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Pathology I Final > NMS pathology section > Flashcards

NMS pathology section Flashcards

2
Q

What is the normal mechanism of Achondroplasia?

A

Activation of FGFR3.

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3
Q

What is the pathologic mechanism of achondroplasia?

A

mutation leads to r/c being in constant state of activation

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4
Q

What disease is also caused by a defect in FGFR3?

A

Thanatophoric dwarfism

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5
Q

What will the FGFR3 do once activated?

A

Inhibit cartilage proliferation.

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6
Q

What fails to grow in achondroplasia?

A

longitudinal bone growth, leads to short limbs

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7
Q

What kind of trait is Achondroplasia?

A

Autosomal-dominant

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8
Q

What is the prognosis in achondroplasia?

A

normal life span and fertility

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9
Q

What is osteopetrosis?

A

thick bones resulting from defect in the function of osteoclasts

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10
Q

Is membranous ossification affected in achondroplasia?

A

no

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11
Q

Osteopetrosis is caused by what?

A

A genetic deficiency of carbonic anhydrase II.

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12
Q

what is the most common lethal form of dwarfism?

A

Thanatophoric dwarfism

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13
Q

What is the prevalence of T.D?

A

1/20,000

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14
Q

What are some physical characterisitics of a person with TD?

A

micromelic limbs, frontal bossing with relative macrocephaly, small chest cavity, bell shaped abdomen. (Gummi bear)

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15
Q

what leads to death at birth in TD?

A

underdeveloped thoracic cavity leads to respiratory insufficiency

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16
Q

What is osteopetrosis AKA?

A

marble bone disease, and Albers-Schonberg disease

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17
Q

What is osteopetrosis a failure of?

A

failure of normal bone resorption → thickened, dense but brittle bones

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18
Q

What would levels of serum Ca, P and alkaline phosphatase be like in Osteopetrosis?

A

normal

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19
Q

What can x-rays of osteopetrosis show?

A

Erlenmeyer flask bones.

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20
Q

Erlenmeyer flask bones that flare out can result in what?

A

Cranial nerve impingment, and palsies due to narrowed foramina.

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21
Q

What is the most common fracture with aseptic bone necrosis?

A

Femoral head.

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22
Q

What are some known causes of aseptic bone necrosis?

A

trauma, emboli, drugs, radiation

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23
Q

What is the most common fracture with aseptic bone necrosis in the carpal bones?

A

Navicular (scaphoid).

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24
Q

What are patients with autoimmune rheumatic disorders at increased risk of?

A

atherosclerosis

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25
Q

What is the cause of EF?

A

Unknown.

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26
Q

Eosinophilic fascitis often begins after what?

A

Strenuous activity.

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27
Q

What is a common sign of eosinophilic fascitis?

A

Orange-peel configuration.

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28
Q

What areas of the body does EF typically not involve?

A

fingers and toes (acral areas)

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29
Q

is muscle strength impaired with EF?

A

no, but myalgia and arthritis may occur

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30
Q

Cutaneous manifestiations with eospinophilic fasciitis may suggest what?

A

Systemic sclerosis.

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31
Q

Patients with systemic sclerosis usually also have what?

A

Raynaud’s syndrome, acral involvment, telangiectasia, and visceral changes.

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32
Q

Will patients with eosinophilic fascitis also have Raynaud’s syndrome, acral involvment, telangiectasia, and visceral changes?

A

No.

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33
Q

What will blood tests show with a patient with eosinophilic fasciitis?

A

Serum protein electrophoresis shows polyclonal hypergammaglobulinemia.

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34
Q

What % of females and males get Mixed connective tissue disease (MCTD)?

A

females-80%. Males-20%.

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35
Q

With mixed connective tissue disease what signs and symptoms may precede other manifestations by years?

A

Raynaud’s syndrome.

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36
Q

Some of the first manifestations of mixed connective tissue disease resemble what?

A

Early SLE, Sytemic sclerosis, polymyositis, dermatomyositis, or RA.

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37
Q

What is the most frequent finding with mixed connective tissue disease?

A

Sausage-like appearance of the fingers.

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38
Q

Renal disease happens how often and how serious with mixed connective tissue disease?

A

10% (rare) and is often mild.

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39
Q

what kind of neuropathy frequently occurs in MCTD?

A

trigeminal sensory neuropathy

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40
Q

Mixed connective tissue is diagnosed how (without doing labs)?

A

Overlapping features are present in patients appearing to have SLE, systemic sclerosis, polymyositis, or RA.

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41
Q

What will lab work show with a patient that has mixed connective tissue disease?

A

RNP antibodies very high, positive ANA.

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42
Q

What type of antibodies are present with mixed connective tissue disease?

A

ENA.

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43
Q

85% of mixed connective tissue disease patients have what else involved?

A

Lungs.

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44
Q

What are some main causes of death associated with MCTD?

A

pulmonary HTN, renal failure, MI, colonic perforation, disseminated infection, cerebral hemorrhage

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45
Q

Which HLA subtypes are associated with polymyosistis and dermatomyositis?

A

DR3, DR52, DR6

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46
Q

what are the subtypes of polymyositis and dermatomyositis?

A

primary idiopathic,

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47
Q

What are some possible ways polymyositis and dermatomyositis are incited?

A

Viral myositis and underlying cancer.

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48
Q

Dermatomyositis is considered what?

A

A complement-mediated vasculopathy (disease of blood vessels).

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49
Q

What is the abnormality in polymyositis?

A

Direct T-cell mediated muscle injury.

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50
Q

What skin changes occur with dermatomyositis?

A

Periorbital edema with a purplish appearance (heliotrope rash).

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51
Q

What would another relatively specific finding be with a patient that has dermatomyositis?

A

Gottron’s papules (pink patches on the knuckles).

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52
Q

What is a way to diagnose someone who has polymyositis?

A

Proximal muscle weakness with or without muscle tenderness.

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53
Q

polymyositis and dermatomyositis share clinical findings with systemic scerosis or less frequently SLE or vasculitis so what should be done to diagnose polymyositis and dermatomyositis correctly?

A

Include as many of the following 5 criteria as possible:

  1. proximal muscle weakness.
  2. Characteristic skin rash.
  3. Elevated serum muscle enzymes.
  4. Characteristic electromyographic or MRI abnormalities.
  5. Muscle biopsy changes.
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54
Q

What is a way to diagnose someone who has dermatomyositis?

A

Heliotropic rash or gottron’s papules.

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55
Q

Of the 5 tests to determine if a patient has polymyositis and dermatomyositis which one is the definitive test?

A

Muscle biopsy changes.

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56
Q

What else should be tested with polymyositis and dermatomyositis patients?

A

Cancer screening is recommended.

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57
Q

What is the prognosis for poly and dermato?

A

long remissions occur in up to 50% of treated patients. Overall 5 year survival rate is 75% and higher in children.

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58
Q

Relapsing polychondritis has what signs and symptoms?

A

Acute pain, erythema and swelling.

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59
Q

What is the most common and second most common place for acute pain, erythmea, and swelling with relapsing polychondritis?

A

1st pinna cartilage. 2nd- nasal cartilage.

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60
Q

What joints will have arthritis with relapsing polychondritis?

A

Costochondral joints.

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61
Q

What are some criteria for diagnosing relapsing polychondritis?

A

1) Bilateral chondritis of external ears
2) inflammatory polyarthritis.
3) nasal chondritis
4) ocular inflammation
5) respiratory tract chrondritis
6) auditory or vestibular dysfunction

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62
Q

Bouts of inflammation in relapsing polychondritis heal over what time frame?

A

Over weeks to months with recurrences over several years.

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63
Q

How many diagnostic criteria must be present for a diagnosis of relapsing polychondritis?

A

3 or more of 6 manifestations.

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64
Q

Sjogren’s syndrome occurs most frequently amoung who?

A

Middle-aged women.

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65
Q

What happens with sjogren’s syndrome?

A

Salivary, lacrimal, and other exocrine glands become infiltrated with CD4+ T helper cells and with some B cells.

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66
Q

What happens to the exocrine glands once infiltrated with CD4+ T cells and some B cells?

A

They are damaged and atrophy.

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67
Q

What will lacrimal glands that are damaged and atrophy cause to happen?

A

Keratoconjunctivitis sicca.

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68
Q

What is a way to diagnose sjogren’s syndrome?

A

Gritty or dry eyes or dry mouth.

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69
Q

What is needed to officialy diagnose someone with sjogren’s syndrome?

A

3 or more of 6 manifestations.

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70
Q

What are the 6 manifestations of sjogren’s syndrome?

A
  1. Eye symptoms. 2. Oral symptoms. 3. positive eye tests. 4. Salivary gland involvment. 5. autoantibodies. 6. Histopathology.
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71
Q

How is histopathology of sjogren’s syndrome done?

A

Biopsy of minor salivary glands.

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72
Q

How is a histopathology of sjogren’s syndrome confirmed?

A

LabialmMinor salivary gland will show multiple large foci of lymphocytes with atrophy of acinar tissue

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73
Q

What type of people will get Systemic Lupus erythematosus (SLE)?

A

70-90% in females. More common amoung blacks, and Asians than Whites.

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74
Q

How quickly will SLE develop?

A

Abruptly or insidiously.

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75
Q

SLE will develop with episodes of what?

A

Arthralgias (joint pain), and Malaise (General body weakness or discomfort).

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76
Q

What are some of the initial findings of SLE?

A

Vascular headaches, epilepsy, or psychoses (Mental disorder).

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77
Q

What happens to the skin with SLE?

A

Malar butterfly erythema.

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78
Q

What is the most common cardiac problem with SLE?

A

pericarditis (inflammation of pericardium).

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79
Q

Name the 11 clincal findings of SLE?

A
  1. Malar rash.
  2. Discoid rash.
  3. Photosensitivity.
  4. Oral ulcers.
  5. Arthritis.
  6. Serositis.
  7. Renal disorder.
  8. Leukopenia.
  9. Neurolgic disorder.
  10. Positive Anti-DNA or anti-smith antibodies.
  11. Antinuclear antibodies ANA ih high titers.
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80
Q

What type of endocarditis is seen with SLE patients?

A

Libman-Sacks endocarditis.

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81
Q

How many of the 11 criteria for calssification of SLE are needed to classify the patient as having SLE?

A

At least 4.

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82
Q

What will anti-Sm and Anti-double-stranded DNA antibodies tell us about SLE?

A

They are very specific but not sensitive.

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83
Q

What will blood tests be like for SLE?

A

Serum complement levels (C3-C4) are often depressed. ESR is elevated.

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84
Q

Renal involvment with SLE will be screened with a urinalysis and it will show what?

A

RBC and WBC casts suggest active nephritis.

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85
Q

What will the prognosis of SLE be?

A

Chronic relapsing and unpredictable.

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86
Q

Improvments of SLE often take how long?

A

4-12 weeks.

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87
Q

What should be tested on pregnant women with SLE?

A

Antiphospholipid antibodies.

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88
Q

Discoid lupus erythematosus will lead to skin changes as part of lupus and the skin changes will cluster where?

A

In light-exposed areas of the skin. Such as face scalp and ears

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89
Q

Drug-Induced lupus erythematosus will show what in lab work?

A

Extremely high antihistone antibodies.

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90
Q

Systemic sclerosis pathophysiology involves what?

A

Vascular damage.

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91
Q

What is pathophysiology?

A

Study of normal changing to abnormal caused by a disease.

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92
Q

Systemic sclerosis is aka?

A

Scleroderma.

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93
Q

What happens to the skin with systemic sclerosis aka scleroderma?

A

More compact collagen fibers in the reticular dermis, epidermal thinning, loss of rete pegs, and atrophy of dermal appendages.

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94
Q

What is systemic sclerosis called that is isolated to skin involvment?

A

Limited cutaneous scleroderma or Crest syndrome.

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95
Q

What is a sign of systemic sclerosis aka scleroderma?

A

Raynaud’s syndrome, and swelling of distal extremities.

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96
Q

What is Raynaud’s syndrome?

A

Cold hands.

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97
Q

How will Systemic sclerosis aka scleroderma affect the joints?

A

Polyarthralgias, or mild arthritis, flexion contractures.

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98
Q

What is a common cause of death from systemic sclerosis aka scleroderma?

A

Lung involvment, and pulmonary hypertension.

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99
Q

Which serum and antibodies should be tested in Scleroderma?

A

Serum ANA and SCL-70

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100
Q

What is the prognosis of systemic sclerosis?

A

unperdictable.

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101
Q

What is the 10 year survival rate like with systemic sclerosis?

A

65%.

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102
Q

What type of systemic sclerosis can be limited and nonprogressive for long periods?

A

Crest syndrome which is aka cutaneous scleroderma.

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103
Q

What can BCP crystals destroy?

A

joints and can cause severe intra-articular or perarticular inflammation

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104
Q

Calcium pyrophosphate dihydrate crystal deposition disease is transmitted in an autosomal dominant pattern with complete penetration by when?

A

Age 40.

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105
Q

With Gout what is the most common cause of hyperuricemia?

A

Decreased renal excretion.

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106
Q

In gout, increased production of urate may be caused by what?

A

increased turnover in hematologic conditions. And in conditions with increased rates of cellular proliferation and death.

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107
Q

What is lesch-Nyhan syndrome?

A

A complete deficiency of the enzyme called hypoxanthine-guanine phosphoribosyltransferase.

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108
Q

Lesch-nyhan syndrome is associated with what disorder?

A

Gout.

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109
Q

intake of what kind of foods can contribute to hyperuricemia?

A

Purine-rich foods.

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110
Q

With gout urate crystals will precipitate out as what

A

Needle-shaped monosodium urate.

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111
Q

What is podagra?

A

Gouty inflammation of the metatarsophalangeal joint of the great toe.

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112
Q

What is tophi?

A

Firm yellow or white papules or nodules that occur in patients who have had chronic gout or who have never had gout.

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113
Q

How will tophi be present in gout?

A

Single or multiple.

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114
Q

About 20% of chronic gout patients will develop what?

A

urolithiasis with uric acid stones or Ca oxalate stones.

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115
Q

Palindromic rheumatism (gout) is acute, recurrent attacks of inflammation in or near one or several joints and these attacks happen how?

A

Attacks subside spontaneously and completely in 1 to 3 days.

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116
Q

What are serum urate levels like with an acute attack of gout?

A

at leaste 30% of patients have normal serum urate at time of attack.

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117
Q

With new gout patients the serum urate levels should be measured 2 or 3 times to establish a baseline if it is elevated what can also be measured?

A

24-h urinary urate excretion.

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118
Q

What is the normal amount of urinary urate excretion in 24 hours?

A

600-900.

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119
Q

X-rays of gout patients are taken to look for what?

A

Tophi.

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120
Q

What is the shape of monosodium urate (gout crystal)?

A

Needle- or rod-shaped.

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121
Q

What is the shape of Ca pyrophosphate dihydrate (gout crystal)?

A

Rhomboid- or rod-shaped.

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122
Q

What is the shape of Ca oxalate (a rare gout crystal)?

A

bipyramidal.

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123
Q

What is the shape of Basic Ca Phosphate (gout crystal)?

A

Shiny, coinlike or slightly irregular.

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124
Q

With achilles tendon enthesopathy what can be done to minimize stress to the achilles tendon?

A

Night splints, Heel lifts.

125
Q

What are the signs and symptoms of anterior achilles tendon bursitis?

A

Pain, swelling, and warmth around the heel are common.

126
Q

What will cause pain to a patient with anterior achilles tendon bursitis?

A

Use thumb and index finger, side to side compression anterior to achilles tendon will cause pain.

127
Q

A bunion is what?

A

A adventitious bursa due to pressure from tight shoes.

128
Q

A bunion is often caused by what?

A

Hallux valgus.

129
Q

a bunion that has swelling and mild inflammation that affects the entire joint would be called what?

A

Osteoarthritic synovitis.

130
Q

Osteoarthritic synovitis is more what?

A

Circumferential.

131
Q

Epiphysitis of the calcaneus is aka?

A

Sever’s disease.

132
Q

What is ephiphysitis of calcaneus aka sever’s disease?

A

Cartilaginous disruption in calcaneal epiphysitis.

133
Q

When will Pain will develop for people with epiphysitis of the calcaneus aka sever’s disease?

A

between 9-14 usually.

134
Q

What is the usual cause of Hammer toe deformity?

A

Misalignment of the joint surface due to genetic predisposition toward aberrant foot biomechanics and tendon contractures

135
Q

What is another cause of Hammer Toe Deformity?

A

Charcot-Marie-Tooth disease.

136
Q

What is the most common digit affected with hammer toe deformity?

A

2nd.

137
Q

Painful corns often develop from hammer toe and they affect what toe?

A

5th.

138
Q

Inferior calcaneal bursitis can develop at the inferior calcaneous near what?

A

the insertion of the plantar fascia.

139
Q

What is a symptom or sign of medial plantar nerve entrapment?

A

Almost constant pain.

140
Q

What is a treatment of medial plantar nerve entrapment?

A

Physical therapy and cryotherapy (treatment by means of application of cold).

141
Q

What is the most common cause of metatarsalgia?

A

Freibergs disease, interdigital nerve pain, Morton’s neuroma

142
Q

What is morton’s neuroma?

A

It includes Freiberg’s disease and interdigital nerve pain.

143
Q

What is Freiberg’s disease?

A

avascular necrosis of the metatarsal head.

144
Q

What disease is Freiberg’s disease seen with?

A

Metatarsalgia.

145
Q

How is metatarsalgia diagnosed?

A

With X-rays.

146
Q

What will be seen on X-rays of a metatarsalgia patient?

A

head of 2nd metatarsal is widened and flattened.

147
Q

What are the signs and symptoms of metatarsalgia?

A

Burning or lancinating(stabing) quality or paresthesias.

148
Q

What can?€?t patients do with metatarsalgia?

A

Wear most shoes.

149
Q

What causes tissue changes with metatarsalgia?

A

Tissue changes due to aberrant foot biomechanics.

150
Q

To diagnose metatarsalgia take the patients foot and 1st toe is dorsiflexed and then inspect the metatarsal head and palpate each sesamoid. Tenderness is localized where?

A

To a sesamoid usually the tibial sesamoid.

151
Q

Plantar fasciosis is caused by a shortening or contracture of the calf muscles and plantar fascia and what are the things that can lead to this?

A

Sedentary lifestyle.

152
Q

Plantar fasciosis is common amoung sedentary people and which other population and situations?

A

People who are standing or walking on hard surfaces for prolonged periods.

153
Q

What is a sign or symptom of plantar fasciosis?

A

Pain at the bottom of the heel on weight bearing particularly when first arising in the morning.

154
Q

What happens to pain at the bottom of the heel for plantar fasciosis in the morning, does the pain return?

A

It usually improves within 5 to 10 minutes only to return later in the day.

155
Q

How is plantar fasciosis diagnosed?

A

Confirmed if firm thumb pressure applied to calcaneus when the foot is dorsiflexed elicits pain.

156
Q

What are the most effective treatments of plantar fasciosis?

A

in-shoe heel and arch cushioning, calf stretching exercises, and night splinting devices that stretch the calf and plantar fascia.

157
Q

With plantar fibromatosis what is seen while the foot is dorsiflexed?

A

Nodules displayed most easily when the foot is dorsiflexed against the leg

158
Q

What is Haglund’s deformity and what is condition is it associated with?

A

bony prominence on the calcaneous seen with many posterior achilles tendon bursitis patients.

159
Q

what are the signs and symptoms of posterior achilles tendon bursitis?

A

Cystic nodules 1-3 cm in diameter.

160
Q

Enthesopathy(A disease occurring at the site of attachment of muscle tendons and ligaments to bones or joint capsules) is differentiated from posterior achilles tendon bursitis how?

A

by the absence of a soft-tissue lesion.

161
Q

What is another name for Tarsal Tunnel Syndrome?

A

Posterior tibial nerve neuralgia

162
Q

What nerve and where is the nerve compressed to cause Tarsal Tunnel Syndrome?

A

At the level of the ankle, the posterior tibial nerve passes through a fibro-osseous cnaal and divides into the medial and lateral plantar nerves

163
Q

What are the signs and symptoms of tarsal tunnel syndrome?

A

Pain (occasionally buring and tingling).

164
Q

Where will pain be found with tarsal tunnel syndrome?

A

Retroballeolar and sometimes in the plantar medial heel and may extend along the plantar surface as far as the toes.

165
Q

How is tarsal tunnel syndrome diagnosed?

A

TAPPING or palpating the posterior tibial nerve below the medial malleolus at the site of compression or injury, and this will often cause distal tingling.

166
Q

When tapping of the posterior tibial nerve to diagnose tarsal tunnel syndrome and the patient gets distal tingling what is this called?

A

Tinel’s sign.

167
Q

What is the treatment for tarsal tunnel syndrome?

A

Foot inversion, injection, surgery or a combination

168
Q

What is tibialis Posterior Tendinosis?

A

Degenration resulting from long-standing biomechanical problems such as excessive pronation (often in obese people) or involved with primary inflammatory disorders ie: RA or gout

169
Q

What are some signs and symptoms of Tibialis Posterior Tendinosis?

A

Early on, occasional pain behind the medial malleolus but over time pain becomes severe with painful swelling behind the medial malleolus

170
Q

What is the treatment for Tibialis Posterior Tendinosis?

A

Orthotics and braces or surgery

171
Q

What are the 5 different joint disorders?

A

1) Juvenile Idiopathic arthritis (JIA).
2) Neurogenic arthropathy.
3) Osteoarthritis (OA).
4) Rheumatoid arthritis (RA).
5) Seronegative Spondyloarthropathies

172
Q

With tibialis posterior tendinosis a treatment could be corticosteroid injections what will this do?

A

Exacerbate the degenerative process.

173
Q

What is the cause of juvenile idopathic arthritis?

A

Unknown.

174
Q

What seems to be the cause of Juvenile idopathic arthritis?

A

Genetic predisoposition and autoimmune pathophysiology.

175
Q

What are the 3 possible patterns of Juvenile idiopathic arthritis?

A
  1. Systemic onset.
  2. Pauciarticular onset aka oligoarticular.
  3. Polyarticular onset.
176
Q

How many possible patterns are there of Juvenile idiopathic arthritis?

A

three.

177
Q

What is the difference between pauciarticular (oligoarticular) and polyarticular onset of juvenile idiopathic arthritis?

A

Pauciarticular (oligoarticular) onset- less than 4 joints are involved.
Polyarticular onset- more than 5 and often more than 20 joints are invovled.

178
Q

Systemic onset of juvenile idiopathic arthritis is aka?

A

Still’s disease.

179
Q

How will Still’s disease be diagnosed by lab work?

A

RF and ANA are absent.

180
Q

What will lab work show for pauciarticular onset JIA?

A

ANA are present in up to 75% and RF is absent.

181
Q

What will the lab work show for polyarticular-onset?

A

RF usually negative.

182
Q

What type of patients with polyarticular-onset JIA will RF be positive?

A

Adolescent girls.

183
Q

What is iridocyclitis and what disorder is it associated with?

A

Inflammation of the iris and ciliary body found with juvenile idiopathic arthritis

184
Q

What complications can iridocyclitis cause?

A

Pain, photophobia but can be asymptomatic leading to scarring and glaucoma with band keratopathy

185
Q

What is the pathophysiology of neurogenic arthropathy?

A

Impaired deep pain sensation or proprioception.

186
Q

What are the signs and symptoms of neurogenic arthropathy?

A

Pain is the first symptom, but ability to sense pain is impaired and therefore the degree of pain is often unexpectedly mild for the degree of joint damage.

187
Q

What are some of the late signs and symptoms of neurogenic arthropathy?

A

Fractures and bony healing may produce many loose pieces of cartilage or bone BAG OF BONES.

188
Q

What will neurogenic arthropathy simulate in its early stages?

A

Osteoarthritis.

189
Q

How can neurogneic arthropathy be distinguished from osteoarthritis?

A

Neurogenic arthropathy progresses more rapidly than OA and frequently causes proportionately less pain.

190
Q

How is neurogenic arthropathy treated?

A

Treatment of the underlying neurologic condition may slow progression.

191
Q

What is the most common joint disorder?

A

Osteoarthritis (OA).

192
Q

What is neuropathic arthropathy also known as?

A

Charcot’s Joints

193
Q

What is the most common joint disorder?

A

Osteoarthritis

194
Q

What are the two types of Osteoarthritis classifications?

A

Primary (idiopathic) or Secondary (some known cause)

195
Q

What is a primary Osteoarthritis that involves multiple joints classified as?

A

Primary Generalized Osteoarthritis

196
Q

What are some other names for Osteoarthritis?

A

Degenerative Joint disease, Osteoarthrosis, Hypertrophic osteoarthritis

197
Q

How does the process of Osteoarthritis begin?

A

Begins with tissue damage from mechanical injury, transmission of inflammatory mediators from the synovium into cartilage or defects in cartilage metabolism

198
Q

What happens to synovial fluid with OA?

A

The synovium becomes inflamed and thickened and produces synovial fluid with less viscosity and greater volume.

199
Q

What is symptom or sign of OA?

A

Pain is usually worsened by weight bearing and relieved by rest but can eventually become constant.

200
Q

Stiffness following awaking with OA lasts how long?

A

less than 30 minutes.

201
Q

What are the joints most often affected by OA?

A

DIP and PIP (although RA has more effect on PIP)

202
Q

What are names for the nodes on the DIP and PIP joints ?

A

DIP- distal interphalangeal aka Heberden’s nodes. PIP-proximal interphalangeal aka Bouchards nodes.

203
Q

How can OA affect back pain?

A

Lower back or leg pain that is worsened by walking or back extension

204
Q

What is a treatment of OA of the hip?

A

Prolotherapy.

205
Q

How is Osteoarthritis diagnosed?

A

X-rays, generally reveal marginal ostephytes, narrowing of the joint space, increased density of the subchondral bone, subcondral cyst formation, bone remodeling, and joint effusions. (standing x-rays of knees are more sensitive at detecting joint space n

206
Q

What are 2 treatments of OA?

A

Rehabilitation techniques and weight loss.

207
Q

What is a cause of Rheumatoid arthritis?

A

Autoimmune reactions although the precise cause is unknown

208
Q

What is the pathophysiology of Rheumatoid Arthritis?

A

Prominent immunologic abnormalities include immune complexes produced by synovial lining cells and in inflamed blood vessels

209
Q

What happens to the synovium with Rheumatoid arthritis aka RA?

A

normally thin synovium thickens.

210
Q

Lots of inflammatory mediators are released with Rheumatoid arthritis and they are released by what?

A

Hyperplastic synovial tissue (pannus)

211
Q

In what percentage of patients with RA do rheumatoid nodules develop?

A

30%

212
Q

What is a symptom or sign of Rheumatoid arthritis?

A

Symmetric joint symptoms, stiffness that lasts 60 minutes or more after rising in the morning, and the stiffness may occur after any prolonged inactivity.

213
Q

In which joints does rheumatoid arthritis affect?

A

Virtually any joint except uncommonly the distal interphalangeal (DIP) joints and the axial skeleton is rarely involved except for the upper cervical spine

214
Q

What do popliteal cycsts cause?

A

Found with Rheumatoid Arthritis and they are cysts that can cause calf swelling and tenderness suggestive of deep vein thrombosis

215
Q

What are popliteal cycsts also named as?

A

Baker’s cysts

216
Q

How can Rhematiod arthritis be diagnosed?

A

Check for Anti-cyclic citrullinated peptide antibody (ccp) antibodies and serum rheumatoid factor (RF).

217
Q

You need 4 of 7 criteria to diagnose someone with RA what are the 7 criteria?

A
  1. Arthritis in 3 or more joints.
  2. Arthritis in hand joints.
  3. Morning stiffness for more than 1 hour.
  4. Rheumatoid nodules.
  5. Serum rheumatoid factor.
  6. Symmetric arthritis.
  7. Imaging changes.
218
Q

What are some differential diagnosis that can simulate RA?

A

1) Crystal-induced arthritis
2) Osteoarthritis
3) SLE
4) Sarcoidosis
5) Reactive arthritis
6) Psoriatic arthritis
7) Ankylosing spondylitis

219
Q

Anti-ccp is more sensitive for RA than what?

A

RF.

220
Q

What would the Rheumatoid factor aka RF be like in labs of a patient that has seronegative spondyloarthropathies?

A

RF is negative.

221
Q

What disorders will be included in seronegative spondyloarthropathies?

A

Ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and others.

222
Q

In what population is ankylosing spondylitis more frequent?

A

3 times more frequent in men than in women and begins most often between ages 20 and 40

223
Q

What is common in untreated ankylosing spondylitis patients?

A

Kyphosis.

224
Q

What is the spine like with ankylosing spondylitis?

A

Bamboo spine.

225
Q

What are some systemic neurologic signs that can result from ankylosing spondylitis?

A

Compression radiculitis or sciatica, vertebral fracture or subluxation, or cauda equina syndrome

226
Q

What is a cardiovascular manifestation that can result from ankylosing spondylitis?

A

Dyspnea, cough or hemoptysis can occur

227
Q

What can cause a secondary infection associated with ankylosing spondylitis?

A

Aspergillus

228
Q

How is ankylosing spondylitis diagnosed?

A

Lumbosacral spine imaging and blood tests (ESR, C-reactive protein and CBC)

229
Q

Is ankylosing spondylitis equivalent to diffuse idiopathic skeltal hyperostosis (DISH)?

A

No

230
Q

What comorbity is opten associated with idiopathic skeletal hyperostosis (DISH)?

A

Diabetes Mellitus type II

231
Q

Reactive arthritis is aka?

A

Reiter’s syndrome.

232
Q

What can’t you do with reactive arthritis?

A

can’t see, can’t pee, and can’t dance with me.

233
Q

What is joint involvment like with reactive arthritis aka reiter’s syndrome?

A

generally asymmetric.

234
Q

With reactive arthritis when would urethritis develop?

A

7-14 days after sexual contact.

235
Q

What else might develop over the next few weeks with reactive arthritis after sexual contact?

A

Conjunctivitis.

236
Q

How is reactive arthritis diagnosed?

A

Asymmetric arthritis affecting the large joints of the lower extremities or toes.

237
Q

Disseminated gonococcal infections can closely simulate reactive arthritis so how can they be distinguished?

A

Disseminated gonococcal infection tends to involve upper and lower extremities equally, be more migratory and not produce back pain, and reactive arthritis affects the lower extremities or toes.

238
Q

What else can simulate reactive arthritis?

A

Psoriatic arthritis.

239
Q

How can we distinguish between psoriatic arthritis and reactive arthritis?

A

psoriatic arthritis affects mostly upper extremities especially the distal interphalangeal joints and RA-affects lower extremities.

240
Q

Psoriatic arthritis develops in 5-40% of patients with what?

A

Psoriasis.

241
Q

What associated disorder is the autoantibody antinuclear antibodies (ANA) a predisposition for?

A

SLE, but not exclusive.

242
Q

What associated disorder is the autoantibody anti-ds(double stranded)DNA and anti-smith a predisposition for?

A

Specific for SLE.

243
Q

What associated disorder is the autoantibody Antihistone a predisposition for?

A

Drug-induced lupus.

244
Q

What associated disorder is the autoantibody Anti-IgG a predisposition for?

A

Rheumatoid arthritis.

245
Q

What associated disorder is the autoantibody Anticentromere a predisposition for?

A

Scleroderma (CREST).

246
Q

What associated disorder is the autoantibody Anti-Scl-70 a predisposition for?

A

Scleroderma (Diffuse).

247
Q

What associated disorder is the autoantibody anti-jo-1 a predisposition for?

A

Polymyositis, dermatomyositis.

248
Q

What associated disorder is the autoantibody Anti-SS-A a predisposition for?

A

Sjogren’s syndrome.

249
Q

What associated disorder is the autoantibody Anti-SS-B a predisposition for?

A

Sjogren’s syndrome.

250
Q

What associated disorder is the autoantibody Anti-U1 RNP a predisposition for?

A

Mixed connective tissue disease.

251
Q

What associated disorder is the autoantibody Anti CCP a predisposition for?

A

Rheumatoid arthritis.

252
Q

What is another name for Anti-IgG antibody?

A

Rheumatoid factor.

253
Q

What will osteoporosis do to bone?

A

Cortical thickness and number and size of trabeculae decrease resulting in increased porosity.

254
Q

What will decrease with osteoporosis?

A

Total bone mass.

255
Q

What type of deficiency in men and women is linked with osteoporosis?

A

Estrogen deficiency.

256
Q

Osteoporosis is impaired formation response during bone remodeling probalby caused by what?

A

Age-related decline in the number and activity of osteoblasts.

257
Q

Where is the most common site for fragility fractures with osteoporosis?

A

Distal radius and vertebral compression fractures.

258
Q

What are some risk factors associated with osteoporosis?

A

Ciagrette smoking and excessive caffeine or alcohol use.

259
Q

What drugs can cause osteoporosis? (NB question)

A

Corticosteroid, Ehtanol, Phenytoin (Dilantin)/anticonvulsants, tobacco, barbiturates, heparin

260
Q

What is the specific kyphosis accompanied by exaggerated cervical lordosis found in osteoporosis known as?

A

Widow’s hump or dowager’s hump

261
Q

What is the cause of dowager’s hump?

A

Multiple thoracic compression fractures that eventually cause dorsal kyphosis, with exaggerated cervical lordosis

262
Q

what are some common consequences of osteoporosis?

A

vertebral crush fractures (acute back pain, loss of heigh, kyphosis), distal radius (Colles’) fractures and femeoral neck fractures

263
Q

What is seen with an osteoporotic vertebral body when compared to a normal vertebral body?

A

Loss of horizontally oriented trabeculae but thickened the vertical trabeculae

264
Q

What is DEXA and what is it used for?

A

Dual-energy x-ray absorptiometry used to measure bone density often a diagnostic tool for osteoporosis.

265
Q

What do plain x-rays of osteoporosis show?

A

A loss of horizontally orientated trabeculae increases the prominence of the cortical end plates and of vertically orientated, weight bearing trabeculae

266
Q

What other bone disorders are included in Osteopenia?

A

Osteoporosis or Osteomalacia

267
Q

what is a DEXA result of >1 defined as?

A

osteopenia and suggests an increased risk of osteoporosis

268
Q

what is a DEXA result of >2.5 defined as?

A

Diagnostic for osteoporosis

269
Q

What is osteomalacia?

A

softening of bones as a result of inadequate mineralization of the organic matrix (osteoid). Caused by vitamin D deficiency (inadequate intake, inadequate exposure to sunlight, or abnormal intestinal absorption)

270
Q

What are some pathologies of osteomalacia

A

1) Excess non-mineralized osteoid
2) Bone deformities and fractures
3) Rickets

271
Q

What can cause Vitamin D deficiencies?

A

Inadequate metabolic processing and activation of vitamin D, or disturbances of phosphate metabolism

272
Q

What are some symptoms of rickets?

A

1) Bowlegs
2) widened costochondral junction
3) craniotabes (softening of skull bone)
4) delayed definition

273
Q

What is rickets?

A

Osteomalacia in children

274
Q

what is renal osteodystrophy caused by?

A

Caused by chronic renal failure and compensatory hyperparathyroidism

275
Q

What are some pathologic findings of renal osteodystrophy?

A

1) Resorption of bone 2) osteofibrosis 3) Osteomalacia 4) Osteitis cystica 5) Brown tumors of hyperparathyroidism (rare)

276
Q

What is a synonym for hyperparathyroidism?

A

Osteitis fibrosa cystica

277
Q

What is hyperparathyroidism and what will happen with serum values?

A

Anatomical change due to severe pth elevation that leads to increased serum Calcium, and decreased serum phosphate leading to bone breakdown and fractures

278
Q

What is Renal osteodystrophy?

A

Term that collectively describes all skeletal changes of chronic renal failure including:
1) Increased osteoclastic bone resorption mimicking osteitis fibrosa cystica
2)delayed matrix mineralization (steomalacia)
3) Osteosclerosis
4) Growth retardation
5)

279
Q

What are some pathogeneic features of renal osteodystrophy?

A

1) Chronic renal failure -> phosphate retention -> increased PTH to balace Ca/PO4 (2:1 ratio)
2) Chronic renal failure -> decreased vit D activation in kidneys -. Decreased PTH suppression and decreased Ca absorption
3) Chronic renal failure -> metabolic

280
Q

What lab values would be present with hyperparathyroidism?

A

High serum calcium, low serum phosphorus, and high ALP (signifies bone fractures and breakdown)

281
Q

About 80% of osteomyelitis results from what?

A

contiguous spread or from open wounds it is often polymicrobial.

282
Q

What are some of the common infecting organims with osteomyelitis?

A

S. aureus, MRSA(methicillin-resistant S. aureus), Pseudomonas aeruginosa, serratia sp (IV drug users), salmonella sp (sickle cell disease), histoplasmosis, blastomycosis, or coccidioidomycosis (valley fever)

283
Q

What bones are often involved with osteomyelitis?

A

The vertebrae are often involved

284
Q

what pathophysiology tends to occur with osteomyelitis?

A

Tends to occlude local blood vessels causing bone necrosis and local spread of infection therefore infection may expand through the bone cortex and spread under the periosteum

285
Q

What are some signs and symptoms of osteomyelitis?

A

Acute: usually experience weight loss, fatigue, fever and localized warmth, swelling, erythema and tenderness. Chronic: intermittent bone pain, tenderness and draining sinuses.

286
Q

What are x-rays like for osteomyelitis?

A

they become abnormal after 2-4 weeks showing periosteal elevation, bone destruction, soft-tissue swelling, and in the vertebrae it shows loss of body height or narrowing of the adjacent infected intervertebral disk space, and destruction of end plates abo

287
Q

What will show abnormalities earlyer than x-rays with osteomyelitis and what are the limitations?

A

Bone scans show abnormalities of osteomyelitis earlier than plain x-rays but does not distinguish among infection, fractures, and tumors

288
Q

What is a characteristic presentation of long standing osteomyelitis?

A

A drainage tract into the subperiosteal shell of viable new bone (involucrum) and an inner native necrotic cortex (sequestrum)

289
Q

Paget’s disease is aka?

A

Osteitis deformans.

290
Q

What is a common feature of Paget’s disease?

A

Charaterized by irregular restructuring of bone and subsequent thickening and dformities of bones

291
Q

What is the histologic hallmark of paget’s disease aka osteitis deformans?

A

Mosaic bone pattern. (histologic hallmark)

292
Q

How is Paget’s disease diagnosed?

A

Radiologically

293
Q

what are 3 phases in the evolution of Paget’s Disease?

A

1) Destructive (osteolytic) phase
2) Mixed phase
3) Osteosclerotic phase

294
Q

What can paget’s disease lead to?

A

Osteogenic sarcoma

295
Q

Why are the 3 phases of evolution of Paget’s disease pertinent?

A

Because all three of the phases can be seen on the same radiograph of a single long bone (light to dark)

296
Q

What are some common yet obscure symptoms of paget’s disease?

A

Hat size can be increased and hearing loss due to auditory foramen narrowing

297
Q

What is a benign tumors of the bone?

A

Osteoma

298
Q

What is a benign tumors of the cartliage?

A

chondroma

299
Q

What is a benign tumors of connective tissue?

A

Fibroma

300
Q

What is a malignant tumors of the bone?

A

Osteosarcoma and Ewing’s sarcoma

301
Q

What is a malignant tumors of the cartliage?

A

chondrosarcoma

302
Q

What type of primary bone tumor (both benign and malignant) are found in the epiphysis?

A

Benign: Giant cell tumor (osteoclastoma) Malignant: none

303
Q

What are Giant cell tumor is aka?

A

Osteoclastoma.

304
Q

What type of primary bone tumor (both benign and malignant) are found in the metaphysis?

A

benign- osteochondroma. Malignant- Osteosarcoma.

305
Q

What type of primary bone tumor (both benign and malignant) are found in the Diaphysis?

A

Benign- osteoid osteoma. Malignant- Ewing’s sarcoma.

306
Q

What type of primary bone tumor (both benign and malignant) are found in the intramedullary area?

A

Benign- enchondroma. Malignant- chondrosarcoma.

307
Q

With osteosarcoma the periosteum has been lifted and laid down a shell of reactive bone known as what?

A

Codman triangle.

308
Q

What is an enchondroma?

A

Typically a benign cartilage tumor that is found on the inside of typically small bones like the hands and feet and can cause pathologic (spontaneous, non tramatic) fractures

Pathology I Final (3 decks)

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