DLA 12; lecture 17+18 Flashcards

1
Q

porta hepatis of the liver?

A

contains the hepatic A, portal vein, and hepatic ducts

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2
Q

what does a classic hepatic lobule look like histologically

A

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

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3
Q

hepatocyte surfaces of the classic lobule?

A
  1. adjacent
    form small, tunnel like canaliculi
    used for movement of bile
  2. basal surface
    adjacent to the sinusoids
    has contact with space of disse
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4
Q

Kupffer cell

A

found in the liver
derived from monocytes

phagocytic cells; immune function

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5
Q

peri-sinusoidal space of disse

A

functions to exchange material between the blood and the hepatocytes

have Ito cells:
used for fat storage and vitamin A storage
modified pericytes

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6
Q

functional lobule of liver

A

triangular region

have three points which are the portal veins

portal area in the middle of triangle

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7
Q

bile canaliculi and canals of herring

A

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)

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8
Q

Liver acinus of rappaport

A

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

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9
Q

CHF and liver

A

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

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10
Q

fatty liver disease

A

associated with chronic alcohol intake and metabolic syndrome

increased lipid droplets, thus hepatomegaly

reversible!

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11
Q

liver cirrhosis

A

diffuse liver damage

have collagen deposition due to ito cells
blood restriction
have nodular appearance

not reversible

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12
Q

gallbladder constriction?

A

facilitated by CCK

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13
Q

histology of gallbladder

A

simple columnar epithelium

have false lumens
mucosal folds

have sinuses of Rokitansky Aschoff:
invaginations of the mucosa into the deeper layers

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14
Q

regulation of pancreatic secretion

A

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

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15
Q

Acute pancreatitis

A

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

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16
Q

cystic fibrosis and the pancreas

A

can lead to obstructions in the pancreatic duct due to thickness

also malabsorption

17
Q

hormone sensitive lipase

A

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

18
Q

role of epinephrine and breaking down TAGs

A

activates PKA

PKA is going to phosphorylate HS lipase

stimulates hydrolysis of the TAG into glycerol and FFA

19
Q

tissues that use FFA’s?

A

liver and muscle (skeletal and cardiac)

brain and RBC’s DO NOT use FFA’s

20
Q

activation of the Fatty acid?

A

the fatty acid is converted into fatty acyl CoA by fatty acid CoA synthetase (thiokinase)

needs two high energy bonds

21
Q

transport of the fatty acid into the mito?

A

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

22
Q

reactions of beta oxidation

A
  1. oxidation (need FAD)
  2. addition of water
  3. oxidation (need NAD)
  4. cleavage

two C’s at a time
Acetyl CoA is produced for the TCA cycle

23
Q

Acyl CoA dehydrogenase

A

Needs FAD

converts fatty acyl CoA to enoyl CoA

24
Q

LCAD, MCAD, SCAD?

A

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

25
Q

systemic fatty acid oxidation disorders

A

MCAD deficiency
carnitine deficiency
CPT-1 deficiency

have hypoglycemia (no gluconeogenesis) 
hypoketosis 

BC LESS acetyl coA

26
Q

myopathic fatty acid oxidation disorders

A

muscles

cramps during low intensity exercise 
high blood lactate 
elevated Ck-MM's 
lipid droplets in muscle 
myoglobinuria
27
Q

MCAD deficiency

A

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

28
Q

Carnitine deficiency

A

systemic:
early age of presentation
hypoglycemia
hypoketosis

myopathic:
muscle weakness and cardiomyopathy
elevated CK-MM
lipid droplets in muscle

29
Q

CPT-I deficiency

A

hypoglycemia and hypoketosis

affects liver isoform

30
Q

CPT-II deficiency

A
cardiomyopathy and muscle weakness 
lipid deposits 
myoglobinuria
high CK-MM 
affects muscle isoform
31
Q

Jamaican vomiting sickness

A

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

32
Q

oxidation of odd chain fatty acids

A

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