Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Imm/Musculoskel/Skin > Osteoporosis (2) > Flashcards

Osteoporosis (2) Flashcards

1
Q

What is osteoporosis?

A

Bone disorder
low bone density, impaired bone architecture, and compromised bone strength
Predisposes to increased fracture risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors (6)

A
  1. Age
  2. Genetics
  3. Diet/lifestyle … smoking, 3 or more alcoholic drinks/day, low calcium intake, limited exercise
  4. Hormonal status … postmenopausal, premature menopause
  5. Diseases (RA, Vit D deficiency)
  6. Medications (glucocorticoids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Medical conditions associated with osteoporosis

A

Endocrine/hormonal
-ovarian failure
-testosterone deficiency
-hyperthyroidism
-Cushing’s syndrome
-growth hormone deficiency in children
-primary hyperparathyroidism
-diabetes

Gastrointestinal
-nutritional disorders (anorexia)
-malabsorptive states
-chronic liver disease

Disorders of calcium/phosphate balance
-hypercalciuria
-vitamin D deficiency
-hypophosphatemia

Inflammatory disorders
-RA

Chronic illness
-CKD
-Malignancies
-HIV/AIDs
-organ transplant

Disuse/immobility
-muscular dystrophy
-MS
-stroke/cerebrovascular accident

Genetic
-osteogenesis imperfecta
-cystic fibrosis
-hemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some medications that increase risk of osteoporosis (5)

A

Antiseizure therapy (phenytoin, carbamazepine, phenobarbital, and valproic acid)

Antiretroviral therapy (NRTIs, NNRTIs, protease inhibitors)

Furosemide

Glucocorticoids (long term oral therapy)

PPIs (long term therapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When does bone loss occur?

A

When bone resorption exceeds bone formation or due to high bone turnover
-accelerated bone turnover increases the amount of bone that is not adequately mineralized (so its not good quality bone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 2 types of bone

A

Cortical - long bones (make up 80%) , hard bones

Trabecular - vertebrae and end of long bones, spongey bones
-these are metabolically more active and have a higher bone turnover rate because of large surface area and honeycomb like shape
-they are more susceptible to estrogen deficient bone loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Functions of bone

A

Mechanical support
Transmission of forces generated by muscles
Protection of viscera
Mineral homeostasis
Place for blood cell production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Constituents of bone

A

Extracellular matrix
-made of organic component - osteoid (35%) - which is made of protein, collagen mostly
-and a mineral component (65%)

Embedded in the matrix are a variety of specialized bone cells…
osteoblasts - synthesize bone
osteocytes - lay down bone
osteoclasts - resorb bone
The balance between these maintains homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The unique feature of bone, its hardness, is imparted by what component?

A

The inorganic components - hydroxyapatite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Osteoblasts

A

Located on the surface of matrix
Synthesize, transport, and assemble bone matrix and regulate its mineralization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Osteocytes

A

These are derived from osteoblasts, but these are located within the bone (whereas osteoblasts are on the surface)

They help control calcium and phosphate levels, detect mechanical forces, and translate them into biological activity - mechanotransduction

(also help lay down bone?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Osteoclasts

A

These are located on the surface of bone

They are specialized macrophages derived from monocytes - they are responsible for bone resorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Vitamin D

A

This is a fat soluble vitamin
A lot of vitamin D is synthesized endogenously in the skin (powered by light)

The active form of vitamin D…
-stimulates intestinal absorption of calcium
-stimulates calcium resorption in renal distal tubules
-collaborates with PTH to regulate blood calcium
-promotes mineralization of bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Parathyroid hormone (PTH) formation

A

Peptide (protein) hormone
Made from a precursor produced in the parathyroid gland that is cleaved by a protease to form PTH

This is calcium sensitive protease - presence of calcium therefore limits the production of PTH

Also, there is a calcium sensing receptor (CaSR) which when simulated by calcium limits the production and secretion of PTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PTH activity (2 functions)

A

PTH regulates calcium and phosphate flux across membranes in bone and kidney leading to… increased serum calcium and decreased serum phosphate
(makes sense, calcium and phosphate will form a precipitate, so to increase calcium concentration, need to decrease phosphate)

In the bone… PTH increases the activity and number of osteoclasts (which are responsible for bone resorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do PTH and active vitamin D both effect bone in 2 ways

A

Both PTH and 1,25(OH)2D regulate bone formation and resorption (each is capable of stimulating both processes)

They contribute to the preosteoblast proliferation and differentiate into osteoblasts (resulting in bone formation)

But, they also stimulate the expression of RANKL by the osteoblast
-RANKL (on osteoblast) binds to RANK on osteoclast precursors, causing them to produce functional osteoclast (resulting in bone resorption)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bone remodeling/demodeling regulation

A

Bone remodeling/demodeling in balance by action of osteoblasts/osteoclasts

Osteoblasts release MCSF (macrophage colony stimulating factor) which binds binds receptor on osteoclasts - this is one signal

Osteoblasts ligand - RANKL, binds RANK receptor on osteoclasts, boosting differentiation of osteoclasts into active form

MCSF and RANKL induce bone resorption

Osteoblasts also synthesize an antagonist to RANKL - osteoprotegerin (OPG) - this binds to the RANK receptor preventing the binding of RANK (so OPG neutralizes RANKL), inhibiting osteoclast differentiation, and thus inhibiting bone resorption

Different systemic factors affect this balance
-hormones, vitamin D, inflammatory cytokines, growth factors
-PTH and glucocorticoids (promote osteoclast differentiation and bone turnover)

The mechanisms are complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Sex hormones (estrogen and testosterone) generally have what effect on the bone?

A

Block osteoclast differentiation or activity by favoring OPG expression (inhibit bone resorption)

(this is why when women go through menopause, there is less estrogen, so increased RANKL expression and increased osteoclast activity, since there is less OPG to neutralize the RANKL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the most common cause of osteoporosis?

A

Postmenopausal (estrogen deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Postmenopausal osteoporosis pathophysiology

A

-estrogen deficiency > significant bone density loss

-increased proliferation and activation of new osteoclasts and prolonged survival of mature osteoclasts occurs

-Interleukins, prostaglandin E2, TNF-α, and interferon γ also increase resulting in more RANKL and less OPG

-There is increase in calcium excretion and decrease in calcium gut absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some causes of estrogen deficiency

A

Menopause
Anorexia nervosa
Lactation
Medications (prolonged medroxyprogesterone implants, aromatase inhibitors, gonadotropin releasing hormone agonists)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Menopause related osteoporosis timeline

A

Bone loss (mass and strength) begins during perimenopause and continues up to 8 years after menopause

note - early menopause increases loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Male osteoporosis

A

Males have a lower risk of developing osteoporosis and osteoporotic fractures

They have larger bone size, greater peak bone mass, and an increase in bone width with aging

Also fewer falls and shorter life expectancy may contribute to this

There are secondary causes (medical conditions) that can increase the risk of males developing osteoporosis

Other risk factors include smoking, alcohol abuse, low body weight, weight loss, age, long term glucocorticoid use, androgen deprivation therapy, low testosterone concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Clinical presentation and consequences of osteoporosis

A

Silent disease

Vertebral fractures can occur
-may be asymptomatic or cause mild back pain, multiple vertebral fractures can cause decrease in height and curve the spine

Most common sites for fractures are hip, spine, and wrist

Results in pain and physical deformity and decreased quality of life
Compression of thoracic region can cause respiratory and GI complications
Hip fracture has the highest mortality rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which type of fracture has the highest mortality rate?

A

Hip fractures
(about 20% die within a year)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

FRAX tool

A

This is a assessment tool that tells us the probability of a patient having a major osteoporotic fracture and hip fracture in the next 10 years

We use this when we consider treatment decisions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Bone mineral density assessment

A

Peripheral bone mineral density (BMD) devices:
-DXA or QUS (quantitative ultrasonography)

The gold standard is DXA (central dual-energy x ray absorptiometry)
-measures BMD at hip or spine
-assesses fracture risk and establishes the diagnosis (T score) and severity of osteoporosis

(should be done for all women aged 65 years or older, men aged 70 years or older, postmenopausal women younger than 65 years old and men 50 to 69 years old with risk factors for fracture, and patients with an identified secondary cause for bone loss - most insurance will pay every 2 years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Central DXA scores

A

T score and Z score

T score
-assesses severity in reference to the general population
-below -2.5 is considered osteoporosis, from -1 to -2.5 is considered osteopenia

Z score
-more useful for men and children
-compares patient’s BMD to the mean BMD of sex and age matched population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is osteoporosis diagnosed?

A

Diagnosis is established by measurement of BMD (from central DXA) OR if there is assurance of adult hip or vertebral fracture in the absence of major trauma

Normal T score is -1 and above
Osteopenia (low bone mass) is -1 to -2.5
Osteoporosis is diagnosed when T score is less than -2.5

It is considered severe/established osteoporosis if T score is less than -2.5 and there has been one or more fractures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the main goal of therapy for osteoporosis

A

Prevention

Once it has developed…
-stabilize, improve bone mass and strength
-prevent fractures/falls
-reduce pain, improve QOL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Nonpharm therapy

A

Proper nutrition (adequate amounts of calcium, vitamin D and protein), moderation of alcohol intake, caffeine, and salt

Maintain a healthy weight

Exercise: moderate-intensity weight bearing activities (walking, jogging, stairs) and resistance activity (free weights, elastic bands)

Smoking cessation

Fall prevention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Recommended calcium intake

A

Men + women 19-50 … 1000 mg/day

Men 51-70 … 1000 mg/day
Women 51-70 … 1200 mg/day

Men + women 71 and over … 1200 mg/day

But anything below 2000-25000 mg/day is safe and not considered a risk (anything above that we think about CV risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which form of calcium supplement is preferred?

A

Calcium carbonate
-has highest percent of elemental calcium and is the least expensive
(also used as an antacid- Tums)

Should be taken with meals to enhance absorption- needs acidic environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Calcium citrate considerations

A

Acid independent absorption (unlike calcium carbonate) - so good for those taking H2RA or PPI

Can also be taken without regards to food (unlike calcium carbonate)
And has less GI upset than calcium carbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a big ADR from calcium supplements, what should patients be counseled to do when taking calcium because of this?

A

Constipation
Counsel patients to increase water, fiber, and exercise

36
Q

Use of __________ may decrease calcium absorption

A

PPIs (specifically calcium carbonate, calcium citrate can be used)

37
Q

Calcium drug interaction considerations

A

Calcium may decrease absorption of other drugs including…
-iron
-tetracyclines
-quinolones
-bisphosphonates
-thyroid supplements

so administration should be separated by 2-4 hours

38
Q

Vitamin D therapy considerations

A

If someone is vitamin d deficient, we need to replace the deficiency with a higher treatment dose first, then continue on a maintenance dose

vitamin D is usually well tolerated, monitor for hypercalcemia

the half life of vitamin D is 1 month, so about 3 months of therapy should be completed before repeating level

The goal is to maintain an active vitamin d of at least 20 ng/mL

39
Q

Vitamin D drug interaction considerations

A

Some medications may induce vitamin D metabolism
-rifampin
-phenytoin
-carbamazepine

And some may decrease vitamin D absorption
-cholestyramine
-orlistat
-mineral oil

so in both of these cases you may need higher doses of vitamin D

40
Q

Which patients should receive prescription drug therapy?

A

Any man or postmenopausal woman over 50 years old presenting with at least one of the following…
-a hip or vertebral fracture
-T score of -2.5 or less at neck, total hip, or spine
-low bone mass (t score -1 to -2.5) with a FRAX 10 year probability of a hip fracture of 3% or higher, or a FRAX 10 year probability of any fracture of 20% of higher

41
Q

Prescription therapy should be used in addition to what?

A

Calcium and vitamin D
(every patient should get these!)

42
Q

Estrogen and testosterone considerations for osteoporosis

A

These are NOT prescribed for just osteoporosis treatment
But, if they are needed for other conditions, may have benefit of osteoporosis as well

43
Q

Which drugs are first line pharmacological options for osteoporosis and why? (4)

A

Bisphosphonates
1. alendronate
2. risedronate
3. zoledronic acid (IV)
(not ibandronate is a bisphosphonate but is second line)

  1. denosumab

These drugs are first line because they have efficacy data for the reduction of both hip and vertebral fracture risk

44
Q

Bisphosphonate MOA

A

They are analogs of pyrophosphate (a natural metabolite in the body), but they have longer half lives because the P-O-P bond has been replaced with a non-hydrolysable P-C-P bond

They have many effects on bone mineral homeostasis
Major function: retard formation and dissolution of hydroxyapatite crystals within and outside the skeletal system

Also…
-inhibit active vitamin D production
-inhibit intestinal calcium transport
-cause metabolic changes in bones - inhibition of glycolysis
-inhibition of cell growth
-changes in acid and alkaline phosphate activity

45
Q

Bisphosphonates have low ___________

A

Absorption
(bioavailability is less than 1% and is decreased with food/beverage consumption… important counseling point)

46
Q

Bisphosphonate ADRs

A

Oral: esophageal and gastric irritation (because they are acids)

Muscoloskeletal pain

Acute phase reactions… fever, flu like symptoms, myalgia, arthralgia (more with IV form than oral)

Rare but serious: severe GI events (esophageal erosion, ulcer, GI bleeding), osteonecrosis of the jaw (ONJ), subtrochanteric femoral (atypical) fractures

47
Q

Binding strength of different bisphosphonates

A

The different bisphosphonates have different binding strengths to bone …
greatest is zolendronic acid > alendronate > ibandronate > risedronate

48
Q

Bisphosphonate duration of therapy

A

The ideal duration of therapy is not known
But should last less than 5 years

49
Q

Bisphosphonate contraindications (3)

A

CrCl < 30-35 ml/min (drug is absorbed into bone within first 24 hours, the rest is renally excreted)

Serious GI conditions (abnormalities of esophagus)

Pregnancy

50
Q

Bisphosphonate monitoring parameters

A

Bone density
Fractures
GI symptoms
Muscle aches
Serum calcium and SCr for zoledronic acid prior to each infusion

51
Q

ORAL bisphosphonate patient education points

A

Oral tablet should be taken with 6 ounces of plain water at least 30 minutes before consuming food, supplements, or medications (60 minutes with ibandronate) (no juice, coffee, mineral water, etc.)

Remain upright for at least 30 minutes (60 minutes for ibandronate)

For swallowing difficulties - there is an effervescent form of alendronate, must be dissolved in 4 ounces of water, follows same food/medication restrictions

There is a delayed release form of risedronate - give immediately following breakfast with 4 ounces of plain water

52
Q

Oral bisphosphonate missed dose counseling points

A

Most dosing is once weekly (sometimes once monthly)
-if missed once weekly dose - take the next day, if more than 1 day has passed, just skip that dose
-monthly doses can be taken up to 7 days before the next administration

53
Q

IV bisphosphonate counseling points

A

Serum calcium concentration must be checked and corrected if needed prior to each infusion

Needs to be administered by health care provider

Can take acetaminophen prior to infusion to decrease fever, flu like symptoms, myalgias, and arthralgias (acute phase reactions)

54
Q

Denosumab MOA

A

Humanized monoclonal antibody that binds to and prevents the action of RANKL (inhibiting osteoclast formation and activity)

55
Q

3 concerns with denosumab

A
  1. some immune cells express RANKL, so there can be an increased risk of infection with denosumab use
  2. bone turnover suppression is similar to that of potent bisphosphonates, so risk of osteonecrosis
  3. denosumab can lead to transient hypocalcemia
56
Q

Denosumab place in therapy

A

Treatment of osteoporosis in patients at high risk for fractures - including…
- glucocorticoid induced osteoporosis
- men receiving androgen deprivation therapy (for prostate cancer)
- women receiving aromatase inhibitor (for breast cancer) with high risk of fracture

57
Q

Denosumab administration

A

60 mg SQ every 6 months
-must be administered by health care professional (can be done by pharmacist in some states)

58
Q

Denosumab renal function consideration

A

NO renal dose adjustment is currently required
But, hypocalcemia is more common in patients with renal impairment - so monitor patient’s serum calcium within 14 days of administration if CrCl < 30

59
Q

Denosumab duration of therapy

A

After 5-10 years patients should be reevaluated for medication continuation, discontinuation, or switching to a different medication

60
Q

Denosumab ADRs

A

Common: back pain, arthralgia, eczema, cellulitis, infection

Rare: osteonecrosis of the jaw, atypical femoral shaft fracture

61
Q

Denosumab monitoring parameters

A

Bone density
fractures
Serum calcium (hypocalcemia should be corrected prior to dose)

62
Q

What are the alternative pharm therapy agent options? Why are they considered alternatives?

A

Parathyroid hormone analogues
1. Abaloparatide
2. Teriparatide

  1. Ibandronate (second line bisphosphonate)
  2. Raloxifene (second generation mixed estrogen agonist/antagonist)
  3. Romosozumab (humanized monoclonal antibody that binds to sclerostin)

These are considered alternative because they have evidence for decreasing vertebral fracture risk but NOT hip fracture risk

63
Q

What is a last line option for osteoporosis?

A

Intranasal calcitonin

64
Q

Teriparatide MOA

A

Recombinant form of PTH (analog of PTH)
First approved “anabolic” - bone building drug
-increases osteoblast formation and inhibits osteoblast apoptosis
(counterintuitive of what PTH does, but this is what PTH administration has shown)

65
Q

Teriparatide duration of therapy

A

Only approved for use for 2 years
-intermittent administration has shown to increase the number of osteoblasts, but continuous administration has shown to increase the number of osteoclasts (which is why duration is limited)

66
Q

Abaloparatide MOA

A

Synthetic analog of parathyroid hormone related protein (PTHrP)
-acts similar to PTHrP, binds to and activates PTH1 receptor on osteoblasts and bone stromal cells increasing bone growing and bone density conserving activities

67
Q

Abaloparatide and teriparatide place in therapy

A

Both:
postmenopausal women with osteoporosis at high risk for fracture defined as multiple risk factors for fracture, a history of osteoporotic fracture, or failed or intolerant to other therapies

Teriparatide also has an indication for men…
men with idiopathic or hypogonadal osteoporosis who are at high risk for fracture, men intolerant to other osteoporosis medications, and patients with glucocorticoid-induced osteoporosis

68
Q

Abaloparatide and teriparatide administration

A

SQ daily injections for 2 years max

(80 mcg for abaloparatide, 20 mcg for teriparatide)

69
Q

Abaloparatide and teriparatide ADRs and BBW

A

Orthostatic hypotension
Transient hypercalcemia
Urolithiasis (calcium)
Increased uric acid (keep this in mind if patient has history of gout)
Injection site reactions

BBW: osteosarcoma (data from animal studies)

70
Q

Abaloparatide and teriparatide monitoring parameters

A

Orthostatic hypotension
Serum calcium
Urinary calcium (for patients with suspected urolithiasis or preexisting hypercalcemia)
BMD at baseline and 1-2 years following initiation of therapy

71
Q

Raloxifene MOA

A

SERM - selective estrogen receptor modulator
It is a mixed agonist/antagonist at the estrogen receptor depending on the tissue (partial agonist of ERalpha and pure antagonist or ERbeta)
-estrogen activity in liver and bone
-anti-estrogen activity in breasts and uterus

72
Q

Raloxifene place in therapy

A

for patients who are unable to take bisphosphonates and denosumab, or in patients with a high risk of vertebral fracture and a high risk of invasive breast cancer

73
Q

Raloxifene administration

A

PO once daily (60 mg)

74
Q

Raloxifene ADRs

A

Hot flashes
Leg pain, cramps, spasms
Peripheral edema
VTE (do not use in high risk patients)

75
Q

Raloxifene monitoring parameters (2)

A

Lipid profile
BMD at baseline and every 1-3 years

76
Q

Raloxifene drug interaction consideration

A

Highly protein bound, so has interaction with other protein bound drugs… can displace and cause higher concentrations of those drugs in the serum (e.g. warfarin)

77
Q

Romosozumab MOA

A

Humanized monoclonal antibody that binds to sclerostin
-sclerostin is a glycoprotein produced by osteocytes that inhibits the Wnt (growth factor) signaling pathway leading to inhibition of osteoblast differentiation/function

By binding to sclerostin, romosozumab prevents the sclerostin from inhibiting the Wnt pathway, so the Wnt pathway will be stimulated - resulting in increased osteoblast formation and therefore increased bone formation

(also decreases bone resorption but to a lesser extent)

78
Q

Romosozumab place in therapy

A

postmenopausal women at very high risk for fracture defined as multiple risk factors for fracture, a history of osteoporotic fracture, or failed or intolerant to other therapies

79
Q

Romosozumab administration/duration

A

SQ administration, monthly for up to 1 year
-must be administered by health care professional

80
Q

Romosozumab ADEs/BBW

A

Headache, arthralgia, hypercalcemia, injection site reaction, hypersensitivity

Theoretical risk of increased malignancy

BBW - Serious cardiovascular events (myocardial infarction, stroke, and cardiovascular death)
-do not use within 1 year of MI or stroke

81
Q

Romosozumab monitoring parameters

A

Hypersensitivity
Signs/symptoms of cardiovascular events
Serum calcium
BMD

82
Q

Calcitonin MOA

A

Calcitonin is a hormone, its function is to counteract PTH - lowers serum calcium and phosphate levels and inhibits osteoclastic bone resorption

Bone formation is not impaired at first with calcitonin administration, but overtime, both formation and resorption of bone are reduced

83
Q

Calcitonin place in therapy

A

Last line therapy

for women who are at least 5 years past menopause; rarely used and should only be considered if no other therapies are appropriate due to cancer risk

Note- short-term treatment may provide analgesic effect in patients with acute painful vertebral fractures (it is the only agent that has analgesic effect, so can be used short term for painful fractures)

84
Q

Calcitonin administration

A

IM, SQ, or intranasal spray … daily

85
Q

Calcitonin ADRs

A

Rhinitis (with intranasal spray)
Depression
Rash
Nausea
Injection site reactions
Back pain
Malignant neoplasm (this is why it is last line)

Imm/Musculoskel/Skin (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions