SKIN DISORDERS (1).ppt pathology present

When creating a description for uploading content about a skin disorder, it's important to provide clear, informative, and sensitive details. Here’s a structured outline you can use:

### Title:
- **Understanding [Specific Skin Disorder Name]** (e.g., Understanding Psoriasis)

### Description:
1. **Overview:**
- Begin with a brief introduction to the skin disorder.
- Example: “This resource provides an in-depth look at [Specific Skin Disorder], a chronic condition that affects millions of people worldwide.”

2. **Symptoms:**
- Describe the common symptoms associated with the disorder.
- Example: “Common symptoms include [describe symptoms, e.g., red patches of skin, itching, scaling, etc.]. These symptoms can vary in severity and may impact daily life.”

3. **Causes and Risk Factors:**
- Explain the potential causes and any known risk factors.
- Example: “While the exact cause of [Skin Disorder] is still being researched, factors such as genetics, environmental triggers, and immune system responses may play a role.”

4. **Diagnosis:**
- Outline how the disorder is diagnosed.
- Example: “Diagnosis typically involves a physical examination by a healthcare professional and may include skin biopsies or other tests to rule out similar conditions.”

5. **Treatment Options:**
- Discuss available treatments and management strategies.
- Example: “Treatment options may include topical therapies, phototherapy, and systemic medications. It's important to work with a healthcare provider to find the best approach for individual needs.”

6. **Living with the Disorder:**
- Provide tips or advice for managing the condition.
- Example: “Managing [Skin Disorder] can be challenging, but support groups, lifestyle changes, and education about the condition can greatly improve quality of life.”

7. **Conclusion:**
- Offer encouragement and resources for further information.
- Example: “For more information on [Skin Disorder] and to connect with others affected by it, visit [resource links or organizations]. Remember, you are not alone in this journey.”

### Keywords (for SEO):
- Skin disorder, [specific disorder], symptoms, causes, treatment, management, healthcare.

### Example Description:
“**Understanding Psoriasis** - This resource provides an in-depth look at psoriasis, a chronic skin condition that affects millions of people worldwide. Common symptoms include red patches, itching, and scaling, which can vary in severity and significantly impact daily life. While the exact cause is still being researched, genetics and environmental factors may play a role. Diagnosis typically involves a healthcare professional’s examination and may include skin biopsies. Treatment options vary and can include topical therapies and systemic medications. Managing psoriasis can be challenging, but support and education can enhance quality of life. For more information and resources, visit [links]. Remember, you are not alone in

2. Acne
- A physical change in the skin caused by a disease process in the sebaceous follicle
- Acne is the term for plugged pores(comedeons)(blackheads and whiteheads), papule
(pimples), and even deeper lumps (cysts or nodules) that occur on the face, neck,
chest, back, shoulders and even the upper arms
Types of Acne
•Comedo, papule, pustule, nodule and cyst.
•Sebaceous glands: Glands in the skin that produce an oily substance called sebum--
these glands are the sites of acne lesions.
•Sebaceous glands are attached to hair follicles and are found mostly on the face,
neck, back and chest.
•Sebum: The oily substance produced by sebaceous glands.

3. Classification of Acne Vulgaris/cystic acne/acne
•Obstructive Acne
•Open Comedones (Black heads)
•Closed Comedones (White heads)
•Inflammatory Acne (in order of lesion formation)
•Papules
•Pustules
•Nodules
•Cysts
•Scars

5. Mechanism
•Acne occurs when androgen hormones cause sebaceous glands to grow
and produce more sebum. In concert with this change, there are
changes in the skin lining the hair follicle to which sebaceous glands are
attached.
•The skin cells of the follicle lining shed more quickly, in clumps, and are
sticky. These cells and increased sebum output are likely to cause
clogged pores that can become comedones.
• Finally, a kind of bacteria, P. acnes, which is a normal resident on the
skin, invades the clogged follicle and begins to multiply rapidly.
•The result is acne in all its forms.

6. Acne Treatment
•Given the way acne occurs, acne treatments do one or
more of the following:
•Reduce sebum production
•Reduce P. acnes
•Normalize the shedding of skin cells
•Drugs used in Acne
–Azelaic Acid
–Clindamycin Topical
–Erythromycin Topical
–Tetracycline Topical
–Benzoyl Peroxide
–Tretinoin
–Isotretinoin

7. IMPETIGO
•The most common bacterial skin infection in children
•Superficial infection of the epidermis
•Most commonly involves the face (mouth and nose), extremities,
hands, and neck
•Peak incidence in summer and early fall
•Children with poor hygiene and malnutrition
•Contagious and will spread from one part of the body to another
through scratching
•Usually appears on previously traumatized skin or skin that has a
preexisting break in its integrity (psoriasis, eczema, atopic dermatitis)

8. IMPETIGO--IMPETIGO--Nonbullous formNonbullous form
•ETIOLOGY:
–1. Staph (S.aureus)
–2. Combo Strep and Staph
–3. Strep (S.pyogenes)
–Usually on predisposed skin (bites, cuts, burns)
•CLINICAL FEATURES:
–Discrete (clear shape), fragile (easily damaged) vesicles surrounded by an
erythematous border. The vesicles become pustular, rupture, and discharge a
honey colored fluid that quickly forms a crust.
–Little or no erythema, pruritis(Itch (pruritus)
is a sensation that causes the desire
or
reflex to scratch)
, or constitutional symptoms( that effect many body systems
like wt loss, fatigue, fever)
–Regional adenopathy(enlargement
of a lymph node.)
(90%)
–Leukocytosis ( inc wbc)(50%)

9. IMPETIGO--IMPETIGO--Nonbullous formNonbullous form
Mubin
Mustafa Kiyani

10. IMPETIGO--IMPETIGO--Bullous FormBullous Form
•ETIOLOGY:
–Staphlococcus aureus
–Occurs sporadically(sometimes happening) on intact skin as a manifestation of
localized toxin production
–These
bacteria produce a toxin causing separation between the top skin
layer
(epidermis) and the lower layer (dermis). that reduces cell-to-cell
stickiness
(adhesion
•CLINICAL PRESENTATION:
–Flaccid, transparent bullae (having clear yellow colour fluid) that quickly become purulent and
rupture spontaneously
–Most commonly on the skin of moist intertriginous areas(an
area where two skin areas may touch or
rub
together eg axilla)
–No regional adenopathy, erythema, or constitutional symptoms

11. IMPETIGO--IMPETIGO--Bollous FormBollous Form

12. IMPETIGO--IMPETIGO--DIAGNOSISDIAGNOSIS
•History
•Physical exam
•Culture, gram stain, biopsy using
histopathic evaluation when unsure

13. IMPETIGO--IMPETIGO--TreatmentTreatment
•Mupirocin (Bactroban) ointment
–Apply to affected area TID for 10 days
•Cephalexin (Keflex)
–25-50 mg/kg/day for 10 days for children
–500 mg BID for adults
•Alternatives
–Pen VK
–Second generation Cephalosporins
–Macrolides
•Bullous Impetigo of a NB
–Oxicillin, Augmentin…PO

14. IMPETIGO--IMPETIGO--ComplicationsComplications
•Can persist for months if untreated
•Pigmentary changes with or without scarring
•Acute glomerulonephritis (Group-A- Beta hemolytic Strep)
–3 weeks after pyoderma (any skin
disease
 that
is 
pyogenic) -children 2-6 years old
–headache, anorexia, dull back pain, edema, proteinuria, hematuria, ( presence
of red blood
cells
in the urine)
and RBC casts
•Cellulitis Cellulitis
is a bacterial infection of the skin and tissues beneath the skin. 
–Rapidly spreading infection of the dermis and subcutaneous tissue
–Warmth, tenderness, localized erythema
–No sharply demarcated borders
•Lymphangitis
–Inflammation of the lymphatic channels from invasion by pathogenic organisms (Group-A-
Beta-hemolytic Strep)
–Erythematous, irregular linear streaks from primary site to regional lymph nodes

15. ECTHYMAECTHYMA
•Deeper and more chronic infection than impetigo
•More frequently on the legs
•S. pyogenes
•Initial vesicles with erythematous base==>erode through dermis to
form a thick crusted ulcer with elevated margins surrounded by a
red rim.
•Tx= same as impetigo

16. ERYTHEMA
MULTIFORME
Erythema
multiforme is a type of
hypsersensitivity
reaction that occurs in
response
to medications, infections, or
illness

17. ERYTHEMA MULTIFORME
•Mucocutaneous
disease
(A mucocutaneous
zone is
a region of the body in which 
mucosa
 transitions
to 
skin.eg
body orifices like
lips, nostrils, 
conjunctivae, urethra, vagina.

epithelium transitions

to epidermis, lamina
propria
 transitions
to 
dermis,

and smooth
muscle transitions to skeletal muscle.
•Males
adolosents , young adults are affected
more

18. ERYTHEMA MULTIFORME
AETIOLOGY /PATHOLOGY
•Unclear
aetiology and pathogenesis
•Infections
like HSV and mycoplasma can trigger this disease
•Drugs
like Sulphonamides ,barbiturates
•Suggested
cause is also given as to a
type
III hypersensitivity
reaction

19. Herpes simplex virusHerpes simplex virus

20. ERYTHEMA MULTIFORME
CLINICAL FEATURES
•Upper
respiratory infection
•Headache
•Nausea
and Vomiting

21. ERYTHEMA MULTIFORME
Signs during the disease:
•Red
macules – 1cm or more in diameter with cyanotic center
•Lips
grossly swollen ,split crusted bleeding

•Widespread
fibrin covered erosions and erythema in the mouth.
•Mild
fever
•Conjunctivitis
may be associated
•Attacks
recur at the intervals of several months
•Usually
self limiting.

22. ERYTEMA MULTIFORME

23. ERYTEMA MULTIFORME
HISTOPATHOLOGY
•Necrosis
of the kertinocytes
•Inter
& intra cellular odema.
•Subepithelial
blisters are common
•Infiltration
of inflammatory cells.

24. ERYTEMA MULTIFORME

25. ERYTEMA MULTIFORME
•MANAGEMENT
•No
specific treatment required .
•Systemic
steroids may give relief to the fever.
•In
severe cases antibiotics are used to prevent secondary
infections.
•Symptomatic
–analgesics, antipyretics, antihistamines.

26. PEMPHIGUS VULGARIS
•Pemphigus is an autoimmune disorder. The immune system
produces
 antibodies against specific proteins in the skin and mucus membranes.
These antibodies break the bonds between skin cells. This leads to the formation of a
blister.
•Autoimmune disease.
•Common
in Ashkenazi and Mediterranean jews .
•Middle
aged females.
•Other
variants are:


Pemphgius
Vegitans


Pemphigus
Foliaceus & Erthematosus


Paraneoplastic
pemphigus.

27. PEMPHIGUS VULGARIS
CLINICAL FEATURES:
•Painful
ulcers or bulla are formed which are fluid filled.
•They
can be formed any where in the oral cavity .
•they
may be located:
•In
the mouth
•On
the scalp, trunk, or other skin areas
•The
bulla is rapidly ruptured leaving a
collapsed
roof of
grayish
membrane
with
a red ulcerated base.The ulcer
may
look like large map shaped.

28. PEMPHIGUS VULGARIS
•Some
time the ulcers are joined together to make a
confluence
this condition is very painful.
•It
has a variable course might involve skin, oesophagus,
cervix.

•Protein/fluid,electrolyte
and weight loss /secondary
infections.
(complications)
•Fatal
if untreated.

29. PEMPHIGUS VULGARIS

30. PEMPHIGUS VULGARIS
PATHOGENESIS:
•It
is an autoimmune disease
•There
are circulating antibodies of type IgG.
•These
antibodies are reactive against the
desmosomes(structures
that adhere cells) or the
tonofilament
complex.
•There
destruction or disruption of these tonofilament
complex
,resulting in the loss of attachment from cell to cell


path.cont…d

31. PEMPHIGUS VULGARIS
•The
epithelial damage is directly proportion to the
number
of the circulating antibobies.
•The
tonofilament or desmosomes are disrupted by a
proteolytic
enzyme which is released by these
antibodies
.
•The
cell to cell break down also takes place through a
complement
system but this process is not clearly
understood
.

32. PEMPHIGUS VULGARIS
Mubin
Mustafa Kiyani

33. PEMPHIGUS VULGARIS
HISTOPATHOLOGY:
•Intra
epithelial vesicles or bulla and cleft like spaces are
produced
by acantolysis(
 loss
of intercellular connections, such
as desmosomes,
resulting in loss of cohesion between keratinocytes,
[1]
 seen
in diseases
such
as pemphigus vulgaris)
•These
changes are in the
stratum
spinosum
or
the prickle
cell
layer
•The
basal cell remain attach to the lamina propria and
project
into the bulla like tombstones.
•Inflammatory
cells are very scanty however eosinophils
may
be seen.
•Acantholytic
statum spinosum cells occur singly or are in
the
forms of clumps lying freely within the blister fluid.
These
cell loose there polyhedral morphology rather
they
are small rounded and contain hyper chromatic
nuclei
called the TAZANK CELLS.
Mubin
Mustafa Kiyani

34. PEMPHIGUS VULGARIS
DIFFRENTIAL DIAGNOSIS:
•Pempegiod
(rare autoimmune blistering skin
diseases.)
•Erthema
multiforme
•Bullous
lichen plannus (
 development
of vesicles
and bullae with
the 
skin
lesions
)

35. PEMPHIGUS VULGARIS
TREATMENT:
•High
mortality rates previously
•Introduction
of systemic corticosteroids like
prednisolone
in stable cases.
•Prednisolone
plus azathioprine, methotrexate
and
cyclophospamide in progressed or
advance
cases.

36. Verruca Vulgaris
•“common wart”
•Benign, hypertrophied areas of the skin
•Papilloma
viruses
•Types
–common warts
–plantar warts

37. Background
Information
•Warts are small harmless lesions of the skin
•caused by a virus: the human papilloma virus.
•The appearance of warts can differ based on the
type of wart and where it is located on the body.
•Warts are common in children. Most cases occur
between ages 12-16 years.
•Up to 30% of warts disappear by themselves
within 6 months. Most will disappear without any
treatment within 3 years.

38. Background
Information
•Warts are caused by the DNA-containing human
papillomavirus (HPV). There are at least 63
genetically different types of HPVs.
•The virus enters the skin after direct contact with
recently shed viruses kept alive in warm, moist
environments such as a locker room, or by direct
contact with an infected person.
•The entry site is often an area of recent injury.
The incubation time—from when the virus is
contracted until a wart appears—can be 1-8
months.

39. Types
of warts
•Common warts (verrucae vulgaris):
These common warts typically develop on
the hand, especially around the nail. They
are gray to flesh colored, raised from the
skin surface, and covered with rough,
hornlike projections.

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49. Types
of warts
•Plantar warts (verrucae plantaris): Plantar
warts, by definition, occur on the plantar surface,
or bottom, of the foot.
•They usually occur in high pressure areas such
as the heel and the metatarsal heads (just
behind the toes).
•They usually grow into the skin, not outward like
common warts.
•This growing into the skin makes them more
difficult to treat.

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53. •Flat warts (verrucae plana): Flat warts are
most commonly seen on the face, the
back of the hands, and lower legs.
•They usually appear as small individual
bumps about 1/4 inch across.
•Flat warts may spread rapidly on the face
and lower legs from the activities involved
in shaving.
Types
of warts

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57. Treatment
•Home care is effective in making the wart
or warts go away. No matter what
technique you use, warts will disappear
60-70% of the time.
•Techniques may be done with and without
medication.

58. Treatment
•The ultimate goal of the medical therapies
(not the surgical treatments) is to get your
body to recognize the wart as something
foreign and to destroy it, much like the
body destroys a cold virus.

59. Adhesive
tape therapy
•Place several layers of waterproof
adhesive tape over the wart region (even
duct tape).
•Do not remove the tape for 6-1/2 days.
Then take off the tape and open the area
to the air for 12 hours.
•Reapply tape for another 6-1/2 days.

60. Adhesive
tape therapy
•The tape works best in the region around
the fingernail.
•Tape works because the air-tight, moist
environment under the tape does not allow
the virus to grow and reproduce

61. Salicylic
acid therapy
•Salicylic acid is available by many different trade
names at the drug store.
–Dual Film
–Wart-Off
–Dr. Scholl’s Wart Medication
–Medi-Plast
•It comes either as a liquid to paint on the wart or
as a plaster to be cut out and placed on the wart
tissue.

62. Salicylic
acid therapy
•The area with the wart should be soaked
in warm water for 5-10 minutes.
•The wart should then be pared down with
a razor. A simple razor works fine for this,
then throw it away.
•Do not shave far enough to make the wart
bleed.

63. Salicylic
acid therapy
•Apply the salicylic acid preparation to the
wart tissue.
•Do not apply it to other skin because of
salicylic acid's potential to injure normal
tissue.
•Follow directions on the package for how
long to apply the acid.

64. Cryosurgery
•Liquid nitrogen or cryotherapy is used to deep
freeze the wart tissue.
•With liquid nitrogen applied to the wart, the water
in the cells expands, thus exploding the infected
tissue.
•The exploded cells can no longer hide the
human papillomavirus from the body's immune
system.
•The immune system then works to destroy the
virus particles.

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67. Laser
Therapy
•Laser therapy: Lasers are simply very
intense light sources.
•This light has an enormous amount of
energy that heats the tissue enough that it
vaporizes.
Mubin
Mustafa Kiyani

68. Shave
Removal
•Shave removal and electrodessication of
the base may be necessary when other
treatment methods fail.
•This would involve numbing the region
around the wart and shaving the wart flat
with the surface and light
electrodessication of the base.