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Musculoskeletal Exam 2 > Pathology - Bone, cartilage, soft tissue > Flashcards

Pathology - Bone, cartilage, soft tissue Flashcards

1
Q

What is the cause of Cretinism?

What type of growth is impaired?

A
  • Maternal iodine deficiency
  • Linear growth severely impaired, failure of fontanel closure of skull, and chondrocytes do not follow orderly progression resulting in failure of ossification.
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2
Q

What are some features of cretinism?

What is the treatment/

A
  • hypotonic posture, coarse facial features, and umbilical hernia.
  • Treated with thyroid hormone
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3
Q

What is Morquio syndrome a deposition of?

What are its manifestations?

A
  • A deposition of glucosaminoglycans in developing bones.
  • severe form of dwarfism:
    • ->dental defects
    • -> MR
    • -> Corneal opacities
    • -> Hearing defects
    • ->Cardiac valve disturbances
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4
Q

What is the mode of transmission of Achondroplasia?
Where is there a stop in growth?
What type of signaling is deficient?

A
  • Autosomal dominant trait, short linked dwarfism.
  • Caused by an arrest of growth at the growth plate (most common disease of growth plate).
  • paracrine signaliing
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5
Q

What is the most type I collagen disorders?
What areas does it effect?
What is the mode of transmission?

A
  • osteogenesis imperfecta. “brittle bone disease”
  • Joints, eyes, ears, skin, and teeth
  • Autosomal Dominant
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6
Q

What is Osteopetrosis?

A

It is a rare genetic disease, that pathologically lays down more bone.
- There is diffuse skeletal sclerosis and a “stone-like” quality of bone, however these bones are abnormally brittle and fracture easily. Also known as “marble bone disease” and albers-Schonberg disease

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7
Q

What occurs in the juvenile form of Osteopetrosis that can cause death?

A
  • The calvaria can become thick and push the brain down.
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8
Q

What are the classification types of Osteopetrosis?

What are the 4 types ?

A
  • Autosomal recessive “malignant”
  • Autosomal dominant “benign”
  • i. infantile malignant, ii. type II carbonic anhydrase deficiency, iii. autosomal-dominant type I iv. Type II
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9
Q

What occurs with to porosity of bone in osteoporosis?

What are the most common forms of osteoporosis?

A
  • increased porosity: (i. locally due to disuse or osteoporosis ii. diffuse–>metabolic bone disease iii. susceptibility to fractures)
  • senile form or the post-menopausal form
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10
Q

Peak bone mass is achieved by young adulthood, when does bone loss begin to occur? What is the process?

A
  • 30-40 years bone loss occurs at 0.7%/year
  • Old osteoblast have decreased replicative capacity, loss of osteoblast regulating proteins, this is typical of senile osteoporosis.
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11
Q

What is the main lack of that causes increases in bone loss in the elderly?

A
  • Decreased physical activity, treatment would be to increase weight loading - weight lifting exercise.
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12
Q

What is a genetic factor of osteoporosis?

What are the roles of PTH and Calcitonin?

A
  • Vit. D receptor that reflects increased or decreased bone mass.
  • PTH (given alone) will exacerbate osteoporosis and calcitonin will form more bone. Play a role in senile osteoporosis
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13
Q

When is it most important for women to take calcium?

What are the 3 ways that the body increases low calcium amounts?

A

As adolescent girls, because if they are deficient in calcium intake, shunting peak bone mass and increasing susceptibility to osteoporosis
- Calcium is low and will increase levels by increasing Ca absorption in GI, in kidney, and breaking down bone.

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14
Q

After menopause - how much of cortical bone mass might they lose? Trabecular bone mass?
What is the main hormone suspected?

A

35% of cortical and 50% of trabecular in 40 years following menopause. 1 out of 2 woman suffer fractures due to this.
- decreased estrogen levels

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15
Q

How do estrogen effect bone mass?

What does prolonged usage of glucocorticoids treatment do?

A
  • Estrogen’s effect on bone mass is mediated via cytokines, thereby decreasing IL-6; IL-1; and TNF all of which are potent stimulators of osteoclast
  • Glucocorticoids: decreases bone resorption and increases bone formation. Treat by giving biphosphonates
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16
Q

What is the diagnostic for osteoporosis?

What are treatments available?

A
  • bone density radiographs

- Calcium, Vit. D, estrogen replacement, PTH, bisphosphanates (focused on increasing bone mass levels)

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17
Q

What are characteristic symptoms of Osteoporosis?

A

Osteoporosis hump, Hip fractures, Compression fractures

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18
Q

What is the most prominent disease caused by osteoclast dysfunction?
What are the 3 stages of Paget’s Disease?

A
  • Paget Disease - haphazard bone resorption and synthesis. Fractures occur easier despite a smaller mass.
    i. initial osteolytic stage,
    ii. mixed osteoclastic - osteobalstic stage,
    iii. predominant osteoblastic activity, ending into a quiescent osteosclerotic stage. Resulting in increased bone mass disordered and architecturally unsound.
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19
Q

When is the normal onset of Pagets?

What is the only current cause of Pagets disease?

A

Adulthood

  • Paramyxovirus that produces IL-6 which is a potent osteoclast stimulator/recruiter
  • possibly genetic 18q
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20
Q

How are most cases of Pagets found?

A
  • Incidentally, will not present with any clinical sign or symptom.
  • Many patients exhibit increased serum alkaline phosphate, and increased urine hydroxyproline
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21
Q

Where does Pagets occur?
Where is pain the most common problem?
What are some complications?

A
  • in 1 or more bones; in axial skeleton or proximal femur in >80% of cases
  • microfractures and bone overgrowth (nerve)
  • weight bearing causing anterior/lateral bowing of femur/tibia. severe secondary OA
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22
Q

What are common types of fractures seen?
What is a feature of the skin?
What effect might it have on the heart?

A
  • “Chalkstick - in femur (most common)
    Compression fractures in spine
  • Hypervasularity
  • Heart failure may result from high output due to A-V shunt
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23
Q

What can tumor-like lesions associated with Paget’s disease result in?

A
  • .7-.9% incidence results in sarcoma-
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24
Q

What groups do Rickets and Osteomalacia occur?
How do both deficiencies occur?
What is a characterisitic bone deformity in RIckets?

A

Rickets is vitD deficiency in kids
Osteomalacia is vit D deficiency in adults.
- Both occur by (ineffective mineralization of bone, increase in nonmineralized osteoid)
- Lateral bowing

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25
Q

What disorder can be associated with decreased vit D deficiency?

A
  • Hypophosphatemia which is X-linked
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26
Q
  • What plays a central role in calcium homeostasis?

- What regulates PTH?

A
  • PTH stimulates osteoclasts which increases bone resorption and calcium mobilization.
  • Mediated via increasing RANK production ligand on osteoblasts.
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27
Q

What structures does PTH act on to effect Calcium change?

A
  • Acts directly on kidney
  • Acts directly on bone to cause breakdown
  • Acts indirectly on GI by activating vit D which allows calcium absorption
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28
Q

All skeletal changes associated with chronic renal disease?

A
  • increase osteoclast activity (bone resorption)
  • osteomalacia
  • osteosclerosis
  • growth retardation
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29
Q

What is Osteomyelitis?

A
  • inflammation of the bone and marrow via bacterial induced inflammation (pyogenic and mycobacteria, mycobacterium tuberculosis).
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30
Q

What is pyogenic osteomyelitis?

A
  • bacteria reach bone by 3 routes
    i. blood borne (major)
    ii. neighboring tissue
    iii. traumatic (fractures) Staph Aureus **- anaerobe and aerobes seen mainly after bone trauma
  • Salmonella is an important causative agent in patients with sickle cell anemia.
31
Q

Why is osteomyelitis difficult to sample for?

A
  • previous antibiotic therapy
  • inadequate samplling for culture
  • suboptimal culture methods
32
Q

What type of infection is tuberculosis osteomyelitis?

- where does the infection occur

A
  • Mycobacterial infection (therefore granulomatous inflammation w/ caseous necrosis) - with a 1-3% complication rate
  • Long bones and vertebrae (Pott disease)
33
Q

What are the common primary sites for metastatic bone tumors?
Where will an adenocarcinoma of the prostate metastasize?

A

1) prostate (most common)
2) Breast
3) Lung
4) Kidney
5) GI tract
6) Thyroid (least common)
- To the prostate

34
Q

What are the three types of bone disease that are malignant with the suffix “-oma”

A

Malenoma, lymphoma, glioma

35
Q

What is an osteoma?

What part of the bone is an osteoma more common?

A

Benign lesions in bone (not invasive)

- more common in head and neck

36
Q

What can you distinguish between an Osteoid osteoma and an osteoblastoma?

A
  • Distinguished from each other by their size and site of origin. An osteoid osteoma is most often in the femur and tibia
  • Osteoid osteoma - more often in males (2:1), <cm in dimension, found on leg
  • osteoblastomas are larger in the spine
  • Pain relief: Osteoid osteoma can be relieved with NSAID and an osteoblastoma cannot be treated and is more difficult to localize. ***
37
Q

What is an osteosarcoma?

A
  • Malignant and the most common malignant tumor of bone, primary de novo and secondary forms from other diseases such as Pagets. Rapidly progressing.
38
Q

Where does a primary osteosarcoma present when compared to Pagets.

A

Primary Osterosarcoma - presents most often in the second decade of life above and below the knee. Pagets moves to the spine

39
Q

What is the frequency of osteochondroma?

A
  • most common benign bone tumor, 33% of all benign tumors of the bone.
40
Q

What is a condroma?

A

A benign tumor composed of mature hyaline cartilage.

41
Q

Where does a condroma present?
When does a condroma present?
Where in the bone does it present?

A
  • Presents on the small bones of the hands and feet
  • 3rd to 5th decades
  • Occurs in the medullary cavity of bone
42
Q

What is Ollier disease?

A
  • Multiple chondroma. Proliferation of cartilage in the metaphases of several bones, most commonly of the hands and feet, causing distorted growth in length or pathological fractures; chondrosoma frequently develops:(
43
Q

What is Maffucci Syndrome?

A
  • Multiple Chondromas associated with benign vascular tumors (angiomas) of SOFT TISSUE.
44
Q

What types of chondromas are usually innocuous?
What percentage of patients with a multiple chondroma syndrome develop a chondrosarcoma?
What age group does a Chondrosarcoma normally present in?

A
  • Solitary chondromas
  • 1/3
  • Occurs in older patient (peak at 6th decade)
45
Q

What are some common sites that Chondrosarcoma arise?

A
  • in the central portion of skeleton (shoulder, pelvis, proximal femur, ribs); Most arise de novo
46
Q

What age range does giant cell tumors of the bone present in?
What part of the bone is t located in?

A

Rare, aggressive benign tumor that presents between ages of 20 and 40 years.
- isolated almost entirely in epiphysis (head of tibia or in the femur

47
Q

For Ewing Sarcomas and primitive neuroectodermal tumors:

- How common are they in children
- What is the common gene problem
- Where do they occur?
A
  • second most common form of bone tumor in kids
  • common gene translocation (t11;22) (q24;q12)
  • metadiaphysis (femur); flat bones of the pelvis
48
Q

What is Osteoarthritis?

What is it’s etiology?

A
  • Most common disorder of joints; it is a degeneration of articular cartilage.
  • Arises without any causative agent, therefore it is called a “primary” osteoarthritis
49
Q

What is secondary osteoarthritis?

Is osteoarthritis an inflammatory disease?

A
  • refers to changes developing previously injured joint.

- Hell No! Inflammation may occur secondarily

50
Q

What function is lost in osteoarthritis and what are the factors exacerbating it?

What risk does osteoarthritis directly relate to?

A

Chondrocytes lose the capacity to maintain articular cartilage due to :

1) Aging
2) Mechanical effects (major factors on joints)
3) Genetic factors ( primarily in hands and hips) 
 4) decreased levels of estrogen *** - Bone density
51
Q
  • What type of changes does osteoarthritis result in?

- What joints are commonly affected by osteoarthritisis?

A
  • Weakening and breakdown of type II collagen
  • TNF, IL-1, and NO possible mediators as well as increased apoptosis
  • Hips, knees, lower lumbar, and cervical vertebrae.
52
Q

What type of disease is Rheumatoid Arthritis (RA) and what factors are important?
What is affected in RA?

A
  • It is a chronic systemic inflammatory disorder also know as an autoimmune disease. It is mediated by HLA-DR4.
  • Skin, blood vessels, heart, lungs, muscles, but mainly affects joints.
53
Q

What is its general pathophysiology?

What is found in the synovial membrane of rheumatoid arthritis?

A
  • A lack of HLA-DR4 is designated by the immune system as non-self and there is a destruction (mostly of joints) of articular cartilage and akylosis (bent, crooked, stiff) of the joints
  • Edematous, CD4+, vasodilation due to angiogenesis, fibrin, hemosiderin, macrophages, fibroblast, neutrophils.
54
Q

What is juvenile idiopathic arthritis (AKA juvenile rheumatoid arthritis)?
How does it differ from RA?

A
  • Any and all forms of arthritis before age 16.
  • 1) More large joints affected
    2) Systemic disease more common
    3) Rheumatoid factor/nodules absent
    4) ANA sero + is common
    5) Oligoarthritis more common
    - 4 or fewer joints during first 6 months
    - absence of psoriasis and HLA-B27 (diagnostic for inflammatory arthritis)
55
Q

What is gout a buildup in?

What are recurrent episodes of arthritis due to ?

A
  • it is an increase in uric acid in tissues.

- due to crystalline aggregates caused by precipitation of monosodium urate crystals

56
Q

What causes an increase in uric acid in tissues?

A
  • Increase in uric acid production with normal excretion (most common- unknown cause), or normal uric acid production with decreased excretion at the kidneys
57
Q

What does the precipitation of monosodium urate crystals evoke?

A
  • crystals are chemotactic and activate complement system C3a and C5a, and also increase accumulation of neutrophils and macrophages in joints. Phagocytosis of crystals cause release of toxic free radicals and leukotrines–> B4; finally proinflammatory mediators are released (IL-1, IL-6, TNF)
58
Q

What is pseudo-gout ?
What is the age group that it is most common in.
- What occurs is different about the hereditary form of Pseudo-gout?

A

Unknown etiology for a buildup in Calcium pyrophosphate crystal deposit disease (CPPD), chrondrocalcinosis

  • > 50 yrs
  • Occurs earlier in life, associated with osteoarthritis, AD form germ line mutation in ANKH affecting pyrophosphate channel
59
Q

What disorders are associated with the secondary form of pseudo gout?

A

1) Previous joint damage
2) Hemochromatosis
3) Hypomagnesemia
4) Hypothyroidism
5) Diabetes

60
Q

Where does psudogout occur in?

Gout vs Pseudogout

A
  • Knees
  • Wrist
  • Elbows
  • Shoulders
  • Ankles

-Besides for crystal type- gout is chronic and pseudogout is acute.

61
Q

Where are soft tissue tumors derived from?

What is the proportions of Benign soft tissue tumors to malignant?

A
  • Soft tissue tumors are derived from extraskeletal mesenchymal cells
  • Benign outnumbers malignant by 100:1
62
Q

What are some etiologies of soft tumors/ lesions?

A
  • unknown, possibly from burns, radiation therapy, trauma –>implicated in sarcoma development
  • Chemicals
  • Kaposi Sarcoma associated with herpes virus 8
  • viruses not important in most sarcomas
63
Q

How do most of the soft tumors occur?

What are the genetic factors that might effect soft tumor lesions?

A

Sporadically

  • Neurofibromatosis type 1 (neurofibroma, malignant schwannoma,
  • Garner syndrome
  • Li-Fraumerie syndrome (p-53 deficiency, sarcoma, soft tissue)
  • Osler-weber-Rendu syndrome ( hereditary telangiectasia) - autosomal dominant, dialated capillaries/viens, present from birth, widely distributed.
64
Q

Where can soft tumors appear?
What sex is more prone?
What is the percent pervailance in kids?

A
  • Anywhere, 40% in lower extremities, 20% in upper extremities, 10% in head and neck, 30 % in trunk
  • male
  • 15-20% arise in children
    • ->4th most common malignancy
65
Q

What is the most common types of soft tissue tumors in children?

A

rhabdomyosarcoma

66
Q

What is the most common types of soft tissue tumors in young adults?

A
  • synovial sarcoma
67
Q

For Lipoma what is the location in the skin?
When does it occur (agewise)?
What are some physical characteristics of a lipoma?
What is it’s treatment

A
  • SUBCUTANEOUS
  • Adulthood
  • Soft, mobile, and painless (except for an angiolipoma)
  • Cured by excision
68
Q

What does a midline mass of fatty tissue also indicate?

A
  • a tethered spinal cord
69
Q

When might a Liposarcoma occur?
Where does it arise?
How does it progress?

A
  • In adulthood (40-60 years) - uncommon in children.
  • Arise in deep soft tissues of proximal extremities and RETROPERITONEUM; abdominal cavity
  • develop into a very large masses
70
Q

What are the 3 types of liposarcomas?

A
  • well differentiated (indolent), myxoid type (intermediate malignant behavior), pleomorphic (aggressive and readily metastasize. All types recur
71
Q

What is a Rhabdomyosarcoma?
Where do they occur?
What genetic mutations predispose for Rhabdomyosarcoma?
Treatment?

A
  • Most common soft tissue sarcoma in children and adolescence (prior to age 20)
  • Most often occur in: head and neck or genitourinary tract
  • mutations which involve dysregulation of muscle differentiation.
  • Surgery plus chemotherapy and radiation
72
Q

What are the subtypes of Rhabdomyosarcomas?

A
  • Botryoides (<10yrs) Grape like lesion in young girls
  • Embryonal (most common)- typical in nasal cavity, orbit, middle ear, prostate, vagina, bile ducts, paratesticular. Best prognosis
  • Pleomorphic
  • Alveolar
73
Q

What is a Leiomyoma?

A

A tumor of the soft muscle, benign, often arise in uterus, may also arise inother genital regions
- Never progresses to be malignant

74
Q

What is a Leiomyosarcoma?

A
  • 10-20% of soft tissue sarcomas
  • occurs in adults, women>men
  • most oftern develop in skin and deep soft tissues of extremities and retroperitoneum

Musculoskeletal Exam 2 (8 decks)

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