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Gastrointestinal Module > Biochem > Flashcards

Biochem Flashcards

1
Q

Functions of porphyrin

A

Oxygen transport in hemoglobin and myoglobin

Electron transport in cyrochrome a,b,c

Breakdown of peroxide as catalase

Hydroxylation in cytp450

Light absorption in chlorophyll

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2
Q

Porphyrin structure

A

4 pyrrole
Carbon bridges
Metal ion in center
Propionate and methyl attached

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3
Q

Metal Ion in porphyrin in hb

A

Iron

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4
Q

Metal Ion in porphyrin in chlorophyll

A

Magnesium

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5
Q

Forms of iron

A

Heme Fe2+ - ferrous

Hemin Fe3+ - ferric

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6
Q

Heme synthesis overview

A

In mitochondria :
(I)
Succinyl coa + glycine —> delta-aminolevulinic acid
Enzyme : ALA synthase

In cytosol

(II)
2 Delta aminolevulinic —> porphobilinogen
Enzyme : ALA dehydrogenase

(III)
Porphobilinogen —-> uroporphyrinogen I or III
Enzyme : HMB synthase

(IV)
Uroporphyrinogen I and III —> coproporphyrinogen I and III
Enzyme : uroporphyrinogen decarboxylase

In mitochondria
(V)
coproporphyrinogen III —> protoporphyrinigen IX
Enzyme : coproporphyrinogen oxidase

(VI)
Protoporphyrinogen IX—> protoporphyrin IX
Enzyme : protoporphyrinigen oxidase

(VII)
Protoporphyrin IX —-> heme
Enzyme : ferrochelatase

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7
Q

Rate limiting step of heme synthesis

A

Ala synthase

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8
Q

Form of control of ALA synthase

A

Transcriptional regulation
Heme and hemin repress transcription of enzyme

Coordination with glob in chain synthesis

Allosteric inhibition by heme and hemin

Inducers of enzyme : aromatic drugs, xenobiotics, steroids

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9
Q

Enzymes that can get deactivated by lead and other heavy metal

A

Ala dehydratase

Ferrochelatase

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10
Q

What enzyme is bifunctional in heme synthesis

A

HMB synthase

Uroporphyrinogen I and III synthase activity

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11
Q

What reaction in heme synthesis requires cysteine and ascorbic acid as reducing agents

A

Ferrochelatase

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12
Q

Iron deficiency impact on ferrochelatase

A

Insertion of zinc leading to zinc protoporphyrin - used clinically to determine iron deficiency

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13
Q

Porphyria

A

Hereditary or acquired defects in heme synthesis

Mostly autosomal dominant

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14
Q

Exception in porphyria that is autosomal recessive

A

Congenital erythropoietic porphyria

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15
Q

Location of porphyria in body

A

Hepatic or erythropoietic

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16
Q

2 major locations of heme synthesis

A

Liver

Bone marrow

17
Q

Lead poisoning

A

Inhibit ferrochelatase and ALA
Dehydratase

Coproporphyrin III and ALA accumulates in urine

18
Q

Symptoms of lead poisoning

A 
In children : 
Developmental defects 
IQ drop
Hyperactivity 
Insomnia

Adults:
Severe abdominal pain
Mental confusion

19
Q

Acute intermittent porphyria

A

HMB synthase defect

porphobilinogen and ALA accumulations in Uribe

Dark urine in light and air
NO photo sensitivity

20
Q

Congenital erythropoietic porphyria

A

Uroporphyrinogen III synthase defect

Accumulation of uroporphyrinogen I and coproporphyrinogen I in urine

PHOTOSENSITIVITY

21
Q

Porphyria cutanea tarda

A

Uroporphyrinogen decarboxylase deficiency

Uroporphyrin accumulates in urine

PHOTOSENSITIVE

22
Q

Most common form of porphyria

A

Porphyria cutanea tarda

23
Q

Hereditary coproporphyria

A

Coproporphyrinogen oxidase deficiency

Intermediates before this block accumulate in urine

PHOTOSENSITIVITY

24
Q

Variegated porphyria

A

Protoporphyrinogen oxidase deficiency

Intermediate before block accumulate

PHOTOSENSITIVITY

25
Q

Erythropoietic porphyria

A

Ferrochelatase deficiency

Protoporphyrin accumulate in erythrocytes, plasma and bone marrow

PHOTOSENSITIVITY

26
Q

Where do you find most heme

A

RBC (85%)

27
Q

Component formed after heme degradation

A

Biliverdin which forms bilirubin

28
Q

How is bilirubin transported

A

By serum albumin

29
Q

Excretion of bilirubin pathway

A

RBC with heme

RBC with heme degraded and release of bilirubin

Bilirubin transported by albumin to liver

Bilirubin in liver conjugated with glucuronic acid

Bile formed excreted into small intestine

In intestine , bacteria remove glucuronic acid and bilirubin is converted to urobilinogen

One part of urobilinogen is converted to stercobilin and excreted through feces

Other part of urobilinogen reabsorbed from gut and enter portal blood
Some of it also do enterohepatic cycle
Rest of it transported to kidney and converted to yellow urobilin and excreted in urine

30
Q

Types of jaundice

A

Hemolytic jaundice
obstructive jaundice
hepatocellular jaundice
jaundice in newborns

31
Q

Hemolytic jaundice

A

Massive hemolysis of red blood cell leads to more bilirubin than can be processed
More unconjugated bilirubin in blood which can’t be excreted so form jaundice

32
Q

Obstructive jaundice

A

Obstruction of bile duct (Tumors, bile stones)

Lead to 
nausea
 pain
 Pale clay colored stools 
liver damage 
increase in conjugated Bilirubin
33
Q

Hepatocellular jaundice

A 
Liver damage (cirrhosis, hepatitis) 
Cause increased bilirubin level in blood due to decreased conjugation

Decreased urobilinogen so urine is dark and stool is pale
High AST And ALT level due to liver damage
Nausea
Anorexia

34
Q

Jaundice in newborns

A

Premature babies have low expression of bilirubin glucuronyltramsferase

So excess bilirubin
Can cause toxic encephalopathy
Treatment with blue fluorescent light ( conversion of bilirubin to polar version)

35
Q

Crigler naijar syndrome

A

Deficiency in bilirubin glucuronyltramsferase

36
Q

Gilbert’s syndrome

A

Liver does not properly process bilirubin due to defect in enzyme for conjugation.

Overall mild
Light eye jaundice

37
Q

Techniques to determine bilirubin concentration

A

Van den bergh réaction

REaction when unconjugated bilirubin in aqueous solution

Reaction when unconjugated or conjugated in methanol => gives total bilirubin

CAn substract one from the other to find unconjugated bilirubin

Gastrointestinal Module (15 decks)

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