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BMS292 > Topic Two: Endocrine Function - Pituitary Gland Disorders > Flashcards

Topic Two: Endocrine Function - Pituitary Gland Disorders Flashcards

1
Q

Where are most hormonal endocrine processes regulated?

A

Hypothalamic-pituitary axis

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2
Q

Hypothalamic control begins with the secretion of hormones that directly target organs. What does the hypothalamus produce and how is it transported?

A

Two hormones
Transported along neurons to the posterior pituitary gland before being released into the blood stream.

  • Oxytocin (OXT) for uterine contractions
  • Antidiuretic hormone (ADH) for water retention and blood volume
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3
Q

The second stage of hypothalamic control = the release of regulatory hormones that control secretion of hormones from the pituitary gland, how does this occur?

A
  • Neuroendocrine cells in the hypothalamus secrete hormones that stimulate endocrine cells in the pituitary to secrete trophic hormones.
  • These travel to target glands to stimulate hormone release
  • Hormones exert an action on the tissues and causing physiological effect
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4
Q

Mention some regulatory hormones that are produced in the hypothalamus and control release of hormones from the anterior pituitary gland.

A
  • Prolactin (releasing hormone)

- Prolactin (inhibiting hormone)

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5
Q

Briefly mention communication between the hypothalamus and the adrenal gland.

A

Autonomic neurons project from the hypothalamus to the adrenal gland
Sympathetic nervous system activation stimulates the release of hormones from the adrenal gland

Hormones such as
Epinephrine
Norepinephrine

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6
Q

How does endocrine regulation occur?

A

By physiological stimuli or by feedback loops that depend on the circulating concentration of the hormones themselves

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7
Q

How is endocrine dysfunction classified?

A

It reflects ‘hyper-‘ (too much) or ;hypo-‘ (too little) function of endocrine signalling

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8
Q

Endocrine dysfunction occurs because?

A

Direct dysfunction of the endocrine process
OR
Dysfunctional regulation of the process

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9
Q

When effecting the endocrine gland itself - hypofunction can arise due to?

A
  • Absence or impaired development of gland (congenital defects)
  • Absence or dysfunction of an enzyme needed for hormone synthesis or release
  • Gland destruction or atrophy - from blood flow disruption, infection or inflammation, autoimmune diseases, neoplastic growth
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10
Q

When effecting the endocrine gland itself - hyperfunction can arise due to?

A
  • Overdevelopment of the gland (congenital defects)
  • Over production or hyperfunction of an enzyme needed for hormone synthesis or release
  • Para neoplasia: Hormone producing tumour of gland.
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11
Q

Regarding hormone circulation HYPOfunction can arise due to?

A

Hormone destroyed by circulating antibodies
Absence or dysfunction of a carrier protein.
Overactivity of metabolic clearance of hormone.

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12
Q

Regarding hormone circulation HYPERfunction can arise due to?

A

Hyperfunction can arise due to:
Underactivity of metabolic clearance
Dysfunction of a carrier protein (promoting too much release of free hormone).

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13
Q

Regarding regulation, hyppfunction can arise due to?

A

Hypofunction can arise due to:
Increased production of a regulating hormone or increased presence of a regulating substrate.
Increased negative receptor expression on endocrine cells or reduced positive receptor expression.
Increase endocrine cell responsiveness to negative regulatory signalling.

HYPERfunciton can arise due to the opposite of the above.

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14
Q

What is hyperpituitarism?

A

Most commonly due to pituitary tumour (adenoma)

These are usually benign and usually of one type of pituitary cell only.

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15
Q

Hyperpituitarism has characterised high levels of what hormones?

A 
Thyrotrophs		
Corticotrophs	
Somatotrophs		
Gonadotrophs		
Lactotrophs
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16
Q

What is hyperpituitarism?

A

Most commonly due to pituitary tumour (adenoma)

These are usually benign and usually of one type of pituitary cell only.

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17
Q

Hyperpituitarism has characterised high levels of what hormones?

A 
Thyrotrophs		
Corticotrophs	
Somatotrophs		
Gonadotrophs		
Lactotrophs
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18
Q

What are some of the symptoms for hyperpituitarism?

A 
Vision problems (due to pressure on optic nerve)
Headaches
Symptoms of hypopituitarism if tumour ends up damaging the other functioning tissue
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19
Q

What is prolactinoma?

A

Prolacting secreting tumor

20
Q

What is a therapy for hyperpituitarism?

A

Long term replacement of target gland hormones

21
Q

What is therapy for prolactinoma?

A

Medical: inhibit PRL secretion with dopamine agonist.
Must be one that does not cross blood brain barrier (avoid side effects), e.g bromocriptine or cabergoline

Surgical: radiotherapy or excision of tumour

22
Q

Remind me about growth hormone.

A

Growth hormone producing cells of the anterior pituitary are known as somatotrophs. Growth hormone is released from somatotrophs in response to GHRH release from the hypothalamus

23
Q

Growth Hormone secretion is stimulated by?

A

hypoglycaemia, fasting, starvation, high amino acid levels, trauma, excitement, stress, heavy exercise

24
Q

Growth Hormone is inhibited by?

A

hyperglycaemia, fatty acid release, cortisol, obesity

25
Q

What are the three types of GH deficiency in children?

A
  • Primary GH deficiencies
  • Secondary GH deficiency
  • Congenital GH deficiency
26
Q

Briefly outline Primary GH deficiencies

A

Pituitary agenesis during development leads to a lack of somatotrophs (growth hormone producing cells of the anterior pituitary).
Idiopathic GH deficiency: lack of GHRH yet have adequate somatotrophs

27
Q

Briefly outline Secondary GH deficiency.

A

Pan-hypopituitarism: conditions that cause deficiencies of all anterior pituitary hormones

28
Q

Briefly outline Congenital GH deficiency

A

Genetic abnormality in the production of, or response to GH. Normal birth length, decreased growth rate evident by age 1-2 years

29
Q

How does GH manifest its deficiency in children?

A 
Normal intelligence
Short stature
Immature facial features
Delay in skeletal maturation
Puberty often delayed
30
Q

What are the two types of GH deficiencies in adults?

A
  1. GH deficiency that was present in childhood and continued

2. GH deficiency that developed during adulthood usually due to pituitary tumour or its treatment

31
Q

GH deficiency results in a metabolic syndrome characterised by what?

A

Central adiposity
Increased visceral fat
Insulin resistance
Dyslipidaemia

32
Q

Metabolic syndromes such as Central adiposity, Increased visceral fat, Insulin resistance and
Dyslipidaemia effect what?

A

These effects increase the risk of cardiovascular mortality in GH deficient adults

33
Q

When GH is in excess in children what occurs?

A

Gigantism

  • GH excess occurring before puberty and fusion of epiphyses
  • Results in increased linear growth
34
Q

When GH is in excess in adults what occurs?

A

Acromegaly
- GH excess occurring after puberty and fusion of
epiphyses
- May result in localized abnormal growth.

35
Q

GH excess in adults is mostly caused by?

A
  1. Somatotropic (growth hormone producing cell) adenoma (95%)
  2. Excess GHRH; ectopic GHRH (small cell lung carcinoma); ectopic GH secretion from non-endocrine tumours
36
Q

How is excess GH manifested in adults?

A
  • Soft tissues continue to grow & small bones of hands, face and skull bones enlarge
  • Laryngeal and bronchial cartilages enlarge - voice deepens/bronchitis
  • Arthropathy
  • Skin thickening, hypertrophy of sebaceous and sweat glands
  • Hypertension due to cardiac hypertrophy (cardiomegaly)
  • Effects associated with hypophyseal tumour e.g. severe headache
  • Sleep apnoea
  • Increased risk of various cancers (e.g. colorectal)
37
Q

What is the metabolic effect of an excess of GH?

A

Increased free fatty acids = Accelerated atherosclerosis
Decreased skeletal and adipose tissue uptake of glucose/increased liver glucose conversion

Increased BGL → overstimulation of pancreatic β cells → increased insulin secretion → GH induced insulin resistance → increased BGL
β cell burnout → insulin deficiency → diabetes mellitus

38
Q

What is the metabolic effect of an excess of GH?

A

Increased free fatty acids = Accelerated atherosclerosis
Decreased skeletal and adipose tissue uptake of glucose/increased liver glucose conversion

Increased BGL → overstimulation of pancreatic β cells → increased insulin secretion → GH induced insulin resistance → increased BGL
β cell burnout → insulin deficiency → diabetes mellitus

39
Q

What are treatment options for excess GH?

A
  • Surgical excision of tumour
  • Radiotherapy
  • GH receptor antagonists
  • Octreotide acetate - somatostatin analogue
  • Lower blood levels of GH and IGF-1 in persons with acromegaly
  • Reduces tumour size
  • Also inhibits GIT hormones including insulin and glucagon
40
Q

What is ADH also known as?

A

Vasopressin or arginine vasopressin

41
Q

What does ADH act on?

A
  • Acts on kidneys to promote water reabsorption
  • Promotes insertion of aquaporins (water channels) into membrane of collecting ducts in kidney tubules
  • Secretion promoted by increased plasma osmolarity
  • Minor effect to promote vasoconstriction (more in other species)
42
Q

What is deficiency in ADH called?

A

Diabetes insipidus
Diabetes = overflow, insipidus = tasteless
Symptoms: polyuria (excessive urination), dehydration & polydipsia (excessive thirst)
Treatment synthetic ADH (desmopressin), intranasal

43
Q

What is ADH excess also known as?

A

SIADH (Syndrome of inappropriate antidiuretic hormone secretion)

44
Q

What causes SIADH?

A

Range of common causes including medication side effects (including anaesthetics & antidepressants) and lung disease

45
Q

What is treatment for SIADH?

A
  • Discontinue the medication causing the problem
  • Fluid restriction
  • Hypertonic saline if sodium levels too low
46
Q

Diabetes Insipidius VS SIADH

BMS292 (13 decks)

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