a study guide for the pathology quiz on male genitalia. we started with a review of various conditions that can affect the male genitalia: phimosis refers to an inability to retract the foreskin of the penis, often due to adhesions formed from undifferentiated tissue in children less than 3 years old. paraphimosis is an inability of the foreskin to fold over the glans. condyloma acuminata are genital warts, caused by HPV strains 6 and 11, appearing as sessile or pedunculated, red papillary outgrowths on the coronal sulcus, inner prepuce, glans, or perianal area.
bowen's disease is commonly caused by HPV 16 and 18 and manifests as single, gray-white plaques with shallow ulcerations and crusting, either on the shaft of the penis or the scrotum. histologically, one might see dysplastic epithelium, scattered mitosis above the basal layer, and nuclear atypia.
bowen's might lead to squamous cell carcinoma, which might also be caused by HPV strains 16 / 18, or simply poor hygeine. SCC typically affects men 40-70 and manifests as painless lesions that may bleed. early lesions may just be epithelial thickening with some fraying / fissuring, while late or untreated lesions may develop into papules, ulcers with ragged and heaped up margins.
some assorted testicular disorders that we've already covered in CPD: cryptorchidism is an undescended testicle which can be associated with hormonal disorders of deficient LHRH and "trisomy 13". it might also be related to exposure to anti-androgenic compounds such as phthalates in plastics and tagamet, which is used to treat plantar warts and peptic ulcers. cryptorchidism increases the risk for infertility as well as testicular cancer of the fully descended side. hydroceles are serous fluid filled masses that can be caused by inflammation (sports) as well as structural / developmental abnormalities. varicoceles result from dilatation of the panpiniform plexus and is also associated with sports such as extreme mountain biking or soccer.
benign prostatic hypertrophy is nodular hyperplasia of the periurethral region of the prostate. it is associated with some dietary factors: deficiency of lycopene, nettles, zinc, EFA's, and amino acids- as well as dietary excess of alcohol, cadmium, cholesterol, and pesticides. the main growth factor for the prostate is DHT, which is converted from testosterone by 5-alpha reductase; cadmium and cholesterol both increase 5-alpha reductase activity, thus contributing to BPH. two other hormonal influences: estrogen increases stroma susceptibility to hyperplasia and prolactin increases androgen uptake.
prostate cancer is the most common type of cancer in men, generally of the type adenocarcinoma. it affects men over 50 with some racial demographic trends: asians tend to have a lower incidence and african americans have a higher incidence. genetic factors that have been identified are the p53 gene and hypermethylation of glutathione S-transferase. a diet high in arachidonic acid (found in meat products) can also be a risk factor. dietary protective factors might include lycopene, vitamin A and E, selenium, soy, and possibly fish oil. the lesions themselves are gritty and firm nodules on the posterior aspects of the lateral lobes, and if metastasis occurs, the bones are a high possibility-- osteoblastic lesions are a common finding in the lumbar / thoracic spine, femur, pelvis, ribs.
questions
various conditions...
1. what is phimosis?
2. how is phimosis related to age?
3. what is paraphimosis?
4. what is the etiology of condyloma acuminata?
5. what is the morphology of condyloma acuminata?
6. what locations are condyloma acuminata commonly found?
7. ∂escribe the histopathology of condyloma acuminata.
bowen's disease...
8. what age does bowen's disease usually affect?
9. what are the most common etiological agents for bowen's disease?
10. describe the morphology of the lesions in bowen's disease.
11. what locations are affected in bowen's disease?
12. what are some histopathological features of bowen's disease?
SCC...
13. what are the most common etiologies for SCC?
14. where are SCC lesions located?
15. describe the morphology of early SCC lesions.
16. describe the morphology of late SCC lesions.
17. what age does SCC generally occur in?
18. what is the relationship to regional lymph nodes and metastasis of SCC?
19. what is the clinical presentation of SCC?
various testicular disorders...
20. what are some intrinsic risk factors for cryptorchidism?
21. what are some extrinsic risk factors for cryptorchidism?
22. what are the sequelae for cryptorchidism?
23. what is a hydrocele and what is it commonly due to?
24. how common in a varicocele?
25. what are examples of types of hobbies that are associated with varicoceles?
26. which side is more commonly affected by varicoceles?
benign prostatic hypertrophy...
27. what are some etiological factors for BPH related to dietary deficiency?
28. what are some etiological factors for BPH related to dietary excess?
29. what is the mechanism by which cadmium and cholesterol are related to BPH?
30. what are DHT and 5-alpha reductase and how are they involved in BPH pathophysiology?
31. what is the effect of estrogen and prolactin in the prostate?
prostate cancer...
32. how common is prostate cancer?
33. what age group does prostate cancer affect?
34. what are the demographic groups that have high and low risks for developing prostate cancer?
35. what are two genetic factors that have been identified as etiological agents in prostate cancer?
36. what is a dietary risk factor for prostate cancer?
37. what are some protective factors for prostate cancer?
38. what is the most common location for prostate cancer?
39. what is the morphology of the lesions in prostate cancer?
40. what is a common area for metastasis and what are the type of lesions found?
testicular cancer...
41. testicular cancer cells are most commonly derived from which cell line?
42. germ cell vs. non germ cell derived testicular cancer: which is more likely malignant?
43. what is the racial trend for incidence of testicular cancer?
44. what is the serum marker for a seminoma?
45. which condition is a seminoma associated with?
46. what is the prognosis for a seminoma?
47. what is the prognosis for an embryonal carcinoma?
48. what are the serum markers for an embryonal carcinoma?
49. which age group does the yolk sac tumor affect?
50. what are the serum markers for a yolk sac tumor?
51. are teratomas considered benign or malignant?
52. what are the serum markers for a teratoma?
53. what is the prognosis for a choriocarcinoma?
54. which age group is lymphoma most common?
answers
1. abnormal tightness of the prepuce that prevents retraction over the glans.
2. may be related to adhesions from lack of tissue differentiation that occurs before ~3 years.
3. tissue gets stuck behind the glans.
4. HPV 6 and 11
5. sessile or pedunculated, red papillary outgrowths that may be verrucous or flat.
6. coronal sulcus, inner prepuce, glans, perianal.
7. acanthosis, koilocytosis, intact basement membrane.
8. over 35yo.
9. HPV 16 and 18.
10. solitary thickened gray/white plaque with shallow ulcerations and crustin.
11. the shaft or scrotum.
12. dysplastic epithelium
scattered mitosis above basal layer
nuclear abnormalities: large, odd shaped, or multiple.
13. bowen's disease, HPV 16 + 18
14. most on the glans or the inner surface of the prepuce.
15. epithelial thickening with fraying and fissuring.
16. papules and large, infected ulcers with ragged, heaped up margins.
17. 40-70yo.
18. regional nodes may be swollen without spread of SCC.
19. painless lesions that bleed.
20. hormonal disorders of deficient LHRH
trisomy 13
21. phthalates (in plastic)
tagamet (used to treat plantar warts and peptic ulcers)
22. increased risk for testicular cancer
increased risk for infertility
23. build up of serous fluid in the scrotum, from trauma or due to structural abnormalities.
24. 10% of men have them.
25. extreme mountain biking and soccer players.
26. mostly left side.
27. lycopene
nettles
zinc
EFA's
amino acids
28. alcohol
pesticides
cadmium
cholesterol
29. increase in 5-alpha reductase activity.
30. testosterone is converted by 5-alpha reductase to DHT, which is the main prostatic growth factor.
31. estrogen increases stroma susceptibility and prolactin increases androgen uptake.
32. the most common cancer in males.
33. after 50 years old.
34. low risk in asians, high risk in african americans.
35. loss of p53 gene, hypermethylation of glutathione S-transferase.
36. high arachidonic acid content.
37. lycopene
vitamin A, E
fish oil
soy, selenium
38. posterior aspect of lateral lobes.
39. gritty, firm nodules.
40. osteoblastic bone lesions characteristic of boney metastasis to lumbar/thoracic, femur, pelvis, ribs.
41. germ cells.
42. germ cells.
43. whites: blacks 5:1
44. HCG.
45. cryptorchidism.
46. good with removal of affected testes. >95%.
47. worse than seminoma; tends to grow rapidly and spread outside the testicle.
48. HCG or AFP.
49. children under 3yo.
50. AFP.
51. benign until puberty, malignant afterwards.
52. no increase in HCG or AFP levels.
53. poor; fast growing.
54. over 65yo.
Showing posts with label SCC. Show all posts
Showing posts with label SCC. Show all posts
Friday, April 30, 2010
Wednesday, February 24, 2010
pathology III: esophageal and gastric disorders quiz review
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.
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.
Monday, February 1, 2010
CPD II: esophageal disorders part II
this lecture is a continuation of the esophageal disorder lecture, the second in the GI series by Dr. Thom. we finished up the obstructive esophageal disorders: extrinsic compression, esophageal cancers, barrett esophagus, schatzki ring, plummer vinson, inflammation, candida. extrinsic compression of the esophagus causes dysphagia and results from a number of sources such as abnormal subclavian artery, diverticulosis, mediastinal masses, enlarged heart, cervical spurs. cancer of the esophagus is divided into two main categories: 75% of cases are squamous cell carcinoma, which affects the non keratinizing stratified squamous epithelium and is from tobacco, alcohol, and other carcinogens. adenocarcinoma results from metaplasia of stratified squamous cells, which then turn into barrett's epithelium, which can then undergo more dysplasia and turn into adenocarcinoma. adenocarcinoma does not have a clear link to alcoholism but is connected with smoking, scleroderma/other motor disorders, obesity, drugs, diet. schatzki rings and plummer vinson both involve an extra esophageal growth of some sort; schatzki rings are lower esophageal rings that cause intermittent dysphagias while plummer vinson is an esophageal web, accompanied by fe deficiency anemia.
GERD is gastric reflux caused by relaxation of the LES for various reasons. normally the regurgitation of gastric contents is protected by the LES constriction, downward peristaltic motion, and alkaline saliva mixing. the LES tone can be decreased by a number of factors such as drugs, hormones, certain foods, and GERD symptoms can be worsened with smoking, obesity, and pregnancy. a patient with GERD often experiences heartburn symptoms in addition to possible respiratory complaints due to aspiration of gastric contents, dysphagia / odynophagia, and waterbrash, which is copious salivary secretions in response to GERD. diagnosis is made by endoscopy with biopsy, esophagram with barium swallow, EGD to detect esophagitis (associated in 50% of cases), barrett's esophagus, and to rule out peptic ulcer disease.
the last two esophageal disorders are related to bleeding: mallory weiss is upper GI bleeding caused by lacerations at the gastroesophageal junction and can result in hematemesis, vomiting, or in more severe cases, blood in the stool. it has been shown to be correlated to high consumption of alcohol and aspirin. esophageal varices are varicose veins in the esophagus caused by increased portal hypertension (hep B, C, cirrhosis, alcoholism, fatty liver can all cause), which might rupture and cause massive bleeding in the stomach and out of the mouth.
questions
obstructive esophageal disorders, cont'd...
1. what is esophageal extrinsic compression due to? †
2. what percentage of esophageal cancers are due to SCC vs. adenocarcinoma? √
3. what is the etiology of SCC of the esophagus and what tissue layer does it affect? †
4. what is the treatment of SCC in the esophagus? √
5. what part of the esophagus is adenocarcinoma likely to affect? √
6. describe the pathogenesis of adenocarcinoma of the esophagus. †√
7. what is barrett epithelium? √
8. patients with barrett esophagus are more likely to have... √
9. what are the risk factors for esophageal adenocarcinoma? XX
10. what is a schatzki ring? †√
11. how common is a schatzki ring and what is the prognosis? †√
12. what is plummer vinson syndrome? X√
13. what is the etiology of plummer vinson syndrome? √
14. plummer vinson is resolved by treatment of... √
15. what are some factors that cause inflammation of the esophagus? X√
16. ∂escribe the clinical picture of a patient that has esophageal inflammation due to candida. X†
17. describe the imaging findings of the above patient. X
GERD...
18. what is GERD? √
19. reflux of acid into the esophagus is normally protected by... √
20. what are the causes of GERD? †
21. what can decreased LES pressure be caused by? X
22. what are some typical symptoms of a patient with GERD?
23. what are some extra-esphageal symptoms of a patient with GERD? X
24. patients with GERD are often misdiagnosed with... √
25. what are the imaging techniques used to diagnose GERD? †
26. what is the EGD technique useful for in the diagnosis of GERD? √
27. what are the complications of GERD? X
28. what are the treatments for GERD? X
bleeding problems...
29. what is mallory weiss syndrome?
30. what are the symptoms of mallory weiss?
31. what are the less common symptoms of mallory weiss?
32. what are two substances that have been linked to mallory weiss?
33. what are esophageal varices due to?
34. esophageal varices might lead to...
answers
1. mediastinal masses, aberrant right subclavian artery, enlarged heart, cervical spurs, divertuculi.
2. 2/3 SCC 1/3 adenocarcinoma.
3. tobacco, alcohol, other carcinogens, affects non keratinizing stratified squamous cell epithelium.
4. if surgery, involves removing most of the neck because of the high lymph node concentration.
5. mid and distal esophagus.
6. gastric reflux causes metaplasia of normal stratified squamous cells, turning them into "barrett epithelium", then dysplasia, then adenocarcinoma.
7. specialized intestinal epithelial layer containing goblet cells.
8. lower LES pressure and worse esophageal peristalsis, therefore more acid reflux.
9. not alcohol (!), smoking, scleroderma/other motor disorders, obesity, drugs, diet.
10. a lower esophageal ring that causes intermittent dysphagias.
11. 6-14% of patients who undergo GI exams; usually asymptomatic.
12. dysphagia for solids, esophageal webs (thin mucosal membrane that grows across lumen), fe deficiency anemia.
13. excess smoking and drinking.
14. anemia.
15. chronic debilitating disease, steroids, antibiotics, immunosuppresants, chemo, estrogen. [chronic drugs drugs drugs rays boobs]
16. dysphagia with intense pain of short duration, often tolerate only liquids, oral thrush.
17. barium swallow would show shaggy mucosa or filling defects, endoscopy would show white mucosa and swelling.
18. gastric esophageal reflux disease, a common condition characterized by heartburn and acid regurgitation symptoms.
19. LES, downward peristaltic motion, alkaline saliva.
20. decrease of LES pressure, smoking, pregnancy, obesity.
21. drugs (morphine, diazepam, calcium channel blocker, nitrates, beta-blockers), hormones (secretin, cholecystokinin, glucagon), foods (alcohol, caffeine, lipids, chocolate).
22. heartburn felt usually after eating or bending over, respiratory complications from regurgitation, dysphagia, odynophagia, waterbrash. [heartburn, breathe, swallow, swallow, water]
23. coughing/wheezing, aspiration pneumonia, fatigue, chest pain. [cough, pneumonia, tired, pain]
24. asthma because of the cough which is caused by aspiration.
25. endoscopy with biopsy, barium esophagram, esophagogastroduodenoscopy.
26. identifying esophagitis, barrett esophagus, ruling out peptic ulcer.
27. esophagitis (50% of cases), barrett's esophagus, stricture of distal esophagus, respiratory complications.
28. improve diet, cut out alcohol, stay elevated, heel drops, avoid constricting clothing. [diet, elevation, dropping, clothing]
29. gastroesophageal junction lacerations and upper GI bleeding.
30. hematemesis, followed by wretching / vomiting.
31. hematochezia, melena, syncope, abdominal pain.
32. exceess alcohol and aspirin.
33. anything that increases portal hypertension: Hep B, Hep C, cirrhosis, alcoholism, fatty liver.
34. rupture, massive bleeding into the stomach and out of the mouth (a life threatening emergency).
GERD is gastric reflux caused by relaxation of the LES for various reasons. normally the regurgitation of gastric contents is protected by the LES constriction, downward peristaltic motion, and alkaline saliva mixing. the LES tone can be decreased by a number of factors such as drugs, hormones, certain foods, and GERD symptoms can be worsened with smoking, obesity, and pregnancy. a patient with GERD often experiences heartburn symptoms in addition to possible respiratory complaints due to aspiration of gastric contents, dysphagia / odynophagia, and waterbrash, which is copious salivary secretions in response to GERD. diagnosis is made by endoscopy with biopsy, esophagram with barium swallow, EGD to detect esophagitis (associated in 50% of cases), barrett's esophagus, and to rule out peptic ulcer disease.
the last two esophageal disorders are related to bleeding: mallory weiss is upper GI bleeding caused by lacerations at the gastroesophageal junction and can result in hematemesis, vomiting, or in more severe cases, blood in the stool. it has been shown to be correlated to high consumption of alcohol and aspirin. esophageal varices are varicose veins in the esophagus caused by increased portal hypertension (hep B, C, cirrhosis, alcoholism, fatty liver can all cause), which might rupture and cause massive bleeding in the stomach and out of the mouth.
questions
obstructive esophageal disorders, cont'd...
1. what is esophageal extrinsic compression due to? †
2. what percentage of esophageal cancers are due to SCC vs. adenocarcinoma? √
3. what is the etiology of SCC of the esophagus and what tissue layer does it affect? †
4. what is the treatment of SCC in the esophagus? √
5. what part of the esophagus is adenocarcinoma likely to affect? √
6. describe the pathogenesis of adenocarcinoma of the esophagus. †√
7. what is barrett epithelium? √
8. patients with barrett esophagus are more likely to have... √
9. what are the risk factors for esophageal adenocarcinoma? XX
10. what is a schatzki ring? †√
11. how common is a schatzki ring and what is the prognosis? †√
12. what is plummer vinson syndrome? X√
13. what is the etiology of plummer vinson syndrome? √
14. plummer vinson is resolved by treatment of... √
15. what are some factors that cause inflammation of the esophagus? X√
16. ∂escribe the clinical picture of a patient that has esophageal inflammation due to candida. X†
17. describe the imaging findings of the above patient. X
GERD...
18. what is GERD? √
19. reflux of acid into the esophagus is normally protected by... √
20. what are the causes of GERD? †
21. what can decreased LES pressure be caused by? X
22. what are some typical symptoms of a patient with GERD?
23. what are some extra-esphageal symptoms of a patient with GERD? X
24. patients with GERD are often misdiagnosed with... √
25. what are the imaging techniques used to diagnose GERD? †
26. what is the EGD technique useful for in the diagnosis of GERD? √
27. what are the complications of GERD? X
28. what are the treatments for GERD? X
bleeding problems...
29. what is mallory weiss syndrome?
30. what are the symptoms of mallory weiss?
31. what are the less common symptoms of mallory weiss?
32. what are two substances that have been linked to mallory weiss?
33. what are esophageal varices due to?
34. esophageal varices might lead to...
answers
1. mediastinal masses, aberrant right subclavian artery, enlarged heart, cervical spurs, divertuculi.
2. 2/3 SCC 1/3 adenocarcinoma.
3. tobacco, alcohol, other carcinogens, affects non keratinizing stratified squamous cell epithelium.
4. if surgery, involves removing most of the neck because of the high lymph node concentration.
5. mid and distal esophagus.
6. gastric reflux causes metaplasia of normal stratified squamous cells, turning them into "barrett epithelium", then dysplasia, then adenocarcinoma.
7. specialized intestinal epithelial layer containing goblet cells.
8. lower LES pressure and worse esophageal peristalsis, therefore more acid reflux.
9. not alcohol (!), smoking, scleroderma/other motor disorders, obesity, drugs, diet.
10. a lower esophageal ring that causes intermittent dysphagias.
11. 6-14% of patients who undergo GI exams; usually asymptomatic.
12. dysphagia for solids, esophageal webs (thin mucosal membrane that grows across lumen), fe deficiency anemia.
13. excess smoking and drinking.
14. anemia.
15. chronic debilitating disease, steroids, antibiotics, immunosuppresants, chemo, estrogen. [chronic drugs drugs drugs rays boobs]
16. dysphagia with intense pain of short duration, often tolerate only liquids, oral thrush.
17. barium swallow would show shaggy mucosa or filling defects, endoscopy would show white mucosa and swelling.
18. gastric esophageal reflux disease, a common condition characterized by heartburn and acid regurgitation symptoms.
19. LES, downward peristaltic motion, alkaline saliva.
20. decrease of LES pressure, smoking, pregnancy, obesity.
21. drugs (morphine, diazepam, calcium channel blocker, nitrates, beta-blockers), hormones (secretin, cholecystokinin, glucagon), foods (alcohol, caffeine, lipids, chocolate).
22. heartburn felt usually after eating or bending over, respiratory complications from regurgitation, dysphagia, odynophagia, waterbrash. [heartburn, breathe, swallow, swallow, water]
23. coughing/wheezing, aspiration pneumonia, fatigue, chest pain. [cough, pneumonia, tired, pain]
24. asthma because of the cough which is caused by aspiration.
25. endoscopy with biopsy, barium esophagram, esophagogastroduodenoscopy.
26. identifying esophagitis, barrett esophagus, ruling out peptic ulcer.
27. esophagitis (50% of cases), barrett's esophagus, stricture of distal esophagus, respiratory complications.
28. improve diet, cut out alcohol, stay elevated, heel drops, avoid constricting clothing. [diet, elevation, dropping, clothing]
29. gastroesophageal junction lacerations and upper GI bleeding.
30. hematemesis, followed by wretching / vomiting.
31. hematochezia, melena, syncope, abdominal pain.
32. exceess alcohol and aspirin.
33. anything that increases portal hypertension: Hep B, Hep C, cirrhosis, alcoholism, fatty liver.
34. rupture, massive bleeding into the stomach and out of the mouth (a life threatening emergency).
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