The Liver and Bililary Tract Flashcards

1
Q

the average weight of a normal adult liver is between

A

1400-1600 grams

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2
Q

capsule covers the surface of the liver

A

Glissons

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3
Q

The liver has ______ lobes designated as______,_______,_______, and _______.

A

Right, left, quadrate, caudate

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4
Q

two microscopic structural units of the liver are the _____and the_____.

A

Lobule and acinus

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5
Q

Define and differentiate the sinusoids from the canaliculi.

https://histology.siu.edu/erg/liver.htm

A

Between the plates of hepatocytes are vascular sinusoids. Arterial and portal venous blood traverses the sinusoids and exits into the terminal hepatic vein through orifices in the vein wall. Between abutting hepatocytes are bile canaliculi, which are channels 1-2 micrometers in diameter, formed by grooves in the plasma membranes of the facing hepatocytes and delineated from the vascular space by tight junctions.

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6
Q

The monocytic-phagocytic cells lining the sinusoids are known as

A

Kupffer cells

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7
Q

The liver has a dual vascular supply coming from the _______ and the ______.

A

Portal vein and hepatic artery

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8
Q

Disturbances of bilirubin metabolism cause ______and _______.

A

Jaundice and cholestasis

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9
Q

Disturbances of bilirubin metabolism cause ______and _______.

A

Jaundice and cholestasis

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10
Q

Define jaundice and cholestasis.

A

Jaundice – yellow discoloration of the skin and sclerae due to bile formation, disruption, and retention of pigmented bilirubin.
Cholestasis – systemic retention of not only bilirubin but also other solutes eliminated in bile.

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11
Q

Describe the five pathophysiological mechanisms that produce jaundice and give examples of each.

A

acronym REDII
1. Reduced hepatic uptake – drug interference with membrane carrier system
2. Excessive production of bilirubin – hemolytic anemia
3. Deficiency of canalicular membrane transporters – Dubin-Johnson syndrome
4. Impaired conjugation – physiologic jaundice of the newborn
5. impaired bile flow – obstruction (intrahepatic or extrahepatic); manifestations relate to intestinal malabsorption including nutritional deficiencies of the fat soluble vitamins A, D, and K

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12
Q

The alterations that cause liver failure fall into what three categories

A

ACH

1) Acute liver failure - massive hepatic necrosis
2) Chronic liver disease – cirrhosis
3) Hepatic dysfunction without overt necrosis – tetracycline toxicity

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13
Q

Describe the pathophysiology of hepatic encephalopathy.

A

Hepatic encephalopathy is caused by abnormal neurotransmission in the central nervous and neuromuscular systems and appears to be associated with elevated blood ammonia levels, which impair neuronal function and promote generalized brain edema.

google:
Hepatic encephalopathy is deterioration of brain function that occurs in people with severe liver disease because toxic substances normally removed by the liver build up in the blood and reach the brain.

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14
Q

discuss hepatorenal syndrome

A

Hepatorenal syndrome refers to the appearance of renal failure in patients with severe chronic liver disease, in which there are no intrinsic morphologic or functional causes for the renal failure.

google
portal hypertension=> splanchnic vasodilation (responsible for the hypoperfusion of the renal system which leads to the activation of the renin-angiotensin-aldosterone system ) => decreased effective circulatory volume => activation of renin-angiotensin-aldosterstone system=> renal sodium avididity (acsites) and renal vasoconstriction (hepatorenal syndrome)

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15
Q

Discuss the similarities and differences between passive congestion and centrilobular hemorraggic necrosis of liver

A

Right sided cardiac decompensation leads to passive congestion of the liver. The liver is slightly enlarged, tense, and cyanotic with rounded edges. On microscopic examination, there is congestion of the centrilobular sinusoids. With time, centrilobular hepatocytes become atrophic, resulting in markedly attenuated liver cell plates. Left sided cardiac failure or shock may lead to hepatic hypoperfusion and hypoxia. In this instance, hepatocytes in the central region of the lobule undergo ischemic necrosis (centrilobular necrosis). The combination of hypoperfusion and retrograde congestion acts synergistically to generate centrilobular hemorrhagic necrosis.

note on picture that bottom is congestion/right sides heart failure and top is left sided heart failure/centrilobular necrosis

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16
Q

Define and discuss Budd-Chiari syndrome and differentiate this from portal vein obstruction.

A

Budd-Chiari syndrome (hepatic vein thrombosis) - The obstruction of two or more major hepatic veins, characterized by hepatomegaly, weight gain, ascites, and abdominal pain.

Hepatic vein thrombosis is associated with polycythemia vera, inherited disorders of coagulation, Paroxysmal nocturnal hemoglobinuria, and intra-abdominal cancers.

google: think backflow vs occulsion
portal vein obstruction- Obstruction of this vein can be caused by a tumor or growth pressing on the vessel, or by a clot in the vessel

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17
Q

most common cause of liver disease in the US is

A

nonalcoholic fatty liver disease

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18
Q

which stains for fat and glycogen

A

FAT-sudan IV or Oil red O
glycogen-PAS
it also says “done on frozen”? dont know what that means

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19
Q

Prolonged severe chronic passive congestion or centrilobular hemorrhagic necrosis of the liver associated with heart failure leads to ___________ also known as ________.

A

liver fibrosis
cardiac sclerosis

google:
Cardiac sclerosis or cardiac cirrhosis is the end-point of passive hepatic congestion from heart failure.

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20
Q

What disease is characterized by inflammation and obliterative fibrosis of intrahepatic and extrahepatic bile ducts with dilation of preserved segments – “onion skin” fibrosis?

A

google:
Primary sclerosing cholangitis (answer) (PSC) is a chronic liver disease in which the bile ducts inside and outside the liver become inflamed and scarred, and eventually narrowed or blocked

Primary sclerosing (skluh-ROHS-ing) cholangitis (koh-lan-JIE-tis) is a disease of the bile ducts. Bile ducts carry the digestive liquid bile from your liver to your small intestine. In primary sclerosing cholangitis, inflammation causes scars within the bile ducts. These scars make the ducts hard and narrow and gradually cause serious liver damage. A majority of people with primary sclerosing cholangitis also have inflammatory bowel disease, such as ulcerative colitis or Crohn’s disease.

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21
Q

Define and differentiate predictable and unpredictable drug reactions and give examples of each.

A

Predictable drug reactions may occur in anyone who receives a sufficient dose of an agent - acetaminophen, tetracycline, antineoplastic agents.

Unpredictable reactions depend on idiosyncrasies ( a way of behaving or thinking that is characteristic of a person) of the host, particularly the host’s propensity to mount an immune response to the antigenic stimulus and the rate at which the host metabolizes the agent – chlorpromazine, halothane, methyldopa

22
Q

Define and differentiate neonatal hepatitis from extrahepatic biliary atresia.

A

Neonatal hepatitis – prolonged neonatal cholestasis with variable degrees of hepatic synthetic dysfunction such as hypoprothrombinemia.

Biliary atresia is defined as a complete obstruction or partial obstruction of the lumen of the extrahepatic biliary tree within the first three months of life. (Not in Robbins, p. 857)

23
Q

Define cholangitis and give some etiologies.

A

Cholangitis is the term used for bacterial infection of the bile ducts. Cholangitis can result from any lesion creating obstruction of bile flow, most commonly choledocholithiasis. Other causes- tumors, acute pancreatitis, fungi, viruses, or parasites.

24
Q

what are the 4 phases of acute symptomatic viral hepatitis with recovery

A

1) Incubation period
2) Symptomatic preicteric phase
3) Symptomatic icteric phase (the patient develop yellow discoloration of the eyes and urine (icteric phase).)
4) Convalescence (p. 836)

acronym ISS covalescence

google:
Acute viral hepatitis is diffuse liver inflammation caused by specific hepatotropic viruses that have diverse modes of transmission

25
Q

define chronic hepatits

A

Chronic hepatitis is defined as symptomatic, biochemical, or serologic evidence of continuing or relapsing hepatic disease for more than 6 months.

26
Q

Define cirrhosis and give the three characteristics features.

A

Cirrhosis – the liver is subdivided into nodules of regenerating hepatocytes surrounded by scar tissue.

Three characteristics:
Bridging fibrous septa
Parenchymal nodules
Disruption of the architecture of the entire liver (

27
Q

Discuss the pathophysiology of portal hypertension, including the three main causes, and the four main clinical consequences.

A

Increased resistance to portal blood flow may develop in a variety of circumstances, which can be divided into prehepatic, intrahepatic, and posthepatic causes.

Prehepatic – obstructive thrombosis and narrowing of the portal vein or massive splenomegaly

Intrahepatic – cirrhosis

Posthepatic – severe right sided heart failure, constrictive pericarditis, and hepatic vein outflow obstruction
Four major clinical consequences -
1) Ascites ( fluid collects in spaces within your abdomen. As fluid collects in the abdomen, it can affect your lungs, kidneys, and other organs.)

2) Formation of portosystemic venous shunts (google : rare vascular anomalies that occur secondary to abnormal development or involution of fetal vasculature)
3) Congestive splenomegaly
4) Hepatic encephalopathy (er doesn’t work properly, toxins build up in the blood. These toxins can travel to the brain and affect brain function)

27
Q

Discuss the pathophysiology of portal hypertension, including the three main causes, and the four main clinical consequences.

A

Increased resistance to portal blood flow may develop in a variety of circumstances, which can be divided into prehepatic, intrahepatic, and posthepatic causes.

Prehepatic – obstructive thrombosis and narrowing of the portal vein or massive splenomegaly

Intrahepatic – cirrhosis

Posthepatic – severe right sided heart failure, constrictive pericarditis, and hepatic vein outflow obstruction
Four major clinical consequences -
1) Ascites ( fluid collects in spaces within your abdomen. As fluid collects in the abdomen, it can affect your lungs, kidneys, and other organs.)

2) Formation of portosystemic venous shunts (google : rare vascular anomalies that occur secondary to abnormal development or involution of fetal vasculature)
3) Congestive splenomegaly
4) Hepatic encephalopathy (er doesn’t work properly, toxins build up in the blood. These toxins can travel to the brain and affect brain function)

28
Q

what are 3 distinctive forms of liver disease associated with chronic alcohol consumption?

A
  1. hepatic steatosis
  2. alcoholic hepatitis
  3. cirrhosis
29
Q

Eosinophilic cytoplasmic inclusions dispersed about the nucleus in alcoholic cirrhosis are known as_

A

mallory bodies

google:
Mallory bodies (MB), also known as Mallory-Denk bodies (MDB), are cytoplasmic hyaline inclusions of hepatocytes, once thought to be specific for alcoholic hepatitis now occur in other liver diseases which include nonalcoholic steatohepatitis (NASH), cholestatic liver diseases, primary biliary cirrhosis (PBC

30
Q

What are the five proximate causes of death in the end-stage alcoholic?

A

1) hepatic coma
2) massive gastrointestinal hemorrhage
3) an intercurrent infection
4) hepatorenal syndrome
5) hepatocellular carcinoma

31
Q

Define Wilson disease

A

Wilson disease is an autosomal recessive disorder caused by the ATP TB gene resulting in impaired copper excretion in the bile and a failure to incorporate copper into ceruloplasmin. It is marked by the accumulation of toxic levels of copper in many tissue and organs, principally the liver, brain, and eye.

32
Q

hat is the name of the eye lesions found in patients with Wilson disease?

A

Kayser-Fleischer Rings

33
Q

Define and differentiate the two forms of biliary cirrhosis.

A

Primary biliary cirrhosis is an inflammatory autoimmune disease affecting the intrahepatic bile ducts.
Secondary biliary cirrhosis results from uncorrected obstruction of the extrahepatic biliary tree.

google:
Secondary biliary cirrhosis. This results from prolonged bile duct obstruction or narrowing or closure of the bile duct for other reasons, such as a tumor.

34
Q

discuss the pathophysiology of focal nodular hyperplasia

A

Focal nodular hyperplasia presents as a spontaneous mass lesion in a noncirrhotic liver, most frequently in young to middle-aged adults. The lesion appears to be due to heterogeneity in hepatic blood supply arising from focal obliteration of portal vein radicals and compensatory augmentation of arterial blood supply.

the f is this saying i dunno but eh cant get every concept

35
Q

What major protease inhibitor is frequently elevated in primary cancers of the liver?

A

Alpha-fetoprotein

google: protease prevents the virus from making copies of itself

36
Q

Most metastatic tumors of the liver generally arise from what primary organs?

A

breast, lung, colon, pancreas

37
Q

four histological layers of the GB

A

1) Mucosal lining with a single layer of columnar cells
2) Fibromuscular layer
3) Layer of serosal fat with arteries, veins, lymphatics, nerves, and paraganglia 4) Peritoneal covering (Not in Robbins)

38
Q

The spiral valves in the neck of the gallbladder are known as the

A

spiral valves of heister

google: mucosal folds located on the endoluminal surface of the cystic duct

39
Q

outpuchings of the mucosal epithelium with a diagnosis of chronic cholecystitis

A

Rokitansky-Aschoff sinuses

google:
The term Rokitansky-Aschoff sinuses, or Luschka’s crypts of the gall bladder, is applied to deep outpouchings of mucosa extending into or through the muscular coat and into the perimuscular layers, leading to separation of the interstices and delicate walls of the muscle bundles.

40
Q

folding of the fundus of the gallbladder

A

answer: Phrygian cap
google: Phrygian cap is a congenital anomaly of the gallbladder

41
Q

two main types of gallstones are __ and __ with __ being the most common

A

Cholesterol stones and pigment stones
Cholesterol stones

google: pigment stone are made of bilirubin

42
Q

The four major factors associated with the formation of gallstones are__

A

Age and sex, environmental factors, acquired disorders, hereditary factors

43
Q

Cholesterol gallstone formation involves a tetralogy of simultaneous defects which are

A
  1. Bile must be supersaturated with cholesterol
  2. Gallbladder hypomotility promotes nucleation
  3. Cholesterol nucleation in bile is accelerated
  4. Mucus hypersecretion in the gallbladder traps the crystals, permitting their aggregation into stones. (p. 876)
44
Q

Briefly describe the morphologic types of carcinomas of the gallbladder.

A

The infiltrating pattern is more common and usually appears as a poorly defined area of diffuse thickening and induration of the gallbladder wall that may cover several square centimeters or may involve the entire gallbladder.

Deep ulceration may cause direct penetration of the gallbladder wall or fistula formation to adjacent viscera into which the neoplasm has grown. These tumors are scirrhous (scirrhous reaction resulting in a small fibrosed and contracted gallbladder) and have a firm consistency. The exophytic pattern grows into the lumen as an irregular, cauliflower mass but at the same time invades the underlying wall. The luminal portion may be necrotic, hemorrhagic and ulcerated. Most common sites are the fundus and the neck.

google:
Incidental gallbladder cancer in routine cholecystectomy specimens can be grossly subtle, with areas of mucosal granularity / irregularity, minimally raised / polypoid mucosal lesions or focally thickened fundus / body (Am J Surg Pathol 2019;43:1668)
Frank tumors may have one or more of the following features:
Thickened and indurated gallbladder wall
Exophytic or polypoid friable mucosal lesions (especially those arising from intracholecystic papillary neoplasm)
Firm, gritty, tan-white to yellow-gray cut surface

45
Q

hydrops of the gallbladder

A

Progressive mucosal removal of luminal lipids in obstructed, inflamed gallbladders may have clear mucinous secretions.

google:Gallbladder hydrops or mucocele 5 refers to marked dilatation of the gallbladder due to chronic obstruction of the cystic duct resulting in accumulation of sterile non-pigmented mucin.

46
Q

Describe the appearance of a gallbladder with cholesterolosis.

A

The mucosal surface is studded by yellow flecks; also known as strawberry gallbladder.

47
Q

Describe the pathophysiology of cholesterolosis.

A

Cholesterol normally entering the gallbladder mucosa by free exchange with the lumen may be esterified by acyl CoA, cholesterol acyltransferase. Cholesterol hypersecretion by the liver promotes excessive accumulation of cholesterol esters within the lamina propria of the gallbladder.

48
Q

Define Courvoisier’s Law.

A

Courvoisier’s law states that, in the presence of jaundice, an enlarged gallbladder is unlikely to be due to gallstones; rather carcinoma of the pancreas or the lower biliary tree is more likely

49
Q

cholelithiasis vs choledocholithiasis

A

Cholelithiasis involves the presence of gallstones (see the image below), which are concretions that form in the biliary tract, usually in the gallbladder. Choledocholithiasis refers to the presence of one or more gallstones in the common bile duct