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ALU 201 > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

Define the term Rheymatism

A

soft tissue and/or musculoskeletal disorders such as tendonitis, bursitis and fibromyalgia.

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2
Q

Define the term “arthritis”

A

joint inflammation characterized by swelling pain, and loss of motin.

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3
Q

Name 4 examples of rheumatic diseases

A
  1. rheumatoid arthritis (RA)
  2. osteoarthritis (OA) * most common
  3. crystal-induced arthritis (gout)
  4. systemic lupus erythematousus (SLE)
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4
Q

How is arthritis type diagnosed?

A

assessing petter of the arthritis in conjunction with age, and gender. Lab tests are not always useful. There is no gold standard.

  • RF+ factor, CRP, normocutic anemia, elevated ESR- can be present.
  • can look at Xrays, CT and MRI to help make dx.
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5
Q

How is rheumatic diseases treated?

A

multi-disciplinary and multi-factorial approach.
Cure is not possible, therefore disease is controlled and in remission for sxs.
- NSAIDS, analgesics, are used as basic therapies, then move to systemic corticosteroids, and DMARDs are also used.

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6
Q

Which joins are commonly affected by osteoathritis and psoriasis

A

DIP joints ( distal interphalangeal )

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7
Q

Which joints are commonly affected by osteoarthritis and rheumatoid arthritis?

A

PIP joints. (proximal interphalangeal)

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8
Q

Which joints are commonly affected by RA?`

A

MCP joints- metacarpal-phalangeal

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9
Q

Which disorder is commonly associated with the thump joint attached with the wrist (CMC joint)

A

Osteoarthritis.

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10
Q

Which disorder involves the wrist, elbow and shoulder joints?

A

RA, but if the pt does heavy manual labour OA is involved.

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11
Q

Which arthritis commonly affects the spin, neck or cervical spine?

A

RA and OA, it can also be affected by sernoegative spindyloarthritis, such as ankylosing spindylitits.

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12
Q

Are the thoracic and lumber spines involved in R.A ?

A

no, but the lumbar spine is a common site for OA and DDD.

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13
Q

What are spondyloarthritides (SpA)

A

a group of seronegative (RF -ve) disorders that involve the spine, sacroiliac joints, and sometimes peripheral joints quite diffusely.

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14
Q

Which disorder affects the following:

  1. hips
  2. knees
  3. ankles
  4. subtalar and mid-tarsal joints (hindfood/midfood)
  5. MTP joints (toes joint foot)
  6. small toe joints
A
  1. OA/RA
  2. systemic forms of arthritis, OA
  3. RA, and only OA after fractures.
  4. RA
  5. RA, and only the first and 5th MTP joints involved with OA (bunion)
  6. OA, RA and psoriasis.
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15
Q

The following can indicate which kind of arthritis:

  1. skin inflammation
  2. inflammatory eye or bowel involvement
  3. nodules
A
  1. psoriasis
  2. seronegative arthritis rather than RA
  3. RA/gout
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16
Q

Define Osteoarthritis:

A

a group of joint disorders where the balance between synthesis and destruction of the joint cartilage is disturbed. This leads to the destruction of the joint.

X-rays shows joint space narrowing, and formation of bony spurs, and thickining of bone adjacent to joint cartilage.

sxs: pain, stiffness, loss of range of motion, deformity, inactive gelling, low-grade and intermittent inflamation.

more common in F, and ^ age. Some genetic component.

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17
Q

What are some risk factors for osteoarthritis?

A

previous damage to a join
developmental abN of the join
obesity
metabolic disorders (acromegaly/hemochromatosis)

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18
Q

How is osteoarthritis txed?

A 
multi-factorial: 
weight loss/exercise
use of walking aid 
physiotherapy for muscle strengthening 
occupational therapy. 
emotional support (pain)
Rx: simple analgesics (tylenol)
and some anti-inflammatories + gastroprotective rx. 
opioids (with caution)
SNRI- antidepressant for back pain. 
local steroid injections

surgery in end-stage oseteoarhritic joins with replacements

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19
Q

What are the most common sites affected by spinal osteoarthritis?

A

lower cervical and lower lumbar spine, d/t stresses. This is referred to DDD.
the discs betwee the vertebrae change over time and become compressed.

sxs of pain arise

tx;ed with surgery if a nerve root or cord is compressed. otherwise most people use analgesics, anti-inflammatory, physio and weight loss/posture modifications.

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20
Q

Define DISH (diffuse idiopathic Skeletal Hyperostosis)

A

variant of OA
formation of large flowing osteophytes connecting vertebral bodies (anterolaterally). this causes large bony spurs at tendon or ligament insertions.
involves thoratic spine, usually
comon in older people.
sxs: spinal stiffness and reduction in spinal range of motion, but little pain.
- associated with DM
- no mortality implications

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21
Q

Define R.A.

A
  • most common inflammatory polyarthritis.
  • no single dx- its characterized by a scoring system, and needs to be over 6/10.
  • more common in F
  • heterogenous illness,
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22
Q

What are the sxs for RA?

A

starts with fatigue, morning stiffness, swelling and pain in joints, and disturbance of normal joint function.

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23
Q

What are factors associated with poor RA prognosis?

A
  1. male gender
  2. early functional disability
  3. high titer of Rheumatoid factor or antibodies to CCP
  4. early development of radiologic erosions
  5. extra-articular manifestations
  6. smoking
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24
Q

What are some examples of extra-articular manifestations of R.A?

A

rheumatoid nodules over pressor points/organs
vasculitits
pulmonary disease
cardiac disease/pericarditis
dry eye/mouth
eye inflamation (rare)
Felty’s syndrome (componation of splenomegaly, low WBC count and arthritis)

> > Rare d/t new therapies

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25
Q

How is R.A. treated?

A

releave sxs, preserve funtion and prevent structural damages. local steroid injections, sometimes oral steroid therapy but its controversal.
physiotherapy, early aggressive tx, occupational therapy, analgesics, NSAIDs, and use of remittive or DMARDS and/or Biologic therapies.
*biologic therapies are usually combined with methotrexate or DMARDS and are through IV.

use DAS, SDAI and CDAI scoring to determine the disease activity- goal is to get it back in remission.

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26
Q

What are some markers of reduced survival in combination with R.A hx?

A
  1. poor functional capacity
  2. multiple joint involvement
  3. need for hospitalization

Most common cause of death in pt with RA is cardiovascular disease.

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27
Q

Define SpA (spondyloarthropathies)

A

group of arthritic disorders is comprised of 4 related disorders that share common features of -RF, ^ frequency of genetic harker HLA-B27, and predilection for involment of the spine and peripheral joints.

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28
Q

Name the 4 kinds of spondyloarthropathies

A
  1. Ankylosing spondylitis (AS)
  2. psoriatic arthritis (PsA)
  3. arthritis of inflammatory bowel disease
  4. reactive arthritis
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29
Q

Define Ankylosing spondylitis.

A

Inflammatory disorder of the spine that can also involve peripheral joints.

  • common in M
    sxs: inflammatory-type back pain, in lumbar spine and sacroiliac join regions and works it way up. Joint eventually fuse and limitations of moition are permanent.
  • associated with a genetic marker HLA-B27.
30
Q

What are the extra-articular manifestations associated with AS

A

accute eye inflammation
heart block or aortic regurg
pulmonary fibrosis (rare)

31
Q

How is AS dxed?

A

clinical ft. including loss of spine motion and decreased chest expansion and inflammatory back pain.
mild anemia of chronic inflammation type
Xrays eventually show joint changes

MRI is used to check the spine and SI joints when disorder is suspected.

32
Q

How is AS treated>

A

exercise/physio to maintain spinal posture and range
anti-inflammatory drugs are used
remittive drugs -occasionaly with sulfasalazine and methotrexate if peripheral arthritis is present.
TNF-alpha immunomodulators to reduce pain and stiffness

33
Q

Deine psoriatic arthritis

A

benign skin condition chracterized by scaly plaques developing over the skin.
arthritis risk increased.
- some genetic composition
- psoriatic-type arthritis develops before the onset of skin lesions in about 15% of people
- elevated serum uric acid can be seen
- -RF

34
Q

How is psoriatic arthritis treated?

A 
NSAIDS
typical remittive drugs for R.A. including anti-TNF-alpha biologic therapies
Methotrxate
anti-malarial therapies (less used)
sulfasalazine/ leflunomide.
  • mortality is dependent on increased risk of cardio diseases, if PA is moderate/severe
35
Q

Define Reactive Arthritis

A
  • begins after an acute diarrheal illness caused by bacteria, or venereal infection.
  • common in males
  • scaly skin lesions can be seen over penis and soles of feet
  • pain at tendon and ligament insertions into bones
  • associated with HLA-B27 antigen.
  • 1/3 develop condition that is disabling
  • no impact on mortality.
36
Q

What is the classic trial of reactive arthritis (3)

A
  1. arthritis- leads to be an asxs oligoarthritis of lower extremity joints and can also involve spine,
  2. urethritis
  3. conjunctivitis
37
Q

How is reactive arthritis txed?

A

anti-inflammtory drugs

chronic forms can benefit from abx as well as DMARDS.

38
Q

Define Arthritis and IBD (inflammatory bowel disease)

A

UC and chrons associated with arthritis

  • mild, non-destructive arthritis involving large joints.
  • tx’ed with anti-inflammatories,
  • people with arthritis and IBD can develop spondylitits identical to idiopathic ankylosing spondylitits
  • Anti-TNF agents are used in IBD,
  • mortalitis impact is based entirely on the IBD.
39
Q

How is Gout characterized?

A

recurrent attacks of acute joint inflammation wiht the involved joint being red, hot, swollen, and painful.

  • lower extremities affected
  • more common in male
  • sometimes 1- ++ attacks in life time.

dx by the detection of crystals of monosodium urate in the joint fluid. There can also be corelated arthritis, and CPPD deposition disease.

tx: Acute: NSAIDS, colchicine and ora intra-anticular steroids.
chronic: rx with urate lowering therapies.

40
Q

What are tophi?

A

dopsits of uric acids that develop in the joints and over pressure joints.

  • they are composed of pure monosodium urate
  • dx by polarizing light microscopy
41
Q

What is the etiology of gout?

A
  • most people have idiopathic form, where there are subtle abN in uric acid metabolic that leads to over production or under excretion.
  • 10% is secondary to orther problems.
  • some dietary factors contribute to gout (high-purine foods and corn syrup)
42
Q

Define SLE

A

chronic overactive autoimmune disease in which increased amount of abN antibodies are produced that react with the individuals own itssues.

  • genetic composition + environmental and hormonal factors.
  • More common in F
43
Q

How is SLE dx’ed?

A

based on clarification criteria, usuallly 4 of the following:

  1. oral ulcers
  2. athritis that is usually non-erosive
  3. proteinuria or abN urinalysis and cellular cast
  4. pleurisy or pericarditis
  5. malar rash
  6. discoid rash
  7. photosensitivity
  8. seizures, psychosis
  9. blood disorders, (anemia, L ABC, thrombocytopenia)
  10. positive anti-nuclear antibody (ANA)
  11. other immunologic abN ie: p+ve LE cell prep or presence of certain antibodies
44
Q

How is SLE treated?

A

baseline: education and F/u with NSAIDS.
Anti-malarial drugs are requently used for rashes, arthritis and fatigue.
oral corticosteroids are required for severe inflammation and maintenance.
immunosuppressive drugs can be used.
Cyclophosphamide used fro severe renal or neurological manifestations.
biologic drugs

45
Q

What is the prognosis for SLE?

A

used to be bad, but now is better d/t better recognition of the disease, milder cases, and better therapy.

cause of death:

  1. active lupus with end-organ damage such as heart, lungs, kidneys and CNS
  2. infection
  3. atherosclerotic complications.
46
Q

Define Scleroderma (systemic sclerosis)

A

chronic immune disease that typically affects the skin and various internal organs.

  • skin thickens over the fingers, arms, legs trunks and/or face.
  • there is localized and systemic forms. Localized is better.
  • more common in Females
  • cause unknown
  • death/disability is usually by lung, heart, kidney involvement.
47
Q

What are the sxs of Scleroderma?

A

Raynayds’ phenomenon
renal crisis- which can cause HTN and acute renal failure.
scarring and fibrosis of lungs, heart, and GI tracts as well as pulmonary HTN.

48
Q

What is Raynaud’s Phenomenon?

A

Circulatory disorder characterized by cold induced color changes in the hands and feet. This is d/t spasm of the small blood vessels in response to cold.

49
Q

How is Scleroderma diagnosed?

How is it treated?

A

clinical manifestation as well as presence of certain specific antinuclear antibodies.

Symptomatic treatment for HTN to prevent renal amage. GI sxs tx’ed with PPI
pulmonary HTN tx’ed with infusions of synthetic prostaglandins

50
Q

Define Polymyositis and dermatomyositis

A

inflammatory diseases of muscle, which causes weakness usually in shoulder, pelvic girdles and neck muscles.

  • etiology unknown
  • rare, more common in F.

dermatomyosis is associated with skin rash, and skin leasions where as polymyositis doesnt have the rash

51
Q

How are Polymyositis and dermatomyositis diagnosed?

A

compatible clinical picture as well as muscle inflammation, ^ CK, and ^ aldolase levels.
EMG testing can be done
but dx is confirmed by muscle biopsy.

They are usually associated with underlying malignancy

52
Q

How are Polymyositis and dermatomyositis treated?

A

high-dose oral steroids and immunosuppresive drugs.

prognosis is variable.

53
Q

Define Sjogren’s syndrome

A

an inflammatory disease that can affect different parts of the body but mostly affects the lacrimal and salivary glands.

sxs appear between age 45-55.
more common in Females
Corelated to RA or other connective tissue disease.
- most complications arise d/t decreased tears and saliva d/t inflammation/destruction of glands, (^ infection risk) there are other sxs related to rashes, inflammation of organs and numbness/weakness
- prognosis fairly good

54
Q

How is Sjogrens syndrome dx’ed?

A

typical sxs, physical examination, blood tests and special studies that assess decreased tear/saliva production.
Eye exam is helpful.
Biopsies can also be done

55
Q

How is Sjogrens syndrome tx’ed?

A

symptomatically
Dry eyes= articial tears + reduce inflammation
increase fluid intake, chew gum, or saliva substitutes.
px Rx to stimulate saliva slow.
antifungal therapies for yeast infections.

hydroxychloroquine, an antimalarial may be helpful for reducing joint pain and rashes.

prednisone or immosuppresants agents can be used for severe sxs.

56
Q

Define Polymyalgia Rheymatica (PMR) and giant cell arteritis

A

related conditions that occur in people >50 yo.

PMR- characterized by pain and stiffness involving the neck, shoulder girdle, and pelvic girdle muscles. ^ EAR, normal CK, and no true muscle weakness. it mimics RA,

GCA- is a form of vasculitis involving inflammation fo the large arteries. can lead to blindness, claudication and organ dysfunction.
biopsy appearance is typical and is bassi of dx, as well as u/s.

57
Q

T or F: 10-15% of patients with PMR have GCA where as 40% of patients with GCA have associated PMR

A

True

the onset of the two conditions can be separated by quite a gap in time.

58
Q

What are the sxs associated with Polymyalgia Rheymatica (PMR) and giant cell arteritis

A

PMR: weight loss, fatigure, low-grade fever, inflammation of small blood vessels in the muscle and around joints

GCA: pain in jaw muscles on eating or speaking, severe temporal headaches and tenderness of the scalp and the area of the temples.

59
Q

How are Polymyalgia Rheymatica (PMR) and giant cell arteritis diagnoses?

A

PMR: by exclusion based on clinical hx associated with ESR.
Also a dramatic response to low-dose corticosteroid

GCA: biopsy

60
Q

Polymyalgia Rheymatica (PMR) and giant cell arteritis treated?

A

corticosteroids for blindness in GCA and sxs of PMR.

low does steroids, can be use.

Once tx begins the risk of blindness decreases alot, but there is risk of long-term steroid therapy.

61
Q

Define Vasculitits

A

disorders characterized by inflammation in the walls of blood vessels of various sizes.

depending which vessels are affected, the organs can manifest differently.

unknown etiology though some are linked to hep infections.

tx’ed with high doses of oral steroids and immunosuppressive drugs.
can also do plasma exchange and IVIG.

Mortality and morbidity is high

62
Q

Name a few examples of vasculitits (forms)

A 
PEN
GPA
MPA 
EGPA 
temporal arteries

difficult to dx and depends on biopsy proof of inflammation in the blood vessels.

63
Q

define osteoporosis

A

disorder characterized by decreased bone mass which can result in spinal deformity

common in F.

64
Q

Osteoporosis can be divided into several types. Name them

A
  1. post-menopausal in F
  2. age-related osteoporosis
  3. secondary to endocrine disorders.
  4. malignant causes.
65
Q

What are 5 risk factors associated to primary osteoporosis ?

A
  1. increased age
  2. female gender
  3. early menopause
  4. smoking
  5. ETOH abuse

physical inactivity, thin body types and some Fx.

66
Q

What are the sxs of osteoporosis

A

asxs until a gracture, which then results in deformities which include thoracic kyphosis.

common sites of fracture: spin, hip, wrists.

67
Q

How is osteoporosis diagnosed?

A

Bone mass assessment. This is done by bone densitometry, the assessment standards is known as DXA (dual energy x-ray absorptiometry) this compared to the age creates a T-score.
DXA tscore not lower -1. is a normal DMB
DXA t-score btween -1 and -2.5 is osteopenia (mild)
anything -2.5 or lower is osteoporosis

68
Q

What is FRAX?

A

online calculator that integrates risk factors (BMD, fracture hx, steroid use, age, gender) to calculate the fracture risk for next 10 years.

69
Q

How is osteoporosis treated?

A

good preventive care in younger ages (^ Ca+ intake)

then bisphosphonate tx, biologic agent denosumab, raloxigene and synthetic parathyroid hormones.
Ca and vit D supplements have limited role.

70
Q

Define Osteomalacia

A

a metabolic done disease in which mineralization of the skeletal matrix is defective.

  • presents insidiously, fractures are esily done.,
  • sxs: diffuse skeletal pain, and bony tenderness and altered gait. Possible proximal muscle weakness.
  • Xray shows pseudo-fractures, and bone scans show increased weakning of the bone at sites where arteries cross the surface.
  • tx’ed with Vit D administration, with Ca+ and inorganic phosphate
71
Q

What causes osteomalacia?

A

Vit D deficiency or disorders of Vit D metabolism
- genetic causes and relation to GI disorders, malabsorption or renal disease.
can also be caused by drugs and toxins

72
Q

Define paget’s disease of bone

A

metabolic disorder in which there is accelerated bone turnover. the bone that is formed in abN and weaker.

  • Xray: bone appears coarsened and thickened.
  • examination can show palpable done enlargement.
  • sxs: Asxs, and disease is dx’ed incidentally when x-ray shows pagetic changes or when a seium alk phos is found to be elevated.
  • some may have boen pain, and fracture through weakend bone.
  • Hearing loss can develop in skull involvement. Can also develop congestive heart failure.
  • in aSxs individuals, no tx required. In those with sxs or ^ allk. phos, bisphosphonate drugs are often used. Calcitonin injections can be given prior to orthopedic surgery .
  • life expectancy is not really affected.

ALU 201 (16 decks)

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