Pcol 2 Exam 3 Flashcards
Donezepil
Ari
Central choliesterase inhibitor
So more ACH in the synpase therefore improving neurotransmission and increase activation of central nicotinic receptors
Treat alzeihmer a neurodegenerative disease
AE periphery:
-Bradycardia
-Bronchoconstriction
-Increase gland secretion
-Increase urine
AE central:
Insomnia
Aricept
Rivastigmine
Exe
Centrall cholinesterase inhibitor
So inhibit cholinesterase so increase ACH in the synapse –> improve neurotransmission and increase activation of post-synaptic central nicotinic receptors
Treat alzeihmer a neurodegenerative disease
AE periphery:
Bradycardia
Bronchoconstriction
Increase salivation
Increase urine
AE central:
Insomnia
Exelon
Galantamine
Raza
Central cholinesterase inhibitor –> so increase ACH in the synapse therefore increase activation of post-synaptic centrall nicotinic receptors
Treat alzeihmer
Peripheral AE:
-Bradycardia
-Bronchoconstriction
-Increase urination
-Increase salivation
Central AE:
-Insomnia
Razadyne
Memantine
Namen
NMDA receptor antagonist
MOA:
-Block glutamate from binding to NMDA receptors –> so prevent the death to cholinergic neurons that is caused when too much activation of AMPA and NMDA receptors
-It protects the cholinergic neurons
Thera use
-Memantine (namenda) slows the progression of the alzeihmer disease
-Is use in combo with cholinesterase inhibitors
Namenda XR
Donanemab
DonaKi LecaLeq
anti-amyloid monoclonal antibody
MOA:
Bind to the amyloid plaque and clear it out from the brain preventing neuronal death
The amyloid plaques are derived because of incorrect cutting at the amyloid precursor protein
Thera use
-Treat alzeihmer
AE:
-Intracranial bleeding
Kisunla
Lecanemab
DonaKi LecaLeq
Anti-amyloid monoclonal antibody
MOA:
-Bind to the amyloid plaque and will remove it from the brain preventing neuronal death
-The amyloid plaque are form because of incorrect cutting in the amyloid precursor protein
Thera use:
-Treat alzeihmer pt will take it for 3-4 months and then as needed when the symptoms return
AE:
-Intracranial bleeding
Leqembi
Riluzole
THINK Rilu Eda Radica
NMDA receptor antagonist
It will reduce the excitation of glutamate to the neuron–> therefore reduces the death to the motor neurons in the cerebral cortex and the lower motor neurons
-It will extend the life of a pt that suffers from ALS by 2 months
Rilutek
Edaravone
Think: Rilu Eda Radica
Is a antioxidant –> is a free radical scavenger –> it will reduce the ability of oxidants to attack the nerves
Can treat ALS
Radicava
Avonex
AVO REBI BETA EXTAVIA
Interferon Beta
MOA:
-It will bind to the interferon receptor in the Tcells and will reduce the activity of the Tcells so less T cells in the CNS –> less release of cytokines –> so less activation and release of macrophages –> so no demyelination of the neuron
-But over time the pt that receives interferon beta injection will start to produce neutralizing antibodies and will bind to the avonex interferon and neutralize it –> therefore decreases its acitivity
Thera:
-Treat MS –> they are disease modifying agents –> the will try to reduce the frequency and relapse of an acute MS atack a relapse -remmiting MS
AE:
-Reduce wound healing
-Reduce immune system
-Increase risk of severe infection
-Hepatotoxicity –> need to monitor LFT
-Decrease WBC–> Need to monitor blood counts
-Decrease RBC
-Increase risk of seizure
-Increase risk of depression
-Increase risk of suicide thought
-Increase risk of HF
-Flu like symptoms–> body aches
-injection site rxn
Rebif
AVO REBI BETA EXTAVIA
Interferon beta
MOA:
-Will bind to the interferon receptor on the T cells and will reduce the activity of the T cell so less Tcell to CNS –> less release of cytokines less activation of macrophages so reduces the demyelination of the neuron
-but over time in a pt receiving a interferon beta injection it will produce neutralizing antibodies that will neutralize the activity of the interferon
AE:
-Injection site rxn
-Flu like symptoms–> muscle aches
-increase risk of seizure
-Incrase risk of depression
-Increase suicide thoughts
-Decrease WBC
-Decrease RBC
-Hepatotoxicity – check LFT
-Increase riks of HF–> decrease CO
-Decrease wound healing
-Decrease immune system
-Increase risk of severe infection
Betaseron
AVO REBI BETA EXTAVIA
nterferon beta
MOA:
-Will bind to the interferon receptor on the T cells and will reduce the activity of the T cell so less Tcell to CNS –> less release of cytokines less activation of macrophages so reduces the demyelination of the neuron
-but over time in a pt receiving a interferon beta injection it will produce neutralizing antibodies that will neutralize the activity of the interferon
AE:
-Injection site rxn
-Flu like symptoms–> muscle aches
-increase risk of seizure
-Incrase risk of depression
-Increase suicide thoughts
-Decrease WBC
-Decrease RBC
-Hepatotoxicity – check LFT
-Increase riks of HF–> decrease CO
-Decrease wound healing
-Decrease immune system
-Increase risk of severe infection
Extavia
AVO REBI BETA EXTAVIA
nterferon beta
MOA:
-Will bind to the interferon receptor on the T cells and will reduce the activity of the T cell so less Tcell to CNS –> less release of cytokines less activation of macrophages so reduces the demyelination of the neuron
-but over time in a pt receiving a interferon beta injection it will produce neutralizing antibodies that will neutralize the activity of the interferon
AE:
-Injection site rxn
-Flu like symptoms–> muscle aches
-increase risk of seizure
-Incrase risk of depression
-Increase suicide thoughts
-Decrease WBC
-Decrease RBC
-Hepatotoxicity – check LFT
-Increase riks of HF–> decrease CO
-Decrease wound healing
-Decrease immune system
-Increase risk of severe infection
Capaxone
Gla
MOA:
-Capaxone (Glatiramer acetate) will reduce T cell activity because they have a MBP component and will protect from the Tcell to attack the MBP
AE:
-Chest pain, flushing, SOB –> Following injection
-Decrease wound healing
-Predispose to severe infection
-Decrease immune system
Glatiramer acetate
Tisabri (Natalizumab)
Natali-
MOA:
-It will bind to the A4B1 integrins on the T cell and will prevent the T cells from binding to VCAM-1 a cell adhesion molecule that allow movement of the T cell throught the endothelial but because Tisabri prevents it –> results in decrease T circulating T cell so less T cell entering to the CNS
Thera:
-Treat MS
AE:
-Decrease wound healing
-Decrease immune system
-Predispose pt to severe infection
-PML–> Progressive multifactorial Leukoencephalopathy –> is a severe brain infection that causes speech defects, blurry vision and can cause death.
-It has a REMS–> Need to check pt doesn’t have risk for PML
Natalizumab
Lemtrada
Alem-
MOA:
-Is a monoclonal antibody against the CD-52 on the surface of the T cells and B cells and when lemtrada binds it will cause a antibody dependent cell mediated toxicity causing the B cell and T cells to die —> so get reduction in circulating T cells and B cells so less immune response
Thera:
-Treat M.S
AE:
-Hemorragic stroke–> Due to the release of cytokines when lymphocytes are dying off
-Decrease wound healing
-Decrease immune system
-Predispose pt to severe infection
Alemtuzumab
Ocrevus (Ocrelizumab)
Ocrelizumab
Is a monoclonal antibody
MOA:
-It will bind to CD-20 in the B cells and will cause a antibody dependent cell mediated toxicity –> reduces circulating B cells and reduce immune response
Thera:
-Treat MS
AE:
-Decrease wound healing
-Decrease immune system
-Predispose pt to severe infection
Ocrelizumab
Briumvi (Ublituximab)
Ubli
Is a monoclonal antibody
MOA:
-It will bind to CD-20 on the Bcells and will cause a antibody dependent cell mediated toxicity –> reduces circulating B cells and immune system
Thera:
-Treat MS
AE:
-Decrease wound healing
-Decrease immune system
-Predispose pt to severe infection
Ublituximab
Kesimpta (Ofatumumab)
Ofatu-
Is a monoclonal antibody
MOA:
-It will bind to CD-20 on the surface of B cell and will cause a antibody-dependent cell mediated toxicity –> so reduces ciruculating B cell number and reduces immune response
Thera:
-Treat MS
AE:
-Decrease wound healing
-Decrease immune response
-Predispose pt to severe infection
Ofatumumab
Novantrone
mito-
Novantrone is use to treat MS
MOA:
-It will inhibit topioisomerase so inhibit DNA replication –> therefore decreases the number B cells and T cells
AE:
-Alopecia–> affects rapid dividing cells
-Agranularcytosis-anemia
-Cardiotoxicity –> can cause HF–> Dose is based on the pt BSA and if the pt reach the limit dose they wont be able to receive novantrone anymore because it can cause cardiactoxicity
-D/V
-Decrease wound healing
-Decrease immunesystem
-Predispose to severe infection
Mitoxantrone
Gilenya
-imob
S-1-P-1 agonist
MOA:
-When S-1-P-1 receptor is active in the thymus it will allow the immature T cells to move out from the thymus into circulation
-at the begining the symptoms of MS worsens because of the increase in circulating T cells –> but with the prolonged activation of the S-1-P-1 Receptor it causes desensitization of the receptor –> receptor down regulation and –> so eventually it will reduce the number of circulating T cells because less will be move to circulation
Thera:
-Treat MS
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
-HTN
-Macular papular edema –> fluid accumulated in the eye
-Pulmonary edema
-Cardiac edema
-Hepatotoxicity –> increase LFT
-Bronchitis
-First dose bradycardia –> drop HR only in the first dose so need to monitor the pt in the first dose. Bradycardia happens because Gilenya (Tingolimob) is less selective to the S1P1 receptor on the thymus –> so it can activate other S1P1 receptors on the heart
Tingolimob
Mayzent
Sip- imob
S1P1 agonist
MOA:
Activation of the S1P1 receptor in the thymus will allow the immature T cells to move from the thymus into circulation at the begining the number of circulating T cells increases therefore the symptoms gets worse but eventually receptor desensitization causing down regulation of the receptors –> decreasing the number of circulating T cells
Thera: treat MS
AE:
-Decrease wound healing
-Predispose pt to infection
-Decrease immune system
-HTN
-Macular papular edema–> Fluid in the eye
-Pulmonary edema
-Cardiac edema
-Hepatotoxicity –> Increase LFT
-Bronchitis
Siponimob
Zeposia
oza -imob
Zeposia (Ozamimob)
MOA:
-S1P1 agonist –> Activation of the S1P1 receptor will allow the movement of the immature T cells from the thymus to circulation but because of prolong activation of the S1P1 receptor it will cause desensitization of the receptor –> down regulation –> eventually decreases the circulating T cells
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
-HTN
-Cardiac edema
-Macular papular edema–> Fluid accumulation in eye
-Pulmonary edema
-Bronchitis
-Hepatotoxicity –> Increase LFT
Ozanimob
Ponvoy
Pone -imob
S1P1 agonist
MOA:
-Activation of the S1P1 receptor in the thymus will allow for the movement of the T cells from the thymus to circulation so at the begining the number of circulating T cells increases and the symptoms get worse –> but prolonged activation of the S1P1 receptor will cause desensitization of the receptor –> receptor down regulation
So circulating T cells decreases
Thera: Treat MS
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
-HTN
-Bronchitis
-increase liver enzyme –> hepatotoxicity
-Macular papular edema–> accumulation of fluid in the eye
-Pulmonary edema
-Cardiac edema
ponesimob
Aubagio
Teri-
MOA:
-It will inhibit dihydrorate dehydrogenase pyrimidine –> so less pyrimidine bases available for DNA replication of T cells –> therefore it will reduce the synthesis of new T cells
Thera:
-It will treat m.s –> because less t cells available to go to circulation then to the CNS so no release of cytokines that will activate macrophages so no demyelination
AE:
-Predispose pt to severe infection
-Decrease immune system
-Decrease wound healing
-Alopecia –> because it will also affect the DNA replication of rapidly dividing cells
-N/V
-Diarrhea–> Because it will cause sloghting of the GIT lining
-Agranylarcytosis–> Decrease WBC
-Anemia–> Decrease RBC
Teriflunomide
Tecfidera
Tecfi-Dime Vume-Diro Bafi-monome
Is a Fumeric acid derivative
MOA:
-Exact mechanism is unknown but it said to decrease the # of T cells by causing oxidative damage to the T cells
Thera
-Treat MS
AE:
-Predispose pt to severe infection
-Decrease immune system
-Decrease wound healing
Dimethyl fumarate
Vumerity
Tecfi-Dime Vume-Diro Bafi-monome
Fumeric acid derivative
MOA
-Exact mechanism is unknown but is said to decrease T cells by causing oxidative danger to the T cells
Thera:
Treat MS
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
Diroximel fumarate
Bafiertan
Tecfi-dime Vume-diro Bafi-monome
Fumeric acid derivative
MOA:
-Exact mechanism is unknown but it said to decrease # of T cells by causing oxidative danger on T cells
Thera:
-Treat MS
AE:
-Predispose pt to severe infection
-Decrease wound healing
-Decrease immune system
monomethyl fumarate
Maveneclad
Clad-
Is not a monoclonal antibody
MOA:
-It will cause apoptosis of B cells and T cells –> so reduce the number circulating B cells and T cells
Thera:
-Treat M.S
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
Cladribine
Ampyra
Dalfa-
Block K+ channels in the demyelinated neuron
MOA:
-In a pt with MS the demyelinated neuron will exposed the K+ channels and allows the K+ to leave causing hyperpolarization –> decreasing conduction of A.P so decrease neuronal function
But Ampyra will block K+ channels so no K+ leaves no hyperpolarization
Thera:
-Improve neuronal function in pt with MS
-Improve walking and muscle strength
AE:
-Increase risk of seizure
-UTI
Dalfampridine
Cyclosporine
Calcineurin inhibitor
MOA:
-It will bind to cyclophilin and will be able to inhibit calcineurin –> so no dephosphorylation of NFAT –> no IL2 production, no proliferation of T cells
Thera:
-For maitainence phase to prevent organ rejection transplant once the transplant organ is in the pt
-Rheumatoid arthritis
-psoriasis
AE:
-HTN
-Gingival hyperplasia–> increase growth of teeth gum so pt should increase hygiene
-Nephrotoxicity–> monitor kidney function
-Muscle tremors
-Hirsutism –> increase facial and body hair
-Diabetes mellitus –> it causes damage to the beta cells in the pancrease so increase blood glucose
-decrease wound healing, decrease immune system, predispose to severe infection
DDI:
-Avoid 3A4 and PGP inhibitors –> Ritonavir, azole antifungals, erythromycin, clarithromycin, verapamil, diltiazem, grapefruit
Sandimmune, neoral
Tacrolimus
Calcineurin inhibitor
MOA:
-Binds to FKBP protein and will be able to inhibit Calcineurin –> so no dephosphorylation of NFAT so no production of IL2 –> no proliferation of T cells
Thera:
-For maitainence phase to prevent organ rejection once the transplant is done
-Protopic –> can treat psoriasis
-Rheumatoid arthritis
AE:
-HTN
-Diabetes mellitus–> it will destroy beta cells of the pancrease so increase blood glucose
-Hirsutism–> increase facial and body hair
-Gingival hyperplasia–> Increase growth of teeth gum so pt should maintain oral hygiene
-Nephrotoxicity –> need to monitor kidney function
-Muscle tremors
-decrease wound healing, predispose pt to severe infection, decrease immune system
DDI:
-Avoid PGP and 3A4 inhibitors
Ritonavir, azole antifungals, erythromycin, clarithromycin, grapefruit, verapamil, diltiazem
Prograf, Protopic
Pimecrolimus
Eli
Calcineurin inhibitor
thera:
-For maitainence phase to prevent rejection of the organ transplant
-Rheumatoid arthritis
-Psoriasis
AE:
-HTN
-Hirsutism –> increase facial and body hair
-Gingival hyperplasia
-Nephrotoxic
-Muscle tremors
-Diabetic mellitus–> because it can destroy beta cells of the pancrease so increase blood glucose
-Decrease wound healing, predispose pt to severe infection, decrease immune system
Elidel
Sirolimus
Rapa
CDK-2 inhibitor
MOA:
Sirolimus will bind to FKBP protein and then it will form a complex with m-TOR (Mammalian target of Rapamycin (aka sirolimus)) and will inhibit CDK-2 (Cyclin dependent kinase) –> so will reduce the T cell proliferation
Thera:
-For maitenance –> once the pt receives the organ transplant want to prevent rejection of the organ
-Rheumatoid arthritis
-Psoriasis
-Is also coated in the stents–> place a stent on the coronary artery to open the artery and improve blood flow. Coating the stent will prevent restenosis of the coronary artery
AE:
-Hypercholesterolemia
-Hypertriglycemia
-Decrease WBC counts –> So need to monitor Blood counts on the pt
-Decrease immune system, decrease wound healing, predispose pt to severe infection
-If give also Calcineurin inhibitor like Cyclosporine (Sandimmune, neural) it will increase the risk of nephrotoxicity caused by Calcineurin inhibitors
DDI:
3A4 and PGP inhibitors
Ritonavir, azole antifungals, erythromycin, clarithromycin,grapefruit, amiodarone, verapamil, diltiazem
Rapamune
Everolimus
Zor-, Afin-
CDK-2 inhibitor
MOA:
-Everolimus (Zortess, afinitor) will bind to FKBP and then will form complex with mTOR (Mamalian Target Of Rapamycin) and will inhibit CDK-2 –> slows the proliferation of T cells
Is use for cancer
AE:
-Hypertriglyceride
-Hypercholesterolemia
-Reduction in WBC counts –> Need to do periodical blood counts
–Decrease immune system, decrease wound healing, predispose pt to severe infection
Zortess, afinitor
Azathioprine
Imu
Is a prodrug is converted to 6-mercaptopurine and then to 6-thioguanine –> 6-thioguanine will be incorporated to DNA instead of guanine and when DNA replication occurs the replicated enzymes wont be able to continue so DNA replication stops –> Stop DNA replication of T cells and rapid dividing cells
Decrease T cells
Thera:
-For maintenance phase to prevent organ rejection transplant
-Rheumatoid arthritis
-Psoriasis
AE:
-Allopecia
-Agranularcytosis –> Decrease WBC
-Decrease blood counts
-Teratogenic
-Diarrhea
-Decrease immune system, decrease wound healing, predispose pt to severe infection
Ci: Pregnant
DDI:
-Allopurinol (Zyloprim) and Febuxustat (Uloric) will inhibit xanthine oxidase –> and xanthine oxidase is needed for metabolism of purines to uric acid –> so inhibit metabolism of Azathioprine (is converted to 6-mercaptopurine) so the levels of azathioprine increases in serum therefore it can cause severe agranularcytosis
TPMT (Thiopurinemethyltransferase) –> if pt lacks of it wsont be able to metabolize azathioprine. If the pt has low levels of TPMT just need to lower the dose
Imuran
Mycophenolate
Cell- , myfor-
ionosine monophosphate dehydrogenase inhibitor
MOA:
It will inhibit ionosine monophosphate dehydrogenase –> enzyme responsible for the synthesis of purine bases –> so if inhibit ionosine monophosphate dehydrogenase there will be reduction in formation of pyrimidine bases –> so slows DNA replication so slows T cell proliferation and other rapid dividing cells
-Cannot co admin with azathioprine (Imuran) because it will results in severe drop in WBC
-But can coadmin Calcineurin inhibitors: Cyclosporine (Sandimmune, neoral) or Tacrolimus (Prograf) or Pimecrolimus (Elidel)
Can also coadmin CDK-2 inhibitors –> Sirolimus (Rapamune) or Everolimus (Zortress, afinitor)
AE:
-Allopecia
-Drop in WBC
-Decrease blood counts
-Diarrhea
-Teratogenic
-Decrease immune system, decrease wound healing, predispose pt to severe infection
CI: pregnant
Cellcept, myfortic
Basiliximab
Simu-
Monoclonal antibody against the IL-2 receptor
So reduce T cell proliferation
Is use for the induction phase –> before receiving a antibody
AE:
-Anaphylaxis rxn
Simulect
Muromonab CD3 (OKT 3)
Monoclonal antibody against CD3 on the surface of T cells
-It will decrease circulating T cells by causing a antibody dependent cell toxicity rxn
thera:
-Is use for acute rejection of organ transplant
Only use for short term
Lifetegrast
Inhibits LFA-1 cell adhesion molecule on the surface of T cells
So will prevent the movement of the T cells from the blood to the eye
reduces circulating T cells
Treat dry eye syndrome
Xiidra
Methotrexate
traditional DMARD
Traditional DMARD
Inhibit dihydrofolate reductase
MOA
Inhibit dihydrofolate folate reducatase–> Enzyme responsible for synthesis of pyrimidine –> so is inhibit so decrease synthesis of pyrimidines so less pyrimidines available for DNA replication –> So decreases T cell proliferation and synthesis of T cells and rapid dividing cell
Thera:
-Treat rheumatoid arthritis–> take it once a week
AE:
Allopecia
Decrease WBC count –> decrease blood counts so need to check blood levels
Teratogenic
Diarrhea
Pulmonary toxicity
Hepatoxicity
CI
Pregnant
Leflunomide
is a pro drug
Ara
Traditional DMARD
Inhibits dihydrooptarate
MOA:
Leflunomide is a pro-drug and is converted to Teriflunomide that is acid –> when is converted to teriflunomide it will inhibit dyhydro-opterate that is essential for synthesis of DNA therefore decreasing T cell proliferation
Thera:
-Treat rheumatoid arthritis
AE:
-Allopecia
-Diarrhea
-Decrease in WBC count
-Weight loss
-Teratogenic–> Leflunomide is a pro-drug and is converted to teriflunomide that has a long half life and goes through entero hepatic circulation –> If give cholestyramine (bile acid sequestran) it will bind to teriflunomide in the GIT and will excrete it so the pt can get pregnant without concern of teratogenic
Arava
Sulfasalazine
Azul
Traditional DMARD
Is a prodrug
MOA
Is broken down in the colon to 5-aminosalicylic acid (Mesalamine) and Sulfapyridine –> The sulfapyridine component will inhibit T cell activity so reduces the cytokine production into IL-1 so treat Rheumatoid arthritis
Mesalamine component –> is in the colon and has a local effect in the large intestine in the colon and treat ulcerative colitis inflammation of the colon
Thera:
-Treat rheumatoid arthritis
AE:
-Discoloration of urine, saliva and skin –> it looks orange
-Photosensitive
-Skin rash
-Reduction in WBC counts –> Pt can take folic acid
Azulfine
Hydroxychloroquine
plaqu
Traditional DMARD
Inhibits IL-1 release from T cells
MOA:
Inhibits IL-1 release from T cells –> so prevent the damage to Bone, cartilage and joints cause by IL1
Plaquenil
Penicillamine
Injection in joint is a traditional DMARD
treat rheumatoid arthritis
Gold salts
injection in joint is a traditional DMARD
treat rheumatoid arthritis
Recamide (Infliximab) –> increases risk of HF so avoid in pt with HF
Enbrel (Etanercept) –> not monoclonal
Humira (Adalimumab)
Cimzia (Certolizumab)
Simponi (Golimumab)
R En Hu Cim Sim
TNF alpha antagonist is a biological DMARD
MOA:
-They will bind to the extracellular portion of TNF alpha receptor and will prevent TNF from binding–> Neutralazing the activity of TNF so prevent the destruction of joints, bone, cartilage
Thera: they are use for
-Rheumatoid arthritis
-Ezcema
-Psoriasis
-Ankylosis spongitis
-IBD
-Crohns
-Ulcerative cohlitis
-Eosonophilic asthma
AE:
-Biological dmards suppress the immune system so much that it puts the pt at risk of severe infections like: sepsis, tuberculosis
-Reduce wound healing
-Injection site rxn
Kineret (Ankira)
Ilaris (Canakinumab)
IL-1 inhibitors is a biological DMARD
Kineret –> Antibody against the IL-1 receptor –> it will bind to the IL-1 receptor in the extracellular portion and will prevent IL-1 from binding
Ilaris–> Antibody against the IL-1 protein itself will bind to the IL-1 and will prevent it from binding to its receptor
Thera:
-Rheumatoid arthritis
-Ankolosis spongitis
-Ulcerative colitis
-Crohns
-IBD
-Eosonophilic asthma
-Atopic dermatitis
Ezcema
Psoriasis
AE:
-Severe infection–> Sepsis, tuberculosis
-Decrease wound healing
-Cannot give live vaccine to a pt on a immunosupressant
Actemra (Tocilizumab)
Kevzara (Sarilumab)
IL-6 receptor antagonist is a biological DMARD
Thera:
-Treat rheumatoid arthritis
-Psoriasis
-Eptopic dermatitis
-Crohns
-IBD
-Ulcerative colitis
-Ezcema
AE:
-GI perforation –> Wholes in GIT
-Hepatotoxicity
-Reduce blood counts –> Drop WBC and RBC
-Increase cholesterol and lipids
-Demylinated disorders–> Leads to reduce neuropathy and can lead to multiple sclerosis
Abacet (Orencia)
T cell inhibitor is a biological DMARD
MOA:
-It will bind to CD80 and CD86 in the surface of antigen presenting cells and will prevent presentation of the antigen to the T cells–> Therefore it results in no activation of the T cells
Treat autoimmune conditons like rheumatioid arthritis, ezcema, ankilopongitis, IBD, crohns, eosonophilic asthma, Ulcerative colitis, contact dermatitis
AE:
-Decrese wound healing
-Predispose to severe infection
-Decrease immune system
Rituxan (Rituximab)
It will bind to CD-20 on the surface of B cells and will cause a antibody-dependent cell mediated toxicity causing depletion of circulating B cells
Treat autoimmune conditions
AE:
-Skin rashes
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
Xelijanz (Tofacitinib)
Olumiant (Baricitinib)
Rinvoq (Upadacitinib)
Cibinqo (Abrocitinib)
Opzelura (ruxolitinib) –> topical for atopic dermatitis and psoriasis
JAK inhibitors
MOA:
-Inhibit post-receptor signaling –> inhibit JAK (a enzyme) so no phosphorylation of STAT, no formation of dimer and no trasnlocation of STAT to nucleus –>so inhibits post receptor signaling
Thera:
-Treat rheumatoid arthritis
-Atopic dermatitis
-Psoriasis
-Ezcema
-IBD
-Crohns
-Ulcerative colitis
AE:
-CV risk
-MI
-Stroke
-Reduce wound healing
-Reduce immune system
-Predispose pt to severe infections
CI:
-History of MI or unstable angina
Otezla
apre-
PDE-4 inhibitor
MOA:
-Will inhibit PDE4 so no breakdown of CAMP –> so get increase in CAMP –> And the increase in CAMP will activate PKA and the PKA will cause less release of Cytokines from dermatological areas
Thera:
-Treat atopic dermatitis
AE:
-Weight loss
-Depression
Apremilast
Eucrisa
Crisa
PDE4 inhibitor
MOA:
-Will inhibit PDE4 so no breakdown of CAMP –> increase CAMP in dermatological sites will cause activation of PKA –> That will decrease the release of cytokines
Thera:
-Treat atopic dermatitis
AE:
-Weightloss
-Depression
Cristaporole
Taltz (ixekizumab)
Cosentyx (sexukinumab)
Bimzelx (Bimekizumab)
Siliq (brodalumab)
IL-17 inhibitors
Taltz, Cosentyx, Bimzelx –> monoclonal antibodies against the IL-17 protein so it will bind to it and will reduce its activity
Siliq–> Monoclonal antibody against the IL-17 receptor so prevent IL-17 from binding
Thera:
-Treat rheumatoid arthritis
-Ezcema
-Crohns
-Psoriasis
AE;
-Reduce wound healing, decrease immune system, predispose pt to severe infection
Nucala (mepolizumab)
Cinqair (reslizumab)
Fasenra (benralizumab)
Nucal and Cinqair –> Monoclonal antibodies against IL-5 protein and it will cause decrease signaling of IL-5
Fasenra–> Monoclonal antibody against IL-5 receptor and will prevent IL-5 from binding
Thera:
-Treat eosonophilic asthma
Adbry (tralokinumab)
Edglyss (Lebrikizumab)
IL-13 antagonist
-They bind to IL-13 protein and prevent it from binding to its receptor
Thera:
-for autoimmune conditions
Dupixent (Dupilumab)
IL-4 antagonist
Inhibits IL-4 subunit
So reduces signaling of IL-4 in the IL-4 receptor because IL-4 will not bind
and
IL-4 subunit is also in IL-13 –> so reduce signaling of IL-13 because IL-13 also has IL-4 subunit and the IL-4 will not bind.
Treat RA, ezcema, psoriasis, atopic dermatitis
Tremfya (guselkumab)
Skyrizi (Risankizumab)
Ilumya (tildrakizumab)
Omvoh (mirikizumab)
IL-23 antagonist
They are monoclonal antibodies against IL-23 protein and will reduce its signaling preventing IL-23 from binding to its receptor that contains P-19 subunit
Thera:
-For Rheumatoid arthritis
-Ezcema
-Psoriasis
-Ulcerative colitis
-Crohns
-IBD
AE:
-Decrease wound healing
-Decrease immune system
-Predispose pt to severe infection –> sepsis or tuberculosis
Stelara (Ustekinumab)
IL-12 and IL-23 antagonist
Monoclonal antibody against P-40 subunit that is in both IL-12 and IL-23 therefore will prevent IL-12 and IL-23 from binding to its receptor –> Reduces IL-12 and IL-23 signaling
For autoimmune conditions like: rheumatoid arthritis, ulcerative colitis, IBD, Crohns, ezcema, psoriasis
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
Olsalazine
Dipen
Mesalamine component
MOA:
-Olsalazine (Dipentum) has a azo link that is broken down in the colon to mesalamine
Thera:
-Treat ulcerative colitis –> inflammation of the colon
Dipentum
Basalazide
Cola
Mesalamine component
MOA:
-Basalazide (Colazal) has a azo link that is broken down in the colon to mesalamine
Thera:
-Treat ulcerative colitis –> Inflammation in the colon
Colazal
Pentasa (DR)
Mesalamine component delayed release of mesalamine
MOA:
-Pentasa is a enteric coating delayed release of mesalamine –> So it gets to the stomach and will start to release mesalamine in the small intestine jejenum and ileum
Thera:
-Treat crohns disease–> inflammatory disease of the small intestine
Asacol
Lialda
Mesalamine pH sensitive coating release tablets
MOA:
-Asacol and lialda are pH sensitive coating tablets and will start to dissolve in the ileum –> and release mesalamine in the ileum (The small intestine)
Thera:
Treat Crohns disease –> inflammation in the small intestine
Rowasa –>Enema
Rowasa is a enema of Mesalamine
Thera:
-Can give rowasa for inflammation in the colon–> Treat ulcerative colitis
Canasa –> Suppository
Canasa is a suppository of mesalamine
Thera:
-Can give Canasa for inflammation in the rectum
Budesonide
Ento-
Glucocorticoid steroid
MOA:
-Budesonide is given orally is a glucocorticod steroid and will activate glucocorticoid receptors along the GIT –> reducing inflammation of GIT
-Budesonide can be absorb from the GIT –> To the liver and it has high first pass metabolism so very little gets into the blood stream therefore less risk of AE
Thera:
-Can use it for chronic use for IBD
Entocort EC
Hydrocortisone
Corte
Glucocorticoid steroid
MOA:
-Hydrocortisone (Cortenema) is given as a enema and works locally in the colon and will activate glucocorticoid receptors in the colon and reduce the inflammation in the colon
Thera:
-Is only use when someone has a relapse to IBD because some of hydrocortisone can get absorb and get systemic AE
AE:
-Hyperglycemia
-Increase BP
-Osteoporosis
-Fat redesposition
-Decrease bone mass
-Decrease muscle mass
-Weight gain
-insomnia
-Psychosis
-glaucoma
-Catarats
-thining of skin
-decrease wound healing, decrease immune system, predispose pt to severe infection
Cortenema
Entyvio (Vedolizumab)
Monoclonal antibody against A4B7 integrins on surface of T cells
MOA:
-A4B7 integrins on the activated T cell in the GIT will interact with MAD-CAM-1 on the endothelial cell and the process of diaepedisis will occur –> so the T cells squeeze out from the endothelial to the blood stream
But Entyvio will bind to A4B7 on the surface of the T cells in the GIT and will prevent the interaction of the T cells with MAD-CAM-1 integrin –> So reduces the movement of circulating T cells to the tissues to the GIT
Thera:
-Treat IBD
AE:
-Decrease wound healing
-Predispose pt to severe infection
-Decrease immune system
Estradiol
Estrace
Estring
Climara
Femira
Vivelle
Estrogen receptors agonist
MOA:
They need to cross the nucleus and bind to the Estrogen receptor inside the nucleus (a nuclear hormone receptor) and the HSP part leaves and the ER + Estrogen agonist form a homodimer and will recreuit CoA activators protein and bind to them
–> Then the Estrogen agonist + ER + CoA activators –> will bind to the promoter region on the gene and will increase transcription of that gene ultimately resulting in increase protein synthesis
Thera:
-They are use for Hormonal replacement therapy in post-menopause women that have low levels of estrogen:
Treat the hot flashes –> in a post menopause women the low levels of estrogen will cause dilation of the blood vessels on the skin causing them to be very warm and sweaty –> but estrogen agonist will cause constriction so treat hot flashes
-Decrease risk of osteoporosis–> In post menopause women the low levels of estrogen will cause decrease in bone mineral density and increase osteoporosis–> but estrogen agonist will prevent osteoporosis
-Treat vaginal dryness –> use as topical
-Decrease cholesterol
-Decrease LDL
-Increase HDL
AE:
-Increase transcription of clotting factors –> can cause blood clots –> So increases the risk of blood clots, stroke, MI, angina, PE, VTE
-Increases risk of breast cancer and endometrial (uterus) cancer –> because the increase in estrogen levels will increase growth of estrogen dependent tissues
-Decrease milk production –> so CI if lactating
CI:
-Uncontrolled HTN
-History of MI, TIA, stroke, angina, PE or VTE
-Smoker
->35yrs
-Lactating female
-History of breast cancer or uterus (endometrial) Cancer
DDI:
-Estrogen is metabolize by P450 so need to avoid strong inducers because they will decrease the concentration of estrogen in the blood so decrease its effectiveness
Avoid: Phenytoin, carbamazepine, valproic acid, topiramate, phenobarbital
Progesterone (Prome- , Crino-)
Medroxyprogesterone (Depo-
Levonorgestrel (Plan B)
Norgestrel
Norethindrone (Ayen-
Norgestimate
Ethynodiol
Drospirenone
Desogestrel
Segesterone
Progestin receptor agonist
MOA:
-They need to enter the nucleus and bind to progestin receptor in and will form a homodimer –> will recruit CoA activator proteins and bind to the promoter region in the gene and increase transcription of gene ultimately increasing protein sysnthesis
Thera:
-Use in combination with estrogen agonist for Hormonal replacement therapy and will decrease the risk of uterus cancer
-Can be use as contraceptive mini pil or in combo–> Increase mucus secretion in the cervix will prevent sperm from entering. Inhibit ovulation by 90% and is 99% contraceptive. If patient miss just one dose she will loose the local effects of progestin so no mucus in cervix and sperm can enter and pregnancy occur
-Can support pregnancy if implantation already occur–> it will provide fluids nutrients for the embryo
-For endometriosis –> that is enlargement of the endometrium because of overgrowth causing pain
-Decrease risk of uterus (endometrial) cancer
AE:
-Increase cholesterol
-Increase LDL
-Decrease HDL
-Decrease bone mineral density
-Osteoporosis
-Virolent effects –> the older ones are non selective (Medroxyprogesterone, Levonorgestrel, Norgestrel)and can bind to androgens receptor where testosterone binds and causes –> deepening of voice, increase facial and body hair, increase muscle weight, acne
Veozah
Neurokin 3 receptor antagonist
-Blocks neurokinin 3 receptor
blocks NKB from binding on hypothalamic KnDy receptors
Fezolinetant
Raloxifine
Evi-
SERM
MOA:
-Works as antagonist in the uterus and breast tissue
Thera:
-Decrease risk of uterus and breast cancer
-Can treat osteoporosis
AE:
-Hot flashes
Evista
Tamoxifen
Nolva-
SERM
Has antagonist effect in breast tissue –> so decreases risk of breast cancer
AE:
-Increase risk of uterus cancer–> has agonist effects on the uterus so can increase growth of uterus tissue
-Hot flashes
Nolvadex
Toremifen
Fare-
-ifen SERM
-Toremifen (Fareston) will treat and prevent breast cancer –> it will act as antagonist in breast tissue so will not cause growth of breast tissue
AE:
-Increase risk of uterus cancer –> act as a agonist in uterus tissue so will cause increase growth of the uterus tissue
-Hot flashes–> Act as a antagonist in blood vessels and causes hot flashes in pre and post menopause women
Fareston
Ospemifene
Osphe
-ifene SERM
-Act as a estrogen agonist
Use for dyspareunia –> painful intercourse due to vaginal dryness
AE:
-Hot flashes –> act as a antagonist in the blood vessels
Osphena
Bazedoxifen + Conjugated estrogens (Premarin) = Duavee
Bazedoxifen works as a estrogen antagonist in uterus and breast tissue –> so decreases the risk of uterus and breast cancer
-Reduces hot flashes because has conjugated estrogen (Premarin)
Fluvestran
faslo-
-estran
SERD (Selective Estrogen Down Regulators)
MOA:
-It binds to the estrogen receptor alpha and will cause a change in confirmation exposing the proteolytic site and the proteolytic enzyme will be able to bind and attack the receptor causing receptor down regulation
Thera:
-Treat and prevent breast cancer
Faslodex
Elacestran
Orse-
SERD (Selective Estrogen Receptor Down Regulators)
-estran
MOA:
-It binds to the estrogen alpha receptor and will cause a change in confirmation exposing the proteolytic site and the proteolytic enzyme will be able to bind and attack it causing receptor down regulation
Thera:
-Treat and prevent breast cancer
Orsedu
Uliprista
SPRM
Selective Progestin Receptor Modulators
It will bind to the Progestin receptors in the uterus and will activate them and increases the mucus in the cervix uterus lining and prevent sperm entry
-Is use as emergency contraceptive
Ella
Mifepristone
Progestin receptor antagonist
MOA:
-It will block progestin receptors in the uterus and will cause change in the uterus lining and will cause contraction of the uterus and expel the egg
-Is use as abortification
Misoprostol
Clomiphen
Clomi-
SERM
Selective Estrogen Receptor Modulator
MOA:
-It works as a antagonist and will block estrogen receptors in the HPA-Axis and the Hypothalamus will think there is low estrogen so will increase release of GNRH –> pituitary increase release of FSH and LH
And the increase in FSH and LH will accelerate ovulation and will release the mature egg to be fertilize by sperm
Thera:
-Is the first line option for infertility –> it causes early release of the egg. Use alone not in combo
AE:
-Hot flashes –> because act as a antagonist in blood vessels
-Increase risk of multiple birth
-Can cause harm to fetus –> cannot take while pregnant
Clomid
