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RED - Endocrine Pharmacology & Therapeutics > E1 - Review of Hormonal Mechanisms > Flashcards

E1 - Review of Hormonal Mechanisms Flashcards

1
Q

What are the characteristics of a hormone?

A
  • Chemical messengers that normally ‘arouse/excite’
  • Secreted directly into the bloodstream from (ductless) endocrine gland
  • Target cell/tissue is a long distance from gland
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2
Q

What are the 4 types of intercellular messengers in the body and their characteristics?

A
  • Endocrine (internal/ductless/distance to target/in blood circulation e.g. insulin)
  • Autocrine (affects own cell locally e.g. prostaglandins) & Paracrine (within interstitial fluid to neighbouring cell e.g. somatostatin)
  • Neuroendocrine - nerve fibres/endo (e.g. hormone made in nerve cell then stored in secretory granules of the axon terminus; e.g. from posterior pituitary gland releasing ADH; arginine vasopressin)
  • Neurotransmitter (made by neurones, travels short distance across synaptic cleft e.g. ACh, Glu)
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3
Q

What are the 3 main types of hormones according to chemical structure?

A
  • Peptide hormone
  • Steroid hormone
  • Hormones derived from tyrosine (starting hormone)
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4
Q

What do peptide hormones consist of? Give examples.

A
  • Chains of amino acids, from 3AAs to 180AAs

- Includes those from hypothalamus, anterior/posterior pituitary gland, pancreas, GIT.

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5
Q

What are steroid hormones derived from? Give examples.

A
  • Cholesterol
  • E.g. Adrenal cortex: cortisol, aldosterone
    Gonads: sex hormones
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6
Q

Give examples of hormones derived from tyrosine and their characteristic properties.

A
  • Thyroid hormones

- Catecholamines (e.g. adrenaline/noradrenaline/dopamine; has catechol group - lots of NH2)

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7
Q

What are the 5 steps of peptide hormone synthesis?

A
  1. ) Gene > mRNA (transcription), mRNA > protein (translation; making a protein from mRNA
  2. ) PREPROHORMONE made in ribosomes (on RER/in cytoplasm), peptide chain also undergoes protein folding/disulphide bridging and glycosylation attachment of carbohydrates)
  3. ) Peptide travels through RER stack and ‘pre’ signal peptide bit is cleaved; leaving a PROHORMONE which is packaged into vesicles to the Golgi complex
  4. ) Peptide undergoes further processing through Golgi complex stack, packaged into secretory granules to form the mature HORMONE
  5. ) Hormone stored in secretory granules until its required/stimulus; where secretory granule moves towards plasma membrane, fuses then expulsion of hormone into circulation (exocytosis)
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8
Q

What does the ‘pre’ part of the preprohormone entail?

A

Hydrophobic short sequence; signal peptide (telling cell the protein needs processing/packaging for exporting)

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9
Q

What is the difference in hormone release re. peptide and steroid hormones?

A

Peptide; release dependent on exocytosis (hormone stored in secretory granules)

Steroid; release dependent on hormone synthesis (biosynthetic enzyme activity) and is via simple diffusion; not stored.

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10
Q

How are steroid hormones released via simple diffusion?

A

Due to the lipophilicity of steroid hormones; they are attracted to the phospholipid bilayer (plasma membrane) and are led out of the cell that way.

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11
Q

How do steroid hormones travel in the blood?

A

Once release from an endocrine cell via simple diffusion, they are bound by plasma proteins.

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12
Q

Why do peptide hormones circulate as free hormones/how does it affect half-life?

A
  • Due to solubility; hydrophilic, water soluble nature; likes aqueous environments
  • But proteases present in the blood/at target tissue, thus half-life is matter of minutes
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13
Q

What is half-life?

A

Time taken for initial concentration to fall by 50%

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14
Q

How do steroid/thyroid hormones achieve the longer half-life of hours - days and what advantages does this pose?

A
  • Bound reversibly to plasma proteins (weak bonding; can’t travel as free hormone as lipophilic - not water soluble)
  • Protects hormone, delaying metabolism and providing a circulating reservoir
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15
Q

Do peptide hormones act intracellularly at the target cell?

A

No; they are hydrophilic and thus cannot cross the fatty plasma membrane.

They interact via cell surface receptors in the plasma membrane.

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16
Q

What are the two main types of cell surface receptors for peptide hormones? Give examples of their substrates.

A
  • G-protein e.g. glucagon

- Tyrosine kinase e.g. insulin

17
Q

What changes occur upon peptide hormone docking?

A
  • Signal transduction of hormone via 2nd messenger
  • Physiological changes; altered activity of enzymes or ion channels
  • Altered gene expression of specific proteins
18
Q

Where are intracellular receptors located for steroid hormones?

A
  • Cytosolic

- Nuclear (usually)

19
Q

What are the consequences of steroid hormone binding?

A
  • An increase or decrease in gene expression (depending on whether stimulating/inhibiting)
20
Q

What does an increase in gene expression from a stimulating steroid hormone entail?

A
  • Upregulation of gene = increased transcription/translation = more protein present = greater enzyme activity/more ion channels present etc)
21
Q

Where are hormones metabolised?

A

Most hormones metabolised by enzymes in liver, kidney and/or blood; little metabolism by target tissues (most of the hormone already metabolised before arriving to target)

22
Q

How are hormones excreted?

A
  • Via the kidney = urine

- Via the gut = faeces

23
Q

What are the two feedback regulation processes?

A
  • Negative feedback; consequence (B) negatively controls process (A) to maintain a set point; narrow range maintained.
  • Positive feedback; consequence (B) amplifies/enhances process (A) further
24
Q

What is simple feedback regulation?

A
  • Gland releases hormone, hormone acts at target tissue, target tissue’s response influences OG gland.
25
Q

What is the endocrine axis?

A

Interactions between hypothalamus (releasing hormone), anterior pituitary (tropic hormone) and peripheral endocrine glands (peripheral hormone) in series with feedback regulation of hormone secretion

26
Q

What occurs re. the endocrine axis if the level of peripheral hormone is too high?

A
  • Negative feedback loop to anterior pituitary (direct) and hypothalamus (indirect)
  • Thus less release of releasing hormone from hypothalamus
  • Thus less release of tropic hormone from the anterior pituitary
  • Restoring peripheral hormone level to the set point
27
Q

What are neuroendocrine reflexes?

A

Regulatory input from higher centres in the brain above the hypothalamus e.g. STRESS on cortisol release = more produced to deal with stress situation.

28
Q

What do diurnal and circadian mean?

A
  • Day-night

- Around a day

29
Q

How does diurnal rhythm influence hormone release in relation to cortisol?

A
  • Body prepares you with high levels of cortisol at the start of the day (to deal w/mini-stresses)
  • Body produces more cortisol at late-evening period to deal with rest of the day
  • Body produces cortisol during sleep in preparation for the next day
30
Q

What are the 3 endocrine disorders?

A
  • Hypersecretion (hormone excess) e.g. tumour or immunological factor like Graves’ disease
  • Hyposecretion (lack of hormone) e.g. lack of enzyme genetically, immunological attack, destruction by disease, surgical removal
  • Decreased target-cell responsiveness; at receptor level or downstream enzyme
31
Q

What is the difference between a primary disorder and a secondary disorder (relating to endocrine)?

A
  • Primary; dysfunction originating in the peripheral endocrine itself (the OG)
  • Secondary; under/overstimulation of the anterior pituitary one above the endocrine axis/excess production of preceding tropic hormone from external source
32
Q

What investigations/tests are undertaken for suspect endocrine abnormalities?

A
  1. ) Signs & symptoms
  2. ) Endocrine investigations (hormone levels)
  3. ) Imaging (CT scan etc)
33
Q

What endocrine investigations/hormone level tests are available?

A

a. ) Single-point (baseline)

b. ) Dynamic/provocative; checking integrity of feedback control

34
Q

What testing method is used for suspected hyposecretion and how does it show it?

A

Stimulation; hormone levels rise in the norm, failure to stimulate indicates hormone insufficiency (often regarded as confirmatory test)

35
Q

What testing method is used for suspected hypersecretion and how does it show it?

A

Suppression; hormone levels fall in the norm, failure to suppress indicates autonomous secretion (tumour).

36
Q

What is the treatment for hormone deficiency?

A

Synthetic hormone replacement

37
Q

What is the treatment for excess hormone?

A

Drugs to block productoin

38
Q

What is the treatment for decreased target-cell responsiveness?

A

Drugs to enhance cellular response to hormone

RED - Endocrine Pharmacology & Therapeutics (7 decks)

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