Name two mechanisms that regulate hepatic arterial blood flow: _____ and _____ Neural regulation and Humoral regulation Metabolic regulation and Hepatic buffer response Vasodilation and Vasoconstriction Intrinsic regulation and Extrinsic regulation

Metabolic regulation and Hepatic buffer response

1.2 Liver

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Medicine - Hepatology

user_kumartyv Created by 9 mon ago

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Name two mechanisms that regulate hepatic arterial blood flow: _____ and _____

In a healthy patient, _____% of hepatic blood volume can be transferred to central circulation.

Why is PT a useful lab for detecting *acute* liver failure? Due to the short half-life of liver-derived _____

Most common blood-borne infection in the U.S.? _____

Which organ systems does advanced cirrhosis affect? _____

Which volatile anesthetic best preserves hepatic blood flow and oxygenation? _____

Your patient is coming in for an elective surgery. The patient has acute hepatic disease. Do you delay the case? _____

Glucagon is a vaso(dilator/constrictor)? _____

High concentrations will decrease the liver's response to _____; _____ may be a more effective way to vasoconstrict the patient.

How much of a patient's cardiac output goes to the liver? _____

The hepatic artery is responsible for _____% of the blood supply to the liver.

The hepatic artery is responsible for _____% of the O2 supply to the liver.

The portal vein is responsible for _____% of the blood supply to the liver.

The portal vein is responsible for _____% of the O2 supply to the liver.

Tributaries of the portal vein include gastric, esophageal, mesenteric, and _____ veins.

Hepatic flow regulation allows the liver to get what it needs so that it can serve its purposes for what part of the body? _____

Intrinsic hepatic blood flow regulation is based on _____ and local metabolic needs.

Extrinsic regulation of hepatic blood flow involves neural (sympathetic) or humoral (epi, NE, vasopressin, etc...) mechanisms. True or False? _____

Intrinsic regulation only occurs with the (portal venous/hepatic arterial) flow. _____

What is the hepatic buffer mechanism? Decreased portal vein flow leads to decreased washout (increased build-up) of _____, which dilates the hepatic artery.

What is the maximum response of the hepatic buffer mechanism? _____% increase in hepatic artery flow in response to a 50% decrease in portal vein flow.

What can diminish or abolish the hepatic buffer mechanism? (3) _____

Decreased portal blood pH and O2 content or increased PCO2 leads to (increased/decreased) hepatic artery blood flow. _____

Metabolic regulation of hepatic arterial flow is most active in a (postprandial/fasted) state. _____

Portal venous pressure is dependent upon splanchnic arteriolar tone, portal venules, and post-sinusoidal tone (hepatic venules). True or False? _____

Stimulation of α1 receptors in the liver will (increase/decrease) blood volume. _____

Stimulation of α1 receptors in the liver will (increase/decrease) blood flow. _____

Which has a greater effect on hepatic blood flow: epi & NE or dopamine? _____

Hepatic arterial beds contain (α/β) adrenergic receptors. _____

Portal venous beds contain (α/β) receptors. _____

_____ produces long-lasting arteriolar dilation and antagonizes arterial constriction from other responses (like catecholamines).

This is an example of (intrinsic/extrinsic) (neural/humoral) regulation. _____

Marked constriction of _____ and _____ vasculature is caused by angiotensin.

Reduced _____ outflow is a result of angiotensin's effect on the liver.

Reduced total _____ blood flow is a consequence of angiotensin's action.

_____ causes intense vasoconstriction of splanchnic arterial vessels while decreasing portal venous resistance.

In high doses, _____ and _____ reduce portal hypertension and esophageal variceal bleeding.

Vasopressin and octreotide help with portal hypertension by (increasing/decreasing) arterial inflow and (increasing/decreasing) portal venous pressure. _____

This will result in (increased/decreased) pressure on esophageal varices. _____

Which one is used more often for reducing portal hypertension? _____

Is hepatic innervation more sympathetic or parasympathetic? _____

PNS stimulation of the liver causes blood glucose to (increase/decrease) due to increased _____ synthesis and glucose uptake. _____

Effects of SNS stimulation in the liver: Hepatic vascular resistance (increases/decreases). _____

Hepatic blood volume (increases/decreases) due to SNS stimulation. _____

Blood glucose (increases/decreases) due to increased gluconeogenesis and glycogenolysis. _____

Functions of the liver include blood reservoir, bilirubin excretion, protein synthesis, metabolic, endocrine, drug metabolism, immunologic, and _____.

Up to _____% of the total blood volume is stored in the liver.

In a patient with severe liver dysfunction, you will transfuse blood (more/less) readily. _____

SNS suppression by anesthetic agents attenuates the auto transfusion response of the liver and predisposes the patient to _____ decompensation.

Severe liver disease impairs the normal vaso(dilatory/constrictive) response of the body, exacerbating hypovolemia and hypotension. _____

_____% of hepatic blood volume can be transferred to central circulation within seconds.

Which coagulation factors are not produced in the liver? _____

Which coagulation factors are vitamin K dependent factors? _____

The liver synthesizes _____, thereby modulating platelet production.

What modulators of fibrinolysis & clotting does the liver produce? _____

The liver produces clotting factors and modulates their _____.

The half-lives of liver-derived coagulation factors are (short/long). _____

Which is the shortest liver-derived coagulation factor? _____

What test may be a useful monitor in acute liver failure? _____

A patient is on Coumadin, and Vitamin K is given. Failure of normalization of PT/INR following vitamin K indicates underlying _____ dysfunction.

Bilirubin is the end product of _____ degradation; about _____% comes from _____ breakdown.

Endocrine function of the liver includes synthesis & secretion of what 3 endocrine hormones? _____

Biotransformation of what endocrine component occurs in the liver? _____

Unconjugated bilirubin is bound to albumin and transported to the _____, where albumin & bilirubin are separated.

Bilirubin is primarily conjugated with what acid? _____

Conjugated bilirubin is excreted into what? _____

Conjugated bilirubin passes into _____, converted to _____ and excreted.

~10% absorbed in intestine and returns to liver via the _____ vein, where it is sent back through bile to the small intestine. What's another name for this? _____

Dietary carbs arrive in the liver via the _____ vein.

After a meal (postprandially) glucose is extracted from the _____ vein with the help of _____.

Excess glucose is converted to what? _____

How much glycogen can the liver store? _____

Initially, you're going to use _____ to break down glycogen.

Later, you're going to get glucose via muscle & fat catabolism and _____.

Primary reason we have hyperglycemia in chronic liver disease? _____

Hyperglycemia is a(n) (early/late) symptom of chronic liver disease. _____

Primary reason we see hypoglycemia in chronic liver disease? (3) _____

Hypoglycemia is a(n) (early/late) symptom of chronic liver disease. _____

Hypoglycemia is also seen with a large hepatocellular cancer due to (increased/decreased) uptake by the tumor. _____

Excess carbs, lipids, and proteins get synthesized into what? _____

Fatty acids are then esterified to (3) _____

After this, they're packaged into _____ for transport to _____.

The liver is capable of synthesizing (essential/non-essential) amino acids. _____

In the liver, proteins are degraded to amino acids in hepatic _____.

Then they're used to produce _____ and metabolize _____.

They're further deaminated to (3) _____

In the liver, ammonia is converted to _____, which is then excreted by the kidneys.

Patients with liver failure can't degrade ammonia properly, leading to increasing serum ammonia levels and what? _____

Does a normal BUN mean good kidney function? _____

_____ is the major plasma protein synthesized by the liver.

Albumin is the primary determinant of colloid _____ pressure and is an important transport mechanism that binds many anesthetic drugs.

Half life of albumin? _____

Are albumin levels a useful indicator for acute liver disease? _____

Where is pseudocholinesterase made? _____

Can patients with liver disease receive succinylcholine? _____

Pseudocholinesterase is required for degradation of: (3) _____

What are Kupffer cells? _____

Kupffer cells make up about _____% of the hepatic mass.

An impairment in Kupffer cell function is often a precursor to _____ and _____, particularly following splanchnic ischemia or severe GI pathology.

Initially, give (more/less) NDNMB to a patient with severe liver disease. _____

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