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Boards: GI > The Liver > Flashcards

The Liver Flashcards

(73 cards)

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1
Q

Liver Anatomy

A
  • Largest gland in the body: 1-4% total body weight
  • 4 main lobes: L (medial, lateral), R (medial, lateral), quadrate, caudate
  • Each lobe: own arterial supply, venous drainage, biliary system
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2
Q

Biliary System

A

GB: absent in horses, rats

Bile duct terminates in duodenum of dog, bovine

Others share common bile ducts with pancreas: cats, horses, SR

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3
Q

Brief Summary Species Differences

A

–SA: left, right divided into medial, lateral; enlarged caudate lobe that contacts R kidney

–Equine: left divided, entirely within ribcage

–Porcine: deep interlobular fissures (4 lobes - R, L, M, lat) + small caudate lobe that does not contact R kidney

–Bovine: fused lobes, R of midline

–SR: two papillary processes, deeper umbilical fissure

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4
Q

Portal Triad

A

hepatic arteriole, portal venule, bile duct – define perimeter of lobule

hepatocytes radiate outward from central vein

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5
Q

Hepatic Blood Supply

A

Portal vein/circulation: receives blood from GIT, supplies majority of blood flow to liver
 Hepatic Artery = second blood supply
 Portal veins: low PO2, provides O2 DT large volume

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6
Q

Hepatic Blood Flow

A

Hepatic artery blood enters sinusoid directly or through peribiliary capillary plexus, mixes with portal venous blood in low‐pressure sinusoid microvasculature

Blood from gut, spleen, pancreas –> portal vein –> liver sinusoids –> hepatic vein (central vein) –> cava

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7
Q

Three zones sinusoidal hepatocytes?

A

Zone 1 = peritubular
Zone 2 = transitional
Zone 3 = centrolobular

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8
Q

Zone 1

A

peritubular, largest amt of mitochondria/site of most oxidative processes
* Most oxygen

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9
Q

Zone 2

A

Transitional Zone

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10
Q

Zone 3

A

centrolobular, large amount of smooth ER/microsomal enzyme activity
* Major role in metabolism
* Least oxygen

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11
Q

Consequences of increased pressure through portal system?

A

o Increased pressure through portal system –> neovascularization, acquired shunts

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12
Q

MOA Maintenance of Low Portal Pressures

A

 Low basal resistance
 Distensible pre, post sinusoid resistance sites
 Highly compliant hepatic vasculature
 Hepatic artery buffer response (HABR)

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13
Q

HABR

A

 Hepatic artery buffer response (HABR): accumulation of adenosine when blood slows, causes vasodilation of hepatic artery

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14
Q

Blood Supply

A

o **Receives 20-30% CO, ~12% total blood volume received at any given time **

Portal vein: provides 75% blood flow, relatively low oxygen saturation (from GIT)
 Large volume of blood, importance oxygen source for hepatic tissue

Hepatic artery: 25% blood flow
 Helps sustain hepatocellular function (majority O2)
 Blood enters, mixes with portal blood – sinusoidal delivery or via peribiliary capillary plexus

Regulation of HBF largely depends on preportal factors affecting portal vein BF

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15
Q

What are the 6 reflexes involved in maintenance of HBF autoregulation?

A
  1. Pressure flow regulation
  2. Hepatic artery buffer response
  3. Hepatorenal reflex
  4. Metabolic control
  5. Vascular Escape
  6. Reduced portal vein pressure (arteries dilate to compensate)
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16
Q

Pressure Flow Regulation

A

drop in intrahepatic pressure causes liver to expel up to 50% blood volume to increase CO

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16
Q

Hepatorenal reflex

A

hypotension sensed in liver –> renin release from kidney, angiotensinogen I from liver

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17
Q

Metabolic Control of HBF

A

high CO2, low O2 increase arterial blood flow
* Hypercapnia = vasodilation

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18
Q

Vascular Escape

A

arterial VC from SNS stimulation opposed by NO, adenosine release, arterial dilation

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19
Q

Causes Increased HBF

A

Post prandial, glucagon
Beta agonists
Hypercapnia
P450 enzyme induction (barbiturates)
Hepatitis

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20
Q

Causes Decreased HBF

A

Upper abdominal sx
Beta blockade, alpha 1 agonism
Hypocapnia, hypoxia
P450 inhibition (H2 blockers)
Cirrhosis
IPPV/PEEP

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21
Q

Function: protein synthesis

A

Albumin: major contributor to plasma oncotic pressure, transport, binding

Globulins: 75-90% alpha, 50% beta, Immunoglobulin synthesis = endocrine function

Coag Factors:
▪ Fibrinogen
▪ Prothrombin (FII)
▪ Factors V, VII, IX, X, XI, XII, XIII
▪ Prekallikrein
▪ High molecular weight kininogen
▪ Plasminogen
▪ Plasminogen activator inhibitor -1
▪ Alpha 2 antiplasmin
▪ Antithrombin
▪ Protein C/S
▪ Performs vitamin K dependent carboxylation of 2, 7, 9, 10, protein C/S

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22
Q

Metabolism

A

Carbohydrates: gluconeogenesis, glucose oxidation
 Glycogenesis, glycogenolysis, glycogen store

Lipids: lipogenesis, lipolysis, FA oxidation
 Ketogenesis, cholesterol/TG synthesis and breakdown
 Lipoprotein synthesis, breakdown

Vitamin absorption, storage, activation

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23
Q

Detoxification, Excretion of Waste Products/Xenobiotics

A

o Synthesis, degradation of amino acids
o Conversion of ammonia to urea
o Filtration, storage of blood – iron, copper, RBC storage
o Bile acids, bilirubin metabolism

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24
First Pass Metabolism
reduces concentration esp after enteral administration, ultimately decreases bioavailability/amt available to systemic circulation
25
Phase I Metabolism
introduces polar groups to drugs, typically inactivates but sometimes activates pro drug Conversation of relatively lipophilic compounds into hydrophilic metabolites = Oxidation, reduction, hydrolysis **CYP450**
26
Induction of CYP450
pentobarb, phenobarb, barbiturates, dexamethasone, omeprazole, rifampin, tramadol
27
Inhibition of CYP450
diltiazem, amiodarone, erythromycin, ketoconazole, itraconazole, omeprazole, ranitidine
28
Phase II Metabolism
CYSTOL conjugation, further hydrophilicity to facilitate drug excretion Primary mechanism: glucuronidation * Cats: reduced ability to form glucuronide conjugates DT limited glucuronyl transferases
29
Role of Kupffer Cells
bacteria, toxins in portal circulation processed by phagocytic Kupffer cells
30
Hepatic Fetal Circulation
* Oxygenated blood travels from placenta via umbilical vein * Mostly bypasses liver via ductus venosus o Closes early in horses, pigs * Flow of blood controlled by sphincter --> enables proportion traveling to heart via liver to be altered * Closure of DV becomes permanent at 2-3 weeks, remnants form ligamentum venosum
31
Abnormalities Present with liver dysfunction?
Low serum albumin, glucose, BUN usually present in liver dysfunction +/- coat factors, globulins
32
ALT
Liver specific cytosolic enzyme – hepatocellular injury in dogs, cats ▪ NOT good indicator of liver dz in LA o Small amt in kidney, heart, muscle
33
ALT Increases
1. Anticonvulsants, CS in dogs 2. Primary, secondary hepatic dz with altered cell permeability (inflammation), necrosis +/- EDO DT toxic effects of retained bile salts on hepatocytes 3. Muscle injury in LA (main source in horses = SkM) 4. Hyperthyroid cats
34
AST
Cytosolic enzyme in wide variety of tissues: muscle, heart, kidney, brain, plasma ▪ Indicator for liver +/- muscle injury in LA, SA ▪ Not organ specific: SkM > liver > CaM Increased AST with normal CK suggestive of hepatic insult
35
AST Increases
Myopathies – muscle trauma/prolonged recumbency, vitamin E/selenium deficiency, infectious myositis ● Persist for longer than increases in CK activity Liver dz: similar to ALT, levels not as high as muscle damage ● More sensitive marker of liver dz injury in cats Mildly increased in hyperthyroid cats
36
ALP
Produced by bile duct endothelium – BDO increases production, cholestatic marker ▪ Cats: specific indicator of liver dz ▪ Cholestasis in dogs, increases before bilirubin ▪ Less utility in large Also produced in bone, kidney, intestines, placenta – multiple isoforms
37
Physiologic ALP Elevations
▪ Age: higher in younger, growing animals, decrease ~3mo, normalize by 15mo – bone isoform, colostrum ▪ Siberian Huskies (familial, benign) ▪ Endogenous corticosteroid release from chronic stress
38
Drug Related ALP Elevations
▪ Dogs only: Glucocorticoids induce production of isoenzyme of ALP ▪ L-ALP induced by anticonvulsants (pheno, pentobarb), steroids
39
Pathophysiologic Increases ALP
▪ Hepatobiliary dz in SA – structural cholestasis (extra or intrahepatic), functional cholestatsis ▪ Neoplasia (DT localized cholestasis), non-hepatic neoplasia ▪ Acute hepatocellular injury ▪ Dogs: hyperadrenocorticism ▪ Increased non-neoplastic osteoblastic activity
40
Sorbitol Dehydrogenase
Cytoplasmic enzyme with highest concentrations in liver, specific indicator of liver dz in all species – indicative of hepatocyte damage ▪ Enzyme of choice for detecting hepatocellular injury in horses, cattle
41
GGT
o Transmembrane protein, expression restricted to luminal surface o Increased with bile flow impairment o Many non hepatic sources: lung, kidney, spleen, intestines, muscle, RBC, mammary gland, repro tract
42
GGT Increases Assoc with Drugs
increase with steroids in dogs
43
GGT Physiologic Increases
▪ Neonates – colostrum, sensitive indicator of passive transfer in cattle ▪ Some donkeys, burros have 2-3x GGT of horses
44
GGT Pathophysiologic Increases
Secondary to biliary hyperplasia - release secondary to damage/necrosis of biliary epithelial cells SA: sensitive indicator of biliary hyperplasia, structural cholestasis LA: biliary hyperplasia, structural cholestasis ● Elevated with GI issues, primary liver dz in horses, high GGT syndrome in race horses Renal injury: expression on membrane of proximal renal tubular epithelial cells, cell injury cases GGT to be shed into urine (not blood) Hyperadrenocorticism in dogs
45
Serum Bilirubin
o Ability of hepatocyte to take up unconjugated bilirubin in blood, conjugate it (render it water soluble), excrete into bile – broken down in GIT by bacteria o Used primarily as a marker of liver dz, supportive evidence of hemolytic anemia
46
Unconjugated/Indirect Bilirubin
Bound to albumin, dominant form of total bilirubin in blood Produced in macrophages from breakdown of heme groups (porphyrin ring) ● Normal metabolism or intravascular/extravascular hemolysis Non-RBC sources ~20% unconjugated bilirubin Water insoluble DT hydrogen bonds btw hydrophilic groups
47
What is the rate limiting step with bilirubin conjugation?
excretion into biliary canaliculi
48
Conjugated/Direct Bilirubin
▪ Renders bilirubin water soluble, normally excreted into bile ● Bile salts form micelles facilitating fat absorption ● Urobilinogen: conjugated bilirubin reduced by bacteria, intestinal enzymes – resorbed, broken down ▪ Form in urine – normal finding in dogs, ferrets ▪ Can pass through glomerular filtration barrier, increase in conjugated bilirubin in blood rapidly spills into urine
49
DDx Increased Total Bilirubin
▪ Horses: fasting, off feed ▪ Neonates, esp foals ▪ Anorexia – horses, cattle ▪ Hemolytic anemia ▪ Liver disease ▪ Cholestasis ▪ Inherited: some sheep, monkeys, rats
50
Bile Acids
▪ Steroids synthesized by hepatocytes from cholesterol, excreted into bile ▪ Emulsify fat in intestine, facilitate nutrient absorption – highly conserved ▪ Increased with: ● Hepatocellular dysfunction ● Abnormal portal flow ● Cholestasis
51
Changes in albumin levels
~80% loss of hepatic function
52
Ammonia
▪ Produced from dietary amino acids, catabolism of amino acids, amines, nucleic acids, glutamine, glutamate in peripheral tissues ▪ Converted in liver via urea cycle to urea, excreted into GIT and urine
53
Ddx Increased Ammonia
● Physiologic following high protein means, strenuous exercise ● Decreased uptake of ammonia DT abnormalities in hepatic portal blood flow, hepatic dysfunction ● Decreased conversion to urea: hepatic dysfunction/abnormal blood flow, inherited disorders in urea cycle, lack or decreased availability of urea cycle ● Increased ammonia production
54
Cholesterol
▪ Most common steroid in body – precursor of cholesterol esters, bile acids, steroid hormones
55
DDX increased cholesterol
● Increased numbers of cholesterol-rich lipoproteins ● Iatrogenic following exogenous corticosteroids in fasted dogs, cats ● Nephrotic syndrome ● Hypothyroidism ● Cholestasis – normally excreted in bile ● DM ● Hyperadrenocorticism – peripheral insulin resistance ● Pancreatitis ● Excessive negative energy balance ● Inherited lipid metabolism disorders
56
Ddx decreased cholesterol
● Decreased production, absorption, genetic defect ● Altered metabolism ● Increased uptake lipoproteins
57
Main Keys for Anesthetizing Liver Patients
Mentation: animals with liver dz may be obtunded (HE) – reversible agents, lower doses, potential for increased context-sensitive half life
58
ACP
negative effects on platelet aggregation in potentially coagulopathic patient, may increase HBF, vasodilation/hypotension; 99% protein bound
59
BZD
Advanced liver dz: potential to cause HE DT accumulation of ammonia, NMDA hyperactivity, decreased ATP  Benzos may aggravate – contraindicated in HE  Flumazenil may minimize
60
Induction Agents
--Only TP avoided --Ket: decreases HBF/DO2, primarily hepatic metabolism - caution when conduction with benzos --Propofol: extra hepatic metabolism, maintains HBF --Etomidate: decreased HBF, DO2 - esterase metabolism
61
Inhalants
o Impairs autoregulatory functions, alteration of HBF in dose-dependent manner  Decrease in HBF  decreased DO2, exacerbated with hypotension  PPV: decrease VR, especially in hypovolemic patients o Decreased drug clearance, hepatocellular damage
62
Halothane
HEPATOTOXIC
63
Ascites
Negative Prognostic indicator with liver dz
64
Anesthetic Concerns Assoc with Liver Dz
o HE: high concentrations of endogenous benzodiazepine receptor agonists, uniquely sensitive to drugs that exert action on GABA receptors o Hypokalemia o Hypoglycemia o Hypoalbuminemia o Ascites o Coagulopathy o Hypotension o Impaired drug metabolism
65
US-Guided BX under sedation
o Ideal to have reversible protocol: benzos +/- opioids +/- a2s o Monitoring, flow by oxygen important o **Vasovagal hypotension reported after cutaneous liver bx** o **Bleeding = risk, should be monitoring**
66
Cholecystectomy, EHBDO
o High morbidity and mortality o Creatinine, low blood pressure associated with mortality ▪ Especially with pancreatitis and bile peritonitis o Often hypercoagulable o Dogs with Cushings often predisposed
67
Hepatic Neoplasia
o Hemorrhage = concern, consider blood typing/cross matching o Decisions to transfuse based on several factors: HCT, speed/amt of blood loss, hemodynamic stability o Venous return should be evaluated: CVP, ABP waveform o Hepatocellular carcinoma ▪ Increases in ALT/AST negative prognostic indicator ▪ Coagulopathies can complicate
68
PSS
Anomalous vessels flowing from portal circulation without passing through liver ▪ No liver metabolism when bypassing liver o Non-specific signs: hypoglycemia, low albumin, coagulopathies, altered drug response HE, seizures seen with PSS ▪ Humans: flumaz may improve mental status DT intrinsic BDZ like compounds o CRP may be elevated: supports involvement of inflammatory process
69
Interventional Radiology
o Must ensure complete immobilization during coil placement for PSS ▪ NMBA: Atricurium or cisatricurium often used ▪ Inspiratory hold may be used as well o Patients may be hypothermic o Monitor ABP, CVP; support with IV fluids and inotropes
70
LAs
Amides: directly metabolized by liver, potential for prolonged effect
71
Opioids
Humans: morphine causes **spasm of sphincter of Oddi,** increases pressure in gallbladder - not demonstrated in veterinary patients o May take longer to metabolize opioids vs healthy patients, analgesic intervals altered o **Remifentanil:** plasma esterase hydrolysis, rapid elimination, short context sensitive half life
72
NSAIDS
All have potential to cause hepatic injury ▪ Intrinsically – aspirin, acetaminophen ▪ Idiosyncratic – Particularly Cox2 selective, unpredictable- not dose related Unknown if administration safe in patients with preexisting hepatic disease ▪ May also impair coagulation and hemostasis o Should be avoided or closely monitored

Boards: GI (4 decks)

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