Hepatic Failure

Front 1

what processes lead to portal HTN

Back 1

1. increased resistance leading to increased sinusoidal pressure due to deposition of collagen
2. endothelial cell dysfunction resulting in decreased NO production and increased endothelin-1 production
3. vasodilation of splanchnic arterioles secondary to increased NO production increased blood flow through portal system and decreases effective intravascular volume which activates RAAS

Front 2

what deposits ECM resulting in increased resistance blood flow through the liver

Back 2

stellate-derived myofibroblasts

Front 3

differentiate intrahepatic portal vein obstruction from prehepatic portal vein obstruction on physical exam

Back 3

intrahepatic will show caput medusa on exam while prehepatic will not

Front 4

3 physical exam findings that indicate the presence of portal HTN

Back 4

splenomegaly
caput medusa
jaundice

Front 5

why does ascites develop intrahepatic and posthepatic but no prehepatic portal HTN

Back 5

ascites develops due to increased sinusoidal pressure and allow fluid and protein to leak into the peritoneal cavity, prehepatic does not lead to increased sinusoidal pressure

Front 6

what is hepatic wedge pressure (HVPG)

Back 6

measures the difference between the portal vein pressure and the SVC pressure
*normal is 3-5 mmHg

Front 7

in what two situations will HVPG be increased

Back 7

cirrhosis - intrahepatic sinusoidal blockade
radiation therapy - post-sinusoidal blockade

Front 8

in what situations (and cause) will HVPG be normal in the presence of portal HTN

Back 8

pre-sinusoidal - schistosomiasis
pre-hepatic - portal vein thrombosis
post-hepatic - Budd-Chiari syndrome

Front 9

what histilogic features of hepatic sinusoids differentiate them from other capillary beds

Back 9

contain fenestrae and lack a BM so they are more permeable to protein

Front 10

calculate SAAG

Back 10

(serum albumin concentration) - (ascetic albumin concentration)

Front 11

differentiate a SAAG of greater than or less than 1.1 mg/dL

Back 11

SAAG > 1.1 mg/dL seen in portal HTN (transudative)
SAAG < 1.1 mg/dL seen in peritoneal malignancy or infection (exudative)

Front 12

differentiate between sinusoidal portal HTN seen in cirrhosis from post-sinusoidal portal HTN because both have a SAAG of > 1.1 mg/dL

Back 12

cirrhosis (sinusoidal) - ascitic albumin is < 2.5 mg/dL
RHF or veno-occlusive disease (post-sinusoidal) - ascitic albumin is > 2.5 mg/dL

Front 13

why does cirrhosis have less ascitic albumin than that found in RHF or veno-occlusive disease

Back 13

between the ECM accumulation caused by stellate-derived myofibroblasts cause less protein to be able to traverse the hepatic sinusoids

Front 14

what causes hepatic encphalopathy

Back 14

accumulation of toxins in the CNS due to impaired urea cycle leading to increased systemic levels of NH3

Front 15

what causes astrocytic dysfunction and proliferation leading to Alzheimer type II astrocytosis

Back 15

build of NH3 causes the astrocytes to convert it to glutamine, this is the only mechanism in the CNS to clear ammonia

Front 16

how does ammonia accumulation lead to decreased excitatory neurotransmission (3)

Back 16

1. neurons are unable to convert glutamine to glutamate due to excessive NH3
2.increased GABA production by intestinal bacteria which bypasses the liver
3. increased aromatic AA serve as precursors for false excitatory neurotransmitters and cause depletion of true ones

Front 17

what causes asterixis

Back 17

neuroinhibition due to increased GABA and decreased glutamate, NE, and E

Front 18

how do the following precipitate hepatic encephalopathy: hypokalemia, metabolic alkalosis, GI bleeding, high protein diet, constipation, and infection

Back 18

hypokalemia - stimulates renal PCT to increase NH4 synthesis as well as stimulating development of metabolic alkalosis
metabolic alkalosis - increases conversion of NH4 --> NH3
GI bleeding - increased substrate for NH3 production
high protein diet - increases NH3 production
constipation - increase production of NH3 by bacteria
infection - increases tissue catabolism

Front 19

what test is useful for predicting the severity of acute liver injury

Back 19

PT - increased PT indicates that the vitamin K dependent clotting factors are not being made

Front 20

hemodynamid findings seen in chronic liver failure

Back 20

low systemic vascular resistance (AV shunting)
high CO
increased HR

Front 21

what two things cause low SVR in patients with chronic liver failure

Back 21

NO and substance P - causes AV shunting

Front 22

what is the mechanism of hepatorenal syndrome

Back 22

renal vasoconstriction of afferent arteriole secondary to sympathetic nervous system responding to decreased vascular resistance and decreased PGE2 production

Front 23

expected serum findings in hepatorenal syndrome

Back 23

hypervolemic hyponatremia - due to stimulation of vasopressin secondary to decreased effective intravascular volume
increased creatinine > 1.5 mg/dL

Front 24

what is orthodeoxia

Back 24

deoxygenation in the upright position

Front 25

what is the mechanism behind orthodeoxia

Back 25

1. intrapulmonary shunts due to increased pulmonary vascular angiogenesis
2. decreased time for O2 to diffuse
3. increased distance between the RBC and alveolus from vasodilation

Front 26

what are the characteristic blood findings in hepatopulmonary syndrome

Back 26

increased (A-a)O2 gradient
PaO2 < 70 mmHg
PaCO2 30-35 mmHg

Front 27

which gonadal hormone is increased in men with liver failure

Back 27

estrogen due to increased peripheral conversion of androgens to estrogen

Front 28

which gonadal hormone is decreased in women with liver failure

Back 28

progesterone

Front 29

why do patients with cirrhosis and ascites develop hyperglycemia

Back 29

seen postprandally due to decreased glucose utilization in muscle and decreased glucose extraction

Front 30

why do patients with end-stage parenchymal failure develop hypoglycemia

Back 30

hepatic glycogen depletion and decreased gluconeogenesis

Front 31

two acid-base abnormalities that commonly develop in chronic liver failure

Back 31

anion-gap metabolic acidosis - build up of lactate due to AV shunting
respiratory alkalosis - CNS stimulation because of mild hypoxemia

Front 32

at what pressure does portal HTN exist

Back 32

portal pressure > 12 mmHg

Front 33

what is a predisposing factor for developing spontaneous bacterial peritonitis

Back 33

large volume of ascites with low albumin content (<1.5 g/dL)

Front 34

patient with ascites presents with fever, abdominal pain, worsening encephalopathy and > 250 PMNs in ascitic fluid

Back 34

bacterial peritonitis

Front 35

serum cholesterol in hepatic failure

Back 35

decreased due to decreased hepatic synthesis along with decreased intestinal absorption

Front 36

manifestations of systemic vascular dilation that occur in areas drained by the SVC

Back 36

spider telangectasias

Front 37

ethanol abuse and effects on phase I and II hepatic enzymes

Back 37

increases phase I leading to conversion of benign medications to more toxic intermediates
decrease phase II resulting from glutathion deficiency
*increased phase I and decreased phase II make it difficult to handle drugs like acetaminophen