Temporal Arteritis + Osteoporosis (32) Flashcards

1
Q

What is GCA?

A

Inflammatory disease of blood vessels (large and medium) of the head, mainly branches of ECA.

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2
Q

Which part of the the vessel is affected most for GCA?

A

Tunica medium

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3
Q

What are the pathological changes in microscopic picture of GCA?

A
  • Involved arterial segments develop intimal thickening (with occasional thromboses) that reduces the luminal diameter.
  • Classic lesions exhibit medial granulomatous inflammation centered on the internal elastic lamina that produce elastic lamina fragmentation.
  • There is an infiltrate of T cells (CD4+ > CD8+) and macrophages.
  • Although multinucleated giant cells are seen in approximately 75% of adequately biopsied specimens, granulomas and giant cells can be rare or absent.
  • Inflammatory lesions are only focally distributed along the vessel and long segments of relatively normal artery may be interposed.
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4
Q

What is one simple blood test to prove GCA?

A

ESR (elevated)

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5
Q

Why does blindness occur in GCA?

A

Ophthalmic artery involvement

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5
Q

What is the most confirmatory test for GCA?

A

Temporal artery biopsy

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5
Q

Why did the patient develop osteoporosis?

A

Steroid therapy and post-menopausal status.

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6
Q

What is the treatment for GCA?

A

Corticosteroids. Start prednisolone 60mg/d PO immediately or IV methylprednisolone if evolving visual loss or history of amaurosis fugax. Typically a 2-year course.

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6
Q

What are the pathological changes in osteoporosis?

A
  • Histologically normal bone that is decreased in quantity.
  • Postmenopausal osteoporosis, the increase in osteoclast activity affects mainly bones or portions of bones that have increased surface area, such as the cancellous compartment of vertebral bodies.
  • The trabecular plates become perforated, thinned, and lose their interconnections, leading to progressive micro fractures and eventual vertebral collapse.
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7
Q

What is osteoporosis and what is its pathogenesis?

A
  • Metabolic bone disease characterized by low bone mass, micro architectural deterioration of bone tissue, increase bone fragility, and loss of bone matrix.
  • Three main mechanisms: inadequate peak bone mass, excessive bone resorption, and inadequate formation of new bone during bone turnover.
  • Mechanisms by which corticosteroids cause osteoporosis: direct inhibition of osteoblast formation, direct stimulation of bone resorption, inhibition of GIT calcium absorption, stimulation of renal calcium losses, and inhibition of sex steroids.
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8
Q

How can multiple myeloma be diagnosed?

A

Punched-out lytic skull lesions on x-ray, M spike on protein electrophoresis, Ig light chains in urine (Bence Jones proteins), and CRAB (hypercalcemia, renal insufficiency attributable to myeloma, anemia, and bone lesions).

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8
Q

What are the causes of osteoporosis?

A
  • Primary: idiopathic, postmenopausal, and senile.
  • Secondary: endocrine disorders (Addison disease, diabetes type 1, hyperparathyroidism, hyperthyroidism, hypothyroidism, pituitary tumors, neoplasia, carcinomatosis, and multiple myeloma), gastrointestinal (hepatic insufficiency, malabsorption, malnutrition, and vitamin C and D deficiencies), drugs (alcohol, anticoagulants, anticonvulsants, chemotherapy, and corticosteroids), and miscellaneous (anemia, homocystinuria, immobilization, osteogenesis imperfecta, and pulmonary disease).
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9
Q

What are the other causes of pathological fracture?

A

Skeletal metastasis, Paget’s disease, multiple myeloma, rickets, osteomalacia, osteogenesis imperfecta, and radiotherapy.

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10
Q

What is multiple myeloma?

A
  • t’s a plasma cell neoplasm commonly associated with lytic bone lesions, hypercalcemia, renal failure, and acquired immune abnormalities.
  • It produces large amounts of IgG 55% or IgA 25%.
  • It is the most common primary bone tumor in elderly.
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11
Q

What are Bence Jones proteins?

A
  • They are monoclonal globulin proteins or immunoglobulin light chain found in the urine.
  • The proteins are produced by neoplastic plasma cells.
  • Bence Jones proteins are present in 2/3 of multiple myeloma cases.
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12
Q

What are the concerns if going to surgery (on steroids)?

A

Addisonian crisis (see Steroids station, ASSCC).

13
Q

How can Addisonian crisis be prevented?

A

Increase the patient steroid dose prior to surgery or convert to IV hydrocortisone.

13
Q

What caused the patient’s sudden death in POD1 after THA?

A

Fat embolism.

14
Q

What are the causes of fat embolism?

A

Long bone fracture (closed), major burns, acute pancreatitis, DM, orthopedic surgery (intramedullary nailing, joint reconstruction), decompression sickness, and CPBG (cardiopulmonary bypass graft).

15
Q

How can fat embolism be managed?

A
  • Mainly supportive/prevention of complications like ARF, ARDS.
  • Respiratory (O2/mechanical ventilation), fluid and electrolytes balance, general (DVT, sepsis, nutrition).
  • Specific unproven: ethanol, dextran, and heparin.