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Phase 1 mine > Liver > Flashcards

Liver Flashcards

1
Q

what is the diaphragmatic surface

A

anterolateral = contains bare area

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2
Q

what is the visceral surface

A

posteroinferior = covered with peritoneum, except gallbladder/porta hepatis

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3
Q

what is the bare area of the liver

A

large triangular area on diaphragmatic surface = no peritoneum

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4
Q

what is the falciform ligament

A

double fold of peritoneum = forms a natural anatomical division of right/left lobe of liver and attaches liver to diaphragm

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5
Q

what is the ligamentum teres

A

free edge of falciform ligament = remnant of umbilical vein

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6
Q

what are the coronary ligaments

A

attach the superior surface of liver to posterior diaphragm = anterior/posterior

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7
Q

what are the triangular ligaments

A 
left = union of anterior/posterior layers of coronary ligament at apex of liver = left lobe to diaphragm
right = attaches right lobe to diaphragm
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8
Q

what is the functional division of the liver

A

line down gall bladder/ivc

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9
Q

what is the porta hepatis

A

point of entry into liver for hepatic arteries and portal vein/exit for hepatic ducts

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10
Q

where is calot’s triangle

A

at porta hepatis

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11
Q

what are the contents of calot’s triangle

A

right hepatic artery
cystic artery
lymph node of Lund
lymphatics

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12
Q

what is the liver’s fibroud layer known as

A

glisson’s capsule

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13
Q

what supplies blood to the liver

A

25% hepatic artery proper from coeliac trunk to non-parenchymal structures
75% hepatic portal vein

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14
Q

wha tdoes the hepatic portal vein supply the liver with

A

partially deoxy blood + nutrients from small intestine to liver parenchyma = allows detoxification

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15
Q

what does the portal triad contain

A

proper hepatic arterioles
hepatic portal venules
bile ducts

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16
Q

what are the structural units of the liver

A

lobules

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17
Q

what are the functional units of the liver

A

acini

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18
Q

what are acini

A

divided into zones according to distance form arteriole blood supply = hepatocytes closest better oxygenated

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19
Q

what is the nerve supply to the liver

A

parenchyma = hepatic plexus = sympathetic (coeliac plexus) and parasympathetic (vagus)

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20
Q

what is the nerve supply to glisson’s capsule

A

lower intercostal nerves

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21
Q

with what organs does the pancreas have anatomical relations

A 
stomach
duodenum
transverse mesocolon
common bile duct
spleen
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22
Q

what vessels is the pancreas associated with

A

aorta/IVC posteriorly
superior mesenteric artery behind neck
hepatic portal vein behind neck
splenic artery travels superior border

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23
Q

describe the duct system of the pancreas

A

acini connected by intercalated ducts = unite into lobules = drain into intralobular collecting ducts = become main pancreatic duct

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24
Q

what forms the hepatopancreatic ampulla of vater

A

pancreatic duct unites with common bile duct

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25
Q

what is Hartmann’s pouch

A

mucosal fold in neck of gallbladder = common site for gallstone lodging

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26
Q

what supplies blood to the gallbladder

A

cystic artery

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27
Q

what is the venous drainage of the gallbladder

A

cystic veins to portalto portal vein

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28
Q

what structures are found in the porta hepatis

A

portal vein
r/l hepatic artery
r/l hepatic duct
microscopically = lymphatics/vagus nerve branches/greater splanchnic nerves branches

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29
Q

where is the bare area of the liver

A

under central tendon of right side of diaphragm

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30
Q

what is the surface marking of the fundus of the gall bladder

A

tip of 9th costal cartilage

where midclavicular line crosses costal margin

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31
Q

what degenerates to become ligamentum venosum

A

ductus venosus

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32
Q

what innervates the gall bladder

A

coeliac plexus = sympathetic and sensory fibres

vagus nerve = parasympathetic innervation

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33
Q

where would disease of gall bladder be felt

A

rubbing on diaphragm so pain carried by c3,4,5 = right shoulder

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34
Q

where do hepatic veins drain

A

IVC

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35
Q

which fat soluble vitamins are stored in the liver

A

KADE

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36
Q

what substances are stored in the liver

A

iron
glycogen
minerals
fat soluble vitamins

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37
Q

where is iron used

A

haemoglobin
myoglobin
bone marrow

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38
Q

name 4 sources of iron

A

meat
liver
egg yolk
shell fish

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39
Q

how much of ingested iron is absorbed in duodenum

A

about 10% = changes according to needs

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40
Q

what is ferritin

A

protein-iron complex acting as intracellular store for iron in kupffer cells in liver

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41
Q

how does iron travel in the blood

A

bound to transferrin

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42
Q

what cells in the liver store iron

A

kupffer cells

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43
Q

what 2 things occur when body has reached iron capacity

A
  1. increased free iron in plasma/intestinal epithelial cells = increased ferritin production = increased iron binding and therefore reduce amount released into blood
  2. hepatocytes release hepcidin = inhibits ferroportin so reduce amount of iron in blood
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44
Q

what occurs when iron is absorbed

A
  1. actively transported into duodenal enterocytes
  2. then incorporated into ferritin and stored intracellularly
  3. most bound to ferritin = released back to lumen and excreted in faeces
  4. absorbed iron not bound to ferritin = released into blood via ferroportin then bind with transferrin
  5. iron bound to transferrin = to liver
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45
Q

what occurs when iron stores are low

A

production of intestinal ferritin decreases = decrease amount of iron bound to ferritin = increase free iron released into blood

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46
Q

what is the most abundant plasma protein

A

albumin

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47
Q

what are the functions of albumin

A
  1. binding/transport of large, hydrophobic compounds = bilirubin/FA/hormones/drugs
  2. maintenance of colloid osmotic pressure
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48
Q

what is colloid osmotic pressure

A

effective osmotic pressure across blood vessel walls permeable to electrolytes but not large molecules = almost entirely due to plasma proteins

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49
Q

how does albumin maintain the osmotic pressure of the blood

A

presence in blood = water conc is lower than in interstitial fluid = net flow of wate rout of interstitial fluid into blood plasma

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50
Q

what are the 4 starling forces

A
  1. capillary hydrostatic pressure = fluid out of cap
  2. interstitial hydrostatic pressure = fluid into cap
  3. osmotic force due to plasma protein conc = fluid into cap
  4. osmotic force due to interstitial fluid protein conc = fluid out of cap
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51
Q

what occurs to fluid at the arterial end of capillarires

A

interstitial fluid has high conc of proteins bc fluid loss to lymphatics so has higher osmotic pressure = bulk fluid filtration out of capillaries into interstitial fluid

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52
Q

what occurs to fluid at venous end of capillaries

A

capillary hydrostatic pressure decrease die to resistance of blood flow but all other starling forces same = bulk fluid absorption into capillaries

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53
Q

what causes a decrease in albumin

A 
decreased synthesis
decreased catabolism
increased loss = haemorrhage
liver failure
nephrotic syndrome = albumin filtered into urine
burns
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54
Q

what is hypoalbuminaemia

A

decrease of albumin in blood = caused by liver failure = leads to oedema because decreases capillary oncotic pressure

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55
Q

what are globulins

A

work as antibodies = alpha/beta made in liver

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56
Q

what is the role of the liver in producing clotting factors

A

produces all except calcium (IV) and vWF (VIII)

produces bile salts essential for vitamin K absorption

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57
Q

what is the role of vitamin K

A

essential for synthesis of clotting factors 10, 9, 7 ,2 = 1972

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58
Q

what are complement factors

A

= plasma protein

sticks to pathogens = mark for neutrophils for killing

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59
Q

what water soluble vitamin is stored in the liver

A

B12

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60
Q

what are xenobiotics

A

foreign chemical substance not normally found of produced in body which cannot be used for energy requirements = DRUGS
= absorbed across lungs/skin/ingested
= excreted in bile/urine/sweat/breath

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61
Q

describe pharmacologically active compounds

A

lipophilic = can pass through memranes
non-ionised at pH 7.4
bound to plasma proteins to be transported in blood

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62
Q

what are microsomal enzymes

A

enzymes found in small particles consisting of piece of endoplasmic reticulum to which ribosomes are attached

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63
Q

where are microsomal enzymes found

A

on smooth endoplasmic reticulum mostly in liver hepatocytes

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64
Q

where are non-microsomal enzymes found

A

cytoplasm/mitochondria of hepatocytes in the liver (+ other tissues)

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65
Q

what processes are microsomal enzymes involved in

A

oxidative, reductive, hydrolytic
mainly phase 1 reactions = biotransform substances
can be involved in phase 2 = glucuronidation

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66
Q

what are microsomal enzymes induced/inhibited

A 
drugs
food
age
bacteria
alcohol
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67
Q

what processes are non-microsomal enzymes involved in

A

non-specific = can be phase1 or 2
involved in all conjugation reactions
NOT in glucuronidation

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68
Q

what is the aim of liver detoxification

A

to transform a drug into less toxic/more water soluble so can be excreted

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69
Q

what is the aim of phase 1 reactions

A

make substance more hydrophilic by adding/exposing a hydroxyl group

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70
Q

give 3 examples of non-synthetic catabolic reactions

A

oxidation
reduction
hydrolysis
= introduce reactive group to drug ready for conjugation

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71
Q

give 4 examples of oxidation of drugs

A

hydroxilation = adding OH
dealkylation = remove CH side chains
deamination = remove NH
hydrogen removal

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72
Q

what occurs in hydrolysis

A

split amide and ester bond

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73
Q

what occurs in reduction

A

addition of a hydrogen

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74
Q

what is functionalisation

A

introducing reactive group to drug/adding/exposing oH, SH, NH2, COOH
= occurs mainly in liver catalysed by cytochrome P450 enzyme

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75
Q

what are cytochrome P450 enzymes

A

microsomal
in phase 1
uses haem group to oxidise substances = products are more water soluble

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76
Q

what is the overall reaction for phase 1 reactions

A

NADPH + H+ + O2 + RH = NADP+ + H2O + R-OH

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77
Q

give 2 examples of non-microsomal enzymes used in phase 1 reactions

A

alcohol dehydrogenase

aldehyde dehydrogenase

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78
Q

what are the outcomes of phase 1 reactions (4)

A
  1. inactivate drugs
  2. further activate drug
  3. activate drug from pro-drug
  4. make drug into reactive intermediate
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79
Q

what are phase 2 reactions

A

synthetic anabolic reactions

= conjugation reactions

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80
Q

what is a conjugation reaction

A

attachment of substituent groups
usually inactive products
catalysed by transferases
= increase hydrophilicity for renal excretion

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81
Q

what is a glucuronidation reaction

A

adding glucuronic acid to make more hydrophilic

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82
Q

what enzymes are used in glucuronidation reactions

A

glucuronosyltransferase (UGT) = microsomal

uridine diphospho-glucuronic acid (UDPGA) = coenzyme for conjugation of glucuronic acid

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83
Q

give an example of an active drug to inactive metabolite

A

phenobarbital to glucuronides

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84
Q

give an example of an active drug to active metabolite

A

codein to morphine

85
Q

give an example of an inactive drug to an active metabolite

A

loratidine to active drug

86
Q

give an example of an active drug to a reactive intermediate

A

paracetamol to NAPQI = toxic

87
Q

how is paracetamol metabolised

A

predominantly via phase 2 glucuronic acid/sulphate conjugation

88
Q

how does paracetamol become toxic

A

low glucuronic acid/sulphate = undergo phase 1 metabolism via oxidation = NAPQI
= removed by glutathione but if low levels glutathione then = toxic!!

89
Q

what is the equation for alcohol metabolism

A

ethanol to acetaldehyde by ADH
acetaldehyde to actetate by ALDH
acetate to CO2 + H2O

90
Q

what is protein turnover and degradation

A

continuous degradation and resynthesis of all cellular proteins = variable and reflects usage/demand

91
Q

when is protein turnover increased

A

tissue damage
pregnancy
starvation
severe burns

92
Q

what are the 2 primary methods of protein breakdown

A

lysosomal

ubiquitin-proteosome pathway

93
Q

where does lysosomal protein breakdown take place

A

through sinusoidal endothelial cells to Kupffer cells

94
Q

describe lysosomal protein degradation through

A
  1. soluble proteins from blood through sieve plates of sinusoid
  2. phagocytosed by kupffer cells
  3. packeaged into lysosomes in kupffer cells
  4. lysozymes breakdown proteins
95
Q

where does the ubiquitin-proteasome pathway take place

A

cytoplasm of cells

96
Q

describe protein degradation in the ubiquitin-proteasome pathway

A
  1. ubiquitin binds to protein = acts as target for proteosomes
  2. proteosome encases protein and destroys it
  3. amino acids can be recycled
97
Q

where does amino acid degradation/catabolism take place

A

in hepatocytes in liver

98
Q

what is amino acid catabolism

A

nitrogen containing amino group removed to produce nitrogen and carbon skeleton
N = excreted/incorporated into other compounds
C = metabolised/krebs

99
Q

name the 2 main catabolism processes

A

oxidative deamination

transamination

100
Q

what is oxidative deamination (in the glucose alanine cycle)

A

in liver

alanine to pyruvate gives an amine group to alphaketoglutarate to form glutamate

101
Q

what is the enzyme used in oxidative deamination

A

glutamate dehydrogenase

102
Q

what are the implications of oxidative deamination being a reversible reaction

A

excess ammonia produced = can cross BBB = react with alphaketoglutarate = decrease ATP = dangerous

103
Q

what is transamination (in the glucose alanine cycle)

A

transfer of alpha amino group from glutamate to pyruvate to make alanine
glutamate goes to alphaketoglutarate

104
Q

what is the enzyme for transamination

A

alanine aminotransferase

105
Q

where are the enzymes for the urea cycle found

A

mitochondria/cytosol of hepatocytes

106
Q

describe the urea cycle in 3 steps

A
  1. arginine to ornithine by arginase with generation of urea
  2. ornithine to citrulline with addition of ammonia and CO2 (carbomyl phosphate)
  3. citrulline to arginine with addition of ammonia
107
Q

what is generated from the urea cycle

A

urea only (= 2 x ammonia)

108
Q

what occurs if there are enzyme deficiencies of the urea cycle

A

leads to higher levels of ammonia in blood

no enzymes = no life

109
Q

why is ammonia associated with neurotoxicity

A

able to cross BBB
once inside converted to glutamate (glutamate dehydrogenase) = depletion in alpha-ketoglutarate = oxaloacetate reduces = no krebs cycle = cell damage/death

110
Q

what does 1 cycle of urea cycle consume

A

3ATP

4PO4-

111
Q

how is fat stored

A 
most = adipocytes forming adipose tissue
some = in hepatocytes
112
Q

what are lipids

A

ester of fatty acids and certain alcohol compounds

113
Q

name 3 functions of a lipid

A

energy reserves
structural cell membrane
hormone metabolism

114
Q

what is the role of lipoproteins

A

transport cholesterol in blood

115
Q

what is HDL

A

high density lipoprotein = formed in liver

removes excess cholesterol from blood/tissue then deliver to liver which secretes as bile/convert to bile salts

116
Q

what is LDL

A

low density lipoprotein =
produced by hepatic lipase in hepatocytes
main cholesterol carriers = take to tissues for endocytosis

117
Q

why is LDL bad

A

high plasma concentrations associated with increase cholesterol deposition in arterial walls

118
Q

why is LDL needed

A

essential in supplying cells with cholesterol needed for steroid hormone synth/plasma membranes

119
Q

what is VLDL

A

very low density lipoprotein
synthesised in hepatocytes
transport triglycerides from liver to tissues

120
Q

how much of the energy used by muscle/liver/kidneys is derived from catabolism of fatty acids

A

under resting conditions = approx half

121
Q

what is the function of adipocytes

A

synthesise/store triglycerides during food uptake
release FA/glycerol into blood when food not being absorbed from small intestine
FA/glycerol in blood for uptake in cells = energy for ATP

122
Q

describe the 4 step process of fat catabolism

A
  1. FA across cell membrane
  2. bind to coenzyme A by acyl CoA synthetase to form acyl CoA
  3. acyl CoA through mitochondrial membrane by cartinine shuttle
  4. in mitochondria = Beta oxidation = 2C removed to repeat cycle and acetyl CoA, NADH, FADH formed for Krebs/oxidative phosphorylation
123
Q

what is the role of lipoprotein lipase

A

hydrolyses triglycerides in lipoproteins into 3 x FA and 1 x glycerol

124
Q

what is the role of hepatic lipase

A

converts intermediate density lipoprotein into LDL = packaging with more triglycerides to be released into body

125
Q

where is hepatic lipase found

A

expressed in liver/adrenal glands

126
Q

where is bile secreted

A

in liver by hepatocytes continuously

127
Q

what is the role of bile

A

emulsify fats

excretory pathway for most steroid hormones/drugs

128
Q

where is bile stored

A

in gall bladder = concentrated bc NaCl/water absorbed into blood

129
Q

what is the space of disse

A

space separating hepatocytes and sinusoids

130
Q

what are hepatic lobules

A

wedge-like arrangements of hepatocytes around 1 to 2 cells deep surrounded by sinusoids = mixed portal/hepatic artery blood

131
Q

what are the contents of bile

A 
bile salts - mostly cholesterol and waste products
lecithin = phospholipid
HCO3-
bile pigments
trace metals
132
Q

how is bile stored in the gall bladder

A

bile salts, cholesterol, lecithin = aggregated to mixed micelles

133
Q

what cells secrete the components of bile

A

hepatocytes = bile salts, cholesterol, lecithin, bile pigments
epithelial cells lining bile ducts = most of HCO3- rich solution = stimulated by secretin

134
Q

describe the production and storage of bile

A
  1. bile produced in hepatocytes
  2. transported in micelles through canaliculi
  3. actin filaments contract around canaliculi to move bile to hepatic ducts
  4. hepatic duct to cystic duct to gall bladder
135
Q

what is the enterohepatic circulation

A

recycling pathway of bile salts

136
Q

what happens to bile salts during digestion of a fatty meal

A

most that enter intestinal tract = absorbed by specific Na+ coupled transporters in terminal ileum

137
Q

what happens to absorbed bile salts

A

returned via portal vein to liver
uptake to hepatocytes driven by secondary AT coupled to Na+
then secreted into bile

138
Q

what occurs to lost bile salts

A

5% lost in faeces

liver synthesises new bile salts from cholesterol

139
Q

what occurs to bile in the fasted state

A

bile synthesised/recirculated in liver
sphincter of Oddi shut
bile diverted back to be stored in gall bladder

140
Q

what occurs to bile in the fed state

A

fat stimulates release of CCK
CCK relaxes sphincter of Oddi and contracts gall bladder
stored bile shoots into duodenum

141
Q

what is CCK

A

cholycystokinin

142
Q

describe the role of cholesterol in bile

A

cholesterol extracted from blood = to liver = secreted into bile
solubility achieved by incorporation into micelle

143
Q

what is ezetimibe

A

enzyme which blocks protein-mediated transport of cholesterol across membrane of cells of wall of duodenum

144
Q

what happens to cholesterol in the digestive system

A

50% absorbed = bile

50% excreted in faeces

145
Q

what are bile pigments

A

substances formed from haem portion of haemoglobin when old/damaged erythrocytes break down in spleen/liver

146
Q

what is bilirubin

A

predominant bile pigment which is extracted from blood by hepatocytes and actively secreted into bile

147
Q

what colour is biliverdin

A

green

148
Q

what colour is bilirubin

A

orange/yellow

149
Q

what colour is stercobilin

A

gives faeces brown colour

150
Q

what colour is urobilin

A

responsible for yellow of urine

151
Q

what is jaundice

A

yellow discolouration of skin caused by high serum bilirubin level

152
Q

what occurs in pre-hepatic jaundice

A

increased total bilirubin in blood
increased unconjugated bilirubin bc exceed amount liver can conjugate
enlargement of spleen due to haemolysis

153
Q

what are the clinical signs of pre-hepatic jaundice

A

normal faeces

normal urine = unconjugated = insoluble so bound to albumin so dont filter into urine

154
Q

what occurs in hepatic jaundice

A

problem with liver itself = cannot take up/conjugate/excrete bilirubin
enlargement of spleen = trying to help liver break down RBCs
all levels bilirubin increase = no conjugation + leaky liver
decreased urine urobilinogen

155
Q

what are the clinical signs of hepatic jaundice

A

normal faeces

dark urine = raised conjugated bilirubin but decreased urine urobilinogen

156
Q

what occurs in post hepatic jaundice

A

= obstruction
high conjugated bilirubin bc liver is fine
no enlarged spleen
increased urine bilirubin

157
Q

what are the clinical signs of post hepatic jaundice

A

pale faeces

dark urine = increased urine urobilinogen as hepatic system still working

158
Q

name 3 causes of prehepatic jaundice

A

malaria
sickle cell anaemia
thalassaemia

159
Q

name 3 causes of hepatic jaundice

A

liver cirrhosis
liver cancer
drugs

160
Q

name 3 causes of post hepatic jaundice

A

gallstones
pancreatic cancer
gall bladder cancer

161
Q

why do gallstones form

A

if concentration of cholesterol in bile becomes too high compared to phospholipids/bile salts = cholesterol crystallise out of solution

162
Q

what blood vessel is closely related to the duodenum

A

superior gastroduodenal artery runs in close proximity to duodenum

163
Q

what does the pancreas secrete

A

HCO3-

digestive enzymes

164
Q

how do secretions leave the pancreas

A

secretions arise from acinar tissue = secreted into ducts = converge into pancreatic duct = joins common bile duct = enter duodenum

165
Q

where is the accessory pancreatic duct

A

emerges above ampulla of vater in duodenum

166
Q

what does HCO3- do

A

secreted by epithelial cells lining ducts = duct cells
protect duodenal mucosa from gastric acid
buffers material entering duodenum to pH suitable for enzymes

167
Q

what is the production of HCO3- from pancreas stimulated/inhibited by

A

stimulated by release of secretin produced in small intestine in response to acid in duodenum
secretin also stimulates CCK + inhibits acid secretion/gastric motility of stomach

168
Q

how is HCO3- secreted into the pancreatic duct lumen

A

by Cl-/HCO3- exchanger

169
Q

describe the process of HCO3- secretion from pancreatic ducts (5)

A
  1. bicarbonate reaction within cell = H+ + HCO3- produced
  2. H+ out of basolateral to capillary exchanges for Na+ - H+ to portal vein
  3. Na+/K+ATPase pumps K+ in and Na+ out = provide energy for secretion of HCO3- (K+ out again)
  4. Cl- in an apical side i exchange for HCO3- out
  5. Cl- does not accumulate in cell = leaves via cystic fibrosis transmembrane conductance regulator (CFTR channel)
170
Q

what types of enzymes are secreted by the pancreas

A

active or precursors secreted by gland cells at pancreatic end of duct system

171
Q

what does CCK do

A

stimulates secretion of digestive enzymes
potentiates action of secretin = stimulate bicarb secretion from pancreas
stimulates contraction of gall bladder/relaxes sphincter of oddi

172
Q

where and why is CCK secreted

A

produced in small intestine = in response to presence of amino acids/FA in small intestine

173
Q

give 2 examples of active enzymes secreted by pancreas

A

alpha amylase = starch to maltose

lipase = triglycerides to monoglycerides and FA

174
Q

give 3 examples of enzymes precursors secreted by pancreas

A

zymogen = trypsinogen to trypsin
= mediated by enterokinsases
= trypsin activates other enzymes = chymotrypsin

175
Q

what is somatostatin

A

produced in D cells of pancreatic islets/islets of langerhans
= powerful inhibitor of exocrine secretion

176
Q

what do the isles of langerhans contain

A

alpha cells
beta cells
D cells
PP cells

177
Q

what do alpha cells produce

A

glucagon

178
Q

what do beta cells produce

A

insulin/amylin

179
Q

what do delta/D cells produce

A

somatostatin

180
Q

what do PP cells produce

A

pancreatic polypeptide

181
Q

what are the phases of pancreatic secretion

A

cephalic phase

gastric phase

182
Q

what occurs in the cephalic phase

A

initiated by sensory experience of eating/smelling food etc

= parasympathetic vagus nerve stimulation of acinar cells

183
Q

what occurs in the gastric phase

A

initiates by presence of food in stomach

= parasympathetic vagus nerve stimulation of acinar cells

184
Q

what has happened by the end of the cephalic and gastric phases

A

pancreatic ducts filled with inactive zymogens ready for release with HCO3- via sphincter of Oddi
amino acids/FA in duodenum = CCK released = gallbladder contract = sphnicter relax

185
Q

what is the hepatic diverticulum

A

cellular expansion of the foregut which gives rise to the parenchyma of the liver
= appear in middle of 3rd week as outgrowth of endodermal epithelium at distal end of foregut

186
Q

how does the bile duct form embryologically

A

forms when connection between liver diverticulum and foregut narrows

187
Q

how are the gallbladder and cystic duct formed embryologically

A

small ventral outgrowth developing from bile duct

188
Q

when does bile production begin

A

12th week - subside during last 2 months

189
Q

how is the lesser omentum formed

A

formed due to rotation of liver and stomach

190
Q

where does the pancreas develop from

A

endodermal lining of duodenum as 2 buds = dorsal/ventral

when duodenum rotates to become C shaped = fuse together

191
Q

how is the main pancreatic duct formed

A

by union of ventral pancreatic duct with distal part of dorsal bud

192
Q

how are the islets of langerhans formed

A

develop from pancreas parenchyma at 3rd month

193
Q

describe the histology of sinusoids

A

thin discontinuous fenestrated epithelium
no basement membrane
contain scattered kupffer cells but cannot see this on h&e

194
Q

describe the order of vessels that carry bile

A

canaliculi
bile ductules
trabecular ducts
bile ducts

195
Q

describe the histology of hepatocytes

A

polyhedral epithelial cells
abundant mitochondria = granular cytoplasm
large central spherical nuclei
may be binucleate

196
Q

what are the 3 layers of the gall bladder wall

A
  1. simple columnar epithelium on bm
  2. specialised mucosa of loose fibrous connective tissue
  3. thick muscularis propria
197
Q

describe the histology of the pancreas

A

poorly defined fibrous capsule
septa divides glands into acini
pacinian corpuscles

198
Q

do liver cells replicate

A

yes because binucleate cells so regeneration capable

199
Q

what are pacinian corpuscles

A

onion shaped connective tissue built up around nerve endings = reduce mechanical sensitivity of nerve

200
Q

describe the histology of acinar cells

A

pyramidal shape
rich rER basally
zymogen granules apically
single nucleus

201
Q

do liver cells replicate

A

yes because binucleate cells so regeneration capable

202
Q

what are ito cells

A

in sinusoids
fat storing cells
play role in FA regeneration

203
Q

what cells produce kupffer cells

A

circulating macrophages derived from monocytes

204
Q

what is the role of insulin in the liver

A

liver stores glycogen
insulin promotes conversion of excess glucose to glycogen
glycogen can be broken down and released as glucose in response to glucagon

205
Q

how is iron stored in the liver

A

transferrin in hepatocytes

ferritin in kupffer cells

206
Q

what are the consequences of high fatty acid beta-oxidation

A

too much acetyl CoA produced = too much for Krebs = increased ketogenesis = results in acetone and hydroxybutyrate

207
Q

how is high beta oxidation regulated

A

high levels of glycerol-3-phosphate indicate high levels beta oxidation = insulin released to inhibit (glucagon stimulates beta oxidation)

208
Q

what 2 ways can ketoacidosis occur

A 
diabetic = not enough insulin
alcohol = high glucagon

Phase 1 mine (12 decks)

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