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279 Cards in this Set

  • Front
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Enzyme co-factor for insulin action
Chromium
Inhibits Vitamin K (anticoagulant)
Warfarin (Coumadin)
most widespread micronutrient deficiency in the world
iodine-- goiters and cretinism (kids), hypothyroidism
Role: Connective tissue/collagen formation, promotion of iron absorption by keeping iron in the absorbable state (ferrous Fe2+)
Vitamin C/Ascorbic Acid
micronutrient synthesized in the liver from trypthophan
Niacin (Vitamin B3)
Cofactor for folate function
Cobalamine (Vitamin B12)
2 things absorbed in the terminal ileum
bile acids and vitamin B12 (cobalamine)
1. Acute: papilledema, bulging fontanelles, vertigo, diplopia, skin exfoliation
2. Chronic: anorexia, headache, dry skin, hair loss, hepatosplenomegaly
Vitamin A/Retinol excess
Role: increase intestinal absorption of calcium and phosphorus, increase renal reabsorption of calcium
Vitamin D (Ergocalciferol)
1. decreased calcium absorption from small intestine
2. decreased reabsorption of calcium from the kidneys
3. stimulates PTH release
4. PTH- increases calcium absorption from the gut but also leaches it from bones
Vitamin D (Ergocalciferol) deficiency
seen in granulomatous disease: sarcoidosis, lymphoma
1,25 dihydroxyvitamin D excess--> hypercalcemia
1. increased calcium reabsorption from the gut
2. hypercalcemia-stones, moans, psychological overtones
3. hypercalcuria (stones)
vitamin D excess
Excess Sx:
1. dec platelet aggregation
2. interferes with vitamin K metabolism (don’t use with warfarin—too much anticoag effect)
Vitamin E (alpha tocopherol) excess
Zollinger Ellison syndrome
gastrinoma- tumor that secretes gastrin causing parietal cells to release HCl and intrinsic factor-- this leads to high levels of acid secretion and peptic ulcer disease.
Functions of Cholecystokinin
1. Gallbladder contraction
2. sphincter of Oddi relaxation
3. delayed/dec gastric emptying
4. stimulation of pancreatic acinar cells
Stimulants of CCK release
fatty acids and protein- CCK-releasing peptide and monitor peptide (panc acinar cells)
Why does eating fatty foods potentially make the pain of cholelithiasis worse?
Fatty foods stimulate the release of CCK which stimulates the contraction of the gallbladder
Where is CCK released from?
I cells of the duodenum
Where is secretin released from and what are it's function.
Released from S cells of duodenum
1. Stimulates the release of HCO3- (bicarb) from pancreatic ductular cells. Water follows. This allows pancreatic enzymes to flow into duodenum and function (alkaline pH)
2. decreases gastric acid secretion
3. increases bile secretion
What stimulates the release of secretin?
The entry of acid from the stomach along with food
Where is somatostatin released from?
D cells in the antrum of the stomach and pancreatic islets (delta cells--endocrine-release somatostatin into blood)
What are the functions of somatostatin?
Turns everything off...
1. dec gastric acid (parietal cells) and pepsinogen (chief cells) secretion
2. dec pancreatic and small intestine fluid secretion
3. dec gallbladder contraction
4. dec insulin and glucagon release
What is a type of synthetic somatostatin and what is it used for?
Octreotide/Sandostatin
1. carcinoid tumors
2. VIPomas
3. esophageal varices-- GI hemorrhage
4. chronic pancreatitis
What is GIP and what are its endocrine and exocrine functions?
Glucose dependent Insulinotropic Peptide stimulated by oral glucose load
endocrine: increase insulin release- pull glucose intracellular
exocrine: decrease gastric H+ secretion
What is VIP and what does it do?
Vasoactive Intestinal Peptide- relaxation of intestinal sphincter and smooth muscle, increase intestinal water and electrolyte secretion
VIPoma-- massive diarrhea (relaxation + H20 and lytes secretion)
What is motilin and what does it do? What can stimulate it?
Motilin is secreted by the small intestine during the fasting state. It produces Migrating Motor Complexes to clear the gut of undigested food (less than size of nickel). Stimulated by erythromycin-- can clear gut of blood prior to scope.
What is intrinsic factor? What does it do and where it is release from?
secreted by parietal cells of the stomach (in addition to HCl), it is a vitamin B12 binding protein needed for the absorption of vit b12 in the terminal ileum
What is autoimmune gastritis what does it lead to?
autoimmune destruction of gastric parietal cells-- less HCl, but high gastrin levels, lack of intrinsic factor--> pernicious anemia (macrocytic)
What stimulates gastric acid secretion in the stomach? What inhibits it?
stimulate HCl release: gastrin (g cells in antrum), ACh, histamine (ECL cells)
inhibit HCl release from parietal cells: somatostatin, glucose dependent insulinotropic peptide (GIP), prostaglandin, secretin
What is pepsinogen? Where is it released?
Pepsinogen is released from gastric chief cells-- it cleaved by H+ to its active form= pepsin--degrades protein (not nearly as important as pancreatic proteinases)
Where is Bicarb (HCO3-) produced/released in the GI tract? What is its purpose?
pumped out by pancreatic ductular cells (secretin), brunners gland of duodenum, mucus that covers gastric epithelium (protects epithelium from damage from acid)
Neutralizes acid and prevents autodigestion of pancreatic enzymes (only work in alkaline env)
What pancreatic enzyme is secreted in its active form?
amylase
what characteristic histological feature do you see with Hep B infection?
"ground glass" hepatocytes--> HBsAg
What activates trypsinogen and where is it located?
enteropeptidase/enterokinase on the intestinal brush border
How must carbohydrates be absorbed?
As monosaccharides (glucose, galactose, fructose)
How is glucose absorbed into enterocytes?
Via the Sodium-Glucose-Galactose co-transporter (SGLT-1) -- so when someone is dehydrated you should give sodium glucose in 1:1 concentrations.
How is fructose absorbed by enterocytes?
By facilitated diffusion (GLUT-5)
Plummer Vinson Syndrome
Triad of
1. dysphagia from esophageal webs
2. glossitis
3. iron deficiency anemia
Risk Factors for Esophageal Cancer
ABCDEF
Alcohol/Achalasia
Barret's esophagus from GERD (LES)
Cigarrettes
Diverticuli (Zenker's above the upper eso sphincter)
Esophageal web (plummer-vinson syndrome), esophagitis
Famlial
most common type of esophageal cancer worldwide and where found in the esophagus?
squamous cell carcinoma, in the upper and middle esophagus
most common type of esophageal cancer in the U.S. and where found in the esophagus?
adenocarcinoma in the lower 1/3 of esophagus. Barret's (intestinal metaplasia is risk factor)
celiac sprue
autoantibodies to gliadin (in wheat, barley, rye)-- causes 1. blunting of villi in the proximal small bowel
2. massive malabsorption and diarrhea
3. lymphocytes in the lamina propria in the epithelium
4. crypt hyperplasia
Blood test- alpha1 gliadin and tissue transglutaminase (TTG)
Treatment- gluten free diet
associated with dermatitis herpetiformis
at slightly increased risk for T cell lymphoma
disease associated with dermatitis herpetiformis
celiac sprue
Acute gastritis (erosive)
disruption of the mucosal barrier--> inflammation
Causes:
1. stress
2. NSAIDs (block PGE2-- which stimulates mucous production)
3. burns = Curling ulcer-- dec plasma volume--> sloughing of gastric mucosa
4. brain = Cushing's ulcer-- inc vagal stimulation--> inc ACh--> in parietal cell H+ secretion
Chronic gastritis (nonerosive)
Type A- body of stomach
two types: A (body) and B (antrum), AB Pairing to help remember

A (Body)- Autoimmune gastritis-attacks parietal cells--> Achlohydria, pernicious Anemia (lack of intrinsic factor)
chronic gastritis
Type B- antrum of the stomach
caused by H. pylori Bacterium infection--affects Antrum
increased risk for MALT lymphoma
Menetrier's disease
gastric hypertrophy with protein loss, parietal cell atrophy, and inc mucous cells--precancerous condition. Rugae of the stomach are so hypertrophied they look like the gyri of the brain
common features of gastric adenocarcinoma
1. signet rings (looks like class ring) and 2, acanthosis nigricans (dark brown/black hyperpigmentation of the skin that is also associated with endocrine dysfunction--DM, hypothyroid etc)
things associated with stomach cancer
1. nitrosamines (smoked foods)
2. chronic gastritis
3. achlorhydria (lack of stomach acid)
linitis plastica
thickened leathery appearance of the stomach when gastric adenocarcinoma is diffusively infiltrative ("leather bottle")
virchow's node
gastric adenocarcinoma mets to the left supraclavicular node
krukenberg's tumor
gastric adenocarcinoma with bilateral mets to the ovaries- abundant mucus and signets rings
compare and contrast gastric ulcers and duodenal ulcers
Gastric ulcer- pain is Greater with meals, 70% caused by H. pylori infection, chronic NSAID use also implicated (block PGE2--dec mucus production/protection)
Duodenal ulcer- pain Decreases with meals--> weight gain, almost 100% caused by H. pylori infection. See hypertrophy of Brunner's gland (secrete alkaline mucus), clean punched out margins (bleeding, perforation, penetration of pancreas, and obstruction can occur)
crohn's disease
granulomas,
skip lesions-seen as cobblestoning on imaging, transmural inflammation,
fistulas and fissures
creeping fat/mesentery-from trans inflam,
smoking,
rectal sparing,
extraintestinal manifestations of crohn's
1. migratory polyartheritis,
2. erythema nodosum (inflammation of fat cells on the skin--causing nodules often on the shins),
3. ankylosing spondylitis (cannot extend or flex spine),
4.uveitis,
5. immunologic disorders
ulcerative colitis
-continuous inflammation of the colon always involving the rectum
-only mucosal and submucosal inflammation
-pseudopolyps, ulcers, bleeding
-increased risk for colorectal cancer, severe stenosis, toxic megacolon
-"lead pipe" appearance on imaging- major continuous inflammation
extraintestinal manifestations of ulcerative colitis
1. primary sclerosing cholangitis (alternating areas of stricture and dilatation intra and extrahepatic bile ducts-- cholestasis)
2. pyoderma gangrenosum (tissue becomes necrotic forming deep ulcers--usually on the legs)--can also be seen in crohns though
appendicitis presentation
periumbical pain (visceral-- non localizing) that then localizes the RLQ- McBurneys point. Can perforate-- peritonitis
rule out diverticulitis and ectopic pregnancy
diverticulum
(true vs false)
blind outpouching of the GI tract
true- involves all layers of the gut wall
false- involves only mucosa and submucosal layers, often where vasa recta penetrate muscularis propria/externa
diverticulosus
many diverticuli, often asymptomatic or vague discomfort
-very common (50% of ppl over 60)
-arise from increased intraluminal pressure, low fiber diet-hard stools
- most common in sigmoid colon
diverticulitis
-inflammation of diverticula causing LLQ pain, fever, leukocytosis
-may perforate-- peritonitis, abscess formation, or bowel stenosis
- give Abx
- may cause bright red blood per rectum, colovesical fistula (colon to bladder-->pneumaturia)
Zenker's diverticulum
false diverticulum located above the upper esophageal sphincter. presents with halitosis (trapped food), regurgitation of undigested food, dysphagia, obstruction
Meckel's diverticulum
persistence of the vitelline duct or yolk sac,
may contain acid-secreting gastric mucosa or pancreatic tissue
can cause bleeding, volvulus, intussusception, or obstruction near the terminal ileum
the 5 twos
1. 2 inches long
2. 2 feet from ileocecal valve
3. 2% of population
4. often present within first 2 years
5. may have 2 types of epithelia (gastric, pancreatic)
most common congenital anomaly of the GI tract
Meckel's diverticulum
possible outcomes of Meckel's diverticulum
bleeding, volvulus, intussusception, or obstruction near the terminal ileum
intussusception
telescoping of 1 bowel segment into a distal segment
can compromise blood supply
often due to intraluminal mass or stricture causing one part to get stuck and the other to slide inside it
usually seen in infants--constipation
volvulus
twisting of portion of the bowel around its mesentery/stalk
can lead to obstruction and infarction
may occur at sigmoid colon cuz of redundant mesentery
usually in elderly
Hirschsprung's disease
congenital megacolon characterized by lack of myenteric/Auerbach's plexus in segment of bowel
due to failure of neural crest cells to migrate
presents as chronic constipation early in life (failure to pass meconium)
dilated portion of the colon proximal to aganglionic segment
involves rectum
pts with Down syndrome at inc risk
duodenal atresia
causes early bilious vomiting with proximal stomach distention = "double bubble"
Associated with down's syndrome
meconium ileus
in cystic fibrosis, meconium plug obstructs intestine, preventing stool passage at birth
necrotizing enterocolitis
necrosis of intestinal mucosa and possible perforation
colon usually involves but can involve entire GI tract
in neonates- more often in preemies
ischemic colitis
reduction in intestinal blood flow causes ischemia
commonly occurs at the splenic flexure--watershed region/border zone
typically seen in elderly
adhesion
acute bowel obstruction
usually after surgery
can cause well demarcated necrotic zones
angiodysplasia
tortuous dilation of vessels--> bleeding
most often seen in cecum and ascending colon
more common in elderly
colonic polyps
which type is most likely to be malignant?
90% are benign hyperplastic hamartomas, not neoplasms--remove them anyway
grow into the intestinal lumen- can be flat (sessile) or pedunculated (on stalk)
The more villous (colon does not usually have villi--only small bowel, since villi are for absorption)
Colorectal cancer
gene involved
3rd most common cancer
most are sporadic (APC gene mutation)
presentation of right sided vs left sided CRC
right bleeds- Iron deficiency in man over 50 is CRC until proven otherwise
left obstructs (lumen is more narrow on the left)
risk factors for CRC
1. age
2. villous adenomas
3. chronic IBD, esp ulcerative colitis
4. family hx
5. FAP (100% chance of developing CRC)
6. HNPCC (80% develop CRC)
CRC screening
all people over 50 unless hereditary condition--then earlier
stool occult blood and colonoscopy
FAP (familial adenomatous polyposis)
gene involved, presentation, and other cancers
thousands of polyps throughout entire colon
always involved the rectum--carpeted (100% risk of developing CRC)-- do colectomy
gene: APC
at risk for duodenal and thyroid cancer (many die from duodenal ca if colon removed)
Gardener's syndrome
FAP with osseous and soft tissue tumors, retinal hyperplasia
SODD
sebaceous cyts
osteomas
dental caries
desmoid tumors
Turcott's syndrome
FAP with possible brain involvement (glioma, medulloblastoma)
TURcott = TURban
HNPCC = Hereditary Non-Polyposus Colorectal Cancer = Lynch syndrome
presentation, gene, other cancers
80% go onto develop CRC
proximal colon always involved
gene= DNA mismatch repair genes
other cancers: esop's gu
ENDOMETRIAL, stomach, ovarian, pancreas, genitourinary
Peutz Jegher Syndrome
inheritance pattern?
presentation, other cancers
at risk for?
Autosomal Dominant
benign polyposis syndrome
hyperpigmentation macules on oral mucosa, hands and feet (mucocutaneous lesions-abnormal freckling)
other cancers- colon, breast, lung, pancreas, ovary, uterus, stomach
Risk: intussusception
Carcinoid tumor
tumor of endocrine cells
50% of small bowel tumors
most common in small intestine
often produce 5-HT which can lead to carcinoid syndrome-- right sided valvular disease, wheezing, flushing, diarrhea.
carcinoid syndrome only happens if there are mets outside the GI tract (otherwise liver metabolizes excess 5-HT)
met is often in liver
Carcinoid syndrome
carcinoid tumor produces 5-HT--leading to...
flushing
wheezing
diarrhea
right sided valvular disease
small bowel adenocarcinoma
where does it usually occur?
risk factors?
presentation?
usually in the duodenum
risk factors: IBD, HNPCC, FAP, celiac, Peutz Jegher, juvenille polyposis
present: obstruction--> jaundice, blood loss
cirrhosis
histology?
presentation?
histo: diffuse fibrous bands/septae and regenerative nodules
presentation: portal HTN--> esophageal varices (hematemesis), caput medusa (umbilical veins), internal hemorrhoids (painless)
jaundice, sceral icterus, ascites, edema, asterexis (arms outstretched, hand's flap)
hyperestrogen state- spider angiomata, gynecomastia, testicular atrophy
Measurements of Liver Function (3)
1. albumin
2. bilirubin
3. prothrombin time (INR) - liver makes clotting factors
TIPS
transjugular intrahepatic portosystemic shunt (relieves portal HTN but may exacerbate encephalopathy if present)
micronodular cirrhosis
nodules <3 mm uniform in size
due to metabolic insult: alcohol, hemachromatosis, wilson's dz
macronodular cirrhosis
nodules > 3mm varied in size
usually due to significant liver injury leading to hepatic necrosis (post-infectious or drug induced hepatitis) inc risk for HCC
LFTs: AST and ALT
when elevated? which is elevated more when?
viral hepatitis (ALT > AST) more liver specific
alcoholic hepatitis (AST > ALT) ratio > 2:1 S= sauced
Myocardial infarction (AST)
Markers of cholestasis
what else could cause these elevations?
Alkaline Phosphatase (ALP)- bone, bile duct dz, obstructive liver dz,
Gamma Glutamyl Transpeptidase- (GGT)- liver dz, heavy EtOH
Markers of acute pancreatitis
Amylase- up in 2 hrs peaks quickly
Lipase- up in 4 hrs-- stays elevated longer, best marker
Labs indicating Wilson's dz
low serum ceruloplasmin, high serum and urine copper
Reye's syndrome
presentation, cause, histo
rare, often fatal childhood hepatoencephalopathy
present: hypoglycemia, coma
histo: microvesicular steatosis (drug)
cause: virus (esp VZV or influ B) treated with aspirin/salicylates
hepatic steatosis
histo?
short-term change with moderate alcohol intake
macrovesicular fat, reversible
alcoholic hepatitis
histo?
requires sustained, long term consumption of alcohol
Mallory bodies- intracytoplasmic eosinophilic inclusions), chickenwire fibrosis in zone 3 (near central vein)
alcoholic cirrhosis
irreversible
micronodular, irregularly shrunken liver
sclerosis around the central vein (EtOH in zone 3)
(drugs and bugs in zone 1 around portal vein)
Hepatocellular carcinoma (HCC)
risk factors?
chronic Hep B or C
alcoholic cirrhosis
NASH
Wilson's
hemochromatosis
alpha-1-antritrypsin deficiency
aflatoxin in peanuts!
HCC findings
1. hypoglycemia
2. tender hepatomegaly
3. ascites
4. polycythemia (inc HCT--lost fluid from circ due to low albumin)
What may be elevated in HCC?
50% of the time alpha-fetoprotein levels are elevated
Nutmeg liver
cause?
blood backing up into liver caused by right sided heart failure or Budd-chiari syndrome
liver appears mottled like nutmeg-- if persists centilobular congestion and necrosis may occur
Budd-Chiari syndrome
what is it? what is it associated with?
clot in hepatic vein or IVC leading to centrilobular congestion and necrosis--congestive liver disease (ascites, hepatomegaly, portal HTN)
associations: pregnancy, polycythemia vera, HCC
alpha1- antitrypsin deficiency
histo?
misfolded protein accumulates in the liver (PAS positive globules) (protease inhibitor of neutrophil elastase)-- there is no inhibition of neutrophil elastase so lungs are destroyed-- emphysema
PAS positive globules seen in the liver
alpha-1-antitrypsin deficiency
Gilbert's syndrome
hereditary hyperbilirubinemia- 30% less less UGT1A1 to conjugate bilirubin. Asymptomatic--but may have jaundice and scleral icterus with stress, dehydration or fasting
Criggler-Najjar Syndrome Type I
absence of UDP glucoronyl transferase (UGT)-- cannot conjugate bilirubin. unconjugated hyperbilirubinemia.
Findings: jaundice, kernicterus (bilirubin deposition in the brain)- will die without liver transplant
tx: plasmaphoresis and light therapy
what can be given to increase liver synthesis of UGT1A1 ?
phenobarbital (good tx for Criggler Najjar type 2-- less severe than type 1- with 70% reduction in UGT1a1 levels.
what drug is metabolized by UGT1A1 and can have impaired metabolism with Gilbert or Criggler Najjar
Irinotecan- chemotherapy drug
Dubin Johnson syndrome
hereditary conjugated hyperbilirubinemia-- can conjugate bilirubin but not excrete it into bile ductules--leads to grossly black liver (pigmented) . benign
Rotor syndrome
similar to dubin-johnson syndrome- hereditary caonjugated hyperbilirubinemia-- milder and no liver pigmentation
Wilson's disease
aka? characterized by? tx?
copper accumulation in brain, kidneys, liver, joints, cornea
characterized by ABCD:
Asterexis
Basal ganglia degeneration- movement disorder (parkinsonian)
Cirrhosis, dec ceruloplasmin, corneal deposits (Kaiser-Fleysher rings), chorea, copper accumulation, Carcinoma (HCC)
Dementia
tx: penicillamine (copper chelation)
hemochromatosis
gene? sx?
accumulation of iron because of continuous absorption-defect in HFE gene
Sx: dilated cardiomyopathy-CHF
deposition in pituitary-- melanin-bronze discoloration of skin, and dec gonadotropins-- testicular atrophy, gynecomastia
deposition in the pancreas- diabetes
increased risk for HCC
tx: repeated phlebotomy
causes of acute pancreatitis
IGET SMASHeD
Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune dz
Scorpion bite
Hypercalcemia, hyperlipidemia, hypothermia
e
Drugs-steroids, sulfazalazine, a , NSAIDs, diuretics, DII (HIV drug)
primary sclerosing cholangitis
ERCP? histo? lab findings? associations?
inflammation and fibrosis of intra and extrahepatic bile ducts
ERCP: beading of bile ducts--alternating areas of strictures and dilatations
histo: onion skinning- thick layers of collagen deposition around bile ducts
lab: inc ALP and/or GGT
assoc: ulcerative colitis in 80%
Abdominal Zones, names and blood supply
1. foregut =
2. midgut =
3. hindgut =
1. foregut= epigastrium- celiac artery- stomach--> ampulla of vater in D2
2. midgut = periumbilical- superior mesenteric artery- ampulla of vater--> proximal 2/3 of transverse colon
3. hindgut- hypogastrium/suprapubic- inferior mesenteric artery- distal 1/3 of transverse colon--> rectum above pectinate line
pain derived by the autonomic nervous system that is midline and generalizes to a zone but it is not focal-- due to wall tension, dull cramping
visceral pain
pain at site of origin, sharp, severe, persistent, due to acute pH or temperature changes
somatic nervous system
parietal pain
referred pain
left shoulder
left diaphragm irritation-- spleen
esophagus
heart
referred pain
right shoulder
right diaphragm irritation -liver, gallbladder, duodenum
referred pain, right subscapular
biliary tree
referred pain, flank
kidney, pancreas
referred pain, groin
ureters, bladder
retroperitoneal structures
SAD PUCKER
* S = Suprarenal glands (aka the adrenal glands)
* A = Aorta/IVC
* D = Duodenum (second and third segments [some also include the fourth segment] )
* P = Pancreas (tail is intraperitoneal)
* U = Ureters
* C = Colon (only the ascending and descending branches)
* K = Kidneys
* E = Esophagus
* R = Rectum
causes of upper GI bleeds
peptic ulcer eroding into vessels
(duodenal ulcer can erode into gastroduodenal artery--huge bleed)
esophageal/gastric varices
Mallory-Weiss tear- tear of mucosa at gastroesophageal junction (retching-alcohol)
esophagitis
causes of lower GI bleeding
1. colon cancer (occult bleeding)
2. internal hemarrhoids (painless)
3. external hemarrhoids (painful)
4. ulcerative colitis
5. diverticular bleeding- not associated with diverticulitis
6. infections- bloody diarrhea- shigella etc
what is the largest lymphoid organ in the body?
GI tract (peyer's patches - ileum has more than jejunum)
name the layers of the GI tube
lumen--> epithelium--> lamina propria--> muscularis mucosa--> submucosa (messeners plexus)--> muscularis externa/propria circular--> myenteric plexus of Auerbach--> longitudinal--> serosa
what type of muscle is the upper 1/3 of the esophagus? the rest of the GI tract?
striated muscle
smooth muscle
what part of the GI tract lacks serosa? what is a consequence of this?
esophagus- esophageal cancers (adenocarcinoma) can spread easily to other retroperitoneal structures
what is the pain purpose of crypts? villi?
small bowel has which?
large bowel has which?
crypts--> secretion
villi--> absorption
small bowel has crypts and villi
large bowel only has crypts-- goblet cells-secreting mucin
Describe the innervation of the GI tract
SNS- inhibitory
PNS- excitatory
ENS- enteric nervous system- main driver of GI tract- myenteric plexus of Auerbach--controls smooth muscle contractions
Achalasia
sx?
etiology?
appearance on imaging?
what disease can mimic this?
sx: dysphagia
lack of inhibitory neurons of myenteric plexus of Auerbach at the lower esophageal sphincter-- LES cannot relax to allow for passage of food (sticks in chest)
imaging- bird beak or rat's tail sign
mimic: Chagas disease
pacemaker cells of the GI track (located between circular and longitudinal muscle layers)-- receive innervation from myenteric plexus of Auerbach?
interstitial cells of Cajal
Basal Electrical Rhythm (BER)
relative rates of stomach and duodenum
rhythmic wave of partial depolarization- uncoordinated/ slow waves of contraction within the GI tract
stomach (3/min)
duodenum (12/min)
peristalsis
coordinated contraction and relaxations of the smooth muscles of GI tract- pushing food along
-controlled by enteric nervous system
oropharyngeal dysphagia
description? signs?
causes?
dysfunction in swallowing at the level of the pharynx, mouth-- usually under voluntary control-- epiglottis covering trachea, palate rising to protect nasopharynx
frequently see aspiration and repeated episodes of pneumonia
signs: aspiration pneumonia, nasal regurg, drooling, facial droop etc
causes: stroke, parkinson's, myasthenia gravis (autoimmune- blocking ACh receptors at motor end plate), ALS (degeneration of motor neurons)
esophageal dysphagia
causes?
dysfunction in the esophagus
causes: achalasia, strictures, rings/webs, esophagitis, connective tissue disease (i.e. scleroderma)
gastroesophageal reflux disease
sx:
possible causes?
consequence?
when is it worse and why?
reflux of gastric contents into esophagus
SX: heartburn/retrosternal burning, dysphagia, worse at night
cause: may have more relaxation of the LES than other people (pregnancy, progesterone), or may have more acidic stomach juices (caffeine/coffee), may eat things that induce relaxation of the LES (chocolate, mint, alcohol)
2. hiatal hernias-sliding of GE jxn
consequence: 10% get Barrett's esophagus-- intestinal metaplasia (which can go onto to become esophageal adenocarcinoma in 10%)
WORSE: at night when lying flat-- decreased peristalsis/gastric emptying, gravity, dec saliva production
esophageal dysphagia: motility vs mechanical/structural, signs
motility- trouble with both liquids and solids (achalasia)
mechanical/structural (strictures etc)-- trouble with solids > liquids
TX for GERD
1. H2 blockers (-dine) -
histamine is released by ECL cells of the stomach and stimulates parietal cell release of HCl
2. Proton Pump Inhibitors- i.e. omeprazole- must take before meal because proton pumps are only induced by presence of food
3. antacids- tums
normal epithelium of the esophagus?
squamous cell epithelium
2 types of hiatal hernias
1. sliding hiatal hernia- GE jxn slides back and forth through diaphragm hiatus (20% of people have it- normally asx, but can get GERD)
2. paraesophageal hernia- cardia, part of stomach herniates through the diaphragmatic hiatus but the GE jxn remains below diaphragm
what radiological test exposes patient to the most radiation and thus should be avoided in pregnant women?
CT
what do the gastric chief cells secrete?
pepsinogen and gastric lipase
What activates trypsinogen so that it can become trypsin and activate all other pancreatic enzymes?
enteropeptidase on the brush border of the duodenum
what is the most common benign liver lesion?
at risk for?
tx?
cavernous hemangioma
at risk for rupture: hemoperitoneum
tx: none, do not biopsy
focal nodular hyperplasia
related to?
characteristic histo lesion?
benign liver lesion
related to congenital malformation of portal vein branches that leads to increased hepatic artery flow-- arterial enhancement with quick venous washout
histo: central fibrous scar
what liver lesion are females on contraceptives at risk for?
why are these risky?
functioning hepatocytes?
histo characteristic?
tx?
adenoma (estrogen dependent)
risk: they can rupture--> hemoperitoneum (especially during pregnancy)
hepatocytes are non-functional
histo characteristic: naked/unaccompanied arteriole
tx: stop birth control and resect tumor as it may transform into HCC
common benign liver lesion that may be related to ADPKD
appearance on CT?
tx?
liver cysts
round fluid filled cysts
tx: nothing
what is the most common cause of hepatocellular carcinoma worldwide?
chronic hepatitis B infection (especially if maternally transmitted)
Risk factors for HCC?
cirrhosis (alcohol, chronic hep b or c)
hemochromatosis)
presentation of HCC?
right upper quadrant pain, may refer to right shoulder, weight loss, decompensation of liver disease
malignancy symptoms?
fatigue, unintended weightloss, night sweats, low grade fever, anorexia ,diarrhea
What cancers are likely to metastasize to the liver?
Cancers Sometimes Penetrate Benign Livers
Colon > Stomach > Pancreas > Breast > Lung
lactulose is used to treat? mechanism?
hepatic encephalopathy
mech: undigestable--causes diarrhea and traps nitrogen as NH4+ (must be excreted since it is charged and cannot be absorbed)
rifaxamine
used to tx?
travelers diarrhea and hepatic encephalopathy
mech: kills colonic bacteria that produce nitrogenous wastes
mechanism of ascites?
loss of albumin
decreased ECV- revs up RAAS
drugs to treat portal HTN
octreotide- blocks splanchnic vasodilation
non-specific Beta blockers- blocks vasodilation of the gut (propanolol, nadolol)
side effect of ribavirin?
hemolytic anemia
what is the goal of HBV treatment?
decreased HBV DNA and HBV Surface Antigen
what is used to treat HBV?
pegylated interferon and lamuvidine (nucleoside analogue--reverse transcriptase inhibitor)
what is unique about HBV? (the type of virus it is)
DNA virus that uses an RNA intermediate to replicate (needs a reverse transcriptase)
what is the goal of HCV treatment?
eradication of the virus
markers of cholestasis?
ALP- alkaline phosphatase-- also elevated with bone resorption
GGT- gamma glutamyl transpeptidase
manifestations of cholestasis?
jaundice, pruritis, steatorrhea, vitamin D, A, K, E deficiency
primary biliary cirrhosis
who is most often affected?
lab test?
affected: middle aged women
lab test: anti-mitochondrial antibodies
primary sclerosing cholangitis
associated with?
appearance on ERCP?
associated with ulcerative colitis
ERCP: alternating strictures and dilations
large gallstones are most likely to cause what?
cholecystitis
double duct sign is clue for?
pancreatic cancer in head of pancreas- obstructing pancreatic duct and common bile duct
what causes secondary biliary cirrhosis?
in kids?
prolonged obstruction of extrahepatic ducts
kids-- biliary atresia
what can you give reduce jaundice in person with Criggler-Najjar Type II? why?
phenobarbital-- induces UGT1A1-- conjugated bilirubin
Extraintestinal manifestations of Inflammatory Bowel Disease
CHEATS-
cholangitis (UC > CD)
Hematologic- iron deficiency anemia- malabsorption (CD > UC)
Eyes- uveitis--
A- artheritis + ankylosing spondylitis
T
Skin- erythema nodosum (CD) and pyoderma gangrenosum (UC)
hartnup disease
decreased absorption of tryptophan- decreased hepaticc synthesis of niacin (vit B3) from tryptophan--> pellagra
mechanism of methotrexate?
inhibits DNA synthesis by disrupting folate metabolism- must give folate supplement
what is the hallmark histologic feature of primary sclerosing cholangitis?
onion-skinning-- fibrosis around the bile ducts- but still have nice cuboidal epithelium
patients with PSC are at increased risk for?
cholangiocarcinoma and Colorectal carcinoma
histology of primary biliary cirrhosis?
squished bile ducts with abnormal epithelium and vague granulomas (inflammatory infiltrates)
what is the best test for cholelithiasis?
ultrasound
pseudocyst
pancreatic cyst filled with pancreatic juices after acute pancreatitis- no epithelial lining
murphy's sign
have pt breathe in- palpate liver- if they have cholecystitis they will stop breathing in when the liver edge hits your hand because it hurts so bad
If a stone is lodged in the cystic duct, will you see jaundice?
No- the stone is not blocking passage of bile from the liver so bilirubin is still being excrete in the bile
gallstone ileus
gallstone erodes through the gallbladder into the duodenum and causes obstruction- usually at the ileocecal valve
ascending cholangitis
stone in the common bile duct causes infection
what size stones are most likely to cause acute pancreatitis?
small stones because they are able to make their way through the cystic duct into the common bile duct and obstruct outflow of pancreatic enzymes/juices
risk factors for gallstones?
four F's
Fat
Female
Forty
Fertile
2 types of gallstones? which is most common?
cholesterol and pigmented
most common = cholesterol
overall most common is mixed
what are pigmented stones made out of?
two types of pigmented gallstones? where are each formed? what are they associated with?
calcium and unconjugated bilirubin
black pigmented- formed in gall bladder- hemolysis
brown stone- formed outside of the gall bladder due to infection
what does bacteria do to bilirubin
unconjugates it
courvosier's sign
palpable gall bladder with painless jaundice-- usually do pancreatic malignancy obstructing the common bile duct
porcelain gallbladder
what is it? what does it increase risk for?
calcification of the gallbladder that increases risk of developing gallbladder adenocarcinoma
kernicterus
unconjugated bilirubin is fat soluble and can cross the BBB leading to mental status changes
risk factors for cholangiocarcinoma
blockage, primary sclerosing cholangitis, chronic infection
klatskin tumor
cholangiocarcinoma arising from the confluence of the hepatic ducts- will not see gallbladder dilation since it is upstream from gallbladder
what is the difference between small bowel and colonic mesenteric ischemia?
small bowel- usually from embolus in the background of atherosclerotic disease-- develops suddenly, pain with eating (intestinal angina), occult bleeding (obvious bleeding is late- bad sign- necrosis), periumbilical pain, do angiography
colonic ischemia- usually in older people, atherosclerosis or unknown mechanism, obvious blood in stool, non-painful or suprapubic pain, often in watershed regions, do colonoscopy to look for source
where do emboli get lodged in mesenteric ischemia?
distal superior mesenteric artery (angle and diameter)
how do drugs cause ischemic colitis? what drugs do this?
vasospasm
drugs: triptans (for migraines), cocaine (blocks reuptake of NE), pseudoephedrine (a 1 agonist), birth control
Describe HCO3- secretion from the ductular cells of the pancreas.
what stimulates it?
What drives it?
Cl- is pumped out through CFTR and this creates gradient for it to be pumped back in in exchange for HCO3-
Describe cystic fibrosis in the context of the GI tract/pancreas etc.
CFTR channels are defective so Cl- cannot be pumped out into the lumen creating a gradient for an antiporter whereby Cl- is reabsorbed and HCO3- is pumped out with water and Na+ following. There is plugging of the pancreatic ducts leading to pancreatic insufficiency-- acinar cells are working but enzymes are not making it into the duodenum.
what stimulates release of secretin?
where is it released from?
gastric acid stimulates release
released from S cells of duodenum
how long is the small bowel?
how long is the large bowel?
small bowel: 20 ft- 6m
large bowel: 5 ft- 1.5 m
What are paneth cells? where are they located?
cells with eosinophilic granules contain lysosyme- contribute to host defense
describe the vascular supply of the rectum. why is this relevant for cancer mets?
the upper rectum is supplied by the IMA and drained by the IMV so mets from this part of the rectum will go to the liver through portal circulation.
the lower rectum is supplied by the inferior rectal artery off of the internal iliac artery and drained by iliac vein into the IVC so mets will go through heart to lungs
What is the major stimulatory neurotransmitter of the GI tract?
inhibitory neurotransmitters?
stimulate: ACh (contraction)
inhibit: Vasoactive Intestinal Peptide, NO (relaxation)
what is contracted and what is relaxed during flatulence?
pooping?
flatulence: internal and external anal sphincters relax, puberectalis contracts
pooping: internal, external anal sphincters and puborectalis muscle all relax
what are essential fatty acids?
must be obtained from diet- linolenic and linoleic acid
what are micelles necessary for?
what is required to make micelles?
digestion of cholesterol, fat soluble vitamins (D, A, K, E) and some LCFA
required: bile salts
what creates greater fat malabsorption and subsequent steatorrhea, lack of pancreatic lipase? lack of bile salts?
lack of pancreatic lipase-- only can digest 30% of fats
with no bile salts-- can still digest 60% of fats
discuss the differences in fat absorption for SCFA and MCFA vs LCFA, cholesterol and fat soluble vitamins
SCFA and MFCA- portal venous sx
others: emulsion droplet--> micelles--> absorption-->re-esterification--> packaging with apoproteins to make chylomicrons--> lymphatics--> venous circ via thoracic duct into subclavian
what electrolytes are involved in absorption?
secretion?
absorption: water follows Na+ IN
secretion: water follows Cl- out
how does cholera toxin work?
stimulates Cl- secretion from CFTR, water follows--> secretory diarrhea
what is the normal osmolality of stool?
290mOsm/kg water
how do you calculate the stool osmotic gap?
if gap is high what does this mean?
290 - (Na+ + K+) x 2

high gap (>50)-- there are ions that are unaccounted for (like lactose, polyethylene glycol, sorbitol) causing water to be drawn into lumen
what kind of diarrhea do bile acids cause?
secretory- they are an irritant-- do not draw water in (not an ion)
which requires further digestion in cells: proteins or monosaccharides?
proteins
what breaks down disaccharides?
brush border enzymes- isomaltase (can break 1,6 glycosidic bond, which amylase cannot),
lactase, etc
hydrogen breath test
test for lactose intolerance-- if cannot digest lactose it gets to the colon and the bacteria ferment it producing H+ and CO2 gas
which enzyme is not affected by celiac sprue/blunting of brush border?
amylase-- secreted in its active form- does not need to be activated by trypsin which requires enteropeptidase
risk factors for esophageal cancers
Achalasia
Barrett's
Cigarettes
Diverticula (Zenker's)
Esophagitis, Esophageal webs (Plummer Vinson Syndrome)
Familial
bethanecol
ACh analogue- prokinetic
resists breakdown by AChesterase
SE: cholinergic: SLUDGE
metochlopramide
anti-emetic and prokinetic
dopamine receptor antagonist and ACh agonist
SE: extrapyramidal tardive dyskinesia, dystonia
prochloperazine, chlorpromazine
dopamine antagonists
what kind of receptors are located in the Chemoreceptor trigger zone of the area postrema? what is significant about this area?
histamine, dopamine, serotonin, opiod

this area is responsible for vomitting in response to toxins in the blood-- lacks BBB
ondansetron
anti-emetic
serotonin antagonist
good for chemo, pregnancy and post op
benadryl, diphenhidramine
anti-histamine (H1)- anti-emetic good for motion sickness
SE: anti-cholinergic- mad, red, blind, dry
scopolamine
muscarinic antagonist-- use to treat SLUDGE and good for motion sickness
glucagon
inhibits smooth muscle contraction- used to relax GI tract before endo
erosions vs ulcers
erosions are more shallow
ulcers penetrate the muscularis mucosa
protective factors for the stomach
mucous, HCO3-, prostaglandins, blood flow, cell turnover
damaging factors to the stomach
smoking, NSAIDS, alcohol, H. pylori, acid
misoprostol
SE:
prostoglandin analogue used to induce mucous cells to produce mucus, bicarb and phospholipid--protection against ulcers
ALSO decreases acid production
SE: induces uterine contractions and closes PDA- do not give to pregnant women
sucralfate
bind to ulcer surface--> physical protection
use: traveler's diarrhea, ulcers
bismuth
bind to ulcer surface-- physical protection against stomach acid
use: traveler's diarrhea, gastric ulcers
triple therapy for H. Pylori infection
Please MAke Tummy Better
PPI, Metronidazole, amoxicillin or tetracycline, Bismuth
H. pylori
gram, motility, associated conditions?
where does it take up residence>?
what does it produce?
how can it be tested?
gram negative, spiral shaped, flagella (crawls under mucous layer of stomach)
can cause chronic gastritis, increased risk of gastric cancer, gastric and duodenal ulcers
prevalence is 50%
reside: in stomach- can only survive on gastric mucosa
produces urease: breaks down urea to ammonia-- base that is protective against stomach acid
test: urease breath test- radiolabeled urea is given, if bacteria present they break it down to ammonia and CO2 which is exhaled (labeled), also stool Ag, serology
H. pylori can affect antrum or body of stomach- how does it differ in terms of acid production?
antrum- destroys D cells that make somatostatin-- less inhibition of gastrin and parietal cells- more acid
body- destroys parietal cells- less acid
risk factors for gastric adenocarcinoma
where does it occur?
nitrosamines, nitrates (smoked foods), achlorhydria, H. pylori
antrum of the stomach (usually from intestinal metaplasia)
B cell lymphoma or T Cell lymphoma- which is related to celiacs, which to H pylori
b cell MALT- h pylori
t cell MALT- celiac
high gastrin levels, but low gastric acid
(may be seen with hashimoto's thyroiditis etc)
autoimmune gastritis
acute necrotizing colitis of premature, low birth weight babies-- affects the terminal ileum and ascending colon
necrotizing entercolitis
GI ulcer related to head trauma
Cushing's ulcer (need to cushion the brain)
GI ulcer related to burns
curling's ulcer (curling irons burn you)
Boerhaave's syndrome
complete esophageal rupture
differential for microcytic anemia
TAILS: thalassemia
Anemia of Chronic Disease
Iron Deficiency
Lead poisoning
Sideoblastic anemia- cannot incorporate iron into Hb
Antacids
Calcium, Mg, Al
mech?
SE?
increases pH, binds pepsin,
Ca- kidney stones, rebound high acidity
Mg- diarrhea- Must go to bathroom
Aluminum- a minimum amount of poop
H2 blockers
-tidine
cimetidine etc
PPIs
-prazoles
must be taken before meals because the K+/H+ ATPase pump is only present when parietal cells are stimulated
test for carbohydrate malabsorption
fecal pH- if carbs are not absorbed they are fermented by colonic bacteria producing acid- lower pH
hydrogen breath test- radiolabeled - fermentation- gets into blood-breathed out
if you find alpha-1-antitrypsin in the stool, what other protein may be there too?
albumin
fetal duodenal atresia can cause what during pregnancy? after birth?
during pregnancy- polyhydramnios- fetus cannot swallow amniotic fluid so it spits it out- increased levels of fluid
after birth- repeated vomitting
gastric inhibitory peptide.
released from?
function?
K cells of the duodedum
delays gastric emptying by closing the pyloric sphincter, decreases release of gastrin
tropical sprue
where found?
what deficiency associated?
tx?
where: SE Asia
deficiency: vitamin b12 and folate
tx: tetracycline
causes of macrocytic anemia
vitamin B12, folate deficiency, lack of intrinsic factor
how do intestinal bacteria relate to
vitamin K, folate, vitamin B12, and bile salts?
bacteria synthesize vitamin K and folate- decreased PT with bacterial overgrowth
digest vitamin B12
and deconjugate bile salts
whipples disease
presentation?
histology?
males (8:1), arthralgia, weight loss, diarrhea, abdominal pain, lymphadenopathy
histo: PAS positive macrophages(containing bacteria) in lamina propria
what gene is associated with spontaneous CRC?
APC gene
difference between adenoma and adenocarcinoma
adenocarcinoma- invasion into or beyond muscularis mucosa
what determines prognosis of stomach cancer?
depth of invasion
What is FAP? inheritance pattern?
what gene is associated?
what is risk of CRC?
What other cancers are associated?
Familial Adenomatous Polyposis
Autosomal Dominant
APC gene
100% risk of CRC
duodenal, thyroid
What are FAP variants?
Gardner's syndrome- FAP with
Sebaceous cysts
Osteomas
Dentition abnormalities
Desmoid tumors

Turcott- Turban-- FAP with brain cancers/CNS tumors
hyperplastic colon polyps
incidence, tx, histo?
most common benign polyps in the colon
incidence: 50% of people over 60 have them
tx: must remove for potential malignant transformation
histo: star shaped pattern
HNPCC most commonly presents in which part of the colon?
R> L
cowden's syndrome
inheritance pattern?
where on body?
other cancers?
autosomal dominant
hamartomas on skin (may appear like acne) and in GI tract
other cancers: thyroid and breast
diverticulosis complications
diverticulitis- inflammation/blockage
diverticular bleeding (not associated with diverticulitis)
complications of diverticulitis
abscess, fistula, obstruction, perforation
always operate when pt can
treatment for acute diverticulitis- then later?
bowel rest then high fiber diet
what can be given for pain related to pancreatitis?
uncoated pancreatic enzymes + acid suppression- active in the duodenum and break down CCK-RP--not as much CCK stimulus of exocrine pancreas
what can be given for malabsorption related to pancreatitis?
pancreatic enzymes either uncoated or coated
treatment of acute pancreatitis
fluids, fluids, fluids for third spacing
octreotide
chronic vs acute colitis
edema, crypts, metaplasia?
acute- edema, straight crypts, no metaplasia, PMNs in lamina propria
chronic colitis- no edema, distorted crypts, metaplasia, lymphocytes in crypts
microscopic colitis
colonoscopy?
presentation?
types? distinguishing features?
associations
scope: appears normal
presentation: watery diarrhea
types: lymphocytic (intraepithelial lymphocytes), collagenous (mallory trichome stain, subepithelial collagen band)
associations: NSAIDs, PPIs, SSRI
acute systemic complications of pancreatitis
ARDS/SIRS
shock
renal failure
DIC
most common cause of acute and chronic pancreatitis?
alcohol
how might chronic alcoholism lead to pancreatitis?
concretions develop in ducts that lead to partial obstruction
new onset diabetes in someone > 50
palpable gallbladder and painless jaundice
pancreatic cancer
tumor marker elevated in pancreatic cancer
CA19-9
treatment of diverticulitis
2 ABx: metronidazole and ciprofloxacin

bowel rest in short term