Oral Cavity and GI tract Flashcards Preview

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Flashcards in Oral Cavity and GI tract Deck (82):
1

Aphthous ulcers

Extremely common
Small, painful, shallow ulcers
Soft palate, gums, border of tongue
Unknown etiology
Often triggered by stress
Usually resolve in a few weeks

2

Oral candidiasis

Occurs only in individuals where nl protective mechanisms are compromised
-Immunodeficiency
-Cancer
-DM
-Antibiotic or glucocorticoid therapy
-Denture wearers

3

AIDS oral complications

Herpesvirus infection
Oral candidiasis
Hairy leukoplakia
-White confluent patches, epidermal thickening
-Caused by EBV
-May call attention to HIV infection

4

Kaposi sarcoma

Low-grade malignant tumor caused by KS-associated herpesvirus infection
Red/purple nodular masses in lining of oral cavity and elsewhere

5

Leukoplakia

White patch or plaque caused by epidermal thickening or hyperkeratosis
Cannot be scraped off
Smoking, EtOH abuse

6

Erythroplakia

Red plaque that appears distinct from surrounding mucosa
> 50% transform to cancer

7

Oral cancer

Common
Smoking, chronic alcoholism are risk factors
Avg age at dx is 55-60 yrs
Most oral cancers are squamous cell carcinoma

8

Sialadenitis

Inflammation of the salivary glands
Caused by:
-Infection from bacteria (Staph and strep)
-Infection from viruses (mumps)
-Autoimmune reactions (Sjogren syndrome)
Pain, enlargement of salivary glands

9

Salivary gland tumors

Uncommon
Peak incidence is age 50-60

10

Pleomorphic adenoma

Most common tumor type of salivary glands
Benign
Slow growing, may compress facial structures

11

Mucoepidermoid carcinoma

Tumor of salivary glands
Malignant tumor, mix of mucous and squamous cells

12

Tx for salivary gland tumors

Surgery
Recurrences are common, but prognosis is good

13

Heartburn

Retrosternal burning pain; regurgitation of gastric contents into lower esophagus

14

Sx of esophageal lesions

Dysphagia
Heartburn
Hematemesis
Melena

15

Achalasia

Incomplete relaxation of lower esophageal sphincter in response to swallowing
Myenteric ganglion cells in body of esophagus reduced or absent

16

Sx, causes of achalasia

Dysphagia
Regurgitation
Aspiration
Cause unknown

17

Hiatal hernia

Separation of muscles of esophagus and diaphragm, with protrusion of stomach above diaphragm
Small hiatal hernias: common and usually asymptomatic
Large hiatal hernias: heartburn, nausea, reflux esophagitis
Complications: ulceration, bleeding
95% are sliding, as opposed to rolling

18

Mallory-Weiss syndrome

Longitudinal tears in the esophagus at the gastroesophageal junction
Caused by severe retching, vomiting

19

Sx of Mallory-Weiss syndrome

Bloody stools
Vomiting bright red blood
Pain
Infection

20

Prognosis of Mallory-Weiss syndrome

Usually heals without surgery

21

Esophageal varices

Dilated submucosal veins in lower esophagus
Asymptomatic until rupture, then life-threatening bleeding
Portal htn
Sclerotherapy, balloon tamponade

22

Esophagitis

Inflammation of esophageal mucosa
Usually in adults >40 yoa
Most cases due to GERD

23

Causes and sx of esophagitis

Heartburn
Severe: bleeding, development of esophageal stricture, Barrett esophagus

24

Barrett esophagus

Replacement of distal esophagus stratified squamous mucosa with metaplastic GI-like mucosa (adaptation)
Complication of long-standing GERD
30-100x risk for adenocarcinoma

25

Adenocarcinoma

Most common esophageal cancer in US
Whites > blacks
Risk factor: Barrett esophagus
Distal 1/3 of esophagus

26

Sx of adenocarcinoma

Insidious onset
Late obstruction

27

Squamous cell carcinoma

Most common esophageal cancer worldwide
Blacks > whites
Risk factors: chronic esophagitis (alcohol and smoking), genetics
Middle 1/3 of esophagus

28

Sx of squamous cell carcinoma

Insidious onset
Late obstruction

29

How does blood stemming from stomach diseases differ from esophageal pathologic blood?

Blood congeals and turns brown in stomach acid, so vomited blood looks like coffee grounds

30

Chronic gastritis

Chronic inflammation in gastric mucosa, leading eventually to muscle atrophy and epithelial metaplasia
Most important cause is infection by H. pylori

31

Sx of chronic gastritis

Most are asymptomatic
Risk factors (bile, reflux, NSAIDs, autoimmunity) may develop peptid ulcers, MALT lymphomas, or gastric adenocarcinomas

32

Acute gastritis

Acute mucosal irritation
Causes include NSAIDs, alcohol, smoking, infections, trauma

33

Sx of acute gastritis

Depend on extent of damage and erosion to gastric mucosa
No sx
Epigastric pain with N/V
Hematemesis, melena, and potentially fatal blood loss

34

Peptic ulcers

Chronic, solitary, recurrent lesions in the first portion of the duodenum or in the stomach
H. pylori
Additional risks: NSAIDs, smoking, alcohol

35

Sx of peptic ulcers

Epigastric pain, bleeding

36

Tx of peptic ulcers

PPI
Abx
Rarely surgery

37

Gastric carcinoma

Over 90% of stomach cancers
Two morphological types:
-Intestinal: arises from metaplastic cells following chronic gastritis, males > females
-Diffuse: arises from gastric mucous cells and not associated with chronic gastritis, females > males

38

Intestinal vs diffuse types of gastric adenocarcinoma

Intestinal: H. pylori risk factor, diffuse: none identified
Gland formation in intestinal vs no gland formation in diffuse

39

Atresia

Intestinal lumen does not develop; duodenal atresia is most common

40

Duplication

Saccular structures that may or may not communicate with remainder of lumen

41

Meckel diverticulum

Blind pouch, usually in the ileum

42

Omphalocele

Intestines herniate through abdominal musculature surrounding umbilicus

43

Malrotation

Of developing bowel, causing intestine to develop in abnormal positions

44

Hirschsprung disease

Congenital megacolon
Nerve cells absent from most of the large intestine
Stool moves slowly, causing obstruction
Main threat to life is superimposed enterocolitis with fluid and electolyte imbalances
50%: inactivating mutations in RET gene

45

Ischemic bowel disease

Narrowing of arteries that supply blood and oxygen to intestines
Often caused by atherosclerosis, > 50 yoa
Acute occlusion of a major mesenteric artery can cause transmural infarction

46

Risks of ischemic bowel disease

Age
Recent major abdominal surgery
Recent MI
Afib

47

Hemorrhoids

Enlarged veins located within tissues of the lower portion of the rectum or anus
Common after age 50

48

Risks for hemorrhoids

Straining during constipated bowel movement
Venous stasis of pregnancy in younger women

49

Colonic diverticulosis

Blind pouch that communicates with the lumen of the gut
Usually in the sigmoid colon

50

Causes of colonic diverticulosis

Low-fiber diet
Exaggerated peristaltic contractions and focal weakness in colon wall

51

What is the most affected part of the gut in a bowel obstruction

Small bowel

52

Secretory

Excessive secretion of intestinal fluid; infections, tumors, excess laxative use

53

Osmotic diarrheal disease

Something in bowel is drawing water form the body into the bowel; antacids

54

Exudative diarrheal disease

Presence of blood and pus in the stool; infections, inflammatory bowel diseases

55

Malabsorption-related diarrheal disease

Defective digestion, reduced surface of small intestine, infections

56

Deranged motility diarrheal disease

Surgery, neural dysfunction, infections

57

Viral infections- infectious enterocolitis

Rotavirus
Norovirus
CMV
HSV
Viral hepatitis

58

Bacterial infections- infectious enterocolitis

Campylobacter
Salmonella
Shigella
E. coli

59

Parasites- infectious enterocolitis

Giardia lamblia
Entamoeba histolytica
Cryptosporidium

60

What is an example of a malabsorption syndrome?

Celiac disease

61

Malabsorption syndromes

Defective absorption of fats, vitamins, proteins, carbs, electrolytes, minerals, and water

62

Most common presentation of malabsorption

Chronic diarrhea

63

Causes of malabsorption

Defects in intraluminal digestion, mucosal absorption, nutrient delivery

64

Irritable bowel syndrome

Often causes cramping, abd pain, bloating gas, diarrhea and constipation

65

Risks for irritable bowel syndrome

Young
Female
FHx of IBS

66

Crohn and ulcerative colitis

Chronic relapsing inflammatory disorders
Abnl local immune response against nl gut flora and probably self antigens, in genetically susceptible individuals

67

Epidemiology of Crohn disease

In US: 3-5/100,000
Between 15-30 yoa; can affect any age; minor peak at 60-70 yrs
Females sligthly more than males
Whites > nonwhites
Ashkenazi Jewish > non-Ashkenazi Jews

68

Clinical features of Crohn disease

Onset is usually insidious with a hx of recurrent diarrhea, crampy abd pain, fever, and gradual weight loss
Presentation is highly variable and unpredictable
In most pts, sx remit spontaneously or following therapy, but will recur with varying frequency and severity

69

Genetics of Crohn disease

Multifactorial inheritance
Increased risk: NOD2, HLA-DR7, HLA-DQ4
NOD2 plays a role in regulating the immune response to bacterial infection
Intestinal microenvironment may be an important environmental factor contributing to Crohn disease

70

Ulcerative colitis

Inflamattive disease of the colon, limited to the mucosa and submucosa
Begins in rectum and extends proximally
Granulomas absent
No skip lesions
Ulcers rarely extend below the submucosa
Higher risk of carcinoma development

71

Epidemiology of ulcerative colitis

Usually presents between 25-50 yoa, but can occur at any age
No differences between the sexes
Whites > nonwhites

72

Clinical features of ulcerative colitis

Insidious with cramps, tenesmus, lower abd pain with intense cramping
Highly variable and unpredictable
Bloody mucoid diarrhea may persist for days or mos and subside, then recur after asymptomatic intervals of varying lengths

73

Genetics of ulcerative colitis

Increased risk associated with HLA-DRB1

74

Other differences between Crohn and ulcerative colitis

Crohn: patchy involvement, Ulcerative colitis: Continous involvement
Crohn: transmural inflammation, fistulas, strictures, Ulcerative colitis: Superficial inflammation

75

Tumors of the small and large intestine

Colon and rectum most often affected
Sporadic (85%) or familial (15%)
Benign (75%) or malignant (25%)
Solitary or multiple
Primary > secondary
Adenocarcinomas- 70% of all cancers from the GI tract

76

Etiology of colon cancer

Genetic factors
-Familial adenomatous polyposis
-Lynch syndrome (HNPCC)
Dietary factors, such as a "Western diet"
-Low fiber
-High carb
-High-fat content

77

Classification of intestinal tumors

Non-neoplastic polyps
Benign neoplasms
Malignant neoplasms

78

Non-neoplastic polyps

90% of all epithelial polyps
Present in over half of all people >60 yoa
Hyperplastic polyps most common polyps of colon and rectum
Multiple > single

79

Neoplastic polyps (adenomas)

Benign polyps
75% are tubular adenomas
Often multiple
Incidence increases with age

80

Colorectal cancer

98% of all cancers in the large intestine are adenocarcinomas
Almost always arise in benign adenomatous polyps
-Six or more mutations required for cancer to form
Peak incidence is 60-70 yoa

81

Two distinct pathways for the development of colon cancer

Adenomatous polyposis coli pathway (APC gene)
-Sporadic colon cancer
-Inherited colon cancer
Microsatellite instability pathway (DNA repair genes)
-Sporadic
-Inherited colon cancer

82

Familial adenomatous polyposis

Autosomal dominant
One mutant copy of the adenomatous polyposis coli (APC) gene is limited
2nd nl copy requires a somatic mutation, which causes the development of hundreds to thousands of benign adenomatous polyps
Polyps often develop into malignant growths and cause cancer of the colon and/or rectum, but only after a cell acquires mutations in numerous additional genes