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Endocrine > Week 6 Review Q's > Flashcards

Week 6 Review Q's Flashcards

Pharma of GH (1-35) Physio of GH (36-55) GH and Growth factors biochem (56-88) behavioral science 1 (89-107) behavioral science 2 (108-118) patho lab assessment of growth disorders (119-132)

1
Q

Growth hormone is made up of how many amino acids?

A

191 (2 disulfide bonds connecting them)

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2
Q

How does GH mediate its effects?

A

via IGF-1

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3
Q

Which of the following does NOT increase GH production? a. exercise b. low fatty acids c. high protein meal d. high sugar in blood e. ghrelin

A

d. high sugar in blood (low blood sugar stimulates GH, it has an anti-insulin effect)

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4
Q

During sleep, when is GH the highest?

A

after 60-90 minutes of sleep (stage 3 of 4 of sleep)

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5
Q

Dopamine acts to increase GH release by acting on which receptor? a. alpha 1 b. alpha 2 c. beta 1 d. beta 2

A

d. beta 2

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6
Q

serotonin and adrenergic agonists (ex/clonidine) act to increase GH release by acting on which receptor? a. alpha 1 b. alpha 2 c. beta 1 d. beta 2

A

b. alpha 2 (adrenergic receptors)

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7
Q

Where is somatostatin found? What does it inhibit?

A

found in hypothalamus and pancreas; decreases insulin, glucagon, and growth hormone

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8
Q

Which inhibits the release of GH? a. IGF-1 b. somatostatin c. both d. neither

A

c. both

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9
Q

Which inhibits the synthesis of GH? a. IGF-1 b. somatostatin c. both d. neither

A

a. IGF-1

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10
Q

Which two of the following stages is GH likely to increase in? a. neonate b. childhood c. adolescence d. adults e. elderly

A

a. neonate & c. adolescence (around puberty)

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11
Q

Whats the half-life of GH? What metabolizes it?

A

20 minutes liver and kidney

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12
Q

short term GH uptake VERSUS long term GH uptake (how does each affect carb uptake?)

A

short term causes increase of glucose uptake, but long term causes decrease of glucose uptake

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13
Q

What mediates the actions of growth hormone?

A

IGF-1

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14
Q

How can you determine if a kid has insufficient GH?

A
  1. growth less than 4cm per year
  2. no response to agents that usually increase GH secretion (low response= less than 7 microliters)
  3. delayed bone age
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15
Q

Which of the following is an analog of Growth hormone-releasing hormone (GHRH)? a. Mecasermin b. Somatrem c. Somatropin d. Sermorelin

A

d. Sermorelin

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16
Q

Which of the following is made by adding methionine amino acid? a. Somatropin b. Somatrem c. both d. neither

A

b. Somatrem

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17
Q

Which of the following can be taken orally? a. Somatropin b. Somatrem c. both d. neither

A

d. neither

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18
Q

What is used to treat Laron Dwarfism? explain.

A

Mecasermin is used because it’s an IGF-1 analog. In Laron Dwarfism, the GH receptor is insensitive or not functioning, so we bypass it and directly give IGF-1.

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19
Q

Hexarelin is an analog of … made up of … amino acids

A

Hexarelin is an analog of ghrelin made up of 6 aa’s (can be given intranasally)

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20
Q

How do androgen and estrogens interfere with GH action?

A

they enhance epiphysis closure

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21
Q

How do glucocorticoids interfere with GH action?

A

because they’re catabolic hormones (increase protein degradation) and that goes against GH

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22
Q

Which of the following has the exact AA sequence as GH? a. Somatropin b. Somatrem c. both d. neither

A

a. Somatropin (GH aka Somatropin)

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23
Q

How does GH affect drug concentrations?

A

it increases Cytochrome P-450 activity, and this metabolizes the drugs and decreases their serum level

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24
Q

Octreotide is an analog of what? What does it inhibit?

A

its an analog of somatostatin, so it decreases insulin, glucagon, and GH

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25
Q

Cabergoline & Bromocriptin are analogs of

A

dopamine (used to treat acromegaly)

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26
Q

What drug blocks GH receptors?

A

Pegvisomant

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27
Q

T/F: Octreotide is given orally

A

false, it can be given subcutaneously

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28
Q

When (time of day) should you give GH or GH analogs? Why?

A

in the evening, to mimic body rhythms

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29
Q

What’s the relationship between dopamine analogs and GH?

A

dopamine stimulates GH secretion in normal people, but in patients with acromegaly, Cabergoline & Bromocriptin, (dopamine analogs) it decreases GH secretion

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30
Q

Which is used to treat Pancreatic cell tumors (VIPomas)? a. Somatropin b. Octreotide c. Cabergoline d. Hexarelin e. Pegvisomant

A

b. Octreotide (also to treat carcinoid tumor and GH excess)

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31
Q

What two drugs normalize IGF-I levels in 35% of patients?

A

Cabergoline & Bromocriptin

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32
Q

Which has a side effect of vomiting? explain the mechanism. a. Somatropin b. Octreotide c. Cabergoline d. Hexarelin e. Pegvisomant

A

c. Cabergoline (vomiting due to the activation of the chemoreceptor trigger zone)

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33
Q

Which has a side effect of H. pylori infections? a. Somatropin b. Octreotide c. Cabergoline d. Hexarelin e. Pegvisomant

A

b. Octreotide

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34
Q

Which drug is given once or twice a month via intramuscular methods?

A

Somatrem

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35
Q

Which drug has a side effect of gall bladder contractility?

A

Octreotide

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36
Q

T/F: GH mainly targets the liver

A

true, it does have receptors in many places in the body but the liver is where IGF-1 is secreted which mediates GH activities (GH receptor is enriched in the liver)

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37
Q

What is more, GH in free form or GH bound to its binding protein (GHBP)?

A

they’re equal

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38
Q

What stabilized IGF-1? For how long can it do this?

A

IGF-1/IGFBP/ALS complex works to stabilize IGF-1 for up to 12 hours

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39
Q

What do you measure when you want to evaluate GH in the body?

A

GH’s half-life is very short, so we measure IGF-1, which has a longer half-life and is stimulated by GH (IGF-1 is a good indicator of GH levels)

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40
Q

Explain how GH can lead to the burn out of pancreatic beta cells?

A

GH has an anti-insulin effect, so it reduces glucose uptake and it increases glucose output. This results in high glucose in the blood, and that triggers insulin release. Insulin is getting released more and more (GH acting against it) that the body becomes insulin INsensitive. So now more insulin is needed to make the same progress. beta cells work more and more until they burn out. Just like us in medical school.

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41
Q

What occurs to insulin if no GH is present?

A

lower insulin secretion

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42
Q

GH is anabolic for which of the following? a. carbs b. fats c. proteins

A

c. proteins

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43
Q

How can you remove the lipolytic effects of GH?

A

if you give insulin along with it (long term GH effect becomes ketogenic)

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44
Q

What type of energy do we use when we sleep? why?

A

GH is released during sleep and it shifts the metabolism towards lipolysis conserve carbs and proteins.

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45
Q

How does GH effect urea production?

A

it increases amino acid uptake and helps the body retain nitrogen, thus decreasing urea production

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46
Q

What is the Protein sparing effect?

A

(aka amino acid sparing) is the process by which the body derives energy from sources other than protein. Such sources can include fatty tissues, dietary fats and carbs.

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47
Q

How do high amounts of free fatty acids and hyperglycemia effect GH release?

A

decrease it

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48
Q

Explain how sex hormones affect GH release.

A

sex hormones increase GH release, however, very high levels of sex sterioids- like in pregnancy- inhibit GH stimulation and release

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49
Q

Why are those with pituitary dwarfism likely obese?

A

GH-induced lipolysis lost

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50
Q

What condition is characterized by high GH but no IGF-I production?

A

Laron syndrome (remember: Laron Dwarfism is treated with IGF-I analogs)

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51
Q

What is Simmonds disease?

A

form of hypopituitarism due to pituitary destruction.

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52
Q

give me at least 3 symptoms of Simmonds disease

A
  • Hypoglycemia
  • Increase percentage of fat
  • Decrease percentage of protein
  • Muscle weakness and exhaustion
  • Increased risk of heart disease
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53
Q

Which results in increased brain weight? a. acromegaly b. giantism

A

a. acromegaly

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54
Q

Which results in higher susceptibility to infections? a. acromegaly b. giantism

A

b. giantism

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55
Q

T/F: ketoacidosis is common among patients with giantism

A

false, diabetes can occur, but ketoacidosis is rare

56
Q

What chromosome encodes GH?

A

chromosome 17

57
Q

Using what mechanism does GHRH activate somatotrophs to release GH?

A

via cAMP

58
Q

Using what mechanism does Ghrelin activate the release of GH?

A

Ca

59
Q

Using what mechanism does somatostatin inhibit GH release?

A

by inhibiting cAMP

60
Q

What type of receptors are receptors of the hypothalamus?

A

heptahelical transmembrane receptors that are bound to G proteins

61
Q

Which of the following G proteins activates phosphodiesterase? What occurs after this activation? a. Gs b. Gi c. Gq

A

b. Gi Gi activates phosphodiesterase, which converts cAMP to 5’-AMP inactivating it to stop the GH expression

62
Q

Which activates somatostatin release (negative feedback)? a. GH b. IGF-1

A

b. IGF-1

63
Q

What is one of the reasons that older people lose muscle mass?

A

reduction of GH

64
Q

GH receptor is made up of how many aa’s?

A

620

65
Q

How many binding sites does GH have?

A

two

66
Q

GHBP is made up of which part of the GH receptor?

A

the extracellular domain

67
Q

What does GHBP do and how does it work?

A

it inhibits GH by attaching to the GH ligand (non-productivity binding) it increases GH half-life by binding to it and delaying its elimination

68
Q

how many aa’s make up IGF-I & IGF-II?

A

IGF-I = 70 aa’s IGF-II = 67 aa’s

69
Q

Which of the following mainly comes from the liver? a. IGF-I b. IGF-II

A

a. IGF-I

70
Q

Which of the following is implicates in cancer development? a. IGF-I b. IGF-II

A

a. IGF-I

71
Q

What is des(1-3)IGF-1? What is it made of? How is its activity special? why?

A

It’s made up of IGF-I that has been converted. It’s more potent than IGF-I because of reduced affinity to IGFBP (growth factor binding protein)

72
Q

IGF-I half-life is prolonged by … when …. is administered

A

IGF-I half-life is prolonged by 12 hours when IGFBP is administered (binding protein)

73
Q

What type of IGFBP is the major one found in the serum?

A

IGFBP-3

74
Q

Which of the following effects fetal development? a. IGF-I b. IGF-II

A

b. IGF-II

75
Q

IGFBP-3 concentration is dependent on what?

A

GH dependent

76
Q

Which of the following effects skeletal and cartilage growth? a. IGF-I b. IGF-II

A

a. IGF-I

77
Q

The receptors of which two of the following are similar? What does this mean? a. IGF-I b. IGF-II c. insulin

A

a. IGF-I & c. insulin (parts of each of them can merge and create a receptor)

78
Q

What is more likely to bind to a IGF-I receptor?

A

IGF-I, then IGF-II, then with least affinity it can bind with insulin

79
Q

How is the IGF-II receptor different from IGF-I receptor?

A

no tyrosine kinase domain (the IGF-II receptor is just there to trap and remove the IGF-II)

80
Q

What are the two kinds of receptor tyrosine kinases?

A

monomeric dimeric

81
Q

What activates MAPK (mitogen-activated protein kinase)?

A

SHC (src homologous and collagen)

82
Q

Which of the following controls glucose homeostasis within the cell? a. src homologous and collagen (SHC) b. Phosphoinositide 3-kinase (PI3K) c. mitogen-activated protein kinase (MAPK)

A

b. Phosphoinositide 3-kinase (PI3K) (activated by Insulin receptor substrate 1 (IRS-1))

83
Q

How do intracellular proteins know when to bind to receptor tyrosine kinases?

A

SH2 and/or SH3 domains of proteins recognize the activated phosphotyrosine residues

84
Q

Which two of the following are off switches? (inhibitors of GH intracellular activity) a. SHP-2 b. Shc c. SOCS d. Grb2

A

a. SHP-2 (src homology 2 domain-containing protein tyrosine phosphatase 2) & c. SOCS (suppressor of cytokine signaling)

85
Q

How does SHP-2 & SOCS act?

A

SHP-2 -> dephosphorylates the GH receptor and/or JAK2 SOCS -> inhibits JAK2

86
Q

Which decreases JAK2 activity and which increases JAK2 activity? a. SH2-B b. Shc c. SOCS d. Grb2

A

a. SH2-B -> increases JAK2 c. SOCS -> decreases JAK2

87
Q

African pigmy is characterized by a. GH resistance b. GH deficiency c. IGF-I resistance d. IGF-I deficiency

A

c. IGF-I resistance (due to partial defect in GH receptor. Bad receptor-> delayed rise in IGF)

88
Q

Laron Dwarfism is characterized by a. GH resistance b. GH deficiency c. IGF-I resistance d. IGF-I deficiency

A

a. GH resistance

89
Q

What is the allostatic load?

A

the wear and tear on the body which accumulates as an individual is exposed to repeated or chronic stress

90
Q

Which (one or two) of the following has adrenaline and noradrenaline receptors? a. T cells b. B cells c. Lymphocytes d. Macrophages

A

c. Lymphocytes

91
Q

Which (one or two) of the following glucocorticoid receptors? a. T cells b. B cells c. Lymphocytes d. Macrophages

A

a. T cells & b. B cells

92
Q

How does stress indirectly affect immunity?

A

by encouraging maladaptive behaviors

93
Q

How do stressors affect the immune system?

A

acute stressors stimulate the immune system but chronic ones suppress it

94
Q

T/F: cortisol and epinephrine can promote nerve cell damage in chronic stress

A

true (also encourage deposition of fat, insulin resistance, and hypertension- in chronic stress)

95
Q

How does chronic stress affect cortisol levels?

A

chronic stress makes the body less sensitive to glucocorticoids (ex/cortisol) and when its less sensitive, it takes more glucocorticoid to negatively inhibit the secretion (negative feedback loop). thats why the levels increase. (higher levels lead to inflammation)

96
Q

How does chronic stress lead to reduced cardiovascular health?

A

chronic stress releases cholesterol into the blood, it builds up on arterial walls and restricts blood flow to the heart

97
Q

T/F: cardiac patient outcomes are associated with anger levels

A

true (anger has 20% increased risk for coronary artery disease)

98
Q

Which personality type is associated with anger? a. type A b. type B c. type C d. type D

A

a. type A (main compnents= hostility and anger)

99
Q

Which personality type has an increased risk of adverse cardiac outcomes? a. type A b. type B c. type C d. type D

A

d. type D

100
Q

Which of the following is more likely to have IBS or a gastrointestinal disease? a. stay at home mom b. gym teacher c. soldier d. a high school dropout

A

c. soldier found twice as often in more stressful occupations

101
Q

What bacteria causes ulcers?

A

H. pylori

102
Q

What type of stress is associated with enhanced memory storage and greater concentration on immediate events?

A

short term

103
Q

How does chronic stress affect the brain?

A

shrinking of the hippocampus (due to high long term cortisol exposure)

104
Q

What does antonovsky salutogenic model emphasize?

A

concerned with the relationship between health, stress, and coping. What people do to maintain health? (underlying origin of health)

105
Q

Whats the function of generalized resistance resources (GRRs)?

A

they’re used to adapt and to resist the forces that push towards disease (used in the salutogenic model)

106
Q

What are the three factors of the salutogenic model? explain them. Whats the most important factor?

A

comprehensibility - makes cognitive sense manageability - can use resources to cope with them meaningfulness - makes emotional sense (most important is meaningfulness)

107
Q

What does a weak sense of coherence (SOC) present as? how about a strong SOC?

A

Weak SOC - no hope, everything will go wrong strong SOC - life is complicated and it will work out

108
Q

Why is pain in cancer patients the least reported and treated pain?

A

Patients believe that if they report the pain the physician will focus on the pain rather than the cancer treatment and they will get worst

109
Q

What is an independent risk factor for predicting cancer survival?

A

pain

110
Q

Where does pain perception occur?

A

in the brain not the pain receptors

111
Q

T/F: the more severe the pain is the more likely the patient is expressing it (yelling, crying, etc.

A

false, many factors go into the expression of pain (ex/ culture, believes, mental status, etc

112
Q

Which kind of somatic pain is more intense? a. surface somatic pain b. deep somatic pain

A

b. deep somatic pain

113
Q

Which kind of somatic pain in neoplasms? a. surface somatic pain b. deep somatic pain

A

b. deep somatic pain

114
Q

describe of liver and pancreatic pain

A

sharp and penetrating

115
Q

What’s malingering pain?

A

an exasperated response to pain for secondary gains

116
Q

What is Anorexia-cachexia syndrome?

A

progressive weight loss associated with malignancy and is characterized by loss of appetite (anorexia), skeletal muscle wasting, and reduced adipose tissue

117
Q

T/F: children exposed to repeated painful procedures often experience less anxiety and pain due to acclimatization

A

false, anxiety and pain increases with more procedures

118
Q

Which chemotherapy symptoms does acupuncture help relieve?

A

nausea and vomiting

119
Q

What three organs does GH have a direct effect on?

A

liver, muscle, adipose

120
Q

A patient has spade hand, what is a possible explanation?

A

he has acromegaly (spade hands is when the patient can put his fingers close together due to excess growth)

121
Q

What are two chromosomal abnormalities that cause short stature?

A

turner’s syndrome down’s syndrome

122
Q

Which is more helpful in diagnosis of GH disorders? why? a. baseline GH levels b. dynamic GH levels

A

b. dynamic GH levels (GH is pulsatile, so based on the time you measure it, the basal GH levels may appear normal or abnormal. Dynamic GH levels are measured after a stimulatory agent is given to enhance GH secretion)

123
Q

How do you assess bone age?

A

X-ray of nondominant hand and wrist

124
Q

What does a GH stimulation test indicate?

A

GH deficiency or pituitary tumor

125
Q

What are four things that can stimulate GH secretion?

A

insulin arginine clonidine L-dopa

126
Q

How do you diagnose/confirm GH deficiency?

A

failure of at least 2 stimulation tests and/or IGF-1 levels (this can also confirm GH deficiency)

127
Q

What are two chromosomal abnormalities that cause tall stature?

A

Klinefelter syndrome Marfan syndrome

128
Q

What suppresses GH secretion?

A

glucose (OGTT) (many more ex/ high free fatty acids)

129
Q

Besides GH, what hormone is increased in acromegaly?

A

prolactin (high in 25% of the patients)

130
Q

IGF-1 levels can confirm which of the following? a. GH deficiency b. acromegaly c. both d. neither

A

a. GH deficiency (it can screen for acromegaly, but not confirm it)

131
Q

GH excess in children vs GH excess in adults

A

in children= giantism in adults= acromegaly

132
Q

GH deficiency in children vs GH deficiency in adults

A

in children= pituitary dwarfism in adults= more fat mass (especially in omentum), less lean body mass, cardiovascular risk factors, and social isolation

133
Q

What is the mechanism of somatorem in a child with growth hormone
deficiency?
A. Decrease collagen synthesis
B. Increases proliferation of chondroblasts and osteoblasts

A

B. Increases proliferation of chondroblasts and osteoblasts

134
Q

What is a characteristic of IGF-1 receptor? (Ask Dr.)
A. Exhibits intrinsic tyrosine kinase activity
B. Heterodimerizes with GH receptor
C. Couples with Gi protein
D. Couples with Ras

A

no answer provided

135
Q

Which of the following stimulates growth hormone release?
A. Exercise
B. Glucagon
C. Carbergoline
D. Oral glucose tolerance test

A

A. Exercise

Endocrine (8 decks)

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