Gastrointestinal Flashcards
Pancreatic adenocarcinoma
Risk factors (3) + genetic predispositions (4)
Risks:
age >65
SMOKING
chronic pancreatitis
Genetic: hereditary pancreatitis Peutz-Jeghers MEN1 HNPCC (Lynch)
Pancreatic adenocarcinoma
s/s (lesion location-based)
paraneoplastic sign
weight loss, anorexia
epigastric/back pain (tail tumors > splanchnic plexus)
painless obstructive jaundice (head tumors > Courvoisier)
hepatomegaly / ascites in metastases
Migratory Thrombophlebitis (Trousseau sign) maybe due to procoagulant factors from tumor
True Diverticula
what are they, examples, other characteristics of examples
contain ALL 3 layers of gut wall (mucosa/submucosa, muscularis and serosa)
embryological abnormalities such as:
CONGENITAL COLONIC DIVERTICULA (rare, single large lesion)
MECKEL DIVERTICULUM (heterotopic gastric or pancreatic mucosa; may bleed; located in SI not colon; pain nausea and vomiting in early childhood)
False Diverticula
what makes them “false”, cause + examples
only mucosa + submucosa herniate (NO MUSCULARIS) through areas of focal weakness in muscularis
exaggerated contractions in certain areas of colonic SM
ZENKER DIVERTICULUM - upper esophagus
DIVERTICULOSIS - sigmoid colon in pt over 60; painless hematochezia (vasa recta disruption); inflammation > LLQ pain, low fever, bowel habit change
Abetalipoproteinemia
genetic defect? presentation?
AR loss-of-function in MTP (microsomal triglyceride transfer protein) chaperone for ApoB folding and lipid loading onto chylos and VLDL
presents in first year with malabsorption sx
Abetalipoproteinemia
histo? labs? deficiencies?
histo - normal SI architecture with foamy/clear enterocytes at tips of villi due to lipid accumulation
labs - LOW triglycerides + cholesterol; absent chylomicrons, VLDL and apoB
deficiencies in VITAMIN E and essential fatty acids > acanthocyte RBCs, progressive ataxia and retinitis pigmentosa (other lipid-soluble vitamin defic. possible)
acute appendicitis
peak incidence? underlying cause?
all ages, but peaks at 6-10 years old
LUMINAL OBSTRUCTION - mostly fecaliths, sometimes lymph follicles, FBs, nematodes or carcinoids
retained mucus > wall distension > impaired venous outflow > ischemia > bacterial invasion (may rupture + cause peritonitis)
Pyloric Stenosis
epidem? presentation? tx?
mostly MALE INFANTS
recurrent projectile NON-BILIOUS vomiting with visible peristalsis and an olive-sized mass in distal stomach/pyloric area (hypertrophy of muscularis mucosae)
surgical splitting of muscle for tx
Zollinger-Ellison syndrome
s/s? differential dx?
gastrinoma in SI or pancreas; often malignant
cause parietal cell hyperplasia > peptic ulcer, heartburn and diarrhea (HCl impairs enterocytes)
ulcers are found in DISTAL DUODENUM; gastric rugae are thickened
- “SECRETIN test” - normally increases HCO3 and INHIBITS GASTRIN release from G cells; paradoxically INCREASES GASTRINOMA GASTRIN release (abnormal adenylate cyclase activation)
3 yr old with abd pain, rectal bleeding. Blind pouch from ileum to umbilicus via fibrous band.
What is it? How does it form?
Its layers?
Rule of 2s?
Meckel’s diverticulum
failed obliteration of omphalomesenteric / vitelline duct
true diverticulum
all layers (mucosa, sub-, musc- and serosa) (ectopic gastric mucosa / pancreatic tissue common inside –> HCl –> bleeds)
2% population; 2 ft from IC valve; 2 inches long; 2% symptomtic; 2:1 male
2 types of gastric adenocarcinoma + general characteristics
- SIGNET RING CARCINOMA - cells don’t form glands; abundant mucin droplets marginalize nucleus (“signet ring” look); ILL-DEFINED, DIFFUSE wall involvement via E-CADHERIN LOSS; cause LINITIS PLASTICA
2 INTESTINAL-TYPE ADC - resemble colon cancers > glands of columnar/cuboidal cells; nodular, polypoid, WELL-DEFINED and RAPIDLY EXPAND into lumen; often ulcerate + bleed
2 sites of gastric adc metastases
Virchow node - left supraclavicular
Sister Mary Joseph nodule - periumbilical nodes
Menetrier disease
histo + functional changes
rugal hypertrophy with PARIETAL CELL ATROPHY
decreased acid secretion
Ulcerative Colitis biopsy
diffuse inflammatory infiltrates with NEUTROPHILIC MICROABSCESSES in crypts
(intermittent bloody d and abd. pain)
Whipple disease biopsy
distended macrophages in intestinal lamina propria
GI MALT lymphoma biopsy
ATYPICAL LYMPHOCYTES in the lamina propria
assoc. with H. pylori in stomach
Mesenteric Adenitis
age? cause? s/s?
mostly age 5-14; Yersinia enterocolitica (dog poop)
fever, RLQ pain, nausea/vomiting
Colitis-associated vs. sporadic colorectal cancer
Age? Origin of dysplasia?
Location? # of tumors?
Histo? Mutations?
COLITIS-ASSOCIATED:
younger (40-55)
flat, nonpolypoid lesions
proximal > distal (especially in Crohn’s)
multifocal
mucinous / signet ring cell; poorer differentiation
early p53, late APC mutation
SPORADIC: older (>60) polypoid lesions distal > proximal single lesion rarely mucinous; better differentiation early APC, late p53 mutation
Acalculous Cholecystitis
in whom? s/s? special sign? dx?
in CRITICALLY ILL pts (sepsis, severe burn, trauma, immunosuppression) via GB stasis and ischemia
can be hard to notice if pt intubated/sedated
fever, RUQ pain, leukocytosis, mild LFT elevation
Murphy sign positive - pt breathes in while doc has hand below ribs, R midclavicular. pt will wince + stop inhaling when GB hits doc’s hand
dx by US > large GB with edema and no stones
Choledochal cyst
what is it? in whom? sx?
congenital dilation of common bile duct
present in kids <10
recurrent abdominal pain + jaundice
US in chronic cholecystitis
shrunken, fibrosed GB via repeated mild attacks of acute cholecystitis
incidental GB finding on abdominal XRAY
what? cause? increases risk of?
porcelain gallbladder
rim of calcium deposits visible on xray
caused by chronic cholecystitis
incr. risk of GB carcinoma
Esophageal SCC
histo?
nests of squamous cells with abundant pink cytoplasm
KERATIN PEARLS
INTERCELLULAR BRIDGES
Esophageal SCC
epidem? s/s? progno?
man > 50 with smoking/drinking history
solid food dysphagia (may progress to liquid)
retrosternal burning / discomfort
weight loss
IDA + fatigue via blood loss
poor progno (locally advanced/metastatic common)
gag reflex
efferent + afferent limbs
afferent - glossopharyngeal n. (CN IX)
efferent - vagus (CN X)
Pancreas development
2 buds: which gives what?
how is it different in pancreas divisum?
ventral bud - gives UNCINATE proc. and PROXIMAL MAIN DUCT (Wirsung)
dorsal bud - gives rest of head, body + tail plus ACCESSORY DUCT and distal main duct
in divisum, 2 buds don’t fuse fully > dorsal duct (Santorini) is dominant, ventral duct is accessory
Locating appendix during appendectomy
how?
Follow TAENIA COLI to their origin at the end of the cecum
Psoas sign
what is it?
abdominal pain elicited by thigh extension
positive in acute appendicitis when pt has RETROCECAL appendix > can irritate psoas and any stretching of it causes pain (pt generally sits/lays with hips flexed)
not specific for appendicitis; positive in other retroperitoneal conditions
Meckel diverticulum
what is it and how does it form?
ILEAL outgrowth due to FAILED VITELLINE DUCT OBLITERATION (aka omphalomesenteric duct)
Meckel diverticulum
s/s?
Sometime asymptomatic
Sometimes painless spontaneous lower GI bleed
Can cause INTUSSUSCEPTION > colicky pain and “CURRANT JELLY” poop
Meckel diverticulum
cell types in diverticulum? consequences of this?
specific imaging for Meckel’s?
Can have GASTRIC MUCOSA > acid causes ULCERS + BLEEDING
Can have PANCREATIC TISSUE
99Tc-Pertechnetate (with parietal cell affinity) goes to diverticulum > increased uptake in periumbilical or RLQ is characteristic
2 Ventral wall defects?
Cause?
Gastroschisis - loose herniated bowel loop to right of umbilicus
Omphalocele - sac-enclosed herniated bowel through umbilicus
failed LATERAL BODY FOLD CLOSURE
Imperforate anus
embryological cause
Hindgut (distal 1/3 of transverse colon onward) descends along the inferior mesenteric artery normally
FAILED HINDGUT DESCENT causes imperforate anus
Other than Meckel’s diverticulum…
what are 3 vitelline duct abnormalities?
Persistent vitelline duct - goes all the way to umbilicus from ileum
Vitelline sinus - fibrous band from ileum to umbilicus; deep fibrous sinus inward from umbilicus
Vitelline / entero-cyst - cyst suspended from 2 fibrous bands btwn ileum + umbilicus
“Pancreatic cholera”
what is the main hormone involved? weird syndrome name?
symptomatic tx?
VIPoma (pancreatic islet cell tumor) causes…
“WDHA” syndrome…
Watery D
Hypokalemia
Achlorhydria - low gastric acid
VIP stimulates pancreatic chloride/bicarb, plus it binds enterocytes > cAMP > Na, Cl and water secretion
Tx is SOMATOSTATIN (Octreotide) to inhibit GI hormone production (VIP, gastrin, glucagon and CCK)
TWO things involved in solubilization of cholesterol in GB
would be low in case of cholesterol stones
bile salts and PHOSPHATIDYLCHOLINE
best examination for general screening for the presence of malabsorption due to ANY etiology
fecal fat testing (stool microscopy with Sudan III stain)
Crohn’s complications
3 (+ their consequent complications)
plus ONE SPECIAL HISTO FEATURE of Crohn’s (a type of inflammation seen in many other diseases)
- STRICTURES - wall edema, fibrosis + muscularis mucosae hypertrophy narrows lumen > obstructive ileus
- FISTULAS - ulcer penetrates bowel wall and forms a “sinus tract” to another organ (enterovesicular, -vaginal, -enteric)
- ABSCESS - form when sinus tracts become walled off; may perforate > diffuse peritonitis
CD histo shows NON-CASEATING GRANULOMATOUS inflammation
Esophageal SCC risk factors (5)
- Alcohol
- Tobacco
- N-nitroso foods
- Underlying esophageal disease (achalasia, etc.)
- Hot liquids
Esophageal ADC risk factors (4)
- Barrett esophagus
- GERD
- Obesity
- Tobacco
Primary Biliary Cirrhosis/Cholangitis
in whom? initial presentation (2 sx)?
middle-aged women
fatigue, NIGHT PRURITUS at first
Primary Biliary Cirrhosis/Cholangitis
later s/s? (after pruritus + fatigue)
- HSmegaly + cholestasis (jaundice, pale poo, dark pee)
- fat malabsorption (A, D, E, K defic.)
- impaired cholesterol excretion - HIGH LIPIDS and XANTHELASMA
- very late = cirrhosis and portal htn
Primary Biliary Cirrhosis/Cholangitis
main auto-Ab?
(several others)
antimitochondrial - against pyr DH complex
ANA
anti-glycoprotein-210
anti-centromere
Primary Biliary Cirrhosis/Cholangitis
histo
dense infiltrate in PORTAL TRACTS of macros, lymphos, PLASMA cells and EOSINOPHILS
GRANULOMATOUS destruction of interlobular bile ducts
Primary Sclerosing Cholangitis
in whom? presentation? (sx, lab)
pt with long history of ULCERATIVE COLITIS
fatigue
cholestasis sx
HIGH ALP
(p-ANCA can be seen in many cases; ANA and anti-smooth muscle can be seen in cases with overlapping AI hepatitis)
Primary Sclerosing Cholangitis
histo
diffuse inflammation/fibrosis of LARGE INTRA- AND EXTRAHEPATIC bile ducts
“ONION SKIN” fibrosis around ducts with obstruction
Most specific dx test for ACUTE CHOLECYSTITIS
Radionuclide biliary scan
radiotracer given IV accumulates in liver + bile; if it is only seen excreted into the duodenum and not the GB then positive for acute cholecystitis
(US is the initial test and would show thick wall, fluid around GB and positive sonographic Murphy sign, but IS LESS SPECIFIC; radionuclide used if US is inconclusive)
Lymphatic drainage of colon (cecum to anus) by segment
Cecum + Asc. + 2/3 transverse - SUPERIOR MESENTERIC nodes
1/3 transverse to superior 1/3 rectum - INFERIOR MESENTERIC nodes
middle 1/3 rectum - INFERIOR MESENTERIC + INTERNAL ILIAC nodes
distal 1/3 rectum - INGUINAL nodes (some to inf. mes. and int. iliac)
Type I: familial chylomicronemia syndrome
defect, what’s elevated, s/s
defect in LPL or ApoC-II
high chylomicrons
acute pancreatitis
lipemia retinalis
eruptive xanthomas
HSmegaly
Type IIA: Familial Hypercholesterolemia
defect, what’s elevated, s/s
defect in LDL-R or ApoB-100
high LDL
premature CAD
corneal arcus
tendon xanthomas, xanthelasma
Type III: Familial Dysbetalipoproteinemia
defect, what’s elevated, s/s
defect in ApoE
high chylomicron + VLDL remnants
premature CAD and PVD
tuboeruptive + palmar xanthomas
Type IV: Familial Hypertriglyceridemia
defect, what’s elevated, s/s
defect in ApoA-V (but also polygenic)
high VLDL
increased pancreatitis risk
assoc. with obesity, insulin resistance, and CAD
What are the 2 MCCs of acute pancreatitis?
gallstones - middle-age or older; mostly women; if young then prob due to hemolysis (sickle cell, etc.)
alcoholism
After gallstones + alcoholism…
what are some less common causes of acute pancreatitis?
procedures? drugs? microbes? structural issues etc.?
ERCP or surgery (gastric, biliary or after cardiac surgery)
azathioprine, sulfasalazine, furosemide, valproate
mumps, Coxsackie, Mycoplasma
high triglycerides or hypercalcemia
pancreas abnormalities (stricture, cancer, divisum) or Vater ampulla (Oddi stenosis, choledochal cyst)
Simple mnemonic for remembering the defects in the 4 important familial hyperlipidemia disorders
CBET
Type I = ApoC-2 (or LPL)
Type II = ApoB-100 (or LDL-R)
Type III = ApoE
Type IV = Triglycerides (polygenic)
(If you know the functions of these, you’ll know what’s elevated:
- C-2 activales LPL > no chylo breakdown > high chylos + TGs > pancreatitis
- B-100 binds LDL-R for hepatic uptake > hi LDL
- E binds liver for chylo/VLDL remnant uptake
- Just remember it…)
What does ApoA-1 do?
Deficiency of it or a related molecule results in what?
activates LCAT > esterifies free cholesterol in HDL
ApoA-1 or LCAT defic. leads to low HDL and hi free cholesterol
Diffuse Esophageal Spasm
how do contractions look on manometry?
radiological sign?
periodic SIMULTANEOUS contraction along whole length of esophagus
instead of contractions appearing in sequence down the length of the esoph
radio = “CORKSCREW” esophagus on barium esophogram
Diffuse Esophageal Spasm
pathogenesis
impaired inhibitory neurotransmission in the myenteric plexus
Collagenous (microscopic) colitis
in whom? histo?
older women with frequent diarrhea
thickening of subepithelial collagen band
Colorectal adenocarcinomas:
Right-sided vs. left-sided vs. rectal
S/S?
- Right-sided - EXOPHYTIC mass in large lumen > no obstruction (stool more liquid here); have IRON-DEF ANEMIA via occult loss plus WEIGHT LOSS, anorexia + fatigue
- Left-sided - INFILTRATIVE mass ENCIRCLES lumen > obstruction with CONSTIPATION, pain, DISTENSION and VOMITING
- Rectal - TENESMUS and SMALL-CALIBER stool
what is superior mesenteric artery syndrome?
presentation?
compression of 3rd part (inferior transverse) of duodenum between SMA and aorta
intermittent intestinal obstruction with POSTPRANDIAL PAIN in person with little mesenteric fat (LOW WEIGHT or MALNUTRITION)
gastric chief cells release what? 2
pepsinogen and gastric lipase
(Chief cells are basophilic, lots of RER, deep in pits)
HCl from parietals converts to pepsin
After gastric surgery (Whipple), what can be cut to decrease gastric acid output and resulting jejunal ulcers?
vagal trunks
How is PERISTALSIS and LES TONE affected in esophageal dysmotility of scleroderma?
BOTH are decreased
gastric acid suppressing drug with POTENT CYP450 INHIBITION
what other sfx does it have? (one of which is shared by another drug in its class)
Cimetidine - H2 blocker
anti-androgenic effects - high PRL, gynecomastia, impotence and low libido
crosses BBB > dizziness, HA
cimetidine and RANITIDINE both DECREASE CREATININE CLEARANCE (incr. serum levels)
if a patient has a first degree relative with colon cancer, HOW AND WHEN SHOULD THEY BE SCREENED?
what other method should not be used for screening and why?
start at AGE FORTY (normal low-risk population screening starts at 50) via COLONOSCOPY
or start TEN YEARS BEFORE RELATIVE’S presentation
should not use occult blood screening, due to LOW SENSITIVITY
Gastric vs. Duodenal ulcer
how do meals affect the pain
Gastric - pain is Greater with meals
Duodenal - pain is Decreased with meals
Gastric vs. Duodenal ulcer
Relation to H. pylori?
General pathophys?
Other cause (1 for each)?
Gastric - 70% H pylori; via decreased mucosal protection; other cause is NSAID
Duodenal - 90% H pylori; via low mucosal protection OR increased HCl; other cause is Zollinger-Ellison
How are gastric and duodenal ulcers related to cancer?
Histo considerations?
Gastric - risk of CARCINOMA increases! must BIOPSY MARGINS to rule it out
Duodenal - generally benign, no risk increase; biopsy shows BRUNNER GLAND HYPERTROPHY
1 complication of gastric + duodenal ulcers?
site of ulcer with predilection for this complication?
Hemorrhage - posterior ulcers > anterior
gastric - lesser curvature bleeding from left gastric a. common
duodenal - posterior wall bleeding from gastroduodenal artery common
Complication… more commonly of duodenal ulcers… that may be visible on x-ray?
Predilection site for this?
Related sign?
Perforation - anterior > posterior (opposite of hemorrhage)
may have referred shoulder pain via phrenic irritation
Musculoskeletal complication of IBD, especially when treated with corticosteroids
Aseptic necrosis
common in femoral head; x-ray shows collapse of head with preservation of articular cartilage
A heavy-drinking, heavy-smoking Japanese man who eats mostly traditional Japanese food
what is his main risk for gastric cancer?
the Japanese food
due to smoking of fish + preservation with nitrites
what two things are produced by bacterial overgrowth in SIBO and elevated in serum?
vitamin K and folate
Other than distended bowel loops with air-fluid levels…
what is a MORE SPECIFIC sign of gallstone ileus?
“pneumobilia” - air in the biliary tree
gallstone ileus happens when a large stone enters the GI tract via a CHOLECYSTOENTERIC FISTULA formed btwn the GB and duodenum; air from the GI tract can travel backward into the biliary tree through this fistula
How does Celiac disease affect calcium homeostasis?
malabsorption of fats > low vitamin D
results in low Ca, low Pi and increased PTH > increased ALP due to bone turnover
Cholecystokinin
produced by what in response to what?
effects (3)?
I cells of small intestine via FAs and AAs
- increases panc. enzymes + bicarb
- GB contraction
- Inhibit gastric emptying
(so basic effect is to get food in duodenum digesting well + inhibit more food coming in until current food is dealt with)
Hormone that decreases secretion of many GI hormones
made by what + decreases what
Somatostatin
Delta cells in islets, duodenum, pyloric antrum
decr. VIP, gastrin, glucagon, CCK
Mechanism of ANTRAL H pylori infection pathogenesis
which cells are affected?
where is the ulcer?
DELTA cell depletion > decreased SOMATOSTATIN > elevated gastrin > more HCl release
(cytotoxins also decrease duodenal bicarbonate)
acid into unprotected duodenum > DUODENAL ulcers
Mechanism of GASTRIC BODY H pylori infection pathogenesis
which cells are affected?
where is the ulcer?
associated risks?
multifocal atrophic gastritis > PARIETAL CELL loss > acid is low or normal
GASTRIC ulcers form via direct mucosal damage (ammonia, toxins) and inflammation
assoc. with metaplasia + malignancy (MALT lymphoma and ADC), whereas antral infection is not
two mechanisms by which gastrin increases HCl release
- Direct - via CCK-B receptors on parietals
2. Indirect - via acting on on ECL cells > histamine release
What parts of the LIVER and COLON are most susceptible to ischemic injury?
Liver - area around CENTRAL VEIN (“zone III”)
Colon - splenic flexure + rectum
2 main types of HIATAL HERNIAS
which is more common? which part protrudes?
- SLIDING - more common; GE junction displaced upwards and cardia slides into hiatus; “hourglass” imaging
- PARAESOPHAGEAL - in this case the FUNDUS protrudes into the thorax; less common
Through what muscle (general + two specific parts) does a Zenker diverticulum protrude?
inferior pharyngeal constrictor
thyropharyngeus + cricopharyngeus portions
What nerve innervates the INFERIOR PHARYNGEAL CONSTRICTOR muscles?
vagus nerve
2 types of gastroesophageal mural injury + main feature
cause of both (same)
- Mallory-Weiss tear - MUCOSAL tear (bleeding only)
- Boerhaave syndrome - TRANSMURAL tear (air/fluid leakage into mediastinum + pleura
(both via forceful vomiting)
Mallory-Weiss tear vs. Boerhaave syndrome
Presentation similarities (1) and differences (2)
same - vomiting + retching
M-W tear - hematemesis and EPIGASTRIC pain
BS - CHEST + UPPER ABD. pain and FEVER, DYSPNEA + SEPTIC SHOCK
(because BS has leakage of fluid + air into mediastinum and pleura)
Difference in acid-base balance between excessive VOMITING vs. DIARRHEA
vomiting = HCl loss = metabolic ALKALOSIS
diarrhea = HCO3 loss = metabolic ACIDOSIS
First genetic change in colon cancer?
Later 3 changes (1 activation, 2 inactivations)
First is APC inactivation
Then KRAS activation and p53 / DCC inactivations
What side do a cerebellar lesion’s symptoms manifest on?
IPSILATERAL side
What 3 symptoms can arise from cerebellar HEMISPHERE lesions?
(cerebellar, not cerebral!)
- Dysdiadochokinesia - impaired rapid alternating movements
- Limb dysmetria - over/undershoot
- Intention tremor - during targeted movement
(all are IPSILATERAL!)
Lesions to cerebellar VERMIS cause what sx?
TRUNCAL ATAXIA
wide, unsteady gait
(vermis controls the “medial descending” motor systems - ant. corticospinal, reticulospinal, vestibulospinal, tectospinal)
Lesions to the FLOCCULONODULAR LOBE of the cerebellum cause what?
(bonus: this lobe plus the inferior vermis make up the “_____cerebellum”)
vertigo and nystagmus
“vestibulocerebellum”
Secretin
made by what cells? in response to what? causes what?
by duodenal S cells
in response to H+ in duodenum
pancreatic HCO3 secretion
(NOT enzyme secretion… CCK and cholinergic stimulation stimulates enzymes)