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GI II Midterm > Chapter 18 - Liver And Bile Ducts > Flashcards

Chapter 18 - Liver And Bile Ducts Flashcards

1
Q

What lab tests show hepatocyte integrity?

A

Serum aspartate aminotransferase (AST)

Serume alanine aminotransferase (ALT)

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2
Q

What tests show biliary excretory function?

A

Total, Direct (conjugated), serum bilirubin
Serum alkaline phosphatase
Serum GGT

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3
Q

What tests show hepatocyte synthetic function

A

Serum albumin
Prothrombin Time (PT)
Serum ammonia

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4
Q

What are the reversible degenerative changes of hepatocytes?

A

Fat accumulation (steatosis) and bilirubin buildup (cholestasis)

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5
Q

When hepatocyte injury is not reversible how do they die?

A

Necrosis: predominant mode in ischemic-hypoxic injury and oxidative stress
Apoptosis: acute and chronic hepatitis, shrinkage, pyknosis, karyorrhexis, acidophil bodies

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6
Q

Explain the process of hepatocyte regeneration

A

Primarily occurs by proliferation of hepatocytes adjacent to those that have died
Stem cell replenishment is usually NOT a significant part of parenchymal repair
Hepatocytes are stem-cell like

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7
Q

What hepatic cell once activated, is primarily responsible for liver scar deposition?

A

Stellate cells
Lipid (vit A) storing cell when quiescent
Activated: TNF, Kupffer cells, toxins etc -> highly fibrogenic and contractile myofibroblasts

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8
Q

If chronic injury leading to scar formation is interrupted (like clearance of hepatitis virus infection, or cessation of alcohol use), then what can lead to scar formation being reversed?

A

Stellate cell activation cease

Fibrosis fragmented by Metalloproteinases produced by hepatocytes

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9
Q

When does liver failure occur?

A

When greater than 80-90% of hepatic function is lost

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10
Q

What cytokine is fibrogenesis driven by?

A

TGF-B released by Kupffer cells and lymphocytes

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11
Q 
What cytokine drives
Proliferation of stellate cells:
Contraction of activated stellate cells: 
Chemotaxis of activated stellate cells: 
Fibrogenesis:
A

Proliferation of stellate cells: PDGF, TNF
Contraction of activated stellate cells: ET-1
Chemotaxis of activated stellate cells: MCP-1, PDGF
Fibrogenesis: TGF-B

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12
Q

What is acute liver failure defined as?

A

Liver illness associated with encephalopathy and coagulopathy within 6 months of initial diagnosis
Fulminant hepatic failure: encephalopathy develops w/i 2 weeks of jaundice onset

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13
Q

What is most acute liver failure caused by?

A

Massive hepatic necrosis attributable to
US: acetaminophen overdose
Asia: Hep B and E, A

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14
Q

What is the clinical course of acute liver failure

A

Nausea, vomiting, jaundice
Progressing to encephalopathy and coagulopathy (inadequate hepatic synt of coagulopathy factors)
Liver initially swells d/t edema and inflammation
Liver transaminases elevated - hepatocyte destruction
Liver dramatically shrinks - transaminases decline
Portal HTN

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15
Q

What is hepatic encephalopathy

A

Life-threatening disorder of CNS and neuromuscular transmission
Excess ammonia in the blood impairs neuronal fxn and brain edema -> confusion, coma, limb rigidity, hyperrefelxia, asterisks

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16
Q

What are the MC causes of chronic liver failure worldwide?

A

Alcohol abuse, viral hepatitis, NASH, hemochromatosis

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17
Q

Morphological characteristics of cirrhosis

A

No central vein
Bridging fibrosis
Parenchymal nodules - hepatocyte regeneration encircled by fibrosis
Dense mononuclear infiltrate
Increase portal chronic inflammation gives interface hepatitis appearance

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18
Q

Clinical features of Chronic liver failure/Cirrhosis

A

Clinically silent until far advanced in 40% of pts
Anorexia, WL, weakness, and debilitation
Hyperestrogenemia -> palmar erythema in men, spider angiomata, hypogonadism, gynecomastia
Portal HTN + Sx of acute failure

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19
Q

Cirrhosis death can be due to what?

A

Progressive liver failure with encephalopaty and coagulopathy
Complications of portal HTN - variceal bleeding
Bacterial infections duet o gut mucosal damage and Kupffer cell dysfunction
HCC

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20
Q

What does Portal HTN result from?

A

Combination of increased flow into portal circulation and/or increased resistance to portal blood flow

Prehepatic: thrombosis, portal vein narrowing, massive spenomegaly with increased splenic vein blood flow
Intrahepatic: fibrous tissue (cirrhosis) MC, schistosomiasis, massive fatty change
Posthepatic: RSHF, hepatic vein obstruction

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21
Q

What are the major clinical consequences of portal HTN?

A

Ascites
Splenomegaly - caused by long-standing congestion and can cause thrombocytopenia and pancytopenia due to hypersplenism
Esophageal varices
Hepatic encephalopathy

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22
Q

Describe ascites

A

Collection of excess serous transudate in the peritoneal cavity
Most often a consequence of cirrhosis
500 ml or more to detect - trunkal obesity

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23
Q

Hep A virus

A 
ssRNA
Causes benign, self limited disease; fulminant HAV is rare 
Damage d/t CD8 T cells
Fecal-oral route 
Anti-HAV IgM - acute infection 
IgG - long-term immunity
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24
Q

Hep B virus

A 
dsRNA, Parenteral, PAS-D stain 
risk of hepatocellular carcinoma 
CD8 T cells damage
Ground glass hepatocytes****
Acute, self-limited hepatitis - MC
Fulminant hepatitis with massive liver necrosis - rare 
Nonprogressive chronic hepatitis 
Progressive chronic disease culminating in cirrhosis and increased risk of HCC 
Asymptomatic carrier
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25
Q

Best predictor of chronicity in HBV hepatitis

Geographic distribution and mode of transmission

A

Age at time of infection
Younger age at infection has higher probability of chronicity
Africa, Asia: high-prevalence area, transmission during childbirth MC
Europe: intermediate prevalence, horizontal transmission in childhood by minor cuts or breaks MC
US, Western Europe: low-prevalence, IV drug abuse and unprotected intercourse
> 90% HBV infections acquired early in life in endemic areas result in healthy carrier states

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26
Q

Antigens and Abs in HBV infection

A

HBeAG persistence = progression of chronic disease
HBsAG for 6 months = chronic carrier
IgM anti-HBcAg usually first antibody to appear
Anti-HBsAg signifies end of acute disease and persists for years

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27
Q

Hep C virus

A

Ss RNA, parenteral
HCV RNA polymerase low fidelity -> genomic variability
High titers against HCV does not confer effective immunity
Progresssion to chronic disease occurs in most (80-90%) and cirrhosis in 20%
Morph: lymphoid follicle**

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28
Q

What are the primary risk groups of HCV infection and how is the infection discovered?

A

IV drug abusers and multiple sex partners

Coincidental blood screen detecting elevations of ALT/AST (transaminases)

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29
Q

What Hepatitis virus has a high rate of fatal fulminant hepatitis in pregnant women? Where is it prevalent and what is the clinical course in a non pregnant pts?

A

HEV
HEV epidemics in Asia, Mexico, Africa,
Endemic: India
Usually self limited

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30
Q

What are the key features of autoimmune hepatitis (AIH)

A

Chronic, progressive hepatitis with strong genetic predisposition
Caucasian - DRB1 allele
Female predom
Triggered by viral infections or drugs or component of other autoimmune disorders (RA, Sjogren, UC)
Clusters of periportal plasma cells**
Rosettes
Type I: MC in US; ANA, ASMA; middle aged women; HLA-DR3
Type II: LKM-1, ACL-1; Kids-teens

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31
Q

What are the clinical features of autoimmune hepatitis ? Treatment?

A 
Acute or indolent paths 
Acute fulminant onset of Sx of liver failure in 40% of pts
Early severe fibrosis/scarring 
untreated: 6 month mortality in 40%
Survivors: cirrhosis in 40%
Immunosuppression therapy
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32
Q

What is the leading cause of liver pathology in most Western countries?

A

Alcoholic liver disease

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33
Q

What are the three (overlapping) forms of ALD?

A

Hepatic steatosis (fatty liver)
Alcoholic (steato-) hepatitis
Alcoholic steatofibrosis

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34
Q

Key features of hepatic steatosis

A 
Fatty liver 
Microvesicular lipid droplets w/i hepatocytes 
Can occur with moderate alcohol intake 
Enlarged, soft, greasy, yellow 
Little-no fibrosis 
Reversible
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35
Q

Key features of alcoholic (steato) hepatitis

A

Ballooning degeneration and hepatocyte necrosis
Mallory-Denk body (intracellular eosinophilic aggravates of intermediate filaments)
Neutrophilic rxn
Portal and periportal mononuclear inflammation
Fibrosis

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36
Q

Key features of alcoholic steatofibrosis

A

Stellate cell activation
Hepatic dysfunction
Hypoproteinemia
Coagulation abnormalities

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37
Q

Pathogenesis of ALD

A

Quantity and time
15% of alcoholics develop cirrhosis
Gender: women (pharmacokinetics and metabolism, estrogen increases permeability to endotoxins)
Ethnic: AA
Genetic: polymorphism in aldehyde dehydrogenase (metabolizing enzymes) or cytokine promoters
Comorbid conditions: iron overload, viral hepatitis increase severity

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38
Q

What are the clinical features of ALD ? What are the causes of death?

A

Elevation of AST:ALT 2:1 - unique
Hepatic steatosis: hepatomegaly, elevation of serum bilirubin and alk phos, minimal Sx
Alcoholic hepatitis: after heavy drinking acutely, tender hepatomegaly, bilirubin and alk phos elevated —> cirrhosis in 1/3 pts; slow resolution
Alcoholic cirrhosis: irreversible
Abstained: survival good
Death: hepatic coma, Gi hemorrhage, intercurrent infection, hepatorenal syndrome, and HCC

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39
Q

What is the most acquired metabolic disorder of the liver?

A

NAFLD

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40
Q

What is NAFLD and NASH? What is it d/t?

A

Group of conditions (metabolic syndrome - dyslipidemia, hyeprinsulinemia, insulin resistance) characterized by hepatic steatosis in absence of heavy alcohol consumption
NASH = NAFLD + hepatocyte damage and inflammation
Increasing prevalence of obesity

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41
Q

Pathogenesis of NAFLD?

Morphology?

A

Probably a consequence of hepatocyte fat accumulation and increased hepatic oxidative stress
2 hit Hypothesis: Hit 1 - insulin resistance -> hepatic steatosis-> NAFLD; Hit 2 - hepatocellular oxidative injury -> necrosis and 2* inflammation -> NASH
Morph: hepatocytes filled with fat vacuoles w or w/o inflammatory infiltrates; microvascular steatosis

42
Q

Clinical features of NAFLD and NASH

Treatment?

A

Hispanics>AA>whites
NAFLD only: asymptomatic w little risk of cirrhosis
+ NASH: symptom free or fatique, malaise, RUQ discomfort; serum transaminases levels elevated in 90%

NASH -> possible HCC or cirrhosis
Cardiovascular disease is frequent cause of morbidity and mortality
RX: targeted at obesity, hyperlipidemia, and insulin resistance

43
Q

What is hemochromatosis ?

A

Multi-organ disease
Excessive iron accumulation in parenchymal cells of liver and pancreas mainly
Hereditary (primary) type: homozygous recessive, excessive iron absorption bc regulation abnormal
Hemosiderosis (secondary) type: parental iron admin (transfusions, ineffective erythropoietin, increase iron intake, chronic liver disease)

44
Q

How is Hemochromatosis screened for? What is the treatment?

A

Increase serum iron and ferritin
Liver biopsy
Genetic testing
Prussian blue stain

Rx: regular phlebotomy

45
Q

What is the pathogenesis of hemochromatosis ?

A

Hepcidin (HAMP) mutation (normally lowers plasma iron)

Adult form: almost always caused by HFE gene mutation (cys-tyr, C282Y); causes reduction in Hepcidin expression

46
Q

Morphology of hemochromatosis

A

Iron accumulates as hemosiderin in liver, pancreas, myocardium, endocrine glands, joints, and skin
Cirrhosis and pancreatic fibrosis are the chief additional morphological changes

47
Q

What are the clinical features of hemochromatosis ? Death can result from what?

A

Classic triad; micronodular cirrhosis, DM, and skin pigmentation in sun-exposed areas
Iron->pancreas->DM
Sx appear after age 40 (amenorrhea, m: impotence and loss of libido)
Males predom (women lose iron w menstruation, and pregnancy)
Hepatomegaly
Death: cirrhosis and HCC and cardiac involvement

48
Q

What is Wilson disease

A

Multi-organ disease (liver, brain, eye)
Autosomal recessive
ATP7B gene mutations (copper transporting ATPase)
Copper excretion into bile reduced
Copper not incorporated into cerulopasmin
Ceruloplasmin secretion into blood inhibited
= copper accumulation in liver ->ROS generation

49
Q

Morphology of wilson disease

A 
Liver damage: minor-severe 
Fatty change, acute and chronic hepatitis with Mallory-Denk bodies, cirrhosis, rarely massive necrosis 
CNS toxicity of basal ganglia 
Kayser-Fleischer rings***
Copper toxic to RBC-> hemolytic anemia
50
Q

What are the clinical features of Wilson Disease? How is it Dx?

A

Age of onset and clinical presentation: variable (6-40 YOA; avg 11.4)
MC: acute or chronic liver disease b4 age 40
Mild behavioral changes, psychosis, Parkinson-like symptoms
Dx: decreased serum ceruloplasm, increased hepatic copper content, increased urinary copper excretion

Serum copper lvls are no NO diagnostic value

51
Q

What is the treatment for Wilson disease?

A

Copper chelation

Liver transplantation may be necessary

52
Q

Main mutation in Wilson disease

A

ATP7B

Majority have compound heterozygotes of different mutations on each ATP7B allele

53
Q

What is A1-Antitrypsin deficiency

A

MC diagnosed inherited hepatic disorder in infant and child
Autosomal recessive
2 organ disease: liver and lung
Very low serum lvls of this protein that normally inhibits neutrophil protease
-> emphysema bc of destructive proteases and hepatic disease by hepatocellular accumulation of misfolded protein

54
Q

What is the pathogenesis of A1-AT deficiency?

A 
Most mutations (PiMM) result in no or only moderate reductions in lvls and have no clinical manifestations 
PiZZ homozygotes (Glu->Lys): protein misfolding, ER stress response (UPR) -> autophagy, mitochondrial dysfunction and NF-kB = hepatocyte damage

Additional genetic or environmental factors: only 10% PiZZ homozygotes develop overt liver disease

55
Q

Morphology of a1-AT deficiency

A

PAS positive cytoplasmic globules in periportal hepatocytes

56
Q

Clinical features of a1-AT deficiency

Treatment

A

Neonatal hepatitis with cholestatic jaundice in 10-20% newborns
Adolescence: Acute hepatitis, cirrhosis, lung dz
Adults: HCC in 2-3% of homozygous adults, cirrhosis
Smoking accentuates lung emphysematous damage
Rx: liver transplantation

57
Q

What is neonatal jaundice?

A

Physiologic jaundice
Hepatic metabolic machinery does not mature until 2 weeks of age
Newborn develops transient, mild unconjugated hyperbilirubinemia
Exacerbated by breast-feeding due to bilirubin-deconjugating enzymes in breast milk
Use blue light machine

58
Q

What are the hereditary hyperbilirubinemias unconjugated forms?

A

Crigler-Najjar syndrome type I: Fatal, autosomal recessive, kernicterus, liver transplant, no UGT1A1
Critter-Najjar syndrome type II: autosomal dominant, UGT1A1 deficiency, not usually lethal
Gilbert syndrome: AR, not symptomatic, hyperbilirubemia exacerbated by infection, exercise, or fasting

59
Q

What are the hereditary hyperbilirubinemias conjugated forms?

A

Dubin-Johnson syndrome: AR, Black liver - pigment granules, usually not symptomatic, no bilirubin glucuronide transport protein, jaundice
Rotor syndrome: AR, jaundice, not symptomatic, defective uptake or excretion

60
Q

What are the consequences of cholestasis

A

Intrahepatic: hepatocellular dysfunction or canalicular obstruction
Extrahepatic: d/t duct obstruction
Jaundice, pruritus, xanthomas, intestinal malabsorption with nutritional deficiencies d/t port uptake of A,D,K vitamin

Serum alk phos and gamma-glutamyl transpeptidase (GGT) elevated

61
Q

What is the MC cause of bile duct obstruction in adults?

A

Extrahepatic choleslithiasis (gallstones)

62
Q

Clinical features of Large bile duct obstruction

A

Obstruction may promote ascending cholangitis with 2* bacterial infection of biliary tree: fever, chills, abdominal pain, jaundice

Charcot triad: fever, RUQ pain, jaundice

63
Q

MC cause of bile duct obstruction in neonates ?

A

Biliary atresia: extrahepatic biliary tree obstruction w/i first 3 months of life

64
Q

What is the single most frequent cause of death from liver disease in early childhood and accounts for the majority of children referred for liver transplantation?

A

Biliary atresia

65
Q

Pathogenesis of biliary atresia

A

Extrahepatic ducttst

Severe early fetal form (20%): aberrant intrauterine development of the biliary tree and commonly associated with other anomalies

Perinatal form (80%): secondary to viral infections and/ or autoimmunity; results from postnatal destruction of normal biliary tree

66
Q

Morphology and clinical features of Biliary atresia

A

Inflammation and fibrosing stricture of extrahepatic biliary tree
Fibrosis progressing to cirrhosis in 6 months
Seen in infant of normal birth weight and postnatal weight gain
If left untreated (liver transplantation), death occurs w/i 2 years of birth

67
Q

What is autoimmune cholangiopathy ?

A

Autoimmune disorder of intrahepatic bile ducts

PBC and PSC

68
Q

Key features of Primary Biliary Cirrhosis

A

Age: 50
Gender: F
Clinical course: progressive, insidious, pruritis, hepatomegaly, jaundice, xanthomas -> cirrhosis , variceal bleeding, encephalopaty
Associated conditions: Sjogren
Serology: 95% AMA + for PDC-E2 and 50% ANA +
Florid duct lesions and loss of small ducts only
Alk phos, GGT, cholesterol lvls elevated
Nonsuppurative inflammatory destruction of small bile ducts

69
Q

Treatment of primary biliary cirrhosis

A

Early-stage disease: oral urosodexycholic acid, slows progression

70
Q

Key features of Primary Sclerosing cholangitis

A

Age: 30
Gender: Male
Clinical course: unpredictable but progressive, severe - WL, ascites, variceal bleeding, encephalopathy, chronic pancreatitis and HCC
Ass conditions: IBD (UC)
Serology: P-ANCA
Radiology: strictures and beading of large bile ducts; pruning of smaller ducts
Duct lesion: inflammatory destruction of extrahepatic and large intrahepatic ducts; fibrotic obliteration of medium and small intrahepatic ducts

71
Q

what are nodular hyperplasias?

A

Solitary or multiple benign hepatocellular nodules in the absence of cirrhosis

Focal nodular hyperplasia: young adults, liver normal, single well demarcated mass containing central stellate fibrous scar

Nodular regenerative hyperplasia: diffuse (multiple) nodules without fibrosis, d/t intrahepatic blood flow; can develop portal HTN, ass: HIV, rheumatologic dz and SLE

72
Q

What is the most common benign liver tumor?

A

Cavernous hemangioma

73
Q

What are cavernous hemangiomas?

A

Benign neoplasm
Unencapsulated lesions usually 1-2 cm in diameter
Large, thin-walled vascular spaces
Can be locally destructive and generally DO NOT REGRESS
Female predom
Incidental discovery or cause of hemorrhage

74
Q

What are hepatocellular adenomas?

A 
Benign neoplasm 
30 cm in diameter
Young females 
Associated with OC use and anabolic steroids 
Incidentally discovered
75
Q

What are the three subtypes of hepatocellular adenoma?

A

HFN1-alpha -inactivated hepatocellular adenoma: mutations responsible for AD maturity-onset of diabetes in young, women, no risk of malignancy

B-catenin-activated: very high risk for malignant transformation, respected when found, OC and anabolic steroid use (women, men)

Inflammatory: men and women, NAFLD associated, small risk of malignant transformation, gp130 mutation (IL-6, jakstat)

76
Q

In the US, the vast majority of tumors involving the liver are benign or metastatic?

A

Metastatic

77
Q

What is the most common primary liver cancer?

A

HCC

78
Q

What is the most common liver tumor of early childhood? Key features?

A

Hepatoblastoma
Rare after age 3
Wnt-B-catenin pathway
Ass.: FAP and Beckwith-Wiedemann syndrome

Epithelial type and mixed epithelial and mesenchymal type

fatal if untreated, good prog if resected

79
Q

HCC predominately found in what people and geography?

A

Male predom
Developing countries with high rates of HBV
Exposure to aflatoxin (aspergillosis toxin)
Western pop: Increase HCV infection increasing HCC incidence
Chronic alcoholism, NASH, Hemochromatosis, a1-AT def
Background of chronic liver disease

80
Q

Morphology of HCC

A

Solitary mass, multifocal nodules or diffuse infiltrative cancer with massive liver enlargement in the background of cirrhosis often

Intrahepatic and vascular invasion common
Metastases more likely after 3 cm
Satellite tumor nodules

81
Q

What is a distinctive variant of HCC? Key features?

A 
Fibrolamellar carcinoma 
5% of HCC
Single scirrhous, hard tumor
20-40 yo (85% under age 35)
ABSENCE of chronic liver disease 
Cells in cords or ness separated by dense lamellar collagen bundles 
Rich in mitochondria - oncocytes
82
Q

Clinical features of HCC and prognosis

A

Hepatomegaly
RUQ pain
WL
Elevated serum AFP (alpha-fetoprotein) **
Prognosis depends on respectability of tumor
Mortality 2* to cachexia, GI or esophageal variceal bleeding, liver failure with hepatic coma or tumor rupture and fatal hemorrhage

83
Q

What is a cholangiocarcinoma ? Associations?

A

2nd MC 1* malignant tumor of liver
Chronic inflammation and cholestasis increasse risk
Arise from intrahepatic and extrahepatic biliary tree
Most perihilar (Klatskin tumors)
Can be associated w PSC, stones, NAFLD, HBV, and HCV

84
Q

What is a major risk in Southeast asia for cholangiocarcinoma?

A

Parasitic infection by Op=isthorchis sinensis

85
Q

Morphology of CCA

A

Single large mass, multifocal nodules or diffusely infiltrative
Contrast to HCC: typically pale, bc no bilirubin pigment
Desmoplastic w dense collagenous stroma

86
Q

Describe metastasis to the liver

A

Typically multiple implants are present with massive hepatic enlargement
Large implants tend to have defective vascular supplies and become centrally necrotic

87
Q

What are the congenital anomalies of the gallbladder? What is most common?

A

Absent
Aberrant location (embedded in hepatic substance)
Folded fundus (phrygian cap) MC***
Duplicated, bilobed

88
Q

More than 95% of biliary tract disease is attributable to what?

A

Cholelithiasis

89
Q

Majority of calculus are what kind of stones?

A

Cholesterol (90%)

90
Q

What are the main risk factors for cholesterol gallstones ?

A

Native americans: 75% of Hopi, Navajo, Pima groups

Fair, Fat, Female, Fertile, Family History

91
Q

What are the most common gallstones in US and Western Europe?

A

Cholesterol stones: supersaturation; hard, pale yellow

92
Q

What are the most common stones found in African americans?

A

Pigment stones, setting of unconjugated bilirubin due to chronic hemolytic conditions
I.e sickle cell disease
Black if sterile or brown with infection, soft

93
Q

What are the clinical features of cholelithiasis?

A

Majority asymptomatic
Pain = biliary colic (RUQ or right shoulder pain)
Sx: spasmodic, colicky pain d/t passing stones in bile ducts; inflammation causes RUQ pain

More severe complications: emphysema, perforation, fistula, cholangitiss, obstructive cholestasis or pancreatitis
Increased risk for gallbladder carcinoma

94
Q

What is acute cholecystitis and the MC cause?

A

Acute inflammation of gallbladder mostly d/t gallstone obstruction

95
Q

What is the pathogenesis of acute cholecystitis ?

A

Acute calculous cholecystitis: gallstones causing irritation -> inflammatory mediators–> gallbladder dysmoltility

Acute Acalculous cholecystitis: d/t ischemia, decrease flow in end-arterial cystic arter circulation; setting of sepsis w hypotension and multiorgan failure, immunosuppression, major trauma or burns, DM or infections

96
Q

What is the morphology of acute cholecystitis?

A

Enlarged, tense, bright red - blotchy green/black gallbladder with serosal fibrinous exudate

–> gangrenous cholecystitis in severe cases

97
Q

What are the clinical features of acute cholecystitis ?

A

Mild or surgical emergency

Sx: RUQ or epigastric pain in 6 hrs, pain, fever, anorexia, tachycardia, diaphoresis, and N/V

98
Q

What is chronic cholecystitis d/t?

A

Repeated bouts of acute cholecystitis
Often develops w/o antecedent attacks
90% gallstones but do not play a direct role in initiating inflammation
Chronic bile supersaturation with cholesterol-> inflammation

99
Q

What is the morphology of chronic cholecystitis

A

Contracted (fibrosis)
Normal in size or enlarged (from obstruction)
Gray-white wall -
Cholesterol-laden Mo in lamina propria (Cholesterolosis) and gallstones freq
Rokitansky-Aschoof sinuses
porcelain gallbladder (mural dystrophic calcification - rare) -> risk of cancer

100
Q

What are the complications of acute and chronic cholecystitis?

A

Bacterial superinfection, gallbladder perforation and abscess formation or peritonitis
Formation of biliary-enteric fistula

101
Q

What is the MC malignancy of extrahepatic biliary tract?

A

Adenocarcinoma

102
Q

Key feature of carcinoma of the gallbladder

A

Women predom
Age 70
Gallstones (95%)
Chronic gallbladder inflammation with or without stones is a critical risk factor
Asians: parasitic disease dominate vs stones
Infiltrating (diffuse thickening) or exophytic (cauliflower)
Local invasion of liver, extension to cystic duct and portohepatic LN
Metastatic seeding in peritoneum, viscera and lungs
Sx: insidious and indistinguishable from cholelithiasis - unresectable when discovered = poor prognosis

GI II Midterm (5 decks)

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