PORTAGE PATHOPHYSIOLOGY
Module 9: Exam Questions with Answers
,Q1. Differentiate between the three major chemical classes of hormones
and give one example of each.
Answer:
Hormones are classified by chemical structure into three groups. (1)
Peptide/protein hormones (e.g., insulin, growth hormone, ADH) are
water-soluble, stored in secretory vesicles, act via cell-surface receptors and
second messengers (e.g., cAMP), and have a rapid onset with short half-life.
(2) Steroid hormones (e.g., cortisol, aldosterone, estrogen, testosterone)
are derived from cholesterol, lipid-soluble, not stored (synthesized on
demand), travel bound to carrier proteins, cross the cell membrane, and bind
intracellular/nuclear receptors to directly alter gene transcription, giving a
slower but more sustained effect. (3) Amine hormones (e.g., thyroid
hormone, epinephrine, norepinephrine) are derived from amino acids
(tyrosine); thyroid hormone behaves like a steroid (lipid-soluble, nuclear
receptor) while catecholamines behave like peptides (water-soluble, surface
receptor).
Q2. Explain the concept of negative feedback in endocrine regulation
and why it is clinically important.
Answer:
In negative feedback, the hormone (or the physiological effect it produces)
inhibits further hormone release, keeping levels within a homeostatic range.
For example, rising cortisol suppresses hypothalamic CRH and pituitary
ACTH secretion. This is clinically important because measuring both the
trophic hormone and the target-gland hormone together allows localization of
a pathology: e.g., high cortisol with low ACTH suggests an adrenal source
(primary), whereas high cortisol with high ACTH suggests a pituitary or
ectopic source (secondary/tertiary). Loss of normal feedback suppression is
the basis of most endocrine stimulation and suppression tests.
Q3. What is the difference between primary, secondary, and tertiary
endocrine gland dysfunction?
Answer:
, Primary dysfunction originates in the target/peripheral gland itself (e.g.,
primary hypothyroidism from thyroid gland failure) — trophic hormone (TSH)
is high because feedback inhibition is lost. Secondary dysfunction
originates in the pituitary (e.g., low TSH causing hypothyroidism). Tertiary
dysfunction originates in the hypothalamus (e.g., low TRH causing low TSH
and low thyroid hormone). Distinguishing these levels requires measuring
the hormone at each level of the axis (hypothalamic releasing hormone,
pituitary trophic hormone, and peripheral gland hormone).
Q4. Describe the hypothalamic-pituitary-target organ axis using the
thyroid axis as an example.
Answer:
The hypothalamus releases thyrotropin-releasing hormone (TRH), which
stimulates the anterior pituitary to secrete thyroid-stimulating hormone
(TSH). TSH stimulates the thyroid gland to produce T4 (thyroxine) and T3
(triiodothyronine). Circulating T3/T4 then exert negative feedback on both
the hypothalamus (decreasing TRH) and the anterior pituitary (decreasing
TSH), maintaining stable circulating thyroid hormone levels. This three-tier
axis (hypothalamus pituitary target gland) is the general template for
most endocrine systems, including the adrenal (CRH-ACTH-cortisol) and
gonadal (GnRH-LH/FSH-sex steroids) axes.
Q5. What are 'up-regulation' and 'down-regulation' of hormone receptors,
and how do they affect tissue sensitivity?
Answer:
Down-regulation occurs when chronic exposure to high hormone
concentrations decreases the number or sensitivity of receptors on target
cells, reducing tissue responsiveness (e.g., insulin resistance in type 2
diabetes, where chronic hyperinsulinemia down-regulates insulin receptors).
Up-regulation occurs when low hormone levels or increased need cause
target cells to increase receptor number/sensitivity, enhancing
responsiveness to the available hormone. These adaptive mechanisms
explain why hormone effect does not always correlate linearly with
circulating hormone concentration and are central to the pathophysiology of
receptor-based endocrine disorders.
Module 9: Exam Questions with Answers
,Q1. Differentiate between the three major chemical classes of hormones
and give one example of each.
Answer:
Hormones are classified by chemical structure into three groups. (1)
Peptide/protein hormones (e.g., insulin, growth hormone, ADH) are
water-soluble, stored in secretory vesicles, act via cell-surface receptors and
second messengers (e.g., cAMP), and have a rapid onset with short half-life.
(2) Steroid hormones (e.g., cortisol, aldosterone, estrogen, testosterone)
are derived from cholesterol, lipid-soluble, not stored (synthesized on
demand), travel bound to carrier proteins, cross the cell membrane, and bind
intracellular/nuclear receptors to directly alter gene transcription, giving a
slower but more sustained effect. (3) Amine hormones (e.g., thyroid
hormone, epinephrine, norepinephrine) are derived from amino acids
(tyrosine); thyroid hormone behaves like a steroid (lipid-soluble, nuclear
receptor) while catecholamines behave like peptides (water-soluble, surface
receptor).
Q2. Explain the concept of negative feedback in endocrine regulation
and why it is clinically important.
Answer:
In negative feedback, the hormone (or the physiological effect it produces)
inhibits further hormone release, keeping levels within a homeostatic range.
For example, rising cortisol suppresses hypothalamic CRH and pituitary
ACTH secretion. This is clinically important because measuring both the
trophic hormone and the target-gland hormone together allows localization of
a pathology: e.g., high cortisol with low ACTH suggests an adrenal source
(primary), whereas high cortisol with high ACTH suggests a pituitary or
ectopic source (secondary/tertiary). Loss of normal feedback suppression is
the basis of most endocrine stimulation and suppression tests.
Q3. What is the difference between primary, secondary, and tertiary
endocrine gland dysfunction?
Answer:
, Primary dysfunction originates in the target/peripheral gland itself (e.g.,
primary hypothyroidism from thyroid gland failure) — trophic hormone (TSH)
is high because feedback inhibition is lost. Secondary dysfunction
originates in the pituitary (e.g., low TSH causing hypothyroidism). Tertiary
dysfunction originates in the hypothalamus (e.g., low TRH causing low TSH
and low thyroid hormone). Distinguishing these levels requires measuring
the hormone at each level of the axis (hypothalamic releasing hormone,
pituitary trophic hormone, and peripheral gland hormone).
Q4. Describe the hypothalamic-pituitary-target organ axis using the
thyroid axis as an example.
Answer:
The hypothalamus releases thyrotropin-releasing hormone (TRH), which
stimulates the anterior pituitary to secrete thyroid-stimulating hormone
(TSH). TSH stimulates the thyroid gland to produce T4 (thyroxine) and T3
(triiodothyronine). Circulating T3/T4 then exert negative feedback on both
the hypothalamus (decreasing TRH) and the anterior pituitary (decreasing
TSH), maintaining stable circulating thyroid hormone levels. This three-tier
axis (hypothalamus pituitary target gland) is the general template for
most endocrine systems, including the adrenal (CRH-ACTH-cortisol) and
gonadal (GnRH-LH/FSH-sex steroids) axes.
Q5. What are 'up-regulation' and 'down-regulation' of hormone receptors,
and how do they affect tissue sensitivity?
Answer:
Down-regulation occurs when chronic exposure to high hormone
concentrations decreases the number or sensitivity of receptors on target
cells, reducing tissue responsiveness (e.g., insulin resistance in type 2
diabetes, where chronic hyperinsulinemia down-regulates insulin receptors).
Up-regulation occurs when low hormone levels or increased need cause
target cells to increase receptor number/sensitivity, enhancing
responsiveness to the available hormone. These adaptive mechanisms
explain why hormone effect does not always correlate linearly with
circulating hormone concentration and are central to the pathophysiology of
receptor-based endocrine disorders.
