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Dermatology Board Prep > DERM (12) Medical Therapy > Systemic Immunomodulators > Flashcards

Systemic Immunomodulators Flashcards

1
Q

What is the mechanism of apremilast?

A

PDE-4 inhibitor

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2
Q

What are the indications for apremilast?

A

Psoriasis and psoriatic arthritis

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3
Q

What are the most common side effects of apremilast?

A

Diarrhea and nausea (usually go away spontaneously in 4 weeks)

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4
Q

What is a serious medical history item that should be screen for apremilast?

A

Depression/suicidality. There have been reports of depression on the medication

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5
Q

Renal adjustment of apremilast?

A

Yes, in severe renal impairment, halve the dose

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6
Q

Laboratory monitoring needed for apremilast?

A

None!

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7
Q

What JAK’s are affected by tofacitinib?

A

JAK 1 and 3

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8
Q

What are the most common side effects for JAK inhibitors?

A

URI, mild headaches, and nausea. May have decreased hgb and neutrophil count but normalizes on treatment.

Also may have increased LDL, HDL, CK, TGs, and LFTs

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9
Q

What JAK inhibitors are affected by Ruxolitinib?

A

JAK 1 and 2

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10
Q

What is azathioprine’s active metabolite?

A

6-TG (thioguanine)

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11
Q

What is azathioprine’s mechanism of action?

A

Active metabolite is produced by hypoxanthine-guanine phosphoribosyltransferase (HGPRT) pathway and shares similarities w/ endogenous purines. So, it gets incorporated in the DNA and RNA and inhibits purine metabolism and cell division. This is particularly true if the cells are fast-growing and don’t have a purine salvage pathway (like lymphocytes).

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12
Q

What enzymes break azathioprine into its inactive metabolites?

A

Xanthine oxidase and thiopurine methyltransferase

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13
Q

What is the clinical effect of azathioprine?

A

It diminishes T-cell unction and antibody production by B-cells

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14
Q

What medications can lead to life-threatening myelosuppression in people taking azathioprine?

A

Xanthine oxidase is involved in the conversion to inactive metabolites, so allopurinol or febuxostat can inhibit this and lead to elevated levels of azathioprine

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15
Q

What other medications besides allopurinol and febuxostat can increase the risk of myelosuppression with azathioprine?

A

ACEi, sulfasalzine, and concomitant use of folate antagonists

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16
Q

What test must be checked before starting azathioprine?

A

TPMT activty

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17
Q

Important side effects of azathioprine?

A

Leukopenia, thrombocytopenia, and immunosuppression (correlates with low TPMT activity)

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18
Q

What cancer risks are increased in azathioprine?

A

Squamous cell carcinoma and lymphoma (non-Hodgkin’s B-cell lymphoma)

No clear evidence that this actually occurs with doses used in dermatologic dz

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19
Q

What are the most common side effects of azathioprine?

A

Gastrointestinal side effects: nausea, vomiting, and diarrhea (often between first and tenth day of therapy), gastritis and pancreatitis

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20
Q

When does hypersensitivity syndrome usually occur?

A

Usually between first and fourth week of therapy and more common in those getting MTX or cyclosporin

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21
Q

What effect on the killed hepatitis B vaccine do azathioprine and prednisone have?

A

These have been shown to decrease the response of the vaccine

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22
Q

If azathioprine is given with a TNF-a inhibitor, what cancer is the person at risk for?

A

Increased risk of hepatosplenic T-cell lymphoma

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23
Q

What baseline tests should be done before starting azathioprine?

A

Pregnancy test, tuberculin skin test

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24
Q

What is the mechanism of action for mycophenolate mofetil?

A

Binds and inhibits inosine monophosphate dehydrogenase

This is an important enzyme for de novo synthesis of purines - which is essential in activated lymphocytes

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25
Q

What medications or things can decrease the absorption of mycophenolate mofetil?

A

Requires gastric acidity –> needed for cleavage into its active version

things like antacids, H2 blockers, PPI’s things that decrease acidity will decrease serum levels

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26
Q

What are absolute contraindications for mycophenolate mofetil?

A

Pregnancy and drug allergy

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27
Q

What is the risk of skin cancer or other cancers in those taking mycophenolate mofetil for dermatologic conditions?

A

Unknown, risk is increased in transplant patients but these patients often have more than one medication on board.

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28
Q

What are the most common side effects of mycophenolate mofetil?

A

Diarrhea, abdominal pain, nausea, and vomiting

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29
Q

What is the neutrophil dysplasia that can be seen with the administration of mycophenolate mofetil, and what can it signify?

A

Pseudo-Pelger-Juet anomaly = nuclear hypolobulation w/ a left shift. This may predict the development of neutropenia

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30
Q

What baseline tests should be performed for mycophenolate mofetil?

A

Baseline hepatitis B/C panel, tuberculosis screen, and pregnancy test

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31
Q

What lab monitoring should be done for patients on mycophenolate mofetil?

A

CBC/ w diff, CMP at baseline and then every 2-4 weeks after starting treatment or dose escalation and then every 2-3 months once the dose is stable

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32
Q

What is the mechanism of action for cyclosporine?

A

Forms a complex w/ cyclophilin, which inhibits calcineurin (intracellular enzyme), –> decrease in NFAT activity (this transcribes various cytokines, such as IL-2)

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33
Q

How does cyclosporine affect CD4 and CD8 cells?

A

Decreases IL-2 production leads to decreased numbers of CD4 and CD8 cells

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34
Q

What is the maximum dose for dermatologic disease for cyclosporine?

A

5 mg/kg and can be used continuously for up to 1 year (FDA, 2 years for worldwide consenses)

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35
Q

In what patients is cyclosporine contraindicated in?

A

Lymphoma, risk of progression

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36
Q

What are the two most noted side effects of cyclosporine?

A

Hypertension and nephrotoxicity

these are dose and duration dependant

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37
Q

How can kidney damage be avoided in using cyclosporin?

A

Not exceeding doses of 2.5-5mg/kg, not using for more than 1 year, and dose adjusting when creatine increases by 30%

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38
Q

Is HTN a reason to discontinue cyclosporine?

A

No, the HTN that develops is thought to be 2/2 renal vasoconstriction. When it occurs it can be controlled with blood pressure medications.

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39
Q

What are the preferred blood pressure medications for cyclosporine-induced HTN and why?

A

CCB’s like nifedipine and isradipine because these do not affect serum levels of cyclosporin

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40
Q

Important side effects of cyclosporine?

A

Increased risk of NMSC (other malignancies is unclear), hyperlipidemia, hypertrichosis, gingival hyperplasia, myalgia, paresthesia, tremors, malaise, hyperuricemia (can precipitate gout), hypomagnesemia and hyperkalemia

Bilirubin, uric acid, lipids, potassium (all of these go up)

For the main labs think BULK-UP

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41
Q

What should be done if Cr increases by more than 30% while on cyclosporine?

A

Re-check Cr levels. If it is still >30% then decrease dose by at least 1mg/kg for 4 weeks. Then re-check the Cr. If it <30% increase over baseline then therapy can be resumed. If Creatine does not drop then discontinue therapy. If the creatine returns to within 10% of baseline, cyclosporine can be resumed at a lower dose

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42
Q

What should be done if creatine levels increase by >50% while on cyclosporine?

A

Cyclosporine must be decreased until the Cr has returned to baseline

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43
Q

What baseline measurements/labs should be done prior to starting cyclosporine?

A

2 baseline blood pressure at least 1 day apart

2 baseline creatine values at least 1 day apart

Baseline: BUN, CBC, LFTs, fasting lipid profile, magnesium, potassium, and uric acid

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44
Q

Monitoring for cyclosporin?

A

Labs (CBC, CMP, lipids, uric acid, magnesium) and blood pressures should be checked every 2 weeks for the first 1-2 months then every 4-6 weeks with blood pressure checked at each visit (encourage pt to take a home log of blood pressures)

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45
Q

What is the mechanism of action for methotrexate?

A

Binds dihydrofolate reductase with more affinity than folic acid. This prevents dihydrofolate from being converted to tetrahydrofolate which is a required cofactor for purine synthesis. Ultimately this inhibits cell division

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46
Q

What medications can be given to reduce side effects or rescue the patient from adverse effects of methotrexate?

A

Leucovorin (folinic acid) or thymidine. Folinic acid is the naturally occurring version of folic acid (synthetic). Both of these decrease side effects

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47
Q

Does giving folate or folinic acid decrease the efficacy of methotrexate?

A

No!

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48
Q

At what cumulative doses of methotrexate is there concern for hepatic fibrosis and how is this assessed?

A

> 1.5-5g of methotrexate, especially with preexisting live dz like HCV, psoriasis, EtOH abuse, or those not getting folate (reduces the risk of LFT abnormalities by 76%).

Presence of cirrhosis is tested w/ liver biopsy for now

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49
Q

Absolute contraindications of methotrexate?

A

Pregnancy and lactation

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50
Q

What are the idiosyncratic adverse reactions of methotrexate?

A

Acute pneumonitis (rare), methotrexate must be stopped early or can be life-threatening

Pancytopenia: usually occurs early (4-6 months), and may be idiosyncratic

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51
Q

What are the risk factors for pancytopenia in methotrexate tx and when does pancytopenia occur?

A

Usually occurs early (4-6 weeks), old age, poor renal function and lack of oflic acid supplementation are risk factors

52
Q

Why should Bactrim be avoided in patients on methotrexate?

A

3 main issues with the Bactrim MTX combination: 1. Both inhibit dihydrofolate reductase, so folate metabolism goes way down and increases the risk of myelosuppression. 2. Both drugs can cause nephrotoxicity and this impairment can lead to elevated levels of either or both drugs. 3. Competitive protein binding, usually MTX is highly bound to albumin, Bactrim displaces this and increases the serum levels of free MTX (increases levels by 30% and decreases excretion.

  • For dermatology, the myelosuppression is likely more likely (kidney toxicity is with higher doses, and less common)
53
Q

Most common side effects of methotrexate?

A

GI side effects common, include nausea, anorexia (both of these more common than diarrhea), vomiting, and ulcerative stomatitis

*Other side effects include alopecia, HA, fatigue, dizziness, accelerate d nodule development in patients with RA (usually on the fingers, smaller than normal RA nodules), and phototoxicity (including UV and radiation recall reactions

54
Q

What agents can increase the risk of myelosuppression when given with methotrexate?

A

Agents that also inhibit folic acid metabolism: trimethoprim, sulfonamides, and dapsone

Agents that displace methotrexate plasma proteins leading to increased levels: tetracyclines, phenytoin, phenothiazines, sulfonamides, NSAIDs, salicylates

55
Q

What agents can increase the risk of myelosuppression when given with methotrexate?

A

Agents that also inhibit folic acid metabolism: trimethoprim, sulfonamides, and dapsone

Agents that displace methotrexate plasma proteins leading to increased levels: tetracyclines, phenytoin, phenothiazines, sulfonamides, NSAIDs, salicylates

56
Q

What baseline and monitoring labs are needed for methotrexate?

A

CBC w/ diff, CMP, viral hep panel, then repeat these weekly for the first month (except the viral panel), and then gradually decrease the frequency to every 3-4 months (q 2weeks for 2 months, q month for 2 months, q 3 months after

57
Q

What should be given if significant myelosuppression is seen?

A

Leucovorin rescue

58
Q

In what population can injectable methotrexate be considered?

A

Pediatric population, they may have reduced oral absorption of methotrexate or the underlying diseases may alter this as well

59
Q

What is UV and radiation recall?

A

Methotrexate causes toxic cutaneous reactions to reappear on previously affected skin

60
Q

What is the mechanism of hydroxyurea?

A

Impairs DNA synthesis through inhibititor of ribonucleotide diphosphate reductase; hypomethylates DNA and results in altered gene expression

61
Q

What is hydroxyurea used for within dermatology?

A

severe recalcitrant psoriasis, Sweet’s syndrome, erythromelalgia, and hypereosinophilic syndrome

62
Q

Mechanism of action for IVIG?

A

Decreased antibody production, complement activation, neturalization of pathogenic antibodies and bacterial superantigens, binds immune receptors and leads to immunomodulation, decreases TNF-alpha and other proinflammatory cytokines, antioxidant, blocks Fc receptors, decreases T-cell activation through various pathways, increases regulatory T-cells and contains anti-Fas receptor antibodies which decreases keratinocyte apoptosis, and decreases migration fo immune cells to target tissues.

63
Q

Dermatologic uses for IVIG?

A

autoimmune blistering disorders, dermatomyositis, SJS/TEN, Kawasaki disease, SLE, chronic autoimmune urticaria, scleroderma, and livedoid vasculopathy

64
Q

What are the side effects of IVIG?

A

Must screen for IgA levels, deficiency can lead to anaphylaxis w/ IVIG

  • Infusion-related adverse effects include headache, myalgia, flushing, fever, wheezing, and pretreatment w/ antihistamines/NSAIDS/corticosteroid can help, fluid overload can occur in cardiac and renal failure patients, aseptic meningitis, thromboembolic events, and dyshidrotic hand eczema
65
Q

What conditions can increase the risk of renal failure w/ tx of IVIG?

A

Elevated rheumatoid factor and cryoglobulins

66
Q

What is the mechanism of action for antimalarial medications (hydroxychloroquine, chloroquine, quinacrine)?

A

Several mechanisms:

  • Inhibits UV-induced cutaneous reactions by binding to DNA and inhibiting superoxide production
  • Raise intracytoplasmic pH and stabilize microsomal membrane which leads to decreased ability of macrophages to express MHC complex antigens on cell surface
  • Reduce lysosomal size and impair chemotaxis
  • Impair platelet aggregation and adhesion
67
Q

How long does it take for the antimalarial to reach a steady-state in the blood?

A

3-4 months, important to remember when looking at the clinical effect

68
Q

Absolute contraindications for antimalarials?

A

Hypersensitivity to the drug (can have cross-reactivity between chloroquine and hydroxychloroquine), continued use is contraindicated for patients who get retinopathy

69
Q

Relative contraindications for antimalarials?

A

Severe blood dyscrasias, significant hepatic dysfunction, significant neurologic disorders, retinal or visual field defects/changes, pregnancy, and lactation (in SLE benefits might outweigh risks to the fetus of stopping) and psoriasis

70
Q

What neurologic disease is a contraindication for chloroquine?

A

Myasthenia gravis

71
Q

What mucocutaneous side effects can the anti-malarials cause?

A

Yellow pigmentation of the skin (quinacrine), drug-induced LP, morbilliform hypersensitivity eruption (risk higher in certain types of Dermatomyositis), psoriasis exacerbation (chloroquine in particular)

Bluish-gray to black hyperpigmentation in 10-30% of pts treated more than 4 months. Usually affects the shins and is indistinguishable clinically from minocycline induced hyperpigmentation. Can also occur on the face and palate

  • Nail hyperpigmentation
72
Q

What occular toxicities can be seen in the antimalarials?

A

Corneal deposits (keratopathy), neuromuscular eye toxicity (ciliary body dysfunction), retinopathy (maculopathy)

  • All except maculopathy are reversible w/ stopping med
73
Q

What are the eye monitoring requirements for the antimalarials?

A

Baseline exam w/ visual field testing

  • Dilated exam and visual acuity testing within the first year of starting therapy
  • Dilated exam and visual acuity testing yearly after 5 yrs of treatment
74
Q

What side effects are seen in the antimalarials?

A

GI side effects are the most common and the most common reason for stopping (chloroquine > hydroxychloroquine). restlessness, excitement, confusion, and seizures (usually high dose). Rare but can be severe bone marrow toxicity w/ quinacrine and agranulocytosis w/ chloroquine

75
Q

Screening tests for antimalarials?

A

G6PD not necessary for hydroxychloroquine and chloroquine or quinacrine.

  • baseline ocular exam, CBC w/ diff, CMP, LFT’s periodically
76
Q

Can the use of antimalarials delay the onset of SLE if a patient has cutaneous/limited lupus erythematosus?

A

Yes

77
Q

If you need more clinical effect and the patient is maxed out on hydroxychloroquine or chloroquine what can be added?

A

Quinacrine

78
Q

What is the mechanism of action for dapsone?

A

Inhibits myeloperoxidase

  • This leads to decreased oxidative damage to normal tissue in various neutrophilic dermatoses (affects eos and monos to a lesser extent).
  • Decreases hydrogen peroxide and hydroxyl radical levels
  • Can potentially also decreases chemotaxis of neutrophils (not shown in therapeutic dosing regimens
79
Q

What part of the dapsone is responsible for the hemolytic effect that can be seen?

A

The methylated metabolite (hydroxylamine metabolite DDS-NOH

80
Q

How long does a single dose of dapsone stay in the system?

A

30 days

There is significant enterohepatic recirculation leading to long half-life

81
Q

Dermatologic uses for dapsone?

A

FDA approved: dermatitis herpetiformis and leprosy

Off-label: LABD, bullous SLE, erythema elevatum diutinum, PG, sweets, neutrophilic urticaria, subcorneal pustular dermatosis/IgA pemphigus, and Behcets syndrome, vasculitides

82
Q

Is cross-reactivity between dapsone and other sulfa-drugs like sulfapyridine or sulfonamide-type drugs occur frequently?

A

No, it is very rare

83
Q

What patients should dapsone be used in with great caution/not used?

A

G6PD deficiency, cardiopulmonary dz, liver dz, or renal dz

  • Pts w/ preexisting neuropathy should also be carefully considered as well
84
Q

What is the dosing patter for hemolytic anemia and methemoglobinemia in dapsone use?

A

It happens to all patients to some degree. It is related to oxidate stress from N-hydroxy metabolites

  • It is dose-dependent however
  • Problem because increased methemoglobinemia decreases the oxygen-carrying capacity and may worsen cardiopulmonary dz or hemotologic dz
85
Q

What is the most severe idiosyncratic reaction to dapsone?

A

Agranulocytosis

86
Q

When is the agranulocytosis most likely to happen w/ dapsone?

A

Usually, 7 weeks in (3-12 weeks range) and can manifest as fever, pharyngitis, and sepsis

87
Q

Side effects w/ dapsone?

A

Peripheral neuropathy (mostly distal motor and some sensory) can occur, look for wasting of the muscles on the hands as it can be reversed if stopped early)

  • Nausea, gastritis, reversible cholestasis and hepatitis, and hypersensitivity syndrome
88
Q

What monitoring should be performed for dapsone?

A

Baseline: G6PD (lower doses if levels are low), CBC w/ diff, LFTs, renal function and UA

Monitoring: Weekly CBC’s for the first 4 weeks and every two weeks thereafter for 3 months to look for agranulocytosis

After 3 months, renal fxn, LFT’s, and UA every 3-4 months

check methemoglobin if there is clinical suspicion of decreased O2 circulation or anemia

89
Q

What can be given to decrease the risk of methemoglobinemia w/ dapsone?

A

Cimetidine and maybe Vitamin E

90
Q

What should be used in a methemoglobinemia emergency?

A

Methylene blue

91
Q

What can be used in the worsening of methemoglobinemia seen after surgery or during surgery after both local amide and general anesthetic is given?

A

Vitamin C

92
Q

How quickly do patients with DH respond to dapsone?

A

Very quickly usually within 24-36 hours. Bullous lupus patients also respond quickly whereas EBA patients do not

93
Q

What is the mechanism of etanercept?

A

It is a soluble fully human dimeric fusion protein (TNF receptor linked to Fc portion of IgG)

  • Binds to TNF-alpha and TNF-beta
94
Q

How is etanercept given?

A

Subcutaneously

95
Q

What type of antibody is infliximab?

A

Chimeric monoclonal IgG antibody binding TNF-alpha only targets soluble and transmembrane TNF-receptor

96
Q

How is infliximab given?

A

IV

97
Q

What type of antibody is Adalimumab?

A

Fully human monoclonal IgG antibody against transmembrane TNF receptor

98
Q

How is adalimumab given?

A

Subcutaneous injection

99
Q

What TNF-alpha inhibitors have the most injection site reactions?

A

Etanercept (14%)>adalimumab (3.2%)

100
Q

When are injection site reactions often the worst in those receiving etancerpt?

A

Usually the most pronounced during the 2nd injection (delayed-type hypersensitivity?)

101
Q

What do the infusion reactions of infliximab look like?

A

Nausea, headache, flushing, dyspnea, injection site infiltration and taste perversion

slowing the infusion rate, and premedication can help wiht this.

102
Q

If you see the efficacy of infliximab waning or stop what could be one source of the issue?

A

Can have infliximab-associated-antidrug antibodies. This increases infusion reactions and decreases efficacy.

103
Q

A family history of what disease would make you more cautious in giving TNF-alpha inhibitors?

A

A family history of demyelinating disease should make you give caution. Cases of patients on these medications getting these.

104
Q

Increased risks of what conditions may be seen with TNF-alpha inhibitors?

A

Malignancy: lymphoma and maybe skin cancer, also hepatosplenic T-cell lymphoma if given azathioprine at the same time

Increased risk for reactivation of tuberculosis or primary infection, invasive fungal disease, opportunistic infections like legionella and listeria

105
Q

What about TNF-alpha inhibitors in congestive heart failure?

A

There is mixed evidence, may increase the risk of developing or exacerbating CHF. Should be used w/ caution (especially infliximab)

106
Q

Baseline and monitoring labs for TNF-alpha inhibitors?

A

Screen for tuberculosis, viral hepatitis panel at baseline

CBC w/ diff and LFT’s q 3 months w/ infliximab and q 12 months for others given risk of rare hematologic toxicity and liver failure/autoimmune hepatitis

107
Q

Can TNF-alpha inhibitors be used in hepatitis C + individuals?

A

Yes, it can be used w/ active hepatitis C infection, caution is advised w/ HBV however because there have been reports of reactivation.

108
Q

What is the target of ustekinumab (Stelara)?

A

IgG1 antibody against P40 subunit of both IL-12 and IL-23

109
Q

What are the most common SE for ustekinumab?

A

URI most common, increased risk of some infections including TB, fungal dz, and viral illnesses

110
Q

What is the mechanims of rituximab?

A

Chimeric IgG targeting CD20–> Depletes B-cells within 2-3 weeks of initial treatment, with sustained depletion for 6 months.

111
Q

How long after Rituximab does it take for B-cells to return to normal?

A

1 year

112
Q

What are the main relative contraindications for rituximab?

A

History of bronchospasm, hypotension, or angioedema

113
Q

What are the common side effects of Rituximab?

A

Hypertension, nausea, upper respiratory tract infections, arthralgia, pyrexia, pruritus.

Most common are infusion reactions = generally, mind and more often occurs with the first infusion. Patients with cardiac or pulmonary conditions are more likely to have severe reactions.

  • Serious SE’s include: HBV reactivation, progressive multifocal leukoenceaphloapty, SJS/TEN, serious infection, hepatic failure and myelosuppression
114
Q

What are the IL-1 inhibitors?

A

Canakinumab, Anakinra, Rilonacept, and Gevokizumab

115
Q

What are some off-labe uses of IL-1 inhibitors in dermatology?

A

PG, PAPA syndrome, HS, lamellar ichthyosis, Sweet’s syndrome, panniculitis, Muckle-Wells syndrome, and other autoinflammatory syndromes and SAPHO syndrome

116
Q

What are the most common S/E of the IL-1 inhibitors?

A

Injection site reactions; important to monitor absolute neutrophil count as neutropenia can occur

117
Q

What are the 3 main IL-17 inhibitors and what are their targets?

A

Ixekizumab (Talz) and Secukinumab (Cosentyx): Neutralize IL-17A

Brodalumab (Siliq): neutralizes IL-17 receptor

118
Q

What are the most commonly reported SE in the IL-17 inhibitors?

A

Most common: Nasopharyngitis

Other common S/e: URI, injection site reactions, HA, Candidiasis and HSV infections

119
Q

What is the efficacy of the IL-17 inhibitors as compared to the IL-12/23 inhibitor ustekinumab and TNF inhibitor etanercept?

A

IL-17 inhibitors are more effective than both of these mediations.

120
Q

What is one important effect of IL-17 inhibitors in regards to speed of clearance?

A

They are faster than the other psoriasis medications

121
Q

Which class of psoriasis biologics should be used in caution with inflammatory bowel disease?

A

IL-17 inhibitors, there are reports of worsening IBD with these and IL-17 is important in maintaining the gut lining

122
Q

What is the mechanism of action for omalizumab?

A

Monoclonal antibody against IgE antibody

123
Q

Side effects of omalizumab?

A

Anaphylaxis, malignancy, and injection site reaction

124
Q
A
125
Q

What are some symptoms of methemoglobinemia from dapsone?

A

Tachypnea, low oxygen saturation (usually in the high 80’s), and a bluish hue to the skin

126
Q

What are the treatments for dapsone-induced methemoglobinemia?

A

Mild cases can consider cimetidine

Moderate to severe cases will need methylene blue

127
Q

What immunomodulator is known to cause gastrointestinal bleeding?

A

Mycophenolate mofetil

Most occurs w/ solid organ transplant dosing (3+ grams), however, can occur in blistering disorders

DERM (12) Medical Therapy (7 decks)

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