GI Flashcards
The digestive tube is derived from what embryonic structure?
the yolk sac (later endoderm)
the lining of the GI tract and visceral organs is derived from which primary germ layer?
endoderm; GI epithelium, glands; many organs bud off: liver, pancreas and trachea
The stroma (CT) and muscles of the GI tract are derived from which primary germ layer?
mesoderm; stroma, muscles, peritoneum and spleen
The IMA is derived from which embryonic structure?
hindgut; transverse colon to rectum
The transverse colon to the rectum is supplied by which artery and is derived from what embryonic structure?
the IMA and the hindgut
The SMA is derived from which embryonic structure?
midgut; ampulla of vater to the transverse colon
the ampulla of vater to the transverse colon is supplied by which artery and is derived from what embryonic structure?
the SMA and the midgut
The celiac trunk is derived from which embryonic structure?
the foregut; mouth (oral cavity) to the ampulla of vater
The mouth (oral cavity) to the ampulla of vater is supplied by which artery and is derived from what embryonic structure?
the foregut and the celiac trunk
Mesentery is derived from which germ layer?
mesoderm
Dorsal mesentery
greater omentum; gut moves away from posterior wall in development and covers most abdominal structures
Structures that the ventral mesentery cover?
the lesser omentum and falciform ligament; bottom of the esophagus, stomach and upper duodenum; liver grows into it; derived from the septum transversum
ventral mesentery are what structures in an adult?
lesser omentum and falciform ligament; derived from the septum transversum
What structure divided the foregut structures (respiratory diverticulum which forms the lung buds and the esophagus)?
tracheoesophageal septum; abnormal septum development leads to esophageal atresia (closed esophagus) when the septum deviates posteriorly
Characteristic findings in a neonate with esophageal atresia
esophagus does not connect to stomach, fetus will not be about to swallow fluids leading to polyhydramnios; when born baby will present with drooling, choking and vomiting (unable to swallow secretions building up in oral cavity); diagnosis with NG tube unable to go into stomach because of closed cavity
Physiology herniation of the midgut
6th week of development, abdomen becomes too small so intestines herniate through umbilical cord; visible on fetal ultrasound; reduction of herniation by 12th week
Omphalocele vs Gastroschisis
both are pediatric abdominal wall defects
- omphalocele - abnormal rotation of the midgut; contents will be covered by peritoneum (membrane) and will be midline
- gastroschisis - full thickness abdominal wall defect; contents will NOT be covered by membrane, elevated maternal AFP because it leaks out, and will be paraumbilical (typically to the R) - note that insertion site is usually normal and separate from the defect
omphalocele
pediatric abdominal wall defects; abnormal rotation of the midgut; contents will be covered by peritoneum (membrane) and will be midline
associated congenital abnormalities to omphalocele
trisomy 21 (few associated abnormalities with gastroschisis)
gastroschisis
full thickness abdominal wall defect; contents will NOT be covered by membrane, elevated maternal AFP because it leaks out, and will be paraumbilical (typically to the R) - note that insertion site is usually normal and separate from the defect; pt will later have poor GI function after repair
the midgut rotates around what structure in development?
the SMA
Where should the cecum be located after midgut rotation has taken place?
cecum should be in right lower quadrant where it is normally located
malrotation of the midgut can lead to what defect?
volvulus - small bowel twist around SMA, there is vascular compromise leading to ischemia; presents with vomiting, sepsis, distended abdomen and blood in stool; tx w urgent surgery
L sided colon (cecum) can develop from which malformation?
malrotation of the midgut during development
persistence of the vitelline duct results in what abnormality?
Meckel’s diverticulum - outpouching or “bulging” that occurs at the ileum
Meckel’s diverticulum
outpouching or “bulging” that occurs at the ileum; formed due to the persistence of the vitelline duct (disappears by week 9); known as a TRUE diverticulum because contains ALL layers of the bowel (mucosa, submucosa and muscular); contain ectopic gastric tissue - can be diagnostic using a technetium scan
Rule of 2’s
Meckel’s diverticulum; occurs in 2% of the population, male to female ratio is 2:1, located within 2 feet from the ileocecal valve and usually 2 inches in size
duodenal atresia
most common type of GI atresia; results in failed “recanalization”; associated with Down syndrome; can see the Double Bubble Sign on imaging - dilation of duodenum and stomach with a tight pylorus in the middle
jejunal-ileal-colonic atresia
causes due to vascular disruption leading to ischemic necrosis that is reabsorbed and a blind end of the bowel is left; “apple peel atresia” - bowel distal to blind end may be curled
pyloric stenosis
hypertrophy of the pyloric leading to stenosis; projectile “non-bilious” vomiting; olive mass felt on palpation; usually in first born children
spleen embryology
arises from dorsal mesodermal tissue; NOT from endoderm!!; blood supply is the celiac trunk; gastrosplenic ligaments carries the short gastric arteries and the left gastric epiploic vessels
If there is a IVC or abdominal aorta rupture where would blood pool?
in the back of the abdomen - retroperitoneal bleeding; they are retroperitoneal strcutres along with the kidneys, 2nd/3rd parts of duodenum, ascending/descending colon, part of the rectum and head and body of the pancreas
Pectinate line
part of the anal canal
above the line - derived from the hindgut; columnar epithelium simulator to stomach; supplied by superior rectal artery (branch of IMA); venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids; lymph drainage of internal iliac nodes
below the pectinate line - derived from proctoduem (ectoderm); stratified squamous epithelium similar to skin; supplied by inferior rectal artery (to internal pudenal to internal iliac to IVC); lymph drainage is superficial inguinal nodes; painful external hemorrhoids
above the pectinate line
derived from the hindgut; columnar epithelium simulator to stomach; supplied by superior rectal artery (branch of IMA); venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids; lymph drainage of internal iliac nodes
portal HTN affects what part of the pectinate line?
above the pectinate line; venous drainage is superior rectal veins (IMV to portal system); can swell in portal HTN and lead to internal hemorrhoids
below the pectinate line
derived from proctoduem (ectoderm); stratified squamous epithelium similar to skin; supplied by inferior rectal artery (to internal pudenal to internal iliac to IVC); lymph drainage is superficial inguinal nodes; painful external hemorrhoids
lymph drainage above the pectinate line
nternal iliac nodes
Imperforate anus
handout and ectoderm meet to form anus but there is an absence of an anal opening; commonly associated with GU malformations (renal agencies and bladder exstrophy); baby will fail to pass meconium; can be a urethra or vagina fistula present
3 main branches of the celiac trunk
common hepatic, left gastric and splenic
the right gastric arteries originates from which artery?
the proper hepatic artery, which comes from the common hepatic artery which is one of the 3 branches off of the celiac trunk
The 2 most common perforated ulcers and their bleeding source
gastric ulcers at the lesser curvature of the stomach - bleeding from left gastric artery (celiac trunk)
posterior duodenal ulcers - bleeding from gastroduodenal artery ( branch off common hepatic artery - celiac trunk)
Short gastric arteries
branches of the splenic artery (celiac trunk); supply funds and upper cardiac portions of the stomach; vulnerable to ischemia if splenic artery is occluded; no dual blood supply
Pringle’s maneuver
clamping of the hepatoduodenal ligament in the OR to find the source of bleeding in a pt with internal hemorrhaging; used to control liver bleeding (via portal vein or proper hepatic artery), if bleeding continue then most likely IVC or hepatic veins
the 3 structures contained within the hepatoduodenal ligament?
part of the lesser omentum; contains the common bile duct, the portal vein and proper hepatic artery
SMA syndrome
rare cause of bowel obstruction; SMA can press downward and obstruct the duodenum leading to obstruction; classic pt - recent massive weight loss (fat pad shrinks)
dual blood supplies (abdominal collaterals) of the celiac trunk and the SMA
protects against ischemia if one is occluded; via superior and inferior pancreaticoduodenal arteries - supplies the duodenum and pancreas
dual blood supplies (abdominal collaterals) of the SMA and the IMA
protects against ischemia if one is occluded; via marginal artery of Drummond
dual blood supplies (abdominal collaterals) of the IMA and the iliac artery
protects against ischemia if one is occluded; via superior rectal and middle rectal arteries; rectal ischemia occlusion is RARE
pt with belly pain from ischemic colitis, where should you look next?
check the heart for A Fib - mostly caused by emboli from cardiac origin - typically affect jejunum the most due to traveling to the SMA; don’t look for somewhere in the abdomen; pt will have “pain out of proportion to exam” and occult blood in stool
Watershed areas of the colon
- splenic flexure - marginal artery of Drummond - vulnerable to under perfusion
- Rectosigmoid junction - narrow branches of IMA
Chronic mesenteric ischemia
intestinal angina; usually older pt with vascular dz; they have recurrent abdominal pain after eating so develops a fear of eating that results in weight loss; they will have sudden worsening on top of history of recurrent pain and may suggest acute thrombosis
Submucosa of the GI
CT that contains the meissner’s plexus - clinical correlation to Hirschsprung’s disease (missing this layer - aganglionic)
Auerbach’s plexus is found in which layer of the GI tract?
controls GI motility; in the muscular layer between the inner and outer muscular layers; controls peristalsis; abnormality can lead to achalasia (esophagus) and also absent in kids with Hirschsprung’s dz
epithelium of esophagus
non-keratinized stratified squamous epithelium; esophagus is the collapse structure filled with air behind the trachea on the CAT scan
epithelium of stomach
simple columnar epithelium; you will see gastric pits and gastric glands
histology of the small intestine; simple columnar epithelium; villi - MUCOSA extensions (finger-like) into the lumen - increase SA for absorption; crypts of Lieberkuhn - contain goblet cells; microvilli - microscopic extensions- epithelial cell membrane
the villi of the small intestines are extensions of what layer?
extensions of the mucosa layer into the lumen; increases surface area for absorption
Plicae circulares
folds of mucosa and submucosa found throughout the small intestines (most abundant in jejunum); increases surface are for absorption
Brunner’s Glands
only found in duodenum in the submucosa; produces alkaline fluid to protect from acidic stomach fluid; will be increased thickness in PUD
Peyer’s patches
lymph cell aggregates found in ileum; contain M cells collect antigens and presents the to initiate an immune response
Slow waves of the GI tract
maximum # of contractions per time
Stomach 3/min
Duodenum 12/min
ileum 8/min
Sphincter of Oddi dysfunction
narrowing that can occur after pancreatic or gallstone disease, contents (pancreatic enzymes and bile) are unable to be released via the Ampulla of Vater; presents with episodic RUQ pain and can see recurrent pancreatitis due to buildup of pancreatic enzymes
Sphincter of Oddi dysfunction
narrowing that can occur after pancreatic or gallstone disease, contents (pancreatic enzymes and bile) are unable to be released via the Ampulla of Vater; presents with episodic RUQ pain and can see recurrent pancreatitis due to buildup of pancreatic enzymes
Sphincter of Oddi Spasm
smooth muscle contractions caused by opioids (morphine); drug of choice in patients with pancreatitis is Meperidine (Demerol) because believed to not cause muscle spasms
the portal triad consists of what 3 vessels?
portal vein, hepatic artery and bile duct
Which hepatic zone is affected by viral hepatitis first?
zone 1 - right next to the portal blood coming from the intestines
Which hepatic zone is affected by ischemia first?
zone 3 furthest away from the hepatic artery
Pancreas embryology
two buds from foregut - ventral and dorsal - retroperitoneal organ (secondarily)
ventral - main pancreatic duct, part of head and uncinate process
dorsal - body, tail, accessory duct and the rest of the head
Annular pancreas
ventral bud fuse around the duodenum (ring of pancreatic tissue) and causes bowel obstruction; presents distention and abdominal pain
pancreas Divisum
dorsal and ventral ducts to not fuse leading to 2 senate ducts; often asymptomatic but can cause pancreatitis
Ampulla of Vater
where biliary and pancreatic ducts merge; empties into major duodenal papilla; anatomical transition from foregut to midgut; celiac trunk transitions to SMA
the 3 main salivary glands
submandibular glands
sublingual gland
parotid gland
submandibular glands
AKA Wharton’s duct; located at floor of the mouth;
sublingual gland
located at floor of the mouth
parotid gland
located behind angle of the jaw below and in front of ears;
saliva contains a large amount of which antibodies
IgA antibodies; also lysozymes - disrupt bacterial cell walls and lactoferrin - prevent bacterial growth
saliva contains a large amount of which antibodies
IgA antibodies; also lysozymes - disrupt bacterial cell walls and lactoferrin - prevent bacterial growth also found in breastmilk)
Sjogren’s disease
autoimmune dz resulting in loss of saliva leading to infections and dental carries (cavities)
Saliva electrolytes
becomes hypotonic as it travels passed the ductal cells (secreted as isotonic by acinar cells) due to the removal of Na and Cl and addition of K+ and HCO3
regulation of saliva
increased by both sympathetic (smaller effect) and parasympathetic (major effect) - M1 and M3 receptors; also activated by food smell and sight
muscarinic antagonist on saliva
causes dry mouth; atropine, scopolamine - motion sickness
muscarinic agonists on saliva
increase saliva production; pilocarpine (use in Sjögren’s syndrome - causes excessive sweating) and organophosphate poisoning - nerve gas or famers exposed to pesticides
Sialadentitis
inflame of salivary gland usually secondary to an obstructing stone (sialolithiasis) most often to Staph aureus or anaerobes; treatment is Nafcillin (stop coverage) or Metronidazole or Clindamycin (anaerobes)
Mumps
caused by RNA mumps virus; largely prevented by MMR vaccination; key feature is parotitis - often b/l leading to facial swelling
Pleomorphic adenoma
most common salivary tumor mainly affecting the parotid gland; benign mixed tumor (BUZZWORD: epithelial and storm tissue cells) with rare malignant transformation; painless mobile mass at the angle of the jaw
Warthin’s Tumor
2nd most common salivary tumor mainly affecting the parotid gland; AKA papillary cyst adenoma lymphomatosum; key risk factor is SMOKING 8x); key findings - presence of cyst filled fluid that are surrounded by dense lymphoid infiltrates and this lymph tissue can aggregate into germinal centers
Mucoepidermoid carcinoma
most common malignant salivary tumor; risk factor of prior radiation (child w lymphoma that was treated w radiation); occur in parotids; can cause facial nerve paralysis; look for squamous (epidermoid) cells AND mucus screwing cells
femoral triangle borders
superior - inguinal liagment
medial - adductor longus
lateral - sartorius
Femoral vessels
lateral to medial - “NAVeL”
nerve, artery (pulse), vein and then lymphatics
Contents of femoral sheath
below the inguinal ligaments; contains the femoral vein, artery and ring (opening to femoral canal) NOT the nerve
the 3 fascial layers of the spermatic cord
external spermatic fascia, cremasteric fascia and internal spermatic fascia
Inguinal contents in males vs females
males - spermatic cord
females - round ligament
Indirect inguinal hernia
“indirectly” through abdominal wall; LATERAL to epigastric vessels; covered by all layers of the spermatic fascia; due to congenital defect that causes bowel to protrude through the processes vaginalis (should have closed after the descent of the testes - to become tunica vaginalis testis); defect more common on the R
typically pt that presents with an indirect hernia
males are most common; adulthood pt who are heavy lifters (contraction workers) or straining (constipation) and newborns on mechanical ventilation
Key points on indirect inguinal hernias
Direct inguinal hernias
bowels bulges “directly” through the abdomen wall through Hesselbach’s triangle; MEDIAL to epigastric vessels; through the external ring; only covered by external spermatic fascia only and never bulges into the scrotum; usually older man of years of CT stress
Borders of Hesselbach’s triangle
inguinal liagment
inferior epigastric vessels
rectus abdominis
on the floor is the transversals fascia
Borders of Hesselbach’s triangle
inguinal liagment
inferior epigastric vessels
rectus abdominis
on the floor is the transversals fascia
Femoral hernias
herbal through the femoral ring medial to the femoral vessels; protrudes through the inguinal ligament; more common in women (but indirect is MOST common for both genders); high risk of incarceration - bowel trapped in hernia sac - can lead to strangulated (blood flow cut off and bowel becomes ischemic and necrotic)
Hiatal hernias
hernia where stomach herniates into the thorax leading to GERD; major risk factor is obesity; most common is the sliding hiatal hernia (95%); both due to phrenoesophageal membrane - laxity in sliding and defect (hole) in paraesophageal
sliding hiatal hernia
most common type of hiatal hernia; displacement of the GE junction above the diaphragm; funds remains below the GE junction; gives “hourglass” appearance on imaging
sliding hiatal hernia
most common type of hiatal hernia; displacement of the GE junction above the diaphragm; funds remains below the GE junction; gives “hourglass” appearance on imaging
CDH - Congenital diaphragmatic hernia
development defect in diaphragm - pleuroperitoneal membrane; basically a hole in the diaphragm; abdominal organs protrude into chest resulting in pulmonary hypoplasia; often fatal
GI barium contract showing and “hour-glass” appearance seen with a sliding hiatal hernia; protrusion of the stomach through the diaphragm into the thoracic cavity
Splenic vein thrombosis
splenic vein runs along the posterior surface of the pancreas and develop a clot from pancreatic inflammation (as in pancreatitis); short gastric vein drains fungus of stomach; splenic vein thrombosis can increase pressure in short gastric veins and cause gastric varies ONLY in the fundus; stomach and esophagus are spared
Meckel diverticulum; intestinal outpouching shows gastric mucosa due to failure of the vitelline duct to obliterate; various ectopic (heterotopic) tissues can be present - most common is gastric tissue - can secrete HCl and pt will present with lower GI bleeding and anemia
surgical landmark in removal of the appendix
pt with appendicitis - during the procedure, the tenure coli can be used as a surgical landmark - following it to its origin at the cecal base
External hemorrhoids
below the pectinate line; covered by squamous epithelium and have cutaneous innervation from the inferior recta nerve - branch off the pudendal nerve; sensitive to touch, temperature and pain
Internal hemorrhoids
above the pectinate line; covered by columnar epithelium; have autonomic innervation from inferior hypogastric plexus - only sensitive to stretch and NOT pain, temperature or touch
Which part of the GI is ALWAYS involved in Hirschsprung disease?
rectum is always involved - neural crest cells migrate caudally; newborn will fail to pass meconium within 48 hours of birth
Stool incontinence
internal and external sphincter or more commonly the puborectalis muscle fails to relax resulting in chronic constipation
Retroperitoneal organs
SAD PUCKER
Retroperitoneal hematomas
commonly associated with blunt abdominal trauma and typically reflect injury to retroperitoneal organs; pancreatic injury a frequent cause - high-riding seat belt; can lead to life-threatening blood loss
Pernicious anemia
autoimmune disorder involving cell-mediated destruction of parietal cells predominantly found in the upper glandular layer of the gastric body and fundus
Which two structures are added to cholic acid in conjugation to make it a better surfactant ?
taurine - an organic acid - this forms taurocholic acid
glycine - an amino acid - this forms glycocholic acid
what is the rate limiting enzyme in the synthesis of bile acid?
7 alpha hydroxylase (classic pathway - P450 enzyme - requires NADPH and O2); converts cholesterol to 7-alpha hydroxycholesterol which later turns into cholic acid - a major form of bile acid
Enterohepatic circulation of bile acids
most lipid absorption occurs in the jejunum (conjugated BA not absorbed); bile salts remain behind and are passed to distal small intestine and absorbed by active transporters in the terminal ileum (95%); the rest are secreted in the stool - a way cholesterol is excreted from the body
Main mechanism in which cholesterol is secreted from the body?
excreted in stool; cholesterol is NOT water soluble so can’t be passed in the urine; cholesterol drugs such as bile acid resins will encourage more excretion in stool by preventing bile reabsorption (largely replaced by statins)
Antimicoribal effects of bile salts
disrupts bacterial cell membranes
Cholestasis
disrupted bile flow to the intestines; lab findings - direct hyperbilirubinemia and elevated alkaline phosphatase; symptoms - jaundice, pruritus (itching due to bile salts in skin), dark urine, clay colored stools no stercobilin); can lead to fat malabsorption and decrease fat soluble vitamins
Alkaline phosphatase
alk phos - produced by the bile duct epithelial cells; obstruction of bile flow will cause increase all phos synthesis - you will see a more elevated alk phos than AST/ALT in cholestasis because the primary site of dysfunction is the bile ducts
patterns of bile/liver damage
example 1 - AST/ALT are 2x norm limit but alk phos is about 5x normal limit - cholestatic pattern (gallstone)
example 2 - AST/ALT 10x norm limit and alk phos 2x norm limit - hepatocellular pattern (cirrhosis)
magnitude of liver function test
rises in AST and ALT; only about 2 causes of 10,000 rise in these enzymes - a shock liver and acetaminophen toxicity
best first test in a pt with cholestasis?
RUQ ultrasound; differentiates extrahepatic (dilated bile ducts) from intrahepatic (normal bile ducts)
Intrahepatic cholestasis of pregnancy ICP
sometimes called pruritus gravidarum; reversible form of cholestasis (lack of bile flow) that affects women in 2nd and 3rd trimesters; believed to be caused by elevated estrogen and progesterone levels decreasing bile flow in the liver
Heme is converted to biliverdin via which enzyme?
heme oxygenase - turns it green color
Biliverdin is metabolized by which enzyme into bilirubin?
biliverdin reductase - turns it brown/yellow color
unconjugated bilirubin (carried by albumin in the blood) in converted to conjugated bilirubin via which enzyme?
UDP glucuronyltransferase (UGT); converts bilirubin from insoluble to soluble
bacterial enzyme in the small intestine that converts conjugated bilirubin back into the unconjugated form?
bacterial beta-glucuronidase; this unconjugated bilirubin is converted into urobilinogen
fate of urobilinogen?
fate 1 - excretion in the feces as stercobilin (90%); makes stool dark
fate 2 - reabsorbed by intestines, converted to urobilin and excreted in urine (10%); makes urine yellow
fate of bilirubin
direct and indirect bilirubin
Van den Bergh reaction
direct - measurement of conjugated bilirubin
indirect - measurement of unconjugated bilirubin
dark urine
seen in elevated conjugated bilirubin; also seen in rhabdomyolysis (breakdown of skeletal muscle), hematouria and dehydration (common)
the 6 special causes of hyperbilirubinemia?
- Rifampin/Probenecid
- Gilbert’s Syndrome
- Crigler-Najjar Syndrome (more severe Gilbert’s)
- Dubin-Johnson Syndrome
- Rotor’s Syndrome (milder form of Dubin-Johnson)
- Neonatal jaundice
Rifampin/Probenecid cause of hyperbilirubinemia
Rifampin (antibiotic commonly used to treat TB) and Probenecid (used to treat gout); both compete with bilirubin for uptake of the liver; causes an increase with unconjugated bilirubin but all LFTs will be normal - look at the pt meds list
pt present with elevated unconjugated bilirubin levels after being successfully treated w gout or TB, but all other LFT are normal.
first thing you should do is look at med list; Rifampin (antibiotic commonly used to treat TB) and Probenecid (used to treat gout); both compete with bilirubin for uptake of the liver; causes an increase with unconjugated bilirubin
Gilbert’s Syndrome cause of hyperbilirubinemia?
there is decrease UGT function (defect in UGT promoter gene); when there is an increased bilirubin production due to stress, menses, illnesses or fasting - pt can present w jaundice; no serious consequences
Crigler-Najjar Syndrome cause of hyperbilirubinemia?
more severe form of Gilbert’s Syndrome; severely reduced/absent UGT enzyme; pt cannot conjugate bilirubin; type 1 presents in infancy and often fatal due to kernicterus (neurotoxin - basal ganglia and brain stem nuclei); type 2 is less severe - tx with phenobarbital or clofibrate
Dubin-Johnson Syndrome cause of hyperbilirubinemia?
causes CONJUGATED hyperbilirubinemia; defective liver excretion; abnormal gene that codes for multi drug resistance proteins (MRPs) that is necessary for bilirubin excretion to bile; BLACK LIVER - benign condition and no tx necessary
Neonatal Jaundice
takes about 14 weeks for UGT to reach adult level of function; results in increased unconjugated bilirubin that can lead to kernictrus; preterm babies are most at risk; tx w phototherapy (converts bilirubin to lumirubin - more water soluble - excretion w/o conjugation)
Where are parietal cals found in the stomach?
in the gastric glands; more so in the upper layers
Gastrin binds to which receptor on parietal cells to activate the secretion of HCl?
CCKb; gastrin is released from G cells found in the mucosa of the antrum (distal) in the stomach
Why is it that if you block acetylcholine release (w atropine), you will not block the vagus nerve input on the stomach?
the vagus nerve at the stomach does NOT secrete Ach, instead secretes gastrin releasing peptide (GRP); activated G cells to secrete gastrin; so tx with vagotomy rather than atropine
Why does the bicarbonate levels in serum rise slightly after someone has just eaten a meal?
due to the alkaline tide; H+ needed to for HCl production in the stomach releases HCO3 as a by product that is secreted in the serum
Why does vomiting produce metabolic alkalosis with low urinary chloride
you are losing lots of HCl so Cl will be low; there will be an increased production of HCl by parietal cells (if urinaryl Cl is high then think diuretic use); bicarb will build up in the serum as a byproduct causing a metabolic alkalosis
young women with an unexplained metabolic alkalosis, she has low urinary chloride, what should you suspect as her diagnosis?
surreptitious vomiting; loss of HCl from stomach so the HCl production will be increased and this will generate lots of bicarb in the serum (alkaline tide) causing metabolic alkalosis
Second messengers on parietal cells
Ach and Gastrin - Gq with PLC/IP3/Ca2+
Histamine, Somatostatin and PGE’s - Gs with AC/cAMP
Which amino acids can stimulate gastric release in the stomach?
phenylalanine and tryptophan
Gastrinoma
Zollinger-Ellison syndrome; gastric secreting tumor that occurs in the duodenum or pancreas (G cells are found in the pancreas in fetus); excessive acid secretion of acid and hypertrophy/hyperplasia of the mucosa; presents w abdominal pain and diarrhea; may see distal duodenal ulcers (far beyond where most ulcers are seen)
treatment for a gastrinoma
Octreotide (somatostatin) - inhibits gastrin release; high does PPI’s (omeprazole, lansoprazole, pantoprazole) or surgical excision
Pernicious anemia
autoimmune gastritis; loss of parietal cells; loss of intrinsic factor so cannot absorb B12; high gastrin levels are a typical finding along with G-cell hyperplasia
Cholecystokinin (CCK)
stimulated by FA’s and monoglycerides (NOT triglycerides) released by I cells in the small intestine; hormone for gallbladder contraction and pancreatic enzyme secretion; makes the sphincter of Oddi to relax
HIDA scan
Hepatic iminodiscetic acid (HIDA) scan; often done when a pt has RUQ pain and a US is non-diagnostic such as with gallstones; sometimes CCK is administered for gallbladder ejection fraction determination
Secretin
released by S cells of the duodenum; increases HCO3 in pancreatic duct cells to neutralize gastric acid in the small intestine (increases pH); used as a secretin stimulation test in gastrinoma
Why is oral glucose metabolized faster than IV glucose?
because of the GIP (glucose-dependent insulinotropic peptide) hormone; stimulated by glucose, FA’s and AA’s (only one stimulated by all 3); stimulates insulin release from pancreas; IV glucose does not stimulate GIP release (does not go through the intestines)
VIP
Vasoactive Intestinal Peptide; its a neurocine (synthesize by neurons); relaxation of smooth muscles; raises pH and inhibits gastrin; can cause a tumor - VIPoma
VIPoma
VIP from islet cells in the pancreas; presents with a watery diarrhea, tea-colored odorless diarrhea (resembles cholera sometimes called the pancreatic cholera syndrome); pts will have hypokalemia and achlorhydria (absences of gastric acid)
VIPoma
VIP from (increases pH) islets cells in pancreas; presents with a watery diarrhea, tea-colored odorless diarrhea (resembles cholera sometimes called the pancreatic cholera syndrome); pts will have hypokalemia and achlorhydria (absences of gastric acid)
WDHA syndrome
watery diarrhea, hypokalemia and achlorhydria as seen in a VIPoma
adults (30-50 yrs) with long-standing diarrhea (no blood or pus), no response to diet changes and endoscopic sampling shows elevated pH in the stomach
VIPoma - VIP secreting tumor of islet cells of the pancreas; there will be elevated VIP on serum testing; no response to diet changes eliminates lactose intolerant; tx with Octrotide (somatostatin)
Which antibiotic can be used to treat gastroparesis (as seen in diabetes) and why?
Erythromycin - because it binds to motilin receptors in the stomach, intestine and colon; promotes motility in the fasting state
GERD
decreased lower esophageal sphincter (LES) that allows gastric juice to back flow into the esophagus; causes reflux esophagitis; classic history findings - basal zone hyperplasia, lamina propria papilla elongate and increased eosinophils (do not confused and think it is an allergic rxn)
Histamine H2 blockers
Famotidine, Ranitidine, Nizatidine, Cimetidine; all block histamine receptors on parietal cells; used in GERD
Proton Pump Inhibitors (PPI’s)
Omeprazole, Pantoprazole, Lansoprazole, Esomeprazole; inhibit H+/K+ pump on parietal cells; used in GERD
Ingestion of Lye
alkali substances that contain Na+ or KOH - found In household cleaners; typically invested accidentally by children; rapidly injuries wall of esophagus and causes liquefactive necrosis; child usually recovers but can result in strictures that lead to dysphagia
Barrett’s Esophagus
METAPLASIA of the esophagus due to long-standing GERD; diagnosed with endoscopy; can lead to esophageal cancer
Esophageal Cancer
two types - SCC - upper esophagus - **hoarse voice and cough (most common worldwide) and adenocarcinoma - distal esophagus (more common w GERD); both have increased risk with smoking and present with “progressive dysphagia” - solids and then liquids as tumor grows;
Lymph nodes with esophageal cancer
Upper esophagus (neck) - as seen in SCC esophageal cancer - cervical lymph nodes
Middle esophagus (chest) - mediastinal and tracheobronchial nodes
Lower esophagus (abdomen) as seen in adenocarcinoma of the esophagus - celiac and gastric nodes
Esophagitis of infectious causes
Candida - white membranes and pseudohyphae on biopsy
HSV-1 - causes oral herpes, can involve esophagus and present with “punched out” ulcers
CMV - AIDS pt (CD4 <50) and linear ulcers
pt presents with dysphagia, GERD treatments are not working and predominance of eosinophils on biopsy
Eosinophilic esophagitis - allergic rxn of unknown antigen; immune-mediated; MUST EXCLUDE GERD
Achalasia
inability to relax lower esophageal sphincter (LES); loss of ganglion cells in Auerbach’s plexus (muscular layer); often idiopathic but can be caused by Chana’s Disease - protozoa: Trypanosoma cruzi; pt suffers from bad breath
Esophageal varices
dilated submucosal veins (usually lower 1/3rd - left gastric veins) typically due to portal HTN; tx w/ emergent endoscopy for banding/ligation
Mallory-Weiss Syndrome
esophageal mucosa damage at the GE junction; causes PAINFUL hematemesis; caused by severe chronic vomiting - alcoholism or bulimia
BoerHaave Syndrome
more severe than Mallory-Weiss Syndrome; transmural rupture of the esophagus and air is able to exit the esophagus; can see air in mediastinum on cxr “pneumomediastinum” and air under the skin in the neck ** subcutaneous emphysema! - when you press on the skin you can hear bubbling and cracking from the air underneath the skin
Schatzki Ring
ring at the squamocolumnar junction in the esophagus; common cause of dysphagia to solids; located usually lower esophagus
Triad of Plummer-Vinson Syndrome
iron deficiency anemia
beefy red tongue
esophageal web
-common in middle-age white women
Zenker’s Diverticulum
a false diverticulum (does not contain all layers; not the muscular layer); chronic swallowing that occurs at the esophagus and pharynx junction problem due to **cricopharyngeal muscle failure to relax; classic located at the **Killian’s Triangle; pt presents w/ dysphagia and halitosis
Gamma-glutamyl transpeptidase (GGT)
liver function test similar to alkaline phosphatase (alk phos) but is not elevated in bone disease unlike alk phos; used to determine the origin of elevated alk phos; if both are elevated then there is a hepatobiliary cause to the elevated alk phos; also elevated after heavy alcohol consumption
Alcoholic Fatty Liver Disease
accumulation of FA’s in liver; usually asymptomatic, may cause hepatomegaly; abnormal AST>ALT; often reversible w/ cessation of alcohol but increased risk of cirrhosis w/ continued use; zone 3 (centrilobular) most at risk
Non-Alcoholic Fatty Liver Disease
fatty liver not due to alcohol; NASH - fat and inflammation; ALT>AST (contrast with alcoholic liver dz AST>ALT); associated with obesity; improves w/ weight loss
Acute Hepatitis
classically after heavy, binge drinking on top of a long hx of alcohol consumption; toxic effects from buildup of **actealdehyde!; there is damage of **intermediate filaments that gives the appearance of **Mallory bodies
pt goes out on a big binge drinking of alcohol then presents with fever, jaundice and RUQ pain/tenderness
Acute Hepatitis; toxic effects from buildup of **acetaldehyde!; there is damage of **intermediate filaments that gives the appearance of **Mallory bodies
Reye’s Syndrome
rare cause of liver failure and encephalopathy in children with viral infections (chicken pox - varicella zoster/ influenza B) who take aspirin to tx their infection; they present w/ rapid serve liver failure; aspirin **inhibits beta oxidation; AVOID aspirin in children
Staining of the liver in a alpha-1 anti-trypsin (AAT) pt
Liver abscess; walled-off infection of the liver; usually bacteria in the US 80% of cases (Staph aureus - hematogenous route; entamoeba histolytica (protozoa) - ascends through biliary tree - transmitted from contaminated water - bloody diarrhea as well; Echinococcus (helminth) - fecal/oral transmission of eggs - will show massive liver cysts
Autoimmune Hepatitis
autoimmune inflammation of the liver; most common in women in their 50s/60s; most specific antibody test - Anti-smooth muscle antibodies (ASMA); tx w/ steroids and immunosuppressants
Liver cirrhosis
shrunken liver that is replaced by fibrosis tissue and nodules; hyperammonemia (elevated ammonium levels can lead to neurotoxicity - asterixis, confusion and coma); can tx w/ Lactulose (laxative); cam present w/ jaundice, hypoglycemia (loss of gluconeogenesis), coagulopathy, and hypoalbuminemia (low oncotic pressure), elevated estrogen (normally removed by the liver)
Consequences of elevated estrogen in liver cirrhosis
normally removed by the liver; gynecomastica in men, spider angiomata and palmer erythema (remember saying - estrogen can make your skin red)
Hemodynamics in liver cirrhosis
increased vasodilators (NO), leads to decreased SVR leading to decreased BP and CO (decreased effective circulating volume) - sympathetic activation - increased RAAS and ADH, increased Na+/H20 retention = increased total body water (edema/ascities)
Esophageal varices in Portal HTN
multiple dilated engorged blood vessels around the esophagus, collaterals between the esophageal veins and left gastric veins; they can rupture
Gastric varices in Portal HTN
multiple dilated engorged blood vessels around the upper stomach (fundus); collateral between the left gastric veins (branch of the coronary vein - systemic) and short gastric veins (splenic vein - portal)
Caput Medusa
engorged veins around the umbilicus; collaterals between the paraumbilical vein and the epigastric veins
Internal Hemorrhoids in Portal HTN
multiple dilated engorged blood vessels above the dentate line; collaterals between the superior rectal vein (portal system) and the middle/inferior rectal veins (to IVC)
Mechanism of low platelets in portal HTN
due to engorgement of the spleen - Hypersplenism via the splenic vein
pt with portal HTN symptoms but the liver biopsy is normal, what should you suspect?
portal vein thrombosis
SAAG
Serum Ascites Albumin Gradient (SAAG)
SAAG >1.1 g/dL (HIGH) - there is a big difference between the serum and ascites albumin = portal HTN
SAAG <1.1 g/dL (LOW) - there is NO difference between the serum and ascites albumin = malignancy ascites
** perform on ALL pt with ascites to rule out malignancy
Drug of choice for Ascites Tx
Spironolactone - K+ sparing diuretic that blocks aldosterone at the distal tubule; and large volume paracentesis
Infectious complication of ascites
Spontaneous Bacterial Peritonitis (SBP) - ascitic fluid infections; usually E. coli and Klebsiella (gram negatives); fever, abdominal pain, and increased PMNs; tx with Cefotaxime (3rd generation cephaloporins)
Stellate cells
perisinusoidal cells in the liver that are a major contributor to cirrhosis; storage site for Vit A metabolites; secreted TGF B to produce fibrosis tissue;
Aspergillus in relation to liver
fungus that produces **aflatoxin; contaminate in CORN; high dietary intake is associated with hepatocellular carcinoma (HCC); non-industrialized countries
Common metastatic site for hepatocellular carcinoma (HCC)
**lung and bone (usually solitary tumor if primary); metastasis TO the liver most commonly come from the GI (colon, stomach, pancreas) and will see multiple nodules
Hepatic Adenoma
benign; solitary in right liver lobe, common in young women (20s and 40s); associated with **contraceptive use; can be a clinical problem during pregnancy (tumor can rupture)
Hepatic Angiosarcoma
Rare malignant vascular tumor associated with toxic exposures:
Vinyl chloride - used in plastic - inhalation
Arsenic - rock, soil, water
Wilson’s Disease
AR disorder (mut in ATP7B - chr 13) with dysfunction in copper metabolism; Excess copper is mostly excreted in bile; incorporated into serum via ceruloplasmin; copper accumulates - increased free radical production, deposits in the brain and cornea (Kayser-Fleischer Rings) - slit lamp exam; diagnostic hallmark: low ceruloplasmin level (defect); usually a young pt (12-23yrs); tx with Penicillamine (copper chelator)
Pt with suspected Wilson’s Disease, what test should you order next?
**Slit lamp exam - detectable for Kayser-Fleischer Rings in the eye; don’t pick liver function test; also a low ceruloplasmin is a hallmark for Wilson’s Disease; tx with Penicillamine
Two special features of Hemochromatosis
iron overload (hereditary C282Y mut - pts should avoid (never) alcohol consumption because it accelerated liver disease AND avoid Vitamin C supplements because it increased iron absorption
Elderly pts with gallstone symptoms should make you suspect what?
cancer; gallstones typically occurs in 40s
Crohn’s Disease in relation to Gallstones
Crohn’s disease commonly involves inflammation of the ileum which causes abnormal resorption of bile salts
Biliary Colic
episodic RUQ pain, radiate to ** right shoulder pain, usually occurs after fatty meals and lasts for about 30 mins; CCK stimulates gl
Chronic Cholecystitis
long-standing untreated cholecystitis; chronic inflammation causes a **porcelain gallbladder (Ca2+ deposition - can be seen on imaging); increased risk for gallbladder carcinoma
Acalculous cholecystitis
acute cholecystitis NOT due to gallstones; caused by gallbladder ischemia and stasis; pt will have thickened gallbladder wall and a + Murphy’s sign; ** Biliary sludge: thickened bile - slow/incomplete gallbladder emptying (hypomotility); this usually occurs in critically ill pts
AIDS Cholangiopathy
complication of end-stage HIV infection; result from chronic infection involving biliary tree cause biliary obstruction from *strictures; common bugs - Cryptosporidium (most common) and CMV infection
Cryptosporidium seen with biliary obstruction
Cryptosporidium is a protozoan - transmitted fecal/oral route usually through contaminated water and causes infectious diarrhea; pts who are healthy experience self-limited watery diarrhea but those who are immunocompromised (HIV) can cause life-threatening diarrhea; diagnosed with modified acid-fast stain showing oocytes
Charcot’s triad
clinical features of ascending cholangitis - fever, abdominal pain and jaundice (can progress to Reynolds pentad)
Reynolds pentad
clinical features of a severe ascending cholangitis - fever, abdominal pain, jaundice, confusion and hypotension
Microbiology of ascending cholangitis
usually caused by gram - organisms: E. coli, Klebsiella, Enterobacter
Watch for Chinese liver fluke, may have just consumed sushi - Clonorchis sinensis - helminth found in infected fish; you will see peripheral eosinophilia
Gallstone ileus
massive gallstone that erodes the gallbladder wall creating a fistula with the small intestine; will cause bowel obstruction at the ileocecal valve looks for air in biliary tree on imaging (should never be filled with air, but bile)
Gallbladder carcinoma
adenocarcinoma from chronic inflammation or from chronic salmonella infection (S. typhi)
Biliary atresia
idiopathic biliary obstruction in neonates; on US *gallbladder is absent or abnormal; jaundice, dark urine, pale stools; tx with surgical procedure - Kasai procedure
Primary Biliary Cirrhosis
Biliary cirrhosis w/o extra hepatic obstruction; autoimmune disorder where T-cells attack interlobular bile ducts; will see granulomatous inflammation; imaging will show absence of biliary obstruction (WILL BE NORMAL contrast with Primary Sclerosing Cholangitis); more common in women; two common symptoms - fatigue and pruritus - REMEMBER ITCHING; commonly associated with Sjogren’s
Why is it important to remember ITHING with Primary Biliary Cirrhosis?
itching may be before the development of jaundice and can be misdiagnosed with a skin condition - initial complaint! look for the two most common symptoms of itching and fatigue together, more common in women and itching may be severe and often worse at night
pt is a women who presents with severe itching and physician orders alk phos, alk phos is elevated, what should you order to confirm your diagnosis?
should suspect Primary Biliary Cirrhosis and order anti-mitochondrial antibodies to confirm diagnosis
Treatment for Primary Biliary Cirrhosis?
Ursodeoxycholic acid is the only effective tx; it is similar to bile acids (so replaced endogenous bile acids) but less toxic hepatocytes
Primary Sclerosing Cholangitis
do not confuse with Primary Biliary Cirrhosis; this disorders has fibrosis and strictures that obstructs bile flow; involves intra and extra-hepatic bile ducts; STRONGLY associated with ulcerative colitis; labs: elevated IgM and positive p-ANCA
Primary Sclerosing Cholangitis - fibrosis and strictures that obstructs bile flow; involves intra and extra-hepatic bile ducts; STRONGLY associated with ulcerative colitis; labs: elevated IgM and positive p-ANCA
pt has hx of ulcerative colitis and now presents with jaundice and elevated alk phos levels what should you suspect and what labs do you want?
Primary Sclerosing Cholangitis; order a cholangiogram to confirm diagnosis - see biliary stricture and dilations “beading” “beads on a string”
Curling’s Ulcer
occurs in burn pts; there is loss of skin/fluids resulting in dehydration and hypotension to the stomach; resulting in mucosal damage (decreased mucosal perfusion) leading to acute gastritis and ulcers; place on PPI
Cushing’s Ulcer
caused by increased intracranial pressure due to a tumor or hemorrhage; increased vagal stimulation leading to increased Ach released on the stomach; excess acid production resulting in gastritis/ulcers; place on PPI
Stress Ulver’s
common among critical ill pt (shock, sepsis, trauma) leads to decreased mucosal perfusion leading to acute gastritis and ulcers; place on PPI
Autoimmune Gastritis
pernicious Anemia; chronic inflammation of gastric body/fundus; more common in women; associated with HLA-DR antigens and is also associated with gastric adenocarcinoma
Type B chronic gastritis
bacterial gastritis due to H. pylori; gram negative rod that is urease positive causes ulcers in acute and chronic gastritis; mostly occurs in antrum
MALT Lymphoma
Tx for H. pylori
triple therapy:
PPI
Clarithromycin
Amoxicillin/Metronidazole
Brunner’s Gland Hypertrophy
seen in pts with PUD; it is only in the duodenum and found in the submucosa; produces alkaline fluids that protects from the acidic stomach fluid; there will be increased thickness in PUD
Arterial supply that can erode in a duodenal ulcer?
gastroduodenal artery
air under the diaphragm on CXR; occurs with gastric or duodenal ulcers; causes pneumoperitoneum
Arterial supply that can erode in a gastric ulcer?
left gastric artery; courses the lesser curvature of the stomach
Risk factors for intestinal type gastric carcinoma
adenocarcinoma (95% of all gastric carcinomas); older men and smoking (no proven association with alcohol); nitrosamines (smoked meats) and Type A blood (mechanism unclear)
signet ring that is characteristic for diffuse type gastric carcinoma; will also see a diffusely thickened stomach (like a leather) - linitis plastica
Special clinical findings in Gastric carcinoma?
Acanthosis Nigricans
Leser-Trelat sign (explosive onset of multiple itchy seborrheic keratoses)
Virchows node (enlarged left supraclavicular node - drains stomach)
Sister Mary Joseph nodule (metastasis to periumbilical region - palpable on exam)
Krukenverg tumor (ovarian tumor secondary to another site)
Menetrier’s Disease
a hypertrophic gastropathy; more common in men, **hyperplasia of mucous cells leading to excessive gastric mucous secretions; there will be a loss of acid (achlorhydria); albuminemia because of a loss of protein
look for pt with edema, facial swelling with abdominal pain - labs will show low serum albumin and a cat scan will show a very large stomach - increased risk for gastric adenomcarinoma
Fat malabsorption clinical manifestations
steatorrhea
pale if bile absent (no bilirubin)
voluminous stools
stools that float
greasy, foul smelling
loss of fat soluble vitamins (ADEK)
Give examples of what causes which type of diarrhea.
steatorrhea - malabsorption of high fat content; can occur in gallbladder issues and short bowlel syndrome w/ resection of the terminal ileum
inflammatory - WBC/RBC present on microscopy; happens in infection
water secretory - infection with cholera
watery osmotic - lactose intollerant
Carbohydrate malabsorption clinical manifestations
watery diarrhea
osmotic effect of sugar molecules
Proteins malabsorption clinical manifestations
edema (loss of albumin)
Celiac Sprue
AKA Celiac disease; destruction if the small intestine triggered by gluten (Gliadin) exposure; tissue transglutaminase (tTG) auto T-cell antibodies (anti-tTG) - type IV hypersensitivity; associated w/ HLA-DQ2 and HLA-DQ8
Three Key Histological features in Celiac Sprue
Blunting of Villi - much smaller
Crypt hyperplasia
Lymphocytes in lamina propria
Celiac Sprue; Three Key Histological features:
Blunting of Villi - much smaller villi in right photo
Crypt hyperplasia
Lymphocytes in lamina propria
Celiac Sprue Clinical manifestations
duodenum commonly affected (contrast w/ tropical sprue that affects the entire small bowel); flatulence, bloating and steatorrhea; children - failure to thrive w/ iron deficiency anemia (iron is primarily absorbed in duodenum); can present with Dermatitis Herpetiformis - herpes-like lesions on skin (IgA deposition in dermal papillae)
pts are at risk for T-cell lymphoma; pt who has been adherent to celiac diet and now symptoms are getting worse
pt develops chronic diarrhea after recent travel to the Caribbean, all celiacs test will be negative (anti-tTG), there is blunting of the villi in all segments of the small intestine. What condition do you suspect and supplementation you should give?
Tropical sprue; tx w/ antibiotics (usually tetracycline) and give **folate supplementation
Whipple’s Disease
infection w/ Tropheryma whipplei (gram + rod related to actinomycetes); systemic infection involving the small intestine, joints, brain and heart; **HALLMARK: PAS + foamy macrophages seen in the lamina propria of the small intestine
PAS + foamy macrophages seen in the lamina propria of the small caused by an infection w/ Tropheryma whipplei (gram + rod related to actinomycetes) as seen in Whipple’s Disease
D-xylose Test
test carbs absorption in the small intestine; D-xylose is a monosaccharide that is absorbed directly w/o an enzyme there only needs to be an intact mucosa; abnormal results are seen in bacterial overgrowth and Whipple’s disease
Drugs that can trigger acute pancreatitis
GLP-1 agonists (diabetics) - Exenatide and Liraglutide
Sulfa drugs
6-Mercaptopurine (6-MP)
Pancreatic pseudocyst; a complication of pancreatitis; walled-off collection of edema/fluid with granulation/fibrous tissue that surrounds the fluid; found usually OUTSIDE of the pancreas (most common in the lesser sac); required 4 weeks to mature after pancreatitis (can always develop in people w/ chronic pancreatitis) diagnosed by CT or MRI
Chronic Pancreatitis
fibrosis/calcification of the pancreas; chronic abdominal pain that can result in a fear of eating; two main complications -
1. Splenic vein thrombosis resulting in gastric varices (left gastric vain and left gastric vein)
2. Pancreatic insufficiency leading to fat malabsorption and steatorrhea, fat-soluble vitamin deficiencies and diabetes (loss of insulin)
Pancreatic cancer
most common in the head (near the duodenum where bile drains); vague abdominal pain and weight loss “painless jaundice” tumor grows slowly; Courvoisier’s sign - PE finding of an enlarged, non-tender gallbladder plus jaundice
Pancreatic Cancer genetics
K-RAS gene (chr 12) - 90%
SMAD4 gene (chr 18) - 60%
Pancreatic Cancer genetics
K-RAS gene (chr 12) - 90%
SMAD4 gene (chr 18) - 60%
Pathogensis of appendicitis
opening ig the cecum becomes **obstructed; due to fecaliths (hard fecal masses) - more common in adults OR lymphoid hyperplasia - more common in children
The “Acute Abdomen”
acute onset of abdominal pain with rebound tenderness; reflects peritoneal inflammation; requires urgent surgical intervention; need to avoid life-threatneing complications of perforation
Diverticular Disease
blind pouch extending out from the GI tract due to breakdown of the muscular layer (occur where vasa recta penetrate muscularis of colon); it is a false diverticulum (does NOT contain all layers); usually occurs in sigmoid colon; caused by straining to pass stool; lower GI bleeding; if gets infected - Diverticulitis
Diverticulitis
inflammation of the diverticulum; presents with fever and increased WBCs, LLQ pain (sigmoid colon); occult blood in stool; complications of an abscess, bowel obstruction, fistula, and perforation
Adhesions
bands of scar tissue in peritoneal cavity commonly formed after surgery (C-section in women, appendicitis or bowel obstruction); most common cause of short bowel obstruction; tx would be to surgically lysis the adhesions (risk for more adhesions)
Intussusception
telescoping of the intestine; intestine folds into lumen; can compromise blood supply and lead to ischemia; GI bleeding with “currant jelly” appearance; medical emergency; common in children <1 yrs; most causes are idiopathic but the most common pathological cause is Meckel’s diverticulum (incomplete obliteration of the vitelline duct) - look for ectopic gastric mucosa in intestines; also strong association with adenovirus
Hirschsprung’s disease
failure of neural crest cells to migrate leading to an absence of ganglion cells in the nerve plexuses; child will have failure to pass meconium; barium imaging has characteristic finding go “transition zone”; diagnosis is made by biopsy rectal “suction” biopsy; RECTUM is ALWAYS involved
Ogilvie Syndrome
acute “pseudo-obstruction” of intestines; dilated colon in absence of a lesion; usually in hospitalized or nursing home pts after an illness or surgery. Often associated w/ narcotics
Irritable Bowel Syndrome
FUNCTIONAL bowel syndrome (problem w/ the function not the structure); normal intestine structure (biopsy is normal); recurrent abdominal pain for 3 days per month for 3 months; relief w/ defeaction
Necrotizing enterocolitis; occurs in preterm infants due to GI and immune immaturity; bacterial in bowel causes inflammation and ischemic necrosis; bowel becomes congested and gangrenous with formation of intramural gas collections; pneumatosis intestinal can be seen on abdominal x ray (air in bowel wall); tx w/ bowel rest
Necrotizing enterocolitis
occurs in preterm infants due to GI and immune immaturity; bacterial in bowel causes inflammation and ischemic necrosis; bowel becomes congested and gangrenous with formation of intramural gas collections; pneumatosis intestinal can be seen on abdominal x ray (air in bowel wall)tx w/ bowel rest
Angiodysplasia
aberrant blood vessels in GI tract; commonly in cecum and right sided colon; caused by high wall stress; can present w/ lower GI bleeding
Crohn’s disease
one of the IBDs; relapsing, remitting course “flares”; noncaseating granulomatous inflammation; affect entire wall (transmural); any portion of the GI can be affects (mouth to anus); terminal ileum is affects (B12 deficiency and loss of bile salts); RLQ pain (terminal ileum); often skips the rectum; can see cobblestone mucosa and transmural inflammation can lead to fistulas; creeping fat and strictures “string sign”
Ulcerative colitis
one of the IBDs; relapsing, remitting course “flares”; ulcers of the intestinal tract specifically in the colon; inflammation of the mucosa and submucosal (not full thickness); ALWAYS starts in the rectum and works it way upward; does NOT involve the small intestine; presence of pseudopolyps, loss of haustra “lead pipe appearance” and crypt abscesses (PMNs); p-ANCA
Pseudopolyps - healing of ulcers as seen in Ulcerative colitis
seen in Ulcerative colitis
Extra-intestinal features of ulcerative colitis
Pyoderma gangrenous - deep necrotic skin ulceration (causes ulcers of the colon, can also cause ulcers of the skin)
Primary sclerosing cholangitis
Ankylosing spondylitis - inflamed spine
Uveitis - inflamed eye
Feared complication of ulcerative colitis
Toxic megacolon - colon stop contracting (increased NO) leading to intestinal dilation (rapid distention occurs) the wall thins and it is prone to rupture and perforation; pt can go into shock and die; obtain a flat plate x ray of the abdomen
noncaseating granulomas in the small intestine
Crohn’s disease
Crohn’s disease
Extra-intestinal features of Crohn’s disease
Migratory poly arthritis - most common - arthritis of the large joints
Kidney stones - calcium oxalate stones; high oxalate levels, so oxalate Is free to be absorbed in the gut
Immunology of the inflammatory bowel disorders
Ulcerative colitis - Th2 mediated = no granulomas
Crohn’s disease - Th1 mediated = granulomatous disease
Immunology of the inflammatory bowel disorders
Ulcerative colitis - Th2 mediated = no granulomas
Crohn’s disease - Th1 mediated = granulomatous disease
Tx of UC w/ Sulfasalazine with side effects
GI upset
Sulfa hypersensitivity
Oligospermia in men - problem w/ men trying to conceive (is reversible)
Hyperplastic Polyp
most common
Hyperplastic Polyp
most common type of colon poly; it is benign; often found in the rectosigmoid colon; classically has a “sawtooth” or serrated pattern; no special screening required after biopsy
pt has a colonoscopy and a polyp is identified and removed, analysis comes back and it is a hyperplastic poly, what are next steps?
no special screening required after biopsy
Colon Polys that are high risk for development into colon cancer
adenomatous villous polyps (tubular polyps are less common)
Peutz-Jeghers Syndrome
AD disorder of juveniles; multiple hamartomas are found throughout the GI tract; will present with pigmented spots on lips and buckle mucosa; increased risk for gastric, small intestinal and colon cancer
adolescent is brought in due to multiple pigmented spots on lips and buccal mucosa
Peutz-Jeghers Syndrome; multiple hamartomas are found throughout the GI tract; increased risk for gastric, small intestinal and colon cancer
Genetics of colon cancer (3 things)
- two well-defined pathways
- chromosomal instability pathway - APC mut 1st and then KRAS mut and finally a p53 mut = tumor cell growth (FAP and FAP variants)
- micro satellite instability - de novo w/o polyp (less common mechanism) (HNPCC/Lynch Syndrome)
- Cyclooxygenase-2 (COX-2) expression is increased*** (tx w/ aspirin)
- Deleted in Colorectal Cancer (DCC) gene mutated in advanced colorectal cancers
Familial Adenomatous Polyposis (FAP)
AD disorder involving a germline mut of APC gene; ALWAYS 100% progresses to colon cancer; tx; colon removal (colectomy)
Gardner’s Syndrome
FAP variant - remember is forms bumps all over the body; benign bone growth (osteomas) - esp mandible; skin cysts (epidermal, fibromas, lipomas); CT growths and hypertrophy of the retinal pigment (children are born with flat dark spot in retina)
Turcot Syndrome
FAP variant - polyposis of the colon plus brain tumors (mostly medulloblastomas and gliomas)
Hereditary Non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome
inherited mut in DNA mismatch repair enzymes leading to colon cancer via micro satellite instability; 80% lifetime risk; usually R sided tumor
pt w/ R sides colon cancer with multiple 1st family members also w/ cancer that person may have what?
inherited mut in DNA mismatch repair enzymes leading to colon cancer via micro satellite instability as seen in Hereditary Non-Polyposis Colorectal Cancer (HNPCC)/Lynch Syndrome
Step Bovis
normal colonic bacteria; gram + cocci and gamma hemolytic; Lancefield group D; cases bacteremia and **endocarditis; STRONGLY associated w/ colon cancer
pt w/ Step Bovis organism identified (endocarditis), what test should you do next?
Colonoscopy; STRONGLY associated w/ colon cancer
Carcinoid Tumors
neuroendocrine tumor that secrete the NTM serotonin (5-HT); caused diarrhea and flushing (these pts are miserable!!); may also develop valvular heart disease (fibrous deposits on tricuspid and pulmonic valves); when symptoms present they now have the carcinoid syndrome; liver and lung metabolize (inactive) serotonin (left sided lesions are rare); altered **tryptophan metabolism (deficiency) needed for Niacin (B3) = pellagra; measure 5-HIAA in the urine and elevated levels is diagnostic; tx w/ octreotide
HCV tx
chronic HCV infection is tx w direct-acting antivirals (DAAs) meds such as ledipasvir and sofosbuvir; these meds target specific HCV enzymes which inhibits viral replication and and assembly; results in cute in >97% pts
Hepatitis A infection
transmission of HAV occurs through fecal-oral route and is common in areas w overcrowding and poor sanitation; outbreaks frequently result from contaminated water or food, and *raw/steamed shellfish
pancreatic cancer
pancreatic ductal adenocarcinoma is almost always due to an early activating mut in the KRAS oncogene (KRAS = pan CRE ASS); this leads to constitutively active proteins that allows for uncontrolled proliferation of tumor cells
