ICM - Rheum 2 Flashcards

(56 cards)

1
Q

factors that determine peak bone mass

A

genetics, nutrition (calcium/VitD), endocrine status (early menopause, decreased gonadal activity), physical activity/health during growth

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2
Q

these are associated with increased bone loss

A

aging, hypogonadism/menopause, high bone turnover

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3
Q

pathology of osteoporosis (in cancellous bone)

A

thinning of trabeculae, loss of trabecular plates (architecturally weakened)

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4
Q

lifestyle risk factors for osteoporosis

A

alcohol, smoking, inadequate diet (low Ca/VitD, excess VitA, salt), inadequate physical activity

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5
Q

this kind of diet will increase risk of osteoporosis

A

low Ca/VitD, excess vitA/salt

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6
Q

rheumatologic disease risk factors for osteoporosis

A

RA, SLE, ankylosing spondylitits

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7
Q

endocrine risk factors for osteoporosis

A

adrenal insufficient, Cushing’s syndrome (corticosteroid excess), excess thyroid, diabetes, hyperparathyroid, central adiposity

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8
Q

hypogonadal risk factors for osteoporosis

A

menopause, androgen insensitivity, hyperprolactinemia, anorexia nervosa, Turners (XO), Klinefelters (XXY), panhypopituitarism

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9
Q

areas of predilection for fracture in osteoporosis

A

hip, wrist, vertebral spine

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10
Q

asymptomatic fractures of dorsal spine can lead to this

A

kyphosis

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11
Q

main screen and diagnostic study for osteoporosis; what does this measure?

A

DEXA (dual xray absorbiometry); bone density

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12
Q

BMD T score >-1 (bone one standard deviation below young adult mean)

A

normal

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13
Q

-1

A

osteopenia

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14
Q

BMD T score > -2.5 standard deviation below young adult mean

A

osteoporosis

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15
Q

women above this age, and men above this age, should be tested for osteoporosis

A

65, 70

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16
Q

impaired mineralization of bony matrix

A

osteomalacia

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17
Q

osteomalacia conditions that are DDX for osteoporosis

A

VitD deficiency/dysfunction, phosphate deficiency, acidosis, hypophospatasia, mineralization inhibition

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18
Q

cornerstone for pharmaceutical therapy of osteoporosis –> decrease hip/spine fracture by 50%

A

bisophosphonates (Fosamax, Boniva, Actonel/Atelvia, Reclast)

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19
Q

what do bisophosphonates inhibit?

A

osteoclast function (some osteoblast)

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20
Q

possible adverse effects of bisophosphonates

A

irritate esophagus/stomach, renal insufficiency

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21
Q

possible late side effects of bisophosphonates

A

osteonecrosis of jaw, atypical femur fractures (not at neck)

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22
Q

pharmaceutical therapy for osteoporosis….reduces vertebral fracture 30% (intranasally or w/ subcu injection), decrease pain vertebral fracture, could have allergic reaction (if allergic to salmon)

A

calcitonin

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23
Q

exercise recommended in osteoporosis

A

weight-bearing and muscle strengthening

24
Q

women >51 and men>71 should get this much calcium per day

25
recommended daily calcium for men 50-70 yo
1000 mg/day
26
recommended VitD daily allowance for adults \>50
800-1000u VitD/day
27
% of patients that regain full prefracture functioning
40%
28
possibly complications of vertebral fractures
loss of height, restrictive lung disease, constipation, abdominal pain, bloating, early satiety
29
these are responsible for cell mediated immune resopnse in RA
CD4 in synovial membrane
30
white patients with RA express this MHC haplotype more than non RA patients (nonwhite RA patients also seem to share amino acid sequences with this MHC)
HLA DR4
31
pathology of RA
hypertrophied/hyperplasia synovial membrane, angiogenesis, CD4 and B cell infiltrate, synovial membrane invades cartilage
32
this forms as synovial membrane transformed to inflammatory tissue --\> tissue invades/destroys cartilage and bone
pannus
33
these make up pannus in RA
type A/MP like and type B/FB like synoviocytes, plasma cells
34
history of RA
gradual/palindromic onset swelling/pain, symmetric distribution (usually small joints, but some larger), constitutional symptoms
35
peak onset age of Ra
30-55 (3:1 women)
36
corticosteroids as treatment for RA can cause these ocular problems
glaucoma and cataracts
37
hydroxychloroquin as treatment for RA can cause this ocular problem
retinal pigment epithelial toxicity
38
acute phase proteins measured in RA
ESR, CRP, HgB
39
antibodies are directed at this in rheumatoid factor
fc portion IgG
40
if patient has inflammatory polyarthritis AND positive rheumatoid factor, more predictive of these future conditions
erosions and subcu nodules
41
seronegative spondyloarhtropathies that are DDX for RA
psoriatic arthritis, Reiter's syndrome, enteropathic arthritis (Chrons, Sprue), reactive arthritis
42
acute onset of pain in shoulders and hips in patients \>50 yo...ESR very high...\*responsive to corticosteroids\* (DDX for RA)
polymyalgia rheumatica
43
infectious causes of inflammatory polyarthritis --\> DDX for RA
parvovirus B19, rubella, Hep B, gonoccal arhtritis, polyarticular septic arthritis
44
gold inhibits these enzymes (DMARD)
acid phosphatase, collagenase, PKC, phospholipase C
45
possible side effects of gold therapy for RA
myelosuppresion, oral ulcers, rash proteinuria
46
DMARDS that affect purine NT synthesis
methotrexate and azathiprine
47
this DMARD affects pyrimidine NT synthesis
leflunomide (Arava)
48
side effects for methotrexate
oral ulcers, pneumonitis, hepatic toxicity, myelosuppression
49
side effect for azathioprine
myelosuppression
50
side effects for leflunomide
myelosuppression, hepatic toxicity, hair loss, diarrhea, weight loss
51
this DMARD causes fusion of TNF receptor and Fc portion IgG (TNFa antagonist)
etanercept (Enbrel)
52
this DMARD is recombinant fully human IgG Ab to TNF (TNFa antagonist)
adalimumab (Humira)
53
this DMARD TNFa antagonist is binding region of mouse Ab to TNF fused to Fc portion of human Ig
infliximab (Remicade)
54
possible future targets for RA treatment
MP, IL 4/10
55
triple drug therapy that is considered more effective in treatment of RA with no increase in toxicity
methotrexate, sulfasalazine, hydroxychloroquin
56
these are indicated for early control of pain and inflammation in RA
NSAIDs and corticosteroids