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142 Cards in this Set
- Front
- Back
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describe the prescribing cascade
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tendency to prescribe a med that is used to tx the sns or sxs of another medication
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how does the change in volume distribution of lipophilic and hydrophilic drugs change in elderly?
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elderly: dec volume of distribution of hydrophilic drugs and an increase in lipophilic drugs
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which phase of metabolism is greater in the elderly? lesser? what does each phase entail?
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Phase 1: greater in elderly-->oxidation, hydroxoylation and reduction w/ active metabolites.
phase 2: conjugation w/ INACTIVE metabolites |
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what drugs are elderly pts more sensitive to?
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Opioids
benzos CNS- drugs anesthetics |
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what two CV drugs prescribed to elderly pts cause dec sensitization?
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ACE-I and nondihydropyridines
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when is HCTZ NOT an effective antihypertensive?
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when CrCl <30
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what is one of the greatest indicators of anticoagulant response?
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age
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ACE-I + K supplements=
ACE-I + spironolactone= |
Hyperkalemia
Hyperkalemia |
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Digoxin + verapamil=
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slowed impulse and dec contractility
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define drug error:
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inappropriate/incorrect admission, omission, administration or dose (includes giving to do the wrong pt)
just FYI: this is what the FDA says: "any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the health care professional, patient, or consumer." |
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define adverse drug event
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any drug related event incident that results in harm to the pt (does not necessarily mean that an error was made)
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define adverse drug reaction
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rxn implies a casual/ temporal link before the drug and event
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NMS vs Serotonin syndrome:
onset: pupils: Bowel sounds: Neuromuscular tone: reflexes: mental status: rhabdo and elevated transaminases: |
NMS: O: Days- weeks, P: normal, BS: normal or decreased, NM: Lead pipe- rigid everywhere, R: bradyreflexia, MS: alert--> coma, R&T: yes and yes
SS: O: mins to hours, P: Mydriasis, BS: hyperactive, NM: increased in LE, R: hyperreflexia, MS: agitated--> coma; R&T= no and no |
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why would you need to increase the amount of PCN that you give to a premie?
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bc penicillin is an acid labile drug and premies don't have the normal pH drop off that term babies do, so they stomachs are more alkalytic.
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how is percutaneous absorption of medication altered in newborns?
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increased absorption d/t underdeveloped stratum corneum.
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why do newborns require a larger loading dose of a protein drug?
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bc they have a lower amount of protein concentration and therefore a lower amount of drug binding.
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why do newborns require a smaller lipophilic loading dose?
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bc they have an increase in body fat so the distribution will be more diffuse.
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high risk pts for immunosuppressive tx
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African america, pediatrics, broadly presensitized persons, repeat transplants
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ALG toxicity can cause?
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Histiocytic lymphomas, serum sickness
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how are monoclonal abs generated?
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hybridoma: B cells from immunized animals are fused w/ a tumor (myeloma) cell line.
fused: HAT medium (Hypoxanthine, aminopterin, thymidine)- aminopterin inhibits de novo synthesis of nucleotide. --> myeloma cells lack HGPRT |
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what does the muromonab - CD3 induce?
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TCR rapid internalization
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major toxicity muromonab-CD3? how do you lessen the sxs?
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cytokine release syndrome-- 30 min after infusion--> inc in TNF-alpha, IL-2, IL-6 and INF-g
lessen sxs: admin GCs before injection |
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two immunomodulating agents that block IL-2? which one has more toxicity and why?
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Daclizumab and Basiliximab. Basiliximab has more toxicity bc it is a human-mouse IgG1 mAb which has an increased risk of side effects compared to the humanized Daclizumab
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how do calcineurin inhibitors shorten their graft 1/2 life?
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via their nephrotoxicity
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how does cyclosporine work?
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cyclosporine binds cyclophillin which inhibits calcineurin which can then no longer dephosphorylate NFAT--> leading to an inhibition of IL-2
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how does NFAT usually work? what drugs interrupt NFAT?
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cyclophillin activates calcineurin which induces dephosphorylation of NFAT and NFAT translocates into the nucleus and induces a transcription of IL-2 and over cytokines.
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how does Tacrolimus work?
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binds to both cyclophillin and FKBP --> leads to calcineurin inhibitions--> blocks NFAT--> blocking IL-2.
this makes tacrolimus far more potent. |
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what is the problem w/ calcineurin inhibitors?
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Tacrolimus and cyclosporine are very toxic to the body--> causing neurotoxicity, nephrotoxicity, hyperglycemia, HTN and hyperK.
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what cells are affected by calcineurin inhibitors?
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B-cells, T cells and granulocytes
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how does sirolimus work?
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also binds to FKBP but this FKBP binds to mTOR which blocks downstream signalling through TCR and inhibits proliferation.
does NOT inhibit IL/ cytokine production by IL-2 |
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what are the toxicities a/w sirolimus?
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BMS (esp thrombo)
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How do Glucocorticoids (GC) cause in increase in apoptosis of activated cells? which cytokines are downreg by GC?
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by increasing IKB expression which curtails activation of NF-KB
IL-1, IL-6 |
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what six immunosuppressant drugs (besides mono and polyclonal drugs) are approved for use in transplantation?
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Sirolimus, cyclosporine, tacrolimus, GCs, azathrioprine, mycophenylate mofetil
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How does mycophenylate mofetil work? What are the associated toxicities?
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inhibits de novo synthesis of purines--> inhibits T and B lymphocyte responses.
tox: BMS (mainly neutropenia) |
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how does azathrioprine work? what are the associated toxicities?
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Metabolized to 6-thioinosinic acid which inhibit inosinic acid--> inhibiting DNA replication
tox: BMS (leukemia, anemia and thrombocytopenia) |
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What immunosuppressant should you be cautious giving to a pt w/ gout?
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Azathioprine
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which immunosuppressant is used to tx ITP and Autoimmune hemolytic anemia?
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Azathioprine
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how does cyclophosphamide work? a/w what toxicities?
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destroys proliferating lymphoid cells, alkylates some resting cells.
hemorrhagic cystitis and pancytopenia |
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which immunosuppressant presents mass cell degranulation? what is its use?
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Vincristine: used for ITP refractory to prednisone
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what does MTX block?
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thymidine synthesis
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what is the thx for established rejection?
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GCs in high doses (pulse), biologics (polyclonal abs and muronomab)--> attack T cells
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What are the drugs used for induction thx? maintenance?/
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induction: antilyphocyte induction w/ either muronomab or polyclonal
maintenance: calcineurin inhibitor, GCs and an antimetabolite (Azathioprine or Mycophenylate Mofetil) |
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Name the drugs that fit each category:
A) specifically Renal transplants: B) GVHD c) steroid resistant solid organ transplant D) steroid resistant GVHD e) AI F) Derm disorders |
a) ATG, Daclizumab, Dactinomycin
b) cyclosporine, GCs, MTX c) ALG, muronomab D) Sirolimus, Mycophenylate Mofetil E) GCs, Mycophenylate mofetil, Azathioprine, Cyclosporine, anti-TNF-alpha F) Tacrolimus, Sirolimus, Mycophenylate MOfetil |
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what 5 AI dzes can experience remission thanks to immunothx?
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Hemolytica anemia, DM-1, ITP, Hashimoto's, temporal arteritis
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DOC for ITP, AIHA, AGN?
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Prednisone
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which immunosuppressent is CI w/ CHF pts?
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infliximab
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what is MOA of etanercept? toxicities a/w?
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anti-TNF-alpha: blocks TNF-alpha and beta
tox: RTI, infex. +ana, + anti-dsDNA ab |
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what is decreased when a pt is adalimumab?
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ESR, CRP, Matrix Metalloproteinases, IL-6
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what are the two pathways that are necessary for T cell activation?
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pathway 1: via TCR
signal 2: via Costimulatory receptor ligand pair: CD28 on T cell and B7-1 (CD80) & B7-2 (CD86) on APC--> after activated it exposes CD154 (CD40L) which it interacts w/ CD40 on the costimulatory pair |
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what is abatacept composed of? what should abatacept NEVER be taken w/?
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extracellular domain of CTLA-4 fused to human IgG Fc.
CTLA-4 (costim molecule found on T cells that bind to CD80/86). --> inhibits T cell activation--> anergy never take w/ anakinra or other anti-TNF drugs |
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what is the MOA of INF-B? what does it cause?
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acts on BBB by interfering w/ T cell adhesion to endothelium by binding VLA-4 on T cells or by inhibiting T cell expression of MMP.
causes an immune deviation of Th2 over Th1 |
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what drug do you use for a pt w/ MS who is refractory to IFNb?
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Glatiramer acetate
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what immunostimulant is used to tx DUkes class C colorectal CA after sx? toxicitieS?
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Levamisole
tox: Severe agranulocytosis, metallic taste |
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what immunostimulant is currently being used to tx multiple myeloma that is a teratogen? how does it work? tox?
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Thalidomide--> inhibits TNF-alpha and angiogenesis
tox: teratogenicity, peripheral neuropathy, inc risk of DVT |
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what immunostimulant is used to tx bladder Ca?
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BCG
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who do you give GMCSF or GCSF to?
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preterm neonates and neutropenic pts
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what neoplasms are tx w/ TNFalpha?
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hairy cell leukemia, CML, Malignant melanoma, kaposi's sacroma, HBV >6 months, and HCV
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what neoplasms are txed w/ INF-gamma?
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CGD
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what neoplasms are txed w/ IL-2?
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metastatic renal cell CA and malignant melanoma
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specific immune globublin preps are available for what 6 infections?
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hep B, rabies, Tetanus, CMV, VZV, RSV
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how do you tx follicular B cell or nonhodgkin's lymphoma? what if the pt is resistant to that drug?
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Rituximab (binds CD20).
resistant: Ibritumomob tuxetan |
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how do you tx metastatic breast cancer? CLL?
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Breast: Trastuzumab
CLL: Alemtuzumab |
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what is the prophylaxis for RSV?
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Palivizumab
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How does abciximab work>?
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binds GP2b/3a on activated platelet--> inhibits fibronogen, vWF Preventing platelet aggregation.
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what are the 5 common unintentional poisonings?
what are the 4 common intentional poisoninigs? |
opioids, cocaine, heroine, acetaminophen, benzos
opioids, acetaminophen, BZDs, sedatives |
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acetaminophen, how does it cause damage? when does toxicity present? tx?
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the 5% that undergoes CYP450 oxidation is changed to NAPQI which reacts w/ glutathione to form an inactive product. NAPQI when it builds up destroys hepatocytes and renal tubular cells.
tox: 12-24 hours after ingestion tx: activated charcoal, N-acetylcysteine (glutathione precursor), antiemetic PRN |
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what can OD of ethanol glycol cause? what does methanol turn into? what does it cause? tx?
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calcium oxalate crystalluria--> rhabdo and renal failure
methanol--> formic acid--> irreversible blindness tx: Fomepizole. For ethylene glycol add pyridoxine and thiamine. For methanol add leucovorin |
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tx of organophosphate poisoning?
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Atropine and Pralidoxime (breaks covalent bond b/w organophosphates and AChE.
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what are the anticholinergics? sxs of anticholinergic toxicity? tx?
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benztropine, antihistamines, phenothiazines, jimson weed and mushrooms
sxs: dry as a bone, red as a beet, hot as a pistol, mad as a hatter, blind as a bat tx: physostigmine |
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tx of lead poisoning?
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EDTA and dimercaprol, mannitol, bzds
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how does arsenic poisoning work?sxs? tx?
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disruption of enzymes req for oxidative phosphorylation.
sxs: abd pain, N/V, GI hemorrhage, cardiogenic shock, hypotension, delirium ,polyneuropathy tx: dimercaprol |
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"garlic breath and rice water stools?
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Arsenic poisoning
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how does Iron poisoning work? sxs? tx?
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disrupts oxidative phosphophorylation--> forming FRs which causes lipid peroxidation & cell death.
sxs: GI sxs, shock tx: deferoxamine mesylate. |
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how do you tx asphyxiant poisoning? what about CN specifically? what if the pt is spontaneously breathing?
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hyperbaric oxygen thx.
CN: sodium nitrite, sodium thiosulfate. spontaneously breathing= hold amyl nitrite pearls under nose. |
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relaxation of jaws and ankles + sustained rapid eye movement. what is it and how do you antagonize this?
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Serotonin syndrome
antagonize: Cyproheptadine |
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what is the urinary metabolite of cocaine? How does cocaine work? what is produced when you mix cocaine and alcohol?
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Benzoylecgonine
cocaine blocks the reuptake of NE and DA. Benzoylecgonine + etoh --> cocaethylene--> death |
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what should you never give to a person w/ a cocaine overdose?
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B-blocker= will cause significant alpha adrenergic overdrise
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how do you tx bupoprion overdose or body stuffers for cocaine ?
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bowel irrigation
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What should you never do to a person w/ corrosives poisoning? how do you tx?
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induce emesis or give charcoal
tx: dilyte w/ water or milk. |
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what is the tx for rattlehead, copperhead or cottonmouth snake bite?
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restrict blood flow/ perfusion. Antivenom: crotaline polyvalent Fab.
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what are the four abnormalities that lead to acne?
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Hyperkeratinization (increase in loose cells in follicle),
sebum production: androgens bacterial component (p. acnes--> produces lipases that form FFA) Inflammation: response d/t irritation by FAs |
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when are topical txs for acne CI? what do you give the pt instead?
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if likelihood of scarring. give oral pills instead.
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how do you tx mild/ moderate localized acne? how about severe, widespread- back, arms, etc?
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localized: topical
diffuse: oral |
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what is the MOA of benzoyl peroxide for acne? SE?
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Kerolytic/ comedolytic, antibacterial and antiinflammatory.
se: salicylism (+ all the irritation ones) |
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what is the MOA of topical sulfur compounds for acne?SE?
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Keratolytic
se: odor, stain, comedogenic w/ LT use |
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what is the MOA of azeliac acid for acne?
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inhibits thioredoxin and tyrosinase, scavenges FR.
keratolytic, anti-inflammatory se: hypopigmentation (used to tx hyperpigmentation)--> antimitochondrial and antityrosinase activities |
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1st/ 2nd gen retinoids vs 3rd gen?
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1st/2nd gen= more flexible and more SEs; 3rd gen: less flexible and less SEs
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how do retinoids regulate gene trascription?
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by having an endogenous ligand for RARs and RXRs (retinoic X receptors) (RARs= positive, RXRs= negative). These ligand/ receptor complexes (RA/RAR) form a complex which forms a transcription factor--> binds directly to DNA gene promoter regions (DNA--> mRNA)--> new proteins.
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MOA of tretinoin. SEs?
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binds to RARs and induces mitosis (increased cell turn over--> dec cell adhesion--> keratolysis). prevents formation of new microabscesses.
SE: worsening acne before getting better, degrades in UV light, and have anti-wrinkle effects. |
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all topical retinoids are?
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keratolytic and anti-inflammatory
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MOA of adapalene. SEs
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Binds to RARs and acts sim to tretinoin and delivers it to the pilosebaceous unit. Milder SEs than tretinoin and resistant to degradation by UV light.
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Topical retinoid txs? Oral retinoid txs?
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topical: tretinoin, adapalene
PO: Tazarotene, Isotretinoin |
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MOA tazarotene. SE
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prodrug that is converted by esterases in the skin. 3rd gen. UV stable.
Dec mitosis and normalizes keratocyte production by binding to ornithine decarboxylase SE: Pregnancy cat X + tretinoin sxs |
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MOA: Isotretinoin. SEs
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Only drug that covers all four areas for acne formation (K, B, I, S).Binds RARs. This is a/w cis retinoic acid.
SE: epistaxis, ALopecia, conjunctivitis... severe: aboid sunlight, Cat X (craniofacial, cardiac, thymic, CNS abnormalities). |
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which drug to tx acne has a tetracycline interaction? what does it cause?
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ISotretinoin. Causes pseudotumor cerebri.
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which antibiotic tx for acne inhibits translocation and binds at 50s? which antibiotic tx for ance inhibits protein synthesis and binds at 50 s/ which antibiotic tx for acne inhibits translation and binds 30s?
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1) Erythromycin
2) Clindamycin: also inhibits translocation, peptidyl transferase, and peptide bone. 3) tetracycline: blocks amino acid-acyl tRNA binding to A site (inhibiting elongation). |
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wht drug can cause pseudomembranous colitis as a SE?
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clindamycin
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what drug binds to Ca ions and is decreased by concurrent use of antacids?
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Tetracycline: also inhibits effectiveness of OCP.
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what are the two cousins of tetracycline used to tx acne? what makes them different
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Doxycycline: 2x greater potency--> incr incidence (except Ca)
minocycline: 2-4x greater potency--> dec incidence but also ototox, vestibular effects, CNS effects |
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what SE is a/w ethinyl estradiol and norgestimate for acne tx? MOA?
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incr clotting. risk of MI in high risk pts is increased.
moa: inc SHBG and dec Testosterone |
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what is the AI process of psoriasis?
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T cells in the LN are activated by APC and then they enter the blood stream until they get to the dermis where they (esp Th1) are activated by APC again. --> psoriasis
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tx drugs for psoriasis?
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emollients & keratolytics (salicylic acid)
immunosuppressants: CS, cyclosporine, alfacept, eflaizumab, adalimumab |
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tx for hyperproliferation of keratinocytes in relation to psoriasis?
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Topical: Coal tar, Vit D, retinoids
system: retinoids, MTX |
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what is an alternative to CS for txing psoriasis?
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Tar compounds
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where do you use very high potency CS on for acne? high potency?
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very high- not on face
high: on face for short periods of time |
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SE of CS for acne?
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iatrogenic cushings, suppression of pituitary adrenal axis
local: purpura, ecchymosis, steroid rosacea, contact dermatitis |
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what are the SEs for cyclosporine? what about D/D interactions?
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renal dysfxn, hirsuitism, HTN, Gum hyperplasia
D/D: additive nephrotox w/ (prednisolone, digoxin, statins) |
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MOA of alefacept, SE?
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interfers w/ interactive w/ APC--> dec active T cells.
SE: CD4 lymph count. |
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adalimumab SE:
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susceptibility to infxn (latent TB), allergic rxn, lupus like syndrome
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what retinoid drug has a worse side effect profile than isotretinoin?
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Acitretin: more teratogenic.
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acne tx: Transient epidermal hyperplasia followed by cytostatic effect and epiderma thinning
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tar compounds
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MOA of calcipotriene? SE?
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inhibit keratocyte differentiation and proliferation--> dec Th1 stim cytokines
se: transient increase in Ca |
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MOA of MTX? SE?
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inhibit dihydrofolate reductase (DHFR)--> blocks DNA synthesis.
SE: hepatic fibrosis |
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what is required w/ PUVA thx?
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psoralen-methoxalen (intercalates DNA base pairs)
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Describe schedule 1-5
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1) highest abuse risk, no safe med use (heroin, MJ)
2) high abuse risk, safe & accepted (Morphine, oxy) 3) abuse risk <C2 safe & accepted (Vicodin) 4) abuse risk <C3, safe & accepted (diazepam) 5) Abuse risk <C4, safe & accepted (loperamide) |
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schedule 3 drug: how many refills? Schedule 2?
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3: 5 refills in 6 months
2: no refills |
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when do legend drugs expire? schedule 3-5? 2?
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legend: 1 yr
3-5: 6 months 2: 7 days |
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what is "sig"?
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directions to the pt
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abbreviations, what do they mean?
1) PRN 2) ggt (s) 3) q 4) tid 5) qid 6) qhs 7) hs 8) p.o. 9) o.u. 10) o.s. 11) o.d. |
1) As needed
2) drop(s) 3) once 4) three times a day 5) four times a day 6) once at bedtime 7) At bedtime 8) by mouth 9) both eyes 10) left eye 11) right eye |
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define: cellular tolerance? Metabolic tolerance?
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changes in NT levels and receptor # and activity
met: allows for inc drug elimination w/ longer use. |
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ethanol works on what receptors?
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facilitates GABA, inhibits NMDA receptors
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what drugs are CI w/ ethanol?
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benzos and barbs
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fetal alcohol syndrome:
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mental retardation, growth deficiencies, microcephaly, underdev of midface region. (epicathal folds, short palpebral fissures). EtOH--> Free fatty acids
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tx of alcoholism
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disulfram: acetaldehyde dehydrogenase inhibitors
acamprosate: dec glutamate receptors= dec craving propranolol: alcohol withdrawal (tremors, HR) |
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what is crack?
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cocaine + hydrochloride
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what does cocaine block? sxs of cocaine
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DA transport, and NE and 5-HT reuptake
sxs: inc alertness sexual drive, HR, bp, Temp, mental alertness. Mydriasis dec appetite, |
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what can ingested cocaine cause?
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severe bowel gangrene
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how does cocaine cause malignant HTN in preggers?
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by inhibiting uteroplacental circulation
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Mescaline and psilocybin are another name for? MOA?
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LSD
moa: stim of presynaptic and postsynpatic 5-HT receptors |
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what readily destroys cocaine?
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plasma cholinesterase
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Mydriasis + color seems more intense and shapes are altered. dx
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LSD
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what agents cause dissociation?
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PCP (Phencyclidine) and ketamine
dextramethorphan at high doses can cause this too. |
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MOA of dissociative agents?
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Blocks NMDA-type glutamate recptors in cortex and limbic structures (like alcohol)
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MOA of meth?
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DA and adrenergic reuptatke inhibitor (blocks MAO-a)
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what is the most addictive part of meth?
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the rush (intense euphoria) that comes immediately after the spree.
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Pt exudes increased alertness and self-confidence. Hasn't eaten in the past 12 hours and is incredibly provacative acting. Dx
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MEth
a/w meth mouth |
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sxs of MDMA "ecstasy"? what can high doses of MDMA do?
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acute: tachycardia, dry mouth, jaw clenching, muscle aches. insomia, confusion.
high doses can interfere w/ ability to regulate body temp (Liver, kidney and CV sys failure) -sim to NMS. |
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MOA of opiates?
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mu receptors. Gi receptors--> dec cAMP--> dec presyn firing in SC and post syn firing in brain.
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when does abstinent withdrawal from opiates peak? tx? maintenance?
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48-72 hrs. Muscle spasm, autonomic hyperexcitability.
tx: initial: buprenorphine--> methadone [ short term (30 days) or long term (180)] maintenance: buprenorphine + naloxone. |
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What causes a precipitated withdrawal of opiates?
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induction of administered opioid antagonist
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"date rape drug"?"z-bars"?
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benzodiazepines
date rape: flunitrazepam Z-bars: Alprozolam (dec desire for alcohol but when taken w/ alcohol--> CNS depressant) |
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benzo OD tx? withdrawl/detox?
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flumazenil
withdrawal: chlodiazepoxide or lorazepam (5-7 days) |
