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Block 1 Week 2 > Connective Tissue > Flashcards

Connective Tissue Flashcards

1
Q

cytoskeleton vs. connective tissue?

A
  • cytoskeleton is inside the cells

- connective tissue is outside the cells

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2
Q

How define connective tissues when blood vessels are involved?

A
  • can have a region claimed as connective tissue & it can contain small blood vessels
  • BUT when blood vessels become large; various layers of their wall are made of connective tissue
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3
Q

How do we distinguish between a tissue or organs function cells vs connective tissue?

A
  • the organs functional cells=parenchymal; the rest of stuff in-between is connective tissue
  • parenchymal & connective tissue can be separately targeted by disease processes
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4
Q

Parenchymal cells?

A
  • cells within an organ/tissue that are identified with the function of the organ/tissue
  • organs can have many cell types; hepatocytes=only liver so are Parenchymal
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5
Q

What are the components of connective tissue (3)?

A

1) ground substance
2) fibers (elastic vs collagen)
3) cells (citizen, recruited resident, transient effectors)

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6
Q

Citizen cells in connective tissue?

A
  • fat cells, smooth muscle cells, cells of small vessels & nerves, stem cells
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7
Q

recruited resident cells in connective tissue?

A

macrophages, mast cells, some dendritic cells

define inflammatory process w/ transient cells

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8
Q

transient effectors cells in connective tissue?

A

lymphocytes, derived plasma cells, neutrophils, eosinophils, basophils, other macrophages & dendritic cells
define inflammatory process w/ recruited resident cells

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9
Q

Recuited resident cells vs transient effectors in inflammation process?

A
  • recruited residents are acutely recruited during inflammation event
  • transient stay around for weeks/month regardless of inflammatory event
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10
Q

ground substance composed of? role in connective tissue?

A

1) proteoglycans
2) peptidoglycan
3) glycosaminoglycans
4) large glycoproteins
& other stuff in plasma filtrate

  • help w/ tissue hydration
  • provides in between glue/stickyness
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11
Q

What is glycosaminoglycans?

A
  • a poly amino sugar

- has repeating disaccharide unit of hyaluronate; this links to peptide= peptidoglycan; links to protein= proteoglycan

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12
Q

ground substance role in connective tissue?

A

1) made of polymer/carbs
2) are polar & have charge
3) help w/ hydration & structural components of connective tissue
4) provide filling in (sticky shit) material for connective tissue

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13
Q

glycosaminoglycan physical properties?

A

1) has hyaluronate, important non-sulfated GAG
2) hyaluronate absorbsH20, jello like complex
3) found in all tissues prevalent in skin
* gelatanous due to H20 absorption but not jello*
* help w/ tissue hydration*

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14
Q

sulfated gags?

A

-hyaluronate is an UNSULFATED GAG

  • sulfated GAGs impart charge to ground substance
  • have wide distribution; seen in keratin in skin, heparan is crucial for function of basal laminae in kidneys
  • is filling material for connective tissue*
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15
Q

proteoglycans?

A
  • part of ground substance
  • can be large complexes of different molecules attached together;
  • provide components that can contribute to elements like the basement membrane
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16
Q

functions of ground substances x5)

A

1) hold waters: (tissue resilience)
2) acts as a charge & size barrier (regulates access to cells)
3) contributes to physical properties of connective tissue (reinforced concrete)
4) regulate morphogenesis
5) facilitates cell migration by coating cells

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17
Q

Ground substances & age

A

-are in young tissue; go away in old tissue

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18
Q

how does ground substances holding water help the connective tissue?

A

helps with:

1) protection
2) reduces fluid loss
3) limits pathogenic invasion
4) tissue plumpness & resillience

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19
Q

what is morphogenesis?

A
  • migration recognition
  • growth factor activation
  • development of tissue
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20
Q

ground substances disorders (x4)

A

1) problems w/ nutrient/waste product flow
2) improper tissue development (morphogenesis)
3) improper tissue growth
4) cell malfunction due to ground substance accumulation in lysosomes

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21
Q

autosomal recessive disorders & ground substances?

A
  • -Auto rec. diseases involved in lysosomal storage cause defects in ability to metabolize/recycle ground substances
  • get accumulation of macrophages in lysosome
    ex: hurler’s syndrome
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22
Q

Hurler’s syndrome?

A
  • lysosomal storage disease
  • caused by absence of lysosomal degradative enzyme
  • heparan sulfat+ dermatan sulfate accumulate in tissue
  • accumulation in tissue & CNS lead to organ failure & progressive mental retardation.
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23
Q

Fibers of connective tissue (x3)? How see under light microscope level? Type of stain used?

A

1) reticular fibers: can only see if specially stained
2) elastic fibers: just easier to see if specially stained
3) type 1 collagen fibers: easily seen w/ routine stain

are proteins…use Eosin stain

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24
Q

Why can fibers not always be discerned?

A
  • they are embedded in a lot of hyaluronate
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25
Q

types of collagen fibers and presence in connective tissue fiber?

A
  • collagen has many types & several types may be present together
  • Reticular fibers= type 3
  • elastic fibers = collagen-like fibrillar protein
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26
Q

reticular fiber collagen, structure? elastic fiber collagen, structure??

A
  • Reticular fibers= type 3 collagen, good for structural rigidity
  • elastic fibers = collagen-like fibrillar protein, good for elasticity
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27
Q

collagen structure?

A

-trimeric, repeating appearance, helical
-3 alpha chains wrapped together
-

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28
Q

how do the collagens differ? process to differentiate x4)

A

1) each made of Dif combos of 3 alpha chains wrapped together
2) combo dictates the postrtanslational modifications inside the cell
3) PTM inside distracts PTM outside cells
4) PTM outside dictates physical properties necessary for tissue/region of tissue

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29
Q

fibroblasts

A

are cells in connective tissues that produce collagen & other fibers
-help w/ tissue damage & involved in scaring

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30
Q

the secretion of collagen?

A
  • almost every cell is capable of secreting a collagen, glycoprotein & GAGs
  • not sole responsibility fo fibroblasts, but they are a major producer in most tissue
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31
Q

Biosynthesis of collagen 1?

A

1) uptake AA
2) trxn, make mRNA for pre-pro-alpha chains
3) rough ER makes pre-chains
4) cotranslationally pre-piece is severed
5) form pro-alpha into triple helix, end alpha pieces crosslink=procollagen
6) transfer to Golgi
7) packaged into vesicle that can fuse w/ PM
8) vesicle moved by microtubule to PM, pro collagen exocytosed
9) pro collagen cleaved to tropocollagen
10) Lysyl oxidase crosslinks tropocollagen

32
Q

Lysol oxidase:

A

enzyme that crosslinks tropocollagen using non-glycosylated hydroxylysines
-dependent on Cu

33
Q

hydroxyprolines

A

-help make & stabilize the pro-alpha triple helix

34
Q

Type 2 collagen fibers?

A
  • more highly glycosylated than type 1

- more jello-y than type 1

35
Q

why are collagen fibers sometimes wavy?

A

to allow skin to stretch even though the fibers themselves don’t
-usually have elastin fibers as well here

36
Q

tendon collagen?

A

-collagen is lined up, provides mechanical structural resistance

37
Q

type 3 collagen?

A

1) glycosylation state between type 1 and 2
2) forms co-fibers w/ Type 1, helps regulate Type 1 thickness
3) has glycoprotein coat

38
Q

type 4 collagen?

A
  • pro-pieces not removed; are highly glycosylated

- results in no fibers, but randomly arrayed procolagen molecules which forms a FILTER

39
Q

Goodpasture’s Syndrome

A
  • autoimmune antibody response against Type IV collagen

- causes blood and protein in urine, cough up blood from disrupting basal membrane in lungs

40
Q

scurvy

A
  • vit C needed to help the 3 alpha chains form in to the collagen helix
  • w/o vit C, are collagen deficient
  • poor wound healing, can’t replace collagen well (loose teeth)
41
Q

osteogenesis imperfecta

A
  • brittle bones & blue sclera since eyes translucent & seeing aqueous part of eyeball
  • due to Type 1 Collagen deficiency
  • autosomal dominant (rarely recessive)
  • mild to severe
42
Q

Ehlers-Danlos Classification

A
  • disorder in collagen production, autosomal dominant or recessive
  • can be caused by mutations that affect collagen genes, & genes affect processing
  • causes fragile skin, internal organ structural integrity issues
43
Q

6 Ehlers-Danlos classifications

A

1) classical:
2) hyper mobility:
3) vascular:
4) kyphoscoliosis
5) arthrochalasia:
6) dermatoparaxsis:
- can be due to defects in collagen protein coding sequence, enzymes or processing

44
Q

how does diabetes have effect on glycosylation?

A
  • diabetes=hyperglycemia
  • over/abnormal glycosylation so over stimulation/production of collagen
  • tissue (collagen) turnover enzymes can’t keep up, get extremely thick basement membrane
45
Q

issues that come with accumulation of basement membrane

A

contributes to:

1) an anaerobic env
2) cardiovascular disease
3) peripheral neuropathy
4) poor nutrient exchange between capillaries & epithelial cells
- crucial to kidney failure

46
Q

what do elastic fibers do?

A
  • cause skin to ping back when stretch it
  • have a lot of hydrophobic AA, so prefer hydrophobic env
  • use FIBRILLIN layer to protect themselves in hydrophilic env
47
Q

Marfan’s syndrome?

A
  • mutation in fibrillin , fucks up elastic fibers
  • have poor structural integrity in tissues
  • patients= susceptible to heart defects, aneurysms, &abnormally tall
48
Q

effects of aging on GAGs?

A
  • production rate declines, molecular weight decrease can’t hold as much H20= dehydrate
49
Q

effects of aging on collagen?

A

-lower turnover, more cross linking, collagen gets stiff, coarse & stringy

50
Q

effects of aging on elastic fibers?

A

-loose elasticity due to lower turnover & UV damage

51
Q

effect of aging on connective tissue?

A
  • poor turnover of collagen components & elastic fibers

- cause old people to look way you do

52
Q

what are the 3 cell types of connective tissue?

A

1) citizens
2) recruited residents
3) transient effectors

53
Q

Citizen cells of connective tissue?

A
  • fat cells, fibroblast, smooth muscle cells, stem cells
54
Q

recruited resident cells of connective tissue?

A
  • from bone marrow;
  • include macrophages, dendritic cells, mast cells
  • enter tissue & stay for long time (weeks-years)
  • can be activated, then activate dendritic cells, which leave to do immune response
55
Q

transient effectors?

A
  • from bone marrow
  • include plasma cells, macrophages, dendritic cels
  • are recruited during an acute inflammatory response, tissue healing or remodeling g
56
Q

getting nutrients to the epithelium?

A
  • nutrients come form diffusion from capillaries; not every cell type/tissue is in contact with a capillary
  • way connective tissue organizes the cell (fibers, found substances etc) is important for structural resilience & nutrient ability of capillaries.
57
Q

Fibroblasts

A
  • producers of collagen & ground substances in connective tissue
  • but ALL fibroblasts regardless of location produce some collagen & GAGs
  • active in embryonic tissue, less so in adults
  • wait for tissue damage, then secret type 1 and 3 collagen before becoming active
58
Q

smooth muscle cells?

A
  • produce elastic fibers or group together to form smooth muscle (contraction + elastin production)
  • present in smooth muscle, arteries & arterioles
59
Q

elastic fibers vs collagen?

A

-elastic fibers turn over more rapidly

60
Q

promotion of cells/fibers in connective tissue?

A

-is variable depending on the tissue & what trying to hold together

61
Q

white fat cells?

A

-unilocular (one large lipid droplet)
-involved in calorie storage, insulation/cushing, hormone production
-# is determined prenatally
distribution= based on gender& genetics
-distribution of fat associated w/ disease

62
Q

how does weight gain/loss work?

A
  • per tissue; you have a set number of white cells that was determined prenatally
  • weight gain= filling in pre-exisitng cells
  • weight loss= shrinkage of the cells
  • exception: hyper plastic obesity*
63
Q

brown fat cells

A
  • in capillaries, have very large mito
  • deposited in specific areas
  • involved in thermogenesis s, or heat production
  • diet doesn’t effect amount of brown adipose tissue, respond to thermogenic stimuli
64
Q

stem cells

A
  • (pericytes) are around small b mood vessels
  • help in angiogenesis (production of new capillaries)
  • give rise to all other connective tissue cells & elsewhere
  • can be resident or induced `
65
Q

why need stem cells in connective tissue?

A

-to help produce differentiated cells in repsonse to wound repair, inflammation or tissue damage

66
Q

mast cells

A
  • in bone marrow
  • long lived & abundant ; very fragile
  • have many varieties due to differentiation in diff tissues
  • when degranulated by IgE; cause histamine releases, changes in smooth muscle & get more blood flow
  • involved in allergic reactions
  • graulated= no histamine release
  • deganulated= releasing histamine in response to allergen
67
Q

what mast cell granules release in connective tissue? How do granules cause tissue damage?

A
  • histamine

- mass cell granules have digestive enzymes; when have too much degranulation for too long you get tissue damage

68
Q

macrophages

A
  • scavengers w/ receptors to capture bacteria & cell debris
  • use proteases & GAGases
  • cover themselves w/ GAG slime to help move through connective tissue
  • have secretory granules in addition to lysosomes
69
Q

peroxisomes?

A

-fuse w/ endocytotic vesicle to affect killing of ingested bacteria in macrophages

70
Q

macrophages and secretory granules

A
  • contain secretory granules in addition to lysosome

- have many components involved w/ immune response (including inflammatory cells)

71
Q

lymphocytes

A
  • T & B lymphocytes stimulated to divide in lymphoid tissues
  • differeitate into memory or effector cells, recruited to target tissue
  • activated B cells become plasma cells (release immunoglobulins)
    • differenitates & take up residence in Dif tissues
72
Q

granulocytes

A
  • neutrophils, eosinophils, basophils with very brief life space
  • appearance of tissue if from rapid recruitment in blood
73
Q

neutrophils

A

are phagocytes, use granules, lysosomes, peroxisomes to kill ingested bacteria

  • very short life & fragile
  • increase number when connective tissue has bacterial infection
  • first responders to any kind of inflammatory response
  • dead neutrophil +dead bacteria=PUS
74
Q

Eosinophil

A
  • have parasite-digesting granule contents that communicate & activate immune cells
  • number increases w/ parasite infection & allergies
75
Q

Basophils

A
  • similar to mast cells functionally
  • play major role in anaphylaxis
  • very fragile, low abundance in tissue, hard to find in tissue section

Block 1 Week 2 (9 decks)

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