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SP 16 - Gen Path Final > L1, L2: Gastrointestinal Pathology > Flashcards

L1, L2: Gastrointestinal Pathology Flashcards

1
Q

oral manifestations of GI disease may:

A
  • precede onset of lower GI disease
  • be similar to lower GI disease
  • persist after disease resolution
  • reflect systemic changes 2° to GI disease (ex: malabsorption affects tissues)
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2
Q

mucous or serous?

  • parotid acini = _______
  • sublingual acini = _______
  • submandibular acini = ________
  • minor glands = _______
A
  • serous
  • mucous
  • mixed
  • mixed
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3
Q
  • what is sialadenitis?

- causes?

A
  • inflammatory salavary gland lesion
  • sialoliths (stones –> retrograde flow)
  • mumps (viral)
  • sarcoidiosis (systemic inflammation)
  • Sjogren syndrome (autoimmune inflammaton, loss fxn)
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4
Q

what are symptoms of sialadenitis?

A
  • dry mouth
  • swelling
  • pain
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5
Q
  • Sjogren syndrome is what type of disease?
  • who does it most commonly effect?
  • symptoms?

+ increased risk for?

A
  • autoimmune
  • females, middle aged (40 - 50s)
  • dry mouth and dry eyes
  • *** keratoconjunctivitis sicca (dry eyes w/ inflammation)

+ lymphoma (40x)

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6
Q
  • how does Sjogren’s present clinically?

+ what are the two types of Sjogren’s disease?

A
  • either unilateral or bilateral parotid enlargement

+ primary SS (sicca syndrome) = just dry mouth, eyes, lacrimal, salivary glands; xerostomia

+ secondary SS (60%) = occurs when other autoimmune diseases are present (ex: rheumatoid arthritis, SLE)

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7
Q
  • salivary tumors most commonly affect which gland?

+ distinguish b/w benign and malignant

A
  • parotid gland (75% total; 75% of those are benign)

+ benign: plemorphic adenoma = mixed tumor
~ also may present as Warthin tumor

+ malignant = muco-epidermoid carcinoma

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8
Q
  • what is pleomorphic adenoma?
  • to what degree is it encapsulated?
  • how commonly does it recur?
  • what kind of transformation may occur if un-tx?
A
  • benign neoplasm of salivary glands (60% parotid)
  • variable to poor
  • 10%
  • can become malignant
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9
Q
  • what is a Warthin tumor?
  • with what behavior is it associated?
  • what gender is most commonly affected?
  • presents most commonly as (uni/bi)lateral?
A
  • benign neoplasm of SG’s, almost exclusively parotid
  • smoking
  • males (4:1)
  • mostly unilateral; continued smoking can make multifocal or bilateral
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10
Q
  • what is mucoepidermoid carcinoma?
  • what does it affect?
  • how does it present clinically?
A
  • malignant SG tumor
  • parotid and minor SG
  • bluish color from mucin and cystic growth pattern
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11
Q

what are 2 types of obstructive esophageal diseases?

A
  • mechanical = post-inflammatory fibrosis/stenosis (narrowing)
  • functional = muscle spams that may cause diverticula
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12
Q
  • how do esophageal varices occur?

- what risk is associated with them?

A
  • caused by portal hypertension (common in cirrhotic pt)

- asymptomatic; can rupture, cause massive hemorrhage and death

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13
Q
  • what are some extrinsic agents of esophagitis (inf)?

- what are some intrinsic agents?

A
  • chemicals, iatrogenic (intubation, chemo, radiation, grafting [bone]), infections (immune suppressed; viral and fungal), trauma, heavy smoking, pill lodging (acid burns)
  • refux/GERD (gastric esophageal reflux disease)
    + also related to PMN/lymphocyte inflammation
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14
Q

what is Barrett esophagus?

A

histological metaplasia of distal esophagus into mucus-like structure of stomach due to acidic reflux. can lead to neoplasia.

+ divided into “long segment” and “short segment”

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15
Q

how might GI reflux manifest orally?

A
  • erosion of enamel on lingual/palatal surfaces

- extent of loss reflects frequency/duration

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16
Q

what are 2 types of benign esophageal neoplasms?

A
  • leiomyoma

- mucosal polyps

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17
Q

what are 2 types of malignant esophageal neoplasms?

A
  • adenocarcinoma (Barrett)

- squamous cell carcinoma

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18
Q
  • what commonly causes esophageal squamous cell carcinoma?
  • in which population is it most prevalent?
  • what is the prognosis?
  • which area of esophagus most commonly affected?
  • regional variation (causes) include?
A
  • smoking and alcohol abuse
  • males, esp. black males
  • 9% 5 year survival rate
  • middle 1/3
  • diet, environment, genetics
    + diet areas are China, Brazil, South America
    ~ vitamin/ trace metal deficiency
    ~ fungal contamination
    ~ nitrates and nitrosamines
    + “Plummer Vinson(?),” achalasia (?), esophagitis
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19
Q
  • prevalence: more esophageal adenocarcinoma or SCCa?
  • which area of esophagus most commonly affected by adenocarcinoma?
  • most common population?
  • histological sign?
  • clinical signs?
A
  • SCCa > adenocarcinoma prevalence
  • distal 1/3
  • white males
  • Barrett’s esophagus
  • dysphagia, “chest pain,” weight loss (malabsorption or cytokines leading to cachexic metabolism)
20
Q

what is gastritis, and what 3 types are there?

A
  • gastritis = inflammation of stomach lining
  • acute = transient; may be involved in ulceration
  • chronic = longer duration
  • autoimmune = lose parietal cells –> decrease intrinsic factor –> decreased B12 absorption –> pernicious anemia
21
Q
  • pathogenesis of acute gastritis?
  • range of symptoms?
  • pathological presentation?
A
  • cigarettes, alcohol
  • stress, ischemia
  • NSAIDs, aspirin, infection
  • asymptomatic to epigastric pain to hemorrhage
  • punctate (tiny holes) hemorrhage, erosion
  • edema, acute inflammation
22
Q
  • pathogenesis of chronic gastritis?
  • pathological presentation?
  • clinical course of disease?
A
  • infection; 90% cases (Heliobacter pylori)
  • autoimmune 10% cases (pernicious anemia)
  • atrophic epithelium, chronic inflammation, intestinal metaplasia
  • ulceration, cancer risk 2-4% (intestinal metaplasia)
23
Q
  • what causes peptic ulcer disease?
  • symptoms?
  • where are the effects shown?
  • what is the % risk for males VS females?
A
  • H. pylori, NSAID use, stress
  • gastric hyperacidity, recurrent ulcers w/ intermittent healing
  • 98% duodenum or stomach
  • lifetime risk: 10% males, 4% females
24
Q

complications of peptic ulcers?

A
  • intractable pain
  • hemorrhage
  • perforation (5%)
  • obstruction - edema, fibrosis (2%)
25
Q

what 4 diseases of the small intestine were mentioned?

A
  • celiac disease (gluten allergen)
  • tropical sprue (aerobic bacteria)
  • lactase (disaccharidase) deficiency
  • abetalipoproteinemia: transepithelial transport defect (mono and triglycerides)
26
Q
  • which race has gluten sensitivity most, and what is the prevalence?
  • what is the hypersensitive molecule?
  • what is the morphological presentation?
  • how can the prognosis be improved dietarily?
A
  • caucasians; 1:100 - 1:200
  • gliadin
  • blunted villi, inflammatory infiltrate
  • withdraw wheat gliadin and related grain proteins
27
Q

what (4) clinical consequences occur from malabsorption deficiencies of the small intestine?

A
  • anemia (deficient: iron, pyridoxine, folate or B12, bleeding from lack of Vitamin K)
  • osteopenia, tetany: defective Ca, Mg, Vit D, and protein absorption
  • amenorrhea, impotence, infertility: generalized malnutrition
  • A and B12 deficient: peripheral neuropathy, nyctalopia (decreased Vitamin A impairs night vision)
28
Q

how might malnutrition manifest orally?

A
  • iron malabsorption: iron deficiency anemia, B12 malabsorption, pernicious anemia
  • if severe, initial oral sign = atrophic glossitis (bald/reddish tongue results from loss of filiform architecture of tongue)
    + patchy (loss?), or involvement of entire dorsum (?)
  • overt tongue lesions are tender; glossopyrosis (burning sensation) is common complaint
29
Q

how does colon anatomy differ from SI anatomy?

A
  • no villi
  • tubular crypts present
  • surface absorptive cells
  • goblet, endocrine, undifferentiated cells
  • some Paneth cells
30
Q
  • what is a colon polyp?

- what are some types?

A
  • an extension into the colonic lumen
  • hyperplastic
  • inflammatory
  • hamartomatous (“controlled neoplasm, non-cancerous”)
  • adenomatous (neoplastic, tumor)
31
Q

what types of hyperplastic colon polyp characteristics are monitored?

A
  • neoplastic (normal type) VS dysplastic (abnormal type)
  • shape: tubular, tubulo-villous, villous
  • SIZE (most important indicator of malignant change)
32
Q

what are the clinical features of familial adenomatous polyposis (FAP) (glandular origin)?

A
  • > 90% penetrance
  • risk of extracolonic tumors (upper GI, desmoid, osteoma, thyroid, brain)
  • presence of CHRPE (congenital hypertrophy of pigmented epithelial cells)
  • untreated polyposis = 100% risk of cancer
33
Q

what additional features does Gardner syndrome exhibit beyond FAP?

A
  • epidermoid cysts (often on head –> afroman)
  • jaw osteomas
  • supernumerary and/or unerupted teeth
  • increased odontomas
34
Q

how might a dentist be alerted that a patient needs screening for GI diseases such as FAP and Gardner’s?

A

oral manifestations such as osteomas and delayed tooth eruption

35
Q
  • what is Peutz-Jeghers syndrome?

- what are some oral (and other) clinical manifestations?

A
  • a genetic disease characterized by development of hamartomatous polyps of the GI tract and hyperpigmented macules of the lips and oral mucosa (melanosis)
  • GI hamartomatous polyps + intussusception (colonic telescoping)
  • polyps not precancerous, but pt at greater risk for GI adenocarcinoma
  • perioral/oral pigmentation (melanin) in childhood
    + non-sun dependent freckling of vermilion zone
    + nose, lips, buccal mucosa, hands/feet, genitals, perianal
    + present at birth in 95% of cases
36
Q

what are 4 types of intestinal obstruction?

A
  • hernitation
  • loop adhesion
  • volvulus (twisting)
  • intussusception (telescoping)
37
Q
  • what are two types of ulcerative inflammatory diseases?

- subtypes (2)?

A
  • infectious and idiopathic IBS (unknown/spontaneous)
  • idiopathic IBS –> exhibit chronic architectural changes:
    + Crohn’s disease
    + ulcerative colitis
38
Q

what pathological findings are associated with Crohn’s disease?

A
  • any portion of GI tract, commonly terminal ileum
  • transmural (very patchy “skip” lesions)
  • common oral involvement
  • can be thick, stenotic (narrow) bowel wall or
  • fissures/fistulas w/ noncaseating granulomas (infection-related regions of inflammation)
  • mucosal “cobble-stoning” = diseased tissue lower than normal
39
Q
  • what are pathological findings associated with ulcerative colitis?
    + what oral lesions are associated w/ ulcerative colitis?
A
  • affects rectum and proximal colon
  • CONTINUOUS pseudo-polyps
  • mucosal ulceration
  • related: pseudomembranous colitis (C. difficile)

+ oral lesions less common than in Crohn’s
+ scattered, arc shaped pustules on an erythematous mucosa at multiple sites w/ variable severity
~ “snail track” pyostomatitis vegetans)
+ long-standing lesions can become granular, polypoid, or fissured and mimic Crohn’s
+ 10% pt dev IBD-associated arthritis of TMJ’s

40
Q
  • types of benign stomach tumors?

- types of malignant stomach tumors?

A
  • inflammatory or reactive
  • leiomyomas
  • adenocarcinoma (90-95%)
  • lymphoma (4%)
  • carcinoid (3%)
  • spindle cell tumors (2%)
41
Q

what are the characteristics of gastric carcinoma (epithelial/internal lining)?

A
  • 3% of all cancer settings
  • incidence/mortality decreasing
  • risks: regional variation
    + diet (nitrites), genetics, adenoma
    + chronic gastritis, H. pylori
  • 5 year survival
42
Q

(?) what are 3 types/characteristic gastric cancers?

A
  • adenocarcinoma (glandular originating epi cancer; stomach lining)
  • linitis plastica (“leather bottle stomach”)
  • diffuse “signet ring cells” (often carcinoma, nucleus smashed to side by mucin content of cells)
43
Q

what are some epidemiological characteristics of colonic adenocarcinoma?

A
  • most common malignancy of GI tract
  • great heterogeneity
  • 15% of all cancer deaths
  • 2 important prognostic factors:
    + depth of invasion
    + lymph node metastases
44
Q

what are the risk factors for colorectal cancers?

A
  • high-fat, low-fiber diet
  • age >50 y.o.
  • personal or family history of adenoma/colorectal carcinoma
  • IBD’s
  • hereditary colon cancer syndromes (FAP)
45
Q

what are some clinical manifestations for colorectal cancers? (???)

A
  • large cecal cancer?
  • “napkin ring” left-sided cancer
  • villous adenoma with cancer:
    + villous adenoma (?)
    + invasive adenocarcinoma
46
Q

what is the TNM classification of colorectal cancer?

A 
- T = tumor invasion depth
\+ 1: submucosa
\+ 2: muscularis propria
\+ 3: subserosa or pericolic fat
\+ 4: contiguous structures
  • N = lymph nodes
  • M = metastasis
  • higher stage = lower survival
47
Q
  • is H. pylori more common in gastric or duodenal ulcers?

- Rx for H. pylori?

A
  • duodenal ulcers (85-100%) > gastric ulcers (65%)

- Rx = antibiotics and proton pump inhibitors

SP 16 - Gen Path Final (2 decks)

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