Dermatology Textbook

HOW TO DEAL WITH
ADERMATOLOGICAL CASE
Functions of Skin
. h largest organ of the body since:

Skin IS t e
e adult it covers about 3000 square inches.
In the averag
in weighs around 2. 7 kilogram, which is nearly double th e weight of th h
Human sk e uman brain
or liver.
The skin receives about 1/3 of the blood that circulates through the body
functions of skin:
l. Protection: against any injury either mechanical as stab wound or thermal as hot objects or
chemical as acids . . .
mperature regulation: through skin sweati ng
2. Tie · f I · k.
_Sensation: all types of sensations are et ~,a s _1n
3• Excretion: minute amounts o~ ure~ an~ uric acid are ex~ret~d via sweat
4 Synthesis of vitamin O: pro-v1tam1n D 1s converted to v1tam1n Don exposure to UVR in the
s.
skin
. UVR Screening: melanin in the skin reflects the UVR and protects the internal organs
6. Regulation of blood pressure: this is achieved via the arteriovenous shunts in the skin
7 Absorption: of systemic medication can be administrated via the skin as in nicotine patch
s.
. Psychogenic function: skin is the mirror of the body feeling. Fear may induce hair erection
9
For management of a dermatological disease, certain items must be fulfilled;
1- History taking
2- Clinical examination
3- Investigations (if needed)
4- Treatment
History Taking
1-Personal History:
A) Name: for patient identification
B) Age & sex: certain diseases occur in certain age and sex. (acne in adolescent & C.T diseases are
more common in females)
C) Occupation: skin exposed to external environment. (house wives eczema)
D) Residence: endemic disorder such as leprosy in upper Egypt & cutaneous leishmaniasis in Iraq
2-Present History:
A) Complaint: may be disfigurement, itching or burning sensation.

B) Onset: acute, chronic or acute exacerbation on top of chronic illness.
C) Course: progressive, stationary or regressive.
3-Past History:
Important In recurrent disorders shplex
4-Family History:
Important in con . I . .
genita and infestation disorders (as ichthyosis & Scabies)
Scanned by TapScanner
Initial lesions
5-Drug History:
Drugs taken before appearance of the disease may cause drug eruption
B) Clinical Examination
1- General examination:
Skin disorders associated with syst emic disorders as leprosy may be associated with he a
splenomegaly and lymph adenopathy P to-
2- Local examination:
I) Examination of skin:
1- Examination from distance: to comment of skin lesion distribution

2- Close-up examination: to describe the details of skin lesions
II) Examination of skin appendages:

Mucus membranes, nails and hair.
Examination of the skin

A) From distance:
Shows the distribution of lesions that may be:
1) Discrete distribution: multiple lesions separated from each other by normal skin with bizarre
arrangement
Discrete Distribution
2 J Unitateral distribution:
Lesions involving only one side of the body. ~
Unilateral Distribution
3 ) ~eneralized distribution·
les10 · - ·
. ns involving more than 50% of body surface area .
Generalized Distribution
4) Grouped distribution:
Lesions are restricted to a localized area.
Grouped Distribution &

-") \ \':)~ ,l ~
SJ Linear distribution: \ ['l)v'\Lwfl.U)v,.~"~u.

Lesions are arranged a long a line. It may be koebnerization which is appearance of isomorphic
lesions along the site of blunt trauma.
Linear Distribution
Koebner Phenomena
7) Follicular distribution:
6) Zosteriform distrib\Jtion: . dermatome. Lesions are arranged along hair f n·
Lesions are rest ricted to cert~,n-=-=- - - 0 lt1'.i
•
Zosteriform Distribution Follicular Distribution
'
B) Close-up examination
Shows the border of lesions that may be:
1) Well defined border: 2) Ill defined border:

Marked separation between the edge of the Difficult to identify the separation line be-
lesion and normal skin. tween the lesion and normal skin.
Lesion with well defined border

Lesion with ill defined border
3) Circinate border:
The lesion increases in size by peripheral extension and healing at the centre
Lesion with circinate border
-
I .
--__;,-~~-...- Types of Skin lesions<----------..;

'' , . .-~--"-,- - - ~ -
-
111:;_=- ...
; ~
... - . .
Skin lesions may be: ~ --~~----

...
.,,,._, ,
!-Initial (primarY) lesions: n ean.s the first fesi n to appear or important lesion
l-Sccor.dary lesions: means lesion that appears on top of primary lesion or less important lesion
3-Sp zjfic lesions: means diagnostic lesion
tia .: 'n lesions are:

L\- ac:u e & patch
S-P'a e & aque
C odue
O-\'es.ide & Bulla
A) Initial Lesions
1) Mactde:
It is discolouration of skin less than one cm in diameter. If larger than one cm, it is called patch.
Macules and Patches
2) Papule: _ · · II d I
Solid elevation of the skin less than one cm in diameter. If more than one cm, ,t 1s ca e P aque
Types of Papufe
a) Dome shaped:
Papule with smooth convex surface·--~-----:------:::;-7
I I ., ., 3 4
O.:a 1 - J 0 (Ill l •
Papule
Plaque
Dome shaped papule
d) Verrucous Pap
) umbilicated: I with 1
c e shaped papu e Pa pule with fi "•:
b) Flat topped: oom ne rtia
ce ntral notch . surface. Fllll'\11,
Papule with flat su~face. It Is
described as licheno1d papule.
B) !
1
It
t
Umbillcated Papule Verrucous Papule

Flat topped papule
3) Nodule: . . I . ·th dermal extension. Usually better felt than seen.

Elevated solid skin es1on w1
Nodule
4) Vesicle:
Fluid containing lesion less than one cm in diameter. If larger than one cm, it is called bulla. The
bulla may be tense or flaccid. The flaccid bu Ila is intraepidermal so it has a thin wall while the
tense bulla is subepidermal so it has a thick wall.
--
a
- Q"
Tense Bulla Flaccid Bulla Vesicle
-
B) Secondary Lesions
1) Pustule= . 2) Scales: It ls dry surface dllC to ~bnor,nJI k r tin,

ft .IS e lev,,,ted fluid filled lesion con-
(ii zation (differentiation of epidern,al cellc. to form ker -
taining pus. atin) . when skin kerat1nization Is rapid, keratin will
accumulate and separate in thick. masses noueed.
Scales
Types of Scales:
a) Fine branny: ·~ b) Greasy:

Fine sca les that easy detached on
Oily grey yellow scales. Example: seb-
scrapping. Example: pytriasis versi- orrheic Dermatitis
co1or
Fine branny scales

Greasy scales
c) Lamellar: d) Fish scales:

Multiple layers of scales. Example: Scales are grayish brown and fixed in
• •
psor1as1s
the center and free at the periphery.
Example: ichthyosis
Lamellar scales Fish scales
fnftisf Lesions .~
. - '·- .
ffHorn (Kera1"oticf:
T er co a scales
ent. £12 p e. Ok<.oid
Colfarette scares Ho~ny(Keratotic)Sc.a1',s

3) Crust: d
It is dned exudates, either pus or bloo . Crust
4J Erosion:
It is loss of part of epiderml_s. It heals with norma_l skin.
Erosion
SJ Ulcer:
It is loss of the whole epidermis ang part of_dermis, it has characteristic edge. It heats llirr~
tissue.
Ulcer
Initial lesion~
6) Fissure:
It is longitudinal disconti ·t
nu, Y of th e skin .
Fissure
7) Atrophy:
It is th inning of skin due to thinning of epidermis or dermis or both . Atrophic skin is th in, wrink\ed,
transparent and fragile. Sometimes it is described as cigarette paper like.
-·- - ---- ---
Atrophy •
8) Scar:
It is replacement of the skin by fibrous tissue.
Scar •
9) Lichenification: •
It is a descriptive term of 3 criteria:

A) Thickening of skin
B) Hyper~mentation
C) Acien u ted skin markings
Skin lichenification is a feature of •~ronic eczema
Lichenificatton
Ifi e Initial Lesion
C) SpCC
(Sulphu/sullu Cup) ;
2) scutu Ium
. or faW5 (c.lfnical type of t1nta ,;;,p,rt~) - ft
It is specific f t u re w ith concavo#c.o nve..< ~urf~r.,t.;~,
h ped struc
is cup s a . colo ur and stuck to scalp,
golden yellow in
3) eomedone: . . .
It is specific to acne. ft ,s erther.
A) Black head: dome shaped papule, fol-

licular in postion with central black spot
7r~ r_,.,,.6'- r-c_~
r- e,~
Black head comedone White head comedone
4) Tunnel (Burrow):
It is specific for It is a curved line due to burrowing of fem ale mite to skin. It is linear
structure or slightly curved, 7-12 mm in length w it h two ends1 one is a vesicle or papule and the
odk!.r one is blind.
Tunnel or Burrow
5) Target lesion:
It is specifi c to erythema multif .

A) Central zone: cyanotic. orme. It consist s of 3 zones:
B) Intermediate zone : pale.
C) Outer zone: erythematous
Herpes iris is the same as target lesion but t h . .
erytherna multif o rme e ,n the center there ,s a vesicle. \t is a\sa specific
Herpes iris Target lesion
6) Herald patch:
It is specific for Pttyriasis res.ea.
It is a patch that has 3 concentric zones:
A) Central zone: cafe au lait.
B) Peripheral zone: erythematous.
C) Intermediate zone: collaret scales.
Herald patch
Examination of Mucus Membranes

A) Examination of mucus membranes d ·talia are inspected for:
The mucus membranes of mo~th, eye, ~os:~~~:;~treaks (Lace Like)
Erosions, Ulceration, Plaque, Pigmentation
\
E art1in ti tl t NJII ·
h : I l-: t t1 ( 1~ t...' I ' t I l l i t \ > ' ' , I I II l ' •I >(' ( l ( ~ I I ) I :
I 1(
,, 1 P,ttr, ~- ,.1 ,t t ,~t ~, >t11 , ,t1() 11> ,.,\ ,, 1 11yl t1l l, (N t1ll t olcl
N ail Dystrophy PJrorlyct,11..1 Nufl

t-old Sw llltlf:
Examination of Hair
I} Hair loss: it is either:
1- Diffuse hair loss. Hair is lost from all scalp aspects.
2- Patchy or alopecia: Hair is lost from loca lized area, it may be
A} Non cicatrical: hair follicles are still intact and visible. The sca lp morphology 1s normal.
BJ Cictrical: hair follicles are destroyed and sca lp morphology ls abnormal.
Patchy Clcatrlcal Alopecia DiffuM hair fal

Patchy Non Clcatrlcal Alopecla
INVESTIGATIONS
lfll'I(' ,JI('< c 1f,IIII ll1vr••,lfJ1,1f l11 11• 11• t•cl f
1 1I1 1 11 1
1
1
Ir, tl1c 1 cfl,IHl1c>•,/•, ell '1t 1111, 1 •,~1 , 1 ill·,,•I ,•.• •.,I ,';I 1I I.,'' " ll >1{y 111 ,11 1 d tl '1,+!1)
1 1
.I• '
1 Wood ·.., IIHltl , '
2 ~k/r I 11( I I lf)J)ll1H .

3 l\1l I) l(':,t/1111,
4 /111r1l ll r1 o f1t>ltrc '\( c' rl , 1 ,
r, kl,1 IJIOfJ'lY 1.lllll l1l•,lt)f >di l1 ,lc),~y.
1- Wood's Light:
It I"., ~µ 'Clt1I ult, tlVlol(1 t llHl1t wl1 lc l1 It I l1r-ow11 10 :
.. Normal kin, It r •f1oct ~ ti , ,~, vlc")lt•t olot-11 ,
• Pftyrlasls verslcolour, It r ,n , ,~
t5olrl ,, yr llow coloL,r,
• Erythrasma, It , ctl1 1 r t de 'P red oloL1r.. .. /1 , , , , \ , ol\
- Tlnea Capltfs, fl l l1 fl ' ,~ brllllant g r •1•1l olot-Jr.
- Jt ~ I\\ I ..,. • I•• \. ' ·" \ • ' \ \ ••
2- Skin Scrapping:
It i:, used for dlJgr,o!>i~ of 1L1r1gJI Infection of kin .
Procedure:
Skin Is scrt.1tchcd by sca lpel. Th result d co lcs :-ir pln ccd on glass slide, then one drop of 10%
KOH Is added Jnd xJmln d under tl1e rnlcroscopc. Diagnosis of skin and nail fungus Infections
depends on detection of fungal hypli ac while In tinea czi pltis diagnosis depend on detection of
spores either outside the hair (ectothrlx) or Inside the hair (cndothrlx).
' ., l ,\
Hyphae of Dermatophytes Scrapping of skin by scalpel
3- Patch Testing:
It is used for diagnosis of contact dermatitis.
Procedure:
Aluminum strip with multiple holes Is fixed or, the
back. The antigens are placed each In one hole.
Then, another blind aluminum strip Is placed over
the previous one and left for 48 hours.
on removal of the strip, we examine the sites of dif-
ferent allergen for erythema and vesicles. If pres-
ent, the test Is positive.
Patch test
- 1i ts ·
4-lmmunoflourescent es . t 1mn1un<' dlsor
T~1ey are used for diagnosis of au o
ders. They .3re eithe r :
1- Direct test :_ . Ski n biopsy is taken Path1
It detects antibody In the skin: lace d on it.
and flourescent anti-antibody is p l •Hv1
l •P11
Positive lmmuno.
2- Indirect t est: t 3-Hv
. O f atient. F1ourescen fl ou re see nee
It detects antibody in the se rum P . 4-Ac
anti-antibody is added to t he serum of the patient . S- S1
6-A
5- Skin Biopsy:
It d emonst rates the pathological changes in the diseased area. It is usually diagno ti
. Th .d . . s c SL
sist s of epidermis, dermis and subcutaneous tissue. e ep1 erm1s is separated from .de~~ c~~-
basem ent membra ne. ll)\s~
Histology of epidermis:
1- Horny layer (stratum coneum): multiple layers

of non nucleated cells full of keratin protein
2- Granular cell layer (stratum granulosum):

2-3 layers of diamond shaped cells containing ker-
atohyline granules
3- Prickle cell layer (stratum spinosum): 3-5 lay-

ers of polygonal cells with central vesicular nu-
clei. These cells are firmly attached together with
spines or desomsomes.
4- Basal cell layer (stratum basale): single raw of

elongated cells with elongated nuclei. Melano-
cytes are found in between these basal cells
Histology of dermis:
The dermis is generally thicker than the epidermis. It is a flexible connective tissue. It contains:
1- Skin appendges as hair follicles, sweat glands and sebaceous glands.
2- Nerves and nerve endings.
I
3-Rich plexuses of capillaries
The dermis consists of two layers:

- Papillary layer: This forms the superficial dermal papillary layer that lies in between the epider·
mal interpapillary pegs. It consists of loose connective tissue rich in cells and blood capillaries,
and contains collagenous, reticuJar and elastic fibers.
tha
- Reticular layer: This forms the deep thick dermal layer. It is more fibrous and less vascular n
the papillary layer.
Subcutaneous tissue:
It lies beneath the dermis. It is a layer of loose areolar connective tissue rich in fat cells.
Hyperlceratosis, hypergranulosi s Parakeratosis
and acanthos is
Acantholysjs Spongiosis
Therapy in Dermatology
Principles of Topical Therapy:
■ Type of skin lesion: wet lesions needs creams while dry lesions need ointments
■ Never do any harrr,~ do not use irritant and sensitizers

■ Never overtreat: this usually occurs when a patient ask a friend and use many medications
■ Instruct the patient adequately: it is not important to tell a patient how to swallow a pill but
it is essential to tell patients how to apply local medications
■ Prescribe the correct amount of medication for the area and dermatoses to be treated
■ Change the therapy as the response indicates

■ If the prescription is expensive, explain this fact to the patient .
. . ti to apply the r,tedicafiORS for
■ Therapy plus is usually indicated, advise the patient ~u~,s to prevent f'el.U'
to conThis
tly cleared ___ ..-nee_
' '""- -
a specific period after the dermatoses apparen ·
■ Ask the patient to contact you if there is any question or if the .
the dermatoses med1c1ne appeared
to Irr,,
Effects of Locally Applied Drugs:I~::_~::::_~::__ ~

■ Antipruritic Agents: relieving itching in various ways. Ex.ample C
. . . a1am,ne lotion
■ Keratoplastic Agents: increase the thickness o f horny layer. Exam le
p . 1ar preparati
■ Keratofytic Agents: remove or soften horny layer. Example Salic 1. . 00
s
. . Y 1c aad 4%- 6%
40% & factioaod 20% c o, u'ea 2.
()1,;,-
• Antieczematous: stop the secretions by various actions. Example corn ~~ _ .
c-->t-~ ro1 ds
■ Antiparasitic Agents: destroy o r inhibit living infestations. Example· po .. ··"'th .
. - ----- ;f l'l'} 5%
■ Antiseptics: destroy or inhibit bacteria, viruses or fungi
■ Antibacterial topical medications: destroy or inhibit bacteria. Example: genta .

. . . . . myc1n f, . _.
1
acid, erythromyc,ne, t etracyc tne, mup1rc1n, neomycin, and chlorampt,enicol ' ~ •t11t
■ Antiviral Topical Agents; inhibit virus replication. Example: acyclovir
■ Emollient Agents: soften skin surface. Example: cold cream and voseline
Compresses: remove the crust. Example: potassium permenganat e 1/8000 and saline
Drying Agents: dry oozing skin. Example: gentian violet 1%
Creams:
They are semisolid emulsion systems contain!ng both o~I and water. They are water miscible,
cooling and soothing, and are well absorbed into the skin.
They are used in acute oozing skin disorders.
Ointments:
They have oil or grea~ They are semisolid and anhydrous substances. They are used in chronic,
dry skin disorders.
Gels:
They are semisolid preparations gelled with high molecular weight polymers, such as methylcel-
lulose. They are non-gr~a~~ water miscible, easy to apply and wash off.
They are especially suitable for treating hairy parts of the body
Paints:
T~ey are J.i.Q.µig_ preparations, either aqueous, or alcoholic (tinctures), which are usually applied
wit~ a b~ush to the skin. They evaporate, and are therefore cooling as well as astringent and
antiseptic.
They may also be used as protective to seal abrasions
lotions:
They are combination of_Qowder and wate h
to increased evaporating surface Th r. T ey_are able to cover wide surface area of skin due
Example: calamine lotion. . ey are not suitable for xerosis pruritus
,,,,aa• e-sions
Quantity of Creams to Prescribe
Factors affecting the quantity:
Type of dermatoses: acute lesions usually
consume excess topical medications
Base of topical medication: ointments
spread over skin more than creams
Intelligence of the Patients: educated patients
usually consume smaller amounts of topical
medications
Finger tip unit
How to assess the quantity of topical medications r a certain body surface

.
Use the fingertip . of cream needed
unit to assess the quantity . to cove of index finger. It .is ap-
halange
area. One fingertip unit is a column of cream along the diSt al P. f lesions on both hands.
proximately soo mg and it is sufficient for once topical applica_tioni°tion affected body surface
This table shows the average amounts of topical medications m re a
area
Duration of Application Frequency of Application

1 Amount Needed
days 14 Twice/day
2 grams 15
days 14 Twice/day grams 30
3 days 14 Twice/day grams 60
4 days 14 Twice/day grams 480-960
17
Genodermatoses
-
Definition: Inherited genetic skin conditions often grouped ~nt o three categories: chrorn
~~ ,
single gene, and polygenetic. Most genodermatoses show single gene (Mendelian,·nhenta
lcthyosis ~
Group of diseases in which t here is disordered differentiation and cornification of e .
resu lti ng .1n c11
·n1
.ca I appearance o f sea Ies. Ptdel'l't >
lchthyosis vulgaris
• This is the commonest form of inherited icht hyosis
• Autosomal dominant of filaggci-n.,ggQe ( keratin aggregating protein)
• lchthyosis vulgaris has been found to be due to a gene defect in filaggrin, which is a pr .
· formation
the skin that impairs the skin barner · · factors that ote,n
. an d t h e nat ura I mo,·stur1s1ng are I0
to keeping the skin hydrated. key
• Defect also detected in subset of patients with AD
·-------,•
••
SG
ss
I I ' I Piofilaggrin J
1~12 filaggrin repeats
SB
BM
Clinical Picture:
• Onset: delayed onset after 3months usually early childhood
• Fine scales paste on the skin with variable degree of dryness especially during winter with great
improvement in summer
• Scales are coarser on lower limb than trunk attached centrally and detached outward rim
• Extensor aspect of extremities are most prominent while major body folds (eg axillary fold) are
spared
• Palmer and soles show exaggerated skin markings and mild hyperkeratosis
• Ass atopic manifestation and keratosis pilaris~~
• H&E: Compact orthokeratosis reduced granular cell layer
• Benign course improve by time limited finding in adulthood
•
'
Treatment: It can be treated w ith regular application of moisturisers/emollients
X-linked ichthyosis
• Th is condition occurs in males mainly from heterozygous mother
• X linked recessive inheritance
• Defect in an enzyme known as steroid sulphatase
• Lead ing to a lack of breakdown and thus accumulation of cholesterol sulfate, a steroid that
stabilizes cel l membranes and adds cohesion
Clinical Picture:
• Onset: Early onset before 3months
• Dark large tan or grey scales on the limbs and anterior neck all across the trunk.
• It may affect the ears and face. Sides of the neck are usually involved gives dirty neck /unwashed
look
• It varies in its severity and improves in sunny weather.

• It changes very little with age.
• Palms and soles usu spared
• No keratosis pilaris
• No increased AD
19
Lamellar ichthyosis
• A.utosomal recessive
• Present at birth as collodion membrane desquamates 1n 2-3 ,,ks or appear soon ~-
a.~r b,
• Involve ennre cutaneous surface
• Sc.ales are thick large about 1cm in diameter, brown pJate like quad ril ateral adh
erem c
and free edge entr~•,,
• Hvperkeratosts of palm and sole
• Ectropion is almost always present
• H&E: Marked/ massive compact orthohyperkeratosis intact granular cell layer
Treatment of lchthyosis:
In the milder types of ichthyosis the main treatment is regular application of moisturisers or
emollients.
A very wide selection of emollients is available (creams, ointments, lotions, bath oils). Paraffin
containing emollient (occlusive) , urea containing creams( humectant)
These moisturisers are most effective when applied on wet skin within a couple of minutes of
havj ng a shower or bath .
Peeling creams (keratolytics, e.g. salicylic acid) are sometimes used but they can irritate the skin
and can be helpful on the palms and soles.
Severe types of ichthyosis, systemic retinoid (synthetic vitamin A) oral tablet treatment may be
suggested yet side effect makes it difficult for long term use.
Xeroderma pigmentosum
• An inherited condition characterized by an extreme sensitivity to ultraviolet (UV) rays from
sunlight.
• Mutations in genes that are involved in repairing UVR induced damage in DNA called DNA
• • •
exc1s1on repair
20
-
I recessive
tosorna
• AU . Skin- ocular- Neurological
crnical
1 picture. . 1· . I f
. ;de varia bility 1n c 1n1ca eatures
,here is w ...
• .. I first 2ys: photosens1tiv1ty easily sun burn is acut
• Earl~ 1,fer delayed onset lentigines/freckles e profonge1 spa ·'lg
he chin o e: a.rf:-G ~ - ,,._ ,,
t er before age of l Oys
• Skin cane
• sec-s CC- less freq uent MM most tumors occur on H&N

. .
dd·tion
1 to the very large increase 1n skin cancer there is ~ .
• 1~ a 1neoplasms, especially of the centra l nervous syste an opprox,'llatety 50--fo d -.:::r=-
·n ,nterna
1 m. ~
h absence o f r igoro us protecti on from t he sun areas of h
• Int e
ollowed by acce
Iera t e d Photo- age1ng,
. ' cutaneoiYDer- and
multiple . hrp0-P·-c'li~~ - 'h.
resu It, f us m_a 1ignanoes
la r abnorma lities are almost as common as the cutaneo ,.
• ocu . us aonormal....: ,
.k. gly limited to the anterior, UV-exposed structures of the e,,e (l.d Cl5, c..-e
str1 1n . . . 1 , s, co-nea, c: ~ co.....)J :-;c,,..,..,.. _
• ocular affection : photophob1a-corneal o pacity -ectropion and neoplasms tc
• Severe keratitis, leading to corneal opacification and vasculariza ·o

(epithelioma, squamous cell carcinoma, and melanoma}
• Neurological : progressive neural degeneration in 20% of cases
• Diagnosis is made clinically by the presence, from birth, of an acute a :u! "5a:f->--
response at all exposed sites, unusually early lentiginosis in s u n ~ areas - ~ c:;: --
cancers at a young age
Management:
• As the skin changes are all caused by UV light, complete protection from e.'QX)StL.--e -
prevent further skin changes completely. Protective measures include the ,vo. • s-
• All windows should be covered with UV-resistant film

• When outside during daylight hours, exposed skin should be co ered s-~'\SUES" ~
trousers, long sleeves and gloves should be worn together wrth a UV-resistant face ll,- ~
-
• Systemic retionoids can prevent appearance of new cance rs yet should be used - r ~ sc - ~
side effects and rebound when stopped
- --------t~\....---------2
EPIDERM
. OLYSIS BULLOSA:
Ep1dermolysis b . v e in commor1 thf fo r mdtion
of blisters• ullosa (EB) ts a group of rare ge netic disorde rs that h a
in respons e t o minor
. . .
physical lnJury.
Inherited ty .
pes of ep1dermolysis bullosa (EB)
A. lntraepid erma 1("1ntraepidermal separation)
8
• Junctional (intralamina lucida)
C. Dermolytic or dystrophic (sublamina densa)
Keratin 5/14
-
Hemldesffl09ome
Plasma
membrane
Type )(VII c ollagon
Lamina luclda
Type ,v collagen
1.81nfMd•••
Anchoring
I'll>,.. ~P• 1/fll c;ollagen
~ .
,ype 1111 colaa•n C
. ( idermolysis bullosa simplex) .

a. 1ntraep1dermal forms ep _ . 5 and l4, causing the production of
· m utations · keratins - ·d I bl . ·
M ost cases are caused by keratin gene .. ~ haracterized by intraep1 erma 1ster1ng.
. fil t The condition is c d . ti . h .
defective intermediate amen s. . 1these diseases are om1nan Y 1n er,ted,
Lesions typically heal without scarring. Most com~on y,
but recessively inherited cases have been reporte .
. is bullosa simplex11 generalized
Ep1dermolys . ·th generalized blisters that occurs at or shortly after
• The condition typically pres~ti~ts w~ t:e most common sites of involvement. Palmoplantar
b 1"rth Hands feet and extrem1 es ar b ·1 d
•
hyperkeratos1s'.
an d, erosions
- are common · Blisters heal without atrophy,
b ut na, s an mcosal
involvement can take place, more commonly in the more severe su types.
Epidermolysis bullosa simplex~ localized type: limited to hands and feet.
Epidermolysis bullosa simplex (Ogna variant): Generalized bruising and hemorrhagic
blisters occur.
Epidermolysis bul/osa simplex with mottled pigmentation: scattered
hyperpigmented and hypopigmented macules that fade slowly after birth.
Epidermolysis bullosa simplex with muscular dystrophy: Generalized blistering at
birth, followed by later onset of muscular dystrophy. The condition is inherited as an autosomal
recessive trait. , ,. . /' ~
E~iderm~lysis bullosa with pyloric atresia: severe generalized blistering associated

w,t~ pylo_r,c atresia at birth. At other times it is placed in the junctional category due to a6- or
34-,ntegr,n.
. lucida blist ering. M utations in genes cod ing for
I forrTl S b intralam1na . .
,nona racterized Y SO) 6 i ntegrin, and b4 1ntegr1n have been demonstrated,
8, Jl.1'1 dition is c~a collagen XVII (BP l ,a
,he c?n 32 sLJbun1ts, ·ve inherita nce • •
amio1 f1- 3 ,.,.,al recess 1 severe generalized (Herl,tz)
l utoso 1 , • -s bul1osa,
with a epidermo1~s, ra lized blistering at birth with characteristic perio rificial
0 8I
J 11 ,,cti " . characterized by gened na res often accompanied by significant hypertrophic
d•tion
I ,5 th eyes, an , .
rhe con nd the rn ou ' . osal involvement is p resent. Panents often have hoarse cry,
. s arou lti 5 ystem1c muc . . fa
erosion . tissue. Mu . . Patient s usua lly do not su rvive past 1n ncy.
ranulation iratorv difficulties.
g h and resp
coug '
Junctional epidermolysis bullosa, 9.e~~~alize~ intermediate . . .

These patients ca n still display the same per~or1~_c1 al erosive hypergr~nulation nssue as t~~se with
the severe va riant, and they can also show s1gn1ficant mucosaI affection . Tooth abnormalities, and
nail dystrophy can occur. Patients survive infancy, but life expectancy is often reduced .
Another subtype in this category are pati ents with generalized atrophic benign epidermolysis
bullosa. Generalized cutaneous blist ering at birth that heal with a distinctive atrophic appearance.
Extracutaneous involvement is rare. Patients have a typical life expectancy.
6. Dystrophic forms
The cause of dystrophic EB in both autosomal dominant and autosomal recessive inherited forms
is mutation in the COL7AL gene encoding for type \LIi collagen . The anchoring fibrils in these
patients are defective or deficient resulting in sublamina densa plane cleavage. Blisters heal by
dystrophic scarri ng. Formation of milia results as a consequence of damage to hair follicles.
Dominant dystrophic epidermolysis bullosa
Vesicles and bullae are most pronounced over the joints, especially over the toes, fingers, knuckles,
ankles, and elbows. Spontaneous, fle sh-colored, scarlike (albopapuloid) lesions may appear on
the t runk, often in adolescence, with no previous trauma (more severe form) . The formation of
contractures and clawlike hands can occur. The nails and mucosa are frequently involved. The
teeth are normal. The type formerly known as Cockayne-Touraine is more limited in extent and
severity, and no albopapuloid lesions are seen.
l\art syndrome: variant of dominant dystrophic EB that describes congenital localized defects
of the skin, mechanoblisters, and nail deformities.
Recessive dystrophic epldermolysls bullosa
The severer variety characteristically begins at birth with generalized cutaneous and mucosal
~lis~;ring. Di~ital fusion with encasement of the fingers and toes in scar tissues, forming a "mitten
like deformity, is characteristic. There is a high risk of developing cutaneous squamous cell
carcinomas.
Approach :
• ·J.. ir) t,11.'>P~ · n._"'II lC o n{' ~· p"'c
l
in'lf>l l t i 111 ~ c lc ctro r1 rni croscopy (EM) and the othe r llSII)&
,n1nlt1nf,tltJorf' er,t t11 1 ros opy.
. L,... •
• E\1Jlu.3te rn,c.·cnan L
, Ing bact eria l cL1lt urC's fro ,11 poorly l1ea ling wou n ds or wounds that QPPeQr
., .
infuc-ted.
• ln1aging studies for GI dysfunctio n
• DN A mt,tation analysis .
Management:
• Gene t herapy is prom ising.
• Family education
• Palliative treatment.
a. Avoid trauma
b. Gentle and proper wound care
c.. Proper nutrition.
d. Aggressive dental intervention.
e. Surgical intervention
NEUROFIBROMATOSIS (VON RECKLINGHAUSEN'S DISEASE)

Neurofibromatosis is an autosomal dominant inherited syndrome manifested by developmental
changes in the nervous system, bones, and skin.
• Type 1 neurofibromatosis (NF-1, von Recklinghausen's disease)
• Type 2 neuroftbromatosis (NF-2), central or acoustic neurofibromatosis, is distinguished by

bilateral acoustic neuromas, usually in the absence of cuta eous lesions.
• Type 3 (mixed), type 4 (variant): resemble type 2 but have cutaneous neurofibromas.
Neurofibromas: are soft tumors that can be pushed down into the panniculus by light pressure
with the finger (''buttonholing'') and spring back when released. Neurofibromas result from
proliferation of all supporting elements of the nerve fibers including Schwann, perineurial,
endoneurial, and mast cells and blood vessels. ~ ·~ - ·- ..........'
•
su&ar••t•oer••s plexlfocm ""
palpat1on, thesC' rt' '> rnl) I<' .. 1.ltOHbJ:sun~.,
1J• 111. C) f
\ 1 0
W .,.., •Jrc• 11 t
m•v resemblt' rl gl,Jnt C.,lf('\ ,)lJ l1.1lt m I ,u rr,, •, ."
' r. l l (: •
I ~l e• f)\Jr•rl, Ir tJ,JI\ /
y t11~ ',Yin
fJ,Jt.,vY.r C
. , I Jrn,Jr11r~ 'J1
1
Iberet••••laltmacyles·
- • ir 1 11 h t ._•Jrow Ci {',
,,,J·. •J.,,, 1 h 1p,•,p•;,
~r, ,.,Ft ,•1 ~(;,A
1 Iways pr sent by 1 Yt'il r o f Ju <' n rr,dc 1JI, .., r ,ncJ rncJ:.,t vft ,•n "-.J
o .
MHl;a,cy kes;kllo1 (CCQWe's sl1 )· m· [>r v,~r,t 01 l,,rtf, or d air, 'f '
genital, and perinea I area!>. 'Jy oc..c.ur, 'xt, r1c.J lnu(> to th ~ f'11 , , I , ~rid
D a 1
I
,f _.,.,. "' 1r1 1c,l

£a ocrlnal anomalies; Acrom . ,,r,g tr~ ln?,J,n;,,
. ga ly, crc:tinl,,m, hype ~ •
pheochromocytom a (<1%), or Prccoc,ous puberty rp<l rat~1 roidi· ro 1
Bone chanees (usually erosl may be pre~ent.
) rr / / I;.d~rra, J I
. b'fid . ve may produce lord 0 51.5 k

sp1na I a, dislocations, and atra umatic f ractures. , ypho~is, and p· eudo~ h . d:. v,et~ as
art ro:.,:,, J
~~~;nts
1 ren
wi\~
WI
N:; 1 a re four times ~ore Ii kely to develop malignancies than the general population
1 are 200-50~ times more likely to develop malignant myeloid disorders tha~
-
age matched controls, and the risk for CML may be higher for those with xanthogranulomas.
Ne~rolo~ical changes: Mental retardation, dementia, epilepsy, and a variety of intracranial
mal1gnanc1es may occur.
The gene for NF-1 codes for neurofibromin, a protein that negatively regulates signals transduced
by Ras proteins (proto-oncogene products).
The diagnosis of NF-1 requires two or more of the following criteria to be fulfilled:
1. Six or more cafe au lait macules with a greatest diameter of more than 5 mm in prepubertal
individuals, and a greatest diameter of more than 15 mm in postpubertal individuals
2. Two or more neurofibromas of any type or one plexiform neurofibroma
3. Freckling in the axillary or inguinal regions
4. Optic gliomas ~
5. Two or more Lisch nodules . h' . of the long-bone cortex
6. Distinctive osseous lesion, such as a sphenoid dysplas1a or t inning
with or without pseudarthrosis .
. 'bl' or offspring) with the disease
7. First-degree relaave (parent, s, ,ng,
BACTERIAL SKIN DISEASES
The normal skin flora

Normal skin is heavily colonized by bacterial flora (harml~ss cor:nmensals) such as• 0
1 ·Coa
A. .• tive.5taphylocOCO(CoNS). Colonization 1s more dense In 1ntertng1nous and oc c Uded su~u1~
1
Coagulase positive staphylococci is not a resident on healthy skin although it is frequ t1ace
in anterior nares and peri-anal area In 35% and 20% of normal population. ent1y fau no
Common Babcterial skin Pathogens

• Staphylococcus aureus and group A (3-hemolytic streptococcus colonize can inf
ect the sk; "·
They cause a variety of skin and so~ tissue infections, bacteremia, and systemic.,ntoxicati
A • d f · • C>ns
• ...n intact stratum corneum Is the most important e ense against invasion b ·
bacteria ben,c
y Pathoo .
Methicillin-resistant Staphylococcus aureus

Over the past few decades, eeiderolfs_of methicillin-resistant S. aure us infectio h .
1
frequency throughout the world especially in hospitals and health care cente n( ave increased .
· · · h h rs. opera+-- 0 n
1ntens1ve care units, .cancer c emot erapy wards, newborn nurseries , ch ron .1c ca l,ng ro ills
urrent y, Many osp,tals have had to control measures to reduce th e spread of there . faciliti es).'
C I h
Skin Defense Against bacteria infection.
1-Dry surface.
2- Intact surface.
3- Desquamating surface. \,_s'--eM--~>
4- Sebum with its unsaturated fatty acids.
5- Normal Flora which secrete antibiotics.
Predisposing factors
1. Chronic S. aureu s carrier state {nares . .
2. Warm weather and hu 'd 1· , ax1llae,per1neurn vagina)
3 . m1 c ,mate ,
4 •P
Social. . situation : poor hyg1ene,
. ·
crowded liv·
. rur1tic skin disease, ato ic d . . ing condition ,malnutriti
5 .Neglected minor traum: ermatitis,Scabies, Pediculosis and ch·o~ and anaemia
6 .Chronic disease· obe ·t d. ic en pox.
· s, Y, 1abetes
7 · lmmu nosupp ress,on
· and cancer c h emotherapy,
Involvement
.., . of St aphylococcus aure .
"" Primary infection (D" . us in cutaneous infection
• Impetigo irect infection of skin and ad" . .
• Ecthyma Jacent tissues)
• Folliculitis
• furunculosls
• Carbuncle
• cellulitis.
)( Secondary infection (on top of preexisting skin diseases such as)

• Eczema, 1nfest ations,scab1es, pedicutosis ulcer"' t
, >, e c.
)( Cutaneous disease due to effect of bacterial toxin
• Staphylococcal scalded skin syndrom e
• Toxic shock syndrome .
involvement of streptococci (mostly group A beta hemo\vt,c) in cutane-

ous infections.
Direct infections of skin or subcutaneous tissue
• Impetigo
• Ecthyma
• Erysiples
• Perianal infection.
Secondary infection
• Eczema, infestations,dulce_rsfl etc ced by streptococcal infection (mechanism uncertain)
• Skin disease provoke or ,n uen
Psoriasis, especially guttate form
Impetigo
ti o
Im pe g . . .
f the skin.
Definition: tagious superficial pyogen1c infection o
. o is a common con .
• 1mpeng. 1· .cal forms are recognized: . f Tilbury fox or crusted imetigo).
• Two main c 1n1 . (" petigo contag1osa o
Non bullous impengo im
1.
2. Bullous impetigo ·
Epidemiology --
Impetigo
bullous impetigo
Staphyloeoccus aureus
27
The peak seasonal incidence of impetigo is in summer and children are most often affected. 1
adults, males predominate. Poor hygiene and existing skin disease e.g. scabies, predispose to i n
fection Bullous impetigo occurs at all ages, and be especially widespread in the newborn. Min~,
abrasions and other skin lesions may predispose to infection if the patient carries the staphylo~
coccus.
Impetigo contagiosum (non bullous impetigo)
Loca Iization
• The face especially around the nose and mouth and the limbs are the sites most commonly af,
fected, but involvement of the scalp and the body can occur especially in children with ato .
. . b. d . I b Pre
dermatitis or sea ,es an ,n new y orn .
\ ry'l"
.1n1ca
. I pictures
. ~(
Cl
' ~ \,.. ~ '-" ,r \ Q. • ~
..\ .,..\~
.
.,. ,_ -"
~
---..r_r,Jr_.1..- •,.;
t-<,,.,'" ..,
• The early lesion is erythematous macule which is soon turn into a very thin-walled ves·1c1eon
an erythematous base, the vesicle may rapidly change into a pustule then ruptures so .
. . Id rapidly
th at 1t 1s se om seen as such the oozing serum dries giving rise to a crust which is g 0 Id
low in colour. en Yel-
• When it is removed a weaping red surface is seen( erosion) which rapidly crusts · .
5t 7d h f · . again, within
.o ays t . e crust alls off leaving normal skin or slight hyper pigmentation h · .
without scarring. w ich fades
Non bullous or crusted impetigo.

Non bullous Impetigo
•
Im petigo contagiosum
•
d prognosis
coLlrse an t ·n
1
the vesicular stage and this helps the spread 0 f
resen the ct·1
.5 usuallY P . contagiosum usually runs an acute course and sease throu h
t,ing , . impetigo . cornp\et h g
1tc . oculation- 10 da_ys with no residual scar . The course of the dise e ea\ing usu-
autoin place in ,2...t o -=--- ase rnay be Pro\o
allY takes sive crops. nged
w succes
bY ne of Impetigo
Clinical Types
prirnarY . um (Non bullous, crusted, Telbery Fox.)
tigo contag1os
1rnPe . 0
u11ous impetJg_ .
B · petlgO
Circinate ,m
fct~vm, a~ Bock hart impetigo.

FolhcU a ,
secondary impeti_go .
scabies ped1culos1s,wound, .. ).
{eczema, ,
eullous Impetigo
., , _,. ~s--c>~ ~~'<" C>Y-Ole ~ ,ow)
Clinical features~~-£> .
• In bullous impetigo, the bullae. are less rapidly ruptured and persist for 2-3 days.(Bullae are
large and a diameter of 2-3 cm ts common . After rupture thin crusts are formed . Central heal-
ing and peripheral extension may give rise to circinate lesions. Although the face is most often
affected, the lesions may occur anywhere. The buccal mucosa may be involved.
• The lesions may occur anywhere.
Impetigo neonatorum
Its impetigo of the newborn and is a variety of bullous impetigo .
It usually begins between 4th and 10th day after birth , it is highly contiguoy_~ ~nd f!l_ay fa~\~ qe_
Associated with constitutional symptoms as malaise and fever with extensive large buttae ~nd
the mm may be involved. Diarrhea frequently occurs. Bacteraemia ,pneumonia or meningitis mav
rapidly develop with fatal termination . Isolation and treatment with IV antistaph. should be done
Cirinate impetigo
Bullous Impetigo Circinate impetigo
-
pathology
bullou• Impetigo \
1Non t bullou•
almllar t ~hat bllater formation
exc•P d transient.
\ In bullev• lmp•tlgo \ llt• b•loW Is ,Ught an
Th• eplderml• Juel •P or Granuloaum
Th• ,tratum corn•""'
formlng lorg• bulla•through ,ponglotlc
Neuttophll• migrate lty which may
Epidermis Into bllater cov
Contain cocci. t Ins Inflammatory
Th• upper dermis con a d lympho·
tnftltrot• of neutrophll• an
cvte••
Complications:
1. Eczematization. . and cellulitis.
2. Furunculosis ,erysep1las t "or the majority
. tigo accoun s '1
3. Streptococca I ,mpe I u..e glomerulone-
t ptococca ac 1.1
of cases of post-s re . d for development of ne-
phritis. The latent per10 I . &ection is 18-21 days,
. . ft t eptococca in,,
phr1t1s a er s r . . . n might offer a bet-
early treatment of sk1_n ,ntf:;~:nal disease.
ter chance of prev~nt,~g d erythema multiforme
4.Scarfet fever, umcar,a an .
may follow streptococcal impetigo.
Impetigo contagiosum.
Treatment
1- Removal of the crusts by:
• washing with soap and water. . . . .
@ . Topical compresses with warm potasssium r.,ermanganate solution 1/8000 1s used ,1t 1s a cle-
anising agent , mild antiseptic and drying.
• Applying drying agent as gentian violet 1% in water.
2- Topical Antibiotic
• In mild and localized infection, a topical antibiotic
• alone may be sufficient
• Mupirocin ointment . Good results have been achieved with it in both staphylococcal and
streptococcal impetigo,
• fusidic add is also effective against both organisms .
• Topical aeomycin is effective in staphylococcal infections, but tess
• Active against streptococci; Bacitracin has activity against both,
• And the two drugs are often used in combination.
ic Antibiotic
,- svst~ ft:<non is w,d~spread or severe .
_ _tf rt,e
'~nlpanied by fymphadenopathy,
8. ot as a re ls reason t o su spect a nephrit ogeni
,t the 'b . . h - c
c. ot tJS .1n oral an ti 1o ttc s u e as fluclQ)(ac·n·
streptoeocc , , tn or erythromyctn is indicated.
-.nahylaxis _ _ _
r•-r hygten1c measures and eradication of di .
proper . pre s pos1ng facto h
• . scab ies and minor t raum a reduce the t . rs sue as Insect bites, pedic-
ufos1s, . ransm1s- ,......__~
sion of infection. = --..
(dhYR'i
oefinition:
• 15 a Primary bacteriaJ infection of the skin characterized
by the for mation of adherent crusts ,beneat h which ul-
ceration occurs.
•
• Recurence occures rn some cases.
• It was formerly regarded as a st reptococca l infection, it
is now known to be caused by streptococci group A and/
or staph.
• The disease may affect ch ildren and adults.
• Poor h~giene a~d malnutri~on are predisposing factors and minor injuries or scabies may
deterrr11ne the site of the lesions.
Clinical features:
• The primary lesion is a vesicle or a vesiculo-pustule located on an erythematous base that

is soon covered by hard crusts of dried exudates which becomes dark brownish in color and
- --
firmly attached to the margins ,beneath the crust a superficial ulcerative process proceeds.
• The margin of the ulcer is indurated , raised and a red violaceous areola is often present. The
crust is removed with difficulty to reveal a purulent irregular ulcer.
• Healing occurs slowly beneath the crust,the latter being exfoliated, leaving a slight scar, with
some pigmentation.
• The course may be prolonged for 2 - 3 weeks or more.
~ \..,_ e-aL.~ oy S Q)..V'Y.-1n Cj . .
• Recurrence can occur especially with persistance of pred1spos1ng factors.
Ecthyma
Impetigo of Bockhart. Folliculitis Folliculiti')
Treatment: .
• Antibiotics topical or systen1ic may be required .
• ff the infection is persistent or recurrent, the usual sites of st aphylococca l ca rriJg (no ~nd
perineum) should be thought of in the patient and his or her co ntacts.
Furuncle {boil)
• Folliculrtis is a superficial infection of the hair follicles characterized by e ryth ematous, follic-
ular-based papules and pustules / Furuncles are deeper infectio ns of the hair follicl e charac-
terized by inflammatory nodules with pustular drainage, whi ch can coalesce to form larger
draining nodules (carbuncles). ,..,_) .,.··~le \\1,).:, , t'l0 t
Furuncle boil
Furuncle
oefinition; . . . . -
• A furuncle is an acute, usually necrotic infection of a hair follicle with staph aureo,._
Etiology: . . . .
• common iro adolescence and ear_!y _ad~lt~ the infecting stram of staphylococcus is usually
also pre sent in the nares or the perineum .
• From the sites of carriage

h k. the infection
h f . is· disseminated
f by the fingers and by clothing. Me-
c hanical damage
. tot es m event e nction o collars and belts may determine the distribu-
tion of the lesions.
• Malnutrition is an important predispo_sing factor in some countries. however in a high propor-

tion of Cases no conv1nc1ng pred1spos1ng factor can be responsible.
Clinical features~~--t::>v~-v""21.Jos..-_,\.. ,v •o bOo ... o ~OJ4..
A furuncle first presents as a small follicular inflammatory nodule soon becoming pustular
• nd then necrosis occurs, healing takes place after discharge of a necrotic core to leave a vio--
~aceous macule and/or a scar. The rate of development varies greatly, and necrosis may occur
within 2 days or only after 2-3 weeks.
derness is invariable and there may be throbbing pain especially in lesions of the nose or
• exter nal auditory canal. The lesions may be single or multiple, and tend to appear in crops
Ten
• On the upper lip and cheek cavernous sinus thrombosis is a rare and dangerous complication.
Furuncle in between the eye brows
Treatment: .. •
• Allaoxacilli,rsystemically or another pen,c, 11 ,nase res istant antibiotic.
• Hot water compresses . . n of the surrounding skin.

• A topical antibacterial agent redu~es contam,natio . the a-
• Occlusive dressings should be avoided. d . al carriage should be sought '" P
• In recurrent cases exclude diabetes. nasal an per,ne
tient and other household members.
carb 11ncle
Etiology:
• A carblJncl(' is a deep infection of a group of contigl1ou!, follicles wi th s~aph. aureu~ accornpa,
,,ied by intense inflammatory changes In th~ surrounding and und erlying connective tissues.
ThE.'y occur predominantly in men of middle or old age . f .
rd1 1 nd
• And are n,ore common in the presence of di abet es ,malnutrition, ca ac ai ure a during
prolor,ged steroid the rapy.
Clinical features: f few days to reac

h d'
a 1 ame
t
er o
f3
-10 cm
• Painful , hard red swel ling th at increases In s1ze or a . d. harged from the multiple f
or more . Suppuration beginning after 5-7 days and pus is ,sc o1-
hcular orifices.
• Necrosis of the intervening sk in usua lly occurs.
Carbuncle Carbuncle after rupture
• Most lesions are on the back of the neck,the shoulders or the hips and thighs.
• Constitutional symptoms may accompany or precede the development of the carbuncle.
• In bad general condition, death may occur from toxaemia .
Treatment:
• Flttdexacillin or another penicillinase resistant antibiotic should be given.
• Diabetes or other possible underlying conditions should be thought of.
• Surgical intervention may be needed.
Cellulitis and erysipelas

Bacterially:
• Erysipelas is predominantly a streptococcal disease.
• In cellulitis, staph is occasionally implicated alone or together with strept.
Definition:
• Cellulitis is strictly an acute b
tissue , su acute or chronic bacterial inflammation of the b
· su cutaneous
• Erysipelas is a bacterial infection of the d .
• =~:sr
Its main feature is a well -defined raised a~d u~per subcutaneous tissue (legs and face),
e ecting the more superficial (dermal)
erysepilas
•
involvement
cellulitis erysipelas
cellulitis
Clinical features
• Erythema,heat ,swelling and pain or tenderness are constant features.

•
• In erysipelas the edge of the lesion is well demarcated and raised but in cellulitis it is diffuse.
• In erysipelas blistering is common and there may be superficial hemorrhage into the blisters
or in intact skin especially in elderly people.
• In cellulitis the skin shows erythema, oedema, hotness, pain and tenderness with ill defined
border.
Complications
• Without effective treatment,complications are common: fasciitis, myositis,subcutaneous
abscesses,septiceamias and in some streptococcal cases nephritis and the more severe infec-
tion may be fatal in infants and in the debilitated or immunosuppressed. ,:2.,.,.vr~'.-.~
• Periorbitaf and orbital celf uf itis may be complicated by cavernous sinus thrombosis. ~
Treatment:
• s the treatment of choice and should be continued for 10 days.
• In recurrent cases long acting penicillin can prevent attacks.
• In Patients allergic to penicillin another drug commonly erythromyeiA- should be taken.
• Some patients may require life long prophylaxis.
fcvtbcasma
Definition:
. . kin caused by sr.am p~jtive rod5 ,ocvnebecterium Minut:i■••-
lt 1s a superficial Infection of th e 5 fl O ra and some shift In the host-parasite relati
~ . It Is frequently a member of the norma 1
o".
ship results in the development of th e disease.
Epidemiology h hlldren \.4 iabetes,obesity and warm humid climat~ are

• More common among adult~ t an c ''C
predisposing factors .
erythrasma
Epidemiology
• More common among adults than children,diabetes,obesity and warm humid climate are
predisposing factors.
• Clinical features: ~
• It occurs most commonly fn the groins,axillae and the intergluteal and submammary flexures.
~~ The patches are of irregular shape and sharply marginated,at first red but later becoming
brown, new lesions are smooth but older lesions tend to be finely wrinkled or scaly.
D.D. of erythrasma:
• lntertrigo: Frictional dematitis.
• Tinea cruris.
• Pityriasis versicolour
• Candidiasis.
Fluorescence under wood's light:

• Coral red fluorescence.
erythrasma
Treatment:
• Erythrasm~ responds well to most topically ap lied i l .
zole and m1conazole(although it is a bacte . .Pf . ole annfungal agents such as clotrima-
1
rial preparations as fucidic acid The r1a in ection), also it responds to local antibacte-
azole group has antibacterial effect. response to azole group depends on the fact that the
• "' ,li,ytt,,~,.,icu. for 2 weeks is probably th .
e most effective approach.
Leprosy
Hansen's disease
1
Chronic lnfcctlou!> dl SC'i\"'< wlt t, rlrom1n,,nt lt1vc)lv, 1n1,•nt c,f tt,0 ,,kin ,1r1d nf'lrVP~ that 1,, t,JU'.f•d by
the bacllluc; Myco ~,nct<'t l1 1m lrpr1.1P.
The bacillus M. leprae

• Is a very sma ll, slightly curvc:?d ac.ld fc15t nlcohol fnr.t rod
• It can't be cultured In vitro, ca n be c:ult1vnt c-d In rr1ou!.c foot pad and In e>rmadello!:t
• Stained by zlehl-neclscn ~nd f1to stnln (whlc.h ,;tnln thC" bac.1111 a bright red color again:i-t blu,!
background)
It Is an obligate Intracellular microorganism that ha~ a predllcct1on for m acrophages. and

• Schwann cells (which can express TLR2 that have the ability to recognize antigenic compo-
nents of M.lepra with subsequent nerve dam age).
1n atients it survives In cooler b.ody areas (skin, nerves, eyes, respiratory t ract, testes, some
• p
lnterna I organs) b eca u se the bacillus requires a temperature of "'35°C to grow.
Routes of infection
• • fection : (lee of n asa l secretion contains 1-2 million viable bacilli)
Drop Iet 1n
Skin contact: rare
•
P thogenesis . .
a Th re .is var1a
. b I'l'ty
I in susceptibility/resistance,. depending upon genetic factors, so the ma-
• e of expose d individuals do not develop disease .
.ority .
J ending upon t h e Ievel of specific cell-mediated immunity, the disease can progress
• Dep
without . t ' limit itself' or resolve spontaneously.
restrain
TT BT BB BL u
een ,.;a1.,.,..
.,,~ Aaarco:ty
r ■ JF ■•
~,---;1JL:.:;-2'ii™=~;---,
:.:..
L._ _.:::;::
-
li■■ w._
• .::.w;'!:I.;.;..J______ , ~
d
-~=---.,,.
~ -~':':'--
-re-w
---::._:-7, 1Li'i'..: i1no-,1
••
____ _ __________ l,___:~..;.;;....;.--
,._ lrpme tn 11,MFSUl-
••, <:::== =====t=='

__
L v any a ■ litJ •
........
T)_,. l .11 : • ~
- ... .,. ___ _
~ 111 2 1 , rcna
tllnl I RJU1Jre1
The nerve destruction Is tharactarestt, tn lep,mv fffettian.
• In tubertuloid lepros,~untfatral and / or a.s,",,,1t.11tt.af pe,;t;f",-,?taf ~~e
ea,:ty_ln the ftlse~se ,.;J/11 •.,_. ,,,. ,_ ,P .,_
• In tepromatous leprosy: bltaterat symmetrJc.af pe,1pt,er3f r,Pf'le ~,, ~ .,

~,.n $ t•' "'' " 'I
• Th e nerve d vsfunctlon otturs tn the form of tass of sen>6'~""'' · ' ...
atrophy, ulceration, bone resorption and to.ss of dJgitS
Tuberculold leprosy 11 s ,114 1,. ~:ea
• cf p JaqUe"S -,/
• Few well-demartated erythematous or hypoprgment.e
ders, alopecla and ane.sthesia.
• Sometimes only neural involvement is present~
Lepromatous leprosy h atous m~utes, ~ J~ ; , ,.,,,
"d read ervt em
• Multiple, poorly defined, symmetric., w• esp '
and plaques. ,eonine f;k.ies.
f head can tead to a
• Infiltration of the skin of th e ore ·, . ~ddle nose, ac.qufred k L.......__1,v ,k o,,
f •ncJude mada ,os,s, . . d ,.
• Additional signs and fate seque ~e .' a stocklng or glove distttblltiOn, enlarge C)e"l' . jf
the lower extremities, anesthesia ,n
nerves and neuropathic changes.
N,_ r:.
Borderline leprosy r •
et ·c annular ___ .., J
infiltrated papuJonuuu ar Je:>JV,o., •--=-- -c
• Cutaneous lesions are usually asymm r , - . .i
d eripheraf nervous system abnorrr,almes depends upo,,
• The severity of the cutaneousg''
. • ,J, an P
· towatds lepromatous pole ( BL ) ,or t h e w~,wKn
&....... •-:d pate (Bl}
whether the patient ,s ean,n - .,;
Diagnosis
Depends on:
1-Charecteristic skin lesions
2-Nerve involvement
3-Demonstration of M.leprae in slit skin smear
4-Biopsy from skin lesion stained by ziehl neelsen stain
rnvestigations
\• Slit skin smear (ZN STAIN): earlobes, forehead, chin, extensor forearms, and dorsal fi"C't•S
2• Skin biopsy:
- In the tuberculoid pattern of leprosy, a dermal granulomatous infiltrate that may have a linear
pattern as it follows the course of a nerve. Epithelioid cells and Langhans giant cells are sur-
rounded by lymphocytes.
- In lepromatous leprosy: a band of normal-appearing de,11,is (Grenz zone) separates the epi-
dermis from the infiltrate, which is composed of plasma cells and lymphocytes in addition to
Virchow cells -'> ~~ VV"uCro?'-'J5
3• Molecular methods: The detection of M. leprae DNA in fresh skin samples and split sldn
smears by PCR
JREATMENT . .
.d ug therapy (MDT) regimen 1s established by WHO th t.: dose and d
The multi r . d f . , Uration of tr m
. to number of lesions an o bac1ll1 1n the lesions
is accord ,ng . . .
. d es included ,n th,s regimen :
_Ma•o _ru --
• oapsone
.
• Rifampac,n
• clofazimine
• Minocycline
• ofloxacin
Follow up
-• Close follow up clinically and bacteriologically of the treated patients are needed
• Fol/ow up may be extended for years in case of lepromatous leprosy
• Rehabilitation (foot drops, claw hand, bone resorption)
Tuberculoid leprosy
Bord rr,n I pro v
.. ~ , ; . ; -... :, ......
-
.- . . -
Viral infections
. i,. • r • , • • •
~~.-~~. ,.._,_. - .
Viruses are obligatory i~tracellular organism s. Two main groups of viruses are distinguish ed ac -
cording to central nucleic acid core :DNA &RNA
EXamples:
i -DNA viruses:
_ Herpes viruses
e.g:herpes simplex and varicella zoster viruses
-Pox viruses
e.g: molluscum contagiosum
-Papova viruses
e.gHPV(warts)
l-RNA viruses:
-Retroviruses: e.g HIV
-Paramixovirus :e.g measles
Herpes simplex
Etiology
Herpes virus hominis type 1 (mainly face non-genital areas)
or type 2 (ano-genital) .
•
Pathogenesis
• Primary infection: in infants and childr~ where no immunity exists against the virus . Percuta-
neous infection occurs and the virus ascend~ the peripheral nerves to the dorsal root ganglion.
After healing the virus remains latent in the dorsal root ganglion .
• secondary infection: latent virus particles descend from the dorsal root ganglion along the
nerves causing recurrent infection
Pathology:
0 Ballooning
-- _......,....____,. and reticular degeneration of the epidermis with
giant cells.
0 Dermal cellular infiltration and vasculitis.
A- Primary Herpes simplex

• constitutional symptoms with fever and malaise and usually wide spread.
• Morphology
0 Grouped eaif}fl!I vesicles on erythematous base which rupture leading to erosions and crusta-
-
tion and liable to secondary infection.
• Course
o 2-6 weeks.
• clinical types
o Primary gingivostomatitis: j
• Erosions on the mouth interfere with feeding. May
coalesce into yellowish plaque.
o_Keratoconjunctivitis:1 .
• Dentritic painful keatitis and conjun,tivitis and corneal opacity
·ns · gina an
o vuf\'ov.ailf:-' ··th vesicles on the va
• Pain, dysunadw~tis .
• Urthef1tl5 an be affected
• Groin skin may
. f ction in the mafe
o p,;marv genital .' "n: on the penis and pubic area
• 1 and erosio
• vestc es I phadenopathy.
with tender vm
I tion herpes (whittow):
o Prirnarv [nocu a
. ts and surgeons. I
• In denns (fi rs with supratroch ear or
• At the site of trauma nge
·tiarv lymph nodes.) _
ax, . . ·t aon :
o Kaposi var1cefl1 om erup . d titis and Darier's
• In children suffering from atop,c erma '
disease. -- eruption with umblicated

• Generalized vaccinifonn
center.
8- Recurrent Herpes simplex

• Precipitating factors: ..
common co Id , ·nt1uenza and other febrile condition.
l
0
0 Sun exposure.
o trauma including sexual relations
0 Psychological stress or anxiety.
• Localization
o Fae~
• Orificial, periorifcial: lips, nostrils, and
Cheeks ( common sites).
o Mucous membrane:
• Buccal mucosa, tongue, pharynx, larynx and
Conjunctiva (uncommon sites)
o Genitalia:
• Glans penis, clitoris, labia, cervix and urethra.
• Morphology
o Grouped vesicles on an erythematous base.
o Vesicles contain clear fluid that may become purulent that rupture ( in few days) or undergo
crust formation under which epithelialization occurs.
o Or leave erosion within 4-12 hours and heal spontaneously
within
- .,-..,. -
5-7.... days.
t_Diagnosis ,--;z
"--~--- -
o Clinical picture
st
• Tzank te : scraping the vesicle base stained with Giemsa reveals giant multinucleated ce1ts
o Viral culture - - -
oDirect immunofluorescence -
oPCR
• Differential diagnosis: other cause of vesiculobullous erupa·

on.
aonent
• rre ures
nera1 meas
o Ge . disposing factors .
• ,Avoid pre ses of primary infection: hos pi tat ization
, In severe ca
ocal measures:
0
l resses: to remove crust
• comP anate/saltne).
(I( perrneln':viral therapy: (acydovir, iodoxurdidine ,pencyclovirJ.
, t.oe,aa · 1 C • f.
. agent: gentian v10 et ,or oozing es,ons.
· h secon dary ·1n f eetion.
• orying ntibiotics: ·1n cases wit · .1.,_ w:-r
~~s ,
• LOCa I a _q._,,.V"'<'•.,,...
• Local analgesic creams.
systemic:
•
.
- ~<;-le r -b~V\
0
• USllilllYneeded in the first attack and severe recurrent _ f-)CP\..-.c::, \-\:cl,.;n9
cases:
• Aql(lovir (Zovirax~) : 200 mg 5 times daily for 5-10
days; 200 x 5 x 5 . In' • •
•or Famcyclovir (Famv,r®) 125 twice daily for 5 days.

c- Herpes zoster (Shingles)
• Etiology:
0 Varicella zoster virus.
• Pathogenesis:
o reactivation of a latent virus that has been dormant in the sensory ganglion since a primary
infection. ~--- -
Orarely infection may spread to anterior horn cells causing paralysis.
• Predisposing factors: (usually not present)
o Trauma.
o Acute inflammation.
0
Debilitating diseases.
0
lmmunosupression.
• Pathology:
~ Ballooning degeneration of basaJ ..c~ell 19~ by marked
cantholysis due to damage of intercellular bridges with
seofParation and formation of unilocular vesicle with the presence
mutt;
0 . nucleated cells (characteristic) .
Reticular de .
tell d' st. generation due to increased intracellular edema and
one tstenchan
rma1 on and .rupture and coalescence of nearby cells forming multilocular vesicles. ,
Qpiffary nd ges: inflammatory cellular infiltrate, damage of
e othelium (haemorrahgic).
• Clinicat p·1
0~ cture:
• Pa; Ptorns•.
~ (l!llld to se · n
vere) usually at the site of eruption, may precede, associate or follow eruptio •
Viral it1 rrior1S
. . heral or cranial nerve o r several nerves.
.
Localizations. of a per1p
. I along the cou rse nest site but o ther sites include
o /ly unilatera the commo
• usua ctoral region : Is ·nal nerve) limbs or genitals
• The pe facial, tr1gem1 rves)or lower
• face( along ostals or lumbar ne
k( interc I t conte t
• trun fl .d with puru en n s
ho/ogy: matous base, w hich contain clear u1
o Morp d vesicles on erythe . the others may dry up .
• Groupe with crustation
an d 5O rne rupture
• Clinical Types: .
0 Accord '
·ng to the site:
r es zoster pectoralis: ,
• He P e of the intercostals nerves a
• Involve ~n 'de of the chest and back.
eruptions ,n one s1 .
• Pain may be mistaken for chest pain .
• HZ cervicalis:
• Along the cervical nerves .
• HZ abdomenalis:
• Abdominal nerves may be mistaken for renal or
gall bladder or even appendicitis .
• HZ lumbosacral:
• In genitals, groin and sacral regions. . .
• herpes sine herpetica with urinary manifestation but no
cutaneous lesions may occur.
o HZ cranialis:
• Frontalis:
• Involvement of supra-orbital nerve (trigeminal
TG branch) in forehead and scalp.
• Ophthalimicus:
• the ophthal1mic division of TG affect eye ( manifests as conjunctivitis or keratitis) may be af-
fected
side of and is evidenced by involvement of the nasociliary branch affected with vesicles on the
the nose.
• MaKillary branch of TG with vesicles on uvula and
tons,llar area .
• Mandibular branch of TG with vesicles on posterior

tongue, buccal mucosa.
• Fieial:
..__....._1¥,..
&enteutate •s 1· ~ due to involvement of
.,"I ton Wtth e1, ,-3 · .
external ear+ 1.-:_, 111 ind vesicles on
( . 1 and I°""'" h-.- .
·~tai..,
iUdttory nerve). 'Ql't '""'41rAng
Bilateral: . •
. t d with constituoona I ma nlfestation In
o o :are and is assoc,a e d ·mmunocompromised
•debilitating
"Q . diseases an t
patients.
rd . g to n,orphology:
o AcCO in
,. Classical
• Abortive 1·
• d papular with hea 1ng
• Groupe
,. Haemorrahgic . d . d bilitated & immunocompromised subjects.
• vesicles filled with bloo in e
Gangenerous . . d t
•• Gangrene develops at the site of infection ue o
throm bos is of dermal vessels.
• Complications . .
0
Secondary bacterial infections.
0 Eczematization.
0 Gangrene.
~ Post hereptic n~uralgia.
0 Systemic affection
0 Occular
• Keratitis
0 Neurological
• Facial palsy, meningitis& myelitis.
0 Urinary bladder
• Cystitis
• Treatment
o Systemic:
• Analgesic for the relief of pain and for the anti-inflammatory effect
• Acydovir (Zovirax®J 800 mg 5 times daily for 7-10
days.
• ~dovir (Famvir®J 500mg daily for 5 days may help
to decrease post herpetic neuralgia {antiviral).
• Antibiotics : for secondary bacterial infections.
o Local treatment
• Analgesic creams.
• Anesthestic eream.
• Antibiotics if there is secondary infection
• Drying agents.
Claldaen PGx (vancella)

• Organism
0 Vancena .
zoster virus primary infection
• Intubation Period
o 2 Weeks.
• Clfn/cal plctl1re:
Age: tJSlJallY In children
synipton1s ti ,sand rarely severe In adults
Mild cor1stitutional mar1lfest<-1 or
"~ ttch lnB is common .
o Localization fa ce oral mucous mem b rane an d

• on tl1e trun k, sea Ip,
fxtre,n/ties
• Morphology
Papules or macules , vesicles or bullae that form pustules and crust.
0
Lesions in various stages are present at the same time (polymorphism) and usually he I .
a Wtth,r.
7-10 days with normal skin.
• Differential diagnosis
Other exanthems, drug eruption, papular urticaria and erythema multiforme
• Complication
o Secondary infection
o Systemic involvement ( pneumonia) is uncommon.
• Treatment ~ \ ~ (~ \VV\.~ t0-,11\.L VUl)\., - \_o J ,.)OJ.A \i, .9_

o Bed rest
v.Qf)\ ~ (_} J , ' Q Cxc:->--\t:::>'/--'' v, C.\ ~ ~
J ~
o Systemic antibiotics J J
o Local drying agents or antibiotic % QJ\.R)Q~ ; , , ~ 0 ' ~ ~ -~

o In severe cases: -'> Y--__,t_ ~~ \)~\\)~ \.0:. ~ °'- ~ : 1 . ~ . 1 '
• AGydovu- or gammaglobulins.
\~ ·,Y'\~~,.J:_ \/\Jbt ~ ·•'-''~-C:Of~ \.\r.~

•
'(,~ L ~ 3c1t~ ~ \ ~\.-\->0. ·
WARTS
oefinition:
Warts are benign prohf rations of skin and 111ucosa caused by th t1un,_jon P"' -
• • • • •<ii ~p1 11 omav1rus (Hl'V)
warts are trans~1tte~ by direct or 1nd1rect contJct, and predisposing factors lnclud dlsrupno.n
to the normal ep1thettal barrfer.
The causative agent:

HPVs are small, non-enveloped double-stranded DNA viruses belonging to the fam ily o f Papova
viruses.
currently, about 130 serotypes of HPV have been Identi fied and given nu mbers 1,2,3 ...... Certain
HPV types t end t o infect skin at particular anatomic sites; however, warts of any HPV type may
occur at any site. Some serotypes exhibit a potenti al carci nogenic effect. HPV types are often
referred to as ''low-risk'' or ''high-risk'' based on th eir pot ential for oncogenesis.
HPV establishes infection only with in the stratified epithelia of the skin, oral cavity, and anogenltal
tract.
Mode of transmission:
HPV infection usually occurs via ~ ct skin or mucous m embrane contact with infect ed sites
It can also be transmitted indirectly through cont act with contaminated surfaces such as
gymnasium floors or around swimming pools.
Autoinoculation is another means of spread of HPV infection, as evidenced by the linear

- -
arrangement of flat skin warts.
Anogenital HPV infections are usually transmitted sexually and are often detected at several sites
simultaneously (multifocal infection).The most imp~ tant risk factor in transmission of genital
HPV is t he number of sexual partners .
In very rare cases, infections in newborns from an infected birth canal can lead to la-ryngecu
papill~sii.
Th~ incubation period for genital HPV infection is a few weeks or months.
Pathophysiology
The HPV virus infects the epithelium without any systemic dissemination .
The virus enters the cell then unco;ts and delivers its genome to the hoSt cell nucleus to be
eitpressed as autonomous replicating elements (extrachromosomal).
1lle hail
....__ mark of malignant transformation
· h · t gration of the viraf
by high-risk HPV types is t e in e
-'Wlfle .
•nto the host cell genome.
Usina h0st ated into progeny cells.
5'.bse cell machinery viral DNA is replicated and th en segreg ,•r for the replication
quentlu ' 11 to serve as a reservo . h
""ore Vi I'' one daughter cell remains in the basa ayer
Of .,, h
basally w ere
HPV inhibits t e
Clll frorn .ra DNA While the other daughter cell migrates supra- '
•ts normal exit from the cell cycle.
. ;cal presentations: . . . .
Cltn,naJor•·ry of infections
are subclln1cal. In 80 % of frank clln,cal cases the lnfe- ti
. c on re
T,, e sly within 12 months (due to a cellular immune response) solves
spontaneou
Clinical tVPes: .
s warts (Non genital warts)
cutan eou
!-Verruca vulgaris (Common warts):
TheY occur largely between the age of 5 and 20. HPV types 1, 2, 4, 27, 57 and 63 cause co
warts. Frequent immersion of hands in water is a risk factor for common warts. Meat ha:rnon
fish handlers, and other abattoir workers have a high incidence of common warts of the han~ers,
combination of maceration and trauma seems to be a predisposing factor. s. ~
common warts are usually located on t he dorsa of the hands. They also favor the fingers an
palms. They are usually symptomless, but may be tender especially if growing beneath the na~
plate.
Fissuring may lead to bleeding and tendernes~. Lesions range in size from pinpoint to more than
1 cm, most averaging about 5 mm . They grow in size for weeks to months and usually present
as elevated, rounded skin coloured , greyish or brownish pap~les with a ro~h, greyish surface,
which is so characterized that it has been given the name 'verrucous'.
2- Plane warts (flat warts):

Plane warts, due mainly to HPV-3 and HPV-10, are smooth, flat or slightly elevated and are usually
skin colored or greyish-yellow but may be pigmented pa pules . They are -{Ound or polygonal in
shape and vary in size from 1 to 5 mm or more in diameter. The face and t he dorsa of the hands
are the sites of predilection. •
Plane warts may display the Koebner phenomenon - ie. a line of warts may develop along a
scratch mark.
Fflltorrn warts:
J- , th• fa<,, ,111d llml>!» oflt•r, ,l'>S lllllf'
0 1
w.arts ~, ,h, ,,r , .,,n,1II thtC',td or finHc r like-
1
, fill for,, ,
pr0Jtct1ons )
4- 0111tftorm warts:
or finger like w Jrt~, wl1l ch usuolly
threa d tc in !>mc1 II grolips occur most
aggrega ly on the face, r• spccl.._1lly near the
common
eyelids and lips.
5- Plantar hWarths: h bit of rubbin g thei r feet against rough surfaces while bathing or otherwise,
people who ave t edevelop
a such lesions. The lesions are mainly seen over t h e pressure po Ints
are more prone to
such as the heels or metatarsal heads.
The wart appears as a small, shiny, deep seated papul e. Gradually it becomes a sharply defined
rounded lesion with rough keratotic surface surrounded by a smooth collar of thickened horn.
The common types causing plantar warts are HPV types 1, 2, 4, or 57.
Mosaic warts occur when palmar or plantar warts coalesce into large plaques. When the surface
is pared, the angular outlines of tightly compressed individual warts can be seen.
Planta_r warts may be conf~sed with callosities or corns. The diagnosis is made by appearance of
break 1n _the d~rmatoglyph1c pattern over the lesion, p9.in on lateral pressure and the ap earance
of bleeding points. p
.....
Ucw;a- .....
(c>:j -d
-,
Genital warts
Mostly
· transmitted
. by sexual contact • Th ey can occur on the e t .
1
per,~na 11 Y, ,n the anal canal (rarely beyond the d . x er~a or internal genitalia,
pubis and inguinal fold. entate line), the perineum, and on the mons
Could be either:
1- Flat genital warts
Are often multi I d
or b P e: an flat . Lesions may be flesh-colored
rown sometimes h' '
regions)· ;he k . . w ite and macerated (in moist
, d eratin1zed surface of skin warts is absent
Often Pro uced b · ·
18 and 31. Y carcinogenic serotypes commonly 16,
2- Condyloma accuminatum
Larger ca uliflo w er like m asses wh ich are p ed icled, soft
based and have irregular surface w ith crypts harbo ring
bacteria and often produ cing foul sm ellin purul en t
d ischarge . Commonly caused by the non-carcinogenic
serotypes 6 and 11 .
Complications of warts
1- Transmission of infection.
2- Recurrence after removal
3- Bacterial infection in condyloma accuminata
4- Malignant transformation: in lesions caused by high risk types (16,18) starts as ce rvical
vaginal intraepithelial neoplasia (CIN,VIN) and progresses to invasive carcinoma by tim e. 0r
Risk factors for malignant transformation:

HPV infection alone does not cause malignant transformation of infected ti ssue. Cofact ors are
needed, such as tobacco use,
@ pregnancy,
@ folate deficiency,
@ immune suppression (Drugs, HIV)
HPV Vaccines
Developed to guard against genital warts and to diminish the incidence of cervical cancer.
@ Gardasil (quadrivalent vaccine for HPV types 6, 11, 16, and 18.) Administered IM at o, 2,
and 6 months.
® Cervarix (bivalent vaccine for HPV 16 and 18 types).
Diagnosis:
Mostly clinical, rarely a biopsy is indicated to exclude other clinical similar lesions or to detect
dysplasia
Histology:
Common warts are
show acanthosis, papillomatosis, and hyperkeratosis. The rete ridges
elongated and, at the periphery of the verruca, are often bent inward so that they appear to
point radially toward the center.
The characteristic features

vacuolated cells f d that ~distinguish
e>
.verruca vulgaris from other papillomas are foci ol
, ,, , ..,')
and .1n the granular

, re laye
erre Th
to as
k ko11ocytotic
. cells, which are located in the upper stratum malpighii
01 1
by a clea h I d r. e ocytes possess small, round, deeply basophilic nuclei surrounded
r a o an pale-staining cytoplasm.
Large capillary loops are seen in th . .

underneath the lesion. e dermal papillae with mononuclear dermal cellular infiltrate
DD:
For cutaneous warts· Sebo h .
Uchen pianus . rr e1c keratoses actin,·c k t
· ' era oses I corns,callosities, skin tags, and
·tal
l lesions: condylomata lafa of secondary syphili5, M ollusca contaR10, ,1r1d pearly pen~
For gen
paputes.
rreatment
physical destruction: '\
_ Electrodesiccation : \\. ~ ~ Cj.,..n,,cnl\ \-1,rt.C'<Ar-eMu. . . . . .
1
rgery which involves freezing th e w art (generally with liquid nitrogen), creatin g a
2_ cryosu , . d
blister between the wart and epiderm al layer, after whi ch th e w art and th e surrounding dea
~ ~ )\CU-~t.c·,.x)
skin fall off by t hemse Ives.~
,....v\.f°'cn.) l~~ . .
_ Laser treatment - often with a pulse dye lase r or ca rbon d1ox1de (CO 2 ) l~~e r. Pulse dye las~rs
3
(wavelength 582 nm) work by selective absorption by blood cells (specifica lly haemoglob_1n)
leading to occlusion of va scular spaces supplying the wart. CO 2 lasers work by selective
absorption by water molecules and is ablative.
oyod ~,CA.,'--"~)
,-t>U"- 0 ~ "" . .
4_ surgical curettage of the wart is not recommended and must be avoided 1n plantar wart
because of possible reccurence within a painful scar
Chemical cautery:
Ointments or solutions or plasters incorporated with salicylic acid (plantar warts and common
warts) and trichloroa,e~etic acid solution.
1-Podophyllin/Podophyllotoxin{ for external genital warts)

The agent is used extensively in the treatment of anogenital warts. It works as an antimitotic
agent. It is contra indicated in pregnancy and breast-feeding.
2-Topical 5-fluorouracil (for flat warts)
lmmunomodulatory measures
1-lmiquimod 5% cream (for ~~ern~enital w~):
It acts by cytokine secretion from monocytes/macrophages leading to a T-helper 1 dominance
and cell-mediated immunity through the stimulation of toll-like receptors.
2-lntralesional immunotherapy (for resistant cases):

It u~lizes the abil ity of the immune system to mount a delayed type hypersensitivity response to
various antigens and also the wart tissue. Many agents have been used for intralesional injection.
The~e include Candida antigen, mumps antigen,trichophytin skin test antigen, tuberculin, BCG
vaccine and MMR vaccine-.-d__-\}.,...l. --.o~ u:ca""~)
: : • Chnetidine and levamisole for alleged immunomodulatory effects mostly for children.
1zinc sulfate supplementation often reduces or eliminates warts. Dose: 5-10 mg/kg/day.
Molluscum contagiosum
~~
Etlo~~viral infection caused by Po>< Mollusci virU6. bl tranded
5
~-~ay: Pox mollusci virus is an unclassified member of the Poxviridae family (~ou e
viruses).
. h . f cted persons (direct contact) or contaminated
contact wit tn e . ObJAr..
MOT·• Infection follows. may sprea d by autoinoculation. '\.,•
(indirect contact). Lesion 5
h I'ld n sharing a bath and between athletes sharing gyn-.

b tween c re • • • '' •f'lasi
Direct skin contact e b n reported to transmit infection. In adults rn u,...
d b ches has ee ' o11 us
equipment an en . sexually transmitted disease (STD). tu,-.
contagiosum most common 1y is a
. . k'
Reported indirect s tn co ntact includes that with fomites, such as bath towels, spong es, aria
gymnasium equipment.
Epidemiology: A worldwide disease. The greatest incid_ence is in chi~dren younger than age,
years (although rare below 1 year) and in young adults. It 1s commoner 1n males than in fernat~
'
Pathophysiology:
The Pox mollusci virus replicates in the cytoplasm of epithelial cells, producing cytoplasrr ~
inclusions and enlargement of infected cells. The initial infection seems to occur in the ba
~-----.
layer, and the incubation period is usually 2-7 weeks. Following infection, cellular prolrfe~
produces lobulated epidermal growths that compress dermal papillae. The basal layer r ~
intact. Cells at the core of the lesion show the greatest distortion and are ultimately destroyec
resulting in large hyaline bodies (ie, molluscum bodies, Henderson-Paterson bodies) contaip•"'-
cytoplasmic masses of virus material. These bodies are present in large numbers and appear asas
white depression at the center of fully developed lesions.
Cinical picture:
Distribution:
Depends on the mode of transmission. Lesions typically occur on the chest, arms, trunk, and face.
Hundreds of lesions may develop in intertriginous areas, such as the axillae and crural region. ~
palms are usually spared . Patients with atopic dermatitis may develop large numbers of lesions.
Healthy adults with genital molluscum tend to have few lesions, which are limited to the perine1....,.
genitalia, lower abdomen, or buttocks.
Widespread, persistent, and atypical molluscum contagiosum may occur in patients wh"' a~
significantly immune-compromised . , -
.
Lesions are
, . ,> v :'\
asymptomati~ d1scre~, non lender, single or, more often, r12_ul_
"---->
~ ple, r_Q!Jnded, daJrr
shaQed, pin , or pearly white glistening_waxy pa~ that are 2-5 mm in diameter (rarely up~:
1.5 cm in the case of a giant molluscum). The papuiesa re umbilicated and contain a caseous
-
ec,n,plications . .
,tation, ;nflammatton, and secondary lnfect1on.
trr imosis: The disease is usually benign and self-limited. Spontaneous resolution generally occurs
~ months ,n immune-competent individuals; however, lesions have been reported to persist
8
for as long as 5 years.
Recurrences occur in as many as 35% of patients after initial clearing. The disease ofte~ becomes
generalized in patients who are infected with HIV or are otherwise immune-compromosed.
oo:
plane warts, verruca vulgaris, keratoacanthoma,other benign skin tumours
Diagnosis: Histologic or microscopic confirmation of molluscum contagiosum is indicated in
patients who are immunocompromised because several life-threatening opportunistic infections
may clinically mimic molluscum contagiosum.
fJ(amination of H&E preparation reveals a cup-shaped indentation of the epidermis into the dermis.
0ownward proliferation of the rete ridges with envelopment by the connective tissue forms the crater.
Within the region of the indent ation, the epidermis appears thickened (acanthosis), and the
cornified layer typically is disintegrated. The striking feature is the presence of intracytoplasmic,
eosinophilic, granular inclusions within the keratinocytes of the basal, spinous, and granular
layers of the epidermis (molluscoid bodies).
Treatment:
Direct Lesional Trauma
Minor trauma to molluscum lesions frequently produces an inflammatory response and resolution
of the lesion due to activation of th e alternative complement pathway on exposure to the tissue
fluids; furthermore, the Henderson-Paterson bodies release proinfiammatory cytokines and
other neutrophil chemotactic factors upon decomposition.
Various forms of physical trauma and ca ustic topi ca l agents can achieve thi s.
1-Aoin, ia~'k acid, and po t assium hydroxide m ay be used. Cantharidin, silver nitrate,
tnrtel•ro1~acjd, and phenol also are options. Children may tolerate therapy with these agents
better than curettage or cryotherapy. No ne of these ca ustic agents has been approved by the FDA
btreatment of molluscum contagiosum .
"'vsical trauma to individual molluscum contagiosum lesions can be performed with cryotheraPY«
'curettage, expression of the central core with tweezers rupture of the central core with a
or a toothpick, electrodesiccation, shave removal, ~r d~ct ta_ge occlusion.
•office
ftrmsetting' curettage of ind1v1dual
.. lesions is easy and very effective. With a sharp curette and
motion, small, Individual lesions can be removed completely, with little or no bleeding.
0 _ ,..-- ,,.echanical methods. s~ch as expression of the contents int e papule by sq
t forceps held parallel to the skin surface or shaving off the lesions ·th a sharp sc~.aa, pe.
e Prti~•
Les· .s ma afso be treated with 1·ght electrodesiccation. At very tow voltage settings, anesthesaa
__,. not be required.
As or cryotherap , a brief freeze, which causes icing of the lesion and a thin rim of surrounding
·n. is usuall adequate.
Immune Response Stimulation

rntralesional interferon alfa, and topical injections of streptococca\ antigen
iffl1!0Clt: crea1:n,
have been sho n to be effective in treating patients with resistant molluscum contagiosum. lhe
· h cost of these products limits their use to more extensive or resistant infections.
tmiQuimod is a novel topical immune response modifier that is a potent inducer of interferons
- -- • ·- -- '!'' : ':'~ --~-~;-- •• ,
- - - - -- _.,_,_ _~ .• -
SUPERFICIAL FUNGAL INFECTION ' ~ .. f:'~,::·-
~ - .. - - , --..: : '"-'--" ~-....:.t:.--~.:..:..i~-~\
..
Funai can be classlfled Into:

1 Moulds
Thev art' ftla1nC'r1tous fungi that mainly form hyphae. They can be
Pathosenic (dcrmatophytes) or sa prophytic(non dermatophyticmoulds) .
2-Yeast
They are semi spt1erlcal cells which form pseudo hyphae when pathogenic.
Yeast ca n be pathogenic like Candida albicans or non pathogenic like pityriosporum ovale and
orbtculare .
oermatophytes
They are keratinophilic fungi which attack keratin so affect skin ,hair and nails. There are 3 genus,
which contain different species.
• Tricophyton (eg:T.rubrum)
• Epidermophyton (E. tloccosum)
• Microsporum (eg: M. canis)
Classification of superficial fungal infections:

1- hair affection
It is common in school age and rare in infants and adults ,with direct or indirect mode of trans-
mission. ( '3.~\o~COivJ) ~ <.r<..uo""' - ":> ~-~ ~~) )---.. ~Wl..r) ~-~o-1 e~~cJ.>
a. Ring worm:
• Non lnflamatory (black dot and Grey patch)
• lnflamatory (pustular folliculitis and kerioncelzi)
b. Favus
2- skin affection:
• Tinea circinata or Tinea corporis
• Tinea cruris
• Tinea manus and pedis
3- Nails affection (Onychomycosis)
T.Capitus
Non inflammatory ring worm
a-Black dot
Causative organism: Trichophyton violacium
Oinical picture:
• A patch of alopecia with multiple black dots
and scales.
• Hair is cut at the level of scalp.Hair follicles os-
tea are blocked with black dots which are the
remains of the broken hair. Long hairs may
be found in the center of the patch.It may be
single,multiple or diffuse
.figure 1:black dot
55
:,sVP~,.,c.J.-"-'·••-;;:.....~ ~ .
...JttJflf':CftON ..,.·-• -
· cx.1mlnat1o n : ( d h I )
Microscopic . . . •d ·tt, fungal spores form ing a sac. en ot r x
Tt,e hair matrix is fillt w1
'°S of non clca tricla l alopecia.
oD: ott,er caus ..
b-Grav patch
Orga nism· Mlcrosporum audonll
causati ve ·
Clinical picture:
A patch of alopecia with scales. Hairs are cut few mm
above the scalp.The covering sca les are small and dry.
Multiple patches may be dispersed on the sca lp.
,< , ....
Microscopic examinatio~\\,P 1\w":) """;:o>j

Fungal spores surround the hair in an irregular mosaic
pattern in the mid shaft "Ectothrix". figure 2:gray patch
Prognosis
The condition is self-limited at puberty, healing occurs by normal skin.
lnflamatory ring worm
Causative organism :T. mentagrophytes and M.canis
Age: children
Mode of transmission: usually from cats or dogs
Types :
(1) Mild (pustular folliculitis1
Clinical picture:
Multiple pustules at hair follicles, it should be differentiated from bacterial folliculitis. There is
slight erythema of skin in the affected patch .
Hairs are stuck together and broken.
(2) severe [kerion celzi]
Clinical picture :
Marked edema and redness and tumefaction of hair
with formation of boggy soft swelling which on pres-
sure, pus comes out from hair follicle.
Each hair is surrounded by a pool of pus and easily
detached.
Inflammatory ring worm affection heals by scar tissue.
Microscopic examination:
The hair is surrounded by regularly arranged fungal
spores like a column [Ectothrix] figure 3:kerion celzi
Differenttal diagnosis:
l·Abcess
2· other causes of cicatricial alopecia
• Causative organism: T.shoenlelnli
• Clinical picture: the Initial IC' .
s1on 1n tlie
scotulum
A crust like lesion of yellowlc;h "su lphur" colour
with a concave convex surface with Its convex-
ity to the scalp making an erosion or depres-
sion in the epidermis which is firmly adherent
to the scalp and on detachment It givessero-
sanginous discharge.
The scotulum is cup shapedwith mousy

odour,with a size of few mm to few cm figure 4:favus
The affected hair is of normal lenPth thin dry friable lu t I d .
. . - q: , , , , s er ess, u11 gray 1n colour.
The hair appears as ,f dusted with powder.
• • •
Microscopic examination
The fungal elements are present within hair (endothrix hyphae) Th h h
. . . . . e yp ae are arranged parallel
to long1tud1nal ax,s of hair
Tinea circinata
Cause: any dermatophyte
Age: any age
Site: any site except special sites
Symptom: itching & disfigurement
Morphology:
Single or multiple, well definite erythematous
-
scaly circinate patches
which spread eccentrically with healed center
and active margin. If the__cents;r js r~acti\lat~ it
- 1
gives@ polycyclic lesioiiJ The margin is elevated,

erythematous and scaly with vesicles or pus-
tules. The center may show hyperpigmentation.
figure S:T. circinata
Differntial diagnosis
From other superficial circinate lesions.
Tinea cruris
Causative organism: Trichophyton rubrum, Epidermophyton Floccosum and Trichophyton
mentagrophytes..::, ,~--~.
0
_ (..Ml\'- ·CP--\".. -t 's
Sites:
ft affects the upper inner thigh and it may extend to pubic area,lower abdomen& gluteal fold,
upper thighs, rarely it may affect the scrotum or genitalia.
Clnical picture
The lesion is itchy and brownish red in colour with well defined margin with circinate
suPF!tF.IICJAl ,,u111mAl
tNPICT'iON-- -
. h tive margin and healed center.
corlfiguration wit ac
I n1i 11t1tC' scJlcs.
Tl1 e sL1rface s ,o, ~ t11tous scaly lesions Jffccting flex-
oo~Otl1er c ryt l ( I '
l rytfirds,,,a (bacterial infection)

1.
Flc'<tJr.-11 psoriasis
2.
3. 1,,te rt rigo
4. Moniliasis .
c;; Neurodermatitis figure 6:T cruris
-.
6. seborrheic dermatitis
T. man us& T. pedis

causative dermatophytes: T Rubrum , E. Floccosum and T. mentagrophyte.
Types
1. Inter-digital type of tinea pedis(macerated type)
(erosion-interdigita Iis-mycotica) G
The skin b~tween toes or fingers beco~e moist,
whlte, peeled off and ma~ rated with fissure in the
-
center.
It is common among athletics [athletic foot].
2. Erythematous scaly type.
It affects dorsum of hands and feet. It presents by
diffuse erythema and scales. It may be circinate.
3. Eczematous or vesiculobullous type
Present by multiple vesicles and bullae on sole &
sides of toes figure 7 :toe web maceration
4. Hyperkeratotic type
Plaques of hyperkeratosis, Commonly on palms and soles.
Symptom
Mild itching & burn ing sensation.
Pityriasisversi color
Etiology: Malassezia furfur or globosa
Ace: any age but common in adults.
hofogV . •
tf1orP d rnacules or patches which oval or rounded
I define , . . .
wel h popigrnented or cafe-aulatt 1ncolour (hyperpig
y are Y . mented) and cove d ·
;he d heal commonlyw1th post-eruptive hypopigment . re with fine branny
scales- An ation .lt may be perlfollicu\ar (f 11· ..; ,.>
pe). . . 0 ICU-
lar tY •hyperpigmented TVC M1croscop1c examination:
fi g uresa. es and hyphae can be seen giving the characteri sti h _
00th spor c spag .:_tti ~ _meat b~Uappearance
• •
onvchomycos1s . D ,-...,n,'c-'
1·nfection of the nail) ~ \,.. ,'f'.c:,.,,v---~
(Fu nga , L """~ ~ J'( ~ 'b\:e ~ :-:, ~ - t.ll~·,'
Etiology -c. ..,.,..~~t-~'
m atophytes (commonly caused by
1- oer r=----- ~''~ \ ,, ...,.,ycc::,'),',
r.mentagrophytes) (Tine~ungium}
_saprophytic eg: As~erglllus} .
2
_Yeast (Candida alb1cans}.
3
Types
1. Distal subungual onychomycosis.
2. Proximal subungual onychomycosis.

3. White superficial type which affects the
nail
plate.
4_ Total dystrophic type of onychomycosis. figure 9:distal subungual-
Clinical picture: onychomycosis
The nail affected is dry, brittle & lusterless with pitt d &
rated from its bed. e grooved surface. The nail may be sepa-
DD:
Other causes of nail dystrophy.
Diagnosis of fungal infection:
1. History
2. Clnical picture
3. investigations:
- wood's light which is used for screening.
•
..,. scrapping
- culture or culture and sensitivity on Sabaraud Dextrose Agar
Treatment of Mycoses (fungal infection)
A) systematic:
indications:
onychomycosis, tenia capitus and extensive skin infection , extensive TVC and chronic recurrent
tinea pedis and tinea manus. .
1) Griseofulvin
• Fungistatic
• Active against dermatophytes.
• Dose: 10 mg/kg /day
- Duration of treatment:
-
" ::c e : epatoto ,c {not used}.

~uCQI@2t e : octi~ against dermatoph rtest yeast and some non dermatophytic ~
~ z o l e~
gista~ ar.d it Ss active against dermatophytes, yeast and most of non dermat~
mDiU dS
fine
• •
- f _g7et a-
_ cove Aga ·nst der,r,atophytes only.
-
B- Topical
tjAzole
e.g etoc.onazole ,itraconazole (yeast and dermatophyte) ,clotrimazole,
econazole ,isoconazoJe and myconazole
2J Tt:tbeilafirie
3)14
I the for, r, of cream, powder or spray.
-
PARSITIC SKIN DISEASES
.. , e ,.-gma e , te Sarcoptes scabiei

.., ,. r, _ -: , ,.._, ~ ~te .... -- a parasite t l1at
- -., : .. .:: , ., ·n ~ t~e e pide rm is
....~r. nu' sun l .
-tage tunne l tnt o t he
raece s be hind them ;
f'l els.
a ·tch mite (Sarco.p tes
of the mite, .:. scabiei1 seen on a s'kin scraping from scabetic patient
~ --ss: _:-3 .... es ~ ere 2rre on · about 11-12 female mites p.er case.
~ -~~ . . -: ~ ·n . . ~
·n lediate and delayed types to the mite or its products has been
~t
-=~e.: - : e ce e oment of lesions other than burrows.
ode of transmission
..(Jose :>e"'S "'--:o-oe"'Sor') contact.
-Se.;a ...:e~""S€ •
,es a\ . _ .:.:""s~i e infection.
t.~ -+\' \,0 ,:-u """"
Clinical picture _ :::..c. , ~V\.J.
: oc:.. . al scratchjng Th e affected sites : Delicate skin as in the web space between the
I
iw4tfs, per- _,oil ca . anterior axillary fold and medial aspect of the thigh
om of t e es·on : poly morphic; Multiple linear scratch marks,Excoriated papu\es
,5econda bacter·a ·nfection
Ascabies urrow nder magnification
f cabies
•
•
. .. -
•
re .
. -
-
....
-
..
Crusted ·an) scabies
a ost i • u~e resooPse to ... e sarcop~es sca~·ei. e cc-·
... ---- _....,. ..... .. , ~g grouos:
- "- =-
---eta""'Ge-0 Do , '"' s ~ a"'() f'T" e
r- c . . ta..., ~s sens.a-on eprosy S) r·Pgore ,·a a d ta bes dor-~ 5 . )
•
t.:r e Suu u-eSStOn
Diagnosis of scabies
History
Examination
1,,westigations :
• Scraping -
• Skin biopsv
Complications of scabies
Bacter,a1 infecnons
-
- fczematii:ation
-Urticaria
-Acarophobla ( ~ o.. · - ' · r .. ,<~,.,\)
Treatment of scabies
Instructions
-Drugs : Topical and systemic.
· Topical scablcides
1-Benzyl benzoate 10% and 25% lotions
2-Pyrethrlns: permethrin 5% cream, lotion
3-Malathion 0·5% lotion
4-Sulphur (precipitated) 2-10% in petrolatum
5-Crotamiton 10% cream (Eurax )it is anti pruritic
6-Gamma benzene hexachloride 1% cream or emulsion .
Special care fore Infant------ Pregnant
Systemic drug for scabies

,Wr,r,ectin. (200 µg/kg once and repeated after 1-2 weeks) .
1-The full benefit becomes evident when
eradication of scabies in e idemic or endemic situations
2-in nur::sing homes and prisons is needed since ivermectin leads to reliable disease control.
3-Along the same lines, crusted scabies has been effectively treated with ivermectin in adults and
children, sometimes in combination with topical permethrin.
Mechanism of action
ivermectin interrupts the GABA-induced neurotransmission of many parasites.leading to paralysis
of the parasites.
Novel drug
Recently, the essential oil of the tea tree (Melaleuca alternifolia), containing oxygenetic terpenoids,
was found to have rapid scabicidal and antibacterial activity
vaccine development
The multifunctional enzyme glutathione S-transferase of S scabiei could represent a specific target
for vaccination against human scabies.
Pediculosis
Pediculosis is an infestation of lice - blood-feeding ectoparasitic insects of the order Phthiraptera.

The condition can occur in almost any species of warm-blooded animal (i.e., mammals and birds),
induding humans.Although ''pediculosis'' in humans may properly refer to lice infestation of any
,art of the body, the term is sometimes used loosely to refer to pediculosis capitis, the infestation
« the human head with the specific head lice
humanus capitis ( ~ }Lice are small gray brown,blood sucking insects which crawl among
hairs
I 11, 1,,
l l)t'lfll l lltl'> I-.. ',lJ)lt f, (111 •. ,(t II< t ' ii)fl' <.. l ,,tl<)ll)
) f'<',11< ltl,,,1 1~ , ,)rl>'.) 11 (l'1 1 cll<iilt)" I', v1 1 1,ll1111 1 1111 ,
\ v..-.,.,,l)(\1\tf', til,'4,. , ) \ Yt>l)l I \ & I ,,1,,~)•,1!111 f( 1 Vt •r
\ r''-'ti11. l,t'")'l'- 11t~b1, (t , ,1l)\, ) " 11 >
t, <,,if t l ti,),, 1-.. , () , I ) l 1, t' I11 f 1'" t •\t l t) r,, , t, 11, . 1In r..
,l\t\' <)1 h.iw l< lt' f) I (>t,1,,,,, . l t1<' li e t ' ll\ ,lt l11t< 1 c.. t
l1l1111 ,111 l)r'l1,,~, ,,, ,, ,1ln1l)">l .,tw,,yc.. \ ltLkl11t~ lieC'
t h,1t llv.- In <10,1, ,1•,,ocl,111 0 11 wllll t II<' ho ~t ;ind lay I h •Ir egg~ on h,1lr ~h, fl~ or In th(• ~~am,
, Of C.\c,t
H ad lous nit 1: tt ch d to holr hoft
Identifying characteristics of a crab louse
Treatment
•
• Anti scabetic drugs
Eczema
Definition of eczema: r;
~ma is a pattern of, ~ammatory response of the skin characterized clinically itc~l'}g, red~ess,
scafing and c~stered l)apulo-:Yesicles, and Histopathologically by Presence of a lymphocytic
infiltrate around B.V., associated with spongiosis & varying degrees of acanthosis.
Classification of eczema:
1. Exogenous eczemas
• Irritant contact dermatitis
• Allergic contact dermatitis.
• Photo-allergic and phototoxic C.D (contact dermatitis).
• Infective dermatitis. ! cu\.>J(~v...! _..., ~t:j-'>~tJr 0 -o""ullN'-'..,"'"'"')
2. Endogenous eczema :
• Atopic
• dermatitis and pityriasis alba.
.
• Seborrheic dermatitis and infantile Seborrheic dermatitis.
• Gravitational dermatitis.
• Pompholyx (eczema of palm & sole)
• Asteototic (senile) dermatitis.
• Id eruptions.
Histopathology of eczema:
Acute eczema:
• Spongiosis (intercellular epidermal edema).
• Epidermal vesicles.
• Lymphocytic infiltrates.
• lntercellular vaculation.
• Mild acanthosis.
Sub-acute eczema:
• Spongiosis diminishes.
• Vesiculation diminishes.
• Acanthosis increases.
• Lympho-histocytic infiltrates.
Parakeratosis.
-ma:
ratosis replaces parakeratosis.
·s increases.
I vascular dilatation.
istocytic infiltrates.
is & papillomatosis
____ ... ., __
Clinical features of eczema:

Symptoms:
Itching.
• Disfigurement .
• Psychic upset.
Signs: \
• Edema.
•
• Scaling.
Erythema.
'
• Papulo-vesicles.
• Pustules (2ry infection)
• Crustation.
• Lichenification .
• Erosions.
• Fissures.
• Oozing.
In the acute stage ( wet stage) there are acute features including erythema, and vesiculation and
in the chronic stage (dry stage) there are lichenification and fissuring.
Although sometimes overlapping features can occur in the same patients
Infective dermatitis:
Infective dermatitis:
Definition:
It is caused by contact with micro-organisms or their products.
Id eruptions:
It can occur as an allergic reaction to a dermatophyte, bacterial or monilial infections elsewhere
in the skin. The dermatophytid eruption commonly occurs on the hands
Criteria:
1. Proven focus of acute dermatophytosis, bacterial or monilial infection.
2. +ve skin test to responsible antigen.
3. Absence of the infective agent in the Id eruption.
4. Clearing of Id after the infection has been eradicated.
Non dermatophyte id eruptions may occur as a type ofwide spread dermatitis following
acute eczema in a localized area e.g active stasis dermatitis of the feet. It is supposed to be
hypersensitivity response to altered tissue protein in the original site of inflammation
Seborrhoeic Dermatitis:
Definition:
It occurs as red , sha rp IV marg1nated
· Ies1ons
· covered with greasy-looking scales & localised ·in
areas
with with
bo a rich. sup PY · d
I Of se baceous glands (scalp, face &upper trunk). It is usually associate
se rrhoe1c state.
Infantile seborrhoeic dermatitis
Deftnltton:
It is a morphologically distincti .
napkin area or flexures In infa:: co nd1ti 0 n In which erthematous scaly lesions occur in the scalp,
(senile eczema)
_ASteatotiC eczema d crease in skin surface lip ids, sebum
nofioftton : . ted with and possibilly caused by a e
.,.. ma assocra
ft is an eae
& ceramide.
(d . oid) eczema
._.ummutar ,sc
,.,. ..
.
holog1cal
f
eature,
a coin -shaped or discoid
oefinltion: . b unique, non-specific morp
.
haracterrzed y a
ft ,s c . f plaques of eczema .
configuration o
Pftyriasis alba . d
.. . . . k- round (minor feature) tr1ggere
~fin1t1on:specific dermatitis in patients with an atop1c ba~ ti gally produces erythematous scaly
It 1s a ~on &.-.. t rs (eg · sun, soap) which character1s c
nvrronmenta 1 ,oc o , . .
by e h'ch subside to leave areas of hypo-p1gmentat1on.
patches w 1
Oinical featu res of pityriasis alba:

Age: 3-16 years
• in both sexes equally. . II branny scales
• Round, oval, irregular plaques, red, pink or skin col~red with lame ar or ·
• Later, it leaves post-eruptive hypo- or depigmentatlons.
• Single or multiple.
• Face, cheeks, forearms, neck,& shoulders .
Gravitational eczema {Stasis or varicose eczema)

Pathogenesis:
High a,m bulatory venous pressure within the calf muscle pump is transmitted to the capillary
circulation in the skin and subcutaneous tissues of the calf. This distends the local capillary bed
and widens the endothelial pores, thus allowing fibrinogen molecu~es to escape into interstitial
fluid where they form fibrin complexes around the capillaries forming peri-capillary barrier to the
diffusion of oxygen.
Oinical features of gravitational eczema:

• Middle aged male or elderly female.
• Sudden or insidious onset.
• Inner aspect of lower legs.
• Edema, purpura, haemosiderosis, diffuse brown pigmentation, ulceration, and atrophie
blanche . Appearance(whitish atrophic areas)
• Well-fitted supporting stocking and elevation of the legs are essentials for treatment.
pholyx ( Vesicular eczema of palms& soles)

Vesicular eczema of palms& soles)
on:
tt is eczema of the palms a d I hi h . ..
edema fl .d n so es w c 15 modified by its special location and in which
u, accumulates to form vesicles or bullae.
Crops of clear vesicles deepl t d d .
V'aSod'lt . ' Y sea e an sago-11~ preceded by sensation of heat and
. • ation. No er:\1,bema.
les may beco fl-
me con uent & present as large bullae.
: id reaction, contact d · · .
ermatitis, excess sweating, and psycogenic.
Contact dermatitis: f t he skin due to d irect contact with an exogenous agen
It n,cans acute 1nnan1 111at1on ~ d ith sun exposure. t (c0nb.....
or allergcr, ). In some cases, tl11s associate w ·- -g
Eti ological classlncation:
1. Irritant contact derm atiti s (I CD) .
Allergic contact derm atiti s (ACD).
2
_ Photo-toxic, photo-allergic.
3
1. Irritant contact dermatitis . .

It includes several 1nnamn:1atory reaction patterns which follow non -immunological (us
chem ic.al) da mage t o the skin . ua1~
• An accidental exposure to acid or alkali for sufficient time and in sufficient co
ca uses a non-l mmunolgical reaction and dermatitis occurs without prior sensitiza~~ '?~
• M any chemicals penetrate the skin, and many substances alter skin cells includin g don.
ete ~
and house hold care products rgen4
• Dermatitis occurs when the repair capacity of the damaged skin is exhausted 0
penetration of the chemicals excites an inflammatory response . 'When ~
~ '- \ .....v-- • '-
2. Allergic contact dermatitis (ACD) ~ '( - -.t..
It is a delayed or cell mediated type of immunity caused by a contact sensitizer s
most common sensitizers are nickel( e.g:rings and hand watches), perfumes ' neom.Yc1n sul ofh the
~rne
Balsam of Peru and chromates in cement. P ate,
Induction of sensitivity passes into 3 stages:
1. The formation of protein-hap_ten conjugates where the sensitizer acts as the--hapteri.
2. The recognition of the complete or conjugated sensitizer by the immune sysytem.
3. The proliferation of sensitized lymphocytes and their return back to the skin to i d
. n~
inflammation.
3. Photo-sensitization reaction
Photo-sensitive activation of a substance is a physical phenomenon and may occur in vit
. h . . h h t t · ( · ro. If ~
happens in livings k,n t e activation may ave a P o o- ox1c non-immunological)
or a photo-allergic (immunological) basis and thus may be related to a primary irritant effect or
to a hapten formed in situ .
Atopic Dermatitis -
A.O., is a chronic relapsing inflammatory skin disease associated with cutaneous hyper reactimy
to environmental triggers.
Diagnostic Features of Atopic Dermatitis:

Major Feat ures:
• Pruritus.
• Chronic or relapsing dermatitis.
• Personal or family history of Atopic disease e.g: allergic rhinitis or bronchial asthma.
• Typical distribution and morphology of A.O. rash
• Face in infants,
• Extensor surfaces in young children .
• Flexural lichenification in older children and adults.
Minor Features:
1- Eyes
• Anterior subcapsular cataract.
• Keratoconus.
• Infra orbital folds affected.
2- Facial pallor.
3- Palmar hyper linearity.
4- Xerosis.
s- Pityriasis alba.
6- lchthyosis.
-
7- follicular hyperkeratosis (keratosis pilaris)
8 - Non specific dermatitis of the hands and feet.
9- Nipple eczema.
10- Multiple_ Positive type I hypersensitivity skin tests reactions.
11- Propensity for cutaneous infections.
12- Elevated serum lgE level.
- -- -
13 -Food
- intolerance
14- Early age _of onset (before 2 years) .
-
Diagnosis of Atopic Dermatitis:
The Diagnosis of A.D. can be made if three major criteria and three minor criteria are present.
Causes of atopic dermatitis:
. Inherited tendency.
Triggering factors:
1- Physical factors: excess atmospheric humidity and sweat retention in hot weather and skin
dryness in winter
2- Allergic stress.
3- Emotional stress.
4- Exposure to soap, woolen or synthetic fabrics or food.
MANAGEMENT OF ECZEMA:
1. Avoidance of the causative factor ( irritants or allergens}.
-
2. Antihistamines.
3. Antibiotics (infective dermatitis or secondary infections}.
4. Anti-seborrheic agents ( sulphur) or shampoo ( ketoconazol ).
5. Drying agents for acute stage.
6. Emollients for chrQ.nic or dry types.
7. local steroids ( mild or moderately-potent).
8. Systemic steroids if necessary.
MANAGEMENT OF ATOPIC DERMATITIS:

1. Avoidance of triggering factors and skin irritants.
2 Avoidance of emotional stress.
3. Moisturizers and emollients.
•· Early treatment of super-added staph., fungal, or viral infections.
Topical low to mid-potency steroids
Topical Calcineurin inhibitors.
ledating antihistaminics to promote sleep.
therapy for resistant cases. f . t nt cases
notherapy (cyclosporine A) and systemic steroid or resis a
triene antagonist (Montelukast).
Urticaria
Urticaria, also referred to as hives or wheals, is a common and distinctive reaction P tt

may occur at any age; up to 20% of the popu Iation · w,·11 have at least one episode. a ern · urilv~
1
Pathophysiology
• Histamine is the most important mediator of urticaria. Histamine is produced
mast cel ls. There are several mechan isms for histamine release: and stored ii)
• Im munologic (lgE mediated)
• Non immunologic:
o Physical stimuli:
o Direct mast cell degranulation: NSAIDs
o Foods conta ining high levels of histamines: strawberries, tomatoes, shrim
• Histam ine ca uses endothelial cell contraction, which allows vascular fluid to leak b~~w
cells th rough the vessel wall, contributing to tissue edema and whe%1 formafio'n~ een the
'- f c..
Classification:
Ordinary urticaria
• acute (up to 6 weeks of continuous activity)
-
• chronic (6 weeks or more of continuous activity)
• chron ic urticaria is either spontaneous or inducible
Causes of Urticaria:
Acute urticaria:
causes:
Food: tree nuts, legumes, fish, eggs, milk, soy, wheat ....
- Drugs: penicillin, cephalosporin, aspirin, NSAIDs (lgE mediated), Acetylsalicylic acid
Infections, mostly acute viral upper respiratory infections
Chronic urticaria:
causes:
1-ldiopathic (spontaneous) _
2-Autoreactivity: autoimmune CU with anti-lgE and anti-lgE antibodies,cietected by autologous
serum skin test (ASSTfl associated with autoimmune disorders (thyroiditis), characterized~
d~ ~tion and__blg~e~ se activit .
3-lnfection: bacterial (streptococci, helicobacter pylori), parasitic and fungal.
4-lntolerance: non-allergic, dose-dependent and delayed (4-12 h) onset hypersensitivity to food
pseudoallergens such as food colorants, preservatives, taste intensifiers . CU due to intoleran~e
is diagnosed in patients who show decreased disease activity following a 3-4-week diet low ,n
pseudoallergens ·
5-Physical urticaria (reproducibly induced by the same physical stimulus):
• Cold contact urticari~ : ~liciti~~ factor: cold objects/air/ fluids/wind I
• Delayed pressure urticaria: El1c1ting factor: vertical pressure (weals arising with a 3-12 h latencY
t contact urticaria: Efic1t1ng factor: localtsed heat
• H~:r urticaria : Eliciting factor: UV and/or visible light
• SO n,ograph1c urticaria : Eliciting factor: mechanical shearing forces
: :~nown cause, whealmg usually develops within 5-10 minutes of strok ,ng t h fik
r5ists for 15-30 minutes.
• : uagenic urticaria: Eliciting factor: water
q 1· ergic urticaria : Elicitation by increase in body core temperature due to phystc.al exerc,~,
• Cho ,n . . k t,
s icy food. Characterized by: small papules mainly on the trunk, with pr1c Y sensa on
• c~ntact urttcaria: Elicitation by contact with urticariogenic substance
Clinical Manifestations ..
urticaria! lesions are polymorphic, round or irregularly shaped prur1t1c weals.
A wheal consists of three typical features:
(i) A central swelling of variable size, almost invariably surrounded by a reflex erythema;
{ii) Associated itching rubbing in character or sometimes burning sensations . .
(iii) A fleeting nature, with the skin returning to its normal appearance, usually w1th,n 1-24 h.
Clinical variants:
_ Polycyclic (annular) with peripheral extension and central clearing ·
- Vesiculobullous
Angioedema:
Angioedema, which can occur alone or with urticaria, is characterized by nonpitting, nonpruritic1
weJl-defined, edematous swelling that involves subcutaneous tissues (e.g., face, hands, buttocks1
genitals), abdominal organs, or the upper airway (i.e., larynx). Angioedema tends to occur on
the face and may cause significant disfigurement. Laryngeal angioedema is a medical emergency
requiring prompt assessment
Angioedema is characterized by:

(i) Sudden, pronounced swelling of the lower dermis and subcutis.
(ii) Sometimes pain rather than itching;
(iii) Frequent involvement of mucous membranes
(iv) Resolution that is slower than for wheals and can take up to 72 h .
Subtypes:
'• Idiopathic angioedema
·• AJlergic angioedema: often associated with urticaria. It is typically observed within 30 minutes
to 2 hours a~er ~~pos~re to the allergen (eg, food, drug, venom, latex)
ai,AfOs, ACE ,nh•b1tor-1nduced angioedema
Angioedema caused by Cl inhibitor deficiency (Cl-lNH):
Hereditary angioedema
.
Acquired angioedema: decrease of Cl-lNH due to increase metabolism as rn
o4tferative disorders, autoantibodies against Cl-lNH.
111Ciq,;al vasculitis "' Ii " .. \t \ •\ ,a ~

~rial va 5culitis is characterized by pruritic, burning or painfully raised, superficial,
et,'the~atous or edematous, circumscribed wheals .
~~idual u_rticarial lesions last frequently more than 24 hours and leave a residual
~ hyperp1gmentation.
l~ . ~l ~j \Je.r{ - V,..i ~
involvement. S~iri
•
ber of arthropods, including bitin
btt es of a num g
• I ,e porr-e to the . I d
-·•-"' , ,, t J) ' ded by a tiny ves,c e, an are so itch
• . l ... , rutt"'-· flea.). o ften surroun y
.,~,.. •ti: ,. L r ti( ate<.i p l pules,
' ~ 'l) , coriJted. tigens in the arthropods.
• r._,,:, "'t> r..1 •d v t'"X si tivi ty response to an
. e,t•tt cif a hypersen
'-t , t_' ... ~
•
f urticaria and angioedema:
• ~ !O~ d' .
c- _3 • e'\Jrni flat1on lude m ajor internal con ttion
• .... count ESR, CRP: to exc
. b l -~A
• D ~re,'1tta vvv ' ·
.. . for hel1cobacter and parasites
.J Si~
• tc
-• • h roid tests
• ~"~~ te ear ant1bodV,_ t y ST . (anti lgE a ntibodies)
• ~... t••-.. us serum skin te 5t (AS }h
i ~ sence of lgE antibodies for the suspect food .
C'""C test (SPT): to measure t e pre
• _, • ~ ·--..tema without wheals
• c- .~ .
V
C: es:er.a.se ·'lhtbito, level and funcnon

•
Delk, ential Diagnosis:
c~---:. 0 ~ a e: 5=.c dermatitis
... _ _
.., ...
e ....... ~ -'4,J
Treaba.ent
asi1:-es~
?anents sfioutd be advised to avoid factors that trigger relapses: eg, food, drugs.
--rea::.."""'erit with calamine lotion, 1% menthol in aqueous cream have been proved to
scPt:--ess r•sramine induced itching.
~.,-.,,.,.1.atk treatment:
1- A.tdJist«nu..es;
• s«Orld pnet.Jtion Hl-receptor antagonist:
, 5 to 10 mg per day for several weeks I
... f enad1ne, 180 mg per day or 60 mg twice daily

Oesloratad·ne , 5 mg per day
Lot atadine, 10 mg per day
I. fifirir.stst-11Ne!f'lneer;ca1tn-ic·on111 sedatinc Ht-receptor antagonist:
roxyz,ne, 10 to 50 mg at night
Diphenhydramine, 25 to SO mg at night
•HJ· 11M HZ·ce~Rtor 1ota1onist:
Ooxepcn, 10 to SO mg at night
°o CYPfoheptadine 4
Gmetidi . , "'L up to three times dail
ne, titrated to 400 mg th . Y
ree times daily
2• 1.mmunosuppressiye drues; Patients with autoimmu . . ' .
. . h . ne urticaria, Cyclosp . .
only for patients wit severe disease refractory to high d orine 1s recornrnendect
3- .
Qral corticostero1 'd ; ( PrednisoneJ as short-term therapy oses(3oft oral antih'IS.t arn1nes.
.
g d . . I unresponsive . to antihistamines. Not indic ot 7d .days)
eneralize urticaria h in. ac ut e, severe,
4_ I•
Mast cell stabi 1zer: .1n some cases of cholinergic urticaria! a e 1n c ron1c urn car,a · .
5- Leukotriene modifier:
Montelukast, 10 mg: Antileukotrienes may be tak . d . .
. . . for poorly controlled Urticaria
Hl ant1h1stam1ne . . but there is little evidence en in th
that a d1tion to an
as monotherapy.
ey are useful
6- Biological drugs: Omalizumab.
Angioedema:
• Severe cases: Subcutaneous epinephrine (adrenaline) is the main treatment
• Moderate cases :
J. Close monitoring is often necessary.
2. Diphenhydramine (SO) mg intramuscular (IM)/intravenous (IV).
3. Hydrocortiso ne (200 mg) may reduce the possibility of relapse.
• For laryngeal swelling and airway obstruction, close monitoring of the airway is mandatory.
Epinephrine (1:1000) should be administrated subcutaneous or intramuscular.
• Prevention of attacks :The administration of androgen derivatives (Danazol) or antifibrinolytics
(Tranexamic acid) may be considered.
G~ o\c..~,c. drl-3 ~
~
Cy o pc>''~~
f' t_Jf I I f
11,,•11 • ,, , t ,tttJt ltt R c't l('·(fl , l, /ll f >\ ,ll( 1 t lt .
{)4.ll Jt ~( } c1 f ~1,)t1, ,,1f \ w ith i>" ()r/,) I l\,)V( 1 t.l fft•,t•('~8f('( ' r ' lctl lV(' wi th t h ,,,., t.'l • c, .
r.\ 1 1,♦ \ts w,i <'"- .,,1rl w,ltl(' ~ c1l1rl tl8 ,l JJ,1tfr 11t' llf, 1 t fr11 1
, I oft n ,nodlffc,d by t r l1trncnt lnlti
,1c.j ., ,,, ..,nc,,l J rlcl l),l ~ f('W µ rl t\.l t1 t'Otl , 1 r11l~slo t1!i. at1on
PathOB nesls:
Con1µI x 8 'n('ti di C'J <-' wltfl m ..1,1y ' nvlror1 rnc1 ntt-ll fJ ctor~.
Hyp rprollferJt1v ·t ..ltc r t1ltit1g /rt t f1 fck kin Jnd xc • scn l .,,
Skin pro/;feranon I ..l lJ!>t2d by cytokl,, s r ,, '"1s d by lmn,un ' c tis.
PA THOPHYSIOLOGY
....._ •NICTIC. A&rr
- -- - --- - - _- - - _ -- - - - -
.
- - · - - ---=--~- -- - - -- - -- - - · - ---
•
•
scafy, erythematous patches.. f)af)Ules, and J)laQues._

ppl; erythematous patches Aocated , the s,u"" ~ •ds
~ n t s with dew drop like 6esions 110
,.,..-- • mm sa m.cr~~ .'.},aOJ es• .,_ a ~,e sc:3,e
generalized erythema COYeriFlg nearh,
e enrue ooct, s:...·'"ace ~:ea • •► 3- ~
tt?S of se,af ,ng. .., .... - -
- . .
cJ;n,caffy apparent pustules. lndudes : Ra~, §e,e""a zed va--ie~ ca. ec .. «JO l umow&J
, •.
which is localized invotVing pa•'llS and so's..
. _ findings in patients
,,,(JlliC3 _ _ frequently. oven.ap rri more a o ... ~ ca_....
0 __ ~, _
1 0
ptrerent rypes of psorrasrs may requ re differen t tr&:~e,-1....
• Can affect an) part

of the bod} -
ey·picall} scalp.
I I
e[bo\\'. knees and

sacnun -
--L,.
• Extent of disease
.
\'afles
,,
II
-
(lnical Manifestations:
1-Plaque psoriasis:,,.. ,~ _r<.:i

·Wei-demarcated eryth~~atous plaques with overlying silvery sca!e.
Olronic plaque psoriasis is typically symmetric and bilateraJ.
fllrs may exhibit:
• · sign (bleeding after removal of scale).
0 1oebnerphenomenon (fes;ons induced by trauma).
~ psoriasis is the most common form, affecting 80-90% of patients.
'-<:.imately 80% of patients with plaque psoriasis have mild to moderate disease - oca "red
~ed lesions covering tess than 5% of the body surface area (BSA).
!shave moderate to severe disease affecting more than 5% of the BSA or affecting crucial bodv
such as th e hands, feet, face, scalp, or genitals.
• •
2-(iqHF!' DSOCYSIS: . .
c- •e . •set of ra,. orop-5 ,•zed lesions on the trunk and extremities.
JJ
,. Ofte receded b streptococcal pharyngitis.
3 Erytllfude, ,,,ic pspriaisis:

a "'lOst e entire skin surface; skin is bright red.
Associa ed · ~ chuls, and malajse .
. .~stular psoriasis, hospitalization is sometimes required.
§-Pustular psoriasis;
(:haracterized by psoriatic lesions with pustules.
Often triggered by corttcosterolct withdrawal.
W hen generalized, pustular psoriasis can be l'f 1
_h .
e t reaten,ng
-n....c.se patients should be hospitalized and a der . ·
:, , n:: mato 1ogrst consulted.
,-psoriatic arthritis:
A.r-!'... in the presence of psoriasis. ~~ ?~vJ:.e:J
n·ns
Member of the seronegative spondyloarthropathies.
~-,... percent of patients with psoriasis.
~ ~
Ca'") occur at any age, but most commonly appears between the ages of 30 and so years.
c:. ;-nnto-ns can range from mild to severe.
- .
Da~cterized by stiffness, pain, swelling and tenderness of the joints and surrounding ligaments
a,: te,dons (dactylitis, enthesitis).
uassica worse after inactivity, then better with movement.
Seue--ity of skin disease and arthritis may not correlate.
;2~ and remissions usual fy characterize the course of psoriatic arthritis.
PSORIATIC ARTHRITIS
This is the condition
which involve both
psoriasis and joint
.inflammation
•The bue arrow= a normal joint space

• Red arrow = ~cup and saucef effect of the
fourth metatarsal bone beilg jammed into the
base of the fourth toe
•The yelow circle= ·Penci appearanm·
deslrudia, characteristic of the diaease
6-Flexural psoriasis;
Erythematous plaqu es in th e axill a, groin, infra mammary region, and other skin fold
M ay lack sca le due to moistness of area.
Unde1· the breasts

Armpits
Buttocks crease Groin are&

, IJsls , an occur In all p~orla~ls subtyp ~-
.., ,ii psor c 1,,volvt,d In 50% of ,1II pnt1cnt~ with pto 1 1
,,, . 11s ar ") r as s.
t rria
r111S • in 35%.
foe l1 ails 1s co mmon IY f oL1n d ,n
' P,ltit'nt~
· w ith PsA C'Sp cl II h
disease ' J Y t os() with DIP JO1
..1Jil tate depressions of the nail plate surfJee nt lnvolvcmunt
,.. , . pun C • ·
,'lpittlriS· .. se paration of t~,c nail plt:1te f rom the nail bed
ho1vs1s. . .
iJr1Yc hyperkeratos1s: abnorma l kerati nlzation of the dista l 11 b d
ungua I na e .
)SUb ·gn· irregular area of yellow- orange discoloration visi ble th h h
• droP 51 · __ __ _ _ roug t e nail plate.
f 001 1
s-scalo psoriasis:
It is a form of psoriasis that affects the sca lp. --v~ , \:. ~-\:G"'c.½ \...fe,/DV\c:J '.,c.~ ""'~?S"'>:i.
It can be detected in 50 % of patients.
9-Palmoplantar psoriasis:
or pustular type.
May occur as either plaque type
Often very functionally disabling for the patient. th palms and soles and are indistinguish-
. . . typically occur on e
The skin lesions of reacnve arthritis
able from this form of psoriasis.
I..OC1llo'I
~--
""-t 'Id
...,~ -
==-.c11a-..-.
Sld,tlold· Smooe,. e1ry.,.,
tnllll. bla:da o,g,ua, inllrned ........
EnhbOCtf
E,..bGdy
Loclll9d puaAa,
Histopathology:
Histopathology of psoriatic lesions is diagnostic.
1-Parakeratosis of the stratum corneum.
2-Accum lation of neutrophils in the stratum corneum surrounded by parakeratotic cells ( Mt.~:
microabcess ).
3-Absent stratum granulosum.
4-Acanthosis of the epidermis with elongation of rete ridges giving a test tube acanthosis •·
very thin suprapapillary ridges.
5-ln derm is: Capillaries are dilated and increased in number and length. Papillae are raised
edematous.
6-There is a mixed mononuclear cellular dermal infiltrate.
PATHPIE.DtA,COM
nty <>f d<>ttt'd bl 00d vc~sels
Differential Diagnosis:
Seoor-rr\eic dermatitis.
Ecze~a.
p·•ryasis Rose a.
Lia en Planus.
Superficial fungal infections.
Pitryasis rubrapilaris.
Secondary stage of syphilis.
Drug eruption.
Treatment:
Stnc.e the psoriasis is localized (less than 5% body surface area), topical treatment is appropriate.
first line agents: high potency topical steroid. May be used in combination or in rotation with a
t a , i r e t ~ o an.log.
Other topical Qptions: taiarotene, tar, calcineurin inhibitors .
.,.,1"'"91H,oidfj
High efficacy and safety.
d long-term. st emic medications.
Use can be Intermittent an ith UV light or sy
d
. tfvely in patients treated w I tions gels, foams, tape, sprays, shampn..
Also used a June . t s creams, so u ' ""'·
Vehicle types are numerous (01ntmen '
oils lotions). . egular examinations as unsupervised us,
' . roids should receive r Of
Patients using topical corttcoste mended.
. is not reco m
potent topica l m edicati ons
• Iu de··
Local cutaneous side effects inc
Skin atrophy
Telangiectasia
Striae distensae
Acne
Folliculitis
Purpura
Topical Treatment:
Uses Side effects
Medication
All types of psoriasisSkin atrophy,
Topical steroids hypopigmentatlon,
striae
Use in combination or Skin irritation,
Calcipotriene (vitamin
rotation with topical photosensitivity [but
D derivative) no contraindication
steroids
with UVB
phototherapy1
• •
Tazarotene ( Topical Plaque-type psor1as1s. Skin irritation,
retinoid) Best when used with photosensitivity
topical
corticosteroids
Coal tar Plaque-type psoriasis. Skin irritation, odor,
staining of clothes
Caldneurln inhibitors Off-label use for facial Skin burning and
and intertriginous itching
• •
psor1as1s.
Systemic Treatment:
In moderate to severe disease, systemic treatment can be considered and should be supple·
mented with topical treatment.
Oral steroids should never be used in psoriasis as they can severely fl are psoriasis upon discOfl·
tinuation.
1. Phototherapy: narrow-band ultraviolet B light (nbUVB}, broad-band ultraviolet B light (BB·
UVB), or psoralen plus ultraviolet A light (PUVA)
2. Traditional/new oral medications:
Methot,exate 7.5 to 25 ':'g/ week, acitretin, cydosporin 2.S to 5 mg/ kg/ day , .i,athioP'1pe-50
to 100 mg/ day, apra muast.
3. Biologic Agents: TNf•a inhibitors (etanercep.t, a.dalumimab, b1ocke'
iQfllximab ), IL 12/23
(ustekinumab), IL-17 blocker (secuklnumab)
111< 'l)olLP o f ~v. . t ~mlc- t t1t'1 Jpy d P~nds on ,11ultiplp factors:
t ,,nvt'tlh"'ncc
',IUC'
J pffl' f t rl ... ~ pro ft Ir
"'"l t" or nb\ net\ of psorlutic arthritis
p,~!)l"
com<)r l)idlt1P'l
. trrnic t ft=, trl1t'nt for psorl~sls should be given ft
O I
'.)y-.
ehototheragy. • n V a er consultation with a dermatologist
s:ifr, rffectiv<', <1nd cost-offective.
Up to io 25 t re.1tments given 2 to 3 times per week
15
n1r•nt . usua 11 Y req uired for significant improve-
Broadbtlnd UVB photothernpy .
Nb UVB tr('a trncnts n1ay occur In some dermatology offices or at h
PUVA topical or systemic . ome.
Other forms of UV exposure, Including sun exposure, may be beneficial in select patients.
"Spcctalty" dcu1s for psoriasis;
•
Mathotr xatc - Cyclo porlne - Acitretin:
Requires careful considerations of patient medical history, severity/ type of psoria sis, and previ-
ous treatment.
Requires close monitoring of blood work and side effects by an experienced prescriber .
Qlolo&iCSi
Used to treat psoriasis and psoriatic arthritis.
lnfllximab, etanercept, adalumimab, ustekinumab, secukinumab.
Requires careful considerations of patient medical history, severity/type of psoriasis, and previ-
ous treatment.
Requires close monitoring for infection and other side effects.
Factors that influence type of treatment;

Age
Type of psoriasis
Distribution
Extent of psoriasis
Previous treatment
Other medical conditions
Cgmor1>ldlt1es; · ·
I I
atients with moderate-severe psor1as1s.
Caraievaieufar risk factors are more preva ent n P . d' and should be en-
Patients with psoriasis may have an Increase d risk for. card1ovascu 1ar rsease
fi bl diovascular risk factors.
couraged to address their modi a e car h ce and severity of pso-
There Is a positive correlation between 1ncrease d BMI and bot preva Ien
rlasls. • dastr1.1Ction.
. art h rt'tis' which can lead to jotftl
Up to 30% of psoriasis patients have psoriatic
Drug thag W9EMn PIQtlasls;

5¥1ttm1c corttcosterold treatment or with drawal
C\t' t,1 l>lock<.'t l.i
Lft/1/11111
A11ti n1 ., I.,l r l,1I~
l11t(1 ff('IOll S
NSAIDS
Jake Ham.e Points;

Psori ..isis Is ,1 cl,ro,,lr disease wltl1 predominantly skin and joint manifestat1o
111 Lrltisystc m
. About 1/3 of p,JtiC' r1ts w ltl1 psorla !>ls hnve a 1st degree relative with psoriasis. ns.
Dlffcre, 1t typC's of pso riasis ar~ based o n morphology: plaque, guttate, inverse P
, ustula
erytt1rodrrmlc. r, a~d
Plaqu e p~orlasls is tl1 e most com mor1, affecting 80-90% of patients.
Hec.1 ltl1 ca re providers are er1couraged to actively seek signs and symptoms of psoriat1
· ·
at eac,I v,s,t. c arthr·'h•
Topical treatment alone is used when psoriasis Is loca lized

Psoriasis with moderate to severe disease often requires systemic treatment in addition tot .
0
treatment. P1ca1
' 7. "·
Systemic treatment includes phototherapy, oral n]_edlcation~ and biol~gJcal therapy.
Oral steroids should never be used in psoriasis

A successful treatment plan should include patient education as well as provider awareness
. , . Of
t he patients experience.
Psoriasis is a lifelong disease and can affect all aspects of a patient's quality of life.
. hen planus is a cell- mediated .
uc1 . irnrnun
d seases of altered immunity su h e response f
. • . . ' c as ala . 0 Unkn
ith hepatitis C virus infection Pec,a areat . ..0 Wn origin. It m b
w . a, lfJtihgo_ Ith b ay e found With oth
as een found to &..- • er
Epidemiology ~ asSOc,ated
frequency
lnternational:No significant geog h·

rap icat v · .
Mortality/Morbidity anation in frequency .
cutaneous lichen
. planus does not . exists for lichen planus ·
h. h . . carry a risk O f k· ... ...
do have a 1g er incidence of mar s 1n cancer b t - . '"'-•_' •- • •~
ignant transformation. , u u1cerative lesions in the mouth,
Race
No racial predispositions have been t d .
Sex no e for lichen planus ·
No signifi cant differences in incidenc f .
e or 1tchen planus
patients.
Age are noted between male and female
More than two thirds of lichen planus patie t

occur at any age. n s are aged 30·60 years; however, lichen planus can
Clinical Presentation (c;y_
Lesions usually develop on flexural surfaces of the limbs, such as the wrists .After a week or more,
a generalized eruption develops with maximal spreading within 2-16 weeks.
Pruritusofisinvolvement.
extent common in lichen plan us but varies in severity depending on the type of lesion and the
Lichen planus (LP) can involve the mucous membranes, the genitalia, the nails, and the scalp.
The papules are violaceous, shiny, and polygonal; varying in size from 1 mm to greater than 1 cm
in diameter with central umbilication.
They can be discrete or arranged in groups of lines or circles.
Characteristic fine, white lines, called Wickham striae, are often found on the papules.
. n and may be found in patients who do not have skin

Mucous membrane involvement is comma f d the tongue and the buccal mucosa; they
Involvement. Lesions are most commonly f oun_ on linear or reticular pattern on a violaceous
are characterized by white or gray st reaks orm,ng a
background. .k t ophic papular, erosive, and bullous. Oral

Oral lesions are classified as reticular, plaq~e II e, ati~on o; they may even be painful if erosions
lesions may be asymptomatic . or have a burning sensa ,
are present.
hiaher incidence of . nant transformation in meo-

maJag
le1iw may have a "
. a also be fo und on t he conjunctivae, t ~e lary_nx, th e esophagus, the tonsils, the blad
Lesions m Yd h gi na· t hrougho ut th e gastro1ntest1n al t ract; and around the anus. der,
the vu lva, an t e va ' .
. • em ent is commo n in lichen planus. Typica lly, m en develop annular lesions
Gen1ta 1 1nvo 1v . --- ........, on th
. kham striae m ay also be observed o n these 1es1o ns. e
glans. W 1c
vulvar invo lvemen t can ra nge from reticulat e papules to severe erosions.
Nail fin dings are most com mon ly lo ngitudinal gro oving and ridging. Hyperpigmentation, subu
· an d Iong1tu
hyperkerat osis, onycholys1s, · d ·1na I me Ianonych·1a. ngua1
c uta neous lesions m ay be accompanied by follicular and perifollicular lesions on the scalp wh·
' . papu Ies. Th ese Ies1ons
m ay be violaceous, sea Iy, an d prur1t1c · ' ..Ith
can progress to atrophic cicat
r1c1a1
alopecia, kn own as LICHEN PLANOPILARIS.
Variations in lichen planus include the following:

Hy pertrophic lichen planus
Atroph ic lichen planus
Erosive/ulcerative lichen planus
Follicular lichen planus
Annular lichen planus
Linear lichen planus
Vesicular and bullous lichen planus
\. ~ctinic lichen planus
~.k.~
Histologic Findings: 0
,€',
~
1>30-l'-._)
~
~~ ~
The epidermis ~ hyperkeratotic with irregular acanthosis and focal thickening in thegr_anula!:Jayer.
Degenerative keratinocytes, known as colloid or Civatte bodies, are found in the lower epidermis.
The upper dermis has a band like infiltrate of lymphocytic and histiocytic cells with many
Langerhans cells . The infiltrate is very close to the epidermis and often disrupts the dermal-
epidermal junction
Laboratory Studies
Direct immunofluorescence study in lichen planus (LP) reveals globular deposits of immunoglobulin
M (lgM ) and complement mixed with apoptotic keratinocytes.
Medical Care
Lichen planus (LP) is a self-limited _Eise_a~ that usually resolve s within 8-12 months. Mild cases
can be treated with fluorinated topical steroids. More severe cases, especially those with scalp,
nail, and mucous membrane involvement, may need more Intensive therapy.
The first-line treatments of cutaneous lichen planus are topical steroids. A second choice would
be systemic steroids for symptom control and possibly more rapid resolution . Many practitioners
prefer intramuscular\..=- = , o-so m~ every 6-8 weeks.
Other modelities
oral metronidazole
Oral acitretin
mycophenolate mofetil at 1-1.5 g twice
t Up to :>
/d Y fo 6 \f\ .
Fo, lach
u Of 1h c 1 1 r: llt <J' , op1 a1 st r d
Top,c.at nd ~Y ter ic c. ye 'osc<> n n1 ( 11 ( i Lr l d .
Other opbon$ ,net udt 01 , or t, , ,... 1, 11 t ·d
" ,... _ , re r <✓ ~•
E n w ith th s <>ff< <. tivt tr

Patient w,t h wtdE:>~f>t< ad ,c
Complications
Orat ulc rations a soc1at d 1111th lt(hen plarus {LP t'a •et e poterra ~o bec-o~ - .g,..",...,
nf ecn.on, o~teoporo)t S, adrenat ,nsufflc•e c ~ bo ~arro Sl,P9'e5S s... rcr -..n--.ag .,
- -~ r-°'
yperl1pidem1a, and growth retardatio n in ch 1'dren a occ1...r c __..e torr.er.:: GC::-,-:>"
tlapacta 1s often perm anent.
Hypertrophtc lesions may leave res,dual hyperp!gmer.taticn
Vulvar lesions can be pruritlc and painful
Prognosis
The prognosis for lichen planu s is good, as most cases regress vit
recur.
Uchen Planus Differential Diagnoses

firaft Versus Host Disease
Psprifsis. Gutt.ate
PIOl;ia,;s. Plague
5zphJlis
Dou Corpor,s
p·
•tvrias·
is rubra .
and Pit . P•laris
. riasis Rubra Pilaris (PRP) Vr1asis r
p,n' osea
e disease .
, Rar
ffects both sexes and occurs in
• p.. . I all race
f unknown etio ogy and Path s.
•0 . . ogenes·
, onset: ins1d1ous or rapid is.
ciassification
, rype 1: Classic Adult
• Generalized, begins on head
and ne k
• rype 2: Atypical Adult c ·
• Generalized with sparse hair
• rype 3: Classic Juvenile
• Generalized & appears within th .
e first 2
• Type 4: Circumscribed Juvenile Years of life .
• Localized, occurs in prepubertal h"I
. c I dren .
• Type 5: Atypical Juvenile
• Generalized, familial, onset in first f
. ew Years of lit
• Type 6: HIV -Associated e
• Generalized, associated with acn~ co I b .
O
ng ata, h1dradenitis s • .
•
Clin1ca I M "f t n·
an, es a on uppurativa, and hchen spinulosus
Skin Lesions (All types of PRP}

• Follicular hyperkeratotic papules
• Reddish-orange in color
• Begin on the head and neck
• Usually spreading in a cephalocaudal direction.
• Confluence to a reddish-orange psoriasiform, scaling dermatitis
..-. Sharply demarcated islands of unaffected normal skin.
• In darker skin tones, papules are brown
Distribution:
• Types 1, 2, 3, 5, and 6 are Generalized.
• Type 4 is localized.
' " ,,, '' '•l'' ••• ti ( ,llt(l,,I\V,
I , 1,,i,\ll 1111 1 l1 ~• '
• ( ,.,.,,,\ ,111-v '',•'t-tll ''. ,, :,,\'l II,,,"~I tt'M' t,l rvtl,r d r
• t , ,~, t,11 ..,,.t " J. ~,,, •
•IP & Hair I
l, , )l ~ ,111111h1tli)\\ ()I lit<'
• )\ ~l,l'',t,,•, Il "' \ I
• c,,,,
1,, tv,~(' ~ • I) '', l ' •,t'l llt >
1 • •
1,,, '
Mucou• Men1br•n••
• ,,.,, <i
P•lm• a Sol•• clltf ''"''' wt,xv y('l\llWI Ii/or ltlR<' hyp<,rkl r..1tu\ls
• ,,, t yp,, , : r\,11,, . I,t,w'- ' ...!
N11II
• 01 t,,1 y<'IIOW l1ruWI) <11 0 10 1 t1 0 1i, 11, II pl(,t ' thick nlns, c;ubunBLlc I hyp
1, rr, r, 1,,,.\0 .
Associated Conditions
• Typl' ,.
• tct,1 ~,yo iforrn I slons ori I gs
• Typ 5 ( \ \~,')\1.,..:0.\. ~ ,N:)
• Sclcroderma-llk appearance of hands and feet
• Type 6 \.\.. \ ,101
• Acne conglobata
• hidradenitis suppurativa
• lichen splnulosus
Differential Diagnosis
• Psoriasis
• Follicular ichthyosis
• Erythrokeratodermia variabills
• lchthyosiform erythrodermas
Histopathology; Not diagnostic but suggestive

I
• Hyperkeratosis: Alternating ortho and hyperkeratosis and Localized parakeratosis
• Prominent granular layer \.:i -"'>◊':O'f,c..✓.>\ ~ qn'.,
. . . y•I>"
• Acanthos1s with broad and short rete ridges( \c• ,.,,.a') ,\ 1, •.\ , , }~Y;.;t'J~ ( •.n...J .\.c,Q \"'--'> l,~~
• Perifollicular areas of parakeratosis .
.. • Keratinous plugs of follicular infundibula
• Superficial lymphocytic perlvascular Infiltrate
course And Pco1nosis

• A socially and psychologically disabling condition.
• Long duration:
-••Type 3 often resolves after 2 years;
-••Type 4 may clear.
-•• Type 5 has a very chronic course.
-••Type 6 may respond to highly active antiretroviral therapy (HAART).
,raceroeot
a1
• ToP'
cal therapies (Not very ..H tllvr J
• Emollients
• Keratolyt1c agents
• catcipotr,ol
• Gfucocomcoids
• raz.arotene
• pt,ototherapy (Effective in some cases )
. uvA
• NB-UVB
• Photochemotherapy
• Systemic treatment (Most effective)
• MTX
• Retinoids
• Anti-TNf agents: infliximab & etanercept
Pityriasis Rosea
• l\gP.:10 to 43 years.
_,...,Rare in infants and old persons.
-..►Season : Spring and fall.
ts associated with reactivation of HHY:,7 or HHV~ two closely related '3-herpes viruses.
Clinical Manifestation
Sirin lesions
l· Hera d Patch;
--+O«urs in 80% of patients, preceding exanthem.
~ be multiple. __,.'" -
-+Oval, slightly raised plaque or patch 2 to 5 em,
- salmon-red, fine collarette scale at periphery;
l-banthem.
"Appear 1-2 weeks after herald patch.
•ftnesc.aliqg papules and patches with marginal collarette
• Oat Pmk or tawny.
~.....
Kaltered, with characteristic distribution following the lines of cleavage in a #Christmas
on the face.
.,_ ...
•
-
• "'e e
•
•-
•
•
...
• ..........,....
"""' , -+ aan OSJS
• ~s's and microvesicles

•
• .__. :.>..;~:: occ rs · in 6 to 12 weeks or less.

• Rea ■ iier«es are ,.a.,,u,,,.,-non ~ ha been reported ..
reass ra ce
•ap1.:oma
•Oral a or ~ic.al antipruritic lotions to relieve pruritus.
• ~ro.1-:uste1oids. ,
• ~ be · by tNB phototherapy or natural sunlight exposure if treatment is bet"
the&stweetof .
• A shuit c0t■1e of systemic c.ortkosteroids may be needed.
Epldemlologv
Acne vu lgarls affect~approximately 40-50 million individual'; ea,h yr:ar ,n th': u-:; ;; i:,r,.t;, n 4; pE'.; ...
c,dence occurs during adolescence, aff<.:ctine approYlmawly 85% of 1ouni p':opr': be•,,~r. 12
111
and 24 years of age, making lt a physiologic oc,urr nee in thi~ eroup, 12% of 1,amer. ar11¾ of
men will continue to have clinical acne until the fffth decade,'''
Pathogenesis
The pathophysiology of acne involves a complex interaction of multiple factors.
The role of genetic predisposition in the development of acne is uncertain, but ,s decided fr""' " 10 .
factorial. It is known that the number and size of sebaceous glands and their subsequent actv11t7
1sinherited. It is also widely held that acne, including nodulocystfc acne, runs ,n families.
One of the first steps in the production of acne is the formation of the m,crocomedo. This beg,ns
'" the keratinized lining of the upper portion of the follicle, the infund,bulum. Comedo formation
OCcurs when the corneocytes wh ich are normally shed into the lumen of the follicle and extrud-
tdthrough the follicular ostfu~, are retained and accumulate, leading to hyperkerat~•s. {Fig. lA)
lnc.r~a~ed cellular cohesion and prolifera tion occurs in the proximal portion of the infunclibulum,
the •nfrainfundibulum, and it creates mlcrocomedo. (Fig. 18 )
~ hi'\ . L-d atfno whorled 1a,,wna,

r& __ •~ans,on of the comedo the contents become closely pacru: , ere . 0
_,vttlon ' dO II w,th extrusion of the ,mmunc,.

llnic s. As the forces increase rupture of the come wa
ktrat1n and sebum occurs with resultant inflammation. (Fis. lC,D)
Ii
•
• I
• •
.
(NON,
Nrzw•rr ,,,,,, r tt
. ,·~ ~ . ,_
u-(1)
tr,ftarllrn •ti 11 l, not or1ly th r r ul t of comedo rupture seen early In acne lesio f
, n orrnatt
ntpf , ~ 11 nl,mbrr ,1nd IL 1 activity have been shown to Increase prior to h on. For
~ .,. • ... nt pr or, , r J . ( ] ) Th type of Inflammatory response determines the ci·
,, r1 ,n YPerkeraH
, l,n,.
f n1cal le510.
ri I ,, \.ltr phLI pr cctomlnate (typica l of ~arly lesions), a suppurative pustule Is formed n
t Pr«J n1ir,~1t ly 1 h Ip r lymphocyt\'S, foreign body type giant cells, and neutrophilS-re· 1nn~~
fl
tn n, d p pul t nodule nnd cysts, The type of Inflammatory response also plays a role In su 1ts rn
d v I pn1 nt of c,1rring. Early, nonspecific Inflammation results In less scarring than does a~:~
I y d , ,. p""'"'lfi inflnn1matory re pon e,(3)
ft-opionib ct rlum ncnes contributes significantly to the production of acne. These Gram-positive
non m ttl rod.. rt' foltnd deep with in the sebaceous folli cle, along with P. granulosum and'
ra fy. P. P rvum. The pathogeniclty of these microorganisms st ems from several of their proper-'
ti • including t he production of lip9~~s, enzymes contributing to comedo rupture, and several
pro,nfl mmatory mediat ors. (4)
The kin' own innate immune system also Interacts with P. acnes to induce inflammation, One
m h nism ts via toll•like receptors, a class of receptors that mediates the recognition of micro-
bi I p t hogen by immune cells such as monocytes, macrophages and PMNs.
Toll- fik r cept or 2 (TLR2) is found on the surface of monocytes surrounding acne follicles, P.
c~ ha bPPn shown to release pro-Inflammatory mediators (IL-la, IL-8 and TNF-a) through this
TLR2 p thway The increa e in IL-8, In particular, results in neutrophif recruitment, the releaseof
tysosomal nzymc:..>, and subs quent disruption of the follicular eplthelium.(5)
Hormonal eff cts on sebum secretion are key to the production of acne/ An_dro_gens are produced
both outsid th sebaceou unit, primarily from the gonads and adrenal glands, and focally within
the atand via the ction of androgen-metabofizlng enzymes such as 3b-hydroxysteroid dehydro·
pnase (HSO), l 7b-HSD nd Sa•reductase, Androgen receptors, found in the cells of the basal
layer of the ebaceous gland and the outer root sheath of the halr follicle, are responsive totes-
tost,rone and dthydrotestost ron , the most potent androgens/ Dlhydrotestosterone (DHT) has
1 5· 10 fold 1reater • ffinity for the androgen receptor than has testosterone.(6)
. ·cal features
c,,,,, .
. t1arnmatory acne 1s character ized by both op
Non-in . h d . en and clo">ed
dones, or wh rt e ea s, are t ypically small -approx,mat I 1 co1nC1do torn,Mti o1 I
come nt foll icular openi ng. ( Fig. 2A} e V mm ~k,n colored l:J.i pul<': '"it1l)~Pcl
appare fii~~ ~ ~ iiiiiili-~--.7,---~~-----~-- vv , t,o
Figure (2A)
Open comedones, or blackheads, are dome-

shaped papules with a conspicuous dilated fol -
• •
• • •
licular outlet/This open ing is filled with an inspis-
sated co~ of shed
? :a =keratin/
a •
Melanin©deRosition
- - .,..,..,,,.-
• .. •
•
••
and Ii iaoxidation within the debris may be re -
sponsible for the black coloration / lce-pick-t'f.Pe •
•
scarring may result from comedones alone.(Fig. •
2B)The inflammatory lesions of acne originate

with comedo formation but then expand to form •
•
papules, pustu les, nodules and cysts of varying
Figure (28)
severity/ Erythematous papules range from 1 to 5 mm in diamet e'1 PL1stules tend to be approxi -
mately equal in size and are filled with sterile,
wh·
ite pus/ As the severity of lesions progresses,
nodules form and become markedly inflamed, in -
durated
ar&d fil an~ tender/ The cysts of acne are deeper
0
... led with a combination of pus and serosan-
~ neous fl u1'd/ In patients with severe
1
llOduloeysti
alesce c acne, these lesions frequently co-
Plaq,..... to form massively inflamed complex
..-.c:s that can ·include sinus tracts.(Fig. 2C,D,E)
figure (2C)
t lgurP. (70) Figure (2E)
F t of. cne
t ,:ir ly trP, t m()nt of acnP le; e ,sPntiJI for the prevention of lasting cosmetic disfigurern
• tPd wi t 11 ~c.1rri r1g.f Post -Inflammatory h,yperpigmentatlon as well as persistent erythent a~~o':
cornpllc ,1lP'~ ffl'iolv(ld ln flilrnm atory acne/ Although the pigmentary changes usually reerna Oft~,
rn,1 11y montll'i if tl1c acne Is brought und er control, occasionally they can be permanen;;~e o-,'"r
nod1~l, r l1yp<1r t rophlc scars arc the often unfortunate sequelae of both nodular and itte1,,r
;ind on the uppPr trunk, soft, hypopigmented, anetoderma -like lesions. (Fig, 3A,B) cystic acr.~
Figure (3A) Figure (3B)
Acne variants
• Acne fulminans
Acne fulminan s is the most severe form of cystic acne and
is characterized by the abrupt onset of n~dular and suppu-
rative acne in association with variable systemic manifesta-
tions. (Fig. 4)
-
Osteolytic bone lesions may accompany the cutaneous find- -
ings. Systemic manifestations includel_!ev~r arthr_algias, mtal-
glas, hepatospl~nomegaly and severe Q.Wstration]
Treatment of this variant depends on clinical severity and
includes top!_cal, intrae~onal or oral cgrticosteroids, oral
isat~noin and oral 4..!ltibiotics/ DapsOfne in conjunction
with isotumnoin was reportedly beneficial in the treatment
of acne fulminans associatewd with erythema nodosum .
Figure (4)
~ conglobata
• re eruptve nodulocystic acne without systPmic
~rest.anons is termed acne conglobata/ These re cal -
~ leSJOnS are part of the foJftcula r occlusion tetrad
ra w•th dissectlng cellulrtis of the scal p, hidradeniti~
~ n·= and pilonidal cysts. (Fig. 5)
si,P9~ra yr;, ,
• AC"e mechanica Figure (S)

mechan1a occurs secondary to repeated me-
""'=ica) and frictional obstruction of the piloseba-
~s outlet. Com~do formatio~ is the result. Well-
cif5Cnbed mechanical factors include rubbing by
1ne -r,ets, chin straps, suspenders, collars and sca rfs.
:ig 6)
Figure (6)
• Acne excoriee des jeunes filles
~ excoriee des jeunes filles, as the name implies, occurs primarily in young womerY. Typi-
~ rornedones and inflammatory papules are systematically and neurotically excoriated, leaving
:-as:ed erosions that may scar.
unear erosions suggest self-mutilation, and an underlying psychiatric component should be sus-
~ - Patients with an anxiety disorder, obsessive-compulsive disorder or personality disorder
a:-e particularly at risk. Antidepressants or psychotherapy may be indicated in such patients.
• Drug-induced acne
"--""le lesions or eruptive acneiform lesions can be
se,'"' as a side effect of a number of medications,
txiaa,ng anabolic steroids (e.g. danazol, testos-
~one,, corticosteroids, corticotropin, phenytoin,
""°"\tum, 1soniazid, iodides, bromides, azathioprine,
~'V~,:-m onomorpnous eruption of irill_ammator_y
~,f...._ - .... 11-....,. I ,(J\ 1vy.r>
-,,u_~_and pustules is often observea in drug-in-
1
auted oene, some clinicians use the term "follicu-

..-.(Fig. 7)
Figure (7)
~ s dexamethasone and high-dose oral corticosteroids commonly induce characteriSttc

,c-ifor
""" meruptions with a concentration of lesions on_,1be. . .~h~ t a_n.d b~k.
e to . k I ce is responsible for occupa-

.
.... •nsotuble, follicle-occluding substances tn the wor Pa hi . ted ~romat-
len@,Qff b s products c or,na =--- ,.
, ' ending agents include cutting oils, petroleum- ase . ' . ith varvinl
' of
"-·
n -
s, and coal tar derlvatives/ k9ffied_
d · te the clinical picture, w
on~s omina
Papules, pustules and cystic lesions d1str1buted in expose
d as well as typically covered
Acne Vulgaris ·
• Chloracne
d fi e occupational acne caused by exposure to chlorin
Chloracne, the term used to e n k f exposure{. The following age ts f ateo arOh...
. h d b d I after several wee s o n ound . . -~
tc Y rocar ons eve ops . . . fun icides herbicides and wood prese . ,n eta... .
cal con ductors and insulators insecticides, g -'--- f'Vatives ~
-
• Neonatal acne
Neonatal acne occurs in more than 20% of heal y th
newborns. Lesions appear at about 2 weeks of a_ge
and generally resolve within the first 3 months of
life. Typically, small inflamed papules arise on the
cheeks and across the nasal bridge. (Fig. 8) The
pathogenesis of neonatal acne is currently a mat-
ter of debate. Several species of Malassezia (e.g.
sympodiatis, furfur) have been proposed as the eti-
Figure (8)
ology by some investigators.
Topical 2% ketoconazole and benzoyl peroxide have been shown to be effective therapies.
~:-. ~ \_ ~
• Infantile acne
If acne presents at 3-6 months of age, clinically,
come do formation is much more prominent than
in the neonatal form and may lead to pitted scar-
ring. Deep systic lesions and suppurative nodules
are occasionally seen. (Fig. 9) The pathogenesis of
infantile acne reflects the hormonal imblanaces in-
trinsic to this stage of development, and maternal
hormones play only a minor role.
Figure (9)
Infantile acne typically resolves within 1-2 years and remains quiescent In unusual cases. l'Ot-
ever, the acne may persist well into and throughout adolescence. Topical tretioow or ~ -,
~ is usually prescribed for comedonal infantile acne to obviate the risk of permanent sea~
Treatment
• Topical treatments
• • I (aU-trans-retinolc acid) was the first topical comedolytic agent used for the tre~
' I
the
of acne . Its mechanism of action involves normalizing follicular keratinization; it aids in - :
sion o~ existing com~~ones and prevents the formation of new ones/ Tretinoin has t,een; : : .
have s1gn1ncant anti-inflammatory properties may be used as monotherapy for both c
and mild to _m oderate inflammat~ry acne vulgaris. . (Jttllil'
The synthetlc ret1no1d adapalene 1s an aromatic naphthoic acid derivative with a unique
structure, the irritancy profile is also less.
Tazarotene is a synthetic acetylenic retinoid that, like adapalene, is receptor-specific.
. . lftde· ft iSf
Is a potent bacter1ocidal agent that reduces P. acnes within the fo . ; ; ,
ticutarty effective when used in combination with other therapies. In contrast to toJ>iC"
ics, microbial resistance to benzoyle peroxide has not been reported.
. · i · are w idely used f
th
1 . anon with benzoyle pero .dor e treatrn .
f11 blf1 I .. x1 e or t ent of -
cov,,v "·,1"1ost common Y utilized antibioti retinoin c1· acne and are
cs and f · lndarn .
.
available 1
t iedgets. orrnul . vein and a one as well .
a(lJ p attons vary f erythromycin r as in
. .d rom ere epresent th
~ ~1 c 1s a w1 ely used com d
e olvtic and ·1
ams and gels t . e
o solutions
rr11 d anti-· fl
, c· is a naturally occurrin d' in ammatory ag
.~ · hh b g 1carbo . ent.
cream, wh1c as een shown t b xyl1c acid f .
ca I h f P o e eff . ound in
the growt o . acnes, azelaic . ecttve in infl cereal grains It .
ing1·1y and its use is reported to havacf1d reduce s infla ammatory and com~do1s avl ailable as a topi-
d0 . e ew mmato na acne By · h'b•
aY help to lighten postinflammat er Iocal side ff ry acne. Azelaic acid . . . ,n , ,t-
r,, ory hyperpig e ects than topical . . is applied twice
mentation• retino1ds. In additio .
• oral treatment n, ,t
Antibiotics
oral erythrornycin and tetracyclin e, or .its d •
. f orh mo d. erate to severe .in fl ammat
rescribed er1vatives doxyeye1.ine and min 1·
P
this setting, t e primary mechanism f
. action
ory acne unrespo .
f h nsive to
ocyc ine, are usually
topical b'
0
acnes, there bY re d ucing bacterial Pro duction . of0 inflam
t ese agents is suppression
. ofcom mations.
the growth of In
P
matory mediators. ·
Hormonal
-Hormonal therapy is an established second-ltne
. treatm
Hormonal therapies seem to work best. d ent for female patients with acne.
. 1na ultwome · h .
nodules that commonly involve the lowe r f ace and neck.
n wit persistent inflammatory papules and
Oral
gens.contraceptives initiated, because they bl ockb oth ovarian
. and adrenal production of andro-
The progestational antiandrogen cyproterone acetate is currently used in Europe and d c

The standard formulation combines cyproterone acetate (2 mg) with ethinyl estradiol (3~na a.
SOµg) in an oral contraceptive formulation. µg or
Spironolactone functions as both an androgen receptor blocker and an inhibitor of Sa-reductase.

In doses of 50-100 mg twice daily, it has been shown to reduce sebum production and improve
acne . Side effects are dose-related and include potential hyperkalemia, irregular menstrual peri-
ods, breast tenderness, headache and fatigue.(7)
.
lsotretinoin . . . . h been available in Europe for the treatment of
Since 1971, isotretinoin (13-c1s-ret:1noic acid) as . ts w·ith severe nodulocystic acne retrac-
ed it for pat1en '
acne. Twelve years later, the FDA approv .
·b. ucs over 0.me, other clinical forms .of acne
..
have also
-
tory to treatment' including oral antth 10 e of· 1sotret1n°
. • ·n
1 • These include any significant
• I
acne un
motional
been shown to benefit greatly from t e u~ . . ) that results in significant phys1ca or e
. I ant1b1ot1cs
responsive to therapy (including ora
scarring.
The oral retino,d acts upon the sebaceous gland, prohibiting maturation of the basal cell
1
results in sebaceous gland atrophy and reduced sebum production by up to 90%. As a res. his
acnes, which are dependent on the glycerol resulting from the hydrolysis of sebum triglyc:~lt, P.
are unable to thrive. Normalization of follicular keratinization also occurs, and this initial st lde_i,
acnegenesis is significantly inhibited. ep '"
Dosing of isotretinoin varies, but typically 0.5-2.0 mg/ kg/day for 16-20 weeks is recomme d
Although lower-dose regiments (0.1 mg/kg/ day) over the same period may be equally effe~ed.
repeat treatment is necessary in approximately 40% of patients. However, lower daily dosesgi ve,
over a longer period of time, with a total cumulative dose of 120-150 mg/kg, have been show ver,
reduce the risk of relapse .(8) This cumulative dosage can be reached over a period of 4-5 mo n~o
with 1 mg/ kg/d ay. nt s
The side effects of isotretinoin are numerous, the most common adverse effects involve the ski
and mucous membranes and are dose-dependent. These include cheilitis, dryness of the oral a ~
nasal mucosa, generalized xerosis, and skin fragility. Alopecia and eczematous dermatitis ace~
less frequently. Xerophthalmia is common. r
Myatgias are the most common neuromuscular complaint seen with isotretinoin use. Other re-
ported neuromuscular complaints include headache, fatigue and lethargy. Benign intracranial
hypertension, or pseudotumour cerebri, may present with nausea, vomiting and blurred vision.
Concomitant use of tetracyclines increases the risk of developing this complication.
Teratogenicity is a serious potential complication when isotretinoin is used in women of child-
bearing age.
Laboratory studies should be performed for all patients using isotretinoin. Elevated serum tri-
glyceride levels occur fairly frequently (25-45%) of patients, along with an increase in total cho-
lesterol levels (31%), these changes are typically mild and do not require an al·~eration in dosage.
Increased levels of transaminases are also possible.(9)
• Surgical treatment
Comedo extraction can improve the cosmetic appearance and aid in therapeutic responsiveness
- -- - -
to prescribed comedolytic agents.
,,--.I',
For deep and inflamed cystic lesioni)lntralesional in_Lecti_on of corticos!_eroi~ can quickly improve
~oth the appearance and the tenderness of these lesions. Larger nodulocystic lesions may re-
quire incision and drainage prior to steroid injection.
Low-concentration_fhe,rucal _peels are also beneficial for the reduction of comedones. The a·
hydro~ a~ids (including glycolic acid), salicylic acid and trichloroacetic acid are the most common
peeling agents.
d . h . , k' type) and th

. ti n glycolic acid p~els (20-70%, depen 1ng on t e panent s s 1n . 1
H1gher-c~ncentra ho I el-may also be performed in the office setting. Risks of chemical pee
less predictable P eno pe.
include irritation and scarring.
e
• e a a~er
e s a e n
•
C: r s~ e e
J. ~,- va e ce of facial ac- ,e in adu s. J m cad Der-

-- • a
e nts are i d in acne
.
~~~1 ~ -
es
a n • acne scar,·ng: a comparison
ro e and ...._ rone to scare. Br J Der a ,
;l :72-81.
, cG- KJ, - LS O , g a . r · ~ibacte · m e els in ents
acne ga ·s.. J I \'\IP''1" De..._atol. 1975; 65: 382 ..
-3 . G a· , - RSI et a .
I
a n beta efens. g-1 an -2 ex ress n"' 1
-- - aceo~
c i a~ e ga ·s es· ns. J Invest ~
1. · : : 7: _1.20-5.
.. .- ......--g F . s &-~ --ta~ is o& tcStoste'"O o 5 a p a-di
€ eo -tr a..,.aroge a_ ·o,.., · '"' e s ·n? Br J De-a: . 19 2~ . .. 3 :
7-53 ..
7~ Gooafcl ,
-sa
· Areata
Alopecta , immune mediated, neural non scarring
0 fi,ilti.on AA ss a complex genetlc, '
• Alopec1a areat a ( ) . hair follicles.
t - acti"'ely growing
t~rgt? ~ . ff t
crv . overall AA likely a ects ma es and fernatllk
Ep1def'T'10 o&, dwide d isease. ' o ... ~ ~
• AA, a' comn1on worl s about 20% of cases, and as man~ as 60¼ of patients . ~-,.,
• Pediatric AA constitute b f re lO years of age. The disease prevalence noaL A.A
. first patch e o . ~ ars ~
present \v1th their decades of life. It is however rarely reported 1n infants and -
the second and fourth ~~-t
Etiology . _ not exactly known. However factors such as genetic pred~
15
• The etiology of AA • fe ti us agents had been suggested. .._~,. ~
immuruty, stress and in c o
The genetic theory

The genetic theory is supported by
A}familial clustering . . . .
• It h a dbeen rep Orte
d that a positive fa mily history 1s present 1n an average of 20% o~ Pa"-~
• Concordance with twins.
• A ten fold increase of affected fi rst degree relatives .
B} HLA association .
_ HLA has been linked w ith certain human leukocyte antigen (Ht.A) classes. e.g. HLA-Bu_
The immunological theory

( jrcumstantial evidence in support of an autoimmune mechanism underlying AA comes .·..,,...
several sources.
1- The associations between AA and classic auto immune disorders such as auto
thyrokfjtis and vitiligo.
2- Loss of hair during disease activity is coincidental with an infiltrate of activated CD4al5
aro und the hair follicles, along with a CD8 + intra foll icular infiltrate.
3- Hair regrowth with the use of immunosuppressive agents is possible.
4- The infilt ration of antigen presenting cells such as macrophages and Lange,hanS~
around and within t he dystrophic hair follicles has also been observed. This is potentialf~
sistent wit h a response to auto antigens within the hair follicles. . (iii
5- It ~as been demon_strated by immunohistochemistry that there is abn~r~I ~....
ant:Jsen on hair follicle keratinocytes. Fas antigen is a membrane protein anvotved-ess ,;
6- •otecte,,kin 1 beta and other potent inhibitors of hair follicles are aberrantly exi
fected ar__eas of_!h~ sca lp in M. of~--
7- The presence of hair follicle specific lgG auto antibodie~ in the peripheral ~lood ,
ther reinforces the hypothesis that the development of AA could be auto wnmune
ologic factors (theory)
..ieLlr c th eory 1s support~d by th
01081
,.. eur . e folio
,ne fl AA pat:1ents experience occas, wing observ
l Nian¥ n their hai r. onal itching anct/ at1on~:
1ori o . . or ttchi
tens ati ons ,n neuropeptide and neu ng during co b
i. Alters have been r ep o rte d suggesti ng rotroph in expressio . rn ing, touch,na
(fltlf'l f . a neurog n 1n ani b or
ntJ . heral nerve unction in the ci enic role rna1 rnoctel
per1P and v1 d · s of A.A.
3. found to be abnorm al as compared t er rnatornes b as wen as
0 c.ontr I 0 th of
vJ
as .
ssful life events m ay act as a trig . o s. ' wh'1ch inn
4· strexletY and depression .
m ay play a
ger 1n the
. onset and/or
ervate
scalp skin,
as ari rn a1or role , exacerbati
results). in t he etiopat hoge on_of the disease wh
• f n· nes1s of AA ( , ere-
ft,e role of ~n _ec ous agents controversial
. The association of AA and infecti .
1 . ous foe, of d
b
explained on as,s of a common i ental ori • .
rnrnune . in is relati I
• It has been reported that infection . h me iator. ve Y common a d
2 . W1t heli b n may b
gestive au~o,_m mune disorders includin . co acter PYiori can . e
1
3 _ The association of Epstein _ Bar v· . g SJogren's svndr ...""'"'!:.,.~~t ~1ved in Yariou
irus infecti . ome, aut6tmm--> -tr-o,~ -4 ,.,~ s extra di-
on Wtth oc une thyroiditis
Clinical picture currence of AA was suggested and AA_
Here we shall go through the followin . ·
• complaint. g Points:
• Morphology.
• Localization
• Clinical types.
• Course and prognosis.
• Disease associations.
figure 2 alopecia universalis figure 1 alopecia areata
Complaint
The main complaint here is disftgurem~ The disease is frequently asymptomatic, although few
patients report some degree of p rurit~s, tingling or burning before hair loss begins. The disease
may have a psychological passive impact on patients, leading to a high life time rate of anxiety or
depression which in turn may aggravate the disease coarse.
Morphology . .
- Th . i . ble from a single patch of hair loss to complete scalp hair loss in alo-
e presentation s varta . . lo ecia universalis (AU).
1
pecia totalis (AT) or even whole body hair loss ~ a P
- The morphological description of a patch of AA is: I'
• Well demarcated round, oval or with an irregular out ,ne.
'd o f h ,11r.
• rl
Cornp/t,t<.' IY C'VOI
• ~,,c~
Of v,1ricJ l'JI<'
1
ok~ apparently normal.
• Th<" /ec;ional sea P od of th e bald patch are short, tapered proximally and w·d
• Tl 1e /1a/rs at t/1<.__,, bor e r ' er dist
, t erm e c/amation mark ha irs . a11v !>
h~ n cc th(. q~~
localization
. . t is the most common site. Eye Ias h es, eye b rows, b eard area
sc.1 /p ,nvo1verncn , rnoust
I ha iry region of body m ay be also affected . ache
actuJ I Y .1ny ~~d
Clinical tvpes of AA
1- Areata type of AA
The most common type' here the patient present with just one or few small isolated
2- Subtotalis type Patc:nes
Here a considerable portion of the sca lp hair is loSt either initially or following the ·
cence of previously existing isolated patches. coales.
3- Totalis type
Here all of the scalp hair is lost. The onset may be acute or along years.
4- Universalis type
Here all of the body hair is lost.
5- Reticular type
In this clinical variant, several patches are present in various stages of the disease ..
Simultaneous regrowth in one region of the scalp and extension of alopecia to oth ers activity.
lead
to the development of a reticulate pattern. s
6- Ophiasis (_opL"';s-t7 ':)V"\_~
This is a band like, special type of AA affecting the tempero-occipital scalp margin. It usual
affects children and may develop into more severe forms. ly
Note
Nriil involvement particularly pitting as well as lens opacities are sometimes reported With th
severe clinical types of AA namely AT and AU. e
Course and prognosis

The disease usually runs a course characterized by remissions, sometimes spontaneous
relapses. ' and
The following are regarded as poor prognostic signs:
1• Early onset of the disease before puberty.
1. ■ The association with immunological mediated disease and atopic dermatitis.
Familial clustering.
Alopecia totalis and universalis.
Particularly long lasting cases.
b• The presence of nail abnormalities and/or lens opacities.
Hyperinsulinemia.
Signs of disease activity

1- The reticulate attern is an indicator of an . . .
2- The biopsy will show peribulbar activated ToJ~;;:1~g activ~ty _of the disease.
3- lmmunohistochemical studies show that the
relation to the chronic.
c6
ocyte tn~tr~te._
4/COB ratio 1s ~g_!ler in tbe acute phase in
4- ~ay exd,imatio_Q rnarks hair at the bord
O
f h ~ -~ - ~
5- Positivej)ai[S2!Jlltest:- · er t e patch.
6- Abnormal tri~~'D-
e associations
01.eas .
rr,aY occur In ot h<•rw1 s<' h<'dlthy individual:, or ,t m
AA 11 a<,: a ( ouur 1n ~-~, ~.~.....
-••u-.,i]
i
w. •
.utr
sue Atoplc diseases: allergic rh in,ti, a' thrna ~, . \er du,,....a,,~
l· d' ' ; , -~ 0Plt dormat1t1•
2. Autoimmune 1sea~es e.g. thyrolditJ',, vihl 1go - >-
_ oown's syndrome.
3
_ Fournler's syndrome.
4
oeferential diagnosis .
Ca ses of AA should be essentially deferentially diagn ,. d f
. . ~ • f
O.;,e rom other ca u.,e.,
patehy alopec1a . o nr,.. lica• '"f.(.-ta
Like AA they are considered as patchy non sca rring alo .
the main differential diagnosis form cases of AA. pecias, acco rciingJy the-tar~ con:.1de..-~d ai
causes of non cicatricial patchy alopecia

1- AA.
2· Gray patch. '(,u~ ~
3- Black dot. ~
4- Late 2ry stage syphilis(moth eaten alopecia}.
5. Trichotillomania. - v \1.1 ~ \..1v~:.J ~"
6- cryptotillomania --v ,. , (?"->._, ~ , \:"
As regards trichotillomania and cryptotillomania, both are of a psychological orig;n and r.au.r-e ir
which the patients develops in trichotillomania the tic of continuously pulling his hair anrl n ~e
second the tic of continuously rubbing his hair. The cumulative end result of such a scerai·a 15
patchy non cicatricial alopecia.
Investigations
1-Hair pull test ,
Approximately 60 hairs are grasped between the thumb, index and middle f.nge~ -..01·"" t~e
base near the scalp, there are firmly but not forcibly t~~ged away from _the f~,p~• ~~~
than 10% (6 hairs) are pulled away, this indicates a pos,nve pull test and ,mo es a
shedding.
2-Trichogram .
I' f the hair shaft 1n terms of caliber, fragiJ..
th 1 O
Trichogram is concerned with studying e qua hty g,·nal lesional hair ,s a bad progr'osb(
I · h
ity, length and shape. Abnorma tr1c og ram at t e mar
.
sign.
3-Screening for autoimmune diseases .
4-Scalp biopsy in difficult cases Hl st010 gy \nic infiltration that consists pnm~r,ty ot ac;
h
ibulbar lymp oc, ... f present ,s m nima
Most scalp biopsies will show per . the inflammatory infi1trate'
I standing cases
tivated T lymphocytes. In o~g . to tools are not re-
around the miniaturized folltcles. b . 5 and further 1nvest1ga ry
. 0
f AA are o v1ou
However, most presentations
Quired in the vast majority of cases.
5- Trlchoscopy may be also of value . fe<'t,OII>
nonal upsets and ,n
Tra~- stress, ern<>
---unent . itating factor e.g. .
1- Correction of any presenting prec1p ·cal asents-as
. ch top•
aaents. •,toct sensitivity to su}
2- C0unter irritants: .,ndu1..L,o
,.... n of con LO fDNC&,.
- . ,, or
3- Short contact topical Anttiraliri cream 1/2 - 1 %.
4- •
•
• Topical or intradermal.
• Oral: in rapidly progr~siv and wide pread di ea . , ·
5- PUVA therapy, tn refractory and wide spr ad dis•• .... s ·
Clcatriclal alopecia
ucatricial alopecia is the generic term applied to per-
manent areas of hair loss that are associated witt, de-
struction of hair follicles following healing from the ini-
tJat injury or inflammatory insult. There is little if any
potential for hair regrowth . .
Histologically the follicles are replaced by fibrous tissu~,
this replacement is the final result for a number of di-
verse conditions affecting the scalp including: figure 3 cicatricial alopecia
1- Favus. , - ~\)
2- Kerion celzi .
3- Tertiary syphilis.
4- Chronic discoid lupus erythematosis.
5- [)e.ep bacterial infections.
6- Lichen planopilaris (follicular type).
7- D~ep traumas.
8- Burns.
Androgenetic alopecia .
Both male pattern (common male baldness) and female pattern do ex,st.
Common male baldness
Male pattem androgenetic alopecia commonly shows during the teens, 20s or early 30s with
gradual loss of hair. Several patterns occur, but the most frequent is the biparietal recession with
loss of hair on the vertex.
There is no doubt that inherited factors and the effect of androgens particularly ditv-1drot-est~~
one, t he active form of testosterone, are important.
Data regarding the effect of androgens are supported by several observations:
1- Eunuchs do not develop common baldness if they are castrated before adolescence, if they .
are given androgen therapy, baldness may develop.
2- The Sa reduction of testosterone is increased in the scalp of the balding individuals yielding
an increase ,n dihydrotestosterone, the active form of testosterone.
3- In congenital Sa reductase deficiency, baldness does not occur.
4- lack of baldness in individuals with androgen increase senstivity syndrome.
•on the other hand, data regarding the role of a genetic factor is supported by the following
observations:
1- Increase risk with a number of affected relatives.
2- There is an association of male pattern baldness with a polymorphism of the androaen recep-
tor gene on X chromosome.
Figure 4(8)
androgenetic atopecia in female
f common male baldness

1,.,,ent o .
tte1 ,n idtl, an oral hyp~tens,ve drug that cause hypertrichosis when given systemically,
l- 3 3ble as topical preparation as a 2% or 5% solution. The exact mechanism of action is not
~ ' h d'l
_~..,:" defined, ho~ ever t e vaso I atory mechanism is the most acceptable. Regrowth can oc-
~~ ,.35ea~
,J ,,, as 2 months from
. . the start of therapy. Those who respond must continue to use mi-
~-d •,ndefinitely to ma1nta1n a response.
"' f,tnast1 ide, a type 2 Sa reductase competitive inhibitor, also used in treatment of prostate
~ ~r, given as a_1 mg tabl~t daily _is effective i~ preventing further hair loss and in increasing the
'-a,. counts, continued use ,s required to sustain a beneficial result. Clinical trials have shown a
('{'la: increase in sexual dysfunction in men taking finastride for male baldness.
Female pattern hair loss
t~ough maintenance of the frontal hair line is the rule in women, a progressive decrease in the
~ir density from the vertex to the front of the scalp does occur. The mid line part is an important
:: · ·GI due revealing a Christmas tree pattern of hair loss.
~ principal differential diagnosis is chronic telogen effluvium in which the affected women ex-
~tience diffuse hair shedding without noticeable widening of the central (mid line) area.
~ ira the male pattern hair loss, the cause is believed to be a genetic predisposition Wlth an exces-
S.:-1e response to androgens. Most affected women show no signs of v1rihzation, however ,f the
a r loss is sudden or rapidly progressive, investigations should be done for a viril,zing tumour.
"'vestigation is also indicated in such cases accompanied by menstrual dtSturbances. htrsutlsm or
recrudescence of acne even in presence of a gradual onset.
The treatment follows the same mentioned for MPH, however here fini.Jtoif.k contraindicated
th pregnan('l and oral antiandrogens such as si,,ron~ne and may be --., , ,._
tned " cases w' ith evidence of excess an drogen w here they act through block.~ of androaen
receptors.
Diflnse hair loss {T~logen and anagen effluvium hair loss) f (Th)ov .n.MHW"I hairs to te'°len
. h
Refffi to a group of causes resultlng 1n emature con"ers1on ' ......_......
t e pr ~ d n,,g ~ ~ t v v and resuft en a
1~- han,sm thJt occu-~ .,.. ..,..._.._,
t01rs. Prolonganon of telogen ,~ another mec
wave of ha r loss that m n1fest~ after deli\/ fl. pportlve root ~heath In the cont,-y,
·• -
.-v1agen hair has a pigmented bulb an d 1')~ \ urrounlied su th
by 9.......
b b
tetagen hair has a non p,gmented ul an d l ck!) a root )11C'a -
h ..... r umm;atety lost ~t the root.
n.
Whatever the cause and mechan,~m Of t e logen lo · t e..''°' .i.. h
,~ .it tr.-c
more pr0flltnent .._central
exce~l\re shedding of telogen has resutts ,n a d1ffu·
e \o s ~ 1,1c
IJ'\d frontal scalp. . ,ttu~e hair lo~ ,ndude.
The P0SS1ble triggers of telogen effiu um d
- Cmset of androgenetic alopeciia.
Anaemia particularly .iron d efi ci,ency anaemia.
tre ~ nd emotion I upset.,.
P~ nc mcul rfy the postpartum st age.
- D 7 • • ntifong I (fluconazole, and itraconaz,ole), an~coa~~a~t (h~par!dn, coumadine)
--·-·d P s_ nt (amphet m,ne),androgens anabo ic stero, s, a on s ero, al anti-inflarn:
tory dru s.
rrheic dermatitl of the scalp.
H nd hyper thyroid1sm.
- v~ght loss.
·S\fge c acute and chronic illness.
- Po t ope~ tive.
- 810 n efiaency and hypervitaminosis A.
n ·um\Jsually results from-:-ha_ir s~c!_f t frac_!ure as occurring in systemic lupus erythema-
t:OSJiS ·~ -·,..1, and with the use of antim1totic drugs.
tre~~-. ent of diffuse hair loss resulting from hair cycle abnormalities (telogen and ana
e·...,. n.,.,n- ,r oss) is based on the treatment of the cause, in addition to the use of such ag gen
, g10 h factors, vita mins or antioxidants that claim to induce vasodilatation, angiogen~
an" _.,,..,uction of scalp inflammation.
1
es.ts
Bullous Dermatoses
fiititiof1 : diseases presenting mainly by bullous eruptio

O' 6'e skin n
;r,,e"
c:,a55ification =.
1\~is bullosa
'.Aerrno ,-
fpiv ~ . .
rnphigus
1. pe titiS herpetiformis
derrna
1- •
, nrbeCS,.
~ 4 s-syndrome --
1. . pidermal necrolysis T c \J
2. to,c1c e
pathology:
ma lly the polygonal cells of the prickle cell layer tt h
1Nor , are a ac ed together by dei11io.sorr~
· fi'ament-ous plates
wno• .
2. Damage to th_ese des~o~omes by _immunological factors leads to space formaoon f. ed w·
transudation fluid resulting 1n formation of bullae or vesicles
oifferent types()~!..e~mphigus :
1_pemphigus vulgaris: The severest and most common form
2_pemphigus vegetans
3_pemphigus fallacious
4. pemphigus erythematosus
Pemphigus vulgaris & pemphigus vegetans : there are deep lesions with supra-basa, oearr•.-.. -..
lytic bullae
Mucous membrane affection occurs in most cases.
Pemphigus follacious& pemphigus erythematosus : there are superficial lesions wt >uh g\aa-
uJar acantholytic bullae
Mucous membrane affection is rare
PEMPHIGUS VULGARIS
Definition : Chronic bullous life threatening disease affecting the skin & mucous •raecttb. .a1e
Pathogenesis : Autoimmune reaction
Pathology : Supra-basal acantholytic bullae
Incidence~
l. Age :> 40 years
2.Sex : F>M (below 40}, F=M ( above 40)
3-Race : more in Jewish
Dlniql Picture :
1
· very bad general condition
2
· SVrnptoms related to mucous membrane affec-
tion·•
· Pain
· ~essive salivation
..,,.1,.,,,,,,,..,,---
· Interference with feeding
3
~ 5Ymptoms related t o skin affection :
- Presence of painful bullous eruption
-<><>zing o f fluid
4. SVm ptoms related to complications : of the disease itself & of drugs used in treatment
S. sign s :
A, morphology ;
d- M ultipleh flaccid bullae , usually not pruritic, they break easily leaving raw areas with l<>v.,
ency to eal leaving t ran g_ent post eruptive hyperp1gmen. tatr·on ten.
-They are variable in size & shape ( linear or rounded ) .
- the skin between lesions is apparently normal but histologically There is autoimmune reaction
that needs a precipitating factor like trauma to appear.
e, localization ;
- bullae usually begin on t he m ucous membranes
- later, skin lesions appear
skin lesions can occur anywh ere but commonly on chest, ba~k, scalp , face & axilla
C. Nicolisky sign: by lateral pressure by a finger on the skin, the epidermis slides over the derrn1s
in the skin in between lesion.
figure 2 pemphigus vulgaris

figure 3 oral erosion in pemphigus vulgaris
Complications :
A, in the skin :
1. secondary bacterial infection :
- toxaemia , bacteraemia &septicaemia
- streptococcal infection
2. secondary eczematisation due to oozing from raw areas
3. secondary a1.110o,jdosj~ of the kidney leading to ~cute renal failure
4. hypoproteinemia :due to protein loss in bullae
5. dehydration& electrolyte upsets
s, in tbe mucous membrane ;
L ulcers
2. nutritional disturbances & malnutrition
I
PEMPHIGUS VEGETANS
Present by blisters or pustules which lead to vegetating lesions
Usually in intertriginous areas as groin & axillae
- mucous membrane affections are common
- histopathologicalfy, there are 'i''pt:a&asal acanthofytic buflae
FOLACIOUS:
PEp.1ptftGUS fi cial blist ers lead ing to sca les & crusts
super d
There are allzed or generalize
I
are oc h I .
. 1es1ons •callY sub corneal acant o ys1s
atho 1og1 ,
. hlstoP branes are less affected
. rnucou s mem
tGUS ERYTHEMATOSUS
PEMPH superficial blisters
There are h .
h
on t e fa ce there are lupus eryt ematos1s or seborrheic dermatitis like le .
.1 . SIOns
·. on t he trunk, lesions are slm1 ar to pemph1gus
. follaclous
_histopathologically, sub corneal acantholys1s
- rnucOus membranes are rarely affected
Treatment of pemphigus:
(l) corticosteroid : drug of choice (life saving) dose :
-initial dose: 120-180 mg / day
or 1-1.Smg\kg body weight
-Gradual withdrawal with complete recovery.
- Maintenance dose may be needed.
complications of treatment :
- osteoporosis -OM -hypertensio6}
2) other immunosuppressive drugs
- methotrexate
-cyclosporine A
- a2athioprine
They are used with corticosteroid to decrease its dose
(3) other adjuvant therapies :
-treatment of secondary infection
- fluids
- proteins
- diuretics
-management of side effects of drugs e.g DM, HTN
DERMATITIS HERPETIFORMIS
Dcftoitioo ;
O.:onic severely pruritic relapsing skin disease char-
a_aer,tzed by polymorphism
PMl:n1e;na;s ~
4ut0tmmune with auto antibodies formation
btttoloo~
~basal buJ'-e ,.e. below the basal layer
~
{1 Pkture ·
. figure 4 d1r1na
) age = 30-SO years
l!'S\'mJJtoms : s1wr1 china Ii scratchrnc
}"'°'Phoiosv :Polymorphic eruptions
· ""-41 1 that are variable 1n size , colour
.. '111iic1-!s
._._
ompll •tt,,n~ :
( 1) ?.t'l t>ll<f,,r y lr1 t,·l tfc,11
( ~) "( l ,,,,,1.,,y ('l ., nlilt1,.1t1u11 t
' ·.) , , ~ I Il ()It lH Il '' I l II')'. I , ,~) t ~) '1 1I( Itf l I l t t f ' I tl I)l ,, cf lJ
I I I ' 0
s (' V •I c• It ( Il II l l-i
\ ( \
\ (\ I I
rreatm~nt : '. ~
( t} f ,,,t <i1 \I, <>f l 11t)I( is 1
cii.,'- 1 •I{)() Ot> 111f(/<1,,y

..,i : ,,. ,1,l°'ly, 1, (,<) 11,<)rlit<.'>1 H~3 !l) & IIV('r In ult (so moni tor c;crum
( ) it t t1t f>,1ttt ,,t
1, \ 'rl\r t 1v(' to \LJ l f J Lise• CST
(l) with cu1t' 11<) 11t'ld tor rn"1l 11tcnt1ncc
(4} lo I\() . th,ng & dr y111g <-1Rcnts
(" )Glutcr1 tr:'.\<.' di<'t 1 ,ldvl ed.
\l~'C"l...,> \. \. ,, \i t! \ ~.,.._c0\ ttl.•"")
STAPHYLOCOCCAL SCALDED SKIN SYNDROME (4 S)
n, inly ,n n wborr,s
• ,nf cr, n with taph occurs through the umbilica l stump
5 t ph produces toxin which ca uses bullous eruption of the skin
... ch r cter, t,cally there is very large single bu Ila that involve the trunk & may involve both 10
nd upper limbs, its rupture ca uses severe agonizing pain & scalding of the skin
- bulfa are filJed with pus
ry bad general condition, so need ICU care
To:ftmcnt : ,n the ,cu :
-(1) Fluids to replace fluid loss by oozing
-(2)annb,otic~ (anti -staph) : Cloxacillin in large dose
TOXIC EPIDERMAL NECROLYSIS (TEN)

S1mif r to 4 S - yndrome, but:
--occurs t school g
- rt is not du to inf ctton , it is drug Induced :
anafges,c ,NSAIDS, nti onvulsants , anxiolyt-
1cs
• Iara~ bull e which re fill d with serum not
pus.
Tre•t11c•nt : figure 6 toxic epidermal necrofVSiS

1. stop th offending drugs
2 .corticosteroids
II h ~ t ,. ' 111 ~ 'v c., , t o i' wIcI•' , .11 i ~ • ' , , I ,~I·.<) r' I, .,., " 11 ,,tI' I Iloll 111 11•1 ln•d It
111 y I lll ,t1tNJli' I,
rti ' ocvi,1, () I1r,1,,.,11 1ft t ,,, 1,1, •l.111 tJl1l,1• I 11 . • y1,,,,,1v.rr1r-r1t4
r,i!Pl,111 • 1
t rt' <, t orh -t I,, • t,, .. I , <) n' t I
J1• • , , 1' tI~ ' u ct ,
• '· u'Y"11 • d1 ,,lv,,d I
J <I'' , I , Ii , I Il , ,' I i j I I I I r, ', , ,
111 t•1,1 ,ty,, I I I I1Iii · •. PIt 'ii I P, " ' 1',ri f ' t 1
'11 i1• ,,,..11, f
'
1~ln, ,1 1111J <)' ,li,' ,,11<• 11v1 1,1 tr nc l ,lf 11 111c1y,, ' f>r•II ,,1Iy uf M••l,1111,r,,.Y"" r lr,,il
I d111,t1r1i,t lr' ;• ,.,,. h111,,. •
~ ELANOGEN ESIS
ill l)lli10 11
i.l 11 I ,11 <' •, ' fl I1,,, •.Yl11 I•, tl11• ,,.,m,, 1,
C-:~
":":---::::::::~ ~ ,r
111ro11Ah ,1 on1pl<'X pro ,,.,' Clf ,uu '"•,lvr• t<·.iclIon•, .,r.tlr1H 011
,1ir ~mlno ,, id ( 1v1 o In<' ) In th1 prP ,PIICP of ly ""'Y'"''',(
,ostna,(', 11yd, oxylJ c .ind OxldJ•, ) tyro•,lno h I r,111•,fprtnNI
,nto Mrl;-inln.
ryroslnc ~ DOPA ~ooP,e_ulr1ono(!ODOPAchromor'° OHI ... OHi-
CA~ M(\lanln.
Thcrf• are two typ of 1Tl<'I, r1l1,; 111 r)ll<on1t l:.i1lln whlc l, 1 1
- - ---
s rcspo11sibl c nbout llght olor (blur, grrr,1 Iris .ir1d y ,11 0w
1
hnir), and t l10 eu1110IJ11ln wl1l cl1 proclL1cr cll~1rr brown or
blJck colors.
Melanocyte - keratinocyte (Melanocytc -epldermol) unit:
Each Mcl~nocytc di tributes It melanin content (Inside cl

small, oval structurescalledmelanosome>s) to 36 keratin!
cytes.
TYPES OF LEUKODERMA
• INFANCY (Diffuse-CIRCU MSCRIBED).
• CHILDHOOD (Diff use/ CIRCU MSCRIBED). th 101
' ADULTHOOD (D iffuse/ CIRCU MSCRIBED). , I othl'r word,. not ,111 d1,ca.,... * ,n
1
• The followlng hler~rchY Is only tor Jllu ; Jtl ~'~ 1 :;,nonrd 111
110
bncl.
lowing hlt> rarchy you ~hould know th!'nt, onlY ~'
LEI..I
LEUKODERMA
LE
os leukoderm41:
..-t "'ff(dO f ngaf nfecoons.
,.,.- tfi ,al u r---,
.· ~rsi color.
:• . unsatura~ d fatty acids - ~
•
~ . htbit tyrQ.Slllase activity..

J(tS7 1n
cJtlll Others: rTTl .
cv· (the lndeterrT11nate# and the tuberculoid cl,nacal t oa ) on h •

lll)CO-r• _ .. ..~. · \p I It\
· t aonematoses: lb'Pinta
. .Yaws. BeJel.Secondary stage Syph1hs (leucometanodermacoth l 1
()c\lfo'Utan~us A . tnts~: .
•
~ rute hairs.Milky white skin .Blue-grey eyes .
(hfdiak- Higashi Syndrome:

. P.are syndrome.Inherited as an autosomat recessive .Bleeding ten-
dency.
Prog"es.srve neurologic dysfunction.
'T"unodeficiency. (markedsusceptibility to respiratory and cutane-
..,_ "'fections) .
.....a' y fatal before the age of 10 years.later on,death from a malignant lymphoma.
PiH>atdrsm:
•
Autosomal dominant.Since birth .
• --
•
Mainly forehead, trunk, and extrimities.Triangular or diamond shaped areas .
•
Usually on front of the body.Specially on midline distribution.
Wh forelock.May be ~ poliosis of eyebrows and eyelashes .
,~,d b
en urg Syndrome:
fl.are, autosomal dominant or A. reces,ive h perplJ •·
A.chromia of hair and/or skin.M d.ia I side eyebrow
ochromi lrtd l
'
nit
8road nasal root • dystop1acant hOrurl1 •Heter
Voct-Koyanaal syndrome (HARADA):
- A di ea e of unknown etiology.It aff•cts 4 orgJns In succession:
1- Meninges encephahtic or meningitic symptoms+ lymphocytosis of CSF.
2- Eyes bilateral uveitis. choroiditi , optic neuritis(some recovery of visual acuity}.
3- Inner ears deafness and/or tinnitus (over 50% of cases} completely restored .
4- Skin (permanent changes) -+vitiligo (60% of cases}, poliosis (80% of cases} and alope .
areata (in SOil\, of cases). cia
VITILIGO
Genetic element:
: Positive family member affection In about 25-33% of cases.
No p~ove of autosomal (recessive-dominant) trait .
•Vitiligo theories: inheretance geneti c pa ttern .is postul ated (on chromosomes 1-2-and 4).
Multifactorial
Au to-immu11e
theory
lkt~nous- Auto-cytq_tQxi<:.i~
Convergence the o ry
theory
Neural the o ry
I- Auto-immune th eory:
- Association
A with some aut .
. 1'nt>body activity is more o-1mmune diseases.
- Antibodies against m pronounced in active
tissue) ,:8AO:tibodies against co::ocyte surface antig.::her than stable disease.
of v1tiltg
't, on tissue ·
Autow,th ad ecreaseo In
v1t1hgo
It- cases, 1' Level of ant1-tyroslnas
T-h~lp• . antigens (thYro·td, gastric . parietal cells and adrenal
~r cell e a ntib 0 d.
-Melan -cytotox· ·
•_city theory: '· •es.T, cell profil es are abnorrnal ·in
ocyte activity Mel
anocyte death.
•
•
•
•
... JAenced by:LlevJt
t'""' I ontrol .
~(•tl C
AfHOLOGY: Vlt1ll50 arc.is Ab nt M IJnocyt ~-Compl<-t~ ub~ nc, of m IJnocyrcs in ,1

~1sTOP01 'th O total lo~s of p1d rmal pigmentation.
'"'1ari \ w~ul,ir and pcrifoll icul<1r lymphocyt;.c lnfiltrat s mJy b o_b rvcd Jt the t11Jrein of vltt-
• ~cnv u lesion con 1st nt with a ccll-rned1at d proccs d strovms mclanocytcs.
son,rtin,e , ~1
ltgino . s melanocyte with giant rn lano ome Is pre ent at the edg of the d pigment
• ed clrea. (H&E).
,, N
' •
0
~
• A B
Histopathology (H$E stain) lmmunot,istochcmlstry
. ,s peripherles may show -+

• Cultured Melanocytes at lesion
"""' \~l•<'r•""'J •, "\' , !"f

l >\ ' IJ;, \.\.
C I rt'J1ilng ,1ge.
_. .J_, with ,,c JI \tre s.
LINICALLY: oung adu Its. Incldcncc
~even' ernot1oi10 1or Ic ).
phy\,1ncr
onder
• Onset + childhood or V ere sunburn or . ts (77 fJlse prep
• In ~20% +develops after sev In female patten
• Gender _. prepondera nce
• Symptoms: disfigurement. d ven genltalla).
• Localizations: ose ears, eyes, an e
·Perl-orificial (Around mou th , n '
• Pressure points.
· ~"Ywhere.
Morphology of lesion · )
• t le s than h cm
- Variably sized (but no "'$-
Variably shaped (rounded , oval e, er
tic linear geographic, etc ... )
cen , '
1 ( pt 1n lo-
'F' Bilateral and syn1metr1ca exce
calized types) .Very well demarcated.
- Oepigmented (milky white in color} .
,.c.
Otherw ise affected skin is completely normal in all other J pect
-1- Skin thickness
, (neither hypertrophy, nor atrop hy ).2 Skin te tur ' . EIJ ti , " 011 \1nd ~1n t ,,,1
ience.4- Skin sensations.
- HAIRS:
1- Early ------- normally pigmented. .
2- Late in the course -------poliotic (premature graying of
hairs).
Clinical types:
• According to the extent of involvement:
1- Generalized (not more than 50% of the body surface area).
2- Universal (not more than 80% of the body surface area).
3- Acrofacial (distal fingers+ facial orifices).
4- Focal (localized non-dermatomal).
5- Segmental (dermatomal-a'symmetric . ~ ~ ~ ~~
6- Vitiligogradata (trichrome type, tetra, penta}!o
7- Vitiligo with raised borders. ~- . ~-"~ ~?Y<'J~'i
8- Drug induced vitiligo - rare type (Chloroquine- Clofazimine).
9- Chemical- induced leukoderma (occupational in house keepers):
Phenolic compound s (p-TBP}-monomethyl ether of hydroquinone). d
Sulfhydryls (S.Ulfanilic acid - Mercaptoethylamine MEA in dentists, dental technition!>, an
dental assistants).
Others: arsenic- corticosteroids - azelaic acid - mercurials,
Focal (localized non-dermatomal) typeAcrofacial type
• . 0 with raised borders
viti 1,g Viti I.
•go gradata type
Segmental (d
errnatomal)
. 'ligo with melanoma: <:>..,, · ,c\ \
«) .., ,. • ,.
0 v1t1 'ff
1 . Halo nevus.B- D1 use depigmentati ) ,, ,, r _, \ r/.1
N)f':,\P 4fll. (~ \ ....

ri--')l,r (.
"'· on and/or h . ..J ~ y '-"'' l~,.1-·,~
,.. ) YPo p1gmentati (
rurnor ·-------:;;;~~ ~~~;;;::;::=-, on remote areas from the
Halo nevus (with)

and without melanoma
CLINICAL SYSTEMIC ASSOCIATIONS:

A· Autoimmune diseasaes:
Addison's disease, Thyroid disease, Diabetes, Alopecia areata. : ~ o,-~
8- Uveitis. C- Auditory problems.D- Vogt-Koyanagi (Harada) Syndrome.
(.
TREATMENT:
PhototherAP)
• • p:,oralen U\ A
Cosmetic
• Narr0\\1b~nd U\13
camouflage
5urgic.il
Topical ~nd tre•tn1enl
systemic
steroids
- ~ufla_&e:
.!:.- ~~ r - , m-a-L oermablend Oermacolor, and Dermage.
Type of dyes. l..,VYer 1
" · ,
fa liaftion: exposed areas. . .
s,tes Of!'
orawbac~ · perso
na t ,.eJ·ecn·on severe reaction, ,mpracncal for wide areas.
•· ,
,,_ ,yy~ therae,-_

-
Syste,,,ic PUVA:
• 8 methoxy-psoralen 0.5 mg/kg.
• used for exte~sive vitiligo.
Topical PUVA
• 8 methoxy-psora fen 0.05- 0.1% solution.
• used in cases with less tha n 200/4 total surface are a depigmentation.
Mechanism
• PUVA increase the size but not the number of Melanosomes.
1-Photoadducts:
UV light
• Psoralen + DNA - photoadducts (w ith t hymine bases) - DNA inhibition-+ RNA+
protein synthesis. - i
2- lmmunologjc.:
• Decreasing the antibodies d irected against Me la nocyte s.
Side effects of PUVA;
Immediate: pigmentapon- fatigue - xerpsis - ptutitus,
Delayed: skin aging - catar~ct -skjn malignancy (BCC).
Narrowband UVB (NB-UVB):
• Usualfy 311-312 nm wavelength, 2-3 times / week.
• Treatment of choice for adults and children with generalrzed vitiligo.
• 250 mJ/ c.m l • increments by 15% at each exposure • till appearance of erythema.
es: 1- Can be used in children.
2-Can be used in lactating and pregnant women.
3- Can be used in hepatic or kidney dysfunction.
_T~I and ~mic ~roids
• For localized lesions.Face and neck may respond better.
• High potency topical corticosteroid preparations (0.1% betamethasone -0.05% clobetasol
propionate) are effective.1-2 months e tapering.
• IM corticotropins may also help.
~
~-tre~Jrt: ---
le!QKATJONS:
1-Segment.al or local ized vitif igo.
2-Non progressive-inactive disease.
AutologusMinigtafting:
Before
rn,al Grafting:
S· fpi de
Fixation by fine stitches
· Transplantation of non-cultured Melanocytes:
and fter
0-
Before
After
l UJ> • 'V h
I Ip M .. Ind A
vc~~,,I!:.
IJ-IPYl.lf,Ylbtmll.OlYS;
l. Aclttc,: ~v t nli lltpu, rylh rn ,to~l•'
1. uh,,c,JtC' form
I. Chronic : di cold lupu t1nd rc·l<1t ·d var! ·t1 -~ ·.g. h¥P4-rtroi;hic, ~ pc:GIL'4d.,~. r.~
, (Sll) I~ ,1n uutolmmun • di ·a~ · th;,t can aff(:ct almo-,t any ori1,an ,..,:~m __,'
, clinic.ii ymptom mo<t commonly found in c0dult$, including rrlaia; ra~ti, uke-~/r..UCOclu!e-
ou lnvolv •mont, r<:n, 1lnvolv(:m<;nt, prot<:inuria, urinary u,llular ca~, ~zurei, 11<.r~
top nia, h )molytic c.1nemla, fever, and lymphadenopathy,
Ettoloo
~coettc factors;
• Po!>it1ve associations with HLA-87, -88, -Cw7, ·DR2, ·DR3 and -DO.wt are reported
Environmental factors;
• trauma in 11%, with mental stress in 12%, sunburn In
• 5%, infection (EBV) In 3 %, exposure to cold in 2% and pregnancy in 1%.
• Occasionally, drugs (e.g. lsonlazid , penicillamine, griseofulvin and da~one)
4 t Bt 7 CI •
CtQ,C?,c-4
tt.A,(n)j
Mil
,di' jA.lA,21
ll•tO
MC,'
........,.
'lPNn
....,...,... .....
Mt:~
--·
t j.
LI 7 ,
c:NI•
C ,.
7
UYlf'I
1l1•dr
,_
ft:ILRV
S,
• a vC• C
5 FF
..
C 4
O&srt
• More than 90% of cases of SLE occur in women, freQuently starting at dlildbean,. ii!
female-to-male ratio is 9: 1 during the childbearing years.
• 2
Onset of SLE is usually after puberty, typically in the 0s a
nd 3
0s, wi
th 2
°" of an cases di.fs-
nosed during the first 2 decades of fife.
• SLE does not have an age predilection in males . , -
~~
0 ,
Patients may present with any of the following manifestations: ~J:'A• ·1 ,~ M.1J
• Constitutional (eg, fatigue, fever, arthra)gia, weight changes) ,~
• Musculoskeletal (eg, arthrafgia, arthropathy, myalgia, frank arthritis, avascular necrosis) ~
of SlE patient witl have arthralgia.
• Derrnatologic (eg, malar rash, photosensjtivity, disco1d lupus)
• Renal (eg, acute or chronic renal failure, acute nephritic disease)
• Neuropsychiatric (e&, seizure, psychosis)
~
• Pulmonary (eg, pleurisy, pleural effusion, pneumonitis, pulmonary hypertension interstitial

lung disease) '
•
•
Gastrojntestinal (eg, nausea, dyspepsia, abdominal pain)
Cardiac (eg, pericarditis, myocarditis)
-
• Hematologic {e& cytopenias such as leukopenia, lymphopenia, anemia, or thrombocytopenia
Systemic lupus erythematosus

- Mouth and Skin
nose u lc:err. bulU!rfly rash
and red p a ~
Heat
· ~ndocardttn
- athetOKIHOSol~
Lungs • infl.s I I U i 1e11tJon of
• pleur1t,r. Che?fitwo~ScK
- pn~mon,.~
• puJmonary emboll
· pulmonary ,,,.. ~n!
~(hiMjp f abdom,natpaan
Kidney.
Blood
b&ood •n ~ urine- ....... , 1. .
. hagh blood
P'Ntour•
• Muldeand
.Jo'•ts
· ~n•nd
· antv,t•~~
~wol~njOint~
• Dermatotoeicmanifestation of $LE
• Photosensitivity
• Malar rash
• Raynaud phenomenon
• macuJopapular rash
• Bullous lesions······ ··> to)(•·c eP•.dermaf . .,.
• Vasculitic purpura -~\ ,,~a ,j(ft 1 necrolys,s
r,1:>
• mucosa! ulceration
• Telangiectasias , ·~r1.-_ ~w-.~,
• Urticaria
• O:ifhJse hair k>ss• •
,.. ,,, 1
n sI
Ova-
• r, I)
~
~...,
...........,
•• .saas•
~
11t691'1I ~
.... ,
IJoodlow IO
•
,apcawh-eci..u.a
andna.,we,
Cain
_ . I] I)
•nc:..cae;
•,. -
tJa
Q
C!'l11l 7 'fllDocl
dlla.yge, 3 'lll0ocl
.......
.,. ., .err ts r ff- n s , , ,,"'
occtuson / I ,11 M
Mr(
~--
,..:;.._ G. ~ =a Z"«I
• The di11001ls of Slff
iocv ev1deoce,
1.ANA
) .ANTf d!) DNA
J.ANTI RO. LA
4.COMPl EM£NT TE~ T
5.Rr (AfR) ( 1it

6 CRP C liege of RhE'Llf)latology
. f t 11 Americ,111 o
7. ThC' pre!)er,ce of 4 o t ,e % f SL[
of 85% and a specificity of 95 or .
TREATMENT; system(s) involved:

di on t he organ dt •
• Treatment of depen ng
erosltis-type m an
ife stations gPnera lly ref,pon o l- re~ tr11er,1With
• Sk.in musculoskeletal, an d s .
( antin,alcJrlal) hydroxychloroqu1ne ti ??7? t \\
. . fl 11matory medica o ns
• nonsteroidal ant1~in ar h CNS Involvement or rentl l disPase1 often nera,~
· olvement sue as h Id h
• More serious organ ,n~
tates imn1unosuppres ion wit
5
h hi
g
h•dose
.
steroids r1nd cy lophoi p am e, m t otrf!,-.-r,
1
,
.
alsthiopr,ne, mycop hen olate' cyclospor1ne
Consultation with the following specialists may be helpful:
• Rheumatologist - For Joint involve m ent
• Nephrologist - For re nal involvem ent
• Internist - To evaluate for syst emic invo lve m ent
• Ophthalmologist_ To m on itor th e rapy with hydroxychloroqulne or chloroquine
tJ.f
• OLE (DISCOID LUPUS)+++++
• Verrucous LE
• Lichen Planus-LE overl ap.
• Chillblain LE
• Lupus Panniculitis (LEprofundus)
DISCOJD LE
• Discoid lupus erythematosus (DLE) is responsible for 50~85% of cases of CLE and occurs 2 3
times more frequently in women tha n in men.
• It common ly develops in persons aged 20 -40 years. Se
• < 5-10% of patients with OLE progress to SLE. •P
• Exacerbation Is common with increased sun exposure, particularly In the spring and summer.
,,,
Clinic:al oiaure: .,mi •1,
• Discoid lupus erythematosus (OLE) primary leiion Is an erythematous papukt or plaQUf
slight-to-moderate scale. ""' l.
• . progresses, the scale may thicken and become adherent. P1gmentarv
As the lesion . chan r·
ntatiO" ·F
may develop, with hypoplgmentation in the central, or Inactive area, and hyperpiame
at the active border. "'
• In OLE, characteristic lesions are wefl•defined erythematous plaques with partiiHv 1
scales entering a patulous follicle.
,
' '/~ . .,. .. .

.. ---.. Pc:tients ha ,e d.
,J:,, c."t a fe,v h- •sease limited to the head ,ned- and 1-;l;aPE area of. e ,, , o,-_., Zf;d
-~- "'is~d Ji..f}. dve much more e.rtensive disease, potentia ty affecn41g a 'far a o' i.,,.,. -" n (d,s.
1..,..,..,
c: ~--t: .,,itn .d
'x.·e •e I to d~ w, espread
f involvement often ha'✓e hemato og c and ,e,otogic ao. orma1 ~' re
•
•
ie op systemic lupus erythemato~Js SLE). a'"~d are rT;ore u,,j1a.\l1u o ea
~-Th r
ed ~ ·
11
i Lv P dermis
..:; Of ll()
1F rrna1rete radges
Ol lLuta
4 ,.. Plugging _
Vdropic h
~ ~ c, anges of ba~l layer
G If\(
)
~ Perivasc.utar infiltrate
r~ase "'Ucin
-OV- ts ....0nc_;-.
_.;7luve more than 7S% of case wnh lgs IO<.ated atJlE.J
Histopathology of OLE:
a. Liquefaction degeneration of the lasili.ell llYer
b. Hyallnlzatlon, Edema & Flbrinold change below epidermis
c. A patch,y dermal lymphocytic Infiltrate around the appendages
Follicular plug _ ____

(•carpet tack") 1'!~
Liquefaction degeneration - - •
•
' .
•
Thick basement ------"
membrane
Liquefaction Degeneration _
Melanin Incontinence _
h'' .taneous nodules 1-4c.m th
st.>".,., at end- ·
~t" e and upper arms , •n atrophy
, -' fal '
r-1eav, zo-45
,, ,µo rra'1g'(age
snows fymphocytic panniculiti .
~-,r~IO over lying epidermis shows hyd ropic
, ..,,o,es- s, ~yaltne
cha degeneration of th
u-- fflent witli Anti,nalai:ials nges and folhcul ar plugging
e fat, h·1al,ne pap,lla"I
rreat
' oLEtesions may become hypertrophic or verrucous Thi b .

sions, rnost often on t~e ~x:te nsor _arm2., · s su set is manifested by wartfike fe-
, can be treated with Accuta ne or Plaq_uenil.
IREATMENT
, sun-protective measures, including sunscreens, protective clothing, and behavior alteration.
•
T<'picilf steroid, high potency with occlusion if needed.
• top1cal
. glaAeJ.l:fin iohjbitors.. c. . .Jao~•-"'
•• •••• •in resistant cases or wide-spreaded lesions
• 1mm
- d.
: safest and most beneficial system theraPY ..ct ,n.e ,teroi96 "'ethot1 acote,
4- ; " WRRU:59ntS.and ,jm[IIUl'lornodufators, inclu in!f- s,.-e '
0
' 0 ,henotate1,1ofetil, and t~atiele11,tae
Eryth ,m, n do um
Pathogenesl
•t l. ,11 •·1 , t 't'PtJI i,,1n,,,t uht1 \ \ . ,. \ \ ' '
tt ,. \\'. ,d ,, I ~---)rdt'd ,1 ,, 1r•l,,\t d h

p.~ ~t') ' \O\ It • - ~p t, t ,._\ "''' it: ty f
anti'<: t'\\ ch.lllt. ,,gt' :
• bacteri-1( t~rpt .),
• ,n.1se~ ►
• drug"(Or3\ ontraceptiv .,
NSA\D, lJ\fonnmid~s,lodtd ,
bron,ld~ ,penlcHH,,.),
• pregnar,cy,
• sarcoidosis ,
• systemic diseases(IBD,HIV,MALIGNANCY) ....
• or it may be Idiopathic .
Clinical picture:
• Painful, eryth ematous SL1bcutaneous 11odules
Usually distributed symmetrically over pretiblal areas; occasionally elsewhere(trunk,forarm~,
etc)
•
In later stages, lesions acquire a characteristic bruise-like appearance .
• May be accompanied by fever, arthralglas and malaise
Treatment
Discontinue possible ca usative medlcilt\o ns

Treatment of underlying infectious dlt>oa!>es
• Bed rest and leg elevation

NSAIDs and salicylates
• Potassium iodide (inhibit cell mediated Immunity, Inhibit PNL)
• Colchiclne
'
Erythema Multiforme (EM) ~
Erythema multiforme (EM) is an acute, .s~l:-limited_, and sori:,etimes_recurri~~ ~lkin condition t

= c::::,...,associated with certain infections, rned;.hat
. cons,.dere d t o be a_ type IV hypersensitivity reaction
1s
cations, and other various triggers.
ETIOLOGY AND PATHOGENESIS

EM arises as a consequence of immune-complex mechanisms involving antigen-antibody
reac.
tions that target small blood vessels in the skin or mucosa.
Ellologlc famws for developing erytha:w multiforme

Infections Viral in descending Herpes viruses; HSV 1 and Hsv.2, E,>st
Approximately order of incidence Barr virus, cytomegalovirus, ~arit
in 90~ of cases zoster virus
Adenoviruses
Enterov1ruses; coxsackie virus BS, echo
Bacteria I in descending M)<opla_sma pneumoniae
order o f incidence Corynebc1cterium diphtheriae
Hemolytic streptococci
Legionellu pneumophila
Salmonella
Mi,<obiJcterium leprae
Pneumococcus
Drugs Oeu than Highly suspected in Sulfonamid~ (trimethoprim,
10% of cases) descending order sulfa methoxazole)
of incidence Nonsteroidal anti inflammato,y dr~
Penicillins
Anticonvulsants (barbiturates,
carbamazepine)
Hydantoids
Val proic acid
Ail opurinol
Antifungal (TerbinafiM)
Others Oxicam• (piroxicam. teno»cam)
lmidazole
Chlormezanone
S)1tero1c cortic ~roids
Cepha losporins
Quinolones
IIIWtil#W c.ondlbOn
Tetra cl,ne
Graft versus host desNSe
lnftMVnato,y bo\Nel disease
Po'Yartent,s nodoY
San:oidosas
lnnuniz•aon Systw:aic Iupus e,ythemafOUS ,_ I
a.die Calmeae-Guerin. """'
OIMn food lddi._
-:;:::------;:::;=::::::--------........~s!!nwl!f! x i111t1.miz•iofl
hnz0ate
CAL clASSIFICATtON
cuNI ·t,ed according to the foll o win g crit er,a : M
EM ,~ class, . . , >•
EM minor: tygical target s or raised oedematou s papulcs acrally distributed .
~: EM rnaJor: as above, with involvement of one or more mucous membranes.
_SJS: widespread blisters predominant o n the che st, prese nting with erythematou s or purpur,c
3 sand one or more mucous membrane erosion s.
n,acu1e
DIFFERENTIAL DIAGNOSIS
conditions considered ~n the differential diag~osis are primary HSV gingivostomatitis, autoim-
une vesiculobullous diseases, such as pemph1gus vulgari s, bullous pemphigoid or paraneopla_s..-
;, pemphigus, urticaria, or a fixed drug eruption.
TREATMENT
Treatment of EM varies according to disea se severity. The cl inical course of an episode of EM is
variable. Complete healing of lesions may take up to 3 t o 6 w eeks and the disease may recur.
1- Identification and treatment of precipitating factors:
For example, treatment should be instituted as appropriate for management of an active viral
infection. Any drug suspected to have precipitated EM sh ould be promptly discontinued .
2- Treatment of mild EM:
Treatment o mild disease (limited oral and cutaneous involvement), should be focused on symp-
tomatic relief using [opical anti-inflammatory, anesthetic, or analgesic agents. Some of the drugs
that can be used are as follows:
_ Topical sterojd agents applied to involved areas 2 times per day.
_ Mouthwash containing equal parts of viscous lid-0caine 2%, diphenhydramine (12.5 mg/5 ml),
and a~ lumjnum hydroxide and magnesium hydroxide mixture spit, up to 4 times per day.
3- Treatment of severe EM :)
In the severe form of EM, there may be extensive lesions and inability to ingest foods. Systemic
ster.oids may be advised depending on the etiology and severity of disease. The most commonly
used steroid is prednisone [o to 60 mg per day, which is tapered over 2 to 4 week~
4- Recurrence and supportive care:
Depending on the case, recurrence of EM should be avoided by providing antiviral therapy or
irnrnunosuppressive !herapy. Continuous antiviral therapy is effective for the prevention of recur-
rent HSV-associated EM/ 'A 6-month trial of either acyclovir (400 mg twice daily), valacyclovir (500
mg twice daily), or famciclovir (250 mg twice daily) has been suggested . Supportive care should
be provided in the form of a liquid diet, intravenous fluids, electrolytes, and nutritional support.
SJs With skin and major mucous membrane involvement. (8) Widespead blisters of the chest in a child
I
I
I
I
I
I
I
(A) Typical targets of EM associated with raised oedematous papules on hand. (B) Typical targets of EM I
acrally distributed in a child with labial herpes. /

I
~I
Cutaneous manifestations
of HIV infection
an ,mmunodefic1ency virus (HIV) is the causative orga
::,ome (AIDS)
1
n sm of acquired immunodeficiency
IV Is a double stranded RNA virus belonging to the genus Lenti . . .
If
dae virus W1th1n the famifuJ Ret~v· .-
•v Ir,,
suuaucc of HIY virus;

gp120
hosl OSI !)lot Lt ra

- p 17 ITWOtx &J CJger I
~·,g;
-
HIV-RNA
p7gag r81IW'Se
b&dlc;.4.Aase
Pathoghvsioloey of HIV infection:

C04+T lymphocytes are th e main target .
Progressive and sever depletion of CD4+T lymphocyte s
--
-
Mede ot transmission;
Se-xual intercourse
lloodtransfusion
Transplacental
Contaminated needle and syringes
filmIC for disease control (CPCI sta&ID&
· of HIV ·10fection
a-.. 1:acute retroviral syndrome ( primary
,..,uup ·
.
HIV infeetion a
~ fter 2-4 weeks-- incubation period
Group 11 :asymptomatic infection (S-10 years}
"-P 111: persistent generalized lymphadenopath y
lllouP IV: symptomatic HIV infection (AIDS)
.-ouJ) IVa :AIDS related complex
•'-er > 1 month
• • as.s>l base i e
♦
• D ar-hea > 1 TPOT' 1. •

~euro og,cal otS:ease
G~u · &. ctions
Grou Ve : secondary Jn,e
Grou d : neoplastic diseases
_ mtations
CU,:1NJ?US man ---
of HN infection
d. rders
• 1,fection HIV rEJated cutaneous l50 . d
nfectious HlV related cutaneous d1sor ers
: :plastic HJV related cutaneous disorders
Infection HIV related cutaneous disorders:
Viral tnfec;tions • 1 d ome)
_µanthem of primary KfV infection {acute retroVJ~ ~n r
2-4 weeks after HN ex posure; symptoms are self-hm1ted
fever, fatigue . - h I · I · · h
Morbifliform rash, headche, lymphadenopathy, pharyngitis, art ra g1a, mya g1a, n1g t sweats,
gastrointestinaJ symptoms and oral or gen ital ulcers
llerpes simplex virus (HSV)

chronic. non-heali ng, deep ulcerations involving the perianal region , genitalia and tongue
Varicella zoster virus (VZV} :
HN-infected patients have a 7-15 times greater relative risk of developing herpes zoster
~
lV--associated roster can also be mu ltidermatomal, ulcerative, chronic, verrucous and/ or widely
disseminated w ith systemic involvement
Poxvirus:
Moiluscum contagiosum in HIV-infected patients may develop classic dome-shaped umbilicated
papufes as welJ as Jarge.r (>1 cm) c 1

.
Human papillomav;rus (HPV); oa escent and disfiguring plaques
HPV-·nduced lesions are more prevale t . H .
1
Lesions may be w idespread with mu~ ~ IV-infected individuals .
coalesce into large plaques. Pe verrucae on the face, limbs and genitalia that rnaY
In addition~ HIV-infected patients have a h. h .
sia (OH and aoaJ intraepithelia! neoptasia'fA:)~isk of developing cervical intraepitheJjaJ neof>la--
Emtcin Barr virus (EBY>;

• Oral hairy leukopJaloa is an early sign of HIV . . %of
infected indivjduaJs. infection that develops in approximately 25
• The ,u sua'l ly asymptomatic lesions a,p pear . rtons
afong the lateral aspect of the tongue . as corrugated White plaques with hair-like proJec
• Lesions have no malignant potential
. HIY related cutaneous disorders
l!]feSt!QO .
iJirial Infections
hylococcus aureus ~ . •
~P t,ylococcus aureus is the most common bacterial pathogen in patients infected with HN fo
s :litis,impetigo,cellulitis and abcesses
Bacillary angiomatosis
: Gram-negative bacilli in the genus Bartonella are responsible for this disease
• Lesions of variable size and shape seen, including red to purple 'vascular-appearing' papules or
nodules and ulcers
• Diagnosis is usually based on histologic features, i.e. vascular proliferation and numerous bacilli
visualized by Warthin-Starry staining.
• antibiotic therapy (macrolides or tetracyclines)

• a minimum of 2 months is recommended
Mycobacteria;
Cutaneous tuberculosis can develop during advanced stages of HIV infection. Erythematous pap-
ules and nodules, ulcers, verrucous plaques and deep nodules can all be observed
Syphilis :
Syphilis is caused by Treponema pallidum .
Although the classic papulosquamous secondary lesions are often seen, unusual presentations
may be observed in immunocompromised hosts, including rapidly progres.s ive noduloulcerative
forms, papular eruptions th at mimic molluscum contagiosum, and lues maligna .
Luei ma\igna is an aggressive, widespread variant of secondary syphilis with a prodrome of fever
headaches and myalgia, in association with a papulopustular eruption '
infection HIV related cutaneous disorders

Euoeal Infections
Ctostidiasis
Candidiasis is t he fungal infection most frequently enc~unt~red in association with HIV infection
Ni~ety percent of patients with AIDS will develop cand1d,as1s of the_o~opharynx
Painful fissures at the oral commissures and persistent cand1dal ,nfectlons of intertriginous zones
are also seen in HIV-\nfected individuals.
Other signs suggesting immune suppression include chronic paronychia, O¥hodvstroph
r f ractorv vaginal candid iasis. V, a d
Dermatoghvtoses;
Cutaneous involvement can be at_y.Pical in appearance, and lesions m ay be more widespread and
resi stant to therapy.
Systemic tun,a\ infections ;
O\sseminated cryptococcosis and histoplasmosis are seen most comm only, Th ese infections Pres.
ent with a w\de range of morphologies, including pustules, papulonod ules, and less often, Patch-
es, plaques and mucocutaneous ulcerations
Pneumocystis iiroveci;
Disseminated cutaneous P. jiroveci infection i~extremely ra r~ and m ay appear as molluscum con-
tagiosum-\ike papules, bluish ce\\ulitic plaques, and/or deeply seated abscesses in !!}~_external
auditory canal or naJes
intravenous t rimethoprim- sulfamethoxazole (TMP-SMX) is given fo r disseminated Pneumocystis
infection
Infection HIV related cutaneous disorders
Parasitic Infections
Leishmaniasis
Multiple o rgans may be parasitized, and, when t he skin is involved, the lesions typically present
as ulcerated nodules (up to 2 cm in diamet er) on th e extremitie s; in at ypical presentations, the
lesions are disseminated. Erosions and ulcerations of t he lips, palate and nasal mucosa can also
be seen
Infection HIV related cutaneous disorders
Ectooarasitic Infections
~;3:~~~emore sever and ext ensive in AIDS patients with involvement of atypical sites like tace
Crusted scabies is more common with advanced immunosuppresion with thick crusted plaques
on the hands and feet , subungual debris and gross nail thickening
Non infectious HIV relat ed cutaneous disorders
5eborrheic dermatitis ; . . . . .. s (uP to

rrheic dermatitis 1s the most common skin disorder to affect HIV-infected 1nd1V1dual
eb o dis seen in all stages o f t h e d.1sease .
• S'¾) d yel·
85 ~ ~~I tindings_ros!V be simil~to_those seen in the general population, i.e. erythem~:i chest
• Cl~n n the face as well as involvement of extrafacial locations such as the cen
lowish sea Ie 0
and inguinal creases.
Ll~~er, exauerated prffenldtlOflS Wtth obv1ou~ f Ctal nla
• r,v••
_..t p011ibitrtv of HIV tn f~c1.,on,
M
as lhould a ~udden ons-"' ques ca" a ·so occur and sho' !d
, . , , , lT' ,,_; \ or acut4! 'M:>n~ ~
s. ~ofSf.bor,~
fM'G 1aecttous HJV related , utaneou~disordeci

••
, The overall incidence of p~oriasis ts probably not increased ,n t he settin Of . .

hough ,ts clinical presentat1 on can be seve r. g HJV 1nfect1on, al-
~ Al\ 'anverse' dt>lribution 1nv~lv1.ng ingu in al cr eases and genit alia m ay be observed .. -
• it mav be associated w ith s1gn 1fl can t na it d ystro p hy, arthr itis.
• HIV-a5sociated psoriasis may be refractory to topical therapies,
• systemic retinoids or ph~totherapy may be required lmmunosuppressive agents such as
rn,tt1otrexate and cyclospor1n e should be avoided, if possible, in HIV-infected patients
I r J' .,/ . , , .r #'
rmo infectious l;jlV r~lated cutaneous disorders

• Ageneral,ze.d xetos,s can be see n in HIV-infected patients and may be associated with refractory
pruritus
• generalized acquired ichthyosis w it h large p late-l ike scales may develop, beginning on the legs
• P.cyrtMis rubra pilaris can also occur in conjunction w ith HIV infection .
hl'!lar pruritic eruptian of AIDS
• Papular prur1tic eruption (PPE) of AIDS is characterized by marked pruri tus and a greater in-
volvement of the extremities than the trunk or face .
• Some authors b elieve PPE represent s an exaggerated response to arthropod antigens.
• Clinically, the lesions are symmetrically distributed, non -fo llicula r papules, often with secondary
changes (e.g. ex_coriations, form ation of p ru rigo nodularis).
friioophilic folliculitis _
• Eos,nophilic folliculitis is o ne o f th e m o st characteristic and common pruritic dermatoses associ-
ated with HlV disease
• One theory i s that it is an exaggerated reaction t o M alassezia yeast or other organisms normally
present w ithin the fo llicu lar infundibula in HIV-infected patients and is a reflection of abnormal
Th2/Thl immune responses.
• fxcor,ated follicular p ap u les and rare intact pustule s are found primarily on the face and upper
trunk. Cultur es are negative and p er ip heral eosinophilia may be present .
• C04+cou nts are usually <200 cells per_cuqjc roiUim et er
lllmia'1k HIY related cutaneous disorders

• e1moys and bas~J ,ell carcinoma: .
In HIV-infected individuals, as compared with th e general. populati on, these tumors appear ear-
._ and more often 1n site~ such as the trunk and xtrem,ttes
. I h0 mas are non Hodgkin 8-cell type, Addinonal

.,..._ in immunocompetent patie nt~, mo 5t y m p d
..,encft I d
inc u e a younger ag
e of onset m ore a vance
.'
d stages and most importantly, extra-
,
h CNS 1ntestine and skin
involvement at presentation, 1n pamcular t e - ' -
. • a ules to large plaques to ulcerated nodules

~ . lkin lesions vary f rom small viotaceous Pk _P hnes ,n a p1tyrias1s rosea-like patte.rn and
llllllaly, the upper body is involved, often along s ,n don oral mucosa! surfaces, ind ud1ng the
develop on the face, an part1cular the nose, an
Ind hard palate. t he pstrointesnnal tract and lymphatics,
Molt common 5jtes of internal involvement are
nd "' tymphedema
l11d1n& to occlusion with seco a. '
Laboratory investigations:
•ELISA for the dettection of lgG antibody to envelope glycoprotien gp120
• Non-reactive results are obtained during a seronegative 'window' that usually lasts 1-3 months
after the initial infection. Thus, if HIV infection is strongly suspected, methods for detection of
viral antigens rather than anti-HIV antibodies need to be employed
• HIV p24 antigen test
• PCR for the detection of HIV nucleic acid
• CD4 count is low ,CD4/CD8 is less than one
Treatment:
• nucleoside reverse transcriptase inhibitors (2i dovudine,lamivudine)
• non-nucleoside reverse transcriptase inhibitor (oevirapine)
• Protease inhibitors ( iodjnavir)
• Fusion inhibitor
• the most important was the development of a combination drug regimen known as HAART.
Of the various HAART regimens, the most common ones comprise two nucleoside reverse
transcriptase inhibitors (NRTls) combined with either a protease inhibitor or a non-nucleoside
reverse transcriptase inhibitor (NNRTI)
Svphills
·· d. ase with great chronicity. It ls a ystemlc dise se from th onset nd cap bl of

1
ft,rlous t,sruecture in the body during lts course.
1 • . anV s
••
~ t,....
reponema pa\\idum
~ .ed b~ se ua\ : maternal-feta\ ,blood transfusion and rarely by other means of both tran -
1iss,on .h
•. , " nd getting inf-ected wit HIV
,., rt1nS aLl\\: testlng in a\\ patients
· . h syp h·1
wit 1 ·1s.
, )1''11 n
·-
slender ,he\ica\\y tight\y coiled bacteria
J
cram-negative
·c rnicroaerophilic or anaerobic
.Aerob• •
-()(ksCrew motility
"".can be tree living or parasitic
..
.5cst-known are those which cause disease: Syphilis and Lyme's disease
1reoonema pallidum:
S'plroche t-.
0 5 2 .• •
Sph1Uwn
Sprial spirochete that is mobile or spirals varies from 4 to 14 length S to 20 microns and very thin
Ol to 0.5 microns.
Can be seen on fresh primary or secondary lesions by dark-field microscopy or fluoresc nt anti-
techniques
Morpholoo
· ave axial filaments ,which are otherwise similar to bacterial flag Ila
.tt\aments enable movement of bacterium by rotating ln place
rktl Id p
penetration.:.
. th body via skin and mucous mem branes t h rough abrasions
- dur·
-T.palhdum enters e 'I'll
contact
-Also transmitted transplacentally
Dissemination; . regional lymph nodes and then throughout the..,_,._

-Travels via the lymphatic system to ~ ,_~a~
. -
blood steam '"'
-Invasion of the CNS can occur during any stage of syphilis
-The bacteria rapidly enter the lymphatic's, are widely disseminated via the bloodstream and
lodge in any organ . ma.,

-The exact infectious dose for man is not known, but in experimental animals fewer tha
gan isms are sufficient to initiate infection . n ten or-
The bacteria multiply at the initial entry site forming a chancre, a lesion characteristic f .
syphilis, after an average incubation period of 3 weeks . a prunarv
Syphilis
Acquir.t
Congenital:
Trw11111illld ttw~ 111
Tr1mmiltld ftt>111
11othlf to child In utlfO
or blood .,...n
, - - -~ ~
!a,ty(flrsl2
fH11ollle)
Pnrury
Eatlylltera
Prima~ syphilis (The Chancre l

-Incubation period is from 2-4 wees
k
-Develops
Cl . at site of contact /inocul al1on.
+,i
. 11 y: single, painless ' cl ean-based, .indur t d

, - ass1ca .
-Atypical presentations may occur. ' ,, ' a e ulcer ' with firm • raised borders.
Mostly anogenital ' but may occur at any site (t

-Non-tender regional adenopathy ongue • pharynx ' lips. fingers ' nipples ' elc---l
"' -Very infectious.

-May be darkfield positive but ser I
-Untreated' heals in several o ogically negative,
Sile of Chi DCCC weeks ' leaving a faint scar. ' ' ,,..._.,.
Genital;
Males:
• coronal sulcus.
• Glans peins,
• shaft,
(condom chan cre)
• roo1
,_,,,111es:
"''i,< (hidden).
• ce,.. .
mlnora or maJora
• t.ab1a
• Fou rchette
Clit oris.
t,rifCOital;
• pupic area
•
• perineu1rn.
• perianal.
• inner thigh.
,xsca genital:
• LiPS
• Tongue
• Fingers .
• Nipples. •
•
. painless, tenderless, firm, discrete, mobile, no tendency fo r breaking down
Reg1ona 1, ·
Rare types of ch~ncre_

• Ulcerative (mixed infection) .
• Edema only.
• painful (digita l, meata l) . .
• Multiple (on abrasions of scabies & tattoos).
Primary Syphilis- Penile

Ch......,.
dary syphilis
1he skin reaction (rash) appears after 6-8 wee ks after appea ranee of the chancre, 8-12 week from
ure to infection .
•
stage persi 5t for about 2 years can be divided to
brty 2 '
late ry stage ( 6 months from infection) .
2ry stage (after 6 months - 2 years).
dary syphilis at 6-8 weeks - diffuse
. symptoms :
H rJ;t h,•
. 3~1n pu· t1Jl,j~
-U•uJIIY dl'- ,JPP' 'dr', ,,v, n wlthr1ut tr, ,Jfn t tl
CJlnicat maott,,ian°n• t r.. t r ,,J.~ 1

r .,,, ~ 'I'
ta-:'OOJ' h()Jdd' h<• '~<;r1• t r 1r<J,J
l /
t d If ..
Generaj,ze_man_g~_ w___ • • ' ' , , ' ,
hair fall, gonerallr d lymph nod' ~nlarg m,,r,1,
suecJff, manJfeJtal1on,.
Skin rash
Gen ral chardctcr~: a'.>ymptom::Jt1C., non ;t,,hv, n cJ r1 l'' ',f!rlJf ,J ~ ,, (j J ~,,,1 ,. /'.J-r~
Early rash :
small lesions, num rou:i , , ymmetric..al with no ~p,,,,at arra ~" rr"/
Late rash :
Large, few, asymmetrical, ~how:; '-'P~cial conhgur3tion '.!e: V!r,, 311: c,,r ~ ' ~ ~,
Types of ra sh:
• Macules: small faint red spots (ro~eolar),
• Papules: ~e~J~ indurated, smooth .
• Papulo squamous: papule covered by ~cale~. Sc-<1fe-J rna / b~ profu,;,~, arr ~ ~ t v.//~ .-,1..,,... .... ~/
single scale arranged as ring (pityriasi-forrn) .
• Pustule: papu1es w ith central necrosis
• Circlnate arrangement of the lesion.
' Muc.ous membrane Jesions

• o;ffuse taryog,tis,
Diffuse oharyng,p~
Ordinary mucoio oatch~:
Smalt lesaons as s~in paputes, modified by co . ,
Slrghttv raised ~ns covered ~ Jtion of mUW1J!. tneT"'" . nes.
base~ p a ~ -4,,ar ~
0
inner auwarl
""'~""" of th ' 'Y •naJ ite me-mb rane,
e laps & checks & va I •!> ·rated
-
. Bald Pilches; g mucous me branes
Occur on the dorsum of the tr..-
~• - •~ue~red< oath
•~t@ckuJcco;Ocwrinthenasoptaa ;, _ , satedpl~sde.odcf~
lake the track left by a ~ 11
•
r, m tne form of supe fi iai .._
• <l UEC:e'S
-
■ te'
ar l'iJtl6 7
Mucocutaneous junction eruption
• Split papules at the angle of mouth
• Moist papules: indurated papules with moist grayish ~urlace.
Co.!!51ylomp
•covered lata : disc
by a grayish shaped lesion
membrane . , sessile with Ind u rat d ba e • nil t w Ith 1no1,1 11 , th l ll l .
1
11
• Hair: moth eaten alopecia 11
-
•.eteot sVP,hljls
Stagi which follow !> "'C011d(.1 ry t<.111 1( Ion· o f conclary sl,tg,:, h 11 on1 t-,lntnlt; J
1
,
1
,. , ,WfJtt,,.
sion d v lop d Ir, kin or mucoU!> 111 n, b ran an ddl r. ar, bftrotr, 'I cJottn, tit. ',,,,,,.
Only m nlf .-+... tion in form of poc,ltiv r I gy,
Tertiarv ~phiUs •
" • • ' ·t
-Skin & rr1ucous membrane (gumma), -5 y dr of lat 1 n y

-CVS , 7-10 years of latency
-Nervous system , 12-15 years of latency
Skin gumma
Circumscribed infiltration by lym phocytes, plasma cells,glant c 11 , necrosis & ndJJr 11 ,r1 ..
----""""' ~ JJ
erans
clinical picture:
Starts as subc·u taneous nod ule. The overlying the skin at first normal then blui;h t d jr, w 'it
adherent, necrosis occurs & t he lesion ulce rate.
Gummatous ulcer
• Serpiginous outline
• Punched out edges
• lndurated base
• Floor covered by yellowish necrotic sloughs heals by th in~~_aJ
• If occurs on the hair gives circumscribed clcatri.cial alopecla
Tertiary Syphilis
(,3
Tor11ue
• Gumma on the dorsum of the tongue.
• Typical gummatous ulcer.
• Diffuse interstitial glossitis.
• Necrotic areas of epithelium.
• Leukoplakja like patches.
1at '
0
~ P' rous ;nf,ftration .
•ourfltfl
, 0 rn11 tY•
ocf . k of malignancy.
' (I S
, High late
~,rd pa cosal gum ma '
tJbfflu
, atous ulcer ,
gun1m
, ioration
, per11
Mother to Child Transmission

-Infection in uter~ may ~ave serious consequences for the fetus. Rarely, 5 hilis has b
quired by transfusion of infected fresh human blood. YP een ac-
What Congenital Syphilis Means
-If a pregnant woman has syphilis and is not treated quickly, these tiny bacteria travel with her
blood to the death and spontaneous abortion or can result in the delivery of the dead baby, or
the baby can d ie w ithin several days of life.
f the baby survives, there is a high risk that this baby will have copious nasal discharge (snuffles)
packed with Treponemes and severe inflammatory reaction as a consequence, destroying n~
cartilage and bones.
The baby will likely suffer from liver and spleen enlargement and dysfunction, men1ngit1s or
meningoencephalitis, and inflammatory skin rash - all of these are symptoms of early congen1ta1
syphilis.
Coneenital Syphilis
·Passed from mother to fetus during pregnancy.
·Abnormally shaped teeth
·Nasal septum collapse.
·Skeletal abnormalities.
CongttnitaJ yphiJi • ..
Hutch.int0n'' ~ th
1 r I r,. t • ~'J'y
] i> , .., <.. ,1 ,1~rr • ,,,n
J. L... ~_,,:,r, t,Jr I <J c,~n" • ·
H,, \ ')r 1 of ', /ph, ,,

Yno 11 n ton ,,, t o ,J r, , ;.,r I ,. ·, of ·, / P' al ·
1 /p t( I C,l~n:. o r :, / '11p1orr-~ c,f ~ /0 ~ ,r t,,. D" :. t "' r~ r
v1o=>t r ·<.'•nt ~' ·rol0g r- ti.,.•, for • /pr 11·

f>lMlcat £emloat100
OrcJI tav1t I
lyrnph nod •:,
Palms c.1nd ~ol,,•.
G ·n1tcJl lcJ and p •rtdn, I , , ·a
'"Purolog1c. )Yam,n~ on
\ah<>ratory Piaeomi$
Id nt1 f1CcJtlon o f Tr ·pon,·m,J p,Jll1durr1 1n 1,-~1or ~
• DcJrkfi •Id m1lro·,cop /
• Dir .. ct fluor ,, c jn dntibod / r pc,ll1dum (Oft TP1
S rolog1c t .. ~l'..
• r ontr pon mc,I ti•; ~
• Treponernal t ,, !J
Dark field MJcrQK.Ooy

Wha to loor f or.
• T. pallidum morphology and motih y
• The sample •~ tc.1r!!n from th oozing I :.ion or from a Lt a~p1rat(:
-
Advantage:
• D fin,tlve 1m rn d1ate d iagnosis ~pec.ially in th arly ~tag~r- whr:n the:, rolog,cal te-;t~ arf !; If
negative.
Disad .1antages :
• Require~ ~pecic>llzed equ,pm •nt and an e:1p ,,, ;nc.ed mic.ro~c.op,~t
• Possible confusion v;ith oth r pathog"nic and nonpa hogr,n1c ~plroch<•tr•~
• Mu~t be p rform d immE:dictt Iv
• Possib ility of fals >-n •gatlv --~
- - -;: - .._.l!..i.. - • .::: -~- -- - - ,,,---~~

~~-:-
- - - -
.
-
u o fluorescence
t h dar e "Ct m cro copy
tt ua ,tati,e)
• NO!rttrep() l~at (qual,t ame and q uantitative)
use on o e t)-pe of serologcc test is insufficient fo r d iagnosis.
.,__ bl-.
I -
I -na.-..,,YII Serolocic Te.ts
•
I
s
• .a i.;'l? anobodV d irected against a cardiolipin-lecithin-cholest erot-antigen
• IW)t soec·fk for T. paltidum
• r ,ters us.ualty cor re late with d isease activity and results are reported quantit ative!~
• be reactive for life
-t·eponemal tests inclu de VDRL, RPR .
• URL: venereal d isease resea rch laborato r ies
• oo · rapid plasma regain t est
• Raptd and inexpensive

• Easy to perform and can be done in clinic or office
• Quantitanve
• Used to foltow respo nse to therapy
• canbe used t o evalu ate possible reinfection
• 80-100%-Sensttivity
• F~IS!;~ s_t_t,l !~ reactions m ay occur

• fal~ negative reactio n (rare )
•~ - specrfic it cannot r ule in the d isease
TtllpOnemal ~ Tests
Principies
• Measure antibody d irect ed against T. palliduro antigens
• Qualitative
• Usually reactive for life
T111pane1nal tests include Tp.HA, FTA--ABS.
• TP-HA: Treponema pallidu~ -heam aggl~tinatio~ teSt sefWJtN• _,.. tM Roost _...... .._.
• Fto.escent Treponema annbody- absorption
_ _ ...
test. the most . po- wve b years
,· a1. And r.n~ an5 i:Mlt
te5l far the cardiowvuw .. "" n.-.
a.._ lor earty latent syphilis:
• Docum ented seroconvers,on or 4-fold ,nc.rea~ in compa, :,Ori w h a ~ r ?tog ~ ~
within the year preceding the evafua o n
• Unequivocal symptoms of pri mary or sec.ondary syphilis repor1..et1 by p ;Jtlent PM 12
• Contact to an infectious case of syphrfis
• Only possible exposure occurred wrthin p~st 12 months
Patients w ith latent syphilis of unk nown duratio n should be managed clinic.ally as 'f they~ -
latent syphilis.
IBf AJMENT Of $YPHl11$ :

-Earty syphilis
• 2.4 milljon units intramuscularly once
-procaine penicillin 600,000 units intramuscularly daily for 10 days
- if the patient is unable to take penicillin , then give mouth - or do»fOICMe 100 mg X2-tor
days. 15
-Ceft ri9AOr'le , 2gm qd IM/IV for 10- 14 d is a new alternative t reatment
- 1are$mbilis
- genid 2.4 million units intramuscularly weekly for 3 weeks -:. ... ,,, ..l;.,,
-pproca ine penicillin 1.2 million units intramuscularly daily for 21 days.
-Tetracycline or erythromycin 500 mg 4 times a day - or doxycycli ne 100 mg x2-by mouth for 30
days
-Jarrisch-Herxheimer reaction
Jarisch-Herxheimer Reaction
• Self-limited reaction to anti-treponemal therapy
• Fever, malaise, nausea/vomiting; may be associated with chills and exacerbation of secondary
rash
• Occurs within 24 hours after therapy
• Not an allergic reaction to penicillin
• More frequent after treatment with penicillin and treatment of early syphilis
• Pregnant women should be informed of this possible reaction, that it may precipitate early la-
bor, and to call obstetrician if problems develop
Therapy for 5mbilis io Pceenancy

Treat with penicillin according to stage of infection.
Erythromycin is no longer an acceptable alternative drug in penicillin-allergic patients.
Patients w·h o are skin-test-reactive to penicillin should be desensitized in the hospital and treated
with penicillin .
Gonorrhea
c,use onorrhea (Neisser 1879)

•
, er g . ' .
c· gram statna gram -ve 1ntracel-
.. ,er0<COP 1 . .
• ,
d ne shape d1plococc1
.., 1 .
..o · n,yer Martin
CU tv,-..:. . .
• •dase Fermentation, fluorescent AB
• es·: 0 1
'
' •..
Mode of infection
1 D --e,et :
• sen,al 95"
• Accidental
I 2\ d,.re('t:
• rawels
• Toilets
• uncterwears
• anstnrments
incubation period
• 3-5 days (2-14d)
• ;ection spread along mucosa! surface (columnar epith)
t
Acute anterior urtheritis
Symptoms
• BuP'ling micturition
• p.-ofJse Yellowish green discharge
• it.rb;d urine
Signs
• Red oedmatous, Meatus oozing pus
• Sta,ned underwear
Untreated
• Posterior urethrios
Acute posterior urtheritis

Symptoms
• frequent m,cturition.
• Urgency, Dysuria
• Terminal hematurta
Constitut1onal manrfestatlons
Untreated: Complication
ti I diqno i of Urethral dlsch '1
I
•
•
•
(2) ~~,
• f\ n, 1,at
• in.. t tl'l'\entano,1
• C tt, t rrzatior,
• Urinary tone
• Urett,ra·l lavage
• Urin re.tentior,
• anisn1al
• Gan rrt,ea
• Chlamydia
• Mycoplasma
• Cand1da
• Trichomonas vaginalis
• Viral {wart, HSV)
• Chancre
• Non specific
Gonorrhea in females
• U rethra➔ St sq epith ➔ heal ing
• utva & vagi na ➔St sq/ acidic
• Cervix➔sou rce of infection.
• Bartholin gland ➔ chronicity
• Skene's gla nd➔ ch ronicity
• Uterus by instru ment, labour
• Faltopian tubes➔ vaginal douch
Cinicat picture
• 50% :Asymptomatic
• Uretrhra l: Dysuria, discharge, burning, freq uency
• Vulva I: Discharge, sorness
• Cervical :Discharge, heaviness
Signs
1- Purulent discharge soaking vulva, introitus, vaginal pouch
2- Edema, redness of mucosa.
3- pus com ing from urethra, cervix
Differential diagnosis of Vaginal dlsca11e

(1) Physiolo&ical
• Sexual activity
• Around m(1 n~truatlon
• PrtFJnt1nc.y, lactc1tlon
• Pub~rty
• OCP
(2 )P1tholo1lc1 I
• Non or1anl1m1I
• In trum<'ntatlon
• Forel9n body
• Chcmlcal vaglnltls
• Erosion, polyp
• N oplasm
• Organltmal
• Gonorrh ea
• Trlchomon-; vaglnalls
• Chlamydl,a
• Chlamydia gard enclla vaglnalls
• Mycoplosma
• Cand ida
• Vlral (wart, HSV)
• Chancre
• Non sp clttc
D111noat1
A M, rory
8 CK.tmin Mon
C Inv i.t11at1on~
l IJr,n • nctly~I, & cultur
1 r>1 <h•r d1r ct \m~ r&c.ultlJr
HIV I ~YJ>hil, .-rolocv
• lffl\lre f r r ht n,yd1 , mycopl•\ m
''"'
unrthlal
• Sk ntn & c~tin
• P r,ur thr,n P r,u~ thr I b C
• Salping,tis, pyo~alp,nx
• PIO
• Infertility
a-Metastatic
• Arthritis, Periarthrit,s
• Tenomyosltis
• Skin rash : maculopapular
• Myocard ltis, endocarditis
• lritis, iridocyclitis
• Meningitis
• Speticaemia
C-Accideotal
~ .,. ..
Proctitis or Conjunctivitis
Treatment
- Education
- Partner treatment
- Condoms
- Drug therapy
Ceftria)(one 250mg IM single dose.
Cefe¥4Me 500 mg oral single dose.
C'iproflo,tacif'l ➔soo mg oral single dose
Spectinomyc+n ➔2gm IM single dose
Gonorrrhea in children
• Female> male
• Acute gonococcal vulvovaginitis
• Vulva & vagina ( thin st sq epith & decreased acidity)
• Rectum could be affected
• Other glands are underdeveloped
• Direct infection or indirect
• Soreness of vulva increased by walking or urination

• Pus discharge from vagina➔soak underwear
• Dysuria, frequency.
• Edema, redness, tenderness, purulent discharge

• Prognosis➔good drainage early symptoms➔rapid healing
• Complication➔metastatic or extragenital
• 4000001U/day for 4-Sdays
"''' " "'v
d,1 t fr tt l ii t.1 l\lt•, ,,lr1t,,

I
O;i dU t t1' ,I t,, ltlt'· 11

and ljr, XJ}l'-,11, '<i.
Cl
( U g '' rdlly '"'" ' (' dlvlcl ' t ltll1 ;
1· Pr ·t ti ullr ,IU\t' , (II n11 11,11tJr b1.. 11 ,,,, IO'K, )
2• 11 ti ular JU ' , ( t> •rm 1)1 od u lion Ill ol,I, , ,,:
60%). 11
3- Po t-t ti ul'-lr Ju ' . (Ulo k. ,8(' of •,p 11,,1 t,, ,,

111
port: 30% ,( , ... m n d 'Po lti 11 probl ,,,,. : ':>%).
4- Idiopathic.
1- Pre-testicular causes
Pre-testicular causes of Inf rtility include 0 118 )nltul or
acquired diseases of th \ hypothalamu , pltultJry, or
peripher~I organs that alter th hypothalamic pltult ry ,1XbJ
Disorders of the hypothalamus I ad to hypogon dotropl, hypoaon.1dl m,
Congenital
a. Prader-Willi syndrome
b. Laurence-Moon-Biedl syndrome
c. Kallmann syndrome.
Acquired
a. CNS tumors,
b. Temporal lobe seizures, and
. antagonists).
c. Many drugs (eg, dopamine us ,nt rt J fY
d pituitary e•c.
Both pituitary insufficiency an I I or acquired
b congen ta
Pituitary failure may e~._-....-~ ~
C~nltal
. I ofJted LH d ftciency (fertll unuch)
b, I olat d FSH dcftc,erlcy
C Thala . emlJ
Acquired
Tun,or, Infarction, Radiation, Infection, or Granulomatous disease, Prolactinoma.
Primary testicular causes
Prin,ary testicular problems may be;
1- Chromosomal
Abnor1,,c1lities of the sex chromosomes
Klinefelter syndrome 47, XXY karyotype
Mixed gonadal dysgenesis (45, X0/46, XY)
Y chromosome microdeletion syndrome
Autosomal disorders
Down syndrome
Myotonic dystrophy
Bilateral anorchia (vanishing testis syndrome)
2- Nonchromosomal
► Gonadotoxic drugs,
► Radiation and chemotherapy
► Orchitis
► Trauma, or torsion.
► Sickle cell disease
► Sertoli-cell-only syndrome (germinal ce ll aplasia)
► Granu/omatous disease; Leprosy and sarcoidosis
► Excessive use of alcohol, cigarettes, caffeine, and marijuana.
Teslis
retaned
Patflll
~
AtnJir: 6lf ·1tN 13 11
end u.,-i <:I ', a IS Oosoondoo but
nolk>bobn
:>! aorotUm
~-.......,.
~
a-.-.
1'¥).ft!IIVJ
Vaicocele Cryptorchidism
Post-testicular causes of infertility include;
1- Blockage of sperm transportation through the ductal system
Congenital
Congenital blockage of the duetal system
a syndrom e
--,rtle c•
''
111"'.., -"t,rosls
~C ''
~•,-d ch as chlamydia, gono rrhea, tu berc ulosis, and
,,ttct1ons, su
I
81I ox.
sf11 P such as Inguinal or scro t al su rgery.
rraurtia, .
rn antibodies.
p.ntlsper
n deposition problems
z. serne
semen
depositim
problems
•
eJ aculatory
erect,te
PTOblem.s peni le problerts
dysfunctia,
anejaaJlatioo a
ej acula11>rydua retrograde
Obstructia, ej aculatia, hn>ospedas micropenis
Prnc;tae
gland
EFk)'atory
I
duct
Urethra Cowper·s
~
Clinical evaluation of male infertility
1. History
• Medical history .
D. b tes Obe ity Sickle ce II di sea Se, Chronic renal failure, Liver disease, Post pubertal mumps, My~
ta e , Smallpo
coplasma, ' , prostati'ti s, orchitis ' sem inal vesiculitis, and urethritis.
• Sexual history
The frequency, timin~ and methods of coitus, Lubricants which may be spermatotoxic.
• Social history
Ogarette , Alcohol and marijuana smoking lead to a decrease in sperm density, motility, and morphol-
ogy.
Excessive heat exposure from saunas, hot tubs, or the work environment may cause a temporary
decrease in sperm production.
• Medicines
Spironolactone, cyproterone, ketoconazole, and clmetidine have antiandrogenlc properties.

Tetracycline lowers testosterone levels 20%.
Nitrofurantoin depresses spermatogenesis.
Colchicine, methotrexate, phenytoin and calcium channel blockers have all be associated with infer-
tility.
• FamllV history
congenital m•dline defects, cryptorchidism
members may be a sign of a congenrta/ d , hypogonadotrop1sm and t
1sease. , es-ncufar at,.
04
A history of CF or hypogonadism should be . ,op

e 1,c,ted.
• Spinal cord injury
severe spinal cord injury may lead to anejacufation.
2• £,camination
• The testis
The testicles should be palpated individually betw h
een t e thumb and first 2 fi
The examiner should note the presence size and . ngers.
, , consistency of th t . 1
be compared w ith each other. e estic es, and the testides should
The testicular volume, normal testis is considered to b
e greater than 20 ml (orchido
meter)
---
• Epididymis
The head, body, and tail of the epididymis should be palpated
and assessed for;
; Their presence bilaterally.
, Note induration and cystic changes. (duetal obstruc-
tion).
.,. Tenderness may be due to epididymitis.
• Vas deferens
Evaluate the vas for its presence (cord like) bilaterally and
palpate along its entire length to check for defects, (segmental dysplasia, induration, nodularity, or
swelling.)
• Spermatic cord
Check patients for the presence of a varicocele, (bag of worm).
\ Al,0,1.r $ I 1 YI
SICJl>IO'• d_..
• Penis
The examination should focus on the locatio n and patency of the Uret
of meatal strictures. nraJ rT'ea L.S c""'o eP
Patients with hypospadias or epispadias may not deposit semen ap .
propnatety at t~-
•~ cerv
• Rectal examination
The prostate should be of normal size and without cysts,
induration, o r masses.
The seminal vesicles are usually not palpable.
A midline prostatic cyst or palpable seminal vesicles m ay
be due to obstruction of the ejaculatory ducts.
Secondary sexual characters

Hair d istribution, muscle mass, body contour, breast size,
wide pelvis.
3- Laboratory Studies
• Semen analysis
The semen analysis is the cornerstone of the male infertility workup.
The patient should be abstinent for 2-3 days prior to maximize sperm number and quality.
A specimen is collected by masturbation into a clean, dry, sterile container or during coitus using
special condoms (containing no spermicidal lubricants).
The sample should be processed within 1 hour, and 2-3 samples (at a minimum of 2-3 days apart)
should be evaluated because of daily variations in sperm number and quality.
Various parameters are measured, such as ejaculate volume and sperm density, quality, motility, and
morphology.
A)Volume
Normal ejaculate volume is 1.5-5 ml. A small ejaculate volume may be o bserved In patients wilh:
• Retrograde ejaculation,
• Absence of the vas deferens or seminal vesicles,
• Ductal obstruction,
th
~ .
~ An d '1 nt J , \ t
• }! t u
~ QU'lltY (llquifac:.t1on)
~ f t l ltia1'v
n \5 n c.oa ulum th l1ou fie,~ In
t/f"' ,n0t1llty
~ t, de rib d a lh P r <'nl of \ P"rm prp ~n, WI h f\ II
'➔rrl
t1fllY f'.a ~lr rn,1- ''"j r1
r,lO r11sl n,otllllV I defi n d a m r" I ha n r O'A, of ;p rm h, "ng for pr r -,r,.n
Nilf pld forward pr gr~~ lon 1
t,.avl"8 ra
henotoospermla
~ 'Iii of sp rm having forward progr \' ion.
< 25 %of sperm having rapid forward progre~ slon
O)Sperm density
Normal sperm density Is gredt r thanl!:>- 20 million sp rm/ml and great r than S0-60 m,tho" tc,•
sperm. 1
Ollgospermla Is d fin ed a!> the sp rm count fewer than 15 million ~p rm/ml, sev re ohgo~~nfna ,~
less than 5 mllllon/ml, Azoospcrmla i~ d fined as no sperm pr s nt w1th1n ejaculate.
To verify azoo perm la, the semen should be centrifuged and evaluated und'er a fight microscope for
the presence of sperm .
Patients with azoospermla should have a post-ejaculatory ur1ne sample analyzed for sperm, shoold
be evaluated for ejaculatory duct obstruction, and should undergo a hormonal evaluanon
E)Sperm morphology
The head, acrosome, mid piece, and tail of the spermatozoa are analyzed. At least 200 sperm are
analyzed. More than 30% of sperm should be normal. Teratospermia is defined as less than 30% of
sperms are of normal morphology.
Ht1d -
:J-- Atr osomt
Jlpcs2a M ■ ,,-c W
T1t1 -
Mt~
G dSi I ■ I •• &I
♦An Increased
Infection
number of white
bl 00
d cells In the ~emen may be ob5erved in pa~ts With infiecll<M
or ,inflammatory proces5es. (Leucospermla).
55
• Hormonal 1naly l and prolact1n.
H LH testosterone,
Which usually lncludes FS , ' . h pothalamlc, pituitclry, or testtcutar ~Se,.,.
Abnormalities mav be a 5 Ign f a primary Y
°
• Telttcular blop1y men with a normal-filed 1estts and normal fl..cletp on
d in azoo~permIc
Tttt1cular biopsy is lndicate f ductal obstruction.
hot st tet to evaluate or
Normal Semen Parameters
men Parameters
Normal Values
Semen Parameter
1.5-5 ml / ejaculate
Volume
Semen quality (liquefaction) 5-25 minutes
> 15-20 million sperm/ml
Sperm density
SO% with forward progression
Sperm motility
Or 25% with rapid forward progression
l
i L.~Sp~e~r:.,:,m,:,:,,,:,m~o~rp~h~o~l~o~gy~===~ >;;,.;3;,;0;,,;%
;;o,.;;o~f,.;;s~p;,,;;e;,;,,r,;,,,m=sh=o
=u=ld=be=n=o=r,,,,,m=a=l==~J
Male infertility diagnosis and treatment strategies
History, Clinical Ex. And Investigations
Semen analysis
.. Normal
Subnormal
----1~---
Female partner Ex.
Hormonal assay
Low Normal
Normogonadotroph ic HypergonadotroJ
Hypogonadotroph ic
Infertile male hypogonadisrr
Hypogonadism
• r - - - - - -' •:...,__
Human gonadotrophins No availabletreatr
Etiologic treatment
Non etiologic treatment (hormonal)
Assisted reproductive techniques
Hormonal treatment of infertility
GnRH /Gonadoc,apin
releo,ing hormone)
therapy
-
~;._J HlghProlactin
- (Prolodnomo}
Gonadotrop1n replacement. lH FSH

{LHor/and FSH)
T
n
DHT E
Etiologic treatment
► Antibiotics and anti-inflammatory drugs for adnexal infections.
► High ligation varicocelectomy.
► Corrective anastomosis for obstructed ca ses.
I
ted reproduction t chniqu s
With low semen parameters

1· Artificial insemination
'
~rtilization (IVF)
2- ln Vitro~
I
Incubation
In obstructed azoospermia
Sperm retrieval techniques
Testicular sperm aspiration (TESA)

Testicular sperm extraction (TESE)
3- lntraCytoplasmic Sperm Injection (ICSI)
Incubation
It
M latl~f11 ttl
I11 l•v f•Jtt ti •••
'
FIRllr (1) Ar,utotrty of tt, t, rll .
'•"u ,f
,1111111111111111
( Gl!!l ll!t\11
'"'' "'' .,.,..,~,m

l, r•''
'"''' ul1111,
I
( I ,-..:.-.n•••"
I I , I' ,_*"'.,.. """"
'~
Flgur (2) Moleculor control of smooth muscl contr ctton nd retnadon
t1fj ,,I a, I ...
frtct111 dysfunction (ED) affects 50% of men older than 40 years, 1xerttn1 substantfat eff«b
on qu1llty of 11ft Thi& common probl m Is complex nnd lnvolv multiple pathways. Peoite
•rect1on\ are produc d by an Int gration of phy~lologlc procc~se~ involving the ~ntral nervOU$,
Pt'ripherdl nervous, hormonr.l, ond vascular syst ms.
Factors mediat1n1 contraction and relaxation

~ t9&ru
Pin' T
of contraction of cavernoul i mooth mUida determinn the functioN' ..... of IN
nhA a,
fa 1t9. he balance between contraction and relaxat1on Is controlled by central and per,.,,_,
ctor~that involve many transmitters and transmi tte r sy~tems.
ftcto" th at mediate contraction In the pents include noradrenaline, endothehn-l, neur~ptide Y, ,._
,1..1 °t ~.
Dr<>itan Id angiotensin II and others not yet identified. Factor, that mediate relautton__...,
1
'-' 0 lne I I , ' .
indude ac.f'tt Ode
d _,.", cyclase a1;;,,..._,,. Pi'Jr ,
' _ tr c ox1d..!__(~Q), va~oactive intestinal polypeptide, p1tu1tary a e"'''
"dullin, adc no~1 n tr1phO\f>~1 , f'J , nil ,d rlO! r r,,,,,......
relat d pepttde, ()dr nom ...in
calc1tonln gene-
oxide
N1tr1cIIIO
pathwav (figure 2)
wav I or , r, ttcal 1mportanc.e 111
th phys1olog1c, 1nduc..t1on of , , •
s a rcsu It of cxp cnmr-ntJ I •n d c I1nir" I w or, , h ~ o,,,., ,
•'>''
ThP d,u, l .
1~~• ,, , ,,,.,'
, , •,
T1' p3111t ED were dcvelopPd a I d corporal ~rnooth m l1' c.l" c,.,#lf~ of t, ,. P' r i, .,, . , ,
used to trea s the vascu af an • • • "•
I
trabeculae, resultingrein_a~
from nerve endings a erect1Qn , th,,., (NOS) NOS pldys man, rol<~, r<Jng1ng 1 frum h'>m,,,,. , .
--- rurne NO syn ° · h d 1
OS 0 ' ,., '
- produced by the en~, d t subtypes have been 1d nn ' nN , ,rf .,, drd (t'J'J':, ,,~
I 1at1on. To a e, 3 I Th , I • , ' t
to 1, no menc uh H ,, dt·nv~d t,,,rr ,, ,
Noimmune
S system regu NOSl ,NOSl, and NOS3, respec11ve y.
are produced by the genes . neuronal t1ssu e (nNOS), immunoac~vated rnacroph08" cr ll iln,.., (illo:
sources of the original isolates. S) Th subtypes are no t, how ever, hm ltr•d to tht:! n-,,,u -~ from wh,,f ';
and vascular endotheltum (eNO . e t. I
were first isolated. 'd ti·on of L-arginine to NO and L-cltrullint>. Endogenou':> bfoc.k,,,, f
01
inside the cell, catalyzes . Thea gaseous NO that Is produ ce d acts as a n c uro tran,,m,ttl r
the ox1
. ntified ,, o
P•r,
Nos
this pathway have been ,de f i·t . only 5 seconds. NO may act w1th1n th e cell or d,ffu >P and ,nt"'
b. ·c hal - , e ,s r.,,
crine messenger. Its 101og• e cor ora cavernpsa, NO activates guanvlate cyclase, whteh In turn Inc,"• '
with nearby target cells. In th h fe
(cGMPf. Relaxation of va scular smooth muscles by cGMP l• ad~ lo
es cydie-guanosine monophosp a
.
vasodilation . he
and increased focusflow.
blood of several approaches to the treatment of ED. lnh1b1tors
. . o f phoapho.
Alteratton of N_O lev~ls ,s _t h d ze cGMP types, provided the ba sis for the develo pm ent of the P0£S
11
I
diesterase, which pr1mar Y Y ro Y
inhibitors.
Normal
. erectile
. process
to tactile .
ol(acto"' and visuJ!!,snmuh. . . to achieve
The ab1hty . and maintain a
Erecttons. occurd ,n response
d t only on_ the - ~~
- , penile portion of the process but also on the status of the pf:riph-
full erectton epen • t s no
·ty of the vascula r supply and biochemical , events w1th1
. .n the corpora: The auto-
.
era I nerves, t hes1nstem
egr1 ·s ·,nvolved in erection o,rgasm, and tumescence. The parasympathetic . nervous
nom1c nervous
system y involved
is primarily 1
in sustaining and' mamtam1ng
. . . an erectton,. . IS
wh1Ch . denved
. from s~ 51 ne,y~
roots. stimulation causes the release of neurotransmitters from cave rn osal nerve endings and relaxation
-sexual
factors from endothelial cells lining the sinusoids/ NOS produces NO from L-arginine, and this, in turn,
produces other muscle-relaxing chemicals, such as cGMP and cyclic adenosine monophosphate (cAMP),
which work via calcium channel and protein kinase mechanisms (see the image below) . This results in
the relaxation of smooth muscle in the arteries and arterioles that supply the erectile tissue, producing a
dramatic increase in penile blood flow/Relaxation of the sinusoidal smooth muscle increases its compfi-
ance, facilitating rapid filling and expansion / The venules beneath
r the rigid tun ica albuginea are com-
pressed, resulting in near-total occlusion of venous outflow,lniese events produce an-erection with an
intracavemosal pressure of 100 mm Hg.

Additional sexual stimulation initiates the bulboc;werno_!!s reflJ!x / The ischiocavernous muscles force-
fully compress the base of the blood-filled corpora cavernosa, and the penis reaches full erection and
hardness when intracavernosal pressure reaches"200 mm Hg or more. At this pressure, both inflow and
outflow of blood temporarily cease. J
. (,J
Oetumescence results from ~essa11on of neurotral]}mitter release, breakdown of second messeoger> by
phosphodiesterase, and sympathetic nerve excitation during ejaculation Contraction of the trabecular
smooth muscle reopens the venous channels, allowing the blood to be expelled and thereby resulting in
flacc1d1ty.
~:;~:::~~~::~:;igger th ese vascular changes: psych~enic, reflexogenic and centrally originated
Psychogenic
travel erections
from the occur through
spinal erection centresstimulato
(Tll-LZ ~::~h~ay: (e.g._, sound, smell, s_ight and touch) that
2 54
tion from the medial ere-91>tic area and induce a dopamrnerll,!£ m,oanon of ere<·
..-.en•C e
rections, induced by direct genital ,t,mul-'ti t, ' n•'
"'
c:)
~I\ H l n,. . t '
-11v-- nte~ and direct me sages to the aut nom,c nucl I wt, h •.~£ ~ ;g:..:.a.. I\ ' ll ' I ' t I ,I
fl'S' . .. ,, ce . I _ _. • . • fp •n• "'!'\''' 1 "r~
rt'-\'0 -th wQIIII!. spena '"v-u ,nJunes. t ,,
~ erections, inltlated 1n the pontine reticular forrnalJon 3110 arnyod 1
..~-
...rt"'°'d1,re believe d to be ca usedbya relative decrea e 1r, syn'l 1 c3tl, t, "',l,,r . ·~ r c t\t l1r 1t1 '''M
,r,1-il Ill 111
1 11
1eeP an . A-ii centers. t,n w ·' ilt,,r ,, , ,\\t 11
s pro-ere\..\' e
of tht
Table 1: Cc1u e of er~ tile dy f,1n(tion

Cau~es [ .1mpl ·s
--------.....;;_.------------=-=;;;:...;_--
Aging
Ps)'Chologica I disor~rs Depress! n, anx1 't}(
Neurol03ica I disorders Cerebral dis ,a~2 . ~p111al t>I d lr,jur , IJll111
diSt'ase, periphet al 11 1nr'l)ath~,, J1ll c~,,1rf , I
nerve ,n JU ry
Hormonal disorders Hypogona<lism, 11 perprtJl.i i nt'1n1a,
1
ldepresses libido) t1yper- or h}pothyro1d1s111, u hi11~ ,
synclrome. ddison' r. dise,,
Vascular Ath ro clero ls, is h,•mic IYJ,1rt di~oc1 ,
- disorders periph rJI vascula, d1 t > ~• 1, vi>nc>u
incompetPnce, cav •rnosJ I d1, 01dr-1rr.
MediCJtions Antihypt1tensi,,r• , ant1d,•pt• • sants
f depresse, libidoJ, 5trrJJ?,en' ~rirl nt I-
androgens fdepresse~ libldoi, dl~oxin
,\.larij~ana use, alcohol alJus1.J, nar r,tlr9
use, cigarette smoking
Othef d isea.ses Diabetes mellitus, rt11 I fa.llure,
- -
hyperlipidemla, hypertension, chr,,n,,
ob~tructive _euJmo!!ary d, • -se
C:agrostic approach
• JJ.JSt a decade or 2 ago, the routine eva,luation of erectil~ dysfunction c.onsl~ted of an e.11h.1u•.1-1v_ blo
de, ..ca• screening panel, psyc.hologjcal a.s.sessments and occa:;io nal vas!.Ular ,.stln~. rhl· apprr a, 11
.was j'ustJfied as reasonable at the time, because the treatment options avallabl~ w ~tP lrtVRi~lvct
00 1
• COtltrast, wrrent recommendations for management rely on hlst ory-ta~ lrtg an•J ba;J, 9., t 1 htt
tests..
medicatt9ns the patient may be taking should be reviewed.
me<fttal ilfnesses an d • "Y -
• c~t nent of generalized m,e dical illness and may represent the Initial
dysfunction ts often a compo
• £~ rd c I r disease or diJbetes.
peestntition of ca '9YI rt 'n rev rsible or modifiable risk factors, such as tobacco use or lnad-
• TM his.tOfV mav .,~ ~~•I ce a•
..... ditMte control.
Examination ld focus on the vascular, neurological and endocrine systems.

nw ph-..c•• t. m•n non hou - - . - .
note-d and th..e penis sh~ft e-xamined to rule out a penile deformity (Peyronie's di~
. .......,,4 kA
~~ ~~"' '"~
...
ubc,ratory investiptions
• ~ ~ to ~boratory ,nvesngations, recommendations vary and investigations should follow
sU\Pkaon of specific disorders.
• Al< and serwn awcose may be measured to detect occult diabetes, and a lipid screen
pc,lutnM!!d to the presence of dyslipidemia.
cs c ntro\.-ersial; however, it is reasonable to measure t estosterone and prolactin
• Y.f"Ee'l
erectile dysfunctJon combined with loss of libido.
~t~
- or hypothyroidism is suspected should have their thyroid-stimutating hor-
• ~m-
1ei,,e1
Spaicllctests
ba:,sce~ and rigidity assessment
•
•
• -
•
tie dysfunction
•
•
•
•
•
.....
. .....
•
. o....,.
• De,gf - -
Treatment Strategy for erectile dysfunction
fht phys,cian should start to draw a pla n <or t erapy f 0r ~'1<: sr.,<er tflr c,:..,..il-',f ......~
mind
• patient's age.
• Patient generat health status.
• Reaction of the partner and h€r involvement in dee s10 rria1<1~
• Reasonable goal of therapy
• cost effectiveness and risk beneflt ratio
oral pharmacotherapy
. Hormonal therapy:
• Androgen repla cement therapy.
• Prolactin lowering drugs.
- Yoh1mbine:
• Central a2- adrenoceptor blocker.
• Peripheral a2- adrenoceptor blocker in penile arteries .
-Apomorphine _r ( ~-- ' r - ,
• Dopamin e D1, D2 agonist.

• Sublingual formulation 2-3 mg
&e S Jnhlbitors (Slldinafil, Tadalall,
Contraindications:
Organic Nitrites:
Severe cardiac disease
Ritinitis pigmentosa
Incorrect use ➔ treatment failure
Patients should b e advised that:
• Sexual stimulatio n is needed
• A number of drug t rials m ay be required
• Sildenafil may be taken with f ood but onset of action may be de1ayed
• Testosterone augm entatio n sh ould b e prescri bed in documented hypogonadrs.,11-
• Risk factor modrfication may improve t reatm ent outcomes
• Follow-up visits are essential
Manacemeot of PDE inhibitors non-responders

• Recouncelling.
• Treatment of concomitant diseases.
• Treatment of hypogonadlsm .
• Higher doses.
• Shifting to other PDE-5 inhibitor.
• Dally dosing
Dally dpsi111
• Daily dosing is a successful option in sexu al rehabilitation in nerve sparing PfOSt~lOf•'f.
• Successful optio·n for no n-respo nders. . . fur ooa ..,i"d c,nj(
• It Is speculated t hat chronic dally dosing could result in improvement ,n eodotneu .,c
cavernous bodies, but also the whole vascular syst em.
_ Oth,ee:s (Tra,oclone Phentolamine) .
•
• PGEl
•
• I
Thee apy Alprostadii - MUSE

, - . lnjKtion Thc>apy (Papaverine, Prostaglandin El, Bimix, Trimix)
• haiwe failed other therap.ies

• · s disease
• · 1eoeptor agunist. Metanotan II and its active metabolite under investigations for 10
•
• -S AvanafiJ .
• I o<ide releasing POE-5 inhibitor:
• avtivators
•
• (ieoe

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HOW TO DEAL WITH

. h largest organ of the body since:

A) Complaint: may be disfigurement, itching or burning sensation.

1- Examination from distance: to comment of skin lesion distribution

II) Examination of skin appendages:

Examination of the skin

Grouped Distribution &

SJ Linear distribution: \ ['l)v'\Lwfl.U)v,.~"~u.

Zosteriform Distribution Follicular Distribution

1) Well defined border: 2) Ill defined border:

Lesion with well defined border

Lesion with circinate border

--__;,-~~-...- Types of Skin lesions<----------..;

Skin lesions may be: ~ --~~----

tia .: 'n lesions are:

Macules and Patches

Umbillcated Papule Verrucous Papule

3) Nodule: . . I . ·th dermal extension. Usually better felt than seen.

Tense Bulla Flaccid Bulla Vesicle

1) Pustule= . 2) Scales: It ls dry surface dllC to ~bnor,nJI k r tin,

a) Fine branny: ·~ b) Greasy:

Fine branny scales

c) Lamellar: d) Fish scales:

Lamellar scales Fish scales

Colfarette scares Ho~ny(Keratotic)Sc.a1',s

It is a descriptive term of 3 criteria:

A) Black head: dome shaped papule, fol-

Black head comedone White head comedone

It is specifi c to erythema multif .

Herpes iris Target lesion

Examination of Mucus Membranes

N ail Dystrophy PJrorlyct,11..1 Nufl

Patchy Clcatrlcal Alopecia DiffuM hair fal

2 ~k/r I 11( I I lf)J)ll1H .

Hyphae of Dermatophytes Scrapping of skin by scalpel

1- Horny layer (stratum coneum): multiple layers

2- Granular cell layer (stratum granulosum):

3- Prickle cell layer (stratum spinosum): 3-5 lay-

4- Basal cell layer (stratum basale): single raw of

The dermis consists of two layers:

■ Never do any harrr,~ do not use irritant and sensitizers

■ Change the therapy as the response indicates

Effects of Locally Applied Drugs:I~::_~::::_~::__ ~

■ Antibacterial topical medications: destroy or inhibit bacteria. Example: genta .

Finger tip unit

How to assess the quantity of topical medications r a certain body surface

Duration of Application Frequency of Application

• It varies in its severity and improves in sunny weather.

• H&E: Marked/ massive compact orthohyperkeratosis intact granular cell layer

• sec-s CC- less freq uent MM most tumors occur on H&N

• ocular affection : photophob1a-corneal o pacity -ectropion and neoplasms tc

• Severe keratitis, leading to corneal opacification and vasculariza ·o

cancers at a young age

• All windows should be covered with UV-resistant film

. ( idermolysis bullosa simplex) .

E~iderm~lysis bullosa with pyloric atresia: severe generalized blistering associated

Junctional epidermolysis bullosa, 9.e~~~alize~ intermediate . . .

NEUROFIBROMATOSIS (VON RECKLINGHAUSEN'S DISEASE)

• Type 2 neuroftbromatosis (NF-2), central or acoustic neurofibromatosis, is distinguished by

,f _.,.,. "' 1r1 1c,l