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BRS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is a hormone?

A

A chemical messenger carried from the organ it’s produced to its target organ through the bloodstream

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2
Q

Compare and contrast peptide hormones and steroid hormones

A

Peptide hormones are synthesized as prohormones (inactive) requiring further processing to activate. They are stored in vesicles (regulatory section). They travel free in the blood and when activated bind to receptors on the cell membrane and transducer signal uniting 2nd messenger systems.

Steroid hormones are synthesized from cholesterol. They are released immediately and aren’t stored (constitutive secretion). They travel bound to proteins in the blood and bind to intracelular receptores to change gene expression directly

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3
Q

Where does the pituitary gland sit?

A

Sella turcica of the sphenoid bone

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4
Q

What is another name for the anterior pituitary gland?

A

Adenohypophysis

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5
Q

Which pituitary gland needs to be told what to produce by the hypothalamus?

A

Anterior pituitary

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6
Q

How does the hypothalamus regulate anterior pituitary function?

A

Hypothalamic parvocellular neurons release hypothalamic releasing hormones (RHs) or inhibitory hormones (IHs) into the capillary plexus in the median eminence. These RHs/IHs are then carried by portal circulation through the hypophyseal-pituitary portal system to the anterior pituitary to inhibit or stimulate the release of hormones from anterior pituitary cells. The anterior pituitary hormones then leave the gland via the blood

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7
Q

What are the 5 types of endocrine cells in the anterior pituitary and what hormones do they produce?

A

Somatotrophs-> growth hormone (somatotrophin)
Gonadotrophs-> luteinizing hormone (LH) and follicle-stimulating hormone (FSH)
Corticotrophs-> adrenocorticotrophic hormone (ACTH/corticotrophin)
Thyrotrophs-> thyroid stimulating hormone (TSH/thyrotrophin)
Lactotrophs-> prolactin

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8
Q

How are each of the hormones produced by the anterior pituitary regulated?

A

Growth hormone-> growth hormone releasing hormone (RH) and somatostatin (IH)
Prolactin-> dopamine (IH)
LH and FSH-> gonadotrophin releasing hormone (RH)
TSH-> thyrotrophin releasing hormone (RH)
ACTH-> corticotrophin releasing hormone (RH)

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9
Q

What is bitemporal hemianopia and what causes it?

A

Loss of peripheral vision due to compression of optic chiasm (e.g. because of pituitary tumor). This happens because the fibers of the nasal retinae decussate at the center of the optic chain and if the optic chiasm is compressed so will they. Since these fibers transmit sensory information from the lateral visual fields, peripheral vision is lost.

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10
Q

Outline the neuroendocrine reflex arc of milk production

A
  1. Mechanical stimulation of the nipple and surrounding area activates afferent pathways.
  2. Afferent signals are integrated into the hypothalamus and inhibit dopamine release from dopaminergic neurons.
  3. Less dopamine in the hypophyseal-pituitary portal system causes less inhibition of anterior pituitary lactotrophs, increasing the production of prolactin.
  4. Increased plasma prolactin increases milk secretion in mammary glands
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11
Q

What is gigantism?

A

A condition where a person is bigger and taller than normal due to over-production of GH. Only happens if this over-production of GH happens before the end of puberty

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12
Q

Why is there no gigantism in adults with acromegaly?

A

Adults already have fused epyphesial plates and therefore can no longer grow in height

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13
Q

What is acromegaly?

A

It’s caused by overproduction of GH and leads to gradual coarsening of facial features, macroglossia (big tongue), prominent nose, deepening of the voice, prognathism (enlargement of the jaw), increased hand and feet size, sweatiness, headache, carpal tunnel syndrome, and obstructive sleep apnea (soft-tissue changes surrounding upper airway leading to narrowing → Collapse during sleep) but there is no increase in height.

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14
Q

What is the posterior pituitary also known as?

A

Neurohypophysis

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15
Q

What hormones does the posterior pituitary produce?

A 
Oxytocin
Arginine vasopressin (AVP/anti-diuretic hormone)
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16
Q

What is the pituitary gland suspended by from the brain?

A

Pituitary stalk (infundibulum)

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17
Q

Outline the process of thyroid hormone production

A

Hypothalamic neurosecretory cells release Thyrotropin Releasing Hormone (TRH) into the hypophyseal-pituitary portal system, which travels to the anterior pituitary.
TRH stimulates the release of TSH (thyroid-stimulating hormone; aka thyrotrophin) by anterior pituitary thyrotrophic cells.
TSH leaves the anterior pituitary via the blood to travel to the thyroid gland to stimulate thyroid hormone release (T4- thyroxine)

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18
Q

Which hypothalamic regulator inhibits somatotrophs from releasing somatotrophin and which regulator activates the release of growth hormone?

A

Somatostatin (inhibit)

Growth hormone releasing hormone (GHRH)

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19
Q

What effect does dopamine have in terms of hypothalamo-pituitary regulation?

A

High levels of dopamine inhibit the release of prolactin from lactotrophs in the anterior pituitary gland

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20
Q

Where are the receptors for gonadotrophins (LH and FSH) in males?

A

Testes

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21
Q

What is the target gland for prolactin?

A

Mammary gland (located in the breast)

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22
Q

The adrenal cortex is the target organ for which hormone?

A

Adrenocorticotrophic hormone (ACTH) released by corticotrophs from the anterior pituitary gland

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23
Q

Explain the pathology behind bitemporal hemianopia and how the defining symptom arises.

A

A pituitary tumor (adenoma) compresses the optic chiasm. It also covers the sella turcica (suprasellar tumor as it occurs above the sella turcica). The optic chiasm is the region where the nerve fibers transmit sensory information from lateral visual to the occipital lobes.
Compression of the optic fibers from the nasal retinae leads to loss of stimulation from lateral fields to occipital lobe (this is where the primary visual cortex) → Loss of peripheral vision

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24
Q

Outline the mechanism of growth hormone action

A

Secretion of growth hormone by endocrine somatotrophs from anterior pituitary directly binds to complementary target within general tissue (muscle and bone)
Growth hormone can bind to growth hormone receptors of liver → Synthesis of IGF-1 and IGF-2 (Insulin-like Growth Factor - Somatomedin)
IGF-1 is a mediator of growth hormone-stimulated somatic growth, binding to target receptors

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25
Q

What is the difference between gigantism and acromegaly?

A

Gigantism → Growth hormone excess happens before epiphyseal plate fusion (puberty ends) so the patient is VERY tall
Acromegaly → Growth hormone-producing tumor appears after epiphyseal plate fusion. Somatotrophs secrete excessive concentration of growth hormone (same mechanism as gigantism). This causes increased facial features, tongue, hands, and feet, and more but there is no increase in height

26
Q

What type of neurons from the hypothalamus have axon fibers sending signals to the posterior pituitary gland?

A

Hypothalamic magnocellular neurons

27
Q

Which nuclei do magnocellular axons extend from?

A

Supraoptic (AVP) and paraventricular (oxytocin) nuclei of the hypothalamus

28
Q

Outline the regulation of the posterior pituitary gland in terms of the hypothalamic neurons and the hormones that are concerned

A

Supraoptic and paraventricular neurons (hypothalamic magnocellular neurons) produce AVP and oxytocin respectively.
Excitation of these 2 hypothalamic magnocellular neurons stimulates the release of AVP and oxytocin into the posterior pituitary where they diffuse into blood capillaries.
They then leave the posterior pituitary via the blood.

29
Q

What is diuresis?

A

Production of urine

30
Q

Outline the physiological action of ADH (antidiuretic hormone; aka arginine vasopressor -> AVP) for stimulating water reabsorption.

A

The main physiological action of ADH is the stimulation of water reabsorption in the renal collecting duct. This concentrates urine.
ADH increases the permeability of the distal convoluted tubule and collecting duct to water.
ADH binds to V2 G protein-coupled receptors of the cell-surface membrane, which leads to the formation of cAMP. cAMP production enables protein kinase A to activate aquaporin-2 and 3 genes. Aquaporins insert into the tubule membranes, increasing permeability.
Water leaves renal collecting ducts making the urine more concentrated and reabsorbing water into the blood plasma.
When ADH levels fall the level of cAMP production also decreases, causing a withdrawal of water channels → Cell becomes impermeable

31
Q

How many lobes does the thyroid gland consist of?

A

2 lobes (wrap around the trachea and connected in the middle by an isthmus)

32
Q

Which nerve supplies the vocal cords?

A

Left recurrent laryngeal nerve (supplies intrinsic muscles of the larynx); it is a branch of the vagus nerve

33
Q

What is the main function of the thyroid gland?

A

Metabolic regulation through the action of thyroxine synthesis

34
Q

What do parafollicular cells release?

A

Calcitonin; involved in the regulation of calcium metabolism in the body.

35
Q

Which glands are embedded in the thyroid gland and what is their function?

A

Parathyroid glands (superior and inferior on both sides); Responsible for secretion of parathyroid hormone → Elevate Ca2+ levels by degrading bone and stimulating calcium release, which increases the body’s ability to absorb calcium from food.

36
Q

Where does the thyroid gland originate from?

A

Base of the tongue.

37
Q

Where does the thyroid gland originate from?

A

The base of the tongue.

38
Q

Explain the process of thyroid hormone synthesis.

A

TSH secreted by thyrotrophic cells of the anterior pituitary enters the circulation and binds to target TSH receptors (TSH-R) on the cell surface membrane of follicular cells.
Na+ and I- also enter from the blood through the sodium-iodide co-transporter, and the I- ions pass through to the colloid where they are oxidized (iodination) to produce iodine.
Because of the TSH binding to the TSH-R, the prohormone thyroglobulin (TG) is produced and transported to the colloid as well as thyroperoxidase (TPO).
The TG produced binds to the iodine produced (iodination), resulting in monoiodotyrosine (MIT) and diiodotyrosine (DIT). TPO + H2O2 catalyzes the iodination reactions and the coupling reaction.
Then, a coupling reaction occurs:
Coupling of MIT + DIT = T3 (triiodothyronine)
Coupling of DIT + DIT = Tetraiodothyronine (T4) → Thyroxine
The T3 and T4 produced are still bound to TG and move to the follicular cell lysosomes where the protein bonds are broken down, and the T3 and T4 then enter the bloodstream

39
Q

What thyroid hormone is more active?

A

triiodothyronine (T3)

40
Q

What is the major hormone product of the thyroid gland?

A

Thyroxine (T4; tetraiodothyronine)

41
Q

When is T4 deiodinated into reverse T3 and why?

A

Under circumstances requiring reduced metabolism (starvation).
rT3 is the biologically inactive form of T3.

42
Q

Where does most circulating T3 come from?

A

80% from deiodination of T4 by a deiodinase enzyme (T4→ T3)

20% from directly from thyroid secretion

43
Q

How are thyroid hormones (iodothyronines) transported?

A

Transported by 3 plasma proteins:
Thyroid-binding globulin (70-80%)
Albumin (10-15%)
Prealbumin (transthyretin)

44
Q

What are the half-lives of T3 and T4?

A

T3 ~ 2 days

T4 ~ 7-9 days

45
Q

What percentage of T3 and T4 are bioactive components (unbound)?

A

T3 - 0.5%

T4 - 0.05%

46
Q

List 3 thyroid hormone actions?

A

Increased basal metabolic rate.
Increase protein, carbohydrate, and fat metabolism
Have effects on CNS → Important for brain development (Maturation of CNS)
Essential for fetal growth and development.
Enhance the effects of catecholamines leading to tachycardia, glycogenolysis, and lipolysis
Effects on the GI and reproductive systems
Increased heat production

47
Q

What is cretinism?

A

Untreated congenital hypothyroidism.

48
Q

How do you measure TSH levels in a newborn infant?

A

Heel-prick test

49
Q

Explain the hypothalamo-pituitary-thyroid negative-feedback system?

A

TRH in the hypothalamus → hypophyseal-pituitary portal system → anterior pituitary (thyrotropic cells) → TSH → blood → thyroid (TSH-Rs in follicular cells) → T3 & T4.
Production of T3 and T4 causes a negative feedback effect, decreasing the production of TRH (indirect, acts on hypothalamus) and TSH (direct; acts on anterior pituitary).
Somatostatin can also inhibit the production of TSH.

50
Q

What is the Wolff-Chaikoff effect?

A

Iodide in large quantities inhibits the production of T3 and T4 via inhibition of thyroid peroxidase.

51
Q

Are thyroid disorders more common in men or women?

A

Women (4:1 ratio)

52
Q

What causes primary hypothyroidism?

A

Autoimmune thyroid diseases - most common is Hashimoto’s thyroiditis (Presence of one autoimmune disease increases the risk of others)
Thyroidectomy (removal of the thyroid gland)

53
Q

What effect does hypothyroidism have on TSH levels?

A

T3 and T4 levels decrease, causing TSH levels to increase due to negative feedback loop (not enough T3 & T4 present to inhibit TSH)

54
Q

Give 3 symptoms and signs of a patient presenting with primary hypothyroidism.

A 
Bradycardia
Deepening voice
Depression and tiredness
Constipation
Weight gain and reduced appetite
Cold intolerance
Eventual myxoedema coma
Low sexual desire, diminished potency, and fertility
Hair loss (receding hairline), shaggy hair
Dry/rough skin, paresthesia
Memory impairment
Swollen face
Swelling of the eye socket
Enlarged thyroid gland
Muscle cramps
Menstrual cycle disorders
55
Q

How can you treat hypothyroidism and what is a common dose?

A

Levothyroxine (T4 equivalent pill and can be deiodinated into T3 by the body); administered orally - Lifelong treatment.
Usually 100 micrograms (less if the patient is older or has heart problems)

56
Q

What are some potential implications of this treatment?

A

Potential heart attack, weight loss, headaches, rapid HR (tachycardia) but only if taken in very high doses.

57
Q

What are some complications of combined thyroid hormone replacement treatment (T3 + T4)?

A

Symptoms of toxicity → Palpitations, tremor, and anxiety (combination treatment often suppresses TSH)

58
Q

What effect does hyperthyroidism have on your thyroxine levels?

A

Thyroxine levels rise

59
Q

What are the causes of hyperthyroidism?

A

Graves’ disease - Autoimmune condition → Whole gland smoothly enlarged and overactive.
Toxic multinodular goiter
Solitary toxic nodule (toxic adenoma → single nodule undergoes hypertrophy)

60
Q

Explain the pathophysiology of Graves’ disease.

A

Antibodies (thyroid-stimulating immunoglobulins) bind onto TSH-Rs in the thyroid and activate them, leading to excessive thyroid hormone release (increase T4 and T3).

61
Q

What are the common features of Graves’ disease?

A
  • *Smooth goiter**
  • *Exophthalmos** → Antibodies bind to muscles of the eye causing the eye to project forward.
  • *Pretibial myxoedema** → Antibodies stimulate the growth of soft tissue on the shin. (Hypertrophy)
62
Q

Give 3 signs and symptoms of a patient presenting with hyperthyroidism

A 
Heat intolerance 
Weight loss with increased appetite 
Myopathy 
Mood swings 
Diarrhea 
Sore eyes, goiter 
Palpitations 
Tremor of hands 
Muscle cramps/weakness 
Increased HR + high BP, arrhythmia
Broken hair, hair loss, fragile fingernails
Insomnia
Depression
Warm, moist skin
Increased body temperature
Menstrual cycle disorders

BRS (9 decks)

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