This document discusses different types of skin conditions including erythema, telangiectases, urticaria, and purpura. It provides detailed information on each condition including causes, clinical features, types, management, and differential diagnoses. Henoch–Schönlein purpura is mentioned as a type of purpura that mainly affects children and is associated with IgA vasculitis.

1. * Erythema
* TELANGIECTASES
* Urticaria
* PURPURA
HENOCH – SCHÖNLEIN PURPURA
By: Dr. Faraedon Kaftan
College of Medicine
Sulaimani University
2011 - 2012

2. 1. Erythema:
* is redness of the skin due to dilatation & an increase
blood within the small skin blood vessels and leads
to hyperemia in specific area of the skin in response
to endogenous or exogenous factors
* Fades on pressure
Flushing:
is Transient Erythema usually of the face
Blushing: is Flushing caused by Emotional Factors
Erythema: is of 2 types
1- Localized erythema
2- Diffuse (Generalized) erythema

3. 1- Localized erythematous eruptions are due to:
a. Trauma, friction & sweating→ (Erythema intertrigo)
b. Heat: (Erythema-Ab-Igni), (Erythema caloricum)
c. Chemical irritants
d. Light: exposure to sun: (Erythema solare)
e. Cold: Erythema pernio:(affects the acral parts )
f. Neoplasm
g. Reticulosis.
h. Collagen diseases
i. Urticaria
j. Pemphigoid (Pd)
k. Liver cirrhosis:→ (Erythema palmare)
Other types of erythema may occur in response to
certain types of food, drugs, vaccines, stress,
gastro-intestinal disturbances and vasomotor
liability.

4. 1- Localized erythema
Erythema intertrigo: Erythema Ab Igne:
friction & sweating (heat)
Erythema solare : Erythema palmare Erythema pernio
(exposure to sun: Light)

5. 2- Diffuse erythematous eruptions due to systemic factors.
a. Drugs
b. Virus infection
c. Bacterial infections
d. Pregnancy.
Types of Diffuse (Generalized) erythema
 E. Toxicum Neonatorum (ETN):(Toxic E. of the newborn)
 Exanthematous E. (EE)
 E. Infectiosum (EI): (Fifth disease):(Margarine disease)
 E. Annulare Centrifugum (EAC)
 E. Chronicum Migrans
 Erythema due to drug reaction (Corticosteroids)
 E. Multiforme (EM): (E. exudativum)
 E. Nodosum (EN)
 Erythroderma
 E. Annulare Rheumaticum
 E. Elevatum Diutinum (EED)

6. E. Toxicum Neonatorum (ETN):
(Toxic E. of the newborn)
 appears in the 1st 3 or 4 days of life & disappears by the 2nd wk
 erythematous blotchy macules, papules or pustules
 mainly on the trunk , face and proximal parts of the limbs
 The papules may be surmounted by small pustules, 2-4 mm
 In more severe cases, urticarial papules arise within the erythematous
areas, on the back and buttocks.
 The infant’s general health is good
 usually the lesions fade away without treatment .
D. D. Toxic erythema of the newborn:
1. Pustular miliaria,
2. Herpes simplex virus infection .
3. Incontinentia pigmenti .
4. Neonatal pustular pyoderma

7. Exanthematous E. (EE): (Viral Exanthem)
* Erythema is variably generalized and specific
* Viral and bacterial diseases are common causes in infants
& children
* Types: Measles, erythema infectiosum (fifth disease), roseola
and scarlet fever

8. E. Infectiosum (EI):
(Fifth disease):
(Margarine disease)
- Viral epidemic types of
generalized erythema, slightly
infectious in spring & summer
- The erythema appears on the
proximal parts of the extremities,
the face (butterfly appearance)
and spread to cover the entire skin
surface.
- Itching is severe,
- on the fifth day erythema
regresses & itching becomes less.

9. Erythema Annulare Centrifugum

10. ERYTHEMA CHRONICUM MIGRANS /
LYME DISEASE

11. Erythema due to drug reaction (Corticosteroids)
generalized red papular lesions without comedones

12. E M : Erythema Multiformis
 is a common recurrent distinctive skin reaction
 incidence is in the 2nd & 3rd decades of life
 characterized by lesions of the
1- Face 2- Hands & 3- Feet.

13. EM

14. Causes of EM:
1- Virus infections: H. S. (frequently), atypical
pneumonia, Mycoplasma infection, Lymphogranuloma
ingunale
(LGI), psittacosis, Variola, Vaccinia, Hepatitis, Milker’s
nodules, Orf, Infectious mononucleosis (IM), Mumps &
Poliomyelitis
2- Histoplasmosis
3- Bacterial infections
4- X- ray therapy
5- LE
6- P. A. N. (Polyarteritis nodosa)
7- Wegener’s granulomatosis
8- Carcinoma, Reticulosis & Leukemia
9- Pregnancy, premenstrual.
10- Drug reactions.
11- Sarcoidosis
12- Contact reactions
13- Unknown.

15. Clinical features of EM:
1- Papular form:
2- Vesiculo- bullous form:
3- Sever bullous form
1- Papular form:
* dull red, flat maculo- papules
* reach a diameter of 1-2 cm in 48hs.
* IRIS or (target lesion): is a characteristic sign
A- The periphery of the papules remains red
B- The centre becomes cyanotic or purpuric
* These lesions fade in 1-2 wks
* The sites affected are the:
1- Face
2- Backs of the hands, palms, wrists, forearms & elbows
3- Feet & Knees

16. 2- Vesiculo- bullous form:
* is intermediate in severity between:
a. The papular type &
b. Sever bullous type.
* MMs are severely involved
3- Sever bullous form
(Stevens – Johnson syndrome):
* is a very characteristic &
sever type of E. M.
* onset is usually sudden
* numerous organs are affected:
oral cavity, eyes, skin,
male genitalia, anal mm,
renal & Respiratory systems

17. SJS: Stevens Johnson’s Syndrome:
Severe Bullous EM + Organs & mms involvement

18. D.D. of EM:
1. Drug eruption
2. L.E.: Lupus Erythematosus
3. Pemphigoid
4. TEN: (Toxic Epidermal Necrolysis)
Treatment:
*- In the papular type: Symptomatic
*- In sever E.M.:
1- Prednisolone (small) 30- 60mg daily &
decreasing over a period of 2-4 wks.
2- Systemic antibiotic
to prevent 2ndary infections
3- Zovirax tablet or syrup:
when the cause is H. simplex

19. E. Nodosum (EN)
 most cases appear between 20 and 30 years of age
 3-6 times more frequently in women than in men
 erythema nodosum is seen in younger patients than
erythema induratum of Bazin.
 The typical eruption is quite characteristic and consists of:
a sudden onset of symmetrical, tender (painful),
erythematous, warm nodules and raised plaques usually
located on the shins, ankles and knees.
 The eruption lasts from 3 to 6 weeks
Causes:
 3 S (streptococcal, Sulfa, Sarcoidosis) + Tb

20. The nodules in E. Nodosum (EN):
 Are bilateral 1 to 5 cm or more in diameter
 may become confluent resulting in erythematous plaques
 May involve thighs, extensor aspects of the arms, neck, and
even the face.
 At first, show a bright red color and are raised above the
skin. Within a few days, they become flat, with a livid red or
purplish color. Finally, they exhibit a yellow or greenish
appearance often taking on the look of a deep bruise,
which is quite characteristic of erythema nodosum and allows a
specific diagnosis in late stage lesions.
 Ulceration is never seen & heal without atrophy or scarring.
Treatment
 Treatment of underlying associated condition
 Usually, nodules regress spontaneously within a few weeks,
 bed rest is often sufficient treatment.
 Aspirin and nonsteroidal anti-inflammatory drugs

21. Erythroderma
 Is intense and usually widespread reddening of the skin due to
inflammatory skin disease often precedes or is associated with
exfoliation (skin peeling off in scales or layers) known as exfoliative
dermatitis (ED).
Causes:
 Dermatitis especially atopic dermatitis, contact dermatitis
(allergic or irritant) and stasis dermatitis (gravitational eczema) and in
babies,seborrhoeic dermatitis,
 Psoriasis
 Pityriasis rubra pilaris
 Pemphigus and bullous pemphigoid
 Cutaneous T-cell lymphoma (Sezary syndrome)
 Drugs….
 idiopathic called: red man syndrome
may also be a symptom or sign of a systemic disease:
 Internal malignancies eg Ca. of rectum, lung, fallopian tubes, colon
 Haematological malignancies eg lymphoma, leukaemia
 Graft vs Host disease
 HIV infection

22. Management:
 Discontinue all unnecessary medications
 Monitor fluid balance and body temperature
 Maintain skin moisture with wet wraps, other types of wet
dressings, emollients and mild topical steroids
 Antibiotics if secondary infection is present
 Antihistamines for severe itch
 If a cause can be identified then specific treatment should be started
eg topical steroids for atopic dermatitis; acitretin or methotrexate for
psoriasis.
prognosis?
 depends on the underlying disease process. If the cause can be removed
or corrected then prognosis is generally very good.

23. 2. Telangiectasia:
are Permanently Dilated Skin Small Vessels
* Fades on pressure
* Appears on the skin & mms as a small, dull red
linear, stellate or punctate markings

24. Causes of Telangiectasia:
1- Primary Telangiectasia:
Vascular (Cherry angioma)→
Angioma & Angiokeratoma
Angiokeratoma Circumscriptum→
Ataxia Telangiectasia
HHT: Hereditary Hemorrhagic T.

25. Spider angioma

26. 2- Secondary Telangiectasia:
• Prolong vasodilatation as in:
- Rosacea
- Varicose Veins (V Vs)
• Raynaud’s disease.
• XP (Xeroderma pigmentosa)
• Prolong exposure to sunlight or tar
• Post – traumatic
• Radio dermatitis
• Atrophy e.g.: topical Cs.
• L.E., Dermatomyositis, Scleroderma &
Morphea.
• Urticaria Pigmentosa (mastocytosis)

27. 3. URTICARIA: Nettle rash or Hives
 Is an eruption of Transient Erythematous or
edematous swelling of the Dermis or S.C.
tissues for less than 48hs
 Fades on pressure
 While the similar but larger swellings
of the S.C. tissues are called:
- Angioedema or (Angioneurotic edema)
- Quincke’s edema or (Giant Urticaria)
* Urticaria & Angioedema are often associated

28. * Basic mechanism of Urticaria is Local permeability
of capillaries & small venules by Mediators
* Mediators are large No. of substances present in
the body, they are:
1- Histamine: is most important mediator & derived
from mast cells
2- Kinins
3- Prostaglandin
4- Leukotriens
5- Complement
6- Others (but not serotonin in man)
Clinically there are 3 forms of Urticaria:
1- Ordinary Urticarias: about 80% (last few hours)
2- Physical Urticarias: 20% (last few minutes)
3- Herediatory Angioedema
* Sometimes Urticaria is classified in to:
1- Acute Urticaria: less than 1.5 months
2- Chronic Urticaria: more than 1.5 months

29. Provoking causes of Urticaria:
1. Drugs:
A- Histamine – releasing drugs as:
* Codine, Curare, Dextran, Morphine & Polymyxin
B- Drugs for unknown reason aggravate URTICARIA &
Asthma:
* Salicylates, Indomethacin & Benzoates
2- Foods: eggs, nuts, chocolate, fish& shellfish &
tomatoes
3- Food additives: as
a. The yellow azo dye tartarazine b. Benzoate
4- Inhalants: as
a. Grass pollens, b. Mould spores, c. Animal
dander’s & d. House dust

30. 5- Infections & Infestations.
6- Psychological factors:
7- General medical disorder as
a. L. E. b. Reticulosis c. Polycythemia
d. Carcinoma e. macroglobulinaemia
Cl fs of Urticaria:
The lesions are: Weals(Wheals)
* may occur at any site,
* of various sizes,
* few or numerous,
* characteristically intently itching,
* have a white palpable centre of edema with a
variable halo of erythema

31. * Weals are:round, irregular, annular or serpiginous
* Weals last for a few hours in Ordinary Urticaria But in
physical Urticaria Weals last for a few minutes only
Clinical patterns of Physical Urticarias: are AC DC PSH
1- Aquagenic Urticaria (Water)
2- Cold Urticaria
3- Dermographism
4- Cholinergic Urticaria
5- Pressure Urticaria
6- Solar Urticaria (Sun)
7- Heat Urticaria
In general, Spontaneous improvement occurs even
in the absence of Diagnosis or Treatment
D.D. of Urticaria: PU (Insect bites), Pemphigoid, D.H., Atopic
Eczema, Toxic erythema, E. M., Henoch- SchÖenlien
Purpura or Follicular mucinosis

32. Treatment of Urticaria:
1- Careful assessment of the cause
2- Avoidance of salicylates & food additives
3- Anti-candidia regime: Nystatin tablets
4- Anti Histamines
5- Systemic Corticosteroids (Cs):
6- S.C. Adrenaline injection: in sever acute Urticaria
7- Psychotherapy & sedative or tranquilizing
drugs in psychogenic Urticarias

33. 4. Purpura:
- is longlasting appearance of red or purple discolorations on
the skin or mms due to Extravasations of RBCs
- is normally distinguished from Erythema when pressure by
finger or Diascopy fails to blanch the lesion (does not fade
on pressure)
- Is a physical sign with many causes

34. * Extravasated blood is usually broken down to
various other pigments derived from haem
within 2 or 3wks
* in 2 or 3 wks the red color of the blood
changes to: purple, orange, brown, blue or
green which occur in many purpuric lesions
- Normal platelet count is:
150.000- 400.000 per microlitre of blood
- Purpura due to Thrombocytopenic
purpura occurs with a platelet count less
than 50.000 per microlitre of blood

35.  Petechiae: (pinpoint red spots)
are small, purpuric lesions up to 2 mm across,
occurring in crops (groups)
 Ecchymoses or bruises:
are larger extravasations of blood
more than 2 mm across

36. HENOCH – SCHÖNLEIN PURPURA
HSHP: Synonymous: (Anaphylactoid purpura)
is Small - Vessel Vasculitis associated with
Systemic manifestations

37. Predominantly in children, There is particular association of
1- Skin rash (an erythematous-uriticarial & purpuric) with
2- arthritis
3- G. I. Symptoms or both
Nephritis: Is particular complication of HSHP
In other word Nephritisgives HSHP a special
importance.
The cause is undetermined
1. upper respiratory tract infections:
- viruses, streptococcal infections food & drugs (may be
important) but
2. immune complex disease (ICD) (is at present most in favour)
Diagnostic tests:
1- Raised serum Ig A or
2. Ig A deposition in the skin

38. Cl. f.: -
* Prodromal symptoms of (headache, anorexia &
fever) may precede an acute onset of
1- Skin rash (Skin)
2- Abdominal pain & (Abdomen)
3- Arthralgia (Joints)
 These may occur together or all three may not be
present in any one patient
1- Skin Rashes:
The sites of predilection(Skin Rashes) are:
1- External aspects of the limbs
2- Buttocks
3- Face (occasionally)
4- The oral mucosa (Rarely)

39. The eruption begins as a crop (group) of
Erythematous Macules & most macules become
1- Papular
2- Uriticarial: Uriticarial component of the general
picture is characteristic in HSHP
3- Purpuric: A shower of purpura may be the
presenting sign
* Purpura may be the only symptom & always an
outstanding (prominent) feature in HSHP
* The diagnosis of HSHP must be suspected whenever
Purpura occurs in children with a normal platelet
count

40. 2- Abdominal Symptoms:
* In two- thirds or more:
- colic,
- vomiting &
- diarrhea may be accompanied by hematamesis or
(the passage of bloody stools)
The onset may be sever enough to suggest an (acute
abdomen)
* A serosanguineous & Edematous involvement of a
section of the bowel is more common than true
Intussusceptions
* There may be scrotal swelling due to torsion &
subsequent hemorrhage.

41. 3- Polyarthralgia
* Occurs in most cases
* Joints affected are :
1- The ankles
2- knees
3- Elbows &
4- Small joints of the hands & wrists are most
frequently affected
Renal involvement:
• Is the most serious feature of HSHP
* Should receive the most careful attention because
of its prognostic significance;
1- hematuria or 2- proteinuria (usually both)
*Patients with renal involvement must be watched
carefully for 5years.

42. D.D. of HSHP: * Skin lesions:
1- Insect bites (Papular Urticaria)
2- Drug eruptions
3- E.M.
4- Urticaria
5- Gianotti-crosti syndrome: (Papular acrodermatitis):
*Profuse eruption of a symmetrical red papules
5 -10 mm on the thighs & buttocks then on the
extensor aspects of the arms, & finally on the face
*Associated with
A- Generalized lymphadenopathy mostly axillary & inguinal
B- Hepatomegaly
6. Transient recurring circinate erythema of Rheumatic
fever

43. * Abdomen
1- Appendicitis 2-Mesenteric adenitis
*Joints: Rheumatic fever
* Meningococcal septicemia
(if the systemic manifestations are sever)
Course of HSHP:
- Individual episodes usually last 3- 6 wks
- but recurrences are common.
Prognosis of HSHP:
- Of each attack is good
- For life depends on the
1- degrees &
2- severity
of renal involvement

44. Treatment of HSHP:
1- There is no specific treatment
2- Rest is the best therapy
3- Penicillin if there is evidence of
concomitant streptococcal infection
4- Cs: * decrease the symptoms
* have no effect on the
a- purpura or
b- The nephropathy
5- Dapsone if a- steroids fail or
b- Cs: contraindicated

45. It is essential that a
urine analysis be carried out:
1. When the diagnosis is made
2. Weekly during the attack
3. At the end of the attack
4. 1- 3 months after the attack has
subsided
* When persistent proteinuria is
present, further regular tests are
obligatory at intervals for at least 5
years.