Week 10 - Endocrine System and Disorders Flashcards

1
Q

Differentiate an endocrine gland from an exocrine gland

A
  • Endocrine glands are ductless and produce hormones (e.g. oestrogen) that travel to target cells via the bloodstream
  • Exocrine glands produce substances (e.g. enzymes, bile) and release them via ducts
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2
Q

Define the term “hormone”

A
  • Chemical messengers that travel via the blood to act on specific receptors of target cells
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3
Q

List the differences between hormonal and nervous communication. In what ways are they similar?

A

Differences:

  • Transmission Speed
    • Hormone - slow
    • Nerves - fast
  • Length of Effect
    • Hormone - long
    • Nerves - short
  • Mechanism of Action
    • Hormone - travel via bloodstream, to act at specific receptors at target cells
    • Nerves - changes in membrane potential push transmission from one neuron to another, where neurotransmitters act on target receptors

Similarities

  • Both act on specific receptors in target cells
  • Both can cause a change in the activity of a cell
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4
Q

Explain how hormones may be classified based on chemical structure.

A
  • The chemical structure of a hormone determines its mechism of action on a target cell
  • For example, hormones derived from amino acids generally act via secondary messenger systems, whilst hormones that are lipid/steroid-based generally act via direct gene activation
  • This is why they are classified differently
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5
Q

List the hormones that are referred to as steroid hormones. What nutrient are steroid hormones synthesised from?

A
  • Steroid hormones are synthesised from lipids
  • Examples:
    • Aldosterone
    • Oestrogen
    • Testosterone
    • Cortisol
    • Progesterone
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6
Q

Describe how amino acid based hormones differ to steroid hormones in terms of their (i) solubility in water and (i) ability to cross target cell membranes

A
  • Amino acid based hormones
    • soluble in water
    • therefore, cannot diffuse across cell membrane
    • must use secondary messenger systems
  • Steroid based hormones
    • not soluble in water
    • therefore, can diffuse directly across cell membrane
    • can use direct gene activation
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7
Q

Provide some examples of eicosanoids. What nutrient are eicosanoids synthesised from?

A
  • derived from fatty acids (arachidonic acid)
  • e.g. prostaglandins and leukotrienes (involved in allergic response of respiratory tract)
  • generally act as paracrines
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8
Q

List four general actions of hormones. Can you provide an example for each?

A
  • stimulate synthesis or secretion (e.g. leutenising hormone -> testosterone production)
  • increase permeability or exciteability of cell (antidiuretic hormone -> increase water uptake)
  • activation/deactivation of enzymes (e.g. trypsin -> activates pancreatic zymogens to pancreatic enzymes)
  • stimulation of mitosis (e.g. growth hormone -> stimulate somatic growth)
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9
Q

Explain the difference (at the cellular level) between a second messenger system and direct gene activation – you may wish to use diagrams to illustrate your point

A
  • second messenger system
    • hormone is water-soluble and unable to diffuse across membrane
    • binds to a receptor within cell membrane
    • causes a cascade of events involving second messengers within the cell
    • this results in changed cellular activity
  • direct gene activation
    • hormone is lipid-soluble and able to diffuse across membrane
    • binds to receptor within a cytosol, creating a receptor-hormone complex
    • this complex enters the nucleus, and causes a change in cellular activity (e.g. transcription of mRNA)
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10
Q

Which class of hormones relies on second messenger systems? Can you explain why these hormones need to work in this way?

A
  • amino-acid based hormones rely on second messenger systems
  • they are water-soluble / lipid-phobic, meaning they are unable to diffuse across the cell membrane
  • in cyclic amp second messenger system, this leads to the reliance on the activation of G protein to activate a cascade of events to execute the change in cell activity (ATP is involved)
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11
Q

Provide some examples of molecules that are used as second messengers

A
  • cyclic AMP (e.g. in FSH, LH and glucagon mechnanisms)
  • tyrosine kinase (e.g. in insulin activity)
  • PIP2 and calcium (e.g. oxytocin, ADH)
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12
Q

Which hormones are capable of direct gene activation? Can you explain why these hormones are capable of achieving this?

A
  • steroid hormones and T3, T4 are capable of direct gene activation
  • steroid hormones are lipid soluble, therefore, they are able to easily diffuse through the cell membrane
  • T3 and T4 are transported into target cells by membrane-bound transporter proteins, and therefore, are also capable of direct gene activation
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13
Q

How do the receptors for thyroid hormone differ to the receptors targeted by other hormones?

A
  • receptors for thyroid hormones are located within the nucleus of the target cell
  • whilst, in steroid hormones, these receptors are located within the cytosol
  • also, other amino-acid based hormones bind to receptors located on the cell membrane
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14
Q

Describe the three main types of stimuli that can trigger an endocrine gland to synthesise and release hormones. Provide examples for each type of stimuli.

A
  • humoral stimulus (altered blood levels of ions or nutrients)
    • e.g. insulin released in response to high blood glucose levels
  • nervous stimulus
    • e.g. stimulation of SNS leads to release of adrenaline (from adrenal medulla)
  • hormonal stimulus
    • e.g. hypothalamis-pituitary axis - gonadotrophin-releasing hormone (hypothalamus) stimulates secretion of FSH and LH (anterior pituitary gland)
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15
Q

What is meant by the term negative feedback control? Provide an example to illustrate your point.

A
  • when hormone levels rise sufficiently to cuse target organ effects
  • target organ sends feedback to reduce the initial stimulus for hormone release
  • results in inhibition of further hormone release
  • example:
    • testosterone released in response to low levels
    • testosterone produced by interstitial (Leydig) cells provides feedback to anterior pituitary gland to stop releasing FSH and LH
    • sustentacular cells, which are producing androgen-binding protein, produce inhibin to act on hypothalamus to stop releasing gonadotrophin-releasing hormone
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16
Q

Differentiate the terms adenohypophysis and neurohypophysis

A
  • adenohypophysis refers to the action of the anterior pituitary gland, via vessels connected to the hypothalamus
  • whilst, neurohypophysis refers to neurological regulation between hypothalamus and the posterior pituitary gland
17
Q

Describe how the hypothalamic connections of the adenohypophysis differ to those of the neurohypophysis

A
  • posterior pituitary receives the axon terminals of neurons (hypothalamic neurosecretory cells) that project from two nuclei located in the hypothalamus
  • anterior pituitary has a vascular connection to the hypothalamus via the hypophyseal portal system (a network of capillary plexuses connected by veins)
18
Q

Identify the hormonal secretions of the hypothalamus and anterior pituitary gland. Include the effects that these hormones have on their target organs.

A

Hypothalamus-Pituitary Axis

  • hormonal stimulus: growth hormone-releasing hormone in response to low levels of GH
    • target: anterior pituitary gland
    • release: growth hormone
    • function: stimulates somatic growth and mobilises fats for use as an energy source, in preference over glucose
  • hormonal stimulus: corticotrophin-releasing hormone in response to fever or hypoglycaemia or stress
    • target: anterior pituitary gland
    • release: andrenocorticotrophic hormone
    • function: stimulates release of hormones from adrenal cortex e.g. glucocorticoids, androgens, mineralcorticoids
  • hormonal stimulus: thyrotrophin-releasing hormone in response to low levels of T3
    • target: anterior pituitary gland
    • release: tetraiodothyronine (T4) and triiodothyronine (T3)
    • function: regulates of metabolism and heart rate
  • hormonal stimulus: gonadotrophin-releasing hormone
    • target: anterior pituitary gland
    • release: FSH and LH
    • function:
      • FSH -
        • M - stimulates production of androgen-binding protein by sustentacular cells (to support sperm production)
        • F - stimulates maturation of ovarian follicle and production of oestrogens
      • LH -
        • M - stimulates production of testosterone by interstitial (Leydig) cells
        • F - triggers ovulation and converts the ruptured follicle into the corpus luteum

Hypothalamus production

  • oxytocin
    • transported to posterior pituitary gland
    • function: uterine contractions, milk ejections, bonding and nutrients
  • antidiuretic hormone
    • transported to posterior pituitary gland
    • function: RAAS
19
Q

How would you introduce the adrenal glands (structure/function/location) in the setting of a lab exam?

A
  • structure:
    • the adrenal glands are paired glands that are enclosed in a fibrous capsule and a cushion of fat
  • location:
    • they are located atop the right and left kidneys in the upper quadrants of the abdomen
  • function:
    • the adrenal glands have a signficant endocrine role, including releasing hormones such as aldosterone for blood pressure regulation and cortisol, for gluconeogensis.
20
Q

What is the vascular supply of the adrenal glands? Can you explain why these glands have such an abundant vascular supply?

A
  • adrenal glands have an abundant vascular supply, due to their significant endocrine output
  • they are supplied by:
    • superior adrenal arteries
    • middle adrenal arteries
    • inferior adrenal arteries
21
Q

Conceptually map the hormonal secretions of the adrenal cortex. Your concept map should make reference to (i) the regions of cortex where these hormones are produced (ii) the types of stimuli that cause the release of these hormones and (iii) the functions of these hormones

A

Zona glomerulus

  • mineralocorticoids e.g. aldosterone
    • stimuli: low blood pressure; high plasma levels of K+, stress response, atrial natriuretic peptide
    • effect: Na+ reabsorption and K+ secretion

Zona fasciculus

  • glucocorticoids e.g. cortisol
  • stimuli: prolonged stress
  • effect:
    • gluconeogenesis
    • SNS response on smooth muscles of blood vessel walls
    • regulation of immune response

Zona reticularis

  • androgens supplementing gonads e.g. oestrogen after menopause or during puberty
  • stimuli: puberty; menopause

Medulla

  • Chromaffin cells
    • stimulus: short term stress
    • effect: produce adrenaline and noradrenaline - increased HR and heart contractility; peripheral vessel constriction; increased BP; increased blood glucose
22
Q

Describe the cells of the adrenal medulla. Why are these cells referred to as modified postganglionic sympathetic neurons?

A
  • preganglionic sympathetic fibres, leaving the cord at T10-L1, do not synapse at the prevertebral ganglia
  • instead, they terminate at the adrenal medulla, where they synapse directly with chromaffin cells
  • as a result, chromaffin cells are considered to be modified postganglionic sympathetic neurons
23
Q

What is meant by the term “catecholamines”? List five functions of catecholamines.

A
  • definition - catecholamines are neurotransmitters that augment the activity of the SNS
    • adrenaline and noradrenaline functions:
      • increase HR and cardiac contractility
      • vasoconstriction of peripheral blood vessels
      • increased BP
      • increased blood glucose levels
      • increased basal metabolic rate
24
Q

Discuss the role that adrenal glands play in the short-term and long-term stress response.

A
  • short term response:
    • nerve impulse travel via preganglionic sympathetic fibres to adrenal medulla
    • synapse with chromaffin cells results in production and release of adrenaline and noradrenaline
    • these catecholamines:
      • increase HR
      • increase BP
      • dilate bronchioles
      • convert glycogen to glucose in liver (increase blood glucose level)
      • reduce blood flow to peripheral blood vessels (vasoconstriction)
      • increase metabolic rate
  • long term response:
    • zona glomerulus releases mineralocorticoids (aldosterone)
      • kidneys retain sodium and water
      • blood volume and blood pressure rises
    • zona fasciulus release glucocorticoids (cortisol)
      • proteins and fats converted into glucose or broken down for energy
      • blood glucose levels increase
      • immune system is suppressed
25
Q

Differentiate Cushing’s Disease from Cushing’s Syndrome. What is the most common cause of Cushing’s Syndrome?

A
  • Cushing’s Disease
    • hypercorticolism resulting due to increased adrenocorticotrophic (ACTH) hormone secretion (anterior pituitary gland)
  • Cushing’s Syndrome
    • hypercorticolism occurring independently of pituitary adrenocorticotrophic secretion secretion
    • most common cause: iatrogenic (e.g. glucocorticoid hormone therapy)
26
Q

Summarise the clinical features of hypercortisolism. Can you explain the pathological basis of each feature?

A
  • effects on metabolism
    • truncal obesity
    • lemon on toothpicks appearance
    • moon face with flushed red cheeks, buffalo hump
    • muscle weakness/wasting, myalgia, arthralgia
    • osteoporosis, pathological fracture
    • hyperglycaemia -> insulin resistance
  • effects on blood pressure
    • hypertension
  • effects on immunity
    • poor wound healing, skin infections
  • involvement of zona reticularis may produce features of hyperandrogenism
    • hirsutism
    • menstrual irregularity
27
Q

Differentiate Primary Adrenocortical Insufficiency from Secondary Adrenocortical Insufficiency. What is another term given to primary adrenocortical insufficiency?

A
  • Primary - due to intrinsic dysfunction of adrenal cortex (a.k.a Addison’s disease)
  • Secondary - due to pituitary or hypothalamic dysfunction
28
Q

List the causes of Addison’s disease. Which cause is most common?

A
  • 80% most common cause = autoimmune attack
    • damage to adrenal cortex - ZG and ZF are usually affected
    • although, medulla is rarely involved
  • less common causes:
    • infection
      • tuberculosis
      • viral e.g. HIV
    • metastatic disease
    • bilateral adrenalectomy
29
Q

Summarise the clinical features of hypercortisolism. Can you explain the pathological basis of each feature?

A
  • decreased mineralocorticoid (aldosterone) activity
    • severe dehydration (low blood volume due to lack of water reabsorption)
    • hypotension (low blood volume)
    • hyperkalaemia (inability to respond to excessive K+)
  • decreased glucocorticoid (cortisol) activity
    • hypoglycaemia (proteins and fats are no longer converted to glucose, or broken down for energy)
    • postural hypotension
    • systemic features: severe fatigue, weakness, weight loss, GI disturbances
30
Q

Define the term phaeochromocytoma

A
  • malignancy/tumour arising from chromaffin cells of adrenal medulla
31
Q

Summarise the clinical features of phaeochromocytoma. How might an osteopath be able to detect this disorder?

A
  • related to hypertension or complication of hypertension
    • AMI
    • stroke
    • heart failure
    • AAA
  • intermittent catecholamine secretion causing episodes of:
    • pallor, palpitations, sweating, severe headaches, anxiety, tremours
    • abdominal pain, vomiting, constipation, weight loss, hyperglycaemia