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AS - N935 Advanced Patho II > Hepatic Physiology > Flashcards

Hepatic Physiology Flashcards

1
Q

Liver Functions

A

Removes potentially toxic byproducts of certain medications
Metabolizes or breaks down nutrients from food to produce energy when needed
Helps body fight infection by removing bacteria from the blood
Prevents nutrient shortages by storing vitamins, minerals, and sugar
Produces most proteins needed by the body
Produces bile a compound necessary to digest fat and absorb vitamins A/D/E/K
Produces clotting factors

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2
Q

How many lobules in the liver?

A

50,000-10,000

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3
Q

Liver Lobule Structures

A 
HEXAGON CYLINDER
Portal vein
Sinusoids (capillaries)
Central vein
Hepatic artery
Bile canaliculi & bile duct
Space of disse & lymphatic duct
Hepatic cellular plates
Kupffer cells (macrophages)
Interlobular septa
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4
Q

Lymph Production

A

20mL lymph/day

50% liver

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5
Q

Hepatic Blood Flow

A

Liver receives its blood supply from the portal vein and hepatic artery
≈ 1,500mL/min (25-30% CO)
8-9 seconds blood to traverse from portal vein to the central vein; promotes sufficient time blood in contact with hepatocytes & Kupffer cells

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6
Q

Portal Vein

A

Brings blood from the intestines
Supplies 50-55% liver O2 requirement
SaO2 85%
≈ 1,100mL/min (70-75%)
Blood flow dependent on GI tract & spleen (ΔP upstream blood flow)
α1 adrenergic & D1 dopaminergic receptors

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7
Q

Hepatic Artery

A 
Brings fresh blood from the heart
Supplies 45-50% liver O2 requirement
SaO2 98-100%
≈ 400mL/min (25-30%)
Blood flow dependent on metabolic demand
Autoregulation
α1 β2 adrenergic, D1 dopaminergic, & cholinergic receptors
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8
Q

Portal Vein Pressure

A

Average 9mmHg

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9
Q

Hepatic Vein Pressure

A

Average 0mmHg leaving the liver & entering inferior vena cava

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10
Q

Resistance

A 
LOW
Δ P / Q
9mmHg / 1,500mL/min ≈ 6mmHg/L/min
Cirrhosis ↑resistance to blood flow
- Destruction liver parenchymal cells → fibrous tissue that contracts around the blood vessels (bridging fibrosis impedes portal vein blood flow)
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11
Q

Liver Disease Stages

Alcohol-Induced

A

Fatty liver → fibrosis → cirrhosis
Fat deposits cause liver enlargement; strict abstinence can lead to full recovery
Scar tissue forms; recovery possible but scar tissue remains
Connective tissue growth destroys liver cells; irreversible damage

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12
Q

Cirrhosis CAUSES

A 
Most common = alcoholism
Viral hepatitis A/B/C
Bile ducts obstruction
Bile ducts infection
Poison ingestion (Carbon tetrachloride CCl4 - dry cleaning)
Non-alcoholic fatty liver disease
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13
Q

Alcoholic Fatty Liver

A

Lipid deposits w/in hepatocytes
Repeat exposure to toxins can directly lead to fibrosis & cirrhosis
Micronodular cirrhosis - non-functioning liver cells

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14
Q

Non-Alcoholic Fatty Liver Disease

A

NAFLD

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15
Q

Non-Alcoholic Steatohepatitis

A

NASH

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16
Q

SNS Activation →

A

Hepatic artery & mesenteric vessel vasoconstriction ↓hepatic blood flow

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17
Q

Vascular Functions

Blood Reservoir

A

EXPANDABLE organ
Able to store large quantities of blood in hepatic vessels
Normal liver blood volume ≈ 450mL
Liver expands in response to ↑R atrium pressure → back pressure
0.5-1L blood storage in hepatic veins & sinusoids (commonly occurs w/ CHF)
Low pressure (ex: hemorrhage) blood shifts from hepatic veins & sinusoids into the central circulation as much as 300mL (blood “donation”)

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18
Q

Vascular Functions

Blood Cleansing

A

Portal vein blood +bacteria
Hepatic macrophages - Kupffer cells
Kupffer cells line hepatic venous sinusoids cleanse the blood
- Phagocytose debris, viruses, proteins, & particulate matter
- Release enzymes, cytokines, & other chemical mediators
Monocyte-macrophage system aka reticuloendothelial system

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19
Q

Vascular Functions

Lymph Flow

A

Sinusoid pores = extremely permeable & allow easy fluid & protein passage into the spaces of Disse
↑3-7mmHg above normal hepatic venous pressure results in excessive amounts lymph fluid → back-up
Lymph fluid leaks through outer liver capsule surface into the abdominal cavity
↑10-15mmHg hepatic venous pressure ↑lymph flow 20x normal → “sweating” from the liver surface w/ large amounts free fluid entering abdominal cavity = ascites
Portal vein blockage ↑GI tract pressure w/ fluid transudation via gut into the abdominal cavity = ascites

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20
Q

Metabolic Functions

Carbohydrate Metabolism

A

Glucose metabolism
All cells utilize glucose to produce ATP energy
Glycogen storage
When glycogen storage at max capacity glucose converted to fat
Insulin enhances glycogen storage
Epi & glucagon enhance glycogen breakdown (glycogenolysis)
Hepatic glycogen stores depleted after 24hr fast
Gluconeogenesis (↓glucose → new glucose released from fat breakdown)
Able to convert amino acids, glycerol, pyruvate, & lactate to glucose (all compounds contain carbon)

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21
Q

↑Gluconeogenesis

A

Glucocorticoids
Catecholamines
Glucagon
Thyroid hormone

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22
Q

↓Gluconeogenesis

A

Insulin

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23
Q

Metabolic Functions

Fat Metabolism

A

When carbohydrate storage capacity saturated, the liver converts excess CHOs ingested into fat
Fatty acids used as fuel or stored in the adipose & liver (triglycerides)
Able to used fatty acids directly as energy source

  • Fatty acid oxidation to supply energy (derive energy from triglycerides via β oxidation)
  • Synthesis of large amounts cholesterol, phospholipids, & lipoproteins
    80% cholesterol converted to bile salts & secreted into bile (emulsifies fat)
  • Fat synthesis from CHO & proteins
    After fat synthesized transported in lipoproteins to adipose tissue to be stored
24
Q

Metabolic Functions

Protein Metabolism

A

CRITICAL LIVER FUNCTION w/o protein metabolism death will occur w/in days

  1. Protein deamination - required to utilize energy or before converted to carbohydrates or fats
  2. Urea formation to remove ammonia from body fluids - w/o urea ammonia plasma concentration will rapidly rise → hepatic coma → death
  3. Plasma protein formation 90% 15-50g/day - Albumin, α1 antitrypsin, coagulation factors
  4. Amino acid synthesis & other compound synthesis from amino acids - transamination
25
Q

Metabolic Functions

Drug Metabolism

A

Hepatic biotransformation - end products are inactivated or ↑H2O solubility to excrete via urine or bile
Phase 1: CYP450 90% oxidation & reduction (hydrolysis, hydration, dehalogenation)
Phase 2: Conjugation (sulfation, glucoronidation, glutathione conjugation, acetylation, amino acid conjugation, methylation)

26
Q

CYP450 Induction

A

Ethanol (alcohol), barbiturates, ketamine, benzodiazepines
↑enzyme production that metabolizes drugs
Enzyme induction → tolerance & cross-tolerance

27
Q

CYP450 Inhibition

A

Ranitidine, Amiodarone, & Ciprofloxacin

Prolong other drug effects via CYP450 inhibition

28
Q

Phase 1 Cytotoxic

A

Phase 1 reaction products may be more active than the parent compound or rendered cytotoxic

  • Acetaminophen → glutathione
  • Isoniazid
  • Halothane (hepatitis)
29
Q

Drugs Dependent on Hepatic Blood Flow

A

Lidocaine, Morphine, Verapamil, Labetalol, & Propranolol high rate hepatic extraction from circulation
↓metabolic clearance typically d/t ↓hepatic blood flow NOT hepatocyte dysfunction

30
Q

Normal Lidocaine Metabolism

A

1st pass pulmonary effect
Half-life = 1.8hr
Vd = 1.32L/kg
Clearance = 10mL/kg/min

Liver disease ↑half-life ↑Vd ↓clearance

31
Q

Phase 2 Reactions

A

May or may not follow Phase 1 reaction
Substance conjugation w/ H2O soluble metabolite
Most common = glucuronide (large, charged molecule) → polar & water-soluble
Sulfate, taurine, glycine
Conjugated substances are then excreted via urine or bile

32
Q

Metabolic Functions

MISCELLANEOUS

A

Vitamin storage site - A, B12, D, E, & K
Fe storage as Ferritin
Coagulation factors - vitamin K required cofactor to synthesis Factors II (prothrombin), VII, IX, & X
Primary degradation site thyroid hormone, insulin, steroid hormones, glucagon, & ADH

33
Q

Bile Formation

A

Hepatocytes continuously secrete bile salts, cholesterol, phospholipids, & conjugated bilirubin into the bile canaliculi
Bile ducts form L & R hepatic ducts → hepatic duct → cystic duct → common bile duct
Flow via the common bile duct controlled by Sphincter of Oddi
Gallbladder = bile reservoir
Cholecystokinin - hormone released from intestinal mucosa in response to fat & protein that causes gallbladder contraction, Sphincter of Oddi relaxation, & bile ejection into the small intestine

34
Q

Bilirubin

A

Hgb degradation → bilirubin

Excreted into the bile & eliminated via feces

35
Q

Hemoglobin →

A

Globin + Heme

36
Q

Heme →

A

Fe + Pyrrole rings

37
Q

Pyrrole Rings →

A

Biliverdin

38
Q

Biliverdin →

A

Free bilirubin

39
Q

Free Bilirubin →

A

Bilirubin + Albumin
Unconjugated or indirect bilirubin
Absorbed via hepatocytes & released from Albumin
Bilirubin then conjugated w/ glucuronide & sulfate

40
Q

Conjugated Bilirubin

A

Direct bilirubin = TOXIC

Excreted from hepatocytes via active transport process into bile canaliculi & then into intestines

41
Q

Hemoglobin BINDING

A

O2 binds to Fe
CO2 binds to Nitrogen
Carbon monoxide preferentially binds to Fe (kicks off oxygen)
- Treatment = hyperbaric chamber ↑atmospheric pressure to drive off CO

42
Q

Jaundice

A

Excess bilirubin in the ECF
Total bilirubin >3mg/dL
- Unconjugated or conjugated
Common causes: ↑RBC destruction (hemolytic), bile duct obstruction, or damage to hepatocytes preventing excretion into GI tract (obstructive)

43
Q

Hemolytic Jaundice

A

RBCs rapidly hemolyzed
↑bilirubin production ↑unconjugated bilirubin (free/indirect) hepatocytes unable to process (conjugate) d/t overwhelmed
1° ↑unconjugated bilirubin
2° ↑conjugated (direct) bilirubin
Normal excretion
↑urobilinogen formation & urinary excretion

44
Q

Obstructive Jaundice

A

Most often d/t common bile duct obstruction (i.e. gallstone or malignancy)
Also caused by damage to hepatic cells (hepatitis - hepatocyte inflammation)
Normal conjugated bilirubin formation but unable to pass from the liver to intestines
Conjugated bilirubin enters blood d/t back-up → rupture bile canaliculi & directly emptying bile into the lymph system
1° plasma bilirubin = conjugated form
↑conjugated (direct) bilirubin
TOTAL obstruction - NO conjugated bilirubin able to reach intestines to be converted into urobilinogen ჻ no urobilinogen reabsorbed into blood & excreted via kidneys → urobilinogen urine test = completely negative

45
Q

Liver Function Tests

A 
Not sensitive or specific
Liver synthetic function:
- Serum albumin
- Prothrombin time (PT or INR)
- Cholesterol 
- Pseudocholinesterase
Large functional reserve ჻ lab tests may be NORMAL in present cirrhosis
Parenchymal (hepatocellular dysfunction) vs. obstructive (biliary excretion) disorders
46
Q

Serum Bilirubin

A

Total 0.3-1.1 (<1.5mg/dL) reflects balance b/w production & biliary excretion
Unconjugated 0.2-0.7
Conjugated 0.1-0.4 TOXIC

47
Q

Serum Aminotransferases (Transaminases)

A

Measurements reflect hepatocellular integrity
Aspartate aminotransferase AST 10-40u/mL
Non-specific (heart, skeletal muscle, kidneys)
Alanine aminotransferase ALT 5-35u/mL
More specific primarily located in the liver

Mild elevations >300iu/L (cholestasis or metastatic disease)
Absolute levels poorly correlated w/ hepatic injury degree in chronic liver disease
Absolute levels in acute liver disease - drug overdose, ischemic injury, or fulminant hepatitis

48
Q

Serum Alkaline Phosphatase

A

10-30u/mL
Alkaline phosphatase produced by liver, bone, small bowel, kidneys, & placenta
Excreted via bile
1° circulating comes from bone
Biliary obstruction Alk Phos synthesized & released into circulation
2x normal elevation associated with hepatocellular injury (blockage) or hepatic metastatic disease
↑elevations indicate intrahepatic cholestasis or biliary obstruction

49
Q

Serum Albumin

A

Synthetic function
3.5-5.5g/dL
Long half-life (20 days)
Value initially normal in acute liver disease
Serum albumin <2.5 generally indicates chronic liver disease, acute stress, or malnutrition
Hypoalbuminemia also occurs d/t ↑albumin loss via urine (nephrotic syndrome) or GI tract (enteropathy w/ protein loss)

50
Q

Blood Ammonia

A

Normal NH3 47-65mmol/L (80-110mg/dL)
↑NH3 reflects hepatic urea synthesis disruption
Marked elevations usually severe hepatocellular damage → hepatic encephalopathy

Ammonium = NH4

51
Q

Prothrombin Time

A

12-14sec
PT >3-4sec as compared to control = significant
Corresponds to INR 1.5 (international normalized ratio)
Measures fibrinogen, prothrombin (factor II), factor V, VII, & X
Factor VII short half-life therefore PT useful to evaluate hepatic synthetic function in patients w/ acute or chronic liver disease

52
Q

Pre-Hepatic

A

Bilirubin overload
↑unconjugated bilirubin
No change: AST/ALT, alk phos, PT, albumin
Causes: 1° hemolysis, hematoma reabsorption, bilirubin overload (whole blood transfusion)

53
Q

Intra-Hepatic

A

Parenchymal/hepatocellular dysfunction
↑conjugated bilirubin
Markedly ↑AST/ALT
No change alk phos (slight ↑ w/ disease progression/duration)
Prolonged PT
↓albumin
Causes: Hepatitis, drugs, sepsis, arterial hypoxemia, CHF, cirrhosis

54
Q

Post-Hepatic

A 
Cholestasis
↑conjugated bilirubin
Normal to slightly ↑ AST/ALT
Markedly ↑alk phos
No change to prolonged PT
No change to ↓ albumin
Causes:  Cancer, stones, sepsis → inflammation
55
Q

Anesthesia Effects on Hepatic Function

A

↓hepatic blood flow (direct & indirect)
Overventilation → vasoconstriction
Anesthetic drugs α1 adrenergic agonist, β adrenergic blockers, vasopressin
Endocrine stress response ↑catecholamines, glucagon, cortisol (response blunted d/t anesthesia)
Carbohydrate & protein stores are mobilized → hyperglycemia & negative nitrogen balance
Opioids cause Sphincter of Oddi spasm ↑biliary pressure
Mild postop liver dysfunction d/t ↓hepatic blood flow, SNS stimulation, & surgical procedure
Most common cause postop jaundice = bilirubin over-production d/t large hematoma reabsorption & RBC breakdown following transfusion
Halothane hepatitis - Methoxyflurane, Enflurane, Isoflurane (typically after second exposure w/in 28 days)

56
Q

Anesthetic Agent Metabolism

A 
Halothane 20%
Enflurane 2.5%
Sevoflurane 1%
Isoflurane 0.2%
Desflurane 0.02%

AS - N935 Advanced Patho II (20 decks)

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