PATHO 2 final

Differentiate between lobar and broncho- pneumonia

**pneumonia** -develop as a primary acute infection in the lungs or may be secondary to another respiratory or systemic condition which tissue resistance is reduced -it is a risk following any aspiration or inflammation in the lung, when fluids pool or defense mech asuch as cilia is reduced -occasionally it is blood borne -may involve multiple microbes following aspirations -pathophysiologic changes occur primarily in the itnersitital tissue or avelor space -mixed bacteria are usually isolated from the resultant infection Legionnaires' disease Unknown until 1976 outbreak among American Legion convention attendees Legionella pneumophila (gram - bacteria) Resides in pulmonary macrophages Pneumocystis carinii pneumonia Fungus—often cause of fatality among AIDS patients Produces exudate (because of damaged tissues) Infectious inflammation of the lungs "...infectious Inflammation of lungs." (Inflammation of lungs: "pneumonitis") Bacterial & viral agents Breathed in Hematologic spread (septic bacteremia) → spread through the blood 2 categories dependent on exudate location Bronchopneumonia & lobar pneumonia → exudate collects in alveoli Interstitial pneumonia → edema in your tissues and does not get in alveoli Pneumonia is an infectious inflammation of the lungs. It can be caused by a variety of bacteria and some viral agents. The pathogens may be breathed in or may come from being transported in the blood stream. This can always be a complication from a hospital acquired infection. There are two main categories depending up the location of the exudate created (which often obstructs the airways)—broncho- and lobar pneumonia; and interstitial pneumonia. This poor person has every type of pneumonia in existence! Lobar pneumonia features a lobe in which the alveoli are filled with consolidation—a solidified exudate of debri, neutrophils, red blood cells, and fibrin. No gas is exchanged in these alveoli. Broncho pneumonia features consolidation in clumps of alveoli at the ends of bronchioles. It generally is more diffuse throughout the lungs. Interstitial pneumonia—usually of viral or mycoplasmic (see the infection chapter) origin, affects those interstitial cells that comprise the alveoli. The exudate usually causes swelling in the cells themselves. Some cases of this are termed walking pneumonia. Lobar pneumonia features a lobe in which the alveoli are filled with consolidation—a solidified exudate of debri, neutrophils, red blood cells, and fibrin. No gas is exchanged in these alveoli. Broncho pneumonia features consolidation in clumps of alveoli at the ends of bronchioles. It generally is more diffuse throughout the lungs. Interstitial pneumonia—usually of viral or mycoplasmic (see the infection chapter) origin, affects those interstitial cells that comprise the alveoli. The exudate usually causes swelling in the cells themselves. Some cases of this are termed walking pneumonia. LOBAR: -usually is bacterial -anatomic distribution of lesions may be diffuse and patchy throughout both lungs or lobar, meaning consolidated in one lobe -all of one or two lobes -inflammation of alveolar wall and leakage of cells, fibrin, and fluid into alveoli causing consolidation -pleura may be inflammed -sudden and acute onset -signs (high fever and chills, productive cough with rusty sputum, rales) -caused by strept. pneumoniae and is localized in one or more lobes -first stage in development is congestion and develops in the alveolar wall and exudate forms -second stage is consolidation (neutrophils RBCs and fibrin accumulare in the alveolar exudate forming a solid mass) -bc complete lobe is usually involved in inflam process the adjacent pleurae are frequently involved, producing pleuritic pain in affected site -empyema (can cause adhesions bw the pleural membranes restricting ventilation) -filling of alveoli with exudate reduces the diffusion of gases, with o2, and dec blood flow through the affected lobe -hypoxia results and is more marked bc the demand fir o2 increases with higher metabolic rate associated w the infection -o2 def leads to metabolic acidosis MANIFESTATIONS: -sudden onset -confusion and disorentation -treatment involves admin of antibacterial drugs Localized in one or more lobes Neutrophils, RBCs, Fibrin, mix w/alveolar exudate and form solid mass (consolidation) lobar pneumonia in which consolidation of the entire left upper lobe has occurred. Most lobar pneumonias are due to pneumococcus and for decades, these have responded well to penicillin therapy so that advanced, severe cases are not seen as frequently. However, pneumoccoci, like most other bacteria, are developing more resistance to antibiotics. Severe pneumococcal pneumonia still occurs, even in young to middle aged persons (not just the very young and the very old) and has a mortality rate of 20%!

Understand the general physiological causes of anemia

Anemia causes a reduction in oxygen transport. Basic problem is hemoglobin deficit Oxygen deficit leads to: Less energy production in all cells Cell metabolism and reproduction diminished Compensation mechanisms Tachycardia and peripheral vasoconstriction General signs of anemia Fatigue, pallor (pale face), dyspnea, tachycardia Limited o2 in blood cells Anemia causes you to be tired (not enough o2) Oxygen deficit leads to: Decreased regeneration of epithelial cells Digestive tract becomes inflamed and ulcerated, leading to stomatitis Inflamed and cracked lips Dysphasia Hair and skin may show degenerative changes. Ulcer develop on skin (necrotic tissue) Severe anemia may lead to angina or congestive heart failure (CHF). --Heart is working so hard / races so fast and it does not have enough time to fill up with blood and gets heart failure (output of heart is not sufficient) Anemias Anemias Not enough hemoglobin or blood cells -reduce o2 transport in the blood due to a decrease in hemoglobin content -may result from declining production of the protein, a decrease in the number of erythrocytes or combination of these factors -less energy is produced in all cells -general signs of anemia: 1. fatigue 2. pallor (pale face) 3. dyspnea (inc. effort to breathe) 4. tachycardia (rapid heart rate) -severe anemia may lead to angina during stressful situations if the o2 supply to the heart is reduced -- can cause CHF -may also occur when there is a deficiency of a required nutrient, bone marrow function is impaired, or blood loss/excessive destruction of erythrocytes occurs Anemias reduce oxygen transport in the blood due to a decrease in hemoglobin content. The low hemoglobin level may result from declining production of the protein, a decrease in the number of erythrocytes, or a combination of these factors. Anemias may be classified by typical cell characteristics such as size and shape (morphology) or by etiology—for example, the hemolytic anemias. The oxygen deficit leads to a sequence of events: ~ Less energy is produced in all cells; cell metabolism and reproduction are diminished. ~ Compensation mechanisms to improve the oxygen supply include tachycardia and peripheral vasoconstriction. ~ These changes lead to the general signs of anemia, which include fatigue (excessive tiredness), pallor (pale face), dyspnea (increased effort to breathe), and tachycardia (rapid heart rate). ~ Decreased regeneration of epithelial cells causes the digestive tract to become inflamed and ulcerated, leading to stomatitis (ulcers in the oral mucosa), inflamed and cracked lips, and dysphagia (difficulty swallowing); the hair and skin may show degenerative changes. ~ Severe anemia may lead to angina (chest pain) during stressful situations if the oxygen supply to the heart is sufficiently reduced. Chronic severe anemia may cause congestive heart failure. Anemias may also occur when there is a deficiency of a required nutrient, bone marrow function is impaired, or blood loss/excessive destruction of erythrocytes occurs. This section of the chapter covers a few examples of different types of anemias Insufficient iron impedes the synthesis of hemoglobin, thereby reducing the amount of oxygen transported in the blood (see Fig. 10.16A, presented later in the chapter, for a diagram showing four heme groups). This results in microcytic (small cell), hypochromic (less color) erythrocytes owing to a low concentration of hemoglobin in each cell (Fig. 10.12). Iron deficiency anemia is common; it ranges from mild to severe and occurs in all age groups. An estimated one in five women is affected, and the proportion increases for pregnant women. Because iron deficiency anemia is frequently a sign of an underlying problem, it is important to determine the specific cause of the deficit. There is also a reduction in stored iron, as indicated by decreased serum ferritin, decreased hemosiderin, and decreased iron-containing histiocytes in the bone marrow An iron deficit can occur for many reasons: Dietary intake of iron-containing vegetables or meat may be below the minimum requirement, particularly during the adolescent growth spurt or during pregnancy and breastfeeding, when needs increase. Normally, only 5% to 10% of ingested iron is absorbed, but this can increase to 20% when there is a deficit Chronic blood loss from a bleeding ulcer, hemorrhoids, cancer, or excessive menstrual flow is a common cause of iron deficiency. Continuous blood loss, even small amounts of blood, means that less iron is recycled to maintain an adequate production of hemoglobin Duodenal absorption of iron may be impaired by many disorders, including malabsorption syndromes such as regional ileitis and achlorhydria (lack of hydrochloric acid in the stomach) Severe liver disease may affect both iron absorption and iron storage. An associated protein deficit would further impede hemoglobin synthesis. In the form of iron deficiency anemia associated with some infections and cancers, iron is present but is not properly used, leading to low hemoglobin levels but high iron storage levels. Mild anemias are frequently asymptomatic. As the hemoglobin value drops, the general signs of anemia become apparent: ~ Pallor of the skin and mucous membranes related to cutaneous vasoconstriction ~ Fatigue, lethargy, and cold intolerance as cell metabolism decreases ~ Irritability, a central nervous system response to hypoxia ~ Degenerative changes, such as brittle hair, spoonshaped (concave) and ridged nails ~ Stomatitis and glossitis, inflammation in the oral mucosa and tongue, respectively ~ Menstrual irregularities ~ Delayed healing ~ Tachycardia, heart palpitations, dyspnea, and perhaps syncope (fainting) as the anemia becomes more severe

Discuss the pathophysiology of adult (or acute) respiratory distress syndrome (ARDS)

Adult Respiratory Distress Syndrome (ARDS) Widespread lung tissue damage, especially the lining of alveoli Often secondary or even tertiary reaction to other disease states Lungs FAILING People would go into shock Can be caused by inhaling smoke Not getting gas exchange Causes of ARDS Non-infectious interstitial disease Affects interstitial tissue between alveoli Diffuse alveolar damage Septal wall thickening from inflammation Exudate into alveoli Shock Formally called "shock lung" Blood contents leak into interstitium and alveoli Try to do vasoconstriction; acidosis does vasodilation Miscellaneous causes Hypoxia, anoxia, inhalation of toxins, chemicals, drugs, DIC, and heat from fire Signs, Symptoms, and Treatment of ARDS Extreme dyspnea—gasping Low PO2 (hypoxemia) and high PCO2 (hypercapnia) CXR (Chest X-ray) shows diffuse consolidation End result: respiratory failure Must be placed on a ventilator About a 30-40% case fatality rate -aka shock lung, wet lung, stiff lung -restrictive lung disorder predisposing conditions -systemic sepsis, prolonged shok, burns, aspirations, and smoke -basic changes in the lungs results from injury to the alveolar walls and cap membrane, leading to elease of chemical mediators, inc perm of alevelor cap mem, inc fluid and protein in theintersitial area, and damge to the surf producing cells --these events result in dec diffusion of o2 reduced blood flow to the lungs, difficulty in expanidng the lungs, and diffuse atelcelasis -damage to the lung tissue progresses as inc numbers of neutrophils migrate to the lungs, releasing prtesases and other mediators -excess fluid in the lungs predisposes to pneumonia as a complications -chf may develop Adult or acute respiratory distress syndrome (ARDS) is also known as shock lung, wet lung, stiff lung, postperfusion lung, and a variety of other names related to specific causes. It is considered to be a restrictive lung disorder. A multitude of predisposing conditions such as systemic sepsis, prolonged shock, burns, aspiration, and smoke inhalation may cause ARDS. The onset of respiratory distress usually occurs 1 to 2 days after an injury or other precipitating event. In many cases, it is associated with multiple organ dysfunction or failure secondary to a severe insult to the body The basic changes in the lungs result from injury to the alveolar wall and capillary membrane, leading to release of chemical mediators, increased permeability of alveolar capillary membranes, increased fluid and protein in the interstitial area and alveoli, and damage to the surfactant-producing cells (Fig. 13.29). These events result in decreased diffusion of oxygen, reduced blood flow to the lungs, difficulty in expanding the lungs, and diffuse atelectasis. Reductions in tidal volume and vital capacity occur. Damage to lung tissue progresses as increased numbers of neutrophils migrate to the lungs, releasing proteases and other mediators. Hyaline membranes form from protein-rich fluid in the alveoli, and platelet aggregation and microthrombi develop in the pulmonary circulation, causing stiffness and decreased compliance. If the patient survives, diffuse necrosis and fibrosis are apparent throughout the lungs. Excess fluid in the lungs predisposes to pneumonia as a complication. Congestive heart failure may develop

Identify three sources of cerebral vascular accidents (CVAs)

Cerebral Vascular Accident (CVA) a.k.a. Stroke Three types: Thrombus (pictured) Embolus (from other part of body, e.g. heart) Hemorrhage -thrombus: athero in cerebral artery; graudal-- may be preceded by TIA & often occurs at rest; minimal inc ICP; localized effects-- may be less permanent damage if collateral circulation has been established -embolus athero (carotid artery) or systemic source (ex: heart); sudden onset; minimal increased ICP; localized effects unless multiple emboli are present -hemorrhage hypertension-- arteriosclerosis; sudden onset-- often occurs with activity; present inc ICP and often high; widespread effects and severe-- often fatal -CVA stroke is an infarction of brain tissue that results from lack of blood -tissue necrosis may be an outcome of total occlusion of a cerebral blood vessel by atheroma or embolus, which causes ischemia, or may be the consequence of a ruptured cerebral vessel, which causes hemorrhage and inc intracranial pressure -occlusion of an artery by an atheroma is the most common cause of CVA (atherosclerosis) -atheromas develop in the large arteries, such as the carotid arteries (causes gradual narrowing of the arterial lumen by plaque and thrombus, leading to TIAs and eventually infarction) -sudden obstruction causes by an embolus lodging in the cerebral artery -- second type of stroke -thrombi may break off an atheroma, or mural thrombi may form inside the heart after a MI -intracerebral hemorrhage caused by a rupture of a cerebral artery in a patient with severe hypertension -frequently more severe and destructive than other CVAs because they affect large portions of the brain -b/c of the greater inc in ICP with hemorrhages the effects are evident in both hemispheres and are complicated by secondary effects of bleeding, in addition to the disrupted blood supply -collateral circulation may develop in areas gradually affected by atherosclerosis -b/c neurons do not regenerate, an area of residual scar tissue and often cysts remains, with a permanent loss of neurons in that area -In many cases, because specific functions result from integrated output from many areas, it is possible with intensive therapy for a person who has experienced a stroke to develop new neural pathways in the brain or to relearn a task, thus recovering some lost function. Complications are common. These include recurrent CVA; secondary problems related to immobility such as pneumonia, aspiration, and constipation; or contractures related to paralysis -Risk factors for stroke include diabetes, hypertension, systemic lupus erythematosus, elevated cholesterol levels, hyperlipidemia, atherosclerosis, a history of TIAs, increasing age, obstructive sleep apnea, and heart disease. The risk factors for atherosclerosis (see Chapter 12) apply similarly to CVA. The combination of oral contraceptives and cigarette smoking has been well documented as an etiologic factor. Emboli may arise from atheromas in the large arteries, such as the carotids, or from cardiac disorders of the left ventricle, such as acute myocardial infarction, atrial fibrillation, or endocarditis or from an implant such as a prosthetic valve. Severe or long-term hypertension and arteriosclerosis in the elderly increase the risk of intracerebral hemorrhage. Signs and symptoms depend on the location of the obstruction, the size of the artery involved, and the functional area affected (see Figs. 14.3 and 14.13A). The presence of collateral circulation may diminish the size of the affected area. There are "silent" areas of the brain, in which dysfunction resulting from small infarctions is not obvious. Obstruction of small arteries may not lead to obvious signs until several small infarctions have occurred. In some cases, the effects of a stroke develop slowly over a period of hours (termed evolving stroke) Occlusion of large arteries, such as the internal carotid artery or the middle cerebral artery, or a hemorrhage may cause severe, widespread effects, including coma, loss of consciousness, or death, almost immediately. Hemorrhagic strokes usually begin suddenly with a blinding headache and increasingly severe neurologic deficits Rapid treatment with "clot-busting agents," such as tissue plasminogen activator (tPA) (see Chapter 12), has reduced the effects of CVA in some individuals, but initial screening to rule out hemorrhage or other contraindications for anticoagulant drugs is essential. Surgical intervention may be possible to relieve carotid artery obstruction. Glucocorticoids may reduce cerebral edema. Supportive treatment to maximize cerebral circulation and oxygen supply is usually initiated. Assisting the patient's return to a sitting or standing position as soon as the vital signs are stable helps to maintain muscle tone and minimize perceptual deficits

Describe and differentiate between the manifestations of gonorrhea, syphilis, and Chlamydia

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. 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.

Discuss the pathophysiology of Parkinson's disease

Chronic Degenerative Disorders: Parkinson's Disease (Paralysis Agitans) Parkinson's involves a dysfunction of the extrapyramidal motor system, due to degenerative changes in usually the substantia nigra of the basal nuclei. This results in decreased secretion of dopamine--an inhibitory neurotransmitter. Older onset (> 60 yo) Imbalance between neuron excitation and inhibition S/S: tremors, muscle rigidity, slow movement Parkinson's disease is a progressive degenerative disorder that affects motor function through loss of extrapyramidal activity. In Parkinson's disease, dysfunction of the extrapyramidal motor system occurs because of progressive degenerative changes in the basal nuclei, principally in the substantia nigra. In this condition, a decreased number of neurons in the substantia nigra secrete dopamine, an inhibitory neurotransmitter, leading to an imbalance between excitation and inhibition in the basal nuclei. The excess stimulation affects movement and posture by increasing muscle tone and activity, leading to resting tremors, muscular rigidity, difficulty in initiating movement, and postural instability. Many patients with Parkinson's disease have a reduced number of cortical neurons, which is characteristic of dementia. Diagnosis depends on the physical manifestations and clinical history Primary or idiopathic Parkinson's disease usually develops after age 60 and occurs in both men and women. Several genes have been identified in cases of familial Parkinson's disease, but a common focus of research is the possible damaging effects of viruses or toxins on cells. Early signs include fatigue, muscle weakness, muscle aching, decreased flexibility, and less spontaneous change in facial expression. More obvious signs are tremors in the hands at rest and a repetitive "pill-rolling" motion of the hands. Tremors cease with voluntary movement and during sleep. As the disease advances, tremors affect the hands and feet, the face, tongue, and lips. Further motor impairment, increased muscle rigidity, difficulty in initiating movement, slow movements (bradykinesia), and a lack of associated involuntary movement occurs— for example, loss of arm-swinging when walking or spontaneous postural adjustments when sitting. The characteristic standing posture is stooped, leaning forward with the head and neck flexed Festination, or a propulsive gait (short, shuffling steps with increasing acceleration), occurs as postural reflexes are impaired, leading to falls. Complex activities, such as getting up out of a chair, become slow and difficult Other functions are affected as the voice becomes low and devoid of inflection (the person speaks in a quiet monotone) and dysarthria develops. Chewing and swallowing become difficult, prolonging eating time and causing recurrent drooling. The face of the patient resembles a mask, and blinking of the eyelids is reduced, resulting in a blank, staring face. Autonomic dysfunction is manifested in the later stages by urinary retention, constipation, and orthostatic hypotension. As orthostatic hypotension develops, the threat of falls increases. Urinary tract and respiratory infections are common complications. Dementia develops late in the course of the disease in 20% of affected persons.

Describe peptic and gastrointestinal ulcer pathophysiology

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.

Define encephalitis

Generalized infection of the brain or spinal cord usually viral but it also may be caused by bacteria, fungi, and other organisms the mode of transmission may be the bite of the mosquito a rabid animal or ingestion characterized by fever, headache, and nuchal rigidity, but also neurologic disturbances , such as authority, disorientation, seizures, focal paralysis, delirium, and coma Encephalitis Inflammation of brain Typically viral cause How do you treat a virus? Outcomes?? Causes: chickenpox, measles, mosquitoes, prions Herpes simplex (HSV-1) encephalitis Encephalitis is considered an infection of the parenchymal or connective tissue in the brain and cord, particularly the basal ganglia, although various viruses demonstrate an affinity for particular types of cells. The infection may include the meninges. Necrosis and inflammation develop in the brain tissue, often resulting in some permanent damage. Early signs of infection include severe headache, stiff neck, lethargy, vomiting, seizures, and fever Encephalitis is usually of viral origin but may be related to other organisms. In some cases, there may be considerable delay before signs appear. A few examples of specific diseases follow Western equine encephalitis is an arboviral infection spread by mosquitoes, which occurs more frequently in the summer months and is common in young children. St. Louis encephalitis is found throughout the United States and affects older persons more seriously than younger ones Encephalitis is considered an infection of the parenchymal or connective tissue in the brain and cord, particularly the basal ganglia, although various viruses demonstrate an affinity for particular types of cells. The infection may include the meninges. Necrosis and inflammation develop in the brain tissue, often resulting in some permanent damage. Early signs of infection include severe headache, stiff neck, lethargy, vomiting, seizures, and fever. Encephalitis is usually of viral origin but may be related to other organisms. In some cases, there may be considerable delay before signs appear. A few examples of specific diseases follow. Western equine encephalitis is an arboviral infection spread by mosquitoes, which occurs more frequently in the summer months and is common in young children. St. Louis encephalitis is found throughout the United States and affects older persons more seriously than younger ones West Nile fever is a form of encephalitis that originated in the northeastern United States but has now spread to a number of states across the country and into Canada. It is caused by a flavivirus, spread by mosquitoes, with certain birds as an intermediate host. The focus for control has been to track the spread and reduce the risk of mosquito bites in affected areas. The infection initially causes flulike symptoms with low-grade fever and headache, sometimes followed by confusion and tremors Neuroborreliosis (Lyme disease) is caused by a spirochete, Borrelia burgdorferi, transmitted by tick bites insummertime. The site of the tick bite is red with a pale center, gradually increasing in size to form the unique marker lesion, a "bull's eye" that may become quite large and persist for some time. The microbes then disseminate through the circulation, causing first, sore throat, dry cough, fever, and headache, followed by cardiac arrhythmias and neurologic abnormalities (eg, facial nerve paralysis) related to meningoencephalitis. Last, pain and swelling may develop in large joints, sometimes progressing to chronic arthritis. The effects may persist for months. Prolonged therapy with antimicrobials such as doxycycline is prescribed Herpes simplex encephalitis occurs occasionally and is dangerous, arising from the spread of herpes simplex virus type 1 (HSV-1) from the trigeminal nerve ganglion. This virus causes extensive necrosis and hemorrhage in the brain, often involving the frontal and temporal lobes. Early treatment with an antiviral drug, such as acyclovir, may control the infection. Otherwise, treatment is supportive. Amoebic meningoencephalitis can be caused by the amoeba Naegleria fowleri, which thrives in warm water and is typically found in the summer months in the southern United States. This is a rare infection that results in inflammation and swelling of the brain or spinal cord. Unless diagnosed and treated early, this infection is almost always fatal.

Define polyuria, oliguria, uremia

Increased urinary output (polyuria), manifested as frequency and nocturia Polyuria an abnormally large volume of urine excreted within a given period. Oliguria (decreased urine output) indicates that compensation mechanisms to conserve fluid in the body are taking place ~ Urine output decreases (oliguria) as GFR declines. d oliguria (reduced urine output Oliguria abnormally small volume of urine output. Uremia the end result of renal failure when waste products accumulate in the blood and fluid/electrolyte imbalance develops Uremia, or end-stage renal failure (more than 90% of nephrons lost), occurs when GFR is negligible. Fluid, electrolytes, and wastes are retained in the body, and all body systems are affected. In this stage, marked oliguria or anuria develops. Regular dialysis or a kidney transplant is required to maintain the patient's life. A comparison of acute and chronic renal failure may be found in

Describe Cardiac shunts (L to R, R to L, which one is cyanotic)

Left-to-right shunt Of less consequence—blood gets oxygenated again Involve a hole in the heart Heart muscle and left ventricle is bigger and stronger Blood from left side of heart pumps into right side of the heart Shunt → transfer of the fluid Still get perfusion of o2 in the system Recycling blood that does not need to be recycled Acyanotic (o2-ed blood) (blue) or cyanotic (unoxygenated hemoglobin in the blood--> produces blueish color) -the blood from the left side of the heart is recycled to the right side and to the lungs, resulting in an increased volume in the pulmonary circulation, a decreased cardiac output, and an inefficient system -large opening promote this -blood can flow in only ONE direction, from high pressure and therefore blood flows through the septal defect from the left ventricle to the right ventricle -effect is that less blood leaves the left ventricle, reducing stroke volume and cardiac output to the systemic circulation -A diversion of blood from the left side of the heart to the right, as through a septal defect. A diversion of blood from the systemic circulation to the pulmonary circulation, as through a patent ductus arteriosus. Right-to-left shunt More serious—cyanosis—more oxygenated blood in systemic flow Stores o2 blood in left and back into right ventricle Builds up pressure from left side into right side Gets stronger, and over powering the left side of the heart Pushes blue blood into left ventricle (cyanosis) - unoxygenated blood from the right side of the heart bypasses the lungs directly and enters the left side of the heart **the direction and amount of the abnormal blood flow determines the effects on the individual -right-to-left shunt allows deoxygenated systemic venous blood to bypass the lungs and return to the body. cyanotic Atrial Septal Defect (ASD) (hole b/w right and left atria) Blood usually flows from L to R due to higher pressure in left Produces a murmur Septum → dividing walls between the heart Ventricular Septal Defect (VSD) Increases workload of left ventricle Increases workload of right ventricle Increases circulation to lungs Results in pulmonary hypertension Gradually increases pressure in R Ventricle R pressure > L pressure R to L shunt Cyanosis develops Inefficient but will still work -most common congenital heart defect and is known as "hole in the heart" -opening in the interventricular septum -more blood enters the pulmonary circulation --> reduces the efficiency of the system and in time overloads damages to the blood vessels, causing pulmonary hypertension --this would lead to high BP in the right ventricle and a reversal of right to left shunt, leading to cyanosis - Tetralogy of Fallot is the most common cyanotic congenital heart condition. It is more complex and more serious than the others described so far because it includes four (Greek tetra) abnormalities and is a cyanotic disorder (infants suffering from this condition are sometimes called "blue babies"). The four defects are pulmonary valve stenosis, VSD, dextroposition of the aorta (to the right over the VSD), and right ventricular hypertrophy (see Fig. 12.24C). This combination alters pressures within the heart and therefore alters blood flow. The pulmonary valve stenosis restricts outflow from the right ventricle, leading to right ventricular hypertrophy and high pressure in the right ventricle. This pressure, now higher than the pressure in the left ventricle, leads to a right-to-left shunt of blood through the VSD. The flow of unoxygenated blood from the right ventricle directly into the systemic circulation is promoted by the position of the aorta, over the septum or VSD. for repairing , Tetralogy of Fallot showing the four characteristic abnormalities: pulmonary stenosis, ventricular septal defect, overriding aorta, and right ventricular hypertrophy. Tetralogy of Fallot is a cyanotic defect

Describe osteoarthritis (degenerative joint disease or DJD)

Osteoarthritis or growth stunting (in children) Epiphyseal plates grow -- fracture can delay this Bad wear and tear on the bone Degenerative change in a joint Erosion of articular cartilage Underlying bone begins to get damaged Cysts and bone spurs (osteophytes) develop in response Osteophytes break off into synovial fluid Synovial space appears smaller on X-rays Compensation injuries to other areas of the joint or other joints Gets holes and exposure to bone Erosion of bones Results in joint replacement -Osteoarthritis or growth stunting (in children)**Epiphyseal plates grow -- fracture can delay this**Bad wear and tear on the bone Osteoarthritis (OA) may be called a degenerative, or "wear and tear," joint disease. The incidence of osteoarthritis is increasing. It is estimated that one in three adults in the United States has some degree of osteoarthritis. Men are affected more often than women. It is a major cause of disability and absence from the workplace. In this condition the progression is as follows: 1. The articular cartilage, of weight-bearing joints in particular (eg, hips, knees), is damaged and lost through structural fissures and erosion resulting from excessive mechanical stress (Fig. 9.10), or breaks down for unknown reasons. 2. The surface of the cartilage becomes rough and worn, interfering with easy joint movement. 3. Tissue damage appears to cause release of enzymes from the cells, which accelerates the disintegration of the cartilage. 4. Eventually the subchondral bone may be exposed and damaged, and cysts and osteophytes or new bone spurs develop around the margin of the bone. 5. Pieces of the osteophytes and cartilage break off into the synovial cavity, causing further irritation. 6. The joint space becomes narrower (easily seen on x-rays). 7. There may be secondary inflammation of the surrounding tissues in response to altered movement and stress on the joint. No systemic effects are present with osteoarthritis The primary form of osteoarthritis is associated with obesity and aging, whereas the secondary type follows injury or abuse. Genetic changes in joint cartilage have been identified in research studies now underway. These genetic changes result in accelerated breakdown of articular cartilage. Osteoarthritis often develops in specific joints because of injury or excessive wear and tear on a joint. This is a common consequence of participation in sports and certain occupations. Congenital anomalies of the musculoskeletal system may also predispose a patient to osteoarthritis. Once the cartilage is damaged, joint alignment or the frictionless surface of the articular cartilage is lost. A vicious cycle ensues, because uneven mechanical stress is then applied to other parts of the joint and to other joints. The large weight-bearing joints (eg, the knees and hips) that are subject to injury or occupational stress are frequently affected The pain of osteoarthritis, which is often mild and insidious initially, is an aching that occurs with weight bearing and movement. Pain becomes more severe as the degenerative process advances. It may be unilateral in some cases Joint movement is limited. Frequently the joint appears enlarged and hard as osteophytes develop. Walking becomes difficult if the joint is unstable, and the muscles atrophy, causing a predisposition to falls, particularly in older individuals. When the temporomandibular joint is involved, mastication becomes difficult, there is difficulty opening the mouth to speak or yawn, and preauricular pain may be severe. In some cases, the hands are involved, with bony enlargement of the distal interphalangeal joints (Heberden nodes; Fig. 9.11). Usually little soft tissue swelling is seen Crepitus may be heard as the cartilages become irregular, grating against each other. In some cases, other joints are affected as the individual exerts more stress on normal joints to protect the damaged joints Osteoarthritis is not a systemic disorder; therefore there are no systemic signs or changes in serum levels. Diagnosis is based on exclusion of other disorders and radiographic evidence of joint changes consistent with the clinical signs. Radiographic evidence often shows lesser progression of joint changes than the clinical effects of disease.

Describe Paget's disease

Paget's Disease (Osteitis Deformans) Excessive bone destruction with replacement by fibrous, abnormal bone Thickening of bones Causes pathological fractures Skull enlargement compresses cranial nerves Can lead to cardiovascular disease and heart failure Metabolic disorders Bone is fibrous and not as strong→ they get thick but are not that strong ; they can get pathologic fractures from it (in the upper part of the femur is a common place) --occurs in adults older than 40 -childhood infection with a virus has been implicated of a genetic factor -excessive bone destruction occurs with replacement of bone by fibrous tissue and abnormal bone -pathologic fractures are common -skull involvement leads to signs of increased pressure such as headache and compression of cranial nerves -causes cardiovascular disease and heart failure Paget disease is a progressive bone disease that occurs in adults older than 40 years. The cause has not yet been established; however, childhood infection with a virus has been implicated and there is evidence of a genetic factor. Excessive bone destruction occurs, with replacement of bone by fibrous tissue and abnormal bone. Structural abnormalities, evident on x-rays, and enlargement (or thickening) are apparent in the long bones, vertebrae, pelvis, and skull. In some cases, the disease is asymptomatic. Pathologic fractures are common. When the vertebrae are affected, compression fractures and kyphosis result. Skull involvement leads to signs of increased pressure such as headache and compression of cranial nerves. Paget disease also causes cardiovascular disease and heart failure. Treatment goals are to reduce the risk of fractures and deformity

Discuss the development of 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.

. Differentiate between pericarditis and endocarditis

Pericarditis may be acute or chronic and is usually secondary to another condition in either the heart or the surrounding structures. Pericarditis can be classified by cause or by the type of exudate associated with the inflammation. Acute pericarditis may involve a simple inflammation of the pericardium, in which the rough, swollen surfaces cause chest pain and a friction rub (a grating sound heard on the chest with a stethoscope). In some cases, an effusion may develop, with a large volume of fluid accumulating in the pericardial sac (Fig. 12.29). This fluid may be serous as with inflammation, may be fibrinous and purulent as with infection, or may contain blood (hemopericardium) as with trauma or cancer Small volumes of fluid in the pericardium have little effect on heart function, but a large amount of fluid that accumulates rapidly may compress the heart and impair its expansion and filling, thus decreasing cardiac output (cardiac tamponade). The right side (low-pressure side) of the heart is affected first, causing increased pressure in the systemic veins and, if acute, distended neck veins. If fluid accumulates slowly, the heart adjusts, and a very large amount can build up before signs appear. A radiograph would show the enlargement of the heart. Chronic pericarditis results in formation of adhesions between the pericardial membranes that may become constrictive, causing the pericardium to become a tight fibrous enclosure, thus limiting movement of the heart. Pericarditis Infectious inflammation of pericardium or epicardium Exudate builds up in pericardial sac Painful heartbeats Can lead to cardiac tamponade (heart expansion restricted—"P.E.A.") -may be acute or chronic and usually secondary to another condition in either the heart of the surrounding structures -acute p. may involve a simple inflammation of the pericardium, in which the rough, swollen surfances cause chest pain and a friction rub --in some cases, an effusion may develop , with a large volume of fluid accumulating in the pericardial sac -large amount of fluid accumulates rapidy may compress the heart and impair its expansion and filling, thus decreasing cardiac output -right side of the heart is affected first(low pressure side), causing inc pressure in the systemic veins and if acute, distended neck veins -chronic p. results in formation of adhesions bw the pericardial membranes that may become constrictive, causing the pericardium to become a tight fibrous enclosure, thus limiting movement of the heart -tachy. can be a sign -inflammation of the outer layer may include effusion (excessive fluid accumulation) which impairs filling Infective Endocarditis Inflammation of inner lining and valves Usually Streptococcus viridans or Staphylococcus aureus (acute type) "vegetations"—ulcers deform valves and chordae tendineae—valvular insufficiency Infection on the inside of the heart Can be caused by systemic infection brought on by: Tooth abscesses Skin infections UTI's Respiratory infections -two types: subacute type in which defective heart valves are invaded by organisms of low virulence such as strepto viridans; and the acute type in which normal heart valves are attacked by highly virulent organisms such as staphylo. aureus which tends to cause severe tissue damage and may be difficult to treat successfully -micororganisms in the general circulation attach to the endocardium and invade the heart valves, causing inflammation and formation of vegetations on the cusps --vegetations interefere with the opening and closing of the valves -pieces may break away, frming infecting septic emboli that then can cause infarction and infection in other tissues -heart murmors are a common indicator -presence of abnromal tissues in the heart and microbes in the blood and reduced host defenses -anorexia, and childsm and septic emboli, and CHF are some signs and symptoms -blood cultures are treatments -effects the valves which become edematus and verrucae form (rows of small vegetations along the outer dg of the valve cusps) Infective endocarditis, formerly called bacterial endocarditis, occurs in two forms: the subacute type, in which defective heart valves are invaded by organisms of low virulence such as Streptococcus viridans (part of the normal flora of the mouth); and the acute type, in which normal heart valves are attacked by highly virulent organisms such as Staphylococcus aureus, which tend to cause severe tissue damage and may be difficult to treat successfully. It is now recognized that many types of organisms can cause infective endocarditis, and it is important to identify and treat the specific organism promptly The basic effects are the same, regardless of the causative organism. Microorganisms in the general circulation attach to the endocardium and invade the heart valves, causing inflammation and formation of vegetations on the cusps. Vegetations are large, fragile masses made up of fibrin strands, platelets and other blood cells, and microbes. In the acute stage, these may interfere withthe opening and closing of the valves. Pieces may break away, forming infective or septic emboli that then cause infarction and infection in other tissues. This process causes additional destruction and scarring of the valve and the chordae tendineae.Pericarditis may be acute or chronic and is usually secondary to another condition in either the heart or the surrounding structures. Pericarditis can be classified by cause or by the type of exudate associated with the inflammation. Acute pericarditis may involve a simple inflammation of the pericardium, in which the rough, swollen surfaces cause chest pain and a friction rub (a grating sound heard on the chest with a stethoscope). In some cases, an effusion may develop, with a large volume of fluid accumulating in the pericardial sac (Fig. 12.29). This fluid may be serous as with inflammation, may be fibrinous and purulent as with infection, or may contain blood (hemopericardium) as with trauma or cancer

Define hemothorax

accumulation of blood in the pleural space. -hemothorax is when the fluid is blood resulting from trauma, cancer, or surgery Hemothorax is the term used when the fluid is blood resulting from trauma, cancer, or surgery. Empyema occurs when the fluid is purulent as a result of infection, often related to pneumonia.

Discuss the development of cerebral palsy

Most common crippling dz of children Trauma, hypoxia, teratogens Cause of paralysis (but doesn't get worse) Balance & coordination affected Intellectual disability common Impaired CNS function due to injury early in life Frequent cause—lack of oxygen to brain during difficult deliveries Does not "progress" Can cause intellectual disability and motor difficulties Spastic (65-75% of cases) Dyskinetic (20-25% of cases) Ataxic (5% of cases) Mixed (13% of cases) (See Table 23-1) Cerebral palsy (CP) is a group of disorders marked by some degree of motor impairment, caused by genetic mutations, abnormal fetal formation of functional brain areas, infection, or brain damage in the perinatal period. In addition, damage usually occurs in other areas of the brain, resulting in a clinical presentation that is highly variable, depending on the specific areas affected and the severity of the trauma The damage may occur before, during, or shortly after birth and is nonprogressive Pathologically, the brain tissue is altered by malformation, mechanical trauma, hypoxia, hemorrhage, hypoglycemia, hyperbilirubinemia, infection, or some other factor, resulting in necrosis. In some cases, generalized necrosis and atrophy of brain tissue have occurred, whereas in other cases only one or two localized areas of the brain are affected. Although all children have some degree of altered mobility, which provides the basis for classifying cerebral palsy, an assortment of other problems is present in individual cases. ■ Etiology Single or multiple factors may be implicated in the development of cerebral palsy. Hypoxia or ischemia is the major cause of brain damage; it may occur prenatally, perinatally, or postnatally. Hypoxia may be caused by placental complications or a difficult delivery or by vascular occlusion, hemorrhage, aspiration, or respiratory impairment in the premature infant. High bilirubin levels, resulting from problems such as prematurity or Rh blood incompatibility, may cause kernicterus, in which accumulated bilirubin crosses the blood-brain barrier and damages the neurons. Other causes of cerebral palsy include infection or metabolic abnormalities, such as hypoglycemia, in either the mother or the child. The first and largest group includes those with spastic paralysis, which results from damage to the pyramidal tracts (diplegia) or the motor cortex (hemiparesis), or from general cortical damage (quadriparesis). As the name indicates, this form is characterized by hyperreflexia (excessive reflex response). For example, crossed legs are apparent when the child is held up or a child with some mobility walks with a typical scissors gait (ie, on the toes and with crossed legs). The second group is dyskinetic disease, which results from damage to the extrapyramidal tract, basal nuclei, or cranial nerves. This form of cerebral palsy is manifested by athetoid or choreiform involuntary movements and loss of coordination with fine movements The third group, ataxic cerebral palsy, commonly develops from damage to the cerebellum and manifests as loss of balance and coordination. Spastic; 65%-75%; Motor cortex or pyramidal tracts; Paralysis Hyperreflexia and increased muscle tone Dyskinetic; 20%-25% ; Basal nuclei or extrapyramidal tracts ; Loss of motor control and coordination Athetoid or choreiform movements Ataxic ; 5% ; Cerebellum ; Gait disturbance Loss of balance Mixed ; 13% ; All of above ; Some of each of above Spasticity is manifested by increased muscle tone or resistance to passive movement, with excessive reflex responses. Unilateral use of the hands or feet and asymmetric body movements are indications of abnormality. Writhing movements or facial grimaces may indicate athetoid cerebral palsy. Feeding difficulties and constant tongue thrusting are signs of motor dysfunction and may interfere with nutrition and growth. The position of the child's limbs when resting or when held up is often unusual (eg, scissors position of the legs). In addition to the motor deficit, cerebral palsy may be accompanied by many other problems, which depend on the other areas of brain damage. A few common areas of dysfunction are as follows: Intellectual function ~ Communication and speech ~ Seizures ~ Visual problems Communication and speech development are difficult because of motor disability, possible impaired mentation, and visual or hearing deficits. A number of children have learning disabilities and behavioral problems, such as attention deficit disorder, spatial disorientation, and hyperactivity Seizures, primarily of the generalized tonic-clonic (grand mal) type, are common. Visual problems, such as astigmatism and strabismus, occur frequently.

Understand the pathophysiology of sickle cell anemia

--Sickle cell anemia is caused by a mutation in the gene that tells your body to make the iron-rich compound that makes blood red and enables red blood cells to carry oxygen from your lungs throughout your body (hemoglobin --Sickle cell disease is an inherited disease caused by defects, called mutations, in the beta globin gene that helps make hemoglobin. ... The mutations in the gene cause a problem when oxygen levels in the blood are lower, which occurs once the hemoglobin has delivered oxygen to the cells in the body's tissues Affects people of Med. and african descentTend to be resistant to malaria Get eaten up very quickly (what causes anemia)Causes necrosis red blood cell elongates and hardens in a sickle shape when O2 levels are low-- short life span, recessive inheritance, painful crises with multiple infarcation sickle cell anemia CARRIES OXYGEN OUT OF THIS CELL (still carries o2) The problem: 20 days Spleen eats these things up; gets congested with all these cells Excessive hemolysis Explain beta chain defect --Sickle cell disease is an autosomal recessive disorder caused by mutations in the hemoglobin beta (HBB) gene, the hemoglobin gene that is specifically used after birth. ... Absence of the hemoglobin beta chain causes beta-zero-thalassemia, while reduced amounts of hemoglobin beta causes beta-plus-thalassemia --The mutation in the HBB gene in sickle cell anemia changes one of the amino acids, the building blocks of proteins, in the beta chain of hemoglobin. This defect causes the hemoglobin protein to stick together and form stiff fibers. These fibers distort the shape of the red blood cells and make them more fragile. --in Hbs, one amino acid in the pair of beta-globin chains has been changed from the normal glutamic acid to valine--- deoxygenated and changes into a sickled shape -- cell membrane is damaged and has a shorter life span (20 days) o The reason why patients become anemic --Sickle cell anemia is caused by a mutation in the gene that tells your body to make the iron-rich compound that makes blood red and enables red blood cells to carry oxygen from your lungs throughout your body (hemoglobin --Sickle cell disease is an inherited disease caused by defects, called mutations, in the beta globin gene that helps make hemoglobin. ... The mutations in the gene cause a problem when oxygen levels in the blood are lower, which occurs once the hemoglobin has delivered oxygen to the cells in the body's tissues o Effects --multiple infarctions occur throughout the body, leading to affects in the brain, bones, or organs -Infections, pain, and fatigue are symptoms of sickle cell disease. --Early signs and symptoms of sickle cell disease include swelling of the hands and feet; symptoms of anemia, including fatigue, or extreme tiredness; and jaundice. Over time, sickle cell disease can lead to complications such as infections, delayed growth, and episodes of pain, called pain crises o Sickle cell trait --Sickle cell trait describes a condition in which a person has one abnormal allele of the hemoglobin beta gene (is heterozygous), but does not display the severe symptoms of sickle cell disease that occur in a person who has two copies of that allele (is homozygous). Sickle Cell Anemia Affects people of Med. and african descent Tend to be resistant to malaria Sickle Cell Anemia Get eaten up very quickly (what causes anemia) Causes necrosis -representative of a large number of similar hemoglobinpathies -inherited charac. leads to the formation of abnormal hemoblogib -when the altered hemoglobin is deoxygenated, it crystallizes and changes the shape of the RBC from a disc to a crsent shape -cell membrane is damaged, leading to hemolysis and the cells have a much shorter life span than normal -probelm of sickling process is the obstruction of the small blood vessels by the elongated and rigid RBCs, resulting in thrombus formation and repeated multiple infarctions or areas of tissue necrosis -damage and loss of function occur in many organ systems -besides anemia, high rate of hemolysis leads to hyperbilirubinemai, jaundice, etc -clinical signs occur only with severe hypoxia -enlargement of the spleen is common in young people bc the cells cause congestion -painful and perm. damage to tissue -acute chest syndrome -growth and develp. are delayed -CHF may develop -frequent infections occur -can be detected by blood test Sickle cell anemia is representative of a large number of similar hemoglobinopathies. In this anemia, an inherited characteristic leads to the formation of abnormal hemoglobin, hemoglobin S (HbS). In HbS, one amino acid in the pair of beta-globin chains has been changed from the normal glutamic acid to valine (Fig. 10.16). When this altered hemoglobin is deoxygenated, it crystallizes and changes the shape of the RBC from a disc to a crescent or "sickle" shape. The cell membrane is damaged, leading to hemolysis, and the cells have a much shorter life span than normal, perhaps only 20 days, instead of the normal 120 days. Initially the sickling may be reversible when increased oxygen is available, but after several episodes, the damage to the RBC is irreversible and hemolysis occurs. Hemoglobin S can transport oxygen in the normal fashion, but the erythrocyte count is very low, resulting in a low hemoglobin level in the blood. A major problem resulting from the sickling process is the obstruction of the small blood vessels by the elongated and rigid RBCs, resulting in thrombus formation and repeated multiple infarctions, or areas of tissue necrosis, throughout the body (Fig. 10.17). The deoxygenation of hemoglobin may occur in the peripheral circulation as the oxygen content of the blood is gradually reduced, leading to repeated minor infarctions. A serious crisis may occur in individuals with lung infection or dehydration when basic oxygen levels are reduced. During a sickling crisis, many larger blood vessels may be involved, and multiple infarctions occur throughout the body, affecting the brain, bones, or organs. In time, significant damage and loss of function occur in many organ systems In addition to the basic anemia, the high rate of hemolysis leads to hyperbilirubinemia, jaundice, and gallstones

Describe the development of metastatic breast cancer

-Alterations (mutations) in breast cells -Invasive - infiltrating -Noninvasive - in situ -Most frequent - Invasive ductal carcinoma 1. Primary tumor 2. Lymph node 3. Vein 4. Tumor cells lodge in hospitable capillary bed 5. Secondary tumor grows and spreads 6. Multiple tumors 1. Primary breast cancer 2. Spread to axillary lymph node 3. Follow lymphatic to vena cava 4. Lung metastasis- secondary 5. Aorta carries tumor cells from lungs to all organs 6. Ovary metastasis 6. Liver metastasis 6. Brain metastasis

Know the four major types of leukemia

Acute lymphocytic leukemia (ALL) B lymphocytes Young children Acute myelogenous (or myelocytic) leukemia (AML) Granulocytic stem cells Adults Chronic lymphocytic leukemia B lymphocytes Adults older than 50 years Chronic myelogenous leukemia (CML) Granulocytic stem cells Adults 30-50 Acute monocytic leukemia Monocytes Adults Hairy cell leukemia B lymphocytes Males older than 50 years Depending on the particular stem cell affected, both acute and chronic leukemias can be further differentiated according to the cell type involved—for example, lymphocytic leukemia. The four major types are acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML). Most cases of ALL involve the precursors to B lymphocytes. Myelogenous leukemia affects one or more of the granulocytes. The neoplastic stem cell may, in some cases of myelogenous leukemia, involve all blood cells. The major groups are then further differentiated—for example, acute monoblastic leukemia, which is a type of myelogenous leukemia. In some severe forms of acute leukemias, only undifferentiated stem cells can be identified. When the cells are primitive, the term blast may be used in the name. Several detailed classifications for the leukemias are available. A brief summary can be found in four major types: ALL—acute lymphocytic leukemia (B Lymph) Most common childhood cancer -b lymph and young kids CLL—chronic lymphocytic leukemia → makes lymphs (B Lymph) Adults over 50 -b lymph and adults older than 50 AML—acute myelogenous leukemia (Granulocytic stem cells) Most common acute leukemia in adults Centered on bone marrow CML—chronic myelogenous leukemia (Granulocytic stem cells) Adults age 30-50

Discuss the pathophysiology of acute glomerulonephritis

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 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.

Discuss the pathophysiology of acute (autolysis via enzymatic necrosis) 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. 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

Differentiate between Addison's disease and Cushing's syndrome

Addison's Disease Adrenocortical secretion deficiency Autoimmune reaction most common cause Manifestations: Poor stress response Fatigue Weight loss Low serum Na+ Anorexia, nausea, diarrhea Hypotension, syncope Hyperpigmentation Anorexia Addison disease refers to a deficiency of adrenocortical secretions, the glucocorticoids, mineralocorticoids, and androgens. An autoimmune reaction is the common cause. The gland may be destroyed by hemorrhage with meningococcal infection or by viral, tubercular, or histoplasmosis infections. Destructive tumors may also cause hypoactivity. The major effects of these hormonal deficits include the following: ~ Decreased blood glucose levels ~ Poor stress response ~ Fatigue ~ Weight loss ~ Frequent infections Low serum sodium concentration, decreased blood volume, and hypotension, accompanied by high potassium levels, result from the mineralocorticoid (aldosterone) deficit and lead to cardiac arrhythmias and failure. Other manifestations include decreased body hair due to a lack of androgens and hyperpigmentation in the extremities, skin creases, buccal mucosa, and tongue, because of increased ACTH resulting from low cortisol secretion. Addison disease results from a deficit of glucocorticoids, mineralocorticoids, and androgens, affecting blood glucose levels, fluid and electrolyte balance, and the stress response. adrenal Cortex Disorders Cushing's syndrome Too many steroid s(being overly treated; excessive cortisol) Appear puffy; thin hair Excessive glucocorticoids Causes of Cushing's If it is a pituitary gland/tumor, stimulate adrenal gland (cushing's disease) -- pituitary disorder Causing inc cortisol secretions You won't see it bc overwhelming it in bloodstream with cortisol Can get it in lung cancer Iatrogenic (too much steroids) Cushing syndrome is caused by an excess of glucocorticoids (eg, hydrocortisone or cortisol). The mechanism for the excess amount of hormone and the effect on related hormones depends on the cause. Excess glucocorticoids may result from various conditions: Adrenal adenoma (Fig. 16.16) ~ Pituitary adenoma (Fig. 16.17) or Cushing disease ~ An ectopic carcinoma that causes paraneoplastic syndrome (see Fig. 16.17C and Chapter 20) ~ Iatrogenic conditions, such as the administration of large amounts of glucocorticoids for many chronic inflammatory conditions Glucocorticoids are essential for the stress response and essential for life. They perform many important functions in the body. But in excess amounts, they produce many unfortunate effects. This is why prolonged treatment with these drugs is not recommended Typical changes associated with Cushing syndrome include the following: Characteristic change in the person's appearance; a moon face (round and puffy) and a heavy trunk with fat at the back of the neck (buffalo hump) and wasting of muscle in the limbs Fragile skin that may have red streaks as well as increased hair growth (hirsutism) ~ Catabolic effects such as osteoporosis and decreased protein synthesis, which will delay healing ~ Metabolic changes include increased gluconeogenesis and insulin resistance, which may lead to glucose intolerance; this may result in diabetes mellitus or exacerbate an existing diabetic state ~ Retention of sodium and water (mineralocorticoid effect), leading to hypertension, edema, and possible hyperkalemia ~ Suppression of the immune response and the inflammatory response with atrophy of the lymphoid tissue, predisposing the client to infection ~ Stimulation of erythrocyte production ~ Emotional lability and euphoria Health care professionals will have two concerns: 1. The risk of infection in the patient with Cushing syndrome and the need for precautions; infection may be local or systemic (eg, tuberculosis) 2. A decreased stress response in a patient with iatrogenic Cushing syndrome because of the atrophy of the adrenal cortex; therefore the doses of medication may have to be increased before and during a stressful event; similarly dosage must be gradually reduced over a period of time to permit resumption of normal secretory function by the gland Treatment depends on the underlying cause. Cushing syndrome is caused by excess glucocorticoids resulting from a pituitary or adrenal cortical tumor, an ectopic tumor, or ingestion of glucocorticoids. The major effects include catabolic action on bone, muscle, and skin and depressed inflammatory and immune responses

Discuss the development of dry and wet age-related macular degeneration

Age-related macular degeneration (AMD) -- degenerative changes to focus and vision Degeneration of the fovea centralis in the macula lutea Retina is no longer nourished by choroid Two types Dry Retinal cells destroyed by deposits Destroying centralis More common and related to age Wet Abnormal neovascularization Blood vessels are not well formed and start to leak Cannot see (can sense and have some vision but not much) Age-related macular degeneration (AMD) is a common cause of visual loss in older persons. It appears to arise from a combination of genetic factors and environmental exposure (eg, ultraviolet rays and drugs). A similar condition found in younger persons has a stronger genetic basis. Degeneration occurs at the fovea centralis in the macula lutea, with its high density of cones, at the central point of the retina. There are two types of degeneration: The more common type is the dry or atrophic AMD, in which deposits form in retinal cells, gradually destroying them In the wet or exudative form, neovascularization occurs, with the formation of abnormal, leaky blood vessels, rapidly destroying the retina In both types, nutrients can no longer pass from the choroids to the retina. Central vision with high acuity first becomes blurred and then is lost. There is no treatment to reverse the effects. Depth perception is also affected. There is no pain. Peripheral vision is not affected Visual field tests and angiography assist diagnosis. For the dry type of AMD, nutrition is assessed to ensure that vitamin, mineral, and antioxidant intake are sufficient. A high-dose formulation of antioxidants and zinc has been shown to reduce the risk of advanced AMD and its associated vision loss. In the wet type of AMD, photodynamic therapy (photosensitive drug plus laser) may help seal off neovasculature. The older method, laser photocoagulation, may also be used to seal vessels without the photo-activated drug Visudyne, which is used in photodynamic therapy. The new drug, pegaptanib (Macugen) may slow vascular growth in cases of the wet type, and therapy using the drug antivascular endothelial growth factor (anti-VEGF) has shown promise. An intraocular shot of an anti-VEGF drug inhibits the formation of new blood vessels behind the retina and may keep the retina free of leakage.

Describe the pathophysiology of cirrhosis of the liver

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 development of Alzheimer's disease

Alzheimer's Disease (AD) Idiopathic, aka 'senile dementia' Affects 10% > age 65 ; 25% > age 85 Atrophy of cerebrum & neuron loss Short term memory, personality, wandering/lost Severe: bedridden Alzheimer's Disease cerebral atrophy mainly in the frontal & parietal regions narrowed gyri & widened sulci Approximately 10% of the population greater than 65 years of age has Alzheimer's disease (AD), and this increases to over 25% in the age group greater than 85 years. Females are affected more than males. In Alzheimer's disease there is a progressive loss of intellectual function that eventually interferes with work, relationships, and personal hygiene. Personality changes, lack of initiative, and repetitive behavior and impairments in judgment, abstract thinking, and problem-solving abilities are characteristic of the disease. Typical changes in Alzheimer's disease include progressive cortical atrophy, which leads to dilated ventricles, and widening of the sulci Neurofibrillary tangles in the neurons and senile plaques are found in large numbers in the affected parts of the brain. The plaques, which disrupt neural conduction, contain fragments from beta-amyloid precursor protein (βAPP); the role of this protein is a focus of research. Some neurofibrils and plaques have been found in the brains of elderly people whose cognitive function is not impaired, and therefore it appears that the numbers and distribution of the plaques are the significant factors. A deficit of the neurotransmitter ACh also occurs in the affected brain. The specific cause is unknown. At least four defective genes located on different chromosomes have been associated with AD. Three gene mutations on chromosomes 1, 14, and 21 are inherited as autosomal dominant traits resulting in early onset AD. The genetic factor is also supported by the high incidence in older persons with Down syndrome (trisomy 21). One form of late onset AD has been linked to a mutation on chromosome 19. Other forms of Alzheimer's disease appear to be multifactorial in origin. The National Institute on Aging has launched major research investigations into genetic and other suspected factors, including exposure to metals, viruses, and metabolic syndrome. Onset tends to be insidious. The course may extend over 10 to 20 years: In the early stage, gradual loss of memory and lack of concentration become apparent. Ability to learn new information and to reason is impaired and behavioral changes, such as irritability, hostility, and mood swings, are common Cognitive function, memory, and language skills continue to decline. Problem solving, mathematical ability, and judgment are poor. Apathy, indifference, and confusion become more marked. Managing the activities of daily living becomes difficult, affecting meal preparation, dressing, and personal hygiene. Wandering is common and the person may become confused and lost, even in familiar territory In the late stage, the person does not recognize his or her family, lacks awareness or interest in the environment, is incontinent, and is unable to function in any way. Degenerative changes may gradually interfere with motor function.

Identify Atrial (ASD) and ventricular septal defects (VSD)

Atrial Septal Defect (ASD) (hole b/w right and left atria) Blood usually flows from L to R due to higher pressure in left Produces a murmur Septum → dividing walls between the heart Ventricular Septal Defect (VSD) Increases workload of left ventricle Increases workload of right ventricle Increases circulation to lungs Results in pulmonary hypertension Gradually increases pressure in R Ventricle R pressure > L pressure R to L shunt Cyanosis develops Inefficient but will still work -most common congenital heart defect and is known as "hole in the heart" -opening in the interventricular septum -more blood enters the pulmonary circulation --> reduces the efficiency of the system and in time overloads damages to the blood vessels, causing pulmonary hypertension --this would lead to high BP in the right ventricle and a reversal of right to left shunt, leading to cyanosis Atrial septal defect. Blood flow through the defect is usually left to right and produces an acyanotic shunt. Ventricular septal defect. Blood flow through the defect is usually left to right and produces an acyanotic shunt Ventricular septal defect (VSD) is the most common congenital heart defect and is commonly called a "hole in the heart." It is an opening in the interventricular septum, which may vary in size and location. (Septal defects may also occur in the atrial septum when the foramen ovale fails to close after birth.) Small defects do not affect cardiac function significantly but increase the risk of infective endocarditis Large openings permit a left-to-right shunt of blood (see Fig. 12.24A). Blood can flow in only one direction, from the high-pressure area to the low-pressure area. In this case, the left ventricle is the high-pressure area, and therefore blood flows through the septal defect from the left ventricle to the right ventricle. The effect of this altered flow is that less blood leaves the left ventricle, reducing stroke volume and cardiac output to the systemic circulation. More blood enters the pulmonary circulation, some of which is already oxygenated; this reduces the efficiency of the system and in time overloads and irreversibly damages the pulmonary blood vessels, causing pulmonary hypertension. This complication, which may occur in untreated VSD, would lead to an abnormally high pressure in the right ventricle and a reversal of the shunt to a right-to-left shunt, leading to cyanosis Treatment typically involves both medications and surgical repair. The medications involved may be used to do the following: ~ Increase strength of contractions ~ Decrease amount of fluid in circulation ~ Keep a regular heartbeat Surgical methods include the following: ~ Direct open heart surgery to close the hole in the septum ~ Catheter procedure where a catheter is inserted into a blood vessel (typically in the groin) and is used to place a mesh patch in the hole ~ Hybrid procedure where a small incision is made in the heart and a catheter is inserted to place the patch in position to seal the hole A congenital deformity; a hole in the septum between the ventricles that results in a left-to-right shunt of blood;

Describe the pathophysiology of 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

Differentiate between mechanical and paralytic ileus

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. 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. 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 general pathophysiology of acute leukemia

Bone marrow disorder affecting cells that create WBCs Normal stem cells replaced by immature, non-functioning, cancerous stem cells Result: lack of functional WBCs (& also affects RBC/platelet production) Cancer of the bone marrow (depends on which cells are being cancerous) Are not normal functioning cells Get infections Spleen starts to eat up blood cells as you can become anemic Four major types: ALL—acute lymphocytic leukemia (B Lymph) Most common childhood cancer -b lymph and young kids CLL—chronic lymphocytic leukemia → makes lymphs (B Lymph) Adults over 50 -b lymph and adults older than 50 AML—acute myelogenous leukemia (Granulocytic stem cells) Most common acute leukemia in adults Centered on bone marrow CML—chronic myelogenous leukemia (Granulocytic stem cells) Adults age 30-50 Complications of Leukemia Opportunistic infections, including pneumonia Sepsis Congestive heart failure Hemorrhage Liver failure Renal failure CNS depression and coma The Leukemias Diagnostic tests Peripheral blood smears Immature leukocytes and altered numbers of WBCs Numbers of RBCs and platelets decreased Bone marrow biopsy for confirmation Treatment Chemotherapy ALL in young children responds well to drugs Biological therapy (interferon) May be used to stimulate the immune system Leukemias Malignant white blood cells -one or more leukocyte types are present as undiff. immature cells that multiply uncontrollably in the bone marrow and released into the circulation -most cases of ALL involve the precursors ti B lymoh. -when cells are primitive, word blast may be used One or more of the leukocyte types are present as undifferentiated, immature, nonfunctional cells that multiply uncontrollably in the bone marrow, and large quantities are released as such into the general circulation (Fig. 10.22). As the numbers of leukemic cells increase, they infiltrate the lymph nodes, spleen, liver, brain, and other organs. Acute leukemias are characterized by a high proportion of very immature, nonfunctional cells (blast cells) in the bone marrow and peripheral circulation; the onset usually is abrupt, with marked signs and complications. Chronic leukemias have a higher proportion of mature cells (although they may have reduced function), with an insidious onset, mild signs, and thus a better prognosis Depending on the particular stem cell affected, both acute and chronic leukemias can be further differentiated according to the cell type involved—for example, lymphocytic leukemia. The four major types are acute lymphocytic leukemia (ALL), chronic lymphocytic leukemia (CLL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (CML). Most cases of ALL involve the precursors to B lymphocytes. Myelogenous leukemia affects one or more of the granulocytes. The neoplastic stem cell may, in some cases of myelogenous leukemia, involve all blood cells. The major groups are then further differentiated—for example, acute monoblastic leukemia, which is a type of myelogenous leukemia. In some severe forms of acute leukemias, only undifferentiated stem cells can be identified. When the cells are primitive, the term blast may be used in the name. Several detailed classifications for the leukemias are available. A brief summary can be found in The proliferation of leukemic cells in the bone marrow suppresses the production of other normal cells, leading to anemia, thrombocytopenia, and a lack of normal functional leukocytes (Fig. 10.23). The rapid turnover of cells leads to hyperuricemia and a risk of kidney stones and kidney failure, especially in patients who are receiving chemotherapy. The crowding of the bone marrow causes severe bone pain resulting from pressure on the nerves in the rigid bone and the stretching of the periosteum. As the malignancy progresses, the increased numbers of leukemic cells cause congestion and enlargement of lymphoid tissue, lymphadenopathy, splenomegaly, and hepatomegaly. Death usually results from a complication such as overwhelming infection or hemorrhage

Describe the epidemiology of bronchogenic carcinoma

Bronchogenic carcinoma, arising from the bronchial epithelium, is the most common type of malignant lung tumor (Fig. 13.16). A number of subgroups occur. Squamous cell carcinoma usually develops from the epithelial lining of a bronchus near the hilum and projects into the airway (see Fig. 20.3A). Adenocarcinomas (from glands) and bronchoalveolar cell carcinomas are usually found on the periphery of the lung, making them less symptomatic and more difficult to detect in the early stages. The cells of adenocarcinomas may secrete mucin. Small cell or "oat cell" carcinomas are a rapidly growing type of lung cancer often located near a major bronchus in the central part of the lung. They tend to be invasive and metastasize early in their development. Large cell carcinomas are usually found on the periphery and consist of undifferentiated large cells that have a rapid growth rate and metastasize early. An aggressive and deadly cancer called mesothelioma has recently received increased attention from the media and legal firms. Although it is not yet clear what genetic mutations cause mesothelioma, asbestos exposure has been implicated as a possible environmental cause, which has led to numerous law suits being filed on behalf of people who worked with asbestos but were never warned of the potential dangers. Pleural mesothelioma most often affects the pleura surrounding the lungs. Unless diagnosed in the early stages this cancer is usually fatal. Early treatments are the same as for those of any cancer. The first change in the lungs is usually metaplasia, a change in the epithelial tissue, associated with smoking or chronic irritation, which is reversible if the irritation ceases. The loss of normal protective, ciliated, pseudostratified epithelium leaves the lung tissue morevulnerable to irritants and inflammation from smoking. Various chemicals in cigarette smoke are carcinogenic and act as initiators and promoters. Dysplasia or carcinoma in situ then develops. These changes are difficult to detect. Lung cancer is staged at the time of diagnosis based on the tumor size-node involvement-metastases (TNM) classification (see Chapter 20). Stage I tumors are localized, whereas stage III lesions are disseminated. Common sites of metastases from the lungs include the brain, bone, and liver Tumors in the lungs have many effects: ~ Obstruction of airflow by tumor growth into a bronchus causes abnormal breath sounds and dyspnea. ~ Inflammation surrounding the tumor stimulates a cough and predisposes to secondary infection. Frequent infections may occur because secretions pool distal to the tumor. ~ Pleural effusion, hemothorax, pneumothorax, or a combination of these is common with tumors located on the lung periphery owing to inflammation or erosion of the pleural membrane. ~ Paraneoplastic syndrome may accompany bronchogenic carcinoma when the tumor cell secretes hormones or hormone-like substances such as antidiuretic hormone (ADH) or adrenocorticotropic hormone (ACTH). The endocrine effects may complicate both diagnosis and treatment. This syndrome may include neuromuscular disturbances or hematologic disorders such as disseminated intravascular coagulation (DIC) (see Chapter 10). ~ Tumors in the lungs also cause the usual systemic effects of cancer. The incidence of lung cancer continues to rise and is now very high in women as well as men. Cigarette smoking is the major factor in its development. "Second-hand smoke" in the environment has been implicated in a significant number of cases. The risk of developing cancer is higher in persons who begin smoking early, persist for many years, and are considered heavy smokers (ie, they smoke more than a pack per day). Not all smokers develop lung cancer, and therefore there is probably a genetic factor involved that also influences the cellular changes (see Chapter 20). Tumors may develop in persons with chronic obstructive pulmonary disease (COPD), also associated with smoking Occupational or industrial exposure to carcinogens such as silica, vinyl chloride, or asbestos is the other major cause of lung cancer, and the risk is greatly increased if a second factor such as cigarette smoking is also present in an occupationally exposed individual. In addition to the direct carcinogenic effect, any irritant such as smoke leads to chronic inflammation and frequent infections in the respiratory tract, which in turn cause cellular changes. For example, in the mucosa, cigarette smoking causes a change from ciliated columnar epithelium to squamous cell epithelium. The alterations in the respiratory mucosa as it changes through metaplasia to dysplasia demonstrate the cell mutations caused by carcinogens and could perhaps lead to earlier diagnosis. EPIDEMOLOGY: The lungs are common sites of both primary and secondary lung cancer. Benign lung tumors are rare. Lung cancer ranks as the third most common cancer in the United States. The incidence has declined slightly, but the mortality rate remains high. Estimates for 2017 indicate 222,500 individuals will be diagnosed in the United States with lung cancer and more than 155,870 patients with lung cancer in the United States will die. Incidence and mortality rates are similar in Canada. Black men are more likely to develop lung cancer than white men. Both black and white women still have a lower rate of developing lung cancer, but the gap is definitely closing. Despite the serious prognosis of lung cancer, some patients with early stages of cancers are cured (American Cancer Society). Secondary metastatic cancer develops frequently in the lungs because the venous return and lymphatics bring tumor cells from many distant sites in the body to the heart and then into the pulmonary circulation. The hospitable environment within the small blood vessels in the lungs provides a lodging point for tumor cells

Describe 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 tumor 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

Describe the pathophysiology of endometrial carcinomaCervical

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 hypertension

Pathophysiology of breast cancer

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

Know the major cellular components of a hematocrit

Cells (formed elements) 45% Leukocytes Erythrocytes Thrombocytes Granulocytes Agranulocytes Neutrophils Eosinophils Basophils Lymphocytes Monocytes Plasma 55% Proteins Fluid/chemical components Water Other Albumin Globulins Fibrinogen Other The hematocrit shows the percentage of blood volume composed of RBCs and indicates fluid and cell content. A low RBC count may be an indicator of anemia. Hemoglobin is measured, and the amount of hemoglobin per cell is shown by the mean cellular hemoglobin (MCH). as well as an increased hematocrit (the percentage of red blood cells in a volume of blood) due to hemoconcentration Hematocrit refers to the proportion of cells (essentially the erythrocytes) in blood and indicates the viscosity of the blood. Males have a higher hematocrit, average 42% to 52%, than females, 37% to 48%. An elevated hematocrit could indicate dehydration (loss of fluid) or excess red blood cells. A low hematocrit might result from blood loss or anemia The hematocrit shows the percentage of blood volume composed of RBCs and indicates fluid and cell content. A low RBC count may be an indicator of anemia. Hemoglobin is measured, and the amount of hemoglobin per cell is shown by the mean cellular hemoglobin (MCH). Hematocrit (HCT) indicates the percentage of erythrocytes in a specific volume of blood. The number of white blood cells (WBCs) is not significant in measuring the cell volume. Hematocrit can indicate fluid imbalance or anemia percentage of erythrocytes in a blood sample.

Discuss the pathophysiology of polycystic kidney disease (PKD)

Chronic renal failure is the gradual irreversible destruction of the kidneys over a long period. It may result from chronic kidney disease, such as bilateral pyelonephritis or congenital polycystic kidney disease, or from systemic disorders, such as hypertension or diabetes. As mentioned, long-term exposure to nephrotoxins is a cause. The gradual loss of nephrons is asymptomatic until it is well advanced because the kidneys normally have considerable reserve function. Once advanced, the progress of chronic renal failure may be slowed but cannot be stopped because the scar tissue and loss of functional organization tend to cause further degenerative changes. Chronic renal failure has several stages (Fig. 18.17), progressing from decreased renal reserve, to insufficiency, to end-stage renal failure or uremia. In the early stages of decreased reserve (around 60% of nephrons lost) there is a decrease in GFR, serum creatinine levels that are consistently higher than average but within normal rang serum urea levels that are normal, and no apparent clinical signs. The remaining nephrons appear to adapt, increasing their capacity for filtration. The second stage (around 75% of nephrons lost), or that of renal insufficiency, is indicated by a change in blood chemistry and manifestations. At this point, GFR is decreased to approximately 20% of normal and there is significant retention of nitrogen wastes (urea and creatinine) in the blood. Tubule function is decreased, resulting in failure to concentrate the urine and control the secretion and exchange of acids and electrolytes. Osmotic diuresis occurs as the remaining functional nephrons filter an increased solute load. This stage is marked by excretion of large volumes of dilute urine (low fixed specific gravity). Erythropoiesis is decreased, and the patient's blood pressure is elevated. The cardiovascular system must compensate for these effects (see Chapter 12). Uremia, or end-stage renal failure (more than 90% of nephrons lost), occurs when GFR is negligible. Fluid, electrolytes, and wastes are retained in the body, and all body systems are affected. In this stage, marked oliguria or anuria develops. Regular dialysis or a kidney transplant is required to maintain the patient's life. A comparison of acute and chronic renal failure may be found Polycystic (polly-SIS-tick) kidney disease (PKD) is a genetic disease. This means that it is caused by a problem with your genes. PKD causes cysts to grow inside the kidneys. These cysts make the kidneys much larger than they should be and damage the tissue that the kidneys are made of. PKD causes chronic kidney disease (CKD) , which can lead to kidney failure, or end-stage renal disease (ESRD). PKD causes about 2 percent (2 out of every 100) of the cases of kidney failure in the United States each year.

Discuss the development of chronic renal failure—signs and symptoms

Chronic renal failure is the gradual irreversible destruction of the kidneys over a long period. It may result from chronic kidney disease, such as bilateral pyelonephritis or congenital polycystic kidney disease, or from systemic disorders, such as hypertension or diabetes. As mentioned, long-term exposure to nephrotoxins is a cause. The gradual loss of nephrons is asymptomatic until it is well advanced because the kidneys normally have considerable reserve function. Once advanced, the progress of chronic renal failure may be slowed but cannot be stopped because the scar tissue and loss of functional organization tend to cause further degenerative changes. Chronic renal failure has several stages (Fig. 18.17), progressing from decreased renal reserve, to insufficiency, to end-stage renal failure or uremia. In the early stages of decreased reserve (around 60% of nephrons lost) there is a decrease in GFR, serum creatinine levels that are consistently higher than average but within normal range serum urea levels that are normal, and no apparent clinical signs. The remaining nephrons appear to adapt, increasing their capacity for filtration The second stage (around 75% of nephrons lost), or that of renal insufficiency, is indicated by a change in blood chemistry and manifestations. At this point, GFR is decreased to approximately 20% of normal and there is significant retention of nitrogen wastes (urea and creatinine) in the blood. Tubule function is decreased, resulting in failure to concentrate the urine and control the secretion and exchange of acids and electrolytes. Osmotic diuresis occurs as the remaining functional nephrons filter an increased solute load. This stage is marked by excretion of large volumes of dilute urine (low fixed specific gravity). Erythropoiesis is decreased, and the patient's blood pressure is elevated. The cardiovascular system must compensate for these effects Uremia, or end-stage renal failure (more than 90% of nephrons lost), occurs when GFR is negligible. Fluid, electrolytes, and wastes are retained in the body, and all body systems are affected. In this stage, marked oliguria or anuria develops. Regular dialysis or a kidney transplant is required to maintain the patient's life. A comparison of acute and chronic renal failure may be found in The early signs of chronic renal failure include: ~ Increased urinary output (polyuria), manifested as frequency and nocturia ~ General signs such as anorexia, nausea, anemia, fatigue, unintended weight loss, and exercise intolerance ~ Bone marrow depression and impaired cell function caused by increased wastes and altered blood chemistry ~ High blood pressure As the kidneys fail completely (end-stage failure), uremic signs appear: ~ Oliguria ~ Dry, pruritic, and hyperpigmented skin, easy bruising ~ Peripheral neuropathy—abnormal sensations in the lower limbs ~ Impotence and decreased libido in men, menstrual irregularities in women ~ Encephalopathy (lethargy, memory lapses, seizures, tremors) ~ Congestive heart failure, arrhythmias ~ Failure of the kidney to activate vitamin D for calcium absorption and metabolism, combined with urinary retention of phosphate ion, leading to hypocalcemia and hyperphosphatemia with osteodystrophy (a defect in bone development related to calcium and phosphate metabolism; see Fig. 18.18), osteoporosis, and tetany (see Chapter 9) ~ Possibly uremic frost on the skin and a urine-like breath odor in the terminal stage or if infection is present Systemic infections such as pneumonia (common) due to poor tissue resistance related to anemia, fluid retention, and low protein levels

Pathophysiology (including signs and symptoms) of liver failure/cirrhosis

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

Discuss the etiology of colon 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.

Define inflammatory bowel disease (ulcerative colitis and Crohn's 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

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.

Differentiation between IDDM (Type I or juvenile diabetes) and NIDDM (Type II or adult-onset diabetes)

Diabetes Mellitus -- typical diabetes -- something wrong w the insulin (not enough insulin or body cannot produce it) When insulin gets in blood, signal that cell should take in glucose Helps cells absorb things Disorder involving insulin's control of glucose metabolism May be caused by... An absolute insulin deficiency -- not making insulin in the pancreas Not enough insulin produced in beta cells A relative insulin deficit -- tissues have become insensitive to insulin Lack of sensitivity in tissues to insulin Two types of DM: Type I (juvenile) -- more severe Insulin-dependent diabetes mellitus (IDDM) Also known as juvenile diabetes Involves a genetic factor and results from the autoimmune destruction of beta cells Absolute insulin insufficiency Can show up any time in life Treated with insulin replacement Type II Non insulin-dependent diabetes mellitus (NIDDM) Relative insufficiency -- pancreas not making much insulin Also known as mature-onset diabetes More common type Relative insulin insufficiency Increasing prevalence (9% of population) and higher in African Americans, Hispanic Americans, and Native Americans. Associated with obesity Treated by diet and exercise, oral hypoglycemic agents (keep glucose levels down), sometimes insulin Effects of Diabetes Lower blood pH (due to excessive ketones) Ketoacidosis -- semi acute Atherosclerosis Vascular issues Poor circulation Poor healing/infection Vision problems Altered Metabolism Proteins, lipids, carbohydrates Affects nervous system - bad circulation (prone to getting ulcers, fungal infections, etc, and cataracts) Can cause blindness DM may result in hypoglycemia (insulin shock)-- too much insulin Treat with concentrated carbohydrate if conscious or IV glucose if unconscious DM may result in diabetic ketoacidosis (DKA)-- happens over several days and can happen w type 2 diabetes Too much glucose in blood Lots of glucose in the urine -- means thirsty - becomes dehydrated Treat with insulin, fluids, and IV sodium bicarbonate Why is it important to know whether a diabetic patient is experiencing hypoglycemia or ketoacidosis? Because they have opposite causes. What happens if you treat someone for the wrong cause? That person may die! Diabetes mellitus is caused by a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by the lack of response by cells to insulin (insulin resistance). To simplify the text, insulin deficit is used to cover both decreased secretion of the hormone and insulin resistance Insulin is an anabolic hormone (building up or synthesis of complex substances from simple molecules). Deficient insulin results in abnormal carbohydrate, protein, and fat metabolism because the transport of glucose and amino acids into cells is impaired, as well as the synthesis of protein and glycogen. In turn, these metabolic abnormalities affect lipid metabolism. Many tissues and organs in the body are adversely affected by diabetes Some types of cells are not affected directly by the deficit of insulin. Insulin is not required for the transport of glucose into brain cells. This is fortunate, because neurons require glucose constantly as an energy source. In the digestive tract, insulin is not required for glucose absorption. Exercising skeletal muscle can utilize glucose without proportionate amounts of insulin. This can be significant because excessive exercise can deplete blood glucose and result in hypoglycemia. Conversely, exercise is helpful in controlling blood glucose levels in the presence of an insulin deficit. There are two basic types of diabetes: types 1 and 2 The classification system has been revised to better reflect the pathology. Type 1, formerly insulindependent diabetes mellitus, type I, or juvenile diabetes, is the more severe form. It occurs more frequently in children and adolescents but can develop at any age. Although there is a genetic factor in the development of the disease, the insulin deficit results from destruction of the pancreatic beta cells in an autoimmune reaction, resulting in an absolute deficit of insulin in the body and therefore requiring replacement therapy. The amount of insulin required is equivalent to the metabolic needs of the body based on dietary intake and metabolic activity. Acute complications such as hypoglycemia or ketoacidosis are more likely to occur in this group. About 1 in every 400 to 500 children has type 1 diabetes; type 1 diabetes occurs in approximately 10% of all individuals diagnosed with diabetes. It is a major factor predisposing to strokes (cerebrovascular accident), heart attacks (myocardial infarction), peripheral vascular disease and amputation, kidney failure, and blindness. Type 2 diabetes, formerly referred to as non-insulindependent diabetes mellitus, type II, or mature-onset diabetes, is based on decreased effectiveness of insulin or a relative deficit of insulin. This abnormality may involve decreased pancreatic beta cell production of insulin, increased resistance by body cells to insulin, increased production of glucose by the liver, or a combination of these factors. This form of diabetes may be controlled by adjusting the need for insulin by taking the following steps: ~ Regulating dietary intake ~ Increasing the use of glucose, such as with exercise ~ Reducing insulin resistance ~ Stimulating the beta cells of the pancreas to produce more insulin Type 2 is a milder form of diabetes, often developing gradually in older adults, the majority of whom are overweight. However, there has been an increased incidence in adolescents and younger adults who are identified with metabolic syndrome, a complex of several pathophysiologic conditions marked by obesity, cardiovascular changes, and significant insulin resistance due to increased adipose tissue The prevalence of type 2 diabetes increases with age, with approximately half the cases found in persons older than 55 years of age. There is a higher prevalence among African Americans, Hispanic Americans, and Native Americans Gestational diabetes may develop during pregnancy and disappear after delivery of the child (see Chapter 22). Approximately 5% to 10% of women who have gestational diabetes develop type 2 diabetes some years later. A number of other types of diabetes and glucose intolerance vary in cause and severity. Prediabetes—an early manifestation of type 2 diabetes ~ Latent autoimmune diabetes in adults—a slow-onset type 1 autoimmune diabetes ~ Maturity-onset diabetes of the young—a rare form caused by a mutation in an autosomal dominant gene -Diabetes insipidus—diabetes not related to blood sugar levels, but an insensitivity of the kidneys to ADH TYPE 1: -Children and adults -Acute onset -Autoimmune destruction; family history - Thin body weight - Very low plasma insulin level - Insulin replacement - Occurrence of hypoglycemia or ketoacidosis: frequent TYPE 2: - Older but also younger adults - Insidious onset - Familial, lifestyle, and environmental factors, obesity - Obese - Decreased or normal plasma insulin level - Diet and exercise or oral hypoglycemic agents or insulin replacement - Occurrence of hypoglycemia or ketoacidosis: less common

Describe the development of 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.

. Discuss the pathophysiology of Meniere's syndrome

Disorder of the labyrinth Excess endolymph stretches membranes. Disturbs hair cell function in vestibule and cochlea S/S of an attack: Vertigo, tinnitus, nausea, sweating, nystagmus (eyes are twitching all over the place) Has exacerbations (changes to blood flow) and remissions Repeated occurrences leads to permanent hair cell damage Brought on by changes to blood flow: stress, changes in barometric pressure, others To keep our sensory balance Ménière's syndrome is an inner ear or labyrinth disorder occuring in adults 30 to 50 years of age. It usually affects only one ear. Excessive endolymph develops intermittently, stretching the membranes and interfering with the function of the hair cells in the cochlea and vestibule Rupture of the labyrinth membrane may allow perilymph to mix with endolymph, increasing volume and causing an attack. The increased fluid may also be of vascular origin. Each attack may last minutes or hours and causes the following conditions: Severe vertigo: a sensation of whirling and weakness, is often accompanied by loss of balance and falls ~ Tinnitus (excess noise like a roaring motor or ringing) ~ Unilateral hearing loss ~ Nausea and sweating ~ Inability to focus ~ Nystagmus: an involuntary, rapid movement of the eyeball ~ A feeling of pressure in the ear. Repeated occurrences lead to permanent damage to the hair cells, with permanent loss of hearing and vertigo The acute episodes occur over several months, followed by a brief period of relief, and then the cycle repeats. Stress is a predisposing factor, as are other conditions that affect blood flow. Changes in barometric pressure may precipitate an attack. Improvement occurs with stress reduction; avoidance of smoking, alcohol, and caffeine; observance of a low-sodium diet; and use of a mild diuretic. Treatment of attacks consists of drugs such as dimenhydrinate, diazepam, or antihistamines. Home exercise programs have assisted in reducing the individual's sensitivity to motion. In severe cases surgery may be helpful to provide a shunt, remove excess endolymph, or resect the vestibular nerve.

Discuss the signs and symptoms of pulmonary emboli

Embolus flows in pulmonary circulation Obstructs potential infarction The closer to the beginning, the worse the case DVLT (deep vein leg thrombosis) Start to get infarctions in lung tissue (stopping process) closer you are to the heart, the worse the cases -a blood clot or a mass of other material that obstructs the pulmonary artery or branch of other material that obstructs the pulmonary artery or a branch of it, blocking the flow of blood through the lung tissue -most of them are thrombi or blood clots originating from the deep leg veins -due to deep vein thrombosis (DVT) is a leading cause of deaths -infarcation does not follow obstruction of the pulmonary circulation unlesss the general circulation is compromised or there is prior lung disease --usually invovles a segment of the lung and the pleural membrane in the area -small pulmonary emboli are silent -emboli that block moderate-sized arteries cause respiratory impairments bc fluid and blood fill the alveoli of the involved area -large emboli affects the cardiovascular system, causing right sided CHF and decreased cardiac output -resistance to the output from the right ventricle cuases acute cor pulmonale A pulmonary embolus is a blood clot or a mass of other material that obstructs the pulmonary artery or a branch of it, blocking the flow of blood through the lung tissue. Most pulmonary emboli are thrombi or blood clots originating from the deep leg veins (see Chapter 12). An embolus to the lungs travels from its source through larger and larger veins until it reaches the heart and pulmonary artery. It then lodges as soon as it reaches a smaller artery in the lungs through which it cannot pass. The effects of a pulmonary embolus depend somewhat on the material, but largely on the size and therefore the location of the obstruction in the pulmonary circulation (Fig. 13.23). Because lung tissue is supplied with oxygen and nutrients by the separate bronchial circulation, infarction does not follow obstruction of the pulmonary circulation unless the general circulation is compromised or there is prior lung disease. Infarction usually involves a segment of the lung and the pleural membrane in the area. Small pulmonary emboli are frequently "silent" or asymptomatic. However, multiple small emboli (a "shower") often have an effect equal to that of a larger embolus With small emboli, manifestations may include the following: ~ A transient chest pain ~ Cough ~ Dyspnea (this is often unnoticed but can be significant because it may be a warning of more emboli developing) For larger emboli, manifestations may include the following: ~ Chest pain occurs, which increases with coughing or deep breathing ~ Tachypnea ~ Dyspnea develops suddenly ~ Later, hemoptysis and fever ~ Hypoxia stimulates a sympathetic response, with anxiety and restlessness, pallor, and tachycardia Massive emboli cause the following: ~ Severe crushing chest pain ~ Low blood pressure ~ Rapid weak pulse ~ Loss of consciousness Fat emboli are distinguished by the development of acute respiratory distress, a petechial rash on the trunk, and neurologic signs such as confusion and disorientation.

Describe the pathophysiology of infectious mononucleosis

Epstein-Barr virus (very rare that people don't get this 20's) Transmitted in saliva, airborne droplets, blood Attacks B-lymphocytes (impedes antibody production) -commonly shared by drinks (saliva) -can be transferred by droplets -leukopenia (low WBCs) Signs/symptoms: Sore throat, headache, fever, fatigue, malaise Lymphadenopathy Splenomegaly Increased lymphocytes & monocytes Presence of atypical T-lymphocytes Complications: Ruptured spleen Hepatitis meningitis -acute infection affecting lym caused by epstein-barr virus (which is a herpes virus) -common in young adults -agent is transmitted by direct contact with infected saliva, airborne droplets -invades epithelia cells -incubation period is abt 4-6weeks MANIFESTATIONS: -sore throat, headache, fever, rash on trunk, inc in lymph, -possible complications include hep, ruptured spleen, and meningitis -atypical t lymph Infectious mononucleosis is an acute infection affecting lymphocytes caused by the Epstein-Barr virus (EBV, which is in the herpes group). It is common in adolescents and young adults. The infection is usually mild and self-limiting, but occasionally it is marked by complications. The agent is transmitted by direct contact with infected saliva (hence the term kissing disease), airborne droplets, and blood. Epstein-Barr virus invades epithelial cells in the nasopharynx and oropharynx and penetrates to lymphoid tissue, targeting the B lymphocytes and producing typical antibodies. The incubation period is approximately 4 to 6 weeks approximately 4 to 6 weeks. The manifestations include the following: ~ Sore throat, headache, fever, fatigue, and malaise ~ Enlarged lymph nodes (lymphadenopathy) and spleen (splenomegaly) ~ A rash on the trunk ~ An increase in lymphocytes and monocytes in the blood, and the presence of atypical T lymphocytes (Fig. 23.4) ~ A positive heterophil antibody test (Monospot test) Possible complications include hepatitis, ruptured spleen, and meningitis. Because no effective treatment for viral infections is available, supportive measures, particularly bed rest, are indicated. As with many viral infections, recovery may be prolonged, and fatigue and malaise may be persistent. Fitness students and trainers should be aware of an important safeguard against rupture of the spleen—that is, ensuring that the spleen has returned to normal size before an individual participates in sports or strenuous exercise programs.

Describe Osteoporosis

Extensive loss of bone tissue Related to deficiencies in calcium, vitamin D, estrogen, and lack of exercise Osteoporosis, loss of bone density due to loss of calcium salts, is common in older people, particularly women Osteoporosis is a common metabolic bone disorder characterized by a decrease in bone mass and density, combined with loss of bone matrix and mineralization (see Fig. 24.1). Estimates for prevalence run as high as 10 million in the United States, with many more having low bone mass, and therefore increased risk. Although women have a higher risk of osteoporosis, a significant number of men also have been diagnosed. Osteoporosis is a factor in an estimated 1.5 million fractures annually, of which 300,000 involve the hip. Regular bone mass density tests are recommended for all individuals older than 50 years of age. This procedure requires resting on the scanner table for 10 to 15 minutes and is noninvasive. Osteoporosis occurs in two forms: primary, which includes postmenopausal, senile, or idiopathic osteoporosis, and secondary, which affects men and women and follows a specific primary disorder such as Cushing syndrome During the continuous bone remodeling process, bone resorption exceeds bone formation, leading to thin, fragile bones that are subject to spontaneous fracture, particularly in the vertebrae (see Fig. 24.2). Although bone density and mass are reduced, the remaining bones are normal. Osteoporosis affects the bones consisting of higher proportions of cancellous bone, such as the vertebrae and femoral neck. The early stages of the condition are asymptomatic but can be diagnosed using various bone density scans and x-rays to demonstrate the bone changes. Bone mass normally peaks in young adults, and then gradually declines, depending on genetic factors (such as vitamin D receptors), nutrition, weight-bearing activity, and hormonal levels. It appears that calcium intake in the child and young adult is critical to maintenance of bone mass later in life. A number of factors predispose people to osteoporosis. These include the following: ~ Aging: ~ Osteoporosis is common in older individuals, particularly postmenopausal women with estrogen deficiency (see Chapter 24). ~ Osteoblastic activity is less effective with advancing age. ~ Decreased mobility or a sedentary lifestyle: ~ Mechanical stress on bone by muscle activity is essential for osteoblastic activity. Decreased mobility is a factor with aging, but it can also occur if a patient is on bed rest for a prolonged time with a chronic illness or has limited activity due to rheumatoid arthritis. One limb or area of the body may be affected by osteoporosis when it is immobilized because of conditions such as a fracture (disuse osteoporosis). ~ Hormonal factors such as hyperparathyroidism, Cushing syndrome, or continued intake of catabolic glucocorticoids such as prednisone ~ Deficits of calcium, vitamin D, or protein related to diet or history of deficits in childhood or malabsorption disorders ~ Cigarette smoking ~ Small, light bone structure, as in Asian and Caucasian persons ~ Excessive caffeine intake deficiency in bone matrix Thinning of bone cortex Resorption of calcium, mineral salts Etiology: Aging Sedentary lifestyle/decreased mobility Hormonal factors (menopause) Calcium/Vit D deficiency Small bone structure (Caucasian/Asian) Thyroid issues Shows up w/ a compression fracture -common metabolic bone disorder characterized by a decrease in bone mass and density, combined with a loss of bone matrix and mineralization -bone reabsorption exceeds bone formation, leading to thin, fragile bones that are subject to spontaneous fracture -affects bones consisting of higher proportions of cancellous bone -calcium intake in the child and young adult is critical to maintain bone mass later n life -bone mass peaks in young adults and gradually declines with aging and genetic factors AGING: common in older people with estrogen deficiency and osteoblastic activity is less effective with advancing age DECREASED MOBILITY: mechanical stress on bone by muscle activity is essential for osteoblastic activity -- dec. mobility is a factor with aging and can occur if a pt us on bed rest HORMONAL FACTORS: cushing syndrome DEFICITS of calcium cigarrete smoking small, light bone structure excessive caffeine intake SIGNS -back pain is a sign -abnormal curves of the spine -spontaneous fractures treatment: -bone cannot be restored to normal structures, but it can be helped bt therapy -dietary supplement of calcium

Discuss the pathophysiology of oral cancers (mainly squamous cell carcinoma)

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. 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. 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

Describe the development of narrow angle and wide angle glaucoma

Glaucoma Too much fluid build-up in aqueous humor -- front chamber behind cornea lens Pressure builds up Causes increased intraocular pressure Glaucoma results from increased intraocular pressure caused by an excessive accumulation of aqueous humor. Narrow-angle glaucoma occurs when the angle between the cornea and the iris in the anterior chamber is decreased by factors such as an abnormal anterior insertion of the iris. With aging, the lens enlarges, pushing the iris more forward and to the side Narrow angle (acute) Abnl ant. Insertion of iris Happens when someone is in dark for awhile and pupils dilate and cannot drain aqueous humor Build up of pressure This anatomic position may block the outflow of aqueous humor when the pupil is dilated and the thickened iris fills the narrow angle Pressure inside the eyeball can increase significantly within an hour of pupil dilation, blocking drainage of fluid. This leads to acute glaucoma, in which there is a sudden marked increase in intraocular pressure Chronic glaucoma develops frequently in older individuals, usually beginning after age 50. Narrow-angle glaucoma may be caused by a developmental abnormality, aging, or scar tissue in the eye from trauma or infection. Congenital glaucoma occurs as an inherited disorder of several types, both recessive and dominant. wide angle (chronic) Obstruction of trabecular network and canal of Schlemm Chronic and insidious Degeneration Chronic glaucoma, sometimes referred to as wide-angle or open-angle glaucoma, is a common degenerative disorder in older persons, affecting 1% to 2% of the population in the United States. The trabecular network and canal of Schlemm become obstructed, and the outflow of aqueous humor gradually diminishes. Intraocular pressure increases slowly and usually asymptomatically. The increased pressure compresses the blood flow to the retinal cells, causing ischemia and damage to the retinal cells. The anterior portion of the retina is affected first, including the receptor cells for peripheral vision. If pressure inside the eyeball continues to increase, more of the retina and the optic nerve will be damaged. When observed through the pupil, the optic disc appears eroded or "cupped" as the optic nerve fibers are compressed Damage to the retina and optic nerve is irreversible, and eventually blindness results.

Discuss the pathophysiology of Graves' disease

Hyperthyroidism (Graves' disease) Bulgy eyes (enlargement of muscles-- can get optic nerve damage) Can get heart failure More common in women > age 30 years Involves an autoimmune factor S/S: Hypermetabolism Exophthalmos Thyroid storm Dangerous Results in hyperthermia, tachycardia, heart failure, delirium There are various forms of hyperthyroidism, with increased T3 and T4 secretion. Graves disease provides an example Graves disease occurs more frequently in women older than 30 years of age and is related to an autoimmune factor. It is manifested by the signs of hypermetabolism, toxic goiter, and exophthalmos (Table 16.5). Increased stimulation of the sympathetic nervous system magnifies the metabolic effects. Exophthalmos is evident by the presence of protruding, staring eyes and decreased blink and eye movements (Fig. 16.15). It results from increased tissue mass in the orbit pushing the eyeball forward and from increased sympathetic stimulation affecting the eyelids. If untreated, visual impairment may result from optic nerve damage or corneal ulceration. Graves disease is treated by a course of radioactive iodine, surgical removal of the thyroid gland,

Differentiate between hepatitis A & B

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.

Differentiate between hepatitis C, D, and E

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. 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 infectio

Describe the development of hiatal hernias

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; hiatal hernia-- stomach that is herniated 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.

Describe the signs and symptoms of Hodgkin's disease and non-Hodgkin's lymphoma

Hodgkin's Disease—staging (Ann Arbor staging system) Hodgkin's Disease Presence of Reed-Sternberg cell On the decline Est. 2017 cases 8260 Two ages of occurrence: Age 20-40 (Men = Women) Age 50+ (mostly men) Signs & Symptoms: Lymphadenopathy, with later splenomegaly Malaise, loss of appetite, weight loss, fever, anemia Recurrent infections overall 5-year survival rates in the US from 2004-2010 were 85.3%.* -type of lymphoma starting in lymphocytes -originates in lymph nodes in the upper part of the body -onset of the disease occurs primarily in adults from 20-40 -malignancy involves a single lymph node in the neck area -atypical cell used as a marker for diagnosis is REED STERNBERY CELL (a giant cell present in the lymph node) -this charac. this type of lymphoma -ann arbor staging system defines a stage 1 cancer as affecting a single lymph node and etc -stage 2multple regions on same side -stage 3 (regions on both sides of diaphragm) -stage 4 widespread liver, spleen -first indicator is enlarged lymph nodesa and is mainless Non-Hodgkin's Lymphoma Absence of Reed-Sternberg cell Many different types Unlike Hodgkin's—on the increase! 80% involve B-Lymphocytes Increased incidence associated w/HIV infection Increased incidence & mortality w. age Intestinal nodes & organs involved early-on Spread beyond nodes is common -increasing in incidence partly due to the numbers associated with HIV infection -about 80% of cases involve B lymph -initial manifestation is an enlarged painless lymph nodes -distinguished by multiple node involvement scattered throughout the body and a nonorganized pattern of widespread metastates, often present after diagnosis The primary difference between these two categories of lymphatic cancer is the type of lymphocyte that is affected. Hodgkin lymphoma is marked by the presence of Reed-Sternberg cells, which a physician can identify using a microscope. In non-Hodgkin lymphoma, these cells are not present. Hodgkin lymphomas are more likely to arise in the upper portion of the body (the neck, underarms, or chest). Non-Hodgkin lymphoma can arise in lymph nodes throughout the body, but can also arise in normal organs. Patients with either type can have symptoms such as weight loss, fevers, and night sweats. The first indicator is usually an enlarged lymph node, often cervical, that is painless, and nontender. ~ Later splenomegaly and enlarged lymph nodes at other locations may cause pressure effects; for example, enlarged mediastinal nodes may compress the esophagus. ~ General signs of cancer, such as weight loss, anemia, low-grade fever and night sweats, and fatigue, may develop Generalized pruritus is common. ~ Recurrent infection is common because the abnormal lymphocytes interfere with the immune response. The onset is usually insidious and the malignancy well advanced before diagnosis. Frequent infections may be the initial sign related to impaired production of antibodies. ~ Pain, related to bone involvement, is common and is present at rest. ~ Pathologic fractures may occur as bone is weakened. ~ Anemia and bleeding tendencies are common because blood cell production is affected. ~ Kidney function, particularly the tubules, is affected, leading to proteinuria and kidney failure.

Discuss the pathophysiology of hyperparathyroidism

Hyperparathyroidism (have an extra tumor/growth) Often caused by parathyroid adenomas or hyperplasia Results in hypercalcemia Calcium leaves bone tissue leading to osteoporosis Increase likelihood of developing kidney stones Hyperparathyroidism may be caused by an adenoma, hyperplasia, or secondary to renal failure. It causes hypercalcemia, or high serum calcium levels. Hypercalcemia leads to forceful cardiac contractions (see Table 2.7 for signs of calcium imbalance). The most serious effects of hyperparathyroidism occur in the bone tissue. Increased parathyroid hormone (PTH) causes calcium to leave the bone, leading to osteoporosis, weakening the bone so that it fractures easily (see Chapter 9). Hypercalcemia also increases one's predisposition to kidney stones Decreased neuroexcitability Apathy, fatigue Personality change Muscle weakness Decreased tone Forceful cardiac contraction Arrhythmias, bradycardia Hypertension Kidneys Polyuria, thirst Renal insufficiency Renal calculi Decreased peristalsis Constipation, nausea Bone Osteoporosis, fractures Hyperparathyroidism may be caused by an adenoma, hyperplasia, or secondary to renal failure. It causes hypercalcemia, or high serum calcium levels. Hypercalcemia leads to forceful cardiac contractions (see Table 2.7 for signs of calcium imbalance). The most serious effects of hyperparathyroidism occur in the bone tissue. Increased parathyroid hormone (PTH) causes calcium to leave the bone, leading to osteoporosis, weakening the bone so that it fractures easily (see Chapter 9). Hypercalcemia also increases one's predisposition to kidney stones Hyperparathyroidism is a cause of osteoporosis and renal calculi. Often due to an adenoma, it causes hypercalcemia and osteoporosis

Discuss the pathophysiology of Hashimoto's thyroiditis

Hypothyroidism Hashimoto's thyroiditis Autoimmune destruction of thyroid Onset is a storm Inflammatory response Destroys thyroid after Mild hypothyroidism is common and is easily treated by replacement doses of thyroid hormone. Severe hypothyroidism occurs in several forms: ~ Hashimoto thyroiditis is a destructive autoimmune disorder Severe hypothyroidism is present in Hashimoto thyroiditis, an inflammatory autoimmune disorder Hashimoto thyroiditis is a destructive autoimmune disorder Severe hypothyroidism is present in Hashimoto thyroiditis, an inflammatory autoimmune disorder, and cretinism, an untreated congenital condition impairing mental and physical development, or in myxedema with hypometabolism in adults.

Describe the pathophysiology of congenital hydrocephalus

Hydrocephalus is a condition in which excess cerebrospinal fluid (CSF) accumulates within the skull, compressing the brain tissue and blood vessels. The condition is sometimes called "water on the brain." Because the cranial sutures have not yet closed, the infant's head enlarges beyond the normal size as the amount of fluid increases. Excess CSF accumulates because more is produced than is absorbed, often because of obstruction to the flow at some point. In the majority of cases, production of CSF is normal, but there is a reduction in the amount reabsorbed. Most cases are apparent shortly after birth, but some may not be diagnosed until later in childhood There are two types of hydrocephalus. Noncommunicating or obstructive hydrocephalus occurs in babies when the flow of CSF through the ventricular system is blocked, usually at the aqueduct of Sylvius or the foramen magnum (Fig. 14.25). This condition usually results from a fetal developmental abnormality, such as stenosis or a neural tube defect. In many neonates, an associated myelomeningocele or Arnold-Chiari malformation is present. The obstruction leads to increased back pressure of fluid in the ventricles of the brain, which gradually dilates or enlarges the ventricles and compresses the blood vessels and brain tissue In the second type, communicating hydrocephalus, the absorption of CSF through the subarachnoid villi is impaired, resulting in increased pressure of CSF in the system. In neonates, the skull can expand to some degree in the early stages of hydrocephalus to relieve the pressure, but if the condition is not treated quickly, the brain tissue is permanently damaged. In older children and adults, intracranial pressure (ICP) increases more rapidly than in neonates, because the fused sutures of the skull prevent expansion to accommodate the increased volume of CSF. The amount of fontanelles bulge in the early stages of hydrocephalus. Recording head size is a standard procedure after birth and often is done during routine examinations. With the currently brief periods of hospitalization after childbirth, this measurement may not be taken, but it can provide a basic reference point if a problem is suspected. In the patient with hydrocephalus, scalp veins appear dilated and the eyes show the "sunset sign," in which the white sclera is visible above the colored pupil. Pupil response to light is sluggish. The infant is lethargic but irritable and difficult to feed. A high-pitched or shrill cry often occurs when the infant is moved or picked up. The condition must be diagnosed and treated as soon as possible to minimize brain damage. In older children and adults, the head cannot enlarge and the classical signs of increased ICP develop as the volume of CSF expands. These may include decreased memory, difficulty in coordination, and impaired balance. Often urinary incontinence is present. Depending on the underlying cause, other manifestations may be present. Excess CSF Two types Noncommunicating CSF is blocked (usually aqueduct of Sylvius or foramen magnum) Caused by CSF canal atresia or stenosis, or neural tube defect Communicating Impaired absorption of CSF via arachnoid villi Impacts ventricles & brain tissue Babies -head enlargement Older children & Adults -ICP Ventricles become overfilled with CSF Enlarged head, dilated ventricles Compression of brain

Differentiate between interstitial and broncho- pneumonia

Interstitial pneumonia → edema in your tissues and does not get in alveoli Primary atypical pneumonia (PAP) differs in both the causative organisms, often viral or mycoplasmal, and the pathophysiology, which involves interstitial inflammation. Mycoplasma pneumoniae is a small bacterium that lacks a cell wall and can appear in varying shapes. It is found normally in the upper respiratory tract. Mycoplasmal pneumonia is common in older children and young adults. It is transmitted by aerosol but is not considered highly contagious. Frequent cough is a prominent sign. Mycoplasma responds to erythromycin or tetracycline therapy Interstitial inflammation around alveoli Necrosis of bronchial epithelium -scattered small patches -influenza virus -mycoplasma -interstitial inflammation around alveoli -necrosis of bronchial epithelium -variable onset -variable fever, headache -aching muscles -nonproductive hacking cough primary atypical pneumonia -differes in both causative organisms, often viral or mycoplasmal and pathophysiology which involves interstitial inflammation -mycoplasma pneumoniae is a small bacterium that lacks a cell wall and can appear in varying shapes -common in older kids and young adutls -transmitted by aerosol but it is not considered highly contagious -viral pneumonia is often caused by flu a or b and rsv -chalmydia pneumonia is caused by the organism chlamydia pneumoniae -- caused by a PAP and pharyngititis Interstitial pneumonia → edema in your tissues and does not get in alveoli Interstitial pneumonia—usually of viral or mycoplasmic (see the infection chapter) origin, affects those interstitial cells that comprise the alveoli. The exudate usually causes swelling in the cells themselves. Some cases of this are termed walking pneumonia. At higher magnification, the pattern of patchy distribution of bronchopneumonia is seen. Bronchopneumonia is classically a "hospital acquired" pneumonia seen in persons already ill from another disease process. Most common type Staphylococcus aureus, Streptococcus pneumoniae, and pneumococcus. patchy infiltrates consistent with bronchopneumonia from a bacterial infection. Lung Abscess two lung abscesses, one in the upper lobe and one in the lower lobe of this left lung. An abscess can be a complication of severe pneumonia, most typically from virulent organisms such as S. aureus. Abscesses also are complications of aspiration, where they appear more frequently in the right posterior lung. --Lung abscesses often are result of bacterial pneumonia and can also result from aspiration of food or stomach contents. Notice for bronchopneumonia the consolidation (light spots) is more spread out throughout the lung. See the light patches in what is suppose to be a dark lung field. That is consolidation blocking (attenuating) the X-rays. -scattered small patches -multiple bacteria -inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritations -insidious onset -muld fever -productive cough w yellow-green sputum and dyspnea -occurs as a diffuse pattern of infection in both lungs, more often in the lower lobes -begins at the bronchial mucuousa and soreads into the local alveoli -exudate interferes with o2 diffusion -recovery usually occurs without residual lung damage Broncho pneumonia features consolidation in clumps of alveoli at the ends of bronchioles. It generally is more diffuse throughout the lungs. Interstitial pneumonia—usually of viral or mycoplasmic (see the infection chapter) origin, affects those interstitial cells that comprise the alveoli. The exudate usually causes swelling in the cells themselves. Some cases of this are termed walking pneumonia. Notice for bronchopneumonia the consolidation (light spots) is more spread out throughout the lung. Inflammation and purulent exudate in alveoli often arising from prior pooled secretions or irritation Productive cough with yellow-green sputum Dyspnea

myocardial infarct (MI)

MI: Coronary artery occluded -Results in anoxia to tissues Affects Myocardium -Muscle necrosis (coagulation necrosis) -Inflammation/Granulation tissue -Fibrosis (myocardium doesn't regenerate) -Loss of muscle function Affects conduction tissues -Affected tissue loses conductivity -Arrhythmias develop Can result in heart failure and death MI can cause Ventricular Fibrillation which results in no cardiac output or even asystole (no rhythm). Both situations often lead to death. Collateral circulation may reduce damage. -Has neutrophils because of inflammation going on -Disrupts rhythm MI Consequences Eventual heart failure Brain damage if cardiac arrest occurred Infarct gets bigger if heart not rested Hypertrophy to make up for lost tissue Other problems: -Rupture of infarcted area -Ventricular aneurysm -Embolism with stroke MI Warning Signs Feeling of chest pressure, heaviness, or a burning sensation (particularly with increased exertion) SOB, perspiration, weakness, fatigue Nausea or feeling of indigestion Onset of anxiety or feeling of impending doom Manifestations of Progressing MI Pain -Unrelieved by ntg -Men—severe. Women—often milder Pallor, diaphoresis, nausea, dizziness , weakness, and dyspnea Marked anxiety or fear Hypotension (common) -CO decreases—rapid & weak pulse -Development of shock Low-grade fever -MI is also known as a heart attack, involves the death of the myocardial tissue due to ischemia (def of blood) -most common cause is atherosclerosis, usually with thrombus attached 1. thrombus may build up to obstruct the atery 2. vasospasm may occur 3. part of the thrombus may break away, forming an emboli -at point of obstruction, heart tissue becomes necrotic and the area of injury is inflammed -presence of collateral circulation may reduce the size of the infarct -signs: dizziness, pallor, nausea, dyspnea, low grade fever, weakness MI Consequences Eventual heart failure Brain damage if cardiac arrest occurred Infarct gets bigger if heart not rested Hypertrophy to make up for lost tissue Other problems: Rupture of infarcted area Ventricular aneurysm Embolism with stroke -sudden death shortly after MI occurs (ventricular arr. and fibrillation -area of necrosis and inflammation outside the conduction pathway may stimulate additional spontaneous impulses at an ectopic site, causing premature ventricular contrations that lead to tachy. -cocaine users may suffer fatal heart attacks -cardiogenic shock -CHF -rupture of necrotic heart tissue -thromboembolism A myocardial infarction (MI), also known as a heart attack, involves the death of myocardial tissue due to ischemia (deficiency of blood). For those who survive a myocardial infarction, there is notably greater risk of a second MI, congestive heart failure, or stroke occurring within a short time An MI, or heart attack, occurs when a coronary artery is totally obstructed, leading to prolonged ischemia and cell death, or infarction, of the heart wall (Fig. 12.15). The most common cause is atherosclerosis, usually with thrombus attached (see previous discussion under Coronary Artery Disease). Infarction may develop in three ways: 1. The thrombus may build up to obstruct the artery. 2. Vasospasm may occur in the presence of a partial occlusion by an atheroma leading to total obstruction. 3. Part of the thrombus may break away, forming an embolus or emboli that flows through the coronary artery until lodging in a smaller branch, blocking that vessel (see Fig. 12.11). Most infarctions are transmural— that is, all three layers of the heart are involved. A majority involve the critical left ventricle. The size and location of the infarct determine the severity of the damage.

Describe the pathophysiology of meningitis

Meningitis Inflammation of meningeal layers Pia mater arachnoid Original dz or secondary effect Bacterial, viral causes, and even fungal (AIDS) Fever, neck pain, neck muscles rigid, coma (worse-case) Meningitis is an infection, usually of bacterial origin, in the meninges of the CNS. Many microbes can infect the CNS, and all age groups are susceptible. Early diagnosis and treatment is essential to prevent deficits or death. Microorganisms reach the brain via the blood, by extension from nearby tissue, or by direct access through wounds. Microbes such as meningococcus can bind to nasopharyngeal cells in an individual, cross the mucosal barrier, attach to the choroid plexus, and enter CSF. Because the membranes are continuous around the CNS and CSF flows in the subarachnoid space, infection spreads rapidly through the coverings of the brain. Focal signs are absent because there is no localized mass of infection. The inflammatory response to the infection leads to increased ICP, and the pia and arachnoid layers become edematous. The common bacterial infections lead to a purulent exudate that covers the surface of the brain and fills the sulci, causing the surface to appear flat. The exudate is present in the CSF, and the blood vessels on the surface of the brain appear dilated Meningitis is an infection, usually of bacterial origin, in the meninges of the CNS. Many microbes can infect the CNS, and all age groups are susceptible. Early diagnosis and treatment is essential to prevent deficits or death. Microorganisms reach the brain via the blood, by extension from nearby tissue, or by direct access through wounds. Microbes such as meningococcus can bind to nasopharyngeal cells in an individual, cross the mucosal barrier, attach to the choroid plexus, and enter CSF. Because the membranes are continuous around the CNS and CSF flows in the subarachnoid space, infection spreads rapidly through the coverings of the brain. Focal signs are absent because there is no localized mass of infection. The inflammatory response to the infection leads to increased ICP, and the pia and arachnoid layers become edematous. The common bacterial infections lead to a purulent exudate that covers the surface of the brain and fills the sulci, causing the surface to appear flat. The exudate is present in the CSF, and the blood vessels on the surface of the brain appear dilated

Discuss the pathophysiology of muscular dystrophy

Muscular Dystrophy Duchenne's (or pseudohypertrophic) is most common X-linked recessive disorder (but not always) Deficit of dystrophin (muscle cell membrane protein) Muscle function is gradually lost Affects all muscles Muscular Dystrophy Signs/symptoms May first appear as elevated serum creatine kinase About 3 years of age—early signs Weakness in pelvic girdle Waddling gait Difficulty climbing stairs or gaining upright positioning Gower's maneuver → pelvic muscles are too weak to raise themselves (show up in the way they walk) Usually affects males -group of inherited disorders charac. by degeneration of skeletal muscle. they differ in type of inheritence, area affected, age at onset, and rate of progression **duchenne is the most common type PATHOPHYSIOLOGY: -metabolic defect, a deficit of dystrophin (muscle cell membrane protein),leads to degeneration and necrosis of the cell -skeletal muscle fibers are replaced by fat and fibrous connective tissue -muscle function is gradually lost (cardiomyopathy is common) SIGNS/SYMPTOMS: -appear at around 3 years old -when motor weaknesses and regression become apparent in the child -initial weakness in the pelvic girdle causes a waddling gait and difficulty with climbing stairs -weakness spreads to other muslce groups and eventually to the shoulder girlde -tendon reflexes are reduced -respiratory insuff. and infections are common -develop cardiac abnormalities Outcome Vertebral deformities, contractures Respiratory insufficiency with infections Eventually causes cardiac and respiratory failure Muscular dystrophy (MD) is a group of inherited disorders characterized by degeneration of skeletal muscle. The disorders differ in type of inheritance, area affected, age at onset, and rate of progression. Common types are summarized in Table 9.1. Duchenne or pseudohypertrophic muscular dystrophy is the most common type, affecting young boys, with a prevalence of about 3/100,000 males. X-linked inheritance has been demonstrated in most cases of Duchenne muscular dystrophy. Some cases appear to be spontaneous gene mutations. Serum CK is elevated in many but not all carriers of the abnormal gene and appears before the first signs. The basic pathophysiology is the same in all types of muscular dystrophy. A metabolic defect, a deficit of dystrophin (a muscle cell membrane protein), leads to degeneration and necrosis of the cell. Skeletal muscle fibers are replaced by fat and fibrous connective tissue (leading to the hypertrophic appearance of the muscle; Fig. 9.9). Muscle function is gradually lost. Cardiomyopathy is common. With the Duchenne type of muscular dystrophy, early signs appear at around 3 years of age, when motor weakness and regression become apparent in the child. Initial weakness in the pelvic girdle causes a waddling gait and difficulty with climbing stairs or attaining an upright position. The "Gower maneuver," in which the child pushes to an erect position by using the hands to climb up the legs, is a typical manifestation (see Fig. 9.9). The weakness spreads to other muscle groups and eventually to the shoulder girdle. Tendon reflexes are reduced. Vertebral deformities such as kyphoscoliosis and various contractures develop. Respiratory insufficiency and infections are common. The majority of patients with muscular dystrophy develop cardiac abnormalities and mental retardation.

Discuss the pathophysiology of pancreatic adenocarcinoma

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. 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 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. 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.

Understand the stages of fetal development and the basic effects on the mother

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

Definition of coronary artery disease (CAD)

Plaques build up on inside of coronary arteries → opening of arteries get more narrow Artery loses flexibility Decreases the lumen of the arteries Results in ischemia of myocardium Eventually proceeds to heart failure Symptoms/signs: -Pain from oxygen deprived myocardium -Electrical conduction problems due to ischemic tissues -includes angina pectoris or temporary cardiac ischemia and MI (or heart attack) -MI results in damage to part of the heart muscle bc of the obstruction in a coronary artery -Insuff. o2 for the needs of the heart muscle -CAD may lead to heart failure, serious dysrhythmias, or sudden death Sometimes called coronary heart disease, coronary artery disease includes angina pectoris or temporary cardiac ischemia and myocardial infarction or heart attack. Myocardial infarction results in damage to part of the heart muscle because of obstruction in a coronary artery. The basic problem is insufficient oxygen for the needs of the heart muscle A common cause of disability and death, coronary artery disease may ultimately lead to heart failure, serious dysrhythmias, or sudden death. It is the leading cause of death in men and women in the United States, causing approximately 365,000 deaths each year. Statistics for 2015 reveal that one in four deaths are the result of some form of heart disease, and the incidence for new or repeated heart attacks is 735,000 Americans. It is estimated that 27.6 million live with coronary artery disease in the United States. An additional 6 million are currently diagnosed with congestive heart failure (there is some overlap within these figures). The Centers for Disease Control and Prevention (CDC) reported that in 2013, high blood pressure was listed as a factor in 360,000 deaths and affects 68 million Americans. Males tend to develop heart disease at an earlier age than women, but women tend to have more complications, likely due to later diagnosis. The current statistics show a decrease in numbers of individuals being diagnosed with heart disease, which many attribute to prevention awareness programs

Discuss the pathophysiology of prostate cancer

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)

Describe the pathophysiology of Castleman's disease

Rare illness -lymphoid tissues Involves overgrowth of lymphoid tissue Two types Unicentric form Affects a single lymph node Multi centric form Affects multiple lymph nodes and tissue—may have severe effects on the immune system Signs, symptoms, and treatment depend on the type of the disease -involves overgrowth of lymphoid tissue -higher risk of lymphoma -giant lymph node hyperplasia and angiofollicular lymph node hyperplasia and is a lymphopro. disorder -unicentric: **affects only a single lymph node -multicentric **affects multiple lymph nodes and tissue and may lead to a severe weakening of the immune system -anorexia, difficulty breathing and eating due to chest pressure, enlarged spleen or liver, fever, night sweats, numbness or weakness in hands and feet Castleman disease is a rare illness that involves the overgrowth of lymphoid tissue. Although this disease is characterized by overgrowth of lymphatic cells, it is not considered a cancer but is associated with a higher risk of lymphoma. Castleman disease is also known as giant lymph node hyperplasia and angiofollicular lymph node hyperplasia and is classified as a lymphoproliferative disorder. There are two types of Castleman disease: unicentric, which affects only a single lymph node, and multicentric, which affects multiple lymph nodes and tissue and may lead to a severe weakening of the immune system. Unicentric manifestations include: ~ Difficulty breathing or eating due to fullness or pressure in the chest or abdomen ~ A large lump in the neck, armpit, or groin ~ Unexplained weight loss and anorexia ~ Persistent cough Multicentric manifestations include: ~ Fever and night sweats ~ Nausea and vomiting leading to a loss of appetite and resulting in weight loss ~ Weakness and overall fatigue ~ Enlarged spleen, liver, or peripheral lymph nodes in the neck, groin, or armpits ~ Numbness or weakness in the hands and feet due to nerve damage

. Describe the pathophysiology of prostatitis

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

rheumatoid arthritis

Rheumatoid arthritis Possible autoimmune with genetic predisposition, and perhaps viral infections Developed antibody to yourself Attacks synovial membrane Affects the whole body (systemic science) S/S include systemic effects Fatigue Weight loss Fever Iron deficiency anemia depression Often affects young women crippling deformities Has exacerbations and remissions Stress and getting sick can trigger this Presents symmetrically (affect same joint on both sides of the body) → tends to run in families Major cause of disability (1% of people in the US have it) ankylosis → bones grow together (wear and tear) Diminish bodies immune response to keep the autoimmune disorder from happening It is insidious -it is considered an autoimmune disorder causing chronic systemic inflammatory disease- major cause of disability (higher incidence in woman than in men and increases with age) -remissions and exacerbations lead to progressive damage to the joints -disease often commences insidiously with symmetric involvement of the small joints such as the fingers, followed by inflammation and destruction of additional joints -first step of develop. is an abnormal immune response causing inflammation of the synovial membrane with vasodilation, increased perm, and formation of exudate, causing painful joints -the synovitis appears ti result from the immune abnormality -rheumatoid factor, an antibody against imm. G is present in the blood DURING EXACERBATIONS: 1. synovitis (inflamm. recurs and synovial cells proliferate) 2. pannus formation (gran. tissue spreads over articular cartilage) 3. cartilage erosion 4. fibrosis (limits movement- calcifies and the joint space is obliterated) 5. ankylosis (joint fixation and deformity develop. -acute inflammation leads to disuse atrophy of the muscles and stretching of the tendons and ligaments -alignment of the bones in the joints shifts -inflammation and pain may cause muscle spasms -contractures and deformity with subluxation develop -mobility is greatest impaired as the various joints become damaged and deformed -systemic effects arise from circulating immune factors that cause fatigue, depression, anorexia, etc -iron therapy Rheumatoid arthritis (RA) is considered an autoimmune disorder causing chronic systemic inflammatory disease. It affects more than 1% of the population and is a major cause of disability. Rheumatoid arthritis has a higher incidence in women than men and increases in older individuals Remissions and exacerbations lead to progressive damage to the joints. The disease often commences insidiously with symmetric involvement of the small joints such as the fingers, followed by inflammation and destruction of additional joints (eg, wrists, elbows, knees). Many individuals also have involvement of the upper cervical vertebrae and TMJ. The severity of the condition varies from mild to severe, reflecting the number of joints affected, the degree of inflammation, and the rapidity of progression Mobility is greatly impaired as the various joints become damaged and deformed. Walking becomes very difficult when the knees or ankles are affected. The inflammatory process has other effects on the body. Rheumatoid or subcutaneous nodules may form on the extensor surfaces of the ulna. Nodules also may form on the pleura, heart valves, or eyes. These are small granulomas on blood vessels. Systemic effects are thought to arise from the circulating immune factors, causing marked fatigue, depression and malaise, anorexia, and low-grade fever. Iron deficiency anemia with low serum iron levels is common; when it results from rheumatoid arthritis, this anemia is resistant to iron therapy Although rheumatoid arthritis is considered an autoimmune disorder, the exact nature of the abnormality has not been fully determined. A genetic factor is present, with familial predisposition. The abnormality seems to be linked to several viral infections. Rheumatoid factor is not present in all patients with rheumatoid arthritis, yet it may be present in certain other disorders as well. Rheumatoid arthritis is more common in women than men, and the incidence increases with aging.

Describe the development of secondary brain cancer (metastasis from other primary cancers— Lung, breast, melanoma

Secondary brain tumors are common, usually metastasizing from breast or lung tumors, and they cause effects similar to those of primary brain tumors. -secondary brain tumors are common metastasizing from brain to lungs Other factors that may cause secondary brain damage include infection, which is usually a significant risk in persons with open head injuries, and hypoxia, which is related to systemic injury or shock. Respiratory or cardiovascular impairment may cause additional ischemia in the brain

Discuss the development of 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.

Define pneumothorax

Spontaneous (basic) → don't know why it happens (air leaks out and fills space where lungs should be) The normal lung: negative pressure to make the pleura stick to the lungs Air enters through the lungs Open → air comes in from the outside (there is a hole in the chest) Lungs inflate ; space increases ; suck in air through the hole (not helping w gas exchange) Tension → hole; breathe and chest expands and sucks air through hole; flap of tissue (puncture injury); closes off flap so air cannot get out ; causing air to build up really quick ; big mediastinal shift (bending of the trachea) Medical attention asap Air in chest cavity Lung collapse Penetrating wound Painful Dangerous! Relieved by pleurocentesis (withdrawing air) -refers to air in the pleural cavity -fluid or blood may be present in the cavity CLOSED - air can enter the pleural cavity through an opening directly from the internal airways (no opening in the chest wall) -- can be simple of spontaneous -spon, idiopathic, ruptured bleb, from inside of lung, one lung is impaired, breath sounds are absent SIMPLE OR SPON - occurs when a tear on the surface of the lungs allows air to escape from the inside of the lung through a bronchus and visceral pleura -simple occurs in men who have no prior lung disease SECONDARY - associated with underlying respiratory disese resulting from rupture of an emhys bleb on the surface of the lung or erosion by a tumor OPEN - atmospheric air entering the pleural cavity through an opening in the chest wall -puncture wount through chest wall, air entry from outside of body through opening in thorax, mediastinal flutter impaurs venous return to the heart, sucking noise, tracheal swing, dec BP, moderate hypoxemia SUCKING WOUND -large opening in the chest wall where the sound of air moving in and out makes a typical sucking sound TENSION: -most serious form -results from an opening thoruh the chest wall and parietal plerua or from a tear in the lung itssue and viseral pleura that causes ateletaisi -damage creates a flap of tissue or a one way valve effect (opening enlarges on inspiration, promoting airflow into the pleural cavity) -on expiration, opening is sealed off preveting removal of air -severe hypoxia develops - open (pun through thorax) -close (tear in lung surface) -both with flap of one way valve -pleural paun -breth sounds absent on affected side -shock PneumothoraxSpontaneous (basic) → don't know why it happens (air leaks out and fills space where lungs should be)The normal lung: negative pressure to make the pleura stick to the lungsAir enters through the lungsOpen → air comes in from the outside (there is a hole in the chest)Lungs inflate ; space increases ; suck in air through the hole (not helping w gas exchange)

Discuss the pathophysiology of esophageal carcinoma

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.

Identify the causes of acute renal failure

The kidneys may fail to function for many different reasons. Either directly reduced blood flow into the kidney or inflammation and necrosis of the tubules cause obstruction and back pressure, leading to greatly reduced GFR and oliguria (reduced urine output) or anuria (no urine output). Both kidneys must be involved. The failure is usually reversible if the primary problem is treated successfully. Dialysis may be used to replace the kidney function during this period. In some cases, the kidneys sustain a degree of permanent damage. Acute renal failure has numerous causes (Fig. 18.16): ~ Acute bilateral kidney disease, such as glomerulonephritis, which reduces GFR. ~ Severe and prolonged circulatory shock or heart failure, which results in tubule necrosis. Shock associated with burns or crush injuries or sepsis frequently causes renal failure. With burns, the damaged erythrocytes break down in the circulation, releasing free hemoglobin that may accumulate in the tubules, causing obstruction. Hemoglobin also is toxic to tubule epithelium, causing inflammation and necrosis (see Chapter 5, Burns). When skeletal muscle is crushed in an accident, myoglobin is released with similar effects. ~ Nephrotoxins such as drugs, chemicals, or toxins, which cause tubule necrosis and obstruction of blood flow. Industrial chemicals such as the solvent carbon tetrachloride may cause acute renal failure when exposure is intense. Long-term, low-level exposures may cause gradual damage, eventually leading to chronic renal failure. The list of frequently used drugs possibly causing tubule damage is growing longer and now includes sulfa drugs, phenacetin, nonsteroidal antiinflammatory drugs (NSAIDS), acetaminophen and aspirin, and penicillin. When patients take these drugs, fluid intake should be greatly increased to reduce the risk of kidney damage. ~ Occasionally mechanical obstructions such as calculi, blood clots, or tumors, which block urine flow beyond the kidneys and cause acute renal failure. Acute renal failure usually develops rapidly. Blood tests show elevated serum urea nitrogen (BUN) and creatinine as well as metabolic acidosis and hyperkalemia, confirming the failure of the kidneys to remove wastes.

Discuss the pathophysiology of anencephaly and spina bifida

There is a high familial incidence of spina bifida and associated defects, such as anencephaly (absence of the cerebral hemispheres and superior cranial vault). (absence of the cerebral hemispheres and superior cranial vault). absence of the fetal cranial vault exposure of cerebral tissue to amniotic fluid precludes brain development form of neural tube defect typically an isolated birth defect that is not related to chromosomal abnormalities Stillborn incidence reported to occur as frequently as 1 to 5 in 1000 live births in the past. dietary folic acid supplementation by mothers-to-be before and during pregnancy can reduce the incidence Rate is now less than 1 in 10,000 live births in some places. Anencephaly congenital condition where most of the brain and skull are absent Incomplete closure of spine (neural tube) Failure of joining of midline structures Part of spinal cord may protrude out of vertebra 1992- the USPHS recommended women of childbearing age supplement their daily diet with 400 micrograms folic acid. 1996-the FDA ordered the addition of folic acid to enriched cereal grain products Source: CDC.gov: http://www.cdc.gov/Features/dsSpinaBifidaTrends/ Spina bifida refers to a group of neural tube defects that are congenital anomalies of varying severity. They are a common developmental defect, myelomeningocele occurring in an estimated 1500 to 2000 of the 4 million live births per year in the United States The neural tube develops during the fourth week of gestation, beginning in the cervical area and progressing toward the lumbar area. The basic problem in spina bifida is failure of the posterior spinous processes on the vertebrae to fuse, which may permit the meninges and spinal cord to herniate, resulting in neurologic impairment. Any number of vertebrae can be involved, and the lumbar area is the most common location Three types of spina bifida are common: Spina bifida occulta develops when the spinous processes do not fuse, but herniation of the spinal cord and meninges does not occur. The defect may not be visible, although often a dimple or a tuft of hair is present on the skin over the site. The defect may be diagnosed by means of routine x-ray examination or when mild neurologic signs manifest owing to tension on the cord during a growth period. Meningocele is the same bony defect, but herniation of the meninges occurs through the defect, and the meninges and CSF form a sac on the surface. Transillumination confirms the absence of nerve tissue in the sac. Neurologic impairment is usually not present, although infection or rupture of the sac may lead to neurologic damage Myelomeningocele is the most serious form of spina bifida. Herniation of the spinal cord and nerves along with the meninges and CSF occurs, resulting in considerable neurologic impairment (see Fig. 14.26C). The location and extent of the herniation determine how much function is lost. This defect is often seen in conjunction with hydrocephalus ■ Diagnostic Tests Alpha-fetoprotein (AFP) that has leaked from the defect into the amniotic fluid surrounding the fetus results in an elevated level in maternal blood in a specimen obtained at 16 to 18 weeks' gestation. Amniocentesis detects the presence of the elevated AFP, and the presence of spina bifida can also be diagnosed prenatally by ultrasound Spina bifida appears to have a multifactorial basis, with a combination of genetic and environmental factors contributing to its development. Environmental factors include exposure to radiation, gestational diabetes, and deficits of vitamin A or folic acid. Folic acid supplements are recommended before conception and for the first 6 weeks of pregnancy as a preventive measure. Research has shown that such supplementation reduces the incidence rate of the disorder. ■ Signs and Symptoms Meningocele and myelomeningocele are visible as a protruding sac over the spine. In myelomeningocele, the extent of the neurologic deficit depends on the level of the defect (see Fig. 14.4) and the status of the nerve tissue; sensory and motor function at and below the level of the herniation is impaired. Some degree of muscle weakness or paralysis is present. Bladder and bowel control is usually impaired. Depending on the level of damage and the availability of reflex and sphincter control, there may be fecal and urinary incontinence. ■ Treatment Some surgical repair of spina bifida has been done successfully in utero before birth.

Differentiate between subluxation and dislocation

Trauma Subluxation Partial displacement with partial contact with articulating surfaces Still contact but really out of place the bone is only partially displaced, with partial loss of contact between the surfaces, the injury is subluxation Trauma Dislocation -- separate bones and joint they are not touching anymore Separation of two bones at a joint Loss of contact between articulating surfaces Considerable damage to ligaments, nerves, blood vessels Bleeding, inflammation, swelling follow Requires reduction to fix separation of two bones at a joint with loss of contact between the articulating bone surface (usually one bone is out of position, whereas the other remains in its normal location) can cause soft tissue damage

Discuss the development and signs and symptoms 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) 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.

Differentiate between volvulus and intussusception

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 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. 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 Intussusception may occur secondary to polyps or tumors that pull a section of bowel forward with them (the telescoping of a section of bowel inside an adjacent section)

Differentiate between valvular stenosis and valvular insufficiency

Valvular Stenosis (scarring, calcium deposits) → scar is not as flexible Increased resistance to blood flow Heart works harder (to get blood through stiff valve) Hypertrophy develops Mitral Valve Stenosis Different from prolapse Blood impeded from filling left ventricle Can cause left sided congestion signs Can lead to thrombi It is a scarring / stiffening of the mitral valve Does not easily flow / not complete filling -stenosis is the narrowing of a valve, which restricts the forward flow of blood -if the opening is narrow, as in pulmonary stenosis, the myocardium must contract with more force to push the blood through -mitral stenosis and its effects are demonstrated in ECG --left atrium is enlarged from the backup pressure and the inc workload had produced the thickened atrial wall Diseases of the valves Valvular Insufficiency (regurgitative valve) → not closing all the way (floppy and leaking) → back flow to the chamber → inefficient Allows blood to regurgitate back into chamber Increases heart workload Hypertrophy develops Mitral Valve Prolapse 1-2% of Americans have this (most common) "floppy" regurgitation valve Blood leaks back into atrium instead of going out through aorta Regurgitation valve Build up pressure When left ventricle builds up pressure, shuts off (becomes inefficient) -incompetence is when there is a failure of the valve to close completely, allowing blood to regurigitate or leak backwards -mitral valve prolapse is a common occurence; it refers to abnormally enlarged and floppy valve leaflets that balloon backwards with pressure or to posterior displacement of the cusp, which permits regurgitation of blood -valvular defects reduce the efficiency of the heart to pump and reduce stroke volume -if valve leaks and blood regurgitates forwards, the heart must also increase its efforts to maintain cardiac output -treatment is surgical replacement

uIcerative 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.

Describe the condition of 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.

Discuss the development of bladder and renal 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. 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.

describe the pathophysiology of 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. Painful menstruation—endometriosis

Define diverticulitis

inflammation of the diverticula Diverticulitis refers to inflammation of the diverticula. It is a common problem in the Western world, primarily affecting older individuals

Define cholecystitis

inflammation of the gallbladder cholecystitisCholecystitisLiterally -- "Inflammation of the bile-containing bladder"Acute--obstruction of biliary treeChronic—no obstruction, but presence of gallstones or dysfunctional GB-- Cholecystitis refers to inflammation of the gallbladder and cystic duct. 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. 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.

Define 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

Pathophysiology of congestive heart failure (CHF)

heart is unable to pump its required amount of blood Insufficiency of cardiac output Usually starts with one side (L or R) and ends up involving both Causes? CAD (ischemia, MI) → heart attack Myocarditis and cardiomyopathy (not CAD) → inflammation of the heart tissue Excessive cardiac burden Anemia, heart valve problems, hyperthyroidism (overactive thyroid → tachycardia) Arrhythmias Hypertrophy Either left sided or right sided (insufficient output) Left side gets backed up; then goes to right side (both sides not working= CHF) -occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. usually CHF occurs as a complications of another condition **Young Children with CHF** Often secondary to congenital heart disease Feeding difficulties often first sign Failure to gain weight or meet developmental guidelines (to "thrive") Short sleep periods Tripod position to play Cough, rapid grunting respirations, flared nostrils, wheezing Radiographs show cardiomegaly. Arterial blood gases used to measure hypoxia Get it from congenital heart disease Congestive heart failure is a common occurrence when the contractility of the ventricle is reduced and stroke volume declines. This may occur a few days after the MI or much later as activity is resumed Congestive heart failure occurs when the heart is unable to pump sufficient blood to meet the metabolic needs of the body. Usually CHF occurs as a complication of another condition. It may present as an acute episode but usually is a chronic condition. It may result from a problem in the heart itself, such as infarction or a valve defect; it may arise from increased demands on the heart, such as those imposed by hypertension or lung disease; or it may involve a combination of factors. Depending on the cause, one side of the heart usually fails first, followed by the other side. For example, an infarction in the left ventricle or essential hypertension (high blood pressure) affects the left ventricle first, whereas pulmonary valve stenosis or pulmonary disease affects the right ventricle first. It is helpful in the early stages to refer to this problem as left-sided CHF or right-sided CHF s left-sided CHF or right-sided CHF. Initially various compensation mechanisms maintain cardiac output (Fig. 12.20, top part). Unfortunately, these mechanisms often aggravate the condition instead of providing assistance: The reduced blood flow into the systemic circulation and thus the kidneys leads to increased renin and aldosterone secretion. The resulting vasoconstriction (increased afterload) and increased blood volume (increased preload) add to the heart's workload. The SNS response also increases heart rate and peripheral resistance. Increased heart rate may decrease the efficiency of the heart and impede filling, as well as increasing work for the heart. The chambers of the heart tend to dilate (enlarge), and the cardiac muscle becomes hypertrophied (cardiomegaly), with the wall of the ventricle becoming thicker. This process demands increased blood supply to the myocardium itself, and eventually some myocardial cells die, to be replaced with fibrous tissue There are two basic effects when the heart cannot maintain its pumping capability: 1. Cardiac output or stroke volume decreases, resulting in less blood reaching the various organs and tissues, a "forward" effect. This leads to decreased cell function, creating fatigue and lethargy. Mild acidosis develops, which is compensated for by increased respirations (see Chapter 2). Because the affected ventricle cannot pump its load adequately, the return of blood to that side of the heart is also impaired. 2. "Backup" congestion develops in the circulation behind the affected ventricle (Fig. 12.21). The output from the ventricle is less than the inflow of blood. ts blood into the systemic circulation, the normal volume of blood returning from the lungs cannot enter the left side of the heart. This eventually causes congestion in the pulmonary circulation, increased capillary pressure, and possible pulmonary edema, in which fluid is forced into the alveoli. This situation is termed left-sided CHF. In right-sided CHF, the right ventricle cannot maintain its output, so less blood proceeds to the left side of the heart and the systemic circulation (forward effect). The backup effect, or congestion, is apparent in the systemic circulation, as shown by increased blood volume and congestion in the legs and feet and eventually also in the portal circulation (liver and digestive tract) and neck veins. Right- and left-sided cardiac failures are compared

Discuss the effects of hypertension and arterioscelerosis on kidneys (ischemia, necrosis, fibrosis, renal failure: fig 18.14)

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 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 kidney 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. 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.

Discuss primary (vera) and secondary (erythrocytosis) polycythemia

o Primary (p. vera) o Secondary (erythrocytosis) Two main types: Polycythemia vera Bone marrow overactivity Considered a neoplastic disorder Erythrocytosis Caused by prolonged hypoxia Considered as a neoplastic disorder Blood is so thick -- lots of clots Sometimes have too many platelets -Polycythemia: Signs and Symptoms Distended blood vessels, sluggish blood flow Increased blood pressure Hypertrophied heart Hepatomegaly Splenomegaly Dyspnea Headaches Visual disturbances Thromboses and infarctions Trying to clear out excess blood Too many blood cells -secondary: erythorcytisus is an increase in RBCs that occurs in response to prolonged hypoxia and inc erythorprotein secretion -primary, poly. vera, is a condition where there is an an increased production of erythrocytes and other cells in the bone marrow (NEOPLASTIC DISORDER) --marked inc in eryth, and in ganulocytes and thrombocytes -blood vessels are distended and blood flow is sluggish -hemorrhage is frequent in places where the blood vessels are distended Primary polycythemia, or polycythemia vera, is a condition in which there is an increased production of erythrocytes and other cells in the bone marrow. It is considered a neoplastic disorder. Serum erythropoietin levels are low. Secondary polycythemia, or erythrocytosis, is an increase in RBCs that occurs in response to prolonged hypoxia and increased erythropoietin secretion. Usually the increase in RBCs is not as marked in secondary polycythemia, and more reticulocytes appear in the peripheral blood. In polycythemia vera, there is a marked increase in erythrocytes and often in granulocytes and thrombocytes as well, resulting in increased blood volume and viscosity. Blood vessels are distended and blood flow is sluggish, leading to frequent thromboses and infarctions throughout the body, especially when platelet counts are high. Blood pressure is elevated and the heart hypertrophied. Hemorrhage is frequent in places where the blood vessels are distended. The spleen and liver are congested and enlarged, and the bone marrow is hypercellular. In some patients, the bone marrow eventually becomes fibrotic, hematopoiesis develops in the spleen, and anemia follows. In a few patients, acute myeloblastic leukemia develops in the later stages, especially if treatment has involved chemotherapy.

Describe the pathophysiology of multiple sclerosis

progressive random degeneration of peripheral nerves Demyelination = destruction of myelin sheath Adults < 50 yo Found in white matter of CNS Slow nerve impulses Site & symptoms vary according to area of destruction S/S: tremors, diff. Speaking, weakness, incontinence, vision problems (scotomas) Multiple sclerosis (MS) involves a progressive demyelination of the neurons of the brain, spinal cord, and cranial nerves. There are a number of types of MS, with considerable variation in the effects, severity, and progression in any one individual. Multiple sclerosis is characterized by remissions and exacerbations, but nevertheless it is marked by progressive degeneration Loss of myelin interferes with the conduction of impulses in the affected fibers. It affects all types of nerve fibers— motor, sensory, and autonomic—and occurs in diffuse patches throughout the nervous system Research has shown that cognitive function can be impaired in the individual with MS, particularly with respect to attention to tasks and memory The earliest lesion occurs as an inflammatory response as cells that normally do not enter the brain or spinal cord do so and attack neurons, with loss of myelin in the white matter of the brain or spinal cord. Research has identified a protein in the body's blood clotting mechanism as a potential trigger of the immune response Later larger areas of inflammation and demyelination, termed plaques, become visible, frequently beside the lateral ventricles in the brain, in the brain stem, and in the optic nerves. Initially the area of plaque appears pinkish and edematous, but then it becomes gray and firm. Each plaque varies in size, and several may coalesce into a single patch. The initial inflammation may subside, and neural function may return to normal for a short time, until another exacerbation occurs. In time neural degeneration becomes irreversible, and function is lost permanently. With each recurrence, additional areas of the CNS are involved. Multiple sclerosis varies in severity, occurring in mild and slowly progressive patterns in some individuals and in rapidly progressive forms in others CEREBELLUM Loss of balance Ataxia and tremor CRANIAL NERVE Diplopia Loss of vision MOTOR NERVE TRACTS Weakness Paralysis DAMAGE TO SENSORY NERVE TRACTS Paresthesia—prickling, burning sensation The cause is unknown, although many researchers believe it is an autoimmune disorder. However, it may be even more complex in its origins. Multiple sclerosis appears to have genetic, immunologic, and environmental components. Multiple sclerosis occurs more frequently in people of European descent, and there is an increased risk for close relatives of affected individuals. The environmental factors have not yet been determined, although it is thought that climate may play a role because the disease is more common in temperate zones (northern United States and Canada) and in individuals who grow up in temperate climates. However, there are exceptions to this factor, where MS occurs in warm climates. Viral infection and an abnormal immune response have also been suspected.

Describe the development of 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)

Discuss the development of 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.

Describe the development of toxic goiter

Hyperthyroid condition resulting from hyperactivity of thyroid gland toxic goiter Hyperthyroid condition Etiology: excessive TSH stimulation Toxic goiter is a hyperthyroid condition resulting from hyperactivity of the thyroid gland, perhaps due to excessive stimulation by TSH, which produces a large nodular gland. Goiter treatment depends on the size of the goiter, the signs and symptoms, and the underlying cause. Various treatments are available: ~ Hyperthyroidism and hypothyroidism medications such as levothyroxine (Levothroid, Synthroid) ~ Surgery—total or partial thyroidectomy ~ Radioactive iodine—hormone replacement may become necessary as this method may result in an underactive thyroid Toxic goiter is a hyperthyroid condition resulting from hyperactivity of the thyroid gland, perhaps due to excessive stimulation by TSH, which produces a large nodular gland. Goiter refers to an enlargement of the thyroid gland, which is often visible on the anterior neck. Goiters are caused by various hypothyroid and hyperthyroid conditions. A goiter can become very large, compressing the esophagus and interfering with swallowing, or it can cause pressure on the trachea. It can also be of cosmetic concern

Differentiate between type of Brain cancer (including astrocytoma and glioblastoma multiforme)

Neoplasia Malignant (gliomas—many types) Benign (meningioma, neuroma) Brain Tumors: Malignant Glioma (glial [supportive] cells) Astrocytoma Glioblastoma Oligodendroglioma Ependymoma Neoplasia of CNS Benign v. malignant Metastases (secondary cause) Do brain tumors metastasize? Benign tumors can causes trouble too! Malignant tumors named for affected cells/tissue -space occupying lesions that cause inc ICP bc of space constraints within the rigid skull and localized dysfunction related to their location -benign and malignant tumors can be life threatening -glimos form the largest category of primary malignant tumors -arise from glial cells, the parenchymal cells in the CNS -tumors may develop in the meninges or pituitary gland causing similar effects from the pressure on the brain -primary mal. tumors rarely metastasize outside the CNS, but multiple tumors may be present within the CNS -secondary brain tumors are common metastasizing from brain to lungs -as the mass expands, it compresses and distorts the tissue around it, eventually resulting in herniation malignant brain tumor of immature glial cells (most malignant form of astrocytoma) Brain Tumors: Malignant Glioma (glial [supportive] cells) Astrocytoma Glioblastoma Oligodendroglioma Ependymoma Glioma, MR This T2 weighted magnetic resonance imaging (MRI) scan in transverse view demonstrates an infiltrative mass involving the posteromedial right frontal lobe and parietal lobe, consistent with a glioma. -gliomas form the largest category of primary malignant tumors. They arise from one of the glial cells, the parenchymal cells in the CNS -further classified according to the cell of derivation (astroytomas are the most common) and the location of the tumor Glioblastoma, also known as glioblastoma multiforme (GBM), is the most aggressive type of cancer that begins within the brain. Initially, signs and symptoms of glioblastoma are nonspecific. They may include headaches, personality changes, nausea and symptoms similar to those of a stroke. The largest category of primary malignant brain tumors that arise from cells in the central nervous system (CNS) are called: gliomas Primary malignant brain tumors, particularly astrocytomas, do not usually have well-defined margins but are invasive and have irregular projections into adjacent tissue that are difficult to totally remove (Fig. 14.12). There is usually an area of inflammation around the tumor, adding to the pressure. In some cases, obstruction of the flow of CSF or of the venous sinuses increases ICP. As the mass expands, it compresses and distorts the tissue around it, eventually resulting in herniation. A relatively small tumor in the brain stem or cerebellum can compress the medulla within a short time. However, tumors in the cerebral hemispheres, particularly in "silent" areas (without obvious function), may grow quite large before their effects are noticeable.

Differentiate between compound, comminuted, greenstick, and transverse fractures (from written description)

Open fracture → compound fracture (protrudes through the skin → danger is infection) *open-closed: open/compound fracture results when the skin is broken-- more damage to soft tissue, like blood vessels and nerves, and there is a higher risk of infection *comminuted fracture: there are multiple fracture lines and bone fragments Greenstick → one end breaks but not the other end (common in kids) *complete-incomplete: when the bone Is broken to form two or more separate pieces, whereas in an incomplete fracture, the bone is only partially broken. --example: greenstick fracture ** common in the softer bones of children in which the shaft of the bone is bent, tearing the cortical bone on one side but not extending all the way through the bone Comminuted fractures consist of several fracture lines but may not be complicated. ~ Compound fractures involve trauma in which the brain tissue is exposed to the environment and is likely to be severely damaged because bone fragments may penetrate the tissue and the risk of infection is high. Complete-incomplete. A complete fracture occurs when the bone is broken to form two or more separate pieces, whereas in an incomplete fracture the bone is only partially broken. An example of the latter is a greenstick fracture, common in the softer bones of children, in which the shaft of the bone is bent, tearing the cortical bone (outer layer of compact bone) on one side but not extending all the way through the bone. Transverse fracture is a fracture across the bone. ~ Linear fracture is a break along the axis of the bone.

Define cholelithiasis

cholelithiasis (gallstone); CholelithiasisGallstones main causes of GB inflammation....Formed from cholesterol, bilirubin, calciumPotential for obstruction of a duct (Choledocholithiasis)-- blockage of a ductIncreases CholestasisBile is still -- not movingNot good, setting up for infectionsFormed 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 Cholelithiasis refers to formation of gallstones, which are masses of solid material or calculi that form in the bile.

Define atelectasis

collapsed lung; incomplete expansion of alveoli Atelectasis → crushed lungs Lung collapse Usually the result of another condition Causes of collapse Obstruction of air passages (blocking air from filling in the alveoli) Compression of lung Air (pneumothorax) fluid (eg pleural effusion) Mass (compression and obstructive) -nonaeration or collapse of a lung or part of a lung leading to dec gas exchange and hypoxia -occurs as a complication of many primary conditions -ventilation and perfusion are altered and affects the o2 diffusion -the inc respiratory rate can control co2 levels bc this gas diffuses easily -if lungs are not reinflated quickly, the lung tissue can become necrotic and infected -obstructive it reabsorption atectasis develops when total obstruction of the airway -compression results when a mass such as a tumor exerts pressure -inc surface tension -fibrotic tissue in the lungs or pleura may restrict expansion -posteoperative Absence of breath sounds indicates nonaeration or collapse of a lung (atelectasis).

Describe the development of diverticulosis

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. Diverticulosis is asymptomatic diverticular disease. Usually multiple diverticula are present

Tetralogy of Fallot (know the four components)

congenital malformation involving four distinct heart defects -most common cyanotic congenital heart condition -includes four (tetra) abnormalities and is a cyanotic disorder -four defects are pulmonary valve stenosis, VSD, dextroposition of the aorta (to the right over the VSD), and right ventricular hypertrophy -this combo alters pressures within the heart and therefore alters blood flow -pulmonary valve stenosis restricts outflow from the right ventricle, leading to right ventricular hypertrophu and high pressure in the right ventricle -- this pressure leads to a right to left shunt of blood through the VSD -the flow of un-o2-ed blood from the right ventricle directly into the systemic ciruclation is promoted by the position of the aorta, over the septum or VSD -surgery is the only effective treatment for the t.o.f. --done during the first year of birth and involves a number of individual repairs: closing the VSD, reparing the pulmonary valve, and widening the pulmonary arteries to increase the flow Tetralogy of Fallot (TEST QUESTION) → which of these are included? VSD Ventricular septal defect Hole between the two ventricles Dextroposition of aorta Aorta shifted to the right Push up blue and red blood through aorta Pulmonary stenosis Pulm. artery is too narrow Compounds things A lot of back pressure R V Hypertrophy Because of all this back pressure Tetralogy of Fallot is the most common cyanotic congenital heart condition. It is more complex and more serious than the others described so far because it includes four (Greek tetra) abnormalities and is a cyanotic disorder (infants suffering from this condition are sometimes called "blue babies"). The four defects are pulmonary valve stenosis, VSD, dextroposition of the aorta (to the right over the VSD), and right ventricular hypertrophy (see Fig. 12.24C). This combination alters pressures within the heart and therefore alters blood flow

Describe the pathophysiology of multiple myeloma

eoplastic disease that involves increased production of plasma cells in bone marrow Unknown cause Occurs in older adults Production of other blood cells is impaired Multiple tumors in bone Loss of bone Severe bone pain Prognosis poor, with short life expectancy Multiple myeloma Too many plasma cells in the bone marrow -neoplastic disease of unknown etiology involving the plasma cells -inc number of malignant plasma cells replace the bone marrow and erode the bone -multiple tumors and bone destruction develip in the ribs, skills, etc fractures at weakened sites in the bone are common -hypercalcemia develops as the bone breaks down SIGNS: -onset is insideous -frequent infections -pain related to bone involvement -pathologic fractures -anemia and bleeding -kidney function -chemo is usually encouraged for remission; median survival is 3 years -blood transfusions are required in the late stage Multiple myeloma is a neoplastic disease of unknown etiology involving the plasma cells (mature B lymphocytes involved in production of antibodies). An increased number of malignant plasma cells replace the bone marrow and erode the bone (Fig. 11.10). Blood cell production is impaired, as well as production of antibodies. Multiple tumors with bone destruction develop in the vertebrae, ribs, pelvis, and skull. Pathologic or spontaneous fractures at weakened sites in the bone are common. Hypercalcemia develops as bone is broken down. The tumor cells can spread throughout the body, into lymph nodes and infiltrating many organs. Extensive testing is required for the diagnosis. The onset is usually insidious and the malignancy well advanced before diagnosis. ~ Frequent infections may be the initial sign related to impaired production of antibodies. ~ Pain, related to bone involvement, is common and is present at rest. ~ Pathologic fractures may occur as bone is weakened. ~ Anemia and bleeding tendencies are common because blood cell production is affected. ~ Kidney function, particularly the tubules, is affected, leading to proteinuria and kidney failure.

Define pleural effusion

fluid in the pleural space Pleural effusion (fluid in pleural space → exudate or water) Pleural Effusion → tumors can cause this (cancer) Hydrothorax Fluid is transudate CHF a frequent cause Pleural effusion (fluid in pleural space → exudate or water) Fluid is exudate Inflammation of the pleura or pleurisy (inflam. Of the pleura) → can be an infectious process Adhesions- scar tissue binding both sides of the pleura—limiting lung expansion Empyema—purulent exudate (ON THE TEST) -the presence of excessive fluid in the pleural vacity -pleurisy or pleuritis may preced or follow pleural effusion or occur independently -- inflamed swollen and rough -large amts of fluid first inc the pressure on the cavity and then cause separation of the membranes, preventing their cohesion during inspiration -a large amount of fluid causes atelectasis on the affected side and shift of the medsstinal contents towards the unaffected lungs -exudative effusions are a response to inflammation, perhaps from a tumor, in which inc capillary perm allows fluid containing protein and white blood cells to leak into the pleural cavity --transudates are watery effusions called HYDROTHORAX (result from inc hydrostatic pressure or dec osmotic pressure in the blood vessels, leading to a shift of fluid out of the blood vessels into the potential space in the pleural cavity) -hemothorax is when the fluid is blood resulting from trauma, cancer, or surgery -empyema occurs when the fluid is purulent as a result of infection often related to pneumonia Pleural effusion (excess fluid in the pleura) A pleural effusion is the presence of excessive fluid in the pleural cavity. Normally a very small amount of fluid is present to provide lubrication for the membranes. Effusions vary in type and mechanism according to the primary problem. Both lungs may be involved, but more often only one lung is affected because each lung is enclosed in a separate pleural membrane. The effects of effusion depend on the amount, type, and rate of accumulation of the fluid. Pleurisy or pleuritis may precede or follow pleural effusion or occur independently. Pleurisy is a condition in which the pleural membranes are inflamed, swollen, and rough, often in association with lobar pneumonia. Small amounts of fluid are drained from the pleural cavity by the lymphatics and have little effect on respiratory function. Large amounts of fluid first increase the pressure in the pleural cavity and then cause separation of the pleural membranes, preventing their cohesion during inspiration. These effects prevent expansion of the lung, leading to atelectasis, particularly when fluid accumulates rapidly (see Fig. 13.24A). A large amount of fluid causes atelectasis on the affected side and a shift of the mediastinal contents toward the unaffected lung, limiting its expansion also. A tracheal deviation indicates this shift. Venous return in the inferior vena cava and cardiac filling may be impaired because large effusions increase pressure in the mediastinum.

myocardial ischemia

loss of blood supply to heart muscle tissue of myocardium due to occlusion of coronary artery; may cause angina pectoris or myocardial infarction Myocardial ischemia occurs when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (atherosclerosis). If the plaques rupture, you can have a heart attack (myocardial infarction) Cardiac ischemia refers to lack of blood flow and oxygen to the heart muscle. ... If ischemia is severe or lasts too long, it can cause a heart attack (myocardial infarction) and can lead to heart tissue death. In most cases, a temporary blood shortage to the heart causes the pain of angina pectoris.

Define Chronic Obstructive Pulmonary Disease (COPD)

permanent, destructive pulmonary disorder that is a combination of chronic bronchitis and emphysema OPD--Umbrella term for various disorders Reaction to primary disease or chronic irritation Considered a secondary condition Bronchi & bronchioles obstructed (or plugged) Inflammation due to debris & irritation Mucus production as response obstruction Changes to lung, destruction → changes in structure (form of the lungs) All forms result in ineffective ventilation (affects air getting down into lungs) Can be life long and is usually a destructive process going on Is irreversible -group of common chronic respiratory disorders that are characterized by progessive tissue degeneration and obstruction in the airways of the lungs -restrictive lung diseases (irritant causes interstitial inflammation and fibrosis, resulting in the loss of compliance of stiff lung) -causes irreversible and progressive damage to the lungs -repsiratory failure may result because of severe hypoxia -leads to the development of cor pulmonale (right sided CHF due to lung disease) COPD diseases Emphysema Chronic Bronchitis 90% due to cigarette smoke Defined as productive cough 3 months in a year for 2 consecutive years Bronchiectasis → associated with CB Also asthma is often included in this category (your text seems confused about this) Chronic obstructive pulmonary disease (COPD), sometimes also called chronic obstructive lung disease (COLD), is a group of common chronic respiratory disorders that are characterized by progressive tissue degeneration and obstruction in the airways of the lungs. They are debilitating conditions that affect the individual's ability to work and function independently. Examples of these disorders are emphysema, chronic bronchitis, and chronic asthma. Their characteristics are compared in patients, several primary diseases overlap—for example, asthma and bronchitis. Other conditions such as cystic fibrosis and bronchiectasis may lead to similar obstructive effects. In contrast, many occupational lung diseases, such as silicosis, asbestosis, and farmer's lung, are classified as restrictive lung diseases because the irritant causes interstitial inflammation and fibrosis, resulting in loss of compliance, or "stiff lung." Chronic obstructive pulmonary disease causes irreversible and progressive damage to the lungs. Eventually, respiratory failure may result because of severe hypoxia or hypercapnia. In many patients, COPD leads to the development of cor pulmonale, right-sided congestive heart failure due to lung disease The prevalence of COPD is probably underestimated because many people are unaware they have it, particularly in the early stages when symptoms are minimal or masked by the primary problem. The percentage of females has greatly increased, as has the number of deaths. In 2002 there were 124,816 deaths in the United States. In 2005 the breakdown by disease showed approximately 4.1 million persons had emphysema, 9.5 million had chronic bronchitis, and 16 million had asthma in the United States. The CDC states that COPD is the fourth most common cause of mortality in the United States, and WHO estimates that COPD will become the fourth cause of deaths globally by 2020; the current global mortality is 2.74 million.

Discuss the potential problems with the varying degrees of hypertension during pregnancy

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 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 n 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.

Describe the development of 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 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