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PA School Pharm

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Glatiramer acetate is a SQ injection used in the management of MS. Its ADRs include post injection rxn ({{c1::SOB}}, palpitations, flushing, anxiety, {{c1::angina::cardiac}}), injection site rxns, and hypersensitivity.
Natalizumab Black Box Warning: progressive multifocal {{c1::leukoencephalopathy}}
Natalizumab ADRs include hepatotoxicity, {{c1::meningitis::neuro}}, infusion rxns, and HAMonoclonal ab for MS
Which MS therapy has an ADR of first dose effect of <u>bradyarrhythmias</u>? <br><br>{{c1::Fingolimod}}Occurs 6 hours after 1st dose
ADRs of <u>fingolimod</u> include opportunistic infx, lymphopenia, {{c1::Macular edema::occular}}, HTN, hepatotoxicity, progressive multifocal leukoencephalopathy (rare)therapy in MS 
<u>Dimethyl fumarate</u> is used in the management of MS. Its ADRs include flushing, N/V/D, abdominal pain, lymphopenia, {{c1::progressive multifocal leukoencephalopathy}} (rare)
Humanized monoclonal ab against CD20 (Ocrelizumab & Ofatumumab) is a type of management for MS. Its ADRs include infection, local injection site rxns, HA, and {{c1::URI::respiratory}}.
<u>Alemtuzumab</u> is used in the tx of MS. Its ADRs include immunosuppression, {{c1::thyroid}} CA, melanoma, {{c1::herpes}} viral infx, HA, rash, N, fatigue, arthralgia, {{c1::thrombocytopenic purpura::heme}}, glomerulonephritis, and amenorrhea
What drug in the management of MS has an ADR of thrombocytopenic purpura and amenorrhea? <br><br>{{c1::Alemtuzumab}}
What two MS drugs can be taken PO? <br><br>{{c1::Fingolimod + Dimethyl fumarate}}
Hydroxychloroquine is first line in the tx of SLE. One unique ADR is {{c1::ophthalmic toxicity}}.
What SLE drug has ADRs of nasopharyngitis, URI, bronchitis, and cough? <br><br>{{c1::Anifrolumab-fnia}}
<u>Efgartigimod alfa-feab</u> is a drug used to manage MG. Its ADRs include {{c1::respiratory tract}} infx, HA, UTI, myalgia, {{c1::parasthesia::neuro}}.
ADRs to 6-MP include hepatoxicity, {{c1::bone marrow}} toxicity, N/V, stomatitis, pregnancy cat. {{c1::D}}, and {{c1::allopurinol}} interaction.
What immunosuppressive therapy for transplants has ADRs of pancreatitis and gastritis? <br><br>{{c1::Azathioprine}}
Like 6-MP, azathioprine is another immunosuppressive therapy that has a drug interaction with {{c1::allopurinol}}Allopurinol significantly decreases the metabolism of azathioprine
Which immunosuppressive therapy for transplants can have an ADR (rare) of pulmonary fibrosis? <br><br>{{c1::Mycophenolate mofetil}}
Cyclosporine is an immunosuppressive drug used for transplants. It has many ADRs. Some unique ones are {{c1::nephrotoxicity::major concern}}, {{c1::CNS}} toxicity, {{c1::gingival}} hyperplasia, and {{c1::hirsutism::endocrine}}.
Tacrolimus is an immunosuppressive agent used in transplants. Its ADRs include nephrotoxicity, neurotoxicity, and {{c1::IDDM}}IDDM = insulin dependent diabetes mellitus, aka T1DM
One advantage to sirolimus and everolimus in immunosuppressive tx for transplants is that they have low {{c1::nephrotoxicity}} potential
Which two immunosuppressive agents for transplant therapy have ADRs of hyperlipidemia and hypertriglyceridemia? <br><br>{{c1::Sirolimus & Everolimus}}
ADRs to bortezomib include {{c1::neuropathy}} & {{c1::thrombocytopenia}}Proteasome inhibitor
What immunosuppressive agent cannot be used for both women and men trying to conceive? <br><br>{{c1::Leflunomide, Teriflunomide}}
Infliximab has infusion related ADRs of fever, chills, hives, hypotension, {{c1::CP}}
What immunosuppressive therapy has ADR of thyroid d/o in around 16% of patients? <br><br>{{c1::Alemtuzumab}}Same therapy for MS, but in the context of other immune ds
Which immunosuppressive agent can have an ADR of ITP? <br><br>{{c1::Alemtuzumab}}
Omalizumab is an immunosuppressive agent w/ relatively few ADRs. They are pain and inflammation rxn at site of injection & risk of {{c1::infx}}. 
Dupilumab ADRs include injection site rxn, {{c1::conjunctivitis::occular}}, and {{c1::oral herpes}} reactivation
All {{c1::JAK inhibitors}} have a black box warning for serious infections, mortality, malignancy, CV events, and thrombosis
Acitretin is a retinoid used in the tx of psoriasis. Its ADRs include {{c1::alopecia}}, xerosis, photosensitivity, {{c1::hyper}}cholesterolemia, {{c1::depression::psych}}, HA, joint pain, and elevated liver enzymes.
What tx for psoriasis has a black box warning: avoid in pregnancy, breastfeeding or wishing to become pregnant; must use two forms of birth control for one month prior to tx initiation and THREE years after stopping therapy? <br><br>{{c1::Acitretin}}
Ustekinumab is a drug used in the tx of psoriasis. It has a newly reported risk of severe {{c1::cardiovascular}} events early in therapy.More commonly seen in patients tx for psoriasis than Crohn's ds
Second-line biologics for psoriasis include <u>IL-17A blockers</u> (Secukinumab, Ixekizumab, Brodalumab) & <u>IL-23 inhibitors</u> (Guselkumab, Tildrakizumab, Risankizumab). ADRs include infx such as URIs, {{c1::candida}}, herpes, staph skin infx, and {{c1::Crohn's}} disease flare.
What biologic for psoriasis has an ADR for suicide warning and is considered a REMS drug? <br><br>{{c1::Brodalumab}}
Which drug for psoriasis has an ADR of CYP450 pathway drug interactions (phenytoin, and rifampin)? <br><br>{{c1::Apremilast}}PDE4 inhibitor
ADRs to apremilast include N/D, depression, and {{c1::weight loss}}
ADRs to using IFNs for immunotherapy include {{c1::chills}}, {{c1::fever}}, {{c1::myalgia}}
Which immune activating drug has ADRs of blisters, bloody dry eschar, and pain of treated area? <br><br>{{c1::Imiquimod}}
Main ADRs to exogenous immune globulin? <br><br>Transmisison of {{c1::infectious}} ds<br>{{c1::Aseptic meningitis}}<br>{{c1::Hemolysis}} <br>{{c1::Thrombosis}}<br>Injection site rxnsNote that thrombosis is the black box warning
ADRs to caplacizumab? <br><br>{{c1::Bleeding}}
ADRs to colony stimulating factors? <br><br>{{c1::Fever}}, chills, {{c1::GI}} distress, {{c1::muscle}} & {{c1::bone}} pain
<u>IL-2</u> is used in {{c1::kidney}} CA and {{c1::melanoma}} tx
Which IFN attracts & stimulates NK cells? <br><br>{{c1::Alpha}}
Which IFN is secreted by fibrocytes & slows inflammation? <br><br>{{c1::Beta}}
Which IFN is secreted by T cells & NK cells and stimulates <u>macrophage activity</u>? <br><br>{{c1::Gamma}}
Which IFN is used in managing severe malignant osteopetrosis? <br><br>{{c1::IFN-gamma}}
Which IFN is used in management of idiopathic pulmonary fibrosis? <br><br>{{c1::IFN-gamma}}
What types of tissue are used for autografting? <br><br>{{c1::Skin, hair, blood vessels::3}}
Tissue transplantation b/w genetically identical individuals<br><br>{{c1::Isograft}}
Transplantation b/w individuals of the same species who are not genetically identical<br><br>{{c1::Homograft}}
Tissue transplant b/w different species<br><br>{{c1::Xenograft}}Avascular structures have some success (e.g. cornea, heart valves)
Occurs in the OR as the new organ is connected<br><br>{{c1::Hyper-acute organ}} rejectionPreformed ab in the recipient react w/ donor antigens
Occurs w/in a few weeks of organ transplantation due to immune vasculitis<br><br>{{c1::Acute organ}} rejection
Most common form of organ rejection? <br><br>{{c1::Acute-organ}} rejection
Rejection that develops over a period of months to years due to immune vasculitis that slowly starves the donated organ<br><br>{{c1::Chronic transplant}} rejection
Is T-cell or antibody (B-cell)-mediated (TCMR/AMR) rejection more difficult to treat? <br><br>{{c1::AMR}}B-cell mediated rejection
"<div>Develops as
a result of the transfer of donor immunocompetent lymphocytes </div><div><br></div><div>{{c1::Graft vs. Host Reaction}}</div>"
What type of hypersensivity reaction occurs in Graft vs. Host ds? <br><br>{{c1::Type IV immune reaction (T-cell)}}
S/S of Graft vs. Host rxn include {{c1::severe dermatitis}}, diarrhea, fever, and jaundice"Difficult to tx; high mortality<br><img src=""paste-6d27e45a15a7dba78c06ca3d8be6029a5ff00990.jpg"">"
What is the principle approach to immunosuppressive therapy? <br><br>{{c1::Alter lymphocyte function}}
Potency of a glucocorticoid is based on what property? <br><br>{{c1::Vasoconstriction}}The more vasoconstricting the more potent
There are 5 MOAs of glucocorticoids: <br><br>1. Cause {{c1::lymphocytes}} in the blood to be re-distributed into the bone marrow (results in leukopenia to decrease immune response)<br>2. {{c1::Decrease}} the amount of lymphoid tissue and cells in the lymph nodes and spleen<br>3. Decrease capillary {{c1::dilation}} and vascular {{c1::permability}}<br>4. Decrease activity of {{c1::macrophages}}, {{c1::T-cells}}, and {{c1::B-cells}}<br>5. {{c1::Inhibit}} the synthesis of cell-derived inflammatory mediators (e.g. prostaglandins, leukotrienes, thromboxanes)
Can glucocorticoids cause tendon rupture? <br><br>{{c1::Yes}}
Glucocorticoids can cause increased {{c1::appetite}} and weight {{c1::gain}}
{{c1::Endocrine}} ADRs of <u>glucocorticoids</u> are seen more with long term useAmenorrhea, growth suppression in children, new onset DM
Can glucocorticoids cause exophthalmos? <br><br>{{c1::Yes}}Can also lead to cataracts and increase IO glaucoma
Glucocorticoids can alter sperm {{c1::motility}} and {{c1::number}}
Glucocorticoids can cause increased ICP w/ {{c1::papilledema}}
Cushing syndrome is an ADR to {{c1::chronic}} use of glucocorticoids
What is the first thing that a provider should ask a patient before Rx glucocorticoids? <br><br>{{c1::Are you a diabetic?}}Glucocorticoids (any dose) will increase blood glucose levels
"<div>Even
short courses ≤1 week of steroids will increase risk of {{c1::fractures}}, {{c1::venous
thromoboembolism}}, and
{{c1::sepsis}} for 3 months</div>"
Do not use short term steroids for {{c1::sinusitis}}, {{c1::bronchitis}}, {{c1::sore throat}}, or {{c1::CAP}}Low benefit for the risk
For what <u>three conditions</u> are short term oral steroids indicated? <br><br>{{c1::Asthma & COPD exacerbations, acute gout flare}}Benefit is worth the risk
Most potent topical corticosteroids are class {{c1::I}} while least potent are class {{c1::VII}}
Can vaccines be given to patients receiving topical corticosteroids? <br><br>{{c1::Yes}}
Limit application of class I topical corticosteroids to {{c1::50 grams}} per week to minimize the risk of systemic effects
<b><i>Acute</i></b> exacerbations of <u>multiple sclerosis (MS)</u> are managed with {{c1::systemic steroids}}KNOW THIS
Disease modifying treatment (DMT) agents have the greatest impact on what subtype of MS? <br><br>{{c1::Relapsing-remitting MS}}
DMT agents are for {{c1::maintenance}} of MS sx
{{c1::Pegylated}} therapies add proteins to solution to make it heavy and have a slower absorptionThis is beneficial for pt as this means they do not have to be injected as often
What <i>three</i> MS therapies are classified as <u>higher effectiveness for initial treatment</u>? <br><br>{{c1::IV natalizumab, IV ocrelizumab, and SQ ofatumumab}}
What <i>two</i> MS therapies are classified as <u>intermediate effectiveness for initial treatment</u>? <br><br>{{c1::Oral dimethyl fumarate and oral fingolimod}}These are really good, middle of the road options. These would also be beneficial for patients who do not want / are opposed to injections.
What <i>two</i> MS therapies are classified as <u>lower effectiveness for initial treatment</u>? <br><br>{{c1::IM/SQ interferon beta 1a and SQ glatiramer acetate}}
"<div>A
synthetic protein that stimulates <u>myelin production</u> while blocking T cell activity against myelin sheaths </div><div><br></div><div>{{c1::Glatiramer acetate}}</div>"
"<div>A
humanized monoclonal antibody against the cellular adhesion molecule
<u>α4-integrin</u></div><div><br></div><div>{{c1::Natalizumab}}</div>""<div>Reduces the ability of inflammatory immune cells to attach to and pass through the cell
layers lining the intestines and blood–brain barrier</div>"
Natalizumab is used in the tx of MS and Crohn's ds that are not responding to {{c1::TNFi}}
"<div>A
sphingosine 1-phosphate receptor agonist </div><div><br></div><div>{{c1::Fingolimod}}</div>""Sphingosine 1-phosphate is a signaling G-protein for T & B cells<br><br><div>Keeps
lymphocytes in lymph tissue, preventing lymphocyte migration to sites of
inflammation</div>
<div>The
agonism of S1P directly causes its <u>internalization and degradation</u> through the ubiquitin-proteosome
pathway. The
loss of S1P leads to a decrease in the total lymphocyte count in circulation,
specifically CD4+ and CD8+ T cells.</div>"
<u>Siponimod</u> is approved for both {{c1::secondary progressive}} MS and {{c1::relapsing-remitting}} MSSphingosine-1-phosphate receptor agonist
<u>Ozanimod</u> is approved for {{c1::secondary progressive}} MS, {{c1::relapsing-remitting}} MS, and ulcerative colitisSphingosine-1-phosphate receptor agonist
"<div>Activates nuclear
factor (erythroid-derived 2)-like 2, also known as NFE2L2 </div><div><br></div><div>{{c1::Dimethyl fumarate}}</div>""<div>Transcription factor protein that regulates the expression of antioxidant
proteins (good) that protect against oxidative damage (bad) triggered by injury
and inflammation  </div>"
<u>Diroximel fumarate</u> and <u>monomethyl fumarate</u> are both approved for both {{c1::secondary progressive}} and {{c1::relapsing-remitting}} MS
Humanized monoclonal antibody against CD20<br><br>{{c1::Ocrelizumab & Ofatumumab::2}}Decrease lymphocyte population
Only MS therapy that is FDA-approved for <u>primary progressive</u> MS<br><br>{{c1::Ocrelizumab}}IV infusion Q6months
"<div>A
monoclonal antibody that binds to CD52 receptors on the surface of mature
lymphocytes</div><div><br></div><div>{{c1::Alemtuzumab}}</div>""<div>After
treatment, these CD52-bearing lymphocytes are targeted for destruction</div>"
While alemtuzumab is indicated for MS therapy, it is also used in the tx of {{c1::CLL}}, {{c1::cutaneous T-cell lymphoma}}, and {{c1::bone marrow transplant}}IV infusion QD for 5 days and then a year later, one infusion QD for 3 days<br><br>To help avoid infusion rxn, corticosteroid premedication may be given for the first 3 days of therapy
"Known as ""HIV in a vial"" <br><br>{{c1::Alemtuzumab}}"
First line tx for SLE? <br><br>{{c1::Hydroxychloroquine}}
"<div>B-cell
activating factor inhibitor (a type of TNF inhibitor) that prohibits B cell activation to prevent B cell conversion to plasma cells --> prevents ab formation </div><div><br></div><div>{{c1::Belimumab}}</div>"Indicated in the management of SLE<br><br>This is great for preventing those ab-ag complexes that form in SLE
<u>Type 1 interferon receptor antagonist</u> monoclonal ab that inhibits signaling activity of lymphocytes<br><br>{{c1::Anifrolumab-fnia}}Approved for moderate to severe SLE<br><br>IV infusion
Mainstay tx for myasthenia gravis (MG)? <br><br>{{c1::Physostigmine}}This is AChE inhibitor --> allows more ACh to stay in synapse
{{c1::IVIG}} can be used in rescue or bridge therapy for MG
{{c1::Thymectomy::surgical procedure}} can be performed to tx MG
<u>Fc receptor blocker</u> approved for tx of generalized MG in adults who are anti-acetylcholine receptor antibody positive<br><br>{{c1::Efgartigimod alfa-feab}}Binds to Fc receptor reducing circulating IgG; blocking Fc portion of ab prevents ab from fitting to receptor on motor end plate<br><br>IV infusion
{{c1::Post}}-transplant steps are done in every patient, while {{c1::pre}}-transplant steps are done in only certain patients
"Maintenance protocol for post-transplant: {{c1::2-3::#}} immune modulating drugs utilizing the lowest dose possible for life"
Polymorphisms in these <i>three</i> drugs alter metabolism affecting bioavailability <br><br>{{c1::Tacrolimus, cyclosporine, and mycophenolate}}
{{c1::6-MP}} is an antimetabolite that interferes w/ lymphocyte production. It is orally administered for maintenance therapy in transplant therapy.Purine antagonist
6-MP is an <u>antimetabolite</u> used in the tx of {{c1::ALL}} and {{c1::Crohn's ds}}
6-MP has an <u>allopurinol interaction</u>: reduce 6-MP {{c1::1/3}} or {{c1::1/4}} of the usual dose to avoid severe toxicity
{{c1::Azathioprine}} is an <u>antimetabolite</u> that is rapidly converted to 6-MP in vivo
<b>Azathioprine</b> is an <u>antimetabolite</u> that is inactivated by {{c1::thiomethyltransferase}} enzymes"<div>Patients
with a TMPT *2, *3A, or *3C gene mutation will have <i><u><b>decreased metabolic
activity</b></u></i> resulting in increased drug concentrations – ADRs</div><div><br></div><div>This is an area of pharmacogenomics</div>"
<b>Azathioprine</b> is an <u>antimetabolite</u> used in organ transplantation to prevent {{c1::rejection}}Largely replaced by mycophenolate mofetil
Azathioprine has an <u>allopurinol interaction</u>: reduce azathioprine dose by {{c1::60-75%}}
Azathioprine can be used in the tx of autoimmune ds such as Crohn's disease, MG, {{c1::pemphigus::derm}}, and RA
Mycophenolate mofetil is an antimetabolite primarily used in {{c1::transplant rejection}} protocolsHeart, kidney, liver
{{c1::Mycophenolate mofetil::antimetabolite}} may be used in recalcitrant autoimmune diseasesMeaning MMF is last-line therapy for autoimmune ds
Is MMF or azathioprine better for transplant rejection protocols? <br><br>{{c1::MMF}}Mycophenolate mofetil
MMF is primarily {{c1::renally}} eliminated
<b>MMF</b> has <i>decreased</i> absorption when administered with {{c1::antacids}} (Mg, Al) or {{c1::cholestyramine}}Mycophenolate mofetil
"<img src=""paste-8604aff9340dc080a2514d855c0f8b03e18cd91f.jpg""><br>What is being shown can be caused by administration of MMF in some patients. <br><br>{{c1::Pulmonary fibrosis}}"Mycophenolate mofetil
Potent immunosuppressive that is a derivative of <i>Beauveria nivea</i> (soil fungus)<br><br>{{c1::Cyclosporine}}
Calcineurin inhibitor that prevents synthesis of IL-2<br><br>{{c1::Cyclosporine & Tacrolimus}}IL-2 is stimulator for T cell proliferation
Cyclosporine is used to prevent {{c1::organ rejection}} post transplant Kidney, liver, cardiac
Cyclosporine is most effective for preventing organ rejection post transplant when combined with {{c1::corticosteroids}} and {{c1::MMF (or another antimetabolite)}}Mycophenolate mofetil
Can cyclosporine be used in the tx of autoimmune ds? <br><br>{{c1::Yes}}SLE, RA, psoriasis
TDM for cyclosporine? <br><br>{{c1::Trough only}}
Cyclosporine is a CYP{{c1::3A4}} substrate
Major concern w/ cyclosporine use? <br><br>{{c1::Nephrotoxicity}}
If patients are going to use a calcineurin inhibitor for transplants, which one are the more likely to use? <br><br>{{c1::Tacrolimus::Cyclosporine/Tacrolimus}}*Tacrolimus is preferred over cyclosporine due to greater potency, efficacy, and lower corticosteroid dose needed*
{{c1::Tacrolimus}} is derived from <i>Streptomyces sp.</i> soil species
Tacrolimus is used in {{c1::transplant rejection}} prevention via oral administrationLiver, kidney
Tacrolimus can be used topically in the management of {{c1::eczema}} and {{c1::vitiligo}}
<b>Tacrolimus</b> is highly {{c1::protein}} bound and primarily eliminated in {{c1::feces}}
Predominant enzymes responsible for the metabolism of tacrolimus? <br><br>CYP{{c1::3A4}} and CYP{{c1::3A5}}Knowledge of the genotypes would be useful in selecting appropriate tacrolimus doses to avoid overexposure
Like cyclosporine, tacrolimus is often used in combination with {{c1::corticosteroids}} and an {{c1::antimetabolite}} for organ rejection prevention
Prevents activation of T cells and B cells by inhibiting their response to IL-2<br><br>{{c1::Sirolimus and Everolimus::2}}Slightly different mechanism than the calcineurin inhibitors (cyclosporine and tacrolimus)
{{c1::Everolimus}} is a derivative of sirolimus with a higher bioavailability and lower plasma protein binding
A <u>high fat meal</u> with administration of {{c1::everolimus}} may decrease abosorption by 60%I believe high fat meal with sirolimus would also not be good
Sirolimus and everolimus are orally administered and are for the prevention of {{c1::transplant rejection}}
Used in coronary stent coating to prevent restenosis<br><br>{{c1::Sirolimus, Everolimus}}
Advantage to sirolimus/everolimus? <br><br>{{c1::Low nephrotoxicity potential}}
{{c1::Bortezomib}} is a <u>proteasome inhibitor</u> that reversibly binds the chymotrypsin-like subunit of the 26S proteasome, resulting in its inhibition and prevents the degradation of various pro-apoptotic factors
Bortezomib is a proteasome inhibitor that induces plasma cell {{c1::apoptosis}} and blocks {{c1::anti-HLA}} antibody production
Proteasome inhibitor approved for the tx of multiple myeloma<br><br>{{c1::Bortezomib}}Off-label use in antibody-mediated rejection
Pyrimidine synthesis inhibitor that has a very long half-life <br><br>{{c1::Leflunomide}}
"<div>Monoclonal
antibody that binds to and inhibits the activity of TNF; Used in the management of Crohn's disease, ulcerative colitis, and RA</div><div><br></div><div>{{c1::Infliximab}}</div>"
For organ transplant rejection prevention in <u>corticosteroid-avoidance protocols</u> and antibody-mediated rejection tx<br><br>{{c1::Alemtuzumab}}
Monoclonal ab indicated for Graft vs. host disease<br><br>{{c1::Alemtuzumab}}
Recombinant monoclonal ab targeting free and membrane bound IgE<br><br>{{c1::Omalizumab}}Increases threshold for activation of mast cells to undergo degranulation = increased stability
Used in the reduction of the severity and frequency of asthma attacks not controlled by other treatments<br><br>{{c1::Omalizumab}}
Third-line therapy in addition to high dose antihistamine agents for management of chronic idiopathic urticaria<br><br>{{c1::Omalizumab}}
Inhibits IL-4 and IL-13 in the tx of eczema<br><br>{{c1::Dupilumab and Tralokinumab::2}}
{{c1::Dupilumab}} may be used for children 6 months+ with eczema
Dupilumab is also used for {{c1::asthma}} and {{c1::nasal polyps}} – different dosing guidelines
{{c1::Tralokinumab}} is used for moderate to severe <u>eczema</u> in adults
"Intracellular messenger inhibition resulting in suppression of
<u>IL-13, IL-4, and IL-33</u> signaling = decreased lymphocyte activity<br><br>{{c1::JAK inhibitors}}"
JAK inhibitors are administered PO for patients with moderate/servere {{c1::atopic dermatitis}}
MOA unclear, but thought to slow the growth and shedding of skin cells<br><br>{{c1::Acitretin}}
Oral retinoid used in the tx of psoriasis<br><br>{{c1::Acitretin}}Works best when combined with phototherapy<br><br>Can be used with biologics, cyclosporine, or methotexate
First-line biologics for psoriasis – psoriatic arthritis? <br><br>{{c1::TNFi / Ustekinumab}}Etanercept, infliximab, adalimumab, certolizumab
IL-12 & IL-23 inhibitor used in the management of plaque psoriasis, psoriatic arthritis, and Crohn's ds<br><br>{{c1::Ustekinumab}}SQ
Carefully screen patients for underlying <u>cardiac ds risk</u> when Rx {{c1::ustekinumab}}Cardiac ds ADR more commonly seen in patients tx for psoriasis than Crohn's ds
Second-line biologics for psoriasis? <br><br>{{c1::IL-17A or IL-23 blockers}}
IL-17A blockers for plaque psoriasis? <br><br>{{c1::Secukinumab, Ixekizumab, and Brodalumab::3}}
IL-23 inhibitors for psoriasis? <br><br>{{c1::Guselkumab, tildrakizumab, risankizumab::3}}
"PDE4 inhibitor that results
in increased intracellular cAMP, which helps to modulate the balance between
pro-inflammatory and anti-inflammatory mediators<br><br>{{c1::Apremilast}}"
First oral medication approved for tx of psoriatic arthritis? <br><br>{{c1::Apremilast}}
<u>JAK 1 + 3 inhibitor</u> indicated for psoriasis tx<br><br>{{c1::Tofacitinib}}Oral admin
Some biologics increase the risk of {{c1::skin CA}}, so it is important to remind patients to wear sunscreen, get regular skin checks
Induces IFN-alpha, IL, and TNF to increase response of T cells; also activates Langerhans cells of the epidermis<br><br>{{c1::Imiquimod}}
Topically used in the mangement of actinic keratosis, superficial basal carcinoma, HPV genital warts, and molluscum contagiosum<br><br>{{c1::Imiquimod}}
Labeled use in primary immunodeficiency disorders (PIDD) <br><br>{{c1::Exogenous immune globulin}}IgA, IgD, IgM, IgG, IgE
Most uses for exogenous immune globulin are {{c1::off-label}}Accounts for 75% of all IVIG use
Used in the tx of Kawasaki ds<br><br>{{c1::Exogenous Immune Globulin}}
When we give {{c1::exogenous immune globulin}}, it triggers the immune system to shut off endogenous ab productionHelps tx autoimmune ds
Used for tx of Gullian-Barre syndrome, MS, MG, dermatomyositis, autoimmune hemolytic anemia<br><br>{{c1::Exogenous immune globulin}}Can also be used for CMV, and severe sepsis
Tx for Thrombotic Thrombocytopenic Purpura? <br><br>{{c1::Plasma exchange and high dose steroids}}
Inhibits interaction between vWF multimers and platelets, preventing platelet aggregation <br><br>{{c1::Caplacizumab}}Used in the tx of TTP
Stimulate the formation of macrophages, granulocytes, and/or erythrocytes<br><br>{{c1::CSFs}}
{{c1::CSFs}} are used to speed the recovery of patients with <u>myelosuppression</u> from BM transplant, chemotherapy, renal disease, or anemia
{{c1::Filgrastim}} is a G-CSF 
{{c1::Sargramostim}} is a GM-CSF
{{c1::Epoetin}} is a CSF for erythrocytes
Brand name for methylprednisolone? <br><br>{{c1::Medrol Dosepak}}
Generic name for Medrol Dosepak? <br><br>{{c1::Methylprednisolone}}
Dosing schedule for methylprednisolone? <br><br>{{c1::4mg tabs – taper from 24mg to 4mg over 6 days}}
Prednisone dosing schedule? <br><br>{{c1::5-60mg po 1-4x per day}}Highly dependent on indication
Infliximab brand name? <br><br>{{c1::Remicade}}
Remicade generic name? <br><br>{{c1::Infliximab}}
Infliximab dosing schedule? <br><br>{{c1::5-10mg/kg IV infusion every 8 weeks}}Crohn's ds
Epoetin alpha dosing schedule? <br><br>{{c1::50-100 units/kg IV 3 times weekly initially; target Hgb > 10 g/dL}}
Cyclosporine brand name? <br><br>{{c1::Sandimmune}}
Sandimmune generic name? <br><br>{{c1::Cyclosporine}}
Brand name for triamcinolone? <br><br>{{c1::Kenalog}}
Generic name for kenalog? <br><br>{{c1::Triamcinolone}}
Dosing schedule for triamcinolone? <br><br>{{c1::0.1% apply BID-QID}}Very dependent on indication
Brand name for omalizumab? <br><br>{{c1::Xolair}}Dosing based on pretreatment serum IgE and body weight
Xolair generic name? <br><br>{{c1::Omalizumab}}
Ustekinumab brand name? <br><br>{{c1::Stelara}}For plaque psoriasis
Stelara generic name? <br><br>{{c1::Ustekinumab}}
Ustekinumab is only indicated for patients weighing < {{c1::220}} lbs
Dosing schedule for ustekinumab? <br><br>{{c1::45mg SQ initially, then 4 weeks}}Maintenance 45mg SQ Q 12 weeks
Dupilumab brand name? <br><br>{{c1::Dupixent}}
Dupixent generic name? <br><br>{{c1::Dupilumab}}
Dosing schedule for dupilumab? <br><br>{{c1::300mg SQ QOW}}This is for adults with atopic dermatitis – maintenance
At ANC < {{c1::500}} cells/µL there is severe risk of infection
Antineoplastic drugs can be given in a series of treatments w/ {{c1::drug free}} periods of 1-6 weeks
Used to monitor myelosuppression and risk of infection in pt on antineoplastic therapy<br><br>{{c1::ANC}}ANC = (bands + segs)/100 * (total WBC)
Generally, hold chemotherapy dose if ANC < {{c1::1500}}
Use prophylaxis {{c1::colony-stimulating factors}} if chemotherapy regimen is highly myelosuppressive or patient has history of myelosuppression
Stop using CSFs for chemotherapy regimen of high myelosuppression when ANC > {{c1::4000}}
An inactive period when CA cells are not reproducing; Disappearance of all clinical evidence of active ds for at least 4 weeks<br><br>{{c1::Remission}}
Combo drug therapy is used to prevent the development of {{c1::resistance}} in chemotherapy 
VAD protocol for {{c1::multiple myeloma}}Vincristine, adriamycin (doxorubicin), and dexamethasone
CAF protocol for {{c1::breast}} cancerCyclophosphamide, adriamycin (doxorubicin), and 5-FU
Sole use of chemotherapy agents; used most often for palliation of CA sx<br><br>{{c1::Primary induction chemotherapy}}
"Chemotherapy used
before surgery to reduce tumor size; improving surgical resection<br><br>{{c1::Neoadjuvant chemotherapy}}"
Surgery followed by chemotherapy <br><br>{{c1::Adjuvant chemotherapy}}
"<div>Inhibit cell reproduction by irreversibly binding DNA (CCNS); form
cross-links in DNA that alter the double helix structure</div><div><br></div><div>{{c1::Alkylating agents}}</div>"
Alkylating agents are vesicants – severe skin damage with extravasation. What is the antidote? <br><br>{{c1::Sodium thiosulfate}}"<img src=""paste-d7456b53ee832488ba3556399328b79d3989f6cb.jpg"">"
{{c1::Mechlorethamine::Nitrogen mustard}} is used in Hodgkin's lymphoma regimens
Increased {{c1::fluid}} intake and {{c1::MESNA}} administration can minimize hemorrhagic cystitis ADR of cyclophosphamide/ifosfamideHematuria, cystitis, bladder toxicity, and increased risk of bladder CA
Unique ADR to carmustine is {{c1::pulmonary fibrosis::resp}}Nitrosourea
Heavy metal platinum derivatives are primarily indicated for the tx of {{c1::solid tumors}}Cisplatin, Carboplatin, Oxaliplatin<br><br>All admin IV
What do you want to make sure your patients are doing when they are taking platinum derivatives? <br><br>{{c1::Aggressively hydrating}}There may also be Mg wasting, so replacement may be needed
Procarbazine is a misc. alkylating agent used in both {{c1::non-Hodgkin's}} and {{c1::Hodgkin's lymphoma}}, brain tumors, and melanomaGood penetration into most tissues
{{c1::Dacarbazine}} is a misc. alkylating agent used in Hodgkin's lymphoma regimensSkin rashes, GI distress, myelosuppression, phototoxicity are ADRs
Antimetabolites are {{c1::CCS::CCS/CCNS}} S phase
Intrathecal administration of this medication is used when the meninges are involved and as a prophylaxis in ALL<br><br>{{c1::Methotrexate}}
Toxicity of this medication is treated with <u>leucovorin</u> <br><br>{{c1::Methotrexate}}
Main uses of methotrexate: {{c1::acute leukemia}}, {{c1::lymphoma}}, and {{c1::choriocarcinoma}} (uterine CA)
"<div>Indicated
for treatment of mesothelioma and non-squamous, non-small cell lung cancer </div><div><br></div><div>{{c1::Pemetrexed}}</div>"
MOA of pemetrexed? <br><br>{{c1::Folic acid antagonist – antimetabolite}}Similar MOA to methotrexate
{{c1::Pemetrexed}} is administered IV with <u>folic acid</u> & <u>B12 supplementation</u>
Main ADR to pemetrexed? <br><br>{{c1::Myelosuppression}}
Folinic acid used with high dose methotrexate to prevent/treat folic acid deficiency<br><br>{{c1::Leucovorin}}Readily available form of folic acid
6-MP is an antimetabolite antineoplastic agent used in the tx of {{c1::ALL}}
Two antimetabolites used in the tx of hairy cell leukemia? <br><br>{{c1::Cladribine & Pentostatin}}
Antimetabolite used in the tx of CLL? <br><br>{{c1::Fludarabine}}
Main ADR to fludarabine? <br><br>{{c1::CNS toxicity}}
"<div>Pyrimidine antagonist used
for treatment of solid tumors involving the <u>colon</u>, stomach, <u>pancreas</u>, breast,
and ovaries; can also be used topically for BCC & actinic keratoses</div><div><br></div><div>{{c1::5-FU}}</div>"
"Unique ADR to 5-FU? <br><br>{{c1::Palmar-plantar rash (""dirty palms"" with banding nails)}}"
{{c1::Capecitabine}} is metabolized to 5-FU by tumor enzymes
A mitotic inhibitor that binds microtubules arresting cell division leading to apoptosis<br><br>{{c1::Ixabepilone}}
This medication retains activity in cases where tumor cells are insensitive to paclitaxel<br><br>{{c1::Ixabepilone}}
{{c1::Ixabepilone}} is administered IV with <u>capecitabine</u> in the tx of advanced, metastatic breast CA
Liposomal product approved for AML<br><br>{{c1::Cytarabine}}
Unique ADRs to <b><u>cytarabine</u></b> include {{c1::cerebellar ataxia}} & {{c1::capillary leakage syndrome}}Capillary leakage syndrome – systemic and pulmonary edema
Pyrimidine antagonist adminstered IV in the tx of <b>pancreatic</b>, bladder, breast, and non-small cell lung CA<br><br>{{c1::Gemcitabine}}
Vinca alkaloids (vincristine, vinblastine, vinorelbine) are derived from the {{c1::periwinkle}} plant
"Inhibit mitosis by binding to microtubules – ""spindle poisons"" <br><br>{{c1::Vinca alkaloids}}"Vincristine, vinblastine, vinorelbine
Which vinca alkaloid has ADR of neurotoxicity? <br><br>{{c1::Vincristine}}
Which vinca alkaloid(s) are myelosuppressive? <br><br>{{c1::Vinblastine, vinorelbine}}
Vinca alkaloids are primarily used for lymphomas, leukemias, and {{c1::nephroblastoma::renal}}
Derived from the mandrake plant<br><br>{{c1::Etoposide}}
Which phase(s) of the cell cycle does <u>etoposide</u> act on? <br><br>{{c1::S & G1}}
Etoposide has been used to tx {{c1::testicular}} CA
What antineoplastic has been used for tx of mycosis fungoides? <br><br>{{c1::Etoposide}}
Protocol for aggressive lymphomas & progressive neuroblastoma is ICE<br><br>ICE = {{c1::ifosfamide, carboplatin, and etoposide}} +/- rituximab
Binds mitotic microtubules in mitosis & used in the tx of breast, ovarian, lung, bladder, prostate, melanoma, and esophageal CA<br><br>{{c1::Paclitaxel}}
Derived from the Yew tree<br><br>{{c1::Paclitaxel}}
The solvent used for {{c1::paclitaxel}} may cause infusion rxn, so must premedicate with H2 antagonist; corticosteroid; H1 antagonist
Unique ADR to docetaxel? <br><br>{{c1::Fluid retention}}Same class as paclitaxel
Severe diarrhea from this antineoplastic<br><br>{{c1::Irinotecan}}Give diphenoxylate/atropine w/in 24 hrs & loperamide after 24 hrs for severe diarrhea
Irinotecan is used in the tx of {{c1::colorectal}} CA
Dactinomycin, doxorubicin, and idarubicin are all derived from {{c1::Streptomyces}}
Dactinomycin, doxorubicin, and idarubicin interfere w/ DNA synthesis via inhibition of {{c1::topoisomerase II::enzyme}}
Used to tx Wilm's and Ewing's tumors, testicular CA, and sarcomas<br><br>{{c1::Dactinomycin}}Etoposide can also tx these conditions
Used in the tx of many blood and solid tumor CA; has maximum lifetime dose at 550mg per m<sup>2</sup> due to <u>cardiotoxicity</u><br><br>{{c1::Doxorubicin}}
Main ADR to idarubicin? <br><br>{{c1::Cardiotoxicity}}Just like doxorubicin
Idarubicin is used in the tx of many {{c1::leukemias}}
Doxorubicin will turn body secretions {{c1::red::color}}
{{c1::Bleomycin}} is also derived from Streptomyces and is used in the tx of Hodgkin's lymphoma, SCC, and testicular CA
Topical administration of <u>bleomycin</u> has also been used in the tx of {{c1::plantar warts}}
Main ADR to bleomycin? <br><br>{{c1::Pulmonary fibrosis and impaired lung function}}Characterized by cough and dyspnea
{{c1::Asparaginase}} is an enzyme derived from E. coli that depletes the CA cell of {{c1::asparagine::AA}} which inhibits the ability of the CA cell to synthesize proteins and nucleic acidsAdministered IV
Asparaginase is well tolerated b/c is lacks {{c1::myelosuppression}}
Main ADR to asparaginase? <br><br>{{c1::Allergic rxn}}
Hormone antagonists are often used in conjunction with {{c1::radiation/surgery}} to prevent the growth of any remaining CA cells
Do hormone antagonists cause cell death? <br><br>{{c1::No}}Non-cytotoxic
Estrogen receptor blocker used in the tx of breast CA<br><br>{{c1::Tamoxifen}}Selective estrogen receptor modulator (SERM)
{{c1::Tamoxifen}} is usually administered over a 5-year period following surgical removal of the primary tumorNew evidence suggests utility with admin up to 10 years
Use of bupropion, fluoxetine, or paroxetine is discouraged w/ {{c1::tamoxifen}} b/c its efficacy will be decreased
Tamoxifen is admin {{c1::orally}} 
Can be used prophylactically in patients with strong family history of breast CA<br><br>{{c1::Tamoxifen}}
Unique ADR to tamoxifen<br><br>{{c1::Post-menopausal syndrome}}N, hot flashes, rash, vaginal bleeding, thromboembolism, proliferation of uterine lining (endometrial CA) 
Tamoxifen acts as an antagonist in {{c1::breast}} tissue, but partial agonist on the {{c1::endometrium}}
Estrogen antagonist similar to tamoxifen used in the tx of <u>post-menopausal</u> breast CA<br><br>{{c1::Toremifene}}unlike tamoxifen, which can be used pre- or post-menopausal
Used to prevent post-menopausal osteoporosis and prophylaxis of breast CA in high risk pt<br><br>{{c1::Raloxifene}}Does not stimulate proliferation of uterine lining – less risk of endometrial CA, but less efficacious in preventing breast CA
Letrozole, exemestane, and anastrozole are {{c1::aromatase inhibitors::MOA}}
{{c1::Aromatase inhibitors::class}} are indicated for the tx of <u>post-menopausal</u> breast CA following surgical removal of the primary tumorAdjuvant chemotherapy<br><br>Not effective for pre-menopausal women due to added estrogen production
Avoid aromatase inhibitors in women with {{c1::osteoporosis}} due to decreased bone mineral density 
Developed as an alternative for tamoxifen-resistant tumors<br><br>{{c1::Aromatase inhibitors}}Letrozole, exemestane, and anastrozole
Off-label use of <u>aromatase inhibitors</u> = decrease {{c1::gynecomastia}} seen with anabolic steroid use
Common ADRs to aromatase inhibitors include N, {{c1::hot flashes}}, {{c1::vaginal}} bleeding, and joint pain"Less common: infertility,
adrenal insufficiency, kidney failure, alopecia, liver dysfunction, aggressive
behavior"
Analogs of {{c1::GnRH}} inhibit the release of FSH & LH
Leuprolide, goserelin, nafarelin, and triptorelin are {{c1::GnRH analogs}} used in the tx of <b>prostate CA</b>, precocious puberty, endometriosis, advanced breast CA, and endometrial CA
ADRs to GnRH analogs (e.g. Leuprolide) include HA, N, hot flashes, and {{c1::hypogonadism}}
Indicated for the tx of prostate CA<br><br>{{c1::Androgen antagonists}}Flutamide, Bicalutamide, Nilutamide, and Enzalutamide
Flutamide, Bicalutamide, Nilutamide, and Enzalutamide are all {{c1::androgen antagonists}}Indicated for prostate CA
ADRs to androgen antagonists include GI disturbances, {{c1::gynecomastia}}, {{c1::impotency}}, jaundice, changes in liver function, and pneumonitis
Which steroid hormone is used in regimens to increase appetite (weight gain)? <br><br>{{c1::Megestrol}}
"<div>Targets the <u>HER2</u> (human epidermal
receptor) growth receptor seen in 25-30% of patients with metastatic breast
cancer</div><div><br></div><div>{{c1::Trastuzumab}}</div>"
Unique ADR to trastuzumab? <br><br>{{c1::HF}}
Main ADR to cetuximab? <br><br>{{c1::Acne-like rash}}Can also cause fever, constipation, and abdominal pain; also hypotension, interstitial lung ds
"<div>Targets
the CD20 antigen found on the surface of normal and malignant B lymphocytes </div><div><br></div><div>{{c1::Rituximab & Obinutuzumab::2}}</div>""Approved
for the treatment of post-transplant lymphoma, in chronic lymphocytic leukemia,
non-Hodgkin’s lymphoma, RA, Wegener’s Granulomatosis"
Monoclonal antitumor ab for Wegener's granulomatosis? <br><br>{{c1::Rituximab}}
No {{c1::myelosuppression::ADR}} seen in the use of rituximab
Infuse rituximab {{c1::SLOWLY::speed}}Pretreat with diphenhydramine, APAP, and bronchodilators
Infusion related toxicity to {{c1::rituximab}} includes fever, chills, hypotension, <u>bronchospasm</u>, <u>angioedema</u>, and <u>arrhythmias</u>
{{c1::Rituximab}} has a long 1/2 life that lasts for 6+ monthsCaution using live vaccines
Tumor lysis syndrome has been reported w/in 24 hours of first dose of this monoclonal ab<br><br>{{c1::Rituximab}}
"<div>The {{c1::cytotoxic T-lymphocyte–associated
antigen 4}} (CTLA-4) and {{c1::programmed death 1}} (PD-1) <u>immune checkpoints</u> are
negative regulators of  T-cell immune
function</div>"
"<div>CTLA-4 is thought to regulate T-cell
proliferation early in an immune response, primarily in {{c1::lymph nodes}}</div>""<div>CTLA-4
is considered the “leader” of the immune checkpoint inhibitors, as it stops
potentially autoreactive T cells at the initial stage of naive T-cell
activation, typically in lymph nodes</div>"
"<div>PD-1 suppresses T cells later in an
immune response, primarily in {{c1::peripheral tissues}}</div>"
"<div>A core concept in cancer immunotherapy is
that tumor cells, which would normally be recognized by T cells, have developed
ways to evade the host immune system by taking advantage of {{c1::peripheral
tolerance}}</div>"
"<div>{{c1::PD1}} is a transmembrane protein expressed
on T-cells, B-cells, dendritic cells</div>""<img src=""paste-92cbfcfa4ef634b2d70b5a6d9dce0494b91ef633.jpg"">"
"<div>Ligation of PD1 with ligands PDL1 and
PDL2 result in {{c1::inhibition}} of the immune cell response</div>""<img src=""paste-92cbfcfa4ef634b2d70b5a6d9dce0494b91ef633.jpg"">"
PDL1 is expressed on the neoplastic cells of many different CA & by binding to PD1 on T cells, tumor cells can {{c1::evade}} immune attack"<img src=""paste-92cbfcfa4ef634b2d70b5a6d9dce0494b91ef633.jpg"">"
"<div>Designed to restore a patient’s own
antitumor immune response that has been suppressed during tumor development</div><div><br></div><div>{{c1::Immune checkpoint inhibitors}}</div>""Activates T cells to attack CA cells<br><img src=""paste-91c0b7790cf119de82ae47ccd535230ac38306fd.jpg"">"
"<div>Monoclonal antibodies directed
against the immune checkpoint programmed death 1 (PD-1) receptor or PD-L1
ligand </div><div><br></div><div>{{c1::Immune checkpoint inhibitors}}</div>""Indicated in tx of melanoma, NSCLC, head/neck CA, Hodgkin's lymphoma, and renal cell carcinoma<br><img src=""paste-91c0b7790cf119de82ae47ccd535230ac38306fd.jpg"">"
Nivolumab<br><br>{{c1::PD1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Pembrolizumab<br><br>{{c1::PD1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Cemiplimab<br><br>{{c1::PD1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Dostarlimab<br><br>{{c1::PD1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Atezolizumab<br><br>{{c1::PD-L1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Avelumab<br><br>{{c1::PD-L1 inhibitor::MOA}}
Durvalumab<br><br>{{c1::PD-L1 inhibitor::MOA}}"<img src=""paste-a8ef56d5ab7eb905198cc541ec7410788c247f05.jpg"">"
Ipilimumab<br><br>{{c1::CTLA-4 checkpoint inhibitor}}
Tremelimumab <br><br>{{c1::CTLA-4 checkpoint inhibitor}}
First-line tx for patients with NSCLC with PD1 expression<br><br>{{c1::Pembrolizumab}}PD1 inhibitor
Rare ADR to immune checkpoint inhibitors? <br><br>Severe immune-mediated inflammation of the lungs, colon, kidneys, as well as immune-mediated {{c1::hypothyroidism}} or {{c1::hyperthyroidism}}, T1DM, pancreatitisRevving up the immune response, so get autoimmune attack manifestations
Improve migration of T cells to the tumor site by normalizing tumor vasculature<br><br>{{c1::VEGF inhibitors}}
"<div>Approved
for use as a first-line drug for <u>metastatic colon cancer</u>, advanced non-squamous
non–small cell lung cancer (NSCLC), metastatic kidney cancer (mRCC),
glioblastoma in combination with other agents </div><div><br></div><div>{{c1::Bevacizumab}}</div>"Key words here are metastatic
Off-label used to manage macular degeneration<br><br>{{c1::Bevacizumab}}
{{c1::Kinase inhibitors}} are oral agents that block specific proteins manufactured in response to oncogenesAct w/in the cell, blocking the messenger activity of various kinases
Kinase inhibitors work to {{c1::slow}} cell growth rather than destroy cells
Mainstay therapy for CML<br><br>{{c1::Imatinib::kinase inhibitor}}Also used in Philadelphia+ ALL, gastrointestinal stromal tumors (GISTs)
"<div>Kinase inhibitor indicated for HER2 + breast cancer in conjunction
with capecitabine or letrozole</div><div><br></div><div>{{c1::Lapatinib}}</div>"
{{c1::Erlotinib}} is a kinase inhibitor used to tx NSCLC and pancreatic CA
Imatinib targets {{c1::BCR-ABL}}
Lapatinib targets {{c1::EGFR}} and {{c1::HER2}}
Erlotinib targets {{c1::EGFR}}
Erdafitinib targets {{c1::FGFR}}Fibroblast growth factor receptor inhibitor
Used in tx of metastatic bladder CA<br><br>{{c1::Erdafitinib}}
Sorafenib, sunitinib, cabozantinib, and axitinib are TK inhibitors with {{c1::anti-angiogenesis}} propertiesBlock VEGFR
Unique ADRs to kinase inhibitors include {{c1::fluid retention}} and leg cramps
Some kinase inhibitors prolong {{c1::QT interval}} and alter liver function
Many kinase inhibitors utilize the CYP{{c1::450 3A4}} system
{{c1::Palbociclib}} is a selective inhibitor of CDK4/6 At G1 checkpoint
Approved for the tx of HR positive/HER 2 negative metastatic breast CA<br><br>{{c1::Palbociclib}}
ADRs to palbociclib include {{c1::diarrhea}}, fatigue, N, and neutropenia
Dinaciclib and Trilaciclib are other examples of {{c1::CDK}} inhibitors
Bortezomib, carfilzomib, and ixazomib are {{c1::proteasome inhibitors}}; they are used in the tx of {{c1::multiple myeloma}}
Avoid {{c1::proteasome inhibitors::drug class}} in pregnancy and 90 days after therapy stops
"""living"" drugs tailor-made for each patient<br><br>{{c1::CAR T-cells}}"CAR = chimeric antigen receptor
"<div>T
cells are taken from the blood of cancer patients and then modified with genes
encoding receptors that recognize cancer-specific antigens; those cells are
infused to attack cancer cells </div><div><br></div><div>{{c1::CAR T-cells – Autologous Cell Immunotherapy}}</div>""<img src=""paste-90659cad9fa2206dfd8c5accc3bb591475d787e0.jpg"">"
CAR T-cells are currently being used in tx failure cases of {{c1::Non-Hodgkin's}} lymphoma, ALL
ADRs to CAR T-cells include {{c1::cytokine release syndrome}} & {{c1::ICANS}}
"<div>May
occur within hours up to 14 days following CAR T infusion; clinical
indicatory include fever (initial symptom), hypotension, respiratory distress,
elevation in CRP</div><div><br></div><div>{{c1::Cytokine release syndrome}}</div>"
Utilize {{c1::anti-IL-6}} (tocilizumab) if sx of cytokine release syndrome progress to grade 2 or higher
Immune effector cell-associated neurotoxicity syndrome (ICANS) presents in 40% of {{c1::CAR T}} recipients and typically occurs after the start of CRSCRS = cytokine release syndrome<br><br>MOA not fully understood but likely involves disruption of the blood-brain barrier and cerebral edema via cytokine release
Neurologic sx of ICANS include tremor, {{c1::dysgraphia}}, expressive aphasia, impaired attention, and seizureICANS = immune effector cell associated neurotoxicity syndrome
"<div>Blocking
this enzyme halts the normal repair in cancer cells and causes cell death; used in tumors with BRAC1, BRAC2,
PTEN or PALB2 mutations</div><div><br></div><div>{{c1::PARP inhibitor}}</div>"
Olaparib is a {{c1::PARP inhibitor}} used in tx of BRAC-mutant ovarian CARucaparib & Talazoparib are other examples of PARP inhibitors
Rare ADR to PARP inhibitors? <br><br>{{c1::Myelodysplastic syndrome}}
Are PARP inhibitors teratogenic? <br><br>{{c1::Yes}}Avoid in pregnancy and for 7 months after therapy stops
Which immunomodulatory agent is preferrred <br><br>{{c1::Lenalidomide::Thalidomide/Pomalidomide/Lenalidomide}}Less toxic
"<div>Inhibition
of osteoclast
maturation;
decreased bone destruction </div><div><br></div><div>{{c1::Lenalidomide}}</div>"Thalidomide and pomalidomide also do same thing
"Used in the management of multiple myeloma; prevent
activation
of tumor
growth factors by impairing transcription factors<br><br>{{c1::Lenalidomide}}"
Main ADR to lenalidomide? <br><br>{{c1::Teratogenicity}}
Vorinostat is a {{c1::histone deacetylase inhibitor}} approved for cutaneous T-cell lymphoma, and multiple myelomaLeads to buildup of acetylated histones which triggers cell-cycle arrest and apoptosis
Gene expression is dependent upon coiling and uncoiling of DNA around histones, so this drug blocks genes that promote uncontrolled growth<br><br>{{c1::Vorinostat}}Histone deacetylase inhibitor
<u>Vorinostat</u> has a narrow TI which could lead to rare events such as {{c1::QT-interval}} prolongation, cardiac arrhythmias, and ischemiaHistone deactylase inhibitor
"{{c1::Protein
kinase inhibitors}} plus {{c1::Cyclin-dependent kinase inhibitors}} induce tumor cell
senescence "Cell growth arrest
"<div>Drugs used
to treat cancer based on the cancer’s genetic and molecular features without
regard to the cancer type </div><div><br></div><div>{{c1::Tumor-agnostic therapies}}<br></div>"
Tuberculosis vaccine that prevents recurrence in up to 67% of cases of superficial bladder CA<br><br>{{c1::BCG}}Must be adminstered intravesical instillation for six weeks<br><br>The patient moves position Q 15 minutes for 1 hour to ensure that the solution has covered the entire bladder
ADRs to {{c1::BCG}} include cystitis, hematuria, rarely disseminated TBSo don't use this in immunocompromised pt
IFN-alpha {{c1::2b}} approved for follicular lymphoma & melanoma2a for CML & both 2a and 2b for hairy cell leukemia & AIDS-related Kaposi's sarcoma
ADRs to IL-2 administration include hypotension, {{c1::capillary leak}} syndrome, thrombocytopenia, neuropsychiatric changes, and Staph infections
Best efficacy for actinic keratosis? <br><br>{{c1::5-FU}}
Dolasetron, granisetron, and ondansetron are {{c1::5-HT3 receptor antagonists}} used for acute onset N/V controlFirst line for antiemetic<br><br>ADRs: HA, diarrhea
Aprepitant is a {{c1::substance P / neurokinin 1 receptor antagonist}} that is effective in both acute and esp. in delayed phases of emesis from chemotherapyFirst line for antiemetic <br><br>ADRs: dizziness, fatigue, hiccups, anorexia
{{c1::Cannabinoids}} like dronabinol and nabilone are second-line agents used in chemotherapy induced N/V
Other adjunct agents such as {{c1::dexamethasone}} and {{c1::olanzapine}} are second-line therapy for chemotherapy induced N/V
High risk of emesis<br><br>Day 1 – {{c1::NK1R antagonist + 5-HT3 receptor antagonist + dexamethsone + olanzapine::4}}
High risk of emesis<br><br>Day 2-4 – {{c1::continue dexamethasone + olanzapine::2}}If aprepitant is used on day 1 continue on days 2 and 3 due to DOA
Moderate risk of emesis<br><br>Day 1 – {{c1::5-HT3 receptor antagonist + dexamethasone}}
Moderate risk of emesis<br><br>Day 2-3 – {{c1::if delayed emesis is probable – 5-HT3 receptor antagonist + dexamethasone}}
Low risk of emesis <br><br>Day 1 – {{c1::dexamethasone OR 5-HT3 receptor antagonist OR prochlorperazine}}Ppx for delayed N is not necessary
Can benzos be used as anticipatory nausea tx? <br><br>{{c1::Yes}}
Tumor lysis syndrome most commonly occurs when tx {{c1::leukemias}} and {{c1::lymphomas}}
Make sure to keep pt {{c1::hydrated}} w/ tumor lysis syndrome
Brand name for ondansetron? <br><br>{{c1::Zofran}}
Generic name for zofran? <br><br>{{c1::Ondansetron}}
Ondansetron dosing schedule before chemotherapy initiation? <br><br>{{c1::8-24mg po 30 minutes prior to chemotherapy}}
Ondansetron dosing schedule after chemotherapy? <br><br>{{c1::8-16mg po Q12h for 1-2 days after chemotherapy }}
Trastuzumab brand name? <br><br>{{c1::Herceptin}}
Herceptin generic name? <br><br>{{c1::Trastuzumab}}
Trastuzumab is used in combination with {{c1::docetaxel}} and {{c1::carboplatin}}
Bevacizumab brand name? <br><br>{{c1::Avastin}}
Avastin generic name? <br><br>{{c1::Bevacizumab}}
Bevacizumab combination therapy with carboplatin and paclitaxel dosing schedule? <br><br>{{c1::15mg/kg Q3W IV infusion up to 6 cycles}}
Bevacizumab single therapy dosing schedule? <br><br>{{c1::15mg/kg Q3W IV infusion up to 22 weeks}}
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