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LCRS Year 1 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is endocrine function?

A

Hormone’s action on target cells distant from the source

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2
Q

What is paracrine function?

A

Hormone’s action on nearby target cells within immediate area around the source

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3
Q

What is autocrine function?

A

Hormone having an effect on it’s own immediate source

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4
Q

What is cryptocrine function?

A

Hormone having effect within it’s own cell of production

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5
Q

What is the adenohypophysis?

A

The anterior pituitary

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6
Q

Where does the pituitary gland attach to the brain?

A

At the base of the hypothalamus

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7
Q

What two structures is the hypothalamus between and what does it surround?

A

Between the optic chiasma and mammillary body

Surrounds the third ventricle

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8
Q

What structure do neurons pass through to reach the neurohypophysis?

A

Pituitary stalk

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9
Q

Where do neurons stop to release transmitters for the adenohypophysis?

A

Region of median eminance

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10
Q

What is the structure of the vascualr system connecting the hypothalamus and the adenohypophysis?

A

Primary capillary plexus
Long portal veins
Secondary capillary plexus

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11
Q

What would happen if you stop the blood flow to the primary capillary plexus?

A

Loss of function of the adenohypophysis

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12
Q

Which is the anterior pituitary and which is the posterior?

A

Anterior: adenohypophysis
Posterior: neurohypophysis

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13
Q

What is the process of release of hormone from the adenohypophysis from stimulation from the hypothalamus?

A

1) Hypothalamus releases neurotransmitters into the primary capillary plexus of the hypothalamo-hypophysial portal system
2) Neurosecretion reaches adenohypophysis and acts on anterior pituitary target cells
Release of adenohypophysial hormone into general circulation

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14
Q

What are the 5 defined cells types in the adenohypophysis?

A 
Somatotrophs
Lactotrophs
Thyrotrophs
Gonadotrophs
Corticotrophs
(Study, Learn, Then Go Clubbing)
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15
Q

What are the 6 hormones released from the adenohypophysis?

A 
Somatotrophin (Growth hormone)
Prolactin
Thyrotrophin (Thyroid stimulating hormone TSH)
LH
FSH
Corticotrophin (ACTH)
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16
Q

Which cells in the adenohypophysis produce which hormone(s)?

A 
Somatotroph- Somatotrophin
Lactotrophs- Prolactin
Thyrotrophs- Thyrotrophin (TSH)
Gonadotrophs- LH and FSH
Corticotrophs- Corticotrophin (ACTH)
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17
Q

Which hypothalamic hormones stimulate or inhibit somatotrophin? Which one is the dominant influence?

A

Stimulate: Somatotrophin releasing hormone (SRH or GHRH) DOMINANT
Inhibit: Somatostatin (SS)

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18
Q

Which hypothalamic hormones stimulate or inhibit prolactin? Which one is the dominant influence?

A

Stimulate: Thyrotrophin-releasing hormone (TRH)
Inhibitory: Dopamine (DA) DOMINANT

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19
Q

Which hypothalamic hormones stimulate or inhibit LH and FSH?

A

Stimulate: Gonadotrophin-releasing hormone (GnRH)
Inhibit: Gonadotrophin-inhibitory hormone (GnIH)

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20
Q

Which hypothalamic hormones stimulate corticotrophin?

A

Corticotrophin-releasing hormone

Vasopressin (VP/ADH)

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21
Q

What are the target tissues of the adenohypophysial hormones?

A

Somatotrophin- Geneneral body tissues, particularly the liver
Prolactin- Breasts (lactating women)
Thyrotrophin- Thyroid
LH and FSH- Testes (men), ovaries (women)
Corticotrophin (ACTH)- Adrenal cortex

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22
Q

What hormones are produced by hepatocytes when stimulated by somatotrophin? What are their function

A

Somatomedins (IGFI and IGF II)

Acts on body tissues to produce growth and development

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23
Q

What are the metabolic effects of somatotrophin via IGFI? (5)

A

1) Stimulation of amino acid transport into cell
2) Stimulation of protein synthesis
3) Increased cartilaginous growth
4) Stimulation of lipid metabolism leading to increased fatty acid production (increased circulating non-esterified fatty acids and glycerol)
5) Decreased glucose utilisation (increased insulin resistance) and increased gluconeogenesis resulting in increased blood glucose concentration

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24
Q

What lifestyles factors can stimulate a release of gonadotrophin-releasing hormone? (6)

A

1) Sleep (stages III and IV)
2) Stress
3) Oestrogens
4) Exercise
5) Fasting (hypoglycaemia)
6) Amino acids

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25
Q

What hormone released from the stomach stimulates somatotrophin release from the adenohypophysis? What is it’s function?

A

Ghrelin (the hunger hormone)

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26
Q

What negative feedback loops affect somatotrophin?

A

Somatomedins (from liver) feedback to adenohypophysis and hypothalamus
Somatotrophin feeds back to hypothalamus
(Direct and indirect feedback loops)

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27
Q

What are the effects of prolactin? (7)

A

1) HYPOTHALAMUS ↓ sexual behaviour (Switches of GnRH affecting LH and FSH. Also a natural contraceptive)
2) Renal Na+/water reabsorption
3) Steroidogenesis
4) BREAST LACTOGENESIS (post-partum women)
5) Effects on immune system (e.g. stimulate T cells)
6) ↑ LH receptors (testes, ovaries)
7) PITUITARY (↓ LH release)

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28
Q

What is prolactinoema?

A

When high prolactin levels decrease the levels of LH in the pituitary

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29
Q

How does prolactin stimulate the production of milk?

A

Tactile receptors around the nipple respond to stretch and activate the afferent nerve pathway in the brain (multi neuron pathway)
Inhibits dopamine and stimulates the production of TRH (thyrotrophin releasing hormone) causing prolactin to be released
Suckling inhibits the inhibitory pathway and stimualtes production of TRH

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30
Q

What are the three types of hormone?

A

1) Protein/polypeptide hormone
2) Steroid hormone
3) Miscellaneous

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31
Q

How is a protein/polypeptide hormone synthesised? Explain using an example

A

e.g. ACTH (Adrenocorticotroph Hormone)
Produced in a pituitary corticotroph cell
1) Capillary delivers amino acids to the cell
2) Stimulus leads to genes producing prohormone mRNA which leaves the nucleus
3) Aligns on rough endoplasmic reticulum and produces prohormone
4) Prohormone released from RER and delivered to Golgi apparatus where processing occurs
5) Prohormone is packaged into vesicles with enzymes which cleave prohormone = vesicles of ACTH
6) Travel to periphery ready for release by exocytosis

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32
Q

Which blood vessels are pituitary hormones secreted into?

A

Pituitary capillary

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33
Q

How is a steroid hormone synthesised? Explain using an example

A

e.g. Cortisol
Produced in adrenal cortical cells
1) LDL rich in cholesterol is transported across cell membrane from the blood stream by endocytosis
2) Stimulation by ACTH activates cholesterol esterase which releases cholesterol ester depots providing substrate for steroid synthetase
3) StAR protein (sterodogenic acute regulatory protein) mediates transfer of cholesterol from outer to inner mitochondrial membraine (RATE LIMITING STEP)
4) Cholesterol undergoes a series of modifications by cytochrome P450 within the mitochondria to produce mature cortisol
5) Mature hormone can then freely diffuse across the cell membrane into the circulation

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34
Q

How does binding capacity impact the clearance rate of a hormone?

A

↑ binding capacity

↓ clearance rate

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35
Q

How is ACTH transported around the body?

A

It is water soluble so it travels freely in the circulation

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36
Q

How is cortisol transported around the body?

A

It is bound to transport proteins creating a reservoir in equilibrium with a small amount of free hormone

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37
Q

What is the benefit of the method of transport used for cortisol?

A

The free hormone is biologically active so acts as a buffer to protect against rapid changes in concentration

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38
Q

What are 3 binding proteins used to transport hormone in the body? What hormone do they transport?

A

TBG- Thyroid hormone
CBG (Corticosteroid binding globulin)- Cortisol
SHBG- Testosterone/oestradiol

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39
Q

During pregnancy why does the amount of cortisol produced increase?

A

Because the number of corticosteroid binding proteins increases, so does cortisol to balance the equilibrium

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40
Q

The binding of a hormone with its receptor activates an effector system resulting in the generation of what?

A

1) Intracellular signal and second messenger effectors

2) Leads to effect on changes in membrane transport. DNA and RNA synthesis, protein synthesis and hormone release

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41
Q

What is the ACTH mechanism of action in an adrenal cortical cell?

A

1) ACTH binds to the Gs-protein coupled receptor
2) Leads to dissociation of a subunit of Gs protein from β, γ subunits
3) Leads to activation of adenylate cyclase which convert ATP to cAMP
4) cAMP activates protein kinase A
5) Protein kinase A phosphorylates the esterase and activates StAR protein which kick starts steroid hormone production

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42
Q

What is the difference between the receptors which protein hormones and steroid hormones bind to to initiate a response?

A

Protein hormone receptors are on the cell surface

Steroid hormone receptors are intra-nuclear

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43
Q

What is the mechanism of action for cortisol in a cell?

A

1) Enters cell by passive diffusion
2) Binds to specific glucocorticoid (GC) receptors in cell cytoplasm
3) Hormone-receptor complex travels to nucleus and binds to DNA binding sites
4) Causes changes in transcription rates of specific genes and production of new mRNA
5) Translation of mRNA to protein within endoplasmic reticulum

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44
Q

What is the feedback mechanism for ACTH and cortisol?

A

1) ACTH production is initiated by stress (↑ ACTH production)
2) Acts on adrenal glands ↑ cortisol production
3) Cortisol feeds back to adenohypophysis, adrenal glands and hypothalamus to switch off production

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45
Q

Which target would cortisol bind to induce negative feedback within the anterior pituitary?

1) Albumin
2) Cholesterol
3) Glucocorticoid receptor
4) Protein kinase A
5) StAR protein

A

Glucocorticoid receptor

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46
Q

What is the role of the suprachiasmatic nucleus?

A

The body timer (day/night etc)

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47
Q

What hormones are released from the neurohypophysis?

A

Vasopressin (ADH)

Oxytocin

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48
Q

Where are the cell bodies in the neurohypophysis?

A

In the supraoptic and paraventricular nuclei

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49
Q

What neurones terminate in the neurohypophysis?

A

Magnocellular neurones

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50
Q

What are the main features of supraoptic neurones?

A

1) Leave hypothalamic supraoptic nuclei
2) Pass through median eminence
3) Herring bodies along axon
4) Terminate in neurohypophysis
5) They are either VASOPRESSINERGIC or OXYTOCINERGIC

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51
Q

What are the different types of paraventricular neurones?

A

Originate in paraventricular nuclei

1) Some (parvocellular) neurones pass to other parts of the brain
2) Some of the neurones are magnocellular and these pass down to the neurohypophysis
3) Some (parvocellular) VP neurones terminate in median eminence
4) They are either vasopressinergic or oxytocinergic

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52
Q

What is the mechanism of vasopressin synthesis?

A

Pre-prohormone produced and cleaved within the axons and put into granules. All three components are released together

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53
Q

What molecules make up the vasopressin pre-prohormone?

A

Vasopressin + Neurophysin + Glycopeptide (copeptin)

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54
Q

What are the actions of vasopressin? (7)

A

1) Stimulates water reabsorption (Antidiuretic)
2) Vasoconstriction (arterioles have vasopressin receptors)
3) Corticotrophin release (together with CRH)
4) CNS effect
5) Acting as neurotransmitter (or hormone) e.g. on aspects of behaviour
6) Synthesis of blood clotting factors (VIII and Von Willbrandt factor)
7) Hepatic glycogenolysis (stimulates glycogenolysis)

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55
Q

What are the vasopressin receptors?

A

V1a, V1b (V3) and V2

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56
Q

Where is the V1a receptor found? (3)

A

1) Arterial/ arteriolar smooth muscle (vasoconstriction)
2) Hepatocytes (glycogenolysis)
3) CNS neurones (behavioural and other effects)

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57
Q

Where is the V1b (V3) receptor found?

A

Adenohypophysial corticotrophs (corticotrophin production)

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58
Q

Where are the V2 receptors found? (3)

A

1) Collecting duct cells (water reabsorption)
2) Probably other presently unidentified sites (e.g. endothelial cells, vasodilator effect?)
3) Factor VIII and Von Willbrandt factor

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59
Q

What is the mechanism of action of a V1 receptor?

A

Linked via G proteins to phospholipase C
Phospholipase C acts on membrane phospholipids to produce inositol triphosphate IP3 (and DAG)
These increase cytoplasmic [Ca2+] and other cellular mediators (PKC)
Produces cellular response

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60
Q

What is the mechanism of action of a V2 receptor?

A

Linked via G proteins to adenyl cyclase
Adenyl cyclase acts on ATP to for cAMP
cAMP activates protein kinase A (PKA)
This activates other intracellular mediators which produce cellular response (aquaporins)

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61
Q

How does vasopressin cause water reabsorbtion?

A

1) Vasopressin binds to V2 receptor on collecting duct cell basolateral membrane
2) G protein activates adenyl cyclase which converts ATP to cAMP
3) cAMP activates protein kinase A (PKA)
4) PKA activates other intracellular mediators
5) These cause synthesis of AQP2
6) Migration of aggraphores
7) AQP2 insertion into apical membrane
8) Water enters cell from tubule lumen
9) AQP 3 and 4 Allow water to flow into plasma

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62
Q

What is the main stimulus of vasopressin release? What is the mechanism?

A

Increased plasma osmolality

1) Osmoreceptors detect ↑ plasma osmolality in hypothalamus
2) Vasopressin released from neurohypophysis
3) Vasopressin action on V2 receptors in collecting duct
4) Increased water reabsorption
5) Decreased plasma osmolality

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63
Q

What is the mechanism of vasopressin action in response to decreased arterial blood pressure?

A

1) Baroreceptors and volume receptor stimulation decreases inhibiting inhibition of vasopressin
2) Vasopressin release from neurohypophysis
3) Vasopressin action on V1 receptors on arterial smooth muscle
4) Increased vasoconstriction
5) Increased blood pressure

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64
Q

What does oxytocin produce?

A

Contraction

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65
Q

Where are baroreceptors located?

A

In the carotid sinus and the aortic arch

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66
Q

What cells does oxytocin act on in the uterus to aid delivery of baby?

A

Myometrial cells

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67
Q

What cells does oxytocin act on in the breast during lactation?

A

Myoepithelial cells

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68
Q

What two hormones work together in lactation? How?

A

Prolactin produces milk and oxytocin causes contraction of cells to eject the milk

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69
Q

What stimulates a release of oxytocin during lactation?

A

Suckling

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70
Q

What conditions are associated with vasopressin?

A

Diabetes insipidus

SIADH (Syndrome of Inappropriate ADH)

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71
Q

What are the main symptoms of diabetes insipidus?

A

Polyuria

Polydypsia

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72
Q

What are the different types of diabetes insipidus?

A 
Central DI (no VP)
Nephrogenic DI (tissue insensitivity)
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73
Q

What is a normal glucose range?

A

Between 4-6mmol/L

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74
Q

What hormone(s) lower blood glucose?

A

Insulin

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75
Q

What hormone(s) raise blood glucose?

A

Glucagon
Catecholamines
Somatotrophin
Cortisol

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76
Q

What are the different types of diabetes?

A

Type I diabetes mellitus
Type II diabetes mellitus
Maturity onset diabetes of the young

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77
Q

What is the most common type of diabetes?

A

Type II diabetes mellitus

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78
Q

What happens if the blood glucose falls below 2mM?

A

Unconsciousness, coma and death

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79
Q

How much of pancreatic cells are associated with exocrine secretions?

A

98%

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80
Q

How much of pancreatic cells are associated with endocrine secretions?

A

2%

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81
Q

What are the cells of the pancreas associated with endocrine function called?

A

Islets of Langerhans

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82
Q

What is the exocrine function of the pancreas?

A

Releases pancreatic juices into the intestine to aid digestion

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83
Q

What structure allow cell-cell communication between islets of Langerhans?

A

Gap junctions

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84
Q

What are the different cell types that make up the islets of Langerhans?

A

α-cells
β-cells
δ-cells

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85
Q

What do the different islets of Langerhans produce?

A

α-cells- Glucagon
β-cells- Insulin
δ-cells- somatostatin

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86
Q

What effect does somatostatin have on insulin and glucagon?

A

Decreases both

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87
Q

What does insulin do in utero?

A

Stimulates growth and development

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88
Q

What stimulates and inhibits the release of insulin from β-cells? (8)

A 
Stimulated by:
1) Glucagon
2) Certain gastrointestinal horomones
3) Certain amino acids
4) Increased blood glucose
5) β-receptors
6) Parasympathetic activity
Inhibited by:
1) α-receptors
2) Somatostatin
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89
Q

What effect do α-cells have on β-cells?

A

Secretes glucagon which stimulates β-cells to produce insulin

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90
Q

What effect do δ-cells have on β-cells?

A

Secretes somatostatin which inhibits β-cells from secreting insulin

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91
Q

What does insulin do?

A

1) Increased amino acid transport and increased protein synthesis
2) Decreased lipolysis
3) Increased lipogenesis
4) Increased glycogenesis
5) Increased glycolysis
6) Increased glucose transport into cells via GLUT4
7) Decreased blood glucose

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92
Q

What stimulates and inhibits the release of glucagon from α-cells? (7)

A 
Stimulated by:
1) Certain gastrointestinal hormones
2) Certain amino acids
3) Decreased blood glucose
4) Sympathetic activity
5) Parasympathetic activity
Inhibited by:
1) Insulin
2) Somatostatin
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93
Q

What effect do β and δ cells have on α cells?

A

Inhibit release of glucagon

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94
Q

What is the function of glucagon?

A

1) Increased hepatic glycogenolysis
2) Increased lipolysis which causes increased gluconeogenesis
3) Increased amino acid transport into liver which causes increased gluconeogenesis
Which all lead to increased blood glucose

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95
Q

What hormone is released after a meal?

A

Glucagon and insulin

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96
Q

What is glucokinase?

A

The “glucose sensor”
Converts glucose into glucose-6-phosphate
This is the rate limiting step

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97
Q

What occurs if there is an abnormality in glucokinase?

A

Glucose levels are higher and the feedback loop is defective

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98
Q

What transports glucose into cells?

A

GLUT2

Glucose transporter 2

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99
Q

What is proinsulin made up of?

A

Insulin and C-peptide

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100
Q

Measuring C-peptide can be diagnostic of what?

A

Diagnose a rare cancer of the pancreas
Insulinoma
Making insulin inappropriately

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101
Q

What is the mechanism of insulin release?

A

Occurs in β-cells

1) Glucose enters β-cell through GLUT2 and is converted to glucose-6-phosphate by glucokinase
2) The ATP produced blocks the ATP-sensitive K+ channels. 3) This causes an influx of Ca2+ through voltage-dependent K+ channels.
4) This causes the release of premade insulin and synthesis of insulin over the next couple of hours

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102
Q

What causes type II diabetes?

A

There are not enough cells so there is no premade insulin but it can be made over a few hours

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103
Q

What is the difference between stimulation of insulin with oral and iv glucose?

A

Someone who ingests glucose orally produces much more insulin than iv glucose

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104
Q

What is glucagon-like peptide-1 (GLP-1)?

A

A gut hormone that is secreted in response to nutrients. It stimulates insulin and suppresses glucagon.
Increases satiety
Mimics the effects of oral glucose

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105
Q

What gene transcribes GLP-1?

A

Proglucagon gene (mostly from L cells)

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106
Q

What enzyme degrades GLP-1?

A

Dipeptidyl peptidase-4

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107
Q

What is first phase insulin release?

A

The release of stored insulin

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108
Q

What does first phase insulin release do?

A

Switches off hepatic glucose output and prepares muscle for a second phase of insulin

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109
Q

If you have no first phase insulin response what does this mean in terms of diet and insulin?

A

No stored insulin
Problem dealing with refined carbohydrates
Complex carbohydrates are slow release so give them time to respond

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110
Q

What cells can take up insulin without using a receptor?

A

Brain and red cells

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111
Q

What tissues does insulin go to?

A

Liver
Muscle
Adipocytes

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112
Q

How does the insulin receptor work?

A

1) Insulin from the interstitial fluid binds to the α-subunit of the insulin receptors.
2) β-subunits cross the membrane and tyrosine kinase domains allow for post-receptor signalling of the metabolic pathways of insulin
3) This recruits GLUT4 allowing glucose transport into a cell

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113
Q

What is the function of insulin? (8)

A

1) Glucose
- Decrease hepatic glucose output
- Increase muscle uptake
2) Protein
- Decrease proteolysis
3) Lipid
- Decrease lipolysis
- Decrease ketogenesis
4) Growth
5) Vascular effects
6) Ovarian function
7) Clotting
- PAI-1
8) Energy expenditure
- Relation to leptin

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114
Q

Where is the GLUT4 receptor located?

A

Muscle and adipose tissue

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115
Q

How much does the GLUT4 receptor increase glucose uptake?

A

7 times

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116
Q

Insulin plus insulin-like growth factor cause what?

A

Protein synthesis

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117
Q

Lack of insulin and what hormone cause breakdown of protein?

A

Cortisol

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118
Q

What happens to amino acids produced during proteolysis?

A

Enter the circulation and transported to the liver where they are used to support hepatic glucose output

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119
Q

What does insulin do to proteolysis when eating a meal?

A

Stops the breakdown of protein

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120
Q

When is glucose present in the blood?

A

All the time

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121
Q

Where is glycogen found? What is it?

A

In the liver

Stored glucose

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122
Q

What effect does glucagon have on gluconeogenic amino acids entering the liver?

A

Makes it happen at a faster rate

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123
Q

When does gluconeogenesis occur?

A

In the fasting state

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124
Q

If you have eaten a meal what does insulin do in muscle?

A

Stops the breakdown of protein and increases protein production with IGF-1

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125
Q

In the fasting state what happens to the amino acids produced from proteolysis? What are they called? What hormones cause this process?

A

They are transported to the liver for gluconeogenesis
Gluconeogenic amino acids
Cortisol and lack of insulin

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126
Q

What is the process of gluconeogenesis?

A

1) Gluconeogenic amino acids are transported to the liver and glucagon causes them to enter the liver at a greater rate
2) Glucagon (+protein deficiency) causes protein to be broken down into amino acids in the liver
3) Glucagon, catecholamines and cortisol (counter-regulatory hormones) cause amino acids to be converted into glucose
4) This supports hepatic glucose output

Also two glycerol molecules in the liver are joined together to make glucose

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127
Q

How long does carbohydrate last as an energy store?

A

It is a store term energy store (16 hours)

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128
Q

How long does protein last as an energy store?

A

15 days (intermediate energy store)

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129
Q

How long does fat last as an energy store?

A

It is a long term energy store (30-40 days)

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130
Q

What is the mechanism by which insulin causes storage of glucose in adipocytes?

A

1) Triglyceride in blood vessel is broken down by lipoprotein lipase and insulin into fatty acids and glycerol (which is left in the blood)
2) The non-esterified fatty acids (NEFA) then enter the adipocyte
3) Glucose enters the adipocyte using a GLUT4 receptor and is broken down to glycerol-3-phospahate
4) Insulin causes these two molecule to join and form triglyceriade
Glucose can also be converted into NEFA.

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131
Q

What can be used to measure the risk of ischaemic heart disease?

A

Waist circumference

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132
Q

Adipocytes where are more metabolically and endocrinologically active than peripheral adipocytes?

A

In the gut

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133
Q

After a 10 hour fast, how much of your hepatic glucose output comes from hepatic gluconeogenesis?

A

25%

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134
Q

What is the mechanism for production of ketone bodies? When does this occur? Where and why?

A

Occurs in the liver
1) NEFA enter the liver and are converted into Fatty acyl CoA
2) They enter mitochondria stimulated by glucagon
3) Acetyl CoA converted to Acetoacetate
4) Acetoacetate converted to Acetone + 3 hydroxybutyrate (3 OH-B
5) Ketone bodies are produced
They are used as fuel for the brain in the fasting state

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135
Q

What is the cause of high blood sugar and ketones in their urine?

A

They have insulin deficient diabetes

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136
Q

What is the process of hepatic glycogenesis?

A

1) Glucose enters the liver and is converted into glucose-6-P
2) Insulin causes glucose-6-phosphate to be converted into glycogen

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137
Q

What is the process of glycogenolysis?

A

1) Glucagon and catecholamines break down glycogen into glucose-6-phosphate
2) Glucose-6-phosohate is converted into glucose

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138
Q

How does glucose enter muscle?

A

Insulin recruits GLUT4 transporters allowing it to enter

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139
Q

What happens to glucose once it is taken up into muscle after eating?

A

It is converted and stored as glycogen or it is converted into acetyl CoA where is is oxidised (β-oxidation) when muscles are used to provide energy

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140
Q

What happens to a healthy individual when they fast?

A

1) Low insulin: higher glucagon ratio
2) Glucose between 3-5.5mmol/l
3) ↑ [NEFA] (lipolysis occurs)
4) ↓ [amino acid] when prolonged (don’t want to lose all protein)
5) ↑ Proteolysis
6) ↑ Lipolysis
7) ↑ Hepatic glucose output from glycogen and gluconeogenesis
8) Muscle uses lipid for energy
9) Brain uses glucose but will move to ketones
10) ↑ Ketogenesis when prolonged (made from fatty acids

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141
Q

What happens in the fed state after eating a meal?

A

1) Stored insulin released then second phase
2) High [insulin] to [glucagon] ratio (glucose entering gut causes insulin secretion, glucose in circulation causes B-cells to make more insulin
3) Stop hepatic glucose output
4) ↑ Glycogen (store glucose)
↓ gluconeogenesis
5) ↑ protein synthesis (store amino acids)
6) ↓ Proteolysis
7) ↑ Lipogenesis (store fatty acids and glycerol

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142
Q

What occurs in type 1 diabetes?

A

1) No insulin produced
2) Protein is broken down, and amino acids released from muscle
3) Fat stores are broken down (lipolysis)
4) High hepatic glucose output and ketones made from the liver due to low insulin
5) High blood glucose
6) Glycosuria (>10mmol/l leaks out into the urine bringing the water with it- osmotic diuresis- takes ions out too)
7) Ketonuria

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143
Q

What would you find in the urine of an undiagnosed diabetic?

A

Ketones
Glucose
Smell of acetone

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144
Q

What occurs metabolically in insulin-induced hypoglycaemia?

A

1) ↑ insulin (can’t be switched off)
2) ↑ glucagon
3) ↑ Catecholamines
4) ↑ Cortisol
5) ↑ Growth hormone
6) Glucose does enter muscle
7) ↑ hepatic glucose output later with glycogenolysis and gluconeogenesis (patient will recover if they have stored glycogen)
8) ↑ Lipolysis

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145
Q

What would need to be administered if a patient induces hypoglycaemia by injecting too much insulin?

A

Intramuscular glucagon

injected

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146
Q

Where are the main sites of insulin resistance in type II diabetes?

A

Liver
Muscle
Adipose tissue
(where there are metabolic effects of insulin)

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147
Q

Would a person with type II diabetes mellitus have ketogenesis and proteolysis?

A

No

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148
Q

What two symptoms does a patient with type I diabetes that differentiates them from type II diabetes?

A

Ketogenesis

Proteolysis

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149
Q

What effect does insulin resistance have on the mechanism of insulin binding to it’s receptor?

A

T2D inhibits the PI3K-Akt pathway so insulin can’t work and B-cells make more insulin to keep the glucose normal
Homeostatic loop is based on glucose so increased insulin concentration causing compensatory hyperinsulinaemia
A second pathway involved in the insulin receptor is not inhibited in type II diabetes: the MAPK pathway which leads to growth and proliferation

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150
Q

What are the two effects caused by insulin action in T2D?

A

Metabolic (insulin resistance effect)

Mitogenic on growth (hyperinsulinaemia effect)

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151
Q

What are the metabolic effects of insulin resistance in T2D?

A

1) Lowers glucose
2) Stops breakdown of protein
3) Stops breakdown of lipid

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152
Q

What are the mitogenic effects of hyperinsulinaemia in T2D?

A

1) Dyslipidaemia
2) Smooth muscle hypertrophy (hypertension causing ischaemia heart disease)
3) Ovarian function (polycystic ovary disease)
4) Clotting
5) Energy expenditure

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153
Q

What are the symptoms of T2D associated with insulin resistance?

A

1) High [TG] Low [HDL] (dyslipidaemia)
2) Insulin resistance (hyperglycaemia). Fasting glucose (>6.0mmol/l)
3) 60-80% obese. Waist circumference (Men >102, Women >80)
4) Hypertension (>135/80)
5) Insulin resistance, adipocytokines, inflammatory state, energy expenditure
6) Less osmotic symptoms

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154
Q

What dietary changes improve T2D?

A

1) Reduce fat
2) Reduce refined carbohydrate
3) Increase complex carbohydrate
4) Increase soluble fibre
5) Decrease sodium (helps hypertension)

155
Q

Where is the thyroid gland? How big is it?

A

Sits in the neck over the trachea

∼20g

156
Q

What structures make up the thyroid gland?

A

Follicles

157
Q

What is the structure of a follicle in the thyroid?

A

Colloid in the centre surrounded by follicular cells

158
Q

What cells are found in between follicles in the thyroid?

A

Parafollicular cells

159
Q

What is the colloid in the thyroid?

A

A large three month store of iodothyronines still bound to protein

160
Q

What are iodothyronines?

A

Hormones produced in follicles in the thyroid

161
Q

How much higher is iodide in follicular cells than in the blood?

A

25-50 times higher

162
Q

How does the brain stimulate the release of thyroid stimulating hormone?

A

Brain releases thyrotrophin releasing factor which stimulates a release of thyrotrophin (TSH) and prolactin from the anterior pituitary

163
Q

What is the mechanism of release of T3 and T4 from follicular cells?

A

1) TSH (thyrotrophin) binds to TSHR and activates the Na+/I- symporter (NIS). Na+ and I- enter the follicular cell
2) TSH stimulates thyroglobulin production (a genomic pathway) which is then secreted into colloid (2 amino acid strands linked)
3) Thyroid peroxidase enzyme + hydrogen peroxide activates I- → I. I and tyrosil amino acids aligns the thyroglobulin molecule to bind in one or two specific places to form mono/di-iodotyrosils
4) Coupling reaction→ reconfiguration of MIT/DIT-link together → tyrosine T3 or T4
5) When T3/T4 needed TSH facilitates transfer to the blood- endocytosis into cell and proteases and deiodinases remove protein, then transferred into the blood

164
Q

What precursor molecules produce one thyroxine molecule?

A 
Thyroxine= T4
Two DIT (diiodotyrosine)
165
Q

What precursor molecules produce one T3 molecule?

A

DIT + MIT

Diiodotyrosine + monoiodotyrosine

166
Q

How are T3 and T4 mostly transported around the body?

A

Bound to plasma proteins

167
Q

What plasma proteins transport T3 and T4 around the body? And what percentages are carried on each protein?

A

TBG (Thyroxine-binding globulin) ∼70% T4 and ∼80% T3
Albumin ∼10% T4 and ∼15% T3
Prealbumin ∼15% T4 and ∼2% T3

168
Q

How much T3 and T4 is unbound?

A

Only 0.05% T4 and 0.5% T3 unbound (bioactive components

169
Q

What are the latent periods of T3 and T4?

A

T3 around 12 hours

T4 around 72 hours

170
Q

What are the biological half-lives of T3 and T4?

A

T3 around 2 days

T4 around 7-9 days

171
Q

What is a latent period or a hormone?

A

The time it takes from entering the blood to produce a biological effect

172
Q

What is the main hormone product of the thyroid gland?

A

T4

173
Q

What happens to T4 to make it more bioactive, and what is the product of this process? Where does this occur?

A

Deiodinated to produce T3

Occurs in target tissue

174
Q

What is the biologically inactive product that can be produced from T4? What process produces this?

A

Deiodination in a different position

Produces reverse T3 (rT3)

175
Q

When is more rT3 produced than T3? Why is this?

A

In starvation, because the processes that thyroid hormones work on are not needed

176
Q

What are the main actions of iodothyronines?

A

1) Increase basal metabolic rate
2) Increase protein, carbohydrate and fat metabolism
3) Potentiate some of the actions of the catecholamines (e.g. tachycardia, glycogenolysis, lipolysis)
4) Interact with other endocrine systems (e.g. oestrogens)
5) Have effects on the CNS
6) Increase vitamin A (and retinal) synthesis

177
Q

What is BMR?

A

Basal Metabolic Rate

The level of metabolic activity going on when you are inactive

178
Q

What is the name of the condition associated with lack of iodothyronines during foetal development and after birth?

A

Cretinism

179
Q

What is the mechanism of action of iodothyronines?

A

1) T4 is converted to T3 (as more bioactive)
2) Transport systems pump them into the cell
3) Main way they work is genomic: bind to chromosomes, switch different genes for enzymes on and off for different metabolic processes

180
Q

What is the process from brain to thyroid for release of T3 and T4?

A

1) Hypothalamus: TRH (Thyrotrophin releasing hormone)
↓
2) Adenohypophysis: thyrotrophin (TSH)
↓
3) Thyroid gland: Iodothyronines (T3 and T4)

181
Q

What feedback mechanisms are involved in the production of T3 and T4?

A

Thyrotrophin gives auto negative feedback to the hypothalamus
T3 and T4 give direct negative feedback to the adenohypophysis and indirect negative feedback to the hypothalamus

182
Q

What effect does somatostatin have on thyrotrophin?

A

Inhibitory

183
Q

What effect do glucocorticoids have on production of iodothyronines?

A

Inhibits production

184
Q

What nerves are found near the thyroid and would change the voice and prevent breathing if damaged?

A

Internal branch and external branch of superior laryngeal nerve

185
Q

What is the function of the parathyroid glands?

A

Involved in calcium metabolism and nothing to do with thyroid function

186
Q

What is the origin of the thyroid in utero?

A

Foramen caecum at the back of the tongue

Descends bringing with it the parathyroid gland

187
Q

Where is the foramen caecum?

A

The dimple at the back of the tongue (disappearing thyroglossal duct

188
Q

How many lobes make up the thyroid?

A

4

189
Q

At what week is the thyroid in it’s final position in utero?

A

Week 7

190
Q

Which lobe of the thyroid is larger?

A

Right

191
Q

How big is each lobe?

A

4 x 2.5 x 2.5 cm

192
Q

What are the three problems that can occur with thyroid development?

A

1) Agenesis
2) Incomplete descent
3) Thyroglossal cyst

193
Q

What is thyroid agenesis? What is the prognosis?

A

Complete absence of thyroid

Cannot survive for long

194
Q

What causes a thyroglossal cyst?

A

Segment of thyroglossal duct persists and presents as a lump years later

195
Q

What is a lingual thyroid? What problems can it cause and what is the treatment?

A

Thyroid in the wrong place

Can prevent swallowing but if removed will be on thyroxine for life

196
Q

What is a cretin?

A

Neonates with thyroxine deficiency in utero who have irreversible brain damage

197
Q

What are the feature of an elderly cretin?

A 
Short
Low IQ (60-70)
198
Q

How is cretinism prevented in the UK? What would it show?

A

All babies have a heel prick test for thyroid function (measuring TSH) and a Guthrie test (for phenylketoneuria) at 5-10 days of age
Given thyroxine immediately if TSH is found to be high

199
Q

Where is thyroglobulin found?

A

Inside thyroid glands

200
Q

What is the main function of the thyroid?

A

Regulates your BMR
Responsible for synthesis, storage and secretion of thyroid hormones
Regulates growth, development and metabolic rate

201
Q

How many people are affected by thyroid disease?

A

5% of the population

202
Q

What is the female:male ratio of people with thyroid disease?

A

4:1

203
Q

What is myxoedema?

A

Primary hyperthyroidism

204
Q

What is primary hyperthyroidism? What causes it and what happens to thyroxine and TSH levels if you have it?

A

Primary thyroid failure
Autoimmune damage to thyroid (or operation)
Thyroxine levels decline
TSH levels climb (to stimulate thyroxine release)

205
Q

Why are TSH levels high in primary hypothyroidism?

A

Normally TSH produces thyroxine which feeds back to hypothalamus and pituitary to switch off TSH production. This doesn’t happen so TSH continues to be produced

206
Q

What are the symptoms of primary hypothyroidism?

A 
Deepening voice
Depression and tiredness
Cold intolerance
Weight gain and reduced appetite
Constipation
Bradycardia (
207
Q

What is the treatment for hypothyroidism?

A

Take thyroxine daily

Monitor TSH and adjust dose until TSH is normal

208
Q

What is thyrotoxicosis?

A

Hyperthyroidism

209
Q

What is hyperthyroidism? What happens to thyoxine and TSH if you have it?

A

Overactive thyroid gland
Thyroxine is high
No TSH

210
Q

What are the symptoms of hyperthyroidism?

A 
Make too much thyroxine
Raised BMR
Raised temperature (pyrexia)
Burn up calories and lose weight
Increased heart rate
Diarrhoea
Mood swings
Tremor of hands
Goitre (swelling of the neck due to enlarged thyroid)
Sore eyes
Every cell in the body speeds up
211
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

212
Q

How would you diagnose Grave’s disease?

A

Radioactive iodine scan

The whole gland will take in iodine which shows it is overactive

213
Q

What is Grave’s disease?

A

An autoimmune disease where antibodies bind to and stimulate the TSH receptor in the thyroid
Causes goitre (smooth) and hyperthyroidism
Antibodies bind to muscles behind the eye and cause exophthalmos
Antibodies stimulate growth of the shins and cause pretibial myxoedema (hypertrophy)

214
Q

What is pretibial myxoedema?

A

Swelling (non-pitting) that occurs on the shins of patients with Grave’s disease: growth of soft tissue

215
Q

What is the structure of an adrenal gland?

A 
Adrenal medulla (sympathetic nervous system)
Adrenal cortex:
Zona glomerulosa
Zona fasciculata
Zona reticularis
216
Q

What is produced in the adrenal medulla?

A

Catecholamines

217
Q

What is produced in the adrenal cortex?

A

Corticosteroids

218
Q

What are the cells of the adrenal medulla?

A

Chromaffin cells

219
Q

What are the percentages of catecholamines produced in the adrenal medulla?

A

Adrenaline 80%
Noradrenaline 20%
Dopamine

220
Q

What are the types of corticosteroid produced in the adrenal cortex?

A

Mineralocorticoids: Aldosterone
Glucocorticoids: Cortisol
Sex steroids: Androgens and oestrogens

221
Q

What type of corticosteroid is cortisol?

A

Glucocorticoid

222
Q

What two enzymes are involved in production of both aldosterone and cortisol?

A

21 hydroxylase

11β-hydroxylase

223
Q

What is the starting molecule for production of aldosterone, cortisol, androgens and oestrogens?

A

Cholesterol

224
Q

How is cortisol transported in the blood? (include percentages)

A

75% Cortisol/corticosteroid binding globulin (CBG or transcortin)
15% Albumin
10% Free → bioactive

225
Q

How is aldosterone transported in the blood?

A

60% bound to Corticosteroid binding globulin (CBG)

40% Free → bioactive

226
Q

When are cortisol levels higher? In the morning or afternoon? What are the values?

A

Cortisol is much higher in the morning than at night (biological rhythm)

8am: 140-690nmol/l
4pm: 80-330nmol/l

227
Q

How do aldosterone levels vary in an individual?

A

Aldosterone has varying levels when upright compared to supine

228
Q

What are the differences in circulating levels of cortisol and aldosterone?

A

1000 times more cortisol than aldosterone

229
Q

What does aldosterone do?

A

Regulates Na+ concentration in the blood controlling blood pressure
Stimulates Na+ reabsorption in distal convoluted tubule and cortical collecting duct (in sweat glands, gastric glands and colon)
Stimulates K+ and H+ secretion in same locations

230
Q

What is the mechanism of action of aldosterone?

A

1) Enters cell and binds to receptor in the cytoplasm forming a complex
2) Complex enters the nucleus and binds to genes along chromosomes: activates or deactivates genes and regulates protein synthesis
3) Increases Na+K+ pump in basolateral membrane
4) Increases synthesis of Na+, K+ and H+ ion channels on apical membrane
5) Increases reabsorption of Na+

231
Q

What are macula densa cells responsive to?

A

Changes in Na+ concentration in the tubular fluid in the loop of Henle

232
Q

What stimulate renin release? Explain

A

1) Decreased renal perfusion pressure (decreased pressure in the afferent arterioles will stimulate release- associated with decreased ABP)
2) Increased renal sympathetic activity- direct to JGA cells (↓ BP will amplify the effects of decreased BP and assist in causing renin release)
3) Decreased Na+ load to top of loop of Henle (macula dense cells pick up decreased Na+ causing renin release)

233
Q

What is renin?

1) Prohormone
2) Enzyme
3) Hormone
4) Product of Angiotensin cleavage
5) Molecule produced by adrenals

A

2) Enzyme

234
Q

What is the process of the renin-angiotensin-aldosterone system?

A

1) Liver produces plasma proteins which are released into the circulation (Angiotensinogen)
2) ↓ BP stimulates juxtaglomerular cells (and sympathetic nervous system) to release renin
3) Renin converts angiotensinogen into angiotensin I
4) ACE (angiotensin converting enzyme) is produced in the lungs and converts angiotensin I to angiotensin II
5) Angiotensin II stimulates zona glomerulosa in adrenal cortex to release aldosterone
6) Angiotensin II is also a very powerful vasoconstrictor
= ↑BP

235
Q

What does cortisol stimulate in a normal stress response?

A

METABOLIC EFFECTS
- Peripheral protein catabolism
- Hepatic gluconeogenesis
- ↑ blood glucose
- Fat metabolism (lipolysis in adipose tissue)
- Enhanced effects of glucagon and catecholamines
SOME MINERALOCORTICOID EFFECTS (in large amounts)
RENAL AND CARDIOVASCULAR EFFECTS (e.g. excretion of water load, increased vascular permeability)
Other effects (e.g. on bone, CNS, growth etc)

236
Q

What is the pharmacological effect of large amounts of cortisol?

A

1) Anti-inflammatory
2) Immunosuppressive action (used in transplant)
3) Anti-allergic action
4) ↓ production of prostaglandins, leukotrienes, histamine etc

237
Q

What syndrome is associated with excess cortisol?

A

Cushing’s

238
Q

What receptors bind cortisol?

A 
Glucocorticoid receptors (GR)
Aldosterone receptors (MR)
239
Q

How does the binding affinity of cortisol compare to the binding affinity of aldosterone for aldosterone receptors?

A

Equal binding affinity

240
Q

How does the body overcome the significantly higher levels of cortisol preventing aldosterone binding it’s receptor?

A

11β-hydroxysteroid dehydrogenase 2 (enzyme) converts cortisol into inactive cortisone to prevent is swamping receptors

241
Q

What is the mechanism of release from brain to gland of cortisol, including the feedback mechanisms?

A

1) Stress stimulates the release of corticotrophin releasing hormone (CRH) and vasopressin (VP) from the hypothalamus and they are transported to the adenohypophysis
2) This stimulats a release of corticotrophin (ACTH)
3) ACTH stimulates production of cortisol from adrenal cortex
Feedback
ACTH has auto negative feedback to the hypothalamus
Cortisol has direct negative feedback to the pituitary and indirect negative feedback to the hypothalamus

242
Q

What is the mechanism of action of cortisol?

A

1) Enters cell and binds to receptor in the cytoplasm forming a complex
2) Complex enters nucleus and targets over 200 genes
3) Synthesises new proteins such as Annexin 1 which has an autocrine effect

243
Q

What is Cushing’s syndrome?

A

Elevated levels of ACTH in the body
↑ corticotrophin so ↑ POMC and ↑ ACTH
Also ↑ melanocyte stimulating hormone

244
Q

What is dehydroepiandrosterone? (DHEA)

A

A precursor for androgens and oestrogens which is converted into active hormones within target cells (which have the appropriate enzymes)

245
Q

What is Addison’s disease?

A

Primary adrenal failure
UK: Autoimmune disease where immune system destroys the adrenal gland
Worldwide: Tuberculosis of the adrenal glands

246
Q

How many veins supply the adrenal glands?

A

1

247
Q

Roughly how many arteries supply the adrenal glands?

A

50

248
Q

Where does the left adrenal vein drain into?

A

The right adrenal vein

249
Q

Where does the right adrenal vein drain into?

A

Inferior vena cava

250
Q

What is the risk associated with left adrenalectomy?

A

Cutting the spleen (a medical emergency)

Spleen must be removed if this occurs so vaccinated (Haemophilus B and pneumovax) beforehand

251
Q

How are protein hormones administered to a pateint?

A

Cannot be given by mouth as stomach destroys them so much be injected

252
Q

What hormone regulates the production of cortisol?

A

ACTH

253
Q

Why does high ACTH make you more tanned?

A

POMC (precursor to ACTH) is cleaved into ACTH, melanocyte stimulating hormone and endorphins
High ACTH means high MSH

254
Q

What are the symptoms of Addison’s disease?

A 
Cortisol deficiency
Increased pigmentation (even in the mouth- not a tan)
>50% adrenal atrophy
40% tuberculosis
Salt loss
Low blood pressure: feeling dizzy (no cortisol or aldosterone)
Loss of appetite
Very weak
Autoimmune vitiligo may coexist
Eventually fatal
255
Q

Why do people with Addison’s have pigmentation?

A

When you don’t have enough cortisol you don’t have any negative feedback so the pituitary starts making more ACTH. This also produces more MSH which causes pigmentation

256
Q

What is the urgent treatment of Addison’s disease?

A 
Rehydrate with normal saline
Give dextrose (or glucose) to prevent hypoglycaemia which could be due to the glucocorticoid deficiency
Give hydrocortisone indefinitely (or another glucocorticoid to replace missing hormone)
257
Q

What are the biological actions of excess cortisol? (10)

A

1) Impaired glucose tolerance (diabetes)
2) Weight gain (increase fat, lose protein)
3) Thin skin and easy bruising
4) Striae (stretch marks)
5) Proximal myopathy (muscle weakness)
6) Mental changes (depression)
7) Hypertension
8) Fat redistribution
9) Moon face
10) Buffalo hump (interscapular fat pad)

258
Q

List four of the possible causes of Cushing’s syndrome

A

1) Taking steroids by mouth (common)
2) Pituitary-dependent Cushing’s disease (pituitary adenoma)
3) Ectopic ACTH (lung cancer) (from the wrong place)
4) Adrenal adenoma or carcinoma

259
Q

What is the clinical presentation of Cushing’s?

A 
Thin skin
Proximal myopathy
Centripetal obesity (lemon on sticks)
Diabetes, hypertension and osteoporosis
Immunosuppression (reactivation of TB and other cause of sepsis)
Moon face
260
Q

What are the side effects of “steroids”?

A 
Hypertension
Diabetes
Osteoporosis
Reactivation of infection (immunosuppression)
Easy bruising
Poor wound healing, thin skin
Myopathy
261
Q

What is Conn’s syndrome?

A

An aldosterone-producing adenoma

Tumour on the outside of the adrenal gland can make aldosterone autonomously

262
Q

What are the symptoms of Conn’s syndrome?

A

Hypertension (that doesn’t respond to treatment)
Oedema
Hyperkalaemia

263
Q

What is spermatogenesis?

A

Production of mature spermatozoa

264
Q

What is oogenesis?

A

Production of ripe ova

265
Q

What steroid hormones are produced in males?

A

Main: Androgens

Small amounts: oestrogens and progestogens

266
Q

What steroid hormones are produced in females?

A

Main: Oestrogens and progestogens

Small amounts: Androgens

267
Q

During activation of germ cells, when are the maximum number of germ cells?

A

Week 24, then atresia

268
Q

What happens to germ cells after birth?

A

They are quiescent until puberty

269
Q

How many germ cells do men have throughout life?

A

Stays at the same amount throughout life

∼6million

270
Q

How many germ cells do women have thoughout life?

A 
Start with ∼6 million during gametogenesis. Atresia occurs:
At time of birth ∼2 million
Around 400,000 eggs at puberty
Depleted at menopause
Only 300-400 eggs mature to be released
271
Q

How long does spermatogenesis take?

A

70 days

272
Q

What is the process of spermatogenesis?

A

GERM CELL: 44+XY (multiply and differentiate to produce)
SPERMATOGONIA: 44+XY (mitotic division)
PRIMARY SPERMATOCYTES: 44+XY (first meiotic division)
SECONDARY SPERMATOCYTES: 22X or 22Y (second meiotic division)
SPERMATIDS: 22X or 22Y
SPERMATOZOA: 22X or 22Y

273
Q

In males, what triggers gametogenesis at puberty?

A

Raised levels of FSH and testosterone

274
Q

When does atresia occur in women?

A

All the time

275
Q

What is the process of oogenesis?

A

GERM CELL: 44XX
OOGONIA: 44XX (mitotic division)
PRIMARY OOCYTES: 44XX (first meiotic division)
SECONDARY OOCYTES: 22X (and 22XX) (+ first polar body) (second meiotic division)
OVUM (+second polar body): 22X (and 22X)

276
Q

At what stage of development are female gametes at the time of birth?

A

It is a primary oocytes arrested in prophase of meiosis

277
Q

When ovulation occurs, at what stage of development is the female gamete?

A

It is a secondary oocyte

278
Q

When does a female gamete become an ovum?

A

After fertilisation

279
Q

What is a polar body?

A

Following a meiotic division the genetic material is halved equally but the cytoplasm is not. One egg keeps the majority of the cytoplasm and continues with oogenesis, the polar body undergoes atresia

280
Q

When do testes descend into scrotum? Why is this important?

A

At birth
Scrotum a few degrees below body temperature- essential for spermatogenesis
If testes don’t descend = infertility

281
Q

What are coiled seminiferous tubules?

A

Found in the testes
Lined with spermatogonia and Sertoli cells
Spermatozoa are produced, then drained into ducts and concentrated

282
Q

Where are the sperm concentrated?

A

In the rete testis

283
Q

What is the structure of a seminiferous tubule? How does this structure relate to spermatozoa development?

A
  • Spermatogonia around the outside of the tubule
  • Protected and given nutrients to help them develop into primary and secondary spermatocytes then they move into a tight junction and towards the lumen
  • Develop into spermatids in fold of Sertoli cells then move into the lumen for drainage
284
Q

What are the steroidogenic cells in the testes?

A

Leydig cells (found in between tubules)

285
Q

What is the function of Sertoli cells?

A

Provide physical and metabolic support for development

286
Q

What do Sertoli cells synthesise?

A

FSH

Androgen receptors

287
Q

What do Sertoli cells produce in response to FSH?

A

Various molecules including inhibin

288
Q

What does inhibin do?

A

Has a feedback effect on the pituitary and hypothalamus and produces androgen binding globulin

289
Q

What do Leydig cells synthesise?

A

LH receptors

290
Q

What do Leydig cells do in response to LH?

A

Are the principal source of testicular androgens (mainly testosterone)

291
Q

What is the structure of the ovary?

A

Ovarian stroma contains follicles which are undergoing atresia
Also contains remnants of the last corpus luteum
Contains the graffian follicle embedded in the stroma of the ovaries

292
Q

What is the structure of the graffian follicle?

A

Follicular fluid containing the ovum
Surrounded by granulosa cells
Surrounded by thecal cells

293
Q

How long is the menstrual cycle?

A

Usually 28 days

20-35+

294
Q

When does the menstrual cycle begin?

A

On the first day of menstruation

295
Q

On what day of the menstrual cycle does ovulation occur?

A

Around day 14

296
Q

What two cycles make up the menstrual cycle?

A

Ovarian cycle and endometrial cycle

297
Q

What two phases make up the ovarian cycle?

A

Follicular phase

Luteal phase

298
Q

How are the ovarian cycle and endometrial cycle linked? (2)

A

1) During the follicular phase oestrogen (17β-oestradiol) is released which causes the proliferative phase of the endometrial cycle (making it thicker and increasing receptors)
2) In the luteal phase progesterone and 17β-oestradiol are release which causes the secretory phase (reduces the proliferative effect of oestradiol by reducing receptors)

299
Q

What is the function of FSH in the ovarian cycle?

A

Stimulates recruitment of follicles which start developing and producing oestradiol

300
Q

What is the function of LH?

A

Triggers ovulation

301
Q

What causes a change in the levels of 17β-oestradiol and progesterone in the ovarian cycle?

A

Empty follicle converts to corpus luteum and produces large amounts of oestradiol and progesterone
If ovum is not fertilised in luteal phase the levels will drop- no loner negative feedback on gonadotrophins so levels start to rise

302
Q

Describe the development of follicles in the ovaries

A

1) Pre-antral follicle
2) Early antral follicle
3) Late antral follicle
4) Graffian follicle
5) Ovum + Corpus luteum

303
Q

Which follicle is selected for development and ovulation in the ovaries?

A

The follicle most sensitive to FSH

304
Q

How and were are hormones produced in the Graffian follicle?

A

1) LH binds to LH receptors in thecal cells and causes them to start synthesising steroids (only up to andorgen level)
2) Androgens diffuse into granulosa cells where they procude 17β-oestradiol

305
Q

What is the endometrial cycle?

A

Day 6-14: PROLIFERATIVE PHASE- dominant oestrogen influence (Endometrium thin, starts to thicken. Glands thin, begin to enlarge, coil, increase blood supply)
Day 15-28: SECRETORY PHASE- dominant progesterone influence plus oestrogen (Endometrium becomes secretory. Glands secrete glycogen, mucopolysaccharides, etc; mucose engorged with blood)
Day 1-5: SECRETORY PHASE- Endometrium becomes necrotic and is shed

306
Q

What occurs to testosterone to make it more potent? What does it form?

A

Reduction by 5α-reductase to the more potent dihydrotestosterone (DHT)

307
Q

In what tissues is testosterone converted to DHT? (men) (6)

A 
Prostate
Testes (seminiferous tubules)
Seminal vesicles
Skin
Brain
Adenohypophysis
308
Q

What occurs to oestrogens to make them more potent? What does it form?

A

Aromatisation by aromatase to produce 17β-oestradiol (E2)

309
Q

In what tissues is oestrogen converted into 17β-oestradiol? (men) (5)

A 
Adrenals
Testes (Sertoli cells)
Liver
Skin
Brain
310
Q

How are testosterone and DHT transported in the blood? Give percentages

A

Sex hormone binding globulin (60%)
Albumin (38%)
Free (2%) bioactive

311
Q

How are testosterone and DHT transported in seminiferous fluid?

A

Androgen binding globulin (ABG)

312
Q

What are the principal actions of androgens in a male foetus? (3)

A

1) Development of male internal and external genitalia
2) General growth- generally boys are bigger than girls at birth (acting with other hormones)
3) Behavioural effects (development)

313
Q

What are the principal actions of androgens in an adult man?

A

1) Spermatogenesis
2) Growth and development of : male genitalia, secondary (accessory) sex glands (seminal vesicles, blabourethral gland, prostate etc), secondary sex characteristics
3) Protein anabolism
4) Pubertal growth spurt (with GH)
5) Behavioural (CNS) effects
6) Feedback regulation

314
Q

What is an oestrogen?

A

Any substance (natural or synthetic) which induces mitosis in the endometrium

315
Q

What are the principal actions of oestrogens? (13)

A

1) Stimulate proliferation (mitosis) of the endometrium
2) Final maturation of follicle during follicular phase of menstrual cycle
3) Induction of LH surge resulting in ovulation
4) Effects on vagina and cervix
5) Stimulates growth of ductile system of breast
6) Decreased sebaceous gland secretion
7) Increases salt (and water) reabsorption
8) Increases plasma protein synthesis (hepatic effect)
9) Metabolic actions (e.g. on lipids: HDL and LDL)
10) Stimulates osteoblasts
11) Influences the release of other hormones (e.g. prolactin, thyrotrophin)
12) Behavioural effects
13) Feedback regulation (-ve and +ve)

316
Q

What is a progestogen?

A

Any substance (natural or synthetic) which induces secretory changes in the endometrium

317
Q

What are the principal actions of progestogens? (5)

A

1) Stimulates secretory activity in endometrium and cervix
2) Stimulates growth of alveolar system in breast
3) Decreases renal NaCl re-absorption (competitive inhibition of aldosterone)
4) Associates with increase in basal body temperature
5) Negative feedback regulation

318
Q

Where are steroid hormone receptors found?

A

In the nucleus

319
Q

What is the hypothalamo-pituitary-testicular axis?

A

1) Gonadotrophin-releasing hormone in the hypothalamus is released
2) Stimulates the release of LH and FSH from adenohypophysis
3) LH acts on Leydig cells in the testes to stimulate production of testosterone and stimulate Sertoli cells
4) FSH acts on Sertoli cells (+Leydig cells) to stimulate production of inhibin and (with testosterone) stimulate spermatogenesis
5) Testosterone also produces virilisation (male characteristics)
6) Testosterone and inhibin give direct -ve feedback to adenohypophysis and indirect -ve feedback to hypothalamus which slows the pulse generator

320
Q

What occurs in the early follicular phase of the ovarian cycle?

A

LH release starts the production of a few follicles

Oestrogens and progesterone are low at the beginning of the cycle

321
Q

Describe the hypothalamo-pituitary-ovarian axis in the early follicular phase

A

GnRH release
Stimulates release of LH and FSH
Stimulates the ovaries to produce oestrodiol which gives direct and indirect negative feedback

322
Q

What occurs in the early-mid follicular phase of the ovarian cycle?

A

Same as early follicular phase (LH release starts follicle production and progesterone and oestrogen low)
BUT oestrogen levels are beginning to rise

323
Q

What is the positive feedback loop seen in the ovary during the early-mid follicular phase?

A

LH binds LH receptors in thecal cells and produces androgens
FSH binds FSH receptor and produces aromatase
Androgens passed to neighbouring granulosa cells where aromatse converts then to 17β-oestradiol
17β-oestradiol binds to oestrogen receptors which produce more aromatase to produce more 17β-oestradiol

324
Q

What occurs in the mid-follicular phase of the ovarian cycle?

A

Lots of developing follicles under the influence of oestrogen
One follicle more developed than the others and autocrine effects produce enough oestrogen to be self suffiecient- no longer needs FSH to produce aromatase
Oestrodiol and inhibin -ve feedback causes FSH levels to fall
When FSH falls only the Graafian follicle will survive (and grow fast) others undergo atresia

325
Q

What occurs in the late follicular phase of the ovarian cycle?

A

If the high levels of oestrogen are maintained for 36 hours it causes final maturation of the ovum
LH surge caused by high oestrogen levels leads to ovulation (No LH surge = no ovulation)

326
Q

What hormone triggers ovulation?

A

LH

327
Q

What occurs in the luteal phase of the ovarian cycle?

A

Ovum has been released
LH and FSH must be high enough to produce oestrogen but now progesterone levels start to rise
At peak of luteal phase massive negative feedback effect (mainly due to progesterone)- switches off LH and FSH production
No stimulus for oestrogen and progesterone so their levels drop
No negative feedback ready for next cycle to start

328
Q

What causes menstruation?

A

If no fertilisation progesterone, oestradiol and inhibin exert a negative feedback on LH and FSH release leading to luteolysis (degradation of corpus luteum) and menstruation

329
Q

What is amenorrhoea?

A

Absence of menstrual cycles

330
Q

What is primary amenorrhoea?

A

Absence of menstrual cycles if have never happened

331
Q

What is secondary amenorrhoea?

A

Absence of menstrual cycles that have previously happened but have stopped

332
Q

What is oligomenorrhoea?

A

Infrequent menstrual cycles

333
Q

What are the roles of calcium in the body? (7)

A 
NEUROMUSCULAR EXCITABILITY
Muscle contraction
Strength in bones
Intracellular second messenger
Intracellular co-enzyme
Hormone/neurotransmitter stimulus-secretion coupling
Blood coagulation (factor IV)
etc
334
Q

How is most calcium present in the body? Where is it found

A

As calcium salts in bone (99%, ∼1kg)

335
Q

How much calcium is lost in the faeces and urine each day?

A

Faeces: ∼850mg/24hr
Urine: ∼150mg/24hr

336
Q

What is the total blood Ca2+ concentration?

A

∼2.5mM

337
Q

In what state is the Ca2+ in the blood?

A

50% free (biologically active) ∼1.25mM
45% bound to plasma proteins ∼1.13mM
5% as diffusable salts (e.g. citrate, lactate) ∼0.13mM

338
Q

What causes an increase in [Ca2+]?

A

1) Parathyroid hormone

2) Calcitriol- 1,25 (OH)2 Vitamin D3 (dihydroxycholecalciferol)

339
Q

What causes a decrease in [Ca2+]?

A

Calcitonin

340
Q

Where is PTH produced? What is it?

A

In the parathyroid glands

Parathyroid hormone

341
Q

How many parathyroid glands do you have?

A

4 (can have more or less)

342
Q

Where is calcitonin produced?

A

In parafollicular cells in between follicles in the thyroid

343
Q

What is the precursor molecule of PTH?

A

Pre-proPTH

344
Q

What type of receptor does PTH bind? What is it’s action once bound?

A

G-protein linked receptor

Activates adenyl cyclase but also phospholipase C as second messenger system

345
Q

What are the actions of PTH?

A

1) Increased bone resorption (stimulates osteoclasts and inhibits osteoblasts)
2) Increases Ca2+ reabsorption and PO43- (phosphate) excretion in the kidneys (reduced phosphate in urine increases calcium)
3) Stimulates 1α hydroxylase activity from the kidneys which increases synthesis of calcitriol
4) Calcitriol increased Ca2+ absorption and phosphate absorption in the small intestine

346
Q

What is calcitriol?

A

Hormone which regulates calcium and phosphate absorption in the intestine

347
Q

What effect does PTH have on the blood?

A

Increases Ca2+ from kidneys, small intestine and bone resorption so increases the [Ca2+] in the blood

348
Q

How does PTH act on bone?

A

PTH increases Ca2+ resorption from bone
No receptors on osteoclasts
PTH acts on osteoblasts- inhibits them and stimulates production of activating factor RANKL which stimulates osteoclasts

349
Q

What is the mechanism for regulation of PTH?

A

1) Ca2+ receptors respond to decreased plasma [Ca2+]
2) Ca2+ receptors and catecholamines stimulates parathyroid gland
3) Produces PTH
4a) PTH produces calcitriol
4b) Increased plasma [Ca2+]
5) -ve feedback to parathyroid gland

350
Q

What are the actions of calcitriol?

A

1) MAIN: Increased Ca2+ and phosphate absorption in the small intestine
2) Increased Ca2+ and decreased phosphate reabsorption in the kidneys
3) Increased osteoblast activity in bone

351
Q

What type of transporter is used for phosphate reabsorption?

A

Na+/PO43- cotransporter

352
Q

What effect do calcitriol and PTH have on Na+/PO43- cotransporter?

A

Both inhibit it

353
Q

What is the precursor molecule to calcitonin? What receptor does calcitonin bind to?

A

Synthesised from pre-procalcitonin

Binds to transmembrane G-protein linked receptor

354
Q

What are the actions and regulatory mechanisms of calcitonin?

A

1) Increased plasma [Ca2+] and gastrin stimulate the parafollicular cells of the thyroid to produce calcitonin
2) Calcitonin inhibits osteoclast activity
3) Calcitonin increases urinary excretion of Ca2+, Na+ and phosphate
4) Decreased plasma [Ca2+]

355
Q

What are endocrinological causes of hypocalcaemia?

A

1) Hypoparathyroidism
2) Pseudohypoparathyroidism
3) Vitamin D deficiency

356
Q

What is tetany?

A

Spontaneous muscle contraction

357
Q

Name three causes of hypoparathyroidism?

A

1) Idiopathic
2) Hypomagnesaemia
3) Suppression by raised plasma calcium concentration

358
Q

What is pseudohypoparathyroidism?

A

Target organ resistance to PTH (multiple underlying causes)

Believed to be due to defective Gs protein

359
Q

What are the features of pseudohypoparathyroidism?

A

1) Short stature, round face
2) Low IQ
3) Subcutaneous calcification and various bone abnormalities (e.g. shortening of metacarpals)
4) Associated endocrine disorders (e.g. hypothyroidism, hypogonadism)

360
Q

What happens to Plasma [Ca2+], Plasma [PO4] and PTH in hypoparathyroidism?

A

Plasma [Ca2+]: ↓
Plasma [PO4]: ↑
PTH: ↓

361
Q

What happens to Plasma [Ca2+], Plasma [PO4] and PTH in pseudohypoparathyroidism?

A

Plasma [Ca2+]: ↓
Plasma [PO4]: ↑
PTH: ↑

362
Q

What happens to Plasma [Ca2+], Plasma [PO4] and PTH in vitamin D deficiency?

A

Plasma [Ca2+]: ↓
Plasma [PO4]: ↓
PTH: ↓

363
Q

What is the disease associated with vitamin D deficiency in children and adults? What are the clinical features?

A

Children: Rickets
Adults: Osteomalacia
Clinical features: Decreased calcification of bone matrix resulting in softening of bone (bowing of bones in children; fractures in adults)

364
Q

What are three endocrinological causes of hypercalcaemia?

A

1) Primary hyperparathyroidism
2) Tertiary hyperparathyroidism
3) Vitamin D toxicosis

365
Q

What is the cause and mechanism of primary hyperparathyroidism?

A

Adenoma
Parathyroids produce PTH which causes ↑ [Ca2+] however negative feedback mechanism does not work as adenoma produces massive amounts of PTH so [Ca2+] continues to increase

366
Q

What is the cause and mechanism for tertiary hyperparathyroidism?

A

Persistent negative feedback causes the parathyroid to ignore the signal and become autonomous so Ca2+ increases

367
Q

What effect does PTH excess have on the kidneys?

A

1) ↑ Ca reabsorption
2) ↑ PO4 excretion
3) Polyuria
4) Renal stones
5) Nephrocalcinosis
6) ↑ calcitriol synthesis

368
Q

What effect does PTH excess have on the GI tract?

A

1) Gastric acid

2) Duodenal ulcers

369
Q

What effect does PTH excess have on bone?

A

1) Bone lesions
2) Bone rarefaction (reduction in density)
3) Fractures

370
Q

In what condition do you see clubbing of the fingers?

A

Primary hyperparathyroidism

371
Q

What causes short stature?

A

1) Genetics
2) Emotional deprivation
3) Growth hormone deficiency
4) Vitamin D deficiency
5) Cushings disease (excess cortisol)
6) Thyroid disorders (hypothyroidism causes slower growth)

372
Q

What is the difference in growth between boys and girls?

A

Boys are expected to be taller than girls

373
Q

How could you test growth hormone stimulation?

A

1) Insulin induced hyperglycaemia (Blood sample before and after)
2) GH released in large pulses throughout the day (Patient does vigourous exercise, blood sample before and after, should measure marked rise in hormone to check pituitary is releasing hormone)

374
Q

What happens to the osmolarity of urine during a water deprivation test?

A

Urine osmolality would increase since high blood glucose level exerts an osmotic pressure which draws water out of the plasma and into the renal filtrate. This leads to:

  • Polyuria: increased urine volume
  • Polydipsia: excessive thirst
375
Q

What is DDAVP? Why would the osmolarity of her urine rise after the administration of DDAVP?

A

DDAVP is vasopressin.
DDAVP stimulates water reabsorption in the principal cells of the renal collecting ducts. Increased water reabsorption in the renal collecting ducts causes the osmolality of her urine to rise. More normal result after administering DDAVP.

376
Q

A patient presents with a continuous unquenchable thirst and a need to urinate frequently. Her fasting serum glucose is normal. In a water deprivation test DDAVP gave more normal results. What is a likely diagnosis?

A

Sensitive to vasopressin since DDAVP has the desired physiological effects. Cause of disease is a lack of vasopressin due to any of the following:

  • Central diabetes insipidus: this results in the production of dilute urine (as opposed to diabetes mellitus or nephral diabetes insipidus)
  • Genetic disorder
  • Hypothalamic disorder which affects vasopressinergic neurones: e.g. due to trauma or a tumour
  • Hypophysial disorder: e.g. due to inflammation
377
Q

If someone has a lack of vasopressin what test should be conducted to diagnose the condition?

A

Vasopressin may be measured following stimulation of vasopressin release using hypotonic saline
Scan to ensure they do not have a tumour

378
Q

A patient has 2 months of weight loss, drinks 3.5L of water a day and passes the same amount of urine. Urine has ++++ glucose and ketones. Capillary blood glucose is 23mmol/l. What is the diagnosis?

A

Type I diabetes mellitus

379
Q

Why would someone with undiagnosed diabetes mellitus have glucose in their urine and a larger urine volume?

A

Lack of insulin – glucose uptake (via Glut 2 and glut 4) stopped, glycogenesis does not occur (glucose glycogen) therefore glucose remains in the plasma and is passed out in the urine
Increased glucose concentration in the urine exerts and increased osmotic pressure, therefore more water is drawn out into the urine (due to increased osmolarity) therefore urine volume increases

380
Q

A 58 year old has angina pectoris due to coronary artery disease. They are overweight and have a fasting glucose of 12mmol/l. What is the diagnosis and why?

A

Type II diabetes mellitus
BMI is obese. Plasma insulin concentration likely to be normal/high. Not caused by lack of insulin, but unresponsiveness to insulin. Body tries to compensate by increasing insulin secretion, but no effect

381
Q

What are important features in the diet of a patient with type II diabetes mellitus?

A 
Overall calorie control:
- Reduce fat calories
- Reduce refined carbohydrate calories
- Increase complex carbohydrate calories
- Increase soluble fibre
- Reduce sodium intake
Energy restriction will ensure that glucose is taken up into cells as a necessary energy source, therefore preventing hyperglycaemia
382
Q

If a patient has been diagnosed with type II diabetes mellitus and controls their diet what other factors would reduce their risk of CVD?

A

1) Physical activity
2) Weight loss
3) Quit smoking
4) Check BP
5) Can give drugs to lower lipid levels

383
Q

What signs and symptoms would you expect a patient with Addison’s disease to present with?

A

Pigmentation
Low blood pressure: feeling dizzy (no cortisol or aldosterone)
Loss of appetite
Very weak

LCRS Year 1 (2 decks)

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