GI Pathology Flashcards
What is the cause of the pathology shown below?
This is a cleft lip and palate. This is due to failure of facial prominences to fuse.
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?
Aphthous ulcer. Note the grayish base (granulation tissue) surrounded by erythema. These tend to arise due to stress and resolve spontaneously.
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?
Behçet Syndrome is the triad of recurrent apthous ulcers, genital ulcers and uveitis. It is due to immune complex vasculitis involving small blood vessels.
What causes Behçet Syndrome?
Unknown etiology. May sometimes be seen after a viral infection.
A 29 year old man presents with the shallow, painful, red ulcer shown below. How did he get this honker on his lip?
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.
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?
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.
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?
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)
A 16 year old boy presents with bilateral inflamed parotid glands. What is your main concern in treating this patient?
Mumps presents with bilaterally inflamed parotid glands. The virus can also cause orchitis in teenagers which may result in sterility.
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?
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.
A 66 year old man presents with right sided sublingual salivary gland inflammation. What is most likely causing his condition?
He has sialadenitis, characterized by unilateral blockade of salivary gland by a stone and subsequent S. Aureus infection.
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?
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.
What would you expect to see on microscopic examination of the parotid tumor shown below?
This is a pleomorphic adenoma, characterized by stromal (cartilage) and epithelial (glands) tissue.
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?
Rarely, pleomorphic adenomas can transform from a benign tumor to a malignant tumor. Facial nerve involvement indicates infiltration of the parotid gland and malignancy.
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?
He has a Warthin tumor. This is characterized by a benign cystic tumor with abundant lymphocytes and germinal centers (like a lymph node).
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?
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.
What are the 4 common clinical presentations in patients with the condition shown below?
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.
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?
An esophageal web. This presents with dysphagia for poorly chewed food because a thin protrusion of esophageal mucosa catches some of the food.
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?
Plummer-Vinson syndrome is characterized by severe iron deficiency anemia, an esophageal web and a beefy-red tongue due to atrophic glossitis.
A patient presents complaining of dysphagia when eating food and really bad breath (halitosis). What acquired defect could be causing this?
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.
A 37 year old woman presents with painful hematemesis. She has a history of alcohol abuse and bulimia. What is causing her symptoms?
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.
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.
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.
A 37 year old woman presents with painless hematemesis. She has a history of alcohol abuse. What is causing her condition?
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.
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?
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.
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?
He has achalasia. Most common causes are idiopathic and Chagas disease (virus damages myenteric ganglion).
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.
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.
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.
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.
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.
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).
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.
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.
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.
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).
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.
What causes this condition?
This is gastroschisis. The abdominal contents are exposed because of failure of abdominal wall folds to fuse properly during development.
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.
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.
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
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
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).
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.
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.
Binding of what receptors on the parietal cells of the stomach can cause increased acid production?
ACh, gastrin and histamine.
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.
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.
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.
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.
What is the most common cause of vitamin B12 deficiency?
Autoimmune chronic gastritis
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)
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.
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)
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.
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.
Most common location and cause in peptic ulcer disease?
90% in duodenum from H. pylori.
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)
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).
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.
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
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.
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.
Is this a benign or malignant ulcer?
Benign: 1) It is small 2) Punched out appearance 3) Flat mucosal margins
Is this a benign or malignant ulcer?
Malignant: 1) Large 2) Irregular shape 3) Heaped up borders
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.
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.
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.
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
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.
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.
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.
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.
Histologic hallmark of ulcerative colitis
Crypt abscesses with neutrophils
How do ulcerative colitis and Chron’s disease differ in each of the following categories?
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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)
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.
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)
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.
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.
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)
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
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.
