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Anatomy and Physiology I > anatomy and physiology exam three > Flashcards

anatomy and physiology exam three Flashcards

1
Q

compound fracture

A

penetrates the skin

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2
Q

comminuted fracture

A

breaks into pieces

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3
Q

transverse bone fracture

A

perpendicular to medullary cavity

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4
Q

linear bone fracture

A

parallel to medullary cavity

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5
Q

oblique non-displaced bone fracture

A

diagonal to medullary cavity

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6
Q

oblique displaced bone fracture

A

diagonal and a “clean cut”

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7
Q

spiral bone fracture

A

leg is planted, but body has twisted severely

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8
Q

greenstick bone fracture

A

bone bends before breaking

*typically happens in the very young

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9
Q

what are 2nd messengers?

A

found inside the cell

cAMP, cGMP, IP3, DAG, NO, Calcium

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10
Q

what is a kinase?

A

an enzyme that adds a phosphate group to a molecule; phosphate is responsible for stabilizing (turning “on”) or destabilizing ( turning “off”) and enzyme

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11
Q

central dogma

A

gene (DNA) - transcription - mRNA - translation - protein

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12
Q

epigenetics

A

regulates transcription by turning genes on or off without changing DNA

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13
Q

histones

A

found in groups of eight; DNA wraps around histones

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14
Q

inflammatory pathways with acetylation of histones

A

HAT and HDAC

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15
Q

histone acetyl transferases (HAT

A

adds acetyl group to histones and promotes inflammation

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16
Q

histone deacetylase (HDAC)

A

inhibits acetyl groups into histones and inhibits inflammation

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17
Q

corticosteroid injection (cortisone shot)

A

decreases inflammation, pressure, and pain when a tissue is injured

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18
Q

cortisone shots in relation to inflammatory pathways

A

inhibits HAT and promotes HDAC

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19
Q

pre-capillary sphincter (PCS)

A

circular band of tissue that is smooth or skeletal muscle; controls the amount of blood flow into the capillaries

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20
Q

capillary bed

A

site of exchange of nutrients, gases, wastes, blood cells, etc.

so thin it is clear

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21
Q

pre-capillary sphincter vasoconstriction

A

smooth muscle is contracting; resistance and pressure increase

ex: epinephrine/adrenaline

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22
Q

pre-capillary sphincter (PCS) vasodilation

A

resistance and pressure decrease

ex: histamine

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23
Q

hemodynamics

A

increased or decreased blood flow to certain areas of the body based on what is happening

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24
Q

what happens when we are scared?

A

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)

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25
Q

cardiac output formula

A

cardiac output = stroke volume x heart rate

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26
Q

ΔP (change in pressure) formula

A

ΔP = Q (flow) x R (resistance)

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27
Q

MAP (mean arterial pressure) formula

A

D + ((S - D)/3)

D = diastolic
S = systolic
pressure units = mmHg

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28
Q

what are the major locations of baroreceptors?

A

aortic arch and carotid vessels

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29
Q

medulla oblongata

A

holds centers for heart rate, respiration rate, and blood pressure; received signals from change in pressure from baroreceptors

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30
Q

what happens when we stand up to quickly?

A

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

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31
Q

if we are standing for long periods of time, should we lock our knees?

A

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)

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32
Q

to increase ΔP, what needs to happen?

A

increase in heart rate and resistance (vasoconstriction)

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33
Q

what does it mean to increase heart rate?

A

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

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34
Q

rheumatoid arthritis

A

long-term autoimmune disorder that affects joints, typically in the wrist and hands

self-attacking antibodies or immunoglobulin (Ig)

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35
Q

dendritic cells

A

antigen presenting cells (APCs) that “sound the alarm,” and ramp up the immune response by presenting antigens that are foreign to other cells

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36
Q

where are dendritic cells typically found in high numbers?

A

tumor :(

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37
Q

what is an autoimmune disorder?

A

a lot of immune system activity that is not needed, so it attacks itself; antibodies or immunoglobin (Ig)

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38
Q

osteoarthritis

A

an impingement (bone on bone); progressive thinning of hyaline cartilage that leads to formation of osteophytes

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39
Q

osteophytes

A

a bone outgrowth, most commonly bone spurs of the heel (calcaneus); exacerbating makes it worse

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40
Q

“FLAT PEG”

A

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)

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41
Q

vasopressin (ADH)

A

hormone that is against urine formation: ADH levels go up so urine volume goes down

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42
Q

caffeine and C2H5OH

A

inhibit ADH so urine production goes up

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43
Q

gouty arthritis (joint gout disease)

A

deposition of needle-like crystals of uric acid joints

factors: diet, genetic matters, under-excretion of uric acid by the kidney

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44
Q

what are the functions of the skeletal muscle?

A

movement, posture, joint stability, thermogenesis, nutrition

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45
Q

movement (skeletal muscle)

A

produces tension to move things; pulling and squeezing

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46
Q

posture (skeletal muscle)

A

baseline tension exerted at all times

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47
Q

joint stability (skeletal muscle)

A

constant tension exerted that holds joint together

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48
Q

thermogenesis (skeletal muscle)

A

HEAT! shivering is involuntary

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49
Q

nutrition (skeletal muscle)

A

starvation: we have taste bud receptors that bind to glutamate in meat so we taste “savory” (umami)

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50
Q

what is the most prevalent amino acid in higher vertebrates?

A

glutamate

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51
Q

what are the two excitable tissues (RMP to AP)?

A

muscle and nervous

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52
Q

true or false: all tissue types have resting membrane potentials

A

true

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53
Q

how are skeletal muscle fibers classified?

A

1) by how fast fibers contract relative to others and 2) how fibers regenerate ATP

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54
Q

what are the different types of skeletal muscle fibers?

A

type 1, type 2A, type 2B

*there are cultural and geographical components to these

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55
Q

type 1 skeletal muscle fibers

A

slow oxidative; THINK marathon runners of Kenya; slow to fatigue and slow twitch; a lot of mitochondria and capillary bed density

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56
Q

type 2A muscle fibers

A

fast oxidative; faster to fatigue and fast twitch

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57
Q

type 2B muscle fibers

A

fast glycolytic; THINK sprinters in Jamaica (the founder effect); fatigue the fastest

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58
Q

sarcos

A

greek for flesh

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59
Q

myo

A

latin for muscle

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60
Q

myoblast

A

makes or builds muscle

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61
Q

protein filaments of muscle fibers

A

myofilaments (actin or myosin)

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62
Q

sarcoplasm

A

cytoplasm of muscle fibers

63
Q

sarcolemma

A

cell membrane of muscle fibers

64
Q

sarcoplasmic reticulum (SR)

A

stores calcium (sequesters calcium)

65
Q

fascia

A

band or sheet of connective tissue, primarily collagen, beneath the skin that attaches to, stabilizes, encloses, and separates muscles and other internal organs

66
Q

whole muscle

A

fascicles

67
Q

fascicle

A

bundle of muscle fibers

68
Q

what are the three names for ONE muscle cell?

A

muscle cell, myofiber, myocyte

69
Q

myofibers

A

made of myofibrils

70
Q

myofibrils

A

made of myofilaments

71
Q

what is the significance of t-tubules?

A

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

72
Q

what are the four steps of the muscle contractile cycle?

A

cross bridge formation, power stroke, detachment, ATP hydrolysis

THINK tug-o-war!!!

73
Q

cross bridge formation - step one

A

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

74
Q

power stoke (sliding filament theory) - step two

A

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

75
Q

detachment - step three

A

new ATP binds to myosin causing the myosin head to detach from actin

*myosin ATPase

76
Q

what happens when there is an issue in step three (detachment - heads won’t let go) of the muscle contractile cycle?

A

when having low (or NO) ATP, we get cramps when alive or rigor mortis when dead

77
Q

cramp (dehydrated + electrolyte ion balance)

A

gastrocnemius undergoes mechanical detachment: pushing toes toward nose to get heads to detach!

78
Q

hydrolyze ATP - step four

A

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)

79
Q

what does shorten during muscle contraction?

A

H-band, I-band, actual sarcomere

80
Q

what does NOT shorten during muscle contraction?

A

A-band, actin, myosin

81
Q

resting membrane potential (RMP)

A

charge inside of the cell is more negative to the positive outside; ALL tissues have an RMP

82
Q

action potential (AP)

A

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

83
Q

what proteins are involved in action potentials?

A

sodium IN and potassium OUT

84
Q

how do action potentials start and end?

A

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

85
Q

SNAPs and SNAREs

A

vesicle of neurotransmitter can bind to pre-synaptic membrane then exocytose contents into synapse; BOTOX interferes with this

86
Q

what are the three basic types of muscle soreness?

A

immediate, 24-28 hour, weeks

87
Q

causes of muscle soreness

A

over usage, injury, certain viruses (interferons) or for no reason at all due to tension or stress

88
Q

immediate muscle soreness (within seconds)

A

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

89
Q

cori cycle in liver

A

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

90
Q

24-48 hour muscle soreness (days)

A

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)

91
Q

soreness that lasts for weeks

A

usually extreme overextension coupled with engaging in activity the body has NOT adjusted to previously; tendons and ligaments are stretched

92
Q

myopathy

A

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

93
Q

neuropathy

A

nerve (nervous) disease; type of muscular disease that affects the peripheral nerves

94
Q

muscular diseases can be classified as neuromuscular or musculoskeletal in nature do to what factors?

A

genetics, environment, virus (interferons), bacterial exotoxins *lyme disease

95
Q

interferons

A

turn on the p53 gene resulting in an achy feeling

96
Q

p53 gene

A

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

97
Q

muscular dystrophy

A

refers to a group of more than thirty genetic diseases that cause progressive weakness and degeneration of skeletal muscles used during voluntary movement

98
Q

atrophy

A

opposite of hypertrophy; cell size decreases

99
Q

muscular dystrophy causes what diseases?

A

muscle degeneration, progressive weakness, fiber death, fiber branching and splitting, phagocytosis, chronic or permanent shortening of tendons and muscle

100
Q

phagocytosis

A

muscle fiber material is broken down and destroyed by scavenger cells

101
Q

chronic (long-term) or permanent shortening of tendons and muscle

A

overall muscle strength and tendon reflexes lessened of lost due to replacement of muscle by connective itssue and fat

102
Q

what does EPSP stand for?

A

excitatory post-synaptic potential

sodium or calcium in (CATIONS) = closer to threshold

103
Q

what does IPSP stand for?

A

inhibitory post-synaptic potential (let anion in)

chloride in (ANION) = away from threshold

104
Q

voltage-gated channel

A

gates that hinge: open or close; amino acid short sequences hinge

105
Q

summation

A

waves of EPSP and EPSP that lead to threshold; made up of ligand-gated receptors that will turn into channels at threshold

106
Q

depolarization

A

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

107
Q

repolarization

A

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

108
Q

hyperpolarization

A

goes below resting membrane potential so the inside of the cell is even more negative; less active because we are further fro threshold

109
Q

molecular interaction facilitates conformational change (MIFCC)

A

a receptor becomes a channel (example: ligand-gated receptors become channels)

110
Q

voltage-gated channels

A

ION SPECIFIC! made up of amino acid residues that are associated with a protein; in short chains that can open and close

111
Q

what can happen during hyperpolarization?

A

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

112
Q

opiates/narcotics

A

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)

113
Q

integral proteins

A

proteins that are embedded within the cell membrane

114
Q

what are the four main types of integral proteins?

A

channels, pumps, carriers, receptors

115
Q

voltage gated sodium channel

A

opens at threshold, closes at +35 millivolts

116
Q

voltage gated potassium channel

A

opens at +35 millivolts, starts to close around resting membrane potential, actually closes at -90 millivolts

117
Q

action potentials and depolarization roll down the cell membrane like a _____

A

wave

118
Q

what is a ligand?

A

molecule that binds to a receptor

119
Q

what is a ligand-gated receptor or channel?

A

channels will be ion specific and relate to ion movement

ex: acetylcholine receptor

120
Q

how can acetylcholine facilitate different physiological responses?

A

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

121
Q

receptors for acetylcholine

A

nicotinic acetylcholine receptor and muscarinic acetylcholine receptor

122
Q

nicotinic acetylcholine receptor

A

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)

123
Q

muscarinic acetylcholine receptor

A

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)

124
Q

actin

A

thin myofilament

125
Q

myosin ATPAse

A

thick myofilament that binds ATP and hydrolyzes ATP (ATP to ADP + PO4 does not want to happen but does)

126
Q

tropomyosin

A

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)

127
Q

troponin

A

binds calcium

128
Q

sarcomere

A

one functional unit: Z line to Z line

129
Q

A-band

A

length of myosin body; dark; has both actin and myosin

130
Q

I-band

A

between A-bands/myosin bodies; light; has actin only

131
Q

H-band

A

in the A-band where actin and myosin do not overlap; myosin only

132
Q

Z-line or disc

A

dark line in the I-band separating sarcomeres

133
Q

NA+/glucose Co-Transporter CARRIER!!!

A

from cells in the gut (eat and drink) to the blood vessels where absorption of glucose and sodium takes place (glucose flips in)

134
Q

neuromuscular junction (NMJ)

A

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

135
Q

acetylcholine neurotransmitter

A

released from motor neuron terminal

136
Q

where are acetylcholine receptor located?

A

sarcolemma; bind to acetylcholine to initiate muscle contraction

137
Q

voltage gated sodium channels (NMJ)

A

located in muscle fiber membrane; open in response to depolarization caused by acetylcholine binding and allow sodium to enter the cell

138
Q

calcium channel (NMJ)

A

receptors in t-tubules that sense the change in membrane potential and trigger the release of calcium

139
Q

neuromuscular junction ions

A

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

140
Q

creatine

A

first energy source used; creatine shuttles into muscle cell with water following leading the muscle to swell

141
Q

takin exogenous creatine does what to skeletal muscle?

A

creatine kinase adds phosphate to make ADP + PO4 which regenerate ATP

good at repairing tissue but can also interfere with sleep

142
Q

off creatine results in what?

A

muscle shrinks lol

143
Q

true muscle building

A

satellite stem cell recruitment, adding nuclei, and increasing gene transcription to produce more actin and myosin filaments

144
Q

cardiac muscle action potential

A

plateau phase due to potassium out and calcium in counteracting each other

145
Q

plateau phase

A

lengthened time associated with refractory period that prevents cardia tetany and no new action potentials

146
Q

pacemaker of hear in the S.A. node

A

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)

147
Q

smooth muscle action potential

A

rounded due few fast voltage-gated sodium channels within smooth muscle: ROLLS NO SPIKES!!! spike potential indicate long periods of contraction

148
Q

antihistamines

A

swelling of smooth muscle in respiratory tree… inhalers block H1 and inhibit mast cells to decrease histamine

149
Q

muscle relaxants

A

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

150
Q

huntingston’s disease (huntingtin gene)

A

autosomal dominant: short arm chromosome four

huntingtin gene = too many CAG repeats that lead to neuro tissue issues

151
Q

what issues of neuro tissue are associated with huntingston’s disease?

A

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

152
Q

gene p53

A

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 :(

153
Q

ATPase

A

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

154
Q

do humans have a jugular artery?

A

NO! we have SIX jugular veins (three pairs)

Anatomy and Physiology I (13 decks)

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