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STEP 1 STUFF > Pathoma - GI pathology > Flashcards

Pathoma - GI pathology Flashcards

1
Q

cleft lip and palate

A

failure of facial prominences to fuse

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2
Q

aphthous ulcer

A

superficial, painful ulceration

greyish base, surrounded by erythema

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3
Q

behcet syndrome

A

recurrent aphthous ulcers + genital ulcers and uveitis

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4
Q

oral herpes remains dormant in

A

the ganglia of the trigeminal nerve

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5
Q

Leukoplakia

A

white plaque that cannot be scarped away. it often represents squamous cell dysplasia.

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6
Q

hairy leukoplakia - associated virus and prognosis

A

shaggy rough patch on the lateral aspect of the tongue. Due to EBV. Associated with an immunocompromised state and represents hyperplasia –> not dysplastic cells, NOT precancerous.

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7
Q

erythroplakia

A
  • vascularized leukoplakia. suggesting some new blood vessel growth, HIGHLY suggestive of squamous dysplasia.
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8
Q

salivary major glands

A

parotid
submandibular
sublingual gland

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9
Q

Mumps - presentation and complications

A

infection with mumps virus giving bilateral inflammed parotids.
Orchitis leading to sterility is a complication.
Pancreatitis is also a complication
- amylas may be elevated due to pancreatitis or inflammation of oral salivary glands.

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10
Q

Sialadenitis

A
  • usually due to a staph aureus infection.
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11
Q

Pleomorphic adenoma - presentation and prognosis

A
  • most common tumor of the salivary gland
  • often presents at the parotid is a mobile, circumscribed, painless mass.
  • -> benign tumor composed of stromal and epithelial tissue.
  • has a high rate of recurrence due to incomplete resection (tumor has irregular borders making resection difficult)
  • can rarely progress to carcinoma, will present with facila nerve symptoms signifying invasion.
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12
Q

Warthin tumor

A
  • cystic tumor with lymph node tissue. almost always arises in the parotid. 2nd most common tumor of the parotid.
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13
Q

mucoepidermoid carcinoma

A

mucus producing cells and squamous cells. It is a malignant tumor and will commonly involve the facial nerve.

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14
Q

esophageal web

A

protrusion of the mucosa
presents of dysphagia for poorly chewed food
increased risk of squamous cell carcinoma of the esophagus

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15
Q

Plummer Vinson syndrome

A 
severe iron deficiency anemia 
esophageal web 
atrophic glossitis (beefy red tongue)
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16
Q

Zenker diverticulum

A

outpouching of mucosa through acquired defect in the muscular wall. Found at the junction of the esophagus and the pharynx.
–> a false diverticulum

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17
Q

Achalasia
presentation
cause
complications

A

dysphagia for both solids and liquids due to loss of esophageal motility.
Also have inability to relax LES.
–> bird beak sign on barium swallow

  • will have high lower esophageal sphincter pressure on manometry.

–> damage to ganglion cells of the myenteric plexus. Damage can be idiopathic or Chagas disease

increased risk of esophageal squamous cell carcinoma.

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18
Q

GERD

A

LES is not as tight as it should be. Acid and gastric contents go into the lower esophagus.
–> metaplasia of the cells from non-keratinzing squamous epithelium to non-ciliated columnar cells with goblet cells.

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19
Q

Clinical/complications features of GERD

A
  • heartburn
  • adult onset asthma
  • damage to enamel of the teeth
  • ulceration with stricture of lower esophagus
  • Barret esophagus
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20
Q

Esophageal carcinoma - subtypes

A
  • adenocarcinoma most common in the West. Malignant proliferation if glands. Found in the lower 1/3rd of the esophagus. arises from barrets esophagus.
  • squamous cell carcinoma, the most common esophageal cancer worldwide. upper portion of the esophagus. it is from IRRITATION.
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21
Q

causes of esophageal squamous cell carcinoma

A
  • alcohol tabacco
  • very hot tea
  • achalasia (rotting backed up food irritates)
  • esophageal web (this protrusion of the mucosa blocks food, rots, irritates the mucosa)
  • esophageal injury (lye ingestion)
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22
Q

presentation of esophageal carcinoma

A
  • poor prognosis as it presents late, they have progressive dysphagia (solids then liquids). weight loss may also be a presenting symptom.
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23
Q

Gastroschisis

A

congential malformation of the abdominal wall. exposure of contents without covering of peritoneum. to the right of umbilicus.

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24
Q

Omphalocele

A

persistent herniation of the bowel into the into the umbilicus, does not return to the body cavity during development. this herniation is covered by peritoneum.

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25
Q

Presentation of pyloric stenosis

A

2-4 weeks after birth, not immediately. takes time for the stenosis to develop.

clinically:
palpable olive
visible peristalsis
projectile non-bilious vomiting

26
Q

risk factors for acute gastritis

A

Severe burn (Curling ulcer)- hypovolemia from the severe burn leads to decreased blood supply to the stomach, the stomach mucosa does not receive proper nutrients and cannot ‘sweep’ away the acid the builds up there.

NSAIDs - decreased PGE2 (prostaglandin decreases acid production)

Heavy alcohol consumption - will directly damage the mucosa

Chemo therapy - knocking out the turning over cells in the stomach mucosa, loss of strong mucosal surface protection of the stomach

Increased intracranial pressure - Cushing ulcer. with increased ICP there is increased vagal stimulation leading to increased ACh which binds parietal cell receptor leading to increased acid production.

Shock - decrease in blood flow to vital organs

27
Q

Results of acid damage in the stomach

A

Erosion - loss of epithelium

Ulcer - loss of mucosal layer

28
Q

Chronic autoimmune gastritis
pathophysiology
risk for cancer

A

CD4 t-cells attack parietal cells in the body and the fundus (type 4 hypersensitivity). this can result in antibodies to parietal cells or intrinsice factor –> not the cause if the damage, but a consequence of the damage.

  • -> as you have t-cell mediated damage to the parietal cells you disrupt the thickness of the mucosa.
  • -> achlorhydria - low acid in the stomach due to loss of parietal cells. SO gastrin levels will increase due to loss of negative feedback. leading to G-cell hyperplasia in the antrum (these are the cells that make gastrin).
  • -> megaloblastic anemia due to loss of intrinsic factor. (pernicious anemia). NOTE: chronic autoimmune gastritis is the most common cause of vitamin B12 deficiency.

increased risk for adenocarcinoma
–> intestinal metaplasia first. (will see goblet cells in the stomach that should not be there).

29
Q

Chronic H Pylori gastritis
pathophysiology
complications

A

H pylori induces acute and chronic inflammation by producing ureases and proteases which inflame and weaken the mucosal defenses.

Antrum is the most common site.

  • intestinal metaplasia with risk to progression of adenomcarcinoma
  • ulceration
  • MALToma
30
Q

Triple Therapy for H.Pylori

A

amoxicillin
clarithromycin
proton pump inhibtor

31
Q

Two types of gastric carcinoma

A

gastric carcinoma is a malignant proliferation of surfacee epithelial cells. sub-divided in to two types:

  • intestinal
  • diffuse
32
Q

Gastric Carcinoma - Intestinal type

A
  • presents as large irregular ulcer with heaped up margins. it most commonly involves the lesser curvature of the antrum.
  • -> risk factors include intestinal metaplasia (i.e. H pylori and autoimmune gastritis), nitrosamines in smoked food, blood type A.
33
Q

Gastric carcinoma - diffuse type

A
  • characterized by signet ring cells that diffusely infiltrate the gastric wall. Desmoplasia results in thickening of the stomach wall –> linitus plastica.

It is NOT associated with H pylori, intestinal metaplasia, or nitrosamines.

34
Q

Gastric carcinoma presentation

A
  • -> acanthosis nigricans

- -> Leser-Trelat sign (erruption of many serborrheic keratosis on the body)

35
Q

Metastasis of gastric carcinoma

A
  • Virchow node
  • Sister mary joseph nodule
  • liver
  • Bilateral ovaries (Krukenberg tumor)
36
Q

duodenal atresia

A
  • failure of the small bowel to canalize

- associated with Trisomy 21

37
Q

Meckel Diverticulum

Rule of 2’s

A

True diverticulum - outpouching of all the layers of the bowel wall.
–> failure of the vitelline duct to involute.
2’s
- 2 percent of the population
- 2 inches long
- 2 feet from the ileocecal valve
- presents first 2 years of life (but often asymptomatic.

38
Q

Volvulus most common location

A
  • young adult: cecum

- elderly patient: sigmoid colon

39
Q

pathologic component of gluten

A

gliadin

  • -> gliadin is deamidated by tissue transglutaminase
  • -> deamidated gliadin is presented by MHC class to helper T-cells.
  • t cell mediated tissue damage.
40
Q

Dermatitis herpetaiformis

A

Seen in celiac disease. IgA deposition at the tip of dermal papillae. Results in destruction of the connection of the dermis and epidermis.

41
Q

Lab findings in celiac disease

A
  • IgA against tissue transglutaminase, endomysium, or gliadin.

NOTE IgG might be helpful in diagnosis as a subset of these patients are IgA deficient.

42
Q

Celiac disease - diagnosis

A

biopsy flattening of villi and hyperplasia of the crypts, epithelial lymphocytes.
–> note damage is mostly in the duodenum, the jejunum and ileum are LESS INVOLVED.

43
Q

Tropical sprue

A

damage to intestinal villi that arises after infectious diarrhea and responds to antibiotics. pathogen unknown.

in tropical sprue: the damage is more in the jejunum and the ileum. (contrast with celiac).

44
Q

whipple disease

A
  • systemic tissue damage from macrophages loaded with tropheryma whippelii.
  • -> this partially destroyed organism is present in macrophage lysosome and stains PAS positive.

classic involves the lamina propria of the small bowel. Macrophages compress lacteals preventing chylomicorns from being transferred from enterocytes to the lymphatics. This gives the symptom of malabsorption and steatorrhea.

45
Q

whipple disease some important symptoms

A
  • malabsorptive diarrhea
  • arthritis
  • cardiac valves
  • lymph nodes
  • CNS
46
Q

Carcinoid tumor

A

check urine 5-HIAA
carcinoid syndrome involves most the right side of the heart compared to the left because the lung (like the liver) has MAO.
–> cardiac symptoms include tricuspid valvular fibrosis from increased collagen leading to regurg. Also pulmonary valve stenosis.

serotonin –> MAO –> 5-HIAA in the urine

47
Q

causes of acute appendicitis

A
  • fecalith in adult

- lymphoid hyperplasia in a child

48
Q

IBD with crypt abscesses with neutrophils

A

UC

49
Q

IBD lymphoid aggregates with grnaulomas

A

Crohn

50
Q

IBD gross appearance pseudo-polyps

A

UC

51
Q

IBD gross appearance cobblestoning, creeping fat, strictures

A

Crohn

52
Q

Associations with UC

A

PSC

positive P-ANCA

53
Q

Associations with Crohn

A

ankylosing spondylitis
erythema nodosum
uveitis

54
Q

Smoking and IBD

A

protects against UC

increases risk for Crohn `

55
Q

Hirschprung disease

A
  • defective relaxation and peristalsis of the rectum and distal sigmoid colon. Associated with down syndrome.
56
Q

Myenteric (auerbach) plexus

A

controls motility and relaxation. found between the inner and outer layers of the muscularis propria.

57
Q

Submucosal (meissner) plexus

A

regulates blood flow, secretions, and absorption. located in the submucosa.

58
Q

Hirschprung disease - clinical features

A
  • failure to pass meconium
  • empty vault on DRE
  • megacolon

–> rectal suction biopsy will show absent ganglion cells in the muscularis propria. important that it is suction so that you get deeper than the mucosa.

59
Q

Hirschprung disease - treatment

A

resect involved area of bowel

60
Q

adenoma carcinoma sequence

A

APC mutation develops –> KRAS –> p53, COX increased

61
Q

Gardner syndrome

A

FAP with fibromatosis with osteomas

62
Q

Turcot syndrome

A

FAP with CNS tumors (medulloblastoma, glial tumors)

STEP 1 STUFF (15 decks)

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