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Life Cycle and Reproduction Systems (LCRS) > Endocrinology 1 > Flashcards

Endocrinology 1 Flashcards

Adenohypophysis, Neurohypophysis, Diabetes Mellitus, Thyroid Gland

1
Q

Contrast endocrine signalling and nervous signalling.

A

Endocrine: release of chemical into blood.
Nervous: release of chemical across synapse.
E: effect on many target cells, spread through body
N: effect limited to target cells actually innervated
E: long time span, form seconds to days
N: effect generated within milliseconds

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2
Q

What are the 3 hormone classifications?

A

Protein/polypeptide, steroid, miscellaneous.

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3
Q

How are protein hormones stored?

A

They are stored in vesicles as prohormones. The vesicles contain enzyme to cleave the prohormone to activate it when stimulated. Exocytosis upon stimulation.

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4
Q

How are steroid hormones stored?

A

These are lipid soluble, so diffuse into the bloodstream. Plasma proteins, e.g. CBG and albumin, bind to steroid hormones in the blood. Bound and free hormone are in dynamic equilibrium, ensuring the amount of free hormone available to the tissues remains constant.

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5
Q

What is the pars distalis?

A

The body of the anterior pituitary lobe (adenohypophysis).

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6
Q

What is the pars tuberalis?

A

The part of the adenohypophysis which wraps around the pituitary stalk.

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7
Q

What is the median eminence?

A

The part of the hypothalamus which abuts the pituitary gland.

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8
Q

What are the 5 types of adenohypophyseal cells and the hormones they produce?

A

Somatotrophs, releasing somatotrophin (growth hormone).
Lactotrophs, releasing prolactin.
Thyrotrophs, producing TSH (thyrotrophin).
Gonadotrophs, producing LH, FSH
Corticotrophs, producing adenocorticotrophic hormone (ACTH, corticotrophin).

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9
Q

Which hormones released from the adenohypophysis have both ‘on’ and ‘off’ hypothalamic hormones?

A

Somatotrophin and prolactin.

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10
Q

Which adenohypophyseal hormone is under negative control?

A

Prolactin: its regulatory hormone, dopamine, inhibits its secretion.

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11
Q

What’s involved in a neural-endocrine reflex arc?

A

An afferent neural pathway and efferent endocrine pathway.

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12
Q

What are herring bodies?

A

Stores of hormones in vesicles at points along supraoptic and paraventricular neurones terminating in the neurohypophysis.

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13
Q

Where do paraventricular neurones terminate?

A

Some terminate in the neurohypophysis, some at the median eminence and some pass to other parts of the brain.

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14
Q

Which neurones can be described as either oxytocinergic or vasopressinergic?

A

Supraoptic neurones and paraventricular neurones.

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15
Q

What is cleaved from pre-provasopressin to form provasopressin?

A

A signal peptide.

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16
Q

What are the 3 components of provasopressin?

A

(Arginine) vasopressin, a glycopeptide and neurophysin.

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17
Q

What are V1 receptors?

A

Receptors linked via G protein to phospholipase C which acts on membrane phospholipids to produce inositol triphosphate (IP3) and diacyl glycerol, increasing cytoplasmic calcium ions.
V1a = arterial / arteriolar smooth muscle (vasoconstriction).
V1b = Corticotrophs (ACTH production).

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18
Q

What are V2 receptors?

A

Receptors linked via G proteins to adenyl cyclase, which acts to form cAMP, activating protein kinase A (PKA), activating other intracellular mediators. Response = aquaporins (AQP2) inserted in apical membrane.
V2 = collecting duct cells (water reabsorption).

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19
Q

What are AQP3 and AQP4?

A

Aquaporins in the basolateral membrane of collecting duct cells which let water pass down its osmotic gradient from the cell to the blood plasma.

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20
Q

What are 2 major stimuli for vasopressin release?

A

Increased plasma osmolarity, detected by osmoreceptors.

Decreased arterial BP, detected by baroreceptors. Vasoconstriction increases BP.

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21
Q

What is the difference between central/cranial diabetes insipidus and nephrogenic diabetes insipidus.

A 
Central = lack of circulating vasopressin.
Nephrogenic = end organs (kidneys) resistance.
22
Q

Which artery feeds into the primary capillary plexus of the adenohypophysis? Which feeds into the neurohypophysis?

A

The superior hypophyseal artery.

The inferior hypophyseal artery.

23
Q

What is a portal network?

A

Blood from the systemic circulation drains from one capillary network to another, before returning to the heart.

24
Q

What does somatostatin, released from delta cells, do?

A

It inhibits release of insulin and glucagon (paracrine function).

25
Q

Give some effects of insulin.

A

Increased glycogenesis.
Increased glycolysis.
Increase glucose transport into cells by GLUT4
Decreased lipolysis
Increased lipogenesis.
Increase protein synthesis and amino acid transport.

26
Q

Give some effects of glucagon.

A

Increased hepatic glycogenolysis.
Increased lipolysis –> increased gluconeogenesis
Increased amino acid transport into liver –> increased gluconeogenesis.

27
Q

Give a brief mechanism of insulin release from a beta-islet cells.

A

Glucose taken into beta-cell by GLUT2 transporter. It is converted by glucokinase (hexokinase IV) to gluose-6-phosphate. This causes ATP production, closing ATP sensitive K+ channels and causing voltage dependent Ca2+ channels to open, which results in insulin synthesis and release.

28
Q

What can you measure to assess pancreas function?

A

C-peptide. Proinsulin is comprised of insulin and c-peptide, but insulin is hard to detect, so an assay for c-peptide is used.

29
Q

Why do blood glucose levels decrease when dipeptidyl peptidase-4 (DPP-4) inhibitors are taken as tablets?

A

A gut hormone, glucagon like peptide-1 (GLP-1), is secreted in response to nutrients in the gut. It suppresses glucagon secretion and hence stimulates insulin release. Endogenous GLP-1 is rapidly degraded by DPP-4, so inhibiting this enzyme decreases blood glucose levels.

30
Q

What is the term given to the stored insulin which is released to cope with a meal?

A

First phase insulin release (FPIR).

31
Q

Give the structure of the insulin receptor.

A

2 alpha subunits bound to 2 transmembrane beta subunits by disulphide bridges. The cytoplasmic domains of the beta-subunits each have a tyrosine kinase domain which phosphorylate cell protein substrates.

32
Q

How does insulin resistance lead to high BP (due to smooth muscle hypertrophy) and ischaemic HD even in the absence of diabetes?

A

Two proteins are associated with the insulin receptor: IPS (insulin receptor substrate) and Shc. IRS activates the PI3k-Akt pathway responsible for metabolic actions. Resistance affects this pathway and leads to compensatory hyperinsulinaemia. The Shc protein activates the MAPK pathway, which leads to growth and proliferation. Hyperinsulinaemia means this pathway is over-activated, leading to hypertrophy.

33
Q

What is the name of the tissue connecting the right and left lobes of the thyroid, and in 10-30% of the population, also connects the pyramidal lobe?

A

The isthmus.

34
Q

How are T3 and T4 produced by the thyroid gland?

A

Thyroid Stimulating Hormone (TSH) from the adenohypophysis binds to the TSH receptor (TSHR) on the basolateral membrane of follicular cells. This causes the follicular cell to produce thyroglobulin. This is transported into the colloid. TSH also stimulates iodide channels to transport iodide from the blood into the colloid. Thyroperoxidase (TPO) catalyses the iodination of thyroglobulin (TG) to form MIT and subsequently DIT (mono- and di- iodotryosine). T3 is produced by the biding of a MIT and DIT molecule in a coupling reaction: T4 (thyroxine) is produced when 2 DIT molecules are bound. These are released into the blood.

35
Q

What three proteins do thyroid hormones (iodothyronines) bind to in the blood?

A

Thyroxine-binding globulin (TBG) (70-80%)
Albumin (10-15%)
Prealbumin (transthyretin).

36
Q

What % of T3 and T4 are unbound in the blood?

A

0.5% and 0.05% respectively.(These are bioactive).

37
Q

What is the process by which T4 is converted into T3 in the peripheral tissues called?

A

Deiodination. T4 is essentially a prohormone, acting as a reservoir for T3 - the active hormone.

38
Q

What is reverse T3?

A

An inactive form of T3 produced by the deiodination of T4 at a different position.

39
Q

Give some actions of thyroid hormones.

A

Foetal growth and development.
Increased basal metabolic rate.
Increased protein, carbohydrate and fat metabolism.

40
Q

Contrast the latent period and half-life of T3 and T4

A

T3 has a latent period of 12 hours and half-life of 2 days

T4 has a latent period of 72 hours and half-life of 7-9 d.

41
Q

What is the Wolff-Chaikoff effect?

A

Iodide ions inhibit the production of T3 and T4.

42
Q

Describe negative feedback regarding the thyroid gland.

A

There is a direct negative feedback loop inhibiting TSH release from thyrotrophs in the adenohypophysis. There is an indirect negative feedback loop inhibiting release of TRH from the hypothalamus.

43
Q

Describe the embryological development of the thyroid.

A

Formed at back of tongue. Descends down the throat to form the thyroglossal duct. Replaced by foramen caecum: a dimple at the back of the tongue.

44
Q

Which nerve runs close to the thyroid?

A

The left recurrent laryngeal nerve: damage can change quality of voice or even lead to difficulty talking.

45
Q

Give 3 common thyroid disorders of neonates.

A

Agenesis (complete absence) - 1 in 4000 babies
Incomplete descent
Thyroglossal cyst (segment of duct persists and presents as a lump).

46
Q

Why do foetuses without thyroids not suffer irreversible brain damage in utero?

A

T4 can cross the placenta, so they have a thyroxine supply.

47
Q

What is a cretin and how is cretinism prevented.

A

A person with no thyroid gland, hence leading to brain damage and a low IQ.
All babies have a heel prick for a blood test for thyroid function (TSH levels) at 5-10 days old.

48
Q

Describe the epidemiology of thyroid disease.

A

5% of the population affected.
Female to Male ratio = 4:1
Overactive to Underactive = 1:1

49
Q

What is primary hypothyroidism (primary thyroid disease)?

A

Autoimmune damage to the thyroid (or due to an operation). Thyroxine levels decline; TSH levels climb.

50
Q

Give symptoms of primary hypothyroidism.

A

Deepening voice, depression & tiredness, cold intolerance (low BMR), weight gain with reduced appetite, constipation, bradycardia. Eventual myxoedema coma.

51
Q

What is hyperthyroidism? What are the causes?

A

Thyroxine levels rocket: adenohypophysis stops making TSH.
Graves’ disease: makes 3 antibodies.
One binds to the TSHR, stimulating thyroxine production.
2nd binds to muscle behind eye - exophthalmos.
3rd stimulates growth of shin - pretibial myxoedema.

52
Q

Give symptoms of hyperthyroidism.

A

Raised temperature (heat intolerance), high heart rate, myopathy, mood swings, losing weight and hungry all the time, sore eyes, goitre, tremor, can’t walk up stairs.

Life Cycle and Reproduction Systems (LCRS) (4 decks)

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