patho 2 test 4

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Urinary Tract Obstructions

-Interference with urine flow -Causes urine backup behind obstruction of urinary system -Damage occurs to structures behind blockages -increased urinary tract infection -Obstruction can be **Functional **Anatomic *Also known as obstructive uropathy Urolithiasis Hydronephrosis Tumors (neoplasia) In older men, the urinary tract is frequently obstructed by benign prostatic hypertrophy or prostatic cancer. These topics are discussed in Chapter 19. Common causes of obstruction in men and women include tumors, inflammation, scarring, stenosis, congenital defects, and renal calculi

Describe the following pregnancy hypertensive conditions—pregnancy induced hypertension (PIH)

140/90 persistently (usually after 20 weeks gestation) Returns to normal after delivery Can damage vessels in kidneys and retinas, or result in heart failure and stroke regnancy-induced hypertension (PIH; see Chapter 12) refers to a state of persistently elevated blood pressure (more than 140/90) that develops after 20 weeks of gestation and returns to normal after delivery. A specific cause has not been determined, although numerous risk factors have been identified. PIH, if not controlled, may lead to damaged blood vessels in tissues such as the kidneys and retina of the eye or to stroke or heart failure. The decreased blood flow to the uterus may cause premature degeneration of the placenta and presents a risk to the fetus. The efficacy of low doses of aspirin (ASA) in controlling PIH continues to be investigated

Urethritis & Cystitis

2 Categories of *Lower* tract UTIs: Lower urinary tract infections Cystitis Urethritis With cystitis, the bladder wall, and with urethritis, the urethra are inflamed, red, swollen, and in some cases, ulcerated. The bladder wall is irritated and hyper reactive, and bladder capacity is usually reduced. ■ Signs and Symptoms In some cases, the manifestations are very mild and may be unnoticed. ~ Pain is common in the lower abdomen. ~ Dysuria (painful urination), urgency (need to void immediately), frequency (short intervals between voiding), and nocturia (need for urination during the sleep period) occur as the inflamed bladder wall is irritated by urine. ~ Systemic signs of infection may be present (fever, malaise, nausea, and leukocytosis). ~ The urine often appears cloudy and has an unusual odor. ~ Urinalysis indicates bacteriuria (the presence of bacteria in the urine), pyuria, and microscopic hematuria ■ Signs and Symptoms The signs of cystitis, such as dysuria, are also present, because infection is present in both kidneys and bladder. Pain associated with renal disease is usually a dull aching pain in the lower back or flank area, resulting from inflammation that stretches the renal capsule. Systemic signs are usually more marked in pyelonephritis. Urinalysis results are similar to those for cystitis except that urinary casts, consisting of leukocytes or renal epithelial cells, are present, reflecting the involvement of the renal tubules.

Describe the development and complications of gestational diabetes mellitus

2-5% of pregnancies Due to increased glucose intolerance Women w/family history of DM or high birth-rate babies are prone to this Managed by diet or even insulin Increase of fetal abnormalities, stillbirths, or other complications if occurs in 1st trimester Often a large baby is delivered May resolve after delivery, but propensity for mother's later development of DM Diabetes mellitus develops in 2% to 5% of women during pregnancy (see Chapter 16 for more information on diabetes). This condition involves increased glucose intolerance and leads to increased glucose levels in blood and urine. Glucose levels should be closely monitored in women in whom there is a family history of diabetes or who have previously had high-birthweight infants. Dietary management is important, and insulin may be necessary in some cases. Oral hypoglycemic drugs are contraindicated as potentially teratogenic. There is a higher risk of fetal abnormalities if blood glucose is increased in the first trimester, as well as an increase of other complications and stillbirth. The newborn born to a woman with diabetes is usually larger in size and may experience problems regulating blood glucose immediately after birth. Gestational diabetes may resolve after the pregnancy, but in many cases diabetes develops in that individual at a later time.

Describe Celiac Disease

A disease in which one's villi are damaged and the absorption will plummet A.K.A. Sprue Probably genetic etiology Enzyme defect Can't digest gliadin Break-down product of gluten Gluten found in wheat, barley, rye, and oats Toxic effect on villi Malabsorption results SS: steatorrhea, muscle wasting, failure to gain weight Celiac disease, also called celiac sprue or gluten enteropathy, is a malabsorption syndrome that is considered to be primarily a childhood disorder. However, it may also occur in adults, usually at middle age. There is a related disorder, tropical sprue, which is bacterial in origin and often occurs in epidemics in tropical areas. Celiac disease appears to be linked to genetic factors and consists of a defect in the intestinal enzyme that prevents further digestion of gliadin, a breakdown product of gluten. Gluten is a constituent of certain grains: wheat, barley, rye, and oats. The combination of a digestive block with an immunologic response in the person results in a toxic effect on the intestinal villi. The villi atrophy, resulting in decreased enzyme production and less surface area available for absorption of nutrients (Fig. 17.32). Thus the result of celiac disease is malabsorption and malnutrition, which typically manifest as follows: Steatorrhea ~ Muscle wasting ~ Failure to gain weight ~ Irritability and malaise In an infant, the first signs of the disorder usually appear as cereals are added to the diet, at around 4 to 6 months of age. The condition can be diagnosed by a series of blood tests (celiac blood panel) that check for autoantibodies, a duodenal biopsy, and, lastly, adopting a gluten-free diet to assess if health improves under the new conditions. Fortunately celiac disease can usually be treated by maintaining a gluten-free diet, using corn and rice for grains. The intestinal mucosa returns to normal after a few weeks without gluten intake. Patients should be monitored because of an increased incidence of intestinal lymphoma.

acute pancreatitis

Acute pancreatitis involves autodigestion of the pancreas and surrounding tissue, resulting in severe pain, hemorrhage, shock, or peritonitis. Acute Pancreatitis S/S: pain [moderate to severe] in the upper abdomen that is felt through the back (acute abdomen) rigidity [guarding] nausea/vomiting BP decreases HR increases cold extremities possible LOC Digestive effects: Maldigestion malabsorption Most severe—acute hemorrhagic pancreatitis The autodigestion follows premature activation of the pancreatic proenzymes within the pancreas itself. It appears that activation of the proenzyme trypsinogen into trypsin is the trigger; in turn, trypsin converts other proenzymes and chemicals into active forms. The activated enzymes, trypsin, and the proteases amylase and lipase digest the pancreatic tissue, leading to massive inflammation, bleeding, and necrosis The pancreas is composed of delicate tissue and lacks a fibrous capsule that might contain the effects of autodigestion. In some cases, pseudocysts or pancreatic abscesses may develop if the local inflammatory response is successful in localizing the injury. Otherwise, destruction by trypsin and other enzymes progresses into tissues surrounding the pancreas. Lipase causes fat necrosis, binding calcium ions (see pancreatic calcification in x-ray in Ready Reference 5). Blood vessels are eroded by elastase (a protease), leading to hemorrhage Damaging products—for example, cytokines and prostaglandins—released by tissue necrosis lead towidespread inflammation of the peritoneal membranes, or chemical peritonitis. The inflammatory response, including vasodilation and increased capillary permeability, leads to hypovolemia and circulatory collapse. Severe pain, caused by the autodigestion of nerves and the inflammation, contributes to shock (neurogenic shock). Chemical peritonitis results in bacterial peritonitis as intestinal bacteria escape through the more permeable membranes (see Fig. 17.44, presented later in the chapter). Septicemia or general sepsis may result from the escape of bacteria and toxins from the intestines into the general circulation if the inflammatory process is not controlled quickly. Other complications, which may cause death, are adult respiratory distress syndrome and acute renal failure. Although many factors may precipitate acute pancreatitis, the two major causes are gallstones and alcohol abuse. Gallstones may obstruct the flow of bile and pancreatic secretions into the duodenum or cause reflux of bile into the pancreatic duct, thus activating trypsinogen. Alcohol appears to stimulate an increased secretion of pancreatic enzymes and to contract the sphincter of Oddi, blocking flow, but there may be other mechanisms. Alcoholics may have chronic pancreatitis, and the acute episode may be an exacerbation of the chronic form, rather than a separate entity. Sudden onset of acute pancreatitis may follow intake of a large meal or a large amount of alcohol. ~ Severe epigastric or abdominal pain radiating to the back is the primary symptom. Pain increases when the individual assumes a supine position. ~ Signs of shock—low blood pressure, pallor and sweating, and a rapid but weak pulse—develop as inflammation and hemorrhage cause hypovolemia. ~ Low-grade fever is common until infection develops, when body temperature may rise significantly. ~ Abdominal distention and decreased bowel sounds occur as peritonitis leads to decreased peristalsis and paralytic ileus.

Discuss the pathophysiology of acute and chronic gastritis

Acute gastritis-irritants-- some sort of toxin or food Infection/allergies/spicy foods/alcohol/meds SS: nausea/vomiting/epigastric pain/cramps, sometimes fever, headache, diarrhea Lose appetite Pain is base of xiphoid process Chronic gastritis irritation & atrophy Loss of parietal cells Achlorhydria Loss of intrinsic factor-- need for absorption of vitamin b 12 and also autoimmune disorder Genetics, autoimmune, bacterial causes Helicobactor pylori (H. pylori) present-- culprit (very destructivee) Can eventually result in cancer Presents as dyspepsia (indigestion) Loss of secretions due to mucosal atrophy Gastritis is an inflammation of the stomach that may occur in many forms. Gastritis may be acute or chronic; these terms represent two different diseases. Acute gastritis may be a mild, transient irritation with only vague signs, or it may be a more severe ulcerative or hemorrhagic episode Acute Gastritis -- In acute gastritis, the gastric mucosa is inflamed and appears red and edematous. It may be ulcerated and bleeding if the mucosal barrier (the tightly packed epithelial cells and layer of thick mucus) is severely damaged or the circulation is poor, which reduces tissue resistance. Acute gastritis may result from the following: ~ Infection by many types of microorganisms (eg, bacteria and viruses) ~ Allergies to foods such as shellfish or drugs ~ Ingestion of spicy or irritating foods, such as hot peppers, particularly if the person is unaccustomed to a spicy diet ~ Excessive alcohol intake ~ Ingestion of aspirin or other ulcerogenic drugs (especially on an empty stomach) ~ Ingestion of corrosive or toxic substances ~ Radiation or chemotherapy Acute gastritis is usually self-limiting, with complete regeneration of the gastric mucosa in 1 or 2 days. In persons with severe or prolonged vomiting, there is a danger of dehydration, electrolyte loss, and metabolic acidosis, all of which require supportive treatment. Certain infections may require treatment with antimicrobial drugs. Chronic gastritis is characterized by atrophy of the mucosa of the stomach, with loss of the secretory glands. The loss of the parietal cells leads to achlorhydria and lack of secretion of intrinsic factor, which is required for the absorption of vitamin B12. Infection with Helicobacter pylori is often present. Chronic gastritis is often seen in individuals with chronic peptic ulcers, those who abuse alcohol, and the elderly. Autoimmune disorders—for example, pernicious anemia—are associated with a type of chronic gastric atrophy. Many cases are idiopathic. The signs of chronic gastritis, which are often vague, include mild epigastric discomfort, anorexia, or intolerance for certain foods, usually spicy or fatty foods. Persons with chronic gastritis have an increased risk of peptic ulcers and gastric carcinoma. Treatment involves appropriate antibiotics and proton pump inhibitors.

Alcoholic liver disease (Laennec's cirrhosis)

Alcoholic liver disease ("portal" or Laennec's cirrhosis) Portal Hypertension Related to liver failure Distended veins-- backflow Increased pressure in portal system Obstruction in liver causes back-up Blood into other organs (swelling) varices Causes: Cirrhosis Fibrosis Cirrhosis: Alcoholic Liver Disease Initial stage—fatty liver Enlargement of the liver Asymptomatic and reversible with reduced alcohol intake Second stage—alcoholic hepatitis Inflammation and cell necrosis Fibrous tissue formation—irreversible change Third stage—end-stage cirrhosis Fibrotic tissue replaces normal tissue. Little normal function remains. Cirrhosis will continue (signs of liver not working) In patients with alcoholic liver disease, or portal cirrhosis, there are several stages in the development of hepatocellular damage related to the effects of alcohol. Alcohol and its metabolites, such as acetaldehyde, are toxic to the liver cells and alter many metabolic processes in the liver. Secondary malnutrition may aggravate the damaging effects on liver cells. 1. The initial change in alcoholic liver disease is the accumulation of fat in liver cells, causing fatty liver. Other than enlargement of the liver or hepatomegaly, this stage is asymptomatic and is reversible if alcohol intake is reduced. 2. In the second stage, alcoholic hepatitis, inflammation and cell necrosis occur. Fibrous tissue forms, an irreversible change. Acute inflammation may develop when alcohol intake increases or binge drinking becomes more excessive. This second stage may also be asymptomatic, or it may manifest with mild symptoms, such as anorexia, nausea, and liver tenderness. In some patients, after an episode of excessive alcohol intake, there may be sufficient damage to precipitate liver failure, encephalopathy, and death. 3. The third stage, or end-stage cirrhosis, is reached when fibrotic tissue replaces normal tissue, significantly altering the basic liver structure to the extent that little normal function remains. Signs of portal hypertension or impaired digestion and absorption are the usual early indicators of this stage. Alcoholic liver disease, or Laënnec cirrhosis, develops in persons with chronic alcoholism or long-term excessive alcohol intake. In 2010 there were 15,990 liver disease deaths due to alcoholism. Alcohol is a hepatotoxin, an irritant that causes metabolic changes in the liver cells, leading first to lipid accumulation in the cells (fatty liver), then to inflammation and necrosis (alcoholic hepatitis), and finally to fibrosis or scar tissue formation (see Chapter 17 for a discussion of cirrhosis). Destruction of the liver takes place insidiously, with only mild signs and symptoms until the condition is well advanced and irreversible.

Describe the menstrual disorders amenorrhea (primary & secondary)

Amenorrhea Primary No menstruation @ puberty Ovarian problem, hormonal development off Secondary > 12 months Hormone imbalance, pituitary dz, ovarian dz, endometrial dz, (may also be psychosomatic—stress, anxiety, depression) Amenorrhea, or absence of menstruation, may be primary or secondary. In the primary condition, menarche has never occurred. This may result from a genetic disorder such as Turner syndrome (a chromosome abnormality, XO, in which the ovaries do not function). Congenital defects affecting the hypothalamus, central nervous system, or pituitary or congenital absence of the uterus and congenital uterine hypoplasia (infantile uterus) may also interfere with the normal process. Secondary amenorrhea is the cessation of menstruation in an individual who previously experienced menstrual cycles. It frequently results from an impediment in the hypothalamic-pituitary axis. The hypothalamus may be suppressed by conditions such as tumors, stress, sudden weight loss, eating disorders, or participation in competitive sports, leading to reduced body fat. Systemic factors such as anemia or chemotherapy may also cause secondary amenorrhea.

Congenital anal atresia

Anus Atresia. Imperforate anus is a congenital defect in which the opening of the anus is absent or misplaced, usually fistulizing anteriorly to the perineum or GU tract. Anal atresia is an imperforate anus. (Also see Overview of Congenital Gastrointestinal Anomalies.) In anal atresia, the tissue closing the anus may be several centimeters thick or just a thin membrane of skin

ascites

Ascites* Excess fluid in the Peritoneal Cavity Three kinds Transudate Cirrhosis—from liver Nephrotic syndrome—from kidneys CHF—causes back-pressure in liver From disease process or necrotic syndrome Bloody exudate Usually from metastatic cancer to the peritoneum Fluid comes out of heart vessels Chyle Milky fat-containing fluid from blocked lymph flow Blocked lymph nodes Less albumin production (hypoalbuminemia) Ascites Ascites, a complication that occurs when fluid accumulates in the peritoneal cavity, leading to marked abdominal distention; hepatomegaly and ascites may impair respiration if upward pressure on the diaphragm impairs lung expansion. Increased risk of peritonitis This excessive fluid throughout all tissues impairs appetite (ascites) abnormal accumulation of fluid in the abdominal cavity.

Neoplasia

Renal cell carcinoma

Benign tumors are rare in urinary tract Malignant tumors Renal cell carcinoma (vast majority of renal cancers) Unknown etiology & no set risk-factors Asymptomatic in early stages: fever, hematuria, pain Often metastasizes to: liver, ureter, lungs, bone, CNS Usually 50 yo, male, smokers, analgesic use 5-yr survival 96% Stage I 23% Stage IV Renal Cell Carcinoma Usually from tubule epithelium Cortical "Silent" tumor Diagnosis usually after mets Renal cell carcinoma (adenocarcinoma of the kidney) is a primary tumor arising from the tubule epithelium, more often in the renal cortex (Fig. 18.13). The American Cancer Society estimated that there would be 62,700 new cases of renal cell carcinomas in 2016, resulting in 14,240 deaths. It tends to be asymptomatic in the early stage and often has metastasized to liver, lungs, bone, or CNS at the time of diagnosis. This cancer occurs more frequently in men and smokers and is uncommon in people 45 years old or younger. The initial sign is usually painless hematuria, either gross or microscopic. Other manifestations include dull, aching flank pain; a palpable mass; unexplained weight loss; and anemia or erythrocytosis (depending on the tumor's effects on erythropoietin secretion). Paraneoplastic syndromes such as hypercalcemia (increased parathyroid hormone) or Cushing syndrome (increased adrenocorticotropic hormone) are common. cotropic hormone) are common. This tumor tends to be silent; therefore diagnosis is made in one-third of cases after metastasis to lungs, liver, or bone has occurred. Removal of the kidney (nephrectomy) is the treatment because the tumor is usually unresponsive to radiation or chemotherapy. The 5-year survival rate varies from 96% in stage I to 23% in stage IV; newer treatment measures and diagnostic technology may result in higher survival rates.

Fully describe the female reproductive benign tumor disorders—leiomyoma

Benign, estrogen-dependent tumor in uterine muscle Post-menopausal women—becomes fibroid mass Usually small, can become large Can cause pressure damage—infertility S/S: pain, bleeding, UT difficulties Leiomyoma (Fibroids) A leiomyoma is a benign tumor of the myometrium, the cause of which is unknown. These uterine tumors are common in women during the reproductive years, occurring in more than 30% of women, particularly Asian and African American women. After menopause the tumors tend to shrink. As benign tumors, they are not considered precancerous Fibroids are classified by location, developing in the uterine wall (intramural), beneath the endometrium (submucosal), or under the serosa (subserosal). The two latter forms may develop as polyps, with the submucosal type projecting inward into the uterine cavity and the subserosal type growing outward into the pelvic cavity Fibroids usually occur as multiple well-defined but unencapsulated masses, which vary widely in size. Large leiomyomas degenerate in the central region, undergoing necrosis and forming cysts. These benign tumors are hormone dependent, growing rapidly during pregnancy and decreasing in size with increasing fibrosis after menopause Fibroids are often asymptomatic until they grow large enough to be palpated. Abnormal bleeding such as menorrhagia may be an indicator of fibroid development. Large tumors may cause pressure on adjacent structures, leading to urinary frequency or constipation and a heavy sensation in the lower abdomen. Large fibroids may interfere with implantation of the fertilized ovum or the course of pregnancy Treatment of large tumors involves hormonal therapy or surgery

Describe the congenital disorder biliary atresia

Biliary Atresia (Congenital) Does not Develops later in life Biliary tree is not well formed Everything is shriveled up (connects to pancreatic duct) Shows up not long after birth Biliary atresia is a rare disease of the liver and bile ducts that occurs in infants. Symptoms of the disease appear or develop about two to eight weeks after birth. Cells within the liver produce liquid called bile. Bile helps to digest fat.

All types of ileus (intestinal obstruction)

Blockage of intestine (ileus) due to: Mechanical Paralytic (lack of normal peristalsis) Hirschsprung's disease Back up, increased pressure (infarction/pressure necrosis) Can lead to gangrene Rupture Contents spill into peritoneum (peritonitis) Volvulus: 'twisting' of the bowel imagine the impact on GI function as well as blood supply it actually looks like a corkscrew Intussusception: telescoping of bowel into itself common in children can be reduced (fixed) with a barium enema Paralytic ileus is caused by... Severe pain—intestinal sphincters respond by spasm and restrict contents Peritonitis—pus surrounds intestine and prevents peristalsis. Sever enteritis—inflammation blocks neuromuscular transmission Spinal cord trauma—portions of intestine are denervated Hirschsprung's disease (congenital megacolon) Lack of PNS innervation Intestinal obstruction refers to a lack of movement of the intestinal contents through the intestine. Because of its smaller lumen, obstructions are more common and occur more rapidly in the small intestine, but they can occur in the large intestine as well. Depending on the cause and location, obstruction may manifest as an acute problem or a gradually developing situation. For example, twisting of the intestine could cause sudden total obstruction, whereas a tumor leads to progressive obstruction. Intestinal obstruction occurs in two forms. Mechanical obstructions result from tumor, adhesions, hernias, or other tangible obstructions (Fig. 17.41). Functional, or adynamic, obstructions result from neurologic impairment, such as spinal cord injury or a lack of propulsion in the intestine, and are often referred to as paralytic ileus. Although the result can be the same, these types manifest somewhat differently and require different treatments.

Describe the testicular cancers—seminomas and teratomas

Cancer of the Testes—1/300 men affected Seminoma Malignancy of seminiferous tubules Most common Does not metastasize 90% 5 year survival rate Teratoma Malignancy of germ cell (like female but malignant) Mets through blood & lymph to lungs, liver, brain Survival rate for 5 yrs <50% if metastasis is present Benign tumors of the testes are extremely rare, and the majority of tumors that occur in the testes are malignant, arising from germ cells. Although testicular cancer is not common, with about 1 in 263 men being affected during their lifetime, there is concern because it occurs primarily in the 15- to 35-year-old age group and the incidence is increasing. The cause for the increase in cases is not known, and the rate of increase has slowed recently. Testicular cancer is the most common solid tumor in young men. Certain types of testicular cancer may occur in other groups, such as younger children or older males. Testicular cancer may originate from one type of cell, for example, a seminoma, or may be mixed, consisting of cells from a variety of sources and with varying degrees of differentiation. A teratoma consists of a mixture of different germ cells (Fig. 19.7). A common mixed tumor is a teratoma, derived from one or more of the germ cell layers, combined with an embryonal carcinoma, which has poorly differentiated cells. Some malignant tumors secrete human chorionic gonadotropin (hCG) or alpha-fetoprotein (AFP), which serve as a useful serum marker for both diagnosis and follow-up monitoring Some testicular neoplasms may spread at an early stage, for example, choriocarcinoma, whereas others, such as seminomas, remain localized for a more prolonged period. Testicular tumors follow a typical pattern when spreading, first appearing in the common iliac and paraaortic lymph nodes and then in the mediastinal and supraclavicular lymph nodes. Metastases spreading through the blood to the lungs, liver, bone, and brain occur at a later time. Several staging systems are used, based on the extent of the primary tumor, the degree of lymph node involvement (retroperitoneal or otherwise), and the presence of distant metastases. This tumor has a heredity pattern with a change in chromosome number 12 in some families, and there is a possible relationship with infection or trauma. An established predisposing factor is cryptorchidism, or maldescent of the testes. Testicular tumors present as hard, painless, usually unilateral masses. The testis may be enlarged or may feel heavy. Eventually there may be a dull aching pain in the lower abdomen. In some cases, hydrocele or epididymitis may develop because of inflammation, or gynecomastia (enlarged breasts) may become evident if hormones are secreted by the tumo

Discuss the pathophysiology and complications of malignant breast carcinoma

Carcinoma of the Breast #2 cause of mortality 20-40% of masses that become cancerous are NOT palpable mammography could prevent 30% of breast cancer deaths Most originate in ductal epethilium Ductal carcinoma in situ (DCIS) Lump is moveable at first, then becomes fixated when it invades surrounding tissues Metastasis through lymph and blood to bone, liver, lungs, and brain Risk Factors: Family history of breast cancer (BRCA-1 & -2 genes) Hormonal influence Estrogen and/or progesterone receptors may be present in tumor cells Early onset menstruation + late menopause No childbearing (estrogen suppressed during pregnancy) History of other estrogen-linked cancers For example ovarian and endometrial Other carcinogenic influences Chemicals Oncogenic viruses Radiation Carcinoma of the breast is a common malignancy in women and a major cause of death. Rarely breast cancer occurs in males. The incidence of breast carcinoma continues to increase after age 20, and more women are developing the malignancy at a younger age. The National Cancer Institute of the NIH reports that in 2015 there were 231,840 new female cases in the United States resulting in 40,290 female deaths, and a 2016 report estimated 2600 new male cases and 440 male deaths. The overall incidence and mortality rate for this cancer have been increasing for a period of years, but now seem to be decreasing. The American Cancer Society estimates that there are currently 15.5 million survivors of breast cancer living in the United States. Malignant tumors develop in the upper outer quadrant of the breast in approximately half the cases; the central portion of the breast is the next most common location (see Fig. 20.2B). Most tumors are unilateral, although bilateral primary tumors may develop in some cases There are different types of breast carcinomas, but the majority arises from cells of the ductal epithelium. This cancer infiltrates the surrounding tissue and frequently adheres to the skin, causing dimpling. The tumor becomes fixed when it adheres to the muscle or fascia of the chest wall The malignant cells spread at an early stage, first to the nearby lymph nodes. Tumors in the upper outer quadrant and central breast area spread to the axillary lymph nodes. In most cases, several nodes are affected at the time of diagnosis. Widespread dissemination follows quickly, including metastases to the lungs, brain, bone, and liver (see Fig. 20.5 for illustration of breast cancer metastases). Tumor cells are graded on the basis of the degree of differentiation or anaplasia (see Chapter 20). The tumor is then staged based on the size of the primary tumor, the involvement of lymph nodes, and the presence of metastases The presence of estrogen or progesterone receptors on the tumor cells is a major factor in determining how to treat the individual cancer. Such a tumor is hormone dependent because its growth is enhanced by the particular hormone. The majority of cases occur in women over age 50. A strong genetic predisposition has been supported by the identification of specific genes related to breast cancer, BRCA-1 and BRCA-2. Familial occurrence that is proportional to the numbers of affected relatives and the closeness of the relationships has been well documented. The other major factor in the etiology of breast cancer is hormones—specifically, exposure to high estrogen levels. Circumstances such as a long period of regular menstrual cycles (for example, from an early menarche to late menopause), nulliparity (no children), and delay of the first pregnancy, all of which are associated with longer exposure to estrogen, appear to promote cancer development. The role of exogenous estrogen in oral contraceptives or postmenopausal supplements remains controversial. Current formulations for oral contraceptives containing reduced levels of estrogens have considerably reduced the risks. Other factors predisposing to breast carcinoma include fibrocystic disease with atypical hyperplasia, prior carcinoma in the uterus or in the other breast, and exposure of the chest to radiation (particularly in young women). Lack of exercise, smoking, and a high-fat diet have been identified as risk factors in some studies. Prior abortion does not increase the risk of developing breast cancer. Considerable research continues to identify nongenetic risk factors that may be modified during the woman's life. The usual initial sign is a single small, hard, painless nodule. The mass is freely movable in the early stage but later becomes fixed. Other signs as the tumor becomes more advanced include dimpling of the skin, retraction of or discharge from the nipple, and a change in breast contour. Biopsy confirms the diagnosis of malignancy

Discuss the pathophysiology and complications of cervical and endometrial carcinoma

Cervical Carcinoma Women at risk: Oncogenic STDs (HSV-2, HPV) Multiple sex partners Smokers Death rate decreased by 74% through development of Pap smear This is a large cervical squamous cell carcinoma which spread to the vagina. A total abdominal hysterectomy with bilateral salpingo-oophorectomy was performed 1. Normal squamous epithelial cells in transformation zone of the cervix - exposure to irritant or carcinogen changes cell DNA 2. Dysplasia - mild - detected by Pap test; removal of irritant or carcinogen or DNA repair gene 3. Dysplasia - severe - additional exposure to carcinogen; eg, viral infection (STD) alters DNA in dysplasic cells 4. Malignant neoplasm - proliferation of undifferentiated cells 5. Carcinoma in situ - superficial, small localized mass remains for some years 6. Invasive carcinoma - decreased cell adhesion and invasion of local tissues, lymph nodes Cervical Cancer Staging Stage 0: Cervical mucus only—"in situ" Stage 1: Invasive but still confined to cervix Stage 2: Moved to upper vagina Stage 3: Moved into lower vagina/upper pelvis Stage 4: Abdominal invasion/possible mets Uterine Cancer (Endometrial Carcinoma) Most common reproductive tract cancer (not including breast) Adenocarcinoma—from endometrial glands of the epithelium Possible hormonal, viral, chemical etiology Most commonly affects post-menopausal women Prolonged estrogen exposure (either natural or artificial) Early warning sign—unusual bleeding The number of cases of invasive cancer and the number of deaths from cervical cancer have declined by 74% with the increased use of the Papanicolaou (Pap) smear for screening and early diagnosis while the cancer is still in situ. The American Cancer Society estimated 12,990 new cases of cervical cancer resulting in 4120 deaths in the United States in 2016. The average age at onset for carcinoma in situ is 35, whereas invasive carcinoma manifests at approximately age 45. Nearly one in five cancers is diagnosed after age 65; thus women need to be screened after menopause. More cases are occurring in women in their 20s and 30s. Hispanic American women have twice the risk of developing cervical cancers than women in other ethnic groups. Five-year survival rates for noninvasive cancer are 90%—with invasion the rate drops to 70%. The early changes in the cervical epithelial tissue consist of dysplasia, which is initially mild but becomes progressively more severe (Fig. 19.18). This dysplasia usually occurs at the junction of the columnar cells with the squamous epithelial cells of the external os of the cervix (the transformation zone). The majority of cervical carcinomas arise from squamous cells. Cervical intraepithelial neoplasia is graded from I to III based on the amount of dysplasia and the degree of cell differentiation. Grade III consists of carcinoma in situ in which many disorganized, undifferentiated, abnormal cells are present (severe dysplasia). Because the time span from mild dysplasia to carcinoma in situ may be 10 years, there are many opportunities for detection in this early stage. The Pap smear allows an examination of scrapings of the cervical cells and those that slough from the site and are present in the local secretions. These cells indicate the presence of dysplasia long before any signs of cancer appear Carcinoma in situ is a noninvasive stage, to be followed by the invasive stage. Fig. 19.19 illustrates the stages. Invasive carcinoma has varying characteristics, sometimes appearing as a protruding nodular mass or perhaps as ulceration, and sometimes infiltrating the wall. Eventually all characteristics are present in the lesion. As the carcinoma spreads in all directions into the adjacent tissues, including the uterus and vagina, it may also invade the uterine wall and extend into the ligaments, bladder, or rectum. Metastases to lymph nodes or distant sites occur rarely and at a very late stage. Staging of the carcinoma begins with stage 0, representing carcinoma in situ; stage I represents cancer restricted to the cervix; and stages II to IV indicate further spread to the surrounding tissues. Cervical cancer is strongly linked to oncogenic STDs such as herpes simplex virus type 2 (HSV-2) and human papillomavirus (HPV) strains 16, 18, 31, 34, or 45. The Centers for Disease Control and Prevention (CDC) defines cervical carcinoma as a sexually transmitted infection. The virus may exert direct effects on the host cell or may cause an antibody reaction; increased viral antibodies Cervical cancer is asymptomatic in the early stage but can be detected by the Pap test. The invasive stage is indicated by slight bleeding or spotting or a slight watery discharge. Anemia or weight loss may accompany the local signs. Carcinoma of the Uterus (Endometrial Carcinoma and Uterine Sarcomas) Carcinomas of the uterus remain a common cancer in women older than 40 years, with the majority of cases occurring in the 55- to 65-year age range. The American Cancer Society estimated that there would be 60,050 new cases diagnosed in the United States in 2016, resulting in 10,470 deaths. A simple screening test is not available for this cancer; the Pap test does not screen for it. However, the early indicator is excessive vaginal bleeding, which in a postmenopausal woman is a significant sign demanding investigation. Uterine cancers are derived from connective tissue or muscle and are termed leiomyosarcomas. These tumors have a poor prognosis and frequently have metastasized to the lungs by the time diagnosis is made. For more information on sarcomas The majority of endometrial carcinomas are adenocarcinomas arising from the glandular epithelium. The malignant changes develop from endometrial hyperplasia, with the cells gradually becoming more atypical. Excessive estrogen stimulation appears to be the major factor in the development of hyperplasia. This cancer is a relatively slow-growing tumor and may infiltrate the uterine wall, leading to a thickened area, or it may mushroom out into the endometrial cavity (Fig. 19.20). Eventually the tumor mass fills the interior of the uterus and extends through the wall into the surrounding structures. Endometrial cancers are graded from 1, indicating well-differentiated cells, to grade 3, indicating poorly differentiated cells Staging of the cancer is based on the degree of localization. In stage I, tumors are confined to the body of the uterus. In stage II, cancer is limited to the uterus and the cervix. In stage III, the cancer has spread outside the uterus but remains within the true pelvis; and in stage IV, the tumor has spread to the lymph nodes and distant organs. Five-year survival rate for stage I is 99%, stage II is 80%, stage III is 60%, and stage IV is 32% Individuals with a history of increased estrogen levels have a higher incidence of uterine cancer. Exogenous estrogen taken by postmenopausal women is associated with an increased risk of endometrial cancer, and currently the guidelines for use and the dosage of estrogen have been reduced to minimize this danger. Other causes of hyperestrinism include infertility or the earlier ingestion of sequential oral contraceptives. The current practice of combining estrogen with progestin reduces the risk of hyperplasia in the uterus, but is still associated with an increased risk of breast cancer. There is also an increased incidence of cancer in obese women and in those with diabetes or hypertensio

Describe the development and complications of bacterial sexually transmitted diseases (STD) Chlamydia and gonorrhea and their presentations in males and females

Chlamydia Chlamydia trachomatis Males Urethritis with whitish discharge from penis Epididymitis and proctitis possible complications Females Sometimes urethritis or other reproductive tract infection Usually PID results, sometimes without other signs Gonorrhea N. gonorrhoeae Males Dysuria w/purulent discharge Sometimes epididymitis Females Often asymptomatic May result in anal/rectal infections, PID, gonococcal arthritis, STDs, formerly called venereal diseases, encompass a broad range of infectious diseases that are spread by sexual contact. Although the incidence of gonorrhea has decreased a little, the incidence of other STDs has increased, resulting in an overall increase. The actual figures are probably much higher than those stated because many cases of STD are not reported. The increased numbers have been attributed to societal changes in many countries, including factors such as increased participation in premarital sex, particularly among young adults; an increased divorce rate; and an increased number of sexual partners on the part of some individuals. Many people do not take protective measures against STDs, especially when hormonal contraceptives are used to prevent pregnancy. In addition to the standard STDs such as gonorrhea, syphilis, and chlamydial infection, there is evidence that infections such as hepatitis B may be spread by sexual contact. HIV is spread by both heterosexual and homosexual exchange of body fluids Chlamydial infection is considered one of the most common STDs and the leading cause of PID. The pathogen is the bacterium C. trachomatis, a gram-negative obligate intracellular parasite, which requires a host cell to reproduce (see Fig. 6.8). As in gonorrhea, chlamydiae invade the epithelial tissue of the urogenital tract, causing inflammation In most males chlamydial infection becomes evident in several weeks after exposure as urethritis (nongonococcal urethritis) and epididymitis. Manifestations of urethritis include dysuria, itching, and a whitish discharge from the penis. Epididymitis manifests as a painful, swollen scrotum, usually unilateral, accompanied by fever. The inguinal lymph nodes are swollen. Proctitis (rectal inflammation with bleeding and discharge) may occur in anyone practicing anal intercourse Females are often asymptomatic until PID develops. A few experience urethritis, bartholinitis, cervicitis, or salpingitis. Signs of urethritis include dysuria and urinary frequency. Infection in Bartholin glands causes a purulent discharge and cyst formation. Cervicitis may be asymptomatic, or a purulent discharge with inflamed tissues may be evident at the cervical os. Spread to the fallopian tubes leads to the development of PID. Newborns may be infected during passage through the cervix and vagina, resulting in infection in the eyes (conjunctivitis) or in the lungs because of aspiration of infected secretions (pneumonia). The usual treatment for chlamydial infection is tetracycline or azithromycin for the infected person and any sexual partners. Chlamydia and gonorrhea are often seen together in the same client, and thus newer protocols call for treatment of both infections simultaneously with a combination of doxycycline and azithromycin. Gonorrhea is caused by N. gonorrhoeae, a gram-negative aerobic diplococcus (gonococcus). Many strains of N. gonorrhoeae have become resistant to penicillin and tetracycline. The bacteria use pili to attach to the epithelial cells and then damage the mucosa, causing an inflammatory reaction and formation of a purulent exudate. The most common site of inflammation in males is the urethra, which results in dysuria and a purulent urethral discharge. Epididymitis may follow (Fig. 19.21). Some men are asymptomatic. In females, the infection usually involves the endocervical canal and frequently is asymptomatic. It may also affect Skene and Bartholin glands, causing more visible manifestations such as a change in the appearance of the vaginal discharge from clear, slightly white to thick greenish, yellow, or creamy white. PID, a serious complication, frequently follows as the infection ascends along the mucosa. Females may experience infection in the anus and rectum when infected exudate spreads from the vagina. Women are prone to develop bacteremia and gonococcal arthritis, with multiple joint inflammations. Orogenital contact leads to pharyngeal infection manifested as pharyngitis, tonsillitis, or lymphadenopathy. Gonococcal conjunctivitis may be seen in Fig. 15.3. The newborn may become infected during the birth process, resulting in the eye infection called ophthalmia neonatorum. Considering the resistant strains of the organism, the suggested drugs are ceftriaxone and doxycycline. Culture and sensitivity tests may be required to determine effective drugs.

Describe the pathophysiology of biliary obstruction and cholecystitis

Cholecystitis Literally -- "Inflammation of the bile-containing bladder" Acute--obstruction of biliary tree Chronic—no obstruction, but presence of gallstones or dysfunctional GB The gallbladder and biliary tract are frequently affected by one or more interrelated problems involving the formation of gallstones (Fig. 17.18). At least 10% of the population has gallstones, and 500,000 surgical procedures are done per year in the United States to treat gallbladder disease. ~ Cholelithiasis refers to formation of gallstones, which are masses of solid material or calculi that form in the bile. Cholecystitis refers to inflammation of the gallbladder and cystic duct. Cholangitis is inflammation usually related to infection of the bile ducts. ~ Choledocholithiasis pertains to obstruction by gallstones of the biliary tract. Chronic cholecystitis is manifested by milder signs, although the course may be punctuated by acute episodes. Signs often include intolerance to fatty foods, excessive belching, bloating, and mild epigastric discomfort. The presence of gallstones may cause irritation and inflammation in the gallbladder wall (cholecystitis), and this susceptible tissue may then be infected. Infecting organisms are usually Escherichia coli or enterococci, which gain access to the gallbladder through the sphincter of Oddi or from the portal veins or adjacent lymph nodes. When a stone obstructs bile flow in the cystic or common bile duct, biliary colic develops, consisting of severe spasms of pain resulting from strong muscle contractions attempting to move the stone along. Obstruction of the biliary system at the sphincter of Oddi may also cause pancreatitis because the pancreatic secretions are backed up or bile refluxes into the pancreatic ducts. Acute cholecystitis is usually associated with some degree of obstruction and inflammation. Severe pain is often precipitated by eating a fatty meal; fever, leukocytosis, and vomiting accompany the pain. Small stones may be "silent" and excreted in the bile, whereas larger stones are likely to obstruct the flow of bile in the cystic or common bile ducts, causing pain. Note the comparative size of the stones and the bile ducts When a stone obstructs bile flow in the cystic or common bile duct, biliary colic develops, consisting of severe spasms of pain resulting from strong muscle contractions attempting to move the stone along. Obstruction of the biliary system at the sphincter of Oddi may also cause pancreatitis because the pancreatic secretions are backed up or bile refluxes into the pancreatic ducts. Gallstones are frequently asymptomatic. However, larger calculi may obstruct a duct at any time, causing sudden severe waves of pain (biliary colic) in the upper right quadrant of the abdomen or epigastric area, often radiating to the back and right shoulder. Nausea and vomiting are usually present. The pain increases for some time and then may decrease if the stone moves on. If the pain continues, and jaundice develops as the bile backs up into the liver and blood, surgical intervention may be necessary. There is also a risk of a ruptured gallbladder if obstruction persists.

Know difference between cholelithiasis, choledocholithiasis, cholestasis, cholecystitis, cholangitis

Cholelithiasis (gallstone); Cholelithiasis Gallstones main causes of GB inflammation.... Formed from cholesterol, bilirubin, calcium Potential for obstruction of a duct (Choledocholithiasis)-- blockage of a duct Increases Cholestasis Bile is still -- not moving Not good, setting up for infections Formed from cholesterol --Cholelithiasis refers to gallstone formation, commonly due to excess cholesterol in the bile. Severe colicky pain results when gallstones obstruct a bile duct. --Cholelithiasis Formation of gallstones, consisting of cholesterol or bilirubin, which may obstruct the biliary tract; --Cholelithiasis refers to formation of gallstones, which are masses of solid material or calculi that form in the bile (Choledocholithiasis)-- blockage of a duct --Choledocholithiasis pertains to obstruction by gallstones of the biliary tract. cholestasis- Increases Cholestasis Bile is still -- not moving Not good, setting up for infections -- cholestasis (obstructed flow of bile) --Cholestasis obstructed flow of bile in the liver or biliary tract. cholecystitis Cholecystitis Literally -- "Inflammation of the bile-containing bladder" Acute--obstruction of biliary tree Chronic—no obstruction, but presence of gallstones or dysfunctional GB -- Cholecystitis refers to inflammation of the gallbladder and cystic duct. cholangitis Infection of gallbladder and biliary tree One of ducts is obstructed, bacteria comes up into liver and biliary tree Can get liver abscess A complication of obstruction Colonizing bacteria can move up into the liver via the biliary tree and form abscesses --Cholangitis is inflammation usually related to infection of the bile ducts.

Cirrhosis and Liver Failure

Cirrhosis is a disorder in which there is progressive destruction of liver tissue leading eventually to liver failure, when 80% to 90% of the liver has been destroyed. It is the result of a number of chronic liver diseases. About 28,000 persons die of cirrhosis each year in the United States, and 50% of these deaths are alcohol related. Cirrhosis may be classified by the structural changes that take place (eg, micronodular or macronodular) or the cause of the disorder. In some cases, cirrhosis may be linked to specific underlying disorders, particularly congenital problems or inherited metabolic disorders. 1. Alcoholic liver disease (the largest group, also called portal or Laënnec cirrhosis) 2. Biliary cirrhosis, associated with immune disorders and those causing obstruction of bile flow, for example, stones or cystic fibrosis, in which mucous plugs form in the bile ducts 3. Postnecrotic cirrhosis, linked with chronic hepatitis or long-term exposure to toxic materials 4. Metabolic, usually caused by storage disorders such as hemochromatosi Cirrhosis is a disorder in which the liver demonstrates extensive diffuse fibrosis and loss of lobular organization (see Fig. 17.20). Nodules of regenerated hepatocytes may be present but are not necessarily functional because the vascular network and biliary ducts are distorted (Fig. 17.24). Even if the primary cause is removed, further damage is likely because fibrosis interferes with the blood supply to liver tissues or the bile may back up, leading to ongoing inflammation and damage. Initially the liver is enlarged, but it becomes small and shrunken as fibrosis proceeds. In many cases degenerative changes are asymptomatic until the disease is well advanced. Liver biopsy and serologic tests may determine the cause and extent of the damage. The progressive changes that occur in biliary and postnecrotic cirrhosis are directly linked to inflammation, necrosis, and fibrosis associated with the primary condition. The pathophysiologic effects of cirrhosis evolve from two factors: the loss of liver cell functions and interference with blood and bile flow in the liver. Major functional losses in persons with cirrhosis include the following: ~ Decreased removal and conjugation of bilirubin ~ Decreased production of bile ~ Impaired digestion and absorption of nutrients, particularly fats and fat-soluble vitamins ~ Decreased production of blood clotting factors (prothrombin, fibrinogen) and plasma proteins (albumin) ~ Impaired glucose/glycogen metabolism ~ Inadequate storage of iron and vitamin B12 ~ Decreased inactivation of hormones, such as aldosterone and estrogen ~ Decreased removal of toxic substances, such as ammonia and drugs Altered blood chemistry, including abnormal levels of electrolytes or amino acids, and excessive ammonia or other toxic chemicals affect the central nervous system, leading to hepatic encephalopathy. Serum ammonia levels correlate well with the clinical signs of encephalopathy. Ammonia is an end product of protein metabolism in the liver or intestine, and then it is converted by liver cells into urea for excretion by the kidneys. The ingestion of a meal high in protein or an episode of bleeding in the digestive tract may cause a marked elevation in serum ammonia concentration and may precipitate severe encephalopathy. The second group of effects is related to the obstruction of bile ducts and blood flow by fibrous tissue as follows: ~ Reduction of the amount of bile entering the intestine, impairing digestion and absorption ~ Backup of bile in the liver, leading to obstructive jaundice with elevated conjugated and unconjugated bilirubin levels in the blood ~ Blockage of blood flow through the liver, leading to high pressure in the portal veins, or portal hypertension ~ Congestion in the spleen (splenomegaly), increasing hemolysis ~ Congestion in intestinal walls and stomach, impairing digestion and absorption ~ Development of esophageal varices (see Figs. 17.25 and 17.26) ~ Development of ascites, an accumulation of fluid in the peritoneal cavity that causes abdominal distention and pressure Cirrhosis Fibrosis & scarring due to continued damage Insidious then irreparable Nodules, fibrosis/scar tissue, loss of function Effects of Cirrhosis Table 17.6 Sex hormones are not being activated Skin Pruititis Itchiness Edema -- back up of fluid (congested) Ascites

Colorectal cancer

Colon Neoplasia (Colorectal Cancer) Adenocarcinoma 3rd leading type of cancer, 2nd leading cause of cancer death Etiology: probably genetics, diet Benign: polyps (though can predispose to cancer) Adenocarcinoma of Colon barium enema demonstrating sigmoid region note how the lumen is narrowed due to constricting lesion described as 'apple core' lesion common & surgically resectable In the United States, colorectal cancer ranks high as a lethal cancer in individuals older than age 50, and it is the second leading cause of cancer-related deaths. According to information collected in 2013, 136,119 persons in the United States were diagnosed with colorectal cancer, with 51,813 deaths. Overall 1 in 21 to 23 Americans will develop colon cancer if preventive measures do not improve. Many of the deaths could be prevented by early treatment of precancerous lesions, such as polyps, and early detection of malignancy. The American Cancer Society recommends fecal tests for occult blood (FOBT), every year for those older than 40 years old and a sigmoidoscopy every 3 to 5 years for those older than 50 years old. Following a survey, the CDC and American Cancer Society are promoting a routine screening for all persons greater than age 50—to include FOBT, sigmoidoscopy, and colonoscopy—to ensure more early detection and treatment Most malignant neoplasms develop from adenomatous polyps, of which there are diverse types. A polyp is a mass, often on a stem, that protrudes into the lumen, and many polyps represent genetic abnormalities (Fig. 17.38). As polyps increase in size, they carry an increased risk of dysplasia and malignant changes. These adenocarcinomas are distributed about equally in the right (or ascending) colon, the left (or descending) colon, and the distal sigmoid colon and rectum. In recent years, an increasing number of tumors have been found in the right colon using barium enema or CT scans. Lesions in this location are more difficult to diagnose at an early stage because a routine rectal digital examination or proctosigmoidoscopy does not suffice. Tumors in the sigmoid colon and rectum are more easily accessible Carcinomas may manifest differently—for example, as circumferential or annular constrictive "napkin-ring" growths, which are common in the left colon, or as projecting polypoid masses, which are common in the right colon. Flat ulcerating lesions occur less frequently. All types of carcinomas invade the wall, the mesentery, and the lymph nodes and metastasize to the liver. Staging is based on the degree of local invasion, lymph node involvement, and the presence of distant metastases Most adenocarcinomas release carcinoembryonic antigen (CEA) into the blood. Detection of this antigen has limited value as a screening tool because it is also elevated in other conditions, such as ulcerative colitis. However, the presence of the antigen is useful to monitor for recurrence after removal of a tumor This cancer occurs primarily in persons older than age 55. It is more common in the Western hemisphere. The presence of familial multiple polyposis or long-term ulcerative colitis in a patient increases the risk of cancer developing, often at a younger age. Genetic factors are responsible for the increased occurrence of colorectal cancer among close relatives. Environmental factors, such as diet, also appear to play a major role in carcinogenesis. Diets high in fat, sugar, and red meat are thought to produce carcinogenic substances, particularly long term. Low-fiber diets increase risk because they prolong the contact time of the mucosa with carcinogens.

Liver Failure

Condition in which all normal functions of the liver are severely deficient Due to variety of diseases including cirrhosis Loss of function Less albumin production (hypoalbuminemia) Ascites Fibrinogen & prothrombin decrease Blood clotting Detoxification fails Hepatic encephalopathy-due to ammonia build-up General liver failure (no longer becoming functional) Cirrhosis is a disorder in which there is progressive destruction of liver tissue leading eventually to liver failure, when 80% to 90% of the liver has been destroyed. It is the result of a number of chronic liver diseases Liver failure, resulting from hepatobiliary obstruction, is often the cause of death. Cirrhosis Gradual destruction of liver tissue with loss of function and ultimately liver failure

Describe the male congenital abnormalities of epispadias

Congenital Abnormalities of the Penis Epispadias and Hypospadias Urethral opening on dorsal penis Epispadias refers to a urethral opening on the dorsal (upper) surface of the penis, proximal to the glans. If the urethral defect extends proximally and affects the urinary sphincter, incontinence may result. Infections may result from stricture at the opening. In some cases, this condition is associated with exstrophy of the bladder, which is a failure of the abdominal wall to form across the midline.

hypospadias (also chordee)

Congenital Abnormalities of the Penis Epispadias and Hypospadias Urethral opening on ventral penis May result in chordee Hypospadias is a urethral opening on the ventral (under) surface of the penis. If the opening occurs in the proximal section of the penis, it is considered more severe and may be accompanied by chordee, ventral curvature of the penis. Other abnormalities such as cryptorchidism are often associated with hypospadias. Surgical reconstruction, which may be performed in stages, is recommended for both epispadias and hypospadias to provide normal urinary flow and normal sexual function

Crohn's disease

Crohn disease may affect any area of the digestive tract, but it occurs most frequently in the small intestine, particularly the terminal ileum and sometimes the ascending colon. Inflammation occurs in a characteristic distribution called skip lesions, with affected segments clearly separated by areas of normal tissue Initially inflammation occurs in the mucosal layer with the development of shallow ulcers. The ulcers tend to coalesce to form fissures separated by thickened elevations or nodules, giving the wall a typical cobblestone appearance. The progressive inflammation and fibrosis may affect all layers of the wall (transmural), leading eventually to a thick, rigid "rubber hose" wall. This change leaves a narrow lumen ("string sign"), which may become totally obstructed. Granulomas indicative of chronic inflammation may be found in the wall and the regional lymph nodes. The damaged wall impairs the ability of the small intestine to process and absorb food. The inflammation also stimulates intestinal motility, decreasing the time available for digestion and absorption. Interference with digestion and absorption in the small intestine may lead to hypoproteinemia, avitaminosis, malnutrition, and possibly steatorrhea Other complications are common. Adhesions between two loops of intestine may develop when the subserosa is inflamed. The ulcers may penetrate the intestinal wall, causing abscesses to form. Fistulas, a connecting passage between two structures, may form as the ulcer erodes through the intestinal wall. Fistulas may be found between two loops of intestine (see Fig. 17.33D), the intestine and the bladder, or the intestine and the skin. Perianal fissures and fistulas are common. The course of Crohn disease is variable. Exacerbations are marked by diarrhea with cramping abdominal pain. The stool is typically soft or semiformed. Melena may occur if the ulcers erode blood vessels. Pain and tenderness are often centered in the right lower quadrant. Anorexia, weight loss, anemia, and fatigue are associated with malabsorption and malnutrition. Children experience delayed growth and sexual maturation resulting from a lack of adequate protein and vitamins, particularly fat-soluble vitamins A and D. Treatment with glucocorticoids also hampers growth. In addition, many psychological implications are characteristic of this type of chronic illness.

Chronic inflammatory bowel disease

Crohn's disease and ulcerative colitis are chronic inflammatory bowel diseases (IBDs). Causes unknown Genetic factor appears to be involved. Crohn's disease—often during adolescence Ulcerative colitis—second or third decade Many similarities between Crohn's disease and ulcerative colitis -idiopathic and entire wall thickening, fibrosis, lumen stenosis, adhesions Crohn disease and ulcerative colitis are chronic inflammatory bowel diseases, the causes of which are unknown. Prevalence is estimated in the range of 500,000 cases in the United States, ranging from mild to severe. A genetic factor appears to be involved because there is a high familial incidence, and inflammatory bowel disease (IBD) is much more common among certain groups, namely whites, particularly Ashkenazi Jews (from Eastern Europe). Investigative studies on an immunologic abnormality continue because many individuals have high levels of various antibodies or human leukocyte antigen (HLA) and a cytokine, interleukin (IL) in the blood, and T lymphocytes that are cytotoxic to the mucosa. Two genes have been identified, which, if defective, are linked to Crohn disease. In many patients, particularly those with ulcerative colitis, there are manifestations of immune abnormalities elsewhere in the body, including iritis, ankylosing spondylitis, arthritis, and nephrolithiasis. There are many similarities between Crohn disease and ulcerative colitis, and there may be an overlap in their clinical presentation in some individuals (Table 17.7). Both diseases occur in males and females. Crohn disease often develops during adolescence, whereas ulcerative colitis more frequently appears in the second or third decade. These diseases are characterized by remissions and exacerbations as well as considerable diversity in the severity of clinical effects

Describe the different presentations of ovarian carcinoma

Cystadenocarcinomas May be benign, or low or high malignancy Endometrioid Carcinomas Highly malignant Prognosis based on tumor type and time of diagnosis Often goes undetected until it's too late (25% early diagnosis) 2/3 diagnosed after age 55 years S/S—bloating, fullness, indigestion, frequent urination, back ache, dyspareunia There are different types of ovarian cancer tumors, which vary in virulence. These types include serous, mucinous, and endometrioid tumors. The serous tumors account for the majority of malignant cases of ovarian cancer. Early indications of ovarian cancer include feeling of bloating and fullness, indigestion, frequent urination, backache, and pain with intercourse. The lack of a reliable screening test and the hidden nature of the cancer hinder early diagnosis. A large mass may be detected by pelvic exam. Transvaginal ultrasound CT scans, MRI, pelvic exams, and CA125 (a protein whose high levels indicate ovarian cancer) tests are current tools for diagnosis. Treatment involves surgery and chemotherapy

Periodontal disease (gingivitis, periodontitis)

Dental/Periodontal Disease Plaque-bacterial sheet Caries (cavities) Gingivitis-- gums (wraps around bones and goes around roots of your teeth; kind of dull)-- outer gum Build up plaque on outside and spreads Periodontal disease Tartar/calculus-hardened plaque Periodontal Disease --The periodontium consists of the gingivae (gums) and the anchoring structures for the teeth, which include the alveolar bone around the teeth, the cementum (or outer covering of the root of the tooth), and the periodontal ligament joining the cementum to the bone. Periodontitis is the infection and damage to the periodontal ligament and bone by microorganisms and the subsequent loosening and possible loss of the teeth. There are currently eight categories of periodontal disease, ranging from mild gingival disease to severe periodontitis. Periodontal disease is often caused by poor oral hygiene but can also be aggravated by systemic diseases and medications. Gingivitis --Normally the gingiva, or gums surrounding the teeth, are firm, light pink with a stippled appearance, well shaped, and anchor the teeth firmly (Fig. 17.7A). Changes in the gingiva may reflect local or systemic problems. Gingivitis, or inflammation of the gingiva, causes the gingival tissue to become red, soft, and swollen and to bleed easily. This may result from accumulated plaque, which is a mass of bacteria and debris adhering to the tooth, particularly near the gingiva. The involved microbes secrete substances that enable them to adhere to the tooth surface and to plaque. Calculus, or tartar, refers to calcified plaque, which is more irritating to tissue because of its hard, rough surface (see Fig. 17.7C). Poor oral hygiene also predisposes to gingivitis. However, toothbrush trauma (see Fig. 17.7B), resulting from improper or excessive brushing or use of abrasives, can create extensive grooving on the tooth surface, increase plaque retention and damage to the gingivae, and amplify tooth sensitivity Periodontitis --More serious forms of periodontal disease develop when there is an increase in activity of gram-negative anaerobic bacteria as they enter the plaque. Major destructive microbes in periodontal disease include Porphyromonas gingivalis (formerly Bacteroides oralis), Actinobacillus actinomycetemcomitans, and Bacteroides forsythus. These microbes secrete toxins and enzymes destructive to the tissues and white blood cells (WBCs). Such infection is not contagious. In addition to poor oral hygiene, periodontitis is aggravated by smoking, which promotes calculus formation (see Fig. 17.7D); cancer and chemotherapy; diabetes mellitus with decreased tissue resistance and poor healing (see Fig. 16.8A); and HIV infection (AIDS), in which periodontitis is rapidly progressive and often resistant to treatment (see Fig. 17.17D, presented later in the chapter). When periodontal disease develops, plaque and calculus have progressed on the tooth beneath the gingival margin, causing inflammation in the tissues around the root of the tooth. The subgingival areas are colonized by these gram-negative anaerobic bacteria, which ultimately destroy the periodontal attachment of the tooth and the surrounding alveolar bone. An enlarging periodontal pocket forms around the tooth, promoting more anaerobic bacterial activity and active infection. The mucosa is red and swollen and bleeds easily, and the teeth feel loose (see Fig. 17.7E, presented later in the chapter). Major treatment, including drugs and surgical procedures, is required to eradicate the infection and prevent loss of teeth

cryptorchidism

Disorders of the Testes and Scrotum Cryptorchidism Hydrocele, inguinal hernia, spermatocele, and varicocele Torsion Disorders of the Testes and Scrotum Cryptorchidism Congenital disorder Failure of testicle to descend into scrotum from abdomen in developing fetus Infertility results if both fail to descend (Abdominal temperature too high for sperm production) Increased risk for testicular cancer Maldescent of the testis, or cryptorchidism, occurs when one or both of the testes fails to descend into the normal position in the scrotum during the latter part of pregnancy (Fig. 19.2). The testis may remain in the abdominal cavity or discontinue the descent at some point in the inguinal canal or above the scrotum. In some cases, the testis assumes an abnormal position outside the scrotum; this is called an ectopic testis. In many cases, spontaneous descent occurs during the first year after birth The reason for maldescent is not fully understood. Possible factors include hormonal abnormalities, a short spermatic cord, or a small inguinal ring. If the testis remains undescended, the seminiferous tubules degenerate, and spermatogenesis is impaired. Of concern is the increased risk of testicular cancer in cryptorchid testes (see Chapter 23). Therefore surgical positioning of the testes in the scrotum before age 2 is advisable.

Describe the testicular and scrotal disorders of hydrocele

Disorders of the Testes and Scrotum Cryptorchidism Hydrocele, inguinal hernia, spermatocele, and varicocele Torsion Excess fluid in tunica vaginalis space Hydrocele occurs when excessive fluid collects in the potential space between the layers of the tunica vaginalis (Fig. 19.3A). This may occur around one or both testes and can be distinguished by transillumination Hydrocele may occur as a congenital defect in a newborn when peritoneal fluid accumulates in the scrotum. This fluid may be reabsorbed in time. The fluid may continue to escape from the peritoneal cavity if the proximal portion of the processus vaginalis, a section of peritoneal membrane, does not close off as expected after descent of the testes. Usually the scrotum fills with more fluid during the day, becoming larger and firmer, and then the fluid subsides during the night The other common finding in an infant in whom the processus vaginalis remains open is an inguinal hernia, which is a loop of intestine that passes through the abnormal opening (see Fig. 17.41A). Such a hernia usually leads to intestinal obstruction. Surgical repair is recommended if the opening remains patent or herniation persists because there is a risk that the herniated intestinal loop may become strangulated Acquired hydrocele may result from scrotal injury, an infection, a tumor, or unknown causes. Acquired hydroceles are more common after middle age. Large amounts of fluid may compromise the blood supply to the testis, requiring aspiration.

Discuss how disseminated intravascular coagulation (DIC) can become a complication of pregnancy

Disseminated Intravascular Coagulation (DIC) May develop w/preeclampsia & abruptio placentae Usually related to excessive bleeding DIC is not a primary problem, but is a serious complication of events such as abruptio placentae and preeclampsia. In DIC, an increased activation of the clotting mechanism occurs, resulting in diffuse blood clots and excessive consumption of all clotting factors. Diagnosis is confirmed by the low serum levels of clotting factors. This situation leads to hemorrhage as the clotting factors are no longer available for normal clotting. The formation of multiple thrombi in the tissues causes organ damage in later stages, but the signs of DIC are related to hemorrhage in the early stages. Bleeding may occur from the uterus, at injection sites, from the nose or mouth, under the skin (purpura), or internally

Dumping syndrome

Dumping Syndrome Lack of pyloric sphincter (e.g. partial gastrectomy)-- can cure people with type 2 diabetes Food moves directly into small intestine Abnormal chyme Hyperosmolar-draws water and results in diarrhea, cramps, and hypoglycemia-- not enough water in it (absorbs water out of intestine) -- results in diarrhea Crash from too much sugar Stomach removed Lacking pyloric sphincter Dumping syndrome, in which control of gastric emptying is lost, may occur after gastric resection (eg, partial gastrectomy) because the pyloric sphincter is removed. Large quantities of ingested food are rapidly "dumped" into the intestine.The storage stage in the stomach, which includes appropriate dilution of chyme by gastric secretions, is missed. The hyperosmolar chyme draws more fluid from the vascular compartment into the intestine (Fig. 17.17), adding to the intestinal distention and increasing intestinal motility. These changes lead to signs that occur during or shortly after meals, including abdominal cramps, nausea, and diarrhea. The concurrent hypovolemia causes dizziness or weakness, rapid pulse, and sweating. In addition, individuals with dumping syndrome may experience hypoglycemia 2 to 3 hours after meals. The rapid gastric emptying and absorption lead to high blood glucose levels and increased insulin secretion, which results in a rapid drop in blood glucose level with no reserve nutrients advancing slowly from the stomach. Rebound hypoglycemia then develops several hours after eating, with tremors, sweating, and weakness. These problems can usually be resolved by dietary changes, including consumption of frequent small meals that are high in protein and low in simple carbohydrates. Also, fluids should be taken between meals rather than with meals. These measures reduce the hypertonicity of the chyme and the fluctuations in blood glucose. In some cases, medication may be used to decrease intestinal motility.

Describe dysphagia and achalasia

Dysphagia-- difficulty swallowing Difficulty swallowing Achalasia Loss of innervation of lower esophageal sphincter Nervous condition (something wrong with nerves controlling swallowing mechanisms) Congenital atresia Stenosis-- scarring Get fibrosis (fiber tissue)-- narrows diameter of esophagus Esophageal diverticula Get a pouch that develops and food can get caught in it Tumors Pushing in on the esophagus and cannot swallow food Dysphagia, or difficulty in swallowing (Fig. 17.11), has many causes. It may result from a neurologic deficit, a muscular disorder, or a mechanical obstruction. Dysphagia may manifest as pain with swallowing, an inability to swallow larger pieces of solid material, or difficulty swallowing liquids, depending on the cause of the problem. Neurologic causative factors include infection, stroke, brain damage, and achalasia, which results from failure of the lower esophageal sphincter to relax owing to loss of innervation. This leads to an accumulation of food and dilation of the lower esophagus as entry of food into the stomach is delayed. Often chronic inflammation develops in the esophagus, and reflux of this food may lead to aspiration when the person assumes a supine position. There is an increased risk of esophageal carcinoma in an individual who has had long-term achalasia.

Discuss the development and consequences of an ectopic pregnancy

Ectopic pregnancy On increase—possibly due to increase in pelvic inflammatory disease (PID) Results in spontaneous abortion or rupture, which can cause severe hemorrhaging or peritonitis Ectopic pregnancy due to obstructed fallopian tube (due to scarring) Commonly called tubal pregnancy, an ectopic pregnancy occurs when the fertilized ovum (zygote) is implanted outside the uterus. In most cases of ectopic pregnancy, implantation occurs in the fallopian tube. The incidence has been increasing over the past 20 years, perhaps because of an increase in pelvic inflammatory disease that may scar the tube, restricting movement of the zygote to the uterus. Spontaneous abortion may follow in the early stages of pregnancy, or the embryo may continue to develop, eventually causing the tube to rupture. This may lead to severe hemorrhage or peritonitis (a serious infection in the peritoneal cavity; see Chapter 17) with loss of the fallopian tube. The pregnant woman experiences severe pelvic or abdominal pain as blood irritates the peritoneal membranes. Ectopic pregnancy is considered a medical emergency and requires prompt treatment, usually surgical removal of the embryo and associated tube, to prevent hemorrhage and shock. It is currently not possible to maintain a tubal pregnancy to the time the fetus would be viable outside the uterus.

Describe GERD

Esophagus is a tube with muscles (get food from oral cavity to stomach) Sphincter keeps things in stomach -- contents are being pushed up back into the esophagus Stomach lining (mucosa) is made to tolerate the acid Causes heartburn Gastroesophageal reflux disease (GERD) involves the periodic flow of gastric contents into the esophagus. It is often seen in conjunction with hiatal hernia as well as other conditions. The severity of GERD depends on the competence of the lower esophageal sphincter (LES) or the relative pressures on either side of the LES. For example, either a decrease in LES pressure or an increase in intraabdominal pressure allows more of the gastric contents to reflux back into the esophagus. Delayed gastric emptying may also be a factor. Episodes of reflux causing heartburn frequently occur 30 to 60 minutes after eating or at night. Frequent reflux of gastric acid leads to inflammation and ulceration of the mucosa and eventual fibrosis and stricture in the esophagus. Eliminating factors that reduce LES pressure, such as caffeine, fatty foods, alcohol intake, cigarette smoking, and certain drugs, may relieve the discomfort. Avoidance of spicy foods and use of medication may reduce reflux and inflammation.

Etiology of oral cancers (SCC)

Factors that can increase your risk of mouth cancer include: Tobacco use of any kind, including cigarettes, cigars, pipes, chewing tobacco and snuff, among others. Heavy alcohol use. Excessive sun exposure to your lips. The common cancer of the oral cavity is squamous cell carcinoma. These cancers are more common in persons older than age 40, particularly smokers, those with preexisting leukoplakia, or those with a history of alcohol abuse Malignant tumors inside the oral cavity have a poor prognosis because they tend to be hidden and painless. Routine dental care is important in identifying these lesions in an early stage. Common sites are the floor of the mouth and the lateral borders of the tongue (Fig. 17.9). There may be multiple lesions. The carcinoma appears initially as a whitish thickening and then develops into either a nodular mass or an ulcerative lesion, which persists. Intraoral cancer spreads first to the regional lymph nodes and nodes in the neck.

cleft palate

Failure of hard and soft palates to fuse 7-12 weeks into gestation More serious Hard palate does not form -- not coming together-- corrected surgically Unilateral cleft palate Cleft palate involves failure of the hard and soft palates to fuse between 7 and 12 weeks of gestation, creating an opening between the oral cavity and the nasal cavity. The infant has feeding problems because there is insufficient force developed in the mouth to suck and a high risk of aspirating fluid into the respiratory passages. Speech development is also impaired. Temporary measures include the use of special nipples or dental appliances that close off the nasal cavity. Surgical repair of the defect is necessary, and additional plastic surgery to correct growth defects or improve appearance is usually indicated (see Fig. 17.4D). Therapy with a speech-language pathologist and orthodontist promotes normal development. A multidisciplinary team is frequently required over a prolonged period when major clefts are present

Define steatorrhea and what it can tell us about the patient's digestion

Fat-rich, foul smelling stool Steatorrhea (bulky, fatty, foul stools) occurs Steatorrhea is "fatty diarrhea," marked by frequent bulky, greasy, loose stools, often with a foul odor. These stools are characteristic of malabsorption syndromes, such as celiac disease or cystic fibrosis, in which the food intake is not digested or absorbed. Fat is usually the first dietary component affected, and the presence of fat interferes with the digestion of other nutrients. The abdomen is often distended because of the bulk remaining in the intestines. Malnutrition is apparent in other tissues, unless disguised by edema caused by hypoproteinemia.

Common Manifestations of Liver Disease

Fatigue, anorexia, indigestion, weight loss Metabolic dysfunction in the liver, such as decreased gluconeogenesis; decreased bile for digestion and absorption; portal hypertension, leading to edema of intestinal wall and interfering with digestion and absorption Ascites Portal hypertension, elevated aldosterone and ADH levels, decreased serum albumin level, lymphatic obstruction in liver General edema Elevated aldosterone and ADH levels, decreased serum albumin level Esophageal varices, hemorrhoids Portal hypertension and collateral circulation Splenomegaly Portal hypertension Anemia Decreased absorption and storage of iron and vitamin B12, malabsorption, splenomegaly, bleeding Leukopenia, thrombocytopenia Splenomegaly, possible bone marrow depression by ammonia and other toxins Increased bleeding, purpura Decreased absorption of vitamin K, decreased production of clotting factors by liver, thrombocytopenia Hepatic encephalopathy, tremors, confusion, coma Metabolic dysfunction with inability to remove ammonia from protein metabolism and other toxic substances Gynecomastia, impotence, irregular menses Impaired inactivation of sex hormones (eg, estrogen) leads to imbalance Jaundice Impaired extraction and conjugation of bilirubin; decreased production of bile and obstruction of bile flow Pruritus Bile salts in the tissues resulting from biliary obstruction

Peptic ulcer disease (PUD), gastrointestinal ulcers, and their complications

Form of inflammation w. erosion of gastric mucosa H. pylori usually underlying cause Crater with area of surrounding necrosis Affected by gastric acid Pain relieved by........ Epigastric pain (by eating something) Bleeding Melena Hematemesis Penetration Cicatrization Pyloric stenosis Duodenal ulcer—perforation (hole through duodenum) Food empties into abdominal cavity Peritonitis PUD-- peptic ulcer disease Peptic ulcers occur most commonly in the proximal duodenum (duodenal ulcers) but are also found in the antrum of the stomach (gastric ulcers) or lower esophagus Peptic ulcers usually appear as single, small, round cavities with smooth margins that penetrate the submucosa. Once acid or pepsin penetrates the mucosal barrier, the tissues are exposed to continued damage because acid diffuses into the gastric wall. Ulcers may erode more deeply into the muscularis and eventually may perforate the wall. An area of inflammation surrounds the crater. When the erosion invades a blood vessel wall, bleeding takes place. Bleeding may involve a persistent loss of small amounts of blood or massive hemorrhage, depending on the size of the blood vessel involved. Chronic blood loss may be detected by the presence of iron-deficiency anemia or occult blood in the stool; one of these may be the first indicator of peptic ulcer. The mucosal barrier is composed essentially of the tightly packed epithelial cells with tight junctions that can regenerate quickly and are covered by a thick layer of bicarbonate-rich mucus. The development of peptic ulcers begins with a breakdown of the mucosal barrier, which results from an imbalance between the mucosal defense system and forces that are potentially damaging to it. Given the material that is ingested by the stomach and the fact that the powerful and highly acidic gastric secretions can digest protein in food, it is remarkable that the gastric defenses can maintain the integrity of the tissues as well as they do Many factors may contribute to the decreased resistance of the mucosa or excessive hydrochloric acid or pepsin secretion. Impaired mucosal defenses seem to be a more common condition in gastric ulcer development, whereas increased acid secretion is a predominant factor in duodenal ulcers. Currently considered to be of major significance is infection with the bacteria Helicobacter pylori, found in most persons with peptic ulcer disease, although their precise role is not totally understood. Not all persons with H. pylori infection develop ulcers, but eradication of the infection promotes rapid healing of the ulcer. Helicobacter pylori are known to secrete cytotoxins and the enzymes protease, phospholipase, and urease (which releases ammonia), all of which cause damage to mucosal defenses. In addition, the mucosal barrier may be damaged by the following: An inadequate blood supply (eg, vasoconstriction caused by stress, smoking, or shock; circulatory impairment in elderly persons; scar tissue; or severe anemia), which interferes with the rapid regeneration of the epithelium and the production of sufficient mucus, as well as reducing the secretion of alkaline bicarbonate Severe or prolonged stress appears to affect both sides of the balance, reducing mucosal blood flow and motility, leading to stasis of chyme, and increasing glucocorticoid effects. Also, stress may promote behaviors that are often implicated in ulcer development, such as increased caffeine and alcohol intake, cigarette smoking, and altered eating patterns, which often include both irregular hours for meals and ingestion of irritating foods. Healing of peptic ulcers is difficult because the lesion cannot be isolated from the irritants in the environment. During the healing process, granulation tissue forms deep in the cavity, and new epithelial tissue regenerates from the edges. This granulation tissue often breaks down because it is subject to damage by the chyme. Because a longer time is often required for healing, more fibrous scar tissue develops at the site. The ulcers tend to recur because predisposing factors remain or the scar tissue itself interferes with the blood supply to the area. Several complications may accompany peptic ulcer. The ulcer may erode a blood vessel, causing hemorrhage, a common complication (Fig. 17.14B). Rupture of a small blood vessel causes continued loss of small amounts of blood, usually apparent as occult blood in the stool, whereas erosion of a large blood vessel leads to massive hemorrhage, indicated by hematemesis and shock. Hemorrhage may be the first sign of a peptic ulcer A second potential complication, perforation, occurs when the ulcer erodes completely through the wall, allowing chyme to enter the peritoneal cavity (see Fig. 17.14D). This process results in chemical peritonitis, inflammation of the peritoneal membranes and other structures in the abdominal cavity. Eventually this inflammation causes increased permeability of the intestinal wall, passage of bacteria and their toxins into the peritoneal cavity, and bacterial peritonitis. Hemorrhage is not necessarily present when perforation occurs. Third, obstruction of the digestive tract may result later from stricture caused by scar tissue around the pylorus or duodenum, particularly in people with protracted or recurrent ulceration. Etiology Infection with H. pylori is considered an underlying cause of the majority of cases of peptic ulcers. Peptic ulcers are more common in men than women, and people in developed countries have a higher incidence, perhaps because of lifestyle factors. A genetic factor seems to be involved in the frequent familial incidence of duodenal ulcers; also, these ulcers are more common in persons with blood group O. Gastric ulcers are more common in older individuals, those with scar tissue, and those who regularly take ulcerogenic antiinflammatory medications (aspirin or NSAIDs). Multiple factors, such as those listed, are usually involved in the cause. Stress Ulcers Stress ulcers result from severe trauma, such as burns or head injury, or occur with serious systemic problems, such as hemorrhage or sepsis. Ulcers in the presence of burns are often called Curling ulcers, those seen with head injury are termed Cushing ulcers, and others may be referred to as ischemic ulcers. Multiple ulcers, usually gastric ulcers, form within hours of the precipitating event, as the blood flow to the mucosa is greatly reduced, leading to reduced secretion of mucus and epithelial regeneration (see Fig. 17.16). The mucosal barrier is lost, and acid diffuses into the mucosa. In people with Cushing ulcers, increased vagal stimulation of acid secretion often occurs. The first indicator of stress ulcers is usually hemorrhage because of the rapid onset and masking by the primary problem. Prophylactic medications are usually administered as soon as possible to minimize the risk of stress ulcer development in cases of trauma.

Paralytic (lack of nerve stimulation or exterior stifling of peristalsis)

Functional obstruction or paralytic ileus is common in the following situations: After abdominal surgery, in which the effects of the anesthetic combined with inflammation or ischemia Intussusception may occur secondary to polyps or tumors that pull a section of bowel forward with them (see Fig. 17.41C) ~ Volvulus (twisting of a section of intestine on itself), which may be linked to adhesions; in many cases, the cause of intussusception or volvulus is unknown ~ Hirschsprung disease, or congenital megacolon, a condition in which parasympathetic innervation is missing from a section of the colon, impairing motility and leading to constipation and eventually obstruction; Hirschsprung disease often occurs in conjunction with other anomalies ~ Gradual obstruction from chronic inflammatory conditions, such as Crohn disease or diverticulitis in the operative area interfere with conduction of nerve impulses ~ In the initial stage of spinal cord injuries (spinal shock) ~ With inflammation related to severe ischemia ~ In pancreatitis, peritonitis, or infection in the abdominal cavity ~ With hypokalemia, mesenteric thrombosis, or toxemia Mechanical obstruction may result from the following: ~ Adhesions (from previous surgery, infection, or radiation) that twist or constrict the intestine, the most common cause of obstruction ~ Hernias (protrusion of a section of intestine through an opening in the muscle wall; Fig. 17.43) ~ Strictures caused by scar tissue ~ Masses, such as tumors or foreign bodies ~ Intussusception (the telescoping of a section of bowel inside an adjacent section)

Describe the pathophysiology of gastric cancer (adenocarcinoma)

Gastric cancer arises primarily in the mucous glands; most tumors occur in the antrum or pyloric area, and some affect the lesser curvature of the stomach or cardia (see Figs. 17.14 and 17.15). There has been an increase in tumors in the upper stomach near the entrance to the esophagus. Adenocarcinoma occurs most frequently. The lesion is most often an ulcerative type with an irregular crater and a raised margin. Other forms of gastric cancer may infiltrate the gastric wall, causing thickening, or may appear as a protruding mass or polyp. Early gastric carcinoma is a lesion confined to the mucosa and submucosa, whereas advanced gastric carcinoma involves the muscularis layer. Eventually the tumor extends into the serosa and spreads to the lymph nodes (regional and supraclavicular) and to the liver and ovaries. Gastric cancer is asymptomatic in the early stages and usually is not diagnosed until it is well advanced, at which point the prognosis is poor. Adenocarcinoma malignant tumor arising from glandular epithelial cells

Describe the etiology of gastroenteritis

Gastroenteritis-- with viral infection or allergy Usually infection, allergy possible Gastric mucosal inflammation stimulates vomiting and diarrhea Often food or water-borne illness Handwashing helps avoid this Involves more than the stomach Gastroenteritis is the involvement of the stomach and the intestines in an inflammatory process. It is usually caused by infection but may also result from allergic reactions to foods or drugs. Inflammation of the gastric mucosa stimulates vomiting, whereas diarrhea results when the inflammation of the intestines causes increased motility, impaired absorption, and in some cases, increased secretions. Nausea and abdominal cramps are usually present. Fever and malaise are common. Many microorganisms may be transmitted by fecally contaminated food and water. Common causes of foodborne infections are summarized in Table 17.4. Most infections are mild and self-limiting, but occasionally serious illness results when the host is immunosuppressed or the agent is more virulent Often a food- or water-borne illness will involve a large number of cases; in some outbreaks, entire communities may be infected. It is imperative that in times of disaster clear instructions be given about the safety of food and water. Safe sanitation must be put in place as quickly as possible to prevent further illness requiring the use of scarce health resources Some infections are seasonal or occur as epidemics. For example, rotaviruses cause serious infection, with vomiting and watery diarrhea, sometimes with ulceration and bleeding, in young children in temperate climates during the winter months. Epidemics of viral gastroenteritis are common in day care centers and institutions. Careful handwashing and food handling can reduce outbreaks. The infection is usually self-limiting, although supportive treatment may be needed for fluid and electrolyte losses, particularly in young children and the elderly. A stool culture is helpful in identifying the causative organism in persistent cases.

Describe the viral STDs genital herpes (HSV2)

Genital herpes HSV2 Blister-like lesions appear (vesicles) on genital areas or buttocks or thighs Acute stage presents with systemic signs Travels up dermatome to spinal ganglia where it resides until triggered again (stress, respiratory infections) May be transferred to infant during vaginal delivery and cause nervous system damage and even death Places women at high risk for cervical cancer Herpes genitalis is usually caused by HSV-2, although some cases result from HSV-1. HSC-1 is the agent that also causes herpes labialis, or cold sores (discussed in Chapter 8), and may cause genital lesions if oral sex is practiced or if it is autoinoculated by the hands. The lesions are similar, and a tingling and burning sensation at the site usually precedes the appearance of the actual lesion. The lesion characteristic of herpes is a vesicle (blister) surrounded by an erythematous area (Fig. 19.23). The vesicle ruptures after several days, leaving a painful ulcerated area and watery exudate. Eventually a crust forms over the ulcer, and it heals spontaneously in 3 to 4 weeks. Sometimes the initial episode is very mild and not noticed. In women, the lesion is usually found on the cervix, vulva, or urethra. Men have lesions on the penis, scrotum, or urethra. Vesicles may also appear on the buttocks or thighs Systemic signs may be present during the acute stage, including fever, headache, and lymphadenopathy. Following this acute stage, the herpes virus usually migrates along the dermatome to the dorsal sacral root ganglion and there enters a latent stage. Body secretions may contain viruses for a time after the visible lesion heals When reactivated, the virus migrates back to the mucosa or skin and enters the host cells for replication, forming a new vesicle. Reactivation may be triggered by many factors, such as respiratory infections or stress. Recurrent herpes is more common with HSV-2 than with HSV-1. Prodromal signs, such as tingling or burning, signal recurrence before the lesion appears The fluid in the vesicles contains many viruses and may spread the infection to the eyes or skin elsewhere if caution and careful handwashing are not practiced. Active lesions in the vagina or cervix may transmit herpes virus to an infant during a vaginal delivery, frequently causing death or severe central nervous system damage. Delivery by cesarean section is advocated Cervical cancer frequently develops in women with genital herpes. Frequent Pap tests are suggested to monitor any tissue changes. An antiviral agent such as acyclovir (Zovirax) may be applied topically or taken orally to lessen the active stage of infection and reduce the shedding of viruses to some extent; drug-resistant strains of HSV have been identified. This treatment may lessen the symptoms but does not cure the infection Genital Herpes Virus Herpes simplex 2 (HSV-2) Vesicles and ulcers Recurs Meningitis Fetus/neonate damage No cure Antiviral drug, e.g., oral acyclovir, reduces activity and shedding

Define pregnancy associated terms gestation, parity, and gravidity

Gestation Time after 1st day of LMP + 280 days (10 lunar months) (Actually about 2 weeks longer than after conception) Gravidity Refers to number of pregnancy First-time pregnancy would be primigravida Parity Refers to number of pregnancies reaching viability Ex: woman completing 2 or more pregnancies to viability: multipara Trimesters Each about 3 months long surrounding significant changes to mother and fetus Gestation refers to the length of time since the first day of the LMP and equals 280 days (40 weeks) or 10 lunar months. Gestational age is 2 weeks longer than the actual age of the child from the time of fertilization—266 days or 38 weeks Gravidity and parity are terms used to describe a woman's history of pregnancy and childbirth. Gravidity refers to the number of pregnancies; for example, a primigravida is a woman who is pregnant for the first time. Parity refers to the number of pregnancies in which the fetus has reached viability (approximately 22 weeks of gestation). A multipara has completed two or more pregnancies to the point of fetal viability. Coding systems are available to document histories. For example, a fivedigit system records, in sequence, the number of pregnancies, the number of deliveries, the number of premature deliveries, the number of abortions of any type, and the number of children living. The history of a woman in her second pregnancy who has one child living and no other experiences would be recorded as 2-1-0-0-1.

Hepatitis

Hepatitis (viral)- inflammation of the liver Liver inflammation Viral cause Hep A, B, C, D, E Be able to know transmission of each type Exposed through hep B virus (transmitted through blood and body fluids) -- blood transfusions or drug infusions Some people have acute inflammation Hep a is most common -- does not last that long Hep c-- more recent and chronic and tends to spread through blood and goes through its path- no cure (antiviral treatment)-- asymptomatic Hepatitis refers to inflammation of the liver. It may be idiopathic (such as a fatty liver) or result from a local infection (such as viral hepatitis), from an infection elsewhere in the body (eg, infectious mononucleosis or amebiasis), or from chemical or drug toxicity. Mild inflammation impairs hepatocyte function, whereas more severe inflammation and necrosis may lead to obstruction of blood and bile flow in the liver and impaired liver cell function. Given the many functions of the liver, damage to the liver cells has extensive effects in the body. Fortunately, the liver has a good functional reserve and excellent regenerative powers. Although a number of viruses may affect the liver cells, hepatitis is considered to result from infection by a group of viruses that specifically target the hepatocytes. These include hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV). Other viruses that cause hepatitis have not yet been fully identified; meanwhile they have been temporarily designated F and G or non-A-E hepatitis virus The liver cells are damaged in two ways: by direct action of the virus (eg, hepatitis C) or via cell-mediated immune responses to the virus (eg, hepatitis B). Cell injury results in inflammation and necrosis in the liver. Both the hepatocytes and the liver appear swollen, and diffuse necrosis may be present. With severe inflammation, biliary stasis may develop, leading to backup of bile into the blood. Chronic inflammation occurs with hepatitis B, C, and D and is defined as persistent inflammation and necrosis of the liver for more than 6 months. This type of disease eventually causes permanent liver damage (fibrosis) and cirrhosis. There is also an increased incidence of hepatocellular cancer associated with chronic hepatitis. Hepatitis B, C, and D may exist in a carrier state, in which asymptomatic individuals carry the virus in their hepatocytes but can transmit the infection via their blood or body fluids to others. Carriers may be individuals who have never had active disease or have a chronic low-grade infection

Differentiate between A, B, C, D & E hepatitis

Hepatitis A. Also called infectious hepatitis, hepatitis A is caused by a small RNA virus called the hepatitis A virus, or HAV. It is transmitted primarily by the oral-fecal route, often from contaminated water or shellfish. Outbreaks may occur in day care centers. Sexual transmission has occurred in the homosexual population. Hepatitis A has a relatively short incubation period of 2 to 6 weeks. It causes an acute but self-limiting infection and does not have a carrier or chronic state --Fecal shedding of the virus (the contagious period) begins several weeks before the onset of signs (Fig. 17.22A). At this time, the first antibodies, IgM-HAV, appear, followed shortly by the second group of antibodies, IgG-HAV, which remain in the serum for years, providing immunity against further infection. A vaccine is available for those who are traveling to an endemic area or anyone with any liver disease; this vaccine is administered to both children and adults. Gamma globulin provides temporary protection and may be administered to those just exposed to HAV. Hepatitis B. In 2006 the Centers for Disease Control and Prevention (CDC) received reports of 4758 new cases in the United States but estimate the occurrence rate is 10 times that number, with many cases being asymptomatic. Further, there are more than 1 million carriers in the country and 4000 to 5000 deaths annually from associated cirrhosis and cancer. More than 50% of those who test HIV-positive are also positive for hepatitis B. Global estimates are more than 2 billion cases, with 350 million of those being carriers. Unfortunately, 50% of cases are asymptomatic, facilitating transmission to others. --Formerly called serum hepatitis, this form of hepatitis is caused by the hepatitis B virus (HBV), a partially double-stranded DNA virus. The whole virion is often called a Dane particle. This virus is more complex and consists of three antigens: two core antigens (HBcAg and HBeAg) and one surface antigen (HBsAg). Each antigen stimulates antibody production in the body (see Fig. 17.22). These serum antigens and antibodies are useful in diagnosing and monitoring the course of hepatitis, including the development of chronic hepatitis. For example, early in the course of the infection, infected liver cells produce large amounts of HBsAg. When this antigen persists in the serum, it poses a high risk of continued active infection and damage to the liver (chronic disease). A carrier state is also common for HBV, in which the individual is asymptomatic but is contagious for the disease. --Hepatitis B has a relatively long incubation period, averaging about 2 months. Long incubation periods make it more difficult to track sources and contacts for infections. A window, or prolonged lag time, occurs before the serum markers or symptoms become present, during which time the virus cannot be detected but can be transmitted to others --Hepatitis B virus infection is transmitted primarily by infected blood but is found in many body secretions. Blood transfusions are currently processed to reduce the risk of transmission. Intravenous drug abusers have a high incidence of HBV infection. Hemodialysis increases the risk, as does exposure to blood or body fluids in health care workers if barrier precautions are not taken. Sexual transmission has been noted, and HBV can be passed to the fetus during pregnancy. Activities such as tattooing and body piercing may transmit the virus. An HBV vaccine is available for long-term protection for those in high-risk groups, including health professionals, and is now routinely administered to children. Hepatitis B virus immune globulin is available as a temporary measure. Hepatitis C. -- Formerly called non-A-non-B (or NANB) hepatitis, hepatitis C is the most common type of hepatitis transmitted by blood transfusions. The virus is a singlestranded RNA virus. Approximately half the cases enter a chronic disease state. The World Health Organization estimates that 130 million to 170 million people are infected globally, and the CDC estimates the prevalence rate in the United States to be 3.2 million cases. Hepatitis C virus infection increases the risk of hepatocellular carcinoma. This form of hepatitis may exist in a carrier state. Hepatitis D. The agent for hepatitis D is also called delta virus. This incomplete RNA virus requires the presence of hepatitis B virus (HBsAg) to replicate and produce active infection. The hepatitis D virus infection usually increases the severity of HBV infection. Hepatitis D virus is also transmitted by blood; there is a high incidence of infection in intravenous drug abusers. Hepatitis E. Hepatitis E is caused by HEV, a singlestranded RNA virus, and is spread by the oral-fecal route. It is similar to HAV and lacks a chronic or carrier state. It is more common in countries in Asia and Africa, where it causes a fulminant hepatitis that produces a high mortality rate in pregnant women.

Hiatal hernias (particularly "sliding)

Hiatal hernia-- stomach that is herniated Big diaphragm -- hole in the middle for esophagus Stomach can move up to the hole Relatively asymptomatic-- might get caught and filled with food and starts to get inflammation going on with this In patients with hiatal hernia, part of the stomach protrudes through the opening (hiatus) in the diaphragm into the thoracic cavity. Normally the digestive tract is loosely attached to the diaphragm. There are two types of hiatal hernia (Fig. 17.13). With a sliding hernia, the more common type, a portion of the stomach and the gastroesophageal junction move above the diaphragm, particularly when the person is in the supine position. In the standing position, the herniated portion slides back down into the abdominal cavity. In a rolling or paraesophageal hernia, part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm. In this type of hernia, the blood vessels in the wall of the stomach may be compressed, leading to ulceration Food often lodges in the pouch created by the herniated portion, resulting in inflammation of the mucosa, reflux of food up the esophagus, and dysphagia, as the mass of food enlarges and obstructs the passageway. Chronic esophagitis eventually may cause fibrosis and stricture. Often an incompetent gastroesophageal sphincter is seen in individuals with hiatal hernia, which increases the risk of reflux. Factors contributing to hiatal hernia include shortening of the esophagus, weakness of the diaphragm, or increased abdominal pressure (eg, from pregnancy). The signs of hiatal hernia include heartburn or pyrosis, a brief substernal burning sensation, often accompanied by a sour taste in the mouth, which occurs after meals and results from reflux of the gastric contents up the esophagus. Frequent belching (gas) often accompanies this regurgitation. The discomfort is increased by lying down after eating, bending over, or coughing. Dysphagia is common, either because of inflammation of the esophagus or because the mass of food collected in the pouch compresses the esophagus. Persistent, mild, substernal chest pain after meals is a frequent complaint because of inflammation or distention of the pouch. The symptoms can often be reduced by eating frequent, small meals and avoiding a recumbent position after meals. Sliding hiatal hernia- Part of fundus above diaphragm Paraesophageal hernia- Sac and peritoneum in mediastinum Part of the stomach protrudes above the diaphragm, either temporarily or permanently, causing reflux and inflammation;

human papilloma virus (HPV)

Human papillomavirus (HPV) HPV causes genital warts (condylomata acuminata) Up to 6 months incubation Pregnancy promotes growth/spread Appearance may be cauliflower-like or flat and difficult to visualize Males Usually appear on penis Females Found in vagina or on the cervix A cause of cervical cancer Condylomata Acuminata (Genital Warts) Certain types of HPV cause genital warts, an STD that is increasing in frequency. HPV is a circular, doublestranded DNA virus. There are many types of HPV, of which several affect the genital tract. Several of these types also are considered to be a cause of cervical cancer. The incubation period for this infection may be as long as 6 months, and the disease may be asymptomatic, depending on the location of the lesions. Pregnancy promotes the growth and spread of genital warts The condylomata, or warts, vary in appearance from soft, fleshy projections or cauliflower-like masses to flat lesions, to small pointed masses. Flat condylomata require preliminary treatment with acetic acid before they can be visualized. Biopsy is useful in differentiating condylomata from other causes of dysplasia or hyperkeratoses. In women the lesions may be present in the cervix or vagina, and in men they frequently are found on the penis. Genital warts may be removed by a number of different methods, including surgery, laser, cryotherapy, and topical caustics, but they tend to recur. Genital Warts Virus Human papillomavirus (HPV) Soft gray mass or polyp None Can be removed, but rarely cured

Recognize the components of the acronym HELLP

In some patients with preeclampsia, a complication develops. This condition is known for its manifestations by the acronym HELLP (for Hemolysis, Elevated Liver enzymes, and Low Platelets). In a few cases, HELLP progresses to coagulation disorders such as disseminated intravascular coagulation (DIC), as indicated by excessive bleeding. Also, preeclampsia may progress to eclampsia, in which the blood pressure becomes extremely high and generalized seizures (grand mal) or coma develops. Immediate hospitalization is required for adequate treatment of eclampsia.

Intestinal Cancer

Intestinal Obstruction Blockage of intestine (ileus) due to: Mechanical Paralytic (lack of normal peristalsis) Hirschsprung's disease Back up, increased pressure (infarction/pressure necrosis) Can lead to gangrene Rupture Contents spill into peritoneum (peritonitis) There are five types of small intestine cancer. The types of cancer found in the small intestine are adenocarcinoma, sarcoma, carcinoid tumors, gastrointestinal stromal tumor, and lymphoma. This summary discusses adenocarcinoma and leiomyosarcoma (a type of sarcoma)

Urolithiasis (development of urinary tract stones)

Kidney stone (urolithiasis) Urolithiasis (Calculi, or Kidney Stones) Kidney stones are a common problem and frequently recur if the underlying cause is not treated. Calculi can develop anywhere in the urinary tract. Stones may be small or very large (eg, staghorn calculus, a very large stone that forms in the renal pelvis and calyces in the shape of a deer's antlers). Calculi tend to form when there are excessive amounts of relatively insoluble salts in the filtrate or when insufficient fluid intake creates a highly concentrated filtrate. Once any solid material or debris forms, deposits continue to build up on this nidus, or focus, and eventually form a large mass. Cell debris from infection may also form a nidus. Immobility may result in calculi in the kidney because of stasis of urine resulting in chemical changes in the urine (see Chapter 25). Increasing fluid intake (at least eight glasses of water per day) can assist in removing small stones quickly from the urinary tract. Stones usually cause manifestations only when they obstruct the flow of urine (eg, in the ureter). Calculi may lead to infection because they cause stasis of urine in the area and irritate the tissues. This may be an early indication of calculi formation. When located in the kidney or ureter, calculi may cause the development of hydronephrosis, with dilation of calyces and atrophy of renal tissue related to the back pressure of urine behind the obstructing stone Approximately 75% of calculi are composed of calcium salts, with the remainder consisting primarily of uric acid (a breakdown product of purine nucleotides) or urates, struvite (magnesium ammonium phosphate), or cystine (rare), depending on the predisposing factor. Calculi should be examined and urinalysis completed to determine the content of the stones and the predisposing factors Calcium stones (phosphate, oxalate, or carbonate) form when calcium levels in the urine are high due to hypercalcemia, perhaps due to a parathyroid tumor or other metabolic disorder (see Fig. 18.6C). The solubility of calcium salts and uric acid also varies with the pH of the urine. Calcium stones form readily when the urine is highly alkaline. Inadequate fluid intake is a major factor in calculus formation. Calcium oxalate stones may develop in people following vegetarian diets high in oxalate that lead to increased levels of oxalate in the urine. Uric acid stones develop with hyperuricemia (due to gout, high-purine diets, or cancer chemotherapy), especially when the urine is acidic. Infection may cause stones consisting of mixed inorganic salts because in such cases the urine pH is alkaline and debris from the infection may act as a focus for the deposition of crystals.

Discuss the development of Rh incompatibility

Mother is Rh- & baby is Rh+ Placental tear during birth exposes mom to baby's Rh+ Mom develops antibodies to Rh+ Antibodies will attack future fetuses Results in hemolysis, increased bilirubin, jaundice, and possible neurologic damage Indirect Coombs test screens during pregnancy A yet-unsensitized mother can be given Rh immunoglobulin (RhoGam) within 72 hrs of delivery to suppress her own immune system's response to the baby's Rh+ antigen Blood incompatibility can develop when the Rh factor antigens on fetal red blood cells differ from those on maternal red blood cells. Rh incompatibility can be more serious when it leads to hemolytic disease of the newborn (erythroblastosis fetalis). Rh incompatibility results when the mother is Rh negative and the fetus is Rh positive (Fig. 22.2). During the first pregnancy there are usually no problems unless the mother has been exposed to Rh-positive blood at some prior time through a blood product or abortion. At the end of the first pregnancy, when the placenta tears during delivery, some Rh-positive fetal blood enters the maternal circulation, stimulating the formation of antibodies to Rh-positive cells in the mother. During subsequent pregnancies, the maternal Rh antibodies cross the placenta to the fetus. The resulting antigen-antibody reaction in the fetus destroys the fetal red blood cells. Hemolysis of red blood cells leads to severe anemia or low hemoglobin and possible heart failure and death in the child. Hemolysis also causes high serum bilirubin levels in the child, resulting in jaundice (yellow color in the eyes and skin; see Chapter 17) and potential neurologic damage (kernicterus) as bilirubin enters brain tissue If the fetus experiences severe hemolysis in utero, an early birth or intrauterine transfusion may be recommended. After birth, an exchange transfusion may be required. When the neonate is jaundiced, phototherapy (exposure of the newborn's body to fluorescent or blue light) can reduce serum bilirubin levels by promoting conjugation of bilirubin and excretion in the bile Routine screening of maternal blood for Rh antibodies (indirect Coombs test) is carried out early in pregnancy and at regular intervals during the pregnancy. If the mother has not become sensitized and developed antibodies, for example, during the first pregnancy, she can be given passive immunity at the time of delivery to suppress the immune response temporarily. This is done by administering Rh immunoglobulin (RhoGAM) to the mother within 72 hours of delivery. This process prevents sensitization of the mother as a result of fetal red blood cells entering her body during labor and delivery

Nephrosclerosis

Nephrosclerosis (Arteriosclerosis) Plaque build up on vessels supplying kidneys Reduced blood flow ischemia Glomeruli damaged Harden Atrophy Lost nephrons replaced by fibers Glomerulosclerosis Nephrosclerosis involves vascular changes similar to those of arteriosclerosis in the kidney. Some vascular changes occur normally with aging, but these excessive changes cause thickening and hardening of the walls of the arterioles and small arteries and narrowing or occlusion of the lumina of the blood vessels. Such changes reduce the blood supply to the kidney, causing ischemia and atrophy, and stimulate the secretion of renin, ultimately increasing the blood pressure (Fig. 18.14). Continued ischemia can lead to gradual destruction of renal tissue and chronic renal failure. Often such damage is asymptomatic until a late stage. It is often difficult to determine whether the primary lesion has developed in the kidney or if it is secondary to essential hypertension (see Chapter 12), diabetes mellitus (see diabetic nephropathy and Fig. 16.6 in Chapter 16), or another condition. In any case, a vicious cycle can develop with the kidneys and hypertensive changes, and this must be broken to prevent renal failure or other complications of hypertension such as congestive heart failure. Drugs such as antihypertensive agents, diuretics, ACE inhibitors, and beta blockers (which block renin release) all can assist in maintaining renal blood flow and reducing blood pressure. These drugs are discussed in Chapter 12 (see Table 12.1). Sodium intake should be reduced as well.

Pancreatitis

Pancreatitis acute chronic Cystic Fibrosis Neoplasia (cancer) lots of swelling & inflammation around the pancreas Digestive enzymes in pancreas begin to 'eat self' (autolysis) Normally pancreatic enzymes become active in the intestines Causes enzymatic necrosis If acute, it is incredibly painful Pancreas secretes enzymes -- have to be activated Autodigestion (breakdown)- self digestion (death of cells due to enzymes breaking apart) Acute Pancreatitis S/S: pain [moderate to severe] in the upper abdomen that is felt through the back (acute abdomen) rigidity [guarding] nausea/vomiting BP decreases HR increases cold extremities possible LOC Digestive effects: Maldigestion malabsorption Most severe—acute hemorrhagic pancreatitis Necrotic areas and inflamed areas Chronic Pancreatitis Pancreas that is not function-- associated with chronic alcoholism Pancreatic insufficiency Often associate with chronic alcoholism Destruction of exocrine/endocrine glands Gradual loss of normal function Called pancreatic insufficiency Permanent malabsorption and diabetes Fats not absorbed Steatorrhea Fat-rich, foul smelling stool

Discuss the pathophysiology and complications of female reproductive infections and pelvic inflammatory disease (PID)

Pelvic Inflammatory Disease (PID) Infection of entire reproductive tract Follows ascending path through vaginal entry Agents: Staphylococcus, Streptococcus, E. Coli Viruses (such as herpes) Gonorrhea and chlamydia Clinical presentation: Lower abdominal pain Fever Vaginal discharge Sources other than STDs: Bad abortion or delivery practices Complications: Abdominal abscesses and peritonitis Septic shock (and death) Adhesions, fallopian scarring infertility Ectopic pregnancy due to obstructed fallopian tube (due to scarring) Many infections of the vagina (vaginitis) and cervix (cervicitis) are considered STDs and are included in the section on these diseases later in this chapter. Other inflammations of the female reproductive organs often caused by infections include salpingitis (inflammation of the oviduct or fallopian tube), urethritis (inflammation of the urethra), oophoritis (inflammation of the ovaries), and mastitis (inflammation of the mammary gland). In addition to infections caused by organisms passed on through sexual contact, other infections may arise through non-sexually transmitted organisms such as Staphylococcus aureus, which is the bacteria primarily responsible for toxic shock syndrome and mastitis. Candidiasis is one form of vaginitis that is not sexually transmitted. It is a yeast infection caused by C. albicans (Monilia) and usually occurs as an opportunistic superficial infection of mucous membranes or skin (see Fig. 6.7). Infection may follow antibiotic therapy for an unrelated bacterial infection elsewhere in the body (which creates a more alkaline pH and upsets the balance of resident flora) or may develop because of decreased resistance (e.g., in immune-deficiency states) or increased glycogen or glucose levels in the secretions (e.g., with pregnancy, use of oral contraceptives, or diabetes) PID is an infection of the reproductive tract, particularly the fallopian tubes and ovaries. The condition includes cervicitis endometritis (uterus), salpingitis, and oophoritis. The infection may be acute or chronic. PID is a common problem and is a matter of concern because of the potential acute complications such as peritonitis and pelvic abscess as well as the long-term problems of infertility and the high risk of ectopic pregnancy The infection usually originates as a vaginitis or cervicitis and is polymicrobial, often involving several causative bacteria. The microbes ascend through the uterus into the fallopian tubes (Fig. 19.13). The early stage of inflammation promotes additional invasion of bacteria into the mucosa. The tubal walls become edematous, and the lumen is filled with purulent exudate, effectively obstructing the tube and restricting drainage into the uterus. The exudate drips out of the fimbriae onto the ovary and surrounding tissue. The peritoneal membranes attempt to localize the infection initially, but peritonitis may develop (see Chapter 17). Abscesses may form as the inflammatory response struggles to contain or wall off the infection. Pelvic abscesses may be life threatening if not quickly drained surgically. Infection may spread, resulting in septicemia. The most common cause of death in women with PID is septic shock. Adhesions and strictures are common sequelae; they affect the tubes and ovaries, leading to infertility or ectopic pregnancy (implantation of the fertilized ovum in the fallopian tube). Adhesions or scar tissue may also affect the surrounding structures such as the colon. The majority of infections arise from STDs such as gonorrhea (Neisseria gonorrhoeae) and chlamydiosis (Chlamydia trachomatis). Multiple organisms are present in many cases. Other potential agents include Bacteroides, Gardnerella vaginalis, group B streptococci, E. coli, Pseudomonas, Haemophilus influenzae, and Enterococcus A prior episode of vaginitis or cervicitis, often with few signs, frequently precedes the development of PID. Infection is likely to become acute during or immediately after menses, when the endometrium is more vulnerable. PID may also result from insertion of an intrauterine device (IUD, a contraceptive device) or other instrument contaminated by organisms from the lower reproductive tract or other source. Any instrument or device is likely to traumatize the tissue or perforate the wall, leading to inflammation and infection (see Fig. 19.13B—note the adhesions around the IUD). Infection may also be associated with abortion or childbirth.

Explain why varicose veins and hemorrhoids develop during pregnancy

Physiologic Changes & Their Implications Weight Gain & Nutrition About 25-30 lbs (11-14 kgs) Mostly in last trimester Mom's increased metabolic rate = increased appetite Cravings often for snacks—nutritional concerns plus development of dental caries (due to diet, fatigue) Digestive System 1st trimester nausea/vomiting common If severe (hyperemesis gravidarum) may lead to electrolyte imbalance and nutritionally impair fetal development—requires hospitalization Progesterone relaxes smooth muscle so gastro-intestinal motility is affected resulting in reflux, bloating, constipation (which may also lead to hemorrhoids) Nausea and vomiting are common in the first trimester because of the hormonal changes that occur in pregnancy. Changes in eating patterns often reduce discomfort. Frequent small meals, avoidance of fatty or spicy foods, and a reduced fluid intake with meals are suggested. Medication is recommended only in severe cases. The combination drug doxylamine-pyridoxine has been studied extensively and appears to be a safe treatment during pregnancy. Severe uncontrollable vomiting, or hyperemesis gravidarum, may lead to dehydration and electrolyte imbalances and may affect nutrition at a critical point in fetal development. Hospital care is often necessary to maintain fluid and electrolyte balance. The relaxation of smooth muscle in the stomach and intestines by progesterone results in decreased motility in the digestive tract, slower emptying of the stomach, reflux of stomach contents into the esophagus (heartburn), and feelings of bloating and abdominal discomfort. The pressure of the expanding uterus interferes with digestive function also. Constipation is common due to decreased gastric motility and iron supplements. If chronic, constipation may lead to hemorrhoids, which are dilated veins in the anal canal. These can become very painful and may bleed or become infected. A diet high in fiber is recommended to avoid constipation and straining during defecation Physiologic Changes & Their Implications Musculoskeletal Relaxation of pelvic joints results in loss of stability and waddling Increased weight causes increased anterior curvature of lumbar spine (lordosis) resulting in chronic back pain Cardiovascular Increased blood volume (fluid & erythrocytes) resulting in edema, respiratory congestion, and pregnancy gingivitis Progesterone decreased vascular resistance resulting in hypotension during 1st trimester Uterine pressure restricts lower extremity blood flow and causes varicose veins, increasing risk for blood clots—particularly after delivery Supine reclining puts pressure on inferior vena cava resulting in hypotension (women should recline left side) Blood volume, including the relative volumes of both fluid and erythrocytes, is greatly increased to meet the metabolic needs of the fetus. For example, blood flow to the uterus and kidneys must increase to supply more oxygen to the fetus and uterine tissue and remove wastes. Vascular resistance tends to decrease because smooth muscle in the arterioles is somewhat relaxed as a result of increased progesterone. The heart rate may increase slightly, and blood pressure frequently drops slightly in the first two trimesters but then rises again to normal levels during the last trimester The increased blood volume leads to congestion and edema in many tissues. For instance, there may be nasal congestion, which affects breathing. Gingivitis, or inflammation of the tissues around the teeth/gums (see Chapter 17), is common, causing bleeding. Fatigue or stress may impede daily oral hygiene, resulting in more severe pregnancy gingivitis and caries The increased production of red blood cells for the fetus requires increased iron intake by the mother. Iron supplements are frequently required. Because of a relatively greater increase in fluid, the hematocrit decreases slightly, and the woman appears to have a low hemoglobin level (physiologic anemia). Varicose veins frequently develop during pregnancy (see Chapter 12 and Fig. 12.33 for more information on varicose veins). Either the superficial or the deep veins of the legs may be involved. The superficial veins appear large, distended, and purplish. Varicose veins result from restriction of blood flow in the veins to the heart due to the pressure of the uterus, particularly in women who must stand for long periods or who are predisposed to this condition by defects in the vein walls or valves. Varicosities can cause sensations of heavy or aching legs. Legs should be elevated whenever possible, and restrictive clothing such as tight stockings should be avoided to enhance the flow of venous blood. The risk of dangerous blood clots and emboli to the lungs is increased, particularly after delivery

Describe the placental problems placental previa and abruptio placentaie

Placenta previa Placenta over opening between uterus and cervix Is prone to rupture near end of pregnancy with painless bright red bleeding as a sign Hemorrhaging possibility places mother & child in danger Placenta previa occurs when the placenta is implanted in the lower uterus or over the cervical os (the passage between the uterus and the cervix). In the case of placenta previa when the uterus expands and contracts near the end of pregnancy, the placenta is torn and bleeding occurs. The sign is bright red bleeding that is painless. Diagnosis is confirmed by ultrasound. Although in some cases the leak may close, any hemorrhage during pregnancy places both mother and fetus at risk and requires immediate assessment and intervention Abruptio placentae Premature separation of placenta from uterus, usually during 3rd trimester Dark red vaginal bleeding (sometimes) with abdominal pain Abruptio placentae refers to premature separation of the placenta from the uterine wall, resulting in bleeding that may or may not be evident vaginally, depending on where the tear occurs. The blood is often dark red, and abdominal pain is common. Abruptio placentae occurs more commonly during the last trimester.

Portal hypertension

Portal Hypertension Related to liver failure Distended veins-- backflow Increased pressure in portal system Obstruction in liver causes back-up Blood into other organs (swelling) varices Causes: Cirrhosis Fibrosis Portal hypertension increases the hydrostatic pressure in the veins and lymphatics; the increased serum aldosterone levels result in increased sodium ion and water in the extracellular compartment; and the decreased serum levels of albumin lower the plasma osmotic pressure. All these factors contribute to a shift of fluid out of the blood and into the peritoneal cavity. Signs of portal hypertension or impaired digestion and absorption are the usual early indicators of this stage Blockage of blood flow through the liver, leading to high pressure in the portal veins, or portal hypertension Portal hypertension is an increase in the pressure within the portal vein (the vein that carries blood from the digestive organs to the liver). The increase in pressure is caused by a blockage in the blood flow through the liver

Know the ins-and-outs of jaundice (icterus)—what causes it

Pre-hepatic Hepatic Post-hepatic Sign of disease Yellow staining of skin due to excessive bilirubin in circulation Typically, bilirubin is secreted via bile-- hemoglobin gets broken down -- left over stuff that gets conjugated-- come off through skin 3 types of jaundice: (ON EXAM) Pre-hepatic (excessive RBC breakdown) Hepatic (hepatocyte damage)-- PRODUCE BILE-- caused by liver Post-hepatic (obstructive) (bile cannot flow)-- after liver Can see it in the whites of the eyes Complications of Obstructive Jaundice Infection in biliary tree due to cholestasis Bacteria from intestines colonize due to lack of movement Malabsorption Fat not being emulsified Bleeding Vitamin K is fat-soluble, fats remain insoluble Vitamin K deficiency (V.K needed for prothrombin synthesis) Pressure necrosis Backup of bile into tissues (hepatocytes) Foul smelling stool Jaundice (icterus) refers to the yellowish color of the skin and other tissues that results from high levels of bilirubin in the blood. The color is usually apparent first in the sclera, or white area of the eye. Bilirubin is a product of the hemolysis of red blood cells (RBCs) and the breakdown of hemoglobin (see Fig. 17.4). Jaundice, or hyperbilirubinemia, is not itself a disease but rather is a sign of many different types of primary disorders. These disorders are classified into three groups 1. Prehepatic jaundice results from excessive destruction of red blood cells and is characteristic of hemolytic anemias or transfusion reactions. Liver function is normal, but the liver is unable to handle the additional bilirubin. Physiologic jaundice of the newborn is common 2 to 3 days after birth. Increased hemolysis of red blood cells, combined with the immature infant liver, leads to a transient mild hyperbilirubinemia. 2. Intrahepatic jaundice occurs in individuals with liver disease, such as hepatitis or cirrhosis. It is related to an impaired uptake of bilirubin from the blood and decreased conjugation of bilirubin by the hepatocytes. 3. Posthepatic jaundice is caused by obstruction of bile flow into the gallbladder or duodenum and subsequent backup of bile into the blood. Congenital atresia of the bile ducts, obstruction caused by cholelithiasis, inflammation of the liver, or tumors all result in posthepatic jaundice. The type of jaundice present in an individual may be indicated by increases in the serum bilirubin level and changes in the stoolsIn patients with liver disease, both intrahepatic and posthepatic jaundice may be present because inflammation or infection both impairs hepatocyte function and obstructs the bile canaliculi, leading to elevations in the blood of both unconjugated and conjugated bilirubin. In persons with posthepatic jaundice, the obstruction prevents bile from entering the intestine, interfering with digestion and resulting in a light-colored stool. Also, the bile salts that enter the blood and tissues as bile backs up cause irritation and pruritus (itching) of the skin. Treatment depends on removing the cause. Phototherapy is effective in mild forms, whereby exposure to ultraviolet light promotes the conjugation of bilirubin

Hepatic cancer (Differentiate between primary and secondary (metastatic))

Primary & secondary Primary<secondary Primary (hepatoma) Cirrhosis Although secondary tumors are common in the liver, primary malignant tumors are relatively rare, making up less than 2% of all cancers. However, the number of cases and deaths are climbing for unknown reasons. The American Cancer Society has predicted 40,710 new cases and 28,920 deaths in the United States in 2017. There has not been a significant decrease in either incidence or mortality rates for liver cancer The most common primary tumor is hepatocellular carcinoma, developing in cirrhotic livers (Fig. 17.29). Cirrhosis may be secondary to metabolic disorders or hepatitis. Tumors may also result from prolonged exposure to carcinogenic chemicals. Secondary or metastatic cancer often arises from areas served by the hepatic portal veins or that spread along the peritoneal membranes The signs of liver cancer initially are mild, general, and similar to those of other liver diseases; they include anorexia and vomiting, fatigue, weight loss, and hepatomegaly. Portal hypertension and splenomegaly are common. Paraneoplastic syndromes occur with this cancer, with tumor cells producing substances similar to erythropoietin, estrogen, or insulin (see Chapter 20). Because of the minimal early indications, the cancer is usually advanced at diagnosis. Chemotherapy is the usual treatment. If the tumor is localized, a lobectomy or radiofrequency ablation procedure may be used to remove it.

Discuss the pathophysiology of prostate cancer and its complications

Prostate Cancer adenocarcinoma Most frequently diagnosed cancer site (men—1 in 7) #2 cause of cancer mortality, men Prostate Cancer 5-10% HPC1 mutation Silent grower S/S come late Spreads quickly in prostate but slow to metastasize Mets: regional lymph nodes, bone, blood, liver, lung Confined to posterior part of prostate Treatment: surgery, radiation Prostate Cancer Note the irregular yellowish nodules, mostly in the posterior portion (seen here superiorly). Prostate glands containing adenocarcinoma are not necessarily enlarged Prostate cancer is common in men older than 50 years and ranks high as a cause of cancer-related death in men. The American Cancer Society estimated that in 2017 there will be 161,360 new cases of prostate cancer in the United States resulting in 26,730 deaths, which is the secondleading cause of death from cancer in American men. One in seven men is expected to develop prostatic cancer during their lifetime Most tumors are adenocarcinomas arising from the tissue near the surface of the gland (rather than in the central area, as in BPH). There may be more than one focus of neoplastic cells. Tumors vary in degree of cellular differentiation; the more undifferentiated or anaplastic tumors are much more aggressive, growing and spreading at a faster rate. Many tumors are androgen dependent. Prostate cancer is both invasive to regional tissues such as lymph nodes or urethra and metastatic to bone (Fig. 19.6). With better screening of men older than 50 years for this cancer, many more individuals are being diagnosed in earlier stages than in the past. Five-year survival rates vary considerably: Localized cancers have a 100% survival rate, whereas regional spread reduces the rate to 89%, and distant metastases of bone or other organs have a 37% survival rate. Five to ten percent of prostatic cancers are caused by inherited mutations, and the mutation in the HPC1 gene, which has been identified as the cause of these cancers. Other causes include high androgen levels (either intrinsic or extrinsic), increased insulin-like growth factor, and recurrent prostatitis. Prostatic cancer is common in North America and Northern Europe but not in countries farther east. The incidence is higher in the African American population than in Caucasians, indicating a possible genetic factor. Testosterone receptors are found on cancer cells. A hard nodule in the periphery of the gland, often in the posterior lobe, may be detected on digital rectal examination. The tumor tends not to cause early urethral obstruction because of its location. As the tumor develops, some obstruction occurs, producing signs of hesitancy, a decreased stream, urinary frequency, or bladder infection (cystitis)

Discuss the pathophysiology of prostatitis and balanitis

Prostatitis subject to infection due to direct access via urinary tract Usually older men—incomplete bladder emptying If bacterial* — usually e. coli, UTI, gonorrhea S/S: burning urination, pain, WBC in urine, pus in urine & around urethra, fever, chills Fibrosis and/or inflammatory enlargement can lead to urethral obstruction *1) Acute bacterial, 2) chronic bacterial, 3) nonbacterial, 4) asymptomatic inflammatory It is considered an ascending infection or inflammation with multiple causes. The prostate is somewhat protected from ascending infection by the flushing action of urination and ejaculation and by an intact mucous membrane. Also, the prostatic secretions contain antimicrobial factors. However, the close association of the male reproductive tract with the urinary tract, including the continuous mucosa, promotes the spread of infection through the structures, and prostatitis is therefore closely associated with urinary tract infections. The causes of the common nonbacterial form of prostatitis and prostatodynia (painful prostate) have not been established. Acute bacterial prostatitis causes a tender, swollen gland, typically soft and boggy on palpation. The urine contains large quantities of microorganisms, pus, and leukocytes. Expressed prostatic secretions also contain many organisms, confirming the source of the infection. However, this process may be painful and may actually spread the infection or cause bacteremia in acute cases. Nonbacterial prostatitis is indicated by large numbers of leukocytes in the urine and prostatic secretions, although the prostate gland is not markedly enlarged. In patients with chronic prostatitis the prostate is only slightly enlarged, irregular, and firm because fibrosis is more extensive. In most cases of prostatitis the urinary tract is infected and signs of dysuria, frequency, and urgency occur. Other parts of the reproductive tract (e.g., the epididymis or testes) may be involved as well. Acute bacterial prostatitis is usually an ascending infection (it progresses up the urethra) and is caused primarily by Escherichia coli (E. coli) but sometimes by Pseudomonas, Proteus, Enterobacter, Klebsiella, Serratia, or Streptococcus faecalis Balanitis Fungal infection of the glans penis Sexually transmitted Caused by Candida albicans Vesicles develop into patches Severe burning and itching Treatment—topical antifungal medication Balanitis is a fungal infection of the glans penis that can be transmitted during sexual activity. The fungus, Candida albicans, causes the infection primarily in uncircumcised males. Balanitis first appears as penile vesicles that later develop into patches that cause severe burning and itching. Diagnosis is accomplished by the identification of the presence of Candida. Treatment involves topical antifungal medications such as miconazole, tolnaftate, and clotrimazole.

Describe the development and presentation of the protozoan STD trichomoniasis in both males and females

Protozoan STD Trichomoniasis Trichomanas vaginalis—a flagellated protozoa Males: Urethral infection—usually asymptomatic (why is this bad?) Females: Vaginal, urethral, and Bartholin's glands infected Produces inflammation, pruritus, and foul-smelling yellowish discharge Trichomoniasis Protozoa T. vaginalis Asymptomatic, or women may have discharge and dysuria None Antimicrobial drugs, e.g., metronidazole Trichomoniasis is caused by Trichomonas vaginalis, an anaerobic flagellated protozoan, which is an extracellular parasite (see Fig. 6.8). The infection is usually asymptomatic in men, with the organisms residing primarily in the urethra. In women the infection may be subclinical and then flare up when the microbial balance of the vagina shifts. Trichomoniasis is a localized infection, with the organism attaching to the squamous epithelium of the vaginal and urethral mucosa and to Bartholin glands. Active infection causes a copious yellowish, foul-smelling discharge as well as inflammation and itching of the mucosa. Systemic treatment of both partners is necessary with drugs such as metronidazole (Flagyl) or tinidazole Although rare, infections of the male genital tract have also been attributed to Trypanosoma species, Leishmania donovani, Entamoeba histolytica, Acanthamoeba species, Toxoplasma gondii, and Plasmodium falciparum.

Hernias

Protrusion of a loop of an organ or tissue through an abnormal opening hiatal hernia-- stomach that is herniated Big diaphragm -- hole in the middle for esophagus Stomach can move up to the hole Relatively asymptomatic-- might get caught and filled with food and starts to get inflammation going on with this Tissue where it shouldn't be Inguinal Hiatal Umbilical inguinal hernia Mostly in males -- natural weakness When a mass, such as a blood clot or tumor, becomes large enough, it may displace brain tissue, leading to herniation. There are several different types of herniation (see Fig. 14.8). In transtentorial (central) herniation, the cerebral hemispheres, diencephalon, and midbrain are displaced downward. The resulting pressure affects the flow of blood and CSF, the RAS, and respiration. Uncal (uncinate) herniation occurs when the uncus of the radionuclide such as technetium may be added to track perfusion in CNS. Lumbar puncture is used to check pressure and analyze the CSF for altered components. Clinical assessment routinely includes tools such as the assessment of normal reflexes and the Glasgow coma scale to assess the level of consciousness. In patients with hiatal hernia, part of the stomach protrudes through the opening (hiatus) in the diaphragm into the thoracic cavity. Normally the digestive tract is loosely attached to the diaphragm. There are two types of hiatal hernia (Fig. 17.13). With a sliding hernia, the more common type, a portion of the stomach and the gastroesophageal junction move above the diaphragm, particularly when the person is in the supine position. In the standing position, the herniated portion slides back down into the abdominal cavity. In a rolling or paraesophageal hernia, part of the fundus of the stomach moves up through an enlarged or weak hiatus in the diaphragm. In this type of hernia, the blood vessels in the wall of the stomach may be compressed, leading to ulceration. Food often lodges in the pouch created by the herniated portion, resulting in inflammation of the mucosa, reflux of food up the esophagus, and dysphagia, as the mass of food enlarges and obstructs the passageway. Chronic esophagitis eventually may cause fibrosis and stricture. Often an incompetent gastroesophageal sphincter is seen The signs of hiatal hernia include heartburn or pyrosis, a brief substernal burning sensation, often accompanied by a sour taste in the mouth, which occurs after meals and results from reflux of the gastric contents up the esophagus. Frequent belching (gas) often accompanies this regurgitation. The discomfort is increased by lying down after eating, bending over, or coughing. Dysphagia is common, either because of inflammation of the esophagus or because the mass of food collected in the pouch compresses the esophagus. Persistent, mild, substernal chest pain after meals is a frequent complaint because of inflammation or distention of the pouch. The symptoms can often be reduced by eating frequent, small meals and avoiding a recumbent position after meals.

Discuss the development of a puerperal infection and its complication

Puerperal infection Reproductive tract infection within 6 weeks of delivery Signs: fever, vomiting, low abd. Pain, foul vaginal discharge Causes: Cervical lacerations, episiotomy repairs, or wounds remaining from placental separation Microbes: Streptococcus, E. coli, S. Aureus, mycoplasma, C. trachomatis May progress to pelvic cellulitis May progress to peritonitis Localized wound infections are usually contained if they are treated quickly. Puerperal infection (childbed fever) is infection of the reproductive tract at any time during the 6 weeks after birth. It may be endogenous (because of vaginal flora) or exogenous (because of causes in the environment). Cervical lacerations or episiotomy repairs are vulnerable to infection. Common organisms include group B hemolytic Streptococcus, Escherichia coli, Staphylococcus aureus, Mycoplasma, and Chlamydia trachomatis A predisposition to endometritis (inflammation of the uterine lining) can be caused by the separation of the placenta, which leaves raw tissue open to easy access of organisms from the vagina. Any retained placental fragments also promote infection. Signs of infection include fever, vomiting, lower abdominal pain, and foul-smelling discharge from the vagina. The infection may spread to cause pelvic cellulitis (infection in the connective tissues or broad ligament of the pelvis) or peritonitis (infection of the peritoneal membranes) (see Chapter 17). Peritonitis results from infection that spreads directly along the fallopian tubes into the peritoneal cavity and is a serious complication of childbirth. Peritonitis is manifested by severe pain, high fever, tachycardia, and abdominal distention. Scar tissue resulting from infection that involves the fallopian tubes or ovaries may cause infertility. Pelvic abscess, a localized infection, may persist after peritonitis. Potential Complications Adolescent Pregnancy Often prone to complications Metabolic needs of adolescents is higher Erratic hormonal activity Adolescents delay seeking help with their pregnancies Adolescents are prone to poor dietary intake, and may be conducting behavior harmful to developing babies The musculoskeletal structure of the adolescent is not yet mature Often result in premature deliveries, difficult labor, and low birth weight babies Good prenatal care minimizes complications

pyloric stenosis

Pyloric Stenosis Opposite problem-narrow pylorus Fullness, bloating, vomitus has undigested food Stomach is all together-- scarring going on (affecting sphincter) Bloating Narrowing and obstruction of the pyloric sphincter may be a developmental defect in infants, or it may be acquired later in life, usually because of the presence of fibrous scar tissue. In the congenital form, the pyloric muscle is hypertrophied and can be palpated as a hard mass in the abdomen. Signs of stenosis usually appear within several weeks after birth, first as episodes of regurgitation of some food and then as projectile vomiting occurring immediately after feeding. Vomitus may be ejected some distance from the infant and does not contain bile. Stools become small and infrequent. The infant fails to gain weight, is dehydrated, and is irritable because of persistent hunger. Surgery is required to remove the obstruction. In persons with acquired pyloric obstruction, interference with gastric emptying leads to a persistent feeling of fullness and then to an increased incidence of vomiting with or after meals. The vomitus typically contains food from previous meals.

Discuss the pathophysiology and prognoses for male breast cancer

Rare (about 1% of all breast cancer) Similar to female breast cancer Usually detected very late because of no routine screening

Different types of kidney stones

Renal Calculi Kidney stone (urolithiasis) Crystallization of minerals in urine & filtrate Calcium (75%) Struvite Uric acid Cystine Variety of shapes/sizes May move & lodge Causes: Abnormal Calcium metabolism & bone dz Extended bed rest Chronic UTI Gout Abnormal amino acid metabolism (rare) Signs/symptoms Hematuria Flank pain Treatment Allow stone to pass Lithotripsy Laser Stones in the kidney or bladder are frequently asymptomatic, unless frequent infections lead to investigation. Sometimes flank pain occurs because of distention of the renal capsule Obstruction of the ureter causes an attack of "renal colic," consisting of intense spasms of pain in the flank area radiating into the groin that last until the stone passes or is removed. This pain is caused by vigorous contractions of the ureter in an effort to force the stone out. The severe pain may be accompanied by nausea and vomiting, cool moist skin, and rapid pulse. Radiologic examination confirms the location of the calculi. Small stones can be passed eventually and the urine strained to catch stones for analysis. Newer methods of fragmentation of larger stones—such as extracorporeal shockwave lithotripsy, which uses sound waves to break up the stone, and laser lithotripsy, which uses a ureteroscope to locate the stone and a scope-mounted laser to destroy it—have been quite successful and have decreased the need for invasive surgery, which is a procedure called percutaneous nephrolithotomy. In some cases, drugs may be used to partially dissolve the stones Prevention of recurrence related to specific risk factors is of primary importance. Treatment of the underlying condition, adjustment of urine pH by ingestion of additional acidic or alkaline substances, and increased fluid intake all minimize the risk of recurrence.

Alcoholic hepatitis

Second stage—alcoholic hepatitis Inflammation and cell necrosis Fibrous tissue formation—irreversible change In the second stage, alcoholic hepatitis, inflammation and cell necrosis occur. Fibrous tissue forms, an irreversible change. Acute inflammation may develop when alcohol intake increases or binge drinking becomes more excessive. This second stage may also be asymptomatic, or it may manifest with mild symptoms, such as anorexia, nausea, and liver tenderness. In some patients, after an episode of excessive alcohol intake, there may be sufficient damage to precipitate liver failure, encephalopathy, and death.

End-stage cirrhosis

Shrunken nodular liver (here- macronodular liver) Third stage—end-stage cirrhosis Fibrotic tissue replaces normal tissue. Little normal function remains. Cirrhosis will continue (signs of liver not working) The third stage, or end-stage cirrhosis, is reached when fibrotic tissue replaces normal tissue, significantly altering the basic liver structure to the extent that little normal function remains. Signs of portal hypertension or impaired digestion and absorption are the usual early indicators of this stage.

Sialadenitis and infectious parotitis (mumps)

Sialadentitis Infectious or non-infectious Inflammation of salivary gland Can be infectious or noninfectious Infectious parotitis (Mumps) Sialadenitis refers to inflammation of the salivary glands, infectious or noninfectious. The parotid gland is most frequently affected, both by infectious agents and tumors. Bacterial infection may spread from the mouth. Mumps, infectious parotitis, is a viral infection leading to marked, usually bilateral, swelling of the gland (Fig. 17.10). Although a vaccine has been available since the early 2000s, mumps outbreaks have occurred in college-aged adults; in such outbreaks, revaccination is recommended to limit the spread of the disease. Noninfectious parotitis may develop in debilitated or elderly patients who lack adequate fluid intake and mouth care. Tumors such as benign adenomas tend to affect the parotid glands of older individuals. The most frequent malignant tumor of the salivary gland is mucoepidermoid carcinoma, occurring primarily in the parotid glands.

Ischemic bowel disease and its complications

Small Intestine: Ischemic Bowel Disease* Infarction Atherosclerosis Thrombosis Shock—systemic hypotension CHF—systemic hypoperfusion and hypotensive episodes Signs/Symptoms: Intestinal angina (rigid abd. due to pain) Bloody diarrhea Weight loss (from malabsorption) Ischemic Bowel Disease Mild Edema, some hemorrhaging, but heals with minimal fibrosis Moderate Scarring, cicatrization, stenosis or stricture Severe Can lead to infarction, necrosis, gangrene, and finally a strong possibility of rupture and death In more-severe cases, complications can include: Tissue death (gangrene) resulting from diminished blood flow. Hole formation (perforation) in your intestine or persistent bleeding. Bowel inflammation (segmented ulcerating colitis) Ischemic bowel disease occurs when an artery that supplies blood becomes blocked or narrowed. There are several possible causes of ischemic bowel disease, including: Blockage in the arteries due to a tumor or blood clot. Narrowing of the arteries supplying blood to the bowel from atherosclerosis.

Esophageal cancer

Squamous cell carcinoma (worldwide); adenocarcinoma (U.S.) Esophageal cancer. SCC -- see in any kind of lumen Rapidly dividing cells Very malignant and quick to metastasize-- takes a long time to show up Usually discovered late S/S: dysphagia due to narrowed lumen, weight loss, obstruction Esophageal cancer is primarily squamous cell carcinoma and is most commonly found in the distal esophagus. Tumors in the esophagus either form circumferential strictures or grow out into the lumen of the esophagus; both types cause significant dysphagia in later stages Esophageal cancer is associated with chronic irritation— for example, from chronic esophagitis, achalasia, hiatal hernia, alcohol abuse, and smoking. Unfortunately, the initial signs of dysphagia occur relatively late in the course of the disease, and the prognosis currently is poor.

Discuss the pathophysiology of the bacterial STD syphilis, including its various stages

Syphilis Treponema pallidum Systemic infection with four stages: Primary—chancre on genitalia (or cervix) Secondary—widespread symmetrical rash and fever, malaise, sore throat, stomatitis, anorexia (all gone in a few weeks) Latent—May last years, sometimes skin lesions, still present in the blood (may still be spread) Tertiary Gumma formation (eats bones and arteries away) Cirrhosis-like liver damage, dementia, blindness, arterial damage The prevalence of syphilis had been decreasing in the period between 1990 and 2000. The rate increased from 2001 to 2009 but again showed a decrease in 2010. Reasons for the increase vary, but it has also been noted that there has been an increase in antibiotic-resistant strains of the pathogen. The causative organism of syphilis is Treponema pallidum, an anaerobic spirochete (so called because of its corkscrew shape). Dark-field or electron microscopy is required for identification (Fig. 19.22A). Serum antibodies also provide a diagnostic test. Syphilis is a systemic infection that consists of four stages, and the organism can be isolated from lesions in the first two stages. 1. The primary stage is identifiable by the presence of a chancre, a painless, firm, ulcerated nodule that develops at the point of contact on the skin or mucosa about 3 weeks after exposure The organisms reproduce in the chancre and initiate an immune response. This lesion heals spontaneously (without treatment) in several weeks. Such lesions are frequently missed because they may not be visible (e.g., they may be in the cervix in the female) and are asymptomatic. Regional lymphadenopathy may also be present in this stage 2. By the time the chancre heals, the organisms have entered the general circulation, and if untreated, the second stage of the infection begins with a widespread symmetric rash, usually maculopapular and reddish, on the skin and mucous membranes, particularly the palate. This typical rash may be found on the palms of the hands and the soles of the feet. Mucous patches (loose, white, necrotic material) may appear on the tongue. General signs of infection—malaise, low-grade fever, sore throat, stomatitis, and anorexia—are common. Again, these lesions are self-limiting and disappear spontaneously in a few weeks. 3. The patient then enters the latent stage, which may persist for years. Sometimes the skin lesions recur, but usually the person is asymptomatic, although serologic evidence of disease remains 4. Some untreated patients never develop tertiary syphilis, and treatment has reduced the incidence of this stage. The typical lesion of this stage is the gumma, an area of necrosis and fibrosis. Bone gummas lead todestruction (e.g., in the hard palate) and pathologic fractures, whereas gummas in the liver manifest as nodules similar to those of cirrhosis. The cardiovascular system is most frequently affected by gummas, showing damage to the arterial wall and development of aortic aneurysms. Neurosyphilis damages the central nervous system, resulting in dementia, blindness, and motor disabilities (tabes dorsalis) A concern with syphilis is the development of congenital syphilis if the fetus is infected after the fourth month of gestation. The child may die in utero or survive with active infection or multiple abnormalities, particularly in the bones (e.g., saddlenose). Malformations of the teeth (e.g., Hutchinson incisors and mulberry molars) are typical. Inflammation and fibrosis damage the liver and lungs. Transmission occurs by contact with exudate from the skin and mucosal lesions or by body fluids, including semen, blood, and vaginal secretions, during sexual contact. It is likely that syphilis can be transmitted during the first few years of the latent stage as well as during the first two stages. Treatment consists of long-acting benzathine penicillin G or doxycycline and tetracycline for patients who are allergic to penicillin. For neurosyphilis infections, ceftriaxone is recommended.

Identify the nephron as the functional unit of the kidney and discuss its components

The Glomerulus The glomerular capillary loops are thin and delicate. Cells are normal in number. Selectively permeable membrane produces "primary filtrate" (normally no RBC or protein) Blood comes in through here-- microscopic Where the renins produce Tubules Primary filtrate passes thru tubules Capillaries draw some substances back into blood (resorption) Capillaries secrete other substances into filtrate Filtrate becomes urine and is passed through the collecting duct to the renal calyces and pelvis Life in the Tubules Too many hydrogen ions-- getting acidic Resorbed: glucose Secreted: drugs Both reabsorbed and secreted: H+ ions Blood too acidic—secreted Blood to alkaline--resorbed Exchanged: Potassium for sodium The organization of the nephrons within a kidney is complex and must be maintained for effective renal function. The blood vessels and the collecting tubules and ducts for the filtrate must be functionally integrated to fulfill the purpose of the system. Scar tissue can interfere with blood or filtrate flow and thus can lead to secondary damage and progressive destruction of the kidney.

Congenital esophageal atresia

The lack of the development of the esophageal lumen resulting in a blind pouch Biliary Atresia (Congenital) Does not Develops later in life Biliary tree is not well formed Everything is shriveled up (connects to pancreatic duct) Shows up not long after birth Mechanical obstructions include the following: ~ Congenital atresia is a developmental defect in which the upper and lower esophageal segments are separated; the upper section ends in a blind pouch. Reflux of feedings occurs in the infant with congenital atresia, leading to aspiration. In many cases there is a connecting fistula from one of the segments to the trachea. Surgical correction is required as soon as possible to prevent aspiration and provide fluid and nutrients to the infant

Discuss the development and consequences of thrombophlebitis and thromboembolism during pregnancy

Thrombophlebitis Blood clots (thrombi) develop in legs and pelvis of mother after childbirth due to blood stasis or increased coagulability If clot forms in inflamed vein wall it's called thrombophlebitis Thromboembolism If clot breaks away it's called an embolus Flows to right side of heart and then to lungs where it gets lodged and forms a pulmonary embolism Thromboembolisms, or blood clots (see Chapter 10), are common after childbirth and usually develop in the veins of the legs or pelvis (see Chapter 12). To prevent the formation of clots in the legs, the new mother is encouraged to be up and walking immediately after sedation or anesthesia has worn off even in a cesarean section birth. Thrombus may form spontaneously (phlebothrombosis), usually because of stasis of blood or increased coagulability. In some cases, the clot forms over an inflamed area in the vein wall (thrombophlebitis). If a piece of the thrombus breaks away (an embolus), it will flow with the venous blood to the right side of the heart and then into the lungs, where it will lodge in a pulmonary artery or smaller branch, obstructing blood flow in the lungs. This is a pulmonary embolus (see Chapter 13 for more information), which can be very serious and can affect respiratory and cardiovascular function. It is important not to massage a leg that is painful or red until the risk of thrombus has been eliminated. Antiembolic stockings and bed rest may be helpful, as well as careful management of the coagulation problem

Discuss the pathophysiology and complications of benign prostatic hypertrophy (or hyperplasia) (BPH)

Tumors BPH Benign prostatic hypertrophy (actually hyperplasia) Most common, usually > 50 years Hormonal change association w/ aging Smooth prostate bumpy, irregular, enlarges Some fibrosis S/S: frequent, difficult, sometimes painful urination (dysuria) Benign prostatic hypertrophy (BPH) is a common disorder in older men, with an estimated 50% of men over 65 years experiencing some form varying from mild to severe. Although called hypertrophy, the change is actually hyperplasia of the prostatic tissue with formation of nodules surrounding the urethra (Fig. 19.4). These changes lead to compression of the urethra and variable degrees of urinary obstruction. Thus hyperplasia appears to be related to an imbalance between estrogen and testosterone that results from the hormonal changes associated with aging. No connection between BPH and prostatic carcinoma has been identified. Rectal examination reveals an enlarged gland. Incomplete emptying of the bladder due to the obstruction leads to frequent infections (Fig. 19.5). Continued obstruction causes a distended bladder, dilated ureters, hydronephrosis, and possible renal damage (see Chapter 18). If significant obstruction and urinary retention develop in the patient, surgical intervention, using one of several techniques, is required The initial signs indicate obstruction of urinary flow. Hesitancy, dribbling, and decreased force of the urinary stream are direct results of the narrowed urethra. Incomplete bladder emptying leads to frequency, nocturia, and recurrent urinary tract infection. **Complications of benign prostatic hypertrophy.** NODULES (hyperplasia and hypertrophy) FORM IN THE INNER PROSTATE URETHRA IS COMPRESSED OBSTRUCTION TO FLOW OF URINE (Difficulty initiating micturition Dribbling) INCOMPLETE EMPTYING OF BLADDER (Frequency, Bladder distention -- HYDRONEPHROSIS-- KIDNEY DAMAGE) INFECTION (cystitis) (ASCENDS TO KIDNEYS (pyelonephritis)

Mechanical (usually a physical blockage—know different kinds)

When mechanical obstruction of the flow of intestinal contents occurs, a sequence of events develops (Fig. 17.42) as follows: 1. Gases and fluids accumulate in the area proximal to the blockage, distending the intestine. Gases arise primarily from swallowed air, but they also result from bacterial activity in the intestine. 2. Increasingly strong contractions of the proximal intestine occur in an effort to move the contents onward. 3. The increasing pressure in the lumen leads to more secretions entering the intestine and also compresses the veins in the wall, preventing absorption, as the intestinal wall becomes edematous. 4. The intestinal distention leads to persistent vomiting with additional loss of fluid and electrolytes. With small intestinal obstructions, there is no opportunity to reabsorb fluid and electrolytes, and hypovolemia quickly results. 5. If the obstruction is not removed, the intestinal wall becomes ischemic and necrotic as the arterial blood supply to the tissue is reduced by pressure. If twisting of the intestine (eg, volvulus) has occurred or immediate compression of arteries (eg, intussusception or strangulated hernia) results from the primary cause of obstruction, the intestinal wall becomes rapidly necrotic and gangrenous. 6. Ischemia and necrosis of the intestinal wall eventually lead to decreased innervation and cessation of peristalsis. A decrease in bowel sounds indicates this change. 7. The obstruction promotes rapid reproduction of intestinal bacteria, some of which produce endotoxins. As the affected intestinal wall becomes necrotic and more permeable, intestinal bacteria or toxins can leak into the peritoneal cavity (peritonitis) or the blood supply (bacteremia and septicemia). 8. In time, perforation of the necrotic segment may occur, leading to generalized peritonitis. Functional obstruction or paralytic ileus usually results from neurologic impairment. Peristalsis ceases and distention of the intestine occurs as fluids and electrolytes accumulate in the intestine. In this type of obstruction, reflex spasms of the intestinal muscle do not occur, but the remainder of the process is similar to that of mechanical obstruction. With mechanical obstruction of the small intestine, severe colicky abdominal pain develops as peristalsis increases initially. ~ Borborygmi (audible rumbling sounds caused by movement of gas in the intestine) and intestinal rushes can be heard as the intestinal muscle forcefully contracts in an attempt to propel the contents forward. The signs of paralytic ileus differ significantly in that bowel sounds decrease or are absent, and pain is steady. ~ Vomiting and abdominal distention occur quickly with obstruction of the small intestine. Vomiting is recurrent and consists first of gastric contents and then bile-stained duodenal contents. No stool or gas is passed. ~ Restlessness and diaphoresis with tachycardia are present initially. ~ As hypovolemia and electrolyte imbalances progress, signs of dehydration, weakness, confusion, and shock are apparent. Obstruction of the large intestine develops slowly and signs are mild. Constipation and mild lower abdominal pain are common, followed by abdominal distention, anorexia, and eventually vomiting and more severe pain.

Ulcerative colitis

a chronic condition of unknown cause in which repeated episodes of inflammation in the rectum and large intestine cause ulcers and irritation Ulcerative Colitis large intestine Idiopathic Ulceration, mucosal atrophy, polyps, adhesions, only lining of colon 30% lead to Cancer The inflammation commences in the rectum and progresses in a continuous fashion proximally through the colon. The small intestine is rarely involved The mucosa and submucosa are inflamed, commencing at the base of the crypts of Lieberkühn (mucus-secreting goblet cells). The tissue becomes edematous and friable, and ulcerations develop (Fig. 17.34). In an attempt to heal, granulation tissue forms, but it is vascular and fragile and bleeds easily. When the ulcers coalesce, large areas of the mucosa become denuded, but there are residual "bridges" of intact mucosa over the ulcers. This tissue destruction interferes with the absorption of fluid and electrolytes in the colon In severe acute episodes, a serious complication, toxic megacolon, may develop, as inflammation impairs peristalsis, leading to obstruction and dilation of the colon, usually the transverse colon. A concern with long-term ulcerative colitis is the increased risk of colorectal carcinoma, which may be predicted by detection of metaplasia and dysplasia in the mucosa. Diarrhea is present, consisting of frequent watery stools marked by the presence of blood and mucus and accompanied by cramping pain. During severe exacerbations, blood and mucus alone may be passed frequently, day or night, accompanied by tenesmus (persistent spasms of the rectum associated with a need to defecate). Rectal bleeding may be considerable and contributes to severe iron-deficiency anemia. Fever and weight loss may be present.

Irritable bowel syndrome

a common condition of unknown cause with symptoms that can include intermittent cramping, abdominal pain, bloating, constipation, and/or diarrhea Irritable bowel syndrome (IBS, a.k.a. spastic colon) Irritable bowel syndrome (IBS) is a gastrointestinal disorder with manifestations of abdominal pain/discomfort and changes in normal bowel habits. This disorder affects up to 20% of the worldwide population, and statistics show it is more common in young and middle-aged women. The types of IBS are identified based on the primary symptoms of diarrhea, constipation, or pain The different types of IBS are as follows: ~ Abnormal gastrointestinal motility and secretion: Those with diarrhea-type IBS experience rapid transit time of feces through the bowel, whereas those with constipation/bloating IBS have delayed transit time through the bowel. The cause may be hypersensitivity or the effect of serotonin on the enteric nervous system. ~ Visceral hypersensitivity: This type causes increased sensitivity to visceral pain. Causes are similar to those of abnormal motility and secretion but may also include the involvement of activated mast cells and T lymphocytes and effects on the autonomic and central nervous systems in processing information, resulting in increased pain. ~ Postinfectious IBS: This type may cause low-grade inflammation and abnormal immune response in the gut. It is often associated with bacterial enteritis. ~ Overgrowth of flora: This form of IBS may cause constipation and bloating due to methane gas production. This gas production is a result of the overgrowth of the normal intestinal flora found in the gut. ~ Food allergy or intolerance: Certain food antigens may activate the immune response in the mucosa, causing a hypersensitivity reaction and IBS symptoms Psychosocial factors: The IBS symptoms in this case may be caused by factors such as emotional stress, which in turn affects the autonomic nervous system, the neuroendocrine pathway, and pain responses. Manifestations of IBS may include: ~ Lower abdominal pain ~ Diarrhea ~ Constipation ~ Alternating diarrhea and constipation ~ Gas ~ Bloating ~ Nausea There may also be fecal urgency and incomplete evacuation of the bowels. After defecation the symptoms usually subside. Diagnosis of IBS is based on the established signs and symptoms and the exclusion of any structural or metabolic problems that can produce similar manifestations. Test for food allergies, bacterial or parasitic infections, and problems such as lactose intolerance may also be used to confirm the disorder. A protocol referred to as Rome III criteria has been established as a guideline for diagnosing IBS.

Pancreatic insufficiency

a condition characterized by inadequate production and secretion of pancreatic hormones or enzymes. Note that it's caused by destruction of pancreatic endo- & exocrine glands Gradual loss of normal function Called pancreatic insufficiency

Fatty liver

a condition in which fats build up in the liver and cannot be broken down Fatty Liver (Lipidosis) slightly enlarged pale yellow Excessive build-up of fat Excessive fat impacts normal cell function Obesity & alcoholism Initial stage—fatty liver Enlargement of the liver Asymptomatic and reversible with reduced alcohol intake The initial change in alcoholic liver disease is the accumulation of fat in liver cells, causing fatty liver. Other than enlargement of the liver or hepatomegaly, this stage is asymptomatic and is reversible if alcohol intake is reduced.

spermatocele

a cyst that develops in the epididymis and is filled with a milky fluid containing sperm Cyst of fluid/sperm between testis and epididymis A spermatocele is a cyst containing fluid and sperm that develops between the testis and the epididymis outside the tunica vaginalis. It may be related to an abnormality of the tubules. If the cyst is large, it may be surgically removed.

fibroadenoma

a round, firm, rubbery mass that arises from excess growth of glandular and connective tissue in the breast Fibroadenoma—single, moveable, benign One category is nonproliferative lesions, which include microcysts and fibroadenomas. These are not considered precancerous. Fibroadenomas are specific benign tumors that appear as singular, movable masses. These tumors are usually excised

Hydronephrosis

abnormal condition of water in the kidney Dilation of ureters or renal pelvis Necrosis & deterioration of renal tissue Uni- or bilateral Tumor, stone, stricture, enlarged prostate Hydronephrosis occurs as a secondary problem, a complication of calculi, but also of tumors, scar tissue in the kidney or ureter, and untreated prostatic enlargement. Developmental defects are common in the urinary tract and may cause obstruction by kinking or stenosis of a ureter. Obstructive uropathy can be diagnosed by ultrasonography in the fetus, allowing for immediate or neonatal corrective surgery, thus preventing major kidney damage Urine is continually forming. Any prolonged interference with urine outflow through the system results in back pressure and a dilated area filled with urine in the ureter or kidney (see Fig. 18.12B). In the kidney, continued buildup of urine, particularly over a prolonged period, causes necrosis of the tissue because of direct pressure and compression of the blood vessels. Hydronephrosis is frequently asymptomatic unless mild flank pain occurs as the renal capsule is distended or unless infection develops. It can be diagnosed with ultrasonography, radionucleotide imaging, CT scan, or IVP. If the cause is not removed, bilateral hydronephrosis could lead to chronic renal failure

inguinal hernia

above the abdominocrucral crease - direct or indirect greater than 98% male Opening in processus vaginalis allows small intestine to drop in The other common finding in an infant in whom the processus vaginalis remains open is an inguinal hernia, which is a loop of intestine that passes through the abnormal opening (see Fig. 17.41A). Such a hernia usually leads to intestinal obstruction. Surgical repair is recommended if the opening remains patent or herniation persists because there is a risk that the herniated intestinal loop may become strangulated.

Diabetic nephropathy

accumulation of damage to the glomerulus capillaries due to the chronic high blood sugars of diabetes mellitus Excess glucose in vascular basement cells draw in fluid and swell, causing microangiopathy Has to do with people with diabetes Affect arterioles that supply glomeruli Glomerulosclerosis Changes permeability of capillary bed Tubules atrophy Proteinuria Nephrotic syndrome and chronic renal failure Papillary Necrosis Medullary ischemia results in necrosis and sloughing off of the medullary papillae. Dead tissue obstructs ureters Hydronephrosis results Prone to Pyelonephritis Dialysis or transplant a common outcome Diabetic nephropathy, or vascular degeneration in the kidney glomeruli, eventually leads to chronic renal failure (Fig. 16.6). It is responsible for 40% of patients in end-stage renal failure.

Urinary Tract Infections (UTI)

an infection involving the structures of the urinary system that usually begins in the bladder nfectious/Inflammatory Urinary Tract Infections (UTI) Cystitis and Urethritis Pyelonephritis Inflammatory Disorders Glomerulonephritis Nephrotic Syndrome Urinary Tract Infections (UTIs) Very common infections Urine is an excellent growth medium. Lower urinary tract infections Cystitis Urethritis Upper urinary tract infections Pyelonephritis Common causative organism Escherichia coli UTI Causes Bacterial spread via: Blood Exogenous (urethra) S/S Flank pain Pyuria Proteinuria Pain upon urination Urinary Tract Infections (UTIs) (Cont.) More common in women because of: Shortness of urethra Proximity to anus Older men Prostatic hypertrophy Urine retention Congenital abnormalities in children Other common predisposing factors Incontinence Retention of urine Direct contamination with fecal material Urinary tract infections (UTIs) are extremely common. It is estimated that 6 million Americans are affected annually. Urine generally provides an excellent medium for growth of microorganisms. Cystitis and urethritis are considered infections of the lower urinary tract, whereas pyelonephritis is an upper tract infection (Fig. 18.8). Most infections are ascending, arising from organisms in the perineal area and traveling along the continuous mucosa in the urinary tract to the bladder and then along the ureters to the kidneys. Occasionally pyelonephritis results from a blood-borne infection. The common causative organism is Escherichia coli, which is one of the resident flora of the intestine (approximately 85%). The virulent forms of E. coli can adhere to the mucosa of the bladder by means of fimbriae or pili and therefore are not washed out when the bladder empties. Other organisms associated with UTIs include Klebsiella, Proteus, Enterobacter, Citrobacter, Serratia, Pseudomonas, Enterococcus, coagulase-negative Staphylococcus, Chlamydia, and Mycoplasma. In men, urethritis and prostatitis may accompany lower tract infections. Women are anatomically more vulnerable to infection than men because of the shortness and width of the urethra, its proximity to the anus, and the frequent irritation to the tissues. The irritation may be caused by sexual activity, baths, and the use of some feminine hygiene products. Improper hygiene practices during defecation or menstruation also increase risk. Older men with prostatic hypertrophy and retention of urine frequently develop infections. Because the male reproductive tract shares some of the structures of the urinary tract, any infection of the prostate or testes is likely to extend to the urinary structures Congenital abnormalities are a common cause of infection in children, particularly where obstructions to flow or reflux are present. The elderly are at increased risk because of the tendency toward incomplete emptying, reduced fluid intake, impaired blood supply to the bladder, and immobility Common predisposing factors for UTIs in both men and women include incontinence with incomplete emptying of the bladder, retention of urine in the bladder, and any obstruction to urine flow, which tends to result in growth of organisms because bacteria are not promptly flushed out of the bladder by voiding. Pregnancy, scar tissue, and renal calculi (kidney stones) all contribute to infection because the urine and any contaminants do not flow freely through and out of the system. Infection may also result from decreased host resistance present with immunosuppression or diabetes mellitus (vascular impairment and glucosuria). Direct contamination of the urethra and bladder may result from fecal incontinence. As mentioned, instruments or catheters may directly introduce bacteria into the bladder and frequently traumatize the bladder wall, breaking the barrier to infection.

Acute post-streptococcal glomerulonephritis

common in children and young adults. develops 5-21 days after a strep A infection. Glomerular Disease Glomerulonephritis Immune-mediated Type III (immune complex) Acute poststreptococcal glomerulonephritis Antigen/Antibody complex Lodge in glomerular capillaries Inflammatory response Decreased GFR Increased BP Signs & symptoms Flank/back pain Urine (dark & cloudy) Oliguria Elevated BP Diagnostic tests Blood-elevated serum urea & creatinine Blood levels of strep antibodies elevated Urinalysis-proteinuria, gross hematuria, erythrocyte casts Note the extra cells ("hypercellularity") due to post-streptococcal infection. This disease may follow several weeks after infection with certain strains of streptococci. There are many forms of glomerulonephritis. A representative form of glomerular or nephritic disease is acute poststreptococcal glomerulonephritis (APSGN), which follows streptococcal infection with certain strains of group A beta-hemolytic Streptococcus. These infections usually originate as upper respiratory infections, middle ear infections, or "strep throat." Certain strains of Staphylococcus are occasionally responsible for initiating the immune disorder in the kidney Acute glomerulonephritis develops 10 days to 2 weeks after the antecedent infection. Primarily APSGN affects children between the ages of 3 and 7 years, especially boys The anti-streptococcal antibodies, formed as usual from the earlier streptococcal infection, create an antigen- antibody complex (type III hypersensitivity reaction) that lodges in the glomerular capillaries and activates the complement system to cause an inflammatory response in the glomeruli of both kidneys (Fig. 18.9). (See Chapter 7 for a review of the immune response.) This leads to increased capillary permeability and cell proliferation (Fig. 18.10) and results in leakage of some protein and large numbers of erythrocytes into the filtrate. The specific mechanisms of damage are not totally clear, but immunoglobulin G and C3 (complement) are present in glomerular tissue and serum C3 is reduced When the inflammatory response is severe, the congestion and cell proliferation interfere with filtration in the kidney, causing decreased GFR and retention of fluid and wastes. Acute renal failure is possible if blood flow is sufficiently impaired. The decreased blood flow in the kidney is likely to trigger increased renin secretion, which leads to elevated blood pressure and edema (see Fig. 18.14, presented later in the chapter). Severe prolonged inflammation causes scarring of the kidneys. Signs and Symptoms ~ The urine becomes dark and cloudy ("smoky" or "coffee-colored") because of the protein and red blood cells that have leaked into it. ~ Facial and periorbital edema occur initially, followed by generalized edema as the colloid osmotic pressure of the blood drops and sodium and water are retained. ~ Blood pressure is elevated due to increased renin secretion and decreased GFR. ~ Flank or back pain develops as the kidney tissue swells and stretches the capsule. ~ General signs of inflammation are present, including malaise, fatigue, headache, anorexia, and nausea. ~ Urine output decreases (oliguria) as GFR declines.

fibrocystic breasts

benign condition of the breast consisting of fibrous and cystic changes that render the tissue more dense; patient feels painful lumps that fluctuate with menstrual periods Benign Tumors Fibrocystic breast disease Inappropriate response to estrogen/progesterone Multiple cysts develop & accumulate fluid Scar tissue surrounds cysts Lumpy nodules (hard) Bilateral May possibly progress to ductal hyperplasia and carcinoma Three categories (based on cancer risk) Fibroadenoma—single, moveable, benign Proliferative lesions w/ductal hyperplasia—may develop into cancer with + family hx Proliferative changes w/ atypical cells—requires monitoring Also called benign breast disease or fibrocystic change, this includes a broad range of breast lesions. There is some confusion between the normal physiologic changes in the breast that occur during the menstrual cycle and abnormal or pathologic changes. Fibrocystic disease refers to the presence of nodules or masses in the breast tissue that change during the menstrual cycle in response to fluctuating hormone levels, particularly estrogen. The connective tissue of the breast is gradually replaced by dense fibrous tissue. Increasing fluid in the breast during the secretory phase of the menstrual cycle accumulates in cysts bound by fibrous tissue, unable to escape. In addition, the epithelial cells in the ducts proliferate in response to hormones. The cysts enlarge over time, often causing more degeneration of normal tissue. Three categories of lesions have been designated, based on the risk of development of breast cancer: One category is nonproliferative lesions, which include microcysts and fibroadenomas. These are not considered precancerous. Fibroadenomas are specific benign tumors that appear as singular, movable masses. These tumors are usually excised. The second category includes proliferative lesions (with epithelial hyperplasia in the ducts) in which there are no atypical cells. The risk of developing breast cancer in this group increases if there is also a family history of breast cancer The third category, a small one, requires monitoring, particularly if a family history of breast cancer is present. These lesions show proliferative changes with atypical cells. Breast biopsy can detect atypical cells and can differentiate benign from malignant cells. The cysts or nodules feel firm and movable and vary in size during the cycle. The effects are more marked before menstruation, with the breasts becoming heavy, painful, and tender Treatment is largely symptomatic but may include dietary changes such as reduction of caffeine and fat intake and drugs such as the androgen danazol. Fluid may be aspirated from cysts. Cysts may be removed if they manifest premalignant changes. Often there is some improvement after menopause.

metrorrhagia

bleeding from the uterus at any time other than normal menstruation Irregular cycles—from hormonal imbalance ~ Metrorrhagia (bleeding between cycles)

bladder cancer

cancerous tumor that arises from the cells lining the bladder; major sign is hematuria Malignant tumors Bladder cancer Most common in the urinary system, males >50 yo. Epithelium of bladder wall Multiple tumors, may tend to recur Invasive! Metastases to pelvic lymph nodes, liver, bone S/S: hematuria; however, present earlier Cigarette smoking!!! Also, analgesics, NSAIDS, & recurrent infections 5-year survival 85% Stage I 16% Stage IV Malignant tumors of the bladder commonly arise from the transitional epithelium lining the bladder in the trigone area. This cancer often develops as multiple tumors and tends to recur. It is diagnosed by urine cytology (malignant cells in the urine) and biopsy. The tumor is invasive through the wall to adjacent structures, and it metastasizes through the blood to pelvic lymph nodes, liver, and bone. Staging categories range from an in situ tumor through the degree of bladder wall invasion to metastasis. The early sign is hematuria, gross or microscopic. Dysuria or frequency may develop, and infection is common Bladder cancer has a high incidence in individuals working with chemicals in laboratories or industry, particularly with dyes, rubber, and aluminum. More than 50% of patients are cigarette smokers. Other predisposing factors are recurrent infection and heavy intake of analgesics Treatment includes surgical resection of the tumor in 90% of cases, chemotherapy, and radiation. Urinary diversion (eg, ileal loop, the creation of an alternative internal or external urine-collecting unit using part of the ileum) may be required after surgery. Photoradiation (a combination of drug and laser treatment) has been successful in some early cases. Instillation of bacillus Calmette-Guérin vaccine (BCG—a biologic response modifier intended to strengthen the immune response) into the bladder after resection has reduced recurrences of superficial tumors (see Chapter 20). Continued monitoring is necessary to detect recurrences in an early stage. Five-year survival rates vary from 85% in stage I to 16% in stage IV.

ovarian cysts

collections of fluid within a sac (cyst) in the ovary Fluid-filled enlarged corpus luteum or unruptured follicle Insufficient FSH & LH leads to polycystic ovary syndrome Estrogen takes over and becomes excessive Endometrial hyperplasia & infertility Treated with hormone therapy Polycystic ovarian syndrome A.K.A. Stein-Leventhal syndrome Large ovaries covered w/cysts Hypothalamic-pituitary dysfunction A variety of cysts occur frequently on the ovaries. Follicular and corpus luteal cysts are common and develop unilaterally in both ruptured and unruptured follicles. These functional ovarian cysts last approximately 8 to 12 weeks and disappear without complications. They are usually multiple small, fluid-filled sacs located under the serosa covering the ovary. On occasion, a cyst may become large enough to cause discomfort, urinary retention, or menstrual irregularities (Fig. 19.15). Bleeding resulting from rupture can cause more serious inflammation in the peritoneal cavity and requires surgical intervention. With a large cyst there is also risk of torsion of the ovary. Ultrasound examination or laparoscopy can be used to identify a cyst. In polycystic ovarian syndrome, or Stein-Leventhal syndrome, large ovaries containing cysts and covered with a thick capsule develop (Fig. 19.16). Associated hormonal abnormalities include elevated androgen, estrogen, and LH levels and decreased FSH levels. The usual fluctuations or peaks in FSH and LH are missing. Ovulation does not occur. The basic problem is a dysfunction in the hypothalamic-pituitary control system. The cause is unknown, although in some women an inherited factor has been demonstrated. Young women manifest hirsutism (abnormal hairiness), amenorrhea, and infertility. Medications such as clomiphene, an antiestrogen agent, may stimulate ovulation, or surgical wedge resections of the ovaries may help control the hormone levels. Oral contraceptives are used to reduce androgen secretions and masculinization effects. In women who have insulin resistance, treatment with an antihyperglycemic drug such as metformin may result in ovulation.

Diverticular Disease

condition in which bulging pouches (diverticula) in the gastrointestinal (GI) tract push the mucosal lining through the surrounding muscle large Intestine: Diverticula Outpouchings of large intestine Weakening of wall (straining, low fiber diet) Fill up with feces and other debris inflammation Outpouchings of the large intestine (poor diets) Diverticulosis v Diverticulitis Esophageal diverticula Get a pouch that develops and food can get caught in it Diverticular disease refers to various problems related to the development of diverticula (singular, diverticulum). Diverticula may be congenital or acquired. A Diverticulum is a herniation or outpouching of the mucosa through the muscle layer of the colon wall, frequently in the sigmoid colon. Diverticulosis is asymptomatic diverticular disease. Usually multiple diverticula are present Diverticulitis refers to inflammation of the diverticula. It is a common problem in the Western world, primarily affecting older individuals. Diverticula form at gaps between bands of longitudinal muscle that coincide with openings in the circular muscle bands that permit blood vessels to pass through the wall. Longitudinal muscle also occurs in three bands, rather than as a continuous sheet. Congenital weakness of the wall may also be a contributing factor These weaker areas of the wall bulge outward when pressure increases, frequently inside the lumen of the intestine, for example, in the presence of strong muscle contractions. Consistently low-residue diets, irregular bowel habits, and aging lead to chronic constipation and then to muscle hypertrophy in the colon, with elevated intraluminal pressures, and finally to the gradual development of diverticula. Potential complications include intestinal obstruction, perforation with peritonitis, and abscess formation In many cases, diverticular disease remains asymptomatic. Sometimes there is mild discomfort, diarrhea, or constipation and flatulence, which can be excused for other reasons. With diverticulitis, inflammation, related to stasis of feces in the pouches, develops in the diverticula. Lower left quadrant cramping or steady pain and tenderness with nausea and vomiting indicate inflammatory disease. A slight fever and elevated white blood cell count accompany the discomfort.

endometriosis

endometrial tissue located outside the uterus Endometrial tissue outside uterus—probably through fallopian tubes during menstruation Ectopic tissue responds to hormones Painful menstruation (dysmenorrhea) is a common sign Adhesions/fibrous formation/blood filled cysts may result in infertility Endometriosis affects about 5 million women in the United States and is defined as the presence of endometrial tissue outside the uterus on structures such as the ovaries, ligaments, or colon (Fig. 19.12). On occasion, it may affect distant sites such as the lungs. This ectopic endometrium responds to cyclic hormone variations, growing during the proliferation and secretory stages of the menstrual cycle and then degenerating, shedding, and bleeding. Because there is no exit point for this blood and blood is irritating to tissues when it does not belong there, local inflammation and pain result. The inflammation recurs with each cycle and eventually causes the development of fibrous tissue. Although it may be possible to palpate nodular tissue, the diagnosis is confirmed by laparoscopy Fibrous tissue may cause adhesions and obstruction of the involved structures, such as the urinary bladder or colon. When the uterus is pulled out of its normal position (e.g., into retroversion) by adhesions, infertility frequently results. The fallopian tube may be blocked or the ovary covered by fibrous tissue, preventing movement of the ovum into and through the tube, ultimately causing infertility. When endometrial tissue occurs on the ovary, a "chocolate cyst" develops, a fibrous sac containing old brown blood The primary manifestation of endometriosis is dysmenorrhea. The pain may persist throughout menses and typically becomes more severe each month. Dyspareunia, or painful intercourse, may occur if the vagina and supporting ligaments are affected by adhesions. The cause of endometriosis has not been established. Proposed mechanisms include migration of endometrial tissue up through the fallopian tubes into the peritoneal cavity during menstruation, development from embryonic tissue at other sites, spread of endometrium through the blood or lymph, or transplantation of tissue during surgery such as a cesarean section Treatment measures include hormonal suppression of the endometrial tissue, with relief of the pain associated with the monthly cycle, or surgical removal of the ectopic endometrial tissue. Pregnancy and lactation also result in amenorrhea and atrophy of the ectopic tissue. These measures do not cure endometriosis, but they do delay further damage and alleviate the symptoms.

varicocele

enlarged veins of the spermatic cord Varicose veins in spermatic cord A varicocele is a dilated vein in the spermatic cord, usually on the left side. It frequently develops after puberty and results from a lack of valves in the veins, permitting backflow of blood and increased pressure in the veins. Varicocele may be mild, and scrotal support minimizes the heavy feeling. If it is extensive, the varicocele is painful or tender and leads to infertility because of the impaired blood flow to the testes and decreased spermatogenesis. In this case, surgical treatment of the abnormal veins is necessary

menorrhagia

excessive menstrual bleeding Excessive bleeding (amount) & duration Carcinoma, PID, hormone imbalance, anovulation—endometrial hyperplasia Abnormal menstrual bleeding is a common concern. Examples of abnormal patterns include: ~ Menorrhagia (increased amount and duration of flow)

Nephrotic syndrome (nephrosis)

group of clinical signs and symptoms caused by excessive protein loss in urine Abnormal glomerular capillaries resulting in increased permeability allowing escape of plasma proteins (including albumin). Usually secondary to other disorders Edema Hypertension Hematuria Proteinuria Hypoalbuminemia Hyperlipidemia and lipiduria S/S frothy urine, anasarca (massive edema), wt. gain, pallor, loss of appetite due to ascites, pleural effusion, skin break down. Inflammatory Disorders Glomerulonephritis Nephrotic Syndrome The nephrotic syndrome is secondary to a number of renal diseases as well as to a variety of systemic disorders (eg, systemic lupus erythematosus, exposure to toxins or drugs). However, lipoid nephrosis, also known as minimal change disease, is a primary disease in young children ages 2 to 6 years. The pathogenesis is not well established, but the following sequence develops: 1. There is an abnormality in the glomerular capillaries and increased permeability that allows large amounts of plasma protein, primarily albumin, to escape into the filtrate. 2. This results in marked hypoalbuminemia with decreased plasma osmotic pressure and subsequent generalized edema. 3. Blood pressure may remain low or normal in many cases because of hypovolemia, or it may be elevated depending on angiotensin II levels. 4. The decreased blood volume also increases aldosterone secretion, leading to more severe edema. 5. The other significant components of nephrotic syndrome are the high levels of cholesterol in the blood and lipoprotein in the urine. The cause of the hyperlipidemia and lipiduria is not totally clear, although it appears to be related to the response of the liver to heavy protein loss. ■ Signs and Symptoms Urinalysis indicates marked proteinuria, lipiduria, and casts (fatty, epithelial, and hyaline). Cells may be present with certain primary diseases. Urine is often frothy. The significant sign of nephrosis is the massive edema (anasarca) associated with weight gain and pallor. This excessive fluid throughout all tissues impairs appetite (ascites), breathing (pleural effusion), and activity (swollen legs and feet). Skin breakdown and infection may develop because arterial flow and capillary exchange are impaired

Hypertension pathway

juxtaglomerular apparatus secreting renin causing vasoconstriction The relationship between hypertension and the kidney.: 1. Hypertension 2. Decreased blood to nephrons 3. Renin-angiotensin-aldosterone 4. Systemic vasoconstriction 5. Sodium and water retention Increased blood pressure 7. Renal vascular damage Nephrosclerosis 8. Chronic renal failure Decreased blood flow

Peritonitis

inflammation of the peritoneum Contents spill into peritoneum (peritonitis) Peritonitis—pus surrounds the intestine and prevents peristalsis. Peritonitis Inflammation of peritoneal cavity Infectious Bacteria—often from GI tract Chemical irritation A.k.a. sterile peritonitis Bile in peritoneum Pancreatic enzymes Surgical materials Peritonitis is an inflammation of the peritoneal membranes that may result from chemical irritation or directly from bacterial invasion of the sterile peritoneal cavity. Chemical irritation, unless resolved quickly, ultimately leads to bacterial peritonitis. It is usually an acute condition and requires treatment of the primary cause as well as the effects. The incidence of peritonitis and septicemia has decreased with the prophylactic use of antibiotics, but peritonitis remains a threat in many situations. Inflammation of the peritoneal membranes may commence with the presence of chemical irritants, such as bile, chyme, or foreign objects in the peritoneal cavity. This inflammation then increases the permeability of the intestinal wall, permitting enteric bacteria to enter the peritoneal cavity (Fig. 17.44). Necrosis or perforation of the intestinal wall also allows infection directly by enteric organisms. Initially when local inflammation develops in the abdominal cavity, the peritoneum and omentum tend to produce a thick, sticky exudate, which helps the adjacent tissues to stick together and temporarily seal the area, localizing the source of the problem. In some cases the inflammation subsides and an abscess forms that may flare up at a later time. This local inflammation may also reduce peristalsis in the area, decreasing the risk of spreading toxins or bacteria at the time. However, unless the original cause of the problem is removed, it is likely that the inflammation or infection will spread. The peritoneum consists of a large sterile expanse of highly vascular tissue that covers the viscera and lines the abdominal cavity. This peritoneal structure provides a means of rapid dissemination of irritants or bacteria throughout the abdominal cavity. Abdominal distention is evident, and the typical rigid, boardlike abdomen develops as reflex abdominal muscle spasm occurs in response to involvement of the parietal peritoneum. Whatever the cause, this membrane is rapidly involved in the inflammatory response, which leads to vasodilation and increased permeability. The membrane becomes edematous and red. The many blood vessels in the membranes can leak large volumes of fluid into the peritoneal cavity. Hypovolemic shock results as this process of "third-spacing" occurs (see Chapter 12). The fluid, protein, and electrolytes sequestered in the peritoneal cavity are not recycled into the circulating blood and therefore are of no value to the maintenance of body fluid balance. This fluid becomes purulent as infection spreads. Nausea and vomiting, resulting from the intestinal irritation and pain, add to the fluid loss. Two complications may develop if intervention is delayed. When inflammation persists, nerve conduction is impaired and peristalsis decreases, leading to obstruction of the intestines (paralytic ileus). The inflamed membranes permit intestinal bacteria and toxic materials to migrate into the blood and then into the general circulation, which may lead to septicemia. Peritonitis develops secondarily to many conditions, some of which are the following: ~ Chemical peritonitis may result from the enzymes released with pancreatitis, urine leaking from a ruptured bladder, chyme spilled into the peritoneal cavity from a perforated ulcer, bile escaping from a perforated gallbladder, or blood or any other foreign material in the cavity. ~ Bacterial peritonitis may be caused by direct trauma affecting the intestines (eg, penetrating injury), a ruptured appendix, or intestinal obstruction, particularly when blood vessels are compressed and the wall becomes gangrenous. ~ Any abdominal surgery may lead to peritonitis if foreign material remains in the abdomen or infection develops at the site. ~ Pelvic inflammatory disease in women, in which infection ascends through the uterus and into the fallopian tubes, providing direct access to the peritoneal cavity, may result in peritonitis Sudden, severe, generalized abdominal pain occurs with localized tenderness at the site of the underlying problem. The pain tends to increase with any movement, and the individual often restricts breathing. Other manifestations include the following: ~ Vomiting ~ Signs of dehydration and hypovolemia ~ Decreased skin turgor ~ Dry buccal mucosa ~ Pallor ~ Low blood pressure ~ Agitation and tachycardia ~ Fever and leukocytosis as the inflammation and infection develop ~ Abdominal distention, and a rigid abdomen signaling involvement of the parietal peritoneum ~ Decreased bowel sounds, indicating the onset of paralytic ileus and secondary obstruction Peritonitis resulting from a perforated ulcer or ruptured bladder may initially be termed chemical, but infection and bacterial peritonitis follow as intestinal bacteria leak out of the intestines. Severe generalized pain and abdominal rigidity are significant signs.

Pyelonephritis

inflammation of the renal pelvis and the kidney —pyogenic infection of the renal pelvis and parenchyma of one or both kidneys One or both kidneys may be involved. The infection extends from the ureter into the kidney, involving the renal pelvis and medullary tissue (tubules and interstitial tissue). Purulent exudate fills the kidney pelvis and calyces, and the medulla is inflamed. Abscesses and necrosis can be seen in the medulla and may extend through the cortex to the surface of the capsule. If the infection is severe, the exudate can compress the renal artery and vein and obstruct urine flow to the ureter. Bilateral obstruction is likely to result in acute renal failure Recurrent or chronic infection can lead to fibrous scar tissue forming over a calyx, leading to loss of tubule function and hydronephrosis. If severe and bilateral, it can eventually cause chronic renal failure. Purulent exudate and abscesses block flow of blood and urine Upper urinary tract infections Pyelonephritis

Wilm's tumor (Nephroblastoma)

is linked to a bad gene on chromosome 11 Wilms Tumor (nephroblastoma) Cancer Source is kind of genetic Wilm's Tumor found predominantly in children Many are now known to be associated with genetic defects on chromosome 11. children with Wilm's tumor usually present with abdominal enlargement from the mass effect. Nowadays, treatment gives a better than 90% 5 year survival. This is a rare tumor occurring in children. It is associated with defects in tumor-suppressor genes on chromosome 11 and may occur in conjunction with some other congenital disorders. It is usually unilateral. The tumor presents as a large encapsulated mass. Wilms tumor is usually diagnosed at ages 3 to 4 years, when the large abdominal mass becomes obvious (often a waistband on clothes does not fasten or a unilateral bulge appears). In some cases the child develops high blood pressure. Pulmonary metastases may be present at diagnosis. The prognosis for the child depends on the histologic results as well as the stage of the tumor at diagnosis. Tumors showing a favorable histology (less aggressive) have an average 5-year survival rate of 90%.

Pancreatic cancer

malignant tumor of the pancreas Adenocarcinoma Very deadly (Mortality about 95%) Associated with: Cigarette smoking Diabetes obesity S/S: location dependent Often: Pressure on the duodenum and common bile duct cause early signs of obstructive jaundice males (60%) In the pancreatic head blacks > whites pancreatic head in 66% infiltrates locally, obstructs ducts & encases vessels mets to liver, local nodes Pancreatic (exocrine) cancer is increasing in incidence in North America with an estimated 53,670 cases and 43,090 deaths in the United States for (American Cancer Society) 2017. The major established risk factor appears to be cigarette smoking. Pancreatitis and dietary factors have also been implicated. The common form of the neoplasm is adenocarcinoma, which arises from the epithelial cells in the ducts A tumor at the head of the pancreas usually causes obstruction of biliary and pancreatic flow, leading to weight loss and jaundice as early manifestations. Cancer of the body and tail of the pancreas frequently remains asymptomatic until it is well advanced and involves the nearby structures, such as the liver, stomach, lymph nodes, or posterior abdominal wall and nerves. Pain becomes severe as the cancer progresses, eroding tissues Unless the tumor is diagnosed early and can be removed surgically, it is usually not diagnosed until later in the disease. Metastases occur early, and effective treatments for metastatic disease are still in clinical research trials. Mortality is close to 95%. Liver failure, resulting from hepatobiliary obstruction, is often the cause of death

teratoma

monster tumor Malignancy of germ cell (like female but malignant) Mets through blood & lymph to lungs, liver, brain Survival rate for 5 yrs <50% if metastasis is present Teratoma ("Terrible Growth") A.k.a—dermoid cyst Germ cell (ovum) contains DNA for all body tissues Problem—needs DNA from sperm to make complete set to form a human being Germ cell tumor contains various body tissues

Dysmenorrhea

painful menstruation Painful menstruation—endometriosis Dysmenorrhea refers to painful menstruation and may be primary or secondary. Primary dysmenorrhea has no organic foundation and develops when ovulation commences. The majority of women experience some discomfort, but for many the pain is sufficient to interrupt normal activities. In many cases, dysmenorrhea is relieved after childbirth. The severe cramping pain is related to the excessive release of prostaglandin during endometrial shedding. This prostaglandin causes strong uterine muscle contractions and ischemia. Pain develops 24 to 48 hours before or at the onset of menses and lasts for 24 to 48 hours. In addition, nausea and vomiting, headache, and dizziness may accompany the cramps as the prostaglandins enter the systemic circulation. Some relief may be afforded by the use of a heating pad, exercise, or medications such as ibuprofen (Advil), a nonsteroidal antiinflammatory drug, that inhibits prostaglandin synthesis. An alternative treatment is the use of oral contraceptives, which lead to anovulatory cycles that are not painful. Secondary dysmenorrhea results from pelvic disorders such as endometriosis, uterine polyps or tumors, or pelvic inflammatory disease (PID)

colonic polyps

polyps (benign growths) protrude from the mucous membrane of the colon A colon polyp is a small clump of cells that forms on the lining of the colon. Most colon polyps are harmless. But over time, some colon polyps can develop into colon cancer, which is often fatal when found in its later stages Most malignant neoplasms develop from adenomatous polyps, of which there are diverse types. A polyp is a mass, often on a stem, that protrudes into the lumen, and many polyps represent genetic abnormalities (Fig. 17.38). As polyps increase in size, they carry an increased risk of dysplasia and malignant changes

cleft lip

position on back or in infant seat to prevent trauma to the suture line. while feeding hold in upright position. Failure of maxillary processes to fuse with nasal elevations or failure of upper lip fusion (4-8 weeks into fetal development) During fetal development (get exposed to teratogen) Fusion that goes on in the maxilla Outer lip remains open Cleft lip and cleft palate are common developmental abnormalities of the mouth and face and arise in the second or third month of gestation (Fig. 17.4). Cleft lip and cleft palate appear to be multifactorial in origin and are related to a number of inherited and environmental factors. One or both defects may be present in various degrees of severity Cleft lip, which may be unilateral or bilateral (on either side of the midline), results from failure of the maxillary processes to fuse with the nasal elevations or failure of the upper lip to fuse at some time between 4 and 8 weeks of fetal development.

preeclampsia and eclampsia

preeclampsia More serious—kidney dysfunction, edema HELLP (Hemolysis, Elevated Liver enzymes, Low Platelets) May progress to Disseminated Intravascular Coagulation (DIC) or eclampsia (see slide 18) Preeclampsia and eclampsia are more serious conditions in which the blood pressure is higher, and kidney dysfunction is indicated by proteinuria, weight gain, and generalized edema (face, hands, feet, and legs). In some patients with preeclampsia, a complication develops. This condition is known for its manifestations by the acronym HELLP (for Hemolysis, Elevated Liver enzymes, and Low Platelets). In a few cases, HELLP progresses to coagulation disorders such as disseminated intravascular coagulation (DIC), as indicated by excessive bleeding. Also, preeclampsia may progress to eclampsia, in which the blood pressure becomes extremely high and generalized seizures (grand mal) or coma develops. Immediate hospitalization is required for adequate treatment of eclampsia. Eclampsia Extremely high BP Grand mal seizures develop and even coma

chronic pancreatitis

pulmonary disease state characterized by the presence of airflow obstruction caused by chronic bronchitis or emphysema; clinical use of the term indicates the presence of chronic bronchitis and/or emphysema; includes asthma, chronic bronchiectasis, chronic bronchitis, and emphysema. Pancreas that is not function-- associated with chronic alcoholism Pancreatic insufficiency Often associate with chronic alcoholism Destruction of exocrine/endocrine glands Gradual loss of normal function Called pancreatic insufficiency Permanent malabsorption and diabetes Fats not absorbed Steatorrhea Fat-rich, foul smelling stool

Acute appendicitis

sudden inflammation of the appendage attached to the cecum A common acute problem in young adults, occurring in 10% of the population, appendicitis is an inflammation and infection in the vermiform appendix The development of appendicitis usually follows a pattern that correlates with the clinical signs, although variations may occur because of the altered location of the appendix or underlying factors: 1. Obstruction of the appendiceal lumen by a fecalith, gallstone, or foreign material or from twisting or spasm is commonly an initiating factor. 2. Fluid builds up inside the appendix and microorganisms proliferate. 3. The appendiceal wall becomes inflamed and purulent exudate forms. The appendix is swollen. Blood vessels in the wall are compressed (Fig. 17.35). 4. The increasing congestion and pressure within the appendix leads to ischemia and necrosis of the wall, resulting in increased permeability. 5. Bacteria and toxins escape through the wall into the surrounding area. This breakout of bacteria leads to abscess formation or localized bacterial peritonitis. 6. An abscess may develop when the adjacent omentum temporarily walls off the inflamed area by adhering to the appendiceal surface. In some cases, the inflammation and pain subside temporarily but then recur. 7. Localized infection or peritonitis develops around the appendix and may spread along the peritoneal membranes. 8. Increasing pressure inside the appendix causes increased necrosis and gangrene in the wall (infection in necrotic tissue). The wall of the appendix appears blackish. 9. If the appendix ruptures or perforates, it releases its contents into the peritoneal cavity. This leads to generalized peritonitis, which may be life threatening Acute appendicitis is a severe and sudden case of appendicitis. The symptoms tend to develop quickly over the course of one to two days . It requires immediate medical treatment. If left untreated, it can cause your appendix to rupture. This can be a serious and even fatal complication.

Hemorrhoids

swollen, twisted, varicose veins in the rectal region Hemorrhoids-varicose veins of rectum Irritable bowel syndrome (IBS, a.k.a. spastic colon) Overactive large bowel Peristaltic disturbance Cramping, diarrhea, gas which are dilated veins in the anal canal. These can become very painful and may bleed or become infected. A diet high in fiber is recommended to avoid constipation and straining during defecation

esophageal varices

swollen, varicose veins at the lower end of the esophagus Varices-enlarged veins of esophagus Dilation due to liver dysfunction See these due to liver dysfunction Get giant thin, dilated veins in esophagus Could potentially bleed to death Potential to rupture Due to portal hypertension Blood backs up into vessels around esophagus Potential for rupture & bleeding Back pressure-- pushes back on veins -- pushes on intestines (tissues get congested with fluid) Due to portal hypertension Blood backs up into vessels around esophagus Potential for rupture & bleeding Hemorrhage of these esophageal varices is a common complication of cirrhosis. Complications involve ruptured esophageal varices, leading to hemorrhage, circulatory shock, and acute hepatic encephalopathy. Varicosities are irregular dilated and tortuous areas of the superficial or deep veins (see Fig. 10.2). The most common location is the legs, but varicosities are also found in the esophagus (esophageal varices)

premenstrual syndrome

syndrome involving physical and emotional symptoms occurring in the 10 days before menstruation Recently medically verified—affects some women mid-cycle lasting until onset of menstruation Theory: ovarian hormones interfere w/ normal body chemistry (neurotransmitters) Emotional effects: Hostility, irritability, anxiety, depression Physical effects: Headaches, breast soreness, abdominal bloating Premenstrual syndrome (PMS) is a condition that begins a week or so before the onset of menses and ends with the onset of menses. The cause is not completely understood, but research on hormonal factors continues. In most women PMS causes nuisance symptoms such as breast tenderness, weight gain, abdominal distention or bloating, irritability, emotional lability, sleep disturbances, depression, headache, and fatigue. Some women have increased mental concentration and activity, whereas others are lethargic. These manifestations are severe in 3% to 8% of women reporting PMS; the more severe form of the disorder is termed premenstrual dysphoric syndrome. Treatment measures are tailored to the individual and may include hormonal therapy and the use of diuretics or antidepressants as necessary

Enzymatic necrosis

tissue death brought on by enzymes Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes. In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.

Autodigestion (or autolysis)

tissue destruction by an organ's own secretions Digestive enzymes in pancreas begin to 'eat self' (autolysis) Pancreatitis is an inflammation of the pancreas resulting from autodigestion of the tissues. It may occur in acute or chronic form. Acute pancreatitis is considered a medical emergency The autodigestion follows premature activation of the pancreatic proenzymes within the pancreas itself. It appears that activation of the proenzyme trypsinogen into trypsin is the trigger; in turn, trypsin converts other proenzymes and chemicals into active forms. The activated enzymes, trypsin, and the proteases amylase and lipase digest the pancreatic tissue, leading to massive inflammation, bleeding, and necrosis Autodigestion abnormal destruction of tissues by activated digestive enzymes

Carcinoid

tumor derived from the argentaffin cells in the intestinal tract, bile duct, pancreas, bronchus, or ovary Small Intestine Neoplasia* Uncommon—large intestine more common Carcinoid is most common for small intestine Neuroendocrine tumor Slow growing--nodules Metastasizes to liver Carcinoid syndrome Secretes hormone like chemicals from liver Causes respiratory problems, diarrhea, abdominal cramps, fibrosis of heart valves A carcinoid (also carcinoid tumor) is a slow-growing type of neuroendocrine tumor originating in the cells of the neuroendocrine system. In some cases, metastasis may occur. Carcinoid tumors of the midgut (jejunum, ileum, appendix, and cecum) are associated with carcinoid syndrome

testicular torsion

twisting of the spermatic cord causing decreased blood flow to the testis Twisting of spermatic cord Torsion of the testis occurs when the testis rotates on the spermatic cord, compressing the arteries and veins. Ischemia develops, and the scrotum swells. Immediate treatment is required manually and surgically to restore blood flow to the testis. Testicular torsion frequently occurs during puberty, both spontaneously and after trauma.

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