Endocrine Intro, Male And Female Sex Hormones

Front 1

What are 3 endocrine hormone classes?

Back 1

Peptide, cholesterol derivatives, amino acid derivatives

Front 2

Define the terms: endocrine, paracrine, autocrine, juxtacrine, neuroendocrine

Back 2

Endocrine: substance released into bloodstream to interact with cells elsewhere in the body.
Paracrine: Hormone secretion locally and arrives at target cells via diffusion.
Autocrine: Like paracrine, only target cell is same as secreting cell, this is an autoregulation.
Juxtacrine: Direct cell to cell contact uses hormones as cell-cell communication.
Neuroendocrine: Hormones released from nerves into special circulations that interact with targets in an endocrine like manner

Front 3

What are the major determinants of duration of a hormonal response?

Back 3

Duration of Hormone Availability (duration of secretion, amount secreted, half life, receptor availability and turnover),
Mode of Cellular Response (genomic expression, time to synthesize mRNA, mRNA half life, turnover of proteins),
Rapidity in Onset of Compensatory Processes (counter regulatory systemic responses, local cell receptor inactivation or downregulation)

Front 4

Explain the relationship between the hypothalamus and the anterior pituitary gland.

Back 4

Specific hypothalamic neurons in the median eminence secrete specific neurohormones that serve different endocrine purposes into a special portal circulation called the hypothalamic-hypophyseal portal circulation, which then interact with specific cells in the anterior pituitary, of which there are 5 types, that secrete different hormones into the blood stream. Some target glands will secrete a hormone that negatively feeds back on the pituitary and/or hypothalamus.

Front 5

What are the 5 types of anterior pituitary cells, what hormones do they secrete, and how do they influence physiology?

Back 5

Gonadotrophs: Leutinizing Hormone and Follicle Stimulating Hormone (LH and FSH), involved in sex steroid hormone synthesis and gametogenesis.
Lactotrophs: Prolactin, stimulates milk production in breast
Somatotrophs: Growth Hormone, postnatal growth and metabolic actions
Thyrotrophs: Thyroid Stimulating Hormone (TSH), metabolism, brain development, and growth
Corticotrophs: Adrenocorticotropic Hormone (ACTH), modulates stress and metabolic responses via adrenal glands

Front 6

How is the posterior pituitary different from the anterior and what hormones does it secrete and what are their actions?

Back 6

The cell bodies of posterior pituitary hormone secreting cells reside in the hypothalamus, the terminals are in the posterior pituitary. They secrete Antidiuretic Hormone (ADH, vasopressin) that stimulates water retention in kidney and oxytocin which contracts the uterus and allows milk to flow in lactation.

Front 7

What is Kallman's syndrome?

Back 7

Developmental disorder in which GnRH neurons fail to migrate to correct hypothalamic location. Gonadotrophs get no stimulation and atrophy. Gonads don't generate gametes or sex steroids. Patients don't hit puberty, need exogenous hormone replacement therapy.

Front 8

Explain the oral contraceptive birth control theory.

Back 8

Exogenous synthetic estrogens/progesterones negatively feedback on hypothalamus and pituitary maintaining low FSH/LH, preventing ovulation. Sexual development should remain normal due to presence of synthetic hormones, despite low level of hormone production in ovaries.

Front 9

Discuss differences between the cell types and hormone sequence of the posterior pituitary hormones

Back 9

ADH - released from vasopressinergic magnocellular hypothalamic neurons. 9 AA peptide
Oxytocin - released from oxytocinergic magnocellular hypothalamic neurons. Also a 9 AA peptide.

High structural overlap, thus can get crossover of effects.

Front 10

Briefly describe the development of the anterior pituitary.

Back 10

Derived from Rathke's pouch ultimately giving rise to 5 cell lineages. Primordial cells express different transcription factors to differentiate into corticotrophs (T-pit), gonadotrophs (Prop-1 + GATA), somatotrophs, lactotrophs, thyrotrophs (Prop1 + Pit1)

Front 11

What's the significance of pulsatile release of hormones?

Back 11

Avoids desensitization of tissue and pituitary cell receptors.
Frequency and amplitude of pulses can relay phsyiological messages?

Front 12

Causes and effects of hyperprolactinemia

Back 12

Hyperprolactinemia (elevated prolactin secretion) is normal in lactation, but is also a relatively common endocrine disorder in nonlactating individuals. Causes include prolactin-secreting pituitary tumors, iatrogenic causes (therapy with dopamine receptor blockers, or conditions which elevate TRH (such as primary hypothyroidism). Hyperprolactinemia can cause galactorrhea, ie, inappropriate milk synthesis. Hyperprolactinemia can also lead to a loss of libido and fertility in both men and women. Hypoprolactinemia is rare, but might follow pituitary damage.

Front 13

What are the glycoprotein hormones?

Back 13

TSH, LH, FSH, hCG. All have 2 subunits. The alpha is the same in all of them. Beta is specific to each hormone and confers the activity. Both subunits required for activity.

Front 14

Contrast hypo and hyper thyroidism and how could be diagnosed clinically.

Back 14

Hyperthyroidism (excess thyroid hormone) and hypothyroidism (insufficient thyroid hormone) are relatively common endocrine disorders. Knowledge of feedback relationships helps in diagnosing thyroid diseases. If thyroid function is deficient and thyroid hormone synthesis compromised, TRH and TSH levels increase (due to loss of negative feedback). Elevated TSH plus low T4/T3 are diagnostic of primary hypothyroidism.

Front 15

What is POMC?

Back 15

Proopiomelanocortin (POMC) is a prohormone named for its encoded peptides: endorphin, (endogenous opioid), melanocyte stimulating hormone (MSH) and corticotropin (ACTH). In intermediate lobe (not found in adult humans), ACTH is cleaved to αMSH, which regulates pigmentation in many animals.

Front 16

Clinical disorders of growth hormone?

Back 16

Disorders of GH include dwarfism, and can be caused by defects in GH synthesis, or defects in GH receptors, IGF-1, or IGF-1 receptors. Excess GH in adults leads to acromegaly, which causes continued growth of the few bones that remain capable of post-pubertal GH-induced growth (jaw, nose, orbital ridges, knees, elbows, and fingers).

Front 17

What are Herring bodies?

Back 17

Neurosecretory vesicle storage site in nerve terminals of magnocellular neurons. Bulges in the terminals where ADH and oxytocin are stored prior to release.