Exam 3 Flashcards
Rheumatoid arthritis
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
Osteoarthritis
Impingement (bone on bone); Thinning of hyaline cartilage; Formation of osteophytes; Can lead to bone spurs on heel
Gout arthritis
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
Bone fractures:
Compound, Comminuted, Transverse, Linear, Oblique, Green Stick, Spiral
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
Dendritic cells
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
Autoimmune disorder
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
Fascia
A band or sheet of connective tissue that attaches, stabilizes, encloses, and separates muscles
Sacros, Myo, Pathy
Sarcos: Flesh
Myo: Muscle
Pathy: Disease
Types of skeletal muscle fibers
-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)
“FLAT PEG”
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
Osteophyte
An overgrowth of the bone; Bone is not supposed to be there; Most commonly a bone spur of the heel (Calcaneus)
Anterior Pituitary
Adenohypophysis; 7 hormones made and released by the anterior pituitary gland;
FSH, LH, ACTH, TSH, Prolactin, Endorphins, GH
Posterior Pituitary
Neurohypophysis; 2 hormones made in the hypothalamus and release in the posterior pituitary;
ADH and oxytocin
ADH
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
Interferons
Proteins produced by the body’s cells in response to viral infections and other pathogens
p53 gene
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
Muscular Dystrophy
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
Atrophy
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
Muscular Dystrophy Can Cause
-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
Myopathy
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
Neuropathy
Nervous/nerve disease; Damage or dysfunction of the peripheral nerves
Most Prevalent Amino Acid
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
Functions of Skeletal Muscle
-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
SNAP Proteins
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
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
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)
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
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
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
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
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
Allergic Reaction Causes
Vasodilation and bronchoconstriction
Location of major baroreceptors
Aortic arch and carotid sinus
Blood pressure center in brain
Medulla oblongata and hypothalamus
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
Creatine kinase
An enzyme found in creatine; Adds phosphates to creatine; Creatine + PO4 turns into ADP which regenerates ATP (energy source)
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
True Muscle Building
Satellite cell recruitment, adding nuclei, and increasing gene transcription to produce more actine and myosin filaments
Same 3 terms for muscles
Skeletal muscle cells
Myocyte
Myofiber
Muscle fascicles
Largest muscle structure; Bundle of muscle fibers
Myofibrils
Make up myofibrils; Are made up of myofilaments
What shortens during muscle contraction
Sarcomere can shorten to varying degrees; H band; I band
What does not shorten during muscle contraction
A band; Actin; Myosin
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
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.
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
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
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
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
Integral proteins
Proteins that are embedded within the cell membrane; Channels, carriers, pumps, receptors (all are found within AP and RMP)
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
K+ leak Channels
Allow K ions to move across the membrane to maintain RMP
Na+/K+ ATPase
Actively pumping 3 Na+ ions out 2 K+ in using 1 ATP to establish RMP
Voltage-gated Na+ Channels
Open in response to AP allowing sodium ions to rush into cell
Voltage-gated K+ Channels
Open as membrane potential peaks allows K+ ions to flow out of the cells
Voltage-gated Channels (general)
Allows for ions to move through
Ligand-gated receptors
Turn into channels when a neurotransmitter hits the receptor
When does AP start
AP starts when we get to threshold
Depolarization
Na+ in; Starts making cell more positive; Voltage-gated Na+ channel will open at threshold and close at +35
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
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
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
When does AP end
AP ends when we get back to the resting value, or -70mV
Actin
Thin myofilament; I-band and A-band
Myosin
Thick filament; A-band and H-band; Binds ATP and hydrolyzes ATP
Troponin
Binds calcium (Ca++)
Tropomyosin
Blocks the myosin head binding sites until troponin binds with Ca++
Steps of contractile (summary)
- Binding: Myosin head binds to an exposed myosin-binding site on the actin filament
- Power stroke: sliding filament theory; ADP and P are released from the myosin head; Myosin head pulls actin over the top
- Detachment: ATP binds to the myosin head
- Cocking: Catalyze ATP (hydrolysis): ATP ADP + P
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
Proteins involved with AP
Na+ out and K+ in
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
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
Ligand
The molecule that binds to a receptor
Ach receptors
On the motor end plate; Muscarinic vs Nicotinic receptors
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
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
Summation
The waves of EPSP and IPSP that lead to threshold; Made up of ligand-gated receptors that turn into channels and threshold
Imagine an Acetyl group
CH3
|
C=O
|
R
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
Histone
Proteins that help package DNA into nucleosomes; DNA wraps around them; Found in groups of 8 (octets)
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
Jugular artery
Not an artery; Humans have 6 jugular veins, or 3 pairs
IPSP
Inhibitory Post-Synaptic Potential; Getting farther/moving away from threshold; Adding Cl- to the cell
EPSP
Excitatory Post-Synaptic Potential; Getting closer/moving towards threshold; Adding Ca++ and/or Na+ to the cell
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
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
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
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
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++
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
Ca++ Binding Proteins
2 Voltage-gated calcium channels
Ca++ ATPase pumps
Troponin BINDs
Voltage-gated Ca++ channels
2 Ca++ ATPase Pumps
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
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
Immediate Soreness
Muscle burns during act of muscle contraction; Lactate to liver = Cori cycle
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
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
Satellite Stem Cell Recruitment
Happens during 24-48 Hour Soreness; Testosterone turns on genes for muscle repair, which is true muscle building
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
HAT
Histone Acetyl Transferases; Add Ac (acetyl group); Promotes inflammatory pathways
HDAC
Histone Deacetylases; Remove or does not put on Ac (acetyl group); Inhibits inflammatory pathways
Epigenetics
Affects transcription but does not change DNA; Can turn a gene on or off
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
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
Soleus AOI
Plantar Flexion of foot; Proximal shaft of tibia and fibula; Calcaneus
4 Rotator Cuff Muscles
Subscapularis, infraspinatus, supraspinatus, teres minor
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
Gastrocnemius AOI
Plantar flexion of the foot and flexion of the leg; Medial and lateral condyle of femur; Calcaneus
Neuromuscular Junction
Site where motor neurons communicate with skeletal muscle fibers to facilitate contraction
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
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
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
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
Pathways
Series of enzymes; 2nd Messengers go down pathways; Need pathways to be “on” and reciprocal pathway to be “off”
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
Inflammatory Pathways
Gene (DNA) —(transcription)–> mRNA —(translation)–> Protein
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
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
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
Absolute Refactory Period
Happens during plateau phase within the cardiac muscle action potential; No new action potentials; Prevents cardiac tetany
“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
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
Glycolysis with O2
Glucose turns into 2 (3c) pyruvates; Goes to mitochondria; Pyruvate dehydrogenase complex; Krebs cycle
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
Antihistamine
Swelling and inflammation of smooth muscle of respiratory tree; Inhaler blocks H1 and inhibits mast cells, which decreases Histamine
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
PG I2
Wound stage 2
Causes vasodilation for increased blood flow/healing
Demotes platelet aggregation
PG D2
Pain, sleep/wake cycles, pyretic (fever inducing);
Mediates inflammation
PG E2
Main inflammation prostaglandin;
Causes pain, redness, swelling, inflammation
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
PG H2
Wound stage 1;
Thromboxane (substance produced by platelets);
Vasoconstriction and increased clotting/platelet aggregation;
Don’t want to endure massive blood loss
Skeletal Muscle Units Smallest to Largest
Myofilament, myofibril, myofiber, fascicle
Na+/Glucose Co-Transporter System is what type of integral protein
Carrier
