Hypothalamic Pituitary Axis - 2/2 Lopez Flashcards

(51 cards)

1
Q

What is the connection between the hypothalamus and posterior lobe like?

A

Neural

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2
Q

The connection between the hypothalamus and anterior lobe are what?

A

Neural and endocrine

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3
Q

How do hormones get from the hypothalamus to the anterior lobe of the pituitary?

A

Hypothalamic-hypophysial portal vessels

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4
Q

What is a primary endocrine disorder due to a defect in?

A

Peripheral endocrine gland (target tissue i.e. Thyroid gland)

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5
Q

What is a secondary endocrine disorder due to?

A

Defect in pituitary gland

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6
Q

What is a tertiary endocrine disorder due to?

A

Defect in hypothalamus

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7
Q

What are some examples of primary endocrine disorders?

A

Thyroid, adrenal cortex, liver, gonads

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8
Q

What are the most prominent cell types within the pituitary gland?

A

Somatotrophs (50%)

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9
Q

What do corticotrophs release?

Somatotrophs?

A

ACTH

growth hormone

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10
Q

What hormone has melanocyte-stimulating hormone activity?

INC in blood levels of what can cause skin pigmentation?

A

ACTH

MSH

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11
Q

What disease is associated with INC levels of ACTH?

Symptoms?

A

Addison’s disease

Skin pigmentation

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12
Q

What is a main regulator of the HPA axis that stimulates it?

A

Stress (physical, emotional, chemical)

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13
Q

What does ACTH cause the release of in the adrenal gland that can cause negative feedback of the system?

A

Cortisol or aldosterone

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14
Q

What 2nd messenger does the HPT axis use once TRH is released?

What does this activate?

A

PLC

INC in Ca and PKC

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15
Q

After the pituitary thyrotrope has been activated, what does it release?

A

TSH

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16
Q

Once TSH has been released from the pituitary thyrotrope what does it stimulate?

What are its effects?

Ultimate end secretion product?

A

PKA

Thyroid hormone synthesis and secretion, cell growth

T3, T4

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17
Q

What inhibits TRH secretion?

What end product can also inhibit the HPT axis via negative feedback?

A

Stress

T3

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18
Q

What stimulates the synthesis and secretion of GH And where is this initial stimulus located?

What does this hormone act on to release GH?

A

GHRH from the hypothalamus

Acts on ant. Pituitary

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19
Q

What inhibits the secretion of GH?

How?

A

Somatostatin

Blocks response of ant. Pituitary to GHRH

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20
Q

When GH acts on target tissues (liver) what is produced?

How do they inhibit further secretion of GH?

A

Somatomedins (IGF)

Inhibit release from ant. Pituitary AND stimulate secretion of somatostatin from hypothalamus

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21
Q

How is GH secreted?

A

Pulsatile pattern, burst of secretion every 2 hours

22
Q

What tissues are the main targets of direct effect of GH?

Indirect?

A

Skeletal m., liver, adipose

Liver

23
Q

What are the direct effects of GH?

What is the net result?

A

Diabetogenic: DEC glucose uptake into cells
INC lipolysis in adipose
INC protein synthesis in muscle
INC production of IGF

INC in blood [glucose] and blood insulin levels

24
Q

What are the indirect effects of GH?

A

INC Protein synthesis and organ growth (INC uptake of a.a.)

INC linear growth (INC metabolism in cartilage-forming cells and chondrocytes)

25
What causes GH deficiency?
Lack of ant. Pituitary GH DEC GHRH due to hypothalamic dysfunction Failure to generate IGF in liver GH receptor deficiency
26
GH excess causes what? Mostly due to what?
Acromegaly GH-secreting pituitary adenocarcinoma
27
What does excess GH cause before puberty? After?
Gigantism (INC linear growth) INC periosteum bone growth, INC organ size, glucose intolerance
28
How to treat GH deficiency? Excess?
HGH Somatostatin analogue (octreotide)
29
What does lactogenesis induce the synthesis of?
Lactose, casein and lipids
30
What inhibits lactation during pregnancy even though prolactin levels are high?
High levels of estrogen and progesterone down-regulate prolactin receptors
31
What does prolactin suppress? How?
Ovulation DEC synthesis and release of GnRH
32
What causes prolactin deficiency? Result?
Destruction of ant. Pituitary or lactotrophs Inability to lactate
33
What causes prolactin excess? Result?
Destruction of hypothalamus or hypophysial tract, prolactinomas, Galactorrhea and infertility
34
How to treat prolactin excess?
DA receptor agonist (bromocriptine)
35
What is Sheehan syndrome?
Pituitary in pregnancy is enlarged and more vulnerable to infarction
36
What is Cushing's disease?
Pituitary tumors stimulating an increase in cortisol
37
Pituitary adenomas develop in 25% of patients with what?
MEN 1
38
What is the precursor peptide for ADH? Oxytocin?
Preprossophysin Prepro-oxyphysin
39
What are the triggers for ADH secretion?
DEC BP DEC arterial stretch due to low blood volume INC Osmolarity (>280) MAIN stimulus
40
What are the actions of ADH? Ultimate result?
INC H20 reabsorption via V2 receptors Vasoconstriction via V1 receptor INC BP and INC blood volume
41
What mechanism do the V1 receptors work through? V2?
IP3/Ca cAMP
42
What channel does ADH activate? Where?
aquaporin 2 (AQP2) Principal cells of the late DCT and CD
43
What is ADH secretion like in hyper osmolarity? Urine concentration?
ADH INC urine more concentrated
44
What happens to ADH in hypoosmolarity? Urine concentration?
Less ADH secreted Urine more dilute
45
What are the characteristics of General DI?
Lack of effect of ADH Frequent urination Large volume of urine is diluted
46
What is the cause of central DI? From what?
Lack of ADH Pituitary damage or destruction of the hypothalamus
47
What is happening nephrogenic DI? Cause?
Kidneys unable to respond to ADH (INC plasma ADH) Lithium, polycystic kidney disease, sickle cell anemia
48
What drug is used to treat central DI? Nephro DI?
Desmopressin NONE
49
What is SIADH? What is it characterized by?
excessive secretion of ADH, excessive water secretion Hypoosmolarity and hyponatremia
50
How to treat SIADH?
Fluid restriction IV hypertonic saline (3%) V2 receptor antagonist Demeclocycline (inhibits cAMP)
51
What are the 3 hypothalamic-pituitary axises? What do they control?
thyroid, adrenal, gonads (HPT, HPA, HPG) Growth, milk production/ejection, osmoregulation