2024 CASE CONFERENCES

Biochemistry Finals
OLFU MEDICINE

OBESITY DETERMINE PATIENT’S ACTUAL CALORIC INTAKE, IDEAL BODY WEIGHT

AND THE TOTAL CALORIC REQUIREMENT BASED ON THE PATIENT’S
• Defined as an increase in body weight beyond the limits of physical IDEAL BODY WEIGHT
requirement, as the result of an excessive accumulation of fat.
• A chronic condition defined by an excess amount of body fat that can lead to 1. ACTUAL CALORIE INTAKE
diabetes, high blood pressure and obesity associated cardiovascular diseases CASE: Food intake is 135g of proteins, 115g of fat, 590g of carbohydrates
such as heart disease, gallstones, and other chronic illnesses. • 135g CHON x 4 kcal/g= 540 kcal
• Actual body weight is >120% of IBW •  115g Fat x 9 kcal/g= 1035 kcal
In clinical practice, BMI is commonly used to assess obesity • 590g CHO x 4 kcal/g= 2360 kcal

CAUSES OF OBESITY TOTAL ACTUAL CALORIC INTAKE

= CHON + FAT + CHO
1. Physical inactivity = (540 kcal) + (1035 kcal) + (2360 kcal) = 3935 kcal/day
2. Overeating
3. Genetics REMEMBER: *Kilocalorie (kcal)
4. A diet high in simple carbohydrates Standard Conversion: -  Standard unit for measuring energy
5. Medications Alcohol = 7 kcal/g -  Refers to unit of food energy
6. Psychological factors Carbohydrates = 4 kcal/g
7. Social issues Fats= 4 kcal/g
8. Diseases Proteins = 4 kcal/g

TYPES OF OBESITY 2. IDEAL BODY WEIGHT

ANDROID TYPE GYNOID TYPE Weight that is believed to be maximally healthy for a person and based chiefly
on height but modified by certain factors.
• Apple shaped • Pear shaped
Two methods:
• Body's extra fat gets distributed • Body's extra fat gets accumulated in
1.Tannhauser’s Method
over the abdominal region of the the lower body parts like thighs,
2.Fernando’s Method
body because of which the person's hips of which the person's body's
body's shape seems to be apple shape seems to be pear shaped
TANHHAUSER’S METHOD
shaped • Gynoid fat is a lower risk factor for
• Related to high cardiovascular cardiovascular disease than android
FORMULA
disease and mortality rate fat
(height in cm-100) - (height in cm-100) (10%) = weight in kg

GIVEN:
5feet 8inches to cm= 172.72cm

IBW = (172.72-100)-(172.72-100)(.10)
= 72.72 - 7.272
= 65.45 kg

FERNANDO’S METHOD

FEMALE: 100 lb for the rst 5ft + 5 lb for each additional inch
MALE: 101 lb fo the rst 5ft + 6lb for each additional inch

GIVEN
The patient is 250 lbs, converted to kg (divide it by 2.2) = 113.64 kg
IBW = 106 lbs + 48 lbs (5’8)
= 154 lbs/ 69.8 or 70 kg

3. TOTAL CALORIE REQUIREMENT

CASE
A. Using the patient’s ideal body weight:
A medical student, 5 feet 8 inches tall and weighing 250 lbs, damaged his knee
while playing basketball. Towards the end of his recovery period, he was Basal Metabolic Rate (BMR)
convinced that he needed to make an effort to correct his obesity. He was Male = (1 kcal/kg)(IBW/hr)(24hr)
referred to a dietitian by the student health services. His food intake was found Female = (.95 kcal/kg)(IBW/hr)(24hr)
to be composed of 135 grams of proteins, 115 grams of fats, 590 grams of
CHO on the average per day. He expressed his desire to reduce his weight Case:
without significantly changing his level of activity. IBW = 65.45kg
BMR= (1 kcal/g)(65.45 kg)(24hr)
BMR= 1570.8 kcal/day

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 B. For correcting the BMR for sleep: (cBMR)

Deduct 10%/kg of sleep from the previous BMR

Case:
(10%)(65.45)(8hrs) = 52.36 kcal
cBMR= 1570.8 kcal/day - 52.36 kcal
cBMR= 1518.44 kcal/day

C. Calculating for Physical Activity (PA)

Moderate physical activity = 75% cBMR
= (.75)(1518.44 kcal/day)
PA = 1138.8 kcal/day

PHYSICAL ACTIVITY CORRECTED BMR (cBMR)

BED REST 10% cBMR

SEDENTARY 30% cBMR

LIGHT 50% cBMR

MODERATE 70% cBMR

HEAVY 100% cBMR

D. Calculate Speci c Dynamic Action (SDA) LEPTIN

(10%)(cBMR + PA) •  “SATIETY HORMONE”

Case: • Leptin is secreted from fat cells in the adipose tissue
= (.10)(1518.44 kcal/day+1138.8 kcal/day) =(.10)(2657.24) • Adipocyte-derived protein that signals information to the hypothalamus to
SDA = 265.72 kcal/day “stop eating”
• The more fat you have, the more leptin is produced
E. Calculating for Physical Activity
LEPTIN RESISTANCE - Leptin is made but the receptor protein in the
TCR = cBMR+ PA + SDA hypothalamus failed to respond to it
Case:
= (1518.44 kcal/day) + (1138.8 kcal/day) • When there is high production of
+ (265.72 kcal/day) leptin, the food intake receptors
TCR = 2922.96 kcal/day that receives the leptin starts to
down-regulate protecting itself until
SUMMARY Role of Leptin in the Development it becomes leptin resistant
of Obesity • So instead of leptin signaling you to
1.IBW “stop eating”, instead will lead to
Tannhauser = (height in cm-100)-(height in cm-100) (10%) = weight in kg increased appetite.
Fernando’s • ➔ Your brain is starved while your
M (106 lb + 6lb/inch) body is obese
F (100lb + 5 lb/inch)
• Leptin has a role in the
2.BMR = (IBW)(24HRS) development of early menstruation
3.cBMR = (.10)(IBW)(SLEEP)-(BMR) in terms of it as to having an
4.PA = (% OF PHYSICAL ACTIVITY) (cBMR) important role in regulating the
5.SDA = (10%)(cBMR + PA) onset of puberty.
Role of Leptin in the Development
6.TER = cBMR+ PA + SDA • Increasing the secretion of
of Early Mensturation
Gonadotropin-releasing hormone
(GnRH), follicle-stimulating hormone
BODY MASS INDEX (BMI) (FSH) and luteinizing hormone (LH)
all that are necessary for
• Used to identify adults and adolescents that have an abnormal weight in
reproduction.
proportion to their height.
• Measure indicating nutritional status of an individual

BMI = weight (kg) ÷ height (m2)

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 HORMONES THAT ACCUMULATES IN THE PERIPHERAL FAT
• Peptide hormone produced almost
exclusively in adipose tissue
•  It circulates in the blood and
powerfully affects the metabolism of
fatty acids and carbohydrates in the
liver and muscles
• It triggers phosphorylation and
activation of AMP-activated protein
kinase
ADIPONECTIN
• It reduces levels of FFAs in the
blood and has been associated with
improved lipid profiles, increased
insulin sensitivity resulting in better
glycemic control and reduced
inflammation in diabetic patients
• Adiponectin levels decrease as
body weight increases, and leptin
levels increases
• Regulates body fat distribution
• Directly interacting with the Leptin
signaling pathway or through
activation of estrogen receptors
• Estrogen causes a typical female fat
distribution pattern in breasts,
ESTROGEN buttocks, and thighs, as well as its
more feminizing effects. During the
reproductive years, women get
additional fat deposition in the
pelvis, buttocks, thighs, and breasts
to provide an energy source for
eventual pregnancy and lactation.
• Adipose derived peptide hormone
that in humans is encoded by the
RETN gene in Chromosome 19
• Primarily produced in peripheral
RESISTIN
blood monocytes in humans
• Shown to cause “high levels of bad
cholesterol (LDL)”, increasing the
risk of heart disease
DISEASES CORRELATED TO OBESITY
• Obesity can cause resistance to
insulin, the hormone that regulates
blood sugar. When obesity causes
DIABETES MELLITUS TYPE 2 insulin resistance, the blood sugar
becomes elevated. Even moderate
obesity dramatically increases the
risk of diabetes
• Atherosclerosis is the process that
gradually hardens the walls of the
arteries making them lose their
elasticity and finally blocks them up
HEART DISEASE
or narrows them down to impair
blood flow
• Heart = coronary artery disease and
heart attacks
• Non-alcoholic fatty liver disease
(NAFLD) is one of the types of fatty
liver, which occurs when fat is
deposited in the liver due to causes
other than excessive alcohol use
FATTY LIVER DISEASE • NAFLD is related to insulin
resistance and the metabolic
syndrome and may respond to
treatments originally developed for
other insulin-resistant statesasing
the risk of heart disease
• Overweight women has an
increased risk of developing various
cancers including breast, colon,
gallbladder, and uterus
• Overweight men has an increase risk
CANCER
of colon and prostate cancers
The increase of cytokines that are
release by immune cells leads to
inflammation increasing cell
division.
•  Obesity hypoventilation syndrome
also known as Pickwickian
syndrome is a common condition in
which severely overweight people
fail to breathe rapidly enough or
deeply enough, resulting in low
SLEEP APNEA blood oxygen levels and high blood
carbon dioxide (CO2) levels
• The disease puts strain on the heart,
which eventually may lead to the
symptoms such as heart failure, leg
swelling and various other related
symptoms
• Obesity causes osteoarthritis by
increasing the mechanical stress on
OSTHEOARTHRITIS the cartilage.
• Obesity is the most powerful risk
factor for osteoarthritis of the knees
DIETARY REGIMENTS FOR WEIGHT REDUCTION
• The controlling of energy intake or
having a strict diet is a critical
component of weight-loss programs
that influences the rate of weight
loss. Activity accounts for only about
15 to 30 percent of daily energy
expenditure, but food intake
accounts for 100 percent of energy
CONTROL OF ENERGY INTAKE
intake.
• Examples of Popular weight loss
Diets:
Paleo diet
Vegan diet
Low carb diet
Intermittent fasting
Ketogenic diet
• Increased physical activity is an
essential component of a
comprehensive weight-reduction
strategy for overweight adults who
are otherwise healthy. One of the
best predictors of success in the
long-term management of
overweight and obesity is the ability
to develop and sustain an exercise
REGULAR EXERCISE program
• When strength training or resistance
exercise is combined with aerobic
activity, long-term results may be
better than those with aerobics
alone
• Because strength training tends to
build muscle, loss of lean body mass
may be minimized and the relative
loss of body fat may be increased
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 • The use of behavior and lifestyle AMYLOID CASCADE HYPOTHESIS

modification in weight management
is based on a body of evidence that
Amyloid ß → Amyloid Plaques → Neuron Death → Death
people become or remain
BEHAVIORAL MODIFICATIONS overweight as the result of
• Alpha Secretase → cleaves the APP → no formation of Amyloid ß → Non-
modifiable habits or behaviors and
amyloidogenic pathway
by changing these behaviors weight
can be lost and the loss can be
• Beta Secretase → cleaves the APP → cleaved by gamma secretase into
maintained.
either 40 amino acid amyloid peptide (Aß40) or 42 amino acid amyloid
peptide (Aß42) → Amyloidogenic pathway
• Control your home environment -
buy or consume less of tempting
foods like junk foods or avoid them
TAU HYPOTHESIS
if necessary
• Control your work environment -
• Tau protein abnormalities initiate the disease cascade
DO NOT SKIP MEALS, skipping
In this model, hyperphosphorylated tau when paired with other threads of tau
meals may result in overeating at
eventually will form neurofibrillary tangles inside
CHANGE ENVIRONMENT the next meal
nerve cell bodes
• Control your meal time environment
• When this occurs, the microtubules disintegrate, collapsing the neuron’s
- use smaller plates when eating a
transport system
smaller proportion will look large.
• Daily food and health management
- do not arrive hungry on social AMYLOID PLAQUES NEUROFIBRILLARY
gatherings, limit alcoholic TANGLES
beverages and don’t smoke.
Amyloid Precursor Tau Protein
• For people that are severely obese PRECURSOR PROTEIN
Protein
surgeries like gastric bypass are
effective in losing weight. Gastric ROLE Unknown Function Stabilizes microtubules
SURGERY bypass involves creating a small
pouch from the stomach and Increases Ca2+ Destabilizes
connecting the newly created pouch concentration → Alters microtubules
EFFECTS ON
directly to the small intestine Tau protein kinase  Induce inflammation →
NEURONS
activity Cell death → Impaired
synaptic transmission
ALZHEIMER’S DISEASE
• β-secretase Tau Protein Kinase
• insidious, progressive, neurodegenerative ENZYMES INVIOLVED • γ-secretase
• most common cause of dementia
• prominent feature is the presence of β-amyloid plaques and neuro brillary
tangles, and loss of connection between the neurons SITE OF FORMATION Extracellular Intracellular
Characterized by:
neuronal cell dysfunction or death
STRUCTURAL CHANGES IN ALZHEIMER’S DISEASE
shrinkage of brain tissue
progressive cognitive, motor, behavioral impairment
• The cortex shrivels up, damaging areas involved in thinking, planning and
remembering
RISK FACTORS
• Shrinkage is especially severe in the hippocampus, an area of the cortex that
Modi able: plays a key role in formation of new memories
Unavoidable: • Ventricles (fluid-filled spaces within the brain), grow larger
• Head trauma
•  Age: >65 yrs old • As neurons die, large scale changes started to take place in the brain. There
• Smoking
• Gender: >women will be atrophy or shrinkage. Gyri get narrower. Sulci between gyri get
• Obesity
• Family history wider and ventricle gets larger
• Limited physical activity
• Lack of mental activity
• Poor diet Amyloid beta has a toxic effect on the cells. Once one amyloid beta molecule
has been generated, it affects the proteases in the cell to promote the
GENETIC DETERMINANTS
generation of more amyloid beta molecules. Eventually, the toxic amyloid beta
forms plaques within the brain, which drive the development of Alzheimer’s
FAMILIAL AD (early onset) SPORADIC AD (late onset)

•  5 to 10% • 90 to 95%
• autosomal dominant inheritance • unknown cause
• signs first appear between 30s and • genetic and environmental risk
mid-60s (very rarely in the late 20s) factors
• 1% (age 60-65 and 50% (age over
Amyloid precursor protein 85)
(APP) gene - chromosome 21
(+ Down Syndrome) ApoE ε4
Presenilin-1 (PSEN1) - -  chromosome 19
chromosome 14 - proteolytic - less effective allele in the break
subunit of γ-secretase
Presenilin-2 (PSEN2) -
chromosome 1 proteolytic
down β-amyloid
- ApoE ε4 x1 = increased risk
- ApoE ε4 x2 = most-at-risk
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subunit of γ-secretase



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 ALZHEIMER’S DISEASE AND ASSOCIATION WITH:
BIOCHEMICAL CHANGES IN ALZHEIMER’S DISEASE
• increase the risk of AD by enhancing
• Plaques - these clumps of protein called beta-amyloid may damage the formation and/or deposition of
and destroy brain cells in several ways, including interfering with cell- amyloid beta, or that it may affect
to-cell communication non amyloid factors such as
• Tangles - threads of tau protein twist into abnormal tangles inside cerebrovascular risk, local
LIPOPROTEIN AND CHOLESTEROL
brain cells, leading to failure of the transport system. This failure is inflammation, or tau metabolism
strongly implicated in the decline and death of brain cells • Apo E bound to HDL inhibits the
• Improper APP processing - The proteases responsible for cleaving APP aggregation of amyloid beta
begin to malfunction • Free Apo E promotes the
• Disruption of Signaling - amyloid beta changes the signal transduction aggregation of amyloid beta
events within the cell to change cell behavior and contribute to the
development of Alzheimer’s; GSK-3 (Glycogen Synthase Kinase 3) begins to Astrocytes - increased in number and
take on other functions within the cell that contribute to the progression of become activated to produces
Alzheimer’s INFLAMMATION & IMMUNE prostaglandins/arachidonic acid to
• Breakdown of Cellular Structure - changes within the signal transduction of RESPONSE mediate inflammation  
GSK-3 lead to a breakdown of the structure of the cell, and ultimately lead to Microglia - activated microglial cells
cell death produces damage free radicals
• Continuing the Cycle - After the formation of NFTs within a cell, and the
proceeding cell death, any amyloid beta that accumulated within that • Zinc, Copper, and Iron – associated
diseased cell is released into the brain, where it can affect neighboring cells with aggregation of Aß
and lead to more cell death • Sequestration of Copper –
generation of ROS, mediates Aß
toxicity
•  Zinc – inhibits toxicity
METAL TOXICITY & FREE RADICALS
If tau becomes inactive, cytoskeleton is weakened, and the fibers can twist and •  Cu2+ and Fe3+ converted to Cu+
tangle with each other, damaging the cell and forming structure called and Fe2+ (generate free radicals)
neurofibrillary tangles (NFT). The development of NFTs causes brain cell death • Free radical molecules - injure
neurons (Oxidative damage)
IMBALANCES OF HORMONES / NEUROTRANSMITTERS INVOLVED IN AD • Elevated homocysteine – increased
risk of AD
• Growth hormone inhibiting
• Smoking - risk factor for AD
hormone
• Causes vascular and
• Decreased levels in brains of CIGARETTE / TOBACCO SMOKING
neurodegenerative pathways to be
patients with AD
SOMATOSTATIN activated
• Increased growth hormones
• Decreased TSH
• Increased insulin. Decreased fasting TREATMENT AND PREVENTION OF ALZHEIMER’S DISEASE
blood glucose
• reduce acetylcholine breakdown
• Increases cerebral blood flow, ACETYLCHOLINESTERASE
Donepezil, Rivastigmine,
prevents neuronal atrophy and INHIBITORS
Galantamine
reverses nerve damage, particularly
in the area of the forebrain • Inhibit overstimulation of glutamate
damaged by Alzheimer’s disease NON-COMPETITIVE NMDA Memantin - binds to NMDA
• Has a protective effect in the INHIBITORS receptor channels and produces
ESTROGEN
development of AD a noncompetitive blockage
• Introduction of exogenous
estrogen may prevent or delay the • Addresses low mood & irritability
onset of AD ANTIDEPRESSANRS Citalopram, Fluoxetine,
 Decreased level in menopausal Paroxetine, Setraline, Trazodone
women
• Addresses hallucinations, delusions,
• Catecholamine agression, agitation, & hostility
• Provides an endogenous anti- Aripiprazole, Clozapine,
ANTIPSYCHOTICS
inflammatory agent around glial Haloperidos, Olanzapine,
NOREPINEPHRINE
cells and blood vessels Quetiapine, Resperidone,
• Decreased with patients with AD Ziprasidone

• Addresses anxiety, restlessness,

• Excitatory neurotransmitter verbally disruptive behavior &
• Severely affected ANXIOLYTICS resistance
ACETYLCHOLINE
• Decreased choline acyltransferase Lorazepam, Oxazepam,
activity Diazepam

•  Involved in the regulation of mood, • No definitive prevention

appetite, and sleep Regular exercise, Mental
• Decreased activity in patients with PREVENTION stimulation, Healthy diet,
SEROTONIN AD Quality sleep, Stress
• Deficiency may be the result of management, Active social life

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reduction in receptor sites of the
cells that receive serotonin









 ROLE OF ANTIOXIDANTS DELETERIOUS EFFECTS OF FREE RADICALS

WHAT ARE FREE RADICALS? HOW ARE THEY FORMED AND WHATA RE • Chain of reactions of oxidative
THEIR DELETERIOUS EFFECTS TO THE BODY? degradation of lipids.
• It is the process in which free
LIPID PEROXIDATION
FREE RADICALS radicals "steal" electrons from the
• Molecular species capable of independent existence that contains an lipids in cell membranes
unpaired electron • Results in cell damage
• in an atomic orbital.
• Short life-span • Can be classified as Endogenous or
•  Unstable and highly reactive Exogenous
• OXIDATIVE STRESS - tissue damage caused by oxygen radicals OXIDATIVE DNA DAMAGE • Provides direct routes to mutations
• OXYGEN RADICALS (ROS)- The most damaging radicals in biological • Pose a serious threat for genetic
systems are oxygen radicals integrity
○ Superoxide,Peroxide, Hydroxyl Radical and Hydroxyl ion
• Associated with cancer, atherosclerosis, Alzheimer's disease, Parkinson's • Reactive Oxygen Species
disease ENDOGENOUS • Replication errors
• Poor Repair System
FREE RADICALS FORMATION
• Ionizing Radiation (Ultraviolet
PHYSIOLOGIC PATHOLOGIC radiation, X-rays)
• Chemicals (Iron, Copper)
•  Oxidative Phosphorylation • Inflammation EXOGENOUS
• Smoking
• Normal: Oxygen has 4 electrons to ○ Nadph oxidase • Pollution
be converted to water ○ Nitric oxide synthase • Diet (fatty and processed foods)
• Oxygen Free Radicals: Unpaired • Respiratory burst
electron ○ Superoxide dismutase
HOW ANTIOXIDANTS REDUCE FREE RADICALS
FREE RADICAL CHAIN REATION

• Breaking of covalent bonds

INITIATION • Result in a net increase of free
radicals

• The intermediate reacts with a

stable molecule to produce another
PROPAGATION
reactive intermediate (and a product
molecules)

•  Involve the combination of two ROLE AND GENERAL FUNCTIONS OF ANTIOXIDANTS

radicals without replacing
them by new ones
TERMINATION
• 2 radicals react to form a δ bond,
removing reactive radicals & hence
preventing further propagation
• Body's defense mechanism against toxic effects of free radicals
Prevent initiation of chain reactions
Scavenge free radicals generated in chain reactions
Remove peroxides
• Act on SUPEROXIDES AND HYDROGEN PEROXIDES
Superoxide dismutase (SOD)
Glutathione Peroxidase
Catalase

MINERALS ANTIOXIDANT SYSTEM

VITAMINS ANTIOXIDANT SYSTEM

• Tocopherol (Vitamin E)
•   carotenes (Vitamin A)  
• Ascorbic Acid (Vitamin C)
** Bioflavonoids

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 GLUTATHIONE • Reduces inflammatory oxidants

inhaled in air
preventing respiratory related
PULMONARY DISEASE
disease such as asthma,
emphysema and other chronic
obstructive pulmonary diseases

• Glutathione levels are significantly

reduced in the substantia nigra of
patients with Parkinson’s disease
• Increases dopamine sensitivity, so
PARKINSON’S DISEASE
that even though dopamine level is
decreased, it is still effective by
increasing sensitivity of dopamine
Potent antioxidant receptors
● Tripeptide
○ Glutamate, Cysteine, Glycine AGING Glutathione levels decline with age
■ Glu and Cys are bonded by a gamma-peptide bond
■ Cys and Gly are bonded by normal peptide bond • Reduced glutathione inhibits the
enzyme TYROSINASE
WHITENING
• Tyrosinase = Important enzyme in
GLUTATHIONE SYNTHESIS
Melanin Synthesis

FLAVONOIDS

• Bioflavonoids, Vitamin P, Citrin

• Latin word: flavus (yellow)
• Polyphenolic compounds processing 15 carbon atoms
○ two benzene rings joined by a three-carbon linear chain with the carbon
skeleton C6 – C3 – C6
• Class of plant secondary metabolite found in fruits, vegetables and certain
beverages that have diverse beneficial antioxidant effects

FOOD SOURCE
• Fruits - blueberries, apples, oranges
• Vegetables - broccoli, cabbage, cauliflower
• Green tea
• Wine
• Dark chocolates

• Inhibits enzymes associated with the

life cycle of viruses, causing viral
ANTIVIRAL PROPERTY intracellular replication to be
disrupted
TWO ATP-dependent steps:
• Inhibits viral polymerase
1st: gamma-glutamylcysteine is synthesized from L-glutamate and cysteine
• Gamma-glutamylcysteine synthetase • Inhibits cyclooxygenase and
• Rate limiting step ANTI-INFLAMMATORY PROPERTY lipoxygenase activities in the
2nd: glycine is added to the C-terminal of gamma-glutamylcysteine eicosanoid synthesis
• Glutathione Synthetase
ANTIOXIDANT ACTIVITY • Free radicals scavenging activity
2 FORMS OF GLUTATHIONE
• Downregulates mutant p53
REDUCED GLUTATHIONE OXIDIZED GLUTATHIONE ANTICARCINOGENIC PROPERTY Inhibits cell proliferation = cell
cycle arrest = DNA repair
● GSH ● GSSG
● Active Form ● Inactive Form

FUNCTIONS & USES OF GLUTATHIONE

• Activation of T-lymphocytes,
polymorphonuclear leukocytes as
well as for cytokine production
• Inhibits infections by the influenza
IMMUNITY & INFECTION virus
• Neutralizes FREE RADICALS and
PEROXIDES
• ↓Reduced Glutathione = ↑
Oxidative Stress

• Anti-atherogenic property
• Protects against lipid peroxidation
Lipid peroxidase attacks the lipids
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CARDIOVASCULAR DISEASE
in blood vessel cell membranes,
causing cholesterol deposits in the
vessel wall








 BETA CAROTENE AS ANTIOXIDANT FUNCTIONS OF COENZYME Q

• CoQ10 has a key role in cellular

energy supply, via its essential role
ENERGY METABOLISM
in oxidative phosphorylation within
mitochondria.

• Reported to exert anticancer

properties against human breast/
lung cancer cell
• Oral high-dose coenzyme Q10 is
• Antioxidative properties= Long chains of conjugated double CANCER
usually effective to treat
• bonds
mitochonrial disorders that are
• The chelation of free radicals inhibits the peroxidation of
causd by mutations in coenzyme
• lipids.
Q10 biosynthetic genes
• Most important as the precursor of vitamin A
• Acts as a scavenger of lipophilic radicals within the membranes of every cell
• Heart failure patients found that low
compartments.
plasma coenzyme 0 concentration
• It also presents an oxidative modi cation of LDL.
was a good biomarker of advanced
heart disease
CARDIOVASCULAR DISEASE
SELENIUM AS ANTIOXIDANT • It has an antioxidant, a free radial
scavenging and a vasodilator effect
• Selenium is a trace mineral, meaning your body only needs a small • It inhibits LDL oxidation and thus
amount.  It’s also available as a supplement, yet, most diets include the progression of atherosclerosis
selenium making it easy to get.
• Antioxidants like selenium help reduce oxidative stress by keeping free • CoQ10 is able to directly modulate
radical numbers in check the action of genes involved in
• They work by neutralizing excess free radicals and protecting cells from inflammation and may have a role in
damage caused by oxidative stress IMMUNE SYSTEM controlling the release of pro-
inflammatory cytokines in disorders
where this may be required.
COENZYME Q

ANTIOXIDANT VITAMINS A, C, E

A. FOOD SOURCE

VITAMIN C (ASCORBIC VITAMIN E (ALPHA-

VITAMIN A (RETINOL)
ACID) TOCOPHEROL)

• Broccoli • Plant oils (Peanut oil

• Egg
• Strawberries Cottonseed oil,
• Yoghurt
• Kale sunflower oil Soya oil,
• Chees
• Citrus fruits such as rapeseed oil, corn oil,
• Liver and liver
oranges olive oil)
products
• Lime, lemon • Whole grains (Brown
• Yellow/red green
• Tomatoes rice, Quinoa, Corn
vegetables
• Bell peppers grain, Barley, Oatmeal)
• spinach
• Cabbage • Nuts and seeds like
UBIQUINONE • carrots
• Watermelon almond, Nutmeg,
• Oil soluble in nature • sweet potatoes
• Potatoes peanut
• A quinone derivative with a long hydrophobic isoprenoid tail • red bell pepper
• spinach • Green leafy vegetable
• Vitamin-like substance • Yellow fruits (Mango,
• Banana • Shrimp
• Present in most eukaryotic cells Papaya and apricot)
• Kiwi • Egg
• Primarily in Mitochondria
B. RECOMMENDED DIETARY INTAKE

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 C. RECOMMENDED DAILY INTAKE TOXICITY & ADVERSE EFFECTS

VITAMIN C (ASCORBIC VITAMIN E (ALPHA-

VITAMIN A (RETINOL)
ACID) TOCOPHEROL)

• Headache, Nausea, • Formation of oxalate Least toxic of the fat

Ataxia, Anorexia, kidney stones at soluble vitamins, No
Hepatomegaly, megadoses toxicity
hyperlipidemia, Calcium has been observed at
Homeostasis, doses of 300mg/day
hypercalcemia,
• Calcification of soft
tissues and the skin

ROLE IN INFECTION AND IMMUNITY

D. RECOMMENDED DITARY INTAKE TO AVOID DEFICIENCY
VITAMIN C (ASCORBIC VITAMIN E (ALPHA-
VITAMIN A (RETINOL)
ACID) TOCOPHEROL)

Keeps the integrity of Aids in preventing many Inhibit damage to lung

the skin (smoothness
and moisture), that
serves as barrier to
protect the body from
the entry of
microorganism
types of virals and tissue from oxidants in
bacterial infections by the environment
potentiating the
immune system

ROLE IN CARDIOVASCULAR DISEASE & CANCER

VITAMIN C (ASCORBIC VITAMIN E (ALPHA-

VITAMIN A (RETINOL)
ACID) TOCOPHEROL)

• Involves in Break the lipid chain

Hydroxylation of reaction process by
cholesterol to cholic reacting with lipid
acid, which in turn peroxide radicals
VITAMIN DEFICIENCIES
Prevent or slow down excrete by the body
the development of through stool,
VITAMIN A DEFICIENCY
atherosclerosis by preventing deposition
• Nyctalopia/Night blindness preventing oxidation of of cholesterol in the
- nability to see in low light or near darkness conditions due to LDL wall of blood vessel
insuf cient amount of vitamin A, that affects the production of •  Prevents formation of
rhodopsin which is the necessary pigment for night vision. various cancer causing
substance like
• Xerophthalmia nitrosamines
- Dryness of the conjunctiva and cornea within Iflammation and ridge
ROLE IN STRESS, AGING, AND WOUND HEALING
formation brought about by irregular growth and differentiation of many
cell types within skin, and leads to abnormal epithelial keratinization
VITAMIN C (ASCORBIC VITAMIN E (ALPHA-
VITAMIN A (RETINOL)
ACID) TOCOPHEROL)
• Keratinization of skin
- Due to abnormal differentiation of non squamous epithelium, leads to
• Act as coenzyme in Anti-aging vitamins,
keratinization of the skin
Hydroxylation of slow down aging
• Regulate growth and
proline and lysine, process, by preventing
VITAMIN C DEFICIENCY tissue differentiation,
which is responsible radical formation
keeping the normal
Scurvy for strength
integrity of the skin
- Vitamin C de ciency disease, begins with symptoms of appetite loss and • Vitamin C aids in
fever, but progresses with more serious complications faster wound healing
 Skin problems, large bruises around hair follicles that break off easily
 Oral problems, gum swelling, bleeding and teeth loss
Musculoskeletal problems, bleeding in joint causing pain
Anemia, reduced number of RBC
Heart and lung problem, shortness of breath, low blood pressure and
chest pain
• In severe vitamin C deficiency, collagen or intracellular cement is of
abnormal quality and brittle leading to capillaries that are fragile resulting to
tendency to bleed even under minor pressure.

VITAMIN E DEFICIENCY

Hemorrhagic Disease
• Due to vitamin e deficiency, there is no inhibition of free radicals in RBC
membrane, oxidation will occur, leading to decrease membrane structure
integrity which will increase the fragility of RBC leading to erythrocyte
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hemolysis that can progress to anemia.
• Muscular Dystrophy
• Hepatic Necrosis
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 XENOBIOTICS PHASE 2

• Comes from the Greek xenos (foreign) and biotics (of or pertaining to life) The formed slightly polar metabolite from Phase 1 [X-OH] will now undergo
• Foreign chemical matters  Phase 2 for Conjugation.
• Not commonly naturally produced by or expected to be present within. In this phase conjugation of the metabolite produce from phase 1 with
glucuronic acid, sulfate, acetate, glutathione, or amino acids produces more
• Produce biological effects: polar compounds that are more water soluble and can therefore readily be
Pharmacological responses excreted in urine or bile. 
Toxicity
Immunological responses GLUCURONIDATION
Cancers Cofactor: UDP-glucuronic acid
Enzyme: glucuronosyltransferases
Examples: Pharmaceuticals, Pesticides, Cosmetics, Food Additives / Flavorings, • The glucuronide may be attached to oxygen, nitrogen, or sulfur groups of the
Industrial Chemicals, and Environmental Pollutants substrates
• Glucuronidation is probably the most frequent conjugation reaction
EXOGENOUS UDP- glucuronic Acid + X → Glucuronides
• Not normally ingested or utilized by an organism, but they access the body
SULFATION
through dietary food or in the form of therapeutic drugs
Cofactor:  3’- phosphoadenosine 5’-phosphosulfate (PAPS)
Examples: drugs, food additives, pollutants, insecticide, chemical carcinogens
Enzyme: sulfotransferases
In general, these enzymes catalyze the transfer of sulfate from the sulfate donor
ENDOGENOUS
3’- phospoadenosine 5’-phosphosulfate (PAPS)
• Have effects similar to exogenous xenobiotics.
PAPS + X → X-
• Synthesized in the body
• Produced as metabolites
CONJUGATION WITH GLUTATHIONE
Examples: Bilirubin, Bile Acids, Steroids
Cofactor: tripeptide glutathione (γ-glutamylcysteinylglycine) 
SIGNIFICANCE TO MAN Enzyme: Glutathione-S-Transferase
Products excreted in urine and bile.
• Knowledge of the metabolism of Xenobiotics is essential for an X-OH + GSH → X-S-G (Glutathione-S-Conjugate)
understanding of Pharmacology, Toxicology, and the Management of
disease ACEYTLATION
• Many of the Xenobiotics in plant foods have potentially bene cial effects Cofactor: Acetyl Coenzyme A 
and knowledge of their metabolism will permit extrapolation from in vitro Enzyme: acetyltransferases
measurement of antioxidant activity to in vivo protective action X-OH + Acetyl-CoA → Acetyl-X + CoA-SH
• Understanding the mechanisms involved in Xenobiotic metabolism will
METHYLATION
permit the development of transgenic microorganisms and plants
Cofactor: S-adenosylmethionine (SAM)
containing genes
Enzyme: methyltransferases
X-OH + SAM → X-CH3
METABOLISM& DETOXIFICATION OF XENOBIOTICS

• Xenobiotic metabolism and detoxification occurs mainly in the Liver

Other site of biotransformation (Extrahepatic) includes the ff:
Intestinal walls, lungs, Kidneys, Placenta, Brain, Skin, Adrenal glands 
‣
• The metabolism of xenobiotics is generally considered in two phases. 

Phase 1, the major reaction involved is hydroxylation, catalyzed mainly

by members of a class of enzymes referred to as monooxygenases or
cytochromes P450. 
Hydroxylation may terminate the action of a drug, though this is not
always the case. 
In addition to hydroxylation, these enzymes catalyze a wide range of
reactions, including those involving 
‣ Deamination
‣ Dehalogenation
‣ Desulfuration
‣ Epoxidation
‣ Per-oxygenation
‣ Reduction.
PHASE 1

• Reactions convert the parent drug (Hydrophobic) into slightly polar

(Hydrophilic) or slightly water soluble metabolites through introduction or
exposing OH, -SH, or -NH2 functional groups. 
• This results in activation or inactivation of the parent drug 
Catalyzed by Cytochrome P450 (oxidases) which uses NADPH from the
pentose phosphate pathway as a reducing agent.
X-H + O2 + NADPH2 CYP450 X-OH + H-O-H + NADP
Phase 1 metabolism renders compounds more reactive

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 CYTOCHROME 450 DEPRESSION

• The major enzymes involved in drug metabolism (xenobiotic) • Characterize by a pervasive and persistent low mood that is accompanied
Present in highest amount in liver and small intestine especially in the by low self-esteem and loss of interest and pleasure in normally enjoyable
membrane of SER activities
• A hemoprotein – containing a heme cofactor • Major depressive episode – for at least 2 weeks
• The most common reaction catalyzed by cytochromes P450 is a 4 symptoms:
monooxygenases reaction Changes in appetite and weight
Catalyze insertion of one atom of molecular oxygen Changes in sleep and activity
• Substrates are numerous and diverse compounds Lack of energy
Endogenous – cholesterol, steroid hormones, and fatty acids Recurring thoughts of death or suicide
Exogenous – drugs, food additives, and environmental contaminants (ex. • Impaired work ability
cigarette smoke)  • Poor social functioning Pessimism
• Often linked to suicide attempts
Biologic Functions of Cytochrome P450
A. Production of steroid hormones, vitamins A and D, lipid-like eicosanoid HORMONE VS NEUROTRANSMITTER
molecules involved in signaling
B. Metabolism of fatty acids and eicosanoids (e.g. P450 CYP51, essential in CHARACTERISTICS HORMONES NEUROTRANSMITTER
eukaryotic sterol biosynthesis.)
C. Detoxification Hormones are Neurotransmitters are
D. Many substrates are lipid-soluble; hydroxylation increases solubility regulatory chemical
substances which are substances which are
Cytochrome P450 effects in medicine. It is involved in: produced in released at
A. Inactivation or activation of therapeutic agents an organism & the end of a nerve cell
B. Conversion of chemicals to highly reactive molecules, which may DEFINITION transported in by the arrival of nerve
produce unwanted cellular damage, cell death, or mutations; tissue fluids like blood impulse,
C. Production of steroid hormones; and or sap, stimulating transmitting the impulse
D. Metabolism of fatty acids and their derivatives. specific cells or tissues into another neuron,
into action. muscle or some
Drug interaction of Cytochrome P450: other structure
A. Major role in drug detoxification type CYP3A4 estimated to act on ~
ORGAN SYSTEM
50% of known drugs (e.g. the antibiotic erythromycin) Endocrine System Nervous Sten
INVOVLED
B.  Some reactions are harmful
C. CYP3A4 catalysis of acetaminophen (Tylenol) MODE OF
D. Cytochrome P450 – Pigment with an absorbance at 450 nm Through blood Across the synaptic cleft
TRANSMISSION
o This is the characteristic absorbance of CYP450 when bound to carbon
monoxide (CO) TRANSMISSION
Slow Fast
SPEED

TRANSMISSION Act on distant site from In direct appostion to

FACTORS AFFECTING XENOBIOTICS METABOLISM DISTANCE where it is produced the target cells

1. Age, sex & other factors SIGNALS Endocrine Signaling Paracrine Signaling
2. Species, genetics
3. Intake of various xenobiotics can cause enzyme induction Growth and
4. Metabolites of certain xenobiotics can inhibit/stimulate the activities of development,
xenobiotic-metabolizing enzymes maintenance of sexual
5. Various diseases (e.g. Cirrhosis) can affect drug-metabolizing enzyme development, food Transmission of nerve
FUNCTION
activities  metabolism, signals
body temperature,
mood
MAJOR EFFECTS OF XENOBIOTICS
regulation
1. Cell Injury - Covalent binding of xenobiotics to cell macromolecule →
Steroids, Polypeptides & Proteins, Amino acids,
macromolecules targets DNA, RNA and protein → Cell injury → Cell TYPES
Amines Gases
death
2. Hapten - If the xenobiotic binds to protein altering its antigenicity, the
Only stimulate the
xenobiotic is said to act as Hapten Capable of Regulating
UNIQUE CAPABILITY postsynaptic
3. Mutation - Important in chemical carcinogenesis target organs or tissues
neurons
Monooxygenases or xenobiotic → metabolize enzyme present in
endoplasmic reticulum→ determine whether such compound become LOCATION Glands Synaptic Vesicle
“carcinogenic” or “detoxified”
Serotonin, Dopamine,
Oxytocin, Testosterone,
Norepinephrine,
EXAMPLE Cortisol,
Epinephrine,
Estrogen
Glutamate

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 NEUROTRANSMITTERS THAT PLAYS A ROLE IN EMOTION
• Controls many function including behavior,
emotion and cognition.
• Associated with pleasure and reward
• Affects the sleep-wake cycle, goal-directed
DOPAMINE
behaviors and reward-learning, and modulates
the control of movement via the basal ganglia
• Decrease of dopamine: loss of mental energy,
the loss of drive, and the fatigue
• Precursor of serotonin is tryptophan (AA)
• Plays a role in sleep and depression
SEROTONIN
• Major role in the body’s essential function
including appetite, arousal and mood
Norepinephrine is synthesized from the amino acid
tyrosine
NOREPINEPHRINE / Primary role in the body’s stress response
NORADRENALINE May be related to alertness and energy as well as
anxiety,
attention, and interest in life
HORMONES THAT AFFECT EMOTION
Maintain the level of serotonin and endorphins
Associated with positive mood state
ESTROGEN Excitatory
Low levels of estrogen = depression, anxiety &
mood swings
Counterbalances the action of estrogen
PROGESTERONE Has a calming effect
Activates GABA
Cuddle / Love Hormone
Inhibit brain areas associated with behavioral
control of fear & anxiety
OXYTOCIN
Protects us against stress
DEFICIENCY = poor communication, anxiety, fear,
disturbed sleep, irritability
Helps in muscle building, increasing libido, bone
mass, muscle strength and energy level
TESTOSTERONE
High levels = less activity in the prefrontal brain
regions and less communication with amygdala
Stress hormone
CORTISOL Causes an increase in heart rate and blood pressure
Elevated level = depression
MONOAMINE SYNTHESIS
An interconnected pathway of dopamine, epinephrine,
norepinephrine and serotonin
Involves the conversion of amino acid precursors: Tyrosine & Tryptophan
This pathway involves the synthesis, reuptake and degradation of
monoamines.
MonoamineTheory / Hypothesis
May serve as a basis of Depression
Depletion of the available 5-HT, NE and/or DA is used as a model to test the
involvement of monoaminergic systems
Over-expressed MAO-A isoform in the brain degrades serotonin and
norepinephrine
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OTHER NEUROTRANSMITTERS / HORMONES RELATED TO EMOTIONS
• Excitatory neurotransmitter
• Neurotransmitter that triggers muscle
contraction and stimulates the
ACETYLCHOLINE excretion of certain hormones. In the central
nervous system, it is involved in wakefulness,
attentiveness, anger, aggression, sexuality, and
thirst, among other things
• Inhibitory neurotransmitter
• Regulates brain by inhibiting excess firing of
neurons.
GABA
• Lower levels of this neurotransmitter has been
linked to mood challenges, difficulties with self-
control and excessive worry
• A major excitatory neurotransmitter that is
associated with learning and memory.
• Precursor of GABA
GLUTAMATE
• It is also thought to be associated with
Alzheimer’s disease, whose first symptoms
include memory malfunctions
CAUSES & RISK FACTORS IN DEVELOPING DEPRESSION
1.  Biochemistry: differences in certain chemicals in the brain
2. Genetics: can run in the families
3. Personality: people with low self-esteem, easily overwhelmed with
stress; sensitive to personal criticism; perfectionist; self-critical; pessimistic
4. Environmental factors: continuous exposure to violence, neglect, abuse
or poverty
5. Serious medical illness
6. Drug and alcohol abuse
GENETICS OF DEPRESSION
• No single genetic variation has been identi ed
• Genetic variants have only small effects on overall disease risk
• Multiple genetic factors in conjunction with environmental factors are likely
for development of depression
• Twin studies suggest a heritability of 40% to 50% and family studies indicate
a 2-fold to 3-fold increase in lifetime risk of developing MDD among first
degree relatives
• SLC64A and 5-HTTLPR – serotonin gene transporters
• Polymorphism in Brain derived neurotrophic factor (BDNF)
• THP2 gene-associated with tryptophan hydroxylase
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 COVID-19 VACCINE TECHNOLOGY

MEDICAL ILLNESSES ASSOCIATED WITH DEPRESSION

• Stroke • (COVID-19) is an infectious disease caused by a newly discovered

• Heart disease coronavirus. Most people infected with the COVID-19 virus will experience
• Alzheimer’s disease mild to moderate respiratory illness and recover without requiring special
• Parkinson’s disease • treatment.
• Cancer • Older people, and those with underlying medical problems like
• Depression in association with nonspecific somatic complaints, chronic pain, cardiovascular disease, diabetes, chronic respiratory disease, and cancer are
fibromyalgia, chronic fatigue more likely to develop serious illness.
• Endocrine diseases
HOW DOES COCVID 19-SPREAD BETWEEN PEOPLE
• HIV infection

• The virus can spread from an infected person’s mouth or nose in small liquid
MANAGEMENT OF DEPRESSION particles when they cough, sneeze, speak, sing or breathe.
• These particles range from larger respiratory droplets to smaller aerosols.
PHARMACOLOGIC TREATMENTS
• INITIAL SYMPTOMS: Fever, chills, cough, muscle ache, fatigue, loss of taste/
• The most commonly smell
prescribed Fluoxetine
antidepressants Escitalopram
• Treat depression by Paroxetine DEFINITION OF TERMS
increasing levels of Sertraline
SELECTIVE serotonin in the brain • Virion - a complete virus particle that consists of an RNA or DNA core with a
SEROTONIN • SSRIs block the protein coat sometimes with external envelopes and that is the extracellular
REUPTAKE INHIBITORS reuptake of serotonin infectious form of a virus
(SSRIs) into the presynaptic
nerve terminal via the • Virus - are the smallest infectious particles which cannot be seen by an
serotonin uptake site ordinary microscope. They are an obligate intracellular parasites that requires
• Selective because it
host cells for replication. They lack the capacity to thrive and reproduce
mainly affects
outside of a host body
serotonin

SELECTIVE • May be an effective Venlafaxine • Cytokines - are polypeptide products activated cells that the control a variety
NOREPINEPHRINE form of treatment for Desvenlafaxine of cellular response and thereby regulate the immune response; this are
REUPTAKE INHIBITORS people who’ve had Duloxetine synthesize and secreted by the cells assoc with innate and adaptive immunity
(SNRIs) unsuccessful treatment in response to microbial and other antigen exposure.
with SSRI
• Moderately selective
• Antigens - is a substance that stimulates antibody formation and has the
blockade of NET and
ability to bind to an antibody or a T lymphocyte Ag receptor but may not be
SERT
• Inhibit the reuptake of able to evoke an immune response initiall
both serotonin and
norepinephrine • Antibody - is a protein produced by the body's immune system when it
detects harmful substances, called antigens
TRICYCLIC • TCAs block Imitrapine
ANTIDEPRESSANTS norepinephrine and Amitrptyline
• Complements - The complement system plays a critical role in inflammation
serotonin reuptake Desipramine
and defence against some bacterial infections. Complement may also be
into the neuron Nortriptyline
• Blocks action of activated during reactions against incompatible blood transfusions, and
acetylcholine and during the damaging immune responses that accompany autoimmune
histamine disease

MONOAMINE • Blocks monoamine Selegiline

OXIDATE INHIBITOR oxidase enzyme Phenelzine
• Increases
concentration of NT

NON-PHARMACOLOGIC TREATMENTS

• Non-invasive
REPETITIVE
• Magnetic impulses are delivered to the brain to
TRANSCRANIAL
stimulate the nerve cells related to mood and
MAGNETIC
depression
STIMULATION
• Unresponsive patients to therapy and medication

• Shock Therapy
ELECTROCONVULSIVE
• Moderately invasive, results in a seizure while
THERAPY
under anesthesia

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 WHAT IS A VACCINES?
SARSCOV-2 VIRAL STRURTURE
• A product that stimulates a person’s immune system to produce
immunity to a speci c disease, protecting the person from that disease.
• Usually administered through needle injections, but can also be
administered by mouth.

a. Spike/S glycoprotein - transmembrane protein located at the outer surface

of the virus where it forms homotrimers protruding in the surface which
facilitates the binding of the virus to the host by attraction with angiotensin
converting enzymes which are expressed by cells in the lower respiratory tract.

b. Nucleocapsid/ N protein- structural component of the virus localized in the

endoplasmic reticulum-Golgi region that is bound to the viral nucleic acid HOW DOES IT WORK?
material. Because this viral protein is attached or bound to the viral RNA it is
involved in the process related to viral genome, viral replication cycle and
response of the cell against viral infection.

c. M protein- most structurally structured protein which plays an important role

in determining the shape of the virus envelope. This protein binds to all other
structural proteins including the N proteins thus promoting the completion of
the viral assembly by stabilizing the N protein-RNA complex.

d. E protein - smallest protein that plays a role in production and maturation of

the virus

TYPES OF IMMUNITY

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 TYPES OF COVID-19 VACCINES

• Contain killed SARS-CoV-2 virus

• The killed virus is recognized by the immune FACTORS THAT INFLUENCES THE EFFICACY OF VACCINE
system to trigger a response without causing
illness.
INACTIVATED
• This response builds immune memory, so your
VACCINE
body can fight off SARS-CoV-2 in future
• May need to be administered with an adjuvant to
boost immune response.
• Examples: Sinovac/Coronavac Bharat Biotech

• Uses a living but weakened version of the virus or

one that’s very similar.
LIVE-ATTENUATED • The weakened virus is recognized by the immune
VACCINE system to trigger a response without causing
illness.
• In clinical trial for COVID-19 – Codagenix
• 1st dose - presents antigen to the IS; stimulating response; “Priming”
• Use an unrelated harmless virus, modified to • 2nd dose - “Booster” Ensure that the Ab and T cells mediated response are
deliver SARS-CoV-2 genetic material. The delivery competent
virus is known as a viral vector. • Interval: “Vaccine Spacing”; immune response it not strong immediately;
• Our cells use the genetic material to make a gap is needed
specific SARS-CoV-2 protein, which is recognized
VIRAL VECTORS by the immune system to trigger a response.
• Generate strong immune response. SAFETY CONCERNS IN VACCINE
• May need to be stored at specific low
temperatures. • New technology
• Example: AstraZeneca/Oxford Gamaleya • Age
Janssen • Pregnant and Lactating Mothers
• Children & Adolescences
• Only uses the very speci c parts (the subunits) • Immunosuppressed / Immunocompromised individuals
of a virus or bacterium that the immune system • Side effects
needs to recognize. Thrombosis with Thrombocytopenia
SUBUNIT VACCINES
• It doesn't contain the whole microbe or use a Local & Systemic Reactions - pain at the injection site, fever, myalgiaa
safe virus as a vector. The subunits may be Anaphylaxis
proteins or sugars.  Myocarditis
https://www.who.int/news-room/feature-stories/detail/safety-of-covid-19-
• Contain proteins from the SARS-CoV-2 virus, vaccines
which are recognized by the immune system to
trigger a response. STRATEGIES TO OPTIMIZE VACCINE EFFECTIVENESS
• Can be whole proteins, protein fragments, or
many protein molecules packed into • Antigen Characteristics - foreignness, structural stability and molecular weight
nanoparticles. • Adjuvants
PROTEIN VACCINES
• This response builds immune memory, so your • Epitope Enhancement
body can fight off SARS-CoV-2 in future. • Delivery Approaches - gene gun, electroporation, DC targeting, Lipid
• Have good previous safety records. nanoparticle
• Usually administered with an adjuvant to boost
immune response.
• Example: Sano Pasteur Novavax

• Contain a segment of SARS-CoV-2 virus genetic

material that codes for a specific protein. Can be
GENETIC VACCINES / DNA or RNA.
NUCLEIC ACID • Low cost and fast to develop.
VACCINES • May need to be stored at specific low
temperatures.
• Examples: P zer/BioNtech & Moderna

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 SUMMARY

• COVID-19, accdg to who coronavirus disease (covid-19) is an infectious

disease caused by a newly discovered coronavirus.most people infected with
the covid-19 virus will experience mild to moderate respiratory illness and
recover without requiring special treatment.
• Symptoms may appear 2-14 days after exposure to the virus
• Definition of terms for the ff: virion, virus, antigen, antibody and complement
• Structurally, sars-cov-2 has four main structural proteins including spike (s)
glycoprotein, small envelope (e) glycoprotein, membrane (m) glycoprotein,
and nucleocapsid (n) protein, and also several accessory proteins.
• Innate or native immunity is acquired by birth through the genes. it is a more
general or nonspecific component of the immune system- i.e., it attacks any
germs that threaten the body. if the pathogens successfully evade the innate
immune system, the next level of immunity that comes into action is the
adaptive or acquired immune system.
• As the name suggests, adaptive immunity develops as we encounter
exposure to pathogens throughout our life. the adaptive immune system is
specific, i.e. it targets a specific pathogen and takes some time to develop.
• The complement system plays a critical role in the rapid host innate immune
response to bacterial, viral, and fungal infections [1]. complement activation
allows antibodies and phagocytic cells to detect and clear microbes at the
site of infection and stimulates the recruitment of inflammatory cells,
including macrophages, neutrophils, and mast cells
• Vaccine is a tiny weakened non-dangerous fragments of the organism and
includes parts of antigen.
• Development of Vaccines: PRE CLINICAL PHASES, PHASE 1, PHASE 2,
PHASE 3 COVID-19 VACCINES IN EUA: RNA BASED (Pfizer-BioNTech &
Moderna); INACTIVATED (Sinovac); VIRAL VECTOR VACCINES (AztraZeneca,
Gamaleya Sputnik V, Janssen); PROTEIN SUBUNIT (Bharat BioTech&
Novavax)
• Factor that influences the efficacy of vaccine: Instrinsic host, Perinatal,
Extrinsic, Behavioral, Nutritional, Vaccine and administration factors.
• mRNA vaccine can't alter our genetic make-up due to the absence of the
Reverse transcriptase enzyme.
• Vaccines can be theoretically mixed together as long as both vaccines have
the same technology or the principle of the technology is the same
• As of now, it is not recommeneded to mix two difference vaccines togerther
due to the limited data.
• Vaccine are given in 2 doses where the 1st dose serve to prime the immune
system while the 2nd dose serve to boost the immune system.
• Interval between multidose vaccine or called vaccine spacing are needed for
a stronger and longer lasting immunity
• Vaccination of post COVID patient are still recommended due to the
inadequacy of data regarding the length of natural immunity in COVID.
• Immunosuppred individuals even if vaccinated won't produce a competent
immune system but vaccines have an indirect protection to them via others.
• mRNA vaccine technology although new to the COVID 19 vaccine the
technology itself is not new but it still it is considered as safety concerns for
vaccine development due to the data is still limited.
• Thrombosis with Thrombocytopenia and myocarditis are examples of the
reported side effects but the reason is still unknown until this day
• Anaphylaxis and local & systemic reactions such as Pain in the injection site,
fever and myalgia are examples of common side effects in majority of
vaccines
• Adjuvant are compounds used to increase the efficacy of vaccines.

REFERENCES:
• BESHYWAP
• E2 2024 CONFERENCES
• WHO

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