Module 7 - GI Tract Disorders Flashcards

1
Q

What is saliva made up of

A

Saliva is a hypotonic solution of water and solutes with the enzyme amylase that can break down starches. May also contain mucus, lysozyme to break down bacteria, IgA to inhibit bacterial growth, and electrolytes.

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2
Q

Describe the two types of digestion that takes place in the stomach:

A

Chemical digestion - pepsinogen is a proenzyme, or inactive enzyme. The stomach acid is going to activate pepsinogen into its active form pepsin, which can digest proteins into smaller peptides or amino acids.

Mechanical digestion via muscular contractions - 3 layers of smooth muscle. Mechanical digestion breaks food down into smaller pieces and gives the food a greater surface area. The enzymes can then work on chemical digestion.

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3
Q

What are the three main cells in the stomach necessary for digestion?

A

The parietal cells (HCl and intrinsic factor), chief cells (pepsinogen), and G cells (Gastrin)

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4
Q

What functions does the liver have?

A

It produces bile; metabolizes hormones and drugs; synthesizes proteins, glucose, and clotting factors; stores vitamins and minerals and converts them to be usable by the body; changes ammonia ot urea; and converts fatty acids to ketones. The liver can store large amounts of glucose as glycogen; synthesize glucose from amino acids, glycerol, and lactic acid during times of fasting or increased demand; convert excess carbohydrates to triglycerides for storage in adipose tissue; major site for protein synthesis and degradation.

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5
Q

What is the structure and function of the 4 layers of the GI wall?

A

The mucosal layer - it is made up of epithelium, connective tissue, and smooth muscle cells. It produces mucus that lubricates and protects the inner surface of the alimentary canal. It secretes digestive enzymes and substances that break down food. It absorbs the breakdown products of digestion. It maintains a barrier to prevent the entry of noxious substances and pathogenic organism.

The submucosal layer - contains dense connective tissue and some adipose tissue. Has blood vessels, nerves, and structures that secrete digestive enzymes.

The muscularis externa - consists of an inner layer of ciruclarly arranged muscle cells and an outer layer of longitudinally arranged smooth muscle layers. THese layers alternately contract to help move the contents through the GI tract via peristalsis.

The serosal layer - the outermost layer of organs and also called the visceral peritoneum. The peritoneum is the largest serous membrane in the body. It is comprised of two continuous layers, the visceral and parietal peritoneum. The parietal peritoneum lines the wall of the abdominopelvic cavity. Between the two layers is the peritoneal cavity, a potential space containing fluid secreted by the serous membranes. This serous fluid keeps a moist surface to prevent friction between the moving abdominal organs.

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6
Q

What does the pancreas produce?

A

Pancreatic juice with enzymes (proteases - protein, lipases - lipids, amylase - starch) and alkaline buffer to neutralize stomach acid so doesn’t harm the lining of the small intestine as chyme enters from stomach. Pancreas also secretes insulin and glucagon to regulate blood glucose levels. Insulin signals cells to take in glucose after we eat and that drops our blood glucose levels. Secretes glucagon to increase glucose levels between meals.

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7
Q

What is the role of the stomach in digestion

A

Holds food in storage during the early stages of digestion and carbohydrate and protein digestion occur.

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8
Q

What is the role of the small intestine in digestion

A

Duodenum, jejunum, and ileum.

Majority of digestion and absorption take place. Bile and pancreatic juices enter the intestine through the common bile duct and main pancreatic duct. Fat is broken into smaller pieces so enzymes can act on the surface molecules (emulsification).

The small intestine has a lot of surface area (villi, circular folds) which allows absorption of nutrients.

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9
Q

What is the role of the large intestine in digestion

A

Cecum, ascending/transverse/descending/sigmoid colon, rectum, anal canal.

Absorbs mainly water and a storage for waste until defecation.

The microflora help produce vitamins B & K

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10
Q

What is the mesentery?

A

The mesentery is the double layer of peritoneum that encloses some or all of the abdominal viscera and attaches it to the abdominal wall. There are also blood vessels, nerves, and lymphatic vessels that supply the intestinal wall. It also holds the organs in place and stores fat.

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11
Q

What is the omentum?

A

The omentum is a double layered extension or fold of peritoneum that passes from the stomach to adjacent organs in the abdominal cavity or wall. The greater omentum contains fat and has a lot of mobility to follow the movements of the intestines.

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12
Q

What’s the difference between rhythmic and tonic movements?

A

Rhythmic movements are intermittent contractions that help to mix and move food along - esophagus, antrum of the stomach, and small intestine.

Tonic movements have a constant level of contraction or tone without regular periods of relaxation - lower esophagus, upper region of stomach, ileocecal valave, and internal anal sphincter.

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13
Q

What is the enteric nervous system?

A

The myenteric and submucosal plexuses both make up the enteric nervous system. These two plexuses are networks of nerve fibers and ganglion cell bodies. Interneurons connect afferent sensory fibers, efferent motor neurons, and secretory cells to form reflex circuits.

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14
Q

What are the myenteric and submucosal plexuses.

A

The myenteric plexus is a chain of neurons that are involved in GI motility situated between the muscular layers of the GI tract.

The submucosal plexus plays a role in controlling secretions, absorption, and contraction of each segment of the intestinal tract. It is situated between the mucosal and muscular layers of the intestinal wall.

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15
Q

Explain how the stomach churns food.

A

The stomach churns and mixes food in a peristaltic fashion of 3-5 contractions per minute, each lasting 2-20 seconds. Contraction of the antrum pushes food toward the closed pyloric sphincter. Larger particles are returned to the body of the stomach for further churning. The other contents are emptied into the duodenum between contractions.

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16
Q

Describe the two patterns of contractions in the small intestine.

A

Segmentation waves are slow contractions of the circular muscle layer. They occlude the lumen and push digestive contents back and forth, using small portions of the intestine at a time. Chyme gets mixed with digestive enzymes from the pancreas and all surface area is exposed to the intestinal surface for absorption. Segmentation activity is higher after a meal.

Peristaltic contractions are rhythmic movements designed to propel the chyme along toward the large intestine, one direction. When they reach the ileoccecal junction, the stretching of the ileum elicits a reflex which relaxes the sphincter, allowing fluid to move into the cecum.

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17
Q

What are the two types of movements in the colon?

A

Haustral churning is in the compartments of the colon called haustra and these movements fill and expel contents from the haustral, to ensure the entire surface area of the fecal mass is exposed to intestinal surface.

Propulsive mass movements contract a larger segment of the colon to move a collective amount of fecal matter. This is what triggers a need for a bowel movement.

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18
Q

Explain how the GI tract is involved in both endocrine and paracrine regulation

A

Alhough the GI tract is the largest endocrine organ in the body, it is involved in both endocrine (distant) and paracrine (cell-to-cell) regulation. Endocrine regulation begins by releasing a hormone (or protein) into the blood stream. Once in the circulatory system, it travels until reaching the appropriate target cell, which then responds by releasing another hormone or chemical messenger. For example, once stomach acid (present in chime) enters the intestine, it stimulates the release of secretin. In contrast, paracrine regulation only occurs locally, for example a hormone reaches a target cell by crossing a neighboring cell membrane.

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19
Q

What is CCK

A

It is a hormone in the duodenum and jejunum.

It is stimulated by products of protein digestion and long chain fatty acids.

It stimulates contraction of the gallbladder & secretion of pancreatic enzymes; slows gastric emptying; inhibits food intake.

20
Q

What is gastrin

A

It is a hormone in the antrum of the stomach and duodenum.

It is stimulated by vagal stimulation; epinephrine; neutral amino acids; calcium containing foods; alcohol. Secretion is inhibited by acid content of stomach antrum (pH<2.5).

It stimulates secretion of gastric acid and pepsinogen; increases gastric blood flow; stimulates gastric smooth muscle contraction & growth of gastric & intestinal mucosal cells

21
Q

What is ghrelin

A

It is a hormone in the fundus of the stomach. It is stimulated by nutritional fasting and decreased levels of growth hormone.

It stimulates secretion of growth hormone; acts as an appetite stimulating signal from stomach when an increase in metabolic efficiency is necessary.

22
Q

What is GLP-1

A

It is a hormone in the distal small intestine.

It is stimulated by a high carb meal.

It stimulates augmentation of insulin release; suppresses glucagon release; slows gastric emptying; decreases appetite and body weight

23
Q

What is GIP

A

It is a hormone in the small intestine, mainly jejunum

It is stimulated by a high carb meal

It augments insulin release

24
Q

What is secretin

A

A hormone in the duodenum

It is stimulated by acid pH or chyme entering the duodenum (pH<3)

It inhibits gastric acid secretion

25
Q

What are the different types of diarrhea?

A

Acute: less than 14 days; infectious microbes, self limiting, will clear on own.
Acute - noninflammatory (large volume): pathogens secrete toxins that promote fluid retention which increase volume of stool.
Acute - inflammatory (small volume): dysentery; c difficile or E coli; injury and inflammation to the eipthelium, bloody stools, fever.

Chronic: 4+ weeks; assoc with IBS, IBD, malabsoprtion syndromes, and endocrine disorders
Chronic osmotic - osmotic gradient disrupted and lumen contents have hyperosmolarity so it pulls water into the small intestine that cannot be absorbed by the colon; lactose intolerance
Chronic secretory - secretory processes of the small intestine increase, the intestine itself releasing electrolytes causing the hyperosmolarity. Due to bacterial overgrowth, cancers, bioacids, laxatives; fat malabsorption
Chronic inflammatory - IBD
Chronic Infectious - protozoans

26
Q

How do you diagnose and treat diarrhea

A

Diagnosis - symptoms of frequent stools and history of concurrent illness, medication use, travel, exposure to potential intestinal pathogens.

Treatment - some people need nothing; fluid and electrolyte replacement. Meds include lomotil and loperamide to slow GI motility and stimulate electrolyte absorption. Pepto bismol inhibits intestinal secretions and works to decrease frequency of unformed stools. Antibiotics if pathogens identified

27
Q

Describe the different types of constipation

A

Constipation is infrequent, incomplete, or difficult passage of stools.

Common causes - failure to respond to the urge to defecate, inadequate fiber in the diet, inadequate fluid intake, weakness of the abdominal muscles, inactivity and bed rest, and pregnancy.

Normal transit - perceived difficulty in defecation and usually responds to increased fluid and fiber intake.

Slow transit - infrequent bowel movements usually caused by changes in the motor function of the colon. E.g. Hirschsprung disease, defect causes absent ganglion cells in distal bowel.

Disorders of defecatory or rectal evacuation - lack of muscle coordination in the pelvic floor or anal sphincter.

28
Q

What is diverticulosis and diverticulitis?

A

Diverticulosis refers to herniation of mucosa and submucosa through the muscular layer of the colonic wall. When these pouches become inflamed or infected, it is called diverticulitis, which can cause left lower abdominal pain, fever, and GI bleeding.

29
Q

What are some of the causes, diagnoses, and treatments for constipation

A

Causes - narcotics, anticholinergics, calcium channel blockers, diuretics, calcium and iron supplements, aluminum antacids. People with longstanding constipation and straining may develop dilation of the rectum and colon which can cause stool to accumulate with little or no senstation.

Diagnosis - history of infrequent stools, straining, hard or lumpy stools. Rule out other diseases. Rectal exam for fecal impaction, anal stricture, or rectal masses, and check for occult blood in stool. Colonic transit time tests for severe cases.

Treatment - responding to the urge to defecate, adequate fluid and dietary fiber intake, moderate exercise, sparing use of laxatives and enemas.

30
Q

What is irritable bowel syndrome

A

IBS symptoms include recurrent abdominal pain or discomfort that is associated with a change in stool frequency or form. The pain or discomfort may be relieved by defecation. The pain is usually intermittent, cramping, and in the lower abdomen. There may be varying complaints of flatulence, bloating, nausea and anorexia, constipation or diarrhea, and anxiety or depression.

31
Q

What is the etiology, diagnosis criteria, and treatment of IBS

A

Etiology: altered transit due to muscle changes in GI tract; infection (giardia or gastroenteritis) might change the microflora in the gut; immunologic changes increase inflammation; neural changes cause dysregulation between the enteric and CNS in its modulation of the GI tract processes; food, hormones, stress.

Diagnosis: patient history
Rome criteria - abdominal pain and discomfort at least 1 day a week in the last 3 months; pain related to defecation; altered frequency and consistency of stools.
Continuing or recurrent symptoms of at least 12 weeks duration of abdominal discomfort or pain in the preceding 12 months, with 2/3 features - relief with defecation, onset associated with a change in bowel frequency, and onset associated with a change in form of stool.
Lactose intolerance

Treatment - reassurance, stress management, increased fiber, avoid offending foods, antispasmodic or anticholinergic drugs.

32
Q

What is inflammatory bowel disease

A

Crohn’s disease & ulcerative colitis. Inflammatory response, systemic symptoms, familial occurence.

Etiology: genetic predisposition, immune dysfunction, and environmental factors.

Both result from inflammatory cells and mediators that cause tissue damage.

33
Q

What is Crohn’s disease

A

Form of IBD - an inflammatory response that can affect any part of the GI, mostly the terminal ileum or cecum. It is a recurrent, slowly progressive disease that affects people in their 20-30s, and more women.

Granulomatous lesions surrounded by normal mucosal tissue. Skip lesions.

All layers of the bowel are affected; has a cobblestone appearance from fissures and crevices that develop around the submucosal edema. Pathology of the submucosal layer includes inflammatory and fibrotic changes; the bowel wall becomes thickened and inflexible; the adjacent mesentery becomes inflames; regional lymph nodes and channels may become enlarged.

34
Q

Describe the clinical presentation, diagnosis, and treatment of Crohn’s Disease

A

Exacerbations & remissions.
Main symptoms depend on involved locations - diarrhea, abdominal pain, weight loss, fluid and electrolyte disorders, malaise, low grade fever.
Less bloody diarrhea than ulcerative colitis due to it affecting the submucosal layer more than the mucosal layer. Severe diarrhea causes ulceration of the perianal skin. Nutritional deficiencies may occur due to damage in the absorptive surface of the intestines.
Fistulas can form, abdominal abscesses, and intestinal obstruction.

Diagnosis - visualize small intestine with a capsule endoscopy; colonoscopy for colon; stool cultures for infectious causes; CT scans for inflammatory mass or abscess.

Treatment - stopping inflammatory response, promoting healing, maintaining adequate nutrition, preventing and treating complications. Medications - suppress inflammation like corticosteroids, immunosuppresants, and immunomodulators. Surgical intervention for damaged bowel, drainage of abscesses, or repair of fistula tracts. Fatty food should be avoided.

35
Q

What is ulcerative colitis

A

Ulcerative colitis is an inflammatory disease of the colon, common in US and Western countries. Affects the rectum and colon only. The inflammation is continuous. The ulcers form in the crypts of Lieberkuhn which lead to the formation of pinpoint mucosal hemorrhages and end in crypt abscesses. The lesions can become necrotic and ulcerate. The mucosal layer can develop tongue like projections that resemble polyps called pseudopolyps. Because of inflammation, the bowel wall thickens.

36
Q

Describe the clinical presentation, diagnosis, and treatment of UC

A

Clinical presentation: relapsing bouts of diarrhea usually with blood and mucus. Mild abdominal cramping, incontinence, anorexia, weakness, and fatigue.
Severity is defined as mild, moderate, severe, or fulminant dpeending on how much of the colon is affected and the extent of inflammation. People with fulminant disease are at risk of toxic megacolon, which is dilation of the colon with signs of systemic toxicity due to the vast inflammatory response.
Other complications include perforation, homorrhage, and colonic carcinoma.

Diagnosis: sigmoidoscopy, colonoscopy, biopsy, negative stool cultures for infectious disease.

Treatment: dependent on severity, symptoms, geared to control acute manifestations and prevent recurrence. Mild to moderate can avoid irritating foods. Fiber supplements to decrease diarrhea. Meds like corticosteroids, immunosuppresants, and immunomodulators. Surgery to remove rectum and colon if needed.

37
Q

Explain the process of neurotransmitters activating in the GI tract

A

The stomach produces a proenzyme called pepsinogen that is activated by gastric juice to become pepsin. Pepsin starts to digest proteins in the stomach. The gastric juice is made of hydrochloric acid. It’s produced by parietal cells in the walls of the stomach.
Numerous neurotransmitters like histamin, gastrin, and acetylcholine bind to receptors on the parietal cells and that leads to intracellular signaling pathways that are going to activate the proton pump. The proton pump is going to be moving hydrogen ions into the lumen of the stomach, where they’re going to be able to bind to chloride ions and form the hydrochloric acid which has a very low pH. Because there are neurotransmitters involved, we can see that the nervous system is helping to guide this process in digestion.
This acid and pepsin would actualy damage the cells that are releasing it. The pepsin could digest proteins in the surface of these cells. And the acid would destroy these cells. Thus the stomach cells have a mucus lining that’s protecting them called the mucosal barrier.
So along with the cells for the neurotransmitters, these stomach cells have receptors for prostaglandin B2, which inhibits stomach acid production and encourages the secretion of mucus.
Drugs like NSAIDs can disrupt that prostaglandin signals and make patients prone to ulcers and gastric bleeding because we decrease the mucosal barrier.

38
Q

What is GERD

A

GERD is the severe and frequent backwards movement of gastric contents into the esophagus, occurring at least 2x/week.

The esophagus enters into the cardiac region of the stomach close to the heart, which is why it feels like the chest is burning. Can affect people after they have a large meal, eat spicy or acidic foods, consume too much coffee or alcohol. The lower esophageal sphincter relaxes from stomach distension or high fat meals and then allows the stomach acid to reenter the esophagus. The issue is corrected by esophageal peristalsis and salvia neutralizes the acid (bicarbonate).

Two types of GERD:
Erosive esophagitis - mucosal damage to the esophagus
Nonerosive Reflux Disease (NERD) - no mucosal damage

Complications: bleeding and ulcers, strictures (narrowing esophagus from repeated injury and scaring), Barrett Esophagus - The normal squamous mucosa that lines the esophagus is gradually replaced by abnormal columnar epithelium (as seen in the stomach or intestines). Barrett esophagus is a major risk factor for developing esophageal adenocarcinoma.

39
Q

How do you diagnose and treat GERD

A

Belching, chest pain, dyspahgia, bloating or early satiety, laryngitis, chronic cough, sour taste in mouth, dental erosion. Alarming symptoms are weight loss, persistent vomiting, dysphagia, odynophagia, or blood in stool.

Patient history
Acid suppression trial - proton pump inhibitor for 14 days
Esophagoscopy
Esophageal pH monitoring

Treatment:
Lifestyle changes: lose weight, avoid aggravating foods, eat smaller meals, don’t laydown for 3-4 hours after meals, elevate bed
Pharmaceuticals: antacids (alkaline, neutralize stomach acids), H2 receptor antagonists (histamine), proton pump inhibitors (limit production of stomach acid), gastrointestinal stimulants (increase motility of stomach to prevent damaging gastric juices from reaching the esophagus)

40
Q

What is peptic ulcer disease (PUD)

A

Peptic ulcers are open sores in mucosal lining of stomach and duodenum. H. Pylori causes most of them via inflammatory mechanisms, cytokines contribute to mucosal damage. Duodenal (more common) and gastric ulcers.
NSAIDs or steroids inhibit the production of prostaglandins that generate the mucosal barrier in the stomach.
Zollinger-Ellison syndrome - hypersecretory state where too much stomach acid is secreted because of a gastrin secreting tumor.
Smoking, alcoholi, caffeine, emotional stress, genetic predisposition.

Once a patient has an ucler they can reoccur because of incomplete healing or scar tissue. Ulcers can go through any tissue in the GI tract wall and if it goes through smooth muscle, it does not regenerate completely which can lead to further exasperations.

41
Q

How do you diagnose and treat PUD

A

Symptoms: many are asymptomatic, pain that in upper abdomen, burning, cramp like. Gastric ulcers are worsened by eating; duodenal are worse when stomach is empty. Pain may be present for weeks and then remit.

Complications: gastroduodenal bleeding (tissue bleeding or erosion of an ulcer into artery or vein); weakness, dizziness, dehydration, cool moist skin, dark tarry stools. Perforation is less frequent but life threatening (when ulcer erodes through all layers and GI contents enter the peritoneum and cause peritonitis - abdominal pain radiating into the back, night distress, inadequate pain relief - appear on xrays).

Diagnose: endoscopy to visualize the ulcer, biopsies for H pylori, and exclude malignancies. History to evaluate for NSAID use. Lab results for anemia and check stool for occult blood. Barium radiography if needed.

Treatment: eradicate cause and heal the ulcer. PPI, antibiotics if needed. Prostaglandin analog for NSAID associated ulcers to stimulate mucus and bicarbonate secretion.

42
Q

What is jaundice

A

Jaundice is caused by high levels of bilirubin in the blood and is associated with yellowing of the skin, sclera, and mucus membranes (hyperbilirubinemia).

It is an issue of another liver disease - treat the liver disease not the jaundice.

As red blood cells breakdown, the heme in hemoglobin is metabolized into bilirubin which can be toxic, has a yellowish pigment, and it gets processed to the liver where it binds to bile to be eliminated via the stool. When red blood cells are destroyed, the final product of heme breakdown is bilirubin. This free bilirubin, which is insoluble in plasma, is transported in the blood attached to plasma albumin. As it goes through the liver, it is released from albumin and converted to conjugated bilirubin, which is soluble in bile. In the intestine, conjugated bilirubin is converted into a highly soluble urobilinogen by the intestinal flora. Approximately one fifth is absorbed into portal circulation while the remaining amount is excreted in the feces. Normal serum bilirubin is a small amount, less than 1.5 mg/dL.

Pre-hepatic (excessive red blood cell destruction) - hemolytic blood transfusion reaction, sickle cell disease, thalassemia, acquired or autoimmune hemolytic disorders, hemolytic disease of the newborn.
Intrahepatic (with the liver itself) - decreased bilirubin uptake by liver or decreased conjugation, liver damage via hepatitis, cirrhosis, cancer, drug induced cholestasis.
Post-hepatic (obstruction of bile flow) - bile duct structural disorders, cholelithiasis, congenital atresia of the extrahepatic bile ducts, tumors blocking the bile duct.

43
Q

What is neonatal jaundice

A

Hyperbilirubinemia caused by increased production of bilirubin and the neonate’s inability to excrete it. Greater risk of neurotoxicity - encephalopathy, cerebral palsy, sensorimotor deficits, kernicterus (brain damage from bilirubin accumulation in the basal ganglia and brainstem)

Etiology:
Physiologic hyperbilirubinemia - most infants; the bilirubin increases with the destruction of red blood cells and those have a shorter lifespan in neonate. Less efficient at removing the bilirubin because there is going to be more enterohepatic circulation (bile reabsorbed in liver, resecreted into the bile)
Breastfeeding jaundice - take in less milk in beginning, dehydrated, increase enterohepatic circulation
Breast milk jaundice - molecule in milk increases bilirubin reabsorption
Liver disease
Pathologic hyperbilirubinemia from hemolytic disease (red blood cells destroyed, increase heme), hypothyroidism, sepsis, or hematoma resportion.

Treatment based on bilirubin level, age, prematurity, health. Phototherapy - using white or blue light to photo-isomerize unconjugated bilirubin into a water soluble form that can be excreted by the liver and kidneys.

44
Q

How do you diagnose and treat jaundice

A

Lab liver function tests to diagnose liver disease to look for enzymes ALT and AST. ALT is liver specific, both are elevated in liver damage. Serum bilirubin, GGT, alkaline phosphatase measure hepatic excretory function.

45
Q

What is cirrhosis

A

Cirrhosis is the process of continued liver damage and injury leading to fibrosis and nodules that decrease the normal functions of the liver tissue. Many chronic liver disease lead to cirrhosis. Some patients might be asymptomatic and have typical life expectancy, some are at the end stage of liver disease.

Cirrhosis is characterized by diffuse fibrosis and nodules that cause scarring which disrupts blood and bile flow in the liver. Disruption of blood flow leads to portal hypertension; disruption of bile flow causes bile stasis and a loss of liver cells, leading to liver failure. Cirrhosis is associated with an increased incidence of hepatocellular carcinoma.

Nonalcoholic fatty liver disease is now the most common cause of chronic liver disease in the Western world and is associated with obestiy and metabolic syndrome.

Etiology: viral hepatitis (BCD), alcoholic liver disease, non alcoholic fatty liver disease (NAFLD).

Clinical manifestations: decreased liver function, fatigue, anorexia, weight loss, muscle wasting, jaundice, purpura, portal hypertension and can see veins around stomach, aceites, edema in lower limbs, testicular atrophy leading to gynecomastia, hemorrhoids. Hepatomegaly, jaundice, with abdominal pain most common signs.

Diagnosis: history and physical exam, full panel of blood tests, upper GI endoscopy to rule out other causes of disease. Signs of advanced cirrhosis detected using ultrasound, CT scan, and MRI. Liver biopsy most specific and sensitive test.

Treatments: aimed at controlling symptoms and trying to stop progression. Antivirals for hepatitis. Steroids for autoimmunity.

46
Q

What is cholecystitis

A

The gallbladder is a pear-shaped muscular sac located on the ventral surface of the liver. It functions to store and concentrate bile. Bile contains bile salts, cholesterol, bilirubin, lecithin, fatty acids, and the water and electrolytes normally found in plasma.
When food enters the intestine, the gallbladder contracts and the sphincter of the bile duct relaxes, so that bile can flow from the gallbladder to the duodenum. The GI hormone, CCK, is released during food digestion and aids in stimulating gallbladder contraction.

Inflammation of the gallbladder with more than 95% caused by gallstones (cholelithiasis). Gallstones block the cystic duct causing inflammation and fluid to gather in the lumen of gallbladder. The stones form because of biliary sludge becoming static or not moving as it should due to patient becoming pregnant, being given nutrition intravenously.

Cholesterol stones most common. Also black and brown stones. The two major factors that contribute to gallstone formation are increased cholesterol in bile and stasis of bile. Also 40s, obesity, female (esp multinup and oral contraceptives)

Acute cholecystitis is diffuse inflammation of the gallbladder. Eighty-five to ninety percent of acute cholecystitis is due to obstruction of the gallbladder outlet from gallstones. The other cases are due to sepsis, severe trauma, or infection of the gallbladder.
Chronic cholecystitis occurs from chronic irritation by stones or multiple attacks of acute cholecystitis. The presence of gallstones and chronic inflammation of the gallbladder are commonplace with this condition.
When gallstones block the common bile duct (the duct shared by the gallbladder and pancreas), acute pancreatitis can occur. Acute pancreatitis is a reversible inflammatory condition commonly brought on by gallstones or alcohol abuse. It presents with mid-epigastric or left upper quadrant pain that radiates to the back, with nausea and vomiting. When damaged, the pancreas will release amylase and lipase – these lab values will be elevated during this process.

Symptoms include vomiting, anorexia, malaise, fever, pain or tender upper right quadrant. Gallstones cause symptoms when they obstruct bile flow or cause inflammation. Small stones (< 8 mm in diameter) pass into the common duct, producing symptoms of indigestion and biliary colic. Larger stones are more likely to obstruct flow and cause jaundice. The pain of biliary colic presents as right upper quadrant or epigastric pain, sometimes radiating to the back or shoulder. Pain is acute, lasting more than 3-6 hours and is often associated with mild fever, anorexia, nausea, and vomiting. Lab values will often show an elevated white blood cell count, and mild elevations of AST, ALT, alkaline phosphatase, and bilirubin. With chronic cholecystitis, the patient may have an intolerance to fatty foods, belching, and colicky pain.

Worrying complication is perforation of the gallbladder.

Diagnosis via ultrasound and CT scan.

Treatment: pain management, antibiotics, cholecystectomy.