Week 5 Flashcards

1
Q

The Pituitary Gland

A

Small outgrowth of the forebrain
Size of half a pea

Two functional parts
 Adenohypophysis (anterior pituitary)
 Neurohypophysis (posterior pituitary)

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2
Q

Blood and nerve supply pituitary gland

A

Hypothalamus
• Hypothalamic neurons release hormones directly into capillary plexus

Anterior pituitary
• Blood supply from median eminence 
of hypothalamus – portal system
• Hormones from hypothalamus to pituitary
• Sympathetic/parasympathetic nerves

Posterior pituitary
• Supraoptic and paraventricular nuclei
in hypothalamus

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3
Q

Hypothalamus releasing hormones

A

CRH: Corticotrophin releasing hormone (ACTH)
TRH: Thyrotropin releasing hormone
GHRH: GH releasing hormone
Somatostatin: GH inhibition
GnRH: Gonadotrophin (LH, FSH) releasing hormone
Dopamine: Prolactin inhibition
Vasopressin: ACTH release

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4
Q

Pituitary Stimulating Hormones

A

The anterior pituitary produces six major
hormones:
 (1) prolactin (PRL)
 (2) growth hormone (GH)
 (3) adrenocorticotropic hormone (ACTH)
 (4) luteinizing hormone (LH)
 (5) follicle-stimulating hormone (FSH)
 (6) thyroid-stimulating hormone (TSH)

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5
Q

Pituitary Disorder Introduction

A

Can malfunction in several ways, usually as a
result of developing a noncancerous tumour
(adenoma)

Prolactin-secreting adenomas are divided into 2 groups:
 Microadenomas (more common in premenopausal women), which are smaller than 10 mm)
 Macroadenomas (more common in men and postmenopausal women), which are 10 mm or larger.

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6
Q

Pituitary Malfunction

A

Disorders that result from overproduction of pituitary hormones include
 Acromegaly or gigantism: Growth hormone
 Cushing disease: Adrenocorticotropic hormone ( ACTH),
 Galactorrhea (the secretion of breast milk
by men or by women when not pregnant): Prolactin
 Erectile dysfunction: Prolactin
 Infertility (particularly in women):
Prolactin

Disorders that result from underproduction of
pituitary hormones include
 Central diabetes insipidus: Vasopressin
 Hypopituitarism: Multiple hormones

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7
Q

Prolactin secretion

A
Prolactin secretion is controlled 
primarily by inhibition from the 
hypothalamus and it is not subject to 
negative feedback directly or 
indirectly by peripheral hormones.
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8
Q

Prolactin Regulation

A
Dopamine serves as the major prolactin-
inhibiting factor or brake on prolactin 
secretion. 
 Dopamine is secreted into portal blood 
by hypothalamic neurons, binds to 
receptors on lactotrophs, and inhibits 
both the synthesis and secretion of 
prolactin. 
 In addition to tonic inhibition by 
dopamine, prolactin secretion is 
positively regulated by several 
hormones, including thyroid-releasing 
hormone, gonadotropin-releasing 
hormone and vasoactive intestinal 
polypeptide.
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9
Q

Complications of high Prolactin

A

Excess prolactin, or hyperprolactinemia, can lower levels of sex hormones in both women and men.
Related complications can include
 infertility
 bone loss (osteoporosis)

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10
Q

Hyperprolactinaemia in Male

A
High blood prolactin concentration interferes with the 
function of the testicles, the production of testosterone (the 
main male sex hormone), and sperm production
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11
Q

Hyperprolactinaemia in Male Pathophysiology

A

Prolactin inhibits pulsatile GnRH secretion and
consequently inhibits the pulsatile release of
FSH, LH and testosterone.
 This results in marked effects on
spermatogenesis ranging from alteration
in sperm quality to complete
spermatogenic arrest.
 As a result, the patient may present with
secondary hypogonadism or male
infertility.

Furthermore, prolactin may also impact male
fertility through a direct effect on
spermatogenesis.

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12
Q

Hyperprolactinaemia in Male

High prolactin and gynecomastia

A
Defined as benign proliferation of 
male breast glandular tissue, is 
usually caused by increased 
estrogen activity, decreased 
testosterone activity, or the use of 
numerous medications

Imbalance between estrogen action
relative to androgen action at the
breast tissue level appears to be the
main etiology of gynecomastia

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13
Q

Hyperprolactineamia in Females

A

(high prolactin)
This usually manifests with oligomenorrhoea or
amenorrhoea, and diagnosis in such cases is
straightforward.
Another common symptom is “galactorrhoea”, which is the
occurrence of a milky discharge from the breast in a woman
who has not recently been pregnant.
The discharge is the result of persistent high PRL levels
stimulating the mammary gland for milk production.

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14
Q

Hyperprolactineamia in Females, Macroprolactinoma

A

Is the apparent increase in serum prolactin without
symptoms

Serum prolactin molecules can polymerize and
subsequently bind to immunoglobulin G (IgG).
 This form of prolactin is unable to bind to prolactin receptors
and exhibits no systemic response.
 In the asymptomatic patient with hyperprolactinemia, this
condition should be considered.

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15
Q

Complication of Macroprolactinoma

A

Vision problems, caused when the tumour presses on
the optic nerves or optic chiasm, the part of the brain
where the two optic nerves cross over each other
headaches
low levels of other pituitary hormones, such as thyroid
hormones and cortisol

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16
Q

Growth hormone (GH)

A

Promotes growth: skeleton, muscles, viscera
Effects mediated by somatomedins
Released at night during growth

Variety of metabolic effects
 Anabolic, positive nitrogen balance
 Anti-insulin

17
Q

Regulation of Growth Hormone

A

Somatostatin (SS) is a peptide produced by
several tissues in the body, including the
hypothalamus.
Somatostatin inhibits growth hormone
release in response to GHRH and to other
stimulatory factors such as low blood glucose
concentration.
Ghrelin is a peptide hormone secreted from
the stomach.
Ghrelin binds to receptors on somatotrophs
and potently stimulates secretion of growth
hormone.

18
Q

Metabolic actions of Growth Hormone

A
Increase rate of protein synthesis in 
most of cells
Increase mobilization of fatty acids 
for energy production 
Decrease rate of glucose utilization 
throughout body
19
Q

Mediator of Growth hormone IGF-1

A

One of several growth factors necessary for normal
human development.
IGF-1 is synthesized mainly by the liver but also locally in
many tissues.
 Activation of the growth hormone receptor stimulates the
synthesis and secretion of insulin-like growth factor-1 (IGF-
1), a small peptide (about 7.5 kD) structurally related to
proinsulin.
 IGF-1 circulates in the blood at high concentrations and acts as a mitogen, stimulating DNA, RNA and protein synthesis.

20
Q

Clinical Syndrome of GH

A
 Giantism is the result of excessive 
growth hormone secretion that 
begins in young children or 
adolescents. It is a very rare 
disorder, usually resulting from a 
tumour of somatotrophs. 
 Acromegaly results from excessive 
secretion of growth hormone in 
adults, usually the result of benign 
pituitary tumours. The onset of this 
disorder is typically insidious, 
occurring over several years. 
 Growth hormone deficiency
21
Q

Acromegaly pathophysiology

A

Is a disorder of disproportionate skeletal, tissue,
and organ growth.
 Characterized by hypersecretion of growth
hormone (GH),which is caused by the
existence of a secreting pituitary tumour in
more than 95% of acromegaly cases.
 In rare instances, elevated GH levels are
caused by extra pituitary disorders.
 Hypersecretion of GH in turn causes
subsequent hepatic stimulation of insulin-like
growth factor-1 (IGF-1) leading to enlarge
physical features.
 Peripheral neuropathies occur commonly
because of compression of nerves by
adjacent fibrous tissue and endoneural
fibrous proliferation.

22
Q

Gigantism pathophysiology

A

Like Acromegaly however occurs

in adulthood

23
Q

GH excess and Glucose Metabolism

A
GH excess affects insulin 
sensitivity and gluconeogenesis 
and can alter pancreatic β-cell 
function, leading to a derangement 
of glucose metabolism in a 
considerable percentage of 
acromegaly patients.
 Induces hyperglycaemia by 
increasing endogenous 
glucose production and 
decreasing peripheral glucose 
disposal in muscle.
24
Q

Diagnosis of excess GH

A
Functional tests for GH 
1. Basal plasma GH level: High 
2. Plasma Prolactin level: High 
3.  Glucose tolerance suppression 
test: 75 grams of glucose to be 
given orally, GH and blood glucose 
level to be measured 2 hourly 
 Normal: Suppression of GH by 
hyperglycaemia 
1. Acromegaly or gigantism: No 
suppression 
2. Visual field defects: Due to pressure 
by pituitary adenoma 
3. CT scan skull
25
Q

Growth Hormone deficiency (GHD)

A

s a rare condition in which the body does not make enough growth hormone (GH). Also known as dwarfism or pituitary
dwarfism/achondroplasia

GHD can be present:

  1. From birth (congenital), resulting from genetic mutations or from structural defects in the brain.
  2. Acquired later in life as a result of trauma, infection, radiation therapy, or tumour growth within the brain.
  3. No known or diagnosable cause (idiopathic).
26
Q

Dwarfism pathophysiology

A

Hereditary (Autosomal Dominant)
 An autosomal dominant disorder that is the most frequent form of short-limb dwarfism.

 Cartilage-hair hypoplasia is a 
disorder of bone growth 
characterized by short stature 
(dwarfism) with other skeletal 
abnormalities; fine, sparse hair 
(hypotrichosis)
 Abnormal immune system function 
(immune deficiency) that can lead 
to recurrent infections.
27
Q

GH deficiency and glucose

A
Fasting hypoglycaemia and marked 
insulin sensitivity have sometimes 
been observed in GHD children due 
to diminished hepatic output through 
decreased gluconeogenesis or 
abnormal glucose mobilisation
28
Q

Diagnosis of GH deficiency

A

Low IGF-1 can indicate GH
deficiency, but many people with
GH deficiency have normal or low
-normal IGF-1 levels.

GH stimulation test is often used 
as an initial screen for GH 
deficiency.
 Test is performed by 
administering the amino acid 
arginine in a vein to 
raise GH levels. 
 The test measures the 
ability of the pituitary to 
secrete growth hormone in 
response to the arginine.
29
Q

Primary IGF-1 deficiency

A

Can be classified:
 Primary IGFD may happen when IGF-1 levels are low, even
though growth hormone levels are normal or even high
 Secondary IGFD happens in children whose IGF-1 levels are low; this may be due to their bodies’ inability to produce enough growth hormone, poor nutrition, thyroid problems or other factors
 Severe primary IGFD is a type of primary IGFD in which IGF-1
levels are exceptionally low, despite sufficient or high growth hormone levels