SM: Week 4 Flashcards

Question

What is the most commonly fractured bone in the wrist?

Answer 1

Scaphoid bone

Answer 2

- Dorsal Interossei, Palmar Interossei, Lumbricals - Joints: • MP: flex • PIP: extend • DIP: extend

Answer 3

* HPV - Warts * Poxvirus - MOlluscum contagiosum, smallpox * Orf virus * Herpes virus: Varicella Zoster, Herpes Zoster, Herpes Simplex 1 & 2, 6 & 7 (Roseola), EBV * Picornaviruses: Coxsackie A&B, Echovirus * Parvovirus B19: Fifth disease (erythema infectiosum) * Paramyxovirus: Measles (Rubeola) * Togavirus: Rubella * Flavivirus: Dengue Fever, West Nile Virus

Answer 4

1. Sham tenderness: superficial and diffuse tenderness and/or nonanatomic tenderness 2. Simulation tests: based on movements which produce pain, without actually causing that movement, such as axial loading and pain on simulated rotation 3. Distraction tests: positive tests are rechecked when the patient's attention is distracted 4. Non-anatomic pain distribution 5. Inappropriate affect

Answer 5

- Mechanical LBP - Causes: muscle spasm, facet joint inflammation, SI joint dysfunction - Frequently followed by an inciting event 1-2 days before pain

Answer 6

- Early mobilization, PT, core stability, adjustment/manipulation, massage - Pain management: NSAIDs, steroids, narcotics, muscle relaxants, Ice/heat/E stim - Change lifestyle and improve fitness to actually improve LBP long term

Answer 7

- Gradual narrowing of spinal canal and/or neural foramina | - Osteophyte formation, facet hypertrophy, bulging disks, hypertrophy of ligamentum flavum

Answer 8

- may have numbness, tingling, foot drop (esp. when standing) - may manifest as hip, knee, ankle or foot pain exclusively - imaging will reveal a narrowing of spinal canal

Answer 9

- PT - Medications: corticosteroids, NSAIDs, narcotics - Dorsal column stimulators (implanted device) - Surgery

Answer 10

Spondylolithesis is a forward slipping of one vertebrae on another, usually due to bilateral pars interarticularis defect on the vertebral spinous process

Answer 11

- often asymptomatic unless after deconditioning + new activity - may have radicular symptoms with nerve root irritation

Answer 12

- Non-operative: pain medication, PT/activity, TENS/stimulator - Surgical: for patients with progressive slips, uncontrolled pain

Answer 13

- LBP, radicular symptoms (sciatica), identifiable precipitant, numbness/tingling, motor symptoms (e.g. foot drop) - Physical exam findings: splinting, +/- tenderness, positive straight leg raise

Answer 14

- Active rest, oral steroids, pain medication, +/- PT, time (takes 3-6 months to resolve) - Surgery o Indications: pain, lesion on MRI, radicular symptoms, motor weakness o Microdiscectomy o Fusion: remove disc, place bone between vertebral bodies -- lose motion, sets up for further injury elsewhere - 10 year follow up surgery vs non-surgical treatment shows no significant difference, but surgery is helpful in shorter term for many

Answer 15

- Sciatica involves the general compression or irritation of one the five spinal nerves forming the sciatic nerve - Caused by disc disease, spinal stenosis, piriformis or peripheral entrapment, neurogenic claudication, other

Answer 16

- Mechanical (less common than in adults) - Spondylolysis/Spondylolithesis (common in gymnasts -- hyperextension of back) - Disc disease - Tumor - Infection - Rheumatologic - Visceral - Psychosomatic

Answer 17

Tests disc herniation (when positive, a disc is herniated)

Answer 18

This test puts stress on the pars interarticularis which is fractured in Spondylolysis; positive test would indicate a patient has Spondylolysis

Answer 19

- Shows active areas of growth in bones, esp. growth plates - If other areas of bone have intense areas of black that are not growth plates, this indicates the presence of a stress fracture

Answer 20

- It occurs when the pars interarticularis is fractured which typically results in L5 - Scottie Dog collar

Answer 21

- Activity modification, time, bone stimulator - Rarely use bracing anymore - Surgery is possible -- activity modification is usually sufficient

Answer 22

- Striated - Voluntary - Multinucleated with nuclei at cell periphery - Well-developed sarcoplasmic reticulum with T-tubule system located at A-I junction o Triads = T-tubule + 2 terminal cisternae

Answer 23

- Striated - INvoluntary - Sarcoplasmic reticulum less developed and T-tubule system is wider in diameter in comparison to skeletal muscle o T-tubules located at Z-disks o Diads = T-tubule + 1 terminal portion of sarcoplasmic reticulum - single nucleus/cell located in the center of the cell - Intercalated disks present; sometimes don't stain - Presence of atrial granules specific to atrial cardiac muscle cells -- contain atrial natriuretic peptide

Answer 24

- NO striations - NO t-tubules; instead have caveolae that store/release Ca2+ - INvoluntary - fusiform in shape - external lamina formed by reticular fibers and are involved in harnessing the force of contraction - Dense bodies attach actin and myosin not arranged in any precise order - Ca2+ - calmodulin complex activates myosin light chain kinase to phosphorylate the light chains on the myosin heads; this exposes the 'actin-binding' sites on myosin head

Answer 25

single muscle cell; composed of multiple myofibrils

Answer 26

composed of myofilaments; tiny, cylindrical rods within the sarcoplasm of muscle cells

Answer 27

components of myofibrils; actin (thin) and myosin (thick) filaments, associated proteins

Answer 28

G-actin that dimerizes to form F-actin; F-actin becomes helically wound in strands; bound to Z-disk by (α-actinin) and extends to H-band

Answer 29

composed of 4 light chains and 2 heavy chains and into heavy and light meromyosin; the heavy chains are polarized towards Z-disk

Answer 30

Troponin is a complex with three different subunits: TnT, TnC, TnI o TnT: binds troponin complex to tropomyosin o TnC: has great affinity for Ca2+ o TnI: binds troponin complex to actin; prevents actin-myosin interactions

Answer 31

anchors actin filaments to Z-disk and holds the actin filaments in parallel array

Answer 32

part of sarcoplasmic reticulum and is responsible for storage/release of Ca2+ o Skeletal muscle – located at A-I junction o Cardiac muscle – located at Z-disk

Answer 33

long, non-elastic protein that wraps around actin filaments and helps anchor them to the Z-disk; regulates the length the actin filaments achieve

Answer 34

large, elastic protein that position myosin filaments precisely within the sarcomere; acts like a spring

Answer 35

small vesicles that store/release Ca2+ in smooth muscle; equivalent to T-tubules in skeletal/cardiac muscle

Answer 36

found in smooth muscle scattered throughout the sarcoplasm and underneath the sarcolemma; serve as Z-disks in smooth muscles and anchor actin filaments and intermediate filaments

Answer 37

ONE motor neuron and ALL the muscle fibers it innervates o smaller the ratio of motor neurons to number of muscle fibers results in finer muscle control - i.e. 1:1 = very fine control; 1:1600 = very coarse control

Answer 38

o A band remains constant o I-band becomes smaller; may disappear as muscle shortens o Z-disks come closer together (sarcomere shortens!) o H-band narrows and eventually is not seen

Answer 39

- consist of small specialized muscle fibers enclosed in two CT capsules: internal and external - central intrafusal cells contain nuclei with different arrangements: • nuclear bag fibers = nuclei mixed around • nuclear chain fibers = nuclei in a straight line - fusiform shaped (bigger in the middle, tapered towards ends)

Answer 40

- Act as miniature strain gauges - Sensory: • annulospiral/primary endings – located around mid-portions of nuclear bag and chain fibers; large diameter • flower spray/secondary endings – around the distant regions from the mid-region; smaller diameter - Motor: • efferent fibers form motor end plates on either side of mid-region of intrafusal fibers

Answer 41

o Structure: spindle shaped bodies, enclosed by a thin capsule o Function: have afferent fibers (Ib) that penetrate between collagen fibers and are sensitive to stretching forces on muscle tendons • prevents over-contraction of muscle

Answer 42

- Structure: • non-myelinated axon terminal branches occupy recesses in surface of muscle fiber; these recesses are called synaptic troughs/primary synaptic clefts • In the muscle, the subneural apparati/secondary synaptic clefts are made by infolding of the sarcolemma and have ACh receptors (aka nicotinic receptors) that react to ACh from the axon terminal • ACh was released via synaptic vesicle fusion with the axon terminus - Function: nerve impulse conduction to muscle to elicit an action

Answer 43

- "Leak" channels - Voltage gated channels: o Na+: activation voltage must be ~ -40mV; activating o K+: activation voltage ~ -20 to 0 mV; NOT inactivating - Selective/non-selective channels

Answer 44

- RMP = -70mV to relative to outside - Graded potentials: vary in amplitudes due to strength of stimulus (may be depolarizing (EPSP) or hyperpolarizing (IPSP)); bidirectional - Action potentials: "all or none" - amplitude independent of initiating event; starts with depolarization and ends with repolarization/hyperpolarization

Answer 45

- Length constants are determined by membrane resistance and axial resistance o membrane resistance: amount of channels open/closed -- closed channels = greater resistance, greater length constant o axial resistance: > diameter of axon results in decreased resistance, ions flow further, increased length constant - It can transmits potential changes over long distances - when the amplitude has decayed away to a particular height - 37% of original amplitude

Answer 46

- Different stages: • #0: RMP • #1: EPSP sufficient to reach #2 • #2: Action potential threshold: change from graded potential to AP • #3: "Rising phase" • #4: Peak (usually between 0 and +40mV) • #5: Falling phase - rapid repolarization (Vm > RMP) • #6: Afterhyperpolarization (Vm < RMP) • #7 Repolarization to RMP - Actions of channels during stages: • #0: primarily K+ leak channels are open; some Na+ leak open • #1: ligand gated and non-selective cation channels open • #2: VG Na+ activated and open • #3: VG Na+ channels open, some K+ channels open around 0mV • #4/5: DR K+ channels open, VG Na+ become deinactivated (closed) below -40mV • #6: DR K+ channels overshoot • #7: VG K+ channels close

Answer 47

- Hyperkalemia is a condition where there is persistent depolarization of a neuronal membrane - Caused by increased extracellular [K+] which causes depolarization of Vm. Thus VG Na+ channels cannot become deinactivated (closed) and are unable to generate APs resulting in no heart beat.

Answer 48

increase conduction velocity = increase in axon diameter Conduction velocity depends on spacing of VG channels - myelinated fibers > unmyelinated fibers

Answer 49

- Myelinated fibers = motor neurons | - Unmyelinated fibers = sensory neurons (esp. pain)

Answer 50

- Electrial - passage of graded potential from one cell to another; passive - Chemical - active process, involves diffusion

Answer 51

- NT release - Receptor activation - NT inactivation

Answer 52

- Depolarize terminal membrane - Activation of VG Ca++ channels - Ca2+ entry - Change in conformation of docking proteins - Fusion of vesicles to plasma membrane

Answer 53

- It is an autoimmune disease in which peripheral VG Ca2+ channels are attacked which causes a decrease in Ca2+ triggered by NT release. - Manifests as muscle weakness that goes away with repeated contraction. - Treated with Diaminopyridine (DAP), a K+ channel blocker which prolongs APs in the presynaptic nerve by increasing the amount of Ca2+ that enters the cell

Answer 54

- Botox toxin: destroys docking proteins in cholinergic nerves which results in decreased muscle contraction - Tetanus toxin: is transported across the synapse in a retrograde manner and results in decreased transmission and increased muscle contraction

Answer 55

In general, all axonal branches of a neuron release the same neurotransmitter substance or substances from each nerve terminal . - Applies only to axons, as dendrites can release different NTs than their associated axon terminal - Primary NTs have associated neuromodulator peptides that influence the action of the primary NT

Answer 56

- nAChR - AMPA - NMDA - 5HT3 - P2X (NT = ATP, involved in fast nociception) - GABA (IPSP) - Glycine (IPSP)

Answer 57

- Agonist = ACh - 5 subunits with 2 binding sites for ACh, which cause the channel to open - Non-selective cation channel - permits K+, Na+, and Ca2+ to enter o Na+ has the largest driving force at RMP (furthest from Erev of Na+) o As depolarization continues, the driving force for Na+ decreases and the driving force for K+ increases (causes K+ to leave the cell)

Answer 58

Myasthenia Gravis is an autoimmune disease in which antibodies attack the nicotinic ACh receptor (nAChR) which causes rapid muscle fatigue and muscles that cannot sustain a muscle contraction. - Treatment involves preventing ACh degradation (aka AChE inhibitors) -- allows the amount of ACh that is available to work on the rest of the available receptors

Answer 59

- AMPA: excitatory neurotransmitter in brain | - NMDA: receptor for learning and memory

Answer 60

- It is a non-selective cation channel - Once glutamate binds, the channel opens; thus it is ligand gated - Opens/closes quickly due to desensitzation

Answer 61

- Both voltage regulated and ligand gated!!!!! -- very unique to these receptors!! involved in memory and learning - Structure: binding sites for glutamate and an Mg2+ block within channel - Upon depolarization, the Mg2+ block is pushed away, glutamate is able to bind (released previously from presynaptic cell upon depolarization), the NMDA channel opens o Na+ keeps the NMDA channel open (positive feedback loop) o Ca2+ induces Ca2+ release which changes the function of the channel and leads to long-term potentiation and long-term changes in gene expression

Answer 62

- Ligand gated - Predominant inhibitory receptor in the brain (spinal cord uses glycine) - It is a Cl- channel that elicits an IPSP upon influx of Cl- - IPSP occurs only if cell is depolarized above Erev of Cl- (-61mV) - If cell is hyperpolarized, then Cl- leaves the cell and causes the membrane to become depolarized o Net effect: stabilizes membrane potential around -61mV - Many drugs take action on the GABA receptor: barbituates, benzodiazapenes, ethanol (general anesthetics), etc.

Answer 63

- Diffusion (NTs diffuse out of synaptic cleft) - Enzymatic degradation (i.e. AChE action on ACh) - Reuptake (i.e. Monoamines, such as serotonin, are taken back up in the presynaptic cell terminus)

Answer 64

- Monoamines: dopamine, norepinephrine, serotonin - Terminated by reuptake o Drug targets: • tricyclic antidepressants: block reuptake of NE and serotonin • cocaine and amphetamine: block all three monoamines from reuptake • Specific Serotonin Reuptake Inhibitors (SSRIs): block serotonin (5HT) reuptake; used to treat depression

Answer 65

- Motor neuron axon terminal, at NMJ, becomes depolarized due to saltatory conduction vis VG Na+ channels along axon - VG Ca2+ channels open upon depolarization reaching the axon terminus and cause an influx of Ca2+ - The influx of Ca2+ in the presynaptic cell causes the synaptic vesicles to bind to the presynaptic end plate and exocytose their contents (ACh) into the synaptic cleft - ACh diffuses passively across the synaptic cleft and binds to the nAChR on the muscle end plate, resulting in the opening of the nAChR as a Na+ channel (lidocaine blocks these Na+ channels) - Na+ entry causes depolarization of the muscle endplate to occur; if depolarization is great enough this will propagate an AP throughout the muscle - The AP in skeletal muscle results in opening of VG Ca2+ channels (aka L channels) which are physically coupled to Ca2+ release channels (aka ryanodine receptors) - Ryanodine (and caffeine) bind to these ryanodine receptors and cause the release of Ca2+ intracellularly within the muscle o Note: intracellular [Ca2+] > 10^-6 induce muscle contraction - Ca2+ binds to troponin C (TnC) - this initiates muscle contraction

Answer 66

i. Motor neurons releasing acetylcholine ii. Acetylcholine interactions with skeletal muscle nicotinic receptors to: • Increase sodium permeability and depolarize skeletal muscle • Skeletal muscle depolarization causes activation of L calcium channels (dihydropyridine receptors) iii. Calcium entry into muscle releases calcium from intracellular storage sites (sarcoplasmic reticulum) via calcium-induced calcium release (ryanodine receptors – Ry1) iv. Elevated intracellular calcium concentrations result in calcium binding to troponin C v. Calcium binding to troponin C releases inhibition of actin-myosin interactions vi. Myosin heads then contact actin to create muscle shortening and force generation, provided energy in the form of ATP is present