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BMS 460 Exam #4 > Exam 4 Practice Questions > Flashcards

Exam 4 Practice Questions Flashcards

1
Q

Hypothalamic-pituitary-adrenal axis hormones released at nerve terminals:

A
  1. Vasopressin (ADH)
  2. Oxytocin.
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2
Q

What is the target tissue of vasopresssin?

A

Kidney and vascular tissue.

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3
Q

What is the target tissue of oxytocin?

A

Mammary gland and uterus.

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4
Q

Vasopressin and oxytocin are released from the _________ _________, at the ______ ________.

A
  1. Posterior pituitary.
  2. Nerve terminals.
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5
Q

Hormones released from the anterior pituitary:

A
  1. Growth hormone. (GH)
  2. Prolactin (PRL)
  3. Thyrotropin (TSH).
  4. Follitropin (FSH).
  5. Luteotropin (LH).
  6. Corticotropin (ACTH).
  7. Melanocyte stimulating hormone. (MSH).
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6
Q

Hormones released from the anterior pituitary gland are released into the __________.

A

Blood.

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7
Q

Paraventricular nuclei (PVN) primarily secrete _____________.

A

Oxytocin.

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8
Q

Supraoptic neuclei (SON) primarily secretes _____________________, also called ______________________.

A
  1. Anti-diuretic hormone (ADH).
  2. Arginine vasopressin.
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9
Q

What is it called when oxytocin and vasopressin accumulate in axon dilations?

A

Herring bodies.

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10
Q

Oxytocin and vasopressin are transported along the _______ together, via the carrier protein _________.

A
  1. Axons.
  2. Neurophysin.
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11
Q

What is the hypothalamic-hypophyseal portal system?

A

Blood flow between the hypothalamus to the anterior pituitary, that transports hormones.

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12
Q

What is the hypothalamic-hypophyseal tract?

A

A nervous tract between the paraventircular nuclei (PVN) and supraoptic nuclei (SON), to the herring body, that stimulates release of hormones into the blood at the posterior pituitary.

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13
Q

Of GnRH, LH, and FSH, which hormone will start the pulsatile wave of release?

A

GnRH - gonadotropin releasing hormone. This makes sense because LH and FSH are both gonadotropins, that need GnRH to stimulate their release.

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14
Q

True or false: Hormone release is hgihly regulated by a intricate system of negative feedback controls, but does not utilize positive feedback mechanism.

A

FALSE - Hormone release can have positive and negative feedback.

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15
Q

What are the functions of oxytocin?

A
  1. Allows people to experience love and trust.
  2. Can be used for many other things - such as muscle maintenance and repair.
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16
Q

A mutation in the oxytocin receptor may cause:

A

An inability to trust people - single forever.

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17
Q

In normal function, what occurs when ADH binds to vasopressin II receptor?

A
  1. cAMP-mediated translocation of aquaporin-2 to the apical surface of the cell.
  2. Subsequent increase in water permeability.
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18
Q

If there is an abscence of ADH, and water cannot be reabsorbed due to a lack of aquaporins on the apical cell surface, what will occur?

A
  1. Hyperosmality.
  2. Hypernatremia - high plasma Na+ conc.
  3. Polyuria - excessive urination.
  4. Polydipsia - Increased thirst.
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19
Q

How does alcohol inhibit ADH?

A
  1. Alcohol will inhibit the release of ADH from the supraoptic nuclei (SON).
  2. Alcohol acts as an antagonist for ADH in the kidneys, preventing aquaporins from binding to the collecting ducts.
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20
Q

During pregancy, the placenta will secrete _______________, causing breakdown of ______, resulting in inability to reabsorb H2O.

A
  1. Vasopressinase.
  2. ADH/vasopressin.
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21
Q

SIADH stands for:

A

Syndrome of Inappropriate ADH secretion.

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22
Q

What condition is considered to be the opposite of diabetes insipidus?

A

SIADH

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23
Q

Diabetes insipidus is caused by:

A

A lack of ADH, causing decreased ability to reabsorb water.

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24
Q

In SIADH, patients will have abnormally _____ levels of ___________.

A
  1. High.
  2. Vasopressin/ADH.
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25
Q

In SIADH, what occurs due to high levels of ADH?

A
  1. Very highly urine osmolatlity.
  2. Kidneys salvage inappropriately lareg volumes of H2O.
  3. Blood becomes hypo-osmolar.
  4. Plasma Na+ drops (hyponatremia).
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26
Q

What are the 2 mechanism by which hyponaturemia occurs?

A
  1. Dilution of plasma.
  2. Increased excretion of sodium by the kidneys.
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27
Q

Growth hormone induces growth via ____________ _________ ________, produced by ______________.

A
  1. Insulin-like growth factor-1 (IGF-1).
  2. Hepatocytes.
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28
Q

What stimulates the release of growth hormone from acidophils?

A

GHRH - Growth hormone-releasing hormone.

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29
Q

What two thing may inhibit the release of growth hormone?

A
  1. Somatostatin.
  2. High blood glucose.
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30
Q

True or false: IGF-1 stimulates growth of long bones by stimulating hyperplasia of chondrocytes at the epiphyseal plate.

A

TRUE.

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31
Q

What is the most common cause of hypersecretion of growth hormone?

A

An adenoma of the anterior hypophysis AKA anterior pituitary.

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32
Q

What are the two most common consequences of hypersecretion of growth hormone?

A
  1. Gigantism in children.
  2. Acromegaly in adults.
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33
Q

True or false: A mutation in the acidophil-interacting protein is a predisposing factor to hypersecretion of growth hormone.

A

FALSE: A mutation in the aryl hydrocarbon-interacting protein is a predisposing factor to hypersecretion of growth hormone.

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34
Q

________ ________ has an acute anti-insulin metabolic effect and chronic growth-promoting effects.

A

Growth hormone.

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35
Q

What is the mechanism of the acute anti-insulin effects of growth hormone?

A

Binding of growth factor to a tyrosine kinase receptor on the target tissue - causing downstream effects.

Antagonizes the hepatic and peripheral effects of insulin on glucose metabolism, as a defense against hypoglycemia.

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36
Q

What is the major source of IGF-1 in the circulation?

A

The liver.

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37
Q

What happens to IGF-1 as it travels through the blood?

A

IGF-1 travels bound to IGF-binding protein.

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38
Q

What happens in the bone from growth hormone?

A

Growth hormone, parathyroid hormone, and estrogen all stimulate further release fo IGF-1.

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39
Q

A drop in serum levels of IGF-1 or glucose stimulates:

A

Release of growth hormone, via GHRH.

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40
Q

Function of IGF-1:

A

Stimulates the growth of long bones by stimulating the hypertrophy of chondrocytes at the epiphyseal plates.

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41
Q

In endochondral ossification, the growth in length of the long bones depends on what?

A

Interstitial growth of the epiphyseal growth plates.

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42
Q

What are the epiphyseal growth plates made of?

A

Hyaline cartilage.

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43
Q

In endochondral ossification, the _________ ____________ _________ forms as a result of vascularization of the bone collar, and _____________ of the diaphyseal chondrocytes.

A
  1. Primary ossification center.
  2. Hypertrophy.
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44
Q

Explain the mechanism by which the epiphyseal growth plates form:

A
  1. Blood vessels enter the newly formed medullary cavity of the bone.
  2. Vessels grow toward either epiphyseal ends of the bone.
  3. Subsequent formation of the epiphyseal growth plates.
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45
Q

True or false: In adults, the bones reach maximum length and width, so the epiphyseal growth plates become ossified - forming the epiphyseal line.

A

TRUE!

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46
Q

__________ zone of the bone: Primitive hyaline cartilage responsible for growth in length of the long bones.

A

Reserve zone.

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47
Q

___________ zone of the bone: Proliferating chondrocytes line up as vertical and parallel columns of cells.

A

Proliferating zone.

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48
Q

____________ zone of the bone: Apoptosis of chondrocytes and calcification of the matrix occurs here.

A

Hypertrophic zone.

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49
Q

_____________ zone of the bone: Blood vessels penetrate the calcified septa, carrying osteoprogenitor cells with them.

A

Vascular invasion zone.

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50
Q

Layers of the periosteum:

A
  1. Fibrous layer - Outer layer, with fibroblasts and dense irregular C.T.
  2. Osterogenic layer - inner layer, contains progenitor cells that develop into osteoblasts.
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51
Q

What are the four major zones of endochondral ossification?

A
  1. Reserve zone.
  2. Proliferative zone.
  3. Hypertrophic zone.
  4. Vascular invasion zone.
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52
Q

What is the primary stimulator of chondrocyte activity and bone growth?

A

IGF-1

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53
Q

Other than IGF-1, what can stimulate chondrocytes and bone growth?

A
  1. Insulin.
  2. Thyroid hormones.
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54
Q

_____ _________ influence a steep amount of bone growth in adolescence.

A

Sex Steroids - by stimulating secretion of GH and IGF-1.

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55
Q

Sex steroids stimulate:

A

Growth promotion via secretion of GH and IGF-1.

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56
Q

While sex hormones can stimulate bone growth, they can also stop bone growth by:

A

inducing ossification of the epiphyseal plates - epiphyseal closure.

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57
Q

Indian Hedgehog Homolog (IHH) protein regulates:

A

Growth of epiphyseal plate hyaline cartilage.

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58
Q

Indian Hedgehog Homolog (IHH) proteins are secreted by:

A

Proliferating chondrocytes.

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59
Q

True or false: IHH inhibits the secretion of parathyroid-related peptide (PTH-rP) by the chondrogenic layer of the perchondrium - effectively regulating epiphyseal plate growth.

A

FALSE - IHH stimulates the secretion of parathyroid-related protein (PTH-rP) by the chondrogenic layer of the perichondrium - effectively regulating epiphyseal plate growth.

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60
Q

What is the function of Parathyroid-related peptide (PTH-rP)?

A

parathyroid-related peptide stimulates chondrocyte proliferation and delay hypertrophy - maintaining the amount of proliferating chondrocytes.

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61
Q

How do we balance between proliferating anf hypertrophy of chondrocytes?

A

Feedback loop between IHH and PTH-rP.

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62
Q

What condition in mice will a lack of IHH protein expression result in?

A

Dwarfism and a lack of endochondral ossification.

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63
Q

Bone growth for ______ of a bone requires an osteoclastic ______, followed by a chondrocyte ______.

A
  1. Length.
  2. Chase.
  3. Run
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64
Q

Explain the steps of growing the length of a bone:

A
  1. The ossification front invades and destroys chondrocytes - as it passes thru the area.
  2. Calcification of the cartilage matrix occurs, surrounding hypertrophic chondrocytes.
  3. Proliferating chondrocytes in front from the ossification front increase length of the cartilage.
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65
Q

Where do osteoclasts come from, and what is their function?

A
  1. Osteoclasts are derived from monocytes.
  2. Osteoclasts enlarge the bone marrow.
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66
Q

Cbfa1/Runx2 stimulates what?

A

The transition of mature chondrocytes to hypertrophic chondrocytes.

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67
Q

What inhibits the transition of mature chondrocytes into hypertrophic chondrocytes?

A

Sox9.

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68
Q

Where do osteoprogenitor cells come from, and what is their function?

A
  1. Derived from the perivascular mesenchyme.
  2. Go to the primary ossification center to generate osteoblasts.
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69
Q

Function of an osteoblast:

A

To deposit osteoid along the calcified cartilage of the bone, this osteoid will become calcified. They travel with the ossification front.

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70
Q

_________ chase and invade the zone of bone that was previously occupied by __________.

A
  1. Osteoclasts.
  2. Chondrocytes.
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71
Q

True or false: As the bone grows in length, new layers form on the outer portions of the diaphysis via appositional growth.

A

TRUE!

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72
Q

Ossified bone, that has undergone initial formation via endochondral or intramembranous ossification, can only grow by:

A

Appositional growth.

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73
Q

Cycles of appositional deposition and resorption will result in:

A

Increase in bone width, diameter, and thickness.

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74
Q

What will happen to the marrow cavity during appositional cycles of bone deposition and resorption?

A

The marrow cavity enlarges by removal of bone at the endosteal surface.

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75
Q

Periosteum:

A

A membrane that covers the outer surface of all bones, except at the joint of long bones.

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76
Q

Endosteum:

A

A membrane that lines the inner surface of all bones.

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77
Q

New Haversian system bone is added _________ the __________ by its osteogenic layer.

A
  1. Beneath.
  2. Periosteum.
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78
Q

How will ossification present when IGF-1 is absent?

A

There will be a massive reduction in the width of the hypertrophic zone, causing a decrease in longitudinal bone growth.

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79
Q

_________ ________ AKA ________-_______ ________ Is an autosomal recessive disorder that is caused by an insensitivity to growth hormone (GH).

A
  1. Laron syndrome.
  2. Laron-type dwarfism.
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80
Q

True or false: Laron-type dwarfism is associated with mutations in the gene for the IGF receptor.

A

FALSE: Laron-type dwarfism is associated with a mutation in the gene for the GH receptor.

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81
Q

Which condition will present with very low levels of IGF-1 and its carrier protein - IGF-binding protein 3?

A

Laron syndrome.

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82
Q

Clinical manifestations of Laron Syndrome?

A
  1. Short stature.
  2. Resistance to diabetes and cancer.
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83
Q

_______ _______ - there will be a shortened epiphyseal growth plate.

A

Laron syndrome.

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84
Q

What is the most common disease of the growth plate, and a major cause for dwarfism?

A

Achondroplasia.

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85
Q

_______________ is an autosomal dominant disorder, where homozygous cases are fatal.

A

Achondroplasia.

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86
Q

What pathological factor causes achondroplasia.

A

A mutation in the fibroblast growth factor receptor 3 gene, causing impaired proliferation of cartilage at the growth plate and preventing endochondral ossification.

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87
Q

In which condition, does the likelihood of the etiological mutation increase with paternal (dad) age?

A

Achondroplasia.

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88
Q

Clinical manifestations of achondroplasia include normal sized of enlarged ________ _______, shortened ______ and _____, skeletal abnormalties, and normal levels of ________ and ______.

A
  1. vertebral column.
  2. Arms and legs.
  3. Growth hormone (GH) and IGF-1.
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89
Q

True or false: Achondroplasia is a disease that is caused by defect in paracrine cell signalling.

A

TRUE.

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90
Q

In achondroplasia, there is a _________ in the proliferation of chondrocytes in the growth plate.

A

Reduction.

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91
Q

In achondroplasia, which receptor is in a constant state of activation, limiting growth?

A

FGFR3

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92
Q

In a healthy individual, the FGFR3 receptor will:

A

inhibit cartilage proliferation, in appropriate amounts.

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93
Q

True or false: In achondroplasia, both longitudinal and appositional growth are disrupted.

A

FALSE - Only longitudinal growth is. Appositional growth will be normal, and bones will have a normal thickness with a shortened length.

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94
Q

What is the normal pattern of growth hormone (GH) secretion?

A

GH is released into the blood in pulses throughout the 24 hour sleep-wake cycle, with peak secretion happening during the 1st two hours of sleep.

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95
Q

When there is a growth hormone (GH) secreting adenoma on the pituitary gland, what happens to GH release?

A

GH release will not have a pulsatile pattern, and will secrete high levels of GH at all hours.

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96
Q

What is the major consequence of a GH secreting adenoma on the pituitary gland, in children.

A

Gigantism.

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97
Q

What is the major consequence of a GH secreting adenoma in the anterior pituitary gland in adults?

A

Acromegaly.

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98
Q

In a glucose GH test, patients with somatotropic adenomas will show:

A

GH levels that are not suppressed by glucose consumption, and may even rise. In this case IGF-1 can be measured instead of GH.

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99
Q

In a healthy individual, the glucose GH test will show:

A

An hour after the patient has eaten glucose, there will be a suppression of GH levels to 2 ug/L or less.

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100
Q

What type of tumor is often associated with excess secretion of GH?

A

Functional somatotroph adenomas.

101
Q

Pre-pubertal GH tumors to the pituitary gland, may impair:

A

gonadotrophs and epiphyseal plates will continue to grow abnormally.

102
Q

True or false: Nonfunctional pituitary adenomas do not cause any distortion to anatomy.

A

FALSE - Nonfunctional pituitary adenomas distort overlying brain tissue.

103
Q

Excess GH in adults causes ___________.

A

Acromegaly.

104
Q

Excess GH in children causes ___________.

A

Gigantism.

105
Q

Gigantism will affect which tissues?

A
  1. Cause linear and periosteal growth of long bones.
  2. Cartilage, membranous bones, and soft tissues.
106
Q

What disease is due to post-pubertal GH excess?

A

Acromegaly.

107
Q

Acromegaly will affect which tissues?

A

Long bones do not grow in length, but cartilage and membranous bones grow abnormally, causing soft tissues to become enlarged.

108
Q

What will the labs of someone with acromegaly present?

A
  1. Increased GH.
  2. Increased IGF-1.
  3. Increased insulin.
  4. Increased calcium and phosphorus ions.
  5. Increased glucose.
  6. Abnormal (increased or decrease) ACTH.
109
Q

Which hormone regulates the plasma concentration of free calcium ions?

A

Parathyroid hormone (PTH)

110
Q

Functions of calcium:

A
  1. Enzyme activation/inactivation.
  2. Intracellular second messenger.
  3. Exocytosis.
  4. Nerve conduction.
  5. Muscle contraction.
  6. Structural integrity of the bone.
111
Q

True or false: Since parathyroid hormone regulates the concentration of free calcium ions, it will also regulate enzyme activation/inactivation and structural integrity of the bone.

A

TRUE!

112
Q

99% of total body calcium is found in the _________.

A

Bones

113
Q

Explain how parathyroid hormone increases calcium ion influx into the plasma:

A
  1. Directly - by stimulating bone and kidneys to increase influx into plasma.
  2. Indirectly - Increases absorption from the gut.
114
Q

How does parathyroid hormone decrease the concentration of phosphate in the plasma?

A

By inhibiting the renal tubular reabsorption of phosphate, increasing its excretion in urine.

115
Q

Location of the parathyroid glands:

A

Posterior surface of the thyroid, between the thyroid capsule and cervical C.T.

May also be found in the mediastinum or neck.

116
Q

The ______ _______ _______ differentiates into the inferior parathyroid gland and thymus.

A

3rd branchial pouch.

117
Q

The _______ _________ ________ differentiates in to the superior parathyroid glands and the ultimobranchial body.

A

4th Branchial pouches.

118
Q

What are the two cell types of the parathyroid gland, and what is their function?

A
  1. Chief cells - secrete parathyroid hormone.
  2. Oxyphil cells - a transitional form of chief cells.
119
Q

What is DiGeorge Syndrome, and what is it caused by?

A
  1. An absence of the parathyroid glands or thymus - associated with hypocalcemia and birth defects.
  2. Is caused by the deletion of a piece of chromosome 22.
120
Q

Which disease is caused by a “catch-22”

A

DiGeorhe Syndrome (velo-cardio-facial syndrome) - causes by deletion of a portion of chromosome 22.

121
Q

In which condition, are infections common in children due to problems with T-cell mediated response, because of a loss of the thymus?

A

DiGeorge Syndrome (velo-cardio-facial-syndrome)

122
Q

What is a major consequence of thymus loss or hypoplasia?

A

A loss of T-cell maturation, impairing T-cell mediated immune responses.

123
Q

__________ cells: Contain an abundance of mitochondria, which make the cell acidophillic staining in H&E. Additionally, does not have rough ER or golgi apparatus.

A

Oxyphil cells.

124
Q

True or false: Chief cells are responsible for PTH secretion, while oxyphil cells have no relevant secretions.

A

TRUE!

125
Q

_____________________ is activated by a reduction in serum calcium, and causes subsequent increase in PTH secretion to increase serum calcium.

A

Ca2+-sensing receptor (CaSR)

126
Q

Pre-pro-parathyroid hormone is a precursor to the parathyroid hormone, that is synthesized in the:

A

Rough endoplasmic reticulum of chief cells.

127
Q

When extracellular concentrations of calcium ions is _______, PTH synthesis will be ________.

A
  1. low.
  2. Increased.
128
Q

What will be inhibited by an increase in the concentration of extracellular calcium ions?

A

parathyroid hormone synthesis and release.

129
Q

When calcium binds to CASR, it will cause inhibition of ________________ and stimulate ____________________ action.

A
  1. Adenyl cyclase.
  2. phospholipase C (PLC)
130
Q

When calcium binds to CASR, what will be the end responses?

A
  1. Suppression of PTH gene expression.
  2. Acceleration of intracellular degradation of PTH.
  3. Inhibition of PTH release.
130
Q
A
131
Q

What are the two methods to suppress PTH gene expression and synthesis?

A
  1. Calcium binding to CaSR.
  2. 1,25 - dihydroxy vitamin D by causing up-regulation of CaSR gene expression and directly inhibiting PTH gene.
132
Q

How does activation of phospholipase c (PLC) cause inhibition of release of granules containing parathyroid hormone?

A
  1. Activation of PLC causes the production of secondary messengers (IP3, DAG, PIP2)
  2. IP3 increases levels of cytosolic calcium - from intracellular storage.
  3. DAG stimulates protein kinase C (PKC) activity.
  4. inhibited release of granules containing parathyroid hormone.
133
Q

A high concentration of _________ __________ will inhibit the fusion of vesicles containing PTH.

A

cytosolic calcium

134
Q

What kind of mutation will result in the prevention of chief cells to sense an increase in serum calcium?

A

Inactivating mutations of one allele of CaSR.

135
Q

True or false: If chief cells are unable to sense an increase in serum calcium levels, there will be a lack of parathyroid hormone.

A

FALSE - there will be an excess of PTH.

136
Q

Familial benign hypercalcemia - cause, effects, and treatment:

A
  1. Cause: Inactivating mutation of alleles of the CaSR gene.
  2. Effects: Skeletal changes + unremitting hyperparathyroidism.
  3. Treatment: Need to do a parathyroidectomy in newborns with this condition.
137
Q

What will occur if chief cells assume that serum calcium levels are high, when it is not? What is it caused by?

A
  1. A decrease in parathyroid hormone production.
  2. Can cause hypocalcemia, with seizures.
  3. Treatment: Supplemental PTH.
  4. Cause: An activating mutation in the CaSR gene.
138
Q

True or false: Autoimmune diseases that effect the calcium-sensing receptor (CaSR) can either inactivate CaSR or activate CaSR

A

TRUE.

139
Q

Increased PTH will cause:

A

Increased serum calcium.

140
Q

Decreased serum calcium vs increased serum calcium:

A
  1. Decreased serum calcium: No activation of CASR, leading to PTH release, which causing increase in serum calcium.
  2. Increased serum calcium: Calcium binds CaSR, which inhibits PTH release, causing a decrease in serum calcium.
141
Q

Action of PTH in the bones:

A

Promotes demineralization and calcium release by acting on stromal osteoblasts in the bone marrow - causing a net resorption.

142
Q

Action of PTH in the kidneys:

A
  1. Stimulates reabsorption of calcium in the proximal tubules of the renal cortex in the distal nephron.
  2. Stimulates synthesis 1,25-dihydroxy-vitamin D3 (activated calcitriol).
143
Q

Activated 1,25-dihydroxy-vitamin D3 (calcitriol) will cause what to happen?

A

Facilitates increased Ca2+ absorption in the intestinal mucosa.

144
Q

PTH causes calcium re-absorption in which organs?

A
  1. Bone marrow.
  2. Kidneys.
  3. Intestines.
145
Q

Plasma vitamin D will be converted to 25-OH D via ______________ in the kidney, and then further converted to 1,25 OH2D via ______________ in the kidneys.

A
  1. 25-hydroxylase.
  2. 1-hydroxylase.
146
Q

Plasma 1,25-OH2D is the form of calcium that is:

A

Reabsorbed as calcium and phosphate from the GI tract into the blood.

147
Q

Another name for calcitriol?

A

1,25-dihydroxycholecalciferol.

148
Q

True or false: Calcitriol causes reabsorption of calcium in the kidneys, intestines, and bones. While 1,25-Dihydroxycholecalciferol causes utilization of calcium.

A

FALSE: They are the exact same thing.

149
Q

What will have a negative feedback on the liver, preventing over-action of vitamin D3 when it is too high in concentration?

A

25-Hydroxycholecalciferol.

150
Q

Via PTH both __________ and __________ will be resorpbed from the bones.

A

Calcitriol and cortisol.

151
Q

Via PTH which form of calcium will be reabsorbed by the kidneys?

A

Calcitonin.

152
Q

Via PTH which form of calcium will be reabsorbed from the small intestines?

A

Calcitriol.

153
Q

What is calcium homeostasis?

A

Calcium balance in the body - total intake and output.

154
Q

What are the 4 stages of bone remodeling? What is the general goal?

A
  1. Activation.
  2. Resorption.
  3. Reversal.
  4. Formation.

Replacement of old bone with newly formed bone, by a resorption + production sequence.

155
Q

In bone remodeling osteoclasts do ____________, while osteoblasts _______________.

A
  1. Resorption.
  2. Reversal.
156
Q

True or false: Bone remodeling is a continuous process throughout life, occuring at random location.

A

True!

157
Q

What is function of Bone remodeling?

A

To create an optimum bone strength by repairing microscopic damage and maintain calcium homeostasis.

158
Q

________-__________: Microscopic damage to bone tissue.

A

Micro-cracking.

159
Q

Activation stage of Bone remodeling:

A

Osteoclast precursors are recruited, and differentiate into osteoclasts. Active osteoclasts will start bone remodeling toward the outer lamella.

160
Q

What are the residuals from remodeling of the osteon called?

A

Interstitial lamellae.

161
Q

Resorption phase of Bone remodeling:

A

More recruitment of osteoclasts occurs, and resorption expands past the original osteon.

162
Q

Reversal stage of Bone remodeling:

A

Osteoblasts Revere the resorption by secreting osteoid. There will be a “cement line” indicates a boundary of new lamella and old lamella. Reversal continues toward the center of the osteon.

163
Q

Formation phase of bone remodeling:

A

Osteoblasts continue laying down new bone, and become trapped within the mineralized bone matrix. This causes osteoblasts to become osteocytes.

164
Q

In which condition is more bone resorbed than produced, due to dysfunction of bone remodeling?

A

Osteoporosis.

165
Q

What allows for communication between osteoblasts and osteoclasts?

A

Hormones, cytokines, growth factors, and signal-transducing molecules.

166
Q

Systemic factors and local cytokines can controlled the coupled process of bone remodeling, these are deposited in the:

A

bone matrix.

167
Q

Osteoprogenitor cells will proliferative and mature into _________________, via ______, ______, _______.

A
  1. Active osteoblasts.
  2. Runx2, Wnt, and bone morphogenic protein (BMP).
168
Q
A
169
Q

Surface osteoblasts are mediators of:

A

Osteoclastogenesis.

170
Q

Step 1 of osteoclastogenesis:

A

A monocyte derived from bone marrow reaches an area of bone formation, and a receptor for M-CSF is expressed on it.

171
Q

Step 2 of osteoclastogenesis:

A

Monocytes becomes a macrophage. M-CSF bind to its receptor on the macrophage, and induces expression of RANK for its ligand RANKL on the surface of osteoblasts.

172
Q

Step 3 of osteoclastogenesis:

A

The osteoblast-expressed transmembrane protein ligan RANKL, binds to the osteoclast RANK receptor. The cell commits to to osteoclastogenesis. The monocyte becomes a multinucleated osteoclast precursor.

173
Q

Step 4 of osteoclastogenesis:

A

A resting (non-functional) osteoclast uncouples from the osteoblast.

174
Q

Step 5 of osteoclastogenesis:

A

The maturation of osteoclasts is complete when the sealing zone and ruffled border appear. Bone resorption can occur.

175
Q

For maturation from a resting osteoclast to a function osteoclast to occur, what must we use?

A

ayb3 (alpha-gamma-beta-3) integrin. Which causes formation of the sealing zone.

176
Q

What mechanism allows an osteoblast to regulate the population of functional osteoclasts?

A

Osteoblasts will present a RANKL decoy protein called osteoprotegerin, which blocks RANKL from binding to RANK - stopping osteoclastogenesis.

177
Q

RANKL receptor is on the ____________, while the RANK ligand is on the ______________.

A
  1. Osteoblast
  2. Osteoclast.
178
Q

True or false: PTH - parathyroid hormone stimulates osteoclastogensis.

A

TRUE: PTH stimulates M-CSF and RANKL expression, in turn stimulating osteoclastogenesis.

179
Q

Which condition will impair the balance between osteoprotegerin and RANK, which allows for osteoclastogenesis to occur?

A

Hypercortisolism.

180
Q

Vitamin D and PTH can both stimulate:

A

Osteoblasts to do secretions that benefit osteoclastogenesis.

181
Q

In the osteoclast, what prevents excessive rise in intracellular pH?

A

A chloride shift.

182
Q

Explain the anatomy of a mature osteoclast:

A
  1. Actin filaments accumulate to form a sealing zone, where the plasma membrane is close to the bone.
  2. Has a ruffled border.
  3. Sealing zone is made up of actin filaments, ayb3 Integrin, and osteopontin.
183
Q

By which mechanism do osteoclasts break down mineralized bone?

A
  1. Carbonic anhydrase II will create H+ ions from CO2 and H2O.
  2. H+ is released into the howship’s lacuna by an H+-ATPase pump to create an acidic environment. (lower than 4.5) - This degrades mineralized tissue.
  3. Cathepsin K is release into Howship’s lacuna to degrade exposed organic material. - This degrades collagen and noncollagenous proteins.
184
Q

Subosteoclastic compartment is another name for:

A

Howship’s lacuna.

185
Q

What will occur due to abnormal function of osteoclasts?

A
  1. Absent bone remodeling.
  2. Can result in Osteopetrosis - where the bone is abnormally brittle and the marrow canal is not developed.
186
Q

Which cell is considered “a one-cell epithelium”?

A

Osteoclasts.

187
Q

What is the cause of osteopetrosis?

A

A mutation in the M-CSF gene, because without M-CSF there cannot be normal osteoclast differentiation.

188
Q

What will occur due to a deficiency in carbonic anhydrase II?

A

Marble bone disease - a variant of osteopetrosis.

189
Q

Symptoms of marble bone disease?

A
  1. Exophthalmos.
  2. Deafness.
  3. Facial paralysis.
  4. Speech impediment.
  5. Small size of medullary canal of the bones.
190
Q

Cancer metastasis to bone is extremely frequent in which types of advanced cancer? Which type of cancer is it less common in?

A
  1. Breast and prostate cancer.
  2. Lung cancer.
191
Q

Describe an osteolytic bone metastases:

A

Activation of excessive osteoclast number and activity.

192
Q

Describe osteoblastic bone metastases:

A

A result of osteoblast activation or excessive bone deposition.

193
Q

List the factors that account for frequent bone metastasis:

A
  1. Tumor cells have humoral factors that stimulate osteoclast formation.
  2. Tumor cells arrive in bone marrow often, cause it is an area with high blood flow.
  3. Tumor cells stimulate neovascularization and promote more tumor growth, causing more release of humoral growth factos, which are locally liberated by osteolysis.
194
Q

What are the consequences of tumor cells causing neovascularization?

A

Further tumor growth, where bone is a site for growth factors they get liberated there, causing bone metastasis.

195
Q

In osteolytic bone disease, metastatic tumor cells release factors that stimulate ______________ _____________ and _________________

A
  1. Osteoclastic.
  2. Recruitment.
  3. Differentiation.
196
Q

What is the step-by-step mechanism of osteolytic bone disease?

A
  1. Metastatic tumor cells release factors that stimulate osteoclastic recruitment and differentiation.
  2. Osteoclasts break down bone unnecessarily.
  3. Bone resorption causing the release of growth factors that stimulate tumor growth.
  4. As the tumor grows, it produces substances that increase osteoclast-mediated bone resorption.
197
Q

What is the step-by-step mechanism of osteoblastic bone disease?

A
  1. Metastatic tumor cells release growth factors that promote the activity of osteoblasts and osteoclasts.
  2. Excessive new bone formation occurs around the tumor cell deposits.
  3. Osteoclastic activity releases growth factors that stimulate tumor cell growth.
  4. Osteoblastic activity releases unidentified osteoblastic growth factors that also stimulate tumor cell growth.
198
Q

Osteosclerosis:

A

When excessive new bone formation occurs around tumor-cell deposits - a consequence of osteoblastic bone disease.

199
Q
A
199
Q

Parathyroid hormone-related peptide (PTHrP) is encoded is encoded by what type of gene?

A

A gene that is completely distinct from the PTH gene.

200
Q

What peptide can cause hypercalcemia in certain malignancies?

A

PTHrP. - Parathyroid hormone related peptide.

201
Q

PTHrP is made in a variety of ________ and __________ tissues, while PTH is only made in the __________ _______.

A
  1. Normal and malignant.
  2. Parathyroid gland.
202
Q

True or false: PTH and PTHrP are encoded by different genes and found in different tissues, but have the same function on the kidney and bones.

A

TRUE.

203
Q

__________ ____________ is a clonal proliferation of neoplastic plasma cells, or their precursors that are committed to plasmacytic differentiation.

A

Multiple myeloma.

204
Q

Multiple myeloma plasma cells will produce pro-osteoclastogenic (induces osteoclastogenesis) cytokines. These include:

A
  1. IL-3
  2. Macrophage inflammatory protein-1 alpha and beta.
  3. Tumor necrosis factor alpha.
205
Q

How does multiple myeloma affect the bones?

A

it forms multiple foci of plasma cell proliferation in the bone.

206
Q

In multiple myeloma, only _____________ bone lesions develop.

A

osteolytic.

207
Q

In most cancers, bone metastasis can have both ___________ and ___________ forms.

A

Osteolytic and osteoblastic.

208
Q

How do multiple myeloma plasma cells inhibit new bone formation?

A

Multiple myeloma cells produce Dickkopf-1 (DKK1) which inhibits beta-catenin-dependant Wnt signalling, ultimately inhibiting osteoblast activity.

209
Q

How do multiple myeloma plasma cells activate osteoclasts?

A

Multiple myeloma plasma cells produce RANKL, which binds to RANK, ultimately activating osteoclast activity.

210
Q

______________: When bone resorption exceeds bone deposition, and bone bone matrix and minerals are lost.

A

Osteoporosis.

211
Q

Which hormone can normally inhibit excess production and action of osteoclasts, while also enhancing osteoblast activity? Preventing excess resorption of bone.

A

Estrogen.

212
Q

A lack of estrogen will cause:

A
  1. Increased osteoclastic activity.
  2. Decreased osteoblastic activity.
  3. Increased resorption of bone.
  4. Decreased formation of new bone.
213
Q

What puts older women at a higher risk of developing osteoporosis?

A

Estrogen deficiency post-menopausal.

214
Q

How does hypercortisolism lead to osteoporosis?

A

An increase in glucocorticoids increases the production of RANKL, and decreases production of osteoprotegerin, ultimately increasing osteoclastogenesis and causing more bone resorption.

215
Q

What is the most common metabolic abnormality of bone?

A

Osteoporosis.

216
Q

In osteoporosis, there will be a loss of bone matrix and minerals, anatomically this will present as:

A
  1. Decreased bone mass and density.
  2. Decreased thickness of the cortical and trabecular bone.
217
Q

Why is osteoporosis more common in women than in men?

A
  1. men have a greater starting bone mass, taking longer to develop osteoporosis.
  2. Postmenopausal decrease of estrogen in women.
218
Q

What falls under primary osteoporosis?

A
  1. Common type.
  2. Idiopathic type in children + young people.
  3. Post-menopausal (mmost common)
  4. Senile type.
219
Q

What causes fall under secondary osteoporosis?

A
  1. Underlying disease - like hypercortisolism or renal disease.
  2. Drugs - heparin.
  3. Hypogonadism - caused by hypopituitarism.
  4. Malnutrition - anorexia.
  5. Space travel - lack of stress on the bones in no gravity.
220
Q

What are preventative measures for osteoporosis?

A
  1. Ca+ and Vitamin D supplements.
  2. No smoking - it inhibits osteoblast activity.
  3. Weight baring activity.
221
Q

Treatments for osteoporosis:

A
  1. Biphosphates - to inhibit bone resorption.
  2. Antibodies against RANKL - Inhibits osteoclastogenesis.
  3. Calcitonin or estrogen supplementation - inhibits osteoclast activity.
222
Q

In __________ __________ __________, normal handling of calcium and phosphate is disrupted, causing osteoporosis and calcifications.

A

Chronic renal disease.

223
Q

What is the primary cause of secondary hyperparathyroidism?

A

End-stage renal disease.

224
Q

In __________ there will be a lack of reabsorption of calcium, causing ___________. This leads to overproduction of ______, ultimately causing differentiation and multiplication of ___________. This is the process by which renal disease leads to osteoporosis.

A
  1. Nephropathy.
  2. Hypocalcemia.
  3. Parathyroid hormone PTH.
  4. Osteoclasts.
225
Q

In failing kidneys, they cannot excrete __________ properly, or convert enough __________ to its active form.

A
  1. Phosphate.
  2. Vitamin D.
226
Q

In which condition does insoluble calcium phosphate form and cause hypocalcemia, leading to excess PTH release, and eventually leading to formation of osteoporosis?

A

End-stage renal disease.

227
Q

True or false: Chronic renal disease —> secondary hyperparathyroidism —-> Osteoporosis.

A

TRUE.

228
Q

Inadequate dietary vitamin D3 or excessive phosphorus in the diet can cause:

A

long-term over stimulation oof the parathyroid glands - AKA nutritional secondary hyperparathyroidism.

229
Q

Bone ossification includes ______, _________, and ___________ of bone.

A

Growth, modeling, and remodeling.

230
Q

Which two bone diseases have a defect in the mineralization of the bone matrix?

A
  1. Rickets.
  2. Osteomalacia.
231
Q

What separates rickets and osteomalacia?

A
  1. Rickets is seen in children.
  2. Osteomalacia is seen in adults.
232
Q

In which type of rickets is it due to a mutation in the receptor for calcitriol.

A

Hereditary vitamin-D resistant rickets.

233
Q

A parathyroid adenoma can cause hyperparathyroidism, this can clinically present as:

A
  1. Broken bones - osteitis fibrosa cystica.
  2. Kidney stones - Nephrolithiasis and nephrocalcinosis.
  3. Depression and seizures.
  4. Gallstones, acute pancreatitis, and peptic ulcers.
234
Q

What is one of the primary consequences of hypoparathyroidism?

A

Hypocalcemia that causes sodium channels to open in cell membranes, leading to spontaneous firing of action potentials causing spasms - this is called hypocalcemic tetany.

235
Q

What is the cause for hypocalcemic tetany?

A

Hypoparathyroidism.

236
Q

What is a developmental cause for hypoparathyroidism?

A

DiGeorge Syndrome - where parathyroid glands and thymus are completely absent.

237
Q

What are the genetic causes for hypoparathyroidism?

A

Activating mutations of CaSR, so chief cells assume serum calcium is elevated when it is not, ultimately decreasing PTH.

238
Q

What is the autoimmune causes for hypoparathyroidism?

A

Targeting antibodies toward CaSR which constantly activates it, decreasing PTH.

239
Q

Accidental removal of the parathyroid glands during a thyroidectomy can cause:

A

Iatrogenic hypoparathyroidism.

240
Q

What cells produce calcitonin? Where are they found?

A

Neural crest-derived parafollicular C-cells, found in the medulla of thyroid gland.

241
Q

An increase in _____________ will cause increased release of calcitonin from C-cells.

A

Serum calcium.

242
Q

True or false: The main function of calcitonin is to inhibit the effects of parathyroid hormone.

A

FALSE - The main function of calcitonin is to antagonize the effects of parathyroid hormone.

243
Q

Calcitonin will decrease ______ ________, and increase _________ _______ ________.

A
  1. Bone resorption.
  2. Renal calcium excretion.
244
Q

What genes and tissues is calcitonin expressed b?

A

By a gene located on chromosome 11p, and is also expressed in the tissues as calcitonin gene-related peptide (CGRP).

245
Q

Calcitonin gene-related peptide (CGRP) is associated with:

A

Neurotransmitter and vasodilator functions, involved in testicular descent.

246
Q

Hyper-calcitoninemia is caused by:

A
  1. Nutritional disorders - High Ca+ causing mineral imbalance.
  2. Osteopetrosis - In the vertebrae and tibia of bull.
  3. Thyroid neoplasia - In humans is medullary thyroid carcinoma, in bulls it is ultimobranchial tumors.
247
Q
A

BMS 460 Exam #4 (2 decks)

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