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Pathophysiology > Unit 2: PNS, CNS, bone, muscle, circulatory system > Flashcards

Unit 2: PNS, CNS, bone, muscle, circulatory system Flashcards

1
Q

what constitutes the CNS?

A

brain and spinal cord

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2
Q

how many spinal nerves are there?

A

31, 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

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3
Q

what are 4 cellular constituents of a neuron?

A

nissl substance, microtubules, neurofibrils and neurofilaments (intermediate filaments)

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4
Q

what does the nissl substance do?

A

RER, translates and secretes neurotransmitter packages

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5
Q

what are some of the glial cells/supporters of neurons in CNS?

A

astrocytes, oligodendrocytes, microglia, ependymal cells

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6
Q

what are some glial cells/supporters of neurons in PNS?

A

schwann cells=myelination

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7
Q

what do astrocytes do?

A

lots of stuff, connect neurons to vasculature (and may regulate vasodilation/constriction), also contribute to blood brain barrier this way, may regulate synaptic formation and maintenance (thus consolidating memories/influence plasticity) also may release their own neurotransmitters at synapse and modulate APs and influence memories, can communicate with each other via gap junctions, regulate/buffer K ions

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8
Q

what do oligodendrocytes do?

A

lay down myelin in cns

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9
Q

what do ependymal cells do?

A

line surfaces of cavities filled with csf

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10
Q

what is the difference between schwann and oligdendrocytes, besides their locations?

A

schwann only myelinate one axon, oligodendrocytes do many

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11
Q

what is the schmidt langerhans cleft?

A

a trapped portion of cytoplasm of a schwann cell

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12
Q

what structure moves nutrients from body to axon of neuron?

A

microtubules

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13
Q

what cells are degenerated in parkinsons?

A

dopamine producing cells in basal ganglia in substantial nigra of midbrain, thus dopamine cannot inhibit certain pathways and you get an overactive subthalmic nucleus, this is why it is treated with L-dopa

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14
Q

what is the cone shaped, organelle/nissl free area of axon where it leaves the cell body?

A

axon hillock

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15
Q

where do APs always start in a neuron and why?

A

it has the lowest threshold potential, so AP always start here

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16
Q

which protein brings nutrients back to cell body along microtubule and which one brings nutrients away from body along microtubule?

A

anterograde (toward axon) by kinesin, retrograde (away from axon) by dynein

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17
Q

what factors make nerve regeneration more feasible?

A

nerve is cut distal to cell body, nerve is in PNS (CNS is too crowded), nerve it cut close to effector organ, no scar tissue, less inflammation, the type of injury (whether severed or crushed)

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18
Q

what part of the schwann cell forms the myelin sheath?

A

the plasma membrane

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19
Q

what allows saltatory conduction of APs?

A

nodes of ranvier

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20
Q

what happens distal to a cut nerve in wallerian regeneration?

A

swelling, neurofilaments hypertrophy, myelin sheath disintegrates and shrinks, axon degenerates and disappears, muscle also atrophies

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21
Q

what happens proximal to a cute in wallerian regeneration?

A

swelling and dispersal of nissl substance, cells increase metabolic, mitochondrial, and protein synthesis activity (to get nutrients to cut), new terminal axon segments sprout, schwann cells help them find their way back

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22
Q

what are some sensory receptors of nerve impulses?

A

muscle spindles, sensory receptors, mechanoreceptors, golgi tendon organs, free nerve endings

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23
Q

what are golgi tendon organs?

A

dendrites near tendon of a muscle at neuromuscular jcn, if tendon tapped/moved, these will fire

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24
Q

a cells dendrites (or axon or cell body) may receive many impulses and signals, but what must be reached before an AP can be sent on to influence other cells?

A

threshold potential

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25
Q

what would hyper polarizing a membrane with chlorine channels do?

A

inhibit an action potential

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26
Q

what is the function of a synaptic bouton?

A

to increase the surface area of the synapse and continue propagating the AP

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27
Q

what are the 3 different types/kinds of summation?

A

temporal (lots of signals in a short amount of time), spacial, (lots at same space), facilitation (excitatory post synaptic potentials help it get closer to threshold)

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28
Q

how are neurotransmitters like acetylcholine recycled? and why are they taken away?

A

back to cell by receptor mediated endocytosis? or degraded by enzyme; taken away so there is not a continuous stimulus

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29
Q

where are the cell bodies of presynaptic sympathetic neurons located?

A

thoracolumbar: lateral horn of spinal levels T1-L2

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30
Q

where are the bodies of post synaptic sympathetic neurons located?

A

in the sympathetic chain, near the vertebrae, post ganglionic symapthetics have a long way to go to get to effector organ

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31
Q

where are the cell bodies of preganglionic parasympathetic neurons located?

A

in certain nuclei of cranial nerves and sacral nerves

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32
Q

where are the cell bodies of post ganglionic parasympathetic neurons located/

A

in ganglia associated with cranial or sacral divisions, near effector organ

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33
Q

when both parasympathetics and sympathetics are communicating with an effector organ, which one will win out?

A

whichever one is sending the most signals

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34
Q

what area of the body is only innervated by sympathetics?

A

extremities, and also the control of blood pressure, thus to lower BP you need to block the sympathetic beta-receptors

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35
Q

which neuron of the 2 neuron system of autonomics is unmyelinated?

A

postganglionic neuron

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36
Q

T or F: there are different types of adrenergic receptors for the postganglionic neuron of sympathetics (i.e. receptors that respond to norepinephrine or epinephrine)

A

T: the different receptors respond to catecolamines (norepi and epic) but the receptor type is what causes the different types of responses throughout the body

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37
Q

what are some of the functions of the skeletal system?

A

forms body, supports tissues, protects organs, permits movement via muscle attachments, blood cell formation, mineral storage of calcium

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38
Q

what are the three types of joints (classified by movement) and what kind of movements do they allow?

A

synarthrosis-not movable, amphiarthrosis-slightly moveable, diarthrosis-really movable

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39
Q

what are the kinds of joints classified by connective structures?

A

fibrous, cartilaginous, and synovial

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40
Q

what are some types of fibrous joints?

A

syndesmosis (radius and ulna interosseus), sutures, gomphoses (teeth)

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41
Q

what are some examples of cartilaginous joints?

A

symphysis (pubis) connected by disc of fibrocartilage, synchondrosis-hyaline cartilage connects the two bones i.e. ribs and sternum

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42
Q

what are some of the components of a synovial joint?

A

articular cartilage covering bone, joint cavity, synovial membrane, synovial fluid (lube), joint capsule

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43
Q

what are some important ECM components of cartilage? which helps absorb water to make it more hydrated/cushy?

A

proteoglyans, GAGS, elastic fibers, type II collagen fibers, the GAGs attach to water because they are negatively charged

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44
Q

what do the main cells of cartilage do? where do they receive their blood supply?

A

chondrocytes, they secrete matrix components, they use anaerobic glycolysis and get nutrients from surrounding blood vessels in perichondrium (CT sheath)

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45
Q

what protein connects chrondrocytes to the ECM?

A

chondronectin-connects chondrocytes to integrin, GAGs, and collagen

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46
Q

what are the 3 types of cartilage?

A

hyaline, elastic, fibrocartilage

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47
Q

what are some identifying components of hyaline cartilage?

A

in movable joints, no perichondrium, high concentration type II collagen, most common, chondrocytes in lacunae

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48
Q

what are some identifying components of elastic cartilage?

A

lots of elastin fibers and type II collagen in ears

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49
Q

what are some identifying components of fibrocartilage?

A

strong, not as hydrated as hyaline, type I collagen, still does shock absorption and weight bearing
example: intervertebral disc

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50
Q

why does cartilage not regenerate well?

A

no internal blood supply, low metabolic activity

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51
Q

how are chondroblasts stimulated to become chondrocytes for growth/regeneration?

A

somatrotropin is released from pituitary which acts on liver to release insulin like growth factors which stimulates chdonroblasts into chondrocytes

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52
Q

what proteins are important in aggregation of chondrocytes?

A

aggrecans

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53
Q

how many bones are in the appendicular and axial skeletons?

A

80 in axial (cranium + thorax+ spine) 126 in appendicular (extremities plus girdles)

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54
Q

what are the different types of bones?

A

long (extremities), flat, irregular, short/cuboidal(i.e. tarsals)

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55
Q

what are some of the identifying features of long bones?

A

shaft=diaphysis, head=epiphysis, metaphysis=neck, medullary cavity with yellow and red marrow

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56
Q

what is the epiphyseal plate?

A

the plate that helps our bones grow with us, in children i is cartilage, but calcifies as we get older, just shows as a line in adults

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57
Q

what is the inner lining of the medullary called that produces bone precursor cells?

A

endosteum

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58
Q

what are the different types of bone tissue?

A

spongy (cancellous) and compact

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59
Q

what are some of the identifying features of compact bone?

A

haversian system, concentric lamellar organization of osteons

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60
Q

what are some of the identifying features of spongy bone?

A

trabeculae, formed in direction of stress on bone, allow blood vessels through, make the bone lighter

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61
Q

what is the layer of blood vessels and CT of bone called?

A

the perioosteum

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62
Q

how is the periosteum related to shin splints?

A

with excessive use of a muscle after inactivity, like tibialis anterior, it pulls on the periosteum and causes swelling=use NSAIDSs to reduce inflammation and pain (stops production of prostaglandins) and rest

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63
Q

what hormone stimulates mesenchymal cells to become osteoblasts?

A

bone morphogenic proteins of the Transforming Growth Factor beta family

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64
Q

what do osteoblasts do?

A

secrete non mineralized bone matrix (osteoid), respond to parathyroid hormone to secrete MCSF and make more osteoclasts, produce osteocalcin when stimulated with vitamin D (binds calcium) which is the start of mineralization

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65
Q

how does an osteoblast turn into an osteocyte?

A

by being surrounded with calcified bone matrix

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66
Q

what do osteoclasts do?

A

precise function unknown, although they do release cytokines and sclerostin which seems to be involved in bone remodeling, they can also communicate with their neighbors via gap junctions

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67
Q

where are osteoclasts derived from? how could osteoblasts be stimulated to make more of these?

A

derived from monocyte lineage in BM, osteoblasts can be stimulated to differentiate into these by parathyroid hormone in with monocyte colony stimulating factor and RANKL (receptor activator of nuclear factor kB ligand)

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68
Q

what do osteoclasts do?

A

resorb bone like macrophages, bind calcitonin (released by thyroid)

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69
Q

how do osteoclasts resorb bone?

A

they attach to integrins on bone cells (osteoclasts/blasts?) and surround them with their cytoplasm and digest it with their lysozymes filled with hydrolytic enzymes

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70
Q

what kind of problems could inefficient bone resorption cause?

A

filling of medullary cavity with bone=anemia, called osteopetrosis

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71
Q

T or F: both thyroid and parathyroid are involved in regulation of osteoclasts

A

T: parathyoird hormone stimulates osteoblasts to secrete monocyte-colony stimulating factor and thyroid regulates osteoclasts with calcitonin

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72
Q

what is contained in the bone ECM?

A

collagen type I, ground substance, proteoglycans-large negative sugar protein complexes (absorb water, more of these are prevalent in cartilage), hydroxyappetite (calcium+phosphate minerals), glycoproteins (regulate collagen fibril assembly, calcification, and resorption)

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73
Q

which protein is analogous to fibronectin in cartilage, and binds cells to matrix?

A

osteonectin

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74
Q

what causes bone to remodel?

A

stress on bone, weight training/exercise, continuous until age 30

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75
Q

what are bone remodeling units? where do they reside?

A

they are precursor cells that differentiate into osteoblasts and osteoclasts that repair microscopic injuries and maintain bone integrity, they are found in periosteum along vascular channels and free surfaces

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76
Q

what are the phases of bone remodeling?

A

apoptosis of osteocytes, reabsorption by osteoclasts, formation of new bone (osteoblasts forming matrix and differentiating into osteocytes?) in concentric circles to fill space

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77
Q

what regulates bone remodeling?

A

osteoclasts-calcitonin, and parathyroid-osteoblasts

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78
Q

what two ions help the formation of hydroxappatite which is important for crystallization and mineralization of bone?

A

calcium and phospahte

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79
Q

what bone cell is primarily responsible for the ossification process, and how?

A

osteoblasts, because they secrete collagen, proteoglycans, glycoproteins, and calcitonin (binds calcium, increase its concentration locally), some of which can bind calcium. they also secrete vesicles of matrix that have enzymes that hydrolyze phosphate from other molecules, also increasing its concentration locally. these local concentrations form nanocrystal around the vesicle and keep forming with hydroxyappetite until a solid full matrix

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80
Q

what kinds of things can a mesenchymal stem cell turn into?

A

fibroblast (to collagen), chondroblast (to chondrocyte) osteoblast (to osteocyte and osteoclast)

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81
Q

what constituents make up the haversian system/

A

A central canal with a nerve, artery, and vein, concentric lamellae around that, lacunae with osteocytes in them (the osteocytes reach out to others via canaliculi)

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82
Q

what kind of cartilage does endochondral bone formation use as a template?

A

hyaline

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83
Q

where are the primary and secondary ossification centers?

A

primary by blood vessels in medullary cavity, secondary by capillaries to epiphysis in ends of bone, the cartilage dies and becomes replaced by bone

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84
Q

how might a teenager who broke their femur have growth problems?

A

if it interfered with the epiphyseal plate, they may not be able to have their femur/humerus grow normally

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85
Q

how does periosteal bone formation work?

A

osteoblasts differentiate directly from mesenchyme and forms bone between two periosteums

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86
Q

what are the 5 steps to bone remodeling from injury?

A

hematoma (fibrin and platelets), pro callus (fibroblasts and osteoblasts and capillaries grow into hematoma, start laying down cartilage), callus formation (woven bone from calcium and phosphate) , callus replacement (woven bone replaced by compact or spongy bone), bone remodeling (collar forms to incorporate new growth back into existing bone)

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87
Q

what role does bone have in controlling blood calcium levels?

A

parathyroid hormone stimulates osteoblasts to secrete paracrine factors that stimulate osteoclasts to resorb bone and free calcium; calcitonin binds and inhibits osteoclasts from turning over bone if blood calcium is too high

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88
Q

what are some clinical manifestations of osteoporosis?

A

bone that has less mass, density way down (833-648=osteopenic and >648 is osteoporosis)

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89
Q

what are some causes of osteoporosis?

A

lack of vitamin d, mg, and c; inactivity(no stress for remodeling), decreased levels of hormones like estrogen and testosterone, imbalance of bone resorption/creation

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90
Q

what are some potential causes of post menopausal osteoporosis?

A

same as osteoporosis, with an emphasis on changing levels of osteoprotegerin and insulin like growth factor and family history and excessive phosphorous intake through soda/junk food interferes with calcium balance

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91
Q

what are some clinical manifestations of degenerative joint disease/osteoarthritis?

A

damage to synovial joint/idiopathic/hereditary breaks down articular cartilage, synovial membrane starts to break down/deform, joint capsule becomes deformed, more bone begins to form at margins, causing deformity of joint, inflammation, pain, sometimes new bone growth that “locks” a joint

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92
Q

what are some clinical manifestations of inflammatory joint disease/arthritis?

A

autoimmune attacking of CT and synovial membrane of joints; presence of rheumatoid factors and antibodies IgG and IgM, usually bilateral or in at least 3 joints at once; ulnar drift, lots of same symptoms as osteoarthritis

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93
Q

what is ankylosing spondylitis?

A

stiffness and fusion of spine and SI joints

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94
Q

what is gout/

A

inflammation in response to excretion/surplus of uric acid

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95
Q

what disease is marked by widespread muscle and joint pain, fatigue, and increased sensitivity to touch?

A

fibromyalgia

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96
Q

what is the functional unit of muscle contraction?

A

myofibril

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97
Q

what are muscles mostly made of, molecules wise?

A

75% water, 20% protein, 5% organic and inorganic compounds

98
Q

what do the epimysium, perimysium, and endomysium do?

A

CT that surrounds the muscle, fascicle, and fiber, respectively to supply nerves, lymphatics, vessels

99
Q

what fiber helps transmit forces since most fibers don’t run the whole length of the muscle?

A

collagen

100
Q

which protein of the troponin/tropomyosin/actin complex binds calcium to let myosin act on actin?

A

troponin binds calcium

101
Q

what molecules are elevated in blood if there has been damage to muscle?

A

troponin and Creatine Kinase – adds P to ADP from phosphocreatine

102
Q

what molecule acts as a spring to recoil muscle and is the largest protein in the body?

A

titin

103
Q

what protein causes myosin filaments to aggregate?

A

myomesin

104
Q

what enzyme supplies ATP to cell?

A

creatinine kinase-adds P to ADP from phosphocreatine (why people eat “protein” after to give them substrates for muscle energy)

105
Q

what is the functional unit of the neuromuscular system?

A

one motor axon and all the fibers it innervates

106
Q

what is the innervation ratio and how does it relate to endurance?

A

the number of motor units per muscle, the higher the number of motor units, the greater the endurance

107
Q

why might one axon to one muscle fiber be useful?

A

gives you greater control (i.e. hand) although less endurance

108
Q

what are the steps of muscle contraction?

A

activation/excitation, coupling, contraction

109
Q

which muscles are the fast twitch and which the slow twitch?

A

fast ones are type II large alpha, rely on anaerobic glycolysis, thus make lactate, less endurance

slow ones are like intrinsic muscle of back , fire regularly, don’t tire easily, type I small alpha

110
Q

what is the cerebral cortex made of?

A

cell bodies

111
Q

where is the precentral gyrus located and what do it do?

A

located anterior to central sulcus; houses cell bodies of motor neurons to skeletal muscle

112
Q

what does the premotor/brodman area 6 do?

A

programs motor movements, thus it works with percentile gyrus and basal ganglia to modify those signals?

113
Q

what do the eye fields (brodmann area 8) do and where ar they located?

A

control eye movements, located in middle frontal gyrus

114
Q

what kinds of functions does the prefrontal cortex do?

A

inhibition of limbic, goal oriented behavior, planning, analytical, relationships, concentration, short term memory

115
Q

what cranial nerves are associated with brocas area, the motor speech area?

A

vagus for voice, and hypoglossal for muscles of tongue, if damaged in stroke cannot fine tune these=expressive aphasia

116
Q

what does the post central gyrus do and where is it located?

A

primary center for input of sensory info; located posterior to central sulcus in parietal lobe (=primary lobe for sensory)

117
Q

what is the temporal lobe responsible for?

A

long term memory, balance, smell, hearing

118
Q

what is located in the parietal lobe?

A

general sensory info; taste area; sensory speech (wernicke), post central gyrus

119
Q

what does the thalamus do?

A

primary center for relaying of sensory info and deciding what to do with it

120
Q

what is the hypothalamus responsible for?

A

homeostasis, regulating: hormones, temp (and thus fever), ions, thirst, regulation of emotional expression

121
Q

what does the epithalamus do?

A

circadian rhythms and light/dark schedule

122
Q

which supporting nerve cell (neuroglia) is most common in brain tumors? what’s a marker for it?

A

astrocytes=astrocytomas; marker=glio fibrillar acidic protein

123
Q

what is different about the ependymal epithelial as opposed to other epithelium?

A

it lacks a basement membrane

124
Q

what type of junctions do vessels in brain have? in other parts of body?

A

in brain they have tight junctions, everywhere else they have adherent junctions

125
Q

what is the purpose of the blood brain barrier? what cell contributes to it by wrapping its feet around vessels?

A

keeps out toxins/bacteria=immunological advantage; astrocytes

126
Q

what are some of the functions of CSF?

A

bathes brain, provides ions for action potentials,

127
Q

what is the flow of CSF?

A

choroid plexuses, lateral ventricles, interventricular foramina, 3rd venticle, cerebral aqueduct, 4th ventircle, aperatures to subarachnoid space, taken up by dural venous sinuses in arachnid granulations

128
Q

what are the two layers of the dura mater?

A

periosteal, meningeal, meningeal forms sinuses

129
Q

whats the space called between the dura and the skull?

A

epidural space

130
Q

what’s the space called between the pia mater and arachnoid mater?

A

subarachnoid space

131
Q

how is CSF formed at the choroid plexus?

A

vessels close to pia mater help form it, travels through ependymal cells to cavity of ventricle

132
Q

which part of the brain is the most evolutionarily advanced with higher reason and problem solving? fore, mid or hind brain?

A

forebrain

133
Q

what structures make up the forebrain?

A

telencephalon (cerebrum and corpus striatum: basal ganglia), diencephalon (hypothalamus, epithalamus, subthalamus, thalamus), amydala

134
Q

what is in the corpus striatum of the forebrain?

A

putamen, lentiform nucleus, caudate nucleus, (amygdala?), globus pallidus

135
Q

what structures are in the midbrain?

A

corpora quadrigemmina (superior colliculi-eye tracking), inferior colliculi-moving head to hear sound), tegmentum (red nucleus and substantial nigra), basal pedunculi (basal pedunculi+tegmentum=cerebral peduncles)=receives info and makes decisions

136
Q

what structures are in the hindbrain?

A

cerebellum, pons, medulla oblangata (called the myelencephalon)

137
Q

what does the cerebellum do?

A

combine motor info, balance, muscle synergy of iPSALATERAL side

138
Q

what does the pons do?

A

communicates with cerebellum, transmits info from there to contralateral side

139
Q

what does the medulla do?

A

transmits info; HR, BP, respiration, balance, homeostasis, posterior part of reticular formation

140
Q

what is in the reticular formation?

A

nuclei within brainstem (pons, medulla) that communicate with each other; maintains wakefulness, cardiovascular function, respiration; in conjunction with cerebrum it is called the reticular activating system=consciousness

141
Q

which is more likely to result in recovery-destruciton of upper or lower motor neurons?

A

destruction of upper motor neurons, if there cell bodies are destroyed they are more likely to regenerate

142
Q

what are 4 motor pathways?

A

reticulospinal (reticular formation), rubrospinal (red nucleus), vestibulospinal (motor function for balance), lateral corticospinal

143
Q

what are 4 sensory pathways?

A

lateral spinalthalamic tract, posterior column (like fasciculus gracilis or fasciculus cuneatus, stops in nucleus gracilis and through medial lemniscus), anterior spinothalamic, posterior /dorsal

144
Q

what are the 4 components to a reflex arc? how is this more complicated in real life?

A

receptor, afferent, efferent, effector; in real life there are lots of modifications and interneurons that can excite or inhibit; i.e. in the patellar reflex you want to excite the extensors but also need to relax the flexors

145
Q

what are two pain theories?

A

gate theory: gate in spinal cord that either lets signals through or doesn’t, gate is interneurons in substantial gelatinous in dorsal horn that act as the gate; specificity theory: pain is proportionate to amount of tissue damage (doesn’t explain psychologic contributions)

146
Q

what are the three important types of sensory fibers in nociceptors of the gate theory?

A

gate can be “opened” via fast, localized, a-delta fibers, or slow, diffuse, unmyelinated c fibers, or closed via a-beta fibers (non-nociceptive)

147
Q

what are the 4 classifications of pain?

A

nociceptive, non nociceptive, acute, chronic`

148
Q

what’s the difference between pain threshold and pain tolerance? which varies the most over time?

A

pain tolerance=amount of time enduring pain before pain response is initiated (varies over time); pain threshold is amount of pain signals that come in before pain is perceived

149
Q

how are nociceptors characterized? what molecules can stimulate them?

A

they are primary sensory neurons; usually bare nerve endings in skin, muscle, viscera or receptors that respond to chemical, mechanical or temp stimuli; can be stimulated via bradykinins or prostaglandins

150
Q

what are some ways to modulate pain?

A

segmental inhibition (a-beta fibers, low threshold mechanical, touch, distracting info, bite thumb), diffuse noxious inhibitory controls (acupuncture, cause lower amounts of pain to crowd out signals from larger pain stimuli), chemicals and neurotransmitters, direct excitation (via threshold depolarization from direct stimuli) or indirect via prostaglandins, bradykinins

151
Q

the signals from what 3 pathways/neurons converge on the spinal dorsal horn?

A

axons from sensory receptors, spinal interneurons, top/down control mechanisms

152
Q

what chemicals are excitatory for pain?

A

glutamate and aspartate

153
Q

what chemicals are inhibitory for pain?

A

sertotonin, GABA, endorphins=endogenous pain inhibitors (opiates)

154
Q

how do opiates (i.e. endorphins) inhibit pain?

A

they fit in receptors that second order pain neurons in substantia gelatinous have and thus inhibit the continuation of the AP or inhibit release of pain excitatory neurotransmitters like glutamate and aspartame

155
Q

how do indirect excitation of nociceptors work?

A

bradykinins and prostaglandins (products of inflammation/tissue damage)depolarize the membrane of pain neurons

156
Q

what fibers are responsible for somatic and visceral pain?

A

GSA, and GVA respectively

157
Q

why is visceral pain poorly localized?

A

the GVAs synapse in a similar area of the spinal cord as the GSAs, (maybe on the same interneuron?? and it causes a depolarization of something nearby?) and the brain receives a signal from whatever that interferon synapsed at, say to the arm, and could not discriminate precisely where it came from

158
Q

what are the physiologic responses to pain?

A

increased HR, respiratory rate, and BP, pallor, flushing, dilated pupils, blood sugar elevated, gastric stuff decreased, blood flow to viscera and skin decreased (all sympathetic responses)

159
Q

what are some possible causes of chronic pain?

A

nerves regenerating and spontaneously firing, lower pain threshold, loss of inhibiting interneurons in substantial gelatinosa, alterations in DRG in response to peripheral nerve injury, up regulation of nociceptive chemokines or their receptors

160
Q

how do NSAIDs work? what are some examples?

A

they are antiinflammatants which thus inhibits formation of prostaglandins and bradykinins which can depolarize free nerve endings, examples=naproxen, aspirin, ibuprofen

161
Q

how does acetaminophen/tylenol work?

A

it blocks connections at substantia gelatinosa

162
Q

what vessel controls the systemic circulation?

A

arterioles

163
Q

what is an anatomic distinction of arterioles?

A

4 or less layers of smooth muscle

164
Q

which part of the arterial system is controlled by sympathetics via epinephrine and norepinephrine?

A

arterioles

165
Q

what is the name of the smooth muscle that constricts flow to capillaries? what’s the vessel called that bypassed capillaries?

A

just about one layer of smooth muscle cells (tunica media) that is the precapillary sphincter; arteriovenous shunt

166
Q

how many layers of epithelial cells to capillaries have?

A

one

167
Q

what are the layers in a capillary?

A

tunica intima=endothelium+basement membrane; NO tunica media, tunica adventitia

168
Q

do capillaries have smooth muscle?

A

no

169
Q

what are the 3 types of capillaries and where might they be found?

A

continuous, very tight jcns, in brain; fenestrated (holes in cells) muscle/in liver/GI, sinusoidal in BM (holes in cells and in between cells)

170
Q

which of the three capillary types has the largest lumen?

A

fenestrated, large lumen and large holes to get cells in and out

171
Q

what structure allow the escape of WBCs?

A

venules; blood is moving slower here, still a small enough vessel that it perfuses tissues

172
Q

folds of which layer contribute to the valves of veins?

A

tunica intima

173
Q

what comprises the tunica intima? what part is missing in arterioles, venues, and capillaries?

A

endothelium, basement membrane (basal lamina to connect cell to CT, elastic lamina to connect basement membrane to CT) and underlying CT; arterioles, venules and capillaries don’t have the CT

174
Q

what layer is present between tunica intima and media in large veins and arteries?

A

internal elastic lamina-has holes to allow more passage of things from deeper in the wall

175
Q

what kinds of fibers are found in tunica media of elastic arteries?

A

elastic fibers, reticular fibers, proteoglycans

176
Q

what is the function of elastic arteries?

A

to keep BP constant (and also monitor it) by expanding with contraction of blood and recoiling in diastole

177
Q

what are two examples of muscular vessels?

A

femoral artery and vein

178
Q

which vessels have the most tunica adventitia?

A

veins

179
Q

what is the function of the tunica adventia?

A

supply nerves/arteries/veins since vessel is too large to get nutrients from diffusion; and also provide new cells via fibroblasts, responds to injury and inflammation

180
Q

what is the name of the blood vessels and nerves to the largest vessels?

A

vasa vasorum and perivascular nerves

181
Q

what layer may separate adventitia from tunica media in large vessels?

A

external elastic lamina

182
Q

does blood speed up or slow down in capillaries?

A

it slows down, think like a wide river slows down as opposed to a narrow one; good for diffusion

183
Q

what are some factors that affect blood flow?

A

pressure; resistance; viscosity; laminar vs. turbulent flow, compliance

184
Q

what kinds of receptors are baroreceptors?where are they found?

A

mechanical; respond to stretch; at bifurcation of carotid artery and in aorta; it is a swelling with less tunica media so it is more responsive to stretch

185
Q

what cranial nerves are associated with baroreceptors and chemoreceptors?

A

vagus for aortic-can then slow stuff down if need to; glossopharyngeal for carotid sinus and carotid body

186
Q

how would the body respond to high bp in carotid artery?

A

glossopharyngeal starts firing, body inhibits sympathetics and activates vagus to slow down HR and slow down contractility

187
Q

how would the body respond to low o2 at aorta?

A

vagus starts firing its GVAs, body then activates sympathetics to increase respiration

188
Q

where is the vasomotor center located that controls the bar and chemo receptors?

A

reticular formation

189
Q

what are some vasoconstrictors/increasers of BP?

A

vasopressin, angiotensin II, epinephrine, norepinephrine,

190
Q

what are some vasodilators/ decreases of BP

A

aldosterone, nitric oxide, prostaglandins, endothelium derived relaxing factor

191
Q

what kind of surface does endothelium have in arteries? what molecules are involved in this?

A

non thrombogenic; via heparin sulfate, plasminogen activating factor (stops fibrin from making clots), thrombomodulin

192
Q

what kinds of functions can the endothelium do/

A

vasoconstrict/vasodilate, non thrombogenic, immune responses: secretes cytokine: interleukins (recruit WBCs) and allows adhesion of WBCs via p-selectin; secrete growth factors

193
Q

what are some of the vasoconstrictors endothelium produces? vasodilators?

A

angiotensin converting enzyme, endothelin-1; nitric oxide, prostacyclin

194
Q

what are some of the growth factors endothelium secretes

A

monocyte colony stimulating factor for WBCs, vascular endothelial growth factor (for new cells from mesenchyme), angiopoietin

195
Q

what is angiogenesis?

A

sprouting of new vessels from capillaries, endothelium can do this

196
Q

how does the endothelium promote new growth?

A

secreting angiopoietins which stimulate endothelial cells to recruit smooth muscle and fibroblasts to form the other tissues of the vascular wall

197
Q

what is contained within lymph?

A

water, proteins (mostly albumin), APCs, lymphocytes

198
Q

what creates the valves in lymph vessels?

A

endothelial cells

199
Q

what kind of layers are present in lymph vessels?

A

single layer epithelium on a incomplete basal lamina

200
Q

what is hemostasis?

A

ability to stop ourselves from bleeding out

201
Q

where do the right lymphatic ducts and thoracic ducts drain?

A

R and L subclavian veins, respectively

202
Q

what is inside a lymph node?

A

APCs, T and B lymphocytes

203
Q

what are the steps to hemostasis?

A

vasoconstriction, formation of platelet plug (primary hemostasis), activation of coagulation cascade, formation of stronger fibrin (secondary hemostasis), degradation of plug

204
Q

what begins the start of hemostasis?

A

blood hitting underlying matrix/collagen

205
Q

how are platelets aggregated with damage to an endothelial cell?

A

the endothelial cells become activated and release von willbebrand factor-which binds and activates platelets to inner surface of endothelium, the platelets then aggregate and are activated (?)which starts the extrinsic/damage part of coagulation cascade

206
Q

how does the endothelium prevent clotting?

A

by continuously inhibiting or converting pro-clotting factors to inactive forms: i.e. VIIIa and Va, inhibiting Xa (does prothrombin to thrombrin), Va/TF

207
Q

what functions do platelets have? what is healthy level?

A

platelets form clots to prevent bleeding, activate coagulation cascade to further stabilize plug, initiate repair processes via clot retraction and dissolution, normal count is 140-340

208
Q

at what level is thrombocytosis?

A

> 340 platelets

209
Q

at what level is thrombocytopenia?

A
210
Q

what allows platelets to adhere to von willebrand factor?

A

GPib

211
Q

what do platelets secrete when activated to recruit other platelets?

A

ADP, thromboxane (TX2)

212
Q

what inhibits TX2/

A

aspirin=can have clotting issues

213
Q

what does endothelium secrete to activate coagulation cascade?

A

tissue factor

214
Q

what are the two ways to initiate the coagulation cascade?

A

extrinsic from injury that exposes tissue factor on endothelial cells or intrinsic pathway from inflammation via hangman factor, factor XII

215
Q

what are a few antithrombotic mechanisms?

A

block tenase so it cannot make pro thrombin (Xa); block tissue factor via tissue factor pathway inhibit-blocks Xa also, block thrombin, protein c which binds thrombin (inhibits it?) and protein S which breaks down/inhibits Va

216
Q

what are the parts of the fibrinolytic system?

A

as soon as fibrin clot it formed, plasminogen is activated by tissue-plasminogen activator (which resides on epithelial cells and gets activated itself by fibrin) to become plasmin, which breaks down fibrin clots

217
Q

what happens in arteriosclerosis?

A

arterial walls harden via fibroblasts and collagen fibers migrating to tunica intima

218
Q

what happens in atherosclerosis?

A

hardening occurs with endothelial damage in conjunction of macrophages that digest lipids and form fatty streaks and fibroblasts that migrate to tunica intima and form collagen caps which may or may not burst=could be deadly clot

219
Q

what can cause inflammation and damage of the endothelium?

A

smoking, high BP, diabetes, high LDL, low HDL, autoimmunity

220
Q

what are some risk factors for coronary artery disease?

A

atherosclerosis, diabetes, HTN, smoking, high LDL, defect in LDL receptors, improper

221
Q

what are some nontraditional risk factors of coronary artery disease?

A

markers of inflammation and thrombosis: c-reactive protein, fibrinogen, protein c, plasminogen activator inhibitor

222
Q

what is a temporary loss of blood supply to heart called/

A

myocardial ishemia-vessels cannot dilate enough to give heart the 02 it demands, usually from atherosclerosis

223
Q

what is a longer term loss of blood to heart called?

A

myocardial infarction

224
Q

what are the different kinds of angina pectoris?

A

silent-no chest pain felt, just feel off and fatigued, etc, stable: transient-build up of lactic acid (from anaerobic glycolysis?) or abnormal stretching, prinzmetal : unexpected and at rest,

225
Q

what do you test for in blood if someone is having chest pain?

A

troponin=muscle necrosis; creatine kinase=another sign of muscle necrosis (enzyme heart uses to make energy)

226
Q

what is a transmural infarct?

A

an infarct all the way through endocardium to epicardium

227
Q

what is a subendocardial MI?

A

just the myocardium just below the affected endocardium will be affected

228
Q

what are the layers around the heart? where do the purkinje fibers run?

A

epicardium (outermost layer) pericardium-serous and fibrous(adventitia), myocardium (muscle), endocardium =epithelium plus CT, the fibers fun in the CT

229
Q

what two layers make up the epicardium?

A

serous pericardium: the parietal (outermost) and visceral layers; these lubricate the heart’s space for movement; fibrous pericardium (outermost),

230
Q

what does the cardiac skeleton do? what’s it made of?

A

it anchors the hearts valves, makes the septa, insertion points for cardiac muscle, insulates from depolarization going everywhere; made of dense CT

231
Q

what is the physical feature that helps myocardial cells transmit electrical impulses?

A

intercalated discs=gap junctions

232
Q

how are myocardial cells held together?

A

desmosomes

233
Q

which cells are responsible for the generation of a spontaneous electrical impulse?

A

sinoatrial node heart cells, their supporting cells= P cells

234
Q

where is the SA nodes found?

A

at the junction of the superior vena cava and right atrium

235
Q

where do parasympathetics and sympathetics influence the heart?

A

parasympathetics at AV node, sympathetics at SA node

236
Q

where are the cell bodies of the pre ganglionic sympathetic fibers to the heart located?

A

lateral horn of T3-T4

237
Q

where are the dorsal motor control centers of vagus and sympathetics for heart?

A

medullary control center/cardiovascular center in reticular formation

238
Q

what is preload and how is it affected by starlings law?

A

amount of end-diastolic pressure in left ventricle, affected by blood left in ventricle and venous return; more blood=more stetching=higher ability to contract

239
Q

what are the volume receptors in the atria and aorta called/

A

bainbridge

240
Q

how is the heart an endocrine organ?

A

it releases atrionatriuetic hormone if pressure gets too high, which is a diuretic-causes salt excretion and water excretion to lower BP

Pathophysiology (2 decks)

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