Class: Liver path Flashcards

(135 cards)

1
Q

Portal triad is made up of?

A

bile duct, Portal vein, hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How are lobular and acinar liver units different by what is at their center?

A

lobular: Portal vein at center
acinus: Central vein at center

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

acinus/lobule which is structural which is functional

A
lobule = structure
acinus = functional
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

In a liver bx, what ix poorest px:

  1. focal necrosis
  2. fatty degeneration
  3. lymphocytic infiltration
  4. Bridging fibrosis
  5. Single cell necrosis
A

bridging fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the mildest form of injury in the liver?

A

Hydropic degeneration or swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

WHat organelles does Hydropic degeneration affect and what is the pathogenesis of injury?

A

lack of adequate energy supply (ATP) inhibits the activity of the ATP-pump that maintains water homeostasis across the cell membrane . This leads to intracellular water retention (swelling).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The next step in hepatocellular injury after hydropic degeneration is due to a further inability to do what? and results in an increased level of one thing and a decrease in another?

A

inability to produce ATP–>
increased Triglycerides
decreased lipoprotein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

WHt is the result of fatty degeneration (aka fatty metamorphosis) is a progression from one pathilogical state to another. Nme those 2 states

A
retained lipids (from lack of lipoprotein synth) are packaged into vesicals:
early = microvesicular steatosis
later/chronic = macrovesicular steatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are 3 etiologies of microvesicular steatosis

A

Reye’s syndrome (inborn error of ASA mtb)
Pregnancy
tetracycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are 3 etiologies of macrovesicular steatosis?

A

Alcohol
Diabets
Obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which can be life threatening via hepatic failure, micro- or macrovesicular steatosis?

A

micro

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHat is the pathogenesis of steatohepatitis

A

in macrovesicular steatosis, some cells rupture and die –> inflammatory reaction = steatohepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 4 types of hepatocellular necrosis and the progession from mild to severe

A
  1. single cell necrosis
  2. Focal necrosis
  3. zonal necrosis (zones 1-3)
  4. diffuse necrosis (submassive and massive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what zone of the acinus is the first to be affected by ischemia?

A

zone 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what zone of the acinus is the first to be affected by viral hepatitis and ingested toxins

A

ZOne 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what zone of the acinus is the first to be affected by Yellow fever

A

Zone II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

healing by secondary intention (scar formation) occurs in the case of what two types of injury to the liver?

A

Extensive acute necrosis as well as chronic (repetitive) injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

healing by secondary intention (scar formation) involves activation of what cell types?

A

stellate cell, kupfer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

in cirrhosis: Fibrosis is mediated by what cytokine/cell

A

Transforming Growth Factor-beta (TGF-β) acting on stellate cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the morphological hallmark of end-stage liver disease/cirrhosis.

A

bridging fibrosis and nodular regeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is chronic hepatits defined? as evidenced by elevated what?

A

necroinflammatory dz of liver lasting >6 months

as evidenced by high ALT (and others)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

two ddx of cirrhotic liver? and what are they in terms of fibrosis and nodules?

A

chronic hepatic fibrosis (fibrosis wothout nodules)

partial nodular transformation (nodules without fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What antigen is used to dx HBV?

A

HBVsAg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Presence of what 2 markers in blood indicate that you are infectious with HBV?

A

HBeAg (need an envelope to infect)

HBV DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Is HAV acute, chronic, or both
only acute illness- full recovery always occurs
26
What antibody marks active infx of HAV
Anti-virus IgM (non-specific response)
27
What antibody marks protection agaisnt or immunization against HAV
Anti-virus IgG
28
What Hepatitis Viruses are there vaccines fro?
HAV, HBV
29
HEV infection in pregant women is assc with what?
Extremely dangerous- fulminant hepatitis: liver failure with massive liver necrosis
30
WHat marker is used to determine infx/recovery/chronic form of HCV? (only one marker)
HCV-RNA: if present = infx if declining = recovery if persistent = chronic
31
If you don't have this marker, then you have the chronic form of HBV? *******
Absent IgG Anti-HBsAB
32
********recovery from HBV is indicated by what?
negaqtive for HBsAg
33
What are the 3 progressions from Chronic hepatitis with HBV
Recovery: negative HBsAg Healthy carrier state: +HBsAg, -HBeAg Cirrhosis: (might lead to hepatocellular CA
34
IgG anti-HCV and IgM anti-HCV indicate what?
only past infx - not protective
35
WHat indicates Chronic disease in HCV
HCV RNA
36
HDV can only infect with what help?
Needs HBV surface antigen for it's viral coat
37
What is more severe: HDV co-infection with HBV or superinfection upon existing HBV
superinfection upon existing HBV
38
What does each represent in terms of infx: IgG anti-delta virus IgM anti-delta virus
IgG anti-delta virus = chronic superinfx | IgM anti-delta virus = recent infx of either kind
39
What are the 2 mechanisms of drug toxicity? and how is injury mediated in each?
``` direct = toxic metabolite of drug causes injury indirect = toxic metabolite acts as an antigen and the immune response invokes injury ```
40
bile duct obstruction (cholestasis) leads to high levels of what? (2)
ALP, gamma-glutamyl transpeptidase
41
what disease state is a mallory body chc of?***********
Alchoholic hepatitis
42
What is a mallory body?
damaged cytokeratin filaments in heptocytes
43
What are the liver enzyme derangments seen in Alchoholic hepatitis? why this?
AST > ALT AST is in mitochondria and EtOH is toxic to mitochindria
44
What is EtOH metabolized into (3)
Acetic acid plus NADH, H+
45
EtOH metabolism results in what 3 changes
``` hypoglycemia (via GNG prevention) Triglyceride syntyhesis (fatty liver) lactic acidosis ```
46
What are the 3 patterns of liver damage in Alcohol-related liver disease
1. Fatty liver disease 2. Alcoholic hepatitis 3. Cirrhosis
47
Is fatty liver reversible?
yes
48
What mediates the damage in alcoholic hepatitis?
Acetaldehyde
49
What are 4 histological changes chc of alcoholic hepatitis
1. Mallory bodies******** 2. swelling of hepatocytes 3. necrosis 4. acute inflammation (neutrophils)
50
How does alcoholic hepatitis present (2)
1. painful hepatomegaly | 2. AST > ALT
51
what type of change is seen in Fatty liver (aka hepatic steatosis): macro- or microvesicular
macrovesicualr
52
What causes primary hemochromatosis? (gene, chromo, and AA replacement)
HFE gene, chromo 6, C282Y = cysteine replaced by Tyrosine at AA 282
53
What causes secondary hemochromatosis (in what circumstance)
multiple transfusions - as in Beta-thallasemia major
54
What mediates tissue damage in Hemochromatosis
Iron generates free radical via Fenton reaction
55
What stain distinguishes Fe from lipofuscin (and color of Fe)
Prussian Blue stain = Fe is blue
56
what genetic defect (gene and affected function) causes Wilson disease?
recessive mutation in (ATP7B gene) ATP-mediated hepatocyte copper transport
57
What is the pathogenesis of Wilson's disease
lack of excretion of Cu into bile--> buildup in liver, brain, cornea. Cu --> free radical generation and dmg
58
How does Wilson's disease present: age
as a kid or at least < 40
59
How does Wilson's disease present: 3 system/organ manifestations
1. Cirrhosis 2. Neurological manifestations (behavior, dementia, chorea) 3. Kayser-Fleisher rings in cornea
60
4 sequelae of portal HTN seen in cirrhosis
1. Ascites 2. Congestive splenomegaly 3. poto-systemic shunts (varices, caput medusae, etc) 4. hepatorenal syndrome (renal failure)
61
What changes are seen in the hand in cirrhosis (2)
asterixis (tremor when extended) | palmar erythema
62
What causes the coma seen in cirrhosis
buildup of NH3 (liver normally mtbolozes it- it is toxic to brain)
63
decreased protein synthesis in cirrhosis --> what 2 things
1. hypoalbuminemia --> edema | 2. Coagulopathy (lack of vitamin K and others)
64
Which: PT or PTT is followed in cirrhosis
like warfarin - PT (even though lack of vitamin K knocks out 2, 7, 9, 10
65
What cuases non-alcoholic fatty liver?
metabolic syndrome (insulin resistnace)/obesity --> necrosis of hepatocytes
66
What are the liver enzyme levels in non-alcoholic fatty liver?
ALT > AST
67
what is the earliest sign of jaundice
scleral icterus
68
Where does UCB come from
1. RBCs are consumed by reticuloendothelial macrophages 2. Hb is broken down into Heme and globin 3. Heme is broken down into Fe and protoporphyrin 4. protoporphyrin in converted into UCB
69
What enzyme conjugates UCB into CB
uridine glucuronyl transferase
70
Where does urobilinogen come from
intestinal bacteria convert CB into urobilinogen
71
What causes jaundice
increased bilirubin
72
what causes conjugated hyperbilirubinermia (1)
biliary tract obstruction
73
What is increased in Dubin-Johnson and Rotor syndromes?
Conjugated bilirubin (in blood)
74
What cuases both Dubin-Johnson and Rotor syndromes?
defective transport of bilirubin to the cannaliculi (thus the bile) causing CB to build up in blood
75
What is the difference between Dubin-Johnson and Rotor syndromes?
Dubin JOhnson has a super dark liver that has no clinical significance
76
What is elevated in Crigler-Najjar and Gilbert syndromes?
both show elevated UCB
77
What is the mechanism in Crigler-Najjar and Gilbert syndromes? (one is slightly different than the other)
Crigler-Najjar: absent uridine glucuronyl transferase Gilbert syndrome: low uridine glucuronyl transferase activity
78
How do Crigler-Najjar and Gilbert syndromes present
Crigler-Najjar: kernicterus and death | Gilbert syndromes: jaundice with infx/stress, otherwise not significant
79
What is kernicterus
UCB deposition in the brain, particularly the basal ganglia--> neurological deficits and death
80
What is tx for kernicterus in newborn?
Treatment is phototherapy
81
What is the MOA of phototherapy in kernicterus tx of newborn************?
it does not conjugate bilirubin it makes UCB water soluble, allowing it to be excreted in urine
82
What is pathology of Primary biliary cirrhosis
autoimmune granulomatous destruction of bile ducts in liver
83
********what serum marker is present in Primary biliary cirrhosis
Anti-mitochondrial Ab
84
How does Primary biliary cirrhosis?
with features of obstructive jaundice
85
Primary sclerosing cholangitis: what is it
onion-skin fibrosis of both intra- and extra-hepatic bile ducts
86
What is the classic appearance of Primary sclerosing cholangitis on contrast imaging?
beaded appearance with alternating strictures and dilations of bile ducts
87
********What are 2 associations of Primary sclerosing cholangitis?
ulcerative colitis | p-ANCA +
88
what are the 2 pathological events in Reye's syndrome
Fulminant liver failure and encephalopathy
89
though etiology is unclear for Reye's, what is ti likely related to?
mitochondrial damage of hepatocytes
90
How does Reyes present? (type of liver change- micro/macro)
microvascualr change (the severe kind)
91
What is hepatic adenoma associated with?
Oral contraceptive use
92
What is a possible coomplication of hepatic adenoma
tumor may rupture --> intraperitoneal bleeding
93
What 2 viruses are risk factors for hepatocellular CA
HBV, HCV
94
what are 3 risk factors for hepatocellular CA*******
1. chronic hepatitis 2. cirrhosis 3. aflatoxins from aspergillus**********
95
How do aflatoxins from aspergillus cause hepatocellular CA
they induce p53 mutations
96
what is the serum marke for hepatocellular CA
AFP
97
what can hepatocellular CA lead to
Budd-Chiari syndrome
98
What is Budd-Chiari syndrome
liver infarction dt hepatic vein obstruction
99
How does Budd-Chiari syndrome preswet (2)
ascites, painful heptomegaly
100
what is the pathology in acute pancreatitis
autodigestion of the pancreas by it's own enzymes
101
****What is the first enzyme activated in acute pancreatitis?
trypsin--> activation fo the others
102
what are the 2 types of necrosis that result from acute pancreatitis
``` liquefactive hemorrhagic necrosis (of pancreas) fat necrosis (of peripancreatic fat) ```
103
2 MC causes of acute pancreatitis?
alcohol and gallstones
104
Clinical presentatin of acute pancreatitis (2)
epigastric pain radiating to back, elevated serum lipase (and amylase- though this comes from mouth too)
105
4 complications from acute pancreatitis
1. Pseudocyst formation 2. pancreatic abscess 3. Shock 4. DIC/ARDS
106
what are 3 cuases of chronic pancreatitis
1. recurring acute pancreatitis 2. alcohol 3. Cystic fibrosis
107
Chronic pancreatitis also shows epigastric pain radiating to back (like acute). What is different about it's CP? (2)
1. lipase and amylase are not elevated (bc most of pancreas has been destroyed) 2. calcification is seen on imaging ("chain of lakes" pattern)
108
Chronic pancreatitis may lead to what 2 conditions
secondary diabetes mellitus | pancreatic carcinoma
109
what tumor marker is seen in pancreatic carcinoma
CA 19-9
110
What part of the pancreas gives rise to pancreatic CA
ducts
111
2 major risk factors for pancreatic CA
smoking and chronic pancreatitis
112
CP of pancreatic CA (4)
pain radiating to back weightloss (malabsorption) Trousseau syndrome Obstructive jaundice
113
What is Trousseau syndrome -
redness and tenderness on palpation of extremeties
114
What are the 2 signs of obstructive jaundice (besides the obvious yellowing)
pale stools | palpable gallbladder
115
WHat is surigical procedure called that treats Pancreatic CA
Whipple procedure
116
3 cuases of cholelithiasis (gall stones)****
1. increased cholesterol or bilirubin 2. decreased bile acids (aka salts)***** 3. stasis (of glalbladder)
117
2 types of gall stones and their color (which is MC)
MC = cholesterol - yellow | bilirubin (aka pigment stones) = black
118
Which type of stone is radiolucent? opaque
``` cholesterol = radiolucent bilirubin = opaque ```
119
4 risk factors for gall stones
Female Forty Fat Fertile (pregnant)
120
Why does being pregant/Fertile increase chance of gall stones? and MOA
1. estrogen --> increased activity of HMG CoA reductase --> increased cholesterol synthesis
121
How does Crohn's disease increase risk of gall stones
damage to terminal ileum --> decreased uptake of bile salts/acids
122
What is a major risk factor for increased bilirubin stones
chronic extravascular hemolysis
123
What is biliary colic
waxing and waning RUQ pain
124
What is the etiology of biliary colic
gall bladder is contracting agaisnt a stone lodged in cystic duct
125
What is acute choilecystitis
inflammation of the gall bladder wall usually from stone at neck of GB
126
what causes acute cholecystitis
usually dt stone at neck of GB
127
How does acute cholecystitis present? (2)
with RUQ pain that raditates to scapula | increased ALP
128
What is pathogenesis of gallstones causing a ileocecal valve obstruction (aka gallstone ileus)?
a fistula occurs between the GB and the GI tract which allows gallstones to travel into the intestines and lodge in the ileocecal valve
129
What causes chronic cholecystitis
chemical irritation of GB dt longstanding cholelithiasis
130
what is the chc histo finding in chronic cholecystitis*****
rokitansky-aschoff sinus: herniation of GB mucosa into the muscular wall
131
What is a chc late complication of chronic cholecystitis?
porcelain gallbladder
132
What is tx for porcelain gallbladder and why
cholecystectomy - dt high rate of carcinoma progression
133
What is the cause of ascending cholangitis
bacterial infx of bile ducts dt stone obstruction (stops normally clearing flow of bile which allows bact to grow)
134
What is the major risk factor for GB carcinoma
stones (especially with porcelain GB)
135
What cell does GB CA arise from and what type of cancer is it
adenocarcinoma arising form glandular epithelium that lines the GB wall