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Musculoskeletal and oral pathology review

Shylla T Englisch 200 Karten

Karten in diesem Stapel (200)

  1. 1“Brown” tumor of boneHyperparathyroidism or osteitis fibrosa cystica (deposited hemosiderin from hemorrhage gives brown color)
  2. 2“Soap bubble” in femur or tibia on x-rayGiant cell tumor of bone (generally benign)
  3. 3Raised periosteum (creating a “Codman triangle”)Aggressive bone lesion (eg, osteosarcoma, Ewing sarcoma, osteomyelitis)
  4. 4“Onion skin” periosteal reactionEwing sarcoma (malignant small blue cell tumor)
  5. 5Anti-IgG antibodiesRheumatoid arthritis (systemic inflammation, joint pannus, boutonniere and swan neck deformities)
  6. 6Rhomboid crystals, ⊕ birefringentPseudogout (calcium pyrophosphate dihydrate crystals)
  7. 7Needle-shaped, ⊖ birefringent crystalsGout (monosodium urate crystals)
  8. 8↑ uric acid levelsGout, Lesch-Nyhan syndrome, tumor lysis syndrome, loop and thiazide diuretics
  9. 9“Bamboo spine” on x-rayAnkylosing spondylitis (chronic inflammatory arthritis: HLA-B27)
  10. 10Antinuclear antibodies (ANAs: anti-Smith and anti-dsDNA)SLE (type III hypersensitivity)
  11. 11Anti-topoisomerase antibodiesDiffuse scleroderma
  12. 12Keratin pearls on a skin biopsySquamous cell carcinoma
  13. 13Osteoporosis treatmentCalcium/vitamin D supplementation (prophylaxis); bisphosphonates, PTH analogs, SERMs, calcitonin, denosumab (treatment)
  14. 14Osteomalacia/rickets treatmentVitamin D supplementation
  15. 15Chronic gout treatmentXanthine oxidase inhibitors (eg, allopurinol, febuxostat); pegloticase; probenecid
  16. 16Acute gout attack treatmentNSAIDs, colchicine, glucocorticoids
  17. 17Vertebral compression fractureOsteoporosis (type I: postmenopausal woman; type II: elderly man or woman)
  18. 18HLA-B27Psoriatic arthritis, ankylosing spondylitis, IBD-associated arthritis, reactive arthritis (formerly Reiter syndrome)
  19. 19Death in SLELupus nephropathy
  20. 20Tumor of infancyStrawberry hemangioma (grows rapidly and regresses spontaneously by childhood)
  21. 21Actinic (solar) keratosisPrecursor to squamous cell carcinoma
  22. 22Full thickness defect of lip and palateCleft lip and palate
  23. 23What causes cleft lip and palate?Failure of the five facial prominences to fuse
  24. 24How does the face form?During early pregnancy, facial prominences (one superior, two from side, two inferior) grow together and fuse to form face
  25. 25Do cleft lip and palate usually occur together?Yes; isolated cleft lip or palate is less common
  26. 26What is an aphthous ulcer? How does it appear?Painful superficial ulceration of the oral mucosa;
    Grayish base surrounded by erythema
  27. 27When does aphthous ulcer arise?In response to stress
  28. 28Treatment for aphthous ulcerResolves spontaneously, but can recur
  29. 29What is the grayish base of the aphthous ulcerGranulation tissue
  30. 30Triad of Behcet SyndromeRecurrent aphthous ulcers, genital ulcers, uveitis
  31. 31What causes Behcet Syndrome?Immune complex vasculitis involving small vessels
  32. 32Etiology of Behcet SyndromeUnknown; can be seen after viral infeciont
  33. 33Oral herpes definitionVesicles involving oral muscosa that rupture resulting in shallow, painful red ulcers; due to HSV1
  34. 34When does primary HSV1 infection occur, and where does it lay dormant?Usually primary infeciton occurs in childhood; Virus remains dormant in ganglia of trigeminal nerve
  35. 35What cause reactivation of HSV1 leading to "cold sore"Stress, sunlight
  36. 36Squamous cell carcinoma of oral mucosaMalignant neoplasm of squamous cells lining the oral mucosa
  37. 37What are risk factors for squamous cell carcinoma of the oral mucosa?Tobacco and alcohol
  38. 38What is the most common location for squamous cell carcinoma of the oral mucosa?Floor of mouth
  39. 39What are two precursor lesions to squamous cell carcinomaOral leukoplakia and erythroplakia
  40. 40What is leukoplakia?White plaque that cannot be scraped away (in contrast to candidiasis) that can (but does not always) represent a squamous cell dysplasia that can be a precursor to squamous cell carcinoma
  41. 41How does leukoplakia differ from oral candidiasis and hairy leukoplakia?Oral candidiasis: white deposit on tongue that is easily scraped away and is typically seen in immunocrompromised
    Hairy leukoplakia: white rough patch on LATERAL tongue that is seen in immunocompromised people; due to EBV-induced squamous cell hyperplasia and IS NOT premalignant
  42. 42Is hairy leukoplakia premalignant?No
  43. 43What causes hairy leukoplakia?EBV
  44. 44What is erythroplakia?Vascularized leukoplakia that is highly suggestive of squamous cell dysplasia; more of a concern than leukoplakia
  45. 45How do you determine if leukoplakia and erythroplakia are dysplastic/cancerous?Biopsy
  46. 46Are salivary glands endocrine or exocrine glands?Exocrine; they secrete saliva
  47. 47What are the divisions of salivary glands?Major (parotid, submandibular, sublingual) and minor (hundreds of microscopic glands)
  48. 48Name the three major salivary glandsParotid, submandibular, sublingual
  49. 49What is a virus that often results in bilateral inflamed parotid glands?Mumps
  50. 50Other than inflammation of parotid gland, what can mumps cause (3 things)?1. Orchitis
    2. Pancreatitis
    3. Aseptic meningitis
  51. 51What is the worry about mumps in teenage boys?Orchitis leading to sterility
  52. 52What enzyme is elevated in mumps?Serum amylase (can be due either to salivary gland or pancreatic involvement)
  53. 53SialadenitisInflammation of the salivary gland (usually unilateral)
  54. 54What is the most common cause of sialadenitis?Sialolithiasis (obstructing stone in salivary gland) leading to S. aureus infection
  55. 55What nerve runs right through the parotid gland?Facial
  56. 56What is the most common tumor of the salivary glands?Pleomorphic adenoma
  57. 57Pleomorophic adenomaBenign tumor composed of stromal (cartilage) and epithelial (sometimes with glands) tissue in salivary glands
  58. 58Where does pleomorphic adenoma usually arise?Parotid gland
  59. 59How does pleomorphic ademona usually present as?Mobile, painless circumscribed mass at the angle of the jaw
  60. 60Recurrent rate of pleomorphic adenoma, and why?High because of irregular borders that surgeons can miss (incomplete resection)
  61. 61Can pleiomorphic adenoma transform into carcinoma? If so, how does it presentyes, but rarely; presents with facial nerve damage (facial nerve palsy) [remember, facial nerve runs right through the parotid gland!]
  62. 62Warthin tumorBenign cystic tumor with abundant lymphocytes and germinal centers (lymph node like stroma)
  63. 63What is the 2nd most common tumor of the salivary gland?Warthin tumor
  64. 64Where does a Warthin Tumor most commonly arise, and why?Parotid because the parotid is often associated with lymphoid tissue
  65. 65What is the most common malignant tumor of salivary glands?Mucoepidermoid carcinoma
  66. 66What cells is the mucoepidermoid carcinoma composed of?Mucus and sqamous cells
  67. 67Where does mucoepidermoid carcinoma usually arise and what does it commonly involve?Usually arises in parotid gland and commonly involves the facial nerve
  68. 68Congenital defect resulting in a connection between the esophagus and the trachiaTracheoesophageal fistula
  69. 69What is a fistula?Abnormal connection between two tubes
  70. 70What is the most common variant of tracheoesophageal fistula, and how does it present (4 signs)?Proximal esophageal atresia with distal esophagus arising from trachea
    Presentation: aspiration, vomiting, polyhydramnios, and abdominal distension
  71. 71Esophageal webThin protrusion of the esophageal mucosa, often in the upper esophagus
  72. 72Where is esophageal web most common?Upper esophagus
  73. 73How does esophageal web present?Dysphagia for poorly chewed food due to obstruction or partial obstruction caused by the web
  74. 74What risk goes along with esophageal web?Increased risk for esophageal squamous cell carcinoma
  75. 75Triad of Plummer-Vinson SyndromeSevere iron deficiency anemia, esophageal web, and beefy red tongue due to atrophic glossitis
  76. 76What are the layers of the GI tract?Lumen, mucosa, submucosa, muscularis propria, serosa
  77. 77Zenker diverticulum:Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall;
    Zenker diverticulum is a false diverticulum
    Zenker diverticulum most often arises above the upper esophageal sphincter (UES) at junction of esophagus and pharynx
  78. 78False diverticulumOnly one part of the wall has protruded (most GI diverticulum are false, like Zenker)
  79. 79What is one contributing factor to Zenker diverticulum?Abnormal pharyngeal pressure
  80. 80Presentation of Zenker DiverticulumDysphagia, obstruction, halitosis (bad breath due to food rotting in diverticululm)
  81. 81Mallory Weiss SyndromeLongitudinal laceration of mucosa at the Gastroesophageal (GE) junction
  82. 82What causes Mallory Weiss syndrome?Vomiting, so often seen in alcoholism or bulimia
  83. 83How does Mallory Weiss Syndrome present?Painful hematemisis (compared with esophageal varices that have ruptured, which presents with painless hematemesis)
  84. 84What is a risk associated with Mallory Weiss Syndrome?Boerhaave Syndrome; it is a rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema
  85. 85Air bubbles under skin in neck; when you push you hear crackling; diagnosis?Boerhaave syndrome
  86. 86Esophageal varicesDilated submucosal veins in the lower esophagus
  87. 87What does esophageal varices arise secondary to?Portal hypertension; because in portal hypertension, left gastric vein backs up and prevents drainage of esophagus, causing varices
  88. 88Venous drainage of esophagus1. Azygous vein to SVC
    2. Left gastric vein to portal vein
  89. 89How does esophageal varices present?Asymptomatic, but risk of rupture exists; presents with painless hematemesis
  90. 90What is the main risk of esophageal varices?Rupture
  91. 91What is the most common cause of death in cirrhosis?Ruptured esophageal varices
  92. 92Disordered esophageal motility with inability to relax the LESAchalasia
  93. 93What causes achalasia?Damage to ganglion cells of the myenteric plexus
  94. 94What are the two layers of the muscularis propria, and what lies between them?Inner circular layer and outer longitudinal layer; myenteric plexus lies between them
  95. 95What are the two regulatory functions of the myenteric plexus?Important in relaxing LES and regulating bowel/esophageal motility
  96. 96What can cause damage to ganglion cells of myenteric plexus leading to achalasia?Idiopathic or known insult (i.e. Trypanosoma cruzi in Chagas Disease)
  97. 97Clinical features of Achalasia1. Dysphagia for solids and liquids due to loss of esophageal motility
    2. Putrid breath (due to solid accumulation in esophagus)
    3. High LES pressure on esophageal manometry
    4. Bird beak sign on barium swallow
    5. Increased risk for esophageal squamous cell carcinoma
  98. 98Bird beak sign on barium swallowAchalasia
  99. 99GERDReflux of acid from the stomach due to reduced LES tone
  100. 100Name risk factors for GERDAlcohol, tobacco, obesity, fat-rich diet, caffeine, hiatal hernia
  101. 101What is the normal lining of esophagus and what can it become due to GERDNormal: non-keratinizing squamous epithelium
    Metplasia: non-ciliated columnar epithelium with goblet cells
  102. 102What are two common hiatal hernias, and which is most common?Most common: sliding hiatal hernia (cardia of stomach into esophagus leading to GERD)
    Other: paraesophageal hernia (next to esophagus)
  103. 103What is the hourglass sign indicative of?Sliding hiatal hernia
  104. 104How does paraesophageal hernia present?Bowel sounds in lung field, lung hypoplasia; does not necessarily have GERD
  105. 105Clinical features of GERD1. Heartburn that mimics cardiac chest pain
    2. Asthma (adult onset) and cough
    3. Damage to enamel of teeth
    4. Ulceration with stricture and Barrett's Esophagus (late complications)
  106. 106How does ulcer due to GERD lead to stricture?Ulcer takes out all of mucosa (and some submucosa); stem cells are in mucosa, so it must heal with fibrosis, which will contract
  107. 107Barrett EsophagusMetaplasia of the lower esophageal mucsoa from stratified squamous non-keratinizing epithelium to nonciliated columnar epithelium with goblet cells
  108. 108What percent of patients with GERD have Barrett's?10%; Metaplasia (Barrett's Esophagus) occurs in longstanding GERD in response of lower esophageal stem cells to acidic stress
  109. 109How can Barrett's Esophagus Progress?From metaplasia to dysplasia to adenocarcinoma
  110. 110What are the two types of esophageal carcinoma?Adenocarcinoma, squamous cell carcinoma
  111. 111What is the most common type of esophageal carcinoma in the west vs. worldwide?West: adenocarcinoma (proliferation of glands)
    World wide: squamous cell carcinoma
  112. 112Where does adenocarcinoma arise from?Arises from barrett's esophagus (metaplasia --> dysplasia --> cancer) because without metaplasia, the esophagus does not make glands
  113. 113Location in esophagus of adenocarcinomaLower 1/3 (GE junction)
  114. 114Where does squamous cell carcinoma usually arise in the esophagus?Upper or middle 1/3
  115. 115What are the major risk factors for squamous cell carcinoma of the esophagus?(Irritation)
    1. Alcohol and tobacco (most common)
    2. Hot tea (very hot)
    3. Achalasia (due to rotting food)
    4. Esophageal web (Plummer vinson syndrome, rotting food)
    5. Esophageal injury (lye ingestion)
  116. 116When does esophageal carcinoma present?Late
  117. 117Symptoms of esophageal carcinomaProgressive dysphagia (solids to liquids), weight loss, pain, hematemsis
  118. 118What additional symptoms can squamous cell carcinoma of esophagus present with?1) Hoarse voice (recurrent laryngeal nerve involvement)
    2) Cough (tracheal nerve involvement)
  119. 119What dictates lymph node spread of esophageal carcinoma?Where it is located in esophagus
    1. Upper 1/3- spreads to cervical lymph nodes
    2. Middle 1/3- spreads to mediastinal or tracheobronchial nodes
    3. Lower 1/3- spreads to gastric and celiac nodes
  120. 120GastroschisisCongenital malformation of anterior abdominal wall leading to exposure of abdominal contents
  121. 121OmphalocelePersistent herniation of bowel into umbilical cord
  122. 122What causes omphalocele?Failure of herniated intestines to return to body cavity during development (herniation is a part of development, but the bowel should return)
  123. 123What covers the bowel in omphalocele?Peritoneum and amnion of umbilical cord
  124. 124Pyloric stenosisCongenital hypertrophy of pyloric smooth muscle
  125. 125When and in who does pyloric stenosis present?Two weeks after birth; more common in males
  126. 126Treatment for pyloric stenosisMyotomy (cut away the pyloric sphincter)
  127. 127Presentation of pyloric stenosisNonbilious vomiting, visible peristalsis, olive like mass in abdomen
  128. 128Where does bile mix with food?Duodenum
  129. 129What are the different types of gastritis?1) Acute; due to acidic damage to stomach mucosa due to either --
    a) decrease in mucosal defenses, or
    b) increase in acid production
    2) Chronic; due to chronic inflammation of stomach mucosa due to either --
    a) autoimmune, or
    b) h pylori
  130. 130What causes acute gastritis?Acidic damage to stomach due to either decrease in mucosal defenses or increase in acid production
  131. 131Name three defenses to protect the stomach from acid damage and acute gastritis1) Mucin layer produced by foveolar cells
    2) blood supply (provides nutrients and picks up leaked acid)
    3) bicarbonate secretion by surface epithelium
  132. 132What lines the mucosa of the stomach?Epithelium, called foveolar cells, which produce acid and secrete bicarb to protect the stomach
  133. 133What cell makes stomach acid?Parietal cells
  134. 134What are the three receptors on parietal cell?Ach, gastrin, histamine (so all three can induce acid production)
  135. 135Name the four parts of the stomachCardia, fundus, body, antrum
  136. 136Where are parietal cells located in the stomach?Fundus and body
  137. 137How do prostaglandins protect stomach from acid? What produces prostaglandins?1) Decrease acid production
    2) stimulate cells to secrete bicarb and mucus
    3) stimulate blood flow
    foveolar cells produce prostaglandins (via COX)
  138. 138Name six risk factors of acute gastritis1. Severe burn
    2. NSAIDs (decrease PGE2)
    3. Heavy alcohol consumption
    4. Chemotherapy (prevent cellular regeneration of cells of stomach that create mucosal surface to protect against acid)
    5. Increased intracranial pressure
    6. Shock
  139. 139What is a Curling Ulcer?Ulcer in the stomach as a result of severe burn; hypovolemia after a burn leads to decreased blood supply; so acid can now do damage in stomach
  140. 140What is a Cushing Ulcer?Ulcer in the stomach as a result of increased intracranial pressure, which stimulates vagus to increase production of ACh, which stimulates parietal cells to produce acid.
  141. 141How does shock increase risk of acute gastritis?Decreased blood supply in shock
  142. 142What are the results of acute gastritis acid damage (3)?1) Superficial inflammation
    2) erosion (loss of superficial epithelium), or
    3) ulcer (loss of mucosal layer)
  143. 143Chronic gastritisChronic inflammation of stomach mucosa
  144. 144What are the two types of chronic gastritis, and which is more common?Autoimmune and H pylori (most common form of gastritis)
  145. 145What are the two types of chronic gastritis, and which is more common?Autoimmune and H pylori (most common form of gastritis)
  146. 146Pathogenesis of autoimmune chronic gastritis?Mediated by T cells (Type IV hypersensitivity reaction)
    Associated with antibodies against parietal cells and/or intrinsic factor, which is useful for diagnosis but is not the cause of disease
  147. 147Clinical features of chronic autoimmune gastritis1. Atrophy of mucosa with intestinal metaplasia (pathologic) (Foveolar cells become replaced by goblet cells due to chronic inflammation -- this is seen in BOTH types of chronic gastritis)
    2. Achlorhydria with increased gastrin levels and antral-G cell hyperplasia
  148. 148part 23. Megaloblastic (pernicious) anemia due to lack of IF (MOST COMMON CAUSE of B12 deficiency)
    4. Increased risk for gastric adenocarcinoma [intestinal type]
  149. 149Where are G cells in stomach primarily located, and what do they make?Located in antrum; make gastrin which stimulates parietal cells to secrete acid
  150. 150Why does achlorhydia lead to increased gastrin levels?Achlorhydia = low acid production; no neg feedback; Gastrin stimulate parietal cells in body and fundus to produce acid!
  151. 151Where is B12 absorbed?Terminal ileum
  152. 152B12 absorption pathwayIntrinsic factor (released by parietal cells) binds B12; B12 transported to terminal ileum where it is absorbed
  153. 153Intestinal metaplasia due to chronic gastritisFoveolar cells become replaced by goblet cells due to chronic inflammation
  154. 154What causes chronic H pylori gastritis?H pylori induced acute and chronic inflammation
  155. 155What is the most common site of h pylori gastritis?Antrum
  156. 156How does h pylori weaken mucosal defenses in antrum in order to cause chronic gastritis?Ureases and proteases along with inflammation
  157. 157Does h pylori invade the epithelium?No!
  158. 158How does H pylori chronic gastritis present?How does H pylori chronic gastritis present?
  159. 159H pylori chronic gastritis increases risk for what 3 things?1) Ulceration [peptic ulcer disease]
    2) Gastric adenocarcinoma [intestinal type]
    3) MALT lymphoma
  160. 160What type of lymphoma is MALT lymphoma?B cell
  161. 161How does MALT lymphoma develop from H pylori chronic gastritisH Pylori --> Chronic inflammation ---leads to---> germinal center formation in gastric wall ---leads to--> post germinal center B cells from the marginal zone (zone only associated with inflammation)
  162. 162What is treatment for H pylori chronic gastritis/what does it reverseTriple therapy; resolves gastritis/ulcer and reverses any intestinal metaplasia
    amoxicillin (metronidazole if penicillin allergy)
    +
    clarithromycin
    +
    PPI
  163. 163How do you know h pylori has been eradicated?Negative urea breath test and lack of stool antigen
  164. 164Peptic ulcer diseaseSolitary mucosal ulcer involving proximal duodenum or distal stomach
  165. 165What part of GI system does PUD usually affect?Proximal duodenum (90%) or distal stomach (10%)
  166. 166What is the usual cause of duodenal ulcer?H pylori (95%); sometimes due to ZE [Zollinger-Ellison] syndrome
  167. 167What is ZE [Zollinger-Ellison] Syndrome?Condition that causes 5% of PUD due to gastrinoma, which produces gastrin and causes parietal cells (in body and fundus) to produce acid, causing PUD with a duodenal ulcer
  168. 168Presentation of PUD in duodenum (clinical symptoms, histology, location)1. Epigastric pain that IMPROVES with meals
    2. Hypertrophy of Brunner Glands (to reduce acid)
    3. usually anterior duodenum [sometimes posterior duodenum - when present in posterior duodenum, rupture may lead to bleeding from the gastroduodenal artery or acute pancreatitis]
  169. 169Glands in the wall of the duodenum that produce mucusBrunner's glands
  170. 170What are Brunner's Glands?Glands in the wall of the duodenum that produce mucus; hypertrophy in duodenal PUD
  171. 171Where do duodenal ulcers in PUD usually arise, and what are complications of the less common location?Usually arise on anterior duodenum
    When they arise on posterior duodenum rupture can lead to bleeding from gastroduodenal artery or acute pancreatitis
  172. 172Where does bleeding come from if PUD in posterior duodenum ruptures?Gastroduodenal artery
  173. 173What is the most common cause and other less common causes of gastric PUD?H pylori (75% compared to 95% in duodenum)
    Other causes include NSAIDs and bile reflux
  174. 174How do gastric ulcers in PUD usually present?1. Epigastric pain that WORSENS with meals
    2. Ulcer in lesser curvature of antrum [distal stomach -- so 10% of PUD ulcers are gastric ulcers, other 90% are duodenal ulcers]
    3. Rupture leads to bleed of left gastric artery
  175. 175PUD: epigastric pain that worsens or improves with mealsWorsens: [distal stomach] gastric PUD
    Improves: [proximal duodenum] duodenal PUD
  176. 176Bleeding from gastroduodenal artery vs. bleeding from left gastric arteryGastroduodenal artery = proximal posterior duodenal PUD rupture
    Left gastric artery = distal stomach gastric PUD rupture
  177. 177What is included in ddx of PUD?Carcinoma; more often from gastric ulcers than duodenal ulcers; duodenal carcinoma is very rare, hence duodenal ulcers area almost never malignant. gastric ulcers can be caused by gastric carcinoma - intestinal subtype
  178. 178What can cause gastric ulcers?1) H pylori (75%)
    2) NSAIDs
    3) bile reflux
    4) Gastric carcinoma (intestinal subtype)
  179. 179How do you diagnose gastric ulcers caused by gastric carcinoma definitively?Biopsy
  180. 180How do you differentiate from benign peptic ulcers and peptic ulcers caused by gastric carcinoma?Benign: small (< 3cm), sharply demarcated (punched out), surrounded by flat mucosa
    Malignant: Large, irregular, heaped up margins
  181. 181Gastric carcinomaMalignant proliferation of surface columnar epithelial cells in the stomach (adenocarcinoma)
  182. 182What are the two types of gastric carcinoma?What are the two types of gastric carcinoma?
  183. 183What type of gastric carcinoma is more common?Intestinal
  184. 184Where does intestinal gastric carcinoma most commonly present, and how?Most commonly presents in the lesser curvature of the antrum (like stomach ulcers); presents as a large irregular lesion with heaped up margins
  185. 185What are risk factors for intestinal gastric carcinoma?1) Intestinal metaplasia (chronic gastritis) [for example, due to H pylori and autoimmune gastritis]
    2) nitrosamines in smoked foot (Japan)
    3) blood type A
  186. 186What blood type is associated with a risk for intestinal gastric carcinoma?Blood Type A
  187. 187What characterizes diffuse gastric carcinoma?Signet ring cells (Cell with nucleus off to the side due to production of mucus) that diffusely infiltrate the gastric wall
  188. 188DesmoplasiaReaction of the tissue to diffuse stomach cancer, it causes thickening of the stomach wall (linitis plastica)
  189. 189Are H pylori, intestinal metaplasia, and nitrosamines related to diffuse gastric carcinoma?No relation
  190. 190How do both diffuse and intestinal gastric carcinomas present?presents late with:
    1) weight loss
    2) abdominal pain
    3) anemia
    4) early satiety [especially in diffuse due to linitis plastica]
    rarely presents with:
    5) Acanthosis nigricans (thick skin in axillary area)
    6) Leser-Trelat Sign (dozens of suborrheic keratosis)
  191. 191Where does gastric carcinoma (diffuse and intestinal) commonly spread?Left supraclavicular node (Virchow node)
  192. 192What distant metastasis occur after primary gastric carcinoma?1. Liver [most common]
    2. Sister Mary Joseph Nodule in periumbilical region [due to intestinal]
    3. Bilateral ovaries, aka Krukenberg tumor [due to diffuse]
  193. 193What genetic condition is duodenal atresia associated with?Down syndrome
  194. 194Cause of duodenal atresiaCongenital failure of duodenum to canalize
  195. 195Clinical features of duodenal atresia1) Polyhydramnios (bc baby can't swallow or digest amniotic fluid)
    2) double bubble sign (distension of stomach and blind loop of duodenum)
    3) bilious vomiting
  196. 196What is the double bubble sign and what is it associated with?On x-ray, distention of stomach and blind loop of duodenum
  197. 197Meckel DiverticulumOutpouching of all three layers of the bowel wall due to failure of vitelline duct to involute. It is a true diverticulum.
  198. 198What is the vitelline duct?Provides nutrients to the midgut from the yolk sac during gestation
  199. 199What is the most common congenital anomaly of the GI Tract?Meckel Diverticulum
  200. 200Rule of 2s (and associated disease)Associated with Meckel Diverticulum
    1. Present in 2% of population (most common congenital anomaly of GI tract)
    2. 2 inches long and located within 2 feet of ileocecal valve
    3. Can present in the first 2 years of life w bleeding (due to heterotopic gastric mucosa), volvulus, intussusception, or obstruction (mimics appendicitis); however, most cases are asymptomatic.

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Karteikarten am Ohne Titel, erstellt von Shylla T am 11/06/2021.
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Shylla T · Jun 2021
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