney Injury
Sudden loss of renal function (often critically ill hospitalized patients), is generally reversible. Risk factors: advanced age, autoimmune disorders, and liver disease Diagnosis: history, physical examination, blood chemistry, arterial blood gases, urinalysis, complete blood count, renal ultrasound, and biopsy Treatment: Correct fluid and electrolyte imbalances Dialysis A diet high in calories and restricted in protein, sodium, potassium, and phosphates Hypertension management Anemia treatment with synthetic erythropoietin Infection prevention strategies
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Disorders of the upper GI tract:
``` congenital defects (cleft lip and palate and pyloric stenosis) dysphagia vomiting hiatal hernia gastroesophageal reflux disease gastritis peptic ulcers cholelithiasis. ```
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Chronic Kidney Disease
Gradual loss of renal function that is irreversible Causes: diabetes mellitus, hypertension, urine obstructions, renal diseases, renal artery stenosis, ongoing exposure to toxins and nephrotoxic medications, sickle cell disease, systemic lupus erythematosus, smoking ``` Manifestations Hypertension Polyuria with pale urine (early) Oliguria or anuria with dark-colored urine (late) Anemia Bruising and bleeding tendencies Muscle twitches and cramps Electrolyte imbalances Pericarditis, pericardial effusion, pleuritis, and pleural effusion Congestive heart failure Respiratory distress and abnormal breath sounds Sudden weight change Edema of the feet and ankles Azotemia Peripheral neuropathy, restless leg syndrome, and seizures Nausea and vomiting Anorexia Malaise Fatigue and weakness Headaches that seem unrelated to any other cause Sleep disturbances Decreased mental alertness Flank pain Jaundice Persistent pruritus Recurrent infections ``` Diagnosis: history, physical examination, urinalysis, blood chemistry, computed tomography, magnetic resonance imaging, renal ultrasound, biopsy, complete blood count, and arterial blood gases Treatment: manage and prevent complications and alternative medication dosing
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Chronic gastritis
Develops gradually May be asymptomatic, but usually accompanied by a dull epigastric pain and a sensation of fullness after minimal intake Gastritis can be further categorized as erosive or nonerosive Complications of chronic gastritis: peptic ulcers, gastric cancer, and hemorrhage Treatment strategies for chronic include etiology-specific interventions, antacids, acid-reducing agents, and mucosal barrier agents Other strategies include those for GERD
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Acute gastritis
Can be a mild, transient irritation, or it can be a severe ulceration with hemorrhage Usually develops suddenly and is likely to be accompanied by nausea and epigastric pain
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Gastroenteritis
Inflammation of the stomach and intestines, usually because of an infection or allergic reaction
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Helicobacter pylori
Most common cause of chronic gastritis Embeds itself in the mucous layer, activating toxins and enzymes that cause inflammation Genetic vulnerability and lifestyle behaviors (e.g., smoking and stress) may increase the susceptibility
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Acute hepatitis
Proceeds through four phases: asymptomatic incubation phase, three symptomatic phases
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Chronic hepatitis
Characterized by continued hepatic disease lasting longer than 6 months Symptom severity and disease progression vary depending on degree of liver damage Can quickly deteriorate with declining liver integrity
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Diverticulitis
diverticula become inflamed, usually because of retained fecal matter (often asymptomatic until it becomes serious) hemorrhage, and shock. Potential for fatal obstruction, infection, abscess, perforation, peritonitis and shock Manifestations: abdominal cramping, passing frank blood, low-grade fever, abdominal tenderness (usually left lower quadrant), abdominal distension/mass, constipation, obstipation, nausea, and leukocytosis Diagnosis: history, exam, stool analysis (including for occult blood), abdominal imaging, colonoscopy, barium enema, and biopsy Treatment: high-fiber diet, omitting foods with seeds or popcorn, decreased food intake when active bleeding is present, adequate hydration, proper bowel habits, stool softeners, antibiotics, analgesics, colon resection, and blood transfusions
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Gastric ulcers
less frequent but more deadly, Typically associated with malignancy and nonsteroidal anti-inflammatory drugs Pain typically worsens with eating
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Duodenal ulcers
most commonly associated with excessive acid or H. pylori infections Typically present with epigastric pain that is relieved in the presence of food