Exam revision Flashcards
1
Q
types of congenital adrenal hyperplasia
A
- 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
2
Q
Most common forms of congenital adrenal
hyperplasia
A
21-hydroxylase
deficiency
11beta-
hydroxylase
deficiency
3
Q
Congenital Adrenal Hyperplasia
A
Congenital Adrenal Hyperplasia (CAH) is
a family of inherited disorders affecting
the adrenal glands.
Autosomal recessive (mutation on chromosome 6)
4
Q
why is cortisol high in Cushing disease
A
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
5
Q
what is hypothyroidism?
A
Hypothyroidism is
a condition in which the thyroid
doesn’t make enough thyroid
hormones.
6
Q
what is Hyperthyroidism?
A
Hyperthyroidism
is a condition in which the thyroid
makes too much of certain thyroid
hormones.
7
Q
most common cause for hypo and hyper thyroidism
A
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
8
Q
3 types of hypothyroidism
A
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.
9
Q
most common cause of PRIMARY HYPOTHYROIDISM
A
Hashimoto’s thyroiditis
10
Q
Diagnosis for Primary
Hypothyroidism
-Hashimoto
thyroiditis
A
High TSH with low Free T4/T3
High Thyroid autoantibodies
11
Q
Diagnosis for Subclinical Hypothyroidism
A
Elevated TSH and Normal T4/T3 level
12
Q
Diagnosis for SECONDARY HYPOTHYROIDISM
A
Low levels of T4/T3 with high
level of TRH
13
Q
3 causes of hyperthyroidism
A
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
14
Q
best way to determine thyroid dysfunction
A
Measuring serum TSH
15
Q
What are the key players for
Thyroid hormone regulation?
A
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)
16
Q
Purpose of T3 and T4
A
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).
17
Q
Three Types of Hypoparathyroidism
A
Deficient parathyroid hormone
secretion
Inability to Make Active Parathyroid
Hormone.
Resistance to Parathyroid Hormone
(pseudo-hypoparathyroidism).
18
Q
Deficient Parathyroid Hormone Secretion
A
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.
19
Q
Inability to Make Active Parathyroid Hormone.
A
Deficient PTH secretion without
a defined cause (e.g. surgical
injury) is termed Idiopathic
hypoparathyroidism
20
Q
Resistance to Parathyroid Hormone (pseudo-hypoparathyroidism)
A
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.
21
Q
Three types of
hyperparathyroidism
A
Primary
Secondary
Tertiary
22
Q
Primary Hyperparathyroidism
A
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
23
Q
Primary hyperparathyroidism is
caused by
A
parathyroid adenoma – 80%
parathyroid hyperplasia – 15%
parathyroid carcinoma – 1-2%
24
Q
Secondary hyperparathyroidism
A
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
25
Tertiary Hyperparathyroidism
Occurs when prolonged parathyroid stimulation from
a secondary cause results in autonomous
parathyroid hyperfunction.
26
Pathogenesis of primary Hyperparathyroidism
bone thinning and kidney stones (high calcium levels
27
PTH
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.
28
Prolactinoma
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.
29
Macroprolactinoma
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.
30
Complication of Macroprolactinoma
Macroprolactinomas may press
against nearby parts of the
pituitary gland and the brain.
31
FUNCTION of thyroid
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).
32
Testosterone function
Male sexual differentiation
Secondary sex characteristic in puberty and adult
Spermatogenesis
Muscle strength, Muscle volume
Bone density
Erythropoeisis
33
LH and FSH in men and women
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
34
Posterior vs anterior pituitary hormones
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
35
Tropic vs non tropic hormones
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
36
regulation of LH and FSH
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
37
ACTH dependent vs independent Cushing
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.
38
what is Cushing syndrome
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.
39
Diagnosis of Cushing's disease
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.
40
hypogonadism
The term “Hypogonadism” designates a deficiency in
ovary or testicular function
41
3 forms of female hypogonadism
Primary hypogonadism
Secondary hypogonadism
Menopause.
42
Male hypogonadism
A decrease in either of the two major
functions of the testes:
sperm production
testosterone production
43
Male hypogonadism primary vs secondary
Primary hypogonadism
Testes
Serum Testosterone↓, FSH & LH ↑
Secondary hypogonadism
Pituitary gland or Hypothalamus
Serum Testosterone↓, FSH & LH
↔ , ↓
44
Estradiol
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.
45
Female hypogonadism
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).
46
Primary
ovarian
insufficiency
Ovaries do not regularly release eggs
and do not produce enough sex
hormones despite high levels of
circulating gonadotropins
47
Follicle-stimulating hormone
activates aromatase in granulosa cells around the
developing oocytes to convert androgens
to estradiol.
48
Estrogen
stimulates the endometrium,
causing it to proliferate.
49
Luteinizing hormone
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.
50
Progesterone
changes the endometrium
into a secretory structure and prepares it
for egg implantation (endometrial
decidualization)
51
Hypergonadotropic
hypogonadism
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.
52
Acromegaly (occurs in adults)
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.
53
Hyperprolactinaemia in Male
High blood prolactin concentration interferes with
the function of the testicles, the production of
testosterone (the main male sex hormone), and
sperm production.
54
GH
Promotes growth: skeleton,
muscles, viscera
Effects mediated by
somatomedins
Released at night during growth
Variety of metabolic effects
Anabolic, positive nitrogen
balance
Anti-insulin
55
Primary IGF-1 deficiency
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
56
Mediator of Growth hormone
IGF-1
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.
57
Diagnosis of
excess GH
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
58
GH excess
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
59
Metabolic
Functions of
Copper
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.
60
Copper
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.
61
Wilsons disease (Copper toxicity)
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.
62
Vitamins
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
63
3 Water Soluble Vitamins
Some B vitamins
Riboflavin (Vitamin B2)
Thiamin which is vitamin B1)
vitamin C
64
3 Fat Soluble Vitamins
Dissolve in fat, vitamins A, D, E
65
Thiamin
(Vitamin B1)
Functions as the coenzyme
thiamin pyrophosphate (TPP) in
the metabolism of carbohydrate
and in conduction of nerve
impulses.
66
Niacin
(Vitamin B3)
There are two coenzyme forms of
niacin: nicotinamide adenine
dinucleotide (NAD+) and nicotinamide
adenine dinucleotide phosphate
(NADP+).
67
Riboflavin
(Vitamin B2)
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.
68
Pantothenic
Acid
(Vitamin B5)
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.
69
Vitamin B6
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
70
Folic Acid,
Folate,
Folacin
(Vitamin B9)
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.
71
Vitamin C
(Ascorbic
Acid)
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.
72
Vitamin A
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.
73
Vitamin K
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.
74
Malignant vs benign tumours
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.
75
Types of TM
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)
76
Dilemma of tumour markers
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).
77
An ideal tumour marker
The quality should be included
High sensitivity
High specificity
Can be qualified
Safe
Convenience
Low price
78
Zinc and cell mediated immunity
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.
79
The role of Selenium in HIV /
AIDS
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.
80
Extensive Metabolizers (EM) - Inhibitors
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.
81
Poor Metabolizers (PM) - Inhibitors
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.
82
Extensive Metabolizers - Inducers
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.
83
Poor Metabolizers - Inducers
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.
84
inhibitor vs inducer
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.
85
Slope calculation
The slope formula is m=(y2-y1)/(x2-x1)
