BIOCHEMISTRY

MR.JESSIN GEORGE
ASSISTANT PROFESSOR
DEPARTMENT OF BIOCHEMISTRY
 Digestion and Absorption of
carbohydrates

Process of breaking down of food into simpler

compounds

• Digestion in Mouth

• Stomach

• SI
 Mouth
Mechanical Digestion:

Chewing, also known as Mastication crumbles

the carbohydrates food into smaller and
smaller pieces to form bolus.

Chemical Digestion;

Salivary glands in oral cavity secrets Saliva.

Saliva contains enzyme Salivary amylase

Salivary amylase hydrolyses starch into Maltose
and dextrin @ pH of 6.8 to 7

Only about 5% starch are broken down in

mouth.
 Digestion in Stomach
Mechanical Digestion :A Strong peristaltic
contractions of the stomach mix the
carbohydrates into the more uniform mixture of
Chyme

Chemical Digestion:

The action of Salivary amylase contains only

inside bolus
About 30-40% of dietary starch is digested
before bolus, is broken down and acidified.

The action of salivary amylase is blocked by

acidic nature of stomach(pH 1.5)

Further breakdown of carbohydrates takes place

when the chyme is passed downn to the small
intestine.
 Small Intestine
No mechanical digestion

Chemical Digestion:

The pancreas releases Pancreatic Juice through

a duct.

Pancreatic Juice contains the enzyme Pancreatic

amylase.

Enzymes are also secreted by intestinal cells that

line the villi
 Action of pancreatic amylase and
intestinal enzymes.
Starch----🡪 Maltose + isomaltose(Pancreatic
amylase)

Maltose---🡪 Glucose + Glucose(maltase)

Isomaltose----🡪 Glucose + Dextrin(isomaltase)

Dextrin----🡪 Glucose(dextrinase)

Sucrose---🡪 Glucose + Fructose(Sucrase)

Lactose----🡪Glucose + Galatose(lactase)
Undigested Carbohydrates:

Certain carbohydrates like cellulase are

undigested by human due to lack of enzymes
like Cellulase.

But, it provides fibers for absorption of water

into the large intestine, Expand the Muscle walls
and trigger the muscle contractions for egestion

Cure for constipation.

 Absorption of Carbohydrates
Digested food from Alimentary canal to blood
stream

Monosaccharide is absorbed in S.I

Sodium Glucose Transport Protein in membrane

helps absorb glucose and galatose.

Fructose absorbed is converted to glucose inside

cell.
 regulation of blood glucose
The regulation of blood glucose, also known as
blood sugar, is a crucial process in maintaining
proper physiological function. The body carefully
controls blood glucose levels within a narrow
range to ensure a steady supply of energy to
cells. Two hormones, insulin and glucagon, play
key roles in blood glucose regulation. Here's an
overview of how blood glucose is regulated
 Pancreatic Islets:
Pancreatic Islets: The pancreas contains
clusters of cells called pancreatic islets (or islets
of Langerhans). These islets contain different
types of cells, including beta cells and alpha
cells, which produce insulin and glucagon,
respectively.
 Insulin Release:

• Insulin Release:
– When blood glucose levels rise, such as after a meal, beta
cells in the pancreatic islets release insulin into the
bloodstream.
– Insulin acts on target tissues, such as liver, muscle, and
adipose tissue, to facilitate the uptake of glucose from the
bloodstream into these tissues.
– Insulin promotes the storage of excess glucose as glycogen
in the liver and muscles, and as fat in adipose tissue.
– Additionally, insulin suppresses the production of glucose
by the liver (gluconeogenesis).
 Glucagon Release:

• Glucagon Release:
– When blood glucose levels decrease, such as during
fasting or between meals, alpha cells in the
pancreatic islets release glucagon into the
bloodstream.
– Glucagon acts on the liver to stimulate the
breakdown of glycogen into glucose (glycogenolysis)
and the production of new glucose from non-
carbohydrate sources (gluconeogenesis).
– Glucagon also promotes the release of glucose into
the bloodstream.
 Feedback Mechanisms:

– Blood glucose levels are monitored by specialized

cells in the pancreas called glucose-sensing cells
(also known as beta cells).
– If blood glucose levels rise too high, these cells
sense the increase and release insulin to lower
blood glucose levels.
– Conversely, if blood glucose levels drop too low,
the glucose-sensing cells reduce insulin release
and stimulate the release of glucagon to raise
blood glucose levels.
 GLYCOLYSIS
GREAT GRANDMOTHER THROWS FRESH FRUIT
DISH AND GO BY PICKING PUMPKINS TO
PREPARE PIES

HE PUT THE PHONE AND TRIED TO GET THE

PLASTIC PLATE TO EAT PIE
• Step 1: Glucose phosphorylation Glucose, a
six-carbon sugar, is phosphorylated by the
enzyme hexokinase, using one molecule of
ATP, to produce glucose-6-phosphate.
• Step 2: Glucose-6-phosphate isomerization
The glucose-6-phosphate molecule is
converted into its isomer, fructose-6-
phosphate, by the enzyme phosphoglucose
isomerase.
• Step 3: Phosphorylation of fructose-6-phosphate
Fructose-6-phosphate is further phosphorylated by the
enzyme phosphofructokinase-1, using another
molecule of ATP, to produce fructose-1,6-bisphosphate.
• Step 4: Cleavage of fructose-1,6-bisphosphate The
fructose-1,6-bisphosphate molecule is cleaved into two
three-carbon molecules: glyceraldehyde-3-phosphate
(G3P) and dihydroxyacetone phosphate (DHAP). This
reaction is catalyzed by the enzyme aldolase.
• Step 5: Isomerization of DHAP Dihydroxyacetone phosphate
(DHAP) is converted into another molecule of
glyceraldehyde-3-phosphate (G3P) by the enzyme triose
phosphate isomerase. Now, there are two molecules of G3P.
• Step 6: Oxidation and ATP generation Each glyceraldehyde-
3-phosphate (G3P) molecule undergoes oxidation, producing
1 molecule of NADH. At the same time, a phosphate group is
added, and high-energy electrons are transferred to ADP,
producing ATP. This reaction is catalyzed by the enzyme
glyceraldehyde-3-phosphate dehydrogenase.
• Step 7: Conversion of 1,3-bisphosphoglycerate to 3-
phosphoglycerate The high-energy phosphate from
the previous step is transferred to a molecule of
ADP, forming ATP. The resulting molecule, 3-
phosphoglycerate, is produced by the enzyme
phosphoglycerate kinase.
• Step 8: Conversion of 3-phosphoglycerate to 2-
phosphoglycerate The enzyme phosphoglycerate
mutase catalyzes the conversion of 3-
phosphoglycerate to 2-phosphoglycerate.
• Step 9: Dehydration and ATP generation The
enzyme enolase catalyzes the conversion of 2-
phosphoglycerate to phosphoenolpyruvate
(PEP) by removing a water molecule.
• Step 10: Conversion of PEP to pyruvate The
final step of glycolysis involves the enzyme
pyruvate kinase, which transfers a high-energy
phosphate group from PEP to ADP, generating
ATP and pyruvate.
 TCA CYCLE
After glycolysis, pyruvate enters the
mitochondria, where it undergoes a series of
reactions to enter the citric acid cycle, also
known as the Krebs cycle or the tricarboxylic
acid (TCA) cycle. The steps involved in the
conversion of pyruvate to acetyl-CoA and its
entry into the citric acid cycle are as follows:
After glycolysis, pyruvate enters the
mitochondria, where it undergoes a series of
reactions to enter the citric acid cycle, also
known as the Krebs cycle or the tricarboxylic
acid (TCA) cycle. The steps involved in the
conversion of pyruvate to acetyl-CoA and its
entry into the citric acid cycle are as follows:
Transport into the mitochondria: Acetyl-CoA
cannot directly cross the mitochondrial
membrane. Instead, it is converted to citrate by
combining with oxaloacetate, which is a four-
carbon molecule. This reaction is catalyzed by
the enzyme citrate synthase, forming citrate.
Citric acid cycle: Once inside the mitochondria,
citrate undergoes a series of reactions in the
citric acid cycle. The cycle involves several
enzyme-catalyzed reactions that ultimately
result in the regeneration of oxaloacetate, which
can react with another molecule of acetyl-CoA
to continue the cycle.
• The citric acid cycle involves the following key steps:
• Citrate is isomerized to isocitrate by the enzyme aconitase.
• Isocitrate is oxidized and decarboxylated to alpha-ketoglutarate
by the enzyme isocitrate dehydrogenase, generating NADH in
the process.
• Alpha-ketoglutarate is further oxidized and decarboxylated to
succinyl-CoA by the enzyme alpha-ketoglutarate
dehydrogenase complex, producing NADH and carbon dioxide.
• Succinyl-CoA is converted to succinate with the release of a
molecule of GTP (which can later be converted to ATP) by the
enzyme succinyl-CoA synthetase.
• Succinate is oxidized to fumarate by the
enzyme succinate dehydrogenase, generating
FADH2 in the process.
• Fumarate is hydrated to malate by the enzyme
fumarase.
• Malate is oxidized to oxaloacetate by the
enzyme malate dehydrogenase, producing
NADH in the process.
At the end of one round of the citric acid cycle,
one molecule of acetyl-CoA has been completely
oxidized, producing three molecules of NADH,
one molecule of FADH2, one molecule of
GTP/ATP, and two molecules of carbon dioxide.
These high-energy molecules will go on to
participate in the electron transport chain,
where they will generate more ATP through
oxidative phosphorylation.
Diabetes mellitus: Diabetes is a chronic disorder
characterized by high blood glucose levels. It
occurs due to inadequate insulin production
(Type 1 diabetes) or ineffective use of insulin by
the body (Type 2 diabetes). Insulin is responsible
for regulating glucose levels in the blood, and its
dysfunction leads to impaired glucose
metabolism.
Glycogen storage diseases: These are a group of
inherited disorders that affect the storage and
release of glycogen, the storage form of glucose
in the body. Different types of glycogen storage
diseases are caused by deficiencies in specific
enzymes involved in glycogen metabolism.
Examples include Von Gierke's disease (Type I)
and McArdle's disease (Type V).
Galactosemia: Galactosemia is a rare genetic
disorder characterized by the inability to break
down galactose, a sugar found in milk and other
dairy products. It occurs due to the deficiency of
enzymes involved in galactose metabolism, leading
to the accumulation of galactose in the body.
Galactosemia can cause severe complications if not
managed properly, including liver damage,
developmental delays, and cataracts.
Lactose intolerance: Unlike galactosemia, lactose
intolerance is not a genetic disorder but rather a
common digestive disorder. It is caused by the
deficiency of lactase, the enzyme responsible for
breaking down lactose, the sugar found in milk
and dairy products. People with lactose
intolerance experience digestive symptoms such
as bloating, diarrhea, and abdominal pain when
they consume lactose-containing foods.
Hereditary fructose intolerance: This is a rare
genetic disorder caused by the deficiency of the
enzyme aldolase B, which is necessary for
metabolizing fructose. Individuals with
hereditary fructose intolerance cannot properly
process fructose, leading to the accumulation of
fructose-1-phosphate in tissues. Symptoms can
include severe abdominal pain, vomiting,
hypoglycemia, and liver and kidney damage.
• Diabetes Mellitus Type 1:
• Symptoms: Type 1 diabetes is an autoimmune disease in which
the immune system attacks and destroys the insulin-producing
cells in the pancreas. It often develops during childhood or
adolescence. Common symptoms include increased thirst,
frequent urination, extreme hunger, unexplained weight loss,
fatigue, blurred vision, and slow wound healing.
• Complications: If left untreated or poorly managed, type 1
diabetes can lead to various complications over time. These may
include diabetic ketoacidosis (DKA), hypoglycemia (low blood
sugar), eye problems (diabetic retinopathy), kidney disease
(diabetic nephropathy), nerve damage (diabetic neuropathy), and
cardiovascular diseases.
Management: Individuals with type 1 diabetes
require lifelong insulin therapy to regulate blood
sugar levels. Daily monitoring of blood glucose
levels is crucial, and insulin is typically
administered through injections or an insulin
pump. Additionally, a healthy diet, regular
physical activity, and close collaboration with
healthcare professionals are important for
managing type 1 diabetes effectively.
• Diabetes Mellitus Type 2:
• Symptoms: Type 2 diabetes is characterized by insulin resistance,
where the body's cells do not respond effectively to insulin or the
pancreas does not produce enough insulin. Symptoms may
develop gradually and include increased thirst, frequent urination,
fatigue, blurred vision, slow wound healing, recurrent infections,
and areas of darkened skin.
• Complications: Similar to type 1 diabetes, uncontrolled type 2
diabetes can lead to various complications. These can include
heart disease, stroke, high blood pressure, kidney disease
(diabetic nephropathy), eye problems (diabetic retinopathy),
nerve damage (diabetic neuropathy), foot problems, and an
increased risk of infections.
Management: Type 2 diabetes management focuses
on lifestyle modifications, including adopting a
healthy diet, engaging in regular physical activity, and
maintaining a healthy weight. Medications may also
be prescribed to help regulate blood sugar levels. In
some cases, insulin therapy may be necessary. Regular
monitoring of blood glucose levels, cholesterol levels,
and blood pressure is important. Management may
also involve addressing other risk factors, such as
smoking cessation and stress management.
• The Oral Glucose Tolerance Test (OGTT) is a diagnostic test
used to evaluate how well the body processes glucose. It is
primarily indicated in the following situations:
• Diagnosis of Diabetes: The OGTT is used to confirm a diagnosis
of diabetes when other blood glucose tests, such as fasting
plasma glucose or HbA1c, are inconclusive. It helps identify
impaired glucose tolerance (prediabetes) or diabetes.
• Gestational Diabetes: During pregnancy, some women
develop a temporary form of diabetes called gestational
diabetes. The OGTT is commonly used to diagnose gestational
diabetes and assess how the body handles glucose during
pregnancy.
• The procedure for an OGTT typically involves the following steps:
• Preparation: Before the test, the person undergoing the OGTT is
usually advised to have a high-carbohydrate diet for a few days
(approximately 150 grams of carbohydrates per day). It is
important to follow any specific instructions provided by the
healthcare professional conducting the test.
• Fasting Period: The test begins with an overnight fast, typically
for 8 to 12 hours. During this fasting period, the person should
not eat or drink anything except water.
• Baseline Measurements: When the person arrives at the testing
facility, the healthcare professional will measure the fasting
blood glucose level using a blood sample taken from a vein.
• Glucose Solution: After the fasting blood sample is collected,
the person is asked to drink a glucose-rich solution, usually
containing 75 grams of glucose dissolved in water. The solution
is consumed within a specified time (often within 5 minutes).
• Monitoring Blood Glucose Levels: Blood samples are taken at
regular intervals, typically every 30 minutes to 2 hours,
depending on the specific protocol used. The blood samples are
collected to measure the blood glucose levels during the test.
• Waiting Period: During the waiting period, the person is usually
asked to rest and avoid strenuous physical activity. It is
important to remain at the testing facility during the entire
duration of the test.
• Final Blood Sample: The last blood sample is
typically collected 2 hours after consuming the
glucose solution.
• Post-Test Monitoring: After the final blood
sample is collected, the healthcare
professional will evaluate the blood glucose
levels to determine the results of the OGTT.
Normal GTT Curve: A normal GTT curve shows a
gradual rise in blood glucose levels after
consuming the glucose solution, followed by a
steady decline to near-fasting levels. In a healthy
individual, the blood glucose levels should
return to normal within 2-3 hours after the
glucose load. This pattern indicates good glucose
tolerance and is typically seen in individuals
without diabetes or prediabetes.
Impaired Glucose Tolerance (IGT): An IGT GTT curve
shows a higher and prolonged elevation of blood
glucose levels compared to a normal curve. Blood
glucose levels may remain elevated for a longer
duration before returning to normal. This pattern
suggests impaired glucose tolerance, indicating a
higher risk of developing diabetes in the future.
People with IGT may not meet the diagnostic
criteria for diabetes but have higher than normal
blood glucose levels.
Diabetic GTT Curve: A diabetic GTT curve shows
significantly elevated blood glucose levels
throughout the test, with little to no decline.
Blood glucose levels may remain high or
continue to rise after the glucose load. This
pattern indicates impaired glucose metabolism
and is consistent with a diagnosis of diabetes.
 HbA1C
• HbA1c, also known as glycated hemoglobin, is a form of
hemoglobin that is chemically bound to glucose. It
provides a measure of average blood glucose levels over
a period of approximately two to three months. HbA1c
is commonly used as a diagnostic and monitoring tool
for diabetes mellitus.
• The HbA1c test measures the percentage of glycated
hemoglobin in the total hemoglobin present in the
blood. It reflects the average blood glucose
concentration during the lifespan of red blood cells,
which is typically around 120 days.
• The American Diabetes Association (ADA) has
established diagnostic criteria for diabetes and
prediabetes based on HbA1c levels. The current
diagnostic thresholds for HbA1c are as follows:
• Normal: HbA1c level below 5.7%
• Prediabetes: HbA1c level between 5.7% and
6.4%
• Diabetes: HbA1c level of 6.5% or higher
Hypoglycemia refers to a condition characterized
by abnormally low blood glucose levels. It occurs
when the concentration of glucose in the
bloodstream falls below the normal range, which
is typically defined as a blood glucose level below
70 mg/dL (3.9 mmol/L). However, the specific
threshold for hypoglycemia may vary slightly
depending on factors such as age, individual
circumstances, and the presence of diabetes.
• Hypoglycemia can be caused by various factors, including:
• Diabetes Medications: Hypoglycemia is a common side effect
of certain medications used to treat diabetes, such as insulin
and certain oral hypoglycemic agents. These medications
work to lower blood glucose levels, but excessive doses,
incorrect timing, or poor coordination with meals can lead to
hypoglycemia.
• Inadequate Food Intake: Skipping meals, fasting, or
inadequate carbohydrate intake can deprive the body of the
glucose it needs to maintain normal blood sugar levels. This
is particularly relevant for individuals with diabetes who are
on medication or insulin therapy.
• Excessive Physical Activity: Engaging in intense or
prolonged physical activity without adjusting insulin
doses or carbohydrate intake can cause hypoglycemia,
especially in individuals with diabetes. Physical activity
increases glucose utilization by muscles, which can lead
to a drop in blood glucose levels.
• Alcohol Consumption: Alcohol can interfere with the
body's ability to regulate blood glucose levels. It can
cause a delayed release of stored glucose from the liver
and impair the counter-regulatory response to low blood
sugar, increasing the risk of hypoglycemia.
• Other Medical Conditions: Certain medical
conditions, such as liver disease, kidney disorders,
hormonal imbalances (e.g., insulinoma), and
pancreatic disorders, can affect glucose regulation
and lead to hypoglycemia.
• Reactive Hypoglycemia: Some individuals may
experience symptoms of hypoglycemia after
consuming a high-carbohydrate meal due to an
excessive insulin response. This is known as
reactive hypoglycemia.
 Fatty acids
Fatty acids are organic compounds that consist
of a long chain of hydrocarbon molecules with a
carboxylic acid group (COOH) at one end. They
are a fundamental building block of lipids, which
are essential components of living cells and
organisms
 Saturated Fatty Acids (SFAs):

• Saturated Fatty Acids (SFAs):

• Structure: These fatty acids have single bonds
between all carbon atoms in the hydrocarbon
chain, making the chain "saturated" with hydrogen
atoms.
• Properties: SFAs tend to be solid at room
temperature and are commonly found in animal
fats and some vegetable oils.
• Example: Stearic acid is a common saturated fatty
acid found in many animal and plant fats.
 Unsaturated Fatty Acids
• Monounsaturated Fatty Acids (MUFAs):
• Structure: MUFAs have one double bond in
the hydrocarbon chain.
• Properties: They are typically liquid at room
temperature and can be found in various
vegetable oils.
• Example: Oleic acid is a common
monounsaturated fatty acid found in olive oil.
• Polyunsaturated Fatty Acids (PUFAs):
• Structure: PUFAs have two or more double
bonds in the hydrocarbon chain.
• Properties: PUFAs are liquid at room
temperature and are commonly found in
vegetable oils and fatty fish.
• Example: Linoleic acid and alpha-linolenic acid
are essential polyunsaturated fatty acids.
• Monounsaturated fatty acids (MUFAs) have several
clinical significances and health benefits when
incorporated into the diet. Some of the key clinical
implications of MUFAs include:
• Cardiovascular Health: MUFAs have been shown to
have a positive impact on cardiovascular health. They
can help reduce LDL cholesterol levels (often referred to
as "bad" cholesterol) while maintaining or even
increasing HDL cholesterol levels ("good" cholesterol).
This effect can contribute to a decreased risk of heart
disease and stroke.
Inflammation and Oxidative Stress: MUFAs
have anti-inflammatory properties and can help
reduce oxidative stress in the body. Chronic
inflammation and oxidative stress are linked to
several chronic diseases, including
cardiovascular disease, diabetes, and certain
types of cancer. By including MUFAs in the diet,
individuals may lower their risk of these
conditions.
Insulin Sensitivity and Diabetes: MUFAs can
improve insulin sensitivity, which means the
body can use insulin more effectively to regulate
blood sugar levels. This can be beneficial for
individuals with diabetes or those at risk of
developing the condition.
• Weight Management: Including MUFAs in the diet has
been associated with improved satiety and appetite
regulation. This can potentially help with weight
management by reducing overall calorie intake and
promoting a feeling of fullness.
• Brain Health: Some studies suggest that MUFAs,
particularly oleic acid (a common MUFA found in olive
oil), may have a neuroprotective effect and could be
beneficial for brain health. They may play a role in
reducing the risk of cognitive decline and
neurodegenerative diseases like Alzheimer's.
• Anti-Cancer Properties: There is evidence to
suggest that MUFAs may have anti-cancer
properties, particularly in reducing the risk of
certain types of cancer, such as breast cancer and
colorectal cancer.
• Liver Health: MUFAs can be beneficial for liver
health, especially in cases of non-alcoholic fatty
liver disease (NAFLD). They may help reduce liver
fat accumulation and improve liver function.
• Nutrient Absorption: MUFAs can enhance the
absorption of fat-soluble vitamins (A, D, E, and
K) and other nutrients, promoting overall
nutrient bioavailability.
• Anti-Aging Effects: Some research suggests
that MUFAs may play a role in slowing the
aging process and promoting skin health due
to their antioxidant properties.
Polyunsaturated fatty acids (PUFAs) also have
significant clinical implications and health
benefits when incorporated into the diet. The
two main types of PUFAs, omega-3 and omega-6
fatty acids, offer different advantages:
• Omega-3 Fatty Acids:
• a. Cardiovascular Health: Omega-3 fatty acids, particularly
eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA),
have been extensively studied for their cardiovascular benefits.
They can reduce triglyceride levels, lower blood pressure, and
improve overall heart health, potentially reducing the risk of
heart disease and related events.
• b. Anti-Inflammatory Effects: Omega-3s have strong anti-
inflammatory properties, which can help alleviate chronic
inflammation associated with various diseases, including
rheumatoid arthritis, inflammatory bowel disease (IBD), and
metabolic syndrome.
• c. Brain Function and Mental Health: DHA, in particular, is a
critical component of brain tissue and is essential for proper
brain development and function. Omega-3s have been
associated with a reduced risk of cognitive decline, depression,
and anxiety.
• d. Eye Health: DHA is also a major component of the retina,
and a sufficient intake of omega-3s may contribute to
maintaining good vision and reducing the risk of age-related
macular degeneration (AMD).
• e. Pregnancy and Development: Omega-3s are crucial for fetal
brain and eye development during pregnancy. Adequate intake
is associated with improved cognitive development in infants.
• Omega-6 Fatty Acids:
• a. Skin Health: Omega-6 fatty acids, such as linoleic acid (LA),
play a role in maintaining healthy skin by supporting the skin
barrier function and helping to retain moisture.
• b. Inflammatory Response: While omega-6s can promote
inflammation in some contexts, they are also necessary for a
proper inflammatory response, which is essential for wound
healing and defense against infections.
• c. Hormone Regulation: Omega-6 fatty acids are precursors to
certain signaling molecules (eicosanoids) that regulate various
physiological processes, including blood clotting and immune
responses.
Good sources of omega-3 fatty acids include fatty
fish (e.g., salmon, mackerel, sardines), flaxseeds,
chia seeds, and walnuts. Omega-6 fatty acids are
found in various vegetable oils (e.g., soybean oil,
corn oil) and nuts and seeds. For optimal health
benefits, it's advisable to consult with a
healthcare professional or registered dietitian to
develop a balanced dietary plan that meets
individual needs and health goals.
• Essential fatty acids (EFAs) are a subset of
polyunsaturated fatty acids (PUFAs) that are vital for
human health but cannot be synthesized by the human
body. Therefore, they must be obtained through the
diet. There are two main types of essential fatty acids:
• Alpha-Linolenic Acid (ALA):
– ALA is an omega-3 fatty acid and is considered essential
because the human body cannot produce it on its own.
– Dietary Sources: Flaxseeds, chia seeds, hemp seeds,
walnuts, and certain vegetable oils (e.g., flaxseed oil, canola
oil) are good sources of ALA.
• Linoleic Acid (LA):
• LA is an omega-6 fatty acid and is also
classified as essential because it must be
obtained from the diet.
• Dietary Sources: Vegetable oils (e.g., soybean
oil, corn oil, safflower oil, sunflower oil), nuts,
and seeds are rich sources of LA.
Once ingested, ALA and LA can be converted
into longer-chain fatty acids with additional
double bonds, such as eicosapentaenoic acid
(EPA) and docosahexaenoic acid (DHA) for
omega-3s, and arachidonic acid (AA) for omega-
6s. These conversions are not very efficient in
the human body, so it's important to obtain
preformed EPA, DHA, and AA directly from
dietary sources in addition to ALA and LA.
• Essential fatty acids play critical roles in various
physiological processes, including:
• Cell Membrane Structure: EFAs are essential
components of cell membranes, where they help
maintain membrane fluidity and integrity, ensuring
proper cell function and communication.
• Brain Function: DHA, an omega-3 fatty acid, is especially
important for brain development and function. It is
highly concentrated in the brain and plays a role in
supporting cognitive function and mental health.
• Inflammation and Immune Response: EFAs are
precursors to eicosanoids, which are signaling molecules
that regulate inflammation and immune responses in
the body.
• Skin Health: EFAs are involved in maintaining skin barrier
function, promoting moisture retention, and supporting
overall skin health.
• Cardiovascular Health: Omega-3 fatty acids have been
associated with numerous cardiovascular benefits,
including reducing triglyceride levels, improving blood
vessel function, and reducing the risk of heart disease.
• TFAs can occur naturally in small amounts in certain
animal products, but the majority of trans fats in the
human diet are industrially produced through the
process of partial hydrogenation of vegetable oils. This
hydrogenation process converts liquid vegetable oils into
semi-solid or solid fats, making them more stable and
suitable for use in food manufacturing and food
preparation. As a result, TFAs are commonly found in
processed foods, including baked goods, fried foods,
margarine, and snack products.
• There are two primary sources of trans fatty acids:
• Industrial Trans Fats: These are artificial trans fats created
during the partial hydrogenation process of vegetable oils.
These fats have been widely used in the food industry to
enhance the texture, shelf life, and flavor stability of
processed foods.
• Natural Trans Fats: Small amounts of trans fats can also
occur naturally in the digestive systems of ruminant animals
like cows, sheep, and goats. The trans fats produced in the
stomachs of these animals are then found in their meat and
dairy products. However, the amount of natural trans fats in
animal products is relatively low compared to industrially
produced trans fats.
Clinical Significance and Health Concerns:

• Cardiovascular Disease: Consumption of trans fats

has been associated with an increased risk of heart
disease. Trans fats raise levels of LDL cholesterol
("bad" cholesterol) and lower levels of HDL
cholesterol ("good" cholesterol), contributing to an
unfavorable cholesterol profile.
• Inflammation: Trans fats promote inflammation in
the body, which is a contributing factor to various
chronic diseases, including cardiovascular disease,
diabetes, and obesity.
• Type 2 Diabetes: High intake of trans fats has
been linked to an increased risk of developing
type 2 diabetes.
• Adverse Pregnancy Outcomes: Consuming
trans fats during pregnancy may be associated
with an increased risk of adverse pregnancy
outcomes, such as preterm birth.
 The digestion and absorption of lipids

The digestion and absorption of lipids (fats) is a

complex process that involves several steps and
specialized enzymes. The primary site of lipid
digestion is the small intestine, where most of
the fat absorption takes place. Here's a step-by-
step overview of the digestion and absorption of
lipids:
Emulsification: Lipids are hydrophobic (water-
insoluble) substances, and they cannot mix directly
with the watery environment of the digestive tract.
To facilitate digestion, bile salts produced by the
liver and stored in the gallbladder are released into
the small intestine when fat enters the digestive
system. Bile salts emulsify large fat globules into
smaller droplets, increasing the surface area for
the action of digestive enzymes.
Pancreatic Lipase Action: In the small intestine,
pancreatic lipase, an enzyme secreted by the
pancreas, acts on the emulsified fat droplets.
Pancreatic lipase breaks down triglycerides (the
main form of dietary fat) into free fatty acids and
monoglycerides.
Formation of Micelles: The products of fat
digestion (free fatty acids and monoglycerides)
have both water-soluble and water-insoluble
parts. To enhance absorption, these products
combine with bile salts to form tiny structures
called micelles. Micelles are small enough to
remain suspended in the watery environment of
the small intestine, allowing for efficient
absorption.
Absorption: The micelles move to the surface of
the intestinal lining, where the free fatty acids
and monoglycerides are absorbed into the cells
of the small intestine (enterocytes). Once inside
the enterocytes, they are reassembled into
triglycerides.
Formation of Chylomicrons: Within the
enterocytes, the newly formed triglycerides are
combined with cholesterol and other lipids to
form larger particles called chylomicrons.
Chylomicrons are specialized lipoproteins that
transport dietary fats through the lymphatic
system, bypassing the liver initially.
Transport through Lymphatic System:
Chylomicrons are too large to enter the
bloodstream directly, so they are transported
through the lymphatic vessels and eventually
enter the bloodstream via the thoracic duct,
which empties into a large vein near the heart.
Circulation and Utilization: Once in the
bloodstream, chylomicrons circulate throughout
the body, delivering triglycerides to various
tissues. Lipoprotein lipase, an enzyme present
on the walls of blood vessels, breaks down the
triglycerides in chylomicrons into free fatty acids
and glycerol. These fatty acids are then taken up
and utilized by cells for energy or stored as fat in
adipose tissue.
It's important to note that while most dietary
fats are absorbed into the body, some portion of
the fats that escape digestion, along with some
breakdown products, is excreted in feces.
 Metabolism
The metabolism of lipids involves the various
processes by which fats are broken down,
utilized, and stored in the body. Lipid
metabolism plays a crucial role in providing
energy, maintaining cell structure, and
regulating various physiological functions. The
key aspects of lipid metabolism include:
Digestion and Absorption: As mentioned earlier, lipid
metabolism begins with the digestion and absorption of
dietary fats in the small intestine. Triglycerides are
broken down into fatty acids and monoglycerides by
pancreatic lipase, and these products are absorbed into
the enterocytes of the small intestine. Inside the
enterocytes, they are reassembled into triglycerides and
combined with other lipids and proteins to form
chylomicrons, which are transported through the
lymphatic system and eventually released into the
bloodstream.
Transport of Lipids: Once in the bloodstream,
lipids are transported in lipoproteins.
Chylomicrons transport dietary fats, while other
lipoproteins like very-low-density lipoproteins
(VLDL), low-density lipoproteins (LDL), and high-
density lipoproteins (HDL) play roles in the
transport of endogenously synthesized lipids
and cholesterol.
Lipolysis: Lipolysis is the process of breaking
down triglycerides stored in adipose tissue into
fatty acids and glycerol. This process is
controlled by hormones, such as adrenaline and
glucagon, which activate lipase enzymes to
release stored fats when the body needs
additional energy.
Beta-Oxidation: Fatty acids released through
lipolysis enter the mitochondria of cells, where
they undergo beta-oxidation. In beta-oxidation,
fatty acids are broken down into acetyl-CoA
molecules through a series of reactions. Acetyl-
CoA can then enter the citric acid cycle (Krebs
cycle) to produce energy in the form of ATP.
Ketogenesis: During periods of prolonged
fasting or low carbohydrate intake, the liver
produces ketone bodies (acetoacetate, beta-
hydroxybutyrate, and acetone) from excess
acetyl-CoA. Ketone bodies serve as an
alternative energy source for tissues, especially
the brain, when glucose availability is limited.
Synthesis of Lipids: Lipid metabolism also
involves the synthesis of lipids when the body
needs to store energy. Excess glucose or other
energy sources can be converted into
triglycerides and stored in adipose tissue for
later use.
Cholesterol Metabolism: Cholesterol is another
important lipid that plays a vital role in cell
membrane structure and serves as a precursor
for hormones, vitamin D, and bile acids.
Cholesterol synthesis occurs mainly in the liver.
HDL and LDL particles are involved in
transporting cholesterol to and from various
tissues.
Regulation by Hormones: Lipid metabolism is
highly regulated by hormones such as insulin,
glucagon, adrenaline, and various other factors.
These hormones control processes like lipolysis,
lipogenesis, and ketogenesis to maintain energy
balance and respond to metabolic demands.
• Disorders in lipid metabolism can have significant
impacts on an individual's health and may
contribute to various medical conditions. Some of
the related disorders in lipid metabolism include:
• Hyperlipidemia: This refers to elevated levels of
lipids, such as cholesterol and triglycerides, in the
blood. Hyperlipidemia is a major risk factor for
atherosclerosis, which can lead to heart disease
and stroke.
• Dyslipidemia: Dyslipidemia encompasses a range of
lipid-related abnormalities, including high levels of LDL
cholesterol (bad cholesterol), low levels of HDL
cholesterol (good cholesterol), and high triglyceride
levels. Dyslipidemia is often associated with metabolic
syndrome, obesity, and diabetes.
• Atherosclerosis: Atherosclerosis is a condition in which
fatty deposits, cholesterol, and other substances build
up on the inner walls of arteries, forming plaques.
These plaques can restrict blood flow and lead to heart
attacks, strokes, and other cardiovascular problems.
• Familial Hypercholesterolemia (FH): This is a
genetic disorder characterized by extremely high
levels of LDL cholesterol due to a mutation in the
LDL receptor gene. FH significantly increases the risk
of premature cardiovascular disease.
• Hypertriglyceridemia: Elevated levels of
triglycerides in the blood can increase the risk of
pancreatitis, a painful inflammation of the pancreas.
It is often associated with obesity, poorly controlled
diabetes, and excessive alcohol consumption.
• Lipoprotein Lipase Deficiency: Lipoprotein lipase (LPL)
is an enzyme that plays a key role in breaking down
triglycerides in the blood. Deficiency in LPL activity can
lead to severe hypertriglyceridemia and increased risk
of pancreatitis.
• Lysosomal Acid Lipase Deficiency (LAL-D): LAL-D is a
rare genetic disorder characterized by a deficiency of
lysosomal acid lipase, an enzyme responsible for
breaking down lipids in cells. Accumulation of lipids in
tissues can lead to organ damage, including the liver
and spleen.
• Tangier Disease: This rare genetic disorder is
characterized by extremely low levels of HDL
cholesterol. It can lead to an increased risk of
atherosclerosis and cardiovascular complications.
• Cholesteryl Ester Storage Disease (CESD): CESD is
another rare genetic disorder that leads to
impaired lipid metabolism, particularly the
accumulation of cholesteryl esters in cells. It can
affect the liver and lead to liver disease.
• Lipodystrophy Syndromes: Lipodystrophy syndromes are
a group of rare genetic or acquired disorders
characterized by abnormal fat distribution and
metabolism. These conditions can lead to insulin
resistance, diabetes, and other metabolic abnormalities.
• Nonalcoholic Fatty Liver Disease (NAFLD) and
Nonalcoholic Steatohepatitis (NASH): These conditions
involve the accumulation of fat in the liver, which can
progress to inflammation and liver damage. They are
closely linked to obesity and insulin resistance.
Xanthomas: Xanthomas are fatty deposits that
can accumulate under the skin or within
tendons due to lipid metabolism disorders. They
are often associated with conditions like familial
hypercholesterolemia.
• Cholesterol is a lipid molecule that serves as a
precursor for the synthesis of various important
compounds in the body. Some of the
compounds formed from cholesterol include:
• Steroid Hormones:
– Corticosteroids: These include hormones such as
cortisol, which regulates metabolism and immune
responses, and aldosterone, which controls
electrolyte balance and blood pressure.
Sex Hormones: Cholesterol is a precursor for
both male and female sex hormones. In males,
cholesterol is converted into testosterone, and
in females, it is used to synthesize estrogen and
progesterone.
Bile Acids: Cholesterol is converted into bile
acids, which play a critical role in the digestion
and absorption of dietary fats. Bile acids are
synthesized in the liver and stored in the
gallbladder before being released into the small
intestine to aid in the emulsification and
absorption of fats.
Vitamin D: Cholesterol is a precursor for vitamin
D synthesis. When the skin is exposed to
ultraviolet B (UVB) radiation from sunlight,
cholesterol is converted into a precursor
molecule that eventually forms active vitamin D
(calcitriol). Vitamin D is essential for bone
health, immune function, and various other
physiological processes.
Sterols: Cholesterol itself is a sterol, and it
serves as a structural component of cell
membranes, influencing their fluidity and
stability.
Neurosteroids: Cholesterol is also involved in
the synthesis of neurosteroids, which are steroid
hormones that affect neural function and can
have effects on mood, behavior, and other
neurological processes.
Cholesterol Esters: Cholesterol can be stored in
the body as cholesterol esters, which are less
reactive and more soluble forms of cholesterol.
These esters are stored in various tissues,
including adipose tissue.
Ketone bodies are a group of three water-soluble
compounds produced as byproducts of the
breakdown of fatty acids in the liver. They are
synthesized when the body's glucose supply is
limited, such as during prolonged fasting,
carbohydrate restriction, or in conditions like
diabetes. Ketone bodies provide an alternative
source of energy, particularly for the brain and other
tissues, when glucose availability is reduced. The
three main types of ketone bodies are:
• Acetoacetate (AcAc): Acetoacetate is the first
ketone body produced during ketogenesis. It can be
converted into both of the other ketone bodies, β-
hydroxybutyrate and acetone.
• Beta-Hydroxybutyrate (β-Hydroxybutyric Acid or
BHB): Beta-hydroxybutyrate is the primary ketone
body that serves as an important energy source,
especially for the brain and heart. It can be
converted back into acetoacetate and further into
acetyl-CoA for energy production in cells.
Acetone: Acetone is the simplest and least
abundant of the three ketone bodies. It is
produced as a minor byproduct of ketone
metabolism and is mostly exhaled through the
breath. This is why people with high levels of
ketone bodies in their blood may have a
characteristic fruity breath odor.
 Significance of Ketone Bodies:
Alternative Energy Source: Ketone bodies serve
as an alternative fuel source for tissues,
especially the brain, when glucose availability is
limited. This is crucial during fasting, prolonged
exercise, or when carbohydrate intake is
restricted.
Brain Function: The brain typically relies on
glucose for energy, but it can readily use ketone
bodies as an energy source during periods of
glucose scarcity. This is particularly important
because some individuals, like those with
uncontrolled diabetes, may experience impaired
glucose uptake by brain cells.
Preservation of Muscle Protein: Ketone bodies
can help spare muscle protein from being
broken down for energy, as they provide an
efficient source of fuel that reduces the need for
amino acids to be converted into glucose.
Weight Loss and Ketogenic Diets: The
production of ketone bodies is a hallmark of
ketogenic diets, which are low-carbohydrate,
high-fat diets used for weight loss. The presence
of ketone bodies in the blood indicates that the
body is in a state of ketosis, where fat is being
metabolized for energy.
Regulation of Insulin and Glucose Levels:
Ketone bodies can have effects on insulin
sensitivity and glucose metabolism. In some
cases, increased levels of ketone bodies may
improve insulin sensitivity and glycemic control.
Medical Applications: Ketone bodies have been
used in the treatment of certain medical
conditions, such as epilepsy and other
neurological disorders.
Lipoproteins are complex molecular assemblies
that transport lipids (fats and cholesterol) through
the bloodstream. They are composed of lipids on
the inside and proteins on the outside, allowing
them to be soluble in the watery environment of
the blood. Lipoproteins play a crucial role in lipid
metabolism by facilitating the transport of lipids to
and from various tissues. There are several types of
lipoproteins, each with distinct functions and roles
• Chylomicrons:
• Function: Chylomicrons are the largest and
least dense lipoproteins. They are synthesized
in the small intestine after the ingestion of
dietary fats (triglycerides) and are responsible
for transporting dietary triglycerides to various
tissues, including adipose tissue (for storage)
and muscle tissue (for energy).
• Very Low-Density Lipoproteins (VLDL):
• Function: VLDLs are produced in the liver and
contain mainly endogenous triglycerides. Their
primary role is to transport triglycerides
synthesized in the liver to other tissues for energy
storage. As VLDLs lose triglycerides through
lipolysis, they become denser and eventually
transform into intermediate-density lipoproteins
(IDLs) and then low-density lipoproteins (LDLs).
• Intermediate-Density Lipoproteins (IDLs):
• Function: IDLs are intermediate products
between VLDLs and LDLs. They still contain
some triglycerides and cholesterol, and their
fate is to either be further metabolized to LDLs
or taken up by the liver.
• Low-Density Lipoproteins (LDL):
• Function: LDLs, often referred to as "bad
cholesterol," transport cholesterol from the
liver to tissues throughout the body. However,
if LDL levels are elevated and not properly
regulated, excess LDL cholesterol can
accumulate in arterial walls, contributing to
the development of atherosclerosis and
increasing the risk of cardiovascular disease.
• High-Density Lipoproteins (HDL):
• Function: HDLs, often referred to as "good
cholesterol," have a protective role in
cardiovascular health. They transport
cholesterol from peripheral tissues back to the
liver for excretion (a process known as reverse
cholesterol transport). High levels of HDL are
associated with a reduced risk of
cardiovascular disease.
• Lipoprotein(a) [Lp(a)]:
• Function: Lp(a) is structurally similar to LDL
but has an additional protein component,
called apolipoprotein(a). Elevated levels of
Lp(a) are considered a risk factor for
cardiovascular disease as it may contribute to
the formation of atherosclerotic plaques.
• A lipid profile, also known as a lipid panel, is a blood
test that measures the levels of various types of
lipids (fats) and cholesterol in your bloodstream. This
test provides valuable information about your
cardiovascular health and risk factors for heart
disease and other related conditions. The
components typically measured in a lipid profile
include:
• Total Cholesterol: This is the sum of all cholesterol in
your blood, including both LDL and HDL cholesterol.
• Low-Density Lipoprotein Cholesterol (LDL-C): Often
referred to as "bad cholesterol," high levels of LDL-C are
associated with an increased risk of atherosclerosis and
heart disease.
• High-Density Lipoprotein Cholesterol (HDL-C): Often
referred to as "good cholesterol," higher levels of HDL-C
are associated with a lower risk of heart disease.
• Triglycerides: These are a type of fat that circulates in
the blood. Elevated triglyceride levels are also
associated with an increased risk of cardiovascular
disease.
• In some cases, the lipid profile may also include calculations or
measurements of additional parameters, such as:
• Non-HDL Cholesterol: This is calculated by subtracting HDL-C from total
cholesterol. Non-HDL cholesterol provides information about all the
cholesterol carried by atherogenic lipoproteins (those associated with
atherosclerosis).
• LDL Particle Number (LDL-P): This measures the actual number of LDL
particles, which can be a better indicator of cardiovascular risk compared
to LDL cholesterol levels.
• LDL Particle Size: This measures the size of LDL particles, which can have
implications for cardiovascular risk.
• Triglyceride/HDL Ratio: This ratio is calculated by dividing triglycerides
by HDL cholesterol. It provides insight into insulin resistance and
cardiovascular risk.
The normal range for lipid profile values can vary
slightly depending on the laboratory and the
units of measurement used. However, here are
generally accepted reference ranges for a
standard lipid profile in milligrams per deciliter
(mg/dL):
• Total Cholesterol:
• Desirable: Less than 200 mg/dL
• Borderline High: 200-239 mg/dL
• High: 240 mg/dL and above
• Low-Density Lipoprotein Cholesterol (LDL-C):
• Optimal: Less than 100 mg/dL
• Near Optimal: 100-129 mg/dL
• Borderline High: 130-159 mg/dL
• High: 160-189 mg/dL
• Very High: 190 mg/dL and above
• High-Density Lipoprotein Cholesterol (HDL-C):
• Low: Less than 40 mg/dL (for men), less than
50 mg/dL (for women)
• Higher levels are generally better for HDL-C.
• Triglycerides:
• Normal: Less than 150 mg/dL
• Borderline High: 150-199 mg/dL
• High: 200-499 mg/dL
• Very High: 500 mg/dL and above
Atherosclerosis is a chronic and progressive
cardiovascular disease characterized by the
accumulation of fatty deposits, cholesterol, cellular
waste, calcium, and other substances within the
walls of arteries. This buildup forms plaques that
can narrow and harden the arteries, reducing blood
flow to vital organs and tissues. Atherosclerosis is a
major cause of various cardiovascular problems,
including heart attacks, strokes, and peripheral
artery disease.
• The process of atherosclerosis involves several
stages:
• Endothelial Dysfunction: The inner lining of
arteries, called the endothelium, becomes
damaged or dysfunctional due to factors like
smoking, high blood pressure, high
cholesterol, and diabetes. This damage allows
LDL cholesterol and other substances to
infiltrate the arterial wall.
Fatty Streak Formation: LDL cholesterol
particles penetrate the damaged endothelium
and accumulate in the arterial wall, leading to
the formation of fatty streaks. These streaks
consist of cholesterol-laden foam cells.
Plaque Formation: Over time, the fatty streaks
can progress into more complex plaques.
Immune cells, smooth muscle cells, and
connective tissue also accumulate in the area,
contributing to plaque growth. Plaques may
become inflamed and rupture, leading to the
release of clot-forming substances into the
bloodstream.
• Calcification: The accumulated material in the
plaque can calcify, causing the plaque to
harden and become less flexible.
• Narrowing of Arteries: As the plaques grow,
they can narrow the arteries and reduce blood
flow. This can lead to angina (chest pain) when
the heart muscle doesn't receive enough
blood, or to peripheral artery disease when
other body tissues are affected.
Plaque Rupture and Blood Clots: Ruptured
plaques can expose their contents to the
bloodstream, triggering the formation of blood
clots. If a blood clot blocks a coronary artery, it
can lead to a heart attack. If it blocks an artery in
the brain, it can result in a stroke
Complications: Severe atherosclerosis can lead
to various complications, including acute
coronary syndrome (unstable angina or heart
attack), stroke, kidney problems, and reduced
blood flow to the legs and feet.
• Risk factors for atherosclerosis include:
• High levels of LDL cholesterol
• Low levels of HDL cholesterol
• High blood pressure (hypertension)
• Smoking
• Diabetes
• Obesity
• Sedentary lifestyle
• Unhealthy diet
• Family history of heart disease
Prevention and management of atherosclerosis involve
adopting a heart-healthy lifestyle, including regular exercise, a
balanced diet, maintaining a healthy weight, managing blood
pressure and cholesterol levels, avoiding smoking, and
managing diabetes. Medications such as statins, aspirin, and
antihypertensive drugs may be prescribed to control risk
factors and reduce the progression of atherosclerosis. In some
cases, medical procedures like angioplasty and stent
placement may be necessary to restore blood flow in blocked
arteries. Early detection and appropriate management are
essential for reducing the impact of atherosclerosis on
cardiovascular health.
 UNIT -4 Enzymes
Enzymes are biological molecules that act as
catalysts in living organisms. They play a crucial
role in various biochemical reactions by
speeding up the rate at which these reactions
occur. Enzymes are essential for maintaining the
processes of life, and they are involved in a wide
range of physiological functions, including
digestion, energy production, and DNA
replication.
• Oxidoreductases: These enzymes catalyze oxidation-
reduction reactions, involving the transfer of electrons
between molecules. Examples include dehydrogenases
and oxidases.
• Transferases: Transferases catalyze the transfer of
functional groups, such as amino groups or phosphate
groups, between molecules. Kinases and transaminases
are examples.
• Hydrolases: Hydrolases catalyze hydrolysis reactions,
where a molecule is broken down by the addition of
water. Examples include lipases and proteases.
• Lyases: Lyases catalyze reactions where functional groups
are added to or removed from molecules without
hydrolysis or oxidation. Decarboxylases and dehydratases
are lyases.
• Isomerases: Isomerases catalyze the rearrangement of
atoms within a molecule to convert it into its isomeric
form. An example is an isomerase that converts glucose-6-
phosphate into fructose-6-phosphate.
• Ligases: Ligases, also known as synthetases or synthases,
catalyze the joining of two molecules by forming a new
chemical bond. DNA ligase is an example.
Isoenzymes, also known as isozymes or
isoenzymes, are a group of enzymes that have
the same or similar catalytic activities but differ
in their amino acid sequences and are often
encoded by different genes. Isoenzymes are a
result of gene duplication and divergence during
evolution.
Enzymes play a crucial role in various diagnostic
tests and assays to assess health and disease
conditions. Monitoring the activity levels of
specific enzymes in biological samples (such as
blood or urine) can provide valuable information
about the functioning of various organs and
tissues. Here are some enzymes of diagnostic
importance and the conditions they are
associated with:
Alanine Aminotransferase (ALT) and Aspartate
Aminotransferase (AST): ALT and AST are
enzymes found in liver cells. Elevated levels of
these enzymes in the blood can indicate liver
damage or disease, such as hepatitis, cirrhosis,
or liver injury.
Alkaline Phosphatase (ALP): ALP is found in
various tissues, including the liver, bones, and
bile ducts. Elevated ALP levels may indicate liver
or bone disorders, such as liver disease, bone
disease, or blocked bile ducts.
Creatine Kinase (CK): CK is involved in energy
metabolism in muscles. Elevated CK levels can
indicate muscle damage or injury, such as in
cases of myocardial infarction (heart attack) or
muscle diseases like muscular dystrophy.
Lactate Dehydrogenase (LDH): LDH is found in
many tissues, including the heart, liver, muscles,
and red blood cells. Increased LDH levels can be
a sign of tissue damage or disease, such as
myocardial infarction, liver disease, or hemolysis
(destruction of red blood cells).
Amylase and Lipase: These enzymes are
involved in digestive processes. Elevated levels
of amylase and lipase in the blood may indicate
pancreatitis, an inflammation of the pancreas.
Gamma-Glutamyl Transferase (GGT): GGT is
found in the liver, biliary tract, and other tissues.
Increased GGT levels can be associated with liver
or bile duct disorders, such as cholestasis or
alcohol-related liver damage.
Prostate-Specific Antigen (PSA): PSA is
produced by the prostate gland. Elevated PSA
levels may indicate prostate cancer, although
other factors can also affect PSA levels, such as
prostate enlargement (benign prostatic
hyperplasia) or infection.
Troponins (Troponin T and Troponin I):
Troponins are specific to cardiac muscle and are
used as markers of cardiac damage. Elevated
troponin levels are a key indicator of myocardial
infarction (heart attack).
Acid Phosphatase: Acid phosphatase levels can
be used as a marker for prostate cancer.
However, it is less commonly used today
compared to PSA testing.
• Cholinesterase: Cholinesterase levels can be
used to assess organophosphate pesticide
exposure or to diagnose certain conditions like
liver disease or muscle disorders.
• D-dimer: D-dimer is an indicator of blood clot
formation and breakdown. Elevated D-dimer
levels can suggest conditions like deep vein
thrombosis (DVT), pulmonary embolism (PE), or
disseminated intravascular coagulation (DIC).
Glucose-6-Phosphate Dehydrogenase (G6PD):
G6PD deficiency is a genetic disorder that can
lead to hemolytic anemia. Testing for G6PD
activity is important in diagnosing and managing
this condition.
 Alanine Aminotransferase (ALT)
• Alanine Aminotransferase (ALT) is an enzyme primarily found
in the liver. It plays a crucial role in the metabolism of amino
acids. ALT levels in the blood can be measured through a
simple blood test.
• 1. Normal Range: The normal range for ALT can vary slightly
between different laboratories and geographic regions due
to differences in measurement techniques and reference
populations. However, in general, ALT levels are typically
considered normal when they fall within the following range:
• For adults: 7 to 56 units per liter (U/L)
• For children: 7 to 35 U/L
• Interpretation:
• Normal ALT Levels: When ALT levels are within the
normal range, it generally indicates that the liver is
functioning normally, and there is no significant
liver damage or inflammation.
• Elevated ALT Levels: Elevated ALT levels can
indicate liver injury or disease. The degree of
elevation can vary, and the specific cause should
be determined through further evaluation and
testing.
• Symptoms Associated with Elevated ALT:
• Liver Diseases: Elevated ALT levels are often associated with various
liver conditions, such as hepatitis (both viral and non-viral), fatty liver
disease, alcoholic liver disease, cirrhosis, and liver tumors.
• No Symptoms: Importantly, elevated ALT levels themselves do not
typically cause symptoms. Instead, they serve as a marker of
underlying liver damage or disease. Symptoms, if present, are more
likely to be related to the underlying liver condition causing the ALT
elevation.
• Possible Symptoms of Liver Disease: Symptoms of liver disease can
include fatigue, jaundice (yellowing of the skin and eyes), abdominal
pain or discomfort, dark urine, pale stools, unexplained weight loss,
nausea, vomiting, and loss of appetite, among others.
It's essential to remember that while elevated
ALT levels can be indicative of liver disease, they
are not specific to a particular condition. Further
testing, including additional liver function tests,
imaging studies (such as ultrasound or MRI), and
sometimes liver biopsy, may be required to
determine the underlying cause of the ALT
elevation and the severity of liver disease
Aspartate Aminotransferase (AST),
Aspartate Aminotransferase (AST), also known
as serum glutamic oxaloacetic transaminase
(SGOT), is an enzyme found in various tissues
throughout the body, with higher concentrations
in the liver and heart. It plays a role in amino
acid metabolism and is important for various
biochemical processes. AST levels in the blood
can be measured through a simple blood test.
• Interpretation of AST Levels:
• Normal Range: The normal range for AST
levels can vary slightly depending on the
laboratory and measurement units, but it
typically falls within the range of 10 to 40 units
per liter (U/L) of blood. However, it's essential
to note that the reference range can vary, so
it's best to rely on the specific reference range
provided by the laboratory conducting the test
Elevated AST Levels: Elevated AST levels in the
blood are generally indicative of tissue damage,
particularly damage to the liver, heart, or
skeletal muscles. The degree of elevation can
vary, and the underlying cause needs to be
determined through further evaluation and
testing.
Common Symptoms Associated with Abnormal
AST Levels:
Liver Disease: Elevated AST levels can indicate
liver damage or inflammation. Common liver
conditions associated with elevated AST include
hepatitis, cirrhosis, and fatty liver disease.
Symptoms may include fatigue, jaundice
(yellowing of the skin and eyes), abdominal pain,
and changes in appetite.
 Alkaline Phosphatase (ALP)
Alkaline Phosphatase (ALP) is an enzyme found
in various tissues throughout the body, with
particularly high concentrations in the liver,
bone, bile ducts, and placenta during pregnancy.
It plays a role in several physiological processes,
including bone mineralization and the transport
of compounds across cell membranes. ALP levels
can be measured through a blood test,
Normal Range: The normal range of ALP can vary
depending on the laboratory and the specific
testing methods used. However, in general, the
normal range for ALP in adults is approximately
20 to 140 units per liter (U/L) of blood. Keep in
mind that age, gender, and other factors can
influence these reference ranges, so it's essential
to refer to the specific reference range provided
by the laboratory conducting the test.
• Interpretation of ALP Levels:
• Normal ALP Levels: If ALP levels fall within the
normal range, it generally indicates that there
is no significant underlying liver or bone
disease. ALP is typically elevated during
periods of rapid bone growth (e.g., childhood
and adolescence), and it may also be slightly
higher in pregnant women.
• Elevated ALP Levels: Elevated ALP levels can
be indicative of various conditions, including:
• Liver Disorders: ALP levels may rise in liver
diseases such as hepatitis, cirrhosis, or biliary
obstruction. Elevated ALP, along with elevated
bilirubin and other liver function tests, may
suggest liver dysfunction.
• Associated Symptoms: The presence of symptoms often
depends on the underlying cause of elevated ALP levels.
Common symptoms that may be associated with conditions
leading to elevated ALP levels include:
• Jaundice (yellowing of the skin and eyes)
• Abdominal pain, especially in the upper right side
• Fatigue and weakness
• Bone pain or deformities in bone disorders
• Itching
• Dark urine
• Pale-colored stools
 Gamma-Glutamyl Transferase (GGT)
Gamma-Glutamyl Transferase (GGT) is an enzyme
found in various tissues in the body, with the highest
concentrations typically in the liver and bile ducts.
GGT plays a crucial role in the metabolism of
glutathione, a substance that helps protect cells from
oxidative damage. Elevated GGT levels in the blood
can indicate various underlying health conditions,
and its interpretation should be considered in
conjunction with other liver function tests and
clinical symptoms.
Normal Range for GGT: The reference range for
GGT can vary slightly depending on the
laboratory and the population being tested.
However, a general guideline for the normal
range of GGT in adults is usually considered to
be less than 30 IU/L (international units per
liter).
• Interpretation of GGT Levels:
• Normal GGT Levels: GGT levels within the
normal range are typically a good indicator of
healthy liver function. However, it's essential
to consider GGT results alongside other liver
function tests and clinical information.
• Elevated GGT Levels: Elevated GGT levels can indicate
various underlying conditions, including:
• Liver Diseases: GGT is often elevated in liver diseases, such
as hepatitis, fatty liver disease, alcoholic liver disease, and
cirrhosis.
• Biliary Diseases: Conditions that affect the bile ducts, such
as cholestasis (bile flow obstruction), gallstones, or
pancreatic disorders, can lead to elevated GGT levels.
• Alcohol Use: GGT is sensitive to alcohol consumption, and
chronic alcohol use can significantly increase GGT levels,
even before other liver function tests show abnormalities.
• Medications: Some medications, including
certain anticonvulsants, statins, and anti-
inflammatory drugs, can cause GGT elevation.
• Obesity: Elevated GGT levels can be
associated with obesity and metabolic
syndrome.
• Clinical Symptoms: Elevated GGT levels alone may
not cause noticeable symptoms since it's primarily a
marker of underlying conditions. However, the
symptoms associated with GGT elevation are typically
related to the underlying disease. For example:
• In liver diseases, symptoms may include jaundice
(yellowing of the skin and eyes), abdominal pain,
fatigue, and changes in urine and stool color.
• In biliary diseases, symptoms may include abdominal
pain, nausea, vomiting, and pale-colored stools.
It's important to remember that GGT is not a
specific marker for any one condition, and
further evaluation is needed to determine the
underlying cause of elevated levels. Your
healthcare provider will consider your medical
history, other liver function tests, imaging
studies, and clinical symptoms when
interpreting GGT results and making a diagnosis.
 Creatine Kinase (CK)
Creatine Kinase (CK), also known as creatine
phosphokinase (CPK), is an enzyme found
primarily in muscles, including skeletal muscles
and the heart. It plays a crucial role in the
energy metabolism of muscle cells. CK levels in
the blood can be measured through a blood
test, and the interpretation, normal range, and
symptoms related to CK are as follows:
Interpretation: Elevated CK levels in the blood
can indicate muscle damage or injury. CK levels
can rise in various conditions, including muscle
trauma, strenuous exercise, muscle disorders
(myopathies), and heart conditions, such as
myocardial infarction (heart attack). The
interpretation of CK levels depends on the
clinical context and the patient's symptoms.
• Normal Range: The normal reference range for
CK levels in the blood can vary slightly from one
laboratory to another, but a general range is as
follows:
• Male: 39-308 units per liter (U/L)
• Female: 26-192 U/L
It's important to note that CK levels can vary
based on age, sex, and muscle mass, so what is
considered normal may differ for individuals
Heart-Related Symptoms: In the context of a heart
attack (myocardial infarction), significantly elevated
CK-MB (creatine kinase isoenzyme specific to the
heart) levels may be seen. Symptoms of a heart
attack can include chest pain or discomfort,
shortness of breath, radiating pain in the arm, jaw,
or neck, and sweating. CK-MB levels can be used in
combination with other cardiac markers like
troponin to diagnose a heart attack.
 Troponin
Troponin is a cardiac biomarker used to
diagnose and assess heart muscle damage,
particularly in the context of myocardial
infarction (heart attack). Here's some
information about interpreting troponin levels,
its normal range, and associated symptoms:
• Interpretation of Troponin Levels:
• Normal Range: Troponin levels are typically very low
or undetectable in the blood of healthy individuals.
The exact normal range can vary slightly depending on
the laboratory and the type of troponin assay used,
but it is generally less than 0.03 ng/mL.
• Elevated Troponin Levels: Elevated troponin levels
indicate damage to the heart muscle. The degree of
elevation is often proportional to the extent of
damage. Troponin levels can start to rise within 3-4
hours after the onset of a heart attack and peak within
24-48 hours. High-sensitivity troponin assays can
detect even smaller elevations, allowing for earlier
diagnosis.
• Symptoms Associated with Elevated Troponin:
• Elevated troponin levels are often associated with
symptoms of myocardial infarction (heart attack).
These symptoms can include:
• Chest Pain: Severe, crushing, or squeezing chest
pain or discomfort is a hallmark symptom of a
heart attack. This pain may radiate to the arms,
neck, jaw, back, or stomach.
• Shortness of Breath: Difficulty breathing or shortness
of breath, often accompanied by chest discomfort.
• Nausea and Vomiting: Some individuals experience
nausea and may vomit during a heart attack.
• Sweating: Profuse sweating, sometimes described as
"clammy" or "cold" sweats.
• Weakness and Fatigue: Feeling unusually weak,
fatigued, or lightheaded.
• Anxiety or Restlessness: A sense of impending doom,
anxiety, or restlessness.
 Lactate Dehydrogenase (LDH)
Lactate Dehydrogenase (LDH) is an enzyme
found in various tissues throughout the body,
including the heart, liver, muscles, kidneys, and
red blood cells. It plays a role in converting
lactate to pyruvate, which is important in
cellular energy production. LDH levels can be
measured through a blood test
Normal Range: The normal range for LDH levels
can vary slightly depending on the laboratory
and the method used for testing. Generally, the
normal range for LDH in adults is approximately
140 to 280 international units per liter (IU/L).
However, it's important to note that normal
ranges can vary among different age groups and
populations.
• Interpretation:
• Elevated LDH Levels: Elevated LDH levels can indicate
various medical conditions or tissue damage.
Interpretation of LDH levels should be done in
conjunction with other clinical findings and tests. Some
conditions that can lead to increased LDH levels include:
– Tissue injury or damage, such as in myocardial infarction
(heart attack) or muscle injury.
– Hemolysis (destruction of red blood cells), which can be seen
in conditions like hemolytic anemia.
– Liver disease or hepatitis.
– Certain cancers, such as lymphoma.
– Infections, including pneumonia.
– Kidney disease.
Decreased LDH Levels: Decreased LDH levels are
not commonly encountered in clinical practice
and are less informative than elevated levels.
They may be seen in rare genetic conditions
affecting LDH production.
• Symptoms Associated with Elevated LDH:
Elevated LDH levels are not specific to any one
condition, so the symptoms associated with LDH
elevation will depend on the underlying cause.
• In the context of a heart attack (myocardial
infarction), elevated LDH levels may be
accompanied by chest pain or discomfort,
shortness of breath, and other cardiac
symptoms.
 AST
• Symptoms of Heart Disease: When interpreting AST levels in the
context of heart diseases, it's crucial to consider the overall
clinical picture, including symptoms. Common symptoms of heart
disease or a heart attack (myocardial infarction) can include:
• Chest pain or discomfort (angina)
• Shortness of breath
• Fatigue
• Rapid or irregular heartbeat
• Dizziness or lightheadedness
• Nausea or vomiting
• Pain or discomfort radiating to the arms, neck, jaw, or back
Other Cardiac Enzymes: AST is often measured
along with other cardiac enzymes, such as
troponin and creatine kinase-MB (CK-MB), to get
a more comprehensive picture of cardiac muscle
injury. Troponin, in particular, is a more specific
marker for heart muscle damage and is
considered the gold standard for diagnosing
myocardial infarction.
 CK
• Interpretation of Muscle Enzymes:
• Elevated CK Levels: Elevated CK levels can
indicate muscle damage or disease. CK is found
in various muscle tissues, including skeletal
muscle and cardiac muscle, so elevated CK
levels can be associated with both muscle
diseases (myopathies) and heart conditions.
The degree of CK elevation can vary depending
on the severity of muscle damage.
• Symptoms of Muscle Diseases: The symptoms of muscle
diseases can vary widely depending on the specific condition
and the muscles affected. Common symptoms include:
• Muscle weakness: Difficulty in performing everyday
activities or lifting objects.
• Muscle pain or tenderness: Discomfort or soreness in the
affected muscles.
• Muscle stiffness: Difficulty moving the muscles, especially
after periods of rest.
• Fatigue: Feeling tired or exhausted, often due to the extra
effort required for muscle movement.
• Muscle cramps or spasms: Involuntary muscle
contractions or twitching.
• Difficulty swallowing or breathing: In some muscle
diseases, muscles involved in these functions can be
affected.
• Gait abnormalities: Altered walking patterns due to
muscle weakness or imbalance.
• Contractures: Permanent shortening of muscles,
leading to joint deformities in some cases.
• Muscle atrophy: Shrinkage or wasting of muscle tissue.
Cardiac involvement: Some muscle diseases may
affect the heart muscle, leading to symptoms
such as chest pain, shortness of breath, and
irregular heartbeats.
 Aldolase
Aldolase is an enzyme found in various tissues in
the body, including muscles and the liver. It plays
a role in the breakdown of glucose for energy
production. Elevated levels of aldolase in the
blood can be indicative of muscle damage or
certain medical conditions.
Normal Range: The normal range for aldolase
levels can vary slightly depending on the
laboratory and the units used for measurement.
In general, the reference range for aldolase is
around 1 to 8 units per liter (U/L). However,
specific reference ranges may differ between
labs.
• Interpretation:
• Normal Levels: Aldolase levels within the normal
range are typically not a cause for concern.
• Elevated Levels: Elevated aldolase levels can
indicate muscle damage or certain medical
conditions. It's important to note that aldolase is
not a specific marker for a particular disease, so
further evaluation is usually necessary to
determine the underlying cause of the elevation.
• Symptoms Associated with Elevated Aldolase:
• Muscle Weakness: One of the primary reasons for elevated
aldolase levels is muscle damage. Conditions that cause
muscle injury or breakdown, such as muscular dystrophy,
myositis, or rhabdomyolysis, may be associated with muscle
weakness and pain.
• Pain and Swelling: Muscle pain and swelling can occur along
with elevated aldolase levels, particularly in conditions that
lead to muscle inflammation or injury.
• Fatigue: In some cases, individuals with muscle disorders or
conditions associated with elevated aldolase may experience
fatigue and reduced exercise tolerance.
• Difficulty Moving: Depending on the underlying cause,
individuals may have difficulty with certain movements or
tasks due to muscle weakness.
Additional Testing: Elevated aldolase levels are
usually a signal to healthcare providers to
investigate further. This may involve additional
tests such as creatine kinase (CK) levels,
electromyography (EMG), muscle biopsy, or
imaging studies to assess the extent of muscle
damage and determine the underlying cause.
Alkaline phosphatase (ALP) is an enzyme found in
various tissues in the body, including the liver,
bones, and intestines. It plays a crucial role in bone
mineralization and liver function. Elevated or
decreased levels of ALP in the blood can indicate
different medical conditions, including bone
diseases. Here's some information on interpreting
ALP levels, the normal range, and symptoms
associated with bone diseases related to ALP:
Normal Range: The normal range for ALP levels
can vary depending on factors such as age, sex,
and the laboratory performing the test.
However, in general, the reference range for ALP
is around 20 to 140 units per liter (U/L) in adults.
Children and teenagers tend to have higher ALP
levels due to growth, so their reference ranges
may be different.
• Interpretation:
• Normal Levels: ALP levels within the normal
range are typically not a cause for concern.
• Elevated Levels: Elevated ALP levels can have
various causes, and bone diseases are one of
the potential reasons for higher ALP. However,
elevated ALP alone does not provide a specific
diagnosis; further evaluation is necessary to
determine the underlying cause.
• Symptoms Associated with Bone Diseases Related to
ALP:
• Bone Pain: Bone diseases that affect ALP levels can lead to
bone pain, which may vary in intensity and location.
• Fractures: Weakened bones due to certain bone diseases
may result in an increased risk of fractures.
• Deformities: In some cases, bone diseases can cause
deformities or changes in bone structure.
• Difficulty in Mobility: As bone health deteriorates,
individuals may experience difficulty in movement and
mobilit
• Conditions Associated with Elevated ALP:
• Paget's Disease of Bone: Elevated ALP levels are often
seen in Paget's disease, a condition characterized by
abnormal bone remodeling. It can cause bone pain,
deformities, and fractures.
• Osteomalacia: Osteomalacia is a condition where bones
become soft and weak due to a deficiency in vitamin D or
calcium. Elevated ALP may be observed in this condition.
• Bone Metastases: In cases of cancer that have spread to
the bones (bone metastases), ALP levels can be elevated
due to increased bone turnover.
 Prostate-specific antigen (PSA)
Prostate-specific antigen (PSA) is a protein
produced by the prostate gland in males. A blood
test measuring PSA levels is commonly used as a
screening tool for prostate cancer, as well as for
monitoring the progression of prostate cancer in
individuals who have been diagnosed with the
disease. Here's some information on interpreting
PSA levels, the normal range, and symptoms
associated with prostate cancer:
Normal Range: The normal range for PSA levels
can vary slightly depending on the laboratory
and the units used for measurement. In general,
PSA levels in the blood are typically low in
healthy individuals. A PSA level of 4.0
nanograms per milliliter (ng/mL) or lower is
often considered normal. However, what's
considered a "normal" level can vary based on
age and other factors.
• Interpretation:
• Normal Levels: PSA levels within the normal range are
generally considered a positive sign. It suggests a lower
likelihood of prostate cancer, though it doesn't rule it
out entirely. Other factors, such as age and family
history, should also be considered.
• Elevated Levels: Elevated PSA levels can indicate various
conditions, including prostate cancer, but they are not a
definitive diagnosis on their own. Further evaluation is
needed to determine the cause of elevated PSA levels.
• Symptoms Associated with Prostate Cancer:
• Early-Stage Prostate Cancer: In its early
stages, prostate cancer often does not cause
noticeable symptoms. Routine PSA screening
and digital rectal examinations (DRE) by a
healthcare provider are essential for early
detection.
• Advanced Prostate Cancer: As prostate cancer
advances, it can lead to symptoms such
as:Increased urinary frequency and urgency
• Difficulty starting or stopping urination
• Weak urine flow
• Blood in the urine or semen
• Erectile dysfunction
• Bone pain, particularly in the lower back, hips,
or ribs (indicative of metastasis to the bones)
"ACP" commonly refers to "Acid Phosphatase,"
which is an enzyme found in various tissues in
the body, including the prostate gland, red blood
cells, and bone. Acid phosphatase levels in the
blood can be measured for diagnostic purposes,
primarily to assess prostate health and
investigate certain medical conditions.
Normal Range: The normal range for acid
phosphatase (ACP) levels can vary depending on
the laboratory and the units used for
measurement. In general, the reference range
for ACP in adults is around 0 to 3.7 units per liter
(U/L) for males and 0 to 2.9 U/L for females. It's
important to note that reference ranges may
differ between labs.
• Interpretation:
• Normal Levels: ACP levels within the normal range
are typically not a cause for concern.
• Elevated Levels: Elevated ACP levels can have various
causes, and the interpretation depends on the clinical
context. Elevated ACP levels can occur in conditions
such as prostate cancer, bone metastases, and some
other disorders. However, elevated ACP alone does
not provide a specific diagnosis; further evaluation is
needed to determine the underlying cause.
• Symptoms and Conditions Associated with Elevated ACP:
• Prostate Cancer: Elevated ACP levels can be seen in cases of
advanced prostate cancer. It can indicate the presence of
cancer cells in the prostate gland.
• Bone Metastases: In cases where cancer has spread to the
bones (bone metastases), ACP levels can be elevated due to
increased bone turnover.
• Paget's Disease of Bone: This bone disorder can also lead to
elevated ACP levels as it affects bone remodeling.
• Prostate Disorders: Conditions other than prostate cancer,
such as prostatitis or benign prostatic hyperplasia (BPH), may
also cause elevated ACP levels.
• Blood Disorders: Some blood disorders, such as hemolysis
(destruction of red blood cells), can lead to increased ACP
levels.
 UNIT-5 Acid-base balance
Acid-base balance refers to the delicate
equilibrium between acids and bases (alkaline
substances) in the body's fluids, particularly the
blood. Maintaining this balance is crucial for
normal physiological function because even
slight deviations can have significant clinical
consequences.
• The body tightly regulates its acid-base
balance through several mechanisms,
primarily involving the respiratory and renal
systems:
• Buffer Systems: The body contains chemical
buffers, such as bicarbonate (HCO3-),
phosphate, and proteins, which can quickly
bind to excess acids or bases to prevent rapid
changes in pH.
• Respiratory Regulation: The respiratory system
controls the levels of carbon dioxide (CO2) in the
blood. When CO2 levels increase, the body
becomes more acidic, and when they decrease, it
becomes more alkaline. Faster breathing eliminates
CO2, while slower breathing retains it.
• Renal Regulation: The kidneys help maintain acid-
base balance by excreting hydrogen ions (H+) or
reabsorbing bicarbonate ions. They can also
synthesize new bicarbonate ions.
• There are four primary types of acid-base
disturbances:
• Respiratory Acidosis: This occurs when the
lungs cannot remove enough CO2, leading to
increased levels of carbonic acid in the blood.
Causes can include respiratory conditions like
chronic obstructive pulmonary disease
(COPD), pneumonia, or impaired respiratory
function due to drugs or neurological issues.
Respiratory Alkalosis: This happens when the
lungs excrete too much CO2, causing a decrease
in carbonic acid levels and making the blood
more alkaline. Hyperventilation, anxiety, or high-
altitude exposure are common triggers.
Metabolic Acidosis: This occurs when there is an
accumulation of metabolic acids in the body,
such as lactic acid in lactic acidosis, ketoacids in
diabetic ketoacidosis, or when the kidneys
cannot excrete enough hydrogen ions. Causes
can include kidney disease, diabetes, or severe
dehydration.
Metabolic Alkalosis: This results from excessive
loss of metabolic acids (e.g., through vomiting or
excessive use of diuretics) or excessive intake of
bicarbonate. It leads to an increase in blood pH.
 Clinical Significance:
• Physiological Function: Proper acid-base balance is
essential for the normal functioning of enzymes,
proteins, and other biochemical processes in the body.
Even minor imbalances can disrupt these processes.
• Clinical Diagnosis: Measuring the blood pH and levels
of bicarbonate and carbon dioxide can provide
important diagnostic information. Abnormal acid-base
values can indicate underlying medical conditions,
guide treatment decisions, and help monitor the
progress of a patient.
• Respiratory and Metabolic Compensation: The
body can often compensate for minor acid-base
imbalances by adjusting the other component
(respiratory or metabolic) to partially correct the
pH. This compensation can give valuable insights
into the underlying cause of the imbalance.
• Treatment: Understanding acid-base balance is
crucial for effective medical interventions. For
example, treating respiratory acidosis may involve
improving lung function, while metabolic acidosis
may require addressing the underlying cause and
providing bicarbonate supplementation in severe
cases.
 pH
pH (potential of hydrogen) is a measure of the
acidity or alkalinity of a solution. It quantifies the
concentration of hydrogen ions (H+) in a
solution, which determines whether the solution
is acidic, neutral, or alkaline (basic). The pH scale
ranges from 0 to 14, with 7 considered neutral.
A pH less than 7 indicates acidity, while a pH
greater than 7 indicates alkalinity (basicity).
• The normal value for pH in various parts of the
body can vary:
• Blood: The normal pH range for arterial blood
(the pH of oxygenated blood) is approximately
7.35 to 7.45. A pH below 7.35 is considered
acidemia, while a pH above 7.45 is considered
alkalemia. It's important to maintain blood pH
within this narrow range for proper
physiological function.
• Stomach: The stomach's acidic environment
typically has a pH of around 1 to 3 due to the
presence of hydrochloric acid (HCl), which aids
in digestion.
• Small Intestine: The pH in the small intestine
is more neutral, ranging from 6 to 7.4, to
facilitate the digestion and absorption of
nutrients.
• Urine: Urine pH can vary depending on factors
such as diet and hydration. A normal urinary
pH typically ranges from 4.6 to 8, with
variations in response to dietary changes and
metabolic conditions.
• Skin: The skin's pH is mildly acidic, with a
normal range of around 4.5 to 5.5. This acidity
helps protect the skin from harmful
microorganisms.
The regulation of blood pH is a complex process
involving multiple mechanisms, with the primary
players being blood buffers, the respiratory
system, and the renal system. These systems
work together to maintain the blood's pH within
a narrow range, typically between 7.35 and 7.45.
• Blood Buffers:
• Blood contains chemical buffers, including bicarbonate
(HCO3-), phosphate, and proteins like hemoglobin. These
buffers can quickly bind to excess hydrogen ions (H+) to
prevent rapid changes in pH.
• The bicarbonate buffer system is particularly important.
It involves the reversible reaction between carbonic acid
(H2CO3) and bicarbonate ions (HCO3-):
– H2CO3 ⇌ H+ + HCO3-
• If there is an increase in H+ (acidity), the excess H+ ions
can combine with HCO3- to form H2CO3, which helps
neutralize the excess acid. Conversely, if there is a
decrease in H+ (alkalinity), H2CO3 can dissociate into H+
and HCO3- to release hydrogen ions and increase acidity.
• Respiratory Regulation:
• The respiratory system plays a crucial role in regulating
blood pH by controlling the levels of carbon dioxide (CO2)
in the blood.
• When CO2 levels increase, such as during conditions like
hypoventilation or lung disease, the body becomes more
acidic because CO2 combines with water to form carbonic
acid (H2CO3), which releases hydrogen ions (H+).
• Conversely, when CO2 levels decrease, such as during
hyperventilation, the body becomes more alkaline because
there is less carbonic acid and fewer hydrogen ions.
• Renal Regulation:
• The kidneys play a longer-term role in regulating blood pH
by excreting excess hydrogen ions (H+) or reabsorbing
bicarbonate ions (HCO3-).
• When the blood is too acidic, the kidneys can excrete more
H+ ions and retain HCO3-, which helps raise blood pH.
• When the blood is too alkaline, the kidneys can excrete less
H+ ions and excrete more HCO3-, which helps lower blood
pH.
• The kidneys can also synthesize new bicarbonate ions to
help maintain pH balance.
 ABG
Arterial blood gas (ABG) analysis is a test that
measures the levels of various gases, such as oxygen
(O2) and carbon dioxide (CO2), as well as the pH
and bicarbonate (HCO3-) concentration in arterial
blood. These values provide important information
about the respiratory and metabolic status of a
patient. Normal ABG values can vary slightly
depending on the laboratory and the specific
reference ranges they use, but generally, the
following are considered normal values:
• pH: 7.35 to 7.45
– A pH below 7.35 is considered acidemia (acidosis).
– A pH above 7.45 is considered alkalemia (alkalosis).
• Partial Pressure of Oxygen (PaO2): 75 to 100 mm Hg
– PaO2 measures the concentration of oxygen dissolved in the
arterial blood.
• Partial Pressure of Carbon Dioxide (PaCO2): 35 to 45 mm Hg
– PaCO2 measures the concentration of carbon dioxide dissolved in
the arterial blood.
• Bicarbonate (HCO3-): 22 to 28 mEq/L
– Bicarbonate is a measure of the concentration of bicarbonate ions
in the blood and provides information about metabolic status.
• Oxygen Saturation (SaO2): 95% to 100%
– SaO2 measures the percentage of hemoglobin saturated with
oxygen in arterial blood.
• Acid-base disorders are medical conditions
characterized by imbalances in the pH (acidity
or alkalinity) of bodily fluids, particularly the
blood. There are four primary types of acid-
base disorders, each defined by specific
changes in the blood's pH and bicarbonate
(HCO3-) levels. These disorders can have
various underlying causes. Here are the four
types:
• Respiratory Acidosis:
• Definition: Respiratory acidosis occurs when there is an
accumulation of carbon dioxide (CO2) in the blood, leading
to an increase in carbonic acid (H2CO3) and a decrease in
blood pH. This results in blood becoming more acidic.
• Causes:
– Impaired lung function, such as chronic obstructive pulmonary
disease (COPD), asthma, or pneumonia.
– Respiratory depression caused by drugs like opioids or sedatives.
– Chest injuries or neuromuscular disorders that affect breathing.
• Respiratory Alkalosis:
• Definition: Respiratory alkalosis occurs when there is a
decreased level of carbon dioxide (CO2) in the blood,
leading to a decrease in carbonic acid (H2CO3) and an
increase in blood pH. This results in blood becoming
more alkaline.
• Causes:
– Hyperventilation due to anxiety, panic attacks, or high-
altitude exposure.
– Fever.
– Overuse of mechanical ventilators.
• Metabolic Acidosis:
• Definition: Metabolic acidosis occurs when there is an
accumulation of metabolic acids in the blood, resulting in a
decrease in blood pH. This is typically due to a decrease in
bicarbonate (HCO3-) levels.
• Causes:
– Lactic acidosis: Excessive production of lactic acid, often seen in
conditions like sepsis or severe exercise.
– Diabetic ketoacidosis (DKA): Accumulation of ketone bodies in
uncontrolled diabetes.
– Renal failure: Impaired kidney function can lead to decreased
bicarbonate reabsorption and acid buildup.
– Ingestion of certain toxic substances.
• Metabolic Alkalosis:
• Definition: Metabolic alkalosis occurs when there is an
excessive loss of metabolic acids or an increase in
bicarbonate (HCO3-) levels in the blood, resulting in an
increase in blood pH. This makes the blood more alkaline.
• Causes:
– Vomiting or gastric suction: Loss of stomach acid (HCl) leads to
an increase in bicarbonate levels.
– Diuretic use: Some diuretics can lead to loss of potassium and
hydrogen ions.
– Excessive ingestion of bicarbonate-containing antacids.
 Unit-6
Hemoglobin is a crucial protein found in red
blood cells (RBCs) that plays a central role in
oxygen transport and exchange throughout the
body.
• 1. Hemoglobin Structure:
• Hemoglobin is a tetrameric protein composed
of four subunits: two alpha globin and two
beta globin chains in adults (alpha2beta2). In
fetal hemoglobin (HbF), gamma globin chains
replace the beta globin chains.
• Each subunit contains a heme group, which
contains an iron atom that binds oxygen.
• 2. Oxygen Binding and Release:
• Hemoglobin binds oxygen in the lungs,
forming oxyhemoglobin.
• In tissues with lower oxygen levels,
oxyhemoglobin releases oxygen, becoming
deoxyhemoglobin.
• 3. Red Blood Cell Lifespan:
• Red blood cells have a limited lifespan,
typically around 120 days.
• As RBCs age, their hemoglobin undergoes
various changes, including oxidative damage.
• 4. Hemoglobin Breakdown (Hemolysis):
• Aged or damaged RBCs are removed from
circulation by the spleen and liver.
• Hemoglobin is broken down into its constituent
parts: heme and globin chains.
• Heme is further broken down into biliverdin (green
pigment) and then bilirubin (yellow pigment).
• Bilirubin is transported to the liver, conjugated
with glucuronic acid, and excreted into bile.
• Clinical Significance:
• Anemia: Hemoglobin levels are used to
diagnose anemia, a condition characterized by
low RBC count or reduced hemoglobin
content. Anemia can result from various
factors, including nutritional deficiencies,
chronic diseases, or genetic disorders affecting
hemoglobin synthesis.
Hemoglobinopathies: These are genetic
disorders that affect the structure or production
of hemoglobin. Examples include sickle cell
disease and thalassemia, which can lead to
abnormal hemoglobin molecules and cause
severe clinical symptoms.
Jaundice: Elevated levels of bilirubin, a
breakdown product of hemoglobin, can lead to
jaundice, a yellowing of the skin and eyes. This
can be indicative of liver dysfunction or
increased RBC breakdown (hemolysis).
Oxygen Transport: Hemoglobin's primary
function is to transport oxygen, and
abnormalities in its structure or function can
lead to oxygen-carrying deficiencies, causing
tissue hypoxia and various clinical symptoms.
Carbon Monoxide Poisoning: Hemoglobin can
also bind to carbon monoxide (CO) more readily
than oxygen, leading to carbon monoxide
poisoning, which can have severe clinical
consequences due to impaired oxygen
transport.
Transfusion Medicine: Understanding
hemoglobin metabolism is essential in
transfusion medicine, as it helps in selecting
appropriate blood products for patients with
anemia or blood loss.
Monitoring Health: Hemoglobin levels are
routinely measured in clinical practice as part of
a complete blood count (CBC). Changes in
hemoglobin levels can provide important
diagnostic information about a patient's health
and may indicate underlying medical conditions.
Heme degradation is the process by which
heme, a molecule containing an iron atom found
in hemoglobin and other heme-containing
proteins, is broken down into its constituent
parts. This degradation pathway is crucial for
recycling iron and preventing the buildup of
excess heme in the body. The primary steps in
the heme degradation pathway are as follows:
Hemolysis: The first step in heme degradation
typically occurs when old or damaged red blood
cells (RBCs) are removed from circulation, either
in the spleen or the liver. These cells undergo
hemolysis, which is the breaking open of RBCs to
release their contents, including hemoglobin.
• Hemoglobin Release: Hemoglobin is released
from the lysed RBCs and is then acted upon by
enzymes to initiate its breakdown.
• Hemoglobin Oxygen Release: If the
hemoglobin still contains oxygen
(oxyhemoglobin), oxygen is released from the
heme group. This process involves the release
of oxygen molecules from the iron atom in the
heme group.
• Hemoglobin Denaturation: Hemoglobin is denatured, meaning its protein
structure is disrupted. This step is facilitated by various enzymes, including
heme oxygenase.
• Heme Oxygenase Reaction: Heme oxygenase is the enzyme responsible for
breaking down heme into its constituent parts. There are two forms of
heme oxygenase: heme oxygenase-1 (HO-1) and heme oxygenase-2 (HO-2).
The reaction catalyzed by heme oxygenase results in the following products:
• a. Biliverdin: Heme is converted into biliverdin, a green pigment. This
reaction involves the release of carbon monoxide (CO) and the liberation of
iron from the heme molecule.
• b. Iron Release: The iron released during the conversion of heme to
biliverdin is then transported and stored in the body's iron stores (such as
ferritin) for reuse in the production of new hemoglobin or other iron-
containing molecules.
• Biliverdin Reduction: Biliverdin is rapidly converted
into bilirubin by an enzyme called biliverdin reductase.
• Bilirubin Conjugation: Bilirubin is transported to the
liver, where it is conjugated with glucuronic acid to
form conjugated bilirubin, which is water-soluble and
can be excreted in bile.
• Bilirubin Excretion: Conjugated bilirubin is excreted
into the bile and eventually eliminated from the body
through the feces. A small portion may also be
excreted in the urine.
The breakdown of heme is essential for the proper
functioning of the body because it prevents the
accumulation of excess heme, recycles iron, and
produces substances like bilirubin that are eventually
excreted from the body. Any disruption in this pathway
can lead to conditions such as jaundice, where the
buildup of bilirubin in the body results in yellowing of the
skin and eyes. Additionally, understanding heme
degradation is important for diagnosing and managing
various disorders, including hemolytic anemias and
certain liver diseases.
Jaundice is a medical condition characterized by
the yellowing of the skin, eyes, and mucous
membranes due to elevated levels of bilirubin in
the blood. Bilirubin is a yellow pigment
produced during the breakdown of hemoglobin
from red blood cells. There are several types of
jaundice, each with different underlying causes.
The three main types of jaundice are:
• Prehepatic Jaundice (Hemolytic Jaundice):
• Causes: Prehepatic jaundice occurs when the excessive
breakdown of red blood cells (hemolysis) leads to an increased
production of bilirubin. This excess bilirubin overwhelms the liver's
capacity to conjugate and excrete it effectively. Common causes of
prehepatic jaundice include:
– Hemolytic anemias, such as sickle cell anemia or hereditary
spherocytosis.
– Blood transfusion reactions.
– Certain infections, like malaria.
– Genetic disorders affecting hemoglobin, like thalassemia.
• In prehepatic jaundice, bilirubin is typically unconjugated (indirect)
because the liver hasn't had the chance to process it yet.
• Hepatic Jaundice (Hepatocellular Jaundice):
• Causes: Hepatic jaundice results from dysfunction or
damage to the liver, which impairs its ability to process
bilirubin. Causes of hepatocellular jaundice include:
– Liver diseases, such as viral hepatitis (e.g., hepatitis A, B, or C),
alcoholic liver disease, or cirrhosis.
– Medications or toxins that affect liver function.
– Inherited liver disorders, like Gilbert's syndrome.
– Fatty liver disease.
• In hepatocellular jaundice, both unconjugated (indirect)
and conjugated (direct) bilirubin levels may be elevated.
• Posthepatic Jaundice (Obstructive Jaundice):
• Causes: Posthepatic jaundice occurs when there is a blockage or
obstruction in the bile ducts, preventing bilirubin from being
excreted into the intestine. This can lead to a buildup of
conjugated bilirubin in the blood. Common causes include:
– Gallstones, which can obstruct the common bile duct.
– Tumors in the pancreas or bile ducts.
– Biliary strictures (narrowing) due to inflammation or scarring.
– Parasitic infections, such as liver flukes.
• In posthepatic jaundice, bilirubin is typically conjugated (direct)
because it has already been processed by the liver but cannot
be excreted.
• It's important to note that the specific symptoms and treatment
for jaundice can vary depending on its underlying cause.
Diagnosis often involves blood tests to assess bilirubin levels,
imaging studies to identify obstructions or liver abnormalities,
and a thorough medical history and physical examination.
• Jaundice itself is a symptom of an underlying medical condition,
and treatment aims to address the root cause. This may involve
managing liver disease, addressing hemolytic disorders,
removing obstructions, or treating infections, depending on the
type and cause of jaundice. Early diagnosis and appropriate
treatment are essential to prevent complications associated
with jaundice and its underlying conditions.
 Van Den Bergh Test
It is a specific test for identification of increased
serum bilirubin level
Normal serum gives a negative van den bergh
reaction
Van den bergh reagent is a mixture of equal
volumes of sulfanilic acid and sodium nitrite
(Diazo reagent)
Principle:
Diazo reagent reacts with bilirubin to form a
purple coloured azobilirubin
Direct and indirect reaction:
Bilirubin as such is insoluble in water while the
conjugated bilirubin is soluble
Van den Bergh reagent reacts with conjugated
bilirubin and gives a purple colour
immediately(normally within 30 secs)
This is direct positive Van Den Bergh reaction
Addition of methanol or alcohol dissolves the
unconjugated bilirubin and gives the Van den
bergh reaction (normally wihin 30mins) positive
This is indirect positive
If the serum contains both unconjugated and
conjugated bilirubin in high concentration, the
purple colour is produced immediately (direct
positive) which is further intensified by the
addition of alcohol(indirect positive)
This type of reaction is known as biphasic
 The serum of the patient is mixed with diazo
reagent. If a red colour develops immediately it is
called a direct positive. It happens if conjugated
bilirubin is present. In an indirect positive test, the
patient's serum is first treated with alcohol and later
mixed with diazo reagent. This causes development
of a red colour. It is seen if unconjugated bilirubin is
present. If both conjugated and unconjugated
bilirubin are present the reaction is termed a
biphasic reaction.
 Unit VII
• Liver Function Tests:
• Alanine Aminotransferase (ALT): Normal range is typically
7-56 units per liter (U/L).
• Aspartate Aminotransferase (AST): Normal range is
typically 10-40 U/L.
• Alkaline Phosphatase (ALP): Normal range is typically 44-
147 U/L.
• Total Bilirubin: Normal range is typically 0.1-1.2 milligrams
per deciliter (mg/dL).
• Albumin: Normal range is typically 3.4-5.4 grams per
deciliter (g/dL).
• Kidney Function Tests:
• Creatinine: Normal range is typically 0.6-1.3
mg/dL for adults.
• Blood Urea Nitrogen (BUN): Normal range is
typically 7-20 mg/dL.
• Glomerular Filtration Rate (GFR): A GFR
greater than 90 mL/min is considered normal.
• Pancreatic Function Tests:
• Amylase: Normal range is typically 30-110
U/L.
• Lipase: Normal range is typically 0-160 U/L.
• Thyroid Function Tests:
• Thyroid Stimulating Hormone (TSH): Normal
range is typically 0.4-4.0 milli-international
units per liter (mIU/L).
• Free Thyroxine (FT4): Normal range is typically
0.8-1.8 ng/dL.
• Cardiac Function Tests:
• Troponin I: Normal levels are typically below
0.04 ng/mL.
• Creatine Kinase-MB (CK-MB): Normal levels
are typically below 25 U/L.
• Lung Function Tests:
• Forced Expiratory Volume in 1 Second (FEV1):
Normal values depend on age, sex, and height
but are typically around 80-100% of the
predicted value.
• Forced Vital Capacity (FVC): Normal values
also depend on factors like age, sex, and
height but are generally similar to FEV1.
• Hemoglobin and Hematocrit:
• Hemoglobin (Hb): Normal range for adults is
typically 12.0-15.5 grams per deciliter (g/dL)
for women and 13.5-17.5 g/dL for men.
• Hematocrit (Hct): Normal range for adults is
typically 36-46% for women and 39-50% for
men.
 Renal
Renal function tests are a group of blood and
urine tests used to assess how well the kidneys
are functioning. These tests provide valuable
information about the overall health of the
kidneys and can help diagnose various kidney
disorders and monitor their progression. Here
are some common renal function tests and how
to interpret their findings:
• Creatinine Blood Test:
• Creatinine is a waste product produced by the
muscles and excreted by the kidneys. A blood test
measures the level of creatinine in the bloodstream.
• Interpretation:
– Elevated Creatinine: High levels of creatinine in the
blood may indicate impaired kidney function because
the kidneys may not be effectively filtering and
removing it from the body. This can be a sign of acute or
chronic kidney disease.
• Blood Urea Nitrogen (BUN):
• BUN is a measurement of the amount of urea
nitrogen in the blood, which is a waste product
formed during the breakdown of proteins.
• Interpretation:
– Elevated BUN: An elevated BUN level can indicate
kidney dysfunction or other conditions affecting
the kidneys. However, BUN levels can also be
influenced by factors like diet and dehydration
• Glomerular Filtration Rate (GFR):
• GFR is a calculated value that estimates how well
the kidneys are filtering waste products from the
blood. It is considered one of the most reliable
indicators of kidney function.
• Interpretation:
– Decreased GFR: A lower GFR suggests reduced kidney
function. Chronic kidney disease is staged based on
GFR values, with lower GFR values indicating more
advanced stages of the disease.
• Urine Albumin-to-Creatinine Ratio (ACR):
• This urine test measures the amount of albumin
(a protein) relative to creatinine in the urine. It is
used to detect early signs of kidney damage.
• Interpretation:
– Elevated ACR: An increased ACR suggests the
presence of excess albumin in the urine, which is a
sign of kidney damage. It may be an early indication
of conditions like diabetic nephropathy or
hypertensive nephropathy.
• Urine Dipstick Test:
• This simple test checks for the presence of
protein, blood, glucose, and other substances
in the urine.
• Interpretation:
– Positive findings on the dipstick for protein or
blood may indicate kidney problems. Further
evaluation is usually needed to determine the
cause.
• Serum Electrolytes (Sodium, Potassium):
• Electrolyte levels in the blood are monitored
because the kidneys play a crucial role in
maintaining electrolyte balance.
• Interpretation:
– Abnormal electrolyte levels can be indicative of
kidney dysfunction or other underlying conditions.
 LIVER
Liver function tests (LFTs), also known as hepatic
function tests, are a group of blood tests that
assess the health and function of the liver. The liver
is a vital organ responsible for many essential
functions in the body, including metabolism,
detoxification, and the production of proteins
necessary for various bodily processes. LFTs provide
valuable information about the liver's overall health
and its ability to perform these functions.
• Common liver function tests include:
• Alanine Aminotransferase (ALT): ALT is an enzyme
found primarily in the liver cells. Elevated ALT levels
often indicate liver damage or injury, which can be
caused by conditions like hepatitis, fatty liver disease, or
medication side effects.
• Aspartate Aminotransferase (AST): Like ALT, AST is an
enzyme found in the liver, but it's also present in other
organs, such as the heart and muscles. Elevated AST
levels can be a sign of liver damage, but they can also be
elevated in conditions affecting those other organs.
• Alkaline Phosphatase (ALP): ALP is an enzyme found in the
liver, bones, and other tissues. Elevated ALP levels may
suggest liver or bone disease. In the context of liver
function, ALP is often used to assess the biliary system (bile
ducts), and elevated levels can indicate a blockage or
obstruction.
• Total Bilirubin: Bilirubin is a waste product formed when red
blood cells break down. It is processed by the liver and
excreted in bile. Elevated levels of total bilirubin can result
from various liver disorders, such as hepatitis or cirrhosis, or
from conditions that cause an excess breakdown of red
blood cells.
Albumin: Albumin is a protein produced by the
liver. It helps maintain proper fluid balance in
the body and plays a role in transporting various
substances in the blood. Low albumin levels can
be indicative of chronic liver disease or
malnutrition.
• Interpreting Liver Function Test Results:
• Normal Results: Normal LFT results fall within the reference
ranges provided by the laboratory. However, it's important to
note that these ranges can vary from one laboratory to
another.
• Elevated ALT and AST: Elevated ALT and AST levels often
indicate liver damage or inflammation. The degree of
elevation may provide clues about the severity of liver injury.
Further evaluation is necessary to determine the underlying
cause, which could be viral hepatitis, alcoholic liver disease,
non-alcoholic fatty liver disease (NAFLD), or others
• Elevated ALP: Elevated ALP levels can suggest biliary
(bile duct) obstruction or bone disease. Additional tests
and imaging may be needed to identify the exact cause.
• Elevated Total Bilirubin: Elevated bilirubin levels may
indicate liver dysfunction or excessive breakdown of red
blood cells. The cause could be hepatitis, gallstones, or
other liver-related issues.
• Low Albumin: Low albumin levels may indicate chronic
liver disease, malnutrition, or kidney problems. It can
also be a sign of inflammation or chronic illness.
Thyroid function tests are a group of blood tests used
to assess the functioning of the thyroid gland, a
butterfly-shaped gland located in the neck that
produces hormones that regulate various metabolic
processes in the body. The primary hormones
produced by the thyroid gland are triiodothyronine
(T3) and thyroxine (T4), which play a crucial role in
controlling the body's metabolism, energy production,
and overall health. Thyroid function tests typically
include the measurement of several parameters:
• Thyroid Stimulating Hormone (TSH): TSH is produced
by the pituitary gland and stimulates the thyroid gland
to produce T3 and T4. A high TSH level usually indicates
an underactive thyroid (hypothyroidism), while a low
TSH level suggests an overactive thyroid
(hyperthyroidism).
• Free Thyroxine (FT4): FT4 is the active form of T4, and
it represents the amount of unbound T4 hormone
available to the body's cells. High FT4 levels are often
seen in hyperthyroidism, while low levels may indicate
hypothyroidism.
• Total Thyroxine (T4): This measures the total
amount of T4 in the blood, including both free
and bound T4. Elevated total T4 can occur in
hyperthyroidism, while decreased levels may
suggest hypothyroidism.
• Triiodothyronine (T3): T3 is another thyroid
hormone, but it is less commonly tested than
T4. Elevated T3 levels can be seen in
hyperthyroidism.
• Interpreting Thyroid Function Test Findings:
• Normal Thyroid Function:
– TSH within the reference range (typically 0.4-4.0 mIU/L).
– FT4 and total T4 within the reference range.
• Hypothyroidism (Underactive Thyroid):
– Elevated TSH level (typically above the reference range).
– Low FT4 and total T4 levels (below the reference range).
• Hyperthyroidism (Overactive Thyroid):
– Low or suppressed TSH level (typically below the reference range).
– Elevated FT4 and/or total T4 levels (above the reference range).
– In some cases, elevated T3 levels may also be observed.
• Subclinical Hypothyroidism or
Hyperthyroidism:
• TSH is outside the reference range, but FT4
and total T4 remain within the reference
range. This may indicate early thyroid
dysfunction.
 UNIT VIII
Immunoglobulins, also known as antibodies, are a
group of proteins produced by B cells (a type of
white blood cell) as a critical component of the
immune system. These proteins play a central role
in the immune response by recognizing and
neutralizing foreign invaders, such as bacteria,
viruses, and other pathogens. Immunoglobulins
have a specific structure and function that enables
them to perform their immune-related tasks
effectively.
Structure of Immunoglobulins:
Immunoglobulins have a Y-shaped structure
composed of four polypeptide chains, organized
as two identical heavy chains (H) and two
identical light chains (L). The basic structure of
an immunoglobulin includes the following
components:
• Variable Regions (Fab): These regions, located at the
tips of the Y-shaped molecule, are highly variable
between different types of immunoglobulins and
individuals. They are responsible for recognizing and
binding to specific antigens (foreign substances).
• Constant Region (Fc): The stem of the Y-shaped
molecule contains the constant region, which
interacts with various immune system components to
mediate different effector functions of antibodies.
• Heavy Chains (H): There are five different types of
heavy chains (IgM, IgD, IgG, IgA, and IgE) that
determine the class or isotype of the
immunoglobulin. Each heavy chain type has
distinct properties and functions.
• Light Chains (L): There are two types of light
chains (kappa and lambda) that are associated
with immunoglobulins. They play a role in
stabilizing the antibody structure and antigen
binding.
• Function of Immunoglobulins: Immunoglobulins function as
key components of the adaptive immune response. Their
primary functions include:
• Antigen Recognition: The variable regions of immunoglobulins
contain antigen-binding sites, also known as antigen-binding
fragments (Fab). These regions recognize and bind to specific
antigens on pathogens, such as viral proteins or bacterial cell
surface molecules.
• Neutralization: By binding to antigens on pathogens,
antibodies can neutralize their activity. This prevents the
pathogens from infecting host cells and spreading within the
body.
• Opsonization: Antibodies can enhance the process of
phagocytosis, where immune cells such as
macrophages and neutrophils engulf and destroy
pathogens. This occurs through the binding of
antibodies to the surface of pathogens, marking them
for destruction by phagocytes.
• Complement Activation: Some immunoglobulins,
particularly IgM and IgG, can activate the complement
system, a group of proteins that enhance the immune
response. Complement activation leads to the lysis of
pathogens and promotes inflammation.
Antibody-Dependent Cellular Cytotoxicity
(ADCC): Antibodies can recruit immune cells,
such as natural killer (NK) cells, to target and kill
infected cells. This process is known as ADCC
and is important in the defense against virus-
infected cells and some cancer cells.
 Enzyme-Linked Immunosorbent Assay
(ELISA)
Enzyme-Linked Immunosorbent Assay (ELISA) is a
widely used laboratory technique for the
detection and quantification of specific proteins
or antibodies in a sample. ELISA can be employed
for various purposes, including the diagnosis of
diseases, monitoring immune responses, and
assessing the presence of particular antigens.
Here's an overview of how an ELISA investigation
is conducted and how to interpret the results:
• 1. Sample Collection:
• Start by collecting the biological sample you want to
analyze. This could be blood, serum, plasma, urine,
saliva, or any other appropriate sample depending on
your research or diagnostic needs.
• 2. Plate Coating:
• In a 96-well microplate, specific antibodies or antigens
are immobilized on the surface. These antibodies or
antigens serve as capture molecules that will bind to
the target protein or antibody in your sample.
• 3. Blocking:
• To prevent nonspecific binding, the remaining uncoated
areas on the plate are blocked with a blocking buffer
(usually containing bovine serum albumin or milk
proteins).
• 4. Sample Incubation:
• Add your sample (diluted appropriately) to the
microplate wells. If you're detecting antibodies, the
sample may contain antibodies against a specific antigen.
If you're detecting antigens, the sample may contain the
antigen of interest.
• 5. Primary Antibody Incubation:
• After the sample incubation, add a primary
antibody that specifically binds to the target protein
or antigen. If the target is an antibody, use an anti-
immunoglobulin antibody conjugated with an
enzyme.
• 6. Wash Steps:
• Wash the microplate wells to remove unbound
substances, including any nonspecifically bound
antibodies or antigens.
• 7. Enzyme Conjugated Secondary Antibody:
• Add a secondary antibody that is conjugated
to an enzyme (e.g., horseradish peroxidase or
alkaline phosphatase). This secondary
antibody binds to the primary antibody.
• 8. Wash Steps:
• Wash the plate again to remove any unbound
secondary antibodies.
• 9. Substrate Addition:
• Add a substrate solution that is specific to the
enzyme used. When the enzyme binds to its
substrate, it produces a detectable signal (e.g.,
color change or fluorescence).
• 10. Signal Measurement: - Measure the intensity
of the signal generated by the enzyme-substrate
reaction. This is usually done using a microplate
reader that can measure absorbance or
fluorescence.
• Interpretation of ELISA Results:
• The intensity of the signal is directly proportional to the
concentration of the target protein or antibody in the
sample. A higher signal indicates a higher concentration of
the target.
• Compare the signal of your samples to a standard curve
generated using known concentrations of the target
protein or antibody. This allows you to determine the exact
concentration of the target in your sample.
• Typically, ELISA results are reported in units such as ng/mL
or IU/mL, depending on the type of assay.
 UNIT III
• Amino acids can be classified in various ways
based on their nutritional importance and
metabolic fate within the body. Two common
classifications are:
• Classification Based on Nutritional Importance:
– Essential Amino Acids: These are amino acids that
the body cannot synthesize on its own and must be
obtained through the diet. There are nine essential
amino acids for humans:
• Leucine
• Isoleucine
• Valine
• Threonine
• Methionine
• Phenylalanine
• Tryptophan
• Histidine
• Lysine
• Non-Essential Amino Acids: These are amino acids that the body
can synthesize internally, and dietary intake is not necessary.
However, under certain conditions, they may become
conditionally essential. Some examples include:
• Alanine
• Asparagine
• Aspartic Acid
• Glutamic Acid
• Serine
• Tyrosine
• Arginine (conditionally essential in some situations, such as during
growth)
• Classification Based on Metabolic Fate:
• Glucogenic Amino Acids: These amino acids can be
metabolized to produce glucose through various metabolic
pathways. They can enter the citric acid cycle (Krebs cycle) as
intermediates and be converted into glucose via
gluconeogenesis. Examples include:
– Alanine
– Serine
– Glycine
– Cysteine
– Threonine
– Tryptophan
– Glutamine
– Proline
– Histidine (partially)
– Methionine (partially)
• Ketogenic Amino Acids: These amino acids can be
metabolized to produce ketone bodies (acetoacetate and
beta-hydroxybutyrate) instead of glucose. Ketone bodies
are used as an energy source, especially during periods of
fasting or low carbohydrate intake. Examples include:
• Leucine
• Lysine
• Isoleucine
• Phenylalanine
• Tyrosine
• Tryptophan (partially)
• Both Glucogenic and Ketogenic Amino Acids: Some
amino acids can be both glucogenic and ketogenic, as
they can be converted into either glucose or ketone
bodies depending on the metabolic context. Examples
include:
• Threonine
• Tryptophan (partially)
• Isoleucine (partially)
• Phenylalanine (partially)
• Tyrosine (partially)
 Digestion,Absorption and Metabolism

Proteins are an essential component of the human

diet, and they play a crucial role in various
physiological processes in the body. The digestion,
absorption, and metabolism of proteins are
intricate processes that involve multiple organs
and enzymes. Disorders related to these processes
can have significant health implications. Here's an
overview of how proteins are digested, absorbed,
metabolized, and some related disorders:
• Digestion of Proteins:
• Protein digestion begins in the stomach, where the enzyme pepsin
is released in its inactive form, pepsinogen. When pepsinogen
comes into contact with the acidic environment of the stomach, it is
activated to pepsin. Pepsin breaks down proteins into smaller
peptides.
• The partially digested food then moves to the small intestine, where
pancreatic enzymes, including trypsin, chymotrypsin, and
carboxypeptidase, further break down the peptides into smaller
peptides and individual amino acids.
• Enzymes produced by the brush border of the small intestine, such
as aminopeptidases and dipeptidases, complete the digestion
process by breaking down peptides into free amino acids.
• Absorption of Amino Acids:
• Amino acids, the end products of protein digestion,
are absorbed in the small intestine.
• Active transport mechanisms and co-transport with
sodium ions facilitate the absorption of amino acids
across the intestinal epithelial cells into the
bloodstream.
• Once absorbed, amino acids are transported via the
portal vein to the liver and distributed throughout
the body for various metabolic processes.
• Metabolism of Amino Acids:
• Amino acids serve several metabolic roles in the body:
– They are used as building blocks for the synthesis of new
proteins (protein biosynthesis).
– They can be converted into glucose through
gluconeogenesis when needed for energy.
– Some amino acids can be converted into intermediates of
the citric acid cycle (Krebs cycle) for energy production.
– Amino acids can be used to synthesize important molecules
like neurotransmitters and hormones.
• The fate of amino acids depends on the body's
metabolic needs and the specific amino acids involved.
Various biologically important compounds

Amino acids are the building blocks of proteins,

but they also play crucial roles in the synthesis
of various biologically important compounds
beyond just proteins. Here are some of the key
compounds synthesized from various amino
acids:
• Neurotransmitters:
• Dopamine: Derived from the amino acid
tyrosine, dopamine is a neurotransmitter that
plays a role in mood regulation, reward, and
motor control.
• Serotonin: Synthesized from the amino acid
tryptophan, serotonin is involved in mood,
sleep, and appetite regulation.
• Hormones:
• Thyroid Hormones: Thyroxine (T4) and
triiodothyronine (T3) are thyroid hormones
synthesized from the amino acid tyrosine. They
regulate metabolism.
• Epinephrine and Norepinephrine: These
hormones, also known as adrenaline and
noradrenaline, are synthesized from tyrosine and
phenylalanine and play roles in the "fight or flight"
response.
• Nitric Oxide (NO):
– Nitric oxide is a signaling molecule synthesized
from the amino acid arginine. It is involved in
regulating blood vessel dilation,
neurotransmission, and the immune response.
• Glutathione:
– Glutathione is synthesized from the amino acids
glutamate, cysteine, and glycine. It acts as an
antioxidant and plays a critical role in
detoxification processes within cells.
• Creatine:
– Creatine is synthesized from the amino acids arginine,
glycine, and methionine. It plays a crucial role in
supplying energy for muscle contractions and is often
used as a supplement by athletes.
• Heme:
– Heme is a molecule synthesized from glycine and
succinyl-CoA, and it contains iron. It is a crucial
component of hemoglobin, myoglobin, and various
enzymes involved in oxygen transport and metabolism.
• Porphyrins:
– Porphyrins, including heme, are synthesized from
various amino acids and are essential components
of various proteins and enzymes, such as
cytochromes and chlorophyll.
• Melanin:
– Melanin is synthesized from the amino acid
tyrosine and is responsible for the pigmentation of
skin, hair, and eyes. It provides protection against
UV radiation.
• Catecholamines:
– Catecholamines, including epinephrine,
norepinephrine, and dopamine, are synthesized
from the amino acids phenylalanine and tyrosine.
They play roles in the sympathetic nervous system
and stress response.
• GABA (Gamma-Aminobutyric Acid):
– GABA is synthesized from the amino acid
glutamate and serves as the primary inhibitory
neurotransmitter in the central nervous system.
Inborn errors of amino acid metabolism, also known as
inborn errors of metabolism (IEM), are a group of rare
genetic disorders that affect the body's ability to process
and utilize amino acids properly. Amino acids are the
building blocks of proteins, and they play a crucial role in
various biological processes. In individuals with these
disorders, there is a deficiency or dysfunction in one of
the enzymes responsible for metabolizing specific amino
acids. This can lead to the accumulation of toxic
substances and the deficiency of essential compounds,
causing a wide range of symptoms and health problems.
There are many different inborn errors of amino acid
metabolism, each associated with a specific amino acid or
group of amino acids. Some of the well-known examples
include:
Phenylketonuria (PKU): In PKU, there is a deficiency of the
enzyme phenylalanine hydroxylase, which is responsible
for converting phenylalanine into tyrosine. As a result,
phenylalanine levels build up in the body, leading to
intellectual disabilities, developmental delays, and other
neurological problems if left untreated.
Maple Syrup Urine Disease (MSUD): MSUD
affects the metabolism of the branched-chain
amino acids leucine, isoleucine, and valine. It
can lead to neurological problems,
developmental delays, and the characteristic
sweet-smelling urine odor.
Homocystinuria: This disorder is characterized
by a buildup of homocysteine due to defects in
enzymes involved in its metabolism. It can lead
to eye problems, intellectual disabilities, and
cardiovascular issues.
Alkaptonuria: Alkaptonuria is caused by a
deficiency of the enzyme homogentisate
dioxygenase, which results in the accumulation
of homogentisic acid. This leads to darkening of
connective tissues and urine, among other
symptoms.
Tyrosinemia: Tyrosinemia refers to a group of
disorders involving the metabolism of tyrosine.
Tyrosinemia type I is the most severe form,
which, if untreated, can lead to liver and kidney
damage.
Cystinuria: This condition results in the excessive
excretion of cystine, which can lead to the
formation of kidney stones.
• The symptoms and severity of inborn errors of amino acid
metabolism can vary widely, depending on the specific enzyme
deficiency and the buildup of toxic metabolites. Early diagnosis
and management through dietary restrictions, enzyme
replacement therapies, or other interventions are essential to
mitigate the impact of these disorders.
• Treatment often involves special diets that limit the intake of
the amino acid in question or provide cofactors to support
enzyme function. Regular medical monitoring and management
are crucial to preventing complications and improving the
quality of life for individuals with these conditions.
Plasma proteins are a crucial component of the
blood and are primarily synthesized by the liver.
They serve various essential functions in the
body, including maintaining osmotic pressure,
transporting substances, contributing to
immune function, and serving as coagulation
factors. There are three main types of plasma
proteins: albumins, globulins, and fibrinogen.
• Albumins:
• Function: Albumins are the most abundant plasma
proteins and play a vital role in maintaining oncotic
pressure (osmotic pressure within blood vessels)
and regulating fluid balance. They also serve as
carriers for many substances, including hormones,
fatty acids, and drugs.
• Normal Value: The normal range for albumin levels
in the blood is typically between 3.5 to 5.0 grams
per deciliter (g/dL).
• Globulins:
• Function: Globulins encompass a diverse group
of proteins that include transport proteins,
enzymes, and immunoglobulins (antibodies).
They are essential for immune function, transport
of various molecules, and enzymatic activities.
• Normal Value: Globulin levels can vary widely but
generally fall within the range of 2.3 to 3.5 g/dL.
• Fibrinogen:
• Function: Fibrinogen is a clotting factor that plays
a crucial role in the blood clotting process. It is
converted into fibrin during blood coagulation,
forming a mesh-like structure that traps blood
cells to stop bleeding.
• Normal Value: Normal fibrinogen levels range
from 200 to 400 milligrams per deciliter (mg/dL).
• Proteinuria:
• Definition: Proteinuria is the presence of an abnormal
amount of protein in the urine. Normal urine usually
contains a small amount of protein, but significant
proteinuria may indicate an underlying health issue.
• Causes: a. Kidney Disease: Most commonly,
proteinuria is a sign of kidney damage or kidney
disease, which can be caused by conditions such as
glomerulonephritis, nephrotic syndrome, diabetic
nephropathy, or hypertension.
b. Infections: Infections in the urinary tract, like
urinary tract infections (UTIs), can lead to
temporary proteinuria.
c. Systemic Conditions: Conditions like systemic
lupus erythematosus (SLE) and multiple
myeloma can cause proteinuria.
d. Heavy Exercise: Vigorous exercise can
sometimes result in temporary proteinuria, but
it usually resolves on its own.
• Hypoproteinuria:
• Definition: Hypoproteinuria is the presence of a
lower-than-normal level of proteins in the blood,
particularly low levels of albumin and globulins.
• Causes: a. Malnutrition: Inadequate dietary
protein intake can lead to hypoproteinuria. b.
Liver Disease: Liver disorders can impair the
liver's ability to produce proteins, resulting in
hypoproteinuria.
c. Kidney Loss: Excessive loss of proteins through
the kidneys (e.g., in nephrotic syndrome) can
lead to low blood protein levels.
d. Malabsorption: Conditions that affect the
absorption of nutrients in the gastrointestinal
tract can result in hypoproteinuria.
• Hypergammaglobulinemia:
• Definition: Hypergammaglobulinemia is characterized by
elevated levels of gamma globulins (a type of
immunoglobulin) in the blood.
• Causes: a. Autoimmune Diseases: Conditions like
systemic lupus erythematosus (SLE), rheumatoid
arthritis, and Sjögren's syndrome can cause
hypergammaglobulinemia.
• b. Chronic Infections: Some chronic infections, such as
tuberculosis and chronic viral hepatitis, can lead to
elevated gamma globulin levels.
c. Monoclonal Gammopathy: Conditions like multiple
myeloma or Waldenström macroglobulinemia can cause
the overproduction of a specific type of immunoglobulin,
leading to hypergammaglobulinemia.
d. Chronic Inflammatory Disorders: Chronic inflammatory
conditions like sarcoidosis and chronic granulomatous
diseases may result in increased gamma globulin
production.
e. Allergies: Allergic reactions and asthma can sometimes
lead to temporary elevations in gamma globulin levels.
 principle
Electrophoresis is a general term that
describes the migration and separation of
charged particles (ions) under the influence of
an electric field. An electrophoretic system
consists of two electrodes of opposite charge
(anode, cathode), connected by a conducting
medium called an electrolyte.
• Protein Electrophoresis:
• Normal Pattern: In serum protein electrophoresis, a normal
pattern typically shows five main protein fractions: albumin,
alpha-1 globulins, alpha-2 globulins, beta globulins, and
gamma globulins. The proportions and positions of these
fractions are fairly consistent in healthy individuals.
• Abnormal Pattern: Abnormal protein electrophoresis
patterns can indicate various medical conditions, such as
multiple myeloma (a spike in the gamma globulin region),
liver disease (altered albumin/globulin ratios), or
inflammation (elevated alpha globulins).
• RNA Electrophoresis:
• Normal Pattern: In DNA electrophoresis, the normal
pattern depends on the purpose of the analysis. In agarose
gel electrophoresis for DNA, a ladder-like pattern of DNA
fragments of known sizes is typically used as a reference. A
normal DNA ladder shows well-separated, distinct bands.
• Abnormal Pattern: Abnormal DNA electrophoresis
patterns may include smearing, which can result from DNA
degradation or contamination. In genetic testing, the
presence of specific DNA fragments may indicate genetic
mutations.
• RNA Electrophoresis:
• Normal Pattern: For RNA electrophoresis, normal
patterns depend on the RNA sample's purpose. In
denaturing agarose or polyacrylamide gels, distinct
bands of ribosomal RNA (rRNA) and messenger RNA
(mRNA) are typically observed.
• Abnormal Pattern: Abnormal RNA electrophoresis
patterns may show degradation or the presence of
unexpected RNA species, indicating issues with RNA
quality or processing.
• Hemoglobin Electrophoresis:
• Normal Pattern: Hemoglobin electrophoresis is
used to separate different types of hemoglobin. A
normal pattern shows distinct bands for
hemoglobin A, A2, and F, with the majority being
hemoglobin A in adults.
• Abnormal Pattern: Abnormal patterns can indicate
various hemoglobinopathies, such as sickle cell
anemia (presence of hemoglobin S) or thalassemia
(altered ratios of A and A2).
Pyruvate, a product of glycolysis, enters the
Krebs cycle (also known as the citric acid cycle or
the tricarboxylic acid cycle) through a series of
enzymatic reactions. The Krebs cycle takes place
in the mitochondria and is a crucial part of
cellular respiration, where pyruvate is fully
oxidized to produce carbon dioxide, high-energy
electrons, and ATP. Here are the steps involved
in the entry of pyruvate into the Krebs cycle:
• Conversion to Acetyl-CoA:
• In the cytoplasm, pyruvate is first converted to
acetyl-CoA in a reaction catalyzed by the enzyme
pyruvate dehydrogenase complex (PDH complex).
This complex consists of several enzymes and
cofactors.
• During this process, pyruvate loses a carbon dioxide
molecule and releases a high-energy electron in the
form of NADH. Acetyl-CoA is produced as a two-
carbon molecule attached to coenzyme A (CoA).
• Entry into the Krebs Cycle:
– Acetyl-CoA is transported into the mitochondria,
where the Krebs cycle takes place.
• Combining with Oxaloacetate:
– Acetyl-CoA combines with oxaloacetate, a four-
carbon compound, to form citrate, a six-carbon
compound, in a reaction catalyzed by the enzyme
citrate synthase.