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All the things > GI Pathology (10.1 - 10.6) > Flashcards

GI Pathology (10.1 - 10.6) Flashcards

1
Q

What is the cause of cleft lips/ palate?

A

failure of the facial prominences to fuse

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2
Q

True or false: cleft lip and palate usually occur together

A

True

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3
Q

How do the pharyngeal arches fuse in development?

A

Come from all directions to fuse together to form the mouth

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4
Q

Superficial ulcerations of the oral mucosa = ?

A

Aphthous ulcer

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5
Q

What are the gross characteristics of aphthous ulcers?

A

Grayish base surrounded by erythema (granulation tissue)

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6
Q

What is Behcet syndrome? What causes it? What is the classic triad of symptoms?

A

Recurrent aphthous ulcers, genital ulcers, and uveitis caused by immune complex vasculitis of small vessels

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7
Q

When do the symptoms of Behcet syndrome usually recur?

A

After viral infection

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8
Q

What is the virus that usually causes oral herpes?

A

HSV-1

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9
Q

What are the gross characteristics of oral herpes?

A

Shallow, painful red ulcers or vesicles on the lips

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10
Q

When in life does HSV-1 infection usually occur? Where does it lie dormant?

A

Early in childhood, and remains dormant in the ganglia in the trigeminal nerve

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11
Q

What causes the reactivation of the HSV-1 virus?

A

Stress and sunlight

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12
Q

What is the most common location of SCC in the mouth?

A

Floor of the mouth

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13
Q

What are the risk factors for developing SCC in the mouth?

A

EtOH and Tobacco

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14
Q

What are the precursor lesions to SCC in the oral cavity?

A

Leukoplakia or erythroplakia

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15
Q

What is the risk of leukoplakia/erythroplakia?

A

Progression to SCC

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16
Q

What are the diseases that should be in your differential when you see white plaques in the oral cavity? How do you differentiate?

A

Oral candidiasis
Hairy Leukoplakia
Leukoplakia

Scrape it off (candida if it comes off)

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17
Q

Where is hairy leukoplakia usually found? What virus causes this?

A

Lateral aspect of the tongue

EBV

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18
Q

What are the two major differences between oral hairy leukoplakia, and leukoplakia of SCC?

A

Oral hairy leukoplakia is caused by EBV, and is only hyperplasia of the tongue cells

SCC leukoplakia is dysplasia

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19
Q

—-What is erythroplakia? What does this suggest?—-

A

—-Leukoplakia that is vascularized

this suggests squamous dysplasia—–

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20
Q

What are the three major salivary glands in the mouth?

A
  • Parotid
  • Submandibular
  • Sublingual
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21
Q

What is the most feared complication of mumps? Why?

A

Sterility secondary to testicular infection

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22
Q

What is the virus that causes mumps? Family?

A
  • Mumps virus

- Paramyxovirus

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23
Q

What are the two causes of increased serum amylase in Mumps?

A

Increased production from BOTH the salivary gland, and pancreas

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24
Q

What GI organ can be affected with Mumps? What does it cause?

A

Pancreatitis

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25
Q

What are the neurological concerns with Mumps?

A

Meningitis

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26
Q

What is sialadenitis? What is the usual cause? What is the feared complication of this?

A

Inflammation of the salivary gland usually secondary to sialolithiasis and subsequent Staph. Aureus infection

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27
Q

True or false: Sialadenitis is usually bilateral

A

False- usually unilateral

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28
Q

What is pleomorphic adenoma? What are the tissue types that compose this?

A

Benign salivary gland tumor composed of stromal and epithelial tissue

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29
Q

Where do pleomorphic adenoma usually occur?

A

Parotid gland

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30
Q

What are the s/sx of pleomorphic adenomas?

A

Mobile, painless circumscribed mass at the angle of the jaw

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31
Q

What nerve is at risk with parotid gland tumors?

A

Facial nerve issues

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32
Q

Why is there a high rate of recurrence of pleomorphic adenomas?

A

Very irregular margins, thus may lead to leaving in cells during a surgery

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33
Q

What is a Warthin tumor? Histological characteristic?

A

Benign cystic tumor with abundant lymphocytes and germinal centers

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34
Q

Where do Warthin tumors usually arise? Why?

A

Parotid glands–one of the last glands in development to separate from adjacent lymph node tissues

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35
Q

What are the benign tumors of the parotid gland? (3)

A
  • Pleomorphic adenomas
  • Warthin tumors
  • Mucoepidermoid carcinoma
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36
Q

What is the most common malignant tumor of the parotid gland?

A

Mucoepidermoid carcinoma

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37
Q

—–What are mucoepidermoid carcinomas? What type of cells compose it? Where is it usually found?—–

A

—–Malignant tumor composed of mucinous and squamous cells that usually arises in the parotid gland—–

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38
Q

What is the most common congenital defect of the esophagus?

A

Atresia of the esophagus, with a fistula between the distal esophagus and the trachea

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39
Q

What are the signs of esophageal atresia in utero (1), and when born (2)?

A
  • Polyhydramnios
  • Abdominal distention
  • Aspiration
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40
Q

What are esophageal webs? What layer of the esophagus is involved, and where in the esophagus do these usually occr?

A

Thin protrusion of esophageal mucosa, most often in the upper esophagus

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41
Q

What are the signs of esophageal webs? What cancer are these patients predisposed to?

A
  • Dysphagia for poorly chewed foods

- SCC

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42
Q

What causes the abdominal distention and aspiration with esophageal atresia?

A

-Air going into the stomach causes distention, with resulting regurgitation going into the trachea and lungs

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43
Q

What are the four layers of the GI tract?

A
  • Mucosa
  • Submucosa
  • Muscularis propria
  • Serosa
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44
Q

What is the most common complication of esophageal webs?

A

Plummer-Vinson syndrome

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45
Q

What is Plummer-Vinson syndrome? What is the classic triad of symptoms?

A

Severe Fe deficiency anemia presenting with:

  • beefy red tongue
  • dysphagia
  • Fe deficiency anemia
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46
Q

What is a Zenker diverticulum? Where does this usually occur?

A

Out pouching of pharyngeal mucosa through an acquired defect in the muscular wall, arising above the upper esophageal sphincter at the junction of the esophagus and pharynx

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47
Q

What are the s/sx of a Zenker diverticulum? (3)

A
  • Dysphagia
  • obstruction
  • halitosis
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48
Q

What layers of the GI tract are involved in a Zenker diverticulum? Is this a true diverticulum?

A

Pharyngeal mucosa and submucosa–no, since it does not involve the muscularis externa

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49
Q

What is Mallory-Weiss syndrome? Cause?

A

Longitudinal laceration of the mucosa at the gastroesophageal junction, d/t excessive vomiting (alcoholism, and bulimia)

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50
Q

What are the s/sx of Mallory-Weiss syndrome?

A

Painful hematemesis

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51
Q

What disease can Mallory-Weiss syndrome progress to?

A

Boerhaave syndrome

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52
Q

What is Boerhaave syndrome?

A

Rupture of the esophagus, causing air in the mediastinum and subcutaneous emphysema of the neck

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53
Q

What is the cause of esophageal varices?

A

Portal HTN

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54
Q

What are the two veins that the esophageal vessels drain into?

A
  • Azygos vein into the SVC

- Left gastric into the hepatic portal

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55
Q

What is the cause of painful hematemesis? Painless?

A

Painful = Mallory-Weiss syndrome

Painless = esophageal varices

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56
Q

What are the two major reasons esophageal varices 2/2 portal HTN results in profuse hemorrhaging?

A
  • Increased probability of rupture

- Lower coag factors d/t cirrhosis

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57
Q

What is achalasia? What is the cause of this?

A
  • Disordered esophageal motility with inability to relax LES

- Due to damaged ganglion cells in the myenteric nerve plexus

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58
Q

What parasitic infection can lead to achalasia of the esophagus?

A

Chagas disease

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59
Q

What are the s/sx of achalasia (2)? Imaging findings?

A
  • Inability to swallow solid and liquids
  • Halitosis
  • “Bird Beak” sign of the esophagus on Ba swallow
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60
Q

What is the plexus of nerves that runs between the inner circular layer, and outer longitudinal layer of the GI tract? What is the function of this plexus?

A
  • Myenteric

- Controls muscle motility

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61
Q

What neoplastic process can achalasia progress to?

A

esophageal SCC

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62
Q

What is the relative pressure of the LES in achalasia (high or low)?

A

High

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63
Q

What is the change in the cell type of Barrett’s esophagus secondary to GERD?

A

non-Keratinized stratified squamous to non-ciliated simple columnar with goblet cells

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64
Q

What are the two major causes of GERD?

A
  • Hiatal hernia

- lower LES pressure

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65
Q

What are the two types of hiatal hernias?

A
  • Sliding (cardia of the stomach protrudes into the esophagus)
  • Paraesophageal (stomach herniates next to the esophagus in the diaphragm)
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66
Q

What is the appearance of a sliding hiatal hernia on Ba swallow?

A

Hourglass appearance

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67
Q

What is the classic physical exam sign of paraesophageal hiatal hernias?

A

Bowel sounds in the thorax

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68
Q

How does GERD cause asthma and cough?

A

Irritation of the airways from reflux

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69
Q

What are the dental findings of GERD?

A

Increased acid = damaged enamel

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70
Q

Where are the stem cells in the layers of the stomach? What is the significance of this in relation to GERD?

A

Mucosa–if knock out the mucosa, then will heal by fibrosis, causing a loss of the tone present in the LES

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71
Q

What is the most common type of esophageal cancer in the West? What is this usually associated with? Where in the esophagus does this usually occur?

A
  • Adenocarcinoma
  • Barrett’s esophagus
  • Distal 1/3
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72
Q

What is the most common esophageal cancer worldwide? Where in the esophagus does this usually arise?

A
  • SCC

- upper or middle third of the esophagus

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73
Q

What is the cause of SSC of the esophagus?

A

Irritation of the esophagus

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74
Q

How do Achalasia and esophageal webs lead to SCC?

A

Irritation via food degradation sitting in the esophagus

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75
Q

What are the s/sx of SCC of the esophagus? (3)

A
  • Progressive dysphagia
  • Hematemesis
  • Hoarse voice/cough
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76
Q

—–Where does lymph flow in the upper 1/3 of the esophagus? Middle? Distal?—–

A
  • —–Upper = cervical nodes
  • Middle = mediastinal or tracheobronchial nodes
  • Lower = celiac and gastric nodes——
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77
Q

Why is it that esophageal SCC can present with hoarse voice?

A

Invasion of the SCC beyond the BM may lead to compression of the recurrent laryngeal nerve

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78
Q

What is gastroschisis?

A

Congenital malformation of the abdominal wall, causing an exposure of abdominal contents

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79
Q

What is an omphalocele?

A

Persistent herniation of bowel into the umbilical cord, due to failure of herniated intestines to return to the body cavity during development

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80
Q

What comprises the cover of omphaloceles? How about in a gastroschisis?

A
  • Peritoneum and amnion of the umbilical cord

- Nothing for a gastroschisis

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81
Q

What way does the intestines rotate during development, when it is in the umbilical yolk stalk?

A

Counterclockwise 270 degrees

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82
Q

What is the cause of pyloric stenosis? Which gender is this more common in?

A
  • Hypertrophy of the pyloric smooth muscle

- Males

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83
Q

When does the pyloric stenosis usually form relative to birth? What are the s/sx?

A
  • 2 weeks after birth

- Non-bilious projectile vomiting and olive-like mass in the abdomen

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84
Q

What is the treatment for pyloric stenosis?

A

Myotomy of the pyloric sphincter

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85
Q

What is acute gastritis? What are the two ways in which this occurs?

A

Increase acid production or decreased mucosal protection in the stomach, causing degradation of the stomach by acid

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86
Q

What are the two type of chronic gastritis?

A
  • Chronic autoimmune gastritis

- Chronic H.Pylori gastritis

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87
Q

What are the three major components of mucosal protection from stomach acid? (3)

A
  • Mucus (foveolar cells)
  • Bicarb secretion
  • Blood flow (picks up acid)
88
Q

What are Curling ulcers?

A

Stomach ulcers in the context of a severe burn d/t hypovolemia and lower blood flow to the stomach.

89
Q

What is a cushing ulcer?

A

Increased intracranial pressure, causing increased vagal stimulation, and increased ACh, which increases acid production

90
Q

What are the effects of prostaglandins on the stomach? (3)

A
  • Increase mucus and bicarb secretion from foveolar cells
  • Decrease acid secretion
  • Increase blood flow to the stomach to sweep away acid
91
Q

What are the three receptors on parietal cells in the stomach that lead to increased acid secretion?

A
  • Histamine (paracrine)
  • ACh (neurotransmitter)
  • Gastrin (Endocrine)
92
Q

What is the cell in the stomach that creates acid? What other important protein does this secrete?

A
  • Parietal cell

- Intrinsic factor

93
Q

What is the MOA of shock causing ulcers?

A

Hypovolemia causes decreased blood flow to the stomach lining

94
Q

What are the three outcomes of acid damage in the stomach, and how are each of these defined?

A
  • Superficial inflammation
  • Erosion (loss of epithelial layer)
  • Ulceration (loss of mucosal layer)
95
Q

What is the pathophysiology of chronic autoimmune gastritis? What type of hypersensitivity reaction is this? What is the significance of the antibodies produced in this?

A

Autoimmune destruction of parietal cells (and/or intrinsic factor). This is a type IV hypersensitivity rxn
-Antibodies are a consequence of the damage, not the cause of it

96
Q

What are the two places in the stomach that parietal cells are common in?

A
  • Fundus

- Body

97
Q

What is the achlorhydria seen in chronic autoimmune gastritis?

A

Lack of acid production secondary to loss of parietal cells

98
Q

What happens to acid levels, gastrin levels, and G cells in chronic autoimmune gastritis?

A
  • Decrease acid
  • Increased gastrin
  • Antral G cell hyperplasia
99
Q

Pernicious anemia has a high or low MCV?

A

High

100
Q

What is the most common cause of vitamin B12 deficiency? What is this disease called?

A
  • Autoimmune chronic gastritis

- Pernicious anemia

101
Q

Why are pts with chronic, autoimmune gastritis at an increased risk for gastric adenocarcinoma?

A

Chronic irritation / inflammation induces metaplasia of the foveolar cells with goblet cell formation

102
Q

What is the most common cause of chronic gastritis?

A

H.Pylori infx

103
Q

What are the two enzymes that H. Pylori secretes that allow it to live on the stomach lining?

A
  • Urease

- Proteases

104
Q

What is the most common site of H.Pylori infection?

A

Antrum of the stomach

105
Q

Does H.Pylori invade the stomach mucosa?

A

No

106
Q

Why are pts with chronic gastritis at an increased risk for MALT lymphoma?

A

generation of germinal center and post germinal center B cells from the MARGINAL zone

107
Q

What is the treatment for gastric carcinoma/MALT lymphoma secondary to H.Pylori infection?

A

Triple therapy (PPI, Az, Clindamycin)

108
Q

What are the two ways in which you could confirm that the treatment for H.Pylori was effective?

A
  • Negative urea breath test

- No H.Pylori antigen in the stool

109
Q

What is the most common site of peptic ulcers?

A

Proximal duodenum

110
Q

What is the major cause of PUD?

A

H.Pylori infection

111
Q

What are the s/sx of duodenal PUD?

A

Epigastric pain that improves with meals

112
Q

What is Zollinger-Ellison syndrome?

A

CA of the gastrin secreting portions of the stomach, causing increased acid release and ulcer formation

113
Q

Why are the symptoms of PUD improved with meals?

A

Duodenum will increased HCO3 secretion, neutralizing the acid

114
Q

What is the most common complications of PUD rupture?

A

Rupture of the walls of the duodenum

115
Q

What happens if there is a rupture of the anterior wall of the duodenum?

A

Air beneath the diaphragm

116
Q

What happens if there is a rupture of the posterior wall of the duodenum? (What organ and artery are at risk)?

A
  • Acute pancreatitis

- Gastroduodenal artery rupture

117
Q

Why is it that gastric ulcer symptoms worsen with meals?

A

increased acid secretion

118
Q

What are the two most common causes of gastric ulcers?

A
  • NSAID use

- H. Pylori

119
Q

What artery is at risk if a gastric ulcer ruptures along the lesser curvature of the stomach?

A

Left gastric artery

120
Q

True or false: duodenal ulcers are almost never malignant?

A

True

121
Q

What are the gross characteristics of a non-cancerous ulcer in the stomach?

A

Flat. small, with well defined borders

122
Q

What are the gross characteristics of a cancerous ulcer in the stomach?

A

Large, irregular and piled up borders

123
Q

Gastric carcinoma is a malignant proliferation of what cells? What type of cancer, then, does this lead to?

A

Surface epithelial cells (adenocarcinoma)

124
Q

What are the two general types of gastric carcinomas?

A
  • Intestinal

- Diffuse

125
Q

What are the features of the intestinal type of ulcer?

A

large, irregular ulcer with heaped up margins

126
Q

Where are intestinal gastric carcinomas usually found in the stomach?

A

Along the lesser curvature of the antrum

127
Q

What are the 3 risk factors for intestinal type gastric carcinoma? (food chemicals, blood type, etc)

A
  • Nitrosamines
  • Blood type A
  • Intestinal metaplasia
128
Q

What are the histological characteristics of diffuse type gastric carcinomas?

A

Signet rings cells that diffusely infiltrate the gastric wall

129
Q

What causes the thickening of the stomach wall in diffuse type gastric carcinoma? What is this called?

A
  • Desmoplasia

- Linitis plastica

130
Q

True or false: The diffuse type of gastric carcinoma is not associated with H.Pylori infx, metaplasia, or nitrosamines

A

True

131
Q

What are the s/sx of gastric carcinoma? (besides pain and weight loss) (4)

A
  • Early satiety
  • Anemia
  • Abdominal pain
  • Weight loss
132
Q

What is the Leser-Trelat sign? What GI malignancy is this seen in?

A

The Leser-Trélat sign is the explosive onset of multiple seborrheic keratoses often with an inflammatory base.

This can be seen with Gastric carcinoma!

133
Q

Distant mets from gastric carcinomas usually involve what organ?

A
  • Liver
  • Periumbilical region
  • Bilateral ovaries
134
Q

What is the sister Mary Joseph nodule?

A

mets from gastric CA to the periumbilical region

135
Q

—-What is the Krukenberg tumor?—-

A

—-Bilateral mets from gastric CA to the ovaries—-

136
Q

What is duodenal atresia?

A

failure of the small bowel to canalize

137
Q

What genetic disease is duodenal atresia associated with?

A

Down syndrome

138
Q

What are the s/sx of duodenal atresia? (3, in utero and postpartum)

A
  • Polyhydramnios
  • Double bubble sign
  • Bilious vomiting
139
Q

What is the vomiting like in pyloric stenosis? Duodenal atresia?

A
  • Pyloric stenosis = non-bilious

- Duodenal atresia = bilious

140
Q

What is Meckel diverticulum? Is this a true diverticulum?

A

true diverticulum that arises due to a failure of vitelline duct to involute

141
Q

What is the vitelline duct?

A

Pathway that receives nutrients from the yolk sac during development

142
Q

Passing of meconium via the umbilicus at birth = ?

A

Failure of the vitelline duct to involute

143
Q

Soft stool in the periumbilical region of an infant’s abdomen = ?

A

Meckel diverticulum

144
Q

What is the most common congenital anomaly of the GI tract? What percent of births does this occur in?

A
  • meckel diverticulum

- 2%

145
Q

What are the rule of twos for Meckel diverticulum? (4)

A
  • 2% of the population
  • 2 inches long
  • Located within 2 feet of the ileocecal valve
  • Presents within 2 years of life
146
Q

What are the complications with meckel diverticulum? (3)

A
  • Bleeding
  • Volvulus
  • Intussusception
147
Q

True or false: The majority of cases of Meckel diverticulum are symptomatic

A

false– most are asymptomatic

148
Q

What is a volvulus?

A

twisting of bowel along its mesentery, resulting in an obstruction and infarction

149
Q

What is the most common location of a volvulus?

A
  • Sigmoid colon (elderly)

- Cecum (young)

150
Q

What are the stools that occur with intussusception?

A

“Currant Jelly” stools

151
Q

What is a “leading edge” in intussusception?

A

An outpouching of the wall of the intestines that acts for the proximal part of the bowel to hang onto, and pull

152
Q

What is the most common cause of a leading edge in infants? Adults?

A
  • Infants = lymphoid hyperplasia

- Adults = Tumor

153
Q

Why is the small bowel particularly susceptible to ischemic injury?

A

Uses a ton of ATP for transport of nutrients across the mucosa

154
Q

What type of infarction can occur with embolism/thrombosis of the SMA or mesenteric veins?

A

Transmural

155
Q

What is the mechanism by which infarctions of only the mucosa of the intestines occur?

A

Marked hypotension

156
Q

What are the three clinical features of small bowel ischemia/infarction?

A
  • Abdominal pain
  • Bloody diarrhea
  • Decreased bowel sounds
157
Q

What is the pathophysiology celiac disease? What is the most pathogenic component of wheat?

A
  • Immune mediated damage of the small bowel due to gluten exposure
  • Gliadin
158
Q

What are the gene loci that are associated with Celiac disease?

A

HLA DQ2 and DQ8

159
Q

What are the three monosaccharides that are absorbed by the small intestines?

A
  • Fructose
  • Glucose
  • Galactose
160
Q

What is the enzyme that deamidates gliadin? What happens immunologically when this occurs?

A
  • tTG (tissue transglutaminase)

- Deamidated gliadin is presented by APCs and MHC II

161
Q

What immune cells are involved in Celiac disease and mediate the tissue damage?

A

Helper T cells

162
Q

What is dermatitis herpetiformis seen in Celiac disease? Treatment / prognosis for this?

A
  • IgA deposition at the tips of the dermal papillae, causing herpes-like blisters in the skin
  • This resolves with a gluten-free diet
163
Q

What are the three IgA antibodies that can occur with Celiac disease?

A
  1. Endomysium
  2. tTG
  3. Gliadin
164
Q

What antibody subclass is used for celiac diagnosis if the pt does not produce IgA?

A

IgG

165
Q

What are the three histological findings of Celiac disease?

A
  • Flattening of the villi
  • Hyperplasia of the crypts
  • Increased intraepithelial lymphocytes
166
Q

Which part of the small intestines is most affected by Celiac disease?

A

Duodenum

167
Q

What two malignancies should you think of if a pt with Celiac disease presents with similar symptoms, despite good dietary control?

A

Small bowel carcinoma and T cell lymphoma

168
Q

What is the pathophysiology of tropical sprue? When does it classically present?

A

Small bowel villi destruction by an unknown organism, after treatment for infectious diarrhea with Abx

169
Q

What part(s) of the intestines are most affected by tropical sprue? What nutritional deficiencies can occur because of this?

A
  • Jejunum and ileum

- Folate and B12 deficiency, since these are absorbed here

170
Q

What is the difference of location of intestinal changes between Celiac disease and tropical sprue?

A 
celiac = duodenum
Tropical = jejunum and ileum
171
Q

What is the causative agent of Whipple’s disease?

A

Tropheryma Whippelii

172
Q

Where does Tropheryma Whippelii reside in the body (which cells/ which layer)?

A

Within macrophages along the lamina propria of the small bowel

173
Q

What causes the fat malabsorption with Whipple’s disease?

A

Compression of lacteals by macrophages involved in inflammatory response

174
Q

What are the s/sx of Whipple’s disease? Why?

A

Steatorrhea / fat malabsorption d/t accumulation of organisms within the lamina propria of the intestines

175
Q

Where do chylomicrons that are synthesized in the intestinal enterocytes go when absorbed? How does this release to the steatorrhea in Whipple’s disease?

A
  • Lamina propria to Lacteals to lymphatics.

- Deposition of diseases macrophages will clog this up

176
Q

What is the histological appearance of the macrophages in the lamina propria in whipple’s disease? What is the stain that can be used to highlight these?

A

Foamy macrophages that are highlighted by PAS staining

177
Q

What are the four places that Whipple’s disease affects besides the GI tract?

A
  • Synovium of the joints
  • Cardiac valves
  • Lymph nodes
  • CNS
178
Q

What is abetalipoproteinemia, and how is it inherited? What does this cause?

A

AR deficiency of -apoB48 and apoB100

-fat malabsorption and absent LDL

179
Q

What is the function of apoB48? B100?

A
  • B48 = structural protein of the chylomicron

- B100 = structural protein of VLDL and LDL

180
Q

What are carcinoid tumors?

A

malignant proliferations of neuroendocrine cells, causing a low grade malignancy

181
Q

What is the worst type of neuroendocrine tumor?

A

Small lung cell carcinoma

182
Q

What is the immunohistological stain that is used to identify carcinoid tumors?

A

Chromogranin

183
Q

What is Chromogranin?

A

Stain used to identify Carcinoid tumors

184
Q

What is the most common site for the development of carcinoid tumors in the GI tract? What does this appear as?

A

Small bowel–grows as a submucosal polyp-like nodule

185
Q

What is the chemical that Carcinoid tumors secrete? What is the lab test for this?

A
  • 5HT

- 5-HIAA (metabolite of 5HT) will be found in the urine

186
Q

What happens when carcinoid tumors metastasize to the liver?

A

Are now able to dump 5HT directly into the portal vein, without being processed by the liver first

187
Q

What is the cause of carcinoid heart disease?

A

Liver mets of carcinoid tumors dump 5HT directly into hepatic vein/IVC, causing fibrosis of the right heart, leading to tricuspid regurg and valvular stenosis

188
Q

What are the three symptoms of 5HT overproduction by carcinoid tumors? What can trigger these?

A
  • Bronchospasm
  • Diarrhea
  • Flushing
  • EtOH or emotional distress
189
Q

Why is it that carcinoid tumors that met to the liver cause only left sided valvular stenosis and tricuspid regurg, and NOT right sided problem?

A

Lungs have MAO, which will metabolize the excess 5HT

190
Q

—What is the metabolite of 5HT that is made by MAO, and secreted in the urine?—-

A

—-5-HIAA—-

191
Q

What are the two major causes of acute appendicitis? Which is more common to children? Adults?

A

Obstruction via lymphoid hyperplasia (children) or fecaliths (adults)

192
Q

What are the s/sx of a ruptured appendix?

A

Peritonitis that presents with guarding and rebound tenderness

193
Q

What are the three classical characteristics of IBD?

A

Young jewish female with recurrent bloody diarrhea and abdominal pain

194
Q

What parts of the GI wall are involved in ulcerative colitis?

A

Mucosal and submucosal (not muscularis or serosa)

195
Q

What parts of the GI wall are involved in Crohn’s disease?

A

Transmural (all parts of the wall)

196
Q

Where does ulcerative colitis usually begin? What is the most proximal place it can involve?

A
  • Rectum, works its way up

- Cecum is the most proximal it can go

197
Q

Which is contiguous, and which has skip lesions: ulcerative colitis, Crohn’s disease

A

ulcerative colitis is contiguous

Crohn’s disease has skip lesions

198
Q

Crypt abscesses are found in what disease (histologic hallmark)?

A

Ulcerative colitis (PMNs in crypts)

199
Q

What is the gross appearance of ulcerative colitis?

A

Pseudopolyps and loss of haustra

200
Q

What are the complications of ulcerative colitis?

A

toxic megacolon and carcinoma

201
Q

What is the disease that is classically associated with ulcerative colitis?

A

Primary sclerosing cholangitis

202
Q

What is the effect of smoking on ulcerative colitis? Crohn’s disease?

A 
UC = protects against
CD= increases risk
203
Q

What are the two factors that are used to predict the risk of developing carcinoma from ulcerative colitis?

A

Extent of colonic involvement

Duration of the disease

204
Q

What is the antibody that is found in ulcerative colitis?

A

pANCA

205
Q

What parts of the GI tract can Crohn’s disease affect? What is the least common site?

A
  • Mouth to anus

- Rectum is the least common site

206
Q

What are the usual symptoms of CD?

A

RLQ pain with non-bloody diarrhea

207
Q

What is the inflammation seen in UC? CD?

A 
UC = crypt abscesses
CD = Granulomas
208
Q

What is the gross appearance of CD?

A

Cobblestone mucosa

209
Q

What are the complications with CD?

A

Malabsorption

fistula formation

210
Q

What causes the contractions, stenosis, and the “creeping fat” of the GI tract with CD?

A

Fibroblasts in the granulomas cause fibrosis and contraction

211
Q

What is the “string sign” suggestive of?

A

CD

212
Q

What extra-GI disease is CD associated with?

A

Ankylosing spondylitis

213
Q

Why are kidney stones more common with CD?

A

Increased ability for CaCO3 to be absorbed into the blood

214
Q

“lead pipe appearance” on x-ray is suggestive of which IBD? What causes this?

A

Ulcerative colitis d/t loss of haustra

215
Q

Why is it that the emesis is non-bilious with pyloric stenosis?

A

Gastric contents have not yet entered the intestines

216
Q

How can chemotherapy cause stomach ulcers?

A

Decrease cell turnover in the stomach lining

217
Q

What are the two ways of acquiring lactose intolerance?

A
  • Loss of enzymes physiologically

- Temporary loss of enzyme from a GI infection

All the things (36 decks)

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