Overview of Endocrinology Flashcards

1
Q

What are the main hormone products of the Thyroid Gland

A

Tetraiodothyronine (T4)

Triiodothyronine (T3)

Calcitonin (CT)

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2
Q

What are the main hormone products of the Parathyroid Gland

A

Parathyroid Hormone (PTH)

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3
Q

What are the main hormone products of the Pineal Gland

A

Melatonin

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4
Q

What are the main hormone products of the Thymus

A

Thymosin

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5
Q

What are the main hormone products of the Heart

A

Atrial Natiuretic Peptide (ANP)

Brain Natiuretic Peptide (BNP)

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6
Q

What are the main hormone products of the Adrenal Cortex

A

Glucocorticoids

Mineralcorticoids

Androgens

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7
Q

What are the main hormone products of the Adrenal Medulla

A

Epinephrine

Norepinephrine

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8
Q

What are the main hormone products of the Pancreas

A

Insulin

Glucagon

Somatostatin

Pancreatic Peptide

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9
Q

What are the main hormone products of the Kidney

A

Erythropoietin

Calcitrol

Renin

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10
Q

What are the main hormone products of the GI Tract

A

Gastrin

Secretin

Cholecystokinin (CCK)

Gastric Inhibitory Peptide (GIP)

Glucagon-Like Peptides (GLPs)

Motilin

Ghrelin

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11
Q

What are the main hormone products of the Testis

A

Testosterone

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12
Q

What are the main hormone products of the Ovaries

A

Estrogen

Progesterone

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13
Q

What are the main hormone products of the Adipose Tissue

A

Leptin

Adiponectin

Resistin

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14
Q

What are the main hormone products of the Anterior Pituitary

A

Growth Hormone (GH)

Adrenocorticotropic Hormone (ACTH)

Follicle-Stimulating Hormone (FSH)

Leutinizing Hormone (LH)

Prolactin (PRL)

Thyroid Stimulating Hormone (TSH)

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15
Q

What are the main hormone products of the Posterior Pituitary

A

Antidiuretic Hormone (ADH)

Oxytocin (OT)

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16
Q

What are the main hormone products of the Hypothalamus

A

Thyroid Releasing Hormone (TRH)

Growth Hormone Releasing Hormone (GHRH)

Growth Hormone Inhibiting Hormone (GHIH)

Somatostatin (SS)

Gonadotropin Releasing Hormone (GnRH)

Prolactin Releasing Hormone (PRH)

Prolactin Inhibiting Hormone (PIH or Dopamine)

Corticotropin Releasing Hormone (CRH)

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17
Q

What is the function of the endocrine systrem?

A

Regulates growth, development, metabolism, and reproduction through a network of hormones and receptors utilizing endocrine, paracrine, autocrine, neurocrine, and transcriptional signaling mechanisms throughout the body

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18
Q

What does excess secretion of growth hormone (GH) during development lead to?

A

Gigantism - greatly accelerated rate of growth with delayed closure of the epiphyses

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19
Q

What does excess secretion of growth hormone (GH) in adulthood lead to?

A

Acromegaly - causes slow, progressive changes including coarsening of the facial features, protrusion of the lower jaw, and enlargement of the hands and feet

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20
Q

Tell me about the hypothalamus

A

Part of the diencephalon

Contains nuclei - including the supraoptic nucleus (SON), para-ventricular nucleus (PVN), and arcuate nucleus (AN)

Synthesizes neuro-hormones (releasing and inhibiting hormones), which bind to membrane receptors on target cells in the anterior pituitary (AP)

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21
Q

What are the releasing and inhibiting hormones of the hypothalamus?

A

Thyroid Releasing Hormone (TRH)

Gonadotropin Releasing Hormone (GnRH)

Growth Hormone Releasing Hormone (GHRH)

Growth Hormone Inhibiting Hormone (GHIH) or Somatostatin

Prolactin Releasing Factor (PRF)

Prolactin Inhibiting Hormone (PIF) or Dopamine (DA)

Corticotropin Releasing Hormone (CRH)

22
Q

What is Pulsatile Secretion?

A

Hormones made by the hypothalamus, pituitary, and some of the other endocrine glands are released in short pulses or bursts

When used in treatment of disease, they must be administered in a way that mimics the endogenous pattern of release in order to be effective

23
Q

Tell me about the pituitary gland

A

AKA hypophysis

Has two main lobes: anterior lobe (adenohypophysis) and posterior lobe (neurohypophysis or pars nervosa)

24
Q

Tell me about the Anterior Pituitary

A

Mainly the pars distalis, consists of glandular epithelium originating from Rathke’s pouch (an invagination of ectoderm in the oropharynx) with hormone-secreting cells arranged in cords/clusters

Sella Turcica - part of sphenoid bone where pituitary gland sits which limits pituitary expansion - therefore if pituitary enlarges, it puts pressure on adjacent structures (optic chiasm)

25
Q

What are the hormones released from the Anterior Pituitary

A

Thyroid Stimulating Hormone (TSH)

Leutinizing Hormone (LH)

Follicle Stimulating Hormone (FSH)

Growth Hormone (GH)

Prolactin (PRL)

Adrenocorticotropic Hormone (ACTH)

26
Q

What is the Hypothalamic-Hypophyseal Portal System (HHPS)

A

A neurovascular link to the endocrine system

Provides a direct route for hypothalamic hormones to reach the AP - consists of 2 capillary beds (plexuses) connected by long portal veins

i) primary plexus is located in the median eminence; ii) secondary plexus opens up onto its target cells in the anterior pituitary

Purpose: deliver hypothalamic hormones quickly and at very high concentrations

Vessels in HHPS are fennestrated, so substances that would normally be excluded by the blood brain barrier are allowed to pass freely and in both directions

Hypothalamus (Releasing/Inhibiting Hormones) -> Primary plexus (Median Eminence) -> Long Portal Veins -> Secondary Plexus -> -> -> Target cells in the AP

27
Q

Tell me about the Posterior Pituitary

A

Pars nervosa or neurohypophysis

Derives from neuroectoderm

Not a true endocrine gland

Consists of glial cells (or pituicytes) and axon terminals extending from the hypothalamus

Doesn’t synthesize hormones of its own, but stores hormones synthesized in the hypothalamus

28
Q

Posterior Pituitary Hormones

A

Vasopressin (VP) or Antidiuretic Hormone (ADH)

Oxytocin (OT)

*Made in the SON and PVN of the hypothalamus and then delivered to the PP by axonal transport, where they are stored

29
Q

What is the Hypothalamic-Hypophyseal Tract

A

Long axons pass from the hypothalamus and ME through a hypothalamic-hypophyseal tract in the infundibular stalk to the PP

Action Potentials’ carried over this tract have the capacity to trigger the release of hormones from vesicles in the PP

Once released, they can gain access to the bloodstream in order to reach their target cells in the periphery

30
Q

Pituitary Gland Histology

A

Anterior appears darker due to cells that are basophilic in nature

Herring bodies - histologically detectable aggregates that form when hormones accumulate in the posterior pituitary

Somatotropes -> GH = acidophilic

Lactotropes -> PRL = acidophilic

Thyrotropes -> TSH = basophilic

Corticotropes -> ACTH = basophilic

Gonadotropes -> Gonadotropins: LH, FSH = basophilic

Chromophils = acidophils (stain pink; secrete GH, PRL) and basophiles (stain blue; secrete TSH, ACTH, LH, FSH)

31
Q

Tell me about the Adrenal Glands

A

Vital to life

Each adrenal gland has a cortex, originating from mesoderm

A medulla, originating from ectoderm

vital in organisms response to environmental stress

Produce steroids and catecholamines that participate in the sympathetic nervous system (SNS) to bring about the fight or flight response = essential for self-preservation

Also involved in metabolism, fluid homeostasis, blood pressure, vasomotor tone, heart rate, cardiac output, and other processes throughout the body

Clinically, catecholamines are used to counteract cardiac arrest, treat shock, and dilate the bronchioles in asthmatics; Glucocorticoids, like cortisol, are also used in these and other conditions, mainly for their ability to reduce inflammatory- and autoimmune reactions

32
Q

Adrenal Gland Hormones

A

Adrenal Cortex:

Mineralocorticoids = aldosterone from zona glomerulosa

Glucocorticoids = cortisol from zona fasiculata

Adrenal androgens = DHEA, Androstenedione from zona reticularis

Adrenal Medulla:

Catecholamine = Norepinephrine from Chromaffin cells

Catecholamine = Epinephrine from Chromaffine cells

33
Q

Adrenal Cortex

A

Divided into 3 histologic zones:

Zona glomerulosa

Zona fasiculata

Zona reticularis

34
Q

Adrenal Medulla

A

Located at the center of the adrenal gland, surrounded by the cortex

Unlike cortex, originates from ectoderm and cells are Chromaffin cells

Chromaffin cells - considered to be modified postganglionic sympathetic neurons and don’t have axons, dendrites, and don’t make synapses; during development, cortisol promotes differentiation of chromaffin cells and inhibits formation of neuronal processes (axons, dendrites)

35
Q

Explanation of Adrenal Glands

A

After catecholamines are synthesized, they’re stored in granules within chromaffin cells for fast release in response to stressful stimuli

When these stimuli activate the SNS, action potentials travel through preganglionic sympathetic neurons entering the adrenal medulla and trigger the release of acetylcholine, ACh, which acts as a neurotransmitter

Instead of acting at a synapse, ACh acts at a nerve-gland junction by binding to nicotinic receptors on chromaffin cell membranes initiating the release of catecholamines from pre-formed granules into the bloodstream

36
Q

Tell me about Parathyroid Glands

A

Embedded in the connective of the thyroid

Contain principal cells (chief cells) and oxyphil cells

Principal cells secrete PTH, which participates in blood calcium regulation

37
Q

Tell me about the Thyroid Gland

A

Contains follicle cells that synthesize T3 and T3 as well as parafollicular “C” cells, which secrete calcitonin (CT)

Thyroid hormone synthesis is triggered by TSH from the anterior pituitary

TSH levels controlled both by the positive effects of TRH (From the hypothalamus) and by the negative effects of elevated serum levels of T3-T4 via negative feedback

TSH and T3-T4 are reciprocally related

Interplay between hormones in the HPT axis is what keeps T3 and T4 within the normal, euthyroid range

38
Q

Hypothalamic-Pituitary-Thyroid Gland (HPT) Axis

A

When thyroid hormone levels are too high in the blood, they exert a negative feedback over the AP and hypothalamus to prevent further production of TSH and TRH, respectively

When circulating levels of T3-T4 become too low, the inhibitory effects over TRH and TSH are removed, and thyroid hormone levels return to normal

When TRH is released from the hypothalamus it binds to receptors on AP thyrotropes to trigger the release of TSH

TSH causes the size, number, and activity of thyroid follicle cells to increase and it stimulates every step in the pathway of thyroid hormone synthesis

Thyroid hormones travel through the entire circulation, diffuse into target cells, and bind to nuclear receptors in order to activate target gene transcription

Thyroid binding globulin (TBG) is the main transport protein for thyroid hormones traveling through the bloodstream

39
Q

Thyroid Follicle Histology

A

Thyroid follicle is the structural and functional unit of the thyroid gland; thyroid gland contains hundred of ‘thyroid follicles’

Each thyroid follicle consists of a single layer of cuboidal epithelial cells, aka ‘follicle’ cells’ - the cells that produce thyroid hormones and release them into the bloodstream

Follicle cells have 2 functional surfaces: apical and basal; apical side faces the lumen which stores colloid; basal side faces the bloodstream

Main constituent of colloid is “thyroglobulin” (TG); an iodinated glycoprotein that is endocytosed into the follicle cell for cleaved into thyroid hormones and release into the bloodstream

Para-follicular cells, which produce CT, are located between follicles

40
Q

HPT Axis Regulation

A

Defects at any level can lead to increases or decreases in thyroid hormone production (hyper- or hypothyroidism)

Most common cause of thyroid dysfunction originates in the thyroid gland itself = PRIMARY

Secondary dysfunction is used when a problem, originating in the AP, causes thyroid hormone levels to become abnormal; SECONDARY = Anterior Pituitary

Central or Tertiary describe the impact of problems in the hypothalamus or higher brain centers on the thyroid; CENTRAL (TERTIARY) = hypothalamus

Peripheral hypothyroidism = target tissues have become insensitive to the effects of thyroid hormones; results from mutations in the genes encoding thyroid hormone

41
Q

Hypothalamic-Pituitary-Target Organ Axis

A

Feedback signaling: hormones released by the hypothalamus stimulate the pituitary gland hormones that have the capacity to regulate downstream target organs; if hormone secreted by a target organ increases beyond a certain critical upper leve, it exerts feedback inhibition over the anterior pituitary and hypothalamus to prevent continued stimulation for its release

Hormone = Thyroid hormones: T3-T4

Origin = follicle cells in the thyroid gland

Positive Regulator = TSH from the anterior pituitary

Negative Regulator = Feedback inhibition of TRH from the hypothalamus and TSH from the AP, exerted by high levels of T3-T4 in circulation

Targets = thyroid hormones increase oxygen consumption and metabolic rate in nearly every cell in the body

42
Q

Hypothalamic-Pituitary-Adrenal Gland Axis

A

Hypothalamus –CRH–>Antr Pituitary – ACTH –> Adrenal Cortex –> decreased Cortisol

Decreased cortisol -> + Hypothalamus and + Antr Pituitary

Hypothalamus –| CRH –> Antr Pituitary –| ACTH –> increased Cortisol

Increased cortisol -> - Hypothalamus and - Antr Pituitary

Central = Hypothalamus

Secondary = Anterior pituitary

Primary = Adrenal cortex

43
Q

In primary hypocortisolism, cortisol is high and ACTH is low. Where is the problem?

A

Problem with the Adrenal Cortex.

Adrenal cortex is able to make cortisol freely

Negative effects still happening onto Antr Pituitary so ACTH is still low

44
Q

Hypothalamic-Pituitary-Thyroid Gland Axis

A

When TRH is released from the hypothalamus, it binds to receptors on AP thyrotropes to trigger release of TSH

TSH binds to receptors on follicle cell membranes in the thyroid gland to upregulate the synthesis of T3 and T4

Thyroid hormones travel through the entire circulation, diffuse into target cells, and bind to intracellular receptors

Thyroid hormone-receptor complexes will ultimately exert actiosn by up-regulating expression of target genes

45
Q

In an individual with hypothyroidism due to low T3-T4 levels, how would you expect TSH levels to change and why?

A

Low T3-T4 levels will increase levels of TSH in a normal individual; the thyroid is not responsive to TSH

46
Q

If the low thyroid hormone levels are caused by destruction of the thyroid gland (follicles), which of the following terms would you use to describe the patient’s hypothyroidism?

A

Primary

47
Q

A 37yo woman comes to your office with complaints that suggest she may have hypothyroidism. These complaints include fatigue; dry, flaky skin; difficulty concentrating; and feelign cold when everyone else is too warm. Elevated levels of what hormone would best support a diagnosis of hypothyroidism?

A

TSH

48
Q

List four hormones in the HPT axis

A

T3

T4

TRH

TSH

49
Q

In an individual with low T3-T4 levels, how would you expect TSH levels to change?

A

TSH levels will increase

50
Q

What hormones in the HPT axis have the most obvious reciprocal activity? What is the clinical significance of this?

A

TSH and T3-T4

In hypothyroidism: low T3-T4 and high TSH

In hyperthyroidism: high T3-T4 and low TSH

51
Q

If the levels of T4 and TSH in circulation are both below normal, where is the problem most likely to have originated?

A

Anterior pituitary - secondary

52
Q

If the circulating levels of T4 are low or normal, but TSH levels are elevated, where is the problem likely to have originated?

A

Thyroid gland