Endocrine system I - Hormones Flashcards

1
Q

Examples of neurontransmitters;

A

noradrenaline
acetylcholine

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2
Q

Examples of neuroendocrine

A

Oxytocin & ADH

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3
Q

Examples of endocrine

A

Insulin
TSH
Thyroxine
Cortisol

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4
Q

Intracellular messages systems: simple step by step

A

Secreting cell > Blood vessel > target cell (neurotransmitter gets transferred)

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5
Q

From secreting cell >target cell. What is this type of regulation called?

A

Paracrine

e.g. glucagon, somatostatins

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6
Q

Autocrine =

A

chemical released by same cell is taken in by its own use - own function

e.g. prostaglandins

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7
Q

What are hormones + example;

A

chemical substances that act like messenger molecules in the body

e.g.
GIT
Thymud
Adipocyte
Placenta
Kidney
Heart

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8
Q

Properties and functions of hormones;

A

1) “yo arouse” or “excite”
2) glands secretes hormones directly into blood stream (ductless)
3) Carried to target cells/tissure (away from endocrine gland - INTERNAL to body)

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9
Q

Endocrine gland

A

Sylvia gland
Internal to the body
Function - secrete hormone

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10
Q

List 4 types of hormone=

A
  1. Peptide hormones
  2. steroidal hormones
  3. Tyrosine containing hormone
  4. Eicosanoids

DIFFERENT - [structure, storage, transportation, function]

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11
Q

List 4 types of hormone=

A
  1. Peptide hormones
  2. steroidal hormones
  3. Tyrosine containing hormone
  4. Eicosanoids

DIFFERENT - [structure, storage, transportation, function]

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12
Q
  1. Peptide hormones

Size and structure
Location of secretion
Synthesis
Release
Transport

A

Chemical structure : chains of amino acids
[small chains e.g. TRH: contains 3aas / large chains e.g. LH/FSH 80aas]

Mostly secreted from hypothalamus, pituitary, pancreas and GIT

Synthesis (like any other protein synthesis): transcription/translation-preprohormone-prohormone-hormone-secretory granules/vesicles STORED IN CELLS

RELEASE STIMULI : Exocytosis

Transport : Hydrophilic, freely circulate in the blood vessel
No plasma protein binding
Short half-life; minutes

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13
Q
  1. Steroidal hormones

Chemical structure
Synthesis
Release
Transport

A

Chemical structure : cholesterol as the base
cortisol, aldosterone (adrenal cortex) & sex hormones (gonads)

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

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14
Q

Peptide hormones, why not bind to any plasma protein in order to increase its half life?

A

Mostly protein, not freely moving to bind

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15
Q

Where does steroidal hormone bind to?

A

Binding/carrier plasma protein IN the blood vessel

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16
Q
  1. Tyrosine containing

Chemical structure
Synthesis
Release
Transport

A

Chemical structure : tyrosine as the base
thyroid hormones and catecholamines (adrenal medulla)

Synthesis : Thyroxine < Tyrosine > Epinephrine

Release : Stimulus required
Simple diffusion across membrane

Transport : Binds with Plasma protein (Weak and reversible bonds)
Half-life: hours to days

17
Q
  1. Eicosndoids

Chemical structure
Synthesis
Release
Transport

A

Chemical structure : Polyunsaturated fatty acid derivatives
Eg; prostaglandins, leukotrienes, prostacyclins and thromboxanes

Synthesised by stereo- and regio-specific peroxidation of arachidonic acidby three enzyme families namely lipoxygenases, cyclooxygenases, and cytochrome P450

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

18
Q
  1. Peptide hormone FUNCTION
A

for example hormone binds to G-protein receptor [ACTH, glucagon] > signal transduction > physiological response

hormone [insulin, growth hormone] > receptor > tyrosine kinase > signal transduction > physiological response

19
Q
  1. Steroidal hormonal FUNCTION (& thyroid hormones)
A
  • Intracellular receptors & transcription factors

Glucocorticoid receptor - Cortisol
Mineralocortioid receptor - Aldorsterone
Androgen receptor - Testosterone

20
Q

Steroidal hormone step by step = specific proteins & biological effect

A

Hormone > diffusion> nuclear receptor (in nucleus) > DNA > mRNA > specific proteins & biological effects

Hormone > Cytosolic receptor > into nucleus > DNA > mRNA > specific proteins & biological effects

21
Q

Hormonal homeostasis:
feedback regulation types?

A
  • OUTCOME (Y) of a PROCESS (X) acts to regulate the RATE of the PROCESS

Process (x) > [+] Outcome (y) < [-] Process (x) =
-ive feedback : OUTCOME -ively controls PROCESS (maintain a set-treshold)

Process (x) > [++] Outcome (y) < [+] Process (x) = +ive feedback : outcome amplifies the PROCESS

22
Q

Hormonal Homeostasis types;

A

(a) Simple Feedback Axis
(b) Hypothalamus-Pituitary- Axis
(c) Neuroendocrine reflux’s

23
Q

(a) Simple Feedback Axis

A

Endocrine Gland > Hormone > Target cells (glucose-induced insulin secretion

24
Q

(b) Hypothalamus-Pituitary- Axis

A

Higher centres tress > Hypothalamus > releasing hormone (CRH) > Anterior Pituitary > trophic hormone (ACTH) > target cells (bret tissue) / Peripheral Endocrine Gland > Hormone (cortisol) > Target cells (response)

25
Q

Endocrine / Hormonal Disorders

A
  • Can be too much secretion
  • Could need a specific hormone in the circulation
  • Tumour
26
Q

Hormone released from peripheral gland we refer to them as a _________ _________

A

primary defect

27
Q

What’s responsible for stress?

A

Cortisol

If releasing less > e.g. tumour in adrenal gland > cortisol level goes low in blood > more ACTH

Problem is with peripheral endocrine gland

28
Q

How can cortisol be tested?

A

In urine

29
Q

High amount of ACTH > effect on cortisol

A

Increased amount

30
Q

Primary defect

A

CRH
ACTH

31
Q

Secondary defect

A

ACTH
CORTISOL

32
Q

Exception = e.g. lung cancer [ectopic] = need _____

A

ACTH > acts on peripheral gland to release more cortisol

33
Q

Ectopic producing tumour =

A

Small cell lung tumour,
pancreatic, ovarian

34
Q

1) Hyper-secretion
2) Hypo-secretion
3) dysfunction/impaired receptors

A

1) Hormone excess (hyper-secretion)
- Tumour or immunological factor (Graves disease)
2) Lack of hormone (hypo-secretion)
- Genetic, immunological attack, destruction by disease, surgical removal (Type 1 diabetes mellitus)
3) Decreased target-cell responsiveness
- At level of receptor or downstream enzyme (Type 2 diabetes mellitus)

35
Q

Tumour in peripheral gland

A

Primary

36
Q

pituitary or ectopic

A

Secondary

37
Q
A