Life threatening skin conditions Flashcards

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1
Q

fever and skin rash after new medication. CBC with eosinophilia.

A

DRESS syndrome

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2
Q

DRESS is a

when does it start?

A

potentially life threatening drug reaction that happens 2-8 weeks after initial exposure

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3
Q

which drugs cause DRESS?

A

anticonvulsants (phenytoin or carbamazepine), allopurinol and sulfonamides (sulfasalazine) and abx (minocycline and vancomycin)
acabavir (HIV NRTI)

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4
Q

fever, generalized LAD, facial edema and diffuse morbilliform rash that can progress to confluent erythema and follicular accentuation

A

DRESS presentation

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5
Q

DRESS rash

A

morbilliform rash that can progress to confluent erythema and follicular accentuation

can involve the mucosa (mouth and pharynx) and doesn’t cause erosions

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6
Q

what other organ systems are affected in DRESS?

A

can see liver (hepatomegaly and jaundice)
Can see kidney (acute interstitial nephritis)
Can see lung (cough and dypsnea)

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7
Q

labs of DRESS

A

see eosinophilia and atypical lymphocytes and elevated hepatic transaminases

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8
Q

treatment of DRESS

A

stop offending drug and this resolution can take up to 6-9 weeks

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9
Q

hypersensitivity vasculitis clinical presentation

A

fever, palpable purpura and petechiae, arthralgias, LAD and elevated ESR. Seen with anticonvulsants. NO esosinophilia

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10
Q

Hypereosinophilic syndrome HES) is defined by

A

profound eosinophilia >1500 and multi system involvement (Heart, GI, lungs, brain, skin, kidneys) without a identifiable cause.

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11
Q

what is serum sickness like syndrome

A

seen after exposure to new drugs (antiseizure drugs, antibiotics, and infections (hep B or strep)

Can cause systemic symptoms arthralgias, and urticarial or serpiginous macular rash. This happens within 1-2 weeks after drug exposure and NO eosinophilia

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12
Q

Steven Johnson syndrome

A

triggered by new medications and seen with sudden onset of mucocutaneous lesions with subsequent necrosis and sloughing of of skin. NO eosinophilia or elevation in LFTs.

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13
Q

Staph toxic shock syndrome risk factors are:

A

tampon use,
nasal packing,

surgical/post partum wound infection

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14
Q

what causes staph toxic shock syndrome?

A

staph aureus

exotoxin release acting as superantigens

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15
Q

what are clinical features of staph toxic shock syndrome?

A

fever >102 or 38.9
hypotension
diffuse macular rash involving the palms and soles
desquamation 1-3 weeks after disease onset
vomiting and diarrhea
altered mental status without focal neurological signs

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16
Q

treatment of Staph toxic shock syndrome?

A
supportive care (IVF replacement)
removal of foreign body (Tampon or nasal packing)
antibody therapy (clindamycin and vancomycin
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17
Q

pt has progressive lethargy and confusion and has shaking chills and diarrhea. Had nasal packing for a nose fracture. Has fever and hypotension and tachycardia and ill. Has diffuse erythema of mucous membranes and skin and palms and soles and pitting edema of both legs

A

staph toxic shock syndrome

treat with clindamycin and vacomycin

remove nasal packing.

18
Q

desquamating rash, multiorgan failure and hypotension and diffuse erythroderma and encephalopathy

A

staph toxic shock syndrome

encephalopathy occurs due to cerebral edema.

19
Q

are there positive blood cultures in toxic shock syndrome?

A

no but should still get them if someone is septic shock

generally can culture at the infection source.

20
Q

why do we use clindamycin and vancomycin for staph toxic shock syndrome?

A

because clindamycin - helps stop /inhibits toxin production

21
Q

after recovery what is long term management for toxic shock syndrome from nasal packing?

A

eradication of S aureus with mupirocin

22
Q

what staph bacteria causes toxic shock syndrome?

A

group A strep.

23
Q

when to use vancomycin and cefepime to treat someone after a fight?

A

only use this if there’s a basal skull fracture during the fight and they develop meningitis.

24
Q

Side effects of bactrim

A

skin - Steven Johnson syndrome, TEN (toxic epidermal necrolysis) exfoliative dermatitis- seen up to 15% in HIV positive pts

Hematological: megaloblastic pancytopenia (folate deficiency)

Renal: hyperkalemia, impairs tubular secretion of Cr without affecting GFR
see crystalluria
interstitial nephritis

25
Q

difference between SJS and TEN?

A

<10% body surface area: Steven johnson syndrome
10-30% of BSA: SJS/TEN overlap
>30% of BSA: TEN

26
Q

clinical features of Steven Johnson syndrome:

A

4-28 days after exposure to trigger (2 days after repeat exposure)
acute influenzae like prodrome
rapid onset of erythematous macules, vesicles, bullae
necrosis and sloughing of epidermis
mucosal involvement

27
Q

Common triggers for Steven Johnson syndrome and TEN

A
drugs: 
allopurinol
antibiotics like bactrim or sulfonamides
anticonvulsants: carbamazepine, lamotrigene, phenytoin
NSAIDS: piroxicam
sulfasalazine
28
Q

what other common triggers can cause Steven Johnson and TEN?

A

mycoplasma pneumoniae
vaccination
Graft vs host dx

29
Q

which population of people is most vulnerable to developing Steven Johnson syndrome from antibiotics or common triggers?

A

HIV positive pts

3X more common

30
Q

initial prodrome of fever and influenza symptoms with new onset of painful red or purple macules. Skin lesions then progress to bullae formation and necrosis and sloughing

A

presentation of SJS

Can see mucosal lesions - ocular, oral, genital and respiratory surfaces

31
Q

What kills most people with SJS and TEN

A

secondary infection

32
Q

management of SJS?

A

need to be managed in hospital setting in ICU burn unit

all suspected or unnecessary medications should be immediately discontinued as prognosis of SJS or TEN improves with early removal of causative medications

Tx is supportive and wound care. Consider steroids nad IVIG in severe cases.

33
Q

pt takes bactrim for sinusitis. 5 days later states she has improved but has redness and “blisters” on her arms?

A

send to the hospital and stop bactrim immediately.

Concern for SJS

34
Q

fever, rash, LAD, and eosinophilia and elevated LFTs after starting a medication like phenytoin, carbamazepine or phenobarbital

A

anticonvulsant hypersensitivity reaction

subtype of DRESS but has a mortality rate of 10%

35
Q

anticonvulsant hypersensitivity reaction presents how long after starting a new drug?

A

seen up to 2 months after starting and see fever, rash, pharyngitis and LAD, and facial edema and can have hepatitis or nephritis

36
Q

anticonvulsant hypersensitivity reaction labs:

A

eosinophilia and anemia

can have megaloblastic anemia, hepatitis, and rhabdomyolysis

37
Q

anticonvulsant hypersensitivity reaction can be caused by

A

phenytoin, lamotrigene, allopurinol carbamazepine phenobarbital, ACEi, antidepressants, and beta blockers.

38
Q

Medications that need genetic testing prior to starting:

A

allopurinol in asians
oxcarbamazepine in asians
acabavir in HIV pts

39
Q

Rule of Nine’s for Total body surface area:

A

each lower extremity represents 18% TBSA
each upper extremity represents 9% TBSA
anterior and posterior trunk each represent 18% TBSA
head represents 9% TBSA

40
Q

necrotizing dermatitis differential

A

zinc deficiency on TPN
allopurinol toxicity
glucagonoma