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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
Q

SNARE Proteins

A

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

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26
Q

Hemodynamic Formulas

A
  • 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)
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27
Q

Systolic vs. Diastolic in Blood Pressure

A

Systolic blood pressure is the top number
Diastolic blood pressure is the bottom number
Ex: 120 (Systolic)/80 (Diastolic)
Pressure units = mmHg

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28
Q

Precapillary Sphincter

A

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

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29
Q

Scenario: Stand up too quickly

A

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

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30
Q

Formula Scenario: Stand up too quickly

A

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

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31
Q

Scenario: Locked knees while standing

A

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

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32
Q

Allergic Reaction Causes

A

Vasodilation and bronchoconstriction

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33
Q

Location of major baroreceptors

A

Aortic arch and carotid sinus

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34
Q

Blood pressure center in brain

A

Medulla oblongata and hypothalamus

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35
Q

Creatine

A

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

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36
Q

Creatine kinase

A

An enzyme found in creatine; Adds phosphates to creatine; Creatine + PO4 turns into ADP which regenerates ATP (energy source)

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37
Q

Exogenous creatine

A

Swells up muscle; Good at repairing tissue but can interfere with sleep; Only take if working skeletal muscles intensely for 20 hours a week

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38
Q

True Muscle Building

A

Satellite cell recruitment, adding nuclei, and increasing gene transcription to produce more actine and myosin filaments

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39
Q

Same 3 terms for muscles

A

Skeletal muscle cells
Myocyte
Myofiber

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40
Q

Muscle fascicles

A

Largest muscle structure; Bundle of muscle fibers

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41
Q

Myofibrils

A

Make up myofibrils; Are made up of myofilaments

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42
Q

What shortens during muscle contraction

A

Sarcomere can shorten to varying degrees; H band; I band

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43
Q

What does not shorten during muscle contraction

A

A band; Actin; Myosin

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44
Q

Step 1 of muscle contractile cycle

A

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

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45
Q

Step 2 of the muscle contractile cycle

A

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.

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46
Q

Step 3 of the muscle contractile cycle

A

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

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47
Q

Step 4 of the muscle contractile cycle

A

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

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48
Q

RMP

A

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

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49
Q

AP

A

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

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50
Q

Integral proteins

A

Proteins that are embedded within the cell membrane; Channels, carriers, pumps, receptors (all are found within AP and RMP)

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51
Q

ATP Hydrolysis

A

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

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52
Q

K+ leak Channels

A

Allow K ions to move across the membrane to maintain RMP

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53
Q

Na+/K+ ATPase

A

Actively pumping 3 Na+ ions out 2 K+ in using 1 ATP to establish RMP

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54
Q

Voltage-gated Na+ Channels

A

Open in response to AP allowing sodium ions to rush into cell

55
Q

Voltage-gated K+ Channels

A

Open as membrane potential peaks allows K+ ions to flow out of the cells

56
Q

Voltage-gated Channels (general)

A

Allows for ions to move through

57
Q

Ligand-gated receptors

A

Turn into channels when a neurotransmitter hits the receptor

58
Q

When does AP start

A

AP starts when we get to threshold

59
Q

Depolarization

A

Na+ in; Starts making cell more positive; Voltage-gated Na+ channel will open at threshold and close at +35

60
Q

Repolarization

A

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
Q

Hyperpolarization

A

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
Q

Values for AP

A

RMP is -70 mV for a standard neuron; -50 at threshold; +35 is where it peaks; -70mV is where the AP ends

63
Q

When does AP end

A

AP ends when we get back to the resting value, or -70mV

64
Q

Actin

A

Thin myofilament; I-band and A-band

65
Q

Myosin

A

Thick filament; A-band and H-band; Binds ATP and hydrolyzes ATP

66
Q

Troponin

A

Binds calcium (Ca++)

67
Q

Tropomyosin

A

Blocks the myosin head binding sites until troponin binds with Ca++

68
Q

Steps of contractile (summary)

A
  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
Q

ATPase

A

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
Q

Proteins involved with AP

A

Na+ out and K+ in

71
Q

Bigger/smaller APs

A

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
Q

MIFCC

A

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
Q

Ligand

A

The molecule that binds to a receptor

74
Q

Ach receptors

A

On the motor end plate; Muscarinic vs Nicotinic receptors

75
Q

Muscarinic Receptors

A

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
Q

Nicotinic Receptors

A

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
Q

Summation

A

The waves of EPSP and IPSP that lead to threshold; Made up of ligand-gated receptors that turn into channels and threshold

78
Q

Imagine an Acetyl group

A

CH3
|
C=O
|
R

79
Q

Opiates/Narcotics

A

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
Q

Histone

A

Proteins that help package DNA into nucleosomes; DNA wraps around them; Found in groups of 8 (octets)

81
Q

Kinase

A

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
Q

Jugular artery

A

Not an artery; Humans have 6 jugular veins, or 3 pairs

83
Q

IPSP

A

Inhibitory Post-Synaptic Potential; Getting farther/moving away from threshold; Adding Cl- to the cell

84
Q

EPSP

A

Excitatory Post-Synaptic Potential; Getting closer/moving towards threshold; Adding Ca++ and/or Na+ to the cell

85
Q

The gate of a voltage-gated channel

A

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
Q

Why does Na+/K+ ATPase pump need to use ATP

A

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
Q

How can same neurotransmitter have different effects within the body

A

Binding to different receptors will lead to different ions moving; Different signaling pathways are alerted based on different receptors

88
Q

Muscle Relaxants

A

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
Q

Second Messenger

A

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
Q

Vagus nerve effect on SA node

A

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
Q

Ca++ Binding Proteins

A

2 Voltage-gated calcium channels

92
Q

Ca++ ATPase pumps

A

Troponin BINDs

93
Q

Voltage-gated Ca++ channels

A

2 Ca++ ATPase Pumps

94
Q

Cori Cycle

A

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
Q

Muscle Soreness

A

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
Q

Immediate Soreness

A

Muscle burns during act of muscle contraction; Lactate to liver = Cori cycle

97
Q

24-48 Hours Soreness

A

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
Q

Overexertion Soreness

A

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
Q

Satellite Stem Cell Recruitment

A

Happens during 24-48 Hour Soreness; Testosterone turns on genes for muscle repair, which is true muscle building

100
Q

Corticosteroid Injection

A

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
Q

HAT

A

Histone Acetyl Transferases; Add Ac (acetyl group); Promotes inflammatory pathways

102
Q

HDAC

A

Histone Deacetylases; Remove or does not put on Ac (acetyl group); Inhibits inflammatory pathways

103
Q

Epigenetics

A

Affects transcription but does not change DNA; Can turn a gene on or off

104
Q

Cardiac AP

A

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
Q

Smooth Muscle AP

A

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
Q

Soleus AOI

A

Plantar Flexion of foot; Proximal shaft of tibia and fibula; Calcaneus

107
Q

4 Rotator Cuff Muscles

A

Subscapularis, infraspinatus, supraspinatus, teres minor

108
Q

Voltage-gated channels open and close when

A

Voltage-gated channels open and close when acetylcholine is released into the synaptic cleft and binds to the acetylcholine receptors

109
Q

Gastrocnemius AOI

A

Plantar flexion of the foot and flexion of the leg; Medial and lateral condyle of femur; Calcaneus

110
Q

Neuromuscular Junction

A

Site where motor neurons communicate with skeletal muscle fibers to facilitate contraction

111
Q

Neuromuscular Junction Proteins

A

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
Q

Neuromuscular Junction Ions

A

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
Q

Neuromuscular Junction Muscle Contraction Process

A

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
Q

What does p53 gene play a role in

A

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
Q

Pathways

A

Series of enzymes; 2nd Messengers go down pathways; Need pathways to be “on” and reciprocal pathway to be “off”

116
Q

1st vs 2nd Messengers

A

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
Q

Inflammatory Pathways

A

Gene (DNA) —(transcription)–> mRNA —(translation)–> Protein

118
Q

Hemodynamic Formulas Relationships

A

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
Q

T-tubule

A

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
Q

Plateau Phase

A

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
Q

Absolute Refactory Period

A

Happens during plateau phase within the cardiac muscle action potential; No new action potentials; Prevents cardiac tetany

122
Q

“Pacemaker” of heart AP

A

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
Q

Immediate Muscle Soreness Summary

A

GLUT4 helps glucose go in cell –> glycolysis –> 2 (3C) pyruvates → O2 down = burn = lactate → lactate in blood → to liver → CORI CYCLE → lactate → pyruvate

124
Q

Glycolysis with O2

A

Glucose turns into 2 (3c) pyruvates; Goes to mitochondria; Pyruvate dehydrogenase complex; Krebs cycle

125
Q

Glycolysis with no O2

A

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
Q

Antihistamine

A

Swelling and inflammation of smooth muscle of respiratory tree; Inhaler blocks H1 and inhibits mast cells, which decreases Histamine

127
Q

Huntington’s Disease

A

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
Q

PG I2

A

Wound stage 2
Causes vasodilation for increased blood flow/healing
Demotes platelet aggregation

129
Q

PG D2

A

Pain, sleep/wake cycles, pyretic (fever inducing);
Mediates inflammation

130
Q

PG E2

A

Main inflammation prostaglandin;
Causes pain, redness, swelling, inflammation

131
Q

PG F2 alpha

A

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
Q

PG H2

A

Wound stage 1;
Thromboxane (substance produced by platelets);
Vasoconstriction and increased clotting/platelet aggregation;
Don’t want to endure massive blood loss

133
Q

Skeletal Muscle Units Smallest to Largest

A

Myofilament, myofibril, myofiber, fascicle

134
Q

Na+/Glucose Co-Transporter System is what type of integral protein

A

Carrier

Bio 319 (A&P) (10 decks)

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