Viral Diseases

Herpes
Simplex
Virus
(HSV)

Painful, recurrent vesicular

eruption of mucocutaneous
surfaces
HSV-1: Oral-labial lesions
HSV-2: Genital lesions
Virus spreads through
epidermal cells fuse into
giant cells
Local host inflammatory
response erythema +
swelling

Initial infxn passed by direct contact virus

remains dormant in local nerve ganglia
Primary episodes: longer, more severe than
recurrences
Onset: preceded by prodromal tingling, burning,
pain
Can also present w/ lymphadenopathy, fever,
discomfort, malaise, edema
Recurrences: limited to mucocutaneous areas
innervated by involved nerve
Recurrent oral (HSV-1): common cold sorecluster of crusted vesicles on erythematous
base. Trigger: sun, fever
Recurrent genital (HSV-2): Unilateral, cluster
of blisters on erythematous base, less pain +
systemic involvement than primary

Clinical
Tzanck smear of
vesicle base:
multinucleated giant
cells
*VSV has same
appearance on Tzanck,
so cx or direct IF Ab
staining needed for
definitive dx

Oral or IV Acyclovir
Frequency +
severity of
recurrences
Daily acyclovir,
famciclovir
suppressive therapy
Pts w/ >6
outbreaks per
year
Pts w/ EM
In AIDs pts HSV can
persist, ulcers
remaining resistant to
antiviral therapy

Dermatitis
Herpetifor
mis

Associated w/ celiac
disease (15-25% have it)

Pruritic papules + vesicles on elbows, knees,

buttocks, neck, and scalp

Bx: Granular IgA on

dermal papillae

Dapsone

Varicella
(Chickenpo
x)

Transmission: respiratory
droplet or direct

Prodrome: malaise, fever, headache, myalgia

24 hrs before rash onset

clinical

Self-limited in healthy
children- Benadryl

Incubation: 10-20 days

Contagious: 24 hrs before
eruption until lesions crust

Pruritic lesions over 2-3 days (dewdrop on rose

petal)
Lesions in all stages of development
over entire body
Palms and sole SPARED!

In first trimester
Microcephaly
Chorioretinitis
IUGR
Cataracts
Herpes
Zoster

Recurrence of VZV in specific

nerve

Infants, children,
adults: Vaccine
Adults: Acyclovir
Neonates:
VZIG if mom
contracted w/in 5
days of delivery

In adults: More severe

Systemic complications (pneumonia,
encephalitis)
Lesions preceded by intense local pain then arise
as grouped blisters on erythematous base
Dermatomal

Gluten-free diet

clinical

Acyclovir
**Pain control most
important

In immunocompromised: can lead to

severe local dz
Disseminated cuteanous dz
Systemic dz
Older pts: Postherpetic neuralgia
Molluscum
contagiosu
m

Poxvirus infxn

Tiny waxy papules, central umbilication

Clinical

MC in young children +
AIDS pts

Asymptomatic unless inflamed/irritated

Confirmed by
expressing/staining
contents of papules

Giemsa or
Wrights stain
Large inclusion or
molluscum bodies

Spread = physical contact

Children: trunk, extremities, face

Adults: genitalia, perineal region
AIDS: Face, large
**If see giant molluscum contagiosum
HIV

Verruca/co
ndyloma
(Warts)

Pathogen: many different

types of HPV
Location: skin, mucous
membranes, other pithelia
Usually benign, some
subtypes of HPV (16 +
18) squamous
malignancies
Spread: direct contact
HPV hyperproliferation of
infected cells
*Long latency period.
Children sometimes acquire
HPV at birth w/ no
manifestation until years
later

Common warts: Most prevalent HPV

Hands
Palmer + Plantar: grown downward into skin
flatter appearance
Genital: Cauliflower-like papule or nodule
appearing
Glans penis, vulva, perianal region
Mucous membranes: velvety + white
Oral, genital, laryngeal mucosa (transmitted
to infants by mothers w/ genital HPV)

Clinical
Acetowhitening
(mucosal lesions)

Any local destructive

method:
Curetting,
freezing, or
trichloroacetic
acid
Resolve
spontaneously over
months-years
untreated in
children
Destruction of tissue:
Curette,
cryotherapy, or
acid keratolytics
Genital warts:
Local
podophyllin,
trichloroacetic
acid, imiquimod,
or 5-FU
Cervix:
Must be
monitored
cytologically +
histologically for
evidence of
malignancy

BACTERIAL INFECTIONS
Impetigo

Superficial, weeping local infxn

Primarily in children

Common type: Pustules, honey-colored

crusts on erythematous base; Face

Pathogen: Group A strep (B-hemolytic)

and Staph

Bullous type: Acral; Large stable blisters

Almost always caused by S. aureus
Can evolve into SSSS

Spread = direct contact

ERYSIPELAS

Group A Strep

Clinical

Pts have hx of trauma or pharyngitis

Antibiotics w/ anti-staph activity

Penicillin

Small red patch on cheek

Turns into painful, raised, shiny red plaque
Scarlet fever

S. pyogenes

sunburn w/ goosebumps appearance

Penicillin

Strawberry tongue
Salmonella
typhi
Erythrasma

Small pink papules on trunk (rose spots) in

groups of 10-20
PLUS gallbladder disease!
Pathogen: Crynebacterium

Brownish-red patches w/ fine scales

Along major skin folds

Cholecystectomy for chronic

carrier state
Woods light exam:
coral-red fluorescence

Erythromycin (erythrasma =
erythromycin)

More common in diabetics

Gram stain: +
filamentous rods
Cellulitis

Deep, local infxn involving CT, subq

tissue, or muscle in addition to skin
Common pathogen: Staph or group A
strep. Originating from damaged skin or
systemic source of infxn

Red, hot, swollen, tender skin

Clinical

Oral antibiotics 7-10 days

Fever + chills common

Wound culture (may

help aid +
sensitivities)

Systemic toxicity, comorbid

conditions, DM, extremes of age,
hand or orbital involvement:
IV antibiotics

Regional lymphadenopathy

Blood cx (when
bacteremia
suspected)

Community acquired MRSA is

common risk
Risk

Necrotizing
fasciitis

factors:
Diabetes
IV drug use
Venous stasis
Immune compromise

Deep infxn along fascial plan

severe pain followed by anesthesia
Pathogen: S. pyogenes or Clostridium
perfringens
**Fournier gangrene = localized to
scrotum + perineal area

R/o abscess, urticaria,

contact dermatitis,
osteomyelitis, and
necrotizine fasciitis

Hx of trauma or recent surgery to affected area

Sudden onset of pain + swelling at site
anesthesia

Local radiographs or
CT : air in tissue
Biopsy (from edge of
lesion)

Erythema quickly spreads over hrs-days

Margins move into normal skin
Skin becomes dusky/purplish necrosis
If skin is open, gloved fingers can easily
pass btw two layers to reveal yellow-green
necrotic fascia

SURGICAL EMERGENCY!
Early + aggressive surgical
debridement
Strep: Penicillin G
Aerobic: metronidazole or 3rdgen cephalosporin

Most important signs: tissue necrosis, putrid

discharge, bullae, severe pain, gas production,
rapid burrowing through fascial planes, lack of
classical tissue inflammatory signs,
intravascular volume loss
Folliculitis

Inflammation of hair follicle

Tiny pustule- usually has hair penetrating it

Pathogen: Staph, Strep, and Gram

Bacteria, occasionally yeast (Candida,
Pityrosporum ovale)

Furuncle: deeper hair follicle abscess

Larger and more painful
May disseminate to adjacent follicles
carbuncle

*Pseudemonas aeruginosa hot

tub folliculitis

Clinical

Mild: Topical antibiotics

Severe: Systemic antibiotics
Large lesions: incised, drained,
cultured to r/o MRSA

Mechanical (ingrown hairs)

risk: Diabetes, Immunosuppression
Can be critical problem in AIDs pts
(intensely pruritic + resistant to therapy)
Acne

Chronic inflammatory condition of

pilosebaceous unit
Pathogenesis:

Hormonal activation of sebaceous

glands

Comedo (plugged sebaceous follicle)

Propionibacterium acnes in follicle

inflammation

Meds (lithium, corticosteroids)

Begins at puberty
Face, back, upper chest (greatest density of
sebaceous follicles)
Comedo:
Open comedones (blackheads)
Close comedones (whiteheads)
Inflammatory:
Comedo ruptures pustule (large/nodular)
Scar: picking at papules

Clinical

Mild comedonal acne topical

retinoid:

Tretinoin (retin-A) +
benzoyl peroxide
Mild popular or pustular acne
Topical Erythromycin/
clindamycin
Systemic: tetracycline
(photosensitivity),
erythromycin
**Severe acne or moderate
acne, primarily nodulocystic,
failing previous tx or have
scarring Isoretinoin
(Accutane)
Teratogen!!
Associated w/ depression
*Monthly blood tests (B-hcg,
LFTs, cholesterol, TGs)

Pilonidal
cysts

Abscesses in sacrococcygeal region

Repetitive trauma plays role

Abscess at natal cleft tender, fluctuant, warm

and indurated
*May develop into perianal fistulas

Starts as folliculitis abscess

complicated by perineal microbes
(Bacteroides)

Clinical

Incision + Drainage

r/o perirectal and anal

abscess

MC btw 20-40, Men > women

Risk: deep/hairy natal clefts, Obesity,
Sedentary lifestyle

FUNGAL INFECTION
Tinea
versicolor

Infection w/ Malassezia furfur (normal

skin yeast)
Risk: Humid and sweaty conditions,
oily skin, Cushings syndrome,
Immunosuppression

Candidasis

Chest and back

Clinical

Small, scaly patches of varying color

KOH prep:
spaghetti and
metaballs pattern of
hyphae and spores

Pale, velvety pink or whitish, hypopigmented

macules or hyperpigmented (thickened scale)
Do not tan and are NOT scaly
Scale on scraping
Oral: painless white plaques, cannot easily be
scraped off

Risk: antibiotics, steroids, diabetes

Skin: pink, circular, erythematous macules that
converge, with smaller satellete lesions nearby in
skinfolds

Clinical
KOH prep: hyphae +
pseudospores

Topical selenium sulfide daily x

1 week
Ketoconazole shampoo
*Inform pt. change in
pigmentation takes months to
return to normal
Oral: Oral fluconazole; Nystatin
swish and swallow
Skin: Topical antifungals; keep
skin clean and dry
Diaper: Topical nystatin

Infants: diaper area along inguinal folds

Dermatophy
te infections

Dermatophytes live only in tissues

with keratin (skin, nails, and hair)
Organisms: Microsporum,
Trichophyton, Epidermophyton
Risk: Pets, diabetes, peripheral
circulation, immune compromise,
chronic maceration of skin (athetic
activities)

Tinea corporis: scaly, pruritic eruption w/ sharp,

irregular border central clearing
Immunocompromised or children following
contact w/ infected pet

Clinical

Topical or systemic antifungals

KOH prep: hyphae

*Tinea capitis must be treated w/

systemic drugs

Seen on hair follicles

or clothing

Head lice:
OTC pyrethrin (RID) +
mechanical removal of nits

Tinea pedis/manuum: Chronic interdigital scaling

w/ erosions btw toes (athletes foot) or
thickened, scaly skin on soles
Assymmetric involvement of hands typical
Tinea crurus (jock itch): chronic infxn of groin
(spares scrotum)
Tinea capitis (ringworm): diffuse, scaly scalp
eruption similar to sebhorreic dermatitis

PARASITIC
Lice

Live off blood

Head louse: scalp, layes eggs as nits
attached to hair
Body louse: clothing; bites only body
Pubic louse: pubic hair
Spread: body contact or sharing
bedclothes/garments
Secrete local toxins pruritis

Scabies

Pathogen: Sarcoptes scabiei (mates

on skin surface female digs
passage into stratum corneum lays
eggs). Burrowing pruritis
intensity when allergy develops
Spread: close contact

Severe pruritis, secondary bacterial infection of

excoriations
Classroom epidemics common

Body lice:
Wash body, clothes, and
bedding thoroughly
Topical permethrin or
pyrethrin

Body lice: inadequate hygiene, crowded living

conditions
Pubic lice (crabs): anticoagulant in saliva
blue bites

Pubic: RID
Intense pruritis, especially at night + after hot
showers
MC sites: hands, axillae, genitals

Mite may be
identifiable by
scraping intact
tunnels and looking
under microscope

Exam: track seen, erythematous, excoriated

papules

Overnight: 1-2 applications of

5% permethrin cream from
neck down
*Contacts treated as well!
Oral ivermectin
Pruritis may persist 2 weeks
after tx, so provide symptomatic
tx

Hx of pruritis in several family members

ISCHEMIC DISORDERS
Decubitus
ulcers

Continuous pressure on skin restricts

microcirculation Ischemic necrosis
Incontinence of urine or stool
macerates skin ulceration

Grade I: Perisstent redness

Grade II: Ulceration

*Prevention is key!
Routinely move bedridden
pts (special beds)

Grade III: destruction of structures beneath skin

(muscle or fat)

Low grade: wound care

(hydrocolloid dressings)

MC in bedridden pts

Clinical

High grade: surgical

debridement

Risk: underlying bony predominance,

fat, lack mobility, lack cutaneous
sensation
Venous
stasis ulcers

Near lateral or medial malleolus

Associated w/ lower extremity edema

Arterial
insufficiency

Heel + tips of toes

Very PAINFUL

Neuropathic

Underside of foot + toes

Compression (unna boots or

compression sockings)
+ Elevation

ulcers
Gangrene

At pressure points. PAINLESS

Necrosis of body tissue
Dry: insudfficient blood flow to tissue;
atherosclerosis
Wet: baterial infxn w/ skin flora
Gas: clostridium perfringens infxn

Dry:
Early: dull ache, cold, and pallor of flesh
w/ necrosis (usually toe) becomes bluishblack, dry, and shriveled
Risk: Diabetes, vasculopathy, smoking

Clinical

Surgical debridement,
amputation if necessary
*Antibiotics alone do NOT
suffice (d/t inadequate blood
flow) but given as adjuvant to
surgery

Wet:
tissue appears bruised, swollen, or blistered
w/ pus

Gas gangrene:
Hyperbaric O2 (toxic to
anaerobic C. perfringens)
Susceptible pts should
maintain careful foot care
and avoid trauma

Gas:
At site of recent injury/surgery
Swelling around injury, skin turns pale then
dark red
Bacteria rapidly destructive of tissue gas
separates healthy tissue predisposes
to infxn
MEDICAL EMERGENCY!

MISCELLANEOUS SKIN DISORDERS

Acanthosis
nigrans

Sin in intertriginous zones

(genital and axillary regions, nape of
neck) is hyperkeratotic +
hyperpigmented w/ velvety
appearance

Fasting glucose to
r/o insulin
resistance

Topical retinoids but

typically not treated

Histology:
lichnoid pattern
band of T
lymphocytes at
epidermaldermal jxn w/
damage to basal
layer

Mild: topical steroids

Clinical

Avoid triggers that

aggravate vasodilation
(coffee, tea, hot drinks,
spicy foods, chocolate,
alcohol)

Encourage to lose weight!!

Associated w/
DM
Obesity
HAIR-AN Syndrome
Cushing disease
Gi adenocarcinoma
(paraneoplastic syndrome)
Lichen
planus

Chronic inflammatory dermatosis

involving skin + mucous
membranes
Middle-aged women between 30
and 60

Voilaceous, flat-topped, polygonal

papules

Intense pruritis, can be induced by

drugs, associated w/ Hep. C

Koebners Phenomenon: lesions

appear at site of trauma

Rosacea

Wickmans striae (white stripes), esp.

on mucous membranes

disease:
Planar, Polygonal, Purple
Pruritis, Persistent
Penile, Perioral, Koebners
phenomenon

Chronic inflammatory condition w/

facial flushing, localized erythema,
telangiectasia, papules, and
pustules
Women, middle-aged 30-50,
abnormal flushing response to
various substances
Do NOT have comedones (vs. acne)

Early: Central facial erythema w/

telangiectasias
Later: Papules and pustules
Associated findings:
Ocular keratitis (gritty sensation in
eyes)
Rhinophyma (sebaceous gland
hyperplasia of nose)

Urinary 5-HIAA (r/o

carcinoid
syndrome)
Serology (r/o SLE)

Acute dermatitis pink + scaly

Rxn to viral infxn w/ HHV 6 or 7
Tends to occur in miniepidemics among young
adults

Initial lesion: Herald patch (several cm

+ erythematous w/ a peripheral scale)
Days-weeks: multiple tiny, symmetric
papules w/ fine cigarette paper scale.
Christmas tree pattern: papules
arranged alone skin lines on pts back
Pts generally asymptomatic

Vitiligo

Disease of depigmentation
Chronic + Progressive
Serologic markers of
autoimmune dz
Anithyroid Abs, DM, pernicious
anemia
Pts w/ malignant melanoma may
develop antimelanocyte immune

Small, sharply demarcated,

depigmented macules/patches on
otherwise normal skin
Hands, face, genitalia
Peri-orificial lesions or lesions on finger
tips
Total depigmentation (vs. lightened in
tinea versicolor)

Oral mucosa: Tretinoin gel

*Most cases resolve
spontaneously 6-18 mo.
Oral have more chronic
course.

Mild: low-potency topical

steroids or topical
metronidazole
Severe cases: Both oral +
topical therapy

Environmental triggers (infectious

agents, sunlight, certain foods/drinks)
Pityriasis
rosea

Severe: Systemic steroids

Clinical

Heal w/out tx in 2-3 weeks

KOH (r/o fungus)

Skin lubrication, topical

antipruritics, systemic
antihistamines

Differential:
Secondary
syphilis (RPR)
(Systemic sx)
Guttate
psoriasis
(smaller,
thicker scale)
Drug eruptions
Clinical
Histo: total
absence of
melanocytes
r/o:
postinflammatory
hypopigmentation,
scleroderma,
piebaldism, toxin

Severe: short course of

systemic steroids

Topical/systemic psoralens
Exposure to sunlight or
PUVA
Must wear sunscreen
(depigmented skin lacks
protection)

DYSPLASIAS
Seborrheic
keratosis

Benign thickening s of epidermis

MC = back and chest

Clinical diagnosis

Very
common,
in all pts >40
response
almost
vitiligo

>50 years

When may erupt suddenly, may be

part of paraneoplastic syndrome
(d/t tumor production of epidermal
growth factors)

Exophytic, waxy brown,stuck on appearing

papules/plaques

Histo:
hyperplasia of
exposure
benign,
basaloid epidermal
(phenolated
cells
w/
horn pseudocysts
cleaners
= toxic to
(prominent follicular
melanocytes)
openings)

May become irritated spontaneously or by

external trauma (esp. in groin, breast, or axillae)

NO malignant potential!
Actinic
keratosis

Pre-malignant lesion

Predisposes pt to SCC in situ

Squamous cell
carcinoma

2nd MC skin tumor locally destructive

effects + potential for metastasis +
death

Clinical

Dry, scaly papules w/ erythematous base

Bx (r/o SCC):
intraepidermal atypia over
sun-damaged dermis

Face, lower lip, hand dorsum, forearms, bald

scalp, ears

DDx: Bowens disease

(form of SCC in situ)

Arise from actinic keratosis rarely metastasize

Clinical

Lips down or ulcers that wont heal

more likely to metastasize

Confirmation: Biopsy

MCC = UV light
Other:

If carcinoma suspected:

Excision/curettage
Advise pts to use sun
protection
Surgical excision or
radiation

Necessary for dx +
Intraepidermal
atypical
keratinocytes w/
penetration of BM by
malignant epidermal
cells growing into
dermis

sinuses (osteomyelitis)
Older adults w/ sun-damaged skin,
arising from actinic keratosis

Basal cell
carcinoma

Cryosurgery, topical 5-FU,

or topical imiquimod

therapy

Chemical carcinogens
prior radiation therapy
chronically draining infectious

Keratoacantho
ma

Removed for cosmetic

reasons

r/o actinic keratosis, lentigo

(focal in melanocytes),
SCC, and BCC

Middle aged/Older men

Sandpaper-like texture

Outdoor occupation (excessive

sunlight)

No treatment necessary
d/t benign nature

Graded histologically

Benign epithelial tumor

Looks like SCC but develops more rapidly and

may regress spontaneously

Similar to SCCs

Lupus
Multisystem autoimmune dz related
Nonspecific sx: fever, anorexia, weight
erytehmatos
totumor
Ab-mediated cellularVarying
attackdegrees
+
loss, symmetric
joint pain
MC Malignant skin
of pigmentation,
ulceration,
and
Clinical
depth
of
growth
us (discoid,
deposition of Ag-Ab complexes
Slow
growing,
locally
destructive,
Confirmation: biopsy
subacute,
*Have 4 criteria
virtually NO metastatic potential
SLE)
Risk: African AmericansUpper lip up
D Discoid rash
Islands of proliferating
O - border
Oral ulcers
MC Risk: Chronic UV light
Pearly nodule w/ rolled
epithelium resebling
Usually affects women of
P Photosensitivity
basal layer of
childbearing
age
A Arthritis
Multiple lesions on
non-sun-exposed
epidermis
areas more suggestive of arsenic
M Malar rash
exposure or inherited basal cell
Differential:
I Immunologic criteria
nevus syndrome
N Neuro sx (Lupus cerebritis, seizures)
Benign tumors
E Elevated ESR
Location: Face, other sun-exposed

Mild joint sx: NSAIDS

Excision, curettage and
electrodesiccation/cautery
Acute exacerbations:
, deep cryotherapy,
Corticosteroids
superficial radiation
therapy, and Mohs
surgery

Progressive refractory

cases:
Cure rates >95%

Corticosteroids
Hydroxychloroquine
Cyclophosphamide
azathioprine

Hypopigmented

areas

R Renal dz (proteinuria, casts) melanocytic nevi

A ANA + (highly sensitive, not
Melanoma
specific)
S Serositis (pleural or pericardial
Dermatitis
effusion)
H Hematologic abnormalities (Anemia,
Psoriasis
Leukopenia, thrombocytopenia)

Pagets disease

Melanoma

Scleroder
ma

MC life-threatening dermatologic
dz

First growth phase: horizontal-intraepidermal

flat but in diameter (typical of lentigo
maligna or melanoma in situ)

Inflammation excessive
Raynauds, dysphagia, mask-like face, tight skin
Risk:
deposition of type I and III
Later: vertical growth phase (dermal invasion)
Short,
intense bursts of sun
collagen
progressive
Symmetric thickening of skin face and/or distal
Pruritis = early sign of malignant change
tissueexposure
fibrosis (esp. in childhood +extremities
w/

intermittent exposure)
Characteristics:
CREST Syndrome (limited
Associated
w/ CREST Syndrome (limited
Congenital melanocytic nevi,
form)
form):
Irregular pigment
Calcinosis
# of nevi,
Diffuse form: skin, GI, GU,
Raynauds
phenomenon
Irregular
contour + border
renal,Dysplastic
pulmonary,
and
nevi,
Esophageal dysmotility
Nodule
and
ulcer formation
cardiovascular systemis
Sclerodactyly
Immunosuppression
Telangiectasias
Changes in size/shape/color/contour/surface
Risk:
Genetics:
Familial atypical mole,Diffuse form:
Female
Melanoma
(FAM-M) syndrome
Age 35-50
Pulmonary fibrosis

Kaposis
Sarcoma (KS)

Amyloido
sis

Cor pulmonale
Acute renal failure
Vascular proliferative dz attributed to Malignant
Classic variant:
HTN
herpesvirus, HHV-8, also called
Kaposis sarcoma-associated
herpesvirus (KSHV)

Extracellular deposition of
protein fibrils
Dz of elderly

Multicentric vascular macules + coalescent

papules/plaques on lower extremities

Elderly Ashkenazi Jewish or Mediterranean

Mycosis

Malignancy determined
RF
and ANA may be +
histologically

Anticentromere
Staged by Breslows Abs
(specific
CREST)
thickenessfor
and
tumornode-metastasis (TMN)

Anti-Scl-70
Clarks level = another
(antitopoisomerase
1)
classification system linking
Abs
associated
melanoma
depthw/
to
diffuse
dz and poor
prognosis
prognosis

Biopsy: spindle cells

(elongated tumor cells) w/
+HHV-8 staining

Palliative is d/t
*Mortality
pulmonary HTN and
complications of
pulmonary HTN

PrimaryMore
systemic
(AL) and
Seconary systemic
disseminated
cases:
(AA): Kidneys, heart, liver

Bx (confirms):
Congo
cells
red stain apple
green birefringence
under polarized light

African KS (endemic KS)

Immunocompromised

Excision w/

Acute flairs:
margins
Corticosteroids
D-penicillamine
LN dissection for
(for
skin changes
staging
inhibits collagen
Malignant:
cross-linking)
Ca2+
channel
Potential
to relapse
blockers

after several years

amlodipine,
Pts w/ early(for
nifedipine
raynauds)
melanoma at low risk
for relapse
but high
ACEIs
for renal
dz +
risk for subsequent
prevention
of
melanomas
scleroderma renal
crisis
Pt. surveillance
essential

Hx and clinical impression

Dx: Clinical
Presence of viral

descent

Confined to skin:

Macroglossia, waxy papules on face

Alzheimers dz: Brain

Tuberous
sclerosis

Total excision biopsy

protein LANA in tumor

Retinal phacomas, seizures, MR, sebaceous

Epidemic
HIV-associated
KS
adeomas,
ash-leaf
hypopigmented
macules

Seizure control

Aggressive form of dz
Most common HIV-associated malignancy

Slow, progressive neoplastic

Early lesion: nonspiecific, psoriatic-appearing

Clinical + Histology

Stage I: Topical steroids,

Porphyra
cutanea
tarda

Associated w/ Hep. C

NO abd pain
+ red urine
Vesicles on back of hand after drinking alcohol,
drugs, estrogens

Lyme
disease

Tick-borne
Pathogen: Borrelia
burgdorferi
Carrier: Ixodes ticks on
white-tailed deer and
white-footed mice

Onset of rash w/ fever, malaise, fatigue,

headache, myalgias, and/or arthralgias

Summer months
Endemic to northeast

Primary (early-localized):
Erythema migrans (small erythematous
macule/papule at tick-biting site expands
slowly weeks-days)
Border macular or raised, central clearing
(bulls eye)
Secondary (early disseminated):
Migratory polyarthropathy
Neurologic phenomena (bells palsy)
Meningitis
Myocarditis
Conduction abnormalities (3rd deg. Block)
Tertiary (late disease):
Arthritis
Subacute encephalitis (memory loss +
mood change)

Stop EtOH
Then phlebotomy

Clinical dx of erythema
migrans:
ELISA (+ =
exposure)
Western Blot
(confirms)
Tissure cx + PCR
(not routinely done)

Early: Doxycycline
CNS + arthritic:
Ceftriaxone