Module 16: Endocrine System

Endocrine System

Acts with nervous system to coordinate & integrate activity of body cells. Influences metabolic activities is hormones transported in the blood. Response is slower, but lasts much longer longer than signals from nervous system

Exocrine glands

Secrete non-hormonal substances(sweat, saliva) into a network of ducts

Endocrine glands

directly secrete hormones into the bloodstream

How are hormones controlled?

Negative Feedback loop, allowing for only a narrow, desirable range

Hormones

Long-distance chemical signals that work at very low concentrations

Half-life

The rate of hormone breakdown in circulation, the amount of time required to reduce the concentration of hormone by one-half. How long a hormone is active in the body.

Preprohormone

Contains one or more copies of the peptide hormone, including a signal sequence directing movement into the Rough ER

Peptide/Protein Hormones

Made in advance and stored in secretory vesicles. Water-soluble/hydrophilic←degradation enzyme, short half-life, must bind to membrane bound receptors to signal via secondary messenger systems (fast)

Steroid Hormones

Synthesized from cholesterol, hydrophobic, and must be transported by carrier proteins into the blood. Longer half-life and ability to diffuse across the plasma membrane. Hormones secreted by gonads and adrenal cortex, heavily modified with smooth ER

Amino Acid derived Hormones

Derived from either tryptophan (melatonin) or tyrosine

Water soluble hormones

Protein/peptide and all amino acid based hormones except thyroid hormone. A on plasma membrane receptors and work through secondary messenger systems

Lipid soluble hormones

Steroid and thyroid hormones. Act on intracellular receptors that directly activate genes

Up-regulation

Target cells form more receptors in response to low hormone levels, making them more sensitive to the signal

Down-regulation

Target cells loose receptors in response to high hormone levels, making them less sensitive to the signal

Humoral stimuli

Changing blood levels of ions/nutrients directly stimulate secretion of hormones (sensed by chemoreceptors)

Neural stimuli

Nerve fibers directly stimulate hormone release. NS can override endocrine functions esp during periods of extreme stress

Hormonal stimuli

Hormones stimulate other endocrine organs to release their hormones

Trophic hormones

Cause growth in their target tissues

Tropic hormones

hormones that stimulate other endocrine glands to release their hormones

Parathyroid hormone PTH

Controls Ca2+ homeostasis. Detects low [Ca2+] in the plasma

Posterior Pituitary

An extension of the hypothalamic neural tissue where the hormones are synthesized in the cell body (residing in. The hypothalamus) but released from the axon terminals (in the posterior pituitary). Oxytocin and ADH/Vasopressin

Oxytocin

Strong stimulant of uterine contractions as it is released during childbirth, but it also acts a neurotransmitter in the brain & a hormonal trigger for milk ejection

ADH/Vasopresin

Inhibits excessive urine production by regulating water balance in the kidneys

Peptide hormones

Control growth, metabolism, and reproduction

Thyroid-stimulating hormone TSH

Stimulates the normal development and secretary activity of the thyroid. Release of this is triggered by the hypothalamic hormone thyrotropin – releasing hormone (TRH) Inhibited by rising blood levels of thyroid hormones that act by negative feedback inhibition on the pituitary and hypothalamus

Thyrotropin-Releasing hormone TRH

Hypothalamic hormone, triggers, the release of Thyroid-Stimulating hormone TSH

Adrenocorticotropin hormone ACTH

Stimulates the adrenal cortex to release Corticosteroids. Triggered by rising levels of the hypothalamic, hormone, corticotropin, releasing hormone CRH in daily rhythm. Inhibited by rising levels of corticosteroid ids that act by negative feedback inhibition on the pituitary and hypothalamus.

Corticotropin releasing hormone CRH

Hypothalamic hormone, adrenocorticotropin hormone. ACTH is triggered by rising levels of this. Fever, hypoglycemia and stressors can alter the release of this.

Gonadotropins

Triggered by gonadotropin Releasing hormone Gn RH during an after puberty, but are suppressed by gonadal Hormones via negative feedback. follicle-stimulating hormone And luteinizing hormone

Gonadotropin releasing hormone GnRH

Hypothalamus hormone that triggers the release of gonadotropin

Follicle stimulating hormone

Stimulates gamete (Sperm or egg) Production

Luteinizing hormone

Promotes production of the gonadal Hormones (Estrogen or testosterone)

Permissiveness

One hormone cannot exert its full effect without another hormone present

Synergism

More than one hormone produces same effects on the target cell, and their effects are more than additive

Antagonism

One or more hormones oppose the action of another

Hypersecretion

An overproduction and release of hormones. May be caused by tumors, making these cells unresponsive to neg feedback mechanisms

Hyposecretion

Indicates a deficit in a specific hormone. Damage to one of the endocrine tissues or insufficient diet

Primary pathology

If a pathology arises in the last endocrine gland in a complex reflex pathway

Secondary pathology

If a pathology arises in the anterior pituitary

Tertiary Pathology

If a pathology arises in the hypothalamus (very rare)

How is a pathology determined?

Examining the levels of the three hormones involved in the pathway (blood levels)

What are the hormone levels in a Primary Hypersecretion Due to problem with adrenal cortex?

CRH levels-low, ACTH levels-low, Cortisol levels-high

What are The hormone Levels in secondary hypersecretion Due to pituitary problem?

CRH levels – low, ACTH level – high, Cortisol levels – high

What are the hormone levels of tertiary hypersecretion Due to hypothalamic problem (rare)?

CRH levels – high, ACTH Levels – high, cortisol levels – high

Type 1 diabetes

Insulin dependent diabetes, an autoimmune disease caused by the destruction of insulin-producing cells in the pancreas

Type 2 diabetes

Non-insulin dependent, caused by a reduced response to insulin, usually associates with overweight & underactive individuals

Gestational diabetes

Can affect a pregnant woman leading to dangerously large babies & complicated delivery

Insulin

Hormone released when glucose levels are high. Tells cells to glucose in the plasma, & signals liver cells to store the glucose as glycogen. Protect against hyperglycemia

Glucagon

Released during periods of lower glucose levels. Signals the liver to breakdown glycogen & begin gluconeogenesis to ensure homeostasis. Protect against hypoglycemia

Hemoglobin A1C

Indicates Hb exposure to glucose the preceding 8-12 weeks. Examines the levels of glycohemoglobin

Hyperglycemia

Elevated glucose levels in the plasma

Cortisol hormone

Adrenal cortex hormone. Derivative of cholesterol, synthesized on demand, requires transport proteins to move in blood. Mediate long-term stress

What are the 4 targets of cortisol?

Liver→ Gluconegenesis: breakdown of glycogen to breakdown glucose

Muscles→Protein catabolism: breakdown muscle proteins for fuel

Adipose tissues→Lipolysis: breakdown fat for fuel

Immune system→suppressed: reducing inflammation, cytokine signals, AB production. More likely to get sick rn

Endogenous cortisol

Cortisol that you make within the body

Exogenous cortisol

Cortisol put on the outside of the body, you did not make it

Hypercortisolism

Too much cortisol. Caused by tumors-uncontrolled release of cortisol and could be due to medications

Hypercortisolism Symptoms

Hyperglycemia, tissue wasting and lipolysis. Fat deposition in the trunk(abdominal striations) and face (plump cheeks or “moon face”) 1° Cushings Syndrome. 2° Cushings disease

Iatrogenic

Hormone-secreting tumors or from exogenous administration of the hormone

Cushing’s disease

Benign tumor in the anterior pituitary causing excessive levels of ACTH. Secondary pathology

Cushing Syndrome

Primary pathology, something wrong with adrenal cortex (tumor)

Hypocortisolsim

Too little of cortisol. Addisons Disease. Build up of intermediate but cannot make cortisol. Intermediate instead are made into testosterone. Hypoglycemia

Addison’s disease

Hyposecretion of all adrenal steroid hormones. Autoimmune destruction of the adrenal cortex. Hypoglycemia. Masculinization of females

Thyroid hormone

T3,T4. Long term effect on metabolism, helps to manipulate the metabolic rate of the cell and heat production. Affects virtually every cell in the body.

TSH thyroid-stimulating hormone

Stimulates colloid to release thyroid hormone and tell follicular cells to grow. Trophic hormone

Follicular cells

Spherical structure. The hollow center of each one is filled with a colloid. The colloid holds a 2-3 month supply of thyroid hormones.

What are some things the thyroid stimulating hormone T3,T4 target?

All cells→ Increases metabolic rate and heat production: greater demand for fuel & O2. Subsequent increases in cardiac output to ensure these higher “needs” of the tissues. CO^ leads to BP^

Hyperthyroidism

Tumors or Graves Disease. High heat prod. O2 rise. Increase in CO (HR^,SV^), so BP^ mucopolysaccharide deposition in the eye orbit→ buggy eyes GOITER

Hypothyroidism

Damage or low iodine. Low heat prod. less O2 use. Decrease in CO (HR decrease), so BP decrease. Mucopolysaccharide deposition under the skin→ myxedema. GOITER

Mucopolysaccharide in hyperthyroidism

Deposition in eye orbit→ buggy eyes

Mucopolysaccharide in hypothyroidism

Deposition under the skin→ myxedema: puffy appearance

Graves’ disease

Thyroid- stimulating immune proteins (TSI) bind to thyroid gland TSH receptors and cause the gland to hypertrophy. Antibody that mimics TSH

Goiter

An enlargement or hypertrophy of the follicular cells in the thyroid

What are the three hormones of Adrenal Cortex?

Trigger: circadian rhythm or stress target

Hypothalamus: CRH

Anterior Pituitary: ACTH

Adrenal Cortex: Cortisol

What are the three hormones of the thyroid gland?

Trigger: Tonic release

Hypothalamus: TRH

Anterior Pituitary: TSH

Thyroid Gland: T4, T3

What does the TSH effect?

Colloid release of thyroid hormone and tell follicular cells to grow

Osteoblasts

Deposit calcium as they create new bone matrix. Breakdown bone matrix during bone resorption release, stored calcium

Calcitonin

Secreted by the thyroid and opposes PTH, increasing calcium deposition into bone and increasing renal excretion of calcium

When Ca2+ is low = parathyroid gland→ PTH. What are targets of the PTH?

Osteoblast→ Break bone down(Bone resorption)

DCT→ Promote selective reabsorption.

Small intestine→ (Vit D) promote absorption

When Ca2+ is elevated = Thyroid gland(parafollicular cells)→ Calcitonin. What are the targets Calcitonin?

Decrease osteoclast activity→ Results in more Ca2+ Deposition In bone

Prevent Ca2+ reabs.→ promote Ca2+ excretion