Steve Seagal's Gut Punching GI Gospel Flashcards
What is the foregut
pharynx to duodenum
What is the midgut
duodenum to proximal 2/3 of transverse colon
what is the hindgut
distal 1/3 of the transverse colon to the anal canal above the pectinate line
Developmental defects of anterior abdominal wall due to the failure of:
Rostral fold closure: sternal defects
Lateral fold closure: omphalocele, gastroschisis
Caudal fold closure: bladder extrophy
Duodenal atresia: associated with? What is it?
failure to recanalize
trisomy 21
Jejunal, ileal, colonic atresia is mostly due to
vascular accident, like superior mesenteric not developing, makes gut small and twisty, called apple peal atresia
Midgut development
6th week is when midgut herniates through umbilical ring
10th week returns to abdominal cavity and rotates around SMA
Malrotation of the midgut, omphalocele, intestinal atresia or stenosis, volvulus
Gastroschisis
extrusion of abdominal contents through abdominal folds; not covered by peritoneum
Omphalocele
persistence of herniation of abdominal contents into umbilical cord, sealed by peritoneum
Tracheoesophageal atresia
EA with distal tracheoesophageal fistula is most common: drooling, choking, vomiting with first feeding. Fistula allows air into stomach. Cyanosis is secondary to laryngospasm (spasm is to stop reflux aspiration). diagnose by NG not being able to get to stomach
H-type: is the fistula alone
Pure atresia: no gas in stomach
Congenital pyloric stenosis
Hypertrophy of the pyloris causes obstruction
palpable “olive” mass in epigastric region and nonbilious projectile vomiting at 2-6 weeks of age
treat with surgical incision
more often in first born males
Pancreas embryology
derived from foregut
ventral pancreatic buds contribute to the pancreatic head and main pancreatic duct.
uncinate process is formed by the ventral bud alone
dorsal pancreatic bud becomes everything else
Annular pancreas
ventral pancreatic bud abnormally encircles 2nd part of duodenum; forms a ring of pancreatic tissue that may cause duodenal narrowing
Problem with malrotation of ventral bud around duodenum
New born will have bilious vomiting and polyhydramnios
Pancreas divisum
ventral and dorsal parts fail to fuse at 8 weeks
Spleen embryology
arises in mesentery of stomach (hense is mesodermal) but is supplied by foregut (celiac artery)
Retroperitoneal structures
all GI structures that lack a mesentery and non-GI structures
injuries to these can cause blood or gas to build up in space
SAD PUCKER
Suprarenal glands, Aorta and ivc, Duodenum (2nd through 4th parts), Pancreas (except tail), Ureters, Colon (descending and ascending), Kidneys, Esophagus, Rectum
Falciform ligament
Connects liver to anterior abdominal wall
contains ligamentum teres hepatis
this is a derivative of ventral mesentery
Hepatoduodenal ligament
Connects Liver to duodenum
Contains the portal triad: proper hepatic artery, portal vein, common bile duct
Part of the lesser omentum
Pringle maneuver-
hepatoduodenal ligament may be compressed between thumb and index finger placed in omental foramen to control bleeding
omental foramen is what connects the lesser and greater sac
Gastrohepatic ligament
Connects liver to lesser curvature of stomach
contains the gastric arteries
separates the greater and lesser sacs on the right
may be cut during surgery to access lesser sac
Gastrocolic ligament
connects greater curvature and transverse colon
contains gastroepiploic arteries
it is part of the greater omentum
Gastrosplenic ligament
connects greater curvature and the spleen
contains short gastric arteries and left gastroepiploic vessles
Separates the greater and lesser sacs on the left
Splenorenal ligament
connects spleen to posterior abdominal wall
contains the splenic artery and vessels, tail of pancreas
Layers of the gut wall
MSMS
Mucosa- epithelium, lamina propria, muscularis mucosa
Submucosa- includes submucosal nerve plexus (meissner’s)
Muscularis externa- includes Myenteric plexus (Auerbach)
Serosa/adventitia- Serosa when intraperitoneal, adventitia when retroperitoneal
Frequency of basal electric rhythm: stomach, Duodenum, Ileum:
stomach: 3 waves/min
Duodenum: 12 waves/min
Ileum: 8-9 waves/min
Distinctive Histology of the esophagus
nonkeratinized stratified squamous epithelium
Distinctive Histology of the stomach
Gastric glands
Distinctive Histology of the Duodenum
Villi and microvilli which increase absorptive surface
Brunner glands in the submucosa
Cyrpts of Lieberkuhn
Distinctive Histology of the Jejunum
Plicae circulares and crypts of Lieberkuhn
Distinctive Histology of the Ileum
Peyer patches in the lamina propria and submucosa
plicae cirulares in the proximal ileum
crypts of Lieberkuhn
Has the largest Number of goblet cells in the small intestine
Distinctive Histology of the Colon
Colon has crypts of Lieberkuhn but no villi
numerous goblet cells
What is Superior mesenteric artery syndrome
when the transverse portion of the duodenum is entrapped between SMA and aorta
causes intestinal obstruction
GI blood supply and innervation for the Foregut
Celiac artery
Vagus parasympathetic innervation
at vertebral level T12 and L1
structures included are the proximal duodenum: liver, bladder, pancreas, spleen (mesoderm)
GI blood supply and innervation for the midgut
SMA
Vagus parasympathetic
at vertebral level L1
Structures include duodenum to proximal 2/3 transverse colon
GI blood supply and innervation for the hindgut
IMA
Pelvic parasympathetic innervation
at vertebral level L3
Structures include distal 1/3 transverse colon to the upper portion of the rectum
splenic flexure is a watershed region: what does that mean
receives blood from the terminal branches of SMA and IMA, makes it prone to ischemic damage in cases of low blood pressure because it does not have its own primary source of blood
Celiac trunk: branches
common hepatic, splenic, left gastric: make up the main blood supply of the stomach
Anal fissure
Tear in anal mucosa below the pectinate line
Pain while Pooping
Located Posteriorly since this are is Poorly Perfused
Internal hemorrhoids
receive visceral innervation and are therefore not painful
Lymph drains into deep nodes in this area
Blood flow below pectinate line
arterial supply form inferior rectal artery (branch of internal pudendal artery
Venous drainage to inferior rectal vein to internal pudendal vein to internal iliac vein to IVC
Likely cancer of GI above and below pectinate line
above you are more likely to get adenocarcinoma
below you are more likely to get squamous cell carcinoma
Blood flow above pectinate line
arterial from superior rectal which is a branch of the IMA
venous is to the superior rectal vein to the inferior mesenteric to the portal system
External hemorrhoids
below pectinate line
receive somatic innervation via inferior branch of pudendal nerve, making them painful
lymph drains to superficial inguinal nodes
3 zones of Liver anatomy
Zone 1: periportal zone: affected first by viral hepatitis, Ingested toxins
Zone 2: intermediate zone
Zone 3: pericentral vein: centirilobar zone, affected first by ischemia, contains p-450 enzyme, most sensitive to metabolic toxins, site of alcoholic hepatitis
Femoral triangle and lymph
Lateral to Medial you have
Nerve-Artery-Vein-Empty space-Lymphatics (all femoral)
“you have to go lateral to medial to find your NAVEL”
Femoral sheath contains what
Fascial tube 3 to 4 cm below inguinal triangle
contains femoral vein, artery, and canal (deep inguinal lymph nodes) but not the femoral nerve
H2 blockers: names
Cimetidine, Ranitidine, Famotidine, nizatidine
H2 blockers: mechanism
Reversible block of histamine H2-receptors which decrease H+ secretion by parietal cells
Must take before you eat
H2 blockers: Clinical Use of it
Peptic ulcer, gastritis, mild esophageal reflux
H2 blockers: toxicity
cimetidine is a potent inhibitor of cytochrome p450; also has antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males); can cross blood-brain barrier (confusion, dizziness, headaches) and placenta.
Both cimetidine and ranitidine decrease renal excretion of creatinine
Other H2 blockers don’t have these effects
Proton pump inhibitors: names
omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole
Proton pump inhibitors: mechanism
irreversibly inhibit H+/K+ ATPase in stomach parietal cells
must take before meal, only work against active pumps not inactive pumps
Proton pump inhibitors: clinical use
Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome
Proton pump inhibitors: toxicity
increased risk of C Diff infection, pneumonia (get klebsiella infections in the lungs more often), Hip fractures, decreased serum Mg2+ with long term use
Bismuth, Sucralfate: mechanism, clinical use
Bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer
used for increasing ulcer healing, travelers’ diarrhea
Misoprostol
A PGE1 analog. increases production and secretion of gastric mucous barrier, decreases acid production
Used to prevent NSAID induced peptic ulcers; maintenance of a PDA; also used to induce labor (ripens cervix)
Causes diarrhea, contraindicated in women of childbearing potential (abortifacient)
Octreotide
Mechanism: long acting somatostatin analog
Uses: acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors
Toxicity: nausea, cramps, steatorrhea
Antacid use
can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying
all can cause hypokalemia
aluminum hydroxide
antacid
causes constipation, hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
slow onset and no systemic absorption
Calcium carbonate
antacid
causes hypercalcemia and rebound acid secretion
Systemically absorbed, Rapid onset of action, Long duration, Belching (CO2), gastric distension, Mild systemic alkalosis.
Hypercalcemia in pts w/ impaired renal function if taken with dairy products (milk-alkali syndrome)
Magnesium hydroxide
antacid
Osmotic diarrhea, Renal insufficiency causing hypermagnesemia causing CNS and cardio toxicity
give this with aluminum hydroxide (Causes constipation) and boom! less poopy side effects
Diaphragmatic hernia
abdominal structures enter the thorax; may occur in infants as a result of defective development of peuroperitoneal membrane
most commonly a a hiatal hernia, in which stomach herniates upward through the esophageal hiatus of the diaphragm
sliding hiatal hernia
is most common diaphragmatic hernia
gastroesophageal junction is displaced upward; hourglass stomach
Paraesophageal hernia
gastroesophageal junction is normal and fundis protrudes into the thorax
indirect inguinal hernia
goes through the internal (Deep) inguinal ring, external (superficial) inguinal ring, and into the scrotum. enters internal inguinal ring lateral to inferior epigastric artery. Occurs in infants owing to failure of processus vaginalis to close (can form hydrocele). much more common in males
(follows path of descent of the tests, covered by all 3 layers of spermatic fascia)
Direct inguinal hernia
Protrudes through the inguinal (Hesselbach) triangle. Bulges directly through abdominal wall medial to inferior epigastric artery. Goes through the external (superficial) inguinal ring only. Covered by external spermatic fascia. Usually older men
MDs don’t LIe: Medial to inferior epigastric artery=Direct hernia; Lateral to inferior epigastric artery= Indirect hernia
Femoral hernia
protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle. more common in females
leading cause of bowel incarceration
Hesselbach triangle
made from the: inferior epigastric vessels, lateral border of rectus abdominis, inguinal ligament
Cholecystokinin
from I cells in Duodenum, Jejunum
increases: pancreatic secretions, gall bladder contraction, relaxation of sphincter of Oddi
decreases: gastic emptying
Regulation: increased release by fatty acids, amino acids
CCK acts on neural muscarinic pathways to cause pancreatic secretion
Gastrin
released from G cells of antrum of stomach and G cells in duodenum. stimulated by increased stomach distention, alkalinization, amino acids, peptides, vagal stimulation; decreased release if pH
Glucose-dependent insulinotropic peptide (AKA GIP)
Released by K cells in duodenum and jejunum in response to fatty acids, amino acids, oral glucose
Exocrine function: decrease H+ secretion
Endocrine function: increase insulin release
AKA: gastric inhibitory peptide
An oral glucose load is used more rapidly than the equivalent given by IV due to GIP release
Motilin
released from small intestine, produces migrating motor complexes during fasting state
Motilin receptor agonists (e.g. erythromycin) are used to stimulate intestinal peristalsis (also why a lot of antibiotics cause diarrhea)
Secretin
release from S cells in duodenum in response to acid or fatty acids in lumen of the duodenum
acts to: increase pancreatic HCO3- secretion, increase secretion, decrease gastric acid secretion
HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
Somatostatin
released from D cells in pancreatic islets and GI mucosa in response to acid and inhibited by vagal stimulation
Acts to :decrease gastric acid and pepsinogen secretion, decrease pancreatic and small intestine fluid secretion, decrease gallbladder contraction, decrease insulin and glucagon release
Somatostatin is an inhibitory hormone; has antigrowth hormone effects (inhibits digestion, absorption of substances needed for growth)
nitric oxide
causes: increase smooth muscle relaxation including lower esophageal sphincter
Loss of NO secretion in implicated in increase LES tone of achalasia
Vasoactive intestinal polypeptide (VIP)
released from parasympathetic ganglia in sphincters, gallbladder, small intestine in response to distention and vagal stimulation, inhibited by adrenergic input
acts to: increase intestinal water and electrolyte secretion, and increase relaxation of smooth muscle and sphincters
VIPoma:
non alpha, non beta islet cell pancreatic tumor that secretes VIP
Copious Watery Diarrhea, Hypokalemia, and Achlorhydria
WDHA syndrome
Intrinsic Factor
released from parietal cells of the stomach
acts to bind Vitamin B12 which is required for the uptake of B12 in the terminal ileum
Autoimmune destruction of parietal cells leads to chronic gastritis and pernicious anemia
Gastric acid
From the parietal cells of the stomach
released in response to histamine ACh and gastrin
decreased release by stimulation from somatostatin, GIP, prostaglandin, and secretin
Acts to decrease stomach pH
Gastrinoma
gastrin secreting timor that causes high levels of acid secretion and ulcers refractory to medical therapy
Zollinger-Ellison syndrome.
Diagnose by seeing mass on CT, giving patient secretin and their gastrin levels go up.
Pepsin
released from chief cells of the stomach
aids in protein digestion
released in response to vagal stimulation and local acid
released as inactive pepsinogen which is cleaved by acid or pepsin to become pepsin
HCO3- (bicarb) in the GI tract
released from the mucosal cells (stomach, duodenum, salivary glands, pancreas) and the Brunner glands (duodenum)
Neutralizes acids
increased secretion in response to pancreatic and biliary secretion with secretin
HCO3- is trapped in mucus that covers the gastric epithelium
Gastrin increases acid secretion primarily by
ints effects on enterochromaffin-like cells (ECL cells) leading to histamine release which acts on the parietal cells. Gastrin can act on parietal cells, but does not have as much effect
Brunner glands
Located in duodenal submucosa
Secrete alkaline mucus
Hypertrophy seen in peptic ulcer disease
Pancreatic secretions
Isotonic fluid; low flow is high in Cl-, high flow is high in HCO3-
alpha-amylase
pancreatic secretion
works in starch digestion
secreted in active form
Lipase, phospholipase A, Colipase
pancreatic secretion
works in fat digestion
Pancreatic secretion: Proteases
works in protein digestion
Includes trypsin, chymotrypsin, elastase, carboxypeptidases
secreted as proenzymes (zymogens)
Trypsinogen
pancreatic secretion
converted to active form of trypsin
trypsin molecules can convert trypsinogen into active trypsin
also converted into trypsin by enterokinase/enteropeptidase, a brush-border enzyme on the duodenal and jejunal mucosa
Carbohydrate absoprtion
only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes.
Glucose and galactose are taken up by SGLT1 (Na dependent)
Fructose is taken up by facilitated diffusion by GLUT-5
All are transported into the blood by GLUT-2
D-xylose absorption test: distinguishes GI mucosal damage from other causes of malabsoprtion
Iron absorption
only absorbed as Fe2+ in duodenum
Folate absorption
absorbed in jejunum and ileum
B12 absorption
absorbed in terminal ileum along with bile acids, requires intrinsic factor from parietal cells
Peyer patches
Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum. Contains specialized M cells that sample and present antigens to immune cells
B cells stimulated in germinal centers of peyer patches differentiate into IgA-secreting plasma cells, which ultimately reside in lamina propria
IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen
Bile
Composed of bile salts (bile acids conjugated to glycine or taurine, making them water soluable), phospholipids, cholesterol, bilirubin, water, and ions
Cholesterol 7alpha-hydroxylase catalyzes rate-limiting step of bile synthesis
Functions: digestion and absorption of lipids and fat soluble vitamins (ADEK), Cholesterol excretion (only way humans can get rid of cholesterol), antimicrobial activity (via membrane disruption)
Bilirubin
Product of heme metabolism
Removed from blood by liver, conjugated with glucuronate and excreted in bile
direct bilirubin: conjugated with glucuronic acid and is water soluble
Indirect bilirubin: unconjugated; water insoluble
Stercobilin
Bilirubin is excreted with bile and via the gut bacteria turned into urobilinogen and then into stercobilin and excreted in feces. gives poop its brown color
80% of bilirubin in gut is excreted this way, 20% reabsorbed and either peed out or comes back into GI to try again.
Pleomorphic adenoma
benign mixed tumor
Most common salivary gland tumor
Presents as a painless, mobile mass
Composed of chondromyxoid stroma and epithelium
Recurs if incompletely excised or ruptured intraoperatively
Warthin tumor
papillary cystadenoma lymphomatosum
Is a benign cystic tumor with germinal centers
Salivary tumors in general
Generally benign and almost always in the parotid gland
Mucoepidermoid carcinoma
most common salivary malignant tumor and has mucinous and squamous components
Typically presents as a painless, slow-growing mass
Achalasia
Failure of relaxation of LES due to loss of myenteric (auerbach) plexus
High LES opening pressure and uncoordinated peristalsis leads to progressive dysphagia to solids AND liquids (obstruction would by just solids).
Barium swallow shows dilated esophagus with an area of distal stenosis (bird’s beak)
Associated with an increased risk of esophageal squamous cell carcinoma
secondary achalasia can be caused by Chagas disease
Boerhaave syndrome
Transmural usually distal esophageal rupture due to violent retching; surgical emergency
Eosinophilic esophagitis
infiltration of eosinophils in the esophagus in atopic patients.
Keys to this disease: food allergens lead to dysphagia, heartburn and strictures, Unresponsive to GERD therapy.
Esophageal strictures
narrowing or tightening of the esophagus that causes swallowing difficulties
Associated with lye ingestion and acid reflux
Esophageal varices
Painless bleeding of dilated submucosal veins in the lower 1/3 of the esophagus secondary to hypertension
Esophagitis
associated with reflux, infection in immunocompromised (Candida: white pseudomembrane; HSV-1: punched-out ulcers; CMV: linear ulcers), or chemical ingestion
Gastroesophageal reflux disease
commonly presents as heartburn and regurgitation upon lying down. May also present with nocturnal cough and dyspnea, adult-onset asthma. Decrease in LES tone
Mallory-Weiss syndrome
Mucosal lacerations at the gastroesophageal junction due to severe vomiting. Leads to hematemesis. Usually found in alcoholics and bulimics.
Plummer-Vinson Syndrome
Triad of Dysphagia (due to esophageal webs), Iron deficiency anemia, and Glossitis (“Plumbers” DIG)
Sclerodermal esophageal dysmotility
Esophageal smooth muscle atrophy leads to decreased LES pressure and dysmotility which causes acid reflux and dysphagia which can lead to strictures, Barrett esophagus, and aspiration. Part of CREST syndrome
Barrett Esophagus
Glandular metaplasia: replacement of nonkeratinized stratified squamous epithelium with intestinal epithelium (nonciliated columnar with goblet cells) in the distal esophagus. Due to chronic acid reflux (GERD). Associated with esophagitis, esophageal ulcers, and increase risk of esophageal adenocarcinoma
Esophageal cancer
Can be squamous cell or adenocarcinoma. Typically presents with progressive dysphagia (first solids, then liquids) and weight loss; poor prognosis. Squamous is more common worldwide, Adeno is more common in US, squamous is the upper 2/3 and adeno is lower 1/3 of esophagus.
Risk factors are AABCDEFFGH; Achalasia, Alcohol (squamous), Barrett (adeno), Cigarettes (both), Diverticula (squamous), Esophageal web (squamous), Familial, Fat/obese (Adeno), GERD (adeno), Hot liquids (squamous)
Acute gastritis
Erosive
Disruption of mucosal barrier leads to inflammation. Can be caused by stress, NSAIDS (less PGE2), alcohol, uremia, burns (Curling ulcer which decreases plasma volume and causes sloughing of gastric mucosa), and brain injury (Cushing ulcer, increased vagal stimulation increases ACh secretion increasing H+ production)
VERY COMMON in alcoholics and daily NSAID users
Type A chronic gastritis
non-erosive, Fundus and body
Autoimmune disorder characterized by Autoantibodies to parietal cells, pernicious Anemia, and Achlorhydria. Associated with other autoimmune disorders
“A comes before B” (location) and “type A for Autoimmune”
Type B chronic Gastritis
non-erosive, antrum most common type. Caused by H. Pylori infection. increase risk of MALT lymphoma and gastric adenocarcinoma
“Type B is Bacteria”
Menetrier disease
Gastric hypertrophy with protein loss (can lead to hypoalbumenemia), parietal cell atrophy and increase mucous cells. Precancerous. Rugae of stomach are so hypertrophied that they look like brain gyri. Possible cause is increase transforming growth factor (TGF-alpha)
Stomach cancer
Almost always adenocarcinoma. Early aggressive spread and node/liver metastases. Often presents with acanthosis nigricans.
Intestinal: associated with H. Pylori infection, dietary nitrosamines (smoke foods, preservatives), tobacco smoking, achlorhydria, chronic gastritis, pernicious anemia, commonly on lesser curvature; looks like ulcer with raised margins
Diffuse: not associated with bacteria; signet ring cells; stomach wall grossly thickened and leathery (lintis plastica)
acanthosis nigricans
brown to black, poorly defined, velvety hyperpigmentation of the skin. It is usually found in body folds,[1] such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas
Virchow node
involvement of left supraclavicular node by metastasis from stomach
Krukenberg tumor
bilateral stomach cancer metastases to ovaries. Abundant mucus, signet ring cells
Sister Mary Joseph nodule
subcutaneous periumbilical metastasis from stomach cancer. I did not make this up
Gastric Ulcer
Mechanism: decrease in mucosal protection against gastric acid
H. Pylori infection in 70% of cases, NSAIDs another cause
Pain is Greater with meals, might cause weight loss
Often in Older patients
Increases risk of Carcinoma
Duodenal Ulcer
Mechanism is a decrease in mucosal protection or increase in gastric acid secretion
H. Pylori infection in 100% of cases, Zollinger-Ellison syndrome is another cause
Pain Decreases with meals, might cause weight gain
No contribution to carcinoma
See hypertrophy of brunner glands
Ulcer complication: Hemorrhage
Happens in Gastric and duodenal (posterior > anterior) ulcers
Ruptured gastric ulcer on the lesser curvature of the stomach which leads to bleeding form left gastric artery if proximal: distal lesser curvature is right gastric.
An ulcer on the posterior wall of the duodenum leads to bleeding from gastroduodenal artery
Ulcer complication: Perforation
Happens in Duodenal ulcers (anterior > posterior)
May see free air under the diaphragm with referred pain to the shoulder
Malabsorption syndromes normally cause what symptoms
Can cause diarrhea, steatorrhea, weight loss, weakness, and vitamin and mineral deficiencies
Tropical sprue
similar findings as celiac sprue (affects small bowel), but responds to antibiotics. Cause is unknown, but seen in residents of or recent visitors to tropics.
Whipple disease
Infection with Tropheryma whipplei (gram positive); PAS positive foamy macrophages in intestinal lamina propria, mesenteric nodes. Cardiac symptoms, Arthralgias, and Neurologic symptoms are common. most often occurs in older men.
Foamy Whipped cream in a CAN
Celiac Sprue
Autoimmune mediated intolerance of gliadin (wheat) leading to malabsorption and steatorrhea. Associated with HLA-DQ2, HLA-DQ8, and northern European descent. Findings include anti-gliadin antibodies; blunting of villi; lymphocytes in the lamina propria. Decreased mucosal absorption that primarily affects distal duodenum and proximal jejunum. Serum levels of tissue transglutaminase antibodies are used for diagnosis. Associated with dermatitis herpetiformis. increase risk of T cell lymphoma. Treat with gluten free diet
Disaccharidase deficiency
most common is lactase deficiency leading to milk intolerance. Normal-appearing villi. Get osmotic diarrhea. since lactase is located at tops of intestinal villi, self-limited lactase deficiency can occur following injury (e.g. viral diarrhea)
Lactose tolerance test is positive for lactase deficiency if what criteria are met
Administration of lactose produces symptoms, and Glucose rises less than 20 mg/dL
Abetalipoproteinemia
decrease synthesis of apolipoprotein B48 (chylomicron formation) and B100(Makes VLDL and LDL) leading to an inability to generate chylomicrons causing decreased secretion of cholesterol and VLDL into blood stream then fat builds up in enterocytes
Presents in early childhood with failure to thrive, steatorrhea, acanthocytosis, ataxia, night blindness
Pancreatic insufficiency
Due to cystic fibrosis, obstructing cancer, and chronic pancreatitis. Causes malabsorption of fat and fat-soluble vitamins (Vitamins A, D, E, K)
Causes: increase neutral fat in stool
D-xylose absorption test
normal urinary excretion in pancreatic insufficiency: decreased excretion with intestinal mucosa defects or bacterial overgrowth
Crohn Disease: possible etiology
disordered response to intestinal bacteria
Crohn Disease: Location
Any portion of the GI tract, usually the terminal ileum and colon. “Skip lesions”, rectal sparing
Crohn Disease: Gross morphology
transmural inflammation leading to fistulas. Cobblestone mucosa, creeping fat, bowel wall thickening (string sign on barium swallow x-ray), linear ulcers, fissures
Crohn Disease: Microscopic Morphology
Noncaseating granulomas and lymphoid aggreages (Th1 mediated)
Crohn Disease: complications
Strictures (leading to obstruction), fistulas, perianal disease, malabsorption, nutritional depletion, colorectal cancer, gallstones
Crohn Disease: intestinal manifestation
Diarrhea that may or may not be bloody
Crohn Disease: extraintestinal manifestation
migratory polyarthritis, erythema nodosum, ankylosing spondylitis, pyoderma gangrenosum, aphthous ulcers, uveitis, kidney stones
Crohn Disease: treatment
Corticosteroids, azathioprine, methotrexate, infliximab, adalimumab
Ulcerative Colitis: possible etiology
autoimmune
Ulcerative Colitis: location
colitis= colon inflammation, continuous colonic lesions, always with rectal involvement
Ulcerative Colitis: Gross morphology
Mucosal and submucosal inflammation only
friable mucosal pseudopolyps with freely hanging mesentery. loss of haustra leading to lead pipe appearance on imaging
Ulcerative Colitis: Microscopic Morphology
Crypt abcesses and ulcers, bleeding, no granulomas (Th2 mediated)
Ulcerative Colitis: complications
Malnutrition, sclerosing cholangitis, toxic megacolon, colorectal carcinoma (esp. adenocarcinoma) (worse with right sided colitis or pancolitis)
Ulcerative Colitis: intestinal manifestations
Bloody diarrhea
Ulcerative Colitis: extraintestinal manifestations
pyoderma gangrenosum, erythema nodosum, primary sclerosing cholangitis, ankulosing spondylitis, apthous ulcers, uveitis
Ulcerative colitis: treatment
ASA preparations (sulfasalazine, mesalamine, oslalzine), 6-mercaptopurine, infliximab, colectomy
Irritable bowel syndrome
Recurrent abdominal pain associated with 2 or more of the following: 1. pain improving with defecation 2. change in stool frequency 3. change in stool appearance
No structural abnormalities, most common in middle ages women, chronic symptoms. May present with diarrhea, constipation, or alternating symptoms. Pathophysiology is multifaceted. Treat symptoms.
Appendicitis
Acute inflammation of the appendix due to obstruction by fecalith (in adults) or lymphoid hyperplasia (in children).
Initial diffuse periumbilical pain migrates to McBurney point (1/3 the distance from anterior superior iliac spine to umbilicus).
Nausea, fever
May perforate leading to peritonitis; may see psoas, obturator, and Rovsing signs
Differential should be diverticulitis (elderly), ectopic pregnancy (use Beta-hCG to rule out).
treat: appendectomy
Rovsing’s sign
palpation of the left lower quadrant of a person’s abdomen increases the pain felt in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis
Diverticulum
blind pouch protruding from the alimentary tract that communicates with the lumen of the gut. Most diverticula (esophagus, stomach, duodenum, colon) are aquired and are termed false in that they lack or have an attenuated muscularis externa. most often in sigmoid colon
True diverticulum
has all 3 gut wall layers outpouch
False diverticulum
only mucosa and submucosa outpouch. Occur especially where vasa recta perforate muscularis externa
Diverticulosis
Many false diverticula of the colon, commonly sigmoid. Common (about 50% of people over 60 have them). Caused by increase intraluminal pressure and focal weakness in colonic wall. Associated with low fiber diets.
Often asymptomatic or associated with vague discomfort. A common cause of hematochezia. Complications include diverticulitis and fistulas
Diverticulitis
Inflammation of diverticula classically causing LLQ pain, fever, leukocytosis. May perforate leading to peritonitis, abscess, formation, or bowel stenosis. Give antibiotics.
Stool occult blood is common +/- hematochezia. May also cause colovesical fistula (fistula with bladder) leading to pneumaturia.
Sometimes called left sided appendicitis due to overlapping clinical presentation
Zenker Diverticulum
Pharyngoesophageal false diverticulum. Herniation of mucosal tissue at killian triangle tbetween the thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor. Presenting symptoms: dysphagia, obstruction, foul breath from trapped food particles. most common in elderly males
Meckel diverticulum
True diverticulym
persistence of the vitelline duct. May contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue. Most common congenital anomaly of GI tract. Can cause melena, RLQ pain, intussusception, volvulus, or obstruction near the terminal ileum. Contrast with omphalomesenteric cyst=cystic dilation of vitelline duct
Diagnosis: pertechnetate study for uptake by ectopic gastric mucosa.
The five 2’s: 2 inches long, 2 feet from ileocecal valve, 2% population, commonly presents in first 2 years of life. May have 2 types of epithelia (gastric/pancreatic)
Intussusception
Telescoping of 1 bowel segment into distal segment, commonly at ileocecal junction. compromises the blood supply leading to intermittent abdominal pain often with currant jelly stools. Unusual in adults (associated with intraluminal mass or tumor that acts as lead point that is pulled into the lumen). Majority of cases occur in children (usually idiopathic or associated with recent enteric or respiratory viral infection Abdominal emergency in early childhood
Volvulus
Twisting of portion of bowel around its mesentery; can lead to obstruction and infarction. Can occur throughout the GI tract. Midgut volvulus more common in infants and children (usually cecum). Sigmoid volvulus common in elderly.
Hirschsprung disease
congenital megacolon characterized by lack of ganglion cells/enteric nervous plexuses (Auerbach and Meissner) in segment on intestinal biopsy.
Due to failure of neural crest cell migration.
Associated with mutations in the RET gene, and with down syndrome.
Presents with bilious emesis, abdominal distention, and failure to pass meconium in first 48 hours of life. Ultimately manifests as chronic constipation. Dilated portion of the colon proximal to the aganglionic segment, resulting in a transition zone. Involves rectum. treat with resection.
Diagnosed by rectal suction biopsy
Intestinal Disorder: adhesion
Fibrous band of scar tissue; commonly forms after surgery; most common cause of small bowel obstruction. can have well demarcated necrotic zones.
Intestinal Disorder: Angiodysplasia
Tortuous dilation of vessels leading to hematochezia. Most often found in cecum, terminal ileum, and ascending colon. More common in older patients. Confirmed by angiography.
Intestinal Disorder: duodenal atresia
Causes early bilious vomiting with proximal stomach distention (“double bubble” on x ray) because of failure of small bowel recanalization. Associated with down syndrome.
Intestinal Disorder: Ileus
intestinal hypomotility without obstructionleading to constipation and decreased flatus; distended/tympanic abdomen with decreased bowel sounds
Associated with abdominal surgeries, opiates, hypokalemia, and sepsis
Intestinal Disorder: Ischemic colitis
Reduction in intestinal blood flow causes ischemia. get pain after eating leading to patient weight loss. commonly occurs at splenic flexure and distal colon. typically affects elderly.
Intestinal Disorder: Meconium ileus
in cystic fibrosis, meconium plug obstructs intestine, preventing stoll passage at birth.
Intestinal Disorder: Necrotizing enterocolitis
Necrosis of intestinal mucosa and possible perforation. Colon is usually involved but can involve entire GI tract. In neonates, more common in preemies (decreased immunity), get bleeding, look for bottle fed babies, usually first week of life, low birth weight. See signs of shock.
Colonic polyps
masses protruding into gut lumen leading to a sawtooth appearance. 90% are non-neoplastic. often rectosigmoid. can be tubular or villous.
Adenomatous colonic polyps
Are precancerous. malignant risk is associated with increase size, villous histology, increased epithelial dysplasia. Precursor to colorectal cancer (CRC). the more villous the polyp the more likely it is to be malignant (villous villain)
Symptoms: usually none, can be lower GI bleed, partial obstructions, secretory diarrhea (villous adenomas)
Hyperplastic colonic polyps
most common non-neoplastic polyp in colon (>50% found in rectosigmoid colon)
Proliferation of goblet cells, sawtooth appearance, glandular epithelium
90% of colon polyps are this type
Juvenile colonic polyps
mostly sporadic lesions in children
Hamartomatous colonic polyps
Peutz-Jeghers syndrome- autosomal dominant syndrome featuring multiple nonmalignant hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, genitalia. Associated with increase risk of CRC and other visceral malignancies.
Colorectal cancer: Epidemiology
Most patients are over 50 years old and 25% have a family history of CRC
Familial adenomatous polyposis
autosomal dominant mutation of APC gene on chromosome 5q. 2-hit hypothesis. 100% progress to CRC unless colon is resected. Thousands of polyps arise starting at a young age; pancolonic; always involves rectum
Gardner Syndrome
can lead to CRC;
FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium
Turcot syndrome
Can lead to CRC;
FAP + malignant CNS tumor
Hereditary nonpolyposis colorectal cancer
autosomal dominant mutation of DNA mismatch repair genes. ~80% progress to CRC. proximal colon is always involoved
Risk factors for colorectal cancer
IBD, tobacco use, large villous adenomas, juvenile polyposis syndrome, Peutz-Jeghers syndrome
Presentation of colorectal cancer
Rectosigmoid> ascending > descending
ascending: exophytic mass, iron deficiency anemia, weight loss
Descending: infiltrating mass, partial obstruction, colicky pain, hematochezia.
Rarely presents as strep bovis bacteremia
How to diagnose colorectal cancer
iron deficiency in males and postmenopausal women raises suspicion. screen patients over 50 with colonoscopy or stool occult blood test
Apple core lesion seen on barium x-ray
CEA tumor marker: good for monitoring recurrence, not useful in screening
molecular pathogenesis of colorectal cancer
2 pathways that lead to CRC;
Microsatellite instability pathway (~15%): DNA mismatch repair gene mutations leading to sporadic and HNPCC syndrome. Mutations accumulate but no defined morphologic correlates.
APC/beta catenin (chromosomal instability) pathway (~85%) leads to sporadic cancer.
Overall: lose APC gene, Lose K-RAS gene, Lose tumor suppressor (p53).
C. diff infection: Classification, symptoms, what does it look like
Gram +, rod, motile, spore forming, toxin A (attracts granulocytes), Toxin B (cytopathic.
Toxins are how C diff causes psuedomembranous colitis, get it after starting antibiotic
Get greenish, foul smelling watery diarrhea, cramps, fever, leukocytosis.
Treat with metronidazole and add vanco if it is real bad.
Cirrhosis
Diffuse fibrosis and nodular regeneration destroys normal architecture of liver: increase risk for hepatocellular carcinoma (HCC)
Etiologies: alcohol in 60 to 70% of cases, viral hepatitis, biliary disease, hemochromatosis
Portosystemic shunts partially alleviate portal hypertension but lead to esophageal varices, gynecomastia, and caput medusae
what are the effects of portal hypertension
Esophageal varices (leading to hematemesis and melena) Peptic ulcers (leading to melena) Splenomegaly Caput medusae, ascites portal hypertensive gastropathy anorectal varices
What are the effects of liver cell failure
Hepatic encephalopathy scleral icterus Fetor hepaticus (breath smells musty) Spider nevi Gynecomastia Jaundice Testicular atrophy Liver flap=asterixis (coarse hand tremor) Bleeding tendency (decrease clotting factors and increased prothrombin time) Anemia Ankle edema
Serum marker, what does it mean: Alkaline phosphatase ALP
Obstructive hepatobiliary disease, HCC, bone disease
Serum marker, what does it mean: Aminotransferases AST and ALT
Viral hepatitis is ALT > AST Alcoholic hepatitis (AST>ALT)
Serum marker, what does it mean: Amylase
Acute Pancreatitism mumps
Serum marker, what does it mean: Ceruloplasmin
Decreased in wilson disease
Serum marker, what does it mean: gamma-glutamyl transpeptidase (GGT)
increased in various liver and biliary diseases (just like ALP cab), but NOT in bone diseases
Associated with alcohol use
Serum marker, what does it mean: Lipase
Acute pancreatitis (most specific test for it)
Reye Syndrome
Rare, often fatal childhood hepatoencephalopathy
Findings: mitochondrial abnormalities, fatty liver (microvesicular fatty change), hypoglycemia, vomiting, hepatomegaly, coma. Associated with viral infection (especially VZV and influenza B) that has been treated with aspirin.
Mechanism: aspirin metabolites decrease beta oxidation by reversible inhibition of mitochondrial enzyme. Avoid aspirin in children, except those with kawasaki disease.
Hepatic steatosis
reversible change with moderate alcohol intake. macrovesicular fatty change that may be reversible with alcohol cessation
Alcoholic hepatitis
requires sustained, long-term consumption. Swollen and necrotic hepatocytes with neutrophilic infiltration. Mallory bodies (intracytoplasmic eosinophilic inclusions) are present. AST>ALT ratio greater than 2:1
Alcoholic cirrhosis
Final and irreversible form. Micronodular, irregularly shrunken liver with “hobnail” appearance. Sclerosis around central vein (zone III). Has manifestations of chronic liver disease (e.g. jaundice, hypoalbuminemia).
Non-alcoholic fatty liver disease
metabolic syndrome (insulin resistance) leading to fatty infiltration of hepatocytes which causes cellular ballooning and eventual necrosis. May cause cirrhosis and HCC> independent of alcohol use. ALT > AST
Hepatic encephalopathy
Cirrhosis leading to portosystemic shunts which cause decreases in NH3 metabolism causing neuropsychiatric dysfunction. Spectrum from disorientation/asterixis (mild) to difficult arousal or coma (severe).
Triggers: increase in NH3 production (from dietary protein, GO bleed, constipation, infection) or decrease in NH3 removal(due to renal failure, diuretics, post-TIPS)
Treatment: lactulose (increase NH4+ generation), low-protein diet, and rifaximin (kills intestinal bacteria).
Hepatocellular carcinoma/hepatoma
most common primary malignant tumor of the liver in adults. Associated with hepatits B and C, Wilson disease, hemochromatosis, alpha1-antitrypsin deficiency, alcholic cirrhosis, and carcinogens (e.g. aflatoxin from aspergillus). May lead to Budd-Chiari syndrome.
Findings: jaundice, tender hepatomegaly, ascites, and anorexia. Spreads hematogenously.
Diagnose: increase alpha-fetoprotein; ultrasound or contrast CT;
Can get increased EPO causing polycythemia
Cavernous hemangioma
common benign liver tumor; typically occurs at age 30-50 years. biopsy contraindicated because of risk of hemorrhage
Hepatic adenoma
rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use; may regress spontaneously or rupture (abdominal pain and shock).
Angiosarcoma
Malignant tumor of endothelial origin; associated with exposure to arsenic, vinyl chloride (plastics industry, was used as a refrigerant in the past)
Highly aggressive tumor, comes from blood vessels,
Nutmeg liver
Due to backup of blood into liver. commonly caused by right sided liver failure and Budd-Chiari syndrome. The liver appears mottled like a nutmeg. If the condition persists, centrilobular congestion and necrosis can result in cardiac cirrhosis
Budd-Chiari syndrome
Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis, leading to congestive liver disease (hepatomegaly, ascites, abdominal pain, and eventual liver failure). May develop varices and have visible abdominal and back veins. Absence of JVD. Associated with hypercoagulable states, polycythemia vera, pregnancy, and HCC
alpha1-antitrypsin deficiency
misfolded gene product protein aggregates in the hepatocellular ER leading to cirrhosis with PAS + globules in liver. Codominant trait.
In lungs this causes uninhibited elastase in alveoli causing breakdown of elastic tissue leading to panacinar emphysema.
Jaundice
Abnormal yellowing of the skin and/or sclera. Due to bilirubin deposition. occurs at high bilirubin (>2.5 mg/dL) in the blood secondary to increased production or defective metabolism
Unconjugated (indirect) hyperbilirubunemia
increase urine urobilinogen
Disease that cause this: Hemolytic, physiologic (newborns), Criglar-Najjar, Gilbert syndrome
Conjugated (direct) hyperbilirubinemia
decreased urine urobilinogen
Biliary tract obstruction: gallstones, pancreatic liver cancer, liver fluke, can have increased conjugated billirubin in urine.
Biliary tract disease: primary sclerosing cholangitis, primary biliary cirrhosis
Excretion defect: Dubin-Johnson syndrome, Rotor syndrome
Mixed (direct and indirect) hyperbilirubinemia
Normal or increased urine urobilinogen
Hepatitis, cirrhosis
Physiologic neonatal jaundice
at birth, immature UDP-glucuronosyltransferase leads to unconjugated hyperbilirubinemia causing jaundice/kernicterus
Treat: phototherapy (converts unconjugated bilirubin to water-soluble form)
Gilbert syndrome
Mildly decreased UDP-glucuronosyltransferase conjugation activity leading to decreased bilirubin uptake by hepatocytes. Asymptomatic or mild jaundice. Elevated unconjugated bilirubin without overt hemolysis. Bilirubin increased with fasting, stress or infection (stressed medical student on the ward looking jaundice)
Crigler-Najjar syndrome
Type 1: Absent UDP-glucuronosyltransferase. Presents early in life; patients die within a few years. Findings: jaundice, kernicterus (bilirubin deposition in brain), increased unconjugated bilirubin. Treatment: plasmapheresis and phototherapy.
Type 2 is less severe and responds to phenobarbital, which increases liver enzyme synthesis.
Dubin Johnson syndrome
Conjugate hyperbilirubinemia due to defective liver excretion. grossly black liver. benign
Rotor syndrome
is similar to dubin johnson syndrome, but even milder and does not cause black liver
Wilson disease (Hepatolecticular degeneration)
Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin. Leads to copper accumulation. especially in liver, brain, cornea, kidneys, and joints.
Characterized by: decreased Ceruloplasmin, Cirrhosis, Corneal deposits (Kayser-Fleischer rings), Copper accumulation, Carcinoma (hepatocellular), Hemolytic anemia, Basal ganglia degeneration (Parkinsonian syndromes), Asterixis, Dementia, Dyskinesia, Dysarthria
Copper is Hella BADDD
Hemochromatosis
Hemosiderosis is the deposition of hemochromatosis is the disease caused by this iron deposition. Classic triad of micronodular Cirrhosis, Diabetes melitus (islet cells dysfunction), and skin pigmentation leading to bronze diabetes. Results in CHF, testicular atrophy, and increase risk of HCC. Disease may be primary (autosomal recessive) or secondary to chronic transfusion therapy (beta thalassemia major).
Increased ferritin, increase iron, decreased TIBC leading to increased transferrin saturation (>45% transferrin saturation is diagnostic).
Primary hemochromatosis genetics
Due to C282Y or H63D mutation on HFE gene. Associated with HLA-A3
Treatment of hemochromatosis
For hereditary: repeated phlebotomy, deferasirox, deferoxamine
Prussian blue stain
A stain to see iron. In hemochromatosis you take a biopsy, stain with prussian blue and see the iron.
Secondary biliary cirrhosis
Extrahepatic biliary obstruction (gallstone, biliary stricture, chronic pancreatitis, carcinoma of the pancreatic head) leads to increase pressure in intrahepatic ducts causing injury/fibrosis and bile stasis.
Presentation: pruritis, jaundice, dark urine, light stools, hepatosplenomegaly.
Labs: increased conjugated bilirubin, increased cholesterol, Increased ALP
Complicated by ascending cholangitis
Primary biliary cirrhosis
Autoimymune reaction leading to lymphocytic infiltrate + granulomas causing destruction of intralobular bile ducts.
Presentation: pruritis, jaundice, dark urine, light stools, hepatosplenomegaly.
Labs: increased conjugated bilirubin, increased (sometimes massively) cholesterol (can lead to xanthomas), Increased ALP
Increased Serum mitochondrial antibodies, including IgM. Associated with other autoimmune conditions (e.g. crest, sjogren, rheumatoid arthritis, celiac disease)
Primary sclerosing cholangitis
unknown cause of concentric “onion skin” bile duct fibrosis leading to alternating strictures and dilation with “beading” of intra- and extrahepatic bile duct on ERCP.
Presentation: pruritis, jaundice, dark urine, light stools, hepatosplenomegaly, no stones, 90% of patients have ulcerative colitis
Labs: increased conjugated bilirubin, increased cholesterol, Increased ALP
Hypergammaglobulinemia (IgM). Associated with ulcerative colitis. Can lead to secondary biliary cirrhosis and cholangiocarcinoma
Gallstone (cholelithiasis) caused by
increased cholesterol and/or bilirubin, decreased bile salts, and gallbladder stasis all cause stones
Cholelithiasis: cholesterol stones
radiolucent with 10-20% opaque due to calcifications
accounts for 80% of stones
associated with obesity, crohn disease, cystic fibrosis, advanced age, clofibrate, estrogen therapy, advanced age, clofibrate, estrogen therapy, multiparity, rapid weight loss, and native americican origin
Cholelithiasis: pigment stones
black, radiopaque, hemolysis; brown= radiolucent, infection
Seen in patients with chronic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.
Made of unconjugated bilirubin and small amount of cholesterol
Cholelithiasis: causes what conditions
Most often causes cholecystitis; also ascending cholangitis, acute pancreatitis, bile stasis
Also lead to biliary colic: Neurohumoral activation(e.g. by CCK after a fatty meal) triggers contraction of the gallbaldder, forcing stone into the cystic duct. amy present without pain (e.g. in diabetics)
Can cause fistula between gallbladder and small intestine, leading to air in the biliary tree. Gallstone may obstruct ileocecal valve leading to gallstone ileus.
Diagnosis and treatment of cholelithiasis
Dx: ultrasound
Treat with cholecystectomy is symptomatic
Cholecystitis
Acute or chronic inflammation of gallbladder. Usually from cholelithiasis; most commonly blocking the cystic duct leading to secondary infection; rarely ischemia or primary infection (CMV)
Murphy sign + which is inspiratory arrest on RUQ palpation due to pain. increase ALP if bile duct becomes involved (ascending cholangitis). Diagnose with ultrasound or HIDA
Porcelain gallbladder
calcified gallbladder due to chronic cholecystitis; usually found incidentally on imaging. Treatment: prophylactic cholecystectomy due to high rates of gallbladder carcinoma.
Acute pancreatitis: caused by
Autodigestion by pancreatic enzymes
Caused by GET SMASHED: Gallstones, Ethanol (#1 cause), Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hypercalcemia, Hypertriglyceridemia (>1000mg/dL), ERCP, Drugs
Acute hemorrhagic pancreatitis will leave soapy-chalky-white deposits which are from digestion of adipose tissue (fat necrosis)
Acute Pancreatitis: Clinical presentation and labs
Clinical presentation: epigastric abdominal pain radiating to back, anorexia, nausea
Labs: increased amylase, increased lipase (higher specificity)
Acute pancreatitis: can led to
Can lead to DIC, ARDS, diffuse necrosis, hypocalcemia (Ca2+ collects in pancreatic calcium soap deposits), pseudocyst formation, hemorrhage, infection, multiorgan failure
Complication: Pancreatic pseudocyst (lined by granulation tissue, not epithelium; can rupture and hemorrhage)
Chronic pancreatitis:
Chronic inflammation, atrophy, calcification, of the pancreas. Major causes are alcohol abuse and idiopathic. Can lead to pancreatic insufficiency causing steatorrhea, fat soluble vitamin deficiency, diabetes mellitus and increased risk of pancreatic adenocarcinoma. Amylase and lipase may or may not be elevated in chronic
Autodigestion can occur due to enzymes eating pancreas
Pancreatic Adenocarcinoma: Genetics, background
Prognosis averages 1 year; very aggressive tumor arising from pancreatic ducts (disorganized glandular structure with cellular infiltration); already metastasized at presentation; tumors more common in pancreatic head (causing obstructive jaundice). Associated with CA-19-9 tumor marker (also CEA, less specific)
Pancreatic Adenocarcinoma: presentation
Presents with Abdominal pain radiating to back, weight loss (due to malabsorption and anorexia), migratory thrombophlebitis-redness and tenderness on palpation of extremities (trousseau syndrome), obstructive jaundice with palpable nontender gallbladder (courvoisier sign)
Pancreatic Adenocarcinoma: Treatment
Treat: whipple procedure, chemo, radiation
Pancreatic Adenocarcinoma: Risk factors
Tobacco use, chronic pancreatitis, diabetes, age over 50, jewish and african males
Osmotic Laxatives
Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose.
MechanismL provide osmotic load to draw water out
Clinical use: constipation
Toxicity: diarrhea, dehydration; may be abused by bulimics
Lactulose: uses for it
osmotic laxatives
Also used to treat hepatic encephalopathy since gut flora degrade it into metabolites (lactic acids and acetic acid) that promote nitrogen excretion as NH4+
Infliximab
Mechanism: monoclonal antibody to TBF-alpha
Clinical use: crohn disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriasis
Toxicity: infection (including reactivation of latent TB), fever, hypotension
sulfasalazine, mesalamine, Olsalazine
Mechanism: a combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (Anti-inflammatory). activated by colinic bacteria
Clinical use: Ulcerative colitis, Crohn disease
Toxicity: malaise, nausea, sulfonamide toxicity, reversible oligospermia
Ondansetron
Mechanism: 5-HT3 antagonist; decreased vagal stimulation. Powerful central-acting antiemetic
Clinical use: control vomiting postoperatively and in patients undergoing cancer chemotherapy
Toxicity: headache, constipation
Keep on dancing with ondansetron
Metoclopramide
D2 receptor antagonist. increased resting tone, contractility, LES tone, motility. Does not influence colon transport time
Used for: diabetic and post-surgery gastroparesis, antiemetic
Toxicity: increased parkinsonian effects. restlessness, drowsiness, fatigue, depression, nausea, diarrhea. Drug interaction with digoxin and diabetic agents. Contraindicated in patients with small bowel obstruction or Parkinson disease (D1 receptor blockade).
Docusate
anionic surfactant (surface active agent) reduces surface tension at oil-water interfaces of feces, allows water and lipids to penetrate feces Is a stool softener, given with meds that cause constipation
Ursodiol
for medical, non surgical, treatment of cholelithiasis
reduces cholesterol synthesis and secretion in bile duct, allowing for the cholesterol stone the chance to dissolve. Usually combined with lithotripsy.
Prochloperazine
Blocks dopamine receptors, antiemetic
Toxicity: parkinsonian symptoms
elevated alkaline phosphatase is a sign of
bile duct/bile tree injury. enzyme found in these cells.
Ulcerative colitis and Crohns disease: what is the link
There is an unknown genetic link. If a first degree relative has one of these two diseases you are at a higher risk of getting either one! They think the diseases are similar just on opposite ends of a spectrum. Look for that Rectal sparing in crohn and rectal involvement in ulcerative colitis.
Cacinoid tumor
Most commonly in the small bowel, grows as a submucosal polyp like nodule
Made of a proliferation of neuroendocrine cells, low grade malignancy
Positive for chromogranin
Secretes serotonin, which is degraded by the liver into 5-HIAA and nothing bad happens
However, if it has a metastasis at or beyond the liver, then you get carcinoid syndrome
Carcinoid syndrome
Due to serotonin
bronchospasm, diarrhea, flushing of skin
Can be triggered by alcohol or emotional stress which stimulates serotonin release
Carcinoid heart disease
Right sided heart valvular fibrosis (increased collagen) leading to tricuspid regurgitation and pulmonary valve stenosis; right heart valves fine due to presence of MOA in lungs which degrades serotonin.
jaundice with w/ painless palpable gall bladder, no liver tenderness
Think pancreatic carcinoma in the head of pancreas
May obstruct common bile duct leading to increase in alkaline phosphatase and gamma glutamyl transferase
Ca-19-9 positive in most patients but some patients cannot make this protein (better used for following patients than diagnosing)
meconium ileus
First manifestation of cystic fibrosis and happens in neonates
get obstruction in bowel and unable to pass stool/meconium
See air-fluid levels on imaging which is a sign of obstruction
Can cause perforations and peritonitis
Intraperioneal calcifications may be seen on plain films
Give enema and drain the blockage
sublingual gland composition
mostly mucous acini
submandibular gland composition
mixed mucous and serous acini
parotid gland composition
mostly serous acini and fat
