here are some study questions for the quiz on esophageal and gastric disorders.
questions
esophageal disorders...
1. what is the etiology of achalasia?
2. what is the morphology of achalasia?
3. what are the possible sequelae of achalasia?
4. what is DES?
5. what is the morphology of DES?
6. what are the clinical manifestations of DES?
7. what is nutcracker esophagus?
8. what are the clinical manifestations of nutcracker esophagus?
9. what is the etiology of diverticula?
10. what are diverticula called in the proximal vs. distal portion of the esophagus?
11. what are the two types of hiatal hernia? which is most common?
12. what are some complications of hiatal hernias?
13. what is the etiology of mallory weiss syndrome?
14. what is the morphology of mallory weiss?
15. what are the sequelae of mallory weiss?
16. what is the etiology of esophageal varices?
17. what layer of the esophageal wall are esophageal varices?
18. what is a complication of esophageal varices?
19. what is the clinical presentation of esophageal varices?
esophagitis...
20. what are the etiologies for esophagitis that involve external irritation?
21. what are the etiologies for esophagitis that involve decreased LES tone?
22. what are some other etiologies of esophagitis?
23. what are the histomorphological characteristics of esophagitis?
24. what is the morphology of candida esophagitis?
barrett's esophagus, adenocarcinoma...
25. what is the most common etiology of barrett's esophagus?
26. what is the gross morphology of barrett's esophagus?
27. patches that are bigger than what size are at greater risk for developing adenocarcinoma?
28. what is the histomorphology of barrett's esophagus?
29. what is the etiology of esophageal adenocarcinoma?
30. risk of adenocarcinoma might be decreased by...
31. what is the morphology of esophageal adenocarcinoma? where in the esophagus does it affect?
squamous cell carcinoma vs. adenocarcinoma...
32. what is the difference in epidemiological factors in SCC vs. adenocarcinoma?
33. what is the etiology of SCC?
34. what is the difference in location for SCC vs. AC?
35. what is the morphology of SCC?
36. what is the 5 year prognosis for SCC?
37. what is the prognosis for AC?
h. pylori...
38. h. pylori is present in what percentage of chronic gastritis?
39. what are the characteristics of h. pylori that allow it to flourish in the GI system?
40. what are two outcomes of h. pylori infections?
41. what is the morphology of a stomach infected with h. pylori?
42. what are the techniques used to diagnose h. pylori infection?
figure 17-11, robbins 8th ed...
43. what are some "defensive forces" present in normal gastric mucosa?
44. what are injurious forces that can damage gastric mucosa?
45. what are the layers in a gastric ulcer from the lumen to the serosa?
acute gastritis...
46. what are the most common etiologies of acute gastritis?
47. what is the gross morphology of acute gastritis?
48. what kind of exudate is associated with acute gastritis?
49. what are the clinical manifestations of acute gastritis?
chronic gastritis...
50. chronic gastritis is characterized by...
51. what is the incidence of chronic gastritis in the US?
52. what are the etiological mechanisms for chronic gastritis?
53. what are some examples of autoimmune conditions that could result in chronic gastritis?
54. what is the gross morphology of chronic gastritis?
55. what are the clinical manifestations of chronic gastritis?
56. diagnosis of chronic gastritis is made by...
57. what are the complications of chronic gastritis?
58. what is a MALToma?
gastric cancer...
59. which countries does gastric cancer have a particularly high incidence in?
60. which blood type has a high incidence for gastric cancer?
61. which races are particularly affected by gastric cancer?
62. what are some diet related risk factors for gastric cancer?
63. what is the gross morphological difference between a gastric ulcer and gastric cancer?
64. what locations are gastric cancer and a gastric ulcer most prone to affect?
65. what is the histomorphological features of the intestinal and diffuse variants of gastric cancer?
66. both the intestinal and diffuse variants of gastric cancer spread to...
67. describe the stages of pathological progression in gastric cancer.
virchow's node and sister mary joseph nodule...
68. what does virchow's node refer to?
68. what does the sister mary joseph nodule refer to?
answers
1. nerve degeneration causes increased LES tone, decreased LES relaxation, and aperistalsis.
2. progressive dilation, variable wall thickness, loss of myenteric plexus.
3. from increased pressure: SCC, candida esophagitis, diverticula.
4. failure of functional peristalsis: entire esophagus contracts simultaneously.
5. twisted corkscrew shaped esophagus.
6. dysphagia, odynophagia.
7. functional peristalsis but with high amplitude contractions.
8. odynophagia.
9. abnormal motility / spasm.
10. proximal: Zenker. distal: traction.
11. 95% are sliding. 5% paraesophageal.
12. ulceration, hemorrhage, perforation, strangulation, obstruction. [hi. strangle and tear the ham which is perfectly obstructing you]
13. severe alcoholism.
14. longitudinal lacerations, mm to cm in length.
15. inflammatory ulcers, mediastinitis, chronic blood loss.
16. increase in portal hypertension. can be from alcoholic cirrhosis, non-alcoholic cirrhosis, portal vein thrombosis.
17. submucosa.
18. rupture and hemorrhage into into lumen and esophageal wall.
19. asymptomatic until rupture.
20. reflux, radiation, gastric intubation, alcohol, hot fluids, hiatal hernia.
21. hypothryoidism, scleroderma, smoking, obesity, pregnancy.
22. infection / immunosuppression, chemical toxicity, skin disease.
23. eosinophils in the epithelium, basal zone hyperplasia, extended lamina propria papillae.
24. grey/white pseudomembrane loaded with fungal hyphae.
25. long standing GERD.
26. red and velvety patches.
27. 3cm.
28. esophageal epithelium turns into columnar intestinal epithelium with goblet cells.
29. generally occurs in areas of barrett esophagus in patients over 40 years old.
30. h pylori overgrowth.
31. distal esophagus, flat or raised patches that progress to nodular masses that may ulcerate.
32. SCC: older than 50, male, black, iran/china/HK/south africa/PR/eastern europe. AC: older than 40, male, white, US/canada/UK/australia/brazil/netherlands.
33. toxic influences, HPV
34. SCC in mid esophagus, AC in distal esophagus.
35. plaque-like thickenings, tumors that encircle the lumen.
36. superficial: 75%. nodal: 9%.
37. 80%, unless advanced stage: 25%.
38. 90%.
39. motility, urease, protease, adhesion molecules, toxins.
40. antral gastritis / atrophic gastritis, abnormal acid production.
41. intra-epithelial neutrophils, lymphoid aggregates, sub-epithelial plasma cells, hyperplastic / inflammatory polyps.
42. antibody tests, urea breath tests, stool tests, rapid urea test, bacterial culture tests, DNA detection.
43. bicarbonate, mucosal blood supply, mucous secretion, epithelial regeneration.
44. h. pylori
NSAIDs
aspirin
cigarettes
alcohol
hyperacidity
45. necrotic debris
acute inflammation
granulation tissue
scarring (fibrosis)
46. GI irritants, systemic toxins, stress.
47. neutrophils above basement membrane
superficial epithelium erosion
infiltrate and exudate in the lumen
48. fibrin purulent exudate.
49. ulcer like pain
nausea, vomiting
hematemesis
50. chronic mucosal inflammation without erosions that lead to mucosal atrophy and epithelial metaplasia.
51. over 50% in the later decades of life.
52. autoimmune
chronic infection
toxic
mechanical
53. hashimoto, addison's, IDDM.
54. attenuated / flat / reddened mucosa
lymphocytes and plasma cells in lamina propria
metaplasia with intestinal epithelial cells
55. hunger pains
pain at night and with gastric emptying
pain that refers to chest, thoracic spine, left shoulder
56. endoscopy or barium swallow xray.
57. anemia
obstruction
penetration into neighboring organs
perforation
carcinoma in an ulcer [A O P P C] [an outstanding pathologist prevents catastrophe]
58. low grade gastric lymphoma of the MALT tissue.
59. japan and china.
60. type A.
61. african americans, native americans, native hawaiians.
62. food preserved with nitrates
lack of refrigeration
lack of fresh fruits and vegetables
charred foods / polycyclic hydrocarbons
63. gastric ulcer: level margins, smooth base, red/edematous surrounding mucosa.
gastric cancer: raised margins, shaggy/necrotic base, neoplastic tissue extends into surrounding mucosa.
64. GC: lesser curvature, antrum, pylorus. GU: lesser curvature, duodenum.
65. intestinal: broad, cohesive growths, bulky tumors of glandular structures. diffuse variant: signet ring cells, gastric type cells.
66. regional and distant lymph nodes, especially the sentinel node.
67. normal
acute gastritis
chronic gastritis
chronic atrophic gastritis
intestinal metaplasia
dysplasia
gastric adenocarcinoma
68. the sentinel lymph node, the lymph node to which gastric carcinoma often metastasizes.
68. a nodule in the periumbilical region that can be an indicator of metastasis of gastric carcinoma.
Showing posts with label gastritis. Show all posts
Showing posts with label gastritis. Show all posts
Wednesday, February 24, 2010
Monday, February 1, 2010
CPD II: stomach disorders
hiatal hernia is an abnormal prolapse of the stomach above the esophageal hiatus of the diaphragm, caused by increased abdominal pressure, muscle weakening of the diaphragm, and loss of elasticity, usually all exacerbated by age (70% of 70 year olds have hiatal hernia). it can be asymptomatic, or result in increased reflux, a "spare tire" shape above the waist, or increased waist sensitivity. risk factors all involve increasing abdominal pressure such as chronic constipation, low fiber diet, straining during bowel movements, obesity. surgery is ineffective, but vitamin C, cell salts, visceral manipulation have shown some success.
hypochlorhydria is low stomach acid levels, fairly common in elderly, that results from certain foods, medications (antacids in particular), stress, and radical diet changes. the lack of stomach acids causes fermenting of food in the stomach rather than digestion and can lead to manifold symptoms of GI distress such as constipation, bloating, diarrhea, gas, heaviness, fullness, and also pyloric alkali burn. eventually, the insufficient absorption of minerals might lead to joint and muscle problems as well as dry skin and brittle nails. hypochlorhydria is diagnosed via pH tests: a string pH test or a heidelberg pH test, which measures the time the stomach pH takes to come back down after a dose of bicarbonate. a chem screen will also show low Cl levels and a hair test might show low mineral content.
gastritis is a general term for a collection of conditions that result in inflammation of gastric mucosa. erosive gastritis is characterized by erosion of the gastric mucosa and is subdivided into acute and chronic erosive gastritis. acute is caused by medications (NSAID's in particular), trauma / surgery / severe illness, and results in severe symptoms that may include blood in nasogastric aspirate. chronic is caused by drugs as well, or chronic inflammatory disease, or viral infection, and may be asymptomatic, nonspecific, or manifest as mild nausea.
non erosive gastritis is generally caused by h. pylori, which is a gram negative, spiral shaped organism that is likely transmitted via the fecal/oral route or contaminated food/water. following infection, h. pylori burrows into the mucous layer overlying the gastric mucosa and secretes toxins and enzymes which cause inflammation, and ultimately atrophic gastritis, leading to decreased acid production. after the initial inflammation, patients with non-erosive gastritis due to h. pylori might be asymptomatic. there are two categories of tests that can detect presence of h. pylori. non-endoscopy tests include the urease breath test (detecting exhalation of radiotagged urea which is metabolized by urease secreting h. pylori), stool antigen test, and antibody test. all three tests are high specificity and sensitivity- the one downfall is that the antibody test can remain positive for 3 years after eradication of h. pylori. the endoscopy tests involve sampling the gastric mucosa: in the rapid urease test, the sample is put on a plate with urea and a pH sensitive media that changes color upon the reaction of urease. the bacterial culture test is difficult to perform and is only used "when antibiotic susceptibilities are necessary". the histologic detection involves staining the biopsy sample with certain stains.
h. pylori is also commonly associated with peptic ulcer disease, which most commonly occurs in the first few centimeters of the duodenum or the lesser curvature of the stomach. h. pylori is one of many factors that can throw off the balance between stomach acids and protective mucosal measures (such as bicarbonate secretion, mucus secretion), along with various lifestyle factors and NSAID's, that can all ultimately lead to PUD. some hypersecretory states that can also lead to PUD may involve tumors of islet cells that overproduce gastrin as in a gastrinoma or systemic mastocytosis and basophilic leukemias which both result in histamine overproduction. PUD associated with gastric ulcers are differentiated from duodenal ulcers by a different symptom picture. whereas duodenal ulcers are temporarily relieved by food, gastric ulcer symptoms are worsened by food (recall that hypochlorhydria is also worsened with food). duodenal ulcer pain is well circumscribed, intense epigastric pain that comes on 2-3 hours after food, is relieved by antacids, and often causes waking at night. gastric ulcer pain comes in episodes of several weeks and might remit spontaneously, only to recur years later. antacids might not have an effect on gastric ulcer pain.
while PUD has few specific PE findings, the diagnosis can be made with certainty via endoscopy with biopsy, which will yield actual visualizations of the ulcers and allow for h. pylori sample testing. PUD has several possible complications: hemorrhage of blood into the GI tract might manifest as coffee ground emesis and melena. perforation occurs when acid penetrates other organs. obstructive complications that result from fibrosis or spasm results in profuse vomiting long after eating. perforation is an acute abdominal emergency that results in intense spreading abdominal pain, lowered blood pressure, tachycardia, and decreased bowel sounds. despite these possible outcomes, PUD can have an excellent prognosis if the underlying cause is treated; if h. pylori is eradicated, ulcer recurrence rate will drop from 60-70% to 10-20%.
questions
hiatal hernia...
1. what is a hiatal hernia?
2. most people with hiatal hernia are...
3. what are the two types of hiatal hernia?
4. what is the frequency of hiatal hernia in people younger than 40 and older than 70?
5. what is the etiology for hiatal hernia?
6. what are some risk factors for a hiatal hernia?
7. what is the symptom picture of patients with hiatal hernia?
8. what are some effective treatments for a hiatal hernia?
hypochlorhydria...
9. what is the etiology of hypochlorhydria?
10. hypochlorhydria is more common in what age?
11. what are the signs and symptoms of hypochlorhydria?
12. how does the symptom picture contrast from an ulcer?
13. describe what can occur at the pyloric valve in hypochlorhydria.
14. what are some long term effects of hypochlorhydria?
15. what are the tests used to diagnose hypochlorhydria?
16. what is the heidelberg test?
erosive gastritis...
17. what is gastritis? √
18. what symptoms does microscopic inflammation of gastric mucosa correlate with? √
19. what are the two categories of acute gastritis? √
20. what is the etiology of acute erosive gastritis? ††
21. what are the signs and symptoms of acute erosive gastritis? X†
22. what is chronic erosive gastritis characterized by? √√
23. what is the etiology of chronic erosive gastritis? †X
24. what are the symptoms of chronic erosive gastritis? †
non erosive gastritis...
25. what is the etiology of non-erosive gastritis?
26. how does infection with h. pylori get transmitted?
27. what type of bacteria is h. pylori and what is its morphology?
28. describe the pathogenesis of gastritis via h. pylori.
29. what percentage of gastric and duodenal ulcers is h. pylori associated with?
30. describe the symptoms of non-erosive gastritis caused by h. pylori.
31. what are some general diagnostic tests that can aid in the diagnosis of non-erosive gastritis?
31b. what are four radiologic signs of gastritis that are fairly consistent regardless of etiology?
h. pylori tests, non-endoscopy...
32. what are three non-endoscopy based tests for h-pylori?
33. what is the sensitivity and specificity of the stool antigen test?
34. what are the two uses of the stool antigen test?
35. what is involved in the urea breath test?
36. what is the sensitivity and specificity of the urea breath test?
37. when is the urea breath test used?
38. what is the antibody test for h. pylori?
39. sensitivity of the antibody test?
40. what is the drawback of the antibody test?
h. pylori tests, endoscopy...
41. what are the three endoscopy tests for h. pylori?
42. what is involved in the rapid urease test?
43. how sensitive is the rapid urease test?
44. when is the bacterial culture test used?
45. what is involved in the histologic detection of h. pylori?
peptic ulcer disease...
46. where do peptic ulcers most commonly occur? √
47. what are some injurious factors that disturb the pH balance in the pathogenesis of PUD? †
48. what are some factors that protect against the pathogenesis of PUD? †
49. what are the most common etiologies for PUD? √
50. there is a weak association between PUD and which blood type? √
51. what are some hypersecretory states that might lead to PUD? †
52. what is a gastrinoma and how is it diagnosed? √
53. describe the pain that a patient with PUD involving a duodenal ulcer might experience. √
54. what are the common symptoms for PUD involving a duodenal ulcer? †
55. what is a notable difference in symptom presentation between PUD involving gastric vs. duodenal ulcer? X
56. what is the symptom picture of a gastric ulcer PUD? †
57. which is more common in PUD, a gastric or duodenal ulcer? √
58. which type of ulcer is more common in older PUD patients? √
PUD diagnosis, complications, prognosis...
59. what are some PE findings for uncomplicated PUD?
60. what is the imaging technique of choice for diagnosis of PUD?
61. what are possible complications of PUD?
62. hemorrhage might result in...
63. describe the clinical picture of a PUD patient who develops perforation.
64. what is "penetration" in the context of PUD complications?
65. what are the symptoms accompanied by obstructive complications of PUD?
66. what is the prognosis of PUD?
67. curing h. pylori infection changes ulcer recurrence rate from 60-70% to...
answers
1. when a portion of the stomach prolapses through the esophageal diaphragmatic hiatus.
2. asymptomatic, discovered incidentally.
3. sliding or paraesophageal.
4. 10%, 70%.
5. diaphragmatic muscle weakening, loss of elasticity, increased abdominal pressure.
6. low fiber diet, constipation, straining during bowel movement, obesity, chronic esophagitis.
7. asymptomatic, or increased reflux, spare tire bulge above waist, waist sensitivity.
8. vitamin C, cell salts, visceral manipulation. surgery not generally successful.
9. same foods as GERD, TUMS, caffiene / sugar / refined foods / alcohol, drugs, stress, radical diet shifts.
10. gets more common over 30, very common in over 60 year olds.
11. trouble digesting proteins, diarrhea / constipation, bloating, gas, heaviness, fullness.
12. worse from eating, as opposed to an ulcer, which is better from eating.
13. insufficient acid to balance out alkaline duodenum might precipitate alkali burn through pyloric valve.
14. joint/muscle aches, dry skin, brittle nails from malabsorption of minerals.
15. heidelberg pH test, string pH test, hair screen for low minerals, chem screen for low Cl.
16. measuring pH, adding bicarbonate to raise pH, then monitoring how long it takes for pH to lower back to normal levels.
17. inflammation of the gastric mucosa.
18. no correlation.
19. erosive and non erosive.
20. medications- NSAID's in particular. irradiation, alkali ingestion, chronic reflux, trauma / surgery / severe illness.
21. may be too ill to complain of gastric problems, may have blood in nasogastric aspirate.
22. multiple punctate or apthous stomach ulcers.
23. drugs, chronic inflammatory disease such as crohn's, viral infection.
24. may be asymptomatic or nonspecific, mild nausea.
25. most common cause is h. pylori.
26. unclear but likely through fecal-oral, or consumption of contaminated food / water.
27. gram negative, spiral shaped.
28. h. pylori settles into the mucous overlying gastric mucosa and secretes toxins / enzymes that cause inflammation of the gastric mucosa, leading to atrophic gastritis and therefore decreased acid production.
29. 60% gastric, 80% duodenal.
30. usually asymptomatic, maybe mild epigastric tenderness.
31. CBC (check for anemia from GI bleeding), liver/kidney/GB/pancreatic function tests, pregnancy test, occult blood. [anemia, organs, babies, cults]
31b. thick folds, inflammatory nodules, coarse area gastrica, erosions. [folds, nodes, coarse, erodes] [of course my nose erodes when folded]
32. stool antigen test, urea breath test, antibody test.
33. over 90%.
34. both to confirm presence of h. pylori before treatment and to confirm eradication after treatment.
35. patient ingests radiolabeled urea which is broken down by the urease from h. pylori, incorporated into exhaled CO2 which is then measured.
36. greater than 90%.
37. after therapy to confirm eradication.
38. ELISA test to detect IgA and IgG antibodies against h. pylori.
39. ~95%
40. might give false positive for 3 years after eradication of bacteria.
41. rapid urease, bacterial culture, histologic detection.
42. bacteria placed on dish with urea and pH indicator; color of media changes with urease breakdown of urea.
43. 90%.
44. "when antibiotic susceptibilities are necessary".
45. staining of a biopsy specimen with hematoxylin, eosin, Warthin, Giemsa, Genta stains.
46. 1st few cm's of the duodenum or along the lesser curve of the stomach.
47. weakened mucosa (from acid, pepsin, alcohol), drugs/smoking/stress, foods/lifestyle risk factors.
48. mucus, bicarbonate, hydrophobic layer, mucosal blood flow.
49. h. pylori, lifestyle factors, NSAID's.
50. O.
51. gastrinoma, multiple endocrine neoplasia, antral G cell hyperplasia, systemic mastocytosis, basophilic leukemias. [gastrin, MEN, antral, masto, basophils] [gassy men; an antsy mass of phil's]
52. tumor of pancreatic islet cells which results in high gastrin, detected by gastrin level tests or secretin tests (secretin normally should lower gastrin levels but in these patients raises them).
53. well circumscribed, severe, epigastric pain that occurs 2-3 hours after a meal and is relieved by antacids or milk.
54. epigastric pain, dyspepsia, heartburn, anorexia, coffee-ground emesis, melena, hematemesis. [stomach, indigestion, reflux, skinny, coffee, melena, vomiting blood] [yelena drank some coffee which caused indigestion and reflux in her stomach, caused her to lose weight and vomit blood]
55. eating often causes gastric ulcers while temporarily relieving duodenal ulcers; also may have no relief from antacids.
56. several week long episodes followed by disappearance without treatment and possible recurrence years later.
57. duodenal is more common, especially in males.
58. gastric.
59. few / nonspecific findings, may have epigastric tenderness, guaiac positive stool, melena.
60. endoscopy with biopsy.
61. hemorrhage, perforation, penetration, obstruction.
62. coffee ground emesis, melena.
63. acute abdominal emergency: severe spreading pain from right upper quadrant, decreased bowel sounds, hypotension, tachycardia.
64. acid invades other structures such as the pancreas and liver.
65. voluminous vomiting at the end of the day.
66. when underlying cause is addressed, prognosis is excellent.
67. 10-20%.
hypochlorhydria is low stomach acid levels, fairly common in elderly, that results from certain foods, medications (antacids in particular), stress, and radical diet changes. the lack of stomach acids causes fermenting of food in the stomach rather than digestion and can lead to manifold symptoms of GI distress such as constipation, bloating, diarrhea, gas, heaviness, fullness, and also pyloric alkali burn. eventually, the insufficient absorption of minerals might lead to joint and muscle problems as well as dry skin and brittle nails. hypochlorhydria is diagnosed via pH tests: a string pH test or a heidelberg pH test, which measures the time the stomach pH takes to come back down after a dose of bicarbonate. a chem screen will also show low Cl levels and a hair test might show low mineral content.
gastritis is a general term for a collection of conditions that result in inflammation of gastric mucosa. erosive gastritis is characterized by erosion of the gastric mucosa and is subdivided into acute and chronic erosive gastritis. acute is caused by medications (NSAID's in particular), trauma / surgery / severe illness, and results in severe symptoms that may include blood in nasogastric aspirate. chronic is caused by drugs as well, or chronic inflammatory disease, or viral infection, and may be asymptomatic, nonspecific, or manifest as mild nausea.
non erosive gastritis is generally caused by h. pylori, which is a gram negative, spiral shaped organism that is likely transmitted via the fecal/oral route or contaminated food/water. following infection, h. pylori burrows into the mucous layer overlying the gastric mucosa and secretes toxins and enzymes which cause inflammation, and ultimately atrophic gastritis, leading to decreased acid production. after the initial inflammation, patients with non-erosive gastritis due to h. pylori might be asymptomatic. there are two categories of tests that can detect presence of h. pylori. non-endoscopy tests include the urease breath test (detecting exhalation of radiotagged urea which is metabolized by urease secreting h. pylori), stool antigen test, and antibody test. all three tests are high specificity and sensitivity- the one downfall is that the antibody test can remain positive for 3 years after eradication of h. pylori. the endoscopy tests involve sampling the gastric mucosa: in the rapid urease test, the sample is put on a plate with urea and a pH sensitive media that changes color upon the reaction of urease. the bacterial culture test is difficult to perform and is only used "when antibiotic susceptibilities are necessary". the histologic detection involves staining the biopsy sample with certain stains.
h. pylori is also commonly associated with peptic ulcer disease, which most commonly occurs in the first few centimeters of the duodenum or the lesser curvature of the stomach. h. pylori is one of many factors that can throw off the balance between stomach acids and protective mucosal measures (such as bicarbonate secretion, mucus secretion), along with various lifestyle factors and NSAID's, that can all ultimately lead to PUD. some hypersecretory states that can also lead to PUD may involve tumors of islet cells that overproduce gastrin as in a gastrinoma or systemic mastocytosis and basophilic leukemias which both result in histamine overproduction. PUD associated with gastric ulcers are differentiated from duodenal ulcers by a different symptom picture. whereas duodenal ulcers are temporarily relieved by food, gastric ulcer symptoms are worsened by food (recall that hypochlorhydria is also worsened with food). duodenal ulcer pain is well circumscribed, intense epigastric pain that comes on 2-3 hours after food, is relieved by antacids, and often causes waking at night. gastric ulcer pain comes in episodes of several weeks and might remit spontaneously, only to recur years later. antacids might not have an effect on gastric ulcer pain.
while PUD has few specific PE findings, the diagnosis can be made with certainty via endoscopy with biopsy, which will yield actual visualizations of the ulcers and allow for h. pylori sample testing. PUD has several possible complications: hemorrhage of blood into the GI tract might manifest as coffee ground emesis and melena. perforation occurs when acid penetrates other organs. obstructive complications that result from fibrosis or spasm results in profuse vomiting long after eating. perforation is an acute abdominal emergency that results in intense spreading abdominal pain, lowered blood pressure, tachycardia, and decreased bowel sounds. despite these possible outcomes, PUD can have an excellent prognosis if the underlying cause is treated; if h. pylori is eradicated, ulcer recurrence rate will drop from 60-70% to 10-20%.
questions
hiatal hernia...
1. what is a hiatal hernia?
2. most people with hiatal hernia are...
3. what are the two types of hiatal hernia?
4. what is the frequency of hiatal hernia in people younger than 40 and older than 70?
5. what is the etiology for hiatal hernia?
6. what are some risk factors for a hiatal hernia?
7. what is the symptom picture of patients with hiatal hernia?
8. what are some effective treatments for a hiatal hernia?
hypochlorhydria...
9. what is the etiology of hypochlorhydria?
10. hypochlorhydria is more common in what age?
11. what are the signs and symptoms of hypochlorhydria?
12. how does the symptom picture contrast from an ulcer?
13. describe what can occur at the pyloric valve in hypochlorhydria.
14. what are some long term effects of hypochlorhydria?
15. what are the tests used to diagnose hypochlorhydria?
16. what is the heidelberg test?
erosive gastritis...
17. what is gastritis? √
18. what symptoms does microscopic inflammation of gastric mucosa correlate with? √
19. what are the two categories of acute gastritis? √
20. what is the etiology of acute erosive gastritis? ††
21. what are the signs and symptoms of acute erosive gastritis? X†
22. what is chronic erosive gastritis characterized by? √√
23. what is the etiology of chronic erosive gastritis? †X
24. what are the symptoms of chronic erosive gastritis? †
non erosive gastritis...
25. what is the etiology of non-erosive gastritis?
26. how does infection with h. pylori get transmitted?
27. what type of bacteria is h. pylori and what is its morphology?
28. describe the pathogenesis of gastritis via h. pylori.
29. what percentage of gastric and duodenal ulcers is h. pylori associated with?
30. describe the symptoms of non-erosive gastritis caused by h. pylori.
31. what are some general diagnostic tests that can aid in the diagnosis of non-erosive gastritis?
31b. what are four radiologic signs of gastritis that are fairly consistent regardless of etiology?
h. pylori tests, non-endoscopy...
32. what are three non-endoscopy based tests for h-pylori?
33. what is the sensitivity and specificity of the stool antigen test?
34. what are the two uses of the stool antigen test?
35. what is involved in the urea breath test?
36. what is the sensitivity and specificity of the urea breath test?
37. when is the urea breath test used?
38. what is the antibody test for h. pylori?
39. sensitivity of the antibody test?
40. what is the drawback of the antibody test?
h. pylori tests, endoscopy...
41. what are the three endoscopy tests for h. pylori?
42. what is involved in the rapid urease test?
43. how sensitive is the rapid urease test?
44. when is the bacterial culture test used?
45. what is involved in the histologic detection of h. pylori?
peptic ulcer disease...
46. where do peptic ulcers most commonly occur? √
47. what are some injurious factors that disturb the pH balance in the pathogenesis of PUD? †
48. what are some factors that protect against the pathogenesis of PUD? †
49. what are the most common etiologies for PUD? √
50. there is a weak association between PUD and which blood type? √
51. what are some hypersecretory states that might lead to PUD? †
52. what is a gastrinoma and how is it diagnosed? √
53. describe the pain that a patient with PUD involving a duodenal ulcer might experience. √
54. what are the common symptoms for PUD involving a duodenal ulcer? †
55. what is a notable difference in symptom presentation between PUD involving gastric vs. duodenal ulcer? X
56. what is the symptom picture of a gastric ulcer PUD? †
57. which is more common in PUD, a gastric or duodenal ulcer? √
58. which type of ulcer is more common in older PUD patients? √
PUD diagnosis, complications, prognosis...
59. what are some PE findings for uncomplicated PUD?
60. what is the imaging technique of choice for diagnosis of PUD?
61. what are possible complications of PUD?
62. hemorrhage might result in...
63. describe the clinical picture of a PUD patient who develops perforation.
64. what is "penetration" in the context of PUD complications?
65. what are the symptoms accompanied by obstructive complications of PUD?
66. what is the prognosis of PUD?
67. curing h. pylori infection changes ulcer recurrence rate from 60-70% to...
answers
1. when a portion of the stomach prolapses through the esophageal diaphragmatic hiatus.
2. asymptomatic, discovered incidentally.
3. sliding or paraesophageal.
4. 10%, 70%.
5. diaphragmatic muscle weakening, loss of elasticity, increased abdominal pressure.
6. low fiber diet, constipation, straining during bowel movement, obesity, chronic esophagitis.
7. asymptomatic, or increased reflux, spare tire bulge above waist, waist sensitivity.
8. vitamin C, cell salts, visceral manipulation. surgery not generally successful.
9. same foods as GERD, TUMS, caffiene / sugar / refined foods / alcohol, drugs, stress, radical diet shifts.
10. gets more common over 30, very common in over 60 year olds.
11. trouble digesting proteins, diarrhea / constipation, bloating, gas, heaviness, fullness.
12. worse from eating, as opposed to an ulcer, which is better from eating.
13. insufficient acid to balance out alkaline duodenum might precipitate alkali burn through pyloric valve.
14. joint/muscle aches, dry skin, brittle nails from malabsorption of minerals.
15. heidelberg pH test, string pH test, hair screen for low minerals, chem screen for low Cl.
16. measuring pH, adding bicarbonate to raise pH, then monitoring how long it takes for pH to lower back to normal levels.
17. inflammation of the gastric mucosa.
18. no correlation.
19. erosive and non erosive.
20. medications- NSAID's in particular. irradiation, alkali ingestion, chronic reflux, trauma / surgery / severe illness.
21. may be too ill to complain of gastric problems, may have blood in nasogastric aspirate.
22. multiple punctate or apthous stomach ulcers.
23. drugs, chronic inflammatory disease such as crohn's, viral infection.
24. may be asymptomatic or nonspecific, mild nausea.
25. most common cause is h. pylori.
26. unclear but likely through fecal-oral, or consumption of contaminated food / water.
27. gram negative, spiral shaped.
28. h. pylori settles into the mucous overlying gastric mucosa and secretes toxins / enzymes that cause inflammation of the gastric mucosa, leading to atrophic gastritis and therefore decreased acid production.
29. 60% gastric, 80% duodenal.
30. usually asymptomatic, maybe mild epigastric tenderness.
31. CBC (check for anemia from GI bleeding), liver/kidney/GB/pancreatic function tests, pregnancy test, occult blood. [anemia, organs, babies, cults]
31b. thick folds, inflammatory nodules, coarse area gastrica, erosions. [folds, nodes, coarse, erodes] [of course my nose erodes when folded]
32. stool antigen test, urea breath test, antibody test.
33. over 90%.
34. both to confirm presence of h. pylori before treatment and to confirm eradication after treatment.
35. patient ingests radiolabeled urea which is broken down by the urease from h. pylori, incorporated into exhaled CO2 which is then measured.
36. greater than 90%.
37. after therapy to confirm eradication.
38. ELISA test to detect IgA and IgG antibodies against h. pylori.
39. ~95%
40. might give false positive for 3 years after eradication of bacteria.
41. rapid urease, bacterial culture, histologic detection.
42. bacteria placed on dish with urea and pH indicator; color of media changes with urease breakdown of urea.
43. 90%.
44. "when antibiotic susceptibilities are necessary".
45. staining of a biopsy specimen with hematoxylin, eosin, Warthin, Giemsa, Genta stains.
46. 1st few cm's of the duodenum or along the lesser curve of the stomach.
47. weakened mucosa (from acid, pepsin, alcohol), drugs/smoking/stress, foods/lifestyle risk factors.
48. mucus, bicarbonate, hydrophobic layer, mucosal blood flow.
49. h. pylori, lifestyle factors, NSAID's.
50. O.
51. gastrinoma, multiple endocrine neoplasia, antral G cell hyperplasia, systemic mastocytosis, basophilic leukemias. [gastrin, MEN, antral, masto, basophils] [gassy men; an antsy mass of phil's]
52. tumor of pancreatic islet cells which results in high gastrin, detected by gastrin level tests or secretin tests (secretin normally should lower gastrin levels but in these patients raises them).
53. well circumscribed, severe, epigastric pain that occurs 2-3 hours after a meal and is relieved by antacids or milk.
54. epigastric pain, dyspepsia, heartburn, anorexia, coffee-ground emesis, melena, hematemesis. [stomach, indigestion, reflux, skinny, coffee, melena, vomiting blood] [yelena drank some coffee which caused indigestion and reflux in her stomach, caused her to lose weight and vomit blood]
55. eating often causes gastric ulcers while temporarily relieving duodenal ulcers; also may have no relief from antacids.
56. several week long episodes followed by disappearance without treatment and possible recurrence years later.
57. duodenal is more common, especially in males.
58. gastric.
59. few / nonspecific findings, may have epigastric tenderness, guaiac positive stool, melena.
60. endoscopy with biopsy.
61. hemorrhage, perforation, penetration, obstruction.
62. coffee ground emesis, melena.
63. acute abdominal emergency: severe spreading pain from right upper quadrant, decreased bowel sounds, hypotension, tachycardia.
64. acid invades other structures such as the pancreas and liver.
65. voluminous vomiting at the end of the day.
66. when underlying cause is addressed, prognosis is excellent.
67. 10-20%.
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