jdlevenson's version from 2015-06-20 04:07


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Hepatitis B microscopic appearanceGround glass appearance of hepatocytes with ballooning degeneration, hepatocyte necrosis and portal inflammation. The cytoplasm becomes granular and eosinophilic in its appearance because of HBsAg spheres and tubules (hence ground glass).
Hepatitis C liver changesLYMPHOID aggregates within portal tracts and focal areas of MACROVESICULAR STEATOSIS.
Hepatitis under light microscopy (B or C)Apoptosis of hepatocytes, acinar necrosis and periportal mononuclear inflammatory infiltration
All cases of acute viral hepatitis histologically***Diffuse ballooning degeneration/ hepatocyte swelling, mononuclear cell infiltrates, councilman bodies/ eosinophilic apoptotic hepatocytes. Liver biopsy not needed.
Most common cause of acute viral hepatitis in young adultsHAV


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Gilbert syndromeReduced production of UDP-glucuronyl transferases causes a mild unconjugated hyperbilirubinemia during times of stress (fasting or illness). Do not develop liver disease.
Physiologic jaundice vs Hemolytic disease of newbornPhysiologic jaundice – within 24 hours of birth; relatively mild unconjugated hyperbilirubinemia; Hemolytic disease of newborn – within 24 hours of birth as well but unconjugated hyperbilirubinemia accompanied by hemolytic anemia and a positive Coombs test.
Conjugated hyperbilirubinemia with direct bilirubin fraction of at least 50% and no liver diseaseDubin-Johnson syndrome, a benign condition from defect in hepatic excretion of bilirubin glucuronides across canalicular membrane. Not a/w hemolysis. Liver becomes black.
Dubin-johnson syndrome histologyLiver black; may see dense pigment of epinephrine metabolites within the lysosomes.
Dubin-Johnson presentationconjugated hyperbilirubinemia; jaundice; maybe some nonspecific fatigue, abdominal pain and weakness; bilirubin between 2-5 mg/ dl to 20-25 mg/dl.


Acute rise in ammonia affects astrocyte and neuron function.
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Glutamate-Glutamine normal cycleGlutamate released by neuron at synapse is taken up by astrocytes. Astrocytes convert it to glutamine. Glutamine is released by astrocytes and taken up by neurons. Neurons convert glutamine into glutamate for use as neurotransmitter OR transaminated into alpha KG for use in the krebs cycle.
Ammonia interferes with glutamate-glutamine cycle in what 2 ways1. It speeds up astrocyte conversion of glutamate to glutamine, depleting astrocytes and neurons of glutamate and thus interfering with excitatory neurotransmission and neuronal energy production. Increased glutamine also causes a hyperosmolar state in which mitochondria do not work well. 2. Ammonia is metabolized by neurons by glutamate dehydrogenase with help of AKG, depleting the neuron of AKG that could be used for energy metabolism in the brain.
In H Encephalopathy, Oxindole is increased. So what?Normally cleared by liver. It causes sedation, muscle weakness and hypotension and coma.


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HCC diagnosisHigh levels of alpha-fetoprotein and or ultrasound or contrast CT/MRI; biopsy. Clinical symptoms – RUQ pain, malaise, fatigue, weight loss, fullness – are similar to cirrhosis and chronic hepatitis so AFP, even though present in only 50-75% of cases, may help with diagnosis to distinguish from cirrhosis.
HCC, 3 major causesHep (B or C); aflatoxins; chronic alcohol. However others include non-alcoholic fatty liver disease, autoimmune disease, hemochromatosis, A1AT, Wislon.
Patients with stable compensated cirrhosis who suddenly decompensate without apparent reasonevaluate for HCC including with AFP
AFP inHep C and HCC; more often in HCC especially with continuous rise


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Classic triad of hemochromatosisHyperpigmentation/ bronze; DM and cirrhosis (bronze diabetes). AR. Also impotence, arthropathy and cardiac enlargement.
Hemochromatosis lab findingsHigh Ferritin, High Transferrin, Low TIBC, High Iron. Can be as high as 50 g enough to set off metal detectors at airports.
Hemochromatosis typically presenst onceAt least 20 g of iron have been accumulated; usually after age 40; women later due to protective effecst of mensturation and pregnancy


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Reye syndrome hepatic dysfunction appears asMicrovesicular steatosis, small fat vacuous in the cytoplasm of hepatocytes without necrosis or inflammation present in the liver. On EM, swelling, decreased number of mitochondria and glycogen depletion.
Reye syndrome causes hepatic dysfunction (vomiting, hepatomegaly, ALT, AST< ammonia, PT, PTT, bili) andEncephalopathy, probably from hyperammonemia of CNS leading to cerebral edema. Pathogenesis unclear but thought to be related to mitochondrial dysfunction.
Aspirin should not be given to children under 16 except forTreatment of serious illness such as Kawasaki


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Young patient with unexplained chronic hepWilson’s disease. Look for low ceruloplasmin and increased urinary copper excretion and or Kayser-Fleischer rings.
How is copper typically excretedCopper absorbed in duodenum -> bound to albumin -> transported to liver -> incorporated with a globulin to form ceruloplasmin -> secreted into plasma; senescent ceruloplasmin and unabsorbed copper -> secreted into bile and excrete in stool. So, BILE is primary route of copper elimation and stool – 85-95%. (Kidneys secrete copper but only about 5-15% of daily excretion).


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A1AT functionNeutralize proteases such as elastase of neutrophils or pancreatic trypsin. If lost, excessive destruction by inflammation.
PAS-positive pink globules in hepatocyteDiagnostic for A1AT.
A1AT histologyOval to round intracytoplasmic hepatocyte inclusions that appear eosinophilic on H and E and are strongly PAS positive.
PAS positive also in ?T. Whippelii/ Whipple disease


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Excessive alcohol consumption has what effect on beta oxidationImpairs beta oxidation of FA to acetyl coA
Type I HyperlipoproteinemiaI like C -> deficiency of CLPL and or apolipoprotein C2 and excess of Chylomicrons; AR; causes pancreatitis (from vessels filled with chylomicrons rupturing), hepatosplenomegaly, and eruptive pruritic xanthomas (but no risk of developing atherosclerosis). Increased in blood- chylomicrons and TG and cholesterol
Type II HyperlipoproteinemiaSpread out II and put D in it and then its like LDL. Decreased synthesis of LDL receptors/ absent or defective. Increased blood level of LDL and cholesterol. Autosomal dominant* (like Type IV). Heterozygotes – 300 mg/dl vs Homozygotes – 700+ mg/dl. Causes accelerated atherosclerosis (may have MI before 20), tendon (achilles) xanthomas, and corneal arcus.
Acquired causes of Type II?Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.
Type IV hyperlipoproteinemiaIV looks like LV → hepatic over production of VLDL. TG accumulates and causes pancreatitis.
Main complication of Type I? II? IV?I – pancerattis; III and IV – atherosclerosis
Garlic odor + n/v, abdominal pain, diarrhea, and decreased level of consciousnessAcute arsenic poisoning.
Most common cause of night blindnessHereditary retinitis pigmentosa, i.e. not Vit A deficiency. Other causes toxic retinopathy due to chloroquine or phenothiazines; congenital rubella syphilis or other infections and diabetic retinopathy.


Impaired function of CFTR channel protein. Decreased water content in epithelial secretions leads to thick, viscous mucus that causes – chronic airway obstruction and impaired bacterial clearance, - GI maldigestion and malabsorption.
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Clinicalchronic productive cough; recurrent pulmonary infections (pseudomonas, staph aureus), chronic bronchiectasis with reticulonodular pattern on CXR, steatorrhea and failure to thrive; nasal polyps; male infertility (absence of vas deferens). Meconium ileus in newborn.
Diagnosiselevated sweat chloride levels, nasal potential difference measurements and genetic testing. Chromosome 7** and most common is deletion of Phe508. Trysinogen screening of newborn since there is increased immunoreactive trypsinogen in CF patients.
CFTR -> ATP gated Cl- channel that secrets Cl in lungs and GI but REABSORBS Cl- in sweat glands. Most often misfolded protein that remains in RER causing decreased Cl secretion and as a result decreased H20 secretion. Na is absorbed as a result to balance Cl and that brings in more water. That’s why you get abnormally thick secretions in lungs and GI while you get increased levels of Cl in sweat (since its not being reabsorbed). Increased Na absorption also causes more negative transepithelial potential difference (but more on that later).
CF is equivalent to taking loop diuretic because of H20 and Na losses (already have Cl inside; don’t want to take more in so Na K 2 Cl transporter won’t work) and then resulting ENaC leading to K+/ H+ wasting ->> contraction alkalosis and hypokalemia. N-acetylcysteine to loosen mucus plugs (cleaves disulfide bonds within mucus glycoproteins), dornase alfa (DNAse) to clear leukocytic debris.
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CF treatmentMay give Lipase to help with pancreatic insufficiency.


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Antibiotics implicated in C Diff beyond ClindamycinFluoroquinolones, penicillins, broad spectrum cephalosporins
C. Diff toxins a and toxin b act byDisrupting actin cytoskeleton and intracellular signaling. Overlapping and synergistic but toxin a causes more intestinal inflammation (neutrophils included) and fluid secretion and is more enterotoxic and toxin b is more cytotoxic. Both inactivate Rho-regulatory proteins involved in signal transduction and actin cytoskeleton structure maintenance. Toxins disrupt intercellular tight junctions leading to cell rounding/ retraction and increased paracellular intestinal fluid secretion.
C. Diff symptomsFever, abdominal pain, watery diarrhea and leukocytosis and then can range to toxic megacolon/ fulminant colitis plus or minus pseudomembranes
Ribosomal protein synthesis is inhibited by what bugsShigella with its toxin and E. Coli with shiga-like toxin
Loss of cell membrane integrityC. Perfringens
T. Cruzi neurotoxin does whatDestroys myenteric plexus – of esophagus, colon, ureter – and causes intramural parasympathetic denervation of smooth muscle. In esophagus it incapacitates the LES so food gets stuck.
T. Cruzi can cause DCM andMegacolon, ureter and esophagus
Toxoplasmosis causes () in immunocompetentMono-like whereas CNS involvement etc in immunocompromised
2nd most common cause of chronic watery diarrhea in HIV/AIDS and immunocompromised Isospora belli. Treat with Bactrim or pyrameth/sulfa.
REVIEW BRUCELLA. Campylobacter fetus too
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Picornia viruses are made ofRhinovirus and enterovirus.
Which picorna viruses are acid labileRhinovirus. Like most viruses, dies at pH < 5. However, enteroviruses are acid stable. Hence they can colonize GI whereas rhino – upper respiratory tract.
Bacterial toxins that induce cAMPEc – cholera; A – anthrax and cereus (both are bacillius); M = campylobacter; P = pertussis; E = ETEC ADD TO ANKI
What cells inactivate EF-2 by ADP-riBOWsylationC. Diptheriae and Pseudomonas. Inhibit protein synthesis that way (whereas shiga like toxins inactivate the 60s ribosomal subunit in human cells).
E. Coli 0157:H7 does notProduce glucuronidase or ferment sorbitol.
Strongyloides larvae autoinfectionhatch from eggs laid in intestinal wall; repenetrate wall, enter blood stream.
StrongyloidesNematode; roundworm. Transmitted in soil contaminated with human feces. Larvae penetrate skin and migrate hematenously to the lungs -> aspirated -> intestine -> lay eggs, noninfectious rhabditiform larvae that migrate into the intestinal lumen to be excreted in the stool but some rhabiditiform molt directly into filariform larva and within the intestine and reinfect. AUTOINFECTION -> leading to widespread dissemination of the parasites throughout the body via HYPERINFECTION*. Can cause multiorgan dysfunction and septic shock. Occurs most in patients taking immunosuppressants or with HTLV-1 infection. Impaierd TH2 cellular immunity.
What part of immune system for helminthes/ roundwormsEos and Baso
Dx of strongyloidesLarvae in the stool as eggs and adult parasites are usually seen only in intestinal biopsies. NOT EGGS.
Cysts in stools?Intestinal protozoa like giardia and entamoeba.
Proglottids in stool?Intestinal tapeworms like taenia and diphyllobothrium.
Vibrio vs Campylobacter, how to tell differenceMedia. Vibrio –alkaline and Campylobacter not.
Since vibrio does not invade, what will you not see in stoolNo leukocytes or erythrocytes; mucus and sloughed epithelial cells instead.
Diarrhea with leukocytes with monocyte predominanceSalmonella Typhi
Diarrhea with leukocytes with neutrophil predominanceEverything else – shigella, slamonella, c. jejuni, EIEC.
Charcot-leyden crystals (eosinophil breakdown) seen in ?Intestinal parasitic infectiosn that are eosinophilic such as strong, ancylo, ascaris, toxocara, trichinella (but not giardia or entamoeba).
Intraabdominal abscess, two most likely drugs#1. Bacteriodes fragilis and # 2. E. Coli. NOT S. Aureus, which is the usual cause of abscess formation on the skin.