DLA 12; lecture 17+18 Flashcards
porta hepatis of the liver?
contains the hepatic A, portal vein, and hepatic ducts
what does a classic hepatic lobule look like histologically
has a central portal vein
shape of a hexagon; all points of the hexagon are portal areas
hepatocytes:
have at least one centrally located nucleus
foamy cytoplasm
hepatocyte surfaces of the classic lobule?
- adjacent
form small, tunnel like canaliculi
used for movement of bile - basal surface
adjacent to the sinusoids
has contact with space of disse
Kupffer cell
found in the liver
derived from monocytes
phagocytic cells; immune function
peri-sinusoidal space of disse
functions to exchange material between the blood and the hepatocytes
have Ito cells:
used for fat storage and vitamin A storage
modified pericytes
functional lobule of liver
triangular region
have three points which are the portal veins
portal area in the middle of triangle
bile canaliculi and canals of herring
BC receive bile from the liver and convey that bile to the canals of herring
COH are surrounded by cholangiocytes (these sense changes in bile flow)
Liver acinus of rappaport
a functional lobulation based on blood flow
divided into 3 zones:
zone 1:
first to be exposed by blood
zone 3:
last to be exposed to blood
first to be ischemic
CHF and liver
Zone 3 of the acinus is the first to be impacted by this condition due to decreased blood output which deprives this area of the liver of oxygen
fatty liver disease
associated with chronic alcohol intake and metabolic syndrome
increased lipid droplets, thus hepatomegaly
reversible!
liver cirrhosis
diffuse liver damage
have collagen deposition due to ito cells
blood restriction
have nodular appearance
not reversible
gallbladder constriction?
facilitated by CCK
histology of gallbladder
simple columnar epithelium
have false lumens
mucosal folds
have sinuses of Rokitansky Aschoff:
invaginations of the mucosa into the deeper layers
regulation of pancreatic secretion
CCK:
induces the acinar cells to release proenzymes
secretin:
induces the intercalated ducts to secrete large amounts of alkaline fluid; neutralize chyme
sympathetics: regulate blood flow
parasympathetics: stimulate activity of acinar cells and centroacinar cells
Acute pancreatitis
inflammation of the pancreas
most likely due to gallstones or alcohol abuse
can have a gallstone blockage in the pancreatic duct which could lead to this inflammation
cystic fibrosis and the pancreas
can lead to obstructions in the pancreatic duct due to thickness
also malabsorption
hormone sensitive lipase
fatty acids in TAG’s are released as free fatty acids by this enzyme
inhibited by insulin
low levels and insulin and epinephrine stimulate this enzyme
role of epinephrine and breaking down TAGs
activates PKA
PKA is going to phosphorylate HS lipase
stimulates hydrolysis of the TAG into glycerol and FFA
tissues that use FFA’s?
liver and muscle (skeletal and cardiac)
brain and RBC’s DO NOT use FFA’s
activation of the Fatty acid?
the fatty acid is converted into fatty acyl CoA by fatty acid CoA synthetase (thiokinase)
needs two high energy bonds
transport of the fatty acid into the mito?
CPT-1 will take acyl CoA and carnitine and form acyl carnitine (move acyl group)
translocase will then take acyl carnitine and move it into the inner membrane space
CPT-II will remove the acyl group from the carnitine and produce acyl CoA again
carnitine will go back to the intermembrane space
reactions of beta oxidation
- oxidation (need FAD)
- addition of water
- oxidation (need NAD)
- cleavage
two C’s at a time
Acetyl CoA is produced for the TCA cycle
Acyl CoA dehydrogenase
Needs FAD
converts fatty acyl CoA to enoyl CoA
LCAD, MCAD, SCAD?
LCAD:
long chain acyl Co-A
used for 16-C chains
MCAD:
medium chain acyl CoA
used for 10-C chains
SCAD:
short chain acyl CoA
used for 6-C chains
systemic fatty acid oxidation disorders
MCAD deficiency
carnitine deficiency
CPT-1 deficiency
have hypoglycemia (no gluconeogenesis) hypoketosis
BC LESS acetyl coA
myopathic fatty acid oxidation disorders
muscles
cramps during low intensity exercise high blood lactate elevated Ck-MM's lipid droplets in muscle myoglobinuria
MCAD deficiency
hypoglycemia after fasting or after illness
low glucose
Fatty acids are elevated
ketone bodies are low
autosomal recessive
be found between 6-24 months old
medium chain acyl carnitines in urine
dicarboxylic acids in urine
Carnitine deficiency
systemic:
early age of presentation
hypoglycemia
hypoketosis
myopathic:
muscle weakness and cardiomyopathy
elevated CK-MM
lipid droplets in muscle
CPT-I deficiency
hypoglycemia and hypoketosis
affects liver isoform
CPT-II deficiency
cardiomyopathy and muscle weakness lipid deposits myoglobinuria high CK-MM affects muscle isoform
Jamaican vomiting sickness
eating unripe ackee fruit
contains hypoglycin A which inhibits MCAD
thus hypoglycemia due to less gluconeogenesis and lack of beta oxidation
vomiting
medium chain acyl carnitines found in urine
oxidation of odd chain fatty acids
propionyl CoA is converted to methylmalonyl CoA
by propionyl CoA carboxylase (needs biotin)
methylmalonyl CoA is converted to succinyl CoA
by Methylmalonyl CoA mutase (need B12)
can enter TCA cycle
