GI Patient Questions Flashcards
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.
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.
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
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.
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
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.
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
DM
Down Syndrome
Sarcoidosis
Chediak-Higashi/Agranulocytosis/Cyclic Neutropenia
Infective Endocarditis, Pulmonary and Brain Abscesses
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.
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)
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
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
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)
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.
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
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)
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
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
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
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
You have a patient that has Diptheria. What are the Oral Manifestations?
Dirty White, Fibrinosuppurative, Tough, Inflammatory membrane over their tonsils and retropharynx.
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
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)
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
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.
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)
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)
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
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
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
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 are some bacterial causes of sialdenitis?
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.
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.
How would this be seen on histology?
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