Gastrointestinal Flashcards
Retroperitoneal structures:
“SAD PUCKER”
- Suprarenal (adrenal) gland
- Aorta and IVC
- Duodenum (2nd, 3rd, and 4th parts)
- Pancreas (except tail)
- Ureters
- Colon (descending and ascending)
- Kidneys
- Esophagus (lower 2/3)
- Rectum (upper 2/3)
GI ligament that is a derivative of the fetal umbilical vein? what structure does it contain? what does it connect?
Falciform ligament
- contains the ligamentum teres
- derivative of the fetal umbilical vein
- connects liver to anterior abdominal wall
GI ligament that contains the portal triad (hepatic artery, portal vein, common bile duct)?
Hepatoduodenal ligament
Which GI ligament may be compressed to control bleeding by placing fingers in the omental foramen?
Hepatoduodenal ligamentf
Frequency of waves/peristalsis in stomach? duodenum? ileum?
stomach–> 3 waves/min
duodenum–> 12 waves/min
ileum–> 8-9 waves/min
Meissner’s plexus:
- where’s it located?
- other name?
- what’s its function?
- located in Submucosa
- “submucosal plexus”
- controls secretory activity; secretes mucus (so is near the lumen…)
Auerbach’s plexus:
- where’s it located?
- other name?
- what’s its function?
- located in Musculara externa (really, between muscularis externa inner circular and outer longitudinal layers)
- “Myenteric plexus”
- controls muscle contractions; coordinates motility along entire gut wall
Roles of the mucosa of the GI tract?
mucosa = innermost layer of gut wall
- has 3 parts, each with a role:
- epithelium–> absorption
- lamina propria–> support
- muscularis mucosa–> motility
cell type in esophagus?
stratified squamous epithelium
cell type in stomach?
gastric glands
where in GIT are Brunner’s glands?
Duodenum
–>submucosal glands that produce alkaline-rich/bicarb secretion
Where in GIT are Crypts of Lieberkuhn?
Duodenum, Jejunum, Ileum, and Colon
Where in GIT are villi and microvilli?
Small intestine; not Colon (makes sense, b/c villi are there to increase absorptive surface)
Where in GIT are goblet cells?
Ileum–> has most goblet cells in the small intestine; but, also found in other parts of small intestine: as go along the small intestine, # of goblet cells increases
Where in GIT are Peyer’s patches?
only in Ileum
Where does celiac trunk come off the abdominal aorta?
T12
Where does the SMA come off the abdominal aorta?
L1
Where do the renal arteries come off the abdominal aorta?
L1
Where does the inferior mesenteric artery come off the abdominal aorta?
L3
What level is the bifurcation of the abdominal aorta?
L4
Muscle types composing the Esophagus:
- upper 3rd–> striated muscle (voluntary)
- middle 3rd–> striated + smooth muscle
- lower 3rd–> smooth muscle (involuntary)
Artery that supplies the Foregut? Innervation of the foregut?
- Celiac artery
- Vagus nerve
Artery and Nerve that supply the Midgut?
- SMA
- Vagus nerve
Artery and Nerve that supply the hindgut?
- IMA
- Pelvic nerve
Watershed area of the GIT?
=> splenic flexure
-supplied by the terminal branches of the IMA and SMA, so most sensitive to hypoxia
What structures make up the foregut? midgut? hindgut?
- foregut: stomach to proximal duodenum; also: liver, gallbladder, pancreas, spleen
- midgut: Distal duodenum to proximal 2/3 of transverse colon
- hindgut: distal 1/3 or transverse colon to upper part of rectum; inludes splenic flexure (watershed area)
Portal triad:
- Hepatic artery
- Portal vein
- Common bile duct
Branches of celiac trunk?
- celiac trunk comes off abdominal aorta at T12
- branches:
- common hepatic artery
- splenic artery
- left gastric artery
–> these branches make up the main blood supply of the stomach!
Which arteries supply the lesser curvature of the stomach? greater curvature?
- lesser curvature –> L and R gastric arteries (L gastric comes off the Celiac trunk; the two gastrics anastamose)
- Greater curvature: L and R gastro-omental arteries (also anastomose with each other)
3 Portosystemic shunts (alleviate portal hypertension)
1) Esophageal varices –> anastomosis at the esophagus
2) Caput medusae –> anastomosis at the umbilicus
3) Internal hemorrhoids –> anastomosis at the rectum
type of hemorrhoids and cancers seen above and below the pectinate line:
- above pectinate line:
- internal hemorrhoids (not painful)
- adenocarcinoma
- below pectinate line:
- external hemorrhoids (painful)
- squamous cell carcinoma (main risk factor for squamous cell carcinoma here = HPV 16,18,31)
Pathway of bile: from production to secretion into duodenum:
Bile made in liver –> R and L hepatic ducts –> Common hepatic duct –> some into common bile duct, some into cystic duct –> from cystic duct, stored in gallbladder, then released back into cystic duct when needed, into common bile duct –> common bile duct meets pancreatic duct at Ampulla of Vater –> bile released via Sphincter of Oddi into Ampulla of Vater in duodenum!
Lodging of a gallstone where may lead to obstruction of both bile and pancreatic ducts?
if gallstone is lodged in Ampulla of Vater
What sort of tumor may obstruct the common bile duct?
Tumors of head of pancreas –> can compress ampulla, like a gallstone, thus obstructing common bile duct
Lateral to Medial organization of the Femoral Region:
Lateral: “NAVeL” :Medial
- Nerve
- Artery
- Vein
- Lymphatics
Femoral triangle:
- formed by?
- contains?
- formed by:
- inguinal ligament
- sartorius muscle
- adductor longus muscle
- contains:
- femoral nerve, artery, vein (lateral–>medial)
What does the femoral sheath contain?
-Contains femoral vein, artery, and lymphatics, but NOT femoral nerve
Sliding vs Paraesophageal Hiatal Hernias:
- Both are types of diaphragmatic hernias, which occur at the gastro-esophageal jxn; stomach herniates upward through the esophageal hiatus of the diaphragm.
- sliding hiatal hernia: GE jxn is displaced; have an “hourglass stomach”
- paraesophageal hernia: GE jxn is normal; cardia of stomach moves into the thorax
“hourglass stomach”
sliding hiatal hernia
What kind of inguinal hernia occurs in infants?
INdirect inguinal hernia in INfants
–>goes through the INternal/deep inguinal ring, external/superficial inguinal ring, and into the scrotum (Basically, follows the path of the testes)
–>occurs in infants d/t failure of processus vaginalis to close
–> Covered by all 3 layers of spermatic fascia
What type of inguinal hernia passes through the inguinal/Hesselbach’s triangle?
Direct inguinal hernia
- -> only covered by external spermatic fascia (unlike indirect, which is covered by all 3 layers)
- ->usually in older men
Hernia that’s most common in women?
Femoral hernia
Hernia that’s a leading cause of bowel incarceration/obstruction?
Femoral Hernia
Hesselbach’s triangle:
- borders?
- what type of hernia goes through it?
- Borders:
- inguinal ligament
- inferior epigastric artery
- lateral border of rectus abdominis
*Direct inguinal hernias (older men) go through Hesselbach’s triangle
G cells (antrum of stomach) secrete?
Gastrin (“pro-gastric”)
I cells (duodenum, jejunum) secrete?
CCK (“pro-duodenum”, “anti-gastric”–> CCK stimulates pancreatic secretions)
S cells (duodenum) secrete?
Secretin (“pro-HCO3”, “nature’s antacid”)
D cells (pancreatic islets, GI mucosa) secrete?
Somatostatin (inhibits everything!)
Which hormone is increased in Zollinger-Ellison syndrome?
Gastrin
=”gastrinoma”
Which GI hormone is stimulated by Phenylalanine and Tryptophan?
Gastrin
What AAs may stimulate gastrin release?
Phenylalanine and Tryptophan
What does CCK cause?
Stimulates pancreatic secretion, gallbladder contraction, and gastric emptying
What does Secretin do?
Stimulates pancreatic HCO3- secretion, decreased gastric acid secretion, increased bile secretion
–> it’s “nature’s antacid” –> neutralizes gastric acid in duodenum to allow pancreatic enzymes to function
Somatostatin:
- where is it secreted from?
- what does it do?
- secreted from D cells in pancreas (islets) and GI mucosa
- inhibits:
- ->decreased gastric acid and pepsinogen secretion
- ->decreased pancreatic and intestinal secretions
- ->decreased gallbladder contraction (so, if lots of somatostatin, may get biliary stones)
- ->decreases insulin and glucagon release
***so overall inhibits digestion and absorption of substances needed for growth…
What is used more rapidly: oral glucose load or equivalent given by IV?
oral glucose is used more rapidly, d/t GIP = Gastric Inhibitory Peptide = Glucose-dependent insulinotropic peptide
VIP = Vasoactive Intestinal Peptide:
- secreted from?
- actions?
*source: Parasympathetic ganglia in sphincters, gallbladder, small intestine
- actions:
- increases intestinal water and electrolytes secretion
- increases relaxation of intestinal smooth muscle and sphincters
VIPoma:
- origin
- symptoms?
non-alpha, non-beta pancreatic islet cell tumor
- may be associated with MEN I
- secretes VIP
- symptoms:
- ->tons of watery diarrhea (b/c VIP stimulates intestinal water and electrolyte secretion) –> so, as a result also have: dehydration, hypokalemia, etc…
Endocrine tumor that leads to lots of watery diarrhea?
VIPoma (pancreatic tumor, secretes tons of VIP)
Action = binds vitamin B12 to allow uptake of B12 in terminal ileum?
Intrinsic Factor
Which substances are secreted by Parietal Cells of stomach?
- Intrinsic Factor
- Gastric Acid
Gastrinoma
gastrin-secreting tumor; get constant high levels of acid secretions and ulcers
–>=zollinger-ellison syndrome
Secreted by chief cells of stomach
Pepsin
Action of pepsin?
protein digestion
what activates pepsinogen–>pepsin?
Acid (H+)
Which cells secrete HCO3-?
- mucosal cells (in stomach, duodenum, salivary glands, pancreas)
- Brunner’s glands (in submucosa of duodenum)
How do NSAIDs lead to acidic damage in stomach?
- Prostaglandins generate mucus that covers that covers the gastric epithelium
- ->NSAIDs–>decrease PGs–> decrease mucus –> decrease HCO3- –> increased susceptibility to acidic damage in stomach
Which glands secrete saliva? What stimulates saliva secretion (PSNS, SNS?)? When is saliva hypotonic/isotonic?
- secreted from parotid, submandibular, sublingual glands
- stimulated by Sympathetic AND Parasympathetic activity
- Normally is hypotonic, but is more isotonic with higher flow rates, b/c less time for absorption
- **Sympathetic stimulation–> thicker secretions
- **Parasympathetic stimulation–> watery secretions
How does Gastrin stimulate acid secretion in stomach?
G cells in antrum of stomach are stimulated by vagus nerve (via GRP transmitter)–> release Gastrin into circulation –> Gastrin stimulates ECL (EnteroChromaffin-Like) cells to release Histamine –> Histamine induces Parietal cells to secrete HCl
Affects of atropine on GI secretions?
Atropine = anti-cholinergic
- -> blocks vagal stimulation of parietal cells (use ACh as transmitter)
- -> BUT, no effect on G cell stimulation by vagal cells, because G cells use a different transmitter, GRP (not ACh) –> so, Gastrin can still stimulate parietal cells to secrete Intrinsic Facor and (via enterochromaffin-like cells and histamine) to secrete HCl
How do prostaglandins protect the stomach?
- decrease acid secretion (Gi–>decreased cAMP–>decreased proton pumping)
- increase mucus and HCO3- production
3 factors that stimulate G-cells to make Gastrin?
- Hypercalcemia
- Phenylalanine
- Tryptophan
What may cause hypertrophy of Brunner’s glands?
Peptic ulcer disease (b/c lots of acid to deal with)
–>Brunner’s glands are located in duodenal submucosa; function = secrete alkaline mucus to neutralize acid contents entering duodenum from stomach
Trypsinogen:
- secreted by?
- converted to trypsin by?
- action?
- secreted by pancreas
- enterokinase/enteropeptidase converts trypsinogen–>trypsin
- converts other proenzymes/zymogens and more trypsinogen to active form
- trypsin (and other zymogens)–> involved in protein digestion
alpha-amylase
secreted by pancreas
- digests starch
- **also have amylase in saliva, which digests starch in saliva
Lipase
secreted by pancreas
-digests fat
salivary amylase vs pancreatic amylase:
- both digest starch
- salivary: hydrolyzes alpha-1,4-linkages to form disaccharides
- pancreatic: hydrolyzes starch to oligosaccharides and disaccharides
D-Xylose absorption test
Test to distinguish GI mucosal damage from other causes of malabsorption
–>D-xylose is normally easily absorbed by intestines; if problem with intestinal absorption, get low levels of D-xylose in urine and blood
SGTL1 = Sodium-Glucose-Co-Transporter:
Na-dependent transporter; absorbs Glucose and Galactose in enterocytes
GLUT-5
absorbs Fructose (by facilitated diffusion) into enterocytes
GLUT-2
Transports all monosaccharides (Glucose, Galactose, Lactose) from intestines into blood
Where in GIT is Iron absorbed?
Duodenum
Where in GIT is folate absorbed?
Jejunum
Where in GIT is Vitamin B12 absorbed?
Terminal ileum, along with bile acids; requires intrinsic factor (from parietal cells)!
Peyer’s patches:
- where?
- function?
- located in ileum
- Peyer’s patches = lymphoid tissue in lamina propria and submucosa of small intestine
- function:
- ->contain M-cells that take up antigen
- ->B-cells stimulated in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells. IgA ultimately resides in lamina propria. IgA protects gut from pathogens!
Lymphoid tissue of the GIT?
Peyer’s patches
- located in ileum
- B-cells in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells –> IgA lives in lamina propria and protects gut from pathogens!
specialized M-cells that take up antigen in GIT?
-in Peyer’s patches –> the lymphoid tissue of GIT!
IgA in GIT comes from?
Peyer’s patches: have B-cells in germinal centers of Peyer’s patches (lymphoid tissue) that differentiate into IgA-secreting plasma cells
–>IgA protects the gut from pathogens!
Only way body can excrete cholesterol?
Bile
How is copper excreted from the body?
Bile; can’t excrete it in Wilson’s disease though…
3 functions of Bile:
1) Digest and absorb lipids and fat-soluble vitamins
2) Excrete cholesterol
3) Anti-microbial activity (by disrupting membranes)
Pale/Clay-colored stools?
-problem processing bilirubin
Cholestyramine
- Bile Acid Resin –> a lipid-lowering agent
- ->interferes with ability to reabsorb Urobilinogen–> so, more is excreted in stool or kidney; the liver then must use cholesterol to make more…
Colestipol
Bile-acid resin (like Cholestyramine; lipid-lowering agent)
Colesevelam
-Bile-acid resin (like cholestyramine; lipid-lowering agent)
Urobilin
breakdown product of bilirubin, excreted in urine; gives urine it’s color
Stercobilin
breakdown product of bilirubin, excreted in feces; gives color of stool (without it, have pale/clay-colored stool)
Urobilinogen
- breakdown product of conjugated/direct bilirubin, after gut bacteria alter it in the gut; has 3 possible fates:
1) excreted in feces as Stercobilin (about 80% of it)
2) excreted in urine as Urobilin (very little of it –> about 2%)
3) reabsorbed by liver via enterohepatic circulation (about 18% of it)
Biggest risk factor for a malignant salivary gland tumor?
Smoking
most common location of benign salivary gland tumor?
Parotid gland
Pleomorphic salivary gland adenoma:
- most common salivary gland tumor
- painless, movable mass, benign, recurs
Warthin’s tumor
-benign salivary gland tumor; trapped in a lymph node, surrounded by lymph tissue
Mucooepidermoid carcinoma
-most common malignant salivary gland tumor
loss of Myenteric/Auerbach’s plexus?
Achalasia
- ->can’t relax Lower Esophageal Sphincter
- ->get esophageal aperistalsis
- ->progressive dysphagia of solids and liquids (vs obstruction, which is dysphagia to solids only)
- ->increased risk of esophageal carcinoma
Bird’s beak on barium swallow
Achalasia (esophageal aperistalsis; can’t relax LES d/t loss of Myenteric/Auerbach’s plexus)
2 conditions that may lead to secondary achalasia?
- Chaga’s disease (mega-esophagus)
- CREST scleroderma (Esophageal dysmotility)
increased risk of what cancer with Achalasia?
–> esophageal carcinoma
progressive dysphagia of solids AND liquids, vs just solids vs progressive dysphagia first of solids THEN of liquids?
- solids + liquids–> Achalasia
- only solids–> obstruction
- solids, then liquids–> esophageal cancer
Painless bleeding in lower 1/3rd of esophagus?
Esophageal varices
–>associated with portal HTN
Dysphagia + Glossitis (swollen, smooth tongue) + Iron-deficiency anemia
Plummer-Vinson syndrome
- ->Dysphagia is d/t esophageal webs = thin membrane-like protrusion into esophagus
- ->associated with increased risk of Squamous Cell Carcinoma of Esophagus
Boerhaave syndrome:
- TRANSMURAL esophageal rupture d/t violent vomiting
- -> vs Mallory-Weiss which is just lacerations at the G-E jxn
Esophageal pathology associated with lye ingestion and acid reflux?
Esophageal strictures
Barrett’s esophagus: what sort of metaplasia occurs? increased risk of what kind of cancer?
Glandular metaplasia: squamous epithelium of distal esophagus is replaced with columnar/intestinal epithelium
- d/t chronic GERD
- assoc w/increased risk of Adenocarcinoma of esophagus
- also associated with esophagitis and esophageal ulcers
What type of esophageal cancer is most common worlwide? in US?
- worlwide: Squamous cell > Adenocarcinoma
- US: Adenocarcinoma > Squamous Cell
- What part of esophagus is affected in each of these cancers?
- What risk factors cause Squamous Cell Carcinoma?
- What risk factors associated with Adenocarcinoma?
- Squamous Cell: upper 2/3
- smoking
- alcohol
- achalasia
- esophageal webs (ie Plummer-Vinson syndrome)
- Adenocarcinoma: lower 1/3
- Barret’s esophagus
- Esophagitis
- Diverticula (like Zenker’s)
Whipple’s disease:
- Tropheryma whippelii infection (gram +)
- PAS + foamy macrophages in intestinal lamina propria
- mostly older men
- CAN:
- ->cardiac symptoms
- ->Arthralgias
- ->Neurologic symptoms
- **Also, classic malabsorption symptoms: diarrhea, steatorrhea, weight loss, weakness
- treat with antibiotics!
Which part of intestine is affected in Celiac sprue?
-Proximal small bowel, mostly
What part of intestine is affected in lactase deficiency?
only tips of intestinal villi (b/c that’s where lactase is located)
–>so, get normal look villi
fat accumulation in enterocytes + malabsorption in childhood + neurologic manifestations?
Abeta-lipoproteinemia
- ->have decreased synthesis of apo-B –> can’t generate chylomicrons –> decreased secretion of cholesterol and VLDL into bloodstream –> so, fat accumulates in enterocytes
- **this is a malabsorption syndrome
- treat with vitamin E supplementation (helps body produce some apoproteins)
Causes of pancreatic insufficiency? What must be supplemented?
Causes:
- cystic fibrosis
- obstructing cancer
- chronic pancreatitis
- get malabsorption of fat and fat-soluble vitamins (A, D, E, K)
- get increased fat in stool
- treat by pancreatic enzyme replacement, limit fat intake, and supplement A, D, E, K.
List the Malabsorption syndromes:
“These Will Cause Devastating Absorption Problems”
- Tropical sprue
- Whipple’s disease
- Celiac sprue
- Disaccharidase deficiency (like lactose intolerance)
- Abetalipoproteinemia
- Pancreatic insufficiency
Blunting of villi + Crypt hyperplasia in small intestines?
Celiac sprue
Curling’s ulcer
Burning of the esophagus –> can lead to sloughing of gasric mucosa and Acute Erosive Gastritis
Cushing’s ulcer
Brain injury that can lead to Acute Erosive Gastritis:
brain injury–> increased vagal stimulation –> increased ACh –> increased H+ production –> Gastritis
Main causes of Acute Erosive Gastritis:
*Acute Erosive Gastritis = disrupton of mucosal barrier –> inflammation
- Main causes:
- Alcoholics
- Pts taking daily NSAIDs (ie Rheumatoid Arthritis pts)
- Curling’s ulcer = burning esophagus
- Cushing’s ulcer = brain injury resulting in increased vagal stimulation
- Stress
Autoimmune disorder with:
- autoantibodies to parietal cells
- pernicious anemia (b/c no parietal cells, so no IF, so no B12)
- Achlorydia (b/c no acid from parietal cells)
Chronic/Non-erosive gastritis of the Fundus/Body = Type A
Cause of chronic/non-erosive gastritis to the fundus/body of the stomach
Autoimmune disorder with:
- autoantibodies to parietal cells
- pernicious anemia
- achlorydia
Cause of chronic/non-erosive gastritis affecting the antrum of the stomach?
H. pylori
- this is the most common type of chronic gastritis
- increased risk of MALT lymphoma
What part of the stomach does H. pylori affect?
Antrum
Disease in which rugae of stomach look like brain gyrae?
Menetrier’s disease
- ->gastric hypertrophy
- protein loss
- parietal cell atrophy
- increased mucous cells
- precancerous
- ->rugae are so hypertrophied that look like brain gyri!
Main type of stomach cancer?
Adenocarcinoma (almost always)
Acanthosis nigricans
seen in hyperinsulinemia and in visceral malignancies; often seen in gastric adenocarcinoma
Virchow’s node:
metastasis from stomach to left supraclavicular node
Krukenberg’s tumor:
bilateral metastasis from stomach to ovaries
–>see lots of mucus and signet ring cells in ovaries
Sister Mary Joseph’s nodule:
metastasis from stomach adenocarcinoma to subcutaneous periumbilical area
signet ring cells
cells seen in diffuse stomach cancer
- ->filled with mucin; nucleus is pushed to periphery
- ->see in stomach; also see if metastasis from stomach to ovaries (Krukenber’s tumor)
Linitis Plastica
Stomach adenocarcinoma; stomach looks like a leather bottle –> thickened and leathery
Pain is increased with eating? decreased with eating?
- Increased with eating –> gastric peptic ulcer
* Decreased with eating –> duodenal peptic ulcer (b/c have bicarb secretion, which soothes ulcer)
Role of H. pylori in gastric and duodenal peptic ulcers?
- gastric ulcers–> H. pylori in 70% of cases
* duodenal ulcers–> H. pylori in about 100% of cases
Is there an increased risk of cancer with Peptic Ulcer disease?
Trick question:
- If gastric ulcer –> increased risk of carcinoma
- If duodenal ulcer –> NO increased risk of carcinoma
Recurrent ulcers despite treatment?
Check gastrin levels; may be Zollinger-Ellison syndrome
Part of Intestines affected in Crohn’s?
Any part of GIT can be affected; but, usually involves terminal ileum and colon; have skip lesions
–>rectal sparing!
Part of intestines affected in ulcerative colitis?
- always the rectum
- then, have continuous colonic lesions up from there
How much of intestinal wall is affected in Crohn’s? in Ulcerative colitis?
Crohn’s–> transmural
Ulcerative Colitis–> only mucosal and submucosal
Creeping fat
Crohn’s
Cobblestone mucosa
Crohn’s
“string sign” on barium swallow
Crohn’s
“lead pipe” appearance of intestines on imaging?
Ulcerative Colitis (d/t loss of haustra)
IBD with: Noncaseating granulomas and Th1 mediated lymphoid aggegates on microscopy:
Crohn’s disease
no granulomas in UC; also UC is Th2-mediated
IBD that has a higher association with colorectal cancer?
Ulcerative Colitis
Crohn’s also is associated with it; but higher risk with UC
Treatment for Crohn’s?
- Corticosteroids
- Infliximab
Treatment for Ulcerative Colitis?
- Aminosalicylic Acid preparations (like Sulfasalazine)
- 6-MP
- Infliximab
- Colectomy
STD that is commonly mistaken for IBD?
L1,L2, L3 subtypes of Chlamydia –> cause Lymphogranuloma venereum
Dx criteria for IBS?
Recurrent abdominal pain + at least 2 of:
- pain improves with defecation
- change in stool frequency
- change in appearance of stool
McBurney’s point:
1/3 distance from ASIS to umbilicus (or 2/3 distance from umbilicus to ASIS!)
–>pain is localized here in appendicitis
Risk/Complication of appendicitis?
Perforation–> get peritonitis
“true” vs “false” diverticulum?
true: all 3 gut wall layers involved (ie Meckel’s)
false: only mucosa and submucosa outpouch
Most common site of diverticula?
Sigmoid colon
Most common cause of severe left lower quadrant pain?
Diverticulitis (inflammation of diverticula)
Treatment for diverticulitis?
Antibiotics
left lower quadrant pain + bright red rectal bleeding?
Diverticulitis
stinky breath (halitosis) + dysphagia + esophageal obstruction?
Zenker’s diverticulum = “false” diverticulum at junction of pharynx and esophagus
–>have stinky breath d/t trapped food!
Cause of Meckel’s diverticulum?
Persistent vitelline duct or yolk sac
Most common congenital anomaly of GI tract?
Meckel’s diverticulum
Pertechnetate study
Dx for Meckel’s diverticulum
The five 2’s of Meckel’s diverticulum?
- 2 inches long
- 2 ft from ileocecal valve
- 2% of popl
- usually presents during first 2 years of life
- may have 2 types of epithelia (gastric/pancreatic)
currant jelly stools?
Intussusception
Where does intussusception commonly occur?
commonly at ileocecal junction
What age group does volvolus usually affect? Where does volvulus usually occur?
- usually in elderly
- may occur at cecum and sigmoid colon (b/c have redundant mesentery)
Congenital megacolon d/t failure of neural crest migration?
Hirschsprung’s disease
-lack of ganglion cells/enteric nervous plexuses (Auerbach’s and Messner’s) in segment of intestines
What part of GIT is usually affected in Hirschsprung’s?
Involves rectum
Failure to pass meconium?
- Hirschsprung’s
- Cystic Fibrosis
Increased risk of Hirschsprung in people with what other syndrome?
Down syndrome
4 GI conditions associated with Down syndrome:
- Hirschsprung
- Celiac
- Duodenal atresia
- Annular pancreas
Bilous vomiting in baby + “double bubble” (proximal stomach distention)
Duodenal atresia = blind duodenum
–>associated with Down syndrome
Necrotizing enterocolitis: most common in what pt popl?
-preemie infants (b/c decreased immunity)
Pain after eating in elderly + weight loss (but, not a gastric ulcer…)
ischemic colitis
–>usually occurs at splenic flexure (watershed area) and distal colon
Sawtooth appearance of masses in gut lumen?
Colonic polyps
Area often involved in colonic polyps?
-Rectosigmoid
90% of colonic polyps are not malignant; which types are most likely to be malignant?
-Adenomatous, villous polyps (more villous the polyp, more likely to be malignant)
multiple non-malignant hamartomas throughout GIT + hyperpigmented mouth, lips, hands, genitalia (so, hyperpigmented mucosal surfaces) + increased risk of Colorectal cancer?
Peutz-Jeghers syndrome
–>autosomal dominant
autosomal dominant mutation of APC gene on chromosome 5q?
FAP = Familial Adenomatous Polyposis
–>100% of pts progress to colorectal cancer
Lynch syndrome/HNPCC (Hereditary NonPolyposis Colorectal Cancer)
- ->autosomal dominant mutation of DNA mismatch repair genes
- -> 80% of pts progress to Colorectal Cancer
- -> always involves proximal colon
FAP + osseous and soft tissue tumors + retinal hypertrophy?
Gardner’s syndrome
FAP + malignant CNS tumor?
Turcot’s syndrome
“apple core” lesion on barium enema?
colorectal cancer
CEA tumor marker
colorectal cancer
Iron deficiency anemia in older males or post-menopausal females?
Suspect colorectal cancer
Most common sites of carcinoid tumors?
- appendix
- rectum
- ileum
Bronchospasm + Flushing + Diarrhea + Right-sided heart lesion
Serotonin Syndrome (carcinoid tumor that secretes serotonin)
Why is carcinoid syndrome only a “syndrome” once it metastasizes out of GI system?
- -> b/c just tumor alone = carcinoid tumor, not syndrome
- -> if tumor is in the GI, it may secrete serotonin, but don’t see any of the symptoms, b/c the liver metabolizes serotonin
- ->once it metastasizes, usually to liver, then start seen symptoms associated with serotonin secretion; then it becomes “syndrome”
form of bilirubin in bloodstream?
unconjugated bilirubin-albumin complex = indirect (water-insoluble) bilirubin
form of bilirubin in liver?
conjugated/direct (water-soluble) bilirubin
form of bilirubin in stool?
stercobilin
form of bilirubin in urine?
urobilin
uridine glucuronyl transferase = UDP glucuronyl transferase
enzyme, converts indirect bilirubin to direct bilirubin in liver
Effects of Portal Hypertension
- Esophageal varices –> Hematemesis
- Melena
- Splenomegaly
- Caput medusae, ascites
- Hemorrhoids
- Portal hypertensive gastropathy
Effects of liver cell failure:
- Coma–> hepatic encephalopathy; from release of ammonia and other toxic metabolites from liver
- Scleral icterus
- musty smelling breath
- gynecomastia
- jaundice
- testicular atrophy
- asterixis (hand flap)
- bleeding tendency (from decreased prothrombin and clotting factors)
- anemia
- ankle edema
liver enzymes (AST, ALT) in alcoholic vs viral hepatitis?
alcoholic hepatitis: AST>ALT
viral hepatitis: ALT>AST
Lactulose
- Osmotic laxative
- Also: Treatment for hepatic encephalopathy (in liver failure) –> b/c gut bacteria break it down, promoting nitrogen excretion as NH4+
GGT (gamma-glutamyl transpeptidase)
serum marker for liver disease; elevated with heavy alcohol consumption
decreased ceruloplasmin?
Wilson’s disease
elevated amylase?
- acute pancreatitis
- also elevated in MUMPS!
elevated lipase?
acute pancreatitis
elevated Alkaline Phosphatase?
- non-specific:
- obstructive liver disease (hepatocellular carcinoma)
- bone disease
- bile duct disease
*if elevated ALP, can then check GGT. If elevated GGT, then know it’s d/t liver disease
What is Reye’s syndrome? What are the signs/symptoms?
=Childhood Hepatoencephalopathy:
- ->mitochondrial abnormalities
- ->fatty liver (microvesicular fatty change)
- ->hypoglycemia
- ->vomiting
- ->hepatomegaly
- ->coma
Mechanism: aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzymes
One disease when children should be treated with aspirin?
Kawasaki’s (to prevent coronary artery thrombosis)
Best indicators of Liver function and progrnosis?
Prothrombin time and Serum albumin (albumin is made in liver, as are clotting factors)
*hypoalbuminemia + elevated PT = POOR prognosis.
3 stages of alcoholic liver injury:
-Reversible?
1) Hepatic steatosis
- -> Macrovesicular steatosis/fatty change associated with moderate alcohol intake
- ->REVERSIBLE with alcohol cessation
2) Alcoholic hepatitis:
- ->from sustained, long-term alcohol intake
- ->swollen and necrotic hepatocytes; neutrophil infiltration
- ->Mallory bodies (intracytoplasmic eosinophilic inclusions)
3) Alcoholic cirrhosis:
- ->shrunken liver with “hobnail” appearance
- ->sclerosis around central vein
- ->looks like chronic liver disease: hypoalbuminemia, jaundice…
- ->IRREVERSIBLE
Hepatic steatosis:
- macrovesicular fatty change of liver; see hepatocytes filled with lipid droplets
- Reversible effect of moderate alcohol intake; can reverse by stopping to drink alcohol
- **can also get fatty liver from certain HIV drugs; metabolic syndrome; etc…
Mallory bodies
intracytoplasmic eosinophilic inclusions within hepatocytes; see in alcoholic hepatitis
7 diseases associated with increased risk of hepatocellular carcinoma:
- Hepatitis B
- Hepatitis C
- Hemochromatosis
- Carcinogens (specifically Alfatoxin from Aspergillus)
- Alcoholic cirrhosis
- alpha-1-antitrypsin deficiency
- Wilson’s disease
cancer associatd with elevated alpha-fetoprotein?
Hepatocellular carcinoma
Common benign liver tumor in 30-50 year olds?
- Cavernous Hemangioma
- ->DON’T biopsy it! b/c may lead to hemorrhage
Nutmeg liver
Backup of blood into liver; d/t right heart failure and Budd-Chiari syndrome
–>if it persists, may result in cardiac cirrhosis
Condition that looks similar to Right Heart Failure (Hepatomegaly, etc) BUT, absence of jugular venous distension:
Budd-Chiari syndrome
Budd-Chiari syndrome:
- Occlusion of IVC or hepatic veins –> leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventually liver failure)
- ->may have varices and visible abdominal/back veins
- ->Looks kind of similar to Right heart failure, BUT absence of JVD
- ->Associated with:
- hepatocellular carcinoma
- pregnancy
- polycythemia vera
- hypercoagulable state
Liver cirrhosis + Panacinar Emphysema?
alpha-1-antitrypsin deficiency
–>this is a CODOMINANT trait
PAS-positive globules in liver?
alpha-1-antitrypsin deficiency
Cause of physiologic jaundice in neonates? Treatment?
Immature UDP-glucuronyl transferase at birth (physiologic): can’t convert unconjugated bilirubin to conjugated in liver –> get unconjugated/indirect hyperbilirubinemia –> Jaundice
*Treat with phototherapy: converts unconjugated bilirubin to a water-soluble form, so it can be renally excreted! COOL!
What is jaundice? What are the 3 causes/types of pathologic jaundice (not counting physiologic neonatal jaundice)?
Jaundice = yellowing of skin and/or sclerae d/t elevated bilirubin
- Causes:
- Hepatocellular injury
- Obstruction to bile flow
- Hemolysis
Jaundice, elevated bilirubin in response to fasting, stress, exercise?
- -> Gilbert’s syndrome
- -> have mildly decreased UDP-glucuronyl transferase (so decreased conversion of indirect to direct bilirubin) or decreased bilirubin intake
- ->mild disease; quite common, but most pts don’t even know they have it
- ->when flares: have indirect hyperbilirubinemia
pathologic jaundice early in life + kernicterus (bilirubin deposition in brain) + elevated unconjugated bilirubin
Crigler-Najjar Syndrome Type 1
–>absent UDP-glucuronyl transferase (so can’t convert indirect to direct bilirubin) –> get elevated indirect/unconjugated bilirubin
Treatment for Crigler-Najjar syndrome type 1?
- phototherapy (makes Unconjugated bilirubin water-soluble, so can excrete in urine)
- Plasmapheresis (get rid of excess unconjugated bilirubin)
–>Crigler Najjar type 1 is fatal within a few years
Crigler-Najjar type 2:
- what is it?
- treatment?
milder form of Crigler-Najjar type 1; have decreased amount of UDP-glucuronyl transferase (not absent, as in type 1)
–>can treat with phenobarbital (increases synthesis of liver enzymes, including UDP glucuronyl transferase)
Phenobarbital
Treatment for Crigler-Najjar type 2 (and can be used for symptomatic Gilbert’s)
–>increases synthesis of liver enzymes –> so, increases synthesis of UDP-glucuronyl transferase
Conjugated Hyperbilirubinemia + Black liver on gross examination
–>otherwise benign
=Dubin-Johnson syndrome
–>defective liver excretion of bilirubin; so get elevated conjugated bilirubin in blood
Rotor’s syndrome:
mild disorder, similar to Dubin-Johnson syndrome (but less severe); have defective liver excretion of bilirubin, so mildly elevated conjugated bilirubin in blood; unlike Dubin-Johnson syndrome, does not cause black liver
Disease d/t problem with bilirubin uptake into liver?
- Gilbert’s
- ->elevated unconjugated bilirubinemia
Diseases d/t problem with bilirubin conjugation
- Gilbert’s
- Crigler-Najjar types 1 and 2
- physiologic neonatal jaundice
–>elevated unconjugated bilirubinemia
Diseases d/t problem with bilirubin excretion from liver?
- Dubin-Johnson
- Rotor’s
–>elevated direct/conjugated bilirubinemia
Penicillamine
Treatment for Wilson’s disease
Kayser-Fleischer ring
yellow-green-golden brown corneal ring seen in Wilson’s disease
decreased levels of ceruloplasmin?
seen in Wilson’s disease
–>ceruloplasmin=major copper-carrying protein in blood
Signs/symptoms of Wilson’s disease: “CCCCCopper is Hella BADDD”
- decreased Ceruloplasmin
- Corneal deposits = Kayser-Fleischer rings
- Cirrhosis
- Copper accumulation (in liver, brain, cornea, kidneys, joints, etc)
- hepatocellular Carcinoma (increased risk)
- Hemolytic anemia
- Basal ganglia degeneration (specifically, degeneration of PUTAMEN); get parkinsonian symptoms
- Asterixis
- Dementia
- Dyskinesia
- Dysarthria
***Treat with Penicillamine
What part of brain is degenerated in Wilson’s disease?
Basal ganglia, specifically Putamen, degeneration
–>get Parkinsonian symptoms
micronodular Cirrhosis + Diabetes + skin pigmentation?
Hemochromatosis = “Bronze” diabetes
Deferoxamine
Treatment for hereditary Hemochromatosis
–>also do repeated phlebotomy
Causes of hemochromatosis?
- herditary (autosomal recessive)
- secondary to repeated blood transfusions (ie in Beta-thalassemia major)
lab findings in Hemochromatosis: ferritin, iron, TIBC, transferring?
- elevated ferritin (stores iron within cells)
- elevated iron
- decreased TIBC (indirect measure of transferrin, which transports iron in blood)
- elevated transferritin saturation (serum Fe/TIBC)
Which HLA is associated with hemochromatosis?
HLA-A3
Complications/Results of Hemochromatosis:
- CHF
- Testicular atrophy in males
- increased risk of hepatocellular carcinoma
Cause of primary biliary cirrhosis?
- ->Autoimmune reaction: get lymphocytic infiltrate and granulomas
- ->mostly seen in middle-aged women
- ->anti-mitochondrial antibodies
Elevated anti-mitochondrial antibodies?
Primary biliary cirrhosis
Causes and pathophysiology of Secondary Biliary Cirrhosis?
–>Extrahepatic biliary obstruction (like a gallstone, biliary stricture, carcinoma of head of pancreas, chronic pancreatitis) –> so, get increased pressure in intrahepatic ducts –> injury and fibrosis –> bile stasis
“onion skin” bile duct fibrosis?
Primary Sclerosing Cholangitis (a biliary tract disease)
Presentation and Labs in Biliary Tract Diseases (Primary and Secondary Biliary Cirrhosis, Primary Sclerosing Cholangitis):
Presentation:
- Pruritis
- Jaundice
- Dark urine (b/c elevated urobilinogen in urine)
- Pale stools (b/c bile not making it into stools)
- Hepatosplenomegaly
Labs:
- Conjugated/Direct Hyperbilirubinemia
- elevated cholesterol
- elevated ALP
Pruritus in a middle-aged woman + elevated conjugated bilirubinemia?
- ->Consider primary biliary cirrhosis
- ->may also consider primary sclerosing cholangitis
Complication of Secondary Biliary Cirrhosis?
Ascending cholangitis = infection of biliary tree (makes sense, b/c have an obstruction of bile flow; bile stasis; etc…)
What condition is Primary Sclerosing Cholangitis associated with?
Ulcerative Cholitis
-primary sclerosing cholangitis can also lead to secondary biliary cirrhosis
Biliary tract disease with Hypergammaglobulinemia (IgM)?
–>Primary sclerosing cholangitis
5 main risk factors for gallstones/cholelithiasis:
5 F’s:
- Female
- Forty
- Fat
- Fertile (multiparity)
- Feathers (Native Americans)
Charcot’s triad of cholangitis (infection of biliary tree/common bile duct):
1) Jaundice
2) Fever
3) RUQ pain
Murphy’s sign
- ->positive in cholecystitis; good way to dx pain in the RUQ
- ->positive: when deeply palpate, pt has inspiratory arrest b/c such deep pain
Pain on deep palpation, causing inspiratory arrest
Positive Murphy’s sign
–> positive in cholecystitis; way to dx RUQ pain
3 causes of gallstones:
- elevated cholesterol and/or bilirubin
- decreased bile salts
- gallbladder stasis
–>all of these can cause stones
Most common cause of cholecystitis (inflammation of gallbladder)?
Gallstones
–>have positive Murphy’s sign!
Ascending cholangitis =
inflammation of bile duct; usually d/t obstruction of duct by gallstones
What is acute pancreatitis?
=autoingestion of pancreas by pancreatic enzymes. ouch.
Causes of Acute Pancreatitis:
“GET SMASHED”
- ->Gallstones and Ethanol = Most common causese
- Gallstones
- Ethanol
- Trauma
- Steroids
- Mumps
- Autoimmune disease
- Scorpion sting
- Hypercalcemia/Hypertriglyceridemia
- ERCP (Endoscopic Retrograde Cholangiopancreatography = endoscopic technique to dx/treat problems of pancreatic or biliary ducts; but, main risk of it = acute pancreatitis)
- Drugs (ie sultas, HIV drugs…)
#1 cause of chronic pancreatitis? -other main cause?
#1 = alcoholism other main cause = smoking
labs in acute pancreatitis:
-elevated amylase and lipase (lipase = more specific)
steatorrhea, fat-soluble vitamin deficiency, diabetes
pancreatic insufficiency; may be a result of chronic pancreatitis (which is usually d/t alcoholism or smoking)
CA-19-9
specific tumor marker for Pancreatic adenocarcinoma
CEA
less specific tumor marker for pancreatic adenocarcinoma
painless jaundice in male >50 years old?
consider Pancreatic adenocarcinoma
#1 risk factor for Pancreatic Adenocarcinoma? -other risk factors?
1 = Smoking (but, not alcoholism)
- other risk factors:
- chronic pancreatitis (which is usually caused by alcoholism or smoking… kind of contradicts the not alcoholism thing…)
- Jewish and African American males
- > 50 years old
- Diabetes
- Genetics
Courvoiseier’s sign:
- obstructive jaundice with palpable gallbladder
- ->pruritus, dark urine, pale stools (all signs of obstructive jaundice…)
- ->see with pancreatic adenocarcinoma
Trousseau’s syndrome:
- migratory thrombophlebitis–> redness and tenderness on palpation of extremities
- ->see with pancreatic adenocarcinoma
Presentation of pancreatic adenocarcinoma:
- abdominal pain that radiates to back
- weight loss
- redness and tenderness on palpation of extremities (migratory thromboephlebitis = Trousseau’s sign)
- Obstructive jaundice and palpable gallbladder –> pruritus, dark urine, pale stools (=Courvoiseier’s sign)
Asterixis:
See in:
- liver cell failure
- Wilson’s disease
- Uremia (increased BUN and Creatinine, like in renal failure)
Drugs that end in “-dine”
H2 blockers: Cimetadine, Ranitidine, Famotidine, Nizatidine
–> take H2 blockers before you “dine”
Ranitidine
H2 blocker
Cimetidine
H2 blocker
- ->inhibits cytochrome P450!
- ->also:
- gynecomastia, impotence, decreased libido in males (anti-androgen effects)
- can cross BBB (headaches, dizziness, confusion)
- can cross placenta
Famotidine
H2 blocker
Nizatidine
H2 blocker
Drugs that can cause gynecomastia? (random, not necessarily GI)
“Some Drugs Create Awesome Knockers”
- Spirinolactone
- Digitalis
- Cimetidine
- Alcohol
- Ketoconazole
Mechanism of H2 blockers?
- reversibly block Histamine (released from ECL cells, after stimulation by Gastrin) from binding to the H2 receptor on gastric parietal cells
- ->get decreased cAMP, meaning no stimulation of the ATP-ase –> decreased H+ secretion from parietal cells into gastric lumen
What are more potent drugs: H2 blockers or PPIs?
PPIs are more potent than H2 blockers; so, use H2 blockers for less severe cases; PPIs for more severe
*note: H2 blockers are reversible; PPIs are irreversible
drugs ending in “-prazole”
PPIs (proton pump inhibitors)
- Omeprazole
- Lansoprazole
- Pantroprazole
- Esomeprazole
Omeprazole
PPI
Lansoprazole
PPI
1st line treatment for Zollinger-Ellison syndrome?
Proton Pump Inhibitors
Mechanism of PPIs?
Irreversibly inhibit Proton Pump (H/K-ATPase) in parietal cells (so, can’t excrete H+ into gastric lumen from parietal cells)
Bismuth
- treatment of ulcers and traveler’s diarrhea
- mechanism: binds to ulcer base, providing physical protection; thus allowing HCO3- secretion to reestablish pH gradient in mucus layer
Sucralfate
Same mechanism as bismuth; treatment of ulcers and traveler’s diarrhea
- ->bind to ulcers, providing physical protection; allows HCO3- secretion to reestablish pH gradient in mucus layer
- Requires an acidic environment to polymerize; WONT WORK IF TAKING ANTACIDS CONCURRENTLY!
Misoprostol:
- mechanism
- clinical uses
- side effect
- contraindications
- Prostaglandin analog
- Mechanism: binds receptor on parietal cell –> stimulates Gi –> decreased cAMP –> decreased stimulation of Proton Pump –> decreased acid production/secretion into gastric lumen
- Clinical uses:
- Prevent NSAID-induced peptic ulcers (b/c NSAIDs decrease prostaglandins)
- Treatment of PDA
- Induce labor
- Side effect:
- Diarrhea
- Conraindication:
- Pregnant women/women of child-bearing age (b/c induces labor)
Octreotide:
- mechanism
- clinical uses
Somatostatin analog
*Somatostatin/Octreotide –> Gi –> blocks/decrease cAMP –> blocks Proton Pump –> decreased acid secretion into gastric lumen
- Uses:
- secretory diarrhea
- acute variceal bleeds
- acromegaly (inhibits GH)
- VIPoma (pancreatic islet cell tumor that secretes lots of Vasoactive Intestinal Polypeptide, causing lots of diarrhea)
- Carcinoid tumors
Treatment of VIPoma?
Octreotide
Treatment of Carcinoid Syndrome?
Octreotide
Diphenoxylate
opiate-anti-diarrheal drug;
–>binds to Mu opiate receptors in GI tract and slows motility
Side effects of Antacids?
- all can cause hypokalemia (b/c block H/K-ATPase)
- Can chelate and decrease effectiveness of other drugs
Side effects of Aluminum Hydroxide (antacid) overuse?
- “aluMINIMUM of feces”= constipation
- hypokalemia and decrease efficacy of other drugs (all antacids)
- others
Side effects of Magnesium Hydroxide (antacid) overuse:
“Must Go to the bathroom” = diarrhea
- hypokalemia and decrease efficacy of other drugs (all antacids)
- others
Side effects of Calcium carbonate (antacid = TUMS!)
- Hypercalcemia
- may cause rebound increase in acid!
- hypokalemia and decrease efficacy of other drugs (all antacids)
Magnesium hydroxide
- osmotic laxative
- also an antacid (with side effect of diarrhea!)
Magnesium citrate
-osmotic laxative
Polyethylene glycol
Osmotic laxative
Infliximab clinical uses?
- monoclonal anti-TNF antibody
- Uses:
- Crohn’s disease
- Rheaumatoid arthritis
Sulfasalazine:
- mechanism?
- clinical uses?
=combo of Sulfapyridine (antibacterial) + 5-ASA (aminosalicylic acid = anti-inflammatory)
–>activated by colonic bacteria (so, only effective in distal ileum and colon)
- clinical uses:
- Ulcerative Colitis (always)
- Crohn’s (but, only acts in distal ileum and colon; so, only if disease is localized to those areas, which it often is)
Odansetron:
- mechanism
- clinical uses
- side effects
=anti-serotonin and anti-emetic
- Clinical uses:
- pts undergoing chemo, to combat nausea/vominiting
- pregnant women with morning sickness
- side effects:
- headache (think opposite of triptans, which are serotonin-agonists; relieve headaches)
- constipation (think opposite serotonin/carcinoid syndrome, which causes diarrhea)
Metoclopramide:
- mechanism
- uses
- toxicity/side-effects
- contraindications
=D2-receptor antagonist (Dopamine-blocker)
- uses:
- diabetic and post-surgery gastroparesis (delayed gastric emptying)
- Toxicities/Side effects:
- may lower seizure threshold
- parkinsonian symptoms (b/c block dopamine)
- diarrhea, etc…
- Contraindications:
- Parkinson’s disease (duh)
- small bowel obstruction (duh)
4 Drugs that may lower seizure threshold? (random, not specific to GI)
1) Metoclopramide (treats gastroparesis)
2) Buproprion (anti-depressant w/out sexual side effects; increased seizures, especially pts with bulemia or anorexia)
3) Tramadol (used to treat chronic pain; weak opiod-agonist; inhibits serotonin and NE reuptake, but not used to treat depression)
4) Enflurane (inhaled anesthetic)
