Final Exam Case Study on Alcoholism Practice

History: Vincent Miller, a 62-year-old accountant, has had a "drinking problem" throughout most of his adult life. He drinks about a half-case of beer each day. He has lost several jobs over the years for drinking at the workplace or showing up for work drunk. He lost his driver's license for drunk-driving, and his drinking has placed a considerable strain on his marriage. He has tried several self-help programs as well as Alcoholics Anonymous, all with little success. He has been hospitalized on several occasions over the years. Vincent has a severe tremor in his hands (probably a result of excessive alcohol intake), which makes it very difficult for him to use a spoon, fork, and knife to eat. It's your first day on the job as an occupational therapist, and you are consulted by his physician to see if there is any way to help Vincent use eating utensils. Not knowing anything about him, you open up his past medical records, which, incidentally, are quite thick.

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2. Based upon your knowledge of the vomiting reflex, why might severe vomiting tear the mucosa?

2. The following events occur as part of the vomiting reflex:A. The individual inhales deeply and holds the diaphragm in the flattened and contracted position. In this position, the diaphragm pushes against the stomach and raises intra-abdominal pressure.B. The glottis closes to prevent vomitus from entering the respiratory tract.C. The abdominal wall muscles contract (i.e. the "bearing down" or Valsalva maneuver), further increasing intra-abdominal pressure and therefore increasing external pressure on the stomach.D. The lower esophageal sphincter (also called the cardiac sphincter) relaxes to allow the stomach contents to enter the esophagus and be propelled to the mouth.E. The soft palate elevates to close off the opening into the nasal cavity.Thus, the act of vomiting greatly increases the intra-luminal pressure in the stomach and esophagus. This, coupled with the fact that the vomitus is very acidic, causes irritation of the lower esophageal lining. In instances of severe, repeated bouts of vomiting, the esophageal mucosa may actually tear. This phenomenon is called a Mallory-Weiss tear.

First Hospitalization: You note that Vincent was hospitalized at age 32 with a complaint of vomiting up blood after a drinking binge that lasted seven days and was marked by excessive and repeated vomiting episodes. The vomitus was bright red. The hospital chart lists a diagnosis of "Upper GI bleed" due to a Mallory-Weiss tear. You look up "Mallory-Weiss tear" in an internal medicine textbook and see that it is defined as "a longitudinal tear in the mucosa at the gastroesophageal junction -- i.e. in the area of the lower esophageal sphincter -- caused by repeated vomiting."1. Why was the blood bright red, rather than the color of "coffee grounds"?

1. The bright red color of the vomitus indicates that the blood either didn't enter the acidic environment of the stomach, or didn't spend much time in the stomach. Blood that remains in the stomach for longer periods becomes dark and hardens into pieces that resemble coffee grounds, hence the term "coffee ground emesis.

Second Hospitalization: At age 36, Vincent was hospitalized again, this time with complaints of abdominal pain in the upper epigastric region (i.e. just below the xiphoid process of the sternum) and "coffee-grounds" emesis. He also complained of "heartburn" (a burning sensation in the area of the sternum) which was partially relieved with antacids. A diagnosis of "upper GI bleed due to gastritis and reflux esophagitis" is noted in the chart.1. What is causing the pain in the upper epigastric region ? What barrier(s) normally protect the stomach lining from its own acid?

1. The pain in Vincent's upper epigastric region is most likely referred pain due to his gastritis (i.e. inflammation of the stomach lining). The stomach lining is normally protected from the corrosive effects of its own acidic secretions in the following ways:A. There are tight junctions between adjacent epithelial lining cells, making it difficult for secreted H+ ions to be reabsorbed back through the stomach lining.B. The gastric glands secrete a thick coating of HCO3- - rich mucus onto the lining.C. Gastric epithelial cells damaged by the gastric acid are quickly replaced by underlying cells.However, excessive alcohol ingestion can break down this mucosal barrier, thus increasing its permeability to H+ ions. The gastric acid seeping into the stomach wall can cause irritation, inflammation, bleeding, and sometimes ulceration of the gastric lining - - the latter phenomenon being called a peptic ulcer, because of the ability of the stomach digestive enzyme pepsin to digest the wall itself. The presence of "coffee-ground" emesis suggests that Vincent's stomach lining is slowly bleeding, either as a result of the gastritis or peptic ulcer or both.

2. What is reflux esophagitis?

2. Reflux esophagitis is inflammation of the lower esophageal lining due to the excessive reflux of corrosive gastric acid into the duodenum. Esophageal reflux causes referred pain in the sub-sternal region - - the same location where referred pain from ischemic heart disease (i.e. angina pectoris) is felt, hence the term "heartburn." Causes of reflux esophagitis include excessive relaxation (or "incompetence") of the lower esophageal sphincter, impaired esophageal emptying, and delayed gastric emptying. Alcohol has been shown to lower the lower esophageal sphincter pressure, and it is probably a major contributing cause of Vincent's reflux esophagitis. And in Vincent's case, the reflux esophagitis is exacerbated by his repeated alcohol-drinking binges and bouts of vomiting.

3. Can you think of any treatments for Vincent's problems? Explain the mechanisms for those treatments, based upon your knowledge of the regulation of gastric secretions.

3. Treatments for reflux esophagitis include the following:A. Avoid exposure to substances that reduce lower esophageal sphincter pressure, such as alcohol, caffeine, cigarette smoke, and chocolateB. Avoid large meals (i.e. over-distension of the stomach)C. Avoid strenuous activity or lying down for the first two hours following a mealD. Use antacids, which directly neutralize the gastric acid in the stomach lumenE. Use H2-blocking drugs, which block the stimulatory effect of histamine on the gastric glands and therefore decrease gastric acid secretionF. Use drugs that directly increase the lower esophageal sphincter pressure (e.g. cisapride), making it more difficult for gastric contents to reflux into the esophagusG. Use H+ ion pump blockers (e.g. omeprazole), which directly inhibit gastric acid secretion by the stomach liningMany of the treatments listed here are helpful in the treatment of gastritis and peptic ulcers as well. However, if it is determined that Vincent has a peptic ulcer, he should be placed on two weeks of antibiotic therapy to destroy the bacterium Helicobacter pylori, which is implicated in most ulcers.

Third Hospitalization At age 41, Vincent entered the hospital with complaints of a high fever, nausea, loss of appetite, and a dull, continual pain in the left side of the back. In addition, he had diarrhea of a particularly foul odor and yellow color . He had also lost 15 pounds over the last month and a half. Unfortunately, the page in the chart is torn, so you cannot read the diagnosis! But your memory of an anatomy and physiology course you took in college helps you figure out the possible causes of Vincent's problem.1. Excessive exposure to alcohol can cause inflammation of certain digestive organs, such as the stomach. Inflammation of which organ(s) might be causing Vincent's back pain?

1. Chronic exposure to alcohol can cause pancreatitis - - i.e. inflammation of the pancreas. Since the pancreas is a retroperitoneal organ, the dull, throbbing pain associated with pancreatitis is often felt in the back. It is therefore likely that Vincent is suffering from alcohol-induced pancreatitis. The destruction of exocrine cells in the pancreas reduces this organ's ability to secrete digestive enzymes and HCO3- ions into the duodenum during meals. Consequently, many of the nutrients in Vincent's meals will never be completely digested, and therefore never absorbed into the bloodstream. Vincent will slowly lose weight due to this malabsorption syndrome.

2. Based upon the location of this pain, would you guess that the organ in question is a retroperitoneal organ or an organ attached to the abdominal wall by a broad sheet of mesentery? Explain your answer.

2. Chronic exposure to alcohol can cause pancreatitis - - i.e. inflammation of the pancreas. Since the pancreas is a retroperitoneal organ, the dull, throbbing pain associated with pancreatitis is often felt in the back. It is therefore likely that Vincent is suffering from alcohol-induced pancreatitis. The destruction of exocrine cells in the pancreas reduces this organ ability to secrete digestive enzymes and HCO3- ions into the duodenum during meals. Consequently, many of the nutrients in Vincent's meals will never be completely digested, and therefore never absorbed into the bloodstream. Vincent will slowly lose weight due to this malabsorption syndrome.

3. Based upon the function of the organ in question, what is causing the "steatorrhea" and weight loss?

3. Since many of the nutrients Vincent ingests during a meal pass through the intestines unabsorbed, they osmotically draw water from the bloodstream into the intestinal lumen, causing an "osmotic diarrhea." The high fat content of the stool gives it a foul odor and yellowish color - - a condition called steatorrhea. The inability of Vincent to absorb the nutrients of his meal will cause him to slowly lose weight. This malabsorption syndrome can now be treated with the ingestion of pancreatic enzymes with each meal.

Fourth Hospitalization As you read on, you note that Vincent was hospitalized again at age 49 with dull pain in the right, upper quadrant of the abdomen, intermittent fever of 3 weeks duration, and a yellowing of the skin and the whites of the eyes. A diagnosis of "alcohol-induced hepatitis" is listed in the chart.1. Is the diagnosis consistent with the location of the abdominal pain? Explain your answer.

1. With excessive intake of alcohol, the liver switches over from the use of fats and carbohydrates as its primary "fuel" to the use of alcohol as its primary fuel. This can lead to excessive production of lactic acid, which, in turn, can cause inflammation of the liver tissue. The liver occupies the majority of the right upper quadrant of the abdomen, and thus pain of liver origin is often felt over the surface of the abdomen's right upper quadrant. As alcohol-induced hepatitis progresses, the unused fat accumulates in the liver, causing the organ to change in color from a dark, reddish brown to a yellowish color that resembles nutmeg (hence the terms "nutmeg liver" or "fatty liver"). In the final stages, the liver tissue can be destroyed by scar tissue (i.e. cirrhosis of the liver).

2. How are the liver and gallbladder connected to each other and to the duodenum?

2. The right and left hepatic ducts emerge from the undersurface of the liver and combine to form the common hepatic duct. The common hepatic duct, in turn, merges with the cystic duct (coming from the gallbladder) to form the common bile duct. Finally, the common bile duct courses downward toward the pancreas, where it merges with the main pancreatic duct to form the ampulla of Vater, the end of which opens into the duodenum of the small intestine. A small ring of smooth muscle called the sphincter of Oddi regulates the rate at which hepatic, gallbladder, and pancreatic secretions enter the duodenum.

3. If Vincent's liver disorder resulted in the production of a "gallstone," what danger might that present for his pancreas?

3. A gallstone expelled from the gallbladder can be force by peristaltic contractions down through the cystic and common bile ducts. If it gets lodged and stuck near the ampulla of Vater, it could partially or completely block not only the flow of bile from the liver and gall bladder into the duodenum but also the flow of the bicarbonate-rich fluid and digestive enzymes from the pancreas into the duodenum. This may cause bile (a powerful lipid-emulsifying agent) to regurgitate into the pancreas and cause destruction of the tissue. Furthermore, the pancreatic enzymes building up in the pancreas may be converted to their active forms and begin to digest the pancreas, itself. Thus, someone with a gallstone lodged in the ampulla of Vater is at risk of developing severe damage to the pancreas and pancreatitis.

4. Why are Vincent's skin and eyes tinged yellow? What is this condition called?

4. If Vincent has a gallstone obstructing the flow of bile, he may develop "obstructive jaundice." Bilirubin, a breakdown product of the hemoglobin in red blood cells, is primarily excreted from the body through the bile. If the flow of bile is blocked, it is difficult to excrete bilirubin. Thus, bilirubin levels may rise in the bloodstream, causing the typical yellowish appearance of the skin and eyes known as jaundice - - in Vincent's case, "obstructive" jaundice because the jaundice is due to the obstruction of bile flow.

Fifth Hospitalization: At age 58, Vincent was rushed to the emergency room with severe vomiting of bright red blood. On examination, he had a blood pressure of 60 mmHg / 30 mmHg. The bleeding and vomiting started abruptly while Vincent was eating some hard, dry French bread. An endoscope (i.e. a flexible tube equipped with a camera) was placed down Vincent's esophagus, and a diagnosis of esophageal varices was quickly made.1. What are esophageal varices?

1. Esophageal varices are distended veins in the submucosa of the esophagus. Enlargement of these veins causes them to protrude out into the esophageal lumen, where they are at risk of tearing if Vincent swallows food that is particularly hard in texture.

2. Where are esophageal varices typically located? (Be specific.)

2. Esophageal varices are usually located in the lower end of the esophagus, where veins of the portal circulation (i.e. veins ultimately draining blood through the portal vein of the liver) anastomose with veins of the systemic circulation (i.e. veins ultimately draining blood into the superior and inferior venae cavae).

3. On the hospital chart you see two other "secondary diagnoses" listed: (1) cirrhosis of the liver, and (2) portal hypertension. Does this additional information help explain why Vincent developed esophageal varices? Explain your answer.

Yes, it does. Cirrhosis of the liver is a condition that results from chronic excessive ingestion of alcohol. In this condition, the liver tissue is damaged and slowly replaced by scar tissue. The scarring of the liver makes it difficult for portal vein blood to enter the liver. The portal vein, under normal conditions, shuttles venous blood from most of the abdominal organs and the lower esophagus to the liver. In this way, the liver gets a "first look" at the newly absorbed nutrients from the intestinal wall - - a crucial function, since the liver is the body's primary processer of these nutrients.However, in cirrhosis of the liver, the scarred over liver tissue can obstruct the flow of portal vein blood into the liver. This increases the hydrostatic blood pressure in the portal vein and all of its tributaries - - a condition called "portal hypertension." This rise in blood pressure distends the tributary veins, particularly those that have anastomoses (i.e. direct connections) to veins of the systemic circulation. The esophageal veins are particularly vulnerable to this distension, and thus Vincent developed esophageal varices.Another set of veins prone to distension in Vincent are the hemorrhoidal veins in the rectum. This causes hemorrhoids, which like esophageal varices, are prone to rupture.

4. Why is bleeding particularly dangerous for Vincent?

4. A. Cirrhosis of the liver decreases the liver's ability to produce blood-clotting factors 2, 7, 9, and 10. These factors, when activated, help blood to clot in order to minimize bleeding following the rupture of blood vessels.B. Cirrhosis of the liver decreases the liver's ability to produce and release bile. Bile is normally secreted into the duodenum to help us emulsify fatty foods and other fat-soluble nutrients so that they can be properly digested and absorbed through the wall of the small intestines. One fat-soluble nutrient required in our diet is vitamin K. Vitamin K serves as a co-enzyme for the enzymes required to produce blood-clotting factors 2, 7, 9, and 10. Without sufficient bile release, we cannot absorb vitamin K. Thus, vitamin K levels are low, making difficult for the liver to produce blood-clotting factors 2, 7, 9, and 10.Ruptured esophageal varices can therefore be life-threatening for Vincent. An ice-water lavage may be required to quickly stop his bleeding before more permanent measures are taken.