anatomy and physiology exam three Flashcards
compound fracture
penetrates the skin
comminuted fracture
breaks into pieces
transverse bone fracture
perpendicular to medullary cavity
linear bone fracture
parallel to medullary cavity
oblique non-displaced bone fracture
diagonal to medullary cavity
oblique displaced bone fracture
diagonal and a “clean cut”
spiral bone fracture
leg is planted, but body has twisted severely
greenstick bone fracture
bone bends before breaking
*typically happens in the very young
what are 2nd messengers?
found inside the cell
cAMP, cGMP, IP3, DAG, NO, Calcium
what is a kinase?
an enzyme that adds a phosphate group to a molecule; phosphate is responsible for stabilizing (turning “on”) or destabilizing ( turning “off”) and enzyme
central dogma
gene (DNA) - transcription - mRNA - translation - protein
epigenetics
regulates transcription by turning genes on or off without changing DNA
histones
found in groups of eight; DNA wraps around histones
inflammatory pathways with acetylation of histones
HAT and HDAC
histone acetyl transferases (HAT
adds acetyl group to histones and promotes inflammation
histone deacetylase (HDAC)
inhibits acetyl groups into histones and inhibits inflammation
corticosteroid injection (cortisone shot)
decreases inflammation, pressure, and pain when a tissue is injured
cortisone shots in relation to inflammatory pathways
inhibits HAT and promotes HDAC
pre-capillary sphincter (PCS)
circular band of tissue that is smooth or skeletal muscle; controls the amount of blood flow into the capillaries
capillary bed
site of exchange of nutrients, gases, wastes, blood cells, etc.
so thin it is clear
pre-capillary sphincter vasoconstriction
smooth muscle is contracting; resistance and pressure increase
ex: epinephrine/adrenaline
pre-capillary sphincter (PCS) vasodilation
resistance and pressure decrease
ex: histamine
hemodynamics
increased or decreased blood flow to certain areas of the body based on what is happening
what happens when we are scared?
fight or flight! we want increased blood flow to skeletal muscle and brain (vasodilation) BUT decreased blood flow to reproductive organs and gastrointestinal tract (vasoconstriction)
cardiac output formula
cardiac output = stroke volume x heart rate
ΔP (change in pressure) formula
ΔP = Q (flow) x R (resistance)
MAP (mean arterial pressure) formula
D + ((S - D)/3)
D = diastolic
S = systolic
pressure units = mmHg
what are the major locations of baroreceptors?
aortic arch and carotid vessels
medulla oblongata
holds centers for heart rate, respiration rate, and blood pressure; received signals from change in pressure from baroreceptors
what happens when we stand up to quickly?
we become light headed, get a head rush, and the inter-cranial blood pressure drops; baroreceptors pick up on the change in pressure and signal the medulla oblongata to vasoconstrict so heart rate increases which then increases blood pressure
if we are standing for long periods of time, should we lock our knees?
NO! if leg muscles are not continually flexing, there is inadequate blood flow to the brain, so there is not enough blood pressure going to the brain: we then become light headed (HEAD RUSH IS MORE SEVERE)
to increase ΔP, what needs to happen?
increase in heart rate and resistance (vasoconstriction)
what does it mean to increase heart rate?
a higher cardiac output results if the stroke volume remains the same; since cardiac output is the same as Q (flow), an increase in cardiac output would increase blood pressure
rheumatoid arthritis
long-term autoimmune disorder that affects joints, typically in the wrist and hands
self-attacking antibodies or immunoglobulin (Ig)
dendritic cells
antigen presenting cells (APCs) that “sound the alarm,” and ramp up the immune response by presenting antigens that are foreign to other cells
where are dendritic cells typically found in high numbers?
tumor :(
what is an autoimmune disorder?
a lot of immune system activity that is not needed, so it attacks itself; antibodies or immunoglobin (Ig)
osteoarthritis
an impingement (bone on bone); progressive thinning of hyaline cartilage that leads to formation of osteophytes
osteophytes
a bone outgrowth, most commonly bone spurs of the heel (calcaneus); exacerbating makes it worse
“FLAT PEG”
made and released from the anterior pituitary
FSH (follicle-stimulating hormone)
LH (luteinizing hormone)
ACTH (adrenocorticotropic hormone)
TSH (thyroid stimulating hormone)
Prolactin (function to produce milk
Endorphins (pain killers)
GH (growth hormone)
vasopressin (ADH)
hormone that is against urine formation: ADH levels go up so urine volume goes down
caffeine and C2H5OH
inhibit ADH so urine production goes up
gouty arthritis (joint gout disease)
deposition of needle-like crystals of uric acid joints
factors: diet, genetic matters, under-excretion of uric acid by the kidney
what are the functions of the skeletal muscle?
movement, posture, joint stability, thermogenesis, nutrition
movement (skeletal muscle)
produces tension to move things; pulling and squeezing
posture (skeletal muscle)
baseline tension exerted at all times
joint stability (skeletal muscle)
constant tension exerted that holds joint together
thermogenesis (skeletal muscle)
HEAT! shivering is involuntary
nutrition (skeletal muscle)
starvation: we have taste bud receptors that bind to glutamate in meat so we taste “savory” (umami)
what is the most prevalent amino acid in higher vertebrates?
glutamate
what are the two excitable tissues (RMP to AP)?
muscle and nervous
true or false: all tissue types have resting membrane potentials
true
how are skeletal muscle fibers classified?
1) by how fast fibers contract relative to others and 2) how fibers regenerate ATP
what are the different types of skeletal muscle fibers?
type 1, type 2A, type 2B
*there are cultural and geographical components to these
type 1 skeletal muscle fibers
slow oxidative; THINK marathon runners of Kenya; slow to fatigue and slow twitch; a lot of mitochondria and capillary bed density
type 2A muscle fibers
fast oxidative; faster to fatigue and fast twitch
type 2B muscle fibers
fast glycolytic; THINK sprinters in Jamaica (the founder effect); fatigue the fastest
sarcos
greek for flesh
myo
latin for muscle
myoblast
makes or builds muscle
protein filaments of muscle fibers
myofilaments (actin or myosin)
sarcoplasm
cytoplasm of muscle fibers
sarcolemma
cell membrane of muscle fibers
sarcoplasmic reticulum (SR)
stores calcium (sequesters calcium)
fascia
band or sheet of connective tissue, primarily collagen, beneath the skin that attaches to, stabilizes, encloses, and separates muscles and other internal organs
whole muscle
fascicles
fascicle
bundle of muscle fibers
what are the three names for ONE muscle cell?
muscle cell, myofiber, myocyte
myofibers
made of myofibrils
myofibrils
made of myofilaments
what is the significance of t-tubules?
allow action potentials (AP) to go deep within the cell, and when the AP hits the sarcoplasmic reticulum it will open up voltage gated calcium channels so that calcium gets out and troponin binds it
what are the four steps of the muscle contractile cycle?
cross bridge formation, power stroke, detachment, ATP hydrolysis
THINK tug-o-war!!!
cross bridge formation - step one
action potential hits sarcoplasmic reticulum, releasing calcium. troponin binds to free calcium, moving tropomyosin out of the way and exposing the myosin head binding sites that are on actin filaments. once myosin binds it is called the cross-bridge formation
*myosin heads bind to actin
power stoke (sliding filament theory) - step two
myosin heads will pull actin over the top of the myosin when they release ADP and PO4 group on them
*actin and myosin do not shorten
detachment - step three
new ATP binds to myosin causing the myosin head to detach from actin
*myosin ATPase
what happens when there is an issue in step three (detachment - heads won’t let go) of the muscle contractile cycle?
when having low (or NO) ATP, we get cramps when alive or rigor mortis when dead
cramp (dehydrated + electrolyte ion balance)
gastrocnemius undergoes mechanical detachment: pushing toes toward nose to get heads to detach!
hydrolyze ATP - step four
myosin ATPase can bind ATP, and hydrolyze it to ADP + PO4 which re-cocks the myosin head so that is can re-attach to another actin molecule
*pulls (power stroke)
what does shorten during muscle contraction?
H-band, I-band, actual sarcomere
what does NOT shorten during muscle contraction?
A-band, actin, myosin
resting membrane potential (RMP)
charge inside of the cell is more negative to the positive outside; ALL tissues have an RMP
action potential (AP)
a wave of depolarization along or down a membrane (inside of the cell becomes more positive); all or nothing electrochemical response under normal circumstances - ions move! (once an AP starts it cannot be stopped!); only muscle and nervous tissue use RMPs to form APs
what proteins are involved in action potentials?
sodium IN and potassium OUT
how do action potentials start and end?
START at threshold and END when we get back to RMP; AP is the same every single time, meaning they are not bigger or smaller BUT we can have more or fewer being sent
SNAPs and SNAREs
vesicle of neurotransmitter can bind to pre-synaptic membrane then exocytose contents into synapse; BOTOX interferes with this
what are the three basic types of muscle soreness?
immediate, 24-28 hour, weeks
causes of muscle soreness
over usage, injury, certain viruses (interferons) or for no reason at all due to tension or stress
immediate muscle soreness (within seconds)
muscle burns during act of muscle contraction and oxygen concentration decreases while lactic acid increases and pH decreases (lactate to liver = CORI cycle)
ex: wall sits
cori cycle in liver
lactic acid (muscle) to pyruvate (liver) to 1) blood that goes to tissue in need of pyruvate, 2) liver for krebs cycle, or 3) liver for gluconeogenesis
24-48 hour muscle soreness (days)
after heavy lifting or over-exertion; leads to tiny micro-tears in the muscle (actin and myosin) and need to be repaired by testosterone levels going up in BOTH genders (satellite stem cell recruitment vs creatine)
soreness that lasts for weeks
usually extreme overextension coupled with engaging in activity the body has NOT adjusted to previously; tendons and ligaments are stretched
myopathy
muscular disease: diseases of muscle in which the muscle fibers do not function properly, resulting in muscle weakness; primary defect is in muscle as opposed to nerves
neuropathy
nerve (nervous) disease; type of muscular disease that affects the peripheral nerves
muscular diseases can be classified as neuromuscular or musculoskeletal in nature do to what factors?
genetics, environment, virus (interferons), bacterial exotoxins *lyme disease
interferons
turn on the p53 gene resulting in an achy feeling
p53 gene
crucial for regulating apoptosis, mitosis and DNA repair processes, ensuring cellular integrity and preventing tumorigenesis; about 50% of all human cancers have a mutated p53 gene
muscular dystrophy
refers to a group of more than thirty genetic diseases that cause progressive weakness and degeneration of skeletal muscles used during voluntary movement
atrophy
opposite of hypertrophy; cell size decreases
muscular dystrophy causes what diseases?
muscle degeneration, progressive weakness, fiber death, fiber branching and splitting, phagocytosis, chronic or permanent shortening of tendons and muscle
phagocytosis
muscle fiber material is broken down and destroyed by scavenger cells
chronic (long-term) or permanent shortening of tendons and muscle
overall muscle strength and tendon reflexes lessened of lost due to replacement of muscle by connective itssue and fat
what does EPSP stand for?
excitatory post-synaptic potential
sodium or calcium in (CATIONS) = closer to threshold
what does IPSP stand for?
inhibitory post-synaptic potential (let anion in)
chloride in (ANION) = away from threshold
voltage-gated channel
gates that hinge: open or close; amino acid short sequences hinge
summation
waves of EPSP and EPSP that lead to threshold; made up of ligand-gated receptors that will turn into channels at threshold
depolarization
AP starts at threshold; then sodium coming in through voltage-gated sodium channel opened at threshold starts making the cell more positive BUT the channel closes at +35 millivolts
repolarization
potassium comes out through voltage-gated potassium channel opened at +35 millivolts making the cell more negative BUT begins to close around the RMP but ACTUALLY closes at -90 millivolts
hyperpolarization
goes below resting membrane potential so the inside of the cell is even more negative; less active because we are further fro threshold
molecular interaction facilitates conformational change (MIFCC)
a receptor becomes a channel (example: ligand-gated receptors become channels)
voltage-gated channels
ION SPECIFIC! made up of amino acid residues that are associated with a protein; in short chains that can open and close
what can happen during hyperpolarization?
1) we are more negative then resting membrane potential, 2) stronger stimulus is needed to get back to threshold, 3) is tissue or cell is TOO hyperpolarized and we cannot get back to threshold then it becomes completely inactive
opiates/narcotics
hyperpolarize the medulla oblongata: heart rate, respiration rate, blood pressure all decrease and then we die within 6-8 minutes (NEVER reach threshold and action potential)
integral proteins
proteins that are embedded within the cell membrane
what are the four main types of integral proteins?
channels, pumps, carriers, receptors
voltage gated sodium channel
opens at threshold, closes at +35 millivolts
voltage gated potassium channel
opens at +35 millivolts, starts to close around resting membrane potential, actually closes at -90 millivolts
action potentials and depolarization roll down the cell membrane like a _____
wave
what is a ligand?
molecule that binds to a receptor
what is a ligand-gated receptor or channel?
channels will be ion specific and relate to ion movement
ex: acetylcholine receptor
how can acetylcholine facilitate different physiological responses?
1) acetylcholine is binding to different receptors that become channels or is associated with a nearby channel or 2) through ion movement; channels are ion-specific
receptors for acetylcholine
nicotinic acetylcholine receptor and muscarinic acetylcholine receptor
nicotinic acetylcholine receptor
opens sodium channel; found in the skeletal muscle and is an EPSP due to letting sodium into the skeletal muscle (goes towards threshold and cell becomes more positive)
muscarinic acetylcholine receptor
becomes channel; found in the S.A. node (pacemaker of the heart) and is an IPSP due to letting chloride in and potassium out (goes away from threshold and cell becomes more negative)
actin
thin myofilament
myosin ATPAse
thick myofilament that binds ATP and hydrolyzes ATP (ATP to ADP + PO4 does not want to happen but does)
tropomyosin
blocks the myosin head binding sites until troponin binds with calcium and it “rolls” out of they way to expose the myosin head binding site (cross bridge formation: myosin-head attachment)
troponin
binds calcium
sarcomere
one functional unit: Z line to Z line
A-band
length of myosin body; dark; has both actin and myosin
I-band
between A-bands/myosin bodies; light; has actin only
H-band
in the A-band where actin and myosin do not overlap; myosin only
Z-line or disc
dark line in the I-band separating sarcomeres
NA+/glucose Co-Transporter CARRIER!!!
from cells in the gut (eat and drink) to the blood vessels where absorption of glucose and sodium takes place (glucose flips in)
neuromuscular junction (NMJ)
site where motor neurons communicate with skeletal muscle fibers to facilitate contraction
acetylcholine neurotransmitter
released from motor neuron terminal
where are acetylcholine receptor located?
sarcolemma; bind to acetylcholine to initiate muscle contraction
voltage gated sodium channels (NMJ)
located in muscle fiber membrane; open in response to depolarization caused by acetylcholine binding and allow sodium to enter the cell
calcium channel (NMJ)
receptors in t-tubules that sense the change in membrane potential and trigger the release of calcium
neuromuscular junction ions
sodium: enters muscle cell upon acetylcholine binding, causing depolarization of membrane
calcium: released from the sarcoplasmic reticulum
potassium: leaves the muscle cell during repolarization after the action potential
creatine
first energy source used; creatine shuttles into muscle cell with water following leading the muscle to swell
takin exogenous creatine does what to skeletal muscle?
creatine kinase adds phosphate to make ADP + PO4 which regenerate ATP
good at repairing tissue but can also interfere with sleep
off creatine results in what?
muscle shrinks lol
true muscle building
satellite stem cell recruitment, adding nuclei, and increasing gene transcription to produce more actin and myosin filaments
cardiac muscle action potential
plateau phase due to potassium out and calcium in counteracting each other
plateau phase
lengthened time associated with refractory period that prevents cardia tetany and no new action potentials
pacemaker of hear in the S.A. node
vagus nerve is parasympathetic, slowing down heart rate from the original .5 seconds to 1 second by releasing acetylcholine and use of muscarinic acetylcholine receptor (chloride in, potassium out - IPSP)
smooth muscle action potential
rounded due few fast voltage-gated sodium channels within smooth muscle: ROLLS NO SPIKES!!! spike potential indicate long periods of contraction
antihistamines
swelling of smooth muscle in respiratory tree… inhalers block H1 and inhibit mast cells to decrease histamine
muscle relaxants
help with tension and pain of skeletal muscle
1) nicotinic acetylcholine antagonist that does not allow binding and 2) increase GABA in brains which inhibit cerebral pathways
huntingston’s disease (huntingtin gene)
autosomal dominant: short arm chromosome four
huntingtin gene = too many CAG repeats that lead to neuro tissue issues
what issues of neuro tissue are associated with huntingston’s disease?
issues with transcription of genes, cell to cell communicate, cell signaling issues
cognitive and behavioral issues that are not visible after the age of 30, so they may already be passed on
gene p53
crucial for regulating apoptosis, mitosis, and DNA repair processes, ensuring cellular integrity and preventing tumorigenesis
about 50% of all human cancers have a mutated p53 gene :(
ATPase
THINK Na+/K- pump that pumps 3 Na+ out and 2 K+ in (against their gradient); this is considered ATP hydrolysis which takes something that does not want to happen and makes it happen
do humans have a jugular artery?
NO! we have SIX jugular veins (three pairs)
