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Liver, Biliary tract and Pancreas Flashcards

1
Q
  1. Liver failure:

PATTERNS OF HEPATIC INJURY

A
  1. Degeneration and intracellular accumulation:
    - cell swelling + enlargement
    - fat, iron, copper etc. accumulate
  2. Necrosis + apoptosis:
    - coagulative necrosis
  3. Regeneration:
    - mitotic figures
  4. Inflammation:
    - hepatitis
  5. Fibrosis:
    - in response to inflammation or direct toxic insult
    - first around portal tract + central vein + within sinusoids
  6. Cirrhosis:
    - progressive parenchymal injury + fibrosis
    - end-stage liver disease, increases risk of pregnancy
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2
Q
  1. Liver failure:

LIVER FAILURE hepatic failure

A

= total loss (80-90%) of over function as a direct result of injury/disease

  • develops due to insidious destruction of hepatocytes or by repetitive discrete waves of parenchymal damage
  • can also be due to sudden massive destruction of hepatic tissue
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3
Q
  1. Liver failure:

LIVER FAILURE etiology

A
  1. Acute liver failure with massive hepatic necrosis
    - cause: drugs, viral hepatitis, idiopathic
    - massive hepatic necrosis ⇒ shrink
    - need transplant
  2. Chronic liver disease
    - most common route
  3. Hepatic dysfunction without obvious necrosis
    - acute fatty liver of pregnancy
    - tetracycline toxicity
    - Reye syndrome
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4
Q
  1. Liver failure:

LIVER FAILURE clinical features

A
  1. Jaundice
    - due to retention of bilirubin + bile stasis
  2. Malabsorption/ weight loss
    - due to bile, enzyme, vitamin deficiency
  3. Hypoalbuminemia
    - due to impaired synthesis ⇒ edema + muscle wasting
  4. Hyperammonemia
    - due to decreased urea-cycle ⇒ hepatic encephalopathy
  5. Hyperestrogenemia
    - metabolism impaired ⇒ palmar erythema, spider angiomas, hypogonadism, gynecomastia
  6. Palmar erythema, spider angiomas on skin
  7. Ascites, splenomegaly, gastroesophageal varices
  8. Hepatorenal syndrome
  9. Hepatic cardiomyopathy
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5
Q
  1. Liver failure:

LIVER FAILURE complications

A
  1. Hepatic encephalopathy
  2. Hepatorenal syndrome
  3. Coagulopathy
  4. Hepatopulmonary syndrome
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6
Q
  1. Liver failure:

HEPATIC ENCEPHALOPATHY

A

CLINICAL FEATURES:
- behavioral abnormalities
- stupor, deep coma
- death
- rigidity, hypo-reflexia, seizures, asterixis
MORPHOLOGY:
- minor changes in brain - edema, astrocytic reaction
PATHOGENESIS:
- severe loss of hepatocellular function
- shunting of blood from portal to systemic circulation
⇒ exposure of brain to altered metabolic environment
ACUTE: elevated ammonia ⇒ impair neuronal functioning + promote edema
CHRONIC: altered AA metabolism in brain ⇒ deranged neurotransmission

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7
Q
  1. Liver failure:

HEPATOPULMONARY SYNDROME

A
  • vasodilation in pulmonary vessels in patients with acute or chronic liver failure ⇒ blood runs quick ⇒ no gas exchange
  • symptoms: dyspnea, hypoxemia
  • if severe: no transplant
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8
Q
  1. Liver failure:

HEPATORENAL SYNDROME

A

= development of renal failure without any primary kidney diseases
PATHOGENESIS:
- unknown, but splanchnic vasodilation + systemic vasoconstriction ⇒ stasis in venous circulation ⇒ decreased flow to cortex of kidneys
CLINICAL FEATURES:
- oliguria
- azotemia
- hyperosmolar urine

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9
Q
  1. Liver failure:

HEMORRHAGIC DIATHESIS

A
  • liver impairment ⇒ synthesis of clotting factors impaired ⇒ increased bleeding tendency + thromocytopenia
  • can lead to massive hemorrhage in GI + other places
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10
Q
  1. Cholestasis, cholelithiasis, jaundice:

CHOLESTASIS etiology

A
  • primary sclerosing cholangitis
  • primary biliary cirrhosis
  • abdominal mass
  • biliary atresia
  • biliary trauma
  • congenital anomalies of the biliary tract
  • gallstones
  • drugs
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11
Q
  1. Cholestasis, cholelithiasis, jaundice:

PRIMARY BILIARY CIRRHOSIS PBS

A

= chronic progressive (+fatal) cholestatic autoimmune liver disease
AGE: middle-aged women, 40s-50s
MORPHOLOGY:
- destruction of intrahepatic bile ducts
- portal inflammation and scarring ⇒ cirrhosis + liver failure
PATHOGENESIS:
- high titer of antimitochondrial ABs AMA
- onset insidious ⇒ pruritus + jaundice
- hepatic decompensation with portal HT, variceal bleeding, hepatic encephalopathy
- elevated APP + cholesterol

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12
Q
  1. Cholestasis, cholelithiasis, jaundice:

PRIMARY SCLEROSING CHOLANGITIS PSC

A

MORPHOLOGY:
- progressive fibrosis + destruction of extra hepatic + large intrahepatic bile ducts
- segmental changes
- associated with IBD (UC)
PATHOGENESIS:
- linkage with certain HLA alleles
- ANCA ⇒ immunologically mediated disease
CLINICAL FETURES:
- progressive fatigue, pruritus, jaundice
- weight loss, ascites, variceal bleeding, encephalopathy
TREATMENT: transplant

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13
Q
  1. Cholestasis, cholelithiasis, jaundice:

CHOLELITHIASIS pathogenesis

A
  1. Cholesterol stones (80%):
    - cholesterol exceeds solubilizing capacity in bile⇒ cholesterol precipitates into cholesterol monohydrate crystals
    ⇒ supersaturation of bile with cholesterol
    ⇒ establishment of nucleation sites by calcium salts
    ⇒ stasis in gallbladder ⇒ precipitation
    ⇒ mucous hypersecretion to trap crystals
  2. Pigment stones (20%):
    - presence of unconjugated bilirubin ⇒ insoluble calcium bilirubinate salt
    - risk factors:
    ⇒ age (forty)
    ⇒ gender (female)
    ⇒ hereditary (familial)
    ⇒ obesity (fat)
    ⇒ environment
    ⇒ acquired disorders
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14
Q
  1. Cholestasis, cholelithiasis, jaundice:

CHOLELITHIASIS morphology

A
  1. Cholesterol stones:
    - in gallbladder
    - 50-100% cholesterol
    - pale yellow ⇒ grey-white
    - ovoid, firm
    - radiolucent 80%
  2. Pigment stones:
    - anywhere in biliary tree
    - black: gallbladder, small, large quantity, crumble easily, 50-75% radiopaque
    - brown: heptic ducts, big, small quantity, soft, greasy, radiolucent
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15
Q
  1. Cholestasis, cholelithiasis, jaundice:

CHOLELITHIASIS clinical features

A
  • asymptomatic
  • excruciating pain
  • empyema
  • perforation
  • fistulae
  • inflammation of biliary tree
  • obstructive cholestasis or pancreatitis
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16
Q
  1. Cholestasis, cholelithiasis, jaundice:

JAUNDICE definition

A

= yellow discoloration of skin, mucosa and sclera as a result of hyperbilirubinemia and deposition of bilirubin in tissues

  • common sign of liver disease
  • systemic retention of bilirubin ⇒ elevated serum levels
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17
Q
  1. Cholestasis, cholelithiasis, jaundice:

JAUNDICE pathogenesis + clinical features

A 
TYPES:
  - prehepatic (hemolytic anemia)
  - hepatic (liver disease)
  - posthepatic (gallstone, tumor)
MECHANISM:
  - excessive production of bilirubin
  - reduced hepatic uptake
  - impaired conjugation
  - decreased hepatocellular excretion
  - impaired bile flow
INBORN ERRORS CAUSING JAUNDICE:
  - Gilbert syndrome 
  - Criggler-Najjar
  - Dublin-Johnson syndrome
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18
Q
  1. Circulatory disorders of liver:

HEPATIC ARTERY INFLOW IMPAIREMENT

A
  • interruption does not always cause ischemia due to dual blood supply
  • hepatic artery thrombosis in transplanted liver ⇒ ischemia
  • thombosis / compression of intrahepatic branch of hepatic artery due to:
    • polyarteritis nodosa
    • embolism
    • neoplasia
    • sepsis
      ⇒ local parenchymal infarct
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19
Q
  1. Circulatory disorders of liver:

PORTAL VEIN OBSTRUCTION AND THROMBOSIS

A

SYMPTOMS:
- abdominal pain
- ascites
- portal HT
- congestion + bowel infarction
CAUSE OF EXTRAHEPATIC PORTAL VEIN OBSTRUCTION:
- peritoneal sepsis
- pancreatitis ⇒ splenic vein thrombosis
- thromobgenic diseases + post surgical thrombosis
- vascular invasion by cancer

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20
Q
  1. Circulatory disorders of liver:

HEPATOPORTAL SCLEROSIS

A
  • result of myeloproliferative disorder + hyper coagulability, peritonitis
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21
Q
  1. Circulatory disorders of liver:

IMPAIRED BLOOD FLOW THROUGH THE LIVER

A

CAUSES:
- cirrhosis
- sickle cell disease ⇒ sinusoids packed with sickled RBCs
- DIC
- RS-HF
MORPHOLOGY OF LIVER IN HF:
- RS-HF: enlarged, tense and cyanotic liver, congestion of centrilobular sinusoids ⇒ atrophies
- LS-HF: hepatic hypoperfusion ⇒ ischemic necrosis of hepatocytes
- combined: nutmeg liver

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22
Q
  1. Circulatory disorders of liver:

PELIOSIS HEPATIS

A
  • sinusoidal dilation when efflux of hepatic blood is obstructed
  • rare condition
  • associated with exposure to anabolic steroids + oral contraceptives
  • complication: intra-abdominal hemorrhage
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23
Q
  1. Circulatory disorders of liver:

BUDD-CHIARI SYNDROME

A 
= thrombosis of 2+ major hepatic veins
CAUSES:
  - myeloproliferative disease
  - pregnancy
  - postpartum state
  - oral contraceptives
  - paroxysmal nocturnal hemoglobinuria
  - intra-abdominal cancers
SYMPTOMS:
  - hepatomegaly
  - weight-gain
  - ascites
  - abdominal pain
MORPHOLOGY:
  - swollen, red-purple liver
  - tense capsule
  - congestion + necrosis
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24
Q
  1. Circulatory disorders of liver:

SINUSOIDAL OBSTRUCTION SYNDROME

A

PATHOGENESIS:

  • toxic injury to sinusoidal endothelium ⇒ damaged cells slough off ⇒ create emboli
  • damage accompanied by passage of RBCs into space of Disse, proliferation of stellate cells, fibrosis of hepatic vein
  • 20-30 days after bone marrow transplant
  • caused by: drugs, total body radiation
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59. Acute and chronic hepatitis: | ACUTE HEPATITIS etiology
- viral hepatitis - yellow fever - non-viral infection - alcohol - toxins - drugs - autoimmune diseases - metabolic diseases
26
59. Acute and chronic hepatitis: | HEPATITIS A
PATHOGENESIS: - virus invades hepatocytes ⇒ replicates ⇒ apoptosis - feco-oral transmission - short incubation (15-50d) - sporadic / endemic - clinically mild disease + full recovery - no carrier state or chronicity - vaccine available - diagnosis: anti HAV ABs
27
59. Acute and chronic hepatitis: | HEPATITIS B
PATHOGENESIS: - virus incorporate viral genome into host genome ⇒ replicate ⇒ produce viral antigens ⇒ immune response ⇒ apoptosis - transmission by blood and body fluids - long incubation (60-90d) - vaccine available CLINICAL COURSES: 1. acute hepatitis with recovery and clearance of virus 2. non-progressive chronic hepatitis 3. progressive hepatitis ending with cirrhosis 4. fulminant hepatitis with massive liver necrosis 5. asymptomatic carrier state
28
59. Acute and chronic hepatitis: | HEPATITIS C
PATHOGENESIS: - virus encorporate viral genome to host genome ⇒ replicate ⇒ produce antigens ⇒ immune response ⇒ apoptosis - transmission by blood - long incubation (7-8w) - asymptomatic - persistent infection - cirrhosis ⇒ liver cancer - no vaccine
29
59. Acute and chronic hepatitis: | HEPATITIS D
- replication of hepatitis D needs co-infection of hepatitis B - mild / fulminant - incubation: 60-90d - composed of Dane particle with HBV envelope - IgM anti HDV AB - hepatitis B vaccine
30
59. Acute and chronic hepatitis: | HEPATITIS E
- water borne endemic hepatitis - feco-oral transmission - incubation: 4-5w - mortalility in pregancy - self-limiting
31
59. Acute and chronic hepatitis: | CLINICAL FEATURES OF ACUTE HEPATITIS
``` PHASES: 1. incubation period 2. symptomatic preicteric period 3. symptomatic icteric period 4. covalescence SYMPTOMS: - malaise, fever, weight loss, nausea, headache, muscle + joint pain, vomiting, diarrhea, enlarged tender liver, jaundice ```
32
59. Acute and chronic hepatitis: | CHRONIC HEPATITIS general + pathogenesis
``` GENERAL: - inflammation of liver that lasts more than 6 months ⇒ inflammation + necrosis - may progress to cirrhosis CAUSES: - hepatitis virus - Wilson disease - alpha-1 antitrypsin deficiency - chronic alcoholism - drugs - autoimmunity ```
33
59. Acute and chronic hepatitis: | CHRONIC HEPATITIS morphology + clinical features
``` MORPHOLOGY: - periportal inflammation - periportal + bridging necrosis ⇒ fibrosis ⇒ macronodular cirrhosis CLINICAL FEATURES: - mild symptoms/ asymptomatic - spider angiomas - palmar erythema - hepatomegaly - hepatic tenderness ```
34
60. Alcohol- and drug-induced liver disease: | ALCOHOLIC LIVER DISEASE forms
1. Hepatic steatosis ⇒ large, soft, yellow greasy liver 2. Alcoholic hepatitis ⇒ hepatocytes swell, necrosis, Mallory bodies, neutrophilic infiltrate, fibrosis 3. Cirrhosis ⇒ nodular, yellow, fatty and enlarged liver
35
60. Alcohol- and drug-induced liver disease: | HEPATOCELLULAR STEATOSIS pathogenesis + clinical features
PATHOGENESIS: - shunting of normal substrates from catabolism ⇒ lipid biosynthesis due to excess NAD - impaired assembly + secretion of lipoproteins - increased peripheral catabolism of fat CLINICAL FEATURES: - hepatomegaly - elevated bilirubin + APP - tretment: alcohol withdrawal + good diet
36
60. Alcohol- and drug-induced liver disease: | ALCOHOLIC HEPATITIS pathogenesis + clincal features
PATHOGENESIS: - Acetalaldehyde: ⇒ lipid peroxidation, acetalaldehyde-protein adduct formation ⇒ disrupt cytoskeletal + membrane function - ROS: react with membranes + proteins - Cytokines: abnormal regulation, TNF!, from ROS + endotoxin of gut bacteria CLINICAL FEATURES: - 15-20yrs of excessive drinking - malaise, anorexia, weight loss, painful abdomen, tender hepatomegaly, fever - cirrhosis
37
60. Alcohol- and drug-induced liver disease: | CIRRHOSIS pathogenesis + clinical features
``` CLINICAL FEATURES: - increased portal HT ⇒ variceal hemorrhage + hepatic encephalopathy - malaise, weight loss, weakness, loss of appetite - ascites, jaundice, peripheral edema CAUSE OF DEATH: - hepatic failure - massive GI bleeding - infection - hepatorenal syndrome - hepatocellular carcinoma TREATMENT: abstinence from alcohol ```
38
60. Alcohol- and drug-induced liver disease: | REYE SYNDROME
- acute liver failure - no necrosis - small fat vacuoles in hepatocytes - fatty liver with minimal inflammation - no jaundice - cerebral edema - in children <10yrs - lethal young age + viral infection + aspirin ⇒ REYE
39
60. Alcohol- and drug-induced liver disease: | DRUG INDUCED LIVER DISEASE
- can be predictable reaction or unpredictable - immediate / weeks-months - mild reaction / acute liver failure PREDICTABLE AGENTS: - acentaminophen - tetracycline - antidepressants - mushroom toxin - alcohol UNPREDICTABLE AGENTS: - chlorpromazine - halothane - sulfonamides - direct toxicity + inflammation MORPHOLOGY: - necrosis in parts /whole - liver shrinks ⇒ red + wrinkled capsule - collapsed reticulin framework - scarring ⇒ macronocular cirrhosis CLINICAL FEATURES: - hepatocellular necrosis - cholestasis - steatosis - steatohepatitis - fibrosis + vascular lesions
40
61. Metabolic and inherited liver diseases: | METABOLIC LIVER DISEASE general
``` = non-alcoholic fatty liver disease NAFLD + NASH associated with: - insulin resistance - type 2 DM - obesity - dyslipidemia ```
41
61. Metabolic and inherited liver diseases: | METABOLIC LIVER DISEASE pathogenesis + clinical features
``` PATHOGENESIS: - insulin resistance ⇒ accumulation of TAG * impaired oxidation of FA * increased synthesis + take of FA * decreased hepatic secretion of VLDL - release of TNF, IL-6, MCP-1 ⇒ liver damage - fat-laden hepatocytes sensitive to peroxidation products ⇒ apoptosis CLINICAL FEATURES: - asymptomatic - fatigue, malaise, RUQ pain - diagnosis: liver biopsy TREATMENT: - obesity reduction - improve insulin resistance ```
42
61. Metabolic and inherited liver diseases: | HEMOCHROMATOSIS general + pathogenesis
GENERAL: - genetic disorder ⇒ accumulation of iron in tissues - predominantly males (7:1) - primary: AR disease- mutation in HFE gene - secondary: transfusions, ineffective hematopoiesis + increased iron intake PATHOGENESIS: - missense mutation in HFE gene ⇒ less hepcidin ⇒ more uptake of iron⇒ deposition in parenchymal organs - iron toxic to tissues: ⇒ lipid peroxidation by iron catalyses ROS ⇒ stimulation of collagen formation ⇒ direct interaction of iron with DNA
43
61. Metabolic and inherited liver diseases: | HEMOCHROMATOSIS clinical features
- age: 50yrs - hepatomegaly - abdominal pain - grey skin pigmentation - DM by destruction of pancreatic islets - cardiac dysfunction ⇒ cirrhosis, hepatocellular carcinoma, cardiac disease TREATMENT: phlebotomy
44
61. Metabolic and inherited liver diseases: | WILSON DISEASE
- AR disease of copper metabolism⇒ accumulation of copper in liver, eye, brain PATHOGENESIS: - mutation in ATP7B gene on chr. 13 ⇒ ATPase metal ion transporter in Golgi - absorbed copper fails to enter circulation in form of ceruloplasmin ⇒ accumulates in liver ⇒ promotes formation of free radicals ⇒ binding to cellular proteins ⇒ displace other metals in hepatic metalloenzymes CLINICAL FEATURES: - hemolysis - changes in brain, cornea, kidneys, bones, joints, parathyroid glands - acute and chronic hepatic failure⇒ fatty changes, hepatitis, cirrhosis - neuropsychiatric manifestations - Kayser-Fleischer rings
45
61. Metabolic and inherited liver diseases: | ALPHA 1 ANTITRYPSIN DEFICIENCY
- AR disorder ⇒ abnormally low serum level of AAT PATHOGENESIS: - function of AAT is to inhibit proteases (neutrophil elastase) - AAT synthesized by two Z-alleles contains a single AA substitution ⇒ misfolded⇒ cannot be secreted ⇒ accumulation in ER ⇒ excessive lysosomal degradation CLINICAL FEATURE: - newborns with deficiency⇒ 10-20% cholestasis - in older persons ⇒ related to chronic hepatitis, cirrhosis, pulmonary disease - leads to pulmonary emphysema TREATMENT: liver transplant
46
61. Metabolic and inherited liver diseases: | NEONATAL CHOLESTASIS
= persisting conjugated hyperbilirubinemia in newborns - due to impaired bile excretion or impaired bile flow CLINICAL FEATURES: - abdominal pain - palpable liver + enlarged spleen - dilated bile duct system, bile duct proliferation in response to back pressure
47
61. Metabolic and inherited liver diseases: | REYE SYNDROME stages
STAGE 1. Rash on palms on hands + feet. Heavy vomiting, generalized lethargy, confusion, nightmares, headaches STAGE 2. Stupor, hyperventilation, fatty liver, hyperactive reflexes STAGE 3. Possible coma, cerebral edema, respiratory arrest STAGE 4. Deepening coma, dilated pupils, no light response, liver dysfunction STAGE 5. deep coma, seizures, MOF, flaccidity, hyperammonemia, death
48
62. Liver cirrhosis: | CIRRHOSIS definition + etiology
``` = diffuse process characterized by fibrosis and conversion of normal liver architecture into abnormal nodules ETIOLOGY: - chronic hepatitis - toxic damage (alcohol) - NASH - cholestatic disorders - metabolic diseases - cryptogenic ```
49
62. Liver cirrhosis: | CIRRHOSIS pathogenesis
MECHANISM: - hepatocellular death - regeneration - progressive fibrosis - vascular changes - cell death ⇒ fibrosis - loss of sinusoidal endothelial cell fenestrations ⇒ vascular shunts - collagen deposits converts sinusoids to high-pressure, fast-flow vascular channels without free solute exchange
50
62. Liver cirrhosis: | CIRRHOSIS morphology
- bridging fibrous septa - parenchymal nodules - disruption of architecture of entire liver - Diffuse finely nodular (classic Laennec type with atrophy) ⇒ post-hepatitis virus cirrhosis - Diffuse medium-sized nodular. dark purple (classic Hanot type with hypertrophy) ⇒ chronic congestion * green liver ⇒ primary biliary cirrhosis, chronic sclerosing cholangitis * grey-brown ⇒ hemochromatosis, Wilson disease - Diffuse irregularly nodular⇒ autoimmune hepatitis, cirrhosis - Irregular medium- and large-sized nodular ⇒ secondary biliary cirrhosis
51
62. Liver cirrhosis: | CIRRHOSIS clinical features
- clinically silent - anorexia, weight loss, weakness - progression to hepatic failure - leads to death: * progressive HF * complication related to HT * development of hepatocellular carcinoma
52
63. Tumors and tumor-like lesions of liver: | HEPATOCELLULAR NODULES focal nodular hyperplasia
- solitary or multiple benign nodules - localized, well-demarcated but poorly encapsulated lesion - hyperplastic hepatocyte nodules with central fibrous scar - in non-cirrhotic livers - not precursor of malignancy
53
63. Tumors and tumor-like lesions of liver: | HEPATOCELLULAR NODULES macroregenerative nodules
- solitary or multiple benign nodules - in cirrhotic livers - larger than surrounding cirrhotic nodules - contain more than 1 portal tract + intact reticulin framework - not precursor of malignancy
54
63. Tumors and tumor-like lesions of liver: | HEPATOCELLULAR NODULES dysplastic nodules
- solitary or multiple benign nodules - larger than 1mm - in cirrhotic liver - hepatocytes highly proliferative + crowding + polymorphism - precursors of hepatocellular cancer
55
63. Tumors and tumor-like lesions of liver: | HEPATIC CARVERNOUS HEMANGIOMAS
- benign - well circumscribed lesions of endothelial cell-lined vasculature + intervening stroma - red-blue, soft nodules, <2cm - often directly beneath capsule COMPLICATIONS: - compression - rupture - coagulation ⇒ consumptive coagulopathy
56
63. Tumors and tumor-like lesions of liver: | HEPATIC ADENOMA
- benign - women in child-bearing age + used oral contraceptive MORPHOLOGY: - pale, yellow, well-demarcated nodules - often beneath the capsule - may reach 30cm - composed of sheets and cords ⇒ resemble normal hepatocytes CLINICAL FEATURES: - DD: hepatocellular carcinoma - risk of rupture⇒ intra-abdominal hemorrhage - might carry beta-catenin mutation
57
63. Tumors and tumor-like lesions of liver: | HEPATOCELLULAR CARCINOMA pathogenesis
ETIOLOGY: - HBV or HCV infection - aflatoxin exposure - chronic alcoholism / cirrhosis - tyrosinemia - hemochromatosis - small-cell, high-grade dysplastic nodules in cirrhotic liver - cell origin: mature hepatocyte + progenitor cell - presence of structural and numeric chromosomal abnormalities
58
63. Tumors and tumor-like lesions of liver: | HEPATOCELLULAR CARCINOMA morphology + clinical features
``` MORPHOLOGY: - irregular, soft yellowish-green nodules - trabecular and acinar pattern + well-differentiated or poorly differentiated fibrolamellar tumor CLINCAL FEATURES: - silent hepatomegaly - rapid increase in liver size - ascites - fever - pain DEATH DUE TO: ⇒ profound cachexia ⇒ variceal bleeding ⇒ liver failure with hepatic coma ⇒ rupture of tumor with fatal hemorrhage ```
59
63. Tumors and tumor-like lesions of liver: | OTHER MALIGNANT TUMORS
1. Cholangiocellular carcinoma | 2. Hepatoblastoma
60
64. Inflammation and tumors of the biliary tract and gallbladder: ACUTE CHOLECYSTITIS
= acute inflammation of gallbladder that contains stones ⇒ acute calculous cholecystitis PATHOGENESIS: - result of chemical irritation + inflammation of gallbladder wall in setting of obstruction to bile flow - phospholipases ⇒ hydrolysis of lecithin to lysolechitin ⇒ toxic to mucosa MORPHOLOGY: - edematous thickening of wall - neutrophilic infiltration - hemorrhage CLINICAL FEATURES: - fever, nausea, leukocytosis, prostration - conjugated hyperbilirubinemia
61
64. Inflammation and tumors of the biliary tract and gallbladder: ACUTE NON-CALCULOUS CHOLECYSTITIS
- associated with infections in autoimmune vasculitis or secondary to trauma - mostly in seriously ill-patients * post-operative state * severe trauma * severe burn * sepsis
62
64. Inflammation and tumors of the biliary tract and gallbladder: CHRONIC CHOLECYSTITIS
PATHOGENESIS: - associated with gallstones - supersaturation of bile predisposed to cholecystitis + stone formation MORPHOLOGY: - mucosal atrophy, fibrous thickening of gallbladder wall - hypertrophy + hyperplasia of deeper glands - adhesions to nearby organs CLINICAL FEATURES: - recurrent attacks of pain in RUQ COMPLICATIONS: - bacterial superinfection with cholangitis or sepsis - gallbladder perforation + local abscess formation - gallbladder rupture + peritonitis - biliary enteric fistula
63
64. Inflammation and tumors of the biliary tract and gallbladder: CHOLANGITIS
= inflammation of wall of bile ducts - caused by bacterial infection - results from any lesion obstructing bile flow + choledocholelithiasis - Ascending cholangitis ⇒ ascends to intrahepatic biliary ducts - Bacterial cholangitis ⇒ fever, chills, abdominal pain, jaundice - Suppurative cholangitis ⇒ purulent bile fills ⇒ liver abscess
64
64. Inflammation and tumors of the biliary tract and gallbladder: CARCINOMA OF THE GALLBLADDER
- develops from epithelial lining of organ - more common in women, age:70s TYPES: - flat, scirrhous and infiltrative form - polyploid-fungating form - prognosis: 5yrs ⇒ <5% - gallstones in 60-90% - metastasis: regional LN, GI tract organs CLINICAL FEATURES: - abdominal pain - jaundice - anorexia - nausea + vomiting
65
64. Inflammation and tumors of the biliary tract and gallbladder: CHOLEANGIOCARCINOMA
``` = adenocarcinoma with biliary differentiation arising from cholangiocytes in ducts + outside - occur at age: 60-70 - poor prognosis RISK FACTORS: - primary sclerosing cholangitis - fibrocystic disease - Klatskin tumor= extrahepatic choleangiocarcinoma developing at hilum + distally in biliary tree CLINICAL FEATURES: - chronic cholestasis - inflammation ```
66
65. Pancreatitis: | ACUTE PANCREATITIS causes
- alcoholism - bile stone - trauma - hypercalcemia - hyperlipoproteinemia - vater-papilla obstruction - infections - iatrogenic (ERCP)
67
65. Pancreatitis: | ACUTE PANCREATITIS pathogenesis
- autodigestion by inappropriately activated pancreatic enzymes IMPORTANT FACTORS: 1. increased pressure in pancreatic duct 2. duodeno-pancreatic reflux 3. bilio-pancreatic reflux 4. epithel-damage due to biliary acid salts 5. trypsin-activation PATHWAYS: 1. Pancreatic duct obstruction - obstruction ⇒ accumulation of enzyme rich interstitial fluid ⇒ lipase ⇒ fat necrosis ⇒ inflammatory cytokines ⇒ inflammation ⇒ edema ⇒ compromises blood flow ⇒ ischemia 2. Primary acinar injury: - ischemia, viruses, drugs, trauma 3. Defective intracellular transport of proenzymes within acinar cells: - digestive proenzymes + lysosomal enzymes packed together ⇒ proenzyme activation, lysosomal rupture, local release
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65. Pancreatitis: | ACUTE PANCREATITIS clinical features
- abdominal pain - increased vascular permeability - leukocytosis - DIC - ARDS - diffuse fat necrosis - shock due to peripheral vascular collapse
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65. Pancreatitis: | ACUTE PANCREATITIS complications
- infections - shock - sterile pancreatic abscesses or pancreatic pseudocyst - Local: abscess, ascites, fistula, apoplexy ⇒ retroperitoneal hemorrhage, digestion of surrounding organs - Systemic: paralytic ileus, peritoneal shock, peritonitis, acute RF, DIC, ARDS, DM
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65. Pancreatitis: | CHRONIC PANCREATITIS etiology
= longstanding inflammation + fibrosis + destruction of exocrine pancreas ETIOLOGY: - long term alcohol abuse - pancreatic duct obstruction - chronic pancreatitis associated with CF - hereditary pancreatitis (PPSS1/SPINK1 mutation)
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65. Pancreatitis: | CHRONIC PANCREATITIS pathogenesis
1. Ductal obstruction: - inciting agents increase protein concentration of pancreatic secretions ⇒ ductal plug 2. Toxic-metabolic: - direct toxic effect on acinar cells ⇒ lipid accumulation, acinar cell loss, parenchymal fibrosis 3. Oxidative stress: - generates free radicals ⇒ membrane lipid peroxidation + subsequent chemokines expression 4. Necrosis fibrosis: - acute pancreatitis ⇒ local perilobular fibrosis, duct distortion + altered pancreatic secretion ⇒ loss of parenchyma + fibrosis
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65. Pancreatitis: | CHRONIC PANCREATITIS morphology + clinical features
``` MORPHOLOGY: - parenchymal fibrosis - decreased number + size of acini - variable dilation of ducts - ductal epithelium atrophied, hyperplastic, squamous metaplasia - ductal concentration - islets of Langerhans spare ⇒ fuse ⇒ disappear - pancreas is hard, calcified CLINICAL FEATURES: - jaundice - digestion problems - recurrent abdominal + back pain - silent ⇒ DM develops ```
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66. Diabetes Mellitus: | GENERAL
= metabolic disease characterized by hyperglycemia CLASSIFICATION: 1. TYPE 1DM - absolute deficiency of insulin secretion - pancreatic B-cell destruction 2. TYPE 2DM - peripheral resistance to insulin + inadequate compensatory response of insulin secretion COMPLICATIONS: - Acute: hyper- and hypoglycemic shock, acidosis - Chronic: secondary damage in multiple organ systems ⇒ risk for CAD + cerebrovascular diseases
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66. Diabetes Mellitus: | PATHOGENESIS OF T1DM
- autoimmune disease ⇒ T cells react against unknown beta-cell antigen in islets ⇒ hyperglycemia + ketosis - locally produced cytokines damage B-cells which are produced during immune reaction - autoantibodies against a variety of B-cell antigens, including insulin - genetic susceptibility + environmental factors - develops in childhood
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66. Diabetes Mellitus: | PATHOGENESIS OF T2DM
- environmental factors ⇒ life style, dietary habits - Insulin resistance: 1. genetic defect of insulin receptor 2. Obesity + insulin resistance - B-cell dysfunction ⇒ inadequate insulin secretion
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66. Diabetes Mellitus: | COMPLICATIONS OF DM
- atherosclerosis - microangiopathy - renal involvement * AS * inflammation * Kimmelstiel-Wilson syndrome - diabetic foot - pyoderma - candidasis
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66. Diabetes Mellitus: | PATHOGENESIS OF COMPLICATIONS RELATED TO DM
1. Non-enzymatic glycosylation: - glucose attaches to free amino groups on proteins without enzyme - degree directly related to blood glucose concentration - early glycosylation products of collagen + proteins ⇒ advanced glycosylation end product ⇒ accumulates in vessel wall - AGE on proteins ⇒ cross-linkage between polypeptides ⇒ trap non-glycosylated plasma and interstitial proteins ⇒ LDL leads to AS/ albumin leads to diabetic glomerulopathy - circulation plasma proteins ⇒ addition of AGE residues ⇒ bind AGE receptors 2. Activation of protein kinase C: - hyperglycemia ⇒ chronic PKC activation ⇒ vascular changes ⇒ AS/cardiomyopathy/ retinopathy/ nephropathy/ neuropathy 3. Intracellular hyperglycemia: - increased production of ROS
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67. Tumors of the exocrine and endocrine pancreas: | SEROUS CYSTADENOMA
- composed of glycogen-rich cuboidal cells surrounding small cysts containing clear fluid - present in 7th decade - abdominal pain - benign - surgical resection
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67. Tumors of the exocrine and endocrine pancreas: | MUCINOUS CYSTIC NEOPLASM
- arise in women, in body/tail of pancreas - painless, slow-growing mass - cystic spaces filled with thick tenacious mucin + lined by columnar mucinous epithelium - beign/ borderline/ malignant
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67. Tumors of the exocrine and endocrine pancreas: | INTRADUCTAL PAPILLARY MUCINOUS NEOPLASM
- benign/ borderline/ malignant - arise mostly in men - head of pancreas - lack of cellular stroma - structure similar to mucinous cystic neoplasm
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67. Tumors of the exocrine and endocrine pancreas: | PANCREATIC CARCINOMA
PATHOGENESIS: - progressive accumulation of genetic changes in pancreatic epithelium ⇒ non-neoplastic noninvasive lesion ⇒ invasive carcinoma - desmoplastic reaction - mutations: KRAS, p16, SMAD4, p53 - develops from ductal epithelial cells - prognosis 5yrs ⇒ <5% MORPHOLOGY: - mostly in head of pancreas - poorly demarcated, white scarred/ nodular area COMPLICATION: - migratory thrombophlebitis - obstruction of common bile duct METASTASIS: - peritoneum, duodenum, stomach, liver, colon, spleen - regional LN, liver, lungs, bone marrow
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67. Tumors of the exocrine and endocrine pancreas: | SOLID PSEUDOPAPILLARY TUMOR
- in women, 20-40 yrs - large, encapsulated, mix of cystic solid or hemorrhagic components - low malignant potential - metastasis: liver - surgical resection⇒ good prognosis
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67. Tumors of the exocrine and endocrine pancreas: | INSULINOMA
``` - Beta cell ⇒ hypoglycemia - CNS: confusion, stupor, attacks when fasting LABORATORY FINDINGS: - increased insulin - increased insulin:glucagon ratio ```
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67. Tumors of the exocrine and endocrine pancreas: | GASTRINOMA
- increased gastrin - location: duodenum, pancreas or around - Zollinger-Ellison syndrome - invasive - sporadic + single - multiple + MEN 1 syndrome
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67. Tumors of the exocrine and endocrine pancreas: | GLUCAGONOMAS
- increased glucagon - mild DM - necrolytic migratory erythema - anemia
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67. Tumors of the exocrine and endocrine pancreas: | TUMORS OF ENDOCRINE PANCREAS
- MEN 1 syndrome - benign: insulinoma, PPcell tumor - malignant: glucagonoma, gastrinoma, somatostatinoma, VIPoma

PATHOLOGY 2 (11 decks)

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