Liver I Pathology
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| This histologic model is used to describe histopathology of the liver | The Hepatic Lobule
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| this hoistologic model is used to describe the physiologic relationships between hepatocytes and their vascular supply | Hepatic Acinus
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| Describe the hepatic lobule model. | 1-2 cm diameter hexagon oriented around a central vein (terminal tributary of hepatic vein) with portal tracts at the periphery.
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| describe the hepatic acinus model | hepatocytes form a triangular shape, the apex of which is near the central vein and the base is formed by penetrating septal venules; divided into three zones;1-3
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| in the hepatic acinus model, which zone is furthest from the blood supply? | zone 3
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| in the hepatic acinus model, which is the first zone to have toxins and things spread to it? | zone 1
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| blood flows through the liver through these | sinusoids
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| list some functions of the liver | excretory, synthetic, catabolic, metabolic, storage
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| describe the excretory funciton of the liver | it excretes bile
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| describe the synthetic function of the liver | it makes serum proteins, clotting factors, albumin, prothrombin, fibrinoven, factor 8 clotting factor
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| describe the catabolic function of the liver. | it breaks down hormones, amino acids, responsible for etoxification. it breaks down estrogen, ammonia, drugs, and chemicals
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| describe the metabolic function of the liver | responsible for glucose homeostasis: FFA is converted to energy, and triglycerides are secreted as LPP.
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| describe the storage function of the liver | stores glycogen, triglycerides, fat soluble vitamins, iron and copper.
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| ischemic insult will generally show damage to what? why? | the centrilobular hepatocytes because they are furthest from the blood supply.
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| disruption of the excretory function of the liver results in.. | jaundice
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| disruption of the synthetic function of the liver results in... | edema and coagulopathy because albumin is responsible for maintaining oncotic pressure, and if you don't have albumin you get ascites, edema, and coagulopathy
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| disruption of the mcatabolic function of the liver results in... | fetor hepaticus, hyperestrogenemia
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| disruption of the metabolic and storage function of the liver results in... | malnutrition
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| disruption of the catabolic function of the liver results in this in males... | gynecomastia, because they have too much estrogen since they cannot break it down.
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| hepatic failure results from what percent of liver functional capacity loss? | 80-90 percent
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| hepatic failure requires... | liver transplant
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| in hepatic failure, without a liver transplant, mortality rate is what? | eighty percent
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| list the three categories that lead to hepatic failure | acute, chronic, hepatic dysfunction without overt necrosis
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| this cause accounts for about fifty percent of liver failure | acetaminophen toxicity
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| what are some complications of hepatic failure? | hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome
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| this is a complication of hepatic failure which leads to a disorder o fneurotransmission in CNS and neuromuscular system. it may progress over hours or days in acute hepatic failure, and is manifested by a spectrum of disturabances in consciousness | hepatic encephalopathy
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| name some other complications of hepatic encephalopathy | elevated ammonia levels in blood and CNS, impair neuronal transmission and promote generalized brain edema, reversible of the underlying hepatic condition is corrected.
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| the most common cause of fulminant hepatitis in the US is this... | drug and toxin induced liver disease
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| this is a critical factor that influences susceptibility to drug induce dinjury | genetic variability in cytochrome p450 ability to metabolize drugs
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| what is the mechanism of drug induced liver disease | direct tox to hepato or biliary epith cells, causing necrosis, apopto, or disruption of cellular function, through hepatic conversion of a xenobiotic to an active toxin, through immune mechanisms,
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| what are some things that can cause steatosis? | ethanol, methotreate, corticosteroids, total parenteral nutrition
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| what are some things that can cause steatosis | ethanol, methotrexate, corticosteroids, total parenteral nutrition
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| what are some things that can cause steatohepatitis? | amiodarone, ethanol
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| what are some things that can cause fibrosis and cirrhosis? | methotrexate, isoniazid enalapril
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| what is the leading cause of liver disease in most western countries? | excessive alcohol
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| what are the thre forms of alcoholic liver disease? | hepatic steatosis, alcohol hepatitis, cirrhosis
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| hepatic steatosis is also known as this | fatty liver disease
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| how much alcohol is too much? | ingestion of 12 beers or 2 glasses of 80 proof liquor a day for 10-20 years is associated more consistently with severe injury
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| what is the mechanism of hepatic steatosis? | ethanol increases lipolysis and delivery of free fatty acids to the liver
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| what is the metabolic consequence of ethanol consumption? | increased fatty acid synthesis, decreased mitochondrial oxidation of fatty acids, increased production of triglycerides, which impairs release of lipoproteins
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| what is the gross morphology of fatty liver? | it becomes large and yellow
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| describe the characteristics of alcoholic hepatitis.. | hepatocytes swelling and necrosis, presence of Mallory bodies, neutrophilic reactions in the lobule, fibrosis
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| these are cytoplasmic inclusions of cytokeratin intermediate filaments complexed with other proteins and they are present in alcoholic hepatitis | Mallory bodies
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| fibrosis in alcoholic hepatitis results from... | activation of sinusoidal stellate cells and portal tract fibroblasts; fibrosis is sinusoidal and perivenular
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| the end stage of chronic liver disease is characterized by this, and forty percent are asymptomatic until late in the course. | cirrhosis.
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| describe some symptoms of cirrhosis... | anorexia, weight loss, weakness. in advanced cases, signs and symptoms of hepatic fialure are present. patients die due to: progressive liver failure, complication of HTN or development of hepatocellular carcinoma
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| describe the pathogenesis of cirrhosis.. | normally the kupfer cells and macrophages are in the quiescent state, insult causes kupfer and stellate cells to become activated, which release neutrophils and inflammatory mediators, you get deposition of ECM via fibroblasts
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| what is the gross morphology of cirrhosis? | liver is misshapen, and you have surface nodularity with connective tissue septae. with cirrhosis, the regeneration cells are limited to a confined space, which causes a misshapen liver.
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| myofibroblast proliferation in cirrhosis is due to.. | activated stellate cells.
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| in the histology of cirrhosis, you see these.. | bridging fibrous septa, parencymal nodules, diffuce architectural disruption
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| this is described as increased resistance to portal blood flow, or an absolute increase in portal venous pressure above 8mmHG, increase in the pressure gradient between portal and hepatic vein of >5mmHg. | portal hypertension
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| what is the pathophysiology of portal hypertension? | increased resistance ot portal flow at the level of the sinusoids, and increase in portal venous flow due to hyperdynamic circulation.
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| to which part of the microanatomy of the liver does blood flow into from the circulation? | sinusoids
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| list the three causes of portal hypertension | intrahepatic/sinusoidal, post hepatic/post sinusoidal, pre-hepatic/pre sinusoidal
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| what is the pathophysiology of intrahepatic/sinusoidal cause of portal hypertension? | cirrhosis, sinusoidal occlusion
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| what is the pathophysiology of pre-hepatic/pre-sinusoidal cause of portal hypertension? | hepatic artery compromise, portal vein obstruciton and thrombosis. you can have a block caused by a clot, which can increase resistance to blood flow.
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| what is the pathophysiology of the post hepatic/post sinusoidal cuase of portal hypertension? | inferior vena cava thrombosis, hepatic vein thrombosis, (budd chiari syndrome), veno-occlusive disaease
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| these disorders make up the bulk of hte causes of portal hypertension (but the most common cause of portal hypertension is still cirrhosis) | circulatory disorders
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| different manifestations of circulatory disorders in the liver depend on these two different causes: | impaired blood flow through the liver, hepatic venous outflow obstruction through the hepatic vein.
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| a block in the common, right, or left hepatic artery will manifest as a... | local hepatic infarct because you still have the hepatic veins supplying a little oxygen.
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| ischemic insult to the liver will be most pronounced in zone... | 3
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| Now will discuss hepatic manifestations of circulatory disorders causing impaired blood flow to the liver... |
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| is liver infarct common or rare? why? | rare, due to its dual blood supply
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| a localized infarct in the liver can occur from these... | hepatic artery compromise, neoplasia, sepsis
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| what is the gross morphology of a liver infarct? | the distal hepatic tissue is pale tan, and sometimes hemorrhagic.
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| the most common cause of heart failure is left sided or right sided? | left sided. you do not pump enough blood back to the body.
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| this type of heart failure causes congestion | right sided heart failure
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| right sided cardiac decompensation leads to... | passive congestion: enlarged liver, tense, with rounded edges, congestionm of centrilobular sinusoids, centrilobular atrophy.
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| left sided cardiac failure leads to what symptoms in the liver? | shock or decreased blood flow to the liver, resulting in hypoxia and ischemic coagulative necorsis in teh central region of lobule (centrilobular necrosis)
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| this happens due to sustained chronic severe congestive heart failure reflected as centrilobular fibrosis in the liver. | cardiac sclerosis
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| this results from the combination of hypoperfursion and retrograde congestion | centrilobular hemorrhagic necorisis.
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| what is the gross morphology of the liver in passive congestion and centrilobular necrosis | major blood vessels are visible, variegated, mottled, red appearance (nutmeg liver)
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| in the gross morphology of the liver in circulatory disorders, what do light and dark areas represent? | light areas represent ischemia, dark areas are congested.
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| this occurs in any condition where efflux of hepatic blood flow is impeded. It is a rare condition whereby sinusoidal dilation is primary and not secondary to any condition. | Peliosis hepatis
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| what is the pathogenesis of peliosis hepatitis? | unknown
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| peliosis hepatitis is clinically associated with what types of diseases? | many diseases such as cancer, TB, AIDS, post transplantation immunodeficiency, anabolic steroids, etc.
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| what is a potential fatal result from peliosis hepatis? | potentially fatal intra-abdominal hemorrhage
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| hepatic manifestatins of circulatory disorders causing hepatic venous outflow obstruction |
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| This disease is manifested by liver enlargement, pain, and ascites due to obstruciton of two or more major hepatic veins, due to IVC obstruction and its hepatic portion. | Budd-Chiari syndrome
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| what is the treatment for Budd-Chiari syndrome? | prompt surgical creation of portosystemic venous shunt
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| the symptoms of this disease are: tender hepatomegaly, ascites, weight gain, and jaundice. | sinusoidal obstruction syndrome (veno-occlusive disease)
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| what does the sinusoidal obstruction syndrome arise from in sinusoidal obstruction syndrome? | from toxic injury to sinusoidal endothelium, sloughing off the wall, embolizing and obstructing sinusoidal blood flow.
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| sinusoidal obstruction syndrome primarily occurs in what context? | within the first three weeks following allogenic bone marrow transplant.
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| what are the histologic manifestations of sinusoidal obstruction syndrome? | deposition of collagen within the lumen of the central vein.
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| what are four major consequences of portal hypertensin? | hepatic encephalopathy, esophageal varices (PS shunts), congestive splenomegaly, ascites.
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| when liver damage occurs, there is accumulation of excess serous fluid (protein <3 gm/dL) in the peritoneal cavity. it is caused by cirrhosis in 85% of cases, and is clinically detectable when fluid levels reach about 500ml in the abdomen | Ascites
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| yellowing of the skin is known as | jaundice
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| yellowing of the sclerae is known as | icterus
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| a rare type of brain damage that occurs with severe jaundice, and is due to accumulation of unconjugated bilirubin. all the clinical manifestations arise from bilirubin retention | kernicterus
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| systemic retention of not only bilirubin but other solutes eliminated in the bile (like cholesterol, cholic acid, etc) | cholestasis
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| the end product of heme degradation is called... | bilirubin
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| thick, greenish yellow fluid made up of: bilirubin, bile salts, bile acids, taurine/glycine, cholesterol, electrolytes | bile
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| what are two functions of bile | 1. emulsification of dietary fat in the lumen of hte gut through detergent action of bile salts. 2. elimination of bilirubin, excess cholesterol, xenobiotics and other waste products that are insufficiently water soluble to be excreted in urine.
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| bilirubin goes to the bilirubin-protein complex via this enzyme | glutathione-5-reductase
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| the bilirubin-protein complex goes to bilirubin glucuronide via this enzyme | UGT1A1
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| the water soluble form of bilirubin to be excreted is this | bilirubin glucuronide
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| what are three congenital red blood cell diseases which lead to excess hematopoiesis? | sickle cell, thalassemia, spherocytosis
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| what are two causes of unconjugated hyperbilirubinemia? | impaired uptake (cell injury, drugs like rifampin and probenacid, newborn)altered glucoronyl transferease activity (absent UGT1A1 activity-cringler Najjar type I, decreased UGT1A1 activity-Cringler najjar type Ii, gilbert syndrome, newborn
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| what are two causes of conjugated hyperbilirubinemia? | impaired transport into canaliculus, canalicular cholestasis
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| describe impaired transport into the canaliculus | cell injury (viral or alcoholic hep), toxins, dubin johnson syndrome, rotor syndrome.
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| describe canalicular cholestasis | cell injury (viral or alcoholic hep) drugs and toxins, pregnancy.
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| unconjugated bilirubin is also called... | indirect bilirubin
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| give some characteristics of unconjugatd bilirubin | insoluble in water at physiologic pH, exists in tight complex with albumin, cannot be excreted in urine
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| conjugated bilirubin is also known as.. | direct bilirubin
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| give some characteristics of direct bilirubin | water soluble, loosely bound to albumin, can be excreted in urine
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| describe physiologic jaundice in the newborn | transient and mild unconjugated hyperbilirubinemia within the first two weeks of life, but after the first twenty four hours.
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| what causes physiologic jaundice of the newborn? | immature transhepatic clearance of bilirubin
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| physiologic jaundice of the newborn is more pronounced in these two populations: | premature infants (immaturity and increased turnover of RBC), and breastfed babies (presence of bilirubin deconjugating enzymes in breastmilk)
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| what is the treatment of physiologic jaundice of the newborn? | phototherapy-absorption of light by unconjugated bilirubin generates water soluble isomers.
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| list three hereditary unconjugated hyperbilirubinemias. (note: these diseases all have normal liver morphology) | gilbert syndrome, Crigler-Najjar type I, Crigler-Najjar type II.
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| this hereditary unconjugated hyperbilirubinemia is autosomal recessive. It is common and benign, mild, fluctuating hyperbilirubinemia associated with stress. there is no clinical consequence | Gilbert syndrome.
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| this hereditary unconjugated hyperbilirubinemia is autosomal dominant with variable penetrance, generally mild, extroardinarily yellow skin, phenobarbital induces hypertrophy of ER in hepatocytes. | Crigler Najjar type II
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| this hereditary unconjugated hyperbilirubinemia is autosomal recessive and fatal in the neonatal period. Death is secondary to kernicterus within eighteen months without liver transplantatoin | Crigler Najjar type I
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| list the two types of hereditary conjugated hyperbilirubinemias | dubin johnson syndrome, rotor syndrome
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| this hered conjug hyperbili is an AR disorder due to absence of canalic protein MDR2, resp 4 transport of bilirubin glucoronides into bile. it presents as chronic recurrent jaundice of fluctuating intensity, and most are asymptomatic with normal lifespan | Dubin Johnson syndrome
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| this type of hereditary conjugated hyperbilirubinemia is due to impaired bile formation and flow, has normal liver morphology, and patients are jaundiced but have normal lives. | Rotor syndrome
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| what are histologic features of dubin johnson syndrome | abundant cytoplasmic inclusions of coarse dark brown pigment granules, normal hepatocytes, EM shows these lysosomal inclusions.
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| this is a pathologic condition of impaired bile formation and flow | cholestasis
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| cholestasis is caused by... | obstruction of bile channels (intra or extra hepatic),defects in hepatocyte bile secretion
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| what are some signs and symptoms of cholestasis | jaundice, xanthomas, pruritis, deficiencies of fat soluble vitamins KADE
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| what are some lab findings in cholestasis? | increased alkaline phosphatase, increased gamma glutamyl transferase
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| what do you see in the parenchyma in cholestasis? | swollen hepatocytes with bile pigments in cytoplasm, dilated canaliculi, apoptotic cells, kupfer cells with bile.
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| in cholestasis, what do you see in the portal tracks? | bile ductular proliferation, edema bile pigment retention, neutrophilic infiltration
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| list some major causes of extrahepatic biliary obstruction | bile duct carcinoma, enlarged lymph node (ex: Hodgekin disease, metastatic carcinoma), sclerosing cholangitis, postoperative stricture, congenital biliary atresia, pancreatic cancer, gallstones, carcinoma of the ampulla of vater
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| name two types of intrahepatic biliary tract disease | primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC)
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| describe primary biliary cirrhosis | portal tract markedly expanded by lymphocytic infiltrate and plasma cells. granulomatous reaction, bile duct destruction.
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| describe primary sclerosing cholangitis | atrophy of bile duct epithelium, concentric periductal (onion skin fibrosis), lymphocytic infiltrate
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| this is a group of autosomal recessive cholestatic conditions | progressive familial intrahepatic cholestasis
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| in this type of progr famil intrahep cholesta, cholestasis begins in infancy, with severe pruritis and progresses to liver failure before adulthood. there is mutation in the ATP8B1 that causes impaired bile secretion and benign intrahepatic cholestasis | PFIC-1
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| in this type of PFIC, there is extreme pruritis and growth failure progression to cirrhosis in the first decade. high risk of cholangiocarcinoma, and there is mutation in the ABC B11 gene. | PFIC-2
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| in this type of PFIC, there is cholestasis with high serum GGT, absence of phosphatidly choline in bile duct epithelium destroyed detergent actoin mutations in ABCB4 gene. | PFIC-3
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| list some haptic diseases associated with pregnancy | preeclempsia and eclampsia, acute fatty liver of pregnancy, intrahepatic cholestasis of pregnancy
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| list characteristics of preeclempsia | maternal HTN, proteinuria, peripheral edema, coagulation abnormalities and DIC, "HELLP": hemolysis, elevated liver enzymes, low platelets
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| what are some characteristics of eclampsia? | preeclemptic signs/symptoms with hyper-reflexia and convulsion
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| this disease presents with a spectrum from subclinical to hepatic failure and death and presents in the third trimester. symptoms are bleeding, N/V, jaudice and coma. pathogenesis is unkonwn, and mitochondrial dysfunction is implicated. | acute fatty liver in pregnancy
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| how do you diagnose acute fatty liver in pregnancy? | high clinical suspicion confirmed by microvesicular steatosis using special stains on tissues for fat (oil red O or Sudan black) on frozen tissue
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| a third trim occurrence charact by pruritis followed by darkening of the urine and occasionally light stools and jaunndice, its a benign condition w/increased risk for gallstand malabsorp. there is incr inci of fetal distress, stillbirths and prematurity | intrahepatic cholestasis of pregnancy
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| what are some patterns of injury that can happen in metabolic liver disease? | steatosis, steatohepatitis, fibrosis and cirrhosis
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