Peristalsis is a manifestation of two major reflexes within the enteric nervous system that are stimulated by a bolus of foodstuff in the lumen. Mechanical distension and perhaps mucosal irritation stimulate afferent enteric neurons. These sensory neurons synapse with two sets of cholinergic interneurons, which lead to two distinct effects:
One group of interneurons activates excitatory motor neurons above the bolus - these neurons, which contain acetylcholine and substance P, stimulate contraction of smooth muscle above the bolus.
Another group of interneurons activates inhibitory motor neurons that stimulate relaxation of smooth muscle below the bolus. These inhibitor neurons appear to use nitric oxide, vasoactive intestinal peptide and ATP as neurotransmitters.
Segmental peristalsis, GI 1~2 movement per minute
After surgery, see active peristalsis before giving food.
Bloody pleural fluid in the chest => tuberculosis or malignancy
=> post-complication of recurrent pneumonia or infection
Pneumonia
bacterial: unilateral, fever, lower consolidation
viral: bilateral, rhonchi, cough
con·sol·i·da·tion
Function: noun
: the process by which an infected lung passes from an aerated collapsible condition to one of airless solid consistency through the accumulation of exudate in the alveoli and adjoining ducts
| Main Entry: rhon·chus |
-k
/| |
Pneumonia is an illness of the lungs and respiratory system in which the alveoli (microscopic air-filled sacs of the lung responsible for absorbing oxygen from the atmosphere) become inflamed and flooded with fluid. Pneumonia can result from a variety of causes, including infection with bacteria, viruses, fungi, or parasites. Pneumonia may also occur from chemical or physical injury to the lungs, or indirectly due to another medical illness, such as lung cancer or alcohol abuse.
Typical symptoms associated with pneumonia include cough, chest pain, fever, and difficulty breathing. Diagnostic tools include x-rays and examination of the sputum. Treatment depends on the cause of pneumonia; bacterial pneumonia is treated with antibiotics.
Pneumonia is a common illness, occurs in all age groups, and is a leading cause of death among the elderly and people who are chronically ill. Vaccines to prevent certain types of pneumonia are available. The prognosis for an individual depends on the type of pneumonia, the appropriate treatment, any complications, and the person's underlying health.
People with infectious pneumonia often have a cough that produces greenish or yellow sputum and a high fever that may be accompanied by shaking chills. Shortness of breath is also common, as is pleuritic chest pain, a sharp or stabbing pain, either felt or worse during deep breaths or coughs. People with pneumonia may cough up blood, experience headaches, or develop sweaty and clammy skin. Other symptoms may include loss of appetite, fatigue, blueness of the skin, nausea, vomiting, and joint pains or muscle aches. Less common forms of pneumonia can cause a variety of other symptoms. For instance, pneumonia caused by Legionella may cause abdominal pain and diarrhea, while pneumonia caused by tuberculosis or Pneumocystis may cause only weight loss and night sweats. In elderly people the manifestations of pneumonia may not be typical. Instead, they may develop new or worsening confusion or may experience unsteadiness leading to falls. Infants with pneumonia may have many of the symptoms above, but in many cases, they are simply sleepy or have decreased appetite.
Physical examination
Individuals with symptoms of pneumonia need medical evaluation. Physical examination by a health care provider may reveal fever or sometimes low body temperature, an increased respiratory rate, low blood pressure, a fast heart rate, or a low oxygen saturation, which is the amount of oxygen in the blood as indicated by either pulse oximetry or blood gas analysis. People who are struggling to breathe, confused, or who have cyanosis (blue-tinged skin) require immediate attention.
Listening to the lungs with a stethoscope (auscultation) can reveal several things. A lack of normal breath sounds, the presence of crackling sounds (rales), or increased loudness of whispered speech (whispered pectoriloquy) can identify areas of the lung which are stiff and full of fluid, called "consolidation." The examiner may also feel the way the chest expands (palpation) and tap the chest wall (percussion) to further localize consolidation. The examiner may also palpate for increased vibration of the chest when speaking (tactile fremitus). [1]
Chest X-rays, sputum cultures and other tests
An important test for detecting pneumonia in unclear situations is a chest x-ray. Chest x-rays can reveal areas of opacity (seen as white) which represent consolidation. Pneumonia is not always seen on x-rays, either because the disease is only in its initial stages, or because it involves a part of the lung not easily seen by x-ray. In some cases, chest CT (computed tomography) can reveal pneumonia which is not seen on chest x-ray. X-rays can be misleading, because other problems, like lung scarring and congestive heart failure, can mimic pneumonia on x-ray. [2] Chest x-rays are also used to evaluate for complications of pneumonia. (See below.)
If an individual is not getting better with antibiotics, or if the health care provider has concerns about the diagnosis, a culture of the person's sputum may be requested. Sputum cultures generally take at least two to three days, so they are mainly used to confirm that the infection is sensitive to an antibiotic that has already been started. A blood sample may similarly be cultured to look for infection in the blood (blood culture). Any bacteria identified are then tested to see which antibiotics will be most effective.
A complete blood count may show a high white blood cell count, indicating the presence of an infection or inflammation. In some people with immune system problems, the white blood cell count may appear deceptively normal. Blood tests may be used to evaluate kidney function (important when prescribing certain antibiotics) or to look for low blood sodium. Low blood sodium in pneumonia is thought to be due to extra anti-diuretic hormone produced when the lungs are diseased (SIADH). Specific blood serology tests for other bacteria (Mycoplasma, Legionella and Chlamydophila) and a urine test for Legionella antigen are available. Respiratory secretions can also be tested for the presence of viruses such as influenza, respiratory syncytial virus, and adenovirus.
Most cases of pneumonia can be treated without hospitalization. Typically, oral antibiotics, rest, fluids, and home care are sufficient for complete resolution. However, people with pneumonia who are having trouble breathing, people with other medical problems, and the elderly may need more advanced treatment. If the symptoms get worse, the pneumonia does not improve with home treatment, or complications occur, the person will often have to be hospitalized.
Antibiotics are used to treat bacterial pneumonia. In contrast, antibiotics are not useful for viral pneumonia, although they sometimes are used to treat or prevent bacterial infections that can occur in lungs damaged by a viral pneumonia. The antibiotic choice depends on the nature of the pneumonia, the most common microorganisms causing pneumonia in the local geographic area, and the immune status and underlying health of the individual. Treatment for pneumonia should ideally be based on the causative microorganism and its known antibiotic sensitivity. However, a specific cause for pneumonia is identified in only 50% of people, even after extensive evaluation. Because treatment should generally not be delayed in any person with a serious pneumonia, empiric treatment is usually started well before laboratory reports are available. In the United Kingdom, amoxicillin is the antibiotic selected for most patients with community-acquired pneumonia, sometimes with added clarithromycin; patients allergic to penicillins are given erythromycin instead of amoxicillin. In North America, where the "atypical" forms of community-acquired pneumonia are becoming more common, azithromycin, clarithromycin, and the fluoroquinolones have displaced amoxicillin as first-line treatment. The duration of treatment has traditionally been seven to ten days, but there is increasing evidence that shorter courses (as short as three days) are sufficient.[3][4][5]
Antibiotics for hospital-acquired pneumonia include vancomycin, third- and fourth-generation cephalosporins, carbapenems, fluoroquinolones, and aminoglycosides. These antibiotics are usually given intravenously. Multiple antibiotics may be administered in combination in an attempt to treat all of the possible causative microorganisms. Antibiotic choices vary from hospital to hospital because of regional differences in the most likely microorganisms, and because of differences in the microorganisms' abilities to resist various antibiotic treatments.
People who have difficulty breathing due to pneumonia may require extra oxygen. Extremely sick individuals may require intensive care treatment, often including intubation and artificial ventilation.
Viral pneumonia caused by influenza A may be treated with rimantadine or amantadine, while viral pneumonia caused by influenza A or B may be treated with oseltamivir or zanamivir. These treatments are beneficial only if they are started within 48 hours of the onset of symptoms. Many strains of H5N1 influenza A, also known as avian influenza or "bird flu," have shown resistance to rimantadine and amantadine. There are no known effective treatments for viral pneumonias caused by the SARS coronavirus, adenovirus, hantavirus, or parainfluenza virus.
Abdominal fluid
exudate – ascites, protein
cirrhosis -> has ascites
if female has ascites, likely to be an ovarian cancer
-
transudate – no WBC, no protein
In medicine (gastroenterology), ascites (also known as hydroperitoneum or more archaically as abdominal dropsy) is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and severe liver disease, its presence can portend other significant medical problems. Diagnosis of the cause is usually with blood tests, an ultrasound scan of the abdomen and direct removal of the fluid by needle or paracentesis (which may also be therapeutic). Treatment may be with medication (diuretics), paracentesis or other treatments directed at the cause.
Classification
Ascites exists in three grades:[1]
Grade 1: mild, only visible on ultrasound
Grade 2: detectable with flank bulging and shifting dullness on physical examination
Grade 3: directly visible, confirmed with fluid thrill (or fluid wave)
[edit] Diagnosis
In addition to the routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation, a diagnostic paracentesis should be performed to sample about 50 to 100 mL of fluid. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as Gram stain and cytology.[2]
The serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[3] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (<>
Ultrasound investigation is often performed prior to attempts to remove fluid from the abdomen. This may reveal the size and shape of the abdominal organs, and Doppler studies may show the direction of flow in the portal vein, as well as detecting Budd-Chiari syndrome and portal vein thrombosis. Additionally, the sonographer can make an estimation of the amount of ascitic fluid, and difficult-to-drain ascites may be drained under ultrasound guidance. Abdominal CT scan is a more accurate alternate to reveal abdominal organ structure and morphology.
Causes
Causes of high SAAG ("transudate") are:[2]
Cirrhosis - 81% (alcoholic in 65%, viral in 10%, cryptogenic in 6%)
Heart failure - 3%
Budd-Chiari syndrome or veno-occlusive disease
Causes of low SAAG ("exudate") are:
Cancer (primary peritoneal carcinomatosis and metastasis) - 10%
Tuberculosis - 2%
Pancreatitis - 1%
There is an important distinction between transudates and exudates. Transudates are caused by disturbances of hydrostatic or colloid osmotic pressure, not by inflammation. Medical distinction between transudates and exudates is through the measurement of the specific gravity of extracted fluid. Specific gravity is used to measure the protein content of the fluid. The higher the specific gravity, the greater the likelihood of capillary permeability changes in relation to body cavities.
Ascites is the accumulation of nonsanguinous fluid in the peritoneal cavity.
| 16.2 Mechanisms | page 33 |
With significant liver disease, albumin synthesis is reduced. Low serum albumin results in a decrease in intravascular osmotic pressure. This causes renal blood flow changes, resulting in sodium and water retention. Increased aldosterone levels, possibly due to decreased catabolism of this hormone by the liver, also contribute. There is a generalized salt and water retention, but the fluid accumulation may be confined to the peritoneal cavity or may be associated with peripheral edema. Ascites develops because of increased portal pressure and the transudation of fluid from the capillaries in the portal system to the peritoneal cavity. Hepatic lymph production also increases and extravasates directly into the peritoneal cavity.
| 16.3 Signs and Symptoms | page 33 |
Ascites most commonly presents with increasing abdominal girth, often associated with an uncomfortable feeling of distention, and sometimes nausea and anorexia. Shortness of breath may develop, resulting from either elevation of the diaphragm or pleural effusion. Ankle edema may accompany ascites.
Clinical examination reveals flank fullness on inspection. "Shifting dullness" or a "fluid thrill" may be elicited. Smaller amounts of fluid may be detected on ultrasound when clinical signs are absent. One should look for other signs of portal hypertension, such as dilated abdominal wall veins or an enlarged spleen.
| 16.4 Differential Diagnosis | page 33 |
Newly developed ascites must have a diagnostic aspiration to determine the albumin level, cell count and cytology. The fluid should be clear and straw-colored. Occasionally, lymph can accumulate in the peritoneal cavity, causing "chylous ascites," which requires different management. Ascitic fluid may become infected, in which case the white blood cell count will be elevated in the fluid. If the fluid is sanguinous, other causes _ such as infection or malignancy _ must be sought. The serum ascites albumin gradient is the best way of confirming if the ascitic fluid is secondary to portal hypertension. In this situation the gradient is high _ i.e., >11 g/L _ whereas it is low if the ascites is due to peritoneal carcinomatosis. This is far more accurate than our previous assessment of transudative versus exudative ascites.
| 16.5 Approach to Management | page 34 |
Management initially includes bed rest and salt restriction. Most cases also require adding a diuretic such as spironolactone. Careful aspiration of large quantities (up to 8 L) of ascitic fluid may be necessary in some resistant cases; this can be safely performed, and if the serum albumin level is very low an intravenous infusion of albumin is given before the paracentesis.
fluid wave a sign of free fluid in the abdominal cavity; percussion on one side of the abdomen transmits a wave that is felt on the opposite side.
Hypertympany?
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Symptoms of Cirrhosis
spider angioma
Spider angiomas, also known as "nevus araneus," are a type of angioma found slightly below the skin's surface. They often contain a central red spot, and reddish extensions that radiate outward like a spider's web.
[edit] Seen in
Pregnancy.
- They are often associated with high estrogen levels, so they are commonly found on pregnant women.
Liver disease.
- People with impaired liver function may also exhibit spider angiomas, possibly because the liver is not processing excess estrogen properly.
birth control pills
unknown etiology
[edit] Location
Trunk
face
hemorrhoid
Hemorrhoids (also known as haemorrhoids, emerods, or piles) are varicosities or swelling and inflammation of veins in the rectum and anus. (I84.3-I84.5) External hemorrhoids are those that occur outside of the anal verge (the distal end of the anal canal). They are sometimes painful, and can be accompanied by swelling and irritation. Itching, although often thought to be a symptom from external hemorrhoids, is more commonly due to skin irritation.
(I84.3) If the vein ruptures and a blood clot develops, the hemorrhoid becomes a thrombosed hemorrhoid.
(I84.0-I84.2) Internal hemorrhoids are those that occur inside the rectum. As this area lacks pain receptors, internal hemorrhoids are usually not painful and most people are not aware that they have them. Internal hemorrhoids, however, may bleed when irritated.
(I84.1) Untreated internal hemorrhoids can lead to two severe forms of hemorrhoids: prolapsed and strangulated hemorrhoids.
Prolapsed hemorrhoids are internal hemorrhoids that are so distended that they are pushed outside of the anus.
If the anal sphincter muscle goes into spasm and traps a prolapsed hemorrhoid outside of the anal opening, the supply of blood is cut off, and the hemorrhoid becomes a strangulated hemorrhoid. After visual examination of the anus and surrounding area for external or prolapsed hemorrhoids, a doctor would conduct a digital examination. In addition to probing for hemorrhoidal bulges, a doctor would also look for indications of rectal tumor or polyp, enlarged prostates and abscesses.
Visual confirmation of hemorrhoids can be done using a medical device called an anoscope. This device is basically a hollow tube with a light attached at one end that allows the doctor to see the internal hemorrhoids, as well as polyps in the rectum.
If warranted, more detailed examinations, such as sigmoidoscopy and colonoscopy can be performed. In sigmoidoscopy, the last 60cm of the colon and rectum are examined whereas in colonoscopy the entire bowel is examined.
A pathologist will look for dilated vascular spaces which exhibit thrombosis and recanalization.
Medical treatments
Some people require the following medical treatments for chronic or severe hemorrhoids:
Rubber band ligation: elastic bands are applied onto an internal hemorrhoid to cut off its blood supply. Within several days, the withered hemorrhoid is sloughed off during normal bowel movement.
Hemorrhoidolysis/Galvanic Electrotherapy: desiccation of the hemorrhoid by electrical current.
Sclerotherapy (injection therapy): sclerosant or hardening agent is injected into hemorrhoids. This causes the vein walls to collapse and the hemorrhoids to shrivel up.
Cryosurgery: a frozen tip of a cryoprobe is used to destroy hemorrhoidal tissues. Rarely used anymore because of side effects
Laser, infrared or BICAP coagulation: laser, infrared beam, or electricity is used to cauterize the affected tissues. Lasers are now much less popular.
Hemorrhoidectomy: a true surgical procedure to excise and remove hemorrhoids.
Stapled Hemorrhoidectomy: Also called the procedure for prolapse and hemorrhoids, it is designed to resect soft tissue proximal to the dentate line, which disrupts the blood flow to the hemorrhoids. It is generally less painful than complete removal of hemorrhoids and also allows for faster recovery times. It's meant for hemorrhoids that fall out or bleed and is not helpful for painful outside conditions.
Enema: This Practice is only used to clean the rectum in some cases and only done by an M.D. Water is injected into the rectum and then flushed out cleaning the area.
Doppler Guided Hemorrhoidal Artery Ligation : The only evidence based surgery for all grades of hemorrhoids. It does not involve cutting tissues or even a stay at the hospital; patients are usually back to work on the same day. Best treatment for bleeding piles, as the bleeding stops immediately.[citation needed]
[edit] Diseases with similar symptoms
Symptoms associated with rectal cancer, anal fissure, anal abscess, anal fistula, and other diseases may be similar to those produced by hemorrhoids and may be reduced by the topical analgesic methods described above. For this reason, it is a good idea to consult with a physician when these symptoms are encountered, particularly for the first time, and periodically should the problem continue.
carput medussa(?)
azygous vein is compromised in cirrhotic patient, blood vessel rupture, hematemesis(vomiting of blood)
neurological sign, asterixis
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Cirrhosis is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrotic scar tissue as well as regenerative nodules, leading to progressive loss of liver function. Cirrhosis is most commonly caused by alcoholism and hepatitis C, and was the 12th leading cause of death in the United States in 2000.[1] Ascites is the most common complication of cirrhosis and is associated with a poor quality of life, increased risk of infections, and a poor long term outcome. In advanced stages of cirrhosis, the condition is irreversible and the only option would be a liver transplant.
Complications
As the disease progresses, complications may develop. In some people, these may be the first signs of the disease.
Bruising and bleeding due to decreased production of coagulation factors.
Itching due to bile products deposited in the skin.
Hepatic encephalopathy - the liver does not clear ammonia and related nitrogenous substances from the blood, which affect cerebral functioning: neglect of personal appearance, unresponsiveness, forgetfulness, trouble concentrating, or changes in sleep habits.
Sensitivity to medication due to decreased metabolism of the active compounds.
Hepatocellular carcinoma is primary liver cancer, a frequent complication of cirrhosis. It has a high mortality rate.
Portal hypertension - blood normally carried from the intestines and spleen through the portal vein flows more slowly and the pressure increases; this leads to the following complications:
Ascites - fluid leaks through the vasculature into the abdominal cavity.
Esophageal varices - collateral portal blood flow through vessels in the stomach and esophagus. These blood vessels may become enlarged and are more likely to burst.
Problems in other organs. Cirrhosis can cause immune system dysfunction, leading to infection. Fluid in the abdomen (ascites) may become infected with bacteria normally present in the intestines (spontaneous bacterial peritonitis). Cirrhosis can also lead to impotence, brain dysfunction and renal failure (hepatorenal syndrome) and osteoporosis.
Causes
Cirrhosis has many possible causes; sometimes more than one cause are present in the same patient. In the Western World, chronic alcoholism and hepatitis C are the most common causes.
Alcoholic liver disease (ALD). Alcoholic cirrhosis develops in 15% of individuals who drink heavily for more than a decade. There is great variability in the amount of alcohol needed to cause cirrhosis (as little as 3-4 drinks a day in some men and 2-3 in some women). Alcohol seems to injure the liver by blocking the normal metabolism of protein, fats, and carbohydrates. Patients may also have concurrent alcohol hepatitis with fever, hepatomegaly, jaundice, and anorexia. AST and ALT are both elevated but less than 300 IU/L with a AST:ALT ratio > 2.0, a value rarely seen in other liver diseases. Liver biopsy may show hepatocyte necrosis, Mallory bodies, neutrophilic infiltration with perivenular inflammation.
Chronic hepatitis C. Infection with this virus causes inflammation of and low grade damage to the liver that over several decades can lead to cirrhosis. Can be diagnosed with serologic assays that detect hepatitis C antibody or viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used screening test in the US.
Chronic hepatitis B. The hepatitis B virus is probably the most common cause of cirrhosis worldwide, especially South-East Asia, but it is less common in the United States and the Western world. Hepatitis B causes liver inflammation and injury that over several decades can lead to cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but accelerates cirrhosis in co-infection. Chronic hepatitis B can be diagnosed with detection of HBsAG > 6 months after initial infection. HBeAG and HBV DNA are determined to assess whether patient will need antiviral therapy.
Non-alcoholic steatohepatitis (NASH). In NASH, fat builds up in the liver and eventually causes scar tissue. This type of hepatitis appears to be associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications. This disorder is similar to that of alcohol liver disease but patient does not have an alcohol history. Biopsy is needed for diagnosis and appears similar to that in alcohol liver disease.
Primary biliary cirrhosis. May be asymptomatic or complain of fatigue, pruritus, and non-jaundice skin hyperpigmentation with hepatomegaly. There is prominent alkaline phosphatase elevation as well as elevations in cholesterol and bilirubin. Gold standard diagnosis is antimitochondrial antibodies with liver biopsy as confirmation if showing florid bile duct lesions.
Primary sclerosing cholangitis. PSC is a progressive cholestatic disorder presenting with pruritus, steatorrhea, fat soluble vitamin deficiencies, and metabolic bone disease. There is a strong association with inflammatory bowel disease (IBD), especially ulcerative colitis. Diagnosis is best with contrast cholangiography showing diffuse, multifocal strictures and focal dilation of bile ducts, leading to a beaded appearance. Non-specific serum immunoglobulins may also be elevated.
Autoimmune hepatitis. This disease is caused by the immunologic damage to the liver causing inflammation and eventually scarring and cirrhosis. Findings include elevations in serum globulins, especially gamma globulins. Therapy with prednisone +/- azathioprine is beneficial. Cirrhosis due to autoimmune hepatitis still has 10-year survival of 90%+. There's no specific tool to diagnose autoimmune but it can be beneficial to initiate a trial of corticosteroids.
Hereditary hemochromatosis. Usually presents with family history of cirrhosis, skin hyperpigmentation, diabetes mellitus, pseudogout, and/or cardiomyopathy, all due to signs of iron overload. Labs will show fasting transferrin saturation of > 60% and ferritin > 300 ng/mL. If hepatic iron > 71 umol/g, it is highly suggestive of homozygous HH and warrants genetic testing or liver biopsy. Biopsy is stained with Prussian blue and may detect fibrosis. Heterozygotes do not develop cirrhosis.
Wilson's disease. Autosomal recessive disorder characterized by low serum ceruloplasmin and increased hepatic copper content on liver biopsy. May also have Kayser-Fleischer rings in the cornea and altered mental status.
Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive disorder. Patients may also have COPD. Serum AAT will be low.
Cardiac cirrhosis. Due to chronic right sided heart failure which leads to liver congestion.
Drugs or toxins, including chronic use of acetaminophen.
Certain parasitic infections (like schistosomiasis).
Pathophysiology
The liver plays a vital role in synthesis of proteins (e.g. albumin, clotting factors and complement), detoxification and storage (e.g. vitamin A). In addition, it participates in the metabolism of lipids and carbohydrates.
Cirrhosis is often preceded by hepatitis and fatty liver (steatosis), independent of the cause. If the cause is removed at this stage, the changes are still fully reversible.
The pathological hallmark of cirrhosis is the development of scar tissue that replaces normal parenchyma, blocking the portal flow of blood through the organ and disturbing normal function. Iredale (2003) summarises the pivotal role of stellate cell, a cell type that normally stores vitamin A, in the development of cirrhosis. Damage to the hepatic parenchyma leads to activation of the stellate cell, which becomes contractile and obstructs blood flow in the circulation. In addition, it secretes TGF-β1, which leads to a fibrotic response and proliferation of connective tissue. Furthermore, it disturbs the balance between matrix metalloproteinases and the naturally occurring inhibitors (TIMP 1 and 2), leading to matrix breakdown and replacement by connective tissue-secreted matrix.
The fibrous tissue bands (septa) separate hepatocyte nodules, which eventually replace the entire liver architecture, leading to decreased blood flow throughout. The spleen becomes congested, which leads to hypersplenism and increased sequestration of platelets. Portal hypertension is responsible for most severe complications of cirrhosis.
Treatment
Liver damage from cirrhosis cannot be reversed, but treatment can stop or delay further progression and reduce complications. Close follow-up is often necessary. Alcohol and acetaminophen, as well as other potentially damaging substances, are discouraged. A healthy diet is encouraged, as cirrhosis may be an energy-consuming process. Salt restriction is often necessary, as cirrhosis leads to accumulation of salt (sodium retention). High-protein food increases the nitrogen balance, and would theoretically increase encephalopathy; in the past, this was therefore eliminated as much as possible from the diet. Recent studies show that this assumption was incorrect, and high-protein foods are even encouraged to maintain adequate nutrition.
Treatment exists of elimination of the causes and preventing complications:
Elimination of causes: alcoholic cirrhosis caused by alcohol abuse is treated by abstaining from alcohol. Treatment for hepatitis-related cirrhosis involves medications used to treat the different types of hepatitis, such as interferon for viral hepatitis and corticosteroids for autoimmune hepatitis. Cirrhosis caused by Wilson's disease, in which copper builds up in organs, is treated with chelation therapy (e.g. penicillamine) to remove the copper.
Preventing complications. Diuretics may be necessary to suppress ascites. Antibiotics will be prescribed for infections, and various medications can help with itching. Laxatives, such as lactulose, decrease risk of constipation; their role in preventing encephalopathy is limited. For portal hypertension, propranolol is a commonly used agent to lower blood pressure over the portal system.
In severe complications from portal hypertension, transjugular intrahepatic portosystemic shunting is occasionally indicated to relieve pressure on the portal vein.
If complications cannot be controlled or when the liver ceases functioning, a liver transplant is necessary. Survival from liver transplantation has been improving over the 1990s and is now around 90%, depending largely on the severity of disease in the recipient. Transplantation necessitates the use of immune suppressants (ciclosporin or tacrolimus).
Coffee has recently (June 2006) been found to [1]cut cirrhosis risk.
In cellular pathology, steatosis is a condition which is a marker of sublethal cellular injury. It is also known as fatty change. It is characterised by the presence of abnormally large quantities of fat within a cell. Steatosis may affect the cells of a variety of tissues and organs. It reflects an impairment of the normal process of constant synthesis and breakdown of triglyceride fat.
Steatosis may occur in the liver as a result of a variety of stresses, including hepatitis C and exposure to poisons such as ethanol (alcohol) and in obesity. The fat accumulates in vesicles that displace the cytoplasm. When the vesicles are sufficiently large that they distort the nucleus, the condition is known as macrovesicular steatosis. Otherwise the condition is known as microvesicular steatosis.
Urea cycle
blood ammonia normal?
Asterixis is a flapping tremor of the hand that is an early sign of hepatic encephalopathy (damage to brain cells due to toxins not cleared from the blood by the liver). The exact cause of this disorder is not known but it is thought to be related to by abnormal ammonia metabolism.
Asterixis is the medical word to describe flapping tremor (sometimes said to resemble a "bird flapping its wings"). It is best shown in the hand-flapping tremor when the arms are outstretched in extension and the wrist is dorsiflexed. Adams and Foley first described asterixis in 1949 in patients with severe liver failure and encephalopathy. Typically there are brief, arrhythmic interruptions of sustained voluntary muscle contraction causing brief lapses of posture. It is bilateral, and may be asymmetrical with a frequency of 3-5 Hz. Asterixis is seen most often in drowsy or stuporose patients with metabolic encephalopathies, especially in decompensated cirrhosis or acute hepatic failure. It is also seen in some patients with renal failure and azotaemia, and in carbon dioxide narcosis of respiratory failure. Asterixis can also be a feature of Wilson's disease.
The word derives from a- + Greek. stērixis a fixed position.
| Main Entry: frem·i·tus |
Main Entry: crep·i·ta·tion
Pronunciation: 
krep-
-
t
-shn
Function: noun
: a grating or crackling sound or sensation (as that produced by the fractured ends of a bone moving against each other or as that in tissues affected with gas gangrene) <crepitation in the arthritic knee>
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malabsorption from
pancreatitis
cystic fibrosis
celiac disease
deficiency of fat soluble vitamins ADEK
Vitamin B12 deficiency => decreases production of intrinsic factor
vitamin B12 absorbed in fundus, intrinsic factor produced in fundus
Cyanocobalamin is a vitamin commonly known as vitamin B12 (or B12 for short).
Deficiency
The usual daily intake in the Western diet is 5–7 µg (Food and Drug Administration (FDA) Daily Value [6]); the daily requirement is 1–2 µg. B12 is mostly absorbed in the terminal ileum. The production of intrinsic factor in the stomach is vital to absorption of this vitamin. Megaloblastic anemia can result from inadequate intake of B12, inadequate production of intrinsic factor (pernicious anemia), disorders of the terminal ileum resulting in malabsorption, or by competition for available B12 (such as fish tapeworms or bacteria present in blind loop syndrome).
Hematological deficiency is manifested primarily by anemia and macrocytosis; other cell lines such as white blood cells and platelets are often also low. Bone marrow examination may show megaloblastic hemopoiesis. Serum homocysteine and methylmalonic acid levels are also high in B12 deficiency and can be helpful if the diagnosis is unclear.
Neurological signs of B12 deficiency, which can occur without accompanying hematologic abnormalities, include demyelination and irreversible nerve cell death. Symptoms include numbness or tingling of the extremities and an ataxic gait, a syndrome known as subacute combined degeneration of the cord.
The American Psychiatric Association's American Journal of Psychiatry has published studies showing a relationship between depression levels and deficient B12 blood levels in elderly people in 2000 [7] and 2002 [8].
[edit] Diagnosis of B12 deficiency
Serum B12 levels are often low in B12 deficiency, but there does not exist a robust assay, and if other features of B12 deficiency are present then the diagnosis must not be discounted. One possible explanation for normal B12 levels in B12 deficiency is antibody interference in people with high titres of intrinsic factor antibody.[9] Bone marrow aspiration, serum homocysteine and methylmalonic acid levels can also be helpful.[10]
[edit] Treatment of B12 deficiency
Traditionally, treatment for B12 deficiency was through intramuscular injections of cyanocobalamin. However, it has recently been appreciated that deficiency can be treated with oral B12 supplements when given in sufficient doses. When given in oral doses ranging from 0.1–2 mg daily, B12 can be absorbed in a pathway that does not require an intact ileum or intrinsic factor.[11][12] The Schilling test can determine whether symptoms of B12 deficiency are caused by lack of intrinsic factor, though this is being performed less often due to the lack of availability of reagent for the test.
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Intrinsic factor is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 later on in the small intestine.
Upon entry into the stomach, vitamin B12 becomes bound to one of two B12 binding proteins present in gastric juice. In the less acidic environment of the small intestine, these proteins dissociate from the vitamin, enabling it to bind to intrinsic factor and enter the portal circulation through a receptor in the ileal mucosa specific for the B12-intrinsic factor complex.
In pernicious anemia, an autoimmune disease, autoantibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B12, and subsequent megaloblastic anemia. Atrophic gastritis can also cause intrinsic factor deficiency and anemia through damage to the parietal cells of the stomach wall. Pancreatic exocrine insufficiency can interfere with normal dissociation of vitamin B12 from its binding proteins in the small intestine, preventing its absorption via the intrinsic factor complex.
Bariatric surgery is a known risk factor in the development of pernicious anemia. Other risk factors contributing to this condition are stomach tumors, gastric ulcers, and excessive alcohol consumption.
Steatorrhea (or steatorrhoea) is the formation of bulky, grey or light colored stools. Stools may also float and have an oily appearance. There is increased fat excretion, which can be objectivated by determining the fecal fat levels. While definitions have not been standardised, fat excretion in faeces in excess of 0.3 (g/kg)/day is considered indicative of steatorrhea.
Seen in:
malabsorption, e.g. in inflammatory bowel disease, celiac disease, and abetalipoproteinemia
choledocholithiasis (obstruction of the bile duct by a gallstone)
pancreatic cancer (if it obstructs biliary outflow)
parasite
Histoplasmosis, also known as Darling's disease, is a disease caused by the fungus Histoplasma capsulatum. Its symptoms vary greatly, but the disease primarily affects the lungs. Occasionally, other organs are affected—this form of the disease is called disseminated histoplasmosis, and it can be fatal if untreated. H. capsulatum is found throughout the world and is endemic in certain areas of the United States, particularly in states bordering the Ohio River valley and the lower Mississippi River. The fungus has been found in poultry house litter, caves, areas harboring bats, and in bird roosts (particularly those of starlings).
Transmission
H. capsulatum grows in soil and material contaminated with bat or bird droppings. Spores become airborne when contaminated soil is disturbed. Breathing the spores causes infection. The disease is not transmitted from an infected person to someone else. Plants fertilized with bat droppings may contain spores and when burned the smoke becomes infectious.
[edit] Symptoms
If symptoms occur, they will start within 3 to 17 days after exposure; the average is 10 days. Most infected persons have no apparent ill effects. The acute respiratory disease is characterized by respiratory symptoms, a general ill feeling, fever, chest pains, and a dry or nonproductive cough. Distinct patterns may be seen on a chest x-ray. Chronic lung disease resembles tuberculosis and can worsen over months or years. The disseminated form is fatal unless treated. While histoplasmosis is the most common cause of fibrosing mediastinitis, this remains a relatively rare disease.
[edit] Treatment
Antifungal medications are used to treat severe cases of acute histoplasmosis and all cases of chronic and disseminated disease. Mild disease usually resolves without treatment. Past infection results in partial protection against ill effects if reinfected.
Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii. The parasite infects most warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by contact with cat faeces, or by transmission from mother to fetus. The most common means of transmission to humans is raw or undercooked meat. The illness is usually minor and self-limiting.
Between 30 and 60 percent of the world population is estimated to carry a Toxoplasma infection. After the first few weeks of infection (where it typically causes mild or no illness, or a flu-like illness) have passed, the parasite rarely causes any symptoms in otherwise healthy adults. However, people with a weakened immune system, such as those infected with HIV, may become seriously ill, and it can occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases and can affect the heart, liver, and eyes (chorioretinitis).
Transmission may occur through:
Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma cysts. Infection prevalence in countries where undercooked meat is traditionally eaten, such as France, has been related to this transmission method. Oocysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat.[1]
Ingestion, accidental or otherwise, of contaminated cat feces. This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits, or touching anything that has come into contact with cat feces.
Drinking water contaminated with Toxoplasma.
Transplacental infection in utero.
Receiving an infected organ transplant or blood transfusion, although this is extremely rare.[1]
The cyst form of the parasite is extremely hardy, capable of surviving exposure to freezing down to -12 Centrigrade, moderate temperatures and chemical disinfectants such as bleach, and can survive in the environment for over a year. It is, however, susceptible to high temperatures-above 66 Centrigrade, and is thus killed by thorough cooking, and would be killed by 24 hours in a typical domestic freezer.[2]
Although the pathogen has been detected on the fur of cats, it has not been found in an infectious form, and direct infection from handling cats is generally believed to be very rare. Cats excrete the pathogen in their faeces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat faeces are not generally contagious for the first day or two after excretion, after which the cyst 'ripens' and becomes potentially pathogenic. Studies have shown that only about 2% of cats are shedding at any one time, and that shedding does not recur even after repeated exposure to the parasite.
Clinical manifestations
Infection has two stages:
[edit] Acute toxoplasmosis
During acute toxoplasmosis, symptoms are often flu-like: swollen lymph nodes, or muscle aches and pains that last for a month or more. Rarely, a patient with a fully functioning immune system may develop eye damage from toxoplasmosis. Young children and immunocompromised patients, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain or the eyes. Only a small percentage of infected newborns have serious eye or brain damage at birth.
[edit] Treatment
The vast majority of patients with a normal immune system require no treatment.
Patients with HIV/AIDS or patients who are immunosuppressed should be given sulfadiazine and pyrimethamine. Pregnant women who become ill with acute toxoplasmosis should be treated with spiramycin. Folinic acid (leucovorin) is administered in all cases to reduce the bone marrow suppression caused by pyrimethamine (ref: Montoya JG, Liesenfeld O. Toxoplasmosis. Lancet. 2004 Jun 12;363(9425):1965-76. )
[edit] Latent toxoplasmosis
Most patients who become infected with Toxoplasma gondii and develop toxoplasmosis do not know it. In most non-immunodeficient patients, the infection enters a latent phase, during which only bradyzoites are present, forming cysts in nervous and muscle tissue. Most infants who are infected while in the womb have no symptoms at birth but may develop symptoms later in life.
[edit] Treatment
The cysts are immune to the standard acute treatments as the antibiotics do not reach the bradyzoites in sufficient concentration.
The antibiotic atovaquone has been used to kill Toxoplasma cysts in situ in AIDS patients.[3] In mice, a combination of atovaquone with clindamycin seemed to optimally kill cysts.[4]
[edit] Risk factors
Infants born to mothers who became infected with Toxoplasma for the first time during or just before pregnancy.
Persons with severely weakened immune systems, such as those with AIDS. Illness may result from an acute Toxoplasma infection or reactivation of an infection that occurred earlier in life.
TORCH = congenital, vertical to baby, cross placenta
five groups of chronic infections: toxoplasmosis, other viruses, rubella, cytomegalovirus (CMV), and herpes simplex virus (HSV). The "other viruses" usually include syphilis, hepatitis B, coxsackie virus, Epstein-Barr virus (mononucleosis), varicella-zoster virus, and human parvovirus.
granuloma = epitheloid cells + macrophage cells
=> calcified, accumulation of dbris
In medicine (anatomical pathology), a granuloma is a group of epithelioid macrophages surrounded by a lymphocyte cuff. Granulomas are small nodules that are seen in a variety of diseases such as Crohn's disease, tuberculosis, sarcoidosis, berylliosis and syphilis. It is also a feature of Wegener's granulomatosis and Churg-Strauss syndrome, two related autoimmune disorders.
An important aspect of granulomas is whether they are caseating or not. Caseation (literally: turning to cheese) is a form of necrosis at the centre of a granuloma and is a feature of the granulomas of tuberculosis.
rubella crosses blood brain barrier, all TORCH cross brain blood barrier
CIA form the brain of spinal cord
CMV retinitis in immunosuppressed
forscanet, inclusion bodies
malignant melanoma – ABCDE?
A popular method for remembering the signs and symptoms of melanoma is the mnemonic "ABCDE":
Asymmetrical skin lesion.
Border of the lesion is irregular.
Color: melanomas usually have multiple colors.
Diameter: moles greater than 5 mm are more likely to be melanomas than smaller moles.
Evolution: The evolution (ie change) of a mole or lesion may be a hint that the lesion is becoming malignant --or-- Elevation: The mole is raised or elevated above the skin.
deadliest, abdomen, toe
Basal cell carcinoma
“crater” apperance, dimple, same location as SCC but does not metastasize, palasadin, nuclei, bird-flying wings, deeper and bloody looking
Basal cell carcinoma (BCC) is the most common skin cancer. It can be destructive and disfiguring. Risk is increased for individuals with a family history of the disease and a high cumulative exposure to UV light via sunlight or, in the past, carcinogenic chemicals especially arsenic. Treatment is with surgery, topical chemotherapy, x-ray, cryosurgery, photodynamic therapy. It is rarely life-threatening but if left untreated can be disfiguring, cause bleeding and produce local destruction (eg., eye, ear, nose, lip).
Forms
Various forms are recognised:
Nodular: flesh-colored papule with telangiectasis. If it ulcerates, it becomes a "rodent ulcer" (ulcus rodens), an ulcerating nodule with (often) a pearly border.
Cystic: rarer and hard to distinguish from the nodular form. It has a central cavity with fluid.
Pigmented: a variant of the nodular form that may be confused with melanoma.
Sclerosing/cicratising: a scar-like lesion.
Superficial: a red scaling patch
About two thirds of the carcinomas occur in sun-exposed areas and one third occur in non-sun-exposed areas, emphasizing the genetic susceptability of the basal cell cancer patients.
squamous cell carcinoma
may metastasize, keratin peel, PLE popple
In medicine, squamous cell carcinoma is a form of cancer of the carcinoma type that may occur in many different organs, including the skin, mouth, esophagus, lungs, and cervix. It is a malignant tumour of epithelium that shows squamous cell differentiation.
Squamous cell carcinomas account for about 20% of non-melanoma skin cancers, (with basal cell carcinomas accounting for about 80%), but are clinically more significant because of their ability to metastasize. Squamous cell carcinoma is usually developed in the epithelial layer of the skin and sometimes in various mucous membranes of the body. This type of cancer can be seen on the skin, lips, inside the mouth, throat or esophagus. This type of cancer is characterized by red, scaly skin that becomes an open sore.
When associated with the lung, it often causes ectopic production of parathyroid hormone-related protein (PTHrP), resulting in hypercalcemia.
Squamous cell carcinoma strikes more than 200,000 people in the United States alone every year. Smoking is a significant risk factor. Other risk factors include sun exposure, radiation therapy, exposure to carcinogens, chronic skin irritation or inflammation, genetic diseases, and presence of premalignant lesions.
A carcinoma can be characterized as either in situ (confined to the original site) or invasive.
Squamous cell carcinoma of the skin is often caused by long term exposure to the sun. To be diagnosed, a biopsy is done where a sample is taken and examined under a microscope. If it is found to be cancerous, a surgery is done to remove it.
Squamous cell cancer can also occur after organ (e.g. heart, kidney) transplantation. Anti-rejection drugs, that ensure the organ is not rejected by the body, can also lower the immune system. This can be a major factor towards squamous cell skin cancer.
causes of SCC – smoking, arsenic exposure, benzene, UV exposure
causes of BCC – UV
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osteosarcoma, - osteogenic sarcoma – kid 10 ~20 years old, malignant bone tumor
Osteosarcoma is the most common type of malignant bone cancer, accounting for 35% of primary bone malignancies. There is a preference for the metaphyseal region of tubular long bones. 50% of cases occur around the knee. It is a malignant connective (soft) tissue tumor whose neoplastic cells present osteoblastic differentiation and form tumoral bone.
Treatment
Patients with this are best managed by an oncologist and an orthopedic oncologist experienced in managing sarcomas. Current standard treatment is to use neoadjuvant chemotherapy (chemotherapy given before surgery) followed by surgical resection. The percentage of tumor cell necrosis (cell death) seen in the tumor after surgery gives an idea of the prognosis and also lets the oncologist know if the chemotherapy regime should be altered after surgery.
Standard therapy is a combination of limb-salvage orthopaedic surgery and a combination of high dose methotrexate with leucovorin rescue, intra-arterial cisplatin (with or without caffeine(Japan)), adriamycin, ifosfamide with mesna, BCD, etoposide, muramyl tri-peptite (MTP).
Ifosfamide can be used as an adjuvant treatment if the necrosis rate is low.
3-year event free survival ranges from 50% to 75%. and 5-year survival ranges from 60% to 85+% in some studies. Overall, 60-65% treated 5-years ago(2000) will be alive today. Osteosarcoma has one of the lowest survival rates for pediatric cancer despite chemotherapy's success in osteosarcoma of 6 chemotherapies, interferon-alpha, interleukin-2, and being the prototype of solid tumors in cancer.
Treatment studies come from Children's hospital Boston, Memorial Sloan-Kettering, Children's Oncology Group, Italian Oncology Group, Japan, and MD Anderson in Texas.
Fluids are given for hydration.
Drugs like Krytril and Zofran help with nausea and vomiting.
Neupogen, epogen, Neulasta help with white blood cell counts and neutrophil counts.
Blood helps with anemia.
Prognosis is separted into three groups.
Stage I osteosarcoma is rare and includes parosteal osteosarcoma or low-grade central osteosarcoma. It has an excellent prognosis (>90%) with wide resection.
Stage IIb prognosis depends on the site of the tumor (proximal tibia, femur, pelvis, etc.) size of the tumor mass (in cm.), the degree of necrosis from neoadjuvant chemotherapy (beforeoperation chemotherapy), and pathological factors like the degree of p-glycoprotein, whether your tumor is CXCR4 positive, Her2 positive as these can lead to distant metastases to the lung. Longer time to metastases, more than 12 months or 24 months and the number of metastases and resectability of them lead to the best prognosis with metastatic osteosarcoma. It is better to have fewer metastases than longer time to metastases. Those with a longer length of time(>24months) and few nodules (2 or fewer) have the best prognosis with a 2-year survival after the metastases of 50% 5-year of 40% and 10 year 20%. If metastases are both local and regional the prognosis is different unfortunately. (see http://www.osteosarcomasupport.org/prognosis.htm) top two articles.
Initial Presentation of stage III osteosarcoma with lung metastates depends on the resectability of the primary tumor and lung nodules, degree of necrosis of the primary tumor, and maybe the number of metastases. Overall prognosis is 30% or greater depending.
sarcoma – tumor of hard tissue
A sarcoma is a cancer of the connective or supportive tissue (bone, cartilage, fat, muscle, blood vessels).
lipoma – tumor of soft tissue
A lipoma is a common, benign tumor composed of fatty tissue. Lipomas are soft to the touch, sometimes moveable, and are generally painless. They grow very slowly, and have not been found to become cancerous (it should be noted however that malignant liposarcoma also arises from fatty tissue). Many lipomas are small but can enlarge to sizes greater than six centimeters. Lipoma is commonly found in adults from 40 to 60 years of age but can also be found in children. 1/1000 of the general population has a Lipoma.
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The escape of fluid, proteins and blood cells from the vascular system into the interstitial tisssue or body cavities is known as EXUDATION.
An exudate is an inflammatory extravascular fluid that has
- high protein concentration
- much cellular debris
- specific gravity above 1.020
A transudate is a fluid with
- low protein content (most of whom is albumin)
- specific gravity of less than 1.012
- is an ultrafiltrate of blood plasma and results from hydrostatic imbalance across the vascular endotehlium
Edema, excess fluid in the interstitial or serous cavities can be either an exudate or a transudate.
Pus, a purulent exudate is an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris
