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MS1 Fall > Foundations Week 1 > Flashcards

Foundations Week 1 Flashcards

1
Q

Glycogen

A

branched glucose polymer attached to core protein glycogenin (G)

(mature particles in the nucleus have about 55,000 glucose residues!)

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2
Q

Cytoplasmic disease examples

A

PKU, sickle cell anemia, hemolytic anemia, glycogen storage diseases

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3
Q

Components of the cytoskeleton

A

Intermediate filaments, microtubules, and microfilaments

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4
Q

Microfilaments

A

Contain actin. Involved in muscle contraction, cell movement, intracellular transport/trafficking, maintenance of the cell shape, cytokinesis, etc

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5
Q

Intermediate filaments

A

Cell “scaffolding.” Involved in the maintenance of cell shape, anchoring of organelles, some cell-to-cell junctions.

Examples: keratin, lamin, desmin, etc

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6
Q

Microtubules

A

Hollow cylinders (the “9+2” structure). Commonly organized by the centrosome.

Involved in the mitotic spindle, cilia & flagella movement, and intracellular transport

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7
Q

Do membrane carbohydrates span the lipid bilayer?

A

No, they are only present as modifications to lipids and proteins (on the membrane surface facing away from the cytosol)

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8
Q

Cerebroside

A

glycolipid + monosaccaharide

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9
Q

Ganglioside

A

glycolipid + oligosaccharide + sialic acid (an acidic sugar)

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10
Q

Does a uniporter transport ions?

A

No, only molecules down their concentration gradient without energy input.

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11
Q

Normal lab values for Na+ in the blood?

A

136-145 mEq/L (mM)

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12
Q

Normal lab values for K+ in the blood?

A

3.5-5.1 mEq/L (mM)

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13
Q

Normal lab values for Mg2+ in the blood?

A

1.5-2.0 mEq/L (mM)

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14
Q

Normal lab values for Ca2+ in the blood?

A

8.4-10.2 mg/dL (2.1-2.8 mM)

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15
Q

Plasma membrane disease examples

A

Cystic Fibrosis, familial hypercholesterolemia, and Muscular Dystrophy (Duchenne type)

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16
Q

What color does euchromatin stain?

A

Light

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17
Q

What color does heterochromatin stain?

A

Dark

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18
Q

Where does rRNA synthesis and ribosome subunit assembly take place?

A

The nucleolus

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19
Q

Nucleus and nucleolus disease examples

A

Inherited & spontaneous diseases, aneuploidy syndromes, Hutchison-Gilford progeria syndrome, Treacher Collins syndrome

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20
Q

Where does aerobic respiration occur in the mitochondria?

A

Inner membrane and cristae

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21
Q

What happens in the mitochondrial matrix?

A

Catabolic processes (TCA, fatty acid oxidation) and anabolic processes (AA synthesis, steroids). Also where the circular genome is found

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22
Q

Mitochondrial disease examples

A

MCAD, MERRF (myoclonic epilepsy with ragged-red fibers)

Note: mitochondrial diseases present with a wide range of clinical features

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23
Q

Lysosome

A

Low pH, contains acid hydrolases that degrade and recycle.

Fuse with endosomes and phagosomes. Incomplete degradation forms residual bodies (lipofuscin)

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24
Q

Residual bodies/lipofuscin

A

Protect cells from toxic effects of incomplete degradation. Accumulate in cells over times (decades).

Lipofuscin = “lipid dark” without stain

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25
Q

Ceroid

A

abnormal pathological accumulation of lipofuscin or lipofuscin-like bodies

Ceroid accumulation is a hallmark of certain lysosomal storage diseases

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26
Q

Lysosome disease examples

A

storage diseases, mucolipidoses

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27
Q

Functions of the smooth ER?

A

lipid & steroid hormone synthesis, detoxification of xenobiotics, stores Ca 2+ ions

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28
Q

Where are glycans added?

A

the rough ER (NOT the golgi… golgi just modifies)

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29
Q

What side do vesicles enter the golgi apparatus? What side do they exit?

A

Enter on the cis side, exit on the trans side

remember that the golgi is polarized!

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30
Q

What is it called when glucose is spontaneously, and irreversibly, added to protein?

A

non-enzymatic glycation

This does NOT happen in the golgi

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31
Q

Steps in the secretory (exocytic) pathway?

A

rER -> golgi -> vesicle -> plasma membrane

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32
Q

Where does protein “quality control” occur?

A

In the rER before the protein heads to the golgi. Those that are unfolded will be retained in the rER lumen or degraded

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33
Q

Permanent neonatal diabetes mellitus

A

Mutations disrupt folding in the rER, formation of disulfide bonds in the rER, and/or proteolytic removal of C peptide in secretory vessicles

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34
Q

Three main destinations as vesicles exit the trans Golgi network?

A
  1. Lysosome - need a specific sorting signal for this
  2. Regulated secretion - specific signal is needed; stored in secretory vesicle until secretion is initiated (e.g. insulin in beta cell of pancreatic islet)
  3. Constitutitive secretion - proteins without sorting signals follow this default pathway
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35
Q

I Cell Disease

A

Lysosomal enzymes don’t make it there, thus stuff isn’t degraded. Instead these enzymes are secreted by the cell (in the default pathway) and cause damage to cells/the matrix

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36
Q

Internalization pathways

A
  1. phagocytosis - phagosomes fuse with primary lysosome for degradation
  2. Endocytosis - extracellular molecule internalization; traffic to endosomes
  3. pinocytosis - extracellular fluid and dissolved substances are internalized
  4. Receptor-mediated endocytosis - selective endocytosis; cell surface receptors bind specific ligands
  5. Autophagy - degrades cell components in lysosomes; fuses with primary lysosomes; induced by starvation, damage, and stress
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37
Q

Endocytic pathways

A

Recycling

Transcytosis across a polarized cell

Delivery to a lysosome for degradation

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38
Q

What is the only cell pathway for degradation of large internal structures/organelles?

A

Autophagy

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39
Q

What are the two main pathways for degradation in the cell?

A

Autophagy & the ubiquitin proteasome system

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40
Q

What are the main insulin-responsive tissues in the body?

A

Fat, liver, and muscle

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41
Q

What does insulin promote in fat tissue?

A

Uptake of glucose and fats from blood & increases synthesis and storage of lipids

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42
Q

What does insulin promote in the liver?

A

Uptake of glucose, increase glycogen synthesis, and reduces glycogenolysis

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43
Q

What does insulin promote in muscles?

A

Uptake of glucose & amino acids from blood & increased protein synthesis

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44
Q

Tissues

A

cells + extracellular matrix

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45
Q

Specialized functions

A

Specific cells + specific extracellular properties/organization

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46
Q

Four classic tissues

A
  1. Epithelium
  2. Connective tissue
  3. Muscle
  4. Nerve
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47
Q

What embryologic tissue does the epithelial (surface) arise from?

A

Primarily ectoderm and endoderm

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48
Q

What embryologic tissue does the CT and muscle arise from?

A

Primarily mesoderm

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49
Q

What embryologic tissue does the nerve tissue arise from?

A

Primarily from the neuroectoderm (CNS) and neural crest (PNS)

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50
Q

Where is epithelial tissue found?

A

All internal and external body surfaces, alimentary canal from inner lip to anal skin, line all blood & lymphatic vessels, compose all glands

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51
Q

Characteristics of epithelia

A

All cells connected to other cells, polarized (apical, basal, lateral, organelles), specializations (apical, lateral, basal), avascular, and stem cells

Note: basal lamina is the only extracellular matrix associated with epithelia

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52
Q

Basal lamina

A

“Basement membrane”

Extracellular matrix layer synthesized largely by epithelial cells, which adhere to it. The basal lamina is then adhered to connective tissue.

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53
Q

What do desmosomes do?

A

Connect intermediate filaments in one cell to those in the next cell. Located in the lateral plasma membranes

Cell-cell anchoring junctions

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54
Q

What do adherens junctions do?

A

Connect actin filament bundles in one cell with that in the next cell. Located in plasma membranes below tight junctions

Cell-cell anchoring junctions

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55
Q

What do tight junctions do?

A

Seal gaps between epithelial cells near the apical surface

Regulates diffusion between cells & prevents movement of membrane components

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56
Q

What do gap junctions do?

A

Allow the passage of small water-soluble molecules from cell to cell. Located on the lateral plasma membranes

Channel-forming junction

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57
Q

What do hemidesmosomes do?

A

Anchor intermediate filaments in a cell to extracellular matrix. Located on the basal plasma membrane

Cell-matrix anchoring junctions

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58
Q

What do actin-linked cell-matrix adhesions do?

A

Anchor actin filaments in cell to extracellular matrix

Cell-matrix anchoring junctions

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59
Q

What do occluding junctions do?

A

Seal the basal and apical compartments

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60
Q

Do microtubules bind junctions in epithelial cells?

A

No

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61
Q

Types of simple epithelia?

A

Squamous, cuboidal, and columnar

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62
Q

Pseudostratified epithelium

A

All cells adhere to basal lamina, but not all cells reach free (apical) surface

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63
Q

What does normal airway mucus do?

A

It travels up the mucociliary escalator. First, it is secreted by the goblet cells, and then it forms a layer that is propelled by cilia on the epithelial cells

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64
Q

Apical specializations

A

Microvilli, cilia, stereocilia

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65
Q

Function of microvili

A

Increase surface area, absorption

NOT motile

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66
Q

Function of cilia

A

movement/propulsion, ATP hydrolysis (by dynein motor “arms”)

Microtubule core that is motile

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67
Q

Stereocilia

A

Very long micovilli that project from the apical surface of specialized cells present in the male reproductive tract and the inner ear

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68
Q

Infolding

A

Type of basal specialization that increases surface area

Mitochondria found between infoldings in many epithelial cells

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69
Q

Primary Ciliary Dyskinesia

A

Cilia function defect, low or no motility, no or poor clearance of airway mucus

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70
Q

Exocrine glands

A

Secretory product -> duct

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71
Q

Endocrine glands

A

Secretory product -> blood

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72
Q

Serous gland secretion?

A

Watery & protein rich

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73
Q

Mucous gland secretion?

A

Thick + mucin rich

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74
Q

Exocrine secretory mechanisms?

A

Merocrine (most cells, fusion of secretory vesicles with plasma membrane)

Apocrine (specialized cells, lipid droplet secretion)

Holocrine (specialized cells - cell death and rupture)

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75
Q

Endocrine secretory mechanism?

A

Merocrine - fusion of secretory vesicles with plasma membrane

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76
Q

What layer of the epidermis is the transition from living to dead cells?

A

The stratum lucidum

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77
Q

Layers of the epidermis?

A

Come, Let’s Get Sun Burned

(All start with Stratum)

Corneum
Lucidum
Granulosum
Spinosum
Basale
78
Q

What are the most numerous cells in the epidermis?

A

Keratinocytes

79
Q

Where are keratinocyte stem cells (KSC) found?

A

Stratum basale

80
Q

What cells do not arise from keratinocyte stem cells?

A

Langerhans, melanocytes, Merkel cells (function in tactile sensation)

81
Q

What are prickle cells?

A

Keratinocytes in the stratum spinosum

Appearance is due to thousands of desmosomes per cell

82
Q

Epidermolysis bullosa simplex (EBS)

A

Mutation of keratins 5 and 14 (in the basal layer)

Blisters develop soon after birth at sites subject to pressure or rubbing

83
Q

Pemphigus vulgaris

A

Most common Pemphigus blistering disease. Autoantibodies to desmoglein 3 (desmosomes not able to attach properly)

84
Q

Bullous pemphigoid

A

Autoimmune disease where autoantibodies cause hemidesome degradation (separates the stratum basale from the basal lamina and causes blistering on the skin)

85
Q

Three types of skin stem cells

A
  1. Epidermal - stratum basale, form keratinocytes
  2. Sebocyte - in sebaceous gland, secrete sebum
  3. Bulge - in hair follicle sheath, form hair cells
86
Q

Whats the most common form of skin cancer?

A

Basal cell carcinoma

Slow-growing, usually not metastatic, typically from follicular bulge stem cells, surgical removal common

87
Q

Invasive carcinoma (epithelial proliferation)

A

cancer, exits epithelium and crosses the basal lamina to enter the connective tissue

88
Q

Carcinoma in situ (epithelial proliferation)

A

Dysplasia of full thickness of the epithelium (epidermis), pre-malignant

89
Q

Dysplasia (epithelial proliferation)

A

Abnormal epithelial cells and disordered growth; abnormal differentiation/maturation of epithelial cells

90
Q

Metaplasia (epithelial proliferation)

A

Replacement of one epithelium for another by stress or inflammation; usually reversible

91
Q

Hyperplasia (epithelial proliferation)

A

Normal response, increase in epithelial cell #

92
Q

H and E stain

A

Hematoxylin - basic dye - binds acidic (basophilic) molecules like DNA

Eosin - acidic dye - binds basic (acidophilic) molecules like proteins

93
Q

Erythrocyte diameter

A

7.8 micrometers

94
Q

Location of 55S ribosome?

A

Mitochondria

95
Q

Location of 80S ribosome?

A

Cytoplasm

96
Q

Endothelium

A

simple squamous epithelium lining blood and lymphatic vessels

97
Q

Mesothelium

A

simple squamous epithelium lining body cavities

98
Q

The epidermis is composed of what?

A

keratinized stratified squamous epithelium

99
Q

Corneocytes

A

Terminally differentiated, flattened dead cells

AKA keratinocytes in the stratum corneum

100
Q

Tonofilaments

A

Intracellular keratin fibers (intermediate filaments)

Confer strength

101
Q

Eccrine sweat gland

A

Simple coiled; almost all skin, involved in thermoregulation

102
Q

Apocrine sweat gland

A

Simple coiled; secretes proteins, lipids, sugars, and organic compounds into hair follicles

103
Q

Sweat gland ducts have what kind of epithelia?

A

Stratified epithelium (either squamous or cubodial)

104
Q

The secretory portion of a gland has what kind of epithelia?

A

Glandular epithelium (not classified)

105
Q

All epithelial cells secrete what?

A

Collagen Type IV. Secreted at the basal surface via constitutive merocrine secretion; part of basal lamina

106
Q

Exocrine portion of the pancreas

A

Acini + ducts, glandular epithelium, merocrine secretion of zymogens

107
Q

Endocrine portion of the pancreas

A

Islets of Langerhans, epithelioid cells (not polarized, not classified as epithelium), endocrine products like insulin, glucagon, etc

108
Q

Pancreatic acinus

A

spherical cluster of epithelial cells that secrete products at apical plasma membranes into lumen

109
Q

Parenchyma

A

generic term for functional cells of a tissue

110
Q

Stroma

A

generic term for the supporting cells and matrix of a tissue

Ex: Connective tissue in many organs

111
Q

What is Cellulitis?

A

Inflammation of the dermis and subcutaneous tissue. Etiology is a bacterial infection (endogenous or exogenous) from a break in the skin, burn, insect bite, IV, fungal infection.

Clinical signs: redness, swelling, tenderness, warmth

112
Q

Connective tissue

A

Cells + extracellular matrix. Cells are attached to the matrix and not each other. Vascularized, can recruit immune cells.

113
Q

Loose connective tissue

A

More cells, less ECM

Ex: lamina propria of intestinal villus

114
Q

Dense connective tissue

A

More ECM, fewer cells

Irregular = collagen fiber orientation in many directions

Regular =collagen fiber orientation in one direction

115
Q

Connective tissue cell components

A

Fibroblast, undifferentiated cell, plasma cell, adipocyte, macrophage, mast cell

FU PAMM (imagine Dwight from the office saying it)

116
Q

Connective tissue transient (wandering) components

A

neutrophil, eosinophil, basophil, lymphocyte, monocyte

Immune-related!

117
Q

Connective tissue ECM components

A

protein fibers (collagen and reticular elastic), ground substance (proteoglycans, glycosaminoglycans), basal/external lamina, tissue fluid

118
Q

Fibroblasts

A

Most abundant and widely distributed CT cell

Synthesize ECM (fibers and ground substance)

Fibers = collagen and elastic

Ground substance = proteins and polysaccaharides

“All purpose cell”

119
Q

Adipocyte

A

White fat = unilocular, one large lipid droplet

Brown fat = multilocular, many small lipid droplets

Lipid droplet is primarily triacylglycerols

120
Q

Do connective tissue cells synthesize a basal or external lamina?

A

No. Basal lamina is for epithelia

121
Q

Primary function of ECM?

A

Managing extracellular stress (tension, torsion, compression, shear)

122
Q

What is the most abundant protein in the body?

A

Collagen

123
Q

Collagen Type I

A

Fibril, fiber, bundle

Bone, skin, tendons, ligaments, cornea

Synthesized by fibroblast, tendinocyte, osteoblast

124
Q

Collagen Type II

A

Fibril, Fiber

Cartilage

Synthesized by chondroblast, chondrocyte

125
Q

Collagen Type III

A

Fibril, thin fiber (branched networks

Reticular fibers (lymph nodes, spleen, liver, blood vessels, skin)

Synthesized by reticular cell, fibroblast, smooth muscle cell

126
Q

Collagen Type IV

A

Sheet or plaque

Basal lamina, external lamina (bind to ECM molecules like laminin)

Synthesized by adipocyte, epithelial cell, muscle cell, Schwann cell

127
Q

Collagen Type VII

A

Fibril

Anchoring fibrils (skin, eye, uterus, esophagus). Function to connect basal/external lamina to CT

Synthesized by fibroblast

128
Q

Order of Collagen Type 1 organization

A

Tropocollagen triple helix, fibril (68nm is the banding pattern; critical feature of strength is covalent crosslinks here), fiber, bundle

129
Q

Collagen synthesis steps

A
  • Pro-alpha chain synthesis
  • Hydroxylation & Glycosylation
  • Self-assembly of three pro-alpha chains
  • Procollagen triple-helix formation and secretion through merocrine function
  • Extra-cellular: self polymerization to make fibril with 68nm banding pattern & covalent cross-linking
130
Q

Examples of collagen diseases

A
  1. Osteogenesis imperfecta (OI): brittle bone disease (multiple fractures), caused by defects in type 1 collagen
  2. Ehlers-Danlos Syndrome: joint hyper mobility, tissue fragility, and skin extensibility
131
Q

Blue sclera sign

A

Sclera is rich in dense, irregular CT (type I collagen). An issue with type I like OI or EDS will cause bilateral blue sclera

132
Q

Elastic fibers

A

Composed of elastin core (crosslinked monomers like collagen) and microfibrils (fibrillin)

Ex: desmosine. Measure of this in the urine is a clinical measure of tissue damage

133
Q

Marfan syndrome is caused by what?

A

A defect in the fibrillin 1 gene (not elastin!)

134
Q

Ground substance

A

Space filling molecules, fluid-filled. Found between CT fibers, resists pushing (compressive stress)

Examples: glycosaminoglycans (GAGs), proteoglycans (PGs)

135
Q

Hyaluronic Acid

A

Very long GAG; repeating disaccharide; function is to organize water, shock absorption, lubrication in synovial joints

136
Q

Proteoglycans

A

core protein + GAGs

137
Q

Multi-adhesive proteins (MAGs?)

A

Link ground substance molecules in the ECM to each other and cells
Ex: fibronectin

138
Q

What cells exit the blood, enter connective tissue, differentiate, and remain in CT?

A

Resident fixed cells: macrophage, mast cell, plasma cell

139
Q

Extravasation

A

process of exiting blood at post-capillary venules (after mast cell and macrophage stimulation)

140
Q

Simplified inflammatory response

A
  1. Mast cells and macrophages in CT release primary inflammatory mediators that cause vessels to dilates and “leak”
  2. Extravasation of leukocytes into CT (neutrophils, basophils, and eosinophils)
  3. Macrophages phagocytose microbes, dead cells & debris
141
Q

Scleroderma

A

Excess healing by fibroblasts; chronic inflammation. Fibroblasts produce excess collagen and skin becomes thickened and hardened

142
Q

Epidermolysis Bullosa

A

a group of rare inherited skin diseases that are characterized by the development of blisters following minimal pressure to the skin

143
Q

Treatment for epidermolysis bullosa?

A

preventing and treating wounds and infection

144
Q

Four major types of epidermolysis bullosa?

A
  1. Simplex (EBS)
  2. Junctional (JEB)
  3. Dermolytic or Dystrophic (DEB)
  4. Mixed (Kindler syndrome)
145
Q

EB Simplex

A

Intraepidermal cleavage due to defects in keratins 5 and 14

autosomal dominant

146
Q

Junctional EB

A

intra-lamina lucida split, autosomal recessive, least common type, lethal by age 2

147
Q

Dystrophic EB

A

subepidermal cleaveage due to deficient or defective collagen 7 fibrils

148
Q

Research in EB?

A

Protein replacement therapy: replace or boost missing or defective protein

Cell-based therapy: stem cells, fibroblasts, or gene-corrected cells. Bone marrow transplants

Gene therapy: corrected gene transfer via retrovirus or stem cell therapy

149
Q

Where are large amounts of glycogen stored?

A

Liver and muscle cells

150
Q

Glycolipid

A

sphingosine + monosaccharide or oligosaccharide

151
Q

Where is the C chain of insulin removed during the synthesis & secretion pathway?

A

Within the secretory vessicle

152
Q

Types of autophagy

A

macro, micro, and chaperone-mediated

153
Q

Does H&E stain glycogen?

A

Nope. Glycogen isn’t charged so no stain.

PAS does stain it red-pink

154
Q

Forms of specialized connective tissue?

A

Adipose, blood, bone, cartilage, hemopoietic, lymphatic

155
Q

Two types of endocrine glands

A
  1. Secretory portion is classified epithelial cells (e.g. thyroid follicle)
  2. Secretory portion is not classified; epithelioid-like (“glandular epithelium”
156
Q

What do all epithelial cells secrete at the basal surface?

A

Type 4 Collagen; it’s a constitutive merocrine secretion that makes up part of the basal lamina

157
Q

Three types of cartilage

A
  1. hyaline
  2. elastic
  3. fibrocartilage

HEF

158
Q

Hyaline cartilage

A

mechanical support, covers articulating surfaces of bones, model for skeletal bone formation

predominantly type 2 collagen

found in growth plates, trachea, costal cartilages, larynx, tip of nose

surrounded by perichondrium EXCEPT for articular cartilage

159
Q

Elastic cartilage

A

found where resilience and springiness are needed (ear and epiglottis)

contains type 2 collagen + increased amount of elastic fibers

surrounded by perichondrium

160
Q

Fibrocartilage

A

very limited; transitional form

combo of dense regular CT & hyaline cartilage - mostly type 1 collagen with some type 2

plays a role in fracture repair

found in intervertebral disks, pubic symphysis, menisci, and where tendons insert into bones

NO perichondrium

161
Q

Cartilage

A

Specialized CT that is composed of chondrocytes (95%) and ECM

Avascular and aneural

162
Q

Chondrocytes

A

occur singularly or in nests; synthesize the extracellular matrix; housed in lacunae (small cavities in ECM)

163
Q

Perichondrium

A

dense, irregular CT capsule that surrounds hyaline (sans articular part) + elastic cartilages. Source of nutrients and oxygen for avascular cartilage

164
Q

Two types of cartilage growth

A
  1. Appositional growth - new cartilage forms at surface of existing cartilage. Deposition on the outside surface of cartilage
  2. Interstitial growth - new cartilage forms within existing cartilage. This is what chondrocytes do. They divide and create cell nests - get space between them as they divide (note: they are NOT stem cells)
165
Q

What type(s) of cartilage are capable of repair?

A

Fibrocartilage. During bone repair it is formed around the broken bone & then undergoes calcification

Hyaline and elastic cartilage are not capable of repair (avascular!). Hyaline undergoes calcification & gets replace by bone

166
Q

Fibrous outer layer of the bone?

A

Periosteum

Covers the outer surface except at epiphyses

Multilayered

The innercellular layer contains osteoblasts, osteoclasts, osteoprogenitor cells, and bone lining cells

167
Q

Inner layer of the bone?

A

Endosteum

Covers internal bone surfaces (marrow cavity, Haversian canal)

Single cellular layer (osteoblasts, osteoclasts, osteoprogenitor cells, and bone lining cells)

168
Q

Two kinds of bone?

A
  1. Compact

2. Spongy (aka trabecular)

169
Q

Composition of bone?

A

35% cells (osteo- -blasts, -clasts, and -cytes) + ECM of ground substance + 90% collagen 1

65% mineral crystals (primarily calcium phosphate in the form of hydroxyapatite crystals)

170
Q

osteoprogenitor cell

A

Derived from mesenchyme; differentiate into osteoblasts

171
Q

Osteoblasts

A

synthesizes organic components of ECM; found adjacent to bone matrix they have synthesized

172
Q

Osteocyte

A

mature bone cell residing in a lacuna; synthesizes organic components of ECM

completely surrounded by its own matrix

numerous processes allow cell-to-cell communication with osteoblasts and osteocytes

173
Q

How are nutrients and waste transported in bone?

A

Small channels radiate from each lacuna through the mineralized matrix

Act as passage routes from nutrients/waste

** gap junctions are essential

174
Q

How does bone tissue grow?

A

By appositional growth, NOT interstitial

Bone deposition occurs by osteoblasts and osteocytes

Requires vitamin C and oxygen

175
Q

How does bone, the organ, grow?

A
  1. Intramembranous ossification - differentiation of mesenchymal cells into osteoprogenitor cells
  2. Endochondral ossification - involves the erosin of hyaline (or fibrocartilage) cartilage by osteoclasts and deposition of bone by osteoblasts and osteocytes
176
Q

Intramembranous Ossification

A

Mesenchymal cells differentiate into osteoblasts. Osteoblasts deposit osteoid that then becomes mineralized bone.

Bone formation occurs at numerous sites simultaneously in form of spicules which “grow together” as they expand to form trabeculae of bone

Occurs in flat bones of the cranium, face, mandible and maxilla

177
Q

Endochondral Ossification

A

Requires interstitial and appositional growth of cartilage, erosion of that cartilage, vascularization, and bone deposition by osteoblasts and osteocytes

Process associated with bone growth/development. Weight-bearing bones of axial skeleton and bones of the extremities

178
Q

How does bone grow in width?

A

By appositional growth

179
Q

How does bone grow in length?

A

By interstitial growth of cartilage and appositional growth of bone

180
Q

What promotes vascular invasion in bone growth?

A

Hypertrophying chondrocytes secreting VEGF (Vascular Endothelial Growth Factor)

181
Q

What type of collagen forms a “scaffold” around hypertrophying chondrocytes in bone growth?

A

Collagen X

A point mutation in the gene for this causes a form of dwarfism (chondrodysplasia)

182
Q

Regulation of endochondral ossification

A

Nutritional (vitamin C, calcium, oxygen)

Hormonal (IGF-I is produced in the liver in response to growth hormone secretion. Stimulates chondrocyte proliferation and bone growth. FGF is a negative regulator of bone growth by inhibiting chondrocyte proliferation)

183
Q

Bone remodeling

A

Relies on osteoclasts to break down old matrix and osteoblasts to lay down new matrix

(advancing cutting cone & closing cone)

184
Q

What causes an osteoclast precursor to mature?

A

Binding of RANKL to RANK

osteoprotegerin secreted by osteoblasts inhibits RANKL

185
Q

What increases osteoclast numbers?

A

Parathyroid hormone (PTH) increases numbers to resorb bone and increase blood calcium

186
Q

What inhibits osteoclast numbers?

A

Calcitonin inhibits activity and decreases blood calcium

187
Q

Osteopetrosis

A

Thick dense bones, treatment is bone marrow transplant

188
Q

Osteoporosis

A

Decrease in bone mass and increase in bone fragility. Treatment is diet, hormone replacement therapy or anti-RANKL antibodies

189
Q

Paget’s Disease

A

Abnormal bone architecture, enlarged and misshapen bones. Treatment is calcitonin and bisphosphonates

190
Q

Steps in bone repair

A
  1. Granulation tissue from fibroblasts and periosteal cells
  2. Soft callus of dense CT and fibrocartilage forms to help stabilize the bone. At the same time osteoprogenitor cells divide and differentiate into osteoblasts
  3. Hard callus of mixed spicules of calcified fibrocartilage and bone forms. At the same time, endochondral ossification is ongoing
  4. Bone remodeling occurs and Haversian systems are rebuilt

MS1 Fall (23 decks)

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