pituitary gland and thyroid gland Flashcards
1
Q
- What is meant by a hormone?
A
A messenger carried from the organ where they are produced to the organ which they affect by means of blood stream
2
Q
- What are the differences between peptide and steroid hormones?
- Synthesis
- Storage
- Receptors
A
Peptide hormones are synthesised as pro-hormones requiring further processing, whist steroid hormones are synthesised in a chain of reactions from cholesterol
Peptide hormones are stored in vesicle, whereas steroid hormones are not stored
Peptide hormones bind receptors on the cell membrane and transduce signal using 2nd messenger systems
Steroid hormones bind to intracellular receptors to change gene expression directly
3
Q
- Which part of the pituitary gland is continuous with the hypothalamus?
- Where does the pituitary gland sit?
- What is the pituitary gland suspended by from the brain?
A
Posterior pituitary gland; anterior is anatomically distinct with the hypothalamus, with presence of no neural tissue.
Sella turcica (small depression in the sphenoid bone) Pituitary stalk (infundibulum)
4
Q
- What 3 regions can the anterior lobe be divided into?
- What is another name for the posterior pituitary gland?
A
Pars tuberalis
Pars intermedia (thin epithelial layer that separates anterior pituitary from posterior) Pars distalis (responsible for hormone secretion) Neurohypophysis
5
Q
- What type of neurones regulate anterior pituitary function?
- Where do hypothalamic parvocellular neurones terminate and what do they release?
A
Hypothalamic Parvocellular neurons
Regulate it by secretion of hormones into into hypophyseal vessels
Median eminence (these neurones are very short) Hypothalamic releasing/inhibitory factors into capillary plexus in median eminence
6
Q
- Which endocrine cells is the adenohypophysis made up of (5)?
A
Somatotrophs
Lactotrophs Corticotrophs Thyrotrophs Gonadotrophs
7
Q
- Outline the pathway/process of the hypothalamo-pituitary portal system
A
Axon terminals of hypothalamic neurosecretory cells release hormones (regulatory and inhibitory) into the hypothalamo-pituitary portal system
RHs and IHs travel through hypophyseal vessels to the anterior pituitary gland Secondary fenestrated (leaky) capillary plexus leads release of hypothalamic factors. RHs and IHs stimulate or inhibit release of hormones from anterior pituitary cells Anterior pituitary hormones leave the gland via the blood
8
Q
- Outline the process of thyroid hormone production
A
Axon terminals of hypothalamic neurosecretory cells release Thyrotropin Releasing Hormone (TRH) into hypothalamo-hypophysial portal system.
TRH travels to anterior pituitary via portal system. TRH stimulates release of TSH (thyrotropin) from anterior pituitary thryotrophs TSH leaves gland via blood to travel to thyroid gland to stimulate thyroid hormone release (T4- thyroxine)
9
Q
- What hormone do each of the 5 classes of anterior pituitary cells release?
A
Somatotrophs - Growth hormone (somatotrophin)
Lactotrophs - Prolactin Thyrotrophs - Thyroid stimulating hormone (TSH) Gonadotrophs - LH and FSH Corticotrophs - Adrenocorticotrophic hormone (ACTH, corticotrophin)
10
Q
- Where are hypothalamic regulators released from?
- Which hypothalamic regulator inhibits somatotrophs from releasing somatotropin and which regulator activates release of growth hormone?
A
Parvocellular neurosecretory cells within the hypothalamus; subsequently released into the primary capillary plexus of the median eminence
Somatostatin (inhibit) Growth hormone releasing hormone (GHRH)
11
Q
- What effect does dopamine have in terms of hypothalamo-pituitary regulation?
- Gonadotrophin releasing hormone causes the release of which hormones from the anterior pituitary gland?
- Where are the receptor sites for gonadotrophins (LH and FSH) in males?
A
High levels of dopamine inhibit the release of prolactin from lactotrophs in the anterior pituitary gland
Luteinising hormone and follicle stimulating hormone (LH and FSH)
Testes
12
Q
- What is the target gland for prolactin?
- The adrenal cortex is the target organ for which hormone?
A
Mammary gland (located in the breast)
Adrenocorticotrophic hormone (ACTH) released by corticotrophs from the anterior pituitary gland
13
Q
- Explain the pathology behind a bitemporal hemianopia and how the defining symptom arises
A
A pituitary tumour (adenoma) compresses the optic chiasm. It also covers the sella turcica (supra-sella tumour as it occurs above the sella turcica). The optic chiasm is the region where the nerve fibres transmit sensory information from lateral visual to the occipital lobes
Compression of the optic fibres from the nasal retinae leads to loss of stimulation from lateral fields to occipital lobe (this is where the primary visual cortex) → Loss of peripheral vision
14
Q
- Outline the neuroendocrine reflex arc for milk production
A
Mechanical stimulation of the nipple stimulates the touch and sensory receptors, activating the afferent pathways. Action potentials traverse along the axons through the ascending sensory pathways
Afferent signals integrate in hypothalamus and inhibit dopamine release by dopaminergic parvocellular neurones Less dopamine in the hypothalamic-pituitary portal system results in less inhibition of anterior pituitary lactotrophs Increased plasma protein increases milk secretion in mammary glands
15
Q
- Outline the mechanism of growth hormone action
A
Secretion of growth hormone by endocrine somatotrophs from anterior pituitary directly binds to complementary target within general tissue (muscle and bone)
Growth hormone can bind to growth hormone receptors of liver → Synthesis of IGF-1 and IGF-2 (Insulin-like Growth Factor - **Somatomedin**) IGF-1 is a mediator of growth hormone-stimulated somatic growth, binding to target receptors
16
Q
- What is the difference between gigantism and acromegaly?
A
Gigantism → Growth hormone excess happens before epiphyseal plate fusion (puberty ends)o patient is VERY tall
Acromegaly → Growth hormone-producing tumour; after epiphyseal plate fusion. Somatotrophs secrete excessive concentration of growth hormone (same mechanism as gigantism)
17
Q
- List clinical features of acromegaly
A
Coarsening of facial futures
Macroglossia (big tongue) Prominent nose Large jaw (prognathism) Increased hand and feet size (ring and shoe size) Increased sweatiness (clammy hands) Headaches Obstructive sleep apnoea (soft-tissue changes surrounding upper airway leading to narrowing → Collapse during sleep → Causes disruption to sleep patterns) Acromegaly DOESN'T result in increased height.
18
Q
- What type of neurones from the hypothalamus have axon fibres going sending signals to the posterior pituitary gland?
- Which nuclei do magnocellular axons extend from?
- Which hormones does the neurohypophysis release?
- what two functions does ADH have?
A
Hypothalamic magnocellular neurones
Supraoptic (AVP) and paraventricular (oxytocin) nuclei of hypothalamus
Arginine vasopressin (AVP); also known as anti-diuretic hormone (ADH)
Oxytocin
water reabsorption in kidney (via V2 receptor) and vasoconstrictor (via V1 receptor in the kidney)
19
Q
- Outline the regulation of the posterior pituitary gland in terms of the hypothalamic neurones and the hormones that are concerned
A
Supraoptic and paraventricular neurones (hypothalamic magnocellular neurones in hypothalamus) produce AVP and oxytocin respectively
Excitation of these 2 hypothalamic magnocellular neurones stimulates the release of of AVP and oxytocin into the posterior pituitary where they diffuse into blood capillaries They then leave the posterior pituitary via the blood
20
Q
- Outline the physiological action of ADH for stimulating water reabsorption.
A
ADH increases the permeability of the distal convoluted tubule and collecting duct to water
ADH binds to V2 G protein-coupled receptors of cell-surface membrane
Leads to formation of cAMP. cAMP production enables protein kinase A to activate aquaporin-2 and 3 genes Aquaporins insert into the tubule membranes, increasing permeability Water leaves renal collecting ducts making the urine more concentrated and reabsorbing water into plasma When ADH levels fall the level of cAMP production also decreases, causing a withdrawal of water channels → Cell becomes impermeable
21
Q
- What effect does oxytocin have during the delivery of a baby?
- What effect does oxytoxin have during milk ejection?
A
Affects the uterus at parturition
Contraction of the myometrial cells Affects the breast during lactation Contraction of the myoepithelial cells
22
Q
- Outline the steps involved in the neuroendocrine reflex arc of milk ejection
A
Mechanical stimulation of nipple and surrounding area activates afferent pathways
Afferent signals integrated in hypothalamus and stimulate oxytocin-releasing neuron activity Action potentials travel down oxytocin neurons and oxytocin is secreted into the bloodstream Increased plasma oxytocin increases milk ejection in mammary glands
23
Q
- What do parafollicular cells release?
- Which glands are imbedded in the thyroid gland and what is their function?
A
Calcitonin; involved in the regulation of calcium metabolism in the body.
Parathyroid glands (superior and inferior on both sides); Responsible for secretion of parathyroid hormone → Elevate Ca2+ levels by degrading bone and stimulating calcium release, which increases the bodies ability to absorb calcium from food.
24
Q
- Where does the thyroid gland originate from?
- What is the pyramidal lobe?
A
Base of the tongue.
Extension of the thyroid gland (remnant of thyroglossal duct); ~55% of individuals have it.
25
- Explain the process of thyroid hormone synthesis
TSH secreted by anterior pituitary by thyrotroph cells enter circulation → bind to target TSH receptors on the cell surface membrane of follicular cells
Activation of secondary messenger system results in gene expression of thyroglobulin(TG) and thyroid peroxidase (TPO) synthesis
Active transport of iodide ions into follicular cells via sodium-iodide symporter (NIS)
(Sodium grad. maintained by Na+-K+ ATPase)
iodide ions and TG move into the colloid
Iodide binds to aromatic ring on tyrosine residues of TG → 3-monoiodotyrosine (MIT); further iodination forms 3,5-diiodotyrosine (DIT). This iodination of TG is caused by thyroid peroxidase in the presence of hydrogen peroxide in the colloid.
Coupling of MIT + DIT = T3 (triiodothyronine)
Coupling of DIT + DIT = Tetraiodothyronine (T4) → Thyroxine
Endocytosis by apical membrane of iodinated TG into follicular cells → subjected to proteolysis in lysosomes to cleave tyrosine residues from large protein → Liberation of T3 and T4
Both T3 and T4 diffuse into the blood
26
- Which thyroid hormone is more active?
- What is the major hormone product of thyroid gland?
- When is T4 deiodinated into reverse T3 and why?
T3 (3,5,3-**triiodothyronine)**
T4; thyroxine; tetraiodothyronine
Under circumstances requiring reduced metabolism (starvation).
rT3 is the biologically inactive form of T3.
27
- Where does most circulating T3 come from?
| - What are thyroid hormones (iodothyronines) transported by?
80% from deiodination of T4 by a deiodinase enzyme (T4→ T3)
20% from directly from thyroid secretion
Transported by 3 plasma proteins:
Thyroid-binding globulin (70-80%)
Albumin (10-15%)
Prealbumin (aka transthyretin)
28
- What are the half-lives of T3 and T4?
| - What percentage of T3 and T4 are bioactive components (unbound)?
T3 ~ 2 days
T4 ~ 7-9 days
T3 - 0.5%
T4 - 0.05%
29
how does thyroid hormone affect...
- basal metabolic rate
- protein, carb, fat metabolism
- foetal growth
Increased basal metabolic rate.
Increased heat production
Inceased 02 consumption
Increase protein, carbohydrate and fat metabolism (inc glucose absorb, glycogenolysis, protein synthesis, gluconeogenesis, lipolysis)
Have effects on CNS → Important for brain development (Maturation of CNS)
Essential for foetal growth and development- importantly CNS devel
30
- Explain the hypothalamo-pituitary-thyroid negative-feedback system?
Parvocellular hypothalamic neurones release TRH into primary capillary plexus → Hypophyseal portal system
TRH → Secondary capillary plexus → Stimulates thyrotrophs in the anterior pituitary to release TSH → Acts on thyroid gland to release T3 and T4
Elevated levels of T3 and T4 result in a negative feedback effect, directly acting on anterior pituitary to inhibit secretion of thyrotropin and indirectly on the hypothalamus (TRH)
31
- Are thyroid disorders more common in men or women?
- What causes primary hypothyroidism?
- What affect does hypothyroidism have on TSH levels?
Women (4:1 ratio)
Autoimmune thyroid diseases - Hashimoto's thyroiditis is typically associated with hypothyroidism (Presence of one autoimmune disease increases the risk of others)
TSH levels elevated due to reduced inhibitory effect from T3/T4
32
- How can you treat hypothyroidism and what is a common dose?
- What are some potential implications of this treatment?
- What are some complications of combined thyroid hormone replacement treatment (T3 + T4)?
Levothyroxine (T4 equivalent pill); administered orally - Lifelong treatment.
Usually 100 micrograms (less if patient is older)
adjust dosing based on TSH levels
Potential heart attack, weight loss, headaches, rapid HR (tachycardia)
Symptoms of toxicity → Palpitations, tremor, anxiety (combination treatment often suppresses TSH)
33
- What effect does hyperthyroidism have on your thyroxine levels?
- What are the causes of hyperthyroidism?
Thyroxine levels rise
Graves' disease - Autoimmune condition → Whole gland smoothly enlarged and overactive
Toxic multinodular goitre
Solitary toxic nodule (toxic adenoma → single nodule undergoes hypertrophy
34
- Explain the pathophysiology of Graves' disease.
| - What are the common features of Graves' disease?
Antibodies (thyroid-stimulating immunoglobulins) bind onto TSHr in the thyroid leading to excessive thyroid hormone release (^ T4 and T3)
Smooth goitre
Exophthalmos→ Antibodies bind to muscles of eye causing the eye to project forward.
Pretibial myxoedema → Antibodies stimulate growth of soft tissue on shin. (Hypertrophy)
35
symptoms of hypothyroidism?
deepening voice
depression
myxodema coma
enlarged thyroid
opposites to hyperthyroidism
- bradycardia (slow HR)
- cold intolerance
- weight gain
- dry, rough skin
- tiredness
- constipation
36
Symptoms of hyperthyroidism?
```
myopathy
mood swings
palpitations
hand tremor
sore eyes
goitre
```
opposites to hypothyroidism
- tachycardia (fast HR)
- heat intolerance
- weight loss with increased appetite
- wet moist skin
- nervousness, insomnia, irritability
- diarrhoea
37
where does the adenohypophysis originate from?
where does the neurohypophysis originate from?
up growth from the oral ectoderm
of the primitive oral cavity
called Rathke' s pouch
Epithelial origin
downgrowth of the diencephalon
that forms floor of the the third ventricle
neural origin
38
What is TG?
how does T3 affect target cells?
pro hormone of thyroid hormone- subject to iodination
effects nuclear receptors on target cells and impacts gene expression
39
How is the thyroid gland formed?
Midline outpouching from the floor of the pharynx- originates from the base of the tongue
development of the thyroglossal duct
divides into 2 lobes
duct disappears leaving foreman caecum
final position by week seven
thyroid gland develops
40
what is cretinism?
how is TSH measured in babies?
aka untreated congenital hypothyroidism
when baby cant produce their own thyroid hormone after being born
heel prick test
41
how does thyroid hormone affect...
- catecholamine
- GI
- Reproductive system
- growth
Enhance the effects of catecholamines leading to tachycardia, glycogenolysis and lipolysis
Effects on the GI (how fast food is moving) and reproductive systems (period/ fertility)
inc growth formation and bone maturation
