Principles of Nutrition: Food Sources, Energy Requirements and Metabolism

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1-Principals of Nutrition
Food is necessary to normal life, and provides the body with energy
for its physiological functions. The oxidation of carbohydrates, lipids
and proteins leads to the generation of high energy bonds in ATP
(adenosine tri phosphate), the energy currency of the cell. In addition
some of these oxidative products are used to generate the
carbohydrates, lipids and proteins of which the body is composed.
Adequate diet
* It is the diet which is essential for normal growth ,
maintenance of life and reproduction.
* It must supply essential nutrients as vitamins, essential amino
acids and essential fatty acids.
* It must contain :-
1- Carbohydrates 2- Lipids
3- Proteins 4- Vitamins
5- Minerals 6- Water
Energy Requirements
The energy requirement for a 70-kg adult male is 2300- 3100 Kcal,
while it is 1600- 2400 kcal for a female
Energy content of different food sources:
Carbohydrates----------------------- 4.1 Kcal/gm
Lipid ----------------------- 9.3 Kcal/gm
Proteins ----------------------- 4.1 Kcal/gm

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Introduction to metabolism
The functions of cells and tissues in all organisms require :
1) Energy which is obtained from digestion and degradation of
food (carbohydrates, lipids and proteins)
2) Synthesis of complex molecules for building of new structures
Metabolism is the process by which the human body can liberate
stored energy from food and synthesize complex molecules from
simpler one and to degrade and get rid of waste and toxic molecules.
Metabolic pathways
A- Catabolic pathways .........that generate energy
B- Anabolic pathways...........that use energy to synthesize
important molecules
C- Amphibolic pathways ......that are both anabolic and catabolic

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Importance of Carbohydrate
1- Carbohydrates are the principal source of energy in human.
2- They are components of nucleic acids and linked with lipids
(glycolipids) and proteins ( glycoproteins).
3-Some insoluble carbohydrates enter in structure of connective
tissue.
4- Some carbohydrate lubricate skeletal joints as hyaluronic acid.
Chemical structure of Carbohydrates
Carbohydrates are organic compounds composed of Carbon ,
Hydrogen and Oxygen ( carbo = carbon , hydrates = hydrogen and
oxygen in their proportion in water H2O ).
Classification of Carbohydrates
Chemistry and metabolism
of Carbohydrate
Carbohydrates
Monosaccharides Disaccharides Polysaccharides
pentoses Hexoses

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They are simple sugar units , cannot be hydrolyzed into other sugars.
They include :
s
Pentose
-
A
( penta =5) sugars that contain 5 carbons . They are present in fruits
and can be formed in the body .
* Ribose is present in structure of RNA (ribonucleic acid) and ATP
( energy currency of the cell)
* Deoxyribose is present in structure of DNA
(deoxyribonucleic acid )
Hexoses
–
B
( hexa = 6) sugars that contain 6 carbons.
*Glucose (dextrose) is the major sugar in blood , it is present in
fruits and honey
Fructose is very sweet , and present in fruits.
*
Galactose is present in milk , glycolipids and glycoproteins.
*
ٌٌ
Glucose Ribose
1- Monosaccharides

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Disaccharides consist of two monosaccharides joined by a
glucosidic bond.
1- Maltose
* It is called malt sugar , it is found in malt.
* It is formed of two glucose units.
* It is formed by hydrolysis of starch by amylase enzyme.
* It is a fermentable sugar.
Glucose
Glucose
2- Sucrose
* It is called cane sugar (table sugar) .
* It is formed of glucose and fructose.
* It is fermentable
Glucose Fructose
3- lactose
It is the milk sugar
*
It is formed of galactose and glucose .
*
It is synthesized by mammary gland during lactation.
*
* Lactose is considered the best food for infant due to :-
2-Disaccharides

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1- It is the least sweet, so the infant can take large amounts of it.
2- It is non fermentable , so it does not cause abdominal
distention or colic.
3-It is laxative, so it prevents the incidence of constipation.
Polysaccharides contain more than 10 units of monosaccharides.
Glucosans Fructosans
formed of glucose units formed of fructose units
as: starch , glycogen , dextran as; inulin
dextrins and cellulose
1- Starch
* It is the storage form of carbohydrates in plants (never present in
animals).
* It is a branched chain formed of glucose units linked by α 1— 4
glucosidic bond ( a bond between carbon one of one glucose unit and
carbon four of the adjacent glucose unit ) while at the branch point ,
it forms α 1— 6 glucosidic bond . * Starch gives blue color with iodine
.
α1- 4 glycosidic bond glucose units
Branch point α 1—6 glycosidic bond
The branched structure of glycog
Polysaccharides

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2- Glycogen
* It is the animal equivalent of starch in plants and function as the
main storage polysaccharide in human liver and muscles.
* Glycogen is formed of glucose units liked by α 1— 4 glucosidic bonds
in the main chain and α 1— 6 at the branching points. It is more
extensively branched than starch.
* In muscles , it serves as energy reserve for muscle contraction, while
liver glycogen supplies glucose to other tissues through blood.
* Glycogen gives a pink color with iodine.
.
3- Cellulose
*It is the main structural molecules in cell walls of plants .
*It a glucosan formed of β 1— 4 glucosidic bonds.
* It is a straight chain , not branched so it is fibrous , tough and
insoluble in water.
* Cellulose can not be digested by gastrointestinal enzymes of
human and carnivorous animals as the β1— 4 bonds are not
hydrolyzed by amylase ( The only vertebrates able to use
cellulose as source of energy are cattle ,rabbits , sheep, goats and
camel i.e herbivorous animals).
* Cellulose pectin and lignin are present in cell walls of plants
and called Dietary fibers that have very important role in diet :
1- They add bulk to stool , so stimulate intestinal wall and prevent
constipation.
2- They also can absorb 5-10 times as their own weight water , that is
drained into intestinal lumen increasing bowel movement .
3- They bind to toxic compounds present in diet decreasing their
absorption, so they protect against colon cancer.
Average need of dietary fibers is 25-35 gm /day and are present in
cereals, bread , fruits and vegetables.

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In the mouth digestion of starch and glycogen begins during mastication
under the effect of salivary amylase. They are converted to dextrins and
maltose
Salivary amylase
Starch and Glycogen Dextrins + Maltose
pH 6-8
In the stomach the action of salivary amylase stops due to the acidic
medium because the enzyme needs alkaline medium.
In the duodenum starch and glycogen digestion is completed by the action
of : pancreatic amylase , maltase and disaccharidases ( found in the brush
border of intestinal cells ). Finally monosaccharides are obtained.
Pancreatic amylase
Starch + Dextrins Maltose
pH 7
Maltase
Maltose 2 Glucose
Sucrase
Sucrose Glucose + Fructose
Lactase
Lactose Glucose + Galactose
Lactose intolerance
This condition is due to deficiency of lactase enzyme . It may be:
Congenital (Primary) in some people due to genetic defect of the enzyme
Acquired ( secondary ) to gastroenteritis especially in children due to
loss of the brush border of intestinal cells by infectious agents.
In this condition , Lactose accumulates in the lumen of the small intestine .
The osmotic effect of the unabsorbed lactose leads to influx of water in the
Digestion of Carbohydrate

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small intestine . So the clinical symptoms are : intestinal distention ,
nausea , colic, and watery diarrhea.
Absorption of Carbohydrates
The end products of carbohydrate digestion are :
Glucose , Fructose and Galactose
They are absorbed as monosaccharides
1- Facilitated transport
This method of absorption requires specific protein carriers called
glucose transporter proteins GLUT. They combine with glucose and
facilitate its entry into the cell. . These carriers are either insulin- dependant
or insulin – independent. Fructose also is absorbed by this method.
2- Active transport
Glucose and galactose are transported by this method . They are absorbed
against a concentration gradient ( from lower concentration to higher
concentration) , so need energy and carrier protein.
Fate of absorbed sugars
The absorbed sugars pass from intestine to the liver through portal
circulation . In the liver galactose and fructose are converted into glucose.
The liver acts as a blood glucostat i.e It converts excess absorbed glucose
into stored glycogen and reconverts the stores to glucose during starvation
to maintain adequate level of glucose in blood.
Uptake of glucose by peripheral cells
Glucose is absorbed from blood by peripheral body cells by glucose
transport proteins GLUT , that are insulin-dependant or insulin-
independent , as mentioned before . Insulin-independent uptake of glucose
occurs in : Brain , RBC, Liver cells, Renal medulla , Cornea , Lens and
Retina..

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Metabolic fate of glucose
Glycolysis means breakdown of glucose . It occurs in cytoplasm (cytosol)
of all body cells either in presence of oxygen ( aerobic) or in absence of
oxygen ( anaerobic). It results in breakdown of the six-carbon atom of
glucose into two molecules of pyruvate with 3 carbons and 2 ATP
( adenosine triphosphate , the energy currency of the cell)
HMP pathway for
synthesis of pentoses
Glucose
Glycolysis & TCA cycle
to produce energy
Glycogenesis
to form glycogen
Synthesis of other carbohydrates:
* Fructose in semen
* Galactose for lactose synthesis
Provides acetyl CoA for synthesis of:
Fatty acids
Cholesterol
Glycerol
Ketone bodies and steroids
Non essential amino acids
Glycolysis

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Under aerobic conditions glycolysis is considered as a preparatory
pathway for complete oxidation of glucose into CO2 and H2O in TCA
cycle (Kreb’s cycle) in mitochondria to produce ATP .
Under anaerobic conditions , as in case of
-absence of mitochondria , in RBC or
- non functioning mitochondria due to decreased blood supply and oxygen
cornea, lens, retina, renal medulla and during stressful muscular exercise.
Glycolysis is considered the main source of ATP with production of lactic
acid
2 ATP 2 pyruvate 2 NADH+2H2
Glycolysis under Aerobic conditions
Pyruvate will enter the mitochondria to be converted to Acetyl-CoA ,which
enter Kreb’s cycle . 2 NADH(nicotinamide dinucleotide) enter the
respiratory chain in mitochondria to produce 3 ATP for each NADH
molecule ( 6 ATP) . So the overall energy is 8 ATP.
End products of glycolysis

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Glycolysis under Anaerobic glycolysis
In this condition , the mitochondrial fate of pyruvate and NADH is absent
so, the net energy produced is only 2 ATP only .
The tricarboxylic acid cycle is also called citric acid cycle or Kreb’s
cycle. It is the final common pathway for oxidation of carbohydrates,
lipid and proteins because their oxidation give Acetyl-CoA.
All enzymes of the cycle are located in the mitochondria.
Functions of Citric acid cycle
TCA cycle is amphibolic : serves both catabolic ( provides energy,
ATP) and anabolic ( synthesis of important substances), So its
functions include:
1-It provides ATP .
2-It provides citrate that is the precursor for synthesis of fatty
acids.
3-Synthesis of non essential amino acids
4- TCA cycle shares in gluconeogenesis. Gluconeogenesis is
synthesis of glucose from non carbohydrate sources .
5- It gives the precursors for Heme synthesis , that is an important
part of hemoglobin
Tricarboxylic Acid Cycle
(TCA cycle)

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NADH+H & FADH2 ( flavinamide dinucleotide ) will enter the
respiratory chain in mitochondria to produce ATP
One NADH+H 3ATP
One FADH2 2ATP
3 NAD (3 ×3ATP)+ 1 FAD( 2ATP)+ 1GTP 12 ATP So
one molecule of Acetyl-Co oxidation in TCA cycle will give 12 ATP

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Glycogen is the storage form of carbohydrates in mammals. It is
stored in cytoplasm as granules in all body cells, but it is specially
abundant in liver and skeletal muscles .
Liver Glycogen is responsible for maintaining blood glucose level
during fasting and during sleep.
Muscle glycogen is responsible for providing glucose as a fuel for
anaerobic glycolysis during muscle contraction.
Glycogenesis = glycogen synthesis from glucose units during well
fed condition .
Glycogenolysis = glycogen breakdown to give glucose during fasting
‫الصيام‬.
.
This is an anabolic pathway occurs in cytoplasm to form very
important substances. It is active in cells which has a high rate of
nucleic acid synthesis ( rapidly dividing tissues as bone marrow,
skin and gastric mucosa)
or which utilizes NADPH ( nicotinamide dinucleotide phosphate, a
reducing agent ) in large amounts as liver . adipose tissue and
lactating mammary gland
The regulating enzyme of this pathway is:
glucose -6 phosphate dehydrogenase (G6PD).
Glycogenolysis and glycogenesis are separate pathways and
reciprocally regulated by regulating their main enzymes . So
when glycogenolysis is activated, glycogenesis is inhibited and
vise versa .
Pentose phosphate pathway
Glycogenesis & Glycogenolysis

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Importance of Pentose phosphate pathway:
1- It is the only source of pentoses (5C sugars ) used for :
* nucleic acid synthesis DNA and RNA.
* Coenzymes as NAD ( nucotinamide dinucleotide )
* FAD (flavinamide dinucleotide )
* ATP ( adenosine triphosphate ) the energy currency of the cell.
2-It is the major source of NADPH ( a reducing agent ) used for :
* synthesis of fatty acids, cholesterol and catecholamines.
*Keeping the erythrocyte membrane integrity against oxidizing
agents ( with the help of glutathione ).
- It is is deficiency of glucose 6- phosphate dehydrogenase enzyme .
- It is X- linked disease : transferred from carrier mother to her boys
only but girls do not suffer .
- Deficiency of this enzyme leads to decreased rate of Pentose
phosphate pathway with decreased concentration of NADPH required
for integrity of RBC membrane .
- The deficiency is manifested only after intake of certain oxidant ‫مواد‬
‫مؤكسدة‬ drugs like antimalarial drugs , sulfa drugs or ingestion of
fava beans .
- The clinical picture include hemolytic anemia , jaundice and black
urine. ttt : blood transfusion .
Gluconeogenesis is the metabolic process by which glucose is
synthesized from non carbohydrate precursors as lactic acid , amino
acids, glycerol and propionyl CoA.
It occurs mainly in the liver and kidney.
Conditions characterized by active gluconeogenesis:
1-Prolonged fasting and starvation .
2-Periods of intense exercise.
3-With cortisone therapy & Cushing ’s syndrome ( high cortisone ). .
Gluconeogenesis
Favism ‫الفولية‬ ‫مرض‬

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In normal persons , fasting blood glucose level is 70 -110 mg %.
Fasting state means estimation of glucose after an overnight fast of
8- 12 hours.
Following a meal , the blood glucose rises rapidly by about 30-50 mg
% but return to fasting level where it remains until the next meal,
then this pattern is repeated.
Hyperglycemic Factors Hypoglycemic factors
↑ glucose ↓ glucose
Absorption from GIT Glycolysis
Glycogenolysis
glycogenesis
Gluconeogenesis
Hyperglycemic Hormones Hypoglycemic hormones
(Glucagons, adrenaline, ( Insulin )
Cortisol, growth hormone)
The maintenance of stable blood glucose level is one of the finely
regulated mechanisms under the control of the following:
1-The liver ,
2-The kidney
3-Hormones.
1-The Liver
The liver is the principal organ of glucose regulation . It stores
glucose
as glycogen after meals in the post –absorptive state and releases it in
the blood between meals . During fasting more than 90% of glucose
is derived from liver glycogenolysis and gluconeogenesis ( from
lactate , glycerol and alanine) and the remainder from kidney
gluconeogenesis.
Regulation of Blood
glucose
Blood glucose

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2- The kidney
Glucose is continuously filtered by the kidney glomeruli and
returned completely to the blood by the renal tubules. The
capacity of kidney tubules to reabsorb glucose is limited , so when
blood glucose is elevated above a certain limit called renal
threshold , glucose will pass in urine producing glucosuria . Renal
threshold for glucose is 180 mg %.
3- Hormones
Different hormones are involved in regulation of blood glucose .
They include Insulin and Anti-insulin hormones
* Insulin
Insulin is secreted from the β cells of pancreas in response to
hyperglycemia Insulin decreases blood sugar by :
↑ glucose transport into the cells
↑ utilization of glucose by activating glycolysis
↑ glycogensis
↓ glycogenolysis
↓ gluconeogenesis
* Anti- Insulin hormones
Hypoglycemia induces secretion of Epinephrine, glucagons ,
glucocorticoids
Hypoglycemia induces secretion of Epinephrine, glucagons , glucocorticoids
glucagon epinephrine glucocorticoids
secreted from α cells of pancreas secreted from adrenal medulla secreted from
↑ glycogenolysis in liver in response to stress adrenal cortex
↓ glycogenesis ↑ liver and muscle glycogenolysis ↑ gluconeogenesis
↑ glucoeogenesis
↓ glycolysis

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It is the presence of glucose in urine which can be detected by
Beneddict ‫ۥ‬s test or glucose strips. Glucosuria could be due to:
1- Diabetic glucosuria
Diabetic hyperglycemia is the most common cause of glucosuria.
Blood glucose exceeds the renal threshold so glucose will pass in
urine.
2- Alimentary glucosuria
It is a benign type of glucosuria due to ingestion of high carbohydrate
diet . Glucose is rapidly absorbed from the intestine with increasing
blood glucose above the renal threshold resulting in glucosuria.
3- Renal glucosuria
This occurs due to defect in renal tubular absorption mechanisms of
glucose due to diseases of the kidney as glomerulonephritis .
4-Gestational glucosuria
This may occur during pregnancy.
5- Transient ( emotional ) glucosuria
It occurs in some people due to emotional stress that induces
secretion of catecholamines .Once stress is removed ,glucosuria
disappears.
Glucosuria

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Diabetes Mellitus
Definition: metabolic disorder characterized by hyperglycemia due to
an absolute or relative lack of insulin or to a cellular resistance to
insulin
Major classifications
1. Type 1 Diabetes
2. Type 2 Diabetes
Diabetes Type 1
Definition
1. Metabolic condition in which the beta cells of pancreas no
longer produce insulin; characterized by hyperglycemia,
breakdown of body fats and protein and ketosis
2. Accounts for 5 – 10 % of cases of diabetes; most often occurs in
childhood or adolescence
3. Called Juvenile-onset diabetes or insulin-dependent diabetes
(IDDM)
Etiology
Autoimmune reaction in which the beta cells that produce
insulin are destroyed
Risk Factors
1. Genetic susceptibility
2. Viral infections
3. Chemical toxins
Diabetes Type 2
Definition: condition of hyperglycemia occurring despite
availability of body’s own insulin
Known as non-insulin dependent diabetes or adult onset
diabetes
Etiology:
1. Insufficient insulin to lower blood glucose
2. Cellular resistance to insulin

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Risk factors:
1. History of diabetes in parents
2. Obesity
3. Physical inactivity
5. Women: history of gestational diabetes
6. Hypertension
Clinical picture:
Hyperglycemia leads to:
a. Polyuria
b. Glycosuria
c. Polydipsia
d. Polyphagia
e. Weight loss
Treatment:
Type 1:
Insulin therapy
Type 2:
Physical exercise
Diet
Weight loss
Insulin therapy

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Biological lipids are a wide group of compounds characterized by
their insolubility in water and solubility in non polar solvents as ether,
chloroform and benzene.
-
Physiological Importance of lipids include :
1- Triacylglycerol are the stored form of lipids in the body .
2- Phospholipids are major structural elements of biological
membranes.
3- Lipoproteins are important constituents of cell membrane and help
in transporting lipids in blood.
4- Other lipids as steroids act as hormones ( cortisone,
estrogen and testosterone )
5- Lipids in subcutaneous fat provide insulation against external
temperature.
Classification of lipids
Triacylglycerols phospholipids Fatty acids
Waxes Glycolipids Glycerol
Lipoproteins Steroids
Ketone bodies
Fat soluble vitamins
Lipid Chemistry
and Metabolism
Simple lipids Complex lipids Precursor & Derived
lipids

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Fatty Acids
Fatty acids ( F A ) contain one COOH carboxyl group , with a
hydrocarbon chain having different chain length :
CH3– (CH2) n- COOH
- Short chain fatty acids (2-6 carbons)
- Medium chain fatty acids (8-14 carbons )
- Long chain fatty acids ( 16 carbons and above)
The hydrocarbon chain can be fully saturated without double bond
.These are solid at room temperature. Or unsaturated , with one
(monounsaturated ) or more double bonds (polyunsaturated). They
are liquid at room temperature.
*Examples of saturated fatty acids are:
Palmitic acid is saturated with 16 carbon atoms.
Stearic acid is saturated with 18 carbon atoms.
Arachidic acid is saturated with 20 carbon atoms.
* Examples of unsaturated fatty acids:
Oleic acid has 18 carbon atoms with one double bond .
Linoleic acid has 18 carbon atoms with 2 double bonds.
Linolinic acid has 18 carbon atoms with 3 double bonds.
Arachidonic acid has 20 carbon atoms with 4 double bonds.
*Essential Fatty acids
Linoleic, linolenic and arachidonic are called Essential Fatty Acids
because human body can introduce a double bond at carbon 4,5,6
until the 9 position but never beyond C9, so they must be supplied in
diet.
9 8 7 1
CH3 – CH2 – CH2 – CH2 – CH2 – CH2 – C H2 – C H2 – (C H2)6– COOH
Introduction of double bonds Double bond can be introduced

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Does not occur in human in human in this region
Importance of essential fatty acids:
1-They are required for growth and health especially in children.
2-They form esters with cholesterol thus preventing its
precipitation in blood vessels and atherosclerosis.
3-They enter in structure of cell membranes.
4-Arachidonic acid is the precursor for important compounds, such
as prostaglandins, thromboxanes and leukotriens.
These are esters (salts) of fatty acids with various alcohols, They
include:-
Triacylglycerols (TAG)
* Esters of three (tri ) fatty acids with glycerol .
* They represent the storage form of lipids in subcutaneous tissue
and abdominal cavity, that are used as a fuel during starvation .
* Triacylglycerols containing the same kind of fatty acids combined
with glycerol are called simple TAG , e.g tripalmitin and tristearin.
Mixed TAG contain 2 or more type of fatty acid e.g 1-stearyl,2-
linoleyl3- palmityl glycerol.
* Most natural fats are mixtures of simple and mixed TAG having
fatty acids of different chain length and number of double bonds
1-Simple Lipids

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* TAG of vegetable oils (corn and olive oils) are rich in unsaturated
fatty acids and so, are liquid at room temperature. They are converted
industrially into solid fat (artificial butter ) by catalytic hydrogenation
which reduce their double bonds . TAG containing only saturated FA
are solid at room temperature.
* As stored Fuel, TAG have advantages over glycogen because their
oxidation produce more than twice the energy produced by
oxidation of glycogen n. Moreover, the body can store larger amounts
of TAG than glycogen .
Phospholipids
-
A
These are lipids containing Phosphorus
*
* They are formed of Glycerol with 2 fatty acids joined at carbon
1 and 2 with an ester linkages .
* Carbon 3 of glycerol is connected to a phosphate group ,that in turn
is joined to a nitrogenous base that may be ; choline, serine,
ethanolamine or inositol .
Examples :
1-Lecithin
It is composed of glycerol, one saturated F A , one
unsaturated FA , Phosphate and choline. It is present in cell
membrane. Phospholipase A2 is an enzyme present in some snake
G
L
Y
C
E
R
O
L
Fatty Acid
Fatty Acid
4
PO Nitrogenous base
2- Complex lipids

- 26 -
venoms, acting on lecithin present in cell membrane of RBCs
removing one FA so lysolecithin is produced . Cell membrane
becomes fragile and hemolysis of RBCs will occur.
2-Dipalmitolyl lecithin ( Lung surfactant )
It is lecithin containing 2 palmitic acids . It is normally lining the
lung alveoli , preventing adherence due to surface tension. Its
absence from lungs of premature infants causes respiratory distress
syndrome
3-Cephalins
They are phospholipids contain serine and ethanolamine as
nitrogenous bases. They are present in cell membranes.
4-Plasmalogen
It is a platelet activating factor that stimulate platelet aggregation.
Glycolipids
-
B
These are lipids containing sugar units ( glucose , galactose ).
They are widely distributed in every tissue of the body particularly in
nervous tissue and brain e.g cerebrosides and gangliosided.
s
Lipoprotein
-
C
*Lipoproteins are complexes of proteins and lipids which transport
lipids in the blood. All plasma lipoproteins contain phospholipids
and different types of proteins ,which are characteristic for each
lipoprotein.
* Plasma lipoproteins can be separated by electrophoresis and
ultracentrifugation into the following classes:
1- Chylomicrons
2-Very low density lipoproteins (VLDL)
3- Low density lipoproteins (LDL)
4- High density lipoproteins (HDL)

- 27 -
Derived lipids include substances derived from lipids by hydrolysis;
as fatty acids and alcohols ( glycerol & sphingosine ).
Precursor lipids
They include :
1- Steroids
2- Fat soluble vitamins: Vitamin A, D ,E and K.
They are compounds having 17 carbon steroid nucleus, which
consists of four fused rings. They include:
1-Cholesterol
* Cholesterol is the main steroid in animal tissues.
* Cholesterol is synthesized in all cells of human body.
* Dietary cholesterol is derived from food of animal origin as
eggs and meat.
* Cholesterol has several functions:
a- It is involved in membrane structure .
b- It is the precursor of steroid hormones and bile acids.
c- It is converted to 7- dehydrocholesterol , that is present in
subcutaneous tissue . It is converted to Vitamin D by the effect of
ultraviolet rays of sunlight.
Precursor & Derived lipids
Steroids

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2-Steroid hormones
Steroid hormones are divided into 2 classes: the sex hormones and
the adrenal hormones. They are all synthesized from cholesterol and
differ in structure and function.
Sex hormones
Male sex hormones Female sex hormones
Testerone Estrogen & Progesterone
secreted by the testis and involved Estrogen is secreted from the
in development of secondary ♂ ovaries and involved in seco-
sex characters ndary ♀ sex characters
Progesterone is secreted from
corpus luteum, and involved
in preparing the uterus for
implantation of fertilized
ovum.
Adrenal hormones
Glucocorticoids Mineralocorticoids
Cortisol, cortisone and Aldosterone
Corticosterone
They play important role in They are required for
Carbohydrate, protein and normal Na+
and K+
Lipid metabolism. Balanc
3-Bile acids
* They are 24- carbon steroid compounds synthesized in the liver.
* They act as detergent in the intestine emulsifying dietary fat to
make them easily digestible.

- 29 -
* They also help in absorption of lipids and fat soluble vitamins.
Lipid Digestion and absorption
Lipids present in the diet include, triacylglycerol ,cholesterol,
phospholipids, essential fatty acids and lipid soluble vitamins. The
insolubility in water is a problem in digestion and absorption which
could be solved by bile secretion.
The more polar products form mixed micelles of free fatty acids, 2-
monoacylglycerol, cholesterol & bile acids approach the brush border
membrane of the intestinal mucosa for absorption (bile acids pass on
to the ileum for absorption).Once in mucosa cells fatty acids and
monoglyceride are recombined to form triacylglycerol.
Triacylglycerol + cholesterol + phospholipid + proteins form a
lipoprotein complex called a chylomicron

- 30 -
*Fatty acids are synthesized in the cytoplasm of cells in many tissues
including, liver , kidney, brain , lung , mammary gland and adipose
tissue.
*Fatty acids are synthesized from Acetyl-Co obtained from
carbohydrates to produce palmitic fatty acid (16 carbon) . Then all
other fatty acids are made by modification of palmtic acid.
*Insulin stimulates fatty acid synthesis by causing induction of
genes of the enzymes responsible for fatty acid synthesis.
Fatty acids act as source of energy in liver , skeletal muscles and
heart during periods of fasting . Palmitic acid needs seven cycles of β
oxidation which gives rise to 8 acetyl CoA , NADH and FADH2 .
Every acetyl-CoA when oxidized in TCA cycle gives ATP. Also
NADH and FADH2 enter TCA cycle to give ATP when oxidized in
electron transport chain. This oxidation occurs in mitochondria and
gives a large number of ATP . The net energy produced from palmitic
acid oxidation is 129 ATP.
Fatty acid synthesis
Fatty acid oxidation

- 31 -
Acetyl CoA produced by oxidation of fatty acids in liver
mitochondria has many fates :
1- Oxidation in TCA cycle
2- Synthesis of Ketone bodies ( Ketogenesis)
Ketogenesis is the synthesis of ketone bodies in the liver
mitochondria from acetyl –CoA. They include:
1-Acetoacetic Acid
2- Β- Hydroxybutyric acid
3- Acetone
Ketone bodies synthesized in the liver are transported to other tissues
(skeletal muscles , heart, kidney and brain ) .
Ketone bodies are oxidized in TCA cycle in the mitochondria of these
tissues to produce energy.
Ketone bodies are products of normal metabolism of fatty acid
oxidation and serve as source of energy in certain tissues as brain ,
heart , kidney and muscles.
Normally their serum concentration is less than 0.1 mg / dl .
Their level in blood depends on the rate of their production and the
rate of their utilization. When production of ketone bodies exceeds
their utilization , their level in blood increases resulting in ketonemia
Metabolism of Ketone Bodies
Ketogenesis
Ketolysis
Ketosis

- 32 -
and their excretion in urine Ketonuria and this condition is called
Ketosis. This occurs in :
1- Uncontrolled diabetes mellitus
2- Starvation
During starvation and diabetes , Insulin ↓ and glucagon ↑ .
Glucagon stimulates lipolysis and oxidation of fatty acids, so
acetyle-CoA increases and ketogenesis increases exceeding ketolysis.
Lipogenesis = esertification of three fatty acids with the alcohol
glycerol to form triacylglycerol ( tri = 3 , acyl = fatty acid ) TAG.
This occurs in liver and adipose tissues. The liver synthesizes TAG,
partly from glucose and from free fatty acids in excess of its needs.
TAG are stored in fat cells in adipose tissue .
Lipolysis = hydrolysis of TAG into glycerol and three fatty acids
during fasting to release fatty acids for energy production.
Insulin stimulates lipogenesis and inhibits lipolysis .
Lipogenesis And Lipolysis

- 33 -
Anti- insulin hormones (glucagons, catecholamines and growth
hormone ) stimulate lipolysis by activating hormone sensitive
lipase.
During the well fed state lipogenesis is activated
During fasting lipolysis is activated

- 34 -
There are two distinct lipid transport pathways:
* Exogenous pathway (transports dietary lipid absorbed from the
food to the tissues).
* Endogenous pathway (transports lipids synthesized in the liver
to the tissues). Lipids are insoluble in aqueous solutions but still
have to be transported around the body. The insoluble lipids are
transported in association with various proteins (apolipoproteins)
as lipoprotein complexes. There are 4 main classes of lipoprotein
that differ in their:
* Density (protein is denser than lipid so the more protein present
the higher the density)
* Composition (different lipoproteins contain different proportions
of protein, triacylglycerol, phospholipids and cholesterol)
* Size * Function
General structure of lipoproteins: lipoproteins have a central
hydrophobic core of TAG and cholesterolesters. The outer layer
contains more polar lipids ,Phospholipids and free cholesterol and
the protein ( apoproteins).
Lipid transport - Lipoproteins

- 35 -
Plasma lipoproteins include :
1 – Chylomicrones
2- Very low density lipoproteins ( VLDL)
3- Intermediate density lipoproteins (IDL)
4-Low density lipoproteins (LDL)
5- High density lipoproteins (HDL)
Chylomicrons
Chylomicrons are the largest (1000 nm) and least dense of the
lipoproteins. Chylomicrons are produced for the purpose of
transporting dietary triglycerides and cholesterol absorbed by
intestinal epithelia. Chylomicron assembly originates in the intestinal
mucosa. Excretion into the plasma is facilitated through the
lymphatic system.. Once transported to tissues, triglycerides
contained in chylomicrons are hydrolyzed by lipoprotein lipase
contained on the endothelial cell walls. The chylomicron remnant,
including residual cholesterol, is taken up by the liver.
Very Low Density Lipoproteins (VLDL)
Very low density lipoproteins are the next step down from
chylomicrons in terms of size and lipid content. VLDL assembly in
the liver involves the early association of lipids with apo-B100 .
Lipoprotein lipase also removes triglycerides from VLDL in the
same way as from chylomicrons.
Intermediate Density Lipoproteins (IDL)
Intermediate density lipoproteins are smaller than VLDL (40 nm)
and more dense (. They contain the same apolipoproteins as VLDL.
IDLs are derived from VLDL. IDLs can be taken up by the liver for
reprocessing, or upon further triglyceride depletion, become LDL.

- 36 -
Low Density Lipoproteins (LDL) and Lipoprotein(a)
Low density lipoproteins are smaller than IDL and more dense .They
contain the apolipoprotein apo-B100.
LDL is the main transporter of cholesterol and cholesteryl esters
from liver to peripheral tissues . So they are called “bad
lipoproteins” .LDL is absorbed by the liver and other tissues by
endocytosis through LDL receptor. The LDL receptor can be
recycled to the cell membrane.
High Density Lipoproteins
High density lipoproteins are the smallest of the lipoproteins and
most dense . HDL contains several types of apolipoproteins .
HDL is produced as a protein rich particle in the liver and intestine. .
HDL can acquire cholesterol from cell membranes and can transfer
cholesteryl esters to VLDL and LDL . HDL can return to the liver
where cholesterol is transported from tissues to the liver. The liver
can then excrete excess cholesterol in the form of bile acids. So they
are called “good lipoproteins ”.
HEALTH EFFECTS OF LIPIDS Excessive dietary fat intake is
associated with obesity, diabetes, cancer, hypertension and
atherosclerosis.Not more than 35% of energy intake should come
from fat. Saturated fat should not make up more than 15% of the total
fat intake. Atherosclerosis is characterized by deposition of
cholesterol and cholesterol esters of lipoproteins LDL in the
connective tissue of arterial wall resulting in their occlusion.
Prolonged high levels of LDL , is associated with increased risk of
coronary heart diseases and atherosclerosis.

- 37 -
.
Fatty liver
What is Fatty Liver?
Fatty liver is the accumulation of fat (TAG) in the liver. Simple fatty
liver is not a disease, since it does not damage the liver, but is a
condition that can be identified by taking a sample of liver tissue
(liver biopsy) and examining it under a microscope. Another term
often used to describe this condition is fatty infiltration of the liver.
What causes Fatty Liver?
Fat accumulates in the liver usually in the following conditions :
1- Heavy use of alcohol 2- Obesity and high carbohydrate diet
3- Diabetes mellitus 4-Drugs such as corticosteroids.
How is Fatty Liver identified?
The patient may have:
* enlarged liver
*minor elevation of liver enzyme tests.

- 38 -
Proteins are the most abundant biological molecules present in the
cell. Proteins have a large number of functions : including structural
and functional.
Functions of proteins :
1- Catalytic Function
Enzymes catalyze chemical reactions converting a substrate to a
product .
2-Transport function
Hemoglobin and myoglobin transport oxygen in blood and muscles
respectively. Transferrin transports iron in blood. Other transport
proteins bind and carry steroid hormones . Many drugs and toxic
compounds are transported in blood bound to proteins.
3- Contractile function
Myosin and actin proteins are the major components of muscles.
4- Protective function
The immunoglobulins (antibodies) are proteins produced by plasma
cells to act against different bacteria and viruses that invade the body
5- Regulatory function
Many hormones and hormone receptors are proteins. Protein
receptors respond to hormones by initiating complex physiological
response.
6- Structural function
The structural proteins include collagen and elastin which form the
matrix of bones and ligaments and provide structural strength and
elasticity to organs and vascular system. Keratin is present in hair and
other epidermal tissues .
Amino Acids
* All proteins are synthesized from 20 amino acids . These amino
acids have codons in the genetic code. Transcription and translation
Protein Chemistry and Metabolism

- 39 -
of the DNA code results in polymerization of amino acids into a
specific linear sequence characteristic for each protein.
* Each amino acid (AA) has a carboxyl group COOH and an amino
group NH2 bonded to the same carbon. They have the following
general structure:
COOH
|
NH2 C H
|
R
* Amino acids differ from each other in their side chains or R group,
which vary in structure , size , electric charge and the solubility of
amino acid in water.
* These amino acids are :
Glycine, Alanine , Valine , Leucine, Isoleucine, Proline,
Serine , Threonine, Cysteine , Methionine, Aspartic , glutamic,
Lysine , Arginine, Aspargine, Glutamin, Histidine ,
Phenylalanine, Tyrosine and Tryptophan.
* Classification of Amino Acids:
Nutritional classification
- Non Essential A A : They can be synthesized inside the body and
do not have to be taken in diet.
- Essential A A: They are 10 AA ,can not be synthesized in the body
and so they must be supplied in diet .These A A are essential for
normal metabolism , health and growth .Their deficiencies in diet
result in diseases. To remember the 10 essential AA remember the
statement," Any Help In Learning These Little Molecules Proves
Truly Valuable "
Arginine Histidine Isoleucine Leucine Therionine
Lysine Methionine Phenylalanine Tryptophan Valine
Proteins are classified according to their contents of essential AA
into:

- 40 -
1- Proteins of high biological value
These are animal proteins which contain all essential AA needed
by the body.
2-Proteins of low biological value
Vegetable proteins lack one or more essential AA .Two Or more
different proteins are consumed together Which complement each
other in amino acid content.
For example , combination of corn (deficient in lysine)
with legumes ( deficient in methionine but rich in lysine)
approaches the biological value of an animal protein.
Peptides and proteins are polymers of amino acids. This
polymerization occurs intracellular in ribosomes during Translation
of mRNA. Chemically this polymerization is a dehydration reaction
requiring energy. The carboxyl group of an AA forms a peptide bond
with the amino group of the next AA with removal of one molecule
of water producing a dipeptide. Formation of subsequent peptide
bond result from serial addition of AA with the formation of a
tripeptide, tetrapeptide and so on . Repetition of this stepwise
dehydration process will generate a polypeptide.
Peptides & Proteins

- 41 -
R1 R2
| |
NH2 – C H – COOH + NH2 – C H – COOH
AA 1 AA 2
H2O The condensation reaction requires
energy
R1 H R2
| | |
NH2 – C H – C ----- N –C H – COOH
||
O
A dipeptide
H O R2 O H O R4
| || | || | || |
NH3 – C – C ---- N – C – C---- N – C – C ---- N – C – C
OO
| | | | | | |
R1 H H H R3 H H
Amino terminal Peptide bond Carboxy
terminal
A Tetrapeptide

- 42 -
Orders "levels" of protein structure”
‘Four organization levels
1- Primary structure of proteins:
• Is the linear sequence ‘order’ of A.A
‘joined by peptide bonds’
• Abnormal A.A. sequence results in
improper folding and loss of normal
function as in many genetic diseases.
2- Secondary structure ‘arrangement:
• Include α- helix, β-Sheet,
α– helix: The most common type of
helices. It is tightly packed
spiral structure.
β- pleated sheet: It has
pleated zigzag like surface
3- Tertiary structure of
proteins:
• Is the three-dimensional structure of
a protein.
4- Quaternary structure:

- 43 -
• Is the arrangement of the subunits of a proteins consisting of
two or more P.P chains
A protein may be
• monomeric : consists of a single polypeptide chain Or
• Polymeric: consists of more than one polypeptide chain
Each protein is characterized by its final shape which is maintained
by a group of non-covalent bonds.
* Denaturation of the protein is defined as a change in its physical,
chemical or biological properties . Denatured protein looses its
secondary , tertiary and /or quaternary structure . Primary structure is
not affected by Denaturation .
* Denaturating factors which include :
a) Physical factors as
- high temperature
- vigorous shaking
- high pressure
- U.V and X-ray irradiation.
b) Chemical reagents as
- strong acids and bases
- concentrated urea
c) Biological agents
- enzymes
*Effects of Denaturation:
1- Physical changes
- decreased solubility
- increased viscosity
- increased digestibility
2- Chemical changes
- Loss of shape , i.e loss of tertiary ,secondary but not the
primary structure.
- increased susceptibility to hydrolysis by proteolytic enzymes
3- Biological changes
]
Denaturation of proteins

- 44 -
- decrease or loss of biological function
- decrease or loss of antigenic properties
Application of Denaturation:
1 - Heat coagulation test of urine is denaturation of albumin .
2 - Digestion of proteins begins in the stomach by the action of
gastric HCL ( chemical factor ) , to be completed by the
different digestive enzymes ( biological factor).
Digestion and absorption of proteins
1- Stomach
Protein digestion begins in the stomach where gastric HCL denatures
proteins making them more accessible to the action of proteolytic
enzymes.
Proteins HCl denatured proteins
Gastric juice contains 2 proteolytic enzymes : Renin and Pepsin .
Renin is important in digestion of milk in infants .it is absent in
adults
Pepsin is present in stomach as pepsinogen , which is activated to
pepsin by HCL . Pepsin is an endopeptidase that act on denatured
proteins changing them into polypeptides chains.
Denatured proteins Pepsin Polypeptide chains
2- Intestine
- Pancreatic secretion is alkaline and contains three proteolytic
enzymes:
Trypsin , chemotrypsin, elastase and carboxypeptidase
These enzymes degrade proteins and polypeptides into smaller
polypeptides, tripeptides and dipeptides.
Polypeptides chains pancreatic enzymes smaller polypeptides
Tripeptides
dipeptides
- Intestinal juice contains three enzymes
Aminopeptidase , tripeptidase and dipeptidase
These enzymes completedigestion of proteins into amino acids

- 45 -
Polypeptides
Tripeptides intestinal enzymes Amino Acids
Dipeptides
Amino Acids are absorbed through an active process in the intestinal
mucosa that is energy dependant and need carrier molecule.
Proteins are degraded in the following conditions:
1- During normal turnover of tissues , tissue proteins are degraded
into amino acids , which are catabolised if not needed for new
protein synthesis.
2- Proteins of diet are degraded into amino acids ,which are used for
protein synthesis , and if not needed amino acids are catabolised.
3-During starvation and diabetes mellitus , when carbohydrates are
unavailable or can not be utilized, body proteins are catabolised for
energy production.
In these conditions , Amino Acids either enter in synthesis of new
proteins or catabolised because they can not be stored. So firstly
Amino groups are separated from the carbon skeleton of the Amino
Acids . The Amino group passes into a specific pathway called
“Urea cycle ”. The carbon skeleton of the amino acid is converted to
either glucose or ketone bodies.
Although ammonia enters in structure of amino acids , its
accumulation in abnormal high concentration (after catabolism of
amino acids) has toxic effects. Therefore, ammonia must be
eliminated as soon as formed.
Sources of ammonia :
1- Liver:
Catabolism of Amino Acids
Ammonia

- 46 -
Transamination of amino acids followed by deamination of glutamic
acid . It means transfer of an amino group NH2 from an amino acid to
to a keto acid forming a new amino acid and a new keto acid .
Transamination help in amino acid synthesis and catabolism. Two
transaminases are important in clinical diagnosis of liver and heart
diseases :
SGOT = serum glutamic oxaloacetic transaminase
SGPT = serum glutamic pyruvic transaminase
These enzymes are present in high concentration in liver and heart
and are released in serum due to cell injury that occurs in myocardial
infarction and liver diseases as cirrhosis or hepatitis.
Transamination collects amino groups from all amino acids in
glutamic acid which undergo deamination in the liver mitochondria
releasing ammonia NH3.
2- Kidney
releases ammonia from glutamine by glutaminase enzyme.
3- Intestine
a portion of urea diffuses into intestine and hydrolyzed to ammonia
by the action of bacterial urease enzyme.
* Urea is the main end product of protein catabolism .
* Urea is synthesized in liver , released into blood and cleared by the
kidney in urine.
* Measurement of blood urea is a test of kidney function
Blood Urea level 20 - 40 mg / dl
Urea level in urine 20 - 40 gm / day
The main route of elimination of urea is through Urea Cycle
Urea Cycle

- 47 -
Ammonia toxicity
Ammonia is a highly toxic product . Hyperammoniemia is
characterized by comma . It occurs in conditions as liver cell failure
due to defect of urea cycle . Comma of Ammonia toxicity is due to :
1- Removal of excess ammonia involves amination of ketoglutaric
acid into glutamic acid with disturbance of Krebs cycle and ATP
production required for brain function.
2- Elevated levels of ammonia produce an increased permeability to
K+
and Cl-
ions that interfere with electrical activity of the brain.
Protein energy malnutrition
There are two disorders of protein energy nutrition widely spread in
developing countries :
1- Kwashiorkor
This condition occurs after weaning and is defined as inadequate
intake of protein in presence of adequate intake of carbohydrate
.Kwashiorkor is characterized by decreased heart functions , low
serum albumin level . Clinical picture include anorexia , diarrhea ,
edema, growth failure, loss of hair, liver enlargement and ascites
2- Marasmus
This results from deficiency of proteins and carbohydrates as in
starvation . It is characterized by generalized wasting .

- 48 -
.
Nucleic Acids
*They are composed of many nucleotides. Each one consists of :
Nitogenous base ( Adenine ,Guanine, Cytosine ,Uracil, Thymine)
+ Pentose sugar + phosphate
*There are 2 types of nucleic acids:
1-Deoxyribonucleic acid (DNA)
2- Ribonucleic acid ( RNA)
DNA
1-DNA is present in the nucleus of all cells as parts of chromosomal
structure and they carry the genetic information
2-Each chromosome is formed of double strands of DNA turning
around each other.
3-The bases of one strand is liked to those of the other one by
hydrogen bonds( weak bonds).
4-Adenine in one strand is liked to thymine by 2 hydrogen bonds,
while Guanine is liked to Cytosine by 3 hydrogen bonds ( base
pairing rule).
Marasmus
Kwashiorkor

- 49 -
5-The sequence of bases in one strand of DNA is complementary to
that of the second strand.
6-Before cell division , Replication of chromosomes double the
amount of DNA by splitting the two strands . Upon each strand a
complementary one is synthesized. Giving daughter DNA that exactly
resembles the original one.
RNA
There are 3 types of RNA , present mainly in the cytoplasm
1-Messenger RNA ( mRNA):
• It constitutes a small percentage of RNA.
• It is synthesized by transcription in the nucleus under the
control of DNA.
• It carries the genetic information from DNA to the
ribosomes for synthesis of a specific protein.
2-Ribosomal RNA ( rRNA):
• It constitutes 80 % of total RNA
• It is found in the form of granular particles attached to the
endoplasmic reticulum in the cytoplasm.
• Ribosomes act as a centre for protein synthesis
( translation).
3-Transfer RNA (tRNA)
• It is present in cytoplasm represent 15% of all RNA.
• Its nucleotides are arranged to form three loops and two
free ends .
• For each amino acid there is a specific tRNA , so there are
at least 21 different types of tRNA.
• It carries the "anticode" triplet nucleotides that is
complementary to the codon present on mRNA.

- 50 -
DNA RNA
Site Nucleus and
mitochondria
Mainly cytosol
Shape Double helix Variable
DNA
tRNA

- 51 -
Strands 2 Strands Single strand
Sugar Deoxyribose Ribose
Purines A,G A,G
Pyrimidines C,T C,U
Types One type 3 types
Functions Carry genetic
information and
synthesis of RNA
Protein synthesis.
Comparison between DNA and RNA
• Proteins (also known as polypeptides) are
made of amino acids arranged in a linear
chain.
• The sequence of amino acids in a protein is
defined by the sequence of nucleotides in the
gene.
DNA Replication
▪ The DNA duplication.
▪ The transfer the genetic information from a parent
to a daughter cell.
Transcription
• Transcription, is the process of creating mRNA copy of
a sequence of DNA.

- 52 -
Translation
• In translation, (mRNA) produced by transcription is decoded by
the ribosome to produce a specific amino acid chain, or
polypeptide.
• Translation occurs in the cell's cytoplasm, where the ribosomes
are located.
Ribosomes
▪ Factory for protein synthesis.
▪ Composed of ribosomal RNA and ribosomal proteins.
▪ Translate (mRNA) to build polypeptide chains using
amino acids delivered by (tRNA).
Recombinant DNA biotechniques
It is sometimes called "Genetic Engineering". It includes the techniques of
DNA identification ,characterization and manipulation. These techniques can
provide new approaches for diagnosis and treatment of many diseases.
Examples
1-Polymerase chain reaction (PCR)
It is an amplification of DNA in a test tube, in which million of copies of a
specific sequence of DNA can be produced in a few hours. PCR can help in
• diagnosis of genetic diseases
• identification of microorganisms as : hepatitis viruses B and C
and tuberculosis bacteria ‫مرض‬ ‫بكتريا‬
‫السل‬
• forensic medicine ‫بر‬‫ب‬‫الع‬ ‫با‬‫ب‬‫الط‬ uses to identify victims and
criminals.
• archeology to determine mummies DNA ‫المومياوات‬ ‫ل‬ ‫التعرف‬
2- Gene therapy ‫بالجينات‬ ‫العالج‬
It is to replace the defective gene in a patient with genetic disease
with a normal gene. This method of therapy is still under
investigation and research trials.
**********

Obesity
With the term ‘obesity’, we characterize an abnormal
or excessive accumulation of body fat, which
constitutes a great threat to health.
Obesity, and more specifically the central type of
obesity, which is characterized by excess fatty tissue
around the abdominal region, is associated with an
increased risk of developing diabetes and
cardiovascular disease, and perhaps even ‘the
metabolic syndrome’

What is the difference between an overweight and an
obese patient?
• Although, for the majority of people, the terms ‘overweight’ and ‘obese’ seem
to be synonymous, there is a significant difference between them. We can
determine whether a person is overweight or obese by:
combining their age and gender with the anthropometric parameters of their
body weight, body mass index (BMI) and body fat mass. An adult who has a
• BMI of 25–29.9 kg/m2 is said to be overweight, while an adult with a BMI in
excess of 30 kg/m2 is said to be obese.
In the case of children and adolescents, the various BMI and weight ranges are
different from those of adults, and the fact that normal levels of fat in the body vary
depending on gender and age must be taken into account. In the case of children or
teenagers, the various BMI and weight ranges are different from those for adults and
take into consideration the normal differences in body fat, according to gender
(boys or girls) and age group

Table of Weight status categories and
percentile ranges.
Percentile range
Weight Status category
Less than the 5th percentile
Under weight
5th percentile to less than the 85th
percentile
Healthy weight
85th to less than the 95th percentile
At risk of overweight
Equal to or greater than the 95th
percentile
Overweight

Obesity is a complex multifactorial disease that results
from the positive energy balance that occurs when energy
intake exceeds energy expenditure. Lifestyle and
environmental factors, including excessive energy intake,
high fat intake, and physical inactivity, are associated with
the pathophysiology of obesity. Growing evidence suggests
a strong link between genetic factors and the pathogenesis
of obesity. Genes involved in energy regulation such as
leptin, a signal protein for satiety produced in the adipose
tissue, and other hormones or peptides, such as
neuropeptide Y, may have important implications for
understanding the causes of obesity .

1- Genetic predisposition towards
obesity?
• Key genes, which are located on specific
chromosomes (e.g. 2p, 3q, 5p, 6p, 7q, 10p,
11q, 17p and 20q), may influence many
parameters related to energy intake and
energy expenditure, and that they are
associated with the basic metabolic rate,
thermogenesis due to food intake and how
active a person is generally inclined to be

2- Role of dietary fat intake in the
development
of obesity?
a- The increase in fat intake of the modern diet and
reduced physical activity are the two main causes of
the development of obesity in industrialized
countries. Fat is the most energy-dense nutrient in
our diet, producing nine calories per gram, which is
more than twice the calories derived from other
macronutrients such as carbohydrates and proteins
b- dietary fat is more efficiently metabolized and
stored in body fat than carbohydrates are.

c- Very fatty foods provide an intense feeling of
enjoyment and pleasure
d- Fatty foods do not produce a strong feeling of
satiety. For this reason they are usually over
consumed, which encourages the passive over
consumption of calories and the development of
obesity by affecting the body’s total energy
balance

d- Fat can contribute to the development of
obesity by regulation of leptin
levels. Increased dietary fat intake results
in central leptin resistance, whereas the
restriction of dietary fat can lead to a partial
improvement in leptin signaling, resulting in a
spontaneous reduction in appetite and body
weight.

3- Role of sugar and carbohydrate
intake in the
development of obesity?
Carbohydrates represent the most essential energy
fuel for the organism and play a very important role
in our diet. They produce greater satiety, especially
when they are in the form of complex high-fibre
types, a better control of pre- and postprandial
blood glucose levels and a higher dietary-induced
thermogenesis, with a lower energy density (3.75
kcal/g (15.7 kJ/g), than fats (9 kcal/g, 37.68 kJ/g).

4- Overconsumption of calories and
the development of obesity
• An imbalance between energy intake and energy
expenditure is consider the most important factor in
the development of obesity. When we consume more
calories than we expend for our daily needs (basal
metabolic rate, thermogenic processes and activity),
this extra energy is stored in the body, mainly as fat
stored in fat tissue, in order to be used later as an
energy fuel. Therefore, apart from the quality of the
diet and the proportion of fat, protein and
carbohydrates, the total quantity of energy
• intake and energy consumed is most important for the
energy balance of the body

5- Obesity in feeding disorder
Eating disorders and obesity are usually seen as very different
problems but actually share many similarities. In fact, eating
disorders, obesity, and other weight-related disorders may
overlap as girls move from one problem, such as unhealthy
dieting, to another, such as obesity. This information sheet is
designed to help parents, other adult caregivers, and school
personnel better understand the links between eating
disorders and obesity so they can promote healthy attitudes
and behaviors related to weight and eating.
- Over one-half of teenage girls and one-third of teenaged
boys use unhealthy weight control behaviors such as skipping
meals, smoking, fasting, vomiting, or taking laxatives.

Causes of Eating Disorders
• Personality Traits
• Genetics
• Environmental Influences
• Biochemistry

1- Personality Traits
• Low self-esteem
• Feelings of inadequacy or lack of control in life
• Fear of becoming fat
• Depressed, anxious, angry, and lonely feelings
• Rarely disobey
• Keep feelings to themselves
• Perfectionists
• Achievement oriented
– Good students
– Excellent athletes
– Competitive careers

2- Genetic Factors May Predispose People to
Eating Disorders
*Studies Suggest:
• Increased risk of anorexia nervosa among first-degree biological
relatives of individuals with the disorder
• increased risk of mood disorders among first-degree biological
relatives of people with anorexia, particularly the binge-
eating/purging type.
• Twin studies
– concordant rates for monozygotic twins is significantly higher than
those for dizygotic twins.
• Mothers who are overly concerned about their daughter’s
weight and physical attractiveness might cause increase
risk for development of eating disorders.
• Girls with eating disorders often have brothers and a
father who are overly critical of their weight.

3- Environmental Factors
- Interpersonal and Social
• Interpersonal Factors
– troubled family and personal relationships
– difficulty expressing emotions and feelings
– history of being teased or ridiculed based on size
or weight
– history of trauma, sexual, physical and/or mental
abuse
• 60-75% of all bulimia nervosa patients have a history of
physical and/or sexual abuse

Environmental Factors
• Social Factors (media and cultural pressures)
– Cultural pressures that glorify "thinness" and place value on
obtaining the "perfect body”
– Narrow definitions of beauty that include only women and
men of specific body weights and shapes
– Cultural norms that value people on the basis of physical
appearance and not inner qualities and strengths
– People pursing professions or activities that emphasize
thinness are more susceptible
• ie. Modeling, dancing, gymnastics, wresting, long
distance running

Environmental Factors
• Media messages help to create the context
within which people learn to place value on
the size and shape of their body.
– Advertising and celebrity spot lights scream
“thin is in,” defining what is beautiful and
good.
– Media has high power over the development
of self-esteem.

4- Biochemical Factors
• Chemical imbalances in the neuroendocrine system
– these imbalances control hunger, appetite, digestion, sexual
function, sleep, heart and kidney function, memory, emotions,
and thinking
• Serotonin and norepinephrine are decreased in acutely ill
anorexia and bulimia patients
– representing a link between depression and eating
disorders
• Excessive levels of cortisol in both anorexia and
depression
– caused by a problem that occurs in or near the
hypothalamus

I- Anorexia Nervosa
• Description
– Characterized by excessive weight loss
– Self-starvation
– Preoccupation with foods, progressing restrictions against
whole categories of food
– Anxiety about gaining weight or being “fat”
– Denial of hunger
– Consistent excuses to avoid mealtimes
– Excessive, rigid exercise regimen to “burn off” calories
– Withdrawal from usual friends

Anorexia
• Symptoms
– Resistance to maintaining body weight at or above
a minimally normal weight for age and height
– Intense fear of weight gain or being “fat” even
though underweight
– Disturbance in the experience of body weight or
shape on self-evaluation
– Loss of menstrual periods in girls and women
post-puberty

Anorexia Nervosa
*onset and course
• mean age at onset is 17 years
• affects about 1% of all females in late adolescence
and early adulthood
• bi-modal peaks at ages 14 and 18
• rarely occurs in females over age 40
• course and outcome are highly variable
• recover after a single episode
• fluctuation pattern of weight gain followed by
relapse
• chronic deteriorating course of the illness over
many years

Onset often associated with a stressful
life event:
• leaving home for college
• termination or disruption of an intimate
relationship
• family problems
• physical abuse
• sexual abuse

Anorexia Nervosa
*onset and course cot.
• Deluded thinking develops
– some girls believe they can ward of pregnancy by
being thin
– fast track professionals believe the only way they
can compete in a “man’s world” is to be thin
– being thin is the only way to receive attention

Anorexia Nervosa
*onset and course cont..
• Other developments throughout the course of
anorexia
– dramatic weight loss
– preoccupation with food and dieting
– refusal to eat certain foods
• progresses to restrictions against whole categories of food
(i.e.; carbohydrates)
– denial of hunger
– anxiety about gaining weight or being fat
– consistent excuses to avoid meal times
– withdrawal from friends and activities
– development of food rituals
• eating foods in certain orders, excessive chewing, rearranging
food on a plate

Health Consequences of Anorexia Nervosa
• Abnormally slow heart rate and low blood pressure, which mean that the
heart muscle is changing. The risk for heart failure rises as heart rate and
blood pressure levels sink lower and lower.
• Reduction of bone density (osteoporosis), which results in dry, brittle
bones.
• Muscle loss and weakness.
• Severe dehydration, which can result in kidney failure.
• Fainting, fatigue, and overall weakness.
• Dry hair and skin, hair loss is common.
• Growth of a downy layer of hair called lanugo all over the body, including
the face, in an effort to keep the body warm.

Anorexia
• What do counselors look for?
– Rapid loss of weight
– Change in eating habits
– Withdrawal from friends or social gatherings
– Peach fuzz
– Hair loss or dry skin
– Extreme concern about appearance or dieting

Description
• Recurrent episodes of binge eating. An episode of
binge eating is characterized by both of the following:
-eating, in a discrete period of time (e.g., within any
2-hour period), an amount of food that is definitely
larger than most people would eat during a similar
period of time and under similar circumstances
-a sense of lack of control over eating during the
episode (e.g., a feeling that one cannot stop eating
or control what or how much one is eating)

Description
• Recurrent inappropriate compensatory behavior in
order to prevent weight gain, such as self-induced
vomiting; misuse of laxatives, diuretics, enemas, or
other medications; fasting; or excessive exercise.
• The binge eating and inappropriate compensatory
behaviors both occur, on average, at least twice a
week for 3 months.
• Self-evaluation is unduly influenced by body shape
and weight.
• The disturbance does not occur exclusively during
episodes of Anorexia Nervosa.

Symptoms
• Eating large amounts of food uncontrollably (binging)
• Vomiting, using laxatives, or using other methods to
eliminate food (purging)
• Excessive concern about body weight
• Depression or changes in mood
• Irregular menstrual periods
• Unusual dental problems, swollen cheeks or glands,
heartburn, or bloating (swelling of the stomach)

Warning Signs That Counselors Look
For
• Evidence of binge eating
• Evidence of purging behaviors
• Excessive, rigid exercise regimen
• Unusual swelling of the cheeks and jaw area
• Calluses on the back of the hands and
knuckles from self-induced vomiting
• Discoloration or staining of teeth

Warning Signs That Counselors Look
For
• Creation of lifestyle schedules and rituals to
make time for binge-and-purge sessions
• Withdrawal from friends and activities
• In general, behaviors and attitudes indicating
that weight loss, dieting, and control of food
are becoming primary concerns

Developmental Level
• The average onset of Bulimia begins in late
adolescence or early adult life
– Usually between the ages of 16 and 21
• However, more and more women in their 30s
are reporting that they suffer from Bulimia

Prevalence
• The prevalence of Bulimia Nervosa among
adolescent and young adult females is
approximately 1%-3%.
• The rate of occurrence in males is
approximately one-tenth of that in females.

Bulimia Nervosa
*onset and course
• usually begins in late adolescence or early adult life and
affects 1-2% of young women
• 90% of individuals are female
• frequently begins during or after an episode of dieting
• course may be chronic or intermittent
• for a high percentage the disorder persists for at least several
years
• periods of remission often alternate with recurrences of binge
eating
• purging becomes an addiction

Bulimia Nervosa
*onset and course cont..
• occurs with similar frequencies in most
industrialized countries
• most individuals presenting with the disorder
in the U.S. are Caucasian.
• only 6% of people with bulimia receive mental
health care
• the incidence of bulimia in 10-39 year old
women TRIPLED between 1988 and 1993

Health Consequences of Bulimia Nervosa:
• Causes electrolyte imbalances that can lead to irregular
heartbeats and possibly heart failure and death.
Electrolyte imbalance is caused by dehydration and loss of
potassium and sodium from the body as a result of
purging behaviors.
• Inflammation and possible rupture of the esophagus from
frequent vomiting.
• Tooth decay and staining from stomach acids released
during frequent vomiting.
• Chronic irregular bowel movements and constipation as a
result of laxative abuse.
• Gastric rupture is an uncommon but possible side effect of
binge eating.

Management of obesity
An ideal dietary weight-reducing
program must contain all the food
groups, without excluding any of them

• It is a program that includes daily servings of
fruits and vegetables (raw or cooked), fat-free
or low-fat milk and milk products and servings
from starchy foods (e.g. bread, rice, pasta,
cereals) and potatoes, legumes, adequate
protein sources such as lean meat, poultry, fish,
beans, eggs and nuts, with a certain amount of
fat, mainly in the form of monounsaturated
olive oil

• In any diet, adequate protein, derived from both plant
sources and lean sources of animal protein, is essential
to help spare lean body mass. In weight-reducing diet
programs, protein intake should be 0.8–1.5 g/kg
• At the same time, an ideal dietary programme should
be characterized by variety, proportionality, flexibility
and personalization and should cover the nutritional
and energy needs of the dieter, according to their age,
gender, resting metabolic rate, health status, level of
physical activity and their lifestyle. The total reduction
in calories should not exceed 500–1000 kcal/day in
order to achieve a weight loss of 0.5–1 kg/week

What are the very low calorie diets?
Are they useful and healthy
choices? Who should follow them?
• VLCDs are very strict dietary programes that provide a
very low-energy intake of 400–800 kcal and a total
protein intake of 45–100 g per day, in the form of
regular foods and meals, but also as specially prepared
liquid formulas. Being so low in energy, VLCDs are
severely restricted in terms of
their carbohydrate and fat intake A multivitamin
supplement was included in regular foods, rather than a
special formula, in order to provide adequate amounts of
vitamins and minerals. People on a VLCD must drink over
two liters of water and they can drink other non-caloric
fluids (tea, coffee or others).

• These diets are advised for :
• A short period (no more than three months)
• Only under medical supervision. They can be dangerous, as they are
not nutritionally balanced diets and they may produce certain
nutritional
and electrolyte deficiencies, lean body mass loss or development of
medical
problems (e.g. gallstones).
These programes are not suitable for all overweight or obese people,
but only to obese patients that cannot lose weight through conventional
methods and diets of modest caloric restriction, and to patients with
certain medical problems, in whom a rapid weight loss is indicated. They
are often prescribed to the morbidly obese patient, under medical
supervision, prior to their undergoing bariatric surgery, and during
and post-surgery, in order to reduce complications

Are high-protein diets more
appropriate for the treatment
of obesity?
• High-protein diets are the most popular type
of exclusion diets used in the weight-control
industry. The higher intake of protein and the
severe restriction of carbohydrates in the diet,
through the exclusion of fruits, starchy foods
and legumes, had been considered the best
solution for obesity. It is true that protein
provides specific benefits in the diet that are
useful during a weight-reducing diet programe

Advantages of protein diet program
1- Protein is more thermogenic diet
2- Induce satiety and prolonged feeling of fullness
3- Depress hunger
4- Protein metabolism produce higher diuretic effect
• 5- Low carbohydrate contributes to a lower intake of
overall calories, to a lower plasma insulin level and
improved
insulin sensitivity, which leads to a higher fat
oxidation and utilization of fat as energy fuel, by
promoting ketosis, which also leads to weight loss

• These dietary programs seem to be effective and to
contribute to weight
loss only in the short term, while in the long term they have
almost the same effect as low-fat and high-carbohydrate
diets.
Disadvantages:
They can be dangerous, in the case of long-term application,
as they allow and promote the consumption of high-fat and
high-salt protein foods, which can lead to higher levels of
cholesterol and increased levels of blood pressure, and
prohibit the consumption of vitamin and mineral-rich food
sources, such as fruits and starchy vegetables and cereals

Is water beneficial for the treatment of
obesity?
Adequate intake of water can lead to:
1- Before meal it can lead to fullness of stomach
and determine amount of food intake
2- Increase excretion of keton bodies
3- Regulate intestinal functions
4- Increased metabolic rate and daily energy
expenditure through water induced thermogenesis

When is a nutritional supplement
beneficial during a
weight-reducing programe?
• In the cases of stricter programes, when the
caloric level is lower than 1200 kcal,or in the
presence of specific groups of people (e.g.
adolescents, lactating women), a supplement
is usually necessary since the food intake may
be insufficient. The most commonly used
supplements are those of iron, sodium,
potassium, magnesium, phosphorus and
calcium

What is the role of exercise in the
treatment of obesity?
• Exercise is considered a cornerstone of weight
loss and weight maintenance. It represents the
second component of energy balance, which is
the output or the energy expenditure that is
necessary to achieve a positive energy balance
and weight loss. Body weight is determined by
the balance between energy intake and energy
expenditure, and weight loss can only be
achieved by decreasing energy intake and/or
increasing physical activity.

Diet and weight control
• It is widely accepted that in order to achieve
the best weight reduction, a reduction in
calorie intake of 500–1000 kcal per day will
help to achieve a healthy and gradual, weekly
weight loss. The energy allowance should be
lower than 1000–1200 kcal/day for women
and 1200–1600 kcal/day for men.

Are there nutritional supplements
appropriate for weight loss?
• Numerous nutritional supplements claim to
promote weight reduction in parallel with a
low-calorie dietary plan. According to their
function, these supplements have been
organised by the Food & Drug Administration
into the following categories:

• increased energy consumption: supplements such as
ephedra (‫)االفدرين‬, bitter orange, guarana, caffeine,
country mallow , yarbe mate
• increased satiety: guar gum, psyllium, glucomannan
• increased lipid oxidation: L-carnitine, hydroxycitric acid,
green tea, vitamin B5 , liquorice, pyruvate, CLA
(conjugated linoleic acid – naturally occurring fatty acid,
which is found in meat, cheese and dairy products)
• Decreased lipid absorption: chitosan various ways of
function: laminaria, spirulina, apple cider vinegar, etc.

Treatment Strategies:
• Ideally, treatment addresses physical and
psychological aspects of an eating disorder.
• People with eating disorders often do not recognize
or admit that they are ill
– May strongly resist treatment
– Treatment may be long term
• E.D. are very complex and because of this several
health practitioners may be involved:
– General practitioners, Physicians, Dieticians, Psychologists,
Psychiatrists, Counselors, etc.
• Depending on the severity, an eating disorder is
usually treated in an:
– Outpatient setting: individual, family, and group therapy
– Inpatient/Hospital setting: for more extreme cases

Anorexia Treatment
• Three main phases:
– Restoring weight lost
– Treating psychological issues, such as:
• Distortion of body image, low self-esteem, and
interpersonal conflicts.
– Achieving long-term remission and rehabilitation.
• Early diagnosis and treatment increases the
treatment success rate.

Anorexia Treatment
• Hospitalization (Inpatient)
– Extreme cases are admitted for severe weight loss
– Feeding plans are used for nutritional needs
• Intravenous feeding is used for patients who refuse to eat or the
amount of weight loss has become life threatening
• Weight Gain
– Immediate goal in treatment
– Physician strictly sets the rate of weight gain
• Usually 1 to 2 pounds per week
• In the beginning 1,500 calories are given per day
• Calorie intake may eventually go up to 3,500 calories per day
• Nutritional Therapy
– Dietitian is often used to develop strategies for planning
meals and to educate the patient and parents
– Useful for achieving long-term remission

Bulimia Treatment
• Primary Goal
– Cut down or eliminate binging and purging
– Patients establish patterns of regular eating
• Treatment Involves:
– Psychological support
• Focuses on improvement of attitudes related to E.D.
• Encourages healthy but not excessive exercise
• Deals with mood or anxiety disorders
– Nutritional Counseling
• Teaches the nutritional value of food
• Dietician is used to help in meal planning strategies
– Medication management
• Antidepressants (SSRI’s) are effective to treat patients who also
have depression, anxiety, or who do not respond to therapy alone
• May help prevent relapse

Eating Disorder Treatment
• Medical Treatment
– Medications can be used for:
• Treatment of depression/anxiety that co-exists with the
eating disorder
• Restoration of hormonal balance and bone density
• Encourages weight gain by inducing hunger
• Normalization of the thinking process
– Drugs may be used with other forms of therapy
• Antidepressants (SSRI’s such as Zoloft)
– May suppress the binge-purge cycle
– May stabilize weight recovery

• Individual Therapy
– Allows a trusting relationship to be formed
– Difficult issues are addressed, such as:
• Anxiety, depression, low self-esteem, low self-
confidence, difficulties with interpersonal relationships,
and body image problems
– Several different approaches can be used, such as:
• Cognitive Behavioral Therapy (CBT)
– Focuses on personal thought processes
• Interpersonal Therapy
– Addresses relationship difficulties with others
• Rational Emotive Therapy
– Focuses on unhealthy or untrue beliefs
• Psychoanalysis Therapy

• Nutritional Counseling
– Dieticians or nutritionists are involved
– Teaches what a well-balanced diet looks like
• This is essential for recovery
• Useful if they lost track of what “normal eating” is.
– Helps to identify their fears about food and the
physical consequences of not eating well.

• Family Therapy
– Involves parents, siblings, partner.
– Family learns ways to cope with E.D. issues
– Family learns healthy ways to deal with E.D.
– Educates family members about eating disorders
– Can be useful for recovery to address conflict,
tension, communication problems, or difficulty
expressing feelings within the family

• Group Therapy
– Provides a supportive network
• Members have similar issues
– Can address many issues, including:
• Alternative coping strategies
• Exploration of underlying issues
• Ways to change behaviors
• Long-term goals

Prognosis for Improvement
• Anorexia
– 50% have good outcomes
– 30% have intermediate outcomes
– 20% have poor outcomes
• Bulimia
– 45% have good outcomes
– 18% have intermediate outcomes
– 21% have poor outcomes

• Factors that predict good outcomes:
– Early age at diagnosis
– Beginning treatment as soon as possible
– Good parent-child relationships
– Having other healthy relationships with friends or
therapists

• Anorexia
– Poorer prognosis with:
• Initial lower weight
• Presence of vomiting
• Failure to respond to previous treatment
• Bad family relationships before illness
• Being Married
• Bulimia
– Poorer prognosis with:
• High number hospitalizations because of severity
• Extreme disordered eating symptoms at start of
treatment
• Low motivation to change habits

Feeding patients
Encourage long-term care residents to maintain their
independence and feed themselves whenever possible. However,
patients may require feeding assistance for many different
reasons. Physical problems (unable to hold a fork, tremors that
prevent getting the spoon to mouth, etc) or cognitive problems
(just forgetting how to eat) can result in a need for feeding
assistance.

1- Oral feeding assistance
• Definition of oral feeding:
The term ‘oral feeding’ is used here to denote
eating and drinking.
The term ‘oral feeding’ does not imply that the
patient is passive in the organization and timing
of feeding, even if they are totally dependent on
the assistance of careers

– Signs that residents may need feeding assistance
or require feeding by staff:
• Poor meal intake
• Lack of interest in meal trays
• Cognitive impairment (eg, confusion or dementia)
• Physical inability to eat (unable to use arms, tremors
that prevent self-feeding, etc)
• Vision problems that prevent self-feeding
Often feeding problems are a combination of
physical problems and cognitive impairment.

• Benefits of feeding residents:
– Increased oral intake with potential for improved nutritional and
hydration status
– Mealtime interaction with staff
• Levels of feeding assistance:
– Tray setup
– Limited assistance, which may include, assisting with the end of a meal
after residents eat part of a meal, or feeding only certain food items
– Restorative feeding program (residents are encouraged to eat by
themselves with assistance provided as needed)
– Residents are fed by staff

Before setting up the tray or feeding residents:
– Assure dentures and hearing aids are in, glasses
are on, and residents are toileted
– Assure proper positioning of resident:
• Sitting up in the chair, feet on the ground if at a table
• If in bed, head raised and supported with pillows if
needed

• Tray setup techniques:
– Wash hands—bare-hand contact with food is not allowed
Use utensils or tongs
• Wear gloves or use protective paper, such as the paper sleeve bread is served in,
when handling food directly
– Make sure silverware is accessible
– Make sure adaptive feeding equipment, if ordered, is available for residents
– Open milk cartons, salt packets, etc
– Butter bread and season food as needed
– Cut meats or butter bread if needed, always asking residents if they would like
assistance with these tasks
– Cue resident to eat if necessary
– Ask residents if you can do anything else for them before moving on
– If assistance is required, stay with these residents, encourage independent feeding and
use of adaptive equipment, if ordered, and assist them with eating and drinking as
needed
•

Feeding techniques:
– Wash hands—bare-hand contact with food is not allowed
• Use utensils or tongs
• Wear gloves or use protective paper, such as the paper sleeve
bread is served in, when handling food directly.
– Follow any special feeding techniques as instructed by the
occupational or speech therapist
– Feed residents small bites at a time
– Alternate liquids with solids
– Do not mix foods together
– Cue residents to open mouth, if necessary
– Record intake as soon as possible after feeding residents

Clinical issues of relevance to oral
feeding
Four main areas of clinical practice need to be addressed
for a complete understanding of an oral feeding problem:
• The pre-oral phase of eating and drinking, intra-oral
bolus preparation, and swallowing
• Respiratory function
• The diagnosis, treatment and complications of the
underlying medical, neurological, surgical or psychiatric
condition
• The environment, including the availability of careers
and the nature of the food and drink provided.

The pre-oral phase, intra-oral bolus
preparation, and swallowing
• The pre-oral phase includes appropriate and necessary
implement use by patient or career, choosing the order
in which the food is to be presented, salivation and
other anticipatory behavioral responses, and the
traditional social interactions.
• Swallowing, as defined, comprises laryngeal elevation,
laryngeal closure, opening of the upper oesophageal
sphincter, bolus transit from mouth to oesophagus,
and the subsequent return of the involved structures to
their starting positions. The larynx is centre stage in
swallowing: the upwards and forwards movement
leads to opening of the cricopharyngeus, and its
closure is the main mechanism of airway protection.

• Intra-oral bolus preparation depends on
dentition, salivation, chewing (muscles
supplied mainly by the fifth cranial nerve (V)),
and control and manipulation of the bolus by
the muscles of the tongue (XII) and face (VII).

Other routs of assisted feeding
2- Enteral Feeding
• Enteral nutrition generally refers to any method
of feeding that uses the gastrointestinal (GI) tract
to deliver part or all of a person's caloric
requirements.
• It can include a normal oral diet, the use of liquid
supplements or delivery of part or all of the daily
requirements by use of a tube (tube feeding).
• Using the GI tract is closer to normal and can help
the immune system.

Indication for enteral feeding
• Malnourished patients or in those at risk of
malnutrition who have a functional
gastrointestinal tract but are unable to maintain
an adequate or safe oral intake: e.g
1- Critically ill patients, in whom enteral feeding
promotes gut barrier integrity and reduces rates of
infection and mortality
2- Postoperative patients with limited oral intake.
The complication rate and duration of hospital stay
are reduced by early enteral feeding
3- After elective gastrointestinal surgery

4- Gastrointestinal cancer surgery
5- Early post-pyloric feeding (duodenal or jejunal) is
useful as, although gastric and colonic function is
impaired postoperatively, small bowel function is often
normal. Feeding is usually introduced after 1 to 5 days
6- Patients with severe pancreatitis, without pseudocyst
or fistula complication. Enteral feeding promotes the
resolution of inflammation and reduces the incidence of
infection
7- Low-flow enteral feeding may also be useful in
combination with parenteral nutrition to maintain gut
function and reduce the likelihood of cholestasis

8- Patient who has had a stroke and now has
difficulty swallowing (called dysphagia). The
swallowing may normalize over time or in some
instances may not return to normal which could
put the patient at risk for inadvertently
swallowing any solids and liquids consumed into
the lungs which could cause a severe
pneumonia

Enteral access
Tube feeding is nutrition provided through the GI
tract via a tube, catheter, or a surgically made hole
into the GI tract.
- Short-term access is usually achieved using
nasogastric (NG) or nasojejunal (NJ) tubes at an
initial continuous feeding rate of 30 mls per hour.
- For longer use, a tube entering the stomach from
outside the abdomen (a gastrostomy) might be
appropriate

Disadvantages
Advantages
Length of use
Enteral access
device
Not indicated if bleeding
disorder, nasal/facial
fractures and certain
esophageal disorders
Easy to place, variety
of sizes available for
patient comfort
Short-term
use
Nasogastric tube
(NGT; through the
nose)
Not tolerated for long
periods of time in alert
patients; tube may damage
teeth
Lower incidence of
sinusitis than NGTs
Short-term
use
Orogastric tube
(through the
mouth)
May be difficult to position;
smaller size tubes may
make administration of
some medications difficult,
and an infusion pump is
needed
Smaller diameter
than NGTs and less
patient discomfort;
may be used in
delayed gastric
emptying
Short-term
use
Nasoenteric tube
(generally thought
of as a tube beyond
the stomach)

Same as orogastric
tubes
Same as orogastric
tubes
Short-term use
Oroenteric tube
(postpyloric feeding
tube)
Compared with oral and
nasal route, this
technique is more
invasive
Easily cared for and
replaceable; large size
tube allow for bolus
feeding, and
administration of
medications
Short-term
useLong-term
use
Gastrostomy tube
(can be placed
radiologically,
endoscopically or
surgically)
Technically more
difficult to place; smaller
size tubes may make
administration of some
medications more
difficult, and an infusion
pump is needed
Decreases the risk of
food and fluids
passing into the lungs;
allows for early
postoperative feeding
Long-term use
Jejunostomy tube
(can be placed
radiologically,
endoscopically or
surgically)

• These contain all the carbohydrate, protein, fat, water, electrolytes,
micronutrients (vitamins and trace elements) and fiber required by
a stable patient
2- Pre-digested' feeds
• These contain nitrogen as short peptides or free amino acids and
aim to improve nutrient absorption in the presence of pancreatic
insufficiency or inflammatory bowel disease.
• The fiber content of feeds is variable and some are supplemented
with vitamin K, which may interact with other medications.
Nutrients such as glutamine, arginine and essential omega-3 fatty acids
are able to modulate immune function. Enteral immunonutrition may
decrease major infectious complications and length of hospital stay in
surgical and some critically ill patients.
Feed preparations
1- Standard enteral feeds

Complication of enteral feeding
1- General complications:
a- Constipation
b- Nausea, vomiting and diarrhea
c- Improper absorption of nutrients
d- Dehydration and electrolyte disturbance
e- Hyperglycemia
f- Vitamin and mineral deficiency
g- Decrease liver proteins

2- Tube complications
NG tube:
This may cause nasopharyngeal discomfort and later nasal erosions,
abscesses and sinusitis
• Although acute complications such as pharyngeal or oesophageal
perforation, intracranial or bronchial insertion are uncommon, they
may be fatal.
• Longer use may cause oesophagitis, oesophageal ulceration and
stricture.
• Fine-bore tubes should be used and replaced in the alternate nostril
each month. Large stiff tubes are particularly unsafe in the presence
of varices and insertion of any tube should be avoided for three
days following acute variceal bleed.

Percutaneous gastrostomy or jejunostomy tubes:
– These can lead to complications related to endoscopy plus
bowel perforation and abdominal wall or intraperitoneal
bleeding.
– Post-insertion complications include stoma site infections,
peritonitis, septicaemia, peristomal leaks, dislodgement and
gastrocolic fistula formation.
• All feeding tubes should be flushed with water before and
after use, as they block easily. Blockages can sometimes be
removed by flushing with warm water or an enzyme
solution but some tubes may need to be replaced.
•

3- Infection
Bacterial contamination of enteral feed can cause serious infection
4- Gastro-oesophageal reflux and aspiration
• Reflux occurs frequently with enteral feeding, particularly in
patients with impaired consciousness, poor gag reflex and when fed
in the supine position.Patients should be propped up by at least 30°
whilst feeding and should remain in that position for a further 30
minutes to minimize the risk of aspiration. Post-pyloric tubes should
be used in unconscious patients who need to be nursed flat.
• Reflux is more likely with accumulation of gastric residues. Gastric
aspirates should be measured regularly and the feeding regimen
altered or prokinetics added to reduce gastric pooling.

5- Gastrointestinal symptoms
• Gut motility and absorption are promoted by hormones
released during mastication, with co-ordinated stomach
emptying and the in presence of intraluminal nutrients.
• As the usual physiological mechanisms are bypassed during
enteral feeding, gastrointestinal symptoms such as
abdominal bloating, cramps, nausea, diarrhoea and
constipation are common.
• Symptoms may respond to reduced feed administration
rates, continuous rather than bolus feeding, alternative
feed preparation or the addition of prokinetic agents.

6- Re-feeding syndrome
• This occurs in previously malnourished patients who are fed with high
carbohydrate loads.
• Carbohydrates (eg, glucose) in the feed can cause a large increase in the circulating
insulin level. This results in a rapid and dramatic fall in phosphate, potassium and
magnesium - with an increasing extracellular fluid (ECF) volume.
• As the body tries to switch from catabolic (starvation mode) to using exogenous
fuel sources, there is an increase in oxygen consumption, increased respiratory
and cardiac workload (may precipitate acute heart failure and tachypnoea and
make weaning from a ventilator difficult). Demand for nutrients and oxygen may
outstrip supply.
Both of the above can lead to multiple organ failure; respiratory and/or cardiac
failure, arrhythmias, rhabdomyolysis, seizures or coma, red cell and/or leukocyte
dysfunction.
• The gut may have undergone some atrophy with starvation and, with the return of
enteral feeding, there may be intolerance to the feed, with nausea and diarrhoea.
• Feeds should be started slowly and the electrolytes closely monitored and
adequately replaced to avoid these problems developing.

Enteral feeding can be done at home?
Yes

3- Parenteral Feeding
• Refers to the delivery of calories and nutrients
into a vein.
Indications:
Anyone who cannot/will not eat, or cannot
maintain their fluid and/or nutritional status by
oral eating or by tube feeding may be
appropriate for intravenous nutrition

Routes of parenteral feeding
1- Short term central venous catheter:
Which are tubes that are put in place in the hospital and generally removed
prior to discharge
- Many catheters are available in multilumen versions to allow for
simultaneous infusion of multiple fluids and/or medications
- It require routine flushing with a drug called heparin to prevent clotting and
additional site care and also has a higher rate of the catheter moving out of
position than a Hickman catheter
2- Long term central venous catheter:
Located in the upper chest
-A Hickman catheter is a brand of catheter that is tunneled under the skin
and put in place either in a Radiology Department or in an operating room. A
Hickman catheter requires dressing care to be performed by the patient, a
family member or a Home Care Service.

Complications of parenteral feeding
1- Infection 2- clotting (occlusion) 3-Breakage
4- Thrombosis around the catheter
How we can minimize complications:
1- A strict infection control protocol is recommended
regardless of the type of catheter placed and includes the
following:
a- hand washing b- Aseptic site and hub care (wearing
gloves, prepping site with topical antiseptics, etc.)
C- Port sterilization before access
d- Close monitoring of catheter site appearance for redness or
inflammation.

2- Catheter occlusion, or inability to infuse a
solution and/or aspirate a blood sample, may be
prevented by flushing the catheter to keep it
open. Catheter occlusion may arise from blood,
IV fat solutions, or precipitates (abnormal crystal
formation in a solution) and may be treated with
a declotting agent administered by a Registered
Nurse.

3- When a catheter is cracked, leaking, or
broken, the catheter must be repaired or
replaced as soon as possible. A catheter is
clamped between the exit site and the break to
prevent entrance of air or leakage of blood.

Can parenteral feeding done at home?
Yes with training
- Can I work while I am on parenteral feeding?
- Yes

Nutrition in Gastrointestinal
Diseases
I- Upper GIT Diseases

1- Nausea and vomiting
• The most striking hazard is occurrence of dehydration
Ways of restricting nausea and vomiting
- Avoid drinking fluids with meals (drinking water 40–60 min
before or after meal)
- Cold drinks may be better tolerated than warm
- Carbonated drinks or ice cubes may alleviate the sense of
nausea
- Consumption of toast may restrict nausea, especially during
the morning.
- Foods that commonly cause dyspepsia, such as fatty or fried
foods, coffee, foods rich in spices and also vegetables with a
strong odour,such as onions, garlic should be generally avoided

- Small and frequent meals prevent stomach
distension
- Avoid smelling food during preparation/cooking.
- Avoid going to bed straight after consuming
food

2- GASTROESOPHAGEAL REFLUX
DISEASE
The symptomatic reflux of gastric contents particularly acid,
pepsin, and bile into the esophagus which results in damage
to the esophageal mucosa and leads to esophagitis,
regurgitation, and heartburn.
- Ordinarily the esophagus is protected from reflux of gastric
contents by contraction of the lower esophageal sphincter
- Treatment is aimed at modifying the factors that promote
gastroesophageal reflux and irritation. Treatment requires a
multifactorial approach and is aimed at nutrition and lifestyle
modifications, drug therapy

Management goals are as follows:
1. Limit intragastric pressure.
2. Avoid substances that decrease the LES.
3. Decrease acidity of refluxed material to
prevent irritation of the esophagus.

1- Consume small volume meals; this may
necessitate dividing meals into smaller meals and
midmorning and midafternoon snacks, or
consuming fluids between meals
2- Maintain upright posture during and after eating
(Intragastric pressure is increased by mechanical
and postural factors)
3- Reduce weight if needed (Regression of
symptoms is likely to accompany weight loss)
4- Avoid tight fitting clothing, frequent bending

5- Avoid lying down after eating; consume bedtime
snacks or meals at least 2 hours before retiring
6- Elevate head of bed at least 6 inches when sleeping
7- Limit fat in diet
8- Avoid gastric stimulants: (Cigarette smoking, Alcohol,
Chocolate, Coffee, regular Caffeine)
9- Limit food constituents that the patient claims cause
discomfort; these may include citrus fruits and juices,
tomato products, and carbonated beverages

3- Dietary management in peptic ulcer
disease
Diet plays a minor role in peptic ulcer treatment and the main aim is to
alleviate patients’ symptoms.
• Generally, foods that often exacerbate symptoms include spices,
especially red hot pepper and coffee and other caffeine-containing
beverages , as well as large amounts of alcoholic beverages.
• Acid foods, such as vinegar, lemon, orange and other citrus fruits
and their juices have been traditionally avoided by patients with
peptic ulcer on the grounds that these items exacerbate symptoms.
During periods of exacerbation, acid foods should be limited,and
patients may benefit from a soft diet, without large amounts of fat
or fried foods. The thorough chewing of food, the avoidance of
large meals that cause stomach distension and the limited
consumption of carbonated drinks

Principles of Nutrition: Food Sources, Energy Requirements and Metabolism

Principles of Nutrition: Food Sources, Energy Requirements and Metabolism

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Principles of Nutrition: Food Sources, Energy Requirements and Metabolism