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Molecular Mechanisms > Block 2 > Flashcards

Block 2 Flashcards

1
Q

location of actin fibrils in cells

A

filopodia (villi projections); stress fibers bundles (across cells); lamellipodia; amorphous gel; contractile ring

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2
Q

microfilament polimerization

A

ATP + G-actin form trimer (rate limiting) –> filament; + end grows faster. ATP and Mg2+ required for polymerization

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3
Q

profilin

A

promotes G-actin polymerization by binding monomers

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4
Q

thymosin

A

inhibits G-actin assembly into Filamentous Actin—binds G-actin and inhibits polymerization

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5
Q

Arp2/3

A

bind (-) actin; serve as nucleating factors (bypass of rate LS)and allow for formation of branched (70 degrees), dendritic array of tree of actin (think lamellipodium)

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6
Q

formins

A

bind (+) actin filament; cause straight filaments

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7
Q

regulation of MF

A

CDC42 -> Rac -> Rho GTPase (Ras like).
Rac critical for control of lamellipodia (via WASp and Arp2/3)
Rho-GTPase control stress fibers (via WASp and Arp2/3). CDC42 is critical for filopodia ie interact with formins.

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8
Q

myosin 6 and Va

A 
6 = moves to (-) end of actin (exception; all other myosins move towards +)
Va = moves vesicles in cytoplasm
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9
Q

movement of cell via actin

A

(1) Rac -> WASp -> arp2/3 -> polymerization of dendritic arbors of actin
(2) placement of integrins to interact w matrix
(3) depolymerization at back of the cell; myosin contration to move cell and nucleus

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10
Q

MT polymerization

A

originates from centrisome (2 centrioles + clould of gamma tubulin ring-like complexes)
aggreagates of beta+alpha- form 13 protofilaments that then create MT (+ end is fast growing)

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11
Q

stabilization of MT

A

mt-GTP “recruits” EB1. EB1 interacts w plasma membrane via mDia and APC (activated by Rho-GTP)

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12
Q

Tau, MAP2

A

Tau - space MT closer together; MAP2 - space MT further apart

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13
Q

drugs that destabilize MT (5)

A

podophyllotoxin, vinblastine, vincristine, cholchicine, garlic called S-allymercaptocysteine

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14
Q

drugs that stabilize MT (3)

A

Taxol, Epothilone, Cryptophysins

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15
Q

IF in epithelia, neurons, nuclei

A

epi - keratin
neurons - neurofilaments
nuclei - lamins

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16
Q

epidermolysis bullosa

A

a blistering disorder due to autoimmune attack or inherited abnormalities on the desmosome or its components that cause disorganization of dermis-epidermis interface.

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17
Q

plakins

A

allow for cross-bridge of IF to MT and MF

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18
Q

link cytoskeleton into nucleus via lamins

A

nesprins-sun complex

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19
Q

types of junctions that contain cadherins

A

adhesion, desmosomes, hemidesmosomes

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20
Q

general characteristics of cadherins

A

EC domain activated by Ca; homotypic binding; domain swapping

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21
Q

adhesion junctions as signaling molecules

A

intracellular domain of cadherin interacts with beta catenin - alpha catenin - vinculin - actin.
beta catenin is also a transcription factor (cotranscription factor LEF-TCF)
beta catenin degraded by APC (inhibited by Wnt signaling)

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22
Q

desmosomal cadherin

A

desmoglein, desmocollin

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23
Q

pemphigus vulgaris

A

auto-antibodies attack desmoglein 3 (desmosomal cadherin). blistering within keratinocyte layer, skin shedding

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24
Q

tight junction proteins

A

claudins (also impart selectivity)

occludins. both are tetraspanins

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25
Q

gap junctions (proteins and regulation)

A

6 connexins make a connexon -groups of them form gap junction
open in low Ca2+ or high pH
close in high Ca2+ or low pH
synchronize the activity of groups of cells

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26
Q

nectins/syncam

A

heterophilic adhesion junctions; present in eye and ear Nectin1-3 interaction for ex. +/- charges and different chain lengths allow for heteropholic interactions

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27
Q

examples of GAGs

A

hyaluronic acid; chondroitin; dermatan sulfate; keratan sulfate; heparan sulfate; heparin

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28
Q

GAGs - characteristics

A

(think repeating sugars)

sulfated; have carboxyl groups (ie glucouronic acid) - hold water, Na+; firm but not hard - resist compression

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29
Q

hyaluronan

A

type of GAG but: polymerized at cell surface (not made in Golgi); not sulfated

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30
Q

proteoglycan

A

core protein + GAGs

linked via serine (O-linked) -> xylose-galactose-galactose-glucuronic acid (tetrasaccharide primer)

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31
Q

aggrecan

A

type of glycoprotein. long protein core+ thousands of GAG chains.
can link to hyaluronic acid via link proteins –> principal component of cartilage

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32
Q

Laminin

A 
matrix protein (trimer w subunits alpha, beta, gamma) shape of cross; Short arms of laminin “self assemble.” Long arms (1) bind to integrin receptors in focal adhesion spots and in hemi-desmosomes and (2) interact with other components of the matrix.
rich in the basal lamina
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33
Q

Fibronectin

A

matrix protein (dimer) interacts with laminin and with integrins via the RGD sequence recognized by integrins. Self-dimerize when interact with integrins. rich in the basal lamina

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34
Q

collagen IV

A

reticular matrix under laminin matrix (basal lamina)

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35
Q

collagen II

A

cartilage

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36
Q

collagen III

A

spleen; lymphocytes

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37
Q

nicogen and perlecan

A

link laminin matrix to collagen IV

perlecan is a heparin sulface proteoglycan

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38
Q

integrins

A

transmembrane proteins (alpha-beta dimers) that interact w matrix and cytoskeleton of IF or actin. bind to RDG sequence present in most matrix proteins; present in focal adhesions (Cell-Cell and Actin-Linked Cell-Matrix-Adhesion) and Hemidesmosomes (Cell-Matrix) and Desmosomes (Cell-Cell).

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39
Q

focal adhesion

A

Cell-Cell and Actin-Linked Cell-Matrix-Adhesion - all connect to actin fibers in cells. composed of integrins linked to actin cytoskeleton via talin (regulated by mechanical forces that pull on it and reveal vinculin binding site), vinculin, paxillin. β-Catenin and Focal Adhesion Kinases are associated with these junctions

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40
Q

integrin “activation”

A

folded up when inactive.
(1) inside - outside signaling: extracellular signal=>receptor=> second messenger=> Binding of Talin on the inner face of the integrin=> integrin unfolds and interacts with extracellular matrix.

(2)Outside->Inside Signaling: integrins bind to ligands -> send signals for cell survival “anchorage dependent survival.” cells that are not bound die (“anoikis” = “a state of homelessness)

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41
Q

LFA1

A

type of integrin present in white blood cells. binds to Ig superfamily counterreceptors (ICAM); alpha mutation results in impaired recruitment of leucocytes; beta mutation = leucocyte adhesion deficiency; impaired inflammatory response

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42
Q

alpha(iib)beta3

A

integrin present in platelets that ligate to fibrinogen. mutation in alpha = bleeding, no platelet aggregation (Glanzmann’s disease). mutation in beta = Glanzmann’s disease and mild osteopetrosis

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43
Q

A6B4

A

integrin present in hemidesmosomes in epithelia that ligate to laminin. mutation in A or B = severe skin blistering

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44
Q

focal adhesion kindase (FAK)

A

activated by integrin binding of matrix and by growth factor signaling. In turn, they regulate the binding of integrins to the matrix and hence organize the shape of the cell as well as its potential motility

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45
Q

selectin

A

receptors on WBC’s that bind sugars by a lectin domain (recognize carbohydrates); mediate transitory binding; allow for WBC to roll along endothelium. when it has to leave the blood vessel it expresses leukocyte integrin (ex: LFA1) that bind to endothelial ICAM and VCAM

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46
Q

Nernst Equilibrium (basic concept)

A

for charged molecules moving across a semipermeable membrane -> equilibrium between concentration and charge gradients

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47
Q

starling forces

A

hydrostatic pressure and osmotic/oncotic pressures are opposing. in blood vessels - water w nutrients will come out of the capillary in the arterial side (higher pressure) and come into venous side w waste

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48
Q

cyclic changes that allow myosin to “walk” along actin

cross bridge cycle

A

(1) rigor = myosin attached,no ATP
(2) +ATP = myosin released, sliding possible
(3) myosin head is cocked, ATP hydrolized but ADP and Pi still bound
(4) Pi falls off, reattaches weekly at first (force generating/power stroke)
(5) ADP falls, myosin head again locked to actin

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49
Q

anchoring actin in sarcomeres

A
  • Cap Z, alpha actinin -> + end at Z disc
  • tropomodulin -> - end
  • nebulin regulates length of actin filaments
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50
Q

titin

A

anchors thick filaments (myosin II) in Z discs - determines sarcomere length and gives it elasticity

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51
Q

Transverse tubules

A

(t tubules) invaginations of plasma membrane (sarcolemma) in muscle cells that allow for electrical signal to spread quickly (Ca2+ release).
has a voltage sensitive protein L-type, Ca2+ channel (dihydropyridine receptor) that when depolarized forces conformational changes in the ryanodine receptors in the neighboring sarcoplasmic reticulum

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52
Q

ryanodine receptor

A

Ca2+ release channel; releases Ca2+ from sarcoplasmic reticulum after being activate by both mechanical and Ca mediated changes (mechanical>chemical)

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53
Q

SERCA

A

reverses stimulus when skeletal muscle contraction is done by taking up Ca2+. pumps Ca/H+ back into sarcoplasmic reticulum where Ca is stored bound to CALSEQUESTRIN and CALRETICULIN

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54
Q

sarcomere

A

unit of myofilaments (Z-Z; A band and two halfs of I bands).
thin filaments inserted into the Z discs
H band = “center”- myosin but no actin
M zone= center of the H band where thick filaments are suspended and stabilized in register
A band = “all thick” - spans all of myosin (dark band)
I band = actin but no myosin (light band)
Contraction: A band is Always the same length, Z lines get closer, I and H bands shorten and disappear.

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55
Q

*muscle contraction - SA vs nerves

A

SA node cells pace; nerves modulate rate and force of contraction

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56
Q

3 types of glia cells

A

astrocytes (support)
oligodendroglia (myelin)
microglia (defense; macrophage analogue)

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57
Q

pentobarbital

A

drug that prolongs opening of GABA channels, inducing sleep; used to stop seizures

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58
Q

Flux “equation”

A

J(i) = Pi x A x delta(mu)

flux of “i” = pathway x area x driving force

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59
Q

lamins

A

10nm diameter filaments (IF) that form network inside the inner nuclear membrane. can be assembled and disassembled (phosphorylation causes disassembly) during mitosis. Lamin A and B are the two major lamins

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60
Q

Emerin

A

specialized proteins in the internal nuclear membrane near pores that interact w lamin network

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61
Q

nuclear pore

A

ring of 8 subunits, central plug, basket, fibrils directed towards cytoplasm, transmembrane proteins gp120, POM121

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62
Q

NLS

A

nuclear localization signal - PKKKRKV (could also be bipartite KRP…….KKKK). sufficient. can be anywhere in protein

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63
Q

nuclear export sequence

A

leucine rich (L-NES)

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64
Q

nuclear import

A

alpha importin (= alpha karyopherin) recognized NLS. +beta karyopherin. complex binds to Ran-GDP and pore proteins; enter nucleus; important releases cargo when Ran-GTP replaces Ran-GDP. RanGTP-important exit nucleus

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65
Q

nuclear export

A

RanGTP binds exportin+cargo» exit nucleus&raquo_space; RanGDP rebinds

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66
Q

MAN1

A

protein in the inner nuclear membrane that can regulate signaling by classical second messengers (MAN1 turns off SMAD inside nucleus)

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67
Q

steroid signaling (enter cell, bind to receptors which are transcript. factors) is there amplification? what are some examples?

A

no amplification.

ex: cortisol, testosterone, estradiol, thyroid hormone

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68
Q

contact dependent cell surface signaling

A

cell 1 - delta; cell 2 - notch receptor.
delta tries to endocytose notch receptor, pulls on it, reveals notch proteolysis site. notch is proteolyzed, cytoplasmic domain (notch intracellular domain = NICD) goes to nucleus, kicks out CSL receptor, activates tons of genes.
asymmetric. ex: capillaries

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69
Q

Frizzles/Wnt

A

wnt ligand binds frizzles, blocks degradation of beta-catienin, which goes to nucleus and binds TCF/LEF transcript. factor bound to DNA

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70
Q

G-protein linked receptor

A

7trasnmembrane receptor. when ligand binds

(1) GDP is exchanged for GTP in G protein Alpha (A). A and Gamma (G) +Beta (B) dissociate (GB).
(2a) G-A signals by
(i) adenyl cyclase&raquo_space; ATP->cAMP&raquo_space; PKA, which phosphorylates transcription factors
(ii) activating phospholipase C, which cleaves inositol into diacyl glycerol (» PKC) and IP3 (» Ca2+ channel)
(2b) G-GB&raquo_space; K channel

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71
Q

tyrosine kinase receptor

A

ligands are dimers&raquo_space; dimerize receptors, cross phosphorylate, recruit adaptors, activate Ras activating proteins.
Ras GTP&raquo_space; Map-k-k-k&raquo_space; Map k-k&raquo_space; Map-k&raquo_space; many genes; proliferation.
Ras = onco gene

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72
Q

Avastin

A

drug that targets VEGF (vascular endothelial growth factor, a tyrosine kinase pathway). VEGF stimulates vascular developmetn

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73
Q

JAK-STAT

A

ligand binds to receptor&raquo_space; receptor recruits JAK&raquo_space; Jak (tyrosine kinase) phospho receptor, STATs bind to phospho sites, get phosphorylated as well, dimerize, move into nucleus, activate gene expression

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74
Q

SMADS

A

type of STATs - after heterodimerization, move into nucleus, regulate genome

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75
Q

adherens junction

A

connects actin filament bundle in one cell with that in the next (vs. desmosome - connects IF)

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76
Q

PCP

A

glutamate-activated channel - creates hallucinogen/behavior changes

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77
Q

BTx

A

keeps Cl channel open

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78
Q

GABA

A

opens channel

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79
Q

pentobartital

A

keeps GABA channel open; sleep; prevents seizure

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80
Q

how to “address a protein” to apical side of epithelium

A

GpI linkage to lipid raft (cholesterol and glycosphingolypids). GpI linkage added by recognition of 30terminal aa (dominant)

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81
Q

transcytosis

A

directing proteins from basolateral membrane to apical membrane (epithelia)

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82
Q

how to “address a protein” to basolateral side of epithelium

A

protein must have beta turn (hydrophobic-XX-tyrosine). from golgi AP proteins place them in clathrin (mu subunit binds to .XXY., beta subunit binds to clathrin). vessicle interacts with EXOCYST (~10 proteins that lead it to v-snare, t-snare interaction and fusion)

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83
Q

cytoplasmic proteins that aggregate at tight junctions

A

Zo-1, Zonab (carrier protein), cyclins (cell cycle regulator), cytoskeleton. When cell-cell bound&raquo_space; cyclin prevented from going to nucleus. Wound&raquo_space; tight junction broken&raquo_space; cyclin can go into nucleus and promote cell proliferation

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84
Q

example of selective destruction as a way of maintaining cell polarity in epithelium

A

IgG receptor PIGR. it binds antibodies in the basal side, transcytoses them to apical lumen, where it is cleaved

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85
Q

regulation of apical/basal membrane ratio

A

Know: LKB1, PAR1, and PAR3 all stimulate apical identity.
FYI: apical identity defined by PAR1 in basolateral and Par3 in apical surface. LKB1 transmits
extracellular signal à PAR1-mediated phosphorylation events prevent basal invasion by the apical
polarity determinants. Phosphorylated PAR3 binds PAR5 during relocation to apex.

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86
Q

3 components of connective tissue (broad). 3 types

A

(1) matrix - GAG-sulfated and non-sulfated, proteoglycans. H2O
(2) fibers - collagen, elastin
(3) cells - fibroblast/fibrocytes/chondroblast/chondrocytes/osteoblast/osteocytes

types: loose, dense (refers to fibers), embryonic

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87
Q

collagen (typical aa, formation)

A

triple alpha helices, common feature of glycine-x-y.
• formed in ER w N and C-terminal telopeptide to prevent crosslinks&raquo_space; exocytosis&raquo_space; procollagen peptidase takes off telopeptide&raquo_space; fibrils form&raquo_space; lysyl oxidase crosslinks extracellularly to prevent degradation&raquo_space; fibrils combine to form fibers
• post translational hydroxylation of proline and lysine allow for interchain H bonds hydroxylation requires Vit C&raquo_space; SCURVY

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88
Q

collage types I-IV. how many types of alpha chain

A

Type I – skin, bones, tendon.
Type II – cartilage.
Type III – reticular (+skin - think Ehlers Danslos).
Type IV – basement membrane (forms sheet, not fibrils)
» 42 types of alpha chains. 40 types of combinations documented. Types II, III, VII, XVII, XVIII have only one alpha type. Types I, IV, IX, XI have 2 or 3 types of alpha chains

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89
Q

Ehlers Danlos

A

problems with procollagen pepsidase (ADAMTS2) - no mature collagen. Could also result from defect in lysyl oxidase. (TYPE III collagen)

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90
Q

elastin

A

random coiled. FIBRILLIN 1 limits elasticity. (aorta, ear, giraffe’s neck)

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91
Q

Marfan’s syndrom

A

due to defect in fibrillin. Arachnodactyly (very long fingers). Lens dislocate, aorta is floppy, low diastolic BP. will die of aortic rupture

92
Q

loose connective tissue

A
  • areolar (under epithelium of skin, glut, breast ducts, etc) - has immune cells, allows for nutrients through, resistant to compression
  • adipose (white, brown in chest, sternum, vertebral column, babies)
  • reticular (lymphoid organs - nodes, spleen) collagen II. silver stain
93
Q

gynecomastia

A

breast tissue growth in males. can be side effect of medications such as spirolactone

94
Q

white adipose; regulation

A

signet ring cells (one large fat droplet)

  • NE/Epi: TG breakdown upregulated via G-alpha» cAMP»PKA»perilin and hormone stimulated lipase
  • Insulin: TG breakdown downregulated via PDE-3B, which destroys cAMP
95
Q

leptin

A

signals to brain, “satiety hormone”. dysfunction in leptin (ob/ob) or receptor (db/db) can lead to obesity.
- ob/ob mice sutured to WT&raquo_space; ob/ob lose weight, saved.
- db/db mice sutured to WT&raquo_space; stays obese, WT dies
(db=dead battery=no reception)

96
Q

brown fat

A

generates heat and consumes O2. brown fat removed&raquo_space; (-) O2 consumption. Low O2&raquo_space; (-) heat

97
Q

mesenchyme; Wharton’s jelly

A

mesenchyme = embryonic connective tissue

Wharton’s jelly = mucus jelly surrounding umbilical cord

98
Q

cartilage (ratio of fibrous/ground substance and general characteristics)

A

50%fibrous matrix(collage II, a little of IX, XI) 50% ground sub. resists compression; chondrycytes live within their lacunae; communication via ECM (slow)

99
Q

bone (ratio of fibrous/ground substance and general characteristics)

A

99.6% fibrous matrix. resists tension. osteocytes communicate w each other via CANALICULI using gap junction; also interact w matrix
hydroxyappitite

100
Q

development of bone and cartilage

A

1) Initial Mesenchyme Condensations: Wnt&raquo_space; Sox9/Runx1&raquo_space; mesenchymal condensation
2) high pO2 and some tensile stresses» bone tissue. BMP 2, 4, 7, then runx2 and osterix&raquo_space; osteocalcin&raquo_space; bone formation
3) low pO2 and intermittent compression, Indian hedgehog growth factor (Ihh) and FGF&raquo_space; Sox9, Sox5, Sox6 drives the progenitor cell to chondrocytes. (Sox9 creates cartilage but maintains it in a mature, quiescent state)

101
Q

types of cartilage and where they are found

A

Hyaline (trachea, articular surfaces)
Fibrocartilage (intervertebral disks)
Elastic (ear, epiglottis)

102
Q

ways cartilage grows

A
  • Appositional - chondroblasts add to perichondrium

* Interstitial - chondrocytes expand from w/in isogenous nests (lacunae)

103
Q

2 types of ossification

A
  • endochondrial - most bones

* intermembranous - skull and clavicle only

104
Q

endochondrial ossification

A

1) Diaphysis (bone collar): Hyaline cartilage precursor > stress> hypertrophic chondrocytes> VEGF and collagen X> periosteal bone collar > primary ossification center > vascularization/osteoprogenitors > fully ossified diaphysis
2) epiphysis (growth plates - interstitial growth): hyaline cartilage at bone plate > IHH> chondrycytes stimulated to (+) proliferate to proliferative zone from stem cell zone and mature into BONE (-)make PTHrP, which slows down proliferation and bone maturation

105
Q

intermembranous ossification

A

no cartilage precursor; between membranes. growth occurs at suture lines. osteocytes on surface and matrix

106
Q

bone types

A

Woven: disorganized, fetal Lamellar: adult bone - Organized into osteons: lamellae (highly organized collagen) around central canal = Haversian canal (vessel, nerve), osteocytes btwn lamellae. canalliculi oriented in the same direction

  • Grossly categorized as:
    1) Cancellous, aka spongy = trabecular - Bone heads
    2) Compact aka dense = cortical - Bone shafts
107
Q

factors that increase bone resorption

A

parathyroid hormone
glucosteroids
thyroid hormone
high doses of vit D metabolites

108
Q

factors that decrease bone resorption

A

calcitonin

gonadal steroids

109
Q

factors that increase bone formation

A

growth factor
vit D
gonadal steroids

110
Q

factors that decrease bone formation

A

glucocorticoids

111
Q

bone remodeling. (osteocyte regulation)

A
  • baseline: +sclerostin > Wnt OFF> no bone formed

* stress: -sclerostin > Wnt ON >bone formed

112
Q

bone remodeling (osteoclast regulation)

A

osteoclasts are under regulation of MCSF (macrophage colony stimulating factor) > osteoclasts develop, mature, “live in” Howship’s lacunae, use H+pump, express RANK-R.
(+) RankL (from osteoblast)&raquo_space; ++ bone resorption
(+)OPG (osteoprotegerin from osteoblast)»– bone resorption by binding RankL
under inflammation - RANKL increases, reabsorption increases

113
Q

astrycyte

A

type of glia cell - support to neurons. (instead of collagen)
has much IF made of glial fibrillary acidic protein, desmosomal junctions, processes that wrap around blood vessels/neurons

114
Q

microglia

A

macrophages from bone marrow invading the brain.

115
Q

oligodendroglia and schwann cells

myelination

A
  • make myelin or its equivalent. nodes of ranvier/ saltatory action potential.
  • 1 Schwann cell myelinates 1 axon; oligodendroglia myelinate more >1 neuron
  • Myelin = plasma membrane with a few glycoproteins (myelin basic protein in CNS/protein P0 in the periphery)
  • proteolipid protein (plp) holds together the stacks of membrane wrappings (very hydrophobic; located in the “extracellular clefts”)
116
Q

electrical synapse

A

FAST; passive diffusion through GAP; rare - ex: brainstem neurons that control breathing

117
Q

chemical synapse

A

slow and more important
action potentia> Ca2+ channels open> Ca2+ enters> NT vesicles fuse> NT release> NT crosses cleft, bind to receptors

small stimulus - release of small NT from docked vesicles that were packaged regionally (vesicle recycling maintains volume)
large stimulus = release of peptide NT that were packaged in Golgi

118
Q

ionotropic receptors

A

ligand-gated (direct) ON or OFF

nicotinic AchR - fast (present on skeletal m.)

119
Q

metabotropic receptor

A 
GPCR-coupled 
muscarinic AchR (present on smooth m.) >MapKinase... slow
120
Q

synapsin

A

tethers vesicles to actin near the active zone in neurons

121
Q

Ca-calmodulin activation

A

causes docking of reserve vesicles of NT at plasma membrane - activates v-snares called synaptobrevin to interact w t snares syntaxin
synaptotagmin calcium - catalize fusion of t and v snares

122
Q

botulinum

A

cleaves and inactivates SNAREs –> paralysis ACh (excitatory NT and NMJ)

123
Q

alpha-conotoxin

A

blocks Ach gated channels

124
Q

Ach synthesis/degradation

A

synthesized in terminal bouton by choline acetyl-transferase
taken up by H+/Ach exchange
degraded by achetylcholineesterase in baseal lamina in synapse

125
Q

NT amino acids

A

GABA (from glutamate)
Glycine (from serine?)
Glutamine
Aspartate

126
Q

NT amines

A 
DOPA
Dopamine
Norepinephrine
Epinephrine
(all 4 - catecholamines. excitatory. from tyrosine. Sympathetics , motion control, mental health (Parkinsons Dz, BP, Schizophrenia)

serotonin (mood, sex, appetite)

histamine (allergy)

127
Q

action potential

A
  1. Resting MP = Leak K channels
  2. Receptor/Synapse stimulus sums to threshold
  3. Voltage gated Na channels open
  4. Voltage gated K channels open and Na channels inactivate
  5. Voltage gated K channels stay open leading to “undershoot”
  6. Voltage gated K channels close and leak K channels open
128
Q

accounts for no retrograde flow in neuronal action potential transmission

A

Na channel inactivation (latency)

129
Q

accounts for no retrograde flow in neuronal action potential transmission

A

Na channel inactivation (latency)

130
Q

WASp mechanism

A

hormones or other signals=>CDC42=>unfolding of Wasp=>ARP2/3 activation=>actin polymerization=>force for migration of the leading edge of the cell. ex: WBC making podosomes to migrate across endothelial cells through capillaries . magakaryocytes migration to sinusoids within bonoe cavity to deposit platelets there

131
Q

WASp mechanism

A

hormones or other signals=>CDC42=>unfolding of Wasp=>ARP2/3 activation=>actin polymerization=>force for migration of the leading edge of the cell. ex: WBC making podosomes to migrate across endothelial cells through capillaries . magakaryocytes migration to sinusoids within bonoe cavity to deposit platelets there

132
Q

type of connective tissue in dura and arachnoid mater

A

dura - dense fibrous irregularly arranged

arachnoid - loose areolar

133
Q

types of nerons

A

monopolar - sensory
bipolar - special sensory
multipolar - everything else
pseudounipolar - fused processes

134
Q

comparing axons/dendrites

A

axons:
- tau
Dendrites: have Nissl bodies (RNA), ER, ribosome, mRNA; map2

135
Q

vesicular transport in neurons

A

+ end (towards synapse) = kinesin
(fast transport for synpatic vesicles, slow for tubulin, actin and other housekeeping proteins)
- end (towards cell body) = dynein = retrograde transport used to recycle organelles; tenanus toxin and viruses uses this mechanism

136
Q

vesicular transport in neurons

A

+ end (towards synapse) = kinesin
(fast transport for synpatic vesicles, slow for tubulin, actin and other housekeeping proteins)
- end (towards cell body) = dynein = retrograde transport used to recycle organelles; tenanus toxin and viruses uses this mechanism

137
Q

cardiac muscle

A

branched; striated; nuclei in the middle
Intercalated discs: desmosones (IF),adhesion (MF), gap junctions (located laterally)
1 T tubule per sarcomere, thicker than skeletal m.

Excitation-contraction-coupling is dependent on L-type Ca channels’ triggering Ca influx (vs. skeletal muscle -> L-channel mechanical change to ryanodine receptors more important than Ca influx).
Ca2+ entering from the L-type channel promotes Ca2+-induced Ca2+ release (CICR) from the SR via Ca2+ release channels (ryanodine receptors)

138
Q

smooth muscle

A

no striation; nucleus in the middle of cells; caveolae instead of T-tubules

139
Q

myoepithelial cells

A

branced cells made from epithelia under hormonal regulation for contraction (ex: oxytocin for secretion of milk)

140
Q

myoepithelial cells

A

branced cells made from epithelia under hormonal regulation for contraction (ex: oxytocin for secretion of milk)

141
Q

organization of skeletal muscle

A

Muscle fiber = muscle cell. Muscles are bundles of fibers, which are bundles of fibrils, which are bundles of filaments. (Hint: the shorter the name, the larger the structure!)
endomysium around myofiber
perimysium around bunches of myofibers
epimysium around entire muscle

142
Q

effect of Ca2+ release from sarcoplasmic reticulum into skeletal muscle cytoplasm

A

Ca2+ binds TroponinC/I/T
(TnI binds to actin and inhibits biding to myosin; TnT binds to tropomyosin)
Ca binds to TnC&raquo_space; complex swivels, tropomysin moves and opens myosin binding site» allows cross-bridge cycle to occur

143
Q

effect of Ca2+ release from sarcoplasmic reticulum into skeletal muscle cytoplasm

A

Ca2+ binds TroponinC/I/T
(TnI binds to actin and inhibits biding to myosin; TnT binds to tropomyosin)
Ca binds to TnC&raquo_space; complex swivels, tropomysin moves and opens myosin binding site» allows cross-bridge cycle to occur

144
Q

innervation “types” for smooth muscle

A 
Multi-unit: each cell innervated 1:1, precise, fast (vas deferens, some blood vessels)
Unitary: one nerve innervates many cells, slow.
in general (not just smooth m): motor unit = nerve and all of its innervated muscle fibers.
muscle pool = many motor neurons innervating many muscle fibers.
145
Q

bungarotoxin

A

from snake; binds to acetylcholine receptor in muscle (cholinergic nerve junction)

146
Q

excitation-contractrion coupling in smooth m.

A
  1. Extracellular Ca2+ enters though channels in caveolae.
  2. [Ca2+]i increased by CICR and IP3- induced Ca2+ release from SR.
  3. Ca2+ binds calmodulin. 4. Ca2+-calmodulin complex activates myosin light chain kinase (MLCK).
  4. MLCK phosphorylates and activates myosin (II) so that it can interact with actin.
  5. Force is delivered to dense bodies (analogous to Z discs), causing flattening and contraction but no directional force.
  6. SR Ca2+ is repleted by store-operated Ca2+ channels in plasma membrane.
    * K channel involved but not Na dependent action potential!
147
Q

dynein

A

molecular motor that causes retrograde (- end) transport of vesicles along MT tracks. cocking mechanism. only a a couple of variants. dynactin, Lis1=nudE/L modify dynein

148
Q

kinesin

A

motor protein that moves towards +end (NH3 end of proteins)

149
Q

orientation of +/- ends of MT in epithelia

A

+end basolateral

- end apical side

150
Q

lissencephaly

A

“smooth brain” disease caused by mutation in dynein regulator Lis1 (usually cell progenitors in brain migrate from ventricle to cortex; cannot do so w/out lis1)

151
Q

Lis1

A

regulator of dynein; determines force generation to move large structures such as nuclei along MT towards centrosome

152
Q

layers and types of skin

A

epidermis, dermis, hypodermis
glaborous/volar/non hairy (thick)
hairy = thin

153
Q

layers and compositon of epidermis

A

Basale=>Spinosum=>Granulosum=>Corneum

Cells = Keratinocytes, Melanocytes, Langherans cells, Merkel cells

154
Q

keratinocytes

A

divide in the basale layer (stem cells=>transit amplifying cells=>committed to differentiate=>upward migration). In the spinosum- have desmosomes that make the cells look spiny. In the granulosum- filled with granules of lipids and cellular metabolites that cause cell adherence. in the corneum- flattened lipid-waxes made in the granulosum layer. No nuclei in the corneum, cell death and finally shedding within 2 weeks.

155
Q

melanocytes

A

from the Neural Crest; migrate to the skin. make granules and transfer them to different layers of more basal keratinocytes via phagocytosis. The melanin reduces UV-B damage to skin. Melanoma is a cancer of the melanocytes that form clumps in the epidermis and they migrate and form metastasis.

156
Q

langerhan cells

A

in the spinosum layer. They are antigen presenting cells (CD11+, dendritic marker)

157
Q

merkel

A

in stratum basale; derived from keratinocytes. contain granules of neurotransmitters that signal to nerves; innervated by sensory neurons. Useful to detect fine spatial details in touch

158
Q

epidermal appendages

A
  • hair - associated w dermal papilla (cells from dermis); aerector pili muscle; stem cells
  • sebaceous glands - attach to hair follicle
  • eccrine sweat glands - water for thermalregulation
  • apocrine sweat glands - pheromones. urogenital-axillary zones
159
Q

nociceptive nerves

A

detect noxious stimuli

160
Q

pacinian corpuscles

A

nerves; sense high freq vibration encoding fine texture

161
Q

meissner corpuscles

A

sense low freq vibrations -coarse stimuli

162
Q

squamous cell carcinoma (scc)

A

confined to the epidermis or invasive into the dermis. They come from keratinocytes and the image is one of large proliferative cells in the epidermis

163
Q

eczema (atrophic dermatitis)

A

a disorder of the barrier function due to filaggrin mutations

164
Q

mild epidermal bullosa (simplex)

A

caused by mutations in keratin that attach to hemidesmosomes integrines in basal keratinocytes. blisters within epidermis

165
Q

intermediate epidermal bullosa (junctional)

A

antibodies target integrin of hemidesmosome in keratinocytes. blisters form at interaction of epidermis and dermis

166
Q

severe “dystrophic” epidermal bullosa

A

antibodies or mutations affecting collagen VII below dermo-epidermal junction

167
Q

bullos pemphigoid

A

antibodies to BP180 (adhesion protein that holds epidermis to dermis)

168
Q

poly = neutrophil = PMN = segmented

A

50% of wbc in circulation) multilobar nuclei, poor stainers with red and blue dyes ie neutral staining. They do not divide or proliferate. “Bands” are younger version of neutrophils.

for phagocytosis and the release of substances from granules. make “Pus”. respond to Gram+and Gram- bact, also to some parasites and dead tissue

169
Q

monocytes

A

(5-9% of circulating wbc in circulation)
non segmented nuclei, horseshoe shaped or oval shaped nucleus. Not granulocytes; precursor” macrophage
eat dead cells, foreign proteins, and parasites ie Leishmania. Macrophages in spleen and liver eat degraded RBC and become filled with hemosiderin, a iron based brown degradation product.

170
Q

lymphocytes

A

(about 20-30% of circulation)—round big nucleus and little cytoplasm. “adaptive immunity” ie the cells become educated.
T: Acquired immunity ie response to vaccine; Many subtypes
B: Antibody production after antigen presentation.

T cells respond to viral and bacterial infection. For example, viral myocarditis (Coxsackie virus) is infiltrated by lymphocytes not neutrophils. Lymphocytes also infiltrate organs in “autoimmune disease” as in auto-immune thyroiditis

171
Q

eosinophils

A

Segmented nuclei. Terminally differentiated. Granules with “major basic proteins” that form a crystalline array. Recruited to sites of inflammation and defense in parasitic infection (ex “River Blindness” ) or responding to allergic stimuli like asthma and reactions to medications

172
Q

basophils

A

(1% of wbc): Related to mast cells in tissues. Granules contain histamine, heparin. Turned on by IgE receptors that have bound to allergens. Involved in allergies. Think about anti-histamines!

173
Q

serum

A

no coagulation factors; after clotting leaving serum at top.

174
Q

plasma

A

plus coagulation factors and fibrin and fibrinogen that have not clotted yet and is preserved by additives in the blood collection tube. The anticoagulants include heparin and citrate (binds up Ca2+)

175
Q

definition of stem cells

A

1)Self Renewal;
2)Multi-Lineage Differentiation; 3)Proliferate and Reconstitute the hematopoietic system
CD34+ CD38- Kit+ Lin-
Kit = receptor for stem cell factor
Lin-= no binding of monoclonals that recognize early RBC, WBC

176
Q

aplastic anemia

A

killing of stem cells often with antibodies, some medications, chemotherapy.

177
Q

RBC precursors (recognize vs WBC precursors but don’t memorize)

A

Human Stem Cell-HSC=>Burst forming unit-erythyroid, BFU’s (c-kit+)=>Colony forming unit-erythroid CFU’s (GATA1 transcription factor, Erythropoeitin Receptor, EpoR)=>
proerythroblast =>basophilic erythroblast =>polychromatophilic=> normoblast=>nucleus removed=> reticulocyte =>mature RBC
(cell gets smaller and filled w hemoglobin. organelles digested by autophagy)

Proerythroblast progenitor stimulated to proliferate by erythropoietin (Epo-R), and transferrin-iron (Transferrin Receptor1).
process occurs at the surface of macrophages in the bone marrow, an island of cells= stem cell “niche”. macrophage destroys the nucleus of RBC and supplies iron-transferrin to RBC. In bone marrow there are erythroblastic islands, clusters of the erythroid lineage surrounding macrophage.

178
Q

Vasculogenesis

A

DE NOVO formation of blood vessels
-embryo hemangioblasts» become blood or endothelial cells
-tissues that express VEGFR-1, -2 and neuropilin receptors are targets of VEGF-A
-isolated vasculogenic cords form, also include primitive blood cells
-2 signalling pathways give 2 fates:
vascular: VEGF via VEFGR-1, -2 and Angiopoietin via Tie2
or
lymphatic: VEGFC, D via VEFGR-3

179
Q

Angiogenesis

A
  • new sprous from existing vessels
  • VEGF-A induces proteases that make gaps in vessels
  • TIP cells migrate towards VEGF-A
  • trailing cells undergo mitosis to form sprout, which forms a lumen
  • tip cells secrete PDGF, turning mesenchymal cells into pericytes
  • macrophages help prune, form anastamoses
180
Q

hypoxia in vascular growth

A

HIF1-alpha no longer
degraded
-HIF1-alpha binds DNA to upregulate VEGF, Ang2 PDGF
-new sprouts grow, oxygen levels rise

181
Q

Notch in angiogenesis

A
  • tip cell responds to VEGF-A in env ++ Jag/D114
  • stalk sees D114, ++Notch
  • stalk – VEGFR2
  • lower VEGFR2 in stalk prevents sprouting
  • high notch makes arteries, not veins
182
Q

knockouts in VEGF pathway

A 
ko VEGFR2 (flk gene) = no endothelium
ko VEGFR1 (flt gene) = vascular malformation (refiner)
VEGFR3 mutation: inherited lymphedema
183
Q

AVASTIN (bevaxizumab)

A

monoclonal anti-VEGF that treats cancer

184
Q

retinopathy of prematurity

analogous to wet macular degeneration

A

pO2 in atmosphere&raquo_space; in womb -> hyperoxia supresses VEGF

- few blood capillaries > hypoxia > VEGF upregulated > too much blood vessels > leak > retina edema

185
Q

ascites

A

intra periotoneal fluid (abdomen)

186
Q

edema in cavities

A

effusions/hydrothorax

187
Q

total body edema

A

anasarca

188
Q

hematoma

A

massive clot

189
Q

hematoma in thoracic cavity

A

hemothorax

190
Q

petechiae

A

minute (1-2mm) hematoma

191
Q

purpura

A

larger (1cm) hematoma

192
Q

ecchymoses

A

hematoma several cm in size

193
Q

3 causes of thrombosis

A

endothelial injury
abnormal blood flow
hypercoagulability

194
Q

lines of Zahn

A

in blood clots (pale, yellowish lines); indicated thrombus was formed in vivo; microscopically - RBC, platelets, fibrin

195
Q

arterial thrombi

A

coronary, cerebral, aorta and brances

196
Q

venous thrombi

A

9-% deep leg; peri-uterine, peri-prostatic

197
Q

mural thrombi

A

from heart

198
Q

fate of venous thrombi that embolize

A

“right-sided” - lungs

199
Q

fate of areterial thrombi that embolize

A

“left-sided” - brain, spleen, kidneys

200
Q

paradoxical embolus

A

thrombus goes through patent foramen ovale to left side

201
Q

causes of DIC (disseminated intravascular coagulation)

aka consumption coagulopathy

A

obstetrical catastrophe
sepsis
carcinoma
– all of these release tissue factor (tissue thromboplastin)&raquo_space; coagulation via extrinsic pathway
dx: measure fibrin split products (D-dimers)

202
Q

criteria for SIRS (systemic inflammatory response syndrome)

A

2 or more of the following:

  1. body temp 38
  2. HR >90
  3. tachypnea: >20 breaths/min
  4. WBC 12,000 or >10%immature neutrophils (bands) (bone marrow giving out)
203
Q

reverting postmitotic cells

A

hepatocytes, renal tubular

vs. postmitotic, intermitotic

204
Q

how ischemia hypoxia damages the cell

A

impairment of aerobic respiration, conv to anaerobic respiration, lactic acid production, inhibition of NaKATPase, increase in cell osmolarity, swelling

205
Q

hypertrophy vs hyperplasia vs metaplasia, dysplasia

A

hypertrophy - cells get bigger
hyperplasia - increase in cell #
metaplasia - change of one adult cell type to another (ex: squamous metaplasia due to smoking = mucin turned into squamous cell)
dysplasia = pre-malignant cell architectural changes
atrophy = decrease in size; ischemic change

206
Q

necrosis vs. apoptosis

A

necrosis leads to secondary inflammation; apoptosis does not

207
Q

some proteins involved in apoptosis

A

TNF (tissue necrosis factor), FAS, caspases. release of cytochrome C from mitochondria

208
Q

some proteins involved in response to ER stress

A

1) Perk -> eIFalpha -> ATF4 -> **CHOP -| eIF by GADD3
(Chop ++ leads to apoptosis in chronic stress)
CHOP – chaparenos, ERAD, Ca2+ levels, S-S activity

2) ATF6 -> pre-mRNA XBP1 – chaparenos, ERAD, Ca2+ levels, S-S activity
3) IRE1 -> pre-mRNA XBP1 –chaparenos, ERAD, Ca2+ levels, S-S activity

209
Q

oliguria

A

loss of urine output

210
Q

3 stages of shock

A

Stage 1 acidosis and chemical abnormalities

Stage 2 manifestation of kidney damage that used to be called acute tubular necrosis, now called intrinsic Acute Kidney Injury, brain damage

Stage 3 resolution phase

211
Q

transudate

A

low protein extravasation from blood due to (1) osmotic (reduced) and (2) hydrostatic (increased) imbalance. low specific gravity fluids (

212
Q

exudate

A

high protein concentration in fluid usually w inflammatory cells. high specific gravity >1.020
Ex: Inflammatory diseases: cancer, infection, autoimmunity

213
Q

Hashimoto’s Thyroiditis

A

Chronic Lymphocytic Thyroiditis
????=>CD4->INF gamma=>macrophages and CD8 cytotoxic, and many plasma cells make antibodies against thyroid tissues. No neutrophil infiltrates. chronic damage to the thyroid; hypothyroidism

214
Q

what makes up a granuloma

A
  • palisading T Cells (lined up around)&raquo_space; activate macrophages via IFN gamma
  • epitheloid macrophages (activated)
  • giant cells (fused activated macrophages) = Langherans cells
215
Q

causes of granulomas

A
  • infection (TB caesating, syphilis, schistosomiasis)
  • foreign body (silica, talc, suture, etc)
  • unknown (sarcoidosis asteroid bodies crystals, can undergo calcification and form Schaumann bodies, Crohn’s)
216
Q

haptoglobin

A

circulating hemoglobin binding protein (complex is then cleared by liver). low haptoglobin in blood tests = sign of hemolysis

217
Q

tumor markers CK7 CK20 (cytokeratins in epithelia)

A 
CK7+20- = lung
CK7-20- = liver
CK7-20+ = colon
218
Q

plasma tumor markers

A

CEA (carcinoembryogenic antigen –> colon, pancreas, lung, breast)
AFP (alphafetoprotein) = hepatocellular, germ cell, testis ca

219
Q

“hormone tumor markers”

A

calcitonin - medullar thyroid ca
HCG - testis, placenta ca
PTHrP - squamous cell carcinoma; hypercalcenemia

220
Q

“glycoprotein tumor markers”

A

ca125 - ovary
ca19-9 - bile ducts, pancreas
ca-15-3 - breast

221
Q

inherited autosomal recessive syndromes of defective DNA repair

A

Xeroderma pigmentosum - skin ca
ataxia telangiectasia - ATM gene mutation, G1 arrest. immunodef/ lymphoid malign.
bloom syndrome - helicase mutation; osteosarcoma
fanconi anemia - hypoplasia in kidney, spleen, bone

222
Q

trousseau phenomenon

A

multiple thrombi due to cancer production of mucin

223
Q

gleevac

A

chemotherapy drug that binds to mutated kinase in CML (chronic myelogenous leukemia) (BCR-ABL translocation)

224
Q

HERCEPTIN

A

anti-HER2/neu receptor antibody; chemo

225
Q

AVASTIN

A

anti-VEGF
SUNITINIB - also targets VEGFR and other receptors
antiDLL4 - blocks vascularization (chemo)

Molecular Mechanisms (3 decks)

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