W9 Endocrine System Flashcards
What are the different intracellular messenger systems? (5)
Neurotransmission
Neuroendocrine
Endocrine
Autocrine
Paracrine
What is an example of a…
neurotransmitter?
neuroendocrine transmitter?
Endocrine transmitter?
Autocrine transmitter?
Paracrine transmitter?
Neurotransmission- noradrenaline, acetylcholine
Neuroendocrine- Oxytocin and ADH
Endocrine- Insulin, TSH, thyroxine, cortisol
Autocrine- Prostoglandins
Paracrine- Glucagon, somatostatins
What do hormones do?
Where are they secreted?
“Arouse or Excite”
Glands secrete hormones directly into blood stream (ductless)
Carried to target cells/tissue (away) from the endocrine gland
What is the structure of a peptide hormone?
Where are they secreted
Small chains
Large chains
Mostly secreted from hypothalamus, pituitary, pancreas and GIT
Peptide hormones:
How are they synthesised and stored?
How are they transported?
How are they adapted for transport? (4)
Synthesis: like any protein synthesis
Transcription/Translation
preprohormone-prohormone-hormone-secretory
granules/vesicles
Stored in the cells
Release: Require stimuli
Exocytosis
Transport:
Hydrophilic,
Freely circulate in the blood vessel
No plasma protein binding
Short Half-life: minutes
How are steroidal hormones synthesised?
How are they released/transported?
How are they adapted for transport? (3)
Chemical structure- Cholesterol as the base
Synthesis- Like any steroidal synthesis
Enzymatic conversion of precursor (cholesterol base) molecules into hormone
Not stored in the cells
Release:
Stimulus increase precursor level and enzyme activation
Simple diffusion across membrane
Transport:
-Lipophilic
-Binds with Plasma protein
-Half-life: hours to days
When is a molecule inactive?
How can you activate it?
Any molecule BOUND to a PLASMA PROTEIN it becomes inactive.
In order to activate it, steroidal hormone must be released from carrier protein
What is tyrosine?
How is it transported?
How is it adapted for transport?
Chemical structure: tyrosine as the base
thyroid hormones and catecholamines (adrenal medulla)
Release
Stimulus required
Simple diffusion across membrane
Transport
Lipophilic
Binds with Plasma protein (Weak and reversible bonds)
Half-life: hours to days
What are eicosanoids?
How do they travel across the cell membrane?
How are they adapted for transport?
Chemical structure: Polyunsaturated fatty acid derivatives
Eg; prostaglandins, leukotrienes, prostacyclins and thromboxanes
Synthesis:
Precursor- Arachidonic acid (membrane lipid)
Enzymes- Lipase dictates the production of various eicosanoids
Release:
Stimulus required
Poorly diffuse through cell membrane
Transport:
Eicosanoids require transporter (anionic)
Half-life: in seconds: rapidly inactivated: Limited to autocrine and paracrine effects
Synthesized by stereo- and regio-specific peroxidation of arachidonic acid by three enzyme
families namely lipoxygenases, cyclooxygenases, and cytochrome P450
Hormonal homeostasis
Peptide hormone function
Hormonal Homeostasis
What is negative and positive feedback?
Negative- OUTCOME negatively controls PROCESS (maintain a set-threshold)
Positive feedback- OUTCOME amplifies the PROCESS
Hypothalamus -Pituitary axis
Hypothalamus—CRH released— Anterior Pituitary— ACTH released—Peripheral Endocrine Gland—Cortisol—Target cells (response)
What type of hormone is released by anterior pituitary?
Peptide hormone
Hormonal homeostasis consists of what? (4)
Simple Feedback Axis
Hypothalamus-Pituitary- Axis
Neuroendocrine reflux’s
Circadian Rhythms (diurnal- sleep and wake
cycle)
Metabolism of Hormones
Enzymatic processes:
Largely in blood, liver and kidney and some in target
cells/tissues/organs
Excreted in urine.
Hyposecretion example
Type l diabetes
What is an example of Hypersecretion?
Tumors
What is located on the peripheral gland?
Primary defect
High ACTH secreted means..
Increases cortisol production
Negative feedback at hypothalamus (CRH is low)
Secondary defect
What causes an Endocrine disorder?
Give an example
Tumour in peripheral gland (primary) or pituitary (secondary) or ectopic
Immunological (& genetic): Autoimmune disease (eg: T1DM, Hashimoto’s, Graves’, Addison’s)
Treatment strategies:
Hyposecretion
Hypersecretion
Impaired target-cell responsiveness
Tumour
- Hyposecretion/hormone deficiency – Replace the hormone (supplements)
- Hypersecretion/hormone excess – Block the synthesis and release (drugs)
- Impaired target-cell responsiveness – drugs to enhance cellular response to hormone
- Tumour – radiotherapy or surgery
Primary defect
Low ACTH and CRH
High Cortisol
What is a Secondary defect?
Low CRH
High ACTH and Cortisol
Four types of Hormones
Peptide
Steroidal
Tyrosine containing
Eicosanoids
Hypothalamus -Pituitary
Cell bodies and the neurons responsible for the secretion of hypothalamic releasing factors (hormones)
Hypothalamus-Anterior Pituitary
Where do releasing factors pass to?
Releasing factors pass along the portal vessels to reach capillary bed of the anterior pituitary, to control secretion of anterior pituitary hormones
Hypothalamus Posterior-Pituitary
Paraventricular (PVN) and
supraoptic (SON) nuclei,
and the neurons carrying
oxytocin and ADH
(vasopressin) to the
posterior pituitary, where
they are stored/ released
Pituitary gland clinical relevance
Pituitary tumours are mostly benign and slow-growing
Over/under production of hormones (Hyper/Hypo)
Local effects: pressure on surrounding structures
– headaches, visual disturbances
Somatotropin, HGH
What is it secreted by?
How is it stored?
What is its role?
What is its stimulus for growth?
Secreted by acidophilic cells of anterior pituitary glands
It is stored in the cells as granules. Growth hormone production is pulsatile
Peptide hormone: 21.5 K Da single-chain polypeptide (190 AA) with 2 disulphide bridges)
Major role in growth (linear) & metabolism
Drop in blood glucose is the stimulus for the growth of HGH (human growth hormone)
What is gluconeogenesis?
What type of process is it?
endogenous process in the liver
production of glucose from amino acids and glycerol