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Bone > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Acetaminophen

A 
Tylenol
Starting dose: 325-500mg PO TId
Max: 3g/day
max dose decreased in those with kidney or liver dysfunction or alcohol-use disorders
scheduled dosing works better
takes 1-2 weeks to work
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2
Q

Aspirin

A

Bayer, Ecotrin, Bufferin
starting dose: 325mg TID
Max: 2600(pain)-3600*mg/day(inflammation)

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3
Q

diclofenac

A

Voltaren XR
SD: 100mg QD
Max: 200mg/day

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4
Q

Etodolac

A

Lodine
SD: 300mg BID
Max: 800-1000mg/day

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5
Q

Ibuprofen

A 
Motrin, Advil
SD:200mg PO TID
Max: 3200mg/day
OTC & RX
do not give in immediate fracture-repair period
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6
Q

indomethacin

A

indocin
SD: 25mg PO BID or 75mg PO QD
max: 150mg/day

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7
Q

Meloxicam

A

Mobic

  1. 5mg PO QD
    max: 15mg/day
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8
Q

Naproxen

A

Naprosyn- 250 mg PO BID
Anaprox, Aleve, Neprelan- 220mg PO BID
Max: 1500mg/day
OTC & RX; may be safest NSAID w/ CV risk factors

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9
Q

Oxaprozin

A

Daypro
SD: 600mg PO QD
Max: 1200mg/day

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10
Q

Piroxicam

A

Feldene
SD: 10mg PO QD
Max: 20mg/day

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11
Q

Celecoxib

A

celebrex
SD: 100mg/day
Max: 200mg/day
COX-2 selectivity is lost w/ concomitant ASA

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12
Q

osteochonral junction is composed of

A

subchondral bone and cartilage

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13
Q

In OA, Initial

A

thickening of articular cartilage followed by fibrillation, degradation and erosion

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14
Q

osteophytes

A

new bone formation at joint margins in OA

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15
Q

with disease progression in OA, there is

A

vascular invasion & calcifaction of nearby articular cartilage-> decreased thickness of cartilage, bone remodeling & enhanced cartilage deterioration

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16
Q

primary enzymes responsible for the degradation of cartilage are:

A

the matrix metalloproteinases (MMPs)- MMP-13 specificty for collagen type II.
in OA, these are over expressed and inhibitors get overwhelmed

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17
Q

What secretes MMPs?

A

synovial cells and chondrocytes

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18
Q

Inhibitors of MMPs:

A

Alpha-2-macroglobulin and TIMPs

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19
Q

OA symptoms

A

Localized, deep, aching pain; pain on motion and joint stiffness < 30min

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20
Q

Heberden’s nodes

A

bony enlargements of DIP (ends of fingers)

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21
Q

Bouchard’s Nodes

A

bony enlargements of PIP (middle of fingers) 10X more common in women

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22
Q

Crepitus

A

cracking noise caused by bones rubbing each other

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23
Q

Labs in OA are

A

generally normal

ESR may be slightly elevated

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24
Q

X-ray in OA will show

A

narrowing of joint space, appearance of marginal osteophytes, subchondral bone sclerosis or cyst formation->eventually joint deformity

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25
Q

COX-1

A

present in many cells and responsible for housekeeping functions- increase gastric mucus, release of PGE2 to control release of gastric acid, motility, control renal blood flow, produce TXA2 in plateleys

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26
Q

COX-2

A

inducible at sites of injury or damage. Also present naturally in CNS, kidney and bone

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27
Q

first line treatment for OA

A

APAP

- primarily CNS MOA (COX-2)

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28
Q

APAP does NOT

A

produce GI irritation
affect bleeding or excretion of uric acid
respiratory or CV effects

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29
Q

APAP COX MOA

A

scavenges & eliminates peroxide tone

periheral COX protected by excess peroxides produced at sites of inflammation- overcome APAP

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30
Q

Critical radical needed to produce COX activity is generated by abstracting an electron from

A

tyrosine 385

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31
Q

APAP 3 MOA hypothesis

A
  1. inhibition of COX
  2. central serotonergic mechanism
  3. endocannabinoid pathway
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32
Q

____ & ____ block activity of APAP

A

5-HT3 antagonists & antagonists of cannabinoid BC-1

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33
Q

Main elimination of APAP

A

via glucuronide & sulfate conjugation pathways- but can become overwhelmed in high concentrations

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34
Q

too much APAP forces it through:

A

P450-CYP3#4 and CYP2E1 to NAPQI

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35
Q

NAPQI is elimiated

A

by conjugation to GSH and excreted in urine

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36
Q

in APAP overdose, GSH:

A

becoe depleted & NAPQI reacts with critical molecules of the cell

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37
Q

hepatotoxicity of APAP dose

A

10-15g

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38
Q

Death from liver damage of APAP dose

A

> 20g

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39
Q

treatment of APAP overdose

A

N-Acetyl-L-cysteine- GSH precursor; best if given w/in 10 hours

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40
Q

Aspirin chemical name

A

acetyl salicylic acid; developed by Felix Hoffman

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41
Q

Aspirin is a _____ inhibitor

A

irreversible COX-1; acetylates Ser530

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42
Q

NSAIDs block:

A

prostaglandin biosynthesis

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43
Q

Positive effects of NSAIDs by inhibition of _____

A

COX-2 (CV problems)

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44
Q

Adverse effects of NSAIDs by inhibition of ____

A

COX-1 (GI problems)

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45
Q

COX-1 vs COX-2

A

Iso 434 and 523 are substituted for valines in COX-2

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46
Q

COX-2 selective inhibitors tend to be

A

larger V shaped molecules

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47
Q

in pregnancy, COX inhibitors:

A

can block induction of labor

48
Q

treatment of GI symptoms with NSAIDs

A

add PPIs or Misoprostol

49
Q

Altered blood coagulation- COX-1 inhibitors block:

A

platelet function-> bleeding

Platelets cannot make more COX-1 bc they do not have a nucleus

50
Q

Renal function- NSAIDs:

A

reduce renal blood flow and GFR-> water and salt retention-> inc. BP in pts with renal insufficiencies
little effect in healthy pts

51
Q

NSAIDs w/ short half lives

A

<5 hours

aspirin, diclofenac, indomethacin, ibuprofen

52
Q

NSAIDs with long half lives

A

> 10 hours

naproxen, piroxicam, celecoxib, refecoxib

53
Q

primary route of elimination of NSAIDs

A

hepatic metabolism

54
Q

Salicylate clearance from the body follows:

A

nonlinear PK

55
Q

watch for NSAID drug interactions with:

A

lithium, warfarin, oral hypoglycemics, high dose MTX, antihypertensives (ACE-I, Beta-blockers, diuretics)

56
Q

Capsaicin (Zostrix) MOA

A

Depletes substance P- involved in pain transmission

57
Q

Nutritional supplements for OA

A

Glucosamine & chondroitin- little benefit

58
Q

Intra-articular corticosteroids in OA

A

inhibit PG synthesis
Triamcinolone & methylprednisolon most used
can induce osteoporosis
useful in pts w/ effusions, local inflammation
injected intro joint after aseptic aspiration
never into infected joint
mono or combo therapt

59
Q

Intra-articular hyaluronic acid (HA) in OA

A 
HA- shock absorber & lube in cartilage
mild anti-inflammatory 
3-4 injections/yr
knee & hip
not really recommended
60
Q

Opioids in OA

A

LAST RESORT!
Tramadol
low dose, sustained release- oxycodone, morphine, fentanyl

61
Q

Tramadol MOA

A

dual mechanism- mu-receptor
R enantiomer- simulates release of serotonin
S enantiomer- blocks reuptake of NE

62
Q

Goals of therapy in OA

A

Alleviate pain and stiffness
maintain or improve function
maintain or improve QOL
avoid side effects of therapy

63
Q

Topical agents in OA

A

can be used 1st line- small joints

64
Q

Capsaicin OA

A

3-5x/day
no PRN dosing
smaller joints

65
Q

Bio-Freeze OA

A

Menthol 3.5%/Camphor 0.2%

up to 4X/day

66
Q

topical NSAIDs

A

diclofenac 1% topical gel (Voltaren)
Deiclofenac 1.3% patch (Flector)
caution in >75 yo

67
Q

Oral NSAIDs in OA

A

2nd line
PRN or scheduled
takes 2-3 weeks to see benefit

68
Q

bisphosphonates in OA

A

Alendronate (Fosamax)- knee
Risedonate (Actonel)- decrease joint space narrowing; decrease need for joint replacement surgery
may be useful in pts with osteoporosis too

69
Q

RA MOA hypothesis

A
  1. low affinity MHC receptors- no negative selection of T cells
  2. citrullinated proteins- shared epitope HLA-DR molecules bind with higher affinity
70
Q

presense of ___ & ___ in RA synovium

A

PAD and citrullinated epitopes

71
Q

citrullination

A

arginine to citrulline by PAD - autoimmune response to it

change in charge

72
Q

RA has been linked to genetic polymorphisms in

A

PTPN22 & STAT4

73
Q

RA potential triggers

A

smoking- in ACPA+ pts

viruses, bacteria, stress/trauma

74
Q

Series of events in RA

A

Initiating event- APC & T cells
Autoimmune response
Inflammation
autoantibodies

75
Q

Autoantibodies in RA are called

A

rhematoid factors- produced by B cells

form complexes in serum, synovial fluid & membranes-> inflammation & destruction

76
Q

initial changes in RA

A

Microvascular damage & inflammation of synovial space

77
Q

Sjögren’s syndrome

A

a systemic autoimmune disease in which immune cells attack and destroy the exocrine glands that produce tears and saliva

78
Q

extra-articular involvement in RA

A

Rheumatic nodules, vasculitis, ocular manifestations, cardiac involvement, splenomegaly & neutropenia

79
Q

Felty’s syndrome

A

splenomegaly & neutropenia

80
Q

Lab findings in RA

A

Anemia, Thrombocytosis, erythrocyte sedimentation rate, rheumatoid factors antinuclear antibodies (ANA), anticyclic citrullinated peptides antibodies (anti- CCP & ACPA), turbid synovial fluid

81
Q

radiologic evaluation in RA

A

soft tissue swelling, joint space narrowing, osteoporosis near joint, erosions

82
Q

RA vs OA swelling of the joint

A

RA- feels soft and spongy

OA- bony and hard

83
Q

Non-biologic DMARDs

A

small, synthetic molecues

MTX, hydroxychloroquine, sulfasalazine & leflunomide

84
Q

Biologic DMARDs

A

proteins
anti-TNF: infliximab, adalimumab, etanercept, Golimumab, certolizumab
Non-TNF: Abatacept, Rituximab, Anakinra

85
Q

MTX

A 
folic acid antagonist
acts against rapidly proliferating cells
polyglutamated MTX is a high affinity inhibitor for DHFR
inhibits formation of DNA & RNA 
20-30mg/week
86
Q

MTX adenosine MOA

A

MTX inhibits AICAR transformylase-> accumulation of AICAR-> inhbits AMP and adenosine deaminase-> increased extracellular adenosine-> anti-inflammatory

87
Q

MTX polyamine MOA

A

MTX blaocks THF-> reduces polyamine formation-> decrease local toxicity

88
Q

First line treatment in RA

A

MTX
2-3 week onset
can lead to bone marrow suppression & liver/renal insufficiencies
avoid in prego

89
Q

administration of ____ can reduce/prevent some adverse effects

A

folic acid

90
Q

leflunomide

A

converted to A77-1726->inhibits dihydroortate DH
critical for formation of pyrimidines
no bone marrow suppression
do not use in prego for MEN & women or liver diease
100mg po qdX3days then 20mg PO QD

91
Q

hydroxychloroquine

A 
concentrates as cationic base in acidic lysosomes & raises their pH->impedes their function
2-6 months for onset
one of the least toxic DMARDs
ocular toxicity!!- need yearly eye exams
200-400mg PO QD
92
Q

Sulfasalazine (Azulfidine)

A 
cleaved by bacteria in the gut
sulfapyridine is the active compound
inhibits AICAR transformylase & increases adenosine-> decreased inflammation
onset 2 months
hyemolytic anemia in pts w/ G6PD deficiency
interacts w/ warfarin
Stevens-Johnson syndrome
avoid use w/ antibiotics
titrated to 1g PO BID
93
Q

gold salts

A

inhibit maturation & function of macrophages & T cells
6 month onset
reversible renal toxicity/ lots of toxicities
suppression of blood cell production

94
Q

Azathioprine

A

prodrug converted into 6-MP

95
Q

D-Penicillamine

A

metal chelating agent

reduces reactive aldehydes which bind to collagen preventing it from cross-linking and facilitating its degradation

96
Q

minocycline

A

attenuates TNF-alpha production, downregulating pro-inflammatory cytokine production
100mg PO BID
chelation w/ bones & teeth

97
Q

biologic DMARDs cannot be given

A

orally!

98
Q

TNF-alpha antagonists

A 
all prego category B
screen for TB
risk of HF
infliximab- mouse/IV
adalimumab- human/SQ
golimumab- human/SQ; once/month
etanercept-binds 2 molecules of TNF-alpha/SQ; 50mg/week
certolizumab pegol- not a full antibody; no Fc region
99
Q

IL-1 receptor antagonist

A

Anakinra
not glycosylated
4-6 hr half life
prego catecory B

100
Q

Anti IL-6

A

Tocilizumab- mouse
binds to both soluble and membrane receptors
require an effector molecule-GP130

101
Q

Abatacept

A

costimulation blocker
CTLA-4
binds to CD80/86 & inhibites CD28 interaction

102
Q

rituximab

A

B cell depletion
mouse
binds to B cell CD20
60 hr half life

103
Q

glucocorticoids are secreted by

A

Zone F

104
Q

mineralocorticoids are secreted by

A

Zone G

105
Q

cortisol inhbits

A

immune system

106
Q

keto group on glucocorticoids

A

makes it inactive!

i.e. prednisone

107
Q

11 beta-hydroxysteroid DH

A

type 1: reduces keto-> hydroxyl; activation

Type 2: oxidizes back to keto & shuts down glucocorticoid

108
Q

transrepression of steroids

A

repress gene transcription of pro-inflammatory modulators of the host immune system

109
Q

transactivation of steroids

A

increase release of anti-inflammatory factors

110
Q

glucocorticoids are ____ bound to plasma proteins

A

largely

111
Q

adverse effects of glucocorticoids

A 
infection
hyperglycemia
osteoporosis
fluid & electrolyte changes
cataracts
adrenal insufficiency
112
Q

features of poor prognosis in RA

A 
functional limitations
extra-articular disease
positive rheumatoid factor
positive anti-CCP antibodies
bony erosions by radiography
add biologic DMARD
113
Q

Goals of therapy in RA

A

achieve full remission or low disease activity
alleviate pain
maintain QOL
maintain function essential for ADLs & work
slow rate of joint damage
avoid or minimize adverse effects & toxicities of therapies

114
Q

full remission is defined as absence of:

A 
symptoms of active, inflammatory joint pain
morning stiffness
fatigue
synovitis on joint exam
progression of radiographic damage
elevated ESR & CRP
115
Q

tofacitinib

A

targeted DMARD
need to be screened for TB & hepatitis
BBwarning- serious infection & malignancy
DO NOT USE w/ BIOLOGIC

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