Connective Tissue Flashcards

1
Q

CT proper forms supportive

A

Stroma or parenchyma

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2
Q

Ground substance

A

Proteinglycans, glycosaminoglycans, anionic, adhesive glycoproteins

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3
Q

Adhesive glycoproteins found in CT

A

Laminin and fibronectin

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4
Q

Fixed cells (intrinsic)

A

Fibroblasts

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5
Q

Fibroblast origin

A

Hematopoietic cells

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6
Q

Fibroblast fxn

A

-Synthesize and secrete ECM and produce growth factors

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7
Q

Wandering leukocytes of CT (extrinsic)

A
  • Monocytes: become macrophage when localized in CT
  • Plasma cells
  • Mast cells
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8
Q

Monocytes

A

Become macrophages when localized in CT

-AKA histiocytes

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9
Q

Plasma cells differentiate in CT from

A

B-Lymphocytes

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10
Q

Type III collagen

A
  • Reticular fibers

- Support heavily cellular organs

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11
Q

Reticular fibers stain with

A

Silver stains and PAS

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12
Q

Reticular fiber location

A
  • Smooth muscle and hematopoietic organs (bone marrow, spleen, lymph nodes)
  • Parenchymal organs (liver and endocrine glands)
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13
Q

Elastic Fibers

A
  • Central core of elastin with fibrillin surrounding

- Contain desmosine and isodemosine (aa)

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14
Q

Elastic fibers are rich in which AA

A

-Glycine and proline

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15
Q

Elastic fiber location

A

-Vertebral ligaments, larynx, elastic arteries

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16
Q

Fibrillin vs Fibronectin

A
  • Fibronectin has binding sites

- Fibrillin acts as a fibril forming molecule

17
Q

Type I collagen location

A
  • BONE, dermis, organ capsules, fibrocartilage, cementum

- Osteogenesis imperfecta

18
Q

Type II collagen

A

-Hyaline and elastic cartilage

19
Q

Type III collagen

A

-Reticular fibers

20
Q

Type IV collagen

A

Lamina densa of the basal lamina

21
Q

Type V collagen

A

Placenta

22
Q

Tropocollagen

A

Formed by the last pro peptide cleavage of pro collagen

23
Q

Keloid formation

A

Overproduction of type III collagen

-Leads to elevated scarring in dark skinned patients

24
Q

Marfan syndrome

A

Defect in gene coding for fibrillin

25
Q

Collagen synthesis

A
  1. ) preprocollagen in ribosomes on rER
  2. ) in rER, hydroxylation of proline and lysine (Vit. C dependent)
  3. ) Glycoslylation of hydroxylysine
  4. ) triple helix (pro collagen)
  5. ) trasport to golgi
  6. ) Release to ECM
  7. ) in ECM, cleavage of peptides to form tropocollagen
  8. ) Tropocollagen aggregates to form fibrils
  9. ) Fibrillar structure is reinforced by enzyme lysyl oxidase (LOX)
26
Q

Scurvy

A
  • Lack of Vit. C
  • Hydroxylation does not occur
  • Gum ulceration and hemorrhages
27
Q

Osteogenesis imperfecta

A
  • single NT change in a gene for collage type I

- Pontaneous fractions, cardiac insufficiency

28
Q

Ehlers-Danlos IV

A
  • faulty translation of type III collagen

- Aortic and or intestinal rupture

29
Q

Type III collagen disorders

A
  • Keloid formations (overproduction)

- Ehlers Danlos type IV (underproduction)

30
Q

Ehlers Danlos VI

A
  • Faulty lysine hydroxylation

- Increased skin elasticity, rupture of eyeball

31
Q

Ehlers Danlos VII

A

Decrease in pro collagen peptides

-Increased joint mobility with frequent luxation

32
Q

Alport Disease

A
  • Defect in type IV collagen
  • X-linked
  • Blood/protein in urine, progresses to CKD