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Derm Rheum > Acquired Bone Disorders - Gupta > Flashcards

Acquired Bone Disorders - Gupta Flashcards

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1
Q

What is osteoporosis?

A

Reduction in trabecular bone mass leading to porous bone –> increased risk of fracture

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2
Q

What are the most common forms of osteoporosis?

A

Senile and postmenopausal

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3
Q

What is the pathogenesis of osteoporosis?

A

For post-menopausal, all these things are a result of decreased Estrogen

There is also a decrease in OPG that causes the increased osteoclast activity (due to dec regulation)

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4
Q

What does osteoporosis look like microscopically?

A

Normal bone (left) has thick trabeculae

Osteoporotic bone (right) has thinnned trabeculae

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5
Q

Describe estrogen’s influence on bone? What cytokines are involved?

A

Estrogen increases osteoblast activity, decreases osteoclast activity

IL-1, IL-6, TNF modulate osteoclastogenesis (osteoclast differentiation, activation, life span, and function)

Estrogen inhibits secretions of these cytokines

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6
Q

What is the most common fracture in people with osteoporosis?

A

Proximal femoral fractures –> associated with high mortality rate

Gupta notes contradict. Other sources say vertebral fractures more common

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7
Q

What is osteomyelitis?

A

Infection of the bone, typically in children –> Most commonly bacterial

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8
Q

What does acute osteomyelitis look like microscopically?

A

Neutrophils for dayz all up in the bone

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9
Q

What are the symptoms and causes (3 patterns) of osteomyelitis?

A

Bone pain with signs of systemic infection

Caused by direct innoculation (bone trauma), contiguous spread (cellulitis), or hematogenous spread

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10
Q

What are the bacteria (6) associated with osteomyelitis and populations most commonly seen in?

A

Staph aureus –> most common cause (90%)

Nisseria gonorrhoeae –> sexually active young adults

Pasteurella –> Dog/cat bites

Salmonella (encapuslated) –> Sickle cell disease

Pseudomonas –> DM and IV drug abusers, step on nail

TB –> usually invovles vertebrae (Pott’s disease)

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11
Q

What does osteomyelitis look like on X-ray

A

Lytic focus (sequestrum) surrounded by sclerosis (involcrum) on X-ray

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12
Q

What lab value will be very elevated in osteomyelitis?

A

ESR > 100mm/hr

Can also be seen in temporal arteritis and polymyalgia rheumatica

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13
Q

What is osteonecrosis/avascular necrosis?

A

Necrosis of bone and bone marrow due to ischemia

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14
Q

What are the causes of osteonecrosis?

A

1) Fracture/trauma
2) Long-term steroid use
3) Sickle cell –> dactylitis
4) Alcohol abuse
5) Decompression sickness –> N2 emboli lodge in bones (Caisson disease)

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15
Q

What does osteonecrosis look like grossly?

A

Wedge shaped pale area of necrosis in bone

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16
Q

What does osteonecrosis look like microscopically in sickle cell?

A

Diffusely congested, hemorrhagic marrow during sickle cell crisis

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17
Q

What is Pagets disease of bone?

A

Imbalance between osteoclast and osteoblast activity –> osteoclasts are overactive

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18
Q

What is the bone localization of Pagets disease?

A

Localizes to one or more bones –> does not involve entire skeleton

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19
Q

What is the epidemiology of Pagets disease?

A

Usually pts in their 60s

If pt >40 and has isolated elevated AlkPhos, suspect Pagets

Familial link to chromosome 18

20
Q

What are the three stages of Pagets disease?

A

1) Osteoclastic
2) Mixed osteoblastic-osteoclastic
3) Osteoblastic

21
Q

What are the clinical features of Pagets disease?

A

1) Bone pain –> microfractures
2) Increased hat size –> skull is common site
3) Hearing loss –> Impingement on cranial nerve
4) Lion-like facies –> involvement of facial bones
5) Isolated elevated AlkPhos

22
Q

What is seen on biopsy with Pagets disease?

A

Mosaic pattern of lamellar bone –> lots of pieces but none are fused

23
Q

What is osteomalacia(adults)/Rickets(kids)?

A

Inadequate mineralization of bone due to low VitD (“kids need the D” - Jared Fogle) –> leads to weak bones and fracture

24
Q

What lab findings are there in osteomalacia/Rickets?

A

1) Decreased serum calcium
2) Decreased serum phosphate
3) Increased PTH
4) Increased AlkPhos

25
Q

What is the microscopic appearance of osteomalcia?

A

Surfaces of bony trabeculae (black) are covered by a layer of unmineralized osteoid (dark pink) –> van Kossa stain turns calcified tissue black

26
Q

What are the clinical features of Rickets?

A

1) Pigeon-breast deformity –> inward bending ribs with anteriorly displaced sternum
2) Frontal bossing –> osteoid deposition on the skull
3) Rachitic rosary –> osteoid deposition at costochondral joints
4) Bowing of the legs

27
Q

What is hyperparathyroidism?

A

Overactivity of parathyroid glands producing excess PTH

28
Q

What are the causes of primary and secondary hyperparathyroidism?

A

Primary –> Hyperplasia or tumor of parathyroid glands

Secondary –> Prolonged hypocalcemia leading to lots of PTH

29
Q

How does hyperparathyroidism effect bone?

A

Excess PTH detected by osteoblasts –> activate osteoclasts and bone is resorbed causing cyst-like brown tumors in bone

30
Q

What does hyperparathyroidism look like microscopically in bone?

A

Brown tumors show fibroblasts mixed with osteoclasts and numerous activated osteoclasts (large, dark pink multinuclated cells) at the edge of trabecula

31
Q

What is the bone disease associated with hyperparathyroidism called?

A

Osteitis fibrosa cystica - von Recklinghausen disease of bone

32
Q

What is renal osteodystrophy?

A

Term to collectively describe skeletal changes associated with chronic renal disease – kidney fails to convert Vitamin D to active form

33
Q

What is the pathogenesis of renal osteodystrophy?

A

Decreased VitD leads to reduced Ca2+ absoprtion from intestines –> hypocalcemia causes increased PTH and increased bone resportion

34
Q

What is a bone fracture (don’t fuck this up)?

A

A break in the continuity of bone

35
Q

What are the types of fracture?

A

1) Closed (simple) –> doesn’t penetrate skin
2) Open (compound) –> penetrates skin
3) Displaced –> separated in non-anatomic position
4) Pathologic –> bones fracture due to pathologic process (osteoporosis)
5) Spiral –> fracture from torque (child abuse)

36
Q

If a patient has a compound fracture, what should you do before closing the wound?

A

Washout and give antibiotics to prevent infection

37
Q

If a patient has a displaced fracture, what must you do before it can heal?

A

Must reduce the fracture back to anatomical position

38
Q

What is a stress (hairline) fracture?

A

Fracture caused by repeated stress on a bone –> often weight bearing bones

39
Q

What typically causes a scaphoid fracture?

A

Falling on an outstretched hand –> pain in the anatomical snuffbox

40
Q

What is the necessary treatment in scaphoid fracture?

A

Splint the patient to prevent avascular necrosis

41
Q

What causes a basillar skull fracture and how does it present?

A

Secondary to trauma

Presents as periorbital ecchymoses, mastoid ecchymoses, CSF leaking thorugh ears or nose (metallic, salty taste)

42
Q

What fractures in children are suspected for non-accidental trauma?

A

1) Rib fracture
2) Spiral fractures (except Toddler’s fracture of distal tibia)
3) Multiple fractures of different ages
4) Shaken baby syndrome causing subdural hematoma and retinal hemorrhage

43
Q

What happens immediately after a bone fracture?

A

Hematoma fills fracture gap and surroudning area of bone-injury to provide framework –> allows platelets and inflammatory cells to do their part

44
Q

One week after a fracture, what is happening?

A

1) New osteoprogenitor cells
2) Granulation tissue containing vessels and fibroblasts
3) Hematoma is removed

45
Q

What happens 2-3 weeks after a fracture?

A

Early callus formation –> cannot support weight

46
Q

What is the final stage of healing after a fracture?

A

Bony callus mineralizes so controlled weight bearing can be tolerated

47
Q

What are some complications of a fracture?

A

1) Fat emboli
2) DVT and PE
3) Compartment syndrome –> Five Ps: Pain, Pallor, Paresthesias, Pulselessness, Paralysis

Derm Rheum (39 decks)

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