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Block 7; Week 5-Michelle > Walby-Musculoskeletal > Flashcards

Walby-Musculoskeletal Flashcards

1
Q

What is the role of the 206 bones in the human body?

A 
Hematopoiesis
Mineral homeostasis (Ca++, Phos)
Mechanical support, protection of internal organs
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2
Q

What % of bone is inorganic, organic?

A

35% organic

65% inorganic

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3
Q

What is the main inorganic component of bone? What is its fcn? What other inorganic minerals are stored in bone?

A

calcium hydroxyapatite
gives bone its hardness
calcium, phosphorus, sodium, magnesium

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4
Q

What is osteoid?

A

unmineralized bone

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5
Q

What are osteoprogenitor cells? Where are they located?

A

pluripotential mesenchymal cells

**lie near & on bony surfaces

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6
Q

Where are osteoblasts located? WHat is one of their special functions?

A

on the surface of bones
**start mineralization
BUILD BONE

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7
Q

Where are osteoclasts located? What are they derived from?

A

come from: granulocyte-monocyte precursors in bone marrow
Location: Howship’s lacunae
**note; these guys are multinucleated!!

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8
Q

What is the function of osteocytes? How do they communicate b/w one another?

A

role in calcium & phosphorus homeostasis
**communicate via canaliculi
located in lacunae

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9
Q 
From inside to outside...list the locations of the following cell types in the bone...
Osteogenic Cell
Osteoclast
Osteoblast
Osteocyte
A 
Inside:
Osteoclast
Osteocyte
Osteoblast
Osteogenic Cell
Outside
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10
Q

The trabeculae of the bone is located where?

A

in the medullary cavity

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11
Q

What are the 2 layers of the periosteum?

A

outer layer: fibrous

Inner layer: osteogenic

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12
Q

Once again, what are osteoprogenitor cells derived from?

A

derived from mesenchymal cells

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13
Q

What do osteoblasts come from? Where are they located? What can they turn into?

A 
develop from osteoprogenitor cells
line the inner periosteum
endosteum
Haversian canal
**can become osteocytes after they gradually become surrounded by matrix
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14
Q

What is the function of osteocytes?

A

exchange of nutrients & waste w/ blood via canaliculi

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15
Q

What are osteoclasts derived from? What is their function?

A

come from bone marrow precursor

secrete enzymes, concentrate H+ & dissolve bone & calcium crystals. Release minerals into blood.

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16
Q

WHat is the order of cartilage to bone?

A 
resting/reserve
proliferation
hypertrophy
calcification
ossification
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17
Q

What are the proteins of the bone?

A

Type I Collagen–90% of organic component

Non collagen products of osteoblasts

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18
Q

What are the 2 types of collagen deposition?

A
  1. woven bone: random weave, weaker structure

2. lamellar bone: slow deposition, strong

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19
Q

When do you see woven bone?

A

fetal skeleton
adult pathologic states like fractures, tumors, infections
**anything that requires rapid growth

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20
Q

When do you see lamellar bone?

A

in adults, replaces woven bone @ growth plates

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21
Q

What are some of the uncommon congenital malformations that can happen to bone?

A

Absence of a phalanx, rib, or clavicle

Extra bones (supernumary ribs, digits)

Fusion of adjacent joints (syndactylism)

Formation of long, spider-like digits (arachnodactylism) as is seen in Marfan’s syndrome

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22
Q

What is the most common disease of the growth plate? …a hereditary condition of abnormal growth

A

achondroplasia aka osteochondrodysplasia

messed up maturation of cartilage–>disorganized chondrocytes

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23
Q

Which mutation causes achondroplasia? What is the result?

A
  • *caused by Fibroblast Growth Factor Receptor 3 mutation

* *results in dwarfism

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24
Q

Which hereditary pattern of achondroplasia is most common? What are the characteristics of this?

A

Heterozygous more common
aut dom
short extremities, bowed legs, lordosis, normal trunk, big head
normal life span, reproduction etc

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25
Q

What is it that causes the enlarged heads in heterozygous achondroplasia?

A

normal cranium & vertebrae

but frontal bossing & saddle nose

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26
Q

What happens in the less common homozygous achondroplasia?

A

compromised resp capacity
dead in infancy
GH unhelpful

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27
Q

What are mucopolysacchardisoses?

A

lysosomal storage disease
involving acid hydrolyses
**bad hyaline cartilage
**therefore, messed up growth plates & articular surfaces
See: chest wall deformities, short stature, malformed bones

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28
Q

What is osteogenesis imperfecta?

A

brittle bone disease
abnormal Type I Collagen formation–too little bone, multiple fractures
a condition of abnormal matrix

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29
Q

What is the clinical presentation of OI?

A 
lax joints
blue sclera (so thin you can see the veins!)
deafness (fracture inner ear bones)
thin skin
small & discolored teeth
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30
Q

What exactly happens to the bone in OI?

A

cortical thinning
attenuation of bony trabeculae
woven bone instead of trabecular bone

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31
Q

What is OI often misdiagnosed as?

A

child abuse

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32
Q

What are the 4 major types of osteogenesis imperfecta?

A
  1. (aut dom) postnatal fractures w/ blue sclera & deafness
  2. (aut rec) perinatal demise
  3. (aut rec) progressive deformation & growth retardation, hard to survive
  4. (aut dom) postnatal fractures without blue sclera
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33
Q

Survivors of OI usu have an aut dom form. Types I & 4. What are their features?

A

hearing deficits
blue yellow teeth
all have fractures

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34
Q

Give 3 categories of metabolic disorders affecting bone.

A

Nutritional
Endocrine
Osteoporosis

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35
Q

Vit C deficiency can mess with bone as a nutritional metabolic disorder…leading to…

A

Scurvy

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36
Q

Vit D deficiency can mess with bone as a nutritional metabolic disorder…leading to…

A

Rickets & Osteomalacia

Soft bones w/ more osteoid & less mineralization

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37
Q

What is an example of an endocrine metabolic problem with bone?

A

hyperparathyroidism

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38
Q

What is osteoporosis? What are the different subtypes?

A

decreased bone mass & density=increased fragility
normal ratio of minerals to protein matrix
Can be local (w/ disuse) or diffuse
Can be primary or secondary

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39
Q

Which type of people suffer from primary osteoporosis?

A

postmenopausal women
senile people (men)
idiopathic in younger peeps

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40
Q

Which ethnicity is least likely to have osteoporosis?

A

African Americans

higher bone density

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41
Q

What are some osteoporosis risk factors?

A
  • *Excessive alcohol, caffeine, carbonated beverages
  • *Cigarette smoking
  • *Anticonvulsants (phenytoin), Benzodiazepines (valium & xanax) - long term
  • *Hypogonadism (decr. testosterone)
  • *Hypercortisol states, therapeutic or adrenal pathology
  • *Hyperparathyroidism
  • *Inadequate Ca++ and Vitamin D in diet
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42
Q

When would an X-ray show osteoporosis?

A

only after 30-40% of the bone mass is depleted.

USE A DEXA SCAN

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43
Q

T/F Serum Ca++, Phosphorus, Alkaline pHosphatase are helpful in diagnosis of osteoporosis.

A

False.

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44
Q

Where do you often see fractures when you have osteoporosis?

A

painful vertebral fractures in thoracic & lumbar regions
loss of height
deformities: kyphoscoliosis, lordosis
fractures of wrist & weight bearing bones, femoral neck, pelvis, spine

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45
Q

How do people die from osteoporosis? How many people per year do die from it?

A

die from PE or pneumonia after immobility from fall

40K-50K per year die.

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46
Q

When do you reach your peak bone mass?

A

3rd decade of life
b/c with time osteoblasts & osteoprogenitor cells have decreased biosynthetic ability over time
after 30 yo, 0.7% decrease in mass/year

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47
Q

Where does the bone loss begin after the third decade of life?

A

begins in spin & femoral head

increased trabecular bone

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48
Q

What happens if you have calcium intake in adolescence?

A

esp common in adolescent girls
get lower peak bone mass
predisposed to osteoporosis

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49
Q

What are hormonal factors in osteoporosis?

A

deficiency in estrogen
deficiency in testosterone
**increased bone resorption

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50
Q

What is the mechanism of estrogen in healthy bones?

A

decreased estrogen
increased IL-1 from blood monocytes
IL-1 is a potent activator of osteoclasts
osteoblasts activated, but not as much
bones w/ increased surface area (like trabecular bone of vertebral bodies)–>micro fractures!

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51
Q

What is a notable bone disease of osteoclast dysfunction?

A

Pagets Disease aka osteitis deformans

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52
Q

What are the 3 phases of Paget’s?

A

Phase 1: osteolytic (osteoclasts active (10-12 nuclei) & predominate), hypervascular, bone loss
Phase 2: Mixed osteoclast/osteoblast, but osteoblasts predominant.
Osteosclerotic Phase: Burn out!

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53
Q

What happens to the bone marrow in Paget’s disease–phase 2?

A

replaced by CT that has osteoprogenitor cells & blood vessels

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54
Q

What does the bone end up looking like after the phases of Paget’s?

A

mosaic, jig saw puzzle
woven bone present
weak & prone to fractures

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55
Q

What age group & race do you usu seen Paget’s in?

A

Age group: 5th decade

Race: Northern Europe & US, excluding Scandinavians

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56
Q

What is thought to cause Paget’s disease?

A

a slow virus, paramyxovirus-like deal found in osteoclasts

virus induces production of IL-6, activates osteoclasts

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57
Q

What percentage of Paget’s cases are monostotic (1 lesion)? Where are these lesions usu located?

A

10%

tibia, ileum, femur, skull, vertebrae, humerus (more proximal things)

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58
Q

What percentage of Paget’s cases are polyostotic (multiple lesions)? Where are these lesions located?

A

90%

pelvis, spine, skull (more axial skeleton)

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59
Q

What are the symptoms of Paget’s disease?

A 
often asymptomatic
headache, hearing loss, visual problems
pain localized to bone b/c of micro fractures or bone overgrowth into nerve
leonine facies
bowing bones w/ weight
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60
Q

What is leonine facies?

A

overgrowth of craniofacial bones

  • *also seen in leprosy
  • *difficult to stand upright b/c of weight of bone
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61
Q

What can happen to blood flow in severe polyostotic disease?

A

increased blood flow w/ a fcnl AV shunt

high output cardiac failure

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62
Q

Which bone tumors are seen in paget’s disease?

A

giant cell tumor (benign)

sarcomas (seen w/ severe polyostotic disease)

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63
Q

T/F Extramedullary hematopoiesis is seen in Paget’s b/c of depletion of normal bone marrow after the 3 phases.

A

True!

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64
Q

What are the lab findings in Paget’s? Note: not that helpful in diagnosis.

A

Non-specific, but include:
elevated serum alkaline phosphatase
elevated urinary hydroxyproline
Normal serum calcium and phosphate

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65
Q

WHat is the treatment for Paget’s?

A

anti-resorptive agents that inactivate osteoclasts
Bisphosphonates (Fosamax)
calcitonin

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66
Q

What is osteopetrosis?

A

Stone Bone or Marble Bone
abnormally brittle bone
can cause osteosclerosis
**one type exhibits carbonic anhydrase II deficiency (necessary to acidify an environment–osteoclasts can’t do their thing)

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67
Q 
In Osteitis fibrosa cystica...what's the deal with the following:
calcium
phosphate
alkaline phosphatase
PTH
other characteristics?
A

calcium: up
phosphate: down
alkaline phosphatase: up
PTH: up
other characteristics? brown tumors

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68
Q 
In osteomalacia & rickets...what's the deal with the following:
calcium
phosphate
alkaline phosphatase
PTH
other characteristics?
A

calcium: down
phosphate: down
alkaline phosphatase: up
PTH: up
other characteristics? soft bones

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69
Q 
In osteopetrosis...what's the deal with the following:
calcium
phosphate
alkaline phosphatase
PTH
other characteristics?
A

calcium: normal
phosphate: normal
alkaline phosphatase: up
PTH: normal
other characteristics?
thick dense bones aka marble bone

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70
Q 
In osteoporosis...what's the deal with the following...
calcium
phosphate
alkaline phosphatase
PTH
other characteristics?
A

calcium: normal
phosphate: normal
alkaline phosphatase: normal
PTH: normal
other characteristics?
decreased bone mass

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71
Q 
In Paget's disease...what's the deal with the following?
calcium
phosphate
alkaline phosphatase
PTH
other characteristics?
A

calcium: normal
phosphate: normal
alkaline phosphatase: variable by stage
PTH: normal
other characteristics?
abnormal bone architecture

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72
Q

Give an example of a bone problem that has defective mineralization v. defective metabolism. What’s the difference?

A

Vit D deficiency–defective mineralization. Increase in osteoid
Osteoporosis–defective metabolism. Mass decreased, but bone is normal.

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73
Q

What is the precursor to Vit D3 in the skin? In the plant food?

A

Skin: 7-dehydroxycholesterol

Plant Food: ergosterol

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74
Q

What does Vit D bind to for transport in the body?

A

alpha 1 globulin (d binding protein)

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75
Q

What is VIt D converted to in the liver? In the kidney?

A

Liver: converted to 25-OH Vit D
Kidney: 1,25 OH2 active form

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76
Q

What are the 3 mechanisms that regulate Vit D?

A
  1. elevated active Vit D3 inhibits alpha hydroxylase in kidney
  2. hypocalcemia–>PTH up–>alpha hydroxylase activated
  3. hypophosphatemia–>alpha hydroxylase activated
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77
Q

What are the functions of VIt D?

A
  1. stimulates intestinal absorption of Ca++ & phosphate
  2. w/ PTH mobilizes Ca++ from bone
  3. w/ PTH causes reabsorption of Ca++ from renal tubules
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78
Q

What is the function of VIt D during times of hypocalcemia?

A

works with PTH

maintains plasma level of ca

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79
Q

What is the mineralization function of VIt D?

A

required for normal mineralization of epiphyseal cartilage & osteoid matrix

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80
Q

What is the effect of Vitamin D Deficiency?

A

hypocalcemia in blood

**either too much resorption of bone then results or lack of proper mineralization

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81
Q

What are some factors that can cause Vit D Deficiency?

A 
not enough sunlight
decreased intestinal absorption
enhanced degradation b/c of drugs--affects cyt p450
liver disease
renal disease
82
Q

What is the basic lesion of VIt D Deficiency?

A

excess of unmineralized matrix

83
Q

What happens in rickets?

A

overgrowth of epiphyseal cartilage
deposition of osteoid matrix

Disruption of orderly replacement of cartilage by osteoid matrix, with enlargement and lateral expansion of osteochrondral junction

Abnormal growth of capillaries and fibroblasts in disorganized zone because of microfractures

Deformation of skeleton due to loss of structural rigidity of developing bones

84
Q

What are the clinical manifestations of Rickets?

A 
frontal bossing
rachitic rosary
pidgin breast
Harrison's groove
deformities of pelvis, long bones, lumbar lordosis & bowing of legs
85
Q

What is rachitic rosary?

A

deformation of chest from overgrowth of cartilage or osteoid at costochondral junction
**Rickets

86
Q

What is pidgeon breast?

A

anterior protrusion of the sternum
pull of resp muscles on the weak metaphyseal areas of ribs
**Rickets

87
Q

What is Harrison’s groove?

A

girdling of thoracic cavity at lower margin of rib cage due to pull of diaphragm

88
Q

What is osteomalacia?

A

Derangement of remodeling process that occurs throughout life

Newly formed osteoid matrix is inadequately mineralized, with resultant Excess of persistent osteoid
Contours of bone not affected, but Bone is weak and prone to microfractures, most likely affecting vertebral bodies and femoral necks

89
Q

PTH regulates homeostasis of what? Increased Parathyroid hormone levels cause what?

A

Calcium!
stimulate osteoblast receptors
release mediators
increase osteoclast activity

90
Q

Which is more severe..primary or secondary hyperparathyroidism?

A

primary is more severe

91
Q

The changes involved in hyperparathyroidism are collectively known as what?

A

osteitis fibrosa cystica

92
Q

Which type of bone is more affected by hyperPTH…

cancellous or cortical

A

Cortical more affected!

93
Q

What happens to teeth with HyperPTH?

A

subperiosteal resorption produced thin cortex
loss of lamina dura around teeth
teeth are loosened!!

94
Q

What causes the brown tumors of hyperparathyroidism?

A

microfractures & secondary hemorrhages cause influx of multinucleated macrophages & fibrous tissue. Form tumor.

95
Q

What is renal osteodystrophy?

A

skeletal changes due to chronic renal disease
See:

Increased osteoclastic bone resorption which mimics osteitis fibrosa cystica
Delayed matrix mineralization (osteomalacia)
Osteosclerosis
Growth retardation
Osteoporosis

96
Q

What is the mechanism of renal osteodystrophy?

A

renal failure–phosphate retention
hyperphosphatemia causes hypocalcemia–causes secondary hyperparathyroidism
kidneys damaged–less active Vit D
inhibited renal hydroxylase b/c of high phosphate levels
reduced intestinal absorption of Ca++ b/c of that low VIt D

97
Q

What is the result of increased PTH levels in renal osteodystrophy?

A

Increased osteoclast activity
parathyroid glands more sensitive to depressed calcium
PTH retained in body

98
Q

Low levels of VIt D3 & Ca++ in renal osteodystrophy contribute to the progression to what?

A

osteomalacia

99
Q

Strangely, iron accumulation happens in renal osteodrystrophy. What is another deposition in bone due to the drugs used to bind phosphate?

A

aluminum deposition in bone

100
Q

What is a simple fracture? A compound fracture?

A

simple: if overlying tissue is intact
compound: if skin is broken

101
Q

What is a comminuted fracture?

A

if bone is splintered

102
Q

What is a displaced fracture?

A

if ends of bone at fracture site are not aligned

103
Q

What is a stress fracture?

A

if fracture develops slowly b/c of increasing repetitive loads that cause a break

104
Q

Describe briefly the process of a bone fracture healing.

A 
fracture
blood clot
bone near the break is dead
fibroblasts move in & build on the fibrin matrix
osteoclasts & vessels move in
cartilage forms first
then woven bone (non weight bearing)
months later: lamellar bone
105
Q

What is avascular necrosis? What are other names for it?

A 
**necrotic bone due to ischemia--usu in hip
aka
bone infarction
osteonecrosis
aseptic necrosis
ischemic bone necrosis
106
Q

What are possible causes of avascular necrosis?

A

prior steroid admin
idiopathic!
Other possibilities: CT disease, sickle cell (plugs small vessels of bone during crisis), radiation, alcohol abuse, tumors, trauma

107
Q

What are the 2 types of avascular necrosis?

A

subchondral infarct: triangular articular cartilage viable b/c of synovial fluid contact
medullary infarct: cortex uninvolved due to collateral blood flow

108
Q

What is the clinical course of subchondral infarcts? Medullary infarcts?

A

Subchondral: chronic pain, if cartilage collapses-severe osteoarthritis
Medullary: silent & stable
**associated with Gaucher’s disease (sphingolipid accumulation)
dysbarism
hemoglobinopathies

109
Q

What is the cause of pyogenic osteomyelitis?

A

bacteria (extension from acute infection of an adjacent joint)
traumatic implant after fracture
usu staph aureus!

110
Q

In neonates with pyogenic osteomyelitis…what is usu the causative organism? In sickle cell patients? With trauma?

A

Neonates: E coli or group B strep
Sickle Cell: Salmonella
Trauma: Mixed bacterial infections

111
Q

Where do pyogenic osteomyelitis abscesses usu form in children? In adults?

A

Children: the metaphysis
Adults: anywhere
**can sometimes turn into a squamous cell carcinoma if it leaks into a sinus

112
Q

What is chronic osteomyelitis?

A

follows an acute infection
no more neutrophils, now lymphocytes & plasma cells
residual necrotic bone can be resorbed by osteoclasts or surrounded by a rim of new reactive bone

113
Q

What is sequestrum?

A

residual necrotic bone seen in chronic osteomyelitis

114
Q

What is involucrum?

A

big sections of residual necrotic bone surrounded by a rim of reactive new bone

115
Q

What is a Brodie’s abscess?

A

well defined rim of sclerotic bone around a residual abscess

116
Q

What are the symptoms of chronic osteomyelitis? What are the imaging studies? What is the treatment?

A

symptoms: fever, malaise, leukocytosis
Routine radiographic
Radionuclide scan (gallium)
Treatment: vigorous antibiotic therapy

117
Q

What can be some bad results of chronic osteomyelitis?

A

pathologic fractures
bacteremia
endocarditis
**sometimes amyloidosis, squamous cell carcinoma in sinus tracts

118
Q

What is tuberculosis osteomyelitis?

A

spread via blood usu
seen in AIDs patients
bacillus starts the infection in synovium where there is oxygen & then it spreads to the bone
spinal lesions spread to adjacent soft tissue (pott’s disease)

119
Q

What is the most common malignant tumor of the bone?

A

osteogenic sarcoma

120
Q

Usu if you see a bone tumor in the first 3 decades of life…is it benign or malignant? In elderly?

A

Younger people: benign

Elderly: malignant

121
Q

How are bone-forming tumors usu deposited? What are osteomas?

A

deposited as woven trabeculae
variably mineralized
Osteomas: oval projections from subperiosteal or endosteal surfaces of the bone cortex

122
Q

Are osteomas malignant?

A

No! They are benign.
Look like normal bone under histo.
Can impinge on brain, eye function

123
Q

Which syndrome is associated with multiple osteomas on the skull?

A

Gardner’s Syndrome

124
Q

WHile osteoid osteomas & osteoblastomas are identical on histo…they have a size difference. What is it? What are other shared features?

A 
Osteoid Osteomas: 2 cm in size
**occur in 20s & 30s
begin small, round, radiolucent "nidus" that becomes sclerotic or mineralized w/ a rim of bone 
they are well circumscribed
will recur if not excised
125
Q

What are distinguishing features of osteoid osteoma?

A

peripheral skeleton–femur or tibia
painful at night
too much prostaglandin E2
relieved by aspirin

126
Q

What are the distinguishing features of osteoblastomas?

A

spine involved
possibly painful–dull ache
aspirin ineffective

127
Q

How does osteogenic sarcoma form?

A

malignant mesenchymal cells form in the bone matrix
p53 tumor suppressor gene mutates
usu occurs in the metaphysics of long bones, often in the knee
usu <20 yo

128
Q

If osteogenic sarcoma is secondary…what is the original cause?

A

Paget’s disease

radiation

129
Q

WHat does osteosarcoma look like microscopically?

A

islands of primitive bony trabeculae

rim of malignant osteoblasts

130
Q

What is the course of osteosarcoma?

A

aggressive lesions
metastasize via blood
lung mets 20% at the time of initial diagnosis

131
Q

What is osteochondroma?

A

most common benign tumor in bone
mature bone with a cartilaginous cap (cauliflower look)
arise from metaphysics near growth plate of long bones, anchored to the cortex
asymptomatic

132
Q

What is endochondroma aka chondroma?

A

benign lesion of mature hyaline cartilage
usu seen in short tubular bones of hands & feet
asymptomatic, but could be painful
in 1/3 of patients–could be a chondrosarcoma

133
Q

What is Ollier’s disease?

A

multiple endochondromas

on one side of the body

134
Q

What is Maffucci’s syndrome?

A

multiple endochondromas

associated with hemangiomas of soft tissue

135
Q

What is chondrosarcoma?

A 
matrix forming bone tumor
seen in middle-aged & older people
associated with endochondroma
starts in medullary cavity
central skeleton affected
mets to lungs
136
Q

What is the giant cell tumor of the bone?

A

occurs in epihpyses of long bones
usu benign
soap bubble appearance on radiology
neoplastic mononuclear cells–abundance reactive osteoclast-like multinucleated cells

137
Q

What gender & age group does giant cell tumor of bone usu occur in?

A

more often in females

20-40yo

138
Q

What is Ewing’s Sarcoma?

A 
2nd most common childhood malignancy of bone
affects femur, tibia, pelvis usu
pain & inflammation
expanding intramedullary mass
abundant necrosis
139
Q

Due to the abundant necrosis what is ewing’s sarcoma sometimes misdiagnosed as?

A

osteomyelitis

140
Q

Somehow related to Ewing’s Sarcoma…a translocation t(11,22) can cause what?

A

primitive neuroectodermal tumors

141
Q

What does Ewing’s sarcoma look like on histo?

A

small blue cell tumor
sheets of small cells with uniform nuclei
contain glycogen

142
Q

What is multiple myeloma?

A

pockets of plasma cells
abundant cytoplasm, large eccentric nuclei with clock face chromatin
produce Ig

143
Q

What is fibrous dysplasia?

A

benign tumor like condition with possible fractures
fibrous tissue replaces normal trabecular bone–get disorderly islands of deformed bone
mono-ostotic (more common) & poly-ostotic form

144
Q

What’s the deal with the mono-ostotic form of fibrous dysplasia?

A

begins in adolescence

happens in ribs, calvarium, femur, tibia, jaw

145
Q

What’s the deal with the poly-ostotic form of fibrous dysplasia?

A

adulthood issues
craniofacial involvement
associated with endocrine abnormalities
unilateral bone lesions & cafe au lait spots

146
Q

What is osteoarthritis?

A

most common disorder of joints
not inflammation
degeneration of articular cartilage–wear & tear
usu primary
can be secondary to a deformed joint from a metabolic disease

147
Q

What are the changes in composition & mechanical properties of cartilage seen in osteoarthritis?

A

increased water & decreased proteoglycans
weakening of collagen network (type II)
chondrocytes secrete IL-1–this activates proteolytic enzymes & collagenases

148
Q

WHat is the eburnation that happens with osteoarthritis?

A

subchondral bone becomes thickened

gives appearance of ivory

149
Q

HOw can cysts form in the bone with osteoarthritis?

A

form in the bone as cracks in cartilage allows synovial fluid to leak in.

150
Q

What are Herberden’s nodes in osteoarthritis?

A

these are osteophytes on distal interphalangeal joints

151
Q

What is rheumatoid arthritis?

A

systemic chronic inflammatory disease
affects many organ systems, including joints
more often in females, 40s & 50s

152
Q

What is the clinical presentation of rheumatoid arthritis?

A 
morning stiffness
heat & movement alleviate
joint swelling, redness, warmth
neutrophils present
radiology shows erosions
**usu small joints & symmetric joint involvement
not DIP joints
153
Q

What types of cells are seen in the synovium & synovial fluid of a rheumatoid arthritis patient?

A

infiltration of lymphocytes, macrophages, plasma cells in synovium
neutrophils may be in the synovial fluid
synovial lining cells proliferation & become hypertrophic
see villous projections
sometimes see lymphoid follicles

154
Q

Where do subcutaneous nodules form in a rheumatoid arthritis patient? What do they look like microscopically?

A 
at areas of pressure, maybe elbow
microscopically:
fibrinoid necrosis
palisading macrophages
rim of granulation tissue
155
Q

Infectious Arthritis (suppurative) is usu caused by which bacteria? What are some predisposing factors for this ?

A 
most commonly: GC, staph, strep, H influenza, gram neg rods
salmonella-sickle cell patients
Factors:
immunodeficiency
joint trauma
IV drug use
156
Q

Infectious Lyme Disease is caused by which organism? Pathway of infection? AFfect on joints?

A 
Borrelia Burgdorferi
Rodents--Humans via deer ticks
joints: ones that are large
can look like rheumatoid at first
extensive erosion of large joint cartilage
157
Q

WHat is gout?

A

uric acid (from purine metabolism) accumulation as monosodium irate crystals in joints
recurrent episodes of acute arthritis–esp in 1s metatarsal
tophi

158
Q

What do the monosodium urate crystals look like microscopically?

A

needle-shaped

birefringent: look yellow in one direction & blue in another

159
Q

What are tophi?

A

large accumulations of crystalline material in soft tissue

can create a chronic granulomatous reaction

160
Q

Most gout is primary & is caused by what?

A

overproduction of uric acid

unknown enzyme defects

161
Q

10% of gout cases are secondary. to what for example?

A

lymphoma or leukemia treatment
as tumors are lysed–proteins released for degradation
chronic renal insufficiency-can’t get rid of the uric acid
lesch-nyhan syndrome-lack of HGPRT enzyme

162
Q

T/F Urate crystals in synovium of a gout patient are chemotactic & active complement, attract neutrophils & macrophages to joint & synovium & create arthritis.

A

What do you know–true!

163
Q

What is pseudo gout?

A

deposition of calcium pyrophosphate crystals
found in knee after trauma or surgery
can be associated with systemic disease–like hemochromatosis

164
Q

Which joints are often associated with pseudo gout? HOw long do the attacks last?

A

1 day-4 weeks

involves knees, ankles, wrist, elbow, hips, shoulders

165
Q

How do the crystals appear microscopically in pseudo gout?

A

coffin-shaped

weakly bi-refringenet

166
Q

Where do the calcium pyrophosphate crystals of pseudo gout come from?

A

nucleosides in chrondocytes

167
Q

What is a motor unit?

A

motor neuron w/ a peripheral axon that extends to another motor neuron & connects via a neuromuscular junction

168
Q

What is neurogenic atrophy of skeletal muscle?

A

happens when muscle is deprived of normal innervation

progressive atrophy of Type 1 & 2 fibers

169
Q

What are the clinical features of neurogenic atrophy?

A

muscle weakness

in infants: floppy baby syndrome

170
Q

What is the morphology of neurogenic atrophy?

A

atrophy in small group clumps b/c one nerve supplies one motor unit

171
Q

T/F Type I fibers are fast twitch.

A

False. They are slow twitch.

172
Q

It is difficult to distinguish neurogenic atrophy from other types of atrophy related to type II myofibers. What are the causes of fast twitch atrophy?

A

disuse
glucocorticoid use that is longterm
hypercortisol state

173
Q

What is myasthenia gravis?

A

acquired autoimmune disorder of neuromuscular junctions
more common in females
antibodies form to the acetylcholine receptor
some sort of relationship w/ a messed up thymus

174
Q

What are some clinical features of myasthenia gravis?

A

ptosis or diplopia
facial & neck muscles or resp muscles can be messed up
progressed throughout the day

175
Q

What is the treatment for myasthenia gravis?

A

anticholinesterase agent (edrophonium chloride)
cholinesterase inhibitors
thymectomy

176
Q

What’s the deal with Duchenne Muscular Dystrophy?

A

x-linked, affects more males
muscle weakness, proximal
calf muscles weak & large
absence of structural proteins (dystrophin)

177
Q

What does DMD look like microscopically?

A

CT increased
marked variation in muscle fiber size
hypertrophy & atrophy of adjacent fibers

178
Q

WHat’s the deal with Becker Muscular Dystrophy?

A

X linked
mutation in dystrophin
less severe than DMD

179
Q

What is rhabdomyoma?

A

cardiac muscle neoplasm associated with tuberous sclerosis

180
Q

What is rhabdomyosarcoma?

A

most common soft tissue sarcoma in peds

181
Q

What are some other variants of rhabdomyoma?

A

embryonal–head neck GU, retroperitoneal
Alveolar
Pleomorphic Type

182
Q

When a rhabdomyoma is found in the GU tract what is it called?

A

sarcoma botryoides
it looks gelatinous & grape like structures are present
may be primitive small round blue cells with scattered strap cells (skeletal muscle)

183
Q

How are soft tissue tumors classified?

A

fat, muscle, fibrous tissue

184
Q

What are the associative “causes” of soft tissue tumors?

A 
Radiation therapy
Chemical and thermal burns
Trauma
Exposure to some organic chemicals
AIDS/Kaposi’s sarcoma/virus
185
Q

What is a lipoma?

A

most common soft tissue tumor
benign slow growing masses, usu painless
comprised of mature fat cells, yellow in color

186
Q

What is a painful form of a lipoma? How is it cured?

A

angiolipoma: local pain on velar surface of the forearm

* *cured by simple excision

187
Q

What is a liposarcoma?

A

arise in deep tissues of proximal extremities or retroperitoneum
can also be in lower extremities or abdomen
appear in 50s or 60s

188
Q

WHat is nodular fasciitis?

A

a fibrous tissue tumor
most commonly found in upper extremities & trunk
grow rapidly!
hx of trauma sometimes in patients

189
Q

Is a nodular fasciitis a neoplasm? WHat is its sometimes confused with?

A

No, not a true neoplasm. Caused by an over-reaction of fibroblasts.
**can be confused with sarcoma b/c of cellularity

190
Q

What is fibromatosis?

A

group of fibroblastic proliferations
infiltrative
recur after excision
deep form more aggressive than superficial

191
Q

T/F Fibromatosis is an example of a true neoplasm.

A

False.

192
Q

What are the 2 superficial types of fibromatosis?

A

Duptyren’s contracture (palmar fibromatosis)

Peyronie’s DIsease (penile fibromatosis)

193
Q

What is the name of the tumor included in the deep fibromatosis?

A

desmoid tumor

194
Q

WHat is a fibrosarcoma?

A

comprised of fibroblasts
originates in fibrous tissues of bones & invades long or flat bones like femur, tibia, mandible
favors deep tissues of thigh, knee, trunk
metastasizes to the lungs via blood

195
Q

Central fibrosarcoma arises from where?

A

intramedullary canal

196
Q

Peripheral fibrosarcoma arises from where?

A

arising from periosteal tissues

197
Q

What is the infantile-type of fibrosarcoma?

A

usu congenital

presents in first 2 years of life

198
Q

What is the common age & gender for fibrosarcoma?

A

male

30-40

199
Q

WHat are fibrohistiocytic tumors?

A

benign–aggressive malignant tumors
most important type: malignant fibrous histiocytoma
aka pleomorphic sarcoma
favored sites: lower limbs & retroperitoneal areas

200
Q

What is the prompt of a fibrohistiocytic tumor? Which age do you usu see this in?

A

post-irradiation

50s-70s

201
Q

What is a synovial sarcoma?

A

arises from mesenchymal cells around joint cavities–not from synovial cells!
develop in vicinity of large joints of lower extremities, esp the knee

Block 7; Week 5-Michelle (11 decks)

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