Gastroenterology (F.A.) Flashcards
Gastrin
where: G cells in antrum of stomach
action: increase H+ secretion by parietal cell, increase stomach mucus lining, increase stomach motility
regulation (+): food (stomach distension, alklanization, AA/peptides,), vagal stim via GRP,
regulation (-): low pH
how does chronic PPI and chronic atrophic gastrtitis (H Pylori) affect Gastrin levels
increased gastrin levels
Somatostatin
where: D cells of Islet of Langerhans (Pancreas)
action: decrease all secretions: gastrin, pancreatic (glucagon, insulin, enzymes), lowers gallbladder motility
regulation (+): low pH
regulation (-): vagal
Cholecystokinin
where: I cells of duodenum
action: help pancreatic/biliary secretions enter duodenum (increase gall bladder motility, increase pancreatic secretion via neural muscarinic pathway, soften sphincter of Odi) and decrease gastric emptying
regulation(+): presence of FA/AA
Secretin
where: S of the duodenum
action: neutralize acid by secreting HCO3-., decrease gastric acid secretion, increase bile secretion
regulation (+): high acidity, presence of FA
Glucose dependent Insulinotropic peptide
where: K cells of duodenum
action: increase insulin release, decrease gastric acid secretion
regulation (+): FA, AA, oral glucose
Motilin
where: small intestines
action: increase migrating motor complexes
regulation (+): FASTING STATES
Vasoactive Intestinal Peptide
where: parasympathetic ganglia of sphincters, gallbladder, SI
action: increases H20/electrolyte secretion, relaxes sphincters and smooth muslces
regulation (+) : distension and vagal
regulation (-): sympathetics
Ghrelin
where: stomach
action: increase appetite
regulation(+) in fasting state
regulation (-) : food
when is Ghrelin increased pathologically
Prader-Willi
Intrinsic Factor
where: parietal cells of stomach
action: bind B12 for absorption in terminal ileum
Gastric Acid
where: parietal cells of stomach
action: release H+ into lumen
regulation (+): gastrin , AcH, histamine
regulation (-): SST, Secretin, GIP, prostoglandin
Pepsin
where: chief cells of stomach
action: protein breakdown
regulation (+): needs H+ to activate from pepsinogen
Bicarbonate
where: mucosa and Brunner’s glands (SI)
action: neutralize acid
regulation: secretin
what are the pancreatic secretions?
alpha amylase, trypsinogen, lipase, proteases
explain the role of trypsinogen
trypsinogen gets activated by enterokinase/enteropeptidase (brush border enzymes on duodenum/jejunum) and becomes trypsin which can then activate the other zymogens (pro-peptidases) released by pancreas, and further activate itself by cleaving trypsinogen more.
explain the process of carbohydrate absorption at SI
-monosacch only
- glucose and galactose through SGLT1
-fructose through GLUT 5
then everything enters blood via GLUT 2
SI injury leads to deficient absorption of what (3) vitamins/minerals
Fe
Folate
B12
“Iron Fist Bro”
Peyer;s Patches role?
unencapsulated lymphoid aggregates in Ileum
Uses M cells to sample environment and be APC
causes Bcell to become plasma cells that produce IgA
whats in bile, anyways?
bile salts: bile acid (made by 7 alpha hydroxylase) conjugated to taurine or glycine to be water soluble
bilirubin(broken down heme), phosopholipids, cholesterol, water, ions
what does bile do, anywho?
- cholesterol excretion
- digestion of lipids, and absorption of fat soluble vitamins
- antimicrobial
heme—–> biliverdin
which enzyme???
heme oxygenase
direct vs indirect bilirubin
direct: soluble, conjugated w/ glucoronic acid (at liver)
indirect: INsoluble, UNconjugated,
what enzyme conjugates bilirubin?
UDP glucoronysyl transferase
fate of conjugated bilirubin?
becomes urobilinogen. 80% of which becomes stercobilinogen and is pooed out
20% of urobilogen is reabsorbed and most of this is recycled by liver, and a very small amount is peed out via kidney (urobilin)
naaaame the salivary gland tumor:
- most common
- benign
- mixed : chondromyxoid stroma and epithelium
- recurs if partially removed
pleomorphic adenoma
naaaame the salivary gland tumor:
- most common malignant
- has mucinous and squamous components
mucoepidermoid carcinoma
naaaame the salivary gland tumor:
benign cystic w/ germinal centers
smokers
10% bilatera, 10% malignant
Warthrin tumor
Achalasia
“bird’s beak”
very HIGH LES resting pressure, because of loss of Auerbach’s plexus (PSNS) so decreased VIP and NO released, uncoordinated/absent peristalsis
progressive dysphagia of solids AND liquids
achalasia poses an increased risk of what?
esophageal ca
Boerhaave Syndrome?
transmural tear in esophagus due to retching
- pneumomediastinum
- subcutaneous emphysema
“esophageal rings”
“linear furrows”
unresponsive to GERD
eosinophilic esophagitis
caustic ingestions and GERD causes what esophageal problem
strictures
Esophageal varices
dilated lower 1/3 veins, hematemesis
seen in portal htt, cirrhosis
Esophagitis in immunocompromised. Name the cause?
- white plaque
- linear tears
- punched out lesions
- candida
- CMV
- HSV1
GERD symptoms? whats going on with LES?
- heart burn, regurg, dysphagia, hoarse, cough
- transient decreases in LES pressures
What syndome is caused by a mucosal tear in esophagus due to severe vomitting (alcholics, bulemics)
Mallory Weiss Syndrome
Plummer Vinson Syndrome
iron deficiency anemia
esophageal webs
dysphagia
(glossitis)
Plummer Vinson Syndrome causes risk of?
esophageal SCC
esophageal smooth muscle atrophy and fibrous replacement with low resting LES pressures
CREST syndrome (sclerodermal esophageal dysmolitity)
Barrett’s Esophagus has increased risk of?
esophageal adenocarcinoma
Barret’e Esophagus path?
stratified squamous epithelium (normal in esophagus) has metaplasia with nonciliated goblet cells (of intestines)
due to chronic GERD
squamous cell carcinoma of esophagus vs adenocarcinoma
location
risk
prevelance
SCC: upper 1/3
A: lower 1/3
SCC:smoking, alcohol, hot tea, betel nuts
A: GERD/Barrett, obesity, smoking
SCC: world
A: USA
Acute Gastritis (3 causes)– think erosions!
- NSAIDs - b/c they decrease PGE protection
- Curling’s Ulcers- result of burns– hypovol– ischemia
- Cushing’s Ulcers- result of CNS damage– increased vagal output– increased acidity
Chronic Gastritis (2) causes— think inflammation
(1) H Pylori – antrum of stomach, PUD and MALT lymphoma
(2) autoimmine– body/fundus of stomach–parietal cells of stomach attacked
Menetrier’s Disease
excess mucosal hyperplasia causing hypertrophic rugae. Damages parietal cells, decreases acid production
what is “intestinal” gastric cancer associated with
H Pylori, smoked foods, smoking, chronic gastritis
what is “diffuse” gastric cancer associated with
NOT H pylori
it looks like the signet ring
leather bottle stomach, linitis plastica
Virchow Node
sign of gastric cancer
L supraclavicular node involvement by mets from stomach
Krukenberg Tumor
bilat mets to ovaries from gastric cancer
mucin secreting
Sister Mary Joseph nodule
sign of gastric cancer met to the subcut periumbilical area
Gastric Ulcer vs Duodenal Ulcer
food?
HPylori relation?
other causes apart from HPylori
food makes gastric ulcer Greater
food makes duodenal ulcer Decrease
gastric ulcer is 70% relation to HPylori
duodenal ulcer is 90% relation to HPylori
gastric ucler can be caused by NSAID
duodenal ulcer can be caused by ZES
which type of ulcer is generally benign?
duodenal
how do you diagnose a gastric ulcer vs a duodenal ulcer
gastric: biopsy margins to rule out malignancy!
duodenal: just check for hypertrophy of Brunner’s glands (no biopsy required)
if ulcer ruptures on lesser curvature of stomach? wheres the bleed?
how about posterior duodenal wall?
(1) L gastric A
(2) gastroduodenal A
celiac’s disease
autoimmune against gliadin (most present in duodenum+ jejunum).. IgA anti-tissue transglutaminase
path: crypt hyperplasia and villous atrophy
HLADQ2 and HLADQ8
Celiac’s
dermatitis herpetiform
Celiac’s
celiac has increased risk of
T cell lymphoma
Lactose Intolerance
normal villi
decrease stool pH
osmotic diarrhea
breath H test >20 ppm
pancreatic insufficiency
decrease absorption of ADEK and B12
causes: chronic pancreatitis and CF (as well as cancers)
Tropical Sprue
looks like Celiac’s but responds to antibiotics
megaloblastic anemia assn bc of folate and later B12 def
hint: someone from or visitng the tropics
what causes Whipple Disease
cause: TROPHERYMA WHIPPLEI
INTRACELLULAR GRAM + PAS+
foamy macrophages in intestinal lamina propria
what are the symptoms of whipple’s disease?
Foamy Whipped cream in a “CAN”
- cardiac
- arthralgia
- neurologic
with diarrhea and steatorrhea occurring later in the disease
UC vs Crohn’s Disease: where?
UC: continuous lesions, always includes rectum: mucosal/submucosal
Crohn’s: skip lesions (seen in terminal ileum often) and SPARES rectum: transmural
pathological finds: UC vs Crohn’s
UC: bleeding, crypt abcess, no granuloma, TH2, “lead pipe” no haufsta
Crohn’s: granulomatous(noncaseating)TH1, lymphoid aggregates, “creeping fat” “cobblestone mucosa” “string sign” (= a string connecting two parts of GI)
complications of UC vs Crohns
UC: toxic megacolon, fulminant colitis, perforation
Crohn’s: fistulas, strictures, perianal disease
Bloody diarrhea: Crohn’s or UC
UC!
name the common extra-intestinal manifestations of Crohn’s and UC
Pyoderma Gangrenosum
Erythema Nodosum
inflammmation of eye and joints
mouth ulcers
+ ASCA (anti-sacchromyces cervisiae ab)
Crohn’s
what is UC + for? what else is UC associated with
p-ANCA +
primary sclerosing cholangitis (90% have UC)
Crohn’s management
corticosteroids, Azathioprines, antibiotics, infliximab, adalimumab
UC management?
5 ASA (like mesalamine), 6MP, infliximab, colectomy
IBS
- change in form of stool
- change in frequency of stool
- abdominal pain
Appendicitis
caused by obstruction of appendix which leads to basterial invasion and inflammation
what two things present like appendicitis?
diverticulitis
ectopic pregnancy
diverticulum
Meckels: true: has all 3 gut layers
most are acquired: false: have only mucosa and submucosa
Diverticulosis
occurs in elderly, false diverticuli in sigmoid colon, can be due to increased intraluminal pressure, low fiber diet, and weak colonic wall
diverticulitis
inflammationof diverticuli
LLQ pain
Zenker’s diverticulum
a false diverticulum due to cricopharyngeal muscles not moving correctly
seen in Killian’s triangle in inferior pharyngeal constricter
seen in old men
Meckel’s Diverticulum
patency of the vitelline duct prox to the midgut
can be cause of infection due to ectopic tissue (gastric or pancreatic)
true diverticulum
RLQ pain
2x likely in males under 2 yo
diagnosis: pertechnate study
pain location of diverticulosis vs Meckels
diverticulosis– LLQ
Meckel’s– RLQ
Hirschsprung Disease
lack of ncc migration causes no autonomic ganglia in lower GI tract
assn w/ RET, increased risk with Down’s
causes congential megacolon
presentation of Hirschsprung Disease
Bilious Vomit
explosive (squirt sign) feces expulsion
no meconium within 48 hours
Malrotation
anomaly of midgut rotation during detal devlopment causes wrong positioning of bowel
“Ladd bands” are characteristic, they can lead to volvulus and duodenal obstruction
volvulus
twisting of bowel around mesentery
midgut volvulus in children
sigmoid volvulus- in elderly
“coffee bean”
intussusception
lead point causes proximal intestine to fit into distal intestine
common lead points: ilio-cecal junction, Meckel’s, can be associated with virus (like adeno or rota)
“currant jelly stool”
“thumb print sign”
colonic ischemia
h(x) of atherosclerosis+ pain after eating?
chronic mesenteric ischemia
out of proportion abdominal pain+ currant jelly stool
acute mesenteric ischemia
tortuous vessel dilation of right sided colon? older patient?
angiodysplasia
intestinal hypo-motility sans obstruction
ileus
CF+ constipation in baby
meconium ileus
premie baby + formula food+ air in abdomen?
necrotizing enterocolitis
Peutz-Jegher and Juvenile Polyposis causes what kind of polyps in colon?
hamartomatous
what are the two types of colonic polyps with malignany potential
(1) serrated
(2) adenomatous
what are the types of adenomatous polyps?
(1) villous (worse prognosis)
2) tubular (better prognosis
what do serrated colonic polyps look like
saw toothed pattern of crypts
chromosomal instability leads to what kind of polyp
probs w/ APC, KRAS are “chromasomal instability” lead to adenomatous polyps(=neoplastic)
what does microsatellite instability lead to in type of polyp?
cpg methylation, BRAF mutations= microsatellite instability
cause serrated polyps (pre-malignant)
FAP
AUTOSOMAL DOM MUT IN APC
multiple colonic polyps after puberty, 100% will become cancer
what is Gardner’s syndrome
FAP+ bone/soft tissue tumors (+ hypertophy of retinal pigment)
extra teeth or impacted teeth a sign of?
Gardner’s Syndrome
Turcot Syndrome
FAP/ Lynch + malignancy CNS tumor
peutz jeghers apart from hamartomatous GI polyps has increased risk of what cancers?
breast+ GI
many hamartomatous polyps before age of 5
Juvenile Polyposis syndrome
Lynch Syndrome
autosomal dominant mutation in mismatch repair genes (MSH1/2) causes microsatellite instability
linked to ovarian, endometrial, skin and colonic cancers
most common location of colorectal cancer
rectosigmoid> ascending> descending
how do ascending CRC and descending CRC present differently?
ascending:bloody stool, “exophytic mass”
descending : obstruction “infiltrating mass”
whats the marker for CRC
CEA
“apple core lesion”
CRC
molecular pathogenesis of CRC?
“firing order of events” AK53
APC
KRAS
p53/ DCC
why is it thought that NSAIDS can protect against CRC?
bc overexpression of COX2 has been seen in CRC
what does a cirrhotic liver look like
diffuse bridging fibrosis and regenerative nodules distrupting normal liver architecture
cirrhosis increases the risk for what?
HCC
causes of cirrhosis?
(1) alcohol(70%) nonalc fatty liver disease chronic viral hepatitis autoimmune hepatitis biliary disease metabolic diseases
causes of portal htt?
(1) cirrhosis
vascular obstruction of portal v
Budd Chiari
schistosomiasis
what are the neurologic signs of cirrhosis
hepatitis encephalopathy
asterixis
what do AST and ALT show
hepatic injury
alcohol AST»ALT (or progression to advanced cirrhosis)
what do ALP and yGT show?
biliary injury
note ALP is also increased in bone conditions (but not yGT) yGT is also more closely associated with alcohol use
Reye syndrome
when you give a kid aspirin it causes irreversible mitochondrial damage( due to decreased B-ox), encephalopathy, and microvesicular fatty change of liver
what is the progression of alcoholic liver disease
(1) hepatic steatosis : macrovesicular fatty change, reversible with alcohol cessation
(2) alcoholic hepatitis: due to chronic alc use, shows as swollen and necrotic hepatocytes, neutrophilic infiltrate, Mallory bodies
(3) alcoholic cirrhosis: final and irreversible, regen nodules with bands of fibrsosis
what is a mallory body?
its seen in alcoholic hepatitis (intermediates stage of alcoholic liver disease) and its a intracytoplasmic inclusion of an eosinophilic staining keratin filament
NAFLD pathology?
cellular ballooning and necrosis
associated with insulin resistance and metabolic syndrome
can cause cirrhosis and CRC
hepatic encephalopathy physiology?
cirrhosis and shunting of blood away from liver causes decreased metabolism of ammonia. this ammonia can cross BBB
can be exscerbated by increase in ammonia (GI bleed, protein in diet, renal failure)
treatment is: lactulose (increases ammonia to ammonium) and rifaximin (decreases gut NH3 production)
HCC marker?
AFP
HCC caused by?
(1) Hep B
2) cirrhosis and its causes: Hep c, hemachromatosis, NAFLD, alcohol, a1antitrypsin, aflatoxin
whats the most common benign liver tumor
cavernous hemagioma
DONT BIOPSY– it might bleed
what liver cancer is related to OCP and steroid use?
hepatic adenoma
arsenic and vinyl chloride cause
angiosarcoma of liver (malignant)
if you see multiple liver tumors?
METS
Budd-Chiari syndrome
blockage of hepatic veins.
“nutmeg liver”- centrilobular congestion/necrosis
absent JVD
a1antitrypsin deficiency
problem with liver+ lung (dyspnea) panacinar emphysema (bc of no inhibition on elastase) and misfolded proteins(AAT) aggregating in liver (PAS+)
jaundice
yellowing of skin or sclera bc of hyperbilirubinemia
causes of unconjugated hyperbilirubinemia
unconjugated= insoluble = Indirect
- hemolytic
- physiologic : baby doesnt have mature UDP glucoronosyl transferase
- Criggler Najar I- no UDP GT (II is less severe and responds to phenobarbital)
- Gilbert’s– mildly decreased UDPGT
causes of conjugated hyperbilirubinemia
conjugated= soluble=direct
bile tract obstruction (PSC, PBC)
excretion defect: Rotor’s and Dubin-Johnson
causes of mixed hyperbilirubinemia
cirrhosis, hepatitis
black liver + conjugated hyperbilirubinemia is?
DubinJohnson.
the black pigment is epinephrine
(note this is not seen in Rotor’s)
Wilson’s disease?
Copper overload due to decreased Cu excretion in bile bc autorecmut in ATP7B.
decreased serum ceruloplasmin
t(x): penacillamine, or trientine, oral zinc
wilson’s disease symptoms?
Kayser-Fletcher rings, hemolytic anemia, renal problems (Fanconi) liver/neuro/psych involvement
What is the cause of Hemochromatosis
Autosomal recessive mutation in the HFE gene (transferrin receptor accessory) which causes faulty liver sensing of iron- telling the body iron is low when its not. this leads to increased iron absorption from intestines
What are the symptoms of Hemochromatosis
- “bronze diabetes”
- skin pigmentation
- -DM
- arthopathy
- dilated or restrictive cardiomyopathy
- -hypogonad
Hemochromatosis is a risk factor for what?
HCC
Primary Sclerosing Cholangitis
who? histology? assn?
- affects middle aged men
- inflamm and sclerosis (“onion skin thickening”) of biliary tree (“beads of a string”)
- p-ANCA, Ulcerative Colitis , increased IgM
Primary Biliary Cholangitis
who? histology? assn?
- affects middle aged women
- association to autoimmune conditions (Sjogren, Hashimoto, CREST, RA, Celiac)
- histology: lymphocytic infiltrate with granulomas of the bile ducts.. its an AUTOIMMUNE rxn!
- anti-mitochondrial ab +, increased IgM
secondary biliary cholangitis
due to obstructive lesion (gallstone, biliar strictures, head of pancreas tumor) of the extrahepatic ducts. which causes an increased pressure in the intrahepatic ducts, and leads to innjury, fibrosis, and stasis
(can be complicated by ascending cholangitis infection)
black stone=
brown stone =
hemolysis
infection
choledocolithiasis
stone in the CBD, causes increase in ALP, GGT, direct BR, (and or AST and ALT)
cholecystitis and its 2 causes
inflamm of gall bladder usuallly due to stone in cystic duct
(1) calculus: gallstone in fuct
(2) acalculus: being very sick ex: sepsis, burns CMV causes gallbladder STASIS and hypoperfusion
Porcelain Gallbladder
blue and brittle gallblader (lights up on CT) due to calcification from chronic cholecystits.
this risk is gallbladder cancer, so get rid of the gallbladder!!!
whats the traid, and pentad of ascending cholangitis
Charcot triad: jaundice, fever, RUQ pain
Pentad: shock, and altered mental status
acute pancreatitis
(1) gallstone (2) alcohol (high TGs Mumps, autoimmune, scorpion sting, high calcium, ERCP)
- injury causes activation of trypsinogen which activates all other zymogens while still in pancreas causing autodigestion.
what does acute pancreatitis present like
acute epigastric pain radiating to back
INCREASED serum amylase and lipase
can be complicated by formation of a psuedocyst: covered in granulation tissue not epithelium. many other complications like hemorrhage, ARDS etc
chronic pancreatitis
chronic inflamm/atrophy/calcification of pancreas.
cause: alcohol abuse and idiopathic
note that amylase and lipase may not be elevated
pancreatic insuff will cause low ADEK absorption, DM, and steatorrhea
pseudocysts can occur here too
Pancreatic Adenocarcinom
CA19-9
Trousseau Sign- migrating thrombophlebitis
Courvoisier’s Sign- palpable but not tender gallbladder
if at head of pancreas- can cause CBD obstruction
wt loss w/ abdominal pain radiating to back
