Liver, Gallbladder And Pancreas Disease

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anatomy of the liver

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1400 to 1600 gm (approximately 2.5% of body weight)

Dual blood supply-portal vein (60-70%)and hepatic artery (30-40%).

Zonation in liver parenchyma-note gradient of activity of many hepaticenzymes, usually see a lobular architecture.

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physio function of the liver

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-maintains metabolic hemostasis - processes basically everything - carbs, fats, proteins and vitamins

-synthezise serum proteins (for oncotic pressure)

-primary site for detox of xenobiotics and waste

-huge functional reserve of regenerative capacity can mask hepatic injury

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liver's response to injury

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-degeneration of hepatocytes or accumulation of toxic products

-necrosis/apoptosis (toxins?)

-inflammation (impeded and facilitates healing)

-regeneration: functional return, but over TIME fibrosis: reduced/loss of function

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Cirrhosis

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-diffuse, fibrosis, regenerations hepatocytes

-among the top 10 causes of death in the US

-primary role in liver related death

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etiology of cirrhosis

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alcohol, viral, non-alcoholic steatohepatitis (inflammation involved with fatty accumulation), biliary disease and iron overload

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morphologic changes of the liver in cirrhosis

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1) bridging fibrous septa

2) parenchymal nodules

3) fibrosis and parenchymal inury

end result: loss of hepatic funxn and increased risk for Ca

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what are reasons behind increased pressure of portal blood flow?

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1) prehepatic (obstructive thrombi)

2) intrahepatic (cirrhosis)

3) posthepatic (right sided heart failure)

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cirrhosis symptoms

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weight loss

weakness

liver failure

portal hypertension

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portal hypertension can lead to

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-ascites (abdominal swelling from hepatic lymph)

-collateral venous channels that leads to esophageal varices that could rupture or cause anemia

-splenomegaly

-hepatic encephalopathy and hypogonadism

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fatty liver disease (cirrhosis)

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alcohol - deprivation of nutrient or works as a toxin

obesity, DM and medications can cause a fatty liver too

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Jaundice etiology

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overproduction, reduced hepatocyte uptake or obstruction of bile flow (that eliminates billirubin), hepatitis

hemolytic anemia is the number one cause

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jaundice

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excess billirubin (conjugated and unconjugated)- the conjugated for require glucuranic acid from the liver

-yellow color of skin and sclera

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what causes infectious viral infections of the liver?

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usually hepatotropic viruses (A,B,C,D,E and G) but can also be systemic infections like EBV, rubella etc..

**all result in hepatocyte injury that is assoc with inflamm

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Hep A

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RNA virus

benign, self-limiting

NO chronic disease or carrier state

fecal-oral (crowded, unsanitary conditions, with consumption of contaminated water)

usually 2-6 weeks

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Hep B

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DNA virus

-parenteral (blood) or sexual contact with serology that will remain in the blood forever

-usually self limiting (90%)

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vaccine for hep B?

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yes

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Hep B possible results

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1. recovery

2. nonpregressive chronic hep

3. progressive hep ending in cirrhosis

4. asymptomatic carrier

5. liver Ca

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what determines the outcome of Hep B

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host immune response --> damage is from cytotoxic T cells

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Hepatitis C

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-major cause of liver disease worldwide

-chronic liver disease ending in cirhosis is a common end stage

-RNA virus

-parenteral contact/sexual spread

-increased risk for hepatocellular carcinoma

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vaccine for hep C?

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NO!, but there is a tx now!

protease and nucleoside inhibitors (combo drug) is curative in most pts. with some side effects, but very expensive

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acute viral hepatitis

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-usually resolves in 8 wks but can ead to acute liver failure (rare) or transition into a chronic state (esp with hep C)

-symptoms: asymp to fatigue or jaundice

INFLAMMATION by lymphocytes, NOT neutrophils

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chronic hepatitis

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abnormal liver function for more than 6 weeks: definition

determine the etiology, grade the activity and stage and then tx

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alcoholic liver disease

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60% of chronic liver disease is associated with overuse of alcohol

-usually deaths are due to cirhosis

there are 3 main features: hepatic steatosis, alcoholic hepatitis and cirhosis (steatosis an hepatitis are reversible)

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metabolic liver diseases

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most common is non-alcoholic fatty liver disease (obese peoples)

hemochromatosis, wilsons and alpha 1anti-trypsin deficiency

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hemochromatosis

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excessive accumulation of body iron. Most is deposited in liver and pancreas

-hereditary forms: AR missing chromosome 6 that has the gene that absorbs Fe

-acquired form: excess Fe intake

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features of the liver with hemochromatosis

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clinical: micronodular cirrhosis with hepatomegaly, DM and skin pigmentation (bronzed)

morphology of the liver: fibrosis and hemosiderin

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tx of hemochromatosis

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phlebotomy to detect and Fe chelators

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Wilsons disease

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failure to incorporate copper, so there is an accumulation in liver, brain and eyes

acute or chronic liver disease, fatty, necrosis and cirrhosis

AR

presents with a tremor or behavioral changes

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wilsons disease testing and tx

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screening, NOT blood levels

Cu levels in the urine and liver

tx with chelation: D-penicillamine

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alpha 1 antitrypsin deficiency

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develop pulmonary emphysema from protein degrading enzymes

liver disease develops, forming mallory bodies and PAS positive granules within hepatocytes

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hepatic tumors arise from

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-there are a variety of benign and malignant

-cysts, bile ducts, hemangiomas, hepatocytes

**rich blood supply to the liver so many of the tumors are from metastatic (esp. the breast and colon) and only really present as a enlarged liver

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bile duct carcinome

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"Cholangiocarcinoma"

-cancer of the biliary tree - most adenoCa

-very demoplastic tumor-tumors are firm and gritty

-very aggressive, but asymptomatic until late stage

-collision tumor with HCC

-fatal within 6 mo.

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hepatocellular adenoma

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-benign

-usually assoc. with oral contraceptives (reaction mechanism) b/c once removed, regression of the tumor

-NO bile ducts : histo

- presents as an acute abdomen with intra-abdominal bleeds

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hepatocellular carcinoma

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-worldwide: 3rd leading cause of cancer death

-male predominence

-strong propensity for vascular invasion

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etiological factors for hepatocellular carcinoma

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cirrhosis

viral infection, alcoholism, NASH and food contaminants (alfatoxins)

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prognosis and tx of HCC

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grim prognosis

resection if foccal, new Ca foci may develop, liver transplant

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Fibrolamellar Carcinoma

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-distinct, but variant of HCC in young peoples

-generally no underlying disease

-NO etiologic profile

"scirrhous" tumor - scarring tumor

tx thru surgery, better prognosis than HCC (32% 5 year)

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cholelithiasis (gall stones)

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-10-20% of adults. increased risk with age and obesity

-caucasian women mainly

-cholestrol and pigment stones

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complications with gall stones

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colicky pain

inflamm

obstruction of the gall bladder that erodes into the ileum

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pathogenesis gall stone

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supersat --> initiation --> growth

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types of stones

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cholestrol (radiolucent)

bilirubin (radiopaque)

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stone risk factors

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cholestrol: caucasain women, estrogens

pigments: hemolysis, Gi disorders and biliary infection

**hereditary and gall bladder stasis also contribute

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cholecytitis

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assoc with gall stones

-acute or chronic (f>>M)

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acute cholecytitis

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severe RUQ pain

chemical, bacterial, reflux-ischemia

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chronic cholectitis

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-not a dramatic presentation, can be asymp

-stones cause this usually

-fibrosis and inflamm result

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cancer of the gallbladder

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- f>>M

-LOW survival rate (less than 5%)

-risk factors: gall stones or infectious agents

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acute pancreatitis

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-reversible injury associated with inflammation

-release of lipases and inflammatory proteolysis

-necrosis of vessels with hemorrhage

-fat necrosis

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acute pancreaitis clinical presentation

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"acute abdomen" - grabs attn. upper back intense pain, full blown acute pancreatitis is a medical emergency (release of toxic enzymes like amylase and lipase)

-organ failure, abscess and possible death

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acute pancreatitis causes

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80% of the time is biliary tract disease, stones or alcoholism

-could be infections (mumps), trauma, metabolic diseases and medications

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chronic pancreatitis

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irreversible destruciton of exocrine pancreas with ensuing fibrosis and eventual destruction of endocrine parenchyma (later on)

unclear etiology

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symptoms and diagnosis of chronic pancreatitis

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severe ab pain to silent

daignosis - be suspicious, may have already destoryed all of the acinar cells so not an inc in serum amylase

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chronic pancretisis morphology

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-reduced acini

-chronic inflamm

-fibrosis

-obstruciton of ducts and spare islets

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pancreatic exocrine tumors

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-4th leading cause of Ca in the U.S becasue silent growth (in old people)

-mainly adenoCa

-derive from cysts?

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causes pancretic Ca

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DM, smoking and chronic pancreatitis

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pancreatic Ca appearance

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-ill defined gritty and hard

cancers at the head obstruct bile duct (jaundice) and cancers at the body and tail are usually clinically silent