GI Patient Questions Flashcards by Andrew Harold

You have a patient that comes in complainig of mouth pains. You note that his dentition is poor, and that he drinks lots of acidic sugary drinks multiple times a day (and has every day for the past 15 years). He consumes only processed foods, and is significantly overweight. Routine labs were performed, and everything came back normal.

What is the most likely cause of his “mouth pain”?

What would you expect to find when observing his mouth?

Dental Caries (Tooth Decay)

Loss of Teeth, and Rotted teeth.

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On some of his other teeth, you notice a sticky colorless, biofilm, that collects on the surface of his teeth – what is this?

What can this lead too? Is this reversible?

Dental Plaque

Gingivitis (inflammation of the oral mucosa), YES very reversible

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You find later that he has certain bacteria colonizing his good and bad oral mucosa – what is typically seen in the Good mucosa? Bad Mucosa?

What does this “bad” flora usually cause in the mouth?

what specific things?

If this were to continue what is he at risk for?

Good Mucosa – Facultative Gram +

Bad Mucosa – Anearobic/Microaerophillic Gram - Flora

Periodontitis (an inflammatory process affecting the supporting structures of the teeth)

Teeth (*Periodontal L), Alveolar Bone, Cementum

Loss of the Periodontal L, so loss of his teeth

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You assess that he has Periodontitis (as well as a host of other problems), but note that this disease can be a component of systemic diseases as well . . . what are the other disease we need to think about for this patient?

What is this patient at risk for in the future, if untreated?

AIDS,

Leukemia

Chron Dz

Down Syndrome

Sarcoidosis

Chediak-Higashi/Agranulocytosis/Cyclic Neutropenia

Infective Endocarditis, Pulmonary and Brain Abscesses

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A Patient comes into your clinic complaiing of a recurrent and super painful spot in his mouth. Upon inspection you note a single shallow, hyperemic ulceration that is covered by a thin exudate, with a small rim of erythema.

What is the lesion?

What immunologic disorders are associated with these lesions?

In the beginning these lesions are largely ____? and then later after an infection sets in are largely____?

How long will this last?

Apthous Ulcer (Canker Sore)

IBD, Celiac Dz, Behcet dz

First – Mononuclear (Infiltrate)

After Infection – Neutrophilic (Infiltrate)

7-10 days, may last weeks if she is immunocompromised.

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You have a child that has been constantly biting her mouth, and the mother notes that she has developed an “ulcer like lesion” inside her mouth. . . what do you expect this to be?

Where is this lesion usually concentrated?

Irritation Fibroma (Traumatic Fibroma)

Along the bite line (or gingiva)

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You have a pregnant mother who comes in complaining of a disgusting red thing on the top of her teeth. You see an ulcerated, red-to-purple lesions. She states that it has grown RAPIDLY over the past 2 weeks.

What is the most likely lesion?

What would be seen Histologically?

What is the Tx?

Pyogenic Granuloma

A Highly vascular proliferation of organizing granulation tissue.

Surgical Excision – can regress into a dense fibrous mass

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You have a 3 year old child that presents to the clinic for a routine checkup. On inspection you note that he has some ulcerations of his gingiva, that the mother notes came on last week suddleny. She stated that the child had a slight fever a while back, and wasnt eating, and seemed a little irritable, but has since gotten better.

What was most likely the cause?

What is the most likely explanation of his ulcerations?

HSV-1 infection

HSV-1 infxn causing Acute Herpetic Gingivostomatitis

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You have an adult patient come in who has a history of a recent upper respiratory infxn, and who now has small vesicles on their lips, nasal orifices, buccal mucosa, gingiva, and hard palatte.

What is most likely the cause?

What other things could have caused this?

What are the vesicles called here?

HSV-1

Besides an URI, you can have Pregnancy, Menstraution, Immunosuppression, temp extremes, etc. (all can cause recurrent herpetic stomatitis)

Herpes Labialis (usually resolve in 7-10 days)

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You have an adult patient come in who has a history of a recent upper respiratory infxn, and who now has small vesicles on their lips, nasal orifices, buccal mucosa, gingiva, and hard palatte.

Where is this usually latent in?

How can we visualize it on Histo?

What is this type of virus?

What systemic bad things can this cause?

the Trigeminal Ganglia

Tzank Smear

DS DNA Virus

Keratoconjunctivitis. Temporal Lobe Enceph.

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You have an adult patient come in who has a history of a recent upper respiratory infxn, and who now has small vesicles on their lips, nasal orifices, buccal mucosa, gingiva, and hard palatte.

What other viruses can infect the Head and Neck region?

EBV – Mono, Lymphoma, Nasopharyngeal Carcinoma

CMV

Enterovirus – Hand foot and Mouth Dz

Rubeola – Measles

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You have a 58 year old immunocomprised man who comes into your clinic. He has a superficial, gray to white inflammatory membrane with fibrinosuppurative exudate in his mouth. You scrape off a sample, and note a erythematous inflammatory base.

What is the most common cause of this type of scenario?

What subtype causes this? (and what are the others?)

What is another scenario in which someone can get this type of infection?

Candida Albicans Infxn

Pseudomembranous ** (oral thrush)

Erythematous

Hyperplastic

After taking Antiobiotics – can get Oral Thrush (even immunocompetent)

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You have a patient who is a recent organ transplant recipient. He complains of eye and facial pain. He has had blurry vision, with soft tissue swelling. His top of his mouth is also very sore. You get a CBC, and sputum culture and do not find any bacterial organisms. The Lab does not that he apseptate hypae, branching at 90 degrees were found.

What is causing his symptoms?

What are some of ther potential organisms that could cause a similar manifestation?

Mucormycosis Infxn

Histoplasmosis, Blastomycosis, Coccidio, Crpyto, Aspergillosis

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You have a child come in that has Scarlet Fever, what would I expect to find inside this childs mouth?

What causes Scarlet Fever?

A Strawberry Tongue

Strep Pyogenes

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You have a child that comes in who was noted to not have been vaccinated. He now has measles, and your preceptor wants to know what are the most likely oral manifestations of this disease?

What causes Measels?

Spotty Enanthema in the Oral Cavity (before their rash)

and Koplik Spots (Ulcerations of the buccal mucosa)

Paramyxovirus

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You have a 14 year old boy that recently got a new girlfriend, and after making out with her for way too long, he gets diagnosed with Mono.

What are the oral manifestations of this disease?

What causes Mononucleosis?

Acute Pharyngitis, Tonsilits

(may have Gray-White Exudative Membrane)

Palatal Petechiae

Enlargement of the LN

EBV

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You have a patient that has Diptheria. What are the Oral Manifestations?

Dirty White, Fibrinosuppurative, Tough, Inflammatory membrane over their tonsils and retropharynx.

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In your new HIV patient, he asks you what things he needs to be worried about in the future regarding his oral health. You want to counsel him on exactly what problems can arise (or specifically his Oral Manifestations of his HIV) . . . you would say . . .

Predisposition for:

Herpes

Candida (and other Fungi)

Kaposi Sarcoma

Hairy Leukoplakia

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You have a patient that was recently diagnosed with HIV. You note that he has hyperkarototic thickenings on the lateral border of his tongue.

What is the name of this?

What Causes it?

What organism does it look like?

Hairy Leukoplakia

EBV

Looks like Candida – but can’t be scraped off

(Candida can be superimposed ontop of Hairy Leukoplakia sometimes)

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A 55 year old male patient comes into your clinic with a white patch that cannot be scraped off of their mouth. They are a 1ppd smoker for the past 30 years. Their previous history is otherwise normal, with no apparent PMH. They are worried about the change, and want to make sure its not cancerous.

What is the most likely diagnosis?

Is this cancerous?

Leukoplakia

It is considered precancerous until histo eval

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Where in the Oral mucosa is this most likely found?

How would we describe the appearance?

On Histo what do we see?

Buccal Mucosa, Floor of the Mouth, Ventral Surface of the Tongue, Palate, Gingiva

Patches of Sharply demarcated borders, smooth or wrinkled and fissured. May be corrugated, verrucous plaques.

A Spectrum of epi changes; from hyperkeratosis overlying a thickened acanthotic/orderly mucosal epi – to markedly dysplastic (into CIS)

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A 45 year old man comes into your clinic with what another physician describes as a severe dysplastic lesion, with intense subepithelial inflammatory reaction with vascular dilation. He noted that the lesion is slightly depressed with relation to surrounding oral mucosa. He also notes that the patient is 20 year 2ppd smoker.

What is the physician describing?

Is there a possibility of malignant transformation?

Erythroplakia

YES, a higher rate of malignant transformation than Leukoplakia.

**Note can be seen with Leukoplakia (Speckled Leukoerythroplakia)

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You have a 50 year old man with a extensive history of smoking and alcohol abuse show up to your clinic. You note that he has SCC of the oropharnyx.

What virus is associated with this?

What structures are usually associated?

What is seen Histologically?

What can SCC be confused with commonly?

HPV-16

Tonsils, Base of tongue, Pharynx

Epithelial gets replaced by Basal Looking Cells with Hyperchromatic Nuclei

Leukoplakias

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You have a 50 year old man with a extensive history of smoking and alcohol abuse show up to your clinic. You note that he has SCC of the oropharnyx.

What accounts for the poor prognosis of SCC?

Where does SCC of the oropharynx metastisize too locally?

Late Diagnosis, with metastsis to distant sites like: Mediastinal LN, Liver, Lungs, Bone

Cervical LNs

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You have a 50 year old man with a extensive history of smoking and alcohol abuse show up to your clinic. You note that he has SCC of the oropharnyx. What would you have expected him to be complaining of when his cancer was just an HPV precancerous lesion? What mutations are found in this patient with HPV associated SCC? Which one is associated with Squamous Differentiation?

NonSpecific Symptoms (Sore Throat, Ear Infxns, Odynophagia, Weight Loss) E6 --\> p53 (inactivation) E7 --\> Rb (inactivation) P63/NOTCH1 p16 (overexpressed) Squamous Differentiation --\> p63/NOTCH1

A 15 year old male patient presents to your clinic after a radiograph showed multilocular radioluciencies within the posterior mandible, the PCP sent them your way with high urgency. Upon histology you note a cyst with a thin layer of keratinized stratified squamous with a prominent basal cell layer and a corrugated epi surface. What does he have? What ages are most at risk for this? What should he be evaulated for? what mutation causes this syndrome?

Odontogenic Keratocyst (OKC) 10-40 year olds Nevoid Basal Cell Carcinoma Syndrome (GORLIN Syndrome) PTCH (chrom 9q22)

You have a 74 year old patient that is complaining of dry mouth. She has a decrease in the prodution of saliva. What are some complications of this? What are some causes of this?

Xerostomia --\> Dental Caries, Candiadiasis, Difficulty Swallowing and Speaking MEDICATIONS (Anticholingergics, Antidepress, Antipsychotics, Antihistamines, Diuretics, Sedatives, muscles relaxants, analgesics) Sjögrens Syndrome (seen with enlargement of salivary glands)

You have a toddler who is brought in by their mother with a fluid filled lesion on their lower lip that has a blue translucent hue. The child fell a couple of days ago, and she is worried that this might have caused this bump-lesion. What is the lesion most likely? On histo what would be expected? What causes this?

Mucocele Pseudocyst with cyst-like spaces lined with inflammatory granulation tissue (or Fibrous CN tissue), Mucin and Macrophages filled. Trauma, from blockage of the salivary gland duct --\> leakage into the stroma.

You have a toddler who is brought in by their mother with a fluid filled lesion on their lower lip that has a blue translucent hue. The child fell a couple of days ago, and she is worried that this might have caused this bump-lesion. What viral cause of sialadenitis is this toddler at risk for (assuming no vaccinations)? What does this affect?

Mumps Parotids, Pancreas, Testes

S. Aures, S. Viridans --\> causing sialolithiasis REVIEW: \*\*Recall there are Inflammatory (Mucoceles), Viral (Mumps), Bacterial (Sialolithiasis) of Sialadentiis!!

You have a toddler who is brought in by their mother with a fluid filled lesion on their lower lip that has a blue translucent hue. The child fell a couple of days ago, and she is worried that this might have caused this bump-lesion. After treating this toddler and all heals well. 10 years later the same toddler comes in with a ruptured sublingual gland. What do we call this? How would it look on histo?

Ranula A "Plunging Ranula" -- cysts that have dissected through the CN tissue stroma connecting the two bellies of the myohoid muscle.

You have a 43 year old woman who comes in with a painless, slow growing, mobile, and discrete mass within the buccal cavity. You note that it affects the Parotid gland. She was noted to have undergone radiation treatment 5 years ago following a cancer diagnosis. What is the most likely diagnosis? What is this a mixture of? What gene is this associated with?

**Pleomorphic Adenoma** **Ductal (Epi) and Myoepithelial Cells** *(Epithelial and Mesenchymal Differentiation)* PLAG1

You have a 43 year old woman who comes in with a painless, slow growing, mobile, and discrete mass within the buccal cavity. You note that it affects the Parotid gland. She was noted to have undergone radiation treatment 5 years ago following a cancer diagnosis. What would be seen upon histology? What is the malignancy potential of this? What is the name of the caricnoma that arises from this?

a Rounded, well demarcated mass under 6 cm. _GREAT HETEROGENIETY_ Malignancy potential increases with time. (but Pleomorphic is usually benign) Malignant Mixed Tumor (or Carcinoma ex Pleomorphic Adenoma)

You have a 55 year old male smoker that comes into your clinic. You note a oval, encapsulated 3 cm palpable nodule in the parotid gland. What is the diagnosis? What is seen Histologically? What is the nodule filled with? Where is this type of tumor usually seen exclusively?

Warthin Tumor A double layer of lining cells // Upper --\> palisading columnar cells with numerous mitochondria ; Lower --\> cuboidal to polygonal cells Mucinous or Serous Secretions (Dark Brown Fluid -- Motor Oil look) Parotid Gland ONLY!

You have a 55 year old male smoker that comes into your clinic. You note a oval, encapsulated 3 cm palpable nodule in the parotid gland. Benign or Malignant?

Benign

A 75 year old woman comes into your clinic with a large 8 cm circumscribed mall in her parotid gland. She is noted to have some pain along that side of her face. You note a mixture of squamous cells and mucus secreting cell and intermediate cells. What is the diagnosis? What Genes are usually associated? Where else can this grow?

Mucoepidermoid Carcinoma 11:19, q21;p13 (MECT1/MAML2) --\> hurts NOTCH Palatte, Buccal Mucosa, Tongue, Partoid

A 75 year old woman comes into your clinic with a large 8 cm circumscribed mall in her parotid gland. She is noted to have some pain along that side of her face. You note a mixture of squamous cells and mucus secreting cell and intermediate cells. How could we visualize this on histology? If she were noted to have Low Grade, what is the prognosis? Why would this patient be experiencing pain?

With a Mucin Stain Low Grade --\> Rarely would metasize, recur less frequent (High grade metastasizes much more frequently, and reoccurs more often) Because it grows Perineural

You have a patient you are observing, that has a tumor of the palatine glands. It is a slow growing tumor and has invaded some perineural spaces. The patient has had 3 recurrences in the past 10 years, and sadly has now had it disseminate to their bone, liver, and brain. What is the diagnosis? What makes this diagnosis more or less severe?

Adenoid Cystic Carcinoma Whether it affects the Minor Salivary Glands (More severe) or the Major Salivary glands (less severe) -- so this case is more severe, because of it affecting the palatine gland.

Small cells with dark, compact nuclei -- with little cytoplasm. The spaces between the tumor cells are filled with hyaline material.

You have a 1 week old baby who presents with non-billious vomiting, and failure to thrive. The baby also has a fever, and is having trouble breathing. The baby is coughing up a yellow-green sputum. You order a CBC, and note prominent WBC count. What is causing her presentation? Why is she presenting with a fever? What other congenital problems would this baby potentially have?

Esophageal Atreisa, specifically as a Tracheoesophageal Fistula Due to aspiration pneumonia -- and a bacterial infection. Heart Defects, GU, Neurologic Problems

You have a new-born that has yet to pass their meconium. You note a congenital abnormality of failure of the cloacal diaphragm to involute. What is the problem with the child?

Imperforate Anus (most common form of congenital intestinal atresia)

You have a patient who comes in complaining of dysphagia, and odynophagia. They have had to switch to a liquid diet, and have lost some weight because of this diet change. They have also had long bouts of spitting back up their food a little. You note that they are taking Omeprazole. What is the potential problem here? What exactly is causing the problem with swallowing? Besides GERD, what else could cause this?

Esophageal Stenosis (incomplete Atresia) Fibrous Thickening of the Esophagous from long-standing GERD. Systemic Sclerosis, Irradiation, Caustic Injury, (GERD)

You have a patient who comes in complaining of dysphagia, and odynophagia. They have had to switch to a liquid diet, and have lost some weight because of this diet change. They have also had long bouts of spitting back up their food a little. You note that they are taking Omeprazole. If this patient had been a child, and no history of GERD -- would you be thinking same thing? What Artery affects each of the following segments of the Esophagus that you need to be worried about? Upper 1/3 Middle 1/3 Lower 1/3

YES, but a Congenital Form of Esophageal Stenosis. Upper -- Inferior Thyroid A Middle -- Branches of Thoracic Aorta Lower -- Left Gastric A

You are on your OB/GYN rotation and help to delivery a baby, that is found to have a congenital anomalie. They have gastric contents that are found in a ventral membranous sac. You note it is from incomplete closure of the abdominal musculature. What is the problem? What if there was no sac?

Omphalocele Gastroschisis (all layers of abdominal wall are incompletely formed)

You have a patient that comes in complaining of Dysphagia, and GERD. You note that they have Barretts Esophagus, and are thus at risk for Adenocarcinoma. They have uncharecteristic amounts of gastric acid production in the upper 1/3 of the esophagus. What is the problem?

Inlet Patch (Ectopic Gastric Mucosa)

You have a patient on a routine visit that is found to have uncharacteristic tissue in the stomach and esophagus. They did not report any symptoms, but were found on histology to have inflammation and local tissue damage. The doc said that surprisngly the patient was headed toward an obstruction of the pylorus from all the inflammation and scarring, and would have been symptomatic in the near future. What is the cause?

Ectopic Pancreatic Tissue

You have a patient that comes in complaining of diarrhea, and bloody stools. You do an evaluation and find small patches of mucosa in the small bowel and colon. What is the cause? What is being secreted?

Gastric Heterotopia Gastric Juices

You have a 2 year old male that presents with bleeding from the rectum, and abdominal pain in the RLQ. What is potentially on your Dx? Where is it usually found? What causes this (physiologically)? What causes this (Embryologically)? How is the orientation of it?

Meckels Diverticulum (a true Diverticulum -- all 3 layers) Congenital -- Ileum // Acquired -- sigmoid colon Ectopic Pancreatic or Gastric Tissue, Failed Involution of the Vitelline Duct on the ANTI-Mesenteric Side of the Bowel

You have a 5 week year old baby boy who was born uncomplicated. His mother has noted that he has spontaneous regurtitation, projectile vomiting, non-bilious vomiting after feeding -- and then demands to be re-fed. On inspection of the baby you find a firm, ovoid 1-2 cm abdominal mass, and on auscultation of the abdomin you hear hyperactive bowel sounds. The mother was noted to have had a "bad" infection during the pregnancy, and took some left-over medicine she had from a prior infection. What is the cause of the problem? What potenitally caused it? What other types of people have this problem? How would you treat this?

Pyloric Stenosis Taking Antiobiotics : Azithromycin, Erythromycin Associated with: Monozygotic Twins/ Dizygotic Twins, Turner Syndrome, Trisomy 18 Tx with Surgical Splitting of the pylorus.

You have a 55 year old male who has had a long history of peptic ulcers, and antral gastritis. He is noted to have regurgitation, and non-bilious vomiting, and cant seem to stay full. He has lost some weight recently, and is worried. What is the problem? What cancers are associated?

Acquired Pyloric Stenosis -- from Antral Gastritis, Peptic Ulcers Carcinomas of the Distal Stomach and Pancreas are associated with Acquired Pyloric Stenosis

You have a 2 day old infant male who has yet to pass his meconium, but has passed little bits of stool. He is noted to have Down Syndrome, and some other serious neuological abnormalities. He has been having bilious vomiting for the past 2 days upon trying to eat, and upon auscultation you do not hear any bowel sounds. What is the patient most at risk for? Where does this problem usually start and work up too? What is the disease?

Enterocolitis\* Fluid and Electrolyte Disturbances Perforation Peritonitis From Rectum up proximally. Hirschprungs Disease

You have a 2 day old infant male who has yet to pass his meconium, but has passed little bits of stool. He is noted to have Down Syndrome, and some other serious neuological abnormalities. He has been having bilious vomiting for the past 2 days upon trying to eat, and upon auscultation you do not hear any bowel sounds. What is the tx process for this baby? What does the problem stem from? What mutations cause this? What immunologic stain would help me to document this loss?

Surgical Resection of the affected segments Loss of Meissner Submucosal and Auerbach Myenteric Plexus (aganglionosis) RET Gene, Endothelin (and receptor) Acetylcholinesterase stain

You have a 35 year old male coming in with problems swallowing. You find that the person has normal contractions with an increased LES pressure. What is the cause of this persons Esophageal Obstruction?

Nutcracker Esophagus

You have 40 year old woman who is having chest pain, dysphagia, and problems swallowing. She has normal troponin levels, and cardiac enzymes. What is most likely her cause? What physiologically is causing it? What would be seen on radiograph? How is the esophageal sphincter affected?

Diffuse Esophageal Spasm Uncoordinated Esophageal contractions. Corkscrew Appearance LES dysfxn -- its hypertensive

You have a 52 year old man who has been complaining of regurgitation, and his wife has been saying that he has had perpetual bad breath for a while now. He has been complaining of not being able to eat solid foods, and has lost some weight. What is the problem? Where is this usually found?

Zenker Diverticulum Killians Triangle

You have a 42 year old women who has has been complaining of fatigue and problems with eating. She is found to have decreased hemoglobin, and has microctic hypochromic RBC. Her tongue is swollen, and she has inflammation and cracking on the side of her mouth. What is causing her problems eating? What is this apart of, syndrome wise?

Esophageal Mucosal Webs (non-circumferential) Plummer-Vinson Syndrome

You have a man who has a circumferential rings of mucosa and submucosa in his esophagus. Your preceptor wants to know which type of Schiatzki Ring he has if it is just aboe the Gastroesophageal Jxn? What if it was at the squamocolumnar jxn of the lower esophagus?

A Rings -- covered by mucosa B rings -- they have gastric cardia mucosa on their undersurface

A 4 year old child comes in to your clinic with problems of feeding, inability to belch, dysphagia, and chest pain. He is found to have an increased LES tone, and a distinctive Bird Beak sign on radiograph imaging. What is this? Where is the degeneration?

Primary Achalasia In the Extraesophageal Vagus N, or Dorsal Motor Nucleus of the Vagus (in medulla)

You have a 53 year old man who recently got back from a vacation, and is now having problems eating solid foods, and is extremely worried. What is the most likely dx? What are some other (non-infectious) causes of this disease?

Secondary Achalasia -- due to T Cruzi. (Chagas Dz) Malignancy, Amyloidosis, Sarcoidosis, Polio, Down Syndrome, Triple A Syndrome, HSV1,

You have an 18 year old who recently tried alcohol for the first time, and got way too drunk. He starting thowing up, and is now throwing up blood. You diagnose him with a Mallory-Weiss tear, and your attending asks you to list some of the other main causes of esophageal-caused-hematemesis?

Boerhaave Syndrome Mallory-Weiss Syndrome Esophageal varices Esophageal-Aortic Fistula Infectious Esophagitis Benign Strictures Vasculitis Eosinophillic Esophagitis Chemical/Pill Esophagitis Esophageal Ulcers Barrett Esophagus Cancer Hiatal Hernia

You have a man present to the ER with severe mediastinitis, tachypnea, and shock. You find subcutaneous emphysema, and a crunching/rasping sound that follows along the heart beat. What is the disease? What is happening in this disease? What is the crunching/rasping sound called?

Boerhaave Syndrome Transmural Tearing and Rupture of Distal Esophagus Hammans Sign

A 83 year old man comes in with self-limited pain on swallowing, odynophagia and possible perforation. He noted that felt a lumb in his throat all day after taking his morning medications, and that this has been happening a lot recently. What does he have? Where does this usually happen? What accompanies the ulceration?

Pill-Induced Chemical Esophagitis At the site of strictures Superficial Necrosis with Granulation tissue and eventual fibrosis

You have a 31 year old man with no significant medical history present to your clinic with odynophagia, dysphagia, and chest pain when swallowing. After an EDG with Biopsy in which you find an ulcer, you get the results from histology and find that he has abundant neutrophils, and some mild necrosis, you also see nuclear viral inclusions within a rim of degenerating epi cells at the margin of the patients ulcer. What should we expect for the diagnosis? If he were noted to be immunocomprimised instead?

Infectious Esophagitis (with HSV) Same (with HSV, CMV, Candida, Asperg, Mucor)

You have a 31 year old man with no significant medical history present to your clinic with odynophagia, dysphagia, and chest pain when swallowing. After an EDG with Biopsy, you get the results of your histology and find that he has abundant neutrophils, and some mild necrosis. What does Candida look like on EDG? What type of ulcer does HSV make? What type of ulcer does CMV make?

Candida -- gray white pseudomembranes of fungal hyphae and inflamm cells HSV -- punched out ulcer, with herpesvirus nuclear inclusions CMV -- shallower ulceration and cytoplasmic inclusions within capillary endothelium and stromal cells (nuclear and cytoplasmic inclusions)

You have 45 year old woman who is constantly having Heartburn, Dysphagia, and regurgitation of sour tasting gastric contents. You decide to perscribe Pantoprazole, and tell her to modify some aspects of her life. What is her Diagnosis? What problem LOOKS like a GERD patient, but is infact more severe?

GERD, Reflux Esophagitis Hiatal Hernia (with herniation seen on Xray)

A 43 year old man has trouble swallowing his food, and rash on his upper arms, back, wrist, and hands; was seen by his doctor who gave him some Omeprazole, but it hasnt seem to help. He is noted to have asthma, and uses a bronchodilator every day. What is he presenting with? What would be seen under the microscope? What is the tx?

Eosinophillic Esophagitis superficial EOSINOPHILS (intraepithelial) Avoid Food Allergens, Systemic Corticosteroids

You have a patient that has Cirrhosis, and now has painless hematemesis. They have an elevated hepatic nevous pressure, and advanced liver disease. They are diagnosed with Esophageal Varices. What is the treatment for this? What causes this disease? Besides Cirrhosis, what else worldwise causes Esophageal Varices? What is the likelyhood of rupture?

Beta Blockers to reduce portal blood flow and Endoscopic Variceal Ligation Portal HTN causes you to have collateral channels being formed, and allow drainage into the subepithelial and submucosal venous plexi. Schistosomas (S. Mansoni) For Small Varices, that have never bled --\> low risk for bleeding and death For Large Varices, that have bled before --\> medical emergency

A 45 year old white male presents to your clinic with long standing GERD, and subsequent PPI use. He admits to being an alcoholic, but is in AA and is working on it. He is also a smoker 1/2 ppd, but is slowly quitting with perscribed Chantix. What is he at risk for? Which is? How do we diagnose this? What cancer can develop from this?

Barrett Esophagus Intestinal Metaplasia (Squamous to Columnar) ENDOSCOPY and BIOPSY! Adenocarcinoma

A 45 year old white male presents to your clinic with long standing GERD, and subsequent PPI use. He admits to being an alcoholic, but is in AA and is working on it. He is also a smoker 1/2 ppd, but is slowly quitting with perscribed Chantix. He is noted to have a long segment of barretts esophagus. . how does this affect his cancer risk?

It Increases it; Longer Segments of BE = Higher risk of Adenocarcinoma

A 45 year old white male presents to your clinic with long standing GERD, and subsequent PPI use. He admits to being an alcoholic, but is in AA and is working on it. He is also a smoker 1/2 ppd, but is slowly quitting with perscribed Chantix. He is noted to have Severe Cytologic and Archietectural changes, how would you grade his dysplasia?

High Grade Low Grade --\> Gland Archietecture Abnormal (Budding, Irregular Shapes, Cell Crowding)

A 56 year old white male is presenting with pain and difficulty swallowing, he has noted that he has had an unintentional 10 pound weight loss over the past 1 month. He has had some hemetemesis, chest pain, and vomting. On his past medications he has been taking Metformin, Pantoprazole, and Simvastatin. He says that he has had long-standing GERD for the past 10 years. What does he have? What does this arise from? What would I see microscopically in this area? What mutations give rise to this (Early/Late)? What is the prognosis?

Adenocarcinoma of the Distal 1/3 of the Esophagus Barretts Esophagus DIffusely Infiltrative Signet-Ring Cells TP53, CDKN2A (downreg) \<-- Early Amplification of EGFR, ERBB2, MET, Cyclin D1, Cyclin E \<-- Late Poor --\> usually diagnosed after metastasis to distant LN.

A 50 year old African American male comes into your clinic with sudden onset of dysphagia, odynophagia. He says that he has lately had to start going to an all liquid diet, and has lost some weight because of it. He says that he has smoked since he was 16, and that he drinks 5 drinks a week. His diet isn't the best, and doesnt like fruits and vegetables. What does he potentially have? What is the etiology of the disease? What genetics are involved?

Adenocarcinoma - Middle 1/3 of the Esophagus HPV infection can cause it, Plummer Vinson Syndrome can cause it, Tylosis -- LOF: TP53, Cadherin, NOTCH1 -- Amplification of SOX2 Genes

A 50 year old African American male comes into your clinic with sudden onset of dysphagia, odynophagia. He says that he has lately had to start going to an all liquid diet, and has lost some weight because of it. He says that he has smoked since he was 16, and that he drinks 5 drinks a week. His diet isn't the best, and doesnt like fruits and vegetables. What is seen Early in the disease process? What is seen Late in the disease process?

Early --\> small, gray white plaque like thickenings Later --\> thickenings grow to be polypoid or exophytic and can obstruct the lumen they can cause pneumonia and invade the aorta, or mediastinum.

You have a patient that is worried about developing stomach ulcers, because he read online that they kill you. You reassure him that normal things like Surface mucus secretion, bicarb, and epithelial barrier function help to protect from the normal damaging factors like your stomachs own acid and peptic enzymes. You do tell him, if he is that worried to avoid the following causing worse injury that could lead to an ulceration . . . .

NASIDs H Pylori Infxn Tobacco Alcohol Gastric Hyperacidity Duodenal-Gastric Reflux

A 45 year old female patient comes in with epigastric pain, N/V, and melena, and occasional bilious vomiting. On further inspection your find mucosal erosion, ulceration, and some hemorrhage of the gastric mucosa. You take a biopsy and on histology you find an abundance of neutrophils. What is the most likely diagnosis? What is causing her Bilious Vomiting? What would be the morphological sign you would expect? If her biopsy had shown no inflammatory cells would this change the diagnosis?

Acute Gastritis Bile Reflux Foveolar Cell Hyperplasia with a Corkscrew appearance and epi proliferation YES! We would classify it -- Acute Gastropathy

A 45 year old female patient comes in with epigastric pain, N/V, and melena, and occasional bilious vomiting. On further inspection your find mucosal erosion, ulceration, and some hemorrhage of the gastric mucosa. You take a biopsy and on histology you find an abundance of neutrophils. What is the normal layer of protective mechanisms that the stomach has in place to protect itself? Erosion causes a superficial mucosal defect with a fibrin purulent exudate that can progress to what?

Mucus layer over the stomach, Bicarb "Alkaline Tide", an unstirred layer of Neutral pH fluid on top of the mucus, and constant replacement of the foveolar cells Ulcers

You have a man who just recently came to hospital after falling down 3 stories in a burning building. He suffered severe trauma, burns, and intracranial problems - and is admited to the ICU. To stabilize the patient we worry about the "whole patient" -- so naturally we want to know what type of ulcers he is prone to at his stay in the hospital. What type of ulcers is he prone to from his injuries and his prolonged stay in the hospital?

Stress Ulcers Curling Ulcers -- from the burns and trauma Cushing Ulcers -- from the intracranial

You have a man who just recently came to hospital after falling down 3 stories in a burning building. He suffered severe trauma, burns, and intracranial problems - and is admited to the ICU. To stabilize the patient we worry about the "whole patient" -- so naturally we want to know what type of ulcers he is prone to at his stay in the hospital. His Stress ulcer is from what problem? What does these ulcers look like on endoscopy? How long will it take to heal these ulcers?

Ischemia from systemic hypotension or reduced blood flow. (look for splanchnic vasoconstriction) Found anywhere in the stomach; Well Demarcated, rounded, less than 1 cm, base is stained brown-to-black by acid digestion. Days -- to several weeks!

A 72 year old presents with massive, painless hemetemesis, and has significant hypoytension. She has been taking NSAIDs for the past 2 years, and has noticed ever time she takes them she has this bout. Her liver function tests are weirdly normal, and so you move to the next item on your differential; What could be happening here? What causes the bleeding in this?

Dieulafoy Lesion Dilated Submucosal A's along the lesser curvature of the stomach, being exposed causing the bleeding.

You have a 62 year old cirrhotic patient who also has systemic sclerosis come in complaining of hemetemesis, and fatigue. You get a CBC and note that they have Iron Def. Anemia. You decide to do an endoscopy and find longitudinal stripes of edematous erythematous mucosa next to paler mucosa. You also find fibirin thrombi in capillaries. What is the disease? What is the name of the exam findings? What is causing this? What would you find in the stools of this patient?

Gastric Antral Vascular Ectasia (GAVE) Watermelon Stomach Cirrhosis and Systemic Sclerosis (usually idiopathic) Occult Fecal Blood

You have a 62 year old AA patient who comes in with N/V and upper abdominal pain, they deny any hemetemsis, but states that their symptoms have been persistent the past couple of weeks. Their Urea Breath test is +, and have a + fecal bacterial detection. You correctly diagnose them with H. Pylori Chronic Gastritis. Where does this gastritis usually begin? What is the person at risk for (in terms of other ulcers?) What is this called when this affects more than just the orignal site? What are they more at risk for now that it affects more than one site?

Antrum of the Stomach -- not seen with hypergastrinemia Duodenal Peptic Ulcers, and involving the rest of the Stomach (Body and Fundus) Multifocal Atrophic Gastritis Gastric Adenocarcinoma

You have a 62 year old AA patient who comes in with N/V and upper abdominal pain, they deny any hemetemsis, but states that their symptoms have been persistent the past couple of weeks. Their Urea Breath test is +, and have a + fecal bacterial detection. You correctly diagnose them with H. Pylori Chronic Gastritis. What gene is usually found in thses cases? What factors are increased/decreased? How does Iron def. Anemia affect their cancer outlook?

CagA Gene Increased --\> TNF, IL-1B Decreased --\> Il-10 It is a risk factor for H. Pylori associated Gastric Cancer

You have a 62 year old AA patient who comes in with N/V and upper abdominal pain, they deny any hemetemsis, but states that their symptoms have been persistent the past couple of weeks. Their Urea Breath test is +, and have a + fecal bacterial detection. You correctly diagnose them with H. Pylori Chronic Gastritis. Where is the H. Pylori found in the stomach antrum? What transformation do you see occur that leads to a type of cancer in these patients? Is H. Pylori found anywhere else in the GI Tract?

In the Superficial Mucosa overlying the epi cells Lymphoid Aggregates (with Germinal Centers) --\> this MALT can transform into Lymphoma. (MALToma) NO -- only in the stomach -- it can cause duodenal peptic ulcers, but H Pylori doesnt stay in the duodenum.

A 60 year old woman comes into your clinic complainig of a smooth, beefy red tonque. She is noted to have Type 1 DM, and Primary Ovarian Failure. She has been progressively tired lately, and epigastric pain, and malabsorptive diarrhea. What is she suffering from? What is causing her fatigue? What is the name of her tongue complaint, and what causes it? What HLA alleles are associated with this disease?

Autoimmune Gastritis Pernicious Anemia (B12 def) Atrophic Glossitis --\> Vit B12 Def (Pernicious Anemia) NONE -- not Associated with HLA

A 60 year old woman comes into your clinic complainig of a smooth, beefy red tonque. She is noted to have Type 1 DM, and Primary Ovarian Failure. She has been progressively tired lately, and epigastric pain, and malabsorptive diarrhea. What sort of cancer risk does she have? If she were complaing of neurologic changes what would this tell us, and how can we help?

High risk of ADENOCARCINOMA She'd have "Subacute Combined Degeneration of the Cord" -- and we'd treat this with B12 supplementation --\> but it wouldnt reverse the neurological changes.

A 60 year old woman comes into your clinic complainig of a smooth, beefy red tonque. She is noted to have Type 1 DM, and Primary Ovarian Failure. She has been progressively tired lately, and epigastric pain, and malabsorptive diarrhea. What is the pathogenesis? What would we see in immunostain?

Loss of Parietal Cells --\> loss of Gastric Acid/IF --\> Stimulates Gastrin Release from Enterochromaffin cells --\> causes Hypergastrinemia/ Loss of IF means Vit B12 def --\> megaloblastic anemia (a decrease in # of RBC) CD4 T Cells against Parietal Cell components (H/K ATPase) CHROMOGRANNIN A

You have a 67 year old patient that had recent epigastric burning, fatigue. She states it happens 1-3 hours after a meal, and is always worse at night. When she eats it makes it better for just a bit. She also has been belching alot more, and feels bloated. She has been taking NSAID's to help relieve the pain, but it hasnt been working. She is also a long term smoker of 2ppd. What is going on? What is associated with this disease? Where, anatomically, is this located?

Peptic Ulcer Disease H. Pylori Infection (Chronic Gastritis) in The Lesser Curvature of the Stomach (can also occur in the Proximal Duodenum)

You have a 67 year old patient that had recent epigastric burning, fatigue. She states it happens 1-3 hours after a meal, and is always worse at night. When she eats it makes it better for just a bit. She also has been belching alot more, and feels bloated. She has been taking NSAID's to help relieve the pain, but it hasnt been working. She is also a long term smoker of 2ppd. If this patient had a pneumoperitoneum -- what would this tell us?

Perforation --\> Medical Emergency

A 34 year old male comes into your clinic with diarrhea, weight loss, and hypoproteinemia -- seen with edema, and malnutrition. He says that he has had some hemetemesis, and epigastric pain as well. He is noted to have hypochlorhydria, and a positive fecal blood test. And excessive secretion of TGF-Alpha. What is the most likely diagnosis? What would be seen on endoscopy? What is his prognosis? If the patient were a child instead, what would the prognosis be?

Menetrier Disease Giant Gastric Folds (from Hyperplasia of the Foveolar Epi) Needs to be evaluated for risk of gastric adenocarcinoma Self-limited -- usually followed a respiratory infection.

A 50 year old male has duodenal ulcers and chronic diarrhea. You find doubling up of the Oxyntic Mucosal Thickness and a ton of parietal cells. You also note there is excessive mucin production, and proliferation of endocrine cells. On microscopy you find that neutrophils are the main infiltrate. What is the disease? Where does this occur? How do we treat this? What is his prognosis?

Zollinger-Ellison Syndrome (from a gastrin secreting tumor in fundus) Found in the Small Intestine and Pancrease PPI's Most Gastrinomas are malignant (need to be resected), also watch out for MEN I. NOT ASSOCIATED WITH ADENOCARCINOMA

Rapid Fire: Which Polyp is most common in people between 50-60, found in the antrum, with neutrophilic and lymphocytic infiltrate, and will occasionally transofrm into adenocarcinoma? (most common form of polyps)

Inflammatory/Hyperplastic Polyps

Rapid Fire: Which polyp has no dominant age range, found in the body of the stomach, it is mostly mucous cells with a cystic lining, neutrophilic and lymphocytic infilrate, NOT associated with adenocarcinoma!

Gastric Cystica

Rapid Fire: Which polyp is average right at 50 years old, found equally in the body and fundus of the stomach, and has nausea as its major symptom. It is associated with FAP syndrome.

Fundic Gland Polyps

Rapid Fire: Which polyp is present in an average age of 50-60 and is found more in the antrum, with variable inflammatory infiltrate, and is frequently associated with adenocarcinoma?

Gastric Adenomas.

You have a 55 year old man who presents with dyspepsia, dysphagia, nasuea for the past 3 weeks, and recently has noticed he hasnt been hungry, and has lost some weight. When he does eat he gets full pretty quickly, and has been fatigued. He states a different doctor told him he has something called Chronic Gastritis, and gave him some PPI's, but he didnt feel like the doctor treated the "whole person" so he came to you. You want to do an endoscopy to check some things out and find that there are bulky masses in his stomach. What is the potential diagnosis? If his findings had found infiltrates thickening the mucosal wall, and Signet Ring Cells -- would this change your diagnosis?

Gastric Adenocarcinoma -- Intestinal Type YES, it would be GA --\> Diffuse Type

You have a 55 year old man who presents with dyspepsia, dysphagia, nasuea for the past 3 weeks, and recently has noticed he hasnt been hungry, and has lost some weight. When he does eat he gets full pretty quickly, and has been fatigued. He states a different doctor told him he has something called Chronic Gastritis, and gave him some PPI's, but he didnt feel like the doctor treated the "whole person" so he came to you. You want to do an endoscopy to check some things out and find that there are bulky masses in his stomach. You note that the Adenocarcinoma has gone to 5 of the most common LN metasis (how unlucky for him) -- What are the most common sites?

Virchow Node (Supraclaviulcar Sentinel LN) Sister Mary-Joseph Node (Periumbilical LN) Irish Node (Left Axillary LN) Krukenberg Tumor (Ovary) {yes i know I said he was a man] Pouch of Douglas

You have a 55 year old man who presents with dyspepsia, dysphagia, nasuea for the past 3 weeks, and recently has noticed he hasnt been hungry, and has lost some weight. When he does eat he gets full pretty quickly, and has been fatigued. He states a different doctor told him he has something called Chronic Gastritis, and gave him some PPI's, but he didnt feel like the doctor treated the "whole person" so he came to you. You want to do an endoscopy to check some things out and find that there are bulky masses in his stomach. If this man had a familiy history of Gastric Cancer -- what would the LOF Mutation be?

CDH1 Gene (E-Cadherin) TP53 BRCA2 mutations -- have a higher risk as well

You have a 55 year old man who presents with dyspepsia, dysphagia, nasuea for the past 3 weeks, and recently has noticed he hasnt been hungry, and has lost some weight. When he does eat he gets full pretty quickly, and has been fatigued. He states a different doctor told him he has something called Chronic Gastritis, and gave him some PPI's, but he didnt feel like the doctor treated the "whole person" so he came to you. You want to do an endoscopy to check some things out and find that there are bulky masses in his stomach. Since this is a more sporadic intestinal type gastric cancer what are the genetics associated?

LOF -- APC gene, TGF-B, BAX, CDKN2A GOF -- B-Catenin

You have a patient that recently got diagnosed with a MALToma from their H. Pylori Chronic Gastritis. THey are presenting with Dyspepsia, Epigastric pain, and Hemetemesis, Melena and weight loss. The lymphoma arose in the stomach, and he also has a problem with an infection of EBV in the bowel. What is the most common translocation associated here? This MALToma can transform into a more aggressive tumor, what is it? MALTomas express which CD markers?

t(11:18)(q21;a21) -- AP12 gene, with mutated MLT activating NF-kB --\> promoting B Cell growth and survival (MALToma) Diffuse Large B Cell Lymphoma (due to inactivation of p53, p16) -- not responsive to H pylori eradication CD19,20, and CD43 in 25% of cases

A 60 year old man with blood loss, anemia, and a tumor that arose from the Intestinal cells of Cajal presents to your clinic. Your preceptor notes that this tumor is the most common mesenchymal tumor of the abdomen. What is the tumor? You treat with Imatinib which responds well to which mutations? This tumor is more common in which other diseases?

GIST -- Gastrointestinal Stromal Tumor KIT or PDGFRA mutations Neurofibromatosis Type 1, Carney Triad (in young females)

Rapid Fire: Where are GI Carcinoid Tumors most seen in the GI tract?

[MOST COMMON] Jejunum/Ileum, Appendix/Colorectum, Stomach/Proximal Duodenum, Esophagus [LEAST COMMON]

Rapid Fire: Carcinoid Tumors are associated with what? Ileal Carcinoid Tumors have what symptoms? Where embroylogically do most metastasis come from?

Endocrine Cell Hyperplasia, Autoimmune Chronic Gastritis, MEN1, ZES PPI therapy Cutaneous FLushing, Sweating, Bronchospasm, Colicky Abdominal Pain, Diarrhea, Midgut (Jejunum/Ileum)

A 35 year old female comes into your clinic with abdominal pain, distention, vomting and constopation. She had a radical hysterectomy about 5 months ago, and was doing fine up until about a week ago. What is causing her problem?

Adhesions -- causing Intestinal Obstruction

You have a 26 year old male who comes in with distention of the stomach, and abdominal pain, and scrotal pain. Your doctor while helping the patient, explains that this is the most frequent cause of intestinal obstruction world wide. What is the problem? Why is this a problem?

External Herniation through the Inguinal Canal Small bowel loops go through the canal, and impinging on venous drainage and blood flow. This causes stasis --\> can strangle the bowel --\> cause infarction and infection.

A 2 year old male is having obstruction and infarction of his sigmoid colon. On Xray you see an Xray Sign. What is going on? -------------------------------------------------------- What other form of obstruction are children most at risk for? - what would the kid need (association wise) in order for you to think of this? How would you tx this child?

Volvulus -- twisting of the bowel at the mesenteric point. Intussuception. Viral Infection, MALT tissue -- things that create a leading edge to cause Intussuception. (Rotavirus) Contrast or Air Enema

You have a patient that doesnt know how to describe their findings to you. They read on wikipedia the difference between Melena and Hematoschezia -- but have now forgotten. How would you descirbe the difference?

Melena -- from higher up -- dark tarry stools -- digested blood Hematoschezia --\> bright red blood from the rectum usually

A 70 year old woman comes into your clinic with sudden onset of cramping, LLQ pain, passage of blood in the stool, and sometimes bloody diarrhea. She is noted to have COPD, and Cardiac Arrythmias. Upon ausculatation you do not hear any abdominal sounds over the stomach. What are we worried about? What areas are we worried about? Which stage causes the most damage?

Ischemic Bowel Disease Watershed Areas -- Splenic Flexure/Sigmoid Colon, Rectum/ -- specifically the surface epithelium Reperfusion Injury (Stage) -- the bowel is pretty good (with collateral circulation) during the hypoxic stage, but restoration of blood causes free radicals, neutrophils, inflamm mediators etc.

A 70 year old woman comes into your clinic with sudden onset of cramping, LLQ pain, passage of blood in the stool, and sometimes bloody diarrhea. She is noted to have COPD, and Cardiac Arrythmias. Upon ausculatation you do not hear any abdominal sounds over the stomach. What other systemic problems could contribute to this? What specific type of this disease has a higher mortality?? What other things can precipate this general disease?

HS Purpura, Wegener Granumloam, PAN Right Sided Colonic Ischemia (from occlusion of the SMA) Cardiac/Vascular Problems, Vasoconstrictors, Elicit Drugs, CMV, Ecoli, Hernias

A 70 year old woman comes into your clinic with sudden onset of cramping, LLQ pain, passage of blood in the stool, and sometimes bloody diarrhea. She is noted to have COPD, and Cardiac Arrythmias. Upon ausculatation you do not hear any abdominal sounds over the stomach. What would her bowel look like? If she had Chronic Ischemia how would that show up?

Intensely Congested, Darkly-purple-red color, the wall will be edematous, thickened and rubbery. Fibrous Scarring of the Lamina Propria as well as stricture formation (can lead to more obstruction)

You have a 45 year old male post radiation treatment who has aneroxia, abdominal cramps, and malabsorptive diarrhea. You find radiation fibroblasts within the stroma of his bowel. What is the problem?

Bowel Ischemia -- from Radiation Enterocolitis

What is a disorder of the small/large intestines that is a GI emergency for Neonates?

Necrotizing Enterocolitis

A 65 year old women has chronic symptoms of a Lower GI Bleed, specifically found in the right colon. She also is noted to have a meckels diverticulum in her ileum. Upon further inspection you find tortuous venins, venules, capillaries of the submucosa and mucosa. What is her most likely diagnosis?

Angiodysplasia

Which diseases are associated with problems of proteins, carbs, and fats being broken down for absorption?

_Intraluminal Digestion_ ## Footnote **Chronic Pancreatitis** **CF** **Primary Bile Acid Malab** **IBD**

Which Diseases are associated with problems involving hydrolysis of carbs and peptides by disaccharidases.

_Terminal Digestion_ ## Footnote **Celiac Dz** **Env Enteropathy** **Autoimmune Enteropathy** **Diassch. Def** **Viral/Bacterial/Parastitic Gastroenteritis** **IBD**

Which Diseases are associated with problems in lymphatic transport of absorbed lipids?

_Lymphatic Transport_ ## Footnote **Whipple Disease**

Which Diseases are associated with problems withn nutrients, fluid, and electrolytes being transported across and processed withing the SI epi?

_Transepithelial Transport_ ## Footnote ***Look at table 17-7 (pg 781)***

A person that has isotonic stool, that continues with fasting has what type of Diarrhea? A person with lactase def, or excessive osmotic forces exerted by unabsorbed luminal solutes, and goes away when fasting? A person who has steatorrhea, or failure of nutrient absorption -- and is relieved by fasting has what type of diarrhea? A person who has a purulent, bloody stools that continues with fasting -- has what type of diarrhea?

Secretory Diarrhea Osmotic Diarrhea Malabsorptive Diarrhea Exudative Diarrhea CONTINUES with Fasting --\> Secretory/Exudative STOPS with Fasting --\> Osmotic/Malabsorptive

A 35 year old woman has had chronic diarrhea, bloating, chronic fatigue and a itchy rash on her skin for the past 3 months. You find excess plasma cell activation with a ton of IgA abs. She is noted to have been diagnosed with Sjögrens syndrome 5 years ago, and has been slightly depressed. What is the potential etiology of her problems? Which HLA's are helpful in this dz? What is the most diagnostic test for this dz? What would be seen on scope?

Celiac Dz HLA-DQ2, HLA-DQ8 tTG AB serologic test is most Diagnostic for Intraepithelial CD8 T Cells Massive loss of Villi (total villous atrophy), dense plasma cell infiltrates in lamina propria, Crypt Hyperplasia, and loss of brush border surface area.

Gliadin Peptide --\> causes IL15 to be released from Epi Cells --\> causing IE T Cells to be expressed --\> once the cell is stressed, T Cells express MIC-A allowing NKG2D to bind causing DAMAGE to the cells --\> allowing more Gliadin into the cell (causing a cycle)

A 35 year old woman has had chronic diarrhea, bloating, chronic fatigue and a itchy rash on her skin for the past 3 months. You find excess plasma cell activation with a ton of IgA abs. She is noted to have been diagnosed with Sjögrens syndrome 5 years ago, and has been slightly depressed. What other systemic diseases are associated with this dz?

T1 DM, Hashimotos Thyroiditis, Sjogren Syndrome, IgA Nephropathy, Ataxia, Autism, Depression, Epilepsy, Down Sydrome, Turner Syndrome

Rapid Fire: What disease is associated with poor sanitation areas and developing countries, where the people will have defective intestinal mucosal immune function -- and there is no clinical lab or histopath to help diagnose it?

Environmental Enteropathy (Tropical Sprue)

Rapid Fire: This disease is an X-Linked Disorder with severe persistent diarrhea in young children. It is due to a FOXP3 gene mutation on the X chromosome. With defective CD4 T-Reg Cells. These people will have autoabs to enterocytes, Goblet Cells. And abs to Parietal and Islet Cells.

**Autoimmune Enteropathy** IPEX syndrome was the dz mentioned.

Rapid Fire: This disease is a rare AR disorder where you cant secrete triglyceride rich lipoproteins. Usually presents in infancy who is having a problem with diarrhea, steatorrhea, failure to thrive. There is a mutation of the MTP protein -- so you have intracellular lipid accumulation. You will see Burr Cells on peripheral blood smear, and use an OIL-Red O Stain for lipids?

Abetalipoproteinemia

Rapid Fire: Cant drink milk, without diarrhea, frothy stools, abdominal distention.

Congenital Lactase Def Acquired -- happens because of downreg of lactase gene expression.

A 23 year old female comes into your clinic with abdominal pain, bloating and diarrhea She has said that her symptoms seem to get better once she goes to the bathroom, but she has noticed that her stool consistency has changed. You take a thorough HPI, and find that she also had a viral gastroenteritis about 8 months ago, and it has started since then. What do you think is going on here? What could a possible cause be? How can we help her with her symptoms?

She has IBS-D -- but its a diagnosis of exclusion. Too much Bile Acid Creation/Malabsorption -- for IBS-D ONLY Tx with a 5-HT3 Receptor Antagonist (Ondansetron -- the setrons) for IBS-D

Psychological Stressors, Diet, Perturbation of Gut Microbes, Abnormal GI Motility, Increased Enteric System Responses, Brain-Gut Axis problem.

You have a patient that has intermittent attacks of diarrhea, fever, abdominal pain (RLQ), and that he has had to quit smoking, becuase it has made it worse. He has a rash on his knees, and his eyes are slightly inflammed. He also states that his joints have hurt, but it seems to be a different joint all the time. You find on serology that he is + for ASCA ab. What disease does he potentially have? What things do we need to worry about in this patient? Does this person have a risk of cancer?

Inflammatory Bowel Disease -- CHRON Disease Malabsorption, Malnutrtion, Hypoalbuminemia, Iron Def Anemia, B12 def, Fibrosing Strictures -- causing bowel obstruction YES! You need to watch out for Adenocarcinoma! *(if theres colonic involvement)*

You have a patient that has intermittent attacks of diarrhea, fever, abdominal pain (RLQ), and that he has had to quit smoking, becuase it has made it worse. He has a rash on his knees, and his eyes are slightly inflammed. He also states that his joints have hurt, but it seems to be a different joint all the time. You find on serology that he is + for ASCA ab. What type of inflammation is present in this patient? How will the wall appear? How will any ulcer appear? What is a hallmark microscopically of this disease?

Transmural Inflammation (present in SKIP Lesions) THICKENED Deep, Knife Like Non-Caseating Granulomas

You have a patient that has intermittent attacks of diarrhea, fever, abdominal pain (RLQ), and that he has had to quit smoking, becuase it has made it worse. He has a rash on his knees, and his eyes are slightly inflammed. He also states that his joints have hurt, but it seems to be a different joint all the time. You find on serology that he is + for ASCA ab. What genes are associated? Which T Cells are more common? What is the earliest lesion of this disease? What would this disease look like under the microscope?

1) NOD2/NFkB ATG16L1 IRGM 2) Th1/Th17 cells 3) Apthous Ulcer 4) Cobblestone Appearance

You have a patient that has intermittent attacks of diarrhea, fever, abdominal pain (RLQ), and that he has had to quit smoking, becuase it has made it worse. He has a rash on his knees, and his eyes are slightly inflammed. He also states that his joints have hurt, but it seems to be a different joint all the time. You find on serology that he is + for ASCA ab. Where is this disease most common, and what type of lesions are found?

Terminal Ileum, Ileocecal Valve, and Cecum SKIP LESIONS

You have a patient who has had Lower Abdominal pain, cramping that is relieved by defecating, and stringy, mucoid, bloody, diarrhea. They have just recently started chantix to help stop smoking, but have been under such stress that they have started smoking again -- and have found that it is helping their symptoms. Upon serology you find + pANCAs. What is the potential dz? Where does this disease affect? What do we need to watch out for in this patient? What is this patients cancer risk?

Inflammatory Bowel Disease -- Ulcerative Colitis RECTUM --\> works its way up through colon. can affect the whole colon (Pancolitis) and can affect a little part of the ileum (called backwash ileitis) Toxic Megacolon YES, associated with Adenocarcinoma.

You have a patient who has had Lower Abdominal pain, cramping that is relieved by defecating, and stringy, mucoid, bloody, diarrhea. They have just recently started chantix to help stop smoking, but have been under such stress that they have started smoking again -- and have found that it is helping their symptoms. Upon serology you find + pANCAs. How is the wall of the site affected? Where is the inflammation? How would you characterize the Ulcers? Does this patient have any risk of Granulomatous formation?

Serosal surface is normal (no thickening) --\> DIFFUSE distribution Inflammation is limited to the Mucosa. Superifical Broad-Based. NO -- UC not associated with Granulomas

You have a patient who has had Lower Abdominal pain, cramping that is relieved by defecating, and stringy, mucoid, bloody, diarrhea. They have just recently started chantix to help stop smoking, but have been under such stress that they have started smoking again -- and have found that it is helping their symptoms. Upon serology you find + pANCAs. How does the colon look? What genes are associated?

Slightly Red or Granular Colon with broad based superficial ulcers. Pseudopolyps -- that can form mucosal bridges. Mural thickening is not present, so we need to watch out for Toxic Megacolon --\> perforation. ECM1 HNFA

Rapid Fire: This problem is from a complication of a surgery where you get a blind distal segment of the colon, and they develop numerous mucosal lymphoid follicles with germinal centers. It is sometimes seen in UC patients where the problem is because of a diverted segment.

Diversion Colitis

Rapid Fire: You have a middle aged woman with dense subepithelial collagen layer, and increased numbers of intraepithelial lymphocytes and a mixed inflammatory infiltrate within the lamina propria.

Collagenous Collitis (a form of Microscopic Collitis)

Rapid Fire: You have a Person with celiac disease, where the subepithelial collagen layer is normal thickenss, and there is an increase in intraepithelial lymphocyte. You can also have this problem if you have Graves Dz, Rheumatoid Arthritis etc.

Lymphocytic Collitis

Rapid Fire: You have a patient who just got a hematopoietic stem cell transplant, and now has water diarrhea. They will have Epithelial apoptosis, particularly of the crypt cells.

Graft-Vs-Host Dz

You have a patient that comes in with Intermittent cramping, continous lower abdominal discomfort, constipation, distention of the abdomen, and the feeling that they cant fully empty their rectum. What is the disease? What side is most likely affected if this patient is from the western part of the globe? What is the pathogenesis? What is the Tx?

Sigmoid/Colonic Diverticular Disease (Diverticulosis) Left Sided Elevated Intraluminal pressure in the colon -- forms along the taeniae coli. Can cause diverticultis is it becomes inflammed. High-Fiber Diet -- resolves spontaneously.

You have a patient that comes in with Intermittent cramping, continous lower abdominal discomfort, constipation, distention of the abdomen, and the feeling that they cant fully empty their rectum. What would the morphological features be? (NOTE: Most people are asymptomatic with this disease!)

Small, Flask like outpouchings alongside the taeniae coli surrounded by fat containing epiploic appendices A thin wall composed of flattened/atrophic mucosa, compressed submucosa, and attenuated/absent muscularis propria. Hypertrophy of the Circular layer of muscularis propria

Rapid Fire: Which type of polyp occurs sporadically or with a component of a genetic syndrome -- due to germline mutations in tumor suppressor genes or proto-oncogenes. They are usually associated with an increased risk of cancer (considered pre-cancerous)

Hamartomatous Polyps

You have a 3 year old child that is presenting with rectal bleeding; he is also noted to have digital clubbing. The family notes that their family has a history of this type of problem, and that its some sort of polyp problem. What does this child have? What is the inheritance? What will this inheritance require, surgery wise? What genes are associated? Does this child have a potential for malignany transformation?

Juvenile Polyps (Retention Polyps - a type of Hamartomatous polyp) AD Colectomy to limit hemorrhage SMAD4, BMPR1A YES -- lots of types of adenocarcinoma.

A 11 year old child comes into your clinic with Dark Blue-Brown macules on his lips, nostrils, buccal mucosa and on his palms and genitals. He has multiple GI Hamartomatous polyps and mucocutaneous hyperpigmentation. What disease does this child have? What mutation can help with Diagnosis? What should we think about screening him for?

Puetz-Jeghers Syndrome STK11 mutation Gastric and Small Intestine Cancers

The polyps will be large and pedunculated with a lobulated contour (which can cause intussuception) On Histo -- you will see Arborizing network of connective tissue, smooth muscle, lamina propria and glands lined by normal appearing intestinal epi. (The arborizing -- helps to distinguish PJS from Juvenile polyps)

A 11 year old child comes into your clinic with Dark Blue-Brown macules on his lips, nostrils, buccal mucosa and on his palms and genitals. He has multiple GI Hamartomatous polyps and mucocutaneous hyperpigmentation. When this boy is in his 20-30's what do we need to screen him for? What was he screened for when he was a baby?

20-30 -- colon, pancreatic, breast, lung, ovarian, uterine cancers Babies -- Sex Cord Tumors of Testes

You have a patient that is known to have AD Familal Adenomatous Polyposis. Their average polyp size is around 5 cm. They have 100s of polyps that have riddled the colon. They also have Congenital Reinal Pigmented Epithelium Hypertrophy. What are the genes associated with Classic FAP? What are the genes associated with MYH Associated APC?

APC MYH

Rapid Fire: Which Etiology is related to the following: APC/WNT pathway (molecular defect) APC target Gene AD inheritance Tubular, Vilious Typical Adenocarcinoma

Familial Adenomatous Polyposis

Rapid Fire: Which Etiology is related to the following: DNA Mismatch repair (molecular defect) MYH target gene AR inheritance Sessile serrated adenoma, mucinous adenocarcinoma (histology)

MYH Associated Polyposis

Rapid Fire: Which Etiology is related to the following: DNA Mismatch repair (molecular defect) MSH2, MLH1 AD inheritance (Right side predominant of colon) Sessile serrated adenoma, mucinous adenocarcinoma (Histology)

Hereditary Nonpolyposis Colorectal Cancer (Lynch Syndrome)

Rapid Fire: Which Etiology is related to the following: APC/WNT Pathway APC (Left Side of Colon Predominant) Tubular, Villous - Typical Adenocarcinoma

Sporadic Colon Cancer (70-80%)

Rapid Fire: Which Etiology is related to the following: DNA Mismatch Repair MSH2, MLH1 (Right side predominant in colon) Sessile Serrated Adenoma, Mucinous Adenocarcinoma

Sporadic Colon Cancer (10-15%)

Rapid Fire: Which Etiology is related to the following: Hypermethylation MLH1, BRAF (Right side of colon predominant) Sessile Serrated Adenoma, Mucinous Adenocarcinoma

Sporadic Colon Cancer (5-10%)

You have an 85 year old male patient that comes in with fatigue and weakenss. You learn that they have iron deficient anemia. You find that this person has actually been losing weight unintentionally. What do we always need to think about in this patient presentation? What molecular defect/target gene is affected? What were are some risk factors for this patient?

Right Sided Colorectal Adenocarcinoma -- *these symptoms are specific for this type.* DNA Mismatch Repair -- MSH2, MLH1 *(Right sided)* Diet, Decreased Vegetable Fiber, Increased Carbs/Fat

You have an 85 year old male patient that comes in with fatigue and weakenss. You learn that they have iron deficient anemia. You find that this person has actually been losing weight unintentionally. If this person on xray were to have a "napkin ring" obstruction where would the cancer be affecting? If you find that this person has glands that are abundant and are producing excess mucin, how does that affect his prognosis? What are the most important prognosis factors for this patient?

Distal Colon Makes it WORSE Depth of Invasion, Presence of LN metastases

You have a patient that comes in with cramping and LLQ discomfort. They admit to a change in bowel habits, and upon stool testing you find Occult bleeding in the stools. What needs to be at the top of your differential? What Spordaic Molecular Defect/Target Gene is affected? Where is metastases most common for all types?

Left Sided Colorectal Adenocarcinoma APC/WNT pathway -- APC Liver, LN, Lung, Bone (except for Rectum --\> doesnt drain via portal circulation!)

You have a 45 year old female patient that presents with rectal bleeding, and pain on defecation. She says she started getting these when she was pregnant with her 2nd child. She also complains of significant constipation. You notice variceal dilations of the inferior part of the venous plexus. What does she have? if she had had variceal dilations of the superior part of the venous plexus?

**External Hemorrhoids** *(Inferior Hemorrhoidal Plexus)* **Internal Hemorrhoids** *(Superior Hemorrhoidal Plexus)*

You have a patient that has an HPV infection, and has a condyloma acuminatum. This person is most at risk for what? What about if it were in the area of simple columnar? What if it were at the junction between the two?

Squamous Carcinoma (below the pectinate line of anal canal) Adenocarcinoma (above the pectinate line of anal canal) Basaloid Tumors (Mixed Adeno/Squamous)

Rapid Fire: Diagnose: RLQ pain (may start out Epigastric) N/V, low fever, elevated peripheral white count + Mcburney's

Appendicitis (maybe pinworm obstruction, Carcinoid tumors, mucocele --\> obstruction)

Your patient comes in with the most common congenital anomalie of the Gallbladder. What is it?

**Phrygian Cap** Where the fundus is folded inward

Which type of Gallstones are pale yellow, round to ovoid, and have a finely granula, hard external surface -- They may become gray-white to black -- and may be lamellated. There are usually multiple of these? Which type of gallstone are brown-to-black. Usually have spiculated contours and molded -- sometimess seen with Chronic Hemolytic Anemias, Severe Ileal Dysfunction, or bacterial contamination of the biliary tree?

Cholesterol Stones Pigmented Gallstones

A 54 year old patient comes in with Progressive RUQ pain that has lasted for more than 6 hours. He has a mild fever, tachypnea, swewating, nausea, and vomiting. In his RUQ you feel an enlarged and tense mass. What does he potentially have? What is he at risk for?

Acute Cholecystitis Recurrence, Death, Gangrene (perforation)

You have a patient that has recurrent attacks of steady epigastric pain, N/V, and intolerance for Fatty foods. On X-ray you notice a smooth glistening appearance to this specific organ, with a variably thickened wall. What does he have? From what? What is the glistening appearnce of the organ? What are some complications we need to be worried about for this patient?

Chronic Choleocystitis from long standing cholelithiasis Porcelain Gallbladder Bacterial Superinfection, Gallbladder perforation, Porcelain Gallbladder --\> going into Gallbladder Cancer

You have two patients that come in at the same day with similar problems -- 1) He comes in with a failure of fusion of the fetal duct systems of the dorsal and ventral pancreatic primordia. He has already had a couple of bouts of pancreatitis. He notes that another physician told him that only a small amount of the pancreas is drained by the ampulla of vater -- which pancreatic anomalie does he have? 2) A female comes in noting that her pancrease completely encircles a part of her duodenum, and she has had multiple problems with digestion and regurgitation in the past. -- Which pancreatic anomalie does she have?

1) Pancreatic Divisum 2) Annular Pancreas

Acute Pancreatitis Microvascular Leak and Edema, Fat Necrosis, Acute Inflammation, Destruction of Pancreatic parenchyma. NPO for resting the pancreas, than TONS of IV Fluids to help with 3rd spacing.

A 65 year old chronic alcoholic, comes in with abdominal pain. He states that it is constant, intense, and the pain goes up to his back and his left shoulder. He has had N/V and hasnt been eating. You note he has elevated plasma levels of amylase and lipase. You Treat him, but a couple of years later -- he comes back in with mild-to-moderate-severe abdominal pain, He also has jaundice and you note his liver enzymes are elevated. You confirm he has a gallstone induced obstruction, and on HIstology you find Fibrosis, atrophy and droupout of acini with variable dilation of pancreatic ducts. What is his problem now?

Chronic Pancreatitis

Rapid Fire: What are the genes associated with inherited predisposition to pancreatitis?

CFTR -- 7q31 SPINK1 -- 7q34 PRISS1 -- 5q32

**Pseudocysts** -- localized collections of necrotic and hemorrhagic material rich in pancreatic enzymes that lack epithelial lining.

You have a patient who has a unilocular, thin walled cyst that is believed to result from anomalous development of the pancreatic ducts. It is about 4 cm in diameter. He is noted to have Von-Hippel Lindau disease. What does he have?

Congenital Cysts

You are worried about a patient who looks like they have a cyst in their pancreas. The physician over you tells you not to worry, its just cancer. But wants to know the main Cystic looking Neoplasms?

Serous Cystic Neoplasm Mucinous Cystic Neoplasm Intraductal Papillary Mucinous Neoplasms Solid-Pseudopapillary Neoplasm

You have a 67 year old man, with a long history of smoking, who has recently developed pain when he is lying down. He has noticed he has lost some weight, and hasnt been as hungry lately. He also says he is tired and weak alot. You notice a positive Trousseau sign. He also has + CA19-9 ag in his blood. What does he have? What genes are involved? What does the positive Trousseau sign tell you?

Pancreatic Carcinoma (Infiltrating Ductal Adenocarcinoma) BRCA2, CDKN2A (also associated with Puetz-Jeger --STK11) He has Migratory Thrombophlebitis

GI Patient Questions Flashcards

(169 cards)