Liver - Anatomy Flashcards
1
Q
How is the liver divided anatomically?
Physiologically?
A
- Anatomic- clinically insignificant but helps to facilitate segmental resection
- four distinct lobes:
- Right and left with falciform ligament btw
- Caudate and quadrate
- four distinct lobes:
- Physiologic- 8 functionally independent segments known as the french (Couinaud) system
- each segment has its own vascular flow and biliary drainage
- reduces M&M if resections are done by segment
- imaging done to create 3D modes for precision
2
Q
Describe the microscopic anatomy of the liver lobule
A
- Hexagonal shape on cross section
- 6 vertically aligned portal canals at corners and central vein at center
- Each portal canal contains:
- connective tissue
- lymphatics
- nerves
- portal triad
- terminal branches portal vein
- hepatic artery
- bile duct
3
Q
How does the Acinus lobule concept differ from the classic lobule?
A
- Small parenchymal mass arranged around a central axis consisting of: terminal hepatic arteriole, portal venule, bile ductule, lymp and nerves
- blood enters the center of the acinus and flows out (centrifugally) to the hepatic venules
- bile flows opposite direction
4
Q
What are the different zones of the Acinus lobule concept?
A
- Zone 1- Periportal zone
- cells are closest to the portal axis, receive blood that is rich in oxygen and nutrients
- major site of oxidative metabolism and conversion ammonia to urea
- Most prone to reperfusion injury
- cells are closest to the portal axis, receive blood that is rich in oxygen and nutrients
- Zone 2- midzonal region
- the arbitrary intermediary transition zone
- “anatomic reserve”
- Zone 3- pericentral
- cells at margin of acinus- receive blood that has exchanged gases and metabolites with cells in zones 1 & 2
- least resistant to metabolic and anoxic damage
- most prone to ischemic damage
- major site of CYP450 and anaerobic metabolism
5
Q
How is the liver innervated?
A
- Stimulation of SNS post-ganglionic T3-T11
- increases hepatic vascular resistance (decreased blood volume)
- increases glycogenolysis and gluconeogenesis (increased bs)
- Stimulation of PSNS
- increases glucose uptake and glycogen synthesis
6
Q
How much of the CO goes to the liver?
How many ml/min to the portal vein? Pressure?
How many ml/min to the hepatic artery? Pressure?
What arteries feed the which organs that get picked up by the portal vein? (PIC)
A
- High flow with low vascular resistance
- CO = 25-27% = 1350 ml/min
- Portal vein- 1050 ml/min
- 75% blood flow, 50% O2 delivery
- pressure = 9 mmHg
- Hepatic artery- 300 ml/min
- 25% blood flow, 50% O2 delivery
7
Q
How is hepatic blood flow regulated?
A
- Hepatic arterioles have a myogenic response to stretching that keeps local blood flow constant, despite changes in BP
- An increase in transmural pressure (BP) causes vasoconstriction, preventing elevation in local bf
- decrease causes dilation, preserving perfusion
- Autoregulation of the hepatic artery is present in metabolically active liver (postprandial hyperosmolarity)
- usually absen in the fasted state (most OR patients)
- Volatile agents dose-dependently decrease this response
- pressure-flow autoregulation does not exist in the portal circulation
- **decreases in pH or O2 or increased CO2 increase hepatic artery flow.
8
Q
What is the hepatic arterial buffer response?
A
- Changes in portal venous flow induce reciprocal changes in hepatic arterial flow
- As portal venous flow decreases, adenosine builds up in the piriportal region
- increases in periportal adenosine cause decreased arteriolar resistance and hepatic arterial flow increases
- Increases in portal venous flow washes out adenosine from the periportal region, raising arteriolar resistance and lowering hepatic arterial flow
9
Q
What are some extrinsic influences on portal circulation?
A
- Tone of pre-portal splanchnic organ arterioles regulate portal vein flow
- decreases in pH or PaO2 (portal blood) often associated with increases in hepatic arterial flow
- postprandial hyperosmolarity increases both the hepatic arterial and the portal venous flow.
10
Q
What are the humoral influences on portal circulation?
Which one is a good treatment for portal hypertension and esophageal varicies?
A
- Hepatic arterial bed has alpha 1, alpha 2, and beta 2 adrenergic receptors
- Epi will cause vasoconstriction (alpha receptors) and vasodilation (beta receptor)
- Portal vein has alpha receptors only
- Epi injected into portal vein will cause only vasoconstriction (alpha)
- Dopamine- weak vasoactive effects compared to Epi and NE
- Glucagon
- dose dep relaxation of hepatic arterial smooth muscle
- antagonizes vasoconstrictor responses of the hepatic artery to various physiologic stimuli-including increases in SNS tone
- Angiotensin II-
- severely constricts hepatic arterial & portal venous beds
- markedly ↓ both mesenteric & portal venous flow; blood flow to liver may plummet
- Vasopressin
- intensely constricts the splanchnic arterial bed
- lowers portal venous resistance….. effective treatment for portal hypertension/esophageal varacies
11
Q
How is the liver involved with Lymph?
A
- 50% of lymph is made in the liver
- sinusoidal epithelium is extremely permeable, allowing fluid and proteins into the space of Disse
- protein content in lymph is 6 g/dl (similar to plasma)
- Slight increase in IVC pressure (10-15 mmHg) will increase lymph up to 20x
- sweating from liver surface causes ascites
12
Q
What are the alterations caused by cirrhosis?
A
- Liver parenchymal cells are destroyed and replaced with fibrous tissue that impedes portal blood flow through liver
- Secondary to alcoholism, poison ingestion (carbon tetrachloride), viral disease (hepatitis), bile duct obstruction and infection
13
Q
_____% of liver can be regenerated in animal studies.
Normal liver function can occur after ____% has been resected.
A
70% of liver can be regenerated in animal studies.
Normal liver function can occur after 80% has been resected.
**liver disease impairs ability to regenerate
14
Q
Why is the liver considered a blood reservoir?
A
- Liver is an expandable organ
- Hepatic arteries, veins, and capillaries contain 450 ml blood (10-15% TBV)
- with R heart failure or increased R atrial pressure, liver can accomodate up to an extra L of blood.
- Intense SNS response can significantly decrease blood flow and expell 400-500 ml within seconds
- Anesthetics and liver disease impair this response
15
Q
How does liver disease affect the endocrine system?
A
- altered hormone levels and diminished hepatic synthesis of hormone binding globulins with altered metabolism and receptor regulation leads to significant endocrine abnormalities
- Insulin-like growth factor 1 (somatomedin)- mediates actions of hormones from other endocrine glands
- Angiotensinogen- precursor to Ang II, helps w/ fluid and electrolyte balance
- Thrombopoeitin- stimulates bone marrow precursor cells to differentiate into plts
- T4 conversion to T3 or inactivation
- Inactivation of:
- corticosteroids
- ADH
- aldosterone
- estrogen
- androgens
- insulin
*
16
Q
What is the liver’s immunologic function?
A
- Kupffer cells make up 10% of hepatic mass, lining hepatic venous sinuses and clean blood of toxins, abcteria, etc
- takes <0.01 second for the bacterium to pass into the wall of the kupffer cell after coming in contact with it
- Kupffer cell can produce and recruit inflammatory mediators/neutrophils
- Kupffer cells are impaired in advanced disease
- contributes to sepsis/MODS
17
Q
How does the liver metabolize carbohydrates?
A
- Maintenance of normal blood glucose concentration
- Storage of lg amts of glycogen (75 g or 24 hrs worth)
- Conversion of galactose and fructose to glucose
- gluconeogenesis (from aa and triglycerides)
- formation of many chemical compounds from intermediate products of carbohydrate metabolism
18
Q
How does the liver metabolize lipids?
A
- Beta-oxidation of fatty acids to supply energy for body
- Cholesterol, phospholipids and lipoprotein synthesis
- synthesis of fat from proteins and carbohydrates
19
Q
How does the liver metabolize protein?
A
- Deamination of amino acids
- formation of urea
- removes ammonia from bodily fluids
- plasma protein formation
- amino accid synthesis and interconversions
- can produce 12-50 mg protein/day
20
Q
What kind of vitamins does the liver store?
How much?
A
- Vitamin A- 10 months worth
- vitamin D- 3-4 months worth
- Vitamin B12- >1 yr worth
- Iron as ferritin- “blood iron buffer”
21
Q
Which coagulation factors does the liver produce?
Which ones require vitamin K?
A
- All coagulation factors EXCEPT vWF, VIII, III & IV
- Vitamin K dependent: **Bile required for Vit K absorption
- Prothrombin/Factor II
- factor VII
- factor IX
- factor X
- Proteins C and S
22
Q
The liver produces about ___% of hem.
What part of the metabolism of hgb is the liver responsible for?
A
20%
Hepatocytes responsible for conjugating bilirubin and releasing it into bile and eliminated via alimentary tract
23
Q
How much bile does the liver secrete?
A
- Liver secretes 500 ml/day from common bile duct into duodenum
- contains: conjugated bile salds, cholesterol, phospholipids, conjugated bilirubins, electrolytes
- Bile acids help alkalinize and emulsify the large fat particles to increase surface area for digestion/aiding absorption
- Bile is the means for excretion of waste products from blood (xenobiotics, bilirubin, Ca, and cholesterol)
- Opioids (mu agonists) may interfere with biliary flow by increasing pressure in bile duct or causing SOOS
- antagonized by VA, naloxone, nitroglycerine, atropine, and glucagon
24
Q
What is the liver’s role in pharmacokinetics?
A
- Drugs bind to proteins synthesized by the liver which affects how the drug distributes (Vd)
- Hepatic biotransformation = metabolism of drugs by hepatocytes changing them into inactive water-soluble substances that can be excreted and eliminated via the bile or urine
- Phase I- hydrolysis, CYP450
- Phase II- conjugation
- CYP450- liver has more than 20 diff CYP enzymes
- many oxidate drugs, environmental toxins, steroid hormones, lipids, and bile acids
- Hepatocyte of zone 3 have the highest content of CYP proteins
25
Q
What is the intrinsic clearance concept?
A
- Intrinsic clearance reflects the fraction of the delivered drug load that is metabolized or extracted during a single pass through the liver
- High clearance- clearance at or near rates they transverse the liver
- lidocaine, benadryl, metoprolol
- Low clearance- clearance independent of hepatic flow
- diazepam, acetaminophen, warfarin
- This is more significant when dealing with drugs that are highly protein bound
26
Q
How is hepatocellular damage assessed?
A
- AST- present with damaged liver cells, but can also be caused by other organs (heart, skeletal muscle, brain)
- ALT- only produced by liver injury or necrosis
- LDH- Poor diagnostic specificity for liver disease
- GST- found in multiple organs, sensitive indicator for liver damage
- Best to get during a case
- present in different tissues
- iso-enzyme B is specific to liver
- half life of 90 minutes- levels will quickly drop if there is no more hepatocyte damage
27
Q
How is Bile flow assessed?
A
- Alkaline phosphatase (AP) isoenzymes- generalized screening, idea about damage, but can be elevated with other normal situations
- 5’-nucleotidase- more specific info about if issue is extrahepatic or internal
- Gamma glutamyl transferase (GGT)- not useful anymore
- Serum bilirubin
- conjugated- indicates obstruction
- unconjugated- around surgery caused by hemolysis (lots of work to do)
- issue with hepatocellular dysfunction
- congenital problem
28
Q
How can the liver’s synthetic function be assessed?
good indicators of hepatic functions
A
- Albumin (1/2 life 3 weeks)- half life too long to trend for acute situation
- PT/INR (coag factor 1/2 lives 4 hours to 4 days)- better to trend for an acute situation
