Pathophysiology

INVESTIGATIONS
MODULE 2 OUTLINE • skin scrapings, hair, and nail
clippings analyzed with potassium
I. Common Skin Infections hydroxide (KOH) prep (since these fungi live
a. Dermatophytosis as molds, look for hyphae, and mycelia)
i. Tinea Capitis
ii. Tinea Corporis MANAGEMENT
iii. Tinea Cruris • topicals may be used as first line
iv. Tinea Pedis agents for tinea corporis/cruris and tinea
v. Tine Manuum pedis (interdigital type), e.g. clotrimazole or
vi. Tine Unguium terbinafine cream applied bid, continued till
b. Candidiaisis one week after complete resolution of
i. Cutaneous lesions
ii. Oral
iii. Pityriasis Versicolor • oral therapy is indicated for
c. Ectoparasitic onychomycosis, tinea capitus, e.g.
i. Scabies terbinafine (Lamisil) or itraconazole
ii. Pediculosis (Sporanox)
d. Viral
i. Warts • itraconazole is a P-450 inhibitor. It
ii. Herpes Simplex alters metabolism of non-sedating
iii. Chicken Pox antihistamines, cisapride, digoxin, and HMG
e. Bacterial CoA reductase inhibitors
i. Impetigo
ii. Furunculosis and
Folliculitis A. Tinea Capitis
iii. Abscess
iv. Cellulitis DEFINITION
v. Necrotizing Fasciitis • non-scarring alopecia with scale
vi. Gas Gangrene
II. Skin Manifestation of Metabolic ETIOLOGY
Diseases • Trichophyton tonsurans and
a. Jaundice Microsporum species
III. Inflammatory Skin Disorders
a. Psoriasis EPIDEMIOLOGY
b. Urticaria • affects children (mainly black),
immunocompromised adults
I. DERMATOPHYTOSIS • very contagious and may be
transmitted from barber, hats, theatre
DEFINITION seats, pets
infection of skin, hair and nails
caused by a species of dermatophyte (fungi SIGNS AND SYMPTOMS
that live within the epidermal keratin and • round, scaly patches of alopecia
do not penetrate deeper structures) • may see broken off hairs
• if tissue reaction is acute, a Kerion
ETIOLOGY (boggy, elevated, purulent inflamed
• Trichophyton, Microsporum, nodule/plaque) may form - this may be
Pityrosporum, Epidermophyton species secondarily infected by bacteria and result
in scarring
PATHOPHYSIOLOGY
• digestion of keratin by EXAMINATION
dermatophytes results in scaly skin, broken • Wood’s light examination of hair:
hairs, crumbling nails green fluorescence only for microsporum
infection
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
 Pathophysiology
• culture of scales/hair shaft may be
done on Sabourad’s agar
• microscopic examination of a KOH
preparation of scales or infected hair shafts
reveal characteristic hyphae
MANAGEMENT
• griseofulvin 15-20 mg/kg/day x 8
weeks or terbinafine (Lamisil) 250 mg od x
2-4 weeks
(vary dose by weight)
DIFFERENTIAL DIAGNOSIS
• psoriasis, seborrheic dermatitis, alopecia
areata, trichotillomania
B. Tinea Corporis (Ringworm)
DEFINTION AND CLINICAL FEATURE
• pruritic, scaly, round/oval plaque with
erythematous margin and central clearing
• single or multiple lesions
• peripheral enlargement of lesions
• site: trunk, limbs, face
ETIOLOGY
• T. rubrum, E. floccosum, M. cannis, T.
cruris
EPIDEMIOLOGY
• most common in farm children and those
with infected pets
EXAMINATIONS
• microscopic examinations of KOH prep of
scales scraped from active margin shows
hyphae
• scales may be cultured on sabourad’s agar
DIFFERENTIAL DIAGNOSIS
• psoriasis
• seborrheic dermatitis
• nummular dermatitis
• pityriasis rosea
C. Tinea Cruris (“Jock Itch”)
DEFINITION AND CLINICAL FEATURES
• scaly patch/plaque with a well-defined,
curved border and central clearing on
medial thigh
• does not involve scrotum
• pruritic, erythematous, dry/macerated
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
ETIOLOGY
• T. rubrum, T. mentagrophytes, E.
floccosum
EPIDEMIOLOGY
• most common in adult males
EXAMINATIONS
• same as for Tinea corporis
DIFFERENTIAL DIAGNOSIS
• candidiasis (involvement of scrotum and
has satellite lesions)
• erythrasma (coral-red fluorescence with
Wood’s lamp)
• contact dermatitis
D. Tinea Pedis (Athlete’s Foot)
DEFINITION
• pruritic scaling and/or maceration of the
webspaces and powdery scaling of soles
CLINICAL FEATURES
• white vesicles, bullae, scale maceration
• interdigital
ETIOLOGY
• T. rubrum, T. mentagrophytes, E.
floccosum
EPIDEMIOLOGY
• chronic infections are common in atopics
• heat, humidity, occlusive footwear are
predisposing factors
SIGNS AND SYMPTOMS
Acute infection - red/white scales, vesicles,
bullae, often with maceration
• may present as flare-up of chronic tinea
pedis
• frequently become secondarily infected
by bacteria
Chronic - non-pruritic, pink, scaling
keratosis on soles, and sides of foot, often
in a “moccasin” distribution
• sites: interdigital, especially in 4th
webspace
 Pathophysiology
EXAMINATIONS
• microscopic examination of a KOH prep of
scales from roof of a vesicle or powdery
scaling area
• culture of scales on sabourad’s agar
DIFFERENTIAL DIAGNOSIS
• dyshidrotic dermatitis
• allergic contact dermatitis (dorsum/heel)
• atopic dermatitis
• erythrasma, intertrigo (interdigital)
• psoriasis (soles or interdigital)
E. Tinea Manuum
CLINICAL FEATURES
• acute: blisters at edge of red areas on
hands
• chronic: single dry scaly patch
• primary fungal infection of the hand is
actually quite rare; usually associated with
tinea pedis with one hand and two feet
affected = “1 hand 2 feet” syndrome
ETIOLOGY
• same as in tinea pedis
DIFFERENTIAL DIAGNOSIS
• contact dermatitis, atopic dermatitis,
psoriasis (all three commonly mistaken for
fungal infections)
• granuloma annulare (annular)
F. Tinea Unguium (Onychomycosis)
DEFINITION AND CLINICAL FEATURES
• crumbling, distally dystrophic nails;
yellowish, opaque with subungual
herperkeratotic debris
• toenail infections usually precede
fingernail infections
ETIOLOGY
• T. rubrum (90% of all toenail infections)
EXAMINATION
• KOH prep of scales from subungual
scraping shows hyphae on microscopic
exam
• subungual scraping may be cultured on
Sabourad’s agar
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
MANAGEMENT
• terbinafine (Lamisil) 250 mg od (6 weeks
for fingernails, 12 weeks for toenails) or
pulse itraconazole (Sporanox) at 200mg bid
x 7d, then 3 weeks off (2 pulses for
fingernails, 3 pulses for toenails)
DIFFERENTIAL DIAGNOSIS
• psoriasis (pitting, may have psoriasis
elsewhere)
• trauma
• lichen planus
I.II CANDIDIASIS
A. Cutaneous Candidiasis – (Candida
Albicans)
Overgrowth of Normal Commensal of the
mouth, vagina, or lower GIT.)
- Only infects the outer layers of the
epithelium of mucous membrane or
skin.
Presentation:
➢ Red, macerated area
➢ Glistening Surface
➢ Scaling along the advancing border.
➢ The initial lesion is a papule that
then becomes a pustule.
➢ Important clinical feature is the
presence of ‘satellite’ pustules
beyond the border of the main
infection.
Treatment:
➢ Topical Therapy
B. Oral Candidiasis – (Candida
Albicans)
Presents as:
➢ White Patches easily scraped off to
leave a red, raw base.
➢ Chronic red, raw gums, tongue and
buccal mucosa.
Treatment: Topical or Systemic Therapy
C. Pityriasis versicolor – (Candida
Albicans
- Caused by normal Commensals ʹ Eg.
yeasts (Candida).
- Common Superficial Fungal-Induced
Rash
 Pathophysiology
Presentation:
➢ flaky, discolored patches on chest &
back.
➢ Small, well defined, slightly scaly
patches
➢ Either Hyperpigmented or
Hypopigmented
I. ECTOPARASITIC
A. Scabies
Organism:
- Sarcoptes scabiei (Scabies Mite)
Epidemiology:
- Human infestations originating from
pigs, horses and dogs are mild and
self-limiting.
- Scabies infestations from other
humans never cure without
intervention.
Ecology:
- Mites live in stratum corneum (Don’t
get any deeperͿ
- Eat stratum corneal Keratinocytes
- Make “tunnels” by eating
- Mating occurs on the hosts skin
- Fertilized Female Mites Burrow into
the Stratum Corneum (1 mm deep)
- Salivary Secretions contain
Proteolytic Enzymes > Digest
Keratinocytes.
Transmission:
- High prevalence in children (50%)
and adults (25%) in tropical remote
communities
- Spread by close physical contact
Presentation:
- Itch (Exacerbated at night and after
hot showers).
- Itchy, Excoriated Rash on Trunk,
associated with Scaly Burrows on
the fingers and wrists.
- Often vesicles and pustules on the
palms and soles and sometimes on
the scalp.
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
Diagnosis:
Clinical Diagnosis:
➢ Chronic itch with Symmetrical Rash
➢ Burrows
Skin Scraping - Look for Scabies Mites:
➢ Intact larvae, nymphs or adults
➢ Unhatched or hatched eggs
➢ Molted skins of mites
➢ Fragments of molted skins
➢ Mite feces
Treatment:
- Topical Permethrin or Oral
Ivermectin
Environmental Measures:
➢ Mites can contaminate bedding,
chairs, floors, and even walls
(Usually only a problem with crusted
scabies)
➢ Wash, sun, vacuum, surface
insecticide
Community Prevention:
➢ Treat all close contacts – Esp. in
Indigenous Communities
➢ Simultaneous Effective Treatment
TREAT AGAIN IN 7 DAYS
B. Pediculosis - Head Lice
3 Types:
1. Head Lice: Pediculus Humanus Capitis
Epidemiology:
- Common in Primary School Children
in the Tropics
- Higher prevalence in Aboriginal
Children
Diagnosis:
- Conditioner + Fine-Tooth Come
- Wipe combings on white tissue
paper
2. Body Lice: Pediculus Humanus Corporis
- Live on clothes, and come to the body to
feed.
3. Pubic Lice: Phthirus Pubis
- Largely sexually transmitted
- Blood Feeder
 Pathophysiology
- Can infect any Body Hair - HPV 6 & 11 = Genital & Cutaneous
(Pubic/Trunk/Legs/Axilla/Beard) but Warts
rarely head. - HPV 16 & 18 = Cervical & Penile Ca

Lifecycle: Appearance:
➢ Eggs laid in hair (knits) - Verrucous surface
➢ Larvae grow into adults - Can often see a tiny black dot in the
➢ Adults – blood sucking (live in hair) middle due to thrombosed capillary
blood vessels
Transmission:
- head-head contact. Presentation:
Presentation: - Common on back of fingers, toes
- Scalp and Neck can be Itchy and knees
- Nits are noticeable on the hairs. - Common Warts
Diagnosis: (Skin/Plantar/Palmar)
- Best Method = ͚Conditioner + Comb - Genital Warts (Cervix, Vulva, Penis)
Technique͛: - NB: Cervical Papillomas - Can cause
o Very Practical for parents cervical cancer.
o Cost Effective - Laryngeal Papilloma
o High Sensitivity
o Conditioner ‘Stuns’ the lice No Reliable Treatment:
by suffocating them - 50% of childhood warts disappear
o Prevents them from running within 6mths; 90% are gone in 2
away years.
- Many don’t bother with treatment.
Management/Treatment: - Surgical Excision/Chemical
➢ Conditioner & Nit Comb Treatment/Cryotherapy/Electrosurg
➢ Physical Removal ery (Cauterize)
➢ Cut Hair
➢ Topical Insecticidal Cream Clinical Significance
➢ Good idea to wash pillows and hats - Contagious
though – Hot Wash - Central blood vessels > Bleed
➢ (Treat all body hair – for Pubic lice) profusely when the surface is
broken.
Reasons for Treatment Failure:
➢ Inadequate application of the B. Herpes Simplex (Cold Sores/Genital
product Lesions)
➢ Lice are resistant to insecticide
➢ Failure to retreat to kill nymphs What is it?
emerged from eggs - Common Mucosal Viral Infection
➢ Reinfection. that presents with localized
blistering
II. VIRAL - Can reside in a latent state

A. Viral Warts 2 Types:

- Benign Tumors of the skin a. Type 1
- Common in children - Typically facial/oral infections (Cold
- Infectious ʹ (Spread by direct sores/fever blisters)
contact) - Occur mainly in infants & young kids

Organism: b. Type 2
- Typically from HPV (human - Mainly Genital
papilloma viruses) - Occur after puberty (often
transmitted sexually)
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
 Pathophysiology
Pathophysiology:
Presentation: - Incubation Period = 2 weeks
Stages of Infection: - (Chicken Pox) Initial Mucosal
1. Prodromal Stage Vesicle or "blister" Infection > Viraemia > Epidermal
stage Lesions
2. Ulcer stage - May lead to Latent infection of
3. Crust stage Dorsal Ganglion Cells of Sensory
Nerves.
- The virus grows down the nerves - (Shingles) Reactivation of latent
and out into the skin > Localized Varicella Zoster Virus in Peripheral
Blistering Nerves
- Neuralgia
- Lymphadenopathy Signs/symptoms:
- High Fever - Itchy rash or red papules
- Recurrences can be triggered by: - Begins on the Trunk > Face and
Minor trauma/Other Extremities
infections/UV - May cover entire body
radiation/Hormonal - High fever/headache/cold-like
factors/Emotional symptoms/vomiting/diarrhea.
stress/Operations/procedures on Diagnosis:
face - Clinical Diagnosis
- Immunofluorescence
Treatment: - Test for Elevated VZV-Specific
- Mild cases require no treatment Antibodies (IgM - Primary Infection;
- Sun protection to prevent IgG - Second Infection)
- Oral Antiviral Drugs (Stop the virus
multiplying) Treatment:
- Symptomatic
Complications: - Resolves on its own.
- Encephalopathy
- Trigeminal Neuralgia (Neurogenic Complications:
Pain) - Varicella During Pregnancy can
cause Congenital Varicella
C. Chicken pox (Herpes Varicella Syndrome:
Zoster) o Spontaneous Abortion (3-8%
in 1st Trimester) or IUGR
What is it? - Skin: Cutaneous Defects,
- Highly contagious disease Hypopigmentation
- Typically childhood disease (before - Neuro: Intrauterine Encephalitis,
10yrs) Brain Damage, Seizures,
- One infection thought to confer Developmental Delay
lifelong immunity - Eye: Chorioretinitis, Cataracts,
Anisocoria
Organism: - MSK: Limb Hypoplasia
- Varicella zoster virus (HHV3) (AKA: - Systemic: cerebral cortical atrophy
Chicken Pox Virus, Varicella, Zoster) - Renal: Hydronephrosis, Hydroureter
- GI: GORD
Transmission: - CVS: Congenital Heart Defects
- Highly Infectious - Perinatal Varicella Infection:
- From person to person o severe mortality rate of 30%
- Aerosol Droplets
- Direct contact with fluid from open
sore.

[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
 Pathophysiology
IV. BACTERIAL
A. Impetigo (AKA School Sores)
What is it?
- Superficial Bacterial Skin Infection
- Most Common in school kids
- Very Contagious ʹ (Spread by Close
Contact & Poor Hygiene)
- Usually resolves slowly
Organism:
- Mostly Staphylococcus Aureus
- Sometimes Streptococcus Pyogenes
- Can lead to Glomerulonephritis or
Rheumatic Fever if it is Strep
a. Staph. Aureus (Bullous)
b. Streptococcus (Non-bullous)
Presentations:
- Occur most commonly on face
- Fragile vesicles rupture & crust
- Can be confused with HSV
1. Nonbullous/Crusted Impetigo:
- (Most common)
- Yellow crusts and erosions
- Itchy/Irritating (but not painful).
2. Bullous impetigo:
- Always due to S. Aureus
- Mildly irritating blisters that erode
rapidly leaving a brown crust.
3. Ulcerative lesions:
- Always due to S. pyogenes.
- Most common in Aboriginal
Communities
Very Infectious
- Epidemic in young children
- Transmitted through skin contact
- Outbreaks associated with poor
hygiene / crowded living conditions
Treatment:
- Cover Affected Areas
- Abstain from School
- Systemic or Topical Antibiotics
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
B. Folliculitis & Furunculosis (Boils):
What is it?
Folliculitis:
- Acute pustular infection of a hair
follicle
- Commonly after Waxing/Shaving
Boils (Furuncles):
- A deep form of folliculitis.
Organism:
- Staphylococcus Aureus
Presentation:
- Folliculitis: An Erythematous Pustule
centered on a Hair Follicle.
- Boils (Furuncles): Tender, red
nodule which enlarges & may later
discharge pus
Treatment:
- Treated aggressively with antibiotics
and drainage.
C. Abscesses:
- Usually Staphylococcus Aureus
- Begin as superficial infections of hair
follicles (folliculitis)
➢ Organisms travel down Hair Follicles
following Disruption (Eg. After
Shaving)
➢ Development of boils (furuncles)
- Number of boils cluster together =
carbuncle;͟ aka Abscess
D. Cellulitis:
What is it?
- Bacterial infection of the Dermis and
Sub-Cutaneous Tissues
Organism:
- Adults: 90% due to Staph.
Aureus/GAS
- Children: H. influenzae b
- Associated with cat/dog bite:
Pasteurella multocida
Presentation:
- Painful, raised and Edematous
Erythema. (Most commonly on
Lower Leg)
- Possible Blistering
- Lymphadenopathy - & Malaise &
Fever.
 Pathophysiology
Distribution:
- Children - Periorbital Area
- Adults - Lower Legs
There’s usually an underlying cause:
- Lymphoedema
- Tinea, Herpes simplex infection,
- Chronic sinus infection
- Chronic dermatitis
- Poor lower leg circulation
- Wounds
Treatment:
- Antibiotics
E. Necrotizing Fasciitis:
- Medical Emergency - Often needs
Radical Debridement of Necrotic
Tissue
Organisms:
- Group A Strep (GAS)
- Staph. Aureus
- (Both cause severe, systemic
toxicity)
- Others (Vibrio, Clostridium,
Bacteroides)
Pathogenesis:
- The Necrosis is Toxin-Mediated >
YOU CAN’T JUST TREAT WITH
ANTIBIOTICS
- Not due to a Flesh Eating Bacteria
Types:
Type I - Polymicrobial Infection
Type II - Monomicrobial Infection
F. Gas Gangrene:
Organism:
- Clostridium perfringens
Pathogenesis:
- Generally, occurs at site of trauma
or recent surgical wound
- Usually only occurs with Poor Blood
Supply (E.g. Diabetes)
- Anaerobic conditions
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
- Toxins are produced > Cause the
Tissue Death and associated
Symptoms
Presentation:
- Inflammation at the Site of Infection
- Brownish-red and extremely painful
tissue swelling
- Gas may be felt in the tissue when
the swollen area is pressed
- Margins of the infected area expand
rapidly (Within a few minutes)
Prognosis:
- The involved tissue is completely
destroyed (Toxin-Mediated
Destruction)
G. Mycobacterial Infections:
1. Leprosy:
- Tuberculoid and lepromatous forms
- Mainly affect skin and nerves
SKIN MANIFESTATION OF METABOLIC
DISEASES – JAUNDICE
BILIRUBIN
 Bilirubin is a yellow breakdown
product of normal heme catabolism.
 Its levels are elevated in certain
diseases, and it is responsible for the
yellow color of bruises and the
brown color of feces.
 Bilirubin reduction in the gut leads
to a product called urobilinogen,
which is excreted in urine.
 It is thought to be a toxin because it
is associated with neonatal jaundice,
possibly leading to irreversible brain
damage due to neurotoxicity.
 Like these other pigments, bilirubin
changes its conformation when
exposed to light. This is used in the
phototherapy of jaundiced
newborns: the illuminated version of
bilirubin is more soluble than the
unilluminated version.
 Pathophysiology
BILIRUBIN FORMATION
- Erythrocytes (red blood cells)
generated in the bone marrow are
destroyed in the spleen when they
get old or damaged.
- This releases hemoglobin, which is
broken down to heme, as the globin
parts are turned into amino acids.
- The heme is then turned into
unconjugated bilirubin in the
macrophages of the spleen.
- Bilirubin is bound to albumin and
transported in plasma from the
reticuloendothelial system to the
liver, as unconjugated bilirubin.
- In the liver, bilirubin is made water
soluble by hepatocytes which
conjugate bilirubin with glucuronic
acid to form conjugated bilirubin
(BC).
- BC is secreted from hepatocytes to
the bile canaliculi of the liver and is
transported from the liver via the
gall bladder and common bile duct
to the gastrointestinal tract.
- In the ileum and colon, bacteria
convert bilirubin into
stercobilinogen.
- Stercobilinogen is oxidized to
stercobilin, which is excreted in the
feces.
- While most bilirubin is excreted as
stercobilin, a small amount of
stercobilinogen is reabsorbed into
the blood, modified by the kidneys,
and excreted as urobilinogen in the
urine.
JAUNDICE
- Jaundice is a condition in which the
skin, sclera (whites of the eyes) and
mucous membranes turn yellow.
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD
- This yellow color is caused by a high
level of bilirubin, a yellow-orange
bile pigment. Bile is fluid secreted by
the liver.
- Jaundice may be noticeable in the
sclera (white) of the eyes at levels of
about 30-50 μmol/l, and in the skin
at higher levels. Jaundice is classified
depending upon whether the
bilirubin is free or conjugated to
glucuronic acid into:
1. Conjugated jaundice
2. Unconjugated jaundice
- Jaundice also can be classified into
three categories, depending on
which part of the physiological
mechanism and the pathology
affects. The three categories are:
1. Pre-hepatic: The pathology is
occurring prior the liver
2. Hepatic: The pathology is located
within the liver
3. Post-Hepatic: The pathology is
located after the conjugation of
bilirubin in the liver
Pre-hepatic jaundice is caused by anything
which causes an increased rate of hemolysis
(breakdown of red blood cells). As seen in:
- Malaria
- Certain genetic diseases, such as
sickle cell anemia, spherocytosis and
glucose 6-phosphate dehydrogenase
deficiency
- Commonly, diseases of the kidney.
Hepatic jaundice causes include:
- Acute Hepatitis
- alcoholic liver disease.
- Neonatal jaundice, is common,
occurring in almost every newborn
as hepatic machinery for the
conjugation and excretion of
bilirubin does not fully mature until
approximately two weeks of age.
Post-hepatic jaundice, also called
obstructive jaundice, is caused by an
interruption to the drainage of bile in the
biliary system.
 Pathophysiology

- The most common causes are

gallstones in the common bile duct,
and pancreatic cancer in the head of
the pancreas. Also, a group of
parasites known as "liver flukes" live
in the common bile duct, causing
obstructive jaundice.
B. Urticaria (Hives):
Etiology
- Type I hypersensitivity – Allergy
(Food/drug/plant/etc)

- The presence of pale stools and dark Pathogenesis:

urine suggests an obstructive or
post-hepatic cause as normal feces
get their color from bile pigments.
- Patients also can present with
elevated serum cholesterol, and
often complain of severe itching.
INFLAMMATORY SKIN DISORDERS
- Antigen is Re-Exposed to a sensitized
Mast-Cell/Basophila IgE-Bound Mast
Cell Degranulates: § àReleasing
Inflammatory Mediators (Histamine)
of Type-1-Hypersensitivity
Reactions.
- Perivascular inflammatory infiltrate:
lymphocytes, neutrophils or
eosinophils.

A. Psoriasis Clinical Significance

Etiology
- Multifactorial (Genetic & Immune)
Pathogenesis:
- Sensitized T cells infiltrate the skin
and secrete cytokines and growth
factors > Continuous stimulation of
basal cellsa > Increased cell turnover
> Inflammation, Vascular
Proliferation Angiogenesis
- Usually on trunk and extremities.
- Individual lesions are transient,
usually resolve in 24 hr, but entire
episode may last for days.
- All ages, more in 20 – 40y.
********END OF MODULE 2********

Morphology
Gross:
- Plaque covered with Silvery Scales
(Due to Hyperkeratosis &
Parakeratosis)
- Bilateral
- Well-Demarcated
- Erythematous Based

Clinical Significance (List 3x Clinical

Features):
Can cause Multi-System Disorder:
- Arthritis
- Myopathy
- Enteropathy
- Immunodeficiency
- Nail Pitting

Auspitz Sign:
- Micro bleeding when crusts are
removed.
[MODULE 2 – DISORDERS OF THE SKIN] – Prepared by: Michael Angelo O. Sumugat, RMT MD