Path of Liver, Gall Bladder, and Pancreas Flashcards
(111 cards)
1
Q
list four physiological functions of the liver
A
- metabolic hemostasis
- ->processes AA, carbs, lipids, vitamins - synthesize serum proteins
- detoxification of xenobiotics/waste
- regenerative functions
2
Q
why can the liver mask underlying pathologies early on?
A
has an enormous functional reserve
huge regenerative capacity
3
Q
what is the blood supply of the liver
A
portal vein
hepatic artery
4
Q
weight of the liver
A
1400-1600 grams
5
Q
how does the liver respond to injury (5)? what cell is involved?
A
hepatocytes!
- degeneration (accumulate toxic products)
- necrosis (cell death)
- inflammation (affect healing)
- regeneration (functional return)
- fibrosis (loss of functional tissue)
6
Q
what is JAUNDICE?
A
excess bilirubin
>2.0 mg/dl
7
Q
how does JAUNDICE develop?
A
- overproduction of bilirubin
- reduced hepatocyte uptake of bilirubin
- obstruction of bile flow
8
Q
1 cause of Jaundice
A
hemolytic anemia
9
Q
jaundice present clincially as
A
yellow skin (jaundice) and yellow sclera (icterus)
10
Q
two functions of hepatic bile
A
- emulsify fats
2. eliminate excess bilirubin, cholesterol, xenobiotics
11
Q
etiology of hepatitis
A
hepatotrophic virus
autoimmune
drug
toxic agents
12
Q
systemic viruses involving the liver
A
Epstein Barr Virus Cytomegalovirus yellow fever rubella herpesviruses
13
Q
hepatitis definition
A
hepatocyte injury w/ association of inflammation
chronic–>see scarring
14
Q
route of transmission for Hep A
A
fecal oral route
ingesting contaminated water and food
15
Q
Hep A characteristics
A
RNA virus benign incubation 2-6 weeks, avg 28 days transient-->don't usually screen for Hep A in blood donors no carrier state
16
Q
where is Hep A most commonly found, in what areas
A
poorly hygienic areas
17
Q
Hep B characteristics
A
DNA virus
incubation 30-180 days
serology: remains in blood
has carrier state, chronic
18
Q
Hep B causes further disease
A
acute hepatitis
nonprogressive chronic hepatitis
progressive disease w/ cirrhosis
asymptomatic carrier state
causes high risk for development of HCC (hepatocellular carcinoma)
19
Q
what is the main determinant of outcome for Hep B patients
A
host immune response
CD8 cytotoxic T cell damages Hep B infected hepatocytes
20
Q
how is Hep B transmitted
A
sexual spread, parenteral
21
Q
Hep B prevention
A
vaccination exist (95% works)
blood and tissue screening completed
22
Q
Hep C characteristics
A
RNA virus
incubation 7-8 weeks
acute phase: asymptomatic
carrier state, chronic, cirrhosis
23
Q
Hep C transmission
A
sexual spread, parenteral
24
Q
Hep C complications
A
risk factor for HCC (definite)
chronic infection ending in cirrhosis in 80-85% of infected individuals and may develop 5-20 years later
25
Hep C prevention
no vaccine
| genomic instability
26
Hep D characteristics
RNA virus
co infection
-->Hep B must be present first to develop Hep D
27
Hep E characteristics
```
RNA virus
not common in U.S.
self limited
waterborne, animal reserviors
not associated with chronic liver disease
```
28
Hep G characteristics
not hepatotropic
| does not increase liver enzymes such as serum aminotransferases
29
where does Hep G virus replicate
in bone marrow and spleen
30
acute viral hepatitis resolution
in about 8 weeks
31
acute viral hepatitis symptoms
asymptomatic (evidence in the blood only)
| may have fatigue, anorexia, joint aches, jaundice
32
acute viral hepatitis histology
panlobular disarray
inflammation
hepatocyte necrosis
33
acute viral hepatitis progression
- massive necrosis that can result in acute liver failure (rare)
- can become chronic (Hep B, C)
34
what is considered chronic hepatitis
if have abnormal liver function for greater than 6 weeks
35
autoimmune hepatitis
chronic, progressive, hepatitis w/ unknown etiology
| T cell mediated destruction
36
cirrhosis mortality rate
12th most common cause of cancer death in U.S.
| primary route of liver related death
37
cirrhosis etiologies
- alcohol
- viral hepatitis
- non alcohol steatohepatitis
- biliary disease
- iron overload
38
cirrhosis pathologic presentations
hepatocyte death and inflammation causing reduced liver function, portal hypertension, and high risk for HCC
bridging septae
parenchymal nodules
fibrosis--parenchymal injury-->loss of function
39
what is main problem of fibrotic liver?
compromised blood supply
| decreased function
40
cirrhosis symptoms
```
weight loss
weakness
liver failure
portal hypertension
-----splenomegaly
neoplasm--HCC
```
**large reserve of liver may mask symptoms**
41
portal hypertension-->ascites
accumulation of fluid in peritoneal cavity
thin limbs w/ distended abdomen
complication of cirrhosis
42
what is portal hypertension
increased pressure of portal blood flow
43
where can portal hypertension originate
1. prehepatic (obstructive thrombi)
2. intrahepatic (cirrhosis)
3. post hepatic (right sided heart failure)
44
consequences of portal hypertension (5)
1. ascites-->generally serious in nature
2. esophageal varices
3. splenomegaly
4. hepatic encephalopathy
5. hypogonadism
45
drug and toxic injury may be predictable or non predictable and effect which gender more frequently
females
46
three alcoholic liver diseases
1. hepatic steatosis
2. EtOH hepatitis
3. cirrhosis (minority of alcoholic patients)
47
nature of fibrosis in fatty liver from alcohol
little fibrosis at onset then accumulation of alcohol causes further increase deposition of lipid
can be reversed if stop intake of alcohol
48
"mallory bodies"
deposits in fatty liver
| clumps of cytokeratins
49
most common metabolic liver disease
NAFLD--non alcoholic fatty liver disease
50
nonalcoholic steatohepatitis (NASH)
hepatocyte injury
metabolic liver disease
10-20% progress to cirrhosis
70% of obese individuals have some form of liver disease
-->liver biopsy needed, increase in liver enzymes in 90% of affected individuals
51
hemochromatosis
accumulation of excess body Fe
-->deposit in liver, pancreas, heart
usually due to abnormal regulation in absorption at SI
hereditary-->homozygous recessive
52
hemochromatosis onset
slow; don't usually notice until 5-6th decade
53
hemochromatosis gender
more affected in males 7:1
54
classic triad manifestation of hemochromatosis
1. cirrhosis w/ hepatomegaly
2. diabetes
3. skin pigmentation
55
general clinical features of hemochromatosis
increase features in males
- hepatomegaly
- abdominal pain
- increased skin pigmentation
- deranged glucose metabolism
- cardiac arrhythmias
- atypical arthritis
56
diagnosis hemochromatosis
test serum Fe
57
hemochromatosis morphology and tx
morphology:
- hemosiderin
- fibrosis
treatment:
- phlebotomy
- Fe chelators
58
hemosiderosis
non hereditary, acquired disease
causes: ineffective erythropoiesis/myelodysplastic syndromes
increase absorption of Fe
59
Wilson's disease
accumulation of Cu in liver brain and eye
failure to incorporate copper into ceruloplasmin so get toxic levels in unwanted areas
60
wilson's disease onset
see between 6-40 yrs old
61
wilson's disease presentation
acute/chronic liver disease
| may have tremor or behavioral changes
62
wilson's disease screening process
not in serum; so no blood test
test levels of Cu in urine or liver
63
what is alpha1-antitrypsin deficiency?
| what presents within hepatocytes to help diagnosis?
degradation of protein enzymes that develops into pulmonary emphysema and liver disease
mallory bodies and PAS positive granules in hepatocytes
64
bile duct carcinoma--cholangiocarcinoma
- -location
- -characteristics
- -prognosis
- cancer of the biliary tree
- arises in bile duct within and outside the liver
- demosplastic tumor--firm and gritty
- aggressive, asymptomatic until later stage
- fatal within 6 mos
**can get collision tumor with HCC
65
Hepatocellular Adenoma
- associations
- benign or malignant
- presentation
- histology
- complications
benign liver neoplasm (mimic HCC)
associated with oral contraceptives; may regress if discontinue (young women); hormonal stimulation
presents in acute abdomen; intra abdominal bleed
bland hepatocytes and no bile ducts
complications:
- ->may progress to hepatocellular carcinoma
- ->subscapular hemorrhage (rupture and bleed)
66
3rd leading cause of cancer deaths
hepatocellular carcinoma
67
HCC
etiology?
what is elevated in 50% of patients?
prognosis?
complication?
ETIOLOGY:
- ->cirrhosis (chronic alcoholics)--many pts have symptoms
- ->chronic viral infection (hep B and C)
- ->NASH (nonalcohol steatohepatitis)
- ->food contaminants (aflatoxins)
Serum alpha-fetoprotein is elevated
-->but not specific for HCC
Prognosis: poor
-->ressection or liver transplant
Complication:
-->high probability for vascular invasion
68
Fibrolamellar Carcinoma
- who does this affect
- prognosis?
- etiology
- tx
variant of hepatocellular carcinoma--"scirrhous" tumor
affects males and females of younger population (20-40 yrs)
no know risk factors; pts do not have underlying liver disease
better prognosis than HCC
TX: surgery/radiofrequency ablation
69
hemosiderosis
- hereditary?
- causes?
- what is increased in the body?
not hereditary; acquired disease
caused by ineffective erythropoeisis; myelodysplastic syndromes
increased absorption of Fe; if having high number of transfusions can get Fe overload
70
secondary biliary cirrhosis
- what is it?
- how does it happen?
- result?
biliary tree obstruction
-->obstruction of the extrahepatic duct
primary cause is cholelithiasis (gall stones)
-->also caused by malignancies of the biliary tree/pancreas
develop secondary inflammation-->fibrosis and scarring
71
primary biliary cirrhosis
- what is it? what does is affect?
- how does it present?
- etiology
inflammatory autoimmune disease
--affects the intrahepatic bile duct
Presents with nonsuppurative inflammatory destruction of intrahepatic ducts
-->portal inflammation, scarring, cirrhosis
Etiology-->autoimmune
72
Primary sclerosing cholangitis (PSC)
-what happens?
-endpoint?
complications?
fibrosing cholangitis develops luminal obliteration
ends up with biliary cirrhosis much like primary and secondary biliary cirrhosis
increase in chronic pancreatitis and HCC in these pts
73
nodular hyperplasia
- presentation
- what does this cause
single or multiple nodules may develop in liver
non-cirrhotic liver: "focal nodular hyperplasia" or "nodular regenerative hyperplasia"
focal or diffuse alteration of hepatic blood supply
-->results in obliteration of portal veins and compensatory increase in arterial supply
74
cholelithiasis
incidence?
associations?
presentations?
gall stones; common (10-20% adults)
INCIDENCE: higher w/ increasing age
- ->Caucasian women (2:1 over men)
- ->increased w/ obesity
ASSOCIATIONS:
- ->increased risk w/ estrogen (pregnancy, oral contraceptive use)
- ->increased risk w/ gall bladder stasis
- ->hereditary
PRESENTATIONS:
--> 80% are silent--asymptomatic
-->if have symptoms
................colicky biliary pain, perforation, obstruction of gall ................bladder, erosion into ileum-->cause GI obstruction
75
cholelithiasis stone formation
supersaturation-->initiation-->growth
76
two types of stones in cholelithiasis
cholesterol (85%)-->radioloucent
| bilirubin (50-75%)-->radiopaque
77
cholelithiasis risk factors
cholesterol stones: increased in caucaisians, older females, high amounts of estrogen
pigmented (biliary) stones: hemolysis, GI disorders, biliary infection
78
cholecystitis
- onset
- symptoms
- associations
onset: 4-6th decade; more so in females
- ->acute or chronic
ACUTE: severe upper right quadrant pain, low grade fever, anorexia, tachycardia, nausea, vomitting
-->symptoms can arise abruptly
CHRONIC: vague symptoms (not as dramatic), recurrent episodes of colicky epigastric/right quadrant pain
-->fibrosis and inflammation present
many associated w/ gallstones
79
Carcinoma of Gallbladder
- associations
- prognosis
- incidence
ASSOCIATIONS: gallstones (95%)
Prognosis: poor (5 yr survival is 5-12%)
Incidence: common in 7th decade (60s)
- ->higher in whites
- ->higher in females
80
carcinoma of gallbladder
| -->risk factors
1. gallstones
| 2. infectious agents within gallbladder (inflammation)
81
what is the 5th highest prevalence of GI malignancy
cancer of the gallbladder
82
what are the two main physiological functions of the pancreas
1. exocrine--digestion
| 2. endocrine--regulation of glucose via insulin and glucagon
83
what cells produce the pancreatic exocrine enyzmes that aid digestion
acinar cells
84
what are 5 exocrine pancreas pathologies
1. cystic fibrosis
2. congenital anomalies
3. acute/chronic pancreatitis
4. pseudocysts
5. neoplasms
85
what is pancreatitis and what is the cardinal manifestation
reversible parenchymal injury associated w/ inflammation
CAUSES: obstruction, infection
-->mumps, trauma, metabolic disease, meds (estrogen)
CARDINAL SIGN: ABDOMINAL PAIN
- ->complain of "upper back intense pain"
- ->medical emergency because of potential to release toxic enzymes
86
acute pancreatitis associated w/ what other diseases
80% associated w/ choletlithiasis, billiary tract disease, and alcoholism
87
etiology of acute pancreatitis
1. trauma-->blunt force/iatrogenic
2. drugs-->chemo
3. infection-->septisemia, mumps
4. metabolic issues-->hypercalcemia
5. idiopathic reasons--possible connection to genetics
88
pathologic destruction of acute pancreatitis
release lipases that causes fat necrosis
inflammatory proteolysis--inflammation from degradation of proteins
vessels necrose-->hemorrhage presents
89
what is another reference name for acute pancreatitis
"acute abdomen"
90
complications of acute pancreatitis
1. mortality 8%
2. abscess
3. organ failure
91
what are two elevated enzymes in acute pancreatitis
amylase and lipase
92
main difference between chronic and acute pancreatitis
chronic is irreversible destruction
93
pathologic destruction by chronic pancreatitis
destroys acinar cells-->irreversible destruction of exocrine function
late stages-->causes destruction of endocrine parenchyma
94
etiology of chronic pancreatitis
```
unclear
but connections with:
-->alcoholism
-->biliary disease
-->hypercalcemia
-->hyperlipidemia
-->oxidative stress
-->possible genetic?
```
95
histological presentation of chronic pancreatitis
- reduced acinar cells
- chronic inflammation
- fibrosis
- duct obstruction
- spare islets
96
symptoms of chronic pancreatitis
severe abdominal pain
-OR-
silent disease: only detect once person develops diabetes
*requires high level of suspicion to detect....may be difficult because serum amylase levels may not increase because of already destroyed acinar cells
97
pancreatic exocrine tumors can present in two ways
cysts
| carcinoma
98
pancreatic cysts (3 types)
congenital
pseudocysts
neoplastic cyst
99
what is the 4th leading cause of cancer deaths
pancreatic cancers
100
what is serous cystadenoma
example of pancreatic neoplasm
| cystic
101
cystic pancreatic neoplasm
incidence?
complication?
higher in females
seventh decade
95% of mucinous cystic neoplasms arise in women
--CAN BE ASSOCIATED W/ INVASIVE CANCER
INTRADUCTAL PAPILLARY mucinous neoplasms increased prevalence in men
102
what is the precursor lesion for pancreatic cancer
PanINS (pancreatic intraepithelial neoplasia)
103
onset of pancreatic cancer
disease of the elderly
| 60-80 yrs (peak at 6-7th decade)
104
primary risk factor for pancreatic cancer
| -seems to double risk
cigarette smoking (environmental influence)
105
what diagnosis raises concern in older pts for development of pancreatic cancer
diagnosis of diabetes
106
pancreatic cancer
- prognosis
- symptoms
prognosis is poor: most die within 6 mos
symptoms: "silent growth", usually don't show any sign of abnormality until cancer has invaded adjacent structures
107
what is the first sign detected for pancreatic cancer
PAIN..but by then it is already too late
108
what is the trousseau sign of pancreatic cancer
migratory thrombophlebitis
109
what are two diseases that pose risk for pancreatic cancer
diabetes mellitus
| chronic pancreatitis
110
what is the difference if develop pancreatic carcinoma at the head or body/tail of pancreas
head: cause bile duct obstruction-->leads to jaundice
body/tail: remains silent until large enough to cause problems
111
what does pancreatic carcinoma look like
ill defines
gritty, gray white
hard
