UWorld - GI and Hepatobiliary Flashcards
Phosphatidylcholine levels releation to cholesterol gallstones?
Risk INC w/ cholesterolDEC w/ phosphatidylcholine and bile salts.
Rare limiting step of bile acid synth?
Creation of cholesterol 7a hydroxylase
Presentation of colon CA based off right or left side?
Left side - obstructionRight side - systemic symptoms, symptoms of iron def anemia (fatigue). Also perhaps blood. THis is because right colon has larger caliber than left so you dont get obstruction.
What tissue can be found in Meckes?
Ectopic tissue. Gastric mucosa found in 80% of symptomatic Meckes. Acid production lead to ulceration and bleeding. Also called heterotopy. It is not metaplasia, as it was always this way. Ectopia is result of congenital malformation.
Secretory IgA - how is it produced?
Made my plasma cells. But “secretory piece” is synthesized by epithelial cells. Connects the IgAs. IgA composed of 2 Ig, J chain, and Secretory piece.
What titers do you see in pt who has been vaccinated agaisnt HBV?
HBsAg negativeAnti-HBsAgHBsAg - first viral marker - precedes aminotransferases and onset of clinical symptoms. Remains during entire symptomatic phase of acute Hep B. Suggests infectivity (as does HbeAg)Anti-HBs Ab- appears after successful HBV caccination or clearance of HBsAg. Detectable for life. Anti-HBc - appears after emergence of HBsAg, remains detectable for long after recovery. Both IgM and IgG response. However, IgM anti-HBc presnt in “window period” - Important for diagnosis when HBsAg has been cleared and anti-Hbs Ab is not yet detectable. IgM anti-HBc is the MOST SPECIFIC marker for diagnosis of acute hept B. HBeAg - appears shortly after apperance of HBsAg - indicates active viral replication and infectivity. Disappears before hBsAg is eliminated. If it persists more than 3 months - INC risk of chronic hep B. Anti-HBe Ab- suggests cessation of active viral replication and low infectivity.
How is BUN affected in hepatic dysfunction (alcoholic etc).What triggers hepatoencephalopathy?
BUN is INC in kidney failure, HF, and dehydration.BUN is DEC in liver failure because ammonium cannot be converted to urea (BUN)So Ammonium is INC, but BUt is DEC. Ammonium enters circulation through GI tract during enterocytic catabolism of glutamine and bacterial catabolism in the colon. Enters through portal vein. If liver is damaged, ammonia instead accumulates int he blood as hepatoctes dysfunction and shunting of blood through collateral ciruclation may occur.Hepatoencephalopathy triggered by GI bleeding (and corresponding INC in ammonia and nitrogen absorption in gut). Can be triggered by anything that alters ammonia balance. Hypovolemia, , hypokalemia, metabolic alkalosis, hypoxia, sedative use, hypoglycemia, infection.
What is the mech of Vanc resistance in VRE?
D-ala D ala ->D-ala D lactate
What is the mech of N acetyl cystein in acetaminophen intox?
Provides sulfhydryl groupsActs as glutathionine substitute and binds toxic metabolites.Acetamenophen tox and p450 metabolism creates Nacetyl-p-benzoquinoneime (NAPQI). This is metabolized by hepatic glutathione. In tox, sulfation and glucuronide conjugation are saturaetd. Excess NAPQIformed form P450 -> glutathione depleted -> hepatotox.
Hyperammonemia in hepatic encephalopathy results ind epletion of what protein/carb?
Hyperammonemia -. Depletion of a-KG. Which inhibits Krebs cycle. Excess ammonia also depletes glutamate (Excitatory neurotransmitter). Causes accumulation of glutamine -> astrocyte swelling and dysfunction. AKA hepatoecenphalopathy caused by astrocye and neuron dysfunction.
What is the glutamate glutamine cycle?
Glutamate released by neurons for neurotransmissions.GLutamate taken up by astrocytes and gonverted to glutamine (non-neuroactive). Glutamine released by astroyes and taken up by neurons. Converted back to glutamate or transaminated to a-KG to be used in Krebs cycle.
Polysaccharide accumulation in lyososmal vesicles. Hepatomegaly, cardiomegaly, macroglossia, Hypotonia, MR. THink?
T2 Glycogen storage disease. Pompes diseasePolysacch accumulation was glycogen.Normal glycogen structure, but 1,4 glycosidic bonds cant be broken. Due to lack of lysosomal a- glucosidase.Glycogen accmulation in lysoosmal vacuoles is NOT seen in other glyocgen storage isease.
Adenoma to CA sequence. Go.
APC inactivationMethylation abnormalities,COX2 OVER-expressionKRasDCCP53
What GI microbio illnesses only require a few cells?
Entamoeba histolytica - just 1Giardia lamblia - just 1Shigella - 10Campylobacter jejunia 500Clostridium - 500Cholera 10^6Salmonella - 10^7Enterotoxigenic E Coli 10^9
What matenral marker indicates high probability of vertical transmission (90%) - in HBV?
HBeAg. Newborns w/ mothers o active hep B are passively immunized w/ Hep B IG. Followed by active immunization w/ recombinant HBV vaccine.
How do positive predictive value and negative predictive value relate to population sizes?
Both vary w/ population.PPV - INC when disease is more common. Probability is higher that a person who tests positive will ahve the disease in a high prevalence location. If relatively uncommon, then lower PPV.Negative predicitve value has inverse assoc w/ prevalence. As prevalence INC, negative predictive value DEC.
What stimus secretion of Bicarb? Trypsinogen?
Secretin -> BicarbCCK -> Trypsinogen (+ others. Gets pancreas and bile duct going!)
Tubular adenomaVillous AdenomaDescribe. More than just malignancy potential
Tubular - smaller and pedunculated.Villous - larger. Can have velvety or cauliflower like projections (partial obstruction)VIllous can secrete large amount of mucus -> secretory diarrhea.
Likely intestinal Carcinoid tumor location?
Appendix, ileum, rectum. Flushing,WheezingVascular telangiectasiasDIarrhea
Normal intestinal mucosal architecture, w/ tips of villi enterocytes contianing clear/foamy cytoplasm? Inheritance.
Abetalipoproteinemia - AR - impaired formation of Apo-B. Loss of function in MTP gene. Manifests in first year of life - foul smelling, greasy stools. low plasma triglyeride and choletserol levels. Fat soluble vitamin def. Acanthocytes. Neuro symptoms (progressive ataxia, retinitis pigmentosa)
Best way to detect C diff colitis
PCR detection of Toxin A and B genes in stool.
Retroperitoneal hematoma w/ mild ab pain after MVA. Think?
Pancreas. Damage to transverse colon, liver, and spleen would NOT cause retroperitoneal hematoma. They are INTRAPERITONEAL organs. Dmg to any of these would lead to hemoperitoneum - free blood in peritoneal psace. NOT retroperitoneal.
What is the mech of H pylori damage -> ulcers? Wher does it occur?
H pylori damages the somatostatin producing antral cells. Somatostatin inhibits gastrin release. So High gastrin levels -> acid. Not neutralized by bicarb -> duodenal ulcerations.H pylori in gastric antrum and fundus,as well as any ectopic tissue, but does not seem to invade these. Mainly somatostain producing antral cells.
What enzyme allows for glucose synth out of triglyercide breakdown rpoducts?
Glycerol kinase.Triglycerise -> Glyerol + Fatty Acids (Acety Coa -> beta ox/ketogenesis)Only Glyerol can be used for gluconeogenesis. Glycerol + Glycerol kinase -> Glycerol 3 phosphate.
Where is the pancreas derived form?Describe embryology of normal pancreas devo as well as annular pancreas devo.
ForegutVentral pancreatic bud (Attached to gallstone) + DOrsal pancreatic bud. Ventral rotates posteriorly so that gallbladder is now behding duodenum. Ventral and dorsal pancreatic buds fuse. If the ventral bud cleaves into two parts and orms a ring -> annular pancreas. Cna cause dudoenal stenosis (bilious vomiting)Incomplete fusion of ventrla and dorsal pancreatic buds would lead to pancreas divisum -> usu asymptomatic.
Where do most viruses get their plasma membrane (Envelop from?) What is the exception?
Most enveloped acquired lipid bilayer from budding through plasma membrane.Exceptions include Herpes virus - bud through and acquire hot cell nuclear membrane.
Cricopharyngeal dysfunction causes?
High dysphagia - difficulty swallowing - felt at throat - coughing, chocking. Zenker diverticulum can form. May also ead to food aspiration. Diverticulum may be palpated as LATERAL neck mass.
when do you see true divertula of esophagus vs fake?
Fake - Zenker - cricopharyngeal muscle dysfunction (= diminished relaxation -> INC inraluminal pressure -> herniation). True - scarring and traction - seen in mid portion - may result from mediastinal lymphadenitis (TB
Elevated Alk phosph of unclear etiology. What is next?
Elvated alk phos could be Liver, Bone»_space; Intestine, kidney, placenta, leukocytes, neoplasmsNext step should be hepatic GGT (predominantly hepatocytes and biliary epithelia). Useful in determining whether elevated alk phosphatase is hepatic or bony origins.
Diarrhea and constipation w/ draining fistula near coccyx?
Crohns.You can have fistulas anywhere - skin (perianal fistula), urinary bladder, vagina, retroperitoneum, oral apthous ulcers.
Hepatic vs Renal clearance. WHat characteristics favor eac?
Hepatic - high lipophilicity and high volume of distribution, high penetration into CNS. THese qualities make it so that drugs will be filtered, but will be easily be able to be re-enter tissues from tubules. SImilar to how charged and uncharged pass though kidney membrane. However, charged are stuck.
What cell cannot use ketone bodies?
Erythrocytes (lack mito)Hepatocytes as well - do have mito, but lack enzyme succinyl CoA acetoacetate CoA transferase (thiophorase) - CANT use ketones.
What ab organ is not from a foregut derivative, but is supplied by the foregut artery?
Spleen - derived from mesodermal dorsal mesentary - supplied by celiac.
How does urea breath test work?
Give Carbon radiolabeled urea orally. H pylori ureas breaks down urea into carbon dioxide and ammonia. The CO2 is absorbed into bloodstream, and exhaled in pt breath. Do breath samples 30 minutes after ingested urea.
Mech and bugs w/ IgA protease? W Protein A?
IgA protease - cleaves di-gammaglobulin IgA - prevents the prevention of entry. Found in Strep pneumo, H flu, Both NeisseriaProtein A - has higher affinity for IgG than IgG does to bacteria. Binds IgG and prevents it from opsonizing Staph A.
Opioid analgeis can lead to what very rare side effect?
SHould know that common side effect is constipation. Contraction of smooth muscle cells in sphincter of Oddi can lead to constriction and spasm -> INC bile duct pressure - > Biliary colic. Severe cramping and pain in right upper abdomen.
Hepatic abscess - common causes?
Enteric bacteria via ascending biliary tractStaph A - hematogenous seeding to liver.
Told that wife and child are Jehovas witness by husband and not to give blood. Cant get into contact w/ husband, no Jehovas card. What to do?
Give blood - standard of care. No outline, and no contact.If dad was back in contact during the final moments and still said no blood - there would be no blood. This is because some jehovas witness will be okay with life saving treatment.
Why is Hep D defective?
Must be coated by external coat antigen of HBsAg before it can infect hepatocytes and mutlple.
Erosions vs Ulcers ?
Erosions - may not past through mucosa. Do not go past muscularis mucosa (which is in between mucosa and submucosa)Ulcers past mucosa into submucosa.
Common causes of SMA syndrome?
Dimished mesenteric fat that provides a buffer - low body weight, recentlw eight loss, severe burns, prolonged bed rest. Lordosis. Also Surgical correction of scolioisis, which lengthens spine and DEC mobility of SMA> Traps the TRANSVERE part of duodenum.
HIV pt w/ esophageal pain. 3 Major possible endoscopic findings?
Candida - patches of grey/whtei psuedomembranes.HSV1 - small vesicels that evolve into “punched out” ulcers. - EOsinophili intranuclear inclusions (Cowdry type A) in multinuclear squamous cells .CMV - Linea ulcerations - both inranuclear and cytoplasmic inclusions.
What is hyperestrinism in alcoholic cirrhosis due to? 2 things
DEC catabolism of estrogenINC sex hormone (Testosterone) binding globulin. (DEC free testosterone to estrogen ration)Leads to gynecomastia, testicular atrohy, DEC body hair, spider angiomata
Words associated w/ diverticula?
Pulsion. (Opposite of suction) DUe to INC intralumina pressure during straining/constipation.
Where does lipid absorption occur? Where does lipid digestion occur?
DUodenumo - digestion of lipidJejunum -Absorption of lipidIleum - sight of Bile B12 absorption.
Major effect of cholecystectomy on bile flow?
Cholecystectomy has little effect on secretion and absorption of bile. Change is the RATE. With surgery it is constantly released, as there is no storage place.Pt w/ cholecystectomy are less able to tolerate large fatty meals in one sitting - unable to release a large coordinated amount.
When do you use double stranded DNA probe?
Southwestern blot. Looking for DNA BINDING PROTEINS! Such as c-Jun and c-Fos (DNA binding protein).
What is important about the 16S rRNA sequence
Essential for initiation of protein synthesis - contains sequence complementary to SHine Dalgarnoa sequence on mRNA. (Shine Dalgarnoa sequence is located 10 bases upstreak of the AUG start codon on prokaryotic mRNA)So the 16S subunit of 30S ribosome allows for the binding of the mRNA
What is another name for Lactose?How can lactase def present acutely?
Galactosyl B-1, 4 glucose.After viral gastroenteritis that damges intestinal epithelium. Causes ab distention, flatulence, diarrhea after lactose ingestion
Another name for Shiga like toin? Mech?
Shiga = Vero cytotoxin.Inhibit protein synth B - forms pentamers w/ central pore.A - activates catalyses that remove single specific adenine residue -> prevent binding of tRNA to 60S subunit and prevent protein synth.
How does halothane/inhalte anesthetic hepatotoxicity present?How do the signs/labs differ from end stage liver disease (cirrhosis)
Anytime SURGERY and LIVER are involved, consider this. Rapid atrophy -> shrunken. Cannot be histologically distinguished from acute viral hepatitis (widespread centrilobular hepatocellular necrosis and inflammation of portal tracts and parenchyma)Significant elevated aminotransferase levels, INC prothrombin time (PT - F7) - Eosinophilia. Normal albumin levels (half life of 20 days - acute doesnt get to this)Cirrhosis - DEC albumin level due to chronic process - palmar erythema and ab distention w/ ascites. May see splenomegaly from portal hypertension from cirrhosis (would not see in acute setting)
Why do IgGs agaisnt Hep C envelop not confer immnity?
Envelopes are HIGHLY immunogenic.BUUUUUUUUUUUUTTTTVARIETY of antigenic structures of hep C virus envelop proteins. Host Ab lags behind produciton of NEW mutatn starins of HCV. Immunity is not conferred.No 3->5 proofreading built in -> hypervariable .
Salmonella enteritidis (vs Shigella)vsSalmonella Typhi?
Enteritidis - - MANY ANIMAL RESERVOIRS - Dissemiantes hematogenously (sickle cell osteomyelitis), Produces Hydrogen sulfide. Invates and causes monocytic response (eyers patch) + in blood and stool cultures.Shigella (No hydrogen sulfide invades - causes PMN rx. .Typhi - typhoid fever - HUMANS ONLY. rose spots on ab, FEVER, heardache, diarrhea. May remain in gallbladder and cause carrier/chronic state.
Mech diff between cause of HCC w/ Hep B and Hep C?
Hep B - integrates w/ host genome. Codes for HBx protein - substance the distrupts growth control of infected cells by activating multiple growth promoting genes. HBx also binds to p53. Hep C - chronic inflam.
Where is colon adenoA most likely to occur?
Rectosigmoid colon. Rarely Transverse and descending. So “left side obstructs is referring to rectosigmoid” Although left side is smaller, the lumen is smaller.Ascending colon is second most common location of colorectal CA. Right side (Ascending) are large, bulky masses - more likely to bleed.
What is ELISA good for measuring?
Enzym linked immunosorbent assay - commonly sued to measure protein in body fluid - for example - to measure plasma insulin levels
Go deep into the mech of hemochromatosis (genetic)
AR - HFE chr 6. Due to impaired HFE protein expression on basolateral surface of epithelial cell in small intestine crypts.HFE complexes w/ B2 microglobulin to bin to transferrin receptor. HFE usu binds to Transferrin receptor to regulate Iron endocytosis.PT w/ HFE mutation are unable to bind to transferrin receptor - no regulation.
Tx for Hep C? Mech?
INFa and Ribavarin.INFa = immuno stuff.Ribavarin - prevents DNA replication - multifactorial.Ribavarin - Nucleoside Antimetabolite - interferes w/ duplication of viral genetic material. 1. Induces lethal hypermutation2. Inhibits RNA polymerase and inhibits Inosine monophosphate dehdrogenase (Delets GTP)3. Causes defective 5’ cap formation in viral mRNA 4. Modulates a more effective immune response. RIBAVARIN CAN WORK AGINAST A NUMBER OF DNA AND RNA VIRUSES. Currently used for Chronic Hep C and RSV>
Wwater born gastroenteritis - bacteria - able to survive in ALKALINE MEDIA. Think? STool microscopy?
VIBRIO. Noninvasive - mucus and epithelial cells only.Vibrio is INCREDIBLY acid sensitive - this is why you need to inest 10^10 V cholera for them to grow! Or 10^6 if Vibrio is in food (food buffers) So Vibrio more common in Achlorhydria states.
Different Mech of APC vs Microsatellite?
APC - needed for intercellular attachmentLynch (HNPCC) - DNA mismatch repair. - PROXIMAL COLON ALAYS INVOVLED. Also, has TENDENCY FOR EXTRAINTESTINAL MALIGNANCIES.
Location of FAP, HNPCC, Sporadic
FAP - pancolonic - always involves rectum.Sporadic - (adenoma -> Ca sequence) - APC, Kras, P53/DCC- Left sided (Rectosigmoid>ascending» others)HNPCC - Proximal/Right colon always involved.
Estrogens effect on choletserol?
Estrogen INC biosynh of cholesterol by INC hepatic HMG-CoA reductase activity. Suppression of cholesterol 7a-hydroxylase (by fibrates) - DEC the conversion of cholesterol to bile acids. Results in Excess cholesterol (stones)
