D’YOUVILLE COLLEGE
BIOLOGY 307/607 - PATHOPHYSIOLOGY
Lecture 15 - HEPATIC & PANCREATIC DISORDERS
Chapter 14
1.
Review of Liver Anatomy & Physiology:
• anatomy of liver & biliary system (fig. 14 - 1 & ppt. 1):
- largest gland in body; occupies most of the right upper quadrant (right
lobe) & extends across the midline (left lobe)
- biliary tree: the liver secretes bile via right & left hepatic ducts that unite to
form common hepatic duct
- the gall bladder, nestled under the right lobe, communicates with the
common hepatic duct via the cystic duct
- the common bile duct extends inferiorly from union of the common
hepatic and cystic ducts, empties into the duodenal wall, jointly with the pancreatic
duct (= hepatopancreatic ampulla)
- liver lobule: parenchyma is organized into cylindrical columns of
hepatocytes radiating from central vein (fig. 14 - 2 & ppt. 2)
- leaky capillaries (sinusoids) facilitate maximal exchange between
hepatocytes & blood (cleansed by Kupffer cells) (fig. 14 - 3 & ppt. 3)
- hepatic circulation: blood supply furnished by hepatic portal vein &
common hepatic artery
- branches merge to supply sinusoids that drain into central vein of each
lobule
- these drain into hepatic veins & to inferior vena cava (ppts. 4 & 5)
• physiology of liver:
- enterohepatic cycle: hepatocytes release bile into bile canaliculi (fig. 14 - 3
& ppt. 3) that drain into biliary tree
Bio 307/607 lec 15
- p. 2 -
- bile salts are an important constituent of bile (facilitate fat digestion
and absorption by emulsifying fat in the intestine)
- most bile salts are reabsorbed (ileum) and returned to liver for reuse
- 20% excreted in feces (figs. 14 - 4 & ppt. 6)
- metabolic functions: regulates blood glucose levels by absorbing &
storing it as glycogen (glycogenesis) or secreting it by breaking down glycogen
(glycogenolysis) or synthesizing glucose from amino acids (gluconeogenesis)
- regulates protein levels (synthesizes many plasma proteins) to
maintain osmotic balance, provide transport molecules & clotting factors
- maintains amino acid pool & excretes ammonia from protein
breakdown by forming urea
- maintains lipids in blood (formation of lipoprotein) (figs. 14 - 6, 9 - 16
& ppts. 7 & 8); synthesizes or excretes cholesterol (in bile) as needed
- processes bilirubin (bile pigment from hemoglobin breakdown) to
excrete with bile (fig. 14 - 5 & ppt. 9)
- detoxifies drugs (fig. 14 - 7 & ppt. 10) & other chemicals (e.g. alcohol),
stores vitamins and other nutrients, and inactivates several hormones
Bio 307/607 lec 15
2.
- p. 3 -
Hepatic Failure:
- given the liver's extensive reserve & regenerative capacity, disease may be
well advanced before signs & symptoms occur; three main signs are evident:
• jaundice: three main conditions may lead to disruption of bilirubin excretion
(fig. 14 - 8 & ppt. 11)
- excessive red cell breakdown, e.g., in hemolytic anemias, overburdens
liver with bilirubin load
- obstruction of biliary tree, e.g., gallstones, inflammation of ducts,
compressions due to tumors, strictures; causes other damage (fig. 14 - 20 & ppt. 12)
- liver diseases that impair bile formation and excretion
• malabsorption: failure to produce bile results in disruption of fat absorption
& fat-soluble vitamin absorption, leading to steatorrhea, clotting deficiencies
• disturbed hepatic metabolism: protein deficiency leads to weight loss,
widespread edema, ascites (fig. 14 - 14 & ppt. 13), deficient urea formation is believed
responsible for encephalopathies, disrupted lipid metabolism causes fatty change (fig.
1 - 15 & ppt. 14), increased sensitivity to drugs & toxins, and other sequelae of
metabolic deficits
3.
Liver Disease:
• hepatitis: viral infections (fig. 14 - 9 & ppt. 15) & toxic chemicals may cause
both acute and chronic inflammations of liver (hepatitis)
- some viruses are systemic and some attack liver directly (four main types):
Bio 307/607 lec 15
- p. 4 -
- hepatitis A virus produces a usually acute & mild condition; passed
through fecal contamination (polluted water, contaminated seafood); often, confined
populations may experience epidemics
- hepatitis B virus is potentially more serious and spread through blood
and body fluids; at-risk populations include IV drug users, sexually promiscuous
individuals, and health care workers frequently exposed to blood or body fluids or
their products
- hepatitis D virus infects only in presence of existing HBV infection, which
may be exacerbated by HDV
- hepatitis C virus is transmitted by blood; before its identification
transmission through unscreened blood banking was a problem
- chronic hepatitis: most acute cases resolve uneventfully (e.g. HVA
infections); some chronic episodic cases (chronic persistent hepatitis) may also be
resolved without therapy; more serious cases (usually associated with HCV or with
HDV superimposed on HBV infection) are called chronic active hepatitis (fig. 14 - 10
& ppt. 16)
- damage to liver is not usually directly due to the virus but to the immune
response it generates
• cirrhosis: end-stage inflammation accruing from liver damage
- may be gradually progressive (minimal or no symptoms) or aggressive
- involves post-necrotic replacement of tissue with fibrosis & nodular
parenchyma proliferation, until liver failure may be so severe as to be irreversible
(figs. 14 - 11 & 14 - 12)
Bio 307/607 lec 15
- p. 5 -
- two main sequelae are portal hypertension and hepatic insufficiency (fig.
14 - 15 & ppt. 17)
- excessive alcohol consumption is a major cause other than hepatitis
viruses (fig. 14 - 17 & ppt. 18)
4.
Pancreatic Disorders:
• anatomy & physiology: extends from duodenum (head) across to spleen
(tail) behind stomach and transverse colon (ppt. 19); secretes enzymes and
bicarbonate, necessary for normal intestinal digestion, and secretes hormones from
islets
• pancreatitis: acute and chronic forms are recognized, the latter consisting of
recurrent episodes of acute attacks
- alcohol abuse may obstruct pancreatic duct (duodenal mucosal swelling
coupled with pancreatic hypersecretion); accumulation of released enzymes attacks
pancreatic tissue, causing necrosis (often soapy due to salts of fatty acids)
- cholelithiasis (gallstones) is also a frequent cause of pancreatic duct
obstruction (fig. 14 - 22 & ppt. 20)
- released pancreatic enzymes cause numerous systemic effects (fig. 14 - 25
& ppt. 21)