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Year 1 LCRS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is an endocrine gland?

A

A group of cells which secrete messenger molecules into the bloodstream.

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2
Q

What is a hormone?

A

A bioactive messenger secreted by an endocrine gland into the blood.

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3
Q

What are the signalling differences between the endocrine and nervous system?

A

Endocrine:

  • Release chemical hormone into blood
  • Many target cells throughout body
  • Effect takes place over long period of time

Nervous:

  • Release chemical across synapse
  • Target cells must be innervated
  • Effect takes place within milliseconds.
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4
Q

What are the different endocrine glands/tissue in the body?

A

Brain, Hypophysis, Parathyroid, Thyroid, Heart, Liver, Pancreas, Adrenals, Kidneys, Adipose, Gonads, GI Tract, Placenta.

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5
Q

How are protein hormones produced?

A

Synthesised as pro-hormones. Processed in Golgi, and sent off in vesicles with enzymes. Pro-hormone is further processed in vesicles (by those enzymes).

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6
Q

How and where are steroid hormones produced?

A

Starting with cholesterol, stepwise enzymatic conversion in the mitochondria.

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7
Q

How does cholesterol get into the mitochondria?

A

With the help of stAR protein (steroidogentic Acute Regulatory). This is the limiting step in the synthesis of steroid hormone.

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8
Q

How do different tissues produce different steroid hormones?

A

The mitochondria in those tissues have different balances of enzymes.

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9
Q

Where are hormones stored after synthesis?

A

Protein hormones are stored in endocrine cells.

Steroid hormones are stored in the blood, bound by plasma proteins (such as Albumin).

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10
Q

How does ACTH increase steroid hormone production?

A

1) G-protein activation leads to conversion of ATP into cAMP through Adenyl Cyclase
2) cAMP activates enzyme Protein Kinase A
3) PKA phosphorylates esterases (allowing liberation of cholesterol) and stAR proteins (enhancing movement of cholesterol into mitochondria)

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11
Q

What are the differences in receptors for steroid and protein hormones?

A

Protein hormone receptors are on the plasma membrane. Steroid hormone receptors inside the cell.

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12
Q

By what bone structure is the hypophysis enclosed by?

A

The sella turcica

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13
Q

What is the main difference between the adenohypophysis and neurohypophysis?

A

Anterior pituitary is mainly secretory. Posterior pituitary is mainly full of nerve fibres.

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14
Q

How can neural clusters in the hypothalamus be organised?

A

By function, into hypothalamic nuclei.

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15
Q

What is the medial eminence?

A

It is the border of the pituitary stalk, where it meets the hypothalamus. It consists of a wall of capillaries called the primary capillary plexus.

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16
Q

How do hypothalamic neurosecretions reach the pituitary gland?

A

The neurosecretions are released into the hypothalamus-hypophsial portal system via the primary capillary plexus, which connects to the secondary capillary plexus through portal veins.

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17
Q

Why can you not detect hypothalamic secretions in blood?

A

The concentrations are very small

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18
Q

What are the different cell types in the adenohypophysis - and what do they produce?

A 
Somatotrophs - Somatotrophin
Lactotrophs - Prolactin
Thyrotrophs - Thyrotrophin
Gonadotrophs - LH and FSH
Corticotrophs - Corticotrophin (ACTH)
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19
Q

Where are adenohypophyseal hormones stored?

A

As they are protein hormones, they are stored in secretory granules.

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20
Q

What type of hormones are the adenohypophsial hormones?

A

Somatotrophin and Prolactin are proteins.
Thyrotrophin and the gonadotrophins are glycoproteins with an alpha and beta subunit. The alpha subunit is common to all.
Corticotrophin in a polypeptide (only 39 aa long)

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21
Q

What are the stimulatory and inhibitory hypothalamic hormones, along with their linked adenohypophyseal hormones?

A

(S) Somatotrophin Releasing Hormone / SRH and (I) Somatostatin control somatotrophin release.

(S) Thyrotrophin Releasing Hormone (TRH) and (I) Dopamine control thyrotrophin and prolactin release.

(S) Gonadotrophin Releasing Hormone (GnRH) and (I) Gonadotrophin Inhibitory Hormone (GnIH) control gonadotrophin release.

(S) Corticotrophin Releasing Hormone (CRH) and (I) Vasopressin control corticotrophin release.

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22
Q

What are the target cells of somatotrophin?

A

General body tissues, but specially the liver.

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23
Q

What are the target cells of prolactin?

A

Breast tissue

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24
Q

What are the target cells of thyrotrophin?

A

Thyroid cells

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25
Q

What are the target cells of gonadotrophin?

A

Testes and Ovaries

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26
Q

What is the general function of somatotrophin?

A

Growth and development

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27
Q

How does somatotrophin cause metabolic actions?

A

Causes secretion of Insulin-Like Growth Factors (IGF1 and IGF2). IGF1 is the main hormone that leads to metabolic actions.

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28
Q

What are the effects of somatotrophin?

A
  • Stimulation of amino acid transport into cells
  • Stimulation of protein synthesis
  • Increased bone and cartilage growth
  • Stimulation of lipid metabolism leading to fatty acid production
  • Decreased glucose utilisation
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29
Q

How are somatotrophin levels regulated?

A

+ Amino acids promote SRH secretion
+ Hypoglycaemia promotes SRH secretion
+ Exercise promotes SRH secretion
+ Oestrogen promotes SRH secretion
+ Stress promotes SRH secretion
+ Sleep stages III and IV promotes SRH secretion
+ Ghrelin from stomach promotes somatotrophin production
- Somatotrophin has NEGATIVE FEEDBACK on SRH production
- IGF1 has NEGATIVE FEEDBACK on somatotrophin and SRH production

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30
Q

What are the effects of prolactin?

A
  • Breast lactogenesis
  • Increases LH receptors in testes and ovaries
  • HIGH CONCENTRATIONS decreases LH release by decreasing GRH secretion from hypothalamus. Also decreases sexual behaviour.
  • Immune system, steroidogenesis and renal reabsorption effects.
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31
Q

How are prolactin levels regulated?

A

+ Suckling increases levels of TRH and inhibition of dopamine receptors
+ Oestrogens and Iodothyronines increase levels of TRH and secretion of prolactin.

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32
Q

Where do the cell bodies of the neurones in the neurohypophysis lie?

A

In the hypothalamus

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33
Q

Where do nerves from the paraventricular nucleus terminate?

A

Most (magnocellular) terminate in the neurohypophysis. Some (parvocellular) terminate in the primary capillary plexus. Few (parvocellular) terminate in the brain.

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34
Q

What hormones are released from the neurohypophysis?

A

Vasopressin and Oxytocin.

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35
Q

What is the suprachiasmic nucleus associated with?

A

Vassopressic neurones and circadian rhythm.

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36
Q

Which hypothalamic nuclei are associated with magnocellular neurones? What do they release?

A

Supraoptic and Paraventricular. These can either be vasopressinergic or oxitocinergic.

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37
Q

Where are hormones in magnocellular neurones stored?

A

Herring bodies

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38
Q

What are the components of the vasopressin and oxytocin pro-hormones?

A

Vassopressin Prohormone: Argenine Vasopressin, Neurophysin, Glycopeptide
Oxytocin Prohormone: Oxytocin, Neurophysin.

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39
Q

How do the structures of vasopressin and oxytocin differ?

A

Phenylalanine in Vasopressin is replaced with Isoleucine in Oxytocin
Arginine in Vasopressin is replaced by Leucine in Oxytocin.

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40
Q

What are the effects of vasopressin?

A

Stimulates water reabsorption from collecting ducts.
Vasoconstriction
Corticotrophin release
Affects CNS
Synthesis of blood clotting factors VIII and VWF
Hepatic glycogenolysis

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41
Q

Where are the three types of vasopressin receptors found?

A

V1a: Arterial smooth muscle, hepatocytes, CNS neurones
V1b: Adenohypophyseal corticotrophs
V2: Principle cells in nephron

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42
Q

How do V1 receptors work?

A

G-protein linked to phospholipase C. Leads to the production of IP3 and DAG, increasing cytoplasmic Ca2+ and Protein Kinase C.

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43
Q

How do V2 receptors work?

A

G-protein linked to adenyl cyclase, which converts ATP to cAMP, activating Protein Kinase A. This activates AQP2 (aquaporin), released in the apical membrane of the principle cell.

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44
Q

How is vasopressin release controlled?

A
  • Osmoreceptors in hypothalamus stimulate vasopressin release when increased plasma osmolarity
  • Baroreceptors decrease inhibition (thus stimulating vasopressin release) when decreased arterial blood pressure.
  • Various stressors from the brain causes a release of vasopressin.
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45
Q

What are the effects of Oxytocin?

A

1) Oxytocin works on myometrial cells causing contraction of uterus.
2) Behavioural effects
3) Causes myoepithelial cells to contract leading to milk ejection

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46
Q

Describe the diseases associated with abnormal levels of vasopressin

A

Lack of vasopressin is Diabetes Insipidus. Central DI is where no vasopressin is produced. Nephrogenic DI is associated with tissue insensitivity. Two main symptoms are Polyuria and Polydipsia.
Too much vasopressin leads to SIADH (Syndrome of Inappropriate ADH) where plasma sodium concentration is reduced.

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47
Q

What are the distributions of the the different types of diabetes?

A

11% is Type 1
85-95% is Type 2
3% is MODY

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48
Q

What is the normal level of glucose?

A

4-5 mM

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49
Q

What happens if glucose levels drop below normal?

A

Below normal, brain function will be impaired, as the brain mostly runs on glucose. Below 2Mm, unconsciousness, coma and death can result.

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50
Q

What is the distribution of endocrine and exocrine function of the pancreas?

A

98% is exocrine, 2% are endocrine.

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51
Q

What facilitates paracrine signalling between cells of islets of Langerhans?

A

Gap junctions and tight junctions.

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52
Q

What are the different cells in the islet of Langerhans, an their functions?

A

alpha-cells produce glucagon
beta-cells produce insulin
delta-cells produce somatostatin

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53
Q

What is insulin secretion by beta-cells regulated by?

A

Increase in [glucose] stimulates insulin secretion.
Certain amino acids and gastrointestinal hormones stimulate insulin secretion
Parasympathetic activity stimulates insulin secretion
Sympathetic activity inhibits insulin secretion
Somatostatin inhibits insulin secretion
Glucagon stimulates insulin secretion

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54
Q

What are the effects of insulin?

A
  • Increased glycogenesis
  • Increased glycolysis
  • Increase glucose transport into cell (via GLUT-4)
  • Increased amino acid transport and protein synthesis
  • Decreased lipolysis
  • Increased lipogenesis
  • Decreased gluconeogenesis (decreased hectic glucose output)
  • Decreased glycogenolysis
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55
Q

What is glucagon secretion by alpha-cells regulated by?

A

Decreased [glucose] stimulates glucagon secretion
Certain amino acids and gastrointestinal hormones stimulate glucagon secretion
Sympathetic activity stimulates glucagon secretion
Parasympathetic activity inhibits glucagon secretion
Somatostatin inhibits glucagon secretion
Insulin inhibits glucagon secretion

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56
Q

What are the effects of glucagon?

A 
Increased hepatic glycogenolysis
Increased blood glucose
Increase lipolysis
Increased gluconeogenesis
Increased amino acid transport into liver
Increased gluconeogenesis
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57
Q

What is C-peptide?

A

A cleaved off molecule in the production of insulin (from pro-insulin). It is released in equimolar quantities with insulin.

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58
Q

What is the incretin effect?

A

Orally consumed glucose causes a surge of higher levels of insulin compared to IV glucose.

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59
Q

What causes the incretin effect?

A

Glucagon-like peptide-1 (GLP-1) is a gut hormone secreted in response to nutrients in gut. It is a transcription product of proglucagon gene, mostly from L cells. It stimulates insulin and suppresses glucagon.

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60
Q

How can diabetes be treated with dipeptidyl peptidase-4 inhibitors?

A

Dipeptidyl peptidase-4 causes degradation of glucagon-like peptide-1. Inhibition of the enzyme will lead to more GLP-1 and this greater levels of insulin and less glucagon.

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61
Q

Describe the structure and function of the insulin receptor

A

It has two alpha and two beta subunits. The beta-subunits have tyrosine kinase domains which phosphorylates cell protein substrates.

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62
Q

Describe the function of the GLUT-4 protein

A

GLUT-4 is found all across the body, but mainly in muscle and adipose tissue. It is activated by insulin and can cause unto x7 increase in glucose uptake. It is inhibited by cortisol, catecholamines and somatotrophin.

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63
Q

What regulates the process of gluconeogenesis?

A

Glucagon increases amino-acid uptake of the liver (more gluconeogenesis).
Insulin decreases the rate of conversion of glucose from amino acids, decreasing hepatic glucose output.
Glycogen, Catecholamines and Cortisol increase gluconeogenesis.

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64
Q

How does insulin affect fat metabolism?

A

In vasculature, insulin stimulates lipoprotein lipase to breakdown triglycerides
In adipose tissue, insulin leads to the retention of triglycerides by preventing their catabolism.

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65
Q

How can the brain’s energy demand be satisfied?

A

Glucose and ketone bodies

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66
Q

How can fats be converted into glucose?

A

Glycerol can be used in gluconeogenesis in the liver. Fatty acids can also enter the liver, where they are converted into ketone bodies.

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67
Q

How is the production of ketone bodies regulated?

A

Insulin decreases the production of ketone bodies

Glucagon encourages it.

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68
Q

What are the characteristics of the fasted state, and how is it maintained?

A
  • Low [insulin] to [glucagon] ratio
  • High [NEFattyAcids]
  • Low [amino acid]

Maintained by:

  • Increase proteolysis
  • Increased lipolysis
  • Increased glucose output from gluconeogenesis and glycogenolysis
  • Brain using glucose then ketones
  • Muscles using lipids
  • Increase ketogensis when prolongued
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69
Q

What are the characteristics of the fed state, and how is it maintained?

A
  • Stored insulin released
  • High [insulin] to [glycogen] ratio

Maintained by:

  • Low hepatic glucose output
  • Increased glycogen synthesis
  • Decreased gluconeogenesis
  • Increased protein synthesis
  • Decreased proteolysis
  • Increased lipogenesis
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70
Q

What is the clinical presentation of Type 1 Diabetes Mellitus?

A
  • Absolute insulin deficiency
  • Proteolysis with weight loss
  • Hyperglycaemia
  • Glycosuria with osmotic symptoms (Polyuria and Polydipsia)
  • Ketonuria
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71
Q

What is the clinical presentation of Type 2 Diabetes Mellitus?

A
  • Hyperglycaemia
  • Hypertension
  • Increased waist circumference
  • Central adiposity
  • Dyslipidaemia
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72
Q

Where does insulin resistance in Type 2 Diabetes Mellitus usually reside?

A

Liver, muscle and adipose tissue.

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73
Q

Describe lipoprotein metabolism in Type 2 Diabetes Mellitus

A

Decreased lipoprotein lipase activity causes:

  • decreased LDL clearance
  • Increase in triglycerides
  • decrease in HDL
  • increased total LDL
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74
Q

How can Type 1 and Type 2 diabetes be differentiated clinically?

A

Type 2 Diabetes patients usually have enough insulin to suppress ketogeneis. While Type 1 Diabetes patients do not.

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75
Q

What dietary recommendations would you make to a Diabetes Mellitus patient?

A
  • Reduce calories as fats and refined carbohydrates
  • Increase calories as complex carbohydrates
  • Increase soluble fibre
  • Decrease sodium intake.
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76
Q

Where is the thyroid gland located?

A

Inferior to larynx, superior to trachea.

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77
Q

How are the cells of the thyroid gland organised?

A

Follicular cells surrounding colloid in a circular arrangement. Parafollicular cells lie between follicles.

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78
Q

What does Thyroid Stimulating Hormone / Thyrotrophin stimulate the production of?

A

Iodiothyronines (T3 and T4)

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79
Q

Describe the polarity of the follicular cell

A

The apical side faces the colloid. The basolateral side faces the arteriole.

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80
Q

How does thyrotrophin stimulate iodothyronine production?

A

1) Activates Iodide (I-) pump, moving iodide into the cell against gradients. Pendrin pump then moves iodide into colloid.
2) Stimulates production of thyroglobulin (TG), which moves into colloid, associated with apical membrane.
3) Activates enzyme thyroid peroxide (TPO) which oxidises I- into I (Iodine) in the presence of hydrogen peroxide. Iodine immediately reacts with tyrosine residues in thyroglobulin, forming mono and di-iodotyrosils.
4) TPO also couples iodinated thyroglobulin, forming tri or tetra-iodothyroNINE (T3 and T4/thyroxine)
5) Stimulates apical movement of lysosomes and uptake of TG (with T3 and T4) into lysosome. Lysosomal enzymes liberate the T3 and T4 molecules, which move into blood.

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81
Q

What is pendrine disease?

A

A form of hypothyroidism where people lack pendrin pump.

82
Q

How are the iodothyronines transported into the blood?

A
  • Thyroxine-binding globulin (TBG) binds with 70% T4 and 80% T3
  • Albumin binds 10% T4 and 15% T3
  • Prealbumin binds 15% T4 and 2% T3
    0. 05% T4 is unbound, 0.5% of T3 is unbound.
83
Q

What are the latent periods and half-lives of T3 and T4?

A

T3: 12h and HL of 2 days
T4: 72h and HL of 7-9 days

84
Q

What are the functional differences between T3 and T4?

A

More T4 than T3
T3 is more bioactive. Most T4 is converted into T3 in cell. T4 has own effects as well.
T4 can be converted into inactive rT3 (reverse T3)

85
Q

What are the effects of iodothyronines?

A
  • Increased basal metabolic rate (except brain). This results in calorigenesis (heat production)
  • Increase protein, carbohydrate and fat metabolism
  • Important for foetal development
  • Potentiate catecholamines
  • Increase Vitamin A synthesis from retinal
86
Q

Why can severe hypothyroidism lead to yellow colouration of skin?

A

Buildup of retinal (as not converted into Vitamin A).

87
Q

Where are T3 and T4 receptors found on the cell?

A

In cell cytoplasm and nucleus.

88
Q

How is iodothyrodide release regulated?

A
  • Somatostatin decreases production of TSH
  • T3 and T4 have direct negative feedback to adenohypophysis decreasing thyrotrophin (TSH) levels
  • T3 and T4 have an indirect negative feedback effect in hypothalamus, decreasing TRH levels.
  • Thyrotrophin has negative feedback loop on hypothalamus
  • Wolff-Chaikoff effect (increased iodide consumption counterintuitively decreases T3 and T4 levels)
  • Glucocorticoids have negative effect on thyrotroph cells
    + TRH (thyrotrophin releasing hormone) increases secretion of TSH
    + Sympathetic activity
    + Oestrogen have positive effect on TRH
89
Q

Describe the development of the thyroid gland?

A

Starts out from the tongue, it then grows and settles to final position by week 7. It is connected to the tongue by thyroglossal duct.

90
Q

How is the foramen caecum formed?

A

Disappearance of thyroglossal duct.

91
Q

What are the lobes of the thyroid gland?

A

Left lobe, Right lobe (largest), Isthmus and pyramidal lobe.

92
Q

How much does the thyroid gland in an adult weigh?

A

20g

93
Q

Why do patients need to be alerted about potential damage to voice when undergoing thyroid surgery?

A

Left recurrent laryngeal nerve hooks around the thyroid, supplying the vocal cords. If this is cut, one can loose their voice.

94
Q

What are the potential problems associated with thyroid gland development?

A
  • Agenesis (absence)
  • Incomplete descent
  • Thyroglossal cyst (fluid accumulating in thyroglossal duct)
95
Q

What disease describes lack of thyroxine in babies?

A

Cretinism is thyroxine deficiency in utero. Children have irreversible brain damage.

96
Q

How is cretinism detected and treated?

A

Detected by heal prick test at 5-10 days of age. Treated by 100ug thyroxine a day.

97
Q

Who is more likely to be affected by thyroid disease?

A

Women (4:1)

98
Q

What is myxoedema?

A

Primary hypothyroidism (primary thyroid failure) due to autoimmune damage. Thyroxine levels low. TSH levels high (lack of negative feedback)

99
Q

What are the clinical manifestations of hypothyroidism?

A
  • Deepening voice
  • Depression and tiredness
  • Cold intolerance
  • Weight gain and reduction in appetite
  • Constipation
  • Bradycardia
100
Q

What is the sequelae of primary hypothyroidism?

A

Myxodoema coma (loss of brain function). Cholesterol levels too high, death from MI and Stroke.

101
Q

What is thyrotoxicosis?

A

Hyperthyroidism. Too much thyroxine produced, TSH is close to zero. Raised basal metabolic rate; raised temperature.

102
Q

What are the clinical features of hyperthyroidism?

A 
Losing weight
Tachycardia
Myopathy
Mood swings
Feeling hot in all weather
Diarrhoea
Increased appetite but weight loss
Trembling of hands
Paliptations
Sore eyes
Goitre
103
Q

What is Grave’s disease?

A

Hyperthyroidism caused by antibody production stimulating TSHR. Leads to whole gland smoothly enlarged.

104
Q

What is the difference between between myxoedema and pretibial myxoedema?

A

Pretibial myxoedema is a symptom of Graves disease (HYPERthyroidism) - swelling of shins. Myxoedema is HYPOthyroidism.

105
Q

What is another name for the adrenal glands?

A

Suprarenal glands

106
Q

What are the different sections of the adrenal glands?

A

Cortex: Zona glomerulosa, Zona fasciculata, and Zona reticularis
Medulla

107
Q

What homes are produces in the two main sections of the adrenal glands?

A

The adrenal cortex makes corticosteroids

The adrenal medulla makes catecholamines

108
Q

What are the subtypes of corticosteroids and where are they produced?

A

Mineralocorticosteroids (mainly aldosterone) is produced by the zone glomerulosa.
Glucocorticoids (mainly cortisol) and Sex-steroids (Androgens and Oestrogens) are produced by zone fasciculata and reticularis

109
Q

How is cortisol transported and stored in the blood?

A

75% bound to corticosteroid binding globulin
15% bound to albumin
10% unbound

110
Q

How is aldosterone transported and stored in the blood?

A

60% bound to corticosteroid binding globulin

40% unbound

111
Q

How do cortisol and aldosterone levels vary?

A

Cortisol levels vary on the time of day. Usually higher in the morning.
Aldosterone levels are not dictated by the adenohypophysis, rather if one is upright or supine.
Cortisol levels are 1000x greater than aldosterone levels.

112
Q

What are the effects of Aldosterone?

A

Increase osmolarity of blood (>increase vasopressin > increase BP) by:

  • Increase number of Na+ and K+ and H+ ion channels in distal convoluted tubule and cortical collecting duct. This leads to more Na+ reabsorption into these cells and more K+ and H+ secretion to the glomerular fluid. The combined effects allows the Na+/K+ pump to work harder.
  • Increase number of ATPase enzymes to allow pumping Na+/K+ pump on basolateral membrane, increasing Na+ in blood, and K+ in cell.
113
Q

What are the effects of excessive aldosterone?

A

Excessive extra-cellular fluid and hypertension.

114
Q

What stimulates the release of aldosterone?

A
  • Angiotensin II stimulates zona glomerulosa of adrenal glands
  • Increase in K+ and decrease in Na+ (but much less so)
  • Corticotrophin enhances renin-angiotensin system.
115
Q

What cell produces renin?

A

The junta-glomerular cells of the afferent arteriole of the glomerulus.

116
Q

What causes renin secretion?

A
  • Decreased renal perfusion pressure
  • Juxta-glomerular sympathetic activity
  • Decreased [Na+} detected by Macula dense cells
117
Q

Describe the renin-angiotensin system

A

The liver produces angiotensinogen. Renin breaks this down to Angiotensin I. ACE (Angiotensin Converting Enzyme) converts this to Angiotensin II.

118
Q

What are the effects of angiotensin II?

A
  • Vasoconstriction

- Aldosterone release

119
Q

What is the most important stress hormone?

A

Cortisol

120
Q

What are the effects of glucocorticoids?

A
  • Peripheral protein catabolism
  • Fat metabolism
  • Hepatic gluconeogenesis
  • Enhanced effects of glucagon and catecholamines
  • Mineralocorticoid effects
  • Renal and CVS effects (e.g excretion of water and increased vascular permeability)
121
Q

What are the clinical effects of large amounts of cortisol?

A
  • Anti-inflammatory action
  • Immunosuppressive action
  • Anti-allergic action
122
Q

What receptors can cortisol bind to?

A

Glucocorticoid and mineralocorticoid receptors.

123
Q

Why doesn’t cortisol have mineralocorticoid effects on the kidneys?

A

Cortisol is inactivated to cortisone by 11(beta)-hydroxysteroid dehydrogenase 2 enzyme in the kidneys.

124
Q

How does cortisol lead decreased levels of prostaglandins?

A

Cortisol causes the production of Annexin 1, which binds to Annexin 1 receptors in the same or adjacent cells, decreasing the amount of aranchadonic acid (a precursor to prostaglandins)

125
Q

How is cortisol secretion regulated?

A

+ Corticotrophin releasing hormone stimulates corticotrophin secretion.
+ Corticotrophin stimulates cortisol production.
- Vasopressin inhibits corticotrophin secretion.
- Corticotrophin has an auto-negative feedback effect on its stimulation
- Cortisol has a direct negative feedback effect on the adenohypophysis preventing corticotrophin release
- Cortisol has an indirect negative feedback effect on the hypothalamus, decreasing CRH secretion.

126
Q

What is DHEA?

A

Dehydropiandrosterone; It is a precursor to androgens and oestrogens. It is converted to oestrogen in target cells. It is important in post-menopausal women as they don’t produce ovarian steroids.

127
Q

What are the disorders associated with inappropriate amounts of cortisol?

A

Inadequate cortisol is Addison’s disease

Excessive cortisol is Cushing’s syndrome

128
Q

Describe the blood supply to the adrenal glands.

A

Many arteries supply adrenal glands. Blood leaves through one vein only. Right adrenal gland drains directly into IVC. Left adrenal gland drains into the renal vein first.

129
Q

Why are patients immunised with HIB and pneumovax before surgery to adrenal glands?

A

Spleen is right next to left adrenal gland, leaving spleen at risk. Spleen is associated with the immune system.

130
Q

What is the pathway for aldosterone synthesis?

A

Cholestrol -> Pogesterone -21-> 11 deoxy corticosterone -11-> corticosteroid -18-> aldosterone

131
Q

What is the pathway for cortisol synthesis?

A

Cholestrol -> Pogesterone -17-> 17 hydroxy progesterone -21-> 11 deoxycortisol -11-> cortisol

132
Q

What is the pathway for oestrogens synthesis?

A

Cholestrol –> Pogesterone -17-> 17 hydroxy progesterone –> Androgens (testosterone) –> Oestrogens (oestradiol).

133
Q

What is the pro-hormone to corticotrophin? What is it composed of?

A

POMC = ACTH + MSH

134
Q

What causes addison’s disease?

A

Autoimmune condition or tuberculosis of adrenal glands.

135
Q

What are the clinical features of Addison’s disease?

A

Pituitary gland secreting lots of ACTH and MSH:

  • increase skin pigmentation
  • vitiligo
  • no cortisol nor aldosterone, so low BP
136
Q

How is Addison’s disease treated?

A
  • Rehydration with normal saline
  • Dextrose to prevent hypoglycaemia
  • Give hydrocortisone or another glucocorticoid
137
Q

What are the clinical features of Cushing’s syndrome?

A
  • Impaired glucose tolerance
  • Weight gain
  • Thin skin and easy brushing
  • Striae
  • Proximal myopathy
  • Depression
  • Hypertension
  • Central fat distribution (moon face and inter scapular fat pad ‘buffalo hump’)
  • Diabetes
138
Q

What are the four main causes of cushing’s syndrome

A

1) Taking steroids by mouth
2) Pituitary adenoma (Cusing’s DISEASE)
3) Adrenal ademoma or adenocarcinoma
4) ectopic ACTH

139
Q

What are the gonads?

A

Testes in males

Ovaries in females

140
Q

What genetic information determines if one develops testes of ovaries?

A

The sex-determining region of the Y chromosome

141
Q

What are the functions of the gonads?

A

1) Gametogenesis (spermatogenesis or oogenesis)
2) Steroidogensis (males mainly androgens, less oestrogen and progestogens; females mainly oestrogen and progestogens, less androgens)

142
Q

Compare the number of germ cells in males and females

A

Number of germ cells in males stays around the same throughout their lives (6 million). Number of germ cells in females peaks at 24 weeks (6 million), decreases rapidly until puberty, then slowly until menopause by a process called atrasia.

143
Q

What are the intermediate cells between a germ cell and spermatozoa?

A

Germ cell -> Spermatogonia -mitosis-> Primary spermatocyte -meisois1-> secondary spermatocyte -meiosis2-> Spermatids -mature-> Spermatozoa

144
Q

When does gametogenesis begin in males?

A

During puberty, under the influence of FSH

145
Q

What are the intermediate cells between a germ cell and ovum?

A

Germ -> Oogonia -> Primary Oocyte -meisos1-> Secondary Oocyte -meiosis2-> Ovum

146
Q

Where in the development of an ovum are the cells arrested in development and undergo atresia?

A

When they are primary oocytes

147
Q

Where does spermatogenesis take place?

A

In the cytoplasm of sertoli cells, in the coiled seminiferous tubules.

148
Q

What is the fate of a spermatozoa after they are produced?

A

They are collected in the Rete testis, and drained by the vasa efferent into the epididymis where they are stored and matured.

149
Q

How are spermatozoa ejaculated?

A

They are released from the epididymis into the vas deferens before being ejaculated via the urethra

150
Q

What makes up the seminiferous tubules?

A

A sheath of connective tissue containing spermatogonia.. Inner to that lies a layer of elongated sertoli cells, and finally the lumen.

151
Q

How are spermatozoa protected from immune reactions?

A

Sertoli cells have tight gap-junctions preventing access by blood.

152
Q

Where is testosterone produced in the testes?

A

Leydig cells

153
Q

How do the testes react to gonadotrophs?

A
  • Sertoli cells have FSH and androgen receptors; response to FSH will produce molecules including inhibin.
  • Leydig cells have LH receptors, to which in response will produce androgens (mainly testosterone)
154
Q

What is the name given to an ovarian follicle that is ready for ovulation?

A

Graffian follicle

155
Q

What becomes of the ovarian follicle after ovulation?

A

Corpus Luteum that secretes steroids

156
Q

How long does the menstrual cycle last?

A

28 days (20-35)

157
Q

When does the menstrual cycle begin?

A

First day blood and cellular debris from necrotic uterine epithelium is lost.

158
Q

What are the two cycles included in the menstrual cycle?

A
  • Ovarial cycle: Follicular phase -> Ovultaion -> Luteal Phase
  • Endometrial cycle: Proliferative phase -> Secretory phase
159
Q

When in the menstrual cycle does ovulation occur?

A

Day 14

160
Q

How are the two cycles in the menstrual cycle linked?

A

The follicular phase causes the proliferative phase by the release of 17(beta)-oestrodiol, which causes mitosis of endometrium, and increases number of progesterone receptors.
The luteal phase sees the production of progesterone and oestrogen, which endures secretory phase of the endometrium.

161
Q

How does the endometrium change during the proliferative phase?

A

Endometrium gets thicker
Glands become bigger
Blood vessels get larger

162
Q

Describe the levels of FSH during the menstrual cycle

A

FSH levels are slightly raised at the beginning of the cycle to ‘rescue follicles’ by stimulating them to continue their development.
FSH levels decrease as 17-beta-oestrodiol levels rise. FSH levels then spike during ovulation as large 17-beta-oestrodiol increases FSH levels.

163
Q

Describe the levels of 17-beta-oestrodiol during the menstrual cycle

A

As follicles start to grow, they start to produce 17-beta-oestrodiol, and so levels rise. The dominant follicle is chosen and start stop produce large amounts of 17-beta-oestrodiol.
As ovulation occurs, 17-beta-oestrodiol levels decrease. The subsequent corps luteum starts to produce more 17-beta-oestrodiol (around day 20), causing a slower rise in levels.
If fertilisation does not occur, oestrogen levels fall.

164
Q

Describe the levels of LH during the menstrual cycle

A

Follows FSH levels, except LH surge before ovulation caused by large concentration of 17-beta-oestrodiol.

165
Q

Describe the levels of progesterone during the menstrual cycle

A

Progesterone WITH oestrogen produces a negative effect on gonadotrophin levels, so progesterone levels stay low before ovulation (except bump)
Corpus luteum produces progesterone causing a rise and fall after ovulation.

166
Q

How do the gonadotrophs affect the ovarian follicles?

A

FSH is needed for the development of the follicles from pre-antral follicles to late-antral follicles to griffian follicles.
FSH/LH surge causes ovum to leave the graffian follicle.

167
Q

How do the cells in the ovaries react to gonadotrophs?

A

Theca cells have LH receptors, that produce androgens when stimulated. Granulosa cells have FSH receptors and convert androgens into oestrogens as they have aromatase enzymes.

168
Q

What is the more potent version of testosterone, and how is it formed?

A

Testosterone is reduced by a 5(alpha)-reductase enzyme to dihydrotestosterone (DHT).

169
Q

How are oestrogens made?

A

Aromatase activity on testosterone or androstenedione

170
Q

How is testosterone transported in the blood?

A

60% with Sex Hormone Binding Globulin (SHBG)
38% with Albumin
2% Bioactive

171
Q

What are the principal actions of androgens?

A

Fetus:

  • development of male genitalia
  • general growth
  • behavioural effects

Adult:

  • spermatogenesis
  • growth and development of genitalia, secondary sex glands, secondary sex characteristics
  • protein anabolism
  • pubertal growth spurt
  • behavioural effects
172
Q

Define oesterogen and give examples.

A

Anything able to induce mitosis in the endometrium. Such as 17-(beta)-oestrodiol, Oestrone, Oestriol

173
Q

What are the principal actions of oestrogens?

A 
Stimulate mitosis of endometrium
Final maturation of follicle
Induction of LH surge
Effects on vagina and cervix
Stimulate growth of ductile system of breast
Increase salt and water reabsorption in kidneys
Increase plasma protein synthesis
Stimulates osteoblasts
174
Q

Define Progestogen and give examples.

A

Proestrogens are any substance which induces secretory changes in the endometrium. Examples include progesterone and 17(alpha)-hydoxyprogesterone.

175
Q

What are the principal actions of Progestogens?

A

Stimulates secretory activity in endometrium and cervix
Stimulates growth of alveolar system in breast
Decreases renal NaCl re-absorption
Increased basal body temperature

176
Q

Describe the hypathalamo-pituitary-testicular axis

A

The hypothalamus releases Gonadotrophic Releasing Hormone (GnRH) in a pulsatile fashion.
The GnRHs cause gonadotrophs in the adenohypophysis to release LH and FSH.
LH stimulates Leydig cells to produce testosterone. Testosterone has a negative feedback effect on the production of LH.
FSH stiumlates stroll cells to produce inhibit, which have a direct negative effect on FSH release and indirect negative effect on GnRH release.

177
Q

What is amenorrhoea?

A

The absence of menstrual cycles. Can be primary (never occurred) or secondary.

178
Q

What is oligomenorrhoea?

A

Infrequent menstrual cycles

179
Q

What is infertility?

A

An inability to reproduce.

180
Q

What are the roles of calcium in the body?

A
  • Neuromuscular excitability
  • Muscle contraction
  • Strength in bones
  • Intracellular second messenger
  • Intracellular co-enzyme
  • Blood coagulation (Factor IV)
181
Q

How is calcium stored and transported in the body?

A

Stored as calcium salts in bone reserves.

In blood, calcium is transported as ions, plasma proteins and salts.

182
Q

What are the concentrations of calcium in the blood as ionised, proteins and salts?

A

Ionised: 1.25mM
Plasma proteins: 1.13 mM
Salts: 0.12 mM

Total: 2.5mM

183
Q

What causes increased levels of [Ca2+]?

A
  • Parathyroid hormone [PTH or parathormone]

- 1,25 (OH2) Vitamin D3 [Calcitrol]

184
Q

What causes decreased levels of [Ca2+]?

A

Calcitonin

185
Q

Where is PTH produced?

A

Parathyroid gland.

186
Q

What is the secondary messenger effects of PTH?

A

Activation if adenyl cyclase (-> cAMP) AND phospholipase C

187
Q

What are the effects of PTH?

A

Kidney:

  • Increased PO4(3-) excretion (leading to increased levels of Ca)
  • Increased Ca2+ reabsorption
  • Stimulates 1(alpha) hydoxylase activity, increasing the synthesis of 1,25 (OH2) D3

Bone:

  • Inhibits osteoblasts
  • Osteoblasts produce osteoclast activating factors, stimulating osteoclasts to increase bond reabsorption.

Small Intestine:

  • Increased Ca2+ absorption
  • Increased PO4(3-) absorption
188
Q

How is PTH regulated?

A

Parathyroid glands are stimulated by:
+ decreased plasma [Ca2+]
+ Catecholamines

Negative feedback loops:

  • increased [Ca2+] plasma
  • Synthesis of 1,25 (OH2) D3
189
Q

How is Vitamin D3 (cholecalciferol) obtained?

A

1) Through diet

2) When UV hits the skin: 7-dehydro cholesterol is converted to cholecalciferol.

190
Q

How is 1,25-(OH2)-D3 synthesised?

A

cholecalciferol (Vitamin D3) is converted to 25-hydroxy-cholecalciferol in the liver. 1(alpha)hydroxylase enzyme stimulated by PTH, synthesises 1,25,hydroxy-cholecalciferol.

191
Q

What are the actions of 1,25(OH2)D3?

A

Main action in small intestine to increase PO4(3-) and Ca2+ absorption.
Stimulates kidneys to increase Ca2+ reabsorption and decrease PO4(3-) reabsorption.

192
Q

What are the secondary messenger effects of calcitonin?

A

Phospholipase C

193
Q

Why and where is calcitonin synthesised?

A

Calcitonin is synthesised in the parafollicular cells due to detection of increased plasma [Ca2+]. Gastrin can also stimulate cacitonin release.

194
Q

What are the effects of calcitonin?

A

Inhibits osteoclasts and increases urinary excretion of Ca2+ to decrease plasma [Ca2+]

195
Q

What are the potential causes of hypocalcaemia?

A
  • Hypoparathyroidism
  • Pseudohypoparathyroidism
  • Vitamin D deficiency
196
Q

How can tetany be tested?

A

Looking for Trousseau’s sign and Chvostek’s sign

197
Q

What is another name of psudohypothyroidism, and what is the pathophysiology?

A

Allbright hereditary oesteodystrophy. This is where target organs are resistant to PTH due to defective G-proteins.

198
Q

What are the clinical features of pseudohypothyroidism?

A
  • Short stature
  • Low IQ
  • Subcutaneous calcification and bone abnromalities
  • Associated endocrine disorders
199
Q

How do [Ca2+], [PO4] and PTH levels vary between the different causes of hypocalcaemia?

A

They all show decreased levels of [Ca2+].
Hypoparathyroidism shows increased levels of [PO4] and lower levels of PTH.
Pseudohypoparathyroidism has high levels of PTH (as it caused by PTH resistance) in comparison.
Vitamin D deficiency has low levels of [PO4] and high levels of PTH

200
Q

What is vitamin D deficiency called as a condition in adults and children?

A 
Children = rickets
Adults = Osteomalacia
201
Q

What are the causes of hypercalcaemia?

A
  • Primary hyperparathyroidism (adenoma)
  • Tertiary hyperparathyroidism
  • Vitamin D toxicosis
202
Q

What are the consequences of hypercalcaemia?

A

Kidneys:

  • Increased Ca reabsorption
  • Increased PO4 exretion
  • Polyuria
  • Nephrocalcinosis
  • Increase in 1,25-(OH2)-D3 synthesis

GI tract:

  • Gastric acid
  • Duodenal ulcers

Bone:

  • bone lesions
  • bone rarefactions
  • fractures

Year 1 LCRS (2 decks)

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