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213 Cards in this Set

  • Front
  • Back
What structures does the Celiac Artery supply?
Those of Foregut embryonic origin:

Stomach to proximal duodenum
What structures does the SMA supply?
Those of Midgut embryonic origin:

Distal duodenum to proximal 2/3 of transverse colon
What structures does the IMA supply?
Those of Hindgut embryonic origin:

Distal 1/3 of transverse colon to upper portion of rectum
Which artery supplies the structures derived from foregut?
Celiac A.
Which artery supplies the structures derived from Midgut?
Which artery supplies the structures originating from the Hindgut?
What are the main branches of the celiac trunk?
Celiac-> L. Gastric, Splenic, Common hepatic

Common Hepatic -> Hepatic Artery Proper, R. Gastric, Gastroduodenal A.
What are the five portal-systemic anastamoses?
(1) L. Gastric + Azygous --> Esophageal Varices
(2) Superior + Inferior Rectal --> External Hemorrhoids
(3) Paraumbilical + Inferior epigastric --> Caput Medusae
(4) Retroperitoneal + Renal
(5) Retroperitoneal + Paravertebral
What are the common findings in portal hypertension?

1. Esophageal varices
2. External hemorrhoids
3. Caput medusae
What are the layers of the gut wall inside to outside?
1. Mucosa
2. Submucosa
3. Muscularis Externa
4. Serosa/Adventitia
What makes up the Mucosa layer of the gut wall?
[] Epithelium (absorption)
[] Lamina propria (support)
[] Muscularis mucosa (mucosal motility)
What is Meissner's plexus?
(S)ubmucosal nerve plexus that controls (S)ecretions, blood flow & absorption. Contains cell bodies of parasympathetic terminal effector neurons.
What is Auerbach's plexus?
(M)yenteric nerve plexus (found between longitudinal & circular muscle layers) controls (M)otility
Which nerve plexus controls Secretions?
Meissner's Plexus = Submucosal plexus = between mucosa & muscularis externa.
Which nerve plexus controls Motility?
Auerbach's Plexus = Myenteric Plexus = between external & internal muscular layers.
What is Brunner's Glands?
Secrete alkaline mucus to neutralize acid contents entering the duodenum. Located in duodenal submucosa -- only GI submucosal glands. Hypertrophied in peptic ulcer disease.
[Hypertrophied Brunner's Glands]
Peptic Ulcer Disease
What is Peyer's Patch?
Unencapsulated lymphoid tissue found in lamina propria & submucosa of small intestine. Secretes IgA to deal with intraluminal antigens. Specialized M cells take up antigens.
What are the sinusoids of liver?
Irregular "capillaries" with fenestrated endothelium. No basement membrane. Allows macromolecules of plasma full access to basal surface of hepatocytes through perisinusoidal space.
What is the significance of the pectinate line?
It represents the point where hindgut meets ectoderm.
What is found above the pectinate line?
[] Internal hemorrhoids (not painful)
[] bec. Visceral innervation
[] Adenocarcinoma
[] Superior rectal Artery (via IMA)
[] Superior rectal Vein (portal system)
What is found below the pectinate line?
[] External hemorrhoids (painful)
[] bec. Somatic innervation
[] squamous cell carcinoma
[] Inferior rectal artery (via internal pudendal A.)
[] Inferior rectal vein (IVC)
What is found in the Femoral triangle?
Lateral to medial: N-(AVEL):
[] Nerve (outside sheath)
[] Artery
[] Vein
[] Empty space
[] Lymphatics
What is a femoral hernia?
Entrance of abdominal contents through the femoral canal.
What is the sourece of salivary secretions?
Parotid, submandibular, submaxillary & sublingual glands
What is the function of salivary secretions?
(1) alpha-amylase (ptyalin) begins starch digestion; inactivated by low pH of stomach
(2) bicarbonate neutralizes oral bacterial acids, maintains dental health
(3) mucins (glycoproteins) lubricate food
What is the innervation of salivary secretions?
sympathetic (T1-T3) &
parasympathetic (facial, glossopharyngeal)
What is the flow rate of salivary secretions?
low flow rate = hyptonic
high flow rate = isotonic
What are the four GI secretory products?
(1) Intrinsic Factor
(2) Gastric Acid
(3) Pepsin
(4) HCO3-
What is Intrinsic Factor?
Produced by: Parietal cells of the stomach

Action: Required for B12 uptake in terminal ileum

Notes: Autoimmune destruction of parietal cells --> Chronic gastritis & pernicious anemia
What is Gastric acid?
Produced by: Parietal cells of the stomach

Action: lower stomach pH

Regulation: [+]Histamine, ACh, Gastrin; [-]Somatostatin, GIP, prostaglandin, secretin
What up-regulates Gastic acid secretion?
What down-regulates Gastric acid secretion?
What is Pepsin?
Produced by: Chief cells of the stomach

Action: Protein digestion; optimal fxn @ pH 1-3.

Regulation: [+]by vagal stimulation, local acid

Notes: Pepsinogen --> Pepsin by H+
What is HCO3- as a gastric secretion?
Produced by: Mucosal cells of stomach & duodenum

Action: Neutralizes acid; prevents autodigestion

Regulation: [+]Secretin
What are the GI hormones?
[] Gastrin
[] Cholecystokinin
[] Secretin
[] Somatostatin
[] Gastric inhibitory peptide (GIP)
What is Gastrin?
Source: G cells, antrum of stomach

Action: [+]H+ secretion, growth of gastric mucosa, gastric motility

Regulation: [+]Stomach distension, amino acids, peptides, vagal stimulation [-]H+ secretion and stomach acid pH <1.

Notes: [++]in Zollinger-Ellison; phenylalanine & tryptophan are stimulators
<Elevated Gastrin Levels>
What is CCK?
Aka: Cholecystokinin

Source: I cells, duodenum, jejunum

Action: [+]pancreatic secretion, gallbladder contraction, growth of exocrine pancreas & gallbladder; [-]gastric emptying

Regulation: [-]secretin & stomach pH <1.5; [+]fatty acids, amino acids

Notes: In cholelithiasis, pain worsens after fatty food ingestion due to [+]CCK
What is secretin?
Source: S cells, duodenum

Action: [+]pancreatic HCO3- secretion; [-]gastric acid secretion

Regulation: [+]acid, fatty acids in lumen of duodenum

Notes: HCO3- neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function
What is Somatostatin?
Souce: D cells, pancreatic islets; GI mucosa

Action: [-]gastric acid & pepsinogen secretion, pancreatic & small intestine fluid secretion, gallbladder contraction, insulin & glucagon release

Regulation: [+]acid; [-]vagal stimulation

Notes: Inhibitory hormone; antigrowth hormone effects
What is GIP?
AKA: Gastric Inhibitory Peptide

Source: K cells, duodenum & jejunum

Action: Exocrine -- [-]gastric H+ secretion; Endocrine -- [+]insulin release

Regulation: [+]fatty acids, amino acids, oral glucose (only GI hormone stimulated by all 3!)

Notes: [+]GIP is why an oral glucose load is used more rapidly than the equivalent given by IV
What is absorbed in the stomach?
What is absorbed in the duodenum?
[]Glucose, via Na co-transport
[]Vitamins A & D
[]Fatty acids
What is absorbed in the proximal jejunum?
[]glucose, galactose, monosaccharides, disaccharides
[]vit A & D
[]Fatty acids
[]Proteins & Amino Acids
What is absorbed in the terminal jejunum?
[]Water-soluble vitamins
[]fatty acids
[]proteins & amino acids
What is absorbed in the ileum?
[]Proteins & amino acids
[]vitamin B12
[]Bile salts
What is absorbed in the colon?
[]Short-chain fatty acids
Where are proteins & amino acids absorbed?
[]Proximal & Terminal jejunum
Where is glucose absorbed?
[]proximal jejunum
Where are fatty acids absorbed?
[]proximal jejunum
[]terminal jejunum
[]colon (short chain only)
What receptors are found on the parietal cell?
[]H2 histamine receptor (Ranitidine, Cimetidine, Famotidine)
[]M3 ACh receptor (Anticholinergics)
[]Prostaglandin (Misoprostol)
What pancreatic enzyme digests starch?
Alpha amylase -- secreted in active form
What pancreatic enzymes digest fats?
lipase, phospholipase A, colipase
What pancreatic enzymes digest proteins?
Note: Secreted as proenzymes
How are pancreatic proenzymes activated?
Trypsinogen is converted to active enzyme trypsin by enterokinase, a duodenal brush-border enzyme.
What is pancreatic insufficiency?
seen in CF and others. Pts present w/ malabsorption & steatorrhea. Limit fat intake, monitor for signs of fat-soluble deficiency.
What vitamins are fat-soluble?
Vit A, D, E & K
What carbohydrates are absorbed?
Only monosaccharides (glucose, galactose & fructose)
What does salivary amylase do?
Starts digestion. Hydrolyzes alpha-1,4 linkages to yield disaccharides (maltose, maltotriose & alpha-limit dextrans)
What does pancreatic amylase do?
Hydrolyzes starch to oligosaccharisdes & disaccharides. Highest conc. in duodenum.
What does oligosaccharide hydrolases do?
At brush border of intestine. Rate-limiting step in carbohydrate digestion, produces monosaccharides from oligo- and disaccharides.
Where do the hepatocytes face in liver?
apical surface towards bile canaliculi. basolateral surface towards sinusoids.
What is the difference between direct & indirect bilirubin?
Direct is conjugated with glucuronic acid; water soluble. Indirect is unconjugated and not water soluble.
What makes up bile?
[] Bile salts (bile acids conjugated to glycine or taurine to make them water soluble)
[] phospholipids
[] cholesterol
[] bilirubin
[] water
[] ions
What is a diaphragmatic hernia?
Abdominal structures enter the thorax; most commonly a hiatial hernia -- stomach herniates upwards through esophageal hiatus. also may occur in infants as a result of defective development of pleuroperitoneal membrane.
What is the difference in location between a direct and an indirect hernia?
[MDs don't LIe]
[M]edial to inferior epigastric artery = [D]irect hernia.
[L]ateral to inferior epigastric artery = [I]ndirect hernia.
What is an Indirect Inguinal Hernia?
INdirect hernia goes through the INternal (deep) inguinal ring and external (superficial) inguinal ring and INto the scrotum. Lateral to Inferior epigastric A. INdirect hernias occur in INfants owing to failure of processus vaginalis to close. Much more common in males.
What is a direct inguinal hernia?
Protrudes through the inguinal triangle. Direct hernia bulges directly through abdominal wall medial to inferior epigastric artery. Goes through external inguinal ring only. Usually in older men.
What are the borders of Hesselbach's triangle?
Hesselbach's triangle = inguinal triangle:

[] Inferior epigastric artery
[] lateral border of rectus abdominis
[] inguinal ligament
What is achalasia?
Failure of relaxation of LES due to loss of Auerbach's plexus. Progressive dysphagia & [+] risk of esophageal carcinoma. May be secondary to Chagas' disease. "Bird beak" on barium swallow.
<"Bird beak" on barium swallow>
What is a Meckel's Diverticulum?
Persistence of vitelline duct. Most common congenital abnormality of the GI tract.

Five 2's
[] 2 inches long
[] 2 feet from ileocecal valve
[] 2% of population
[] presents in first 2 years of life
[] may have 2 types of epithelia
What are the enzyme markers of GI pathology?
[] Aminotransferases (AST / ALT)
[] GGT
[] Alkaline phosphate
[] Amylase
[] Lipase
[] Ceruloplasmin
What is the significance of Aminotransferase findings?
[] ALT > AST = Viral Hepatitis
[] AST > ALT = Alcoholic Hepatitis
[] AST Only = MI
What is the significance of Alkaline phosphatase findings?
Obstructive liver disease (hepatocellular carcinoma) or bone disease
What is the significance of amylase/lipase findings?
Acute pancreatitis
What is the significance of lowered Ceruloplasmin findings?
Wilson's disease
What is Barrett's Esophagus?
BARRett's = [B]ecomes [A]denocarcinoma, [R]esults from [R]eflux

Glandular metaplasia replacement of squamous epithelium in distal esophagus due to chronic acid reflux.
What are the risk factors for Esophageal cancer?
[B]arrett's esophagus
[D]iverticuli (eg. Zenker's)
[E]sophageal web (eg Plummer-Vinson) / [E]sophagitis

Usually Squamous. Barrett's leads to Adenocarcinoma
What is Congential pyloric stenosis?
Hypertrophy of the pylorus causes obstruction. Palpable "olive" mass in epigastic region and nanbilious projectile vomiting at 2 weeks of age. Treatment via surgical incision. Occurance 1/600 live births, often in 1st born.
<Palpable "olive" mass in epigastric region>
Congenital pyloric stenosis
What is the significance of lowered Ceruloplasmin findings?
Wilson's disease
What is Barrett's Esophagus?
BARRett's = [B]ecomes [A]denocarcinoma, [R]esults from [R]eflux

Glandular metaplasia replacement of squamous epithelium in distal esophagus due to chronic acid reflux.
What are the risk factors for Esophageal cancer?
[B]arrett's esophagus
[D]iverticuli (eg. Zenker's)
[E]sophageal web (eg Plummer-Vinson) / [E]sophagitis

Usually Squamous. Barrett's leads to Adenocarcinoma
What is Congential pyloric stenosis?
Hypertrophy of the pylorus causes obstruction. Palpable "olive" mass in epigastic region and nanbilious projectile vomiting at 2 weeks of age. Treatment via surgical incision. Occurance 1/600 live births, often in 1st born.
<Palpable "olive" mass in epigastric region>
Congenital pyloric stenosis
List the malabsorption syndromes.
[] Celiac sprue
[] Tropical sprue
[] Whipple's disease
[] disaccharidase deficiency
[] pancreatic insufficiency
What is Celiac sprue?
Autoantibodies to gluten (gliadin) in wheat and other grains. Proximal small bowel.
What is Tropical sprue?
Probably infectious.
Responds to antibiotics
Affects entire small bowel
What is Whipple's disease?
Infection with Tropheryma whippelii;
PAS-positive macrophages in intestinal lamina propria. Can only see organisms on EM.
<PAS-positive macrophages in intestinal lamina>
Whipple's disease.
What is disaccharidase deficiency?
AKA Lactase deficiency
What is Pancreatic insufficiency?
Due to CF, chronic pancreatitis.
Causes malabsorption of fat, protein, vitamins A, D, E & K
What is Acute gastritis?
aka Erosive gastritis
Disruption of mucosal barrier -> inflammation.
Caused by stress, NSAIDs, alcohol, uricemia, burns (Curling's ulcer) & brain injury (Cushing's ulcer)
What is Curling's ulcer?
acute gastritis due to burns.
What is Cushing's ulcer?
acute gastritis due to brain injury.
What is type A chronic gastritis?
aka fundal
[four A's]

[A]utoimmune disorder characterized by
[A]utoantibodies to parietal cells,
pernicious [A]nemia
What is type B chronic gastritis?
aka antral

Type B = a Bug = H. pylori
What risk is increased in chronic gastritis?
gastric arcinoma
What are the two types of peptic ulcer diseases?
gastric ulcer & duodenal ulcers
What are the findings associated with peptic ulcer disease?
[] clean "punched-out" margins (vs carcinoma)
[] complications include bleeding, penetration, perforation & obstruction
[] Incidence 2x in smokers
What is a gastric ulcer?
[] pain [G]reater with meals -> weight loss
[] H. pylori 70%
[] also chronic NSAIDs
[] Due to [-]mucosal protection against gastric acid
What is a duodenal ulcer?
[] Pain [D]ecreases with meals -> weight gain
[] 100% H. pylori
[] due to [+]gastric acid secretion or [-] mucosal production
[] hypertrophy of Brunner's glands
What is Virchow's node?
Involvement of left-sided supraclavicular node implies mets from stomach or below
What is a Krukenberg tumor?
bilateral metastasies to ovaries of stomach cancer. Via hematogenous spread. Abundant mucus, "signet-ring" cells in ovaries.
<Thick rigid stomach>
Linitis plastica due to gastric adenocarcinoma.
What is stomach cancer?
[] Adenocarcinoma
[] agressive local spread & node/liver mets
What is associated with stomach cancer?
[] dietary nitrosamines
[] achlorhydria
[] chronic gastritis
Where does stomach cancer like to spread?
[] liver
[] supraclavicular (virchow's) node
[] ovaries (krukenberg's)
What are the possible etiologies of IBD?
CD: Infectious
UC: Autoimmune
Where do you find IBD?
CD: Any portion of GI tract. Usually terminal ileum. Skip lesions with Rectal sparing
UC: Colitis = colonic inflammatioin continuous starting from rectum.
What is the gross morphology of Crohn's Disease?
[] Transmural inflammation.
[] Cobblestone mucosa.
[] creeping fat.
[] bowel wall thickening.
[] linear ulcers
[] fissures
[] fistulas
<"String sign" on barium swallow x-ray>
Crohn's disease
What is the gross morphology of Ulcerative Colitis?
[] Mucosal and submucosal inflammation only.
[] Friable pseudopolyps with freely hanging mesentery.
What is the microscopic morphology of IBD?
CD: Noncaseating granulomas and lympmhoid aggregates

UC: Crypt abscesses and ulcers, bleeding, no granulomas
What are the complications of IBD?
CD: strictures. fistulas. perianal disease. malabsorption. nutritional depletion

UC: sever stenosis. toxic megacolon. colorectal carcinoma
What are the extraintestinal manifestations of IBD?
CD: Migratory polyarthritis. erythema nodosum. ankylosing spondylitis. uveitis. immunologic disorders. kidney/gall stones

UC: pyoderma gangrenosum. primary sclerosing cholangitis
What disease is primary sclerosing cholangitis associated with?
Ulcerative colitis
What are the effects of smoking on IBD?
CD: smoking makes it worse

UC: smoking makes it better
What are the clinical findings in appendicitis?
initially diffuse periumbilical pain -> localized pain at McBurney's point. Nausea, fever; may performate -> perritonitis
What is the differential diagnosis for appendicitis?
[] Diverticulitis (elderly)
[] Ectopic pregnancy (use Beta-hCG test)
What is the most common indication for emergent abdominal surgery in children?
What is the difference between a true and false diverticulum?
True = all 3 gut wall layers outpouch

False = pseudodiverticiulum = only mucosa & submucosa outpouch. occur especially where vasa recta perforate muscularis externa
What is the most frequent location for diverticulum?
sigmoid colon
What is the most frequent location for GI polyps?
sigmoid colon
What is the most frequent location for GI cancer?
sigmoid colon
What is a diverticulum?
blind pouch leading off the alimentary tract that communicates with lumen of gut.

Most lack or have attenuated muscularis externa (ie "False")
What is diverticulosis?
[] Many diverticuli.
[] 50% is pts > 60 y/o
[] low-fiber diets
[] asymptomatic or rectal bleeding
What causes diverticulosis?
increased intraluminal pressure and focal waknesses in the colonic wall.
What is diverticulitis?
[] inflammation of diverticula.
[] Causes LLQ pain.
[] May perforate -> peritonitis, abscess or bowel stenosis.
What is intussusception?
[] "telescoping" of 1 bowel segment into distal segment.
[] Can compromise blood supply
[] Often due to intraluminal mass
What is volvulus?
[] Twisting of portion of bowel around its mesentery
[] May lead to obstruction and infection.
Were is the most frequent occurance of volvulus?
sigmoid colon where there is redundant mesentery
What is Hirschsprung's disease?
[] Congenital megacolon due to lack of nervous plexus in segment (both Auerbach & Meissner).
[] due to failure of neural crest cell migration
[] presents as constipation early in life (failure to pass muconium)
[] dilated portion of colon proximal to aganglionic segment
[] risk increased with Down syndrome
<failure to pass muconium>
[] Hirschsprung's disease
[] stenosis of rectal sphincter
What is the 3rd most common cancer?
Colorectal cancer
What are the risk factors for colorectal cancer?
[] colorectal villous adenomas
[] chronic IBD (esp. UC)
[] high-fat & low-fiber diets
[] [+] age
[] FAP
[] DCC gene deletion
[] personal/family hx of colon cancer
What is Peutz-Jeghers
a benign polyposis syndrome. Not a risk factor for CRC.
<"apple-core" lesion on barium swallow>
Colorectal cancer
What is CEA?
a nonspecific tumor marker. Used to screen for recurrance of CRC.
What is Cirrhosis?
Cirrho (Greek) = tawny yellow
diffuse fibrosis of liver, destroying normal architecture with nodular regeneration.
What are the two types of cirrhotic regeneration?
MICRONODULAR = < 3 mm, uniform size
Due to metabolic insult:
[] alcohol
[] hemochromatosis
[] Wilson's disease

MACRONODULAR = > 3mm, varied size.
Due to significant liver injury with hepatic necrosis:
[] postinfectious or drug induced hepatitis
[+] hepatocellular carcinoma
What is a portacaval shunt?
Shunt between splenic vein and left renal vein to relieve portal htn.
What are the effects of liver cell failure?
[] Coma
[] Scleral icterus
[] Fetor hepaticus (breath like a corpse)
[] Spider nevi
[] Gynecomastia
[] Jaundice
[] Loss of sexual hair
[] Asterixis = liver "flap"
[] Bleeding tendency ([-] prothrombin & clotting factors)
[] Anemia
[] Ankle edema
What is asterixis?
aka Liver "flap" = coarse hand tremor seen in liver failure
What are the effects of portal hypertension?
[] Esophageal varicies -> hematemesis / melena
[] peptic ulcer -> melena
[] splenomegaly
[] caput medusa
[] ascites
[] hemorrhoids
How can you identify alcoholic hepatitis in a lab test?
[A] [S]cotch & [T]onic = AST / ALT > 1.5
What are the clinical findings of alcoholic hepatitis?
[] swollen & necrotic hepatocytes
[] neutrophil infiltration
[] Mallory bodies
[] fatty change
[] sclerosis around central vein
[] elevated AST
<Mallory body>
intracytoplasmic eosinophilic inclusion seen in alcoholic hepatitis
What is another name for SGOT & SGPT?
What is Budd-Chiari syndrome?
Occlusion of IVC or hepatic veins with centrilobular congestion and necrosis leading to congestive liver disease.
What is associated with Budd-Chiari syndrome?
[] polycythemia vera
[] pregnancy
[] hepatocellular carcinoma
What is Wilson's disease?
aka hepatolenticular degeneration

Inadequate hepatic copper excretion and failure of copper to enter circulation as ceruloplasmin. Copper accumulates in:

[] liver
[] brain
[] cornea
[] kidney
[] joints

AR inheritance
Treat with penicillamine
What are the clinical findings in Wilson's disease?

[B]asal ganglia degeneration (parkinsonian sx)
[C]eruloplasmin depressed, [C]irrhosis, [C]orneal deposits (Kayser-Fleischer rings), [C]opper accumulation, [C]arcinoma, [C]horea
<brown pigmentation in a ring around the periphery of cornea>
Kayser-Fleischer rings indicative of Wilson's disease. Often presents with mental deterioration & tremor
<Bronze skin color>
What is hemochromatosis?
disease caused by hemosiderosis = deposition of hemosiderin (iron)

May be primary (AR inheritance) or secondary to chronic transfusion therapy.

Treated with phlebotomy, defroxamine
What are the clinical signs of hemochromatosis?
[] micronodular cirrhosis
[] pancreatic fibrosis
[] skin pigmentation (bronze)
What are the results of hemochromatosis?
[] CHF
[] hepatocellular carcinoma
What are the three types of jaundice?
[] Obstructive (>50% direct)
[] Hepatocellular (20-50% direct)
[] Hemolytic (<20% direct)
What are the clinical findings in hepatocellular jaundice?
(caused by hepatitis):

[] conjugated/unconjugated hyperbillirubinemia
[+] urine bilirubin
[=/-] urine urobilinogen
What are the clinical findings in obstructive jaundice?
(caused by obstruction in common bile duct etc):

[] conjugated hyperbillirubinemia
[+] urine bilirubin
[-] urine urobilinogen
What are the clinical findings in hemolytic jaundice?
(caused by hemolytic anemia, crigler-najjar):

[] unconjugated hyperbilirubinemia
[-] Absent urine bilirubin
[+] urine urobilinogen
What is Gilbert's syndrome?
Mildly [-] UDP-glucuronyl transferase. Asymptomatic. unconjugated bilirubin elevated w/o hemolysis.
What is Crigler-Najjar syndrome?
Absent UDP-glucuronyl transferase. Presents early in life & pts die within a few years. Treatment with plasmapheresis & phototherapy. Type I more severe. Type II responds to phenobarbital.
What is Dubin-Johnson syndrome?
Conjugated hyperbilirubinemia due to defective liver excretion. Grossly black liver. Benign.
What is Rotor's syndrome?
a milder form of Dubin-Johnson
<Black liver>
Dubin-johnson syndrome
What are the three types of hereditary hyperbilirubinemias?
[] Gilbert's syndrome
[] Crigler-Najjar
[] Dubin-Johnson
What is Primary sclerosis colangitis?
[] Inflammation & fibrosis of bile ducts associated with UC.
[] Leads to secondary bilary cirrhosis.
[] Alternating strictures & dilation with "beading" on ERCP
What is Charcot's triad of cholangitis?
[1] Jaundice
[2] Fever
[3] RUQ pain
<"beading" on ERCP>
<Increased AMA>
serum anti-mitochondrial antibodies are indicative of Primary Biliary Cirrhosis
What are the clinical manifestations of PBC?
Primary Biliary Cirrhosis:

[] Intrahepatic
[] Autoimmune disorder
[] Severe obstructive jaundice
[] Steatorrhea
[] Pruritus
[] Hypercholesterolemia (xanthoma)
What serum values are elevated in PBC?
[] Alkaline Phosphatase
[] Serum mitochondrial antibodies
What are the clinical manifestations of SBC?
Secondary Biliary Cirrhosis:

[] Extrahepatic biliary obstruction -> [+] pressure in intrahepatic ducts -> injury/fibrosis
[] complicated by ascending cholangitis (bacterial infection)
[] "bile lakes"
<"bile lakes">
Secondary Biliary Cirrhosis
What serum values are increased in SBC?
[] Alkaline phosphatase
[] conjugated bilirubin
What is the most common primary malignant tumor of the liver in adults?
Hepatocellular carcinoma = Hepatoma
What things are associated with increased risk for hepatocellular carcinoma?
[] hepatitis B & C
[] Wilson's disease
[] hemochromatosis
[] alpha-1-antitrypsin deficiency
[] alcoholic cirrhosis
[] carcinogens
How does Hepatocellular carcinoma present?
[] Tender hepatomegaly
[] ascites
[] polycythemia
[] hypoglycemia
How is hepatocellular carcinoma spread?
hematogenous dissemination
What is elevated in HCC?
alpha-fetoprotein levels
What is Reye's syndrome?
Rare, often fatal childhood hepatoencephalopathy associated with viral infection (VZV & influenza B) & salicylates.

Findings: fatty liver, hypoglycemia & coma
What are the risk factors for gallstones?
Five [F]'s:

[F]ertile (multiparity)
What causes gallstones?
Elevated cholesterol and/or bilirubin overwhelms solubilizing bile acids and lecithin
What are the three types of stones?
[1] Cholesterol stones (10-20% radiopaque)
[2] Mixed stones (radiolucent)
[3] Pigment stones (radiopaque)
What factors are associated with increased risk for cholesterol stones?
[] obesity
[] CD
[] CF
[+] age
[] clofibrate
[] estrogens
[] multiparity
[] rapid wt loss
[] Native American origin
What is the most common type of gallstone?
Mixed cholesterol & pigment
What factors are associated with increased risk for pigment stones?
[] chronic RBC hemolysis
[] alcoholic cirrhosis
[] age
[] biliary infection
What are the causes of acute pancreatitis?

[A]utoimmune disease
[S]corpion sting
[D]rugs (eg sulfa)
What is associated with fatal pancreatitis?
What is the clinical presentation of acute pancreatitis?
epigastric abdominal pain radiating to back; anorexia, nausea

[+] amylase
[+] lipase (more specific)
What can pancreatitis lead to?
[] DIC
[] diffuse fat necrosis
[] hypocalcemia
[] pseudocyst formatioin
[] hemorrhage
[] infection
What is the most common cause of chronic calcifying pancreatitis?
What is the most common cause of chronic obstructive pancreatitis?
What is the prognosis for Pancreatic adenocarcinoma?
[] <6 months
[] Very aggressive
[] usually already metastasized
[] most common in pancreatic head -> obstructive jaundice
What is the clinical presentation for pancreatic adenocarcinoma?
[1] Abdominal pain radiating to back
[2] Weight loss
[3] migratory thrombophlebitis (Trousseau's syndrome)
[4] Obstructive jaundice with palpable gallbladder (Courvoisier's sign)
<Courvoisier's sign>
A palpable gallbladder indicates acute onset of obstructive jaundice (ie not stones -- they cause withered gallbladder)

Associated with: Pancreatic adenocarcinoma.
<Trousseau's syndrome>
Recurrent clots in different superficial veins around the body (aka migratory thromboembolism)

Associated with: Adenocarcinoma of pancreas or lung
{Cimetidine, ranitidine, famotidine, nizatidine}
aka Tagamet, Zantac, Pecid, Azid

H2 Blockers

Mechanism: reversible block of Histamine H2 receptors -> [-] H+ secretion by parietal cells

Clinical use: Peptic ulcer, gastritis, GERD

Toxicity: Cimitidine potent inhibitor of P450 and antiandrogenic effects and [-] renal creatinine excretion
What is the difference in effects of H2 blockers vs Proton pump inhibitors?
H2 blockers: 60-70% reduction in acid. More at night, less at meals

Proton pump: 90% reduction in acid. More at meals (take 30 min before food)
{Omeprazole, lansoprazole}
aka prilosec, prevacid (nexium = S-omeprazole)

Proton Pump Inhibitors

Mechanism: Irreversibly inhibit H+/K+ ATPase in stomach parietal cells. Activated by H+ so only acts in stomach.

Clinical use: Peptic ulcer, gastritis, GERD, Zollinger-Ellison
{Bismuth, sucralfate}
aka pepto bismol

Mechanism: Bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucus layer.

Clinical use: [+] ulcer healing, traveler's diarrhea

Part of triple therapy for h Pylori.
Mechanism: A PGE1 analog. [+] production and secretion of gastric mucous barrier, [-] acid production

Clinical use: Prevention of NSAID-induced peptic ulcers. Also, paintenance of patent ductus arteriosus

Toxicity: Diarrhea. Contraindicated in childbearing women (abortifacient)
{pirenzepine, propantheline}
Muscarinic antagonists

Mechanism: Block M1 receptors on ECL cells -> [-] histamine secretion; Block M3 receptors on parietal cells -> [-] H+ secretion

Clinical use: Peptic ulcer

Toxicity: Bradycardia, dry mouth, difficulty focusing eyes
Mechanism: Monoclonal antibody to TNF-alpha.

Clinical use: CD, UC, RA

Toxicity: Respiratory infection, fever, hypotension
Mechanism: combination of sulfapyridine (antibacterial) and mesalamine (anti-inflammatory); activated by colonnic bacteria.

Clinical use: UC, CD

Toxicity: Malaise, nausea, sulfa toxicity, reversible oligospermia
Mechanism: 5-HT3 antagonist; central-acting antiemetic

Clinical use: control vomiting postoperatively and in chemotherapy pts.

Toxicity: Headache, constipation
What happens in antacid overuse?
Can affect absorption, bioavailability or urinary excretion of other drugs by altering gastric or urinary pH or delaying gastric emptying

Overdose can cause:
[1] Aluminum hydroxide: constipation & hypophosphatemia
[2] Magnesium hydroxide: diarrhea
[3] Calcium carbonate: hypercalcemia, rebound [+] acid

Also can cause hypokalemia
What is the difference between aluminum and magnesium based antacids?
Alu[minimum] amount of feces -> constipation

Mg = [M]ust [g]o to the bathroom -> diarrhea
What are the four types of laxatives?
[1] Osmotic: sorbitol, polyethylene glycol
[2] Bulk forming: metamucil, citrucel
[3] Stool softener: colace
[4] Peristaltic stimulant: Ex-lax, sennecot