Professional Documents
Culture Documents
•• Cholesterol Synthesis
Smile Formula 2
•• Insulin acts in Fed state, so is always an anabolic
•• Enzyme: Lipoprotein LipaseQ
hormone
Catabolic Pathways List •• Glucagon acts in fasting/starvation state, so is
•• Glycolysis (breakdown of glucose to pyruvate) a catabolic hormone
•• Link reaction by PDH complex [Pyruvate (3C) → •• Insulin activates all anabolic pathwaysQ
Acetyl CoA (2C)] –– Exception: Insulin also activates 2 catabolic
•• Glycogenolysis (breakdown of glycogen) pathways:
•• The pathways/ enzyme which are activated by Exception: Two breakdown products of fats can be
glucagon are always active in phosphorylated converted to glucose:Q
state 1. Glycerol → Break down product of TG
Important Information
Substrate Level Oxidative Phosphorylation/
•• Additional of O2 → Oxidation
Phosphorylation ETC
•• Addition of H2 or e- → Reduction In Glycolysis & TCA by Many oxidoreductases
•• H2/H atom/reducing equivalent = e- enzyme Kinase enzymes & ATP synthase
Q. In low insulin: glucagon ratio. What is correct? TCA Cycle / Kreb’s Cycle
(NEET PG 2023) •• 3 Rate Limiting Enzymes
A. Increase activity of HSL 1. Citrate synthase
B. Increase activity LPL
2. α-Ketoglutarate dehydrogenase
C. Increase glycogenesis
3. Isocitrate dehydrogenase: Most important
D. Increase glycolysis
Stimulated By ADP
Exp: HSL is a catabolic enzyme so activity increases
under low insulin (anabolic hormone) and high glucagon Inhibited by ATP and NADH
(catabolic hormone) concentration.
Reciprocal Regulation:
2 opposite pathways never occur together:
1. Glycolysis & Gluconeogenesis: Fructose 2,6 Bisphosphate is the reciprocal regulator, which inhibits
gluconeogenesis and activates glycolysis, as it is formed in fed state.
2. Beta oxidation & Fatty acid synthesis: Malonyl CoA is formed in fed state in Fatty acid synthesis and it
inhibits CPT-1 (RLE of beta oxidation of Fatty acids)
G6PD deficiency Pyruvate kinase deficiency
Hemolysis Hemolysis
1st most common human enzyme deficiency 2nd most common human enzyme deficiency
Heinz bodies present Heinz bodies absent
•• In prokaryotes, RLE of Pyrimidine synthesis is: ATC (Aspartate Trans Carbamoylase)
A. 2 ATP + 2 NAD
B. 2 ATP
C. 2 ATP + 2 NAPH
D. ATP + 2 FADH2
A. 2 ATP + 2 NAD
•• 2 ATP used: Hexokinase, Phosphofructokinase B. 2 ATP
•• 2 SLP give 4 ATPs as phase II of glycolysis C. 2ATP + 2 NADH
starts with 2 molecules of glyceraldehyde-3-
phosphate. D. 4 ATP + 2 FAPH2
•• Total ATPs generated = 7 ATPs (aerobic 2 ATP as net gain of NAD is ‘Zero’.
conditions).
Q. No. of ATP produced in RBCs in fed state, fasting
state, aerobic and anaerobic condition.
Under Anaerobic Condition
Ans. As there are no mitochondria in RBC, so, there
is no ETC. So, no ATP will be produced from NADH via
ETC. Hence, total ATP produced in RBC in fed, fasting,
aerobic or anaerobic state is always 4-2 = 2 ATP
A. 2 ATP
B. 5 ATP
C. 7 ATP
D. 3 ATP
Ans. 5 ATP
Shuttles
•• NADH is starting material for ETC but it is
formed in cytoplasm whereas ETC occurs in
mitochondria.
•• 2 Shuttles help in transport of NADH across
the inner mitochondrial membrane (IMM) of
mitochondria.
Important Information
•• CPS-I is absent in brain
•• Arginase is absent in kidneys, so last product
of urea cycle in kidney is arginine. So, source
of arginine (semi-essential) in body is kidneys.
•• 2 ATP used by Phosphoglycerate Kinase –– In fed state, it does not allow acyl CoA to go
into mitochondria
•• So, 4 ATPs and 2 GTPs or 6 high energy
phosphates are used to make 1 glucose from 2 •• Liver – Mitochondria
pyruvate –– Here activated FA comes for β-oxidation
•• Lactate gets converted to pyruvate and most commonly from Palmitic Acid(16C)
pyruvate is used in gluconeogenesis; no ATP is
used or produced from lactate to pyruvate.
•• Alanine is the most glucogenic amino acidQ
which is converted to glucose; Alanine gets
converted to pyruvate by Alanine transaminase
(here also no ATP used or produced)
A. 21
B. 26
•• 1 NADH = 2.5 ATP
C. 106
•• So, for β-hydroxy butyrate total ATP produced
D. 12.9
will be = 19 (from acetoacetate) + 2.5 (from 1
Ans. B NADH) = 21.5
•• As it will not be used in TCA cycle. So, 80 ATP
Important Information
will not form.
Pathways producing zero ATPQ
•• Instead acetoacetate will form ketone bodies.
•• HMP
•• Hence, only 28 ATP are produced
•• Uronic acid pathway
•• So, net gain = 28-2 (2 ATP required for
activation of FA = 26 ATPs •• RL shunt
Lysosomal Storage Diseases •• This enzyme lies in Golgi apparatus and make
•• If some lysosomal enzyme (Hydrolases) is/ hydrolases reach to lysosomes.
are absent or deficient, then that particular •• If this enzyme is defective, hydrolases will not
substrate (mostly macro-molecule) accumulates reach lysosome.
and get stored in lysosomes giving rise to
lysosomal storage disorders. •• It is also known as protein targeting disorder
as protein do not reach its target organelle
1. Mucopolysaccharidosis (MPS)
•• Clinical features
2. l-cell disease
–– Same as MPS
3. Pompe’s disease (also a Glycogen Storage
Disease) –– Serum hydrolase ↑↑
5. Sphingolipidoses
•• Dermatan sulfate •• Dermatan sulfate
+ Heparan Sulfate + Heparan sulfate
accumulation accumulation
•• AR •• XR (So, mostly males
patients)Q
•• Severe and Inguinal •• Known as Mild Hurler with
Hernia present aggressive behaviour
•• Reilly Bodies •• Reilly Bodies Inclusions
Inclusions found not found mostly
Important Information
•• Fabry’s disease: Only sphingolipidosis which is
X-linked recessive as all others are autosomal
recessive.
•• No Mental Retardation in Gaucher’s disease
(as glucocerebroside is not found in CNS)Q
•• No hepatosplenomegaly in Tay Sach’s disease
as gangliosides are absent in liver
•• All Sphingolipidoses have cherry red spot Clinical feature of Fabry’s disease:
except Fabry’s, Gaucher’s & Krabbe’s disease
Angiokeratomas: Benign cutaneous lesion of capillaries,
•• Sphingolipidoses with angiokeratoma: Fabry’s resulting in small marks of red to blue color &
disease- this also resembles Sickle cell crisis characterized by hyperkeratosis.
•• SLP resembling Rheumatoid arthritis: Farber’s
DiseaseQ
6. Wolman’s Disease
•• Enzyme deficient: Acid lipaseQ
Clinical images related to Sphingolipidoses:
•• It is lysosomal storage disease but not a
sphingolipidosis.
•• It is also k/a cholesterol ester storage disease
as here TG & cholesterol esters accumulate.
•• Pathognomonic feature is calcification of
adrenal glandsQ
•• Other clinical features
–– Watery green diarrhoea
–– Relentless Vomiting and failure to thrive
–– Hepatosplenomegaly
Calcification of adrenals
3. Zellweger Syndrome
•• Most severe peroxisomal biogenesis disorder
•• Organelle affected is peroxisomes, so that no
enzymes reach there (‘ghost’ peroxisomes)
•• In peroxisomes, α-oxidation occurs, which
breaks down Phytanic Acid. And oxidation of
VLCFA (Very Long Chain Fatty Acids)Q
•• In this disease, both these processes do not
occur, causing accumulation of phytanic acid &
VLCFA.
4. Cystic fibrosis
5. Familial Hypercholesterolemia
Clinical features of Zellweger syndrome Type I - Von Gierke’s Disease: most common GSD in
children- Clinical features
•• Severe hypoglycemia
•• Massive hepatomegaly & kidneys also enlarged
due to glycogen accumulation
•• Ketosis
•• Hyperlipidemia
•• Moon like/round/Doll like faces
•• Lactic acidosis
•• Hyperuricemia
High Forehead
Clinical features of Von Gierke’s disease
Garrod’s Tetrad
•• Inborn errors of metabolism
•• 4 diseases MNEMONIC: CAAP
–– C - Cystinuria
–– A - Alkaptonuria
–– A - Albinism
–– P - Pentosuria (Essential Pentosuria) - enzyme
deficient is Xylulose Reductase or Xylitol
Dehydrogenase
1. Acquired
•• Due to vitamin B6, B9 and B12 deficiency
2. Genetic
•• Due to Enzyme Cystathionine beta Synthase
defectQ
•• Here cysteine becomes essential.
•• c/f
–– ↑ Serum Homocysteine (has SH - group)
–– ↑ urine Homocystine (made of two
homocysteine joined by S-S bond)
Cyanide nitroprusside test is positive.
Albinism
•• Enzyme deficient: Tyrosinase (makes melanin
from tyrosine)
•• Tyrosine is an oxidase enzyme & requires copper
for its action.
•• c/f
•• Hypopigmentation (milky white skin, Blonde Important Information
hair, and Red eye color)
•• How to distinguish between vit B6, B9 and B12
deficiency
Vitamin
Substrate accumulated
deficiency
B6 Homocysteine, Xanthurenic acid
Homocysteine, FIGLU (Form Imino
B9
GLUtamate)
B12 Homocysteine, L-methyl malonyl acid
Important Information
Vitiligo
•• Patchy hypopigmentation
•• Tyrosinase is normal
Homocystinuria (HCU)
Two types:
Q. Glycogen stored in liver in all the following Exp: In MSUD, the branched-chain amino acids
conditions except? (FMGE Aug 2020) (leucine, isoleucine, and valine) are restricted in the
diet, due to defect in their catabolism.
A. Gaucher’s disease
B. Cori’s disease Q. Brunt sugar smell of urine is due to the defect of?
C. Mc Ardle’s disease (INICET Nov 2022)
D. Pompe’s disease A. Phenylalanine hydroxylase
Exp: Gaucher’s disease, is a lysosomal storage disorder B. Isovaleryl CoA dehydrogenase
of sphingolipids and not glycogen, but all others Cori’s C. Fumarylacetoacetate hydrolase
disease, Mc Ardle’s disease, or Pompe’s disease are D. Branched chain keto acid dehydrogenase
Glycogen storage disorders.
Exp: Burnt sugar like odor is a characteristic feature
Q. A 40-year-Old Male Patient come in OPD and of Maple Syrup Urine Disease (MSUD) which occurs
complaining of long-standing black Urine ferric due to the inherited deficiency of branched Chain
Chloride and Benedict’s test both were found to be Keto-acid dehydrogenase.
positive in this patient. Pinna and sclera of eyes have
Q. Zellweger syndrome is caused by the defect of
black pigmentation. What is your diagnosis? (FMGE
which of the following organelles? (INICET Nov 2022)
Dec 2020)
A. Mitochondria
A. Phenylketonuria
B. Lysosomes
B. Galactosemia
C. Peroxisomes
D. Nucleus
Isomerism
•• Isomerism is possible due to Asymmetric/chiral
carbon
–– Asymmetric C - When all of 4 valencies of
C are occupied by different atoms/group of
atoms. e.g.
Isomerism is of 2 Types:
1. Structural isomerism a.k.a. stereoisomerism (same
molecular formula, different Structure)
2. Optical isomerism (same molecular formula,
different optical properties)
4. Anomerism
Important Information
•• In case of carbohydrates → D-Form is
abundant.
•• In case of amino acids in Proteins → L-form Important Information
is abundant.
•• Pyranose: Six membered ring with 5 C & 1 Oxygen
•• Free amino acid (Amino acid not in protein) → •• Furanose: Five membered ring with 4 C & 1 Oxygen
can be L or D Form, e.g. D-serine & D-aspartate ○○ Glucose → mainly Pyranose
(Found in brain)
○○ Fructose → mainly Furanose
•• Amino acid synthesized in body → L-form ○○ Hexoses (6C) → Both Pyranose & Furanose exists
•• Source of D-Amino acid → always exogenous ○○ Pentoses (5C) → Only Furanose exists
(Diet or Bacteria flora)
Anomers are of two types- alpha and beta
Ans: Only L
3. Epimerism
Proteoglycan Glycoprotein
A. Rothera’s Test
B. Benedict’s test
C. Seliwanoff’s Test
D. Biuret Test
Exp: The Rothera’s test is used to detect the presence
of ketone bodies (ketones) in the urine, which can be
elevated in conditions like diabetic ketoacidosis.
CARBOHYDRATE METABOLISM
GLYCOLYSIS or EMP (Embden Meyerhof pathway)
•• Inhibitors of Glycolysis
•• Iodoacetate & Arsenite → inhibits glyceraldehyde-
3-P dehydrogenase
PREVIOUS YEAR QUESTIONS –– Na Fluoride → inhibits Enolase (used in blood
glucose estimation)
Q. A patient report is as follows; FPS - 82: PPBS -
140; Urine was found to be positive for benedict test. Important Information
What is the probable diagnosis? (JIPMER - Dec -
•• When arsenite inhibits glycolysis, then no
2019)
ATP is produced but glycolysis continues, and
A. Renal glycosuria pyruvate is formed.
B. Transient glycosuria
C. Alimentary glucosuria Irreversible steps / Substrate level
D. DM Regulatory steps phosphorylation (SLP)
1. Hexokinase 1. PG Kinase
Exp: The presence of glucose in the urine (positive
Benedict’s test) in a patient with normal fasting 2. PFK 1 2. Pyruvate Kinase
and postprandial blood sugar levels suggests renal 3. Pyruvate Kinase
glycosuria, which is a benign condition.
Link Reaction
Q. Which of the following tissues are dependent on
Enzyme - PDH (Pyruvate Dehydrogenase) complex,
insulin for glucose uptake (INICET Nov 2022)
irreversible reaction, occurs in mitochondria
Important Information
Malate (4C): Intermediate of TCA Cycle
Malonate (3C): Inhibitor of TCA Cycle
Malonate / Malonyl CoA is an inhibitor of:
1. TCA Cycle (inhibits Succinate Dehydrogenase)
2. ETC (inhibits Complex II)
3. Beta Oxidation of Fatty Acids (inhibits CPT-1)
Important information
•• 5 coenzymes are required for release of
energy from link reaction & TCA: Lipoic acid,
B1, B2, B3, B5. So, multivitamins are given
•• In B1 deficiency (Beri-Beri) or PDH complex during LethargyQ
deficiency, lactic acidosis will occur due to
excess pyruvate converting in to lactate in ETC
cytoplasm. •• Components of ETC (Located in Inner
Mitochondrial Membrane)
TCA Cycle
–– 5 protein complexes (I to V)- fixed within
•• Vital cycle of cell (occur in fed as well as fasting
the membrane
state), occurs in mitochondria in aerobic state
–– 2 Mobile molecules: Coenzyme Q and
•• TCA depends on 2 things:
Cytochrome C (a Peripheral membrane protein)
–– Energy status of cell: If ATP present, TCA
Note: Coenzyme Q is the only non-protein component
will not occur & vice-versa.
of ETC
–– Availability of oxaloacetate: Oxaloacetate
–– In ETC, oxidation & phosphorylation occur
is also regarded as carrier of TCA cycle or
together (coupled).
1st Substrate of TCA cycle. Also, it plays a
catalytic role in TCA cycle. –– Uncoupling means that oxidation occurs but
not phosphorylation.
Important Information
•• Uncouplers e.g.
•• Only 1 SLP occurs in TCA done by enzyme succinate
thiokinase which mostly produces ATP, but in liver & –– Dinitrophenol (drug)
kidney during fasting/starvation state, it produces –– Natural/Physiological uncouplers
GTP, as during this state, gluconeogenesis occurs & it
1. Thermogenin: present in brown fat in
requires GTP.
hibernating animals & in neonates & is
•• Acetyl CoA is not an intermediate of TCA cycle. responsible for non-shivering thermogenesis
•• 2 CO2 which are removed in TCA comes from
2. Thyroxine
Oxaloacetate. If oxaloacetate not given, then mark
Acetyl CoA. 3. Free fatty acids
•• Malonate (3C) → Inhibits Succinate dehydrogenaseQ Q. ADP to ATP conversion in ETC is inhibited by?
•• Arsenite → Inhibits α-ketoglutarate Ans. Oligomycin (inhibits complex V which converts ADP
dehydrogenaseQ to ATP)
•• Fluorocitrate → Competitively inhibits Aconitase Q. ADP to ATP transfer in ETC is inhibited by?
•• Fluoroacetate → Non- competitively Inhibits Ans. Atractyloside (inhibits ADP-ATP translocase, which
Aconitase transfers ADP & ATP)
•• Present in mitochondria
Pyruvate carboxylase Reciprocal regulation of Glycolysis &
•• Uses ATP
•• Activated by acetyl CoA Gluconeogenesis
PEPCK
(Phosphoenolpyruvate
Both are present is cytoplasm
carboxykinase)
Fructose -1-6-
Bisphosphatase
•• Present in endoplasmic
reticulum (to prevent glucose-
6-P breakdown to glucose in
cytoplasm)
Important Information
•• Common enzyme of
Glucose-6 - •• Fructose 1,6-Bisphosphate compound → Glycolysis
gluconeogenesis and
phosphatase intermediate
Glycogenolysis
•• Present in liver but absent in •• Fructose 1,6-Bis Phosphatase enzyme →
muscles Gluconeogenesis enzyme
Other Names:
•• Debranching enzyme → Amylo-α(1→6)-glucosidase
•• Glucan transferase → oligo-1,4-1,4-glucantransferase
or 4:4 transferase
•• Branching enzyme → amylo-(1,4→1,6)-trans
glycosylase or 1,4-alpha-glucan-branching enzyme
•• Acid maltase also called as Lysosomal acid alpha
glucosidase
HMP
•• Glucose 6–P (a hexose phosphate) is the
TIGAR- TP-53 Induced Glycolysis and Apoptosis starting material hence the name Hexose
Regulator Monophosphate Pathway
Q. A Mediterranean person didn’t receive Primaquine. Q. All are features of gluconeogenesis except?
Which pathway gets affected by G6PD deficiency? (JIPMER Dec 2019)
A. Gluconeogenesis is synthesis of glucose from non-
Ans: HMP, as antioxidant drugs like Anti-malarials carbohydrate source
increase the oxidant stress, which further increases B. Mainly takes place in liver
H2 O 2 C. Seen in fasting state
D. Step are simple reversal of glycolysis
Sorbitol Pathway
Exp: Gluconeogenesis involves different enzymatic
reactions from glycolysis, including bypass reactions
to overcome the irreversible steps of glycolysis.
•• Enzymes are not heat stable This graph is for Simple enzymes
•• Enzymes are stereo-specific •• Michaelis-Menton constant [Km]Q
–– Km is defined as that substrate concentration
at which velocity of reaction is half of Vmax
–– Km is signature of Enzyme as it is a constant
value for a particular enzyme
–– Km does not change with change in either
enzyme or substrate concentration
–– So, in case of competitive inhibition; affinity↓
so, Km ↑
Important Information
•• Chymotrypsin cuts at C- terminal of large
hydrophobic amino acids like Phe, Tyr and Trp
•• Trypsin cuts at carboxy terminal of basic amino acids
like Lys and Arg
•• Elastase cuts at carboxy terminal of small neutral
amino acids e.g. glycine, serine.
Enzyme Classification
Enzyme Class (EC no.) Distinguishing Feature
1. Oxidoreductases
•• Oxidases •• Use O2 as an electron acceptor like cyt C Oxidase
•• Dehydrogenase •• Use molecules other than O2 as electron acceptor (NAD, FAD, NADP); e.g. PDH in
link reaction.
•• Use H2O2 as electron acceptor; e.g., Glutathione peroxidase
•• Peroxidase
•• Incorporate O2 into the substrate; 2 types:
•• Oxygenase
○○ Dioxygenase: incorporates 2 atoms of molecular O2 into the substrate e.g.
homogentisate dioxygenase
○○ Monooxygenases/Hydroxylases/mixed function oxidases: incorporates 1 atom of
molecular O2 into the substrate. e.g. phenylalanine hydroxylase (converts Phe to
Tyr)
•• Reductase •• Example: Glutathione Reductase
2. Transferases
•• Methyltransferase •• Transfer one carbon units
•• Aminotransferase •• Transfer amino groups
•• Kinase •• Transfer phosphate from ATP
•• Phosphorylase •• Transfer phosphate from Pi
3. Hydrolases
•• Phosphatase •• Remove phosphate from a substrate using water
•• All digestive enzymes •• Any enzyme that breaks macromolecule e.g. amylase, maltase etc.
4. Lyases
•• Synthases •• Link 2 molecules without using ATP
•• Aldolase A & B •• Produce aldehydes via elimination reactions
•• Simple Decarboxylases •• Produce CO2 via elimination reactions
•• Hydratase •• Add or remove water but do not break bond e.g. Enolase, aconitase, fumarase, PEPCK
5. Isomerases
•• Racemase •• Interconvert L & D stereoisomers
•• Mutase •• Transfer group b/w atoms within a molecule
•• Epimerase •• Interconvert epimers
6. Ligase
•• Synthase
•• Link 2 molecule via an ATP-dependent
•• Carboxylase
•• Use ATP, Biotin and CO2 (Mn- ABC) and also uses Mg2+
A. Competitive
B. Uncompetitive
C. Non-competitive
D. Suicidal
Properties of Enzymes Exp: In the presence of non-competitive inhibitor
Vmax changes while Km remains same.
•• Increase velocity/rate of reaction
•• ↓ Activation energy
AMINO ACIDS & PROTEINS
•• Do not change the equilibrium of reaction
BASICS OF AMINO ACIDS
•• Do not change the free energy of substrates/
products
Important Information
•• AA having max. tendency to bind phosphate →
OH containing amino acid
•• 17 amino acids can take part in transamination
•• AA which is a site for covalent modification
→ OH containing amino acid •• 3 Amino acids that can’t take part in
transamination: Mnemonic: POLYTHENE
•• AA which is involved in O–Glycosidic bonds →
OH containing amino acid –– PO - PrOline
Q. Which AA is involved in N–Glycosidic bonds? –– LY - LYsine
Ans: Asparagine (has CONH which can provide N for –– THENE - THrEoNinE
N-glycosidic bond)
Chaperones
•• These are proteins which help in protein folding
Transdeamination: Transamination (peripheral cells) •• e.g. HSP-10 & 70, Calnexin, Calreticulin
+ Oxidative deamination (liver)
•• HSP-60 class is chaperonins
Proteins •• Calbindin is a Ca binding protein, not a chaperone
•• Protein: polymers of amino acids
•• Mostly present in RER
Important Information
•• Bonds in Enzyme-Substrate interactions
(Mnemonic: HHI)
–– H - Hydrophobic
–– H - Hydrogen
–– I - Ionic
–– Sometimes covalent but Never Van der
Note: In fats, double bond is in cis-configuration Waals Forces
•• Bonds in Protein-DNA interactions (Mnemonic:
HIV)
–– H - Hydrophobic
–– I - Ionic
–– V – Van der Waals Forces
–– Never Covalent bond
Features 1° 2° 3° 4°
S~S Hydrophobic
Hydrophobic H-bond
Bond Covalent/ Peptide/ Amide Hydrogen bond
Hydrogen Ionic
Ionic (Mnemonic- HHI)
Functional
Absent Absent Present Present
activity
•• In carcinoid syndrome, pellagra occurs because Q. Which of the following is not used for protein
too much tryptophan used in the formation of precipitation? (INICET July 2021)
serotonin that very less tryptophan is available A. Heavy metals
for Niacin formation
B. Alcohol & acetone
C. Change in pH other than isoelectric pH
PREVIOUS YEAR QUESTION
D. Trichloroacetic acid
Q. Bends in alpha-helix structure are formed by Exp: Only at isoelectric pH, a protein has no net
which amino acid ? (JIPMER Nov 2017) charge and readily precipitate out of the solution. At
A. Glycine all other pH a protein will remain soluble in solution.
B. Lysine Q. Selenocysteine is present in which of the following
C. Methionine enzymes? (INICET Nov 2022)
D. Glutamine A. Glutathione reductase
Exp: Due to its small side chain, glycine allows for B. Glutathione peroxidase
greater flexibility and can easily accommodate the B. Thioredoxine peroxidase
conformational changes required for bends in the
D. Thioredoxine oxidase
alpha-helix structure.
Exp: Selenocysteine is an essential amino acid
Q. Which amino acid does not include post incorporated into the active site of enzymes such as
translational modification? (AIIMS Nov 2017) glutathione peroxidase
A. Selenocystiene
Q. Levels of D5 – hydroxyl indole acetic acid (5-HIAA)
B. Triiodothyronine in urine are raised: (FMGE June 2022)
C. Hydroxy-proline
A. Carcinoid syndrome
D. Hydroxy-lysine
B. Hartnup’s disease
Exp: Selenocysteine is encoded by a specific codon C. PKU
and is directly incorporated into proteins during
D. Alkaptonuria
translation, without the need for post-translational
modification Exp: Increased levels of 5-HIAA in urine are indicative
of carcinoid syndrome, a condition associated with
Q. Creatinine, NO & urea are synthesized from neuroendocrine tumors.
which, amino acid? (NEET Jan 2019)
Q. Which amino acid is not used for synthesis of
A. Arginine
LIPIDS
Classification of Lipids
Simple Lipids
•• Phosphatidic acid = Glycerol + 2 FAs + P
•• So, product of hydrolysis of Cardiolipin = 3
Glycerol + 4 FA + 2 P
•• Can be antigenic due to its complex nature.
•• Anti-Phospholipid Syndrome - Occurs due to
Anticardiolipin antibodies. It is a thrombotic
condition and diseased female has history
of recurrent abortions. Anti-phospholipid
syndrome patients give false positive VDRL
test, as they have antibodies against cardiolipin
Important information
OH OH P Choline
•• DHA
NH2 NH —FA1
○○ is required for brain development of first 2-3
Amide bond
OH OH years of life so, Health drinks are fortified with
DHA.
C18 C18 ○○ Breast milk always contains DHA.
Sphingosine
(18 C amino alcohol) Ceramide
•• α–Linolenic acid is precursor of ω-3 category means
Sphingomyelin
(present in Myelin sheet of brain) if α–Linolenic acid is taken in diet, other two ω-3 FAs
can be made form it in the body.
Glycolipids / Glycosphingolipids •• Linoleic acid is precursor of ω-6 category and can be
used to make other two ω-6 FAs in the body
•• Made of Alcohol (sphingosine) + FA + Carbohydrate
•• Most Essential FA is - Linoleic acid as it can make
Types: arachidonic acid which is required for PGs and
1. Glucosylceramide / Glucocerebroside Leukotrienes synthesis.Q
•• Never found in CNS but always found in extra •• PUFAs which are cardioprotective: ω-3 PUFAs
neural tissues Signs of Essential fatty acid (EFA) deficiency
2. Galactosylceramide/Galactocerebroside •• Generalized scaly dermatitis composed of
•• Ceramide (Sphingosine + FA) + galactose thickened, erythematous, desquamating plaques,
Acanthosis nigricans
•• Always found in CNS
•• Alopecia, Thrombocytopenia
PUFAs or Essential Fatty Acids •• Failure to thrive, Growth retardation and poor
•• ≥ 2 double bonds wound healing
•• Intellectual disability in children
Lipoproteins
Composition of various lipoproteins
Protein/Apoprotein
Lipoprotein Lipid present
present
Chylomicron TG (exogenous) Apo B48
Chylomicron
TG + Cholesterol Apo B48 + Apo E
Remnant
VLDL TG (endogenous) Apo B100
Tangier’s disease / Familial alpha-
VLDL
lipoprotein deficiency / Hypo alpha
Remnant TG + Cholesterol Apo B100 + Apo E
(IDL)
lipoproteinemia
LDL Cholesterol Apo B100 + Apo E •• Mutation in ABCA-1 gene
Apo-A, Apo-C and •• Decreased HDL
HDL Cholesterol ester
Apo-E
•• Cholesterol accumulation in various body tissues
Like in tonsils → Large orange/yellow tonsils →
Q characteristic featureQ
• • Enlargement of throat, Liver, Spleen
(hepatosplenomegaly) and Lymph Nodes
•• Peripheral Neuropathy (Mononeuritis multiplex)
Important Information
•• Exogenous TG is transported to peripheral tissues by
Chylomicron.Q
•• Endogenous TG is transported from liver to
peripheral tissues by: VLDLQ
•• Cholesterol is transported from liver to peripheral
High density lipoproteins (HDL) tissues by: LDL
•• Cholesterol is transported from peripheral tissues to
Function- Reverse cholesterol TransportQ liver by: HDL
Important Information
Clinical Features to tackle hyperlipoproteinemia
related clinical questions
•• Tendon xanthoma → ↑ Cholesterol
•• Eruptive xanthoma → ↑ TG
•• Palmar & Tubero eruptive xanthoma → ↑ Chylo-
remnant & ↑ VLDL remnant
•• Milky plasma → ↑ Chylomicrons
•• Acute pain in abdomen [Acute pancreatitis] → ↑ TG
Abetalipoproteinemia, or Bassen-
Kornzweig syndrome
•• A stands for Absent (or negligible) beta-
lipoproteins - VLDL , IDL and LDL
•• defective assembly and secretion of (apo)
B-containing lipoproteins → Apo B 48 & Apo B Fatty Acid Synthesis
100
•• Mutation in Microsomal Triglyceride Transfer
Protein - MTP (transfers TGs from intestine &
liver to Chylomicrons & VLDL)Q
•• Decreased plasma TGs (not absorbed from
intestine)
•• Defective absorption of fat-soluble vitamins as
chylomicrons not formed
FA synthase complex - Main enzyme of fatty acid & also in muscles but never occurs in liver, due
synthesis: a multienzyme complex & has 2 monomers to absence of Thiophorase in liver. Q
Important Information
Q. FA is synthesized from?
Ans: Acetyl CoA and not malonyl CoA
•• Because extra Carbon of Malonyl CoA is not
getting added in newly synthesized FA
•• 1st enzyme carboxylase adds one CO2 to form
malonyl CoA but 2nd enzyme FA synthase
removes the CO2. So, only CO2 of acetyl CoA
are used.
•• But, Main Donor of carbon for fatty acid
synthesis – Malonyl CoA
Important information
•• Thiolase is a common enzyme for 4 lipid
metabolic pathways:
1. Ketone body synthesis
2. Ketone body utilization
3. Cholesterol synthesis
4. β-oxidation of FA
Types of Hypoglycemia
Ketotic-hypoglycaemia Non-ketotic hypoglycaemia
Von Gierke’s Disease Insulinoma
Q. Type I hyperlipoproteinemia is characterized by? Exp: Fatty acid transport through the mitochondrial
(NEET Jan 2019) membrane is facilitated by carnitine, which helps
transport long-chain fatty acids into the mitochondria
A. Elevated LDL
for beta-oxidation.
B. Elevated HDL
C. Elevated lipoprotein lipase Q7. For Coronary artery prevention, which needs to
be given: (FMGE Jan 2023)
D. Elevated chylomicrons.
A. Saturated fatty acid
Exp: Type I hyperlipoproteinemia is characterized by
elevated levels of chylomicrons (large triglyceride- B. Omega 3 FA
rich lipoproteins) due to deficiency of enzyme LPL C. Omega 6 FA
which breaks down TG in chylomicrons. D. Omega 9 FA
Q. Ketone bodies are not utilized by? (JIPMER May 2019) Exp: Omega-3 fatty acids, such as eicosapentaenoic
acid (EPA) and docosahexaenoic acid (DHA), are
A. Brain
recommended for coronary artery prevention due to
B. RBC their beneficial effects on heart health.
C. Heart
Q. Liver produces KB but cannot use KB due to absence
D. Skeletal muscle
of which enzyme: (INICET May 2023)
Exp: Red blood cells do not have mitochondria and,
A. Thiophorase
therefore, cannot utilize ketone bodies for energy.
B. Thiolase
Q. A patient has multiple tendon xanthomas. Serum C. HMG CoA synthase
cholesterol (398 mg/dl) & LDL (220 mg/dl) were found
D. HMG CoA Reductase
to be raised. Statins were given to this patient. What
is the diagnosis? Exp: The absence of thiophorase enzyme (first enzyme
(NEET Sep 2021) of KB utilization) in the liver prevents the utilization
of ketone bodies produced by the liver.
A. Lipoprotein lipase deficiency
B. Familial hypercholesterolemia Q. A patient with C/O muscle weakness came to OPD.
C. Tangier’s disease Doctor found he has cardiomyopathy & diagnosed him
to be a case of Barth syndrome, where patient has
D. Huntington’s disease
mitochondrial dysfunction. What is the defect in this
Exp: The presence of tendon xanthomas, along with patient: (INICET May 2023)
elevated serum cholesterol and LDL levels, suggests a
A. Cardiolipin
diagnosis of familial hypercholesterolemia
B. Lecithin
Q. Eicosanoids are formed from? (INICET May 2022) C. Lysolecithin
A. Arachidonic acid D. Cephalin
B. Platelet aggregation Exp: Barth syndrome is characterized by a defect in
C. 4 fused rings the synthesis of cardiolipin, a phospholipid primarily
D. Arginine found in the inner mitochondrial membrane
Exp: Eicosanoids, such as prostaglandins and
leukotrienes, are derived from arachidonic acid, which MOLECULAR BIOLOGY
is an omega-6 fatty acid
Nucleic Acid
Q. Fatty acid transport through mitochondrial
•• Nucleic Acid (DNA/RNA) = Polymer of
membrane is via? (NEET PG 2022)
Nucleotides
A. Carnitine
•• NucleoTide = Nitrogenase base + Sugar +
B. Acyl carrier protein
Phosphate
C. Cholesterol transporter
•• NucleoSide = Nitrogenase base + Sugar
D. LCAT
Nitrogenous Base
N–base Nucleoside Nucleotide form
Ribose to Deoxyribose conversion occur Tip to remember: Thymine matching with Methyl
at Di-Phosphate level Note: Thymine (Pyrimidine) is different from
Thiamine (Vitamin B1)
PURINE SYNTHESIS
1.De novo pathway
•• High energy consuming pathway (15-20 steps)
•• RLE: PRPP glutamyl amido transferase
2. Salvage pathway
•• Less energy consuming pathway (only 1 step)
•• Main enzyme: HGPRT (Hypoxanthine Guanine
Phosphoribosyl Transferase)
PURINE CATABOLISM
OPRT + Decarboxylase
•• Bi-functional enzyme (single protein with 2
enzymatic activities)
Q
•• Deficiency leads to Orotic Aciduria
Orotic aciduria
•• Growth Retardation and developmental delay
–– Neurological defects
Adenosine Deaminase (ADA)
–– Megaloblastic anaemia which is non-
•• Used for conversion of adenosine to Inosine by responsive to B12 or folic Acid Rx
Normal
XX 1 Normal
female
•• Formed by removal of one O atom of OH at 2 nd
Turner Female with no
position carbon of ribose XO 0
Syndrome Barr body
•• But If oxygen is removed from both 2’ & 3’ Klinefelter’s Male with Barr
position, then it is called 2’-3’ dideoxyribose. XXY 1
Syndrome body
If this is used, it will stop DNA synthesis as
Female with two
free 3’ OH is lost, which is required to add next Super Female XXX 2
Barr bodies
nucleotide in a growing DNA/RNA chain
Types of chromosome - Depending upon position of •• Amino acids and proteins also absorb UV light
at 280 nm
centromere
–– It is due to aromatic amino acids
–– maximum for tryptophan Q
•• NAD and NADP absorb light at 340 nm Palindrome definition: same sequence on both strands
(when read in 5’ to 3’ direction)
•• Porphyrin absorb at 400 nm (Soret Band)
Due to conjugated
DNA REPLICATION
Absorption of
Molecule double bonds in the Enzymes of DNA replication
light at:
rings
1. Helicase: Causes strand separation, Use ATP,
DNA 260 nm (UV) Nitrogenous bases Creates positive supercoils
Aromatic amino 2. Topoisomerase- Relieve positive supercoils
Proteins 280 nm (UV) acids (maximum by
tryptophan) 3. Single Strand DNA Binding Proteins (SSBs)-
Prevents reannealing by binding single DNA
NAD/NADP 340 nm (UV) Adenine strands in prokaryotes.
Porphyrins 400 nm (Visible) Pyrrole rings
Note: Helicases, Topoisomerases & SSBs
BONDS IN DNA constitute Unwinding proteins
4. Primase
•• Synthesizes the primers (RNA primer) using
DNA as Template
–– 1 primer is required for leading strand
–– Multiple primers are required for lagging
strand
DNA
•• Right-handed
•• ds in both Prokaryotes and Eukaryotes
–– Prokaryotic DNA is circular (two ends are
joined to form closed circle)
–– Eukaryotic DNA is linear (two ends are free) 5. DNA Polymerase III- Synthesizes both leading
•• Eukaryotic nuclear DNA has introns that & lagging strands
prevents mutations 6. DNA Polymerase I
•• But eukaryotic mitochondrial DNA is like •• Removes RNA primers from both leading &
prokaryotic DNA with no introns, so there are lagging strands
more chances of mutation in it.
•• Fills gap only on lagging strand
Palindrome •• Creates a single gap on leading strand
Q. Which of the following is a palindrome? 7. DNA Ligase- Creates 3’-5’ Phosphodiester bond
A. TAAT to join DNA with DNA, Uses ATP & acts only on
lagging strand
B. GGCC
Ans: B
β DNA repair
δ Lagging strand
DNA-G α Primase
DNA REPAIR
Type of repair Cell cycle phase Damage Cause Disease
Nucleotide excision repair G1 T-T dimers UV radiation damage Xeroderma pigmentosaQ
Spontaneous, heat, IR
G1 mainly but can C → U conversion Rare, MUTYH associated
Base excision repair rays, viral infection,
occur in any phase by deamination polyposis
Nitrous oxide
HNPCC (Hereditary
Mismatch repair G2 Mismatched base Proofreading error Non-Polyposis Colorectal
Cancer)Q
•• Formation of RNA from DNA as template in •• Sense strand: as it has same sense of direction
nucleus as new RNA (see fig)
Q. If 4 bases make 1 codon, then how many codons are –– Misnomer i.e. name indicates that it helps in
possible? release. However, it does not help in release.
It only recognises the stop codon
Ans: Total 44 = 256 codons are possibleQ
•• Peptidyl transferase releases the polypeptide
•• Out of 64, 3 are stop codons i.e. do not code for from P site
amino acids
1. UAA Important Information
2. UAG Q. How many ATP & GTP are used to add one AA in
the growing polypeptide chain
3. UGA
Ans:
•• So, for 20 AA, 61 codons are present
2 ATPs → for the activation of AA
–– or on an average, for each amino acid 3 codons
are present 2 GTPs → 1 GTP used in elongation for adding AA
–– Each amino acid has more than 1 codon, known → 1 GTP used for translocation
as Degeneracy/Redundancy of codon So, 4 high energy phosphates are used to add one
•• AA that do not show degeneracy (only 1 codon AA in the growing polypeptide chain
present):
Crispr-CAS 9 System
1. Methionine - AUG
•• CRISPR-Clustered Regularly Interspersed
2. Tryptophan – UGG Short Palindromic Repeats
•• Have 20 isoenzymes (one for each AA) PCR (Polymerase Chain Reaction)
•• Is the only point of proofreading during Used for amplification of DNA
translation
Components of PCRQ
•• Responsible for fidelity/accuracy of protein
synthesis 1. Heat is used for denaturation and 2 strands
separation
Factors in translation in prokaryotes &
2. DNA to be amplified
eukaryotes
3. 2 primers (1 for each strand)
Prokaryotes Eukaryotes
Initiation IF 1, 2, 3 eIF 1, 2, 3, 4F (RL) 4. Enzyme: Taq polymerase [derived from Thermus
aquaticus bacteria]
Elongation EF– Tu, Ts, G eEF 1α, 1β, 1γ, eEF2
Termination RF 1, 2, 3 eRF 5. Substrates: Deoxyribonucleotides
Factors used in translocation: EF-G (Prokaryotic) 6. Mg2+ in Buffer
and eEF-2 (Eukaryotic) Note: Dideoxyribonucleotide is never the component
•• Releasing factor (RF) of PCR
Real Time PCR / Quantitative PCR Disorders caused due to genomic imprinting
•• Normal PCR is End-PCR i.e. only at the end of 1. Prader Willi Syndrome (PWS)Q
whole PCR process, we get the products and do
•• Paternal allele is deleted, and Maternal allele is
the analysis.
imprinted/inhibited means both copies (father
•• Real time PCR displays the amount of DNA and mother) of gene not working giving rise to
synthesized in real time, as it has SYBR-green sign and symptoms
dye , which gives fluorescence when bound to
the synthesized ds-DNAQ 2. Angel Man syndromeQ
•• Maternal copy of allele is deleted, and Paternal
RT-PCR (REVERSE TRANSCRIPTASE PCR)
allele is imprinted/inhibited leading to various
sign and symptoms
MICRO ARRAY/chip
GENOMIC IMPRINTING
•• It is gene inhibition at the level of transcription
Lot of DNA fragments (probes) are placed on a small
Mechanisms of Genomic Imprinting material looking like a chip.
1. DNA methylation- most common mechanismQ
Uses of chip
•• occurs at CG site/CG Island/CpG sites (C & G •• Can detect multiple mutations
together present on same strands)
•• Can do multiple gene expression analysis
•• cytosine is usually methylated in CG site that
causes inactivation of the gene •• Can do comparative genomic hybridization
•• Can detect SNPs (single nucleotide
polymorphisms)
Limitation
•• Can’t detect aneuploidy (monosomy & Trisomy)
Karyotyping
•• Best technique for detecting monosomy &
•• DNA methylation can be detected by Na- trisomy
bisulfite method •• Limitations
2. PTM of Histones (Post Translational Modifications) –– Lengthy (culture of cell required)
•• Histone Deacetylation –– It can only be done in metaphase arrest
•• Histone Methylation –– Cannot detect micro deletions, amplifications
•• Method to detect PTMs: Chromatin Immuno and complex translocationsQ
Precipitation (ChIP)
Fish (Fluorescent In Situ-
Hybridization)
•• Advantages
AR (Autosomal Recessive)
•• Most of biochemical enzyme defects
•• All MPS disorders except Hunter
•• All urea cycle disorder’s except OTC
•• All sphingolipidoses except Fabry’s disease
•• All amino acid disorders e.g. PKU, Albinism, HCU
etc Severity of damage in point mutation
•• All glycogen storage disorders Frameshift > Non-Sense > Missense
Exp: In a patient with swelling in MCP joints and Q. Which of the following methods uses RNA?
elevated uric acid levels, the enzyme xanthine (INICET July 2021)
oxidase, which converts hypoxanthine and xanthine to
A. Western blot
uric acid, is targeted for treatment.
B. RT-PCR
Q. Mother side uncle has disease... Her son has C. Sangers method
disease. Which type of inheritance is this? (FMGE
D. G-banding
Aug 2020)
Exp: Reverse transcription polymerase chain reaction
A. X-linked recessive
(RT-PCR) is a method that uses RNA as a template
B. X-linked dominant to synthesize complementary DNA (cDNA), which is
C. Autosomal dominant then amplified by PCR.
D. Autosomal recessive
Q. Deamination of methylated cytosine will form?
Exp: In X-linked recessive inheritance, there is (INICET May 2022)
no male to male transmission, but more males are
A. Uracil
affected, and affected son is born to unaffected
mother (carrier). B. Guanine
C. Adenine
Q. All are true about telomerase EXCEPT? (INICET
D. Thymine
Nov 2020)
Exp: Deamination of methylated cytosine results in
A. has reverse transcriptase activity
the conversion of cytosine to thymine.
B. Maintains fidelity of DNA replication
C. Maintains length of DNA Q. Banding technique used for dicentric chromosomes?
(INICET May 2022)
D. Found only in eukaryotes
A. G
Exp: While telomerase has an important role in
maintaining the length of telomeres and compensating B. NOR
for their shortening during DNA replication, it does C. C
not maintain the fidelity of DNA replication which is D. R
mainly done by DNA pol I and III.
Exp: C banding stains heterochromatin which are regions
Q. RNAi acts through? (INICET July 2021) of the chromosomes at or near centromere. So, C banding
will be most useful for dicentric chromosomes.
A. Knock out
B. Knock down Q. DNA-Protein interactions can be studied by using?
C. Knock in (INICET May 2022)
D. Knock up A. DNA fingerprinting
Q. Binding site of miRNA on mRNA? (INICET July Exp: DNA footprinting is a technique used to study
2021) DNA-protein interactions by identifying regions of
DNA protected by protein binding.
A. 5’ UTR
B. 3’ UTR Q. dd-NTPs in Sanger’s Sequencing technique uses?
C. Gene promotor (INICET May 2022)
A. Its fluorescence
–– (Glycine - X - Y) n i.e. every 3rd amino acid is Copper (Cu) as cofactor, so Cu deficiency also
GlycineQ leads to decrease strength in collagen
–– X, Y can be Proline, Hydroxyproline, Lysine,
Plasma Proteins
Hydroxylysine
1. Transthyretin/ Pre-albumin
•• 28 types found in body
•• Used in transport of thyroxine & Retinol Binding
Important Collagen typesQ Protein (RBP)
1. Hydroxylation of proline and lysine residues, to •• ATP-7A is present •• ATP-7B is present in liver
increase H-bonds in intestine for to throw Cu in bile and
absorption of Cu. Its also incorporates Cu in Cp.
deficiency causes: Its deficiency causes:
○○ ↓ Cu (Cu stays ○○ ↑ Cu in liver (due to
in intestinal cell, non-excretion from
unable to enter body)
blood) ○○ ↓ ceruloplasmin
○○ ↓ ceruloplasmin (Cp) (due to non-
(Cp) (due to incorporation of Cu in
insufficient Cu to Cp)
Clinical Significance: The deficiency of vitamin C will form Cp)
hinder these reactions resulting in fragile collagen of
blood vessels of gums which can be easily bruised and Note: ↓ Ceruloplasmin (Cp) is common between Menke
bleed during brushing causing scurvy. and Wilson Disease
1. Glycosylation Menke’s kinky hair syndrome- Clinical
•• Addition of carbohydrate in collagen which features
helps in making Aldol condensation
•• Premature birth
•• Enzyme required is Lysyl oxidase which require
•• Hypotonia
•• Growth retardation
•• Mental retardation
•• Grey depigmented hair:
–– Tyrosinase (an oxidase) is affected as
oxidases require Cu
–– Tyrosinase is required for synthesis of
Melanin.
–– So, melanin synthesis is decreased causing
grey hair
•• Brittle kinky hair
–– As lysyl oxidase affected, so defective and
weak collagen synthesis
•• Decreased Cu in blood and urine
Vitamins
Water soluble Fat soluble
•• Vit B, vit C •• Vit A, D, E, K
•• Usually acts as •• Stored in body & don’t act
coenzyme & are not as coenzyme
Wilson’s hepatolenticular degeneration stored in body •• Exception: Fat soluble
•• Exception: One Vitamin which act as
Clinical features water-soluble vit coenzyme - Vit K
•• Cu accumulates in liver causing liver damage which get stored in
body - Vit B12
•• When excess in liver, ↑ Cu can go to other
extrahepatic tissues and cause following
changes: Important Information
–– In Brain – Neurological degeneration Q. Water Soluble form available for which fat-
soluble vitamin?
–– In Kidneys- Renal damage, urolithiasis
Ans: Vit K - Synthetic form – K3 /menadione is water
–– In Bone marrow & RBC - Hemolytic anemia
soluble
–– In Eyes -
→ Sunflower cataract
→ Kayser-Fleisher (KF) rings - green/golden
ring in Descemet’s membrane of cornea due
to Cu deposition
•• Vitamin B6 - coenzyme •• Vit B12 -progressive Corneal ulcer covering less than 1/3 of the X3A
of heme synthesis enz peripheral neuropathy corneal surface
ALA synthase Corneal ulcer covering greater than 1/3 of X3B
the corneal surface
Important Information Corneal scarring XS
Vitamin D
Hypervitaminoses D
Symptoms
•• Hypercalcemia
•• Hypercalciuria causing Renal stones
•• Calcification of Soft tissues: calcium deposited Vit K deficiency
in blood vessels causing hypertension
•• Easy bruising
Vitamin E •• Bleeding tendencies
•• Most potent lipid phase antioxidant (chain •• ↑ Prothrombin time
breaking antioxidant)Q
•• Haemorrhagic disease of new-bornQ
•• Other antioxidant vitamins: Vit C, A and D
–– Fatal and occurs quite often, so, all new-borns
•• Vit E work synergistically with Se, Glutathione are given vit K injection
and Vit C for its antioxidant role
Important Information
C/F of Vit E Deficiency Reasons of Haemorrhagic disease of newborn
•• progressive peripheral neuropathy •• Intestine of a new-born is sterile (i.e. intestinal
bacteria for Vit K synthesis not present)
•• Hemolysis Q
ONE LINERS
cGMP as second messenger inQ
•• Vitamin A visual cycle
•• NO induced vasodilation effects
•• Activation of ANP and BNP
Lipid deficiency causing retinitis pigmentosa: DHA (DocosaHexaenoic Acid)
Best Investigation for any inborn error of Metabolism (IEM) - Mass spectrometryQ
PREVIOUS YEAR’S QUESTION Exp: Type I collagen is the most abundant collagen
type in the human body, including the skin. It provides
Q. Type of collagen Maximum in skin? (NEET Jan structural support and tensile strength to the skin
2019)
Q. Defect in Menke disease? (NEET Jan 2019)
A. Type I
A. Lysyl hydroxylase
B. Type II
B. Lysyl oxidase
C. Type III
C. Prolyl hydroxylase
D. Type IV
D. Prolyl oxidase