DERMATOLOGICAL CONDITIONS

PAUL NGATIA
STUDENT NURSE.
Sept 2019
KMTC KITALE CAMPUS
 Definition of some terms used in
Dermatology
Dermatosis; any skin disease without inflammation
Dermatitis; inflammation of the skin
Dermatology; the science of skin diseases
Dermatologist; medical specialist in skin diseases
and their treatments
Dermatomycosis; study of fungal skin infection
Dermatoglyphics; study of pattern of ridges of the
skin of the fingers, palms, toes and soles (genetics)
for legal or clinical purposes).
 A lesion is any single area of altered skin which
may be solitary or multiple.
A rash is a widespread eruption of lesions
(greater than 20 lesions).
NB: Skin lesions can be primary or secondary.
 Primary lesions are those, which are not affected
by trauma, manipulations such as scratching,
scrubbing, etc., or regression over time. They arise on
normal skin. Examples of primary skin lesions include;
Macule, Papule, Nodule, Pustule, Vesicle, Wheal, Cyst.
 Secondary lesions are those that are superimposed on
an existing skin lesion. Examples include: scales,
crusts, fissures, excoriations, skin ulcers, scars,
atrophy and sclerosis
 Definitions of Skin Lesions
 Macule; a flat spot or discoloured area of the skin, not
raised above the surface (lack elevation or depression)
 Papule; a palpable lesion or a small solid elevation of the
skin just above the epidermis <5mm in diameter.
 Nodule; a small swelling or protuberance that extends
deeper into the dermis than a papule. >1cm in diameter.
 Pustule; a small inflamed elevation of the skin that is filled
with pus (similar to a pimple or a blister)
 Vesicle; a very small blister (<5mm) usually containing
serum (elevated, palpable mass containing serous fluid).
 Wheal; a small burning or itching swelling/edematous on
the skin usually of brief duration, left by a blow, mosquito
bite or as part of an allergic reaction
 Cont’…
 Purpura; is bleeding into the skin
 Erythema; is red skin due to increased blood supply and it
will blanch on pressure (i.e. redness of the skin caused by
congestion of the capillaries)
 Petechiae: pinpoint red spots that appear on the skin as a
result of blood leakage into the skin (assoc. with bleeding
tendencies or emboli to skin)
 Cyst; skin cysts are encapsulated epithelium-lined cavities
(>5mm diameter) containing fluid or solid material e.g.
blood, pus, sebum, mucus etc. found in the dermis.
 Comedones: are the primary lesions of acne caused by
sebum blockage in the hair follicle.
 Skin tumour; swelling on skin >2.5cm in diameter.
 Common Skin Conditions;
 Bacterial infections (pyodermas); Impetigo, Folliculitis,
Cellulitis, Seborrhea, Seborrheic Dermatoses.
 Viral skin infections; Human Papilloma Virus, Herpes
Viruses (herpes zoster, herpes simplex),
 Fungal infections (mycoses); ringworms, tinea
 Autoimmune skin disorders e.g. Pemphigus.
 Non-infective inflammatory conditions; Dermatitis
(Eczema), Psoriasis, Acne Vulgaris,
 Pressure ulcers/decubitous ulcers
 Burns; degrees, percentages (‘rule of nines’),
complications [a must know for every nurse]
 Tumours of the skin (malignant tumours) e.g. Basal cell
Carcinoma, Malignant melanoma, Kaposi Sarcoma etc.
1. IMPETIGO
Impetigo is a superficial bacterial infection of the
skin caused by staphylococci, streptococci, or
multiple bacteria.
Bullous impetigo is a more deep-seated infection
of the skin caused by Staphylococcus aureus, and
it is characterized by the formation of bullae (i.e.,
large, fluid-filled blisters) from original vesicles.
The bullae rupture, leaving raw, red areas
The exposed areas of the body i.e. face, hands,
neck, and extremities are most frequently
involved.
 Cont’…
Impetigo is contagious and may spread to other
parts of the patient’s skin or to other members of
the family who touch the patient or use towels or
combs that are soiled with the exudate of the
lesions
Although impetigo is seen at all ages, it is
particularly common among children living in
poor hygienic conditions.
It often follows pediculosis capitis (head lice),
scabies (itch mites), herpes simplex, insect bites,
poison ivy, or eczema.
Chronic health problems, poor hygiene, and
malnutrition may predispose an adult to impetigo.
Some people have been identified as
asymptomatic carriers of S. aureus, usually in the
nasal passages.
 Clinical Manifestations of Impetigo
The lesions begin as small, red macules, which
quickly become discrete, thin-walled vesicles that
soon rupture and become covered with a loosely
adherent honey-yellow crust
These crusts are easily removed to reveal smooth,
red, moist surfaces on which new crusts soon
develop. If the scalp is involved, the hair is
matted, which distinguishes the condition from
ringworm.
Impetigo
 Management of Impetigo
Systemic antibiotic therapy is the usual treatment.
 It reduces contagious spread, treats deep infection, and
prevents acute glomerulonephritis (i.e., kidney
infection), which may occur as an aftermath of
streptococcal skin diseases.
 In non-bullous impetigo, benzathine penicillin or oral
penicillin may be prescribed.
 Bullous impetigo is treated with a second-generation
penicillins (e.g., cloxacillin, dicloxacillin).
 In penicillin-allergic patients, erythromycin is an
effective alternative
Cont’...
Topical antibacterial therapy (e.g. mupirocin)
may be prescribed when the disease is limited to
a small area. However, topical therapy requires
that the medication be applied to the lesions
several times daily for a week
 When topical therapy is prescribed, lesions are soaked
or washed with soap solution to remove the central site
of bacterial growth, giving the topical antibiotic an
opportunity to reach the infected site.
Cont’…
 After the crusts are removed, a topical medication
(e.g., Polysporin, bacitracin) may be applied.
 Gloves are worn when providing patient care.
 An antiseptic solution, such as povidone-iodine
(Betadine) may be used to clean the skin, reduce
bacterial content in the infected area, and prevent
spread.
Cont’…
The nurse instructs the patient and family
members to bathe at least once daily with
bactericidal soap.
Cleanliness and good hygiene practices help
prevent the spread of the lesions from one skin
area to another and from one person to another.
Each person should have a separate towel and
washcloth.
Because impetigo is a contagious disorder,
infected people should avoid contact with other
people until the lesions heal.
2. SEBORRHEIC DERMATOSES
Seborrhea is excessive production of sebum (i.e.,
secretion of sebaceous glands) in areas where
sebaceous glands are normally found in large
numbers, such as the face, scalp, eyebrows, eyelids,
sides of the nose and upper lip, malar regions (i.e.,
cheeks), ears, axillae, under the breasts, groin, and
gluteal crease of the buttocks.
Seborrheic dermatitis is a chronic inflammatory
disease of the skin with a predilection for areas that
are well supplied with sebaceous glands or lie
between skin folds, where the bacteria count is high.
Clinical Manifestations
 Two forms of seborrheic dermatoses can occur, an
oily form and a dry form.
 Either form may start in childhood and continue
throughout life.
 The oily form appears moist or greasy.
 There may be patches of sallow, greasy skin, with
or without scaling, and slight erythema (i.e.
redness), predominantly on the forehead, naso-
labial fold, beard area, scalp, and between
adjacent skin surfaces in the regions of the
axillae, groin, and breasts.
Cont’…
 Small pustules or papulo-pustules resembling
acne may appear on the trunk.
 The dry form, consisting of flaky desquamation
of the scalp with a profuse amount of fine,
powdery scales, is commonly called dandruff.
 The mild forms of the disease are asymptomatic
 When scaling occurs, it is often accompanied by
pruritus (itching), which may lead to scratching
and secondary infections and excoriation.
Predisposing factors of Seborrheic
Dermatitis
Genetic predisposition.
Hormones
Nutritional status
Infection
Emotional stress
 Management of Seborrheic Dermatitis
 Because there is no known cure for seborrhea, the
objective of therapy is to control the disorder and
allow the skin to repair itself.
 Seborrheic dermatitis of the body and face may
respond to a topically applied corticosteroid
cream, which allays the secondary inflammatory
response. However, this medication should be
used with caution near the eyelids, because it can
induce glaucoma and cataracts in predisposed
patients.
Cont’...
 Patients with seborrheic dermatitis may develop a
secondary candidal (yeast) infection in body
creases or folds.
 To avoid this, patients should be advised to
ensure maximum aeration of the skin and to clean
carefully areas where there are creases or folds in
the skin.
 Patients with persistent candidiasis should be
evaluated for diabetes.
Cont’...
The mainstay of dandruff treatment is proper, frequent
shampooing (daily or at least three times weekly) with
medicated shampoos.
Two or three different types of shampoo should be used in
rotation to prevent the seborrhea from becoming resistant
to a particular shampoo. The shampoo is left on at least 5
to10 minutes.
As the condition of the scalp improves, the treatment can
be less frequent.
Antiseborrheic shampoos include those containing
selenium sulfide suspension, zinc pyrithione, salicylic acid
or sulfur compounds, and tar shampoo that contains sulfur
or salicylic acid.
 Cont’…
A person with seborrheic dermatitis is advised to avoid
external irritants, excessive heat, and perspiration; rubbing
and scratching prolong the disorder.
 To avoid secondary infection, the patient should air the
skin and keep skin folds clean and dry.
The patient is cautioned that seborrheic dermatitis is a
chronic problem that tends to reappear. The goal is to keep
it under control.
Patients need to be encouraged to adhere to the treatment
program.
Those who become discouraged and disheartened by the
effect on body image should be treated with sensitivity and
an awareness of their need to express their feelings
 3. HERPES ZOSTER
• Herpes zoster, also called shingles, is an
infection caused by the varicella-zoster virus, a
member of a group of DNA viruses (the virus is
a member of the herpes-virus group).
• The viruses causing chickenpox and herpes
zoster are indistinguishable, hence the name
varicella-zoster virus.
• The disease is characterized by a painful
vesicular eruption along the area of distribution
of the sensory nerves from one or more posterior
ganglia.
Cont’...
Itis assumed that herpes zoster represents a
reactivation of latent varicella virus infection and
reflects lowered immunity
After a case of chickenpox runs its course, it is
thought that the varicella zoster viruses
responsible for the outbreak lie dormant inside
nerve cells near the brain and spinal cord.
Later, when these latent viruses are reactivated,
they travel by way of the peripheral nerves to the
skin, where the viruses multiply and create a red
rash of small, fluid-filled blisters
 Clinical Manifestations
The incubation period for herpes zoster is 7-21 days
Manifestations occur in three phases; pre-eruptive, acute
eruptive and post-herpetic neuralgia (PHN)
Pre-eruptive phase is characterized by;
 Previously dormant VZV becomes reactivated within dorsal
root ganglia of the spinal cord and follow the dermatome
that corresponds with the ganglion/ganglia affected.
 Pain, pruritus and paresthesia over the sensory region
following that dermatome.
 This phase lasts 1-10 days, with 48 hours being typical.
NB: a dermatome is an area supplied by a nerve
 Acute eruptive phase characterized by;
 Appearance of unilateral patchy erythematous vesicular swellings
areas (eruptions) in the dermatomal area affected
 Development of initially clear vesicles that become purulent
(cloudy) and eventually rapture and form crusts
 The inflammation is usually unilateral, involving the thoracic,
cervical, or cranial nerves in a band-like configuration.
 The blisters are usually confined to a narrow region of the face or
trunk
 Pain that is severe and unrelenting (burning, lancinating i.e. tearing
or sharply cutting), stabbing, or aching.
 Some patients have no pain, but itching and tenderness may occur
over the area.
 Sometimes, malaise and gastrointestinal disturbances precede the
eruption
 Lasts 10-15 days
Post-herpetic neuralgia is variable in terms of duration
and manifestations.
It is characterized by;
 Pain which is localized to the dermatological area affected
and may be severe for 30 or more days after lesions have
healed.
NB: Herpes Zoster Opthalmicus (HZO) is a rare sub-type
of herpes zoster that causes severe ocular pain and
complications such as blindness.
Management
 The goals of herpes zoster management are to
relieve the pain and to reduce or avoid
complications, which include;
Infection,
Scarring,
Post-herpetic neuralgia and
Eye complications.
 Pain is controlled with analgesics, because
adequate pain control during the acute phase helps
prevent persistent pain patterns.
Cont’...
 Systemic corticosteroids reduce incidence and duration of
PHN
 There is evidence that infection is arrested if oral antiviral
agents such as acyclovir (Zovirax), valacyclovir (Valtrex),
or famciclovir (Famvir) are administered within 24 hours
of the initial eruption.
 Intravenous acyclovir, if started early, is effective and
significantly reducing the pain and halting the progression
of the disease.
Topical agents containing calamine or lidocaine are
helpful, but not in steroid preparations
Antihistamine to control itching
Antibiotics for secondary bacterial infections
Cont’...
In addition to medications, cold compresses may help
to relieve pain and itching
The patient is taught how to apply wet dressings or
medication to the lesions and to follow proper hand
hygiene techniques to avoid spreading the virus
The disease can be prevented by avoidance of person
with herpes zoster, during contagious phase. The
person with varicella is contagious from 1-2 days
before rash onset until the lesions have crusted (until
the rash develops crusts).
Cont’…
Varicella vaccine for children and adults who have
not had chicken pox.
Zostavax vaccine is administered for pts over the age
of 60 years.
 NB: People who have been exposed to varicella
(i.e., chicken pox) by primary infection or by
vaccination are not at risk for infection after
exposure to patients with herpes zoster.
Nursing Management;
Educate patient and family about importance of;
 medication adherence,
 how to apply wet dressings or medications,
 proper hand hygiene to avoid spreading the virus
 diversional activities and relaxation techniques to
encourage restful sleep and alleviate discomfort
Instruct patient and relatives on importance of
having a caretaker incase of self care deficit
especially related to old age.
4. HERPES SIMPLEX
Herpes simplex is a common skin infection caused
by herpes simplex virus.
There are two types of the causative virus, which are
identified by viral typing;
a) Herpes simplex type 1
b) Herpes simplex type 2
Generally, herpes simplex type 1 occurs on the skin
of the lips, mouth, gums or tongue and type 2 in the
genital area, but both viral types can be found in both
locations.
Cont’...
Herpes simplex is classified as a true primary
infection, a non-primary initial episode, or a
recurrent episode.
 True primary infection is the initial exposure to the virus.
 A non-primary initial episode is type 1 or type 2 in a
person previously infected with the other type.
 Recurrent episodes are subsequent episodes of the same
viral type
Cont’…
About 85% of adults worldwide are seropositive for
herpes type 1.
The prevalence of herpes type 2 is lower; type 2
usually appears at the onset of sexual activity.
Serologic testing shows that many more people are
infected than have a history of clinical disease.
Other disorders caused by Herpes Simplex virus
include herpetic whitlow (fingers infxn), labial herpes
(lips), cutaneous herpes (skin), herpetic proctitis (ano-
rectal inflammation by herpes) etc.
 Diagnosis
History Taking
Physical Examination
Signs and Symptoms
Culture of lesion (Tzanck smear test)
 Clinical Manifestations
Following initial infection, the virus lives
dormant in nerve ganglia near the spinal column,
where the immune system cannot destroy it.
So passive in asymptomatic
Recurrence of symptomatic infection happens,
simultaneously or may be triggered by stress such
as fever, sunburn, illness, menses, fatigue or injury
The secondary lesion may appear isolated or a
group of small vesicles or pustules on
erythematous base
Cont’...
Crusts eventually forms and lesion heals, almost
1 week the lesion are contagious
Some patients may have prodromal phase of
burning and tingling at the site for a few hrs
before eruption.
They become erythematous, swollen, there may
be redness with no blistering
Lesions can burn, itch and be painful
 Management of Herpes Simplex
Topical acyclovir ointment for primary lesions
Oral antiviral medications as ordered
Various lotions, creams and ointments may be
prescribed to accelerate drying healing of
lesions, e.g. camphor, phenol, alcohol
Antibiotic for secondary bacterial infection
Analgesics to relieve pain.
5. PEMPHIGUS (Pemphigus Vulgaris)

Pemphigus is a group of serious blistering

diseases of the skin which is autoimmune in
nature and is characterized by the appearance of
bullae (i.e. blisters) of various sizes on
apparently normal skin and mucous membranes.
Pathophysiology of Pemphigus
Available evidence indicates that pemphigus is
an autoimmune disease involving
immunoglobulin G (IgG) whereby the IgG
antibody is directed against a specific cell-
surface antigen in epidermal cells, antigen–
antibody reaction occurs resulting to blister
formation. The level of serum antibody is
predictive of disease severity.
Predisposing factors of Pemphigus;
 Autoimmunity i.e. IgG mediated autoimmune reactions
 Genetic factors may also play a role in its development,
with the highest incidence among those of Jewish or
Mediterranean descent.
 Age; this disorder usually occurs in men and women in
middle and late adulthood.
 Drugs e.g. penicillins and captopril
 Neurological Conditions e.g. Myasthenia Gravis (MG).
 Diagnosis
History of genetics predisposition, esp Jews and
Mediterraneans, drugs, MG.
Inspection and palpation (see CF below;)
– Painful irregularly shaped oral lesions, bullae,
– Offensive odour,
– Nikolsky’s sign,
Investigations;
– Lab specimens from blisters and sorrounding skin shows
acantholysis (separation of epidermal cells)
– Immunofluorescence studies reveals intraepidermal
presence of IgG.
 Clinical Manifestations of Pemphigus
Most patients present with oral lesions appearing
as irregularly shaped erosions that are painful,
bleed easily, and heal slowly.
The skin bullae enlarge, rupture, and leave large,
painful eroded areas that are accompanied by
crusting and oozing.
 A characteristic offensive odor emanates from
the bullae and the exuding serum.
Cont’…
There is blistering or sloughing of uninvolved
skin when minimal pressure is applied (i.e.
Nikolsky’s sign).
The eroded skin heals slowly, and huge areas of
the body eventually are involved.
Bacterial super-infection is common
Fluid and electrolyte imbalance,
hypoalbuminaemia occurs
 Management of Pemphigus
The goals of therapy are to;
i. Bring the disease under control as rapidly as possible,
ii. Prevent loss of serum and the development of
secondary infection,
iii. Promote re-epithelization (i.e. renewal of epithelial
tissue).
Corticosteroids are administered in high doses to
control the disease and keep the skin free of
blisters.
Management cont’…
The high dosage level of corticosteroids is maintained
until remission is apparent.
In some cases, corticosteroid therapy must be
maintained for life.
Corticosteroids are administered with meals or
immediately after a meal and may be accompanied by
an antacid as prophylaxis against gastric
complications.
Essential to therapeutic management are daily
evaluations of body weight, blood pressure, blood
glucose levels, and fluid balance.
NB: Corticosteroid therapy has serious side effects...
Quiz: List some side effects of Corticosteroids
(Hydrocortisone/cortisol);
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
Etc……………………
Did your list include the following;
i. Adiposity of the face (moon face)
ii. Muscle wasting esp. the limbs
iii. Osteoporosis and pathological fractures
iv. Diabetes mellitus due excess gluconeogenesis
v. Immuno-depression
vi. Recurrent infections
vii. Insomnia, excitability, euphoria, depression or
mania
viii.Hypertension
ix. Menstrual disturbances
x. Renal failure
xi. Peptic ulcers
Management of Pemphigus Cont’…
Immunosuppressive agents (e.g. azathioprine,
cyclophosphamide, gold) may be prescribed to
help control the disease and reduce the
corticosteroid dose.
Plasmapheresis (i.e. plasma exchange)
temporarily decreases the serum antibody level
and has been used with variable success, although
it is generally reserved for life-threatening cases
 6. ECZEMA
(Atopic Dermatitis)
Eczema is a non-infectious inflammatory dermatosis
(type I immediate hypersensitivity rxn) also called
Atopic Dermatitis resulting from an inflammatory
reaction of the skin (especially the epidermis) to
physical, chemical or biologic agents/irritants.
A family history is common with highest incidence in
infants and children (10-20% of children in the West)
Primary irritant type is where a non-allergic reaction
results from exposure to an irritating substance
Secondary irritant type is due to allergic rxn as a
result of exposure of already sensitized people to
contact allergens (Contact Dermatitis)
This condition (eczema) is characterized by
significant elevations of serum IgE and peripheral
eosinophilia, pruritus and hyperirritability of the
skin, large amounts of histamine in the skin,
excessive dryness of the skin with resultant
itching related to changes in lipid content,
sebaceous gland activity, and sweating.
Itcan be acute or chronic
In response to stroking of the skin, with immediate
redness and swelling appears on the skin, followed in 15
to 30 seconds by pallor, which persists for 1 to 3 minutes.
Lesions develop secondary to the trauma of scratching
and appear in areas of increased sweating and hyper
vascularity.
Atopic dermatitis is chronic and assoc. with allergy and
mostly affects atopic individuals i.e. those prone to
hypersensitivity disorders, children affected by hay fever
or asthma. Remissions, recurrence and exacerbations may
occur.
Treatment must be individualized.
Causes
Soaps
Detergents
Scouring compounds
Industrial chemicals

Predisposing factors
Family history of allergic diseases
Extremes of heat and cold
Frequent contact with soap and water
Pre-existing skin disease
Persons at risk
Persons whose profession requires repeated hand
washing e.g. nurses
Persons with repeated exposure to food or other
irritants e.g. cleaners, hairdressers, food
preparation workers
Women (more commonly affected than men)
Clinical Manifestations
Eruptions begin when causative agent contacts
the skin; the first reaction include;
 Pruritus
 Burning
 Erythema
Followed closely by;
 Edema,
 papules,
 vesicles,
 oozing or weeping
In sub acute phase, the vesicular changes are less
marked, and they alternate with crusting, drying,
fissuring and peeling
If repeated reactions occur, or if the patient
continually scratches the skin, lichenification
(thickening of the epidemis with exaggerations of
the normal creases) and pigmentation occur.
Secondary bacterial infection may follow.
 Management of Eczema
Remove offending irritant if identified through
detailed history and physical exam
Avoid use of soap until healing occurs
Use of barrier cream containing ceramide for small
patches of erythema e.g. Impruv, Dimethicone
(cetaphil).
Apply cool, wet dressings over small areas of
vesicular dermatitis which also helps to clear oozing
eczematous lesions.
Corticosteroids (although efficacy still in doubt).
Patient education on preventing further bouts of infxn
Patient Education on Prevention of Eczema
Avoid contact with irritants e.g. heat, soap, rubbing,
gloves (such as for washing dishes or general cleaning
unless they are cotton lined).
Choose bath soaps, laundry detergents and cosmetics
that do not contain fragrance
Avoid using fabric softener dryer sheet; fabric
softener added to washer may be used
Avoid topical medications, lotions or ointments
except those specifically prescribed for your condition
Wash skin thoroughly immediately after exposure to
possible irritants
ANY QUESTIONS SO FAR?
 7. PSORIASIS
Psoriasis is a chronic non-infectious inflammatory
disease of the skin in which epidermal cells are
produced by autoimmune reactions at a rate that is
about six to nine times faster than normal
The cells in the basal layer of the skin divide too
quickly, and the newly formed cells move so
rapidly to the skin surface that they become
evident as red, profuse scales or silvery plaques of
epidermal tissue commonly appearing on the skin
over elbows, knees, scalp, lower back and
buttocks sometimes associated with arthritis.
Lesions may appear anywhere including oral
cavity, eyes and joints.
onset at any age, with median 28 years.
The psoriatic epidermal cell may travel from the
basal cell layer of the epidermis to the stratum
corneum (i.e. skin surface) and be cast off in 3 to 4
days, which is in sharp contrast to the normal 26 to
28 days.
As a result of the increased number of basal cells
and rapid cell passage, the normal events of cell
maturation and growth cannot take place.
This abnormal process does not allow the normal
protective layers of the skin to form
Types of Psoriasis
1) Plaque Psoriasis; most common (80% of cases), often
appears on the elbows, knees, lower back, scalp.
Xteristic thick, red patches of skin, often with a silver
or white layer of scale.
2) Guttate Psoriasis; appear as small red spots on the
skin of torso and limbs, face or scalp
3) Nail psoriasis; causes nail pitting, grooves,
discolouration, loosening or crumbling of the nail,
thickened skin under the nail, and coloured patches or
spots under the nail. May resemble but should not be
confused with fungal infections of the nail.
4) Scalp Psoriasis; painful, itchy patches (severe
dandruff) noticeable at hairline.
5) Inverse/Flexural Psoriasis; red, shiny, smooth spots
with few scales appearing in skin folds (under the breast,
armpits or groin/genital area). Sweat and moisture from
skin folds keeps this form of psoriasis from shedding
skin scales; and the skin-to-skin contact can make it very
irritating
6) Pustular Psoriasis; xterized by white pustules
surrounded by red skin. Pus inside the blisters is non-
infectious. Scaling also occurs.
7) Psoriatic Arthritis; painful, physically limiting condition
of the joints and often becomes quite severe in the hands.
8) Erythrodermic Psoriasis; rarest but very serious and
painful form of psoriasis that resembles severe burns to
the skin with exfoliations than small scales typical to
most psoriasis.
 Predisposing factors
Although the primary cause is unknown, a
combination of specific genetic makeup and
environmental stimuli may trigger the onset of dx.
There is some evidence that the cell proliferation is
mediated by the immune system.
Periods of emotional stress and anxiety aggravate the
condition.
Trauma, infections, and seasonal and hormonal
changes also are trigger factors
Obesity.
Women gender more common than in men.
 Pathophysiology of Psoriasis
Autoimmune causes are triggered by periods of
emotional stress, anxiety, trauma, infections, seasonal
or hormonal changes causing infiltration of the
epidermis by activated T cells and cytokines resulting
to vascular engorgement, proliferation of
keratinocytes and epidermal hyperplasia. Epidermal
cells improperly retain their nuclei, crippling ability to
release lipids that encourage cellular adhesion
resulting in turnover of poorly matured cells that do
not adhere well to each other; classic presentation of
plaque-like lesions that have silvery, scaly, flaky
appearance.
 Clinical features
Secondary Lesions appear as red, raised patches
of the skin covered with silvery scales.
If scales are scraped away, the dark red base of
lesion is exposed, with multiple bleeding point
Patches are dry and may or may not itch
The condition may involve nail pitting,
discoloration, crumbling beneath the plate free
edges and separation of the nail plate
In erythrodermic psoriasis, the pt is acutely ill,
with fevers, chills and electrolyte imbalance.
 Diagnosis
Presence of classic plaque-type lesions occurring more
commonly on the outer, extensor surfaces of the body
such as knees and elbows generally confirms the diagnosis
of psoriasis (plague psoriasis)
Also assess signs of nail and scalp involvement and a
positive family history
Red, shiny smooth rashes/lesions hidden on skin folds
(flexures) such as the armpits, genitals, under the breasts
or buttocks limited to smaller patches unlike the scaly,
silvery, pustular spots and crusting skin confirms
inverse/flexural psoriasis. More common in obese or
overweight and middle-aged people.
 Management of Psoriasis
NB: There is no known cure for Psoriasis. The
main Goals of Management are;
1. To slow the rapid turnover of epidermis.
2. To promote resolution of the psoriatic lesions.
3. To control the natural cycles of the disease.
General Mgt …
Manage emotional factors especially stress
Gentle removal of scales by taking baths with
added oils (olive oil, mineral oil) and using soft
brush to scrub psoriatic plaques.
Specific Management of Psoriasis
Topical agents e.g. Corticosteroids
Phototherapy e.g. Narrow-band UV A/B therapy
Systemic agents e.g. cytotoxics (methotrexate,
infliximab).
NB: Monitor for side effects of these agents
 8. ACNE VULGARIS
Is a common skin disorder of the sebaceous
glands and the hair follicles that usually occurs
on the face, chest, upper back and shoulder.
Causes of Acne;
The most common cause is hormonal changes
during puberty
The sebaceous of androgens (in adolescence or
menstrual cycle) in turn stimulates the sebaceous
glands to increase sebum production.
This along with gradual obstruction of the pilo-
sebaceous ducts with accumulation debris,
rupture of sebaceous glands, which causes
inflammation
It may also be due to hereditary, stress or
external irritation (soaps and cosmetics)
 Pathophysiology of Acne Vulgaris
During childhood, the sebaceous glands are
small and virtually non-functioning. These
glands are under endocrine control, especially by
the androgens.
During puberty, androgens stimulate the
sebaceous glands, causing them to enlarge and
secrete a natural oil, sebum, which rises to the
top of the hair follicle and flows out onto the
skin surface.
Pathophysiology Cont’…
In adolescents who develop acne, androgenic
stimulation produces a heightened response in the
sebaceous glands so that acne occurs when
accumulated sebum plugs the pilo-sebaceous ducts.
This accumulated material forms comedones.
Although the exact cause is unknown, some closed
comedones may rupture, resulting in an
inflammatory reaction caused by leakage of
follicular contents (e.g., sebum, keratin, bacteria)
into the dermis.
This inflammatory response may result from the
action of certain skin bacteria, such as
Propionibacterium acnes, that live in the hair
follicles and break down the triglycerides of the
sebum into free fatty acids and glycerin.
The resultant inflammation is seen clinically as
erythematous papules, inflammatory pustules, and
inflammatory cysts.
 Clinical Manifestations
The initial lesions are called comedones; closed
comedones or white heads are small white papules
with tiny follicular openings
These may eventually become open comedones or
blackheads
The color is not caused by dirt but by lipids and
melanin pigment
Scarring occurs, picking can lead to inflammation,
further scarring and keloids formation.
Inflammatory reactions that may lead to papules,
pustules, nodules, bullae and cysts.
 Therapeutic Measures
Need to prevent new lesions and control current
lesion through the following specific measures;
 Effective topical agent (benzoyl peroxide), which is
antibacterial prevents pore plugging. Topical agent may
be applied near eyes, nasolabial folds or corners of the
mouth
 Topical Antibiotics (erythromycin, tetracycline) to kill
bacteria in follicles
 Hormone (estrogen) therapy for young women with
precautions
Benzoyl Peroxide.
Benzoyl peroxide preparations are widely used
because they produce a rapid and sustained
reduction of inflammatory lesions.
They depress sebum production and promote
breakdown of comedone plugs.
They also produce an antibacterial effect by
suppressing P. acnes.
Initially, benzoyl peroxide causes redness and
scaling, but the skin usually adjusts quickly to its
use.
Tretinoin is more effective than benzoyl peroxide
Topical or Systemic Antibiotics
Topical antibiotic treatment for acne is common.
Topical antibiotics suppress the growth of
Propionibacterium acnes, reduce superficial free fatty
acid levels; decrease comedones, papules, and pustules;
and produce no systemic side effects.
Common topical preparations include tetracycline,
clindamycin, erythromycin, sulphur+salicyclic acid
(keratolytic agents)
NB: do not repeat giving the same medicine that the
patient has already been receiving if it has not been
effective; for example, in acne we would not like
to repeat tetracycline if it has shown no response so far.
Hormone Therapy.
Estrogen therapy (including progesterone-estrogen
preparations) suppresses sebum production and reduces
skin oiliness.
 It is usually reserved for young women when the acne
begins somewhat later than usual and tends to flare up
at certain times in the menstrual cycle.
 Estrogen in the form of estrogen-dominant oral
contraceptive compounds may be administered on a
prescribed cyclic regimen.
 Estrogen is not administered to male patients because of
undesirable side effects such as enlargement of the
breasts and decrease in body hair.
Other specific treatments include;
 Comedone extraction: cryosurgery (freezing with
liquid)
 Mild peeling [ultraviolet (UV) light, CO2, liquid
nitrogen]
 Derm-abrasion (deep chemical peel) in which the
epidermis and some superficial dermis are removed
down to the level of the scars.
 Excision of scars and injection of fibrin or collagen
below the scars.
 The treatment depends on severity, age, condition,
physique and patient preference
 Surgical Management of Acne
Surgical treatment of acne consists of;
comedone extraction,
injections of corticosteroids into the inflamed lesions,
incision and drainage of large, fluctuant (i.e. moving
in palpable waves), nodular cystic lesions.
Cryosurgery (i.e. freezing with liquid nitrogen) may
be used for nodular and cystic forms of acne.
Patients with deep scars may be treated with deep
abrasive therapy (i.e. derm-abrasion), in which the
epidermis and some superficial dermis are removed
down to the level of the scars.
Removal of comedones with a comedone
extractor involves cleaning the site first with
alcohol.
The opening of the extractor is then placed over
the lesion, and direct pressure is applied to cause
extrusion of the plug through the extractor.
Removal of comedones leaves erythema, which
may take several weeks to subside.
Recurrence of comedones after extraction is
common because of the continuing activity of the
pilosebaceous glands
 Preventing Scarring
Prevention of scarring is the ultimate goal of
therapy. The chance of scarring increases as the
grade of acne increases.
Grades III and IV (25 to more than 50 comedones,
papules, or pustules) usually require longer-term
therapy with systemic antibiotics or isotretinoin.
Patients should be warned that discontinuing these
medications can exacerbate acne, lead to more
flare-ups, and increase the chance of deep scarring.
Moreover, manipulation of the comedones, papules,
and pustules increases the potential for scarring.
When acne surgery is prescribed to extract deep-
seated comedones or inflamed lesions or to incise
and drain cystic lesions, the intervention itself
may result in further scarring.
Dermabrasion, which levels existing scar tissue,
can also increase scar formation.
Hyperpigmentation or hypopigmentation also
may affect the tissue involved.
The patient should be informed of these potential
outcomes before choosing surgical intervention
for acne
Patients are instructed to avoid manipulation of
pimples or blackheads.
Squeezing merely worsens the problem, because a
portion of the blackhead is pushed down into the
skin, which may cause the follicle to rupture.
Because cosmetics, shaving creams, and lotions
can aggravate acne, these substances are best
avoided unless the patient is advised otherwise.
There is no evidence that a particular food can
cause or aggravate acne. In general, eating a
nutritious diet helps the body maintain a strong
immune system
Summary of Acne Tx
Months!!! – Counsel, Mx stress
Wash face 3X with plain soap – do not scrub!
Do not pick/squeeze
No cosmetics
Avoid junk foods
Get Sunlight
Topical – Sulphur, Benzoyl Peroxide, A/b
Systemic – A/b, Vit. A, Oestrogen for ♀
ANY QUESTIONS SO FAR?
 9. Urticaria
Also known as Hives or Nettlerash
Allergy/anaphylaxis (type I hypersensitivity) disorder
Urticaria is defined as an acute or chronic type I
hypersensitive allergic reaction of the skin
characterized by sudden recurrent appearance of an
eruption of wheals or pinkish, edematous elevations
or varying size and shape causing great irritation and
discomfort.
It is thought to be caused by certain foods, insect
bites, infection, drugs/medications, cold climates,
solar exposure, water or emotional stress
Direct release of histamine from the mast cells may
be due to drugs such as morphine, codeine,
acetylcholine, polymyxin B, ethanol, aspirin;
histamine containing foods such as fish of
Scrombroidae family (tuna, mackerel) and some
bacterial and plant toxins.
Urticaria may affect any part of the body, including
mucous membranes of the mouth, the larynx and GIT.
Each hive remains a few minutes to several hours
before they disappear. They may recur i.e. come, go
and return episodically; and if this sequence persists
for longer than 6 weeks, the condition is called
chronic urticaria
If the condition involves the deeper layers of the
skin resulting in more diffuse swellings than
discrete lesions characteristic of hives, it is called
angioneurotic edema (angioedema).
Urticaria needs to be differentiated from other
medical conditions where wheals, angioedema, or
both can occur as a symptom, for example; skin
prick test, anaphylaxis, auto-inflammatory
syndromes, or hereditary angioedema
(bradykinin-mediated angioedema)
Cold urticaria is a form of urticaria induced by
cold temperature exposure (ACU-Acquired Cold
Urticaria) and also attributed to genetic
inheritance – Familial Atypical Cold Urticaria
(FACU); acquired through an autosomal
dominant inheritance from one affected parent).
Diagnosis/Investigations of Urticaria
Detailed history and physical exam, FBC, ESR,
urine, stool for o/c, LFTs, serum creatinine, to
exclude systemic disease in chronic urticaria.
Change of diet e.g. eliminate food for sometime and
re-introduce to find if food sensitivity is possible
cause of urticaria.
Ice cube test for cold urticaria

Signs and Symptoms of Urticaria

Hives that appear and remains for a few minutes to
several hours before disappearing then recurrence
Wheals/welts-pinkish, edematous, itching elevation
on skin
Management of Urticaria
Avoid allergens (including extreme cold stimuli),
Ensure Warmth
Daily antihistamines e.g. Chlorphenamine 4mg
TID (1st generation) or the 2nd generation e.g.
Fexofenadine which is more effective if 1 st
generations do not show improvement.
2nd generation Corticosteroids to decrease
inflammation.
Bed-rest in severe cases
 10. Tropical Ulcer
Tropical means ‘hot’
Tropical medicine is medicine concerned with diseases
that are more prevalent in hot climates.
Tropical ulcer refers to chronic ulcerative skin lesion
common in tropical climates and thought to be caused
by polymicrobial infection with a variety of
microorganisms, including mycobacteria (M.
ulcerans)
It occurs on exposed parts of the body, primarily on
anterolateral aspect of the lower limbs and may erode
muscles, tendons and sometimes bones.
May develop from a mere scratch or minor trauma.
Signs and symptoms
Painful, chronic slightly raised ulcers with an
undermined border and a yellowish necrotic base.
Ulcers usually occurs below the knee around the
ankle, and sometimes on the arms

Diagnosis
History, physical exam, signs and symptoms,
Lab Isolation of M. ulcerans from lesions
 Management/Treatment
Antibiotics (penicillins-procaine benzylpenicillin,
metronidazole) used with topical antiseptic
Improved nutrition, vitamins and general hygiene.
Non-adherent daily dressings and limb elevation
Debridement of large infected ulcers under
anaesthesia.
Skin grafting in advanced cases to prevent lesion
from progressing to chronic stage
Amputation in extreme cases
 Complications of Tropical ulcers
Changes in skin colour e.g. bright red, blue,
green, orange…
Scar tissue formation and disability.
Deep tissue invasion (including bone) which
leads to amputation [BKA]
Chronic or recurrent ulceration
Squamous cell carcinoma (in chronic cases)
Tetanus infection (occurs by entry of C. tetani
through the ulcer.
Further Reading…
Furuncles, Carbuncles and other Secondary lesions
Fungal and Parasitic skin infections (mycoses);
superficial, subcutaneous and systemic mycoses e.g. tinea,
ringworms, [parasites: scabies, pediculosis, tungiasis]
Pressure ulcers/decubitous ulcers
Burns; degrees, percentages (‘rule of nines’), mgt,
complications [a must know for every nurse]
Tumours of the skin; benign e.g. keloids, cutaneous cysts,
angiomas, and malignant tumours e.g. Squamous Cell
Carcinoma, Basal Cell Carcinoma, Malignant Melanoma,
Kaposi Sarcoma etc.
Skin grafting
Furuncle (boil)
 This is an abscess which involves the hair follicle.
 An abscess is a localized collection of pus within the skin associated with
erythema, tenderness, and showing marked infiltration by polymorphonuclear
leucocytes.
 Staphylococcus aureus is the most common causative organism; streptococci and
Gram-negative organisms may also be present.
Carbuncle
 A carbuncle is a suppurative extension of several contiguous furuncles into the
subcutaneous fat. The maintenance of fascial attachments to the skin results in the
production of multilocular compartments.
NB: Furuncles and Carbuncles are common in ‘berber shops’ and are associated
with unhygienic shaving machines,
Folliculitis
 Inflammation of hair follicles, often in clusters, often due to local infection or
chemical irritation or associated with underlying disease.
 May be superficial or deep.
 Characteristic lesions are small yellow or gray pustules surrounded by erythema
and pierced by a hair.

Cellulitis (erysipelas)
This cutaneous non-suppurative infection of the
connective tissue (dermal) and subcutaneous
layers of the skin may be caused by several types
of bacteria, of which haemolytic streptococci are
the most common.
These are usually group A organisms, but b-
haemolytic streptococci of groups B, C, or G may
also be responsible.
Clinical appearance; Erythema, swelling, and
tenderness spreads rapidly with sharp or vaguely
defined borders.
Sebaceous Cysts
Kaposi’s Sarcoma
THANK YOU