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Stack #213009
Drug Induced Skin Disorders
| Question | Answer |
|---|---|
| Incidence of DI Skin Disorders | 2-3% |
| Clinical Findings of DISD cutaneous | redness, facial edema, skin necrosis, blisters/epidermal detachment, positive Nikolsky's sign, urticaria, swelling of tongue or airway, mucous membrane erosions |
| Clinical Findings of DISD General | high fever, enlarged lymph nodes, arthralgias, shortness of breath, hypotension |
| Laboratory Findings of DISD | Eosinophilia, abnormal LFT |
| Pathogenesis of Drug Rxn | hapten formation, drug-hapten complex processed by APC, elicitation of response from T-cells |
| Most common type of drug rash | Maculopapular eruptions |
| Maculopapular Eruptions due to | possibly due to cell mediated response |
| Maculopapular Eruptions present as | flat or raised reddened lesions, few mm to a lrg confluent area, vesicles may be present |
| Maculopapular Eruptions found on this part of body | trunk area or areas of pressure |
| Drugs that can cause Maculopapular Eruptions | Barbituates, Benzodiazepines, NSAIDs. Phenytoin, Penicillins |
| Urticaria (Hives) caused by | circulating IgE immune complexes |
| Urticaria (Hives)occurs in what time frame | Early Rxn: min to hrs of drug exposure__Accelerated Rxn: 12-36hrs__Late Rxn:8-21days |
| Urticaria (Hives)is a ___________type of allergic rxn | psuedoallergic |
| Urticaria (Hives)presents as | raised pruritic erythematous wheals, varying in size, can be the 1st manifistation of anaphylaxis |
| Drugs that can cause Urticaria (Hives) | PCN, cephalosporins, ACE-I, RCM |
| Fixed Drug Eruptions caused by | unknown pathogenesis, cell mediated |
| Fixed Drug Eruptions present as | erythematous round or oval lesions varying in size, tend to not be confluent, local acute inlfammation, hyperpigmentation (chronic) |
| What type of Skin Rxn occurs in the EXACT location as previous rxn upon re-exposure to the offending agent? | Fixed Drug Eruptions |
| Drugs that can cause Fixed Drug Eruptions | Co-Trimoxazole, phenytoin, phenolphthalein, ASA and NSAIDs, tetracycline |
| Two types of Photosensitivity | Phototoxicity and Photoallergy |
| Phototoxicity MOA | UV light activates the drug to emit energy |
| Phototoxicity dependent on | dependent on [ ], absoprtion, and PK of drug as well as amt of light, thickness of skin, and temp and humidity |
| Phototoxicity is a Type ___ allergic rxn | A |
| Photoallergy MOA | UV light + drug form a hapten, not dose dependent |
| Photoallergy Dependent on | location of drug in skin, degree of melanin, immune system of individual |
| Photoallergy is a Type___ allergic rxn | B |
| Phototoxicity presents as | shortly after exposure to sun, sunburn like, hallmark:occurs on area of skin exposed to skin |
| Photoallergy presents as | "solar urticaria", eruptions usually resolve w/ removale of drug but in some cases (topicals) can persist |
| Drugs that can cause Phototoxicity | *Amiodarone, retinoids, tetracyclines, NSAIDs, Sulfonamides, St. Johns Wort, Phenothiazines, Quinolones (different degrees depending on specific agent) |
| Management of Phototoxicity | avoid direct sunlight, tx like sunburn, use protective clothing, sunscreens, EVENING dose strategy |
| Stevens-Johnson Syndrome caused by | cell mediated? |
| Stevens-Johnson Syndrome presents as | epidermal detachment about 10%BSA hands, feet, limbs, face, and mucous membranes |
| Stevens-Johnson Syndrome occurs in___ resolves in___ and heals in ____ | 1-3wk after exposure (re-exposure may occur in 48hrs), 4-5 days and 2-4 wks |
| Stevens-Johnson Syndrome and TENS Prodrome | fever, flu-like sx 1-3 days prior to lesions, skin tenderness, photophobia, conjunctival burning/itching |
| Stevens-Johnson Syndrome lesions | start as ill-defined erythematous macules with purpuric centers, sloughing of skin can begin within days or macule eruptions |
| Drugs that can cause Stevens-Johnson Syndrome | *Allopurinol*, carbamazepine, sulfonamices, phenytoin, PCN, cephalosporins,NSAIDs, iohexol |
| This group of ppl is more likely to have SJS due to a HLA haplotype | Asian people specifically when taking phenytoin or carbamazepine |
| HIV population tends to see more skin rxns with this drug___ | Bactrim (also see bactrim induced neutropenia) |
| Case reports of Stevens-Johnson Syndrome with these drugs | Prilosec, rifampin, irbesartan, zithromax, herbals |
| SJS can manifest as ________in addition to the lesions | arthralgias, myalgias, fevers, and conjunctivitis |
| Toxic Epidermal Necrosis % detachment | epidermal detachment usually > 30%BSA |
| Toxic Epidermal Necrosis preceded by | malaise, fever, HA, myalgias, hours to days before complete manifestation |
| Toxic Epidermal Necrosis lesions | similar to second degree burn or scald, macular lesions with burning sensation |
| Toxic Epidermal Necrosis: Epidermis regenerates in ____ with complete healing in ____ | 3-4 wks and 6-8wks |
| Complications of Toxic Epidermal Necrosis (5) | 1)fluid and electrolyte imbalance__2)erosion of mucous membranes__3)trachea and bronchial involvement__4)age >50__5)death rates similar to brun victims (30% mortality even with tx) |
| Lamotrigine (Lamictal) Prodromal for skin rash | rates of rash 8-10%, mucous membrane involvement, fever lymphadenopathy, facial edema, vomiting, inc in liver nz. |
| Lamotrigine (Lamictal) occurs within the ______ of therapy | first 8 wks |
| Abacavir (Ziagen)(combined with lamuvidine in Kivexa and Epzicom and with lamuvidine and zidovudine in Trizir)____ MOA | Hypersensitivity rxn (1in25 pt), metabolite transported from the liver to other tissues forming a hapten and becoming immunogenic |
| Abacavir (Ziagen) Manifestation | fever, rash, n,v,d, abdominal pain, malaise, resp disfunction **Sx w/o rash can be overlooked :: RECOGNIZE PRODROMAL phase |
| Abacavir (ziagen) occurs in | first 6 wks of therapy usually in 8days |
| Abacavir (ZIagen) testing | Genetic testing for the HLA-B*5701 haplotype (india>western europe>japan) **Screening for this marker now available** |
| Hyperpigmentation can be caused by the following agents | Anticonvulsants (darkening/brown), Antimalarials (lemon), Phenothiazines (blue/gray), Tetracyclines (blue/black), Clofazime (leporasy and bone marrow tx - red/yellow), BCP (milky spots on face or upper torso, caramel)("Cafe au lait" spots) |
| Amiodarone pigmentation | Blue gray pigmentation of head and face exposed to the sun |
| pyridium and urine | bright orange urin |
| propofol and urine | turns it green |
| Define Extravasation | inadvertant administration of a drug that is a vesicant or irritant into the interstitial tissue |
| Irritant define | causes an inflammatory rxn w/ aching, burning, pain and tightness along the needle insertion site and along the vein. Clinical signs include warmth, erythema, *w/o tissue sloughing or necrosis. Sx short in duration w/ no long ter sequelae. |
| Vesicant define | drug that has the potential to cause severe and long term injury. **May result in full loss of underlying skin |
| What to do if extravasation occurs? | stop infusion immediately, elevate extremity, leave catheter in place?, aspirate fluid from area?, give antidote through catheter if not then remove catheter, attempt to aspirate fluid from tissue, do NOT flush the line, |
| Hyaluronidase (Vitrase brand)- MOA | facilitates absorption of infiltrated solutions |
| Hyaluronidase used for extravasation of following drugs | aminophylline (theophyline), dextrose 10%, nafcillin, parenteral nutrition, lactated ringers, radiocontrast media, concentrated infusions of calsium or potassium (these are all drugs with higher osmolality) |
| Phentolamine MOA | alpha-adrenergic blocking agent to dec local vasoconstriction and the resultant ischemia. |
| Phentolamine used for the extravasation of the following drugs | VASOPRESSORS: dobutamine, dopamine, epinephrine, norepinephrine, phenylephrine |
| Sodium Thiosulfate used for extravasation of | mechlorethamine, decarbazine, and cisplatin |
| Dimethylsulfoxide (DMSO)(topical)used for extravasation of | anthracyclines (doxorubicin, mitoxantrone, Idarubicin) |
| Dexrayzoxane (totect) MOA and used for extravasation of | anthracyclines-- derivative of EDTA it is a potent intracellular chelating agent. It inhibits topoisomerase II :: protecting tissue from anthracycline cytotoxicity |
| Warm Compresses | inc drug distribution and absorption by inducing vasodilation |
| Cold COmpresses | localize the extravated fluid, may be helpful if localized antidote were to be locally injected (**avoid in phenytoin extravsation) Mostly used over heated compress. |
| For Cytotoxic agents _____ compress application recommended for all agents EXCEPT _______ and _______ | cold compresses, vinca alkaloids, and epidophyllotoxins (etoposide) |
| Prevention of extravasation | select large veins, patency of IV line should be determined prior to drug admin by flushing with NSS or D5W, agents should be diluted in NSS or D5W, may need to use central veins in some pt |
| Phenytoin (dilantin) | Purple Glove Syndrome- dependent on its infusion rate |
| Three Stages of Purple Glove Syndrome | 1)Pale blue or dark purple discoloration around the IV insertion site 2-12 hrs after the drug was administered__3)Progression occurs during the next 12-16 hours__4)healing starts from periphery and goes to site of injury |
| Purple Glove Syndrome MOA | ?highly alkaline pH of solution may lead to vasoconstriction and thrombosis, poor water solubility, no blatant or visible extravasation (can also occur with Propylene glycol*) |
| PGS MOA 2 | 1) "occult" extrava 2) alkaline sol +neutral blood lead to precipitations 3) catheter insertion or needlestick can lead to microtears |
| Treatment of Purple Glove SYndrome | d/c phenytoin, elevate arm, apply WARM DRY heat, tx pain |
| Prevention of Purple Glove Syndrome | 1)Do NOT admin >50mg/min (push or IV)_2)Dilute ONLY in NSS and mix IMEDIATELY before giving, discard after 4 hours_ 3) Avoid small hand veins_4)Use 20 gauge catheter or lrger w a 0.22 micron filter_5)DO NOT use Bacteriostatic NSS, or dextrose sol |
| Dysguesia | distortion of a correct taste, pos due to intereference w/ chemical composition, flow of saliva, or direct effects on taste receptors__dose related and resolves in days to wks after dc |
| Hypoguesia | blunting or decreased sense of taste |
| aguesia | total lost of taste |
| Drugs that can cause Dysguesia | Clarithromycin(Biaxin) (metallic taste), metronidazole, ACE-I (impaired salty), Griseofulvin (antifungal--taseless), |
| Gingival hyperplasia | inflamed gingival tissue that has fibroblasts and keratinocytes activated by inflammatroy mediators and growth factors. |
| Drugs associated with Gingival hyperplasia | CYA, CCB (partic nifedinpine), often see these two drugs used together, Phenytoin(CYA>Phenytoin>CCB) |
| MOA of Gingival hyperplasia in Cyclosporine | inc fibroblast production of collagen w decreased collagenase activity |
| MOA of Gingival hyperplasia in Phenytoin | mast cell medicated androgen activity on the gingiva |
| MOA of Gingival hyperplasia in CCB | inhibit macrophage-induced cell death of fibroblasts |
| Treatment and prevention of Gingival hyperplasia | good dental hygeine, baseline and throughout tx, correction may need to be surgical. |
Created by:
stormesk
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