CEll Phys Flashcards
lysosome
digestive
mitochondria
energy, aerobic metabolism
ER
transport/synthesis or proteins and lipids, can be smooth or rough
GA
package and transport, recieves proteins from the ER and packages and transports them, can modify them if needed
histones
proteins that packages and organizes DNA into chromosomes
microtubules
will help with mobility/motility, so therefor if decreased motility or mobility to bring something in then it is the microtubule that is effected, helps clears things or helps bring things in
inclusions
store fats
ribosomes
make proteins
cytoplasm
aqueous solution between plasmalemma & nucleus contains-interconnected filaments and fibers, fluid (cytosol) and organelles (not nucleus)
What are four things found in the cytoplasm
- inclusions2. microtubules3. free ribosomes4. anaerobic metabolism
what are four facts about the plasma membrane
- bilayer2. hydrophillic head, hydrophobic tail3. lipid soluble4. big, water soluble, and ions need additional help (facillitated defusion)
transmembrane
both sides through the membrane
integral
within the membrane, communicates with the ECM; CAM
glycoproteins
used for ID
glycocaylx
it is a cell to cell adhesion, cell to cell communicator, house tissue transplant antigens
periphreal proteins
away from membrane (inside or outside), only attach to membrane when needed
cadherins
CAM, ca dependent
selectin
carbohydrate dependent
paracrine
communicate to adjacent cell
endocrine
communicate distally through blood
autocrine
communicate with self
ligand receptors respond to
hormone/NT
G protein
slow cascade intracellularly
voltage (ion) channel
change in electrical charge
catalytic enzyme channel
kinase cascade
passive diffusion, what about na and K?
H-L, lipid soluble, sodium in and K out
active transport [] movement
L->H, pumped
facilitated diffusion, what needs this?
larger, water soluble, glucose, big proteins
endocytosis
vesicular engulf to move in
exocytosis
vesicular engulf to move out
phagocytosis
engulf solid
pinocytosis
engulf fluid
where does the most immediate ATP production come from?
in cytoplasm, anaerobic, ATP generation
phosphocreatine
ctyoplasm, anaerobic
glycolysis
cytoplasm, anaerobic without O2->lactic acidglucose to pyruvate
KCAC
in mitochondria, aerobic
ETC
in mitochondria, final acceptor, cashes in NADH for ATP, aerobic
ectoderm
nervous tissue
endoderm
epithelia lining of GI tract/respiratroy
mesoderm
connective tissue
simple epithelium
single layer -covers external surfaces, internal surfaces, form glands
stratified
multiple layers protection, lines mouth, tongue, espophagus, vagina
transitional
changes permits stretching, lines urinary bladder
glandular tissue
specialized exocrine and endocrine
connective tissue
bind tissues and organs
skeletal muslce
striated, multinucleated
cardiac muscle
striated, intercalated disc,uninucleated
smooth muscle
non striated, uninucleated, no troponin-calmodulin
astrocytes
structure
ependymal cells
CSF
microglia cells
phagocytic
hypertrophy
increase cell size and then organ size
atrophy
decrease in cell sizeEx: brain size decreasing with age, uterus decreasing size with childbirth
hyperplasia
increase in cell number
compensatory hyertrophy and hyperplasia
when tissue tries to regenerate after injury and tissue loss
metaplasia
different cell type replaces old post injury, replacing cell is less differentiated or functional than the original cell
dysplasia
not true adaptation, precancerous change in cellEx: if you smoke all your life and then you replace the cell with a cancerous cell
hypertrophic
post injury acculmulation of Ca- bone spur
dystrophic
post necrosis- dead tissue replaced by CA
metastatic, as seen in hyperparathyroidism
calcium is high and needs to deposit somewhere, anywhere
obstructive accumulation
ducts get obstructed causing accumulations
exogenous acccumulation
from outside environment, trapped inside coal mine, dust to lungs
explain 2 types of things that can cause cell injury
- physical2. radiation3. chemical
hypoxia
lack of oxygen, most common cause of cell injury
senescence in cells
loss of a cell’s power of division and growth
Telomerases
resistant to cell death, persistent telomerases activity, repair the dna allowing it to live longer
free radical
an uncharged molecule (typically highly reactive and short-lived) having an unpaired valence electron.
apoptosis
cell death, we need it, clears out cells to bring more in, checks and balances system
necrosis
cell death that is bad
Werners syndrome
rapid appearance of aging after puberty, WRN gene that produces Werner protein is mutated and so it can’t repair DNA and replication of dna for cell division so they break down faster
progeria
PREPUBERTY accelerated aging in children due to LMNA which makes LAM A protein that causes deterioration of the nucleur envelope, usually die from cardiovascular disease by 14, prepuberty
proliferate
grow or replicate
differentiate
to gain specialized function
pluripotent stem cells
can differentiate into three germ layers embryonic
multipotent stem cells
give rise to a family of cells, hematiopietic stem cells can become monocytes, lymphocytes ect but not bone cells (non blood cells)
unipotent stem cells
produce only one type of cell but retain the property of self renewal
adult stem cells
in tissues and bone marrow that can produce multiple lineages
what are the 4 properties of a stem cell?
- assymetric2. self renewal3. have various potentials4. growth factor dependent
Order of cell replication and checkpoints
G0G1G1/S checkpoint: monitiors for damaged DNA in chromosomesSG2G2/M checkpoint: prevents entry into mitosis if replication isn’t completeMitosiscytokinesis
explain the function of the G0 phase and cancer cells
rest point, cells leave but come back, however, cancer cells rarely leave
what triggers the cell cycle
growth factors
what makes up granulation tissue?
fibroblasts, angiogenisis, and collagen
function of myofibroblasts
appear to help a wound contraction to bring both sides of the wound together to regenerate epithelium, healing via scar
fibroblasts
lay down the new ECM/collagen, which results in the formation of a FIBROUS or scar
why is ECM important?
regeneration and controlling proliferation
angiogensis
new blood vessel formation, stimulated by angiogenic growth factors
what are the general phases of repair?
- inflammation via neutrophils and phagocytes2. granulation via angiogenisis and fibroblasts3. remodeling
primary vs first is dependent on
amount of tissue loss
primary
little tissue loss, clean cut like papercut
secondary
larger tissue loss, no clean boundaries
dehescence
suture rupture, usually seen in obesity
hemmorage
forces more apoptosis therefor healing takes longer
infection
hemmorage leads to more blood, so more potential for infection
nutrition
need glucose for WBC to work and clean up, poor collagen production if not well nourished
too much collagen forms
keloids, collagenous bands
too little collagen is usually caused from
to little protein in the diet
hypovolemia
decrease in blood volume leads to vasconstriction when you need vasodilation the most
age
less angiogenisis causing hypoxia, less elasticitiy, slower fibroblast reaction
what is the primary site for malignancy or ability to spread?
skin
neoplasia =plasia cell increase=neo=nooooo
abnormal growth of new cells and or abnormal growth of abnormal cells1. when stimuli is gone and keep proliferating2. regulation of cell mechanism no longer function
hyperplasia plasia=cell increasehyper=want to please
- Normal response or adaptation of stimuli2.regulated to enable adaptationstimuli disappears and usually stops, if not abnormality in regulation3. callus formationincrease in NORMAL cells
benign
well-differentiated cells that resemble the normal tissue in structure and functiongrows slowlylow mitotic ratewell differentiatednot invasive, does not metastasize, remain localizednot cancer
malignant
rapid growthhigh mitotic ratenot encapsulated, poor boundariesinvade other tissues and structures, spreads via blood vessels and lymphpoorly differentiated or undifferentiated
carinoma
epithelia
adeno
glandular
sarcoma
muscular
autonomy
proliferate in the absence of growth factors, do it on their own
autocrine example protein
GF to own cell, RAS SIGNALING PROTEIN
immortal because of the
telomerase
anchor independent
doesn’t care if something keeps touching it, it keeps growing
density independent
keeps growing even though full
anaplastic
without differentiation
cancer cells are…
NOT STICKY, makes them slippery so they can spread
6 phases of cancer
- in situ2. invade locally by busting through the basement membrane of the ECM or cell membrane3. spread via blood or lymph4. get lodged5. leave to new tissue6. repeat starting with angiogenisis
what is the most common reported symptom of cancer
fatigue
what are some symptoms of cancer
painfatiguecachexiaanemiainfection leukopenia
cachexia
anorexia, loss of appetite, muscle wasting, loss of weight associated with cancer patients
what are the early detection methods for cancer and which cancer is there no early detection methods for?
observation, palpation, lab tests (papsmears, biopsies, MRI, US, endoscopic examinations)PANCREATIC CANCERS NO METHOD OF EARLY DETECTION OR SCREENING
grading measures….
cancer cell level of differentiation
scaling measures….
size or extent of invasion of original tumor
explain the differences between grading and scaling
GX: grade cannot be assessed (undetermined grade)G1: well differentiated (low grade)-appear close to normal, tend to grow/spread slowlyG2: moderately differentiated (intermediate grade)G3: poorly differentiated (high grade)-do not look like normal cells, grow rapidly and spread fasterG4: undifferentiated (high grade)- do not look like normal cells, grow rapidly and spread fasterTHERE ARE CANCER SPECIFIC GRADING SCALES
TNM staging created by the WHO
T-tumor spreadN-level of node involvementM-presence of distal metasticies
oncogenes are stimulated by _____, and supressed by _______
oncogenes are stimulated by proto-oncogenes and supressed by tumor supressors (anti-oncogenes)
p53
usually allows apoptosis by interfering with G1, however, if mutation here in cancer apoptosis is disabled
Rb
tumor suppressing gene, if there is a mutation here then the tumor suppression no longer works and cancer is able to spread
chemotherapy
limit cell proliferation through chemotoxins
radiation
limit cell proliferation through attacking DNA replication
hormones
limit cell proliferation through blocking hormones that help with growth
surgery
limit tumor by removing before vascularization can continue to spread
immunotherapy
pumps up the immune response to fight it off
targeted
disrupts antiogenisis, signal pathways for GFs, stimulate immune response
cell death that interferes without regeneration
necrosis
what is the number one cause of death in children
cancer
what is the most common in the first two years of life?
embryonic tumors like neuroblastomas
what is the most common from 2-5 years old
acute lymphocytic peak
wilms tumor nephroblastoma
starts in one kidney, ages 3-4, not over 6
what is the most common childhood cancer
leukemia
neoblastoma
occurs in the nerve cells of embryo or developing fetus seen in INFANTS!
