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PHAR 123 > Bones and Joints > Flashcards

Bones and Joints Flashcards

1
Q

What is Osteomalacia?

A

Softening ofd bones as a result of inadequate mineralization of the organic matrix
Caused by deficiency of vitamin D, inadequate metabolic processing and activation of vitamin D, or disturbances of phosphate metabolism

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2
Q

What is osteomalacia called in children?

A

Rickets

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3
Q

What is the etiology of Vitamin D defeciency?

A

inadequate intake
Inadequate exposure to sunlight
abnormal intestinal absorption

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4
Q

What is hypophosphatemia?

A

Renal disease –> Phosphorus lost in urine, losses or failure to add phosphate to bone leads to osteomalacia

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5
Q

What is the pathology of Osteomalacia?

A

Excess nonmineralized osteoid
Bone deformities and fractures
Serum Ca and Phosphorus low

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6
Q

What are the symptoms of Osteomalacia?

A

Bone fractures more easily
muscle weakness
widespread bone pain (hips usually)
Low Ca level symptoms:
- abnormal heart rhythms
- numbness around mouth
- nubness of arms and legs
- spasms of hands and feet

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7
Q

What is the most common joint disease?

A

Osteoarthritis

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8
Q

WHat joints does Osteoarthritis affect?

A

weight-bearing joints
Small joints of hands and feet

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9
Q

What are some characteristics that may increase the risk of osteoarthritis?

A

Larger stature
prior injury

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10
Q

How is OA classified?

A

Primary: cause unknown/ multifactorial
Secondary: related to another disease

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11
Q

What is the pathology of osteoarthritis?

A

Bone cysts form, cartilage fragments present, irregular joint space, loss of cartilage, sclerotic bone, cystic change.
Advanced: osteophytes, periarticular fibrosis, calciifed cartilage

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12
Q

What is the main symptom of OA? how does it effect the pt?

A

PAIN
less use –> less muscle –> less mobility –> impacts wt, exercise, and dependance

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13
Q

How is OA managed?

A

Exercise (range of motion, muscle strength wt loss)
Assitive devices
Analgesics such as NSAIDs, corticosteroids, hyaluronic acid injections
Surgery (joint replacement)

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14
Q

What is Rheumatoid Arthritis?

A

Chronic symmetrical inflammatory synovitis, joint destruction, muscle atrophy, and bone destruction
Multisystem
Can affect other areas of body such as lungs, eyes, blood vessels, and skin

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15
Q

What is the genetic factor related to RA? is it more prevalent in Men or Women?

A

HLA-DR4
3:1 F:M prevalence

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16
Q

What are the characteristics of Rheumatoide Synovium?

A

presence of activated lymphocytes, macrophages, and altered fibroblasts

17
Q

Other than genetics what factors can contribute to RA?

A

Smoking
Infectious Material
Being Female

18
Q

What is Pannus? what does it cause?

A

Abnormal, hypertrophied synovium; abnormal tissue develops in the rheumatic joint
Causes deformity of joint and destruction of tissue via release of damaging enzymesm proteins and acids that break down bone and cartilage

19
Q

What are the treatments for Mild, Moderate, and Severe RA?

A

Mild: NSAIDs, plaquenil, sulfasalazine, minocycline, methotrexate
Moderate: Single or Combo of DMARDS
Severe: Combo of DMARDS, steroids (oral), pulse prsorba, and column cytoxan

20
Q

What are DMARDS used in RA?

A

Methotrexate
Anti-TNF agents
Anti-IL-1 agents
Leflunomide
Azathioprine
Gold
Cyclosporine
ANd Mild Agents

21
Q

Plaquenil MOA?

A

Malaria drug
Raises lysosomal pH in antigen presenting cells –> redices antigen processing efficiency
older DMARd, works slowly

22
Q

Sulfasalazine MOA?

A

Older works slower
prodrug
Multiple mechanisms:
effects gut bacteria
inflammatory cell fucntion, cytokine and antibody prodcution
inhibt of folate-dependant enzymes
inhibit synovial neovascularization
increase free radical scavenging activity

23
Q

Minocycline MOA?

A

Antibiotic w/ anti-inflammatory properties
Reduces IL-10, suppresses B and T cells
Reduces nitric oxide synthase, enzyme that breaks down cartilage
synergistic with NSAIDs

24
Q

Methotrexate MOA?

A

Inhibits purine and pyrimidne synthesis
anti-inflammatory –> adenosine receptor agonist
Reduces IL-6, IL-1, and TNF-alpha
Complex effects on immune cell proliferation and activity
Quick acting

25
Q

What is the difference in stiffness for OA vs RA?

A

RA very stiff lasting longer than 1 hour, pain and stifness gets better w/ mobilisation and as day progresses, may have significant fatigue as well
OA: stiff for seconds to minutes after walking, gets worse through day and on activity

26
Q

What is post rest stiffness called in OA

A

Gelling

27
Q

What is Ankylosing Spondylitis?

A

Chronic inflammation of the spine andf the sacroiliac joints causing pain, stiffness i and around spine, fatigue common during active inflammation

28
Q

What can occur over time of chronic spinal inflammation?

A

Complete fusion of the affected vertebrae

29
Q

What other organs can AS affect?

A

eyes, heart, lungs, kidneys, other joints

30
Q

What genetic component is related to AS? who is it more prevalent in?

A

HL-B27 gene (90% of pts)
More in young men but also children

31
Q

What is the pathogenesis of AS?

A

intial inflammationrelsuts from activation of bodys immune system (possibly from a preceding infection)
Once activated bodys immune system is unable to turn off even when infection is gone
Ligaments more affected than bone

32
Q

What are the 3 categories of DMARDs?

A

Conventional (methotrexate, sulfasalazine, hydroxychlorquine, leflunomide)
Biologic ( TNF inhib, B cell depelting agent, T cell modulator, IL6 inhib, IL-17 inhib)
Targeted Synthetic (Janus kinase inhibtors aka JAK)

33
Q

What TNF inhibtors can be used in RA and AS?

A

Adalimumab
Etaercept
Infliximab
Golimumab
Certolizumab pegol

34
Q

What are some risks for TNF inhibitors?

A

Serious infections and malignancy
allergic reactions
liver toxicity
development of inactivating antibodies

35
Q

Why are bone infections hard to treat?

A

Hard to penetrate bone; need high dose IV antibiotics for extended periods of time
Cna become walled off via abcess formation and stimulation of osteoblasts which form more bone overtop of infection furhter walling it off

36
Q

What is Involucrum?

A

Further walling off of affected area via new bone production

37
Q

What is a Brodie’s abscess?

A

An abscess formed containing live pathogens than can lead to infections later

38
Q

Pathogenesis of osteomyelitis?

A

Infection established in bone
inflammatory response –> pus formation nad tissue destruction and systemic syptoms of acute inflammation
local edema puts pressure on vascular supply compromising blood flow
Local mecrosis can result

39
Q

What is the Sequestrum?

A

Trapped dead area due to local necrosis

PHAR 123 (18 decks)

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