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GI Block > Liver Metabolism BCH & LFTs > Flashcards

Liver Metabolism BCH & LFTs Flashcards

1
Q

__________ is the major source of energy for the liver during the Fed state

A

Glucose (Glycolysis and PPP)

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2
Q

Glucose-6-Phosphate are diverted through the _________ to generate ATP and produce NADPH

A

PPP (Pentose Phosphate Pathway)

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3
Q

______________ is the end-product of glycolysis and is converted to ________ _____ which can enter the TCA cycle to ultimately generate ATP

A

Pyruvate; Acetyl CoA

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4
Q

Excess Acetyl CoA and NADPH in the liver is used to synthesis…

A

fatty acids

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5
Q

Amino acids are used as a major energy source for the liver (True or False)

A

False: used to make liver proteins and other nitrogen compounds

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6
Q

In the early Fasting State, the liver’s main function is to….

A

mobilize glycogen stores to maintain blood glucose

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7
Q

What does the liver use for energy during the Fasting State

A

B-oxidation of fatty acids for Acetyl-CoA

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8
Q

The liver synthesizes __________ __________ from __________ for export to muscles and the brain during the Fasting State

A

Ketone bodies; Acetyl-CoA

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9
Q

The high level of protein catabolism in the liver during the Fasting State generates a large amount of _________, making the Urea Cycle CRITICAL for clearance

A

urea

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10
Q

chemical substances that are NOT normally produced by an organism; pharmaceuticals, antibiotics and pollutants are examples

A

xenobiotics

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11
Q

Xenobiotics are (poorly/very) soluble in plasma

A

Poorly (making them difficult to excrete)

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12
Q

Process by which the liver alters the chemical properties of xenobiotics (unnatural compounds) to change the activity and increase solubility to allow excretion in the urine; involves Phase 1 and 2 reactions

A

Biotransformation

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13
Q

(Phase 1 or Phase 2)
Biotransformation of xenobiotics; carried out by CYP450 enzymes; usually hydroxylation; ROS are an intermediate, which is why massive overdoses can harm hepatocytes

A

Phase 1

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14
Q

(Phase 1 or Phase 2)
Biotransformation of xenobiotics; conjugation reactions to make a xenobiotic more easily excreted (via glucuronidation or sulfate addition)

A

Phase 2

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15
Q

Two primary pathways for the liver metabolism of ethanol

A

1st: Alcohol Dehydrogenases

Back-up: MEOS (CYP2E1 enzymes)

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16
Q

Describe the metabolism of ethanol

A

Ethanol–> Acetaldehyde–> Acetate–> Acetyl-CoA–> Ketone Bodies

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17
Q

(ADH vs. CYP2E1) are the main metabolizers of alcohol at mild-moderate levels; have a low Km for ethanol

A

ADH (Alcohol Dehydrogenase)

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18
Q

(ADH vs. CYP2E1) are the backup metabolizers of alcohol; activated at high ethanol concentrations and produce ROS in the process

A

CYP2E1

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19
Q

Within macrophages, heme oxygenase catalyzes heme into a green pigment known as _____________

A

biliverdin

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20
Q

Biliverdin is a byproduct of heme oxidation, and is subsequently reduced to a red-orange pigment called _____________

A

bilirubin (also called unconjugated bilirubin)

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21
Q

byproduct of heme; red-orange pigment; poorly soluble in the plasma and can cross the blood-brain barrier; bound to plasma albumin the transport from macrophages to hepatocytes

A

Bilirubin

22
Q

How is unconjugated bilirubin safely transported through the blood to hepatocytes?

A

Immediately bound to plasma albumin, and allowed into hepatocytes by Organic Anion Transporting Polypeptides (OATP)

23
Q

What membrane protein allows unconjugated bilirubin into the hepatocytes

A

Organic Anion Transporting Polypeptides (OATP)

24
Q

Enzyme in hepatocytes ER that catalyzes the glucuronization of bilirubin to conjugated bilirubin

A

Uridine Diphosphate Glucuronosyl Transferase (UGT)

25
Q

Conjugated bilirubin is transported into the bile canaliculi via what transporter; RATE LIMITING step of secretion

A

cMOAT (Canalicular Multispecific Organic Anion Transporter) (also known as MRP-2: Multidrug Resistance Protein 2)

26
Q

colon enzyme that removes the glucuronic acid molecules from bilirubin to a colorless compound called urobilinogen

A

beta-glucuronidase

27
Q

Most urobilinogen in colon is converted by bacterial enzymes by…

A

stercobilinogen

28
Q

what gives feces its characteristic dark brown color

A

stercobilinogen (conversion of urobilinogen)

29
Q

Normal concentration of bilirubin in the blood

A

< ~ 1 mg/ml

30
Q

physical characteristic that is due to hyperbilirubinemia; yellow pigmentation of the skin, conjunctival membranes and other mucous membranes

A

Jaundice

31
Q

How does liver get rid of excess cholesterol

A

synthesis of bile acids

32
Q

laboratory tests used to help identify the presence of liver disease; the pattern and degree of elevation can provide information about the underlying etiology, severity, and prognosis of the liver disease; can also be used to monitor response to medical therapy

A

Liver Functions Tests (LFTs)

33
Q

Examples of Liver Function Tests

A 
AST (aspartate)*
ALT (alanine)*
Alkaline phosphatase*
GGT*
Bilirubin
Albumin
PT/INR

*represent liver injury (others represent liver function)

34
Q

Which Liver Function Tests indicate hepatocellular injury

A

AST and ALT (elevations are indicative of injury)

35
Q

Which Liver Function Tests indicate cholestatic injury (bile duct obstruction)

A

Alkaline phosphatase, GGT and Bilirubin

36
Q

markers of hepatocellular injury; “aminotransferases”; they are enzymes that play a role in gluconeogenesis under periods of stress (such as injury)

A

AST and ALT

37
Q

Which is more specific for hepatocyte injury: AST or ALT

A

ALT (AST is present in many tissues besides liver, such as heart, skeletal muscle and brain)

38
Q

LFT that indicates cholestatic injury; is a hydrolase enzyme that is most prominent in the bile canaliculi; an impairment of biliary flow (cholestasis) will result in elevated levels due to back-up

A

Alkaline Phosphatase

39
Q

LFT that indicates cholestatic injury; transfers y-Glutamyl groups between amino acids; concentrated in epithelial cells lining fine ductules; MORE sensitive than Alkaline phosphatase

A

y-Glutamyl Transferase (GGT)

40
Q

In cases of liver injury, levels of ___________ and ___________ will decrease

A

Albumin and clotting factors

41
Q

Pre-hepatic causes of jaundice lead to an elevation of (conjugated/unconjugated) bilirubin

A

unconjugated (or indirect) bilirubin (occurs PRIOR to uptake and conjugation in liver)

42
Q

Post-hepatic causes of jaundice lead to an elevation of (conjugated/unconjugated) bilirubin

A

conjugated (or direct) bilirubin (occurs AFTER the uptake and conjugation in liver)

43
Q

Examples of causes of prehepatic jaundice (unconjugated bilirubin)

A

Hemolysis
Sickle cell crisis
Blood transfusion

(events that occur PRIOR to the uptake of bilirubin and conjugation in the liver)

44
Q

Examples of intrahepatic jaundice (both conjugated and unconjugated bilirubin)

A

Hepatitis
Cirrhosis
Hepatocellular Carcinoma
Primary Sclerosing Cholangitis

45
Q

Examples of post-hepatic jaundince (conjugated bilirubin)

A

Choledocholithiasis
Primary Sclerosing Cholangitis
Pancreatitis
Pancreatic carcinoma (at the head)

46
Q

AR disorder of bilirubin conjugation; caused by alteration of UGT1A1 gene; most common hereditary hyperbilirubinemia syndrome

A

Gilbert Syndrome

47
Q

AR disorder of bilirubin conjugation; caused by alteration of UGT1A1 gene; either absent activity (Type 1) or reduced activity (Type II)

A

Crigler-Najjar

48
Q

AR disorder of bilirubin reuptake and storage

A

Rotor Syndrome

49
Q

In the setting of liver disease, the most important aspect of liver imaging is to evaluate for…

A

biliary duct obstruction

50
Q

If liver imaging does not provide a clear etiology for disease, what else can be done for diagnosis…

A

Biopsy (percutaneous or transjugular)

GI Block (9 decks)

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