Chapter 10 Flashcards

1
Q

Cause of cleft lip and palate

A

Failure of facial prominences to fuse

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2
Q

Aphthous Ulcer

A

painful, superficial ulceration of the oral mucosa that arise due to stress.

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3
Q

Behçet Syndrome

A

Recurrent aphthous ulcers + genital ulcers + uveitis. Due to immune complex vasculitis. Etiology unknown, but can follow viral infection.

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4
Q

Precursors of Squamous Cell Carcinoma of the oral cavity

A
  1. Leukoplakia (cannot be scraped off, so not thrush, and not on sides of tongue in immunocompromised, which is hairy leukoplakia)
  2. Erythroplakia- vascularized leukoplakia. More likely to be SCC….
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5
Q

Mumps infection

A

See bilateral inflamed parotid glands, orchitis (in older than 10 boys), pancreatitis (but Amylases elevated regardless), and aseptic meningitis.

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6
Q

Sialadenitis

A

inflammation of the salivary gland due to obstructing stone (sialolithiasis) leading to Staph aureus infection.

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7
Q

Pleomorphic Adenoma (histology and location)

A

Benign tumor of stromal (cartilage) and epithelial tissue most often in parotid.

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8
Q

Recurrence of pleomorphic adenoma (cause)

A

Incomplete resection, due to extension of small islands of tumor through capsule. Rarely can progress to carcinoma (often see facial nerve involvement).

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9
Q

Warthin Tumor (histology and location)

A

Benign cystic tumor with abundant lymphocytes and germinal centers, often seen in parotid.

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10
Q

Mucoepidermoid Carcinoma (histology and location)

A

Malignant tumor of mucinous and squamous cells, most often in parotid involving facial nerve.

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11
Q

Symptoms of tracheoesophogeal fistula

A

Vomiting, polyhydramnios, abdominal distention (from air) and aspiration.

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12
Q

Zenker diverticulum

A

outpouching of pharyngeal mucosa (false diverticulum) due to acquired defect in muscular wall. Presents with dysphagia, obstruction, and halitosis (bad breath)

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13
Q

Mallory-Weiss Syndrome

A

Longitudinal laceration of mucosa at GE junction. Presents with PAINFUL hematemisis. Due to excessive vomiting (alcoholism/bulimia)

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14
Q

Boerhaave Syndrome

A

Rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema (air bubbles in skin that crackle!)

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15
Q

Esophageal Varices

A

Due to portal hypertension (via left gastric vein). When rupture, cause PAINLESS hematemisis (most common cause of death in cirrhosis)

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16
Q

Achalasia

A

Disordered esophageal motility with inability to relax LES. Due to damaged myenteric plexus. Often due to Chagas Disease!

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17
Q

Symptoms of achalasia

A

Dysphasia for BOTH SOLIDS AND LIQUIDS

  • putrid breath
  • High LES pressure of esophageal manometry
  • bird beak sign of barium swallow
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18
Q

Sliding hiatal hernia

A

Hourglass- GE junction moves up into esophagus. Increased risk for GERD (LES bypassed)

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19
Q

Paraesophageal hiatal hernia

A

stomach perforates the diaphragm. Here bowel sounds in lung fields and lung hyperplasia.

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20
Q

Clinical features of GERD

A
  1. Heartburn
  2. Adult onset asthma and cough
  3. Tooth enamal damage
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21
Q

Histology of Barrett Esophagus

A

Metaplasia from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells.

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22
Q

Adenocarcinoma of the esophagus (most common cause and location)

A

Barrett esophagus. Lower 1/3 of esophagus.

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23
Q

Squamous Cell carcinoma of the esophagus (cause)

A

IRRITATION.

  • Alcohol/tobacco
  • Very hot tea
  • Achalasia (from rotting food)
  • Esophageal web (from rotting food)
  • lye ingestion…
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24
Q

Spread of esophageal carcinoma

A

If upper 1/3 –> Cervical nodes
middle 1/3 –> mediastinal or tracheobronchial nodes
lower 1/3 –> celiac and gastric nodes

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25
Q

Gastrochisis

A

Congenital malformation of anterior abdominal wall resulting in exposure of gut (NO COVER)

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26
Q

Omphalocele

A

PERSISTANT herniation of gut into umbilical cord. COVERED by peritoneum/amnion.

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27
Q

Pyloric Stenosis (who is it most commonly seen in, when does it present)

A

More common in males, presents two weeks after birth (normal at birth)

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28
Q

Projectile non-bilious vomiting
visible peristalsis
olive like mass in abdomen

A

Pyloric Stenosis

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29
Q

Causes of Acute Gastritis

A
  1. Severe burn (Curling ulcer) –> due to hypovolemic shock and decreased perfusion.
  2. NSAIDS (decreased PGE2)
  3. Heavy EtOH
  4. Chemotherapy
  5. Cushing Ulcer (increased intracranial pressure leading to increased vagal stimulation)
  6. Shock
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30
Q

What do you find with Achlorhydria

A

Increased gastrin levels and G-cell hyperplasia…

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31
Q

Risks associated with Chronic H Pylori gastritis

A
  1. Ulceration
  2. Gastric Adenocarcinoma (also true of immune mediated chronic gastritis)
  3. MALT lymphoma
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32
Q

How to determine if H pylori infection present

A

Urease breath test
Stool antigen test
biopsy

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33
Q

Cause and symptoms of duodenal ulcers

A

H pylori! (Zollinger-Ellison Syndrome rare)

Epigastric pain that IMPROVES with meals (contrast with gastric ulcers)

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34
Q

Site of bleeding during posterior rupture of duodenal ulcer

A

Gastroduodenal Artery

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35
Q

Cause and symptoms of gastric ulcer

A

H pylori AND NSAIDS!

Epigastric pain that WORSENS with meals (contrast with duodenal ulcers)

36
Q

Site of bleeding of gastric ulcer

A

Left gastric artery (most often located in lesser curvature of antrum)

37
Q

Signs of benign gastric ulcer (vs. malignant)

A

Small (
normal mucosal surroundings

VS. large, irregular, with heaped up margins

38
Q

Risk factors for intestinal subtype of gastric carcinoma

A
  1. Intestinal metaplasia (H pylori/autoimmune gastritis)
  2. Smoked foods- nitrosamines (japan)
  3. Type A blood
39
Q

Risk factors for diffuse subtype of gastric carcinoma

A

NOT associated with H pylori, smoked foods, or intestinal metaplasia…

40
Q

Histology of diffuse subtype of gastric carcinoma

A

-Signet ring cells that diffusely infiltrate gastric wall. Desmoplasia (reaction) results in thickening of stomach wall (called Linitis Plastica)

41
Q

Symptoms of gastric carcinoma

A
  • Weight loss, abdominal pain, anemia, and early satiety (particularly diffuse type)
  • Acanthosis Nigricans (thickening/darkening of skin, particularly in axilla)
  • Leser-Trélat sign: dozens of sebhorrheic keratosis all at once.
42
Q

Sites of spread of gastric carcinoma (3)

A
  1. Left Supraclavicular lymph node (Virchow’s node)
  2. Periumbilical region (Sister Mary Joseph Nodule, see with intestinal type)
  3. Bilateral ovaries (Krukenberg tumor, see with diffuse type).
43
Q

What congenital disorder is Duodenal Atresia associated with?

A

Down Syndrome

44
Q

Clinical signs of duodenal atresia

A
  1. Polyhydramnios
  2. Distension of stomach and duodenum –> double bubble sign.
  3. Bilious vomiting
45
Q

Rule of 2s for Meckel Diverticulum

A
  1. 2% of population (most common congenital anomaly of GI tract)
  2. 2 inches long located 2feet from ileocecal valve (in small bowel)
  3. Presents during first 2 years of life.
46
Q

Symptoms of Meckel Diverticulum

A

Bleeding (due to heterotrpic gastric mucosa)
Volvulus
Intussesception,
Obstruction

47
Q

Most common location of volvulus

A

Sigmoid colon (elderly) and cecum (young adults)

48
Q

Symptoms of intussesception

A

Current jelly stool due to disruption of blood supply and infarctions

49
Q

Most common causes of intussusception

A

In children –> lymphoid hyperplasia (often following rotavirus)

In adults –> tumor

50
Q

Clinical signs of Small Bowel Infarction

A
  • Abdominal Pain
  • Bloody diarrhea
  • Decreased bowel sounds
51
Q

HLA associations with Celiacs

A

HLA-DQ2 and DQ8

52
Q

Path of gluten in celiacs

A

Absorbed, gliadin then deamidated by TISSUE TRANSGLUTAMINASE (tTG). Deaminated gliadin presented via MHC class II. Helper T cells mediate tissue damage.

53
Q

Most immunogenic component of gluten

A

Gliadin

54
Q

Skin finding associated with Celiac Disease

A

Dermatitis herpetiformis –> Small, herpes-like vesicles. Due to IgA deposition at the tips of dermal papillae

55
Q

Lab findings with Celiac Disease

A

IgA antibodies against endomysium, tTG, or gliadin.

Always test IgG as well in case of IgA deficiency.

56
Q

Where in the GI tract is most of celiac disease damage done?

A

DUODENUM

57
Q

Late complications of Celiac Disease

A

T-cell lymphoma and small bowel carcinoma

58
Q

Where in the GI tract is most of tropical sprue damage done?

A

JEJUNUM and ILEUM (can see secondary folate or Vit. B12 deficiency)

59
Q

Histological findings of Whipple Disease and location

A

Foamy macrophages filled with lysosomes containing organism (PAS +). Found in lamina propria of small bowel.

60
Q

Symptoms of Whipple Disease

A

Fat malabsorption and steatorrhea (due to macrophage compression of lacteals and impaired lymphatic drainage). Can also present as arthritis, cardiac valve involvement, lymph nodes, and CNS

61
Q

Abetalipoproteinemia

A

AR deficiency in apolipoprotein B-48 and B-100. Causes impaired fat absorption (B-48) and absent plasma VLDL/LDL (B-100)

62
Q

Carcinoid tumor stain

A

Chromogranin (also small cell carcinoma of lung)

63
Q

Location of carcinoid heart disease

A

R sided, as lungs filter out serotonin (MAO present). Serotonin increases collagen production, leading to tricuspid regurg and pulm. stenosis.

64
Q

What congenital disease is Hirschprung Disease associated with?

A

Down Syndrome

65
Q

How do you diagnose Hirschprung Disease?

A

You must do a Rectal SUCTION biopsy (to get layers of submucosa).

66
Q

What type of inflammation do you see with Ulcerative Colitis?

A

Crypt abscesses with neutrophils

67
Q

What are the common complications of ulcerative colitis?

A

Toxic megacolon and carcinoma (risk based on extent of colonic involvement and duration of disease)

68
Q

What is Ulcerative Colitis associated with?

A

Primary sclerosing cholangitis and p-ANCA

69
Q

What type of inflammation do you see with Crohn’s Disease

A

Lymphoid aggregates with granulomas

70
Q

What complications is Crohn’s Disease associated with?

A

Malabsorption, calcium oxalate nephrolitiasis (KIDNEY STONES), fistula formation, and carcinoma if colon involved.

71
Q

Complications of colonic Diverticula

A
  1. Hematochezia (bright red rectal blood)
  2. Diverticultiis (think left-sided appendicitis
  3. Fistula
72
Q

Angiodysplasia

A

Acquired malformation of mucosal and submucosal capillary beds that can rupture –> hematochezia

73
Q

Hereditary Hemorrhagic Telangiectasia

A

AD disorder of thin-walled blood vessels, esp. in mouth and GI tract. Presents as bleeding…

74
Q

Hyperplastic colonic polyps (histology and course)

A

Serrated appearance on microscopy. NO MALIGNANT POTENTIAL.

75
Q

Adenomatous polyps (course)

A

Benign, but pre-malignant.

76
Q

Adenoma-carcinoma sequence

A
  1. APC mutation (increased risk for polyp)
  2. K-ras mutation (allows for formation of polyp)
  3. p53 and increased expression of COX (progression to carcinoma)
77
Q

Does aspirin help with colonic carcinoma?

A

YES. Because it inhibits COX… thus helps to impede progress from adenoma to carcinoma.

78
Q

Risk factors for progression from adenoma to carcinoma?

A

Size >2cm, sessile growth (flat, non pedunculated), and villous histology

79
Q

Cause of Familial Adenomatous Polyposis

A

AD inherited defect in APC (Chromosome 5)

80
Q

Gardner Syndrome

A

Familial Adenomatous Polyposis + fibromatosis and osteomas

81
Q

Turcot Syndrome

A

Familial Adenomatous Polyposis + CNS tumors (medulloblastomas and glial tumors)

82
Q

Peutz-Jeghers Syndrome

A

Hamartomatous (benign) polyps throughout GI tract and mucocutaneous hyperpigmentation. AD

See increased risk of colorectal, breast, and gynecologic cancers.

83
Q

Hereditary Nonpolyposis Colorectal Carcinoma

A

Inherited mutation in DNA mismatch repair enzymes (microsatellite instability).

See increased risk of colorectal, ovarian, and endometrial carcinomas

84
Q

What heart condition does colonic carcinoma predispose you to?

A

Strep. bovis endocarditis

85
Q

Most common site of colorectal cancer metastasis?

A

Liver!