Exam II material

Question 1

The endocrine system provides ______ of many tissues

Answer 1

Broadcast regulation

Question 2

The specificity of the endocrine system is due to:

Answer 2

Receptors

Question 3

Compared to the nervous system, the responses of the endocrine system are:

Answer 3

Slower but longer lasting

Question 4

Where does the endocrine system release hormones into?

Answer 4

The blood

Question 5

List the three functions of hormones:

Answer 5

1. Maintenance of Homeostasis
2. Growth & Differentiation
3. Reproduction

Question 6

Endocrine organs can be divided into what two categories:

Answer 6

1. Major endocrine glands
2. Organs containing endocrine cells

Question 7

Primary function is to make a hormone & release it when the stimuli for release are present:

Answer 7

Major endocrine gland

Question 8

Organs that happen to have endocrine cells within them, allowing them to release a hormone although their primary function is NOT endocrine regulation:

Answer 8

Organs containing endocrine cells

Question 9

List the specialized endocrine glands (Major endocrine glands)

Answer 9

1. Parathyroid gland
2. Thyroid gland
3. Pituitary gland
4. Adrenal gland
5. Pineal gland

Question 10

List some organs that contain endocrine cells, but their primary function is NOT endocrine regulation:

Answer 10

1. Hypothalamus
2. Skin
3. Adipose tissue
4. Thymus
5. Heart
6. Liver
7. Stomach
8. Pancreas
9. Small intestine
10. Kidneys
11. Gonads

Question 11

A hormone that causes secretion of a hormone by an endocrine gland

Answer 11

Tropic hormone

Question 12

How do we classify hormones?

Answer 12

Based on their strucutre

Question 13

What are the three classifications of hormones?

Answer 13

1. Proteins & polypeptides
2. Steroids
3. Tyrosine derivatives

Question 14

Describe the time period in which protein/polypeptide hormones are made and released:

Answer 14

Made in advance & stored in vesicles until signaled for release

Question 15

Protein/polypeptide hormones are synthesized first as:

Answer 15

Preprohormones

Question 16

The preprohormone will be converted into a:

Answer 16

Prohormone

Question 17

In protein/polypeptide hormones, what is packed into vesicles in the endocrine cell prior to secretion?

Answer 17

Prohormone

Question 18

After the prohormone is cleaved, it is now:

Answer 18

Active hormone

Question 19

The pneumonic for protein/polypeptide hormones:

Answer 19

Protein/Polypeptide = Pre & Pro hormone (all begin with Ps)

Question 20

In addition to the active hormone, what is released when the prohormone is cleaved?

Answer 20

Inactive fragments

Question 21

What is the first thing to be cleaved from preproinsulin?

Answer 21

Signal peptide

Question 22

After the signal peptide is cleaved from preproinsulin what occurs?

Answer 22

Protein folding

Question 23

Following cleavage of the signal peptide from preproinsulin & protein folding, what results:

Answer 23

Proinsulin

Question 24

Proinsulin is stored in:

Answer 24

Vesicles

Question 25

Upon receiving a signal for release into the bloodstream, what is cleaved from proinsulin to convert it to active insulin?

Answer 25

C-peptide

Question 26

Along with insulin release into the bloodstream, what is also released?

Answer 26

C-peptide

Question 27

If you wanted to measure someones baseline endogenous production & release of insulin you could measure the:

Answer 27

C-peptide levels in the bloodstream

Question 28

Protein & polypeptide hormones are often made as an:

Answer 28

Inactive precursor

Question 29

The inactive precursor of protein & polypeptide hormones:

Answer 29

Preprohormone

Question 30

What does the signal peptide in insulin serve as?

Answer 30

A marker that tells the cell that insulin needs to undergo exocytosis

Question 31

Where are the receptors located for protein/polypeptide hormones?

Answer 31

In the plasma membrane

Question 32

Describe the time period in which steroid hormones are made & released:

Answer 32

Made & released on demand

Question 33

Where are the receptors located for steroid hormones?

Answer 33

Located inside the cell

Question 34

Why are steroid hormone receptors located inside the cell?

Answer 34

Because steroid hormones can cross the plasma membrane & bind to internal receptors on target cells

Question 35

Hormones from the hypothalamus, anterior pituitary, posterior pituitary & pancreas:

Answer 35

Protein/polypeptide

Question 36

Hormones from the adrenal cortex, ovaries & testes:

Answer 36

Steroid hormones

Question 37

Steroid hormones are synthesized from: (derivatives of)

Answer 37

Cholesterol

Question 38

What are two hormones that are derived from cholesterol that are STRUCTURALLY very similar?

Answer 38

Aldosterone & Cortisol

Question 39

DHEA, Androstenedione, Testosterone & Estradiol are all steroid hormones involved in:

Answer 39

Reproduction

Question 40

What determines what steroid hormone will be produced from the precursor cholesterol?

Answer 40

The complement of enzymes present

Question 41

Describe the time period present in which amine hormones are made & released:

Answer 41

Made early and stored until secreted

Question 42

Amine hormones are derived from:

Answer 42

Amino acid Tyrosine

Question 43

Thyroid hormone, Epinephrine & Norepinephrine are all:

Answer 43

Amine hormones

Question 44

Epinephrine & Norepinephrine are both:

Answer 44

Adrenal medullary neurohormones

Question 45

Thyroid hormones bind to the protein:

Answer 45

Thyroglobulin

Question 46

Epinephrine & Norepinephrine are stored in vesicles & released via:

Answer 46

Exocytosis

Question 47

Structurally what is the difference between T3 & T4:

Answer 47

The number of iodide atoms attached

Question 48

What is the precursor to Epinephrine & Norepinephrine?

Answer 48

Dopine

Question 49

Hormones released into circulation can either circulate ____ or ________

Answer 49

Freely or with binding proteins

Question 50

The majority of ____, ____ & ____ hormones circulate in their free form:

Answer 50

Amines, Peptide/Protein hormone

Question 51

What is the exception to most amines circulating in their free form & why?

Answer 51

Thyroid hormone Its double ring structure makes it soluble enough to where it needs help getting through the plasma

Question 52

Describe the solubility of amines and peptide/proteins hormones:

Answer 52

Water soluble

Question 53

_____ & ____ hormones circulate bound to specific transport proteins

Answer 53

Steroid & Thyroid

Question 54

Some binding proteins are specific for a given hormone, but some plasma proteins such as ___ & ____ can bind to many hormones

Answer 54

Globulin & Albumin

Question 55

Prevalent protein in the plasma that functions as transportation for a lot of different things such as lipid soluble hormones & fatty acids

Answer 55

Albumin

Question 56

Most binding proteins are synthesized in the:

Answer 56

Liver

Question 57

Patients with a compromised/dysfunctional liver may show signs of:

Answer 57

Endocrine deficiencies

Question 58

Why might a patient with a compromised liver show endocrine deficiencies?

Answer 58

Because most binding proteins are synthesized in the liver & if you can't make your binding proteins you can't get enough hormone into the blood

Question 59

It is always the ______ version of the hormone that binds to receptors & affects the target cell:

Answer 59

Free version (binding protein stays in blood vessel)

Question 60

The constitutive level of plasma hormones

Answer 60

Basal level

Question 61

The stimulated level of plasma hormones

Answer 61

Peak levels

Question 62

The variable pattern of hormone release (peaks & troughs) is determined by the interaction & integration of multiple control mechanisms which include: (4)

Answer 62

Hormonal Neural Nutritional Environmental

Question 63

When a hormone is constantly secreted in small amounts at a time:

Answer 63

Tonic release

Question 64

Hormone fluctuations that happen dependent on the time of day

Answer 64

Circadian rhythm

Question 65

Give an example of a hormone that follows circadian rhythm release:

Answer 65

Cortisol

Question 66

When does cortisol levels spike?

Answer 66

In the early morning hours

Question 67

What can work in addition to circadian rhythm release to regulate the release of hormones:

Answer 67

Stimuli

Question 68

Growth hormone is released during sleep making it following a circadian rhythm release pattern but also displays:

Answer 68

Pulsatile secretion

Question 69

Secreted in pulses (secretes, stops, secretes, stops)

Answer 69

Pulsatile secretion

Question 70

The location of the hormone receptor depends on the ______ properties of the hormone

Answer 70

Chemical

Question 71

The chemical properties of the hormone that determine the location of the hormone receptor can be:

Answer 71

Lipophobic & Liphophillic

Question 72

Ligand/Receptor binding demonstrates:

Answer 72

1. Specificity 2. Affinity 3. Saturation

Question 73

Which classes of hormones bind to plasma membrane receptors?

Answer 73

Polypeptide/Protein hormones Amine hormones*

Question 74

What amine hormone does not bind to plasma membrane receptors? (except to the rule)

Answer 74

Thyroid hormone

Question 75

Which class of hormones binds to nuclear receptors?

Answer 75

Steroid hormones + thyroid hormone

Question 76

Which amine hormones bind to plasma membrane receptors?

Answer 76

Epinephrine & Norepinpehrine

Question 77

What type of receptors would the following hormones bind to & why? - Glucagon - Angiotensin - GnRH - SS - GHRH - FSH - LH - TSH - ACTH

Answer 77

Plasma membrane receptors- they are peptide/protein hormones

Question 78

In general many of the receptors that proteins/peptide hormones & amine hormone bind to in the plasma membrane are:

Answer 78

G-protein coupled receptors (GPCRs)

Question 79

Involved in turning on or off a protein that is already in the cell:

Answer 79

Plasma membrane receptors

Question 80

What class of hormone receptors are involved in causing a change in gene expression to get a biological response?

Answer 80

Nuclear receptors

Question 81

Class of hormone receptors involved in making new proteins:

Answer 81

Nuclear receptors

Question 82

Thyroid hormone & steroid hormones bind to receptors located in:

Answer 82

Either the cytoplasm or the nucleus

Question 83

Once the steroid hormone or thyroid hormone binds to the receptor located in the nucleus or cytoplasm what occurs next?

Answer 83

Transformation of receptor to expose DNA-binding domain

Question 84

Following binding of the steroid hormone or thyroid hormone to the receptor & transformation of the receptor to expose the DNA-binding domain what next occurs?

Answer 84

Binding to enhancer-like element in DNA

Question 85

Examples of plasma membrane hormone receptors:

Answer 85

1. GPCR 2. Tyrosin kinase

Question 86

Why do plasma membrane hormone receptor numbers vary greatly in different target tissues:

Answer 86

Provides a way to achieve specific tissues activation

Question 87

What are two examples of plasma membrane hormone receptors that are more distributed:

Answer 87

1. Thyroid hormone receptors 2. Insulin receptors

Question 88

Why are thyroid hormone receptors & insulin receptors more sidled distributed?

Answer 88

Because their actions are something that most cells participate in

Question 89

How do IGF-1 & Insulin work?

Answer 89

By activating a tyrosine kinase receptor

Question 90

If it is plasma membrane receptor generally it will activate or inhibit _____ to ______

Answer 90

An existing protein to yield a faster response

Question 91

Where are nuclear hormone receptors located?

Answer 91

Cytoplasm or nucleus

Question 92

Nuclear hormone receptors typically leads to:

Answer 92

Formation of new proteins

Question 93

Nuclear hormone receptors all act to:

Answer 93

Increase or decrease gene expression

Question 94

In a nuclear hormone receptor, the hormone receptor complex binds to a ______ in the _____ region of the gene which leads to either the activation or repression of ______

Answer 94

Hormone responsive element Promotor region Gene transcription

Question 95

Because nuclear hormone receptors binding a hormone leads to the formation of a new protein, describe the timeline involved:

Answer 95

It takes a little bit longer to get the response & the response will last a bit longer

Question 96

Hormones that bind to nuclear receptors (thyroid hormone & steroid hormones) undergo _____ to get through the plasma membrane

Answer 96

SImple diffusion

Question 97

The body often releases multiple hormones:

Answer 97

At the same time

Question 98

What are the effects of combined hormone actions: (4)

Answer 98

1. Antagonism 2. Additive 3. Synergistic 4. Permissiveness

Question 99

When two hormones change one variable in opposite directions:

Answer 99

Antagonsim

Question 100

When the response of hormone is equal to the two portions that each hormone provide (2+3=5)

Answer 100

Additive

Question 101

When the combined hormone response is greater than the individual responses of each hormone added together (2+3=10)

Answer 101

Synergistic

Question 102

The presence of one hormone is necessary for another hormone's maximum affect:

Answer 102

Permissiveness

Question 103

Determine which hormone interaction is being described in the following situation: Parathyroid increases plasma calcium levels; Calcitonin decreases plasma calcium levels:

Answer 103

Antagonism

Question 104

Determine which hormone interaction is being described in the following situation: Glucagon, cortisol & epinephrin all increase blood glucose more than the sum of their individual effects:

Answer 104

Synergism

Question 105

Determine which hormone interaction is being described in the following situation: Thyroid hormone causes expression of B adrenergic receptors in bronchiolar smooth muscle:

Answer 105

Permissive

Question 106

What determines whether the negative feedback will be short loop or long loop?

Answer 106

The location of the hormone that acts as negative feedback in the system

Question 107

When the last hormone in the pathway inhibits the system upstream

Answer 107

Long loop negative feedback

Question 108

When an intermediate hormone in the pathway inhibits the system upstream

Answer 108

Short loop negative feedback

Question 109

Feedback where the hormonal product or an intermediate hormone enhances the hormone secretion:

Answer 109

Positive feedback

Question 110

Causes an endocrine gland to secrete a hormone

Answer 110

Tropic hormone

Question 111

Stabilizes the system & prevents over-secretion:

Answer 111

Negative feedback

Question 112

Hormones that have other endocrine glands as there targets:

Answer 112

Tropic hormones

Question 113

A tropic hormone from the hypothalamus that acts on the anterior pituitary to release TSH

Answer 113

Thyroid releasing hormone (TRH)

Question 114

Thyroid releasing hormone (TRH) comes from:

Answer 114

The hypothalamus

Question 115

TRH acts on the:

Answer 115

Anterior pituitary

Question 116

TSH (Thyroid stimulating hormone) is released from:

Answer 116

The anterior pituitary

Question 117

TSH is released from the anterior pituitary & acts on:

Answer 117

The thyroid gland

Question 118

In the regulation of thyroid hormone, a stimulus causes the hypothalamus to secrete ____ which acts on the ______

Answer 118

TRH Anterior pituitary

Question 119

In the regulation of thyroid hormone, _____ cells in the anterior pituitary release _____

Answer 119

Thyrotropic cells Thyroid stimulating hormone

Question 120

In the regulation of thyroid hormone, TSH stimulates _____ cells of the thyroid gland to release _____

Answer 120

Follicular cells Thyroid hormone (TH)

Question 121

Thyroid hormone produces effects in the body that include:

Answer 121

1. Increase in metabolic activity 2. Increase in body temperature

Question 122

In the regulation of thyroid hormone, thyroid hormone stimulates target cells to increase ____ activities resulting in an increase in basal body temperature

Answer 122

Metabolic activities

Question 123

In the regulation of thyroid hormone, increased body temperature is detected by the hypothalamus & the secretion of _____ by the hypothalamus is ____

Answer 123

TRH Inhibited

Question 124

In the regulation of thyroid hormone, thyroid hormone also blocks TRH receptors on thyroid cells inhibiting synthesis & release of ____. Both effects indirectly dampen _____ production in the thyroid

Answer 124

TSH TH

Question 125

Thyroid hormone working to negatively feedback is an example of:

Answer 125

Long loop negative feedback

Question 126

If hormone levels are NOT kept in balance via negative feedback mechanisms what occurs?

Answer 126

Endocrine disorders/Pathologies

Question 127

Enlargement of the thyroid due to increased or decreased thyroid hormone levels:

Answer 127

Thyroid goiter

Question 128

Disease characterized by increased cortisol levels:

Answer 128

Cushings disease

Question 129

Abnormality in the last endocrine organ secreting the hormone leading to either hypo- or hyper-secretion:

Answer 129

Primary endocrine disorder

Question 130

List the causes of primary hyposecretion:

Answer 130

1. Partial destruction of the gland 2. Dietary deficiency 3. Enzyme deficiency required for hormone synthesis

Question 131

List the causes of primary hypersecretion:

Answer 131

1. Endocrine gland tumor

Question 132

Abnormality in tropic hormone leading to either hypo- or hyper-secretion:

Answer 132

Secondary endocrine disorder

Question 133

List the causes of secondary hyposecretion:

Answer 133

A lack of sufficient tropic hormone

Question 134

List the causes of secondary hypersecretion:

Answer 134

A tumor (either in an endocrine gland that secretes tropic hormones or in a non-endocrine tissues that secretes hormones)

Question 135

When you see an endocrine hormone disturbance as a result of cancer:

Answer 135

Paraneoplastic endocrine syndrome

Question 136

When you think of primary endocrine dysfunction you should think:

Answer 136

LAST gland in pathway

Question 137

Type of diagnostic endocrine function test in which you give something to make hormone levels go up to see if hormone levels actually go up: Type of diagnostic endocrine function test in which you give something to inhibit the hormone levels in question & look to see if that actual works:

Answer 137

Stimulation test Suppression test

Question 138

Suppression test would be used to detect what type of endocrine dysfunction:

Answer 138

Hyperfunction

Question 139

List the types of diagnostic test used to examine endocrine function (7):

Answer 139

1. Plasma hormone levels 2. Autoantibodies 3. Urine hormone/hormone metabolite levels 4. Stimulation tests by administration of tropic or stimulating hormone 5. Suppression tests when hyperfunction of endocrine organ is suspected 6. Measurement of hormone receptor presence , number & affinity 7. Imaging

Question 140

Stimulation tests work by administering a ____ hormone:

Answer 140

tropic or stimulating

Question 141

An example of measuring hormone receptor presence as an endocrine diagnostic function test:

Answer 141

Estrogen receptors in breast tumors

Question 142

What autoantibodies might be tested when doing diagnostic tests of endocrine function:

Answer 142

1. Hashiomoto thyroiditis 2. Type I DM 3. Graves disease 4. Addison disease 5. Autoimmune hypoparathyroidism

Question 143

Glucagon, Angiotensin, Gonadotropin releasing hormone (GnRH), Somatostatin (SS), Growth hormone releasing hormone (GHRH), Follicle stimulating hormone (FSH), Lutenizing hormone (LH), Thyroid stimulating hormone (TSH), Adrenocorticotropin hormone (ACTH) Are all ____ hormones When are they made?

Answer 143

Polypeptide/protein hormones Made in advance & stored until use

Question 144

Epinephrine & norepinephrine are ____ hormones When are they made?

Answer 144

Amine hormones Made in advance and then stored

Question 145

Thyroid hormone (TH) is a ____ hormone When is it made?

Answer 145

Exception: amine hormone Made in advance and then stored but does bind to nuclear receptors

Question 146

Aldosterone, Cortisol, Estradiol, testosterone, also mineralocorticoids, glucocorticoids, and androgens are all _____ hormones When are they made?

Answer 146

Steroid hormones Made on demand

Question 147

List things that stimulate growth hormone (GH) release:

Answer 147

GHRH Dopamine Catecholamines (in times of stress & exercise) Excitatory amino acids Thyroid hormone Fasting (Hypoglycemia)

Question 148

List things that inhibits growth hormone (GH) release:

Answer 148

Somatostatin (SS) IGF-1 (because of negative feedback) Glucose (at high levels- hyperglycemia) Free fatty acids

Question 149

GHRH, Dopamine, Catecholamines, excitatory amino acids and thyroid hormone would cause ______ of growth hormone release

Answer 149

Stimulation

Question 150

Portion of the pituitary that is truly filled with endocrine cells- a true endocrine gland:

Answer 150

Adenohypophysis

Question 151

Adenohypophysis is referring to what portion of the pituitary gland:

Answer 151

Anterior pituitary

Question 152

Portion of the pituitary that contains axon terminals of hypothalamic neurons:

Answer 152

Neurohypophysis

Question 153

Neurohypophysis is referring to what portion of the pituitary gland:

Answer 153

Posterior pituitary

Question 154

The pituitary gland is locked in the ______ ventral to the ______

Answer 154

Sella turcica Diaphragma sella

Question 155

List the hormones secreted by the anterior pituitary: (6)

Answer 155

1. FSH 2. LH 3. Adrenocorticotropin 4. Thyroid-stimulating hormone 5. Prolactin 6. Growth hormone

Question 156

List the hormones secreted by the posterior pituitary: (2)

Answer 156

1. ADH/Vasopressin 2. Oxytocin

Question 157

The pituitary gland secretes _____ hormones

Answer 157

Peptide hormones

Question 158

What are the most prevalent cells in the anterior pituitary & what do they secrete?

Answer 158

Somatotrophs Growth hormone

Question 159

What percentage of cells in the anterior pituitary do somatotrophs comprise?

Answer 159

30-40%

Question 160

What is the second most prevalent type of cell in the anterior pituitary & what do they secrete?

Answer 160

Corticotrophs ACTH

Question 161

What percentage of cells in the anterior pituitary do corticotrophs comprise?

Answer 161

20%

Question 162

Aside from corticotrophs & somatotrophs, what types of cells makeup the anterior pituitary & what do they secrete?

Answer 162

Thyrotrophs - TSH Gonadotrophs- LH & FSH Mammaotrophs- Prolactin

Question 163

Adenomas involving somatotropin cells can cause _____ if occurring in children before the closing of long bones (epiphyseal plates) or _____ in adults with musculoskeletal, neurologic, and other medical consequences

Answer 163

Gigantism Acromegaly

Question 164

Benign tumor of epithelial cells that makes hormones:

Answer 164

Adenoma

Question 165

Endocrine cells are derived from:

Answer 165

Epithelial cells

Question 166

If a benign tumor is involved in somatotropic cells this would cause over secretion of:

Answer 166

Growth hormone

Question 167

Majority of cells in the anterior pituitary are devoted to making _____ & _____

Answer 167

GH & ACTH

Question 168

Neurons in the hypothalamus synthesize & secrete ______ hormones that control endocrine cells in the ______

Answer 168

Hypothalamic releasing/inhibiting hormones Anterior pituitary

Question 169

The hypothalamic hormones are released into the ______ in the ______ (in the hypothalamus)

Answer 169

Primary capillary plexus Median eminence

Question 170

Responsible for carrying the hypothalamic hormones to the sinuses of the anterior pituitary gland:

Answer 170

Hypothalamic-hypophyseal portal blood vessels

Question 171

Hypothalamic-hypophyseal portal blood vessels carry the hypothalamic hormones to the ______ of the anterior pituitary gland

Answer 171

Sinuses

Question 172

Regulation of anterior pituitary secretion 1. ______ releases hormones that enter into the blood 2. Hormones travel through the ________ 3. Hormones will continue down through the capillary bed to the ______ wire they can leave the blood & regulate activity of the endocrine cells

Answer 172

1. Hypothalamus 2. primary capillary plexus 3. Sinus

Question 173

Two capillary beds in series

Answer 173

Portal system

Question 174

The hypothalamic-hypophyseal portal vessel is comprised of:

Answer 174

Primary capillary plexus + sinus

Question 175

The hypothalamic hypophyseal portal allows for:

Answer 175

Communication from the hypothalamus to the anterior pituitary

Question 176

Where do releasing hormones come from?

Answer 176

Hypothalamus

Question 177

Where do stimulating hormones cone from?

Answer 177

Anterior pituitary

Question 178

The hypothalamic regulatory hormones bind to_____ in the various endocrine cells of the anterior pituitary

Answer 178

G-proteins coupled receptors

Question 179

Following the binding of the hypothalamic hormones to the G-protein coupled receptors in the anterior pituitary, what is responsible for stimulating or inhibiting anterior pituitary hormone secretion?

Answer 179

Second messengers (cAMP via Adenylate cyclase, IPs & DAG via Phospholipase C)

Question 180

Growth hormone inhibiting hormone (GHIH) =

Answer 180

Somatostatin

Question 181

Prolactin inhibiting hormone (PIH) =

Answer 181

Dopamine

Question 182

Growth hormone is secreted by somatotrophs in the anterior pituitary. The releasing hormone (secreted by hypothalamus) would be _____ (gas) while the inhibiting hormone would be ______ (breaks)

Answer 182

GHRH GHIH

Question 183

GH, a peptide hormone acts _____ on target tissues and as a ______ to the liver

Answer 183

Directly Tropic hormone

Question 184

GH, a peptide hormone acts directly on target tissues ad as a tropic hormone to the _____ which releases _____

Answer 184

Liver IGF1

Question 185

In what situation might growth hormone significantly increase and quickly?

Answer 185

Prolonged starvation/fasting

Question 186

Growth hormone acts tropically on the liver to activate _____ a cell signaling pathway that causes the release of _____

Answer 186

JAKSTAT IGF1

Question 187

A cell signaling pathway in the liver activated by GH that responds by release of IGF1

Answer 187

JAKSTAT

Question 188

What are some target tissues of growth hormone? (6)

Answer 188

1. Liver 2. Chondrocytes 3. Muscle cells 4. Adipose cells 5. Anterior pituitary (short loop negative feedback) 6. Hypothalamus (long loop negative feedback)

Question 189

If GH acts on chondrocytes what results?

Answer 189

1. increased amino acid uptake 2. Increased protein synthesis

Question 190

GH acting on chondrocytes to increase amino acid uptake as well as protein synthesis is ultimately necessary for:

Answer 190

Linear growth

Question 191

In addition to growth hormone acting on chrondocytes being necessary for linear growth what is also necessary for linear growth:

Answer 191

IGF1

Question 192

GH can act on muscles to:

Answer 192

Increase protein synthesis

Question 193

In addition to growth hormone acting on muscle to increase protein synthesis what is also necessary for protein synthesis:

Answer 193

IGF1

Question 194

In excess how does growth hormone affect adipose tissue?

Answer 194

Anti-insulin action

Question 195

What are two locations of negative feedback of growth hormone:

Answer 195

1. Directly feeding back to anterior pituitary (short loop) 2. Feeding back to hypothalamus (long loop)

Question 196

If negative feedback via growth hormone occurs on the hypothalamus what hormone may be released:

Answer 196

Somatostatin

Question 197

Describe the secretion of growth hormone:

Answer 197

Pulsatile secretion; lower concentration during day with highest levels a few hours after sleep

Question 198

When is growth hormone secreted at the highest levels:

Answer 198

A few hours following sleep

Question 199

GH secretion can be stimulated by: (5)

Answer 199

1. Starvation (protein deficiency) 2. Fasting (hypoglycemia) 3. Acute stress 4. Exercise 5. Excitement

Question 200

The secretion of GH during the neonatal period can be described as: The secretion of GH during childhood can be described as: The secretion of GH during puberty can be described as: The secretion of GH during adulthood can be described as:

Answer 200

1. High secretion 2. Decreased secretion 3. Peak levels of secretion 4. Decreased secretion with age

Question 201

Stimulation of GH release: (5)

Answer 201

1. GHRH 2. Dopamine 3. Catecholamines 4. Excitatory amino acids 5. Thyroid hormone

Question 202

Inhibition of GH release: (4)

Answer 202

1. Somatostatin 2. IGF1 (due to negative feedback) 3. High levels of glucose 4. High levels of free fatty acids

Question 203

Many of the growth & metabolic effects of GH are mainly produced by:

Answer 203

IGFs

Question 204

IGFs may also be called:

Answer 204

Somatomedins

Question 205

IGF1 is produced in most tissues and acts on neighboring cells in a ____ manner

Answer 205

Paracrine

Question 206

The major site of IGF1 synthesis:

Answer 206

The liver

Question 207

How many IGF binding proteins are there?

Answer 207

6

Question 208

_____ in adults is one of the main growth promoting insulin-like growth factors:

Answer 208

IGF1

Question 209

Osteocytes responding to mechanical sensors can release:

Answer 209

IGF1

Question 210

Osteocytes responding to _____ can release IGF1:

Answer 210

Mechanical sensors

Question 211

After osteocytes release IGF1 what happens?

Answer 211

IGF1 binds to receptors on osteoblasts to enhance bone formation

Question 212

Mechanisms of actions of GH & IGF1: Growth in nearly all tissues of the body, mainly IGF1 occurs through what mechanisms:

Answer 212

1. increased cell size 2. mitosis 3. Differentiation of bone & muscle cells

Question 213

Mechanisms of actions of GH & IGF1: What are the overall outcomes of the affects of GH & IGF1 causing growth in nearly all tissues in the body:

Answer 213

1. increased organ size 2. increased organ function 3. increased linear growth 4. increased lean body mass

Question 214

Mechanisms of actions of GH & IGF1: Effect of increased amino acid uptake and protein synthesis result in:

Answer 214

Increased lean body mass

Question 215

Mechanisms of actions of GH & IGF1: How does this effect glucose?

Answer 215

Reduced glucose utilization

Question 216

Mechanisms of actions of GH & IGF1: Reduced glucose utilization is due to:

Answer 216

1. decreased cellular uptake 2. increased hepatic glucose production 3. increased insulin secretion

Question 217

Mechanisms of actions of GH & IGF1: The reduced glucose utilization can lead to:

Answer 217

Insulin resistance; diabetogenic

Question 218

Mechanisms of actions of GH & IGF1: Describe the effects on fatty acids:

Answer 218

Mobilization of fatty acids from adipose tissue (lipolysis)

Question 219

The mobilization of fatty acids from adipose tissue:

Answer 219

lipolysis

Question 220

Mechanisms of actions of GH & IGF1: Lipolysis results in:

Answer 220

Increased FFA in blood and use of FFA for energy

Question 221

Before fusion of the epiphyseal plates, GH & IGF1 stimulate:

Answer 221

1. Chondrogenesis 2. Widening of the epiphyseal plates

Question 222

Following GH and IGF1 stimulating chondrogenesis & widening of the epiphyseal plates, what occurs:

Answer 222

Bone matrix deposition stimulating linear growth

Question 223

In adults, GH and IGF1 play a role in regulating the normal physiology of:

Answer 223

Bone formation

Question 224

In adults, how do GH & IGF1 play a role in regulating normal physiology of bone formation?

Answer 224

By increasing bone turnover

Question 225

How do GH and IGF1 stimulate the increase in bone turnover (thereby regulating bone formation):

Answer 225

1. activation of osteoblasts (mainly) 2. Increase bone resorption via osteoclasts (lesser extent)

Question 226

Kids: GH & IGF1 = Adults: GH & IGF1 =

Answer 226

Chondrogenesis Increased bone turnover

Question 227

Osteoblast are of what origin?

Answer 227

Mesenchymal precursor cells

Question 228

What is responsible for the formation of active osteoblasts from the osteoblasts precursors?

Answer 228

IGF1

Question 229

Gigantism occurs in ____ Acromegaly occurs in _____

Answer 229

Children Adults

Question 230

Excess growth hormone in children leading to gigantism is typically caused by:

Answer 230

Pituitary tumor (90%)

Question 231

What areas are commonly involved in pituitary tumors that give rise to gigantism?

Answer 231

Sella & cavernous sinus

Question 232

Tumor causing excessive growth hormone release:

Answer 232

Somatotropin adenoma of pituitary

Question 233

Describe the facial features that may be associated with gigantism/acromegaly: (4)

Answer 233

Coarse facial features Large fleshy nose Frontal bossing Jaw malocclusion

Question 234

Coarse facial features including a large fleshy nose, frontal bossing & jaw malocclusion are collectively reffered to as:

Answer 234

Acromegalic facies

Question 235

What issue with the thyroid may occur with gigantism/acromegaly?

Answer 235

Goiter

Question 236

Describe the potential effects on the heart & what conditions may result due to gigantism/acromegaly

Answer 236

Cardiomegaly Hypertension Coronary heart disease

Question 237

Describe the chest & spine in individuals effected by acromegaly/gigantistm:

Answer 237

Barrel chest Kyphosis & hyperostosis

Question 238

The abnormal glucose tolerance & secondary insulin resistance in an acromegaly/gigantism effected individual may result in:

Answer 238

Diabetes Mellitus

Question 239

Growth hormone shifts the body from using ___ to ____ for metabolism

Answer 239

Carbs to fats

Question 240

Describe the reproductive consequences on individuals with acromegaly/gigantism:

Answer 240

Male sexual dysfunction & menstrual disorders

Question 241

Describe what can occur due to the thicken skin & hypertrophy of sebaceous & sweat glands in gigantism/acromegaly:

Answer 241

Hyperhidrosis & oily skin

Question 242

Hyperhidrosis & oily skin in acromegaly/gigantism can occur due to:

Answer 242

Thickened skin (hypertrophy of sebaceous & sweat glands)

Question 243

What can occur in the joints of individuals with gigantism/acromegaly:

Answer 243

Degenerative arthritis

Question 244

Describe the neuronal effects caused by gigantism/acromegaly:

Answer 244

Parathesias due to peripheral neuropathy

Question 245

What is a potential treatment for pituitary micro adenoma:

Answer 245

Adenectomy via transphenoidal approach followed by medication

Question 246

Oral manifestations of GH excess: (7)

Answer 246

1. Thick rubbery skin, enlarged nose, thick lips 2. Macrocephaly 3. Macrognathia 4. Disproportionate mandibular growth 5. Anterior bite & malocclusion 6. Macroglossia, Dyspnea, Dysphagia, Dysphonia, Sialorrhea 7. Hypertrophy of pharyngeal & laryngeal tissues

Question 247

Enlarged head= Enlarged jaw=

Answer 247

Macrocephaly Macrognathia

Question 248

The disproportionate mandibular growth cause by excess GH includes:

Answer 248

Mandibular prognathism- jaw gets forward Generalized diastemata- teeth separation

Question 249

The anterior open bites & malocclusion caused by excess GH is due to:

Answer 249

Combination of macrognathia & tooth migration

Question 250

Define each: Macroglossia Dyspnea Dysphagia Dysphonia Sialorrhea

Answer 250

Enlarged tongue Difficulty breathing Difficulty swallowing Difficulty speaking Slobbering/droolinh

Question 251

The hypertrophy of the pharyngeal & laryngeal tissues due to excess GH can lead to ________ & how?

Answer 251

Sleep apnea due to the increased growth of pharyngeal & laryngeal tissues obstructing the airway

Question 252

What are the causes of growth hormone deficiency: (5)

Answer 252

1. Hypothalamic disorders 2. Mutations 3. Combined pituitary deficiencies 4. Radiation 5. Psychosocial deprivation

Question 253

Combined pituitary hormone deficiencies:

Answer 253

Panhypopituitarism

Question 254

What type of mutations may lead to GH deficiency:

Answer 254

GHRH receptor GH gene GH receptor IGF1 receptor

Question 255

A decrease in GHRH or an increased in GHIH can lead to

Answer 255

Growth hormone deficiency

Question 256

What depends on the time of onset & severity of hormone deficiency: (talking about growth hormone)

Answer 256

Clinical manifestations

Question 257

The clinical manifestations caused by complete growth deficiency include: (4)

Answer 257

1. Slow linear growth rates (shorter stature) 2. Normal skeletal proportions 3. Pudgy, youthful appearance (decreased lipolysis) 4. In the setting of cortisol deficiency hypoglycemia

Question 258

The most common form of dwarfism that is caused by an autosomal dominant conditions that results from a mutation in the FGF-3 receptor in cartilage & brain:

Answer 258

Achondroplasia

Question 259

Mutation in the FGF-3 receptor in the cartilage & brain makes the receptor overly active and it inhibits cartilage growth at growth plates so:

Answer 259

Limb growth is reduced (growth of trunk is not impacted)

Question 260

Mutated receptor involved in achondroplasia:

Answer 260

FGF-3

Question 261

Oral manifestations of GH deficiency include: 1. Disproportionate delayed growth of the _____ & ____ = ____ facial appearance 2. _____ & ____ of the ___ regions of the jaws are abnormal & may be disproportionately smaller than adjacent structures 3. Solitary _____ 4. Eruption of primary & secondary dentition & shedding of deciduous teeth are ______

Answer 261

1. Skull & facial skeleton; small 2. Tooth formation & growth; alveolar 3. Median maxillary central incisor 4. Delayed

Question 262

How are the oral manifestations of GH deficiency managed:

Answer 262

Correction of dental & skeletal malocclusions

Question 263

Incisor defects in a child with GH deficiency occurs in both:

Answer 263

Primary & permanent dentition

Question 264

Oral manifestations of GH deficiency includes tooth formation & growth of alveolar regions of the jaw are abnormal & may be disproportionately smaller than adjacent anatomic structures this can cause:

Answer 264

1. Tooth crowding & malocclusion 2. Plaque accumulation 3. Poor oral hygiene 4. Gingivitis & perio disease

Question 265

The posterior pituitary contains ~100,000 _________ whose cell bodies are in the_______

Answer 265

Unmyelinated axons of neurons hypothalamus

Question 266

Areas of concentrated neuronal cell bodies in the hypothalamus that have axons that go through the infundibulum with their synaptic terminals located in the posterior pituitary gland

Answer 266

Paraventricular nucleus & Supraoptic nucleus

Question 267

The paraventricular nucleus produces ______

Answer 267

Oxytocin

Question 268

The supraoptic nucleus produces _____

Answer 268

ADH

Question 269

List all at the names for the abbreviation ADH:

Answer 269

1. Antidiuretic hormone 2. Arginine Vasopressin (AVP)

Question 270

Both ADH and Oxytocin are classified as:

Answer 270

Neurohormones

Question 271

Both ADH and oxytocin are neurohormones made of:

Answer 271

Polypeptides of nine amino acids

Question 272

While the paraventricular nucleus secretes Oxytocin, and the supraoptic nucleus secretes ADH, they both have the ability to:

Answer 272

Secrete some of the other neurohormone

Question 273

Describe the similarities between ADH & oxytocin

Answer 273

VERY SIMILAR STRUCTURE & both amine hormones

Question 274

What are the two primary functions of ADH

Answer 274

1. Vasoconstriction (smooth muscle & blood vessels) 2. Antidiuretic (holds on to water)

Question 275

ADH/AVP mechanism of action: 1. Contraction of vascular smooth muscle via _____

Answer 275

V1 Receptors

Question 276

When ADH causes contraction of vascular smooth muscle through V1 receptors what results?

Answer 276

Increases blood pressure

Question 277

V1 stands for:

Answer 277

Vasopressin-1 receptor

Question 278

When ADH acts on V1 receptors what occurs?

Answer 278

Contraction of vascular smooth muscle (blood vessels) leading to increase in BP

Question 279

ADH/AVP mechanism of action: Functions in the renal renal tubules via:

Answer 279

V2 Receptors

Question 280

Where are the V2 receptors (for ADH) located?

Answer 280

Late distal tubule & collecting duct

Question 281

What results when ADH binds to V2 in the last distal tubule & collecting duct?

Answer 281

AQP-2 proteins are inserted into the apical membrane of tubular epithelial cells

Question 282

Where is aquaporin-2 inserted following ADH binding to V2 receptors?

Answer 282

The apical membrane of tubular epithelial cells

Question 283

Following ADH binding to V2 receptors in the renal tubules and AQP-2 being inserted into the apical membrane of tubular epithelial cells what results?

Answer 283

This allows for water reabsorption (in accordance with AQP3 & AQP4 on the basolateral membrane

Question 284

For water reabsorption to occur through AQP2 what also has to be present?

Answer 284

AQP3 & APQ4 on the basolateral membrane

Question 285

V2 receptors in the late distal tubule and collecting duct are _____ receptors

Answer 285

GPCR

Question 286

Although water can go through the apical membrane via simple diffusion, the aquaporins allow for:

Answer 286

Water channels so a lot more reabsorption can occur

Question 287

_____ allows for water to enter the apical membrane _____ are always on the basolateral membrane and allow for the continuation of the water

Answer 287

AQP-2 AQP-3 & AQP-4

Question 288

Stimuli for ADH secretion (3)

Answer 288

1. Decreased blood volume 2. Increased osmolarity 3. Decreased BP

Question 289

In regard to ADH secretion, decreased blood volume is considered:

Answer 289

Isotonic

Question 290

In regard to ADH secretion, increased osmolarity is considered:

Answer 290

Isovolemic

Question 291

The most potent stimulator for ADH release is:

Answer 291

Increased osmolarity (linear on a graph)

Question 292

If blood volume goes down, ADH will function to _______ to resolve the issue

Answer 292

Keep water

Question 293

If the osmolarity of plasma is too high, ADH will function to ____ in order to ______

Answer 293

Keep water Dilute it

Question 294

If your blood pressure is too low, ADH will function to _____ in order to ____-

Answer 294

Keep water Raise it

Question 295

ADH working to keep water in the body will resolve what three issues:

Answer 295

1. High osmolarity 2. Low BP 3. Decreased blood volume

Question 296

Decreased or absent feeling of thirst:

Answer 296

Hypodipsia

Question 297

Hypodipsia may result in ______ which can cause ______

Answer 297

Reduced intake of water Hypernatremia

Question 298

A common problems in elderly people, but is also associated with lesions in the thirst center of the hypothalamus, head trauma, occult hydrocephalus or subarachnoid hemorrhage

Answer 298

Hypodipsia

Question 299

List causes of hypodypsia: (5)

Answer 299

1. Eldery people 2. Lesions in hypothalamus (thirst center) 3. Head trauma 4. Occult hydrocephalus 5. Subarachnoid hemorrhage

Question 300

Diabetes insipidus is a caused by caused by:

Answer 300

ADH imbalance

Question 301

What are the two types of diabetes insipidus:

Answer 301

Neurogenic (Central) Nephrogenic (Peripheral)

Question 302

What do DI and DM have in common?

Answer 302

Large urine output

Question 303

If you have increased osmolarity you would feel:

Answer 303

Thirst (normal conditions)

Question 304

Disease caused by inability to produce & secrete ADH:

Answer 304

Neurogenic/Central Diabetes Insipidus

Question 305

Describe the ADH levels in an individual with Neurogenic/Central DI:

Answer 305

Low levels of ADH (they are unable to produce/secrete it)

Question 306

Treatment for a patient with neurogenic/central DI would be:

Answer 306

To supplement ADH (likely in the form of medication)

Question 307

Person with a tumor near the posterior pituitary gland has surgical removal of the tumor, causing damage to supraoptic nucleus in the posterior pituitary. What are they unable to to produce, what disease would this result in?

Answer 307

ADH Neurogenic/Central DI

Question 308

Lacking a response to ADH (like a resistance)

Answer 308

Nephrogenic/Peripheral DI

Question 309

Nephrogenic/Peripheral DI occurs in the:

Answer 309

Kidneys

Question 310

When ADH is present but the kidneys either do not respond at all, or response inappropriately to the hormone:

Answer 310

Nephrogenic/Peripheral DI

Question 311

Describe the levels of ADH an individuals with nephrogenic/peripheral DI would have and why:

Answer 311

High levels off ADH because they can produce ADH but the stimulus causing secretion is never satisfied

Question 312

Uncharacteristically, really high levels of ADH secretion & NOT becaue it is needed (Oversecretion of ADH)

Answer 312

Syndrome of inappropriate ADH (SIADH)

Question 313

A patient with diabetes insipidus may present with:

Answer 313

Polyuria

Question 314

Excretion of large volumes of urine

Answer 314

Polyuria

Question 315

Describe the urine in a patient with Diabetes Insipidus:

Answer 315

Hypotonic/tasteless (insipid)

Question 316

Other causes of polyuria (not DI) may include: (2)

Answer 316

1. Primary ingestion of excess fluid 2. Inreased metabolism of ADH (pregnancy)

Question 317

Primary ingestion of excess fluid:

Answer 317

Primary polydipsia

Question 318

Increased and uncontrolled secretion of ADH that causes volume expansion & hyponatremia:

Answer 318

Syndrome of Inappropriate ADH (SIADH)

Question 319

In the case of a patient with SIADH what would the increased secretion of ADH cause: (2)

Answer 319

1. Volume expansion 2. Hyponatremia

Question 320

Relative to a dentist, what can cause excessive ADH release?

Answer 320

Surgery, pain, stress

Question 321

Why do pregnant women have to pee more?

Answer 321

During pregnancy, ADH metabolism is increased so less water is reabsorbed causing her to pee more

Question 322

What hormone causes milk ejection from the breast in lactation?

Answer 322

Oxytocin

Question 323

What hormone stimulates the contraction of the uterus towards the end of gestation:

Answer 323

Oxytocin

Question 324

Where is oxytocin released from?

Answer 324

Posterior pituitary

Question 325

Describe the feedback of oxytocin release:

Answer 325

Positive feedback

Question 326

Describe the relationship between Oxytocin & Prolactin:

Answer 326

Permissive

Question 327

Where is prolactin released from?

Answer 327

Anterior pituitary

Question 328

What does prolactin cause?

Answer 328

Milk production in breasts

Question 329

What causes milk secretion in the breast (mechanism)

Answer 329

Myoepithelial cell contraction

Question 330

What causes uterine contraction (mechanism)

Answer 330

Stretch of cervix at the end of pregnancy

Question 331

Objective evidence of a disease that can be seen or measured:

Answer 331

Sign

Question 332

Enlarged hands, polyuria & tachycardia are all examples of:

Answer 332

A sign

Question 333

Cannot be measured (they are subjective) but are reported by person:

Answer 333

A symptom

Question 334

Headache & numbness are both examples of:

Answer 334

A symptom

Question 335

Plasma Membrane Hormone receptors: List the four plasma membrane hormone receptors:

Answer 335

1. G-protein coupled 2. Tyrosine-Kinase 3. Serine Kinase 4. Cytokine

Question 336

Plasma Membrane Hormone receptors: What are our two types of GPCRs?

Answer 336

Gs & Gq

Question 337

Plasma Membrane Hormone receptors: Elaborate on the types of Gs coupled receptors: (6) What second messenger do they produce?

Answer 337

1. Beta-Adrenergic 2. Calcitonin 3. ACTH 4. Glucagon 5. TSH 6. Vasopressin They produce the second messenger cAMP

Question 338

Plasma Membrane Hormone receptors: Elaborate on the types of Gq coupled receptors: (3) What second messenger do they produce?

Answer 338

1. Alpha-adrenergic 2. Angiotensin-II 3. TRH They produced the second messengers IP3, DAG, Ca2+

Question 339

What type of plasma membrane hormone receptor would insulin and IGF-1 bind to?

Answer 339

Tyrosine-kinase

Question 340

What type of plasma membrane hormone receptor would growth factor bind to?

Answer 340

Tyrosine-kinase

Question 341

After cytokine binds to its plasma membrane hormone receptor (leptin) what second messenger does it activate?

Answer 341

JAK/STAT

Question 342

Why would some receptors such as the receptors for insulin and thyroid hormone be more widely distributed?

Answer 342

Because the effects of these hormones is something that we want a lot of cells to respond to

Question 343

About 93% of the active hormones secreted by the thyroid gland is:

Answer 343

T4

Question 344

About 7% of the active hormone secreted by the thyroid gland is:

Answer 344

T3

Question 345

T4= T3=

Answer 345

Thyroxine Triiodothyronine

Question 346

What thyroid hormone is more potent?

Answer 346

T3

Question 347

Thyroid hormone impact _____ & _____ and also have a _____ action on ______

Answer 347

Metabolism & growth/development Permissive Catecholamines

Question 348

What thyroid cells are involved in making thyroid hormone?

Answer 348

T thyrocyte cells

Question 349

What is stored in the colloid of a follicle?

Answer 349

Thyroglobulin

Question 350

Parafollicular cells secrete:

Answer 350

Calcitonin

Question 351

What is the action of calcitonin?

Answer 351

Tone down plasma calcium (decrease)

Question 352

In the middle of the thyroid follicle=

Answer 352

Colloid

Question 353

Where is thyroid hormone made & stored until it is time to be released?

Answer 353

Colloid

Question 354

What is required for thyroid hormone synthesis?

Answer 354

Iodine (I2)

Question 355

Thyroid hormone requires iodine (I2) because this is needed for:

Answer 355

Thyroid follicular cells to actively transport Iodide (I-) obtained from the diet

Question 356

Iodine synthesis steps: 1. Thyroid hormone synthesis requires _____ 2. ____ comes from the diet 3. Thyroid cells have a transporter called: 4. The follicular cells will: 5. The iodide gets into the cell and a second transporter called ___ removes ___ and brings ____ into the colloid of the follicular cell 6. Once inside the colloid Iodide gets concentrated into ______

Answer 356

1. Iodine (I2) 2. Iodide (I-) 3. NA+/I- symporter (NIS) 4. Concentrate the iodide 5. Pendrin; chloride; iodide (I-) 6. Iodine

Question 357

The Na+/I- transporter is a ____

Answer 357

Symporter

Question 358

The Na+/I- symporter is a _____ transporter

Answer 358

Secondary active

Question 359

Iodide must exit the _____ across the ____ to accesse the _____ where the initial steps of thyroid hormones synthesis occur:

Answer 359

thyrocyte apical membrane colloid

Question 360

What enzyme works in the iodination & coupling process:

Answer 360

Peroxidase

Question 361

What is a general term we give for anion exchangers?

Answer 361

Pendrin

Question 362

Pendrin is a ______ that exchanges ____ for ____ bringing ____ in and ____ out in the process of thyroid hormone synthesis

Answer 362

Anion exchanger Cl-/I- I- Cl-

Question 363

Pendrin is ALWAYS moving:

Answer 363

Two negatively charged substances in opposite directions

Question 364

T3 & T4 are produced in the colloid & complexed with:

Answer 364

Thyroglobulin (TG)

Question 365

The enzyme involved in all of the production steps in the formation of thyroid hormone: (Tyrosine, Monoiodotyrosine, Diiodotyrosine, T3, RT3, T4)

Answer 365

Peroxidase

Question 366

Thyroglobulin is made of:

Answer 366

A bunch of tyrosine amino acids

Question 367

Which works first in making T3 & T4 (pendrin or peroxidase???)

Answer 367

Pendrin then peroxidase

Question 368

T3 & T4 secretion into the blood: 1. ____ is internalized by endocytosis 2. The vesicles fuse with ____ in the cell 3. ____ cleaves T3 & T4 from ____ 4. T3 & T4 diffuse out of the cell & into the ___

Answer 368

1. Colloid 2. Lysosomes 3. Protease; thyroglobulin 4. Capillaries

Question 369

Colloid is a ____ of thyroid hormones

Answer 369

Reservoir

Question 370

Majority if not all of T3 & T4 bind with ____ for transport:

Answer 370

Plasma proteins

Question 371

What are the plasma proteins that T3 & T4 bind to?

Answer 371

Thyroxine-binding globulin (TBG) Transthyretin (TTR) Albumin

Question 372

What causes the long half-life of T4?

Answer 372

The strength of its binding to the transport protein

Question 373

Because T3 doesn't bind as tightly to the transport protein its half life is:

Answer 373

2-3 days

Question 374

For T3 & T4 to be secreted into the blood: Colloid is taken into the follicular cell via:

Answer 374

Pinocytosis

Question 375

For T3 & T4 to be secreted into the blood: T3 & T4 undergo ____ to be secreted into the blood

Answer 375

Simple diffusion

Question 376

Target cells make active T3 by using enzymes called ____ that remove an Iodine from T4

Answer 376

Deiodinases/Iodinases

Question 377

Individual target cells can alter their exposure to T3 by regulating:

Answer 377

Their tissue Deiodinase synthesis

Question 378

What are the three different Deiodinases?

Answer 378

D1, D2, D3

Question 379

All three of the deiodinases contain a rare amino acid called:

Answer 379

Selenocysteine

Question 380

In selenocysteine there is a ___ molecule in the place of _____ which is essential for their enzymatic activity

Answer 380

Selenium in the place of sulfur

Question 381

What are various conditions that inhibit deiodinase activity?

Answer 381

1. Selenium deficiency 2. Burns 3. Trauma 4. Advanced cancer 5. Cirrhosis 6. Chronic kidneys disease 7. MI 8. Febrile states 9. Fasting 10. Stress

Question 382

If someone has a condition that inhibits deiodinase activity they could show signs of: Why?

Answer 382

Hypothyroidism Because they are not able to convert T4 to T3

Question 383

T3 actions occur ____ compared to T4

Answer 383

Sooner

Question 384

When does the maximum activity of T3 hormone occur?

Answer 384

Around 2-3 days

Question 385

Compare the activity of T4 to T3:

Answer 385

T4 has a slower onset but a longer duration of action (can last until about 40 days)

Question 386

A variety of genes have the thyroid hormone response element which can lead to:

Answer 386

Gene transcription & synthesis of new proteins

Question 387

The synthesis of new proteins due to the action of T3 & T4 can lead to what five main responses?

Answer 387

1. Metabolism 2. Cardiovascular response 3. CNS development 4. Growth 5. Many other system responses

Question 388

A big effect of the thyroid hormone is on metabolism, what effects can be seen due to T3 & T4 synthesizing new proteins that effect metabolism: (9)

Answer 388

1. Increased BMR 2. Increased glucose absorption 3. Increased gluconeogenesis 4. Increased glycogenolysis 5. Increased lipolysis 6. Increased protein synthesis 7. Increased O2 consumption 8. Increased mitochondria 9. Increased Na+/K+ ATPase activity

Question 389

Background amount of oxygen utilized by cells; a basic indicator of metabolism

Answer 389

BMR

Question 390

A big effect of the thyroid hormone is on the cardiovascular system, what are some effects relating to this?

Answer 390

1. Increased cardiac output 2. Increased tissue blood flow 3. Increased heart rate 4. Increased heart strength 5. Increased respiration

Question 391

The cardiovascular effects of thyroid hormone are caused by an increase in ____ which is a ____ effect

Answer 391

Beta-receptors; permissive effect

Question 392

The negative feedback of the thyroid hormone is mainly at the level of ____ but can also occur _____

Answer 392

Anterior pituitary Hypothalamus

Question 393

It is T4 that is the circulating form of thyroid hormone that is able to caused the feedback inhibition, but it gets converted into T3 in the _____ & ___ so its actually the T3 that inhibits the secretion of ____ & ____

Answer 393

Anterior pituitary & hypothalamus TSH & TRH

Question 394

What actually causes the feedback inhibition of thyroid hormone:

Answer 394

The anterior pituitary and hypothalamus express deiodinase so when T4 levels in the tissues increases they readily convert it (via deiodinase) to T3 which actually causes the inhibition

Question 395

Describe the secretion of TSH:

Answer 395

Pulsatile with increases in evening hours & peak around midnight

Question 396

Describe the secretion of thyroid hormone:

Answer 396

Thyroid hormone secretion mirrors TSH (pulsatile with increase in evening hours & peak around midnight) but also tonically secreted (small amounts)

Question 397

Thyroid hormone stimulates _____ by most metabolically active tissues:

Answer 397

Oxygen consumption

Question 398

How does thyroid hormone effect the BMR?

Answer 398

Increases it

Question 399

Thyroid hormone stimulates ____ metabolism:

Answer 399

Carbohydrate

Question 400

Thyroid hormone stimulate carbohydrate metabolism by:

Answer 400

1. Uptake of glucose by cells 2. Enhances glycolysis & gluconeogenesis 3. Increases CHO absorption from GI tract

Question 401

Describe the effects of thyroid hormone on metabolism relating to proteins:

Answer 401

Stimulate proteins catabolism & synthesis (but mostly catabolism)

Question 402

Describe the effects of thyroid hormone relating to fat:

Answer 402

Stimulates fat metabolism

Question 403

Thyroid hormone stimulates fat metabolism by:

Answer 403

Increasing lipid mobilization & oxidation of fatty acids

Question 404

Thyroid hormone is required to convert _____ to_____, which is why hypothyroid patients may exhibit yellow skin

Answer 404

Beta carotene to vitamin A

Question 405

Vitamin is important in:

Answer 405

Wound healing

Question 406

Thyroid hormone is responsible for decreasing circulating ____ levels. A person with hyperthyroidism may have ______ due to this

Answer 406

Cholesterol Hyperlipidemia

Question 407

With no thyroid hormone at all, what would the BMR look like?

Answer 407

BMR levels would be around 45-50% of normal rate

Question 408

Thyroid hormone is needed for _____ regarding the nervous system:

Answer 408

Needed for normal development

Question 409

Thyroid hormone impacts ____, so someone with hypothyroidism may have have prolonged _____

Answer 409

Reflex time Prolonged reflex time

Question 410

In someone with hyperthyroidism, due to the increased reactivity of neuronal synapses they may experience:

Answer 410

Muscle tremors

Question 411

If someone feels tired but has difficulty sleeping, and anxiety, worry & paranoia they may have: (relating to thyroid hormone effect on NS)

Answer 411

Hyperthyroidism

Question 412

Hyperthyroidism effects on cardiovascular system include:

Answer 412

1. increased expression of beta-adrenergic receptors 2. increased blood flow, HR and heart contractility

Question 413

Describe the permissive effect of thyroid hormone on the cardiovascular system. What might this cause?

Answer 413

Thyroid hormone increases expression of beta-adrenergic receptors and this would lead to an increased SNS response

Question 414

Thyroid hormone effects on the endocrine system: Increased ___ consumption that results in increased secretion of ____ needed to maintain ____ levels

Answer 414

Glucose Insulin Blood glucose

Question 415

Thyroid hormone effects on the endocrine system: Thyroid hormone causes activation of bone formation so this causes a need for increased:

Answer 415

PTH secretion

Question 416

Thyroid hormone effects on the endocrine system: Thyroid hormone causes increased inactivation of ___ which leads to more ____ release by the _____

Answer 416

Glucocorticoids; ACTH; anterior pituitary

Question 417

Thyroid hormone effects on the GI system: Thyroid hormone causes in increase _____ & ____ intake

Answer 417

Appetite Food

Question 418

Thyroid hormone effects on the GI system: Thyroid hormone causes increased rate of ____ & _____ of GI tract Individuals with hyperthyroidism may have ____ due to this Individuals with hypothyroidism may have ____ to this

Answer 418

Secretion & motility of GI tract Diarrhea Constipation

Question 419

Enlarged thyroid gland=

Answer 419

Goiter

Question 420

Goiter is an enlarged thyroid gland that:

Answer 420

DOES NOT indicate functional status

Question 421

Goiter can be seen in:

Answer 421

Hypothyroidism, Hyperthyroidism & Euthyroidism

Question 422

Normal levels of thyroid hormones

Answer 422

Euthyrodism

Question 423

Goiter can be caused by:

Answer 423

Excessive amounts of TSH secretion

Question 424

High TSH stimulate thyroid to secrete large amounts of _____ into ____ resulting in gland enlargement /goiter

Answer 424

Thyroglobin colloid Follicles

Question 425

The most common of hyperthyroidism

Answer 425

Graves disease

Question 426

Although graves disease is the most common form of hyperthyroidism, hyperthyroidism can also occur due to:

Answer 426

Thyroid adenoma

Question 427

Graves disease is an ____ disease Explain how:

Answer 427

Autoimmune Antibodies to the TSH receptor called thyroid stimulating immunoglobulins are produced and they stimulate the thyroid gland directly to produce too much thyroid hormone (T3 & T4)

Question 428

Describe the category of disorder that Graves Disease is, and how the hypothalamus & anterior pituitary are effected:

Answer 428

Primary Endocrine disorder- because issue is at level of thyroid gland Strong negative feedback causes TSH & TRH levels to be reduced

Question 429

Graves disease is more common in:

Answer 429

The girlies

Question 430

List the signs & symptoms of Graves Disease: (10)

Answer 430

1. Sweating/heat intolerance 2. Increased metabolism 3. Increased appetite 4. Weight lose 5. Fine hair/proteins synthesis 6. Increased NS response (Emo instability, insomnia, nervy, restlessness) 7. Fine tremor 8. Goiter 9. Exophthalmus (bug eyes) 10. Pretibial myxedema

Question 431

Treatment of thyroid disease:

Answer 431

Radioactive iodine to ablate thyroid gland followed by L-thyroxine (T4) to prevent hypothyroidism Antithyroid drugs Beta-blockers to block permissive effect of thyroid hormone (Surgery rarely indicated)

Question 432

Oral symptoms of hyperthyroidism may include:

Answer 432

- Burning mouth syndrome - Gum disease - Excessove salivation - Weakening of mandible - Increased caries risk

Question 433

Elevated thyroid hormone with stressful event or serious illness causing fever, tachycardia, elevated BP, nausea, vomitting, diarrhea, breathing problems:

Answer 433

Thyroid storm (thyrotoxicosis)

Question 434

What can bring on a thyroid storm/thyrotoxicosis?

Answer 434

Trauma, surgery, infection, DKA or MI

Question 435

Overall a thyroid storm can be described as:

Answer 435

Exaggerated sympathetic response

Question 436

In patients with hyperthyroidism or those that exhibit signs/symptoms of it what is extremely important?

Answer 436

Administration of epinephrine is CONTRAINDICATED & elective dental care should be deferred

Question 437

Autoimmune reaction against the thy gland that destroys it rather than stimulating it:

Answer 437

Hashimoto's thyroiditis

Question 438

What is the most common cause of hypothyroidisim:

Answer 438

Hashimoto's thyroiditis

Question 439

Prior to diagnosis of Hashimoto's thyroiditis, most patient first exhibit:

Answer 439

Autoimmune thyroiditis

Question 440

In Hashimoto's thyroiditis, inflammation leads to ____ of the thyroid resulting in ____

Answer 440

Fibrosis Decreased secretion of thyroid hormone

Question 441

What is the target of the antibodies in Hashimoto's thyroiditis?

Answer 441

Peroxidase

Question 442

What class of disorder is Hashimoto's characterized by?

Answer 442

Primary endocrine disorder

Question 443

Another form of hypothyroidism (not Hashimoto's) can be due to:

Answer 443

Low iodine

Question 444

Hypothyroidism due to low iodine is classified as:

Answer 444

Primary endocrine disorder

Question 445

In the absence of iodine describe the levels of T3, T4, TSH, & TRH:

Answer 445

Low T3 & T4 Elevated TRH & TSH

Question 446

In hypothyroid state, goiter is due to _____ while no goiter is due to _____

Answer 446

Iodine deficiency TSH deficiency

Question 447

Hypothyroidism due to iodine deficiency= _____ = _____ deficiency Hypothyroidism due to TSH deficiency= _____ = _____ deficiency

Answer 447

Goiter, Primary No goiter, Secondary

Question 448

Symptoms of hypothyroidism may include:

Answer 448

1. Weight gain 2. Constipation 3. Cold/diminished perspiration 4. Lethargy 5. Impaired memory 6. Lack of NS stimulation 7. Coarse, dry brittle hair 8. Hairloss 9. Loss of lateral eyebrows 10. Slow pulse (bc decreased number of beta receptors) 11. Enlarged heart 12. Facial edema 13. Periperhal edema (hands & feet)

Question 449

Unique symptom seen in sever cases of hypothyroidism:

Answer 449

Myxedema

Question 450

In hyperthyroidism patients where does the myxedema occur? In hypothyroidism patients where does the myxedema occur?

Answer 450

Hyper= Pretibial myxedema Hypo= face

Question 451

Myxedema occurs due to increased quantities of ____ & ____ bound with protein plus water that accumulates in the skin

Answer 451

Hyaluronic acid & Chondroitin sulfate

Question 452

Dull expressionless facies with puffiness of eyelids, swollen, cool waxy dry, coarse & pale skin, with lots of creases describes a patient effected with ______ and the treatment would be _____

Answer 452

Myxedema L-thyroxine (T4)

Question 453

Required for postnatal brain maturation

Answer 453

Thyroid hormones

Question 454

Results from congenital absence of thyroid gland:

Answer 454

Congenital cretinism

Question 455

Results from iodine deficient diet; most common cause worldwide:

Answer 455

Endemic cretinism

Question 456

Cretinism can cause ____ of neonates. Skeletal growth is more inhibited than soft tissue growth resulting in:

Answer 456

Physical & mental retardation Obese, stocky & short with large protruding tongue

Question 457

Cretinism can cause a lack of development of the:

Answer 457

Nervous system

Question 458

List the hypothyroidism oral manifestations: (6)

Answer 458

1. Macroglossia 2. Dysgeusia 3. Delayed tooth eruption 4. Poor wound healing 5. Increased periodontal disease 6. Salivary gland enlargement

Question 459

The poor wound healing and increased risk of infection in a hypothyroidism patient is due to:

Answer 459

Decreased activity of fibroblasts

Question 460

Patients with hypothyroidism are sensitive to:

Answer 460

Central nervous system depressants or barbituates

Question 461

85% of the body's phosphate is stored in the ___ 14-15% of the body's phosphate is stored in the ___ Less than 1% of the body's phosphate is stored in the ___

Answer 461

Bones Cells ECF

Question 462

Only 0.1% of the bodies calcium is found in the _____ 1% of the bodies calcium is found in the _____ The rest of the bodies calcium is stored in the ____

Answer 462

ECF Cells & organelle Bones

Question 463

When levels of calcium are too low:

Answer 463

Neuronal hyper-excitability (tetany due to extra NA+ influx)

Question 464

When levels of calcium are too high:

Answer 464

Neuronal depression (Blocks Na+ influx)

Question 465

Carpal spasms can be due to:

Answer 465

HYPOcalcemia

Question 466

Control points for calcium & phosphate include:

Answer 466

1. Absorption- via intestines 2. Excretion- via urine (calcium & phosphate) & feces (calcium only) 3. Temporary storage- via bone (hydroxyapatite)

Question 467

Ca10(PO4)6(OH)2

Answer 467

Hydroxyapatite

Question 468

What are the hormones that regulate plasma calcium?

Answer 468

PTH, Calcitriol, Calcitonin

Question 469

How does PTH regulate plasma calcium & phosphate?

Answer 469

Increases plasma calcium Decreases plasma phosphate

Question 470

How does PTH work to raise plasma calcium & lower plasma phosphate?

Answer 470

1. Mobilizes calcium from bone 2. Enhances renal reabsorption of calcium 3. Increases intestinal absorption of calcium (indirectly)

Question 471

How does calcitriol regulate plasma calcium & phosphate?

Answer 471

Increases plasma calcium Increases plasma phosphate

Question 472

How calcitriol work to raise plasma calcium & phosphate?

Answer 472

Calcitriol is the primary hormone that enhances intestinal absorption of calcium & it also causes absorption of phosphate

Question 473

The primary hormone that enhances intestinal absorption of calcium and also causes absorption of phosphate

Answer 473

Calcitriol

Question 474

What are the other names for calcitriol?

Answer 474

1,25-dihydroxyxholecaliferol Vitamin D3

Question 475

Calcitriol acts on the intestines ____ to enhance absorption of calcium & also phosphate, while PTH acts on the intestines _____ to enhance absorption of calcium

Answer 475

Directly Indirectly

Question 476

Calcitonin comes from:

Answer 476

Parafollicular cells of the thyroid gland

Question 477

How does calcitonin regulate plasma calcium & phosphate?

Answer 477

Decreases plasma calcium Decreases plasma phosphate

Question 478

How does calcitonin work to decrease plasma calcium & phosphate?

Answer 478

By simulating bone formation

Question 479

What hormones stimulate bone formation?

Answer 479

1. Calcitonin 2. Insulin 3. Growth hormone 4. IGF-1 5. Estrogen 6. Testosterone

Question 480

______ & _____ stimulate bone matrix resorption which functions to increase plasma calcium

Answer 480

Calcitriol PTH

Question 481

Calcitriol & PTH stimulate bone matrix ___ How does this effect plasma calcium?

Answer 481

Resorption Increases plasma calcium

Question 482

Bone resorption: 1. Osteoblasts release _____ 2. _____ binds to the ____ on preosteoclasts and this leads to the activation of ______

Answer 482

1. RANKL 2. RANKL; Rank receptors; osteclasts

Question 483

What is the goal of bone resorption?

Answer 483

To increase plasma calcium levels

Question 484

What type of cell is activated during bone resorption? What activates this type of cell?

Answer 484

Osteoclasts RANKL binding to its receptor on preosteoclasts

Question 485

Factors that stimulate bone matrix resorption: (4)

Answer 485

1. PTH 2. Excessive levels of calcitriol 3. Prolactin 4. Corticosteroids

Question 486

What is the goal of bone deposition?

Answer 486

To form bone- put calcium into bone from the blood

Question 487

_____ stimulates bone matrix deposition and inhbits osteoclasts

Answer 487

Calcitonin

Question 488

Calcitonin stimulates bone matrix deposition and inhibits osteoclasts which ultimately does what to plasma calcium?

Answer 488

Decreases

Question 489

If calcium levels in the blood are sufficient we dont need to:

Answer 489

Breakdown bone

Question 490

Anabolic or anti-resorptive factors (for bone)=

Answer 490

1. Estrogens 2. Calcitonin 3. Testostserone 4. Calcium 5. BMP

Question 491

In order to avoid RANKL further activating osteoclasts ____ will bind to it so it cannot bind to its receptor

Answer 491

OPG

Question 492

OPG binding to RANKL ultimately leads to:

Answer 492

Apoptotic osteoclasts

Question 493

Osteoclast that do NOT function to break down bone:

Answer 493

Apoptotic osteoclasts

Question 494

Affects almost 10 million individuals in the US, though only a small proportion are diagnosed & treated. Occurs when there is an imbalance in bone resorption & bone formation

Answer 494

Osteoporosis

Question 495

Risk factors for osteoporosis: (superficial)

Answer 495

1. Vitamin D deficiency 2. Inadequate calcium intake 3. Glucocorticoid medications 4. Reduced physical activity 5. Estrogen deficiency 6. Cigarette smoking 7. Alcohol

Question 496

Describe why vitamin D deficiency can lead to osteoporosis:

Answer 496

Because this can lead to really high PTH levels (secondary hyperparathyroidism) which leads to excessive bone breakdown

Question 497

Describe why inadequate calcium intake can lead to osteoporosis:

Answer 497

Because this can lead to really high levels of PTH (secondary hyperparathyroidism) which leads to excessive bone breakdown

Question 498

Describe why glucocorticoid medications can lead to osteoporosis:

Answer 498

They suppress the immune response leading to the risk of weak & brittle bones

Question 499

Describe why post-menopausal estrogen deficiency can lead to osteoporosis:

Answer 499

Estrogen stimulates the process of bone matrix deposition so the lack of estrogen would throw the balance off

Question 500

Treatments for osteoporosis include:

Answer 500

1. Excerise 2. PT 3. Estrogen replacement 4. Calcium 5. Vitamin D 6. Bisphosphonates

Question 501

When giving vitamin D to an osteoporosis patient you must make sure ____ levels do not get too high

Answer 501

PTH

Question 502

Four pea-sized glands on the posterior surface of the thyroid glands:

Answer 502

Parathyroid glands

Question 503

PTH is secreted by:

Answer 503

Chief cells

Question 504

What are the effect of PTH & how?

Answer 504

Increased plasma calcium by: indirectly increasing intestinal absorption, decreasing renal excretion & increasing bone resorption

Question 505

How does PTH decrease plasma phsophate?

Answer 505

By increasing renal excretion

Question 506

Describe the renal effects of calcium & phosphate by PTH:

Answer 506

Increases renal excretion for phosphate Decreases renal excretion for calcium

Question 507

Why is PTH's effect on the intestinal absorption of calcium considered indirect?

Answer 507

Because it causes more synthesis of vitamin D which in turn causes increased intestinal absorption of calcium

Question 508

When PTF is secreted due to decreased ECF calcium this leads to:

Answer 508

Hypertrophy of Parathyroid gland

Question 509

How would a decrease in ECF calcium concentration effect the rate of PTH secretion?

Answer 509

Increase

Question 510

What conditions would lead to hypertrophy of the parathyroid gland?

Answer 510

Chronic cases- pregnancy, rickets, lactation

Question 511

Chronically if you hypertrophy the parathyroid gland, it becomes:

Answer 511

Even better at secreting PTH

Question 512

An increased ECF concentration of calcium leads to ___ of the parathyroid gland

Answer 512

Decreased activity

Question 513

If the parathyroid gland has a decrease in activity, it will have a ____ in size

Answer 513

Decrease

Question 514

What conditions can cause a decrease in activity & size of the parathyroid gland?

Answer 514

1. Increased vitamin D intake at excessive levels 2. Excess quantities of calcium in diet 3. Bone resorption caused by factors other than PTH

Question 515

Describe the effect on plasma calcium: Bone resorption

Answer 515

Increases

Question 516

Describe the effect on plasma calcium: Reabsorption of calcium by renal tubules:

Answer 516

Increases plasma calcium

Question 517

Describe the effect on plasma calcium: Conversion of 25-hydroxycholecalciferol to 1, 25-dihydroxycholecalciferol:

Answer 517

Increases plasma calcium

Question 518

Describe the effect on plasma phosphate: Decreased reabsorption by renal tubules:

Answer 518

Decreases plasma phosphate

Question 519

Where do we get Cholecalciferol (vitamin D3) from?

Answer 519

Skin from sun

Question 520

In the process of calcitriol synthesis: Cholecalciferol is converted to ____ by what organ?

Answer 520

25-Hydroxycholecalcierfol Liver

Question 521

In the process of calcitriol synthesis: 25-Hydroxycalciferol is coverted to _____ by what organ?

Answer 521

1,25-dihydroxycholecalciferol (calcitriol) Kidney

Question 522

In the process of calcitriol synthesis: What tells the kidney to do the conversion of 25-dihydroxycholecalciferol to the active form?

Answer 522

Parathyroid hormone

Question 523

Where is the main effect of Calcitriol?

Answer 523

Intestine- absorption of Ca & Phosphate from diet

Question 524

Where can calciferol act although not the main effect?

Answer 524

Kidneys- reduced excretion of Ca & Phosphate Bones- bone deposition (indirectly)

Question 525

Vitamin D3 can be stored in the liver for:

Answer 525

Several months

Question 526

Describe the regulation of calcitriol levels:

Answer 526

Tightly regulated- if someone takes excess vitamin D3 the liver will still only convert so much into the 25-hydroxycholecalciferol

Question 527

Someone with compromised liver and kidney function may exhibit:

Answer 527

Vitamin D deficiency

Question 528

Peptide hormone secreted by parafollicular cells:

Answer 528

Calcitonin

Question 529

Parafollicilar cells reside in the ____ and may also be called ____

Answer 529

Thyroid gland C cells

Question 530

Calcitonin is released in response to:

Answer 530

Elevated free plasma calcium

Question 531

Calcitonin decreases the levels of plasma calcium by decreasing the activity of ___ thus decreasing ____

Answer 531

Osteoclasts Bone resporption

Question 532

Not a major controlled of calcium in humans:

Answer 532

Calcitonin

Question 533

What two systems does calcitonin act on?

Answer 533

Bone & kidneys

Question 534

Excess PTH secretion due to a parathyroid gland tumor would be classified as:

Answer 534

Primary hyperparathyroidism

Question 535

Primary hyperparathyroidism can lead to extreme ____ activity in bones causing _____, more specifically _____

Answer 535

Osteoclastic activity Cystic bone disease Osteitis fibrosa cystica

Question 536

Such excessive bone breakdown that we see scar tissue & fibrosis in bones:

Answer 536

Cystic bone disease (Osteitis fibrosa cystica) (caused by primary hyperparathyroidism)

Question 537

Primary hyperparathyroidism can cause hypercalcemia leading to: (in relation to urine)

Answer 537

Polyuria & Calciuria

Question 538

What phosphate levels and why in patients with primary hyperparathyroidsim?

Answer 538

Low phosphate due to increased renal excretion

Question 539

Describe why someone with primary hyperparathyroidism would exhibit muscle weakness and easy fatigability:

Answer 539

Too much calcium- blocks sodium influx leading to neuronal depression (impedes signaling by neurons)

Question 540

Primary hyperparathyroidism signs and symptoms include:

Answer 540

Stones, bones, abdominal groans & psychic moans

Question 541

Describe the stone component of primary hyperparathyroidism:

Answer 541

1. Renal stones 2. Nephrocalcinosis 3. Polyuria 4. Polydipsia 5. Uremia

Question 542

Describe the bones component of primary hyperparathyroidism:

Answer 542

1. Cystic bone disease 2. Osteomalacia/rickets 3. Arthritis

Question 543

Describe the abdominal groans component of primary hyperparathyroidism:

Answer 543

1. Constipation 2. Indigestion 3. Nausea 4. Vomiting 5. Peptic ulcers 6. Pancreatitis

Question 544

Describe the psychic moans component of primary hyperparathyroidism:

Answer 544

1. Lethargy/fatigue 2. Depression 3. Memory loss 4. Paranoia 5. Personality change 6. Confusion, stupor, coma

Question 545

Other symptoms, not included in stones, bones, moans and groans from primary parahyperthyroidism include:

Answer 545

1. Proximal muscle weakness 2. Keratitis 3. Conjunctivitis 4. Hypertension 5. Itching

Question 546

High PTH levels that occur as compensation for hypocalcemia & NOT due to an issue with the parathyroid gland:

Answer 546

Secondary Hyperparathyroidism

Question 547

What are the two causes of hypocalcemia that lead to secondary hyperparathyroidism?

Answer 547

1. Vitamin D deficiency 2. Chronic renal disease- cannot synthesize Vit D3

Question 548

What disease are you at risk for with high levels of PTH?

Answer 548

Osteoporosis

Question 549

Disease that would results from accidental surgical parathyroid gland removal (not common):

Answer 549

Primary Hypoparathyroidism

Question 550

What increases membrane Na+ permeability leading to neuromuscular excitability & muscle spasma

Answer 550

Hypocalcemia

Question 551

What is the condition for the wonky ass hand:

Answer 551

Carpal spasm

Question 552

How many adrenal glands do we have? Where are they located?

Answer 552

Two adrenal glands One ontop of each kidney

Question 553

Describe the structure of an adrenal gland:

Answer 553

Outer cortex + inner medulla

Question 554

What portion of the adrenal gland is essential for life?

Answer 554

Adrenal cortex

Question 555

The adrenal cortex secretes:

Answer 555

1. Corticosteroids 2. Mineralcorticoids 3. Sex hormones

Question 556

Is the adrenal medulla essential for life?

Answer 556

No

Question 557

The adrenal _____ is a true endocrine organ

Answer 557

Cortex

Question 558

Although it is not essential for life, the adrenal medulla is important in:

Answer 558

Secreting epinephrine & norepinephrine in response to sympathetic nervous system stimulation

Question 559

The adrenal medulla hormones are NOT essential for life but help an individual deal with:

Answer 559

Emergencies

Question 560

The adrenal cortex secretes several hormones that are made from:

Answer 560

Cholesterol

Question 561

What are the three layers of the adrenal cortex?

Answer 561

Zona Glomerulosa Zona Fasciculata Zona Reticularis

Question 562

The largest zone of the of the adrenal cortex:

Answer 562

Zona Fasciculata

Question 563

The Zona Glomerulosa secretes _____ and is regulated by ______

Answer 563

Mineralcorticoids RAAS

Question 564

RAAS stands for:

Answer 564

Renin-angiotensin-aldosterone system

Question 565

The Zona Fasciculata secretes ____ and is regulated by _____

Answer 565

Glucocorticoids HPA (CRH, ACTH)

Question 566

HPA stands for:

Answer 566

Hypothalamic-pituitary-adrenal axis

Question 567

The Zona Reticularis secretes ____ and is regulated by _____

Answer 567

Androgens HPA

Question 568

The adrenal medulla is related to the _______ & secretes ____

Answer 568

Sympathetic nervous system; catecholamines

Question 569

What type of cells secrete catecholamines?

Answer 569

Chromaffin cells

Question 570

The do the chromaffin cells of the adrenal medulla secrete Epi & NE?

Answer 570

Directly into the blood

Question 571

What are the three tissues involved in the HPA?

Answer 571

Hypothalamus, pituitary, adrenal gland

Question 572

Why does the zona glomerulosa secrete so much aldosterone?

Answer 572

Bc enzymes involved in the formation of aldosterone from cholesterol are highly expressed in the zona glomerulosa

Question 573

What enzyme is responsible for the conversion of cortisol to cortisone?

Answer 573

11HSD Beta 2

Question 574

What enzyme is responsible for the conversion of cortisone to cortisol?

Answer 574

11HSD Beta 1

Question 575

The reactions that occur for the synthesis of steroid hormones in the adrenal cortex take place in the ______ or the _____

Answer 575

Mitochondria Endoplasmic reticulum

Question 576

Describe the activity of cortisone at cortisol receptors:

Answer 576

Reduced activity

Question 577

Can be used to make testosterone & androgens:

Answer 577

Androstenedione

Question 578

Aldosterone is classified as a:

Answer 578

Mineralcorticoid

Question 579

Aldosterone functions in the kidneys to:

Answer 579

1. Increase renal reabsorption of sodium 2. Increase renal secretion of Potassium

Question 580

Aldosterone working to increase renal reabsorption of Na+ and increasing renal secretion of K+ results in:

Answer 580

Increase in ECF volume and mean arterial pressure

Question 581

What stimulates aldosterone secretion?

Answer 581

1. Angiotensin II 2. Increased levels of K+ 3. Decreased levels of Na+

Question 582

Aldosterone has effects on:

Answer 582

1. Kidney 2. Sweat glands 3. Salivary glands

Question 583

What portion of the adrenal cortex is responsible for aldosterone secretion?

Answer 583

Zona Glomerulosa

Question 584

What are the main functions of angiotensin-II

Answer 584

1. Vasoconstriction 2. Release of aldosterone

Question 585

What function of angiotensin-II is interrelated to the sympathetic nervous system:

Answer 585

Release of aldosterone

Question 586

Since aldosterone causes increased tubular reabsorption of sodium, ultimately raising blood sodium levels what happens to water?

Answer 586

Water retention occurs because where sodium goes water follows

Question 587

The effects of aldosterone on sweat glands is important to:

Answer 587

Conserve body salt in hot environments

Question 588

The effects of aldosterone on the salivary gland is important in:

Answer 588

Conservation of sodium during high rates of salivary secretion

Question 589

In addition to hyperkalemia ______ causes secretion of aldosterol

Answer 589

Angiotensin II

Question 590

An enzyme release by the cells in the kidneys in response to a variety of stimuli (Example: SNS)

Answer 590

Renin

Question 591

Angiotensin converting enzyme (ACE) is produced by the:

Answer 591

Endothelium

Question 592

List the steps of the RAAS:

Answer 592

Angiotensinogen gets converted to Angiotnesin I by the enzyme Renin Angiotensin I gets converted to Angiotensin II by the enzyme ACE

Question 593

Angiotensin II ultimately causes the secretion of _____ but also does ____, ____ & _____

Answer 593

Ultimately aldosterone secretion but also ADH secretion, thirst stimulation & vasoconstriction

Question 594

What do vasoconstriction, aldosterone secretion, ADH secretion & thirst stimulation all have in common?

Answer 594

These all work to raise BP

Question 595

In RAAS, the nonactive precursor made by the liver and found in the plasma:

Answer 595

Angiotensinogen

Question 596

Where is large amounts of ACE found?

Answer 596

In the lungs

Question 597

Alot of _____ medications target RAAS:

Answer 597

HTN

Question 598

How do ACE inhibitors work?

Answer 598

If you inhibit ACE you will make less angiotensin II= lower BP

Question 599

Primary hyperaldosteronism may also be called:

Answer 599

Conn's syndrome

Question 600

In primary hyperaldosteronism where is the problem?

Answer 600

The adrenal gland

Question 601

What are the causes of primary hyperaldosteronism?

Answer 601

1. Adrenal adenoma (benign) 2. Adrenal hyperplasia 3. Adrenal carcinoma (malignant)

Question 602

Describe the levels involved in primary hyperaldosteronism (Conn's syndrome):

Answer 602

Low levels of renin

Question 603

Signs & symptoms of primary hyperaldosteronism (Conn's syndrome) include:

Answer 603

Hypertension Hypernatremia Hypokalemia Headaches Weakness Fatigue Polyuria HYPOKALEMIC ALKALOSIS LOW PLASMA RENIN

Question 604

Explain why someone with primary hyperaldosteronism would have low levels of plasma renin?

Answer 604

Due to so much aldosterone production we will have strong negative feedback

Question 605

A byproduct of cells trying to regulate the K+ levels in the case of primary hyperaldosteronism (Conn's)

Answer 605

Hypokalemic alkalosis

Question 606

In hypokalemic alkalosis the cells attempt to regulate K+ levels leads to an absence of:

Answer 606

H+ in the ECF

Question 607

Treatment options for primary hyperaldosteronism (Conn's) include:

Answer 607

Surgical removal of tumor or most of the adrenal tissue when hyperplasia is present Mineralcorticoid receptor antagonist

Question 608

Disease caused by decreased blood flow and pressure in the renal artery- in which the kidney thinks BP is low and secretes renin excessively

Answer 608

Secondary hyperaldosteronism

Question 609

Describe the levels of renin in secondary hyperaldosteronism:

Answer 609

High levels of renin

Question 610

What are causes of secondary hyperaldosteronism?

Answer 610

1. CHF 2. Renal artery stenosis

Question 611

How might CHF lead to secondary hyperaldosteronism?

Answer 611

Pumping function of heart is declined, leading to low BP, and aldosterone levels will rise to compensate

Question 612

How might renal artery stenosis lead to secondary hyperaldosteronism?

Answer 612

Renal artery pumps blood to kidney and there can be an atherosclerotic plaque in the vessels resulting in decreased blood flow to kidney. Kidney now thinks BP is low and secretes excessive renin to try to compensate for the "low BP." Extra renin leads to extra angiotensin II which leads to extra aldosterone secretion The other kidney is working just fine

Question 613

Signs & symptoms of secondary hyperaldosteronism include:

Answer 613

1. High plasma renin 2. Hypernatremia w/extracellular volume expansion 3. Edema 4. Decreased cardiac output 5. Similar clinical findings to primary hyperaldosteronism (EXCEPT RENIN LEVEL)

Question 614

Hormone that functions in the mobilization of energy stores & suppresses the immune system:

Answer 614

Cortisol

Question 615

What hormone is secreted in response to stress?

Answer 615

Cortisol

Question 616

Cortisol is categorized as a _____ and comes from the ______ of the adrenal cortex

Answer 616

Glucocorticoid Zona fasciculata

Question 617

More cells in the adrenal cortex make ____ than any other cells because of the size of the Zona Fasciculata

Answer 617

Cortisol

Question 618

What are some examples of stressors that may cause cortisol secretion?

Answer 618

Heat Cold Hypo/Hyperglycemia (Not just psychological stress)

Question 619

Cortisol says "there is a stressful situation, let me throw a bunch of nutrients in the blood" but a consequence of cortisol is that:

Answer 619

It suppresses the immune system

Question 620

When does cortisol levels spike? What hormone is opposite of this?

Answer 620

Early morning hours; Growth hormone

Question 621

Cortisol feeds back and inhibits:

Answer 621

1. ACTH secretion from anterior pituitary 2. CRH secretoin from hypothalamus

Question 622

Describe what type of feedback is seen through cortisol:

Answer 622

Long loop only

Question 623

What are the four main actions of cortisol?

Answer 623

1. Gluconeogenesis 2. Protein mobilization 3. Fat mobilization 4. Stabilizes lysosomes

Question 624

The action of cortisol leads to the suppression of immune function?

Answer 624

Stabilizing lysosomes

Question 625

Why are other hormones secreted when ACTH is secreted?

Answer 625

Because the gene for ACTH forms a larger protein (a preprohormone)

Question 626

What is the name of the preprohormone that ACTH is derived from?

Answer 626

Proopriomelanocortin (POMC)

Question 627

In addition to ACTH being synthesized from POMC what else is secreted?

Answer 627

1. Melanocyte stimulating hormone (MSH) 2. Beta-endorphin 3. Beta-lipotrophin

Question 628

A clinical sign of elevated ACTH pathologically is:

Answer 628

Increased skin pigmentation from melanocytes)

Question 629

What is a byproduct of ACTH production?

Answer 629

MSH

Question 630

Cortisol has a similar affinity for the ____ receptor as _____

Answer 630

Mineralcorticoid receptor (MR) Aldosterone

Question 631

What is found at higher circulating concentrations, aldosterone or cortisol?

Answer 631

Cortisol

Question 632

Since cortisol is able to bind to the MR receptor, why doesn't it cause a mineralcorticoid effect?

Answer 632

11B2HSD enzyme converts cortisol to cortisone in aldosterone responsive tissues making sure the aldosterone binds to the MR receptor, not cortisol

Question 633

____ does not bind to GC or MR receptors with as high of an affinity as _____

Answer 633

Cortisone; Cortisol

Question 634

A genetic deficieny of 11B2-HSD that leads to the syndrome:

Answer 634

AME (apparent mineralocorticoid excess)

Question 635

______ is a compound found in licorice that inhibits the activity of _____

Answer 635

Clycerhetininc acid 11B2-HSD

Question 636

What do we expect under normal conditions when the adolsterone binds the mineralocorticoid receptor in the epithelial cells of the kidney:

Answer 636

Increased sodium reabsorption Increased potassium secretion

Question 637

Where would we find 11B2HSD receptors? Where would we find 11B1HSD receptors?

Answer 637

Kidneys, Salivary gland & Sweat glands Skin

Question 638

High circulating cortisol levels such as in Cushing's syndrome can:

Answer 638

Overwhelm the 11HSDB2 receptor

Question 639

Both AME syndrome & high circulating cortisol levels will ultimately cause:

Answer 639

High blood pressure

Question 640

Effects of Cortisol on metabolism: Stimulation of ____ & _____ in the liver resulting in ______

Answer 640

gluconeogenesis & glycogenolysis Increases plasma glucose

Question 641

Effects of Cortisol on metabolism: ____ action resulting in decreased glucose uptake in the muscle & fat but not the brain & heart

Answer 641

Anti-insulin

Question 642

Effects of Cortisol on metabolism: Makes _____ worse by increasing ____ levels, ____ levels, & ____ formation & ____ secretion

Answer 642

Diabetes Glucose, lipid Ketone body Insulin

Question 643

Describe what two hormones are antagonists when dealing with the carbohydrate effect of cortisol on metabolism:

Answer 643

Cortisol & insulin are antagonist

Question 644

Describe what can happen with a diabetic that is scared of the dentist due to cortisol:

Answer 644

They come in, they get stressed out, their cortisol levels rise and in turn their blood sugar rises (bc cortisol stimulates gluconeogenesis & glycogenolysis)

Question 645

Effects of cortisol on metabolism: Inhibits ____ synthesis & increases ______ especially in skeletal muscle

Answer 645

Protein; proteolysis (provides a source of AA for glycoenogenesis)

Question 646

Effects of cortisol on metabolism: Cortisol excess leads to ____ weakness, pain, ___ skin and abdominal ___ due to the protein catabolic effect

Answer 646

Muscle Thin Abdominal striae

Question 647

Effects of cortisol on metabolism: Promotes ____, and shifts the energy system to utilization of ____ to ____ in times of stress

Answer 647

Lipolysis Glucose to fatty acids

Question 648

Effects of cortisol on metabolism: Causes ____ deposition in certain areas (abdomen, interscapular "buffalo hump" and a rounded "moon face"

Answer 648

Lipid

Question 649

95% of the glucocorticoid activity is due to the secretion of:

Answer 649

Cortisol

Question 650

Absence of cortisol contributes to _____ due to the loss of _____ of _____ on blood vessels

Answer 650

Circulatory failure Permissive action Catecholamines

Question 651

Lack of cortisol prevents mobilization of ______ (glucose & free fatty acids) during stress & can result in _____

Answer 651

Energy sources Fatal hypoglycemia

Question 652

Vasoconstriction of blood vessels occurs via:

Answer 652

Alpha 1 receptors

Question 653

Describe the effect cortisol has on catecholamines (Alpha1 receptor) on blood vessels:

Answer 653

Permissive effect- the presence of cortisol allows the alpha 1 receptors effect to be maximized

Question 654

Why would BP decrease when cortisol levels are low:

Answer 654

The presence of cortisol allows the alpha1 receptors response to be maximized, so without the maximum response BP would be lower

Question 655

How does cortisol effect the immune system?

Answer 655

Suppresses immune system

Question 656

What are a few ways that cortisol suppresses the immune system?

Answer 656

1. Stabilizes lysosomal membrane 2. Opposes inflammation (by decreasing WBC migration & phagocytosis) 3. Suppresses T lymphocytes

Question 657

What property of glucocorticoids allows them to be used in treatment of patients with diseases/conditions involving exaggerated inflammatory response?

Answer 657

Their anti-inflammatory action

Question 658

How can treatment with glucocorticoids cause osteoporosis?

Answer 658

Because cortisol stimulates bone resorption via an increase in RANKL expression by osteoblast

Question 659

Treatment with glucocorticoid promotes apoptosis of _____ & ____ which can further lead to osteoporosis

Answer 659

Osteoblasts & Osteocytes

Question 660

The zona reticularis is responsible for the secretion of:

Answer 660

androgens

Question 661

The zona reticularis begins secreting adrenal androgrens around age _____, peaking around age _____ & ______ with age

Answer 661

8; 20; decreasing

Question 662

Adrenal androgens secreted by the zona reticularis include:

Answer 662

DHEA/DHEAS Androstenedione Testosterone Estrogens

Question 663

Describe the effects of adrenal androgens in males versus females:

Answer 663

Adrenal androgens have only weak effects in males but contribute ~50% of active androgens in females

Question 664

Describe the effects of adrenal androgens in females:

Answer 664

Growth of pubic hair, axillary hair & libido

Question 665

A condition resulting from excess androgen production in pre-pubertal boys:

Answer 665

Precocious pseudopuberty

Question 666

Normally puberty in boys is stimulated by _____ which leads to the secretion of FSH and LH But if the adrenal gland is oversecreting androgens it can lead to:

Answer 666

Hypothalamus secreting GRH Early puberty NOT due to the hypothalamic pituitary axis

Question 667

If boys are effected by precocious pseudopuberty brought on by excessive androgen secretion from the adrenal gland this can cause:

Answer 667

Early development of secondary sexual characteristics (under age 8)

Question 668

______ deficiency can result in virilization in newborn females & pseudo-hermaphroditism

Answer 668

21-hydroxylase deficiency

Question 669

21-Hydroxylase deficiency leads to an overproductionof:

Answer 669

Androgens (DHEA, DHEAS, Androstendione)

Question 670

Androgen secreting tumors producing excess androgen result in: (in females)

Answer 670

Virilization & precocious pseudopuberty in females

Question 671

Precocius pseudopuberty:

Answer 671

Early puberty not caused by HPA secreting GRH, but instead due to adrenal androgens in excess

Question 672

21-hydroxylase is an enzyme critical for making ___ & ____ and in the absence of this enzyme there is buildup of excessive amounts of _____ & _____ precursors resulting in excessive production of ______

Answer 672

Aldosterone & cortisol Aldosterone & cortisol precursors Androgen precursors (DHEA, DHEAS, Andrestenedione)

Question 673

Androstenedione is a precursor to:

Answer 673

Testosterone 5-Dihydrotestosterone Estrogenes

Question 674

Although androstenedione is not the precursor made in the greatest amounts compared to DHEA & DHEAS, it is the precursor with the:

Answer 674

Greatest effect

Question 675

Why does the precursor androstenedione have the greatest effect (compared to DHEA & DHEAS)

Answer 675

Because it is more readily convertied peripherally to testosterone & estrogens

Question 676

In adults, hormonally active, benign adrenal adenomas usually secrete _____ or ____

Answer 676

Aldosterone or cortisol

Question 677

Virilizing tumors in women are more likely to be caused by:

Answer 677

Ovarian tumors

Question 678

Virilizing adrenal tumors are ____ and virilization is usually due to ______

Answer 678

Rare; hypersecretion of adrenal androgens

Question 679

List some signs & symptoms of virilization:

Answer 679

Male-pattern baldness Male muscularture Clitoromegaly Increased libido Rapid linear growth with advanced bone age

Question 680

Primary adrenal insufficiency

Answer 680

Addison's

Question 681

Addison's disease can be caused by primary atrophy or injury to the _____

Answer 681

adrenal cortex

Question 682

In about 80% of Addison's atrophy occurs due to ____ of all cortical zones

Answer 682

autoimmune destruction

Question 683

Describe the level of ACTH in addison's disease:

Answer 683

High levels of ACTH

Question 684

Describe the levels of corticosteroid production in addison's disease:

Answer 684

Low corticosteroids

Question 685

Addison's disease can be characterized by a loss of:

Answer 685

Glucocorticoid, mineralcorticoid, & androgen secretion

Question 686

Secondary adrenal insufficiency is due to low levels of:

Answer 686

ACTH

Question 687

If the pituitary gland is unable to secrete enough ACTH this would restult in:

Answer 687

Low cortisol production (secondary adrenal insufficiency)

Question 688

Often latrogenic due to abrupt cessation of steroid therapy

Answer 688

Secondary adrenal insufficiency

Question 689

What is affected in primary adrenal insufficiency that is NOT affected in secondary adrenal insufficiency:

Answer 689

Mineralcorticoid secretion

Question 690

Would signs and symptoms of glucocorticoid deficiency be seen in primary or secondary adrenal insufficiency or both? Would signs and symptoms of mineralcorticoid deficiency be seen in primary or secondary adrenal insufficiency or both? Would signs and symptoms of androgen deficiency be seen in primary secondary adrenal insufficiency or both?

Answer 690

Glucocorticoid deficiency= both- both have lack of cortisol production Mineralcorticoid deficiency= primary only Androgen deficiency= Both- In addisons there is a loss of androgen & in secondary there is low ACTH leading to low androgen production (bc ACTH stimulates androgen production)

Question 691

Two important symptoms of glucocorticoid deficiency include:

Answer 691

Hypoglycemia- because cortisol normally raises blood glucose Low BP- due to the lack of alpha1 receptor permissive effect

Question 692

Hyperpigmentation in primary adrenal insufficiency is due to excess of ______

Answer 692

POMC

Question 693

Cushing's disease is a _____ disorder its characterized by _____ Cushing's sydnrome is a _____ disorder characterized by ____

Answer 693

Secondary- occurs due to brain- high ACTH Primary- occurs due adrenal cortex- low levels of ACTH

Question 694

Both cushings disease/syndrome is characterized by:

Answer 694

High cortisol levels

Question 695

Cushings Disease or Syndrome? 1. Secondary disorder 2. Primary disorder 3. Due to adrenal cortex 4. Due to brain 5. Oversecretion of ACTH leads to excessive cortisol level 6. Overproduction of cortisol leads to low levels of ACTH

Answer 695

1. Disease 2. Syndrome 3. Syndrome 4. Disease 5. Disease 6. Syndrome

Question 696

To distinguish between Cushing's disease & syndrome, what hormone levels would you look at?

Answer 696

ACTH

Question 697

Conn's syndrome is an issue with _____ Cushing's syndrome is an issue with _____ Pheochromoyctomoa is an issue with ______

Answer 697

Mineralcorticoids Glucocorticoids Catecholamines

Question 698

Sudden release of hormone causing sudden "attack" due to chromaffin cell in the adrenal medulla resulting in excessive secretion of epi & norepi

Answer 698

Pheochromocytoma

Question 699

What cells are involved in pheochromocytoma?

Answer 699

Chromafin cells

Question 700

Can be characterized by an exaggerated sympathetic response:

Answer 700

Pheochromocytoma

Question 701

What hormones are invovled in pheochromocytoma:

Answer 701

Epi & Norepi

Question 702

Entire length of thick filament (some overlapping thin filament)

Answer 702

A-band

Question 703

Includes ONLY thin filaments

Answer 703

I-band

Question 704

Includes only thick filaments

Answer 704

H-zone

Question 705

Where thin filaments are anchored

Answer 705

Z-line

Question 706

Link the central regions of thick filaments

Answer 706

M-line

Question 707

When a sarcomere shortens during contraction, what happens to the zone of overlap

Answer 707

Increases

Question 708

When a sarcomere shortens during contraction , what happens to the I-band?

Answer 708

Decreases

Question 709

When the sarcomere shortens during contraction, what happens to the A-band?

Answer 709

THE A-BAND DOES NOT CHANGE IN LENGTH

Question 710

Dark band: Light band:

Answer 710

A-band I-band

Question 711

In muscle, functions as an ATPase enzyme:

Answer 711

Myosin

Question 712

When myosin binds to ATP what happens?

Answer 712

It hydrolyzes the ATP

Question 713

What regulate when contraction can happen?

Answer 713

Troponin & tropomyosin

Question 714

Protein that connects thin filaments to glycoproteins in the sarcolemma:

Answer 714

Dystrophin

Question 715

Provides scaffolding for sarcomeres:

Answer 715

Dystrophin-glycoprotein complex

Question 716

What is the difference between Duchenne & Beckers muscular dystophy?

Answer 716

Duchennes= more severe, low levels of dystrophin if any at all Beckers= makes some dystrophin but not enough, because of this muscle cells weaken and, better prognosis

Question 717

List some types of muscular dystrophy:

Answer 717

Duchenne Beckers Myotonic Oculopharyngeal Limb girdle