Endocrine system Flashcards
1
Q
Examples of
Neurotransmitters
A
Noradrenaline and acetylcholine
2
Q
Examples of
Neuroendocrine
A
Oxytocin & ADH
3
Q
Endocrine
A
Insulin, TSH, thyroxine, cortisol
4
Q
Example of
Paracrine
A
Glucagon and somatostatins
5
Q
Example of
Autocrine
A
Prostoglandins
6
Q
Hormones
A
- Arouses or exicte cells
- Glands secretes hormones directly into blood stream
- Carried to target cells away from the endocrine glands
7
Q
Types of hormones
A
- Peptide hormones
- Steroidal hormones
- Tyrosine hormone
- Eicosanoids
8
Q
Structure and examples
Peptide hormones
A
- Chains of amino acids
- Small chains such as TRH that contains 3 AAs
- Large chains such as FSH and LH that have 80 AAs
- They are secreated by hypothalmus, pituitary, pancreas and GIT
9
Q
Peptide hormone synthesis and transport
A
- Transcription and translation occour
- Preprohormone (coiled) to prohormone to hormone to secreatory granules to vesicales
- Released by exocytosis
- Hydrophilic so free chains that circulate in the blood (no binding to protien)
- short half life (minutes)
10
Q
Structure and examples
Steroidal hormone
A
- Cholesterol as the base
- Cortisol
- Aldosterone (adrenal cortex)
- Sex hormones
11
Q
Steroidal hormones synthesis and transport
A
- Enzymatic conversion of percursor (cholesterol base) molecules into hormone
- Stimulus increases percursor level of enzyme activation and diffusion occour across the membrane
- Is lipophilic so binds with plasma protien albumin if bound to protien it is active
- Half life is hours to days
12
Q
Struture
Tyrosine Hormone
A
Tyrosine base in the thyroid hormone and catecholamines (adrenal medulla)
13
Q
Tyrosine synthesis and transport
A
- From thyroxine to tyrosine to epinephrine
- Stimulus required and it diffuses across the membrane
- Are lipophilic and binds with plasma protein
- Half life from hours to days
14
Q
Structure
Eicosanoids
A
- Polyunsaturated fatty acids derivatives
- e.g prostaglandins, leukotrienes, prostacyclins and thromboxanes
15
Q
Eicosanoids synthesis
A
- Precursor are arachidonic (lipids)
- Enzyme lipase dictates the production of various eicosanoids
- Synthesised by stereo- and regio-specific peridoxation of arachidonic acid by 3 enzyme families
- lipoxygenases, cyclooxygenases, and cytochrome P450
15
Q
Transport and release of eicosanoids
A
- Stimulus required and poorly diffuses through cell membrane
- Requires transporter which as it is anionic
- Half life is seconds and hormone is inactivated rapidly to limit autocrine and paracrine effects
16
Q
Peptide hormone functions
A
- Hydrophilic hormone bind to receptor act on G-protien couple receptor which stimulates the effector (ACTH and glucagon)
- Elswhere the hormone binds with receptor which stimulates tryosine kinase (insulin growth hormone)
- Causes signal conduction and a physological reponse occours
17
Q
Simple feedback axis
A
- Target cells see more glucose automatically sends signal to stimulate insulin and close the receptor for glucagon
18
Q
Insulin secreation
A
- Release of insulin via endocrine glands by a stimulus
- The insulin activates the target cells to increase its uptake of substrates to produce protien synthesis and glycogen storage
- Negative feedback between target cells to endocrine glands
19
Q
Hypothalamus pituitary axis
A
- Hypothalamus releases Releasing hormone which acts on the anterior pituitary gland
- Trophic hormones are released from the anterior pituitary which can act on the target tissue directly
- Trophic hormones can also send a signal to the peripheral edocrine glands
- Then hormone released from the peripheral endocrine glands act on the target cells
20
Q
Complex feedback axis
(cortical)
A
- The cortisol releasing hormone is released from the hypothalamus
- Stimulates the signal of the antiror pituitary gland to release ACTH
- Acts on peripheral endoctrine gland (adrenal gland) this systhesis the steroidal hormmone cortisol
21
Q
Negative feedback axis
(cortical)
A
- Too much cortisol send signal to adrenal gland to stop sysnthesising release of cortisol in adrenal cortex
- Long fedback axis to anterior piturity gland to stop producing the ATCH
- Send signal directly to the hypothalmus to stop producing CRH
22
Q
Neuroendocrine reflex centres
A
- Emotion control infulence HP acess
23
Q
Metabolism of hormones
A
- Largely in blood liver and kidney some are in target cells and it is exreated by urine
24
Q
Endocrine disorders
Hypersecreation
A
- Excess amount of hormone secreated e.g. Graves disease
25
Q
Endocrine Disorder
Hyposecreation
A
- Tumour in glands may cause hyposecreation as less hormone is released
- Type 1 diabetes or immunological distruction
26
Q
Type 1 diabetes
A
- Autoimmune conditions and genetic conditions
- insulin producing cells can’t produce insulin due to antibodies being generated that stop insulin production so hyposecreation occours
27
Q
Primary defect
A
- Non-funtional peripheral endocrine gland (tumour) in hyposecreation
- Stimulates Antierior pituitary and Hypothalmus more therefore increased secreation of CRH and ACTH
28
Q
Secondary defect
A
- Pituitary tumor could cause hypo or hypersecreation
- if hyper then lots of ACTH is being produced therefore more cortisol is being produced
- Low levels of CRH produced at hypothalamus
29
Q
Ectopic deffect
A
- Signal external to the HPA axis
- Tumour produce ACTH which increases its level
- Increase ACTH stimulate release of cortisol
- Scan to check where tumour is
30
Q
Defect with target cells
A
- Type 2 diabetes where the muscle cells adipose cells and liver cells become insulin resistant due to signal unrecognised by receptor on cell
31
Q
diagnose defective hormones
A
- Dynamic and provocative tests this checks for the integrity of feedback control ( primary secondary or target)
- Stimulation test - suspective hyposecreation
- Supression test - suspective hypersecreation
32
Q
Treatment for hyposecreation, hypersecreation and impared target cell
A
- Replace hormone supplements - hyper
- Block synthesis and release of drugs - hypo
- enhance drug cellular respose to hormone
