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My Pathoma Unit 6 > Chapter 10 GI > Flashcards

Chapter 10 GI Flashcards

1
Q

What is a tracheoesophageal fistula?

A

A congenital defect resulting in a connection between the esophagus and trachea.

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2
Q

Describe the most common variant of a tracheoesophageal fistula?

A

Consists of proximal esophageal atresia with the distal esophagus arising from the trachea.

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3
Q

How does the most common variant of a tracheoesophageal fistula present?

A

With vomiting, polyhydramnios, abdominal distension, and aspiration.

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4
Q

What does atresia mean with respect to a lumen?

A

It means the lumen of a tub ends in a pouch or a blind loop.

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5
Q

What is an esophageal web and how does it present? Where does it typically arise

A

Thin protrusion of esophageal mucosa (ONLY), most often in the upper esophagus, presents with dysphagia for poorly chewed food.

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6
Q

What do esophageal webs carry increased risk for?

A

squamous cell carcinoma

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7
Q

What is plummer vinson syndrome?

A

Characterized by severe iron deficiency anemia, esophageal webs, and beefy red tongue due to atrophic glossitis

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8
Q

What is a Zenker diverticulum? Where does it arise? and how does it present?

A

Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall (False diverticulum). Arises above the upper esophageal sphincter at the junction of the esophagus and pharynx. Presents with dysphagia, obstruction and halitosis (bad breath). Patients feel like they have something stuck in the back of their throat.

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9
Q

What is Mallory-Weiss Syndrome and what is it caused by? How does it present?

A

Longitudinal laceration of mucosa at the GE junction caused by severe vomiting, usually due to alcoholism or bulimia. Presents with PAINFUL hematemesis.

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10
Q

What does Mallory Weiss syndrome carry a risk for? Describe it

A

Boerhaave syndrome - rupture of the esophagus leading to air in the mediastinum and subcutaneous emphysema (you can push on air bubbles beneath the skin and as you can hear “rice crispies” crackling)

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11
Q

What are esophageal varices and what do they arise secondarily to? Describe the anatomy

A

Dilated submucosal veins in the LOWER esophagous. (proximal esophagous drains via azygous vein into SVC). Arise secondary to portal hypertension. The distal esophageal vein normally drains into the portal vein via the left gastric vein. In portal hypertension, the left gastric vein backs up into the esophageal vein, resulting in dilation (varices)

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12
Q

Describe the symptoms of esophageal varices? What complication are patients at risk for and what are the symptoms?

A

Usually asymptomatic. Risk for rupture exists. Rupture presents with PAINLESS hematemesis and is the most common cause of death in cirrhosis. (Most patients also have a coagulopathy due to poor liver function)

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13
Q

What is achalasia?

A

Disordered esophageal motility with inability to relax the LES

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14
Q

What is achalasia due to?

A

Damaged ganglion cells in the myenteric plexus.

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15
Q

Where is the myenteric plexus located and what is its function?

A

Ganglion cells of the myenteric plexus are located between the inner cucular and outer longitudinal layers of the muscularis propria and are important for regulating bowel motility and relaxing of the LES.

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16
Q

What causes damage to myenteric plexus ganglion in achalasia?

A

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

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17
Q

What are 5 clinical features of 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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18
Q

What happens in GERD?

A

Reflux of acid from the stomach due to reduced LES tone

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19
Q

What are 6 risk factors for GERD?

A 
1 alcohol
2 tobacco
3 obesity
4 fat rich diet
5 caffeine
6 hiatal hernia
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20
Q

What are 4 clinical features of 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 complicaitons

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21
Q

What is the most common type of diaphragm hernia?

A

Sliding hiatal hernia where the stomach herniates up into th esophagus and creates an hour glass appearance due to compression of LES.

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22
Q

Describe some possible findings in a paraesophageal hiatal hernia?

A

This is less common. Bowel sounds in lung field. If present congenitally can result in lung hypoplasia.

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23
Q

What is Barrett esophagus? What percentage of GERD patients develop this? What is it due to?

A

Metaplasia of the lower esophageal mucosa from stratified squamous epithelium to nonciliated columnar epithelium with goblet cells; seen in 10 % of patients with GERD. Response of lower esophageal stem cells to acidic stress

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24
Q

What might barrett esophagus progress to?

A

dysplasia and adenocarcinoma

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25
Q

What are the two subclasses of esophageal carcinoma?

A

adenocarcinoma or squamous cell carcinoma

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26
Q

Describe adenocarcinoma of the esophagus, where it is common, what it arises from, and which portion it involves?

A

Adenocarcinoma is a malignant proliferation of glands; most common type of esophageal carcinoma in the West. Arises from preexisting Barrett esophagus; usually involves the lower one third of the esophagus

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27
Q

Describe squamous cell carcinoma, where it is most common, and what portion it affects?

A

Malignant proliferation of squamous cells; most common esophageal cancer worldwide. Usually arises in the upper or middle third of the esophagus; major risk factors are based off of irritation.

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28
Q

What are 5 major risk factors for squamous cell carcinoma of the esophagus?

A

1 Alcohol
2 Very hot Tea
3 Achalasia (rotting food)
4 Esophageal web (i.e. plummer vinson –> food rots)
5 Esophageal injury (i.e. lye ingestion - chemical used to straighten hair)

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29
Q

When does esophageal carcinoma present and what do symptoms include. What addition symptoms may squamous cell carcinoma present with?

A

Symptoms include progressive dysphagia (solids to liquids), weight loss, pain, and hematemesis. SCC may additionally present with horse voice (recurrent laryngeal nerve involvement) and cough (tracheal involvement)

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30
Q

Describe the lymph node spread patterns based on area of the esophagus that is affected.

A

Upper 1/3- cervical nodes
Middle 1/3 - mediastinal or tracheobronchial nodes
Lower 1/3 - celiac and gastric nodes

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31
Q

What is gastroschisis?

A

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

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32
Q

What is a omphalocele? What is it due to? what are the contents covered by?

A

A persistent herniation of bowel into umbilical cord. Due to failure of herniated intestines to return to the body cavity during development. Contents are covered by peritoneum and amnion of the umbilical cord.

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33
Q

What is pyloric stenosis? how does it classically present and how is it treated?

A

Congenital hypertrophy of pyloric smooth muscle; more common in males. Classically presents two weeks after birth as projectile nonbilious vomiting, visible peristalsis, and olive like mass in the abdomen. Treatment is a myotomy

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34
Q

When does pyloric stenosis present?

A

babies are born NORMAL. Develops over the course of 2 weeks after birth

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35
Q

What is acute gastritis? and what is it due to? what doe natural defenses include?

A

Acidic damage to the stomach mucosa. Due to imbalance between mucosal defenses and acidic environment. Defenses include mucin layer produced by foveolar cells, bicarbonate secretion by surface epithelium, and normal blood supply (provides nutrients and picks up leaked acid0

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36
Q

What are 6 risk factors for acute gastritis?

A

1 Severe burn (Curling ulcer)- hypovolemia leads to decreased blood supply.
2 NSAIDs (Decresed PGE2 which normally helps to decrease acid production, and upregulates bicarb, mucin and blood flow)
3 Heavy alcohol consumption (Direct mucosal damage)
4 Chemotherapy (kill stem cells)
5 Increased intracranial pressure (Cushing ulcer)- increased stim of vagus nerve leads to increased acid production)
6 Shock Multiple (stress) ulcers may be seen in ICU patients dues to decreased blood flow

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37
Q

What does acidic damage in acute gastritis result in?

A

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

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38
Q

What is chronic gastritis and what are the 2 types?

A

Chronic inflammation of the stomach mucosa. divided into two types based on underlying etiology: chronic autoimmune gastritis and chronic H pylori gastritis

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39
Q

What is chronic autoimmune gastritis due to and what immunological factors are involved?

A

Due to autoimmune destruction of gastric parietal cells, which are located in the stomach BODY and FUNDUS. Associated with antibodies against parietal cells and/or intrinsic factor; useful for diagnosis, but pathogenesis is mediated by T cells (type 4 hypersensitivity)

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40
Q

What are 4 clinical features of chronic autoimmune gastritis?

A 
1 atrophy of mucosa with intestinal metaplasia (peyer's patches with lymphocytes) 
2 achlorhydria with increased gastrin levels due to G-cell hyperplasia (make gastrin in the antrum)
3 megaloblastic (pernicious) anemia due to lack of intrinsic factor
4 increased risk for gastric adenocarcinoma (intestinal type)
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41
Q

What is chronic H pylori gastritis due to? describe the pathogenesis?

A

Due to H pylori induced acute and chronic inflammationlmost common form of gastritis. H Pylori ureases and proteases along with inflammation weaken mucosal defenses; ANTRUM is the most common site.

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42
Q

How does chronic H pylori gastritis present? What does it increase risk for?

A

Epigastric abdominal pain; increases risk for ulceration (peptic ulcer disease), gastric adenocarcinoma (intestinal type), and MALT lymphoma (marginal zone)

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43
Q

What does treatment of Chronic H pylori gastritis involve? what is the common response. what tests are used to follow up treatment success?

A

TRIPLE THERAPY. resolves gastritis/ulcer and reverses intestinal metaplasia. Negative urea breath test and lack of stool antigen confirm eradication of H pylori.

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44
Q

What is peptic ulcer disease? describe the intestinal involvement?

A

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

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45
Q

What are duodenal ulcers in PUD due to? how do they present? What is the diagnostic study/results? where do the ulcers usually arise? What complications may occur

A

Almost always due to H pylori (>95%); rarely, due to ZE syndrome. Presents with epigastric pain that improves with meals. Diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner Glands (produce mucous like substance to protect from acid). Usually arises in anterior duodenum; when present in the posterior duodenum rupture may lead to bleeding from the gastroduodenal artery or acute pancreatitis.

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46
Q

What are gastric ulcers in PUD usually due to? how do they present? where are they located? and what complications may occur?

A

Usually due to H pylori (75%); other causes include NSAIDs (20%) and Bile reflux (5%). Presents with epigastric pain that worsens with meals. Ulcer is usually located in the lesser curvature of the antrum. Rupture carries risk of bleeding from left gastric artery.

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47
Q

What does the differential diagnosis of peptic ulcers include?

A

carcinoma

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48
Q

Are duodenal ulcers more commonly malignant or benign?

A

Almost always benign, Duodenal carcinoma is extremely rare

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49
Q

What type of gastric carcinoma can cause gastric ulcers? Describe the appearance of both and what is required for a definitive diagnosis?

A

intestinal type. Benign peptic ulcers are usually small (), and surrounded by radiating folds of mucosa. Malignant ulcers are large and irregular with heaped up margins. Biopsy is required for definitive diagnosis.

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50
Q

What is gastric carcinoma and what are the two subtypes?

A

Malignant proliferation of surface epithelial cells (adenomcarcinoma). Sub-classified into intestinal and diffuse types.

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51
Q

Describe how intestinal gastric carcinoma presents (gross appearance) and the risk factors for developing it?

A

More common type. presents as a large, irregular ulcer with heaped up margins; most commonly involves the lesser curvature of the antrum (similar to a gastic ulcer). Risk factors include intestinal metaplasia (e.g. due to H pylori and autoimmune gastritis), nitrosamines in smoked foods (japan) and blood type A

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52
Q

Describe how diffuse type gastric carcinoma is characterized by and its association with H pylori, intestinal metaplasia, or nitrosamines?

A

Characterized by signet ring cells that diffusely infiltrate the gastric wall; desmoplasia results in thickening of stomach wall (linitus plastica). Not associated with H pylori, metaplasia or nitrosamines

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53
Q

what is desmoplasia?

A

reactive response of stroma (fibrous tissue plus blood vessels)

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54
Q

Describe a signet ring cell?

A

Nucleus is pushed to the side of the cell by mucin globules.

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55
Q

How and when does gastric carcinoma present?

A

Presents late with weight loss, abdominal pain, anemia, and early satiety (classic in diffuse type); rarely presents as acanthosis nigricans or leser trelat sign

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56
Q

What is the lesar trelat sign?

A

Dozens of seborrheic keratoses in a line.

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57
Q

What is a classic lymph node that gastric carcinoma can spread to?

A

Left supraclavicular node (Virchows node)

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58
Q

Where do distant metastases of gastric carcinoma involve?

A

Commonly involves liver; other sites include periumbilical region (sister mary joseph nodule); seen with intestinal type. Bilateral ovaries (krukenberg tumor); seen with diffuse type.

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59
Q

What is duodenal atresia and what is it highly associated with? What are 3 clinical features?

A

Congenital failure of duodenum to canalize; associated with Down syndrome. Clinical features include polyhydramnios, distension of stomach and blind loop of duodenum (double bubble sign on XR) and bilious vomiting.

60
Q

What is a meckel diverticulum and what is it caused by?

A

Outpouching of all three layers of the bowel wall (true diverticulum). Arises due to gailure of the vitelline duct to involute

61
Q

What is the vitelline duct and what happens if it remains patent?

A

It connects the small bowel to the yolk sac. If it remains patent you can have passing of muconium via the umbilicus.

62
Q

What are the rule of 2s with meckel diverticulum? How does it present?

A

Seen in 2% of the population (most common congenital anomaly of the GI tract. 2 inches long and located in the small bowel within 2 feet of the ileocecal vlave. Can present during the first 2 years of life with bleeding (due to heterotopic gastric mucosa), volvulus, intussesception, or obstruction (mimics appendicitis); however, most cases are asymptomatic.

63
Q

What is volvulus, what does it result in, and what are the most common locations?

A

Twisting of bowel along its mesentery. Results in obstruction and disruption of the blood supply with infarction. most common locations are sigmoid colon (elderly) and cecum (young adults)

64
Q

What is intussusception and what does it result in?

A

Telescoping of proximal segment of bowel forward into distal segment. telescoped segment is pulled forwards by peristalsis, resulting in obstruction and disruption of blood supply with infarction which can cause currant jelly stools..

65
Q

What is intussusception associated with?

A

Leading edge (focus of traction). Inchildren the most common cause is lymphoid hyperplasia (e.g. due to rotavirus); usually arises in the terminal ileum, leading to intussusception into the cecum. In adults, the most common cause is tumor.

66
Q

Small bowel is highly susceptible to ischemic injury, describe what a transmural infarction occurs with?

A

Occurs with thrombosis/embolism of the SMA (atrial fib or vasculitis [PAN]) or thrombosis of the mesenteric vein (P Vera or lupus anticoagulant)

67
Q

Small bowel is highly susceptible to ischemic injury, describe what a mucosal infarction occurs with?

A

with marked hypotension

68
Q

What are the clinical features of a small bowel infarction?

A

abdominal pain, bloody diarrhea, and decreased bowel sounds.

69
Q

Describe lactose intolerance?

A

Decreased function of lactase enzyme found in the brush border of enterocytes. Lactase normally breaks down lactose into glucose and galactose.

70
Q

How does lactose intolerance present?

A

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

71
Q

Describe how lactose intolerance arises?

A

Deficiency may be congenital (rare autosomal recessive disorder) or acquired (often develops in late childhood); temporary deficiency is seen after small bowel infection (lactase is highly susceptible to injury)

72
Q

What is Celiac Disease? What genetic markers is it associated with?

A

Immune mediated damage of small bowel villi due to gluten exposure; associated with HLA-DQ2 and DQ8

73
Q

What is gluten? what is the most pathogenic component and how does it mediate damage?

A

Gluten is present in wheat and grains; its most pathogenic component is gliadin. Once absorbed, gliadin is deaminated by tissue transglutaminase (tTG). Deaminated gliadin is presented by antigen presenting cells via MHC class II. HELPER T CELL MEDIATE TISSUE DAMAGE.

74
Q

Describe the Clinical presentation of celiac disease?

A

Children classically present with abdominal distension, diarrhea, and failure to thrive. Adults classically present with chronic diarrhea and bloating. Small, herpes-like cesicles may arise on skin (dermatitis herpetiformis). Due to IgA deposition at the tips of dermal papillae; resolves with gluten free diet.

75
Q

Describe the antibodies produced in celiac disease

A

IgA antibodies against endomysium, tTG, or gliadin; IgG antibodies are also present and are useful for diagnosis in individuals with IgA deficiency (increased incidence of IgA deficiency in seen in ciliac disease)

76
Q

What does duodenal biopsy reveal in celiac disease?what part of the gi tract is most commonly affected?

A

flattening of cilli, hyperplasia of crypts, and increased intraepithelial lymphocytes. Damage is most prominent in the duodenum; jejunum and ileum are less involved

77
Q

What two conditions are late complications of celiac disease that present as refractory disease despite good diet?

A

Small bowel carcinoma and T cell lymphoma

78
Q

What is tropical sprue?

A

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

79
Q

Tropical sprue is similar to celiac disease except for what 3 major differences?

A

1 Occurs in tropical regions (e.g.carribean)
2 Arises after infectious diarrhea and responds to antibiotics
3 Damage is most prominent in jejunum and ileum (secondary vitamin B12 or folate deficiency may ensue); duodenum is less commonly involved.

80
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)

81
Q

What is the classic site of involvement in whipple disease? describe the damage?

A

Classic site is the small bowel lamina propria. Macrophages compress lacteals. Chylomicrons cannot be transferred from enterocyte to lymphatics. Results in fat malabsorption and steatorrhea.

82
Q

What are some other common sites of involvement with whipple Disease?

A

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

83
Q

What is Abetalipoproteinemia? What is its inheritance pattern and symptoms.

A

AR deficiency of apolipoprotein B-48 and B-100. Malabsorption occurs due to defective chylomicron formation (requires B-48) and also absent plasma VLDL and LDL is seen (Both require B-100)

84
Q

What is Carcinoid tumor? What grade is it? What do the cells stand for

A

Malignant proliferation of neuroendocrince cells; low grade malignancy. tumor cells contain neurosecretory granules that are positive for chromogranin

85
Q

Where does Carcinoid tumor arise? what form does it take?

A

Can arise anywhere along the gut; small bowel is the most common site, grows a submucosal polyp like nodule.

86
Q

What does carcinoid tumor often secrete? What is the urine marker for this?

A

Often secretes serotonin. Serotonin is released into the portal circulation and metabolized by liver MAO into 5-HIAA which is excreted in the urine.

87
Q

What does metastasis of carcinoid tumor result in?

A

Metastasis to the liver allows serotonin to bypass liver metabolism. Serotonin is released into hepatic cein and leaks into systemic circulation by hepato-systemic shunts, resulting in carcinoid syndrome and carcinoid heart disease.

88
Q

What is carcinoid syndrome? What can trigger symptoms?

A

Characterized by bronchospasm, diarrhea, and flushing of skin; symptoms can be triggered by alcohol or emotional stress, which stimulate serotonin release from the tumor.

89
Q

What is Carcinoid Heart disease?

A

Characterized by right sided valvular fibrosis (increased collagen) leading to tricuspid regurgitation and pulmonary valve stenosis; left sided valvular lesions are not seen due to presence of MAO in the lung.

90
Q

What is acute appendicitis and what is it caused by?

A

Acute inflammation of the appendix; most common cause of acute abdomen. Related to obstruction of the appendix by lymphoid hyperplasia (children) or a fecalith (adults)

91
Q

What are 3 clinical features of appendicitis?

A
  1. Periumbilical pain, fever, and nausea; pain eventually localizes to right lower quadrant (mcBurnery Point)
    2 Rupture results in peritonitis that presents with guarding and rebound tenderness
    3 Periappendiceal abscess is a common complication
92
Q

What is inflammatory bowel disease and what is it possibly due to?

A

Chronic, relapsing inflammation of bowel. Possibly due to abnormal immune response to enteric flora.

93
Q

How does IBD present and where is it most prevalent? Who does it present in?

A

Classically presents in young women (teens to 30s) as recurrent bouts of bloody diarrhea and abdominal pain. More prevalent in the West, particularly in caucasians and eastern european jews.

94
Q

how is a diagnosis of IBD made?

A

diagnosis of exclusion; symptoms mimic other causes of bowel inflammation (e.g. infection)

95
Q

What is IBD subclassified into?

A

Ulcerative colitis or Crohn disease.

96
Q

Describe the wall involvement and location of Ulcerative Colitis?

A

Mucosal and submucosal ulcers. Beginins in the rectum and can extend proximally up to the cecum (involvement is continuous); remainder of the GI tract is unaffected

97
Q

What are the symptoms of UC?

A

Left lower quadrant pain (rectum) with bloody diarrhea

98
Q

Describe the inflammation and gross appearance of UC?

A

Crypt abscesses with neutrophils. Pseudopolyps; loss of haustra (‘Lead pipe” sign on imaging)

99
Q

Describe the complications of UC?

A

Toxic megacolon and carcinoma (risk is based on the extent of colonic involvement and duration of disease; generally nor a concern until >10 years of disease)

100
Q

What effect does smoking have on UC?

A

Protects against UC

101
Q

What are the extraintestinal symptoms of IBD?

A

Arthritis (peripheral joints, ankylosisng spondylitis, sacroiliitis, migratory polyarthritis), uveitis, erythema nodosum, polyderma gangrenosum, primary sclerosisng cholangitis and p-ANCA positive

102
Q

Describe the wall involvement and location of Crohn disease?

A

Full thickness inflammation with knife like fissures. Anywhere from mout to anus with skip lesions; terminal ileum is the most common site, rectum is least common.

103
Q

What are the symptoms of Crohn disease?

A

Right lower quadrant pain (ileum) with non-bloody diarrhea

104
Q

Describe the inflammation and gross appearance of Crohn disease

A

Lymphoid aggregates with granulomas (40% of cases). Cobblestone mucosa (due to healing), creeping fat, and strictures (‘String-sign’ on imaging)

105
Q

What are the complications of Crohn Disease?

A

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

106
Q

What effect does smoking have on Crohn Disease?

A

Increases risk for Crohn disease

107
Q

What is hirschprung Disease? What is it associated with?

A

Defective relaxation and peristalsis of rectum and distal sigmoid colon. Associated with DS

108
Q

What is Hirschprung disease due to?

A

Congenital failure of ganglion cells (neural crest derived) to descend into myenteric and submucosal plexus.

109
Q

What is the myenteric plexus, where is it, what does it doe?

A

Auerbach plexus is located between the inner circular and outer longitudinal muscle layers of the muscularis propria and regulates motility.

110
Q

What is the submucosal plexus, where is it, what does it do?

A

Meissner plexus is located in the submucosal and regulates blood flow, secretions, and absorption.

111
Q

What are 3 clinical features of Hirschprung disease?

A

1 Failure to pass meconium
2 Empty rectal vault on DRE
3 Massive dilation (megacolon) of bowel proximal to obstruction with risk for rupture.

112
Q

What type of biopsy must be done for hirschprung disease and what does it reveal?

A

Rectal suction biopsy reveal lack of ganglion cells.

113
Q

what does treatment of Hirschprung disease involve?

A

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

114
Q

What is a colonic Diverticula?

A

Outpouching of mucosa through the muscularis propria (false diverticulum).

115
Q

What are colonic diverticula related to? what are they associated with and where do they arise?

A

related to wall stress. Associated with constipation, straining, and low-fiber diet; commonly seen in older adults (risk increases with age). Arise where the vasa recta traverse the muscularis propria (weak point in colonic wall): sigmoid colon is the most common section

116
Q

Describe the symptoms and complications of Colonic Diverticula?

A

Usually asymptomatic; complications include rectal bleeding (hematochezia). Diverticulitis - due to obstructing fecal material; presents with appendicitis-like symptoms in the left lower quadrant. Fistula - inflamed diverticulum ruptures and attaches to a local structure. Colovesicular fistula presents with air (or stool) in urine.

117
Q

What is angiodysplasia, where does it arise, and what complication can occur and how does it present.

A

Acquired malformation of mucosal and submucosal capillary beds. Usually arises in the cecum and the right colon due to high wall tension. Rupture classically presents as hematochezia in an older adult.

118
Q

What is Hereditary hemorrhagic telangiectasia and how might it present?

A

AD disorder resulting in thin walled blood vessels, especially in the mouth and GI tract. Rupture presents as bleeding.

119
Q

What is ischemic colitis, what is the most common cause, and how does it present?

A

Ischemic damage to the colon, usually at the splenic flexure (watershed area of the SMA). Atherosclerosis of the SMA is the most common cause, presents with postprandial pain and weight loss; infarction results in pain and bloody diarrhea.

120
Q

What is irritable bowel syndrome, what is it related to, and what may improve symptoms?

A

Relapsing abdominal pain with bloating, flatulence, and change in bowel habits (diarrhea or constipation) that improves with defecation; classically seen in middle aged females. Related to disturbed intestinal motility; no identifiable pathological changes. Increased dietary fiber may improve symptoms

121
Q

What are colonic polyps? what are the two most common types?

A

raised protrusions of colonic mucosa, two common types are hyperplastic and adenomatous

122
Q

What are hyperplastic polyps due to, what due they show on microscopy, where do they arise, and what is there malignant potential?

A

due to hyperplasia of glands; classically show a serrated appearance on microscopy. Most common type of polyp; usually arise in the left colon (rectosigmoid). they are benign with no malignant potential

123
Q

What are adenomatous polyps due to and what are their malignant potential?

A

Due to neoplastic proliferation of glands; second most common type of colonic polyp. Benign, but premalignant; may progress to adenocarcinoma via the adenoma-carcinoma sequence.

124
Q

What is the adenoma carcinoma sequence for colonic polyps? describe it. What is aspirins effect?

A

sequence describes the molecular progression from normal colonic mucosa to adenomatous polyp to carcinoma.
1 APC (adenomatous polyposis coli gene) mutations (sporadic or germline) increase the risk for a polyp.
2 K-ras mutation leads to formation of polyp
3 p53 mutation and increased expression of COX allow for progression to carcinoma; aspirin impedes progression from adenoma to carcinoma.

125
Q

What does screening for colonic polyps involve and what is the goal?

A

Screening is performed by colonoscopy and testing for fecal occult blood; polyps are usually clinically silent, but can bleed. the goal is to remove adenomatous polyps before progression to carcinoma.

126
Q

How are hyperplastic and adenomatous polyps treated and what is the greatest risk for progression to carcinoma (3)?

A

Hyperplastic and adenomatous polyps look identical on colonoscopy, hence all polyps are removed and examined microscopically. Greatest risk for progression is related to size >2cm, sessile growth, and villous histology

127
Q

What is Familial Adenomatous Polyposis (FAP)? What is the inheritance pattern? and what is it due to?

A

AD disorder characterized by 100s to 1000s of adenomatous colonic polyps. Due to inherited APC mutation (Chromosome 5); increases propensity to develop adenomatous polyps throughout the colon and rectum.

128
Q

How is FAP treated once detected?

A

The colon and rectum are removed prophylactically; otherwise, almost all patients develop carcinoma by 40 years of age.

129
Q

What is Gardner syndrome?

A

FAP, fibromatosis and osteomas of the facial bones.

130
Q

What is Turcot syndrome?

A

is FAP with CNS tumors (medulloblastoma and glial tumors)

131
Q

What is a juvenile polyp and how does it present?

A

Sporadic, hamartomatous (benign) polyp that arises in children (<5 years). Usually presents as a solitary rectal polyp that prolapses and bleeds

132
Q

What is juvenile polyposis characterized?

A

Juvenile polyposis is characterized by multiple juvenile polyps in the stomach and colon; large numbers of juvenile polyps increase the risk of progression to carcinoma

133
Q

What is Peutz-Jeghers syndrome? What is the inheritance pattern?

A

Hamartomatous (benign) polyps throughout GI tract and mucocutaneous hyperpigmentation (freckle like spots) on lips, oral mucosa, and genital skin; AD

134
Q

What cancers does Peutz-Jeghers syndrome carry and increased risk for?

A

colorectal, breast, and gynecologic cancer.

135
Q

What is colorectal cancer and what is the peak incidence?

A

Carcinoma arising from colonic or rectal mucosa. peak incidence is 60-70 years of age.

136
Q

What are the two major pathways that colorectal carcinoma arises from?

A

Most commonly arises from adenoma-carcinoma sequence; a second important molecular pathway is microsatellite instability.

137
Q

wrt to colorectal cancer. What are micro satellites, what is stability, what causes instability? What is Hereditary nonpolyposis colorectal carcinoma?

A

Microsatellites are repeating sequences of noncoding DNA; integrity of sequence (stability) is maintained during cell division. Instability indicates defective DNA copy mechanisms (e.g. DNA mismatch repair enzymes). HNPCC is due to inherited mutations in DNA mismatch repair enzymes.

138
Q

What cancers does HNPCC increase risk for?

A

colorectal, ovarian, and endometrial.

139
Q

how does colorectal carcinoma arise in HNPCC?

A

Arises de novo (not from an adenomatous polyp) at a relatively early age; usually right sided.

140
Q

What does screening for colorectal cancer involve and what age does it begin?

A

occurs via colonoscopy and fecal occult blood testing; begins at 50. goal is to remove adenomatous polyps before carcinoma develops and to detects cancer early (before clinical symptoms arise)

141
Q

Where can colorectal carcinoma arise?

A

anywhere along the entire length of the colon

142
Q

Describe Left sided colorectal carcinoma presentation and imaging?

A

usually grows as a ‘napkin-ring’ lesion; presents with decreased stool caliber, left lower quadrant pain, and blood streaked stool.

143
Q

Describe right sided colorectal carcinoma presentation and imaging.

A

usually grows as a raised lesion; presents with iron deficiency anemia (occult bleeding) and vague pain. An older adult with iron deficiency anemia has colorectal carcinoma until proven otherwise.

144
Q

What side do the two pathways to colorectal cancer generally tend towards?

A

Adenoma to carcinoma transformation is more common on the left side. MSI is more common on the right side.

145
Q

What infection does colonic carcinoma carry and increased risk for?

A

Streptococcus Bovis

146
Q

Where does distant spread most commonly occur in colorectal carcinoma?

A

Liver

147
Q

What serum marker is raised in colorectal cancer and what can it be used for?

A

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

My Pathoma Unit 6 (2 decks)

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