GI Flashcards
ursodiol MOA
Nontoxic bile acid. Increases bile secretion + decreases cholesterol secretion and absorption.
ursodiol clinical use
PBC + gallstone prevention or dissolution.
Orlistat MOA
inhibits gastric and pancreatic lipase, thus leading to decreased breakdown and absorption of dietary fats.
Orlistat AE’s
steatorrhea + decreased absorption of fat-soluble vitamins.
metoclopramide MOA
D2 receptor antagonist. Increases resting tone, contractility, LES tone, motility. Does not influence colon transport time.
metoclopramide clinical use
diabetic and postsurgery gastroparesis, antiemetic
metoclopramide contraindications
digoxin + diabetic agents + SBO or Parkinson disease (due to D2 receptor blockade)
metoclopramide AE’s
parkinsonian effects, tardive dyskinesia, restlessness, drowsiness, fatigue, depression, diarhea.
ondansetron MOA
serotonin antagonist + decreases vagal stimulation
ondansetron AE’s
headache + constipation + QT interval prolongation
Loperamide MOA
agonist at mu-opioid receptors; slows gut motility. Poor CNS penetration (low addictive potential)
loperamide AE’s
constipation + nausea
Sulfasalazine – MOA, clinical use, SE’s
Sally Westcott in a sulfur geiser/sulfasalazine. Pyramid with sulfur geiser on top on right + tree with bark and hailing on it/MOA = combination of sulfapyridine (antibacterial) + 5-aminosalicylic acid (anti-inflammatory). Bacteria on counter throwing lasso around her/activated by colonic bacteria. Rachel in wheelchair next to counter/can cause drug-induced lupus. Riding a dead sperm/toxicity = malaise + nausea + sulfonamide toxicity + reversible oligospermia. /clinical use = UC + Crohn disease.
lactulose
osmotic laxative
osmotic laxatives AE’s
diarrhea, dehydration.
octreotide MOA
long-acting somatostatin analog; inhibits secretion of various splanchnic vasodilatory hormones.
Octreotide AE’s
nausea, cramps, steatorrhea + increased rick of cholethiasis due to CCK inhibition.
misoprostol MOA
PGE1 analog. increased production and secretion of gastric mucous barrier, decreases acid production.
misoprostol mechanism as abortifacent
Ripens cervix
Other use of misoprostol.
Maintains PDA.
misoprostol AE’s
diarrhea
bismuth, sucralfate MOA
binds to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer.
another use for bismuth, sucralfate
travelers’ diarrhea.
shared AE of all antacids
hypokalemia
aluminum hydroxide AE’s
constipation + hypophosphatemia + proximal muscle weakness + osteodystrophy + seizures
calcium carbonate AE’s
hypercalcemia (milk-alkali syndrome) + rebound acid production
magnesium hydroxide AE’s
Harvey milk (sean penn) from movie milk in middle of room giving magnus who’s benchpressing a blowjob: he’s shitting on a towel + IV pole next to him + is being shocked + riding a mini motorcycle/SE’s = diarrhea + hyporeflexia + hypotension + cardiac arrest.
What is a proton pump?
H+/K+ ATPase in stomach parietal cells.
ZES treatment
PPI
PPI AE’s
Nate is banging Heidi on the table + magnus strong man on the table + carson with his ski gear at other end of table/SE’s = increased risk of C. diff infection + decreased serum Mg2+ with long-term use + atrophic gastritis + carcinoid tumors + headaches + GI disturbances. Rest of seats filled with skeletons/associated with osteoporosis and osteoporotic hip fractures (decreases calcium absorption;calcium carbonate requires an acidic environment for proper absorption).
H2 blocker MOA
reversible block of histamine H2 receptors –> decreased H+ secretion by parietal cells.
H2 Blocker AE’s
- Cimetidine is the primary concern. Others are relatively free of these effects.
- CYP450 inhibitor + antiandrogen effects + can cross BBB (confusion, dizziness, headaches) and placenta + decreases renal excretion of creatinine.
ranitidine AE
Decreases renal excretion of creatinine.
Foregut region
pharynx t oduodenum
midgut region
duodenum to proximal 2/3 of transverse colon.
hindgut region
distal 1/3 of transverse colon to anal canal above pectinate line.
Midgut development
6th week–physiologic midgut herniates through umbilical ring.
10th week–returns to abdominal cavity + rotates around SMA, total 270 counterclockwise.
Defect in rostral fold closure
Sternal defects
Defect in lateral fold closure
Omphalocele, gastroschisis
defect in caudal fold closure leads to…
bladder exstrophy
gastroschisis
extrusion of abdominal contents through abdominal folds (typically right of umbilicus); not covered by peritoneum.
Most common tracheoesophageal anomalies
esophageal atresia with distal tracheoesophageal fistula (85%)
why does cyanosis occur with esophageal atresia?
Secondary to laryngospasm (to avoid reflux-related aspiration).
H-type esophageal atresia
Pure TEF. see FA
jejunal and ileal atresia pathophys
disruption of mesenteric vessels –> ischemic necrosis –> segmental resoprtion.
characteristic sign of jejunal and ileal atresia.
Bowel discontinuity or “apple peel.”
epidemiology of hypertrophic pyloric stenosis
Most common cause of gastric outlet obstruction (1:600).
hypertrophic pyloric stenosis RF
Exposure to macrolides.
hypertrophic pyloric stenosis acid/base disturbance
hypokalemic hypochloremic metabolic alkalosis (vomiting of gastric acid and subsequent volume contraction).
pancreas embryology
Derived from foregut. Ventral pancreatic buds contribute to uncinate process and main pancreatic duct. Dorsal pancreatic bud alone becomes body, tail, isthmus, and accessory pancreatic duct. Both ventral and dorsal buds contribut to pancreatic head.
annular pancreas
ventral pancreatic bud abnormally encircles 2nd part of duodenum; forming ring of pancreatic tissue that may cause dudoenal narrowing and *nonbilious vomiting.
Pancreas divisum and timeframe
Ventral and dorsal parts fail to fuse at 8 weeks. Common and mostly asymptomatic, but may cause chronic abdominal pain and/or pancreatitis.
pancreas anatomy
codebook
SADPUCKER notes
Aorta AND IVC
2nd-4th parts of duodenum
Pancreas (except tail)
Esophagus (thoracic portion)
falciform connects
Liver to anterior abdominal wall
falciform contains
ligamentum teres hepatis
ligamentum teres hepatis derived from…
fetal umbilical vein
falciform derivative of…
ventral mesentery
hepatoduodenal connects…
liver to duodenum
hepatoduodenal
portal triad
pringle maneuver
Compressing hepatoduodenal ligament between thumb and index finger in omental foramen to control bleeding.
hepatoduodenal borders the…
omental foramen
omental foramen connnects
The greater and lesser sacs.
gastrohepatic connects
liver to lesser curvature of stomach
gastrohepatic contains
- gastric arteries
- separates greater and lesser sacs on the right.
what do you need to cut to access the lesser sac?
gastrohepatic ligament
gastrocolic connects… forms..
- greater curvature and transverse colon.
- part of greater omentum.
gastrocolic contains
gastroepiploic arteries
What separates greater and lesser sacs on the left?
gastrosplenic
gastrosplenic connects…forms…
- greater curvature and spleen
- part of greater omentum
gastrosplenic contains
short gastrics, left gastroepiploic
splenorenal connects….
Spleen to posterior abdominal wall.
Splenorenal contains
splenic artery and vein + tail of pancreas
Layers of gut wall
inside to outside -- MSMS Mucosa Submucosa Muscularis externa Serosa
Mucosa contains…
epithelium, lamina propria, muscularis mucosa.
submucosa includes…function..
- Submucosal nerve plexus (Meissner).
- Secretes fluid.
Muscularis externa includes…
Myenteric nerve plexus (Auerbach)
serosa caveat
Called serosa when intraperitoneal, adventitia when retroperitoneal.
erosions vs. ulcers
Ulcers can extend into submucosa, inner or outer muscular layer. Erosions are confined to mucosa.
Stomach basal rhythm
3 waves/min
Duodenum basal rhythm
12 waves/min
Ileum basal rhythm
8-9 waves/min
Muscularis composition
Inner circular layer, myenteric nerve plexus (Auerbach), outer longitudinal layer
Brunner glands
HCO3- secreting cells of submucosa.
Duodenum contains
Brunner glands + cytps of Lieberkuhn + villi and microvilli
histology of jejunum
Plicae circularis and crypts of Lieberkuhn.
Peyer patches
Lymphoid aggregates in lamina propria, submucosa.
Where are peyer patches?
Ileum
Ileum histology
peyer patches + plicae circulares + crypts of lieberkuhn.
Where are the largest number of goblet cells in the small intestine?
Ileum
Colon histology
Crypts of Lieberkuhn but no villi; abundant goblet cells.
abdominal aorta branches rule
Arteries supplying GI structures branch anteriorly. Arteries supplying non-GI structures branch laterally and posteriorly.
Middle suprarenal anatomic location.
T12
celiac trunk anatomic location.
T12
Fist lumbar anatomic location
L1
Renal anatomic location
L1
SMA anatomic location
L1
Gonadal anatomic location
Just above L2
IMA anatomic location
L3
Bifurcation of abdominal anatomic location
L4 (biFOURcation)
Common iliacs anatomic location
L5
SMA artery syndrome
1) presentation
2) anatomy
3) scenario
1) Intermittent intestinal obstruction symptoms (primarily postprandial pain)
2) Transverse (3rd) portion of duodenum is compressed between SMA and aorta.
3) Conditions associated with diminished mesenteric fat (eg, low body weight/malnutrition).
Foregut
1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied
1) Celiac
2) Vagus
3) T12/L1
4) Pharynx (vagus nerve only) and lower esophagus (celiac artery only) to proximal duodenum; liver, gallbladder, pancreas, spleen (mesoderm)
Midgut
1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied
1) SMA
2) vagus
3) L1
4) distal duodenum to proximal 2/3 of transverse colon
Hindgut
1) arterial supply
2) PS innervation
3) vertebral level
4) structures supplied
1) IMA
2) Pelvic
3) L3
4) distal 1/3 transverse colon to upper portion of rectum.
TIPS procedure
Transjugular intrahepatic portosystemic shunt (TIPS). Creates a shunt between portal vein and hepatic vein, thus relieving portal HTN by shunting blood to the systemic circulation, bypassing the liver.
Varices seen with portal hypertension
(gut, butt, and caput (medusa) –> esophageal, rectal (anorectal varices), caput medusa
portosystemic rectal anastomosis
superior rectal with middle and inferior rectal.
caput medusae anastomosis
Paraumbilical with small epigastric veins of the anterior abdominal wall.
esophageal varices anastomosis
left gastric with azygos
pectinate (dentate) line
Formed where endoderm (hindgut) meets ectoderm.
Venous drainage above pecinate line
Superior rectal vein –> ifnerior mesenteric –> portal system
lymphatic drainage above pectinate line
internal iliac lymph nodes
venous drainage below pectinate line
inferior rectal vein –> internal pudendal vein –> internal iliac vein –> common iliac vein –> IVC
lymphatic drainage below pectinate line
Superficial inguinal nodes.
Anal fissure RF’s
low fiber diet + constipation.
Kupffer cells
Specialized macrophages that form the lining of sinusoids
Hepatic stellate (Ito) cells 1) location 2) function
1) space of Disse
2) store vitamin A (when quiescent), produce ECM when activated.
intermediate zone, pericentral vein (centrilobular) zone, intermediate zone
Zone 1 = periportal zone
Zone 2 = intermediate zone
Zone 3 = pericentral vein (centrilobular) zone
Site of alcoholic hepatitis
Zone III
yellow fever affects…
zone II
ingested toxins (eg cocaine) affect….
Zone I
zone affected 1st by ischemia
Zone III (farthest from arterial supply)
zone affected 1st by viral hepatitis
Zone I
ampulla of vater and 2) clinical significance
1) little widened space behind sphincter of oddi in head of pancreas (FA 347)
2) gallstones that lodge here an block both the common bile and pancreatic ducts causing “double duct sign” –> both cholangitis and pancreatitis.
cystic duct
Duct that drains gallbladder
painless juandice
pancreatic adenocarcinoma (usually ductal) in head of pancreas that causes of obstruction of common bile duct.
femoral region organization
NAVeL –> nerve, artery, vein, lymphatics
femoral triangle
contains femoral nerve, artery, vein
femoral sheath
fascial tube 3-4 cm below inguinal ligament. Contains femoral vein, artery, and canal (deep inguinal lymph nodes) but NOT femoral nerve.
femoral triangle borders
- superiorly by inguinal ligament.
- medially by medial border of adductor longus.
- laterally by medial border of sartorius muscle.
superficial inguinal ring
External obie standing in the middle of a golden ring/formed by opening in the external oblique muscle aponeurosis.
Deep inguinal ring
• Code: hole down to china beneath trannies/opening in the transversalis fascia.
Layers of inguinal canal
Obie Spear on outside, closer to bank with stomach covered in big sperm/external spermatic fascia derived from external oblique. Obie hanging from inside pulling testicles up with a rope/cremasteric muscle and fascia derived from internal oblique. Line of trannies with sperm that have buried into their stomachs/internal spermatic fascia derived from transversalis fascia.
Site of protrusion of direct hernia
abdominal wall
Site of protrusion of indirect hernia
deep inguinal ring
conjoined tendon
formed by transversus abdominis muscle + internal oblique muscle
umbilical hernia defect location
defect at linea alba
incarceration
hernia that can’t be reduced.
strangulation
hernia that becomes ischemic and necrotic
presentation of complicated hernias
tenderness, erythema, fever.
structure defective in congenital diaphragmatic hernia and usual location
- pleuroperitoneal membrane.
- left side (no liver for protection)
Site of protrusion of direct inguinal hernia
Hesselbach triangle. Bulges directly through abdominal wall.
Other details of direct inguinal hernia
- goes through external (superficial) inguinal ring only.
- covered by external spermatic fascia.
- usually in older men.
Femoral hernia epidemiology
usually females.
femoral hernia protrusion
Below inguinal ligament through femoral canal below and lateral to pubic tubercle.
caveat about femoral hernias
More likely to incarcerate or strangulate.
Inguinal (hesselbach) triangle
Inferior epigastric vessels, lateral border of rectus abdominis, inguinal ligament
Gastrin source and location
G cells (**antrum of stomach, duodenum)
gastrin action
increases gastric H+ secretion, growth of gastric mucosa, gastric motility.
gastrin 1) increased by 2) decreased by
1) stomach distention/alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP)
2) ph
what increases gastrin production?
chronic PPI use, chronic atrophic gastritis (H pylori), ZES
Somatostatin source
D cells (pancreatic islets, Gi mucosa)
somatostain actions
decreases gastric acid and pepsinogen secretion + pancreatic and small intestine fluid secretion + gallbladder contraction + insulin and glucagon release
somatostain regulation
increased by acid, decreased by vagal stimulation.
CCK source
I cells (duodenum, jejunum)
CCK action
Increases pancreatic secretion + gallbladder contraction. Decreases gastric emptying. Increases sphincter of oddi relxation.
CCK regulation
Increased by fatty acids, amino acids.
How does CCK cause pancreatic secretion
Acts on neural muscarinic pathways.
Secretin source
S cells (duodenum)
Secretin actions
Increases pancreatic HCO3- secretion + bile secretion. Decreases gastric acid secretion. Functions to neutralize gastric acid in duodenum, allowing pancreatic enzymes to function.
Secretin regulation
Increased by acid, fatty acids in lumen of duodenum.
glucose-dependent insulinotropic peptide
another name for GIP.
GIP source
K cells (duodenum, jejunum)
GIP functions
Exocrine: decreases gastric H+ secretion.
Endocrine: increases insulin release.
GIP regulation
Increased by fatty acids, amino acids, oral glucose.
Why does oral glucose lead to increased insulin compared to IV
GIP secretion.
drug that that acts as a motilin receptor agonist
erythromycin
VIP source
PS ganglia in sphincters, gallbladder, small intestine
VIP functions
Increases intestinal water and electrolyte secretion + increases relaxation of intestinal smooth muscle and sphincters.
VIP regulation
Increased by distention and vagal stimulation, decreased by adrenergic input.
Why is there increased LEs tone in achalasia?
Loss of NO secretion.
Ghrelin source
stomach
Ghrelin clinical relevance
Increased in Prader-Willi, decreased after gastric bypass surgery.
gastric acid positive regulators
histamine, ACh, gastrin
gastric acid negative regulation
somatostatin, GIP, prostaglandin, secretin.
pepsin source and function
chief cells, protein digestion
Pepsin regulation
increased by vagal stimulation, local acid
Bicarbonate source
mucosal cells (stomach, duodenum, salivary glands, pancreas) brunner glands (duodenum)
where does bicarbonate sit?
Trapped in mucus that covers the gastric epithelium.
How does gastrin increase gastric acid secretion?
Indirectly through enterochromaffin-like cells (ECL cells) leading to histamine release rather than through its direct effect on parietal cells.
Pancreatic secretions tonicity + flow variance
1) isotonic
2) low flow –> high Cl-
high flow –> high HCO3-
alpha-amylase caveat
secreted in active form. Doesn’t need to be activated.
name some proteases
trypsin, chymotrypsin, elastase, carboxypeptidase.
How is trypsinogen converted to trypsin?
Enterokinase/enteropeptidase, a brush-border enzyme on duodenal and jejunal mucosa.
Glucose and galactose absorption
Taken up by SGLTI (Na+ dependent).
Fructose absorption
Facilitated diffusion by GLUT-5.
GLUT 2 function
transports all monosaccharides (glucose, galactose, and fructose) to blood.
Functon of D-xylose absorption test
Distinguishes GI mucosal damage from other causes of malabsorption.
B12 absorption caveat
absorbed with bile salts.
peyer patch and location
unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum.
Where do IgA-secreting plasma cells sit? What are they derived from
Lamina propria. Derived from B cells when stimulated in germinal centers.
Composition of bile salts
Bile acids conjugated to glycine or taurine, making them water soluble.
Composition of bile
Bile salts + phospholipids + cholesterol + bilirubin + water + ions.
Enzyme catalyzing rate-limiting step of bile acid synthesis.
Cholesterol 7alpha-hydroxylase.
Bile functions
1) Digestion and absorption of lipids and fat-soluble vitamins.
2) Cholesterol excretion (body’s only means of eliminating cholesterol)
3) Antimicrobial activity (via membrane disruption).
Bilirubin cycle
Heme is metabolized by heme oxygenase to biliverdin –> biliverdin reduced to bilirubin –> unconjugated bilirubin is removed from blood by liver, conjugated with glucuronate, and excreted in bile –> gut bacteria metabolize conjugated bilirubin to urobilinogen –> 80% of urobilinogen is excreted in feces as sercobilin (brown color of stool). 20% of urobilinogen remains in gut. Of that 20%, 10% goes to kidney and is excreted in urine as urobilin (giving urine yellow color) and 90% goes back through enterohepatic circulation to the liver.
Direct bilirubin
conjugated with glucuronic acid; water soluble.
Indirect bilirubin
Unconjugated; water insoluble.
Where does initial part of bilirubin cycle occur?
RBCS –> heme –> unconjugated bilirubin occurs in macrophages.
enzymes that conjugates bilirubin
UDP-glucuronosyl-transfease.
Benign/malignant pattern of salivary gland tumors.
Most commonly benign and in parotid gland. Tumors in smaller glands more likely malignant.
Typical presentation of salivary gland tumor
Painless mass/swelling.
What does facial pain or paralysis in a salivary gland mass suggest?
Malignant involvement of CN VII.
Most common salivary gland tumor
Pleomorphic adenoma
Pleomorphic adenoma characteristics and composition
Benign mixed tumor. Composed of chondromyxoid stroma and epithelium and recurs if incompletely excised or ruptured intraoperatively.
Most common malignant salivary gland tumor
mucoepidermoid carcinoma.
Another name for Warthin tumor
Papillary cystadenoma lymphomatosum.
Warthin tumor
Benign cystic tumor with germinal centers.
Causes of secondary achalasia
1) chagas disease 2) extraesophageal malignancies (mass effect or paraneoplastic)
Barium swallow finding of achalasia
birds break
achalasia characteristics
Failure of relaxation of LES due to loss of myenteric (Auerbach) plexus. High LES resting pressure and uncoordinated or absent peristalsis, leading to progressive dysphagia to solids and liquids.
Obstructive dysphagia presentation vs. achalasia
Obstructive dysphagia only occurs with solids, achalasia occurs with both liquids and solids.
Endoscopy findings in eosinophilic esophagitis
Esophageal rings and linear furrows.
patient presenting with GERD but unresponsive to GERD therapy consider…
eosinophilic esophagitis
Pathophys of food impaction in eosinophilic esophagitis
Food allergens –> dysphagia –> food impaction.
What causes esophageal strictures?
1) Caustic ingestion
2) Acid reflux
esophageal varices
dilated submucosal veins in lower 1/3 of esophagus secondary to portal HTN.
atypical but common presentation of GERD
cough + hoarseness (laryngopharyngeal reflux).
GERD association
asthma
Plummer-Vinson triad
dysphagia + iron deficiency anemia + esophageal webs
plummer vinson association
Glossitis
sclerodermal esophageal dystomility pathophys
esophageal smooth muscle atrophy –> decreased LES pressure and dysmotility –> acid reflux and dysphagia –> stricture, Barrett esophagus, and aspiration.
Barrett’s cancer association
ADENOCARCINOMA
more common esophageal cancer worldwide
squamous cell carcinoma
RF’s for esophageal adenocarcinoma
Chronic GERD, barrett’s, obesity, smoking, achalasia
part of esophagus affected in squamous vs. adeno
Upper 2/3 = SCC
Lower 1/3 = adeno
prostaglandin affected by NSAIDs
PGE2
Curling ulcers
Complications from severe burns. (burned by the curling iron)
Curling ulcer pathophys
hypovolemia –> mucosal ischemia.
Cushing ulcer
Ulcer resulting from brain injury (cushin the brain)
Cushing ulcer pathophys
Brain injury –> increased vagal stimulation –> increased ACh –> increased H+ production.
Chronic gastritis pathophys
Mucosal inflammation, leads to atrophy (hypochlorhydria –> hypergastrinemia) and intestinal metaplasia.
H pylori cancer association
MALT lymphoma
H pylori location
affects antrum first, then spreads to body of stomach.
autoimmune gastritis location of damage
body/fundus of stomach
menetrier benign/malignant?
precancerous
gastric cancer epidemiology
Gastric adenocarcinoma –> lymphoma –> GI stromal tumor –> carcinoid (rare).
Gastric cancer personality + presentation
Early aggressive local spread with node/liver metastases. Often presents late with weight loss + early satiety, acanthosis nigricans, leser-trelat.
Intestinal gastric cancer associations
H pylori, dietary nitrosamines (smoked foods), tobacco smoking, achlorhydria, chronic gastritis.
Intestinal gastric cancer location + what it looks like
Lesser curvature; looks like ulcer with raised margins.
Diffuse gastric cancer associations
NOT associated with H pylori. Signet ring cells; stomach wall grossly thickened and leathery (linitis plastica)
Krukenberg tumor histology
Abundnat mucin-secreting, signet ring cells.
Gastric ulcer pain vs. duodenal ulcer pain
Gastric, Greater with meals. Duodenal decreases with meals.
H pylori association with gastric or duodenal ulcers
Causes pretty much all duodenal ulcers and 70% of gastric ulcers.
Gastric ulcer management
Biopsy margins to rule out malignancy
Gastric ulcer benign/malignant?
Increased risk of carcinoma
Gastric ulcer mechanism
decreased mucosal protection against gastric acid.
Duodenal ulcer mechanism
decreased mucosal protection OR increased gastric acdi secretion
Other causes of duodenal ulcrs
ZES
duodenal ulcer – benign/malignant?
Usually benign.
Duodenal ulcer association
hypertrophy of brunner glands
duodenal area prone to hemorrhaging
posterior more common than anterior.
Most common complication of ulcers
hemorrhaging
Artery associated with ruptured gastric ulcer on lesser curvature of stomach
left gastric
Artery associated with hemorrhaging ulcer on posterior wall of duodenum
gastroduodenal
Potential ulcer complications
1) hemorrhaging
2) obstruction (pyloric channel, duodenal)
3) perforation.
Area of duodenum prone to perforation.
anterior>posterior.
Free air under diaphragm with referred pain to shoulder via phrenic nerve….
perforated duodenum from duodenal ulcers.
cancer and celiac’s?
moderately increased risk of T-cell lymphoma
histo findings in celiac’s
villous atrophy + crypt hyperplasia + **intraepithelial lymphocytosis.
area primarily affected by celiac’s
mucosal absorption decreased in distal duodenum and/or proximal jejunum.
Test for celiacs
1) serology for antibodies
2) d-xylose for malabsorption
d-xylose results
1) if blood and urine levels are decreased –> mucosal defect or bacterial overgrowth
2) if pancreatic insufficiency, then will be normal.
Material that accumulates in clear cell carcinoma
high in glycogen and lipids
lactose intolerance diagnosis + analyzing results
lactose hydrogen breath test. Positive for lactose malabsorption if postlactose breath hydrogen value rises > 20 ppm compared with baseline.
Thing to remember about pancreatic insufficiency
not only malabsorption of fat-soluble vitamins but also B12
Pancreatic insufficiency diagnosis
Decreased duodenal pH (bicarbonate) and fecal elastase.
region of intestine affected in tropical sprue
Duodenum + jejunum but can involve ileum.
anemia relationship to tropical sprue
due to folate deficiency, and, later, B12 deficiency.
ulcers in chrohn’s
linear ulcers
microscopic morphology in crohn’s
noncaseating granulomas + lymphoid aggregates.
Other complications of Crohn’s
1) enterovesical fistula, which can cause recurrent UTI and pneumaturia.
2) phlegmon/abscess
3) strictures (causing obstruction)
4) perianal disease.
5) kidney stones
6) gallstones
antibiotics for Crohn’s patients
Ciprofloxacin + metronidazole
UC gross morphology
1) Mucosal and submucosal inflammation only.
2) Friable mucosal pseudopolyps with freely hanging mesentery.
3) Loss of haustra –> “lead pipe” appearance on imaging
Complications of UC
1) Fulminant colitis
2) Toxic megacolon
3) Perforation
Primary sclerosing cholangitis lab finding
p-ANCA
UC treatment
5-aminosalicylic preparations (eg, mesalamine), 6-mercaptopurine, infliximab, colectomy.
IBS presentatoin
Recurrent abdominal pain associated with 2 of following
1) pain improves with defecation
2) change in stool frequency
3) change in appearance of stool.
- - can be diarrhea-predominant or constipation-predominant or mixed.
appendicitis pathophys
In adults –> obstruction by fecalith.
In kids –> lymphoid hyperplasia.
Test for appendicitis and location
- McBurney point
- 1/3 the distance from right anterior superior iliac spine to umbilicus.
Other signs in appendicits
Psoas, obturator, Rovsing signs. guarding and rebound tenderness on exam.
appendicitis differential
diverticulitis (elderly), ectopic, yersinia
Most common site of diverticulum
Sigmoid colon
What does “false” mean in relation to diverticulum?
Attenuated muscularis externa. Only mucosa and submucosa outpouch.
True diverticulum
all 3 gut wall layers, Meckels
Area prone to false diverticula
Where vasa recta perforate muscularis externa.
diverticulosis
Many false diverticula of the colon, commonly sigmoid.
epidemiology of diverticulosis
1/2 of people over age 60.
diverticulosis pathophys
Increased intraluminal pressure and focal weakness in colonic wall. Low-fiber diets.
Painless bleeding in a person with diverticulosis
Painless hematochezia. *not necessarily diverticulitis.
diverticulitis
Diverticulosis with inflamed microperforations.
Presentation of diverticulitis
LLQ pain + fever + leukocytosis.
Diverticulitis treatment
antibiotics
Complications of diverticulitis
1) abscess
2) fistula (colovesical fistula leading to pneumaturia)
3) obstruction (inflammatory stenosis)
4) perforation (leading to peritonitis)
If diverticulitis is complicated, management is…
Percutaneous drainage or surgery.
Where does mucosal tissue herniate in Zenker’s?
Killian triangle between thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor.
Meckel presentation
melena + RLQ pain.
Meckel complications
intussusception + volvulus + obstruction near terminal ileum.
omphalomesenteric cyst
Cystic dilation of vitelline duct. Not peristence of vitelline duct.
Six 2’s of Meckel’s
2x as likely in males 2 inches long 2 feet from ileocecal valve 2% of population presents in first 2 years of life 2 types of epithelia (gastric/pancreatic).
Hirschsprung etiology
Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner plexuses) in distal segment of colon.
Hirschprung genetic association
mutations in RET
Hirschsprung presentation
Bilious emesis + abdominal distention + failure to pass meconium within 48 hours –> chronic constipation.
Hirschsprung diagnosis
Rectal suction biopsy
Hirschsprung treatment
Resection
Positioning of bowel in malrotation
small intestine in ball in bottom right, large intestine on left side, ladd band between large intestine and liver.
Complications of malrotation
1) volvulus
2) duodenal obstruction
intussusception
PROXIMAL segment telescopes into distal segment.
viral infection and intussusception etiology
adenovirus –> peyer patch hypertrophy –> lead point.
Most common pathologic lead point
Meckel diverticulum.
Usual location of acute mesenteric ischemia
Embolic occlusion of SMA.
chronic mesenteric ischemia pathophys
“intestinal angina”: atherosclerosis of celiac, IMA, or SMA –> intestinal hypoperfusion –> postprandial epigastric pain –> food aversion and weight loss.
colonic ischemia presentation
crampy abdominal pain followed by hematochezia.
Watershed areas
splenic flexure, distal colon.
Most common locations of angiodysplasia
Cecum, terminal ileum, ascending colon.
Most common cause of SBO
adhesions
Adhesion presentation
Fibrous band of scar tissue. Can have well-demarcated necrotic zones.
Ileus
Intestinal hypomotility without obstruction –> constipation and decreased flatus; distended/tympanic abdomen with decreased bowel sounds.
Ileus causes
abdominal surgeries, opiates, hypokalemia, sepsis.
ileus treatment
Bowel rest, electrolyte correction, cholinergic drugs (stimulate intestinal motility).
necrotizing enterocolitis pathophys
formula fed premies –> immature immune system –> necrosis of intestinal mucosa (primarily colonic) with possible perforation, which can lead to pneumatosis intestinalis, free air in abdomen, portal venous gas.
What induces COX-2 production?
IL-2
Inguinal (hesselbach) triangle borders
Inferior epigastric vessels, lateral border of rectus. abdominis, inguinal ligament
hyperplastic polyp location and presentation
non-neoplastic and smaller. Rectosigmoid area.
hamartomatous polyps histology
growths of normal colonic tissue with distorted architecture.
adenomatous polyps + presentation
neoplastic, via chromosomal instability pathway. APC and KRAS mutations.
Usually asymptomatic; may present with occult bleeding.
serrated polyps
1) genetics
2) epidemiology
1) premalignant via CPG hypermethylation phenotype pathway with microsatelite instability and mutations in BRAF.
2) Up to 20% of cases of sporadic CRC.
2 hit hypothesis
You need to lose 2 tumor suppressor genes before getting cancer.
Gardner syndrome
FAP + osseus and soft tissue tumors + congenital hypertrophy of retinal pigment epithelium + impacted/supernumerary teeth.
Peutz Jeghers syndrome
o Coded character: Megan Yeiter. Emerging from jegher bag in basement with hyperpigmented mouth, lips, genitalia and covered in ham/syndrome featuring numerous hamartomas throughout GI tract. /presentation = hyperpigmented mouth/lips/hands/genitalia + bloody stool (due to intestinal hamartomas). Kenny sitting to her left + Mr. Kolkhorst sitting on a toilet behind her + tammy on her right + T with gut next to kenny/associated with increased risk of colorectal, breast, stomach, small bowel, and pancreatic cancers (but hamartomas themselves don’t undergo malignant transformation) + ovary/uterus/cervix/lung. Femdom chick whipping her from right /autosomal dominant. /pedunculated polyps. Intussuscepted bowel hanging over her from left/hamartomas can occasionally serve as the lead point for intussusception.
Peutz jeghers mutation
STK11/LKB1 gene.
Juvenile polyposis syndrome
1) presentation
2) prognosis
- AD syndrome in children less than 5 featuring numerous hamartomatous polyps in colon, stomach, small bowel.
- increased risk of CRC
Epidemiology of cancer progression in lynch syndrome + area of involvement
80% progress to CRC + proximal colon is always involved.
Cancers associated with Lynch syndrome
Associated with endometrial, ovarian, and skin cancers.
genetics of CRC
25% have a family history.
CRC RF’s
1) adenomatous and serrated polyps
2) familial cancer syndromes
3) IBD
4) tobacco use
5) diet of processed meat with low fiber.
Areas most commonly involved in CRC
Rectosigmoid>ascending>descending
Ascending mass in CRC presentation
exophytic mass + IDA + weight loss
descending mass in CRC presentation
Infiltrating mass, partial obstruction, colicky pain, hematochezia.
Caveat about CEA tumor marker for CRC
Good for monitoring recurrence, shouldn’t be used for screening.
Screening for CRC
Colonoscopy, flexible sigmoidoscopy, fecal occult blood test, or fecal DNA test.
Genetic cause of most sporadic CRC
Mutations in APC
Mismatch repair gene
MLH1
Chromosomal instability pathway for CRC
APC –> KRAS –> p53, DCC
Cells responsible for fibrosis in cirrhosis
Stellate cells
histology of fibrosis
diffuse bridging fibrosis + regenerative nodules.
Causes of portal HTN
cirrhosis + vascular obstruction (Budd-Chiari) + schisto
metabolic presentation of cirrhosis and portal HTN
cardiomyopathy + peripheral edema
hematologic presentation of cirrhosis and portal HTN
thrombocytopenia + anemia + coagulation disorders
fetor hepaticus
“breath of the dead.” Late sign of liver failure and feature of hepatic encephalopathy. Breath has a sweet, fecal smell to it.
Reproductive presentation of cirrhosis and portal HTN
testicular atrophy + gynecomastia + amenorrhea
What does AST greater than ALT in nonalcoholic liver disease suggest…
progression to advanced fibrosis or cirrhosis.
ALT, AST pattern in most liver disease
ALT is greater than AST, alcoholic liver disease is the exception
Marker of cholestasis
ALP
gamma-glutamyl transpeptidase
increased in various liver and biliary disease, but not in bone disease.
Albumin as a marker of liver disease
decreased in advanced liver disease
Prothrombin as a marker of liver disease
Increased in advanced liver disease (decreased production of clotting factors)
Platelets as a marker of liver disease
decreased in advanced liver disease
Why are platelets decreased in advanced liver disease?
decreased thrombopoietin, liver sequestration and portal HTN (splenomegaly/splenic sequestration).
viral infections associated with Reye syndrome
VZV + influenza B
Reye syndrome pathophys
aspirin metabolites decrease beta-oxidation by reversible inhibition of mitochondrial enzymes.
alcoholic hepatitis histology
swollen and necrotic hepatocytes with neutrophilic infiltration.
Mallory bodies
intracytoplasmic eosinophilic inclusions of damaged keratin filaments.
alcoholic cirrhosis histology
Micornodular, irregularly shrunken liver with “hobnail” appearance. Sclerosis around central vein.
Non alcoholic fatty liver disease:
Super fat hippos sitting around perimeter + inflating balloons + grim reaper sitting in middle/metabolic syndrome (insulin resistance) fatty infiltration of hepatocytes “cellular ballooning” and eventual necrosis. Ollie sitting in chair holding fetus in front of grim reaper/may cause cirrhosis and HCC. /independent of alcohol use. Huge alan + tiny Trojan Spartan to his right/ALT>AST.
antibiotic treatment for hepatic encephalopathy
rifaximin or neomycin
hepatic encephalopathy trigers
1) increased NH3 production and absorption (due to dietary protein, GI bleed, constipation, infection).
2) decreased NH3 removal (due to renal failure, diuretics, bypassed hepatic blood flow post-TIPS).
lactulose MOA in hepatic encephalopathy
Decreases intraluminal ammonia absorption. Lactulose is metabolized by gut bacteria into lactic and acetic acid. The H+ ions emitted bind to NH3, converting it into NH4+ and thereby preventing it’s absorption. Thus, increase NH4+ generation.
alpha1-antitrypsin deficiency cancer association
HCC
cavernous hemangioma prognosis
benign
hepatic adenoma prognosis
May regress spontaneously or rupture (abdominal pain and shock
Most common liver tumor mets
GI + breast + lung
budd-chiari associations
hypercoagulable states + polycythemia vera + postpartum state + HCC
caveat aboud Budd-chiari
Absence of JVD.
pathophys of alpha1-antitrypsin deficiency in liver
Misfolded gene product protein aggregates in hepatocellular ER, causing cirrhosis with PAS positive globules in liver.
hyperbilirubinemia associated with primary sclerosing cholangitis
conjugated
hyperbilirubinemia associated with PBC
conjugated
Mixed (direct and indirect hyperbilirubinemia) seen in…
hepatitits, cirrhosis
physiologic neonatal jaundice prognosis
usually resolves without treatment in 1-2 weeks.
phototherapy for neonatal jaundice mechanize
Isomerizes unconjugated bilirubin to water-soluble form
hereditary hyperbilirubinemias genetics
all AR
Gilbert syndrome mechanism
Mildly decreased UDP-glucoronysltransferase conjugation and impaired bilirubin uptake.
Treatment for Crigler-Najjar type I
Plasmapheresis and phototherapy
Type II Crigler-Najjar
Less severe and responds to phenobarbital, which increases liver enzyme synthesis.
Rotor syndrome etiology
Impaired hepatic uptake and excretion.
another name for conjugated bilirubin
bilirubin diglucuronide
another name for Wilson’s
hepatolenticular degeneration
gene mutation in Wilson’s
ATP7B
labs in Wilson’s
DECREASED ceruloplasmin
Kaysr-Fleischer rings
deposits in Descemet membrane of cornea
Wilson’s treatment
chelation with penicillamine or trientine, oral zinc.
HFE chromosome
6
hemochromatosis
- ferritin
- TIBC
- transferrin
Increased ferritin, increased iron, decreased TIBC, increased transferrin saturation.
Iron overload also seen in..
chronic transfusion therapy (beta-thalassemia major)
hemochromatosis presentation
Presents after age 40 when total body iron > 20 g.
cardiac presentation of hemochromatosis
dilated cardiomyopathy (reversible)
hemochromatosis treatment
Repeated phlebotomy, chleation with deferasirox, deferoxamine, oral deferiprone.
cholestatic pattern of LFTs (characteristic of biliary tract disease)
Increased conjugated bilirubin, increased cholesterol, increased ALP.
Lab findings in PSC
- p-ANCA positive
- increased IgM
PSC complications
1) biliary cirhosis
2) increased risk of cholangiocarcinoma and gallbladder cancer.
Secondary biliary cirrhosis 1) pathophys
1)Extrahepatic biliary obstruction leads to increased pressure in intrahepatic ducts, leading to injury/fibrosis and bile stasis.
Secondary biliary cirrhosis epidemiology
Patients with known obstructive lesions (gallstones, biliary strictures, pancreatic carcinoma)
Secondary biliary cirrhosis complication
Ascending cholangitis
what causes gallstones
increased cholesterol and/or bilirubin, decreased bile salts, and stasis.
cholesterol gallstone associations
Obestity, crohns, advanced age, estrogen therapy, multiparity, rapid weight loss, Native American.
black pigment stone composition
Calcium bilirubinate
Brown pigment stone etiology
infection
pigment stone associations
Crohn’s, advanced age, chronic hemolysis, alcoholic cirrhosis, biliary infections, total parenteral nutrition.
complications of gallstones
1) cholecystitis
2) acute pancreatitis
3) ascending cholangitis
4) fistula between gallbladder and GI tract (air in biliary tree0
charcot triad of cholangitis
Jaundice + fever + RUQ pain
pneumobilia
air in biliary tree
gallstone ileus
osbtruction of ileocecal valve due to gallstone from fistula
Increased ALP suggests
bile duct involvement (ascending cholangitis)
cholecystitis diagnosis
US or cholescintigraphy (HIDA, or hepatobiliary iminiodiacetic acid scan).
causes of alcalculous cholecystitis
ischemia and stasis or CMV
causes of acute pancreatitis
I GET SMASHED. Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps, Autoimmune disease, Scorpion sting, Hypercalcemia/Hypertriglyceridemia (>1000 mg/dL), ERCP, Drugs (sulfa drugs, NRTIs, protease inhibitors).
acute pancreatitis diagnosis
2/3 criteria: acute epigastric pain often radiating to the back, increased serum amylase or lipase (more specific) to 3x upper limit of normal, or characteristic imaging findings.
another complication of acute pancreatitis
hypocalcemia (precipitation of Ca2+ soaps)
chronic pancreatitis
Chronic inflammation, atrophy, calcification of the pancreas.
chronic pancreatitis caveat
amylase and lipase may or may not be elevated (almost always elevated in acute pancreatitis)
pancreatic adenocarcinoma personality
Often metastatic at presentation with average survival around 1 year.
Trousseau syndrome
migratory thrombophlebitis
Courvoisier sign
palpable, nontender gallbladder, characteristic of pancreatic adenocarcinoma.
Treatment for pancreatic adenocarcinoma
Whipple procedure + chemo + radiation.
gastrin pathway
Gq
somatostatin pathway
Gi
Prostaglandin pathway
Gi
alkaline tide
increased blood pH after gastric acid secretion (eg, after meals, vomiting)
carbonic anhydrase
interconverts CO2 + H2 H2CO3
How is Cl excreted in parietal cells
HCO3-/Cl- exchanger generates Cl- gradient, then diffuses through channels out
Gastrin receptor on parietal cells
CCK3
ACh receptor on parietal cells
M3
Cholera mechanism
He’s on a stationary bike + there’s tents set up all over the room + swat team is breaking into his house/cholera A-B toxin (a for activating, b for binding) activates adenyl cyclase by ADP ribosylation to increase cAMP. *This leads to increased Cl- secretory channels in crypt cells.
CCK has some gastrin-like properties because both CCK and gastrin
Have 5 identical C-terminal amino acids.
Monosaccharide transport caveat
Fructose is the only monosaccharide that that is not absorbed by Na+-dependent cotransport. It it stransported by facilitated diffusion.
Amino acid absorption in the intestine
Na+-dependent cotransport (*except for oligopeptides)
Fatty acid absorption
simple diffusion
Why does ileal resection (such as for Crohn’s patients) cause steatorrhea?
Ileum normally transports bile acids from the lumen of the gut. Thus, with ileal resection new synthesis of bile acids is needed to replace bile acids that are lost in the feces. With ileal resection most of bile acids secreted are excreted in the feces and the liver pool is diminished. ***Bile acids are needed for micelle formation in the intestinal lumen to solubilize products of lipid digestion so that they can be absorbed. So the problem is MICELLES DO NOT FORM in the intestinal lumen.
Where are chylomicrons formed?
Within intestinal epithelial cells and are transported to lymph vessels.
Function of CCK
Mediates digestion in the small intestine by inhibiting gastric emptying and decreasing gastric acid secretion. Lines small intestine.
Saliva characteristics
1) hypotonic
2) high HCO3- concentration
3) alpha-amylase and lingual lipase
control of saliva production
Parasympathetic, thus it is abolished by vagotomy.
What are slow waves in small intestinal smooth muscle cells?
oscillating resting membrane potentials.
