Week 2 Flashcards

Question

Dumping Syndrome

Answer 1

rapid gastric emptying often resulting from gastric bypass surgery, vagotomy, and high sugar-containing meals. Rapid entry of gastric contents into the duodenum represents an osmotic challenge, water moves into the lumen resulting in hypovolemia and reduced blood pressure. Results in nausea, weakness, dizziness, sweating, shakiness, diarrhea, heart palpitations

Answer 2

scarring and ulcers near the pylorus can delay emptying or in duodenal ulcers can lead to rapid gastric emptying due to loss of duodenal negative feedback mechanisms.

Answer 3

The neurotransmitters that regulate vomiting are poorly understood, but inhibitors of dopamine, histamine, and serotonin are all used to suppress vomiting.

Answer 4

Receptive relaxation of the proximal stomach allows the stomach to function as a reservoir The antral stomach uses phasic contractions driven by the basal electrical rhythm of the stomach to grind the meal Emptying of the stomach involves tonic contractions of the proximal portions and pylorus opens only partially and intermittently in response to feedback from the duodenum. Liquids leave most quickly and fats leave the stomach slowly permitting emulsification. During fasting, phase III of the MMC is stimulated by the GI hormone motilin and acts to remove undigested material Vomiting requires somatic and gastrointestinal muscles, and involves retrograde propulsion of the gastric contents out of the body.

Answer 5

Periodontal disease is infectious disease destroying supporting structures of teeth Affects more than 30% of population worldwide Mild and common form: gingivitis. Involves the gums. Irritation Redness Swelling

Answer 6

infection of underlying tissues and bones having periodontitis may be associated with: Heart attack Stroke Lung disease Premature birth or having a baby with low birth weight, in women Diabetes***

Answer 7

Biofilms consist of two or more species of bacterial microcolonies that are enclosed in a glycocalyx. Glycocalyx is composed of polysaccharides and constitutes up to 50-95% of the biofilm Other components of the biofilm include proteins and DNA Can be hundreds of species in a biofilm Formation of a biofilm: Weak adherence of cells to a surface Stronger adherence, likely co-adhesion mediated Multiplication of cells Polysaccharide formation Changing of microbial composition over time Why live in a biofilm: Adherence Protection from the immune system Protection from antibiotics Symbiotic (but also anti-symbiotic) relationships Local conditions of pH, etc, in a normally inhospitable environment

Answer 8

Microbes that cause caries are usually located in plaques on tooth surfaces, often in crevices or between teeth Tip: they’re often gram positive Microbes that cause periodontal disease do their destruction primarily below the gumline – in the subgingival space Tip: they’re often gram negative

Answer 9

``` Gram + Cocci Catalase - Facultative anaerobe a hemolytic optochin resistant ``` Mutans Streptococci have well-known virulence factors: adhesin-like surface-associated proteins (e.g. AgI/II family) that are capable of binding to receptors in the pellicle extracellular glucosyltransferases (Gtfs) are constituents of the pellicle and are capable of synthesizing glucans (a type of polysaccharide) in situ from sucrose. Glucans provide additional S. mutans binding sites, as it binds avidly and in large numbers to these polymers

Answer 10

Mitis is usually benign, mutant causes caries.

Answer 11

Gram (-) bacillus anaerobic Asaccharolytic Black-pigmented colonies on blood agar plates Bacitracin resistant Porphyromonas gingivalis Cause periodontal disease

Answer 12

Oral Thrush (Oral candidiasis Most common in babies, elderly, immunocompromised

Answer 13

Hairy leukoplakia HIV+ Fuzzy white patches on side of tongue Unlike thrush, it cannot be wiped away

Answer 14

Ludwig’s angina complication of severe tooth infection or periodontal disease Skin infection on floor of the mouth, usually results from untreated dental infections. Swelling of infected area may block the airway or prevent swallowing of saliva. ``` Symptoms include: Breathing difficulty Confusion or other mental changes Fever Neck pain Neck swelling Redness of the neck Weakness, fatigue, excess tiredness ```

Answer 15

Creamy white lesions, usually on the tongue or inner cheeks. Sometimes oral thrush may spread to the roof of the mouth, gums, tonsils, or pharynx (or esophagus) Esophageal form is dangerous Diagnosis: May diagnose entirely on symptoms, but scraping on microscope slide can be performed (look for hyphae forms) Treatment: Must treat with prescription antifungal Most commonly a topical treatment: clotrimazole lozenge and nystatin suspension (swish and swallow). Unresponsive cases: a systemic antifungal such as fluconazole Worst case: IV administration of amphotericin B (significant side effects) Untreated infections can lead to an invasive candidiasis.

Answer 16

Hyphael forms Bacilli Non-spore Forming Non-motile Candida albicans

Answer 17

Gram (+) Cocci Catalase (-) b Hemolytic Bacitracin Sensitive S. pyogenes

Answer 18

Bacteria Gram (+) Bacilli Non-spore Forming Non-motile C. diphtheriae

Answer 19

Double stranded Linear DNA enveloped Epstein-barr virus

Answer 20

Gram (-) Flagellated helix-shaped rod (spirilli) Microaerophilic Catalase and oxidase (+) Urease (+) Helicobacter pylori Virulence factors: adhesins, urease (raises pH), immune evasion, motility and chemotaxis, VacA, TFSS, CagA ``` Diagnosis: A variety of methods are available, know the principles behind each test Endoscopy + culture Breath Test Stool test Blood test ``` ``` Diagnosis considerations: For test selection consider: purpose (diagnosis or follow-up) Invasiveness cost ``` Treatment: a week of “Triple therapy” is currently used Antibiotics will be necessary (often clarithromycin and amoxicillin; the 1,2) to remove H. pylori Proton pump inhibitor (3rd arm of triple therapy) to aid in the healing of ulcer

Answer 21

Symptoms of gastritis: Inflammation of the gastric mucosa (transient or chronic) Gnawing or burning ache in upper abdomen. May become either worse or better with eating Nausea Vomiting A feeling of fullness in your upper abdomen after eating Symptoms of gastric ulcer: Open sores that develop on the inside stomach lining. Most common: burning abdominal pain Felt anywhere from navel to breastbone Worse when stomach is empty Flare at night Often temporarily relieved by eating foods that buffer stomach acid Disappear and then return for a few days or weeks

Answer 22

H. Pylori virulence factor | Pore forming cytotoxin that allows leakage of Ca+ from epithelial cell

Answer 23

H. Pylori virulence factor Type 4 secretion system (TFSS) is a needle through which CagA travels into the host cytosol and affects the proliferative activities, adhesion, and cytoskeletal organization of epithelial cells. The entire system is also highly proinflammatory. CagA is now known to interact with at least ten host proteins

Answer 24

1. Attract inflammatory cells 2. Inflammatory cells cannot kill easily 3. Host damages itself by continual, ineffective immune response!

Answer 25

``` Gold standard test …but invasive, $$$ Guided biopsy, then: rapid urease testing histology culture ```

Answer 26

``` urease makes ammonia Detects radioactive CO2 Good for diagnosis Good for confirming cure Requires skilled technician ```

Answer 27

Detects H. pylori antibodies Useful for initial diagnosis only Not useful for confirming cure

Answer 28

Easy Good for diagnosis Good for confirming cure

Answer 29

Less frequently, H. pylori infection results in cancers: Mucosa-associated lymphoid tissue (MALT lymphoma or MALToma) in the stomach is termed “gastric MALT” Indigestion, heartburn (stomach pain) Long term inflammation is culprit Tumors of B cells Antibiotics are still part of the treatment strategy Gastric carcinoma Indigestion, heartburn (stomach pain) Long term inflammation is culprit Cancer of stomach lining (epithelial cells) H. pylori a risk factor in only 65-80% of gastric carcinoma potential mechanism by which CagA could contribute to gastric carcinogenesis: association with inactivation of tumor suppressor proteins Note: Infection with H. pylori is also associated with a reduced risk of esophageal adenocarcinoma. (Can you think of a hypothesis for mechanism??)

Answer 30

Characterized by acute neutrophilic inflammation of the mucosa, often with hyperemia and hemorrhage (acute hemorrhagic gastritis). The inflammatory changes can be complicated by gastric mucosal erosion (loss and necrosis of surface epithelium, confined to the lamina propria, i.e. mucosa) or an acute ulceration (necrotizing process extends beyond the mucosa into the submucosa and even into and through the muscle wall). Many causes: Acute infection with Helicobacter organisms First time use of large doses of NSAIDs and aspirin (cyclooxygenase inhibition) Ingestion of large quantities of alcohol (direct toxic effect) Patients with shock, trauma, sepsis, uremia, severe burns, and intracranial disease can get acute stress ulcers (burns – Curling’s ulcers in duodenum; CNS injury – Cushing’s ulcers) Complications of acute gastric ulceration include bleeding and perforation.

Answer 31

Chronic gastritis demonstrates morphologic findings of chronic inflammation (lymphocytes, plasma cells) or evidence of chronic injury (as in chronic reactive gastropathy). Often varying degrees of acute inflammation may also be present (when acute inflammation is present along with chronic inflammation, the histologic findings are described as active chronic gastritis). Most common causes of chronic gastritis include: H. pylori gastritis Autoimmune gastritis Chronic reactive gastropathy Complications of chronic gastritis include gastric mucosal erosions, peptic ulcer disease, gastric atrophy, intestinal metaplasia, dysplasia, and malignancy.

Answer 32

most common pathologic finding is active chronic gastritis, which typically begins in the antrum and can progress to involve the fundus. Morphologic findings of gastric atrophy can also be present. Patients can have high acid production and can get mucosal erosions and peptic ulcers. Complications also include MALT-lymphoma and gastric adenocarcinoma.

Answer 33

can also cause disease similar to H. pylori; this organism has reservoirs in cats, dogs, pigs, and nonhuman primates.

Answer 34

Due to autoimmune CD4+ T-cell mediated destruction of parietal cells; chief cells are also lost during destruction of the gastric glands (“bystander damage”). Antibodies to parietal cells and intrinsic factor are also produced as part of the autoimmune response, but are not pathogenic (can be used as a diagnostic test). The autoimmune damage results in: Decreased gastric acid secretion (achlorhydria). Compensatory hypergastrinemia and hyperplasia of antral gastrin-producing G cells, along with endocrine cell hyperplasia in the fundus and body of the stomach. Vitamin B12 deficiency due to loss of secreted intrinsic factor (pernicous anemia with increased RBC MCV). Reduced serum pepsinogen I concentration. Inflammatory mucosal damage and atrophy of the gastric mucosa in the body and fundus with sparing of the antrum and cardia. Clinical findings develop after many years and are related to vitamin B12 deficiency: Megaloblastic anemia (macrocytic anemia) Atrophic glossitis Malabsorptive diarrhea Peripheral neuropathy: Secondary to subacute combined degeneration of the dorsal and lateral spinal columns. Patients can present with paresthesias and ataxia associated with loss of vibration and position sense, and can progress to severe weakness, spasticity, clonus, paraplegia, and fecal and urinary incontinence. CNS alterations can also occur, including mild personality changes, memory loss, and psychosis.

Answer 35

Pattern of chronic gastric injury characterized by foveolar hyperplasia, mucin depletion, vascular congestion, edema, and lamina propria fibrosis. Changes are due to chemical mucosal injury, associated with use of NSAIDs, aspirin, bile reflux, and alcohol ingestion. Patients can get gastric erosions and ulceration. Chronic reactive gastropathy is very common, so make sure you understand the implications when a gastric biopsy is signed out as “gastritis with changes of chronic reactive gastropathy.”

Answer 36

Chronic ulceration of the GI tract associated with exposure to gastric type acid, typically occurring in the stomach and first portion of the duodenum (duodenum most common site). Most cases are due to either H. pylori chronic gastritis or due to chronic use of NSAIDs. H. pylori can produce hyperchlorhydric chronic gastritis which then damages the mucosa. NSAIDs cause direct chemical irritation and can suppress prostaglandin synthesis which is necessary for mucosal protection. It is estimated that 70% of patients with PUD have H. pylori infection, although only about 20% of H. pylori infected individuals will develop PUD. Other causes of ulceration associated with exposure to gastric acid include Zollinger-Ellison syndrome, GERD (with esophageal ulceration), and heterotopic gastric mucosa in a Meckel’s diverticulum (small intestinal ulceration). Other factors implicated in ulceration include cigarette smoking, and chronic use of high dose corticosteroids. Complications of chronic ulceration in PUD include: Bleeding (clinical hemorrhage as well as iron deficiency anemia). Perforation Obstruction, particularly when the ulcer is located in the pyloric channel, secondary to edema and fibrosis. Clinically, patients present with epigastric burning or aching pain, (often occurring 1-3 hours after eating and relieved with food), GI bleed, iron deficiency anemia, or perforation. Treatment is eradication of H. pylori if present, and neutralization of gastric acid with proton-pump inhibitors. Limiting use of offending medications such as NSAIDs is also recommended. Perforated ulcers can produce free air in the abdomen which can be seen on upright radiographs. These perforated ulcers may require surgical treatment.

Answer 37

defined as eosinophil rich inflammation, in the absence of a known cause for eosinophilia (e.g. reaction to drugs, parasitic infections, malignancy). Most cases are thought secondary to some type of allergic reaction to a food allergen (e.g. cow’s milk or soy protein in children). Patients may have peripheral blood eosinophilia and elevated IgE levels. Isolated eosinophilic gastritis is rare; most cases have involvement at multiple GI sites (e.g. esophagus, duodenum, in addition to the stomach – “eosinophilic gastroenteritis” when small bowel and stomach are involved). Lesions may present as a mass, large ulcer, or with pyloric obstruction.

Answer 38

gastritis characterized by marked intraepithelial lymphocytic inflammation (CD8+ T lymphocytes). Can be seen as an isolated finding, or in patient’s with either co-existing celiac disease or in patients with co-existing lymphocytic/collagenous colitis.

Answer 39

gastritis that appears morphologically similar to collagenous colitis. It can occur in patients with co-existing collagenous colitis, and also as an isolated disease involving the stomach only.

Answer 40

defined as gastritis with granulomatous inflammation. Most cases are secondary to an underlying disorder, such as Crohn’s disease, sarcoidosis, mycobacterial or fungal infections.

Answer 41

Very rare disorder caused by excessive secretion of transforming growth factor alpha (TGF-α). This results in marked diffuse hyperplasia of the foveolar epithelium of the body and fundus of the stomach. Patients also experience protein losing enteropathy and hypoproteinemia, with diarrhea, weight loss, and peripheral edema. Some cases of Menetrier’s disease are associated with an infection (e.g. CMV in children). Patients are also at risk for gastric adenocarcinoma.

Answer 42

Caused by gastrin secreting tumors (gastrinomas, a functioning type of neuroendocrine tumor, to be discussed later), which are most commonly found in the pancreas and small bowel. Elevated gastrin (diagnostic test) results in marked increase in the number of parietal cells, with increased gastric acid production. In addition, there is hyperplasia of mucus neck cells with mucin hyperproduction, and proliferation of endocrine cells in the stomach which can result in gastric carcinoid tumors. Patients will often present with PUD or chronic diarrhea. Treatment consists of removal of the gastrinoma and administration of proton-pump inhibitors. Gastrinomas are sporadic in 75% of patients, and the remainder are associated with MEN type I. The sporadic tumors tend to be solitary, whereas those associated with MEN type I may be multiple. Overall, 60-90% of gastrinomas exhibit malignant behavior.

Answer 43

Most occur in association with chronic gastritis (H. pylori gastritis, chronic reactive gastropathy, autoimmune gastritis); 75% of all gastric polyps are of this type, and most occur in the gastric antrum, followed by the body. These polyps may represent an exaggerated mucosal response to tissue injury and inflammation. Rarely, dysplasia and adenocarcinoma can develop in hyperplastic polyps.

Answer 44

Most occur in association with the use of proton pump inhibitors, secondary to increased gastrin secretion in response to decreased gastric acid. These polyps can also be seen in individuals with familial adenomatous polyposis (FAP).

Answer 45

Neoplastic polyp morphologically similar to other adenomas found in the GI tract (e.g. colon). Incidence of gastric adenomas increases with age, with most occurring in patients age 50 years and older. Gastric adenomas are also increased in incidence in patients with FAP. Since gastric adenomas often occur in association with chronic gastritis and intestinal metaplasia, some believe they represent polypoid areas of dysplasia.

Answer 46

Mesenchymal polypoid proliferation composed of a mixture of stromal spindle cells, small blood vessels, and inflammatory cells, particularly eosinophils. Can occur anywhere in the GI tract but stomach and small intestine are the most common sites. Usually occur in middle aged females, and are felt to represent a reactive “pseudotumor.”

Answer 47

stomach can be involved by polyps as seen in Peutz-Jeghers syndrome, juvenile polyposis, and Cronkite-Canada syndrome (these will be discussed in the lower GI tract lecture).

Answer 48

ectopic pancreatic rests in the stomach can produce a polypoid lesion.

Answer 49

``` consist of small, sessile, yellow mucosal nodules composed of aggregates of lipid laden macrophages in the lamina propria. Most commonly seen in chronic gastritis, and may represent a reaction to tissue injury. ```

Answer 50

Stenosis is due to hyperplasia of the pyloric muscularis propria. Occurring in 1 of 300 to 900 live births, it is 3-4 times more common in males. Patients typically present in the second or third week of life with new-onset regurgitation and persistent, projectile, non-bilious vomiting. Physical examination may reveal a firm abdominal ovoid mass. Surgical myotomy is curative.

Answer 51

Unusually large-diameter mural arteriole penetrates into the submucosa; these large vessels can erode through the mucosa and cause massive bleeding.

Answer 52

Most common malignancy of the stomach (90%). Significant variation in incidence worldwide, with countries such as Japan having 4-fold higher incidence than North America. This is believed to be secondary to environmental influences. In USA, incidence of gastric cancer has declined dramatically in the 20th century, perhaps because of reduced intake of possible dietary carcinogens as well as decreased H. pylori prevalence (see chart). Risk factors for gastric adenocarcinoma include: - Chronic gastritis, such as H. pylori gastritis and autoimmune gastritis (intestinal metaplasia-dysplasia-carcinoma sequence). - Dietary carcinogens (nitrosamines, smoked foods). - Menetrier’s disease. - Diets lacking in fruits/vegetables (antioxidants). - Patients with familial adenomatosis polyposis (FAP). Patients often present with symptoms of dyspepsia, dysphagia, and nausea (like chronic gastritis). Gastric adenocarcinomas typically occur in adults. Most adenocarcinomas involving the stomach occur at the GE junction, but these tumors are usually considered to be distal esophageal adenocarcinomas if their epicenter is within 5 cm of the GE junction and there is extension into the distal esophagus (typically see Barrett’s esophagus with these). Thus, most true gastric adenocarcinomas occur in the antrum. Morphologic types: Intestinal type: can present as a polypoid invasive mass or invasive ulcer. Microscopically, tumor shows glandular differentiation. Diffuse type: presents as diffuse involvement and thickening of the gastric wall (mucosa, submucosa, and muscularis propria). Microscopically, see signet-ring cells. Sometimes, this type of tumor can occur in younger adults. Diffuse involvement of the gastric wall can produce rigidity and a leather bottle appearance (linitis plastica). Tumors can spread to regional lymph nodes and liver (common occurrence), or exhibit peritoneal spread in the abdomen (Sister Mary Joseph umbilical nodule). Sometimes the first evidence of disease will be metastasis to the left supraclavicular lymph node (Virchow’s node). Treatment is with surgery, including regional lymph node dissection. Chemotherapy is used for those with unresectable disease and/or metastases. Overall survival is poor, with 5-year survival rate of 20%.

Answer 53

Can arise anywhere in the GI tract, but stomach is the most common site (60% stomach, 30% jejunum and ileum, 5% duodenum,

Answer 54

Stomach can be involved by a variety of lymphomas, but the most common lymphoma is the extra-nodal marginal zone B-cell lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma, also known as MALTomas), followed by diffuse large B-cell lymphoma (DLBCL). MALT lymphomas can arise in virtually any mucosal site (e.g. lung, GI tract, salivary gland, with stomach the most common site) and are typically associated with chronic inflammation. In the stomach, most MALT lymphomas are associated with H. pylori infection. It is believed that persistent infection with chronic antigenic stimulation results in activation of transcription factors that promote B-cell growth and survival. In some cases this is due to specific translocations resulting in fusion genes with transcription activation. In other cases, persistent H. pylori antigenic stimulation can activate transcription and induce a MALT lymphoma without genetic translocations. Importantly, eradication of H. pylori infection with antibiotics will cause regression of gastric MALT lymphoma in 60-90% of cases! Gastric MALT lymphomas due to translocations are associated with a lack of response to antibiotic therapy. As with H. pylori infection, patients present with dyspepsia and epigastric pain. Diagnosis is established by findings on the biopsy. Gastric DLBCL is typically seen in older individuals, and may arise de novo or from high grade transformation of a lower grade lymphoma such as MALT lymphoma. These lymphomas may present as large ulcerated masses with transmural involvement.

Answer 55

These are tumors that arise from the diffuse endocrine cells that are found in the GI tract. The more well differentiated tumors have historically been called carcinoid tumors; however, as this term can give the false impression that the tumor will behave in a benign fashion, a revised classification scheme (which is still in evolution) has been proposed based on degree of differentiation, mitotic rate, and other findings that can predict the ability of the tumor to metastasize (i.e. behave in a malignant fashion). The difficulty with GI neuroendocrine tumors is that most of them appear well differentiated histologically, and the appearance under the microscope does not allow one to predict their biological behavior. Mitotic rate is often times measured with these tumors, either by counting the number of mitoses per 10 high power fields (HPF) or by measuring the percent of cells in the proliferative phase with an immunohistochemical stain (Ki-67). The most important factors determining biologic behavior are the grade (as determined above), location, and stage of the tumor. In general, the benign (grade 1) tumors are of small size (2 cm in size, with invasion beyond the submucosa. Functioning tumors of any size that do not show poorly differentiated features are considered to be grade 3. The poorly differentiated grade 4 tumors appear malignant histologically, and look similar to small cell carcinoma or large cell neuroendocrine carcinoma as can be seen in the lung. Tumors are staged by site using the T,N,M classification. GI neuroendocrine tumors/carcinomas can occur throughout the GI tract, but small intestine is the most common site (see chart). Tumors typically occur in middle age or older adults. Tumors may be functioning, resulting in symptoms. For example, tumors producing gastrin can result in the Zollinger-Ellison syndrome. Some tumors may cause the “carcinoid syndrome” of cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right sided valvular fibrosis. In this syndrome, the symptoms are produced by bioactive substances secreted by the tumor, such as seratonin, histamine, and bradykinin . As these substances are typically metabolized by the liver, the presence of carcinoid syndrome strongly suggests that metastatic disease may be present. Most of the neuroendocrine tumors producing carcinoid syndrome are of midgut origin (jejunum and ileum, appendix, ascending colon). A helpful diagnostic test for carcinoid syndrome is the detection of 24 hour urinary 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of seratonin. In the stomach, these tumors typically present as a mass lesion or polyp. Most gastric neuroendocrine tumors are well-differentiated and non-functioning, and are most often confined to the mucosa or submucosa. These lesions rarely metastasize. In autoimmune gastritis, one can see hyperplasia of the endocrine cells in the atrophic fundic mucosa. Neuroendocrine tumors associated with autoimmune gastritis often behave in an indolent fashion. Gastric neuroendocrine tumors that arise without a predisposing condition have a greater likelihood to exhibit malignant behavior.

Answer 56

defined as inflammation of the thin, mesothelial covered layer of tissue that lines the abdominal cavity (peritoneum) and covers most of the abdominal organs (serosa). Many possible causes

Answer 57

can be secondary to perforation of a viscus (e.g. acute appendicitis, peptic ulcer, acute cholecystitis, diverticulitis, ischemic bowel, trauma), acute salpingitis, and peritoneal dialysis. Also can occur as spontaneous bacterial peritonitis (bacterial infection occurring in the setting of ascites, without obvious source of contamination).

Answer 58

defined as the accumulation of excess fluid in the peritoneal cavity. Many causes, but portal hypertension associated with cirrhosis is the most common cause (see list). Mechanisms for the development of ascites include “transudative” processes such as portal hypertension, decreased osmotic pressure (e.g. hypoalbuminemia), and “exudative” processes such as peritoneal disease resulting in extravasation of exudative fluid (e.g. peritoneal malignancy). In portal hypertension with cirrhosis, the mechanisms of fluid accumulation are multifactorial, involving splanchnic vasodilation with increased sodium and water retention, hepatic sinusoidal hypertension with increased hepatic lymph fluid (this process also augmented by hypoalbuminemia), and percolation of the hepatic lymphatic fluid into the peritoneal cavity. In obese individuals, detecting the presence of ascites by physical exam can be problematic. Imaging studies can be used, with abdominal ultrasound preferred over CT scan. A complication of ascites can be spontaneous bacterial peritonitis, a bacterial infection developing in the absence of a known contaminating source. An exudate of acute neutrophilic inflammation and fibrin is present on the serosal and peritoneal surfaces, and the ascitic fluid exhibits increased numbers of neutrophils. Organism is detected with gram stain and culture.

Answer 59

a dense fibrosing process that can result in renal failure due to ureteral obstruction. CT image shows obstructive uropathy (arrowheads) resulting from ureteral involvement that precluded contrast administration. Note that calcified abdominal aorta is not elevated from underlying lumbar spine and relatively smooth peripheral margins of abnormal soft tissue (arrows). Some cases of idiopathic (i.e. not due to some other cause) retroperitoneal fibrosis may be manifestations of IgG4-related autoimmune disease (discussed later).

Answer 60

Prominent circular folds in duodenum and upper jejunum Disappear in ileum May increase surface area by a factor of 3

Answer 61

Forms c.t. core of each villus Contains a central lymphatic vessel (lacteal) Capillaries and venules present Very cellular connective tissue: Lymphocytes, eosinophils, plasma cells, macrophages, fibroblasts, mast cells, smooth muscle cells, etc.

Answer 62

``` Open at base of villi Extend to muscularis mucosae Paneth cells at base of crypts Many mitotic cells present Cells turnover every 3-6 days Cells migrate to tips of villi where they are shed ```

Answer 63

Secrete an alkaline mucus (pH 8.1-9.3) into lumen of duodenum; neutralizes acid chyme arriving from stomach Glands are located in submucosa and lamina propria

Answer 64

Brunner’s glands Secrete an alkaline mucus (pH 8.1-9.3) into lumen of duodenum; neutralizes acid chyme arriving from stomach Glands are located in submucosa and lamina propria Many plicae circulares Adventitia present

Answer 65

Peyer’s patches Aggregates of lymphatic nodules M-cells: in epithelium above patches Endocytose antigen and transport it to underlying lymphatic tissue Provide precursors of intestinal plasma cells that produce IgA Plicae very sparse or absent Goblet cells are increasing in numbers

Answer 66

Exocrine and endocrine gland

Answer 67

Basis for eosinophilic staining of apical cytoplasm Contain enzyme precursors (proenzymes) Trypsinogen; chymotrypsinogen; proelastases; procarboxypeptidases; lipolytic enzymes (lipases); alpha-amylases; nucleases

Answer 68

``` Functions Reservoir for bile Concentrates bile Releases bile to duodenum Attached by cystic duct to common bile duct ```

Answer 69

Enzymatic hydrolysis of carbohydrates and proteins occur in duodenum lumen through pancreatic enzymes, at the microvillous membrane, and in the enterocytes for peptides

Answer 70

What are causes? Lactose in breast milk is major source of carbohydrates for infants Decrease in lactase normal condition for most of the world’s adult population Secondary after injury to absorptive cells due to Crohn’s disease, celiac disease, alcohol Symptoms: Bacterial fermentation of lactose leads to gas accumulation/pain, Lactic acid production increases osmotic load and water enters the lumen resulting in increased peristalsis and diarrhea.

Answer 71

Monosaccharide uptake occurs in duodenum and jejunum Two major apical transportersSGLT1 – sodium-glucose/galactose cotransporter-1GLUT5- fructose transporter Glucose (and galactose) are actively taken up through a Na+-monosaccharide symporter, SGLT1 (2 Na+/1 sugar) This is a secondary active transport process, critically dependent upon low intracellular Na+ generated by the Na+/K+ pump - Fructose uptake is promoted by a facilitated transporter, Glut5. - All monosaccharides leave the basolateral membrane via Glut2 and go to the liver.

Answer 72

7 essential amino acids must be obtained from the diet since they can not be synthesized de novo - Digestion is initiated in the stomach by pepsin (cleaves at neutral aas) and is inactive at pH>4.5-Pancreatic proteases include endopeptidases and carboxypeptidases that require brush border enzyme enteropeptidase (enterokinase) for activation-Glycosylated and proline rich proteins are resistant to digestion Amino acid absorption-Occurs in villi of duodenum and jejunum. - Digestion is aided by brush border endo- and exopeptidases generating single amino acids - Amino acids are transported across the apical membrane by Na+ dependent symporters dependent on the basolateral Na+/K+ pump (secondary active transport). - Many of these enyzmes and transporters are degraded and resynthesized with each meal -Peptide transporter 1 PEPT1 cotransports peptides with protons - Apical sodium/hydrogen exchanger (NHE) supplies the luminal H+ ion and is supported by the basolateral Na+/K+ ATPase. - Absorbed peptides are further digested by cytosolic proteases. - Basolateral transporters export surplus amino acids into the blood. - Peptides are cotransported with H+ - Amino acids are cotransported with Na+ - For first 6 months, intact proteins are absorbed by endocytosis. Mechanism of passive immunity in infants. - M cells take up proteins which are transferred to lymphocytes as antigens

Answer 73

-dense in calories, includes fat soluble vitamins, and add flavor- 90% of dietary lipids are triglycerides - 10% cholesterol, phospholipids, lipid soluble vitamins and toxins - Chewing and churning facilitate emulsification increasing water to oil surface area and reducing surface tension. Emulsfied particles are stabilized by coating with bile salts and phospholipids Chief cells secrete gastric lipase- not required but facilitates 10-30% of lipolysis Gastric lipase optimal pH is 5.4 and has a prominent role in neonates due to developmental delay of pancreatic enzyme expression and in people with pancreatic insufficiency. Free fatty acids in the duodenum trigger the release of CCK that activates pancreatic acinar secretion of lipase and procolipase. Pancreatic lipase activity is inhibited by low pH and bile acids prevent lipase binding to fat droplets.Colipase is activated by trypsin and binds bile acids recruiting lipase to cleave fatty acids. Pancreas acinar cells produce additional enzymes that contribute to lipid digestion and many become active in the duodenum which contains higher levels of calcium. Cholesterol esterase has broad specificity and can hydrolyze the 2-position fatty acid left untouched by lipase Secreted Phospholipase A2 converts phospholipids (cell membranes) into fatty acids and lysophospholipids Bile salts and phospholipids act to break up (emulsify) large fat globules into droplets. - Products are taken up by epithelial cell or are "packaged" into small bile salt-coated cylinders called "micelles”. - Bile salts must be present at a certain minimum level (critical micelle concentration) before micelles will form and fat soluble vitamins must be packaged into micelles for uptake. Lipids enter enterocytes by (1) nonionic diffusion, (2) collision with the membrane, or (3) carrier mediated transport Most of absorbed fatty acids are reassembed into triglycerides and coated with apoproteins to form chylomicrons - Fatty acid-binding protein and a sterol-binding protein transport fatty acids and cholesterol to the smooth ER where the 2-mono-glycerides are re-esterified into triglycerides. - Re-synthesized products are packaged in lipid droplets, coated with -lipoproteins (apoproteins) and then extruded from the cell as chylomicrons. - Chylomicrons are taken up by lacteals in the villi and flow with the intestinal lymph through the thoracic lymphatic duct into the venous circulation

Answer 74

Cholesterol esterase has broad specificity and can hydrolyze the 2-position fatty acid left untouched by lipase

Answer 75

Secreted Phospholipase A2 converts phospholipids (cell membranes) into fatty acids and lysophospholipids

Answer 76

Ezetimibe reduces uptake of cholesterol from the lumen by inhibiting Niemann Pick C1 Like 1 and is used to treat patients with hypercholestolemia

Answer 77

Colipase or lipase deficiency- chronic pancreatitis or congenital mutations (triglycerides only need 10-15% of normal enzyme levels). Treat with pancreatic enzyme supplements

Answer 78

Nutrigenetics – Refers to functional changes in the nucleic acid code that influences a persons response to nutrients Variation may be associated with geographic ancestry A gene variant may allow the better use of a specific nutrient by the organism

Answer 79

If a SNP (or variant) is necessary (required) but not sufficient it would mean that it is always present but is not the only requirement for the condition. Sufficient means that the SNP (or variant) is the actual cause of the condition, could also be assisted by other SNPs in the same gene or in another location, which might modulate its behavior in a positive or negative manner.

Answer 80

seeks to identify environmental factors that effect gene expression (global gene expression/or single gene variants)

Answer 81

The major products of lipid digestion - fatty acids and 2-monoglycerides - enter the enterocyte by simple diffusion across the plasma membrane. A considerable fraction of the fatty acids also enter the enterocyte via a specific fatty acid transporter protein in the membrane. Lipids are transported from the enterocyte into blood by a mechanism distinctly different from what we've seen for monosaccharides and amino acids. Once inside the enterocyte, fatty acids and monoglyceride are transported into the endoplasmic reticulum, where they are used to synthesize triglyeride. Beginning in the endoplasmic reticulum and continuing in the Golgi, triglyceride is packaged with cholesterol, lipoproteins and other lipids into particles called chylomicrons. Remember where this is occurring - in the absorptive enterocyte of the small intestine. Transport of lipids into the circulation is also different from what occurs with sugars and amino acids. Instead of being absorbed directly into capillary blood, chylomicrons are transported first into the lymphatic vessel that penetrates into each villus. Chylomicron-rich lymph then drains into the system lymphatic system, which rapidly flows into blood.

Answer 82

Parenchymal edema and peripancreatic fat necrosis occurs first. This is called acute edematous pancreatitis.

Answer 83

When necrosis involves the parenchyma along with hemorrhage and gland dysfunction it is described as hemorrhagic or necrotizing pancreatitis

Answer 84

Increased Amylase/ lipase Lipase is both more sensitive and specific than amylase Lipase and amylase may often be normal or only slightly elevated in chronic

Answer 85

predict mortality after 48 hours of acquired information. You must wait to get the information at 48 hours. The criteria are not used to predict mortality at admission with only initial labs.