Fatty Liver, Cirrhosis, and Related Disorders

Fatty liver, cirrhosis, primary biliary cirrhosis, primary sclerosing cholangitis, and alpha 1 antitrypsin deficiency are all disorders  that result from  an injury to the liver. Injury can be caused by toxins, including alcohol, some drugs, impurities in foods, and the abnormal buildup of normal substances in the blood. Injury to the liver can also be caused by infection or by a disease in which the body attacks its own tissues. Sometimes it can be idiopathic.

Fatty Liver

Fatty liver is an excessive accumulation of a triglyceride inside the liver cells.

In the US and other western countries, the most common causes of fatty liver are alcoholism, obesity, diabetes, and elevated serum triglyceride levels. Other causes include malnutrition, hereditary disorders of metabolism (such as glycogen storage disease), and drugs (such as corticosteroid, tetracycline, and aspirin).

The mechanism by which these diseases or factors cause fat to accumulate within liver cells is not known. Simply eating a high-fat diet, for example, does not produce a fatty liver. One possible explanation is that these diseases or factors slow the rate at which fat is processed (metabolized) and excreted by the body. The resulting buildup of fat within the body, according to this theory, is then stored inside the liver cells.

Sometimes the cause of fatty liver is not clear, especially when it occurs in newborns; however, it is likely to be a defect in the mitochondria of the liver cells.

In some people, a fatty liver does not due to alcohol abuse or drugs and toxins but associated with obesity, diabetes mellitus, and raised serum triglycerides will progress to scarring (fibrosis) and cirrhosis, possibly because of underlying inflammation. This type of fatty liver is sometimes referred to non-alcoholic steatohepatitis.

Symptoms and Diagnosis

Fatty liver usually produces no symptoms. In rare cases, however, it results in jaundice, nausea, vomiting, pain, and abdominal tenderness.

A physical examination that reveals an enlarged liver without any other symptoms suggests fatty liver. Liver function tests are also performed to determine if there is a liver abnormality, such as inflammation, which sometimes accompanies the extra fat in the liver cells and can be associated with the development of cirrhosis in nonalcaholic steatohepatitis.

Excess fat in the liver can be detected on abdominal ultrasound. The diagnosis may be confirmed by a liver biopsy, in which a doctor inserts a long hollow needle through the skin to obtain a small piece of liver tissue for examination inder a microscope.

Fatty Liver from CT scan

Diffuse lower density compared to spleen
Click on image for larger image

Image taken from http://radiology.med.sc.edu/

Prognosis and Treatment

Although excessive fat in the liver may not in itself be a serious problem (the fat can disappear, for example, if the person stops drinking), its underlying cause might be. For example, repeated liver injury from toxic substances such as alcohol may be eventually progress from fatty liver to cirrhosis (severe scarring of the liver). Therefore, treatment of fatty liver aims at minimizing or eliminating the underlying cause of the disorder.

Next week Article : Liver Cirrhosis

Gastroesophageal Reflux Disease (GERD)

  Image taken from http://www.rush.edu/ 

In GastroEsophageal Reflux Disease (GERD), stomach acid and enzymes flow backward from the stomach into the esophagus, causing inflammation and pain in the esophagus.

The stomach lining protects the stomach from effects of its own acid. Because the esophagus lacks a similar protective lining, stomach acid and enzymes that flow backward (reflux) into the esophagus routinely cause symptoms and in some cases damage.

Acid and enzymes reflux when the lower esophageal sphincter, the ring-shaped muscle that normally prevents the contents of the stomach from flowing back into the esophagus is not functioning properly.

When a person is standing or sitting, gravity helps to prevent the reflux of stomach contents into the esophagus. This explains why reflux can worsen when a person is lying down.

Smoking and certain foods, such as chocolate, interfere with the sphincter muscle, making reflux more likely. Reflux is also more likely to occur after soon after meals, when the volume and acidity of contents in the stomach are higher.

Alcohol and coffee also stimulate acid production.

Delayed emptying of the stomach (for example due to diabetes or use of opioids) can also worsen reflux.

 

 

Symptoms and Complication

 Image taken from http://www.thehealthword.com/

 

Heartburn (a burning pain behind the sternum) is the most obvious symptoms of GERD. Sometimes the pain even extends to the neck, throat, and face. Heartburn may be accompanied by regurgitation, in which the stomach contents reach the mouth.

Inflammation of the esophagus (esophagitis) may cause bleeding that is usually slight but can be massive. The blood may be vomited up or may pass through the digestive tract, resulting in the passage of dark, tarry stools (melena) or bright red blood, if the bleeding is brisk enough.

Esophageal ulcers, which are open sores on the lining of the esophagus, can result from repeated reflux. They can cause pain that is usually located behind the sternum or just below it, similar to the location of heartburn.

Narrowing (stricture) of the esophagus from reflux makes swallowing solid foods increasingly more difficult. narrowing of the airways can cause shortness of breath and wheezing.

Other symptoms of GERD include chest pain, sore throat, hoarseness of voice, excessive salivation, a sensation of a lump in the throat (globus sensation), and inflammation of the sinuses (sinusitis)

With prolonged irritation of the lower part of the esophagus from repeated reflux, the cells lining the esophagus may change (resulting in a condition called Barett's esophagus). Changes may occur even in the absence of symptoms. These abnormal cells are precancerous and progress to cancer rarely.

 

 

Diagnosis

The symptoms point to the diagnosis, and treatment can be started without detailed diagnostic testing. Specific testing is usually reserved for situations in which the diagnosis is not clear or treatment has failed to control symptoms.

Examination of the esophagus using and endoscope of the lower esophageal sphincter, and esophageal pH tests are sometimes needed to help confirm the diagnosis and check for complications.

Endoscopy may confirm the diagnosis if the doctor finds that the person has esophagitis or Barrett's esophagus. Endoscopy also helps to exclude the presence of esophageal cancer.

X-rays taken after a person drinks a barium solution and then lies on an incline with the head lower than the feet may show reflux of the barium from the stomach into the esophagus. A doctor may press on the abdomen to increase the like hood of reflux. The x-rays taken after the barium is swallowed also can reveal esophageal ulcers or a narrowed esophagus.

Pressure measurements at the lower esophageal sphincter indicate the strength of the sphincter and can distinguish a normal sphincter from a poorly functioning one. The information gained from this test helps the doctor decide whether surgery is an appropriate treatment.

Some doctors believe that the best test for GERD is esophageal pH testing. In this test, a thin, flexible tube with a sensor probe on the tip is paced through the nose an into the lower esophagus. The other end of this tube is attached to a monitor that the person wears on his belt. The monitor records the acid levels in the esophagus, usually for 24 hours. Besides determining how much reflux is occurring, this test identifies much the relationship between symptoms and reflux and is particularly helpful for people with symptoms that are not typical for reflux.

The esophageal pH test is needed for all people being considered for surgery for GERD. 

 

 

Prevention and Treatment

Several measures may be taken to relieve GERD.

Raising the head of the bed about 6 inches can prevent acid from flowing into the esophagus as a person sleeps.

Specific foods (for example, fats an chocolate) should be avoided, as should smoking and certain drugs (for example, anticholinergic, certain antidepressants, calcium channel blockers, and nitrates), all of which increase the tendency of the lower esophageal sphincter to leak.

A doctor may prescribe a cholinergic drug (for example, bethanechol or metoclopramide) to make the lower sphincter close more tightly.

Coffee, alcohol, and other substances that strongly stimulate the stomach to produce acid or that delay stomach emptying should be avoided as well.

Many of the drugs used to treat gastritis and peptic ulcers also help prevent and treat GERD.

Antacids taken at bedtime, for example, are helpful. Antacids can usually relieve the pain of esophageal ulcers by reducing the amount of acid that reaches the esophagus.

However, proton pump inhibitors, the most powerful drugs for reducing acid production, are usually the most effective treatment for GERD, because even small amount of acid can cause significant symptoms. Healing requires drugs that reduce stomach acid over a 4 to 12 week period. The ulcers heal slowly, tend to recur, and, when chronic and severe, can leaved a narrowed esophagus after healing.

Esophageal narrowing is treated with drug therapy and repeated dilation, which may be performed using balloons or progressively larger dilators. If dilation is successful narrowing does not seriously limit what a person can eat.

Barrett's esophagus may or may not disappear when treatment relieves symptoms. Therefore, people with Barrett's esophagus are asked to undergo an endoscopic examination every 2 to 3 years to ensure that it is not progressing to cancer.

Surgery is an option for people whose symptoms are unresponsive to drug therapy or for people with esophagitis that persists even after symptoms are relieved. In addition, surgery may be the preferred treatment for people who do not like the prospect of having to take drugs for many years. A minimally invasive procedure performed through a laparoscope is available. However, 20 to 30% of people who undergo this procedure experience side effects, most commonly difficulty swallowing and a sensation of bloating or abdominal discomfort after eating.

Peptic Ulcer

Definition

A hole in the lining of the stomach, duodenum, or esophagus. A peptic ulcer of the stomach is called a gastric ulcer, an ulcer of the duodenum is a duodenal ulcer, and a peptic ulcer of the esophagus is an esophageal ulcer. A peptic ulcer occurs when the lining of these organs is corroded by the acidic digestive juices which are secreted by the stomach cells.

 

 

Types of peptic ulcer

Gastric ulcer. This is a peptic ulcer that occurs in your stomach.

Duodenal ulcer. This type of peptic ulcer develops in the first part of the small intestine (duodenum).

Esophageal ulcer. An esophageal ulcer is usually located in the lower section of your esophagus. It's often associated with chronic gastroesophageal reflux disease (GERD).

 

 

 Symptoms of peptic ulcers

A burning pain in the gut is the most common symptom. The pain feels like a dull ache comes and goes for a few days or weeks starts 2 to 3 hours after a meal comes in the middle of the night when your stomach is empty usually goes away after you eat.

Other symptoms are

1. losing weight

2. not feeling like eating

3. having pain while eating

4. feeling sick to your stomach

5. vomiting

Risk Factors for Ulcer

 

Helicobacter pylori infection — The exact source of Helicobacter pylori is not known, but it may be transmitted by person-to-person contact. Be sure to always wash your hands after using the bathroom and before eating.

 

Over-the-counter pain medications such as aspirin or ibuprofen — Frequent use of these medications can block the production of certain substances that protect the stomach lining. If you have an ulcer, limit or eliminate use of these kinds of drugs.

 

Alcohol consumption — Alcohol irritates the stomach lining and increases stomach acid output.

Smoking — Smoking increases the volume and concentration of acid secreted by the stomach. If you have an ulcer, quit smoking.

 

Family history of ulcers — People with family members with ulcers are more susceptible to getting them; the reason for this is not known

Diagnosis

Diagnosis of peptic ulcer is suggested by patient history and confirmed by endoscopy.

Empiric therapy is often begun without definitive diagnosis. However, endoscopy allows for biopsy or cytologic brushing of gastric and esophageal lesions to distinguish between simple ulceration and ulcerating stomach cancer.

Stomach cancer may present with similar manifestations and must be excluded, especially in patients who are > 45, have lost weight, or report severe or refractory symptoms. The incidence of malignant duodenal ulcer is extremely low, so biopsies of lesions in that area are generally not warranted. Endoscopy can also be used to definitively diagnose H. pylori infection, which should be sought when an ulcer is detected.

Gastrin-secreting malignancy and Zollinger-Ellison syndrome should be considered when there are multiple ulcers, when ulcers develop in atypical locations (eg, postbulbar) or are refractory to treatment, or when the patient has prominent diarrhea or weight loss. Serum gastrin levels should be measured in these patients.

Treatment

Antibiotic medications. Doctors use combinations of antibiotics to treat H. pylori because one antibiotic alone isn't sufficient to kill the organism. For the treatment to work, it's essential that you follow your doctor's instructions precisely. Antibiotics commonly prescribed for treatment of H. pylori include amoxicillin (Amoxil), clarithromycin (Biaxin) and metronidazole (Flagyl). Some companies package a combination of two antibiotics together, with an acid suppressor or cytoprotective agent specifically for treatment of H. pylori infection. These combination treatments are sold under the names Prevpac and Helidac. Other medications prescribed in conjunction with antibiotics generally are taken for a longer period.

Acid blockers. Acid blockers - also called histamine (H-2) blockers - reduce the amount of hydrochloric acid released into your digestive tract, which relieves ulcer pain and encourages healing. Acid blockers work by keeping histamine from reaching histamine receptors. Histamine is a substance normally present in your body. When it reacts with histamine receptors, the receptors signal acid-secreting cells in your stomach to release hydrochloric acid. Available by prescription or over-the-counter (OTC), acid blockers include the medications ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet) and nizatidine (Axid).

Antacids. Your doctor may include an antacid in your drug regimen. An antacid may be taken in addition to an acid blocker or in place of one. Instead of reducing acid secretion, antacids neutralize existing stomach acid and can provide rapid pain relief.

Proton pump inhibitors. Another way to reduce stomach acid is to shut down the "pumps" within acid-secreting cells. Proton pump inhibitors reduce acid by blocking the action of these tiny pumps. These drugs include the prescription medications omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex) and esomeprazole (Nexium). The drug pantoprozole (Protonix) can be taken orally or administered intravenously in the hospital. Proton pump inhibitors are frequently prescribed to promote the healing of peptic ulcers.

If you are admitted to the hospital with a bleeding ulcer, taking intravenous proton pump inhibitors decreases the chance that bleeding will recur. Proton pump inhibitors also appear to inhibit H. pylori. However, long-term use of proton pump inhibitors, particularly at high doses, may increase your risk of hip fracture.

Cytoprotective agents. In some cases, your doctor may prescribe these medications that help protect the tissues that line your stomach and small intestine. They include the prescription medications sucralfate (Carafate) and misoprostol (Cytotec). Another nonprescription cytoprotective agent is bismuth subsalicylate (Pepto-Bismol). In addition to protecting the lining of your stomach and intestines, bismuth preparations appear to inhibit H. pylori activity.

Histology of peptic ulcer 

Figure 1:

Peptic ulcer of stomach (arrow). The whole mucosa and part of submucosa are denuded.(M: mucosa, SM: submucosa, MP: muscularis propria)

Figure2: 

Four zones of active peptic ulcer.The necrotic fibrinoid debris and nonspecific inflammatory infiltrate are labeled by arrowhead. Beneath the necrotic and inflammatory zones, there is granulation tissue (arrow). Below the granulation tissue, fibrotic tissue is seen (F).

Figure 3:

Granulation tissue in the ulcer base. New blood vessels lined byplump endothelial cells (arrow). Edema and inflammatory infiltrate are also seen

Figure 4:

Intestinal metaplasia in chronic gastritis. The gastric foveolar epithelium (arrowhead) is replaced by intestinal type of epithelium (arrow).The intestinal epithelium has goblet cells

(all figures taken from http://pathology.tmu.edu.tw )

Barrett's esophagus

Barrett's esophagus is a condition in which abnormal cells develop on the inner lining of the lower part of the gullet (esophagus). The esophagus is the muscular tube that carries food from the mouth to the stomach.

Barrett's esophagus is not in itself a cancerous condition, but over a period of time it can occasionally lead to cancer developing in the lower part of the esophagus. A cancer happens when cells in the affected area continue to grow and reproduce and become increasingly abnormal.

Diagram of comparison between normal esophagus and Barrett's esophagus

Normal

Barrett's esophagus

  Images taken from www.barrettsinfo.com/

Development of Barret's esophagus

 

Barrett’s oesophagus occurs when the acidic stomach contents are continuously refluxed onto the lining of the oesophagus, causing changes to the structure of the tissue. Over time, your body replaces the normal cells lining the oesophagus with cells of a different type. This new type of cell secretes mucus which makes it more resistant to the acid coming up from the stomach. The presence of these cells in the oesophagus is known as Barrett’s oesophagus or Barrett’s metaplasia.

Sign and symtoms

Barrett's esophagus itself does not cause symptoms. The acid reflux that causes Barrett's esophagus results in symptoms of heartburn. Rarely, Barrett's esophagus can progress to cancer of the esophagus, the symptoms of which may be difficulty swallowing or weight loss

 

 

Diagnosis

Diagnosis of the condition usually requires taking a sample of tissue by endoscopy. Doctors insert a lighted, flexible tube (endoscope) with a camera on its tip through the mouth and into the esophagus. Patients are given a local anesthetic or sedated for the procedure. During endoscopy, doctors may remove tissue samples (biopsies) of potentially abnormal areas for examination under a microscope.

Barrett's esophagus without dysplasia (cancerous changes) — If, at the first endoscopy all biopsies are without dysplasia, a second examination is recommended in one year. This is done to make sure that a very small cancer (also known as a prevalent cancer) was not missed at the first endoscopy. For those without dysplasia at the second examination, follow-up endoscopy is recommended in three to five years.

Barrett's esophagus with low-grade dysplasia — follow-up endoscopy is recommended every six months for a year, than every 12 months. Low grade dysplasia, by itself, is usually not lethal. Follow up is to make sure a serious finding is not missed.

Barrett's esophagus with high-grade dysplasia — If two pathologists agree that biopsies show high grade dysplasia, then intervention is usually suggested. The standard of care treatment is esophagus resection surgery or minimally invasive treatment such asphotodynamic therapy. In cases where the high grade dysplasia is only found in one small bump, an experimental option, endoscopic mucosal resection, may be possible. If a patient is not a good candidate for surgery, the doctor may opt to increase acid suppression medications and repeat an endoscopic examination in three months

 

Treatment

Barrett's esophagus usually is treated with medicines called proton pump inhibitors (one brand name: Nexium). These medicines reduce the amount of acid in your stomach. In some cases, surgery is used to keep stomach acid out of the esophagus. Your doctor may recommend that you make some lifestyle changes, such as quitting smoking if you smoke, exercising, losing weight, and avoiding foods that make your heartburn worse.

Mouth Sores (Pathology of GI System)

Mouth Sores Mouth sores vary in appearance and size. Some may be raised, usually filled with fluid (in which case it is called as a vesicle or bulla); others may be ulcers. An ulcer is a hole that forms in the lining of the mouth when the top forms in the lining of the mouth, when the top layer of cells breaks down and the underlying tissue shows through. An ulcer appears white because of the dead cells and food debris inside the hole. Sores can affect any part of the mouth, inside and outside. Canker sores/aphthous ulcers and cold sores are perhaps the most well know, but there are many other types and causes of mouth sores. Any sore that lasts for 10 days or more must be examined by a dentist or doctor to ensure that it is not cancerous or precancerous.


Canker Sores (aphthous ulcers) Aphthous ulcers are small, painful sores inside the mouth

• Aphthous ulcers are very common. The cause is unknown, but stress seem to play a role - for example, a BMS student may get aphthous ulcers during final exam week.
  
• Aphthous ulcer appears as a round white spot with a red border. The ulcer almost always forms on soft, loose tissue on the inside of the lip or cheek; on the tongue, the floor of the mouth, or soft palate; or in the throat.
• Small aphthous ulcers (less than 1/2 inch in diameter) often appear in clusters of two or three; generally, they disappear by themselves within 10 days and do not leave scars.
  
• Larger ulcers are less common, they are irregularly shaped, can take many weeks to heal, and frequently leave scars.
• People with AIDS often have large ulcers that persist for weeks.
• Many people who get aphthous ulcers get them repeatedly - often several times a year.

Symptoms and Diagnosis

• The main symptoms of aphthous ulcers is pain - far more than would be expected from something so small.
• The pain, which lasts 4 to 7 days, worsens if the tongue or food rubs the sore or if hot or spicy foods are eaten.
  
• Severe ulcers can cause fever, swollen lymph nodes in the neck, and a generally run-down feeling.
• A doctor or dentist identifies aphthous ulcers by its appearance and the pain it causes.

Symptoms and Diagnosis

• Treatment consists of relieving the pain until the sore heals by itself.
• An anesthetic such as dyclonine or lidocaine may be used as a mouth rinse.
• However, because these mouth rinses numb the mouth and throat and thus may make swallowing difficult, children using them should be watched to ensure that they do not choke on their food.
  
• Lidocaine in a thicker preparation (viscous lidocaine) can also be swabbed directly on the aphthous ulcers.
  
• A protective coating gel of carboxymethylcellulose, often combine with a corticosteroid (such as triamcinolone or betamethasone), may be applied to protect the ulcers and temporarily relieve pain.
• Finally, for the most severe cases, a corticosteroid may be prescribed as a dexamthasone mouth rinse or, rarely, as predisone tablets taken by mouth.
• However, before prescribing as corticosteroid, a doctor ensures that the person does not also have oral herpes simplex infection, which can be further spread by corticosteroid given in gel form , so the side effects may be a concern.

Oral Herpes Simplex/Cold Sores

Infection of the mouth with herpes simplex virus causes recurring sore (often called cold sores), in which small fluid-filled sore develop on the skin, lips, or mouth in single or multiple clusters.

• The 1st eruption of sores due to infection with oral herpes simplex virus is called primary herpes. It is usually contracted in childhood. Primary herpes may be mild or severe, but it often affects large areas of the mouth and always the gums.
  
• Any subsequent eruption of the sores is called secondary herpes. Secondary herpes is a reactivation of the virus rather than a new infection.
  
• There are at least two forms of herpes simplex virus. In the past, herpes simplex virus type I only caused sores above the waist, and type 2 only below the waist (genital herpes). Click here to more detail on types of herpes simplex virus.
  
• Now however, either type can cause sores anywhere on the body because of sexual behavior etc. Herpes simplex 2 tends to be more severe than type I.
• Typically, a previously uninfected child acquires the virus from contact with an adult who has a cold sore. In rare cases, a person first acquires herpes simplex virus in adulthood, also after contact with someone with a cold sore.
• A person is capable of spreading the infection (contagious) from the time the tingling sensation that proceeds the development of a sore (the prodorome) is experienced to the time at which the sore has completely crusted over. It is unknown whether herpes can be spread by sharing a glass or touching something that an infected person has touched.

Symptoms

• When primary herpes is acquired in childhood, the infection causes gum inflammation and extensive mouth soreness. Fever, swollen lymph nodes in the neck, and general discomfort may develop.
• A child may be cranky and cry continually. However, many cases are mild and go unrecognized. Parents often mistake the problem for teething or another illness. In more severe cases, small blisters form in the child's mouth. These blisters may not be noticed because they rupture within a day or two, leaving many ulcers. The ulcers may occur anywhere in the mouth but always include the gums. Though the child get better in a week to 10 days, the herpes simplex virus never leaves the body.
• When a primary herpes is acquired in adulthood, symptoms are usually more severe and include multiple rapidly developing painful sores on the gums an other parts of the mouth.
• Unlike primary herpes, which causes widespread mouth soreness, the flare-ups of secondary herpes usually produce a single raw, weeping open sore on the outer lip that later crusts over before healing within 2 or 3 weeks. The sore is sometimes called a cold sore or fever blister. Less commonly, a cluster of blisters (vesicles) forms on the roof of the mouth. These small blisters run together and quickly break down into a sore. There is no crusting stage.
• Flare-ups are commonly triggered by sunburn on the lips, certain foods, anxiety, a cold (hence the name 'cold sore'), fever, or anything that lowers the body's resistance to infection. Certain dental procedures can cause a flare-up as well; if a cold sore already exists, dental visits should be postponed until the sore heals.
• Although merely a painful annoyance for most people, flare-ups of oral herpes simplex infection can be life-threatening for a person with an impaired immune system. Impairment of the immune system can be caused by diseases (such as AIDS), chemotherapy, radiation therapy, or a bone marrow transplant. In such people, large, persistent sores in the mouth can interfere with eating; spreading of the virus to the brain can be fatal.

Treatment

• Treatment for primary herpes aims to relieve the pain so that the person can sleep, eat, and drink comfortably. Pain may keep a child from eating and drinking, which, combined with a fever, can quickly lead to dehydration. Thus, a child should drink as much fluids as possible. An adult or older child can use a prescribed anesthetic mouth rinse such as lidocaine to reduce pain. A mouth rinse containing baking soda may also be soothing.
• Treatment for secondary herpes works best when started before the sore erupts - as soon as the person has the sensation (the prodorome) that an attack is starting. Taking vitamin C (1,000 to 2,000 milligrams per day) during the prodrome may make the attack less severe. A doctor may prescribe penciclovir cream or amlexanox paste, which is applied during the prodorome to shorten the duration and severity of the outbreak. The virus itself cannot be permanently eliminated.
• Protecting the lips from direct sunlight by wearing a wide-brimmed hat or by using lip balm containing sunscreen can reduce the possibility of of a flare-up. Also, a person should avoid activities and food that are know to cause flare-ups. Anyone who suffers frequent, severe flare-ups may try taking lysine (available at food stores) indefinitely.
  
• Levaisole, available by prescription, is another drug that seems to reduce recurrences.
• For people with severe herpes simplex and for people with and impaired immune system, acylovir or penciclovir capsules may be prescribed to prevent or limit the severity of the infection. Corticosteroids are not used for herpes simplex because they may allow the infection to spread.
  

Pathophysiology of Gastrointestinal System (1st Lecture)

OVERVIEW OF MODULE
Pathophysiology of Gastrointestinal System - SMS 2054

By Assoc Prof Dr Samiah Yasmin Abdul Kadir

• Review of the gastrointestinal system
• Diseases of the oral cavity & the oesophagus
• Diseases of the stomach
• Development anormalies
• Intestinal and abdominal vascular disorders
• Diarrhoeal diseases
• Inflammatory bowel diseases & colonic diverticulosis
• Other conditions
i. Gastrointestinal lymphoma
ii. Appendicitis
iii. Tumors of the git
• Diseases of the liver, gall bladder, spleen and the pancrease

ASSIGNMENTS
1. EXPLAIN THE REGULATION OF FUNCTION OF THE GASTROINTESTINAL TRACT

2. DESCRIBE THE PHYSIOLOGY OF THE LIVER, GALL BLADDER, SPLEEN AND PANCREAS

3. ELABORATE ON THE EMBRYOLOGICAL DEVELOPMENT OF THE GASTROINTESTINAL SYSTEM

PLEASE SUBMIT ALL 3 ASSIGNMENTS BY 31ST JULY 2008

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click on pathophysio of Gastro - assigment 1

Pathology of Gastrointestinal System

Mouth

- Normal -
Normal

- Inflammatory Diseases -
Pyostomatitis Vegetans

- Malignant Neoplasms -
Squamous Carcinoma

Salivary Glands

- Normal -
Normal Parotid Gland
Normal Sublingual Gland
Normal Submaxillary Gland

- Inflammatory fghgfhfg
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Diseases -
Sjogrens Disease

- Growth Alteration (non-neoplastic)

Lymphoid Hyperplasia

- Benign Neoplasms -
Pleomorphic Adenoma

Esophagus

- Normal -
Normal

- Inflammatory Diseases -
Candida
Erosion
Esophagitis
Reflux
Ulcer

- Necrosis & Degeneration -
Erosion

- Diseases of the Vasculature -
Varices

- Growth Alterations (non-neoplastic) -
Barretts

- Malignant Neoplasms -
Adenocarcinoma
Squamous Carcinoma In Situ
Squamous Carcinoma in situ
Squamous Cell Carcinoma

- Mechanical Diseases & Trauma -
Stricture

Stomach

- Normal -
Normal
Normal Pylorus

- Congenital Abnormalites -
Abdominal Wall Defect

- Inflammatory Diseases -
Candida
Helicobacter
Ulcer

- Diseases of the Vasculature -
Hemorrhage

- Growth Alterations (non-neoplastic) -
Metaplasia
Polyp

- Malignant Neoplasms -
Adenocarcinoma
Stromal Tumor

Small Intestine

- Normal -
Normal Duodenum
Normal Ileum
Normal Jejunum

- Congenital Abnormalites -
Atresia

- Inflammatory Diseases -
Crohns
Cytomegalovirus
Gluten Sensitive Enteropathy
Mycobacterium
Subtotal Villous Atrophy
Total Villous Atrophy

- Necrosis & Degeneration -
Infarct
Ulcer

- Diseases of the Vasculature -
Hemorrhage
Infarct

- Benign Neoplasms -
Adenoma

- Malignant Neoplasms -
Adenocarcinoma
Carcinoid
Gastrointestinal Stromal Tumor
Metastatic Adenocarcinoma
Myeloma

- Mechanical Diseases & Trauma -
Perforation

- Trauma -
Gunshot

Appendix

- Inflammatory Diseases -
Appendicitis
Fibrosis
Peritonitis

- Malignant Neoplasms -
Carcinoid
Cystadenocarcinoma

Colon

- Normal -
Normal

- Inflammatory Diseases -
Acute Colitis
Ascaris
Collagenous Colitis
Crohns
Cryptosporidiosis
Diverticulitis
Pseudomembranous Colitis
Ulcerative Colitis

- Necrosis & Degeneration -
Infarct
Ischemic Colitis
Toxic Megacolon

- Growth Alterations (non-neoplastic) -
Dysplasia
Repair

- Benign Neoplasms -
Adenoma
Adenoma, Tubulovillous
Adenoma, Villous
Polyposis

- Malignant Neoplasms -
Adenocarcinoma
Carcinoid
Leiomyosarcoma
Squamous Carcinoma

- Mechanical Diseases & Trauma -
Diverticulosis
Pneumatosis

Liver

- Normal -
Normal

- Inflammatory Diseases -
Abscess
Cirrhosis
Hemochromatosis
Herpes
Necrosis

- Necrosis & Degeneration -
Fatty Change
Hemochromatosis
Infarct
Necrosis

- Diseases of the Vasculature -
Chronic Passive Congestion
Hematoma
Thrombus

- Growth Alterations (non-neoplastic) -
Focal Nodular Hyperplasia

- Benign Neoplasms -
Adenoma

- Malignant Neoplasms -
Hepatocellular Carcinoma
Lymphoma
Metastatic Adenocarcinoma
Metastatic Esophageal Carcinoma
Metastatic Small Cell Carcinoma

- Mechanical Diseases & Trauma -
Cyst

- Trauma -
Bullet

Gall Bladder

- Inflammatory Diseases -
Cholecystitis, Acute
Cholecystitis, Chronic
Cholelithiasis

- Necrosis & Degeneration -
Cholesterolosis

- Malignant Neoplasms -
Adenocarcinoma
Papillary Adenocarcinoma

- Mechanical Diseases & Trauma -
Cholelithiasis

Pancreas

- Normal -
Normal

- Inflammatory Diseases -
Pancreatitis Acute Hemorrhagic

- Benign Neoplasms -
Adenoma, Papillary

- Malignant Neoplasms -
Adenocarcinoma

- Mechanical Diseases & Trauma -
Pseudocyst

- Congenital Abnormalites -
Omphalocoele