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LCRS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Properties of the pituitary gland

A
  • small (thumbnail sized) with many functions (‘master gland’ due to multifunctionality)
  • separated into anterior and posterior (structurally and functionally two distinct lobes and not one entity)
  • Difference in lobes also includes their origin(derived from different tissue)
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2
Q

Location of the pituitary gland

A
  • sits at the skull base of the brain

- just underneath the hypothalamus, hanging from a stalk

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3
Q

What is the pituitary gland otherwise known as?

A

Hypophysis

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4
Q

Where is the pituitary gland enclosed?

A

The Sella Turcica(pituitary fossa)= saddle-shaped depression of the sphenoid bone

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5
Q

What is the anterior pituitary gland otherwise known as?

A

Adenohypophysis

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6
Q

What is the posterior pituitary gland otherwise known as?

A

Neurohypophysis

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7
Q

Importance of the Sella Turcica

A

Tumour will be constrained by the walls of the bone cavity

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8
Q

Structure of the neurohypophysis

A
  • Derived embryologically from neural tissue (downgrowth of neurones from the hypothalamic region)
  • does not require circulation of blood to perform its function
  • made mainly of long nerve axons and nerve terminals from the hypothalamus nuclei into the posterior pituitary gland
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9
Q

Structure and purpose of the adenohypophysis

A
  • Upgrowth from the buccal cavity (roof of the mouth)
  • Derived embryologically from glandular tissue(secretory function)
  • requires blood circulation to carry out function and produce hormonal effects
  • contains secretory cells packed full of hormones
  • composes the pars distalis (body) and the pars tuberalis (wrapped round the stalk)
  • contains secretory cells full of anterior pituitary hormones
  • made up of the pars distalis (body) and the pars tuberalis (wrapped around the stalk to the hypothalamus)
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10
Q

Define hypothalamic nuclei

A

Collection of neuronal cell bodies (hypothalamus is composed of these distinct nuclei)

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11
Q

Median eminence

A
  • structure at the base of the hypothalamus

- lacks blood brain barrier so communicates directly with systemic circulation

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12
Q

The three hormone classifications

A

1) protein/polypeptide hormones
2) steroid hormones
3) miscellaneous (hormones which do not fit into previous two categories=typically a mixture of characteristics)

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13
Q

Example of a protein/polypeptide hormone

A

ACTH (adrenocorticotropic hormone)

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14
Q

Where is ACTH produced?

A

The anterior pituitary gland (adenohypophysis)

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15
Q

Key concept of protein/polypeptide hormones

A
  • Many protein/polypeptide hormones were originally produced as precursors
  • The precursors are pro-hormones and in some cases, pre pro-hormones (longer versions of the final hormone)
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16
Q

Pro-hormone of ACTH

A

Anterior pituitary gland initially produces POMC (pro-opiomelanocortin) with 241 amino acids compared to 39 amino acids in ACTH

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17
Q

What happens to the pro-hormone?

A

Cleaved by enzymes at specific sites to give active hormone

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18
Q

Differentiation between protein and polypeptide

A

-Includes both number of amino acids (>50 for proteins) and structural element (more complex structures in proteins compared to a single polypeptide chain)

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19
Q

What does the anterior pituitary gland exclusively secrete?

A

Protein/polypeptide hormones

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20
Q

What are steroid hormones derived form?

A

Precursor is cholesterol

-begin with a cholesterol backbone

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21
Q

Example of a steroid hormone

A

Cortisol

-stimulated by the protein/polypeptide hormone ACTH

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22
Q

Hormone synthesis for protein/polypeptide hormones

A
  • precursor molecule is the building blocks of amino acids (originate from proteins in our diet)present within the blood capillary=delivery of materials for hormone synthesis
  • amino acids diffuse from blood capillaries into the cell via amino acids transporters
  • signal to DNA activates the protein synthesis pathway (transcription to give mRNA of pro-hormone)
  • Translation follows where the mRNA sequence from the nucleus is aligned on the ribosome in the cell and build up (addition of new amino acid is linked to a growing peptide chain) to give the prohormone peptide chain which is released from the ribosome
  • The prohormones are cycled into the Golgi Apparatus which packages the prohormones with relevant enzymes within a vesicle, with the relevant enzymes cleaving the prohormone it into to give/liberate the active
  • Active hormone sits in vesicles at the cell surface membrane
  • When required as promoted by a signal, the vesicles bind to the cell surface membrane and release the active hormone into the bloodstream for the functions of the hormone (by exocytosis)
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23
Q

Example of hormone synthesis for protein/polypeptide hormones is in ACTH production within the pituitary corticotroph cell (corticotrophs in the anterior pituitary gland)

A
  • mRNA of POMC (pro-hormone of ACTH) is originally synthesised from transcription
  • Translation of POMC mRNA at the endoplasmic reticulum gives fully complete POMC
  • POMC is cycled into the Golgi Apparatus, packing the prohormone with relevant enzymes into vesicles which can cleave the protein/polypeptide hormones=liberates ACTH
  • ACTH remains in vesicles close to the cell surface membrane of the corticotroph cell, sitting at this surface until signal promotes exocytosis process when required
  • exocytosis from cell into the bloodstream within the blood capillary
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24
Q

Which blood vessel has a exchange function?

A

Capillaries

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25
Q

Properties of protein/polypeptide hormone action

A

-short lived action in bloodstream (metabolised and cleared quickly from the bloodstream)

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26
Q

Which blood vessels are pituitary hormones secreted into?

A

Pituitary capillaries

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27
Q

How many lobes does the thyroid gland have?

A

Bi-lobed (left and right lobe)

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28
Q

Location of the thyroid gland

A
  • Front of the neck just below the Adam’s apple

- below and anterior to the larynx (in front and below the voice box)

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29
Q

Define isthmus

A

Thin bridge of tissue joining the two lobes together=gives a characteristic butterfly shape

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30
Q

Define pyramid (pyramidal lobe)

A

sits on top of the isthmus and observed in around 10%-30% of the population

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31
Q

What is the thyroid gland made of?

A

Follicles (evenly dispersed)

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32
Q

Follicle structure

A
  • Follicular cells line the follicle with the middle being colloid
  • Around the follicles we have parafollicular cells
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33
Q

Recall the two thyroid hormones

A

T3=3,5,3’-tri-iodothyronine

T4=3,5,3’,5’-tetra-iodothyronine (thyroxine)

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34
Q

Thyroid hormone synthesis-Iodine uptake

A
  • TSH secreted from the anterior pituitary gland into the bloodstream will bind to the TSH receptor on the follicular cells
  • This stimulates the uptake of iodide from the bloodstream into the follicular cells via the sodium-iodide symporter (NIS) on the basolateral membrane
  • The iodide is then transported across the apical membrane into the colloid via pendrin
  • Process of iodine uptake into the colloid of the follicles composing the thyroid gland is stimulated by TSH
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35
Q

What else does TSH stimulate?

A

-the synthesis of thyroglobulin (protein)=protein made by the thyroid gland

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36
Q

Iodination

A
  • add iodine to the tyrosine amino acid/tyrosyl residues of thyroglobulin as catalysed by thyroid peroxidase (TPO)-thyroid peroxidase will simultaneously oxidise iodide into reactive iodine for addition and reduce hydrogen peroxide to water molecules
  • Iodination at one position (addition of one iodine) gives monoiodotyrosine (MIT)
  • Iodination at two positions (addition of two iodine) gives diiodotyrosine (DIT)
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37
Q

Thyroid hormone synthesis

A
  • Uptake of iodide
  • Synthesis of thyroglobulin
  • Iodination
  • Coupling reaction
  • Reabsorption of T3 and T4 into the bloodstream
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38
Q

Coupling reaction in thyroid hormone synthesis

A
  • TPO continues to catalyse the coupling reaction for T3 and T4 to be formed
  • The coupling reaction between an MIT and a DIT gives T3
  • The coupling reaction between two DITs gives T4
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39
Q

Why does deiodination occur?

A

T4 is not bioactive

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40
Q

Recall the two subtypes of T3 and how they differ

A
  • Deiodinated to give active T3 form

- Deiodinated at a different position to give reverse T3 which is biologically inactive

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41
Q

Reabsorption of T3 and T4

A
  • T3 and T4 are reabsorbed into the follicular cells and then secreted into the bloodstream
  • The TSH will stimulate lysosomes within the follicular cell to move towards the apical membrane as well as stimulating the uptake of colloid across the apical membrane
  • The colloid internalised by the follicular cell will fuse with the lysosome and the enzymes will break down the protein (T3 and T4 are part of these larger proteins initially) to liberate the two thyroid hormones
  • T3 and T4 can then leave the follicular cell into the bloodstream
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42
Q

What are thyroid hormones otherwise known as?

A
  • Iodothyronine

- we observe the addition of iodine to the tyrosine amino acid

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43
Q

Which positions does iodination occur at to form MIT and DIT?

A
  • Positions 3 or 5
  • Position 3 for MIT
  • Position 3 and 5 for DIT
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44
Q

How are the thyroid hormones transported into the blood once they have been secreted from the thyroid gland?

A
  • transport through binding to plasma proteins
  • in most cases (70%-80%) is transported by TBG (thyroid-binding globulin)
  • in 10% to 15% of cases, the thyroid hormones are bound to albumin
  • the rest are bound to prealbumin (transthyretin)
  • a small proportion of T3 and T4 (0.05% of T4 and 0.5% of T3 is unbound=bioactive component)
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45
Q

What is a bioactive iodothyronines?

A

-free molecules of T3 and T4 not bound to plasma proteins

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46
Q

Latent period of T3

A

Approximately 12 hours

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47
Q

Latent period of T4

A

Approximately 72 hours

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48
Q

Biological half life of T3

A

around 2 days

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49
Q

Biological half life of T4

A

around 7-9 days

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50
Q

Difference between thyroglobulin and the thyroid-binding globulin

A
  • thyroglobulin=protein from which thyroid hormones are synthesised
  • thyroid binding protein=binds the thyroid hormones
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51
Q

Recall the active form of thyroid hormone

A
  • T3
  • T4 is the predominant product within the thyroid gland so needs to converted to T3 in the target peripheral tissues (peripheral)
  • some T3 is made in the thyroid gland but most is synthesised from deiodination in the peripheral tissues
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52
Q

Define deiodination

A

Removal of iodine from a compound

-catalysed by enzyme

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53
Q

Deiodination of T4

A

Remove an iodine from T4 to give the active T3

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54
Q

Mechanisms of iodothyronine action

A
  • T3 and T4 enter the target cells readily and interact with the nuclear receptors (TH receptor)
  • The receptor-hormone complex stimulates gene transcription leading to protein synthesis (main mechanism of genomic action=expression of genes can be upregulated or downregulated)
  • non nuclear action on ion channels on the cell surface membrane
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55
Q

TH actions in infants

A
  • For fetal growth and development
  • If infant is born with congenital hypothyroidism and is left untreated, it leads to cretinism
  • Hence, thyroid hormones and TSH are measured in the new-born infant’s heel prick test (identifies the congenital hypothyroidism)
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56
Q

General TH actions

A
  • TH increases the basal metabolic rate (min level of energy required to sustain vital functions)
  • Required for protein, carbohydrate and fat metabolism (metabolic purpose)-potentiates the actions of catecholamines leading to tachycardia (cardiac manifestation) and lipolysis
  • has effects on almost every system=gastrointestinal (diarrhoea), CNS (agitation and restlessness),respiratory (breathlessness), reproductive (subfertility and irregular periods)
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57
Q

Hyperthyroidism

A
  • Overactivity of the thyroid gland
  • Leads to increased basal metabolic rate and hence presentation is of unintentional weight loss and increased appetite=accelerated metabolism
  • also present with tachycardia (rapid heartbeat)
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58
Q

Hypothyroidism

A

-Underactivity of the thyroid gland

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59
Q

What do hyperthyroidism and hypothyroidism both affect?

A

The menstrual cycle leading to subfertility (reduced fertility)

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60
Q

Define latent period

A

pause between stimulus and response

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61
Q

What regulates the release of TSH?

A

TRH from the hypothalamus

-TRH stimulates thyrotroph cells in pars distalis of anterior pituitary gland to synthesise TSH

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62
Q

The control of TH production runs with what feedback mechanism?

A

Negative

-T3 inhibits production of TSH

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63
Q

What happens if the T4 levels increase in the thyroid gland?

A
  • Deiodination to T3 which suppresses the TSH levels=inhibitory thyroid hormones
  • increased negative feedback
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64
Q

TSH normal range

A

0.5-5.0

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65
Q

What happens if we reduce the negative feedback response?

A

-TSH levels increase

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66
Q

Where does negative feedback occur?

A
  • At the anterior pituitary gland (direct) and at the hypothalamus(indirect)
  • In the hypothalamus, the TRH levels are impacted
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67
Q

What can inhibit thyroid hormone (T3 and T4) release?

A
  • iodide (Wolff-Chaikoff effect)
  • used clinically for patient going into surgery with hyperthyroidism or in a thyroid storm (abrupt onset of severe hyperthyroidism)
  • given potassium iodide to inhibit release of thyroid hormones
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68
Q

Wolff-Chaikoff effect

A

Iodide inhibits thyroid hormone release

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69
Q

How does oestrogen effect TSH and hence iodothyronine production?

A

stimulates

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70
Q

How do glucocorticoids effect TSH and hence iodothyronine production?

A

decrease

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71
Q

Insulin is the hormone of which state?

A

Postprandial state (period after a meal)

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72
Q

Insulin action on blood glucose levels

A
  • reduces levels through decreased hepatic glucose output (suppresses this process)=liver does not need to synthesise glucose after food consumption
  • increases glucose uptake in the muscles
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73
Q

Insulin action on protein

A

-decreases proteolysis (protein broken down into peptides or amino acids=amino acids can be used to synthesise glucose molecules)

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74
Q

Insulin action on lipids

A
  • decreases lipolysis

- decreases ketogenesis

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75
Q

Define endocrinology

A
  • Study of endocrine glands and their secretions

- Study of the ‘messengers’ carried in the bloodstream

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76
Q

Define endocrine gland

A

A group of cells which secrete ‘messenger’ molecules directly into the bloodstream

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77
Q

Define hormone

A
  • The bioactive ‘messenger’ molecule secreted by an endocrine gland into the bloodstream
  • Not simply a metabolite or energy substrate (biological function), but instead effects a change
  • travels in the circulation
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78
Q

Who first identified a hormone?

A

Baylis and Starling (1902)

  • Against Pavlov’s idea that pancreatic secretion was under neural control (instead of hormones it contains)
  • Provided it was a chemical messenger by sampling the dogs small intestine, denervating it (take nerve supply out)
  • Showed acid chyme arriving into the duodenum (first section of the small intestine) stimulated the release of ‘secretin’ from the duodenal S cells
  • Secretin stimulated the pancreas to secrete bicarbonate to neutralise the acid chyme
  • showed hormones have to carried from the organ where they are produced to the organ which they affect by means of the bloodstream (importance of circulation)
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79
Q

Who discovered insulin?

A
  • Banting and Best (1922)
  • Extracted from dog pancreas and purified
  • Insulin is a treatment for type 1 diabetes mellitus to decrease blood glucose levels to a normal blood glucose range
  • treated first human 14 year old patient with insulin whom had type 1 diabetes mellitus=improvement in blood glucose to near normal glucose levels was shown in individual
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80
Q

Define endocrine

A

Hormone’s action on target cells at a distance from the source (travels via the circulation)

81
Q

Define paracrine

A
  • Hormone’s action on nearby target cells (near to the cell in which the hormone was produced)
  • local effect
82
Q

Define autocrine

A

Hormone having an effect on its own immediate source (effects organ/feedback on organ which synthesises the hormone molecule=acts on self)

83
Q

What are the two messenger systems?

A
  • Endocrine system

- Nervous system

84
Q

Difference between the endocrine system and the nervous system in terms of where the messenger molecule is secreted and travels

A
  • In the endocrine system, we have the release of chemicals (hormones) into the bloodstream where they will travel to the target cell (carried in the circulation)
  • In the nervous system, the chemicals (neurotransmitters) are released across the synapse
85
Q

Difference between the endocrine system and the nervous system in terms of effects on the body

A
  • In the endocrine system (depending on the hormone), effect can be far reaching and on many target cells spread throughout the body
  • In the nervous system, the effect will be restricted to those target cells actually innervated (nerve supply)
86
Q

Difference between the endocrine system and the nervous system in terms of effect duration

A

In the endocrine system (as dependent on the hormone and its half life etc), effect will take place over a relatively long time-span ranging from seconds to days (manifestation of hormones can occur for days)
-In the nervous system, the effect will be generated within milliseconds (neurotransmitter broken down quickly=short half life)

87
Q

Classic endocrine glands

A
  • Gonads
  • Pancreas
  • Gastrointestinal tract (GI tract)
  • Adrenals
  • Thyroid gland
  • Parathyroids (4 glands around the thyroid gland controlling the bodies calcium levels)
  • Pituitary gland
88
Q

Nerve axons

A
  • some axons stretch from the hypothalamic nuclei to the posterior pituitary gland
  • some axons are shorter and so stretch from the hypothalamic nuclei and end on the median eminence
89
Q

Regulation of the anterior pituitary gland

A

-regulated and controlled by the hypothalamus immediately above the anterior pituitary gland (gland does not work in isolation)
-hypothalamus is composed of neural tissue (not a classical endocrine gland) and produces neural secretions
-the neurones release these secretions (hormones) which affect the action of the anterior pituitary gland
-important aspect is a circulation to carry the hormones from the anterior pituitary gland and into the systemic circulation to work
-anterior pituitary hormones are stored in secretory cells which require stimulation for their release into the systemic circulation
-Axons protruding from the hypothalamic nuclei can either be short or long
-The short axons terminate at the surface of the primary capillary plexus
If neurosecretion is released from a hypothalamic neurone, it can enter the primary capillary plexus because of the fenestration
-Once in the primary capillary plexus, the neurosecretion travels in the blood through the portal vessels to the secondary capillary plexus which are also fenestrated
-Due to the fenestration, the neurosecretory molecule can leak out and stimulate the secretory cells to release their hormone products by exocytosis (release of products into the circulation)

90
Q

The hypothalamic-hypophysial portal circulation

A
  • Series of capillary plexus’s are important in the anterior pituitary gland
  • Blood is received by the superior hypophysial artery (branch of the internal carotid artery) which then enters the area around the median eminence to the primary capillary plexus
  • Portal vessels will then carry the blood from the primary capillary plexus to the secondary capillary plexus in the pars distalis (body of the anterior pituitary gland)
  • Both the primary and secondary capillary plexus’s are fenestrated=leaky capillary walls allowing communication in terms of secretions from the hypothalamic nuclei
  • blood will leave the secondary capillary plexus and hence the pituitary gland through the cavernous sinus and then the jugular veins
91
Q

Recall the 5 different adenohypophysial cells (present in the anterior pituitary gland)

A
  • Somatotrophs
  • Lactotrophs
  • Thyrotrophs
  • Gonadotrophs
  • Corticotrophs
92
Q

Somatotrophs

A

-produce growth hormones (somatotropin)

93
Q

Lactotrophs

A

-produces prolactin (important hormone in lactation)-higher reference range in the blood of women, especially lactating women

94
Q

Thyrotrophs

A

-produce thyroid stimulating hormone (TSH, Thyrotrophin)

95
Q

Gonadotrophs

A
  • regulate the gonads (testes and ovaries)

- produce the luteinising hormone (LH) and the follicle stimulating hormone (FSH)

96
Q

Corticotrophs

A
  • produces adrenocorticotrophic hormone (ACTH, Corticotrophin)
  • controls of the adrenal cortex (rich supply of hormones)
97
Q

Chain of command in the thyroid axis

A
  • hypothalamus signals to the anterior pituitary gland which will then stimulate the thyroid gland to release thyroid hormones T3 and T4
  • Within the hypothalamus, the paraventricular nuclei releases neurosecretion of TRH along the hypothalamic neurones to the median eminence (Thyrotropin Releasing Hormone) into the hypothalamo-hypophysial portal system (due to leaky capillary walls of primary capillary plexus)
  • TRH will travel in the bloodstream to the secondary capillary plexus in the anterior pituitary gland
  • The neurosecretion TRH stimulates the release of TSH (thyroid stimulating hormone/thyrotrophin) present in the anterior pituitary gland secretory target cells which are responsive to TRH (thyrotrophs)
  • The TRH is able to act on these target cells because of the leaky capillaries in the secondary capillary plexus in the body of the anterior pituitary gland
  • Once TSH is released from the target cells in the anterior pituitary gland by exocytosis, the TSH will enter the systemic circulation
  • TSH will then travel within the bloodstream to the thyroid gland, stimulating the iodide uptake of the follicular cells and overall the production/release of thyroid hormones
  • In the general case, neurosecretions can either be stimulating or inhibitory hormones in terms of the adenohypophysis hormone production
98
Q

Where do hormones come from?

A
  • Larger precursor molecules called prohormones
  • Prohormones tend to not be biologically active
  • Enzymatic cleavage at specific sites of the prohormone yields the smaller hormone molecule which is bioactive
  • Often cleaving will yield useful molecules and redundant molecules=redundant molecules can sometimes be used in clinical practice
  • 5 different adenohypophysial cell types store adenohypophysial hormones in secretory granules
  • secretory granules must fuse with the cell membrane to release contents into circulation by exocytosis
99
Q

Example of a prohormone POMC cleaving

A
  • POMC is the precursor molecule (ProOpioMelanoCorticotrophin)
  • Cleaved enzymatically to give various peptides including ACTH
100
Q

Protein adenohypophysial hormones

A
  • Growth hormone (191 amino acids)
  • Prolactin (199 amino acids)
  • Similar structures in terms of amino acid content (large and share common amino acids)
101
Q

Glycoprotein adenohypophysial hormones

A
  • Glycoproteins consist of alpha and beta subunits (proteins with carbohydrate molecule attached)
  • alpha subunit is common (92 amino acids) but beta subunit is different
  • TSH=110 amino acid beta subunit
  • The 2 gonadotrophins (LH and FSH)=115 amino acid beta subunit
102
Q

Polypeptide adenohypophysial hormones

A

-ACTH (small with only 39 amino acids)

103
Q

5 key adenohypophysial hormones

A
  • Growth hormone
  • prolactin
  • TSH
  • LH and FSH (gonadotrophins)
  • ACTH
104
Q

Every adenohypophysial hormone has?

A

-A hypothalamic hormone as a regulator

105
Q

Somatrophin (APG hormone)

A
  • Has both a stimulatory and inhibitory hypothalamic hormone
  • stimulation from hypothalamus is GHRH (somatotrophin releasing hormone, growth hormone releasing hormone)=tells anterior pituitary gland to release growth hormone
  • inhibition from somatostatin=inhibits the anterior pituitary gland from releasing growth hormone
106
Q

Prolactin

A
  • only APG hormone under negative control
  • Dopamine inhibits anterior pituitary gland for the release of prolactin constantly
  • To increase prolactin levels, we require a reduction in dopamine
  • Small stimulatory effect of prolactin from TRH also but dopamine is the main focus
107
Q

TSH

A

-TRH stimulates release of TSH from the anterior pituitary gland

108
Q

LH and FSH

A

-Gonadotrophin releasing hormone stimulates release of LH and FSH from the anterior pituitary gland

109
Q

ACTH

A
  • Stimulatory controls from CRH (Corticotrophin releasing hormone) and Vasopressin
  • CRH is the main stimulation for the release of ACTH from the anterior pituitary gland
  • Vasopressin is a posterior pituitary gland hormone
110
Q

Target cells of growth hormone

A
  • makes you grow
  • high relevance in childhood and puberty because of growth
  • Target of general body tissues and particularly the liver
  • Causes secretion of IGF1 (another growth molecule)from the liver
111
Q

Target cells of prolactin

A
  • breast cells in terms of lactation

- for lactating women so little effect in men

112
Q

Target cells of thyrotrophin

A

-thyroid gland to secrete thyroid hormones

113
Q

Target cells of gonadotrophins (LH and FSH)

A
  • testes in men to make testosterone and sperm

- ovaries in women to regulate the entire menstrual cycle

114
Q

Target cells of corticotrophins

A

-regulates the adrenal cortex which synthesises certain hormones

115
Q

Growth hormone axis

A
  • Adenohypophysis releases growth hormone which has direct and indirect effects
  • Direct effects relate to receptors on the skeleton and skeletal muscle lead to growth of body tissue and muscle development (anabolic effects)=promotes growth
  • Growth hormones have metabolic actions also
  • Growth hormones also work via the liver by binding to the growth hormone receptors and stimulating the production of IGF I and IGF II (somatomedins)
  • Somatomedins indirectly regulate growth
  • indirect effect by IGF I leads to metabolic actions: stimulation of amino acid transport into cells and protein synthesis, increased gluconeogenesis (why excess of growth hormone can lead to diabetes development), stimulation of lipolysis (breakdown of fat) leading to increased fatty acid production and increased cartilaginous growth and somatic cell growth
  • Increased growth can predispose to malignancy in growth hormone excess
116
Q

Regulation of growth hormone

A
  • hypothalamic nuclei releases GHRH (positive stimuli) for secretion of growth hormone from anterior pituitary gland
  • Also have the release of somatostatin (negative stimuli for growth hormone release from the anterior pituitary gland)
  • Both hypothalamic hormones enter the anterior pituitary gland and depending on what dominates, we either have a reduction or increase in growth hormone secretion
117
Q

Regulation of growth hormone: GHRH dominates

A
  • GHRH stimulates APG to release the growth hormone into the bloodstream by exocytosis
  • The growth hormone will bind to receptors on the liver to stimulate the production of somatomedins (mediating growth)
  • Other stimuli for the release of GHRH from the hypothalamus include: certain amino acids (eg: arginine), fasting (inducing hypoglycaemia is a biological stressor-leads to release of lots of hormones),exercise, oestrogens, stress, sleep (in stages III and IV)=indirect
  • Ghrelin (from the stomach) stimulates the APG to release growth hormones=direct
  • All stressors listed stimulate the growth hormone production and release
118
Q

Which two groups of hormones do the adrenal glands produce?

A
  • Corticosteroids

- Catecholamines

119
Q

Adrenal gland location

A
  • gland sitting directly above the right and left kidneys (2 kidneys in total)
  • due to location, the left adrenal vein will drain into the renal vein
  • due to location, the right adrenal vein drains directly into the inferior vena cava
120
Q

Adrenal gland anatomy

A

-fibrous capsule on the outside of the cortex
-Inner zone is the adrenal medulla
-Adrenal medulla produces the catecholamines
-Outer zone is the adrenal cortex
-Adrenal cortex produces the corticosteroids
The cortex is made of the zona reticularis, zona fasciculata and zona glomerulosa which all produce different corticosteroids=products have to diffuse through medulla and leave the adrenal via the central vein
-Many arteries perfuse both adrenals to provide nutrients and oxygen but only one central vein leaves (collection in middle of the gland to then leave via the one vein) =hormones travel in the bloodstream out of the adrenals through this vein

121
Q

Anatomy of the thyroid

A
  • located in the neck just below the Adam’s apple
  • shield shaped
  • vascular
  • left lobe, right lobe and pyramidal lobe
  • pyramidal lobe in some people=important in embryology in cases of children with lump of neck resulting from enlarged part of thyroid gland
  • moves up and down when you swallow
  • thyroid gland is needed to survive
122
Q

In what instances do we remove the thyroid gland?

A
  • malignancy

- very overactive

123
Q

Parathyroid glands

A
  • unrelated functionally to the thyroid glands
  • controls calcium metabolism
  • removal of thyroid gland with accidental removal of parathyroids leads to problems with regulating calcium metabolism
124
Q

Damage to the recurrent laryngeal nerve?

A
  • vocal cord supply
  • damage by thyroid surgery
  • nerve going past the thyroid gland
  • innervates the larynx to allow speech
  • impact patients voice with damage/quality of voice
  • thyroid surgeons mention this risk when obtaining consent for thyroidectomy
125
Q

How many parathyroid glands do we have?

A

4

-embedded in corners of the lobes of the thyroid gland

126
Q

Origin of the thyroid gland

A
  • extension from the back of the tongue
  • midline outpouching of the floor of the pharynx (base of the tongue)
  • outpouching forms thyroglossal duct which elongates down
  • migrates down neck and divides into two lobes with final position obtained by week 7
  • thyroglossal duct disappears leaving foramen caecum
  • thyroid gland develops in neck to synthesise thyroid hormones
127
Q

Foramen caecum

A
  • dimple at the back of the tongue

- disappearing thyroglossal duct=leaves dimple

128
Q

Adult weight of thyroid gland and dimensions of lobes

A

20g

-each lobe is 4 x 2.5 x 2.5 (cm)

129
Q

Lobes of the thyroid gland

A
  • Left, right, isthmus and pyramidal (4)
  • right lobe is the largest
  • pyramidal lobe above isthmus is only found in some individuals=left from descent of gland from base of tongue
130
Q

Embryology of the thyroid gland

A 
-originates back of tongue and migrates down in fetus
///////
131
Q

Primary hypothyroidism principles

A

-myxoedema
-thyroid gland fails to synthesise thyroxine
(primary thyroid gland failure)
-caused by autoimmune damage to the thyroid gland or from removal of the thyroid gland via surgery
-leads to thyroxine level decline
-Leads to pituitary gland to increase TSH levels to drive thyroid gland production of thyroxine (gland destroyed by immune system so no stimulation eventually have no thyroxine present)

132
Q

Primary hypothyroidism clinical features

A

SLOWING DOWN

  • Basal metabolic rate falls
  • deepening voice (cartilage vibrations slow down)
  • depressed
  • tiredness
  • cold intolerance (due to lower basal metabolic rate)
  • weight gain with reduced appetite (eat less but put on weight)
  • constipation
  • bradycardia (slow heart rate)
  • abnormal reflexes (long recovery from reflex check)
  • brain slows down so you cannot think clearly
133
Q

Primary hypothyroidism treatment

A
  • Treatable
  • if left, primary hypothyroidism can cause death
  • with slow BMR, cholesterol levels increase which can cause death from heart attacks and strokes
  • replace thyroxine with daily dose of thyroxine tablet (100 micrograms on average)
  • Monitor TSH levels with blood test and adjust thyroxine dose until the TSH level is normal (insufficient thyroxine present if high levels of TSH in the blood)
134
Q

Hyperthyroidism

A

SPEEDING UP=every cell in the body speeds up
-thyrotoxicosis
-autoimmune disease
-overactive gland
-makes too much thyroxine
-pituitary gland stops making TSH (falls to 0) because of excess thyroxine detection
but another stimulus is present to make thyroid hormones (immune system)
-synthesises antibody which stimulates receptor in the thyroid gland to make thyroxine adding to excess T4

135
Q

What happens if primary hypothyroidism is not treated?

A

Eventual myxoedema coma (basal metabolic rate reduces so much that the brain cannot function=lack of thyroxine)
-progressive worsening of features is slow=perform poorly for long time (clue)

136
Q

Hyperthyroidism clinical features

A
  • raised basal metabolic rate
  • raised temperature (hot sweats in all weathers)
  • weight loss (excessive calorie uptake in metabolism)
  • palpitations
  • increased appetite
  • mood swings
  • sleeplessness
  • diarrhoea (frequent bowel movements)
  • myopathy (weakness results from loss of muscle with burning calories)
  • tiredness
  • sore eyes
  • tremor of hands= overactive causes adrenaline effects skeletal muscles
  • goitre (gland swells due to immune system stimulation and causes lump in the front of the neck)
137
Q

Causes of hyperthyroidism

A

-Grave’s disease is the common aetiology

138
Q

Grave’s disease

A
  • whole gland is smoothly enlarged and the whole gland is overactive
  • autoimmune disease
  • immune system produces antibodies which bind to TSH and other molecules
  • first antibody bind to and stimulate TSH receptors in the thyroid gland causing enlargement
  • causes smooth goitre and hyperthyroidism
139
Q

Grave’s disease clinical features

A
  • goitre
  • nervous, excitable, insomnia
  • exophthalmos (bulging eyes)=second antibody binds to muscles behind the eye causing them to swell and push eyes forward
  • symptoms of hyperthyroidism
  • pretibial myxedema=third antibody binds and stimulates growth of the soft tissue on the shins causing swelling of the shin (hypertrophy)
140
Q

Pretibial myxedema

A
  • swelling (non pitting) occurring on the shins of patients
  • growth of soft tissue
  • different to myxoedema (primary hypothyroidism)
141
Q

Origin of parathyroid glands

A

-from different branchial arches

142
Q

Lingual thyroid

A
  • rare condition
  • incomplete migration of the thyroglossal duct so thyroid tissue barely descends and remains close to the back of the tongue and grows
  • development pushes uvula sideways
  • causes problem with breathing and swallowing
  • removal requires long term hormone therapy because it is the only functional thyroid gland
143
Q

Problems with the development of the thyroid gland

A
  • Agenesis=complete absence (gland does not grow at all)
  • Incomplete descent=does not move all the way to the final position (lump)
  • Thyroglossal cyst= fluid filled, segment of duct persists and presents as a lump years later (ensure functional thyroid gland nearby before removal surgery)
144
Q

Thyroid cartilage

A
  • felt

- cartilage moved out the way when gland grows/tumour forms

145
Q

Why is thyroxine important?

A
  • brain development
  • neonates with thyroxine deficiency as a result thyroid agenesis leads to irreversible brain damage without thyroxine supplement from birth (not in uterus because thyroxine passes across the placenta)
  • controls basal metabolic rate (amount of energy expended whilst at rest=HR, temp etc)
  • increased bmr=increased thyroxine
  • Hence, every cell is affected by thyroxine
146
Q

Cretin

A

An individual with irreversible brain damage caused by the lack of thyroxine

147
Q

Cretinism

A
  • Condition present from thyroid agenesis
  • IQ is much lower than normal
  • stunted growth (growth is overall slower too)
  • untreatable
148
Q

Prevention of cretinism

A
  • Screening programme now prevents cretinism
  • All babies have a heel prick for a blood test for thyroid function(measuring TSH levels) at the same time as the Guthrie test for phenylketonuria at 5-10 days of age
  • if we identify the condition, it can be reversible by treatment
  • Given thyroxine immediately if TSH levels are high (little thyroxine)
149
Q

Thyroid follicular cell

A
  • site of thyroxine synthesis
  • blood vessel on outside and colloid (store of thyroxine and contains thyroglobulin) on the inside
  • synthesises and stores thyroxine
  • secretes thyroxine into the circulation (controls brain development, function, heart rate, appetite etc)
150
Q

What happens if thyroglobulin is present in the circulation?

A
  • usually found inside the thyroid glands and not in the circulation
  • if found in the circulation, we can determine there is a leak
151
Q

Thyroxine binding globulin

A
  • circulating plasma protein
  • binds to thyroxine in the circulation
  • bins to 75% of the thyroxine in the circulation (24% also bound to albumin so 1% is free and available for use)
  • lots of stored thyroxine within the circulation too
152
Q

Thyroglobulin

A
  • protein
  • keeps and stores thyroxine in the thyroid gland
  • inside the thyroid gland only
153
Q

Roles of the thyroid gland

A
  • Synthesises, stores and secretes thyroid hormones

- Thyroid hormones released regulate growth, development and basal metabolic rate

154
Q

Epidemiology of thyroid disease

A
  • affects 5% of the population (overactive or underactive thyroid gland)
  • more prevalent in females (thyroid disease typically due to autoimmunity and during pregnancy the immune system is easily altered because of tolerance of fetus with other antigens) but often more severe in men
  • equal ratio of overactive thyroid gland and underactive thyroid gland
155
Q

The Adrenal medulla

A
  • produces catecholamines (mainly adrenaline and small amounts of noradrenaline and dopamine)
  • adrenaline=circulating hormone
156
Q

The Adrenal cortex

A

-produces corticosteroids (mineralocorticoids like aldosterone, glucocorticoids like cortisol and sex steroids like androgens and oestrogens)

157
Q

Where is aldosterone produced?

A

-Zona glomerulosa of the adrenal cortex (outer zone)

158
Q

Where are cortisol and sex steroids produced?

A

-Zona fasciculata and zona reticularis of the adrenal cortex

159
Q

Cortisol secretion

A
  • diurnal rhythm (pattern based on 24 hour cycle=change throughout the day and released in pulses)
  • highest in morning
  • lowest at night
160
Q

Aldosterone secretion

A
  • 1000 fold less aldosterone concentration in the bloodstream compared to cortisol during the day
  • reduced production by adrenals
161
Q

Cortisol binding

A
  • non selective

- Cortisol binds to both the glucocorticoid receptors and the mineralocorticoid receptors

162
Q

Aldosterone binding

A

-can only bind to aldosterone receptor (MR=mineralocorticoid receptor )

163
Q

11b-hydroxysteroiddehydrogrenase 2

A
  • cortisol metabolising enzyme
  • certain tissues possess a lot of this enzyme meaning cortisol is unable to leave this tissue=gives aldosterone relevance
  • high levels of enzyme present in the kidney (key aldosterone function) and in the placenta preventing maternal cortisol getting out of the fetus
164
Q

Renin-angiotensin-aldosterone system linked to aldosterone production

A
  • start with renin production from granular cells lining the afferent arteriole in the kidney
  • decrease in renal perfusion pressure (associated with decreased arteriole blood pressure)=sensed and stimulates increase of renin release
  • Renal sympathetic activity=sympathetic nerves directly innervate granular cells (activation of system when blood pressure falls and hence increase in renin release)
  • macular densa cells (sodium sensors) in the distal convoluted tubule detect low sodium concentration in the fluid which stimulates renin production
  • End result is aldosterone production
165
Q

Function of aldosterone

A

-promotes sodium reabsorption in the kidneys and preserves/restores blood pressure

166
Q

The hypothalamo-pituitary-thyroid axis

A
  • hypothalamus synthesises TRH which stimulates the thyrotrophs in the pituitary gland to produce TSH -THS goes to the thyroid gland which results in the synthesis of T3 and T4
  • T3 and T4 feedback negatively at the level of the pituitary gland (TSH) and at the hypothalamus (TRH)
  • Hence, less T4 made means more TSH is secreted due to negative feedback
  • high TSH indicates little thyroxine naturally, so replacement is required
167
Q

TRH

A

thyrotropin releasing hormone

168
Q

TSH

A

thyroid stimulating hormone (thyrotropin)

169
Q

Negative feedback mechanism in terms of the growth hormone

A
  • negative feedback loop is a natural regulatory mechanism
  • means output has negative feedback to the regulatory sources (APG and hypothalamus), then indirect feedback from the APG to the hypothalamus also
170
Q

Prolactin chain of command

A
  • Regulation of lactation is by neuro-endocrine reflex arc
  • Prolactin is essential for the production of breast milk
  • Prolactin from lactotrophs in the APG
  • Prolactin levels tend to be low in both males and females, although slightly higher in females
  • Dopamine from hypothalamic neurones constantly inhibits lactotrophs in APG
  • Neural part is suckling which stimulates tactile receptors on the breast feedbacking to hypothalamic dopaminergic neurones=suppressing these neurones to release less dopamine
  • less dopamine means less inhibition of the lactotrophs producing prolactin, so more prolactin is secreted from the APG into the circulation and travels to the breast for involvement in milk production
  • Here we have a neuronal input and an endocrine output (afferent neural pathway and efferent endocrine pathway)
171
Q

Primary hyperparathyroidism

A

/

172
Q

Secondary hyperparathyroidism

A

/

173
Q

Tertiary hyperparathyroidism

A

/

174
Q

Principal causes of hypocalcaemia (endocrine causes)

A

/

175
Q

Principal causes of hypercalcaemia (endocrine causes)

A

/

176
Q

Product of the zona glomerulosa (adrenal cortex)

A

/

177
Q

Product of the zona fasciculata (adrenal cortex)

A

/

178
Q

Product of the zona reticularis (adrenal cortex)

A

/

179
Q

Product of the adrenal medulla

A

/

180
Q

Primary amenorrhoea

A

If a women has never had a single period in her life

181
Q

Secondary amenorrhoea

A

If a women has had normal periods but these have stopped

182
Q

Oligomenorrhoea

A
  • infrequent cycles

- less severe than amenorrhoea

183
Q

Infertility

A

The inability for a couple to get pregnant following 12 months of regular unprotected sex

184
Q

Principle causes of infertility

A

/

185
Q

Early follicular phase

A
  • within the first 5 days of the menstrual cycle
  • ovary gets 5-10 eggs which begin to grow as developing follicles=under FSH regulation which is made at low levels
  • follicles begin to make 17b-oestradiol (only small amount because follicles are small in size)=relatively absent negative feedback
  • lots of LH and FSH still present to make follicles grow
186
Q

Early-mid follicular phase

A
  • LH and FSH remain at same levels as early follicular phase
  • 17b-oestradiol increases as follicles continue to grow in size
  • all follicles grow but one follicle grows a lot more and is a lot larger compared to the other follicles (higher 17b-oestradiol contribution)
  • At this point, we see the 17b-oestradiol levels increase because of this specific growing follicle dominating called the Graafian follicle
  • positive feedback loop presents because 17b-oestradiol made by the Graafian follicle stimulates the granulosa cells to grow and synthesise more 17b-oestradiol=amplification in granulosa cells
187
Q

Mid-follicular phase

A

-

188
Q

Late follicular phase

A

/

189
Q

Luteal phase

A

/

190
Q

Amenorrhoea

A

Absence of menstrual cycles

191
Q

Addison’s disease clinical features

A

/

192
Q

Gonad development in males

A

Testes

193
Q

Gonad development in females

A

Ovary

194
Q

Gametogenesis in males

A

Spermatogenesis

195
Q

Gametogenesis in females

A

Oogenesis

196
Q

Spermatogenesis

A
  • primordial germ cells proliferate and differentiate to give spermatogonia (diploid)
  • Spermatogonia remain dormant until puberty when spermatogenesis begins
  • Spermatogonia divide by mitosis to give primary spermatocytes (diploid) and more spermatogonia which join a pool (1:1)
  • Primary spermatocytes enter first meiotic division to give secondary spermatocytes (haploid)
  • Secondary spermatocytes (haploid) enter second meiotic division to give spermatids (haploid)
  • Spermatids mature into spermatozoa
  • 70 days in total
197
Q

Oogenesis

A
  • primordial germ cells proliferate and differentiate to give oogonia
  • Oogonia enter mitosis immediately to give primary oocytes
  • Primary oocytes enter first meiotic division straight away (start gametogenesis as soon as possible)
  • primary oocytes develop layer of cells around them to give follicles early in the fetal life, leading to meiotic arrest in prophase I=follicles contains primary oocytes
  • meiotic arrest lasts for 12-50 years (development will either proceed after puberty=12 or just before menopause=50)
  • meiosis is re-established for primary oocytes (diploid) to complete first meiotic division, producing secondary oocytes (haploid) and the first polar body
  • secondary oocytes enter the second meiotic division and complete at fertilisation stage to give ovum and second polar body
198
Q

Functions of the gonads

A

/

199
Q

Structure of the testes

A

/

LCRS (3 decks)

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