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1
Q

in fx for kids, what is often affected

A

the physis aka growth plate

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2
Q

S A L T E R classification

A 
S: straight across-->TYPE 1
A: above growth plate-->TYPE 2
L: lower than growth plate-->TYPE 3 
T: through growth plate-->TYPE 4
E: Erasure of growth plate/crush injury-->TYPE 5
R: Reaction periosteal-->TYPE 6
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3
Q

MC salter fx

A

type 2— above growth plate

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4
Q

fracture healing

  • requires?
  • involves?
  • typical time in adults
A
  • bony fragments be in contact or in very close proximity
  • involves: bridging structure–>CALLUS

**ADULTS: 6-8 weeks

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5
Q

what is a callus

A
  • bridging structure made of fibrous tissue and cartilage
    1. internal callus
    2. external callus
  • fragile
  • must be protected with immobilization of the limb
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6
Q

what happens if theres motion at the fracture site during healing

A

Bony bridges aka calluses will break— fx can take longer to heal or not heal at all

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7
Q

name the four stages of fracture healing

A
  1. hematoma formation
  2. fibrocartilaginous callus formation
  3. bony callus formation
  4. bone remodeling
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8
Q

fracture healing is also called

A

fracture consolidation

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9
Q

define ossification

A

bone formation via osteoblasts

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10
Q

define osteogenesis

A

bone formation via osteoblasts

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11
Q

define bone remodeling

A

replacement of old bone tissue with new bone tissue

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12
Q

Osteoblasts do?

osteroclasts do?

A

BLASTS– build aka form new tissue

CLASTS–cleave/absorb the old tissue

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13
Q

which vits (3), hormones (3) and minerals (3) are required for bone remodeling

A

Vitamins D, C, and A +

Ca, phosphorous, and magnesium

hormones: parathyroid, GH and calcitonin

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14
Q

up to ___ - ___ % of bone mass is recycled every week

A

5-7%

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15
Q

where is the largest ca store in body

A

bones

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16
Q

list the three hormones that regulate ca [ ]

A

PTH
calcitonin
Vit d

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17
Q

what raises ca levels

A

vit d and PTH

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18
Q

what lowers ca levels

A

calcitonin

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19
Q

how does PTH increase blood [ca]—3 ways

A
  1. stim osteoclasts to b/d bone
  2. increasing reabsorption of ca by kidneys
  3. increasing conversion of inactive vit D to active vit —–which then increases ca reabsorption from GI track
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20
Q

PTH causes elevated blood _____ and decreased ____

A

elev CA and decr Phosphate

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21
Q

Vit D _____ absorption of ____ and ____ from ____

A

increases abs calcium and phosphate from the gut

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22
Q

roles of vit d—3

A
  1. incrs abs of ca and phosphate in gut
  2. incrs bone resporption
  3. incrs phosphate reabs in kidneys
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23
Q

how does calcitonin decrease ca levels

A

using calcium to build bone–>decreasing renal reabsorption of ca.

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24
Q

scoliosis

  • define
  • assoc wit?
  • MC in?
  • MCC
A

*deviation of the spine from the vertical axis (cobb angle)
greater than 10 degrees aka cobb angle >10 degrees
*LATERAL curvature of the spine
*MC in females or ppl with fam hx
*MCC=idiopathic
*can be assoc with kyphosis (humpback) or lordosis (sway back)

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25
Q

screening for scoliosis

  • when?
  • whats test called
  • instrument?
  • abnormal findings
A

occurs during routine pediatric exam

  • adams forward bend test*
  • instrument=scoliometer
  • abnormal finding= anything over 7 degree curve is considered abnormal
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26
Q

most sensitive test for scoliosis

A

adams forward bend test

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27
Q

most definitive diagnosis for scoliosis

-finding?

A

xray–over 10 degreees as measured on the AP and lateral xray

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28
Q

treatment of scoliosis depends on what 3 things

A
  1. how bad the angle is
  2. the progression of the curve
  3. skeletal maturity of patient
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29
Q

Lumbosacral sprain/strain aka?

A

lower back pain

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30
Q

MCC of lower back pain?

A

lumbrosacral sprain/ strain

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31
Q

define lumbosacral sprain/strain

-moa

A

acute strain or tear of paraspinal muscles—-esp after twisting or lifting injuries

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32
Q

s/s of lumbosacral sprain or strain

A
  • back pain (lower)
  • muscle spasms
  • DOES NOT RADIATE to leg
  • NO neuro s/s
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33
Q

Dx for lumbosacral sprain/srain

A

clinical dx

xrays are not needed unless s/s persistnet >1 MO or red flag s/s present

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34
Q

define auto immune dz

A

groups of diseases (that often include joint involvement) where body’s own immune system attacks healthy tissue, skin, organs, joints, etc

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35
Q

what drugs are usually tx for rheum dzs (2)

A
  1. systemic glucocoticoid steorids bc the s/s are from immune system rxn—- steroids tamper down immune system
  2. DMARDS–>disease modifying AntiRheumatoid Drugs–>attempt to slow down dz effects on body
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36
Q

what are the lab tests commonly used with autoimmune dz (6)

A
  1. Erythrocyte Sedimentation Rate (ESR)
  2. C-reactive protein (CRP)
  3. Complement tests (C3, C4)
  4. Antinuclear Antibody (ANA)
  5. Rheumatoid Factor (RF)
  6. Anti-citrullinated protein antibody (ACPA)
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37
Q

what is ESR

  • is it specific?
  • what does high ESR mean
A

measures how quickly RBCs settle at bottom of test tube

  • –settle faster=inflammation
  • **it is non-specific and is elevated in many diff conditions
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38
Q

what is CRP

  • used for?
  • sensitive, specific?
A
  • used to detect or monitor significant inflammation in acute conditions—infections
  • used in monitoring chronic inflamm conditions to detect flare ups and det if tx is effective–EX: RA, Lupus, vasculitis)
  • sensitive but not specific
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39
Q

What is Complement tests

-when does it go up? go down?

A

C3 and C4

  • immune system proteins that normally rise dramatically just after an infection and injury
  • BUT in LUPUS—– where the immune system is constantly activated, the levels go down bc they stop responding as dramatically since there is chronic dz state
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40
Q

what is antinuclear antibody (ANA)

(+) test means?

A

they attack healthy body tissues— specifically targeting each cell’s nucleus
(+) ANA means immune syst has launched misdirected atttack on healthy tissue

41
Q

Rheumatoid factor (RF) what is it

  • diagnose wht?
  • sensitive? specific?
A
  • autoantibody that attacks healthy body cells
  • often used to diagnose RA
  • not sensitive
  • not specific
42
Q

Anti-citrullinated protein antibody (ACPA)

  • what is it
  • diagnoses wht?
A

*autoantibodies that are directed against peptides + proteins that are citrullinated–>test allows for EARLY diagnosis of RA

43
Q

patho for RA

-rf

A

hyperplastic synovial tissue (pannus) leads to destruction of joints
inflammation of the synovium=destruction of joint

**t-cell mediated—type IV **

RF

  • women
  • smoking
  • 20-40yo
  • HLA-DRA 1 and 4
44
Q

RF for RA (4)

A
  1. women
  2. 20-40 YO
  3. smoking
  4. HLA-DRA 1 & 4
45
Q

organsims assoc with reactive arthritis

A

GI: salmonella, shigella, campy, yersinia,
GU: chlamydia

45
Q

organsims assoc with reactive arthritis

A

GI: salmonella, shigella, campy, yersinia,
GU: chlamydia

46
Q

Polyarteritis Nodosa– what causes it

  • MC in who
  • incr assoc with what dz
A

type 3 hypersensitivity rxn–> leads to ischemia and microanurysms of affected vessels (CNS, GI and/or renal MC)

MC in men 40-60YO
incr assoc with Chronic HBV and HCV

47
Q

Polymyositis

  • cause
  • patho
  • RF
A

Unknown cause, but thought to be a genetically susceptible individual plus an environmental trigger leads to immune activation, which results in chronic inflammation.

*inflammatory myopathy due to CD8+ lumphocyte infiltration of endomysium
CD8+ lymphocyte infiltration of endomysium

RF

  • wonen
  • 30-50 YO
48
Q

SLE
patho
rf (8)

A

autoantibody production–deposition of immune complexes, complement activation and accompany tissue destruction/vasculitis

  • **multi-organ autoimmune disorder of CT
  • type III hypersen (Ag-Ab immune complexes)

RF

  • young females— onset=20-40s
  • AA
  • hispanic
  • native american
  • genetic + environmental
  • sun exposure
  • infections
  • estrogen—OCPs
49
Q

Congenital Hip Dislocation/Dysplasia

  • define
  • rf (4)
A

abnormality in shape and/or stability of femoral head and acetabulum

RF

  • breech presentation
  • first born child
  • females
  • fam hx
50
Q

Congenital Hip Dislocation/Dysplasia

  • define
  • when is this diagnosed
  • RF
  • PE
  • Dx
  • tx: <6mo, 6m-2yo
A
  • abnormality of the shape/stability of the femoral head + acetabulum
  • hip is examined at birth + every well-check visit up until 9 MO and/or child is walking independently

RF

  • Breech presentation
  • first born child
  • females
  • +fam hx

PE–looking for hip asymmetry, instability and limited abduction
1. BARLOW MANEUVER–>gentle adduction w.o downward pressure to feel for dislocatability—typically will hear a CLICK or CLUNK

  1. ORTOLANI MANEUVER–>abduction and elevation to feel for reducibility— resulting in a CLICK or CLUNK

OTHER FINDINGS: asymmetry, restricted hip abduction,

DX
*clinical with confirmation imaging (MC is US for kids <4MO)

TX
<6MO: Pavlik harness
6m-2y: closed reduction in OR
*monitoring with routine hip xrays until skeletal maturity

51
Q

RF for SCFE

A
  • children 8-16YO
  • obese
  • AA
  • males during growth spurt
  • if seen in kids b4 puberty–suspect hormonal or systemic disorders –hypothyroidism or hypopituitarism
52
Q

RF for Legg-Calve-Perthes disease (4)

-whats a decr RF?

A
  • age 4-10
  • males—4x more likely
  • obesity
  • coagulation abnormalities (face V leiden)

DECR RF: low incidence in AAs

53
Q

strongest bone in body?

A

femur

54
Q

what is the femur surrounded by

A

hamstrings and quads

55
Q

RF for Patellofemoral syndrome (chondromalacia)

A
  • cyclists
  • runners
  • women
56
Q

Rf for achilles tendon rupture

A

75% from sport related injury/weekend warriors

  • incr risk with fluoroquinolone use, corticosteroid injections
  • 30-50YO
57
Q

three ankle bones

A

tibia
fibula
talus

58
Q

ankle mortise

A

separation b/w end of tibia and talus bone

59
Q

RF for plantar fasciitis (5)

A
  • flat feet
  • high arches
  • heel spurs
  • females 40-60 YO
  • obese
60
Q

Neuropathic (charcot) arthropathy

A

Decrs sensation, autonomic dysfunction and repeptitve microtrauma leads to bone resoprtion and weakening

*seen with DM and tables dorsalis (tertiary syphilis)

61
Q

disruption of the articulation of the medial cuneiform and base of the 2nd metatarsal leading to ligamentous injury and/or fracture

A

Lisfranc injury

61
Q

Lisfranc injury

A

disruption of the articulation of the medial cuneiform and base of the 2nd metatarsal leading to ligamentous injury and/or fracture

62
Q

AC ligament provides ____ stability

A

horizontal

63
Q

muscles of rotator cuff

A

Supraspinatus
Infraspinatus
Teres minor
Subscapularis

64
Q

what nerve runs behind the humerus

A

radial nerve

65
Q

Osteomalacia

  • define
  • MCC
  • CM
  • labs
  • imaging findings
A

*disorder of decr mineralization of new bone growth
“softening of bones”

MCC=severe vit D deficiency–vit D absorbs CA–we need CA to mineralize or harden new bone
*can also be genetic cause—genetic disorder causes hypophosphatemia and chronic kidney dz

CM

  • bone pain + muscle weakness
  • bone tenderness
  • fractures
  • diff walking and waddling gait

LAB findings

  • elev alk phosph
  • elev PTH
  • low serum Ca and VIt d

Radiographic findings
Vertebral body trabeculae have a distinct appearance due to inadequate mineralization

66
Q

Osteogenesis Imperfecta

  • define
  • cm
  • pe
  • dx
  • tx
A
  • rare genetic CT dz
  • autosomal dominant dz
  • defects in gene that encodes for type 1 collagen
  • assoc with fetal perinatal death in severe form

CM
Severe, premature osteoporosis - multiple recurrent spontaneous fractures with minimal or no trauma in childhood, leading to limb deformities & shortening.
Deafness can also occur

PE

  • Blue tinted sclerae is a hallmark
  • Thin skin
  • Hyperextensibility of the ligaments
  • Otosclerosis with significant hearing loss
  • Brown teeth (hypoplastic and deformed as well). ***Not to be confused with *TETRACYCLINE TEETH.
  • Intelligence NOT affected

Dx: Clinical & x-rays; Confirmed with genetic/DNA testing

Management:
Bisphosphonates, physical therapy and surgical interventions. Most people are wheelchair bound.

67
Q

Scoliosis

  • define
  • assoc with?
  • list the four main categories and mc?
  • mc in who
  • CM
A

Scoliosis is characterized by lateral curvature of the spine
*Associated with rotation of the involved vertebrae and classified by its anatomic
location, in either the thoracic or lumbar spine.

*** four main categories of scoliosis:
idiopathic,
congenital,
neuromuscular (associated with a neurological or muscular disease), and syndromic (associated with a known syndrome).
*Idiopathic scoliosis accounts for around 80% of cases
It is more common in girls and typically develops around 10–12 years of age, but can occur earlier.

CM
*Scoliosis in adolescents does not typically cause significant pain.
If a patient has significant pain, she/he should be evaluated to rule out the possibility of some other disorder such as infection or tumor.
*Deformity of the rib cage and asymmetry of the waistline are clinically evident for curvatures of 30 degrees or more.
*Lesser curves may be detected through a forward bending test, which is designed to detect early abnormalities of rotation that may not be apparent when the patient is standing erect. Rotation of the spine may be measured with a scoliometer.
*Rotation is associated with a marked rib hump as the lateral curvature increases in severity.

68
Q

normal curve in lumbar region

A

anterior convexity—-lumbar lordosis

69
Q

normal curve in thoracic region

A

posterior convexiy—-kyphosis

70
Q

excesive kyphosis=?

A

PATHOLOGIC

Hyperkyphosis

71
Q

kyphosis often accompanied by?

A

scoliosis

72
Q

RF (4) for acute osteomyelitis

-mc pathogen

A

sickle cell dz
dm
immunocomp
preexisting joint dz

MC pathogen=staph aureus

73
Q

RF for OA

A

MODIFIABLE: obestiy, trauma, heavy labor

NON-MOD: incr age, female, fam hx

74
Q

gout

  • what is it
  • wht happens
  • what causes it
  • RF
A
  • inflammatory monoarticular arthritis
  • caused by crystalization of monosodium urate in joint
  • hyperuricemia is hallmark of dz but does NOT itself indicate gout
  • MC=men >30 YO
  • ETIOLOGY=incr production of uric acid OR decreased excretion of uric acid (90%)
  • inflamm in joint occurs when uric acid crystals collect in synovial fluid as extracellular fluid becomes saturated with uric acid
75
Q

Pseudogout aka Calcium Pyrophosphate Dihydrate Deposition dz

  • RF
  • define
A

RF

  • hemochromatosis
  • hyperparathyroidism
  • hypomagnesia

*calcium pyrophosphate dihydrate deposition in joints + soft tissue–leads to inflammation and bone destruction

76
Q

define tumor

A

abnormal growth
resulting from uncontrolled proliferation
serves no physiologic function
***Not all tumors are cancerous (malignant)
tumor=neoplasm

77
Q

define cancer

A

= refers to a malignant tumor and is not used to refer to benign growths, such as lipomas or hypertrophy of an organ

78
Q

can benign neoplasm be life threatening?

A

YES–>if they are enlarged in critical locations

EX: benign meningioma at the base of skull–compression of brain tissue

79
Q

Benign tumor

-structure

A
  • encapsulated
  • well differentiated
  • retain some normal tissue structure
  • DO NOT invade the capsules surrounding them
  • DO NOT spread to regional lymph nodes or distant locations

*generally named by tissue they arrise from + suffic -oma

80
Q

what is a benign tumor of smooth muscle of uterus called

A

leiomyoma

81
Q

benign tumor of fat cells

A

lipoma

82
Q

malignant tumor

  • growth rate
  • hallmark microscopic finding?
A

grow more rapidly vs benign
*loss of differentiation and absence of normal tissue organization=microscopically

*hallmark finding under microscope=ANAPLASIA–>the loss of cellular differentiation, irregularities of size/shape of nucleus and loss of normal tissue strcture

83
Q

carcinoma arises from

A

epithelial tissue

84
Q

adenocarcinomas arise from

A

ductal or glandular structure

85
Q

Mammary adenocarcinoma

A

malig tumor arising from breast glandular tissue

86
Q

-sarcoma

A

ca arrising from CT tissue

87
Q

rhabdomyoscarcoma

A

malig CA of skel muscle

88
Q

lymphomas

A

CAA of lympahtic tissue

89
Q

Leukemias

A

CA of blood forming cells

90
Q

two CAs that were not named after cell type from they originate

A

Hodgink dz

Ewing sarcoma

91
Q

transformation

A

process by which a normal cell becomes a CA cell

92
Q

autonomy

A

cancer cell’s independence from normal cellular controls— part of transformational process

93
Q

what do tranformed cells lack

A

normal “social controls” seen in nontransformed cells

94
Q

can CA cells die

A

no they are usually immortal—- unlimited life spand and will cont to divide for years

95
Q

are CA cells anchorage dependent or independent

A

independent— can proliferate suspended without attaching to a surface (unlike normal cells)

96
Q

Benign tumors VS Malignant

  • growth rate
  • capsule definition
  • degree of invasiveness
  • diffferentiated
  • miotix index
  • ability to metastisize
A

BENIGN

  1. grow slowly
  2. well-defined capsule
  3. not invasive
  4. well differentiated–look like the tissue from which they arouse
  5. low mitotic index– dividing cells are rare
  6. do not met

MALIG

  1. grow rapidly
  2. not encapsulated
  3. invade local strucutures and tissues
  4. poorly differentiated–may not be able to determine tissue of origin
  5. high mitotic index–many dividing cells
  6. can spread distantly–often thru BVs or lymphatics
97
Q

Osteoid osteoma

A

benign bone tumor characterized by small, radiolucent nidus—- produces high levels of prostaglandins

Pathophysiology 4 (8 decks)

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