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Dermatology Board Prep > DERM (19) Urticaria, Erythema, and Purpura > Drug Reactions > Flashcards

Drug Reactions Flashcards

1
Q

What are the preformed mediators in mast cells?

A

Proteases (tryptase, chymase), heparin, histamine

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2
Q

What are the synthesized mediators in mast cells?

A

prostaglandins, leukotrienes, platelet activating factor, cytokines

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3
Q

If a pediatric patient gets DRESS on phenytoin for seizures, what medication should they be switched to and what ones should they not be transitioned to?

A

Can transition to Valproic acid, there is no cross-reactivity.

There is cross-reactivity with all aromatic anticonvulsants = phenytoin, carbamazepine, and phenobarbitol

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4
Q

How are cutaneous drug reactions divided?

A

Simple (no visceral/systemic involvement) and complex (systemic involvement)

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5
Q

What is the prevalence of severe cutaneous adverse reactions among patients with drug reactions?

A

2% (SJS/TEN, DRESS/DHS, AGEP, anaphylaxis anticoagulant-induced skin necrosis, and generalized fixed drug)

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6
Q

What are the most common morphologies of drug rash?

A

Morbilliform (92%)>>>urticarial (6%)>vasculitis (2%)

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7
Q

When are HIV patients at the highest risk of getting cutaneous drug reactions?

A

Increased risk across the board, but the highest risk is when CD$ count is 100-400/mm3

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8
Q

What are the most common causes of cutaneous drug rash in patients with HIV?

A

TMP/SMX (rash in 40% of HIV pts), dapsone, beta-lactams, nevirapine, abacavir, and anticonvulsants

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9
Q

What is the timing of a morbilliform drug rash?

A

7-14 days after drug initiation (cell-mediated hypersensitivity)

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10
Q

What are the most common culprits of morbilliform drug rash?

A

Beta-lactams, TMP/SMX, anticonvulsants, and allopurinol

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11
Q

What viral infections significantly increase the risk of rash from medications?

A

HIV: especially true for TMP/SMX (40%)

EBV: ampicillin in pts w/ EBV-mononucleosis gives rash in all children and 70% of adults

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12
Q

What is the clinical presentation of a morbilliform drug rash?

A

The rash starts w/ red-pink macules and papules in the groin/axilla and later progress to symmetrically-distributed red macules and papules on the trunk and upper extremities often w/ pruritus (note that viral exanthems aren’t usually pruritic)

  • Rash becomes more confluent over time and the lesions on the lower extremities can have a purpuric component

Doesn’t affect mucous membranes, no facial edema, no peripheral eosinophilia, no dusky/painful lesions on the skin

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13
Q

What is the progression of simple morbilliform drug rash?

A

Clears after 1-2 weeks after drug cessation (will also stop if the drug is continued… doesn’t progress to angioedema/more serious reaction in vast majority of pts)

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14
Q

What is the histology of a simple morbilliform drug reaction?

A

MIld basal vacuolar and spongiotic changes w/ few necrotic keratinocytes (50%). Can have superficial to mid dermal perivascular lymphohistiocytic infiltrate w/ some eos

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15
Q

What is the prognosis of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

10% mortality

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16
Q

What is the timing of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Occurs later, 2-6 weeks after initiation of a drug

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17
Q

What are the most common sx’s in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Fever (85%), morbilliform skin eruption (75%), arthralgias (>arthritis), multi-organ involvement (liver is most common and severe followed by kidney), peripheral eosinophilia (>1500 absolute eos), mononucleosis-like atypical lymphocytosis

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18
Q

What is the usual progression of the rash in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Starts on the face and upper trunk/extremities; appears morbilliform but can become more edematous (facial edema is important early sign), with follicular accentuation and you can have tense vesicles or bullae, pustules, and purpuric lesions

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19
Q

What are the late sequelae that can occur in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Thyroiditis/Graves, SIADH, and diabetes

Can occur up to a year out from initial rash

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20
Q

What virus is thought to be involved in the pathogenesis of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

HHV-6 reactivation (>HHV-7, CMV, and EBV)

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21
Q

What is the most common classes of meds that are known to cause Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Aromatic anticonvulsants (phenytoin, carbamazepine, and phenobarbital), lamotrigine (especially when coadministered w/ valproate), sulfonamides, minocycline, dapsone, allopurinol, abacavir, and nevirapine

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22
Q

Which medications are more likely to affect the liver in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Dapsone, Minocycline, aromatic anticonvulsants

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23
Q

Which medications are more likely to cause cardiac issues in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Ampicillin, minocycline

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24
Q

Which medications are more likely to cause renal damage in Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Allopurinol, carbamazapine, dapsone

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25
Q

What patients are at higher risk of allopurinol hypersensitivity syndrome?

A

Patients with renal failure, Han Chinese with HLA-B*5801,

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26
Q

What clinical differences can be seen in the allopurinol hypersensitivity syndrome as compared to Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS) in general?

A

Liver involvement in 70%, kidney involvement in up to 80%, can also cause pancreatitis and diabetes

25% mortality

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27
Q

Clinical presentation of dapsone hypersensitivity syndrome?

A

Concomitant hemolysis and methemoglobinemia is common

Look for increased bilirubin, icterus, LAD (80%), lacks eosinophilia, liver involvement can be fatal

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28
Q

What are some important clinical components of minocycline hypersensitivity syndrome?

A

Usually seen in young adults getting tx for acne. Associated with glutathione S-transferase deficiency

Strong association with interstitial eosinophilic pneumonia; liver involvement in 75%; renal involvement in up to 20%

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29
Q

What is the treatment of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?

A

Stop the medication and give superpotent topical steroids for skin-limited dz or systemic steroids if lung and heart involved (questionable efficacy in renal or liver dz)

relapse common if steroids tapered too rapidly (need to give for weeks to months)

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30
Q

What things can induce acute generalized exanthematous pustulosis (AGEP)?

A

Medications most common: beta-lactam antibiotics, NSAIDS, etc

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31
Q

What is the timeline for acute generalized exanthematous pustulosis (AGEP)?

A

Occurs rapidly (<4 days) after drug administration

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32
Q

What are the clinical features of acute generalized exanthematous pustulosis (AGEP)?

A

High fever and small (<5mm) non-follicular, sterile pustules arising on a background of edematous red skin

Commonly begins on the face and intertriginous sites and then generalizes within hours

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33
Q

What clinical findings help distinguish acute generalized exanthematous pustulosis (AGEP) from pustular psoriasis?

A

AGEP more commonly have purpuric or EM-like lesions (50%), mucosal involvement, edema of face/hands, or bullae

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34
Q

What lab findings are seen in acute generalized exanthematous pustulosis (AGEP)?

A

Increased WBC with peripheral neutrophilia +/- eos, hypocalcemia, and renal insufficiency

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35
Q

Most common drugs in acute generalized exanthematous pustulosis (AGEP)?

A

Beta-lactam, macrolide antibiotics, calcium channel blockers (diltiazem most common), and antimalarials (longer latency)

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36
Q

What is the histology of acute generalized exanthematous pustulosis (AGEP)?

A

Subcorneal and intraepidermal spongiform pustules, prominent superficial dermal edema, perivascular mixed inflammatory infiltrate w/ eos

Shouldn’t see eos in psoriasis

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37
Q

What histologic features help distinguish acute generalized exanthematous pustulosis (AGEP) from pustular psoriasis?

A

Edema, eos, and lack of acanthosis helps distinguish AGEP from pustular psoriasis

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38
Q

Treatment for acute generalized exanthematous pustulosis (AGEP)?

A

Stop medication that is causing it, supportive therapy w/ topical steroids and antipyretics

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39
Q

What are two types of photosensitive drug reactions?

A

Phototoxic (most common) or photoallergic

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40
Q

What is a phototoxic reaction?

A

Most common and predictable. Most commonly occurs with systemic medications

caused by direct interaction between UVR (UVA most commonly) and drug/drug metabolites which then produce free radicals and damage to skin cells

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41
Q

What is the clinical presentation of a phototoxic medication reaction?

A

Painful exaggerate sunburn-like eruption that can have blistering. This heals with hyperpigmentation

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42
Q

What is the histopathology of a phototoxic medication reaction?

A

Same as sunburn (necrotic keratinocytes (“sunburn cells”), dermal edema, minimal dermal inflammation, and vasodilation

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43
Q

What are the most common medications to cause a phototoxic medication reaction?

A

Tetracyclines (democlocycline>doxycycline>TCn>>>>>minocycline), NSAIDs (naproxen, piroxicam), fluoroquinolones, amiodarone, psoralens, phenothiazines (chlorpromazine and prochlorperazine), voriconazole (can increase risk of SCC), St. Johns Wort, and HCTZ

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44
Q

What medications can cause pseudoporphyria?

A

This is an exaggerated phototoxic reaction:

Naproxen (#1), thiazides, voriconazole, furosemide, TCN’s, nalidixic acid, and tanning bed exposure

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45
Q

What are some differences between pseudoporphyria and PCT?

A

Unlike PCT, pseudoporphyria does not have: hypertrichosis, sclerodermoid features, and hyperpigmentation

porphyrin studies will be normal, histology is similar

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46
Q

What medications are known to cause photoonycholysis?

A

Another form of phototoxic reaction:

  • Psoralens and tetracyclines
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47
Q

What medications can cause a slate-grey hyperpigmentation?

A

Amiodarone, TCAs, and diltiazem

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48
Q

What medications can cause photolichenoid drug reactions?

A

HCTZ and NSAIDs

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49
Q

What plants can cause phytophotodermatitis?

A

Also a phototoxic drug reaction basically

Furocoumarin-containing plants: parsley, celery, lime, fig, and yarrow

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50
Q

What is a photoallergic drug reaction?

A

It is less common, more chronic, and is idiosyncratic (not dose-dependent). It only occurs in sensitized patients (delayed-type hypersensitivity); often persists after the withdrawal of medications and is most commonly caused by topical photoallergans

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51
Q

What is the mechanism of drug photoallergy?

A

Cell-mediated hypersensitivity; UVR (especially UVA) induces chemical changes in the drug that makes it become a photoallergen; requires sensitization with a 7-10 day incubation period

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52
Q

What is the clinical presentation of a photoallergic reaction?

A

Itchy, eczematous to lichenoid eruption on sun-exposed areas initially but can spread to non-sun-exposed sites

less likely to be bullous/intense than phototoxic

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53
Q

What is the histology of a photoallergic reaction?

A

Spongiotic dermatitis, superficial perivascular inflammation, and eosinophils (not sunburn cells/signs of toxic damage)

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54
Q

What are the most common causes of photoallergic reactions?

A

Oxybenzone (most common)> fragrances (6-methyl coumarin, musk ambrette, and sandalwood oil), NSAIDs (piroximcam and ketoprofen), griseofulvin, quinidine/quinine, sulfonamides, and quinolones

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55
Q

How do you confirm the diagnosis of a photoallergic reaction?

A

Photopathc testing (using UVA)

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56
Q

What patch test is piroxicam sensitive to?

A

Thimerisol

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57
Q

What is the most common presentation of drug-induced pigmentary changes?

A

May be localized or generalized but are often in a photodistribution

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58
Q

What are the mechanisms of drug-induced pigmentary change?

A

1) drug/drug metabolite deposition 2) induction of melanin production 3) post-inflammatory changes due to photosensitive eurptions

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59
Q

What other cutaneous findings aside from skin can be affected in drug-induced hyperpigmentation?

A

Melanonychia (longitudinal, diffuse or transverse) and/or oral hyperpigmentation

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60
Q

What are the most common drugs to cause drug-induced hyperpigmentation?

A

Minocycline, chemotherapeutics, AZT (zidovudine), antimalarials, and heavy metals

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61
Q

What is the time course of drug-induced hyperpigmentation?

A

Is often reversible but takes a long time (months to years)

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62
Q

What types of medications often cause hypopigmentation?

A

Most commonly topical medications, but can also be caused by tyrosine kinase inhibitors like imatinib (inhibits c-KIT)

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63
Q

Why do tyrosine kinase inhibitors cause hypopigmentation?

A

They inhibit c-KIT

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64
Q

What are the most common agents to cause drug-induced hypopigmentation?

A

Phenols/catechols (including hydroquinone, MBEH, MMEH, various phenol derivatives, p-cresol) 2) sulfhydryls (including methimazole) and; 3) miscellaneous drugs like PPI, corticosteroids, azelaic acid, benzyl alcohol, tyrosine kinase inhibitors, mercurials, arsenic, thiotepa, and physostigmine

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65
Q

What agent causes irreversible drug-induced depigmentation?

A

MBEH (permanent at the local reaction and distant)

Methyl benzyl ester of hydroquinone, used for depigmentation therapy of vitiligo

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66
Q

When does coumadin-induced skin necrosis tend to occur?

A

2-5 days after drug initiation (when protein C levels are at nadir)

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67
Q

Why does coumadin-induced skin necrosis tend to happen at 2-5 days after starting therapy?

A

That is when protein C levels are at the nadir

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68
Q

What is the clinical presentation of coumadin-induced skin necrosis?

A

Painful red plaques that then progress to hemorrhagic bullae, ulcers on fatty areas like the breast, buttocks, and thighs

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69
Q

What is the histology of coumadin-induced skin necrosis?

A

Non-inflammatory thrombotic vasculopathy (multiple fibrine thrombi in dermal/SQ vessels with no LCV)

70
Q

What is the mechanism of heparin-induced skin necrosis (HITT syndrome)?

A

Autoantibodies against heparin/platelet factor 4 complexes occur which leads to platelet aggregation and consumption. The resulting thrombocytopenia and clotting (due to platelet aggregates) lead to pathology

71
Q

What is the clinical presentation of heparin-induced skin necrosis?

A

Systemic syndrome with decreased platelet levels, thrombosis and cutaneous necrosis

Note that this occurs with unfractionated heparin more than tractionated LMWH

72
Q

What is the treatment of heparin-induced skin necrosis?

A

Stop heparin, start direct thrombin inhibitor or factor Xa inhibitor

73
Q

What is the histology of heparin-induced skin necrosis?

A

Thrombotic vasculopathy with platelet aggregates (not easy to see on H&E)

74
Q

What is the clinical presentation of bromoderma or iododerma?

A

Acneiform lesions, papulopustules, nodules, vegetating lesions simulating P. Vegetans or blastomycosis; clear or hemorrhagic blisters (iododerma> others)

Skin lesions occur after chronic exposure

75
Q

What is the histology of bromoderma/iododerma?

A

Pseudoepitheliomotous hyperplasia with intraepidermal neutrophilic microabscesses and dense dermal neutrophilic inflmation (r/o deep fungal infxn)

76
Q

What cutaneous reactions can be seen at sites of carmustine and nitrogen mustard administration?

A

Hyperpigmentation at sites of topical application due to increased melanocytes and melanin in keratinocytes

77
Q

What cutaneous findings are caused by bleomycin?

A

linear or flagellate hyperpigmentation in patches on the trunk; hyperpigmentation of palmar creases and skin overlying joints that can be a/w minor trauma/scratching

Can also see transverse melanonychia, sclerodermoid changes

78
Q

What cutaneous side effects can be seen with busulfan?

A

Addison’s-like generalized hyperpigmentation with or w/o pulmonary fibrosis (see an increase in melanin in keratinocytes and dermal melanophages)

79
Q

What cutaneous side effects can be seen from cyclophosphamide?

A

Diffuse mucocutaneous hyperpigmentation or localised hyperpigmentation in nails, teth, palms/soles (resolves within 12 months)

80
Q

What pigmentation changes can occur in ifosfamide administration?

A

hyperpigmentation of the flexural areas, hands, feet, scrotum a,nd under occlusive dressings

81
Q

What is a distinctive pigmentation finding in systemic 5-FU administration?

A

Serpentine hyperpigmentation overlying veins that were infused (histology shows necrotic keratinocytes, pigment incontinence, and increased melanin in basal keratinocytes)

82
Q

What skin findings can be seen in hydroxyurea?

A

Early lichenoid or DM-like reaction overlying joints and can lead to PIH at involved sites; melanonychia, lunula hyperpigmentation

83
Q

What pigmentation change can occur with sunitinib administration?

A

Depigmentation of hair and yellowing of the skin

84
Q

What pigmentation changes can be induced by doxorubicin?

A

Hyperpigmentation of the skin overlying the dorsal hands/joints, palmar creases, and oral mucosa and soles

  • Transverse melanonychia,
  • Increased melanocytes and melanin in keratinocytes
85
Q

Hyperpigmentation occurs in what percent of patients taking antimalarials?

A

25%

86
Q

What is the histology of antimalarial induced hyperpigmentation?

A

Deposition of drug-melanin complexes (Fontana Masson+) and hemosiderin (Perls+) in the dermis

87
Q

What is the presentation of pigmentation changes in pt’s getting chloroquine/hydroxychloroquine?

A

Blue-black to grey hyperpigmentation on the pretibial area that looks like type II minocycline hyperpigmentation of the sins. Can also occur less commonly on the face, oral mucosa and sclera

88
Q

What pigmentary changes can occur in patients getting quinacrine?

A

Diffuse yellow-brown discoloration of the skin and eyes that can mimic jaundice

89
Q

What is the clinical presentation of arsenic exposure?

A

Hyperpigmentation patches with superimposed “raindrops” of hyperpigmentation most commonly on intertriginous sites, palms/soles, pressure points

90
Q

How long after exposure to arsenic do the skin lesions occur?

A

Up to 20 years

91
Q

What are the late features of the cutaneous arsenic exposure?

A

Palmoplantar hyperkeratosis, SCC (after the hyperpigmentation stage)

92
Q

What is the histology of arsenic exposure and the resulting skin findings?

A

Deposits of arsenic in dermis and epidermis + increased melanin in keratinocytes

93
Q

What pigmentation does gold cause?

A

Blue-gray hyperpigmentation on face (periocular is #1)and other sun-exposed sites

94
Q

What is the histology of gold induced hyperpigmentation?

A

Gold deposits in macrophages in perivascular/peri-eccrinedistribution; particles have an orange-red birefringence on polarized light

Does not bind to the BMZ or eccrine membrana propria (distinguishes this from argyria)

95
Q

What is the clinical presentation of argyria (silver-induced hyperpigmentation)?

A

Diffuse slate-gray pigmentation, w/ accentuation in photo-exposed areas; due to silver in alternative medicines and elixirs and silver sulfadiazine on burn wounds

96
Q

What is the histology of argyria?

A

Deposits of silver bound to the BMZ and membrana propria of eccrine glands (best seen with darkfield microscopy)

97
Q

What percentage of patients on amiodarone will get cutaneous changes?

A

60% of patients on amiodarone for more than 3-6 months will get hyperpigmentation

98
Q

What is the clinical presentation of amiodarone-induced hyperpigmenation?

A

Phototoxic eruption (erythema of the face and other photo-exposed areas). In a smaller percentage of patients they can get a slate-gray discoloration that is most common after long-term use. This will go away slowly after drug is discontinued

99
Q

What is the histology of amiodarone-induced hyperpigmentation?

A

Unique yellow-brown granules of lipofuscin (Fontana Masson+) in macrophages in a perivascular distribution

Electron microscopy shows lipid-like lysosomal inclusions which is unique to this condition

100
Q

What pigmentation changes can occur with AZT (zidovudine treatment)?

A

Widespread mucocutaneous hyperpigmentation (reversible) with accentuation in photo-exposed sites and sites of friction

Also frequently see longitudinal melanonychia (more than transverse or diffuse)

101
Q

What is the clinical presentation of pigmentary change from clofazimine?

A

Occurs in the setting o leprosy treatment most commonly. Looks like minocycline-induced pigment changes. Can induce the diffuse red-brown color of the skin and conjunctivae or lesional hyperpigmentation (blue-gray discoloration on face)

102
Q

What is the histology of clofazimine induced pigment change?

A

Birefringent red crystals of clofazimine seen in perivascular distribution on fresh frozen tissue only (missed on H&E)

103
Q

What is the presentation of diltiazem-induced hyperpigmentation?

A

Occurs in Fitz IV-VI patients

Slate-gray discoloration on photo-exposed skin with reticular or perifollicular pattern

104
Q

What is the histology of ochronosis from excessive hydroquinone use?

A

Yellow-brown, banana-like deposits in the dermis

the hyperpigmentation fades after stopping the medication

105
Q

What is type 1 minocycline-induced hyperpigmentation?

A

Focal blue-black hyperpigmentation at sites of inflammation or scars (esp acne scars). This is not dose-related

106
Q

What is type 2 minocycline-induced hyperpigmentation?

A

Circumscribed blue-gray “bruise-like” hyperpigmentation of pretibial area and arms

107
Q

What is type 3 minocycline-induced hyperpigmentation?

A

Diffuse brown hyperpigmentation of sun-exposed areas; due to low-grade phototoxic dermatitis

108
Q

What is the histology of type 1 minocycline-induced hyperpigmentation?

A

Dermal deposits of drug complexes with iron/hemosiderin (Perls+)

109
Q

What is the histology of type 2 minocycline-induced hyperpigmentation?

A

Dermal deposits are drug complexes with both iron/hemosiderin (Perls+) AND melanin (Fontana Masson+)

110
Q

What is the histology of type 3 minocycline-induced hyperpigmentation?

A

Increased melanin in basal keratinocytes, dermal melanophages/melanin (Fontana Masson+)

111
Q

Fetal exposure to tetracyclines stains the teeth at different locations, what are these locations for minocycline and tetracycline?

A

Minocycline: mid-portion of the teeth

TCN = gingival one third

112
Q

What changes can be seen from prostaglandin analogs?

A

Periocular hyperpigmentation, eyelash hypertrichosis, and iris hyperpigmentation may follow the use of glaucoma medications

resolve as the medication is discontinued

113
Q

What medications can cause progressive blue-gray hyperpigmentation in photo-exposed areas?

A

Phenothiazines: thioridazine, chlorpromazine, promethazine

Tricyclic antidepressants

114
Q

What is the histology of blue-gray hyperpigmentation from anti-psychotics?

A

Refractile golden brown granules Fontana Masson+, Perls negative) in macrophages in perivascular distribution

115
Q

What is toxic erythema of chemotherapy?

A

Umbrella term that covers many variants of chemotherapy-induced cutaneous reactions.

Effectively the chemotherapy concentrates into the eccrine glands and produces a direct toxic effect leading to rash

116
Q

What is the general clinical presentation of toxic erythema of chemotherapy?

A

Acral dysesthesia, red swollen hands, morbilliform eruption on trunk, prominent desquamation

117
Q

What is the histology of toxic erythema of chemotherapy?

A

Follows what would be expected: epidermal dysmaturation, scattered necrotic keratocytes and eccrine glandular cells, squamous metaplasia of eccrine glands

118
Q

What is the timeline for toxic erythema of chemotherapy?

A

Days-months after drug initiation

119
Q

What are some specific varients of toxic erythema of chemotherapy?

A

Eccrine squamous syringometaplasia, neutrophilic eccrine hidradenitis, palmoplantar erythrodysesthesia/hand-foot syndrome/acral erythema, Ara-C ears, pseudocellulitis

120
Q

What is the most common medications to cause toxic erythema of chemotherapy?

A

Cytarabine/Ara-C (#1), texanes (atypicla hand/foot syndrome w/ red plaques on dorsalhands/achillies tendon/malleoli, nail toxicity), antracyclines (doxo/duano/idarubicin), 5-FU

121
Q

What is the difference between toxic erythema of chemotherapy and hand-foot skin reaction?

A

Hand-foot skin reaction is similar but has less severe acral dysesthesia and hand swelling and classically has prominent hyperkeratotic plaques on areas of friction

122
Q

What is the treatment for hand-foot skin reaction in chemotherapy?

A

Tazorac, 40% urea and feuded (treats hyperkeratosis)

123
Q

What are the most common causes of hand-foot skin reaction?

A

Multi-kinase inhibitors (sorafenib, sunitinib, VEGF inhibitors)

124
Q

What medication can cause sunburn recall?

A

Methotrexate

125
Q

What medications can cause radiation recall?

A

Methotrexate, other chemotherapeutics, high dose INF-alpha, simvastatin

126
Q

What type of alopecia is induced by chemotherapy?

A

Anagen effluvium. Scalp is the most commonly affected area (>eyebrows, axillary, pubic hairs). Hairs may re-grow more curly

127
Q

What chemotherapy agents can cause irreversible alopecia?

A

Busulfan, docetaxel

128
Q

What is the timeline of chemotherapy-induced mucositis?

A

Starts within the first week usually and resolves within 3 weeks

129
Q

What are the treatments of mucositis if severe?

A

Oral hygiene, antimicrobials to decrease secondary infections, and palifermin (keratinocyte growth factor)

130
Q

What are extravasation reactions from chemotherapy?

A

Ulcerations and or indurated red plaques at sites of chemotherapy leakage from the infusion

5-FU, anthracyclines, carmustine, vinblastine, vincristine, mitomycin C

131
Q

What is chemotherapy recall?

A

Tender sterile inflammatory nodules at the sites of previous chemotherapy drug leakage or prior infusion sites

132
Q

What is the most common chemotherapy causes of nail hyperpigmentation?

A

Doxorubicin (#1), 5-FU, cyclophosphamide, hydroxyurea, bleomycin

133
Q

What medication causes serpentine supravenous hyperpigmentation (overlying infusion veins)?

A

5-FU

134
Q

What chemotherapy agents cause painful and hemorrhagic onycholysis?

A

Taxanes

135
Q

Which chemotherapy agents cause exudative hyponychial dermatitis?

A

Combination of docetaxel and capecitabine in the treatment of breast cancer

136
Q

What chemotherapy agent causes lower extremity ulceration?

A

Hydroxyurea

137
Q

What chemotherapy agent can cause a dermatomyositis-like reaction?

A

Hydroxyurea

138
Q

Which medication can cause necrosis of existing psoriasis plaques with treatment?

A

Methotrexate

139
Q

What medication can cause alternating dark and light bands of hair (flag sign)?

A

Methotrexate

140
Q

What medication can cause oral leukoplakia that looks like flat warts?

A

Palifermin

141
Q

What medication can cause acquired cutaneous adherence “sticky skin syndrome”?

A

Combination of doxorubicin + ketoconazole

142
Q

Which chemotherapeutic agents can cause sclerodermoid reactions?

A

Most common on the lower extremities

Caused by taxanes most commonly

143
Q

Which chemotherapeutic agent can cause palmoplantar hyperkeratosis?

A

Capecitabine

144
Q

What medications can cause flagellate hyperpigmentation?

A

Bleomycin, raw shitake mushrooms (more urticarial), and less commonly docetaxel

145
Q

Which medications can cause Raynaud’s syndrome with digital necrosis?

A

Bleomycin (including injected/intralesional)

146
Q

Which chemotherapy is associated with acral sclerosis?

A

Bleomycin

147
Q

What cutaneous reactions can be induced by interferon therapy?

A

Vasculopathy, necrosis, psoriasis exacerbation, and cutaneous sarcoid

148
Q

What cutaneous reactions can occur from IL-2 therapy?

A

Granulomatous eruption, lobular panniculitis

149
Q

What cutaneous findings can sorafenib generate?

A

Multi-tyrosine kinase inhibitor that can cause PPK, acral/facial erythema, SCC’s, KA’s, fingernail splinter hemorrhages, wart-like squamoproliferative lesions, scalp pruritus, flushing, alopecia, stomatitis, KP-like eruption, nipple hyperkeratosis

150
Q

What cutaneous side effects can be seen in sunitinib?

A

Multi-kinase inhibitor that can cause depigmentation of the hair, facial edema, yellow skin pigmentation, hand-foot skin reactions

151
Q

What is Texier’s disease?

A

Indurated morpheaform plaques caused from vitamin K injection (injection site reaction)

152
Q

What vaccines can lead to granulomatous nodules at the site of injection?

A

Aluminium containing ones

153
Q

What is embolia cutis medicamentosa?

A

Can occur with any intramuscular-injected medication. Due to vascular thrombosis from periarterial injection and it presents with severe pain, ischemia, and pallor of injection site minutes

Progresses to purple livedoid plaques with dendritic borders, then ulcerates

154
Q

What medications can cause gingival hypertrophy?

A

Phenytoin (most common >50%), nifedipine (25%), and cyclosproine (25%)

155
Q

What is the presentation of gingival hypertrophy?

A

Typically occurs within the first year of use of medication. It starts in the interdental papillae of the frontal teeth on the labial side then can progress to involve the rest of the teeth with multinodular overgrowth of gums

Spares edentulous areas

Degree of hyperplasia is highly correlated with oral hygiene

156
Q

What medication can give penile ulcerations?

A

Foscarnet (occurs due to irritant contact dermatitis from the medicine being excreted in the urine)

157
Q

What medications can cause telogen effluvium?

A

Heparin, Beta-blockers, IFN, lithium, retinoids, OCP discontinuation, antidepressants, anticonvulsants, ACE inhibitors, colchicine, NSAIDs

158
Q

What medications can cause pseudolymphoma (cutaneous lymphoid hyperplasia)?

A

Anticonvulsants (phenytoin, phenobarbital, carbamazepine, lamotrigine), neuroleptics (promethazine, chlorpromazine), ARBs, imatinib, antiboitocs

Also arthropod bites, Borrelia, tattoo reaction, HSV, HIV, post-zoster

159
Q

What is the cutaneous presentation of pseudolymphoma (cutaneous lymphoid hyperplasia)?

A

Aberrant proliferation of polyclonal B- and / or T-lymphocytes, hypergammaglobulinemia

Presents w/ solitary or multiple grouped firm red to plum-colored plaques and nodules lacking surface changes; most commonly affecting the “upper half of the body” like the face, neck, upper extremities, upper trunk and it can have LAD

160
Q

What is T-cell pseudolymphoma?

A

Looks like MF w/ nad-like lymphoid infiltrate at DEJ with epidermotropism and lymphocytic atypia (cerebriform nuclei); usually polyclonal though

161
Q

What is B-cell pseudolymphoma?

A

Dense dermal mixed infiltrate (lymphs, eos, plasma cells) with Grenz zone; dermal infiltrate is organized as multiple large blue nodules throughout the dermis and superficial fate w/ pale-appearing germinal centers (with tingible body macrophages) with the follicles; a mantle zone of normal-appearing lymphs surrounding the follicles (unlike in b-cell lymphoma); a mixture of kappa and lambda seen, you never see IGH gene clonality

162
Q

What is the serum-sickness reaction?

A

Morbilliform-urticarial plaques or vasculitis. Presents with fever, arthralgias, arthritis, LAD, renal dz, hypocomplementemia, circulating immune complexes

163
Q

What things cause a serum-sickness reaction?

A

Non-human proteins: anti-thymocyte globulin, infliximab, minocycline

164
Q

What is radiation-induced EM?

A

It happens specifically when pts with brain cancer are given phenytoin + radiation. This leads to edema and red discoloration on the head at radiation ports which then develops into EM or SJS-like lesions whtin 2 days and spreads downward with mucosal involvement in some cases

histologically identical to SJS

165
Q

What is the serum sickness-like eruption?

A

Morbilliform to urticarial eruption that starts 1-3 weeks after drug initiation

presents with edema of face/hands/feet; can have arthralgias, arthritis, LAD, fever, but lacks many of the elements of true serum sickness-like vasculitis, renal dz, hypocomplementemia, circulating immune complexes and is self limited

166
Q

What patient population most commonly gets serum sickness-like eruptions?

A

Kids

167
Q

What are the most common causes of serum sickness-like eruption?

A

Cefaclor (#1) >> other beta-lactams, NSAIDs, minocycline, phenytoin

168
Q

What is the symmetrical drug-related intertriginous and flexural exanthem (SDRIFE, “baboon syndrome”)?

A

The symmetric eruption that presents with well-defined red plaques in the anogenital area and can have it in other areas intertriginous/flexural sites after administration of systemic mediations

169
Q

What medications can cause symmetrical drug-related intertriginous and flexural exanthem (SDRIFE, “baboon syndrome”)?

A

Beta-lactams (aminopenicillins and CSN), radiocontrast, other antibx

170
Q

Causes of flagellate erythema?

A

Bleomycin, raw shiitake mushroom ingestion (more urticarial), Still’s dz, dermatomyositis, docetaxel

171
Q

What causes red-man syndrome from vancomycin?

A

Non-immunologic mast cell degranulation (that’s why it needs to be run slower). Can also pre-treat with antihistamines

DERM (19) Urticaria, Erythema, and Purpura (7 decks)

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