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Endocrine Flashcards

1
Q

Describe the endocrine system

A

Consists of organs and ductless glands that secrete hormones.
Primarily controls activities that require duration rather than speed as well as coordinating diverse tissues.
Closely linked with nervous system.

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2
Q

What are the two main types of cellular communication?

A

Direct (gap junctions) and indirect (secretory cell releases ligand that has to bind to target cell).

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3
Q

What are the different forms of indirect cellular communication?

A 
Paracrine
Autocrine
Neurotransmitter
Exocrine
Endocrine
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4
Q

Compare the differences between the endocrine and nervous system.

A

Nervous - neural secretory cells, targets muscle, neurons and endocrine. Electrical and chemical signals. Transported by synapse. Long intracellular signalling distance, short across synapse. Rapid speed, short response duration.
Endocrine - endocrine secretory cells, target most cells in the body. Signal type is chemical, maximum signalling distance is long. Transported by circulatory system, slow speed with long duration of response.

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5
Q

What is a ligand?

A

Molecule that binds to a protein

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6
Q

Describe the steps of communication via chemical messengers.

A

1) secretory cell releases chemical messenger (ligand) into ECF.
2) messenger binds to receptor on target cell.
3) ligand-receptor binding triggers response in target cell via various transduction mechanisms.

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7
Q

What are the six different functional classifications of chemical messengers?

A

Paracrines - eg. Histamine. Secretory cell sends ligand that binds to target receptor on target (neighbouring) cell.
Autocrines - eg. Amines, peptides (gastrin). Secretory cell is the same as the target cell.
Cytokines. Secretory cell releases ligand, travels via blood to receptor on target cell.
Neurotransmitters - acetylcholine. Neuron sends neurotransmitter out of axon, across synapse, to target receptor and cell.
Hormones - insulin, oestrogen, cortisol. Released from secretory cell, travels via blood to target receptor and cell.
Neurohormones (specifically related to posterior pituitary). Secreted from neuron, travels via blood to target receptor and cell.

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8
Q

What is the difference between primary and secondary endocrine glands?

A

Primary - only work to secrete hormones.

Secondary - secrete hormones and have other functions (eg. Kidney).

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9
Q

What are endocrine glands?

A

Ductless glands that secrete hormones.

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10
Q

What do endocrine glands act to control?

A

Body energy levels
Reproduction
Growth and development
Internal balance of body systems ( homeostasis)
Responses to surroundings (stress, injury)

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11
Q

What are exocrine glands?

A

Release messengers into external (rather than internal) environment for communication.
Eg. Pheromones.

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12
Q

True or false, a single endocrine gland may produce multiple hormones? Eg. Anterior pituitary.

A

True

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13
Q

True or false, a single hormone may be secreted by more than one endocrine gland?

A

True

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14
Q

True or false, a single hormone can have more than one type of target cell and therefore can induce more than one type of target effect?

A

True

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15
Q

True or false, a single target cell may be influenced by more than one hormone.

A

True

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16
Q

True or false, some organs are exclusively endocrine in function?

A

True

AP, thyroid gland.

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17
Q

What are hormones?

A

Chemical messengers that travel via blood.
Function in locations removed from their site of secretion.
Chemical classification is dependant on structure.

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18
Q

What are tropic hormones?

A

Regulate the activity of other endocrine glands.
Often come from thyroid or pituitary gland.
Eg. TSH, ACTH
Stimulate and maintain their endocrine target tissues.

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19
Q

What are the 5 major classes of chemical messengers?

A
  1. Steroids
  2. Eicosanoids
  3. Biogenic amines
  4. Peptides/proteins
  5. Amino acids
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20
Q

Which chemical messengers are hydrophobic?

A

Steroids
Eicosanoids
Transported bound to plasma proteins.

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21
Q

Which chemical messengers are hydrophilic?

A

Biogenic amines
Peptides/proteins
Amino acids
Transported dissolved in plasma (don’t require carrier protein)

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22
Q

Is hydrophilic the same as lipophobic?

A

Yes

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23
Q

Is lipophilic the same as hydrophobic?

A

Yes.

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24
Q

Discuss the synthesis of steroids.

A

Synthesised from cholesterol.
Enzymes of formation found in SER and mitochondria.
Synthesised on demand, released immediately.
Rate of secretion controlled by rate of synthesis.

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25
Q

Where are steroids secreted from?

A

Adrenal cortex and gonads.

Eg. Esterodial, testosterone.

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26
Q

Discuss the synthesis of amines.

A

Derived from AA, particularly tyrosine (catecholamines, thyroid hormone).
Synthesised in cytosol and stored in cytosolic vesicles.
Released via exocytosis.
Can act as neurotransmitters and hormones.

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27
Q

Where are amines normally secreted from?

A

Thyroid gland
Adrenal medulla
Eg. Catecholamines, thyroid hormone.

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28
Q

Discuss the synthesis of protein.

A

Cytosolic mRNA template, ribosomes form AA sequence, translated in RER (forms prepropeptide).
Converted to propertied in Golgi apparatus and then active hormone. Packaged in vesicles and secreted via exocytosis.

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29
Q

What are the 4 AA classified as chemical messengers?

A

Alpha glutamate
Aspartate
Glycine
Gamma-amino-butyric acid (GABA)

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30
Q

What type of chemical messenger does AA form? Where is it synthesised?

A

Neurotransmitter

Synthesised in neuron.

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31
Q

What does the blood concentration of chemical messengers depend on?

A

Rate of secretion
Rate of clearance
Transport proteins

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32
Q

What is a non-tropic hormone?

A

Exerts its effect on no endocrine target tissues

Ex. Thyroid hormone

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33
Q

What is the plasma concentration of hormones affected by?

A

Hormones rate of secretion into the blood.
Rate of metabolic activation (only some).
Lipophilic - extent of binding to plasma proteins.
Rate of removal from circulation by metabolic inactivation and excretion.

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34
Q

What does specificity refer to?

A

Hormone must bind to target cell receptor specific to them.

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35
Q

Magnitude of response to a chemical messenger is affected by what?

A

Messenger concentration
Number of receptors
Receptor affinity

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36
Q

What is an agonist?

A

Ligand binds to receptor causing a response.

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37
Q

What is an antagonist?

A

Ligand binds to receptor resulting in no response.

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38
Q

Where are hormones greatly amplified?

A

At target cell.

One steroid hormone activated gene can form many mRNA molecules.

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39
Q

What are some different types of receptors?

A 
Intracellular
Ligand gated ion channels
Receptor enzymes
G-protein coupled
(Membrane bound or internal depending on hormones solubility characteristics).
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40
Q

What are the four components of signal transduction pathways in terms of receptors.

A

Receiver - ligand binding region
Transducer - conformational change of receptor
Amplifier - increased number of molecules affected by signal
Responder - molecular functions that change in response to signal

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41
Q

What are some different types of membrane bound receptors? Which hormones do they work with?

A

Channel linked (ligand gated)
Enzyme linked
G-protein linked

Hydrophilic peptides and catecholamines.

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42
Q

What is the striking feature of second messenger systems (cAMP)?

A

Signal amplification.

Ability of small changes in the concentration of chemical messenger to elicit marked response in target cells.

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43
Q

Discuss intracellular receptors.

A

Cytosol or nucleus.
Lipophilic steroids and thyroid hormone.
Typically these receptors are transcription factors that regulate specific genes in the target cell that code for formation of new intracellular proteins.
Receptor has a region for binding hormone as well as DNA binding region - forms hormone receptor complex (HRE).

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44
Q

What is negative feedback and give an example of it.

A

Exists when the output of a system counteracts a change in input. Moderates response.
Most common in physiological systems.
Ex. Plasma concentration of free circulating TH drops below set point. AP secretes TSH which stimulates thyroid to increase secretion of TH. TH in turn inhibits further secretion of TSH by the AP.

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45
Q

What does positive feedback do?

A

Amplifies response.

Eg. Oxytocin during parturition.

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46
Q

Describe the antagonistic effect of hormones.

A

One hormone causes the loss of other hormone receptors peg. Progesterone and oestrogen.

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47
Q

Describe the synergistic effect of hormones.

A

Action of several hormones are complimentary and their combined effect is greater than the sum of their individual.
Results from influence on receptors.
Eg. Glucose, GH and glucocorticoids.

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48
Q

Describe the permissive effect of hormones.

A

One hormone is needed for another to produce and effect.
First hormone increases target cells responsiveness to the second.
Eg. Adrenaline, TH

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49
Q

Describe the integrative effect of hormones.

A

Hormones produce different but complimentary results in the one organ.

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50
Q

What are the different classes of abnormalities associated with endocrine disorders?

A

Primary - endocrine gland dysfunction (hypo or hyper secretion)
Secondary - initial disorder is in pituitary gland
Tertiary - problem originates in the hypothalamus.

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51
Q

What is the hypophysis and where is it located?

A

Pituitary gland.
Descends from hypothalamus and consists of two or three lobes.
Sits in a bony cavity at the base of the vertebral brain.
Thin stalk (infundibulum) that contains nerve fibres and blood vessels connecting it to hypo.

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52
Q

What are the primary endocrine glands?

A

Hypothalamus and pituitary

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53
Q

What is the function of the pituitary gland?

A

Exerts direct effects on body organs
Regulates growth and activity of thyroid, adrenals and gonads.
Relay between CNS and peripheral endocrine glands.

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54
Q

What is the function of the hypothalamus?

A

Maintenance of homeostasis.
Gains information from both internal and external sources.
Has two lines of communication, autonomic NS and chemical messengers (endocrine).
Primary site where nervous and endocrine systems meet.

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55
Q

What are the names of the axons present in the PP?

A

Paraventricular nucleus sends axons to PP

Also present in the median eminence of the AP (paraventricular zone)

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56
Q

Where are the neurons that are involved in appetite and reproductive control located?

A

Ventromedial and arcuate nucleus.

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57
Q

Which neurons are mainly responsible for PP function and what do they do?

A

Supra optic neuron - releases Oxytocin, ADH (vasopressin)
Paraventricular neurons - release ADH, OXytocin release and some TRH(thyrotropin releasing hormone), CRH(corticosteroid in releasing hormone).

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58
Q

What does the autonomic NS rely on?

A

Direct nervous connection for electrical messages to be relayed along axons.

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59
Q

What do the secretions from the pituitary and hypothalamus effect?

A 
Reproduction
Body weight 
Thermoregulation
Metabolism
Lactation
Immune system
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60
Q

Discuss the pituitary portal system.

A

Vascular link that allows hypothalamic regulatory hormones to reach AP.
Capillary to capillary connection.
As a result, almost all blood supply to AP must first pass through hypothalamus, allows high concentrations of hypo hormones to reach AP as it is a direct link that bypasses general circulation.

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61
Q

Where is the optic chiasma?

A

Protrudes of base of hypothalamus, rostral to the pituitary gland.

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62
Q

What are the different sections of the anterior pituitary?

A

Pars tuberalis
Pars intermedia
Pars distalis

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63
Q

What are the different sections of the posterior pituitary?

A

Infundibular stalk

Pars nervosa

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64
Q

What is the neurohypophysis?

A

Posterior pituitary

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65
Q

What is the adenohypophysis?

A

Anterior pituitary

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66
Q

True or false, the AP and PP are anatomically and functionally related.

A

False.

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67
Q

What does the AP consist of?

A

Glandular epithelial tissue derived embryonically from an outpouching of ectoderm.

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68
Q

Where does the AP hormones come from?

A

Synthesised in the AP

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69
Q

What are neurohormones? And how do they act on the AP?

A

Hypophysiotropic hormones - stimulate the rate of secretion of hypophysial hormones.
Secreted by hypothalamus neurosecretory cell terminals located at the median eminence of the hypothalamus. Transported along axons to the hypothalamo-hypophyseal portal system.

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70
Q

How many hormones does the AP secrete?

A

7 that largely control the hormonal output of several peripheral endocrine glands.

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71
Q

What effect do hypophysiotropic hormones have on the AP hormones?

A

They increase their synthesis and release.

None are released at a constant rate, either episodic or diurnal. Receive feedback from target organs.

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72
Q

What is a negative feedback loop?

A

Target gland hormone acts to suppress secretion of the tropic hormone that is driving it.

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73
Q

What are e major hormones of the AP?

A 
Prolactin
LH
FSH
TSH
ACTH
GH
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74
Q

True or false. The PP is an endocrine organ?

A 
False.  Connected to and continuous with the hypothalamus and has no true secretory cells. 
Innervated and composed of neural stalks from supra optic and paraventricular nuclei. 
Cell bodies (pituicytes) from which nerve fibres connect back to hypothalamus.
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75
Q

What is the function of the PP?

A

Storage and secretion of oxytocin and vasopressin.

Secretion initiated by action potentials from hypothalamus

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76
Q

What are prohormones associated with?

A

Neurophysins - carrier proteins.

77
Q

What are the two hormones associated with the PP?

A

Vasopressin (anti-diuretic hormone) - supra optical nuclei

Oxytocin - paraventricular nuclei

78
Q

How are pre prohormones transported from the hypothalamus to the PP? How do they then become active hormones?

A

Vesicles pass down axons in infundibulum, stored at nerve endings within neurohypophysis.
Converted to prohormones via enzymatic action.
Prohormones becomes active hormone when neurophysin attaches at gland terminals. Ca mediated action potential allows release of hormone into circulatory system.

79
Q

What is the biological action of oxytocin?

A

Release stimulated by sensory mechanic extorts during suckling and in the cervix (neurohormonal reflex arc).
Milk ejection reflex.
Parturition is positive feedback loop.

80
Q

What is the biological action of vasopressin?

A

Two major functions;
Kidney water retention and arterial pressure (increased blood pressure).
Negative feedback loop.

81
Q

Where is the adrenal gland located?

A

On kidney.

Paired.

82
Q

Describe the anatomy of the adrenal gland.

A 
Outer cortex with four separate regions(from outermost to most medial); capsule, zona glomerulosa, zona fasciculata, zona reticularis.
Inner medulla (20%).
83
Q

What does the adrenal gland produce?

A

Lipophilic hormones derived from cholesterol.

Lipophobic derivatives of catecholamines (tyrosine).

84
Q

What are the three steroid hormones produced by the adrenal glands and where do they originate?

A

Mineralocorticoids - mostly aldosterone. Synthesised in zona glomerulosa.
Glucocorticoids - cortisol, corticosterone. Synthesised in zona fasciculata.
Androgens - DHEA, synthesised in zona fasciculata and zona reticularis.

85
Q

What does the adrenal medulla produce?

A

Catecholamines

86
Q

Discuss the secretion and transport of cortical steroid hormones.

A

Lipophilic, poorly soluble in blood so require carrier (CBG or bind with albumin).
Can’t be stored so their rate of secretion matches their rate of synthesis.
Precursor is cholesterol.
Half life of 60-90mins or less if in form of aldosterone.
Liver deactivates and excreted via urine or bile.

87
Q

What is the action of glucocorticoids?

A

Generally catabolic, released in increased amounts at times of stress to mobilise body fuels.
Actions often permissive and enhancive.
Bind to intracellular receptor, effects transcription and translation.
Metabolic effect - increase blood glucose.

Cortisol and corticosterone.
Carbohydrate, protein and fat metabolism.

88
Q

Discuss the role of glucocorticoids in carb metabolism.

A

Increased hepatic gluconeogenesis.
Increased production of glucose from non CHO sources.
Increased hepatic glycogenesis.
Peripheral antagonism of insulin - decreased glucose uptake and oxidation.

89
Q

Discuss the role of glucocorticoids in protein metabolism.

A

Stimulation of proteolysis for glucogenic AA skeletons.
Inhibition of protein synthesis.
Increased synthesis of gluconeogenic enzymes in liver.
Brain and heart muscle are protected.

90
Q

Discuss the role of glucocorticoids in fat metabolism.

A

Enhance lipolysis.
Enhance lipolytic effects of epinephrine on adipose tissue.
Excess cortisol secretion causes redistribution of fat from periphery to face, shoulders, chest, abdomen (cushings).

91
Q

How are glucocorticoids regulated?

A

Negative feedback loop.
ACTH stimulates adrenal cortex.
ACTH release controlled by CRH.
Feedback occurs at two levels - hypothalamus and AP.

92
Q

Discuss the role of glucocorticoids in inflammation.

A

Stabilise lysosomal membranes and inhibit release of lysosomal enzymes that cause damage to adjacent healthy cells.
Dexamethasone is a glucocorticoid.
Minimise tissue damage surrounding injuries and also involved in delayed healing and immunosuppression.

93
Q

Discuss the immunosuppressive effects of glucocorticoids.

A

Suppress T-cell immunity
Inhibit B-cell immunity
Used in transplants to suppress allergic and immune responses.
Sustained, elevated levels of glucocorticoids can reduce immune response.

94
Q

What is the role of mineralcorticoids and what is the main one?

A 
Aldosterone.
Increase ECF volume by increase Na resorption.
Electrolyte homeostasis
Na resorption and K secretion
Homeostasis of blood pressure.
95
Q

What are the specialised post ganglionic neurons present in the adrenal medulla?

A

Chromaffin cells.
Produce catecholamines (adrenaline and noradrenaline).
Increased secretion during stress.

96
Q

What are chromaffin cells regulated by?

A

Sympathetic NS

97
Q

True or false. Chromaffin cells release their chemical transmitter directly into the circulation as a neurohormone.

A

True

98
Q

What are adrenaline and noradrenaline? What are they derived from?

A

Catecholamines

Tyrosine

99
Q

Discuss adrenaline and noradrenaline.

A

Stored in secretory vesicles, released by exocytosis to circulate in blood.
Target organs are stimulated by direct sympathetic nerves and catecholamines.
High uptake, immediate effects and short half life.
Virtually all cells have receptors on surface membranes.
B1 receptors in heart, B2 in arterioles in skeletal and smooth muscle.
Alpha receptors in skeletal muscle arterioles as well, large increases in adrenaline stimulate these.

100
Q

What are the biological effects of catecholamines.

A

Fight or flight.
Increased HR, BP and cardiac contractility.
Dilation of skeletal muscle blood vessels.
Dilation of pupils and airways.
Increased cellular O2
Increased lipolysis
Increased gluconeogenesis
Increased glycogenolysis
(Last four help mobilise body stores, increased cellular metabolism and increased ability to mobilise fuels).

101
Q

What are some abnormalities of adrenocortical secretion.

A

Addisons disease - primary hypoadrenalism. Atrophy of adrenal gland leading to aldosterone and glucocorticoid deficiency. Treat with synthetic mineralo- or gluco-corticoids.
Cushings disease - hyperadrenocorticism. Hyper secretion of adrenal cortex hormones leading to abnormal function of hypothalamus and adenohypophysis. Adenomas of AP and adrenal cortex. Results in high blood glucose levels, decreased protein synthesis, increased salt retention. Treat by removing tumour, irrigation and drugs that inhibit ACTH and CRH.

102
Q

What is metabolism regulated by?

A

Substrate concentration
Enzyme activity/concentration
Compartmentation

103
Q

Discuss the metabolism of CHO.

A 
Oxidised for energy
Generates CO2.
Is a substrate for other metabolic reactions.
Converted to glycogen.
Recovered from glycogen stores.
104
Q

Discuss the metabolism of proteins.

A

AA’s transported in blood.
AA used for protein synthesis.
Catabolised for energy (proteolysis).
AA recovered from Intracellular proteins.

105
Q

Describe the metabolism of fats.

A

Triglycerides broken down by lipoprotein lipase.
FA taken up by cells and oxidised for energy.
FA combined with glycerol in liver to form triglycerides that are stored as fat droplets.
FA and glycerol can be released back into blood.

106
Q

What is the post-absorptive state?

A

Period between meals

Fasting

107
Q

What is the absorptive state?

A

Period during which nutrients are being absorbed after a meal.

108
Q

What are three important substrates/hormones that act on the pancreas?

A

Glucose
Insulin
Somatostatin

109
Q

When is insulin at its highest?

A

During the ‘fed’ state.

110
Q

When is glucagon at its highest?

A

During the ‘fasted’ state.

111
Q

Where is insulin secreted from?

A

Beta cells of pancreas

112
Q

What is insulin secretion stimulated by?

A

Increased glucose and AA
Increased GIT hormones (gastrin, GLP, GIP) and gut fill.
Autonomic NS input.

Glucose enters beta cells via GLUT2 channels. Converts to G-6-P, increases ATP production, closes ATP gated K channels, cell is depolarised causing activation of voltage gated Ca channels leading to secretion.

113
Q

What kind of receptor does insulin bind to on the cell membrane?

A

Tyrosine kinase receptor.

114
Q

Describe the steps of the binding of insulin to its receptor.

A
  1. Insulin binds to tyrosine kinase receptor.
  2. Receptor phosphorylates insulin-receptor substrates.
  3. Second messenger pathways alter protein synthesis and existing proteins. Via enzymes or transcription factors.
  4. Membrane transport is modified.
  5. Cell metabolism is changed.
115
Q

How is glucose transported into insulin sensitive cells?

A

Insulin binds to receptor causing a signal transduction cascade. Causes exocytosis of secretory vesicles with GLUT4 proteins. Allows entry of glucose into the cell via the GLUT4 proteins (muscle and adipocytes).
In hepatocytes entry is via GLUT2.

116
Q

What are the effects of insulin?

A

Increased glucose utilisation and storage
Enhanced AA utilisation
Increased fat synthesis

117
Q

What inhibits insulin?

A

Hypoglycaemia
Sustained hyperglycaemia
GHIH
Increased FFAs

118
Q

Where is glucagon synthesised?

A

Alpha cells of pancreas.

119
Q

What is glucagon release and synthesis stimulated by?

A

Decreased blood glucose.

Increased plasma AA.

120
Q

What role does glucagon play?

A

Stimulates hepatic glycogenolysis and gluconeogenesis.

121
Q

What role does glucagon play in relation to insulin?

A

Antagonist.

But also stimulates its release.

122
Q

What mediates glucagon effects?

A

Adenylate cyclase.

123
Q

What is type 1 diabetes mellitus?

A

Immune mediated destruction of pancreatic beta cells.

Insulin dependent as none is produced.

124
Q

What is type 2 diabetes?

A

Adult onset.
Insulin resistance or decreased insulin production.
Insulin dependency depends on severity of resistance.

125
Q

Where are the thyroid glands?

A

Ventral trachea, near larynx.

Paired.

126
Q

What does the parathyroid gland do?

A

Ca metabolism

127
Q

Describe the composition of the thyroid gland.

A

Functional unit is follicle, these are the major secretory cells, basically fluid filled spheres.
Follicles appear as rings of follicular cells enclosing an inner lumen filled with colloid.

128
Q

Why is colloid unique and what does it mostly consist of?

A

Functions as extracellular storage.

Consists mostly of thyroglobulin (Tg).

129
Q

What do thyroglobulin molecules contain?

A

Thyroid hormone at various stages of synthesis.

Can be in the form of T4 or T3.

130
Q

What is T4?

A

Tetraiodothyronine

4 iodine atoms.

131
Q

What is T3?

A

Tri-iodothyronine

3 iodine atoms.

132
Q

What does thyroid hormone do?

A

Regulates the development and overall basal metabolic rate.

133
Q

How is thyroid hormone regulated?

A

By the hypothalamus-pituitary axis via TSH.

TSH enhances TH secretion and maintains structural integrity of thyroid gland.

134
Q

What are the two basic ingredients required for TH synthesis?

A

Tyrosine

Iodine - required in diet because it can’t be synthesised.

135
Q

Describe the stages of TH synthesis.

A

Synthesis occurs on Tg molecule.

1) Tg produced in ER/Golgi complex. Tyrosine incorporated and molecule exported from follicular cells into colloid by exocytosis.
2) Thyroid captures iodine from blood and transfers it to colloid via iodine pump(driven by Na conc gradient). Iodine transported against conc gradient.
3) iodine oxidised to active iodide by membrane bound enzyme (thyroperoxidase).
4) coupling occurs between iodinated tyrosine molecules to form TH. Stored in colloid until split off and secreted.

136
Q

What is thyroxine?

A

T4
2 tyrosine
4 iodine

137
Q

What is triiodothyronine?

A

T3
2 tyrosine
3 iodine

138
Q

Describe TH transport.

A

Lipophilic so requires carrier protein;
Thyroxine binding globulin (TBG) binds T3 and 4 in humans, sheep, goats and cattle.
Thyroxine binding prealbumin (TBA) binds in horses and dogs.
Albumin can also bind.
Very low % in free form - this portion is the only pool that can exert biological effect (access to receptors).

139
Q

What % of TH is T4 in mammals?

A

90%

140
Q

Is T3 more potent than T4?

A

Yes, 4x more in biological activity.

141
Q

Can T4 be converted to T3?

A

Yes, liver and kidneys activate T4 and convert to T3.

80% of circulating T3 derived from T4.

142
Q

What is the major biologically active TH at a cellular level?

A

T3

143
Q

What is the action of TH?

A

Affects all tissues.
Primary action is to increase basal metabolic rate.
Increase number and activity of mitochondria, increase K/Na/ATPase, increase or decrease catecholamines.

144
Q

Is TH a fast or slow acting hormone?

A

Slow, takes hours to days to exert effect which generally lasts for days.

145
Q

Binding of TH with receptors alters what?

A

Transcription of mRNA and subsequent protein synthesis.

146
Q

What are some of the intermediary metabolic effects of TH?

A

Increased CHO metabolism - increased cell glucose uptake, glycolysis, glycogenolysis, and GI reabsorption.
Increased fat metabolism - increased lipid mobilisation (lipolysis) and increased hepatic excretion of cholesterol.

147
Q

What are the effects of TH?

A 
Increased basal metabolic rate
Decreased body weight
Increased cardiac output. - increased HR, force of contraction and responsiveness of heart to circulating catecholamines. 
Increased rate and depth of respiration
Skin and hair growth
148
Q

What are the physiological effects of TH?

A

Maturational and differential effects
Effects on growth - required for GH secretion
Neurological effects - foetal development
Metabolic effects - calorigenic, CHO, fat, protein
Reproductive effects.

149
Q

How does TH increase BMR?

A

Regulates Na/K ATPase pumps.

150
Q

Why is TH important?

A

Regulates O2 consumption rate and energy expenditure under resting conditions. Effects on BMR.

151
Q

What level of TH secretion favours fuel consumption?

A

Hyper secretion

Glycogen is converted to glucose.

152
Q

Discuss the sympathomimetic effect of TH.

A

Increased TH secretion has similar effects to the sympathetic NS.
Increases target cell responsiveness to adrenalin and noradrenaline.
Causes proliferation of specific catecholamines target-cell receptors.

153
Q

What is the name for normal thyroid function?

A

Euthyroidism

154
Q

What is hypothyroidism?

A

Sub normal thyroid function.

Primary failure of gland, secondary to deficiency of TRH, TSH or both or inadequate dietary iodine.

155
Q

What is hyperthyroid?

A

Excessive thryroid function.

Increased BMR, increased heat production, decreased BW and increased HR.

156
Q

What is goitre?

A

Enlargement of thyroid gland due to hyperplasia/hypertrophy of follicular epithelium.
May be due to iodine deficiency, goitrogenic substances, hereditary biosynthetic substances.

157
Q

What is the pineal gland?

A

Located within brain, composed of glandular tissue.
Secretes melatonin during hours of dark.
Important for circadian cycle.

158
Q

Discuss circadian rhythm and melatonin.

A

Rod and cone receptors in retina detect light/dark changes.
Retinal ganglion cells communicate with suprachiasmatic nucleus. SCN communicates rhythmic signal to other parts of brain and physiological systems including;
Paraventricular nucleus - PP
Ventromedial nucleus - appetite and feeding behaviour
Periventricular nucleus - hormones affecting AP
Pineal gland - melatonin into CSF and blood in circadian rhythm

159
Q

What are the different factors influencing growth?

A 
Diet
Disease
Environment
Concentration of growth influencing hormones
Day length
160
Q

Which hormones play a role in growth?

A

GH
Insulin
thyroid hormone
Sex hormones

161
Q

What is somatotropin?

A

Growth hormone
Peptide secreted from AP in response to GHRH.
Inhibited by GHIH (somatostatin).

162
Q

What is GH synthesis and release stimulated by?

A

Stress
Exercise
Nutrition (low glucose)
Sleep

163
Q

What is GH inhibited by?

A

GHIH.

GHIH stimulated by nutrients, NTs and ANS an d glucagon.

164
Q

Describe the characteristics of GH synthesis and release.

A

Pulsatile release, peak secretions during teenage years.
Most intense period of release is soon after onset of sleep.
Spikes every 6-8hrs.

165
Q

What is somatocrinin?

A

GHRH
Stimulates Gh production and release
Promotes slow wave sleep
Expressed by hypothalamus, GIT, gonads, immune tissues and placenta.
Under nervous control, stimulated by FAs and increased plasma AA.
Inhibited by somatostatin and decreased plasma glucose.
Changes in plasma concentration act as negative feedback.

166
Q

How do GHIH and GHRH act on the AP?

A

Bind with G- protein coupled receptors linked to the cAMP second messenger pathway.
GHRH increases cAMP, GHIH decreases cAMP.

167
Q

What is somatostatin?

A

GHIH
Synthesis and release under control of neurotransmitters and hormones.
GABA inhibits.
GH and IGF1 stimulate.
Signals AP to decrease GH release but not synthesis.
Inhibits release of GHRH.

168
Q

What is GH binding protein?

A

Weakly attached to plasma protein.
Alters distribution and pharmokinetics of GH
Half life of GH is 20minutes.

169
Q

What are the two functions of GH?

A

Growth - stimulation of chondrocyte proliferation and muscle growth. Mediated by IGF-1 (somatomedin) from liver and other tissues.
Metabolic - mediated directly or indirectly via IGF-1. Protein, fat and CHO metabolism. Overall causes increase of FA and glucose in blood, muscles use FA, glucose used by brain. Protein synthesis is stimulated.

170
Q

What are the major target organs of GH?

A 
Liver
Skeletal muscle
Bone/cartilage
Fat
GH receptors in virtually all tissue
171
Q

What are somatomedins?

A

Insulin like growth factors.
Structurally similar to insulin, small peptides that mediate effects of GH.
Synthesised by liver, pituitary, brain and various foetal organs.
Type 1 and 2, 2 is for foetal development
Stimulate cartilage growth, protein synthesis and mitosis.

172
Q

What is the difference between IGF1 and IGF -2?

A

IGF-1 synthesis is stimulated by GH and mediates most of this hormones growth promoting actions. It’s production is controlled by adequate nutrition, age related factors, tissue specific stimulatory factors.
IGF-2 does not depend on GH, it is important for foetal development and continue to be produced during adulthood.

173
Q

Which type of IGF is the primary biologically active form in adult mammals?

A

1

174
Q

What are the effects of IGF mediated by?

A

Insulin

Receptors for IGF 1 and 2

175
Q

What does GH favour the synthesis of?

A

Proteins

176
Q

What is the function of insulin like growth factor binding proteins?

A

Render IGf-1 inactive in circulation, prevents interaction with insulin receptors, prevents hypoglycaemia and prolongs IGF-1 half life.
6 different forms.

177
Q

What are the metabolic effects of IGF?

A

Liver produces 90% of IGf1 in circulation.
High serum IGF1 acts in negative feedback loop inducing somatostatin release and thus reduced GH.
High IGF1 can induce transient hypoglycaemia and increased glycogen synthesis in liver and muscle.
Induce anabolic metabolism (net increase in glycogen, protein and lipid deposition).

178
Q

How does IGF1 mediate bone growth?

A

Increases protein deposition by chondrocytic and osteogenic cells.
Increased mitotic rate.
Conversion of chondrocytes to osteocytes resulting in deposition of new bone.
Stimulation of osteoblasts to become osteoclasts.
Promotes growth in both thickness and length, proliferation in epiphyseal cartilage and stimulates osteoblasts activity.

179
Q

When GH and IGF are in circulation together, which prevails?

A

GH.

When GH is not present, IGF1 stimulates glucose uptake in muscle cells.

180
Q

Where is IGF1 produced?

A 
Liver
Myoblasts
Satellite cells
Myofibres
Fibroblasts
181
Q

What are the physiological actions of IGF1?

A 
Central role in development, differentiation and maintenance of skeletal muscle. 
Regulates proteoglycans in cartilage
Maintains or increases bone density
Mediates anabolic effects of GH
Increases glucose and AA uptake
Decreased proteolysis
Increased protein synthesis
182
Q

Does GH have a direct anabolic effect on myoblasts, satellite cells or myotubes?

A

No

183
Q

In terms of growth hormone, a defect at pituitary level leads to….

A

Hypo pituitary - dwarfism
Gigantism - infantile, prior to puberty.
Acromegaly - adult, after growth plates have closed.

184
Q

In terms of GH, a defect in the liver leads to….

A

Laron dwarfism.

185
Q

Discuss the use of GH for accelerated production.

A

Growth - increases muscle mass and decreases adipose in swine
Milk production - coordinates metabolism in dairy cows to better meet nutrient needs associated with synthesis of milk components.

186
Q

Discuss the use of bovine somatotropin.

A

Used to allow dairy cows to better meet their metabolic needs during milk production.
bST exogenous is the same as endogenous, broken down into AA and absorbed, no effect on humans or milk composition.
However, increased IGF1 in milk from bST treated cows. IGF1 is bioactive (increased by pasteurisation), is absorbed in GIT(higher in infants), implications for breast and GI cancers.

187
Q

What is ghrelin?

A

Produced by gastric fundic cells.
Stimulates appetite
Increases gastric motility and Hcl secertion
Increase CHO utilisation, decreases fat utilisation.
Increased production before eating.
Stimulates GH via enhancing GHRH.
Receptors are G-protein linked.

188
Q

True or false. Fat tissue is actually an endocrine gland.

A

True. It helps regulate appetite.

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