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Unit 8 > Biomed Review > Flashcards

Biomed Review Flashcards

1
Q

What are the relationships between R(input), size of the neuron, and activation potential? In general, what is this relationship called?

A

Membrane resistance is determined by the number of ion channels. (Think: how many doors.) Resistance to activation is dependent on the SA of the cell. (Think: how long is the hallway of doors??) Smaller neurons: smaller surface area: R(input) is HIGHER. *Think: fills up really easily bc only a few doors and less room. Larger neurons: greater surface area: R(input) is LOWER. *Think: takes a while to fill up bc lots of doors and lots of room. SO: 1) smaller neurons are activated before larger. 2) it takes more time for larger motor neurons to be recruited. *This is called the SIZE principle*

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2
Q

Describe systematic recruitment.

A

Smaller motor units = smaller/slower force. Larger motor units = larger/faster force.

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3
Q

How is volitional activation defined? What is failure and why does it occur?

A

Volitional activation is the interaction bw the CNS and the peripheral CNS. Failure = muscle weakness/inability to generate F from a CNS impairment (SO, there is an impairment of the ability to activated LMNs). This occurs either because 1) incomplete motor unit recruitment (the signal isn’t strong enough) or 2) suboptimal discharge rate of motor units. (the signal isn’t firing fast enough).

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4
Q

What are the potential physiological causes of volitional activation deficits vs. clinically?

A

Physiological: 1. Impaired or altered inputs in the motor neuron from descending pathways 2. Afferent inputs from the sensory receptors 3. Segmental influences Clinically: 1. Pain - impact afferent input to dampen signals. 2. Fear of pain - CNS! 3. CVA - lack of input from CNS 4. SCI/MS - fibers unable to convey info/inputs to muscles 5. Stenosis - narrowing 6. Motivation

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5
Q

Why is it important to record maximum muscle force?

A
  1. To ID CNS deficits 2. Measure progress 3. Insurance 4. Compare sides
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6
Q

How does the NS solve the degrees of freedom problem caused by muscles and joints?

A

Muscle synergies!

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7
Q

____________ muscle can be part of _________ synergies. _______ synergy can activated __________ muscles.

A

One, multiple. One, multiple.

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8
Q

Synergies are observed what types of movements?

A

Voluntary AND reactive (involuntary).

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9
Q

Name 4 ways articular cartilage can get injured.

A
  1. Direct blunt trauma. 2. Indirect blunt trauma. 3. Torsional loading. 4. Loading that occurs too rapidly.
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10
Q

What is the potential for articular cartilage healing? What factors contribute to this?

A
  1. Avascularity 2. Immobility of chondrocytes. 3. Limited proliferation of chondrocytes. 4. No perichondrium.
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11
Q

What are the 4 key aspects for PTs to be mindful of in articular cartilage healing?

A
  1. Allow for healing. 2. Protect the matrix (don’t WB too early). 3. Avoid shear and compressive forces. 4. Minimize impairments. *also possibly -> know what the surgery is and load usually in a range that is acceptable, i.e. stay out of 30-75 - this is when the surface is used most often.
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12
Q

Name the 4 phases of cartilage maturation and rehab considerations for each.

A
  1. Proliferation: limited joint loading 2. Transition: reload the joint 3. Remodeling: progress to functional activities 4. Maturation: return to full activity.
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13
Q

What ROM do you want to stay out of for most articular cartilage injuries?

A

30-70 degrees of knee flexion.

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14
Q

Where is patellar femoral stress most in OKC vs. CKC activity?

A

In OKC, from 45-90 knee flexion contact is most. In CKC, from 0-45 knee flexion contact is most.

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15
Q

What are the two methods commonly used for progressing a patient program and what factors go into deciding when to progress?

A

Time-based progression vs. criterion-based (time since injury determines progression vs. PROM/strength/effusion/pain+activity tolerance)

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16
Q

What are the 4 main ligaments of the knee? And what are the main functions of each ligament? What does this have to do with the healing of each?

A

ACL - resists anterior tibial translation PCL - resists posterior tibial translation MCL - resists valgus LCL - resists varus ACL and PCL are intra-articular MCL and LCL are extra-articular The ACL and PCL take the longest to repair because they are intra-articular and this means that when exposed to synovial fluid (due to injury) tissue will undergo phagocytosis. The MCL and LCL will take the least longest to repair (MCL least longest) because they have good access to blood supply.

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17
Q

What are the three general functions of ligaments?

A
  1. Guide motion 2. Provide sensory feedback 3. Provide stability (bc they are taut at end range)
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18
Q

MCL: 1. Resists what stress? 2. History and MOI? 3. Symptoms? 4. Clinical signs?

A
  1. Valgus 2. Lateral trauma 3. Audible Pop 4. Palpation, Observe Swelling, Valgus Stress Test (know end feels)
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19
Q

What is the general timeline for healing for MCL tears/grades?

A

Grade 1: 10 days Grade 2: 2-3 weeks Grade 3: Non-surgical 1ish to 3 months depending upon healing. Non-surgical then surgical always.

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20
Q

What are the suggested return to play criteria for an MCL injury?

A
  1. Full ROM 2. No instability 3. No tenderness to palpation. 4. No effusion. 5. Quad muscle strength = 85% of contralateral side 6. Hop test = 85% of contralateral side
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21
Q

LCL: 1. Resists what stress? 2. History and MOI? 3. Clinical signs?

A
  1. Varus 2. Usually not isolated - instead, combo injury of PLC (posterolateral corner = LCL, popliteal tendon, popliteofibular ligament and the capsule +/- lateral gastroc) 3. Palpation, Pain, Swelling, Varus Test
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22
Q

What is the treatment for Grade 1 vs. 2 vs. 3 LCL tears?

A

Grade 1 and 2: typically treat non-surgically Grade 3: can sometimes be non-surgical (w/ 1-6 weeks to return due to other lateral support *also with grade 3: Potential for fibular head fx Potential for assoc. ACL tear or PCL tear

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23
Q

PCL: 1. Stress? 2. History and MOI? 3. Symptoms? 4. Clinical signs?

A
  1. Resists posterior tibial translation on femur. 2. MVA or falling on a plantar flexed knee 3. Does not always cause fx deficits and pain. 4. Effusion, posterior sag sign, posterior drawer test.
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24
Q

What is the typical treatment for grade 1 vs. grade 2 vs. grade 3 PCL injuries?

A

Grade 1 and 2 are non-surgical (require 3-4 months of healing, 100% QI, and firm end feel on exam) Grade 3 are usually non-surgical, then surgery. If surgery, knee passive flexion 0-90 in prone in 2-4 weeks, active hamstring exercise delayed (bc hamstrings will cause posterior translation of the tibia) until 12 weeks, QI needs to be 90%. *if just rehabbing no active HS until QI = 90% and all AP motion is in 0-90 of flexion in phase 1.

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25
Q

What stress does the ACL resist? What type of history/MOI do we see? Clinical signs?

A

Anterior tibial translation. Plant and cut (will usually hear a pop). If non-contact, an isolated tear. In females more than males. If contact, ACUTE = ACL/MCL/lateral meniscus, CHRONIC = ACL w/ medial meniscus Combined history, exam, lachman’s and anterior drawer have a +LR of 25

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26
Q

What is the criteria for determining ACL copers?

A

Screen: 44 hops, KOS ADL, and GROC Time hop and/or KOS would be greater than or equal to 80% Global Rating of Changing greater than or equal to 60% Not more than one incidence of giving from initial injury to time screening.

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27
Q

What are the two biggest rehab considerations following surgery?

A

A) Goals: full active/passive extension w/in 1-2 weeks, 90–100 degrees of flexion within first 2-3 weeks and full flexion by 6 weeks. B) Quad activation (assoc w/ fxal recovery).

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28
Q

To protect an ACL graft, what are the recommended exercise motion ranges in the acute stages of rehab?

A

Closed Chain, 0-60 degrees. Open Chain, 40-90 degrees.

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29
Q

What are some general rehab considerations in order to progress patients?

A

Tissue reactivity (swelling, pain) Impairment levels (active and passive ROM, strength) Functional level (gait, running, hop tests, self-report scores)

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30
Q

What are the main functions of the meniscus?

A

Force transmission: congruency between the femur and tibia leading to a decrease in point loading / shock absorption - bc composed of more elastic cartilage than articular cartilage. Stability.

31
Q

How does the central portion and peripheral portion of the meniscus different in terms of blood supply?

A

The peripheral portion has a much greater vascular supply: lateral = 10-25% vascular, medial = 20-30% more vascular. The central portion has no blood supply.

32
Q

What are some indications that a patient may need a meniscal repair?

A

Peripheral, longitudinal tears (bc these can actually heal!) Young patients (they will need their menisci longer). Vascular zone tears < or = 3mm W/ ACLr (you’re already in there, yo).

33
Q

Identify and explain 3 current articular cartilage management options.

A

MACI/ACI - send chondroblasts up to Boston and replace tissue. MACI is with porcine. OATS - a plug (can also be from a cadaver). Marrow Stimulation Techniques (Microfracture) - to stimulate healing/growth. Chondroplasty - smooth the surface.

34
Q

What is the difference between postural control, postural equilibrium, and postural orientation?

A

Postural Control = Balance (for stability and orientation) Postural Equilibrium = ability to control COM over BOS Postural Orientation = POSTURE, maintaining position of the body w/ reference to environment.

35
Q

What is the difference between postural control and automatic postural response?

A

Postural control is feedback or feedforward. Automatic postural response is a reactive mechanism (NOT A REFLEX) that’s driven by muscle synergies (ankle, hip, step strategies). The goal of these is to maintain the COM over the BOS.

36
Q

What is the ankle strategy?

A

You lean forward to turn on your plantarflexors and vice versa - this is usually in response to small perturbations.

37
Q

What is the hip strategy?

A

Proximal to distal - turn on muscles at the hip for larger loss of balance. Usually used when w/ a narrow BOS.

38
Q

What is a step strategy?

A

You will step in the direction of the perturbation. This can happen when the perturbation is especially large, when you are slow, or when other strategies aren’t working. The more steps you take the more unsteady you are.

39
Q

What is the typical ratio of our use of different systems for balance? What is specifically important with reference to the visual system?

A

Somatosensory (70%) Vision (10%) - this plays a greater role in anticipatory balance bc of slower neural conduction Vestibular (20%)

40
Q

What are the three main sensory fix of the vestibular system?

A

Sensation and perception of body position and self-motion. Orients head and body to vertical. Gaze stabilization.

41
Q

What are the 2 main motor functions of the vestibular system?

A

Stabilizes the head during postural movements. Controls position of body’s COM.

42
Q

What are the components of the peripheral sensory apparatus? What does it send info about?

A

Bony and membranous labyrinth Acceleration and orientation of head w/ respect to gravity

43
Q

What is the function of the hair cells?

A

Move w/ fluid - they depolarize or hyperpolarize to provide spatial info. They convert mechanical stimuli into neural firing.

44
Q

What direction do the hair cells deflect to create a depolarization in the otoliths?

A

They move toward the kinocilium (the long one).

45
Q

What type of motion do the otoliths detect? What type of motion do the semicircular canals detect?

A

linear acceleration/static tilt (saccule = vertical, utricle = horizontal) SSC = rotational acceleration / angular motion

46
Q

Describe the push pull mechanism of the SCC.

A

This refers to the fact that head movement will excite one set and inhibit the other.

47
Q

True or False: the otoliths and SCC can only work independent of each other.

A

False. Movement is a combination of input from both!

48
Q

What portion of the brainstem does the vestibular nerve enter?

A

Enters at the pontomedullary junction.

49
Q

What are the 2 main targets of the vestibular nerve?

A

Vestibular nuclear complex and the cerebellum.

50
Q

Name the 3 vestibular reflexes and what they do.

A

Vestibular-ocular: maintains stable vision during head motion and generates eye movements. This is the reading the chart example. Vestibulospinal: maintains head/postural stability, adjusts limb and head on body position and generates compensatory body movements. (Spinning in a chair is VOR, VSR) Vestibulocolic activates neck musculature to stabilize head relative to space: just your neck!

51
Q

How is nystagmus named?

A

Named for the direction of the fast phase.

52
Q

What are the 2 phases of optokinetic nystagmus?

A

Initial slow phase in the direction of the stimulus (smooth pursuit) and followed by a fast phase (corrective saccade).

53
Q

When doing caloric testing how does one determine the direction of the nystagmus?

A

COWS - cold, opposite / warm, same. So, if cold water poured in the left ear, you will get right nystagmus and nauseous. This response is normal.

54
Q

Name some ways (4) the vestibular system has influence within the spinal cord.

A
  1. Activation of anti-gravity muscles. 2. Triggers postural responses. 3. Aids selection of response to environment. 4. Coordinates head/trunk movement.
55
Q

Where is arthrogenic muscle inhibition or arthrogenic muscle response? (AMR)

A

Continuing reflex rxn of the muscles surrounding a joint after distension or damage to the structures of the joint. LOSS OF FEEDBACK FROM MECHANORECEPTORS is thought to be the main mechanism of this.

56
Q

What are the main fxns of skin?

A

Protection Temp Regulation Sensation Metabolism (VitD) Communication and Identity

57
Q

What are the primary anatomical layers of the skin and what are their functions?

A

Epidermis - provides surface protection Dermis - tensile strength, house appendages (glands, hair follicles) Subcutaneous Tissue - provide cushioning

58
Q

What are the two fxns of sebaceous glands?

A

Secrete sebum to lubricate skin. Create an acid mantle to prevent infex.

59
Q

What are the for characteristics of aging skin?

A

Tissue layers become thinner. Dermal-epidermal bond becomes more fragile. Decrease in the quantity of dermal cells, appendages, blood vessels, and nerve endings. Decreased elastin.

60
Q

What is the difference full and partial thickness tissue loss? How does the healing differ?

A

Full vs. Partial: injury through both epidermis and dermis for full vs. partial = only epidermis. Full vs. Partial: healing happens (scar formation) through primary/secondary/or delayed primary intention vs. regeneration of epithelium so NO scar formation.

61
Q

How does scar tissue differ from skin?

A

Collagen fibers have less tensile strength so the skin is less elastic. No elastic fibers = no elastic recoil. No dermal appendages = no lubrication.

62
Q

What are the phases of wound healing? Provide details of each.

A

Inflammation: lasts for 0-6 days, may be longer. Looks painful, red, hot, swollen. Hemostasis. Clean-up. Trigger repair. Proliferation: Day 4-14. Granulation tissue (#beef) + epithelial cells around the edges. Neovascularization/granulation/contraction/epithelialization Maturation: Day 8 - yr., wound closed + pink scar. Collagen maturation and reorganization. Reduction in vascularity (pink -> white). Maturation depends on mechanical stress.

63
Q

What is the role of each cell type: neutrophil, macrophage, lymphocytes?

A

Neutrophils: kill microbes, release cytokines. Macrophages: remove debris, secrete growth factors > start repair. Lymphocytes: bring inflammation down, promote granulation.

64
Q

What three general factors delay wound healing/influence the formation of a chronic wound? Give examples of each.

A

Systemic: Stress, nutrition/obesity, temp, comorbidities Iatrogenic: medications, topical agents, trauma as a result of bad treatment Local

65
Q

What are four signs of infex?

A

Induration (hard swelling) Fever (local or systemic) Erythema (redness; irregular borders) Edema

66
Q

What are three potential complications that can occur during the healing process?

A

Dehiscence Excessive Scarring Arthrofibrosis

67
Q

Name the 3 types of cartilage.

A

Elastic Hyaline (this will include articular cartilage) Fibrocartilage

68
Q

What is the role of GAGs in the ECM?

A

Increasing comprehensive stiffness (they are negatively charged and attract water).

69
Q

What collagen type if most common in cartilage?

A

Type II

70
Q

Based on the material properties of articular cartilage, what happens if you load it quickly vs. slowly?

A

Biphasic nature: loading quickly = water doesn’t move in any way, loading slowly = water diffuses.

71
Q

What type of cartilage is this?

What fiber has the highest concentration in this type of cartilage?

What type of stresses is this cartilage good at resisting?

Where would you find it in the body?

A

Fibrocartilage

Type I collagen bundles in line with the direction of stress.

Resists compression and shear forces.

Menisci, IV discs, pubic symphysis, GH joint

72
Q

What type of cartilage is this?

What fibers have a high presence in its ECM?

Where would you find it in the body?

A

Elastic cartilage

High presence of elastin fibers and type II collagen (50/50 split)

External pinna of the ear, epiglottis

73
Q

What type of cartilage is this?

What does this cartilage type have a high concentration of?

What type of stresses does this cartilage resist?

Name a specific type of this cartilage that we as PTs are most concerned about.

How does this cartilage get its nutrition?

A

Hyaline

GAGs

Compression

Articular

Via compression and release - needs to be loaded or it will degraded.

Unit 8 (2 decks)

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