Pathology Exam 4

Front 1

Icterus

Back 1

Yellowing of eyes usaully caused by jaundice-a build up of Bilirubin. Levels about 2.0- 2.5. Normal is .3- 1.2

Front 2

Unconjugated Bilirubin

Back 2

tightly complexed with Albumin
Insoluble in water
Cannot be excreted in urine
seen in Hemolytic disease

Front 3

conjugated Bilurubin

Back 3

Loosely bound to Albumin
Water soluble
See increase with OBSTRUCTION of bile flow

Front 4

2 main causes of jaundice

Back 4

Gall Stone
Carcinmo of head of Pancrease

Front 5

Jaundice is caused by

Back 5

decreases conjugation
decreased heptocellular excretion
Impaired bile flow
Overproduction of Bilirubin

Front 6

Congenital types of unconjugated hyperbilirubinemia

Back 6

Neonatal Jaundice- decrease UDP-glucoseronyltransferase
(UGT1A1)
Crigler-Najjar- type 1= complete loss of UGT1A1
fatal, secondary to brain damage (kernicterus)
Gilbert Syndrome-mild increase of bilirubin(Asymptomatic)

Front 7

Dubin-Johnson Syndrome
Conjugated Congenital Hyperbilirubinemia

Back 7

Young child with Black Liver(Darkly pigmented Liver)
conjugated and cant remove from the Liver

Front 8

Rotor Syndrome
Conjugated Congnital Hyperbilirubenemia

Back 8

Variant od Dubin-Johnson Syndrome without the Liver pigmentation

Front 9

Cholestasis is

Back 9

Bile not moing due too obstruction or heptocellular dysfunction causing systemic retention of Bilirubin and sloutes (Bile salt retention causes itching of the skin-PRURITIS) elevated serum alkaline phosphatases(ALP)

Front 10

Pruritis

Back 10

Itchy skin- caused by stasis of Bile, specifically Bile salts

Front 11

Hepatic Failure

Back 11

Loss of 80-90% of function

Front 12

Causes of Liver Failure

Back 12

Massive hepatic Necrosis-= TB, drugs, chemicals
Chronic Liver Disease= Cirrhosis
Hepatic dysfuntion without necrosis= Reyes disease(Young child given Aspirin during chickenpox

Front 13

Clinical features of Liver failure

Back 13

Jaundice
Hypoalbunemia
Hyperammonemia
Testicular Atrophy
Spider Angiomas
Coagulopathy
Death within weeks to months

Front 14

Hepatic Encephalopathy

Back 14

Confusoin, Deep coma, death
Seizures(Flapping) , hypereflexia, rigidity
Deranged neurotransmission=GABA and ammonia act as false neurotransmitters cause asterixis(flapping tremor)

Front 15

Cirrhosis is most often the cause of

Back 15

Alcohol Abuse- top 10 killer in Western World

Front 16

3 characteristics of Cirrhosis

Back 16

Bridging of septa(Fibosis)
Perenchymal nodules
Liver architecture disruption- dont get vasculature back w/ the regeneration

Front 17

3 Complications of Cirrhosis

Back 17

Progressie Liver failure
Portal Hypertension
Heptocellular carcinoma

Front 18

Portal hypertention is most often the result of

Back 18

Cirrhosis- causes increase pressure, spleenomegaly, ascites(FLuid in abdomen), heptic encephalopathy
Caput Medusae

Front 19

Hepatitis B is different from the pther types because

Back 19

it is a DNA virus, the others are RNA

Front 20

Hepatitis A is spread by

Back 20

Ingestion of cotaminated food and water, doesnt not progress to chronis hepatitis
antibody againt Hep A= IgM

Front 21

Hepatitis B is the worst type and can lead to

Back 21

Cirrhosis
Cancer (Heptcellular carcinoma)
All body fluids are contaminated*

Front 22

HBV- Hepatitis B Serum markers

Back 22

HBsAG- peaks @ active infection, indicates replication
Igm + antiHBc + antiHBe- seen during "Window period"
IgG and antiHBs denotes a previous exsposure

Front 23

HBC- Hepatitis C uasually caused by

Back 23

Inoculations and transfusions
persistent infection 75%
milder syptoms compared to HBV

Front 24

Hepatitis D is dependent on

Back 24

HBV

Front 25

HEV- Hepatitis E is usaully transmitted by

Back 25

Oral-Fecal means
High mortality rate in pregnant females
not associated with chronic liver disease

Front 26

Carrier state, and is typically seen with what disease

Back 26

is an asymptomatic individual that can still transmit the disease. Typically seen with HBV- Looks like "Ground Glass"

Front 27

Acute viral Hepatitis Preicteric stage is defined as

Back 27

the phase before we see Jaundice- nonspecifc symptoms, malaise, fatigability, loss of appetite, increase serum aminotransferase

Front 28

Acute Viral Hepatitis Icteric stage is defined as

Back 28

Jaundice cause by increase conjugated and non-conjugated bilirubin, Dark urine, Light stool, Pruritis(itchy skin, cause by increase in blie salt)

Front 29

Chronic viral hepatitis os usaully seen with and is defined as

Back 29

HBV and HCV, continuing more than 6 months
Fatigue is the most common symptom
MAY see increase Prothrombin or Hyperglobuminemia

Front 30

Morpholgic changes associated with chronic viral hepatitis include

Back 30

"Ground glass", Hepatocytes "Sand" nuclei
Cholestasis
Apoptosis- "Councilman bodies"
Portal Triaditis
Lobular dissaray

Front 31

"Counsilman Bodies" (Apoptosis)is a morphologically change seen in

Back 31

Chronis Viral Hepatitis

Front 32

In Chronic Hepatitis you usually see

Back 32

Piecemeal necrosis (periportal)
Cirrhosis
Portal lymphoid aggragates

Front 33

(Fulminant) Massive Hepatic necrosis is usaully caused by

Back 33

HBV, drugs, and chemicals

Front 34

(Fulminant) Massive Hepatic necrosis usually presents

Back 34

as a shrunken liver because we destroy the cells and the capsule wrinkles, may present as jaundice and encephalopathy

Front 35

Alcohol Liver disease. three distinctive forms

Back 35

HepaticSteatosis(Fatty Liver)
Alcoholic Hepatitis
Cirrhosis(Not reversible)

Front 36

Hepatic Steosis is characterized by

Back 36

(Fatty Change) Large, Yellow, Greasy Liver
Macrovesicular Lipid Globules
Impaired secretion of Lipoprotiens
Revesible with Alcohol withdraw

Front 37

Alcoholic Hepatitis is chracterized as
(15-20 years of alcoholism to cause)

Back 37

Hepatic Swelling and Necrosis
"Mallory Bodies" seen in hepatocytes
Neutrophilis reaction
Fibrosis
Reversible

Front 38

Alcoholic Hepatitis

Back 38

Weightloss
upper adominal discomfort
Hyperbilirubinemia
elevated ALP
Repeated bouts lead to cirrhosis

Front 39

Viral Hepatitis is distuguished from alcoholic Hepatitis by the presence of _____________ in Alcoholic Hepatitis

Back 39

Mallory Body

Front 40

Alcoholic Cirrhosis is characterized by a ______ &_____ Liver

Back 40

Shrunken, Firm

Front 41

Alcoholic Cirrhosis cause a increase in

Back 41

Serum aminotransferase & ALP
Hypoprotinemia and anemia

Front 42

Hemochromatosis is

Back 42

Too much Iron. Iron is usaully stored in the bone marrow but if you have too much it goes to the liver
Hereditary- defect in intestinal iron absorbption
can also be aquired through iron overload
Deposition of Hemosiderin in the Liver

Front 43

In Hemochromatosis the Liver appears

Back 43

Brown granular pigment, stains with Prussian Blue, leads to Cirrhosis
in the Pancrease it deposits in the Islets

Front 44

Hemochromatosis is usaully seen in

Back 44

Males over 40

Front 45

Bronze Diabetes is

Back 45

Iron deposit in the liver causing classic triad of Cirrhosis and hepatomegally, skin pigmentation and Diabetes Mellitis

Front 46

Wilsons disease is

Back 46

Autosomal recessive associated with accumulation of copper
Decrease in Ceruloplasmin(which is transporter for copper)
Can deposit in basal ganglia in brain
in the EYE you see a Kayser-Fleischner Ring

Front 47

Kayser-Fleischner ring is observed in the eye in what disease

Back 47

Wilsons disease- increase copper deposits

Front 48

Alpha-1- Antitrypsin deficiency(ATT) is

Back 48

the inability of the liver to get rid of ATT, so it builds up
Usaully assocciated with emphysema(young) Cirrhosis(old age)
Abnormal gene on chromosome 14 PIZZ*

Front 49

The combination of Emphysema and Cirrhosis usually indicates

Back 49

Alpha-1- Antitrypsin deficiency(ATT)

Front 50

Reye Syndrome is characterized by

Back 50

Massive Fatty change(Steatosis), usaully in children
Developes 2-5 days after a viral infection(usually aspirin to a child with chicken pox)

Front 51

Primary Bilary Cirrhosis is characterized by?, usaully seen in

Back 51

Pruritis, autoimmune disease against the bile duct,causes fibrosis of duct eventually leads to cirrhosis
AntiMitochondrial Antibodies(90%)
Females, age 40-50

Front 52

Passive congestion is seen in

Back 52

Right sided heart failure
congestion of centrilobar sinusoids
Ischemia
"NUTMEG" liver

Front 53

Hepatic Vein Thrombosis (Budd-Chiari Syndrome) is

Back 53

characterized by hepatomegaly, weight gain, ascites,abdominal pain
Associated w: Oral contracepties, polycytemia Vera, severe centrilobar congestion, can lead to Death if untreated

Front 54

Two major causes of passive congestion

Back 54

right sided heart failure
Budd-Chiari(Hepatic Vein Thrombosis)

Front 55

Most common Benign Hepatic tumor is the

Back 55

Cavernous Hemangioma
(Focal nodular Hyperplasia)
(Liver cell adenoma)

Front 56

Most common malignant Hepatic tumor is

Back 56

Metastatic ( usually starts somewhere else and multiple lesions)

Front 57

Hepatocellular carcinoma is (HCC)

Back 57

the most common primary cancer, HBV seen in more than 85%, more common in black males

Front 58

Hepatocellular Carcinoma(HCC) Etiology

Back 58

1. HBV and HCV
2. Cirrhosis
3. Aflotoxins (moldy grains)

Front 59

Hepatocellular carcinoma (HCC) lesion is usaully

Back 59

Unifocal or multifocal and well differentiated
-Cholestasis
Elevated levels of ALPHAFETOPROTIEN(Tumor marker)
7 month survival rate)Death usually from esophageal varices or liver failure with coma

Front 60

the Primary cancer Angiosarcoma is characterized by

Back 60

Polyvinyl chloride, arsenic, and thorochast exposure
(Cancer of blood vessels)

Front 61

Cholangiosarcoma is

Back 61

Cancer of the Bile duct
incidence higher in china(liver flu)