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
*
