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MSS Gun Show > Lower body > Flashcards

Lower body Flashcards

1
Q

Sartorius

Origin

Insertion

Nerve Innervation

Action

A

ASIS

medial tibia (superior)

Femoral n.

Flexes and laterally rotates thigh and flexes leg

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2
Q

Rectus Femoris

Origin

Insertion

Nerve Innervation

Action

A

AIIS

tibial tuberosity (via quadriceps ligament)

Femoral n.

Flexes thigh and extends leg

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3
Q

Vastus Medialis

Origin

Insertion

Nerve Innervation

Action

A

Postero-medial femoral shaft including linea aspera

Tibial tuberosity (via quadriceps ligament)

Femoral n.

Extends legs

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4
Q

Vastus Lateralis

Origin (2)

Insertion

Nerve Innervation

Action

A

Postero-lateral femoral shaft including linea aspera and Greater Trochanter

Tibial tuberosity (via quadriceps ligament)

Femoral n.

Extend legs

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5
Q

Vastus Intermedius

Origin

Insertion

Nerve

Innervation

Action

A

Anterior and lateral femoral shaft

Tibial tuberosity (via quadriceps ligament)

Femoral n.

Extend legs

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6
Q

Iliopsoas

Origin

Insertion

Nerve

Innervation Action (2)

A

Iliacus - iliac fossa

Psoas major - lumbar transverse processes

Lesser trochanter

Iliacus - femoral n.

Psoas major - Lumbar ventral rami

Flexes thigh; stabilizes hip joint

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7
Q

Adductor longus

Origin

Insertion

Nerve Innervation

Action

A

Pubis

Mid-third post. femur

obturator n.

adducts thigh

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8
Q

Adductor magnus

Origin (2)

Insertion

Nerve Innervation (2)

Action (3)

A

Ischiopubic ramus and ischial tuberosity

Posterior femur

obturator n./sciatic n.

Adducts thigh Upper fibers flex thigh Lower fibers extend thigh

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9
Q

Pectineus

Origin

Insertion

Nerve Innervation (2)

Action (3)

A

Superior pubic ramus (pectin)

Proximal femur, inferior to lesser trochanter

Femoral n./ Obturator n.

Adducts thigh Flexes thigh assists in medial rotation of thigh

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10
Q

Gracilis

Origin

Insertion

Nerve

Innervation

Action (2)

A

Pubis

Superior part of medial tibia

Obturator n.

Adducts thigh; flexes leg

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11
Q

What are the boundaries of the femoral triangle?

Superior?

Lateral?

Medial?

Floor (2)? Roof?

A
  1. Superior - inguinal ligament
  2. Lateral - sartorius muscle
  3. Medial - adductor longus muscle
  4. floor - pectineus, iliopsoas
  5. roof - fascia lata (deep fascia)
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12
Q

What is found in the femoral sheath?

A

glides vessels during hip movement

Compartments:

lateral - femoral a.

intermediate - v

medial - Femoral Canal

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13
Q

Where is the site of femoral hernia’s ?

A

femoral ring —> plug of femoral canal (lymphatics)

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14
Q

What arteries form the ‘cruciate anastomosis of the thigh’?

A

medial and lateral circumflex femoral a. + inferior gluteal a.

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15
Q

What muscles does the femoral nerve supply?

A

all ant. thigh muscles + iliacus

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16
Q

what nerve supplies the skin of the lateral thigh?

A

lateral femoral cutaneous n.

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17
Q

what is essentially the tendon for TFL muscle? what does it attach to?

A

fascia lata –> iliotibial tract (laterally) –> Gerdy’s tubercle

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18
Q

What is synovial joint articular cartilage lacking so that it can ‘glide smoothly’?

What creates the ‘shock absorption’ capabilities of the synovial joint?

A

no perichondrium on articular surface

aggrecan aggregate –> attract H20

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19
Q

What are the contents of synovial fluid?

A

Hylauronan - retains H20

lubricin - coats cartilage nutrients that support chondrocytes

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20
Q

What secretes synovial fluid?

What is the surface layer of Synovium composed of?

A

Synovium Synoviocytes –> Macrophage-like cells (inflammation) and Fibroblast-like cells (hyaluronan)

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21
Q

Why is synovial tissue susceptible to infection?

A

Synoviocytes: no tight junctions no basal lamina

Easier for blood-borne microorganisms from the vasculature underlying the synovium to invade the joint space –> inflammation –> infectious arthritis

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22
Q

interstitial growth

A

chondrocytes –> isogenous groups growth from within

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23
Q

appositional growth

A

chondroblasts –> perichondrium growth from edges

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24
Q

Collagen type of cartilage

A

Type II

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25
Q

What growth factor stimulates osteoprogenitor cells to turn to osteoblasts?

A

Osteoclast activity leads to –> GF release acting on Osteoblasts - Bone Morphogenic Proteins (BMPs)/TGF-Beta

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26
Q

What 3 molecules do osteoblasts produce that play a role in osteoclastogenesis ?

A

M-CSF (macrophage colony - stimulating factor)

RANKL (RANK Ligand)

OPG (osteoprotegrin)

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27
Q

What does M-CSF do?

A

enables osteoclast precursor cells to survive and proliferate

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28
Q

What does RANKL do? where are the receptors found?

A

RANK receptor found on osteoclast precursor cells and RANKL is found on osteoblasts and bone marrow stromal cells.

Binding of both leads to differentiation into a mature osteoclast

RANKL promotes bone resorption

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29
Q

What does OPG do?

A

secreted by osteoblasts and binds to RANKL, preventing RANK binding inhibits bone resorption and indirectly promotes bone formation

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30
Q

What does estrogen do in bone growth?

A

suppresses activity of osteoclasts by acting on OPG –> inhibiting RANKL (osteoblast)

Menopause –> Less OPG –> Less RANKL inhibition –> Greater osteoclast activity

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31
Q

What is used as a serum marker for osteoclast activity?

A

TRAP Tartate-resistant acid phosphatase

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32
Q

What is osteoid?

A

substance secreted by osteoblasts:

ORGANIC

type I collagen

osteopontin

osteonectin

osteocalcin

INORGANIC

hydroxyapatite

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33
Q

Process of endochondral ossification

A
  1. cartilage template during development
  2. Chondrocytes die (no nutrients)
  3. Blood vessels proliferate (bring in osteoblasts/-clasts)
  4. Osteoclasts remove calcified cartilage, osteoblasts deposit bone
  5. Longitudinal growth occurs by replacement of cartilage w/ bone in ordered sequence
  6. secondary ossification center occurs in the ends of long bones; cartilage remains b/w the 2 ossification centers (epiphyseal plate)
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34
Q

What are the 2 classifications of fractures?

What is the difference b/w them?

A

Traumatic and Pathologic Fractures

Traumatic - car accident

Patho - osteoporosis, paget’s disease, osteomyelitis, etc…

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35
Q

What are the essential features that should be included in the description of a fracture?

A

affected bone (femur, radius)

location in bone (epiphsysis, metaphysis)

involvement of articular surface fracture pattern (is there comminution (>3 pieces))

open or closed fracture

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36
Q

What are the reasons to stabilize fractures? (4)

A
  1. reduce pain
  2. facilitate healing
  3. improve function
  4. to enable immediate mobilization of a patient
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37
Q

What are the two types of fracture healing?

A

Primary: ‘intramembranous ossification” relies on RIGID fracture fixation in anatomical alignment

Secondary: “en(do)chondral ossification” is enhanced by motion

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38
Q

What are the 3 phases of fracture healing? (3 R’s)

A

REACTIVE phase: clot –> interleukins/GF’s –> stem cell proliferation –> turn into fibrous, cartilage, bone cells, endothelial cells (angiogenesis–> granulation tissue –> replaces clot)

REPARATIVE phase: cartilage forms (9 days) –> cells proliferate/hypertrophy –> enchondral ossification

REMODELING: couples bone resorption and formation

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39
Q

What are common complications of fracture healing?

What are their causes?

A

Infections, stiffness/pain, growth abnormalities.

Malunion, delayed union, nonunion –> bad blood supply (diabetes, smoking, inadequate fixation of the fracture)

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40
Q

What is osteoporosis?

A

skeletal disorder characterized by compromised bone strength predisposing a person to increased risk of fracture

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41
Q

Clinical characteristics of people with osteoporosis?

What are risk factors?

A

Elderly; female –> Back pain (vertebral fractures)

broken bones

Low bone density (-2.5 T score); trabeculae are thin, have lost connections; porous

Risk factors:

post-menopausal

Ca2+, protein, Vit D,C,K deficiencies metabolic problems ( diabetes, hyperthyroidism, COPD, chronic glucocorticoid use, anti-convulsants)

Lifestyle (alcohol, eating disorders)

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42
Q

How do I diagnose osteoporosis vs. osteopenia?

A

osteopenia: 1 - 2.5 standard deviations from young adult mean DXA
osteoporosis: > 2.5 standard deviations from young adult mean DXA

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43
Q

How do you manage a patient with osteoporosis?

A

Nutrition: add Ca2+/Vit D

Exercise: Stop being a pussy and lift weights

Safety: walkers, canes

Meds: antiresorptive agents

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44
Q

Drug used to treat osteoporosis that acts as an anabolic agent; mimics the effects of PTH

What are you at risk for if you use it long-term?

A

Teriparatide Recombinant form of PTH…binds to PTH receptors on osteoblasts to stimulate RANKL release

Osteosarcoma

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45
Q

What vitamin increases the GI absorption of calcium and phosphate; decreases renal excretion?

Aids in bone building?

Side-effects? Think physiology

A

Vitamin D3

Hypercalcemia

Hyperphosphatemia

Hypercalciuria

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46
Q

What osteoporosis drug acts as a monoclonal Antibody to RANKL?

What would this do? One side-effect?

A

Denosumab Inhibit RANKL —> Inhibit osteoclast maturation –> decrease in osteoclasts

Respiratory/Urinary tract infections

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47
Q

What drug acts as a selective estrogen receptor modulator?

What is the physiology behind this?

side-effects? (Think physiology)

A

Raloxifene

Estrogen receptor agonist –> enhances osteoblast activity

endometrial cancer, hot flashes

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48
Q

How do biphosphonates work to treat osteoporosis?

name 2 biphosphonates

A

works as a pyrophosphate that lines the bones and is absorbed by the osteoclast –> blocks enzyme for cholesterol synthesis –> kills osteoclast

Alendronate

Zolendronic acid

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49
Q

Most common organism that causes bacterial osteomyelitis

What area of the bone is usually most affected?

In IV drug abuse?

In neonates?

In sickle cell disease?

A

S. aureus

children - growth plate; adults - epiphysis

E. coli, Pseudomonas, Klebsiella - IV Drug abusers

H. infuienzae, group B strep - neonates

Salmonella - sickle cell disease

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50
Q

What is the pathophysiology of this disease?

What is the most common organism that causes this?

What 3 bugs lead to this in IV drug abusers? (EPK)

A

Bacterial osteomyelitis; s. aureus

Bone abscess –> travel thru haverian canal –> beneath periostium –> New bone forms (involucrum) over the dead bone (sequestrum)

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51
Q

What is the most common organism that causes Granulmatous osteomyelitis?

Where is this commonly found in the body?

Primary or Secondary seeding?

A

M. tuberculosis (in AZ: Coccidioides)

spine, knee, wrist

Secondary seeding from another source: usually from lungs

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52
Q
A

Granulomatous osteomyelitis of the spine

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53
Q

What is circled?

A

Granulomatous osteomyelitis (coccidiomycosis)

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54
Q

What bacterial organisms cause this in neonates?

A

H. influenzae, group B streptococci

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55
Q

In bacterial arthritis what is the most common location of infection?

What does the joint look like grossly?

What is the most common organism that causes infection?

What is the most common organism that causes infection in adolescents and young adults?

A

knee, hip, shoulder, elbow, wrist

Painful, “hot” swollen joint

  • s. aureus*
  • N. gonorrhoeae*
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56
Q

In bacterial arthritis what is the most common organism to cause it in IV drug abusers?

Neonates?

Sickle cell disease?

A
  • E. coli, Pseudomonas, Klebsiella -* IV drug abusers
  • H. influenzae* - neonates
  • Salmonella* - sickle cell disease
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57
Q

What organisms causes Granulomatous arthritis?

Location in the body?

A

M. tuberculosis, fungi (Coccidioides)

seeding from another source (lungs)

spine, knee, hip, ankle, wrist

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58
Q

What is this?

What is the pathophysiology?

Who is at risk? (water, black people, immunosuppressed, drunks)

A

Avascualr necrosis

loss of blood supply to femoral head –> necrosis of bone beneath articular cartilage –> leads to secondary collapse of bone (sudden exercise)

deep-sea diving, sickle cell disease, corticosteroid therapy, alcoholism

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59
Q

What is this?

What is the pathophysiology?

Who is at risk? (water, black people, immunosuppressed, drunks)

A

Avascualr necrosis

loss of blood supply to femoral head –> necrosis of bone beneath articular cartilage –> leads to secondary collapse of bone (sudden exercise)

deep-sea diving, sickle cell disease, corticosteroid therapy, alcoholism

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60
Q

How does chonic renal disease lead to fucked up mineral homeostasis and bone undermineralization?

What is this disease called?

What is the pathophysiology behing it?

A

Renal Osteodystrophy

  1. impaired kidney f(x) –> phosphate retention/Low conversion of Vit D –>
  2. hyperphosphatemia –> stimulates PTH secretion –>
  3. Low active Vit D –> decreased Ca2+ reabsorption –>
  4. hypocalcemia –> Greater PTH secretion –>
  5. Secondary hyperPTHism –> increased osteoclast activity
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61
Q

Disease?

Type of collagen disorder?

Too little or Too much bone made?

3 other abnormalities (think collagen)

A

Osteogenesis Imperfecta

Type I Collagen

Too little bone made (fragile)

blue sclera (choroid veins); hearing loss; abnormal teeth (dentin)

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62
Q

Disorder of abnormal bone remodeling

name?

What age/gender does it occur in?

pathophysiology?

Is it thin or thicker bone?

A

Paget Disease

Older Men

(early) excessive osteoclast activity –>
(middle) excessive osteoclast/osteoblast activity –>
(late) excessive osteoblast activity –>

Thick, heavy bone; more prone to fracture

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63
Q

What disease is this?

What are the lines pointing to?

A

Paget’s disease

cement lines w/ tiny cracks

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64
Q

Typical patient with Enchondroma and location in body?

is this benign or malignant?

A

Younger adults

small bones of hand and feet

benign - well circumscribed

histo looks like normal cartilage

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65
Q

What disease is this? age? is it benign or malignant?

A

Enchondroma

Younger adults

small bones of hand and feet

benign - well circumscribed

histo looks like normal cartilage

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66
Q

what disease is this?

what age does it occur in?

where in the body does it usually present?

A

osteoid osteoma

randomly arranged trabeculae of woven bone

femur and tibia

benign

teenagers

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67
Q

What disease is this?

Where does it occur?

What age?

A

Osteochondroma

starts with misaligned growth plate? (metaphysis)

long bones

teenagers

stops growing when growth plate closes (growth after –> malignant)

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68
Q
A

Osteochondroma

starts with misaligned growth plate? (metaphysis)

long bones

teenagers

stops growing when growth plate closes (growth after –> malignant)

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69
Q

Are most malignant tumors primary in children or formed from metastases?

A

children = primary

adults = metastases (lung, breast, kidney, prostate) –> axial skeleton

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70
Q

What disease is this?

Where does it occur?

age-range of people?

A

Osteosarcoma

Teenagers (Paget’s disease >60 years)

around the knee (distal femur, proximal tibia)

malignant osteoblasts forming osteoid (bone) matrix

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71
Q
A

Osteosarcoma

Teenagers (Paget’s disease >60 years)

around the knee (distal femur, proximal tibia)

malignant osteoblasts forming osteoid (bone) matrix

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72
Q
A

Osteosarcoma

Teenagers (Paget’s disease >60 years)

around the knee (distal femur, proximal tibia)

malignant osteoblasts forming osteoid (bone) matrix

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73
Q

What disease is this?

age-range?

frquent locations

A

Chondrosarcoma

old adults (> 40)

pelvis, ribs, proximal femur/humerus

bluish-white tissue; malignant cells produce chondroid matrix

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74
Q
A

Chondrosarcoma

old adults (> 40)

pelvis, ribs, proximal femur/humerus

bluish-white tissue; malignant cells produce chondroid matrix

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75
Q

What disease is this?

age?

location?

Orgin of cell tumor?

A

Giant cell tumor

Younger adults

around the knee (distal femur, proximal tibia

abundant multinucleated giant cells + mononuclear cells

osteoclast orgin

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76
Q
A

Giant cell tumor

Younger adults

around the knee (distal femur, proximal tibia

abundant multinucleated giant cells + mononuclear cells

osteoclast orgin

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77
Q

What disease is this?

age?

location?

orgin?

A

Ewing sarcoma

children

around the knee

malignant neoplasm of primitive mesenchymal cells

blue round cell tumor

Differential: other blue small cell tumors (lymphoma, neuroblastoma)

t(11:22)

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78
Q
A

Ewing sarcoma

children

around the knee

malignant neoplasm of primitive mesenchymal cells

blue round cell tumor

Differential: other blue small cell tumors (lymphoma, nuroblastoma)

t(11:22)

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79
Q

Gluteus maximus

orgin

insertion

innervation

action

A

post. ilium and sacrum

iliotibial tract; gluteal tuberosity

inferior gluteal nerve

extends thigh

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80
Q

Gluteus medius

orgin

insertion

innervation

action

A

post. ilium

greater trochanter

superior gluteal nerve

abducts and medially rotates femur; prevents pelvic drop on opposite side during swing phase of walking

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81
Q

Gluteus minimus

orgin

insertion

innervation

action

A

posterior ilium

greater trochanter

superior gluteal nerve

abducts and medially rotates femur; prevents pelvic drop on opposite leg during swing phase of walking

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82
Q

Tensor of fascia lata

orgin

insertion

innervation

action

A

ASIS

lateral proximal tibia via IT band

superior gluteal nerve

Abducts and medially rotates femur; stabalizes hip and knee joints during extension

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83
Q

Piriformis

orgin

insertion

innervation

action

A

anterior surface of sacrum

greater trochanter

ventral rami L5, S1, S2

laterally rotates extended thigh; abducts flexed thigh

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84
Q

semitendinosus

orgin

insertion

innervation

action

A

ischial tuberosity

medial surface of proximal tibia

sciatic nerve (tibial division)

extends thigh; flexes leg

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85
Q

Semimembranosus

orgin

insertion

innervation

action

A

ischial tuberosity

posteromedial surface of proximal tibia

sciatic nerve (tibial division)

extends thigh; flexes leg

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86
Q

Biceps femoris

orgin

insertion

action

innervation

A

long head –> ischial tuberosity (sciatic n. tibial division)

short head –> post. femur (common fibular division)

head of fibula

extends thigh; flexes leg

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87
Q

Plantaris

orgin

insertion

innervation

action

A

Posterolateral aspect of distal femur

achillis tendon - calcaneus

tibial n.

weak plantar flexor of foot

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88
Q

Popliteus

orgin

insertion

action

innervation

A

Lateral femoral condyle

posterior surface of proximal tibia

tibial nerve

unlocks the knee joint by laterally rotating femur on fixed tibia

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89
Q

What are the boundaries of the Popliteal fossa?

A
  1. superolateral = biceps femoris
  2. superomedial = semimembranosus and semitendinosus
  3. inferior = two heads of gastrocnemius
  4. roof = fascia lata
  5. floor = femur, popliteus
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90
Q

What nerve innervates each area (arrow)

A

Top –> lateral femoral cutaneous

posterior femoral cutaneous

saphenous nerve (medial)

sural nerve (lateral)

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91
Q

What muscle is this?

action?

A

Splenius: connects skull to the thoracic spine.

extend head and neck; ipsilaterally flex neck and rotate head

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92
Q

Group of muscles (I love spaghetti)

action?

A

Errector spinae muscles

iliocostalis

longissimus

spinalis

extend vertebral column.

unilateral ctrx –> lateral bending

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93
Q
A

top - semispinalis

lies underneath the splenius muscle, connecting the skull to the thoracic spine. Extends the head and neck (bilateral contraction) and rotates and bends the head/neck contralaterally (with unilateral contraction)

multifidus

rotatores

unilateral contraction results in rotation of the head, cervical and thoracic vertebrae in a contralateral direction while bilateral contraction serves to extend the head and vertebral column

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94
Q

Describe how spinal nerves are formed and their disposition upon passing through the intervertebral foramina.

A

combination of the ventral root (containing somatic efferents) and the dorsal root (containing somatic afferents). The nerve passes through the intervertebral foramina and splits into the ventral ramus and a dorsal ramus, mixed nerves that go to the anterior and posterior aspects of the body, respectively.

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95
Q
A
  1. Transverse ligament of atlas – extends from the lateral masses of the atlas and holds the dens of the axis against the anterior arch of the atlas

Steele’s rule of 3rd’s (1 cm gap b/w spinal cord and other structures)

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96
Q
A
  1. Anterior longitudinal ligament - runs on the anterior surface of bodies extending from the sacrum to atlas; ONLY ligament that limits extension of vertebral column
  2. Posterior longitudinal ligament - runs on posterior surface of bodies within the vertebral canal; it is somewhat weaker than the anterior ligament; helps prevent hyperflexion of vertebral column and helps prevent or redirect herniation of the nucleus pulposus.
  3. Interspinous ligaments/Supraspinous ligaments - connective tissue sheet/cord running between the spinous process bodies/apices respectively
  4. Ligamentum flavum - broad yellow fibroelastic tissue (flavus = yellow) extending between adjacent laminae and forming the posterior wall of vertebral canal.; prevents separation of lamina and thus abrupt flexion of vertebral column which could result in damage to the IV disc. This ligament is responsible for the characteristic “pop” when breached during a lumbar puncture.
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97
Q
A

Ligamentum nuchae - continuation of supraspinous ligament in cervical region, filling in concavity of cervical curvature and serving as site of muscular attachment

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98
Q
A
  1. Anterior longitudinal ligament - runs on the anterior surface of bodies extending from the sacrum to atlas; ONLY ligament that limits extension of vertebral column
  2. Intertransverse ligaments – connect adjacent transverse processes
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99
Q

Joints between articular facets in the vertebrae

name?

are they synovial?

A

zygapophysial joints

Synovial

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100
Q

Which nerve supplies the vertebrae periosteum, ligaments, IV discs, dura mater and accompanying blood vessels

A

recurrent meningial nerve

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101
Q

Level of spinal cord of preganglionic sympathetic neurons

What is the name of the nerve that innervates the sympathetic chain?

Name of nerve that allows postganglionic sympathetic fibers to be distributed to spinal nerve after synapsing on sympathetic chain?

A

T1-L2

white rami communicantes (myelinated) –> sympathetic chain

gray rami communicantes

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102
Q

Name of nerve that supplies the back musculature that stabalizes and moves the vertebral column

branch off the one above that innervates the zygapophysial joints of the vertebral column?

A

dorsal rami

articular branch

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103
Q

What are the red flag symptoms of lower back pain?

A

Infection

Cancer

Fracture

Cauda Equina Syndrome: Compression of the nerve roots in the lumbar spine which disrupts sensory and motor function

Presence of these symptoms warrants further evaluation

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104
Q

Explain the key components of a proper physical examination of a patient with acute low back pain.

A

Inspection/Palpation: observe gait/spinal curvature/muscles/sciatic notch

ROM: usually issues w/ forward flexion

Muscle Strength/Neurologic Exam: Patellar (L4)/Achillis (S1) –> issues w/ dorsiflexion nerve root dysfunction

Straight Leg raise/Lasegue’s sign

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105
Q

Acceptable methods of treatment for mechanical low back pain in the acute setting

A

patient education

trial of NSAIDs or acetaminophen

muscle relaxant or opioid depending

physical therapy

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106
Q

Explain how upright balance is achieved in quiet standing through alignment of bones and activation of muscles?

A

Body is aligned so that the vertical line of gravity passes just posterior to the hip joint and just anterior to the knee joint = little muscle activation to maintain balance

The vertical line of gravity does pass in front of the ankle joint, so plantarflexors are needed to keep the body standing.

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107
Q

How do the ligaments maintain static stability and muscles of the back contribute to dynamic stability of the spine

A

Stacking of the spinal vertebrae minimizes muscle activation in quiet standing

roatatores/multifidus finely tune the spine for stability

curves of spine (thoracic and lumbar) keep head above the pelvis

ligaments connect the spinous processes and laminae tightly connected, allowing the pelvis to carry the weight over the feet with minimal muscle activation

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108
Q

What are the 2 phases of Gait and

subdivisions of each?

A

Stance: This is the period of time where the leg is anchored to the ground and supporting the weight of the body. This phase consists of the heel strike, the loading response, the mid-stance, and the terminal stance.

Swing: This is the part of the cycle where the leg is not on the ground and swings from a posterior to anterior position. This phase consists of the toe-off, the mid-swing, and the terminal swing.

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109
Q

Subdivisons of Stance

A

heel strike

the loading response

the mid-stance

the terminal stance.

110
Q

Subdivisons of Swing

A

toe-off

the mid-swing

the terminal swing

111
Q

Describe the three major mechanical requirements for gait and their correspondence to the subdivisions of gait phases

A

Maintaining upright while standing. This is most difficult during the mid- stance, but hip adductor muscles help to realign the pelvis. In addition, the center of mass moves laterally to keep it over the foot and prevent falling.

A means of progression: this is accomplished via actions of plantarflexor muscles during terminal stand and toe off.

Conservation of energy: the actions of bending the legs and raising the pelvis during walking keeps the center of mass approximately level.

Momentum is conserved by using eccentric muscle contractions, which can provide more force with less neural activation, to slow down moving body parts.

112
Q

Explain muscle action that occurs during the subdivisions of stance. Explain how the muscle activities achieve upright balance, forward propulsion, and control of center of mass.

A

Heal strike: the heel plants on the ground. Dorsiflexors prevent the foot from slapping the ground. Hip extensors are active from the terminal swing to slow down the leg.

Loading response: Knee extensors cushion the leg as the heel strikes the ground, and straighten the leg as the body moves forward. In addition, hip abductors re-align the pelvis to achieve upright balance. In this phase as well, there is a lateral shift of the center of mass to keep it over the foot and maintain balance.

Mid-stance: Hip and knee extensors keep the leg straight; hip abductors keep the pelvis level.

113
Q

Explain muscle action that occurs during the subdivisions of swing phase. Explain how the muscle activities achieve upright balance, forward propulsion, and control of center of mass.

A

Toe off: Plantarflexors provide the force needed to push off from the ground and propel the body forward. Hip flexors help to swing the leg forward.

Mid-swing: Dorsiflexors lift up the foot to clear the ground during the swing.

Terminal swing: Knee flexors slow down the forward acceleration of the leg. The swinging motion provides the momentum to extend the knee.

114
Q

Compare the resting membrane’s permeability to K+, Na+ and Cl- for skeletal muscle vs. neurons

A

Muscle - PK : PCl : PNa = 1: 10: 0.005

Neuron - PK : PCl : PNa = 1: 0.1: 0.01

115
Q

Resting membrane potential for Cl-

for muscle?

A

-85 mv

116
Q

What is the impact of high chloride permeability in skeletal muscle?

A

Means membrane potential is greatly influenced by Chloride (-85mv)

Takes large depolarization to overcome influence of choloride on membrane potential to elicit an AP

repolarization relies on chloride influx, rather than potessium efflux from the cell.

117
Q

Why does it take ALOT of Acetylcholine in the NMJ to generate an Action Potential?

What membrane potential activates the post-synaptic membrane to activate voltage-sensitive Na+ channels, leading to an AP?

A

Chlorides influence on resting membrane potential - 85mV

0mV

118
Q

Illustrate a “typical” action potential for a skeletal muscle fiber; show how the membrane’s permeability to Na+ and K+ changes during the action potential and indicate which channels mediate the permeability changes.

A

Acetylcholine acts at ACh nicotinic receptor channels (these channels allow sodium influx and potassium efflux, and increase sodium permeability about 1000 fold), which depolarize the post-synaptic membrane rapidly to 0 mV, thus activating nearby voltage-sensitive sodium channels.

Na+ channels open rapidly; many channels open at once, making sodium permeability 10,000 fold greater than at rest.

The membrane potential rises very rapidly and almost immediately reaches the Nernst potential for sodium.

Voltage-gated sodium channels rapidly close; chloride influx (due to positive charge inside the membrane) repolarizes the membrane. Voltage-gated potassium channels also open, allowing efflux of potassium to help repolarize the membrane.

There is no hyperpolarization due to the strong influence of chloride on the membrane potential. It is basically impossible to lower the membrane potential below the Nernst potential for chloride, even though some potassium efflux does help to repolarize the cell (it is not the most influential player, but potassium permeability does increase slightly during the repolarization period).

119
Q

Discuss the impact of high resting chloride permeability on muscle excitability

A

High chloride permeability reduces the excitability of muscle cells. It means that stimuli must be large in order to depolarize the membrane enough to generate an action potential. This means that muscles will not activate spontaneously (i.e. muscle twitch), and are under control of the central nervous system.

The resting membrane potential is primarily repolarized via chloride influx. This means that potassium only leaves the cell in small quantities, sparing ATP when it comes time to restore potassium levels via the Na,K-ATPase.

Chloride can quickly diffuse into/out of the cell as needed, allowing for quick action potentials in skeletal muscle (i.e., one for one relationship between pre-and post-synaptic firing). Rapid firing is possible and results in constant contraction of the muscle (i.e. tetanus).

120
Q

Predict the impact of reduced chloride permeability on skeletal muscle

A

Then potassium is relied on to restore resting membrane potential (repolarizing the membrane)

results in spontaneous muscle activation and sensitivity to small changes in extracellular potassium

Potassium builds up in extracellular space in the t-tubules, reducing membrane potential and effectively depolarizing the resting potential. This generates an action potential throughout the muscle fiber and keeps muscles contracted. The excitations result from the t-tubules, rather than from the NMJ.

Na,K-ATPase will restore the resting membrane potential and will give back CNS control of muscles. The pump will catch up to restore resting membrane potential.

At first, muscles are stiff, but with more activity control improves.

121
Q

Myotonia Congenita

A

genetic defect in Cl- channel uniquely expressed in skeletal muscle

suffer from an inability to “relax”

repolarization relies on K+ efflux instead of Cl-

Potassium builds up in extracellular space in the t-tubules, reducing membrane potential and effectively depolarizing the resting potential. This generates an action potential throughout the muscle fiber and keeps muscles contracted (independent of neural input). The excitations result from the t-tubules, rather than from the neuromuscular junction.

122
Q

List the sequence of events that leads to elevation and subsequent reduction of cytosolic calcium in skeletal muscle

A

AP –> t-tuble –> activate DHP (voltage-gated Ca2+ channel) –> activated RyR1 (SR membrane) –> Ca2+ release intracellular space –> muscle ctrx!!! –> High [Ca2+] –> Ca-ATPase pumps calcium back into the SR –> Muscle relaxes

123
Q

Indicate how cytosolic calcium levels regulate cross-bridge cycling

A

When cytosolic calcium levels are low, tropomyosin covers the myosin binding site on actin, effectively preventing muscle contraction.

When cytosolic calcium levels are high, calcium binds to troponin and causes a conformational change in the tropomyosin/troponin complex that uncovers multiple binding sites on actin (each tropomyosin covers 7 myosin-actin binding sites). Thus, an increase in calcium can exponentially increase myosin-actin binding.

Cross-bridges cycle, drawing the Z-lines towards each other and shortening the sarcomere.

124
Q

Malignant Hyperthermia Syndrome

What is mutated?

What tiggers it?

Drug Treatment?

A

A mutation in either calcium channel (DHP or RyR1) can result in unregulated release of calcium from the sarcoplasmic reticulum, which causes muscle rigidity, a hypercatabolic state due to muscle contraction that has increased oxygen consumption and carbon dioxide production (hypercapnia), hyperkalemia leading to tachycardia, hyperthermia due to increased muscle activity (temperature can rise 2 degrees an hour), and muscle breakdown (rhabdomyolysis). Lethal if untreated.

People who have these mutations are fine in day to day life, but anesthetics (volatile and depolarizing) can trigger it. Dantrolene is the cure, by blocking open calcium release channels to terminate the response.

125
Q

Graph the relationship between passive and active tension as a function of sarcomere and muscle length, assuming saturating levels of calcium and ATP are available

A

Saturating calcium levels only occur during tetanic stimulation, i.e. maximum stimulus frequency.

The sarcomere (and by extension, muscle) length has a role in the amount of tension that can be generated when the myosin heads attach to actin and generate a power stroke.

When the sarcomere length is too long, the myosin heads do not overlap the actin and cannot pull the actin filaments in a power stroke; i.e. very little force is generated.

When the sarcomere length is too short, many of the myosin heads can make contact with actin, but the ends of the myosin (and eventually also the actin) run into the Z band, which sterically hinders any further sliding action.

Peak active tension occurs when sarcomere length is between 2 and 2.2 micrometers.

This is the reason that muscles as a whole have optimal lengths where force can be generated actively; if too many sarcomeres are too shortened or too stretched, then the muscle will not operate at peak optimal performance. Passively, a muscle resists stretch the longer it is stretched; if the muscle is not stretched it will have very little resistance to stretching.

126
Q

Discuss the strategies used to modulate force in skeletal muscle

A

Calcium availability

After a single stimulus (action potential), there is a small amount of calcium released into the muscle cell. It is enough to contract the cell, but not to full contraction. Calcium release is delayed, taking 25 ms to reach the cell, while action potentials only last 3–5 ms. Thus, the muscle cell can repolarize, at least locally, and then is available to be stimulated again. The CNS can stimulate the muscle repeatedly, causing rapid successive stimulations that increase the concentration of calcium inside the cell, and therefore increase the force generated by the muscle. This is called summation. Repeated rapid stimulation will lead to tetanus, at which point maximum force and maximum calcium are present. The nervous system controls the speed of stimulation.

Number of active fibers

The nervous system also controls how many muscle fibers are active via motor unit recruitment. For lifting heavy objects, more motor units will be recruited than to type on a keyboard or write with a pencil.

127
Q

What is the etiology and pathology of Osteoarthritits?

Primary vs. Secondary

A

Primary OA: unknown etiology, more common in older adults, possible genetic cause –> breakdown of type II collagen, changing the molecular proteoglycan structure (smaller) –> change in water balance, changing loading/resistance –> cartilage doesn’t bounce back when loaded

Abnormal Box genes –> HMGB2 protein deficiency –> inflammation –> High [cytokine] IL-1, IL-6, prostaglandins –> degeneration of cartilage (chondrocytes)

Overall: Aging, obesity, genetic factors, diabetes, hypertension are risk factors

Secondary OA: identifiable injury/trauma that affects the joint and leads to degeneration

128
Q

What are the patterns of presentation of osteoarthritis, including the clinical characteristics, imaging, and synovial fluid analysis that aid in the diagnosis.

A

Insidious presentation –> gradually increasing pain

Inflammatory episodes –> joint swelling

Imaging: cartialge space narrowing –> asymmetrical alignment; spurs, synovial cyst formation, marginal osteophytes

Synovial Fluid: “non-inflammatory”, clear, yellow, viscous

129
Q

Principles of pharmacologic and non-pharmacologic treatment of osteoarthritis

A

Pain management, with acetaminophen or NSAIDs

Intra-articular treatments of corticosteroids (short term benefit, and don’t recommend more than 3–4 injections)

hyaluronan preparations can provide relief for 6–9 months.

Weight reduction, activity modification, PT, heat/cold, orthotics, excercise

130
Q

Pathophysiology of Rheumatoid Arthritis

A

Initiation begins years before onset of symptoms

Involves adaptive and innate immune system

Cytokines: IL-6, TNF, IL-1

Macrophages, T-cells (Th2), B-cells

Gene: HLA –> autoimmune

Environment: smoking –> 40X increase

Hyperplastic synovial membrane –> degenerate bone

131
Q

Disease?

Location?

A

Rheumatoid arthritis

Synovium

Involves adaptive and innate immune system (may see germinal centers in histo)

Cytokines: IL-6, TNF, IL-1

Macrophages, T-cells (Th2), B-cells

Gene: HLA –> autoimmune

Environment: smoking –> 40X increase

Hyperplastic synovial membrane –> degenerate bone

132
Q
A

Rheumatoid arthritis

metacapophalangeal (MCP)

Proximal interphalangeal joints (ICP)

ulnar drift of the fingers

133
Q

Most highly sensitive test for Rheumatoid arthritis?

Most specific?

Which is associated with faster progression?

A

Rheumatoid Factor (RF) - not always found in patients

Anti-citrullinated cyclic peptide (CCP)

CCP

CCP complexes are deposited in the joints, therefore higher anti-CCP antibodies indicative of how chronic disease is

134
Q

1st line DMARD for RA?

mechanism of action

A

Methotrexate

Irreversibly inhibits Dihydrofolate Reductase (enzyme involved in folic acid metabolism)

Inhibits synthesis of DNA, RNA, Proteins, suppresing the immune system (TNF high in RA)

135
Q

DMARD that acts as a TNF-alpha inhibitor (EIA)

A

Etanercept

Infliximab

Adalimumab

SE: Serious infections - viral, fungi, bacteria

136
Q

What is Tocilzumab used for?

mechanism?

A

RA

Inhibits IL-6 receptor/IL-6 interactions

137
Q

What DMARD works as a T-cell costimulatory blocker?

A

Abatacept

138
Q

Which DMARD works as an antibody to CD20 on B-cells, decreasing cytokine release?

A

Rituximab

decreases cytokine release, T-cell interactions and reduces autoantibody levels

139
Q

What DMARD is a Janus Kinase3 inhibitor?

A

Tofacitinib

140
Q

Gout

What molecule is related to it? (Diet high in?)

Name the enzymes involved

What sugar metabolism leads to higher incidence?

A

Male (post-menopause women)

High purine diet (meat)

High Beer intake

Hyperuricemia

- increase PRPP synthase (purine biosynthesis)

- decreased HGPRT in purine salvage pathway

Fructose metabolism

141
Q

Is Gout involved in the Adaptive or Innate immune system?

Which cell mediators are involved?

What is the gold standard for Gout diagnosis?

A

Innate

Autoinflammatory thru IL-1 (recruits neutrophils, macrophages in the joint)

Toll-like receptors involved w/ inflammasomes

Monosodium urate crystals in synovial fluid (precipitate due to lower solubility in synovial fluid than blood plasma)

142
Q
A

Monosodium Urate crystals visible w/ polarized light –> used to diagnose Gout (above)

CPPD (Psuedogout): Rhomboid, Positive Blue

143
Q

Type of synovial fluid effusion Gout is classified as?

A

Septic

Purulent, Low Glucose, High Lymphocytes

144
Q

Subcategories of Spondylarthropathies

quick definition of spondylarthropathies

A

Ankylosing Spondylitis

Psoriatic arthritis

Reactive arthritis

Enteropathic arthritis (Crohn’s, Ulcerative)

changes in ligament attachments rather than synovium

Sacroiliac joint involvement

Associated w/ HLA-B27

145
Q

Characteristics of Spondylarthropathies

A

Inflammatory Back Pain

Asymmetric joint predominance (unlike RA)

HLA-B27

associated w/ enthesitis, dactylitis, uveitis (HLA associated)

bamboo spine (calcification of transverse ligament)

146
Q

Systemic Lupus Erythematosus

A

autoantibodies

147
Q

What caused this?

A

Displacement of sesamoid bone changes direction of pull of flexor hallicus longus tendon

Hallux valgus or Bunion

148
Q

Function of arches in feet

A

Shock absorption

Surface adaptation

Weight distribution

149
Q

3 arches of the foot

A

medial longitudinal - rigid, shock absorption

lateral longitudinal - surface conformation

transverse arch

150
Q

How are the Arches of the foot maintained?

A

interlocking shape of the bones

plantar ligaments

plantar aponeurosis

muscles and tendons

151
Q
A

Pes Planus (Flat Foot)

Inefficient push off during gait because foot unable to assume supinated position to become a rigid lever; pain arises from strain on muscles and ligaments

152
Q
A

Pes Cavaus (High Arch)

relatively inconsequential may strain lateral ligaments and ultimately affect ability to accommodate varying terrains

153
Q

Deep Fascia of the Leg

A

Continuous w/ fascia lata

compartmentalizes leg

forms retinacula

154
Q

Function of Retinacula of the leg

A

prevent “bow-stringing” of tendon when muscles ctrx

155
Q

Synovial Tendon Sheaths

A

A bursa that wraps a tendon as it passes thru a retinacular tunnel

f(x) as same way as bursa = reduce friction

inflammation - tenosynovitis

156
Q

Seasamoid bone in lateral head of gastrocnemius name?

A

Fabella

157
Q

Tendon positioning @ Tarsal Tunnel

Pneumonic?

From medial malleolus to calcaneus

A

Tom Dick an’ Harry

Tibialis Posterior

Flexor Digitorum Longus

Flexor Hallicus Longus

???

158
Q

Trace path of Great saphenous blood flow from foot –> up

A

Dorsal venous arch –> ant. to medial malleolus –> post. to knee

–> ant. in medial thigh –> passes thru saphenous opening (femoral triangle) –> empties into femoral vein

159
Q

Trace the small saphenous vein from foot –> up

A

dorsal venous arch –> post. to lateral malleolus –> empties in popliteal vein

160
Q

Muscles that the tibial nerve innervates?

List

A

Gastrocnemius/ Soleus/ Plantaris

Popliteus/ tibialis post./ flexor digitorum longus/ flexor hallicus longus

intrinsic muscles in sole of foot

skin of heel and sole of foot

161
Q

Muscles/Skin innervated by Superficial Fibular Nerve

A

Fibularis longus/ Fibularis Brevis

skin of lower anterolateral leg and most of dorsum of foot

No artery found in lateral compartment! (perforating branches)

162
Q

Muscles supplied by Deep Fibular Nerve

A

tibialis anterior/ extensor digitorum longus/ extensor hallucis longus

instrinsic muscles on dorsum of foot

wedge of skin b/w 1st and 2nd toes

163
Q
A

saphenous nerve - purple

sural nerve - orange

superficial fibular nerve - yellow

deep fibular nerve - pink

164
Q
A

saphenous nerve - purple

sural nerve (off deep fib/tibial n.) - orange

tibial nerve - green

165
Q

Gastrocnemius

Orgin

Insertion

Innervation

Action

A

Distal posterior femur

Calcaneus via Achilles tendon

Tibial N.

Flexes leg; Planterflexion of foot

166
Q

Soleus

Orgin

Insertion

Innervation

Action

A

Posterior surface of proximal tibia and fibula

Calcaneus via Achilles tendon

Tibial N.

Planterflexes of foot

167
Q

Tibialis Posterior

Orgin

Insertion

Innervation

Action

A

Posterior surface of tibia, fibula and interosseous membrane

Plantar surface of navicular, medial cuneiform, cuboid, calcaneus, 2nd-4th metatarsals

Tibial N.

Plantar flexes foot; Inverts foot

168
Q

Flexor hallucis longus

orgin

insertion

innervation

action

A

Posterior surface of fibula and adjacent interosseous membrane

Plantar surface of distal phalanx of great toe

Tibial N.

Flexes BIG toe

169
Q

Flexor digitorum longus

Orgin

Insertion

Innervation

Action

A

Posterior surface of tibia

Plantar surface of distal phalanges of lateral 4 digits

Tibial N.

Flexes lateral 4 toes; Plantarflexes foot

170
Q

Fibularis Longus

Orgin

Insertion

Innervation

Action

A

Lateral aspect of proximal fibula

Plantar surface of medial cuneiform and 1st metatarsal

Superficial fibular N.

Everts and Plantarflexes foot

171
Q

Fibularis brevis

Orgin

Insertion

Innervation

Action

A

Lateral aspect of middle to distal fibula

Base of 5th metatarsal

Superficial fibular N.

Everts foot

172
Q

Tibialis Anterior

Orgin

Insertion

Innervation

Action

A

Lateral surface of tibia and interosseous membrane

Plantar surface of medial cuneiform and base of 1st metatarsal

Deep fibular N.

Dorsiflexes foot; inverts foot

173
Q

Extensor digitorum longus

orgin

insertion

innervation

action

A

Upper half of medial fibula and interosseous membrane

Dorsal surface of middle and distal phalanges of lateral four digits

Deep fibular N.

Extends lateral 4 digits; Dorsiflexes foot

174
Q

Extensor hallucis longus

Orgin

Insertion

Innervation

Action

A

Anterior surface of mid-fibula and interosseous membrane

Dorsal surface of distal phalanx of great toe

Deep fibular N.

Extends BIG toe; dorsiflexes foot

175
Q

Explain why swelling in one of the compartments of the leg might cause a sharp rise in intra-compartmental pressure and damage to the structures that lie in the compartment.

A

One is direct trauma, which can result in swelling in the compartment from bleeding.

The second mechanism is called re-perfusion injury. In re-perfusion syndrome, arterial inflow to the compartment is prevented, such as with an embolus within the artery or by a traumatic injury to the artery supplying the compartment. Clamps are placed on both sides of the injured artery essentially stopping flow to the distal compartment while the vessel is fixed. Distal to the occlusion of the artery there is hypoxemia and acidosis locally, which increases permeability of the muscle. When blood flow is re-established, the cell permeability causes fluid to leak into the compartment causing a rise in pressure.

May feel a palpable pulse at the ankle while still suffering from compartment syndrome

When pressure is elevated, capillary blood flow is compromised. Edema of the soft tissue within the compartment further raises the intra-compartment pressure, which compromises venous and lymphatic drainage of the injured area. Pressure, if further increased in a reinforcing vicious circle, can compromise arteriole perfusion, leading to further tissue ischemia

176
Q

Describe what you would see in Atrophied muscle?

2 histological features

A

Atrophy muscles

Atrophy typically occurs with type 2 muscle fibers.

When stained for ATPase, at a pH of 9.4, the type 2 fibers stain darkly and are smaller than the type 1 fibers. In addition, the fiber size among type 2 fibers is not consistent. A collection of nuclei is also evidence of atrophy (nuclear bag).

177
Q
A

Atrophy typically occurs with type 2 muscle fibers. When stained for ATPase, at a pH of 9.4, the type 2 fibers stain darkly and are smaller than the type 1 fibers. In addition, the fiber size among type 2 fibers is not consistent. A collection of nuclei is also evidence of atrophy (nuclear bag).

178
Q
A

Atrophy Muscle

Atrophy typically occurs with type 2 muscle fibers.

When stained for ATPase, at a pH of 9.4, the type 2 fibers stain darkly and are smaller than the type 1 fibers. In addition, the fiber size among type 2 fibers is not consistent. A collection of nuclei is also evidence of atrophy (nuclear bag).

179
Q
A

Denervation Angular Atrophy

Suggestive features for denervation are that the fibers are angular and atrophic, both type 1 and type 2; and grouping of fibers.

Grouping below

180
Q
A

Denervation Grouped Atrophy

Suggestive features for denervation are that the fibers are angular and atrophic, both type 1 and type 2; and grouping of fibers.

181
Q
A

Denervation Angular Atrophy

Suggestive features for denervation are that the fibers are angular and atrophic, both type 1 and type 2; and grouping of fibers.

182
Q
A

Target Fiber

Denervated Muscle

183
Q
A

Muscle Denervation

Infant

184
Q

What are muscular dystrophies?

List 2

A

Muscular dystrophies are diseases that degenerate and weaken the muscles.

Duchenne’s MD

Becker’s MD

185
Q

Duchenne’s Muscular Dystophy

A

most common, with an incidence of 1:10,000 males.

characterized by progressive weakness, with most patients becoming wheelchair bound by age 12.

Death occurs from respiratory failure, pneumonia, heart failure (cardiomyopathy).

The etiology in Duchenne’s is a deletion on the short arm of the X- chromosome (Xp21) in the gene for dystrophin. The result is no dystrophin is made.

186
Q

Relevant Histo in slide (6)

What is it?

A

Duchenne’s MD

Hypertrophy and Atrophy

Fibrosis

Necrosis and regeneration

Some inflammation

187
Q

What process is taking place in this skeletal muscle?

A

Regeneration

188
Q

What process is taking place in this skeletal muscle?

A

Necrosis

189
Q

What process (2) is taking place in this skeletal muscle?

A

Atrophy and Hypertrophy

190
Q
A
191
Q

Becker Muscular Dystrophy

A

Becker’s MD is less common and less severe than Duchenne’s, with some patients having a normal life span.

Pathologically, both are characterized by a variable fiber size due to atrophy and hypertrophy; internal nuclei; necrosis, regeneration; fibrosis; hypercontracted fibers

In Becker’s, the mutation in dystrophin produces variable amounts of the gene product.

192
Q

myotonic dystrophy and explain the genetic abnormality that underlies it.

A

Myotonia is sustained involuntary contraction that causes damage to muscle fibers (and eventual weakness).

The disease can be expressed in other organs –> cataracts, baldness, cardiomyopathy, and dementia. The disease becomes worse in successive generations.

Contains internal nuclei and some ring fibers; other pathology like Duchenne’s.

Mutation is on chromosome 19 for myotonin-protein kinase. A 3–4 nucleotide repeat expands to hundreds of copies, causing buildup of the transcripts in the cell nuclei and eventual cell death. Disease is worse with more repeats (Anticipation)

193
Q
A

Congenital myopathies are those muscle disorders that are present at birth. “floppy baby”

Nemaline rods (excess Z-line material accumulated in muscle fibers; red dots), and centronuclear myopathy are examples (nuclei are in the center of the muscle fibers instead of the periphery (nuclei dont stain)).

194
Q
A

Congenital myopathies are those muscle disorders that are present at birth. “floppy baby”

Nemaline rods (excess Z-line material accumulated in muscle fibers; red dots), and centronuclear myopathy are examples (nuclei are in the center of the muscle fibers instead of the periphery (nuclei dont stain)).

195
Q
A

Congenital myopathies are those muscle disorders that are present at birth. “floppy baby”

Nemaline rods (excess Z-line material accumulated in muscle fibers; red dots), and centronuclear myopathy are examples (nuclei are in the center of the muscle fibers instead of the periphery (nuclei dont stain)).

196
Q

What is this showing?

Name of disease when this is fucked up?

A

Normal Myophosphorylase

Glycogenosis is a defect in the synthesis or degradation of glycogen. It may be hepatic, myopathic, or another type. McArdle’s disease lacks muscle phosphorylase (glycogen phosphorylase). See below

197
Q
A

–> Accumulation of glycogen

Glycogenoses (e.g., McArdle’s disease—no myophosphorlase)

198
Q
A

Lipid myopathy is a deficiency of carnitine or carnitine palmitoyltransferase; the muscles cannot mobilize fats for energy and there is a buildup of fat in muscle fibers.

The defect impairs the transport of free fatty acids into mitochondria

199
Q
A

Mitochondrial myopathy refers to a number of defects in the respiratory chain protein complexes. The fibers are “ragged red” due to buildup of mitochondrial material (trichrome stain). Example is Kearns-Sayre syndrome, which causes weak eye muscles, cardiac problems, cerebellar ataxia, and other systemic problems due to a large deletion of mitochondrial DNA. Railroad car or paracrystalline inclusions in the mitochondria visible in EM.

Normal below

200
Q
A

Dermatomyositis has a characteristic skin rash. It usually occurs in adults but sometimes occurs in children. Histologically, it has perifascicular atrophy, and interfascicular inflammation.

201
Q
A

Dermatomyositis has a characteristic skin rash. It usually occurs in adults but sometimes occurs in children. Histologically, it has perifascicular atrophy, and interfascicular inflammation.

202
Q

Polymyositis

Describe clinical presentation

histology

A

Polymyositis appears in women more frequently than men, with a weeks to months onset of proximal muscle weakness and elevated creatine kinase. The EMG shows myopathy. There is necrosis, regeneration, and inflammation histologically. There is no rash as with dermatomyositis. Responds to corticosteroids.

203
Q
A

Inclusion body myositis occurs in middle-aged to elderly men (more frequently than women). Distal weakness occurs first with the knee extensors and flexors of the wrists and fingers, with a protracted course. Unresponsive to corticosteroids.

vacuole below

204
Q
A

Inclusion body myositis occurs in middle-aged to elderly men (more frequently than women). Distal weakness occurs first with the knee extensors and flexors of the wrists and fingers, with a protracted course. Unresponsive to corticosteroids.

Vacuole

205
Q

What is the incidence of knee and ankle sports injuries?

A

Sprains account for 40% of sports injuries (ligament); strains 22% (muscles)

Most sports injuries occurs in the ankle (42%) with only 16% occurring in the knee. However, 85% of surgeries were due to knee injuries, and 50% for loss of the season.

Incidence is 1/10,000 per day have an ankle sprain

ACL tears in women: most common reason for injury in sports. 2–4 times more common in female athletes than male counterparts.

Meniscal tears: most common injury requiring surgery about the knee. Occurs due to twisting of knee (+ McMurray)

206
Q

Explain the anatomic difference and recovery difference between high ankle sprain and a lateral ankle sprain.

A

Lateral ankle sprain damages the lateral fibular ligaments (anterior talo-fibular ligament and/or the calcaneal fibular ligamentof the ankle). These occur with plantar flexion and inversion. Will have varus laxity (laxity when ankle is inverted). The joint line will not look even on x-ray in varus position.

High ankle sprain damages the interosseus ligament between the tibia and fibula (the tibiofibular syndesmosis) and occurs with external rotation injury to the ankle. Uncommon, but occur in about 30% of ankle injuries in collision sports due to the force exerted on the leg during a collision. Pain will be higher on the leg; squeezing the tibia and fibula will elicit pain.

  • *Valgus** - the part of the body distal to the deformed part is deviated away from the body/midline
  • *Varus** - the part of the body distal to the deformed part is deviated toward the body/midline
207
Q

Explain basic principles of treatment for ankle sprains. Relate these treatment approaches to histology of ligaments and how they heal.

A

Treatment of lateral ankle sprain

RICE

Early weight bearing and Active Range of Motion

Functional ankle braces

Resistive Exercise to Full Strength

Proprioceptive Training

Treatment of High ankle sprain

-If Mortise intact: nonweightbearing in cast or boot

gradual return to motion

-If Mortise widened: Operative stabilization

208
Q

Describe the typical mechanism of injury, clinical presentation, physical exam findings associated with a meniscal tear.

A

Mechanism: axial/shear force during twisting of the knee w/ weightbearing

CP: Pain along the joint line or in popliteal space, acute/recurrent swelling, mechanical issues - locking and occasionally giving way

PE: Tenderness along medial and/or lateral joint line, pain in forced flexion and rotation which may cause discomfort, but also a pop or click (+ McMurray)

209
Q

Explain the most common mechanism of injury for the anterior cruciate ligament, as well as the clinical presentation and physical exam findings.

A

Mechanism: non-contact flexion-extension injury w/ deceleration and rotation

CP: history of a twisting injury w/ a “pop”, rapid swelling developing over 4-6 hrs, loss of function, including stiffness and inability to bear weight

PE: hemarthrosis (bloody joint effucsion), limitation of motion and inability to fully extend the knee, joint line tenderness (lateral side), w/ + Lachman test (ant. drawer w/ 20-30 degrees flexion)

210
Q

Describe the proposed explanation for a higher incidence of ACL injury in female athletes

A

Women have more joint laxity, different limb alignment due to the shape of the pelvis, smaller femoral notch and ligament, and hormonal influences that all predispose them to ACL injuries.

Other factors include muscular strength, neuromuscular control, body movement mechanics, and skill level that seem to cause women more injuries.

211
Q

Describe how tearing of collateral ligaments often occurs. Describe the physical examination.

A

In ACL injuries, there is often high valgus stress, which can damage the medial collateral ligament.

Histroy of sudden onset of force applied to outside or inside of the knee w/ the foot fixed to the ground

PE: valgus or varus stress applied to the knee w/ joint in extension (indicative of cruciate ligament damage as well - possible knee dislocation) and again w/ the joint in 20-30 degress flexion (MCL/LCL damage)

212
Q

Describe the anatomy and histology of tendon and ligaments

A

Tendon

70% water; dry weight is 86% collagen. Type I collagen bundles are arranged in parallel direction to the line of pull, with fibroblasts pushed into lines in between the bundles. Collagen is packed into fibrils and eventually fascicles, which are encased in endotenon. Endotenon runs continuously with epitenon with encompasses the entire tendon and carries blood/lymphatics. Tendons which bend around a joint are encased in sheaths. Insert into bone via enthesis (transition to bone via fibrocartilage and sharpey’s fibers)

Ligaments

Structurally similar to tendon. Lower concentration of type I collagen and have more matrix. Varying amounts of elastin depending on location. Orientation of collagen is less organized. Blood supply originates from the bony insertion sites and tends to have a uniform microvascularity.

213
Q

List the common mechanisms of injury to muscle, tendon and ligament

A

Muscle

  • Lacerations (sharp object transects the muscle); part distal to laceration loses nerve supply
  • Contusions (direct, blunt trauma); intramuscular hematoma results (crush injury to muscle fibers)
  • Strains (acute or chronic); rapid stretch that over-lengthens the muscle fibers (pain, swelling, cramping, weakness)
  • Cramps (involuntary, forcible muscle contraction due to hyperexcitability of the nerves)
  • Delayed-onset muscle soreness (small ruptures of muscle fibers)

Tendon

  • Lacerations
  • Strains
  • Avulsions
  • Partial or complete rupture

Ligament (sprains)

  • Tear or rupture
  • Avulsions
  • Joint has moved into a non-physiologic position
  • Muscular dystrophies
  • Infectious Disease
  • Biochemical toxicities
214
Q

Summarize the steps of the healing process for muscle, tendon and ligament. List the stages of soft tissue healing. Be able to describe the major cell types and growth factors involved in each stage.

A
  • Inflammation: tears down damaged tissue. Pain, redness, swelling, heat. Releases cytokines. Neutrophils within first hour, peak 24–48 hours. Phagocytose necrotic debris and release cytokines IL-1, IL- 8, and TNF-alpha; collateral damage of healthy tissue due to release of free radicals. Macrophages arrive and peak at 7 days and also phagocytose, and release IGF-1, PDGF, and IL-6.
  • Regeneration of muscle fibers: in muscle, satellite cells are activated to regrow muscle fibers by trophic factors released by injured muscle cells (bFGF, TGF-beta, and IGF-1).
  • Collagen synthesis: remodelling. Type I goes to the epimysium and perimysium, while type III is in the perimysium and endomysium.
215
Q

Summarize the steps of the healing process for muscle, tendon and ligament. List the stages of soft tissue healing. Be able to describe the major cell types and growth factors involved in each stage.

A
  • Inflammatory phase: begins with formation of a blood clot, an outpouring of fibrin and inflammatory cells. Fibroblasts and migrating capillary buds enter the clot.
  • Reparative phase: laying down of type I collagen perpendicular to the line of pull of the tendon. Reaches maximum at 4 weeks.
  • Remodeling phase: characterized by collagen synthesis and degradation. Lasts up to 1 year following injury.
216
Q

Summarize the steps of the healing process for muscle, tendon and ligament. List the stages of soft tissue healing. Be able to describe the major cell types and growth factors involved in each stage.

A

Occurs in concert (they overlap; unlike tendon)

  • Inflammation: release of inflammatory mediators, vasodilation, increased blood flow. Clot formation, fibrin accumulation, platelet aggregation; plasma exudation. Migration of inflammatory cells. 48–72 hours.
  • Repair: Begins day 2–3. Fibroblast proliferation, matrix synthesis (water, GAGs, type III collagen). Poor tensile strength; increases as type I collagen is added, increased fibril size, organization along stress lines, elastin.
  • Remodeling: begins several weeks after injury. Increases ratio of type I to type III collagen. Increased collagen organization, decreased cellular content, decreased water and proteoglycan content. Lasts years but tensile strength is only 50–70% normal.
217
Q

Describe common treatment modalities for soft tissue injuries. Explain the biologic rationale for why certain soft tissue injuries are best treated with immobilization, while others are best treated with mobilization.

Specifically: muscle, tendon, ligament

A

For muscle, RICE, NSAIDs, only short immobilization -few days (fiber regeneration of collagen type 3/1)

For tendon, immobilization - will get muscle atrophy and then go to PT

For ligament, RICE, Early movement leads to Better scar formation (more type 3 –> 1 collagen), leading to stronger ligament

218
Q

Explain why muscles and tendons of muscles that cross more than one joint are more susceptible to injury.

A

Muscles that cross two joints are more susceptible to injury because they can stretch more with certain physiologic positions (i.e. the hamstrings when the thigh is in flexion and the knee is in extension).

219
Q

Describe how functional differences between eccentric and concentric muscle contractions account for differences in the likelihood of muscle injury.

A

Eccentric contractions are more prone to injury because when the muscle is stretched and activated, the amount of force is much higher than when the muscle is shortened and activated (concentric)

220
Q

Describe and explain the methods used to prevent sprains and strains. Describe the significance of warm-up exercises.

A
  • Warm up; muscle and tendons and viscoelastic and stretches more when warm.
  • Routine conditioning
  • Adequate rest
  • Balanced nutrition
  • Appropriate protective equipment/bracing Body mechanics
  • Stretching? Not shown to decrease injury
221
Q

Explain the differences between sprains and strains, and describe how to recognize differences in their clinical presentations.

A
  • Sprains affect ligaments
  • Strains affect muscles/tendons
  • They can be differentiated by the type/direction of injury, whether or not joint dislocation was present (suggests sprain if it was), whether popping occurred (may also suggest sprain)
222
Q

Describe the commonly used 3-tiered classification system for both sprains and strains. Be able to estimate the expected recovery time from an injury based on the grade of the injury.

A
  • Grade I injuries typically take days to a week to heal.
  • Grade II injuries typically take 2–4 weeks to heal.
  • Grade III typically take >6 weeks to heal.
  • Grade IV injuries typically take months to heal.
223
Q

What are 2 functions of the foot?

A

Stable base for standing

Absorption of energy and transfer back to the ground

224
Q

What are the components of the subtalar joint?

A

talus and calcaneus

responsible for foot inversion and eversion

225
Q

What are the components of the Chopart joint?

A

also called transverse tarsal joint of midtarsal joint

Calcaneus w/ Cuboid and Talus w/ Navicular

226
Q

What are the components of the Lisfranc joints?

A

aka: Tarsometatarsal joint

articulation b/w the bases of the metatarsals and the cuneiforms and cuboid

227
Q

What is the function of the Spring Ligament?

A
  • Supports the head of the talus
  • Stabalizes the medial longitudinal arch
  • Contributes to the ability of the foot to bear weight.
  • If torn –> acquired flatfoot deformity
228
Q

What is the function of the Lisfranc ligament?

A

connects the medial cuneiform to the base of the second metatarsal and thereby secures the entire tarsometatarsal articulation (Lisfranc joint)

229
Q

What is the function of the Plantar Fascia?

A

stabilize the medial longitudinal arch and provide stabilization of the 1st metatarsal especially during the last part of stance phase.

230
Q

What is pes planus?

A

abnormally low or absent medial longitudinal arch

due to failure to develop (age of 4-6 years) or from collapse

talar head displaces medially –> Spring ligament and posterior tibialis tendon are stretched and may tear

231
Q

Pes cavus?

what is it associated with? (4)

A

abnormally high medial longitudinal arch

inverted hindfoot, a plantarflexed first ray, an adducted forefoot and dorsal toe contracture

seen in neuromuscular diseases (Charcot-Marie-Tooth)

can be idiopathic

232
Q

Clubfoot

describe foot position

Is the leg involved?

Male or Femal more prone?

A

development abnormality

foot is positioned in adduction, varus and plantar flexed

Leg involvement: calf muscle atrophy, tendon tightness

environmental and genetic factors

2:1 Male

Seen in spina bifida

233
Q

Lisfranc Injury

A

Lisfranc injury: a disruption of the articulation between the medial cuneiform and base of the second metatarsal

purely ligamentous or with Fracture

Collapse of the transverse arch

234
Q

Turf Toe

A

Seen in athletes

Caused by forceful hyperextension of the 1st MTP joint and results in a sprain of the ligaments of that joint

tear of joint capsule from metatarsal head

235
Q

What are 2 recommendations that the CDC advises for exercise for individuals?

A
  1. 150 minutes of moderate intensity aerobic activity every week.
  2. Muscle strengthening activities that work all major muscle groups on 2 or more days of the week.
236
Q

Define satellite cells and describe the role of satellite cells in helping muscle fibers produce more sarcomeres. Explain the role of sarcomeres in muscle response to exercise.

A
  • Satellite cells are premature myoblasts that remain as precursors to muscle cells, and contain mainly the nucleus. They live at the edge of muscle cells, just outside the muscle fiber but inside the basal lamina.
  • Satellite cells are stimulated in response to stress on the muscle. They divide and proliferate, creating new myoblasts that fuse with the existing muscle fiber.
  • The fusion of myoblasts allows for more proteins to be made in order to form new sarcomeres.
  • Sarcomeres are added in parallel with existing muscle fibers, which both causes the muscle to get bigger and allows it to generate more force.
237
Q

Explain the contribution to ATP production by creatine phosphate, anaerobic glycolysis and aerobic respiration during exercise of varying intensities and durations.

A

Creatine Phosphate: The most immediate and fastest way to resynthesize ATP is by hydrolysis of creatine phosphate.

Anaerobic glycolysis yields the next highest rate of ATP re-synthesis, followed by mitochondrial respiration (aerobic metabolism) which can be sustained for longer duration by reducing the exercise intensity.

238
Q

Compare substrate use (fat vs. carbohydrate) for ATP production during high-intensity, short duration exercise and low-intensity, prolonged exercise.

A

Fat = low intensity prolonged exercise

Carbs = high intensity short duration

What causes shift?

  1. recruitment of fast fibers (have glycolytic enzymes; few mitochondria for fat metabolism)
  2. increases blood levels of epinephrine (stimulates glycogenolysis and lactate production - specifically inhibits fat metabolism)
239
Q

Explain the changes in bone elicited by exercise and how those changes can result in diminished risk of fracture.

Explain the type of exercise that is needed to elicit bone changes

A

Wolff’s law: bone deposition and resorption occurs in response to the stresses placed upon the bone.

Exercise can stress the bone and stimulate deposition.

Exercise reduces the risk of fracture by enhancing or maintaing bone strength, and reducing the risk for falls.

Bone density can be maintained or increased by icluding high impact exercise with resistive exercises with heavy loads (80–90% of body weight). Adaptive bone responses require dynamic stimulation, high threshold of load, and a pattern of bone loading different from everyday loading.

240
Q

Explain how the bone cell types may mediate the exercise stimulus for changes in bone strength.

A

Stress on the bone is detected as a stretch of the cell membrane and change in fluid flow. The signal is transduced by stretch-sensitive Ca channels or calcium binding protein. Leading to influx of extracellular Ca into Osteocytes followed by mobolization of intracellular Ca. This signal is communicated to other cells via gap junctions or diffusion of messengers such as Ca and ATP. Eventually leading to a proliferation of osteoblasts, resulting in a build-up of bone.

241
Q

Critical Period

A

Weeks 4-8

Critical period of limb development when teratogens can modify limb development

earlier insults affect whole limb or upper limb, whereas later exposure alters forelimb or hand/foot formation.

242
Q

What determines the location of limb buds (upper field) on the body wall?

A

HOX (transcription factors)

HOX genes are expressed in regional patterns within the embryo and confer positional information by inducing a suite of other genes to behave ‘appropriately’ for that position and different from other positions during development (e.g., limb vs. flank, arm vs. leg, or wrist vs. elbow).

243
Q

Proximodistal axis formation

A

Ectoderm at leading edge of limb bud is induced and maintained by growth factors (FGFs) in underlying medoserm.

FGF’s lead to apical ectodermal ridge (AER) formation. This ridge also expresses FGF’s that act on the mesoderm in the progress zone to divide.

This cell division leads to outgrowth of the limb bud –> Further outgrowth (away from AER) leads to cartilage model of bone and its specific proximodistal level

The ectoderm at the leading edge of the limb bud is induced and maintained by growth factors (FGFs) expressed by the underlying mesoderm. These factors induce the apical ectoderm to form a ridge, the apical ectodermal ridge or AER. This ridge also expresses growth factors (other FGFs), which induce the mesoderm in the adjacent progress zone to divide. This cell division leads to outgrowth of the limb bud, and contributes to proximodistal patterning. As the limb elongates, mesoderm is moved out of the progress zone (away from the AER) by cell division. It begins to differentiate into cartilage models of the bones appropriate to the limb and its specific proximodistal level (stylopod = proximal arm/leg;

244
Q

stylopod

A

proximal arm/leg

245
Q

zeugopod

A

distal arm/leg

246
Q

autopod

A

wrist/ankle and finger/toes

247
Q

4th week, rule of 4

A

4 limb buds begin to create the appendicular skeleton at the end of the 4th week.

Mesenchymal core from somatic/parietal mesoderm of LPM covered with ectoderm

Ectoderm at leading edge forms apical ectodermal ridge=AER

AER induces progress zone in adjacent mesoderm

Endochondral bone formation as mesoderm leaves progress zone

248
Q

Development of mediolateral axis (pinky finger to thumb)

What zone regulates this?

A

regulated by Zone of Proliferating Activity - signaling center near the posterior margin of the AER

ZPA excretes signaling proteins that act on mesoderm behind progress zone to pattern

secreted morphogens Sonic Hedgehog (Shh) and Retinonic Acid creat a signaling gradient

  • High duration and concentration of Shh –> pinky finger
  • Low duration and concentration of Shh –> index fingers

Patterning is followed by continued outgrowth of the fingers and apoptosis of the webbing between them due to loss of the AER over these inter-digital areas. Failure to grow out the digits leads to brachydactyly, short digits.

249
Q

Dorsoventral axis formation

A

The difference b/w dorsal and ventral sides is based off of signaling proteins from underlying mesoderm inducing differential gene expression in the overlying ectoderm, which reciprocally induces the underlying mesoderm.

defects no nails (double ventral), or nails on the palmer side of the digits (double dorsal).

250
Q

double ventral

A

no nails (double ventral)

251
Q

nails on palmer side of the digits?

A

double dorsal

252
Q

What do limb muscles derive from?

A

somites

253
Q

Limb Rotation

What week does rotation in opposite directions begin?

What transcription factors direct the legs and arms to be different?

A

Begin similarly but w/ leg about 2 days behind

Tbx4 (leg) and Tbx5 (arm) are transcription factors that help direct legs and arms to be different

Week 7: rotation in opposite directions – arm rotates 90 degrees laterally (extensors post) – leg rotates 90 degrees medially (extensors ant)

254
Q

Amelia

A

absence of an entire limb (early loss of FGF signaling from in the AER or progress zone

255
Q

Meromelia

A

absence of part of a limb

(later or partial loss of FGF signaling)

256
Q

Phocomelia

A

short, poorly formed limb (e.g. partial loss of FGF; or HOX disruption).

May include loss of internal structures (stylopod or zeugopod) without disrupting autopod (e.g., from teratogen Thalidomide damage to vascular development).

257
Q

Ectrodactyly

A

“Lobster-Claw” deformity = variant of adactyly but only the middle digit is lost

258
Q

Brachydactyly

A

short digits = failure of digit AER and progress zone FGF expression

259
Q

Polydactyly

A

extra digits = disruption (usually up-regulation) of Shh gradient from ZPA or misexpression of Shh anteriorly

260
Q

Syndactyly

A

fusion of digits (e.g., failure of interdigital apoptosis)

261
Q

What do you predict will happen if the AER is removed or damaged during stylopod, zeugopod or autopod formation?

A

the limb will be truncated in the upper arm/leg, lower arm/leg or hand/foot, respectively.

262
Q

What do you predict will happen if genes typically expressed in autopod mesoderm were ectopically expressed at the stylopod level in the arm?

A

a hand will form at the shoulder without intervening humerus, radius or ulna.

263
Q

What would happen in the autopod if the ZPA morphogen expression was too high or too low? What if it was also expressed in the anterior limb?

A

a hand with additional digits, or missing one or more digits will form, respectively. A hand with mirror duplication of digits will form.

264
Q

What is the clinical and anatomic significance of psoas sign and why in patients with appendicitis do we at times perform this exam?

A

Elicited by passively extending the thigh of a paitent on his side w/ knees extended, or asking the patient to actively flex his thigh at the hip (right side)

The Psoas border the peritoneal cavity, stretching of psoas causing friction of cavity and therefore, if inflammed, then possible infection.

Right Psoas goes under appendix when the patient is supine –> pain –> appenicitis

Perform becasue patient could be presenting w/ retrocecal appendix in retroperitoneal location, showing no abdominal signs

265
Q

Describe the complications one might see in removing the greater saphenous vein for use in coronary bypass surgery.

A

Damage to the great saphenous nerve - loss of cutaneous sensation in medial leg

large hematomas from even small bleeding (anti-coagulants)

ischemia if leg is closed too tightly

Women? (estrogen?)

Diabetes mellitus

Smoking

Obesity

266
Q

Describe the venous drainage of the lower extremity and where varices (dilated veins) would appear in relation to the leg and thigh.

A

In the lower limbs, venous blood flows from the skin to superficial veins, which drain into the deep veins.

Veins have Valves, if they become incompetent, then blood can backup in the superficial veins leading to Varicose veins

267
Q

Describe the physical findings in L5-L4 and L5-S1 disc herniation and describe MRI findings.

A

L4 = Hip extensors Patellar Reflex

L5 = ankle dosriflextion, eversion/inversion, hip abduction

S1 = ankle plantarflexion and hip extensors Achillis Reflex

S1/L5 = posterior sciatica

268
Q
A

Legg-Calve-Perthes

Idiopathic avascular necrosis

involved growing femoral epiphysis

5-6 year olds

Boys > Girls

269
Q
A

Slipped Capital Femoral Epiphysis

Adolescents

Males that are Overweight

Sometimes bilateral

270
Q
A

O’Donoghue Unhappy Triad

Lateral Force from contact sport

medial meniscus and MCL tear

ACL tear

271
Q
A

Osteoarthritis

  • joint space lost
  • Subchondral sclerosis
  • Subchondral cysts (not seen on this image)
  • Osteophytes (small bone spurs forming)

Joint loss in one place

RA involves the entire joint

272
Q
A

Gout

Marginal erosions

overhanging edges

sclerotic borders

soft tissue density – tophi (50% calcified)

MSS Gun Show (2 decks)

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