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GBA Pathology > PATHOMA10 - Gastrointestinal Pathology > Flashcards

PATHOMA10 - Gastrointestinal Pathology Flashcards

1
Q

What are some diseases that affect the oral cavity?

A

1) cleft up and palate 2) aphthous ulcer 3) Behcet syndrome 4) Oral herpes 5) squamous cell carcinoma

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2
Q

What is cleft lip and palate?

A

Full-thickness defect of lip or palate

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3
Q

What is cleft up and palate due to?

A

failure of facial prominences to fuse

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4
Q

How is face formed?

A

During early pregnancy, facial prominences (one from superior, two from the sides, and two from inferior) grow and fuse together to form the face

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5
Q

Does the cleft lip and palate usually occur together or separate?

A

Usually together, isolated cleft lip or palate is less common.

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6
Q

What is aphthous ulcer?

A

Painful, superficial ulceration of the oral mucosa

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7
Q

When does aphthous ulcer arise?

A

in relation to stress and resolves spontaneously, but often recurs

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8
Q

What is aphthous ulcer characterized by?

A

a grayish base surrounded by erythema

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9
Q

What is behcet syndrome?

A

Recurrent aphthous ulcers, genital ulcers, and uveitis

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10
Q

What is behcet syndrome due to?

A

immune complex vasculitis involving small vessels

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11
Q

When might you see behcet syndrome?

A

after viral infection, but etiology is unknown

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12
Q

What is oral herpes?

A

Vesicles involving oral mucosa that rupture, resulting in shallow, painful, red ulcers

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13
Q

What is oral herpes usually due to?

A

HSV-1

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14
Q

For oral herpes when does the primary infection occur?

A

in childhood; lesions heal, but virus remains dormant in ganglia of the trigeminal nerve.

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15
Q

For oral herpes what might cause reactivation of the virus?

A

Stress and sunlight, leading to vesicles that often arise on the lips (cold sore)

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16
Q

What is squamous cell carcinoma of the oral cavity?

A

Malignant neoplasm of squamous cells lining the oral mucosa

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17
Q

For oral squamous cell carcinoma what are the major risk factors?

A

Tobacco and alcohol

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18
Q

What is the most common location for oral squamous cell carcinoma?

A

Floor of mouth

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19
Q

Regarding oral squamous cell carcinoma what are the precursor lesions

A

Oral leukoplakia and erythroplakia

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20
Q

What is leukoplakia?

A

It is a white plaque that cannot be scraped away; often represents squamous cell dysplasia

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21
Q

What is oral candidiasis?

A

it is a white deposit on the tongue, which is easily scraped away; usually seen in immunocompromised states

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22
Q

What is hairy leukoplakia?

A

it is a white, rough (hairy) patch that arises on the lateral tongue. It is usually seen in immunocompromised individuals (AIDS) and is due to EBV-induced squamous cell hyperplasia; not pre-malignant

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23
Q

What is erythroplakia?

A

(red plaque) represents vascularized leukoplakia and is highly suggestive of squamous cell dysplasia,

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24
Q

Would you biopsy erythroplakia and leukoplakia?

A

they are often biopsied to rule out carcinoma

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25
Q

What are salivary glands?

A

they are exocrine glands that secrete saliva.

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26
Q

What are salivary glands divided into?

A

major (parotid, submandibular, and sublingual glands and minor glands (hundreds of microscopic glands distributed throughout the oral mucosa)

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27
Q

What is the mumps?

A

Infection with mumps virus resulting in bilateral inflamed parotid glands

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28
Q

In mumps, what other infections in addition to the mumps virus may be present?

A

Orchitis, pancreatitis, and aseptic meningitis may also be present.

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29
Q

Why is serum amylase increased?

A

due to salivary gland or pancreatic involvement

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30
Q

What is there a risk of with orchitis?

A

carries risk of sterility, especially in teenagers.

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31
Q

What is sialadenitis?

A

Inflammation of the salivary gland

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32
Q

What is sialadenitis most commonly due to?

A

an obstructing stone (sialolithiasis) leading to Staphylococcus aureus infection; usually unilateral

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33
Q

What is pleomorphic adenoma?

A

Benign tumor composed of stromal (e.g., cartilage) and epithelial tissue;

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34
Q

What is the most common tumor of the salivary gland?

A

Pleomorphic adenoma

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35
Q

Where does pleomorphic adenoma usually arise?

A

in parotid

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36
Q

What does pleomorphic adenoma present as?

A

a mobile, painless, circumscribed mass at the angle of the jaw

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37
Q

What is the rate of recurrence in pleomorphic adenoma?

A

High rate of recurrence;

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38
Q

In pleomorphic adenoma what often leads to incomplete resection?

A

extension of small islands of tumor through tumor capsule

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39
Q

What does pleomorphic adenoma present as?

A

Rarely may transform into carcinoma, which presents with signs of facial nerve damage (facial nerve runs through parotid gland)

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40
Q

What is a warthin tumor?

A

Benign cystic tumor with abundant lymphocytes and germinal centers (lymph node-like stroma);

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41
Q

What is the 2nd most common tumor of the salivary gland?

A

Warthin tumor

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42
Q

Where deos the warthin tumor almost always arise?

A

in the parotid

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43
Q

What is a mucoepidermoid carcinoma?

A

Malignant tumor composed of mucinous and squamous cells

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44
Q

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

A

Mucoepidermoid carcinoma

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45
Q

Where does mucoepidermoid carcinoma usually arise?

A

in the parotid

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46
Q

What does mucoepidermoid carcinoma commonly involve?

A

the facial nerve

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47
Q

What is a tracheoesophageal fistula?

A

Congenital detect resulting in a connection between the esophagus and trachea

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48
Q

What is the most common variant of tracheoesophageal fistula?

A

consists of proximal esophageal atresia with the distal esophagus arising from the trachea

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49
Q

How does a tracheoesophageal fistula present?

A

with vomiting, polyhydramnios, abdominal distension, and aspiration

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50
Q

What is esophageal web?

A

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

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51
Q

What does esophageal web present with?

A

dysphagia for poorly chewed food

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52
Q

What is there an increased risk for with esophageal web?

A

esophageal squamous cell carcinoma

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53
Q

What is Plummer-Vinson syndrome characterized by?

A

severe iron deficiency anemia, esophageal web, and beefy-red tongue due to atrophic glossitis.

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54
Q

What is zenker diverticulum?

A

An outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (false diverticulum)

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55
Q

Where does the zenker diverticulum arise?

A

above the upper esophageal sphincter at the junction of the esophagus and pharynx

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56
Q

What does Zenker Diverticulum present with?

A

dysphagia, obstruction, and halitosis (bad breath)

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57
Q

What is Mallory weiss syndrome?

A

Longitudinal laceration of mucosa at the gastroesophageal (GE) junction

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58
Q

What is Mallory weiss syndrome caused by?

A

severe vomiting, usually due to alcoholism or bulimia

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59
Q

What does Mallory weiss syndrome present with?

A

painful hematemesis

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60
Q

With Mallory weiss syndrome, what is there a risk of?

A

Boerhaave syndrome

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61
Q

What is Boerhaave syndrome?

A

rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema

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62
Q

What is esophageal varices?

A

Dilated submucosal veins in the lower esophagus

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63
Q

What does esophageal varices arise with?

A

It arises secondary to portal hypertension

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64
Q

What does the distal esophageal vein normally drain into?

A

the portal vein via the left gastric vein

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65
Q

What is seen in portal hypertension?

A

the left gastric vein backs up into the esophageal vein, resulting in dilation (varices)

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66
Q

What are the symptoms for esophageal varices?

A

Asymptomatic, but risk of rupture exists

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67
Q

What does esophageal varices present with?

A

painless hematemesis

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68
Q

What is the most common cause of death in cirrhosis?

A

Esophageal varices

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69
Q

What is achalasia?

A

Disordered esophageal motility with inability to relax the lower esophageal sphincter (LES)

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70
Q

What is achalasia due to?

A

damaged ganglion cells in the myenteric plexus

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71
Q

Where are the ganglion cells of the myenteric plexus located?

A

between the inner circular and outer longitudinal layers of the muscularis propria

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72
Q

What are the ganglion cells of the myenteric plexus important for?

A

regulating bowel motility and relaxing the LES.

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73
Q

What causes damage to ganglion cells [of the myenteric plexus]?

A

can be idiopathic or secondary to a known insult (e.g., Trypanosoma cruzi infection in Chagas disease)

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74
Q

What are the clinical features for achalasia?

A
  1. Dysphagia for solids and liquids 2. Putrid breath 3. High LES pressure on esophageal manometry 4. Bird-beak sign on barium swallow study 5. Increased risk for esophageal squamous cell carcinoma
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75
Q

What is there an increased risk for with achalsia?

A

Esophageal squamous cell carcinoma

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76
Q

What is GERD?

A

Gastroesophageal reflux disease - Reflux of acid from the stomach due to reduced LES tone

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77
Q

What are the risk factors for GERD?

A

include alcohol, tobacco, obesity, fat-rich diet, caffeine, and hiatal hernia.

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78
Q

What are the clinical features for GERD?

A
  1. Heartburn (mimics cardiac chest pain) 2. Asthma (adult-onset) and cough 3. Damage to enamel of teeth 4. Ulceration with stricture and Barrett esophagus are late complications.
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79
Q

What is barrett esophagus?

A

Metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells seen in

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80
Q

What % of patients with GERD present with Barrett Esophagus?

A

10%

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81
Q

Barrett Esophagus is a response of what to what stimuli?

A

Response of lower esophageal stem cells to acidic stress

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82
Q

What might Barrett Esophagus progress to?

A

May progress to dysplasia and adenocarcinoma

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83
Q

What is esophageal carcinoma?

A

Subclassified as adenocarcinoma or squamous cell carcinoma

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84
Q

What is adenocarcinoma?

A

a malignant proliferation of glands;

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85
Q

What is the most common type of esophageal carcinoma in the West?

A

Adenocarcinoma

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86
Q

From what does adenocarcinoma arise?

A

from preexisting Barrett esophagus; usually involves the lower one-third of the esophagus

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87
Q

What is squamous cell carcinoma?

A

it is a malignant proliferation of squamous cells

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88
Q

What is the most common esophageal cancer worldwide?

A

Squamous cell carcinoma

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89
Q

Where does squamous cell carcinoma usually arise?

A

in upper or middle third of the esophagus;

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90
Q

What are the major risk factors for squamous cell carcinoma?

A

1) Alcohol and tobacco (most common causes) 2) Very hot tea 3). Achalasia 4) Esophageal web (e.g., Plummer-Vinson syndrome) 5) Esophageal injury (e.g., lye ingestion)

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91
Q

What is the prognosis for esophageal carcinoma?

A

Poor prognosis due to late presentation

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92
Q

What are the symptoms for esophageal carcinoma?

A

progressive dysphagia (solids to liquids), weight loss, pain, and hematemesis.

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93
Q

In addition to the symptoms for esophageal carcinoma what may squamous cell carcinoma additionally present with?

A

hoarse voice (recurrent laryngeal nerve involvement) and cough (tracheal involvement).

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94
Q

In esophageal carcinoma what determines the location of lymph node spread?

A

it depends on the level of the esophagus that is involved

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95
Q

For esophageal carcinoma involvement of the upper 1/3 of the esophagus results in what lymph node spread?

A

cervical nodes

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96
Q

For esophageal carcinoma involvement of the middle 1/3 of the esophagus results in what lymph node spread?

A

mediastinal or tracheobronchial nodes

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97
Q

For esophageal carcinoma involvement of the lower 1/3 of the esophagus results in what lymph node spread?

A

celiac and gastric nodes

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98
Q

What is gastroschisis?

A

congenital malformation of the anterior abdominal wall leading to exposure of abdominal contents

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99
Q

What is omphalocele?

A

Persistent herniation of bowel into umbilical cord

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100
Q

What is omphalocele due to?

A

failure of herniated intestines to return to the body cavity during development, the contents are covered by peritoneum and amnion of the umbilical cord

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101
Q

What is pyloric stenosis?

A

congenital hypertrophy of pyloric smooth muscle; more common in males

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102
Q

How does pyloric stenosis classically present?

A

two weeks after birth as; 1. Projectile nonbilious vomiting 2. Visible peristalsis 3. Olive-like mass in the abdomen

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103
Q

What is the treatment for pyloric stenosis?

A

myotomy

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104
Q

What is acute gastritis?

A

Acidic damage to the stomach mucosa

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105
Q

What is acute gastritis due to?

A

imbalance between mucosal defenses and acidic environment

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106
Q

What do the defenses of acute gastritis include?

A

mucin layer produced by foveolar cells, bicarbonate secretion by surface epithelium, and normal blood supply (provides nutrients and picks up leaked acid).

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107
Q

How is a severe burn a risk factor for acute gastritis?

A

(Curling ulcer) Hypovolemia leads to decreased blood supply.

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108
Q

How are NSAIDs a risk factor for acute gastritis?

A

decreased PGE

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109
Q

How is increased intracranial pressure a risk factor for acute gastritis?

A

(Cushing ulcer) Increased stimulation of vagus nerve leads to increased acid production

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110
Q

What is the relationship between shock and acute gastritis?

A

Multiple (stress) ulcers may be seen in ICU patients

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111
Q

What are the risk factors for acute gastritis?

A
  1. Severe burn 2. NSAIDs 3. Heavy alcohol consumption 4. Chemotherapy 5. Increased intracranial pressure 6. Shock.
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112
Q

In acute gastritis what does acid damage result in?

A

superficial inflammation, erosion (loss of superficial epithelium), or ulcer (loss of mucosal layer)

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113
Q

What is chronic gastritis?

A

Chronic Inflammation of stomach mucosa

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114
Q

What is chronic gastritis divided into?

A

two types based on underlying etiology: chronic autoimmune gastritis and chronic H pylori gastritis

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115
Q

What is chronic autoimmune gastritis due to?

A

autoimmune destruction of gastric parietal cells

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116
Q

Where are the gastric parietal cells located?

A

in the stomach body and fundus.

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117
Q

What is chronic autoimmune gastritis associated with?

A

antibodies against parietal cells and/or intrinsic factor; useful for diagnosis, but pathogenesis is mediated by T cells (type IV hypersensitivity)

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118
Q

What are the clinical features for chronic autoimmune gastritis?

A

1) Atrophy of mucosa with intestinal metaplasia 2) Achlorhydria with increased gastrin levels and antral G-cell hyperplasia 3) Megaloblastic (pernicious) anemia due to lack of intrinsic factor 4) Increased risk tor gastric adenocarcinoma (intestinal type)

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119
Q

What is chronic H pylori gastritis due to?

A

H pylori-induced acute and chronic inflammation

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120
Q

What is the most common form of gastritis?

A

(90%) chronic H pylori gastritis

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121
Q

How does H pylori lead to gastritis?

A

H pylori ureases and proteases along with inflammation weaken mucosal defenses; antrum is the most common site

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122
Q

How does H. Pylori gastritis present?

A

with epigastric abdominal pain; increased risk for ulceration (peptic ulcer disease), gastric adenocarcinoma (intestinal type), and MALT lymphoma

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123
Q

What is the treatment for H Pylori gastritis?

A

involves triple therapy.

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124
Q

What is triple therapy?

A

Proton pump inhibitors and antibiotics

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125
Q

What does triple therapy treatment for H pylori gastritis result in?

A

1) Resolves gastritis/ulcer and reverses intestinal metaplasia 2) Negative urea breath test and lack of stool antigen confirm eradication of H pylori.

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126
Q

What is peptic ulcer disease?

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)

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127
Q

What is the duodenal ulcer due to?

A

almost always due to H pylori (> 95%); rarely, may be due to Zollinger Ellison (ZE) syndrome

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128
Q

What does a duodenal ulcer present with?

A

epigastric pain that improves with meals

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129
Q

What does biopsy of a duodenal ulcer show?

A

Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner glands.

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130
Q

What might happen to a duodenal ulcer?

A

May rupture leading to bleeding from the gastroduodenal artery (anterior ulcer) or acute pancreatitis (posterior ulcer)

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131
Q

What is gastric ulcer usually due to?

A

H pylori (75%); other causes include NSAlDs and bile reflux.

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132
Q

What doses gastric ulcer present with?

A

epigastric pain that worsens with meals

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133
Q

Where is the gastric ulcer usually located?

A

on the lesser curvature of the antrum.

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134
Q

What does rupture of gastric ulcer result in?

A

carries a risk of bleeding from left gastric artery

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135
Q

What is the differential diagnosis of ulcers?

A

includes carcinoma.

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136
Q

Might duodenal ulcers lead to carcinoma?

A

Duodenal ulcers are almost never malignant (duodenal carcinoma is extremely rare).

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137
Q

Is there a relationship between gastric ulcers and carcinoma?

A

Gastric ulcers can be caused by gastric carcinoma (intestinal subtype)

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138
Q

How do benign peptic ulcers usually appear?

A

small (< 3 cm), sharply demarcated (punched-out), and surrounded by radiating folds of mucosa

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139
Q

How do malignant ulcers appear?

A

they are large and irregular with heaped up margins

140
Q

What is required for definitive diagnosis regarding gastric ulcers?

A

biopsy

141
Q

What is gastric carcinoma?

A

Malignant proliferation of surface epithelial cells (adenocarcinoma)

142
Q

How is gastric carcinoma subclassified?

A

into intestinal and diffuse types

143
Q

Which subclassification of gastric carcinoma is more common?

A

Intestinal type

144
Q

How does the intestinal type of gastric carcinoma present?

A

presents as a large, irregular ulcer with heaped up margins;

145
Q

Where does the intestinal type of gastric carcinoma most commonly arise?

A

involves the lesser curvature of the antrum

146
Q

How is gastric carcinoma similar to gastric ulcer?

A

They both involve the lesser curvature of the antrum

147
Q

What are risk factor for the intestinal type of gastric carcinoma?

A

they include intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis), nitrosamines in smoked foods (Japan), and blood type A.

148
Q

How is the diffuse type of gastric carcinoma characterized?

A

by signet ring cells that diffusely infiltrate the gastric wall, desmoplasia resulting in thickening of stomach wall (linitis plasties)

149
Q

What is the diffuse type of gastric carcinoma not associated with

A

its not associated with H pylori, intestinal metaplasia, or nitrosamines

150
Q

What does gastric carcinoma present with?

A

It presents late with weight loss, abdominal pain, anemia, and early satiety; rarely presents as acanthosis nigricans or Leser-Trelat sign

151
Q

What might gastric carcinoma spread to?

A

lymph nodes can involve the left supraclavicular node (Virchow node).

152
Q

For gastric carcinoma what does distant metastasis most commonly involve?

A

Liver

153
Q

For the intestinal type of gastric carcinoma what does distant metastasis involve?

A

Periumbilical region (Sister Mary Joseph nodule)

154
Q

For the diffuse type of gastric carcinoma what does distant metastasis involve?

A

Bilateral ovaries (Krukenberg tumor)

155
Q

What is duodenal atresia?

A

Congenital failure of duodenum to canalize;

156
Q

What is duodenal atresia associated with?

A

Down syndrome

157
Q

What are the clinical features for duodenal atresia?

A
  1. Polyhydramnios 2. Distension of stomach and blind loop of duodenum (double bubble) 3. Bilious vomiting
158
Q

What is meckel diverticulum?

A

Outpouching of all three layers of the bowel wall (true diverticulum)

159
Q

Why does meckel diverticulum arise?

A

due to failure of the vitelline duct to involute

160
Q

For meckel diverticulum what is the rule of 2s?

A

1) Seen in 2% of the population 2) 2 inches long and located in the small bowel within 2 feet of the ileocecal valve 3) during the first 2 years of life with bleeding, volvulus, intussusception, or obstruction (mimics appendicitis); however, most cases are asymptomatic

161
Q

What is the most common congenital anomaly of the GI tract?

A

Meckel diverticulum

162
Q

How long is the meckel diverticulum?

A

2 inches long

163
Q

Where is the meckel diverticulum located?

A

in the small bowel within 2 feet of the ileocecal valve

164
Q

How can meckel diverticulum present?

A

during the first 2 years of life with bleeding, volvulus, intussusception, or obstruction (mimics appendicitis); however, most cases are asymptomatic

165
Q

Why is there bleeding during the presentation of meckel diverticulum?

A

Its due to heterotopic gastric mucosa

166
Q

What is volvulus?

A

Twisting of bowel along its mesentery

167
Q

What does volvulus result in?

A

obstruction and disruption of the blood supply with infarction

168
Q

What are the most common locations for a volvulus?

A

sigmoid colon in the elderly and cecum in young adults

169
Q

What is intussusception?

A

Telescoping of proximal segment of bowel forward into distal segment

170
Q

How does intussusception work?

A

Telescoped segment is pulled forward by peristalsis, resulting in obstruction and disruption of blood supply with infarction.

171
Q

What is intussusception associated with?

A

a leading edge (focus of traction)

172
Q

What is the most common cause of intussusception in children?

A

lymphoid hyperplasia (e.g., due to rotavirus) which usually arises in the terminal ileum, leading to intussusception into the cecum

173
Q

What is the most common cause of intussusception in adults?

A

tumor.

174
Q

What is small bowel infarction?

A

Small bowel is highly susceptible to ischemic injury.

175
Q

When does transmural infarction occur?

A

with thrombosis/embolism of the superior mesenteric artery or thrombosis of the mesenteric vein.

176
Q

When does mucosal infarction occur?

A

with marked hypotension

177
Q

What are the clinical features for small bowel infarction?

A

they include abdominal pain, bloody diarrhea, and decreased bowel sounds,

178
Q

What is lactose intolerance?

A

Decreased function of the lactase enzyme found in the brush border of enterocytes

179
Q

What is the normal function of lactase?

A

It normally breaks down lactose into glucose and galactose.

180
Q

How does lactose intolerance present?

A

with abdominal distension and diarrhea upon consumption of milk products; undigested lactose is osmotically active.

181
Q

How does lactose deficiency develop?

A

it may be congenital (rare autosomal recessive disorder) or acquired (often develops in late childhood);

182
Q

How is lactose deficiency related to small bowel infarction?

A

temporary deficiency is seen after small bowel infection (lactase is highly susceptible to injury).

183
Q

What is celiac disease?

A

Immune-mediated damage of small bowel villi due to gluten exposure

184
Q

What is celiac disease associated with?

A

HLA-DQ2 and DQ8

185
Q

In what is gluten present?

A

in wheat and grains

186
Q

What is the most pathogenic component of gluten?

A

gliadin

187
Q

What happens to gliadin once absorbed?

A

gliadin is deamidated by tissue transglutaminase (tTG).

188
Q

What happens to deamidated gliadin?

A

it is presented by antigen presenting cells via MHC class II where the helper T cells mediate tissue damage.

189
Q

What is the clinical presentation for celiac disease in herpes?

A

Children classically present with abdominal distension, diarrhea, and failure to thrive

190
Q

What is the clinical presentation for celiac disease in adults?

A

It classically presents with chronic diarrhea and bloating

191
Q

What is seen on the skin in celiac disease?

A

Small, herpes-like vesicles may arise on skin (dermatitis herpetiformis).

192
Q

What is dermatitis herpetiformis in celiac diseae due to and how does it resolve?

A

IgA deposition at the lips of dermal papillae it resolves with gluten-free diet

193
Q

What are the laboratory findings for celiac disease?

A

1) IgA antibodies against endomysium, tTG (tissue transglutaminase), or gliadin

194
Q

What lab finding for celiac disease is also used in IgA deficiency?

A

IgG antibodies are also present and are useful for diagnosis in individuals with IgA deficiency

195
Q

What is the relationship between IgA deficiency and celiac disease?

A

increased incidence of IgA deficiency is seen in celiac disease

196
Q

What does duodenal biopsy reveal in celiac disease?

A

flattening of villi, hyperplasia of crypts, and increased intraepithelial lymphocyte

197
Q

In celiac disease where is damage most prominent?

A

in the duodenum (jejunum and ileum are less involved)

198
Q

When would the symptoms of celiac disease resolve?

A

with gluten-free diet.

199
Q

What are late complications that present as refractory disease despite good dietary control?

A

Small bowel carcinoma and T-cell lymphoma

200
Q

What is tropical sprue?

A

Damage to small bowel villi due to an unknown organism resulting in malabsorption

201
Q

How does tropical spure compare to celiac disease?

A

Its similar to celiac disease except 1. Occurs in tropical regions (e.g., Caribbean) 2. Arises after infectious diarrhea and responds to antibiotics

202
Q

In tropical spure, where is damage most prominent?

A

in jejunum and ileum (secondary vitamin B12 or folate deficiency may ensue); duodenum is less commonly involved.

203
Q

What is whipple disease?

A

Systemic tissue damage characterized by macrophages loaded with Tropheryma whippelii organisms; partially destroyed organisms are present in macrophage lysosomes (positive for PAS).

204
Q

What is the classic site of involvement in whipple disease?

A

the small bowel lamina propria

205
Q

What happens in whipple disease?

A
  1. Macrophages compress lacteals. 2. Chylomicrons cannot be transferred from enterocytes to lymphatics. 3. Results in fat malabsorption and steatorrhea
206
Q

What are the other common sites of involvement for whipple disease?

A

they include synovium of joints (arthritis), cardiac valves, lymph nodes, and CNS.

207
Q

What is abetalipoproteinemia?

A

Autosomal recessive deficiency of apolipoprotein B-48 and B-100

208
Q

What are the clinical features for abetalipoproteinemia?

A

Malabsorption due to defective chylomicron formation (requires B-48), Absent plasma VLDL and LDL (requires B-100)

209
Q

What is carcinoid tumor?

A

Malignant proliferation of neuroendocrine cells; low-grade malignancy

210
Q

What do the tumor cells in carcinoid tumor contain?

A

neurosecretory granules that are positive for chromogranin

211
Q

Where can carcinoid tumor cells arise?

A

Can arise anywhere along the gut; small bowel is the most common site

212
Q

What does carcinoid tumor grow as?

A

It grows as a submucosal polyp-like nodule

213
Q

What is the relation between carcinoid tumor and serotonin?

A

The neurosecretory granules often secrete serotonin

214
Q

What is serotonin released into?

A

the portal circulation

215
Q

Where is serotonin metabolized?

A

Its metabolized by liver monoamine oxidase (MAO) into 5-HIAA (5-hydroxyindoleacetic acid)

216
Q

What happens to 5-HIAA?

A

it is excreted in the urine.

217
Q

What does metastasis of carcinoid tumor to the liver result in?

A

it allows serotonin to bypass liver metabolism.

218
Q

What is carcinoid syndrome / heart disease?

A

Serotonin is released into the hepatic vein and leaks into systemic circulation via hepato-systemic shunts, resulting in carcinoid syndrome and carcinoid heart disease.

219
Q

What is carcinoid syndrome characterized by?

A

bronchospasm, diarrhea, and Hushing of skin;

220
Q

What might trigger symptoms of carcinoid syndrome?

A

it can be triggered by alcohol or emotional stress, which stimulate serotonin release from the tumor,

221
Q

What characterizes carcinoid heart disease?

A

It is characterized by right-sided valvular fibrosis

222
Q

In carcinoid heart disease why is there right sided valvular fibrosis?

A

increased collagen

223
Q

What does the right sided valvular fibrosis seen in carcinoid heart disease lead to?

A

tricuspid regurgitation and pulmonary valve stenosis

224
Q

In carcinoid heart diseae are there left-sided valvular lesions?

A

No, they are not seen due to presence of monoamine oxidase which metabolizes serotonin in the lung,

225
Q

What is acute appendicitis?

A

Acute inflammation of the appendix; most common cause of acute abdomen

226
Q

What is the most common cause of acute abdomen?

A

Acute appendicitis

227
Q

What is acute appendicitis related to?

A

obstruction of the appendix by lymphoid hyperplasia (children) or a tecalith (adults)

228
Q

What is McBurney point?

A

It is where the pain for acute appendicitis localizes to lower right quadrant

229
Q

What are the clinical features in acute appendicitis?

A
  1. Periumbilical pain, fever, and nausea; pain eventually localizes to right lower quadrant (McBurney point). 2. Rupture results in peritonitis that presents with guarding and rebound tenderness.
230
Q

What is a common complication for acute appendicitis?

A

Periappendiceal abscess is a common complication

231
Q

What is inflammatory bowel disease?

A

Chronic, relapsing inflammation of bowel

232
Q

What is inflammatory bowel disease possibly due to?

A

abnormal immune response to enteric flora

233
Q

How does inflammatory bowel disease classically present?

A

in young women (teens to 30s) as recurrent bouts of bloody diarrhea and abdominal pain

234
Q

Where is inflammatory bowel disease more prevalent?

A

in the West, particularly in Caucasians and Eastern European Jews

235
Q

How do you diagnose inflammatory bowel disease?

A

It?s a diagnosis of exclusion whose symptoms mimic other causes of bowel inflammation

236
Q

What is inflammatory bowel disease subclassified as?

A

ulcerative colitis or Crohn?s disease

237
Q

What is the wall involvement for ulcerative colitis?

A

Mucosal or submucosal ulcers

238
Q

Where does ulcerative colitis begin?

A

In the rectum

239
Q

What does ulcerative colitis involve after the rectum?

A

It can extend proximally up to the cecum, the remainder of the GI tract is unaffected

240
Q

What are the symptoms of ulcerative colitis?

A

Left lower quadrant pain (rectum) with bloody diarrhea

241
Q

What is involved in inflammation with ulcerative colitis?

A

Crypt abscesses with neutrophils

242
Q

What is the gross appearance of ulcerative colitis?

A

Pseudopolyps, loss of haustra ? lead pipe sign on imaging

243
Q

What are the complications for ulcerative colitis?

A

Toxic megacolon and carcinoma

244
Q

For ulcerative colitis what is the risk based on?

A

Its based on extent of colonic involvement and duration of disease (generally not a concern until >10 years of disease)

245
Q

What are the associations for ulcerative colitis?

A

Primary sclerosing cholangitis and p-ANCA positivity

246
Q

What is the effect of smoking on ulcerative colitis?

A

Smoking protects against it

247
Q

What is the wall involvement for crohns disease?

A

Full thickness inflammation with knife like fissures

248
Q

What is the location for Crohn’s disease?

A

Anywhere from mouth to anus with skip lesions

249
Q

What is the most common and least common site for crohn’s disease?

A

Most common is the terminal ileum and the least common is the rectum

250
Q

What are the symptoms for crohn’s disease?

A

Right lower quadrant pain (ileum) with non bloody diarrhea

251
Q

What is involved with the inflammation in Crohn?s disease?

A

Lymphoid aggregates with granulomas (40% of cases)

252
Q

What is the gross appearance of Crohn Disease?

A

Cobblestone mucosa, creeping fat, and strictures (string sign on imaging)

253
Q

What are the complications for Crohns Disease?

A

Malabsorption with nutritional deficiency, calcium oxalate nephrolithiasis, fistula formation, and carcinoma if colonic disease is present

254
Q

What are the associations for Crohns disease?

A

Ankylosing spondylitis, sacroiliitis, migratory polyarthritis, erythema nodosum and uveitis

255
Q

What effect does smoking have on Crohns disease?

A

It increases the risk for developing Crohns disease

256
Q

What is hirschsprung disease?

A

Defective relaxation and peristalsis of rectum and distal sigmoid colon

257
Q

What is hirschsprung disease associated with?

A

Down syndrome

258
Q

What is hirschsprung disease due to?

A

congenital failure of ganglion cells which are neural crest-derived, to descend into myenteric and submucosal plexus

259
Q

Where is the myenteric (Auerbach) plexus located?

A

between the inner circular and outer longitudinal muscle layers of the muscularis propria and regulates motility

260
Q

Where is the submucosal (Meissner) plexus located?

A

in the submucosa and regulates blood flow, secretions, and absorption.

261
Q

What are the clinical features for hirschsprung disease based on?

A

Obstruction

262
Q

What are the clinical features for hirschsprung disease?

A
  1. Failure to pass meconium 2. Empty rectal vault on digital rectal exam 3. Massive dilatation (megacolon) of bowel proximal to obstruction with risk for rupture
263
Q

In hirschsprung disease what does rectal suction biopsy reveal?

A

lack of ganglion cells.

264
Q

What is the treatment for hirschsprung disease?

A

involves resection of the involved bowel; ganglion cells are present in the bowel proximal to the diseased segment.

265
Q

What is colonic diverticula?

A

Outpouchings of mucosa and submucosa through the muscularis propria (false diverticulum)

266
Q

What is colonic diverticula related to?

A

wall stress

267
Q

What is colonic diverticula associated with?

A

constipation, straining, and low-fiber diet; commonly seen in older adults (risk increases with age)

268
Q

From where does the colonic diverticula arise?

A

where the vasa recta traverse the muscularis propria (weak point in colonic wall)

269
Q

What is the most common location for colonic diverticula?

A

sigmoid colon

270
Q

What are usually the symptoms for colonic diverticula?

A

Its usually asymptomatic

271
Q

What are the complications for colonic diverticula?

A
  1. Rectal bleeding (hematochezia) 2. Diverticulitis 3. Fistula
272
Q

What is diverticulitis due to?

A

obstructing fecal material

273
Q

How does diverticulitis present?

A

with appendicitis-like symptoms in the left lower quadrant

274
Q

What is the relationship between colonic diverticula and a fistula?

A

Inflamed diverticulum ruptures and attaches to a local structure.

275
Q

What does the colovesicular fistula present with?

A

air (or stool) in urine

276
Q

What is angiodysplasia?

A

Acquired malformation of mucosal and submucosal capillary beds

277
Q

How does angiodysplasia usually arise?

A

in the cecum and right colon due to high wall tension

278
Q

How does rupture in angiodysplasia classically present?

A

as hematochezia in an older adult.

279
Q

What is hereditary hemorrhagic telangiectasia?

A

Autosomal dominant disorder resulting in thin-walled blood vessels, especially in the mouth and GI tract

280
Q

What does rupture in hereditary hemorrhagic telangiectasia present as?

A

presents as bleeding.

281
Q

What is ischemic colitis?

A

Ischemic damage to the colon, usually at the splenic flexure, watershed area of superior mesenteric artery (SMA)

282
Q

What does ischemic cholitis present with?

A

postprandial pain and weight loss; infarction results in pain and bloody diarrhea.

283
Q

What is irritable bowel syndrome?

A

Relapsing abdominal pain with bloating, flatulence, and change in bowel habits (diarrhea or constipation) that improves with defecation

284
Q

With who is irritable bowel syndrome classically seen ?

A

middleaged females

285
Q

What is irritable bowel syndrome related to?

A

disturbed intestinal motility; no identifiable pathologic changes

286
Q

What may improve the symptoms of irritable bowel syndrome?

A

Increased dietary fiber may improve symptoms.

287
Q

What are colonic polyps?

A

Raised protrusions of colonic mucosa

288
Q

What are the most common types of colonic polyps?

A

hyperplastic and adenomatous polyps

289
Q

What are hyperplastic polyps due to?

A

hyperplasia of glands; classically show a serrated appearance on microscopy

290
Q

What is the most common type of polyp and where does it usually arise?

A

Hyperplastic polyps and it usually arises in the left colon (rectosigmoid)

291
Q

Can hyperplastic polyps result in cancer?

A

No its benign, with no malignant potential

292
Q

What are adenomatous polyps due to?

A

neoplastic proliferation of glands

293
Q

What is the 2nd most common type of colonic polyp?

A

Adenomatous polyps

294
Q

Can andenomatous polyps lead to cancer?

A

Benign, but premalignant, it may progress to adenocarcinoma via the adenoma-carcinoma sequence

295
Q

What is the adenoma-carcinoma sequence?

A

it describes the molecular progression from normal colonic mucosa to adenomatous polyp to carcinoma.

296
Q

What is APC?

A

APC (adenomatous polyposis coli gene)

297
Q

What do mutations in the APC lead to?

A

either sporadic or germline mutations increase risk for the formation of polyp.

298
Q

Mutations of what leads to increased risk for polyp progression to carcinoma?

A

APC, k-ras and p53

299
Q

How does k-ras mutation affect polyps?

A

leads to formation of polyp

300
Q

What is the effect of p53 mutation and polyps?

A

p53 mutation and increased expression of COX allow for progression to carcinoma; aspirin impedes progression from adenoma to carcinoma.

301
Q

How is screening for polyps performed?

A

by colonoscopy and testing for fecal occult blood

302
Q

How do polyps present clinically?

A

they are usually clinically silent, but can bleed.

303
Q

What is the goal in term of polyps?

A

it is to remove adenomatous polyps before progression to carcinoma

304
Q

On colonoscopy can you tell the difference between hyperplastic and adenomatous polyps?

A

No they look identical. Hence, all polyps are removed and examined microscopically

305
Q

With polyps what is the risk for progression from adenoma to carcinoma related to?

A

size > 2 cm, sessile growth, and villous histology.

306
Q

What is familial adenomatous polyposis?

A

(FAP)Autosomal dominant disorder characterized by 100s to 1000s of adenomatous colonic polyps

307
Q

What is familial adenomatous polyposis (FAP) due to?

A

inherited APC mutation (chromosome 5); increases propensity to develop adenomatous polyps throughout colon and rectum

308
Q

How is familial adenomatous polyposis treated?

A

Colon and rectum are removed prophylacticly ; otherwise, almost all patients develop carcinoma by 40 years of age.

309
Q

What is gardner syndrome?

A

it is FAP with fibromatosis and osteomas

310
Q

What is fibromatosis?

A

it is a non-neoplastic proliferation of fibroblasts

311
Q

Where does fibromatosis arise?

A

in retroperitoneum (desmoid) and locally destroys tissue

312
Q

What is Osteoma?

A

it is a benign tumor of bone that usually arises in the skull

313
Q

What is Turcot syndrome?

A

it is FAP with CNS tumors (medulloblastoma and glial tumors)

314
Q

What is a juvenile polyp?

A

Sporadic, hamartomatous (benign) polyp that arises in children (< 5 years)

315
Q

How does juvenile polyp usually present?

A

as a solitary rectal polyp that prolapses and bleeds

316
Q

What is juvenile polyposis characterized by?

A

multiple juvenile polyps in the stomach and colon; large numbers of juvenile polyps increase the risk of progression to carcinoma.

317
Q

What is peutz-jeghers syndrome?

A

Hamartomatous (benign) polyp throughout GI tract and mucocutaneous hyperpigmentation (freckle-like spots) on lips, oral mucosa, and genital skin; autosomal dominant disorder

318
Q

In Peutz-Jeghers Syndrome what is there an increased risk for?

A

colorectal, breast, and gynecologic cancer

319
Q

What is colorectoal carcinoma?

A

Carcinoma arising from colonic or rectal mucosa

320
Q

What is the 3rd most common site of cancer?

A

Colorectal carcinoma

321
Q

What is the 3rd most common cause of cancer-related death?

A

Colorectal carcinoma

322
Q

What is the peak incidence for colorectal carcinoma?

A

it is 60-70 years of age

323
Q

What does colorectal carcinoma most commonly arise from?

A

adenoma-carcinoma sequence

324
Q

For colorectal carcinoma what is a second important molecular pathway?

A

the microsatellite instability (MSI) pathway

325
Q

What are microsatellites in the MSI pathway?

A

they are repeating sequences of noncoding DNA; integrity of the sequence (stability) is maintained during cell division.

326
Q

What does instability in the microsatellite instability pathway indicate?

A

defective DNA copy mechanisms (eg. DNA mismatch repair enzymes).

327
Q

What is HNPCC

A

Hereditary non polyposis colorectal carcinoma

328
Q

What is HNPCC due to?

A

Inherited mutations in DNA mismatch repair enzymes.

329
Q

With HNPCC what is there an increased risk for?

A

colorectal, ovarian, and endometrial carcinoma

330
Q

Where does colorectal carcinoma arise?

A

de novo (not from adenomatous polyps) at a relatively early age; usually right-sided

331
Q

How does the screening for colorectal carcinoma occur?

A

via endoscopy and fecal occult blood testing

332
Q

When does screening for colorectal carcinoma begin?

A

at 50 years of age

333
Q

What is the goal for screening for colorectal carcinoma?

A

To remove adenomatous polyps before carcinoma develops and to detect cancer early (before clinical symptoms arise).

334
Q

In colorectal carcinoma where can carcinoma develop?

A

anywhere along entire the length of the colon

335
Q

In colorectal carcinoma how does left-sided carcinoma usually grow?

A

as a napkin-ring lesion;

336
Q

In colorectal carcinoma how does left-sided carcinoma present?

A

With decreased stool caliber, left lower quadrant pain, and blood-streaked stool

337
Q

In colorectal carcinoma how does right-sided carcinoma usually grow?

A

as a raised lesion;

338
Q

In colorectal carcinoma how does right-sided carcinoma usually present?

A

with iron deficiency anemia (occult bleeding) and vague pain. All older adults with iron deficiency anemia has colorectal carcinoma until proven otherwise.

339
Q

What infection is colonic carcinoma associated with?

A

an increased risk for Streptococcus bovis endocarditis.

340
Q

What is the T stage for colorectal carcinoma based on?

A

depth of invasion;

341
Q

Do tumors limited to the mucosa generally spread?

A

No they do not spread due to lack of lymphatics in the mucosa

342
Q

What does the N stage for colorectal carcinoma represent?

A

spread to regional lymph nodes

343
Q

What does the M stage for colorectal carcinoma represent?

A

distant spread

344
Q

What does the M stage for colorectal carcinoma most commonly involve?

A

the liver

345
Q

What is CEA?

A

it is a serum tumor marker that is useful for assessing treatment response and detecting recurrence; not useful for screening

GBA Pathology (20 decks)

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