Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology II > Exam 2: Growth Hormone > Flashcards

Exam 2: Growth Hormone Flashcards

1
Q

Where is GH produced/released?

A

GH produced/released from anterior pituitary

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

What stimulates the release of GH from the anterior pituitary? And where does it come from?

A

GHRH (growth hormone releasing hormone) released from the hypothalamus

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

What inhibits the release of GH?

A

Somatostatin

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

What target organs does GH act on?

A

Many but liver, muscle, fat, bone, etc

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

When GH stimulates the liver what does the liver then release?

A

IGF-1 (which then goes to act on muscle, fat, bone, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

GH is made from what type of hormone-producing cells?

A

Somatotrophs (which are the most abundant type)

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

What do malignant somatotrophs often produce?

A

GH and prolactin (often due to pituitary adenoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why would malignant somatotrophs produce both GH and prolactin when prolactin is produced by lactotrophs?

A

GH, prolactin, and human chorionic lactotrophs are considered of the same family

GH can act on prolactin receptors as GH and prolactin share 40% of amino acid sequence homology

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

While a pituitary adenoma can increase release of GH and prolactin, why does it decrease release of TSH, ACTH, and gonadotropins (FSH and LH)?

A

A pituitary adenoma can compress the infundibulum (thus hypophyseal vein) decreasing hypothalamic hormonal stimulation of anterior pituitary hormone release (TSH, ACTH, and gonadotropins)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

If the infundibulum is compressed, why would prolactin release be increased?

A

Prolactin release is suppressed by dopamine from the hypothalamus so if the infundibulum is compressed there is less dopamine getting to anterior pituitary so less inhibition of prolactin, thus more prolactin release

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

Pathway of GH from start to finish?

A

Arcuate nucleus of hypothalamus releases GHRH into hypophyseal portal system

Then GHRH transported to somatotrophs in anterior pituitary which then releases GH to secondary capillary plexus

Then GH travels to target organs of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Somatostatin inhibits the release of GH. Where is somatostatin released from in the hypothalamus?

A

periventricular nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

So GHRH is released from what? And somatostatin is released from what?

A

hypothalamus- arcuate nucleus

hypothalamus- periventricular nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

GH and IGF-1 have positive feedback on what?

A

periventricular nucleus of hypothalamus so release somatostatin to inhibit GH release from anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

GH and IGF-1 have neg feedback on what?

A

arcuate nucleus of hypothalamus so inhibit release of GHRH thus inhibit GH release from anterior pituitary also neg feedback directly on anterior pituitary (see image)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the result of GH deficiency in childhood?

A

dwarfism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of GH deficiency in childhood?

A

congenital functional defect or structural damage of hypothalamus or pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes GH deficiency in adulthood?

A

acquired, not by genetic reasons

tumors destroying/compressing infundibulum

pituitary structural damage of pituitary or hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the purpose of GH in childhood?

A

linear growth (soft tissue, visceral organ, muscle, bone) in growing ages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the purpose of GH in adulthood?

A

maintain lean body mass in adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

While GH is very important in childhood growth, what is important in fetal growth?

A

IGF-1 (late fetal growth: triggered by insulin not GH) and IGF-2 (early fetal growth)

so GH deficient infants have normal birth lengths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does GH achieve its goals of growth and maintenance of lean body mass?

A

cell proliferation and energy metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

GH predisposes cell metabolism to enhance lean body mass production by what three ways?

A

utilize fat as the main energy source

maximize protein deposition for lean body mass

earmark glucose for the use by the brain

(this is why GH receptors are in almost all tissues)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What organs/tissues contain the most GH receptors?

A

liver and cartilage

25
Q

The action of GH on fat (utilization of fat as the main energy source so lipolysis and fatty acid release) is antagonistic to what?

A

insulin

26
Q

What would you expect in your GH deficient patient in regards to fat?

A

elevated plasma LDL

elevated plasma triglyceride

premature atherosclerosis, thus elevated cardiovascular morbidity

mild obesity (increased fat mass)

27
Q

What would you expect least in your GH deficient patient in regards to fat?

A

decreased plasma HDL because GH does not down regulate this

28
Q

The action of GH maximizing protein deposition for lean body mass is synergistic to the action of what?

A

insulin

29
Q

What would you expect in your GH deficient patient in regards to protein?

A

GH should strengthen muscles so:

reduced skeletal muscle cross sectional area

muscle weakness

decreased plasma urea levels

decreased myocardial contractility

decreased exercise performances

decreased left ventricle mass index and internal diameter

30
Q

What would you expect least in your GH deficient patient in regards to protein?

A

Increased pulmonary capacity

31
Q

The action of GH on glucose metabolism is antagonistic to what?

A

insulin

32
Q

So GH and insulin counteract each other in regards to glucose metabolism so what happens when there is a pathologic excessive chronic GH release?

A

action of insulin to decrease plasma glucose is overpowered by GH’s action to increase plasma glucose…thus you get insulin resistance so diabetogenesis

33
Q

Should you treat diabetic patient with GH?

A

No, they are already hyperglycemic and the action of GH is to increase plasma glucose

34
Q

At what time of day could hyperglycemia of DM patients be super severe?

A

morning following nocturnal GH release

35
Q

Is the release of GH constant or pulsatile? And when is it at its greatest?

A

Pulsatile

Throughout the night

36
Q

What would you expect in your GH deficient patient in regards to glucose metabolism?

A

decreased fasting glucose levels

decreased insulin secretion

increased hepatic glucose production

37
Q

How does GH achieve its goals of growth through IGF-1?

A

GH stimulated release of IGF-1 from liver increases cell proliferation via a insulin-like metabolic action (but this is insufficient to override GH’s direct effect on glucose and fat) and proliferative action on body organs such as muscle, bone, soft tissue, visceral organs (so synergistic action with GH in amino acid metabolism to build muscles)

38
Q

Action of GH and IGF-1 action in regards to fat and glucose metabolism is antagonistic or synergistic?

A

Antagonistic (IGF-1 action is insufficient to override GH’s direct effect on glucose and fat)

39
Q

Action of GH and IGF-1 action in regards to protein/amino acid metabolism is antagonistic or synergistic?

A

Synergistic

40
Q

Want a nice visual of GH action?

A

See image

41
Q

What measurements are used to dx GH disturbances?

A

glucose and insulin

42
Q

List four main actions of GH?

A

increase plasma fatty acid for energy source

decrease plasma amino acids by increasing uptake into tissues to build muscle

increase plasma glucose for the brain

promote body growth and repair

43
Q

Things that would increase GH secretion?

A

See image

44
Q

Things that would decrease GH secretion?

A

See image

45
Q

What are some clinical signs of GH deficiency?

A

fatigue

weakness

decreased energy level

mild obesity

decreased muscle mass

high LDL levels

decreased cardiac function

decreased insulin sensitivity

etc

46
Q

How could you test if your patient is GH deficient?

A

Insulin challenge:

Inject insulin into pt

Injecting insulin into healthy pt would inc GH

Injecting insulin into GH deficient pt would not change anything/no inc in GH

47
Q

Insulin challenge to test for GH deficiency is contraindicated in what patients?

A

ischemic heart disease

epilepsy

elderly patients

48
Q

Define acromegaly in regards to GH release?

A

excessive and sustained GH release even during the day (normally just elevated at night)

49
Q

What are the three main causes of excess GH?

A

pituitary adenoma

extra pituitary tumor (pancreatic islet cell tumor, lymphoma, iatrogenic)

excess GHRH (pancreatic islet tumor, bronchial carcinoid, small lung cancer, adrenal adenoma)

50
Q

Excess GH in kids results in?

A

Gigantism

51
Q

Excess GH in adults results in?

A

Acromegaly

52
Q

What are the facial features of acromegaly?

A

increase frontal bossing (enlargement of sinuses)

increase in base of nose

thickening of nano-labial sulcus and lips

parotid hypertrophy

loss of oval facial features

worsening of prognathism (the positional relationship of the mandible or maxilla to the skeletal base where either of the jaws protrudes beyond a predetermined imaginary line in the coronal plane of the skull)

wide tooth spacing

53
Q

What are more features of acromegaly?

A

hypertrophy of soft tissue (thickened tongue and skin, increased skin-folds, enlarged visceral organs particularly the liver and spleen)

HTN if CO is decreased due to cardiomegaly

enlargement of hands and feet

oily skin texture

peripheral neuropathy and pain by connective tissues compressing nerves (i.e. carpal syndrome)

insulin resistance

degenerative joints

deepening voice and sleep apnea (due to soft tissue growth in pharynx)

malignant polyps and colon cancer

54
Q

What is the mortality of patients with acromegaly?

A

2-3x increase in mortality

55
Q

If the cause of acromegaly is enlarged anterior pituitary, what other features can you see?

A

headache

peripheral vision loss

double vision

other anterior pituitary deficits that can cause: impotence, fatigue, amenorrhea, and galactorrhea

56
Q

How is acromegaly dx?

A

measure IGF-1

if elevated, then do glucose intolerance test and GH measure

if this shows inadequate GH suppression, then do pituitary MRI

MRI may show pituitary mass (dx: GH secreting adenoma)

but if not, do chest abdominal CT and GHRH measure (dx: extra pituitary acromegaly)

57
Q

What is the initial test you would order if you suspect acromegaly?

A

IGF-1 level

58
Q
A

Pharmacology II (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions