GI Pathology Flashcards
1
Q
What is the cause of the pathology shown below?
A
This is a cleft lip and palate. This is due to failure of facial prominences to fuse.
2
Q
A 47 year old female present to the clinic with the lesion shown below in her cheek. She is a lawyer and gets these often and they tend to go away after a few days. What is your diagnosis?
A
Aphthous ulcer. Note the grayish base (granulation tissue) surrounded by erythema. These tend to arise due to stress and resolve spontaneously.
3
Q
A 47 year old female present to the clinic with the lesion shown below in her cheek. She is a lawyer and gets these often and they tend to go away after a few days. You diagnose her with Behçet Syndrome. What would lead you to diagnose her with this condition?
A
Behçet Syndrome is the triad of recurrent apthous ulcers, genital ulcers and uveitis. It is due to immune complex vasculitis involving small blood vessels.
4
Q
What causes Behçet Syndrome?
A
Unknown etiology. May sometimes be seen after a viral infection.
5
Q
A 29 year old man presents with the shallow, painful, red ulcer shown below. How did he get this honker on his lip?
A
He has oral herpes. It is usually due to HSV-1 infection during childhood that remains latent in the trigeminal ganglia. Sunlight or stress can cause reactivation of the virus and cause the cold sore seen in our friend.
6
Q
A 66 year old man presents with erythroplakia in his mouth. History reveals smoking and chronic alcohol abuse. Where is the most likely location you will find leukoplakia?
A
Erythroplakia is a precursor to squamous cell carcinoma because is indicates squamous cell dysplasia. Oral squamous cell carcinoma is most commonly found in the floor of the mouth.
7
Q
A patient presents with a white shaggy patch on the lateral aspect of the tongue. You cannot scrape it away. What is your most likely diagnosis?
A
Shaggy leukoplakia from EBV infection in an immunocompromised individual. If the patient had leukoplakia on the floor of the mouth you would be thinking squamous cell carcinoma. If you could scrape the plaque away you would be thinking oral thrush (oral candidiasis)
8
Q
A 16 year old boy presents with bilateral inflamed parotid glands. What is your main concern in treating this patient?
A
Mumps presents with bilaterally inflamed parotid glands. The virus can also cause orchitis in teenagers which may result in sterility.
9
Q
A 10 year old girl presents with bilaterally inflamed parotid glands and stomach pain. She also has a terrible headache and neck stiffness. Labs reveal an elevated serum amylase. What is causing her condition?
A
Mumps presents with bilaterally inflamed parotid glands and can also cause aseptic meningitis and pancreatitis. Her serum amylase is elevated due to increased activity of the parotid glands or the pancreas, both can be elevated by mumps.
10
Q
A 66 year old man presents with right sided sublingual salivary gland inflammation. What is most likely causing his condition?
A
He has sialadenitis, characterized by unilateral blockade of salivary gland by a stone and subsequent S. Aureus infection.
11
Q
A 73 year old woman presents with a mobile, painless, circumscribed mass at the angle of her jaw. It is excised, but comes back when she is 75 years old. What is causing her condition?
A
She has a benign pleomorphic adenoma. This is the most common tumor of the parotid gland. It has a high rate of recurrence due to irregular borders.
12
Q
What would you expect to see on microscopic examination of the parotid tumor shown below?
A
This is a pleomorphic adenoma, characterized by stromal (cartilage) and epithelial (glands) tissue.
13
Q
A 73 year old woman presented with a mobile, painless, circumscribed mass at the angle of her left jaw. She has had it for 10 years and decides to not have it removed. She comes back when she is 75 years old and now complains of weakness on the left side of her face. What is your diagnosis?
A
Rarely, pleomorphic adenomas can transform from a benign tumor to a malignant tumor. Facial nerve involvement indicates infiltration of the parotid gland and malignancy.
14
Q
A 53 year old man presents with a mass in the parotid gland. You biopsy it and diagnose him with the second most common salivary gland tumor. What did you see on biopsy?
A
He has a Warthin tumor. This is characterized by a benign cystic tumor with abundant lymphocytes and germinal centers (like a lymph node).
15
Q
A 44 year old woman presents with a 2 month history of a mass in her parotid gland. She decided to get it checked out because she can no longer drink water without spilling on herself. What would you expect to see on microscopic examination of the parotid mass?
A
Mucoepidermoid carcinoma. This is a malignant tumor of the parotid gland that typically causes facial nerve damage. You would see mutinous and squamous cells in the tumor.
16
Q
What are the 4 common clinical presentations in patients with the condition shown below?
A
This is a tracheo-esophageal fistula. This will present with 1) vomiting from food getting stuck in the proximal atretic esophagus, 2) polyhydramnios from the fetus not being able to recycle amniotic fluid, 3) aspiration from gastric acid coming up the distal esophagus into trachea and 4) abdominal distention from tracheal air flowing into the distal esophagus and on to the stomach.
17
Q
You go to the doctor because whenever you eat pancakes or sandwiches, you feel like food gets stuck if you don’t have a drink to wash it down with. What might you have?
A
An esophageal web. This presents with dysphagia for poorly chewed food because a thin protrusion of esophageal mucosa catches some of the food.
18
Q
You go to the doctor because whenever you eat pancakes or sandwiches, you feel like food gets stuck if you don’t have a drink to wash it down with. Labs reveal severe iron deficiency anemia. What other clinical finding is the doctor likely to have?
A
Plummer-Vinson syndrome is characterized by severe iron deficiency anemia, an esophageal web and a beefy-red tongue due to atrophic glossitis.
19
Q
A patient presents complaining of dysphagia when eating food and really bad breath (halitosis). What acquired defect could be causing this?
A
Zenker Diverticulum (false diverticulum). This happens when there is an abnormality swallowing, causing an out pouching of pharyngeal mucosa through the muscular wall in the pharynx, just above the esophageal sphincter. Food gets trapped in there causing dysphagia and halitosis.
20
Q
A 37 year old woman presents with painful hematemesis. She has a history of alcohol abuse and bulimia. What is causing her symptoms?
A
She has Mallory-Weiss syndrome characterized by persistent vomiting from bulimia and alcoholism, creating a linear longitudinal laceration of the mucosa at the GE junction.
21
Q
A 37 year old woman presents with painful hematemesis. She has a history of alcohol abuse and bulimia. On physical exam you note bumps in the skin of her neck that crackle when you push on them. What is causing her symptoms.
A
Lacerations of the esophageal mucosa puts her at risk for Boerhaave syndrome. This syndrome is characterized by rupture of the esophagus that allows air to enter the mediastinum. Air gets into the fascial planes of the subcutaneous tissue and often travels up to the neck, causing subcutaneous emphysema.
22
Q
A 37 year old woman presents with painless hematemesis. She has a history of alcohol abuse. What is causing her condition?
A
Rupture of esophageal varices is the most common cause of death in people with liver cirrhosis. Portal hypertension causes blood back up in the lower submucosal esophageal veins. When they rupture, they do not stop bleeding because these patients are not producing coagulation factors due to liver disease.
23
Q
A 45 year old man presents with dysphagia when swallowing solid food and liquids. His breath is putrid. He is sent for a barium swallow CT and the results are shown below. What is causing his condition?
A
Achalasia. This patient has damage to the ganglion cells of the myenteric plexus. This results an inability to relax the esophageal sphincter and loss of peristalsis, resulting in dysphagia, food piling up and putrid breath.
24
Q
A 45 year old man presents with dysphagia when swallowing solid food and liquids. His breath is putrid. He is sent for a barium swallow CT and the results are shown below. What are the most common causes of this condition?
A
He has achalasia. Most common causes are idiopathic and Chagas disease (virus damages myenteric ganglion).
25
A 45 year old man presents with dysphagia when swallowing solid food and liquids. His breath is putrid. He is sent for a barium swallow CT and the results are shown below. What findings would you expect on esophageal monometry?
A high lower esophageal pressure.
26
A 41 year old man presents with chest pain. History reveals adult onset asthma and cough. Physical exam reveals damage to the enamel of the teeth. Histological analysis of the cells of the esophageal mucosa would reveal what change?
This patient has GERD. Normally the cells of the esophagus are non-keratinizing squamous epithelium. Movement of gastric acid into the esophagus causes metaplasia to non-ciliated columnar goblet cells.
27
A 41 year old man presents with chest pain. History reveals adult onset asthma and cough. Physical exam reveals damage to the enamel of the teeth. What is causing his symptoms? What are risk factors for this?
He has GERD due to reduced lower esophageal sphincter tone, allowing acid reflux. Risk factors include alcohol, tobacco, obesity, fatty diet, caffeine and a hiatal hernia.
28
Why does this patient have GERD?
This is the most common type of diaphragmatic hernia, a sliding hiatal hernia. The cardiac sphincter of the stomach goes through the diaphragm, into the esophagus and allows acid reflux. Note the hour glass appearance due to residual tone in the lower esophageal sphincter.
29
You are listening to the lung fields in a young child who has suspected pulmonary hypoplasia. You hear bowel sounds in the lung fields. What is causing this?
Paraesophageal hernia. This is due to herniation of a portion of the stomach next to the esophagus, in the lung fields. This takes up space in the thorax and can cause lung hypoplasia.
30
A 41 year old man presents with chest pain. History reveals adult onset asthma and cough. Physical exam reveals damage to the enamel of the teeth. What are late complications of this patient’s condition?
Ulceration with stricture: due to mucosal ulceration followed by fibrosis and narrowing of lower esophageal lumen. Barrett’s esophagus: metaplasia of non-keratinizing squamous epithelium to non-ciliated columnar epithelium with goblet cells (shown below).
31
What type of esophageal carcinoma are people at risk for who have Barrett’s esophagus?
Metaplasia of non-ciliated columnar epithelium with goblet cells puts the patient at risk for malignant proliferation of glands (dysplasia) and development of adenocarcinoma.
32
Where is the most common esophageal carcinoma in the west typically found?
Adenocarcinoma is typically found in the lower 1/3 of the esophagus due to metaplasia in that area from acid reflux.
33
Where is the most common esophageal carcinoma in the world typically found?
Squamous cell carcinoma is most commonly found in the upper or middle third of the esophagus.
34
Why are people in southern China and Iran at high risk for squamous cell esophageal carcinoma? Who else is at risk for this type of cancer?
Esophageal irritation puts people at risk for squamous cell carcinoma. They drink very hot tea in these places. Other irritants include alcohol, tobacco, achalasia (rotting food causes mucosa irritation), esophageal web (rotting food causes mucosa irritation) and esophageal injury (lye ingestion).
35
A 43 year old man presents with progressive dysphagia, weight loss, cough, hoarseness, pain and hemetemesis. He has a long history of alcohol abuse and GERD. Labs reveal esophageal cancer in the upper 1/3 of the esophagus. What lymph nodes will be affected in this patient? What if it were the middle 1/3 of the esophagus? What about the lower 1/3?
Upper 1/3 = cervical nodes. Middle 1/3 = mediastinal or tracheobronchial nodes. Lower 1/3 = celiac or gastric nodes.
36
What causes this condition?
This is gastroschisis. The abdominal contents are exposed because of failure of abdominal wall folds to fuse properly during development.
37
What causes this condition?
This is an omphalocele, note the peritoneum and amnion covering the herniated bowel. During development the bowel herniates into the umbilical cord and normally recedes when the bowel makes its 90 degree counterclockwise turn. The bowel does not recede in this condition.
38
A 2 week old boy is brought to the clinic by his mother. She says that he has nonbilious projectile vomiting whenever he eats. Physical exam reveals peristalsis on the abdomen and an olive-like mass in the abdomen. How do you treat him?
This boy has pyloric stenosis, note that it is more common in boys. You treat surgically by myotomy.
39
What differentiates acute from chronic gastritis?
Acute: acid burning of gastric mucosa due to increased acid production or decreased mucosal protection. Chronic: H. pylori induced or autoimmune
40
What are you key defenses in the stomach that protect the mucosa from the acidic environment?
1) Mucus secretion by foveolar cells 2) Bicarbonate secretion to alkalinize the environment 3) Good blood supply to whisk away acidic materials
41
Risk factors for acute gastritis?
Severe burn (hypovolemia limits ability to eliminate acid and causes a Curling ulcer), NSAIDs (limits production of prostaglandins), Alcohol (direct damage to mucosa), Chemotherapy (killing of mucosal stem cells), Increased ICP and shock (hypovolemia).
42
How are prostaglandins protective for the stomach?
Limits acid production, stimulates mucus production, increases bicarbonate secretion and increases blood flow to whisk away acidic material in the stomach.
43
A patient presents to the ED with an epidural hematoma. Why is he at risk for acute gastritis?
Increased ICP causes vagal stimulation. ACh release stimulates acid production by the parietal cells in the stomach. This is called a Cushing ulcer.
44
Binding of what receptors on the parietal cells of the stomach can cause increased acid production?
ACh, gastrin and histamine.
45
Why are most patients in the ICU for shock place on proton pump inhibitors?
They are at risk for multiple gastric ulcers (Stress ulcers) due to decreased gastric blood flow.
46
Acid damage in the stomach can lead to superficial inflammation, erosion or ulceration. What is the difference between the last two?
Erosion = loss of epithelium. Ulcer = loss of mucosal layer.
47
Why might a patient with autoimmune chronic gastritis have to get IM injections of B12 every day?
Megaloblastic (pernicious) anemia. Autoimmune gastritis results in atrophy of the mucosa and destruction of parietal cells in the fundus and body of the stomach. This results in achlorhydria. Achlorhydria causes hyperplasia of G-cells in the antrum and increased gastrin secretion. Destruction of parietal cells causes decreased intrinsic factor production. With less intrinsic factor, less B12 is bound in the intestine and less is absorbed at the ilium because you must have the B12-intrinsic factor complex for absorption.
48
What lab values would be helpful in diagnosis of autoimmune chronic gastritis?
Autoimmune chronic gastritis is a type IV T-cell mediated hypersensitivity, so you can look for antibodies against parietal cells and/or intrinsic factor.
49
What is the most common cause of vitamin B12 deficiency?
Autoimmune chronic gastritis
50
A patient presents to the clinic with long-standing megaloblastic anemia. Labs reveal increased antibody against parietal cells and intrinsic factor. Why is this patient at risk for gastric adenocarcinoma?
Autoimmune chronic gastritis causes intestinal metaplasia in the stomach (Peyer’s patches w/lots of lymphocytes in the stomach)
51
The image below is taken from a patient with chronic gastritis in the antrum of the stomach. What is causing his condition?
Note the “seagull” shaped H. pylori bacteria sitting on the gastric epithelium. These bacteria produce ureases and proteases that damage the mucosa of the antrum.
52
A patient presents to your clinic with a long-standing history of epigastric pain. You give him a proton pump inhibitor + antibiotic and the pain resides. What is he at increased risk for because of long-term H. pylori chronic gastritis?
Ulceration (chronic inflammation), gastric adenocarcinoma (intestinal metaplasia) and mucosal-associated lymphoid tissue (MALT) lymphoma (germinal centers in gastric walls w/marginal zone production of post-germinal center B-cells)
53
There are 3 serious complications in chronic gastritis from H. pylori. How do you treat to limit this?
Triple therapy resolves ulcers, reverses intestinal metaplasia and risk of lymphoma is eliminated by decrease in inflammatory cells.
54
When giving triple therapy to a patient with chronic H. pylori gastritis, how do you confirm therapy is working?
A negative urea breath test (because H. pylori makes urease) and lack of antigen in stool.
55
Most common location and cause in peptic ulcer disease?
90% in duodenum from H. pylori.
56
What type of cancer presents with multiple duodenal ulcers?
Gastrinomas. These tumors secrete lots of gastrin, which binds to parietal cells, causes increased acid production and causes ZE syndrome (multiple duodenal ulcers)
57
A patient presents to the clinic with epigastric pain that improves with meals. Why might you diagnose her with a duodenal ulcer? How do you confirm your diagnosis?
When you eat, the duodenum initiates production of protective mechanisms as it prepares to receive food from the stomach. This improves symptoms. You confirm with endoscopic biopsy showing ulcer with hypertrophy of Brunner glands (glands that produce mucus to protect the duodenum).
58
You go to the doctor with epigastric pain that improves with meals. He does an endoscopic biopsy and diagnoses you with a duodenal ulcer. Why do you hope the ulcer is on the anterior side of the stomach?
One of the complications of a duodenal ulcer is rupture. If the ulcer ruptures posteriorly it could lead to bleeding from the gastroduodenal artery or acute pancreatitis.
59
A patient presents to the clinic with epigastric pain that worsens with meals. What are the most common causes of this pain?
The most common causes of gastric ulcers are 1) H. pylori 2) NSAIDs 3) Bile reflux
60
A patient presents to the clinic with epigastric pain that worsens with meals. What major complication is the patient at risk for?
Rupture of the left gastric artery because gastric ulcers typically appear on the lesser curvature of the antrum.
61
Why would you rather have a diagnosis of duodenal ulcer of gastric ulcer in peptic ulcer disease?
Duodenal ulcers are almost never malignant. Gastric ulcers can be caused by gastric carcinoma.
62
Is this a benign or malignant ulcer?
Benign: 1) It is small 2) Punched out appearance 3) Flat mucosal margins
63
Is this a benign or malignant ulcer?
Malignant: 1) Large 2) Irregular shape 3) Heaped up borders
64
What type of cancer is gastric carcinoma?
Gastric carcinoma is a malignant proliferation of surface epithelial cells, i.e. adenocarcinoma
65
2 types of gastric carcinoma
Intestinal and diffuse type
66
A patient presents with a large, irregular ulcer with heaped up margins in the lesser curvature of the antrum. What are risk factors for this condition?
This is intestinal type gastric carcinoma. Intestinal metaplasia (from chronic autoimmune and H. pylori gastritis), nitrosamines in smoked foods (carcinogen) and blood type A are all risk factors.
67
A patient presents with weight loss, abdominal pain, anemia and early satiety. Gross biopsy reveals linitis plastica (thickening of stomach walls). His biopsy is shown below. What is your diagnosis?
Linitis plastica (shown below) is a reactive response of the stroma to diffuse type gastric carcinoma. Note the signet ring cells diffusely infiltrating the gastric wall.
68
Why is the nucleus pushed to the edge of the cell in patients with diffuse type gastric carcinoma?
Signet ring cells are producing so much mucin it pushes the nucleus to the side
69
What risk factors are not associated with diffuse type gastric carcinoma?
H. pylori, intestinal metaplasia or nitrosamines.
70
Why do patients with gastric carcinoma, especially diffuse type, experience early satiety?
Thickening of the stomach wall impairs the stomach’s ability to expand.
71
A patient presents with gastric carcinoma. What 2 rare dermatologic presentations might this patient also have?
Acanthosis nigricans (darkening of skin, especially near armpit) and Leser-Trelat sign (dozens of seborrheic keratosis all over skin)
72
On physical exam, where would you palpate a patient who has suspected gastric carcinoma?
Left supraclavicular node (Virchow node)
73
Most common locations for metastasis in patients with intestinal type gastric carcinoma? In patients with diffuse type?
Intestinal type = Sister Mary Joseph nodule in periumbilical region. Diffuse type = Krukenburg tumor (bilateral ovaries)
74
A mother gives birth to a Down syndrome baby. Prior to birth, there was polyhydramnios. She brings her child in two days later because he has bilious vomiting whenever she feeds him. Chest x-ray is shown below. What is your diagnosis?
Duodenal atresia is highly associated with Down syndrome. Atresia causes polyhydramnios because the baby cannot digest amniotic fluid in utero. Bilious vomiting occurs because bile is dumped into the duodenum. The x-ray reveals a “double bubble” sign due to distention of the stomach and duodenum with the pyloric sphincter separating the two.
75
A mother gives birth to a child who passes meconium through the umbilicus at birth. What embryological event causes this to occur?
Failure of the vitelline duct to involute, during development the midgut receives nutrients from the vitelline duct. If the duct has partial closure, but does not involute you have a Meckel diverticulum.
76
A patient presents to the clinic with a mass in the umbilical region that is soft. You determine that stool is in the mass. Ultrasonography reveals bleeding of the mass. What is your diagnosis?
Meckel diverticulum. It is a true diverticulum because all three layers of bowel wall are out pouching. The patient is likely bleeding because you can have ectopic gastric tissue producing acid in the diverticulum.
77
What GI anomaly is associated with the rule of 2’s?
2% of population (most common congenital GI anomaly), 2 inches longs, within 2 feet of ileocecal valve, presents with bleeding, volvulus, intussusception or obstruction in first 2 years of life.
78
What are the most common locations you see this in the elderly? Young adults?
This is a volvulus, note the twisting of the bowel that caused infarction and obstruction. Elderly = sigmoid colon. Young adults = cecum
79
Currant jelly stools
Intussusception. Telescoping of a proximal bowel portion into a distal bowel portion causes infarction and these types of stools.
80
Most common causes of intussusception in children? Adults?
Children: sickness causes leading edge lymphoid hyperplasia (Peyer’s patches) and the terminal ileum gets dragged into the cecum because of the thickness of its wall. Adults: leading edge tumor.
81
Why is the small bowel so susceptible to ischemic injury?
It is very active in nutrient absorption and peristalsis, requiring a lot of ATP.
82
A patient presents with abdominal pain, bloody diarrhea and decreased bowel sounds.. CT imaging of the stomach reveals transmural infarction of the small bowel. Name 3 things that could cause this condition?
1) A-fib -\> clot to SMA 2) Polyarteritis nodosa -\> thrombus lodges in SMA 3) Polycythemia Vera or Lupus anticoagulant increase clotting and block mesenteric vein. All of these result in infarction of the entire wall of the small bowel.
83
A patient comes to the ED after a car accident in shock. He complains of bloody diarrhea, abdominal pain and decreased bowel sounds. His BP is 90/40. What region of the small bowel is at risk for infarction in this patient?
Mucosa, it is furthest from the blood supply and at risk for infarction when blood pressure drops
84
In a normal person, how is lactose broken down to glucose?
1) Amylases (from saliva and pancreas) break down sugar into oligosaccharides & disaccharides 2) Lactase breaks down lactose into monosaccharides (galactose and glucose)
85
A 21 year old man presents with abdominal dissension and diarrhea after consuming milk. What is causing his symptoms?
Congenital or acquired lactase deficiency in the brush border of enterocytes causes accumulation of lactose in the lumen of the intestine. Lactose is osmotically active and pulls water into the intestinal lumen.
86
How do patients become lactose intolerant?
Congenital (rare). 10-15 year olds suddenly become lactose intolerant. GI infection destroys enzyme temporarily.
87
What HLA genes are associated with immune-mediated damage of small bowel villi?
Celiac disease is characterized by villi destruction after hypersensitivity reaction from gluten exposure. Associated HLA genes include DQ2 and DQ8.
88
A child presents with abdominal distention, diarrhea and failure to thrive. His father has chronic diarrhea and bloating. How does gluten ingestion initiate hypersensitivity reaction?
Gliadin in gluten is deamidated by tissue transglutaminase (tTG). Deamidated gliadin is presented by MHC II APCs to CD4 helper T cells. These T cells mediate damage.
89
What skin condition will resolve with a gluten-free diet?
Dermatitis herpetiformis. This condition is due to IgA deposition at the tips of dermal papillae that form small blisters that look like herpes on the skin.
90
What antibodies do you look for in serology of a patient with suspect celiac disease?
IgA antibodies against endomysium, tTG or gliadin. Note that you sometimes need to test IgG antibodies because some celiac patients have an IgA deficiency.
91
A child presents with abdominal distention, diarrhea and failure to thrive. Labs show IgA deficiency and IgG antibodies against endomysium, tTG and gliadin. What are you looking for when you do a duodenal biopsy on the child?
Flattened villi, hyperplasia of crypts and increased intraepithelial lymphocytes. Note that damage won’t be as pronounced in the jejunum or ileum.
92
A patient has a history of celiac disease, but has had good dietary control for the past ten years. He now presents with new onset diarrhea and bloating. What conditions may be causing his symptoms?
Patients may develop small bowel carcinoma and T-cell lymphoma (EATL).
93
You see a patient who complains of diarrhea and abdominal distention. Symptoms started after he had the stomach flu on his trip to the Caribbean. He seems to improve with antibiotics. Where is damage occurring in this patient?
He has Tropical Sprue. Damage to small bowel villi due to an unknown organism causes malabsorption and all of his symptoms. Damage is most pronounced in the jejunum and ileum, the duodenum is rarely involved.
94
What nutritional deficiencies might you see in patients with Tropical Sprue?
If the damage is in the jejunum, you have problems with reabsorption of folic acid. If the damage is in the ileum, you may have vitamin B12 deficiency.
95
A patient presents to the clinic complaining of really foul smelling, slimy stools. Labs reveal fat malabsorption. What infection could be causing his symptoms?
Whipple disease (Tropheryma whippelii organism). Macrophages in the villi lamina propria get loaded with the organism. This causes compression of lactiles and diminishes the small bowel’s ability to transport chylomicrons.
96
How does fat get into the blood?
It is digested by salivary and pancreatic lipases. Then it is emulsified by bile until it becomes a mycele. Myceles pass into the enterocytes where they are packed into chylomicrons. Chylomicrons are sent into the lamina propria’s lactiles where it can access the lymphatics and move on to the blood.
97
The most common site of Whipple’s disease is the lamina propria of the small bowel. What other areas can be involved?
Synovium of joints, cardiac valves, lymph nodes and CNS.
98
A patient presents with fat malabsorption and absent VLDL and LDL levels. What deficiencies exist in this patient?
He has abetalipoproteinemia, an autosomal recessive deficiency in APO B-48 (needed to form chylomicrons) and APO B-100 (needed to form VLDL and LDL).
99
What is the lowest form of neuroendocrine malignancy? What do they stain for?
Carcinoid tumor. They stain positive for chromogranin (stains all neuroendocrine tumors).
100
There really is no common tumor of the small bowel. However, there is a tumor who’s most common site is the small bowel. What is it?
Carcinoid tumor. They grow as submucosal polyp-like nodules in the small bowel.
101
A patient presents with bronchospasm, diarrhea and flushing of the skin. Cardiac exam reveals a murmur. 2 months before these symptoms UA revealed 5-HIAA in the urine. What is causing these symptoms?
He has a carcinoid tumor that originated in the small bowel. When it was localized to the small bowel, serotonin secreted by the tumor went to the portal vein and was metabolized by MAO in the liver to 5-HIAA. Once it metastasized to a location where it could reach the systemic circuit, like the liver w/ access to the hepatic vein, then you see carcinoid syndrome and carcinoid heart disease.
102
When do patients present with carcinoid heart disease?
Once carcinoid metastasizes to the liver. From there it can release serotonin into the IVC and cause fibrosis of the right heart valves (tricuspid and pulmonic valve).
103
What symptoms can trigger serotonin syndrome in patients with a carcinoid tumor?
Alcohol or stress
104
Why don’t you get left-sided valvular disease in carcinoid heart disease?
The lung also has MAO. Hence, serotonin from a carcinoid tumor in the liver can only cause tricuspid regurgitation or pulmonary valve stenosis.
105
What are causes of the most common cause of acute abdomen?
Acute appendicitis is caused by lymphoid hyperplasia in kids and fecalith in adults.
106
A patient presents with periumbilical pain, fever and nausea. Shortly after being admitted to the ED, the pain is localized to the lower right quadrant. Physical exam reveals guarding and rebound tenderness. What complications is this patient experiencing?
These are all indicators of acute appendicitis. Guarding and rebound tenderness hints at peritonitis from rupture. Another complication could be periappendiceal abscess.
107
A 22 year old caucasian woman presents with recurrent bouts of bloody diarrhea and abdominal pain. Social history reveals that she is an Eastern European Jew. When can you diagnose her with IBS?
It is a diagnosis of exclusion
108
Histologic hallmark of ulcerative colitis
Crypt abscesses with neutrophils
109
How do ulcerative colitis and Chron’s disease differ in each of the following categories?
\*
110
A patient presents to the clinic with right lower quadrant pain and non-bloody diarrhea. He also has a history of ankylosing spondylitits. What would you expect the gross appearance of this patient’s ileum to look like?
Cobblestone mucosa with creeping fat and strictures (from fibrosis narrowing the lumen and causing stricure and pulling up of submucosa by myofibroblasts in granulation tissue causing creeping fat)
111
Part of bowel affected in ulcerative colitis?
It always starts in the rectum and works its way up as far as the cecum. It is an ulcer so it only affects the mucosa and submucosa.
112
Why do patients with ulcerative colitis have left lower quadrant pain with bloody diarrhea?
The colon is on the left side.
113
You are doing a proctoscopy of a patient who has ulcerative colitis. What would you expect to see the colon to look like grossly?
Pseudopolyps and loss of haustra (note lead pipe appearance in image below)
114
A patient presents with a long history of ulcerative colitis. He is febrile and the colon is dilated on imaging. What are the major factors you need to consider in diagnosing this patient?
He has toxic megacolon. You want to consider his risk for cancer by assessing the duration (is it \> 10 years) and the extent of colon involved.
115
A patient presents with a long history of ulcerative colitis. He is febrile and the colon is dilated on imaging. What may labs reveal in his blood work?
p-ANCA. Ulcerative colitis is also associated with primary sclerosing cholangitis.
116
What diseases do you think of when you hear p-ANCA.
Microscropic polyangiitis, Churg-Strauss and Ulcerative Colitis
117
What habit is protective against ulcerative colitis?
Smoking. Chron’s disease risk is increased by smoking.
118
You get ulcers in ulcerative colitis, what do you get in Chron’s disease?
Knife-like fissures of inflammation going through the entire thickness of the wall.
119
Where in the GI tract do you find Chron’s disease?
Anywhere from the mouth to the anus, the terminal ileum being the most common site and the rectum the least common site. Note that it has skip lesions.
120
A patient presents with right lower quadrant pain and non-bloody diarrhea. He also has lesions on the mucosa of his mouth. What type of inflammation would you expect to see in the terminal ileum?
He has Chron’s disease, not the right lower quadrant pain indicating the most common site, the ileum, is affected. You see lymphoid aggregates with granulomas in Chron’s disease.
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A patient presents with right lower quadrant pain and non-bloody diarrhea. He also has lesions on the mucosa of his mouth. What are the main complications this patient is at risk for?
Malabsorption and nutritional deficiency, Ca-oxalate nephrolithiasis (due to increased absorption of oxalate during inflammation), fistula formation (due to rupture on plugging into another tube) and carcinoma (especially if colon is involved for long period of time).
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A patient presents with right lower quadrant pain and non-bloody diarrhea. He also has lesions on the mucosa of his mouth. What other diseases are associated with his condition?
Ankylosing spondylitis, sacroiliitis, migratory polyarthritis, erythema nodosum and uveitis.
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A mother gives birth do a Down syndrome baby boy. He could not pass meconium and physical exam revealed an empty rectal vault with massive dilation of the bowel proximal to the sigmoid colon. What is your diagnosis?
He has Hirschsprung disease. Defective relaxation and peristalsis of the rectum and distal sigmoid colon are due to failure of ganglion cells to descend into the wall of the bowel from the neural crest. This causes obstruction of bowel content.
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Which ganglion cells do you need for motility and relaxation?
Auerbach’s myenteric plexus
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Which ganglion cells do you need to regulate blood flow, absorption and secretion?
Meissner’s submucosal plexus
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What do you need to diagnose Hirschsprung disease?
Rectal suction biopsy because you need to pull the submucosa into the biopsy. This will show lack of ganglion cells. You need to do it quick because the child is at risk for bowel rupture.
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A mother gives birth do a Down syndrome baby boy. He could not pass meconium and physical exam revealed an empty rectal vault with massive dilation of the bowel proximal to the sigmoid colon. How do you treat him?
Resect the portion of the aganglionic bowel.
128
What causes the condition shown below?
Colonic diverticulum. These happen from increased pressure in the colon wether it be from constipation or low fiber diets. The mucosa and submucosa will bulge out where the vasa recta traverse the muscularis propria because this is a weak point in the colonic wall.
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What is the most common location you will find colonic diverticula?
Sigmoid colon.
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What are common complications associated with colonic diverticula?
Rectal bleeding (remember the diverticulum runs right next to the vasa recta), diverticulitis (left-sided appendicitis) and fistula (wall ruptures and plugs into another structure, could plug into bladder and cause stool to be present in urine).
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Hematochezia
Bright red blood in stool, associated with colonic diverticula (high stress in left colon) and angiodysplasia (high stress in right colon).
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A patient presents with hematochezia and pain on the right side. What acquired malformation could be causing these symptoms?
Angiodysplasia. This is an acquired malformation of mucosal and submucosal capillary beds in the cecum and right colon due to high wall tension.
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This patient presented to the clinic complaining of blood in his stool. What is causing his condition?
AD Hereditary Hemorrhagic Telangiectasia. This disorder results in thin-walled blood vessels that typically arise in the nasopharynx and GI tract.
134
What region of the colon is most likely affected in patients with atherosclerosis of the SMA?
The splenic flexure, this is the region furthest away from its blood supply, the SMA.
135
A patient presents with left-sided abdominal pain right after eating. He also has weight loss because he doesn’t feel like eating as much. What complications is he at risk for?
He has pain right after eating indicating increased energy demand on regions of the colon with decreased blood flow (postprandial pain). This is indicative of ischemic colitis. He is at risk for infarction, which would present with pain and bloody diarrhea.
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A 43 year old woman presents with abdominal pain, bloating, flatulence and constipation. Symptoms resolve with defecation and get better when she eats more fiber. What is your diagnosis?
Irritable bowel syndrome, this is classically seen in middle-aged females with no known etiology.
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2 common types of colonic polyps
Hyperplastic and Adenomatous
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A 57 year old man comes in for his first colonoscopy. You see a few polyps on the left colon (rectosigmoid colon) and diagnose them as benign with no malignant potential. What would you expect to see on biopsy of these polyps?
Hyperplastic polyps are benign. You would see hyperplasia of glands with a serrated appearance. These are the most common type of polyps.
139
A 57 year old man comes in for his first colonoscopy. You see a few polyps and biopsy is shown below. What is your diagnosis?
Note the raise protrusion of colonic mucosa indicating an adenomatous polyp w/malignant proliferation of glands. These are the second most common type of polyp and are premalignant (may progress to adenocarcinoma)
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How do adenomatous polyps progress to adenocarcinoma?
The adenoma-carcinoma sequence. Low risk -\> High risk mutations: double somatic APC mutation (tumor suppressor gene, RISK for polyps) -\> kRAS (polyp develops) -\> p53 (progresses to malignancy) + increased COX
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Mutation in familial adenomous polyposis syndrome. How do you treat these patients?
They develop thousands of polyps from germline double APC mutation on chromosome 5 (tumor suppressor gene). You must remove the colon and rectum in these patients because the vast majority of them will develop carcinoma by age 40 due to easy mutation of kRAS, p53 and increased COX activity.
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Why do patients who take a baby aspirin every day have decreased risk for colon cancer?
The adenoma-carcinoma sequence requires increased COX activity to progress to carcinoma. Aspirin inhibits COX.
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Why are all polyps removed in colonoscopy?
You can’t tell the difference between benign and malignant polyps grossly and biopsy is required.
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What determines the theoretic risk for an adenomatous polyp to become malignant?
1) \> 2 cm 2) Sessile growth (not pedunculated, flat on wall) 3) Villous histology (lots of villi projections, not tubulous)
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What other conditions are associated with familial adenomous polyposis?
When fibromatosis (benign destructive fibroblast proliferation in retroperitoneum) and osteomas (benign bone proliferation in skull) are present w/ FAP, it is Gardner syndrome. When patients have CNS tumors (medulloblastomas & glial tumors) with FAP, it is Turcot Syndrome.
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A mother brings her 4 year old in because of bloody stool. Physical exam reveals a solitary rectal polyp that prolapses and bleeds. What is your diagnosis?
Juvenile polyp. These are sporadic hamartomatous polyps that arise in kids \< 5 years old.
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A mother brings her 4 year old in because of bloody stool. Endoscopy reveals multiple juvenile polyps in the stomach and colon. What is this child at risk for?
This child has juvenile polyposis. Large numbers of polyps increases risk for progression to carcinoma.
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A woman comes to see you with hyper pigmentation on her lips, oral mucosa and genital skin. Endoscopy reveals hamartomatous polyps throughout the GI tract. What is she at increased risk for?
She has Peutz-Jeghers Syndrome. She is at increased risk for colorectal, breast and GYN cancer.
149
What pathway represents about 20% of colorectal cancers?
Microsatellite instability. Every time your cells copy DNA, you copy microsatellites. When DNA copy mechanisms are impaired, microsatellites are unstable and indicate that other genes are also likely unstable. Adenoma-carcinoma pathway accounts for 80%.
150
What colorectal carcinoma carries an increased risk for ovarian and endometrial carcinoma?
Hereditary Non-polyposis Colorectal Carcinoma (HNPCC). This is due to an inherited mutation in DNA mismatch repair enzymes. Note that these cancers will arise de novo without polyps, typically on the right side.
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How do we screen for colorectal carcinoma?
Colonoscopy (removing adenomatous and hyperplastic polyps) and fecal occult blood testing.
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A 70 year old male presents with left-lower quadrant pain, decreased stool caliber and blood-streaked stool. What is the mostly likely pathogenesis of his condition?
Left-sided carcinoma tends to grow as a napkin-ring lesion and cause decreased stool caliber. Left-sided carcinomas are also associated with the adenoma-carcinoma sequence.
153
A 70 year old male presents with iron-deficiency anemia and vague right-sided pain. What is the most likely pathogenesis of his condition?
Right-sided carcinoma tends to grow as a raised lesion (not a polyp). The right-sided colon has a larger lumen so you don’t really get obstructive symptoms, you get bleeding that causes anemia and vague pain. Note that the right side is associated with microsatellite instability.
154
A patient presents with endocarditis. Blood tests reveal strep bovis. What is your next step in working up this patient?
Analysis for colorectal carcinoma.
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How do you stage colorectal cancer?
T: tumor depth of invasion. N: regional lymph nodes, M: Distant metastasis to liver.
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What serum marker is useful for assessing treatment response or recurrence of colorectal carcinoma but not useful for screening?
CEA.
