A L L C H A P T E R S O F B I O C H E M I S T Y

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 Table of Contents

Contents Page

.
g. Protein 03

2-
Lipid 37

3.
Carbohydrates 55

4 .
Metabolism 66

. .

aaan.ep.io , ,

6. Nutrition 127

7.
Hormones 1-66

8 . Clinical & Molecular

174
Environmental
Amino Acids & Peptides( Harper).
Thursday, 12 September 2019 7:24 PM
Proteins Contd.
Saturday, 14 September 2019 5:28 PM
0. General Amino Acid Metabolism (Urea Cycle)
(Vasudevan)
Thursday, 24 October 2019 11:05 PM
Gastric Digestion of Proteins

In the stomach, hydrochloric acid is secreted. It makes the pH optimum for the action of pepsin and also
activates pepsin. The acid also denatures the proteins.

Rennin

Rennin otherwise called Chymosin, is active in infants and is involved in the curdling of milk. It is absent
in adults. Milk protein, casein is converted to paracasein by the action of rennin. This denatured protein
is easily digested further by pepsin.

Pepsin

It is secreted by the chief cells of stomach as inactive pepsinogen. The conversion of pepsinogen to
pepsin is brought about by removal of 44 amino acids from the N-terminal end, by the hydrochloric
acid. The optimum pH for activity of pepsin is around 2. Pepsin is an endopeptidase, Pepsin catalyses
hydrolysis of the bonds formed by carboxyl groups of Phe, Tyr, Trp and Met. By the action of pepsin,
proteins are broken into proteoses and peptones.

Pancreatic Digestion of Proteins

The optimum pH for the activity of pancreatic enzymes (pH 8) is provided by the alkaline bile and
pancreatic juice. The secretion of pancreatic juice is stimulated by the peptide hormones,
Cholecystokinin and Pancreozymin. Pancreatic juice contains the important endopeptidases, namely
Trypsin, Chymotrypsin, Elastase and Carboxypeptidase.
These enzymes are also secreted as zymogens (trypsinogen, chymotrypsinogen and proelastase), so that
the pancreatic acinar cells are not autolyzed. All the three are serine proteases, i.e. the active centers
of these enzymes contain serine residues.

Trypsin

Trypsinogen is activated by enterokinase (enteropeptidase) present on the intestinal microvillus

membranes. Once activated, the trypsin activates other enzyme molecules. Trypsin is activated by the
removal of a hexapeptide from N-terminal end. Trypsin catalyses hydrolysis of the bonds formed by
carboxyl groups of Arg and Lys.

Acute pancreatitis: Premature activation of trypsinogen inside the pancreas itself, will result in the
auto-digestion of pancreatic cells. The result is acute pancreatitis. It is a life-threatening condition.

Chymotrypsin

Trypsin will act on chymotrypsinogen, in such a manner that A, B and C peptides are formed. These 3
segments are approximated, so that the active site is formed. Thus selective proteolysis produces the
catalytic site.

Carboxypeptidases

Trypsin and chymotrypsin degrade the proteins into small peptides; these are further hydrolysed into
dipeptides and tripeptides by carboxypeptidases present in the pancreatic juice. The
procarboxypeptidase is activated by trypsin. They are metalloenzymes requiring zinc.

Intestinal Digestion of Proteins

Complete digestion of the small peptides to the level of amino acids is brought about by enzymes
present in intestinal juice (succus entericus). The luminal surface of intestinal epithelial cells contains
the following enzymes:

Leucine Amino peptidase :

It releases the N-terminal basic amino acids and glycine.

Proline Amino Peptidase :

It removes proline from the end of polypeptides.

Dipeptidases and Tripeptidases :

They will bring about the complete digestion of proteins

Food Allergy

Dipeptides and tripeptides can enter the brush

border of mucosal cells; they are immediately
hydrolysed into single amino acids. They are then
transported into portal vein. Rarely, larger molecules
may pass paracellularly (between epithelial cells)
and enter blood stream. These are immunogenic,
causing antibody reaction, leading to food allergy.
PROTEASES & PEPTIDASES DEGRADE PROTEINS TO AMINO
ACIDS
The proteasome consists of a
macromolecular, cylindrical complex of
proteins, whose stacked rings form a
central pore that harbors the active sites
of proteolytic enzymes. For degradation,
a protein thus must first enter the
central pore. Entry into the core is
regulated by the two outer rings that
recognize polyubiquitinated proteins
Biosynthesis of
Urea
Non-oxidative Deaminations
1. Dehydratases act on hydroxy amino acids to remove ammonia from
the following amino acids:
a. Serine will give rise to pyruvate
b. Threonine is converted to alpha keto butyric acid.

2. Desulfhydrase: Cysteine undergoes deamination and simultaneous transsulfuration to form

pyruvate.

3. Histidine also undergoes non-oxidative deamination to form urocanic acid; catalysed by histidase.

Ammonia may also be produced in the gastrointestinal tract by bacterial putrefaction.

In the urea cycle 2 ATPs are used in the first reaction. Another ATP is converted to
AMP and PPi, which is equivalent to 2 ATPs.The urea cycle consumes 4 high energy
phosphate bonds. However, fumarate formed in the 4th step may be converted to
malate. Malate when oxidised to oxaloacetate produces 1 NADH equivalent to 2.5
ATP. So, net energy expenditure is only 1.5 high energy phosphates. The urea
cycle and TCA cycle are interlinked, and so, it is called as "urea bicycle”.

Regulation of the Urea Cycle

Coarse Regulation :
The enzyme levels change with the protein content of diet. During
starvation, the activity of urea cycle enzymes is elevated to meet
the increased rate of protein catabolism.

Fine Regulation :
The major regulatory step is catalyzed by CPS-I where the positive
effector is N-acetyl glutamate (NAG). It is formed from glutamate
and acetyl CoA . Arginine is an activator of NAG synthase.
 Amino Acids : Structure and Properties (Vasudevan)
Thursday, 21 November 2019 6:03 PM
21. Lipids & its Physiological Significance
Sunday, 22 September 2019 5:54 PM
13. Cholesterol (Vasudevan)
Thursday, 17 October 2019 9:14 PM
Cholesterol regulates the expression of HMG CoA reductase gene
and LDLR (LDL receptor) gene. A specific recognition sequence known as the
sterol regulatory element (SRE) is present in DNA. SRE binding by sterol
regulatory element binding protein (SREBP) is essential for the transcription of
these genes. When cholesterol levels are sufficiently high, the SREBP remains
as an inactive precursor. It binds and activates an SREBP cleavage activator
protein (SCAP), which is an intracellular cholesterol sensor. When cholesterol
is less, SCAP escorts SREBP to Golgi bodies. Two golgi proteases (S1P and S2P)
sequentially cleave the SREBP to a protein, which activates the transcription
of HMGCoA reductase gene by binding to SRE
 Plasma
lipids
• Total
plasma lipid cis 400
600mg 1dL
-

•
About 40% = cholesterol
30% =

phospholipids
20% =

triglycerides
insoluble in water
•

Lipids are ,
thus complexed with Protein .

Protein Apo protein -1 apolipoprotein

part lipoprotein is
•

q
( apo
-

Lp)

Classification contain
ca ,
any , omicrons Apo protein B 48
-
- -

.
5
major types : -

(
b, VLDL = B -
100

C) I D L
(

(d) L D L = B -
100

(
e) HD L =

Apo
-

As free acid bounded to protein

•

fatty are
loosely thus not

included in
lipoprotein .

ca , Chylomicnns
Synthesis
.
chylo microns are
formed in intestinal mucosal cells .

. Rich in
triglyceride
and apo A
only
contain 48
•
At
first they Apo B - -

later bloodstream added

in
Apo C & E are
from HDL
-
.

during transport .

Metabolism
•
Main sites are
Adipose tissue and skeletal muscle .

• The
enzyme Lpl ( Lipoprotein lipase ) Only on
adipose tissue ,

muscles and heart g

not in liver .

present in che lo micron activates Lpl

•

Apoc -
I .

•
Lpl hydrolyses triglycerides present in chelomicrons into
acids &
fatty glycerol
-
 Function

.ch#micnon are the transport form g dietary triglyceride .

to adipose tissue (
for storage ) and to muscle / heart
(
for energy
need )
b
( ,
Y
LIL
synthesis
•

Tniacye glycerol synthesized in liver is incorporated into

VLDL
along
with hepatic cholesterol .

major lipoprotein present

in VLDL
Apo B wi
.

• -
100

Metabolism
•
Apo CII activates Lpl which liberates fatty acids that
are taken up by Adipose tissue and muscle .

°
Remnant g v LDL → I DL
ten cholesterol
/
↳ has TAG & more .

Loses more
triglyceride and
converted in LDL
function =

VLDL
endogenous from liver to peripheral tissues
°
carries TAG .

(c) Low density lipoprotein :

LDL transports cholesterol from liver to tissue

.

peripheral .

only apo protein present

The in LDL B too
apo
-

•
Most g LDL ins derived from VLDL

Half life in blood 2

days
. -
= .

Metabolism

B- to them →
→ -
②⑥
Coated
Clathrin Lysosome LDL

coated pits
reside
digested
cholesterol c) . a .

deposited
 Function
⑨
About 75% plasma cholesterol iis
incorporated into
LDL
particles .

•
Three major fates :

cas Used for synthesis g

other steroids like steroid
hormone
do cholesterol
,
may
be incorporated into membranes .

(c) Cholesterol may be esterified to a

Muff by a
age cholesterol
a
age transferase ( A CAT ) for storage .

Clinical
lol Toncentrateon blood has
• in
positive correlation with
cardiovascular disease .

o
LDL -s Eaten by -s Deposited in sub → Atheroma tous
endothelial
Macrophages
space
plaque
k
t
( Ham cells )
Atherosclerosis
Thus Bad cholesterol A
LDL = .

Thrombosis
•

(d)
High density Lipoprotein :

HDL transport cholesterol from tissues to liver

°
.

apo protein
in
• The main HDL is
Apo A -
I

Metabolism
-

•
The intestinal cells synthesize components g HDL and
release in blood .

• The
free cholesterol denied from peripheral tissue cells
are
taken up by HDL .

cholesterol
o
Apo A I -

activates LCAT ( lecithin acyltransferase )

in
present plasma .

•
The KAT binds to HDL disk ;
 lecithin
Lecithin
gn liver specific
yso
/
.
,

binds
receptor S R -
Bt

to Apo A
-

I present
~ On HD L
cholesterol ester
✓
-

cholesterol .

Mateen with lot cholesterol taken liver

HDL in
by
•

9 up
mediated
cells by apo A I
receptor mechanism
-

Function
•
HDL in the main
transport form g cholesterol from peripheral
tissue g liver which in later excreted
,
through bile .

This non called cholesterol

reverse
transport n HDL .

body in bile
route cholesterol from
• The
only excretory g .

•
Excretion g cholesterol needs prior esterification with Pu FA .

Po Pu FA in anti a theme
genic
.

Clinical
cholesterol
•
HDL is
good as it or an
hoathenogenic .

• HD L L 35
my 1dL increases risk while > 60
mg Idi protects
diseases
the
person from coronary .

sent
1. General Chemistry
Friday, 15 November 2019 10:06 PM
A glycosidic bond or glycosidic linkage is a type of covalent
bond that joins a carbohydrate (sugar) molecule to another
group, which may or may not be another carbohydrate.
 1,4-α-glycosidic and 1,6-glycosidic linkages in
the glycogen oligomer

Dextrins are intermediates in the hydrolysis of starch.

Cellulose is the chief constituent of plant cell walls. It is insoluble and consists of β-D-
glucopyranose units linked by β1 → 4 bonds to form long, straight chains strengthened
by cross-linking hydrogen bonds. Mammals lack any enzyme that hydrolyzes the β1 →
4 bonds, and so cannot digest cellulose. It is the major component of dietary fiber.
Microorganisms in the gut of ruminants and other herbivores can hydrolyze the
linkage and ferment the products to short-chain fatty acids as a major energy source.
There is some bacterial metabolism of cellulose in the human colon.

Chitin is a structural polysaccharide in the exoskeleton of crustaceans and insects, and

also in mushrooms. It consists of N-acetyl-D-glucosamine units joined by β1 → 4
glycosidic bonds.

Pectin occurs in fruits; it is a polymer of galacturonic acid linked α1 → 4, with some

galactose an/or arabinose branches, and is partially methylated
 Metabolic
Pathways g Glucose
① Describe
digestion
I
and absorption
og Carbohydrates .

→
Carbohydrates are
present as
comp Len polysaccharides and to
some extent Disaccharides ( Gm diets

starts
•

Digestion in Mouth
by salivary 9-
Amylase .

•
gm stomach the process a digestion g carbohydrates shops
due acidic
to
highly environment .

•
In intestine ,
the cells secrete sucrase ,
Maltase ,

g so maltase and lactase , which

hydrolyzes disaccharides .

another
Amylase available
In
pancreatic juice a is
° -

which
hydrolyze the a. 1,4 .
glycosidic linkages randomly .

Clinical :

lactase
lactose Gm tolerance :
hydrolyzes lactose to
glucose e

galactose lactase is in brush border

.

present of
enterocytes -

lactase leads to lactose intolerance

Deficiency
•

g
.

condition lactose accumulates

Gn this in
gut that
°

, ,

leads to diarrhea and

flatulence .

• Condition can be
congenital or
acquired .

• lactose intolerance can also occur when there in a

sudden to milk based diet

change
.

it contains lactobacilli
•
Card in an
effective treatment as

which contains lactase .

Absorbafion :

Only monosaccharides are absorbed

by intestine .

•
Rate max Galactose
moderate Glucose
minimum Fructose .
 Absorb lion g Glucose :

•
Glucose can be absorbed through its specific transporter .

which are transmembrane proteins .

Glatt
. Some transmembrane proteins are
to Glu 77

•
Glucose can also be transported as co
transport from
-

lumen to intestinal cells which mediated

,
is
by
sodium Dependent Glucose Transporter -
t
( SG lat -
t)

•
gn Intestine ,
it is Salut -
I

gn
kidney it in salat 2
-

Clinical
Rehydration Fluid
-

.
Common treatment for diarrhea is Oral
. It contains Glucose and Nat .

•
Presence g Nat helps transporting glucose via co -

transport
be maintained
• That's how Nat
in diarrhea .
and Glucose can in
body
Glucose transporters :

Glee T t -
RBC ,
brain . Kidney ,
Retina ,
Placenta
Glee T z
-
Sens al surface g gmteslinal Cells ,
liver ,
B cells Paneer .

Glut 3 - Neurons Brain

,

Glut 4 -

skeletal ,
heart muscles ,
adipose tissue
Glut 5 - Small intestine ,
testis ,
sperms ,
kidney .

Glut 7 -
liner Endoplasmic Reticulum
S Glatt -
Intestine
sake I 2 -

kidney .

. In Type 2 diabetes mellitus .

membrane Glu 74 is

reduced resistance
.
leading to insulin in muscles
Fat cells .
&

°
Glut 5 is Fructose transporter .
 under
② Kl hat in the major catabolic
pathway y
Glucose

Anaerobic conditions ? Mention the steps in

pathway
and indicate the
key enzymes
.

Pathway :
Glucose
④e Eat:
Glu ! se - 6 -

phosphate
=

( Phospho hexose

isomer those
yn
-
G -

phosphate
Eihl . Bisphosphate
-

( Aldolase)

( Glyceraldehyde
Glycentaldehyde f
NAD #
-
3 -

phosphate t DHAP

43 p (
pi

.it/-mutmeiz.pthosphoglycerate
tht
3- phosphate > NA DH

dehydrogenase) 1.3 is
phosphog ly cerate

i:÷÷÷:÷÷÷÷:i ÷÷i "

phots phenol T
( Eno lane ) ( Mgtt )

I GET: P¥, " IT

lactate
pyruvate teh )

Energy yield from glycolysis in anaerobic condition is

°

to
only equal 2 ATP .

Glucose Lactate
•
Egm ; + 2 Pit 2 ADP → 2 + 2 ATP

Biological significance :
Actively contracting muscles
-

that
rapidly consume ATP also
can
regenerate ATP

entirely by Anaerobic
glycolysis .
 ③ Describe process g glycolysis .

Explain how
many
molecules
conditions .
g ATP are
formed in anaerobic & aerobic

in the which the

Glycolysis pathway in
glucose is
converted to pyruvate ( aerobic condition ) or lactate
( anaerobic condition ) with
production g small
along
quantity g energy .

Emb den
• Also known as
Meyerhof Parmar ( EMP ) Pathway -
-

•
It is the
only pathway that in taking place in the all

cells
g body the .

Glycolysis in only source

n energy
in
Erythrocytes .

Glycolytic pathway provides carbon skeletons for

essential amino acids
synthesis of non -
as well as

glycerol part g fat

.

. Most g the reactions in

glycolytic pathway are

reversible , which are also used

for gluconeogenesis .

Glucose

Is Molecules ATP
formed :

/
phosphate
-
g
is:P'd!
""

Fructose
-

in
G
phosphate
In Anaerobic Condo
- -

④ED÷c±÷
needs
.
.

F- e -
1,6 B- is phosphate
caidolase)
Sete ps Enzyme Source No ATP

¥¥÷÷÷÷÷÷÷÷÷÷÷÷
f .

D
" """

: Hexone none
-

if /
t .
-
i
.

÷÷:÷÷÷÷÷÷÷: " "

s
most:L:c : .
. .

⇐now ? Pt-

Phots
hfspghog 't cerate 6 1,3 bis
phospho
cerate
-

Aep 1×2=2
phenol pyruvate
l¥± g ly kinase
pyntavate C. ¥7 .
Imari
lactate
,
g
pyruvate kinase ATP
-1×2=2
Total 4 -

2=20
 In Aerobic fond :

step No
Enzyme Source .

7 ETP

I Hexokinase -
-

3
Phosphofnechokinase I
-
-

5
Glyceraldehyde -

3 -

NADH 2-5×2=5

phosphate dehydrogenase
bisphosphoglyeerale ATP 1×2=2
6 1,3 -

kinase

kinase
Pyruvate ATP 1×2=2
9
-

Total =
g -
2

-
-
⑦

④ klhat are
factors affecting Glycolysis ?
the

Glycolysis is mainly controlled by Regulatory Enzymes or

key enzymes
:

( d) H exo kinase
(b)
Phospho fnecho kinase
( C)
Pyruvate kinase .

Hexo kinase at
(a) :
High affinity for glucose thus will act even

concentrations
low glucose .

•
Glucose -
G -

phosphate has a
feedback inhibitory effect
on
enzyme
-

Insulin increases the and promotes

no
g enzymes
• .

glycolysis .

Glucagon inhibits the enzyme

•
.

I
• Glucose tire )
→
feedback to Hexokinase
 (b)
Phospho Fratto kinase : ( PFK ) in the most important
rate -

limiting enzyme for glycolysis pathway .

•
ATP and citrate are most important inhibitors .

•
AMP ,
ADP are
promoters ( activators .

fructose
• -

2,6 ,
bisphosphate (F 2,6 -
BP ) increases the
activity g PFK lphosphofneehokinase-TE.IE

oakn.fi?ghec9on/.=. '
.

-2.6 BP

ai:-O I;
Pyruvate
.
kinase
Regulatory
(c)
a

:
enzyme Insulin
Glucagon
for Glycolysis .

97nF;ni¥
°
'

¥6 P
( CFA - CoA * IF-2.co/3PT
°
T

Pof -01Acetyl
AT WA most
imp
④ Regulator
Glucagon
-1 Pyruvate kinase
←
T④ Insulin
fructose
I -96 BP

③ What in BPG shunt and describe its

significance .

In RBC step 6 which is

,

1. 3 bis
phospho glycerite → 3 -

phospho glycerite ; is
bypassed .

phospho glycerite It
"2,3,B
"
And I , 3 bis

3 Iphosphoglycerale
significance :

binds to and reduces the

• 2,3 Bph
hemoglobin ,
affinity
towards Oz So in 2,3 BPG
Oxy hemoglobin
presence 7
.

will unload Oz more

easily in tissues .

Under
•

hypoxia , the 2- 313Pa 9 in RBC ,

thus
favouring
the release g Oz to tissue even when poz I
 °
2.3 BPG 9 in
high altitudes .

circulation
o
B Ph 9 in
fetal
shunt No aerated
pathway Paige
A >
•

In this ,
.

⑥ Explain Gluconeogenesis and state its

significance .

It in the
process by which
glucose molecules are

produced from Non carbohydrate

-

precursors ;
which
include lactate acids
,
Glycogenic amino ,
glycerol part
and
y fat pro pion yl CoA from fatty acid chain -

site
Occurs in liver and to lesser extent Renal cortex
.

mainly
mitochondrial and
party cytoplasmic
in
•

Pathway partly .

Key enzymes :

(
Pyruvate Carboxylase
h

(2) Phosphoenolpyruvate carboxy kinase

(3) Fructose I - G -
bis
phosphatase
(4) Glucose -
6 -

phosphor tape .

•
This
pathway is not Reversal g glycolysis .

circumvented
• The irreversible
stages
which
g glycolysis are

4 enzymes key pathway

'

by are also
enzymes for this .

Significance :

blood
.

only
liver
replenish
can
sugar through glycogen! .
.

because
glucose
-
6 -

phosphate at present mainly in

liver -

starvation maintains blood

•

During .
gluconeogenesis
glucose -

• The stored
glycogen at depleted within iz -
is hrs
g
fasting .
 starvation A and
• On
prolonged .
gluconeogenesis
catabolism substrate
protein provides .

Lactate - Glucose
( Glu neo
genesis
"

6 ATP nos used )

Regulation :

Regulatory steps are : -

ca )
Pyruvate carboxylase Acetyl CoA wi activator -
an

g pyruvate carboxylase
.

cbs fructose I bis

phosphatase Citrate in Activator
-
6 -

while Fructose 2,6

AMP & -

bisphosphate an

inhibitors .

Enhancer
(c ) ATP 7 Gluconeogenesis .

Glucocorticoids A
( d,
Hormonal
Glucagon 2
Gluconeogenesis
Insulin inhibits
Gluconeogenesis .

⑦ Explain Glycogen lysis and Glycogen Synthesis o .

Glycogen lysis in the degradation g glycogen

o .

Glycogen phosphorylase glucose glucose

•
removes as
-

t -

phosphate from glycogen

-

It contains pyridoxal phosphate (

• )
prosthetic PLP as a

group
.

•
The x -

glycosidic unit
1,4
linkages are
hydrolysed
time
and
thus
removing glucose one at a .

It not attack 46
.
can
linkage .

°
a'
gem
G'
17,
+ Glucose -
t -

phosphate .

one
 •

Phospho glee a tone

Converts Glucose -
I -

phosphate → Glucose -
6 -

phosphate
•

Hepatic glucose phosphatase hydrolyses GGP to Glucose

-
G -

and
free glucose is released into bloodstream .

°
Gm muscles .
phosphatase
glucoseand used as is absent Gap will -
G -

undergo glycolysis for ATP production .

Glycogen synthesis
• gt is not reversal
g glycogen breakdown -

•
The steps are :

( A1 Activation
-
9 Glucose : -

glucose
phosphate UDP-glucose Ppi
pp

ut
- -

+
Glu -
t -

u> p
Pyro phosphorylase
( uridine
triphosphate)
Primer
(B ) Glycogensynth :
Glycogen alyaogenin
-

those
Glycogen primer (n )
Glycogen (n ti )

+ u D P -

glucose +
VIP

(c)
Branching me

add units
•
The
glycogen synthase can
glucose only in
in needed to create
a -
1,4 linkage branching enzyme
.
A

the a- 1,6
linkages
.

chain
•
When in y I -

12
glucose molecules the ,
branching
residues
enzyme
will
transfer blocky a 6 -
s
glucose
to
form t -

linkage
6 .
⑧ Explain and its
HMP shunt
Pathway significance .

other Monophosphate Pathway

g HMP
tlexose
names .

. oentose
phosphate pathway
°

Dickens -

Honecker Pathway
. shunt
Pathway
•
Phospho gluconate Oxidative
Pathway
•
In
glycolysis ,
there are
few
bi
phosphate intermediates .

but in this
pathway there are
only monophosphate .

enter this
About 10%
glucose molecules
pathway
.
•
,

•
In liver & RBC it in 30%

has oxidative and oxidative phases

The HMP
pathway non
° -
.

oxidative
phosphate oxidised
°

During phase glucose ,

-
G -
ai

and
with
generation g molecules 2 g NADPH ,
one molecule

g pentose phosphate with one

Ea .

During oxidative
Non the
pentose -

phase , phosphate are

converted to intermediates g
glycolysis .

Glucose -
6 -

phosphate
Glucose
f ( alum kinase )
Dehydrogenase ④ ②
Gluphophak/ ¥16 -

phospho
6¥ 6-
phosp luwnale

# flaw lactone#"

Fructose /
Dpt
A
Appu + CMA
NADPH
6 P f v

gluconate
- -

keto phospho
03,3
-
b -

1
F 1,6 BP
Ribtuhise@5.p ⑤
gift
in
AF
ycgsomerar.es#Epimeryfes.tsBpuczs
Dh GASP us e -
-
-
-

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( 21 Ribose - 5 -

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131 Clinical
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dehydrogenase deficiency
dis induced
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ciiis Methemoglobin emia

reduced tram keto lase

( ius
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Thiamine to
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⑨ Explain Cosi
cycle ? / lactic Acid Cycle .

It in the
process
in which
glucose ai converted to
lactate in muscle ; and in liver this lactate in
converted into
re -

glucose .

•
Muscle cramps in due to lactate accumulation .

•
lactic acid from muscle diffuses into blood .

•
lactate reaches Liver and converted to Pyne rate .

thus it is channeled to
Gluconeogenesis .

cycle / Lactic Acid cycle

whole
.
This cycle is Como -

clinical : Oxygen debt after Exercise .

,
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 Metabolism g
fatty Acid
① short note on
Digestion g lipids and its absorb lion -

The
major dietary lipids TAG ( triglycerides ) cholesterol
→
are ,

and
phospholipids .

STOIA CH
• The
lingual lipase has optimum
pH - 2-5 -
5 ,
so it remains

active in stomach and acts on short chain triglycerides .

. The
gastric lipase ni ace 'd stable with optimum pH 5-4 =
,

it secreted secretion in stimulated

in
by Chief cells ,
the

Gaskin
by .

Upto 30%
digesting TAG occurs in stomach .

INTESTINES

Emulsification requisite for digestion g lipids

in
°
a
pre
-
.

•
The
lipids dispersed into smaller droplets ; surface
are

tension is reduced and is increased

surface area .

This in
favoured Cas Bile salts
process by (b) Peristalsis
(c) Phospholipids .

°
Bile salts ( sodium glycocho late and sodium Launch date )
lower surface tension .

Pancreatic
°

Enzymes cat
Lipase
b
( , cholesterol esterase

( c)
Phospholipase Az
Pancreatic
lipase hydrolyses the TAG and
forms
•

(6 Glycerol and acids ( 144

2 MAG ( 78% ) I M AG %)
fatty
-
-
,
,

•
cholesterol ester
may
be hydrolysed to free cholesterol and
fatty au 'd .

•
The action g phospholipase Az produces lyso phospholipid
and a
fatty acid .
 Absorb lion 9 Lipids
c) absorbed to
long fatty acids ( 14
lymph blood
> are not
•
.

Products n
• Bile salt micelle t
digestion namely 2 mono
acyl -

acids cholesterol 8 Kaew b

long fatty ,
, phospholipids and
ly so
phospholipids into
Mixed Micelle .

°
Micelle
formation essential for absorb lion in g

soluble vitamins such not A. D & K

fat -
as .

Bile salts left behind which reabsorbed

•
are are
mostly
from the ileum and returned to liver -

inside the mucosal cells chain

fatty
Once the
long acids
•

are re -

form triage glycerol

esterified to s .

•
Free glycerol absorbed from intestinal lumen
bloodstream
directly enter .

into .

•
TheTAG cholesterol ester &
,
molecules phospholipid along
with Apo proteins 1348 and apo A are incorporated into
duct
chylo microns The I act eats
chyle
thoracic
→ . →

systemic
circulation
Short chain fatty acids ( ( seen
.

• s CFA ) in milk butter , ,

Medium chain ( Mc FA ) ( in coconut oil

and
ghee ) ,

mother 's milk ) do not need re esterification - .

bloodstream
They can
directly enter ,
and then via

and
portal vein to liver ,
immediately utilized Jor
energy .

rapid and better

absorb h in than
long chain
'

o SCF As on
.

Gn short , Ssteps a Lipid Absorb him :

( 11 Minor digestion
 Major digestion clinical

to
(2)

Bile emulsification and cat

Def digestion
i

:
(3)
steatorrhea
( 41 Formation g
micelles on ,
daily is
excretion og fat in
feces
ii. :i ::÷÷:i::m ::÷:÷:÷÷÷ .

ch 'll omicrons
(7)
Assembly g ab ,
Defectorsorb lion :

(8) Export via

lymphatics .

gf absorb team alone is

be
-

defective fat injeces . may

Fate g
Chylomicrom :
split fatcie fatty , acid e

Mono
glyceride

/
taken Adipose
They by I
•
are
up due to
be
tissue skeletal muscle & liar .
May

: se:L! .de:1?:aeg7hfiIsgcn
,

• can be converted town ad

.

to
are
transported Adipose ciii , obstruction g Bile duct
tissue .

② Explain p oxidation -

og Fatty Acid .

The oxidation and splitting g

two carbon units -
occur

at B -
carbon atom .

doin clinical
mithridate
em
for
-

.
Medium chain e short chain
← acids do not
R
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Fatty Acid
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TACIT ) D2
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. s so R -

ee -
E -
CoA -

su Enoyl way preterm infants .

( Enn
!¥!aYAme 1+420
7 FA Dha X l 5 105
step ②
-
•

°
7 NADU X 2 -
5
l
,

di
(/
Further cycles [ slept Ii "
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G 3>4
-

118 > 2 >

- -

Ross
-
-

'

Auriga
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heda's
Thus in
resulting
tis
①
-

p genip

ihp.FM#ni:eg.g ,÷÷:
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Is:{ ii.
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•
Efficiency g p oxidation ca [P keto
fatty aye CoA ]
hypoglycemia
-

wa .sn
-

on - -

,
in about 33%
[ Acetyl -
WA ]

↳ TCA
cycle lkneb cycle E ?I¥¥n ? III Cio ATP ]
 ③ Short note g
Metabolism g ketone bodies .

•
Carbohydrates are essential for metabolism og
fat .

starvation and diabetes mellitus

acetyl colt takes
During
•
-

the alternate route g formation g ketone bodies .

kehogenes.is
. Aceto acetate in
primary body while beta
the
hydroxy ketone
butyrate and acetone ketone bodies
secondary are .

They synthesized exclusively by Liver mitochondria

are

=
.

Acetyl CoA t
Acetyl WA
keto lysis
[Aceto acetyl
synthase]
wa ① /
it '
CoA -
SH
o ketone bodies are
formed
Aceto
in liver but they are

acetyl wa
utilised tissues
by extra
hepatic
Khao
WA
[ HMG AA
+
Acetyl
② like Renal or ten ,
heart ,

synthase ] ~
, w A skeletal muscle brain etc
,

HMG-CoA Almost tissues and

°
all
③ Emma
/
CoA
lyase]
cell
types can use ketone
③
Aceto acetate bodies
v

-
as
fuel except

Acetone
( No
" liver
/ itai : Dehydrogenase] RBC
&
"
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.

we '

B
hydroxy butyrate Aceto acetate
sycwciyyl
-
r +
.

! acetyl
( Thi
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:/
Ace wit
ketosis
-

i ::::÷::÷: :: :.:c:÷÷:c
there will be accumulation the ketone to
.. :¥÷
produce energy
.
.

g
.

bodies in blood .

• This leads to ketone mia ,

Excretion in
urine ( ketonuria )
and smell g acetone in breath .

.
All these three together →
Ketosis -
 Causes

ca , Diabetes mellitus : Untreated diabetes mellitus in the most

common cause
g ketosis .

As Insulin I Accelerated
lipolysis acids
faythg
→ →
More

More
ketone bodies
bi starvation starvation increased rate to
( -
gn .
the g lipolysis is

provide the alternate source

g fuel .

acetyl-CoA Ketone bodies

•
The →
excess
-

High glucagon Keto

genes
is
→

High glucagon 9ns ul in ratio in

potentially ketogenic
•
-

salient
features g ketosis
in Metabolic acidosis
a Reduced buffer
131 Kuss maul 's
respiration
( 41 smell g Acetone
( 51 Osmotic diuresis
(6) Nat Loss

(71 Dehydration
is , coma -
Dehydration & Acidosis → Lethal
effect 9 Ketosis .

•
Detection Roth era 's Test .

Treatment
• Administration g 9 insulin e Glucose
Administration T Hoos
-

and maintain an Electrolyte and

g
•
ce

fiuid balance are

very important aspects .

② Med Notes (med notes in) .

* Revision Notes med notes site

company
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[ App Available ]
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Glucose Dehydrogenase
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LMT
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C -
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-
CoA su -

[Enoyl CoA
)
•

°
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105

IF -5
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[ Acetyl-CoA ]
↳ TCA
cycle lkneb cycle 77¥72 ? III Cio ATP ]
 =
Citric Acid cycle
Function
oxidative oxidizes
( is The
final common
pathway that

acetyl -

CoA to coz .

( 21 The source
g
reduced
coenzymes
that provide the substrate
for the respiratory chain .

link between and anabolic

③ The catabolic
pathway .

( 41 Provides precursors for synthesis g AA and nucleotides

(5)
Components og the cycle have direct a or indirect

controlling effects key enzymes og on other

pathways .

Glucose
Oxidation
I
Pyruvate - Fatty acid

Fats aid
Ketogenic A- A
engines! ;÷÷s÷:
significance og citric acid cycle
•

Complete oxidation g acetyl co A

•
ATP
generation
o
final common oxidative
pathway
metabolic
•

Integration g major pathway

. No net syn -

D carbohydrates from Jat .

°
Excels carbohydrates → Neutral fat
°
Carbon skeleton og AA enters citric acid cycle
•
Amphibolic
a
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cycle

• a -

kg in co -

factor for Historic demthylase

=L>
control Gene expression .

Mutation
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-

E- oh Glutamate
-
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Farmar Leibman demythlase

•
are
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nuncle
/
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Inhibited
by Arsenite
( Non -

competitive )

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by Malon ate

( competitive )
EFFI .
g tenter ediates

Acetyl YA
m>

Fatty acid
synthesis .

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-
-
oxaloacetate

[
Malate a -
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'd I
1 [ succinyl y
ace

Glutamic Acid
Gluconeogenesis y
CoA
y, t
GABA
Heme Keholgsis
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Pyruvate
→ GNIIUX
→
Tryptophan Alamin?
-
'

!
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wrtiahaeetak # g. hate

f a-
i
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Ketoglutarate
Phenylalawsfuranmate §
(
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I
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Tyrosine
seeing
WA
,
aluytamate
Histidine
§
'

Arginine .

Pnopionge -
wa Proline
Valine ,
/ In
Isoleucine Odd chain
acid
Methionine fatty

② Med Notes (mednotes.in)

* Revision Notes med notes site
company
-
. .

[ App Available ]
 Oxidation
Biological ETC
&
-

High energy compounds :

(t 1 A T P :

ATF in the
• universal
currency g energy
within
lining cells .

•
The hydrolysis g
ATP to A DP releases -
7.3kcal
/ mo L .

The in ATP in used to drive all end mic rkns

energy
•

ergo .

At rest Nat Kt ATPase d

formed
•

113 ATP
- -
-
,
g an
uses
up .

other
requiring
energy processes biosynthesis g
are
°

macromolecules ,
muscle contractions cellular motion , .

•
ATP in
continually being hydrolysed regenerated and .

Average person at rest and

regeneratesconsumes ATP

at rate g 3 molecules
/ i about
a see -
e Irs
kg 1 day .

⑦ Creatine Phosphate
• CP ( phosphocreatine ) provides high energy
a reservoir g
ATP to
regenerate
by
ATP
rapidly ! catalysed by
Lohmann 's r k n
creak
none .

ATP Creatine Phosphocreatine A DP

°
• + → + t DG
( lo 5 kcal mot )
/
transfer
-
.

heart
Energy
to
myo fibrils kinase
by
in creatine
•

shuttle
energy
.

.
CP is smaller molecule than ATP
therefore
, ,
CP can
rapidly
diffuse from myocardium to
myo fibrils .
 Oxidative Phosphorylation : courtiers
.
NADH €4 HAD
+
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+
+ ④
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reductase NADH
• It in also called NADH - co Q or
dehydrogenase .

Tightly bound to inner mitochondria

•
g t consists g flavoprotein ( Fp ) consisting ,
FMN and Fe -
S

and
transferred from NADH to flavin prosthetic
+
2 t H
-

•
e are

group
.

t +
MA D H t H t F M N →
F M MHz t NA D

this to collect electron

• Overall
function g complex in
pair g

from NADH and them to co Q

pars
12kcal Imo l and this used to drive
.

Energy released in is

4 ht out g mitochondria .

"
in
: : :X : : : :÷:÷.xi ..
 Complete II . succinate -
Q - reductase .

The electrons
from FA DH enter the ETC at level
g coenzyme Q
.

•
z

step does liberate proton

This not
enough to act
pump
°

energy
as .

•
Three major systems that transfer their electrons to complex I

are :

( as
succinate
dehydrogenase
cbs
fatty aye
-
coth dehydrogenase
cc ) Mitochondrial
glycerol phosphate dehydrogenase .

Summary succinate
? Ii:: ::X
:
FAD &

e.
)c ...
. .. .

Complex HI

•
Cytochrome Reductase .

both contains heme prosthetic group

• This contains cytochrome b e es
,

4 Ht
• Free energy in -
10 kcal Imo l ( released ) & are
pumped out -

summat : Fest etat, test's

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'

:X , , esta
( Fez t)
.

c. to es ,
( Fes ) ( Fest)

Gm plex II ( cytochrome oxidase )

•
It contains cyt .
a &
az
.

4 accepted from act c and to Oz

-

on
e
panes
•
are
.

During this , 2h
-1
am
pumped out -

:
seminary (feat ) " ta ashes ! can,
Cy t
)(
""
-

cost acres , Cy ta -

az ( feat ,
cut , 02
 Complete I ( ATP synthase )
o g t in protein assembly in inner
a mitochondrial memb .

Proton ATP
synthase in transmembrane protein
pumping
° .

units
.
Two
functional : Ft e Fo

inhibited
°
Fo
, .on
?
O
for Oligomycin , as Fo in
by oligo nyein .

( serves as
proton channel )
.
Fi .
It projects into matrix . It
catalyses Atp synthesis
++
ATP syn -

mg
wins
Mg ions .

"
I NADH → 2.5 AT P E

FA D l I- → I .
5 ATP

Glucose → 32
Tnt
Ace ly - co
A → to

Palmitate → 106

Inhibitors g ATP synthesis

( British Anti lewisite)

-

DNP
2,4 dini
to
phenol

carbonyl cyanide phenyl hydrazone

CCCP chloro .
Extras
:

② Med Notes (med notes in) .

* Revision Notes med notes site

company
-
. .

[ App Available ]
 Heme synthesis and Breakdown
•
Heme in
present in : . Heme in
produced by combination

9 Iron with porphyrin

( al
Hemoglobin
(b)
Myoglobin ring .

(e)
Cytochrome s .
get in a derivative g porphyrin
( di Peroxidase
(e) catalase °
since an atom og
iron in
present ,

if Tryptophan pyrrolase
'
heme in a
fern proto porphyrin .

Nitric oxide
( g, synthase .

Biosynthesis g
Heme

•
site =
Almost all tissues
•

esp
- Norm oblasts ( not
by
matured
erythrocytes )
°

Imp -

steps ( as

b)
PBG
( P BG →
Uno
po
-

phninogen
) U Proto
porphyrin
c
( →
*

/ .F÷÷÷÷
-

(d) Gm corporatism
g
Fe .
Some Great
Doctors

WA Palpate
succinyl -1
Glycine Heart

Cala synthases
coa.ws:
acid ( ALA )
2x S Amino Levulinic
L Pn

znzo #[ ALA dehydratase ] -' 2n

containing ;
gnhibited
by lead .

4 x
Porphobihinogen ( PB h )
' deficiency

Hyjftwnymethglbilane
-

[ Uno porphyrin I synthase]

Acute Inter
en
-

og
-

4 Nh ,
- met tent
lumps )
4717 Porphyria

#orphyrinogen
[porphyrin
Uno
og
em III co
synthase ]
→
deficiency
A P
Y
U HI
( open -
II )
¥¥I congenital
erythnopoeihz
462$
p a

Porphyria .
Cytosol /
~
[ Uno porphyrin og en decarboxylase] Acetyl
t
M p
p
Copnoporphyninogen HI ( CpG Metlife
)mtym
→
-
HI
th NADP p p
Mitochondria
-1¥
!
p m
NADPH [ Co
porphyrin
co 292-7
pro
ogeonwda.gg -

Hereditary cop no
por
physics
Pro porphyrin ogen Mpp Pmopionye
=

HI
( PPG III ) MT TM t

Vinyl
-

TI
-

P v

#
P M
I [Proto
4h porphyrin og en oxidase] -

Deficiency
tho
Va
egate Porphyria
porphyrin II

+ Fe
"µµm[etienne synthase / Ferro chelating →
Deficiency
1
Pro top hernia

*:-

I
inhibits the

:/
.
Heme syn T
StG
.

I [ ALA synthase )
ALA

a co
synthase by acting as

v
repressor
-

GALA
also
! [ ALA dehydratase] o
ALA synthase wi

inhibited
PBG allosteric
hematin
ally by
f EUI -
Curro porphyrin og en
synthase) .

HMB

:÷÷÷÷÷i÷÷÷÷÷÷i :÷÷÷÷÷÷÷÷÷÷÷÷÷ dead

.

PHI by .

So lead toxicity
( P oxidase )
.
causes
I [ Po ] -
-

Anemia .

P
j (F) -

(ferrochelatase)
Heme
→
 Catabolism og Ilene
•

Degradation g Hemoglobin RE
g
liver ,
spleen ,
Bone marrow

•
Macnee phages
Hb
.
uptake g Bilirubin by
f- Globin -
s AA Hepatocytes
Heme
Microsome
.

Conjugation
bile
p og

ftp.fgyne
NA " secretion into
macrophages
)
oxygenase
.

↳ co

( omen Bioliverdin
colour )

( MA "

.nl/CBilinndinRedui.aY!jM
(yellow
Bilirubin ( Unwary 're
Bilirubin )
gated
colour ) ( Toxic)

admin
( Not soluble in water )

- Bilirubin
I ;¥:} ::& :
tcnepatoyl.es )

T
.de/njOpmuntsBaeklowoBilooo-s
o-8.tt
'b}7 :{goat
'T I og Bilirubin to blood .

④ bilirubin in
by facilitated keeps
soluble's ed state Excretion Bilirubin
diffusion ) Active
Process -
g
t water soluble
① conjugated
conjugated
The
Um Bilirubin
-

bilirubin → Bile

1 ( UDP -

glucuronic transferase ) ( Rate limiting step )

( Active Process )
Bilirubin -
Mono
glucuronide ② Excretion g conjugated Bil
f ( UDP -

gluuenonyl transferase) into bile is mediated

by
Bil -

digluwronide ( water soluble )

Nontoxic )
Muelispecilic organic
[ Conjugated Bil I ( Anion Transporter (NOAH
 ③ Intestinal bacteria
dewniugak the conjugated
bit -

⑤ About ①
Urobihinogenlu
g 0134
20 't
CB →
)
Bh
is reabsorbed from
intestine and returned u

stereo bilimogen
blood
to liver
by portal { ( SB h )
Fences ( 250-300
* Normal plasma Bilirubin
level mgldag )
ranges from Img Id '
02 -

⑥ Some
part g UZI
•
The U B 0.2 - o -

7mg Id l t

Coni . B 01 -

0.4
mg 1dL
Kidney
Bilirubin level
butbilin ( Gives Yellow
97 > 1mg 1dL
°

( L 4mg ) colour to
}
Urine )
day )
-

Hyper bilirubin emia

Level Btw I and 2mg 1dL are indicative

y
•

Latent Jaundice .

If Bilirubin >
2mg 1dL ,
it diffuses into tissues ,

producing yellow colour in sclera conjunctiva

, ,
skin and
in Jaundice
mucus memb
resulting .

of V

W t

② Med Notes (med notes .in)

* Revision Notes med notes site
company
-
. .

[ App Available ]
 Hemoglobin
structure g Heb :

Normal level og Hb in males 14

13.1591dL
• = -
16

females =

1dL g
Hb A 213
}
• = 2 a a
adult HBA =
97%
In
Hb F a
,
Hb
2x
zy Az 2%
=
=

Hb Az = 22 e 2 D H b F = I %

.
Each a chain in 141 AA and Beta / Delta - 146 AA -

bonds
p subunits
connected covalent
a e are
by weak non -
•

like van der waals

,
n -
bond and electrostatic
forces .

•
There are
1 heme residues / Hb molecule i. e one
for each
subunit .

•
Iron atom occupies the central position og porphyrin sing
.

•
In Hb , Fe remains in
ferrous state ( Fe "
) .

ordinate
°
Fe in linked to
pyrrole nitrogen by
imidazole
4 co -

valency
bonds and fifth a one to
nitrogen g
histidine
proximal .

•
In
oxy
- Hb ,
the 6th
valency g Fe binds the Oz .

Binding og oxygen
to heme
.

one
M c -
c - v
me c-v

IIc - Hee a residue increases the affinity g

I -
.
. +
+1
"
Hp remaining
heme
( no mono pic
SCH Fe
.

'
CH
n
interaction )
-
H i
/
.

Position
.

's
Cooperatively
.
N i µ .

ten exc
M
T
C l #C Hb Hbo Hbo Hb 06 Hbos
Cyp
-
p c -
M → → → →
/
y , ,
Lys His
'
t time 2 times 9 times shines
# Arg
" n
-
\ Affinity
Globin C -
C -

H H
h
Lmf h
-

M -
-

Methyl ( -
ch
, ) i [ Pyrrole]
"

Vinyl ( Cn Chs )
-

V e -
=

Propionic Acid ( )
P = - Ch - Ch -
WOH
z z
 Clinical applications :

hypoxia decreased
( it In ,
the Oz
affinity in with a
shift in
Obc to right and increase in 2,3 BPG inside RBC .

Adaptation to
high altitudes when
poz in low ;

(a) No .
M R BC A
(b) Comet A
g Hb
-

(c) BPG 9 ( shift in ODC tonight )

In anemia increased Oz
( 27 comet D H b
only I
unloading
-

, ,

will ensure
proper oxygenation g tissues .

(3) In cases Hb corn Ct 9 2,3 B Ph I

many ,
as -

(9 nurse relation )

(4) In chronic diseases and cardiac diseases

+ he 2,3 -
B
pulmonary
PG level is Inc .
cyanotic

stoned blood
(5)
Transfusion g large volumes
of ,
which has
a low level y 2,3 -

BPG can lead to sudden hypoxia .

Fetal Hb ( Mbf )

Hbf has 2x and 2g chains

• .

Differences btw Hbf and HBA are : -

(a) Inc .

solubility og deoxy Hbf

(b) Slower electrophoretic mobility for

Hbf

(c) Increased resistance g

Hbf to alkali denaturation
id ) Hbf has decreased interaction with 2,3 -

BPG .

and newborn to
•
ODC
g fetus are shifted left .

A
diminished
when
Major reason is
binding
saturation
g
2,3 BPG .

p 02=20 Hb F
mmhg ,
= 50% .

starts
•

Synthesis og
Hbf
by 7th week g gestation ,

becomes predominant Hb
by 28 th week .

At birth . so %

First 6 month = Reduced to 5%

 Hemoglobin A 2
( 2x and 2 as chains )
•
get in normal
hemoglobin
•
gt vis about 2%
g
total Hb .

•
g n thalassemia ,
Hb Az A

derivatives
Hemoglobin
°

Oxy - Hb -
Dark Red
deoxy
- Hb -

Purple
met - H be Dark brown

carboxy Heb ( -

co -
Hb)

binds with carbon monoxide to

Hb
form carboxy Hb
°
- .

is times than that

• The
affinity g
co to Hb zoo n Oz .

Gf one molecule binds with one monomer n Hb ,

9 and not be released back

the Oz
affinity Oz can .

thus Oz
availability to hime decreases further .

Normally co Hb level is o 16% in smoker it is 47

-
• -
, , .

Clinical
• 9
f co -
Hb level exceed 20%
, symptoms are breathlessness
and chest
headache ,
nausea ,
vomiting pain in .

• At 40 -
60% a
death can result .

• Administration g Oz in the treatment .

9h severe
cases .

Oz under high premiere

in
helpful .

Met -

Ib
state
When
formed
"
•
Fe → fest ,
met -
Hb cis .

• Small quantities og met

-
Hb
formed an
readily reduced
back by reductase system
"
to Fe met Hb
enzyme
-
.

•
About 75
'

t -

by NADH &
Cy
t b 5 5 20 y .

by NADPH system
and s y .

by Glutathione .
 Sickle cell Disease
°

Hbs / sickle cell hemoglobin in the most common

disorder
monogenic
.

acid
• The
glutamic in 6th Position g B - chain og Hb Avi

changed to valine in Hbs .

I
causing Polymerization g Hb molecules in RBC

A
Distortion
g
cell into sickle shape .

•
Hbs can bind and transport Oz and
sicking occurs

under
deoxygenated state .

•
Sickle cells form plug in capillaries and leads to

infraction T organs like spleen .

Hb#
Glu -

HbSB-6Glu#

Hb D ( Punjab ) p -
121 Glu -
G In

HbM/Pnoximal/His-T#
-
distal -

histidine

thalassemia
9T in the most
genetic disease and has
•
common a

about
carrier
frequency g 7%

but in abnormal
•
gt is normal Hb
proportions .

•
Reduction in X - chain A -
Thalassemia
while 13 - chain if B - Thalassemia .

°
Genetic defects may
be (a)RNA splicing defect
(b) Promoter mutants
 (C)
Poly adenylate
-

-
on
signal
(d) Partial defect
gene
deletion .

B -

Thalassemia thalassemia

.is/.:i: : s
a -

• More common than o less common -

C Rare )

x thalassemia
Dec d Chain
syn ry
. . . - .

chain
• Dec .

synthesis g B -

. Genetic defect in
gene

:÷÷÷÷ :O :÷:÷÷÷n
as
.

If three deleted
genes are ,

severe symptoms came

up
.

Gf all 4 deleted death

Syndromes
-
are
,

- in utero ,
since a - chain
•
Hypochromia Micro cystic in mint
Anaemia .

•
In
homozygous condition ,
clinical
manifestations are

and hence Thalassemia

seven
Major .

•
In heterozygous ,
clinical signs &
symptoms are minimal

+has Thalassemia minor .

B Thalassemia Severe Anemia

Homozygous
° -

•
Hyper sp Lene 's m
o
Hepaho splenomegaly .

•
Repeated Transfusion in the
only treatment .

Myoglobin -

• Seen in muscles
• Mb content g skeletal muscle in
2.5g 1100g
•
Cardiac muscle =
I -

4g 1100g
Smooth muscle
0.3g 1100g
• =

• Human Mb = 152 AA .

( 17500 Da )
 •
Mb one molecule can take 1 molecule
g Oz .

o Mb has high affinity for Oz than Hb .

p Oz Mb saturated
Hg
°
30 mm 90%
}
= =

Hb = 50% saturated

Clinical
•
Severe crush
injury causes release
g
Mb
from damaged
muscle .

small molecular
•

Being weigh protein ,

it is excreted

through urine ( myoglobin ceria )

I
Urine →

Dark Red
o g t is also released in Myocardial Infarction .

Anemia
• Gt in most common medical problem in India
Hb I it condition
log 1dL
to in
9
f- a seven .

•
,

•
Most common cause in Iron
deficiency .

Symphony

② Med Notes (med notes .in)

* Revision Notes med notes site
company
-
. .

[ App Available ]
 Enzymes
6
.

major classes
of Enzymes
class I : Oxidoreductases
-

oxidation
This
group of enzymes
will
catalyze
-

substrate with simultaneous reduction

of one

another substrate
of or
coenzyme
.

A Hz t B → A t B Hz

As :
Alcohol + HAD
+
→
Aldehyde t NADH + Ht
( Alcohol
dehydrogenase )

class 2 :
transferases
- This class
of enzymes transfer one
group from
substrate to another substrate .

A -

R t B → At B -
R

As -
Hexose t ATP → Hexose - G -

phosphate 1- ADP

( H exo kinase )

class 3 :
Hydrolases
This class of enzymes can
hydrolyse by adding water
and then
breaking the bond .

As -

Acetylcholine + H2o →
Choline + Acetate

( Acetylcholine esterase)
Class 4 :
lyase
These
from substrates
enzymes can remove
groups
-

break bonds hydrolysis

or
by mechanisms other than

As -

Fructose -
1,6 -

bisphosphate →
Glyceraldehyde -
3 -

phos
.

dihydroxy acetone phosphate

( Aldolase )

class 5 :
isomerases :

- These
enzymes
can
produce isomers
of the

substrate .

As -

Glyceraldehyde -

3 -

phosphate →
DAP

( Trio se
phosphate isomerase)

Class 6 :
ligases
-

Link two substrates

-

together usually with the

simultaneous
hydrolysis of ATP .

As -

Acetyl CoA t wz t ATP →

Malonyl-CoA +

ADP t pi

( Acetyl-CoA carboxylase )
 Coenzyme :

Enzymes complex enzymes containing

can be a

Non protein part called Prosthetic Group

- .

•
The
prosthetic group
in called
Coenzyme .

Protein Part
* =

Apoenzyme
*
Apoenzyme
+
Coenzyme
=

Holoenzyme
Coenzymes may
be divided in 2
groups
:

associated
(a) Those
taking part in reaction with Ht
As -
N AHP ,
FMN . FAD
associated
lbs those
taking part in rkn with other

than
groups hydrogen .

As -

Coenzyme A

Factors affecting Enzyme Activity

( Brief )

( n
Enzyme Concentration ( directly proportional )
substrate Concentration (
( a
directly )
( 31 Product concentration ( indirectly )
141 Effect of temperature ( first directly then falls )
( 51
Effect g pH ( bell shaped curve) ( Bell shaped curve )

(6) Presence 9 Activators inhibitors

repressor
,
.

(7) Covalent modification ② Med Notes (med notes .in)

-
 immunochemistry
Introduction :

Antigen Any substance which invokes

immunological
°
-

an
response
is an
antigen / immuno
gen
.

Epitopes Antibody
'

will be selective
usually against
. -

response
specific spatial configurations antigen
which called on are

determinants
antigenic known epitopes ,
as .

Immune Response
mediated
in cell -

Immunity
121 Humoral
Immunity
Mechanism
Effector -

in
CeHatedIy : -

Immunity against Infection

IAI -

Against bacteria ,
viruses ,
almost

tries
all
parasites .

CBS
Rejection of Allograft Body to
reject implanted organ
-

destruction
mainly by T -
cell mediated mechanism
(c) Tumor Cell

function
( D,
Helper -
T -

helper cells are

necessary for optimal

antibody production by plasma cells and cyt .
T - cells .

( El
Suppressor function .

Production Kines
of Lymph
CFI .

( Gi Delayed type hypersensitivity .

 ( 21
Humty : -

°
Antibodies
produced by plasma cells
are .

• The
antigen antibody reaction leads to activation of
-

complement
system which destroys the foreign cells
,
.

The antibodies can

destroy the
target cells
by following mechanism
.

in Classical
complement Pathway
in
Antibody dependent cell mediated
cytotoxicity
③
Agglutination
Ops ionization target cells
Cen
of .

Antibody Dependent cell Mediated Cytolysis .

requires antibody but the cytolysis

. A DDC
,

does not
require complement activity .

• The
effector cells are neither 7 nor B cells ,

but are called K -

( Killer) cells .

effector at sites
It is
of Tumors
•
.
 Structure of Immunoglobulins
made and ( L ) chains
• The
Ig in
up of 2 Heavy Lte )
chains 2
light .

combined disulfide bridges

through .

Depending on the
heavy chain make up ,
the
Ig are differentiated
into classes
5
major .

la '
IgG y heavy chain
-

( bi
Ig 'M
-

te heavy chain

chain
(G
IgA = a
heavy .

( di
Ig D= S
heavy chain .

E E ( epsilon ) heavy chain

Ig
=

(e)
.

either (lambda ) classes

• The
light chains are K(
Kappa ) or x in all the .

chain
°
In human
beings ,
60% → K
type light
4 one chain
x
type light
.
→
.

Variable & Constant Regions

chains contain variable
Both
heavy &
light relatively Lv ) and
°

constant ( C )
regions
with
regard to their amino acid
composition .

UH
chain heavy
Y! > General terms for light > for chains
°
. .

we

•
The first tos A As in light chains &

first A As in f chains
Its -

heavy
constitute the variable
region
.

The amino acid

sequence
°
can
vary
in H & L chains so that the,

could
the
body synthesise enormous

varieties antibodies
of different .
 Fab &
E.Portions :

(i'
Papin ( proteolytic enzyme from papaya )
cleaves the
Ig so that
two fab (
fraction antibody ) portions & one Fc ( fraction cystallizable)

portion are
produced .

• The
Antigen binding part of Antibody is in fab
fragment .

other site
ciii Another proteolytic enzyme , Pepsin cleaves Ig at an .

to yield Kab, combined

so as 2
,
where two Fab
portions are .

Fab combine but combination

•

part can with

antigen very weakly
flab )
with z in
stronger .

Different classes :
 Complement system :

Complement factors proteins present in are serum .

°
Cell
lysis by antibody in mediated by complement system .

abbreviated
They
'

[
•
are C
] as c± to cos .

. The
complement activity in abolished if is incubated at serum 56°C ,

for 30 mins
, as most
of the
components are thermolabile .

half life of complement system temp only few

°

The -
at room .
is

hours .

Primary &
Secondary Immune Response :

When
antigen is
injected
°
an
,

Antibodies start in 10
days
appear
-

Reach peak level in 20

days .

Response decline
by
about 30 days .

IgM will be
predominant in this
primary response
.

• When the same

antigen in
injected into the same animal
after a
few
months ,
the
response
in
quicker ( within 3
days ) -

stronger ( too to tooo times )

Secondary
g
-

More avid type

( IgG ) Immune
Response
-
.

-
More
prolonged l for months )
 Induced
by immunization with toxoid killed
•

Active Immunity : , or or

attenuated
organisms .

As -
DPT vaccine .
Polio vaccine etc .

Passive
Immunity Protection
given by preformed antibodies
.

: in .

This is used in
immunotherapy against snake bites ,

tetany .

/
.

g. µ , ,.µ , ,

:
→
£
±
or
→
I

%
I

②
 Biochemistry of Cancer
Introduction
-
:

The term derived Latin

from
'
wi Sanskrit
'

Can crum
°
= n
cancer

Greek =
Kar Kino ma = Kar Kita Kam ( crab)
.
All cancers are
multifactorial in
origin
.

They include Genetics hormonal metabolic

physical chemical &
•

, , ,
,

environmental
factors
.

o Most human cancers are

spontaneous .

•
All cancers
originate from one aberrant cell ,
which
goes
on to

multiply and
produce tumor mass .

Mutagens :
Any
substance which increases the rate
of
mutation can

enhance the rate incidence

also
of of cancer .

All
carcinogens Mutagens
•
are .

Examples -
X -

Rays y rays UV chemicals ( tobacco

rays
-

, .
, ,

aflatoxin
etc )

Antonieta gens
cis Vit A & carotenoids shown to
precancerous conditions
are reverse .

Vit E acts antioxidant

ai; as
,
preventing damage made by free radicals
and oxides
super
.

( iiis tit c
prevents cancers in
working
persons
with aniline .

( in Curren min in Turmeric cis

known to prevent cancers .

diet decreases the risk

as low
protein ,
low
fat of cancer in

animal studies .
 µ, flavin oils are
phytochemicals that
posses
anti
mutagenic properties .

(vill Phenolic
compounds are
effective in
fighting mutagens .

( found in
grapes
,
walnuts )

"" " '

Green tea induced mutations
in
effective against smoke .

Oncogene Viruses
°
Another etiological factor of carcinogenesis in the
integration
of viral
genes
into host DNA .

Oncogenes
Normal Constituents cells
Oncogenes of
°
are .

genes capable of
These
causing
°
are cancer .

and denoted
°
To
distinguish viral
gene
cellular
gene ,
they are V -
src &

C
respectively
src
-

oncogenes present
•
The in normal cells are also called as

proto oncogenes
-
.

Today more than too human

proto -

oncogenes
are
known .
 Growth Factors
Many oncogenes through act
°

the
production of growth factor .

•
These may be considered as

local hormones .

• There are more than too

growth factors .

Interleukin and
interferons growth factors released
by
°

are

lymphocytes / macrophages .

Difference between Normal & Tumor Cells .

in
Doubling Time : gt can
vary widely between lo
days to 450
days
with a mean
of about too
days in Tumors cells .
 (2) Contact Inhibition lost
This
property is in cancer cells
-
.

131
Anchorage Dependence Malignant character is the loss of
-

anchorage dependence in tissue culture system .

( 41 Most cancer cells

carry negative surface charges
more on their
due
cell
surface than their normal
counterparts This in .
to

neurami acid ) content

higher MAMA ( N -

acetyl of cancer
membrane
cell
.

151 Cancer cells have a

tendency to
disintegrate from main mass

and to disseminate to distant

nearby or
organ
This is
.

called Metastasis .

161 Cancer cells have increased and

persistent activity of telomerase ,

the that maintains the

enzyme length g telomeres .

Tumor
Maar Kers
called
They are also tumor indene substances
•
as
.

which could be
•

They are
factors released
from the tumor cells ,

detected in blood and

therefore indicate
presence og
tumor in
body .

They are
useful for the
following purposes
:

and
For
follow -

up of cancer to monitor the

effectiveness of
therapy .

do , To facilitate detection
of cancer .

For
(c)
prognosis
.

(d) Precautions -
Tumor
markers are sometimes elevated in

conditions
nonmalignant .

• lather a
marker in med
for cancer
screening or
diagnosis ,

the test result

physician must
confirm a tire
by using
studies tissue biopsies & other procedures
imaging
.

,
Anti -
cancer
Drugs :
-

② Med Notes ( med notes . in )

-
 Biochemistry
-
og -
AIDS d HN

Transmission :

About so %
by sexually transmitted disease ( STDs )
°

About blood
by
°

15% -

About 5%
by Mother to
fetus ( of infants to
•

-
n 30% born HIV +

mothers
may get the
infection )
Course :

klindowenod -
When virus enters the
body .
it is
multiplied in the

body cell but it cannot be detected

,
easily .

. The Virus
capsid antigen p 24 can be detected in blood .

Few months later antibodies

Sewposikvestage -

, are seen in circulation

This is sew
positivity .

this period in but carrier

During normal
°

person a .

3rd
•
About to %
g Seropositive individual
progress
to
stage
within 5
years
.

About so t within to
yrs
• .
.

About within not treated )

yrs ( if
°
90% 15

AIDS Disease
Third
stage when the clinical
manifestations
-

-
in

start
By this time immune
system di
.

o Commensal microbes IT

Patients die within after 3rd

2
stage
•

years .

°
Some
infections by -

fungi : Candida
Cryptococcus
&

Virus :
cytomegalovirus Herpes simplex &

Parasites :
Pneumocystis carinii

Bacteria :
Mycobacterium & Salmonella
 •
Cancers associated with AIDS an
Kaposi sarcoma and

NHL ( non -

Hodgkin 's lymphoma )

•

Cognitive impairment due to meningitis Neuropathies .

and
Neuropsychiatric manifestations .

Clianifestakons :

lymphadenopathy be 2nd
o and Fever
may
seen
by end
of stage .

related
• AIDS
symptoms ( Ars ) are wide .

. Since
immunity Hi in
,
non -

pathogenic microorganisms enter into

the
body and produce lesions in skin ,
GIT .
lungs .
Urinary tract .

brain etc .

•
Gastroenteritis & Tuberculosis are
predominant in AIDS in India .

Laboratory Analysis :

cis
by ELISA test .

ciii tales fern bolt

-

( confirmatory )
( iii , T -

helper count ( L 300 Camm ) ( Normal -

400 cumin )

( Ivi 24 A
p
cut RTPCK ( real time PCR) -
To detect Hiv
particles in blood .

Value copies 1mL of blood

I 5000 in
good prognosis .

> I lakh 1mi blood in bad

g
prognosis .

His HAT ( Nucleic acid testing )

I,

Involves
amplification and detection of one or more
specific
located
target sequences
in
specific Hiv
genes
.

Detection limit to 400

200
copies 1mL
o =
.
 Virus
Human
#
Immunodeficiency #
:

structure :
-

cis Hiv
belongs to the retrovirus groups RNA containing .

viruses that
replicate with the help of transcriptase ( reverse RT ) or RMA

dependent DNA
polymerase .

iii , Virus has

cylindrical
a core ,

containing two copies

of ss RNA .

Protein
ciii ,
components are named after
its molecular wt .

civl Core contains Reverse transcriptase

( p 66 &
p
55 ) ,
endonuclease
(p 32)

Nucleocapsid ( pg )
protease ( p lo )

Major capsid Antigen ( pm) -

About
copies
200
.

Outer shell
Myn 's to ligated Protein
-

(P 17 )

[ About
pies D
p ]
24
 Virus
Entry :

l " The
binding of Hiv with
target cell in
through a
receptor mechanism

The
envelope with bind with
ciii
gp
120
of vines
specifically CD4

molecule on the
surface of target cell .

CD4 acts as a
receptor for
tins
present
.

molecules
(
iii , The CD4 are on
surface of T -

helper cells &

therefore helper cells receive the maximum attack of Hiv .

and
entering receptors
HIV chemokines
(im uses CD4 as .

[ Replicating de ]
 Immunology of AIDS

ii. The CD4 (T helper) lymphocytes decreased number

leading
-

are in
,

to
immunodeficiency .

unit attach with molecules present

• The
gp
120
surface CD4 on

the
surface of T -

helper cells .

• Hiv
preferentially enters into T -

helper cells and they analysed .

act
ciii
Macrophages and
monocytes as the reservoir
of Hiv
infection .

which disseminate the virus to various

organs .
including CMS .

In turn , macrophage de

1400 blood
ciii , T -

helper ( CD4 ) =
cumin g
.

interleukin
Civ , Lymphokines such as
interferon ,
-
2 etc are lowered .

ANTI -
HIV
Drugs :

inhibitors
- -

① RT

anti Inhibitors
o G - classes og
-
HH
drugs .
② Integrase
[ 4 described
-

③ Protease inhibitors ④
Entry
here
] Inhibitors
④

①
②
 ( is Reverse transcriptase ( RT ) inhibitors :

cis AZT ( di deoxy thymidine azidothymidine .

,
Zidovudine )
Iiis dd I ( di
deoxy inosine ,
did anosine .
Lida no sine )
ciiis ddc ( di deoxy cytidine Zala ta bine )
'

civ , das ( stave dine )

HI 37C ( Lami vaccine )

Il
Aba caviar
''
(

Inhibitors Raltegrayir
ciis
Integrase : cis

ciis
Elvitegrauir
ciii , Dolce te
gravis

( iii , Protease Inhibitors : cis Iopinaneir

dis Indinaniir
( iii , Mel
financier
( in
Ampnnaneir
( is Rito navis
( vis Darien aviv & Atacama .ir ( first line
choice )
( in
Entry Inhibitors : Ma ravine 4 En
fair tide
- .

Prevention :

• Since there in no cure

for AIDS ,
and vaccines are not present ,

public education to limit

awareness &
only means
.

am

° Use
protections .

Using disposable syringes

•
.

inactivate the
•

Boiling for to mins will virus .

② Med Notes ( www.mednotes.in )

the Med Note app
* Download
from Play store !
 Fat-soluble -

Introduction
McCollum Simmonds &
Kennedy isolated Hit A in 1913
•

, .

.
Hit A cis
fat soluble ( Active form is present in Animal Tissue ).

carotene)
°
The
pro
- vitamin
(B
-
is
present in
plant tissue .

°
B carotene has two
-

p ionone
rings
connected
by polyprenoid
chain .

molecules
carotene og wit tf
One 2
13
° -

.
All the
compounds with Hit A
are
referred as
Retinoid .

. Vit A Alcohol =
Retinol
Hit A Aldehyde =
Retinal
Hit A acid -

Retinoic acid .

°
As isomers are
possible ,
all trans

Retinal Hit
variety of AI

Metabolism thot A
-
&
Absorption of

• Intestine is the
major site
of absorption .
 carotene cleaned di to
form Retinal
°

B in
by a -

oxygenase
.

Retinal Retinol
Absorption is along with
fats
° - o

NADH
and bile salts
dependent Retinal
requires .

Reductase

the retinol
Within the mucosal cell in
esterified with
°

, re -

fatty acid
,
incorporated into chylo microns and transported to

Liver where lit in stoned as Retinol palmitate in liver stellate

cells .

Transport from liver to Tissue :

Hit A from liver is to

°

transported peripheral tissues as trans

-
retinol
by the retinol
binding protein or RBP .

binds with
• One molecule g KBP one molecule y Retinol .

¥
"
Sheen)
°
In Vit A
deficiency .
the RBP in blood a,

Uptake by Tissues
The retinol binds to
complex specific
°
-

KBP

receptors on Retina ,
skin ,
gonads & other tissues .

• The KBP does not enter the cell .

. Hit then binds to cellular retinoic acid

binding protein ( Ck BP )
in
cytoplasm &
finally to Hormone Responsive elements ( MKE)

of DNA .

And activated
eventually genes
°

are .
 Biochemical Role og
lit A
-

④ Wald 's Visual -

cycle
Generation of Nerve Impulse :

Rhodopsin ( a membrane
protein ) found in
photoreceptor cells

of Retina .

made retinal
It
of protein opsin
is & I cis
up
° - .

• IN hen
light falls on retina ,
the I cis
- -
retinal isomerize to
all -
trans -
retinal -

° The all -
trans retinal -
in then released
from protein -

The isomerization photo excitation leads to activation

&
of
-

G -

protein a
generation og cyclic
-
GMP .

°
Cyclic GMP acts as the
gate for cation
specific channels .

thus the retina transmitted to

• The nerve
impulse generated in in

visual centers in the brain .

residue
° The
signal in terminated
by phosphorylation of a serine

activated kinase
of rhodopsin ,
by an
enzyme rhodopsin ,
so that
tin bind and inactivate
the
inhibitory protein p -
arms can

rhodopsin .

Regeneration og I -
cis - retinal :

la )
After dissociation ,
opsin remains in retina ,
but trans retinal -

enters the blood circulation .

later
-
cis -
retinal is
generated ,
reaches retina and this reattachment
in critical for shutting off pigment 's catalytic activity .

(b) The all trans - -

retinal in isomerize d to 1 - cis -
retinal in the
retina
itself in dark by retinal isomerase .

cel
Alternatively ,
all - trans - retinal in
transported to liver and
then reduced to all - trans - retinol by alcohol dehydrogenase .
 The all -
trans retinol
- to H -
cis - retinol and finally I -
cis - retinal
in liver .

and then transported to Retina .

• This completes the lnlald 's visual cycle .

② Retinoic acid has a role in

regulation of gene expression

&

tissues
differentiation og .

③ Retinol in
necessary for the reproductive system .

⑨ Antioxidant
property
③ 13 carotene be attacks
may useful in
preventing Heart
-
.

⑥ Vit A is the maintenance epithelium

necessary for of
normal

and skin .

Deficiency of -
Vita

Night blindness
cis or ,
Nyctalopia
121
Xerophthalmia
Bi tot 's
(3)
spots
14 ) Keratomalacia
⑦ Preventable Blindness
161 Skin & Mucous Memb .
Lesions .
 Causes for lit A
deficiency
cis Decreased intake
ciis Obstructive jaundice causing defective absorption .

reduced
iiis Cirrhosis of liver
leading to synthesis g KBP
.

( in severe malnutrition
where RBP
all chronic nephrosis ,
is

excreted
through urine .

Daily Requirement of Iit A

children
600µg / day
cis = 400 -

Men
ii , 750
peg / day
=
tooo
-

iiis Women 750

µg / day
-

( in
Pregnancy = 1000
Mg / day

② MedNmed notes .in )

 Fat solubleYi
Introduction :

Angus &
coworkers isolated wit is in 1931 and named it
calciferol .

Vit is derived dehydro cholesterol

either
from Ergosterol
D
F
•

or
-

action radiations
by g Uv .

vitamin derived from fungus ergot

•

Commercially the is ,
-

Ergosterol →
Ergocalciferol ( Vit D2 )
UH

Some Hit D
imp
:
are
-
• .

resistant to heat oxidation acidic

Vit Ds
relatively and
'
o are
. ,

alkaline medium Thus not

easily destroyed while
cooking
.
.

Metabolism
#
of Vit D

Absorption :
Along with
lipids ,
vit D in
predominantly in
proximal
GIT .
Absorbed wit D enters circulation via
chylo microns .

Activation : Hit D vis hormone

pro
.

l
④ ④
l

( liver )
- -
kidney
25 -

hydroxylase t -
d -

hydroxylase Calcitniol

①
( la 25 -

Dihydnog
① ① i
@ cholecalciferol
( Cholecalciferol ) ( 25 -

hydroxy cholecalciferol )
 Vitamin
• Calcitonin thus
formed in
kidney in the Active form g
.

Regulation :

cis The conversion

of F -

dehydro cholesterol to
cholecalciferol is

dependent on
exposure
to
sunlight .

es 25 -

Hydroxylase in liver is controlled by its feedback

inhibition
by 25
hydroxy cholecalciferol
-

(3) Hypercalcemia ,
hypophosphate mia & PTH stimulate the vito

(41
Estrogen also help regulation
in .

Functions :

It intestinal and
"' increases calcium
phosphorus absorption .

coordinates the
⑦ Calcitriol
remodeling of bone and increases

mineral density .

Active Hit D has action on all three

types
bone cells osteoblasts osteoclasts
og I
Osteocytes
-

, .

ad
is , Cal citniol increases the
reabsorption g
calcium
phosphorous
by renal tubules .

(4)
Regulation of Immune system
is ) Regulates epidermal proliferation og
skin .

Hit
Deficiency og is

The
deficiency diseases rickets in children &
°
are

Osteomalacia in adults .

• Hence wit D in known as

Antirachitic vitamin .

• 25 -

Hydroxy Dz : > 30
my 1mL ( optimal ) 3150
ng 1mL
I
ng 1mL ( insufficient )
20 -

29
Toxic
-

10 -
19
ng 1mL ( deficiency )
 Causes for dit D
deficiency :

not
cis
Deficiency of wit D can occur in
people who are

exposed to sunlight properly .

and steatorrhea )
ciii Malabsorption g
lit ( obstructive jaundice
diii
Abnormality g Vit D activation .

( in Deficient renal absorption og phosphates .

In certain
drugs like pheno barbitone , phenetoin etc can
influence
wit D level .

Requirements -
g
titis

children
cis to
Mg / day
a-

iiis Adults = 5 -
lo
Mgl day
ciiis
Pregnancy ,
lactation = to
teglday
Above
(in
age g
60 = v lo 15
My 1
day
-

Clinical Features :

Rickets : -

cis seen in children

Iiis Bone becomes soft
pliable
&

ciiis Bone deformities

( in eight bearing bones -s Bent )

civ )
Enlargement y Epiphysis
is Harrison 's sulcus

( Vil
Rickety rosary .
 Osteomalacia : -

is More to fracture
(
prone
Iiis Bones are
softened due to

insufficient mineralization .

iiis Serum alkaline phosphatase 9

How to
- diagnose :

1 IU is the biological equivalent of 0.67 mg

② Meditates
( med notes .

)
in
 Fat solublellit.tt
Introduction :

active vitamin isolated wheat oil and

• The was
from germ
named tocopherol .

o Vit E in the most

potent biological antioxidant .

structure elucidated Paul who

• The
of Vit E was
by Karrer .

awarded Nobel
was
prize ( 19371
.

l t -

tocopherol )
Metabolism of Hit E :

Normal blood level

of
°

tocopherol in 0.5 -

t
my 1dL
.

•
gt vis absorbed
along with other
fats and needs the help
of bile salts .

°
Tocopherol is absorbed and transported as chylo microns .

. It in then stored in
Adipose tissue .

During catabolism the chroma ne & side chain be

ring
°

,
may
oxidised and excreted bile
in
after conjugation with

glucuronic acid .

Biochemical Role og
Nit E
-

°
St in the most
powerful natural antioxidant -

o Vit E
protects RBC
from hemolysis By preventing the peroxidation .

it
keeps the structural functional integrity og all cells
& .

Vit E also boosts immune

response
o .

° It is also anti -

aging as it
protects from free radicals .

.
It reduces the risk of anthem sclerosis by reducing oxidation

of LDL -

o Vit E can depress leukocyte oxidative bacterial

activity .
 Deficiency og
Hit E ( General Symptoms )
Increased risk cardiovascular
og
°

diseases
children
Hemolytic anemia in
°
.

Infertility
•

Neurological problems
• Neuromuscular
problems such as

spinocerebellar ataxia ,
myopathies ,

etc .

*
Normal adult
body
In . the
wit E stores can meet the

requirement for several months .

Recommended Daily Allowance :

Males
mg / day
•
=
to

Females 1
8
day
my
=

Pregnancy = to
my day
1

4 act lion
12mg day
a
= 1

Vegetable oils are rich sources

g
Vit E .

( fish liver oils are devoid g

dit E )

Hypervitaminosis -
E

• At
high dose (s tooo Io
per day ) ,
it
may
cause
tendency to

hemorrhage ,
as it is mild anti -

coagulant
.

High Risk og Excessive

bleeding .

② Medi ( med notes . in )

 Fat soluble Vitamin
Introduction :

"

letter vitamin
' '

koagulation
"

a
K -

o Vit K is
naphtha quinone derivatives ,
with a
long isoprenoid chain .

side chain
.
The
length of Hit k ,
will
differ .

•
Vit ki 20C side chain
( phylloquinone ) Vit

Vit Kz 30 C side chain K2

•
Henrik Dam isolated Vit K, ( 1929 )

Edward Dois
y
- vit Kz ( 193g ) } awarded Nobel Prize .

( 19431

Metabolism :

Absorption of wit k occurs in the intestine along with

Chet omicrons .

[ Bile salts are

required for normal absorption ] .

o Vit K
may
be derived from diet or intestinal bacterial
synthesis .

. gt is stored in liver and transported in

plasma with P -

lipop.ronst.ci
Biochemical Role of Vit K

Vit
in K is
necessary for coagulation .

in Factors
dependent on hit k are Factor I ( prothrombin ) ,

Factor VII ( SPCA ) , Factor Ix d I .

required many factors

Hit k
(3) is
factor as co -
in .

K dependent
gamma carboxylate necessary for
141 Vit in also on

the
functional activity of osteocalcin well structural as as

proteins of kidney ,
lung &
spleen .
 Deficiency of Hot K :

°
In normal adults
dietary deficiency seldom occurs since

intestinal bacterial synthesis in

sufficient to meet
body needs .

Deficiency can occur in in

Malabsorption og lipids
'" Gastrointestinal Infection .

Daily Requirements ;

Normal adult So too

lug / day
° = -
.

Green leafy vegetables

°
are

good dietary sources .

Yik Dependent carboxylase :

It is micro som al
enzyme
•
.

gt
.

requires Co2 ,
NADPH and
educed wit .

K .

°
9N this
process
vit
passes through
a
cycle -
 Hypervitaminosis K
•

Hemolysis
°

Hyper bilirubin emia

•

thermic terns
*
.
Brain
damage
1
Manifestations
9
Toxicity .

Administration of
large
°

quantities of Menadione *
I

Toxicity in

children .

② Meditates
(med notes .
in )
 Water Soluble V
Introduction :

Albert Szent extracted and named

Giorgi in 1930
Hexuroniacud
°
-

•
In 1933 ,
Haworth established molecular structure and renamed
it as
Ascorbic Acid .

o
Vit C in water soluble ( easily destroyed by heat .
alkali &
storage )
St has
reducing property due to
°

double bonded carbons ( ene diol ) .

Metabolism
acid absorbed
Ascorbic
readily by GIT
°

in .

o L -
Ascorbic in absorbed
by Active transport and
Dehydro ascorbic in absorbed at a
faster rate .

•
The vitamin is excreted in urine .

Oxidation
.

of ascorbic acid
yields dehydro aerobic acid ,
which
oxidised further to acid
is oxalic
through dike to -
L -

gulonic
acid .

and
.

Ascorbic acid in
partly excreted
unchanged partly as

oxalic acid .

Ascorbic acid level o 7 to

1100mL plasma
. =
-

1.2
my g

my 1100
25
1413C
=
cc
g

level dit
•
The
highest og c in
found in
pituitary .
adrenal ,

leukocytes lens & Brain

,
y eyes
.

. The concentration is lowest in

plasma & saliva .
 Biochemical Functions
-
of dit c

its
Collagen synthesis :

Proline Prolyl hydroxylase

-

Vit c Fe
" Hydroxy proline
, a
ketoglutarate
-

lysine "
Hydroxy lysine
• These
hydroxyl groups
are crucial
for maturation
of collagen .

. Thus wit C in crucial for collagen synthesis .

121 Tyrosine Tryptophan Metabolism

, : The metabolism g Tyrosine
and other A- As Nit
require c .

'
•
Tyrosine →
p Con) Phenyl pyruvate Hit c cu -12
Tteomogentisak

!
Do amine
Dopamine
Hit c Catz
Norepinephrine

Tryptophan -

Vite
5 -

hydroxy tryptophan → Serotonin

steroid
r synthesis in
131 Bile acid synthesis steroid adrenal cortex
oogenesis
& .

( 41 Anti oxidant
- : Vit c in an anti - oxidant that prevents free
radical
damages .

°
9T
may prevent cancer
formation -

Daily intake of Hit c reduces the risk of cancer .

151 Fe Absorption : Vit C enhances iron absorption from gut

state
by maintaining
"
iron in Fe .

161 Immune functions :

Neutrophil chemotaxis macrophage ,
and
 My cell functions . serum
complement levels are
improved
by Vit c .

Hb Metabolism gt useful for met Hb

IF ) : is re conversion
of
-
-

to
hemoglobin .

is ) folic Acid Metabolism : It also helps in maturation g RBC .

Hot
Deficiency Manifestations y
c

a
scurvy
( Infantile
12 ) Barlow 's Disease
Scurvy )
(3) Hemorrhagic Tendency [ Pinpoint
141 Internal
hemorrhage hemorrhages]
151 Oral
cavity damage
161 Bone becomes weak

( 71 Anemia due to blood loss , Fe absorption I ,

met Hb A
-

folic Acid I,

Tite
Dietary Sources g

o
Rich sources are :

700mg 1100g
amla ( )

Guava ( 300 my 1100g )

lime
lemon

leafy Vegetables .

Daily Requirement =

75mg (day
( 50mL
orange
For iuices
pregnant ,
aged
=

100mg / day .
 Therapeutic Use

cis Vit C is used as an

adjuvant in
infections .

dis Beneficial effect of ascorbic acid in Tuberculosis .

ciiis Recommended in treatment g ulcer ,

trauma & burns .

( in Mit c in essential
for wound
healing .

Toxicity
°
Since it in water soluble , excess vit C is excreted ,
not accumul
-

abed .

• >
2000mg y
Vit c
daily can cause
teoveroad .

② Media ( med notes . in )

 Water Soluble fit -

Bi
.

Introduction :

•
Vit Bd in also called Thiamine .

•
Thiamine contains a substituted pyrimidine ring connected to a

substituted thiazole
ring by means
of methylene bridge .

vitamin then converted its active

The in to co
enzyme from by
.
-

addition two It
of phosphate groups ,
with help g ATP .
in

catalyzed by thiamine
pyro phosphotransferase .

Physiological Role
of Thiamine :

cis Pyruvate dehydrogenase : The co -

enzyme form
in
[
TPP thiamine
pyrophosphate
It med oxidative
in in
decarboxylation keto acids
•

a
g
-

eg pyruvate dehydrogenase catalyzes

.
the breakdown of
pyruvate to acetyl CoA Co2 -
& .

ciii d-
ketoglutarate dehydrogenase : An
analogous biochemical reaction
that requires oxidative decarboxylation
TPP in
g a -

ketoglutarate
to
succinyl CoA d coz .

( iiis Trans keto lase :

The second that TPP as
group og enzymes
use

co the trans Ketola see in the

enzyme are
shunt
-

.
HMP .

Liv , The main role thiamine (TPP )

of in in carbohydrates metabolism -

so ,
higher intake of carbohydrates a
requirement g thiamine .

Deficiency Manifestations :

IAI Beriberi :
symptoms include

-
Anorexia

Dyspepsia
Heaviness & Klea Kness .
CBS Inlet Beriberi : Here cardiovascular manifestation are
prominent .

Edema
-

n
legs face trunk
. .
and serous cavities .

Palpitation , breathlessness and distended neck veins

are observed .

Death due to Heart

occurs
failure
-

Beriberi
(c)
Dry : 9N this ,
cats
manifestation
are the major
features . Hae
king becomes

difficult .

Peripheral neuritis with

disturbance Paralysis
sensory
→
.

IM
Infantile beriberi 9 't in infants : occurs born to mothers

suffering from thiamine deficiency . Restlessness &

steepness are observed .

it '
later niche -

Korsakoff syndrome : It in also called cerebral beriberi

-
Clinical
features are those g
encephalopathy plus psychosis .

St when the nutritional status

in seen
only in
severely
-

affected .

IF , Polyneuritis : 9 t in common in chronic alcoholics .

Alcohol
utilization needs dose
large g thiamine and it ( alcohol )
.

inhibits intestinal absorption to

g thiamine
leading
thiamine
deficiency .

Thiamine
deficiency impairment
°

may
cause conversion
g g

pyruvate g acetyl CoA .

. This leads to A plasma pyruvate & lactate concentration → lactic

Acidosis
 Sources :

°
Aleurone
layer of
cereals in a rich source
g
thiamine .
-

-
Yeast in also a
good source .

F-
Thiamine
partially destroyed by heat
°

in .

Requirement mgl day

°

=
I - Irs

Thiamine in
useful in treatment
°

Beriberi .
Alcoholic Polyneuritis .

Neuritis is
Pregnancy and

Neuritis g Old
age
.

⑨ Meditates
( med notes in ) .
 Vitamin -
132

Introduction :

Riboflavin was the

first B
complex component to be isolated in a

state
pure
.

.
This vitamin in
synthesized by green plants and
microorganisms
.

attached
o
Gt has a
dimethyl iso all oxazine
ring to which a ribitol in

Ribitol Alcohol g Ribose Disdain

sugar
° = .

converted to its active

Riboflavin
°

in co
enzyme
-

forms ( FMN & FAD ) with help g ATP .

°
Co -

Enzymes
enzymesA ily
containing
of Riboflavin

riboflavin are
:

called Flavoprotein
D- Ribitol

s
) .
,

The two co ( flavin FMN nucleotide ) and

enzymes
•
-
are mono

FAD ( flavin adenine dinucleotide ) .

oxidation FAD
accepts two
hydrogen atoms
from
During
°

process ,

substrate .
In turn .
FAD in reduced to FADHZ .

-
The two nitrogen atoms
of iso all oxazine nucleus accept the H

atoms .

Amino acid oxidation reduced It oxidized

•

During ,
FMN in .
in re
by
molecular
oxygen
to
produce hydrogen peroxide .

In
Respiratory chain the NADH
dehydrogenase contains
°

, FMN .

"
MAD → FMN →
Cog

Riboflavin Deficiency :

( at Cage : It in uncommon as it in
produced by intestinal
flora .

Riboflavin deficiency usually accompanies

other
deficiency diseases
-

such beriberi and

as
,

pellagra kwashiorkor .
( bi Manifestations :
symptoms are confined to skin and mucous membs

cis Glossitis
iii ,
Magenta colored
tongue
ciii , Cheetos is

cixi stomatitis ( inf lammed

Angular mouth corners )

( ill Circumcorneal vascularized lion -

an
Proliferation g Bulba .
conjunctival capillaries .

[ Glossitis ] [ Cheetos 's ] [ Angular stomatitis] [ ]

Dietary sources :

Rich liver dried

sources
yeast
°
are
. .

and whole milk

egg .

.
Adult daily requirement 1.5mg ( day -
-

In
Pregnancy lactation .

& old
day
1.7 to 2. l
age -

omg .

② Meditates
( med notes in ) .
 Vitamin -

133

Introduction :

°
Hit Bz in also called Niacin con, Nicotinic acid con Vitamin PP

It in also called
Pellagra preventing factor Goldberger
.

g
.

Niacin amine Active form Vitamin

•
-
-

g
.

4¥
- comma

[ Niacin amide ] [ Niacin ]

• Niacin in a
pyridine -
3 -

carboxylic acid .

Niacin amide acid amide

°

in .

•
In NAD -1 or NADP ? the reactive site in C 4 and N atom nicotinamide
of
-

Ring .

Co for my Niacin
enzymes g :
-

Niacin converted to its -1

and '

enzyme forms
• we co - HAD NADP .

.
It in attached to Ribose phosphate to form a Nicotinamide mono -

- nucleotide
AMP + Nicho ninamide Mono nucleotide =
HAD
+

¥÷ie÷÷÷:c :÷÷÷n÷÷÷i!
'
" """"

÷: :*::
.
.

-1
In acid attached to Ribose
case
of NADP one more
phosphoric in
.
.

og

Niacin AMP
Deficiency
.

"'
Pellagra :

Deficiency og
niacin leads to
Pellagra ( rough skin ) .

↳ St
by
also caused
deficiency of Tryptophan
in
the as well .

If we seen more in women

tryptophan metabolism
.

as

inhibited
is
by estrogen metabolites .

Some
symptoms
°

are :
 cis Dermatitis -

Bright red erythema .

Iiis Diarrhea

Iii is htt loss ,

Nausea &
Vomiting
civ, Dementia .

Causes :

cis
Dieting of tryptophan ( GO.gg )
cii , Deficient synthesis 1mg Niacin
ciii , Isom.ae#Anliubrculous drug which
-

prevents tryptophan → HAD -1

cixi Hart
nap
disease :
Tryptophan absorption from intestine in
defective
s
congenital disease .

°
Moreover ,
tryptophan in excreted in Urine in
large quantities .

leads to lack
This
of tryptophan and consequently deficiency
•

nicotinamide
of
.

lui Caridad : The tumor utilizes major portion g available

tryptophan for synthesis of serotonin . So

tryptophan I,

Dietary Sources ng Niacin :

. Dried Yeast Meat

.

Fish
Rice
Polishing a
.

liver

Peanut

legumes
Normal Requirement
1dg
°
=
20mg
.

Pregnancy / lactation = 20+5

my 1 day
 Therapeutic Use g Niacin :

°
It inhibits flung FFA from adipose tissue , so
acetyl CoA pool is

reduced → Cholesterol in serum I,

Niacin
•
High dose , in
useful to reduce
lipoprotein [ lpca ] levels
, .

Toxicity :

Nicotinic acid when Vasodilation Histamine

orally
°

given and release

Itching burning and tingling
. Thus came
. .

350mg / day
Liver
damage
°
=
.

day serious
toxicity liver
damage
> 2
my &
°
a
.

② Med Notes
Tmednotes .in)
 Hater soluble lit .
136

Coenzymes Forry :

applied derivatives
o Vit Ba in term to a
family of 3 related
pyridine
( as
Pyridoxine ( alcohol )
( bi
Pyridoxal ( aldehyde)
H
Pyridoxa mine .

[ Pyridoxine] [ pyridoxamin.it

Active form Hit ( pyridoxal phosphate )

of Bo in PLP
°
.

•
It in formed by pyridoxal kinase ,
utilizing ATP .

Functions of Pyridoxal Phosphate :

acts [ PLP]
enzyme for many
° The PLP as co -

reactions in AA metabolism .

Trans amination
(a)
( catalyzed by Amino transferases which
the
employ PLP as co -

enzyme I
(b) Decarboxylation ( AA in these mkn
require PLP as co -

enzyme)
cc , sulfur containing A- As .

( PIP
plays an
important role in methionine and

cysteine metabolism )

id , Heme
synthase in PLP dependent enzyme)
synthesis ( AIA a

Production g Niacin pep in

les
( required for synthesis a
niacin
from tryptophan )
( fi Glycogen olysis ( Phosphorylase PLP )
enzyme requires

Deficiency Manifestations :

°
In Hit Bo
deficiency ,
PLP dependent enzymes function poorly .
(as Neurological Manifestations : serotonin .
epinephrine ,
noradrenalin
and
gamma
amino
butyric acid ( GABA) are not produced
properly .

°
In children .
136 deficiency leads to convulsions due to decreased
formation g GABA .

PLP in involved in synthesis ns.phingolipids ,

so Bo
deficiency leads
to demyelination y nerves and
consequent peripheral Neuritis .

cb , Dermatological Manifestations :
Deficiency g 136 will also
affect
tryptophan metabolism Since niacin in produced from .

tryptophan Bo Niacin deficiency

, Pelley za
→ - s .

In adults
(c '
Hematological Manifestations : ,
hypochromia micwcy hi
anemia occur due to inhibition
may og heme
synthesis .

The metabolic disorders which

respond to wit
•

Ba
therapy
Xanth uremic aciduria &
homocysteine nd
are
.

Effect D
Dzugs :

cis IN H : Iso nicotinic acid hydroxide → causes Hit Bo

deficiency .

Act
ciis Cyclo serine : as 136
antagonist
(
iiis Oral contraceptives : Causes mild Hit Bo
deficiency .

cixi Ethanol : Bo
deficiency neuritis in
quite common in alcoholics .
 Dietary Sources :

°
Yeast .
Meat

Polishing Rice Fish

.
•

• Wheat
.

Egg
°

legumes
•
Green leafy
-
oil seeds vegetables .

. Hit 136 requirements are

related to Protein Intake .

• Adults -
- I -

2mg lday
Pregnancy / Lactation = 2.5
mgl day .

Toxicity :

°
Doses over too
my
→
Sensory Neuropathy .

• >
100mg Imbalance , numbness ,
muscle weakness & Heme
Damage -

② MedN
( med notes .in )
 Vit -

Bs

Introduction :

.
It in also called Panto thermic acid .

°
Panto the mic acid contains and amide
13 alanine D -

pantie acid in

"
linkage
%
.

Ho -

Chz - - -
co - NH -
CH z
-

Chez -
COOH

- -
Pantai Acid p -
Alanine

I
Pantothenic Acid .

Panto theme: acid and

13 mercapto
•

ethanol -

amine
He
Parts Co A
g enzyme
'
-

t.co At

Coenzyme Activity :

( is The
P mercapto ethanol amine ( Mhz -

cuz cuz
- -
SH ) contains one thiol
or
sulfhydryl ( -
su )
group
.
Thus colt in sometimes abbreviated
as CoA -
SH .

dis choline Acetylcholine

Acetyl CoA t → t
CoA

[ enzyme in
acetylcholine synthase ]
Liii , Pyruvate t CoA t NAD
Acetyl CoA coz
t
→ t + NADH

civ ) Important colt derivatives are

:

Acetyl WA
(a)

bi
(
succinyl CoA
(c ) HMG CoA
id , Acyl CoA .

an co -

enzyme
A in an
important component of fatty Acid
synthase
complex . The
Acyl carrier
protein also contain Pantothenic Acid .
 Deficiency of Pantothenic Acid :

°
Go plan 's
Burning foot
syndrome in
manifested as Paresthesia

boring lighting extremities

( .
pains in lower .
staggering gait
and sleep disturbances .

Ran in humans .

. The
syndrome is seen in

Famine ,

Prison
camps
and in some renal
dialysis patients .

Sources :

Widely distributed Plants &

Animals
°

in .

intestines
By flora in
•
.

•
Yeast
Good
Egg } sources .

Liver

Requirement 10mg ( day

a =
.

② MedN ( med notes .in )

 Hit -

137

Introduction :

9T isolated Vincent du Vigneau d

o
was in 1942
by .

•
Also known as Biotin .

It consists imidazole thiophene ring

ring fused
with
°

of an a

with a valeric acid side chain .

The
carboxylic group forms Amide linkage with epsilon H lysine
°

g
residue .

Coz carriage .

↳
Imidazole
Ring Apoenzyme lysine
→

!
Thiopheneing →

Coenzyme Activity :

Biotin acts for carboxyl lion reactions

•

as co
enzyme
-
a .

°
Biotin captures a molecule
of Co2 which in attached to N g biotin
molecule .

Biotin
Antagonists :

is Avidin . a
protein present in
egg
white has
great affinity to biotin .

Thus raw
egg may
cause biotin
deficiency .

ciii Avidin t molecule can combine with 4 molecules g

biotin .

white contains Avidin

Egg .
Egg yolk contains biotin .

Avidin biden system utilised for detection of

ciin -
in
commonly
pathogen by Elisa .

in streptavidin bind 4 molecules Biotin

( can
of .
 Deficiency g Biotin :

( is
Prolonged use
g Antibacterial drugs .

cii , Biotin
deficiency symptoms include -

(a) Dementia

(
b,
Atrophic Glossitis
14
Hyperesthesia
id , Muscle Pain
(e) Anorexia

if , Hallucinations .

Ig )
fatigue .

eh , Hair loss
cis Dermatitis

lip Pale skin .

Iki Abnormal
Heart Actions .

Sources :

•
Flora g Gut in
sufficient .

°
Yeast

Liver

Peanut

Soya bean
} Rich sources .

Milk
Yolk

•
Requirement -
- 200 -

300mg

② MedN ( med notes .in )

 Water soluble Vit -

Bg

Introduction :
o
gt is also called folic acid .

. Pte n'dine t PABA ( para amino

benzoic 'd )
\ / ace

Pteroic acid

f ,
+ Glutamic acid

Pt enoyl Glutamic acid / folic acid

°
Folic acid in soluble in water and

light rapidly destroyed

in hen exposed to ,
it in .

Absorption :

absorbed
It in
readily by Upper part 7 Jejunum
°
.

•
In blood .
it in
transported by P globulin -

Folic acid not stored rather it liver

in in tissues in taken
by
.

up
IN here co -

enzymes
are
produced .

Co :
enzymes
-

CA ) folic acid in first seduced to 7 ,

s dihydro folic acid

by NADPH dependent 5,6 ¥ s tetra hydro folic acid ( THEA)

folate reductase
-

(B) TH FA in the carrier of one carbon

groups
.
-

NE methyl med for synthesis of active

(c , Methyl group
in Th FA wi

which takes part trans reactions

methionine ,
in
methylation .

of Folate
Cannes
Deficiency :

°
Common in India .

fit
. Most common
deficiency .
 ( is
Pregnancy .

His
Defective Absorption .

ciiis
Drugs
civi Hemolytic Anemia .

( vs
Dietary deficiency
( vis
Folate trap
[ Maczocylic
.

Anemia]
EMegakblmaknkem.az
Deficiency Manifestations :

cis Reduced DNA synthesis

dis Macrocyclic Anemia
Ta Immature Nucleus
looking
(
b, Reliculocytosis
( c )
leukopenia d.
Thrombocytopenia
( iiis Hyper homocysteine mia ( s 15µmol Il g Plasma )
L
Coronary Artery
>
Diseases .

civi Birth defects 1- Neural tube defects like spine bifida in foetus)
(v ) Cancer

sources of folic Acid :

°
Yeast .

Green leafy vegetables

Cereals Pulses Oil seeds &
Eggs
•
.
.
,

• Milk in
poor
source
for folic acid .

Daily requirement 200µg ( day

.

• =

Pregnancy = 400 Pgl day

lactation = 300
Mgl day .
 Toxicity :

Nerve
•
Dose over >
Img :
damage
crystallization in
kidney ( Renal damage )
Folate Antagonists :

( i
, Sulfonamides
a
Pyrimethamine ( antimalarial )
③ Aminopterin e
Amethyst -
erin

methyl folic
Y'
( 4 amino 10 acid )
(
-

4 Amino folic ace 'd )

② Meditates
( med notes .in )
 til ater soluble fit -

Biz

Introduction :

°
Also known as Cobalamin .
extrinsic factor ( EF ) of Castle and
Anti pernicious anemia
factor .

• Hit Biz in water soluble ,

heat stable and red in colour .

Contains cobalt wt
4.35%
by
°
.

°
Hit Biz I cobalt atom coordinated with

a cobalt atom ( Corrin Ring )

and benz imidazole
one
ring .

Absorption of lit Biz :

cis
Absorption of lit Biz requires two binding
protein .

( at
factor (
Intrinsic in
gastric juice )
bi
(
Cobalophilin ( in saliva )

ciii
pepsin release the
Gastrin vitamin

From proteins of food and then

Biz binds with cobalophilin .

ciiis In duodenum cobalophilin fit

. in hydrolysed by trypsin and in

released and binds to Intrinsic factor .

mol.rs Intrinsic combine with molecules

civi One
factor can 2
og Biz .

attached with specific receptor muggy;D

This IF -

Biz complex in on

The whole IF -

complex
Biz internalized It may
in . be noted

absorbed from ileum

that Biz in while
folic acid ,
in
from jejunum .
 In blood
methyl Biz form in
°

predominant .

•
Frans cobalamin ,
a
glycoprotein .
in

specific carrier .

• It is stored in the liver cells ,

as

a do -

Biz form ,
in combination
with trans comin .

Generally B complex are not stored

in
body . Biz in an
exception .

Int hole liver contains about

.

2mg 9 Biz
( sufficient for 2-3
yrs )

Caunes of Vit Biz

Deficiency :

Nutritional India
in - Hit Biz
deficiency very
in common in .

Only source
og Bu in
vegetarian diet in curd / milk .

(2)
becreaseabso-rpk.com Malabsorption syndromes : or
Gastrectomy .

(3) AdcbPm Anemia : Autoimmune disease with

strong
familial background .

Antibodies generated against IF are .

-
so IF I
defective absorption a lit
.
. Biz .

( 41 Giant trophy :
Atrophy a Gastric epithelium → IF I →
Biz it.

requirement of vitamin
153
Pmg : Inc .
in
pregnancy
in

another came
og
Hit Biz
deficiency .

Fishtown Tapeworm has special

16 ) to
affinity Biz causing
:

seduction in available wit

[ Not India ]
'

seen in .
 Deficiency Manifestation :

cis folate trap

iii , Meg aloblaslic anemia

ciiis Abnormal
homocysteine level .

civ , Demyelination
can Subacute combined
degeneration .

His Achlorhydria

Source of lit Biz

° Not present in
vegetables .

• liver in richest source .

•
Curd in
good source .

Requirement -
I -2
Mgl day

Pregnancy =

2mg Hay
 Hormones Mechanism of Action Molecules
-
:
t
&
signaling-
y

[ PART -
I]

Signal molecules are

of different types and the
pnicess of
into
transferring the
signal cell in called
signal Transduction .

. Two
types :

ca , sender cell
og cells
ab ,
Target cell

. All cells have

specific and highly sensitive
signal transducer
ng
conserved
mechanisms ,
which have been
during evolution .

Receptor binds with signal molecule and initiate a

process
that

amplifies the signal integrates with ,

input and transmits the

information in the cell .

persists receptor desensitization ends Induce the

If signal response
° .
.

Classes of Hormones :
 types a Hormone
signaling :

when acts sender

( as Automne -

Signaling occurs same cell as

and Recipient As Growth immune &

Inflammahy
.
-

Response .

cb, Pan -

signaling in
effected by local mediators
site
which have their effect near the
of secretion
without
entering circulation .

Juxta crime two

(c)
-
-

Signaling whenoccurs
type g
cells are

adjacent to each other . so contact established

through gap junctions

.

cd , End between which located

signaling in cells
-

are

distance each other

at a
from and
signal
hormones secreted into circulation
maybe .

Type 9 Signaling mechanisms :

(n G -

protein coupled receptor -

External ligand binding to receptor

activator intracellular GTP -

binding protein ,

which
regulates an
enzyme
that
generates an

intracellular second
messenger
.

ciis
Recywsin -

ligand binding to extracellular domain

stimulates formation of second messenger cyclic -

GMP
His Gated ion channel
- Open -

/ closes in
response
to concentration
g signal ligand or membrane
potential -

( in
Receptor Guanylyl cyclone -

ligand binding to extracellular

stimulates formation g cyclic amp .

( vs
AdhesionReceptegn.nl -

changes conformation .
SEYNE

Hormones classification &

Hierarchy :

in with cell -

surface receptors -

Peptides / Amines
"" with intracellular receptors -
On Nucleus .
Steroid ,
Thyroid
hormones

② Medina ( med notes .in,

 Horizon e - Part 2

Hormones acting through cylic AMP :

discovered Sutherland
•

Cyclic AMP ( cAMP ) was

first by Earl in 1961 .

• Action is
through G -
Protein coupled receptors
( GPCRs )
When binds
any ligand
( is ,
the Gpcrs

activate heterotrimeric GTP

binding regulatory
Proteins (G -
Proteins )

Different G -
Proteins present in the cells
are

that are
coupled with different receptors
and
activating different efforts proteins .

cii , G -

protein activates A deny I cyclase .

Liii ) Aden converts CAMP

( 3,5 cyclic
yl cyclase ATP >
AMP )
- -

and
phosphodiesterase hydrolyses cAMP →
5
'
AMP .

.
Cyclic AMP is a second
messenger produced in the cell in
to activation protein
response of adenylate cyclase by active G -
.

During hormonal stimulation cyclic AMP level cell

°

, in increases
several times .

civ , Second
messenger
activates PKA

. The cAMP activates

enzyme
the PKA ( cyclic AMP
dependent protein
kinase )
tetrameric molecule two
° PKA is a
having regulatory CR)

and two catalytic CC ) subunits ( kzcz)

•
This complex has no
activity . But cAMP binds to the
regulatory
and dissociates the tetramer into
subunit
regulatory
and catalytic subunits . The
catalytic subunit in now
free to act .

Hi kinase
Phosphorylates the
Enzyme .

Catalytic subunit then

transfers phosphate
°

a
group from ATP

to different enzymes proteins .

 •

Phosphorylation usually takes place on OH

groups of serine ,

residues substrates
threonine or
tyrosine of .

Hence these kinase called Ser kinase The

.
are
/ Thr .

enzymes may
be activated inactivated
or
by this
phosphorylation .

° This in an
example of covalent modification .

sensitive
Glycogen phosphorylase & Hormone
lipase controlled
°

are

by cyclic Anap .

G- Proteins :

(G stimulatory)
different
-

About 30

G -

proteins identified
are ,

each
being used (G -

inhibitory )
for different signal
transduction pathways .
wiki
snippet
 Protein kinases :

. More than thousand

protein kinases are now known .

• Some
important are listed below :

Calcium based
signal Transduction :

.
Calcium in an
important intracellular regulator of cell
function
like :

( is contraction muscles
of
secretion hormones
( ii ,
of
(
iii , secretion g
Neurotransmitters
cix , cell division
( vs
Regulation 9 Gene regulation .

Rapid but transient increase

in cytosolic calcium malt

from either
opening 9

Cast channels in

the
plasma membrane /
cast channels in ER .

• The released cat can be

rapidly taken
up by Ek to
terminate the response .
 Phospholipase C
Pathway :
trigger sudden cytoplasmic
"
•

specific signals can a increase in Ca

levels to channels
500 tooo nM
by opening in ER plasma memb
-

or

.
The most common
signaling pathway that increases cytoplasmic cat

in Plc
pathway .

Protein coupled receptors

( is
Many cell surface receptors ,
including
activate
G -

and receptor tyrosine kinases Plc

enzyme
.

ciii Plc uses

hydrolysis of
membrane
phospholipid PI Pa to form IB
and
diacylglycerol ( DAG ) .
two classic 20
messenger
.

iii.is DAG attaches to

plasma memb and recruits Protein kinase c

( PKC )

cixi IB diffuses to ER and in bound to Its receptor .

(in The IPs receptor serves as a ca

- +
channel ,
and release Ca
't

from ER .

evil The cat bind to PKC and other proteins & activate them .

② Med Notes 11 Download Meditates app

Tmednotes .in ) from Play stone

!
 Liver Function Test

Introduction :

Biochemical tests for diagnosis &

monitoring of liver diseases
°
are

referred as liver
function tests ( LET) -

Tests
classified functions of liver
•

were on
major :

Excretion bile salts

pigments
la '
g . bromsulpthalein ,
bile etc
b , Metabolism
(
of carbohydrates and A- As -

(c)
Synthesis of proteins serum

( d,
Detoxification of Ammonia &
flippant acid synthesis
Serum
(e)
enzymes (
as
markers )
•
But
nowadays ,
( Fts are
broadly classified as :

in Tests to detect hepatic injury :

ca ) whether mild / severe

,
acute or chronic .

(b) Nature cholestasis

g
injury -

hepatocellular or .

(2) Tests to assess

hepatic function .

Functions of liver :

(I ,
synthetic functions
Metabolic
(21
functions
13 , Detoxification
( 41 Excretion

(5) Homeostasis

(6 ,
storage
its Production g Bile salts

is ,
Help in
digestion og fat
.

Emulsification )
 Function
Classification of
liver Tests :

[A ] Based on
laboratory findings :

based liver
(a)
GI ( tests on

Excretory Function ) :

Bilirubin der
cis Semen : Van
Bergh Klan

(2) Serum Bilirubin : Ict eric Index

(3) Urine bilirubin and Bile salts

(4) Urine
urobilinogen fecal stercobilinogen
&

ambition
fecal stereo bilin
(5) Urine & -

b, tests biomarkers
( Groupie ( liver
enzyme panel
:
for liver
injury
and chol esta sis )

Alkaline
( 11
phosphatase ( ALP )
( 21 Serum
glutamate pyruvate transaminase ( SG PT ) / ALT

(3) Serum
glutamate oxalate transaminase ( 5907 ) IAST
4 Gamma
( ,
Glutamyl Transferase ( GGT )
isocitrate
is , Senen
dehydrogenase
(6) Choline esterase

(F) 5' nucleotidase .

(C '
Gnup ( Tests for synthetic function g
liver ) ( Plasma Proteins )

in Total
proteins
albumin
(2) Serum
g
globulin . Ala Ratio
(3) Prothrombin time

( Gi flocculation test .

(5) A- As in blood & Urine .

concentration
61
Fibrinogen .
 (d) 9nI ( specific function test )

anti
(n x -

trypsin (
I AAT )

(21 Alpha Fe to protein ( AFP ) as Lt'T

13 ) Cerrato
plasmin
( 41 Ferritin .

[B] Based on clinical aspects :

( as
Groep I ( for liver
dysfunction ) [ summary]
(1) Serum bilirubin
121 Serum : Total Protein ,

Albumin , serum Alg ratio .

131 Urine bilirubin

141 Urine
urobilinogen &

fecal stercobilinogen
cenobite
.

(5) Urine 'm

(6) Prothrombin time

171 Blood Ammonia .

(bi (
Grey . I Markers of
lil SGPT
hepatocellular
121 5907
injury )

lol
Groep TI
( for cholestasis )

(l) ALP ( Alkaline phosphatase )

(2)
Gamma Glutamyl Transferase
( GGT )
 Indications of Lhs :

( 11 Jaundice
liver metastasis
as
suspected
(3) Alcoholic liver disease

(
4, Any undiagnosed chronic illness

151 Annual checkup g

diabetic
patients .

disorders
16 ,
Coagulation
statins to check hyper toxicity
its
Therapy with .

Jaundice Tove iew )

⑤ Med Notes fmednotu.in )
-
 Free Radicals & Antioxidants

Reactive oxygen species ( Ros )

radical
di
Superoxide anion ( OE )
radical (
iis
Hydro peroxyl Hoo )
.

(
iii ,
Hydrogen peroxide ( 4202)

Hydroxyl radical ( on )
.

civi

lipid peroxide radical ( Roo )

.

""

vii
singlet oxygen ( 021
'
(

His Nitric Oxide ( Noo )

Pero xy nitrite ( ON 00 )
°

xiii )
-

Important character skis :

Extreme
( as
reactivity
do, short
lifespan
(a
Generation of new Ros
by chain reaction

(d) to Various tissues

Damage .

Clinical significance :

Rheumatoid
(n Chronic
inflammation : Diseases such as

arthritis . chronic ulcerative colitis etc

Is
Free Radicals
by Neutrophils
Acute Inflammation site
At the
inflammatory
121 :
,

activated
macrophages produce free radicals .
⑦
Respiratory Disease :
Breathing of loot
.

oxygen for > 24hm

.

I,
Destruction Endothelium &
of
edema
buy .

°
9N premature newborn ,

Broncho
prolonged Oz exposure -

pulmonary
dysplasia
( comet )
high
.

.
Adult respiratory distress syndrome CARDS ) is

characterized
by Pulmonary edema .

by Neutrophils
due to
It in
free radicals released

Cigarette smoke contains free Radicals .

141 Disease of Eye : Retro lentalfibroplasia & cataract

⑦ Reperfusion Injury Reperfusion injury after

:

myocardial ischemia in caused

by free radicals .

161 Atherosclerosis &

Myocardial Infarction : ID l are

deposited under the endothelial cells ,

which
undergo
oxidation radicals
by free .

And ultimately came

plaque formation .

cumulative effect radicals

171
Ageing : is free came

gradual deterioration in
Ageing process
.
 Role of Antioxidants
Two
types of antioxidants
°
:

Preventive antioxidants will inhibit the initial

they
ca ' : -

production of free
radicals .

catalase and
They glutathione peroxidase
°

are .

ethylene diamine tetra acetate ( EDTA )

bi chain antioxidants
(
breaking : -

They can inhibit

propagative phase .

• Include -

Superoxide dismutase ,
uric acid .
vit E etc .

Antioxidants :

in Vit E -

lipid phone antioxidant

cu Vit c
Aq -
.
Phone antioxidant .

(3) Cerullo
plasmin -
Antioxidant in ECF .

Carotenoids
(
4,
cysteine ,
glutathione . ,
flavonoids and Vita

are minor antioxidants .

Food with antioxidants

⑦
properly :

cat
Spices
(
b, cur cumin

cel Fruits &

Vegetables ( Berries ,
broccoli .
spinach .

di Resveratrol in
(
grapes
.

asparagus ,
green
tea
etc )
② Med Notes (med notes in) .

* Revision Notes med notes site

company
-
. .

[ App Available ]
 Nucleotides
Chemistry Metabolism
: & .

Introduction :

Nucleotides nucleic acids

of DNA and RNA
°
are
precursors
.

° Nucleotides are also

components of important co -

enzymes
like
-1
and FAD and metabolic
regulators
MAD such
, as cAMP & cGMP .

Composition :

°
3
components -

base (
( as
Nitrogenous a
purine
( bi Pentose
sugar
or a
pyrimidine)
cc , Phosphate groups
.

Bases Present in Nucleic Acids :

o Two
types of Nitrogenous base = Purines 4 Pyrimidines .

Purine
byes :

( as
Adenine ( 6 -
amino
purine)
(
b, Guanine ( 2- amino 6- oxo
purine )

O O
T Purine Ring ]
O

•
other minor Purine bases :

( 6- oxo
purine ) ( 2-6 dioxopunk) ( 2-6-8 tri -
oxo
purine)
 Pyrimidine Base :

(a) Cytosine
( bi Thymine
(C) Uracil

. other modified Pyro imide bases :

(
as
Dihydro uracil
(
b, 5
methyl cytosine
-
.

Basic Names og Nucleosides .

Nucleotides and N Tri
-

phosphates :

Nucleosides : Nucleotides :

Nucleoside
-
triphosphate :

Nucleosides &
Nucleotides :
 Nucleotides
Biosynthesis of Purine :

•
It can be explained in two different pathways :

Novo
(a) De
Pathway
-

cb , salvage Pathway [ Dust

- bin -

Pathway ]

Deone Synthesis :

°
It involves three main steps :

(a) Ribose -
5 -

phosphate → IMP synthesis

( bi IMP → AMP synthesis
( c ) IMP → GMP synthesis

Ribose
-
- 5- Phosphate to IMP
-
synthesis :

step 1 : Amination
# f

material biosynthesis
-

Starling for Purine in Ribose - 5 -

P
,
a

product of HMP shunt .

Ribose
- -
5 -
P in converted into
Phosphor ibosyl pyrophosphate
by Pyro phospho kinase -

step : Addition g
Ng

step 3 :
Incorporation of C4 ,
C 5 and MF

step 4 : Addition g
cs

steps : Addition g
Ns

step 6 : Cyclisation ( closure y

Ring I

step 7 : Addition g
CG .

step to : Addition g Cz

steps Addition of Nt
:
slept :
cyclization .

Step 9 : Removal g
Fura mic Acid
 IMP to AMP :
-
-

the central intermediate both and GMP

IMP in
of AMP
• .

step : IMP to Adenylo Succinate by Adenylo Succinate

synthetase .

step# :
Adenylo Succinate to amp .

IMP to GMP :
-
-

step : IMP to XMP

,
this is
dehydrogenation via

enzyme
IMP -

dehydrogenase .

Step II : AMP in converted to GMP

by enzyme GMP
synthase .

Here Amino donor in Glutamate

group
.
 Salvage Pathway :

( is It ensures the
recycling of Purines formed by degradation of
Nucleotides Nucleosides and deoxy nucleosides also be
safer ;
. -
can

material
cii , PRPP in
starting .

( iii ,
The
free purines are
salvaged by two different enzymes ;

Adenine phosphor ibosyl

transferase ( APR ) Tane

Hypoxanthine guanine phosphor ibosyl transferase ( HG Phase )

( in The
Pathway in
special importance in tissues like RBC and brain
de not
where Novo
pathway in
operating .

Regulationshee -

is
 Degradation of Purine Nucleotides :

The end
product of nucleotide catabolism in acid
purine uric
°

curate )
degradation taking place mainly
.

. The in in liver .

°
Xanthine Oxidase in a

metallo
flavoprotein containing
FAD , molybdenum and Fe .

[ In I
 1) eNsof Pyrimidine :

°
The
pyrimidine ring in synthesized free pyrimidine as and
then it in
incorporated into nucleotide .

• The
pathway can be explained by following steps :

( i, Synthesis of Carbamoyl Phosphate

(2) Synthesis of Carbamoyl Aspartate
(3)
Ring closure form dihydro onotafe
to

of Dihydro
(4 ,
oxidation 0 rotate

Addition
of Ribose Phosphate moiety
⑦ .

161
Decarboxylation to form UMP .
For and
VIP ,
UTP CTP o
.

[ UMP → UDP → UTP → CTP )

Applied in Next Note !

⑥ MedNmed notes in )
 Important Questions g Transcription
① Types og Mammalian RNA
polymerases -

Am : 3
different DNA
dependent RNA
polymerases ( RNAP) -

cis RNAP
type II or B Main
enzyme synthesizing mRNAs .

gnhibited anilin
a
by Am
- -

dis RNAP
type I or A Responsible for syn
.

g rRNA '

( iiis RNAP
type I or c
Responsible for production g tRNA

② Transcription Process .

Am : gt in the
process of formation of RNA
from DNA .

Includes Initiation Termination

•
.
Elongation and

followed by Post -

Transcriptional processing .

( ai Initiation : . gn this ,
DNA helin
partially unwinds .

RNAP binds with promotor on DNA with help

of Sigma factors .

-
On
reaching appropriate site . first nucleotide
of mRNA attaches to initiation site g

p subunit g RNAP
.

'
-

This is 5 g mRNA '

This whole in the initiation og

process
-

transcription .

( Humans 105 initiation

available
-

sites are
 ( b,
Elongation : The RNAP more
along the DNA
-

template and New nucleotides are

incorporated in the nascent mRNA .

to rule
one
by one .

according base
pairing
.

RNAP has DNA

unwinding property
•
.

Topo
-
isomerase will also help in
unwinding .

.
A transcription bubble
containing RNAP .
DNA &

nascent Bubble
RNA in
formed .
in about 20
bp .

← Termination specific signals

:
are
recognised by a

termination
protein the , Rho ( s ) factor .

attaches
lnlhen the Rho factor RNAP cannot
•

move
further .

So dissociates from DNA new mRNA in

enzyme
°
,

formed .

Post-transcriptional Processing
bacteria not Translation
• In ,
mRNA in
changed &
of
starters Transcription
mRNA even
before completion g
.

•
In Eukaryotes .
it
undergoes extensive
processing
to

become mature mRNA .

These
modifications include : -

Poly tailing terminus

poly adenylate d
'
cat -
A : The 3 in

in nucleoplasm . This poly -

A tail may be
 nucleotides
20 -
250
long .

The tail protects mRNA

from attack
by
3
'
exonuclease .

cb , terminus
methyl
by
'
at the
'
7
capping
5 5 -

guanosine triphosphate
Methylation of adenine residue and
hydroxyl
'
( Cl Nb
of 2

ribose
group of are common .

coli Removal of Introns ( non -

coding regions )
cel
splicing of Exons l connect
together ) .

③ Inhibitors of RNA
synthesis :

Am : Actinomycin D and Mito in intercalate with

my
strands
DNA ,
thus
blocking transcription .

med Anticancer drugs

They are as
-

② Med Notes (med notes in) .

* Revision Notes med notes site

company
-
. .

[ App Available ]
 Environmental Pollution &
Heavy Metal Poisons

introduction :
-

.
Pollutant : -

Any substance present in environment which ,

metabolism
may produce abnormality in or

alter
wellbeing .

Poison Substance death harm introduced

if in
:
causes
°
or
-

living body or
brought in contact .

Corrosives acids alkalis salts

.
: .

Strong ,
or .

They remove

water from the tissues the cellular

,
coagulate proteins
and convert hemoglobin into acid hematin .

•
Neurotoxins : .
Act at cerebral level .

As Opium -

,
alcohol ,

ether ,
cholon form -

,
cannabis -
etc .

Act at spinal level . As -

Aconite quinine .
4

Metal Poisons Oleander

Heavy
.

( I
feed Poisoning -

°
lead in the most common environmental poison in India
•
About 30%
population are
already affected by lead

poisoning .

.
Can be found in Paints ,
exhaust of Vehicles .

lead
pipes .
newspapers ,
cigarette ,
etc .

Battery repair .
Radiator repair ,
soldering .
Painting &

to
Prinking are
occupations prone get lead
Poisoning .
 Signs e
symptoms :

cis lead is cumulative and accumulated tissues

a
poison is in

over
years
.

[ 90% in bones ,
9% in blood & I % in brain &
kidney ]
lead
ciii can
pass through placenta &
milk .

Miscarriage ,
still birth
and
premature deaths are
reported in lead
poisoning .

brains susceptible
( iiis
Developing are more to lead .

In children mental retardation

cin
learning disability ,
.

behaviour
problems hyper excitability and seizures
, are seen .

I"
Anemia ,
abdominal colic and loss
of appetite are
very
common -

acute
( vis g f blood level in more than to
my
1dL ,
toxicity is

manifested .

( vill Discoloration
along the gums
& Blue line are character -

-
skis
features of Acute lead Poisoning .

lead inhibits heme

cviiis
synthesis .

Treatment :

Calcium do deaf edetate Penick amine

Dimercaprol
•

, .

are used as Antidotes .

( DAL )

Dinner cap to succinic Acid better but

costly
°

in
.

② Med Notes (med notes . in)

 (2)
Mercury Poisoning
Most industrial
poison
.
common .

Source be Elemental
can
Inorganic Organic mercury
°

, or .

Elemental
Mercury
Hazard inhalation of
°

may
come
from Mercury Vapor -

edema and
o
In acute
poisoning .

pulmonary encephalopathy
result
may
.

Triad
of Oral lesions ( gingivitis salivation stomatitis)
°

ca , &
,

(b) Tremor
cel
Psychological changes ( insomnia shyness , ,

are all hallmark of chronic Elemental memory

loss )

mercury poisoning
.

This is called Erethism .

Inorganic Mercury :

Poisoning may
arise
from calomel .
topical medicines
&
plastic industry
in .

Acute effects include gingivitis ,

gastritis vomiting ,

and edema
pulmonary
.

Organic Mercury ( Also known :

as Minamata disease ) .

Poisoning from paints fungicides and

°

occur
may
.

cosmetics .

Eating fish with

high Methyl the most
°

in
mercury ,

causes
for organic mercury poisoning .
(3)
Aluminium Toxicity :

materials
°

Exposure from packaging and building .

paint pigments cosmetics antacids

, .
a aluminium

cooking vessels .

intake
.

If we >
100mg 1 day ,
toxicity results .

Interferes with heme

synthesis and also blocks

absorption of Calcium , phosphorous & Iron .

• Can lead to Alzheimer 's disease .

Also involved in Parkinson 's .

°
Osteomalacia and microcytes hypochromia anemia

are other manifestations of toxicity .

② Med Notes (med notes .in)

* Revision Notes med notes site
company
-
. .

[ App Available ]
 Environmental Pollution &
Heavy Metal Poisons

②
Pesticides & Insecticides :

DD
(m T
(Dichlorodiphenyltrichloroethane )
°
It in
fat soluble and deposited in Adipose tissue .

°
As it is not excreted ,
concentration keeps increasing .

Signs
e
symptoms :

It endocrine disruptor likely to be human

carcinogen
. in ,
.

Chronic
toxicity ( exposure affect reproductive
°

can

capabilities and
embryo or
fetus .

Can cause Breast Cancer

banned but it
*
Many countries have
already DDT is

still available in India .

121
Org azo phosphorus Compounds :

( organophosphorus ) and carbamates ( Okc )

ORP
Oregano are
o

common
pesticides .

Oregano sulphur compounds are

fungicides .

Sign &
symptoms :

neurotoxic
in
They are
powerful agents .

(2)
They inhibit
Acetylcholinesterase through phosphorylation .

③ Thus
transfer of nerve
impulse across
synapses
and at
 nerve muscle junction is
prevented .

Diagnosis & Treatment :

Depends estimation cholinesterase

of in RBC
•
on serum & .

Antidote cholinesterase machinators

.
is
Atropine sulfate &
.

( di acetyl mon oxime or

prated oxime )

Occupational & Industrial hazards

in
Poly chloro biphenyls -

Widely used in industries various .

°
Bi
phenols from plastic containers teach out in

drinking water .

.
Vinyl phenols are dissolved from Pvc
pipes .

decrease
•
These chemicals will lead to in -

fertility &

alteration in behavior .

121 Fenn & chloro

flaw methane -

Chaz ( CFC ) & CFC 13 Used in

Refrigerators &
Spray -

dissociated
Release atoms when
photo
cam
chlorine
.

° -

•
chlorine destroys Ozone .

131 Methanol -

solvent and anti

°

Organic widely used in

paints -

freezes .

It be consumed ethanol and

in
place
°

in
may g more

toxic than ethanol .

characteristic
•

Optic neuritis and blindness in the

toxicity .