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MSK > MSK Flashcards1-500 > Flashcards

MSK Flashcards1-500

1
Q

What are these hands representative of?

A

Dermatomyositis: inflammation of the skin and muscle over the joints

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2
Q

What is this picture representative of?

A

Vasculitis: inflammation of the muscles of arteries

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3
Q

What is this picture representative of?

A

Gout: deposition of uric acid crystals in the joints

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4
Q

What is this picture representative of:

A

Scleroderma: tightening of the skin over the joints

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5
Q

Do all, some, or zero synovial joints have a meniscus?

A

Some, e.g. the knee

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6
Q

What is this?

A

A meniscus, a fibrocartilagenous washer in certain joints

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7
Q

Which three major joints have a meniscus?

A

The knee, the radiocarpal, and the sternoclavicular

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8
Q

Which layer of the joint capsule is more fibrous? Which is highly vascular?

A

The outer is more fibrous; the inner is highly vascular

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9
Q

What is the color of the synovium in real life?

A

Pinkish (it is highly vascular)

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10
Q

What type of cell coats the surface of the synovium?

A

Synoviocytes

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11
Q

What are the two major types of synoviocytes? What is the function of each?

A

Type A and Type B; Type A is phagocytic, while Type B synthesizes hyaluronate

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12
Q

What does normal synovial fluid look and feel like?

A

Egg whites

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13
Q

Does synovial fluid normally clot?

A

No

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14
Q

What substance makes synovial fluid viscous?

A

Hyaluronate

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15
Q

What does weeping lubrication refer to?

A

The permeability of the cartilage in the joint allows it to be soaked with fluid, and applying pressure causes the fluid to weep out and lubricate the surfaces. Increasing the load increases the weeping.

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16
Q

Where is the fluid involved in boosted lubrication stored?

A

In the peaks and valleys of the cartilaginous surface, so when the joint becomes active, it is dislodged

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17
Q

What properties of synovial fluid might be used to diagnose gout or pseudogout? What about trauma?

A

Presence of crystals; presence of blood or inflammatory markers

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18
Q

What is inflammation of bone and marrow (mostly as a result of infection) called?

A

Osteomyelitis

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19
Q

What class of organisms causes the majority of bone infections?

A

Pyogenic bacteria or mycobacteria

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20
Q

What is the most common organism responsible for adult pyogenic osteomyelitis?

A

S. aureus

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21
Q

What vascular change causes septic arthritis to be more common in adults than in growing children?

A

Closure of the growth plates allows metaphyseal vessels to reunite with the epiphyseal vessels and permits spread of bacteria into the subchondral region

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22
Q

What two organisms should be suspected (besides S. aureus) for neonatal pyogenic osteomyelitis?

A

*H. influenzae *and group B streptococci

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23
Q

The three sources of long bone infection are:

  • {{c1::Soft tissue}}
  • {{c2::Vascular}}
  • {{c3::Direct impact/fracture}}
A
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24
Q

Is hematogenous osteomyelitis common in healthy adults? What does it associate with?

A

No; it is mostly in patients with chronic diseases (e.g., diabetes) or drug addictions

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25
Q

Why are metaphyseal vessel particularly supporting of proliferation of bacteria and abscess formation?

A

They have relatively slow circulation in long sinusoidal vessels

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26
Q

How fast does bone necrosis occur after the acute inflammatory reaction to bacterial proliferation in osteomyelitis?

A

48 hours

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27
Q

How might infection in osteomyelitis spread from a metaphyseal abscess to the periosteum?

A

The Haversian system

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28
Q

What is the dead piece of bone in osteomyelitis called? What about the sleeve of reactive bone around it?

A

Sequestrum; the involucrum

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29
Q

What disease is this? Label the two areas of damaged bone.

A

Osteomyelitis; left: sequestrum (necrotic bone), right: involucrum (reactive bone)

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30
Q

What are these abnormalities on this bone scan called, indicative of either osteomyelitis or round cell tumor?

A

Hot spots

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31
Q

How does osteomyelitis appear on an MRI?

A

Increased signal intensity in the medullary space

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32
Q

What are these called, indicative of osteomyelitis?

A

Brodie abscesses

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33
Q

What pathological changes are seen in this preparation of long bone? What does this indicate clinically?

A

Neutrophils in the Haversian system; acute inflammation and necrosis of the bone, suggesting osteomyelitis

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34
Q

What infiltrating cell types signify the changeover from acute inflammation to chronic inflammation in osteomyelitis?

A

Lymphocytes

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35
Q

What is happening in the reactive bone sleeve (involucrum) seen in osteomyelitis?

A

Resorption of the necrotic bone, fibrosis of marrow, and formation of new bone

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36
Q

What critical step is necessary for adequate diagnosis and specific treatment of osteomyelitis?

A

Bone biopsy and cultures

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37
Q

What is the usual treatment for pyogenic osteomyelitis?

A

Antibiotics and surgical drainage

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38
Q

What is the probability of progression from acute to chronic osteomyelitis?

A

5-25%

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39
Q

Describe the difference between chronic recurrent multifocal osteomyelitis and “typical” osteomyelitis.

A

Chronic recurrent multifocal osteomyelitis is idiopathic, commonly seen in children/young adults, and manifests as multifocal non-pyogenic inflammatory bone lesions that recur over time. Cultures of biopsies will be negative.

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40
Q

What do we see in this MRI of a young adult? He presents with psoriasis and acne fulminans, and complains of pain, tenderness and swelling in his lower extremities over a course of months.

A

Chronic recurrent multifocal osteomyelitis

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41
Q

How is chronic recurrent multifocal osteomyelitis treated?

A

NSAIDs, steroids, and anti-TNF_

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42
Q

How many TB patients develop musculoskeletal involvement?

A

1-3%

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43
Q

In an AIDS patient, what is different about the way tuberculous osteomyelitis usually presents?

A

Multifocal as opposed to one site

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44
Q

What is the gross and microscopic pathologic appearance of tuberculous osteomyelitis?

A

Necrotic tissue with a white “cheesy” appearance, and microscopically, central necrosis is surrounded by granuloma-like cell collections (epithelioid histiocytes, multinucleated giant cells, lymphocytes)

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45
Q

When do bone lesions appear in congenital syphilis?

A

5th month of gestation, and they are fully developed at birth

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46
Q

Which stage of adult syphilis (and at what timepoint) can show development of bone infection?

A

Tertiary, 2 to 5 years after initial infection

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47
Q

How can syphilis infection of the bone be demonstrated on a histological study?

A

Silver stain (Warthin-Starry)

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48
Q

What is this deformity, indicative of skeletal congenital syphilis, called?

A

“boomerang deformity” or “saber shin”

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49
Q

If bacterial osteomyelitis spreads hematogenously into the surrounding joints, what is it now called?

A

Infectious (septic) arthritis

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50
Q

Where do most cases of septic arthritis occur?

A

The knee joint

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51
Q

What are the typical sites of tuberculous arthritis? What is visible in the synovium?

A

Hip, knee, and ankle; caseous granulomas

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52
Q

In young immunocompromised patients, what nonbacterial infection of the joints can occur? How do they manifest?

A

Fungal (blastomycosis, cryptococcosis, aspergillosis, candidiasis); similar to TB, with granulomatous inflammation

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53
Q

This parasitic bone infection, caused by ingestion of substances contaminated with dog feces, is caused by what organism? What is the cyst below called?

A

Echinococcus granulosus; hydatid cyst

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54
Q

What is the etiology of rheumatoid arthritis?

A

Unknown: could be bacterial, viral…

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55
Q

What is the best evidence that rhematoid arthritis actually has an unknown infectious cause?

A

Skeletal remains in Alabama where peripheral erosive arthritis was discovered without axial damage (reminiscent of rheumatoid). This suggests that the agent is endemic to America, and spread to Europe via colonial travels at the end of the 18th century, where it was first described in 1800.

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56
Q

How thick is normal synovium? What has happened here?

A

1 or 2 cells; Inflammation, causing thousands of cells to appear

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57
Q

How many joints need to experience soft-tissue swelling in order to diagnose rheumatoid arthritis?

A

__3

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58
Q

How often is rheumatoid factor present in cases of rheumatoid arthritis? What is it?

A

75%; it is an antibody that can be found in the blood

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59
Q

Is a test for anti-CCP (Cyclic Citrullinated Peptide) antibodies more specific than sensitive for rheumatoid arthritis or vice versa? What about sensitivity?

A

Yes, more specific, less sensitive

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60
Q

What is the appearance of synovial fluid in rheumatoid arthritis? What is the glucose level? Are cultures or crystals positive?

A

Slightly turbid; glucose low; negative cultures and crystals

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61
Q

What is the difference in early symptoms between rheumatoid and osteoarthritis?

A

Rheumatoid: morning stiffness, osteoarthritis: pain increases throughout the day and with use

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62
Q

What is the difference in age of onset between rheumatoid and osteoarthritis?

A

Rheumatoid: childhood and adults, peak incidence in 50’s, osteoarthritis gets more common with higher age

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63
Q

Would arthritis in the MCP, wrists, or PIPs be more suggestive of rheumatoid or osteoarthritis?

A

Rheumatoid

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64
Q

Would pain and swelling in the distal interphalangeal joints, hips, and knees be more suggestive of osteoarthritis or rheumatoid arthritis?

A

Osteoarthritis

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65
Q

Is this presentation more typical for rheumatoid or osteoarthritis?

A

Rheumatoid arthritis, because the PIPs are swollen and not the DIPs

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66
Q

What is seen in this radiographic study that suggests rheumatoid arthritis?

A

Periarticular osteopenia and marginal erosions at the PIP joints

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67
Q

What are these characteristic hand deformities called? What are they significant for?

A

Top: swan neck, bottom: boutonnieres (think button stitchers); Rheumatoid arthritis

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68
Q

What has happened here? Is it painful? What type of arthritis is it typical of?

A

Proliferative synovitis; not really, but function of the fingers is lost; rheumatoid arthritis

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69
Q

What are osteophytes? Are they more typically seen in rheumatoid or osteoarthritis?

A

They are bony projections that form along joint margins; osteoarthritis

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70
Q

If radiographic findings (e.g., in these hip joints) are perfectly symmetrical, is it more suggestive of rheumatoid or osteoarthritis?

A

Rheumatoid arthritis, as osteoarthritis is a disease of wear and tear and rarely presents perfectly symmetrically

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71
Q

What symptom secondary to knee arthritis has happened here? What does it need to be differentiated from?

A

Baker’s cyst, a benign swelling of the bursa behind the knee joint that communicates with the synovial sac of the knee; it needs to be distinguished from DVT by MRI, ultrasound, or Doppler

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72
Q

Is this radiographic study more suggestive of osteoarthritis or rheumatoid arthritis? Why?

A

Rheumatoid arthritis; the MTPs are osteopenic but the more distal joints are well preserved

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73
Q

What distance here in a fixed flexion radiographic study of the neck is concerning? What are implications for general anesthesia?

A

The C1-C2 distance between spinous processes is >3mm; this can cause risk for transecting the spinal cord during the hyperextension applied during intubation

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74
Q

What are the two main strategies of treatment for rheumatoid arthritis?

A

Palliative and remittive

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75
Q

Do palliative treatments for rheumatoid arthritis prevent disease progression (joint destruction)?

A

No

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76
Q

What B-cell-targeted therapy has recently shown promise against rheumatoid arthritis?

A

Rituximab

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77
Q

What is the difference between concentric and eccentric excercise of the upper and lower extremities?

A

Eccentric movements are where you relax a muscle while resisting gravity or a loading force, while concentric movements are when you contract a muscle while resisting gravity or a loading force

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78
Q

What is an isocentric movement of an extremity?

A

When you hold a muscle at the same length while resisting a force: e.g. hanging with arms flexed from a bar

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79
Q

What is the normal cadence for walking?

A

100-115 steps/minute

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80
Q

What is a typical comfortable walking speed?

A

~3mph or about a Manhattan block per minute

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81
Q

When walking (as opposed to running), there is a phase called “double support”, referring to what?

A

Both feet are touching the ground

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82
Q

Where is the position of the center of gravity in an average human? How must it move during walking to use the least energy?

A

A few cm in front of S2; in a straight line

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83
Q

What is the average lateral displacement of the body’s center of gravity during walking? What is the shape of this curve when viewed from above?

A

5cm; smooth sinusoidal curve

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84
Q

During normal walking, does the pelvis drop toward the leg on the ground or the swinging leg? By how much?

A

Toward the swinging leg; 5_

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85
Q

What is the point of the knee flexion in the middle of the stance phase of walking?

A

It shortens the leg, reducing the height of the apex of the curve of CG (and tangentially, makes us about 1 inch shorter while walking)

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86
Q

What is an antalgic gait? What are common causes of it?

A

A lopsided gait (more time spent on one foot); osteoarthritis, fracture, tendonitis, sprain

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87
Q

What is the *Trendelenberg *gait? What are its common causes?

A

Side to side bending of the trunk (kind of like swagger); painful hip, hip abductor weakness (gluteus medius), leg-length discrepancy, abnormal hip joint

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88
Q

When somebody has forward-backward sway while walking, what muscle weakness should be suspect?

A

Hip extensor (gluteus maximus)

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89
Q

What are common natural compensations for a leg length discrepancy that can be observed in a patient?

A

Vaulting gait, high-knee gait, hip circumduction, foot drop

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90
Q

What volume of the body is composed of bone (on average)?

A

9%

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91
Q

What minerals does bone participate in homeostasis of?

A

Ca++, P+++, Na+, Mg++

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92
Q

What is the main constituent of the inorganic mineralized matrix of bone?

A

Calcium phosphate-hydroxyapatite

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93
Q

Identify the cell type in each half.

A

Left__osteoblasts, right__osteoclasts

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94
Q

What are these little pyknotic cells embedded in bone (bottom left)?

A

Osteocytes

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95
Q

What cell type is hanging out in these lacunae, and depicted in yellow in the bottom diagram?

A

Osteocytes

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96
Q

How does assembled triple helix collagen move from the ER to the extracellular space of osteoblasts?

A

Golgi apparatus and secretory vesicles

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97
Q

Are osteoblasts controlled by polypeptide hormones only, steroid hormones only, or both?

A

Both

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98
Q

Label the cell types in this diagram. What process is this?

A

Bone remodeling

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99
Q

What receptor on osteoclast precursors responds to direct cell-to-cell contact to cause differentiation into an osteoclast?

A

RANK (receptor activator for Nuclear Factor _B)

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100
Q

What does the osteoclast pump into the Howship’s lacuna that causes resorption of hydroxyapatite?

A

Protons

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101
Q

Bone remodeling is performed by BMU’s__what does that stand for?

A

Basic multicellular units

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102
Q

Compact bone has canals running parallel to the axis of the long bone, and some perpendicular. What are the parallel ones called? The perpendicular ones?

A

Parallel: Haversian canals; perpendicular: Volksmann’s canals

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103
Q

What attaches the periosteum to the bone?

A

The Sharpey’s fibers

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104
Q

What are the little tunnels through which osteocytes extend their dendritic processes to communicate with one another?

A

Canaliculi

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105
Q

What kind of bone is defined by its layering into flat, parallel bundles, with straight cement lines? What disease involves disruption of these layers?

A

Lamellar; Paget’s disease (below)

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106
Q

Almost all bones are primarily formed via endochondral ossification starting in the 6th embryonic week, but not all. What bones are the exceptions?

A

The flat bones of the calvaria (skull cavity)

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107
Q

Is the center of ossification seen in the middle of this long bone the primary or secondary ossification center? What about the two ones on either end seen starting from the second panel?

A

Middle __ Primary; Ends __ Secondary

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108
Q

What is the structure seen here, which is the primary area where bones grow in length?

A

The epiphyseal growth plate

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109
Q

Can osteclasts resorb material (e.g. cartilage) that is not calcified?

A

No

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110
Q

In intramembranous ossification, does cartilage form before bone calcification occurs? What is it called when bone forms directly on pre-existing bone?

A

No; appositional growth

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111
Q

What types of bone are being contrasted here?

A

Top: compact, and bottom: cancellous or trabecular

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112
Q

What transition in morphology occurs as bone remodeling occurs over the years?

A

Woven to lamellar

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113
Q

What is the color of articular cartilage on a young person? What about an elderly person?

A

Young - left; elderly - right

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114
Q

When you compress hyaline cartilage, what extrudes out of the extracellular matrix giving it its spongy quality?

A

Water and mobile ions

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115
Q

What are the three main types of cartilage, seen here?

A

From left to right: hyaline, fibrous, and elastic

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116
Q

The synovial membrane has two or three layers of cells. What do type B synovicytes do? What about type A?

A

Type B: resorb debris from synovial cavity; Type A: secrete synovial fluid, rich in hyaluronic acid

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117
Q

How much of the skeleton is renewed every year?

A

~10%

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118
Q

What is the most common joint disorder in the world, and which costs the US $60B/yr?

A

Osteoarthritis

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119
Q

How much more likely are obese females to develop knee osteoarthritis?

A

5x

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120
Q

Name two developmental deformities that are risk factors for osteoarthritis.

A

Congenital hip dysplasia, Slipped femoral capital epiphysis (SCFE)

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121
Q

Does osteoarthritis incidence increase with more use of the joint?

A

Yes (for example, as seen in a study with chopstick and non-chopstick hands in Beijing)

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122
Q

What vitamin deficiency increases risk for osteoarthritis?

A

Vitamin D

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123
Q

What tissue is gradually lost in osteoarthritis? What tissue thickens?

A

Articular cartilage; Subchondral bone

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124
Q

What are the bony outgrowths that result from the thickening of subchondral bone in osteoarthritis called?

A

Osteophytes

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125
Q

With age, does __synthesis of proteinases in the ECM of cartilage increase or decrease? What about tissue inhibitors of metalloproteinases (TIMPs)?

A

Proteinases increase; TIMPs decrease

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126
Q

What does this patient have (this is an MCP joint)? What is sticking out to the left?

A

Osteoarthritis; osteophyte

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127
Q

What is it called to look inside a joint?

A

Arthroscopy

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128
Q

What type of osteoarthritis is seen here?

A

Inflammatory, note the redness and swelling

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129
Q

What is seen on the DIP of this patient? What is it a sign for?

A

A synovial cyst; osteoarthritis

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130
Q

The DIPs of this patient are palpated and the bulges seen here are bony, not spongy. Is osteoarthritis or rheumatoid arthritis more likely and why?

A

Osteoarthritis, firstly beause it affects the DIPs and PIPs preferentially, and secondly because the bony outgrowths are osteophytes

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131
Q

What kind of deformity is this?

A

Valgus deformity, where the abductors of the hip are very weak and great pressure is put on the lateral epicondyle of the femur into the knee joint

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132
Q

What is this characteristic appearance of the DIPs and PIPs that suggests osteoarthritis?

A

Seagull appearance__overgrowth of the bone surrounding them

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133
Q

What two conditions of a joint increase its likely involvement in osteoarthritis?

A

Overused and weight-bearing

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134
Q

For osteoarthritis, is pain worse in the early morning, or toward the end of the day? Is there morning stiffness?

A

Toward the end of the day after using the joints; typically no A.M. stiffness

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135
Q

What is crepitus of a joint?

A

When it is moved and air bubbles are heard crackling or popping, a sign that bony edges are protruding

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136
Q

Is there a blood test for osteoarthritis?

A

No

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137
Q

What lifestyle changes can be recommended for an osteoarthritis patient?

A

Avoid traumatic occupational or sports usage of the affected joints, lose weight, avoid fall risks (e.g. walking aids), increase endurance and strength via exercise programs or physical therapy

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138
Q

What is notable about the osteoarthritic cervical spine (right) as compared to the normal?

A

Greater intervertebral disc height, and hypertrophic bone spurs on them

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139
Q

Which is normal, left or right? What is the abnormality? (This is a lumbar vertebral body)

A

Right is normal; Left shows bony outgrowths (spinal stenosis) into the spinal canal, which is the nice trangular center area seen in the right

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140
Q

What is seen in this cross section of intervertebral bodies?

A

Herniation of the discs into the vertebrae, called Schmorl’s nodes

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141
Q

Which hip here is normal? What is wrong with the other?

A

The left (patient’s left) hip shows no space to cushion the joint, revealing end stage osteoarthritis and likely a need to replace the joint

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142
Q

What risk must be carefully managed in older patients with osteoarthritis, both in the hospital and the home setting?

A

Fall risk

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143
Q

What kind of drugs are prescribed to help osteoarthritis patients?

A

Nonopioid analgesics, NSAIDs, topical agents (capsaicin or lidocaine), glucosamine/chondroitin, intra-articular agents, and in the worst cases opioid analgesics

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144
Q

What is the proposed mechanism of glucosamine or chondroitin in treating osteoarthritis? Is there strong evidence for this?

A

Anti-inflammatory activity and “rebuilding” of the cartilage; no, the evidence for this is weak

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145
Q

What is an intra-articular agent? Which might be used for osteoarthritis?

A

It is a drug injected into the joint; steroids or hyaluronic acid

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146
Q

Is this medicine recommended by the FDA for treatment of osteoarthritis?

A

No

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147
Q

Are primary tumors of the spine more common than tumors metastasizing to the spine?

A

No

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148
Q

What pedicle does the L5 nerve root exit underneath? What about C4?

A

L5; C3 (recall that C1 exits over C1, and it switches at C8 where there is no vertebra)

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149
Q

Which spinal root is this exam for?

A

C5

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150
Q

Which spinal root is this exam for?

A

C6

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151
Q

Which spinal root is this exam for?

A

C7

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152
Q

What spinal root is this exam for?

A

C8

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153
Q

What is Hoffman’s sign?

A

Flicking the DIP of one finger into hyperextension causes the others to contract

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154
Q

Of these dermatomes, which landmarks are best to know?

A

T4: nipple line, T10: belly button, L1: groin, L2: thighs, L5: lateral calf, L4: medial calf; C5: upper side of upper arm, C6: upper side of lower arm, T1: lower side of lower arm, T2: lower side of upper arm

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155
Q

Which spinal root controls the patellar tendon reflex?

A

L4

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156
Q

Is there a reflex controlled by L5? What motion?

A

There is no reflex; extending (dorsiflexing) the toes

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157
Q

What reflex is controlled by the S1 spinal root?

A

Achilles tendon

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158
Q

What do superficial tenderness, pain on simulation rotation, and pain on axial loading indicate about a CC of lower back pain?

A

It may not be physiological (instead, psychological)

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159
Q

What proportion of spinal column trauma is due to MVAs? At what level of the column are the most serious injuries?

A

45%; 93% of fatal MVAs with spinal trauma occur between occiput and C3

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160
Q

When neurologic injury occurs with motor deficits (e.g., contusion or compression of the spinal cord), how likely is complete recovery?

A

Very unlikely

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161
Q

What kind of injury is this? Is it survivable?

A

Dislocation of the occiput from the atlas; no

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162
Q

The following are X-rays of what kind of injury? Which involves bilateral facets?

A

Distractive flexion (or dislocation of cervical vertebrae); the rightmost is bilateral facet dislocation

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163
Q

What is the treatment for injuries like the following?

A

For cervical dislocations, the team stabilizes the neck, evaluates neurological function, uses imaging studies, and then reduces the dislocation and decompresses surgically with rigid stabilization

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164
Q

At the level of spinal stenosis, does radiculopathy (nerve dysfunction) only, myelopathy (spinal dysfunction) only, or both occur? What about below this level?

A

At the level both; below, myelopathy only

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165
Q

What kind of disk herniation is more likely to result in radiculopathy? Which is more likely to result in myelopathy? What about both?

A
  1. intraforaminal, radiculopathy;
  1. central, myelopathy
  1. a mixture of both, e.g. posterolateral, will result in both symptoms
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166
Q

What is a laminoplasty?

A

A reshaping of the spinal canal in the case of spinal stenosis that decompresses the spinal cord

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167
Q

What is a spondylolithesis?

A

A slipped disc

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168
Q

What type of cartilage is in the nucleus pulposus? What about the annulus? What disease is shown here?

A

Type II (hyaline); Type I (fibrous); degenerative disk disease

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169
Q

When a patient says “sciatica” what do they mean?

A

A pain, numbness and/or weakness in their leg(s)

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170
Q

What are the most common sites for a lumbar herniated disc?

A

Between L4-5 and L5-S1

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171
Q

What is the surgical technique for relieving pressure from a herniated disc?

A

Discectomy or microdiscectomy, where the disc is shaved via a small incision

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172
Q

What condition is present in 30% of the population over 60, where narrowing of one or more levels of the lumbar spinal canal causes compression of nerve roots?

A

Lumbar spinal stenosis

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173
Q

What is the “shopping cart” sign for lumbar spinal stenosis?

A

The patient likes leaning on a shopping cart like a walker in the supermarket, because it allows them to flex their back, which opens the spinal canal

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174
Q

What is claudication?

A

Limping

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175
Q

When a patient comes in with claudication (limping), how can vascular causes be differentiated from a neurogenic etiology?

A

If patient is relieved while sitting, it is neurogenic; if they are relieved while standing, it is vascular. Lower back pain and spinal motion also point to neurogenic. With neurogenic claudication, one can ride a bicycle__with vascular this is too painful.

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176
Q

What is the success rate for laminectomy in treating spinal stenosis?

A

80-90%

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177
Q

What is this procedure? What is it used to treat?

A

Laminectomy; spinal stenosis

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178
Q

What condition is seen in this patient, which keeps him in this hunched pose?

A

Ankylosing spondylitis

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179
Q

What is this procedure used to correct?

A

Ankylosing spondylitis, where the vertebra fuse in a permanently arched position

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180
Q

This man with ankylosing spondylitis has which symptom? How do we differentiate between this and an inflammatory osteoarthritis of the vertebrae?

A

Kyphosis; it doesn’t matter if the person overuses the joints

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181
Q

What is notable about this hip X-ray? What late-stage disease is represented here?

A

The sacroiliac joints have disappeared; ankylosing spondylitis

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182
Q

What is the finding of this spinal X-ray? What disease is this indicative of?

A

“Bamboo spine”: the ligaments are calcifying; ankylosing spondylitis

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183
Q

We see squaring of the vertebral bodies in this radiograph, indicating progression of what disease?

A

Ankylosing spondylitis

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184
Q

The small, lateral calcifications that originate from ligament attachments into the bone during ankylosing spondylitis are formed from which cell type?

A

Syndesmocytes

185
Q

What is significant on this X-ray, and what disease of the vertebral column does it point to?

A

Inflammation of the periosteum; ankylosing spondylitis

186
Q

Which sensory organ is affected by ankylosing spondylitis?

A

Eyes: acute inflammation

187
Q

Why is physical therapy so important for ankylosing spondylitis sufferers?

A

There is no pharamacological agent to prevent fusion of the joints, so the patient should rather fuse with the vertebral joints in an extended position

188
Q

Why are SSZ and MTX prescribed to ankylosing spondylitis patients?

A

They are antibiotic therapies that may combat some chronic infections thought to associate with the disease, e.g., Klebsiella

189
Q

What arthritis are these hands characteristic of?

A

Psoriasis: note the sausage finger, onycholytic nails, DIPs inflamed

190
Q

What arthritis is associated with these nail abnormalities?

A

Psoriatic

191
Q

Why isn’t this hand likely to be affected by rheumatoid arthritis? What arthritis is it?

A

There is no involvement of the radiocarpal joint; Psoriatic, because of the DIP involvement and the sparing of the wrist

192
Q

These toes are likely to be affected by what kind of arthritis?

A

DIP involvement (soft tissue swelling) points to psoriatic arthritis

193
Q

What presentation of arthritis is this? What type of arthritis is it a progression from?

A

Arthritis mutilans; a late stage of psoriatic arthritis

194
Q

What does DMARD stand for?

A

Disease-modifying anti-rheumatic drug

195
Q

Would you provide plaquenil to a patient with psoriatic arthritis? Why or why not?

A

No, it is contraindicated; it can cause an exfoliative erythroderma

196
Q

What type of arthritis do these features point toward?

A

Reiter’s (reactive) arthritis

197
Q

Is reactive arthritis caused by infection or autoinflammation?

A

Infection

198
Q

How is Reiter’s (reactive) arthritis treated?

A

1) Eradicate the infection (antibiotics)
2) NSAIDs or steroids
3) DMARDs (SSZ, MTX, gold)

199
Q

Does arthropathy of IBD occur with greater prevalence in ulcerative colitis or Crohn’s colitis?

A

Crohn’s colitis

200
Q

How is arthropathy of IBD treated?

A

1) Treat the underlying bowel disease (steroids, antibiotics, etc.)
2) Physical therapy

201
Q

What are the muscles of the rotator cuff?

A

Teres minor, infraspinatus, supraspinatus, subscapularis

202
Q

Which is anterior: the acromion, or the coracoid process?

A

Coracoid process

203
Q

Label the following rotator cuff muscles.

A
204
Q

How long does a tear of the rotator cuff muscles take to heal?

A

>6 months

205
Q

What is the most common cause of shoulder pain?

A

Impingement (bursitis)

206
Q

What type of shoulder problem is seen here? The patient reports shoulder pain, is of younger age, and had good strength in the arm before falling off his skateboard onto it.

A

It is a distal fracture in the clavicle that has caused bursitis and impingement.

207
Q

What is notable about this glenohumoral joint?

A

Calcification in the bursa above the head of the humerus

208
Q

How is a diagnosis of calcific tendonitis made? What is the treatment?

A

X-ray; cortisone injection

209
Q

What is the incidence of rotator cuff tears in patients over 70 years?

A

30%

210
Q

Is fatty atrophy or infiltration of a rotator cuff tear a reversible or irreversible change?

A

Irreversible

211
Q

What priorities are factored in the decision to surgically fix a rotator cuff tear?

A

Acuteness of and trauma causing the tear, age of the patient

212
Q

What is the layman term for “adhesive capsulitis”?

A

Frozen shoulder

213
Q

What is the hallmark of adhesive capsulitis?

A

Limited and passive range of motion of the arm

214
Q

What is the top two differential for a CC of frozen shoulder (adhesive capsulitis)? What can be performed to differentiate between the two?

A

Adhesive capsulitis vs. arthritis; X-ray of shoulder will be normal for adhesive capsulitis

215
Q

What two preconditions cause a 4x increase in incidence of frozen shoulder?

A

Diabetes and thyroid disease

216
Q

What are the two treatments for frozen shoulder? What is the prognosis with therapy?

A

Physical therapy (aggressive stretching) and cortisone injection; 90% of patients regain 90% of function over 3 years

217
Q

Is osteoarthritis or rheumatoid arthritis more common in the shoulder? What type of athlete is most likely to develop shoulder arthritis?

A

Osteoarthritis; weight lifters

218
Q

Which shoulder has osteoarthritis? Which has rheumatoid arthritis?

A

Right: osteoarthritis, with irregular degradation of the bony edges at the joint; Left: rheumatoid (inflammation and hyperdensity at the joint margin)

219
Q

What is the surgery procedure for osteoarthritis of the shoulder that does not improve with treatment? Following this procedure, what can patients NOT do?

A

Shoulder replacement; lift weights or do manual labor (but gentle sports are OK)

220
Q

What is this surgical treatment for the shoulder?

A

Reverse shoulder replacement: the ball and socket is reversed!

221
Q

Do you typically operate on fractures of the humerus that affect the glenohumeral joint? What indicates surgery?

A

No; displacement indicates surgery

222
Q

In which direction is the shoulder joint more unstable following trauma?

A

Anterioinferiorally

223
Q

Are CTs blurred by overlying tissues?

A

No

224
Q

What is the standardized unit of the attenuation values in a CT?

A

Hounsfield units

225
Q

Can a CT detect fractures that conventional radiography cannot?

A

Yes, particularly complex fractures in large bones surrounded by a lot of tissue e.g. hips

226
Q

Can MRI distinguish beween yellow and red marrow? Fat and muscle?

A

Yes to both

227
Q

Does MRI require contrast agents to visualize blood vessels?

A

No

228
Q

What has MRI demonstrated in these proximal femurs that the X-ray could not?

A

Ischemic necrosis (note the black cavities in the heads of the femurs)

229
Q

Bone destruction may not be detected on an X-ray until what percentage of the bone has been destroyed?

A

50%

230
Q

What is the use of radionuclides such as Strontium 85 and Technetium99m (99mTc) labeled phosphate compounds to detect osseous abnormalities? Is this technique more sensitive than specific, or vice versa?

A

They will show increased uptake at those areas; yes, more sensitive than specific

231
Q

What is the most widely used radioisotope in clinical nuclear medicine?

A

Technetium99m

232
Q

What kind of radiographic study is this?

A

Radionuclide study of osseous abnormalities (darker means more bone turnover)

233
Q

In a PET/CT scan, what tracer can detect bone metastases and directly incorporates into the tumor cells?

A

FDG

234
Q

What type of radiographic study detects pairs of gamma rays emitted by a positron-emitting radionuclide?

A

PET

235
Q

Are PET scans 3-dimensional?

A

Yes, they can be

236
Q

What kind of fractures do tumors and metabolic bone disease collectively cause?

A

Pathologic fractures (which are typically transverse)

237
Q

In medicine and orthopedics, is the term “fracture” always equivalent to “broken bone”?

A

Yes

238
Q

What is the immediate treatment for an open fracture?

A

It is a surgical emergency: antibiotics, tetanus injection, NPO, wound debridement in the ER or OR

239
Q

Under the Gustilo & Anderson classification for open fractures, what would a fracture that is 1-10cm, with moderate soft tissue damage, be classified as? Is a Type I fracture most serious or least serious?

A

Type II; least serious

240
Q

When are wounds from open fractures closed?

A

Not until 3-7 days after the initial surgery, when the soft tissues have been thoroughly cleaned and assessed

241
Q

What is the Gustilo & Anderson classification for this open fracture?

A

Type IIIA: >10cm, high energy

242
Q

What is the difference between IIIA and IIIB open fractures?

A

IIIB has periosteal stripping

243
Q

What does a “comminuted” fracture mean?

A

There are more than two pieces

244
Q

Which type of fracture line is most likely to be pathological?

A

Transverse

245
Q

What is the shape of this fracture line? What kind of force produced the fracture?

A

Spiral (see the top ridge of the tibia come around the back of the film); twisting

246
Q

What is the difference betwen an intra-articular and an extra-articular fracture?

A

Intra-articular goes into a joint

247
Q

What assessment must be done before and after reduction of a fracture to ensure best possible recovery of function?

A

Assessment of neurovascular status

248
Q

Why might a bone be woven instead of lamellar, even if it is a mature bone?

A

Pathological overactivity of osteoblasts/clasts

249
Q

What is osteocalcin used as a serum or urine marker for?

A

Bone formation

250
Q

How much of cardiac output do bones collectively receive?

A

5-10%

251
Q

Which growth factors for bone formation are found in fracture hematomas?

A

Platelet-derived growth factors

252
Q

Does estrogen stimulate or inhibit fracture healing?

A

Stimulate healing

253
Q

Do thyroid hormones and glucocorticoids increase or decrease osteoclastic activity?

A

Increase

254
Q

What are “cutting cones”?

A

A mechanism to remodel bone: osteoclasts at the front of the cone, remove bone, trailing osteoblasts lay down new bone

255
Q

Do long bones grow in length via endochondral or intramembranous ossification?

A

Endochondral (because it uses a cartilage precursor, endo + chondral)

256
Q

What are the three stages of fracture healing?

A

Inflammation, repair, remodeling

257
Q

What has appeared at this fracture site during the inflammation stage of healing?

A

A hematoma

258
Q

What is the extracellular matrix formed in this reparative phase of fracture healing called?

A

Soft callus

259
Q

With absolute rigid stability of a fracture, do you see a callus form during healing? What bone remodeling structures traverse the fracture site to join the bone?

A

No; cutting cones

260
Q

How long does a femur fracture take to heal (on average), and so therefore how long is the cast on? What about a finger? Why wouldn’t you immobilize the finger for more than this time?

A

Femur: 12 weeks; Finger: 3 weeks; beyond this point, the capsule might calcify and mobility of the finger may not be regained

261
Q

What is the maximum size of a gap in a fracture after which it cannot be filled with woven bone, and must be filled instead with fibrous tissue that ossifies?

A

500 microns

262
Q

What cavity must be reconstituted to say that fracture healing is complete?

A

The medullary cavity

263
Q

Is direct or indirect bone healing preferred (typically)?

A

Direct, hence stabilization of many open fractures

264
Q

What are some drawbacks of casting?

A

Joint stiffness, disuse osteopenia, and muscle atrophy, difficult to maintain the alignment of bones

265
Q

Smoking increases the time needed for fracture healing. Is this mitigated by a patient using nicotine patches?

A

No, the nicotine is directly responsible for decreasing bloodflow to bone

266
Q

In the case of non-union of a fracture that was internally fixed, what are three surgical options?

A

Incision & draining, revision of the fixation, or bone grafting

267
Q

What disease ties together the pictured symptoms?

A

Systemic Lupus Erythematosus

268
Q

What are the auto-antibodies in lupus selective for?

A

The cell nucleus (anti-nuclear antibodies or ANA)

269
Q

Is SLE (Lupus) more common in females or males? Blacks or whites?

A

Females; blacks

270
Q

Out of 1000 black women, age 15-64, how many will develop SLE?

A

~4

271
Q

What is the 5 year survival rate for SLE (Lupus)?

A

93%

272
Q

What is the usual cause of death in late SLE?

A

Atherosclerosis and/or infection

273
Q

Is SLE (Lupus) inheritable?

A

Partially, it clearly has heritable factors, but heritability is not close to 100%

274
Q

Why is SLE (Lupus) a disease that mostly affects women?

A

Estrogen probably plays a role in the etiology, along with decreased levels of androgens

275
Q

Which two immune cell types are defective in SLE (Lupus)?

A

B and T cells

276
Q

What is the blood test that is one of the criteria for diagnosing SLE (Lupus)?

A

ANA (anti-nuclear antibody)

277
Q

How many of the 11 criteria for SLE (Lupus) must be present to include a patient in a clinical study on Lupus?

A

4

278
Q

If you have a positive ANA and an anti-double stranded DNA antibody test, what is the likelihood that you do not have SLE (Lupus)? Which of these tests is more specific?

A

Very low; the double-stranded DNA antibody is more specific but less sensitive

279
Q

What disease does this histological finding prove? How specific is it? Why is it not typically done?

A

This is the LE cell showing SLE (Lupus) with a PMN containing expanded, coagulated nuclear matter; extremely specific; it is labor intensive and not very sensitive

280
Q

What kind of rash is this? What autoimmune disorder does it form one of the 11 criteria for?

A

Discoid rash; SLE (Lupus)

281
Q

What is this test, used when ANA is negative but SLE (Lupus) is still suspected?

A

Skin biopsy for autoimmune complex deposition at the epidermal basement membrane

282
Q

What kind of rash is this? What is it highly suggestive of? What notable part of the face is spared?

A

Malar rash; SLE (lupus); nasolabial fold

283
Q

What scalp related symptom is common for SLE (Lupus) patients?

A

Allopecia

284
Q

What variant of SLE is this? Is it more or less concerning than other variants?

A

Bullous Lupus; more concerning

285
Q

What kind of rash is this? What autoimmune disorder does it associate with?

A

Interarticular; SLE (Lupus)

286
Q

What kind of arthritis accompanies SLE (Lupus)?

A

Non-erosive, soft tissue inflammation

287
Q

How can this nonerosive arthritis be distinguished from rheumatoid? What is the name of this particular arthropathy? What autoimmune condition is it significant for?

A

It can be reduced into normal position with no pain, because it is due to soft tissue inflammation without bony erosion; Jaccoud’s; SLE (Lupus)

288
Q

What is Jaccoud’s arthropathy?

A

An ulnar deviation of fingers 2-5 that is a sign of SLE (Lupus)

289
Q

Is synovial fluid from an SLE (Lupus) patient inflammatory?

A

No

290
Q

What renal symptoms associate with SLE (Lupus)?

A

Hematuria, proteinuria, cellular casts, possibly nephrotic syndrome

291
Q

What immunofluorescence study that suggests SLE (Lupus) is shown here?

A

IgG in the glomerulus

292
Q

Are the neuropsychiatric manifestations for SLE (Lupus) specific or broad?

A

Very broad, many different manifestions are known

293
Q

Are embolisms and thrombosis commonly associated with SLE (Lupus)?

A

Yes, and they are often a cause of death

294
Q

When SLE (Lupus) does not immediately threaten renal function, organ function, or life, how is it treated?

A

Low dose steroids, antimalarials, NSAIDs, methotrexate

295
Q

When SLE (Lupus) threatens the kidneys, how is it treated?

A

High dose steroids with rapid taper, immunosuppressive therapy, and BP control (diuretics, etc.)

296
Q

When SLE (Lupus) is organ or life-threatening, how is it treated?

A

High dose steroids, immunosuppressants, rituximab (experimental)

297
Q

When SLE (Lupus) manifests primarily as an anti-phospholipid syndrome, how is it treated?

A

High intensity anticoagulants, because there is a significant risk of thrombosis or embolism and sudden death

298
Q

What syndrome does SLE (Lupus) sometimes manifest as, causing a combination of thrombosis, recurrent fetal loss, thrombocytopenia, and livedo reticularis?

A

Anti-phospholipid syndrome

299
Q

What is livedo reticularis?

A

A mottled, reticulated purplish vascular pattern on the skin

300
Q

What is this skin finding? In a patient that presents with this skin, thrombocytopenia, and a positive ANA test, what would you suspect? How would you initiate treatment?

A

Livedo reticularis; SLE (Lupus) manifesting as anti-phospholipid syndrome; high intensity anticoagulation

301
Q

What is the average age of onset of systemic sclerosis? Is it as skewed towards women as SLE (Lupus)?

A

30-50; no, slightly less (4:1)

302
Q

What is the key clinical feature of scleroderma?

A

Skin tightening

303
Q

What is the key histologic findings here that are consistent with scleroderma? Are these pictures unique to scleroderma?

A

Collagen deposition throughout the skin without inflammation; no, this could be found in fibrous scars on normal people, so clinical features are needed

304
Q

Is scleroderma independent of environmental agents?

A

No, there is an unknown external trigger despite some inheritable susceptibility

305
Q

Scleroderma is associated with this vasospastic disorder, which can cause discoloration of fingers and toes or brittle nails. This is a microscopy image of the nail bed. What is it called?

A

Raynaud’s

306
Q

Vinyl chloride, epoxy resins, pentazocine, bleomycin and silicone are all associated with what connective tissue disease?

A

Scleroderma (systemic sclerosis)

307
Q

What connective tissue disorder is graft vs. host (GVH) disease or persistent fetal cells (microchimerism) associated with?

A

Scleroderma (systemic sclerosis)

308
Q

A patient presenting with Raynaud’s, arthralgias, and skin thickening on the distal fingers should be evaluated for what?

A

Scleroderma

309
Q

What is this phenomenon? What connective tissue disorder is it highly suggestive of, assuming the patient doesn’t smoke? What if the patient smokes a lot?

A

Raynaud’s; scleroderma; if the patient is a smoker, consider Buerger’s disease (a medium vessel vasculitis)

310
Q

What kind of environment should somebody with Raynaud’s avoid?

A

Cold weather, since it can cause microinfarcts of bones, renal vessels, etc.

311
Q

What disorder of the joints is seen in these hands?

A

Scleroderma

312
Q

What other underlying condition could help perpetuate this ulcer in a patient with scleroderma?

A

Diabetes

313
Q

Are patients with scleroderma ANA positive? What about dsDNA antibody?

A

ANA positive; dsDNA negative

314
Q

What upper GI symptoms are associated with scleroderma?

A

Esophageal dysmotility causing reflux and dysphasia

315
Q

Do patients with scleroderma have small bowel symptoms?

A

Yes, including bloating, cramps, dysmotility and diarrhea

316
Q

What are these strange abdominal X-ray features (barium contrast was used)? What systemic connective tissue disorder is implicated by them?

A

Wide-mouth diverticula; scleroderma

317
Q

What cardiac abnormality is found in 81% of systemic sclerosis patients?

A

Patchy myocardial fibrosis due to intermittent microvascular ischemia

318
Q

What causes a huge surge in the renin-angiotensin system in scleroderma leading to acute renal failure?

A

Microangiopathy in the renal vessels, similar to Raynaud’s

319
Q

This scleroderma patient died of what renal condition?

A

Cortical infarcts due to renal microangiopathy, causing scleroderma renal crisis

320
Q

If a patient has considerable symptoms of CNS dysfunction like chorea, headache, and seizures, are they more likely to have SLE (Lupus) or scleroderma?

A

SLE (scleroderma does not affect the CNS)

321
Q

What is this variant of scleroderma called? What is the symptom demonstrated on this woman’s face?

A

The CREST variant (Calcinosis, Raynaud’s, Esophageal dismotility, Sclerodactyly, Telangectasia) also called limited scleroderma; telangectasia

322
Q

Is a SBP over 140 in a scleroderma patient concerning, and if so what do you do?

A

Yes, it requires prompt treatment with ACE inhibitors

323
Q

What variant of scleroderma is this?

A

Morphea

324
Q

What disease is this? What is it a rare variant of? What chemical was it associated with in a 1989 epidemic?

A

Eosinophilic fasciitis; systemic sclerosis; L-tryptophan contaminated with 1,1’-ethylidenebis

325
Q

What poison causes this chloracne, which disfigured a Ukrainian president?

A

TCDD or dioxin

326
Q

Where are the greater and lesser trochanter of the femur?

A
327
Q

What nerves do the sciatic split into above the knee?

A

Tibial and common peroneal

328
Q

What nerve innervates the anterior compartment of the thigh?

A

Femoral nerve

329
Q

Is range of motion of the hip governed by the bony socket, or the muscles and ligaments surrounding it?

A

The muscles and ligaments, since the ball and socket provide for a far greater range of motion without such constraints

330
Q

Label the following bursae of the hip:

A

Top__trochanteric, bottom__ischial

331
Q

What are some non-orthopedic causes of hip pain?

A

Hernia, testicular, referred from the spine, gynecological

332
Q

Are all leg length discrepancies due to one leg being anatomically longer than the other?

A

No, functional discrepancies result from lateral pelvic tilt, flexion, etc.

333
Q

Is this a child or adult?

A

Child, notice open growth plates

334
Q

In general, is a CT or an MRI more useful for hip problems?

A

MRI, since the soft tissue detail is good for picking out common diagnoses like osteonecrosis

335
Q

What muscle attaches to the lesser trochanter of the femur?

A

The iliopsoas, the major flexor of the hip

336
Q

What is this cavity in this hip?

A

It is gas in the colon

337
Q

What hip abnormality is seen in this child?

A

Perthes, where there is avascular necrosis of the femoral head

338
Q

A tall boy, age 12, comes in with pain in the groin and hip and knee pain during motion. The following X-ray is taken. What condition is this?

A

Slipped capital femoral epiphyses or SCFE

339
Q

A child comes in with problems walking; his family has not has access to medical care since before he was born. The X-ray reveals the following. What is this called?

A

Developmental dysplasia: a congenital issue where the femur heads grow outside of the sockets

340
Q

What is the typical patient that has a femur neck or intertrochanteric fracture?

A

Elderly patients with osteoporosis that fell

341
Q

How is a intertrochanteric fracture treated in an elderly patient that fell?

A

Surgery is necessary

342
Q

What is the top priority for surgical treatment of a intratrochanteric fracture?

A

Get the patient walking as soon as possible, since it aids in the healing process

343
Q

What kind of fracture to the femur happened in this patient?

A

Intertrochanteric

344
Q

What is the major differentiator between femoral neck fractures that will heal and those that likely will not without hip replacement?

A

Whether the femoral neck was displaced, in which case hip replacement is recommended

345
Q

What kind of fracture was fixed here?

A

Femoral neck

346
Q

What is the etiology of osteonecrosis of the hip?

A

Temporary or permanent loss of blood supply to the femoral head

347
Q

What are the signs and symptoms of osteonecrosis (also called avascular necrosis) of the hip?

A

Joint pain with weight bearing, limited range of motion, osteoarthritis

348
Q

How is avascular necrosis treated surgically?

A

Channels are drilled into the bone to promote vascular regrowth

349
Q

What is the gold standard for diagnosis of avascular necrosis of the hip?

A

MRI

350
Q

When the pain in a hip is related to arthritis of the join as opposed to the sciatic nerve, is it most likely to be described as radiating down the posterior or anterior thigh?

A

Anterior

351
Q

What kind of arthritis of the hip is this?

A

Osteoarthritis, because the joint space is narrow. Subchondral sclerosis produces higher density at the margin, with cysts where the synovial fluid has invaded the head of the femur

352
Q

What is the recommended treatment for arthritis of the hip when lifestyle modification is impossible and pain is significant?

A

Hip replacement

353
Q

In metabolic bone disease, will only some bones in the body be affected?

A

No, all will be affected, but to varying degrees of severity

354
Q

What are the four most common molecular etioligies for metabolic bone disease?

A

Calcium metabolism, phosphate metabolism, vitamin D, and PTH

355
Q

What is this condition, characterized by the deposition of unmineralized osteoid around mineralized bone?

A

Osteomalacia or rickets

356
Q

Does metabolic bone disease generally affect trabecular or compact bone first?

A

Trabecular

357
Q

Why might osteoporosis be localized to one limb?

A

If the limb was immobilized, e.g. due to casting

358
Q

What are the two types of primary osteoporosis?

A

Postmenopausal (type 1) and senile (type 2).

359
Q

Does increased or decreased estrogen cause osteoporosis? Hyper- or hypo-parathyroidism?

A

Decreased estrogen; hyperparathyroidism

360
Q

What class of drugs can cause secondary osteoporosis?

A

Anticonvulsants

361
Q

What is the average rate of age-related bone loss?

A

0.7% per year

362
Q

Is postmenopausal osteoporosis a high turnover or low turnover form of osteoporosis? What about senile osteoporosis?

A

Postmenopausal __ high turnover; senile __ low turnover

363
Q

Why does decreased estrogen cause osteoporosis after menopause?

A

Marrow stromal cells produce cytokines in the absence of estrogen, and the cytokines recruit osteoclasts

364
Q

In general, do blacks or caucasians have higher bone density?

A

Blacks

365
Q

Can osteoporosis be reliably visualized on an X-ray?

A

No, because bone loss is not apparent on X-ray until up to 40% of the mass is gone

366
Q

What is the definitive diagnostic procedure for osteoporosis following X-Ray, CT, or MRI?

A

Bone densitometry (DEXA)

367
Q

Are blood levels of Ca++ or phosphates diagnostic for osteoporosis?

A

No

368
Q

What is the most common type of fracture presenting with osteoporosis in women, occuring 8 times more frequently than in men?

A

Vertebral fractures

369
Q

What is notable about this bone specimen?

A

The cortex is very thin and the interior is fatty, suggesting metabolic bone disorder, e.g. osteoporosis

370
Q

What is the treatment for osteoporosis?

A

Bisphosphonates and calcitonin

371
Q

Upon absorption from the intestine or creation from cholesterol via heat and UVB rays in the skin, vitamin D requires hydroxylation in which two organs?

A

Liver and kidney

372
Q

What is the cause of rickets or osteomalacia?

A

A lack of vitamin D or disturbance of its metabolism

373
Q

What is the difference between rickets and osteomalacia?

A

Rickets is osteomalacia in children, which results in overgrowth of epiphyseal cartilage and deformaties, while osteomalacia in adults results in weak bones and fractures.

374
Q

What skin-related conditions might lead to rickets or osteomalacia?

A

Inadequate exposure to sunlight or dark skin pigmentation

375
Q

What GI conditions can prevent absorption of vitamin D in the intestine? What is the manifestation of this problem?

A

Cholestatic liver disease, pancreatic insufficiency, biliary tract obstruction, and small bowel disease; rickets or osteomalacia

376
Q

What is the overall effect of vitamin D release in its double hydroxylated form from the kidney on serum concentrations?

A

Calcium and phosphate levels go up due to resorption from bones and increased absorption from the intestine

377
Q

What produces phosphatonins at levels which can cause osteomalacia?

A

Bone and soft-tissue low-grade tumors

378
Q

What do we see in this child’s arms?

A

Prominence above the wrist due to flaring and poor mineralization, caused by rickets (vitamin D deficiency or metabolic defect)

379
Q

Why do children show widening above the wrist during rickets?

A

The metaphysis of the radius and ulna flare as the growth plate widens and mineralization slows

380
Q

What is the vitamin deficiency causing this? What is it called?

A

Vitamin D deficiency, or rickets; this is the rachitic rosary

381
Q

Do children with rickets have more or less cartilage at the growth plates of their long bones and costochondral junctions?

A

More

382
Q

Does osteomalacia in adults cause deformities as seen with rickets?

A

No, but the bones are weaker and vulnerable to fractures

383
Q

What is notable about the newly formed osteoid matrix in patients with osteomalacia?

A

It is inadequately mineralized

384
Q

What disease is clearly visualized in this H&E section of bone?

A

Osteomalacia

385
Q

What are these lines in an osteomalacia patient called?

A

Lucent lines representing pseudofractures

386
Q

What mediators are used by osteoblasts to stimulate osteoclastic activity? What hormone upregulates this pathway?

A

RANK-L; PTH

387
Q

When histological studies show osteoclastic resorption of bones, tunneling and dissecting through trabeculae (dissecting osteitis), what hormonal imbalance may be suspected?

A

Hyperparathyroidism

388
Q

Are these normal parathyroid glands?

A

No, there is hyperplasia in some of the glands

389
Q

What is notable about this section of cortical bone? What endocrine disorder may cause this?

A

Osteoclastic tunneling; hyperparathyroidism

390
Q

What is this? Why do these associate with hyperparathyroidism?

A

A brown tumor, a bening lesion that develops in bone; overstimulation of osteoclastic activity by PTH leads to reactive changes and hemorrhage that the bone cannot handle

391
Q

If the parathyroid glands are not overgrown (primary hyperparathyroidism), how could hyperparathyroidism still manifest secondarily?

A

Bone disease or chronic kidney disease that leads to low Ca++ levels

392
Q

What is it called when renal failure leads to osteomalacia and hyperparathyroidism? What serum ions are imbalanced in this situation?

A

Renal osteodystrophy; phosphate retention and low serum Ca++

393
Q

What features of osteomalacia secondary to renal osteodystrophy are seen here?

A

From left to right, brown tumor, pseudofractures, and end plate sclerosis

394
Q

What is Paget’s disease__the one also called osteitis deformans? Are there other diseases named after Paget?

A

It is characterized by marked proliferation of bone cells with abnormal remodeling; yes, there are conditions of the breast and urogenital region that also use this name

395
Q

What bone disease causes these facial deformities?

A

Paget’s disease, or osteitis deformans

396
Q

What disease is suggested by these radiological features?

A

Osteitis deformans (Paget’s disease)

397
Q

What disease is this histological pattern in adult bone most characteristic of?

A

The mosaic pattern of Paget’s disease (osteitis deformans)

398
Q

How is Paget’s disease (osteitis deformans) treated?

A

Bisphosphonates and calcitonin

399
Q

What is the most serious complication of Paget’s disease (osteitis deformans)?

A

Sarcoma

400
Q

How long have patients who present with vasculitis complain of being sick?

A

Usually months, with some kind of fever

401
Q

In which size of vessels affected by vasculitis is there skin involvement? Which sizes will cause marked internal organ involvement?

A

Small to medium vessel vasculitis: skin involvement; medium to large vessel vasculitis: internal organ involvement

402
Q

What kind of vasculitis is represented by these lesions? Describe them.

A

Small vessel vasculitis; palpable purpura with itching or stinging

403
Q

How does this histological preparation of a skin lesion demonstrate vasculitis?

A

The inflammation is centered around the small vessels

404
Q

In a small vessel vasculitis, where do the skin lesions appear?

A

Primarily on the lower extremities

405
Q

What bacterial infections can cause small vessel vasculitis?

A

Meningococcemia, gonococcemia, endocarditis, Rocky Mountain spotted fever

406
Q

What is a frequent iatrogenic cause of hypersensitivity small vessel vasculitis? How long does it take to appear after exposure?

A

Drugs like penicillin which the patient is sensitive to; 1-2 weeks

407
Q

How does hypersensitivity vasculitis manifest?

A

Maculopapular or palpable purpuric rash

408
Q

What common viral infection is known to cause a vasculitis with dependent palpable purpura and some peripheral neuropathy?

A

Hepatitis C

409
Q

What is the age group of Henoch-Sch_nlein purpura patients? What is the common clinical presentation?

A

Peds; Fever with purpura on the skin, arthralgia, and GI pain

410
Q

In Turkey, there is a variant of vasculitis that presents with the following ulcers. What is the syndrome called? What are the ulcers called? Where else do the ulcers appear?

A

Beh_et’s syndrome; aphthous stomatitis or canker sores; genitals

411
Q

Should normal periosteum ever be visible on X-ray?

A

No

412
Q

A child presents with chronic pain in one extremity that increases at night but resolves with NSAID use. X-ray followed by histological study finds a small (<1.5cm) yellowish to red nidus of osteoid and woven bone with interconnected trabeculae. What does this patient have? Is it malignant?

A

Osteoid osteoma; no, but if pain worsens surgical ablation may be considered

413
Q

The two most common kinds of bone tumors, both benign, are seen below__what are they?

A

Left: osteochondroma; right: enchondroma

414
Q

What condition characterized by episodic cartilaginous inflammation of both auricles, nasal cartilage polychondritis, and non-erosive polyarthritis sometimes associates with SLE (Lupus)?

A

Relapsing polychondritis

415
Q

What is relapsing polychondritis caused by?

A

Antibodies for type II collagen

416
Q

How can you treat small vessel vasculitis?

A

Eradicate the antigen, NSAIDs, steroids, and immunosuppression

417
Q

What kind of viral infections are liable to cause medium vessel vasculitis?

A

HIV, Hep B, and Hep C

418
Q

What is another name for Thromboangiitis Obliterans?

A

Buerger’s disease

419
Q

Are there systemic or visceral features of Buerger’s disease? If so, what are they?

A

No

420
Q

What social history is a significant cause of Buerger’s disease?

A

Smoking history

421
Q

What cell type infiltrates the vessel wall with thrombosis in Buerger’s disease?

A

Polymorphonuclear neutrophils

422
Q

What is the most important component of treatment for Buerger’s disease?

A

Smoking cessation

423
Q

What kind of vasculitis is caused by microscopic polyangiitis and granulomatous polyangiitis?

A

A medium vessel, systemic necrotizing vasculitis

424
Q

What does ANCA stand for? What type of inflammatory disease does it help classify?

A

Anti-neutrophil cytoplasmic antibody; medium vessel vasculitis

425
Q

Do ANCA associated causes of medium vessel vasculitis usually involve infection?

A

No

426
Q

What is the postulated mechanism of immune complex mediated vasculitis?

A

Circulating immune complexes deposit in the vessel wall, increase permeability, and activate complement, which causes PMN’s to move in and destroy the vessel wall

427
Q

Where do focal lesions concentrate in polyarteritis nodosa? Is there pulmonary vessel involvement?

A

Bifurcations of arteries; No

428
Q

Is polyarteritis nodosa granulomatous?

A

No

429
Q

Wrist drop or foot drop in the absence of trauma is a sign of what, until proven otherwise?

A

Medium vessel vasculitis

430
Q

These pathological specimens are diagnostic of what condition?

A

Polyarteritis nodosa, due to the thrombus and asymmetric inflammatory infiltrate and/or fibrosis in a medium vessel

431
Q

Could this angiographic study of mesenteric vessels differentiate between polyarteritis nodosa, granulomatous polyangiitis and Churg-Strauss vasculitis?

A

No

432
Q

How is polyarteritis treated?

A

Steroids and immunosuppressants (cyclophosphamide)

433
Q

Children’s polyarteritis nodosa is also known by what name? How is it treated?

A

Kawasaki’s disease; IVIG

434
Q

What differentiates microscopic polyangiitis from polyarteritis nodosa (PAN)?

A

In microscopic polyangiitis, there may be vasculitis in the pulmonary small vessels, which are spared in PAN

435
Q

Are microscopic angiitis and polyarteritis nodosa granulomatous?

A

No

436
Q

What organ system involvement distinguishes granulomatous vasculitis from polyarteritis nodosa?

A

Pulmonary and upper respiratory tract involvement points toward granulomatous vasculitis

437
Q

What parts of the body show symptoms most frequently in Wegener’s granulomatosis?

A

Head and neck (sinusitis, otitis, saddle nose), with pulmonary complaints (SOB, hemoptysis, cough)

438
Q

What two medium vessel vasculitis syndromes associate with the “saddle nose” deformity?

A

Granulomatous polyangiitis and Churg-Strauss

439
Q

What kind of biopsy is necessary to generate this sample which is diagnostic of granulomatous polyangiitis?

A

Open lung biopsy

440
Q

What is another name for granulomatous polyangiitis?

A

Wegener’s granulomatosis

441
Q

What autoantibodies were noticed to be associated with necrotizing vascular inflammation, such as polyarteritis nodosa and Wegener’s (granulomatous angiitis)?

A

ANCA (antineutrophil cytoplasmic autoantibodies)

442
Q

Since medium vessel vascultis is ultimately diagnosed by tissue biopsy, what is the point of doing a test for ANCA?

A

It can narrow down the diagnosis in a critically ill patient, e.g. an infant with renal failure in the NICU with positive ANCA likely has some kind of necrotizing vasculitis

443
Q

What major symptoms distinguish Churg-Strauss from Wegener’s granulomatosis (granulomatous angiitis)?

A

Same manifestation but also with asthma, long history of allergy, and eosinophilia

444
Q

How are Churg-Strauss and Wegener’s granulomatosis treated?

A

Steroids and immunosuppressants

445
Q

What new drug has changed the paradigm for treatment of granulomatous angiitis and microscopic angiitis?

A

Rituximab

446
Q

Why is it counterintuitive that Rituximab has an effect on necrotizing vasculitis?

A

Rituximab is directed at CD20 and thereby wipes out B cells, but vasculitis typically involves neutrophils and T cells

447
Q

What are the two forms of large vessel vasculitis?

A

Takayasu’s and Giant Cell Arteritis

448
Q

What is the easiest differentiator between Takayasu’s and Giant Cell Arteritis? Which is more difficult to treat?

A

Patients’ age: if age is >50, giant cell arteritis; Takayasu’s is much more difficult to treat

449
Q

What is the chronic phase of Takayasu’s characterized by?

A

Ischemia

450
Q

Which are the top three vessels that are most commonly involved in Takayasu’s?

A

Subclavian, descending aorta, renal

451
Q

What is the method of diagnosing Takyasu’s?

A

Angiogram, since biopsy is usually too difficult

452
Q

How is Takayasu’s treated?

A

Steroids and immunosuppressants (cyclophosphamide or methotrexate)

453
Q

Where does giant cell arteritis localize? How does it present?

A

Temporal artery; New headache in temporal region, sometimes with palpable temporal artery

454
Q

How is giant cell arteritis diagnosed? Is this an risky procedure?

A

Positive biopsy; no, it is benign since we do not need our temporal artery (plenty of collateral supply)

455
Q

Can temporal arteritis present without a headache? In this case, what is the usual complaint?

A

Yes; fever of unknown origin

456
Q

What is this an obvious sign of? Does it typically present this grossly?

A

Temporal (giant cell) arteritis; rarely

457
Q

This biopsy of a temporal artery is diagnostic of what disease?

A

Temporal (giant cell) arteritis because of intimal thickening, necrosis and disruption of the internal elastic lamina

458
Q

How is giant cell arteritis treated? Would you proceed with it if the biopsy turns out to be negative?

A

High dose steroids; No, although you may start steroids before the biopsy comes back, because eyesight can be lost

459
Q

Scurvy causes collagen breakdown, which can create a purpuric rash reminiscent of what inflammatory condition?

A

Small vessel vasculitis

MSK (2 decks)

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