Exam revision

Question 1

types of congenital adrenal hyperplasia

Answer 1

• usually congenital; delayed virilising adrenal
  hyperplasia is a variant of congenital adrenal
  hyperplasia.
• Both are caused by a defect in production of
  androgens.
• The defect is only partial in delayed virilising
  adrenal hyperplasia, so clinical disease may not
  develop until adulthood

Question 2

Most common forms of congenital adrenal
hyperplasia

Answer 2

21-hydroxylase
deficiency

11beta-
hydroxylase
deficiency

Question 3

Congenital Adrenal Hyperplasia

Answer 3

Congenital Adrenal Hyperplasia (CAH) is
a family of inherited disorders affecting
the adrenal glands.

Autosomal recessive (mutation on chromosome 6)

Question 4

why is cortisol high in Cushing disease

Answer 4

A noncancerous (benign) tumor of the pituitary gland, located at the base of the brain, produces an excess amount of ACTH , which in turn stimulates the adrenal glands to make more cortisol

Question 5

what is hypothyroidism?

Answer 5

Hypothyroidism is
a condition in which the thyroid
doesn’t make enough thyroid
hormones.

Question 6

what is Hyperthyroidism?

Answer 6

Hyperthyroidism
is a condition in which the thyroid
makes too much of certain thyroid
hormones.

Question 7

most common cause for hypo and hyper thyroidism

Answer 7

Hashimoto disease, also known as
Hashimoto thyroiditis.
 This is an autoimmune disease and
the most common cause
of hypothyroidism.

Graves’ disease.
 This is also an autoimmune disease
and the most common cause
of hyperthyroidism

Question 8

3 types of hypothyroidism

Answer 8

Primary hypothyroidism – when your
thyroid gland becomes diseased and
cannot produce sufficient hormones

Subclinical hypothyroidism- early and mild
form of hypothyroidism

Secondary hypothyroidism – when your
pituitary gland isn’t stimulating your
thyroid to produce enough hormones.

Question 9

most common cause of PRIMARY HYPOTHYROIDISM

Answer 9

Hashimoto’s thyroiditis

Question 10

Diagnosis for Primary
Hypothyroidism
-Hashimoto
thyroiditis

Answer 10

High TSH with low Free T4/T3
High Thyroid autoantibodies

Question 11

Diagnosis for Subclinical Hypothyroidism

Answer 11

Elevated TSH and Normal T4/T3 level

Question 12

Diagnosis for SECONDARY HYPOTHYROIDISM

Answer 12

Low levels of T4/T3 with high
level of TRH

Question 13

3 causes of hyperthyroidism

Answer 13

Grave’s disease
 Autoimmune disease caused by
antibodies to TSH receptors

Toxic multi-nodular goiter
 Active multinodular
goiter associated with
hyperthyroidism.

Thyroiditis subacute
 Abrupt onset due to leakage of
hormones
 Follows viral infection

Question 14

best way to determine thyroid dysfunction

Answer 14

Measuring serum TSH

Question 15

What are the key players for
Thyroid hormone regulation?

Answer 15

Hypothalamus: Thyrotropin-
releasing hormone (TRH)
 control of thyroid stimulating
hormone (TSH)

Pituitary: Thyroid stimulating
hormone (TSH)
 controls production of the thyroid
hormones by binding to TSH
receptors located on cells in the
thyroid gland.

Thyroid: triiodothyronine (T3) and
thyroxine (T4)

Question 16

Purpose of T3 and T4

Answer 16

 The function of the thyroid gland is to take
iodine, found in many foods, and convert it
into thyroid hormones: thyroxine (T4) and
triiodothyronine (T3).
 These cells combine iodine and the amino
acid tyrosine to make T3 and T4. T3 and
T4 are then released into the blood stream
and are transported throughout the body
where they control metabolism (conversion
of oxygen and calories to energy).

Question 17

Three Types of Hypoparathyroidism

Answer 17

Deficient parathyroid hormone
secretion
Inability to Make Active Parathyroid
Hormone.
Resistance to Parathyroid Hormone
(pseudo-hypoparathyroidism).

Question 18

Deficient Parathyroid Hormone Secretion

Answer 18

Lack of PTH leads to decreased
blood levels of calcium
(hypocalcemia) and increased
levels of blood phosphorus
(hyperphosphatemia).
There are no symptoms of too
little parathyroid hormone other
than the symptoms due to
having a blood calcium that is
too low.

Question 19

Inability to Make Active Parathyroid Hormone.

Answer 19

Deficient PTH secretion without
a defined cause (e.g. surgical
injury) is termed Idiopathic
hypoparathyroidism

Question 20

Resistance to Parathyroid Hormone (pseudo-hypoparathyroidism)

Answer 20

Characterised by hypocalcemia
(too low blood calcium levels)
and hyperphosphatemia (too
high blood phosphorus levels)

But they are distinguished by
the fact that they DO produce
NORMAL parathyroid hormone.

Question 21

Three types of
hyperparathyroidism

Answer 21

Primary
Secondary
Tertiary

Question 22

Primary Hyperparathyroidism

Answer 22

Generalized disorder resulting
from excessive secretion of
parathyroid hormone (PTH) by
one or more parathyroid glands.

It probably is the most common
cause of hypercalcemia

Question 23

Primary hyperparathyroidism is
caused by

Answer 23

parathyroid adenoma – 80%
parathyroid hyperplasia – 15%
parathyroid carcinoma – 1-2%

Question 24

Secondary hyperparathyroidism

Answer 24

Occurs most commonly in advanced
chronic kidney disease when decreased formation of
active vitamin D in the kidneys and other factors lead
to hypocalcemia and chronic stimulation of PTH
secretion.

Hyperphosphatemia that develops in response to
chronic kidney disease also contributes

Question 25

Tertiary Hyperparathyroidism

Answer 25

Occurs when prolonged parathyroid stimulation from
a secondary cause results in autonomous
parathyroid hyperfunction.

Question 26

Pathogenesis of primary Hyperparathyroidism

Answer 26

bone thinning and kidney stones (high calcium levels

Question 27

PTH

Answer 27

PTH is synthesized
as a 110 amino
acid polypeptide
called pre-pro-PTH

It is cleaved to
pro-PTH (90 amino
acids) and then
PTH (84 amino
acids)

PTH is the major
storage, secreted
and biologically
active form of the
hormone.Ca
regulates
synthesis, release
and degradation
of PTH

PTH gene is in
chromosome 11

PTH is a critical controller of
calcium and phosphorus
balance.

Question 28

Prolactinoma

Answer 28

Prolactinoma is the most common tumour of pituitary
gland, comprising up to 45% of all pituitary tumours.

Prolactinoma is the most common cause of
hyperprolactinemia, which is a common cause of
infertility in males.

Question 29

Macroprolactinoma

Answer 29

Is the apparent increase in serum prolactin
without symptoms

Serum prolactin molecules can polymerize and
subsequently bind to immunoglobulin G (IgG).
This form of prolactin is unable to bind to prolactin
receptors and exhibits no systemic response.
In the asymptomatic patient with
hyperprolactinemia, this condition should be
considered.

Question 30

Complication of Macroprolactinoma

Answer 30

Macroprolactinomas may press
against nearby parts of the
pituitary gland and the brain.

Question 31

FUNCTION of thyroid

Answer 31

 The function of the thyroid gland is to take
iodine, found in many foods, and convert it
into thyroid hormones: thyroxine (T4) and
triiodothyronine (T3).
 These cells combine iodine and the amino
acid tyrosine to make T3 and T4. T3 and
T4 are then released into the blood stream
and are transported throughout the body
where they control metabolism (conversion
of oxygen and calories to energy).

Question 32

Testosterone function

Answer 32

 Male sexual differentiation
 Secondary sex characteristic in puberty and adult
 Spermatogenesis
 Muscle strength, Muscle volume
 Bone density
 Erythropoeisis

Question 33

LH and FSH in men and women

Answer 33

Male Hormones:
 At the onset of puberty, the hypothalamus causes the release of FSH and
LH into the male system for the first time.
 FSH enters the testes and stimulates the Sertoli cells to begin facilitating
spermatogenesis using negative feedback.
 LH also enters the testes and stimulates the interstitial cells of Leydig to
make and release testosterone into the testes and the blood.

Female Hormones:
As with the male, the anterior pituitary hormones cause the release of the hormones FSH and LH.
 In addition, estrogens and progesterone are released from the developing follicles.
 Estrogen is the reproductive hormone in females that assists in endometrial regrowth, ovulation, and
calcium absorption; it is also responsible for the secondary sexual characteristics of females.
 These include breast development, flaring of the hips, and a shorter period necessary for bone
maturation.
 Progesterone assists in endometrial re-growth and inhibition of FSH and LH release.

LH also plays a role in the development of ova, induction of ovulation, and stimulation of estradiol and
progesterone production by the ovaries.

FSH stimulates development of egg cells, called ova, which develop in structures called follicles

Question 34

Posterior vs anterior pituitary hormones

Answer 34

Neurohypophysis: Posterior lobe hormones
The posterior pituitary does not produce any
hormones of its own, rather, it stores and
secretes two hormones made in the
hypothalamus:
* Oxytocin causes the uterus to contract
during childbirth and immediately after
delivery to prevent excessive bleeding.
* Vasopressin (also called antidiuretic
hormone) regulates the amount of water
excreted by the kidneys and is therefore
important in maintaining water balance in the
body.

Adenohypophysis: Anterior lobe hormones
* Growth hormone (GH)
* Thyroid-stimulating hormone (TSH)
* Adrenocorticotropic hormone (ACTH)
* Follicle-stimulating hormone (FSH)
* Luteinizing hormone (LH)
* Beta endorphin
* Prolactin

Question 35

Tropic vs non tropic hormones

Answer 35

Non-tropic hormones are hormones that directly stimulate target cells to induce effects. This differs from the tropic hormones, which act on another endocrine gland

Question 36

regulation of LH and FSH

Answer 36

Prolactin inhibits pulsatile GnRH secretion
and consequently inhibits the pulsatile
release of FSH, LH and testosterone. This is because gonadotrophin-releasing hormone (GnRH) from the hypothalamus causes stimulation of the anterior pituitary to make LH and FSH

Question 37

ACTH dependent vs independent Cushing

Answer 37

ACTH-dependent disease:
 Pituitary Adenoma (also known as Cushing’s Disease)
In this condition, a small tumour causes increased ACTH production.
 Pituitary adenomas are the most common cause of Cushing’s syndrome and makes up
about 70% of cases.
 Ectopic ACTH-producing Tumour
 In this rare condition, a tumour outside of the pituitary is making too much ACTH.
 These tumours are most found in the lung and thymus gland, but have also been found in the thyroid,
ovary, adrenal gland, and liver.

ACTH-independent Disease
 In this condition, either both adrenal glands are hyperactive or there is an adrenal tumour
that is making too much cortisol.

Question 38

what is Cushing syndrome

Answer 38

Cushing syndrome occurs when there is too much cortisol over time

Hyperfunction of the adrenal cortex may be:
 ACTH- independent of ACTH regulation,
eg, production of cortisol by an
adrenocortical adenoma or carcinoma.
 ACTH-dependent hyperfunction of the
adrenal cortex may be due to
1. hypersecretion of ACTH by the
pituitary gland
2. secretion of ACTH by a nonpituitary
tumor, such as small cell carcinoma
of the lung (the ectopic ACTH
syndrome); or
3. administration of exogenous ACTH.

Question 39

Diagnosis of Cushing’s disease

Answer 39

Measurement of midnight plasma
cortisol or late-night salivary cortisol
 Elevated cortisol between 11:00 p.m. and
midnight appears to be the earliest detectable
abnormality in many patients with this disorder.
Cortisol secretion is usually very low at this time
of the day, but in patients with Cushing’s
syndrome, the value is usually elevated.

24-hour urinary free cortisol test
 Reflect the cortisol secretion throughout an
entire day. Although most patients with
Cushing’s have elevated levels of urine free
cortisol, it is becoming increasingly evident that
many patients with mild Cushing’s syndrome will
actually have normal levels of urine free cortisol.

Dexamethasone suppression
screening test.
Dexamethasone is a synthetic steroid that should suppress the cortisol
production in normal subjects to a very low level.
 Measures whether adrenocorticotrophic hormone (ACTH)
secretion by the pituitary can be suppressed.
 Dexamethasone is given and levels of cortisol are measured.
 Cortisol levels should decrease in response to the administration
of dexamethasone.

Question 40

hypogonadism

Answer 40

The term “Hypogonadism” designates a deficiency in
ovary or testicular function

Question 41

3 forms of female hypogonadism

Answer 41

 Primary hypogonadism
 Secondary hypogonadism
 Menopause.

Question 42

Male hypogonadism

Answer 42

A decrease in either of the two major
functions of the testes:
 sperm production
 testosterone production

Question 43

Male hypogonadism primary vs secondary

Answer 43

Primary hypogonadism
 Testes
 Serum Testosterone↓, FSH & LH ↑

Secondary hypogonadism
 Pituitary gland or Hypothalamus
 Serum Testosterone↓, FSH & LH
↔ , ↓

Question 44

Estradiol

Answer 44

Estradiol and progesterone are steroid hormones that prepare the body for pregnancy.
 Estradiol produces secondary sex characteristics in females, while both estradiol and progesterone
regulate the menstrual cycle.

Question 45

Female hypogonadism

Answer 45

Describes the inadequate function
of the ovaries, with impaired
production of germ cells (eggs)
and sex hormones
(oestrogen and progesterone).
 Primary hypogonadism refers to a
condition of the ovaries (primary
ovarian
insufficiency/hypergonadotropic
hypogonadism).
 Secondary hypogonadism refers to
the failure of
the hypothalamus or pituitary
gland (hypogonadotropic
hypogonadism).

Question 46

Primary
ovarian
insufficiency

Answer 46

Ovaries do not regularly release eggs
and do not produce enough sex
hormones despite high levels of
circulating gonadotropins

Question 47

Follicle-stimulating hormone

Answer 47

activates aromatase in granulosa cells around the
developing oocytes to convert androgens
to estradiol.

Question 48

Estrogen

Answer 48

stimulates the endometrium,
causing it to proliferate.

Question 49

Luteinizing hormone

Answer 49

when it surges
during the menstrual cycle, promotes
maturation of the dominant oocyte,
release of the oocyte, and formation of
the corpus luteum, which
produces progesterone.

Question 50

Progesterone

Answer 50

changes the endometrium
into a secretory structure and prepares it
for egg implantation (endometrial
decidualization)

Question 51

Hypergonadotropic
hypogonadism

Answer 51

Also called primary hypogonadism,
is a disorder of abnormal function of
gonads with decreased estradiol
in females, which results in delayed
sexual development.
 Diagnosis is by measuring FSH
and estradiol levels.

Question 52

Acromegaly (occurs in adults)

Answer 52

Characterized by hypersecretion of growth
hormone (GH),which is caused by the
existence of a secreting pituitary tumour in
more than 95% of acromegaly cases.
In rare instances, elevated GH levels are
caused by extra pituitary disorders.
Hypersecretion of GH in turn causes
subsequent hepatic stimulation of insulin-like
growth factor-1 (IGF-1) leading to enlarge
physical features.
Peripheral neuropathies occur commonly
because of compression of nerves by
adjacent fibrous tissue and endoneural
fibrous proliferation.

Question 53

Hyperprolactinaemia in Male

Answer 53

High blood prolactin concentration interferes with
the function of the testicles, the production of
testosterone (the main male sex hormone), and
sperm production.

Question 54

GH

Answer 54

Promotes growth: skeleton,
muscles, viscera
Effects mediated by
somatomedins
Released at night during growth

Variety of metabolic effects
Anabolic, positive nitrogen
balance
Anti-insulin

Question 55

Primary IGF-1 deficiency

Answer 55

Primary IGFD may happen when IGF-1 levels are low, even
though growth hormone levels are normal or even high
Secondary IGFD happens in children whose IGF-1 levels are
low; this may be due to their bodies’ inability to produce
enough growth hormone, poor nutrition, thyroid problems or
other factors
Severe primary IGFD is a type of primary IGFD in which IGF-
1 levels are exceptionally low, despite sufficient or high
growth hormone levels

Question 56

Mediator of Growth hormone
IGF-1

Answer 56

IGF-1 is synthesized mainly by the liver but also
locally in many tissues.
Activation of the growth hormone receptor stimulates
the synthesis and secretion of insulin-like growth
factor-1 (IGF-1), a small peptide (about 7.5 kD)
structurally related to proinsulin.
IGF-1 circulates in the blood at high concentrations
and acts as a mitogen, stimulating DNA, RNA and
protein synthesis.

Question 57

Diagnosis of
excess GH

Answer 57

Functional tests for GH
1. Basal plasma GH level: High
2. Plasma Prolactin level: High
3. Glucose tolerance suppression
test: 75 grams of glucose to be
given orally, GH and blood
glucose level to be measured 2
hourly

Question 58

GH excess

Answer 58

GH excess affects insulin
sensitivity and
gluconeogenesis and can alter
pancreatic β-cell function,
leading to a derangement of
glucose metabolism in a
considerable percentage of
acromegaly patients.
Induces hyperglycaemia by
increasing endogenous
glucose production and
decreasing peripheral
glucose disposal in muscle

Question 59

Metabolic
Functions of
Copper

Answer 59

 Is component of a cofactor for approximately 50
different enzymes. These enzymes need copper to
function properly.
 Is essential for iron absorption and transport.
 Iron is needed to make haemoglobin, a main
component of red blood cells. Therefore, copper
deficiency is often linked to iron-deficiency anemia.
 Is required to build elastin and collagen, which are an
important components of bones and connective tissues.
Therefore, copper is believed to protect the bones and
joints against degeneration and osteoporosis.
 Is required for melanin (pigment) production. People
with copper deficiency may have pale skin and hair.
 Is a key mineral for the immune system. Copper
promotes wound healing.

Question 60

Copper

Answer 60

3rd most important trace element
 Copper combines with certain proteins to produce enzymes
that act as catalysts to help several body functions.
 Some help provide energy required by biochemical
reactions.
 Others are involved in the transformation of melanin for
pigmentation of the skin and still others help to form cross-
links in collagen and elastin and thereby maintain and repair
connective tissues.

Question 61

Wilsons disease (Copper toxicity)

Answer 61

A genetic disorder characterized by copper accumulation
in various organs due to the inadequate synthesis of
ceruloplasmin (the protein that transports copper through
the blood) by the liver
 Wilson’s disease primarily effects the liver, kidneys,
and brain causing degenerative physiological changes
(including cirrhosis of the liver, muscular rigidity and
spastic contraction, and emotional disturbances) that
are fatal if untreated.
 The treatment of Wilson’s disease involves avoidance
of foods rich in copper and any supplements
containing copper and drug treatment with chelating
agents that remove the excess copper from the body.

Question 62

Vitamins

Answer 62

Vitamins are organic molecules that
function in a wide variety of capacities
within the body. The most prominent
function is as cofactors for enzymatic
reactions.

The distinguishing feature of the
vitamins is that they generally cannot
be synthesized by mammalian cells
and, therefore, must be supplied in the
diet. The vitamins are of two distinct
types:
 Water Soluble Vitamins
 Fat Soluble Vitamins

Question 63

3 Water Soluble Vitamins

Answer 63

Some B vitamins
 Riboflavin (Vitamin B2)
 Thiamin which is vitamin B1)

vitamin C

Question 64

3 Fat Soluble Vitamins

Answer 64

Dissolve in fat, vitamins A, D, E

Question 65

Thiamin
(Vitamin B1)

Answer 65

Functions as the coenzyme
thiamin pyrophosphate (TPP) in
the metabolism of carbohydrate
and in conduction of nerve
impulses.

Question 66

Niacin
(Vitamin B3)

Answer 66

There are two coenzyme forms of
niacin: nicotinamide adenine
dinucleotide (NAD+) and nicotinamide
adenine dinucleotide phosphate
(NADP+).

Question 67

Riboflavin
(Vitamin B2)

Answer 67

 Riboflavin is a component of two
coenzymes—flavin mononucleotide
(FMN) and flavin adenine
dinucleotide (FAD)—that act as
hydrogen carriers when
carbohydrates and fats are used to
produce energy.
 It is helpful in maintaining good
vision and healthy hair, skin and
nails, and it is necessary for normal
cell growth.

Question 68

Pantothenic
Acid
(Vitamin B5)

Answer 68

Coenzyme A is also important in the synthesis of
fatty acids, cholesterol, steroids, and the
neurotransmitter acetylcholine, which is
essential for transmission of nerve impulses to
muscles.

Question 69

Vitamin B6

Answer 69

Pyridoxal phosphate (PLP) is the
predominant biologically active
form.
 PLP participates in amino acid
synthesis and the interconversion of
some amino acids.
 It catalyzes a step in the synthesis of
hemoglobin, which is needed to
transport oxygen in blood.
 PLP helps maintain blood glucose
levels by facilitating the release of
glucose from liver and muscle
glycogen

Question 70

Folic Acid,
Folate,
Folacin
(Vitamin B9)

Answer 70

Found in its free-vitamin form,
called cyanocobalamin, and in
two active coenzyme forms.
 Absorption of vitamin B12 requires
the presence of intrinsic factor, a
protein synthesized by acid-
producing cells of the stomach.

Question 71

Vitamin C
(Ascorbic
Acid)

Answer 71

Collagen is also needed for the healing of
wounds. When added to meals, vitamin C
increases intestinal absorption of iron from
plant-based foods.
 High concentration of vitamin C in
white blood cells enables the
immune system to function
properly by providing protection
against oxidative damage from
free radicals generated during their
action against bacterial, viral, or
fungal infections.

Question 72

Vitamin A

Answer 72

Retinol binding protein (RBP), transports
vitamin A from the liver to other tissues

 Free radicals are unstable, highly
reactive molecules that damage DNA,
cause cell injury, and increase the risk of
chronic disease.
 Lutein and zeaxanthin, yellow
carotenoid pigments in corn and dark
green leafy vegetables, may reduce the
risk of macular degeneration and age-
related cataracts.
 Lycopene, a red carotenoid pigment in
tomatoes, may help reduce the risk of
prostrate cancer, cardiovascular
disease, and skin damage from sunlight.

Question 73

Vitamin K

Answer 73

Helps in the activation of seven
blood-clotting-factor proteins that
participate in a series of reactions
to form a clot that eventually stops
the flow of blood.

Question 74

Malignant vs benign tumours

Answer 74

Benign tumours do not spread
from their site of origin, but can
crowd out (squash) surrounding
cells eg brain tumour, warts.
Malignant tumours can spread
from the original site and cause
secondary tumours. This is called
metastasis. They interfere with
neighbouring cells and can block
blood vessels, the gut, glands,
lungs etc.

Question 75

Types of TM

Answer 75

Circulating tumour markers can be found in the
blood, urine, stool, or other bodily fluids of some
patients with cancer. Circulating tumour markers are
used to:
estimate prognosis
detect cancer that remains after treatment (
residual disease) or that has returned after treatment
assess the response to treatment
monitor whether a cancer has become resistant to
treatment

Tumour tissue markers are found in the actual
tumours themselves, typically in a sample of the
tumour that is removed during a biopsy.
Tumour tissue markers are used to:
diagnose, stage, and/or classify cancer
estimate prognosis
select an appropriate treatment (eg, treatment with a
targeted therapy)

Question 76

Dilemma of tumour markers

Answer 76

1) tumour marker levels can be
elevated in people with benign
conditions;
2) tumour marker levels are not
elevated in every person with
cancer, especially in the early
stages of the disease;
3) many tumour markers are not
specific to a cancer
4) the level of a tumour marker can
be elevated by more than one
type of cancer (NCI, 2006).

Question 77

An ideal tumour marker

Answer 77

The quality should be included
High sensitivity
High specificity
Can be qualified
Safe
Convenience
Low price

Question 78

Zinc and cell mediated immunity

Answer 78

Play a central role in the immune system
and Zn deficient individuals experience
increased susceptibility to a variety of
pathogens.

Affects multiple aspects of the immune
system from the barrier of the skin to
gene regulation within lymphocytes.
 Zn is crucial for normal development
and function of cells mediating non-
specific immunity such as neutrophils
and natural killer cells.
 Zn deficiency also affects development
of acquired immunity by preventing
both the outgrowth and certain
functions of T cells such as activation,
Th1 cytokine production, and B cell
help.

The macrophage, a pivotal cell in
many immunological functions, is
adversely affected by Zn deficiency,
which can dysregulate intracellular
killing, cytokine production, and
phagocytosis.

Zn deficiency affects the
development of acquired immunity by
regulating growth and function of T
and B cells.

Zn is needed for DNA replication,
RNA transcription, cell division, and
cell activation.
 Apoptosis is potentiated by Zn
deficiency and Zn also functions
as an antioxidant and can
stabilize membranes.

Question 79

The role of Selenium in HIV /
AIDS

Answer 79

 Recent reports indicate that selenium status is predictive
of HIV-1 related prognosis and may have an important
role in preventing HIV-1 replication.
 studies in HIV-1 seropositive drug users demonstrate that
selenium is a powerful predictor of HIV-1 disease
progression and mortality.
 These findings suggest that selenium administered as a
chemopreventive agent may effectively modulate HIV
disease progression.

Role of selenium in HIV-1 infection appears to be
multifactorial.
 As a biological antioxidant, selenium is required for the activity
of glutathione peroxidase.
 Adequate selenium status may also be essential in controlling
viral emergence and evolution. In addition, adequate selenium
may enhance resistance to infection through modulation of
interleukin (IL) production and subsequent changes in Th1/Th2
cytokine responses.
 Other nutritional factors may be interacting with selenium status,
and contribute to the HIV-1 progression and mortality.

Question 80

Extensive Metabolizers (EM) - Inhibitors

Answer 80

 Extensive metabolizer —– level of
substrate drug is normally low due to
rapid metabolism by the enzyme.
 An inhibitor to the enzyme will inhibit the
extensive metabolism and cause
significant elevations in the substrate
drug.

Question 81

Poor Metabolizers (PM) - Inhibitors

Answer 81

 In a poor metabolizer, the level of substrate drug
remains high because the metabolism of the
substrate is much less than normal.
 When an inhibitor is added, the additional
inhibition of metabolism is not much greater than is
already occurring in the PM.
 The effect of inhibitor is less in a PM than in
normal metabolizers.

Question 82

Extensive Metabolizers - Inducers

Answer 82

 Level of substrate drug is lower than in a normal
metabolizer due to rapid metabolism.
 The addition of an inducer does not cause a
greater difference in the level of substrate because
the metabolism is already increased greatly.
 The drug interaction might not occur.

Question 83

Poor Metabolizers - Inducers

Answer 83

 Level of substrate drug is higher than expected in
normal metabolizer because of the lower
metabolism of substrate.
 The addition of inducer will cause a signification
increase in the metabolism of the substrate -much
lower level of substrate than expected in a normal
metabolizer.
 Drug interaction may occur to a greater extent.
 Drug interaction may result in substrate levels like
those of normal metabolizers.

Question 84

inhibitor vs inducer

Answer 84

Inhibitor: An enzyme inhibitor is a
molecule, which binds to enzymes
and decreases their activity.
Inducer: An enzyme inducer is a type
of drug that increases the metabolic
activity of an enzyme either by
binding to the enzyme and activating
it, or by increasing the expression of
the gene coding for the enzyme.

Question 85

Slope calculation

Answer 85

The slope formula is m=(y2-y1)/(x2-x1)