RHEUM Pharmacology Flashcards by Rachael Petry

MOA: binds CD80 and CD86 and prevents T-cell co-stimulatory signal engaging with CD28.

Abatacept

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MOA: Binds TNF-alpha; blocks its interaction with p55 and p75 surface receptors

Adalimumab

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MOA: Competitively inhibits IL-1 alpha and IL-1beta binding to IL-1R1.

Certolizumab pegol

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MOA: neutralizes membrane associated and solubule human TNF-alpha

Etancerept

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MOA: Endogenous p75 acts as TNF antagonist but does NOT affect TNF alpha production or serum levels (just binds it up)

Etancercept

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MOA: binds to and neutralizes both soluble and membrane TNF-alpha

Golimumab

Infliximab

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MOA: Fab domain binds CD20 and Fc domain and recruits immune effector function to mediate B-cell lysis

Rituximab

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MOA: binds both soluble (serum and synovial fluid) and membrane bound IL-6 receptors and inhibits signaling

Tocilizumab

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MOA: Inhibition of AICAR transformylase →AICA riboside accumulation (inhibits adenosine deaminase)→ increase in adenosine concentration→ inhibition of lymphocyte proliferation; suppression of IL-1, TNF, INF-gamma, histamine release from basophils, chemotaxis of neutrophils; increases IL-4

Methotrexate

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MOA: Active form (mesalamine) is anti-inflammatory (inhibits prostaglandin and leukotriene prodution.

Sulfasalazine

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MOA: A77 1726 inhibits dihydroorotate dehydrogenaase (DHODH) which is located in cell mitochondria and catalyzes key step in de novo pyrimidine synthesis. T-and B-lymphocytes cell cycle progression is arrested and their interactions are interrupted; Ig production is suppressed; CYTOSTATIC

Leflunomide

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MOA: Increases intracellular vacuole pH and alters processes like digestion of antigenic proteins (so no peptide-MHC protein complexes can be formed to stimulate CD4+ T cells—immune response is down-regulated.)

Hydroxychloroquine

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Side effect:

Immunosuppression
Pulmonary Toxicity
Cat. X Teratogen
NO Breastfeeding
Avoid w/vaccination
Malig. lymphoma
GI toxicity
Dermatologic RXN

Methotrexate

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Side effect:

Hematotoxic
NOT for people with hypersensitivity to sulfa drugs
Increased drug levels in slow acetylators

Sulfasalazine

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Side effect:

Immunosuppression (not for patients with immunodeficiency, bone marrow dysplasia, or uncontrolled infection).
Cat. X Teratogen

Leflunomide

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Side effect:

Corneal opacities, kerato/retinopathy
Hepatotoxicity
Blood dyscrasias
CNS toxicity (ex. ototoxicity, seizure)

Hydroxychloroquine

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Monitoring tests for Methotrexate.

1) CBC with diff.
2) LFTs
3) Serum Creat/ BUN
4) Serum uric acid

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Monitoring tests for sulfasalazine.

1) CBC with diff.
2) LFTs
3) Serum Creat/ BUN
4) Urinalysis

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Monitoring tests for Leflunomide.

1) CBC with diff.
2) LFTs
3) Pregnancy test
4) Serum electrolytes (drug increases uric acid in urine/ lowers blood levels)

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Monitoring tests for Hydroxychloroqine

1) CBCs

2) Opthalmalogic exam.

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Major adverse effects for “biological drugs” used to treat RA.

Immunosuppression (especially with upper respiratory infections, watch out)
Malignancy
CHF or hypotension
Blood dyscrasias
Lupus-like syndrome
SJS/TEN

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Which biological drug for RA requires that you use reliable contraception while you take the therapy and for 4-6 months after?

Rituximab

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Which biological IV solution contains maltose (may complicate blood glucose tests)?

Abatecept IV

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What NSAID is available formulated with misoprostol (PGE1 inhibitor) to reduce the risk of duodenal ulcers.

Diclofenac

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Which NSAID also has a rectal preparation available?

Indomethacin

Whaich NSAID also has a parenteral preparation available?

Ketorolac

Which NSAID is COX-2 selective?

Celecoxib

Depolarizing agents.

Curiums and Curoniums (steroids) and D-Tubocurarine

Non-depolarizing agent.

Succinylcholine

Reversal agents.

"stigmines" Edrophonium Sugammedex

Do depolarizing or non-depolarizing have longer half lives?

non-depolarizing have longer half lives

AE: Non-depolarizing drug that causes seizures by liver metabolism building up laudanosine.

Atracurium

AE: Neuromuscular Blocking Agents that block Cardiac M receptor.

pancuronium | rocuronium

AE: Neuromuscular Blocking agents that block cause histamine release.

Tubocurarine | Atracurium

AE: Neuromuscular blocking agents that block Nictotinic N ganglia.

Tubocurarine

AE: malignant hyperthermia (high temp, muscle pain, brown urine), hyperkalemia, stimulation of Nicotinic N, histamine release, and stimulation of cardiac M receptors (decrease HR).

Succinylcholine

Drug given to treat malignant hyperthermia.

Dantrolene

MOA: Drugs that blocks acetylcholinesterase to reverse neuromuscular block.

Neostigmine, Edrophonium, Pyridostigmine

What are AchE inhibitors given to reverse neuromuscular block given with?

Antimuscarinic agents (to prevent the negative effects of AchE inhibitors like bradycardia, bronchospasm, GI peristalsis, increased bladder tone)

MOA: pore structure into which the steroidal NMB inserts, preventing the blocker from being capable of accessing the binding site on the Ach nicotinic receptor (reverse any depth of NM blockade)

Sugammadex

MOA: inhibit the reuptake of serotonin and norepinephrine | fibromyalgia drug

Duloxetine and Milnacipran

MOA: inhibit presynaptic alpha-2-delta subunits of L-type calcium channels→inbitis excitatory transmission by glutamate (alleviates neuropathic pain, anxiety and pain) (fibromyalgia drug)

Pregabalin

Off label drugs for fibromyalgia.

amitriptyline (tricyclic antidepressant) fluoxetine (SSRI) cyclobenzaprine (muscle relaxer)

MOA: Central (CNS) action in reticular activating system and spinal cord leading to sedation and altered perception of pain. It is believed (but not proven) that generalized sedation is the basis for the muscle relaxation. NO DIRECT EFFECT on neuronal conduction, neuromuscular transmission or muscle excitability.

Carisoprodol

MOA: tricyclic antidepressant-like drug for muscle spasm that has central action; possibly at the level of the brain stem.

cyclobenzaprine

MOA: No direct effect on muscle or excitation-contraction coupling. Effects thought to be due to generalized sedative action. Pain relief due to altered pain perception.

Methocarbamol

MOA: agonist on pre-synaptic α-2 receptor agonist leading to decreased activation of polysynaptic spinal cord motor neurons with concomitant reduction in muscle tone but NOT muscle strength. VERY WEAK anti-hypertensive.

Tizanidine

MOA: acts as GABAB agonist at multiple levels in spinal cord, producing either inhibitory signals or hyperpolarizing and thereby reducing the excitatory (aspartate and glutamate) polysynaptic pathways. Pain relief in spinal cord from inhibition of substance P action.

Baclofen

MOA: decreases muscle contraction by directly interfering (ryanodine receptor) with calcium ion release from the sarcoplasmic reticulum within skeletal muscle cells. Effectively it "uncouples" the excitation-contraction process

Dantrolene

List the skeletal muscle relaxers.

Carisoprodol Cyclobenzaprine Methocarbamol Tizanidine

List the drugs to treat spasticity.

Botulinum Toxin Tizanidine Baclofen Dantrolene

AE: BBW for suicidal ideation; mild increases in HR/BP; hyponatremia secondary to SIADH

SSRIs: Duloxetine, Milnacipran

Which SSRI does NOT have CYP metabolism.

Milnacipran

AE: Rebound symptom worsening upon withdrawal; worsening depression and suicidal thoughts should be monitored; Dizziness, sedation, blurred vision and xerostomia

Pregabalin

AE: Drowziness and dizziness are most common, together with other CNS manifestations like agitation, insomnia, vertigo, ataxia; systemic effects of sedation include asthenia, temporary vision loss, mydriasis, orthostatic hypotension. Additive sedation if combined with other sedative agents.

Carisoprodol

AE: GI problems are major: paralytic ileus; Anticholinergic effects (drowsiness, dizziness, fatigue, N/V, constipation, etc.); additive depression with depressant drugs/alcohol; increase QT interval

Cyclobenzaprine

AE: Increased depression with drugs/alcohol; drowsiness, dizziness, lightheadedness, blurred vision, N/V, HA and irritability.

Methocarbamol

AE: hepatocellular toxicity; rebound hypertonicity, tachycardia and hypertension (need to taper down, especially after high drug doses); additive depression with CNS depressents; additive hypotension; asthenia, xerostomia, dizziness, sedation, hypotension.

Tizanidine

AE: BBW for “rebound” neural activity (seizures, confusion, hallucinations, psychiatric disturbances (especially in those with preexisting CNS conditions!)) and increased spasticity (perhaps advancing to rhabdomyolysis, multisystem failure and death); additive CNS depression; additive hypotension with MAOIs and antihypertensives; increase blood glucose; drowsiness, etc.

Baclofen

AE: floppy baby syndrome; muscle weakness leading to drooling, dysarthria, enuresis, myalgias and backache; additive CNS depression; if combined with CCB→ Vfib and CV collapse

Dantrolene

Fibromyalgia drug that must be monitored for serum creatinine.

Pregabalin

Muscle relaxer that has to be monitored for serum creatinine/BUN.

Carisoprodol

Spasticity drugs that must be monitored for LFTs.

Tizanidine | Dantrolene

MOA: Irreversible acetylation of COX-1 in platelets.

Aspirin

MOA: Produces analgesia and anti-pyretic actions in the CNS by inhibiting COX1 and COX2

Acetaminophen

AE: - Greater GI toxicity than NSAID - Hepatotoxicity - Renal toxicity (rare) - Salicylate poisoning (respiratory alkalosis from hyperventilation)→ CV collapse

Aspirin

AE: | -Acute hepatic failure (metabolic production of highly reactive adducts)

Acetaminophen

``` Drug that you need to monitor: LFTs Serum creatinine/BUN Serum Salicylate concentration Stool Guaiac ```

Aspirin

MOA: reversible, alosteric competitive inhibitor of xanthine oxidase (converts xanthine to hypoxanthine which is converted to uric acid) AND also metabolized (oxidation by XO) to oxypurinol which is a non-competitive inhibitor of XO (when molecule is formed, it binds irreversibly to enzyme and kills it).

Allopurinol

MOA: direct inhibitor of both the oxidized and reduced forms of xanthine oxidase and the enzyme-inhibitor complex is highly stable

Febuxostat

MOA: small molecule that is secreted into the tubular fluid by an organic acid transporter; uric acid is secreted into the tubular fluid by a uric acid transporter (NOT affected by drug)—drug competes with uric acid for reabsorption at the brush border transporter (decreasing the amount of uric acid that is reabsorbed/increases uric acid excretion in the urine).

Probenecid

MOA: This drug works by depolimerizaiton of microtubules of migrating cells so that the cells (PMN/WBC) coming toward the gout cannot move—this prevents the release of pro-inflammatory cytokines and STOPS the gout attack and can be used to prevent recurrence of gouty arthritis.

Colchicine

MOA: COX inhibitor that inhibits leukocyte motility (blocks ability of immune response to attack uric acid crystals→ reduces pain associated with inflammatory response)

Indomethacin

MOA: rapidly lowers serum levels of uric acid and reduces urinary excretion of uric acid; increases serum levels of allantoin and urinary excretion of allantoin (5 times more soluble than uric acid)

Pegloticase

AE: increase incidence of active gout (crystals may dissolve and cause flare-ups—so give NSAID); hypersensitivity reactions (dermatitis, exfoliative dermatitis); effects on liver function (need LFTs every 6 weeks at start)

Allopurinol

AE: transaminase elevations >3 times the upper limit

Febuxostat

AE: patient needs to drink a lot of water to prevent kidney stones as the uric acid crystals in joints break down

Probenecid

AE: GI disturbances (acute—sign you have given too much) and blood dyscrasias (chronic)

Colchicine

AE: occur in 50% of patients: GI (N/V, ulcers); CNS (severe frontal HA); Hematopoietic disorders

Indomethacin

AE: VERY EXPENSIVE; patients need to be prophylactically (with colcicine) protected because crystals can break down in joints and cause gout flares; not for patients with antibodies against the PEG moitey

Pegloticase

Gout drug with longest half life.

Pegloticase

Gout drug that will antagonize furosemide and HCTZ (diuretics).

Indomethacin

Gout drug that's action is inhibited by Salicylates/NSAIDs→ switch to tylenol

Probenecid

Drug with DDIs with: 6-mercaptopurine used for blood cancers (reduce dose to 25%); ampicillin/related antibiotics are contraindicated (because will lead to skin problems)!

Allopurinol

What drug do you use in patients who cannot tolerate allopurinol or have renal dysfunciton?

Febuxostat

RHEUM Pharmacology Flashcards

(85 cards)