Lecture 47: Hypothalamic Pituitary Relationships and Biofeedback Pt.1 Flashcards

1
Q

Pituitary Gland Tumors

A
  • expand and put pressure on OPTIC NERVES

- visual problems and dizziness often associated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the two Posterior Pituitary Nuclei and what do they secrete?

A
  1. Supraoptic Nucleus (SON) –> ADH
  2. Paraventricular Nucleus (PVN) –> Oxytocin
  • cell bodies located in hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the Hypophysial Stalk?

A
  • physical connection between hypothalamus and pituitary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What 6 hormones does the Anterior Pituitary Secrete and how is it connected to the Hypothalamus?

A
  • ACTH, TSH, FSH, LH, Prolactin, GH

- connected by hypothalamic-hypophysial portal blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypothalamic-Hypophysial Portal System

A
  • hypothalamus Hypothalamic-release and release-inhibiting hormones directly delivered to anterior pituitary in HIGH CONCENTRATIONS
  • do NOT appear in high concentrations in SYSTEMIC CIRCULATION
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the difference in connection between the Anterior and Posterior Pituitary to the Hypothalamus?

A

Posterior –> ONLY neural connections

Anterior –> both neural AND endocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do these secrete:

  1. Corticotrophs
  2. Thyrotrophs
  3. Gonadotrophs
  4. Somatotrophs
  5. Lactotrophs (mammotrophs)
A
  1. ACTH
  2. TSH
  3. FSH and LH
  4. GH
  5. Prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What do Somatostatin and Dopamine inhibit in the Anterior Pituitary?

A

Somatostatin = GHIH –> Growth Hormone Inhib. Hormone

Dopamine = PIF –> Prolactin Inhibiting Factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do these indicate:

  1. Primary Endocrine Disorder
  2. Secondary Endocrine Disorder
  3. Tertiary Endocrine Disorder
A
  1. peripheral endocrine gland defect (hi/low hormone lvls)
  2. pituitary gland defect (high/low hormone lvls)
  3. hypothalamus defect (high/low hormone lvls)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

FSH and LH characteristics

A
  • regulated by GnRH (hypothalamus)
  • secreted by gonadotropes

Estrogen/Progesterone in females
Testosterone in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acromegaly

A
  • excessive growth of soft tissue, cartilage, bone in face/hands/feet
  • prolonged and excessive secretion of GROWTH HORMONE in adult life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Growth Hormone characteristics

A
  • produced by somatotrophes (SOMATOTROPIN)
  • targets liver and bone
  • GH receptor linked to JAK-STAT signaling
  • inhibited by Somatostatin and IGF-1 (negative feedback)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What stimulates Growth Hormone? (6)

A
  1. Fasting/Hunger/Starvation
  2. Hypoglycemia
  3. puberty hormones
  4. exercise
  5. sleep
  6. stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Direct Actions of Growth Hormone (3)

A
  1. Growth: hypertrophy –> inc. size/volume of cells
  2. Cell reproduction: hyperplasia
    • inc. cell # or proliferation rate by mitosis
  3. Metabolism: inc. glycogen/fat breakdown for NRG
    • inc. protein synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Indirect Actions of Growth Hormone

A
  • tropic function
  • signals liver to produce IGF (insulin-like growth factors); also known as SOMATOMEDIN C
  • targets almost every body cell (stim. hypertrophy and hyperplasia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do increased levels of GH and IGF-1 cause?

A
  1. inc. GH = dec. GHRH

2. inc. IGF-1 = dec. GH and INC. GHIH

17
Q

Excess Growth Hormone effects BEFORE and AFTER bone epiphyses closure

A

Before = Gigantism (IGF-1 simulated long bone growth)

After = Acromegaly (growth of deep organs/cartilaginous tissue)

18
Q

Unfavorable Growth Conditions

A
  • inc. carbohydrate intake and DEC. protein intake (low AA)
  • GH inhibited, liver produces NO IGF-1
  • causes lipogenesis/carbohydrate storage = WEIGHT GAIN
19
Q

Fasted State Growth Conditions

A
  • DEC. carbohydrate intake and INC. protein intake
  • GH produced, liver produced IGF-1
  • lipolysis, ketogenic metabolism, diabetogenic (can promote INSULIN INSENSITIVITY)
  • GH raise blood sugar (dec. peripheral glucose uptake)
20
Q

GH fluctuation throughout the day and life

A
  • secretion highest during SLEEP (distubances perturb secretion)
  • peaks with exercise
  • highest GH secretion during Puberty and drops with age
21
Q

GH Deficiency vs Excess

A

Deficiency = dec. GHRH, growth hormone sec., failure to generate somatomedins, receptor deficiency

Excess = mostly due to GH-secreting pituitary adenoma

  • Before Puberty = GIGANTISM
  • After Puberty = ACROMEGALY
22
Q

GH and Oral Glucose Test (3 requirements for acromegaly diagnosis)

A
  • acromegalic patient with have consistent serum GH levels after oral glucose administration, rather than a drop in GH like a normal person

Requirements for Diagnosis:

  1. inc. serum IGF-1
  2. failure to suppress serum GH
  3. pituitary enlargement on MRI
23
Q

Prolactin characteristics

A
  • synth by lactotropes
  • under tonic inhibition by hypothalamic dopamine
  • action: stimulate/maintain lactation
  • inhibits GnRH (LH/FSH) –> dec. reproductive function and sexual drive
24
Q

Pituitary Adenomas

A
  • hormone-producing adenomas release active hormone in EXCESSIVE AMOUNTS into bloodstream
  • experience symptoms related to hormone action on body
  • most common is PROLACTINOMA (60%), then Acromegaly/Gigantism (20%), then Cushing’s Disease (10%)
25
Q

Major Causes of Hypopituitarism (3)

A
  1. Brain Damage
  2. Pituitary Tumors = adenomas
  3. Non-pituitary tumors –> craniopharyngioma (most common affecting children)
  • rest: infections, infarctions, autoimmune, pituitary hypoplasia, genetics
26
Q

Actions of Oxytocin (2)

A
  1. Milk Ejection (“Milk Letdown”)
    • stim contraction of cells lining milk ducts
    • major stimulus = suckling, anything w/infant
  2. Uterine Contraction
    • stim by cervix dilation or orgasm
    • stimulates uterine contractions
27
Q

Regulation of Oxytocin Secretion

A
  • stored as preprooxyphysin (cleaved in hypothalamus)
  • pro-oxyphysin released from hypothalamus to posterior pituitary
  • cleavage of neurophysins = oxytocin –> released from posterior pituitary