Endocrine Flashcards

1
Q

What is the endocrine system?

A

The system that integrates and controls organ function via secretion of chemicals (hormones) from cells, tissues or glands
Hormones carried in blood
Can either have slow or fast responses

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2
Q

What is endocrine communication?

A

Hormones travel in blood to their target organs/tissues
Tissues detect hormones through the presence of specific receptors for that chemical on/in cells
No receptor = no response

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3
Q

What is neural communication?

A

Neurotransmitters released from presynaptic neurons travel across synaptic cleft to postsynaptic cell to influence its activity.
A neurotransmitter is the chemical released by the neuron but, in contrast to hormones, acts locally within the synaptic cleft.
The endocrine and nervous systems co-operate intimately to provide further control, particularly for long-term phenomena, e.g. growth.

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4
Q

How does neural communication work with endocrine communication?

A

Nerves release hormones which enter blood and travel to their target cells e.g. hypothalamic – pituitary axis.
Although all hormones circulate throughout the body in the blood, the response to any one hormone is highly specific because only target cells have receptors for the hormone.

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5
Q

What is autocrine?

A

Cells secrete chemicals binding to same cell (cytokines)

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6
Q

What is paracrine?

A

Chemicals diffuse in ECF to affect nearby cells

Eg. Histamine

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7
Q

What is exocrine?

A

Chemicals released from exocrine glands via ducts to external environment including GI tract (saliva)

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8
Q

What are the features of an endocrine hormone?

A

Produced by a cell (or group of them)
Secreted into + transported by blood
Exert effects at very low concentrations
Act by binding to receptors on target tissues
Have their action terminated, often via negative feedback loops

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9
Q

What makes up a peptide/protein hormone?

A

Chains of amino acids

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10
Q

What makes up steroid hormones?

A

Synthesised from cholesterol

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11
Q

What are amine hormones made up from?

A

Either tryptophan

Or tyrosine

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12
Q

When are peptide hormones made?

A

Made ahead of time, then stored until required

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13
Q

How are peptide hormones synthesised?

A

Initial protein produced by ribosomes is large + inactive - perprohormone
>Preprohormones contain 1+ copies of the active hormone in their amino acid sequence
>Cleaved into smaller units in RER to leave smaller, still inactive proteins called prohormones
>packaged into vesicles in the golgi apparatus, along with proteolytic enzymes which break the prohormone down into active hormone and other fragments.

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14
Q

What can clinically be measured in regards to peptide hormones?

A

The inactive fragments in plasma

Eg C-peptide in diabetes

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15
Q

How are peptide hormones stored?

A

Hormones and fragments are stored in vesicles in the endocrine cells until release is triggered
>then all vesicle contents are released into plasma (co-secretion).

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16
Q

What is C-peptide?

A

Inactive fragment cleaved from the insulin prohormone.
Levels of C-peptide in plasma or urine are often measured to indicate endogenous insulin production from the pancreas (produced in equal amounts).
>Because insulin is metabolised faster, levels of C-peptide are typically about 5x higher than endogenous insulin release.

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17
Q

What is the mechanism of peptide hormones?

A

Water soluble - easily transported in blood
Difficult to cross cell membrane, need receptors on target cell
Once bound normally create a fast biological responses (seconds to minutes)

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18
Q

What pathways do peptide hormones activate?

A

Most work via modulating either the G-protein receptors, or tyrosine kinase pathways

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19
Q

How do peptide hormones activate their receptors?

A

Activates either a GPCR:
>rapid response through second messenger system

Or Activates a Tyrosine Kinase Linked Receptor:
> alter gene expression
> slower, longer lasting activity

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20
Q

What effects does the activation of peptide receptors have on the cell?

A

Phosphorylate existing proteins in the cell + modify their function
>open/close ion chanels,
>activate/inactivate enzymes

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21
Q

When are steroid hormones made, how are they transported?

A

Lipid soluble, so need carrier proteins (such as albumin) to carry them
synthesised as needed rather than stored (as would diffuse out of cell otherwise)

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22
Q

Where are steroid hormone receptors found?

A

Receptors located inside cells (cytoplasmic or nuclear receptors) due to easy crossing of membrane
>Trigger with activation/repression of gene function with nucleus (genomic effect)

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23
Q

What is the mechanisms of action of steroid hormones?

A

Genes control synthesis of protein so these hormones increase/decreased protein synthesis
Relative slow process - lag time between release + biological effect (hours - days)
Effect persists for a similar amount of time

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24
Q

What are some examples of amine hormones?

A

Dopamine
Adrenaline
Noradrenaline
Melatonin (only one to not be made from tyrosine)

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25
Q

What are the types of amine hormones?

A

Thyroid hormones - simialr mechanicms to steroid hormones

Catecholamines - stimilar mechanisms to steroid hormones

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26
Q

What is the law of mass action?

A

Dictates that as free hormone leaves plasma, more hormone released via carriers
Only minute Quantities of hormone required for physiological functions

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27
Q

What are the functions of carrier proteins?

A

Increases solubiity -> required for transport
Protects from degegation
Unable, when bound, to enter cells
As steroid taken up by cell, more releaed from carrier
>Creates reservoir of hormone ready for action
>Giving prolonged activity

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28
Q

How are hormones metabolised/secreted?

A

Removal via excretion or metabolic transformation - mainly occurs in the lever + kidneys
Faster for peptide + catecholamine - short life in plasma
Steroids + thyroid takes hours -days to excrete/metabolise as potein bound

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29
Q

How is secretion of hormones controlled?

A

Most via negative feedback
Some by neural feedback loops
Other hormones have additional control mechanisms

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30
Q

What are other factors that contribute to hormone control?

A

By regulating number of hormone receptors, can influnece ability for that cell to respond
>Often after prolonged exposure to low concentration, see upregulation
»Increase in number of receptors in target tissues

> Prolonged exposure to high conentration see down regulation
>Decrease in receptors on target tissues

Not only hormone’s receptors, but receptors for other hormones

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31
Q

What are permissive effects?

A

Presence of one hormone enhances effect of another
>Eg adrenaline causes lipolysis, but massive increase in amount of lipolysis when thyroid hormones also present through increased adrenaline receptors

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32
Q

Where is the hypothalamus located?

A

Hypothalamus part of brain and is directly connected to pituitary gland via a stalk called infundibulum

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33
Q

How does the hypothalamus communicate with the pituitary gland?

A

Hypothalamic communication with pituitary gland both neural (posterior pituitary) and endocrine (anterior pituitary) leads to neuroendocrine function

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34
Q

What type of hormones does the hypothalamus and pituitary gland (both parts) secrete?

A

Anterior pituitary - Endocrine hormones
Posterior pituitary - neurohormes
Hypothalamus - neurohormones

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35
Q

Where are the trophic hypothalamic hormones secreted to?

A

Into capillaries that travel to anterior pituitary

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36
Q

Where are the non-trophic hypothalamic hormones secreted to?

A

Travel to posterior pituitary before being secreted into the blood

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37
Q

What is the hypothalam-hypophyseal portal system and its significance?

A

Hypothalamus - network of tiny vessels which transfer trophic hormones to anterior pituitary
Small numbers of neurosecretory neurones sufficient for control
Hormones released from neurosecretory neurons at the median eminence
> Very small amounts of hormones required
> Short distance – very rapid and dynamic

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38
Q

What are the hypothalamic trophic hormones?

A
Thyrotrophin Releasing Hormone (TRH)
Corticotropin Releasing Hormone (CRH)
Growth Hormone Releasing Hormone (GHRH)
Gonadotrophin Releasing Hormone (GnRH)
Prolactin Releasing Hormone (PRH)
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39
Q

What are the hypothalamic inhibitory hormones?

A

Growth Hormone Inhibiting Hormone (GHIH) aka somatostatin

Prolactin Inhibiting Hormone (PIH) aka Dopamine

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40
Q

Describe the anterior pituitary gland

A
true endocrine tissue
epithelial origin
connected to hypothalamus via capillary portal system
also called adenohypophysis
makes up 2/3rds of the gland
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41
Q

Describe the posterior pituitary gland

A
neuroendocrine tissue
neural tissue origin
neural connection to hypothalamus 
secretes neurohormones made in hypothalamus
also called neurohypophysis
makes up 1/3rd of the gland
42
Q

How does the hypothalamus control the hormone production of the anterior of pituitary?

A

By producing realsing and inhibiting hormones

43
Q

What are the hormones produced by the anterior pituitary?

A

Thyroid Stimulating Hormone (TSH) aka thyrotrophin
Adrenocorticotrophic Hormone (ACTH) aka corticotrophin
Follicle Stimulating Hormone (FSH)
Luteinising Hormone (LH) - Gonadotrophin
+ FSH - gonadadotrophin
Growth Hormone (GH)
Prolactin -non-trophic hormone

44
Q

Where does prolactin act, what does it do?

A

Acts on the breast directly

Stimulates lactation

45
Q

Where does thyroid stimulating hormone act, what does it do?

A

On the thyroid

Stimualtes thyroid hormone release

46
Q

Where does adrenocrticotrophic hormone (ACTH) act, what does it do?

A

In the adrenal cortex,

Stimulatesd cortisol release

47
Q

Where does growth hormone act, what does it do?

A

Acts on liver and tissues

Stimulates tissue metabolism and IGF1 release from the liver

48
Q

Where do FSH (follicle stimulating hormone) and LH (luteinising hormone), what does it do?

A

Act on Gonads

Regulate reproductive function and stimulate sex hormone release

49
Q

How is the hypothalamus controlled by feedback?

A

Both short and long loop feedback inhibits hypothalmus production of trophic hormones
Hormones produced by the anterior pituitary will negatively feedback to the hypothalmus
And the hormone from the endocrine gland will negatively feedback to both the anterior pituitary and the hypothalamus

50
Q

What hormones does the posterior pituitary release and store?

A

Vasopressin (ADH)

Oxytocin

51
Q

Where are the posterior pituitary hormones synthesised?

A

In magnocellular neurones (cell bodies in specific areas of the hypothalamus)
>Different subsets make either vasopressin or oxytocin

52
Q

How does the posterior pituitary release hormones into the blood?

A

axons project down the infundibulum from hypothalamus to posterior pituitary
do not synapse with other neurons, their terminals end directly on capillaries
hormones synthesised in the hypothalamus and transported to the nerve terminal in posterior pituitary ready for release
activity in these neurons results in release of vasopressin or oxytocin directly into the blood stream at the posterior pituitary

53
Q

What is the function of vasopressin?

A

regulates water balance

54
Q

What triggers the release of vasopressin?

A

increase in plasma osmolarity,

Decrease in plasma volume/blood pressure

55
Q

Where does vasopressin act, what does it do?

A

Kidney collecting ducts
>Increase in water reabsoprtion
Vascular smoth muscle
>Leads to increased blood pressure

56
Q

What are the main functions of oxytocin?

A

Milk ejection

Uterine contractions

57
Q

What stimulates oxytocin release?

A

Labour - baby’s head against cervix

Suckling

58
Q

Where does oxytocin act, what are its effects?

A

Milk duct smooth muscle
>Contracts muscle, ejecting milk
Uterine smooth muscle
>Child birth

59
Q

What is a primary endocrine disoder?

A

Where there is a defect in the hormone secreting cells

60
Q

What is a secondary endocrine disorder?

A

Where there is a defect in the amount of the trophic hormone released

61
Q

What is a tertiary endocrine disorder?

A

A defect relating to the hypothalamus

62
Q

What is the usual blood glucose?

A

5mmoles

63
Q

What do alpha islet cells of the pancreas produce?

A

Glucagon

64
Q

What do alpha Beta cells of the pancreas produce?

A

Insulin

65
Q

What do delta islet cells of the pancreas produce?

A

Somatostatin

66
Q

What do F islet cells of the pancreas produce?

A

Pancreatic polypeptide

67
Q

How is insulin produced?

A

Produced by pancreatic cells
Synthesised as preprohomone - preproinsulin, converted to proinsulin in ER
Then packaged as granules in secretory vesicles
Within granules proinsulin –> insulin + c-peptide
Stored until activated.

68
Q

How is insulin released by Beta islet cells?

A

Stimulated by glucose! + amino acids in blood:
b-cells have K+ sensitive to ATP
When glucose is abundant, it enters cells through GLUT proteins increasing metabolism
Leads to increase in ATP, closing KATP channels. Intracellular K+ rises, depolarising cell
Voltage dependent Ca2+ channels open, triggering insulin vesicle exocytosis

69
Q

What is the mechanism of insulin?

A

Binds to tyrosine kinase receptors on cell membrane of insulin sensiive tissues (muscle/adipose) to increase glucose uptake by these tissues
>Hence lowers blood glucose
Stimulates mobilisation of specific transporters, GLUT-4
>When stimulated by insulin, it migrates into the membrane of cell able to transport glucose

70
Q

How is the livers uptake of glucose dependant on insulin?

A

GLUT-2 transporters transport glucose into the cell down concentration gradient
Insulin has no direct effect, but glucose transport into hepatocytes affected by insulin status
>Insulin causes glucose conversion into glucose-6-phosphate keeping intracellular glucose low, allowing more glucose to transport across

71
Q

What are the actions of insulin (10)?

A

> Transports glucose across muscle/adipose cell walls
Increases glycogen synthesis in muscle and liver. >Stimulates glycogen synthase
Inhibits glycogen phosphorylase.
Increases amino acid uptake into muscle, promoting protein synthesis.
Increases protein synthesis and inhibits proteolysis
Increases triacylglycerol synthesis in adipocytes and liver i.e. stimulates lipogenesis and inhibits lipolysis.
Inhibits the enzymes of gluconeogenesis in the liver
Has a permissive effect on Growth Hormone
Promotes K+ ion entry into cells by stimulating Na+/K+ ATPase. Very important clinically.

72
Q

What stimuli increase insulin release?

A
  1. Increased [BG]*****
  2. Increased amino acid concentration in plasma
  3. Glucagon (insulin required to take up glucose created via gluconeogenesis stimulated by glucagon)
  4. Other (incretin) hormones controlling GI secretion and motility eg gastrin, secretin, CCK, GLP-1, GIP.
  5. Vagal nerve activity
73
Q

What stimuli decrease insulin release?

A
  1. Low [BG]
  2. Somatostatin (GHIH)
  3. Sympathetic a2 effects
  4. Stress e.g. hypoxia
74
Q

What do incretin hormones increase insulin release?

A

Released by ileum and jejunem in response to nutrients.

Early insulin release prevents glucose surge when absorption occurs.

75
Q

How does vagus activity increase insulin release?

A

Vagus stimulates release of major GI hormones including insulin
Leads to insulin effect of IV being lesser than oral of same amount
>IV glucose leads to increase in insulin due to increased glucose on b cells
>Oral - direct effect on b cells, vagal stimulation + incretin

76
Q

What is glucagon?

A

Formed from preproglucagon being cleaves to form glucagon + major proglucagon fragment
Raises blood glucose

77
Q

What are the actions of glucagon?

A

Primarily opposes action of insulin - part of glucose counter-regulatory control system
Receptors are G-protein couple receptors linked to cAMP system resulting in
>Increased glycogenolysis
>Increased gluconeogensis
>Formation of ketones from fatty acids
All occur in liver

78
Q

What hormones are part of the glucose counter-regulatory control system?

A

Glucagon
Adrenaline
Growth hormone
Cortisol

79
Q

what stimulates the secretion of glucagon?

A

Low [BG]
High [amino acids] . Prevents hypoglycaemia following insulin release in response to aa.
sympathetic innervation and adrenaline,
cortisol
stress e.g. exercise, infection

80
Q

What inhibits the secretion of glucagon?

A

glucose
free fatty acids (FFA) and ketones
insulin (fails in diabetes so glucagon levels rise despite high [BG] )
somatostatin

81
Q

How does the autonomic nervous system, ANS, stimulate islet cells?

A

Parasympathtic activity (vagus) leads to increase in insulin and lesser extent glucagon to anticipate digestion
Sympatetic activation promotes glucose mobilisation
>Increase in glucagon + epinephrine
>Inhibition of insulin

82
Q

What glucose counter regulatory effects does glucagon have?

A

Liver glycogenolysis

Gluconeogensis

83
Q

What glucose counter regulatory effects does adrenaline have?

A

Muscle glycogenolysis
Liver glycogenolysis
Gluconeogensis
Lipolysis

84
Q

What glucose counter regulatory effects does cortisol have?

A

Gluconeogensis
Inhibition of glucose take up
Lipolysis
Protein catabolism

85
Q

What glucose counter regulatory effects does Growth hormone have?

A

Gluconeogensis
Inhibition of glucose take up
Lipolysis

86
Q

What are the actions of somatostatin?

A

Also known as GHIH - inhibiting GH
Action to inhibit GI tract activity
Function appears to be to slow down absoprtion to prevent exaggerated peaks in plasma concentrations
Not a counter-regulatory hormone in control of blood glucose
>However, strongly supressses both insulin + glucagon

87
Q

How does exercise affect glucose uptake?

A

Normally glucose absorbed through glut 4 receptors with insulin binding to it
In exercise, it increases glut-4 expression by allowing them to migrate to the membrane without insulin being present
>This allows the muscle to uptake glucose more easily

88
Q

What is growth hormone?

A

Growth hormone - aka somatostatin
A peptide hormone bound to a carrier protein in blood which is species specific
Promotes growth
>Requires permissive action of thyroid hormones + insulin before it does so
Maintains tissues

89
Q

How does growth hormone work?

A

Effect mediated through stimulating both cell size (hypertrophy) and cell division (hyperplasia)
Achieves effect on cell division via insulin-like growth factor 1 - IGF1

90
Q

When does growth hormone become prominent in the human body?

A

Becomes prominent at 8-10 months

91
Q

How is growth hormone regulated?

A

IGF 1 released mainly from liver in response to GH release from anterior pituitary
IGF1 controls GH release through negative feedback

92
Q

What are the effects of growth hormone on bone?

A

GH stimulates chondrocyte precursor cells (prechondrocytes) in the epiphyseal plates to differentiate into chondrocytes.
During the differentiation, the cells begin to secrete IGF-1 and to become responsive to IGF-I
IGF-1 than acts as an autocrine or paracrine agent to stimulate the differentiating chondrocytes
>Cuases cell division and production of cartilage, the foundation for bone growth.

93
Q

What are the direct effects of growth hormone?

A

Increases gluconeogenesis by the liver
Reduces ability of insulin to stimulate glucose uptake by muscle + adipose tissue
Makes adipocytes more sensitive to lipolytic stimuli.

However, unlike cortisol and just like insulin, GH:
Increases muscle, liver, and adipose tissue amino acid uptake and protein synthesis.

94
Q

What controls the secretion of growth hormone?

A

Controlled by hypothalamus which secretes GHRH and somatostatin (SS)
Large quantities of GH are present in pituitaries of both adults and children. In both, the rate of secretion undergoes rapid spontaneous fluctuations as well as increase/decrease in response to specific stimuli.
For measurement of GH - 24 hour surveillance
Massive spike in children in early hours of sleep

95
Q

What stimuli increase growth hormone secretion?

A

Actual or potential decrease in energy supply to cells.&raquo_space;Eg fasting, exercise cold
Increased amounts of amino acids in the plasma, eg protein meal.
»GH promotes amino acid transport and protein synthesis by muscle and liver.
Stressful stimuli eg infection, psychological stress
Delta sleep
>may be related to growth spurts in children and adolescents and tissue repair in adults.
>Oestrogen and androgens

96
Q

What stimuli decrease growth hormone secretion?

A

Glucose
Cortisol
FFA
REM sleep

97
Q

What factors contribute towards growth?

A

Hormones
Nutrition
Diet

98
Q

What hormones contribute towards growth?

A

GH, IGF1, thyroid hormones, sex hormones, glucocorticoids + insulin

99
Q

What are the two rapid phases of growth?

A

Infancy and puberty

100
Q

What is the infancy growth phase?

A

Growth spurts arounf 2.5cm
Then nothing for a few days
I.e episodic

101
Q

what is the puberty growth phase?

A

Sex hormones cause spikes in GH secretion

Promote bone elongation before causing epiphyseal plates to fuse

102
Q

What conditions arise from hypersecretion of GH?

A

Gigantism (before fusion)

Acromegaly (after fusion)