FA 2 Flashcards
Diverticulisis - complications/treatment of complications
- abscess
- fistula (colovesical –> pneumaturia)
- obstruction (inflammatory stenosis)
- perforation (–> peritonitis)
treatment: percutaneous drainage or surgery
Acute mesenteric ischemia - presentation
- abdominal pain out of proportion of physical findings
- red currant jelly stools
- decreased sounds
Angiodysplasia - definition, presetation, location
acquired torturous dilation of vessels –> hematoscezia
MC often in cecum, terminal ileum, ascenidng colon
Colonic polyps - histological types (neoplastic or not?)
- hyperplastic - nonneoplastic
- hamartomatous - non-neoplastic
- adenomatous - neoplastic
- serrated - premalignant
Colonic polyps - Adenomatous - types and malignancy
tubular –> less malignant potential
villous –> more malignant potential
tubulovirous –> intermediate malignant potential
Serrated - mechanism/biopsy
premalignant, via CpG hypermethylation phenotype pathway with microsatellite instability
biopsy: saw-tooth pattern of crypts
Polyposis syndromes - types
- familiar adenomatous polyposis (FAP)
- Gardner syndrome
- Turcot syndrome
- Peutz-Jeghers syndrome
- Juvenile polyposis syndrome
Gardner syndrome?
FAP + osseus and sot tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth
Turcot syndrome
FAP + malignant CNS tumor
Peutz-Jeghers syndrome - definition/mode of inheritance/presentation
AD syndrome featuring with numerous hamartomas throughout GI tract, along with hyperpigmented mounth, lips hands, genitalia
Peutz-Jeghers syndrome - cancer
increased risk of breast and GI cancers (eg. CR, stoma, small, panceas)
Juveniles polyposis syndrome - definition/mode of inheritance/presentation
AD syndrome in children (typically under 5) featuring with numerous hamartomatous polyps in large and small intestine, stomach
Lynch syndrome - cancers?
- Colorectal (de novo, not drom adenomatous polyp_
- ovarian
- endometrial
- skin
Colorectal cancer (CRC) - risk factors
- adenomatous polys
- serrated polys
- familiar cancer syndromes
- Inflammatory bowel disease
- tobacco use
- diet of processed meat with low fiber
Colorectal cancer (CRC) - location (in order)
rectosigmoid>ascending>descending
Colorectal Cancer - barium enema x-ray
“Apple core” lesion
Colorectal Cancer - markers/characteristics
CEA tumor marker –> food for monitoring recurrence, should not used for screening
γ-Glutamyl transpeptidase (γ-GT) - increased in
- increased in various liver and biliary disease (just as ALP but not in bone disease
- associated with alcohol use
Functional liver markers
- Bilirubin
- Albumin
- Prothrombin
- platelets
Functional liver markers - platelets (and mechanism)
- decreased in advanced liver disease (low thrombopoietin, liver sequestration)
- decreased in portal hypertension (splenomegaly/splenic sequestration)
hepatic steatosis?
Macrovesicular fatty change, heavy greasy liver, that may be reversible with alcohol cessation
alcoholic hepatitis - histology
- Swollen and necrotic hepatocytes with neutrophilic infiltration
- Mallory bodies
Mallory bodies - appearance
intracytoplasmic eosniphhiic inclusions of damaged keratin filaments
Hepatic encephalopathy - triggers example
- increased NH3 production and absorption –> dietary protein, GI bleed, constipation, infection
- decreased NH3 removal –> renal failire, diuretics, bypassed hepatic flow post-TIPS
Hepatic encephalopathy - treamtnet (and mechanism)
- lactulose –> increases NH4+ generation
2. rifamixn or neomycin –> decreases NH4+ producing gut bacteria
GI bleeding increases ammonia - mechanism
RBCs contain proteins Significant bleeding (esp upper GI) –> increases the protein load in the intestine and the production of ammonia
Diuretic therapy ammonia
Decreased serum potassium levels and alkalosis may facilitate the conversion of ammonium (NH4) to ammonia (+NH3).
Constipation - ammonia
Constipation increases intestinal production and absorption of ammonia
Liver tumors - types (and MC)
- Hepatocellular Carcinoma (hepatoma)
- Cavrnous hemangioma
- Hepatic adenoma
- Angiosarcoma
- Metastases (MC)
cancers that give metastasis to liver
- GI malignancies (Collon»stomach>pancreas)
- breast
- lung
A complication of Hepatocellular carcinoma (may lead to..)
Hepatocellular carcinoma spreads ….
- Budd-Chiari syndrome
- hematogenously
Hepatocellular carcinoma - diagnosis
- increased a-fetoprotein
- US or contrast CT/MRI
- biopsy
Cavrnous hemangioma - frequency/behavior/epidimiology
common, benign liver tumor
typically occurs at 30 - 50
(NO BIOPSY–> hemorrhage)
Liver angiosarcoma - definition/risk factors
Malignant tumor of endothelial origin
associated with arsenic, vinyl chloride
Hepatic adenoma - definition/risk factors
Rare, benign liver tumor, often related to oral contraceptive or anabolic steroid use
- may regress spontaneously or rupture (abdominal pain and shock)
α1-antitrypsin deficiency causes (and mechanism
- misfolded gene product protein aggregates in hepatocellular ER –> Cirrhosis with PAS+ globules in liver
- lings –> low α1-antitrypsin –> uninhibited elastase in alveoli –> low elastic tissue –> panacinar emphysema
(CONDOMINANT TRAIT)
bilirubin - levels
total: 0.1 - 1 mg/dL
direct: 0 - 0.3 mg/dL
indirect: 0.2 - 0.7 mg/dL
jaundice: more than 2.5 mg/dL
Causes of mixed (direct and inderect) hyperbilirubinemia
- Hepatitis
2. Cirrhosis
Wislon disease (hepalenticular degeneration) - mechanism
AR mutation in hepatocyte copper transporting ATPase (ATP7B gene, ch13) –> inadequate copper excretion into bile and blood (low serum ceruloplasmin, low serum copper, high urine copper) –> accumulates in liver, brain, kidneys, joints, cornea
Wislon disease (hepalenticular degeneration) - copper accumulates in (organs)
- liver 2. brain
- kidneys 4. joints
- cornea
Wislon disease (hepalenticular degeneration) - presentation
before 40 with
- liver disease (eg. hepatitis, acute liver failure, cirrhosis),
- neurologic disease (dysarthria, dystonia, tremor, parkinsonism
- psychiatric disease
- Kayser-Fleisher rings
- Hemolytic anemia
- renal disease (eg. Fanconi syndrome)
Hemochromatosis - iron accumulation especially in
- liver 2. pancreas 3. skin
4. heart 5. pituitary 6. joints
Hemochromatosis - lab/diangosis
- increased ferritin and iron, decreased TIBC –> increased transferrin saturation
- Liver MRI
- biopsy with Prussian blue stain
Hemochromatosis - clinical manigestation
classic triad: 1. cirrhosis 2. DM 3. Skin pigmentation (bronze diabetes). ALSO: 4. reversible dilated cardiomyopathy 5. hypogonadism 6. arthropathy 7. HCC
hemochromatosis - mechanism of arthropathy
calcium pyrophosphate deposition –> esp in metacarpophalangeal joints
common cause of death in hemochromatosis
HCC
wilson vs hemochromatosis according to age of presentation
wilson –> before 40
hemochromatosis –> after age of 40 when total body iron > 20g (iron loss through menstruation slows progression in women)
wilson vs hemochromatosis according to treatment
hemochromatosis –> 1. repeated phlebotomy 2. chelation with deferasirox 3. deferoxamine
4. oral deferiprone
Wilson –> 1. chelation with penicillamine or trientine
2. oral zinc
Hepatocellular carcinoma - paraneoplastic
EPO
Biliary tract disease - clinical presentation
- pruritus
- jaundice
- dark urine
- light-colored stool
- hepatosplenomegaly
Biliary tract disease - labs
cholestatic pattern of LFTs:
- increased CB
- increased cholersterol
- increased ALP
Biliary tract diseases - types and epidemiology (what type of patients
- Priamary sclerosing cholangitis –> middle-aged men with IBD (UC)
- Primary billiary cirrhosis –> middle aged women
- Secondary biliary cirrhosis –> Patients with known pbstructive lesions (gallstone, biliary strictures, pancreatic carcnoma)
Priamary sclerosing cholangitis - appearance (histology and gross)
histology –> concentric “onion skin” bile duct fibrosis (intrahepatic and extrahepatic ducts) –> alternating strictures and dilation “beading” on ERCP and MRCP
Primary sclerosing cholangitis is associated with
- ulcerative colitis
- p-ANCA
- high IgM
Primary sclerosing cholangitis can lead secondaty to
- biliary cirrhosis
- cholangiocarcinoma
- gallbpaladder cancer
Primary biliary cirrhosis - mechanism
anti - mitochondrial antibodies –> autoimmune reaction –> lymphocytic infiltrate + granulomas –> destraction of intralobular bile ducts
Primary biliary cirrhosis - associated with
- anti - mitochondrial antibodies
- increased IgM
- other autoimmune conditions (eg. Sjogren, CREST, Hashimoto, RA, celiac disease)
Secondary biliary cirrhosis - mechanism
extrahepatic biliary obstruction (gallstones,, biliary structures, pancreatic Ca) –> high pressure in intrahepatic ducts –> injury/fibrosis and bile stasis
Gallstones (cholelithiasis) - types (MC)
- Cholesterol stones (MC - 80%)
2. Pigment stones
cholelithiasis - definition and types and radiolucent of radiopaque
cholelithiasis: solide round stone in gallbladder
1. Cholesterol stones –> radiolucent with 10-20% radiopaque due to calcifications
2. Pigment stones –> if black –> radiopaque (Ca2+ bilirubinate, hemlyisis), if brown (infection) –> radiolucent
cholelithiasis - cholesterol stones are associated with
- estrogen (female, obesity, multiparity, estrogen therapy)
- Crohn
- advanced age
- rapid weight loss
- Native american origin
- Fibrates
cholelithiasis - pigment stones are associated with
- Crohn
- chronic hemolysis
- Alcoholic cirrhosis
- advanced age
- biliary infections (Ascaris lumbricoides, Clonarchis sinensis)
- total partental nutrition
Mirizzi’s syndrome is a rare complication in which
gallstone in cystic duct of gallbladder –> compression of the common bile duct common hepatic duct –> obstruction and jaundice
acute pancreatitis - diagnosis
2 of 3 critera
- acute peigastric pain (often radiating to the back)
- high serum amylase or lipase (more specific) to 3x upper limit of normal
- characteristic imaging findings
pancreatic pseudocyst risk for
rupture –> enzymes in the abnominal cavity and hemorrhage
Pancreatic abscess - due to, presents with
due to E. Coli
presents with abdominal pain, high fever, persistently elevated amylase
special clinical presentation in necrotic pancreatitis
Periublical (Cullen’s sign) and flank (Grey Turner) hemorrhage
Chronic pancreatitis - serum enzymes
amilase and lipase may or may not be elevated
pancreatic adenocarcinoma - Risk factors
- Tobacco 2. chronic pancreatitis (esp >20 years)
3. Diabetes 4. >50 age 5. Jewish and African amerinan males
pancreatic adenocarcinoma - clinical presentation
- abdominal pain radiating to back
- Weigh loss (malabsrorption and anorexia)
- Migratory thrombophlibitis (Trousseau syndrome)
- Obstrctive jaundice (and pale stool) with Courvoisier sign (if at head)
- secondary DM (if at body or tail)
pancreatic adenocarcinoma - markers
- CA 19-9,
2. CEA (not specific)
pancreatic adenocarcinoma - Courvoisier sign?
presence of a palpably enlarged gallbladder which is nontender and accompanied with mild painless jaundice, the cause is unlikely to be gallstones
CEA as a marker
not specific
- colorectal ca (70%)
- pancreatic ca (70%)
- gastric ca
- breast ca
- medullary thyroid ca
- primary biliary cirrhosis - antibodies
- antoimmue hepatitis type 1 - antibodies
- Biliary tract disease associated with ulcerative colitis
- antimitochondrial
- anti smooth muscle
- primary sclerosing cholangitis
H2 blockers - drugs
- TIDINE
1. Cimetidine 2. Ranitidine 3. Famotidine 4. Nizatidine
H2 blockers - clinical use
- Peptic ulcer
- gastritis
- mild esophageal reflux
H2 blockers - adverse effect
- cimetidine inhibits p-450
- cimetidine has antiandrogenic effects (prolactin release, gynecomastia, impotence, low libido in males)
- cimetidine can cross BBB (confusion, dizziness, headache) and placenta
- Cimetidine and ranitidine –> decrease renal excretion of creatinine
other H2 blockers are relatively free ok all these effects
proton pump inhibitors (PPIs) - adverse effects
- high risk for C. difficile infection
- high risk for pneumonia
- low serum Mg2+ with long-term use
Antiacid affect on other drugs - mechansim
Can affect asbsorption, biovailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastrinc emptying
Antiacids - drugs
- Aluminium hydroxide
- calcium carbonate
- Magnesium hydroxide
Aluminium hydroxide - toxicity
- all antiacids can cause hypokalemia
- constipation and hypophosphatemia, proximal muscle weakness, osteodystrophy, seizures
calcium carbonate - toxicity
- all antiacids can cause hypokalemia
- hypercalcemia (milk-alkali syndrome
- rebound acid increasing
Magnesium hydroxide - toxicity
- all antiacids can cause hypokalemia
- diarrhea
- hyporeflexia
- hypotension
- cardiac arrest
Bismuth - similar drug/mechanism of action
Similar drug: sucralfate
Binds to ulcer base, providing physical protection and allowing HCO-3 secretion to reestablish pH gradient in the moucous layer
Bismuth, sucralfate - clinical use
- increases ulcer healing
2. travelers diarrhea
Misoprostol - mechanism of action
A PGE1 analog –> 1. increases production and secretion of gastric mucous barrier
2. decreases acid production
Misoprostol - clinical use
- Prevention of NSAID-induced peptic ulcers (NSAID block PDE1 production)
- maintenance of PDA
- off label for induction of labor (ripens cervix)
Misoprostol - adverse effect
- Diarrhea
2. contraindicated in women of childbearing potential (abortifacient)
Octreotide - mechanism
- Long acting somatostatin analog
- Inhibits secretion of various splanchnic vasodilatory hormones
Octreotide - clinical use
- acute variceal bleeds
- acromegaly
- VIPoma
- carcinoid tumors
- gastrinoma
- glucagonoma
Octreotide - adverse effects
- nausea
- cramps
- steatorrhea
- increased risk for cholelithiasis (inhibition of CCK)
Sulfasalazine - mechanism
A combination of sulfapyridine (antibacterial) and 5- aminosalicylic acid (anti-inflammatory) –> activated by colonic bacteria
Sulfasalazine - clinal use
- Ulcerative colitis
- Crohn disease
(colitis component)
Sulfasalazine - adverse effect
- malaise 2. nausea 3. sulfonamide toxicity
4. reversible oligospermia
Osmotic lexatives - drugs
- Magnesium hydroxide
- magnesium citrate
- polyethlene glycol
- lactulose
Loperamide - mechanism of action
agonist at μ-opiodi receptor –> slows gut motility
POOR CNS penetration –> low addictive potential
Loperamide - clinical use / SE
Diarrhea
SE: 1. constipation 2. nausea
Ondansetron - mechanism of action
5-HT3 agonists –>a. decreases vagal stimualtion
b. central acting antiemetic
Ondansetron - clinical use
control vomiting:
a. postoperatively
a. in cancer chemotherapy
Ondansetron - adverse effect
- Headache
- constipation
- QT interval prolongation
Metoclopramide - mechanism
D2 receptor agonists –> increased resting tone, conractility, LES tone, motility (does not influence colon transport time)
Metoclopramide - clinical use
- Diabetic and postsurgery gatroparesis
2. antiemetic
Metoclopramide - adverse effects
- increased parkinsonian effects, tardtive dyskenisia
- restlessness/fatique 3. drawsiness 4. depression
- diarrhea 6. Interaxt with digoxin and diabetic agents
Metoclopramide - drug interactions
- digoxin
2. diabetic agents
Metoclopramide - Contraindicated in
patients with small bowel obstruction or Parkinson disease
Orlistat - mechanism
inhibits gastric and pancreatic lipase –> decreases breakdown and absorption of dietary fats
Orlistat - clinical use
weight loss
Orlistat - adverse effects
- steatorrhea
2. decreased absorption of fat-soluble vitamins
Ursodiol (ursodeoxycholic acid) - mechanism
nontoxic bile acid –> increases bile acid secretion and decreases cholesterol secretion and reabsorption
Ursodiol (ursodeoxycholic acid) - clinical use
- primary biliary cirrhosis
2. gallostone prevention or dissolution