Alterations Of Liver Functions

Front 1

Normal liver function: synthesis

Back 1

Triglycerides, cholesterol, plasma proteins, clotting factors, amino acids

Front 2

Normal liver function: Produces and secretes

Back 2

Bile salts

- emulsify fats

Front 3

Normal liver function: Storage

Back 3

Vitamins ADEK, iron, glycogen

- phagocytosis of old RBC

Front 4

Normal liver function: Degrades hormones

Back 4

Estrogen, testosterone, ADH, aldosterone

- conjugates bilirubin

Front 5

Normal liver function: Gluconeogenesis

Back 5

The breakdown of carbs

Front 6

Normal liver function: Detoxification

Back 6

Ammonia-> Urea

Metabolized Hormones such as alcohol.

Front 7

Normal liver function: Activation of Vitamin D

Back 7

Self explanatory

Front 8

Portal Hypertension

Back 8

Effects portal venous system.

I'm normally high blood pressure in the portal venous system primarily caused by a resistance to the portal blood flow.

Front 9

Portal Hypertension

Back 9

Affects portal venous system.

I'm normally high blood pressure in the portal venous system primarily caused by a resistance to the portal blood flow.

Front 10

Causes of portal hypertension

Back 10

Anything that obstructs the blood flow to the liver. Examples are liver fibrosis and right heart failure.

RH failure-> increase resistance to the inferior vena cava.

Front 11

Three consequences of portal hypertension

Back 11

1. Splenomegaly

2. Thrombocytopenia

3. Varices

Front 12

Three consequences of portal hypertension

Back 12

1. Splenomegaly

2. Thrombocytopenia

3. Varices

Front 13

Splenomegaly

Back 13

Enlargement of the spleen due to the back up of blood.

Front 14

Thrombocytopenia

Back 14

Low platelets because of the blockage of platelets leaving the spleen. Leads to an increase risk for bleeding.

Front 15

Varices

Back 15

Collateral veins that provide alternative circulation when normal route is impeded.

Front 16

Varices

Back 16

Collateral veins that provide alternative circulation when normal route is impeded.

Front 17

Problems with varices

Back 17

1. Easily ruptured: if ruptured life threatening.

- lower esophagus, stomach, and rectum are common areas for vessels to form.

2. Blood shunted away from liver.

- liver function less efficient: toxins aren't getting filtered out.

Front 18

Ascites

Back 18

A clinical manifestation of liver disease. An accumulation of fluid in the peritoneal cavity.

Front 19

Ascites

Back 19

A clinical manifestation of liver disease. An accumulation of fluid in the peritoneal cavity.

Front 20

Contributing factors to ascites

Back 20

- Decrease in BOP: no plasma proteins synthesized-> decrease in BOP

- Increase in BHP: hypertension

- Decrease in ADH and Aldosterone degradation leads to an increase in these hormones-> increase BHP and H2O

Front 21

Hepatic Encephalopathy

Back 21

Accumulation of toxins, particularly ammonia, causing disruption of neurotransmission.

Front 22

Hepatic Encephalopathy

Back 22

Accumulation of toxins, particularly ammonia, causing disruption of neurotransmission.

Front 23

Hepatic encephalopathy: two mechanisms for ammonia accumulation.

Back 23

1. Blood shunting away from the liver

2. Dysfunctional hepatocytes

Front 24

Clinical manifestations of hepatic encephalopathy

Back 24

1. Personality changes

- "Nasty" temperament

2. Confusion

3. Memory Loss

4. Stupor, coma, death

Front 25

Two mechanisms of jaundice.

Back 25

1. Hepatobiliary mechanisms

2. Hematologic mechanisms

Front 26

Intrahepatic obstructive jaundice

Back 26

Hepatocellular damage or obstruction of bile canaliculi. Some hepatocytes function normally, while others are not.

Front 27

Manifestations of intrahepatic obstructive jaundice.

Back 27

Decrease liver ability to excrete bilirubin.

Conjugated and unconjugated hyperbilirubinemia.

Front 28

Extrahepatic obstructive jaundice

Back 28

Bile duct obstruction (cholestasis).

Front 29

Extrahepatic obstructive jaundice

Back 29

Bile duct obstruction (cholestasis).

Front 30

Manifestations of extrahepatic obstructive jaundice.

Back 30

- conjugated bilirubin accumulates in the liver and enters the bloodstream.

- conjugated hyperbilirubinemia

- Light colored stool

- increased excretion of bilirubin in urine.

Front 31

Hemolytic jaundice

Back 31

- Excessive lysis of red blood cells.

- Hepatocytes cannot conjugate and excrete bilirubin as rapidly as it is formed, so bilirubin enter the bloodstream.

- unconjugated hyperbilirubinemia

Front 32

Physiologic jaundice of the newborn.

Back 32

- Common in neonates, particularly those born premature.

Front 33

Physiologic jaundice of the newborn.

Back 33

- Common in neonates, particularly those born premature.

Front 34

Physiologic jaundice of the newborn typically results from:

Back 34

A deficiency in a liver enzyme that conjugates bilirubin, plus an increased hemolysis of fetal erythrocytes.

Front 35

Physiologic jaundice of the newborn is often treated with "bili lights" - phototherapy.

Back 35

Unconjugated bilirubin isomerizes when exposed to UV light. The newly formed molecule is water soluble.

Front 36

Diagnosing jaundice with lab values:

1. conjugated and unconjugated hyperbilirubinemia

2. Conjugated hyperbilirubinemia

3. Unconjugated hyperbilirubinemia

Back 36

1. Intrahepatic obstructive jaundice.

2. Extrahepatic obstructive jaundice.

3. Physiologic jaundice of newborns

Front 37

____________ bilirubin is not water soluble.

Back 37

Unconjugated

Front 38

___________ bilirubin is water soluble. _______ is responsible for _______ bilirubin.

Back 38

Conjugated. Bile secretion.

Front 39

Acute Liver Failure

Back 39

Necrosis or severe impairment of liver cells without preexisting liver disease. Not well understood. Leading cause is acetaminophen overdose.

Front 40

Manifestations of acute liver failure.

Back 40

- Hepatic cells become edematous.

- patchy areas of necrosis and inflammatory cell infiltrates and disrupts the functional liver disease.

- irreversible

Front 41

Chronic liver failure: Cirrhosis of liver

Back 41

Irreversible