Drug Reactions Flashcards
(171 cards)
1
Q
What are the preformed mediators in mast cells?
A
Proteases (tryptase, chymase), heparin, histamine
2
Q
What are the synthesized mediators in mast cells?
A
prostaglandins, leukotrienes, platelet activating factor, cytokines
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
4
Q
How are cutaneous drug reactions divided?
A
Simple (no visceral/systemic involvement) and complex (systemic involvement)
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)
6
Q
What are the most common morphologies of drug rash?
A
Morbilliform (92%)>>>urticarial (6%)>vasculitis (2%)
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 occurs when the CD4 count is 100-400/mm3.
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
9
Q
What is the timing of a morbilliform drug rash?
A
7-14 days after drug initiation (cell-mediated hypersensitivity)
10
Q
What are the most common culprits of morbilliform drug rash?
A
Beta-lactams, TMP/SMX, anticonvulsants, and allopurinol
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
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
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)
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
15
Q
What is the prognosis of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?
A
10% mortality
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
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
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
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
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)
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
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
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
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
25
What patients are at higher risk of allopurinol hypersensitivity syndrome?
**Patients with renal failure**, Han Chinese with HLA-B\*5801,
26
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?
Liver involvement in 70%, **kidney involvement in up to 80%**, can also cause pancreatitis and diabetes
## Footnote
*25% mortality*
27
Clinical presentation of dapsone hypersensitivity syndrome?
Concomitant hemolysis and methemoglobinemia is common
## Footnote
Look for increased bilirubin, icterus, LAD (80%), lacks eosinophilia, liver involvement can be fatal
28
What are some important clinical components of minocycline hypersensitivity syndrome?
Usually seen in young adults getting tx for acne. Associated with glutathione S-transferase deficiency
## Footnote
Strong association with interstitial eosinophilic pneumonia; liver involvement in 75%; renal involvement in up to 20%
29
What is the treatment of Drug-induced hypersensitivity syndrome/Drug reaction with eosinophilia and systemic symptoms (DIHS/DRESS)?
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)
## Footnote
*relapse common if steroids tapered too rapidly (need to give for weeks to months)*
30
What things can induce acute generalized exanthematous pustulosis (AGEP)?
Medications most common: beta-lactam antibiotics, NSAIDS, etc
31
What is the timeline for acute generalized exanthematous pustulosis (AGEP)?
Occurs rapidly (\<4 days) after drug administration
32
What are the clinical features of acute generalized exanthematous pustulosis (AGEP)?
High fever and small (\<5mm) non-follicular, sterile pustules arising on a background of edematous red skin
## Footnote
*Commonly begins on the face and intertriginous sites and then generalizes within hours*
33
What clinical findings help distinguish acute generalized exanthematous pustulosis (AGEP) from pustular psoriasis?
AGEP more commonly have purpuric or EM-like lesions (50%), mucosal involvement, edema of face/hands, or bullae
34
What lab findings are seen in acute generalized exanthematous pustulosis (AGEP)?
Increased WBC with peripheral neutrophilia +/- eos, hypocalcemia, and renal insufficiency
35
Most common drugs in acute generalized exanthematous pustulosis (AGEP)?
Beta-lactam, macrolide antibiotics, calcium channel blockers (diltiazem most common), and antimalarials (longer latency)
36
What is the histology of acute generalized exanthematous pustulosis (AGEP)?
Subcorneal and intraepidermal spongiform pustules, prominent superficial dermal edema, perivascular mixed inflammatory infiltrate **w/ eos**
## Footnote
**Shouldn't see eos in psoriasis**
37
What histologic features help distinguish acute generalized exanthematous pustulosis (AGEP) from pustular psoriasis?
Edema, eos, and lack of acanthosis helps distinguish AGEP from pustular psoriasis
38
Treatment for acute generalized exanthematous pustulosis (AGEP)?
Stop medication that is causing it, supportive therapy w/ topical steroids and antipyretics
39
What are two types of photosensitive drug reactions?
Phototoxic (most common) or photoallergic
40
What is a phototoxic reaction?
Most common and **predictable**. Most commonly occurs with systemic medications
## Footnote
*caused by direct interaction between UVR (UVA most commonly) and drug/drug metabolites which then produce free radicals and damage to skin cells*
41
What is the clinical presentation of a phototoxic medication reaction?
Painful exaggerate sunburn-like eruption that can have blistering. This heals with hyperpigmentation
42
What is the histopathology of a phototoxic medication reaction?
Same as sunburn (necrotic keratinocytes ("sunburn cells"), dermal edema, minimal dermal inflammation, and vasodilation
43
What are the most common medications to cause a phototoxic medication reaction?
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
44
What medications can cause pseudoporphyria?
This is an exaggerated phototoxic reaction:
Naproxen (#1), thiazides, voriconazole, furosemide, TCN's, nalidixic acid, and tanning bed exposure
45
What are some differences between pseudoporphyria and PCT?
Unlike PCT, pseudoporphyria does not have: hypertrichosis, sclerodermoid features, and hyperpigmentation
## Footnote
*porphyrin studies will be normal, histology is similar*
46
What medications are known to cause photoonycholysis?
Another form of phototoxic reaction:
- Psoralens and tetracyclines
47
What medications can cause a slate-grey hyperpigmentation?
Amiodarone, TCAs, and diltiazem
48
What medications can cause photolichenoid drug reactions?
HCTZ and NSAIDs
49
What plants can cause phytophotodermatitis?
Also a phototoxic drug reaction basically
Furocoumarin-containing plants: parsley, celery, lime, fig, and yarrow
50
What is a photoallergic drug reaction?
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**
51
What is the mechanism of drug photoallergy?
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
52
What is the clinical presentation of a photoallergic reaction?
Itchy, eczematous to lichenoid eruption on sun-exposed areas initially but can spread to non-sun-exposed sites
## Footnote
*less likely to be bullous/intense than phototoxic*
53
What is the histology of a photoallergic reaction?
Spongiotic dermatitis, superficial perivascular inflammation, and eosinophils (not sunburn cells/signs of toxic damage)
54
What are the most common causes of photoallergic reactions?
Oxybenzone (most common)\> fragrances (6-methyl coumarin, musk ambrette, and sandalwood oil), NSAIDs (piroximcam and ketoprofen), griseofulvin, quinidine/quinine, sulfonamides, and quinolones
55
How do you confirm the diagnosis of a photoallergic reaction?
Photopathc testing (using UVA)
56
What patch test is piroxicam sensitive to?
Thimerisol
57
What is the most common presentation of drug-induced pigmentary changes?
May be localized or generalized but are often in a photodistribution
58
What are the mechanisms of drug-induced pigmentary change?
1) drug/drug metabolite deposition 2) induction of melanin production 3) post-inflammatory changes due to photosensitive eurptions
59
What other cutaneous findings aside from skin can be affected in drug-induced hyperpigmentation?
Melanonychia (longitudinal, diffuse or transverse) and/or oral hyperpigmentation
60
What are the most common drugs to cause drug-induced hyperpigmentation?
Minocycline, chemotherapeutics, AZT (zidovudine), antimalarials, and heavy metals
61
What is the time course of drug-induced hyperpigmentation?
Is often reversible but takes a long time (months to years)
62
What types of medications often cause hypopigmentation?
Most commonly topical medications, but can also be caused by tyrosine kinase inhibitors like imatinib (inhibits c-KIT)
63
Why do tyrosine kinase inhibitors cause hypopigmentation?
They inhibit c-KIT
64
What are the most common agents to cause drug-induced hypopigmentation?
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
65
What agent causes irreversible drug-induced depigmentation?
MBEH (permanent at the local reaction and distant)
## Footnote
*Methyl benzyl ester of hydroquinone, used for depigmentation therapy of vitiligo*
66
When does coumadin-induced skin necrosis tend to occur?
2-5 days after drug initiation (when protein C levels are at nadir)
67
Why does coumadin-induced skin necrosis tend to happen at 2-5 days after starting therapy?
That is when protein C levels are at the nadir
68
What is the clinical presentation of coumadin-induced skin necrosis?
Painful red plaques that then progress to **hemorrhagic bullae, ulcers on fatty areas like the breast, buttocks, and thighs**
69
What is the histology of coumadin-induced skin necrosis?
Non-inflammatory thrombotic vasculopathy (multiple fibrine thrombi in dermal/SQ vessels with no LCV)
70
What is the mechanism of heparin-induced skin necrosis (HITT syndrome)?
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
What is the clinical presentation of heparin-induced skin necrosis?
Systemic syndrome with decreased platelet levels, thrombosis and cutaneous necrosis
## Footnote
*Note that this occurs with unfractionated heparin more than tractionated LMWH*
72
What is the treatment of heparin-induced skin necrosis?
Stop heparin, start direct thrombin inhibitor or factor Xa inhibitor
73
What is the histology of heparin-induced skin necrosis?
Thrombotic vasculopathy with platelet aggregates (not easy to see on H&E)
74
What is the clinical presentation of bromoderma or iododerma?
Acneiform lesions, papulopustules, nodules, vegetating lesions simulating P. Vegetans or blastomycosis; clear or hemorrhagic blisters (iododerma\> others)
## Footnote
*Skin lesions occur after chronic exposure*
75
What is the histology of bromoderma/iododerma?
Pseudoepitheliomotous hyperplasia with intraepidermal neutrophilic microabscesses and dense dermal neutrophilic inflmation (r/o deep fungal infxn)
76
What cutaneous reactions can be seen at sites of carmustine and nitrogen mustard administration?
Hyperpigmentation at sites of topical application due to increased melanocytes and melanin in keratinocytes
77
What cutaneous findings are caused by bleomycin?
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
## Footnote
Can also see transverse melanonychia, sclerodermoid changes
78
What cutaneous side effects can be seen with busulfan?
Addison's-like generalized hyperpigmentation with or w/o pulmonary fibrosis (see an increase in melanin in keratinocytes and dermal melanophages)
79
What cutaneous side effects can be seen from cyclophosphamide?
Diffuse mucocutaneous hyperpigmentation or localised hyperpigmentation in nails, teth, palms/soles (resolves within 12 months)
80
What pigmentation changes can occur in ifosfamide administration?
hyperpigmentation of the flexural areas, hands, feet, scrotum a,nd under occlusive dressings
81
What is a distinctive pigmentation finding in systemic 5-FU administration?
Serpentine hyperpigmentation overlying veins that were infused (histology shows necrotic keratinocytes, pigment incontinence, and increased melanin in basal keratinocytes)
82
What skin findings can be seen in hydroxyurea?
Early lichenoid or DM-like reaction overlying joints and can lead to PIH at involved sites; melanonychia, lunula hyperpigmentation
83
What pigmentation change can occur with sunitinib administration?
Depigmentation of hair and yellowing of the skin
84
What pigmentation changes can be induced by doxorubicin?
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
Hyperpigmentation occurs in what percent of patients taking antimalarials?
25%
86
What is the histology of antimalarial induced hyperpigmentation?
Deposition of drug-melanin complexes (Fontana Masson+) and hemosiderin (Perls+) in the dermis
87
What is the presentation of pigmentation changes in pt's getting chloroquine/hydroxychloroquine?
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
What pigmentary changes can occur in patients getting quinacrine?
Diffuse yellow-brown discoloration of the skin and eyes that can mimic jaundice
89
What is the clinical presentation of arsenic exposure?
Hyperpigmentation patches with superimposed "raindrops" of hyperpigmentation most commonly on intertriginous sites, palms/soles, pressure points
90
How long after exposure to arsenic do the skin lesions occur?
Up to 20 years
91
What are the late features of the cutaneous arsenic exposure?
Palmoplantar hyperkeratosis, SCC (after the hyperpigmentation stage)
92
What is the histology of arsenic exposure and the resulting skin findings?
Deposits of arsenic in dermis and epidermis + increased melanin in keratinocytes
93
What pigmentation does gold cause?
Blue-gray hyperpigmentation on face (periocular is #1)and other sun-exposed sites
94
What is the histology of gold induced hyperpigmentation?
Gold deposits in macrophages in perivascular/peri-eccrinedistribution; particles have an orange-red birefringence on polarized light
## Footnote
**Does not bind to the BMZ or eccrine membrana propria** (distinguishes this from argyria)
95
What is the clinical presentation of argyria (silver-induced hyperpigmentation)?
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
What is the histology of argyria?
Deposits of silver **bound to the BMZ and membrana propria** of eccrine glands (best seen with darkfield microscopy)
97
What percentage of patients on amiodarone will get cutaneous changes?
60% of patients on amiodarone for more than 3-6 months will get hyperpigmentation
98
What is the clinical presentation of amiodarone-induced hyperpigmenation?
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
What is the histology of amiodarone-induced hyperpigmentation?
Unique yellow-brown granules of lipofuscin (Fontana Masson+) in macrophages in a perivascular distribution
## Footnote
*Electron microscopy shows lipid-like lysosomal inclusions which is unique to this condition*
100
What pigmentation changes can occur with AZT (zidovudine treatment)?
Widespread mucocutaneous hyperpigmentation (reversible) with accentuation in photo-exposed sites and sites of friction
## Footnote
*Also frequently see longitudinal melanonychia (more than transverse or diffuse)*
101
What is the clinical presentation of pigmentary change from clofazimine?
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
What is the histology of clofazimine induced pigment change?
Birefringent red crystals of clofazimine seen in perivascular distribution on **fresh frozen tissue only** (missed on H&E)
103
What is the presentation of diltiazem-induced hyperpigmentation?
Occurs in Fitz IV-VI patients
Slate-gray discoloration on photo-exposed skin with reticular or perifollicular pattern
104
What is the histology of ochronosis from excessive hydroquinone use?
Yellow-brown, banana-like deposits in the dermis
## Footnote
*the hyperpigmentation fades after stopping the medication*
105
What is type 1 minocycline-induced hyperpigmentation?
Focal blue-black hyperpigmentation **at sites of inflammation or scars** (esp acne scars). This is not dose-related
106
What is type 2 minocycline-induced hyperpigmentation?
Circumscribed blue-gray "bruise-like" hyperpigmentation of **pretibial area and arms**
107
What is type 3 minocycline-induced hyperpigmentation?
Diffuse brown hyperpigmentation of **sun-exposed areas**; due to low-grade phototoxic dermatitis
108
What is the histology of type 1 minocycline-induced hyperpigmentation?
Dermal deposits of drug complexes with iron/hemosiderin (Perls+)
109
What is the histology of type 2 minocycline-induced hyperpigmentation?
Dermal deposits are drug complexes with both iron/hemosiderin (Perls+) AND melanin (Fontana Masson+)
110
What is the histology of type 3 minocycline-induced hyperpigmentation?
Increased melanin in basal keratinocytes, dermal melanophages/melanin (Fontana Masson+)
111
Fetal exposure to tetracyclines stains the teeth at different locations, what are these locations for minocycline and tetracycline?
Minocycline: mid-portion of the teeth
TCN = gingival one third
112
What changes can be seen from prostaglandin analogs?
Periocular hyperpigmentation, eyelash hypertrichosis, and iris hyperpigmentation may follow the use of glaucoma medications
## Footnote
*resolve as the medication is discontinued*
113
What medications can cause progressive blue-gray hyperpigmentation in photo-exposed areas?
Phenothiazines: thioridazine, chlorpromazine, promethazine
## Footnote
Tricyclic antidepressants
114
What is the histology of blue-gray hyperpigmentation from anti-psychotics?
Refractile golden brown granules Fontana Masson+, Perls negative) in macrophages in perivascular distribution
115
What is toxic erythema of chemotherapy?
Umbrella term that covers many variants of chemotherapy-induced cutaneous reactions.
## Footnote
Effectively the chemotherapy concentrates into the eccrine glands and produces a direct toxic effect leading to rash
116
What is the general clinical presentation of toxic erythema of chemotherapy?
Acral dysesthesia, red swollen hands, morbilliform eruption on trunk, prominent desquamation
117
What is the histology of toxic erythema of chemotherapy?
Follows what would be expected: epidermal dysmaturation, scattered necrotic keratocytes and eccrine glandular cells, squamous metaplasia of eccrine glands
118
What is the timeline for toxic erythema of chemotherapy?
Days-months after drug initiation
119
What are some specific varients of toxic erythema of chemotherapy?
Eccrine squamous syringometaplasia, **neutrophilic eccrine hidradenitis,** palmoplantar erythrodysesthesia/hand-foot syndrome/acral erythema, **Ara-C ears**, pseudocellulitis
120
What is the most common medications to cause toxic erythema of chemotherapy?
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
What is the difference between toxic erythema of chemotherapy and hand-foot skin reaction?
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
What is the treatment for hand-foot skin reaction in chemotherapy?
Tazorac, 40% urea and feuded (treats hyperkeratosis)
123
What are the most common causes of hand-foot skin reaction?
Multi-kinase inhibitors (sorafenib, sunitinib, VEGF inhibitors)
124
What medication can cause sunburn recall?
Methotrexate
125
What medications can cause radiation recall?
**Methotrexate**, other chemotherapeutics, high dose INF-alpha, simvastatin
126
What type of alopecia is induced by chemotherapy?
Anagen effluvium. Scalp is the most commonly affected area (\>eyebrows, axillary, pubic hairs). Hairs may re-grow more curly
127
What chemotherapy agents can cause irreversible alopecia?
Busulfan, docetaxel
128
What is the timeline of chemotherapy-induced mucositis?
Starts within the first week usually and resolves within 3 weeks
129
What are the treatments of mucositis if severe?
Oral hygiene, antimicrobials to decrease secondary infections, and palifermin (keratinocyte growth factor)
130
What are extravasation reactions from chemotherapy?
Ulcerations and or indurated red plaques at sites of chemotherapy leakage from the infusion
## Footnote
*5-FU, anthracyclines, carmustine, vinblastine, vincristine, mitomycin C*
131
What is chemotherapy recall?
Tender sterile inflammatory nodules at the sites of previous chemotherapy drug leakage or prior infusion sites
132
What is the most common chemotherapy causes of nail hyperpigmentation?
Doxorubicin (#1), 5-FU, cyclophosphamide, hydroxyurea, bleomycin
133
What medication causes serpentine supravenous hyperpigmentation (overlying infusion veins)?
5-FU
134
What chemotherapy agents cause painful and hemorrhagic onycholysis?
Taxanes
135
Which chemotherapy agents cause exudative hyponychial dermatitis?
Combination of docetaxel and capecitabine in the treatment of breast cancer
136
What chemotherapy agent causes lower extremity ulceration?
Hydroxyurea
137
What chemotherapy agent can cause a dermatomyositis-like reaction?
Hydroxyurea
138
Which medication can cause necrosis of existing psoriasis plaques with treatment?
Methotrexate
139
What medication can cause alternating dark and light bands of hair (flag sign)?
Methotrexate
140
What medication can cause oral leukoplakia that looks like flat warts?
Palifermin
141
What medication can cause acquired cutaneous adherence "sticky skin syndrome"?
Combination of doxorubicin + ketoconazole
142
Which chemotherapeutic agents can cause sclerodermoid reactions?
Most common on the lower extremities
**Caused by taxanes most commonly**
143
Which chemotherapeutic agent can cause palmoplantar hyperkeratosis?
Capecitabine
144
What medications can cause flagellate hyperpigmentation?
Bleomycin, raw shitake mushrooms (more urticarial), and less commonly docetaxel
145
Which medications can cause Raynaud's syndrome with digital necrosis?
Bleomycin (including injected/intralesional)
146
Which chemotherapy is associated with acral sclerosis?
Bleomycin
147
What cutaneous reactions can be induced by interferon therapy?
Vasculopathy, necrosis, psoriasis exacerbation, and **cutaneous sarcoid**
148
What cutaneous reactions can occur from IL-2 therapy?
Granulomatous eruption, lobular panniculitis
149
What cutaneous findings can sorafenib generate?
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
What cutaneous side effects can be seen in sunitinib?
Multi-kinase inhibitor that can cause depigmentation of the hair, facial edema, yellow skin pigmentation, hand-foot skin reactions
151
What is Texier's disease?
Indurated morpheaform plaques caused from vitamin K injection (injection site reaction)
152
What vaccines can lead to granulomatous nodules at the site of injection?
Aluminium containing ones
153
What is embolia cutis medicamentosa?
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
## Footnote
Progresses to purple livedoid plaques with dendritic borders, then ulcerates
154
What medications can cause gingival hypertrophy?
Phenytoin (most common \>50%), nifedipine (25%), and cyclosproine (25%)
155
What is the presentation of gingival hypertrophy?
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
## Footnote
*Spares edentulous areas*
**Degree of hyperplasia is highly correlated with oral hygiene**
156
What medication can give penile ulcerations?
Foscarnet (occurs due to irritant contact dermatitis from the medicine being excreted in the urine)
157
What medications can cause telogen effluvium?
Heparin, Beta-blockers, IFN, lithium, retinoids, OCP discontinuation, antidepressants, anticonvulsants, ACE inhibitors, colchicine, NSAIDs
158
What medications can cause pseudolymphoma (cutaneous lymphoid hyperplasia)?
Anticonvulsants (phenytoin, phenobarbital, carbamazepine, lamotrigine), neuroleptics (promethazine, chlorpromazine), ARBs, imatinib, antiboitocs
## Footnote
*Also arthropod bites, Borrelia, tattoo reaction, HSV, HIV, post-zoster*
159
What is the cutaneous presentation of pseudolymphoma (cutaneous lymphoid hyperplasia)?
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
What is T-cell pseudolymphoma?
Looks like MF w/ nad-like lymphoid infiltrate at DEJ with epidermotropism and lymphocytic atypia (cerebriform nuclei); usually polyclonal though
161
What is B-cell pseudolymphoma?
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
What is the serum-sickness reaction?
Morbilliform-urticarial plaques or vasculitis. Presents with fever, arthralgias, arthritis, LAD, renal dz, hypocomplementemia, circulating immune complexes
163
What things cause a serum-sickness reaction?
Non-human proteins: anti-thymocyte globulin, infliximab, **minocycline**
164
What is radiation-induced EM?
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
## Footnote
*histologically identical to SJS*
165
What is the serum sickness-like eruption?
Morbilliform to urticarial eruption that starts 1-3 weeks after drug initiation
## Footnote
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
What patient population most commonly gets serum sickness-like eruptions?
Kids
167
What are the most common causes of serum sickness-like eruption?
Cefaclor (#1) \>\> other beta-lactams, NSAIDs, minocycline, phenytoin
168
What is the symmetrical drug-related intertriginous and flexural exanthem (SDRIFE, "baboon syndrome")?
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
What medications can cause symmetrical drug-related intertriginous and flexural exanthem (SDRIFE, "baboon syndrome")?
Beta-lactams (aminopenicillins and CSN), radiocontrast, other antibx
170
Causes of flagellate erythema?
Bleomycin, raw shiitake mushroom ingestion (more urticarial), Still's dz, dermatomyositis, docetaxel
171
What causes red-man syndrome from vancomycin?
Non-immunologic mast cell degranulation (that's why it needs to be run slower). Can also pre-treat with antihistamines
