Lower body Flashcards

Question

What growth factor stimulates osteoprogenitor cells to turn to osteoblasts?

Answer 1

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

Answer 2

M-CSF (macrophage colony - stimulating factor) RANKL (RANK Ligand) OPG (osteoprotegrin)

Answer 3

enables osteoclast precursor cells to survive and proliferate

Answer 4

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

Answer 5

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

Answer 6

suppresses activity of osteoclasts by acting on OPG --\> inhibiting RANKL (osteoblast) Menopause --\> Less OPG --\> Less RANKL inhibition --\> Greater osteoclast activity

Answer 7

**TRAP** Tartate-resistant acid phosphatase

Answer 8

substance secreted by osteoblasts: _ORGANIC_ type I collagen osteopontin osteonectin osteocalcin _INORGANIC_ hydroxyapatite

Answer 9

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)

Answer 10

Traumatic and Pathologic Fractures Traumatic - car accident Patho - osteoporosis, paget's disease, osteomyelitis, etc...

Answer 11

affected bone (femur, radius) location in bone (epiphsysis, metaphysis) involvement of articular surface fracture pattern (is there comminution (\>3 pieces)) open or closed fracture

Answer 12

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

Answer 13

Primary: 'intramembranous ossification" relies on RIGID fracture fixation in anatomical alignment Secondary: "en(do)chondral ossification" is enhanced by motion

Answer 14

**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

Answer 15

Infections, stiffness/pain, growth abnormalities. _Malunion, delayed union, nonunion_ --\> bad blood supply (diabetes, smoking, inadequate fixation of the fracture)

Answer 16

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

Answer 17

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)

Answer 18

osteopenia: _1 - 2.5_ standard deviations from young adult mean DXA osteoporosis: _\> 2.5_ standard deviations from young adult mean DXA

Answer 19

Nutrition: add Ca2+/Vit D Exercise: Stop being a pussy and lift weights Safety: walkers, canes Meds: antiresorptive agents

Answer 20

**Teriparatide Recombinant** form of PTH...binds to PTH receptors on osteoblasts to stimulate RANKL release _Osteosarcoma_

Answer 21

Vitamin D3 Hypercalcemia Hyperphosphatemia Hypercalciuria

Answer 22

**Denosumab** Inhibit RANKL ---\> Inhibit osteoclast maturation --\> decrease in osteoclasts Respiratory/Urinary tract infections

Answer 23

**Raloxifene** Estrogen receptor agonist --\> enhances osteoblast activity endometrial cancer, hot flashes

Answer 24

works as a pyrophosphate that lines the bones and is absorbed by the osteoclast --\> blocks enzyme for cholesterol synthesis --\> kills osteoclast ## Footnote **Alendronate** **Zolendronic acid**

Answer 25

S. aureus children - growth plate; adults - epiphysis E. coli, Pseudomonas, Klebsiella - IV Drug abusers H. infuienzae, group B strep - neonates Salmonella - sickle cell disease

Answer 26

Bacterial osteomyelitis; s. aureus Bone abscess --\> travel thru haverian canal --\> beneath periostium --\> New bone forms (involucrum) over the dead bone (sequestrum)

Answer 27

*M. tuberculosis* (in AZ: *Coccidioides*) spine, knee, wrist Secondary seeding from another source: usually from lungs

Answer 28

Granulomatous osteomyelitis of the spine

Answer 29

Granulomatous osteomyelitis (*coccidiomycosis)*

Answer 30

*H. influenzae, group B streptococci*

Answer 31

knee, hip, shoulder, elbow, wrist Painful, "hot" swollen joint * s. aureus* * N. gonorrhoeae*

Answer 32

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

Answer 33

*M. tuberculosis, fungi (Coccidioides)* seeding from another source (lungs) spine, knee, hip, ankle, wrist

Answer 34

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

Answer 35

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

Answer 36

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**

Answer 37

Osteogenesis Imperfecta Type I Collagen Too little bone made (fragile) blue sclera (choroid veins); hearing loss; abnormal teeth (dentin)

Answer 38

Paget Disease Older Men (early) excessive osteoclast activity --\> (middle) excessive osteoclast/osteoblast activity --\> (late) excessive osteoblast activity --\> **Thick, heavy bone;** more prone to fracture

Answer 39

Paget's disease cement lines w/ tiny cracks

Answer 40

Younger adults small bones of **hand** and **feet** benign - well circumscribed histo looks like normal cartilage

Answer 41

Enchondroma Younger adults small bones of hand and feet benign - well circumscribed histo looks like normal cartilage

Answer 42

osteoid osteoma randomly arranged trabeculae of woven bone **femur** and **tibia** benign **teenagers**

Answer 43

Osteochondroma starts with misaligned growth plate? (metaphysis) **long bones** **teenagers** stops growing when growth plate closes (growth after --\> malignant)

Answer 44

Osteochondroma starts with misaligned growth plate? (metaphysis) long bones teenagers stops growing when growth plate closes (growth after --\> malignant)

Answer 45

children = primary adults = metastases (lung, breast, kidney, prostate) --\> axial skeleton

Answer 46

Osteosarcoma **Teenagers** (Paget's disease \>60 years) **around the knee** (distal femur, proximal tibia) malignant osteoblasts forming osteoid (bone) matrix

Answer 47

Osteosarcoma Teenagers (Paget's disease \>60 years) around the knee (distal femur, proximal tibia) malignant osteoblasts forming osteoid (bone) matrix

Answer 48

Osteosarcoma Teenagers (Paget's disease \>60 years) around the knee (distal femur, proximal tibia) malignant osteoblasts forming osteoid (bone) matrix

Answer 49

Chondrosarcoma **old adults** (\> 40) **pelvis, ribs, proximal femur/humerus** bluish-white tissue; malignant cells produce chondroid matrix

Answer 50

Chondrosarcoma old adults (\> 40) pelvis, ribs, proximal femur/humerus bluish-white tissue; malignant cells produce chondroid matrix

Answer 51

Giant cell tumor **Younger adults** **around the knee** (distal femur, proximal tibia abundant multinucleated giant cells + mononuclear cells osteoclast orgin

Answer 52

Giant cell tumor Younger adults around the knee (distal femur, proximal tibia abundant multinucleated giant cells + mononuclear cells osteoclast orgin

Answer 53

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)

Answer 54

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)

Answer 55

post. ilium and sacrum iliotibial tract; gluteal tuberosity inferior gluteal nerve extends thigh

Answer 56

post. ilium greater trochanter superior gluteal nerve abducts and medially rotates femur; prevents pelvic drop on opposite side during swing phase of walking

Answer 57

posterior ilium greater trochanter superior gluteal nerve abducts and medially rotates femur; prevents pelvic drop on opposite leg during swing phase of walking

Answer 58

ASIS lateral proximal tibia via IT band superior gluteal nerve Abducts and medially rotates femur; stabalizes hip and knee joints during extension

Answer 59

anterior surface of sacrum greater trochanter ventral rami L5, S1, S2 laterally rotates extended thigh; abducts flexed thigh

Answer 60

ischial tuberosity medial surface of proximal tibia sciatic nerve (tibial division) extends thigh; flexes leg

Answer 61

ischial tuberosity posteromedial surface of proximal tibia sciatic nerve (tibial division) extends thigh; flexes leg

Answer 62

long head --\> ischial tuberosity (sciatic n. tibial division) short head --\> post. femur (common fibular division) head of fibula extends thigh; flexes leg

Answer 63

Posterolateral aspect of distal femur achillis tendon - calcaneus tibial n. weak plantar flexor of foot

Answer 64

Lateral femoral condyle posterior surface of proximal tibia tibial nerve unlocks the knee joint by laterally rotating femur on fixed tibia

Answer 65

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

Answer 66

Top --\> lateral femoral cutaneous posterior femoral cutaneous saphenous nerve (medial) sural nerve (lateral)

Answer 67

Splenius: connects skull to the thoracic spine. extend head and neck; **ipsilaterally** flex neck and rotate head

Answer 68

Errector spinae muscles **iliocostalis** **longissimus** **spinalis** extend vertebral column. unilateral ctrx --\> lateral bending

Answer 69

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

Answer 70

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.

Answer 71

7. **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)

Answer 72

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 5. **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.

Answer 73

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

Answer 74

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 6. **Intertransverse ligaments** – connect adjacent transverse processes

Answer 75

**zygapophysial joints** **Synovial**

Answer 76

recurrent meningial nerve

Answer 77

T1-L2 white rami communicantes (myelinated) --\> sympathetic chain gray rami communicantes

Answer 78

dorsal rami articular branch

Answer 79

**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

Answer 80

**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**

Answer 81

patient education trial of NSAIDs or acetaminophen muscle relaxant or opioid depending physical therapy

Answer 82

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_.

Answer 83

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

Answer 84

**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_.

Answer 85

heel strike the loading response the mid-stance the terminal stance.

Answer 86

toe-off the mid-swing the terminal swing

Answer 87

**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.

Answer 88

**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.

Answer 89

**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.

Answer 90

**Muscle** - PK : **PCl** : PNa = 1: **10**: 0.005 **Neuron** - **PK** : PCl : PNa = **1**: 0.1: 0.01

Answer 91

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.

Answer 92

Chlorides influence on resting membrane potential - 85mV 0mV

Answer 93

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).

Answer 94

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).

Answer 95

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.

Answer 96

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.

Answer 97

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

Answer 98

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.

Answer 99

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.

Answer 100

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.

Answer 101

**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.

Answer 102

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

Answer 103

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**

Answer 104

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**

Answer 105

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

Answer 106

**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

Answer 107

Rheumatoid arthritis metacapophalangeal (MCP) Proximal interphalangeal joints (ICP) ulnar drift of the fingers

Answer 108

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

Answer 109

**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**)

Answer 110

**Etanercept** **Infliximab** **Adalimumab** SE: Serious infections - viral, fungi, bacteria

Answer 111

RA Inhibits IL-6 receptor/IL-6 interactions

Answer 112

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

Answer 113

Tofacitinib

Answer 114

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**

Answer 115

**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)

Answer 116

Monosodium Urate crystals visible w/ polarized light --\> used to diagnose Gout (above) CPPD (Psuedogout): Rhomboid, Positive Blue

Answer 117

Septic Purulent, Low Glucose, High Lymphocytes

Answer 118

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**

Answer 119

Inflammatory Back Pain **Asymmetric** joint predominance (unlike RA) **HLA-B27** associated w/ enthesitis, dactylitis, uveitis (HLA associated) bamboo spine (calcification of transverse ligament)

Answer 120

autoantibodies

Answer 121

Displacement of sesamoid bone changes direction of pull of flexor hallicus longus tendon ## Footnote **Hallux valgus or Bunion**

Answer 122

Shock absorption Surface adaptation Weight distribution

Answer 123

medial longitudinal - **rigid, shock absorption** lateral longitudinal - **surface conformation** transverse arch

Answer 124

interlocking shape of the bones plantar ligaments plantar aponeurosis muscles and tendons

Answer 125

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

Answer 126

Pes Cavaus (High Arch) relatively inconsequential may strain lateral ligaments and ultimately affect ability to accommodate varying terrains

Answer 127

Continuous w/ fascia lata compartmentalizes leg forms **retinacula**

Answer 128

prevent "bow-stringing" of tendon when muscles ctrx

Answer 129

A bursa that wraps a tendon as it passes thru a retinacular tunnel f(x) as same way as bursa = **reduce friction** inflammation - tenosynovitis

Answer 130

Tom Dick an' Harry **T**ibialis Posterior Flexor **D**igitorum Longus Flexor **H**allicus Longus ???

Answer 131

Dorsal venous arch --\> ant. to medial malleolus --\> post. to knee --\> ant. in medial thigh --\> passes thru saphenous opening (femoral triangle) --\> empties into femoral vein

Answer 132

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

Answer 133

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**

Answer 134

Fibularis longus/ Fibularis Brevis **skin of lower anterolateral leg and most of dorsum of foot** **No artery found in lateral compartment!** (perforating branches)

Answer 135

tibialis anterior/ extensor digitorum longus/ extensor hallucis longus instrinsic muscles on dorsum of foot wedge of skin b/w 1st and 2nd toes

Answer 136

saphenous nerve - purple sural nerve - orange superficial fibular nerve - yellow deep fibular nerve - pink

Answer 137

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

Answer 138

Distal posterior femur Calcaneus via Achilles tendon Tibial N. Flexes leg; Planterflexion of foot

Answer 139

Posterior surface of proximal tibia and fibula Calcaneus via Achilles tendon Tibial N. Planterflexes of foot

Answer 140

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

Answer 141

Posterior surface of fibula and adjacent interosseous membrane Plantar surface of distal phalanx of great toe Tibial N. Flexes BIG toe

Answer 142

Posterior surface of tibia Plantar surface of distal phalanges of lateral 4 digits Tibial N. Flexes lateral 4 toes; Plantarflexes foot

Answer 143

Lateral aspect of proximal fibula Plantar surface of medial cuneiform and 1st metatarsal Superficial fibular N. Everts and Plantarflexes foot

Answer 144

Lateral aspect of middle to distal fibula Base of 5th metatarsal Superficial fibular N. Everts foot

Answer 145

Lateral surface of tibia and interosseous membrane Plantar surface of medial cuneiform and base of 1st metatarsal Deep fibular N. Dorsiflexes foot; inverts foot

Answer 146

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

Answer 147

Anterior surface of mid-fibula and interosseous membrane Dorsal surface of distal phalanx of great toe Deep fibular N. Extends BIG toe; dorsiflexes foot

Answer 148

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

Answer 149

**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).

Answer 150

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).

Answer 151

**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).

Answer 152

**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

Answer 153

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_.

Answer 154

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.

Answer 155

Target Fiber ## Footnote **Denervated Muscle**

Answer 156

Muscle Denervation Infant

Answer 157

Muscular dystrophies are diseases that degenerate and weaken the muscles. Duchenne's MD Becker's MD

Answer 158

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.

Answer 159

Duchenne's MD _Hypertrophy_ and _Atrophy_ _Fibrosis_ _Necrosis_ and _regeneration_ _Some inflammation_

Answer 160

Regeneration

Answer 161

Atrophy and Hypertrophy

Answer 162

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

Answer 163

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)

Answer 164

**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**)).

Answer 165

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)).

Answer 166

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)).

Answer 167

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

Answer 168

--\> Accumulation of glycogen Glycogenoses (e.g., McArdle’s disease—no myophosphorlase)

Answer 169

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

Answer 170

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

Answer 171

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

Answer 172

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

Answer 173

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.

Answer 174

**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

Answer 175

**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

Answer 176

_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)

Answer 177

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

Answer 178

_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

Answer 179

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)**

Answer 180

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)

Answer 181

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.

Answer 182

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)

Answer 183

**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.

Answer 184

**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

Answer 185

* 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.

Answer 186

* 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.

Answer 187

**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.

Answer 188

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

Answer 189

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).

Answer 190

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)

Answer 191

* 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

Answer 192

* 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)

Answer 193

* 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.

Answer 194

Stable base for standing Absorption of energy and transfer back to the ground

Answer 195

talus and calcaneus responsible for foot inversion and eversion

Answer 196

also called _transverse tarsal_ joint of _midtarsal joint_ Calcaneus w/ Cuboid and Talus w/ Navicular

Answer 197

aka: Tarsometatarsal joint articulation b/w the bases of the **metatarsals** and the **cuneiforms** and **cuboid**

Answer 198

* 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

Answer 199

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

Answer 200

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

Answer 201

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

Answer 202

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

Answer 203

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

Answer 204

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

Answer 205

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

Answer 206

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.

Answer 207

* 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.

Answer 208

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.

Answer 209

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)

Answer 210

_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.

Answer 211

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.

Answer 212

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.

Answer 213

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).

Answer 214

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;

Answer 215

proximal arm/leg

Answer 216

distal arm/leg

Answer 217

wrist/ankle and finger/toes

Answer 218

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

Answer 219

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.

Answer 220

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).

Answer 221

no nails (double ventral)

Answer 222

double dorsal

Answer 223

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)

Answer 224

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

Answer 225

absence of part of a limb (later or partial loss of FGF signaling)

Answer 226

**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).

Answer 227

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

Answer 228

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

Answer 229

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

Answer 230

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

Answer 231

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

Answer 232

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

Answer 233

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

Answer 234

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

Answer 235

_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

Answer 236

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

Answer 237

L4 = Hip extensors **Patellar Reflex** L5 = ankle dosriflextion, eversion/inversion, hip abduction S1 = ankle plantarflexion and hip extensors **Achillis Reflex** S1/L5 = posterior sciatica

Answer 238

**Legg-Calve-Perthes** Idiopathic avascular necrosis involved growing femoral epiphysis 5-6 year olds Boys \> Girls

Answer 239

**Slipped Capital Femoral Epiphysis** Adolescents Males that are Overweight Sometimes bilateral

Answer 240

O'Donoghue Unhappy Triad Lateral Force from contact sport **medial meniscus and MCL tear** **ACL tear**

Answer 241

**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_

Answer 242

**Gout** Marginal erosions overhanging edges sclerotic borders soft tissue density -- tophi (50% calcified)

Lower body Flashcards

(272 cards)