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Liver and friends Flashcards

1
Q

what are xenobiotics?

A

foreign chemical substance not normally found/produced in the body - can’t be used for energy requirements

can be absorbed across lungs, skin or ingested

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2
Q

what are drugs?

A

xenobiotics

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3
Q

how are xenobiotics excreted?

A

in bile, urine, sweat, breath

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4
Q

what are the characteristics of pharmacologically active compounds?

A

lipophilic, non-ionised at pH 7.4, bound to plasma proteins to be transported in blood

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5
Q

what is a lipophilic compound?

A

able to pass through plasma membranes to reach metabolising enzymes

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6
Q

what is a microsome?

A

a small particle consisting of a piece of endoplasmic reticulum to which ribosomes are attached

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7
Q

where are microsomal enzymes found?

A

smooth endoplasmic reticulum

mostly found in liver hepatocytes, but also in kidneys and lungs

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8
Q

what are examples of microsomal enzymes?

A

cytochrome P450, flavin monooxygenase, UDP, glucuronosyltransferase

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9
Q

what types of reactions are microsomal enzymes involved in? what do they do?

A

mainly phase I, also phase II

oxidative, reductive, hydrolytic

phase I: biotransform substances (one chemical to another)
phase II: glucuronidation

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10
Q

what is glucuronidation?

A

addition of glucuronic acid to a substance

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11
Q

what can activity of microsomal enzymes be induced or inhibited by?

A

drugs, food, age, bacteria, alcohol

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12
Q

where are non-microsomal enzymes located?

A

cytoplasm and mitochondria of hepatocytes in liver, in other tissue too

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13
Q

what reactions are non-microsomal enzymes involved in?

A

non specific - both phase I and II

all conjugation reactions except glucuronidation

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14
Q

what are examples of non-microsomal enzymes?

A

protein oxidases, esterases, amidases, conjugases, alcohol dehydrogenase, aldehyde dehydrogenase

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15
Q

what is the aim of drug metabolism? where does it occur?

A

to make drugs more polar so they can’t get across membranes and are easily excreted

liver

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16
Q

where are most drugs excreted? what is an exception?

A

kidneys

lipophilic drugs aren’t effectively removed as they’re passively absorbed, due to them diffusing through cell membranes easily

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17
Q

what is a phase I reaction?

A

aim: make drug more hydrophilic/polar so it can be excreted by the kidneys -unmasks/inserts polar functional group (OH, SH, NH2)

introduce/expose hydroxyl groups/other reactive sites that can be used for conjugation reactions (phase II)

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18
Q

what are the types of reactions in phase I reactions?

A

non-synthetic catabolic, oxidation, reduction, hydrolysis

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19
Q

are hydrophilic molecules usually involved in phase I reactions? why/why not?

A

no - they don’t reach metabolising enzymes as they’re excreted easily

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20
Q

what is involved in oxidation?

A

hydroxylation (add OH), dealkylation (remove CH side chains), deamination (remove NH), hydrogen removal

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21
Q

what is involved in reduction?

A

add hydrogen (saturate unsaturated bonds)

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22
Q

what is involved in hydrolysis?

A

split amide and ester bonds

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23
Q

what is functionalism?

A

introduces reactive group to drug

includes adding/exposing OH, SH, NH2, COOH

product of reaction is usually more reactive

small increase in hydrophilicity

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24
Q

what are phase I reactions mainly catalysed by?

A

p450 enzymes

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25
Q

what are cytochrome P450 enzymes?

A

type of microsomal enzyme

involved in phase I reactions

uses heme group (Fe2+) to oxidise substances

products are more water soluble

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26
Q

naming enzymes in cytochrome P450 family

A

prefix CYP
1st number = family enzyme belongs to
letter = subfamily
2nd number = individual genes involved

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27
Q

what are some important P450 isoenzymes?

A 
CYP 1A2
CYP 2C9
CYP 2C19
CYP 2D6
CYP 2E1
CYP 3A4
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28
Q

what is involved in the overall phase I reaction?

A

cytochrome P450 reductase transfers electrons from NADPH to CYP 450

contains flavoprotein which consists of flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN)

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29
Q

what is FAD? what does it do?

A

flavin adenine dinucleotide

accepts electrons from NADPH

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30
Q

what is FMN? what does it do?

A

flavin mononucleotide

electron donor to CYPs

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31
Q

what is the equation for the overall phase I reaction?

A

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

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32
Q

what is drug metabolism?

A

metabolic breakdown of drugs by living organisms, usually through specialised enzymatic systems

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33
Q

what is xenobiotic metabolism?

A

set of metabolic pathways that modify the chemical structure of xenobiotics (foreign to an organism’s normal biochemistry)

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34
Q

what can phase I reactions do?

A

inactivate drugs, further activate them, activate drug from pro-drug, make a drug into a reactive intermediate (could be carcinogenic or toxic)

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35
Q

what are examples of synthetic anabolic reactions?

A

glucuronidation, sulfation, glutathione conjunction, amino acid conjunction, acetylation, methylation, water conjunction

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36
Q

what is the donor compound in glucuronidation?

A

UDPGA

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37
Q

what is the donor compound in acetylation?

A

acetyl CoA

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38
Q

what is the donor compound in methylation?

A

S-adenodyl methionine

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39
Q

what is a conjugation reaction? what is it catalysed? what does it do?

A

attachment of substituent groups (endogenous molecules)

usually inactive products

catalysed by transferases

significantly increases hydrophilicity for renal excretion

mainly in liver, or other tissues e.g. lungs/kidneys

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40
Q

what is a glucuronidation reaction?

A

essentially adding a glucuronic acid group (glucuronide) to drug to make it more hydrophilic

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41
Q

what is the enzyme involved in glucuronidation?

A

glucuronosyltransferase (uridine 5’-diphosphoglucuronosyltransferase) (UGT) - microsomal enzyme, used in phase II reactions, catalyses reaction

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42
Q

what is required to conjugate glucuronic acid?

A

uridine diphosphoglucuronic acid (UDPGA) - coenzyme/donor compound

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43
Q

what does the glucuronidation reaction form?

A

covalent bonds

uridine diphosphate + drug-glucuronide (more hydrophilic)

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44
Q

what is aspirin?

A

analgesic, NSAID, antiplatelet, prodrug, irreversibly inhibits cyclooxygenase (COX)

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45
Q

role of aspirin in phase I metabolism

A

prodrug - activated upon metabolism

hydrolysis reaction

aspirin + H2O -> salicyclic acid + ethanoic acid

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46
Q

role of aspirin in phase II metabolism

A

conjugated with glycine or glucuronic acid

forms range of ionised metabolite

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47
Q

what is paracetamol?

A

acetaminophen

analgesic, antipyretic agent

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48
Q

metabolism of paracetamol

A

predominantly metabolised via a phase II reaction - conjugated with glucuronic acid and sulphate

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49
Q

toxicity of paracetamol

A

if stores of glucuronic acid and sulfate are running low, paracetamol undergoes phase I metabolism via oxidation to produce toxic NAPQI

removed by conjugation with glutathione

overdose - stores of glutathione can run low -> toxicity

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50
Q

what is paracetamol toxicity treated with?

A

N-Acetyl Cysteine

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51
Q

what is the overall reaction of alcohol metabolism?

A

ethanol -(ADH)-> acetaldehyde -(ALDH)-> acetate -> CO2 + H2O

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52
Q

what is ADH?

A

alcohol dehydrogenase

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53
Q

what is ALDH?

A

aldehyde dehydrogenase

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54
Q

what are effects of acetaldehyde?

A

carcinogenic - indications of high levels are facial flushing, rapid heartbeat, nausea

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55
Q

what are the uses of iron?

A

haemoglobin, myoglobin, bone marrow

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56
Q

what are sources of iron?

A

meat, liver, shell fish, egg yolk, beans, nuts, cereals

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57
Q

where does homeostatic control of iron balance occur? what is it regulated by?

A

intestinal epithelium (duodenum), actively absorbs iron from ingested foods

negative feedback - depending on body’s iron balance

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58
Q

how much of ingested iron is absorbed?

A

about 10%

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59
Q

what happens to iron ions once actively transported into duodenal intestinal epithelial cells?

A

incorporated into ferritin (protein-iron complex) that acts as an intracellular store for iron

most is released back into intestinal lumen (bound to ferritin) - tips of villi disintegrate. iron is excreted into faces

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60
Q

what happens when the body store of iron is enough?

A

increased conc of free iron in plasma and intestinal epithelial cells leads to increased transcription of the gene encoding for ferritin -> increased synthesis

-> increased binding of Fe in cells and reduction in amount of iron released into blood

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61
Q

what happens when body stores of iron are low?

A

production of intestinal ferritin decreases -> decreased amount of iron bound to ferritin -> increasing unbound iron released into blood

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62
Q

what is iron bound to in the blood?

A

plasma protein transferrin

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63
Q

where does transferrin take the iron?

A

to bone marrow to be incorporated into new erythrocytes

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64
Q

how is iron stored?

A

once in blood, there are v little means of excreting it - accumulates in tissues (most in liver in liver ferritin within Kupffer cells)

50% in haemoglobin
25% in heme containing proteins (mainly cytochromes)
25% in liver ferritin

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65
Q

what proteins does the liver produce?

A

plasma proteins, clotting factors and complement factors

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66
Q

what is albumin?

A

most abundant plasma protein

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67
Q

what are the functions of albumin?

A

binding and transport of large hydrophobic compounds e.g. bilirubin, FAs, hormones, drugs

maintenance of colloid osmotic pressure

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68
Q

what is colloid osmotic pressure?

A

effective osmotic pressure across blood vessels that are permeable to electrolytes but not large molecules

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69
Q

how does albumin maintain osmotic pressure?

A

its presence means the water conc. of the blood plasma is slightly lower than that of the interstitial fluid -> net flow of water out of the interstitial fluid, into the blood plasma

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70
Q

what do opposing forces do? what are they called?

A

act to move fluid across the capillary wall

Starling Forces

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71
Q

what are the Starling Forces? what do each of them do?

A

capillary hydrostatic pressure (favouring fluid movement out of capillary)

interstitial hydrostatic pressure (favouring fluid movement into the capillary)

osmotic force due to plasma protein conc. (favouring fluid movement into the capillary)

osmotic force due to interstitial fluid protein conc. (favouring fluid movement out of capillary)

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72
Q

what are forces at the arterial ends of the capillaries?

A

hydrostatic pressure from capillary = 38 mmHg > interstitial fluid HP (0) as fluid is quickly picked up by lymphatics

interstitial fluid protein conc. = 3mmHg, osmotic pressure due to plasma proteins = 28mmHg

net outward pressure exceeds net inward pressure -> bulk filtration of fluid out of capillaries

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73
Q

what are forces at the venous ends of the capillaries?

A

only difference in Starling forces is the capillary hydrostatic pressure - decreased to 15mmHg due to resistance

others are same

net inward pressure exceeds net outward pressure -> bulk absorption into capillaries

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74
Q

what is hypoalbuminea?

A

liver failure -> reduction in albumin in blood -> decreased capillary oncotic pressure -> accumulation of water in interstitial fluid -> oedema

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75
Q

apart from liver failure, why may albumin also decrease?

A

nephrotic syndrome, haemorrhage, gut loss, burns

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76
Q

what is nephrotic syndrome?

A

increased glomerular permeability, allowing proteins to filter through BM -> loss of up to several grams of protein a day

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77
Q

what is gut loss?

A

rare syndrome - wall of gut is unusually permeable to large molecules -> albumin loss

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78
Q

how can burns lead to albumin decrease?

A

extensive tissue damage to capillaries -> loss of proteins through walls of capillaries

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79
Q

what are globulins? what do they transport?

A

antibody functions

most are gamma-globulins (not made in liver), some are alpha/beta globulins (made in liver)

lipids by lipoproteins
iron by transferrin
copper by caeruloplasmin

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80
Q

liver production of clotting factors

A

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

bile salts - essential for vit K absorption

vit K essential for synthesis of clotting factors 10,9,7,2

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81
Q

what are complement factors?

A

plasma protein which stick to pathogens

recognised by neutrophils - mark pathogens to kill

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82
Q

what is protein turnover?

A

continuous degradation and resynthesis of cellular proteins

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83
Q

when does rate of protein turnover increase?

A

tissues are undergoing structural rearrangement e.g. damage due to trauma, uterine tissue in pregnancy and skeletal muscle during starvation

severe burns - attempts at remodelling, significant amounts of protein lost in exudate

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84
Q

what are the primary methods of protein breakdown?

A

lysosomal and ubiquitin-proteasome pathway

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85
Q

what is the lysosomal pathway of protein breakdown?

A

carried out in reticulo-endothelial system of liver

sinusoidal endothelial cells remove soluble proteins and fragments from blood through fenestrations (sieve plates) on luminal surface . in liver, proteins are fused into lysosomes containing lysozyme - hydrolytic enzyme that breaks it down into amino acids

Kupffer cells (resident macrophages) phagocytose particulate matter, packaging them into phagosomes containing hydrolytic enzymes

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86
Q

what do sinusoidal endothelial cells do in the lysosomal pathway? what proteins do they remove?

A

remove soluble proteins and fragments from blood through fenestrations (sieve plates) on luminal surface

fibrin, fibrin degradation products, collagen, IgG complexes

proteins then fused into lysosomes in liver

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87
Q

where does the ubiquitin-proteasome pathway occur?

A

in cytoplasm of cells

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88
Q

what proteins does the ubiquitin-proteasome pathway degrade?

A

those defective due to incorrect amino acid sequences

damage to normal function (denatured)

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89
Q

what does the rate of degradation depend upon in the ubiquitin-proteasome pathway?

A

denatured (unfolded) protein is more readily digested than a protein with an intact conformation

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90
Q

what is the process of the ubiquitin-proteasome pathway?

A

proteins targeted for degradation by attachment of small peptide ubiquitin

directs protein to protein complex (proteasome) - unfolds the protein and breaks it down into small peptides

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91
Q

where does amino acid degradation and catabolism occur?

A

in hepatocytes of liver

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92
Q

what happens to amino acids not required as building blocks for protein synthesis?

A

must undergo degradation to specific compounds

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93
Q

what is catabolism?

A

break down of complex substances to simpler ones accompanied by release of energy

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94
Q

what does amino acid catabolism require?

A

alpha amino group (nitrogen containing) to be removed

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95
Q

what does amino acid catabolism produce?

A

nitrogen - incorporated into other compounds or excreted

carbon skeleton - metabolised and used in Kreb’s cycle

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96
Q

what are the 2 main catabolism processes?

A

oxidative deamination and transamination

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97
Q

what is the reaction of oxidative deamination?

A

liberation of amino group as free ammonia

amine group from amino acid is replaced by an oxygen from water to form an alpha-keto acid

coenzyme involved, in products is bound to 2H from water

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98
Q

what is the overall equation for oxidative deamination?

A

amino acid + water + coenzyme -> alpha-keto acid + ammonia + coenzyme-2H

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99
Q

what is the only amino acid that undergoes rapid oxidative deamination?

A

glutamate

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100
Q

what happens to the alpha-keto acid formed from oxidative deamination?

A

used in Kreb’s cycle for use in glucose production - gluconeogenesis

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101
Q

what are the coenzymes/enzymes involved in oxidative deamination?

A

coenzyme: NAD+ (forwards) and NADPH (backwards)
enzyme: glutamate dehydrogenase

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102
Q

what happens to the ammonium produced in oxidative deamination?

A

quickly dissociates to form ammonia, which can be converted to urea via the urea cycle as it’s toxic

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103
Q

what does oxidative deamination depend on?

A

readily reversible

depends on concentrations of glutamate, alpha-ketoglutarate, ammonia

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104
Q

what is the most abundant amino acid in the body?

A

glutamate

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105
Q

what happens when there is excess ammonia?

A

it can easily cross the BBB and react with alpha-ketoglutarate -> decrease in ATP. dangerous

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106
Q

what is transamination?

A

transfer of an alpha-amino group from an amino acid to a keto-acid to form an alpha-keto-acid

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107
Q

what happens if the amino acid alanine is transaminated?

A

amino group is transferred to alpha-ketoglutarate, forming pyruvate (used in Krebs cycle for gluconeogenesis) and glutamate (oxidatively deaminated)

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108
Q

what is the enzyme involved in transamination?

A

aminotransferase - found in cytosol of mitochondria through body, esp. in kidneys and liver

specific to one or few amino group donors

alanine - alanine aminotransferase (ALT)

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109
Q

what is nitrogen balance?

A

a measure of the equilibrium of protein turnover

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110
Q

what is anabolic/catabolic nitrogen balance?

A

anabolic - positive balance, net gain in amino acids

catabolic - negative balance, net loss in amino acids

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111
Q

what are the essential amino acids?

A

histidine, isoleucine, leucine, lycine, methionine, phenylalanine, threonine, tryptophan, valine

body cannot synthesise them

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112
Q

what are the conditionally non-essential amino acids?

A

arginine, asparagine, glutamine, glycine, proline, serine, tyrosine

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113
Q

what are the non-essential amino acids?

A

alanine, asparatate, cysteine, glutamate

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114
Q

what is the most common cause of an anabolic nitrogen balance?

A

intake > loss

pregnancy

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115
Q

what are the recommended daily intakes of amino acids?

A
  1. 8g/kg (normal men and women)
  2. 3g/kg (pregnant women)
  3. 4g/kg (first few months of life)
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116
Q

what are the causes of negative nitrogen balance?

A

intake < loss

malnutrition, multiple trauma/extensive trauma where there’s lots of tissue damage

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117
Q

action of ALT in muscles

A

utilises pyruvate from glycolysis as an alpha-keto acid for transamination

converts glutamate to a-ketoglutarate

produces alanine and alphaketoglutarate (krebs cycle to produce glucose via gluconeogenesis)

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118
Q

what happens to alanine in the liver?

A

travels via blood to liver

converted back to pyruvate by transamination

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119
Q

what happens to pyruvate produced from alanine in the liver?

A

source of carbons for glucose production via gluconeogenesis

enters blood as glucose, used in muscles to produce pyruvate via glycolysis - used again to remove excess ammonia (NH3)

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120
Q

what is the aim of the glucose-alanine cycle?

A

to remove excess ammonia/ammonium from amino acids from muscle protein

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121
Q

what happens to the glutamate produced from alanine in the liver via reverse transamination?

A

converted to ammonium via oxidative deamination, producing ammonium which rapidly dissociates into ammonia

ammonia can be converted to urea via urea cycle

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122
Q

where are the enzymes involved in the urea cycle found?

A

in liver in the mitochondria/cytosol of hepatocytes

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123
Q

what is the process of the urea cycle?

A

arginine (from diet/protein breakdown) is cleaved by arginase to form urea and ornithine

ammonia and CO2 is added on the ornithine to form citrulline

another molecule of ammonia is added to citrulline to regenerate arginine and let the cycle go around again

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124
Q

what is consumed by one turn of the urea cycle?

A

3 ATP equivalents

4 high energy nucleotides (PO4-)

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125
Q

what is/are the compound(s) produced by the urea cycle?

A

urea

arginine, ornithine and citrulline are recycled

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126
Q

deficiencies/absences of enzymes involved in urea cycle

A

arginase

deficiencies: higher levels of ammonia in blood, neurotoxicity
absences: incompatible with life

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127
Q

enzymes involved in the urea cycle

A 
N-acetylglutamate synthase (NAGS)
carbamylphosphate synthetase (CPS I)
ornithine transcarbamylase (OTC)
argininosuccinate synthetase (ASS)
argininosuccinate lyase (ASL) 
arginase
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128
Q

neurotoxicity due to high ammonia levels

A

ammonia can cross BBB very easily

converted to glutamate by glutamate dehydrogenase

depletion in alpha-ketoglutarate

as alpha-ketoglutarate falls, so does oxaloacetate -> krebs cycle stopping

irreparable cell damage and neural cell death

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129
Q

what is the absorptive state?

A

ingested nutrients are absorbed from GI tract into blood

proportion of nutrients are catabolised and used

remainder converted and stored for future use

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130
Q

what happens during the absorptive state?

A

glucose used to generate ATP

amino acids converted to proteins

glycerol and FAs converted to lipids

glucose converted to glycogen

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131
Q

what is the post-absorptive state?

A

nutrients no longer absorbed in GI tract

nutrient stores must supply energy requirements of body

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132
Q

what is glucose regulation in the post-absorptive state?

A

glucose no longer absorbed from GI tract

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133
Q

why is it essential to maintain the plasma glucose concentration in the post-absorptive state?

A

CNS always using it for fuel

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134
Q

what are the main sources of glucose in the post-absorptive state?

A

glycogenolysis, lipolysis, protein

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135
Q

what is glycogenolysis?

A

hydrolysis of glycogen to monomers of glucose-6-phosphate

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136
Q

where does glycogenolysis occur?

A

liver and skeletal muscles

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137
Q

what happens in hepatic glycogenolysis?

A

in liver, glucose-6-phosphate enzymatically converted to glucose, which enters the blood

begins within seconds of stimulus (e.g. sympathetic nervous activation)

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138
Q

how long can glucose from the liver supply body requirements?

A

several hours

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139
Q

what happens in skeletal muscle glycogenolysis?

A

skeletal muscle doesn’t have enzyme needed to make glucose

glucose-6-phosphate undergoes glycolysis to produce ATP, pyruvate and lactate

140
Q

what happens to the products of skeletal muscle glycogenolysis?

A

ATP and pyruvate used directly by the muscle cell

some lactate enters blood, circulates to liver and is converted to glucose which enters the blood (contributes indirectly to blood glucose)

141
Q

what is lipolysis?

A

catabolism of triglycerides in adipose tissue via hydrolysis of triglycerides to produce glycerol and fatty acids

142
Q

how do glycerol and fatty acids enter the blood?

A

diffusion

143
Q

what happens to glycerol from lipolysis?

A

enters liver which enzymatically converts it to glucose

144
Q

what is a source of blood glucose a few hours into the post-absorptive state?

A

protein

145
Q

what does protein loss during a prolonged fast lead to?

A

disruption of cell function, sickness and death

146
Q

how do proteins produce glucose?

A

supply amino acids, which enter blood and are taken up by the liver and converted to glucose via the alpha-keto acid pathway - then released into blood

147
Q

what is gluconeogenesis?

A

synthesis of glucose from precursors e.g. amino acids and glycerol, i.e. non-carbohydrate precursors

148
Q

how much ATP is consumed per glucose formed?

A

6

149
Q

where is fat stored?

A

mostly in adipocytes - form tissues called adipose tissue

hepatocytes

150
Q

what are triglycerides?

A

3 fatty acids bound to a glycerol molecule

151
Q

what kind of energy is stored in the body?

A

78% - triglycerides
21% - proteins
1% - carbohydrates

152
Q

what do dietary lipids consist of?

A

95% - triglycerides

5 - phospholipids, FFAs, cholesterol, fat soluble vitamins

153
Q

what are lipids?

A

esters of fatty acids and certain alcohol compounds

154
Q

what are functions of lipids?

A

energy reserves, structural part of cell membrane, hormone metabolism

155
Q

what are lipoproteins?

A

used to transport cholesterol in the blood

156
Q

what is HDL? what does it do?

A

formed in liver

remove excess cholesterol from blood and tissue, deliver this to liver which secretes into the bile and converts it into bile salts

157
Q

why is HDL called good cholesterol?

A

removes other forms of cholesterol from bloodstream

higher levels of it is associated with lower risk of heart disease

158
Q

what is LDL? what does it do?

A

formed in plasma

main cholesterol carriers - deliver cholesterol to cells throughout body

bind to plasma membrane receptors specific for a protein component of LDLs - taken up by cells via endocytosis

159
Q

why is LDL called bad cholesterol?

A

high plasma concentrations can be associated with increased deposition of cholesterol in arterial walls and higher incidence of heart attacks

160
Q

what is a good thing that LDL does?

A

essential in supplying cells with cholesterol needed to synthesise cell membranes

steroid hormone production in gonads and adrenal glands - aldosterone and cortisol

161
Q

what is VLDL? what does it do?

A

synthesised in hepatocytes

carries triglycerides from glucose in liver to adipocytes

162
Q

where is half of the energy used by muscle, liver and kidneys derived from under resting conditions?

A

catabolism of fatty acids

163
Q

where is most of adipose tissue deposited?

A

underlying skin or surrounding internal organs

164
Q

what is the function of adipocytes?

A

to synthesise and store triglycerides during periods of food uptake

when food is not being absorbed - release FAs and glycerol into blood to provide energy for ATP formation

165
Q

where does fatty acid catabolism occur?

A

mitochondria of hepatocytes

166
Q

what are the steps of fatty acid catabolism?

A

molecule of coenzyme A links to carboxyl at end of fatty acid

breakdown of ATP -> AMP + 2Pi

coenzyme A derivative of fatty acid goes through beta oxidation

molecule of acetyl-CoA is split off from fatty acid and 2 pairs of hydrogen atoms are transferred to coenzymes (one to FAD and other to NAD+)

hydrogen atoms from coenzymes enter oxidative phosphorylation to form ATP

another coenzyme A attaches to fatty acid, cycle is repeated

167
Q

what does one turn of fatty acid catabolism do?

A

shortens fatty acid chain by 2 carbon atoms until all have been transferred to coenzyme A molecules

lead to production of CO2 and ATP via krebs and oxidative phosphorylation

168
Q

what enzymes are involved in the hepatic metabolism of lipids?

A

lipoprotein lipase

hepatic lipase

169
Q

what does lipoprotein lipase do?

A

hydrolyses triglycerides in lipoproteins (chylomicrons and VLDLs) into 2 free fatty acids and 1 glycerol molecule

170
Q

what does hepatic lipase do?

A

expressed in liver and adrenal glands

converts IDL (intermediate density lipoprotein) into LDL - packages it with more triglycerides to be released into body

171
Q

what is bile? where is it stored and concentrated?

A

secreted in hepatocytes continuously

emulsifies fats

excretory pathway for most steroid hormones, drugs and toxins

stored and concentrated in gall bladder as some NaCl and water are absorbed into blood

172
Q

where does the gall bladder lie?

A

at junction of right-mid-clavicular line and costal margin

173
Q

what is the functional unit of the liver?

A

hepatic lobule - formed by hepatic plates stacked on top of eachother

174
Q

what are hepatic lobules?

A

hexagonal in cross section, portal triad at each corner

wedge-like arrangements of hepatocytes 1-2 cells deep, surrounded by sinusoids

175
Q

what does the portal triad consist of?

A

hepatic portal vein, hepatic artery, bile duct

176
Q

what runs up the centre of the hepatic lobule?

A

central vein - eventually becomes hepatic vein

177
Q

what does the hepatic sinusoid contain?

A

substances absorbed from SI end up in hepatic sinusoid, containing oxygen rich blood from hepatic artery and nutrient rich blood from portal vein

178
Q

what is the structure of a hepatic sinusoid?

A

fenestrated, discontinuous endothelium

179
Q

what is the space of Disse?

A

separates hepatocytes from sinusoid

180
Q

what happens to substances absorbed from the SI from the sinusoid?

A

reach vena cava via central vein or taken up by hepatocytes for modification

181
Q

what is the blood supply of the liver?

A

80% from portal vein

20% from hepatic artery

182
Q

what happens to the blood when it leaves the branches of artery and vein when it leaves the portal triad?

A

blood is mixed as it enters the sinusoids

183
Q

what direction does the bile flow in?

A

opposite direction to the blood

184
Q

what are Kupffer cells? where are they found?

A

resident macrophage population in liver

sinusoids, which are lined by a continuous layer of specialised endothelial cells interspersed with them

185
Q

what are stellate cells?

A

undersurface of sinusoids

produce extracellular matrix in space of Disse

186
Q

what are bile canaliculi? what are their structure? how is bile pumped towards bile ducts?

A

between adjacent hepatocytes

not true vessels - don’t have specialised walls

groove running along side of hepatocytes

bound together by tight junctions, gap junctions, desmosomes which cross both cell membranes

actin filaments are in areas around the canaliculi and pump bile towards bile ducts

187
Q

where do the common bile duct and pancreatic duct join, and enter the duodenum?

A

join at ampulla of Vater

enter duodenum at major duodenal papilla (2nd part of duodenum)

sphincter forms around 2 ducts to regulate entry of bile into duodenum - called sphincter of Oddi

188
Q

what does bile contain?

A

bile salts, lecithin (phospholipids), HCO3- and other salts, cholesterol, bile pigments, trace metals

189
Q

why are components of bile aggregated into micelles?

A

bile salts, cholesterol and lecithin

maintain aggregation even when concentrated

bile salts are powerful detergents (for fat emulsification, anionic) - damage cell membrane

190
Q

what are bile salts produced by?

A

hepatocytes

191
Q

what is the role of HCO3- in bile?

A

neutralise acids in duodenum

192
Q

what are the most important digestive components of bile?

A

bile salts

193
Q

what secretes components of bile?

A

hepatocytes - bile salts, cholesterol, lecithin, bile pigments

epithelial cells lining bile ducts - most of HCO3- rich solution

194
Q

what stimulates secretion of bile/pancreas solution?

A

secretin - in response to presence of acid in duodenum

195
Q

what does secretin do?

A

stimulates secretion of bile/pancreatic solution in response to acid in duodenum

196
Q

concentration of bile

A

hepatic bile enters gallbladder via cystic duct and stored and concentrated here - hepatic bile is dilute

197
Q

what stimulates gallbladder contraction?

A

cholecystokinin due to amino and fatty acids in duodenum by I cells of duodenum

198
Q

what does CCK do? what is it secreted by?

A

stimulates gallbladder contraction and the sphincter of Oddi to relax - causes bile to flow into duodenum

I cells of duodenum, due to amino and fatty acids in duodenum

199
Q

vasculature of gallbladder

A

cystic artery supplies oxygenated blood to gallbladder

no venous drainage - stuck to liver bed and blood drains directly into the liver, no identified pathway

200
Q

what happens to the bile salts during digestion of a fatty meal?

A

most entering the intestinal tract via bile are absorbed by specific Na+ coupled transporters in the jejunum and terminal ileum

returned via portal vein - secreted into bile

uptake of bile salts from portal blood into hepatocytes by secondary active transport coupled to Na+

201
Q

what is the enterohepatic circulation?

A

recycling pathway from the liver to the intestine

often recycles bile salts

202
Q

what happens to bile that doesn’t enter the enterohepatic circulation?

A

small amount (5%) escape recycling and are lost in faeces

liver synthesises new bile salts from cholesterol to replace it

203
Q

bile synthesis

A

liver synthesises it from cholesterol

it secretes cholesterol extracted from blood into bile

204
Q

how is cholesterol homeostasis maintained?

A

bile secretion and excretion of cholesterol in the faeces

205
Q

cholesterol in water

A

insoluble - solubility in bile is achieved via micelles.

in blood, it’s bound into lipoproteins

206
Q

when is bile secretion the greatest?

A

during and just after a meal - liver always secreting some

207
Q

what type of muscle is the sphincter of Oddi?

A

smooth

208
Q

how is bile concentrated? where?

A

dilute bile secreted by liver is shunted into the gallbladder

some of NaCl and water is absorbed into the blood

209
Q

what is adaptive relaxation? how does it apply to the gallbladder?

A

size increases but pressure doesn’t

happens when gallbladder fills with bile

210
Q

what are bile pigments?

A

substances formed from the haem portion of haemoglobin when old/damaged erythrocytes are broken down in the spleen and liver

211
Q

what is the predominant bile pigment?

A

bilirubin

212
Q

what is bilirubin?

A

yellow substance that’s extracted from the blood by hepatocytes and actively secreted into bile

213
Q

what contributes to the colour of bile?

A

yellow bilirubin

214
Q

where are erythrocytes broken down?

A

when old/damaged, they’re broken down by macrophages (phagocytic)

spleen and bone marrow, also Kupffer cells of the liver

215
Q

how is haemoglobin broken down?

A

erythrocytes ingested into macrophages

broken down into haem and globin

globin broken down into amino acids - used to generate new erythrocytes in bone marrow

haem further broken down, under action of hemoxygenase into biliverdin and Fe2+ and CO

216
Q

breakdown of haem. enzymes? products?

A

hemoxygenase

biliverdin and Fe2+ and CO

217
Q

what happens to the Fe2+ generated from haem breakdown?

A

bound to iron transporter transferrin - shuttled to bone marrow, incorporated into new erythrocytes

218
Q

what happens to biliverdin from haem breakdown?

A

reduced by biliverdin reductase (enzyme) into unconjugated bilirubin

219
Q

what is unconjugated bilirubin? what happens to it?

A

produced from reduction of biliverdin (from haem) by biliverdin reductase

toxic - lipid soluble and insoluble in blood

bound to albumin, transported to liver

220
Q

movement of unconjugated bilirubin. what is it bound to?

A

albumin - transported to liver, as it’s insoluble in blood

221
Q

what happens to unconjugated bilirubin in the liver?

A

glucuronidation (addition of a glucuronic acid) by enzyme UDP glucuronyl transferase - converted into conjugated bilirubin

222
Q

what is conjugated bilirubin?

A

formed from unconjugated bilirubin in the liver by glucuronidation by UDP glucuronyl transferase

soluble and able to be excreted

223
Q

what happens to conjugated bilirubin after being formed in the liver?

A

dissolved in bile (as it is soluble) and travels down right/left hepatic ducts, common hepatic ducts and in the cystic duct, and into the common bile duct to enter the duodenum

224
Q

what happens to the conjugated bilirubin in the small intestine?

A

enters duodenum, and reaches ileum/large intestine

reduced through hydrolysis reaction (glucuronic acid group removed) by intestinal bacteria to form urobilinogen

225
Q

what is urobilinogen?

A

formed from conjugated bilirubin in the ileum/large intestine, where it undergoes a hydrolysis reaction by intestinal bacteria

lipid soluble

226
Q

what happens to 10% of urobilinogen?

A

reabsorbed into the blood and bound to albumin, transported into liver - oxidised to urobilin

227
Q

what is urobilin? what happens to it?

A

formed from urobilinogen that’s reabsorbed from the blood - oxidation reaction

recycled into bile/transported into kidneys and secreted in urine - yellow colour

228
Q

what happens to 90% of the urobilinogen?

A

oxidised by different type of intestinal bacteria to form stercobilin

229
Q

what is stercobilin? what happens to it?

A

formed from urobilinogen by oxidation by different type of intestinal bacteria

excreted into faeces - responsible for brown colour

230
Q

what is jaundice?

A

a yellow discolouration of skin caused by a high serum bilirubin level (detectable clinically when bilirubin is above 50 micromole/L)

231
Q

what are the 3 main types of jaundice?

A

pre-hepatic, hepatic/intra-hepatic, post-hepatic/obstructive

232
Q

what is pre-hepatic jaundice? what is its pathology?

A

increased breakdown of erythrocytes -> increased levels of serum unconjugated bilirubin without excess bilirubin in urine

stools brown, urine normal

yellow skin

enlarged spleen (excess breakdown)

233
Q

why may the spleen be enlarged in pre-hepatic jaundice?

A

excess breakdown of erythrocytes -> increased serum levels of unconjugated bilirubin

234
Q

what are the causes of pre-hepatic jaundice?

A

malaria, sickle cell anaemia, thalassaemia, physiological jaundice of the newborn

235
Q

what is physiological jaundice of the newborn caused by?

A

excess breakdown of foetal haemoglobin as it’s no longer required - increase in unconjugated bilirubin and liver can’t conjugate it fast enough due to not being developed properly

236
Q

what is hepatic/intra-hepatic jaundice?

A

due to hepatocellular swelling

impaired cellular uptake, defective conjugation/abnormal secretion of bilirubin by hepatocytes

liver is damaged - unable to metabolise unconjugated bilirubin so it builds up, also raised serum conjugated bilirubin

237
Q

what are the manifestations of hepatic/intra-hepatic jaundice?

A

increased conjugated and unconjugated bilirubin

decreased urobilinogen

dark urine, pale/normal stools

enlarged spleen

yellow skin

238
Q

what is hepatic/intra-hepatic jaundice caused by?

A

viral hepatitis, drugs, alcohol hepatitis, cirrhosis, jaundice of newborn

239
Q

what is post-hepatic/obstructive jaundice? what is its pathology?

A

biliary system is damaged, inflamed or obstructed

elevated serum conjugated bilirubin

dark urine, pale stools

normal unconjugated bilirubin

decreased urobilinogen

no enlarged spleen

yellow skin

240
Q

what are the causes of post-hepatic/obstructive jaundice?

A

gallstones, pancreatic cancer, gallbladder cancer, bile duct cancer, pancreatitis (acute or chronic)

241
Q

why can cancer/inflammation of the pancreas cause jaundice?

A

head of pancreas is situated in duodenal loop, near common bile duct

eventually causes obstruction of the duct -> jaundice

242
Q

where will acute pancreatitis pain be?

A

radiate from the back

243
Q

what is Gilbert syndrome? what is its pathology?

A

shortage of UDP glucuronyl transferase - small amounts of conjugation occur

normal conjugated bilirubin level but raised unconjugated bilirubin level

244
Q

what causes gall stones to form?

A

bile salts, cholesterol and phospholipids are water-insoluble and are maintained in a soluble form as micelles

when conc. of cholesterol becomes high in relation to conc. of phospholipid and bile salts, cholesterol crystallises out of solution forming gall stones

245
Q

small bile stones

A

may pass freely through common bile duct into intestine without complications

246
Q

larger bile stone

A

may lodge in opening of gallbladder -> painful contractile spasms of smooth muscles

serious problems if it’s lodged in common bile duct, preventing bile from entering intestines

247
Q

what can stop bile from entering the intestines?

A

stone becoming lodged in common bile dut

248
Q

what are the consequences of a significant decrease in bile due to gall stones?

A

decreased fat digestion and absorption

impaired absorption of fat-soluble vitamins, clotting problems (vit K) or calcium malabsorption (vit D)

steatorrhea

diarrhea and fluid and nutrient loss

249
Q

what are fat soluble vitamins?

A

A, D, K, E

250
Q

what is steatorrhea?

A

caused by decreased bile due to gall stones

fat that’s not absorbed enters large intestine and appears in faeces

251
Q

what causes diarrhea and fluid/nutrient loss in gall stones?

A

bacteria in large intestine covert some unabsorbed fat into fatty acid derivatives, and alter salt and water movements

leads to net flow of fluid into large intestine

252
Q

is the pancreas intraperitoneal or retroperitoneal?

A

completely retroperitoneal apart from the tail

253
Q

what is the tail of the pancreas attached to?

A

spleen - intraperitoneal

254
Q

what can happen to the body of the pancreas?

A

crushed against vertebral bodies during trauma

255
Q

what can happen to the head of the pancreas?

A

closely related to the common bile duct

carcinoma/inflammation of head of pancreas can block bile duct -> post-hepatic/obstructive jaundice

256
Q

what is the uncinate process?

A

comes from ventral bud (rest of it is from dorsal bud) - SM artery and vein are entrapped between head and uncinate process

257
Q

what is between the head and uncinate process of the pancreas?

A

superior mesenteric artery and vein

258
Q

what artery runs in close proximity to the duodenum? what could happen to it?

A

superior gastroduodenal artery

duodenal ulcer can erode the gastroduodenal artery -> haemorrhage and haematemesis

259
Q

what is haematemesis?

A

vomiting of blood

260
Q

what is the development of the pancreas?

A

develops as 2 separate outgrowths - ventral and dorsal pancreas

ventral pancreas rotates around and fuses with dorsal pancreas - becomes head

biliary bud

261
Q

what forms the main pancreatic duct during development?

A

dorsal - Santorini’s duct

ventral - Wirsung’s duct

262
Q

what is the blood supply of the pancreas?

A

celiac trunk

SMA runs through the head because it’s enveloped during the rotation when dorsal and ventral pancreas fuse

dorsal pancreatic artery (from splenic artery), transverse pancreatic artery (from dorsal pancreatic artery), ant. and post. inferior (from SMA)/superior (from gastroduodenal artery from hepatic artery from CT) pancreaticoduodenal arteries

263
Q

what is the venous drainage of the pancreas?

A

splenic vein - joins superior mesenteric vein to form portal vein

264
Q

what does the exocrine pancreas secrete?

A

HCO3- (bicarbonate)

digestive enzymes

265
Q

what is the process of exocrine pancreas secretion?

A

arise from acinar tissue of the pancreas

secreted into ducts which converge into the pancreatic duct which joins the common bile duct, then enters duodenum at ampulla of Vater

266
Q

what is the function of the sphincter of Oddi?

A

circular smooth muscle

regulates flow into duodenum, prevents mixing of bile and pancreatic juice in duct

267
Q

what does reflux of bile down the pancreatic duct cause?

A

acute inflammation due to detergent properties

268
Q

when does the accessory pancreatic duct usually emerge?

A

above the ampulla of Vater

269
Q

what is pancreatic HCO3- secreted by?

A

epithelial cells lining ducts - duct cells

270
Q

what is the function of pancreatic HCO3-?

A

protect duodenal mucosa from gastric acid

buffers material entering the duodenum to a pH suitable for enzyme action

271
Q

what stimulates the secretion of HCO3-?

A

secretin - due to acid in duodenum. from pancreas and liver. potentiates acion of hormone CCK

272
Q

what is secretin secreted by? what is its function?

A

S cells of duodenum - due to acid in duodenum

stimulates secretion of HCO3- from pancreas and liver

potentiates action of CCK

inhibits acid secretion and gastric motility in stomach

273
Q

how is HCO3- secreted into the duct lumen by pancreatic duct cells?

A

apical membrane Cl/HCO3- exchanger

formed by H+ pumped out

274
Q

where is the energy for HCO3- secretion from?

A

Na+/K+ ATPase pumps on basolateral membrane

275
Q

why does Cl- not accumulate in the cell?

A

ions are recycled into the lumen via the CFTR channel (Cystic Fibrosis Transmembrane Conductance Regulator)

276
Q

what does CFTR stand for?

A

cystic fibrosis transmembrane conductance regulator

277
Q

what is transcellular transport?

A

through membrane porters or channels

lumen to interstitium

278
Q

what is paracellular transport?

A

through tight junctions (spaces between cells)

279
Q

what else moves into the pancreatic duct lumen?

A

Na+ and water via a paracellular route, due to the electrochemical gradient established through the CFTR channel

280
Q

what moves into the capillary from pancreatic duct cells?

A

H+ from H2CO3 and Na+ and K+

281
Q

secretion of digestive enzymes by the pancreas

A

enzymes are secreted by gland cells at pancreatic end of duct system

secreted as active or precursors (in inactive form zymogens)

282
Q

what are zymogens?

A

inactive form of digestive enzymes

283
Q

what do the pancreatic enzymes digest?

A

triglycerides (fat) to fatty acids and monoglycerides, polysaccharides to sugar, proteins to amino acids and nucleic acids to nucleotides

284
Q

what are active pancreatic digestive enzymes?

A

alpha-amylase and lipase

285
Q

what is alpha-amylase?

A

active pancreatic digestive enzyme

converts starch to maltose (glucose disaccharide)

286
Q

what is lipase?

A

active pancreatic digestive enzyme

converts triglycerides to monoglyceride and fatty acids

287
Q

what is the function of zymogens?

A

protects pancreatic cells from autodigestion

288
Q

what is a key step in the activation of precursors secreted by pancreas?

A

enterokinase

289
Q

what is enterokinase?

A

proteolytic enzyme embedded in luminal plasma membranes of intestinal epithelial cells

splits off a peptide from pancreatic trypsinogen forming active enzyme trypsin

290
Q

what is trypsinogen?

A

pancreatic proteolytic enzyme

activated by enterokinase to form trypsin

291
Q

what is trypsin?

A

pancreatic proteolytic enzyme activated by enterokinase

activates other pancreatic zymogens by splitting off peptide fragments

292
Q

what is chymotrypsinogen?

A

pancreatic zymogen which is activated into the enzye chymotrypsin by trypsin

293
Q

what are the functions of trypsin and chymotrypsin?

A

enzymes used to break peptide bonds in proteins to form peptide fragments - digest ingested proteins

294
Q

inhibition of pancreatic exocrine secretion

A

somatostatin produced by D cells in pancreatic islets/islets of Langerhans

295
Q

what is somatostatin produced by? what is its function?

A

D cells in pancreatic islets/islets of Langerhans

inhibits pancreatic exocrine secretion

296
Q

what are the cell types in the islets of Langerhans?

A

alpha, beta, delta/D, PP cells

297
Q

what do pancreatic alpha cells produce?

A

in islets of Langerhans

glucagon

298
Q

what do pancreatic beta cells produce?

A

in islets of Langerhans

insulin and amylin

299
Q

what do pancreatic delta/D cells produce?

A

in islets of Langerhans

somatostatin - inhibitor of insulin and glucagon

300
Q

what do pancreatic PP cells produce?

A

in islets of Langerhans

pancreatic polypeptide

301
Q

pancreas and diabetes

A

autoimmune destruction of islets of Langerhans -> diabetes mellitus

type 1: pancreas fails to produce enough insulin
type 2: cells fail to respond to insulin properly

302
Q

what are the phases of pancreatic secretion?

A

cephalic and gastric phase

303
Q

how does the cephalic phase affect pancreatic secretion?

A

initiated by sensory experience of seeing and eating food

involves parasympathetic vagus nerve stimulation of acinar cells to produce digestive enzymes

304
Q

how does the gastric phase affect pancreatic secretion?

A

initiate by presence of food within stomach - involves parasympathetic vagus nerve stimulation of acinar cells to produce digestive enzymes

305
Q

what happens to the pancreas by the end of the cephalic and gastric phases?

A

pancreatic ducts are filled with inactive digestive zymogens ready for release into the intestinal lumen with bicarbonate, via sphincter of Oddi

306
Q

what stimulates the secretion of digestive enzymes from the pancreas?

A

CCK

307
Q

what empties into the sinusoids?

A

terminal branches of portal vein and hepatic artery

308
Q

how does blood leave the liver?

A

via hepatic vein, which eventually drains into the IVC

blood is deoxygenated, detoxified, contains normal homeostatic nutrient levels

309
Q

what is the primitive gut?

A

made from endoderm (epithelial lining, hepatocytes, endocrine and exocrine cells of pancreas)

visceral mesoderm (muscle and connective tissue)

310
Q

what is the foregut?

A

oral pharyngeal membrane -> liver bud

celiac artery, oesophagus, stomach, liver, biliary apparatus, 1/2 of duodenum

311
Q

what is the midgut?

A

liver bud -> 2/3rds transverse colon

SMA, distal half of duodenum, jejunum, ileum, appendix, cecum, ascending colon, right 2/3rds of transverse colon

312
Q

what is the hindgut?

A

2/3rds transverse colon -> cloacal membrane

IMA, left 1/3 of transverse colon, sigmoid colon, rectum, anal canal

313
Q

what is the hepatic diverticulum?

A

cellular expansion of the foregut which gives rise to the parenchyma (functional part) of the liver

314
Q

when and where does the hepatic diverticulum appear?

A

middle of 3rd week as an outgrowth of the endodermal epithelium at the distal end of foregut (duodenum)

315
Q

what does the liver bud contain?

A

rapidly proliferating cells that penetrate the septum transversum

316
Q

what is the septum transversum?

A

thick mass formed in the embryo that gives rise to parts of the thoracic diaphragm and ventral mesentery

317
Q

when does the bile duct form?

A

when connection between the liver diverticulum and the foregut narrows

318
Q

what develops from the bile duct?

A

cystic diverticulum - ventral outgrowth. dives rise to the gallbladder and cystic duct

319
Q

what gives rise to the gallbladder and cystic duct?

A

cystic diverticulum - ventral outgrowth of the bile duct

320
Q

what develops with further growth of the liver bud?

A

allows epithelial liver cords to intermingle with umbilical and vitelline veins, forming the hepatic sinusoids

321
Q

how are the hepatic sinusoids formed?

A

further growth of liver bud allows epithelial liver cords to intermingle with umbilical and vitelline veins - forms sinusoids

322
Q

what do liver cords differentiate into?

A

hepatocytes (liver parenchyma) and form lining of biliary ducts

323
Q

what forms the hepatocytes and the lining of the biliary ducts?

A

liver cords

324
Q

what does the ventral mesentery develop into? when?

A

haematopoietic cells, Kuppfer cells, connective tissue cells

325
Q

how much does the liver weigh at the 10th week? why?

A

10% of total body weight due to large numbers of sinusoids and involvement of liver in haematopoietic function

326
Q

how much does the liver weigh at birth? why?

A

5% of total body weight due to small numbers of haematopoietic islands in the liver. haematopoietic function is greatly reduced

327
Q

when do hepatic cells start production of bile?

A

12th week

328
Q

when does the haematopoietic function of the liver subside?

A

during last 2 months of intrauterine life

329
Q

what happens to liver structures after birth?

A

left umbilical vein obliterates to form the ligamentum teres

ductus venosus undergoes fibrosis leaving ligamentum venosum

330
Q

what is a mesentery?

A

fold of tissue that attaches organs to the body wall

331
Q

what is intraperitoneal?

A

double layer of peritoneum that completely surrounds the organ

332
Q

what is retroperitoneal?

A

the organ is only covered by the peritoneum on its anterior side

333
Q

where is the ventral mesentery?

A

occurs only in foregut

334
Q

where is the ventral mesentery derived from?

A

septum transversum

335
Q

what mesenteries do the foregut, midgut and hindgut have?

A

foregut has dorsal and ventral mesenteries

midgut and hindgut have only dorsal mesentery

336
Q

formation of lesser omentum

A

stomach rotates 90 degrees along longitudinal axis (left becomes anterior)

posterior wall grows quicker (gives greater curvature)

rotates around anterior-posterior axis - pyloric region moves right and up and cardiac region moves left and down

337
Q

what are the proportions of endocrine cells in the pancreas?

A

beta cells: 65-80%
alpha cells: 15-20%
delta cells: 3-10%

338
Q

where does the pancreas develop from?

A

endodermal lining of the duodenum as dorsal and ventral buds

339
Q

where are the dorsal and ventral buds located?

A

dorsal bud in dorsal mesentery

ventral bud in ventral mesentery close to bile duct

340
Q

what does the ventral/dorsal pancreatic bud form?

A

uncinate process and inferior part of head of pancreas

dorsal - remaining part

341
Q

what forms the main pancreatic duct?

A

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

342
Q

what does the accessory pancreatic duct drain?

A

lower part of head and uncinate process

opens at minor papilla (3cm proximal to main duct)

343
Q

where/when do islets of Langerhans develop from?

A

parenchyma of pancreas at third month

344
Q

when does insulin secretion begin?

A

fifth month

345
Q

where does pancreatic connective tissue develop from?

A

visceral surrounding mesoderm

Peer teaching (10 decks)

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