525 Patho Final Exam

Front 1

What is the exocrine function of the liver?

Back 1

It produces bile, emusifies fats, excreted into a duct.

Front 2

What is the endocrine function of the liver?

Back 2

It produces somatomedin C (IGF-1), stimulates growth hormone and growth of bone.

Front 3

What is the storage function of the liver?

Back 3

It stores glycogen (storage form of glucose) and iron for synthesis of new hemoglobin.

Front 4

What is the synthetic function of the liver?

Back 4

It makes albumin and all other plasma proteins (such as the coagulation proteins), except immunoglobulins.

Front 5

What is the metabolic function of the liver?

Back 5

-removes carbs, lipids, proteins from the blood and processes them for use
-removes substances from the blood and breaks them down
-removes circulating hormones from the blood

Front 6

What are examples of the substances that the liver removes from the blood and breaks down?

Back 6

-immunoglobulins
-antigen-antibody complexes
-circulating inflammatory mediators
-drugs and toxins
-GI derived ammonia
-hormones (like estrogen)

Front 7

How do we know if the liver has been injured?

Back 7

Hepatocytes release enzymes and they appear in the blood. These enzymes are elevated in the serum:
SAST - serum aspartate aminotransferase
SALT - serum alanine aminotransferase

Front 8

What is jaundice?

Back 8

The abnormal formation, processing or excretion of bilirubin (a symptom, not a disease).

Front 9

What are the characteristics of jaundice?

Back 9

-yellow skin, mucosa, sclera of eyes
-caused by hyperbilirubinemia
-bilirubin binds to connective tissue (makes it yellow)

Front 10

What is hyperbilirubinemia?

Back 10

-too much bilirubin in the serum, usually >3 mg/dl.
Classified 3 ways: conjugated, unconjugated, mixed.

Front 11

What is bilirubin?

Back 11

It is the breakdown product of hemoglobin.

Front 12

What causes jaundice?

Back 12

This is caused by:
-too much hemoglobin is being broken down; or
-when the liver fails to process the bilirubin.

Front 13

What is icterus?

Back 13

The yellow skin associated with jaundice?

Front 14

What normally happens to bilirubin?

Back 14

Normally, the liver metabolizes this and excretes it as a component of bile.

Front 15

How is jaundice classified?

Back 15

This is classified according to the initiating cause of the hyperbilirubinemia.

Front 16

Prehepatic Jaundice
aka: hemolytic jaundice

Back 16

"injury before the liver"
In a large hematoma, breakdown of red cells occurs with release of bilirubin, if bilirubin becomes systemic - this occurs (seen in trauma victims).

Front 17

Hepatic Jaundice
aka: intrahepatic jaundice

Back 17

"liver damage"
resulting from liver disease;
liver fails to take up normal circulating bilirubin (ex: cirrhosis);
jaundice results when blood levels reach 3 mg/dl

Front 18

Posthepatic Jaundice
aka: obstructive jaundice

Back 18

Usually this involves the inability of the liver to get rid of bile, as with gallstones or a tumor blocking the bile duct;
liver can't release bilirubin as a component of bile and it releases it back into blood instead.

Front 19

What is conjugated bilirubin?

Back 19

This is joined with gluconeride in the hepatocytes. Associated with obstruction of the biliary system (stones). Posthepatic.

Front 20

What is unconjugated bilirubin?

Back 20

This is caused by excessive hemolysis. Prehepatic.

Front 21

What is mixed bilirubinemia?

Back 21

This is associated with liver cell necrosis and destruction of liver parenchyma. Hepatic.

Front 22

What is brown, foamy urine a symptom of?

Back 22

Viral Hepatitis
-conjugated bilirubin is water soluble and is excreted in urine.

Front 23

Is unconjugated bilirubin water soluble?

Back 23

No - it will not be seen in CSF or urine.

Front 24

Disorders that lead to prehepatic jaundice.

Back 24

-Hemolytic blood transfusion reaction
-Hereditary disorders of the red blood cell (sickle cell, Thalassemia, Spherocytosis)
-Aquired hemolytic disorders
-Hemolytic disease of the newborn
-Autoimmune hemolytic anemias

Front 25

Disorders that lead to hepatic (intrahepatic) jaundice.

Back 25

-Decreased bilirubin uptake by the liver
-Decreased conjugation of bilirubin
-Liver cell damage (hepatitis, cirrhosis, cancer)
-Drug induced cholestasis

Front 26

Disorders that lead to posthepatic jaundice.

Back 26

-Structural disorder of the bile duct
-Cholelithiasis
-Congenital atresia of the extrahepatic bile ducts
-Bile duct obstruction by tumors

Front 27

What is fatty liver?

Back 27

Alcoholic liver disease characterized by infiltration of hepatocytes by fat or lipid material; reversible, does not affect biochemical function of hepatocytes until well advanced. (alcholism is not the only cause)

Front 28

What causes alcoholic liver disease (fatty liver)?

Back 28

Metabolism of alcohol (ethanol) by the liver results in increased NADH and decrease NAD.
ethanol+NAD -->/<-- NADH+H+acetaldehyde;
acetylCoA+NADH -->/<-- fatty acids+NAD
-net result,liver is overwhelmed with fatty acids

Front 29

What are other causes of fatty liver?

Back 29

-decreased fatty acid oxidation and decreased export of lipioproteins from the liver
-diets high in fat can overwhelm the ability of the liver to process fat (foie gras)

Front 30

What are esophageal varicies?

Back 30

Tortuous, highly dilated veins in the esophagus that can hemorrhage; caused by HTN in the hepatic portal system.

Front 31

What is the hepatic portal system?

Back 31

The venous drainage from the entire GI tract.

Front 32

What is a portal system?

Back 32

Connection of 2 capillary beds:
In a portal system, blood leaves the heart, circulates through arterial system and arrives at a capillary bed in the GI system --> venous drainage continues to the liver where another capillary bed is encountered within the liver --> the liver is then drained by a vein that leads back to the heart.

Front 33

Is the hepatic portal system low or high pressure?

Back 33

Low pressure (5-10 mmHg).

Front 34

What is hepatic portal system HTN?

Back 34

Liver becomes diseased --> flow of portal blood is impeded --> pressure increases (>12 mmHg).
-Symptoms of this dysfunction are related to the structural connections that exist between this portal system and systemic circulation.

Front 35

What are the consequences of hepatic portal HTN?

Back 35

With increasing pressure, anastomoses, normally not functional, become functional --> causes portal and systemic blood to mix (not good).

Front 36

What are anastomoses?

Back 36

Venous connections between hepatic portal system and systemic circulation (nonfunctional at normotension).

Front 37

Where are the anastomoses?

Back 37

-rectal/anal junction
-esophagus/stomach junction
-part of the stomach
-anterior abdominal wall

Front 38

What are some symptoms of hepatic portal HTN?

Back 38

Caput medussae, hemorrhoids, esophageal and gastric varicies.

Front 39

What is a dangerous pathological condition that results from hepatic portal HTN?

Back 39

Mixing of systemic and portal blood allows substances in portal blood to mix with systemic blood without first being filtered by the liver. These substances can be toxic.

Front 40

In hepatic portal HTN, what happens if ammonia reaches systemic circulation without being removed by the liver?

Back 40

Ammonia, a normal byproduct of digestion, is very toxic to the brain if it reaches systemic circulation --> hepatic coma or hepatic encephalopathy.
-liver becomes diseased --> liver obstruction --> portal HTN --> anastomoses functional --> ammonia reaches syst. circulation --> hep. coma or encephalopathy

Front 41

With advanced liver disease there is a decrease in the systemic circulation of substances normally secreted by the liver. What would these be?

Back 41

-clotting factors
-albumin

SEE PAGE 935, fig. 40-13, mechanisms.

Front 42

How would decreased clotting factors from liver disease manifest?

Back 42

bleeding varicies, hemorrhoids, etc.

Front 43

How would decrease albumin from liver disease manifest?

Back 43

As Edema
portal HTN and increased pressure in peritoneal capillaries AND decreased albumin --> decreased oncotic pressure in blood --> ascities

Front 44

Advanced liver disease also can lead to an enlarged spleen - why?

Back 44

Portal HTN --> shunting of blood into splenic vein --> splenomegaly and hypersplenism from prolonged transit time of blood through the spleen
-hypersplenism - decreased life span and decrease in number of blood cells, leading to anemia, thrombocytopenia, leukopenia

Front 45

So, the major complications of portal HTN and opening of collateral channels are:

Back 45

-ascites
-splenomegaly
-formation of portosystemic shunts - anastomoses

Front 46

Normally the liver removes estrogen. What happens if the liver cannot remove it?

Back 46

Males - gynecomastia, alopecia, testicular atrophy
Women - menstrual irregularities

Front 47

What are the three catgories of portal HTN?

Back 47

Posthepatic
Intrahepatic
Prehepatic

Front 48

What causes posthepatic portal HTN?

Back 48

Severe right-sided heart failure

Front 49

What causes intrahepatic portal HTN?

Back 49

Blockage of blood flow within the liver (Cirrhosis and fatty liver)

Front 50

What causes prehepatic portal HTN?

Back 50

Blockage of blood flow to the liver (Splenomegaly,tumor formation)

Front 51

What is cholestasis?

Back 51

Biliary blockage [posthepatic] [100% conjugated]
-both intrahepatic and extrahepatic blockages can occur
-adverse affects of digestion of fats and fat-soluble vitamins due to a lack of bile can lead to jaundice

Front 52

What is the type of jaundice associated with cholestasis?

Back 52

Obstructive Jaundice

Front 53

Obstructive Jaundice is also often seen with this disorder:

Back 53

Carcinoma of the head of the pancreas

Front 54

Biliary blockage of the duct can result in this:

Back 54

Reflux of bile back into the pancreas --> pancreas digests (emulsification of fat in cells by bile)

Front 55

What is cholelithiasis?

Back 55

Gallstones - concretions composed of chemicals normally found in the bile
Risk factors - 4F's: female, fair-skinned, over 40, Fat

Front 56

What are gallstones normally composed of?

Back 56

75% of all gallstones are cholesterol stones

Front 57

What are the clinical features of cholelithiasis?

Back 57

-frequently asymptomatic
-inflammation of the gallbladder due to mechanical injury - VAGUE or DULL PAIN
-obstruction of cystic duct - SEVER PAIN due to distension
-JAUNDICE - [posthepatic] [100% conjugated]

Front 58

What do gallstones predispose a patient to?

Back 58

Carcinoma of the gallbladder - cell injury causes chronic inflammation --> unwanted cell proliferation.

Front 59

The liver is the primary site for:

Back 59

metabolic conversion and inactivation of drugs and toxins.

Front 60

How does metabolism of drugs and toxins damage the liver?

Back 60

-DIRECTLY- damage by the compound (ex: phalloidin-toad stools - inhibits RNA polymerase which reads and makes MRNA for protein synthesis
-INDIRECTLY- derivatives of a compound can cause damage (ex: CCCl4, tylenol)

Front 61

What is cirrhosis?

Back 61

A chronic liver disease characterized by a loss of normal liver structure and function.
-end stage disease
-irreversible and incurable
-fibrosis (scarring) and liver cell nodules replace normal architecture

Front 62

What is the etiology of cirrhosis?

Back 62

-alcohol abuse, HBV, HCV infections account for 65% off all cases of cirrhosis in the US
-30% unknown causes
-hereditary metabolic diseases, autoimmune diseases, drugs, biliary obstruction account the rest

Front 63

What is the pathogenesis of cirrhosis?

Back 63

Caused by many years of recurring bouts of necrosis of liver cells and repair by fibrosis with disorganized regeneration of liver cells.
-nodular pattern of liver
-Dx grossly by liver's appearance
-whole liver or regions can be affected

Front 64

The primary malignancy of the liver:

Back 64

hepatocellular carcinoma
-can originate in any liver cell
1 million deaths annually worldwide
-common in far east and africa
-S&S weight loss, pain, resembles cirrhosis
-2% of cancer deaths in US
-HIGHLY MALIGNANT
-SEEN IN ADULT MALES 5:1

Front 65

What causes hepatocellular carcinoma?

Back 65

-consumption of aspergillis flavis-aflatoxin from a fungus that grows on improperly stored (wet) grain
-also seen where HepB virus is endemic
-primary site of metastasis from other cancers

Front 66

What is the link between cirrhosis and cancer?

Back 66

Link between cirrhosis and hepatocellular cancer: unwanted cell proliferation.
-highest incidence in cirrhosis secondary to HBV or HCV

Front 67

What is the link between hepatitis and cancer?

Back 67

Link between hepatitis and hepatocellular cancer: unwanted cell proliferation.

Front 68

What are the clinical features of hepatocellular carcinoma?

Back 68

-nonspecific weight loss, loss of appetite, nausea
-enlarged, tender liver
-portal HTN
-5 yr. survival rate is 10%
-chemo. is ineffective

Front 69

Why is chemotherapy ineffective with hepatocellular carcinoma?

Back 69

Because the liver metabolizes chemotherapeutic agents, chemo. will kill patient before it kills cancer cells in the liver.

Front 70

What are causes of secondary liver tumors?

Back 70

Metastasis from other cancers - primary tumors of the lung, breast, GI (colon).
-multiple round lesions will grow with necrotic centers
-cells resember ORIGINAL TISSUE

Front 71

What are the clinical features of metastatic liver cancer?

Back 71

-liver enlarged and tender
-jaundice, ascites, splenomegaly
-poor prognosis
-death is 6 mos. after Dx

Front 72

What is viral hepatitis?

Back 72

A disease caused by inflammation of the liver from infection by 5 viruses.
-often asymptomatic

Front 73

What is Hepatitis A Virus(HAV)?

Back 73

-RNA virus (r/t polio)
-15-50 day incubation
-followed by acute jaundice
-fecal-oral transmission
-sources: sewage, contaminated food/drink, sushi, shellfish, poor hygeine

Front 74

Who contracts HAV?

Back 74

-common in children in underdeveloped countries
-tourists

Front 75

What are symptoms of HAV?

Back 75

fever
vomiting
jaundice
rapid recovery
favorable prognosis
relatively mild symptoms

Front 76

Is there a chronic or carrier state with HAV?

Back 76

No

Front 77

Is there a vaccin available for HAV?

Back 77

Yes

Front 78

What are lab markers for HAV?

Back 78

-elevated SAST(liver specific) and SALT(other cells release this, too) during acute phase (liver cells relsease these enzymes when damaged)
-elevated serum antibodies: IgM-antiHAV then IgG-antiHAV

Front 79

What does it mean if IgM and IgG specific antibodies are elevated for months after symptoms have gone away?

Back 79

This means virus is still present and the immune system is still defending the body against it.

Front 80

What is Heptatitis B Virus (HBV)?

Back 80

-many phased, serious disease
1)subclinical - evidence of the disease without manifest symptoms - Recovery
2)acute infection - Recovery
3)fulminant - followed by death (entire liver is destroyed)
4)heathy carrier
5)chronic non-progressive or persistent infection in which the patient recovers or moves to next step
6)chronic active that progresses to cirrhosis or hepatocellular carcinoma and death (fibrosis and liver is destroyed)

Front 81

What are lab markers for HBV?

Back 81

-First, Serum IgM-antiHBV
-then, Serum IgG-antiHBV
** persistence of IgG-antiHBV may be the only serological indication of viral infection in persistent infection or in a healthy carrier - MAY PERSIST FOR LIFE

Front 82

The failure to produce antibodies to HBV will lead to what?

Back 82

Patient cannot clear the virus and will develop chronic active hepatitis.

Front 83

Is there a chronic or carrier state with HBV?

Back 83

Yes
5-10% become carriers with no physical evidence of disease but can infect others
(only indication may be elevated serum IgG-antiHBV)

Front 84

Is there a vaccine available for HBV?

Back 84

Yes

Front 85

Can a person with HBV ever give blood?

Back 85

No

Front 86

What are the clinical features of HBV?

Back 86

-DNA virus
-40-180 day incubation
-transferred: blood, exposure to blood or blood products, sexual

Front 87

In HBV profound jaundice is a better clinical outcome than mild jaundice!

Back 87

In HBV profound jaundice is a better clinical outcome than mild jaundice!

Front 88

This develops in 1% of patients with HBV:

Back 88

Acute fulminant hepatitis
- rapid course
- massive necrosis of liver
- death

Front 89

Can a chronic state develop with HBV?

Back 89

Yes - smouldering or persistent infection followed by recovery
-develops in <10%
-asymptomatic in 75%
-25% develop chronic active hepatitis and may progress to cirrhosis

Front 90

Chronic hepatitis has a strong correlation with:

Back 90

This has a strong correlation with rare development of hepatocellular carcinoma (unwanted cell replication).

Front 91

What is hepatitis D Virus (HDV)?

Back 91

-incomplete RNA virus
-requires HBV for replication
can occur simultaneously or as a superinfection following HBV

Front 92

What characterizes HDV from HBV?

Back 92

-more severe symptoms
-progression to cirrhosis is more accelerated

Front 93

What is Hepatitis C Virus (HCV)?

Back 93

-RNA virus
-acquired by blood transfusion or sexually

Front 94

What is the clinical presentation of HCV?

Back 94

-similar to HBV
-acute phase is less severe than HBV
-UNLIKE HBV, may smoulder for years with no symptoms
-UNLIKE HBV, tends to progress to chronic hepatitis (50%) and half of these patients develop cirrhosis

Front 95

What are lab markers of HCV?

Back 95

-serum IgM-antiHCV and serum IgG-antiHCV present throughout course of disease

Front 96

What differentiates HCV from other hepatitis infections?

Back 96

-higher incidence of hepatocellular carcinoma
-liver enzymes remain elevated throughout course of disease

Front 97

Is there a vaccine for HCV?

Back 97

No
-significant public health concern

Front 98

What is Hepatitis E Virus (HEV)?

Back 98

-RNA virus
-fecal-oral transmission
-resembles HAV
-usually asymptomatic and transient symptoms

Front 99

Who is HEV especially dangerous to?

Back 99

pregnant women - high mortality

Front 100

Do chronic hepatitis and chronic carrier states develop with HEV?

Back 100

No

Front 101

Is it possible to differentiate types of hepatitis virus infection histologically?

Back 101

No - it is impossible to distiguish one from another morphologically.

Front 102

Where is the pancreas located?

Back 102

Retoperitoneally in the upper abdomen on the left (behind the peritoneum).
-disease associated with pancreas causes referred pain to the back.

Front 103

What are the digestive enzymes produced by the exocrine pancreas?

Back 103

amylase
lipase
peptidases - trypsin, chymotrypsin
bicarbonate

Front 104

Enzymes of the pancreas are secreted as:

Back 104

proenzymes
-they become activated by enteropeptidases and increased pH in the duodenum

Front 105

What are the major diseases of the pancreas?

Back 105

-pancreatitis
-tumors

Front 106

What is pancreatitis?

Back 106

Acute or chronic inflammation of the pancreas; usually a sterile chemical inflammation (no pathogens).
-tissue destruction is caused by digestive enzymes released

Front 107

What is a very mild form of pancreatitis and rarely diagnosed?

Back 107

Acute edematous pancreatitis

Front 108

What is a serious form of pancreatitis with a high mortality rate?

Back 108

Acute hemorrhagic pancreatitis

Front 109

The premature activatio of pancreatic enzymes results in:

Back 109

autodigestion of the pancreas

Front 110

What are three conditions that can cause acute pancreatitis?

Back 110

1)obstruction of main pancreatic duct, frequently by gallstones with reflux of bile
2)injection of bile or other chemicals into the pancreatic duct
3)mechanical disruption of the pancreatic acinar cells (seatbelt trauma)

Front 111

What is the pathology of acute hemorrhagic pancreatitis?

Back 111

-massive edema, hemorrhage, and necrosis of tissue
peritoneal irritation or chemical peritonitis occurs due to leakage of enzymes
-serum levels of lipase and amylase are high

Front 112

What are the clinical features of acute hemorrhagic pancreatitis?

Back 112

-sudden onset
-seen in patients w/gallstones or alcoholism
-SEVERE abdominal pain - distension, nausea, vomiting (ACUTE ABDOMEN)
-shock
-elevated serum amylase, lipase

Front 113

What is the treatment for acute hemorrhagic pancreatitis?

Back 113

No effective treatment - efforts are spent containing the damage and preventing shock
-20-50% mortality rate

Front 114

Patients who survive an attack of acute hemorrhagic pancreatitis are at risk for what?

Back 114

Risk for recurrence, progression to chronic pancreatitis.

Front 115

What is chronic pancreatitis?

Back 115

Normal parenchyma is replaced by irregular fibrosis after repeated bouts with inflammation.
-irreversible due to tissue destruction
-results in endocrine and exocrine insufficiency

Front 116

What are some causes of chronic pancreatitis?

Back 116

-cystic fibrosis
-acute pancreatitis

Front 117

What other disorders can result after development of chronic pancreatitis?

Back 117

-Diabetes Mellitus
-Malabsorption
-Risk for adenocarcinoma of pancreas - at tail of pancreas (by the time symptoms are noticed, it is too late - 0% 2 year survival rate)

Front 118

What are factors that can lead to chronic pancreatitis?

Back 118

-smoking
-alcohol abuse
-high fat diet
*usually affects people >40

Front 119

What are the clinical symptoms of chronic pancreatitis?

Back 119

-often asymptomatic or vague symptoms
-back pain
-late in disease - jaundice due to biliary blockage
-digestive problems due to blockage of pancreatic duct