ENDO 1 Flashcards
Endocrine Features: (2)
• Provides “broadcast’ regulation of many tissues; specificity due to receptors • Slower but longer lasting responses compared to the NS
We will discuss individual hormones and their specific physiological
functions, but, in general, all hormones regulate three types of things: (3)
(1) Maintenance of Homeostasis
- Thyroid Hormone, Insulin, PTH, Vasopressin, Aldosterone, etc.
(2) Growth and Differentiation
- Growth Hormone, Thyroid Hormone, etc.
(3) Reproduction
- LH, FSH, Estrogen, Progesterone, Testosterone, etc.
Specialized endocrine glands: (5)
– Pituitary Gland – Thyroid Gland – Parathyroid Gland – Adrenal Gland – Pineal Gland
SKIPPED Some organs contain endocrine cells that secrete hormones even though their primary function is not endocrine regulation. (11)
– Hypothalamus (TRH, CRH, etc.) – Skin (Vitamin D) – Adipose Tissue (Leptin) – Thymus (Thymosin) – Heart (Atrial Natriuretic Peptide) – Liver (Insulin-Like GF1) – Stomach (Gastrin) – Pancreas (Insulin, Glucagon) – Small Intestine (Secretin, CCK) – Kidney (Renin, EPO, Vitamin D) – Gonads (Testes, Ovaries)
Classes of Hormones (3)
- Proteins and Polypeptides
- Steroids
- Derivatives of Tyrosine
Protein and Polypeptide Hormones
Hormones from the (4)
Hypothalamus,
Anterior Pituitary,
Posterior Pituitary (ex. Antidiuretic Hormone – 9 Amino Acids),
Pancreas (ex. Insulin – 51 Amino Acids), etc.
process of protein activation
Synthesized first as a Preprohormone, which isthen converted to the Prohormone. Upon packing into vesicles in the endocrine cell, the prohormone is cleaved into the Active hormone and Inactive fragments that are then secreted by the endocrine cell.
Steroid Hormones are from the (3)
adrenal cortex
ovaries
testes
Steroid hormones are synthesized from
cholesterol
when are steroid hormones synthesized?
Hormones are synthesized upon demand rather
than being stored.
Amine Hormones are derived from
aa tyrosine
Amine Hormones includes (2)
thyroid hormone and adrenal medullary
neurohormones (epinephrine and norepinephrine).
when are amine hormones produced?
Amine hormones are produced and then stored until
secreted.
Thyroid
hormones bind
to the protein
thyroglobulin
Epinephrine
and
norepinephrine
are stored in
vesicles and
released by
exocytosis
Hormones released into the circulation can circulate either freely or bound to carrier proteins, also known as
binding proteins
The binding proteins serve as a reservoir
for the hormone and prolong the hormone’s
half-life, the time during which the
concentration of a hormone decreases to 50% of its initial concentration.
The (2) hormone is the active form of the hormone, which binds to the specific
hormone receptor
free or unbound
The majority of amines, peptides, and protein hormones circulate in their —
form.
free
Steroid and thyroid hormones circulate bound to
specific transport proteins.
Some binding proteins are specific for a given hormone but some plasma
proteins, such as globulin and albumin can bind to hormones.
Thyroid hormone travels in the plasma bound to: (3)
Thyroxine-binding Globulin (TBG), Transthyretin (TTR)
and Albumin
Because most binding proteins are synthesized in the liver, changes in liver function (ex. cirrhosis) may alter
binding
-protein levels and could indirectly affect
plasma hormone levels.
Plasma levels of hormones
oscillate throughout the day,
showing peaks and troughs
that are — specific
hormone
This variable pattern of hormone release is determined by the interaction and integration of multiple control mechanisms, which include
hormonal, neural, nutritional, and environmental factors that regulate the constitutive (basal) and stimulated (peak levels) secretion of hormones
The location of the hormone receptor depends on the —
properties of the hormone (lipophobic/lipophillic).
chemical
Ligand/Receptor binding demonstrates (3)
specificity, affinity and saturation.
Plasma Membrane Hormone Receptors (4)
- G-protein Coupled
- Tyrosine Kinase: Insulin
- Serine Kinase
- Cytokine: Leptin
Gs coupled Receptors (β Adrenergic, Calcitonin,
ACTH, Glucagon, TSH, Vasopressin) produce the
second messenger —.
cAMP
Gq coupled Receptors (α Adrenergic,
Angiotensin II, TRH) activate the second
messengers (3)
IP3, DAG and Ca2+.
Receptor numbers vary greatly in
different target tissues. This
provides a way to achieve specific
tissue activation
Some receptors, such as (2) receptors,
are more widely distributed.
insulin
and thyroid hormone
Nuclear Hormone Receptors
A large family of receptors that are located either in the cytoplasm or
nucleus. All act to increase or decrease gene expression.
The hormone receptor complex binds to a hormone responsive element in the promoter region of a gene, which leads to either
activation or
repression of
transcription. Forms
new proteins.
Hormone Interactions
The effects of combined actions: (4)
– Antagonism
– Additive
– Synergistic
– Permissiveness
Which hormone interaction is described in each of the
following situations?
A. Parathyroid increases plasma calcium levels; Calcitonin
decreases plasma calcium levels.
B. Glucagon, cortisol and epinephrine all increase blood
glucose more than the sum of their individual effects.
C. Thyroid hormone causes expression of B adrenergic
receptors in bronchiolar smooth muscle.
Tropic Hormones are hormones that have ---- as their targets.
other
endocrine
glands
Hormone levels must be kept in balance
with negative feedback mechanisms. If this
doesn’t occur,— — occur.
endocrine disorders
Primary Disorders
• Abnormality in the last
endocrine organ secreting the
hormone leading to either
hypo- or hyper-secretion.
Causes of Primary Hyposecretion: (3)
(1) Partial destruction of the gland
(2) Dietary Deficiency
(3) Enzyme deficiency required for
hormone synthesis
A tumor in an endocrine gland can
cause
Primary Hypersecretion.
Secondary Disorders
• Abnormality in tropic hormone
leading to either hypo- or
hyper-secretion
A lack of sufficient tropic hormone
leads to
Secondary Hyposecretion.
A tumor (either in an endocrine gland
that secretes tropic hormones or in
non-endocrine tissue (lung)) can
secrete hormones and cause
Secondary Hypersecretion (Paraneoplastic Endocrine Syndrome)
A PRIMARY endocrine
pathology is one where the
abnormality is in the
endocrine organ secreting the hormone (ex. thyroid gland is either secreting too much or insufficient amount of TH.
A SECONDARY endocrine
pathology is where the
abnormality is in
one of the endocrine glands that secrete trophic hormones (Hypothalamus or Anterior Pituitary).
SKIPPED
Diagnostic Tests of Endocrine
Function (7)
- Plasma hormone levels
- Autoantibodies: Hashimoto thyroiditis, type I diabetes, Graves disease, Addison disease, autoimmune hypoparathyroidism
- Urine hormone or hormone metabolite levels
- Stimulation tests by administration of a tropic or stimulating hormone (ex. ACTH to stimulate cortisol release, glucose load to stimulate insulin release)
- Suppression tests when hyperfunction of an endocrine organ is suspected (ex. response of GH to a glucose load or dexamethasone a synthetic glucocorticoid to suppress ACTH and Cortisol)
- Measurement of hormone receptor presence, number and affinity (ex. estrogen receptors in breast tumors)
- Imaging: Radioactive scanning of the thyroid and parathyroids; MRI of pituitary and hypothalamic imagine, CT scanning of adrenal and abdominal endocrine lesions, etc.
