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Foundations > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What is the pathway for innervation of skeletal muscle by a motor neuron?

A

input via axons from other neurons-> cell body -> axon hillock -> initial segment -> collateral branch of axon -> Node of Ranvier -> Effector (skeletal muscle)

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2
Q

What are the types of sensory neurons?

A

bipolar and pseudounipolar

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3
Q

What are the types of integrative neurons?

A

pyramidal cell, interneurons, and Purkinje cells

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4
Q

What are the cytological contents of the axon?

A

mitochondria, microtubules and neurofilaments

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5
Q

What is ante retrograde transport mediated by?

A

Kinesin

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6
Q

What is retrograde transport mediated by?

A

Dynein

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7
Q

What is the path of anterograde transport?

A

from the perikaryon to the periphery

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8
Q

What is the path of retrograde transport?

A

from axon terminals and dendrites to the perikaryon

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9
Q

What is the mesoaxon?

A

a pair of parallel plasma membranes of a Schwann cell that marks the point of edge-to-edge contact in myelination.

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10
Q

What is the myelin sheath composed of?

A

lipid, cholesterol, and proteins

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11
Q

What are Schmidt-Lantermann clefts?

A

small islands of cytoplasm in the myelin sheath.

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12
Q

What are the satellite cells of PNS?

A

small cuboidal cells surrounding neurons that provide electrical insulation and metabolic exchange

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13
Q

What are the four types of neuroglia cells in the CNS?

A

astrocytes, oligodendrocytes, microglia, and ependymal cells

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14
Q

What is the purpose of astrocytes?

A

proliferate in injury/disease, form blood brain barrier, modulate synapse formation and efficiency, and provide physical support.

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15
Q

What are the types of astrocytes?

A

Fibrous astrocytes and protoplasmic astrocytes

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16
Q

What is the purpose of oligodendrocytes?

A

produce CNS myelin (homolog to schwann cells of PNS)

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17
Q

T/F: One oligodendrocyte can produce multiple myelin Sheaths?

A

T

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18
Q

What is the purpose of microglia?

A

proliferate and become phagocytic in response to CNS injury or disease

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19
Q

What is the purpose of ependymal cells?

A

line the ventricles of the brain and central canal of the spinal cord, part of choroid plexus, and possess cilia to move CSF

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20
Q

What is found in the gray matter of the cerebral cortex?

A

neuronal cell bodies, unmyelinated fibers, and associated neuroglia cells

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21
Q

What is found in the white matter of the cerebral cortex?

A

myelinated fibers and associated neuroglia cells

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22
Q

What are the layers of the cerebral cortex in order?

A

molecular layer, external granular layer, external pyramidal layer, internal granular layer, ganglionic layer, and multiform layer

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23
Q

What are the functions of the cerebellum?

A

coordination of motor impulses, maintenance of muscle tone, and maintenance of equilibrium and balance

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24
Q

The dorsal horn has mainly what type of neurons?

A

interneurons

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25
Q

The ventral horn has mainly what type of neurons?

A

motor neurons

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26
Q

The dorsal root has mainly what type of neurons?

A

sensory neurons

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27
Q

What are the characteristics of autonomic ganglia?

A

eccentric nuclei, multipolar neurons, post synaptic neurons, no neuronal clusters

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28
Q

What are the characteristics of sensory ganglia?

A

centrally located nuclei, pseudounipolar neurons, neuronal clusters, no synapses, and lots of satellite cells.

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29
Q

What is the outflow of sympathetic ganglia?

A

thoracolumbar

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30
Q

What is the outflow of parasympathetic ganglia?

A

craniosacral

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31
Q

What is the enteric division?

A

collection of neurons and their processes within the wall of the alimentary canal

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32
Q

How are PNS axons degraded?

A

axons and myelin degenerate distally (wallerian degeneration) and schwann cells and macrophages clean away debri

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33
Q

How to PNS lesions regenerate?

A
  1. formation of bonds of Bungner
  2. axonal stump thickens and several sprouts form
  3. Sprouts enter bands of Bungner
  4. Single sprout persists and grows
  5. myelin sheaths regnerated
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34
Q

How do nerves in the CNS degenerate?

A

axons and myelin degenerate (Wallerian) and oligodendrocytes die. Microglia can not remove myelin debris and myelin inhibit axon regrowth.

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35
Q

What are the symptoms of ALS

A

gradual onset muscle weakness, slurred speech, outbursts of laughing/crying spells

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36
Q

What does ALS attack?

A

motor neurons

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37
Q

What causes the majority of Spinal cord injuries?

A

road traffic accidents

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38
Q

What is MS?

A

autoimmune disorder in which CNS myelin is attacked

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39
Q

What is the cause of MS?

A

death of oligodendrocytes

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40
Q

What is the joining of the epidermis and dermis called?

A

conspicuous interdigitations

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41
Q

What are the characteristics of thick skin?

A

prominent stratum corner, granulosum and distinct lucid. Lacks hair follicles, sebaceous glands and arrector pili muscles

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42
Q

What are the characteristics of thin skin?

A

less prominent layers, no obvious stratum lucid, contains hair follicles, sebaceous glands, and arrector pili muscles

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43
Q

What is the endocrine function of the skin?

A

synthesis of Vitamin D from UV light

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44
Q

What are the layers of the epidermis?

A

stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum

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45
Q

Cells of the stratum lucidum are rich in what?

A

eleidin (metabolite of keratohyalin)

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46
Q

What is the origin of melanocytes?

A

neural crest origin

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47
Q

What do melanosomes contain?

A

tyrosinase

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48
Q

What is tyrosinase?

A

UV sensitive enzyme involved in melanin synthesis

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49
Q

What are the two forms of melanin?

A

eumelanin (brownish black pigment) and pheomelanin (reddish yellow pigment)

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50
Q

What causes Addison’s disease?

A

lack of cortisol from the adrenal cortex that causes over production of ACTH which increases the pigmentation of the skin

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51
Q

What is albinism?

A

hereditary inability of the melanocytpsto synthesize melanin, which is caused by the absence of tyrosinase activity or the inability of the cells to take up tyrosine.

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52
Q

What is vitiligo?

A

genetically regulated degeneration and disappearance of entire melanocytes

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53
Q

Where are Langerhan’s cells located?

A

stratum spinosum

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54
Q

What do Langerhan’s contain?

A

paddle shipped Birbeck granules that activate T lymphocytes

55
Q

What are the characteristics of Merkel cells?

A

located in stratum basale, near areas that are well vascularized and richly innervated connective tissue

56
Q

What is the dermis composed of?

A

dense irregular connective tissue, Type I collagen fibers, and thick elastic fibers

57
Q

What are Krause’s end bulbs?

A

cold and pressure receptors located in the reticular dermis

58
Q

What are the encapsulated nerve endings?

A

Pacinian, Meissner’s and Ruffini’s corpuscles

59
Q

Where are Ruffini’s corpuscles located?

A

reticular dermis, hypodermic and CT of mesenteries and joints

60
Q

What is the pilosebaceous apparatus?

A

the hair follicle and its associated sebaceous and apocrine sweat glands

61
Q

Where is the infundibulum of the hair follicle found?

A

extends from the surface opening of the follicle to the opening of its sebaceous gland

62
Q

Where is the isthmus of the hair follicle found?

A

from the infundibulum to the level of insertion of the arrector pili muscle

63
Q

What are the three layers of the internal root sheath?

A

cuticle (faces the hair shaft), Huxley’s layer (middle plate), and Henle’s layer (outermost part of hair follicle)

64
Q

What are sebaceous glands?

A

holocrine glands that release the entire cytoplasm upon secretion and produce sebum.

65
Q

What cause acne lesions?

A

increased sebum production with puberty that are associated with focal inflammatory responses

66
Q

How does sebum production occur?

A
  1. mitotically active cells at the periphery divide
  2. As cells mature, a lipid rich secretory product is synthesized and accumulates in the cytoplasm
  3. nuclei shrink and cells disintegrate releasing their secretory product into the pilosebaceous canal
67
Q

What are eccrine sweat glands?

A

not associated with hair follicles and consist of dark cells, clear cells, and myoepithelial cells

68
Q

What are apocrine sweat glands

A

large lumen tubular glands associated with hair follicles that do not begin to function until puberty and respond to hormonal influences

69
Q

What is Epidermolysis bullosa simplex?

A

caused by mutations in genes encoding intermediate filaments, which results in the intercellular separation of the basal epidermal cells

70
Q

What is junctional epidermolysis bullosa?

A

results in separation within the basal lamina. Blisters are common with scarring

71
Q

What is dystrophic epidermolysis bullosa?

A

caused by a mutation for the gene encoding type VII collagen and results in separation in the upper dermis. Blisters common with scarring

72
Q

What causes warts?

A

viral infections that are characterized by epidermal hyperplasia, eosinophilic cytoplasmic inclusions and intensely basophilic nuclei

73
Q

Basal cell carcinoma originate from where?

A

keratinocytes in the stratum basal

74
Q

Squamous cell carcinoma originate from where?

A

keratinocytes in the stratum spinosum

75
Q

What causes psoriasis?

A

decrease in the regeneration of keratinocytes and increase in the number of mitotic cells in the s. basal and s. spinosum. Can be controlled by corticosteriods

76
Q

What are the dominant cytoplasmic organelles of the cell body?

A

RER, Nissl bodies/substance, Golgi apparatus, and numerous mitochondria

77
Q

What is an axodendritic synapse?

A

functional contact between an axon and a dendrite

78
Q

What is an axiomatic synapse?

A

contact between axon and a cell soma.

79
Q

What is an axoaxonic synapse?

A

contact between axons

80
Q

What is a dendrodendritic synapse?

A

electric synapses between retina amacrine inter neurons

81
Q

what happens at the synapse of an axon?

A
  1. action potential reaches axon terminal
  2. synaptic vesicles fuse with presynaptic membrane
  3. neurotransmitter are released into synaptic cleft
  4. neurotransmitters bind receptors on postsynaptic membrane
  5. neurotransmitter receptors initiate bioelectric impulses via changes in intracellular ions
  6. action potential is propagated.
82
Q

What do protoplasmic astrocytes contain?

A

Glial fibrillar acidic protein

83
Q

Describe Muscle Fiber Type I

A

Slow Oxidative Fibers (long distance runners), many mitochondria, large amounts of myoglobin

84
Q

Describe Muscle Fiber Type IIa

A

Fast Oxidative, Glycolytic (sprinters, hockey players, etc.), high glycogen, fatigue resistant, many mitochondria

85
Q

Describe Muscle Fiber Type IIb

A

Fast, Glycolytic Fibers, high anaerobic, fatigue prone (short distance sprinters and weight lifters)

86
Q

What does TnI bind?

A

actin

87
Q

What does TnC bind?

A

Ca2+

88
Q

What does TnT bind?

A

tropomyosin

89
Q

What is myosin II composed of?

A

2 polypeptide heavy chains and 4 light chains

90
Q

What is costamere?

A

a sub membrane Z line associated protein structure that connects the sarcomere of the muscle to the cell membrane

91
Q

What is dystrophin?

A

links actin to laminin in the basal lamina

92
Q

What is desmin?

A

surrounds sarcomere at the Z line attaching them to the sarcolemma

93
Q

What is the cause of Duchenne Muscular Dystrophy?

A

sex linked recessive genetic defect resulting in a decrease synthesis of dystrophin.

94
Q

What is the sliding filament model of muscle contraction?

A

Thin filaments slide past thick filaments resulting in greater penetration into A bands, which remain constant in length. I bands and H bands decrease length as Z disks are drawn closer together.

95
Q

What is Myasthenia Gravis?

A

an autoimmune disease where antibodies block Ach receptors of the motor end plate. Characterized by gradual weakening of skeletal muscles. Clinically characterized symptoms include high circulating titer of antibodies to Ach receptors and may be fatal due to respiratory compromise.

96
Q

What is Botulism?

A

type of food poisoning specifically caused by toxin from Clostridium botulinum, which inhibits Ach release at motor end plates. Clinical signs of muscle paralysis, vomiting, visual disorders and even death if untreated.

97
Q

Describe the knee jerk reflex?

A
  1. tapping the patellar tendon stretches quad femurs and associated spindles.
  2. afferent nerves innervating the intrafusal fibers send impulses to the spinal cord signaling a stretch in the intrafusal fibers.
  3. In SC, afferents synapse with efferent nerves back to extrafusal and intrafusal muscles fibers, causing contraction
98
Q

Inhibition of myostatin causes what?

A

excess muscle growth

99
Q

Where are the cardiac purkinje fibers located?

A

Atrioventricular bundle of His

100
Q

What do the thin filaments of smooth muscle contain?

A

actin, smooth muscle tropomyosin, caldesmon, and calponin

101
Q

what is the function of MLCK?

A

enzyme that phosphorylates one of the myosin regulatory light chains enabling cross binding with actin and initiating the contractile cycle

102
Q

What activates MLCK?

A

calcium-calmodulin complex

103
Q

What is the regulation of smooth muscle?

A

MLCK phosphorylates one of the myosin light chains allowing actin-myosin binding and calmodulin along with Ca2+ activates MLCK

104
Q

How is ACh broken down?

A

Ach is hydrolyzed to choline and acetate and a high affinity, Na+ coupled uptake system recovers the choline for re-synthesis of ACh.

105
Q

What causes and EPP?

A

the neurotransmitter binds to receptors on the post synaptic membrane, non-specific small cation channels open allowing depolarization of the membrane

106
Q

What happens if you just tetrodotoxin or saxitoxin?

A

blockage of voltage gated Na+ channels in both the nerve and muscle membranes that prevents the AP

107
Q

What does dendrotoxin do?

A

blocks the voltage gated K+ channels and prevents depolarization of the presynaptic membrane and prolongs the duration of the AP and facilitates the release of ACh

108
Q

what does w-Conotoxin do?

A

blocks the voltage gated Ca2+ channels and prevents exocytosis of ACh from the presynaptic memrbane

109
Q

What do tetanus and botulinum toxins do?

A

inhibit synaptic vesicle exocytosis

110
Q

what is Succinylcholine?

A

an AChR agonist that is not metabolized by AChE. It causes prolonged depolarization and produces flaccid paralysis as Na+ channels near the end plate become inactive

111
Q

Where are skeletal muscle triads located?

A

over the region where the A and I bands overlap in the sarcomere

112
Q

What makes up a skeletal muscle triad?

A

T tubule and 2 cisterns of sarcoplamis reticulum.

113
Q

Describe excitation contraction coupling in skeletal muscle?

A
  1. increase in intracellular Ca2+.
  2. AP spreads from motor end plate to the sarcolemma, down the T tubules
  3. Depolarization of the L type voltage gated Ca2+ channels (DHPR)
  4. each DHPR is mechanically coupled with a Ca2+ release channel (RYR) in the membrane of the junctional sarcoplasmic reticulum
114
Q

Describe excitation contraction coupling in cardiac muscle?

A
  1. DHPRs act as L type Ca2+ channels allowing external Ca2+ to enter the cell.
  2. When Ca2+ enters the cell it binds to Ca2+ receptors on the RYRs (Ryanodine Receptor)
  3. SR Ca2+ release
115
Q

What is calcium induced calcium release?

A
  1. L type Ca2+ channels open during depolarization
  2. influx of extracellular Ca2+ activates RYRS
  3. RYRs release Ca2+ from SR
  4. As free intracellular Ca2+ increases more RYRs open and Ca2+ increases
116
Q

What is the function of Troponin C?

A

binds calcium to the thin filaments in both skeletal and cardiac muscle

117
Q

What is the function of Calmodulin?

A

complexes with Ca2+ and activates MLCK to increase the force of contraction in heart cells. Also the regulatory protein in smooth muscle when complexed with Ca2+

118
Q

What is the function of Parvalbumin?

A

concentration is related to the speed of muscle

119
Q

What is the function of Calquestrin?

A

binds Ca2+ and localizes them in the JSR

120
Q

What is the function Phospholamban?

A

an SR protein that, when phosphorylated, increases SR Ca2+ ATPase activity in cardiac muscle

121
Q

What band remains constant during muscle contraction?

A

A band

122
Q

What band(s) decrease during muscle contraction?

A

H zone and I band

123
Q

What causes the depolarizing phase in smooth muscle APs?

A

voltage gated Ca2+ channels

124
Q

What is required for the relaxation of smooth muscle?

A

Ca2+ must be sequestered or removed to the ECF and the MLCK must be inactivated by cAMP and the MLC must be dephosphorylated by the myosin light chain phosphate

125
Q

What is the smooth muscle latch state?

A

myosin is dephosphorylated but ATP is not readily bound to the myosin so cross-bridge detachment is slowed. Results in a high tension-low energy consumption state

126
Q

What is isometric contraction?

A

the muscle develops tension, but muscle length does not change

127
Q

What is isotonic contraction?

A

One end of the muscle is free, allowing the muscle to contract isometrically first, until it generates more tension than the load imposed on the muscle, then it will shorten.

128
Q

What does the velocity load relationship imply?

A

The muscle will contract isotonically only if it can generate a greater tension than the imposed load

129
Q

What is temporal summation?

A

increasing the frequency of muscle stimulation will increase the tension developed by the muscle

130
Q

What is a tetanic contraction?

A

a summation of contractions until a continuous, maximal contraction is obtains.

131
Q

What is direct phosphorylation?

A

creatine phosphate + ADP= ATP + creatine

132
Q

What is muscle hypertrophy?

A

muscles rapidly adapte to new functional length by adding sarcomeres in serious or they increase in girth by adding sarcomeres in parallel. Accompanied by angiogenesis

133
Q

What is muscle hyperplasia?

A

increase in the number of muscle fibers per muscle.

134
Q

What is muscle atrophy?

A

reverse of hypertrophy and occurs when a muscle is not used

Foundations (3 decks)

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