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)
2
Q
mucous or serous?
- parotid acini = _______
- sublingual acini = _______
- submandibular acini = ________
- minor glands = _______
A
- serous
- mucous
- mixed
- mixed
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)
4
Q
what are symptoms of sialadenitis?
A
- dry mouth
- swelling
- pain
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)
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)
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
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
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
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
11
Q
what are 2 types of obstructive esophageal diseases?
A
- mechanical = post-inflammatory fibrosis/stenosis (narrowing)
- functional = muscle spams that may cause diverticula
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
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
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”
15
Q
how might GI reflux manifest orally?
A
- erosion of enamel on lingual/palatal surfaces
- extent of loss reflects frequency/duration
16
Q
what are 2 types of benign esophageal neoplasms?
A
- leiomyoma
- mucosal polyps
17
Q
what are 2 types of malignant esophageal neoplasms?
A
- adenocarcinoma (Barrett)
- squamous cell carcinoma
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
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
what 4 diseases of the small intestine were mentioned?
- celiac disease (gluten allergen)
- tropical sprue (aerobic bacteria)
- lactase (disaccharidase) deficiency
- abetalipoproteinemia: transepithelial transport defect (mono and triglycerides)
26
- 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?
- caucasians; 1:100 - 1:200
- gliadin
- blunted villi, inflammatory infiltrate
- withdraw wheat gliadin and related grain proteins
27
what (4) clinical consequences occur from malabsorption deficiencies of the small intestine?
- 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
how might malnutrition manifest orally?
- 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
how does colon anatomy differ from SI anatomy?
- no villi
- tubular crypts present
- surface absorptive cells
- goblet, endocrine, undifferentiated cells
- some Paneth cells
30
- what is a colon polyp?
| - what are some types?
- an extension into the colonic lumen
- hyperplastic
- inflammatory
- hamartomatous ("controlled neoplasm, non-cancerous")
- adenomatous (neoplastic, tumor)
31
what types of hyperplastic colon polyp characteristics are monitored?
- neoplastic (normal type) VS dysplastic (abnormal type)
- shape: tubular, tubulo-villous, villous
- SIZE (most important indicator of malignant change)
32
what are the clinical features of familial adenomatous polyposis (FAP) (glandular origin)?
- >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
what additional features does Gardner syndrome exhibit beyond FAP?
- epidermoid cysts (often on head --> afroman)
- jaw osteomas
- supernumerary and/or unerupted teeth
- increased odontomas
34
how might a dentist be alerted that a patient needs screening for GI diseases such as FAP and Gardner's?
oral manifestations such as osteomas and delayed tooth eruption
35
- what is Peutz-Jeghers syndrome?
| - what are some oral (and other) clinical manifestations?
- 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
what are 4 types of intestinal obstruction?
- hernitation
- loop adhesion
- volvulus (twisting)
- intussusception (telescoping)
37
- what are two types of ulcerative inflammatory diseases?
| - subtypes (2)?
- infectious and idiopathic IBS (unknown/spontaneous)
- idiopathic IBS --> exhibit chronic architectural changes:
+ Crohn's disease
+ ulcerative colitis
38
what pathological findings are associated with Crohn's disease?
- 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
- what are pathological findings associated with ulcerative colitis?
+ what oral lesions are associated w/ ulcerative colitis?
- 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
- types of benign stomach tumors?
| - types of malignant stomach tumors?
- inflammatory or reactive
- leiomyomas
- adenocarcinoma (90-95%)
- lymphoma (4%)
- carcinoid (3%)
- spindle cell tumors (2%)
41
what are the characteristics of gastric carcinoma (epithelial/internal lining)?
- 3% of all cancer settings
- incidence/mortality decreasing
- risks: regional variation
+ diet (nitrites), genetics, adenoma
+ chronic gastritis, H. pylori
- 5 year survival
42
(?) what are 3 types/characteristic gastric cancers?
- 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
what are some epidemiological characteristics of colonic adenocarcinoma?
- most common malignancy of GI tract
- great heterogeneity
- 15% of all cancer deaths
- 2 important prognostic factors:
+ depth of invasion
+ lymph node metastases
44
what are the risk factors for colorectal cancers?
- 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
what are some clinical manifestations for colorectal cancers? (???)
- large cecal cancer?
- "napkin ring" left-sided cancer
- villous adenoma with cancer:
+ villous adenoma (?)
+ invasive adenocarcinoma
46
what is the TNM classification of colorectal cancer?
```
- 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
- is H. pylori more common in gastric or duodenal ulcers?
| - Rx for H. pylori?
- duodenal ulcers (85-100%) > gastric ulcers (65%)
| - Rx = antibiotics and proton pump inhibitors
