Liver, Gallbladder, Pancreas - Dr. Dobson Flashcards
(128 cards)
1
Q
alimentary canal
A
GI tract
2
Q
accessory digestive structures
A
- teeth
- tongue
- salivary glands
- liver
- pancreas
- gallbladder
3
Q
portal triad
A
- Hepatic Artery
- Portal Vein
- Bile Duct (flowing opposite way)
4
Q
Canals of Hering
A
connect to bile ductules and into terminal bile ducts
5
Q
Space of Disse contains what
A
= scattered Kupffer cells
= hepatocyte microville
= Hepatic stellate cells
6
Q
normal indirect bilirubin level
normal direct bilirubin level
A
- 0.2-0.9
2. 0.1 - 0.3
7
Q
Abnormalities in labs showing liver disease
A
- GGT (98% chance of lver disease if not normal level)
2. AST/ALT levels
8
Q
AST > 3000U/L
A
severe HTN episode causing centrilobular necrosis (seen in acetaminophen overdose + acute viral hepatitis)
9
Q
AST = 100 -300 U/L
A
alcoholic liver disease , chronic liver diseases, chronic viral hepatitis
10
Q
AST : ALT = 2:1
A
alcoholic hepatitis
11
Q
high ALP
A
bone disease or liver disease
12
Q
high ALP + high GGT =
A
cholestatic liver disease
13
Q
how to assess liver function
A
- PT : acute liver function changes (since it makes coag factors)
- Albumin : chronic liver function changes
- gamma-globulin levels (only elevated in chronic liver function decline)
14
Q
acute hepatitis pattern
A
elevated AST/ALP, other things are variable levels
15
Q
cirrhosis pattern
A
elevated gamma-globulin (with B-g bridging pn serum electrophoresis), elevated PT, LOW albumin
16
Q
chronic hepatits pattern
A
combination of acute hepatitis and cirrhosis patterns
17
Q
Obstructive liver disease pattern
A
cholestasis : elevated ALP and elevated bilirubin
18
Q
histologic changes that are reversible
A
- fat steatosis
- bilirubin cholestasis
- ballooning (cell swelling)
- Mallory Hyaline filaments
- cytoplasmic clearing
19
Q
coagulative necrosis
A
SEEN : acute toxic or ischemic injuries or severe viral or autoimmune hepatitis
HISTOLOGY : confluent, bridging, pan-acinar
20
Q
how do apoptotic cells look like
A
round / oval mass of intensely eosinophilic cytoplasm + dense nuclear chromatin fragments (seen in HCV)
21
Q
Mechanism of liver repair
A
scar (hepatic stellate cells)and regression and regeneration (hepatocytes are like stem cells)
22
Q
Hepatic stellate cells
A
normal : lipid Vitamine A storing cells
acute of chronic injury conditions : fibrogenic myofibroblasts causing scarring
23
Q
what activates hepatic stellate cells
A
TNF-a
24
Q
Areas that fibrose and scar
A
link 2 portal triads and then continue and cause cirrhosis (nodules are the surviving cells trying to replicate)
25
liver failure happens when how much of the liver isn't functioning and survivor rate
80%-90%
| 80% mortality unless liver transplant is done
26
acute liver failure most common cause and definition of it
1. Acetominophen overdose = massive necrosis
2. liver disease with encephalopathy and coagulopathy within 26 weeks of initial injury in the absence of pre-existing liver disease
27
other causes of Acute liver failure
1. fatty liver of pregnancy (steatosis) no necrosis
| 2. virus infection
28
acute liver failure sx
V, N, icterus, jaundice, itching, HIGH LFTs
= life threatening coag abnormalities*
= hepatic encephalopathy
= can lead to multi-organ failure if not tx
29
Chronic Liver failure is associated mostly with and most common cause of it
1. cirrhosis happens from this
| 2. chronic HBV, chronic HCV, NAFLD, AFLD cause this
30
CTP score of :
1. 5-6
2. 7-9
3. 10-15
1. class A, 15-50 years
2. class B, transplant candidate
3. class C, 1-3 months
31
chronic liver failure sx
```
40% asymptomatic until advanced stage*
WL, weakness, Portal HTN** , jaundice**
1. palmar erythma*
2. Spider angiomata*
3. Hypogonadism*
4. Gynecomastia *
```
32
portal HTN from cirrhosis can cause
1. ascites (85%)
2. varices, hemorrhoids, abd wall vessle dilations
3. splenomegally ----> thrombocytopenia, panocytopenia
33
what organisma can involve the biliary tree and liver as local infections or systemic infections
1. bacteria,
2. fungi
3. halminths : schistomsomaisis, strongyloidiasis
4. protozoa : malaria, cryptosporidium
34
HAV :
TR
Dx
chronic liver disease y/n
ssRNA
1. fecal oral, water contaminated
2. Serum IgM ABs
3. no
35
HBV :
TR
Dx
chronic liver disease y/n
partially dsDNA
1. parenteral, sexual, perinatal
2. HBsAg, HBcAg, , PCR HBV DNA
3. 5%-10% of times yes
36
HCV :
TR
Dx
chronic liver disease y/n
ssRNA
1. Parenteral , Intranasal cocaine use
2. ELISA for HCV AB, PRC HCV RNA
3. more then 80% yes
37
HDV :
TR
Dx
chronic liver disease y/n
ssRNA circular
1. parenteral
2. serum IgM and IgG, PCR for HDV RNA
3. 10% (co-infection), 90%-100% (Superinfection) yes
38
HEV :
TR
Dx
chronic liver disease y/n
```
ssRNA
1. Fecal oral
2. Serum IgM and IgG, PCR for HEV RNA
3. only if immunocompromised yes
= no vaccine
```
39
HAV risk of acute hepatic failure
0.2% , its a benign self limited disease, poor hygiene and sanitation
40
HAV sx and complications
1. jaundice, fatigue, recover in 3mos
| 2. cholestasis, Extrahepatic : rash, arthralgia, vasculitis
41
HBV 4 different disease pathways
1. acute hep ----> recovery + clearance
2. acute hepatic failure + massive liver necrosis
3. chronic hep that can ----> cirrhosis
4. asymptomatic healthy carrier
42
high HBV prevealence places most common TR
childbirth (90% cases + 40% of the infants)
43
main determinant to outcome of HBV infection
the hosts immune response, strong can resolve the acute infection
44
protien formed in HBV that is associated with HCC
HBx
45
HBeAB means what
ACUTE : infection has peaked and on wane
| CHRONIC : not made or at late course of disease
46
HBV and rate of getting liver failure and chance of being chronic
1. 0.3% its self limited
| 2. 5%-10% especially if from childbirth then also high chance of getting HCC
47
chronic HBV TX
INF-g and Antiviral reverse transcriptase inhibitors (tenofovir) = slow detrimental effects
48
most common cause of chronic hepatits
HCV
49
HCV sx
asymptomatic during acute phase(85%)
= persistent infection and chronic hepatitis ****
= cirrhosis can lead to HCC
50
reason its hard for immune system to resolve HCV
many variants formed
51
co-infection of HDV and superinfection of HDV
1. acute HBV + HDV
| 2. chronic HBV + HDV
52
HEV TR and prevalence location, risk of becoming chronic and death risk
water-borne and fecal oral, young middle aged, 30% of acute hepatitis in India
= no chronic liver disease unless immunosuppressed
= 20% in pregnant women
53
chronic hepatitis hallmark
| progressive chronic liver damage hallmark
1. increased portal lymphocytic chronic inflammation + fibrosis (also seen in autoimmune hep and steatohepatitis)
2. scarring
54
HBV chronic infection histology
ground-glass hepatocytes from accumulatino of hep B surface Ag (HBsAg)
55
HCV chronic infection histology
portal tract expansion by a lymphoid follicle
56
toxins that can injure the liver and wherein liver the injury occurs
drugs, herbals, supplements, poisons, household products, shampoo, pestacides, perfumes)
= ZONE 3 (perivenular hepatoctes) injury in the central zone of the nodule where CYP450 is
57
2 ways the liver injury from a toxin can happen
1. direct toxicity : liver converts it to XENOBIOTIC
| 2. immune mechanism : toxin acts as a hapten to convert a cellular protein to an Ig
58
most common type of drugs causing liver injury
AB, cardiovascular drugs, CNS, antineoplastic, NSAIDs
59
2 reversible things that can happen to liver when drinking a lot of alcohol
1. Steatosis : fatty change, periventricular fibrosis
2. Hepatitis : liver cell necrosis, inflammation, mallory bodies, fatty changes
= both can lead to cirrhosis if not reversed (fibrosis + hyperplastic nodules)
60
alcohol is metabolized by what CYP
CYP2E1
61
% of alcoholics that get cirrhosis
10%-15%
62
3 types of alcohol producing liver diseases
1. steatosis
2. steatohepatitis
3. steatofibrosis / cirrhosis
63
steatosis sx and labs
1. hepatomegaly, minimal sx
| 2. high bilirubin and alk phosphate
64
Steatohepatitis sx and labs
1. tender hepatomegaly, can have cholestasis
| 2. high bilirubin, AST : ALP = 2:1 ****, elevated alk phosphate
65
Steatofibrosis / cirrhosis sx and labs
1. hepatic dysfunction, coagulation abnormalities
| 2. hypoproteinemia (low albumin and factors for clotting)
66
acute vs chronic alcoholism
1. effects CNS (and can GI and liver) only and is reversible
| 2. chronic : liver stomach, GI, pancreas, CNS, and all other organs, high morbidity
67
most common causing chronic liver disease
is NAFLD : hepatic steatosis not from alcohol
| common in metabolic syndrome
68
metabolic syndrome
1. DM / glucose or insulin intolorance / high fasting glucose
2. BP over 140/90
3. dyslipidemia, central obesity, pr microalbuminuria
69
steatosis is when how much of the liver cells are involved
5%
70
where does fibrosis start in adults and children with NAFLD
adults : around central vein as fine spider web and then expands
children : portal fibrosis
71
NAFLD dx and what you see on imaging
1. fat accumulation and biopsy needed to dx fibrosis
72
NAFLD labs/sx seen show what and can lead to what
1. elevated LFTs and RUQ pain or fullness, malaise
| 2. cardiac death CAD, HCC
73
Iron amounts is controlled by what
intake + absorption in SI
| not by excretion
74
hereditary hemochromatosis does what to what organ and also sx after how much is stored
liver stores 98% Fe so hepatomegaly + cirrhosis
| = sx after 20g stored
75
hereditary hemochromatosis mutation in what
Ferroportin (HEF gene mutation , C--> T called C282Y) = common in caucasians
76
main regulator of Fe absorption in normal person
Hepcidin (HAMP gene)
77
hereditary hemochromatosis sx
hepatomegaly**, hypogonadism *, amenorrhea *, abd pain, skin pigmentations (sun exposed areas), DM, cardiac dysfunction
78
hereditary hemochromatosis DX how
high serum ferritin and Fe, liver biopsy only not needed anymore with genetic testing
79
hereditary hemochromatosis histology in biopsy
Prussian blue stain, = hepatocytes with iron stained blue
80
hereditary hemochromatosis can lead to what complications
cirrhosis, HCC or cardiac problem
81
hereditary hemochromatosis tx effect on HCC
no effect since genetics are still mutated even if you remove the Fe overload
82
Wilsons disease mutation and cause
ATP7B mutation causing X excretion of Cu into bile and ceruloplasmin
83
Cu accumulates where in wilsons disease
1. liver
2. brain : tremor, chorea, rigid dystonia
3. eye :
4. kidney, bones, parathyroid glands)
5, RBCs : hemolytic anemia
84
Wilsons disease SX presenting with
acute or chronic liver disease
85
Wilsons disease DX
low celuluplasmin , high hepatic Cu or high Cu in urine
86
a1 - Antitrypsin deficiency (a1AT) mutation and cause
PiZ / PiZZ mutation*
= X a1AT* which inhibits proteases (esp N elastase, protease released at inflammation)
= proteases always on
87
a1 - Antitrypsin deficiency (a1AT) SX leads to what conditions
1. pulmonary emphysema,
2. liver disease from accumulation on misfolded proteins a1AT : "toxin gain of function mutation "
3. jaundice, hepatitis
88
most common inherited hepatic disorder
a1 - Antitrypsin deficiency (a1AT)
89
Piz mutation is what
point mutation Glu --> Lys = a1AT-Z
90
cholestasis hallmark seen in histology
green-brown plugs of bile in hepatocytes + dilated canaliculi
91
liver conjugates bilirubin with what
glucuronic acid
92
when can you see jaundice at what level of bilirubin
2mg/dL to 2.5mg/dL
93
3 causes of unconjugated bilirubin
1. hemolytic anemia
2. ineffective erythropoiesis
3. defective conjugation with glucuronic acid
94
high unconjugated bilirubin causes what
accumulation in tissues esp neurologic (kernicterus) , when all albumin is saturated
95
conjugated bilirubin 3 most common causes
1. Hepatocellular disease
2. bile duct injury
3. biliary obstruction
96
common thing to see in conjugated bilirubin
easily excreted in urine so you see it there
97
common sx besides jaundice from elevated bilirubin
1. pruritus
2. skin xanthomas (cholesterol accumulation)
3. malabsorption
98
cholestatic disease shows what
1. high alk phosphate + high GGT
| 2. enzymes at apical (canalicular) membrane of hepatocytes and bile duct cells
99
what causes jaundice in babies
| what is the tx and what can make it worse
1. LOW UGT1A1 : glucuronidation conjugator
| 2. blue light therapy, breast milk can make more bilirubin accumulate
100
hallmark histology in Dubin-Johnson syndrome
black-brown melanin-like pigment in hepatocytes
101
Crigler- Najjar Syndrome type 1 and type 2 :
| mutation and sx and what type of bilirubin
type 1 : X UGT1A1 activity, fatal at neonatal
type 2 : low UGT1A1 activity , mild, occasional kernicterus
= unconjugated
102
Gilbert syndrome : mutation and sx and what type of bilirubin
low UGT1A1 activity : not serious
| = unconjugated
103
Dubin- Johnson syndrome : mutation and sx and what type of bilirubin
MRP2 (canalicular multidrug resistant protein) mutation = X biliary excretion of bilirubin glucuronides , Black liver , not harmful
= conjugated
= cant secrete conjugate bilirubin
104
Rotors syndrome : mutation and sx and what type of bilirubin
low hepatic uptake , storage, excretion , not harmful
| = cant store conjugated bilirubin
105
cholestasis come from an obstruction in the large bile duct, what happens if its not corrected + TRIAD of one of those causes
1. bilirary cirrhosis from fibrosis happening
| 2. ascending cholangitis : -----> fever*, ABD pain,* jaundice* = TRIAD, can lead to abscess and sepsis
106
obstructive and not obstructive causes of neonatal cholestasis
OBSTRUCTIVE : Biliary atresia
| NON-OBSTRUCTIVE : paucity of bile duct (Alegielle syndrome), infection, genetic transporter defect
107
biliary atresia is what
complete or partial obstruction of the extrahepatic biliary tree (1st 3mo of life)
108
biliary atresia tx and prevalence
surgery
| = most common cause of death from liver disease in childhood
109
splitting liver
larger portion given to adult, smaller given to child = saves 2 lives when transplanted
110
Kasai procedure
1. remove biliary tree and gallbladder
2. connect SI to liver to drain bile
3. duodenum attached to the SI you attached to the Liver
111
autoimmune hepatits is what type
type 1 (adults, LMK-1 ABs) and 2 (children)
112
2 types of autoimmune cholangiopathies
1. Primary sclerosing cholangitis
| 2. primary biliary cirrhosis
113
gene associated with autoimmune hepatitis in caucasians, japanese, south americans
HLA **** all
1. DR3
2. DR4
3. DRB1
114
DX autoimmune hepatitis + prevalence in sex
female
1. exclude viral hep and drug hep and other causes
2. AutoABs
3. elevated serum IgG
4. liver biopsy
115
staining of autoABs :
1. homogenous staining in cell
2. centromere stain in cell
3. speckled stain in cell
1. SLE
2. Sjögrens syndrome
3. ag against RNPs and Sm
116
TX of autoimmune hepatitis
prednisone + azathioprine at times
117
Autoimmune Hepatitis sx
high AST/ALP
= looks like viral or drug induced hep, abd pain, N/V
= fibrosis or cirrhosis on biopsy
118
Primary Biliary Cholangitis (PBC) :
1. age
2. gender
3. associated SX
4. serology
5. radiology
6. duct lesions
1. 50yo
2. female
3. Sjögrens syndrome, thyroid disease, scleroderma, Celiac D, RA
4. AMA+ (95%), ANA+ (45%)
5. none
6. florid duct lesions, loose small ducts
119
Primary Scerlosing Cholangitis :
1. age
2. gender
3. associated SX
4. serology
5. radiology
6. duct lesions
1. 30yo
2. male
3. IBD (UC)
4. ANCA+, AMA-, ANA-/+
5. Strictures and beading or large bile duct, pruning smaller ducts
6. inflammatory destructioin of extrahepatic and large hepatic ducts, fibrotic obliteration of medium and small intrahepatic ducts
120
Primary Biliary Cholangitis (PBC) : what happens
autoimmune disease of inflammation to small to medium intrahepatic bile ducts
121
Primary Biliary Cholangitis (PBC) :sx and labs seen
1. pruritus and fatigue increasing slowly, splenomegaly, jaundice, hyperpigmentation, vit D malabsorption, steatorrhea, hypercholesteremia
2. high ALK Phosphatase, ABs against PDH complex in Mitochondria****
122
Primary Biliary Cholangitis (PBC) : TX
oral ursodeoxycholic acid (natural bile), liver transplant
| increased risk of HCC
123
Primary Scerlosing Cholangitis : is what
inflammation and obliterative fibrosis of extrahepatic and large intrahepatic bile ducts and dilation of preserved segments
124
Primary Scerlosing Cholangitis : AB t-cell AND histology
1. HLA -B8
| 2. "onion skin concentric scar"
125
Primary Scerlosing Cholangitis : huge association to what
UC (T-cells travel from GI to liver)
126
Primary Scerlosing Cholangitis : sx
1. high ALK Phosphatase
2. jaundice, pruritus, fatigue
3. chronic pancreatitis, chronic cholecystitis
4. Ascending cholecystitis****
127
Primary Scerlosing Cholangitis : eventually becomes
hepatic fibrosis and cirrhosis, cholangiocarcinoma
128
Primary Scerlosing Cholangitis : gold stanard to dx and TX
1. "beading"in large intrahepatic duct and extrahepatic ducts by ERCP**
2. medical anti-inflammatory MX, liver transplant (all end stage liver diseases need to tx with Liver transplant****)
