Exam 2 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

List the 3 functions of hormones:

Answer 4

1. maintenance of homeostasis
2. growth and differentiation
3. reproduction

Question 5

Endocrine organs can be divided into what two categories?

Answer 5

1. major endocrine glands
2. organs w/ endocrine cells

Question 6

Primary function is to make a hormone and release it when the stimuli are present

Answer 6

major endocrine organ

Question 7

organs that happen to have endocrine cells allowing them to release a hormone although their primary fxn is NOT endocrine regulation

Answer 7

organs containing endocrine cells

Question 8

List specialized endocrine glands (major endocrine organs)

Answer 8

1. parathyroid gland
2. thyroid gland
3. pituitary gland
4. adrenal gland
5. pineal gland

Question 9

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

Answer 9

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 10

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

Answer 10

tropic hormone

Question 11

How do we classify hormones?

Answer 11

based on their structure

Question 12

What are the 3 classifications of hormones?

Answer 12

1. proteins or polypeptides
2. steroids
3. tyrosine derivatives

Question 13

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

Answer 13

made in advance and stored in vesicles until signal for release

Question 14

Protein and polypeptide hormones are synthesized first as ____.

Answer 14

Preprohormone

Question 15

The preprohormone will be converted into:

Answer 15

prohormone

Question 16

In protein and polypeptide hormones what is packed into vesicles of the endocrine cell prior secretion?

Answer 16

prohormone

Question 17

After the prohormone gets cleaved, it is now:

Answer 17

active hormone

Question 18

Mnemonic for protein and polypeptide hormones:

Answer 18

Protein/Polypeptide/Pre & Pro hormones (Everything with P’s)

Question 19

in addition to the active hormone, what gets released in when the prohormone gets cleaved?

Answer 19

inactive fragment

Question 20

What is the first thing that gets cleaved from preproinsulin?

Answer 20

signal peptide

Question 21

After the signal peptide is cleaved from preproinsulin, what occurs?

Answer 21

protein folding

Question 22

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

Answer 22

Proinsulin

Question 23

Proinsulin gets stored in:

Answer 23

vesicles

Question 24

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

Answer 24

C-peptide

Question 25

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

Answer 25

C-peptide

Question 26

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

Answer 26

c-peptide levels in the blood stream

Question 27

protein and polypeptide hormones are often made as an:

Answer 27

inactive precurser

Question 28

The inactive precursor of protein and polypeptide hormones:

Answer 28

preprohormone

Question 29

What does the signal peptide in insulin serve as?

Answer 29

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

Question 30

Where are the receptors located for protein/polypeptide hormones?

Answer 30

In the plasma membrane

Question 31

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

Answer 31

Made and released on demand

Question 32

Where are the receptors located for steroid hormones?

Answer 32

Inside the cell

Question 33

Why are steroid hormone receptors located inside the cell?

Answer 33

steroid hormones can cross the plasma membrane and bind to receptors inside target cells

Question 34

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

Answer 34

protein and polypeptide hormones

Question 35

Hormones from the adrenal cortex, ovaries and testes:

Answer 35

steroid

Question 36

Steroid hormones are synthesized from (derivatives of):

Answer 36

cholesterol

Question 37

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

Answer 37

Aldosterone & Cortisol

Question 38

DHEA, Androstenedione, testosterone, and estradiol are all steroid hormones involved in:

Answer 38

reproduction

Question 39

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

Answer 39

compliment of enzymes present

Question 40

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

Answer 40

made early and stored until secreted

Question 41

Amine hormones are derived from:

Answer 41

amino acid tyrosine

Question 42

Thyroid hormone, Noepinephrine and Epinephrine are all:

Answer 42

amine hormones

Question 43

Epinephrine and norepinephrine are both:

Answer 43

adrenal medullary neurohormones

Question 44

Thyroid hormone binds to the protein:

Answer 44

thyroglobulin

Question 45

Epinephrine and norepinephrine are stored in vesicles and released via:

Answer 45

exocytosis

Question 46

structurally what is the difference between T3 and T4?

Answer 46

the # of Iodide atoms attached

Question 47

What is a precursor to epinephrine and norepinephrine?

Answer 47

Dopamine

Question 48

Hormones released into circulation can either circulate ____ or ____.

Answer 48

Freely or with binding proteins

Question 49

The majority of ____, ____, and _____ hormones circulate in their free form.

Answer 49

amines, peptides and proteins

Question 50

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

Answer 50

Thyroid hormones because its double ring structure makes it soluble enough to where it needs help getting through the plasma

Question 51

Describe the solubility of amines, peptides/protein hormones:

Answer 51

water soluble

Question 52

_____ & _____ circulate bound to specific transport proteins

Answer 52

steroid and thyroid hormones

Question 53

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

Answer 53

globulin & albumin

Question 54

What is a shuttle bus found in the plasma (plasma protein) that transports a lot of things such as lipid soluble hormones and fatty acids:

Answer 54

albumin

Question 55

Most binding proteins are synthesized in the:

Answer 55

liver

Question 56

Patients with a compromised liver may show signs of:

Answer 56

endocrine deficiencies

Question 57

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

Answer 57

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

Question 58

It is always the ____ version of the hormone that binds to the receptors and affect the target cell.

Answer 58

Free version (binding protein stays in blood vessel)

Question 59

The constitutive level of plasma hormones

Answer 59

basal level

Question 60

The stimulated level of plasma hormones

Answer 60

peak levels

Question 61

The variable patterns of hormone release (oscillation) is determined by the interaction and integration of multiple control mechanisms which include: (4)

Answer 61

hormonal, neural, nutritional, and environmental

Question 62

When a hormone is constantly secreted in small amounts all of the time:

Answer 62

tonic release

Question 63

Hormone fluctuations that happen dependent on the time of day:

Answer 63

circadian rhythm

Question 64

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

Answer 64

cortisol

Question 65

When does cortisol spike?

Answer 65

early morning hours

Question 66

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

Answer 66

stimuli

Question 67

Growth hormone is secreted during sleep following a circadian rhythm release pattern but also displays:

Answer 67

pulsatile secretion

Question 68

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

Answer 68

pulsatile secretions

Question 69

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

Answer 69

chemical

Question 70

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

Answer 70

lipophilic/lipophobic

Question 71

Ligand/receptor binding demonstrates:

Answer 71

1. specificity 2. affinity 3. saturation

Question 72

Which classes of hormones bind to plasma membrane receptors?

Answer 72

polypeptide/protein and amine hormones

Question 73

What amine hormone does not bind to plasma membrane receptors (exception)

Answer 73

thyroid hormone

Question 74

Which class of hormones binds to nuclear receptors?

Answer 74

steroids hormones + thyroid hormone

Question 75

which amine hormones bind to plasma membrane receptors?

Answer 75

epinephrine and norepinephrine

Question 76

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

Answer 76

Plasma membrane receptor - they are peptide and protein hormones

Question 77

In general, many of the receptors that protein/peptide hormones and amine hormones bind to in the PM are:

Answer 77

GPCR

Question 78

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

Answer 78

plasma membrane receptors

Question 79

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

Answer 79

nuclear receptors

Question 80

Class of hormone receptors involved in making new proteins

Answer 80

nuclear receptors

Question 81

Thyroid hormone and steroid hormones bind to receptors in the:

Answer 81

cytoplasm or nucleus

Question 82

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

Answer 82

transformation of receptor to expose DNA-binding domain

Question 83

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

Answer 83

Binding to enhancer like element in DNA

Question 84

Examples of plasma membrane hormone receptors:

Answer 84

1. g-protein coupled receptor 2. tyrosine kinase

Question 85

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

Answer 85

this provides a way to achieve specific tissue activation

Question 86

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

Answer 86

1. thyroid hormone receptors 2. insulin receptors

Question 87

Why are thyroid hormone receptors and insulin receptors more widely distributed?

Answer 87

Because there actions are something that most cells participate in

Question 88

How do IGF-1 and insulin work?

Answer 88

By activating a tyrosine kinase receptor

Question 89

If it is a plasma membrane receptor, generally it will activate or inhibit _____ to _____.

Answer 89

an existing protein to yield a faster response

Question 90

Where are nuclear hormone receptors located?

Answer 90

cytoplasm or nucleus

Question 91

Nuclear hormone receptors typically leads to:

Answer 91

formation of new proteins

Question 92

Nuclear hormone receptors all act to:

Answer 92

increase or decrease gene expression

Question 93

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

Answer 93

hormone responsive element; promotor region; gene trasncription

Question 94

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

Answer 94

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

Question 95

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

Answer 95

simple diffusion

Question 96

The body often releases multiple hormones...

Answer 96

at the same time

Question 97

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

Answer 97

1. antagonism 2. additive 3. synergistic 5. permissiveness

Question 98

When two hormones change one variable in opposite directions:

Answer 98

antagonism

Question 99

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

Answer 99

additive

Question 100

Ramps of up the systems response when there is a present of more than one hormone- the combined response is greater than each would give individually (2+3=10)

Answer 100

synergistic

Question 101

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

Answer 101

permissiveness

Question 102

Determine which hormone interaction is being described: Parathyroid increases plasma calcium levels; calcitonin decreases plasma calcium levels:

Answer 102

antagonistic

Question 103

Determine which hormone interaction is being described: Glucagon, cortisol and epinephrine all increase blood glucose more than the sum of their individual effects:

Answer 103

synergistic

Question 104

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

Answer 104

permissiveness

Question 105

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

Answer 105

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

Question 106

When the last hormone in the pathway inhibits the system upstream:

Answer 106

long loops negative feedback

Question 107

When an intermediate hormone in the pathway inhibits the system upstream:

Answer 107

short loop negative feedback

Question 108

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

Answer 108

positive feedback

Question 109

Causes an endocrine gland to secrete a hormone:

Answer 109

tropic hormone

Question 110

Stabilizes the system and prevents oversecretion:

Answer 110

negative feedback

Question 111

Hormones that have other endocrine glands as their targets:

Answer 111

tropic hormones

Question 112

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

Answer 112

TRH

Question 113

TRH comes from

Answer 113

Hypothalamus

Question 114

TRH acts on the:

Answer 114

anterior pituitary

Question 115

TSH (thyroid stimulating hormone) is released from the:

Answer 115

anterior pituitary

Question 116

TSH is release from the anterior and acts on the:

Answer 116

thyroid gland

Question 117

In the regulation of thyroid hormone: A stimulation causes the hypothalamus to secrete _____ which acts on ____.

Answer 117

thyrotropin releasing hormone (TRH); anterior pituitary

Question 118

In the regulation of thyroid hormone: ______ cells in the anterior pituitary release _____.

Answer 118

thyrotropic cells; thyroid stimulating hormone (TSH)

Question 119

In the regulation of thyroid hormone: TSH stimulates _____cells of the thyroid gland to release ______

Answer 119

follicular cells; thyroid hormone

Question 120

Thyroid hormone produces effects in the body that include:

Answer 120

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

Question 121

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

Answer 121

metabolic activities

Question 122

In the regulation of thyroid hormone: Increased body temperature is detected by the hypothalamus and the secretion of ____ by the hypothalamus is ____.

Answer 122

TRH; inhibited

Question 123

In the regulation of thyroid hormone: Thyroid hormone also blocks TRH receptors on thyrotropic cell, inhibiting synthesis and release of ____. Both effects indirectly dampen ____ production in the thyroid.

Answer 123

TSH; TH

Question 124

Thyroid hormone working to negatively feedback is an example of:

Answer 124

long loop negative feedback

Question 125

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

Answer 125

endocrine disorders/ pathologies

Question 126

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

Answer 126

thyroid goiter

Question 127

Disease characterized by increased cortisol levels:

Answer 127

Cushing's Disease

Question 128

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

Answer 128

primary endocrine disorder

Question 129

List the causes of primary hyposecretion:

Answer 129

1. partial destruction of the gland 2. dietary deficiency 3. Enzyme deficiency required for hormone synthesis

Question 130

List the causes of primary hypersecretion:

Answer 130

endocrine gland tumor

Question 131

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

Answer 131

secondary endocrine disorder

Question 132

List the causes of secondary hypersecretion:

Answer 132

A lack of sufficient tropic hormone

Question 133

List the causes of secondary hypersecretion:

Answer 133

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

Question 134

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

Answer 134

paraneoplastic endocrine syndrome

Question 135

When you think of primary endocrine dysfunction, you should think:

Answer 135

LAST GLAND IN PATHWAY

Question 136

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

Answer 136

stimulation test supression test

Question 137

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

Answer 137

hyperfunction

Question 138

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

Answer 138

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

Question 139

Stimulation test work by administering a ____ hormone.

Answer 139

tropic or stimulating

Question 140

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

Answer 140

estrogen receptors in breast tumors

Question 141

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

Answer 141

1. Hashimoto thyroiditis 2. Type I DM 3. Graves Disease 4. Addison disease 5. Autoimmune hypothyroidism

Question 142

Glucagon, angiotensin, Gonadotropin releasing hormone (GnRH), Somatostatin (SS), Growth hormone releasing hormone (GHRH), follicle stimulating hormone (FSH), Lutenizing hormone (LH), Thyroid stimulating hormone (TSH), Adrenocorticoptropin hormone (ACTH) are all _____ hormones. When are they made?

Answer 142

polypeptide/protein hormone made in advance & stored

Question 143

Epinephrine and Norepinephrine are both ____ hormones. When are they made?

Answer 143

amine hormones made in advance and stored

Question 144

Thyroid hormone is a ____ hormone. When is it made?

Answer 144

EXCEPTION: amine hormone made in advance and stored (does bind to nuclear receptor though)

Question 145

Aldosterone, Crotisole, Estradiol and testosterone (mineralcorticoids, glucocorticoids and androgens) are all _____ hormones. When are they made?

Answer 145

steroid hormones made on demand

Question 146

List things that would cause stimulation of growth hormone release

Answer 146

growth hormone releasing hormone, dopamine, catecholamines (in times of stress and exercise), excitatory amino acids, thyroid , fasting (hypoglycemia)

Question 147

List things that would cause inhibition of growth hormone release

Answer 147

Somatostatin (SS), IGF-1 (due to negative feedback), Glucose (at high levels- hyperglycemia), and free fatty acids

Question 148

GHRH, Dopamine, Catecholamines, Excitatory amino acids, and thyroid hormone would cause _____ of growth hormone release:

Answer 148

stimulation

Question 149

Somatostatin, IGF-1, Glucose, and FFA would cause ____ of growth hormone release:

Answer 149

inhibition

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 axons 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 located 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 (ACTH) 4. TSH 5. Prolactin 6. Growth hormone

Question 156

List the hormones secreted by the posterior pituitary:

Answer 156

1. antidiuretic hormone/vasopressin (ADH) 2. oxytocin

Question 157

The pituitary gland secretes _____ hormones:

Answer 157

peptide

Question 158

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

Answer 158

somatotrophs; GH

Question 159

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

Answer 159

30-40%

Question 160

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

Answer 160

Corticotrophs; ACTH

Question 161

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

Answer 161

20%

Question 162

Aside from corticotrophs and somatotrophs what other types of cells make up the anterior pituitary and what do they secrete?

Answer 162

Thyrotrophs-TSH Gonadotrophs- LH & FSH Mammotrophs- prolactin

Question 163

Adenomas involving somatotropic cells can cause ____ if occurring in children before closure of the long bones epiphyseal plates or _____ in adults with musculoskeletal, neurologic, and other medical consequences.

Answer 163

gigantism; acromegaly

Question 164

Benign tumors of epithelial cells that make 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 and secrete _______ hormones that control endocrine cells in the ____.

Answer 168

hypothalamic releasing and inhibiting; 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:

Answer 170

hypothalamic-hypophyseal portal blood vessels

Question 171

The hypothalamic-hypophyseal portal blood vessels carry the hypothalamic hormones to the ____ of the anterior pituitary

Answer 171

sinuses

Question 172

Regulation of Anterior Pituitary Secretion 1. the _____ releases hormones that enter into the blood 2. the hormones travel through the _____. 3. the hormones continue down through the capillary bed to the ____ where they can leave the blood and regulate the activity of 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 vessel allows for:

Answer 175

communication from hypothalamus to anterior pituitary

Question 176

Where do releasing hormones come from?

Answer 176

hypothalamus

Question 177

Where do stimulating hormones come 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-protein coupled receptors

Question 179

Following the binding of the hypothalamic hormones to the g-protein coupled receptors in the anterior pituitary, what will stimulate or inhibit anterior pituitary hormone secretion?

Answer 179

second messengers (examples= cAMP via adenylate cyclase, IP3, and DAG vis 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 hormones would be _____ (BRAKES)

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 hormones acts directly on target tissues and as a tropic hormone to the ____ which releases ____.

Answer 184

Liver; IGF-1

Question 185

In what situation might growth hormone significantly increase and quickly?

Answer 185

prolonged starvation/fasting

Question 186

Growth hormone acts tropically in the liver to activate ____, a cell signaling pathway that causes release of _____.

Answer 186

JAK-STAT; IGF-1

Question 187

A cell signaling pathway in the liver activated by growth hormone that responds by release of IGF-1

Answer 187

JAK-STAT

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 are some effects?

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 GH acting on chondrocytes being necessary for linear growth, what is also necessary for linear growth?

Answer 191

IGF-1

Question 192

GH can act on muscles to :

Answer 192

increase protein synthesis

Question 193

In addition to growth hormone acting on muscles to increase protein synthesis what is also necessary for protein synthesis?

Answer 193

IGF-1

Question 194

In excess, how does growth hormone affect adipose tissue?

Answer 194

anti-insulin action

Question 195

What are two locations of negative feed back of the 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 the GH secreted at the highest levels?

Answer 198

a few hours after sleep

Question 199

Growth hormone 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 neonatal period: The secretion of GH during childhood: The secretion of GH during puberty: The secretion of GH during adulthood:

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. IGF-1 (due to negative feedback) 3. High glucose levels 4. FFA (High levels of free fatty acids)

Question 203

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

Answer 203

IGFs

Question 204

IGFs can also be called:

Answer 204

somatomedins

Question 205

IGF-1 is produced in most tissues and acts on neighboring cells in a _____ manner.

Answer 205

paracrine

Question 206

The major site of IGF-1 synthesis:

Answer 206

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

IGF-1

Question 209

Osteocytes responding to mechanical sensors can release:

Answer 209

IGF-1

Question 210

Osteocytes responding to ______ can release IGF-1

Answer 210

mechanical sensors

Question 211

After osteocytes release IGF-1 what happens?

Answer 211

IGF-1 binds to receptors on osteoblasts to enhance bone formation

Question 212

Mechanisms of action of GH and IGF-1: Growth in nearly all tissues of the body, mainly IGF-1 occurs through what mechanisms?

Answer 212

1. increased cell size 2. mitosis 3. differentiation of bone and muscle cells

Question 213

Mechanisms of action of GH and IGF-1: What is the overall outcome of the effects of GH and IGF-1 causing growth in nearly all tissues of the body?

Answer 213

1. increased organ size 2. increased organ function 3. increased linear growth

Question 214

Mechanisms of action of GH and IGF-1: The effect of amino acid uptake protein synthesis in most cells results in:

Answer 214

increased lean body mass

Question 215

Mechanisms of action of GH and IGF-1: How does this effect glucose?

Answer 215

reduced glucose utilization

Question 216

Mechanisms of action of GH and IGF-1: Reduced glucose utilization is due to:

Answer 216

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

Question 217

Mechanisms of action of GH and IGF-1: The reduced glucose utilization can lead to:

Answer 217

insulin resistance ; diabetogenic

Question 218

Mechanisms of action of GH and IGF-1: Describe the effects on fatty acids:

Answer 218

mobilization of fatty acids from adipose tissue (lipolysis)

Question 219

Mobilization of fatty acids from adipose tissues:

Answer 219

lipolysis

Question 220

Mechanisms of action of GH and IGF-1: Lipolysis results in:

Answer 220

increases FFA in blood and use of FFA for energy

Question 221

Before fusion of the epiphyseal plates, GH and IGF-1 stimulate:

Answer 221

chondrogenesis and widening of the epiphyseal plates

Question 222

Following GH and and IGF-1 stimulating chorndrogenesis and widening of the epiphyseal plates, what occurs?

Answer 222

Bone matrix deposition stimulating linear growth

Question 223

In adults, GH and IGF-1 play a role in regulating the normal physiology of:

Answer 223

bone formation

Question 224

In adult, how do GH and IGF-1 play a role in regulating the normal physiology of bone formation?

Answer 224

by increasing bone turnover

Question 225

How do GH and IGF-1 stimulate the increase in bone turnover (there by regulating bone formation)

Answer 225

1. activation of osteoblasts (MAINLY) 2. increasing bone resorption via osteoclasts (lesser extent)

Question 226

Kids: GH and IGF-1 = Adults: GH and IGF-1=

Answer 226

chondrogenesis increased bone turnover

Question 227

Osteoblasts are of what origin?

Answer 227

mesenchymal precursers

Question 228

What is responsible for the formation of active osteoblasts from the osteoblast precursor?

Answer 228

IGF-1

Question 229

Gigantism occurs in _____; while 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 with pituitary tumors that give rise to gigantism?

Answer 231

sella and cavernous sinus

Question 232

Tumor causing excessive growth hormone release:

Answer 232

somatotropic adenoma of the pituitary

Question 233

Describe the facial features associated with Gigantism/acromegaly: (4)

Answer 233

Coarse facial features, large fleshy nose, frontal bossing, jaw malocclusion

Question 234

Coarse facial features, large fleshy nose, frontal bossing, and jaw malocclusion are collectively referred to as:

Answer 234

acromegalic faces

Question 235

What issue with the thyroid may occur with gigantism/acromegaly

Answer 235

goiter

Question 236

Describe the potential affects on the heart and what conditions may occur as a result due to gigantism/acromegaly:

Answer 236

cardiomegaly; hypertension and coronary heart disease

Question 237

Describe the chest and spine in individuals affected by acromegaly/gigantism:

Answer 237

barrel chest and kyphosis and hyperostosis

Question 238

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

Answer 238

diabetes mellitus

Question 239

Growth hormone shifts the body from utilizing ______ to _____ for metabolisms:

Answer 239

carbs to fats

Question 240

Describe the reproductive consequences of gigantism/acromegaly:

Answer 240

male sexual dysfunction and menstrual disorders

Question 241

Describe what can occur due to the thickened skin and hypertrophy of sebaceous and sweat glands in gigantism and acromegaly:

Answer 241

Hyperhidrosis and oily skin

Question 242

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

Answer 242

thickened skin (hypertrophy of sebaceous and 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 microadenoma?

Answer 245

adenectomy via transphenoid approach followed by medications

Question 246

Oral manifestations of GH excess: (7)

Answer 246

1. thick rubbery skin, enlarged nose and thick lips 2. macrocephaly 3. macrognathia 4. disproportionate mandibular growth 5. anterior open bite and malocclusion 6. macroglossia, dyspnea, dysphagia, dysphonia, sialorrhea, 7. Hypertrophy of pharyngeal and laryngeal tissues

Question 247

enlarged head = enlarged jaw =

Answer 247

macrocephaly macrognathia

Question 248

The disproportionate mandibular growth caused by excess growth hormone includes:

Answer 248

mandibular prognathism- jaw jets forward generalized diastemata- separation of teeth

Question 249

The anterior open bite and malocclusion in caused by excess GH is due to:

Answer 249

combo of macrognathia and tooth migration

Question 250

1. Macroglossia: 2. Dyspnea: 3. Dysphagia: 4. Dysphonia: 5. Sialorrhea:

Answer 250

1. enlarged tongue 2. difficulty breathing 3. difficulty swallowing 4. difficulty speaking 5. slobbering

Question 251

The hypertrophy of the pharyngeal and laryngeal tissues in individuals with excess GH can cause_____ and how?

Answer 251

sleep apnea - because of the increased growth of the pharyngeal and 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, IGF-1 receptor

Question 255

A decrease in GHRH or an increase in GHIH could lead to:

Answer 255

growth hormone deficiency

Question 256

What depends on the time of onset and severity of hormone deficiency? (talking about GH)

Answer 256

clinical manifestations

Question 257

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

Answer 257

1. slow linear growth rates (shorter stature) 2. normal skeletal proportions 3. pudgy, youthful appearance (decreased lipolysis) 4. In setting of cortisol deficiency --> hypoglycemia

Question 258

most common form of dwarfism, autosomal dominant condition, resulting from a mutation in the FGF-3 receptor in the cartilage and brain.

Answer 258

achondroplasia

Question 259

The FGF-3 receptor mutation in achondroplasia 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 is not impacted)

Question 260

mutated receptor in achondroplasia:

Answer 260

FGF-3

Question 261

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

Answer 261

1. skull and facial skeleton; small 2. tooth formation and 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 and skeletal malocclusion

Question 263

Incisor defects in a child with growth hormone deficiency occurs in both:

Answer 263

primary and permanent dentition

Question 264

In oral manifestation of GH deficiency: The tooth formation and growth of the alveolar regions of the jaws are abnormal and may be disproprotionately smaller than adjacent anatomic structures, this can cause:

Answer 264

1. tooth crowding and malocclusion 2. plaque accumulation 3. poor oral hygiene 4. gingivitis and 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 haev axons that go through the infundibulum with their synaptics terminals located in the posterior pituitary gland

Answer 266

paraventricular nucleus and supraoptic nucleus

Question 267

The paraventricular nucleus produces:

Answer 267

oxytocin

Question 268

The supraoptic nucleus produces:

Answer 268

ADH

Question 269

List all the names for the abreviation 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 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 and Oxytocin:

Answer 273

VERY Similar structure

Question 274

What are the 2 primary functions of ADH:

Answer 274

1. vasocronstriction (smooth muscle and blood vessels) 2. antidiuretic (holds on to water)

Question 275

ADH/AVP mechanism of action: 1. Contaction 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

increase in BP

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: ADH functions in the renal tubules via:

Answer 279

V2 receptors

Question 280

Where are the V2 receptors (for ADH) located?

Answer 280

Late distal tubule and collecting duct

Question 281

What results when ADH binds to V2 in the late distal tubule and collecting duct?

Answer 281

AQP2 proteins are inserted into the apical membrane of tubular epithelial cells

Question 282

Where is APQ2 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 tubule, and AQP2 being inserted into the apical membrane of tubular epithelial cells, what results?

Answer 283

This allows for water resabsorption (in accordance with AQP3 and AQP4) on the basolateral membrane)

Question 284

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

Answer 284

AQP3 and AQP4 in the basolateral membrane

Question 285

The V2 receptors in the late distal tubule and collecting duct and _____ 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, and _______ are always on the basolateral membrane and allow for the continuation of the water.

Answer 287

Aquaporin 2; Aquaporin 3&4

Question 288

Stimuli for ADH secretion:

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 BP is too low, ADH will function to _______ in order to raise it.

Answer 294

keep water

Question 295

ADH working to keep water in the body will resolve what 3 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 problem in elderly but is also associated with lesions in the hypothalamus (thirst center), head trauma, occult hydrocephalus or subsrachnoid hemmorhage

Answer 298

hypodipsia

Question 299

List causes of hypodipsia: (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 caused by:

Answer 300

ADH inbalance

Question 301

What are the two types of DI?

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 an increased osmolarity, your would feel:

Answer 303

thirsty (under normal conditions)

Question 304

Disease caused by inability to produce and 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 the ADH (give them ADH)

Question 307

A person with a tumor near the posterior pituitary gland has surgical removal of the tumor causing damage to the supraoptic nucleus in the posterior pituitary. What might this result in if they are unable to produce ADH.

Answer 307

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 respond inappropriotely:

Answer 310

Nephrogenic/peripheral DI

Question 311

Describe the levels of ADH in someone with nephrogenic/peripheral DI; why?

Answer 311

High levels, because they can produce ADH and the stimulus causing the ADH secretion does NOT get corrected (causing the hypothalamus to secrete more and more)

Question 312

Uncharacteristically really high levels of ADH secretion and not because it is needed (oversecretion of ADH)

Answer 312

Syndrome of innappropriate ADH (SIADH)

Question 313

A patient with DI 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 DI:

Answer 315

hypotonic and tasteless (Insipid)

Question 316

Other causes of polyuria may include: (Not DI)

Answer 316

1. primary ingestion of excess fluid 2. Increased 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 and 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 and stress

Question 321

Why do pregnant women pee more?

Answer 321

during pregnancy, ADH metabolism (breakdown of ADH) is increased, so more water is released

Question 322

What hormone causes milk ejection from the breasts in lactation?

Answer 322

Oxytocin

Question 323

What hormone stimulates contraction of the uterus toward 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 and 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

Question 329

What causes the milk ejection in the breast? (mechanism)

Answer 329

myoepithelial cell contraction

Question 330

What causes uterine contraction? (mechanism)

Answer 330

stretch of cervix at end of pregnancy

Question 331

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

Answer 331

sign

Question 332

Enlarged hands, polyuria, and tachycardia are all examples of:

Answer 332

signs

Question 333

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

Answer 333

symptoms

Question 334

Headache and numbness are both examples of:

Answer 334

a symptom

Question 335

Plasma Membrane Hormone Receptors: List the 4 plasma membrane hormone receptors:

Answer 335

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

Question 336

Plasma Membrane Hormone Receptors: What are our two types of G-protein coupled receptors?

Answer 336

Gs and Gq

Question 337

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

Answer 337

1. B-adrenergic 2. Calcitonin 3. ACTH 4. Glucagon 5. TSH 6. Vasopressin The produce the second messenger cAMP

Question 338

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

Answer 338

1. A-adrenergic 2. Angiotensin II 3. TRH They produce the second messengers IP3, DAG and 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 we want a lot of cells to respond too

Question 343

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

Answer 343

T4

Question 344

About 7 % of the active hormones 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 hormones 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 the follicle?

Answer 349

Thyroglobuline

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 thryoid follicle=

Answer 352

colloid

Question 353

Where is thyroid hormone made and 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 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 follicular cells contain 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 6. Once inside the colloid, the Iodide gets converted into ____.

Answer 356

1. Iodine 2. Iodide 3. Na+/I- symporter (NIS) 4. Concentrate the Iodide 5. Pendrin; chloride; iodide 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 access the ___ where the initial steps of thyroid hormone synthesis occur.

Answer 359

thyrocyte; apical membrane; colloid

Question 360

What enzymes works in the iodination and 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- in and Cl- out

Question 363

Pendrin is ALWAYS:

Answer 363

moving two negatively charged substances in opposite directions

Question 364

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

Answer 364

Thyroglobulin

Question 365

The enzyme involved in all of the production steps in the formation of thyroid hormone (tyrosine, monoiodotyrosine, diiodotyrosine, T3, RT3, and 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 and T4 (pendrin or peroxidase???)

Answer 367

pendrin THEN peroxidase

Question 368

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

Answer 368

1. colloid 2. lysosomes 3. protease; TG 4. capillaries

Question 369

Colloid is a _____ of thyroid hormones

Answer 369

reservoir

Question 370

Majority if not all of T3 and T4 bind with _____ for transport

Answer 370

plasma proteins

Question 371

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

Answer 371

Thyroxine binding globulin (TBG) Transthryretin (TTR) Albumin

Question 372

What causes the long half life of T4?

Answer 372

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

T3 and T4 secretion into the blood: Colloid is taken into the follicular cell via:

Answer 374

pinocytosis

Question 375

T3 and T4 secretion into the blood: T3 and 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 3 different deoiodinases?

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 the enzymatic activity.

Answer 380

selenium; sulfur

Question 381

What are carious conditions that inhibit deiodinase activity?

Answer 381

1. selenium deficiency 2. burns 3. trauma 4. advanced cancer 5. cirrhosis 6. chronic kidney 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 action occurs ____ compared to T4

Answer 383

sooner

Question 384

When does the maximum activity of T3 hormone occur?

Answer 384

~2-3 days

Question 385

Compare the activity of T4 to T3

Answer 385

T4 has a slower onset but long 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 and synthesis of new proteins

Question 387

The synthesis of new proteins due to the action of T3 and T4 can lead to what 5 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 and T4 synthesizing new proteins that affect metabolism?

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 HR 4. Increased heart strength 5. Increased respiration

Question 391

The cardiovascular effects of thyroid hormone are caused by an increased in ______ which is a _____ effect.

Answer 391

beta receptors; permissive effect

Question 392

Negative feedback of the thyroid hormone is mainly at the level of ____ but can also occur at ____.

Answer 392

anterior pituitary; hypothalamus

Question 393

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

Answer 393

anterior pituitary and hypothalamus TSH and TRH

Question 394

What actually causes the feedback inhibition of thyroid hormone?

Answer 394

The anterior pituitary and hypothalamus increasing their expression of deiodinase activity so when T4 levels in these tissues increase, they readily convert it (via deiodinase) to T3 which causes the inhibition

Question 395

Describe the secretion of TSH:

Answer 395

pulsatile with increases in evening hours and peak ~ midnight

Question 396

Describe the secretion of Thyroid hormone:

Answer 396

Thyroid secretion mirrors TSH secretion (pulsatile with increases in evening hours and peak around midnight) but also is tonically secreted (small amounts)

Question 397

Thyroid hormones stimulates _____ by most metabolically active tissues

Answer 397

oxygen consumption

Question 398

How does thyroid hormone effect BMR?

Answer 398

increases it

Question 399

Thyroid hormone stimulates ______ metabolism

Answer 399

carbohydrate

Question 400

Thyroid hormone stimulates carbohydrate metabolism by:

Answer 400

1. uptake of glucose by cells 2. enhances glycolysis and gluconeogensis 3. increases CHO absorption from GI tract

Question 401

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

Answer 401

stimulates protein catabolism and synthesis but more catabolism (breakdown)

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 and 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 ---> vitamin A

Question 405

Vitamin A is important in:

Answer 405

wound healing

Question 406

Thyroid hormone is responsible for decreasing circulating _____ levels. A person with hypothyroid may have _____ due to this.

Answer 406

cholesterol levels 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 devleopment

Question 409

Thyroid hormone impacts _____ so someone with hypothyroidism may have prolonged ___.

Answer 409

reflex time; prolonged reflex time

Question 410

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

Answer 410

muscle tremors

Question 411

If someone feels tires, but has difficulty sleeping and anxiety, worry and paranoia they may have: (relating to thyroid hormone)

Answer 411

hyperthyroidism

Question 412

hyperthyroidism effected on cardiovascular system include:

Answer 412

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

Question 413

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

Answer 413

Thyroid hormone increases the 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 needed to maintain ____ levels.

Answer 414

glucose; insulin; blood glucose

Question 415

Thyroid hormone effects on the endocrine system: The 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: 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 increased _____ and _____ intake.

Answer 417

appetite and food

Question 418

Thyroid hormone effects on the GI system: Thyroid hormone causes increased rate of ______ and _____ of GI tract. Individuals with hyperthyroidism may have _____ due to this, while individuals with hypothyroidism may have ____ due to this.

Answer 418

secretion and motility 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 and euthyroidism

Question 422

Goiter can be caused excessive amounts of _____ secretion.

Answer 422

TSH

Question 423

High TSH stimulates thyroid to stimulate larges amounts of _____ into ______ resulting in gland enlargement/ goiter

Answer 423

Thyroglobin colloid into follicles

Question 424

The most common form of hyperthyroidism

Answer 424

Grave's disease

Question 425

Although Grave's disease is the most common form of hyperthyroidism, hypothyroidism can also occur due to:

Answer 425

thyroid adenoma

Question 426

Grave's disease is a _____ disease. Explain this:

Answer 426

autoimmune disease. 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 and T4)

Question 427

Describe the category of disorder that Grave's disease is, and who the hypothalamus and anterior pituitary are affected:

Answer 427

Primary endocrine disorder- bc issue is at level of thyroid gland strong negative feedback causes TSH and TRH levels to be reduced

Question 428

Grave's disease is more common in:

Answer 428

The gals

Question 429

List the signs and symptoms of Grave's dizzzeeeez

Answer 429

1. sweating/heat intolerance 2. increased metabolism 3. increased appetite 4. weight loss 5. fine hair/ protein synthesis 6. increase NS response (emo instability, insomnia, nervy, resletessness) 7.fine tremor 8. goiter 9. exophthalmos (bug eyed) 10. pre-tibial myxedema

Question 430

Treatment for the gravy:

Answer 430

radioactive iodine to ablate the thyroid followed by L thyroxine (T4) to prevent hypothyroidism, surgery rarely indicated antithyroid drugs beta-blockers to block permissive effect of thyroid hormone

Question 431

Oral symptoms of hyperthyroidism may include:

Answer 431

- burning mouth syndrome - gum disease - excessive salivation - weakening of mandible - increased caries risk

Question 432

Elevated thyroid hormone with stressful events or serious illness causing fever, tachycardia, elevated BP, nausea, vomiting, diarrhea and breathing problems:

Answer 432

thyroid storm (thyrotoxicosis)

Question 433

What can bring on a thyroid storm?

Answer 433

-trauma -surgery -infection -DKA -MI

Question 434

Overall a thyroid storm can be described as:

Answer 434

exaggerated sympathetic response

Question 435

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

Answer 435

administration of epinephrine is CONTRAINDICATED and elective dental care should be deferred

Question 436

autoimmune reaction against the thyroid gland that destroys it rather than stimulates it

Answer 436

hashimotos thyroiditis

Question 437

What is the most common cause of hypthyroidism?

Answer 437

Hashimoto's thyroiditis

Question 438

Prior to diagnosis of hashimoto's thyroiditis, most patients first exhibit:

Answer 438

autoimmine thyroiditis

Question 439

In hashimoto's thyroiditis, inflammation leads to ___ of the thyroid resulting in _____.

Answer 439

fibrosis; decreased section of thyroid hormone

Question 440

What is the target of the antibodies in hashimotos thryoiditis?

Answer 440

peroxidase

Question 441

What class of disorder is Hashimoto's characterized by?

Answer 441

primary endocrine disorder

Question 442

Another form of hypothyroidism (not hashimoto's) is due to:

Answer 442

low iodine

Question 443

Hypothyroidism due to low iodine is classified as:

Answer 443

primary endocrine disorder

Question 444

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

Answer 444

T3 and T4 low; and TRH and TSH high

Question 445

In hypothyroid states, goiter is due to _____, while no goiter is due to _____.

Answer 445

iodine deficiency; TSH deficiency

Question 446

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

Answer 446

goiter; primary no goiter; secondary

Question 447

Symptoms of hypothyroidism may include:

Answer 447

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. hair loss 9. loss of lateral eyebrows 10. slow pulse (bc decreased # of beta receptors) 11. enlarged heart 12. facial edema 13. peripheral edema

Question 448

Unique symptom seen in severe hypothyroid cases:

Answer 448

myxedema

Question 449

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

Answer 449

hyper= pretibial myxedema hypo= face

Question 450

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

Answer 450

hyaluronic acid and chondroitin sulfate

Question 451

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

Answer 451

myxedema; L-thyroxine (T4)

Question 452

Required for post-natal brain maturation

Answer 452

Thyroid hormones

Question 453

Results from congenital absence of thyroid gland:

Answer 453

congenital cretinism

Question 454

Results from iodine deficient diet; most common cause world wide:

Answer 454

endemic cretinism

Question 455

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

Answer 455

physical and mental retardation Obese, stocky and short with large protruding tongue

Question 456

Cretinism can cause lack of development of ____.

Answer 456

nervous system

Question 457

List the hypothyroidism oral manifestations: (6)

Answer 457

1. macroglossia 2. dysgeusia 3. delayed tooth eruption 4. poor wound healing 5. increased periodontal disease 6. salivary gland enlargement

Question 458

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

Answer 458

decreased activity of fibroblasts

Question 459

Patients with hypothyroidism are sensitive to:

Answer 459

central nervous system depressants and barbiturates

Question 460

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 460

bones cells ECF

Question 461

Only 0.1% of the body's calcium is found in the: 1% of the body's calcium is found in the: The rest of the body's calcium is stored in the:

Answer 461

ECF Cells and organelles bones

Question 462

When levels of calcium are too low:

Answer 462

neuronal hyper-excitability (tetany due to extra Na+ influx)

Question 463

When levels of calcium are too high:

Answer 463

neuronal depression (blocks Na+ influx)

Question 464

Carpal spasms can be due to:

Answer 464

HYPOcalcemia

Question 465

Control points for calcium and phosphate include:

Answer 465

1. absorption- via intestines 2. excretion- via urine (calcium and phosphate) and feces (calcium only) 3. temporary storage- via bones (hydroxyapatite)

Question 466

Ca(10)PO4(6)OH(2)

Answer 466

hydroxyapatite

Question 467

What the hormones that regulate plasma calcium?

Answer 467

PTH, Calcitriol, and Calcitonin

Question 468

How does PTH regulate plasma calcium and phosphate?

Answer 468

Increases plasma calcium Decreases plasma phosphate

Question 469

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

Answer 469

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

Question 470

How does calcitriol regulate plasma calcium and phosphate?

Answer 470

Increases plasma calcium Increases plasma phosphate

Question 471

How does calcitriol work to raise plasma calcium and phosphate?

Answer 471

Calcitriol is the primary hormones that enhances intestinal absorption of calcium and it also causes absorption of phosphate

Question 472

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

Answer 472

Calcitriol

Question 473

What are the other names for calcitriol?

Answer 473

1,25-dihydroxycholecalciferol Vitamin D3

Question 474

Calcitriol acts on the intestines ______ to enhance absorption of calcium and also phosphate. While PTH acts on the intestines _____ to enhance absorption.

Answer 474

Directly; Indirecty

Question 475

Calcitonin comes from:

Answer 475

parafollicular cells of the thyroid gland

Question 476

How does calcitonin regulate plasma calcium and phosphate?

Answer 476

Decreases plasma calcium and phosphate

Question 477

How does calcitonin work to lower plasma calcium and phosphate?

Answer 477

It stimulates bone formation

Question 478

What hormones stimulate bone formation?

Answer 478

1. calcitonin 2. insulin 3. growth hormone 4. IGF-1 5. estrogen 6. testosterone

Question 479

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

Answer 479

Calcitriol and PTH

Question 480

Calcitriol and parathryoid hormone stimulate bone matrix _______ . How does this effect plasma calcium?

Answer 480

resorption; increases plasma calcium

Question 481

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

Answer 481

1.RANK ligand 2. RANK-L binds to the RANK receptors; osteoclasts

Question 482

What is the goal of bone resorption?

Answer 482

Increase plasma calcium levels

Question 483

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

Answer 483

Osteoclasts; Rank Ligand

Question 484

Factors that stimulate bone matrix resoprtion:

Answer 484

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

Question 485

What is the goal of bone deposition?

Answer 485

form bone, take calcium out of blood and put into bone

Question 486

_____ stimulates bone matrix deposition and inhibits osteoclasts.

Answer 486

calcitonin

Question 487

Calcitonin stimulates bone matrix deposition and inhibits osteoclasts which ultimate does _____ to plasma calcium.

Answer 487

decreases

Question 488

If calcium levels in the blood are sufficient, we don't need to:

Answer 488

break down bone

Question 489

Anabolic or anti-resorptive factors (for bone)=

Answer 489

1. estrogens 2. calcitonin 3. testosterone 4. calcium 5. BMP

Question 490

In order to avoid RANK-L further activating osteoclasts, ____ will bind to RANK-L to prevent it from binding to the RANK-L receptor

Answer 490

OPG

Question 491

OPG binding to RANK-L ultimately leads to:

Answer 491

apoptotic osteoclasts

Question 492

Osteoclasts that do NOT function to break down bone:

Answer 492

Apoptotic osteoclasts

Question 493

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

Answer 493

Osteoporosis

Question 494

Risk factors for osteoporosis: (Superficial)

Answer 494

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

Question 495

Describe why Vitamin D deficiency can lead to osteoporosis:

Answer 495

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

Question 496

Describe why inadequate calcium intake can lead to osteoporosis:

Answer 496

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

Question 497

Describe why glucocorticoid medications can lead to osteoporosis:

Answer 497

They supress the immune response leading to risk of weak and brittle bones

Question 498

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

Answer 498

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

Question 499

Treatments for osteoporosis include:

Answer 499

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

Question 500

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

Answer 500

PTH

Question 501

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

Answer 501

Parathyroid glands

Question 502

Parathyroid hormone (PTH) is secreted by:

Answer 502

chief cells

Question 503

What are the effect of PTH? How?

Answer 503

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

Question 504

How does PTH decrease plasma phosphate?

Answer 504

Increasing renal excretion

Question 505

Describe the renal excretion effects on calcium and phosphate by PTH:

Answer 505

Increases renal excretion for phosphate Decreases renal excretion for calcium

Question 506

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

Answer 506

It causes more synthesis of vitamin D, which in turn causes more intestinal absorption of calcium.

Question 507

When PTH is secreted to to decreased ECF calcium, this leads to:

Answer 507

Hypertrophy of parathyroid gland

Question 508

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

Answer 508

Increase

Question 509

What conditions would lead to hypertrophy of the parathyroid gland:

Answer 509

Chronic cases - pregnancy, rickets, and lactation

Question 510

Chronically, if you hypertrophy the parathyroid gland, it becomes:

Answer 510

even better at secreting PTH

Question 511

Increased ECF concentration of calcium leads to ______ of the parathyroid gland.

Answer 511

decreased activity

Question 512

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

Answer 512

decrease

Question 513

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

Answer 513

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 514

Describe the effect on plasma calcium: Bone resorption:

Answer 514

increases plasma calcium

Question 515

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

Answer 515

increases plasma calcium

Question 516

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

Answer 516

increases plasma calcium

Question 517

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

Answer 517

decreases plasma phosphate

Question 518

Where do we get cholecalciferol (vitamin D3) from:

Answer 518

skin (from sun)

Question 519

In the process of calcitriol synthesis, cholecalciferol is converted to ______ ; by what organ?

Answer 519

25-hydroxycholecalciferol ; liver

Question 520

In the process of calcitriol synthesis, 25-hydroxycholecalciferol is converted to _____; by what organ?

Answer 520

1-25 dihydroxycholecalciferol (Calcitriol); kidney

Question 521

What tells the kidney to do the conversion of 25-hydroxycholecalciferol to the active form?

Answer 521

parathyroid hormone

Question 522

Where is the main effect of calcitriol?

Answer 522

Intestines - absorption of calcium and phosphate from diet

Question 523

Where can calciferol act although not the main effect?

Answer 523

Kidneys (reduced excretion of calcium and phosphate); Bones (indirectly causes bone deposition)

Question 524

Vitamin D3 can be stored in the liver for:

Answer 524

several months

Question 525

Describe the regulation of calcitriol levels:

Answer 525

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

Question 526

Someone with a compromised liver or kidney function may exhibit:

Answer 526

Vitamin D deficiency

Question 527

peptide hormone secreted by parafollicular cells

Answer 527

calcitonin

Question 528

Parafollicular cells reside in the _____ and may also be called _____.

Answer 528

thryoid gland; C-cells

Question 529

Calcitonin is released in response to:

Answer 529

elevated free plasma calcium

Question 530

Calcitonin lowers the level of plasma calcium by decreasing the activity of ____, thus decreasing _____.

Answer 530

decreases the activity of osteoclasts thus decreasing bone resorption

Question 531

Not a major controller of calcium in humans:

Answer 531

calcitonin

Question 532

What two systems does calcitonin act on?

Answer 532

bone and kidneys

Question 533

Excess PTH secretion due to a parathryroid gland tumor:

Answer 533

primary hyperparathyroidism

Question 534

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

Answer 534

osteoclastic activity; cystic bone disease; osteitis fibrosa cystica

Question 535

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

Answer 535

cystic bone disease (osteoitis fibrosa cystica)- primary hyperparathryoidism

Question 536

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

Answer 536

polyuria and calciuria

Question 537

What happens to phosphate levels and why in patients with primary hyperparathyroidism:

Answer 537

low phosphate due to increased renal excretion

Question 538

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

Answer 538

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

Question 539

Primary hyperparathyroidism signs and symptoms include:

Answer 539

Stones, Bones, abdominal groans, and psychic moans

Question 540

Describe the stone component to primary hyperparathyroidism:

Answer 540

1. renal stones 2. nephrocalcinosis 3. polyuria 4. polydipsia 5. uremia

Question 541

Describe the bones component to primary hyperparathyroidism:

Answer 541

1. cystic bone disease 2. osteomalacia/rickets 3. arthritis

Question 542

Describe the abdominal groans component of primary hyperparathyroidism:

Answer 542

1. constipation 2. indigestions 3. nausea 4. vomiting 5. peptic ulcers 6. pancreatitis

Question 543

Describe the psychic moans component of primary hyperparathyroidism:

Answer 543

1. lethargy/fatigue 2. depression 3. memory loss 4. paranoia 5. personality change 6. confusion, suport, coma

Question 544

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

Answer 544

1. proximal muscle weakness 2. Keratitis 3. conjunctivitis 4. Hypertension 5. itching

Question 545

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

Answer 545

secondary hyperparathyroidism

Question 546

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

Answer 546

1. vitamin D deficiency 2. chronic renal disease- cannot synthesize Vit D3

Question 547

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

Answer 547

osteoporosis

Question 548

Disease that would result from accidental surgical parathyroid gland removal, not common

Answer 548

primary hypoparathyroidism

Question 549

What increases membrane Na+ permeability leading to neuromuscular excitability and muscle spasms

Answer 549

hypocalcemia

Question 550

What the condition name for the wonky ass hand:

Answer 550

carpal spasm

Question 551

How many adrenal glands and where are they located?

Answer 551

2 adrenal glands, located on top of each kidney

Question 552

describe the structure of a adrenal gland?

Answer 552

outer cortex + inner medulla

Question 553

What portion of the adrenal gland is essential for life?

Answer 553

Adrenal cortex

Question 554

The adrenal cortex secretes:

Answer 554

1. corticosteroids 2. mineralcorticoids 3. sex hormones

Question 555

Is the adrenal medulla essential for life?

Answer 555

no

Question 556

The adrenal _____ is a true endocrine organ

Answer 556

cortex

Question 557

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

Answer 557

Secreting epinephrine and norepinephrine in resonse to sympathetic nervous system stimulation

Question 558

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

Answer 558

emergencies

Question 559

The adrenal cortex secretes several hormones that are made from:

Answer 559

cholesterol

Question 560

What are the 3 layers of the adrenal cortex?

Answer 560

Zona glomerulosa Zona fasiculata Zona reticularis

Question 561

The largest zone of the adrenal cortex

Answer 561

fasculata

Question 562

The zona glomerulosa secretes ______ and is regulated by ______.

Answer 562

mineralcorticoids; RAAS

Question 563

RAAS stands for:

Answer 563

Renin-angiotensin-aldosterone system

Question 564

The zona fasciulata secretes _____ and is regulated by _____.

Answer 564

glucocorticoids; HPA (CRH and ACTH)

Question 565

HPA stands for:

Answer 565

hypothalamic-pituitary -adrenal axis

Question 566

The zona reticularis secretes ____ and is regulated by ____.

Answer 566

androgens; HPA

Question 567

The adrenal medulla is related to the ____ and secretes _____.

Answer 567

Sympathetic Nervous System; Catecholamines

Question 568

What type of cells secrete catecholamines?

Answer 568

chromaffin cells

Question 569

Where do the chromaffin cells of the adrenal medulla secrete Epi and NE?

Answer 569

into the blood

Question 570

What are the three tissues involved in the HPA?

Answer 570

Hypothalamus, Pituitary, Adrenal gland

Question 571

Why does the zona glomerulosa secrete so much aldosterone?

Answer 571

Because enzymes involve din the formation of aldosterone from cholesterol are highly expressed in the zona glomerulosa

Question 572

What enzyme is responsible for the conversion of Cortisol to corisone?

Answer 572

11HSD Beta 2

Question 573

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

Answer 573

11HSD Beta 1

Question 574

The reactions that occur for the synthesis of steroid hormones in the adrenal cortex take place in the:

Answer 574

mitochondria or endoplasmic reticulum

Question 575

Describe the activity of cortisone at cortisol receptors

Answer 575

reduced activity

Question 576

Can be used to make testosterone and androgens:

Answer 576

Androstenedione

Question 577

Aldosterone is classified as a:

Answer 577

mineralcorticoid

Question 578

Aldosterone functions in the kidneys to:

Answer 578

1. increased renal reabsorption of Na+ 2. increase renal secretion of K+

Question 579

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

Answer 579

Increase in ECF fluid volume and mean arterial pressure

Question 580

What stimulates aldosterone secretion?

Answer 580

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

Question 581

Aldosterone has effects on:

Answer 581

1. kidney 2. sweat glands 3. salivary glands

Question 582

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

Answer 582

Zona glomerulosa

Question 583

What are the main functions of angiotensin II?

Answer 583

1. vasoconstriction 2. release of aldosterone

Question 584

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

Answer 584

release of aldosterone

Question 585

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

Answer 585

Water retention occurs because where sodium goes water follows

Question 586

The effects of aldosterone on sweat glands is important to:

Answer 586

conserve body salt in hot environments

Question 587

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

Answer 587

conservation of sodium during high rates of salivary secretion

Question 588

In addition to hyperkalemia, _____ causes secretion of aldosterone

Answer 588

angiotensin II

Question 589

Enzyme released by the cells in the kidneys in response to a variety of stimui (example SNS)

Answer 589

Renin

Question 590

Angiotensin converting enzyme (ACE) is produced by the:

Answer 590

endothelium

Question 591

List the steps of RAAS

Answer 591

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

Question 592

Angiotensin II ultimately causes secretion of _____ but also does _____, _____, and _____.

Answer 592

ultimately aldosterone secretion but also ADH secretion, thirst stimulation, and vasoconstriction

Question 593

What do vasconstriction, aldosterone secretion, ADH secretion and thirst stimulation all have in common?

Answer 593

All these work to raise BP

Question 594

In RAAS, the non-active precursor made by the liver and found in the plasma:

Answer 594

angiotensinogen

Question 595

Where is large amounts of ACE found?

Answer 595

In the lungs- COVA

Question 596

A lot of _____ medications target RAAS

Answer 596

HTN

Question 597

How do ACE inhibitors work?

Answer 597

If you inhibit ACE you will make less angiotensin II

Question 598

Primary hyperaldosteronism may also be called:

Answer 598

Conn's Syndrome

Question 599

In primary hyperaldosteronism, where is the problem?

Answer 599

adrenal gland

Question 600

What are the causes of primary hyperaldosteronism?

Answer 600

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

Question 601

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

Answer 601

Low levels of renin

Question 602

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

Answer 602

1. HTN 2. Hypernatremia 3. Hypokalemia 4. Headaches 5. Weakness 6. Fatigue 7. HYPOKALEMIC ALKALOSIS 8. LOW PLASMA RENIN

Question 603

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

Answer 603

Due to so much aldosterone being produced and it strongly negatively feedingback

Question 604

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

Answer 604

Hypokalemic alkalosis

Question 605

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

Answer 605

H+ levels in the ECF

Question 606

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

Answer 606

surgical removal of tumor or most of the adrenal tissue when hyperplasia is present, or a minercorticoid receptor antagonist

Question 607

Caused by decreased bloodflow and pressure in the renal artery, (the kidney thinks BP is low and secretes renin excessively)

Answer 607

Secondary hyperaldosteronism

Question 608

Describe the levels of renin in secondary hyperaldosteronism:

Answer 608

High levels of renin

Question 609

What are causes of secondary hyperaldosteronism?

Answer 609

1. CHF 2. Renal artery stenosis

Question 610

How might CHF lead to secondary hyperaldosteronism?

Answer 610

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

Question 611

How might renal artery stenosis lead to secondary hyperaldosteroneism?

Answer 611

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

Question 612

Signs and symptoms of secondary aldosteronism include:

Answer 612

1. high plasma renin 2. hypernatremia with extracellular volume expansion 3. edema 4. decreased cardiac output 5. similar clinical findings as primary hyperaldosteronism

Question 613

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

Answer 613

Cortisol

Question 614

What hormone is secreted in response to stress?

Answer 614

Cortisol

Question 615

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

Answer 615

glucocorticoid; zona fasiculata

Question 616

More cells in the adrenal cortex make ____ than any other cells because of the size of the zona fasiculata

Answer 616

cortisol

Question 617

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

Answer 617

- heat - cold -hypo/hyperglycemia (not just psychological stress)

Question 618

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 618

suppresses the immune system

Question 619

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

Answer 619

early morning hours; growth hormone

Question 620

Cortisol feedsback and inhibits:

Answer 620

1. ACTH secretion from AP 2. CRH secretion from hypothalamus

Question 621

Describe what type of feedback is seen through cortisol:

Answer 621

Long loop

Question 622

What are the 4 main actions of cortisol?

Answer 622

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

Question 623

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

Answer 623

Stabilizing lysosomes

Question 624

Why are other hormones secreted when ACTH is secreted?

Answer 624

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

Question 625

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

Answer 625

Proopiomelanocortin (POMC)

Question 626

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

Answer 626

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

Question 627

A clinical sign of elevated ACTH pathologically is:

Answer 627

increased skin pigmentation (from melanocytes)

Question 628

What is a byproduct of ACTH production?

Answer 628

MSH

Question 629

Cortisol has a similar affinity for the ____ receptor as ____.

Answer 629

mineralcorticoid receptor (MR) as aldosterone

Question 630

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

Answer 630

Cortisol

Question 631

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

Answer 631

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

Question 632

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

Answer 632

cortisone; cortisol

Question 633

A genetic deficiency in the 11B2HSD receptor leads to the syndrome:

Answer 633

AME (Apparent Mineralocorticoid excess)

Question 634

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

Answer 634

glycerrhetinic acid; 11B2HSD

Question 635

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

Answer 635

Increased sodium reabsorption and increased potassium secretion

Question 636

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

Answer 636

kidneys, salivary glands, sweat glands skin

Question 637

High circulating cortisol levels such as in cushings syndrome can:

Answer 637

Overwhelm the 11HSDB2 enzyme

Question 638

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

Answer 638

High BP

Question 639

Effects of cortisol on metabolism: Stimulation of both ___ and _____ in the liver resulting in _____.

Answer 639

gluconeogenesis; glycogenolysis; increases blood glucose

Question 640

Effects of cortisol on metabolism: ____ action resulting in decreased glucose uptake in the muscle and fat but not the brain or heart.

Answer 640

anti-insulin action

Question 641

Effects of cortisol on metabolism: Makes ___ worse by increasing ___ levels, ____ level, and ____ formation and ____ secretion.

Answer 641

diabetes glucose levels lipid levels ketone body formation insulin secretion

Question 642

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

Answer 642

cortisol and insulin are antagonists

Question 643

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

Answer 643

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

Question 644

Effects of cortisol on metabolism: Inhibits ____ synthesis and increases ____ especially in skeletal muscles.

Answer 644

protein synthesis; proteolysis (provides source of AA for glycoenogenesis)

Question 645

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

Answer 645

muscle weakness thin skin abdominal striae

Question 646

Effects of cortisol on metabolism: promotes ____; and shifts the energy system from utilization of _____ to _____ in times of stress.

Answer 646

lipolysis glucose to fatty acids

Question 647

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

Answer 647

lipid

Question 648

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

Answer 648

cortisol

Question 649

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

Answer 649

circulatory failure; permissive action; catecholamines

Question 650

Lack of cortisol also prevents mobilization of _____ (glucose and free fatty acids) during stress and can result in ____.

Answer 650

energy sources; fatal hypoglycemia

Question 651

Vasoconstriction of blood vessels occurs via:

Answer 651

alpha 1 receptor

Question 652

Describe the effect cortisol has on catecholamines (alpha 1 receptor) on blood vessels

Answer 652

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

Question 653

Why would blood pressure decrease when cortisol levels are low?

Answer 653

The presence of cortisol allows the alpha receptors response to be maximized, so without the maximum response, blood pressure would be lower

Question 654

How does cortisol effect the immune system?

Answer 654

suppresses immune system function

Question 655

What are few ways that cortisol suppresses the immune system:

Answer 655

1. stabilizes the lysosomal membrane 2. opposes inflammation (decrease WBC migration and phagocytosis) 3. suppresses T-Lymphocytes

Question 656

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

Answer 656

Their anti-inflammatory action

Question 657

How can treatment with glucocorticoids cause osteoporosis?

Answer 657

because cortisol stimulates bone resorption via an increase in RANK-L expression by osteoblasts

Question 658

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

Answer 658

osteoblasts and osteocytes

Question 659

The zona reticularis is responsible for the secretion of:

Answer 659

androgens

Question 660

The zona reticularis begins secreting adrenal androgens around the age ____ , peaking around age _____, and then _____ with age.

Answer 660

age 8, age 20, decreasing with age

Question 661

Adrenal androgens secreted by the zona reticularis include:

Answer 661

DHEA/DHEAS Andostenodione Testosterone Estrogens

Question 662

Describe the effects of adrenal androgens in males vs. females:

Answer 662

andrenal androgens have only weak effects in makes but contribute ~50% of active androgens in females

Question 663

Describe the effects of adrenal androgens in females:

Answer 663

growth of pubic hair, axillary hair, and libido

Question 664

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

Answer 664

precocious pseudopuberty

Question 665

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 665

Hypothalamus secreting GRH early puberty NOT due to the hypothalamic-pituitary axis

Question 666

If boys are affected by precocious psuedopuberty brought on by excessive androgen secretion from the adrenal gland, this can cause:

Answer 666

early development of secondary sexual characteristics (under age 8)

Question 667

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

Answer 667

21-hydroxylase deficiency

Question 668

21-hydroxylase deficiency leads to an overproduction of:

Answer 668

androgens (DHEA, DHEAS, Androstenedione)

Question 669

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

Answer 669

virilization and and precocious pseudopuberty in females

Question 670

Precocious psuedopuberty:

Answer 670

early puberty not caused by HPA secreting GRH and instead due to adrenal androgens in excess

Question 671

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

Answer 671

aldosterone and cortisol aldosterone and cortisol androgen precursors (DHEA, DHEAS, Androstenedione)

Question 672

Androstenedione is a precursor to:

Answer 672

testosterone, 5-dihydrotestosterone, and estrogens

Question 673

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

Answer 673

greatest effect

Question 674

Why does the precursor androstenedione have the greatest affect (compared to DHEA and DHEAS)?

Answer 674

because it is more readily converted peripherally to testosterone and estrogens

Question 675

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

Answer 675

aldosterone or cortisol

Question 676

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

Answer 676

ovarian tumors

Question 677

Virilizing adrenal tumors are ___, and virilization is usually due to _____.

Answer 677

rare; hypersecretion of adrenal androgens

Question 678

List some signs and symptoms of virilizations:

Answer 678

Male pattern baldness, male musculature, clitoromegaly, increased libido, rapid linear growth with advanced bone age

Question 679

Primary adrenal insufficiency:

Answer 679

Addison's Disease

Question 680

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

Answer 680

adrenal cortex

Question 681

In about 80% of Addison's cases, atrophy occurs due to ______ of all cortical zones

Answer 681

autoimmune destruction

Question 682

Describe the level of ACTH in Addison's dx

Answer 682

High ACTH

Question 683

Describe the levels of corticosteroid production in Addisons disease:

Answer 683

Low corticosteroids

Question 684

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

Answer 684

glucocorticoid, mineralcorticoid and adrogen secretion

Question 685

Secondary adrenal insufficiency is due to low levels of:

Answer 685

ACTH

Question 686

IF the pituitary gland is unable to secrete enough ACTH this would result in:

Answer 686

low cortisol production (secondary adrenal insufficiency)

Question 687

Often latrogenic due to abrupt cessation of steroid therapy:

Answer 687

secondary adrenal insufficiency

Question 688

What is affected in primary adrenal insufficiency that is not affected in secondary adrenal insufficiency?

Answer 688

mineralcorticoid secretion

Question 689

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

Answer 689

Both- both have lack of cortisol production primary only Both- Addisons has loss of androgens; and then secondary has low ACTH leading to low androgen production

Question 690

Two important symptoms of glucocorticoid deficiency include:

Answer 690

hypoglycemia because normally raises blood glucose Low BP due to the lack of alpha 1 receptor permissive effect

Question 691

Hyperpigmentation in primary adrenal insufficiency is due to excess of:

Answer 691

POMC-

Question 692

Cushings Disease is a _____ disorder characterized by ______. Cushings syndrome is a _____ disorder characterized by _____.

Answer 692

secondary- occurs due to brain- High ACTH primary- occurs due to adrenal cortex- low ACTH

Question 693

Both cushings disease and syndrome is characterized by:

Answer 693

high cortisol levels

Question 694

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 694

1. disease 2. syndrome 3. syndrome 4. disease 5. disease 6. syndrome

Question 695

To distinguish between cushings disease and syndrome, what hormone level would you look at?

Answer 695

ACTH

Question 696

Conn's syndromes is an issue with ______ Cushings syndrome is an issue with ____ Pheochromocytoma is an issue with ____

Answer 696

mineralcorticoids glucocorticoids catecholamines

Question 697

Sudden release of hormones causing sudden "attack" due to chromaffin cell tumor in the adrenal medulla resulting in excessive secretion of EPI and NE

Answer 697

Pheochromocytoma

Question 698

What cells are involved in pheochromocytomas?

Answer 698

chromaffin cells

Question 699

Can be characterized by an exaggerated sympathetic response:

Answer 699

Pheochromocytoma

Question 700

What hormones are inovled in pheochromocytoma?

Answer 700

Epi and NE

Question 701

Entire length of thick filament (some overlapping thin filament)

Answer 701

A-band

Question 702

Includes ONLY thin filaments:

Answer 702

I-band

Question 703

ONLY thick filaments:

Answer 703

H-zone

Question 704

Where thin filaments are anchored:

Answer 704

Z-line

Question 705

Links the central regions of thick filaments:

Answer 705

M-line

Question 706

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

Answer 706

Increases

Question 707

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

Answer 707

Decreases

Question 708

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

Answer 708

THE A-BAND DOES NOT CHANGE IN LENGTH

Question 709

Why does the A- band not change length?

Answer 709

Its the length of the thick filament

Question 710

Functional unit of skeletal muscle:

Answer 710

sarcomere

Question 711

The thin filament is composed of what 3 elements?

Answer 711

actin, tropomysin and torponin

Question 712

What type of actin molecules make up the active site in which myosin binds?

Answer 712

G-actin

Question 713

What all does troponin bind?

Answer 713

actin, tropomoysin and calcium

Question 714

Troponin has 3 globular proteins:

Answer 714

T, C and I

Question 715

The C globular protein of troponin binds to:

Answer 715

calcium

Question 716

The thick filament is composed of:

Answer 716

Myosin

Question 717

The myosin filament has multiple cross-bridges where heads can bind to the:

Answer 717

G-actin molecule

Question 718

Dark band:

Answer 718

A-band

Question 719

Light band:

Answer 719

I band

Question 720

In muscle, function as an ATPase enzyme:

Answer 720

myosin

Question 721

When myosin binds to ATP, what happens?

Answer 721

Hydrolyzes the ATP

Question 722

What regulate when contracton can happen?

Answer 722

Troponin and Tropomyosin

Question 723

Protein that connects thin filaments to glycoproteins in the sarcolemma

Answer 723

Dystrophin

Question 724

Provides scaffolding for sarcomeres:

Answer 724

Dystrophin-glycoprotein complex

Question 725

What is the difference between Duchenne's and Becker's muscular dystrophy?

Answer 725

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

Question 726

List some types of muscular dystrophies:

Answer 726

Duchenne, Beckers, Myotronic, Oclulopharyngeal, and limb girdle