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Organ Systems > OS II Exam V > Flashcards

OS II Exam V Flashcards

1
Q

Briefly describe cartilage in terms chondrocytes and matrix.

A

Cartilage is made up of chondrocytes and matrix. Chondrocytes can generate matrix. ECM is richly hydrated; many GAG.

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2
Q

What is the perichondrium?

A

CT layer; inner layer differentiates into chondroblasts (growing cartilage cells)

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3
Q

How do hyaline; elastic and fibrous cartilages differ?

A

The elastic has a perichondrium; whereas the fibrous and hyaline cartilage do not. The hyaline is a permanent cartilage usually where joints articulate. Fibrous generally can withstand weight (knee; symphysis etc.)

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4
Q

Why does cartilage cease to grow?

A

Avascularity; immobility of chondrocytes; limited ability of chondrocytes to proliferate.

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5
Q

When and how does cartilage develop?

A

Cartilage begins in the embryo from the mesenchyme; these cells differentiate into chondroblasts. Ends in late teens. TGFbeta converts to chondroblasts.

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6
Q

What is the difference between interstitial and appositional growth?

A

Interstitial-division of chondrocytes within the distensible matrix. During embryogenesis. Appositional-occurs on the surface of cartilage in later stages of development.

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7
Q

What roles does the perichondrium play in support of cartilage?

A

The perichondrium can provide new chondrocytes; but mostly densely CT. Articular cartilage which has no perichondrium and therefore can not regenerate.

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8
Q

What are the major characteristics of bone?

A

Diaphysis; epiphysis; metaphysis; marrow; outer periosteum.

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9
Q

What are the periosteum and endosteum?

A

Periosteum is the outer bone surface contains the osteoprogenitor cells; LIFEBLOOD! Endosteum simple epithelial layer that produces bone progenitor cells.

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10
Q

What makes osteoclasts different from other bone cells?

A

Multinucleated. Get calcium out of bones.

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11
Q

What do osteoclasts secrete?

A

H+ and enzymes

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12
Q

Osteoprogenitor cells

A

Originally differentiate from mesenchymal stem cells. In mature bone; periosteum and endosteum.

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13
Q

Osteoblasts

A

Retains ability to divide or remain dormant. Secrete bone matrix proteins and alkaline phosphatase (promote mineralization). Become osteocytes once enclosed in matrix.

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14
Q

Osteocytes

A

Send processes through canaliculi to adjacent lacunae; responds to mechanical forces; more related to blood calcium.

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15
Q

Bone-lining Cells

A

Derived from osteoblasts; where the bone is quiescent. Maintenance and nutritional support for osteocytes.

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16
Q

Osteoclasts

A

Large; multinucleated cells used to reabsorb bone. Derived from fusion of hemopoietic progenitor cells. High turnover

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17
Q

What are red and yellow marrow?

A

Red marrow consists of blood cells in development; replaced with the yellow marrow (which consists mostly of fat cells)

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18
Q

How does bone marrow supply blood?

A

Blood vessels enter through epiphyseal plate and move down through bone tissue and out through periosteal vein.

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19
Q

What are the differences between compact and spongy bone?

A

Compact bone has highly dense matrix; have osteons. Spongy bone organized into trabeculae; no osteons; precursor to compact bone during development.

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20
Q

Osteons

A

Cylindrical layerong of concentric lamellae enclosing a central canal; often called lamellar.

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21
Q

What are the differences between intramembranous and endochondral ossification in terms of: location in the body?

A

Endochondral ossification tends to happen in long bones. Whereas intramembranous tends to happen for flat bones.

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22
Q

What are the differences between intramembranous and endochondral ossification in terms of: blood vessels?

A

Intramembranous: Woven bone froms with incoming blood vessels. Endochondral: Perichondrium is invaded by blood vessels to become periosteum.

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23
Q

What are the differences between intramembranous and endochondral ossification in terms of: cell types involved?

A

Osteoblasts/cytes with intramembranous and chondroblasts/cytes with endochondral.

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24
Q

What are the differences between intramembranous and endochondral ossification in terms of: the role of cartilage?

A

Intramembranous does not involve cartilage. Whereas; endochondral does involve an initial cartilage model.

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25
Q

What is the epiphyseal plate and its role in bone growth and growth cessation?

A

Site of bone enlargement via interstitial growth. Plate ossifies in late teen years. Cartilage is calcified by HPA.

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26
Q

What hormones are involved in bone growth?

A

GH and IGF

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27
Q

Describe the hypothalamic-pituitary-GH axis.

A

GHRH from hypothalamus stimulates release of GH from anterior pituitary; whereas GHRH SS inhibits it. Alternations creates regular release of GH from ant pit. GH is released into general circulation.

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28
Q

How is GH release regulated?

A

Positively by GHRH from hypothalamus. Negatively by GH and IGF-1

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29
Q

What is IGF-1 and where is it synthesized?

A

Insulin-like Growth Factor from the liver.

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30
Q

Describe the two functions of GH.

A

Growth and maintain Metabolism

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31
Q

How do GH and IGF affect bone growth?

A

GH initiates cell division amon prechondrocytes and IGF increases further replication of chondroblasts.

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32
Q

Describe the effects of GH deficiency and excess.

A

Deficiency: dwarfism Excess: giantism; acromegaly

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33
Q

Describe how bone is remodeled?

A

Absorption and deposition of bone.

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34
Q

What are somites and what happens to them in development?

A

Somites are mesoderm segments; establish early spinal levels. They become sclerotome; dermatome; myotome.

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35
Q

Describe how vertebrae are formed from somites.

A

Fusion of adjacent somites forms the intersegmental vertebrae.

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36
Q

How do bones develop in the limbs?

A

Endochondral ossification via precartilaginous aggreagates and cartilaginous cells that secrete BMP and Ihh.

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37
Q

What mineralizes collagen/cartilage fibers to Ca and PO4?

A

Hydroxyapatite

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38
Q

Which is produced locally; which migrates from the somites?

A

Bone and CT are produced locally. Myotomal cells and dermatomal cells migrate from somites.

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39
Q

What are the two zones in limbs that are responsible for limb development?

A

AER (Apical Ectodermal Ridge) and ZPA (Zone of Polarizing Activity)

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40
Q

What do they do and what are the principal signaling factors involved?

A

AER uses FGF for growth. ZPA uses Shh for pattern

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41
Q

Describe phocomelia in limb development.

A

Absence of proximal segments. E.g. thalidomide. Disruption of FGF.

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42
Q

Describe syndactyly in limb development.

A

Disruption of Shh limiting interdigital apoptosis; often affects digits 3;4; and 5.

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43
Q

What are the different layers of the epidermis and how do they differ?

A

Stratum basale- stem cells that become keratinocytes. Stratum spinosum- form processes (spines) and progress toward surface. Stratum granulosum- develop granules with filaggrin which aggregate keratin. Stratum corneum- cells flatten; lose nuclei and organelles; fill with keratin.

44
Q

What locally produced hormone drives proliferation of skin cells?

A

IGF (by GH)

45
Q

What are the phagocytic cells in the skin called?

A

Langerhan’s cells

46
Q

What is the primary cell type of the skin?

A

Keratinocytes

47
Q

Give a brief overview of Keratinization.

A

Keratin is synthesized in the basal layer and as the cells move up into the spinosum layer. Granules contribute filaggrin which aggregates keratin into bundles.

48
Q

What are some of the functions of keratin?

A

Mechanical support; cytoarchitectural functions; organelle/vesicle distrubution; regulation of signaling pathways.

49
Q

How does the pH gradient in the epidermis affect desquamation of cells?

A

pH deactivates LETKI (inhibitor) which let’s KLK (peptidase) break down the desmosome connections between cells promoting exfoliation

50
Q

Describe the stratum corneum and how it serves as a barrier to external agents and water loss.

A

The stratum corneum is a combination of intercellular lipids and corneocytes. Together they prevent inward assault; and the lipids prevent water loss. Brick and mortar barrier.

51
Q

Describe the lipid layer between corneocytes; how it arises and what it does.

A

Lipids are synthesized and stored in keratinocytes lamellar bodies in spinosum and granulosum and released in the corneum.

52
Q

What types of lipids are secreted by the lamellar bodies in the stratum granulosum?

A

Cholesterol; FFA; but mainly ceramides (sphingolipids)

53
Q

How is hydration maintained in the stratum corneum?

A

Hygroscopic substances absorb and retain water within corneocytes: AA from filaggrin and glycerol from blood (AQP3 transporter)

54
Q

What causes atopic dermatitis?

A

faulty synthesis of ceramides and thus impaired lipid barrrier and water loss with reduction of stratum corneum hydration.

55
Q

What causes contact dermatitis?

A

Disruption of barrier by irritants and allergens -primary event. Followed by sensitization; inflammation; and increased epidermal proliferation and changes in differentiation.

56
Q

What are the pigments that determine skin color?

A

Melanin (reddish-yellow to brown-black); Oxyhemoglobin (pinkness); Keratin (yellow); Carotene (orange-yellow); Bilirubin (yellow-brown)

57
Q

What are molecules that absorb or reflect various frequenceies of light giving them their color?

A

Pigments

58
Q

What is the primary pigment that absorbs UV light?

A

Melanin

59
Q

What are melanocytes?

A

Cells that produce melanin; derived from neural crest cells; have dendritic processes that distribute melanin.

60
Q

How are melanocytes activated by UV light?

A

UV light causes alpha-MSH to be released from keratinocytes. Binding of this hormone at MC-1R stimulates melanocyte proliferation and synthesis of melanin.

61
Q

What are the two types of Melanin?

A

Eumelanin (brown-black) and Phaeomelanin (reddish-yellow)

62
Q

How are keratinocytes pigmented by the melanocytes?

A

Tyrosinase converts tyrosine into dopaquinone forboth melanins. Melanosomes are transferred to keratinocytes along the melanocyte dendrites and phagocytosis of melanocyte tips.

63
Q

What is the difference between light and dark skin?

A

Melanosomes are larger in dark skin and degradation of melanosomes is slower because they are individualized (not clustered in vesicles in light skin)

64
Q

How does melanosomes protect the nucleus from DNA damage?

A

Cap it

65
Q

How does repeated UV exposure tan the skin?

A

Enhances melanocyte activity; more melanin; more melanocytes.

66
Q

What is the function of eumelanin in keratinocytes?

A

Protects skin and DNA from UV damage

67
Q

Describe the impact of UV light on vitamin D synthesis and intestinal calcium absorption.

A

UV light increases the production of vitamin D which increases the amount of active vitamin D which increases absorption of calcium from the intestine.

68
Q

What are the two primary dangers of excess UV exposure on the skin?

A

Cancer and depletion of folate

69
Q

Why is folate photolysis by UV significant?

A

Folate is part of DNA biosynthese; DNA methylation; AA metabolism; and melanin production. Important to rapidly dividing cells; directly relates to reproductive success.

70
Q

Describe the two layers of the dermis and their functions.

A

Papillary layer-site of neurovascular bundles and thermoregulation. Reticular layer-tensile strength

71
Q

What are Langer_s lines?

A

Collagen and elastic fibers form tension lines. (Look similar to muslces)

72
Q

What is the hypodermis?

A

Superficial fascia with skin liganments; contributes to mobility of skin in response to shear and gravitational forces. *fewer in abdomen and buttocks

73
Q

What are skin ligaments?

A

Connect dermis to deep fascia

74
Q

What is the difference between thin and thick skin?

A

Thicks skin has an expanded epidermal-deral interface to resist stress (palm; soles); deep epidermal ridges extend into dermis. Thin skin is relatively flat.

75
Q

Describe the hair follicle.

A

Extension of the epidermis into the hypodermis. Internal root sheath forms channel for heair. Bulb is the bottom of follicle indented by CT dermal paapill. Matrix consists of bulb cells that differentiate into hair cells and the internal root sheath.

76
Q

What are the layers of a hair?

A

Cortex; cuticle; medulla

77
Q

How do hairs grow?

A

Stem cells migrate from the bulge area down to the matrix. Matrix cells prliferate and displace upward. As they move upward they become keratinized. Melanocytes in matrix provide eumelanin or phaeomelanin to pigment hair.

78
Q

What is the source of hair stem cells?

A

The bulb (Stem cell bulge)

79
Q

Differentiate the three stages of hair growth.

A

Anagen-period of growth; 4 years. Catagen-growth stops; 1-2 weeks. Telogen- rest period; 5-6 weeks; hair shaft is shed.

80
Q

What are two types of follicles?

A

Large follicles and vellus hairs.

81
Q

Arrector pili muscles respond to ________ activity to erect hair and cause goose bumps.

A

sympathetic.

82
Q

Describe sebaceous glands: location.

A

Near top of hair follicle; mostly on the scalp. Also lips; oral surfaces of cheeks; and external genitalia.

83
Q

Describe sebaceous glands: secretion.

A

Secrete sebum into hair follicle; which reduces water permeability; resists acid; lye; and bacteriam contamination.

84
Q

Describe sebaceous glands: clinical relevance.

A

Liable to infection

85
Q

What does holocrine secretion mean?

A

The entire contents of the cell are shed as an oily exudate; sebum. Fill up with lipids until they burst releas the sebum into the hair follicle.

86
Q

How much of blood calcium is protein bound? Bound to anions? Free?

A

40%, 10%, 50%

87
Q

How are plasma levels of active ionized Ca buffered?

A

Proteins, phosphate, and H+

88
Q

Acidosis

A

Excess H+ ions occupy sites on proteins, increasing levels of free, ionized Ca++

89
Q

Alkalosis

A

Deficient H+ ions permits Ca++ bind to proteins, reduced free ionized Ca++`

90
Q

What are the three primary hormone for Ca level regulation?

A

PTH, Vitamin D, Calcitonin

91
Q

How does PTH regulate Ca levels?

A

Ca sensing receptors in PT gland respond to drop in free ionized Ca++ and release PTH. PTH increases bone resorption, renal Ca++ reabsorption, and gut absorption of Ca via vitamin D.

92
Q

How does PTH regulate Pi levels?

A

Increase gut absorption of Pi, decrease renal reabsorption of Pi, increasing Pi resorption from bone.

93
Q

Where can vitamin D be activated?

A

Kidney

94
Q

Why does PTH maintain dissimilar concentrations of Ca and Pi by selectively inhibiting Pi reabsorption in the kidney?

A

Reduce risk of CaPO4 precipitation in soft tissues

95
Q

How does PTH act on bone?

A

Acts on osteoblasts to resorp bone via RANK/RANKL.

96
Q

How does continuous versus intermittent PTH differ in relation to bone?

A

Continuous causes bone resorption while intermittent causes bone formation.

97
Q

What is “the most important” action of vitamin D?

A

To facilitate intestinal absorption of Ca/Pi.

98
Q

Where is calcitonin most often seen and what does it do?

A

Lactating females, inhibits osteoclastic resorption of Ca and Pi from bone. Favors deposition.

99
Q

What equilibrium point maintains adequate calcium levels?

A

PTH and calcitonin

100
Q

Hyperparathyroidism

A

Excess PTH, increase blood Ca++. Bone weakness, kidney stones, constipation, abdominal pain, depression of nervous system.

101
Q

Hypoparathyroidism

A

Low PTH. Decreased blood calcium. Tetany of muscles, Trousseau’s sign, chvostek’s sign.

102
Q

Osteomalacia

A

Demineralization of bone from Ca or Vit D deficiency. Kidney damage can cause deficiency.

103
Q

Osteoporosis

A

Loss of bone matrix. Can be caused by: hyperparathyroidism, inactivity of bones, lack of vitamin C, postmenopausal lack of estrogen, lack of GH, hyperadrenalism.

104
Q

Glucocorticoids and bone health

A

Glucocorticoids decrease bone formation by reducing lifespan of osteoblasts and osteocytes.

105
Q

Why can oxidation of fat only supply 60% of maximal aerobic power output?

A

Restrict blood flow through adipose tissue, insufficient albumin to carry FFA, and glucose oxidation limits muscle’s ability to oxidize lipids.

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