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Unit 3 D&D > DD 03-10-14 10-11am Skin Signs of Systemic Disease - Dunnick > Flashcards

DD 03-10-14 10-11am Skin Signs of Systemic Disease - Dunnick Flashcards

1
Q

Clubbing – defn.

A

Nail plate is enlarged & excessively curved (>180 degree angle btwn proximal nail fold & nail plate)

Caused by enlarge of the soft tissue of the distal digit

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2
Q

Clubbing – etiologies

A

Rarely idiopathic/primary

Pulmonary disease (idiopathic, pulmonary fibrosis, lung cancer)

Cardiac disease (cyanotic congenital heart disease)

GI disease (Crohn disease, Ulcerative colitis, Proctitis)

Malignancies (Thyroid / Thymus cancer, Hodgkin disease)

Hypoxemia (possibly related to long-term cannabis smoking)

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3
Q

Terry’s Nails

A

Liver cirrhosis in 82% (also in normal individuals)

Leukonychia affects entire nail except for 1-2 mm distal band

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4
Q

Half-n-half nails

A

Distal nail is normal, proximal nail is white

In 10% of pts w/chronic renal failure (also in normal individuals)

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5
Q

Proximal Subungual White Onychomycosis

A

Associated w/HIV disease

Usually due to Trichophyton rubrum (more specifically called tinea ungum)

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6
Q

Kaposi’s Sarcoma (KS)

A

Usually related to immunosuppression

ENDOthelial malignancy, triggered by HHV-8

Slowly progressive, not very common

Generally brownish purple/red patches

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7
Q

Classic Kaposi’s sarcoma

A

Occurs mostly in elderly men of Eastern European descent

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8
Q

Lymphadenopathic Kaposi’s sarcoma

A

Aggressive form primarily in equatorial Africa

Affects young men & is rapidly fatal

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9
Q

AIDS-Associated Kaposi’s Sarcoma

A

More frequent in homosexual pts w/AIDS

Incidence declining w/better anti-retroviral therapy against HIV

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10
Q

Therapy for Kaposi’s Sarcoma

A

Radiation therapy
Excision
Interferon alpha
Chemotherapy

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11
Q

Thyroid disease – signs/symptoms

A
  • Exophthalmos
  • Pretibial myxedema
  • May cause alopecia areata (if see alopecia, test TSH)
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12
Q

Alopecia areata – association

A

T cells fighting off hair cells, so…

Associated w/other autoimmune diseases:

  • thyroid
  • vitiligo
  • IBD
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13
Q

Alopecia areata – Clinical Non-Scarring Alopecia

A

Round/oval patches of hair loss
Short “exclamation point” hairs, broader at distal end
Hairs often re-row w/ depigmentation

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14
Q

Alopecia areata – Clinical subtypes

A 
Patch focal
Ophiasis pattern
Diffuse variant
Alopecial totalis (all scalp hair)
Alopecia unversalis (all body hair)
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15
Q

Vitiligo - characteristics

A

Development of total white macules / patches

Histology show complete absence of melanocytes

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16
Q

Vitiligo – Associations

A

Most commonly thyroid disease (Hashimoto thyroiditis, Graves’ disease) – screen TSH levels

Other endocrine disorders (Diabetes Mellitis, Pernicious Anemia, Addison’s disease)

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17
Q

Vitiligo – Treatment

A

Topical steroids

Topical calcineuron inhibitor (protopic ointment)

Narrow-band UVB (311nm) or Excrimer Laser (308 nm) –> repigmentation

Psoralens plus UVA (PUVA)

Minigrafting

Depigmentation (monobenzylether of hydroquinone cream)

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18
Q

Excimer laser

A

UVB ray source (308nm)

Xenon-Chloride lamp emitting non-coherent, monochromatic 308nm light

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19
Q

Erythema Nodosum – clinical manifestations

A

Painful, erythematous subQ nodules (subQ inflammation)

Usually symmetically over pretibial lower extremities

Develop bruiselike appearance in later stages

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20
Q

Erythema nodosum – M vs. F, Associated symptoms, Histopathology

A

More common in women

May also have fever, arthralgias, malaise

Histopathology shows septal panniculitis wit neutrophils (inflame. in subQ fat)

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21
Q

Erythemia nodosum - etiology

A

Delayed hypersensitivity to various antigen stimuli (usually infections)

Most common cause: Strep infections, esp. URI

Other infections (1/3 of the cases) – viral URIs, Mycoplasma, TB

Coccidioidomycosis

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22
Q

Erythema nodosum – other more common associations

A

Idiopathic (35-55%)
Drugs – estrogens, oral contraceptives, sulfonamides, penicillin, bromides, iodides
Sarcoidosis (11-22%)
IBD (esp. Crohn’s)

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23
Q

Treatment of Erythema nodosom

A

Bed rest
Treat underlying condition
NSAIDs – Naproxen, Indomethacin

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24
Q

Pyroderma Gangrenosum - clinical manifestations of lesions

A

Initial lesion often pustule on erythematous base or erythematous nodule

Characteristic lesion is an ulcer w/necrotic, undermined (rolled) border

Painful

Usually on lower extremities

Often begins in sites of minor trauma (pathergy)

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25
Q

Pyoderma Gangrenosum – associations

A
  • 50-70% have underying associated condition
  • IBD (20-30%)
  • Arthritis (seronegative arthritis, RA – 20%)
  • Monoclonal gammopathy (often IgA, up to 15%)
  • Other hematologic disorders (Myelogenous leukemia, hair cell leukemia, myelofibrosis – 10%)
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26
Q

Treatment of Pyoderma Gangrenosum

A
  • Conservative wound care
  • AVOID SURGERY/DEBRIDEMENT (causes more injury, more inflammation, never heals)
  • Oral / topical anti-inflammatory agents like steroids
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27
Q

Lichen Planus – clinical manifestations

A
  • Purple polygonal pruritic papules
  • Wickham’s striae = overlying lace-like pattern of white lines on the surface
  • Mucosal lesions w/out skin findings in 15-25% of pts
  • Nail involvement in 10% (may be only involvement)
28
Q

Lichen Planus – Clinical Variants

A 
Annular or Linear (Koebner)
Hypertrophic or Atrophic
Erosive/ulcerative
Actinic
Bullous
29
Q

Lichen Planus – Associations

A

Hepatits C – screen for

Contact allergy to dental metals (amalgams [mercury], copper, gold)

30
Q

Lichen Planus – Treatment

A

Nothing works very well :(

  • Corticosteroids (Topical, Intralesional, Oral
  • Phototherapy
  • Systemic retinoids (isotretinoin, acetretin)
  • Griseofulvin
  • Dapsone
  • Plaquenil
  • Cyclosporine

*treatment of underlying HepC won’t necessarily make lichen planus go away

31
Q

Acanthosis Nigricans – clinical manifestations

A

Velvety hyperpigmentation of intertriginous surfaces & extensor surfaces (less commonly)

Most often neck, axillae, dorsal hands

32
Q

Acanthosis Nigricans – due to…

A

Due to factors stimulating epidermal keratinocytes & dermal fibroblast proliferations

33
Q

Acanthosis Nigricans – Associations

A
  • Rarely Familial : AD, onset in childhood
  • *Obesity
  • *Diabetes mellitus & Insulin resistance
  • Endocrinopathies (hyperandrogenemia, Cushing’s, polycystic ovary, total lipodystrophy)
  • Drugs (rare) – nicotinic acids, systemic steroids
  • Malignancy
34
Q

Acanthosis Nigricans –Malignancy

A
  • May precede or accompany or follow onset of internal cancer
  • Malignancies include gastric adenocarcinoma (also, lung & breast cancer, others)
  • Rapid onset w/ weight loss (to distinguish from other reasons for acanthosis nigricans)
35
Q

Acanthosis Nigricans – Treatment

A

Treat underlying disorder

Keratolytics like ammonium lactate or urea cream (exfoliate)

36
Q

Dermatomyositis – clinical manifestations

A
  • Photodistributed violaceous poikiloderma
  • favors scalp, periocular & extensor skin sites
  • Heliotrope = eruption on upper eyelids +/- periorbital edema
  • Samitz sign
  • Gottron’s papules
  • Gottron’s sign
  • Shawl sign
37
Q

Dermatomyositis – Samitz sign

A

ragged cuticles in Dermatomyositis

38
Q

Dermatomyositis – Gottron’s papules

A

Lichenoid papules overlying knuckles, elbows, knees in Dermatomyositis

39
Q

Dermatomyositis – Gottron’s sign

A

Poikiloderma over knuckles, elbows, knees in Dermatomyositis

40
Q

Dermatomyositis – shawl sign

A

Poikiloderma across back & shoulders in Dermatomyositis

41
Q

Dermatomyositis – Malignancy prevalence

A
  • Internal malignancy in adults from 10-50%
  • More often in females
  • May be higher in pts w/dermatomyositis sine myositis
  • With new onset dermatomyositis in older adult (usually not kids), think about malignancy
42
Q

Dermatomyositis – Malignancy types

A

Most common: GU malignancies, esp. ovarian
Others: breast, lung, gastric carcinoms
Nasopharyngeal carcinoma in Asian men

43
Q

Dermatomyositis – Malignancy work-up

A

Complete Hx & PE

Age appropriate malignancy screening (mammo, CXR, colonoscopy, Pap, PSA, CBC)

Repeat malignancy screen ever 6-12 mo for 1st 2 yrs or more

Risk of malignancy declines after 1st 2 years & reaches baseline after 5yrs

44
Q

Dermatomyositis – Treatment of Skin disease

A 
Sunscreen
Topical steroids
Hydroxychloroquine
Quinacrine
Methotrexate
Retinoids
45
Q

Dermatomyositis – Treatment of Systemic disease

A
  • Oral prednisone (tapered over 2-3 years)
  • Methotrexate
  • Azathiprine
  • High dose IVIG
46
Q

Acute urticaria – rxn type

A

Immediate type I hypersensitivity rxn by IgE antibodies

47
Q

Urticaria – Acute vs. Chronic

A

Acute: 6 week duration, women

  • most often in women 20-40 yo
  • may be related to circulating autoAbs against Ig-epsilon-R1 or IgE
48
Q

Causes of Urticaria

A

Usually idiopathic/autoimmune

Infection, Drugs, Foods, Vasculitis, Contactants, Inhalants, Pregnancy, Meds

49
Q

Drugs & Urticaria

A

Cause <10% of all urticaria

Commmon drugs : Penicillins, Cephalosporins, NSAIDs, mAbs, Contrast media, Latex

50
Q

Eczematous eruptions

A

Most common type of drug rxn in skin

Usually cell-mediated type IV hypersensitivity

Begins 7-14 days after new med (sooner if receiving “old” med)

51
Q

Exanthematous eruptions - causes

A

Occur all over the body – systemic drug rxn or infection, usually

More commonly drug-induced in adults

Aminopenicillins, sulfonamides, cephalosporins, anticonvulsants, allopurinol

52
Q

Exanthematous drug eruption - treatment

A
  • Discontinue offending med & check of results in three weeks (educated guesswork)
  • Supportive topical steroids & anti-histamines
  • Generally resolves spontaneously after 1-2 weeks (but can take up to 3 mo to resolve completely)
53
Q

Stevens-Johnson Syndrome vs. Toxic Epidermal Necrolysis

A

30% = Toxic epidermal necrolysis

In between = overlap syndrome

54
Q

Stevens-Johnson Syndrome – clinical manifestations

A
  • Eruption on face/upper trunk –> may become confluent
  • Evolves to skin necrosis & flaccid bullae
  • Involves mucous membrane
55
Q

Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis –Cause

A

Due to abnormal drug metabolism & immune-complex mediated hypdersensitivity

56
Q

Stevens-Johnson Syndrome – characterized by

A

Epidermal detachment

57
Q

Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis – Long term sequelae

A

Ocular problems including conjunctival synechiae & blindness

58
Q

Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis – Med causes

A
  • Antibiotics (sulfur, ampicillin)
  • Seizure meds
  • NSAIDS
  • Allopurinol
  • Antiretroviral (Nevirapine, Abacavir)
59
Q

Stevens-Johnson Syndrome – Treatment

A
  • Early withdrawal of all possible offending drugs
  • Symptomatic (dressing, IVF, nutrition)
  • Steroids / High dose IVIG = controversial
60
Q

Toxic Epidermal Necrolysis – SCORTEN

A

Score based on Prognostic factors to determine Mortality:

  • Age >40yrs
  • HR >120 bpm
  • Malignancy
  • Body Surface Area (BSA) >10% at day 1
  • high BUN & Glucose, low Bicarb
61
Q

Skin signs of Thyroid disease

A

Vitiligo
Alopecia areata
Exophthalmos
Pretibial myxedema

62
Q

Signs of immunosuppression

A

Kaposi’s sarcoma

Proximal subungual onychomycosis

63
Q

Skin & GI disorders

A

Hep C virus = Lichen planus

IBD = Erythema nodosum, Pyoderma grangrenosum

64
Q

Skin signs of internal malignancy

A

Acanthosis Nigricans
Dermatomyositis
Clubbing

65
Q

Drug eruptions

A

Urticaria
Morbilliform eruptions
Steven Johnson syndrome
Toxic Epidermal Necrolysis

Unit 3 D&D (18 decks)

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