Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

YEAR 1 - Organisation of the Body (Anton) > 14. Endocrinology (HT) > Flashcards

14. Endocrinology (HT) Flashcards

(314 cards)

Start Studying
1
Q

Give some examples of some hormones that involve a GPCR response.

A
  • Protein hormones (e.g. glucagon)
  • Amines (e.g. adrenaline)
  • Lipids (e.g. prostaglandins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Can a single hormones activate multiple GPCR types?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

State what mechanism each GPCR works by.

A
  • Gq - Activates phospholipase C (PLC)
  • Gi - Inhibits adenylate cyclase (AC) activity and therefore the production of cAMP from ATP
  • Gs - Stimulates adenylate cyclase activity
  • G12/13 - Rho family
  • Gβ - Activates inwardly-rectifying potassium channels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What type of receptor is the insulin receptor and what mechanism does it work by?

A
  • Enzyme-linked
  • Binding causes tyrosine kinase activation, leading to autophosphorylation of the receptor and the insertion of GLUT4 into the membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Draw the structure of a steroid receptor (type IV, intracellular receptor).

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some ways in which a hormone signal is turned off?

A
  • Removal or degradation of the hormone
  • Desensitisation of the receptor
  • Internalisation of the receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is receptor desensitisation?

A

The decreased responsiveness that occurs with repeated or chronic exposure to an agonist.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the mechanisms involved in the desensitisation and resensitisation of a GPCR.

A
  • Desensitisation occurs by the phosphorylation of the receptor by GRK (G-protein receptor kinase)
  • This then recruits arrestin, which prevents G-protein interaction, blocking the downstream effects of the receptor
  • Resensitisation involves dephosphorylation of the receptor
  • Desensitisation may also happen by endocytosis of the receptor (which can be dependent or independent of the arrestin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are the insulin and glucagon receptor pathways integrated?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some effects that disease can have on hormone receptors?

A
  • Failure of ligand binding
  • Failure of signal transduction
  • Constitutively active receptor systems
  • Antibodies to receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the two types of receptor mutations?

A
  • Inactivating -> Receptor does not function despite hormone present
  • Activating -> Receptor continually active without hormone bound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the endocrine system?

A

One of the major control systems that use chemical messengers (the other is the nervous system).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a hormone?

A

A chemical messenger released from an endocrine cell to influence the activity of another/the same cell via a receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

At what order of concentration are endocrine hormones typically present in blood?

A

10-7 to 10-13 M

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is hormone concentration the only way of regulating the response to the hormone?

A

No, the receptors may also be controlled to determine sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define an endocrine gland.

A

A well-defined collection of endocrine cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define a diffuse endocrine system.

A

Many hormone-producing cells not aggregated in a gland, but dispersed (e.g. in the gut).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Define a neuroendocrine system.

A

Neurons releasing hormones both into the blood stream and in the CNS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Show the different routes of endocrine communiaction affecting cells.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is neuroendocrine hormone action?

A

The hormone is released from a neuron into the blood stream.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is paracrine hormone action?

A

The hormone acts on local cells via the extracellular fluid.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is autocrine hormone action?

A

The hormone acts on the cell producing the hormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the functions of the endocrine system?

A

The endocrine system promotes survival of the species by:

  • Promoting survival of the individual
    • Effects on development, growth and differentiation
    • Homeostasis (NOTE: this is often disturbed short-term for long-term gain) -> Including anticipatory responses
    • Response to an altered external environment - especially emergency ‘stress responses’
  • Control of the processes involved in reproduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does the speed and duration of endocrine action depend on?

A
  • Rapidity of release
  • Half-life of hormone
  • Rapidity of action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Give an example of hormone action that is: * Fast * Intermediate * Slow
* Fast -\> Adrenaline in stress * Intermediate -\> Insulin in response to meal * Slow -\> Cortisol in lung development
26
What are the two divisions of hormone effects on a cell?
* Activational - Effects that disappear when the hormone is removed. * Organisational - Effects that cause a permanent change in the behaviour of their target cells.
27
Describe some of the control of the release, synthesis and release of hormones.
* Inputs: can be direct or indirect. * Central integration: The central nervous system (CNS) integrates endocrine control via the pituitary gland and peripheral endocrine systems. * Output: the release of defined amounts of hormone in a certain temporal pattern allows both amplitude and frequency modulation. * Feed-forward control: e.g. from hypothalamus to pituitary to endocrine organ to target organ. * Feed-back control (usually negative) by either hormones or their effects - a homeostatic mechanism. This implies a certain “normal level” of hormone in plasma when ‘at rest’.
28
Explain (using examples) the secretion of hormones in pulses and according to rhythms.
* Hormones are released in pulses, which show up as peaks in a graph of hormone concentration against time * These pulses vary during the day according to rhythms, including diurnal and reproductive rhythms * For example, ACTH (and therefore cortisol) has a very high peak in the release in the morning, to prepare the person for the day
29
What are the two types of hormone rhythm you need to know about?
* Diurnal * Reproductive (e.g. menstruation?)
30
What is a diurnal rhythm?
A biological rhythm that is synchronized with the day/night cycle. It may or may not be a circadian rhythm.
31
What is the clinical relevance of diurnal hormone rhythms?
Comparative blood tests need to be taken at the same time on different days.
32
Describe where feed-forward control occurs in the endocrine system.
From the hypothalamus to pituitary to endocrine organ to target organ.
33
Describe where feed-back control occurs in the endocrine system.
* By either hormones or their effects * Usually negatively effect the hypothalamus and anterior pituitary
34
What are the different chemical types of hormone? Give examples of each.
Synthesised and stored in endocrine glands: * Protein * Peptide * Bioactive amine * Steroid * Thyroid Hormones produced enzymatically as they are needed: * Gaseous mediators * Prostaglandins * Angiotensin II
35
Categorise the different types of hormone based on whether they are hydrophilic or hydrophobic. What is the importance of this?
Hydrophobic: * Steroids * Prostaglandins Hydrophilic: * Peptide, polypeptide, protein, glycoprotein Both hydrophilic and hydrophobic properties, very small: * Catecholamines * Thyroid hormones
36
Give an example of each of these type of hormone: * Bioactive amine * Polypeptide * Protein * Glycoprotein * Steroid * Prostaglandin * Gaseous mediators
* Bioactive amine -\> T3, Catecholamines * Polypeptide -\> Insulin * Protein -\> Prolactin * Glycoprotein -\> Luteinising hormone * Steroid -\> Testosterone * Prostaglandin -\> Prostaglandin E2 * Gaseous mediators -\> NO
37
Describe the range in sizes of the different endocrine hormones.
* Amines, thyroid hormones, steroids and some peptides are very small. * Many polypeptide, protein and glycoprotein hormones are very large.
38
What is constitutive and regulated secretion?
* Constitutive secretion -\> Secretion straight away * Regulated secretion -\> Secretion in a controlled way
39
Describe the biosynthesis of proteins, polypeptides and glycopeptides.
* Translated on the rough endoplasmic reticulum * Secreted by either the regulated pathway (e.g. insulin, prolactin) or the constitutive pathway (cytokines, growth factors) * The original translation product (the prohormone) is usually processed proteolytically to yield the active hormone * Many endocrine cells produce more than one active peptide hormone, in varying amounts. These may be derived) from the same prohormone or from different prohormones.
40
Describe the biosynthesis of steroid hormones.
Synthesized rapidly on demand from cholesterol via enzymes in the mitochondria and smooth endoplasmic reticulum.
41
Describe the biosynthesis of bioactive amines.
Produced from tyrosine via intracellular enzymes
42
Describe the biosynthesis of thyroid hormones.
Iodothyronines are produced by iodination and coupling of tyrosyl residues in a protein (thyroglobulin) which are then released by proteolysis (see Thyroid lecture).
43
Describe the biosynthesis of angiotensin II.
Produced by conversion of plasma angiotensin I by angiotensin-converting enzyme in the lung.
44
Describe the biosynthesis of NO.
Produced from arginine by the intracellular enzyme nitric oxide synthase .
45
Describe the biosynthesis of prostaglandins.
Synthesized rapidly on demand from arachidonic acid via the intracellular cyclooxygenase enzymes.
46
Describe the storage of the different types of hormone in endocrine cells.
* Amines and many peptides -\> Stored in large amounts in intracellular granules. Some peptides (e.g. growth factors) are not stored but released as they are made. * Steroids, prostaglandins, gases -\> Not stored * Large amounts of iodinated thyroglobulin, the precursor for thyroid hormone synthesis, but not the free hormone, are stored in the thyroid follicles. However the blood contains a large reservoir of protein-bound thyroid hormone.
47
Describe the order of the normal concentrations of the endocrine hormones in plasma.
* Protein and polypeptide hormones -\> Nanomolar concentrations in plasma * Steroid hormones -\> Sub-micromolar concentrations, mostly bound to specific proteins
48
Are endocrine hormones in the blood transported freely?
* Hydrophilic peptide/protein and amine hormones can circulate freely in plasma. * Most steroid and thyroid hormones are substantially bound to specific binding proteins in the plasma so there is an equilibrium between bound and free.
49
What is the effect of endocrine hormones binding to plasma proteins?
Binding of hormones to proteins in the plasma substantially reduces their clearance and thus extends their ‘half-life’.
50
Describe the metabolism and excretion of endocrine hormones.
* Hormones have a variable half-life, but most are deactivated rapidly. The first step in their metabolism generally destroys their activity. * Hormones that are internalized with their receptor are usually degraded in the lysosomes of the target cells. * Steroid hormones are degraded in the liver (and in target tissues). * Hormones are also lost by excretion: through the kidneys (water soluble), liver and bile.
51
How are endocrine hormone levels in plasma measured?
Most are measured by some form of binding assay: most common is the radioimmunoassay. (These must however be validated by a bioassay to ensure they measure active hormone).
52
Describe the types of endocrine pathologies and how they are caused.
Defects can involve: * Production of hormone * Release of hormone * Mechanism of action Caused by: * Genetic factors * Tumours * Autoimmune disease
53
For any particular hormone, what do you need to know?
54
Remember to add flashcards about the structure of cells that synthesise and store endocrine hormones.
Do it.
55
What germ layer does the pancreas derive from?
Endoderm
56
Draw the gross and histological structure of the pancreas.
57
What percentage of the pancreas do the Islets of Langerhans make up?
1% - The rest of the pancreas has a moslty exocrine role.
58
From when are Islets of Langerhans distinguishable histologically in the pancreas?
From 12th week of gestation
59
How many cells are in an Islet of Langerhans?
Around 1000
60
How many Islets of Langerhans in the pancreas are there?
Around 1,000,000
61
What are the different cell types in the Islets of Langerhans and what hormone does each secrete?
* α-cells -\> Glucagon * β-cells -\> Insulin * δ-cells -\> Somatostatin Also: * PP-cells -\> Pancreatic polypeptide (PP) * ε-cells -\> Ghrelin
62
Label this.
63
In Islets of Langerhans, what are the percentages of the different cell types?
* β-cells (insulin) -\> 55% * α-cells (glucagon) -\> 38% * δ-cells (somatostatin) -\> Less than 5% * PP-cells (pancreatic polypeptide) -\> 1%
64
On what chromosome is the insulin gene located?
11
65
Which cells produce insulin?
β-cells in the Islets of Langerhans in the pancreas
66
How is mature insulin stored in β-cells?
In secretory vesicles
67
How many insulin granules are there in a β-cell and how much insulin does each contain?
* 10,000 secretory granules per β-cell * Each contains 8 femtograms of insulin
68
Show how glucose sensing works in β-cells of the pancreas. [EXTRA]
69
Is insulin secretion happen all in one go?
No, it is biphasic.
70
What are some things that stimulate and inhibit insulin secretion?
Stimulated by: * Glucose * Amino acids * Fatty acids * Parasympathetic innervation * Hormones: * GLP (glucagon-like peptide) * Glucagon (counter-intuitive) Inhibited by: * Sympathetic innervation * Hormones: * Somatostain (from δ-cells)
71
What are the main metabolic effects of insulin?
On carbohydrates: * Increased GLUT4 mediated glucose uptake (muscle and adipose) * Stimulates glycolysis * Stimulates glycogenesis (liver major store of glycogen) * Inhibits gluconeogenesis (liver) * Inhibits glycogenolysis * Inhibits glucagon production by α-cells (paracrine) On proteins: * Stimulates amino acid uptake * Stimulates protein synthesis On lipids: * Stimulates lipogenesis * Inhibits lipolysis
72
Draw the mechanism of action of insulin in target tissues.
73
Compare and explain the insulin response to oral and intravenous glucose.
The incretin effect: When the glucose is taken orally, incretin hormones (such as GLP, glucagon-like peptide) are released in response to the nutrients in the GI tract. This results in a higher insulin spike.
74
What are the effects of glucagon-like peptide (GLP)? [IMPORTANT]
* Stimulates insulin secretion * Inhibits glucagon secretion * Inhibits appetite * Inhibits gastric emptying
75
What is the effect of incretin hormones (such as GLP) on beta-cells in the pancreas?
Increase insulin secretion via the GLP1 receptor (Gαs-coupled GPCR).
76
For insulin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Protein * Two peptide chains referred to as the A chain and B chain, linked by disulfide bonds * Site and mechanism of production & release * Beta cells of the pancreas * Expressed as preproinsulin, then converted to proinsulin, then insulin * Stimuli that cause or inhibit its release * Stimulated by: * Glucose * Amino acids * Fatty acids * Parasympathetic innervation * Hormones: * GLP (glucagon-like peptide) * Glucagon (counter-intuitive) * Inhibited by: * Sympathetic innervation * Hormones: * Somatostain (from δ-cells) * Pattern of secretion into the blood/extracellular fluid * Biphasic * Mechanism of transport in the blood/extracellular fluid * Freely transported? * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * All cells, especially liver, muscle and fat * Binds to a receptor with tyrosine kinase activity, leading to insertion of GLUT4 transporter into the membrane * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Diabetes * Hypoglycaemia
77
What are sulphonylureas?
Medications that control blood sugar levels in patients with type 2 diabetes by stimulating the production of insulin in the pancreas and increasing the effectiveness of insulin in the body.
78
What cells produce glucagon?
α-cells in Islets of Langerhans in the pancreas
79
What chemical class of hormone is glucagon?
Polypeptide
80
Describe how glucagon is synthesised.
Just like insulin, it is synthesised as preproglucagon, then converted to proglucagon and then finally to glucagon.
81
What are some things that stimulate and inhibit glucagon secretion?
Stimulated by: * Hypoglycaemia * Sympathetic innervation * Specific amino acids * Gastrointestinal hormones Inhibited by: * Somatostatin * Insulin (paracrine)
82
What are the main metabolic effects of glucagon?
Promotes glycogenolysis, gluconeogenesis and lipolysis.
83
Describe the mechanism of action of glucagon on target cells.
* Glucagon receptors are Gs-coupled GPCRs * Mechanism of action involves adenylate cyclase activity and increased [cAMP] and subsequent PKA phosphorylation * Affects both gene expression and post-translational modifications (signalling).
84
What are the main sites of action of glucagon?
* Muscle * Liver * Adipose
85
For glucagon, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide hormone * Site and mechanism of production & release * Alpha cells of the pancreas * Stimuli that cause or inhibit its release * Stimulated by: * Hypoglycaemia * Sympathetic innervation * Specific amino acids * Gastrointestinal hormones * Inhibited by: * Somatostatin * Insulin (paracrine) * Pattern of secretion into the blood/extracellular fluid * ??? * Mechanism of transport in the blood/extracellular fluid * Transported freely in blood? * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Muscle, liver and fat cells * Glucagon receptors are Gs-coupled GPCRs * Mechanism of action involves adenylate cyclase activity and increased [cAMP] and subsequent PKA phosphorylation * Affects both gene expression and post-translational modifications (signalling) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Opposite to insulin
86
What hormones is glucagon synergistic with? [IMPORTANT]
* Catecholamines * Glucocorticoids * Growth hormone
87
What cells produce somatostatin?
* δ-cells in Islets of Langerhans in the pancreas * Brain * GI tract
88
What chemical class of hormone is somatostatin?
Peptide
89
What is the effect of somatostatin in the pancreas?
Paracrine inhibitor of insulin and glucagon secretion (i.e. it is a brake on all islet cell activity)
90
Describe the production of somatostatin.
It is a polypeptide cleaved from prosomatostatin
91
Describe the somatostatin mechanism of action in the pancreas.
* Somatostatin receptor is an inhibitory (Gi-coupled) GPCR. * This decreases adenylate cyclase activity and therefore decreases cAMP * Decreased cAMP leads to decreased secretion of insulin and glucagon
92
For somatostatin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide hormone (paracrine) * 28 amino acid molecule (in pancreas) * Site and mechanism of production & release * Cleaved from prosomatostatin * Produced in the pancreatic islets, brain and GI tract * Add mechanism of release * Stimuli that cause or inhibit its release * Add * Pattern of secretion into the blood/extracellular fluid * Add * Mechanism of transport in the blood/extracellular fluid * Paracrine hormone * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Inhibits insulin and glucagon release * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Add
93
What is an insulinoma?
A tumor of the pancreas that is derived from beta cells and secretes insulin.
94
What are the effects of insulinoma?
* Symptoms of hypoglycaemia -\> Recurrent headache, lethargy, diplopia, and blurred vision, particularly with exercise or fasting. * Severe hypoglycemia may result in seizures, coma, and permanent neurological damage. * Symptoms resulting from the catecholaminergic response to hypoglycemia (i.e. tremulousness, palpitations, tachycardia, sweating, hunger, anxiety, nausea) are not as common. * Sudden weight gain is sometimes seen.
95
What is the 'master gland'?
The pituitary gland -\> Because it secretes hormones that act on lots of other organs.
96
Draw the location of the pituitary gland.
Situated beneath the hypothalamus of the brain, in a depression (‘pituitary fossa') of the skull.
97
What are the two main parts of the pituitary and what are their proper names?
* Anterior pituitary -\> Adenohypophysis * Posterior pituitary -\> Neurohypophysis Note: Sometimes people also talk about a small intermdiate lobe between the anterior and posterior. In humans the intermediate love becomes interspersed with the anterior lobe.
98
Describe the development of the pituitary gland.
Anterior: * **Rathke's pouch** grows up from oropharyngeal ectoderm (roof of the mouth) to form the anterior pituitary. Posterior: * The **infundibular process** grows down from the forebrain vesicle to form the posterior pituitary.
99
Which part of the brain is the pituitary gland related to?
Hypothalamus
100
Describe how the pituitary gland is connected with the hypothalamus.
* Anterior pituitary receives hormones from the hypothalamus via portal veins * Posterior pituitary is formed by neurosecretory neurons that start in the hypothalamus
101
Describe the vasculature of the hypothalamus and pituitary.
* Posterior pituitary receives blood supply direct from internal carotid artery * Hypothalamus receives branches direct from internal carotid artery -\> These form a capillary plexus in the base of the hypothalamus that forms portal veins which supply the anterior pituitary. * Anterior pituitary receives blood from hypothalamo-hypophysial portal veins.
102
How many endocrine cell types are found in the anterior pituitary?
5
103
How can the different endocrine cell types in the anterior pituitary be differentiated?
Immunocytochemistry
104
What are the main endocrine cell types in the anterior pituitary?
* Thyrotrophs * Corticotrophs * Gonadotrophs * Lactotrophs * Somatotrophs
105
Describe the histological structure of the anterior pituitary.
The hormones stored in secretory granules.
106
Describe the different ways in which the activity of the anterior pituitary can be regulated. [IMPORTANT]
* By CNS -\> Specific releasing factors from the hypothalamus reach the anterior pituitary via the portal veins * Negative feedback by target hormones (at pituitary and hypothalamus)
107
What are the different types of hormone involved in the hypothalamo-pituitary-endocrine gland axis?
* The hormones from the hypothalamus are called releasing hormones -\> e.g. GnRH (gonadotrophin-releasing hormone) * The hormones from the pituitary are called trophic hormones -\> Secreted by lactoTROPHS, gonadoTROPHS, etc.
108
Draw the hypothalamus-pituitary-endocrine gland axis, along with the different types of feedback.
109
Name all of the hormones secreted by the anterior pituitary gland.
* TSH -\> Thyroid stimulating hormone (a.k.a thyrotrophin) * ACTH -\> Adrenocorticotrophic hormone * LH + FSH -\> Luteinising hormone + Follicle-stimulating hormone (a.k.a gonadotrophins) * PRL -\> Prolactin (a.k.a. mammotrophin) * GH -\> Growth hormone
110
By what cells is TSH secreted?
Thyrotroph cells (in the anterior pituitary)
111
Describe the chemical nature of TSH.
* Glycoprotein hormone [IMPORTANT] * Made of alpha and beta subunits; the beta subunit is specific to TSH, the alpha subunit is shared with LH and FSH.
112
Describe the actions of TSH.
Acts in the thyroid: * Stimulates thyroid hormone (T3 and T4) production + Increases iodine uptake by the thyroid (required for thyroid hormone production) * Stimulates thyroid growth
113
What are the receptors for TSH?
G protein coupled to cAMP, on thyroid gland follicular cells.
114
Describe the control of TSH release. What is it released in response to?
* Stimulated by thyrotrophin releasing hormone (TRH) from the hypothalamus -\> Secretion of TRH is stimulated by cold and by stress via the CNS. * Inhibited by T3 & T4 (negative feedback)
115
Describe when TSH is released.
* Released in pulses with a diurnal rhythm. * Also released in response to cold and stress.
116
Draw the structure of the hypothalamic-pituitary-thyroid axis.
117
For TSH, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Glycoprotein * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Released in response to cold and stress also * Pattern of secretion into the blood/extracellular fluid * Released in pulses in a diurnal rhythmn * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to thyroid cells * Acts by increasing intracellular cAMP with G-protein * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Rare
118
By what cells is ACTH secreted?
Corticotroph cells (in the anterior pituitary)
119
Describe the chemical nature of ACTH.
Polypeptide hormone
120
Describe the actions of ACTH.
Acts on the adrenal cortex and stimulates the secretion of: * Mostly glucocorticoids (i.e. cortisol) * Some increase in sex steroids
121
What are the receptors for ACTH?
G protein coupled to cAMP, on adrenal cortex cells.
122
Describe the control of ACTH release. What is it released in response to?
* Stimulated by corticotrophin releasing hormone (CRH) from the hypothalamus -\> Secretion of CRH is stimulated by stress via the CNS. * Inhibited by glucocorticoids like cortisol (negative feedback)
123
Describe when ACTH is released.
* Released in pulses with a diurnal rhythm -\> High at 7am, low at midnight. * Also released in response to stress and hypoglycaemia.
124
From what prohormone is ACTH cleaved? [EXTRA]
POMC
125
Describe some dysfunctions of ACTH.
* Cushing's disease -\> Excess ACTH from corticotrophinoma pituitary tumours, leading to excess glucocorticoid secretion * Addison's disease -\> Deficiency of ACTH causes glucocorticoid deficiency
126
For ACTH, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Polypeptide * Site and mechanism of production & release * Released from pituitary gland * Cleaved from POMC prohormone * Stimuli that cause or inhibit its release * Released in response to stress and hypoglycaemia * Feedback inhibition by glucocorticoids * Pattern of secretion into the blood/extracellular fluid * Released in pulses in a diurnal rhythmn * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to adrenal cortex cells * Acts by increasing intracellular cAMP with G-protein * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Cushing's disease -\> Excess ACTH from corticotrophinoma pituitary tumours, leading to excess glucocorticoid secretion * Addison's disease -\> Deficiency of ACTH causes glucocorticoid deficiency
127
Draw the hypothalamus-pituitary-adrenal axis.
128
By what cells are FSH and LH secreted?
Gondaotroph cells (in the anterior pituitary)
129
Describe the chemical nature of FSH and LH.
Glycoprotein hormone
130
Describe the actions of LH and FSH in females and males.
Female (acts on the ovaries): * FSH stimulates follicle development and production * LH stimulates progesterone production Male (acts on the testis): * FSH initiates and maintains spermatogenesis * LH stimulates testosterone production
131
What are the receptors for FSH and LH?
G protein coupled to cAMP, on ovary/testes cells.
132
Describe the control of FSH and LH release. What are they released in response to?
* Stimulated by gonadotrophin-releasing hormone (GnRH) during reproductive life. * In females: * Inhibited by sex steroid oestrogen (negative feedback) * BUT switch to positive feedback triggers LH surge at ovulation. * Ovarian peptides (e.g. inhibin) inhibit FSH * In males: * LH release is inhibited by negative feedback from testosterone
133
Describe when FSH and LH are released.
* Hourly pulses of gonadotrophin releasing hormone (GnRH) during reproductive life maintain FSH and LH * However, there are cyclical variations in LH and FSH in the menstrual cycle due to feedback from the gonads
134
Describe some dysfunctions of FSH and LH.
* Infertility -\> Deficiencies of LH and FSH or receptor dysfunction. * Precocious puberty -\> Excess LH and FSH secretion (nearly always due to inappropriate hypothalamic GnRH secretion) or receptor overactivity.
135
Draw the hypothalamus-pituitary-gonadal axis.
136
For FSH and LH, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Glycoprotein * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Feedback inhibition by gonadal hormones * Pattern of secretion into the blood/extracellular fluid * Released cyclically in menstrual cycle * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to gonadal cells * Acts by increasing intracellular cAMP with G-protein * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Infertility -\> Deficiencies of LH and FSH or receptor dysfunction. * Precocious puberty -\> Excess LH and FSH secretion (nearly always due to inappropriate hypothalamic GnRH secretion) or receptor overactivity.
137
By what cells is PRL secreted?
Lactotroph cells (in the anterior pituitary)
138
Describe the chemical nature of PRL.
Protein hormone
139
Describe the actions of PRL.
* Stimulates the development and growth of breast and milk production * Inhibits the reproductive system at the level of the gonads and pituitary -\> Lactational amenorrhea
140
What is lactational amenorrhoea?
* Natural postpartum infertility that occurs when a woman is not menstruating while breastfeeding. * This is due to PRL negative feedback on the HPG axis.
141
What are the receptors for PRL?
Tyrosine kinase on breast cells.
142
Describe the control of PRL release. What is it released in response to?
* Stimulated by suckling and by oestrogen. * Inhibited by hypothalamus (via dopamine) -\> Only pituitary hormone which is like this.
143
Describe when PRL is released.
Released upon suckling.
144
Describe some dysfunctions of PRL.
Hypersecretion of PRL can occur from PRL-secreting tumours in the pituitary gland termed ‘prolactinomas’ -\> Causes galactorrhoea, infertility and impotence.
145
Draw the hypothalamus-pituitary-breast axis.
146
For PRL, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Protein * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Stimulated by suckling and oestrogen * Inhibited by hypothalamus * Pattern of secretion into the blood/extracellular fluid * Released upon suckling * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to breast cells * Acts via a tyrosine kinase receptor * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * PRL-secreting tumours in the pituitary gland termed ‘prolactinomas’ causes galactorrhoea, infertility and impotence.
147
By what cells is GH secreted?
Somatotroph cells (in the anterior pituitary)
148
Describe the chemical nature of GH.
Protein hormone
149
Describe the actions of GH.
* Stimulates long bone and soft tissue growth -\> Directly and indirectly by stimulating the release of IGFs (insulin-like growth factors) from the liver * Metabolic effects: * Insulin-like effects -\> Promote amino acid uptake and promotes protein synthesis. * However, if GH is chronically increased it has anti-insulin effects. It is one of the hormones that switches metabolism away from glucose use and toward increased oxidation of fat (e.g. in starvation).
150
What are the receptors for GH?
Tyrosine kinase on on various tissues.
151
Describe the control of GH release. What is it released in response to?
* Stimulated by hypoglycaemia, stress and exercise -\> Due to growth hormone releasing hormone (GHRH) from the hypothalamus * Inhibited by somatostatin from the hypothalamus. * Inhibited by GH at the hypothalamus (negative feedback)
152
Describe when GH is released.
Secreted in pulses every 4h, and on entering deep sleep.
153
Describe some dysfunctions of GH.
* Dwarfism -\> GH insufficiency * Gigantism (in children) and acromegaly (in adults) -\> GH excess
154
For GH, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Protein * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Stimulated by hypoglycaemia, stress and exercise -\> Due to growth hormone releasing hormone (GHRH) from the hypothalamus * Inhibited by somatostatin from the hypothalamus * Inhibited by GH at the hypothalamus (negative feedback) * Pattern of secretion into the blood/extracellular fluid * Pulsatile release every 4 hours and upon entering deep sleep * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to various cell types * Acts via a tyrosine kinase receptor * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Dwarfism * Gigantism/Acromegaly
155
Draw the hypothalamus-pituitary-liver/muscle axis (for growth hormone).
156
What is acromegaly?
157
Describe the histological structure of the posterior pituitary.
* There are the axons and terminals of magnocellular neurosecretory neurons originating in the hypothalamus. * Pituicytes (a type of glial supporting cell) surround and support the terminals.
158
Describe how the hormones of the posterior pituitary are released.
The posterior pituitary hormones are synthesized in the hypothalamus, packed into granules, transported down the axons and released by exocytosis into the systemic veins draining the neurohypophysis.
159
What controls the release of hormones from the posterior pituitary?
Entirely controlled by the hypothalamus.
160
Whatm are the main hormones of the posterior pituitary?
* Antidiuretic hormone (ADH) (a.k.a vasopressin) * Oxytocin
161
Describe the chemical nature of ADH.
Peptide hormone
162
Describe the actions of ADH.
* Increases water reabsorption by acting in collecting ducts of kidney (V2) * Constricts peripheral arterioles and veins (V1)
163
What are the receptors for ADH?
* V2 receptors in kidney -\> G protein coupled to cAMP * V1 receptors in vasculature -\> PLC coupled
164
Describe the control of ADH release. What is it released in response to?
Stimulated by increases in plasma osmolarity -\> Sensitive to 1% increase from normal plasma OP - 285mOsm. This is sensed by hypothalamic osmoreceptors. These are also sensitive to decreases in blood volume or pressure.
165
Describe some dysfunctions of ADH.
Diabetes insipidus
166
What are the two types of diabetes insipidus?
* Hypothalamic: Lack of ADH production * Nephrogenic: Lack of ADH action
167
For ADH, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Stimulated by increases in plasma osmolarity * Stimulated by decreases in blood volume or pressure * Pattern of secretion into the blood/extracellular fluid * CHECK * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * V2 receptors in kidney -\> G protein coupled to cAMP * V1 receptors in vasculature -\> PLC coupled * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Diabetes insipidus
168
What are the two types of diabetes insipidus?
* Hypothalamic: Lack of ADH production * Nephrogenic: Lack of ADH action
169
Describe the chemical nature of oxytocin.
Peptide hormone
170
Describe the actions of oxytocin.
* Causes contraction of uterine myometrium in childbirth. * Causes ejection of milk. * Roles in social behaviour.
171
What are the receptors for oxytocin?
G protein coupled receptors coupled to PLC in breast and uterine muscle.
172
Describe the control of oxytocin release. What is it released in response to?
* Stimulated by stretch of cervix/vagina during parturition -\> Ferguson reflex * Stimulated by suckling -\> Stimulation of the nipple causes the milk ejection reflex.
173
Describe some dysfunctions of oxytocin.
Deficit of oxytocin may cause prolonged labour.
174
For oxytocin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * Released from pituitary gland * Stimuli that cause or inhibit its release * Stimulated by stretch of cervix/vagina during parturition -\> Ferguson reflex * Stimulated by suckling -\> Stimulation of the nipple causes the milk ejection reflex. * Pattern of secretion into the blood/extracellular fluid * CHECK * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * G protein couple to PLC in breast and uterus * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Deficit can produce prolonged labour
175
Describe the effects of defects of different pituitary gland receptors.
* ADH -\> Failure leads to nephrogenic diabetes insipidus * GH -\> Failure leads to abnormal short stature * ACTH -\> Not known, receptor failure probably lethal because of role of cortisol in perinatal period * TSH -\> Failure leads to rare form of cretinism * LH -\> Failure leads to infertility, constitutive activity leads to precocious puberty.
176
Describe the position and gross structure of the thyroid gland.
* Isthmus (central part) lies anterior to 2nd to 4th tracheal rings. * The lateral lobes wrap around the trachea.
177
How is the thyroid held in place?
Enclosed in fascia which anchors thyroid to the trachea.
178
Describe the development of the thyroid gland.
* A thyroid diverticulum forms in the midline of the floor of the mouth between the 1st & 3rd branchial arch components of the developing tongue. * It grows caudally over the developing larynx to the anterior aspect of the trachea. * As it descends it associates with the superior/inferior parathyroids which develop from the 4th/3rd pharyngeal pouches, and with neural crest cells which will form the parafollicular C (calcitonin) cells. * Two lateral lobes and a central isthmus form.
179
Describe the blood supply to the thyroid.
* Superior thyroid artery -\> First branch of the external carotid artery. * Inferior thyroid artery -\> Arises from the thyrocervical trunk (which in turn is a branch of the subclavian artery).
180
What is a unique feature of the thyroid gland?
Its requirement for iodine.
181
What is the only source of iodine to the body?
Dietary sources (fish, veg, etc.)
182
What does the thyroid gland need iodine for?
Production of T3 and T4, which contain iodine.
183
How does the thyroid store iodine?
Within the hormone precursor ‘thyroglobulin’ extracellularly.
184
Describe the histological structure of the thyroid.
* Follicular cells (epithelial) form follicles the lumen * The follicles are filled with ‘colloid’ * Outside of the follicles there are parafollicular cells
185
Label this structure of the thyroid.
186
What is colloid?
* The fluid that fills thyroid follicles * It contains thryoglobulin (the precursor to T4)
187
What do follicular and parafollicular cells in the thyroid produce?
* Follicular -\> T4 (and some T3) * Parafollicular -\> Calcitonin
188
What produces thyroglobulin?
Follicular cells synthesise the thyroglobulin and secrete it into the colloid within the follicle.
189
Compare the histological appearance of an active and inactive thyroid gland.
* Active thyroid -\> Follicular cells are tall and the colloid reduced in size * Inactive thyroid -\> Follicular cells are low cuboidal and the follicles are filled with colloid.
190
What is another name for parafollicular cells in the thyroid?
C cells
191
What do parafollicular cells in the thyroid produce? What is its effet?
* Calcitonin (a peptide hormone) * Acts to lower raised plasma calcium.
192
How is iodine taken up into the thyroid from the plasma?
Sodium/iodide symporter on the basal membrane of follicular cells
193
Which is the apical side of follicular cells?
The side that faces the colloid.
194
Does the thyroid produce both T3 and T4?
It produces mostly T4, which is then metabolised to T3 peripherally.
195
Describe how T4 (and T3) are produced in the thyroid.
* Sodium/iodide symporter on the basal membrane of follicular cells pumps in iodide from the plasma * Thyroperoxidase enzyme on the apical plasmalemma: * Oxidises the iodide to iodine * Iodinates tyrosyl residues in the thyroglobulin anc couples tyrosyl residues * This produces the hormones T3 and T4 still bound in the thyroglobulin, hence inactive * Colloid is a store of thyroglobulin * Upon stimulation by TSH, the colloid is endocytosed and digested by lysosomes -\> Frees T3 and T4.
196
What are the full names for T3 and T4?
* T3 = Tri-iodothyronine * T4 = Thyroxine
197
What stimulates the production of T4 (and T3)?
TSH (Thyroid-stimulating hormone)
198
Describe the control of T3/T4 production in the thyroid.
* Stimulated by TSH from the anterior pituitary * TRH (thyrotrophin releasing hormone) controls TSH secretion from the anterior pituitary. * TRH is released in hyperglycaemia and cold * Inhibited by T3 and T4 (negative feedback on TSH production) * Iodide is also required
199
Draw the hypothalamo-pituitary-thyroid axis.
200
By what mechanism does TSH act in the pituitary gland?
Acts via cAMP.
201
Name some plasma binding proteins that bind to thyroid hormones (T3 and T4). Describe their affinities for each. [EXTRA]
* Thyronine-binding globulin (TBG) -\> Glycoprotein with higher affinity for T4 than T3, produced by the liver. * Transthyretin -\> Lower affinity for T4, T3. * Albumin -\> Very low affinity, but high capacity.
202
Where is the inactive T4 converted into the active T3?
In the liver and kidney, mostly.
203
What type of enzyme is involved in the metabolism of T4?
Deiodinases
204
What are the different enzymes that act on T4?
* Type I deiodinase converts T4 to active T3 in the liver * Type II deiodinase converts T4 to active T3 in the pituitary * Type III deiodinase converts T4 to the inactive T3r in the liver
205
What determines whether T4 is deiodinated to the active T3 or inactive rT3?
Controlled by the need for metabolism: * Rreduced in starvation due to raised cortisol * Reduced in severe illness * Reduced by propranolol
206
How are iodothyronines (e.g. T4 and T3) ultimately degraded?
* Iodothyronines are finally deiodinated to thyronine * Iodide is salvaged by the kidney and reused.
207
Describe the mechanism of action of T3.
* T3 is transported into cells and acts on nuclear receptors (TR) which act on response elements (TREs) in gene promoters * This interaction results in stimulation or inhibition of the production of many different mRNAs and therefore proteins
208
On what tissues does T3 act?
T3 acts on almost every tissue of the body but has little metabolic effect in the brain, spleen or testis. It also has developmental effects on some tissues.
209
What are the actions of T3? [IMPORTANT]
* Increases basal metabolic rate: * Increases production of Na+/K+ ATPase (which uses 20-45% of all ATP) * Proteins -\> Increases protein degradation * Carbohydrates -\> Increases glycogenolysis and gluconeogenesis. Potentiates insulin effects increasing glycogenesis and glucose usage. * Lipids -\> Stimulates cholesterol breakdown and enhances lipolysis * Stimulates production of ß adrenergic receptors and TRH receptors * Developmental effects: * CNS -\> Essential for postnatal growth of CNS; stimulates production of myelin, neurotransmitters and axonal growth * Bone -\> Stimulates linear growth by effects on chondrocytes * Stimulates normal development, maturation and eruption of teeth, hair and epidermis * Cardiovascular effects -\> Increases cardiac output, rate and force * Stimulates gut motility * Stimulates bone turnover * Increases muscle contraction
210
How does T3 have cardiovascular effects?
* Increases production of myosin, beta-1 receptors and Ca2+-ATPase * These proteins increase contractility
211
Is T3 anabolic or catabolic?
At low doses, it is more anabolic. At high doses, it is more catabolic.
212
How do T3 and T4 provide negative feedback?
They act on the pituitary and hypothalamus, affecting the hypothalamo-pituitary-thyroid axis.
213
What is enlargement of the thyroid called?
Goitre
214
What can be some causes of goitre (enlargement of the thyroid)?
* Iodine deficiency -\> Lack of T3/T4 means there is no feedback on TRH and TSH secretion (TSH stimulates thyroid growth) * Graves' disease -\> Overactivation of the TSH receptor * Tumour -\> May be functioning or not.
215
What are the causes, indicators and symptoms of hyperthyroidism?
Causes: * Graves' disease -\> Generally due to autoimmune production of immunoglobulins that mimic TSH * Tumours of thyroid follicular cells Indicators: * High T3 and T4 * Low TSH Symptoms: * Raised BMR * Fast, bounding pulse * Heat intolerance * Weight loss despite a large appetite * Increased sympathetic drive * Eye protrusion
216
What is another name for hyperthyroidism? [IMPORTANT]
Thyrotoxicosis
217
What are the causes, indicators and symptoms of hypothyroidism?
Causes: * Failure of production by thyroid * Lack of iodine * Autoimmune inhibition * Failure of thyroid development * Failure of pituitary to produce TSH or hypothalamus TRH (‘central’ hypothyroidism) * Thyroid hormone resistance -\> Inactivating mutation of thyroid hormone receptor * Failure of thyroid hormone transporters Indicators: * Low T3 and T4 * High TSH Symptoms: * Reduced metabolism * Slow mentation * Hypothermia * Constipation
218
What are the prenatal and adult forms of hypothyroidism called? What are the symptoms of each? [IMPORTANT]
* Cretinism (prenatal) -\> Gross deficits in CNS myelination and stunting of postnatal growth if untreated (this is due to the importance of T3 in development) * Myxoedema (adult) -\> Reduced metabolism, slow mentation, hypothermia, constipation.
219
What is thyroid hormone resistance and how does it present?
* A number of genetic defects in the thyroid receptor reduce hormone binding. * The subject is hypothyroid but will have normal levels of plasma hormone.
220
How can hypothyroidism be treated?
Administering thyroxine (T4).
221
How can Graves disease be treated?
* It is caused by autoimmune antibodies that bind and activate TSH receptors. * TSH R stimulates enlargement of thyroid gland. * So you can treat it with radioactive iodine I-131.
222
What are some different drugs that alter thyroid activity?
* Thyroxine is given for hypothyroidism * Iodine: In large doses reduces the activity/vascularity of the gland * Radioactive iodine I-131 can be given to destroy thyroid tissue by local irradiation.
223
For T3, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * CHECK * Site and mechanism of production & release * Released from thyroid gland by exocytosis as T4 * T4 is converted to T3 in the liver by deiodinase I enzyme * Stimuli that cause or inhibit its release * Stimulated by TSH from the pituitary * Stimulated by hyperglycaemia stimulates * Inhibited by hypoglycaemia inhibits * Stimulated by cold stimulates * Pattern of secretion into the blood/extracellular fluid * CHECK * Mechanism of transport in the blood/extracellular fluid * Bound to thyronine-binding globulin (TBG), transthyretin and albumin * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Acts on many different tissues * Binds to nuclear receptors, which affect transcription * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Excess -\> Thyrotoxicosis * Deficiency -\> Cretinism, Myxoedema * Goitre * Thyroid hormone resistance
224
What is PTH?
Parathyroid hormone
225
What is the chemical class of PTH?
Peptide hormone
226
Describe when PTH is released and what its action is.
* Released in response to low plasma calcium * PTH restores low plasma Ca2+ to normal
227
What is stress?
A change that threatens to disturb homeostasis: * Physical * Trauma * Infection * Intense heat or cold * Starvation * Surgery * Severe blood loss * Pain * Dehydration * Psychological * Anxiety * Depression
228
What are the inner and outer parts of the adrenal glands called?
* Inner -\> Medulla * Outer -\> Cortex
229
Describe the histology and function of the adrenal glands.
* Inner medulla * Made up of groups of chromaffin cells packed with catecholamine granules -\> Store large amounts of adrenaline and noradrenaline. * Outer cortex * Made up of sheets of cells surrounded by capillaries and arranged in three zones: * Outer zona glomerulosa -\> Makes aldosterone * Middle zona fasciculata -\> Makes cortisol * Inner zona reticularis -\> Makes androgens
230
Label this histological diagram of the adrenal gland. Include the hormones released by each layer.
Medulla produces catecholamines.
231
Describe the position of the adrenal glands.
Just medial to the upper pole of each kidney.
232
Describe the development of the adrenal glands. [IMPORTANT]
* Medulla develops from neural crest * Cortex develops from mesoderm close to the mesonephros. * Early adrenal gland is composed of a fetal zone and a definitive zone * 'Fetal zone' of the adrenal cortex is very prominent in the fetus but it regresses after birth. The definitive zone is similar to the adult adrenal cortex.
233
What is the importance of the fetal zone of the adrenal cortex?
The fetal zone produces androgens which the placenta aromatizes to oestrogens. It regresses after birth.
234
Describe the blood supply and drainage of the adrenal glands. [IMPORTANT]
Arterial supply: * Branches of the inferior phrenic artery, the renal arteries and the aorta. * These small arteries form an arterial plexus beneath the capsule surrounding the adrenal and then enter a sinusoidal system that penetrates the cortex and the medulla draining into a single central adrenal vein in each gland. Venous drainage: * The veins drain to the inferior vena cava (R) and renal vein (L).
235
Describe the innervation of the adrenal glands.
* Principally to the medulla. * Innervated by thoracic preganglionic sympathetic nerves which release ACh, acts at nicotinic receptors -\> NOTE that this is unusual because there are no post-ganglionic nerves.
236
What is the role of the adrenal medulla?
Enabling the fight or flight response via release of catecholamines into the bloodstream.
237
Draw a diagram to show how the adrenal medulla is stimulated.
238
Describe the sythesis of adrenaline in the adrenal medulla.
* In the cytoplasm of chromaffin cells, tyrosine is converted to DOPA by tyrosine hydroxylase * DOPA is converted to dopamine by DOPA decarboxylase * Dopamine is then pumped into granules and is converted to noradrenaline by dopamine beta hydroxylase * Noradrenaline is then stored or pumped out of the granule for conversion to adrenaline (80% of total) by phenyl-N-methyl transferase (PNMT) in the cytoplasm. * Adrenaline is then pumped into granules for storage and release.
239
Is the adrenal medulla necessary for the emergency response to stress?
The adrenal medulla contributes 10% of the total sympathetic nervous system response to stress so thus it is not vital.
240
Summarise the effects of catecholamines on the body.
241
What is the general function of the adrenal cortex?
The maintenance of essential processes in chronic stress.
242
What type of hormones does the adrenal cortex secrete?
(Cortico)Steroid hormones
243
What are the main hormones produced by the adrenal cortex?
* Glucocorticoids (cortisol) * Aldosterone * Androgens
244
What do the different zones of the adrenal cortex release?
From outside to inside: * Zona glomerulosa -\> Aldosterone * Zona fasciculata -\> Cortisol * Zona reticularis -\> Androgens
245
What are corticosteroids and what are the different types?
* Corticosteroids are hormones produced by the adrenal cortex * The two main types: * Mineralcorticoids * Produced in the zona glomerulosa * e.g. Aldosterone * Glucocorticoids * Produced in the zona fasciculata * e.g. Cortisol
246
How are the steroid hormones in the adrenal cortex synthesised?
Glucocorticoids and mineralcorticoids are synthesised from cholesterol (details are not needed).
247
Describe how each of the adrenal cortex steroids is transported in the blood.
* All adrenal steroids are bound by albumin * Cortisol -\> Bound by cortisol-binding globulin * Aldosterone -\> No high affinity binding protein * Androgens -\> Sex steroid binding globulins
248
How are adrenal cortex steroids cleared from the blood?
* The kidney filters free steroid hormone but reabsorbs 90%. * The liver converts steroid hormones to hydrophilic metabolites by hydroxylation and conjugation reactions.
249
Draw the hypothalamus-pituitary-adrenal axis.
250
How do adrenal cortex steroid hormones act?
They act on intracellular receptors that control gene transcription.
251
What adrenal hormone is involved in the hypothalamus-pituitary-adrenal axis?
Cortisol
252
What are glucocorticoids and what is the main one?
* Adrenal hormones that preserve glucose for the brain * The main one is cortisol
253
What are the actions of cortisol (a glucocorticoid)?
* Accelerate gluconeogenesis in liver * Accelerate lipolysis and protein catabolism in liver and peripheral tissues * Central nervous system activity (appetite, mood) * Increased red blood cell production * Maintenance of circulation * Reduce inflammation and the immune response
254
Describe the metabolism of cortisol.
Cortisol is converted in the liver to the relatively inactive metabolite, cortisone, by 11 ß-hydroxysteroid dehydrogenase.
255
Describe the control of cortisol (a glucocorticoid) output.
* Hypothalamus releases corticotrophin releasing factor (CRF) in response to stress (inhibited by cortisol negative feedback). * CRF acts on anterior pituitary corticotrophs to stimulate ACTH production and release * ACTH stimulates the zona fasciculata cells via cyclic AMP to stimulate cortisol production.
256
What are some clinical uses of glucocorticoids?
* Inflammatory disorders, arthritis, asthma * Inhibit transplant rejection * Chemotherapy * Antenatal to mature the lungs in fetus threatening preterm labour
257
What are some deficiencies of cortisol (glucocorticoid) action?
* Insufficiency -\> Addison's * Excess -\> Cushing's
258
Draw the cause and symptoms of Cushing's disease.
Cause: Excess cortisol (glucocorticoids)
259
Draw the causes and symptoms of Addison's disease.
260
How can the effects of cortisol on the immune system be exploited clinically?
Glucocorticoids have immunosuppressant effects.
261
What type of hormone is aldosterone?
Mineralcorticoid
262
What are the actions of aldosterone?
* In kidney collecting tubules: * Stimulates reabsorption of Na+ in exchange for secretion of K+ , H+ , NH3 + * In salivary and sweat glands: * Regulates ion transport to retain sodium.
263
Describe the receptors (and their location) for mineralcorticoids.
* Mineralocorticoid receptors are present in the nuclei of only a few cell types -\> Kidney collecting tubule epithelia, salivary and sweat glands. * However, cortisol also binds to MR. Therefore, in aldosterone targets cortisol is deactivated to protect MR from cortisol activation.
264
Describe the control of aldosterone secretion.
Renin-angiotensin system: * RAA axis is stimulated by low plasma Na+ or low renal blood pressure. * This stimulates renin release which acts in the lung to stimulate conversion of angiotensin I to Angiotensin II (AII) by activating angiotensin converting enzyme (ACE). * Angiotensin II stimulates output of aldosterone from the zona glomerulosa of the adrenal cortex (it also causes arteriolar constriction and drinking in response to thirst).
265
What are some deficiencies of aldosterone?
* Hypoaldosteronism (in adrenal failure) * Results in sodium loss, low blood volume and low blood pressure. * Hyperaldosteronism (Conn's syndrome) * Results in excess sodium retention, water retention and increased blood pressure.
266
Give an example of a drug that influences aldosterone action.
Spironolactone is an aldosterone antagonist used as an anti-hypertensive.
267
Are adrenal androgens a large part of adrenal secretions?
No, at most times they are a very minor component of secretion.
268
What is the main adrenal androgen?
DHEA = Dehydroepiandrosterone
269
What is the function fo DHEA?
It is a weak androgen which stimulates axillary/pubic hair development at puberty, and libido.
270
Describe how release of DHEA is controlled.
It is stimulated by ACTH.
271
Add flashcards on the individual hormones.
272
For adrenaline, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Amine * Site and mechanism of production & release * Formed by a sequence of reactions * Stored in granules in chromaffin cells of the adrenal medulla * Released by exocytosis * Stimuli that cause or inhibit its release * Stimulated by sympathetic stimulation of the adrenal medulla * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Binds to alpha and beta adrenoceptors * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Adrenal medulla is removed the adrenal medulla stress response is compensated for by the remainder of the sympathetic system. * Tumours of the adrenal medulla (phaeochromocytoma) constantly secrete catecholamines causing hypertension, tremor, anxiety, forceful heartbeat.
273
For DHEA, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Steroid * Site and mechanism of production & release * Produced in zona reticularis * Synthesised from cholesterol * Stimuli that cause or inhibit its release * Stimulated by ACTH from the hypothalamus * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * Binds to sex steroid binding globulin * Binds to albumin with low affinity * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Acts on nuclear receptors to affect transcription * Stimulates axillary/pubic hair development at puberty, and libido. * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * CHECK
274
For aldosterone, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Steroid * Site and mechanism of production & release * Produced in zona glomerulosa * Synthesised from cholesterol * Stimuli that cause or inhibit its release * Stimulated by RAA axis in response to decreased blood pressure * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * No high affinity binding proteins * Binds to albumin with low affinity * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Acts on nuclear receptors to affect transcription * In kidney collecting tubules -\> Increases sodium retention in exchange for potassium * In salivary and sweat glands -\> Increases sodium retention * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Hypoaldosteronism (in adrenal failure) -\> Results in sodium loss, low blood volume and low blood pressure. * Hyperaldosteronism (Conn's syndrome) -\> Results in excess sodium retention, water retention and increased blood pressure.
275
For cortisol, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Steroid * Site and mechanism of production & release * Produced in zona fasciculata * Synthesised from cholesterol * Stimuli that cause or inhibit its release * Stimulated by ACTH (which in turn is stimulated by corticotrophin releasing factor, CRF, from the hypothalamus, which is released in response to stress * Inhibited by cortisol negative feedback on the hypothalamus * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * Binds to cortisol-binding protein * Binds to albumin with low affinity * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Widespread effects in different tissues * Acts on nuclear receptors to affect transcription * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Cortisol insufficiency -\> Addison's disease * Cortisol excess -\> Cushing's syndrome
276
Name the different GI hormones and where they are produced in the GI tract.
The ones highlighted are those mentioned in the spec, along with secretin.
277
What are the 4 major classifications of GI hormones?
* Hormones which regulate digestion * Hormones which regulate digestion and appetite * Hormones which regulate appetite and feeding * Incretins (hormones which regulate insulin secretion)
278
State the main GI hormones that fall under these categories: * Hormones which regulate digestion * Hormones which regulate digestion and appetite * Hormones which regulate appetite and feeding * Incretins (hormones which regulate insulin secretion)
279
What are GI hormones released in response to?
Endocrine cells scattered in the gut epithelium sense the contents of the lumen. Smell and taste also contribute.
280
Describe the polarity of gut endocrine cells.
* Hormone secreted basally * Most have microvilli on apex open to gut lumen to sense the content of the gut
281
What is the chemical class of GI hormones? [IMPORTANT]
Peptides
282
How are GI hormones inactivated?
Cleavage by peptidases (since they are peptide hormones)
283
How do endocrine cells in the GI tract respond to the presence of food in the GI tract?
Enteroendocrine cells are electrically active and fire action potentials in response to the presence of digested food in the GI tract.
284
What is the action of histamine?
Stimulates gastric acid (HCl) secretion from the stomach.
285
What cells in histamine secreted by?
Enterochromaffin-like (ECL) cells of the stomach
286
What is histamine secreted in response to?
Stretch or vagal stimulation of the stomach
287
On what receptors (and cells) does histamine act?
H2 receptors on the oxyntic cells of the stomach
288
For histamine, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * Produced from histidine by histidine decarboxylase * Produced in ECL (enterochromaffin-like) cells of the stomach * Secreted by exocytosis * Stimuli that cause or inhibit its release * Stimulated by stretch or vagal stimulation of the stomach * Stimulated by gastrin (which also has an acid secreting effect of its own) * Inhibited by somatostatin * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Stimulates HCl secretion from oxyntic cells of the stomach * Acts on H2 receptors * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * CHECK
289
Where cells is gastrin secreted by?
G cells of the gastric antrum
290
What are the stimuli and inhbitors of gastrin release?
Stimulated by: * Protein digestion products * Vagus stimulation * Stretch of stomach * Hypercalcaemia Inhibited by: * H+ (negative feedback) * Somatostatin (local negative feedback)
291
What are the actions of gastrin?
* Gastric acid secretion (direct & indirect via stimulating histamine H2 ) * Induces the insertion of K+/H+-ATPase pumps into the apical membrane of parietal cells * Pepsinogen secretion Others (not in spec): * Parietal cell growth * Antral motility (churning) * Mucosal blood flow * Trophic to parts of GI tract * Water & electrolyte secretion in liver, pancreas, intestine.
292
Draw a diagram to show how gastrin, histamine and somatostatin act to regulate HCl secretion in the stomach.
* The parasympathetic (vagal) stimulation of histamine-releasing ECL cells causes release of histamine * Parasympathetic stimulation of gastrin-releasing G cells causes release of gastrin, which also promotes further histamine release * Histamine and gastrin together cause insertion of the H+/K+-ATPase into the apical membrane of the endocrine cells in the stomach lining -\> This acidifies the stomach * These actions are inhibited by somatostatin from D cells
293
For gastrin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * G cells of the gastric antrum * Produced as preprogastrin and released by exocytosis * Stimuli that cause or inhibit its release * Stimulated by: * Protein digestion products * Vagus stimulation * Stretch of stomach * Hypercalcaemia * Inhibited by: * H+ (negative feedback) * Somatostatin (local negative feedback) * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Stimulates gastric acid secretion (direct & indirect via stimulating histamine H2) * Induces the insertion of K+/H+-ATPase pumps into the apical membrane of parietal cells * Stimulates pepsinogen secretion * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * CHECK
294
What cells is secretin secreted by?
* S cells, from duodenum to distal ileum * These are in the neck region of intestinal glands
295
What are the stimuli and inhibitors of secretin release?
* Stimulated by acid in proximal duodenal lumen * Inhibited by somatostatin
296
What are the actions of secretin?
* Stimulates secretion of HCO3- and water from the pancreas and liver * Washes pancreatic secretions into the duodenum * Washes bile too
297
By what mechanism does secretin have its action?
* It leads to secretion of HCO3- and water from the pancreas and liver * This is done by stimulation of Gs-coupled GPCRs that lead to increases in cAMP -\> This acts on CFTR, leading to changes in Cl- conductance that drives Cl-/HCO3- exchange.
298
For somatostatin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * D cells from the gastric antrum to the colon * Released by exocytosis * Stimuli that cause or inhibit its release * Stimulated by meals: amino acids, glucose, fatty acids, gastrin, secretin * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Suppresses secretion of GI hormones * Suppresses their effects (acid etc) * Retards absorption of glucose; protects against post-prandial hyperglycaemia (in liver) * Acts via Gi GPCRs that lead to decreases in intracellular cAMP * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * Somatostatinoma
299
For secretin, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * S cells of the duodenum to ileum * Released by exocytosis * Stimuli that cause or inhibit its release * Stimulated by: * Acid in the duodenum * Inhibited by: * Somatostatin * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * It leads to secretion of HCO3- and water from the pancreas and liver * This is done by stimulation of Gs-coupled GPCRs that lead to increases in cAMP -\> This acts on CFTR, leading to changes in Cl- conductance that drives Cl-/HCO3- exchange. * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * CHECK
300
What does CCK stand for?
Cholecystokinin (a.k.a. pancreozymin)
301
What cells is CCK secreted by?
I cells in the duodenum and jejunum
302
What are the actions of CCK?
* Suppresses appetite * Stimulates pancreatic secretions * Stimulates gall bladder contraction * Inhbits stomach emptying and stimulates gut motility * Potentiates action of secretin (stomach acid secretion)
303
How does CCK act on appetite?
* CCK acts on vagal afferent terminals to signal satiety, acts on vagal terminals -\> Inhibits feeding, therefore neurocrine rather than endocrine * Cholecystokinin 1 (CCK1) receptor on the vagus nerve
304
What are the stimuli for CCK secretion?
Products of protein and fat digestion in the duodenum
305
For CCK, summarise: * Chemical class & broad structure * Site and mechanism of production & release * Stimuli that cause or inhibit its release * Pattern of secretion into the blood/extracellular fluid * Mechanism of transport in the blood/extracellular fluid * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target
* Chemical class & broad structure * Peptide * Site and mechanism of production & release * S cells of the duodenum to ileum * Released by exocytosis * Stimuli that cause or inhibit its release * Stimulated by: * Acid in the duodenum * Inhibited by: * Somatostatin * Pattern of secretion into the blood/extracellular fluid * Released upon stimulation * Mechanism of transport in the blood/extracellular fluid * CHECK * Principal target tissue(s) & receptors -\> Mechanism of action in target tissue(s) * Suppresses appetite * Stimulates pancreatic secretions * Stimulates gall bladder contraction * Inhbits stomach emptying and stimulates gut motility * Potentiates action of secretin (stomach acid secretion) * Principal effects of normal hormone levels, excess and deficiency and hormone resistance in target * CHECK
306
What are incretins and what are the two main ones?
* Hormones which regulate postprandial insulin release * Two main examples: * GLP -\> Glucagon-like peptide * GIP -\> Glucose-dependent insulinotropic peptide
307
For GLP, summarise the release site, stimuli for release and actions.
GLP also has a system-wide positive metabolic effect, e.g. on the heart, etc.
308
What produced erythropoietin?
Kidneys
309
What are the main types of eicosanoids you need to know about?
* Prostaglandins * Prostacyclin * Thromboxanes
310
What are eicosanoids produced from?
Arachidonic acid
311
What are the roles of prostaglandins?
* Vasodilator * Prevent aggregation of platelets * Stimulate uterine contractions
312
What is prostacyclin?
A prostaglandin that plays a role in vasodilation.
313
What is an inhibitor of prostaglandin synthesis?
Aspirin
314

YEAR 1 - Organisation of the Body (Anton) (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions