Transport

Front 1

functional growups of solute transporters of carroiers

Back 1

facilitated transporter (uniporter): via facilatated diffusion (GLUT1)
cotransporters or symprters: Na/Glucose: uses ion gradient of Na to bring glucose into cell - active
exchangers or antiporters: also convert energy from ion gadient to do work - active

Front 2

functional growups of solute transporters of carroiers

Back 2

facilitated transporter (uniporter): via facilatated diffusion (GLUT1)
cotransporters or symprters: Na/Glucose: uses ion gradient of Na to bring glucose into cell - active
exchangers or antiporters: also convert energy from ion gadient to do work - active

Front 3

functional growups of solute transporters of carroiers

Back 3

facilitated transporter (uniporter): via facilatated diffusion (GLUT1)
cotransporters or symprters: Na/Glucose: uses ion gradient of Na to bring glucose into cell - active
exchangers or antiporters: also convert energy from ion gadient to do work - active

Front 4

Vasopressin

Back 4

recruits intracellular pool of vesicles that has AQP2 to plasma membrane -> kidney takes up more water

Front 5

Vasopressin

Back 5

recruits intracellular pool of vesicles that has AQP2 to plasma membrane -> kidney takes up more water

Front 6

Vasopressin

Back 6

recruits intracellular pool of vesicles that has AQP2 to plasma membrane -> kidney takes up more water

Front 7

functional growups of solute transporters of carroiers

Back 7

facilitated transporter (uniporter): via facilatated diffusion (GLUT1)
cotransporters or symprters: Na/Glucose: uses ion gradient of Na to bring glucose into cell - active
exchangers or antiporters: also convert energy from ion gadient to do work - active

Front 8

functional growups of solute transporters of carroiers

Back 8

facilitated transporter (uniporter): via facilatated diffusion (GLUT1)
cotransporters or symprters: Na/Glucose: uses ion gradient of Na to bring glucose into cell - active
exchangers or antiporters: also convert energy from ion gadient to do work - active

Front 9

Vasopressin

Back 9

recruits intracellular pool of vesicles that has AQP2 to plasma membrane -> kidney takes up more water

Front 10

Vasopressin

Back 10

recruits intracellular pool of vesicles that has AQP2 to plasma membrane -> kidney takes up more water

Front 11

From what does the CNS form?

Back 11

neural plate and neural tube
(ectoder)

Front 12

from what does the PNS form?

Back 12

neural crest

Front 13

unipolar neurons

Back 13

have single long axon : sensory ganglion neuron

Front 14

multipolar neurons

Back 14

have synapses with axons of other neurons -> motor neuron or sympathetic ganglion neuron

Front 15

Where does motor and sensory enter/exit

Back 15

sensory enters via dorsal roots and motor exits via ventral roots

Front 16

spinal nerves and their relationship to indiv vertebrae

Back 16

7 cranial, 12 thoracic, 5 lumbar, 5 sacral and rest coccygeal

Front 17

where do nerves come out from?

Back 17

xcept for cervical region, spinal nerves exit below corresposing vertebrae

Front 18

where does the adult spinal cord end?

Back 18

L1

Front 19

dermatome

Back 19

area of skin innervated by single spinal nerve

Front 20

mytome

Back 20

a musce innervated by one spinal nerve

Front 21

Where is the nipple?

Back 21

in the T4 dermatome (over the T4 intercostal erve) + 4th intercostal space

Front 22

what hapens to make a muscle contract? start with AP at motoe end plate

Back 22

first that AP goes into T tubule -> makes the sarcoplasmic reticulm release its Ca -> goes and binds to troponin -> shifts the tropomysoin strand out of the way -> now shows the actins binding site for myosin -> by this time myosin globular head has already taken up ATP and energezided -> binds -> pivots -> another ATP comes and releass myosin head from the biding site -> shotern the sarcomere -> shortens the myofibril -> the muscle fiber
but only that muscle fiber

Front 23

when conductance of Na decreases -> due to inactivation - what do the gates look like?

Back 23

m still open but h closed

Front 24

what is the Na channel like thought out the action potenial stages

Back 24

resting: m closed but h open
risgin phase: m open quickly and h starts to close slowly
falling phase: m still open but h closed
undershoot: h still closed

Front 25

what is the k channel like thoughout action potneial?

Back 25

resting: n closed
rising: n slowly start to open
falling: more ns open
undershoot: still some n open but most start to close

Front 26

why do we need Ca entry in immune repossne?

Back 26

stablize the T cell-APC interaction and signaling downstream to induce T cell proliferation and cytokine production

Front 27

the steps in Ca entry

Back 27

when the T cell receptor binds to MHC and costimulaiton -> IP3 relased form membrane -> goes to its recepotr in ER -> stimulates release of Ca from ER -> when this gets depleted -> STIM1 stimulates CRAC channel by intearcting with Ori1-> lets in Ca -> goes and binds to calcineurim/calmodulin + NFAT -> and dephosphorylates it -. NFAT goes to nucleus and stimulate transcription of cytoknies -> T cell goes and becomes Th1 or Th2 depending on what cytokine is made

Front 28

instead of binding to calcineurin/calmodulin + NFAT where else can Ca bind to?

Back 28

the Ca can go and bind to CAM on K channel -> activate it -> K leaves and Ca comes in -> influx of Ca activates T cells -> goes and make cytokines -> makes Th1 or Th2 cells

Front 29

contraindication

Back 29

a condition which makes a particular treatment or procedure inadvisable
can be relative or absolute

Front 30

absolute contraindication

Back 30

if you have a certain condition - cannot take that dug

Front 31

relatice contraindication

Back 31

have a condition - inadised to take drug but you still can

Front 32

replicative senescent

Back 32

irrevesrible growth arrest - after a certin number of cell diviosn
only for human somatic cells
alter function and gene expression
resistant to apoptosis

Front 33

senescent cells and cancer

Back 33

may help other cells beceom cancer
(fibroblasts - produce enzymes that deestyo cellular matrix and help tumor cells grow fatser and T cells when they beomce senescent - decarese in immune surveliance - don't recognize tumor cells well and increase inflamm where helps tumor cells grow )
seescen T cell- when keep seeing the same antigen come to a point where u can't replicate anymore

Front 34

what measures the end of cell diviospn?

Back 34

telemore - importna tfor chromosome stabilit but shorten after every time cell divide - at critical shortening - signal DNA damga esignal -> cell stops diving
because whne this short - greater chance of becoming a tumor

Front 35

telomerase

Back 35

creates more telomers sequences - in germ cells and stem cell and cancer cells
presented in activated B and T cells - but when unable to upregulate temolerase -> senescent

Front 36

senescent

Back 36

seond signal CD28 on T cel- at senenscent no CD28 - permanent
singalutre change of senescent T cell

Front 37

HIV and senescent

Back 37

increases imunological agingin - always fighting off infections -> lots of seesncent cells - lack CD28

Front 38

correlation between senescent and tumor supressor

Back 38

senescnt and stop divindg they will not become a umor -> helps another cell become a tumor -> can stop killing othe rtumor cells - does this becomes stop the tumor suppressor part inside

Front 39

CD28 and AIDS

Back 39

more sensecnt cells that lack CD28 early in infection -> faster progression to AIDS

Front 40

what cytokines do senewscet cells secrete that has to do with bone?

Back 40

T cells produce RANKL -> causes osteoclasts to become activated early in culture ->
a citvely produce cytokines that favor bone destruction

Front 41

chronic stress

Back 41

decreses teomerase -> shorter temolere -> affect immune system

Front 42

teleomer length reflects

Back 42

health

Front 43

centenarians

Back 43

no specific lifestyle
runs in families

Front 44

PIP2 and its two pathays

Back 44

1) PIP3/ATK-PKB / mTOR / survival prolif
2) DAG+IP3 / PKC

Front 45

TPA

Back 45

agonist of DAG, so instead of DAG activating PKC, it can directly act on PKC to activate it.
Additionally, DAG can be broken down, but TPA cannot, so it is always acting to turn on PKC. For this reason, it is a promoter of carcinogenesis (as opposed to an initiator).