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Chemistry year 2 > Lecture set 2 > Flashcards

Lecture set 2 Flashcards

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1
Q

Liver
divided into?
where does it get blood from where it flow through

A

-Divided into right and left lobes surroundedby Round ligament (falsiform )
-recevied blood from hepatic artery which provided O2 blood from heart and hepatic portal vein brings nutrient rich blood from food we eat
-inferior vena cava brings O2 blood back to heart

Blood in the liver flows through the sinusoids which are lined by hepatocytes and empty into central vein >hepatic vein leading to inferior vena cava

Blood and bile travel in opposite directions

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2
Q

what is the flow pathway of bile

A

-flows out of the liver secreted by hepatocytes into bili canaliculi (the spaces between hepatocytes)
-left and right hepatic duct = common hepatic duct > cystic duct in gall bladder forming the common bile duct
-bile is produced in the liver
-blood flows in and bile flows out
-bile duct has 2 directions
1.empty into duodenum or through the cystic duct into gallbladder for concentration and storage
3L produced a day

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3
Q

What does a liver lobule consist of

A

-functional unit of the liver
-hepatocytes are arranged around a central vein
-lobule periphery has a portal triad Bile duct , hepatic artery and portal vein

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4
Q

What are kupffer cells

A

-clean up cell = fixed marcophages
-protrude into macrophages
-in the reticulo-endothelial system
-phagocytosis of foreign particles and bacteria

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5
Q

What is the main function of a kuphher cell

A
  • engulf/lyse old or damaged RBCs
    -hgb is released
    -irone from heme is preserved and carried through circulation by transferrin
    -Iron in bone marrow is used for RBC production or storage as ferritin or hemosiderin
    -porphyrin in heme is converted to bilirubin (waste produced by liver)
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6
Q

What is the function of the liver

A

1.Excretory & Secretory (Bile produced and secreted)

  1. Metabolism – breakdown of:
    CHO, Protein & Lipid Metabolism
    Synthesis: cholesterol, bile acids
    Vitamin metabolism
  2. Detoxification & Drug Metabolism – breakdown of drugs
  3. Circulatory/Hematologic
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7
Q

how does RBC destruction occur

A

-destruction occurs mainly in spleen
-hgb into iron, globin and heme
-iron binds to transferrin and brought to liver or BM for storage
-globin broken down from AAs
-heme converted into bilirubin and released into circulation

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8
Q

Excretion of toxic bilirubin

Metabolism

A

-bili released into circulation from spleen and BM
-bili-alb complex (unconj bili) goes from circulation to sinusoids = unconjugated bilirubin
-in hepatocytes bili removes itself from the complex, and conjugates with glucuronic acid in smooth ER
-conjugation catalyzed by UDP glucuronyl- transferase. Glucuronyl-transferase enzyme not full developed in newborns
-conjugated bili (or bilirubin diglucuronide) excreted into bile
-in intestine conju bili (bili digluconride) hydrolyzed to free bili and glucuronic acid
-free bili reduced to urobiligen (colorless form) by intestinal bacteria (free isnt found in blood or urine)
-urobilinogen oxidized to produce urobilin = bile pigment that gives poop its color

entero-hepatic circulation: 20% urobilinogen reabsorbed in intestine & back to liver
2-5% urobilinogen enters circulation, filtered by kidney, excreted in urine

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9
Q

What type of reaction occurs at the conjugation of bilirubin

A

esterification
with UDP transferase enzyme .
transfer a glucuronic acid molecule (x2 total) to EACH of the two carboxylic acid side chains to form the conjugated form (bilirubin diglucorinde)

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10
Q

When carbohydrates are ingested the liver will:

A

Use glucose for it’s own energy
Circulate glucose to other tissues
Store glucose as glycogen

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11
Q

Liver maintains glucose [ ] by 3 methods:

A

Glycogenesis (store glucose as glycogen) – during high glu

Glycogenolysis (breakdown stored glycogen) – during need for glucose (low glu)

Glyconeogenesis (create glucose from nonsugar carbon substrates) – when stored glu is depleted.

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12
Q

Liver function:

A

Breakdown carbohydrate and maintain glucose concentration

Breakdown of protein to form other proteins

breakdown of lipids from our diets

produces AND clears cholesterol

processes portal blood (hepatic artery, portal vein) coming from digestive tract before it enters circulation

absorbs nutrients needed for metabolic functions

capacity to store blood, can control blood volume

erythropoiesis: embryonic life & adults under stress (usually occurs in bone marrow but if lots of RBC destruction, liver may help by also producing RBCs)

production of blood coagulation factors (protein synthesis)

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13
Q

how is protein metabolized to form or break other proteins in the liver

A

synthesis
-rough ER
-plasma proteins: albumin, alpha-globulins and beta-globulins (not immunoglobulins)
coagulation factors: I, II, V, VII

Breakdown of protein is:
released into sinusoids, then into circulation maintains liver’s Amino Acid Pool

size of pool controlled by:
amino acids supplied (breakdown of what we eat)
transamination (enzymes: transaminases)
Deamination

Trans/demaination is the breakdown of AA , which produce urea and is excreted by kidneys

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14
Q

Lipid Metabolism in liver

A

-Metabolizes lipids & lipoproteins
-Gathers free fatty acids from diet and breaks them down to acetyl-CoA
-Acetyl-CoA can enter several pathways to form triglycerides, phospholipids or cholesterol

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15
Q

Synthesis of Cholesterol in the liver occurs how

A

-occurs in microsomes of hepatocytes
-derived from Acetyl-CoA
-synthesis of cholesterol esters
conversion of cholesterol to bile acids which are excreted as bile salts

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16
Q

Synthesis of Bile Salts

A

-before secretion cholic acid & deoxycholic acid conjugated with either glycine or taurine
-at bile pH bile acid conjugates exist as bile salts

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17
Q

how are bile salts excreted

A

-excreted into bile canaliculi
-emulsify fat in duodenum & facilitate absorption
90% excreted bile salts reabsorbed via portal vein & return to liver = enterohepatic circulation which allows substances to move between GI tract and liver

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18
Q

what is bile composed of

A

-clear, yellowish pH 7.0-8.5
-bile salts from cholesterol
-Bilirubin - conjugated bili, waste product, bili diglucuronide
-Cholesterol - in bile as a waste product , can form gallstones in excess
-Lecithin - phospholipid
-inorganic salts- bicarb, na, k. neutralizes acidic chyme from duodenum, provides alkaline pH for pancreatic and intestinal enzymes

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19
Q

Vitamin Metabolism in the liver how?

A

-liver stores stores fat-soluble vitamins (A, D, E, K)
converts β- carotene (veg & fruit) into Vitamin A

Vitamin K metabolism
1/2 produced by intestinal bacteria, ½ dietary
liver uses it to synthesize coagulation factors
II VII IX X&raquo_space; VitK dependent

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20
Q

how does the liver detoxify

A
  • can detox drugs, poison or bili and ammonia by binding to inactivate or chemically modify for excretion by

Oxidation – adding O2
Reduction – removing O2
Hydrolysis – cleaved by H20
Hydroxylation – introduce hydroxyl group (R-O-H)
Carboxylation – Adding CO2 to produce a carboxylic acid group (R-C=O)
Demethylation – removing methyl group

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21
Q

What is oxidation

A

liver breakdown of alcohol >aldehydes>carbox acids
-uses alcohol dehydrogenase (non-specific)

-ethanol to acetic acid
-methanol to formic acid

build up for formic acid can cause blindness
so if someone has MeOh OD then you give EtOH so there is completion with liver breaking down the EtOH instead of MeOH

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22
Q

What is hydrolysis and example

A

introduction of H2O
-breakdown of aspirin through hydrolysis and excreted through urine

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23
Q

What is the difference between enzymes, isoenzymes and coenzymes

A

Enzymes- large proteins = biological catalysts

Coenzyme (sometimes needed to drive rxn)
organic compounds or cofactors essential for full enzyme activity (e.g. NAD)

isoenzymes different molecular forms, but have similar chemical activity, identical active centers, different arrangement of aa in a side chain: related to tissue type

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24
Q

If you have increased enzymes in SERUM/PLASMA what does it mean

A

-marker of damaged organ, necrosis, cell damage, amount of enzyme can be proportional to damage

-increase production which occurs in organ obstruction - less common

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25
Q

how are enzymes measured

A

-Product formation (end point)
-substrate (how much used, formation or depletion based on enzyme activity)
-continuous monitoring , instrument takes multiple readings, change in absorbance over time, can use NAD or NADP

26
Q

What are some enzyme units

A

international unit-ne (1) micromole of substance (or substrate) per minute, U/L or IU/L *same thing

-amount of enzymes = activity NOT concentration

27
Q

What is part of the aminotransferanse group

transfer AA

A

-convert AA and alpha keto acids by transfer of AA group
AST transfer amino group between aspartate (substrate) and alpha-ketoglutarate > Product is oxaloacetate

ALT transfer amino group between alanine (substrate) and alpha-ketoglutarate > Product is Pyruvate

both part of Kerb cycle
physiological reactions
-both enzymes are substrate-and stereo specific in that they only act on L forms of AAs

28
Q

Where is ALT and AST most found

A

AST- heart, liver, muscle, kidney, pancreas and RBC (affected by hemolysis false increase)

ALT - most liver specific, kidney, heart, muscle, serum

29
Q

What is the significance of AST

A

increased in
-hepatocellular disorders like viral hep, cirrhosis
-cardiac muscle involvement ; rises in 6-8 hours of heart attack
-skeletal muscles - muscular dystrophies and inflammatory conditions

10-30 U/L

30
Q

diagnostic significance of ALT

A

-hepatic disorders
-viral diseases like hepatitis ALT will be higher than AST except when its alcohol induced

-ALT is elevated longer than AST due to longer half life
0-55u/l

31
Q

how do we analyze AST

A

-through coupled rxn where the analyzer continuously measures change in A at 340 when NADH is oxidized to NAD- a change in absorbance is proportional to enzyme activity

first rxn- aspartate + alpha-ketoglutarate (in the reagent) and PT sample with AST = oxalacetate then in 2nd rxn oxalacetate gets used and analyzer measures for NAD

at 340 NADH absorbs light and while at the same wavelength NAD does not

Optimal pH: 7.3 - 7.8
Sources of error:
Hemolysis: falsely ↑ AST results

32
Q

how is the ALT analysis done

A

coupled rxn
-first reaction produces the product PA
-looking for a decrease proportional to enzyme activity

Optimal pH: 7.3 - 7.8
Sources of error:
Unaffected by hemolysis

33
Q

What is GGT

Gamma-Glutamyltransferase (GGT)

A

transfer of a γ-glutamyl group from glutathione γ-glutamyl peptides to amino acids, H2O & other small peptides

found in kidney, brain , prostate, pancreas and liver (non specific of liver testing)

34
Q

What is the diagnostic significance of GGT increases are found where

A

-most sensitive of all liver enzymes
-increased in hepatobiliary (liver) diseases (this is bc location of GGT is in canaliculi – epithelial lining - of hepatic cells, easy access)
-highest increases seen in biliary tract obstruction - Cholestasis s-slowing of bile due to obstruction
-increased in chronic alcoholism- early marker of abuse even if there is no liver damage, levels can go back to normal after person stops drinking

35
Q

What is the issue with GGT diagnostically

A

-non specific for liver disease because it is increased in diabetes, MI, pancreatitis , in PT that get liver enzyme inducing drugs warfarin barbs

-can differentiate source of increased ALP because ALP is increased both liver disease & musculo-skeletal disease
therefore is GGT is not increased itll rule out liver disease

because in liver disease they are both increased

36
Q

how do we analyze GGT

A

ggt in patient , gamma glutam - reagent
-measure Abs of the dye
P-nitro-aniline is a coloured dye and absorbs light at 405-420
-so increase in A is proportional to GGT activity in pt
-no affect in hemolysis
-Males: 2-30 U/L
-Females: 1-24 U/L

37
Q

What is LD
what are the type of reactions

A

acts as catalyst between Lactate and pyruvate
-Works by transferring hydrogen using the co-enzyme NAD

forward pH 8.3- 8.9
-L -lactic acid oxidized to pyruvic with NAD as electron acceptor LA oxidized and NAD reduced

reverse pH 7.1-7.4, 3 times faster than forward
pyruvic acid reduced to L-LA with NADH as electron donor

38
Q

Where is LD found

A

heart, liver, skeletal muscle, kidney, RBC*☆, lung, smooth muscle, brain

-5 isoenyzmes
-tetramer w/ 4 polypep chains H for heart and M for muscle
LDH-1 is fastest, LDH-5 is slowest (electrophoretic mobility – how fast it migrates to anode )

38
Q

What is the significance of LD

A

non specific for liver disease because its found in too many tissues - not recommend in liver profile
-increased in liver and biliary disease highest in liver carcinoma
-high in cardiac disease = MI
-high in skeletal disease, renal diseases
-hematologic: hemolytic anemias, Pernicious anemia

39
Q

requirements for LD analysis

A
  • hemolysis is UNACCEPTABLE
    -unstable in serum - asap
    -store at PT loss of activity at 4 degrees
    -LD concentration in RBC is high so hemolysis increases it
    -concentration of LD in RBC is 100-150x what is found in serum
40
Q

What are the type of LD reactions

A

Forward - l-LA + NAD = PA +NADH (increase ABs)
and reverse (decrease ABs)

substrate must be in excess
-continously monitored reaction
-measure increase or decrease at 340 because at 340 NAD does not absorb
-NADH formation or depletion proportional to amount of enzyme (LD activity) in the specimen

41
Q

Sources of Error in LD analysis

A

Hemolysis: falsely elevated
improper anticoagulants: falsely decreased
freezing specimen: falsely decreased

reference varies based on forward or reverse reactions

42
Q

how can you test for LD isoenzymes

A

electrophoresis

not done usually because its expensive

43
Q

What is ALP and its tissue source

A

-located on the sinusoids and bile canaliculi membranes of liver
-Bone, ALP is in the osteoblasts so it’s involved in bone formation

-Catalyzes the hydrolysis of various phosphomonoesters

Tissue Source
Found in intestine, liver, bone, spleen, placenta and kidney

44
Q

ALP – Diagnostic Significance

A

-non specific for liver disease
-increased in hepatobiliary disorder
-highest in obstructive (extra hepatic conditions like gallstones
-sensitive to impaired bile flow; cholestasis increases synthesis of ALP
-Moderate increase in hepatrocellular diseases (e.g. hepatitis, cirrhosis)

↑ bone disorders (e.g. Paget’s disease)
↑ pregnancy

45
Q

How is ALP analyzed

A

p-Nitrophenylphosphate (colorless) is hydrolyzed with ALP and h2o at pH10.2 to p-nitrophenol (yellow)
-increase in ABs at 405 proportional to ALP in pt
-RI depends on age/sex, higher in children due to increased bone growth

Sources of error:
Hemolysis may cause slight ↑
Run ASAP – activity in serum increases at RT

46
Q

What is Jaundice/Icterus

A

abnormal accumulation of bilirubin in blood
-bile will accumulate in the skin, eyes mucous membranes and causes yellow discolouration
- Jaundice and icterus can be used interchangeably
-icterus is more for the yellow color of serum and plasma

47
Q

Increased Bilirubin in Plasma/Serum what do you look for first

A
  1. How much is present? (conc’n ?)
    we measure Total Bilirubin = unconjugated + conjugated
  2. What type of bilirubin is present?
    unconjugated: found in serum bound ot ALB and insoluble in water
    conjugated: majority normally excreted into bile

3 types of jaundice: pre-hepatic, hepatic, and post-hepatic

48
Q

What is bilirubin metabolism

A

RBC destroyed conversion of Heme to Biliverdin (intermediate product), then conversion of Biliverdin to Bilirubin (unconjugated)
-Bilirubin will combine with albumin in plasma (this is unconjugated)

-In the liver. Unconjugated is converted into conjugated via UDP glucorinde transferase
-Conjugated is carried through either gall bladder for storage or its in the small intestine
-in the small intestine the conjugated gets converted into URObili and then urobilin secreted into stool
-a little bit of the URO gets reabsorbed to liver, to kidney to be filtered and excreted in urine

49
Q

What is Hemolytic (prehepatic) Jaundice: Causes

A

hemolytic anemias - RBC destruction (ex. Thalassemia, hereditary spherocytosis, hereditary elliptocytosis, autoimmune hemolytic anemia, sickle cell anemia)

transfusion reaction (i.e. incompatible blood leads to increased RBC destruction)

Burns, Poisoning (trauma may lead to increased RBC destruction)

50
Q

Why is it called prehepatic hemolytic jaundice

A

-rate of hgb breakdown exceeded and there is accumulation of unconjugated bilirubin in serum = a pre-hepatic disorder

-conjugated bilirubin stays with RI
-hepatocyte function is normal only capacity for handling bilirubin is overloaded

The liver can conjugated can conjugate up to 2X its normal load. When the liver is working at max, then there will be more un conjugated bili going to the small intestine and kidneys so we will see more urobilinogen in urine and urobilin in stool

51
Q

What does Hemolytic Jaundice cause

A

urine & stool darker in colour
due to increased excretion of urobilinogen & urobilin
-mild jaundice
-bilirubin overproduction causes gallstone formation (composed of bilirubin)

-if there is an increase in RBC then there will be an increase in unconjugated bili causing jaundice

52
Q

Hemolytic Jaundice: Test Results

A

plasma / Serum
total bilirubin ↑ = unconjug + conjug
unconjugated bilirubin ↑
conjugated bilirubin →

Urine
urobilinogen ↑ urine dipstick testing (qualitative testing) – due to increase in load
-conjugated bilirubin (water soluble): negative

feces
urobilin ↑ not routinely performed – due to increase in load

Liver Enzymes: Since liver is operating normally
AST, ALT, ALP, GGT: within reference intervals

53
Q

What is hepatic jaundice causes
Defect in bili metabolism or transport

A

-Crigler-Najjar syndrome Gilbert’s syndrome (difference is where the mutation takes place)
-mutation in gene that produces UDP which affects conversion to conjug
-therefore bili cannot be conjug leading to increase of unconjuga

54
Q

What is hepatic jaundice causes

Defect in conjugated bilirubin excretion

A

-Dubin-Johnson syndrome
-Defect in conjugated bilirubin excretion. Bilirubin conjug is normal but removal from liver and excretion is affected
-Increase in conjug

55
Q

What is hepatic jaundice causes
Viral hepatitis & Cirrhosis

A

-affect depends on level of necrosis or impairment of hepatocytes
-in early phase bili is still getting conjug but not as effectively. Damaged liver cells will prevent reabsorption of urobilinogen, so we expect increase in urine urobilinogen excretion
-in later phases there is more unconjugated because the liver cant do its job so there is alot of both - mixed

56
Q

Hepatic Jaundice: Test Results

A

Plasma/Serum:
total bilirubin ↑
generally unconjugated bilirubin ↑
generally conjugated bilirubin ↑

Urine:
urobilinogen ↑ (later as liver is not functioning, ↓ or absent bc less conjugation occurring thus less conversion into urobilinogen)
conjugated bilirubin: positive (if increased in serum)

Feces:
urobilin ↓ (or absent): depends on degree of obstruction (bc less conjugation occurring thus less conversion into urobilinogen and then into urobilin)

Liver Enzymes:
AST, ALT, GGT: ↑
ALP ↑ or →

57
Q

Obstructive (post-hepatic) Jaundice
causes

A

cholestasis (slowing or stopping of bile flow)
-excretory pathway of bile (intra-hepatic & extra-hepatic ducts) physically obsrtucted preventing flow

carcinoma of pancreas
gallstones - common bile duct obstructed
liver tumor- liver CA

POST hepatic disorder

Liver is still functioning, still getting conjugated bilirubin but it’s not being properly excreted. if bile flow blocked, it accumulates in canaliculi causing rupture & increased permeability of the walls of the small bile passages
-bile mostly conj
-bilirubin diglucuronide leaks into sinusoids then circulation
-high conj in plasma/serum
-very high unconju bili (bound to alb) because of liver backup

58
Q

Obstructive Jaundice: Test Results

A

Plasma / Serum:
total bili ↑
unconjugated bilirubin ↑
conjugated bilirubin ↑ ↑

Urine:
urobilinogen ↓ or absent
conjugated bilirubin: positive

Feces:
urobilin ↓ or absent (stools paler) – bc bile doesn’t enter small intestine

Liver Enzymes:
ALP, GGT: ↑ ↑ (ALT, AST variable)
Increased production of ALP & GGT in bile canaliculi due to blockages in bile flow (cholestasis)

59
Q

What is delta bilirubin

A

-third fraction of bilirubin that contributes to “Total Bilirubin” if present
-conjugated bound to ALB
-the molecule is too large so it cant be filtered by the glomerulus and is not detected in urine so instead you see it in plasma
-you only see if there is SIGNIFICANT hepatic obstruction aka in babies w/o bile ducts

Chemistry year 2 (12 decks)

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