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MEH Sem 1 > Lecture 11 - Pituitary Gland > Flashcards

Lecture 11 - Pituitary Gland Flashcards

1
Q

What is the relationship btw the hypothalamus and the pituitary gland?

A
  • Complex functional unit

- Major link btw the endocrine and nervous system

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2
Q

Where is the pituitary gland?

A
  • Beneath the hypothalamus

- In a socket of bone called sella turcica

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3
Q

Give some examples of processes that are modulated by the hypothalamus & the pituitary gland

A
  • Thyroid gland function
  • Lactation
  • Adrenal gland function
  • Water homeostasis
  • Body growth
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4
Q

What is the distinct embryological origin of the anterior pituitary gland (adenohypophysis) ?

A
  • Primitive gut tissue

- Oral ectoderm

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5
Q

What is the distinct embryological origin of the posterior pituitary gland (neurohypophysis) ?

A
  • Comes from neuroectoderm

- Primitive brain tissue

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6
Q

Which pituitary gland is connected to the hypothalamus?

A
  • Posterior pituitary gland

- Hypo. drops down through the infundibulum

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7
Q

What is the definition of a nuclei?

A
  • A collection of cell bodies w. similar func.
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8
Q

Where is oxytocin & ADH (vasopressin) formed & stored?

A
  • Produced by neurosecretory cells in the supraoptic & paraventricular nuclei of hypothalamus
  • Stored & released from P.P to act on distant targets
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9
Q

How does the hypothalamus control the function of the anterior pituitary gland?

A
  • Hypothalamus synthesise hormones –> stored in median eminence before release into hypophyseal portal system
  • The hormones stimulate/inhibit target endocrine cells in A.P
  • Hormones in A.P act on distant targets (endocrine function) or act on neighboring cells (autocrine & paracrine func.)
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10
Q

What is oxytocin responsible for?

A
  • Ferguson’s reflex

- Milk let down and uterine contractions during birth

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11
Q

Name all 6 tropic hormones of the hypothalamus

All hormone have direct effect on release on A.P hormones

A
  • TRH (Thyrotropin RH)
    Stimulate A.P to secrete TSH
  • CRH (Corticotropin RH)
    Stimulate A.P. to secrete ACTH
  • PIH (Prolactin release inhibiting hormone)
    Prevent prolactin secretion
  • GnRH (Gonadotropin RH)
    Stimulate FSH & LH
  • GHRH (Growth hormone RH/ somatotropin)
  • GHIH (Growth hormone IH/ somatostatin)
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12
Q

What is the hormones produced in A.P?

A
  • TSH (Thyroid stimulating H)
    Secretion of T3 & T4
  • ACTH (Adrenocorticotropic H)
    Secretion of cortisol from adrenal glands
  • LH + FSH
    Stimulate ovulation + development of follicles/sperm
  • PRL
    Milk secretion & mammary gland formation
  • GH
    Growth & energy metabolism + IGF (Insulin-like growth factor/Somatomedin: stimulate growth and decrease B.G)
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13
Q

Name factors that influence growth

A
  • Genetics
  • Nutrition
  • Enviroment
  • Hormones
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14
Q

What is the diff. btw necrosis and apoptosis?

A
  • Necrosis is cell death by damage. (caused by hypoxia, lack of nutrients, cellular damage)
  • Apoptosis is programmed cell death
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15
Q

What is GH? What is it stimulated & inhibited by?

A
  • Protein hormone that has a signal peptide that must be cleaved before proper folding
  • ✅ by GHRH, X by somatostatin
  • ✅ deep sleep, X REM
  • ✅ stress, exercise, ⬇️ F.A. & glucose
  • ✅ fasting, X obesity
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16
Q

What does liver & skeletal muscle produce in response to GH?

A
  • IGF (Insulin-like growth factors)
17
Q

What is the function of GH & IGF?

A
  • Stimulates long bone growth
    (length + width before epiphyseal plate closure, width after)
  • IGF stimulate bone and cartilage growth

Both:

  • Maintain muscle & bone mass
  • Promote healing and tissue repair
  • Modulating metabolism
18
Q

List factors that control GH secretion

A
  • ✅ deep sleep, ❌ REM
  • ✅ stress (trauma, surgery, fever) , exercise
  • ✅ decrease glucose/fatty acids
    N.B. GH stimulates gluconeogenesis, lipolysis
  • ✅ fasting, ❌ obesity
19
Q

How does long loop and short loop feedback regulate GH secretion?

A
  • IGFs inhibit GH by stimulating the release of somatostatin

- Short loop mediated by GH itself via somatostatin release

20
Q

What does GH deficiency lead to in childhood? What is the treatment?

A
  • Pituitary dwarfism: proportionate type of dwarfism
  • Complete or partial deficiency
  • Result in delayed or X sexual development n teen years, slow growth rate, short stature
  • Treatment: GH therapy
21
Q

What does GH excess result in childhood?

A
  • Gigantism: Epiphyseal plates X close, long bones grow

- Rare (often caused by pituitary adenoma)

22
Q

What does GH excess result in adults?

A
  • Acromegaly: occurs after epiphyseal plates close, long bones X grow
  • Large extremities: hands,feet,lower jaw
23
Q

How does GH exert its effects on cells?

A
  • GH receptors activate Janus kinases (JAKs)
  • = know
    1. GH binds to receptor –> receptor dimerisation
      1. Receptor change confirmation
      2. Activates kinase activity of receptor
      3. Phosphorylated tyrosine residues become binding sites for other signaling proteins
    1. Activation of signaling proteins
    1. Transcription factors activated and IGFs produced
24
Q

What type of IGFs are there?

A
  • IGF 1 = adults, IGF 2 = kids

- Binding proteins modulate availability of IGFs

25
Q

What does IGF do?

A
  • Increase protein synthesis
  • Stimulate hyperplasia, hypertrophy
  • Increase lipolysis
26
Q

How do pituitary tumours present?

A
  • Mass effect of tumour on local structures: vision loss, headache
  • Abnormality in pituitary function: Hypo-/Hyper-
27
Q

What causes prolactinoma? How is it treated?

A
  • Pregnancy, Stress, Exercise
  • Treated with tablets not operation (even if tumour is very large)
  • Tumour shrink with dopamine agonist (inhibits prolactin)

**X give dopamine antagonists (anti-sickness/anti-psychotic drugs) = can cause high prolactin

28
Q

What are long-term complications of untreated acromegaly?

A
  • Premature cardiovascular death
  • Increased risk of colonic tumours
  • Hypertension and diabetes
  • Disfiguring of body
29
Q

What are some tests to confirm acromegaly?

A
  • Oral Glucose Tolerance Test with GH response
    (Failure to suppress confirms diagnosis)
  • Elevated IGFs
  • Growth Hormone Day Curve (elevated GH)
30
Q

What are some other treatment for excess GH (acromegaly)?

A
  1. Reduce GH secretion:
    (i) Dopamine agonist (cabergoline)
    (ii) Somatostatin analogues (SSA)
  2. Block GH receptor
  3. Radiotherapy: External beam (short bursts multiple times to remove tumour) or Gamma knife (High conc. once)
31
Q

A 63 year old man who has been suffering from polydipsia and polyuria for the past 12 months is diagnosed with neurogenic diabetes insipidus (central diabetes insipidus).
What would be a clinical consequence of this disease if left untreated?

A
  • Hypernatraemia
  • caused by lack of ADH (vasopressin). This results in the production of polyuria
  • Manifestations of hypernatraemia include confusion, neuromuscular excitability, hyperreflexia, seizures, and coma
32
Q 
Luteinizing hormone (LH) is produced by the anterior pituitary gland and in females plays an important role in triggering ovulation (LH surge) and in the development of the corpus luteum.
What is the role of this hormone in men?
A

Control of the production of testosterone by the testis

33
Q

A surgeon operates on a 56 year old woman to remove a pituitary adenoma. He gains access to the adenoma by inserting an endoscope and his surgical instruments through her nose.
Which surgical procedure was used by this surgeon?

A
  • Transsphenoidal surgery
  • access to the pituitary gland is gained by inserting instruments through the nose and sphenoid bone into the sphenoidal sinus cavity.
34
Q

What is the range of macro- & micro- tumour size?

A
  • Macro-adenoma= > 1cm

- Micro-adenoma = < 1cm

35
Q

What are some examples of dopamine agonists?

A
  • bromocriptine and cabergoline

very effective in reducing size of tumour

36
Q

Symptoms and signs of acromegaly

A
  • Broad nose, coarse facial features, thick lips and a prominent supraorbital ridge (the crest of bone situated on the frontal bone of the skull)
  • Enlargement of the hands and feet
  • skin is often greasy with excessive sweating.
  • Deepening of the voice also occurs due to hypertrophy of the soft tissues of the upper airways.
37
Q

Why can’t acromegaly be diagnosed simply by measuring plasma GH and how should it be diagnosed?

A
  • GH varies a lot during the day
  • IGF-1 would be measured (varies less) + oral glucose tolerance test
  • In a normal person, a high blood glucose would inhibit GH production by the anterior pituitary.
  • in an oral glucose tolerance test you purposely raise blood glucose and determine the plasma GH level.
    (The patient drinks 75 g of glucose solution and over 2 hours plasma glucose and GH are monitored. If GH doesn’t drop to below 1 ng/mL, diagnosis cfm)
38
Q

State mechanism of direct and indirect effects of GH on target cells.

A
  • Direct: Binds to growth hormone receptor on target –> intracellular signaling cascades –> ⬆️ growth and cellular metabolism
  • Indirect: GH stimulate liver + skeletal muscles to secrete IGFs –> ⬆️ growth and cellular metabolism

MEH Sem 1 (18 decks)

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