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Medicine 2 > Week 6 - Pituitary Tumour > Flashcards

Week 6 - Pituitary Tumour Flashcards

1
Q

What are the characteristics of endocrine glands?

A
  • Hormone secreted into circulation
  • Homrone out of circulation to target organ
  • TSH and thyroid hormones T3 amd T4
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2
Q

What are the characteristics of autocrine and paracrine glands?

A

Autocrine:

  • Hormone travels short distance in intersitital fluid to act on same cell than made substance
  • Prostaglandins i.e.

Paracrine:

  • Hormone travels short distance in interstitial fluid to neighbouring cell
  • Somatostatin on insulin secretion i.e.
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3
Q

What are the characteristics of neuroendocrine glands?

A
  • Hormones travel from nerve cell, in circulation, to target cell
  • Neurohormones
  • Oxytocin and arginine vasopressin i.e.
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4
Q

How and where are peptide hormones synthesised, released and metabolised?

A
  • Chains of AAs
  • From hypothalamus and pituitary, pancreas, and gastrointestinal tract
  • Synthesis:
    • Gene transcribed to mRNA, into cytoplasm, translation
    • Preprohormone forms and RER folding and cleavage
    • Prohormone = additional processing and cleavage
    • Hormone in secretory granule = mature
    • Stored until release via exocytosis
    • Controlled by regulating exocytosis
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5
Q

How are steroid hormones synthesised, released and metabolised?

A
  • Derived from cholesterol
  • Cortisol, aldosterone and sex hormones
  • Synthesis:
    • Precursor molecule and biosynthetic enzymes
    • Hormone not stored
    • Released via simple diffusion
    • Lipid soluble so readily crossed plasma membrane via plasma proteins
    • Enter blood
      • steroid hormone release = dependet on hormone synthesis
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6
Q

What hormones are derived from tyrosine?

A

Thyroid hormones

Catecholamines

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7
Q

What are the key differences between peptide and steroid hormone properties?

A

Peptides:

    • Hydrophilic
    • No plasma protein binding
    • Half life = minutes

Steroids:

    • Lipophilic
    • Bind to plasma proteins
    • Half life = days
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8
Q

How is hormone release regulated?

A
  • Feedback regulation
  • Neuroendocrine reflexes
  • Diurnal or circadian rhythm
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9
Q

What is involved in feedback regulation?

A
  • Consequences of a process acts to regulate rate next process occurs
  • Negative feedback = consequence negatively controls next process
  • Positive feedback = consequence enhances next process further
  • Simple or involvement of hypothalamic and pituitary tropic hormones
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10
Q

What are the mechanism by which endocrine disorders may develop?

A
  • Hormone excess
    • Hypersecretion, tumour. Grave’s disease
    • Cushing’s syndrome (excess cortisol)
  • Lack of hormone
    • Hyposecretion, genetic, immunological attack, destruction by disease, surgical removal
  • Decreased target-cell responsiveness
    • At level of receptor or downstream enzyme
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11
Q

How do you investigate endocrine disorders?

A
  • Signs and symptoms
  • Endocrine and hormone levels
    • Baseline, dynamic test, stimulation test, suppression test
  • Imaging
    • Tumour
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12
Q

How can you treat endocrine disorders?

A
  • Hormone replacement
  • Drugs to block hormone production
  • Drugs to enhance cellular hormone response
  • Radiotherapy and surgery if a tumour
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13
Q

What is the role of the posterior lobe in secretion of pituitary hormones?

A
  • Neurohypophysis
  • Neural tissue attached to hypothalamus via pituitary stalk
  • Secretes ADH and oxytocin
  • Hormones synthesised in cell bodies of neuron and stored in terminal ends of axons
    • Secreted by neurosecretion
    • Act on non-endocrine tissues
    • Blood supply = middle and inferior hyophyseal arteries
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14
Q

What is the role of the anterior lobe in pituitary hormone secretion?

A
  • Adenohypophysis
  • Glandular tissue growing from Rathke’s pouch
  • Main bulk = pars distalis = curls around pars tuberalis
  • Piece next to posterior pituitary = pars intermedia = secretes melanocyte stimulating hormone
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15
Q

What are the properties of anterior secreiton of pituitary hormones?

A
  • Mediated by hypothalamic releasing hormones
  • Blood supply is superioe hypophyseal arteries
  • External plexus collects from hypothalamus via pituitary protal system
  • Pituitary hormones secreted into lower capillary bed and drain into hypophyseal veins
  • Blood supply enters via pituitary stalk
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16
Q

What are the 2 main posterior pituitary hormones?

A
  • Arginine vasopression (AVP) / ADH
  • Oxytocin
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17
Q

What is the role of AVP / ADH in the posterior pituitary?

A
  • Stimulated by increase in bodily fluid osmolality
  • Cases vasoconstriction via V1 receptors
  • Act on DCT and CD in kindeys to increade permeability and reabsorption of water via V2 receptors
  • Stimulate ACTH release
18
Q

What is the role of oxytocin in the posterior pituitary?

A
  • Release stimulated by suckling and cervical stimulation
  • Stimulates milk let-down
  • Uterine smooth muscle contraction
  • Sexual behaviour
  • Used in labour to reduce pain
19
Q

What are the role of somatotrophs, lactotrophs, corticotrophs, thyrotrophs, and gonadotrophs?

A

Somatotrophs = somatotropin = growth hormone

Lactotrophs = prolactin = stimulates mammary glands

Corticotrophs = corticotrophin = stimulates cortisol release

Thyrotrophs = thyrotropin = TSH

Gonadotrophs = gonadotropins = LH, FSH, steroid homrone synthesis, follicular development / spermatogenesis

20
Q

What is the difference between tropic and trophic?

A

Tropic = have effect on endocrine gland

Trophic = promote growth and tissue integrity

21
Q

What are the causes, symtpoms, and treatment for hyperprolactinaemia?

A

Cause = prolactinoma

Symptoms = fertility loss, libido loss, galactorrhea, gynaecomastia

High rpolactin = inhibition of GnRH release

Treatment = dopamine receptor agonist, surgery, radiotherapy

22
Q

What are the causes, symptoms, and treatment for acromegaly?

A

Cause = GH-secreting tumour

Symptoms = coarsening facial features, englarged hands + feet, headaches, sleep apnoea, hypertension, glucose intolerance, loss of periods

Treatment = surgery, radiotherapym somatostatin analogues to inhibit GH release

23
Q

What are the causes and treatment of Cushing’s syndrome?

A

Cause = excess glucocorticoid activity, ACTH-secreting anterior pituitary tumour

Treatment = tumour removal and radiotherapy

24
Q

What are the causes and treatment of hypopituitarism?

A

Cause = deficiency of 1+ hormones, pituitary adenoma

Treatment = hormone replacememt

25
Q

What is the difference between synergistic and permissive hormone actions?

A

Synergistic = hormone produces + enhanced response than sum of either hormones alone

Permissive = effects of hormones oppose eachother

26
Q

How does GH act?

A
  • Synthesised in somatotrophs
  • Major growth role
  • Important in metabolism
  • Acts via GH receptors on target cell
27
Q

What is the role of IGF-1?

What is the role of insulin in growth?

A

Required for action of growth hormone

28
Q

What is the role of sex hormones in growth?

A
    • during puberty
  • Liner growth and + muscle
  • Stop bone elongation
  • Promote epiphyseal plate closure
29
Q

What is the role of cortisol / glucocorticoids in growth?

A
    • gluconeogenesis
    • lipolysis
    • protein breakdown
  • Can inhibit GH release
  • Can cause growth retardation in children
30
Q

How does GH act to cause growth?

A
    • gluconeogenesis
    • lipolysis
    • AA uptake and protein synthesis
31
Q

What is the action of thyroid hormones on growth?

A
  • Permissive action
  • Role on GH activity in promoting growth
    • role in CNS development
32
Q

What are causes and treatment of stunted growth?

A
  • Pituitary dwarfism (GH deficiency)
  • Hypothyroidism (insufficient THs for GH activity)
  • Cushing’s syndrome (excess cortisol)
  • Congenital adrenal hyperplasia (+ androgens = early bone maturation)
  • Sexual precocity (F = before 8, M = before 9)

Treatment = human growth hormone therapy

33
Q

What are S&S of GH deficiency in adults?

A
  • Psychological changes
  • Malaise, anxiety, depression
  • Osteoporosis
  • Poor muscle tone
  • Impaired hair growth
  • Increase in adipose tissue
34
Q

What are causes of accelerated growth?

A
  • Gigantism
  • Acromegaly (GH secreting tumour)
  • Hyperthyroidism (excess THs = GH promotion)
  • Sexual precocity (inital + bone gorwth, short adult height, early bone maturation)
  • Eunuchoidism (hypogonadism)
35
Q

What is the role of TSHR-stimulating antibodies in Grave’s disease?

What causes Grave’s ophthalmopathy?

A

Autoantibodies stimulate TSH receptors

  • Swelling behind eyeballs
  • TSH receptors recognised
  • Inflammation
  • Cytokine release
  • Oedema and fibrosis
36
Q

What causes pre-tibial myxoedema?

A

Additional hylauronic acid deposition and liquid retention

37
Q

What happens in atrophic thyroiditis and Hashimoto’s thyroiditis?

A
  • Hypothyroidism
  • TSHR blocking antibodies involved
  • Hypothyroidism
  • Low BMR, weight gain
  • Pain, numbness
  • Goitre
  • Cold sensitive
  • Tissue destruction due to CD8 + T cell activation
  • Macrophage activation and tissue damage
38
Q

What happens during pernicious anaemia and diabetes mellitus?

A
  • Gastric autoimmunity
  • Parietal cells produce intrinsic factor, essential for ileal B12 absorption
  • Parietal cells = targetes to less B12 absorption
  • Autoantibodies to intrinsic factor
  • Autoimmune attack on beta cells of islets of Langerhans in pancreas
39
Q

What happens in myasthenia gravis and autoimmune haemolytic anaemia?

A
  • Autoantibodies inhibit ACh receptors
  • Prevention of neuromuscular signalling
  • Type 2 sensitivity
  • Causes opsonization of RBC
    • Enhances phagocytosis through Fc receptor recognition
  • Active compliment causes RBC lysis
40
Q

What happens during Goodpasture’s disease and Pemphigus vulgaris?

A
  • Type 2
  • Autoantibodies bind directly to glomerular basement membrane
  • Autoantibodies to epidermal cadherin
  • Fragile blisters on skin
41
Q

What happens to kidney, skin, and blood vessels in systemic lupus erythematosus?

A
  • Autoantibodies to DNA, histones, ribonuclear proteins, and cytoskeletal proteins
  • Deposits in kidney glomeruli
  • Red rash on skin (photosensitivity)
  • Inflammation
  • Vasculitis

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