W10. ch.19.BONES&JOINTS Flashcards

1
Q

How many bones?

A
  • more than 200, short and long
  • made of osteocytes and extracellular matrix that is impregnate with calcium phosphate salts
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2
Q

Most NB functions of the bones

A
  • mechanical support for the muscles
  • protection of the internal organs (ribs)
  • support of hemapoesis
  • storage of calcium and phosphe salts
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3
Q

Normal structure and shape of bones: influences

A
  • interaction with the muscles
  • hormonal regulation of phosphate and calcium
  • also bone formation and bone resorption
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4
Q

Osteoblasts and Osteoclasts

A
  • osteoblasts form new bone
  • osteoclasts remove and remodel old bone under the influence of hormones (parathyroid, vit c &D), and various other substances such as interleukins and prostaglandins
  • calcium and phosphate released from the bone enter circualtion and are in balance with ionized calcium and phosphate in the serum. Balance is tightly regulated by PTH and vit D.
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5
Q

What is a joint?

A
  • junction between 2 or more bones. Support, structural firmness, and movement.
  • 2 types: synovial and joints that allow for limited or no movement (synathroses)

synovial joint is enclosed in a connective tissue capsuke composed of ligaments. inside lined with synovial cells which secrete fluid

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6
Q

Developmental Disorders of the Bone

A
  • Achondroplasia:AD, causes dwarfism
  • Osteogenesis imperfecta: several diseases characterized by deffective bone formation
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7
Q

Osteomyelitis

A
  • infection of the bone. May present as acute infection that progresses to osteomyelitis
  • most common causes are pyogenic cocci, most staphylococcus aureus
  • poorly cleansed wounds infected by trauma or GSW
  • sickle cell predisposed to infections caused by salmonella
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8
Q

Asceptic Bone Necrosis

A
  • sudden onset of ischemia caused by desruption of blood flow, causes bone infarct
  • infarcts in growing bones occur mostly in children and adolescents
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9
Q

Pathogenesis of Staphylococcal Osteomyelitis:

Where does it occur most often?

In adults, what does it occur as?

How is it treated?

A

-occurs in metaphysis of bone, typically occurs in growing children. Affects boys more than girls - trauma? Metaphysis is the most vascular portion of the bonehese vessels, known as nutrient arteries, penetrate the cortical bone and deliver blood to the zone of the epiphysial growth platethis “direct access” facilitates entry of bacteria into the bone during bacteremia

In adults, osteomyelitis occuts as a complication of bone fracture or bone surgery, or spread of infection to soft tissues

-suppurative must be tx. with large dose abx. Surgury may be required depending on draninge of pus and destruction of bone.

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10
Q

Osteomyelitis image

A
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11
Q

Circulatory Disturbances in bone: Aseptic Bone Necrosis

what is it

most often in which age group

which bones are more at risk

in elderly, which site?

causes?

A
  • sudden onset of ischemia cause by interruption of blood flow - causes bone infarcts
  • Asceptic infarcts of growing bones are diseases that most often occur in children - occur in ossification centers of various growing bones. Can also occur in the elderly at a high rate.
  • Certain growing bones are more at risk: carpal bones due to limited blood supply
  • In elderly: head of the femur is most nb site - fumur fractures and osteoporosis are often incapacitating
  • cause of most infarcts in unknown, but some may be related to trauma, emboli, radiation, or drugs. Well documented causes include air emboli in decompression disease, and microthrombi and sludges in sickle cell.

-

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12
Q

Metabolic disorders of bones: Osteoporosis

A
  • multifactorial disease characterized by absolute reduction of total bone mass
  • most prevalent bone disease worldwide
  • 1/3 of women older than 65 have some minor fracture related to osteoporosis
  • in those older than 85, 1/3 of all north american women and 1 in 6 men are temp or perm confined to bed b/c of hip fractures
  • hip fractures are the most incapacitating complication of osteoporosis
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13
Q

Primary and Secondary Osteoporosis

A

Primary: No definitive clues of etiology. Accounts for most cases. Is disease of elderly persons, accounts for more women than men

Secondary: occurs at any age, related to identifiable causes, including

  • hormonal disturbances: excess (hyperadrenocorticism), or deficiency (hypogonad, diabetes) of hormones
  • Dietary insufficiency of intake (calcium, vit C), or malabsorption of nutrients (intestinal or liver disease)
  • Immobilization
  • Drugs: anticonvulsants or heparin
  • Tumors: hormones of endocrine glands, or direct damage from tumors such as breast cancer
  • osteoporosis often has multiple causes: age, smoking, alcohol. Cirrhosis of liver affects vitamin D metabolism. Post menopausal - lack of estrogen, nutritional deficiencies r/t alcohol
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14
Q

Causes of Osteoporosis: Image

A
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15
Q

Pathogenesis of Osteoporosis:

Characterized by

A
  • characterized by simultaneous loss of bone mass and minerals
  • pathogenesis of primary osteoporosis remains unknown, but several factors bone loss have been id’d
  • initial bone mass
  • diet and lifestyle
  • hormones
  • age related changes in metabolism
  • certain prescribed medications
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16
Q

Osteoporosis- age

A
  • normal bones undergo remodeling throughout the entire lifespan
  • up to the age of 30, bone formation by osteoblasts exceeds bone resorption by osteoclasts
  • after 30, resportion exceeds formation, resulting in a net bone loss of 0.5% each year. After menopause, this is accelerated for a loss of betweem 1-3% each year. May be related to estrogen. Estrogen therapy can prevent or slow bone loss
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17
Q

Osteoporosis: develops more often in

A
  • gracile white woman of small frame, who have smaller initial bone mass than larger frames
  • denser bones in men, blacks, and athletes
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18
Q

Osteoporosis and nutrition:

Which nutrients are most NB?

Under which conditions may this be impaired?

A

Calcium and vitamin D are important, and are added to meet requirements of north american diet.

-If absorption of calcium and vit D are impaired (intestinal or liver disease), then deficiencies develop

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19
Q

Pathology of Osteoporosis: type 1

Describe osteoporotic bones

What part of the bone is lost?

Which bones predominate?

What is the major complication?

A
  • Osteoporotic bones are thin and brittle, prone to fracture
  • loss involves both cortical and spongy bone
  • In type 1, which occurs in post-menopausal women, trabecular bone loss predominates, occuring most prominently in the vertebrae and distal radius.

Major complication is crush fracture of vertebral bodies and of the distal end of the radius.

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20
Q

Pathology of osteoporosis: Type 2

Characterized by:

Most serious complication:

A
  • In type 2, osteoporosis of old age, characterized by proportunate loss of cortical and trabecular bone of the long bones.
  • Most serious fractures of type 2 are the head of the femur
  • none of the bone is spared, nor is trauma required. A persons body weight alone can cause the fracture.
  • vertebrae are common sites of microfractures, which produce wedge shaped deformity. Multiple make elderly look smaller and bent forward
  • these anatomical changes compromise function of internal organs
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21
Q

Clinical Features of osteoporosis

which bone fractures are most incapacitating?

Are there biochemical markers?

A
  • symptoms are extremely variable and non-specific
  • vertebral fractures cause back pain and kyphosis
  • extensive osteoporosis may reduce a persons height up to 15cm or 10%
  • fractures of long bones may be incapacitating
  • over 1 million hip fractures per year, 25% never heal
  • despite loss of bone, people show no biochemical markers. Serum calcium, phophate, and alkaline phosphatase are normal
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22
Q

Dianosis of osteoporosis

A
  • best diagnosed by radiographic studies
  • xray not very sensitive, and detect signs only after 30-50% reduction. Therefore prevention is essential.
  • Bone mineral density measured by dexa scan, can provide more precise estimate of bone loss
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23
Q

Osteomalacia:

What is it?

What causes it?

What is it called in growing bones?

A
  • softening of bones with deformities related to inadequare mineralization of organic bone matrix
  • Changes are caused by disturbances vitamin D or phosphate metabolism
  • Osteomalacia of growing bones in children is called rickets
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24
Q

Etiology of Osteomalacia

  • r/t which nutrients?
  • Why might they be deficient?
A
  • vitamin D and phosphate are essential nutrients
  • Vit D derived from the diet but also synthesized in skin under uv light

Deficiency of vid D: inadequate intake (many north american foods have fortified with vit D), inadequate exposure to sunlight, abnormal intestinal absorption (diseases of small intesting when vit D not absorbed, or billiary /pancreatic diseases with fat malabsorption

-osteomalacia may also be caused by hypophosphatemia r/t abnormal absorption or excessive loss of phosphates. Malabsorption from intestinal diseases or resection. PTH also prevents tubular resorption of phosphates, thus phosphate wasting in urine during hyperparathyroid

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25
Q

Pathogenesis of Osteomalacia:

Where is vitamin D activated?

What is the 3 functions of the main form?

A
  • Activation of vitamin D occurs in the liver and the kidneys
  • several active metabolites are formed, the most important is hydroxylated 1,25 vitamin D. This form has 3 main functions
  • stimulation of intestinal absorption of calcium and phosphorus
  • Action on the bone, includes deposition of calcium into the osteoid and mobilization of calcium from calcified bone. Vitamin D is essential for mineralization of the osteoid
  • stimulation of the PTH dependent resorption of calcium in the kidney
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26
Q

Pathology of Osteomalacia

Deficiency in ___ results in ____

Typical complication

osteomalacia is characterized by

A
  • Vitamin D deficiency results in osteopenia, which is visible as increased bone lucency on xray. CLinically, bones are soft and pliable.
  • fractures and deformity are typical complications
  • rickets (osteomalacia in children) affects bone development

Osteomalacia is characterized by an excess of osteoid around the calcified core of the trabeculae of spongy bone and on the endocavitary side of compact bones. Fractures are common and heal by exuberant osteoid formation. Softening of the bones may also produce deformities.

These are common in children affected by rickets but are rare in adults.

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27
Q

Pathology of Rickets

A
  • endochondral ossification in the growth plate is most severely disturbed
  • this results in growth retardation, bone deformities, and fracture of long bones
  • bow legs result from the inibility of the soft leg bones to carry the weight of the body
  • widened junction between rib bone and cartilage- the costochondral junction- appears nodulat and can be palpated as beads on the thorax (rachitic rosary)
  • softenin of cranial bones is called craniotabs
  • dentition is delayed and the teeth may be speckled by as a result of incomplete miniralization
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28
Q

Clinical Features of Osteomalacia in Adults

A
  • often asymptomatic, or cause non-specific bone pain
  • muscle weakness is common
  • skeletal deformities develop slowly and are not prominent
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29
Q

Diagnosis of Osteomalacia

A
  • based on clinical, radiographic, and labs
  • in vitamin D related - serum calcium and phosphate are low, but the PTH level is elevated b/c of compensatory parathyroid hyperplasia
  • in osteomalacia resulting from phosphate deficiency, serum phosphate is low, but calcium and PTH normal
30
Q

Renal Osteodysrophy

A
  • renal failure associated with complex bone changes
  • changes related directly or indirectly to altered homeostasis of calcium and phosphates in the body
31
Q

Pathogenesis of Renal osteodystophy

A
  • b/c kidneys can not excrete the phosphorus, serum phosphate levels rise.
  • this is accompanied by hypocalcemia and compensatory hyperparathyroid
  • PTH stimulates bone resorption, and a release of calcium and phosphate into the blood, resulting in hyperphosphatemia, normalization of blood calcium levels, and occasionally hypercalcemia
  • Calcium absorption in the intestines is decreased due to the damaged kidney not being able to produce hydroxylated vitamin D, which is essential for intestinal calcium absorption
32
Q

Pathology of Renal Osteodystrophy

A
  • pathologic changes in the bone is highly variable
  • bone trabeculae are predominantly composed of osteoid and are poorly mineralized (osteomalacia)
  • PTH stimulates osteoblasts and firboblasts, causing medullary osteofirbosis
  • may cause cystic changes
  • aggregates of osteoclasts may form small nodules

renal osteodystrophy may improve with transplantation following dialysis

33
Q

Pagets disease

A
  • unknown origin, irregular restructuing of bone that leads to thickening and deformities of bone
  • 3% of all men and women after 60 show radiologic signs
  • highest prevalence seen in british, lowest incidence is east asian
  • familial form linked to gene locus on chromosome 18
  • pathogenesis- linked to defect in function of osteoclasts
  • cytokines stimulating the formation of osteoclasts, maybe?
  • 3 phases: 1-destructive phase marked by bone resorption

2-mixed- bone resorption balanced by bone formation

3-osteosclerotic phase- trabeculae appear irregularly thickened and normal bone is replaced with wide, sclerotic, dense bone

34
Q

Pagets Disease: Clinical Features

A
  • course is highly variable
  • can involce 1 or more bones
  • cranium, proximal femur, and axial skeleton most commonly affected
  • tibia and fibula are thickend and deformed -bowlegged
  • many pts are asymptomatic or have bone pain
  • thickened cranial bones may cause headaches or vision loss
  • osteosarcoma as late complication- because these are so rare - it is assumed that Pagets is involved in tumors that develop over 50
35
Q

Pagets Disease: image

A
36
Q

Diagnosis of Pagets Disease

A
  • made by xray
  • thickened bones show honeycomb or cotton wool appearance
37
Q

Types of fractures: image

A
38
Q

Joint Dislocation

A
  • bones forming a joint lose contact and become misaligned
  • the trauma may tear the joint support structures (ligaments)
  • may damage blood vessels (lead to hematoma)
  • sports injuries often knee and shoulder
  • may occur at any age, but more often is people with loose joints, or collagen/connective tissue disorders
39
Q

Bone Tumors

A
  • Primary bone tumors rare, account for less than 1%
  • 50% are derived from blood forming cells of the bone marrow
  • tumors of bone cells account for 50%
  • secondary tumors outnumber primary 10:1 - breast, lung, kidney, thyroid, prostate
40
Q

Bone tumors: Benign

A
  • Benign tumors are composed of bone cells (osteoma), cartilage cells (chondroma), or fibroblasts (nonossifying fibroma)
  • appear as bumps or soft defects of the outer surface of the bones, or small nodules on the inside of the bones that are discovered on routine xray, or because of the plane they produce on expansive growth
  • only removed if they cause pain
  • do not tend to undergo malignant transformation
  • exception if chondroma- which occasionally gives rise to chondrosarcoma. Multiple chondromas in genetic conditions are at higher risk for this.
41
Q

Malignant Bone Tumors:

occus most often

image of most important features

A
  • occur most often in males
  • bone tumors are classified by the peak age incidence and anatomical location
42
Q

Osteosarcoma

A

Most common primary malignant tumor involving the bone

  • this bone forming tumor most often involves metaphysis of long bones of the extremities. 50% of these tumors located in the knee. Jaw bone is the most common short bone.
  • tumor of young persons. In adult, most develop as a complication of Pagets.
  • metastasize through blood- most dying pts have lung mets
  • tx. is surgical resection and chemo. w/out chemo, less than 10% survive 5 years. With chemo, 5 year survival is 60-70% with some cure.
43
Q

Chondrosarcoma

A
  • malignant tumor composed of neoplasic cartilage cells
  • Tumors originae in the axial skeleton (bones of trunk -pelvis, ribs, vertebrae), and adjascent portion of long bones (proximal femur and humerus).
  • On basis of maturity and level of differentiation of cells, tumors can be classified as well differentiated, moderately differentiated, or poorly differentiated (Grade, I, II, III). Grade I tumors have better prognosis.

Prognosis for I (90%), II (60%), III (40%)

  • affect adults- peak incidence 35-60 years
  • tx. is surgical resection - tumors cells are insensitive to chemo
44
Q

Ewings Sarcoma

A
  • malignant tumor composed of undifferentiated bone marrow cells
  • rare, but still second most common tumor in bones of children. Age 10-20. More common in males. Most rare in african american and asian.
  • composed of small cells that have hyperchromatic bluish nuclei with very little cytoplasm. Cells are poorly understood but may be in common with primitive mesenchymal and bone marrow cells
  • 85% have translocation between chromosome 11 and 22
  • invade cortical bone and spread to soft tissues and extremities
  • cortical bone reacts and new bone formed under periosteum - onion like apprearance on xray
  • may metastasize via blood- highly malignant and lethal w/out chemo. With chemo -75% of children will survive 5 years, and 50% become longterm survivors.
45
Q

Most Common sites of bone tumors: image

A
46
Q

Giant Cell Tumors

A
  • classified as benign or low grade malignant
  • found as expansible lesions eroding the cortical bone in the epiphysis of long bones
  • most often dx. in young adults 20-40
    tx. of choice is removal

cure rate is 95%, metastases are rare

47
Q

Joint Diseases

A
  • most nb is osteoarthritis, or degenerative joint disease, an rheumatoid arthitis. These account for more than 90% of all cases in rheumatology practice
  • tumors of the joints are rare (synovial sarcoma is soft tissue not joint)
48
Q

Osteoarthritis

A
  • also called djd, is the most common disease of the joints
  • classified as:

Primary: causes unknown

Secondary: develop under conditions which stress the joint surfaces such as repeated trauma, congenital abnormal joints (hips and knees of achondroplasia), structurally abnormal joints (affected by hormonal or metabolic diseases)

49
Q

Pathogenesis of DJD

A

-unknown, though most favor wear and tear, consider articular cartilage the primary site of injury

Facts in support of wear and tear:

  • DJD preferentially affects weight bearing joints (knee, hip, vertebrae). Increased risk in overweight individuals.
  • prevalence increases with age. almost everyone over 65 has some evidence.
  • Mechanical instibility and stress of joint accelerates the disease
  • abnormal connective tissue degenerates quickly. Many abnormal properties are inherited-family patterns. Seen more in Native Americans
50
Q

Pathologic Changes in Osteoarthritis:image

A
51
Q

Pathologic Changes in Osteoarthritis

A
  • not specific
  • Initial changes seen inarticular cartilage- shows softening, thinning, irregular defects.
  • very early shows fibrilation with formation of verticle clefts
  • the cartilage fragments are shed into the cavity, leaving behind the denuded surface of subchondral bone
  • continued pressure induces sclerosis of the subchondral plate, called ebumination b/c the bone appears dense like ivory
  • bone degeneration under stress causes cysts, and a bone defect that communicates with the joint cavity
  • at the margins of the joint, spurs of new bone (osteophytes) form, projecting into adjascent connective tissue
  • the traumatized soft tissue undergoes swelling and inflammation
52
Q

Clinical Features of Osteoarthritis

A
  • non specific
  • even large deformities can result in minor disability
53
Q

Symptoms and Pathology in Osteoarthritis: Table

A
54
Q

Symptoms of osteoarthritis

A
  • most common- pain relieved by rest
  • stiffness for 20-30mins then dissapears
  • joints show reduced mobility and tend to be deformed
  • joint movement associated with crepitus
  • muscle spasm and contractures develop as disease progresses
  • weight bearing joints most affected (hip, knee, cervicle and lumbar spine)
  • hand: distal interphalangeal, proximal interphalangeal and first carpometacarpal joints
  • foot: first metatarsalphalangeal (formation of bunion)

symptoms depend on duration of the disease and the anatomic distribution of the joints involved

55
Q

knee joints in osteoarthritis

A

present with pain or crepitus

deformities result in bowleg or knock knee

56
Q

Hip and osteoarthritis

A

-pain in buttocks, upper thigh and limited mobility - antalgic gait

57
Q

Spine and Osteoarthritis

A

-p.442

58
Q

Diagnosis of Osteoarthritis

A
  • clinical symptoms and radiologic findings
  • typical xray findings include narrowing of joint space, sclerosis of subchondral bone, cystic bone changes, ostephytes
  • DJD produces no lab findings
  • joint fluid analysis cannot confirm osteoarthritis
59
Q

Rheumatoid Arthritis

A
  • very common, affects 1% of worlds population
  • most common in adults 40-79 years old
  • characterized by:
  • chronic, symmetric inflammation of joints
  • significant, but not diagnostic lab findings with seralogic data suggestive of immune disorder
  • variable extrarticular manifestations
60
Q

Rheumatoid Arthritis: Etiology

A
  • Cause of RA is unknown
  • 4x more common among women (could be r/t sex hormones or autoimmune)
  • lifestyle: more in cold climates, and urban
  • genetic component
61
Q

Pathogenesis and Pathology of RA

A

-sysetmic autoimmune disease that involves the synovial joints

62
Q

Clinical Features of RA

A

p.443

63
Q

what is the role of genetics and autoimmunity in the pathology of RA?

A

The pathogenesis of rheumatoid arthritis is unknown; however, it is four times more common in women than in men.

Genetic factors are important. Indeed, 70% of patients share a major histocompatibility complex (MHC) allele

. Serologic studies typically show evidence of autoimmune disease (e.g., rheumatoid factor).

64
Q

What is the pathology of RA?

A

Pannus produces mediators of inflammation that contribute to joint and bone erosion.

Joints become immobilized and the intraarticular space may become obliterated as granulation tissue forms collagen-rich scar tissue (referred to as ankylosis).

65
Q

Clinical Features of RA:

Typically present with

most serious complication

other symptoms

A

Rheumatoid arthritis typically presents with acute onset of joint pain, swelling, and redness.

Symmetric involvement of the small joints is typical.

The most serious complications are joint deformities and contractures.

Because rheumatoid arthritis is a systemic disease, many patients show low-grade fever, loss of appetite, malaise, fatigue, and anemia.

66
Q

What are the main causes of infectious arthritis?

A

Infectious arthritis may result from (1) hematogenous spread of pathogens during sepsis, (2) direct spread from other bones, or (3) direct inoculation from surgery or trauma.

The most common bacterial arthritis is caused by the Lyme disease spirochete (Borrelia burgdorferi).

67
Q

What is gout and what are the features of primary and secondary?

  • Gout denotes
  • Primary classified as
  • Secondary is related to
A

Gout denotes a group of diseases characterized by hyperuricemia and deposition of uric acid crystals in various tissues (e.g., joints and kidneys).

Gout may be classified as primary or secondary.

Primary gout is further classified as metabolic (overproduction of uric acid) or renal (underexcretion of uric acid).

Secondary gout is related to another disease that affects uric acid metabolism or urate excretion.

68
Q

How does hyperuricemia to podagra?

A

The most common sites of uric acid deposition are the joints and periarticular connective tissues.

In most cases, the first symptoms occur in the joint of the big toe. This is clinically known as podagra (foot seizure).

Uric acid is probably released from the joint capsule by minor trauma, where it enters the joint cavity and supersaturates the fluid.

Low temperature in the feet contributes to urate crystallization. The crystals are chemotactic and elicit an acute inflammatory response.

69
Q

What are the clinical features of acute and chronic gout? What are systemic features?

A

Clinical features of an acute gout attack include warm, swollen, and painful toe.

Systemic features include fever, tachycardia, and leukocytosis.

Chronic gout is marked by less inflammation and more pronounced bone deformities.

70
Q

What are trophi?

A

Subcutaneous deposits of uric acid crystals in patients with gout are known as tophi.

They occur most commonly on the ears and exterior surfaces of the arms.

71
Q

What kind of urinary stones are found in people that have gout?

A

Approximately 20% of patients with gout have uric acid stones, which predispose to obstructive nephropathy and/or chronic pyelonephritis.