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Endocrine and Reproduction Systems > Growth Hormone > Flashcards

Growth Hormone Flashcards

1
Q

What is the equivalent of truncal fat distribution? What disease can be associated to it?

A
  1. Visceral = abdominal fat

2. DM2

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2
Q

Dislipidemia

A

Abnormal increased amount of fat in the body

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3
Q

What is the primary source of IGF1 production?

A

Liver

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4
Q

Where is most of glucose stored in the body? How is this associated with anabolic growth?

A

Most glucose is stored in skeletal muscle. Skeletal muscle needs glucose in order to grown in size.

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5
Q

What is the importance of IGF1 and GH with bone?

A

IGF1 and GH work together to allow for favorable bone remodeling and growth.

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6
Q

How does GH and IGF1 affect the heart? The liver?

A
  1. Heart: Allows for generally favorable remodeling, inotropy, and chronotropy
  2. Allows for water retention, as well as RAAS stimulation
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7
Q

How does GH affect the thyroid?

A

Allows for thyroid hormone synthesis

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8
Q

What part of the hypothalamus releases the GHRH, GH secretogague, and Somatostatin? What is the job os somatostatin?

A

Ventromedial nucleus. Somatostatin releeases somatotroph-releasing inhibiting factor (SRIF)

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9
Q

What’s released from the anterior pit?

A

A series of somatotropes.:

  1. GHRH-R
  2. Dopamine-R
  3. Somatotroph-release inhibiting factor (SRIF)
  4. GH secretogogue-R
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10
Q

Where is GH released from? What is the job of somatotropes?

A

Anterior pit….and somatotropes control its release/

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11
Q

What promotes GHRH release?

A
  1. Hypoglycemia (GH puts glucose into the bloodstream. Occurs when you’re asleep)
  2. Arginine (just something you need to know)
  3. Ghrelin (associated with fasting state…like when you are sleeping).
  4. Dopamine and seretonin (you just need to know this)
  5. Seretonin
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12
Q

What happens after GHRH is released?

A

GHRH leads tot he release of somatortrope, which directly causes GH release.

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13
Q

What stops somatotrope (and thus GH) release?

A

Somatostatin

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14
Q

How are GH and IGF1 related?

A

You need both. GHRH causes somatotropes to be released. The somatotropes cause GH to be released, and the increase in GH stimulates IGF1 production. They must both be present for growth to occur.

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15
Q

Where is IGF1 released from? What else does this organ release? What is the importance of the other things (besides IGF1) that are released? How do these things work?

A

Liver. it also releases GH binding protein and IGF binding protein. These things extend GH halflife by cleaving product receptors. Albumin is also a binding protein, just not released from the liver.

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16
Q

How do binding proteins work?

A

Binding proteins bind to the hormone. They release the hormone upon reaching the target location.

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17
Q

How is GH involved in lipolysis?

A

Lypolisis breaks ;ipids into triglycerides, which further breaks into glycerol and FFAs. GH increases FFA production, which promotes B oxidation and leads to acetyl coa, which is shuttled into Krebs to make a crap ton of ATP.

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18
Q

How is GH involved in proteolysis?

A

GH legitimately downregulates the breakdown of proteins into amino acids. It is an anabpolic hormone (prefers to build things). This inherently means that it blocks ATP production from this angle.

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19
Q

How id GH involved in glycolysis?

A

Just like proteolysis, GH also inhibits the break down of glycogen into glucose. This would also cut down ATP production.

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20
Q

What is the difference between insulin and GH?

A

Insulin causes liver and muscle cells to uptake glucose into their systems for glycogenesis. GH causes cells to spit the glucose out and place it into the blood stream. Placement into the bloodstream is favorable for skeletal muscle. Placement into the cells is favorable for the cell (glycolysis beats Beta ox, as it prevents ketoacid formation)

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21
Q

What promotes placement of glucose into plasma?

A

GH, Epi and Cortisol (both from pancrease), Glucagon, gluconeogenesis and glycogenolysis (both from liver)

22
Q

What is the normal protocol for elevated glucose in the plasma?

A

Pancreatic beta cells secrete insulin (Insulin levels INCREASE), leading to glucose being uptaken by both skeletal muscle and liver.

23
Q

Brief definition of an anabolic factor

A

Promotes storage of stuffz (glycogenesis)

24
Q

Describe relationship between GH and insulin resistance.

A

Normally GH opposes insulin, preventing insulin from getting glucose to be taken up by the cells. However, too much GH makes it incredibly hard for insulin to promote any glucose uptake. This is associated with insulin resistance (expect insulin levels to go Up as GH goes up in patients with too much GH)

25
Q

Describe pathway of a hypoglycemic patient with regards to GH.

A

Hypoglycemia leads to GH production (to get glucose into the blood). This allows skeletal muscle to take up cellular amino acids, as well as undergo protein synth and lipolysis. Note that GH still kills glucose uptake.

26
Q

Describe pathway of a hyperglycemic patient with regards to GH

A

Hyperglycemic patients promote insulin production, which causes glucose uptake. uptaking glucose allows for glucose storage in the skeletal muscle, liver, and adipose tissues. This storage then leads to glycogenesis and lipogenesis.

27
Q

How does GH affect the liver?

A

GH allows for increased blood glucose, but it also promotes the presence of IGFs and IGFBPs in the liver.

28
Q

What happens when GH and IGF1 work together? What happens when they do not?

A

GH is borderline useless with IGF1. They need each other. That being said, increased GH production leads to increased IGF1 production. When put together, you get growth and deposition (remodeling) of bone. You also get increased lipolysis of fat into fatty acids and glycerol. The incrase in FAs and glycerol leads the the shift of metabolism away from glycogenolysis to FAs and glycerol. This promotes anabolism and myocyte proliferation.

29
Q

How does GH and IGF1 affect bones?

A

GH and IGF1 affects chondrocytes, which promotes longitudinal growth and IGF1 expression. OsteoBLASTS are also affected, leading to bone deposition (mineralization) and IGF1 expression. Note that bones also make some IGF1. Also note that bone mineralization increases blood Ca and increases Ca filtered load.

30
Q

What do bones express what receptor? Bones produce what hormone? What happens to the bone as a result?

A 
Bones express GH receptors (makes sense...GH would not be able to act on it otherwise) and produce IGF1. Bones Are affected in 3 major ways:
Trabecular (the deep inside part of bone): chronic remodeling is stimulated.
Cortical (most exterior and DENSE part of bone made of minerals and extracellular membrane): Affects the bone shape and strength. There is not as much remodeling at this part. 
Growth plate (at epiphysis): Responsible for longitudinal growth. Is responsible for the overall length of bone. Before Epiphyseal plate fusion, GH + IGF1 promotes bone elongation.
31
Q

How does GH levels change as you age?

A

GH and IGF1 levels start at medium levels until pubery. At puberty, GH and IGF1 spike an dreach max levels at 30 (but ppt says 20) years old. After this point, there is a 14% decline per decade.

32
Q

What happens upon giving GH to older patients?

A

Well, we know they WILL NOT revert in age. Reason is that GH seems to have a specific window of operation. After this time period in life, it loses its effect. However, you can still use GH in GH deficient, older patients to get GH to the normal levels of their respective age.

33
Q

Hypercalemia, high triacylglycerides (TAGs), low but normal levels of K, and truncal fat distribution should prompt you to diagnose:

A
  1. Possible DM2 with initial signs of insulin resistance.
  2. Pituitary adenoma. Confirm with MRI. Note that pituitary cancers can screw up optic chiasm (review this), thus affecting vision.
34
Q

Difference between acromegaly and gigantism

A

Acromegaly occurs after epiphyseal plate closure (adult issue). gigantism occurs before epiphyseal plate closure (kiddie issue). Both occur due to excessive GH secretion.

35
Q

Signs and symptoms of GH excess

A
  1. Insulin resistance (becasue tries to put them into GH puts glucose in to blood and insulin tries to put them into cells). The end result here is an increase in truncal fat distribution (no clear association here. Just know it.)
  2. Excessive bone deposition (mineralization)
  3. Hyperglycemia
  4. Hyperdislipidemia (again, this is by association. Just know it.)
  5. Muscle weakness due to fluid imbalance (GH still affects kidneys by promoting water retention)
  6. Weight gain (due to water retention)
  7. Heart hypertrophy
  8. Increased lipolysis, increasing TAG presence in blood
36
Q

Explain the presence of the following:

  1. Newfound insulin resistance, glucose intolerance, DM
  2. Headache
  3. Double vision/loss of visual fields
  4. Diffuse arthralgias (bone pain)
  5. Resistant hypertension
  6. Ventricular hypertrophy
  7. Sexual dysfunction (oligomenorrhea, amenorrhea, normal menstruation with infertility). (Irregular or lack of period)
A
  1. More GH than Insulin present. So crap ton of glucose is in blood.
  2. Potential tumor of pituitary gland
  3. Potential tumor of pituitary gland
  4. Caused by demineralization of bone, increasing Ca in blood. In excess, can leave Ca deposits in joints and cause joint pain.
  5. Caused by tampering of RAAS and abnormal presence of aldosterone and all else related to hypertension.
  6. Negative effects of GH presence.
  7. Screws up gonandotropins (FSH and LH are also in the pit)
37
Q

What are some physical changes expected as a result of increased GH presence over an extended period of time (talking years here)?

A

Frontal bossing, cranial redging (eye brows), widened hands + feet + nose, mandicular overgrowth (cheeks). Note that these things take years (on avg 9 years) to notice.

38
Q

Can exogenous GH ingestion lead to the same effects as endogenous GH production?

A

Yes.

39
Q

List cardiovascular effects of acromegaly

A
  1. Cardiomyocytes have increased contractility and biventricular hypertrophy (not good).
  2. Increased HR and CO
  3. Increased O2 demand because of the increased size of cardiomyocytes.
  4. Acromegalic cardiomyopathy…leads to heart failure.
40
Q

How does abnormal increased in GH affect the cardiovascular system?

A

Leads to hypertension…

  1. GH increases amount of lean body mass (mostly skeletal muscle) and extracellular H2O (the lean water mass). This increase cuts off RAAS system, but you still end up with hypertension (manifesrts exactly like a secondary hyperaldosteronism…high AII and low PRA…increased TAGs, IGF1s, and fasting glucose…hyperglycemia).
  2. GH also directly stimulates aldosterone, which increases extracellular circulating volume and leads to hypertension, despite lowering RAAS.
  3. GH unfavorably remodels vascular smooth muscle
41
Q

How does one determine GH excess

A
  1. Measure GH directly
  2. Measure IGF1BP, although could be deceiving
  3. Give somatostatin, which NORMALLY inhibits GH secretion. See if GH goes down. If it stays up, pituitary adenoma.
  4. Give patient bolus of sugar (Oral Glucose Tolerance Test…measure IGF1 after administration). Note that GH would go down if blood sugar is high. Negative feedback and normal insulin function…So if it does not go down, think pituitary adenoma
42
Q

What is the challenge with measuring hormone levels?

A

They vary immensely, and thus can be misleading. You need to catch measurements at their peak in order to take them seriously.

43
Q

How to medically hand excess GH circulation

A
  1. Prescribe somatostatin (GH inhibitor)
  2. Prescribe IGF1 inhibitor
  3. Remove the suspected pituitary tumor
44
Q

What hormone is often associated with GH? How do you block its secretion?

A

Prolactin. So if you see abnormally high levels of GH, make sure you check Prolactin too. it may also be increased Block prolactin secretion with dopamine…this is the same treatment used for GH excess. They are both released from anterior pit. Note that blocking porlactin may also block GH.

45
Q

How does dopamine operate under physiologic conditions?

A

Dopamine stimulated GH secretion.

46
Q

What happens if GH is not present enough prior to puberty? What is Laron syndrome?

A
  1. Dwarfism

2. Tissue resistance to GH (you’ll notice increased GH BUT LOW IGF1. Remember that GH does nothing without IGF1)

47
Q

How would you test for GH deficiency/Laron Syndrome?

A
  1. Have patient fast for 12 hours…note that the hypoglycemia would normally spark GH secretion
  2. Give patient GHRH and see if GH is released. If not released, you can predict that there is an issue with the anterior pit.
  3. Lower the patient’s blood sugar by giving them insulin (have sugar on standby) and see if GH levels rise.
48
Q

How would you treat low levels of GH/Laron syndrome?

A
  1. GH replacement in normal cases

2. Prescribing IGF1 for Laron patients

49
Q

What dynamic tests could be used to test for GH deficiency?

A
  1. Prescribe arginine, since it is a known stimulant for GHRH
  2. Conduct a stress test (have patient run in treadmill) since it lowers blood shugar just enough to promote GHRH secretion.
  3. Prescribe GHRH and see if it increases somatotrope production, leading to GH release.
  4. Lower blood sugar with insulin (have sugar on standby)
50
Q

Benefits of treating GH deficient adults: It improves their –>

A
  1. Muscle mass
  2. Strength
  3. Max O2 consumption
  4. Mood
51
Q

If trying to use GH for sports gain in adults, Ii there a significant difference when comparing strength and max O2 consumption vs. a given treatment group?

A

No. Treatment showed only an increase in lean body mass, BUT when the H2o contribution was removed, there is no longer any significant gain in lean body mass…as in, no change in muscle mass. The only legitimate benefit is decreased body fat

52
Q

What is the health risk of GH use in adults?

A
  1. Unfavorable cardiac remodeling
  2. Insulin resistance
  3. hypertension
  4. Edema
  5. Kidney disease
  6. Infertility in both men and women (not reversible in either
  7. Morphogenic changes in jaw and mandible…acromegaly.

Endocrine and Reproduction Systems (8 decks)

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