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Symptoms Midterm > Rash > Flashcards

Rash Flashcards

1
Q

Immunologic – delayed type IV hypersensitivity reaction, occurring 7-14 days after drug has started, but can still occur even after drug discontinuation

A

Exanthematous drug eruption

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2
Q

Morbilliform rash. +/- low grade fever

Monomorphic (individual lesions look very similar to one another) macules and thin papules start on face + trunk & spread to extremities. + pruritic

(reaction typically limited to skin)

A

Exanthematous drug eruption

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3
Q

Tx of Exanthamous drug eruption

A

spontaneously resolves within 1-2 weeks, even with continuation of the culprit drug if necessary

Treatment = supportive for pruritis w/ topical corticosteroids and oral antihistamines

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4
Q

Preceded by prodrom of fever, malaise, + upper respiratory sx before onset of skin lesions.

Tender, dusky red, prupuric macules that progress to flaccid bullae and erosions (areas of necrosis)

A

Stevens Johnsons Syndrome /Toxic Epidermal Necrolysis

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5
Q

Onset between 1-3 weeks of drug initiation

Common drugs: allopurinol, anti-convulsants (lamotrigine, carbamazepine, phenobarbital, phenytoin), antibiotics, NSAIDs, and sulfa drugs

A

Stevens Johnsons Syndrome /Toxic Epidermal Necrolysis

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6
Q

Associated symptoms of Steven Johnson

A

Sx: fever, LAD, hepatitis, cytopenias

ny oral surface may be involved: + buccal, ocular, and genital mucosa >90%

+ Resp tract involvement ~25%

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7
Q

Dx between Steven Johnson and TEN

A

Amount of skin covered is generally what indicates diagnosis (indicating as amount of epidermal detachment of the body surface area):

<10% = SJS

10-30%: SJS-TEN

>30% = TEN

Mortality rate = 35% for severe cases of TEN à primarily from SEPSIS

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8
Q

Tx for Steven Johnson

A

Prompt discontinuation of causal drug is key – supportive care, use of IVIG is controversial.

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9
Q

Pathogenesis for atopic dermatitis

A

- Genetics: mutations in profilaggrin gene, responsible for ichthyosis vulgaris (genetic disorder resulting in severely dry skin) = large predisposing genetic factor

- Epidermal barrier dysfunction: ¯ essential fatty acids, fillagrin mutations, ­ susceptibility to allergins, ­ water loss

- Immunopathology = prototypic type II helper T cell disease (causing ­ IL-4, IL-5, and IL-13; ¯ IL-2 and IFN-gamma)

  • Defects in cell mediated immunity: ­ susceptibility to viral, bacterial, and fungal infections of skin – majority of pts colonized with staph aureus
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10
Q

Onset in infancy typical, but delayed onset in adulthood can be seen. Occurs in setting of other atopic disorders including allergic rhino-conjunctivitis and asthma.

A

atopic dermatitis

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11
Q

Acute, Subacute and Chronic lesions seen in atopic dermatitis

A

Acute lesions: edematous, erythematous papules and plaques, and may ooze.

Subacute lesions: erythematous and scaly, may be crusted. ***less well defined than those of psoriasis

Chronic lesions: thickened with lichenification (exaggerated skin lines)

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12
Q

face most often affected (esp cheeks) & lesions are often exudative w/ sig oozing and crusting + extensor involvemnt (diaper area spared); ­ impetigo as well

A

Infantile AD:

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13
Q

What is seen in Childhood AD:

What is seen in Adult AD:

A

involve flexures (antecubital + popliteal fossae) and some lichenification

similar, but may have evidence of habitual scratching and rubbing with chronic popular skin lesions – may be more resistant to treatment.

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14
Q

What does eczema herpaticum present like and how do we treat it?

A

*most common chronic inflammatory skin disease

**Rapid dissemintation of herpes simplex virus within areas of eczema, reffered to as eczema herpeticum, can complicate AD.

Treatment: topical corticosteroids (actively inflamed AD)

  • avoid triggers, use bland emolients + use of lotions alot
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15
Q

What are some pharmaceutical options to treat atopic dermatitis?

A

- Topical calcineurin inhibitors (tacrolimus + pimecrolimus) can be used in place of lower strength topical corticosteroids, but efficacy for lichenified lesions = limited

severe / recalcitrant dz: phototherapy + immuno-suppressants.

- antihistamines = alleviate pruritis, esp sedating H1 antihistamines (diphen-hydramine, hydroxyzine)

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16
Q

Spread by contact with infected skin or clothing

very large ds DNA virus = poxvirus fam

A

Molluscum contagiosum:

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17
Q

Firm small, pink or flesh colored dome-shaped papules with central umbilication

– large eosinophilic inclusions in cytoplasm = viral ‘factories on histology

A

Histology of lesions include molluscum bodies

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18
Q

Who do we see moluscum contigoiusm in? How do we treat it?

A

most common in children,risk with atopic dermatitis and appears

Lesions persist and are more numerous in those with weakened immune systems

~7 weeks s/p expos

Most have complete clearing in 2-4 months

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19
Q

viral infection of a pre-existing dermatosus

most commonly caused by disseminated HSV infection in pts with atopic dermatitis

A

eczema herpeticum

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20
Q

sudden eruption of painul, edematous, crusted vesicles, pustules and erosions

+/- high temperature, malaise, LAD

A

eczema herpaticum

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21
Q

Tx for eczema herpaticum

A

requires IV acyclovir

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22
Q

Difference between Shingles and chicken pox

A

Chickenpox (varicella): d/t infection by varicella zoster virus = highly contagious disease. (incubation 11-20 days)

Shingles: caused by an eruption of latent varicella zoster virus (VZV). Occurs particularly in adults.

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23
Q

lesions develop in successive crops, so that the rash consist of pocks at different stages of development (thus, papules, vesicles, pustules, crusted lesions, and healing lesions may all be present) = ‘dewdrops on a rose petal’

  • can be extensive and severe, esp if adult
A

Chickenpox (varicella):

24
Q

girdle-like vesicular eruption in thoracic or lumbar region, +/- facial lesions as a result of trigeminal nerve involvement.

  • Dermatomal (zosteriform) eruption on one side of body (unilateral)
  • Grouped vesicles on erythematous base
  • Most common dermatomes affected: trigeminal + T3-L2
  • Usually preceded by pain or burning
A

Shingles:

25
Q

Tx for Shingles

A

Generally shingles occurs only once in the immunocompetent, in contrast to herpes simplex virus (HSV) which frequently recurs

tx with antiviral to decrease neuropathic pain and contagious

26
Q

Test with Tzanck Test: Positive test shows 3 Multinucleated giant Cells in the center

A

Poistive in HSV

27
Q

reactivation of VZV in geniculate ganglion. Causes facial paralysis (bell’s palsy) and ear pain. Can visualize vesicles in ear canal. Associated with vestibular and hearing disturbances.

A

Ramsay-Hunt Syndrome:

28
Q

reactivation of VZV in V1 of trigeminal nerve. Vesicles on tip of nose may raise suspicion. Risk of corneal damage.

A

Herpes Zoster Ophthalmicus:

29
Q

potentiall severe neuropathic pain syndrome, most common in elderly –>Treated with TCAs, gabapentin, opioids, topical anesthetics

A

Post Herpetic Neuralgia:

30
Q

HSV: herpes viruses = _____ viruses

HSV-1: tramsmitted through :

HSV-2:

A

dsDNA

HSV-1: direct contact with infected saliva or with contaminated utensils.

HSV-2: sexual transmission

31
Q

à primary infection usually in childhood, characterized by presence of vesicles usually in lips but may affect oral cavity, pharynx, etc. recurrent lesions most commonly around the lips. = COLD SORES

A

HSV-1: herpes labialis (90%)

32
Q

What do we treat HSV 1 and 2 with

A

Acyclovir

33
Q

Once infected, person will harbor HSV for life. Virus can travel along sensory nerves to infect the neurons in the sensory ganglia. Recurrent disease follows this latency in the sensory gangla and can be stimulated by

A

UV light, trauma, fever, HIV infection, menstruation, and stress.

34
Q

Histopathology: epidermal acantholysis with several multinucleated keratinocytes with g_lassy intranuclear inclusions (_Cowdry type A) and ballooning degeneration

A

HSV!!!

35
Q

Most common human cancer: Slow growing tumor that rarely mestastasizes (when it does mets the pt is normally immunocompromised)

A

Basal Cell Carcinoma

36
Q

pearly papules with prominent dilated subepidermal blood vessels (telangiectasia)

A

Basal Cell carcinoma

(secondary to chronic sun exposure – can be locally destructive)

37
Q

cutaneous bacterial infection caused by G+ bacteria, including: staph aureus and strep pyogenes

A

Impetigo

38
Q

Staph Aureus toxins: exfoliative toxin A and exfoliative toxin B (or D) –> targets

A

desmoglein 1 =transmembrane cadherin like glycoprotein that is a component of desmosomes – important for cell to cell adhesion

39
Q

ransmembrane cadherin like glycoprotein that is a component of desmosomes – important for cell to cell adhesion

A

desmoglein: targeted by exfoliative toxin A and B from S. Aurues

40
Q

Severe S.Aureus infection that has high level of exfoliative toxin A and B can lead to

A

SSS

41
Q

majority of lesions are crusted papules (impetigo contagiosa) –> initial lesions are small vesicles or pustules that rupture and become a honey-colored crust with an erythematous base

A

Impetigo (oftne from S.Aureus) especially if it’s the bullous form

42
Q

What are the causes of Impetigo?

bullous and non-bullous forms

A

Bullous is d/t S.Aureus exofoliative toxins

5% of cases, non-bullous impetigo caused by Strep pyogenes results in acute post-streptococcal glomerulonephritis (APSG) risk NOT altered by treatment with antibiotics

43
Q

What is the tx for Impetigo?

A
  • Topical antibiotics +/- systemic antibitoics: Mupirocin or retapamulin topically
  • First line oral antibiotics: semi-synthetic penicillin, cephalosporin, b-lactam/b-lactamase inhibitor combination
  • Consider coverage for MRSA if no response to above or abscess / cellulitis
44
Q

Staph Aureus toxins: exfoliative toxin A and exfoliative toxin B (or D) – usually belonging to phage Group II, type 71 –> targets desmoglein 1–> causing

A

intra-epidermal splitting

See Staphylococcal Scalded Skin Syndrome

45
Q

Sudden onset of skin tenderness + macular eruption –> followed by development of large, easily ruptured, flaccid bullae.

Desquamation of large areas of the skin occurs in sheets + ribbons.

A

Staphylococcal Scalded Skin Syndrome

from Staph Aureus

46
Q

What sites of the body are involved in scalded skin syndrome?

What are usually left alone?

A

usual sites of involvement: face, neck, and trunk (including axillae and groin)
mucous membranes are NOT involved

47
Q

Epidemiology of SSS

A

At risk: kids <2 yrs and adults with renal disease

*tends to occur in outbreaks in neonatal nurseries or in day care nurseries. Occurance in adults is rare but seen in context of renal disease and inability to clear the toxin.

48
Q

Histopathology: subcorneal splitting of the epidermis. A few acantholytic cells + sparse neutrophils may be present within the blister.

A

Scalded skin sydrome

49
Q

flaking off of stratum corneum, as seen in eczema, psoriasis, or SCC; visible fragments as shed from skin

A

Scale:

50
Q

(i.e. cracks in the skin) as seen in inflammatory disorders; sharly defined, linear, or wedged shaped tears in epidermis with abrupt walls

A

Fissure:

51
Q

thickened, leathery skin usually d/t constant scratching and rubbing. With prolonged rubbing and scratching, the outer layer of the skin (epidermis) becomes hypertrophied (overgrown) & this results in thickening of the skin and exaggeration of the normal skin markings, giving the skin a leathery, bark-like appearance. (exaggerated skin lines)

A

Lichenification:

52
Q

traumatized or abraded skin caused by scratching and rubbing

A

Excoriation:

53
Q

occurrence of impetigo by infection of an area of existing dermatosis

A

Impetiginization:

54
Q

a localized defect in the skin of irregular size and shape where epidermis and some dermis have been lost

A

Ulceration:

55
Q

loss of superficial layers of upper epidermis by wearing away as from friction or pressure

A

Erosion:

56
Q

varying colors of liquid debris (serum or pus) that has dried on the surface of the skin

A

Crust:

Symptoms Midterm (12 decks)

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