my own GI path Flashcards
which serotype is oral herpes? and where does it remain dormant?
HSV-1
remains dormant in trigeminal ganglia
Hairy Leukoplakia: pathogenesis, CP, progression?
it is a white, rough (‘hairy’) patch on the SIDES of the tongue, usually seen in AIDS pts.
arises dt EBV-induced squamous cell hyperplasia = not pre-malignant (because no dysplasia)
WHat is highest risk for SqCC of oral mucosa
smoking plus alcohol abuse have a synergistic effect
What is the MC and 2nd MC tumor of the salivary glands?
MC = pleomorphic adenoma 2nd = Warthin tumor
What is the MC malignant tumor of the oral mucosa
mucoepidermoid carcinoma
What is the makeup of pleomorphic adenoma
mixed tumor of chondromyxoid stroma (cartilage) plus epithelium (glands = adeno).
What is the CP of pleomorphic adenoma
mobile, painless circumscribed mass at the angle of the jaw that hasn’t invaded anything
What is the prognosis for plemorphic adenoma
high rate of recurrence dt incomplete resection when small islands of tumor extend through the tumor capsule
What is the other name for a warthin tumor and what does it look like under micro
papillary cystadenoma lymphomatosum:
looks like heterotropic salivary gland inside a LN- cystic glandualr structures within a benign lymphoid tissue
What is a mucoepidermoid tumor made of
mucinous and squamous components
What causes Plummer-vinson syndrome and what does it present with? (4)
Cuased by chronic iron deficiency
CP: esophageal web, Iron deficiency anemia, dysphagia, and glossitis
Zenker diverticulum: true or false? where does it arise, and how does it present? (3)
a false diverticulum arises at junction of eso and pharynx (weak cricopharyngeus m.) CP: 1. halitosis (trapped food) 2. dysphagia 3. obstruction/regurg food
Where do esophageal varices arise
lower 1/3 of esophagus
What is the difference between esophageal varices and Mallory Weiss syndrome CP?
esophageal varices = painless hematemesis
Malloery-Weiss = painful hematemesis
What cuases Mallory Weiss synd (2)
severe retching dt bulimia or alcoholism
What is pathogenesis of Mallory Weiss and what does it increase the risk of?
longitudinal tear at GE jnct dt severe vomiting –> painful hematemesis.
Increases risk of Boerhaave syndrome (air trapped in mediastinum) = emergency
achalasia: pathogenesis
T. Cruzi (Chagas dz) or idiopathic damage to cells in myenteric plexus (auerbach) –> dysregulation of peristalsis and esophageal motility and inability to relax LES.
Achalasia: CP (4)
- Bird;s beak sign on barium swallow
- putrid breath (rotting food)
- high LES pressure on esophageal manometry
- Dysphagia for solids and liquids
Achalasia –> increased risk of?
squamous cell carcinoma
GERD is dt? risk factors include?
dt decreased LES tone
-risk factors: caffeine, EtOH, HIATIAL HERNIA**
what is the exact change seen in Barret’s esophagus
non-keratinized stratified squamous epithelium of esophagus changes to non-ciliated columnar epithelium with goblet cells
what causes Barret’s and what does it increase risk of
caused by GERD and increases risk of adenocarcinoma of esophagus
Gastrochisis: pathogenesis? covered by peritoneum? location in abdomen
- patho: congenital malformation of anterior abdominal wall
- not covered
- to right of umbilicus
Omphalocele: patho? covered by peritoneum?
patho: persistent herniation of abdominal contents into umbilical cord
OmphaloCELE = SEALED by peritoneum
Pyloric stenosis presents how/when*****
- non-bilious projectile vomiting with “olive” mass in abdomen
- presents 2-6 weeks after birth (takes time for stenosis to develop)
What are 3 etiologies of acute gastritis**
- NSAID use–> decreased PGE2–> decreased gastric mucosa protection
- Burn –> hypovolemia –> mucosal ischemia (Curling ulcer)
- **Brain injury –> ^ICP –> ^ vagal stimulation –> ^ACh production –> ^ H+ secretion
2 etiologies of chronic gastritis
- H. pylori infx
2. Autoimmune destruction of parietal cells
Peptic ulcer disease occurs in 2 locations: which is MC? and what is the CP of each with mnemonic?
- Duodenal ulcer = MC
- Gastric ulcer
CP: Gastric ulcer = Greater pain with eating
Duodenal ulcer = Decreased pain with eating
**can think that wherever the ulcer is, that pH predominates
which is almost always benign: gastric or duodenal ulcer
duodenal ulcers are almost never malignant
what is the secondary cause for each: gastric ulcer and duodenal ulcer
Gastric: NSAID use
Duodenal: Zollinger-Ellison syndrome (gastrinoma)
WHat type of cancer is gastric carcinoma? and what cell type has proliferated
adenocarcinoma- proliferation of surface epithelial cells
What are the 2 types of gastric adencarcinoma? which is associated with H.pylori, smoked foods, tobacco?
Intestinal (still located in lesser curvature)- associated with H.pylori, smoked foods, tobacco
Diffuse type: not associated with those things
What is the look (classic sign maybe**) of each type of gastric carcinoma, respectively
Intestinal: heaped up mucosa around ulcer-looking thing
Diffuse: signet ring cells* that diffusely infiltrate the gastric wall, with a thickened, leathery stomach wall (linitis plastica)
WHat are the 3 sites of metatstasis of Gastric CA (and names of tumors located there when aplpicable) and their “look”
- Virchow node: involves left suporaclavicualr node
- Krukenberg tumor: bilateral ovarian mets with signet ring cells (secrete mucin)
- Sister Mary Joseph nodule: subQ periumbilical mets- (seen with Intestinal type)
Duodenal atresia: associate with what? Has what CP
Down syndrome
“double bubble” on CXR
what is MC congenital anomaly of GI tract and it’s etilogy
Mekel’s diverticulum (true)- dt failure of the viteline duct to involute
what is, and what is the pathogenesis of Celiac disease?
Autoimmune damage of smll bowel villi:
Gliadin (gluten protein found in wheat) is absorbed, deamidated (by tTG) and presented by APCs via MHC II to helper T cells–> mediate damage
What are the HLA (2), and another disease (and it’s pathogenesis) association of Celiac disease?
HLA-DQ2
HLA-DQ8
also associated with dermatitis herpetiformis (small vessicles arise on skin dt IgA deposition at ttips of dermal papillae)
what are the laboratory findings in CEliac disease (3)
IgA antibodies against:
- tissue transglutaminase (tTG)
- endomysium
- deamidated gliadin peptides
What is seen on duodenal bx in celiac disease? (3) and where is this damage MC found?***
-
****MC found in duodenum (less in jejunum and ileum):
1. villous atrophy
2. crypt hyperplasia
3. lymphocytic infiltrate
Celiac dz shows increased risk of what
- T-cell lymphoma
- small bowel CA
What is sequelae of tropical sprue and how/why?***
Damage in tropical sprue is similar to that of celiac dz except it is ***found MC in the jejunum and ileum. This leads to megalobastic anemia dt:
- Folate deficiency (jejunal absorption)
- B12 deficiency (ileal absorption)
Carcinoid tumors: tumor cells contain what and stain for what?
contain neurosecretory granules and stain chromogranin (+)
What is the pathogenesis of carcinoid syndrome and when does it not occur?
carcinoid tumor of the gut releases 5HT which mediates sx of carcinoid syndrome. If the tumor is located only in the gut, 5HT is mtbolized into 5-HIAA (which has no effects)- so carcinoid syndrome requires mets to liver so that metabolization of 5HT can be bypassed
What is the pathogenesis of carcinoid heart disease? what side of the Heart is it seen in and why?
5HT hits RH –> ^collagen –> fibrosis and valvular disease (tricuspid regurg, pulmonary valve stenosis)
Left side is not involved bc the lung contains MAO which metabolizes 5HT so that it never reaches the left heart
Hirschprung disease: what is it associated with and what is the dx technique
Assc with Down Syndrome
Dx = Rectal suction bx
what condition improves with defecation
IBS
what causes diverticulitis? where and how presents?
fecal material obstructs a colonic diverticula, usually in the sigmoid colon
CP: LLQ pain, fever, leukocytosis
what are the 2 MC types of colonic polyps? what is their malignant potential *****and how do they look in micro?
Hyperplastic = MC: hyperplasia of glands gives it a serrated appearance (no malignant potential- duh- hyperplasia only)
Adenomatous = 2nd MC: neoplastic proliferation looks like darker glands (dt hyperchromaticism)- may progress to adenocarcinoma**
1. can be tubular= flat polyp = less malignant
2. villous = fingerlike = most malignant potential
3. tubulovillous = intermediate potential
what are the 3 mutations in the adenoma-carcinoma sequence and what does each cause
- APC = ^risk of polyp formation
- KRAS = polyp formation occurs
- p53 = ^COX production and carcinoma
What can impede progression from adenoma to carcinoma? how?
Aspirin! - it stops COX production increased by p53 mutation
what polyp has higher malignant potential:
tubular or villous?
sessile or pedunculated?
below or above 2cm?
villous, sessile, >2cm
what and where is the mutaiton that causes familial adenomatous polyposis? inheritance pattern? mnemonic
AD mutation of APC gene on chromo 5
mnemonic- all 5 of our family would go on vacations in Van (AD)
wht happens if colectomy is not performed in cases of FAP?
100% progression to colorectal CA by age40
What is gardner syndrome a combo of (3)
FAP + fibromatosis and osteomas
What is Turcot syndrome a combo of?
FAP + malignant CNS tumor (medulloblastoma or glial tumors)
Juvenile polyposis sybndrome:
population affected?
inheritance?
polyp/tumor type? (benign or malignant too)
AD
kids < 5
hammartomous polyp (benign)
Peutz-Jeghers syndrome: inheritance? what is it? what other unique finding? increased risk for what?
- AD
- hammatomas throughout GI tract
- accompanied by hyperpigmented mouth, lips, hands, genitalia
- assc. with increased risk for Breast and GI cancers
what are the 2 pathways that give rise to colorectal CA?
- Chromosomal instability pathway (aka adenoma-CA sequence)
2. Microsatellite instability pathway
What are the mutations in the Microsatellite instability pathway of CRC? (generally and specific?)
mismatch-repair enzymes (MLH1)
What bacteria and what condition is CRC associated with an increased risk for? ****
S. bovis culture positive endocarditis
What syndrome (2 names ) is microsatellite instability assc with? What cancers does this syndrome increase risk of (3-4)
HNCC- hereditary non-polyposis colorectal CA (aka Lynch syndrome) carries increased risk for 3 cancers: 1. ovarian 2. CRC 3. endometrial 4. first aid says: skin cancer too
what is the difference in presentation of CRC that arises on the left with that which arises on right?
Left = obstruction, hematochezia Right = Fe-deficiency anemia
Crohns vs Ulcerative colitis: wall involvement
UC: mucosal and SubM infl/ulcers only
Crohns: transmural infl–> fistulas, fissures
Crohns vs Ulcerative colitis: location (MC and LC in crohns)
UC: continuous involvement always involving rectum up to, but not past cecum. (colitis = colon)
Crohns: any part of GI tract from mouth to anus: terminal ileum is MC, rectum LC. Skip lesions
Crohns vs Ulcerative colitis: sx
UC: LLQ pain (rectum) with bloody diarrhea
Crohns: RLQ pain (ileum) maybe or maybe not diarrhea
Crohns vs Ulcerative colitis: micro inflammation*****
UC: crypt abscesses with neutrophils (no granulomas)
Crohns: lymphoid aggregates with **non-caseating granulomas ***
Crohns vs Ulcerative colitis: Gross appearance (imaging)
UC: psuedopolyps, loss of haustra = “lead pipe sign”
Crohns: Cobblestone mucosa, strictures, “creeping fat”, string sign on imaging
Crohns vs Ulcerative colitis: complications*****(risk based on what?)
UC: Toxic megacolon***(dilated), increased risk for CRC - based on extent and duration
Crohns: malabsorption, fistula formation, Calcium oxalate stones, CRC too (if colon is involved),
Crohns vs Ulcerative colitis: associations **
UC: p-ANCA, primary sclerosing cholangitis
Crohns: kidney stones (Ca-oxalate)
BOTH: joint problems, erythema nodosum
Crohns vs Ulcerative colitis: smoking effects
UC: smoking is protective against it
Crohns: increases risk
