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MCM comp > Exam III new material > Flashcards

Exam III new material Flashcards

1
Q

spontaneous lesion

A

small chemical modifications at a NT
depurination- sensitive to hydrolysis = missing base
deamination- C–> Uracil by addition of H2O
don’t distort backbone

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2
Q

Bulky lesions

A

covalent interactions due to UV, carcinogens, oxidative damage. Distorts double helix

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3
Q

copy errors

A

DNA pol incorporates incorrect base

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4
Q

Mutagen

A

an agent that causes DNA damage
chemical or physical
carcinogenic if causes division

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5
Q

chemical mutagens

A

intercalating agent- in between strands of DNA in helix causing stretching
base analogs- inserts into a base space but not actually a base

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6
Q

Indirect activating mutagens

A

require metabolic process to cause damage

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7
Q

Physical mutagens

A

UV radiation. shorter wavelengths=more damage. A->B->C long->short
A: oxidative
B: induces dimers in adjacent pyrimidines
C: germicide C doesn’t make it to surface of earth
Ionization radiation: ss breaks, ds breaks, cross linking

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8
Q

Ionization radiation

A

electromagnetic we use in medicine. because can travel further.
gamma rays are used in cancer therapy– ds breaks are the purpose to kill cells

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9
Q

Particulate radiation

A

not wavelengths, can’t travel very far. don’t use in medicine

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10
Q

Two types of DNA Repair

A

repair bases directly

repair bases that are incorrectly paired or bulky lesions etc..

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11
Q

3mechanisms of DNA repair

A

reverse, remove, tolerate

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12
Q

Base excision repair

A

DNA glycosylase removes purine/pyrimidine but leaves backbone
AP endonuclease recognizes site and cuts our backbone
results in single NT nick so DNA pol comes along and ligase seals

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13
Q

Nucleotide Excision repair, bulky

A

multienzyme complex
scans for distorted double helix and cleaves on either side of distortion
helicase removes ss between cleavage sites
pol and ligase come through

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14
Q

mismatch repair

A

DNA mismatch by DNA pol. following behind replication fork. To locate new synthesized strand use okazaki fragments. MutS and MutL, direct excision of entire sequence near mismatch

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15
Q

piece of DNA is super damaged what back up mech do we have

A

backup polymerases. less accurate, take guesses

trans-lesion synthesis

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16
Q

Transcription coupled repair

A

coding regions- exons. RNA pol stalls-> mech for nucleotide excision repair proteins to cut out lesion.

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17
Q

Double strand breaks

A

non homologous repair- Ku70/80 proteins recruit DNA PK.always lose NT
homologous repair, sister chromatid nearby and used as template. Holiday junction. Recognized by Rad51 and make 3’ overhangs.

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18
Q

DNA damage checkpoints

A

G1/S
S
G2/M

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19
Q

ATM

A

associates with damage and starts kinase cascade for Chk1 and Chk2 proteins to activate p53–>tumor suppressor

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20
Q

p53

A

usually ubiquitinated my Mdm2

when p53 Pi it will Pi p21 which will inhibit Cyclin/cdk complexes in cell cycle

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21
Q

2 major issues with stem cells

A

technological: Driving differentiation

and applying safety

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22
Q

Stem cells

A

have to be able to differentiate into something else and have to be able to proliferate

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23
Q

totipotent

A

total potential to be anything

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24
Q

pleuripotent

A

more directed than totipotent

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25
Q

multipotent

A

more directed than pleuripotent (bone marrow cells)

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26
Q

unipotent

A

near end of cell proliferation stage. “Transant amplifying cell”
Progenitor cell ex: keratinocytes

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27
Q

embryonic stem cells

A

totipotent. ability to take a single cell and grow a complete organism

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28
Q

post-natally derived

A

new borns. umbilical cord blood.placenta-derived:
pleuripoteny/multipotent
cord blood cell banks

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29
Q

adult derived stem cells

A

bone marrow adipose tissue

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30
Q

Induced pleuripotent cell

A

take a cell, fibroblast, keratinocyte. treat with developmental genes. Ox4 Klf4 Sox2 CMyc

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31
Q

cloning

A

somatic cell nuclear transport. take egg, take out nucleus and put in nucleus from a cell.
concerns: aging of DNA, telomere length

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32
Q

Process of induced pleuripotent cells

A

harvest donor cells, place with feeder cells(provide nutrients). transfect with genes of choice and select after proliferation.
mouse experiment with sickle cell anemia

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33
Q

c-Myc function

A

tumorogenisity function. so take out once grown cells that you want

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34
Q

sources of fat for stem cells

A

from surgeries (like around kidney) or from liposuction

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35
Q

what type of cell is fat stem cell

A

mesenchymal stem cell

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36
Q

potential use of stem cells

A

wound healing, diabetes, cardiac infarcts, bladders

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37
Q

Immunomodulation and stem cells

A

T regulatory cells- replace these using stem cells

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38
Q

Ketchums work with Islets

A

using a combination of mouse islets and hASCs, 5-7 days return to normal glycemic level
these mice become diabetic spontaneously

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39
Q

describe experiment with mouse liver

A

co transfected hASC and MSC and endothelial cells to produce liver buds. bile was produced and hepatic proteins but no biliary tree

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40
Q

hESCs transplant

A

changed medium to drive differentiation In VITRO
then transplanted into diabetic mice 32 weeks post injection
bone had grown too.

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41
Q

prochymal and chonrogen

A

chondrogen- knee reconstruction, causes cartilage growth

prochymal

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42
Q

regenexx

A

not used in USA because of FDA

proliferative in vitro

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43
Q

Cell senescence

A

telomerase activity over time. limited number of cell divisions- hayflick limit

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44
Q

hybridoma

A

inject mouse with antigen. wait till makes ab then select ab in B lymphocytes and insert into a tumor cell. infinite ab

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45
Q

structure of antibody

A

2 fab domains- bind antigen

1 fc- functions in signaling

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46
Q

are lymphocytes specific to antigens

A

yes

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47
Q

polyclonal ab

A

ab produced by inoculating an animal against antigen. from multiple lymphocytes against multiple epitopes

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48
Q

ELISA

A

not microscopy, HIV and pregnancy

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49
Q

Proteins in electrophoresis

A

denatured then add SDS which adds negative charge

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50
Q

northern blotting

A

mRNA

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51
Q

southernblotting

A

DNA

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52
Q

western blotting

A

immunoblotting, antibodies

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53
Q

2 ways to replicate DNA

A

1: restrictive endonucleases on each side
2: mRNA–> cDNA via reverse transcriptase, more efficient for specific gene

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54
Q

DNA vector needs

A

Restriction endonuclease site
Autonomous origin of replication (has own machinery)
A gene for antibiotic resistance

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55
Q

Recombinant proteins

A

produce large amounts of protein for therapeutic use.

Expression Vectors- require sequence to express protein. Need bacterial promoter and start site

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56
Q

gene therapy

A

introduce a normal copy of a gene into defective tissue

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57
Q

Retroviruses gene therapy

A

permanent because incorporate into host genome, problem is it can insert anywhere, not directed
Only used in cells that are actively dividing
no immune response

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58
Q

Adenoviruses gene therapy

A

not integrated in host DNA, very transient, constantly re-treat
can give to senescent cells
large immune response

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59
Q

Transgenic animals

A

insert or delete genes from animals using cDNA.Inject into ovuum and offspring will have the gene in all cells and germ line

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60
Q

Blastocyst

A

offspring is chimeric in somatic and stem cells next generation will not be

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61
Q

2 basic components of connective tissue

A

ECM and cells

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62
Q

ECM 3 constituents

A

fibers, ground substance, tissue fluid

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63
Q

2 types of cells in CT

A

“fixed” and hematogenous

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64
Q

3 traditional basic CT fibers

A

collagen
reticular (type III collagen)
and elastic

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65
Q

characteristics of collagen

A

fibrillar, some globular add tensile strength

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66
Q

Collagen I

A

fibril 67nm most abundant- tendon skin, fascia

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67
Q

Collagen II

A

fibril 67nm cartilage, nucleus pulposus, notochord

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68
Q

Collagen III

A

fibril 67nm skin, blood vessels, lymph nodes, spleen

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69
Q

Collagen IV

A

globular, basal lamina of epithelial cells

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70
Q

Collagen VII

A

small fibers 67nm, anchoring fibrils in basal laminae

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71
Q

procollagen

A

can self assemble. Type I collagen, triple helix formation. 2 chains of 1 alphaprocollagen and 1 chain of 2 alphaprocollagen

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72
Q

collagen fibril

A

show periodicity, staggered alignment of procollagen makes it very strong

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73
Q

collagen fiber

A

collagen fibril bundles

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74
Q

length of repeating banding pattern

A

67 nm

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75
Q

length of tropocollagen helix repeating unit

A

300nm

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76
Q

Elastic fibers composed of

A

elastin(amorphous globule protein) and fibrillin (fibrillar protein forms sheath)
elastin core, glycine and proline
surrounded by fibrillin microfibrils that are held together by desmosine and isodesmosine

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77
Q

Marfans

A

fibrillin mutation because elastin has no elasticity

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78
Q

ground substance of ECM

A

GAGs- unbranched polysacs
proteoglycans: GAGs+proteins covalent
adhesive glycoproteins: large multi-domain glycoproteins that interact with integrins, collagen fibers and proteoglycans

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79
Q

GAGs

A

repeating dissacharides

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80
Q

Types of GAGs

A

hyaluronic acid(HUGE) does not covalently bind because doesn’t have sulfate, keratan sulfate heparan sulfate, heparin, chondroitin-4 sulfate, chondroitin-6 sulfate, dermatan

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81
Q

How GAGs function

A

over 100 units long, GAG has overall (-) charge and attracts cations- high [Na] = H2O content
H2O=turgor- resistance

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82
Q

Linking protein

A

used to attach matrix(other GAGs), which are on the core protein aggrecan(another GAG) onto hyaluronic

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83
Q

types of adhesive glycoproteins

A

fibronectin, laminin, integrins, entactin, tenascin, chondronectin, osteonectin

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84
Q

fibronectin

A

dimer of alpha subunits with weight 220kD. links cells and ground substances via integrins, collagen and heparin sulfate PG
embryonic cell migration

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85
Q

laminin

A

trimer, 1alpha 2 beta. Exclusively in basal laminae. 950kD

binds GAGs proteoglycans and adhesive glycoproteins–Collagen IV! entactin integrins and heparan sulfate PG

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86
Q

Integrins

A

250kD heterodimeric. extracell domain binds parts of ground substance causing intracell cascade
COOH terminal binds to vinculin and talin bind to actin

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87
Q

bonds of integrins

A

much weaker than most R-ligand, so but many integrins together to strengthen btu still be mobile(taken apart easily)

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88
Q

entactin

A

collagen IV

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89
Q

tenascin

A

hexamer binds fibronectin

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90
Q

chondronectin

A

binds collagen II

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91
Q

osteonectin

A

binds collagen I

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92
Q

Mucus CT

A

loose CT with lots of ground substance

jelly like matrix(wharton’s jelly) found in umbilical cord and pulp of developing teeth,

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93
Q

Loose areolar CT

A

abundant ground substance
cells:fibroblasts adipose cells, macrophages and mast cells.
loosely woven collagen and elastic fibers. has small nerves and blood vessels.
Packs in tissues and organs

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94
Q

Dense CT. 2 types

A

greater density of loose fibers

regular and irregular

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95
Q

dense irregular CT

A

random arrangement of collagen bundles
dermis
fascia

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96
Q

dense regular CT

A

ordered arrangement: tendon, ligaments, aponeuroses

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97
Q

Adipose CT

A

low fiber and little ground substance. Few fibroblasts hematogenous cells

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98
Q

unilocular

A

white- single lipid droplet

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99
Q

multilocular

A

brown- multiple lipid droplets

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100
Q

Elastic CT

A

fibroblasts, collagen fibers, elastic fibers
wall of large vessel
nuchal ligament

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101
Q

Reticular CT

A

same as collagen III, liver, adipose, lymph and spleen. fibroblasts and reticular fibers

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102
Q

Blood as CT

A

all CT components: cells, ECM
fibers: fibrinogen–>fibrin
ground substance–>GAGs(heparin) proteins(albumin)
fluid–>plasma

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103
Q

characterizations of cartilage

A

rigid flexible and resilient

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104
Q

3 subtypes of cartilage

A

hyaline, elastic, fibrous

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105
Q

articular cartilage

A

hyaline, collagen type II

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106
Q

elastic cartilage

A

type II cartilage, high [ ] elastic fibers

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107
Q

fibrous cartilage

A

intervertebral disc, tendon with chondrocytes replacing fibroblasts collagen I fibers

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108
Q

cartilage cell types

A

chondrogenic
chondroblasts
chondrocytes

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109
Q

fibers of cartilage

A

collagen II (hyaline and elastic) and elastic

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110
Q

ground substance of cartilage is made up of

A

aggrecan (GAG)

chondronectin (adhesive glycoprotein)

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111
Q

development on cartilage

A

embryological mesenchymal cells-> chondroblasts->aggregate->secrete fibers and ground substance and separate to become chondrocytes surrounded by matrix

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112
Q

perichondrium, 2 layers

A

when mesenchymal cells around primordial cartilage condense

fibrous perichondrium, cellular perichondrium

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113
Q

Cartilage growth mechanisms

A

interstitially (within) and appositionally(periphery and moves down)

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114
Q

hormones controlling cartilage growth

A 
growth hormone, thyroid hormone, gluccocorticoids
sex hormones(testosterone, estradiol) Vitamins
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115
Q

Growth hormone-cartilage

A

stimulate growth thru IGF-1

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116
Q

Thyroid hormone-cartilage

A

hypertrophic growth, acts directly thru IGF-1

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117
Q

Gluccocorticoids-cartilage

A

inhibit cartilage growth, down regulate type I collagen.

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118
Q

Vitamin A deficiency

A

slows cartilage growth and calcification

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119
Q

Vitamin C deficiency

A

(scurvy) inhibits collagen synthesis

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120
Q

Vitamin D deficiency

A

inhibits calcification (rickets and osteomalacia)

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121
Q

Is bone inert?

A

mineralized portion is but the tissue is dynamic

122
Q

2 types of bone

A

compact (cortical)

cancellous (spongy)

123
Q

Wolff’s law

A

bone adapts to forces placed on it

124
Q

Bone matrix composition

A

collagen I, majority inorganic, radially arranged collagen fibers of one lamella are perpendicular to those in next lamina
mostly hydroxyapatite salt-Ca2+: form crystals to increase strength

125
Q

lacunae

A

throughout lamellae, small cavities, osteocytes found in lacunae

126
Q

canaliculi

A

radiate from lacunae to transport nutrients cell to cell

127
Q

4 types of lamallae

A

outer circumferential:below periosteum
inner circumferential: along endosteum
osteon: haversian system (functional unit)
interstitial lamellae: remnants of old osteons

128
Q

Cancellous bone structure

A

trabeculae

spicules-no haversian system

129
Q

Osteon structure

A

6-8 lamellae

connected by Volkmann’s canal which are vascular channels at right angles to long axis of bone

130
Q

Periosteum structure

A

fibrous CT tightly adhering to bone, fibrous (outer) cellular (inner) which contains osteogenic cells

131
Q

Sharpey’s fibers

A

fibrous CT tightly adherent to bone. connects periosteum to bone
attach tendons as well

132
Q

endosteum

A

lines bony cavities like haversian canals and marrow spaces

osteogenic potential

133
Q

types of bone cells

A

osteoblasts, osteocytes, and osteoclasts

134
Q

osteoblasts->osteocytes

A

not via differentiation. depends on surroundings what they are

135
Q

osteoblasts

A

mesenchymal cells and osteoprogenitor (periosteum and endosteum) Lots of ribosomes, ER, golgi near surface. nucleus away from surface

136
Q

Osteocytes

A

reside in lacunae, sparse rER and Golgi, long cytoplasmic processes reach through canaliculi
participates in Ca2+ and PO4- transport

137
Q

Osteoclasts

A

large multinucleate, located in Howship’s lacunae, stimulated by fusion of macrophages

138
Q

osteogenesis specific conditions

A

loose mesenchymal form (development)

cartilagenous model

139
Q

Happens in osteogenesis

A

rearrangement of underlying CT, increased vascularity, osteogenic stem cells

140
Q

deposition of bony matrix

A

osteoid is a thin layer of uncalcified preosseous tissue that surrounds the osteocyte, adjacent to active osteoblast

141
Q

making cancellous bone

A

first deposition of bone is a spicule, trabeculae are the spicules that have merged radiating from ossification centers

142
Q

Intramembranous bone formation

A

flat bones, pre existing scaffold:
mesenchymal cells cluster, proliferate and enlarge
cells differentiate and become osteoblasts and secrete matrix, when the matrix calcifies it becomes osteocytes

143
Q

Endochondral bone formation- long bones

A

pre-existing cartilage, osseus cuff forms, midregion calcifies death and reabsorption of central chondrocytes, blood vessels penetrate cuff and form a cavity(for marrow) and the osteogenic cells migrate into cavity
blood vessels then penetrate epiphysis and epiphyseal cartilage plate forms

144
Q

5 distinct zones of epiphyseal plate

A 
zone of resting
zone of proliferating
zone of hypertrophying
zone of calcifying
zone of resorption/ossification
145
Q

zone of resting cartilage

A

pool of chondrocytes- hyaline cartilage

collagen type II

146
Q

zone of proliferating

A

chondrocytes proliferate- stacked nickel

collagen type II

147
Q

zone of hypertrophying cartilage

A

chondrocyte proliferation slows, cells increase in size
collagen type I
cells secrete VEGF

148
Q

Zone of calcifying cartilage

A

chondrocytes begin to degenerate-apoptosis
matrix calcified, scaffold for bone deposition
VEGF still secreting- osteoprogenitor cells arrive at neovascularization

149
Q

Zone of Resorption/Ossification

A

chondrocytes dissapear, vessels invade cartilage source of osteoprogenitor cells. osteoblasts develop and osteoclasts degrade cartilage so new bone is deposited

150
Q

repairing bone fracture

A

granulation tissue and hyaline tissue laid in wound
new tissue develops, cal us
fracture heals as new bony tissue laid down

151
Q

3 ways to regulate Ca2+ metabolism

A

changes in bone turnover
changes in gut absorption
urinary secretion

152
Q

Calcitonin

A

Increased Ca2+ blood levels: inhibits bone resorption. directly inhibits osteoclasts.
parafollicular cells in thyroid gland

153
Q

Parathyroid hormone

A

low bloodCa2+ levels.
increases Ca resorption from bone
binds osteoblasts->releaseing cytokines which stimulate osteoclasts
chief cells in parathyroid hormone

154
Q

Vitamin D

A

converted to calcitriol. regulates Ca2+ and PO4 in blood. promotes Ca2+ uptake from gut
UV exposure causes skin to produce it
ingested in food

155
Q

where is epithelial found in body

A 
endothelium proper: covers and lines surfaces
endothelium: blood and lymph vessels
mesothelium: lines serous cavities
glands: epithelial invaginations
nerve specializations
156
Q

sterocilia

A

very very long microvilli. no motor used for absorption

157
Q

Microvilli

A

brush border or striate border, membrane bound

rooted down via microfilaments and IFs “terminal web”

158
Q

Apical specialization

A

microvilli and sterocilia cilia and flagella

159
Q

LAteral specializations

A

zona occludens, zona adherens: Terminal bars-LM
gap junctions and macula adherens
fascia adherens

160
Q

zona occludens

A

tight junction- permeable seal

161
Q

zona adherens

A

major resistance to shearing stress. dense plaques of myosin tropomyosin actinin and vinculin and E cadherins extra cell protein

162
Q

different lateral specialization found predominantly in muscles

A

6connexin hydrophilic pore

cell-cell communication- ions, cAMP, cGMP, small proteins

163
Q

“spot weld” in cells

A

lateral specialization-macula adherens- tonofilaments which are IFs that anchor into cytoplasm
primarily desmoglein and desmocollin

164
Q

fascia adherens

A

intercalated discs- stretched adherens

165
Q

Basal specializations

A

Basement membrane, hemidesmosomes

166
Q

Basement membrane

A

not phospholipid bilayer. thin acellular layer that separates epithelial cells from underlying CT

167
Q

layers of BM&collagen found in each

A

reticular lamina: connects to basal lamina via collagen VII

basal lamina: lamina rara(lucida) and lamina densa includes collagen IV

168
Q

reticular lamina collagen

A

I II and III

169
Q

hemidesmosome

A

binds epithelium to BM. IFs

170
Q

glands

A

invaginated epithelial cells that begin to secrete

171
Q

modes of secretion for glands

A

apocrine–>membrane bounds particles release in membrane
merocrine–>eccrine, fusion, exocytosis
holocrine–> whole cell lysed

172
Q

classification of glands

A

unicellular vs multicellular mode of secretion
method of production.
nature of secretion

173
Q

Method of gland production

A

exocrine(via ducts), endocrine(secrete into blood and lymphatics) paracrine(extracell space)

174
Q

glandular morphology

A

tubular and acinar

175
Q

ductal morphology

A

simple, coumpoun or branched, or coiled

176
Q

nature of secretion of glands

A

serous- watery. (exocrine pancreas, parotid salivary gland)
mucus- viscouse (goblet, sublingual salivary glands and palantine salivary glands)
mixed- serous demilunes- submandibular salivary glands

177
Q

2 elements of glands

A

parenchyma- functional tissue

stroma- CT elements (lobes and lobule boundary)

178
Q

parenchyma

A

functional tissue of gland. secretory cells and ducts

179
Q

what suggests that ducts are involved in secretion

A

so much mitochondria is found in the infoldings

180
Q

2 divisions of skin

A

Epidermis and dermis

181
Q

hypodermis

A

subcu, attachment, padding, molds external appearance.

182
Q

epidermis layer

A

stratified squamous epithelium. thick 400-600um hairless and thin 70-150um hairy

183
Q

3 layers of epidermis

A

stratum granulosum(superficial) stratum spinosum and stratum basalis (germinativum)

184
Q

Stratum basalis

A

cuiboidal cells dermal-epidermal junction. hemidesmosomes to attach
intense mitotic activity turnover 50-60 days
IFs

185
Q

Mechanism to regulate stratum basalis

A

vitamin A and D required for differentiation and keratinocytes have R for GFs and synthesize GFs

186
Q

stratum spinosum

A

spiney desmosomes all around it-> resist shear stress.

187
Q

Stratum granulosum

A

very basophilic, keratohyalin granules(H2O barrier), keratinosomes present that function as a cement and create barrier to intracellular transport
these both form cell envelop and lipid envelop for H2O barrier

188
Q

2 layers above granulosum

A 
stratum lucidum(thick skin)
stratum corneum (no identifiable organelles) have tonofilaments with filaggrin to form bundles
189
Q

desquamation

A

removing outer epidermal layer, not only due to abrasive forces- lipolytic enzymes

190
Q

Melanocytes

A

specialized cells of epidermis- dendritic cell morphology that reach between keratinocytes to give melanin. via specialized lysosomes called melanosomes

191
Q

melanin production

A

tyrosine converted to DOPA by tyrosine kinase

192
Q

how many keratinocytes does 1 melanocyte associate with

A

about 36

193
Q

4 stages of production of mature melanin granules

A

Stage I: tyrosine containing melanosomes form in melanocyte
Stage 2: melanin production initiatied by tyrosine kinase
stage 3: melanosomes excreted
stage 4: melanosomes phagocytksed by keratinocytes

194
Q

Langerhans cells

A

marrow derived. Antigen presenting cells (APCs)

migrate to T cells and present antigen so then make IL-1 which induces T cells to make IL-2 to T cell proliferation

195
Q

Merkel cells

A

mechanoreceptors for cutaneous sensation found in stratum basalis, more prominent in thick skin with high acuity(fingers)

196
Q

Dermal-epidermal junction

A

dense irregular CT, epidermal pegs and dermal papillae to amplify contact

197
Q

2 layers of dermis

A

Papillary: CT, blood vessels, Meissners corpuscles(2 pt discrimination)
Reticular: hair follicles, pacinian corpuscles, blood and lymph, glands

198
Q

number 1 regulator of body temp

A

heat evaporation and heat production(muscle)

199
Q

Layers of dermal-epidermal junction

A

basal cell plasmalemma (lowest epidermis)
basal lamina(lucida and dense)
CT fibers of basal lamina: anchoring fibrils to dermis via collagen VII

200
Q

Hair follicles

A

shares characteristic with epidermis
source of new epidermis.
arrector pili muscle goose bumps
sebaceous gland (secrete sebum into hair follicle via holocrine), preventing evaporation

201
Q

Sweat glands

A

thermal regulation. most merocrin(eccrine) cholinergic control
simple coiled tubular glands

202
Q

3 cell types in sweat glands

A

dark-pyramidal : secretion granules
clear-primary cells: no secretion granules but lots of mitochondria and glycogen
myoepithelial cells- contractile

203
Q

Apocrine sweat glands

A

axilla, areola, perianal regions
empty into hair follicle, and can store product in the lumen. odorless product but when degraded by bacteria= odor
adrenergic influence

204
Q

Meissners corpuscles

A

low freq vibration, touch sensation. Neuro sensory organs in dermis

205
Q

Pacinian corpuscles

A

neuro sensory present in dermis
found in deep dermis
sense:high freq vibration and pressure

206
Q

muscle fiber

A

muscle cell or myocyte

207
Q

types of m cells

A

skeletal, cardiac, smooth, myoepithelial, myofibroblast

208
Q

myofibroblasts

A

spindle shaped CT cell- intracell bundled of actin filaments, adherence to PM via vinculin
good for closing wounds and shrinking scars

209
Q

myoepithelial cells

A

specialized and assoc with glandular because contain actin and myosin that contract out gland product

210
Q

what glands utilize myoepithelial cells?

A

mammary gland, lacrimal gland, salivary gland and sweat glands

211
Q

smooth muscle

A

sm mm cells. involuntary contraction. 20-200um 3 to 8 um. centrally located nucleus

212
Q

structure of sm mm.

A

external lamina, exibits like rara and dense

each cell had densa and share rara in middle

213
Q

sm mm contraction

A

intercellular gap junctions: link cells
intracellular fingerlike tubules of sarcoplasmic reticulum.
microfilaments and IFs attach at dense bodies which pull and make cell blebbing and nucleus is pleated or coil

214
Q

skeletal muscle composition

A

voluntary contraction, long cylindrical. variable size 1-4cm and 10-100mm HUGE
peripheral nuclei and multiple nuclei

215
Q

striations in skel muscle cells

A

z line to z line line up

216
Q

contractile unit of myofiber

A

sarcomere

217
Q

very thin dark line in myofibers

A

Z line

218
Q

H line in myofibers

A

light band in middle of A band

219
Q

A band

A

dark band in between z lines

220
Q

I band

A

light band on either side of Z line

221
Q

Endomysium

A

surrounds individual cells (myofibers)

222
Q

perimysium

A

surrounds fasicles (bundles of cells)

223
Q

epimysium

A

surrounds muscles (bundles of fascicles)

224
Q

Cardiac muscle

A

composed of cardiac m, involuntary contraction, pecialized striated muscle

225
Q

characteristics of cardiac muscle

A

elongated 50-100um 15-20um, 1-2 nuclei centrally located
not as defined as skel m but have striations.
intercalated discs-fascia adherens: gap junctions

226
Q

4 events that are involved in m contraction

A

Neuro-muscular junction
excitation-contraction coupling
filament sliding
transduction of contraction(muscle-bone)

226
Q

4 events that are involved in m contraction

A

Neuro-muscular junction
excitation-contraction coupling
filament sliding
transduction of contraction(muscle-bone)

227
Q

Neuro-muscular junction

A

excitation signal transfered from neurons to motor end plate

227
Q

Neuro-muscular junction

A

excitation signal transfered from neurons to motor end plate

228
Q

Impulse at Neuromuscular junction

A

change in membrane potential, Ca2+ released, acetylcholine released into synaptic cleft
free Ach binds to R in myocyte membrane to ligand gated channels- Ach opens channel and Na+ depolarizes myocyte membrane

228
Q

Impulse at Neuromuscular junction

A

change in membrane potential, Ca2+ released, acetylcholine released into synaptic cleft
free Ach binds to R in myocyte membrane to ligand gated channels- Ach opens channel and Na+ depolarizes myocyte membrane

229
Q

Excitation-contraction coupling

A

transmission of nerve impulse down T tubules”triads” located at A/I band junction
Na+ influx->Ca2+ release from sER into cytoplasm to bind myofibrils

229
Q

Excitation-contraction coupling

A

transmission of nerve impulse down T tubules”triads” located at A/I band junction
Na+ influx->Ca2+ release from sER into cytoplasm to bind myofibrils

230
Q

each myosin filament is surrounded by how many actin

A

6 actin thin filaments

231
Q

structure of myosin filaments

A

light meromyosin has 2 heavy chains and a hinge region

232
Q

Muscle-Bone Connection

A

tension induced by m contraction. transmitted into connecting bones. actin filaments(insert at z line) and surrounding CT(tendon bone and sharpeys fibers) facilitate transmission

233
Q

describe contraction of skel muscle

A

binding of myosin head to tropomyosin(uncovered when Ca2+ binds troponin) causes release of ADP and Pi which induces contraction and at low energy state, need ATP to release myosin from actin and eventually converted back to ADP and Pi

234
Q

why is rigor mortis at a contractile state

A

because this is the low energy state of muscle contraction

235
Q

smooth muscle contraction

A

Ca2+ release from sER binds to calmodulin(on myosin light chain kinase) which will phosphorylate myosin allowing it to bind actin

236
Q

Golgi tendon organs

A

sensory, but not motor. sense increased tension in entire muscle

237
Q

Nissl bodies

A

rER stains very darkly

238
Q

MSOs

A

belly of most skel mm, run parallel with main muscle fibers.sense length and tone
have own motor and sensory neurons.
annulospiral

239
Q

Skel mm two types of fibers

A

extrafusal: make up bulk of muscles
intrafusal: modified

240
Q

Golgi tendon organs

A

sensory, but not motor. sense increased tension in entire muscle

241
Q

Nissl bodies

A

rER stains very darkly

242
Q

axonal cytoplasm

A

do not contain organelles

only cytoskeleton, mitochondria, and vesicles

243
Q

antergrade and retrograde transport

A

antero: kinesin. from cell body to periphery
retro: dynein. from periphery to cell body

244
Q

dendritic cytoplasm

A

does not have golgi apparatuses

245
Q

synaptotagmin

A

activates t and v snares for fusion in presynaptic membrane

246
Q

Astrocyles

A

CNS neuroglia: maintain tight junctions at blood/brain barrier. assoc with nodes of rangier and regulate [K+]

247
Q

microglia

A

phagocytic cells-response to disease or injury

248
Q

Inhibition of AP on postsynaptic membrane

A

NT gated Cl- channels–> hyperpolarization

249
Q

types of ependymal cells

A

apical surface microvilli and cilia in production CSF
basal surface: infoldings that assoc with astrocyes
lateral surface: tight junctions
choroid plexus: modified and produce CSF

250
Q

satellite cells

A

analogous to Schwann cells but do not produce myelin.

251
Q

enteric neuroglia

A

located in ganglia, analogous to astrocytes

252
Q

Inhibition of AP on postsynaptic membrane

A

NT gated Cl- channels–> hyperpolarization

253
Q

saltatory conduction

A

in myelinated nerve, voltage reversal takes place at nodes of rangier where Na+ and K+ can be moved across membrane. jumps from node to node

254
Q

Grey matter vs white

A

grey: nerve cell bodies, axons and dendrites and glial
white: nerve axons, assoc glial and blood vessels

255
Q

Epineuriam

A

Dense irregular CT, cover peripheral nerve(vessels within this layer)

256
Q

Blood brain barrier

A

Endothelial cells- elaborate tight junctions- continuous capillaries
endothelial basal lamina has pericytes and BM
astrocytes: foot processes close with BM, important for integrity of tight junctions

257
Q

Endoneurium

A

loose CT, covers individual nerve cells

258
Q

Perineurium

A

specialized CT, covers fascicles. perineurial cells maintain blood nerve barrier

259
Q

Epineuriam

A

Dense irregular CT, cover peripheral nerve(vessels within this layer)

260
Q

blood vessels

A

derived from mesenchymal cells
lined with endotehlial cells- mono layer localize immune response, ischemia etc. can change shape/number depending on stimuli

261
Q

endothelial cell location on capillary

A

interior. usually smaller than RBC, so RBC have to squeeze- increasing contact for exchange of material

262
Q

Do capillaries have sm muscle?

A

no, but have perictyes

263
Q

pericytes

A

specialized cells located next to capillary- have processes to surround capillary

264
Q

When does the sprout cell stop

A

when reach another sprout or vessel that is emitting signals to sprout if its the same type of vessel and can join.

265
Q

angiogenesis

A

Sprout from existing vessel
neovascularization
happens in ischemic conditions, menstration, can be caused by tumor metastization of diabetic retinopathy

266
Q

Capillary sprout

A

vasodialtion will occur, followed by Tip cell sprout, it is an existing endothelial cell that changes phenotype to express “pseudopodial” processes to guide into ECM
not dividing- require guidance signals

267
Q

Tip cells are followed by what cells

A

stalk cells- actively dividing epithelial cells and hollowing out to create lumen of capillary

268
Q

When does the sprout cell stop

A

when reach another sprout or vessel that is emitting signals to sprout if its the same type of vessel and can join.

269
Q

Endothelial precursor cell EPCs

A

undifferentiated in bone marrow- signals can recruit these cells. Like ischemia from MI or other complications. Express VEGFR-2 and VE-cadherin

270
Q

events of angiogenesis

A

vasodialtion via NO and VEGF
degradation: proteolytic cleavage of BM components to allow it to travel.
Migration: direct new growth
Proliferation: endothelial cells in stalk
Maturation: after contact of sprouts- laying down BM and recruiting perictyes(capillaries)

271
Q

Matrix metalloproteinase

A

degrades components of ECM to make room for capillary sprout migration

272
Q

VEGF-A

A

promoter of angiogensis: ligand that acts in paracrine manner(diffuses short distances)
VEGF-2 R which bind circulating isoforms->induce down stream signaling pathways. tyrosine kinase so Ras/Raf and MapK and PI3 signaling

273
Q

VEGF

A

induces Endothelial precursor cells to migrate from marrow to local area. Tip cells detect VEGF and move towards it. Increase vascular permeability.
upregulate expression of proangiogenic proteins

274
Q

Proangiogenic proteins

A

plasminogen activator

collegenase

275
Q

What stimulates VEGF

A

hypoxia- Hif1 gene regulatory. usually ubiquitlyated and degraded. but can upregulate VEGF in hypoxic conditions
TGF beta and alpha
PDGF

276
Q

Notch R signaling

A

juxtacrine, membrane bound
Stalk cells. control branching by regulating proliferation. decrease response to VEGF
delta is endothelial cell specific and expressed by tip cells, induced by VEGF

277
Q

Angiopoietins

A

Ang1: recruit periendothelial cells to promote vessel maturation.
Ang2: endogenous antagonist to Ang 1 R(Tie2)
increase response to VEGF- so not grown completely yet

278
Q

PDGF

A

secreted by endothelial cells. R is on pericytes and sm m cells to function in recruitment for maturation. PDGF released after Ang1

279
Q

bFGF

A

endothelial cells and macrophages express this. secreted and stored in ECM- affinity for heparin to help guide recruitment mech
bFGFR expressed in endothelial cells, fibroblasts, sm mm cells and neurons. Mitogenic Induce mitosis

280
Q

TGF-beta

A

induces VEGF expression- fibroblast and endothelium

281
Q

MMPs matrix metalloproteinases

A

contain zine, necessary for tissue remodeling. Induced by VEGF, GFs and mechanical stress
secreted as zymogens by endothelial cells
degrade BM of vessel and ECM components
release ECM bound proangiogenic factors(VEGF) (FGF)
degrade ECM components into fragments to interact with integrin pathways

282
Q

Integrin pathway

A

fibronectin :degraded fragment bind integrin- start to cluster = FAK focal adhesion complexes.
cytoplasmic sides now start to act as transcription->allows cell to migrate via actin cytoskeleton

283
Q

Thrombospondin-1

A

inhibitor of angiogenesis. Upregulated by p53 in fibroblasts

284
Q

When platelet reaches cloth

A

regulators are released to control neovascularization. pro and then anti angiogenic

285
Q

Angiostatin

A

degradation ECM, inhibitor of angiogensis. plasminogen, found in plasma. this is a fragment that could induce apoptosis and inhibit cell migration

286
Q

Endostatin

A

collagen. BM vessel walls. Inhibits VEGF signaling, blocks tyrosine kinase Phosphorylation

287
Q

Platelets

A

small fragemented portions of cells, sacs of proteins to be released when signaled.
14+ promoters angiogenesis and 12 inhibitors

288
Q

When platelet reaches cloth

A

regulators are released to control neovascularization. pro and then anti angiogenic

289
Q

Turn off angiogenesis

A

Degrade Hif-1 and keep [ ] low, this happens when Oxygen levels are good.
E3 von hippel lindau ligase responsible for marking Hif-1 for degradation

290
Q

one dysfunctional allele Von Hippel Lindau

A

somatic mutation results in no functional VHL-> continually express Hif1, overexpression VEGF, hemanglioblastoma(blood vessel rich tumor)

291
Q

Tumor angiogenesis

A

in order for a tumor to grow, needs more vascularization. there is a switch when it can actually stimulate neovascularization

292
Q

Nonneovascularized tumors

A

not clinically detectable (unless skin) small in size, growth inhibited due to hypoxia–> so growth is slow because diffusion of O2 is limited. 100um
generally not metastatic

293
Q

Bevacizumba Avastin.

A

anti VEGF antibody, no longer able to bind to Receptor

shows increase visual activity in diabetic retinopathy. most effective when combined with laser therapy

294
Q

Inhibiting angiogenesis via drugs

A

direct/indirect and biologics(ab and proteins created in living tissues)

295
Q

direct manner of inhibit angiogenesis

A

inhibit endothelial cells from responding

296
Q

indirect manner of inhibiting angiogenesis

A

inhibiting cells that release stimulatory factors like TGF-beta and GFs

297
Q

Bevacizumba Avastin.

A

anti VEGF antibody, no longer able to bind to Receptor

shows increase visual activity in diabetic retinopathy. most effective when combined with laser therapy

298
Q

Trastazumab

A

indirect inhibitor, breast cancer ab antagonist drug
Her2/neu R are tyrosine kinases that are mutated to be on or over expression
younger women. we use ab antagonist in Her2. so halts production of angiogenesis promoters

MCM comp (2 decks)

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