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Block 7 Week 5 > Musculoskeletal-Dr. Walby > Flashcards

Musculoskeletal-Dr. Walby Flashcards

1
Q

What does the Musculoskeletal system include?

A

Bones, Joints, Soft tissue, Muscle

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2
Q

If you dont have vit C what will you get?

A

scurvy

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3
Q

if you dont have vit D what will you get?

A

rickets, osteomalacia

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4
Q

What are the 2 abnormalities of bone growth?

A

achondroplasia (aka ostechodrydysplasia)

Mucopoysacchardioses

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5
Q

What are the three types of osteomyelitis?

A

pyogenic
chronic
tuberculous

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6
Q

What are the four bone-forming tumors?

A
  1. osteomas
  2. osteoid osteoma
  3. osteoblastoma
  4. osteogenic sarcoma
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7
Q

What are some acquired metabolic disorders affecting bone?

A

osteoporosis
osteopetrosis
Paget’s disease

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8
Q

What is the CT of bone?

A

35% organic matrix

65% inorganic elements

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9
Q

(blank) percent of calcium is stored in the bone.
(blank) percent of phosphorus is stored in bone.
(blank) percent of sodium (Na+) and magnesium (Mg++)

A

99%
80%
65%

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10
Q

un-mineralized bone is known as (Blank)

A

osteoid

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11
Q

What is the inorganic component of bone and what is its function?

A

calcium hydroxyapatite-gives bone hardness

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12
Q

What do the organic components of bone made up of?

A

cells of marrow and proteins of matrix

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13
Q

What are osteoprogenitor cels and where do you find them?

A

pluripotential mesenchymal cells that lienear and on all bony surfaces

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14
Q

What do osteoblasts do?

A

build
(found on the surface of bones, synthesize, transport and arrange proteins of the matrix, starts process of mineralization)

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15
Q

Tell me about osteoclasts

A

derived form granulocyte-monocyte precursor
multinucleated
responsible for bone resorption
-reside in howships lacunae

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16
Q

What do osteocytes do?

A

important role in Ca2+ and phosphorus homeostasis; communicate with sruface and each other via canaliculi

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17
Q

Which has bigger lacunae, osteocytes or osteoclasts?

A

clasts!!!

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18
Q

Which is closer to the outside, spongy bone or compact bone?

A

compact bone

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19
Q

What do you find within the medullary cavity?

A

trabeculae

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20
Q

What is on the outside of ocmpact bone?

A

Periosteal vessels

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21
Q

Osteoprogenitor cells derived from (blank) cells

A

mesenchymal cells

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22
Q

Where do osteblasts develop from?

A

osteoprogenitor cells that line inner periosteum, the endosteum and lining the haversian canal.

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23
Q

Osteoblasts synthesize the (blank) components of bone matrix; some gradually become surrounded by matrix and become osteocytes.

A

organic components

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24
Q

(blank) lie in a lacuna within the matrix; involved in exchange of nutrients and wast with blood via canaliculi

A

osteocytes

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25
Q

(blank) are derived from a bone marrow precursor. They secrete enzymes and biochemically concentrate H ions to dissolve bone and calcium salt crystals thereby releasing minerals into blood.

A

Osteoclasts

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26
Q

(blank) forms 90% of the organic component of bone

A

Type I collagen

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27
Q

What are the 2 types of collagen deposition?

A

1) Woven bone

2) lamellar bone

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28
Q

Where do you see woven bone?

A
  • fetal skeleton
  • adult pathologic states requiring rapid growth (fractures, infections, tumors)
  • pattern is random weave and weaker
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29
Q

Where do you see lamellar bone?

A

seen in adults, replaces woven bone at growth plates, deposited slowlly, more stable and stronger than woven bone

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30
Q

What are these:
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

A

congenital malformations-uncommon

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31
Q

What is the most common disease of the growth plate?

A

Achondroplasia (aka osteochondrodysplasia)

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32
Q

What is achondroplasia?

A

impaired maturation of cartilage leading to disorganized chondrocytes caused by mutation in FGFR3

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33
Q

What does achondroplasia result in?

A

dwarfism

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34
Q

Tell me about heterozygous achondroplasia

A

more common

  • AD
  • infants have shortened extremities , normal trunks trunks and enlarged heads
  • normal life span
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35
Q

What will happen if you have homozygous achondroplasia?

A

-compromised respiratory capcity-> often die in infancy

growth hormone doesnt help!!!

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36
Q

What is this:
lysosomal storage disease invoving acid hydrolases-> results in abnormalities of hyaline cartilage, and hence growth plates and articular surfaces, due to abnormalities of chondrocytes, and hence growth plates, and articular cartilage.

A

Mucopolysaccahridoses

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37
Q

What do mucopolysaccharidoes manifest as?

A

as chest wall deformities, short stature, and malformed bones

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38
Q

What is this:
abnormal type I collagen formation-> afects joins, eyes (blue sclear), ears (deafness), skin and teeth….results in too little bone and results in multiple fractures.

A

Osteogenesis imperfecta

brittle bone disease

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39
Q

In osteogenesis imperfecta, there are four major types, what are they?

A

type 1: postnatal fractures with BLUE SCLERA, Deafness (AD)
type 2: perinatal demise (mostly AR)
type 3: progressively deforming w/ growth retardation (AR)
type 4: Postnatal fractures w/out blue sclerae (AD)

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40
Q

Survivors of osteogenesis imperfecta usually have what?

A
  • hearing deficits
  • blue-yellow teeth
  • all have fractures
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41
Q

What deficiency is this:

defective mineralization and increase in non-mineralized osteoid, bones are softer

A

Vit D deficiency

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42
Q

What is this:

decreased bone mass/densitiy-> increased fragility (no abnormality in ratio of minerals to protein matrix)

A

Osteoporosis

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43
Q

What are the primary types of osteoporosis?

A

postemenopausal women

senile

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44
Q

Who are most likely to get osteoporosis?

A

whites/mexican

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45
Q

What are risks for osteoporosis?

A

alcohol, caffeine, carbonation, smoking, anticonvulsants, benzos, hypogonadism, hypercortical states, hyperparathyroidism, inadequate Calcium and vit D

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46
Q

What is phenytoin (dilatin)

A

anticonvulsant

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47
Q

What is valium and Xane?

A

benzos

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48
Q

What is a test that is specific or sensitive to osteoporosis?

A

there isnt one :(

Using some DEXA bone scans to help

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49
Q

Why dont you use Xrays to diagnose osteoporosis?

A

cuz it wont show anything until 30-40% of bone mass is depleted

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50
Q

What is a scary complication of osteoporosis?

A

Pumonary embolism and pneumonia with a very high mortality (more than CA of the breast and endometrium combined)

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51
Q

When do you have peak bone mass and what affects this?

A

3rd decade

-genetic, vit D receptor, sex, race, activity, diet, hormonal status0

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52
Q

What happen to our osteoblasts and osteoprogenitor cells?

A

have decreased biosynthetic ability over time

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53
Q

Where do you start losing bone density?

A

spine and femoral head (increased trabecular bone here)

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54
Q

LOw (Blank) intake during rapid bone grwoth in girls leads to osteoporosis later in life

A

Calcium

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55
Q

What is postemenopausal osteoporosis?

A

yearly reducion in mass is 2% of cortical, 9% cancellous

  • 35-50% decrease in 30-40 years (80-90 yo)
  • 1/2 women-> osteoporotic bone fracture (1/40 men)
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56
Q

If you have a deficiency in (Blank) hormone that you get increase bone resportion

A

estrogen

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57
Q

What happens if you dont have estrogen?

A

get increases in IL-1 which increases increases osteoclast activity

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58
Q

How do you treat osteoporosis?

A

Medications, hormone replacement/ estrogen receptor modulators, calcitonin, vitamin replacement, exercise/activity, decrease in smoking, alcohol, corticosteroid use

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59
Q

Excercise helps with preventing osteoporosis, which is better, endurance training or weight training?

A

weight training

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60
Q

What is the most potent activator of osteoclasts?

A

IL-1

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61
Q

What bone is most affected by IL-1 induced osteoclast activity?

A

affects bones with increased surface area, such as the trabecular bone of vertebral bodies-resulting in progressive microfractures and vertebral collapse

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62
Q

Paget’s disease (osteitis deformns) is caused by (Blank)

A

osteoclast dysfunction

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63
Q

What are the three phases of Paget’s Disease?

A

1: osteoclast/osteolytic stage- hypervascularity, and bone loss
2: mixed osteoclastic/osteoblastic stage, which ends with a predominance of osteoblastic activity
3: culminates in a burnt-out quiescent osteosclerotic stage

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64
Q

When do you usually see Paget’s disease?

A

5th decade, slight male predominance-> usually white

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65
Q

What is the characteristic histologic feature of paget’s disease?

A

mosaic pattern, making bone appear like a jigsaw puzzle, virtually pathognomonic-> the woven bone is weaker and more prone to fracture

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66
Q

What are the three phases of pagets disease?

A

Osteolytic phase
mixed phase
steosclerotic phase

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67
Q

The (blank) is solid but woven and called “burned out

A

osteosclerotic phase

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68
Q

What causes Paget’s disease?

A

a “slow virus” made up of paramyxovirus like particles, this virus induces production of IL-6 which induced IL-1 which recruits osteoclasts

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69
Q

Many cases of pagets disease are (Blank) and only found incidntally on X-ray

A

asymptomatic

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70
Q

90% of polyostotic cases of Paget’s involve the (blank) (blank) and (blank)

A

pelvis, spine, skull

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71
Q

In paget’s disease what is a cardinal symptom?

A

Leonine faces (bone overgrowth in craniofacial area)

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72
Q

In severe polyostotic disease, the increased blood flow causes a (Blank) resulting in high output cardiac failure

A

functional arterio-venous shunt

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73
Q

In the skull, the cortex is thickened and irregular. The findings probably corresponds to the “cotton wool spots” seen on plain films in the later stages of (blank)

A

Paget’s disease

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74
Q

What are the lab findings of paget’s disease?

A
  • elevated serum alkaline phosphatase
  • elvated urinary hydroxyproline
  • normal serum calcium and phosphate
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75
Q

What is the tx of paget’s disease?

A

success wih anti-resorptive agents
(act to inactivate osteoclasts)
-bisphosphonates
-calcitonin

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76
Q

What is this:

bones are abnormally brittle and fracture despite excess deposits and increased density

A

Osteopetrosis (rare)

-can cause osteosclerosis (bone in bone appearance on radiology)

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77
Q

What causes osteopetrosis?

A

variant with carbonic anhydrase II deficiency

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78
Q

What does carbonic anhydrase do?

A

enzyme necessary for bones and renal tubular cells to excrete hydrogen ions and acidify their environment (this prevents osteoclasts from resorbing matrix)

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79
Q

What is this:
Decreased calcium, phosphate
elevated alkaline phosphatase, PTH

A

osteomalacia and rickets

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80
Q

What is this:

only alkaline phosphatase is elevated-> see thick dense bones also known as marble bone

A

Osteopetrosis

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81
Q

When you have a defect in vit D, you will get defective mineralization and an increase in (blank)

A

non-mineralized osteoid

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82
Q

How can you have a metabolism problem?

A

like in osteoporosis, mass is decreased but bone that is present has normal mineral content

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83
Q

Vit D gets converted to (blank) with UV light/

A

D3

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84
Q

If you get Vit D from plants, the precursor is ergosterol which is converted in body to (blank)

A

Vit D2

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85
Q

What are the three organs involved in vit D metabolism?

A

skin/sunlight, kidney, liver

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86
Q

What does Vit D do?

A
  • stimulates intestinal absorption of Ca and P
  • works w/ PTH in mobilization of Ca from bone
  • stimulates PTH dependent reabsorption of Ca in distal renal tubules
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87
Q

(blank) is required for nomal mineralization of epiphyseal cartilage and osteoid matrix.

A

Vit D

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88
Q

In vit D deficiency, the overall reaction results in (blank) which results in resorption of bone or lack of proper mineralization

A

hypocalcemia

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89
Q

WHat is the mechanisms of deformation in rickets?

A

overgrowth of epiphyseal cartilage

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90
Q

What are the clinical symptoms of rickets?

A
  • excess of osteoid->frontal bossing
  • square head
  • pidgeon breast
  • Harrison’s groove
  • Lumbar lordosis and bowing of the legs
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91
Q

What is this:

  • 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
  • bone is weak and prone to microfractures, most likely affecting vertebral bodies and femoral necks
A

Osteomalacia

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92
Q

What are the first bones that break in osteomalacia?

A

vertebral bodies and femoral necks

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93
Q

(blank) regulates calcium homeostasis

A

PTH

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94
Q

In hyperparathryoidism, what happens?

A

increased PTH levels-> stimulate receptors on osteoblasts

  • release of mediators
  • increase osteoclast activity
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95
Q

Increased osteoclast activity affects (blank) bone more than (blank)

A

cortical bone

cancellous bone

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96
Q

In hyperparathyroidism microfractures and secondary hemorrhages elicity influx of multinucleated macrophages and reactive fibrous tissue to form an (blank)

A

apparent mass known as “brown tumor”

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97
Q

THe changes caused by hyperparathyroidism is collectively known as (blank)

A

osteitis fibrosa cystica

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98
Q

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

A

renal osteodystrophy

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99
Q

What is the mechanism behind renal osteodystrophy?

A

renal failure results in phosphate retnetion-> hyperphosphatemia causes hypocalcemia, which causes secondary hyperparathyroidism

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100
Q

WHy will renal failure cause increase osteoclast activity?

A

renal failure-> lack of vit D and calcium-> upregulate PTH to increase Ca-> increased PTH leads to increase osteoclast activity

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101
Q

Low levels of Vit D and Ca contribute to the (blank)

A

osteomalacia

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102
Q

(blank) is a bone disease that occurs when your kidneys fail to maintain proper levels of calcium and phosphorus in the blood. It’s common in people with kidney disease and affects most dialysis patients.

A

Renal osteodystrophy

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103
Q

What is aluminum deposition in bone (iatrogenic) due to?

A

dialysate solutions and aluminum containing oral meds to bind phosphate (major cause)

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104
Q

Why is aluminum deposition bad?

A

interferes with deposition of calcium hydroxyapatite

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105
Q

What is a simple fracture?

A

(closed) if overlying tissue is intact

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106
Q

What is a compound fracture?

A

if fracture site communicates with skin surface, skin broken-> infection w/ S. aureus

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107
Q

What is a comminuted fracture?

A

if bone is splintered

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108
Q

What is a displaced fracture?

A

if ends of bone at fracture site not aligned

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109
Q

What is a stress fracture?

A

if fracture develops slowly due to increasing repetitive loads which eventually cause break

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110
Q

What happens post fracture?

A
  • bloot clot,
  • fibroblasts move in
  • osteoclasts and vessels move in, -cartilage forms early
  • woven bone forms first
  • after months woven bone changes to lamelar bone
  • healed bone is stronger than original bone
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111
Q

Whats up with cartilage and fractures?

A

found as a early part of healing of a fracture, if fracture is not immobilized then it may stay as cartilage

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112
Q

What are other names for avascular necrosis?

A

bone infarction
osteonecrosis
aseptic necrosis
ischemic bone necrosis

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113
Q

ALL instances of avascular necrosis result from (blank)

A

ischemia-> most commonly occurs in the hip

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114
Q

What are the most common causes of avascular necrosis?

A

idiopathic

prior steroid administrations (mechanism unclear)

115
Q

What can these cause:

CT diseases, sickle cell disease, radiation, alcohol abuse, tumors, trauma (ie joint displacement)

A

Avascular necrosis

116
Q

How come sickle cell can cause avascular necrosis?

A

cuz it can plug the small vessels

117
Q

What are the 2 types of avascular necrosis?

A

1) subchondral infarcts

2) medullary infarcts

118
Q

(blank) are triangular or wedge-shaped, they lay over articular cartilage and remain viable due to contact with synovial fluid for nutrients.

A

subchondral infarcts

119
Q

Subchondral infarcts are triangular or wedge-shaped,(blank) shaped overlying articular cartilage remains (blank) due to contact with synovial fluid for nutrients)

A

wedge shaped/ triangular
viable

(subchondral means under cartilage so just remember the cartilage remains intact and underneath it is messed up and the cartilage remains viable because of the synovial fluid giving nutrients to it)

120
Q

Medullary infarcts are (Blank) and cortex is (blank) involved due to collateral blood flow

A

geographic

not usually

121
Q

What do the symptoms of avascular necrosis depend on?

A

location and extent of infarction

122
Q

SUbchondral infarcts cause (blank)

A

chronic pain->

starts off as pain with movement then becomes persistant

123
Q

What is this:
cartilage may collapse and predisopose to severe osteoarthritis, with eventual joint replacement necessary (10% of all joint replacements)

A

Subchondral infarcts

124
Q

(blank) are clinically silent except for larger ones

A

medullary infarcts

125
Q

In (blank) disease, fatty substances-sphingolipids accumulate.

A

Gauchers disease

126
Q

Which type of infarct remains stable, medullary infarcts or subchondral infarcts?

A

medullary infarcts

127
Q

In pyogenic osteomyelitis, most cases are caused by (Blank) which typically reach bone by (blank)

A 
bacteria
hematogenous dissemination (major)
128
Q

What is the most common organism that causes pyogenic osteomyelitis?
What are some other common ones?

A

staph aureus

129
Q

What organism commonly causes pyogenic osteomyelitis in neonates?

A

E. coli and Group B strep

130
Q

What organism commonly causes pyogenic osteomyelitis in sickle cell patients?

A

salmonella

131
Q

What organisms commonly cause pyogenic osteomyelitis in trauma patients?

A

mixed baterial infections, including anaerobes

132
Q

In pyogenic osteomyelitis, up to (blank) percent of cases, a causative organism cannot be islated, due to prior antibiotic therapy, inadequate sampling or suboptimal culture methods

A

50%

133
Q

In children with osteomyelitis, what three things are common?

A

bone abscess
periosteal lift
extension to the joint

134
Q

Where does pyogenic osteomyelitis commonly occur in children?
Adults?

A

metaphysis

anywhere

135
Q

After an acute infection with pyogenic osteomyelitis, what occurs?

A

chronic osteomyelitis

136
Q

(blank) is a piece of dead bone that has become separated during the process of necrosis from normal or sound bone.

A

sequestrum

137
Q

What do you see in chronic osteomyelitis?

A

sequestrum surrounded by a rim of reactive new bone-> this is called involucrum
-Brodies abscess

138
Q

What is this:
well-defined rim of sclerotic bone surrounds a residual abscess
Where do you see this?

A

Brodies abscess

Chronic osteomyelitis

139
Q

How can you find chronic osteomyelitis?

A

radionuclide scans

140
Q

How should you treat chronic osteomyelitis?

A

vigorous antibiotic therapy +/- debridement

141
Q

What are some complications of chronic osteomyelitis?

A 
bacteremia
endocarditis
Systemic amyloidosis (rare)
squamos cell carcinoma along sinus tracts (rare)
142
Q

What is often seen associated with AIDS, it is spread hematogenously, favors long bones and vertebrae?

A

TB osteomyelitis

143
Q

In TB osteomyelitis, bacillus needs oxygen, infection usually starts at (Blank) then spreads into bone.

A

synovium

144
Q

In TB osteomyelitis, extension of infection to adjacent soft tissues is common in spinal lesions (Pott’s DIsease) and these are called (blank)

A

cold abscesses

145
Q

What are the four kinds of bone forming tumors?

A
  1. Osteomas
  2. Osteoid Osteoma
    3. Osteoblastoma
  3. Osteogenic Sarcoma (osteosarcoma)
146
Q

What are the three kinds of cartilaginous tumors?

A

Osteochondroma (osteocartilaginous exostoses)
Enchondroma (chondroma)
Chondrosarcoma

147
Q

What is the most common malignant tumor of bone?

A

osteogenic sarcoma

148
Q

Benign tumors are most common in the first (blank) decades of life

A

3

149
Q

Malignant tumors are most common in the (blank)

A

elderly

150
Q

What are the four bone-forming tumors?

A
  1. osteomas
  2. osteoid osteoma
  3. osteoblastoma
  4. osteogenic sarcoma (osteosarcoma)
151
Q

Bone forming tumors are usually deposited as (Blank) and are variably mineralized.

A

woven trabeculae

152
Q

Osteomas are bosselated, round to oval, and project from the (blank) or (bank) surfaces of the cortex

A

subperiosteal or endosteal

153
Q

Are osteomas benign or malignant?

A

benign-> but may impinge on brain, eye, or interfere w/ function of oral cavity

154
Q

Can osteomas undergo malignant transformation? WHat do they look like histologically?

A

NO!!!!!

normal

155
Q

Multiple osteomas (skull) may be associated with (blank) syndrome

A

Gardner’s syndrome (familial polyposis)

156
Q

What is the difference between osteoid osteoma and osteoblastoma?
When do they occur?

A

identical histology, but differ in size, location and symptoms
2nd and 3rd decades of life

157
Q

Osteoid osteomas by definition are how big?

what about osteoblastomas?

A

less than 2 cm

greater than 2 cm

158
Q

If you completely excise osteoid osteomas and osteoblastomas what will happen?

A

both will recur

159
Q

What is this:
occur in peripheral skeleton, femur or tibia (~50%)
Painful, usually at night
due to production of excess prostaglandin E2
-characteristically relieved by aspirin

A

Osteoid osteomas

160
Q 
What is this:
involves spine more frequently
sometimes painful
pain when present-dull ache
pain is NOT relieved by aspirin
A

osteoblastoma

161
Q

How do you get primary osteogenic sarcoma?

How do you get secondary osteogenic sarcoma arise from?

A
  • De novo

- in conjunction with Paget’s disease, radiation, etc.

162
Q

In whom does osteogenic sarcoma occur in?

A

people less than 20 years of age

-secondary form occurs in elderly

163
Q

Most osteogenic sarcomas occur where?

A

In metaphysis of long bones (60% about the knee)

164
Q

What mutation is associated with osteogenic sarcomas?

A

p53 tumor suppressor gene

165
Q

If you see primitive bony trabeculae and lung mets what should you be thinking?

A

osteosarcoma

166
Q

What are the three cartilaginous tumors?

A
  1. osteochondroma (aka osteocartilaginous exostoses)
  2. enchondroma (chondroma)
  3. chondrosarcoma
167
Q

What are the most common benign tumors of the bones?

A

osteochondroma (aka osteocartilaginous exostoses)

168
Q

What is an osteochondroma?

A

benign proliferation composed of mature bone with a cartilaginous cap (cauliflower look)

169
Q

Where do osteochondromas occur?

A

at metaphysis near growth plate of long bones, firmly anchored to the cortex (asymptomatic)

170
Q

(blank) percent of osteochondromas occur as hereditary multiple osteochondromas

A

15

171
Q

(blank) are benign lesions formed by mature hyaline cartilage.

A

enchondroma (chondroma)

172
Q

Where do you get enchondromas?

A

short tubular bones of hands and feets-> asymptomatic

173
Q

What is Ollier’s disease?

A

Multiple enchondromas

-PREFERENTIALLY on one side of the body

174
Q

What is Maffucci’s Syndrome?

A

multiple enchondromas

-asso. w/ hemangiomas of soft tissue

175
Q

Is it common to get chondrosarcomas from enchodromas?

A

about 1/3 of patients with multiple tumors can get this

176
Q

What is the 2nd most common matrix forming tumor of bone?

A

chondrosarcoma

177
Q

When do you get chondrosarcomas?

A

4th decade and older

178
Q

Where can you find chondrosarcoma?

A

starts in medullary cavity and spreads in the central skeleton (pelvis, shoulder and ribs)-> clear cell variant arises in epiphyses of long tubular bones

179
Q

THe clear cell variant of chondrosarcoma occurs where

A

epiphysis

180
Q

Who gets giant cell tumor of the bone?

A

females b/w 20-40 usually

181
Q

What kind of cells do you find in giant cell tumor?

A

neoplastic mononuclear cells

-reactive osteoclast-like multinucleated cells

182
Q

Where do you see giant cell tumors?

A

epiphysis of long bones

183
Q

What is the cardinal sign of giant cell tumor?

A

“soap bubble” appearance on radiology

184
Q

What is the 2nd most common childhood malignancy of bone?

A

Ewing’s sarcoma

185
Q

What is the translocation involved with Ewings sarcoma?

A

t(11:22)

186
Q

What does Ewings sarcoma affect?

A

femur, tibia, pelvis (metaphysis and diaphysis)

187
Q

What is this:

small blue cell tumor w/ sheet of small cells w/ uniform nuclei containing glycogen

A

Ewings sarcoma

188
Q

Is ewings sarcoma dangerous?

A

YES, has abundant necrosis and young children a less likely to survive

189
Q

What is this:

  • pockets of plasma cells
  • abundant cytoplasm, large eccentric nuclei, w. clock-face chromatin
  • produces immunoglobulin
A

Multiple myeloma

190
Q

What is this:
benign, tumor-like condition w/ possible fractures
-normal trabecular bone is replaced by proliferating fibrous tissue and disorderly islands of deformed bone

A

Fibrous dysplasia

191
Q

What is the most common form of fibrous dysplasia and what are its clincal manifestations?

A

mono-ostotic form (most common 70%)

-> ribs, calvarium, femur, tibia, JAW are common sites

192
Q

What is the clinical manifestation of polyostotic form of fibrous dysplasia?

A

craniofacial involvement, with deformity

193
Q

YOu can get the polyostotic form of fibrous dysplasia with endocrine abnormalities, what is the clinical manifestation of this?

A

unilateral bone lesions, with cafe au lait spots on same side, precocious puberty, also ass. w/ hyperthyroidism, and cushings disease

194
Q

What are the diseases of joints?

A
  • osteoarthritis
  • rheumatoid arthritis
  • infectious arthritis (supperative, lyme disease)
  • gout
  • pseudogout
195
Q

What is osteoarthritis?

A

degenerative joint disease that is the most common disorder of joints

196
Q

Why is osteoarthritis a stupid name?

A

because there is no inflammation it is caued by degeneration of articular cartilage

197
Q

How do you get primary osteoarthritis?

A

arises w/out predisposing factors

198
Q

How do you get secondary osteoarthritis?

A

arises in a joint previously deformed, or in context of a metabolic disease (i.e. hemachromatosis, DM)

199
Q

What are the most important factors for osteoarthritis development?

A

aging and wear and tear

200
Q

Where does osteoarthritis occur most commonly?

A

in weight bearing joints -> due to abnormal mechanical stress on joints such as obestiy, predispose to degenerative joint disease

201
Q

In (blank) you get changes in composition and mechanical properties of cartilage.

A

osteoarthritis

202
Q

What are the changes in cartilage that occur in osteoarthritis?

A

-increased water and decreased proteoglycans
-weakening of collagen network (type II)
chondrocytes secrete IL-1, which activates proteolytic enzymes, collegnases etc

203
Q

What is eburnation and where do you see it?

A

subchondral bone becomes thickened and gives appearance of ivory-> osteoarthritis

204
Q

(blank) may from within bone as cracks in cartilage alow synovial fluid into bone in OA

A

cysts

205
Q

In RA< osteophytes (bony excresences) called (Blank) are found on distal interphalangeal joints (DIPs). (blank) nodes are found on the PIP

A

Heberden’s nodes

Bouchard’s nodes

206
Q

RA is part of a (blank) disease which affects many organ systms (joints, skin, heart, BVs, muscles, lungs)

A

systemic chronic inflammatory disease

207
Q

WHo is affected by RA more, mles or females and when?

A

females in the 4th and 5th decade of life

208
Q

What are the signs and symptoms of RA?

A

symmetric, small joints affected, morning stiffness with gets better with heat and movement, joint swelling, redness, and warmth

209
Q

What will the labs look like in RA?

A

synovial fluid -> lots of neutrophils, poor mucin, increase ESR, RF

210
Q

What is this:
proliferation and hypetrophy of synovial lining cells (pannus/mantle)
-villous projections
-infiltration of lymphocytes, macrophages, plasma cells
-lymphoid follicles
-neovascularization

A

Non-suppurative (chronic) proliferative synovitis

211
Q 
Where do you see this;
subcutaneous nodules along extensor surfaces of forearm and other points of pressure.
Microscopically:
central focus of fibrinoid necrosis
-surrounded by palisading macrophages
-rimmed by granulation tissue
A

RA

212
Q

How can you get infectious arthritis (suppurative)?

A

ALL infectious agents have been implicated

Most commonly: GC, staph, strep, H. influenza, gram-neg rods

213
Q

What are predisposing factors for infectious arthritis?

A

immunodeficiency
joint trauma
IV drug use

214
Q

Patients with sickle cell who get salmonella have potential to get what?

A

infectious arthritis

215
Q

What is lyme disease caused by?

A

Borrelia burgdorferi (a spirochete)

216
Q

How does lyme disease get transmitted?

A

from rodents to humns by deer rickes (i.e ixodes dammini)

217
Q

What is the major arthropod borne disease in the US and what does it involve?

A

lyme disease

-multiple organ systems as well as joints (skin, heart, lymph nodes, meningitis, arteritis)

218
Q

Most affected joints in lyme disease are large and affected in a (blank) fashion

A

migratory

219
Q

What does early lyme disease resemble?

A

lyme disease

220
Q

In lyme disease you can have extensive erosion of (Blank)

A

large joint cartilage

221
Q

What is gout?

A

when uric acid accumulates in tissue as monosodium urate crystals

222
Q

What does gout look like?

A

needle-shaped birefringent

223
Q

With gout you get recurrent episodes of (blank)

A

acute arthritis of 1st metatarsal

224
Q

What are tophi?

A

large accumulations of crystalline material in soft tissue-> chronic granulomatous reaction that is found in gout

225
Q

GOut crystals may lead to what?

A

joint deformity and renal tubular injury or stones

226
Q

Primary gout (90% of cases) is caused by what?

A

overproduction of uric acid due to HGPRT enzyme defect or something

227
Q

How do you get secondary gout ( i.e gout is not the primary disorder)?

A
  • any large increase in urate production (rapid cell lysis during TX for lymphoma or leukemia)
  • decreased excretion of uric acid
  • Lesch-Nyhan syndrom
228
Q

HOw could you get a large increase in urate production leading to secondary gout?

A

rapid cell lysis during TX for lymphoma or leukemia

229
Q

How can you get decreased excretion of urinc acid leading to secondary gout?

A

Chronic renal insufficiency

230
Q

How can Lesch-nyhan syndrome cause secondary gout?

A

over production and over excretion of uric acid with TOTAL lack of HGPRT

231
Q

Urate crystals (from gout) in synovium are chemotactic are activate (blank) to cause (blank)

A

activate complement

-> generates C3a and C5a-> neutrophils and macrophages in joint and synovium-> arthritis

232
Q

What is this:
deposition of calcium pyrophosphate crystals-> derived from nucleosides in chondrocytes, commonly found in knees after trauma/surgery, may be associatd with other systemic diseases, such as hemochromatosis

A

Pseudogout

233
Q

How is pseudogout clinically manifested?

A

self-limited attacks of acute arthritis lasting 1 day to 4 weeks

234
Q

Pseudogout involves what body parts and what do they crystals look like?

A

knees, ankles, wrist, elbows, hips, shoulders

-crystals are coffin shaped and weakly bi-refringent

235
Q

What are the four skeletal muscle diseases?

A
  • neurogenic atrophy
  • myasthenia gravis (MG)
  • muscular dystrophies
  • skeletal muscle neoplasms
236
Q

What are the three types of skeletal muscle?

A

Type 1: slow twitch

type 2: fast twitch

237
Q

What is this:
Muscle deprived of normal innervation resulting in skeletal muscle fibers undergoing progressive atrophy. Both type I and type II muscle fibers.

A

Neurogenic atrophy

238
Q

What are the clinical features of neurogenic atrophy?

A

muscle weakness is hallmark feature

-infants present as floppy baby syndrome

239
Q

Where do you see “small group atrophy”?

A

In neurogenic atrophy

240
Q

What is the most common type of muscle atrophy?

A

type II myofiber (fast-twitch) atrophy

241
Q

What is type II myofiber atrophy due to?

A
  • disuse (bedridden)
  • glucocorticoid use (long term)
  • Hypercortisol state for any reason
242
Q

What is this:
acquired autoimmune disorder of neuromuscular transmission at the junction (F>M)
- antibodies to the acetylcholine receptor

A

myasthenia gravis

243
Q

What is myasthenia gravis associated with?

A

thymus hyperplasia

thmomas

244
Q

Thymus cells from patients with myasthenia when implanted into immunodeficient mice elicit production of (blank)

A

AChR antibodies

245
Q

What are the clinical features of myasthenia gravis?

A

ptosis and diplopia (double vision) due to involvement of extraocular muscles
-respiratory involvement with subsequent respiratory failure

246
Q

HOw do you treat myasthenia gravis?

A
  • anticholinesterase agent (edrophonium chloride aka tensilon)-> transient improvement
  • cholinesterase inhibitors (e.g. mestinon or progstimin)
  • thymectomy
247
Q

What are the 2 muscular dystrophies?

A

DMD

BMD

248
Q

What is DMD?

A

x-linked, 1/3500, calf enlargement, absence of dystrophin

-progressive degeneration of muscle fibers

249
Q

In DMD, (blank) is increased overall throughout the muscle

A

CT

250
Q

What is becker muscular dystrophy (BMD)?

A

x–linked, mutation in dystrophin (unlike duchenne where it is absent) resulting in abnormal form of the protein
(similiar to duchennes but less severe)

251
Q

What is this

-a skeletal muscle neoplasm, cardiac form associated with tuberous sclerosis (probably a hamartoma)

A

Rhabdomyoma

252
Q

What is the most common soft tissue sarcoma in pediatrics, peak in 1st decade?

A

rhabdomyosarcoma

253
Q

What are the three variants of rhabdomyosarcoma?

A
  • embryonal
  • alveolar type
  • pleomorphic type
254
Q

What do you call rhabdomyosarcoma in the GU tract?

A

sarcoma botryoides (gelatinous grape-like structures)

255
Q

What will you see in embryonal rhabdomyosarcoma morphologically?

A

primitive small round blue cells with scattered skeletal muscle “strap cells”

256
Q

Where do you see alveolar type rhabdomyosarcoma?

A

favors torso and extremities, mets to lungs

257
Q

If you see white grapes hangout out of vagina what is it?

A

sarcoma botryoides varient of rhabdomyosarcoma

258
Q

what are the fatty tumors?

A

lipoma/angiolipoma

lipsarcoma

259
Q

What are the fibrous tumors?

A
  • nodular faciitis
  • fibromatosis
  • fibrosarcoma
  • fibriohistocytic tumors
260
Q

What are the skeletal muscle neoplasms?

A

rhabdomyosarcoma

261
Q 
What are these the associated with:
Radiation therapy
Chemical and thermal burns
Trauma
Exposure to some organic chemicals
AIDS/Kaposi’s sarcoma/virus
A

soft tissue tumors

262
Q

What is the most common soft tissue tumors?

A

lipoma

263
Q

WHen will lipopmas become painful?

A

if it turns into an angiolipoma on volar surface of forearm

264
Q

What is this

benign slow growing mass that are usually painless

A

lipoma

265
Q

WHen do you typically see liposarcomas?

Where do you see them?

A

5th and 6th decades of life

  • usually arise in deep tissues of proximal extremities, but may arise in retroperitoneum
  • lower extremities and abdomen
266
Q

What is this:
most common in upper extremities and trunk
-history of trauma
-rapid growth
-not a true neoplasm, it is an over-reaction of fibroblasts
-may be confused with sarcoma due to cellularity

A

Nodular fasciitis

267
Q

What is this:

a GROUP of fibroblastic proliferations that grow in an infiltrative fashion and RECUR after excision

A

Fibromatosis

268
Q

WHat are the two well-known superficial fibromatosis?

A
  • Dupuytrens contracture (palmar fibromatosis)

- Peyronie’s Disease (penile fibromatosis)

269
Q

What is the difference between deep fibromatoses and what tumor is a deep fibromatoses?

A

growth is more aggressive than superficial types and includes Desmoid tumor

270
Q

If you see contracted fingers and thickened bands, what is the disease?

A

Dupuytrens disease

271
Q

What is this::
favors deep tissues of thick, knee and trunk
-mets usually to lungs via hematogenous route
-comprised of fibroblasts, and may grow slowly

A

Fibrosarcoma

272
Q

Who gets fibrosarcomas and where does it originate?

A

males aged 30-40 and it originates in fibrous tissues of the bone -> invades long or flat bones

273
Q

If you have a central fibrosarcoma, where does it arise from?

A

within intramedullary canal

274
Q

If you have a peripheral fibrosarcoma, where does it arise from?

A

from periosteal tissues

275
Q

If you have a secondary fibrosarcoma where, does it arise from?

A

pre-existing lesion or s/p radiation (with generally a poorer prognosis)

276
Q

In infants, fibrosarcoma is usually (Blank) and so present in the first (blank) years of their life

A

congenital

2

277
Q

What is this:

osteolytic with “motheaten” appearance. No sclerosis with cortical destruction

A

Fibrosarcoma

278
Q

If you see a herringbone pattern on a histo slide what is the issue?

A

fibrosarcoma

279
Q

Are fibrohistiocytic tumors, benign or malignant tumors?

A

they range from benign to aggressive malignant tumors

280
Q

WHat is the most important fibrohistiocytic tumor?

A

malignant fibrous histiocytoma (MFH)

281
Q

What is a pleomorphic sarcoma?

A

It is a fibriohistocytic tumor found in lower limbs and retroperitoneal areas and it is the most common type of post-irradiation tumor
-> common in 5th to 7th decades of life

282
Q

(Blank) accounts for about 10% of all soft tissue sarcomas, and does not arise from synovial cells.

A

synovial sarcoma

283
Q

Where do synovial sarcomas come from?

A

mesenchymal cells around joint cavities

284
Q

Most synovial sarcomas develop in the vicinity of (Blank) of lower extremities, especially the knee

A

large joints

Block 7 Week 5 (8 decks)

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