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Bio 319 (A&P) > Exam 3 > Flashcards

Exam 3 Flashcards

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1
Q

Rheumatoid arthritis

A

Long-term autoimmune disorder that affects joints; Self-attacking antibodies or immunoglobin; Dendritic cells sound alarm against own synovial tissues; Typically in wrist and hands

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2
Q

Osteoarthritis

A

Impingement (bone on bone); Thinning of hyaline cartilage; Formation of osteophytes; Can lead to bone spurs on heel

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3
Q

Gout arthritis

A

A type of inflammatory arthritis; Deposition of needle-like crystals of uric acid into joints; Factors include diet, genetics, and under excretion of uric acid by the kidney

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4
Q

Bone fractures:
Compound, Comminuted, Transverse, Linear, Oblique, Green Stick, Spiral

A

Compound: bone penetrates the skin
Comminuted: bone is in pieces
Transverse: breaks perpendicular with medullary cavity
Linear: breaks parallel with medullary cavity
Oblique: breaks at an angle
Green Stick: small break – usually in young kids; bone bends before it breaks
Spiral: twists wrong; body twists as feet stay planted

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5
Q

Dendritic cells

A

Antigen-presenting cells; Sound the alarm and ramp up the immune response by presenting antigens that are foreign to other cells; Found in high numbers within tumors

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6
Q

Autoimmune disorder

A

A condition where the body’s immune system mistakenly attacks its own cells, tissues, or organs; Immune system (antibodies and immunoglobins) malfunctions and targets healthy body parts as if they were foreign substances; Lost of immune system activity when it is not needed

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7
Q

Fascia

A

A band or sheet of connective tissue that attaches, stabilizes, encloses, and separates muscles

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8
Q

Sacros, Myo, Pathy

A

Sarcos: Flesh
Myo: Muscle
Pathy: Disease

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9
Q

Types of skeletal muscle fibers

A

-Type 1: Slow oxidative; Fatigue slowest; Slow twitch; Lots of mitochondria and capillary bed density; Marathon runners (Kenyans and East Africans)
-Type 2A: Fast oxidative fivers; Fast twitch
-Type 2B: Fast glycolic; Fatigue fastest; Sprinters (The founder effect: Jamaica)

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10
Q

“FLAT PEG”

A

Mnemonic for the hormones that come from the anterior pituitary
FSH: Follicle-stimulating hormone
LH: Luteinizing hormone
ACTH: Adrenocorticotropic hormone
TSH: Thyroid stimulating hormone
Prolactin: Functions to produce milk
Endorphins: Pain killers
GH: Growth hormone

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11
Q

Osteophyte

A

An overgrowth of the bone; Bone is not supposed to be there; Most commonly a bone spur of the heel (Calcaneus)

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12
Q

Anterior Pituitary

A

Adenohypophysis; 7 hormones made and released by the anterior pituitary gland;
FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH

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13
Q

Posterior Pituitary

A

Neurohypophysis; 2 hormones made in the hypothalamus and release in the posterior pituitary;
ADH and oxytocin

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14
Q

ADH

A

Antidiuretic hormone or Vasopressin;
Produced by hypothalamus and stored in posterior pituitary gland;
ADH increases amount of water reabsorbed by kidneys, reducing volume of urine produced; If ADH levels increase, the body is trying to keep water in; Caffeine and EtOH (alcohol) inhibit ADH so urine production goes up; Inverse relationship with urine production

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15
Q

Interferons

A

Proteins produced by the body’s cells in response to viral infections and other pathogens

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16
Q

p53 gene

A

Encodes p53 protein, which is a crucial tumor suppressor involved in regulating cell growth and apoptosis; Directly activated by type I interferons during viral infections; Activation enhances p53’s ability to induce apoptosis in virus-infected cells; 50% of all human cancer have a p53 mutated gene

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17
Q

Muscular Dystrophy

A

Refers to a groups of more than 30 genetic disease that cause progressive weakness and degeneration of skeletal muscles used during voluntary movement; All forms worsen as muscles progressively degenerate and weaken; Most prominently affects the integrity of muscle fibers

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18
Q

Atrophy

A

The wasting away or reduction in size of a body part, organ, or tissue; Occurs when cells shrink and lose functionality; Muscle is not used, so it undergoes atrophy and cell size decreases; Opposite of hypertrophy

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19
Q

Muscular Dystrophy Can Cause

A

-Muscle degeneration
-Progressive weakness
-Fiber death
-Fiber branching and splitting
-Phagocytosis (broken and destroyed by scavenger cell)
-Chronic or permanent shortening of tendons and muscles
-Overall, muscle strength and tendon reflexes are usually lessened or lost due to replacement of muscle by connective tissue and fat

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20
Q

Myopathy

A

Muscular disease; Disease of muscle where the muscle fibers do not function properly resulting in muscle weakness; Primary defect is in muscles as opposed to nerves

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21
Q

Neuropathy

A

Nervous/nerve disease; Damage or dysfunction of the peripheral nerves

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22
Q

Most Prevalent Amino Acid

A

Glutamate: Most prevalent amino acid in higher vertebrates; When glutamate in meat binds to taste bud receptors, it tastes “savory”; Discovered by Japanese scientists who called it umami

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23
Q

Functions of Skeletal Muscle

A

-Movement: Produce tension to move things; pulling/squeezing
-Posture: Baseline tension holds joints together
-Joint stability: Constant tension holds joints together (non-usage leads to muscle atrophy)
-Thermogenesis: Muscle activity generates heat
-Source of nutrition: Metabolism regulation of glycogen

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24
Q

SNAP Proteins

A

Soluble NSF Attachment Proteins; Crucial components in cellular trafficking and vesicle fusion processes; Work with SNARE proteins to ensure proper delivery and release of cellular contents, including neurotransmitters, across membranes

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25
SNARE Proteins
Soluble NSF Attachment Protein Receptors; Essential components involved in the release of neurotransmitters; Facilitate the fusion of vesicles involving neurotransmitters with the target membrane, allowing the release of neurotransmitters into the synaptic cleft
26
Hemodynamic Formulas
- Cardiac output = Stroke Volume x Heart Rate C.O. = S.V x H.R. - Change in Pressure = Flow in System x Resistance ΔP = Q (or C.O.) x R - Mean Arterial Pressure = Diastolic Blood Pressure + 1/3 x (Systolic Blood Pressure - Diastolic Blood Pressure) MAP = D + ((S-D)/3)
27
Systolic vs. Diastolic in Blood Pressure
Systolic blood pressure is the top number Diastolic blood pressure is the bottom number Ex: 120 (Systolic)/80 (Diastolic) Pressure units = mmHg
28
Precapillary Sphincter
Circular band of muscle located at junction where small arteries branch into capillaries; Mostly be smooth muscle but can be skeletal; Controls the amount of blood that flows into capillaries; Vasoconstriction (Epinephrine) leads to increased resistance and pressure; Vasodilation (Histamine) leads to decreased resistance and pressure
29
Scenario: Stand up too quickly
Become lightheaded; Blood pressure goes down; Baroreceptors pick up on the change in pressure and signal to the medulla oblongata to vasoconstrict; Heart rate increases
30
Formula Scenario: Stand up too quickly
To increase blood pressure (delta P), raises resistance by vasoconstriction and heart rate; Increase in heart rate means a higher cardiac output if the stroke volume stays the same; Since cardiac output is the same as Q (flow), an increase in output would also increase blood pressure
31
Scenario: Locked knees while standing
Leg muscles aren't continuously being flexed leading to no jolts of pressure; Causes inadequate blood flow to the brain; Not enough blood pressure to brain, so stroke volume increases; Leads to lightheadedness
32
Allergic Reaction Causes
Vasodilation and bronchoconstriction
33
Location of major baroreceptors
Aortic arch and carotid sinus
34
Blood pressure center in brain
Medulla oblongata and hypothalamus
35
Creatine
First energy source used; Shuttles into muscle; Water follows it; Muscle swells so it looks bigger; Gets off creatine and water will leave; Muscle shrinks; Has an enzyme called creatine kinase
36
Creatine kinase
An enzyme found in creatine; Adds phosphates to creatine; Creatine + PO4 turns into ADP which regenerates ATP (energy source)
37
Exogenous creatine
Swells up muscle; Good at repairing tissue but can interfere with sleep; Only take if working skeletal muscles intensely for 20 hours a week
38
True Muscle Building
Satellite cell recruitment, adding nuclei, and increasing gene transcription to produce more actine and myosin filaments
39
Same 3 terms for muscles
Skeletal muscle cells Myocyte Myofiber
40
Muscle fascicles
Largest muscle structure; Bundle of muscle fibers
41
Myofibrils
Make up myofibrils; Are made up of myofilaments
42
What shortens during muscle contraction
Sarcomere can shorten to varying degrees; H band; I band
43
What does not shorten during muscle contraction
A band; Actin; Myosin
44
Step 1 of muscle contractile cycle
When action potential hits sarcoplasmic reticulum, Ca++ is released from the sarcoplasmic reticulum and the Ca++ will bind to troponin; This moves tropomyosin out of the way exposing the myosin head binding sites that are on the actin filaments; When myosin binds it is called a cross-bridge formation
45
Step 2 of the muscle contractile cycle
Myosin heads will “pull” actin over the top of the myosin- happens when they release the ADP and Po4 group on them; This is called the power stroke – sliding filament theory.
46
Step 3 of the muscle contractile cycle
A new ATP binds to the myosin; This causes the myosin head to detach from actin! If out of ATP – CRAMPS (gastrocnemius)- alive vs RIGOR MORTIS-dead
47
Step 4 of the muscle contractile cycle
Myosin can not only bind ATP but can hydrolyze it to ADP and PO4 which “re-cocks” the myosin head, so it is ready to be reattached to another
48
RMP
Resting Membrane Potential; Charge inside the cell is more negative to the positive outside; All tissues have an RMP but only muscle and nervous system use this to form an action potential; Created with Na+/K+ ATPase pump and slow-leak K+ channel
49
AP
Action Potential; A wave of depolarization along or down a membrane; All or nothing response under normal circumstances; Once an AP starts it can not be stopped; There is NO SUCH THING as a “bigger or smaller” AP; It is the same every time; You can have more or fewer AP!! Depends on the muscles being used or how hard you flex a muscle
50
Integral proteins
Proteins that are embedded within the cell membrane; Channels, carriers, pumps, receptors (all are found within AP and RMP)
51
ATP Hydrolysis
Against gradient – an active process; We need ATP to do this; Will turn a positive delta G into a negative delta G; Can take something that DOES NOT want to happen (Na going out, K going in) and make it happen
52
K+ leak Channels
Allow K ions to move across the membrane to maintain RMP
53
Na+/K+ ATPase
Actively pumping 3 Na+ ions out 2 K+ in using 1 ATP to establish RMP
54
Voltage-gated Na+ Channels
Open in response to AP allowing sodium ions to rush into cell
55
Voltage-gated K+ Channels
Open as membrane potential peaks allows K+ ions to flow out of the cells
56
Voltage-gated Channels (general)
Allows for ions to move through
57
Ligand-gated receptors
Turn into channels when a neurotransmitter hits the receptor
58
When does AP start
AP starts when we get to threshold
59
Depolarization
Na+ in; Starts making cell more positive; Voltage-gated Na+ channel will open at threshold and close at +35
60
Repolarization
K+ out; Starts making cell more negative; K+ channel will open at 35+, starts to close around RMP, but will actually close at about -90 mVs
61
Hyperpolarization
Hyperpolarization goes below resting, it is more negative than RMP; Further away from threshold means tissue will be less active or no activity at all; If VERY hyperpolarized (from narcotics or opiates) then there is no chance to get back to threshold; Voltage-gated K+ closes completely
62
Values for AP
RMP is -70 mV for a standard neuron; -50 at threshold; +35 is where it peaks; -70mV is where the AP ends
63
When does AP end
AP ends when we get back to the resting value, or -70mV
64
Actin
Thin myofilament; I-band and A-band
65
Myosin
Thick filament; A-band and H-band; Binds ATP and hydrolyzes ATP
66
Troponin
Binds calcium (Ca++)
67
Tropomyosin
Blocks the myosin head binding sites until troponin binds with Ca++
68
Steps of contractile (summary)
1. Binding: Myosin head binds to an exposed myosin-binding site on the actin filament 2. Power stroke: sliding filament theory; ADP and P are released from the myosin head; Myosin head pulls actin over the top 3. Detachment: ATP binds to the myosin head 4. Cocking: Catalyze ATP (hydrolysis): ATP ADP + P
69
ATPase
Na+/K+ pump; Pumps out 3 Na+ and 2 K+ in against their gradient; This is considered ATP hydrolysis because it takes something that doesn't want this to happen and makes it happen
70
Proteins involved with AP
Na+ out and K+ in
71
Bigger/smaller APs
Cannot have bigger or smaller AP; Can have more or fewer AP depending on the muscles being used; The more AP, the more intense the pain is
72
MIFCC
Molecular Interaction Facilitates Conformational Change; Example is when a receptor turns into a channels; Ach Ligand-gated receptor/channel; The channel will be ion specific
73
Ligand
The molecule that binds to a receptor
74
Ach receptors
On the motor end plate; Muscarinic vs Nicotinic receptors
75
Muscarinic Receptors
Ach binds to muscarinic receptors; Cl- in and K+ out (IPSP); Cell becoming more negative, or away from threshold, because anion is entering and cation is leaving; Ex: Pacemaker for the SA node of the heart
76
Nicotinic Receptors
Ach binds to nicotinic receptors; Na+ in (EPSP); Found in skeletal muscle; Moves towards threshold because cell has more cations entering, therefore making the cell more positive
77
Summation
The waves of EPSP and IPSP that lead to threshold; Made up of ligand-gated receptors that turn into channels and threshold
78
Imagine an Acetyl group
CH3 | C=O | R
79
Opiates/Narcotics
Hyperpolarizes the medulla oblongata which controls the heart rate, respiratory rate, and the blood pressure centres; These all decrease and one can die after 6-8 minutes if the body cannot bring back to threshold
80
Histone
Proteins that help package DNA into nucleosomes; DNA wraps around them; Found in groups of 8 (octets)
81
Kinase
An enzyme that adds a phosphate group; Phosphate is typically responsible for turning pathways on or off; adding a phosphate may either stabilize ("on) or destabilize ("off") the enzyme
82
Jugular artery
Not an artery; Humans have 6 jugular veins, or 3 pairs
83
IPSP
Inhibitory Post-Synaptic Potential; Getting farther/moving away from threshold; Adding Cl- to the cell
84
EPSP
Excitatory Post-Synaptic Potential; Getting closer/moving towards threshold; Adding Ca++ and/or Na+ to the cell
85
The gate of a voltage-gated channel
Made up of amino acid residues that are associated with a protein; Composed in short chains that can open and close; Can have one gate or two gates
86
Why does Na+/K+ ATPase pump need to use ATP
Needs ATP to engage in ATP hydrolysis; Ions are moving against their gradient (low to high concentration); Would not be able to use active transport without ATP hydrolysis
87
How can same neurotransmitter have different effects within the body
Binding to different receptors will lead to different ions moving; Different signaling pathways are alerted based on different receptors
88
Muscle Relaxants
Diminish muscle stiffness, tension, pain; Nicotinic AcR antagonist; Block acetylcholine at the neuromuscular junction directly inhibiting muscle contraction; GABA (neurotransmitter) to brain; GABA is inhibiting APs sent to the skeletal muscles; GABA inhibits cerebral pathways
89
Second Messenger
Molecule or ion inside a cell that transmits signals from a receptor on the cell's surface to target molecules within the cell, initiating a physiological response; Found inside the cell, there are 6 of them; cAMP, cGMP, IP3, DAG, NO, Ca++
90
Vagus nerve effect on SA node
Vagus nerve decreases heart rate by releasing Ach which binds to the muscarinic receptors of the SA node; Parasympathetic to SA node; Causes resting heart rate to be halved
91
Ca++ Binding Proteins
2 Voltage-gated calcium channels
92
Ca++ ATPase pumps
Troponin BINDs
93
Voltage-gated Ca++ channels
2 Ca++ ATPase Pumps
94
Cori Cycle
A metabolic process that involves the conversion of lactic acid produced in muscles into pyruvate in the liver, and then back to the muscles; Lactate in blood goes through lactate shuttle; lactate goes through LDH (lactate dehydrogenase) and turns into pyruvate; pyruvate can go either to bloodstream to tissues, stays in liver to do Krebs cycle, or stay in liver to do gluconeogenesis
95
Muscle Soreness
Many different causes (over usage, injury, certain viruses interferons!); Can be sore for no reason at all due to tension or stress; Three basic types of soreness: Intermediate, 24-48 hours; Weeks
96
Immediate Soreness
Muscle burns during act of muscle contraction; Lactate to liver = Cori cycle
97
24-48 Hours Soreness
Happens after heavy lifting or over exertion; Leads to tiny micro-tears in the muscle; Needs to be repaired; Testosterone level go UP in both gender); Satellite stem cell recruitment
98
Overexertion Soreness
Usually extreme overexertion couple with engaging in activity the body has NOT adjusted to previously; Tendons and ligaments are stretched; Slow to heal; Can last up to weeks
99
Satellite Stem Cell Recruitment
Happens during 24-48 Hour Soreness; Testosterone turns on genes for muscle repair, which is true muscle building
100
Corticosteroid Injection
Injected when tissue is wounded; Cortisone shot into the joints when they are trying to get pressure down, pain down, inflammation down; Inhibits HAT, promotes HDAC; Used by athletes to continue playing without being in pain; Can cause injury to worsen because cannot feel it worsen
101
HAT
Histone Acetyl Transferases; Add Ac (acetyl group); Promotes inflammatory pathways
102
HDAC
Histone Deacetylases; Remove or does not put on Ac (acetyl group); Inhibits inflammatory pathways
103
Epigenetics
Affects transcription but does not change DNA; Can turn a gene on or off
104
Cardiac AP
Depolarization and Na+ voltage-gate opens so Na+ in; Simultaneously, as Na+ voltage-gate closes, the Ka+ voltage-gate and Ca++ voltage gate opens; Plateau phase occurs due to K+ out and Ca++ in simultaneously leading to them counteracting each other; Ca++ voltage-gate closes and repolarization begins; Ka+ continues to go out until it reaches RMP; K+ voltage-gate closes when it hits RMP
105
Smooth Muscle AP
Occurs within GI tract and enteric nervous system (involuntary); Rounded due to slow voltage-gated Na+ channels; Top of the waves can have little spikes which indicates long periods of contraction; Very few fast voltage-gated Na+ channels within smooth muscle
106
Soleus AOI
Plantar Flexion of foot; Proximal shaft of tibia and fibula; Calcaneus
107
4 Rotator Cuff Muscles
Subscapularis, infraspinatus, supraspinatus, teres minor
108
Voltage-gated channels open and close when
Voltage-gated channels open and close when acetylcholine is released into the synaptic cleft and binds to the acetylcholine receptors
109
Gastrocnemius AOI
Plantar flexion of the foot and flexion of the leg; Medial and lateral condyle of femur; Calcaneus
110
Neuromuscular Junction
Site where motor neurons communicate with skeletal muscle fibers to facilitate contraction
111
Neuromuscular Junction Proteins
Acetylcholine (Ach): Neurotransmitter released from motor neuron terminal Ach receptors (nAchRs): Located on sarcolemma; Bind to Ach to initiate muscle contraction Voltage-gated Na+ Channels: Located in muscle fiber membrane; Open in response to depolarization caused by Ach binding, Allowing Na+ to enter the cell Ca+ channels: Receptors in the T-tubules that sense the change in membrane potential and trigger the release of Ca+ Troponin and tropomyosin: Regulatory proteins on the actin filaments that control muscle contraction by exposing binding sites for myosin Myosin: Thick filament protein that interacts with actin to facilitate muscle contraction
112
Neuromuscular Junction Ions
Sodium (Na+): Enters the muscle cell upon Ach binding, causing depolarization of the membrane Calcium (Ca++): Released from the sarcoplasmic reticulum Potassium (K+): Leaves the muscle cell during repolarization after the action potential
113
Neuromuscular Junction Muscle Contraction Process
Nerve signal transmission: Ca++ ATPase pumps Ca++ out; AP hits voltage-gated Ca++ channel and opens it; Ca++ floods in; Causes vesicles to dedock and bind to the cell membrane; Vesicles exocytose neurotransmitters out (Ach) into synapse to the skeletal muscle Ach binding: 2 Ach binds to the nicotinic Ach receptor on the sarcolemma to activate it and turn it into a channel; Lets in Na+ and causes EPSP and depolarization of the muscle fiber membrane Action potential generation: Depolarization triggers the opening of voltage-gated sodium channels, creating an action potential that propagates along the sarcolemma and down the T-tubules Calcium release: The action potential hits the voltage-gated Ca++ on the sarcoplasmic reticulum; Ca++ leaves and enters the sarcolemma Ca++ into the cytosol Contraction mechanism: Ca++ binds to troponin, causing a conformational change that moves tropomyosin away from the myosin-binding sites on actin; Myosin heads bind to actin, forming cross-bridges and pulling the filaments together (sliding filament theory) Relaxation: When the signal ceases, Ach is broken down, leading to repolarization of the muscle membrane; Ca++ is actively transported back into the sarcoplasmic reticulum, causing the muscle to relax
114
What does p53 gene play a role in
Crucial for regulating apoptosis, mitosis, and DNA repair processes, ensuring cellular integrity and preventing tumorigenesis; 50% of all human cancers have mutated p53 gene
115
Pathways
Series of enzymes; 2nd Messengers go down pathways; Need pathways to be "on" and reciprocal pathway to be "off"
116
1st vs 2nd Messengers
1st Messengers are what bind to the receptor outside of the cell; Ex: Histamine 2nd Messengers are what comes out of receptor and goes down enzyme pathways to either stabilize or destabilize
117
Inflammatory Pathways
Gene (DNA) ---(transcription)--> mRNA ---(translation)--> Protein
118
Hemodynamic Formulas Relationships
If stroke volume is increased, then heart rate is decreased; Flexing legs increases stroke volume; If blood pressure decreased, then heart rate increased; Resistance is vasoconstriction (increased) or vasodilation (decreased); If cardiac output increases, then need to vasoconstrict; If resistance increases, then change in pressure increases
119
T-tubule
Action potential goes through cell membrane, hits t-tubule and depolarization takes action potential deep into the cell; Gets to cytoplasmic reticulum and hits multiple voltage-gated Ca++ channels; They open and Ca++ is released
120
Plateau Phase
Ca++ in and K+ out happens simultaneously within the cardiac muscle action potential, leading to them canceling each other out; Lengthens the absolute refactory period; Ca++ concentration gradient actively
121
Absolute Refactory Period
Happens during plateau phase within the cardiac muscle action potential; No new action potentials; Prevents cardiac tetany
122
"Pacemaker" of heart AP
SA Node; Na+ goes in by slow leak channel; When threshold is met, Ca+ in through voltage-gated calcium channel; Repolarization occurs and voltage-gated potassium channel opens, releasing K+; Originally, .5 seconds between each action potential, leading to 120BPM resting heart rate; Vagus nerve fixes
123
Immediate Muscle Soreness Summary
GLUT4 helps glucose go in cell --> glycolysis --> 2 (3C) pyruvates → O2 down = burn = lactate → lactate in blood → to liver → CORI CYCLE → lactate → pyruvate
124
Glycolysis with O2
Glucose turns into 2 (3c) pyruvates; Goes to mitochondria; Pyruvate dehydrogenase complex; Krebs cycle
125
Glycolysis with no O2
Glucose turns into 2 (3c) pyruvates; Goes through Lactate Dehydrogenase (LDH) and increases lactic acid; Increased lactic acid means decrease pH which can lead to proteins to denature and change their form and function; Increased lactic acid goes into blood stream through lactate shuttle and goes through another lactate shuttle to go into the liver; liver turns lactate into pyruvate through LDH (Cori cycle); pyruvate can exit liver via three ways
126
Antihistamine
Swelling and inflammation of smooth muscle of respiratory tree; Inhaler blocks H1 and inhibits mast cells, which decreases Histamine
127
Huntington's Disease
Autosomal dominant; Short arm of chromosome #4; "Huntingtin" gene; Too many CAG repeats which causes issue with transcription of genes, issue with cell to cell communication, and issue with cell signaling; Disease causes cognitive and behavioral issues; Not visible until after the age of 30, which can lead to it having already been passed on
128
PG I2
Wound stage 2 Causes vasodilation for increased blood flow/healing Demotes platelet aggregation
129
PG D2
Pain, sleep/wake cycles, pyretic (fever inducing); Mediates inflammation
130
PG E2
Main inflammation prostaglandin; Causes pain, redness, swelling, inflammation
131
PG F2 alpha
Corpus luteum (CL) regression, skeletal muscle; End of menstrual Estrogen and oxytocin stimulate the release of oxytocin, which aids in the stimulation of uterine contraction
132
PG H2
Wound stage 1; Thromboxane (substance produced by platelets); Vasoconstriction and increased clotting/platelet aggregation; Don't want to endure massive blood loss
133
Skeletal Muscle Units Smallest to Largest
Myofilament, myofibril, myofiber, fascicle
134
Na+/Glucose Co-Transporter System is what type of integral protein
Carrier

Bio 319 (A&P) (10 decks)

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