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CMS - bone & joints 1&2 Flashcards

1
Q

How does bone growth change with age?

A

Different at stages of aging:
rapid in infants and slows as we age into childhood.

There is a growth spurt during adolescence.

By age 18, adult bone levels have been achieved.

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2
Q

What are the types of bone?

A

Cortical / compact / lamellar bone - outer layer

Cancellous / trabecular bone - inner layer. Contains bone marrow.

Woven bone - immature / pathologic bone. Higher vol of osteocytes.

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3
Q

What is Cortical / compact / lamellar bone ?

A

Bone that forms the shaft of long bones and outer layer of flat bones.

Highly organised.

Arranged in concentric rings of bones, adapted to withstand strain of pressure.

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4
Q

What is cancellous / trabecular bone ?

A

Found in flat bones and end of long bones.

Interconnected network of rods and plates of bones.

Allows for resistance of compression of loads.

Main site of turnover where mineral turnover occurs.

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5
Q

What is woven bone ?

A

A more disorganised type of bone.

Appears in early years or fracture sites. E.g. when sustaining an injury.

Also present in diseases with high bone turnover e.g. Paget’s disease.

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6
Q

What makes bone mineralisation important?

A

If the osteoid (collagen) is not mineralised, it would be soft and “bendy”, leading to bone disorders

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7
Q

What is hydroxyapatite?

A

Bone mineral

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8
Q

What are bones made of?

A

Calcified connective tissue

Matrix of collagen fibres containing osteocytes.

Type 1 collage (osteoid)- main protein forming parallel lamallae - offers different densities.

​
Non-collagen proteins e.g. osteopontin (bone remodelling) and osteocalcin, fibronectin (tissue repair)

Within the bone matrix, Ca and phosphate minerals are found abundantly - adds strength and density to the structure.

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9
Q

What are the receptors found on osteoblasts?

A

Express receptors for (Parathyroid hormone “PTH”, oestrogen, glucocorticoids, vitamin D, inflammatory cytokines and TGF beta) which influence bone modelling

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10
Q

An _______ is derived form local mesenchymal stem cells and synthesises bone. What happens during apoptosis?

A

Osteoblast

After they die, osteocytes will line the bone in its’ place.

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11
Q

What is an osteocyte?

A

cells derived from osteoblasts.

Activate bone formation by responding to mechanical strain. Key roles within bone resorption.​

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12
Q

What is the bone cell involved in bone resorption?

A

Osteoclast

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13
Q

What are the functions of osteoclasts?

A

Rich in Alkaline phosphatase - regulates bone mineralisation.

Also express receptors for hormones etc that influence bone remodelling for instance - oestrogen, PTH, glucocorticoids, vit D, inflammatory cytokines and TGF-B (transforming growth factor beta – tumour suppressor).​

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14
Q

Bone formation, metabolism and blood Ca levels are affected by _______________, ________________ and ___________.

A

parathyroid hormone, Vit D and calcitonin.

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15
Q

What are the effects of bone morphogenic proteins?

A

These proteins affect bone formation - available as recombinant proteins, they are sometimes used in grafting procedures or regeneration procedures in oral surgery.

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16
Q

The ​parathyroid hormone is regulated by blood ________, ____________, and ____________ levels.

A

blood calcium, vit D levels and phosphate levels.

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17
Q

When PTH is secreted, intestinal transport of calcium & phosphate are _________, and removal of Ca from bones is ____________.

A

Ca & phosphate promoted

Removal of CA from bone is accelerated

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18
Q

Dietary Vit D is fat soluble, and absorbed from the upper small intestine – which promotes _____________________________________________________________.

A

intestinal absorption of Ca and phosphate.

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19
Q

Vit D is also synthesised in the skin from UV sunlight. How is it converted from the skin?

A

Vit D in the skin is converted by the liver and then kidney into the most active metabolite.

Skin: 7-dehydrocholesterol
-> Cholecalciferol (Vit D3)
-> Liver: 25- hydroxycholecalciferol
-> Kidney: 1,25 - dihydroxycholecalciferol

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20
Q

How is Vit D from food converted in the body?

A

Ergosterol (Vit D2) is converted in the Liver to 25- hydroxycholecalciferol
-> then Kidney: 1,25 - dihydroxycholecalciferol

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21
Q

What is the active metabolite of Vit D, and its role in bone?

A

1,25 - dihydroxycholecalciferol

  • controls bone metabolism & enhances Ca absorption.

The process is enhanced by the parathyroid hormone and low phosphate levels.

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22
Q

What is the role of calcitonin in bone?

A

​apposes the action of PTH & lowers blood Ca levels mainly by promoting the deposition of Ca in the bones.

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23
Q

Which other hormones may affect bone formation & metabolism?

A

Growth hormone and oestrogen hormones

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24
Q

How does blood Ca level affect on the activity of Parathyroid hormone?

A

Decreased Ca in blood will stimulate parathyroid gland to secrete PTH (increased), leading to:

1) ↑ Osteoclast bone resorption (taking Ca from bone)

2) ↑ Synthesis of 1,25- dihydroxyvitamin D3 (active D3 to absorb Ca and PO4 from intestines)

3) ↑ Intestinal Ca absorption (taking Ca from intestines)

4) ↑ Renal tubular resorption Ca (taking Ca from kidneys)

So increasing Ca in the blood

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25
Q

How does a damage to liver and kidneys lead to Vitamin D deficiency?

A

Vitamin D is converted into the most active form by the liver and kidneys as a result of parathyroid hormone and low Ca and PO4 levels.

So damage leads to deficiency.

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26
Q

What common features of illness are seen in elderly pts?

A
  • Nonspecific presentation​
  • Multiple pathology and consequent polypharmacy​
  • Interaction between conditions and between medications​
  • Loss of functional independence​
  • Impaired homeostasis, resistance to disease and recovery.
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27
Q

What common issues affect elderly pts?
- systemic and mental

A
  • Incontinence​
  • Instability (falls)​
  • Immobility​
  • Intellectual impairment(dementia and delirium).
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28
Q

What considerations should be made prior to prescribing for elderly pts?

A
  • Some antibiotics interact with Warfarin​

​

  • Azole antifungals affect blood clotting – increase INR.​

​

  • Make sure their medications do not react with LA. E.g. anti-parkinsonism drugs – may need to lower dose / avoid adrenaline. Check BNF.
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29
Q

What are the stages of healing of bone fractures?

A

Initial stages: Haemotoma formed with granulation tissue​

Vascular stage: re-vascularisation & resorption​

Primary callus formation: osteoid replaced with mature bone. Fracture is very stable. ​

Mature callus – months to years where new bone is laid down along lines of stress. Unnecessary bone replaced.

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30
Q

When bone fractures, healing occurs. Describe the initial inflammatory Cellular stage.

A
  • When the bone is fractured, the blood will rush into the area, forming Haematoma (source of hemopoietic cells & Growth Factors which are useful for repairing).

Then, inflammatory cells (Macrophages, neutrophils and platelets) will migrate to the fractured area secreting Cytokines which attract more cells (Fibroblasts & mesenchymal cells) into the fractured site, producing Granulation tissue (vascular tissue) around the fracture ends to stabilise it.

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31
Q

What happens in bone healing after the inflammatory cellular stage?

A

Then the inflammatory Vascular stage occurs:
- Neovascularisation occurs (new blood vessels formation), leading to Hyperaemia (increased blood flow). Then, Osteoclasts will absorb the fractured margins.

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32
Q

What happens in the Inflammatory Primary callus “Lump” stage of healing after a bone fracture?

A
  • Osteoblasts (bone-production), chondrocytes (cartilage-production), fibroblasts (CT-production) will proliferate and start to produce their products (bone, cartilage and connective tissue), forming a Callus (primary soft fibrous scar “cartilage” which is not visible radiographically)
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33
Q

What happens in the Reparative Bony callus stage of healing after a bone fracture?

A

4) Reparative Bony callus stage:
- The primary soft Callus (cartilage) is being produced quickly, stabilising the fracture temporarily.

Then, Endochondral ossification converts soft Callus (cartilage “Osteoid”) to hard Callus (woven bone), stabilising the fracture

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34
Q

Remodelling stage during bone fracture healing can take months & years. What happens during this time?

A

Remodelling stage (months & years):
- The hard Bony callus (woven bone) will be resorbed (by Osteoclast) & remodelled (by Osteoblast) into hard lamellar bone (bone’s original cortex structure) and the bone marrow cavity will be restored

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35
Q

What are the different types of bone disease?

A
  1. Genetic
  2. Acquired
  3. Joint disorders
  4. Arthritides
  5. Muscular dystrophies
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36
Q

What are the genetic bone diseases?

A

Osteogenesis imperfecta
Cleidocranial dysplasia
Osteopetrosis (Albers-Schonberg Disease)

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37
Q

What is Osteogenesis imperfecta?

A

A rare, autosomal dominant genetic disorder. Has 4 types.

Causes a defect in collagen. Can cause multiple bone fractures easily.

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38
Q

What are the effects of osteogenesis imperfecta on the body?

A
  • Blue sclera of eyes (connective tissue in eyes thinner)
  • Deafness
  • Easy bruising
  • Loose / hypermobile joints / tendons
  • May have cardiac complications
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39
Q

How can osteogenesis imperfecta affect dental management?

A

Care with extractions – fracture risk​

GA risk – chest deformity / cardiac issues​

Teeth – brown/purple/wear/soft dentine

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40
Q

What is Cleidocranial dysplasia?

A

Rare genetic defect – mainly involving skull and clavicle​.

Autosomal dominant

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41
Q

What are the clinical features of Cleidocranial dysplasia?

A

-Clavicles absent or defective – characteristic look​

  • Brachycephalic (broad short skull)​

-Hypoplastic midface = mandibular protrusion​ +/- clefts ​

Other skeletal defects

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42
Q

What are the dental implications of Cleidocranial dysplasia?

A
  • Hyperdontia​​
  • Supernumeraries​​
  • Retained deciduous dentition​​
  • Abnormalities with dentition e.g root formation, cysts et
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43
Q

What is Albers-Schonberg Disease?
Osteopetrosis

A

Rare genetic disorder​ with variable severity​.

Causes excessive bone density​ - risk of fracture but normal healing

Due to defect in osteoclastic activity and bone remodeling​

44
Q

What are the clinical features of Albers-Schonberg Disease?

A

Often no symptoms​. Incidental finding radiographically​

Symptoms: Bone pain, fractures, osteomyelitis​

+/- anaemia​

Susceptibility to infections (defective macrophages/neutrophils)

45
Q

What are the dental implications of Albers-Schonberg Disease?

A
  • Fractures of the jaw / osteomyelitis​​
  • When infection confirmed difficult to eradicate​​
    • Need to carry out ‘atraumatic’ surgery​​. Consider antibiotics for surgery
46
Q

Rickets / osteomalacia is an acquired, childhood disease. What causes this?

A

inadequate skeletal mineralisation due to lack of vitamin D / calcium from sunlight, foods (oily fish and eggs).

  • Worse in dark skin & premature children.
47
Q

What is the tx for rickets / osteomalacia?

A

Vitamin D supplements and dietary advice such as cod liver oil, salmon, mackerel, tuna, eggs yogurt, fortified foods with vitamin D - orange juice, milk, margarine and breakfast cereals.

48
Q

What are the dental effects of rickets?

A

Dental effects rare - delayed tooth eruption, dentinal defects, large pulp chambers, and enamel hypoplasia.

49
Q

If a person with Rickets is also diagnosed with malabsorption, what are other complications to watch out for?

A

hyperparathyroidism/vit K deficiency

50
Q

What is osteoporosis & who is prone to it?

A

Acquired disorder of bone.

Causes:
-Diminished bone mass​ and low bone density​ = fragile bones​ at risk of fracture.

Common in elderly. From 30 years – 1% bone loss per year​. Females: Post menopausal – 5% loss per year

1 in 3 Caucasian women, 50yo – 17.5% risk hip #, 16% risk forearm #

51
Q

Which factors may cause osteoporosis?

A

Calcium intake​

Reproductive hormones​

Parathyroid gland​

Physical activity

52
Q

What are the symptoms of osteoporosis?

A

Symptoms – often none in the early stages​ until unexpected fracture.​ Then maybe back pain, reduced height (over time), stooped posture, prone to bone fractures.

53
Q

How is osteoporosis diagnosed?

A

FRAX tool - measures risk of bone fracture
DEXA scan - measures bone density

54
Q

What is the tx for osteoporosis?

A

Hormone replacement, bisphosphonates, PTH, fluoride, Vitamin D, Calcitonin, Ca supplements

Avoidance of certain activity

Exercise - weight bearing

55
Q

How is osteoporosis diagnosed?

A

FRAX tool - measures risk of bone fracture
DEXA scan - measures bone density

56
Q

Describe the mechanism of bisphosphonate inhibitor of osteoclast activity.

A
  • Inhibit osteoclast activity & promote osteoclast apoptosis

Modulate signaling from osteoblasts to osteoclasts: increased osteoprotegerin production (OPG- inhibits resorption) , decreased RANKL expression.

  • bisphosphonates are concentrated under osteoclasts & released locally during bone resorption.
57
Q

What is Fibrous Dysplasia?
[acquired]

A

Chronic disorder where scar-like tissue grows in place of normal bone​. The fibrous tissue weakens the bone over time.

*may be more common in Afro-carribeans

58
Q

What are the clinical features of Fibrous Dysplasia?

A

Benign chronic fibro-osseous lesions in cranio-facial region - frequent in this area.​

​Monostotic (single) or Polystotic​ (multiple) bones affected.

59
Q

What is ​McCune Albright Syndrome? – *Fibrous Dysplasia

A

bone, skin and endocrine tissues affected.

Main feature is fibrous dysplasia.

60
Q

How is fibrous dysplasia diagnosed?

A

Radiology – ground glass appearance, poorly defined margins.

Biopsy may be required​ e.g. firm swelling in maxilla

Raised serum ALP and Urinary hydroxyproline (Serum Ca and Po normal)​

*If significant can be surgically reduced - may get a lot of bleeding.

61
Q

What is Pagets disease?

A

Bone disease that causes changes in balance of remodeling of bone​ and causes deformity.

Aetiology generally unknown ? viral / genetic.

Common 3% over 40 years​.

Symptoms: may be asymptomatic in early stages but often bone pain. Multiple systemic effects.

62
Q

What are the complications of Paget’s disease on body systems?

A

Musculoskeletal: bone pain, deformity, osteoarthritis of adjacent joints, fractures, spinal stenosis.

Neurological: hearing loss tinnitus, cranial nerve deficit, increased cerebrospinal fluid pressure, paraplegia.

CVD: congestive HF, increased cardiac output, aortic stenosis, atherosclerosis, endocardial calcification

Metabolic: hypercalcaemia, hyperuricemia (high uric acid), nephrolithiasis (kidney stones)

Neoplasia: sarcoma - osteosarcoma, fibrosarcoma, Giant cell tumour.

63
Q

How is Paget’s disease diagnosed?

A

Osteolysis on radiographs and mixed areas of lysis and sclerosis. ​

Serum ALP raised​

Ca and PO normal​

Raised urinary hydroxyproline and pyridinoline excretion

64
Q

What is the tx for Pagets?

A

Bisphosphonates

Calcitonin for pain relief

65
Q

What are the potential effects of widespread Pagets on the heart?–

A

can get artero-venous fistulas causing high output cardiac failure, can also sometimes develop into osteosarcomas.

66
Q

What are the dental impacts of Pagets?

A

~ ​Enlargement of maxilla, rarely mandible​.

~ Bulging in the zygomatic area (prominent zygomas)​

​~Hypercementosis of teeth sometimes​

67
Q

In a patient with Pagets, dental surgery may be more complex due to following risks.

A

Pt may be highly vascular – causing excess bleeding​

or​

poor vascularisation – leading to osteomyelitis (bone infection)

68
Q

What are the parathyroids?

A

Parathyroids are 4 small glands on the posterior aspects of the thyroid glands.

They produce the parathyroid hormone.​

69
Q

Parathyroids & Vit D control _______ levels.

A

plasma Ca levels.

70
Q

What is the role of parathyroid hormone in bone minerals?

A
  • acts on the kidneys by increasing renal reabsorption of calcium and pairing the reabsorption of phosphate.​

​- increases the absorption of Ca from the gut & also promotes osteoclastic bone resorption which consequently results in the rise of plasma Ca & ALP levels.

71
Q

~What is hyperparathyroidism?

A

Excess parathyroid formation from parathyroid glands.

Primary & secondary forms
1* - female predisposition. Single parathyroid adenoma. 50% asymptomatic, often associated with renal stones.

72
Q

What are the symptoms of primary hyperparathyroidism?

A

​- Hypercalcaemia, bone pain, pathological #, giant cell tumours, peptic ulcers, pancreatitis, hypertension. ​

-Local swelling sometimes in mandible​

  • Corneal calcification​
  • Subperiosteal resorption fingertips​
  • Thinning bone trabeculae​
  • Osteitis fibrosa cystica (fibrous replacement of resorbed bone)
    ​
  • Bone lesiosn in 10-20%​
  • Jaw / Skull lesions​
  • Pepperpot skull appearance.
73
Q

The tx of hyperparathyroidism consists of…

A
  • Surgery for removal of adenoma​
  • Post op issues with hypocalcaemia (may need supplements)
74
Q

Parathyroid hyperplasia in response to a persistently low calcium is known as ___________.

Bone lesions are more common.

A

hyperparathyroidism

75
Q

What causes secondary hyperparathyroidism?

A

Due to chronic renal failure / malabsorption

76
Q

What are the dental impacts of hyperparathyroidism?

A

Giant cell lesions – uncommon and present late​. *Middle aged, renal issues – suspect PT issues​

Brown Tumours ​

Care with other systemic issues eg renal disease etc.

77
Q

List the common joint disorders in bone disease.

A

Marfans syndrome​

Ehlers-Danlos​

Recurrent TMJ dislocation

78
Q

List the common Arthritides in bone disease.

A

Osteoarthritis​

Rheumatoid arthritis​

Felty sun​

Juvenile arthritis​

Ankylosing spondylitis​

Infective arthritis​

Gout

79
Q

What is Marfans syndrome​?
*Rare – 1 in 10,000

A
  • Autosomal dominant​
  • Connective tissue disorder – defect in fibrillin ​
  • Excessive tubular bone, loose joints

​Different sub-types but common feature of Marfans is having ​
Long/tall thin body, thin slender fingers – spider like.​ Huge arm span

*>90% may get cardiac problems e.g. valvular, & occular lesions​

*can sometimes get pneumothorax (collapsed lung) ​

80
Q

What are the 3 key areas of defects​ in Marfans syndrome.

A

Skeletal​

Cardiovascular​

Neuro-ocular

81
Q

What does the acronym MARFANS stand for?

A

Mitral valve prolapse
Aortic dissection
Retinal detachment
Fibrillin-1 mutation
Arachnodactyly - long fingers / toes
Near sighted
Scoliosis

82
Q

Dental effects of Marfans syndrome?

A

High palate​

TMJ dysfunctional subluxation​

Malocclusions

83
Q

Ehlers – Danlos syndrome is a rare disorder of __________ formation. It is autosomal dominant, but recessive also seen.

A

Collagen

84
Q

Symptoms of Ehlers-danlos syndrome.

A

Hyperextensible skin​

Easy bruising​

Loose/hypermobile joints *​

Recurrent spontaneous dislocations​

Poor healing

85
Q

What are the systemic complications of Ehlers-danlos syndrome?

A

Mitral valve prolapse​ (floppy – predispose of heart failure & I.E)​

Haematological issues – bleeding​, platelet defects​

86
Q

What are the oral complications of Ehlers-danlos syndrome?

A

Dental
TMJ​ (can get recurrent dislocation)​

Short teeth / abnormal roots / pulp stones​​

Micrognathia​​ - short mandible.

Anterior open bite

Gingival hyperplasia

87
Q

What is osteoarthritis?

A

Painful & stiff joints. Most common type of arthritis.

Mechanism: Degeneration of articular cartilage (*classic underlying pathology) and proliferation of new bone, cartilage and Connective tissue.

(thickening of exposed underlying bone, with development of peri-articular cysts. The cysts can collapse with continued peripheral bone proliferation = progressive deformity of joints)​

Remodelling at joint contour

88
Q

The symptoms of osteoarthritis include

A

Pain, stiffness and swelling. ​

No systemic symptoms like R A. [no obvious inflammation or serological changes]

89
Q

Who is more likely to get osteoarthritis?

A

More common in women​

Overweight / obese​

Athletes​

Pagets or gout​

Genetic predisposition

90
Q

What is the diagnosis of osteoarthritis?

A
  • Clinical​ features
  • Imaging – narrowing of joint space, sometimes with osteophyte formation (bone lumps/cysts).
91
Q

What is the tx of osteoarthritis?

A

Analgesia​ - topical on joints or systemic NSAIDs.​

Joint replacements

92
Q

The most common form of chronic inflammatory joint disease is _____________.

Discuss mechanism & aetiology

A

Rheumatoid arthritis:
= Characterised by the presence of rheumatoid factor (but not always).​

= Symmetrical, destructive​

Aetiology: All ethnic groups, worldwide. Occurs in genetically predisposed individuals​

F3 : 1M​

? T-lymphocyte activation​

Multi-system, immunologically mediated disease.

93
Q

What are the clinical features of rheumatoid arthritis?

A

*onset insidious – gradual progression​:
- Stiffness of hands/feet ​
- Usually worse in the morning​
- If acute – redness, tenderness and swelling over joints. Spindle shaped (due to joint swelling & muscle wasting).

  • Ulnar deviation – symmetrical. Hands pointed out.​
  • Wrists, elbows, ankles, knees – increasing disability​
  • C-spine involvement – atlanto-axial subluxation (vertebra in neck becomes dislocated)
94
Q

What are the clinical features of rheumatoid arthritis to help with diagnosis?

A

clinical – pain, swelling, heat and stiffness in affected joints +/- nodules, +/- systemic signs. Dislocation of joints. Sometimes Sjogren’s syndrome.​

95
Q

What diagnostic factors can indicate RA?

A
  • Rheumatoid Factor (RF) present in 60—70% of pts. Sensitive immunoglobulin marker.​
  • inflammatory markers (some have normal)- elevated erythrocyte sedimentation rate or C Reactive Protein.
  • Radiographic features – initially widening of joint space followed by narrowing, erosion and destruction.
96
Q

How is RA managed?

A

> Supportive measures​

> Analgesics e.g. NSAIDs, Paracetamol​

> Corticosteroids into joint spaces – long term streroids. [risk of infection, wound healing, and ability to handle stress].​

​> DMARDs (disease modifying anti-rheumatic drugs) – reduce pain & swelling.​
* Methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, azathoprine​

& Biologic agents – reduce pain & swelling.​
* Etanercept, Adalimumab, Infliximab (biologics – immunomodulators) - expensive, toxic side effects. Issues with healing – MRONJ type of effect *

97
Q

What are the dental impacts of RA?

A

Often associated with Sjogrens syndrome​​

Some changes on OPT within TMJ​​

Care with meds – risk of bleeding, infection, MRONJ

98
Q

What is felty syndrome?

A

This is a syndrome associated with rheumatoid arthritis coupled with Splenomegaly & Neutropenia – difficult to manage due to systemic effects.

  • F>M
  • Caucasians
99
Q

What is juvenile arthritis?

  • Symptoms
  • Types
  • Diagnosis
A

Painful joints – associated with fever, nodules, anaemia and malaise​

Mainly affects girls- late childhood​

Variety of types​-
Systemic( 1 or more),
Polyarticular (>5 joints)​,
Pauciarticular​ - juvenile RA affecting less than 4 joints.

Diagnosis – RF is positive in ~75% pts​

Issues similar to that of adults & sometimes ankylosing spondylitis

100
Q

What is Ankylosing Spondylitis?

A

Form of chronic inflammatory arthritis​.

*Mainly seen in young males – family history​

*Affects sacroiliac and spinal joints​

*Causes fusion of vertebrae over time​
* diagnosis - blood test positive for HLA-B27 antigen

Dental – care for GA *positioning difficult.

101
Q

What are the complications of Ankylosing Spondylitis?

A
  • lower back pain and stiffness around sacral iliac joints and sometimes the hip as well. Sometimes limited chest expansion causing issues with respiration. May get anaemia associated with this.​

Also, may develop eye lesions (25%) and cardiac disease (10%)​

102
Q

What is the tx for Ankylosing Spondylitis?

A

Treatment is physiotherapy and exercises​.

NSAIDs for pain (sometimes Anti-TNF)​

103
Q

What is gout?

*Rarely affects TMJ

A

Common form of chronic inflammatory arthritis​

Crystals of monosodium urate monohydrate build in joints - derived from hyperuricaemic body fluids ( caused by release of enzymes from PNM leukocytes).​ Results in swollen & inflamed joints.

This causes inflammatory arthritis, tenosynovitis (inflammation of joint synovium), bursitis (inflammation of fluid filled sacs in joints that cushion joints) or cellulitis (swollen, hot skin), tophaceous deposits (sandy/gritty), urolithiasis (calculi / stones)and renal disease.

104
Q

What causes gout?

A
  • High uric acid from breakdown of purines (red meat, organ meats, some seafood)​
  • High blood pressure, diabetes, obesity.​
105
Q

Tx for gout

A
  • NSAIDS, Allopurinol

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