Exam 1 Ch. 14 Oral And GI Flashcards

1
Q

What is the general name for an apthous ulcer

A

Canker sore

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2
Q

If a patient has a painful ulceration in their mouth characterized by a white exudate and red rim what do they have

A

An aphthous ulcer

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3
Q

How much of the population is affected by an apthous ulcer

A

40%

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4
Q

Who is most likely to get an aphthous ulcer

A

Females less than 20 years old (reproductive age) and those with celiac disease/IBD

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5
Q

What is also known as the extreme version of an apthous ulcer

A

Behcet disease

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6
Q

What are 3 things that increase the likelihood of an aphthous ulcer

A
  • trauma/foods
  • nsaids/corticosteriods
  • vitamin B12
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7
Q

What is HSV-1

A

Oral herpes

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8
Q

Childhood HSV infection are usually symptomatic or asymptomatic?

A

80% asymptomatic

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9
Q

Most adults have what relationship with HSV

A

60% are carriers

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10
Q

Where is HSV dormant in adults

A

Trigeminal ganglion (CN v)

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11
Q

Reactivation of HSV in adults is known as what

A

Recurrent herpetic stomatitis

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12
Q

Childhood HSV can present itself as symptomatic and known as what?

A

Acute herpetic gingivostomatitis

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13
Q

Does location indicate type of HSV

A

No!

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14
Q

What are major symptoms of HSV

A

Grouped vesicles resulting in itching/burn, with HA, sore throat

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15
Q

Is there a cure for HSV

A

No, antiviral drugs decrease replication reducing recurrence

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16
Q

If HSV spreads to the CNS what is it known as

A

Herpesviral encephalitis (life threatening/HSV-1)

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17
Q

What is also known as thrush

A

Oral candidiasis

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18
Q

What is the occurrence of thrush in new borns

A

About 40%

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19
Q

What is the characteristic of oral candidiasis

A

Gray/white pseuodmembranes that can be scraped off

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20
Q

In what ways is oral candidiasis opportunistic

A

Decreases immune status, broad spectrum antibiotics, diabetes

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21
Q

How do physicians make diagnosis of the oral candidiasis

A

Leukoplakia, candidemia, oral CA

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22
Q

What are the two types of an oral proliferative lesion

A

Fibroma and pyogenic granuloma

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23
Q

Where is a fibroma most commonly found

A

Along the bite line

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24
Q

What is a characteristic of a fibroma

A

A nodular mass following chronic irritation

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25
Q

What is another name for a pyogenic granuloma

A

Pregnancy tumor

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26
Q

Why are pregnant women and children likely to get pyogenic granuloma

A

Hormonal factors, irritation, rapid growth

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27
Q

What are characteristicsof a pyogenic granuloma

A

Hemangioma on gingiva, red/purple

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28
Q

What is the treatment of a pyogenic granuloma

A

Remove irritant or excision

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29
Q

What is the difference between thrush and leukoplakia

A

Thrush can be scraped off, leukoplakia cannot

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30
Q

What are characteristics of leukoplakia

A

Raised white patch that can’t be scraped off due to epithelial hyperplasia/keratosis

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31
Q

Who is most likely to get leukoplakia

A

Males (2x) age 40-70 years

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32
Q

What are the risks of leukoplakia

A

Inflammation, tobacco, alcohol, candidiasis

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33
Q

How is leukoplakia diagnosed

A

Rule out cancer through biopsy, 25% are precancerous

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34
Q

If a leukoplakia is precancerous what kind is it

A

Squamos cell carcinoma

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35
Q

What is erythoroplakia

A

Red oral lesion with irregular borders

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36
Q

Who is most likely to get an erythroplakia

A

Males age 40-70

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37
Q

What increases risk of erythroplakia

A

Tobacco use, >50% transition into cancer

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38
Q

What type of cancer is about 2x more common among males

A

Oral cancer

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39
Q

What mutations are common in oral cancer

A

TP53 mutations from sites of dysplasia

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40
Q

Are multiple primary tumors common in squamos cell carcinomas

A

Yes

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41
Q

What is the prognosis of those with squamos cell carcinoma

A

Poor <50% long term survival, early detection best, pain/dysfunction = advanced stages

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42
Q

What are the risks of squamos cell carcinoma

A

Alcohol, tobacco, >30 years old, HPV-16

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43
Q

What are characteristics of oral squamos cell carcinomas

A

Raised firm lesion of white or red with irregular borders

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44
Q

What are the 2 most common places of oral squamos cell carcinoma

A

Ventral (inferior) tongue and floor of the mouth

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45
Q

Where is oral squamo cell carcinoma most likely to invade or metastasize

A

Cervical nodes

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46
Q

HPV associated oral squamos cell carcinoma is most likely located where

A

Base of tongue and tonsillar crypts

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47
Q

Where are primary salivary gland pathologies found

A

Rare but MC in parotid glands

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48
Q

What is indicated by dry mouth due to decreased saliva production

A

Xerostomia

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49
Q

What is an autoimmune attack on salivary AND lacrimal glands

A

Sjogren syndrome

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50
Q

What happens to the tongue from xerostomia

A

It can fissure and ulcerate creating risk for cadidiasis

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51
Q

What is sialadenitis

A

Inflammation and enlargement of salivary glands

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52
Q

What are two causes of sialadenitis

A

Viral and bacterial

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53
Q

Viral sialadenitis is mc caused from what

A

Mumps virus infection

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54
Q

What can viral sialadenitis create in adults

A

Pancreatitis and orchitis

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55
Q

What causes bacterial sialadenitis

A

MC staph. Aureus infection with dehydration being a risk

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56
Q

What is it called when saliva collects within tissue creating an inflamed cyst

A

Mucocele follows ductal obstruction

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57
Q

What is the liklihood of cancers ratio to salivary gland size

A

Smaller salivary glands tumors are less common but are greater cancer risk and vice versa for larger glands

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58
Q

Who is mostly impacted by salivary gland neoplasms

A

MC females 60-80 years old

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59
Q

What is the mc impacted gland from salviary gland neoplasms

A

Parotid

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60
Q

What is a pleomorphic adenoma

A

Mc a benign tummor that is painless and encapsulated

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61
Q

What is an invasive, affixed form of a parotid gland neoplasms that is aggressive

A

Carcinoma ex pleomorphic adenoma

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62
Q

What is Zenker’s diverticulum

A

Lower esophageal outpouching

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63
Q

What causes Zenker’s diverticulum and what does it affect

A

From increased pressure in the pharynx creating uncoordinated swallowing and cricopharyngeus muscle spasm

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64
Q

Why is halitosis associated with zenker’s diverticulum

A

A bolus accumulates within the lower esophageal outpouching

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65
Q

How is zenker’s diverticulum diagnosed

A

Through barium swallowing and video fluoroscopy

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66
Q

Which esophageal lesion is associated with atresia, tracheal fistula, stenosis that produces regurgitation

A

Mechanical esophageal lesion

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67
Q

Which esophagial lesion is produced from achalasia resulting in aperistalsis

A

Functional esophageal lesions

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68
Q

What happens in ectopia esophageal lesion

A

Mostly asymptomatic that is an ectopic gastric mucosa (inlet patch ) located in the upper 1/3

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69
Q

What does esophageal varices of esophageal lesions follow

A

Follows portal HTN

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70
Q

What is achalasia

A

Failure to relax due to functional esophageal obstruction

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71
Q

What are the 3 causes of achalasia

A

Incomplete LES relaxation, increased LES tone, esophageal aperistalsis

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72
Q

How is achalasia treated

A

Dialation or injection of botulinium toxin

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73
Q

Dilated esophagus from achalasia produces what

A

Dysphagia, regurgitation, “heart burn” producing weight loss sometimes

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74
Q

How is achalasia diagnosed

A

Barium swallowing producing “bird beak sign”

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75
Q

What is the most common type of achalasia

A

Primary that is due to loss of inhibitory innervation to LES (idiopathic)

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76
Q

What causes secondary achalasia

A

Co-morbidity impairing LES funx

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77
Q

What are common co-morbidities causing secondary achalasia

A

Chagas disease, diabetes, polio, inflammation near Auerbach’s plexus

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78
Q

What causes esophageal varices

A

Portal venous congestion producing portal HTN

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79
Q

What are 2 causes of portal venous congestion in esophageal varices

A

Blood in esophageal venous plexus making it dilated/tortuous, or cirrhosis from alcohol/flatworm

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80
Q

When are esophageal varices at risk for severe hemorrhage

A

When its asymptomatic

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81
Q

How does advanced cirrhosis affect the CNS

A

Liver failure produces toxins into CNS producing hepatic encephalopathy

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82
Q

What are 2 main symptoms of esophagitis

A

Odynophagia and dysphagia

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83
Q

What is GERD

A

Gastroesophageal reflux disease = idiopathic LES dysfunction

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84
Q

What is the most common cause of esophagitis

A

GERD

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85
Q

What is the MC GI complaint

A

GERD

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86
Q

What are some symptoms of GERD

A

Dysphagia, heartburn, “sour brash”

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87
Q

What are major risks of esophagitis

A

Obesity and increased gastric volume

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88
Q

What are some treatments/managements of GERD

A

Sleep at angle, weight loss, PPI, not laying down within 2 hours of eating, no carbonated drinks

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89
Q

What causes chemical esophagitis

A

Acute, pill induced, chemo, irradiation

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90
Q

Who is most likely impacted by infectious esophagitis

A

Debilitated and immunosupressed

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91
Q

When is infectious esophagitis most likely to hhappen

A

After an ulcer from microbes (fungal/viral)

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92
Q

What cases esophageal lacerations

A

Trauma from coughing or vomiting

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93
Q

What type of tear is most likely a part of esophageal laceration

A

Mallory weiss tear

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94
Q

Where is a longitudinal tear located at in a mallory weiss tear

A

Gastroesophageal jxn

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95
Q

Mallory weiss tear is associated with how many upper GI bleeds

A

50%

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96
Q

What is a hiatal hernia

A

Stomach protrudes to thorax widening esophageal hiatus

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97
Q

What are the characteristics of axial hiatal hernia

A

“Sliding” it is the MC and it is bell shaped

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98
Q

What are the characteristics of non axial hiatal hernia

A

“Rolling” and part of the stomach protrudes causing stragulation and obstruction

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99
Q

Who is mostly affected by hiatal hernia

A

70% are greater than 70 years old

100
Q

What hiatal hernia is symptomatic

A

Non axial which mimics GERD causing possible perforation/hemorrhage

101
Q

What is Barret esophagus

A

Metaplastic columnar epithelium replaces the stratified squamos epithelium after stomach acid damage

102
Q

Where does barret esophagus take place

A

The distal esophagus

103
Q

Who is most at risk for barrett esophagus

A

Caucasian males that are obese and 40-60 years old

104
Q

What symptom of barret esophagus prompts an evaluation

A

GERD

105
Q

What are some complications from barrett esophagus

A

Esophageal adenocarcinoma, ulcerations, strictures

106
Q

How do you diagnose barrett esophagus

A

Esophagoscopy and biopsy under regular surveillance

107
Q

How do you treat barrett esophagus

A

Stop irritants or meds (PPI’s, surgery)

108
Q

What are the 3 types of esophageal tumors

A

Leiomyoma, adenocarcinoma, squamos cell carcinoma

109
Q

Which esophageal tumor is MC in the US and which is MC worldwide

A

Adenocarcinoma = MC in US and squamos cell carcinoma = MC worldwide

110
Q

What are the risks for an adenocarcinoma esophageal tumor

A

Similar to GERD

111
Q

What is an adenocarcinoma esophageal tumor caused by

A

Esophageal metaplasia/dysplasia

112
Q

Which esophageal tumor makes up 90% of all esophageal CA

A

Squamos cell carcinoma

113
Q

What are indicators of an advanced adenocarcinoma

A

Obstruction = dysphagia/odynophagia

114
Q

What are some symptoms of an advanced adenocarcinoma

A

Vomit, cachexia, fatigue

115
Q

Which esophageal tumor has early lymphatic invasion and what is the prognosis

A

Adenocarcinoma, poor <25% at 5 years

116
Q

How do you diagnose an adenocarcinoma

A

Esophagoscopy, endoscopy = if abnormal image shown then biopsy taken

117
Q

What are 3 characteristics of a diffuse infiltration of an esophageal adenocarcinoma

A

Flat/raised, exophytic, ulceration

118
Q

Who is most at risk for a squamos cell carcinoma esophageal tumor

A

African american males older than 45 years with alcoholism, HPV, or taking nitrosamines

119
Q

Where is squamos cell carcinoma going to be impacting most, geographically

A

Rural

120
Q

Why do those with squamos cell carcinoma (esophageal) have a poor prognosis <10% at 5 years

A

Due to lymphatic mets

121
Q

What does a cardio-pulmonary invasion with an esophageal squamos cell carcinoma cause

A

Possible fistula

122
Q

What can also result from a squamos cell carcinoma (esophageal)

A

Strictures, hemorrhage

123
Q

Mucosal ulcerations can produce hemorrhages producing what

A

Hematemesis and melena

124
Q

What is the cause of the most common infection of the stomach

A

Helicobacter pylori

125
Q

What is an inflammation of gastric mucosa

A

Gastritis

126
Q

What are the 2 forms of the gastric inflammatory diseases

A

Acute and chronic gastritis

127
Q

Are neutrophils associated with acute or chronic gastritis

A

Acute gastritis

128
Q

What can cause the acute erosive hemorrhagic gastritis

A

Hemorrhage that is from possible erosion/ulceration

129
Q

Acute gastritis is dose dependent with what

A

Nsaids

130
Q

What meds are associated with acute gastritis

A

PPI’s, H2 receptor antagonists = decrease gastric acidity

131
Q

Hematemsis with acute gastritis is associated with who

A

Alcoholics

132
Q

Acute peptic ulcerations can cause what type of hemorrhage

A

Hematemesis

133
Q

What are 3 causes of acute peptic ulceration

A
  1. Severe physiological stress
  2. High dose of NSAIDS
  3. Intracranial disease(vagal nerve)
134
Q

What is rare with chronic gastritis

A

Hematemesis

135
Q

What are the multifactorial causes of chronic gastritis

A
  • helibacter pylori
  • increased age
  • other stressors
136
Q

What can follow chronic gastritis

A
  • peptic ulcer disease

- gastric adenocarcinoma

137
Q

What are the risks of chronic gastritis

A

Poor childhood sanitation/hygeine

138
Q

Dysplasia/metaplasia from chronic gastritis produces what

A

Carcinogenic = gastric adenocarcinoma, MALT lymphoma

139
Q

Who is most commonly affected by autoimmune gastritis

A

Elderly about 60 years old

140
Q

What antibodies are released from autoimmune gastritis

A

Parietal cells and I.F.

141
Q

Why does autoimmune gastritis complicate erythropoiesis

A

Pernicious anemia

142
Q

What are two identifiers of peptic ulcer disease

A

Pin point pain (granulation tissue), and hemorrhage

143
Q

Where doe peptic ulcer disease affect

A

Proximal duodenum(4x) and gastric antrum

144
Q

Who is more at risk from peptic ulcer disease

A

Males

145
Q

What factors contribute to peptic ulcer disease

A

Increase acidity (ulcerogenic), nsaids (decrease gastric protection), h. Pylori

146
Q

Why can peptic ulcer disease be a medical emergency

A

Possible perforation/hemorrhage

147
Q

What is a major symptom of peptic ulcer disease

A

Epigastric pain 1-3 hours postprandial

148
Q

Which type of peptic ulcer disease is releived postprandial and which type worsens postprandial

A

Duodenal = releif, gastric= worse

149
Q

What are 3 types of gastric polyps and which is MC

A

Inflammatory and hyperplastic polyps (MC), fundic gland polyp, gastric adenomas

150
Q

Who is most commonly afffected by a gastric adenoma

A

Males age 50-60

151
Q

What is associated with 90% of all stomach cancers

A

Gastric adenocarcinomas

152
Q

Who mostly gets gastric adenocarcinomas

A

Males age 55

153
Q

Males from which country are more likley to get gastric adenocarcinomas

A

Japan

154
Q

What is pyloric stenosis

A

Hypertrophy/narrowing of pyloric sphincter

155
Q

What is a characteristic of pyloric stenosis in newborns

A

Non bile stained projectile vomiting

156
Q

Who is most likely to get pyloric stenosis

A

White males, turner syndrome

157
Q

What treatment is associated with pyloric stenosis

A

Pyloromyotomy

158
Q

Intestinal obstructions are most commonly found where

A

In SI

159
Q

What is an abdominal wall defect allowing the intestine to protrude =inflammation

A

Hernia

160
Q

What is an intestinal obstruction with adherent segments

A

Adhesions producing inflammation = fibrosis

161
Q

What is a proximal segment telescoping into a distal segment

A

Intussusception

162
Q

What is a twisting loop of bowel

A

Volvulus, possible infarction

163
Q

What is a congenital outpouching of the SI

A

Meckel diverticulum

164
Q

What is a lack of neurologic ganglia in the rectum

A

Hirschsprung disease

165
Q

What causes hirschsprung disease

A

Defective neural crest cell migration

166
Q

Who is impacted more by hirschsprung disease

A

Females

167
Q

What arteries are impacted by ishemic bowel disease

A

Superior mesenteric, inferior mesenteric, celiac

168
Q

Ischemia in ischemic bowel disease causes what

A

Hypotension/occlusion, mucosal infarction

169
Q

What are 3 types of ischemic bowel disease

A

Thrombosis, arterial embolism, non occlusive ischemia

170
Q

What are characteristics of chronic ischemic bowel disease

A

Episodic bloody diarrhea mimicking IBD

171
Q

What are characteristics of actue ischemic bowel disease

A

Abdominal pain, frank blood in stool, risk for septic shock = 50% mortality rate

172
Q

What is angiodysplasi

A

Vascular lesion

173
Q

Where are angiodysplasias commonly found

A

MC in cecum, or ascending colon

174
Q

What are angiodysplasias hypothesized to develop following what

A

Mechanical stress (constipation)

175
Q

What are the two types of hemorrhoids

A

Internal = above anorectal line, external = below anorectal line

176
Q

When hemorrhoids irritates surrounding tissues what happens

A

Perianal itching, frank blood in stool

177
Q

What are the top 3 malabsorption diseases in the US

A

Celiac, crohn, pancreatic insufficiency

178
Q

What is excessive fat in feces called

A

Steatorrhea

179
Q

What is bloody diarrhea

A

Dysentery

180
Q

What is celiac disease

A

Immune mediated reaction to gliadin

181
Q

What produces villous atrophy and what disease is it associated with

A

B and t cells damaged within celiac disease

182
Q

Where does celiac disease impact

A

Duodenum and jejunum

183
Q

What is dermatitis herpetiformis

A

Celiac disease manifesting on the skin

184
Q

What disease is associated with cycles of mucosal injury, malnutrition, inflammm.

A

Environmental enteropathy

185
Q

Autoimmune environmental enteropathy involves what

A

Villus flattenin

186
Q

When is lactos intolerance acquired

A

In young adulthood MC

187
Q

What is an indication of traveler’s disease

A

> 3 unformed or loose stools within 24 hours

188
Q

What is the mc bacterial enteric pathogen in the US

A

Campylobacter jejuni

189
Q

Campylobacter jejuni may initiate what

A

Reactive arthritis

190
Q

How long does acute self limited colitis last

A

<1 month

191
Q

What is pseudomembranous colitis

A

Antibiotics disrupts flora (antibiotic associated colitis)

192
Q

What causes pseudomembranous colitis

A

Clostridium difficile overgrows = enterotoxins= inflammation/cell death

193
Q

Who is most susceptible to pseudomembranous colitis

A

Old age, hospitilization, decreased immunity

194
Q

What are psuedomembranes

A

Cellular debris and leukocytes

195
Q

What is viral gastroenteritis

A

Infection that leads to superficial injury to the stomach/SI

196
Q

1/2 of all gastroenteritis is associated with what

A

Viral gastroenteritis

197
Q

What causes viral gastrroenteritis in children

A

Rotavirus

198
Q

What causes viral gastroenteritis in adults

A

Norovirus

199
Q

How does one get viral gastroenteritis

A

Direct viral contact via contaminated food/H2O

200
Q

What is treatment for viral gastroenteritis

A

Self limiting, fluid replacement

201
Q

What type of parasitic disease affect greater than 1/2 the world

A

Ascaris lumbricoides

202
Q

What is a flagellated protozoa that resists cold and chlorine

A

Giardia lamblia

203
Q

What is giardia lamblias affect on the body

A

Its non-invasive and alters the SI enzymes

204
Q

What is another name for giardiasis

A

Beaver fever

205
Q

What is giardiasis

A

Malabsorption = diarrhea, anorexia, cramps

206
Q

What is sigmoid diverticulitis

A

Acquired diverticulum usually within the sigmoid colon

207
Q

What increases risk of sigmoid diverticulitis

A

Age and refined foods, decreased fiber = increase strain/pressure

208
Q

What is another possible cause of sigmoid diverticulitis

A

Possible infection = perforation = hemorrhage

209
Q

Who is most susceptible to sigmoid diverticulitis

A

50% of people > 60

210
Q

What is the sensation of inadequate BM and what is it usually associated with

A

Tenesmus with sigmoid diverticulitis

211
Q

What are main treatments for sigmoid diverticulitis

A

Increased fiber = decresed exaggerated peristalsis= reduce intraluminal pressure

212
Q

When does irritable bowel syndrome usually occur

A

Mc females 20-40 years old, psychological stress

213
Q

What is inflammatory bowel disease

A

Abnormal GI immune response = chronic/relapsing

214
Q

What are the 2 types of inflammatory bowel disease

A

Crohn disease and ulcerative colitis

215
Q

Where does crohns disease affect

A

Entire GI, MC in ileum

216
Q

Where does ulcerative colitis usually affect

A

Rectum/distal colon within the mucosa/submucosa

217
Q

What is the body’s reaction during inflammatory bowel disease

A

Microbiota, epithelial dysfunction, aberrant immune response

218
Q

What happens in crohns disease

A

Regional inflammation/fissures/ creeping fat

219
Q

What type of mediated reaction is with crohns disease

A

T cell mediated

220
Q

What does crohns disease open up the GI up to

A

Risk for adenocarcinoma

221
Q

What is ulcerative colitis

A

Superficial inflammation = mucosal ulcerations

222
Q

Where does ulcerative colitis start

A

Always begins in rectum to proximally

223
Q

Who is most likley to get ulcerative colitis

A

20-25 years old

224
Q

What is inhibitory to ulcerative colitis

A

Smoking

225
Q

What is ulcerative colitis associated with

A

Toxic megacolon = polyarthritis, AS, eye irritation

226
Q

What do relapsing episodes of ulcerative colitis look like

A

Stool is grossly bloody/mucoid

227
Q

What can ulcerative colitis lead to

A

Adenocarcinoma

228
Q

What is an autosomal dominant cancer syndrome

A

Familial adenomatous polyposis

229
Q

What does familial adenomatous polyposis affect

A

APC gene on chromosome 5

230
Q

How many people develop cancer from familial adenomatous polyposis

A

100% mc before age 30

231
Q

What is common in the stool. Of those with familial adenomatous polyposis

A

Occult blood with possible anemia

232
Q

How is familial adenomatous polyposis diagnosed

A

> 100 adenomas

233
Q

What is lynch syndrome

A

Hereditary cancer syndrome

234
Q

How does one get lynch syndrome

A

Inherited mutations alter DNA mismatch repair

235
Q

What is the most common type of tumor of the colon

A

Adenocarcinomas next is carcinoid tumors

236
Q

What is the mc malignancy of the GI tract

A

Colorectal adenocarcinoma

237
Q

Who is mc affected with colorectal adenocarcinoma

A

Ages 50-70 males in developed nations with highly processed diets

238
Q

What dietary risks are associated with colorectal adenocarcinomas

A

Low fiber=low stool bulk, low antioxidants, high fat/carbs,

239
Q

Where is colorectal adenocarcinoma mc mets to

A

Liver

240
Q

What are the two types of small intestine tumors

A

1/2=adenocarcinomas, 1/2=carcinoids

241
Q

Where are most of the tumors of the SI

A

Duodenum

242
Q

What is the mc cause of acute abdomen

A

Acute appendicitis

243
Q

How does early compare to late acute appendicitis

A

Early=periumbilical/epigastric discomfort

Late=RLQ tender/deep constant pain progress to sharp

244
Q

Who is mc affected by acute appendicitis

A

Male adolescents

245
Q

What is a common cause of acute appendicitis

A

Obstruction = ischemia = inflammation

246
Q

If acute appendicitis results in a rupture what happens

A

High morbidity/mortality or sepsis

247
Q

What is the mc tumor of the appendix

A

Carcinoid possible site for mucocele