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%.
No comments:
Post a Comment