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Unit 6 > GI - Unit 6 > Flashcards

GI - Unit 6 Flashcards

1
Q

Gastroschisis

A

Gastro = stomach

schisis = splitting

Gastroschisis is the failure of the abdominal wall to fuse during embryological development leading to a “split” in the abdominal wall allowing for the exposure of abdominal contents

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2
Q
A

Gastroschisis - failure for the abdominal folds to fuse in development resulting in the exposure of abdominal contents

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3
Q

Omphalocele

A

Persistent herniation of bowel into umbilical cord

Due to failure of herniated intestines to return to the body cavity during development

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4
Q

Normal development of bowel

A

As it develops, it herniates into the umbilical cord due to the lack of space in the abdomen.

The bowel undergoes a 90 degree counterclockwise rotation which pulls the bowel out and back into the body cavity

  • Omphalocele occurs when this last step fails to complete/occur
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5
Q
A

As it develops, it herniates into the umbilical cord due to the lack of space in the abdomen.

The bowel undergoes a 90 degree counterclockwise rotation which pulls the bowel out and back into the body cavity

  • Omphalocele occurs when this last step fails to complete/occur. You will have an outpouching of abdominal contents surrounded by a peritoneum
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6
Q

How do you distinguish between a gastroschisis and an omphalocele?

A
  • Gastroschisis – no peritoneum surrounding the abdominal contents (failure to close abdominal folds)
  • omphalocele – peritoneum surrounds the abdominal contents (failure to retract the normally herniated contents)
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7
Q

Pyloric stenosis

A

Congenital hypertrophy of pyloric smooth muscle

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8
Q

Pyloric stenosis - more common in what population?

A

males

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9
Q

Pyloric stenosis - why does it not occur until after 2 weeks of birth?

A

Pyloric stenosis is due to hypertrophy of the pyloric sphincter muscle.

Hypertrophy takes time to develop and will not occur until after about 2 weeks

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10
Q

Pyloric stenosis - classical presentation

A
  1. Projectile nonbilious vomiting (increased pressure caused by the stenosis eventually causes regurgitation. It is nonbilious because the food has not yet reached the duodenum where food normally combines with bile)
  2. visible peristalsis (tight + enlarged stomach makes it easier to visibly see the peristalsis)
  3. Olive-like mass in the abdomen (representing the hypertrophic sphincter)
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11
Q

What type of vomitting is seen in pyloric stenosis? Why?

A

nonbilious because the food has not yet reached the duodenum where food normally combines with bile

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12
Q

Pyloric stenosis - treatment

A

Myotomy (excision of the hypertrophic muscle)

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13
Q

Acute gastritis

A

Burning of the stomach by acid. Due to 2 reasons

  1. increased acid production
  2. decreased protection from the mucosa
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14
Q

Acute gastritis - what is it caused by?

A

Due to imbalance between mucosal defenses and acidic environment (resulting in too much relative acid that essentially burns the stomach)

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15
Q

Natural defenses in the stomach against acid (3)

A
  1. mucin/mucous production by the foveolar cells (physical barrier against acid)
  2. bicarbonate secretion by surface epithelium (neutralizes acid)
  3. normal blood supply (provides nutrients and picks up leaked acid)
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16
Q

Why is the blood supply so important to the stomach? What is its role in acute gastritis?

A

Provides nutrients to the stomach and picks up any leaked acid and carries it away (so acid doesn’t build up beyond a certain point)

In cases such as shock where blood flow is decreased, there is an increased risk for stress ulcers due to the buildup of acid

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17
Q

Why is there an increased risk of stress ulcers in ICU patients?

A

Shock can cause loss of or decreased perfusion to the gut reducing its capacity to reabsorb and carry away any leaked acid.

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18
Q

What cells are responsible for the production of mucin protective layer in the stomach?

A

Foveolar cells

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19
Q

Foveolar cells - what do they produce?

A
  1. Mucin
  2. Prostaglandins (PGE2)
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20
Q

Role of prostaglandin (PGE2) in normal stomach protection (3)

A
  1. Decrease acid production
  2. stimulate cells to produce mucin and bicarbonate
  3. increased blood flow to mucosal barrier (vasodilation)

Overall goal is to decrease the acidity of the environment

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21
Q

Acute gastritis - risk factors (6)

A
  1. Severe burn (Curling ulcer) - hypovolemia –> decreased blood supply
  2. NSAIDs (decreased PGE2)
  3. Heavy alcohol consumption (toxin that directly damages the mucosa)
  4. Chemotherapy (knockout of the regenerating cells – can’t regenerate the mucosal layer)
  5. Increased ICP (Cushing Ulcer) – increased ICP –> increased vagal stimulation –> increased ACh == stimulates the parietal cells to increase acid production
  6. Shock (multiple stress ulcers may be seen in ICU patients (due to reduced blood flow)
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22
Q

Parietal cells - what receptors are responsible for regulating acid production

A
  1. ACh receptor
  2. Gastrin receptor
  3. Histamine receptor

Activation of these receptors all stimulate acid production

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23
Q

Where are the majority of the parietal cells located?

A

Body and fundus of the stomach

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24
Q

Why does alcohol affect acute gastritis?

A

Alcohol is a toxin that can directly damage the mucosa

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25
Q

What is the mechanism by which increased ICP (intracranial pressure) increases acid production?

A

Increased ICP –> increased vagal stimulation –> increased release of ACh –> activation of parietal cells

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26
Q

Curling ulcer

A

an acute peptic ulcer of the duodenum resulting as a complication from severe burns when reduced plasma volume leads to ischemia

  • ischemia reduces ability to remove acid
  • ischemia can result in necrosis which knocks out the protection completely
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27
Q

Cushing ulcer

A

a gastric ulcer produced by elevated intracranial pressure

(increased vagal response due to increased ICP –> increased ACh)

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28
Q

What results from acid damage? (3)

A
  1. Superficial inflammation
  2. erosion (loss of superficial epithelium)
  3. ulcer (loss of mucosal layer)
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29
Q

What is the difference between an ulcer and erosion?

A

Erosion is simply the loss of the superficial epithelium

Ulcer is the loss of the mucosal layer as well (deeper)

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30
Q

What is often given to patients in the ICU to preemptively protect against stress ulcers?

A

Proton pump inhibitors

Worried about possible shock or decreased perfusion to the stomach

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31
Q

Chronic gastritis - 2 major causes

A
  1. Autoimmune
  2. H. pylori
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32
Q

Why is there a megaloblastic anemia when there is a loss of parietal cells?

A

Parietal cells also produces intrinsic factor which is vital to the absorption of vitamin B12

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33
Q

Chronic autoimmune gastritis

A

due to autoimmune destruction of the gastric parietal cells, which are located in the body and the fundus of the stomach

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34
Q

Chronic autoimmune gastritis - what type of hypersensitivity reaction is it? Why?

A

Type 4 – b/c it’s mediated by T cells

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35
Q

Chronic autoimmune gastritis - what are 2 indicators that this damage is happening?

A

Antibodies against:

  • intrinsic factor
  • parietal cells

Note: these are NOT causing the damage, but rather an indicator that the damage is happen. The destruction of the parietal cells will release its contents and cause the production of Abs against these factors

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36
Q

Most common cause of vitamin B12 deficiency

A

Chronic autoimmune gastritis

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37
Q

Chronic autoimmune gastritis - clinical features (4)

A
  1. atrophy of the 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 for gastric adenocarcinoma (intestinal type)
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38
Q

Chronic autoimmune gastritis - why is there atrophy of the mucosa?

What else occurs to the cells along with atrophy?

A

Atrophy b/c the autoimmunity is killing the parietal cells

  • The inflammation also causes intestinal metaplasia
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39
Q

Chronic autoimmune gastritis - why is there G-cell hyperplasia?

where does it occur?

A
  • G-cells responsible for producing gastrin. Gastrin stimulates parietal cell production of gastric acid.
    • Loss of parietal cells results in achlorhydria which feedbacks to cause compensatory increase in gastrin levels.
  • G-cells are located primarily in the antrum.
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40
Q

Chronic autoimmune gastritis - why is there a megaloblastic anemia?

A

Parietal cells produce intrinsic factor – required for the absorption of vitamin B12

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41
Q

Most common form of gastritis

A

H. pylori - induced acute and chronic inflammation (~90%)

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42
Q

Where would you find H. pylori during an infection?

A

On the mucosal surfaces.

They do NOT invade the mucosa. They cause their damage by the production of ureases and proteases that weaken/destroy the mucosal defenses

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43
Q

How does H. pylori cause gastritis?

A

Production of ureases and proteases which along with the inflammation (to fight the bacteria) weaken the mucosal defenses

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44
Q

Where does H. pylori infection most commonly occur? How is it different than autoimmune gastritis?

A

Occurs primarily in antrum.

Autoimmune occurs in the body and the fundus

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45
Q

Chronic H. pylori gastritis - classical presentation

A
  1. epigastric abdominal pain
  2. increased risk for ulceration (peptic ulcer disease)
  3. gastric adenocarcinoma (intestinal type)
  4. MALT lymphoma (the chronic inflamation results in generation of germinal centers in the mucosa/gastric wall and the resulting marginal zone which recruits the post germinal center B cells)
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46
Q

Why is there an increase risk for MALT lymphoma with chronic H. pylori gastritis?

A

MALT = mucosa-associated lymphoid tissue

The chronic inflammation develops germinal centers and marginal zones in the mucosal wall. These centers will recruit the necessary cells including B cells that if chronic will increase the risk of MALT lymphomas (aka MALTomas)

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47
Q

Treatment for chronic H. pylori gastritis?

A

Triple therapy (reminds you of the 3 major symptoms)

  • ulcers
  • MALTomas
  • adenocarcinoma (intestinal metaplasia)

The therapy resolves the gastritis/ulcer and reverses intestinal metaplasia. Lastly, the resolution of the infection removes the inciting factor that can induce MALTomas

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48
Q

chronic H. pylori gastritis - how to confirm the therapy worked? (2)

A

Negative urea breath test (remember H. pylori produces ureases)

Lack of stool antigen

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49
Q

Where do peptic ulcers occur?

A

Proximal duodenum (90%)

distal stomach (10%)

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50
Q

Subtypes of peptic ulcers (2)

A

Duodenal ulcer – usually anterior duodenum, but can also occur in posterior duodenum

Gastric ulcers – usually located on the lesser curvature of the antrum

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51
Q

Most common cause of peptic ulcer disease

A

H pylori

Causes:

  • >95% of all duodenal ulcers
  • ~75% of gastric ulcers
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52
Q

Duodenal ulcers - cause(s)

A

H pylori (>95%)

ZE (Zollinger-Ellison) syndrome – gastrinoma

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53
Q

Duodenal ulcers - presentation

A

Epigastric pain that improves with meals (eating stimulates the production of protective substances such as mucin that is secreted in preparation for the acid that comes along with meals)

  • the ulcer is typically downstream of the Brunner glands (glands that secrete mucous) which is why it improves with meals. if it were upstream (ie gastric ulcers), the pain would not subside, but actually worsen (because of increased acid)
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54
Q

Duodenal ulcers - what is characteristically seen on biopsy?

A

hypertrophy of Brunner glands (glands in the duodenum that produce mucous in response to meals/acid)

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55
Q

Duodenal ulcers - Where do they usually arise?

A

Anterior duodenum

However, when they are present in the posterior duodenum (rarer), they may result in bleeding from the gastroduodenal artery or acute pancreatits

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56
Q

Duodenal ulcers - what is at risk if these are found in the posterior duodenum?

A
  • Bleeding from the gastroduodenal artery (runs along the posterior duodenal wall)
  • acute pancreatitis
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57
Q

Gastric ulcers - most common cause(s)

A
  • H pylori (75%)
  • NSAIDs (20%)
  • bile reflux
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58
Q

Gastric ulcers - clinical presentation

A

epigastric pain that worsens with meals (increased acid causes more pain. The ulcer lies above the Brunner glands, so there is no increased protection, but rather suffers from the increased acid)

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59
Q

Gastric ulcers - where are they classically located?

A

lesser curvature of the antrum

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60
Q

Gastric ulcers - if they rupture, what are you worried about?

A

Risk of bleeding from the left gastric artery that supplies the lesser curvature

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61
Q

Which ulcers improves with meals? Which worsens? Why?

A
  • Duodenal ulcers improve with meals
  • Gastric ulcers worsens.

When you eat a meal, there is increased acid production by the parietal cells (located in the body and fundus of the stomach) along with increased production of mucin by the Brunner glands (located in the duodenum). to protect against the increased acid. If ulcer is downstream of Brunner glands (ie duodenal ulcers), then they improve with meals due to increased mucin. If upstream of the Brunner glands, then the increased acid will worsen the pain due to increased acid.

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62
Q

What else is on the Dx of ulcers besides infection and NSAIDs?

A

carcinoma

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63
Q

Where are the majority of peptic ulcers located?

A

Duodenum

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64
Q

What is the risk of carcinoma when a patient has duodenal ulcers?

A

Duodenal ulcers are almost never malignant

Carcinoma in this region is extremely rare

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65
Q

What is the risk of carcinoma when a patient has gastric ulcers?

A

Much greater than the duodenal ulcers.

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

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66
Q

How do you distinguish between benign and malignant peptic ulcers?

A

Benign

  • small (<3cm)
  • sharply demarcated (“punched-out”)
  • surrounded by radiating folds of mucosa

Malignant

  • large
  • irregular w/ heaped up margins
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67
Q

What is required for definitive diagnosis of carcinoma?

A

biopsy

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68
Q

Gastric carcinoma

A

Malignant proliferation of surface epithelial cells (adenocarcinoma)

subclassified into intestinal and diffuse types

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69
Q

Gastric carcinoma - subclassifications (2)

A

Intestinal type (more common)

Diffuse type

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70
Q

Gastric carcinoma (intestinal type) - where does it most commonly appear?

A

The lesser curvature of the antrum (similar to gastric ulcer)

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71
Q

Gastric carcinoma (intestinal type) - risk factors (3)

A
  1. intestinal metaplasia (due to H pylori and autoimmune gastritis)
  2. nitrosamines in smoked foods (Japan)
  3. blood type A
    • an easy way to remember this is carcinoma is typically abreviated “CA”
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72
Q

Gastric carcinoma (diffuse type) - classical characteristics

A
  • Signet ring cells that diffusely infiltrate the gastric wall
  • The infiltration of these cells causes a response in the form of desmoplasia (development of fibrous tissue and blood vessels) that results in the thickening of the stomach wall
  • NOT associated with H pylori, intestinal metaplasia, or nitrosamines
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73
Q

Major differences between the intestinal and diffuse type of gastric carcinomas

A

Intestinal – large irregular ulcers commonly due to intestinal metaplasia, nitrosamines and/or blood type A

Diffuse – no ulcers. Diffuse thickening of gastric wall caused by desmoplasia as a result of infiltration of signet ring cells

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74
Q

What are signet ring cells? Why are they called that?

A

signet ring cells are cells with their nucleus pushed off to one side due to the excessive production of mucuous (stored in the cytoplasm)

Most frequently associated with stomach cancer, but can arise in other tissues such as prostate, bladder, gallbladder, breast, colon, ovarian stroma and testies.

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75
Q

What type of gastric carcinoma is associated with early satiety? Why?

A

Diffuse type. The thickening of the gastric wall impairs the ability to expand the gastric wall.

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76
Q

Gastric carcinomas - clinical presentation

A

Presents late w/

  • weight loss
  • abdominal pain
  • anemia
  • early satiety (occurs with both, but more prominent in diffuse type)
  • acanthosis nigricans
  • Leser-Trelat sign (dozens of seborrheic keratosis under skin that arise all of sudden)
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77
Q

Gastric carcinomas - what are 2 high yield features that are rare, but very highly associated with these disease states?

A
  1. acanthosis nigricans
  2. Leser-Trelat sign (dozens of seborrheic keratosis under skin that arise all of sudden)
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78
Q

What lymph node(s) do gastric carcinomas often spread to?

A

Left supraclavicular node (aka Virchow node – one of the many nodes that drains the stomach)

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79
Q

Gastric carcinomas - distant metastatic sites

A

Intestinal type – periumbilical region (Sister Mary Joseph nodule)

Diffuse type – bilateral ovaries (Krukenberg tumor)

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80
Q

Duodenal atresia

A

congenital failure of duodenum to canalize

associated with Down syndrome

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81
Q

Duodenal atresia - what disease is it associated with?

A

Down syndrome

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82
Q

Duodenal atresia- clinical features

A
  • Polyhydraminos
  • Distension of stomach and blind loop of duodenum (‘double bubble sign)
  • Bilious vomiting
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83
Q

Duodenal atresia - what is seen on xray? (Classic finding)

Why does it exist?

A

“Double bubble”

The atresia causes a blind loop (basically a closing) of the duodenum which ultimately causes distension all upstream.

The pyloric sphincter will remain tight and cause a separate of the distention into 2 bubbles that gives off the classic finding on xray

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84
Q

Duodenal atresia - why is there polyhydraminos?

A

Urine of baby is the major component of AF. The volume is normally decreased via the ingestion.

Without being able to pass it through, there will be less held within the baby and more outside in the AF.

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85
Q

Duodenal atresia - what type of vomiting occurs? Why?

A

bilious vomiting

The vomitting is occurring at a point after the bile has merged with the food.

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86
Q

Fake vs real diverticulum?

A

Real – includes all 3 layers of the bowel wall (ie Meckel Diverticulum)

Fake – does NOT include all 3 layers (ie Zenker Diverticulum – outpouching of only the muscle wall)

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87
Q

Meckel Diverticulum

A

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

Arises due to failure of the vitelline duct to involute

Rule of 2’s

  • seen in 2% of the population (most common congenital anomaly of the GI tract)
  • 2 inches long
  • located in the small bowel within 2 feet of the ileocecal valve
  • can present in the first 2 years of life
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88
Q

In early embryological development, how does the midgut receive nutrients?

A

Receives nutrients from the yolk sac via the vitelline duct

  • duct forms in the 4th week and involutes by the 7th week
  • persistence of the duct –> Meckel Diverticulum
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89
Q

Vitelline duct - what is its purpose?

A

“vital” for receiving nutrients in early life.

Forms ~4th week and supplies the midgut with nutrients from the yolk sac.

Involutes by the 7th week.

  • failure to involute –> Meckel Diverticulum
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90
Q

Vitelline duct - what happens when it fails to involute completely? partially?

A

Partial failure –> Meckel diverticulum

Complete failure –> passing of meconium(the dark green substance forming the first feces of a newborn infant) via the umbilicus

  • basically leaking feces as it descends the gut (due to passage remaining open)
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91
Q

Meckel Diverticulum - rule of 2s

A
  • seen in 2% of the population (most common congenital anomaly of the GI tract)
  • 2 inches long
  • located in the small bowel within 2 feet of the ileocecal valve
  • can present in the first 2 years of life
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92
Q

Meckel Diverticulum - clinical characteristics

A

Most often asymptommatic. However if it does cause symptoms:

Rule of 2s

  • seen in 2% of the population (most common congenital anomaly of the GI tract)
  • 2 inches long
  • located in the small bowel within 2 feet of the ileocecal valve

Can present in the first 2 years of life with:

  • bleeding (due to heterotopic gastric mucosa)
  • volvulus
  • intussusception
  • obstruction (mimics appendicitis)
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93
Q

Meckel Diverticulum - How does bleeding occur?

A

Heterotopic (“in the wrong place”) gastric mucosa present in the diverticulum.

  • gastric mucosa produces gastric acid which will cause bleeding due to lack of protective substances (ie mucin, bicarb, etc…)
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94
Q

Volvulus

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)

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95
Q

Volvulus - biggest concern/complication

A

Twisting of the bowel cuts off blood suply resulting in infarction

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96
Q

Volvulus - most common location in elderly vs young adults. Why do they occur there?

A

Young adults – cecum

Elderly – sigmoid colon

Volvulus occurs in these places most commonly because there is a ton of mesentery that provides the redundancy to allow for twisting w/o clinical symptoms

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97
Q

Intussusception

A

Telescoping of proximal segment of bowel forward into distal segment

  • pulled forward by peristalsis –> resulting in obstruction and disruption of blood supply with infarction
    • infraction will create currant jelly stools
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98
Q

Intussusception - what is required for this to occur?

A

Presence of a leading edge (focus of traction – basically something to hook onto in order to drag the rest forward during peristalsis)

  • Children (most common) – lymphoid hyperplasia (due to rotavirus)
    • Usually arises in terminal ileum, lading to intussusception into the cecum
  • Adults (most common) – tumor
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99
Q

Intussusception - most common cause in children

A

Lymphoid hyperplasia (ie due to rotavirus)

  • viral infection –> massive lymphoid hyperplasia –> development of Peyer’s patches as the leading edges
  • Usually arises in terminal ileum –> intussusception into the cecum
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100
Q

Intussusception - most common cause in adults

A

Tumor - creating the leading edge

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101
Q

Small bowel infarction - why does it occur?

A

Small bowel is high susceptible to ischemic injury because it does a lot of the digestion (requires a lot of ATP)

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102
Q

Small bowel infarction - what is required for the infarction to occur?

A

Transmural infarction (requires the infarction to be transmural or across the entire wall)

  • thrombosis/embolism of SMA (feeds into the bowel)
  • thrombosis/embolism of mesenteric vein (drains the bowel)
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103
Q

What can occur to the small bowel due to marked hypotension?

A

Hypotension reduces the blood flow and can cause the infarction of the mucosa layer while sparing the submucosa and all the other superficial layers that receive blood supply first before reaching the mucosa

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104
Q

Small bowel infarction - clinical features

A
  • abdominal pain
  • bloody diarrhea
  • decreased bowel sounds
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105
Q

Causes of thrombosis in the SMA (superior mesenteric artery)

A

Most commonly:

  • atrial fibrillation (results in stasis in the atrium –> hypercoagulable)
  • vasculitis (ie polyarteritis nodosa – remember that clinical features included melena and abdominal pain)
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106
Q

Causes of thrombosis in the mesenteric vein

A

Most commonly:

  • polycythemia vera (increased viscosity –> increased coagulable state)
  • lupus anticoagulant
107
Q

Lactose intolerance

A

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

  • lactase normally breaks down lactose into glucose and galactose
108
Q

What does lactase normally break down lactose into?

A

glucose and galactose

109
Q

In terms of carbohydrates, what can our gut absorb?

A

We can ONLY absorb monosaccarides. More specifically, we only have the enzymes to absorb:

  • fructose
  • galactose
  • glucose

The other sugars typically are excreted or digested/fermented by bacteria in our gut (creating flatuence)

110
Q

Which sugars can our body absorb?

A

Can only absorb monosaccarides:

  • fructose
  • galactose
  • glucose
111
Q

Lactose intolerance - clinical features

A
  • abdominal distension (fermentation of sugars by bacteria)
  • diarrhea (lactose is osmotically active)

Occurs in consumption of milk products (high in lactose)

112
Q

Lactose intolerance - how does it arise? (3)

A
  1. Congential (rare autosomal recessive disorder)
  2. Acquired (often develops in late childhood)
  3. Temporary deficiency is seen after small bowel infection (lactase is highly susceptible to injury)
113
Q

Celiac disease

A

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

associated with HLA-DQ2 and DQ8

114
Q

Celiac disease - genetic association

A

HLA-DQ2

HLA-DQ8

115
Q

Celiac disease - what is the pathogenic component responsible in gluten?

Why is it pathogenic? (ie how is processed by body that stimulates response?)

A

Gliadin

  1. Once absorbed, gliadin is deamidated by tissue transglutaminase (tTG)
  2. deamidated gliadin is presented by APCs via MHC class II
  3. Helper T cells mediate tissue damage
116
Q

Celiac disease - what type immune reaction is this disease process? What cell type mediates the damage?

A

Type IV hypersensitivity mediated by helper T cells

117
Q

Celiac disease - clinical presentation

A
  1. Children
    • abdominal distension
    • diarrhea
    • failure to thrive
  2. Adults
    • chronic diarrhea
    • bloating
  3. Dermatitis herpetiformis
118
Q

Celiac disease - clinical presentation in children

A
  • abdominal distension
  • diarrhea
  • failure to thrive
  • Dermatitis herpetiformis
119
Q

Celiac disease - clinical presentation in adults

A
  • chronic diarrhea
  • bloating
  • Dermatitis herpetiformis
120
Q

Dermatitis herpetiformis

A
  • Small herpes-like vesicle that arise on the skin
  • Characteristically seen in celiac disease
  • Due to IgA deposition at the tips of the dermal papillae –> results in blistering that resembles herpes
  • Resolves with gluten-free diet
121
Q

Dermatitis herpetiformis - why does it occur? (mechanism)

A

Deposition of IgA at the tips of the dermal papillae –> disruption/destruction of the dermal/epidermal junction –> blister formation at the tips of the dermal papillae – multiple blisters that resemble herpes

122
Q

Dermatitis herpetiformis - treatment

A

gluten-free diet

123
Q

Celiac disease - what antibodies are found on labs?

A

IgA antibodies against

  • endomysium
  • tTG
  • gliadin

IgG antibodies are also present and useful in individuals with IgA deficiency (increased incidence of IgG deficiency in celiac disease)

124
Q

Celiac disease - what is classically seen on histology as a result of this disease’s inflammatory state?

A
  • Flattening of vili
  • hypertrophy of crypts
  • increased intraepithelial lymphocytes

Figure (normal on left, celiac on right)

125
Q

What part of the small bowel does celiac disease preferentially hit?

A

Most prominent in the duodenum.

Jejunum and ileum less involved

126
Q

Celiac disease - treatment

A

gluten-free diet

127
Q

Celiac disease - late complications

A
  • Small bowel carcinoma
  • T-cell lymphoma (EATL – enteropathy associated Tcell lymphoma)

May present despite good dietary control

128
Q

What important vitamin is absorbed in the jejunum?

A

Folic acid

129
Q

What important vitamin is absorbed in the ileum?

A

Vitamin B12

130
Q

Tropical sprue

A

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

131
Q

What disease is tropic sprue similar to? How is it different?

A

Similar to celiac disease

Different in that tropical sprue:

  • occurs in tropical regions (ie Carribean)
  • arises after infectious diarrhea and responds to antibiotics
  • damage is most prominent in the jejunum and ileum; duodenum is less commonly involved
    • secondary vitamin b12 (ileum) and folate deficiency (jejunum) may ensue
132
Q

Whipple disease

A

Systemic tissue damage characterizd by macrophages loaded with Tropheryma whippelii

  • partially destroyed organisms are present in macrophage lysosomes (positive for PAS)
133
Q

Whipple disease - what is the bug responsible?

A

Tropheryma whippelii

134
Q

Whipple disease - What is classicially found on IHC? What stain is used?

A

PAS (periodic acid shift)

positive for partially destroyed organisms present in macrophage lysosomes

135
Q

Where does fat digestion start? By what enzymes?

What occurs in fat digestion?

A
  1. Fat digestion starts with breakdown of lipids via lipases from salivary glands and pancreas
  2. emulsified into smaller droplets in the stomach and the small bowel
    • bile helps in this process
  3. produces a product that can easily diffuse through the enterocyte
    lipid droplets diffuse through the enterocytes
  4. Enterocytes package the lipid droplets into chylomicrons
  5. chylomicrons diffuse into the lamina propria filling up the lacteals (lymphatic spaces)
  6. from the lymphatics, the chylomicrons drain empty into the blood stream via the thoracic duct
136
Q

How does fat (from digestion) get into the blood stream?

A

enterocyte –> chylomicrons –> lacteals (lymphatic spaces in the lamina propria of small bowel) –> lymphatics –> blood (via thoracic duct)

137
Q

Whipple disease - classic site of involvement

A

Most common site

  • Small bowel lamina propria

Other common sites

  • synovium of joints (arthritis)
  • cardiac valves
  • lymph nodes
  • CNS
138
Q

Whipple disease - classic clinical features when there is small bowel involvement(2)

Why do they occur?

A

Fat malabsorption and steatorrhea

  1. Macrophages come into the lamina propria to clean up the bugs. They compress the lacteals (lymphatic spaces – what chylomicrons use to get into the lymphatics and then the blood)
  2. Chylomicrons cannot be transferred from enterocytes to lymphatics
  3. Results in fat malabsorption and steatorrhea
139
Q

Whipple disease - pathogenesis of symptoms

A

Macrophages compress lacteals and block the ability for chylomicrons to be transferred from enterocytes to lymphatics

  • results in fat malabsorption and steatorrhea
140
Q

Abetalipoproteinemia

A

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

Clinical features:

  • malabsorption and steatorrhea – defective chylomicron formation (requires B-48)
  • absent plasma VLDL and LDL (requires B-100)
141
Q

What apolipoprotein is required for chylomicron formation?

A

Apolipoprotein B-48

142
Q

What apolipoprotein is required for VLDL and LDL formation?

A

Apolipoprotein B-100

143
Q

What clinical feature results from lack of apolipoprotein B-48?

A

B-48 required for chylomicron formation –> malabsorption and steatorrhea

144
Q

What clinical feature results from lack of apolipoprotein B-100?

A

B-100 required for VLDL and LDL –> absent plasma VLDL and LDL

145
Q

Neuroendocrine tumors – what cancer has the worst prognosis/grade? the lowest grade?

A

Worst progrnosis: small cell carcinoma of lung

Lowest/best: carcinoid

146
Q

Carcinoid tumor

A

Low-grade malignancy of neuroendocrine cells

  • tumor cells contain neurosecretory granules that are positive for chromogranin

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

  • grows as a submucosal polyp-like nodule
147
Q

Carcinoid tumor – what marker is classically found on IHC?

A

tumor cells contain neurosecretory granules that are positive for chromogranin

148
Q

Carcinoid tumor - what is neuroendocrine hormone commonly secreted?

A

5HT (serotonin)

149
Q

Carcinoid tumor - hormonal effect of a primary tumor (no metastasis)?

A

Nothing…

5HT is released into portal circulation and metabolized by liver monoamine oxidase (MAO) into 5-HIAA which is then secreted in the urine.

The hormonal effect only occurs after either metastasis occurs or the tumor develops to the point where it can overwhelm the liver’s capacity to degrade 5HT

150
Q

Breakdown of serotonin – what is the enzyme responsible? what is the breakdown product?

A

5HT is broken down by monoamine oxidase (MAO) into 5-HIAA

151
Q

Carcinoid tumor - most common site of involvement

A

small bowel; but can occur anywhere in the gut

152
Q

Carcinoid tumor - what is required for the hormones secreted to have an effect?

A

Requires metastasis to liver

  • allows 5HT to bypass liver metabolism
  • released into the hepatic vein (which has tiny connections to the systemic circuit via hepato-systemic shunts)
    • carcinoid syndrome
    • carcinoid heart disease
153
Q

Carcinoid syndrome - classic findings

A

Triad

  1. bronchospasm
  2. diarrhea
  3. flushing (of skin)

Can be triggered by alcohol or emotional stress which stimulate 5HT release from tumor

154
Q

Carcinoid syndrome - what can trigger symptoms?

A

Alcohol or emotional stress which stimulate 5HT release from tumor

155
Q

Carcinoid heart syndrome

A

Due to effect of 5HT secreted by carcinoid tumor

Characterized by right-sided valvular fibrosis (increased collagen) which results in:

  • tricupsid regurgitation
  • pulmonary valve stenosis

Does NOT occur on left side (degraded by MAOs in left lung)

156
Q

Carcinoid heart syndrome - what clinical features would you find?

A

5HT affects the valves only on the right side (degraded before it reaches left by pulmonary MAOs)

  • Right-sided valvular fibrosis (due to increased collagen deposition)
    • tricuspid regurgitation + pulmonary valve stenosis
157
Q

Carcinoid heart syndrome - which part of the heart does it affect? why?

A

Only affects the right side.

5HT goes through the pulmonary circulation in order to reach the left which contains MAOs that will degrade/metabolize the 5HT before it reaches the lung

158
Q

Most common cause of acute abdomen

A

Acute appendicitis – an acute inflammation of the appendix

159
Q

Acute appendicitis - most likely/common cause(s)

A

Related to obstruction of the appendix

  • children –> lymphoid hyperplasia (just like in intussusception
  • adults –> fecalith (stone made from feces)
160
Q

Acute appendicitis - clinical features

A
  • periumbilical pain –> pain eventually localizes to right lower quadrant (McBurney point)
  • fever
  • nausea
  • rupture results in peritonitis w/ guarding and rebound tenderness
  • periappendiceal abscess is a common complication
161
Q

Acute appendicitis - what symptoms would present if there is rupture?

A

Guarding and rebound tenderness

162
Q

Acute appendicitis - common complication(s)

A

periappendiceal abscess

163
Q

Inflammatory bowel disease

A

chronic, relapsing inflammation of the bowel

possibly due to abnormal immune response to enteric flora (but generally it is idiopathic)

164
Q

Inflammatory bowel disease - what population does it classically present?

What does it present as?

A

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
165
Q

Inflammatory bowel disease - how is the diagnosis made?

A

Diagnosis by exclusion

Symptoms mimic other causes of bowel inflammation that need to be first rule out (ie infection)

166
Q

Inflammatory bowel disease - subclassifications (2)

A

Ulcerative colitis

Crohn disease

167
Q

Classic histological finding for ulcerative colitis

A

Crypt abscesses with neutrophils

168
Q

Classic histological finding for Crohn Disease

A

lymphoid aggregates with granulomas (40% of cases) alongside normal crypts

169
Q

Ulcerative colitis - what kind of wall involvment is seen?

A

mucosal and submucosal ulcers

170
Q

Crohn disease - what kind of wall involvment is seen?

A

Full-thickness inflammation with knife-like fissures

171
Q

What locations does ulcerative colitis affect?

A

Begins in rectum and can extend proximally up to the cecum (predominantly affects the colon/large-intestine)

  • will NOT extend into the small bowel
  • involvement in continuous
  • remainder of GI tract is unaffected
172
Q

What locations does Crohn disease affect?

A

Anywhere from mouth to anus with skip lesions

  • Terminal ileum is the most common site
  • rectum is the least common
173
Q

Most common site of involvement in Crohn Disease

Least common?

A

Most common: terminal ileum

Least common: rectum

174
Q

Ulcerative colitis - clinical symptoms

A

Left lower quadrant pain (rectum)

bloody diarrhea

175
Q

Crohn disease - clinical symptoms

A

Right lower quadrant pain (ileum)

non-bloody diarrhea

176
Q

Ulcerative colitis - gross appearance

A

Pseudopolyps (numerous bumps as a response to the healing of ulcerations)

Loss of haustra (‘lead pipe’ sign on imaging)

  • haustra (foldings) – shown in yellow
  • lead pipe (due to loss of the folds) – circled in red
177
Q

Crohn disease - gross appearance

A

Cobblestone mucosa (representative of the healing process)

  • shown in image

creeping fat and strictures (due to myofibroblasts)

  • ‘string-sign’ on imaging
178
Q

Ulcerative colitis - complications

A
  • Toxic megacolon (enlarged colon w/ toxic wastes; risk of rupture)
  • carcinoma (risk is based on extent of colonic involvement and duration of disease – generally not of concern until >10 years)
179
Q

Crohn disease - complications

A
  • Malabsorption (due to damage to small bowel where a lot of reabsorption normally takes place) with nutritional deficiency
  • calcium oxalate nephrolithiasis
  • fistula formation (if wall ruptures, the ruptured opening can form another connection)
  • carcinoma (if colonic disease is present)
180
Q

What factors determine the risk for carcinoma in the inflammatory bowel diseases? (2)

A
  1. extent of colonic involvement
  2. duration of disease (usually not of concern until >10 years of disease)
181
Q

How does smoking affect the inflammatory bowel diseases?

A

Smoking:

  • Protects against ulcerative colitis
  • Increases risk for Crohn disease
182
Q

Inflammatory bowel disease - extraintestinal manifestations

A
  • arthritis (peripheral joints, ankylosing spondylitis, sacrolitis, migratory polyarthritis)
  • uveitis
  • erythema nodosum
  • pyoderma gangrenosum
  • primary sclerosing cholangitis
  • p-ANCA
183
Q

Histological differences between Crohn disease and ulcerative colitis?

A
184
Q

Wall involvement - difference between ulcerative colitis (UC) and Crohn disease?

A

UC: mucosal and submucosal surfaces

Crohn: full-thickness inflammation with knife-like fissures

185
Q

Location - difference between ulcerative colitis (UC) and Crohn disease?

A

UC: begins in rectum and extends proximally up to the cecum (only colonic involvement); remainder of GI tract unaffected. Involvement is continuous

Crohn: anywhere from mouth to anus with skip lesions; terminal ileum most common site

186
Q

Symptoms - difference between ulcerative colitis (UC) and Crohn disease?

A

UC: LLQ (rectum) w/ bloody diarrhea

Crohn: RLQ (ileum) w/ non-bloody diarrhea

187
Q

Histological hallmark - difference between ulcerative colitis (UC) and Crohn disease?

A

UC: Crypt abscesses w/ neutrophils

Crohn: lymphoid aggregates w/ granulomas (~40% of cases)

188
Q

Complications - difference between ulcerative colitis (UC) and Crohn disease?

A

UC: obstruction resulting in toxic megacolon

Crohn: malabsorption w/ nutritional deficiency; calcium oxalate nephrolithasis; fistula formation

Both diseases have carcinoma risk (present in Crohn’s if there is colonic disease)

189
Q

Hirschsprung disease

A
  • Defective relaxation and peristalsis of rectum and distal sigmoid colon
    • associated with Down Syndrome
  • Congenital failure of ganglion cells (neural crest-derived) to descent into myenteric and submucosal plexus
190
Q

What 2 gastrointestinal diseases are associated with Down syndrome?

A

Hirschsprung disease

Duodenal atresia

191
Q

Hirschsprung disease - cause?

A

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

192
Q

What are the 2 sets of ganglion cells in the gut?

A
  1. Myenteric (Auerbach) plexus – regulates motility and relaxation
  2. Submucosal (Meissner) plexus – regulates blood flow, secretions and absorptions
193
Q

Layers of vessel wall

A

Lumen

  • muscosa
  • submucosa
  • musclaris propria
  • serosa

Blood

194
Q

Myenteric (Auerbach) plexus - where is located? what does it do?

A

Located in between the inner circular and outer longitudinal layer of the musclaris propria

Responsible for motility and relaxation

195
Q

Submucosal (Meissner) plexus - where is located? what does it do?

A

Located within the submucosa layer

Responsible for regulating blood flow, secretions and absorptions

196
Q

What are the embryological origins of the ganglion cells of the gut?

A

Neural crest derived

197
Q

Hirschsprung disease - what is the major cause of all the symptoms?

A

The lack of ganglion cells in the gut results in lack of motility and relaxation of the vessel walls.

The lack of motility –> obstruction (bowel doesn’t move)

the lack of relaxation –> creates a choke point making it easier to create an obstruction

In the end, the result in an obstruction that can cause:

  • Failure to pass meconium (the dark green substance that forms the first feces of a newborn infant)
  • Empty rectal vault on digital rectal exam (DRE)
  • Massive dilatation (megacolon) of bowel proximal to obstruction with risk for rupture (inability to relax properly and obstruction from lack of motility –> massive dilatation behind block)
198
Q

Hirschsprung disease - clinical features

A

All based on obstruction (due to lack of good persitalsis/relaxation)

  • Failure to pass meconium (the dark green substance that forms the first feces of a newborn infant)
  • Empty rectal vault on digital rectal exam (DRE)
  • Massive dilatation (megacolon) of bowel proximal to obstruction with risk for rupture (inability to relax properly and obstruction from lack of motility –> massive dilatation behind block)
199
Q

Hirschsprung disease - how is the diagnosis made?

A

Requires rectal suction biopsy – reveals lack of ganglion cells

  • has to be suction biopsy because normal biopsy only captures the mucosa which doesn’t contain any ganglion cells. Suction is to pull the submucosa into the biopsy
200
Q

What kind of special biopsy is needed for diagnosis of Hirschsprung disease?

A

Rectal suction biopsy. Normal biopsy will only get the mucosa without any ganglion cells. Need suction to suck in some of the submucosa which will contain the cells you are looking for (which may be absent)

201
Q

Hirschsprung disease - treatment

A

resection of the involved bowel and leave behind sections that do have ganglion cells

202
Q

Colonic diverticula

A

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

Related to wall stress

Usually asymptomatic; by can have many complications

  • Rectal bleeding (hematochezia)
  • Diverticulitis
  • Fistula
203
Q

Colonic diverticula - what kind of diverticulum is it? Why?

A

False diverticulum – outpouching of only the mucosa and submucosa through the muscularis propria

204
Q

Colonic diverticula - major cause

A

Wall stress

  • Associated with constipation, straining and low-fiber diet – commonly seen in older adults (risk increases with age)
  • Can also arise where the vasa recta traverse the muscularis propria (weak point in the colonic wall) – sigmoid colon is the most common location
205
Q

What factors are associated with vessel wall stress that can cause colonic diverticulum? (4)

A
  1. constipation
  2. straining
  3. low-fiber diet
  4. where the vasa recta traverses the muscularis propria (sigmoid colon)
206
Q

How can the vasa recta cause colonic diverticula? Where does it most commonly occur?

A

The vasa recta traverses the muscular propria which creates a weak point in vessel wall

Sigmoid colon is the most common location

207
Q

Colonic diverticula - complications

A
  • rectal bleeding aka hematochezia (diverticula sometimes right alongside the vasa recta)
  • diverticulitis (obstruction by fecal materials –> inflammation)
    • presents with appendicits-like symptoms in the left lower quandrant
  • fistula – inflammed diverticulum ruptures and attaches to a local structure
    • colovesicular (colon – bladder) fistula with air (or stool) in urine
208
Q

How does diverticulitis present clinically?

A

appendicitis-like symptoms in the left lower quandrant

remember – obstruction results in inflammation behind it causing inflammation of the diverticula (hence diverticulitis)

209
Q

Colonic diverticula fistula – what is a common fistula that forms? How does it present?

A

Colovesicular fistula (colon – bladder)

Presents with air (or stool) in urine

210
Q

Angiodysplasia

A
  • Acquired malformation of mucosal and submucosal capillary beds
  • usually arises in the cecum and right colon due to high wall tension
  • rupture classically presents as hematochezia in an older adult
211
Q

Angiodysplasia - Why and where does it occur?

A

Due to high wall tension

Usually arises in cecum and right colon

212
Q

Angiodysplasia - if there is a rupture, how does it present?

A

hematochezia

213
Q

Results of high stress on the colon?

A

Left colon –> diverticula

Right colon –> angiodysplasia

Both can result in hematochezia

214
Q

Hereditary hemorrhagic telangiectasia

A

Autosominal dominant disorder resulting in thin-walled blood vessels in the mouth and GI tract (can occur anywhere between the nasopharyns to the GI tract)

  • Thin-walled –> more prone to stress –> easier to for blisters/diverticula

Rupture presents as bleeding

215
Q

Ischemic colitis

A

Ischemic damage to the colon – usually at the splenic flexure (watershed area of SMA)

atherosclerosis of SMA is the most common cause

Presents as:

  • postprandial (after meals) pain (increased energy requirement after meals acts like a stressor that will bring about the pain that would otherwise go unnoticed)
  • weight loss (pain from the meals –> less eating –> weight loss)
216
Q

Ischemic colitis - clinical presentation

A
  • postprandial pain (increased energy requirement after meals acts like a stressor that will bring about the pain that would otherwise go unnoticed)
  • weight loss (pain from the meals –> less eating –> weight loss)
217
Q

Ischemic colitis - where does it usually occur? why?

A

Usually occurs at the splenic flexure

Ischemia results in damage to the furthest reached areas. Splenic flexure is the last thing fed by the SMA (SMA is also the longest artery feeding into the colon)

218
Q

Ischemic colitis - most common cause

A

Atherosclerosis of SMA

219
Q

Irritable bowel syndrome

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 pathologic changes (biopsy would appear normal)
  • increased dietary fiber may improve symptoms
220
Q

Irritable bowel syndrome - what is the cause?

A

Related to disturbed intestinal motility, however there are no identifiable pathologic changes (biopsy would appear normal)

221
Q

Irritable bowel syndrome - what can help to improve symptoms? why?

A

syndrome thought to be caused by disturbed intestinal motility

Dietary fiber may improve symptoms (helps to move along the feces)

222
Q

Colonic polyps

A

Raised protrusions of colonic mucosa

Most common types

  • hyperplastic (due to hyperplasia of glands)
  • adenomatous (neoplastic proliferation of glands via adenoma-carcinoma sequence)
223
Q

Hyperplastic polyps

A
  • Due to hyperplasia of glands
  • Classically shows a ‘serrated’ appearance on microscopy
  • Most common type of polyp; usually arises in the left colon (rectosigmoid)
  • Benign, with no malignant potential
224
Q

Hyperplastic polyps - cause?

A

Hyperplasia of glands – benign with no malignant potential

225
Q

Hyperplastic polyps - classic appearance on microscopy

A

‘serrated’

226
Q

Colonic polyps - which ones are benign? malignant?

A

Most common are the hyperplastic and adenomatous polyps

  • Hyperplasic – benign with no malignant potential
  • adenomatous – neoplastic proliferation that can progress to carcinoma via the adenoma-carcinoma sequence
227
Q

Most common type of colonic polyp? 2nd most common?

A

Most common – hyperplastic

2nd most – adenomatous polyp

228
Q

Adenomatous polyps

A

Due to neoplastic proliferation of glands – 2nd most common type of colonic polyp

Benign, but pre-malignant – may progress to adenocarcinoma via the adenoma-carcinoma sequence

229
Q

Adenomatous polyps - how does it progress to carcinoma?

A

Adenoma-carcinoma sequence

  1. APC (adenomatous polyposis coli gene) mutations (sporadic or germline) increase risk for formation of polyp
  2. K-ras mutation leads to formation of the polyp
  3. p53 mutation AND increased expression of COX allow for progression to carcinoma
230
Q

Adenoma-carcinoma sequence

A

Describes the molecular progression of normal colonic mucosa –> adenomatous polyp –> carcinoma

  1. APC (adenomatous polyposis coli gene) mutations (sporadic or germline) increase risk for formation of polyp
  2. K-ras mutation leads to formation of the polyp
  3. p53 mutation AND increased expression of COX allow for progression to carcinoma
231
Q

What gene increases the risk for polyp formation? What role does the gene play in cancer?

What disease is associated?

A

APC (adenomatous polyposis coli gene) – a tumor suppressor gene located on chromosome 5

Familial adenomatous polyposis (FAP) disease

232
Q

What gene is associated with the formation of the colonic polyp? What role does the gene play in cancer?

A

K-ras – proto-oncogene (cell cycle regulator)

233
Q

What gene mutations is required for the progression of a colonic polyp to carcinoma?

What can be done to impede this progression?

A
  • p53 mutation
  • increased expression of COX

Aspirin impedes progression from adenoma to carcinoma

234
Q

Colonic polyps - how is screening done?

What is the goal of the screening?

A
  • colonoscopy
  • testing for fecal occult blood (polyps are usually clinically silent, but can bleed)

Goal is remove adenomatous polyps before progression to carcinoma

235
Q

How do you distinguish between hyperplastic and adenomatous colonic polyp on colonscopy?

A

You can’t. They look identical. Hence, all polyps are removed and examined microscopically.

Greatest risks for progression

  • size > 2cm
  • sessile growth (grows flat rather than outwards)
  • villous histology
236
Q

What characteristics are used to determine the risk of progression from polyp to carcinoma?

A
  • size > 2cm
  • sessile growth (grows flat rather than outwards)
  • villous histology
237
Q

Familial Adenomatous Polyposis (FAP)

A
  • Autosomal dominant disorder characterized by 100s to 1000s of adenomatous colonic polyps
  • Due to APC mutation (chromosome 5) – increases risk/propensity to develop adenomatous polyps throughout the colon and rectum
  • Colon and rectum are removed prophylactically; otherwise all patients develop carcinoma by 40 years of age
238
Q

Familial Adenomatous Polyposis (FAP) - where is disease most likely to hit?

A

Colon and rectum

239
Q

Familial Adenomatous Polyposis (FAP) - If a patient has been found to have this disease, what is the treatment? What happens if not treated?

A

Colon and rectum and removed prophylactically.

Otherwise, almost all patients develop carcinoma by 40 years of age

240
Q

Gardner syndrome

A

Familial Adenomatous Polyposis (FAP) with fibromatosis and osteomas

  • fibromatosis: non-neoplastic proliferation of fibroblasts
    • arises in retroperitoneum (desmoid) and locally destroys tissue
  • osteoma: benign tumor of bone that usually arises in the skull
241
Q

Fibromatosis

A
  • non-neoplastic proliferation of fibroblasts
  • arises in retroperitoneum (desmoid) and locally destroys tissue
242
Q

Osteoma

A

Benign tumor of bone that usually arises in skull

243
Q

Turcot syndrome

A

Familial Adenomatous Polyposis (FAP) + CNS tumors (medulloblastoma and glial tumors)

244
Q

Juvenile polyp

A

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

  • Usually presents as a solitary rectal polyp that prolapses and bleeds
245
Q

Juvenile polyposis

A

Multiple juvenile polyps in the stomach and colon

Large number of juvenile polyps increase the risk of progression to carcinoma (but otherwise normally relatively benign)

246
Q

Peutz-Jeghers Syndrome

A
  • Hamartomatous (benign) polyps throughout the GI tract and mucocutaneous hyperpigmentation (freckle-like spots) on lips, oral mucosa, and genital skin;
  • autosomal dominant disorder
  • increased risk for colorectal, breast, and gynecologic cancer
247
Q

Peutz-Jeghers Syndrome - genetics

A

autosomal dominant

248
Q

Peutz-Jeghers Syndrome - clinical characteristics

A

Hamartomatous polyps throughout GI tract

mucocutaneous hyperpigmentation (freckle-like spots) on lips, oral mucosa, and genital skin (shown in pic)

249
Q

hamartoma

A

focal malformation that resembles a neoplasm in the tissue of origin

250
Q

Peutz-Jeghers Syndrome - what cancers are at increased risks?

A

Colorectal

breast

gynecologic

251
Q

Colorectal carcinoma - statistics

A

3rd most common site of cancer (when you exclude the skin)

3rd most common cause of cancer-related death

Peak incidence is 60-70 years of age

252
Q

Colorectal carcinoma - age of peak incidence

A

60-70 years

253
Q

Colorectal carcinoma - how can it arise? (2)

A
  1. adenoma-carcinoma sequence (most common)
  2. microsatellite instability (MSI)
254
Q

Microsatellite instability pathway of carcinoma development

A

Microsatelittles are repeating sequences of noncoding DNA – integrity of these sequences (stability) is maintained during cell division

Instability indicates defective DNA copy mechanisms (ie DNA mismatch repair enzymes) – if these microsatellites are unstable, it is a sign that other genes are as well.

  • microsatellites basically act as an indicator or “satellite” for the presence of defects that may exist (nonspecific, but gives reason to do more genetic testing)
255
Q

Classic example of microsatellite instability (MSI)

A

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

  • due to inherited mutations in DNA mismatch repair enzymes
256
Q

Hereditary nonpolyposis colorectal carcinoma (HNPCC)

A

due to inherited mutations in DNA mismatch repair enzymes

increased risk for colorectal, ovarian, and endometrial carcinoma

  • colorectal carcinoma arises de novo (not from adenomatous polyps) at a relatively early age; usually right sided
257
Q

What is the difference between the adenoma-carcinoma sequence and the MSI pathways of carcinoma development?

A

adeoma-carcinoma sequence: normal –> polyp –> carcinoma

MSI pathway: normal –> carcinoma

  • arises de novo and not from adenomatous polyps
258
Q

Colorectal carcinoma - screening

A

Same as for polyps

  • colonoscopy
  • fecal occult blood testing

Begins at 50 years of age

Goal is remove any adenomatous polyps before carcinoma can develop and to hopefully detect the cancer early (before clinical symptoms arise)

259
Q

Colorectal carcinoma - where can it develop?

A

Can develop anywhere along entire length of colon

  • Left-sided carcinoma usually grows as a ‘napkin-ring’ lesion (typically associated with adenoma-carcinoma sequence)
    • presents with decreased stool caliber, left lower quadrant pain, and blood streaked stool
  • Right-sided carcinoma usually grows as a raised lesion (typically associated with MSI)
    • presents with iron-deficiency anemia (occult bleeding) and vague pain
260
Q

Colorectal carcinoma – what is the difference of those that develop on the right vs the left side of the colon?

A

Left

  • usually grows as a ‘napkin-ring’ lesion (typically associated with adenoma-carcinoma sequence)
  • presents with decreased stool caliber, left lower quadrant pain, and blood streaked stool

Right

  • usually grows as a raised lesion (typically associated with MSI)
  • presents with iron-deficiency anemia (occult bleeding) and vague pain
  • an adult with iron deficiency anemia has colorectal carcinoma until proven otherwise
261
Q

An elderly patient presents with iron deficiency anemia – what is the Dx?

A

colorectal carcinoma until proven otherwise

262
Q

Colorectal carcinoma - why is there an iron deficiency anemia?

A

Bleeding = loss of RBCs which contain iron, an essential mineral that is normally recycled within the body.

Acutely, it doesn’t make much of a difference, but chronically, it results in insufficient iron resulting in an iron deficiency anemia

263
Q

Colorectal carcinoma and endocarditis association

A

Colorectal carcinoma is associated with an increased risk for Streptococcus bovis endocarditis

264
Q

Colorectal carcinoma - serum markers

What are they used for? (ie prognosis, screening, recurrence, etc…)

A

CEA (Carcinoembryonic antigen)

Used for assessing treatment response and detecting recurrence

NOT useful for screening

Unit 6 (10 decks)

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