Pathology of Skin - Common Disorders

Pathology of common skin disorders for undergraduate medical students.

1. “Life’s battles don’t go always to the
stronger or faster man, sooner or later,
the man who wins is the man who
thinks he can”
Aim for the Moon… even if you miss, you will Aim for the Moon… even if you miss, you will
land among Stars…..!land among Stars…..!

3. DERMATOPATHOLOGY
Acute, Chronic, Infections, Blistering, Neoplastic
Dr. Shashidhar Venkatesh Murthy
Associate Prof. & Head of Pathology

4. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Psoriasis,
•Chronic Eczema,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Actinic Keratosis,
•Seborrheic Keratosis.
•Malignant:
•BCC, SCC, Melanoma.

5. Normal Skin: (Thin)

6. Prominent granular layer
Thick Skin:

7. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Psoriasis,
•Chronic Eczema,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Actinic Keratosis,
•Seborrheic Keratosis.
•Malignant:
•BCC, SCC, Melanoma.

8. INFLAMMATORY disorders: Pathogenesis
Urticaria Acute Chronic Lichen
Eczema Eczema Sclerosis
DermalInfl Epidermal InflHyperplasia Hyperkeratosis
Acute Inflam. Chronic Inflam.
Ep. Hyperplasia

9. URTICARIA (Hives)
•Type I hypersensitivity – Allergy
•All ages, more in 20 – 40y.
•Erythematous papules and
plaques
•Individual lesions are transient,
usually resolve in 24 hr, but
entire episode may last for days.
•Usually on trunk and extremities.

10. Urticaria (Hives)

11. URTICARIA – Histopathology
Perivascular inflammatory
infiltrate: lymphocytes,
neutrophils, eosinophils.
* Note lack of spongiosis
or other epidermal
changes.

12. URTICARIA (Hives)
•Follows exposure to pollens, foods,
drugs, pressure, temperature etc.
•Ag  IgE  Mast cell
Degranulation  Inflam.
•perivascular inflammatory infiltrate:
lymphocytes, neutrophils or
eosinophils.
•Hereditary angioneurotic edema 
Congenital C1 esterase inhibitor
deficiency causes uncontrolled
complement activation and
urticaria.

13. Urticaria – Microscopic features
1.Superficial dermal edema (space between collagen)
2.Dilated blood vessels with perivascular inflammatory cells.
3.Normal Epidermis (no spongiosis or hyperplasia)
1
3
2

14. Acute ECZEMA – Types
•Contact dermatitis
•Atopic dermatitis
•Drug eczema
•Photoeczema
•Primary irritant dermatitis
Intraepidermal
edema & blister

15. ECZEMA dry - (atopic)

16. My ear is dripping on my shirt…!
•A 36y Male, 12wk rash left ear.
•Spreading and becoming
increasingly irritating despite
twice daily applications of
Kenacomb Otic ointment.
•he is otherwise in good health,
with no history of serious
illness, and there are no known
allergies nor rashes anywhere
else.
•DD: contact dermatitis, fungal
infection (Tinea), Imeptigo
(bact), others.
Drug induced
Eczema

17. ECZEMA – histology
•Spongiosis
(Intraepidermal)
edema
•Superficial
perivascular
lymphocytic
infiltrate

18. ECZEMA – pathogenesis:
Hypersensitivity Reaction:
•Initial exposure to antigen:
•Antigen processed by Langerhans cells and presented
to T cells in the lymph node  T cell activation 
memory cells.
•Re-exposure to antigen:
•Quick (memory T cells) response  inflammation 
urticaria, erythema, wet eczema
•Persistence of antigen stimulation:
•Chronic inflammation  Acanthosis, hyperkeratosis
(lichenification) – dry eczema.

19. ECZEMA (irritant)

20. ECZEMA (contact dermatitis)

21. ERYTHEMA MULTIFORME:
•Self limited Hypersensitivity response to,
•Infections: herpes simplex, Mycoplasma
•Drugs: sulfonamides, penicillin barbiturates
•Malignancy: carcinoma, lymphoma
•Auto Immune dis: SLE, SS, dermatomyositis
•Multiple forms - papules, plaques, nodules,
blisters, ulcers etc..
•Characteristic “targetoid” lesions.
•Central grey necrosis, Erythematous raised border.
•Mild to severe forms – spectrum
•EM Minor, EM Major, Stevens-Johnsons
syndrome and toxic epidermal necrolysis.

22. ERYTHEMA MULTIFORME
Target Lesions

23. ERYTHEMA MULTIFORME - Microscopy
•Necrotic
keratinocytes
•Spongiosis
(edema)
•Epidermal
lymphocytes
•Superficial
perivascular
lymphocytes
Note: destruction of basal epidermal layer.

24. Stevens-Johnson Sy.(EM major)
•A 2y black male, who was
started on Phenobarbital after
his third febrile seizure. Seven
days later, he developed
erythematous lesions over his
extremities, hands, face and
trunk with high fever. Bullae,
Erosion and crusting of
mucosal surfaces.
•May be caused by other drugs,
infections, histology same as
EM.

25. Toxic Epidermal Necrolysis (TENs):
•Larger body surface
involvement (>40%)
•Development of bullae &
peeling of epidermis in sheets
>3 cm & the skin becomes
tender within 48 hours.
•Extensive basal layer
degeneration.
•Serious complication of EM
Major & TENs is conjunctival
damage resulting in corneal
drying and opacification
(blindness).

26. "The gem cannot be polished without
friction, nor man perfected without
trials or problems (or exams)…!."
--Chinese proverb

27. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Chronic Eczema,
•Psoriasis,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Actinic Keratosis,
•Seborrheic Keratosis.
•Malignant:
•BCC, SCC, Melanoma.

28. PSORIASIS - pathophysiology
•Multifactorial: genetic and immune
•strong association HLA-C (w 0602 allele)
⋆

•Sensitized T cells infiltrate the skin and
secrete cytokines and growth factors
•Inflammation, Increased cell turnover
•Vascular proliferation angiogenesis
•Trauma precipitates lesions – Koebner phen.
•Multi system disorder:
•Arthritis, myopathy, enteropathy, Immunodef.

29. PSORIASIS - clinical
•Chronic, recurrent elbows, knee, scalp
•well-demarcated, pink plaque covered with loosely
adherent silvery scales.
•Removal of scales  point bleeds – Auspitz sign.

30. PSORIASIS
CLINICAL:
•Pink Plaques
•Silvery scales.
•Koebner Phenomenon
•Auspitz sign
•Arthritis.

31. PSORIASIS – Nail changes
•“Oil-slick” nail discoloration
•Nail pitting
•Onycholysis

32. PSORIASIS – Arthritis.

33. Psoriasis: Histopathology
Acanthosis, Parakeratosis, neutrophilic microabscesses.

34. PSORIASIS - histology
Parakeratosis
Diminished granular layer
Regular elongation of the
rete ridges
Tortuous papillary dermal
vessels
neutrophil abscess in
epidermis

35. Lichen Planus:
•Pruritic, Purple, Polygonal, Planar,
Papules and Plaques.
•Skin & mucosa. Genitals, oral,
•Self limited. 1-2 years.
•Basal layer, Interface dermatitis.
•Degenration, Squamatization
•Anucleate dead epidermal cells in
basal layer – Civatte bodies.
•Similar to EM but chronic with
hyperplasia, hyperkeratosis(scaling).

36. Lichen Planus:
Mucosal involvement

37. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Chronic Eczema,
•Psoriasis,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Actinic Keratosis,
•Seborrheic Keratosis.
•Malignant:
•BCC, SCC, Melanoma.

38. Impetigo: Bacterial Infection
•Staph or Strep
•Superficial, Bacterial
•Oozing & crusting.
•Spongiosis
•Neutrophils.

39. Impetigo:
Epithelium
Ulcer + Inflam

40. Acne: Acne: Pathogenesis
•Inflammation of pilosebaceous units
•Interplay of four factors
•Excessive sebum - sebaceoussebaceous glandgland
hyperplasiahyperplasia
•HyperkeratinizationHyperkeratinization – Microcomedo -
Obstruct pores.
•Lipids and cellular debris accumulate
within the blocked follicle.
•Colonization of PropionibacteriumPropionibacterium acnes acnes
(+ secondary infection)
•InflammationInflammation is further enhanced by
follicular rupture and subsequent
leakage of lipids, bacteria, and fatty
acids into the dermis.

41. Acne: Hair fol. infection:
Neutrophil Abscess
Hair Follicle (infected)
Hair Follicle (infected)Block  sebum  infection
Harmonal, excess/drying/oily
Comedo

42. Bacterial
Skin Infections:
Types

43. Viral Infections:
•Human papillomavirus: Warts (verrucae)
•Keratotic(hard) & condyloma (fleshy)
•Molluscum contagiosum:
•Herpes – Zoster & Shingles.
•HIV – Kaposi sarcoma (HHV 8)

44. Verruca Plana:
•HPV-3 or 10
•Face, young, flat
•Small, hyperkeratotic
•Koilocytic keratinocytes.

45. Palmoplantar warts: Myrmecia
•HPV-3 or 10
•Sole & Palms
•Intradermal hard cyst.
•Inward growth
•Koilocytic keratinocytes.

46. Condyloma accuminatum:
•HPV-6, Genital warts
•Fleshy growths
•Acanthosis, papillomatosis
•Koilocytes- perinuclear
halo. – viral inclusions.
Pap Smear
Cervical
Biopsy

47. Molluscum contagiosum:
•DNA pox virus
•Grouped pearly hypopigmented
flask like papules with central
cupped scaly centre (arrow A).
•Pink cytoplasmic viral inclusions
“Molluscum body” (arrow B)
B A

48. Fungal: Tineasis
•Ring worm, Round, scaly, itchy
dermatitis – Trichophyton sp
•Spreading out with Central clearing.
•Lab: Scrapings in KOH solution
•Tinea cruris.
•Tinea capitis
•Tinea versicolor – pale macules –
•Pityrosporum.
Fungus
Fungus

49. Case Study: Painful, Itchy vesicles:
•A 32y man, itchy and painful
rash on the back of his left leg
•About 7 days ago, he began to
feel an “intense itching &
burning pain” behind his left
knee.
•“small blisters” began to “pop
up” over the area.
•Not responding to antibiotic
ointment and acetaminophen
(Tylenol).
? likely diagnosis?
*Intense, burning pain & blisters along nerve distribution
Cutaneous Herpes - Shingles.

50. “The worst thing in your life may
contain seeds of the best. When you can
see crisis as an opportunity, your life
becomes not only easier, but more
satisfying.”
–Joe Kogel

51. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Chronic Eczema,
•Psoriasis,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Actinic Keratosis,
•Seborrheic Keratosis.
•Malignant:
•BCC, SCC, Melanoma.

52. BLISTERING DISEASES
•Subcornial.
•Suprabasal.
•Subepidermal.
PEMPIGUS FOLIACESOUS PEMPIGUS VULGARIS BULLOUS PEMPHIGOID

53. BLISTERING DISEASES
•Pemphigus :
•vulgaris most common (80%) other variants (vegetans,
foliaceus, erythematosus) are rare
•40-60y, mucosa & skin.
•scalp, face, axilla, groin, trunk.
•Autoimmune, IgG against desmosomes.
•acantholysis, intraepidermal blister, loose cells inside bulla.
•Bullous pemphigoid:
•Elderly, Autoimmune (subepidermal Anchoring proteins).
•thighs, flexor surface of forearms, axilla, groin, 30% oral.
•Large, Tense, Subepidermal bullae, no acantholysis.
•Dermatitis Herpetiformis:
•Rare, very itchy small papules, vesicles, occassional bullae.
Males, associated with celiac disease (gluten sensitivity).

54. Pemphigus vulgaris

55. Pemphigus vulgaris
•Gross: Axilla, flaccid, erythematous base,
easy rupture, crusted ulcers.
•Microscopy: intraepidermal location.
Loose acantholytic cells inside.

56. Acanthocytes - Acantholysis:

57. PEMPHIGUS – Immunoflourescence
Deposition of
immunoglobulin
and complement
along keratinocyte
membranes giving
a “fish net”
appearance

60. PEMPHIGUS
•Four variants: P. vulgaris – most common

61. Intraepidermal bulla:

62. BLISTERING DISEASES
•Pemphigus :
•vulgaris most common (80%) other variants (vegetans,
foliaceus, erythematosus) are rare
•40-60y, mucosa & skin.
•scalp, face, axilla, groin, trunk.
•Autoimmune, IgG against desmosomes.
•acantholysis, intraepidermal blister, loose cells inside bulla.
•Bullous pemphigoid:
•Elderly, Autoimmune (subepidermal Anchoring proteins).
•thighs, flexor surface of forearms, axilla, groin, 30% oral.
•Large, Tense, Subepidermal bullae, no acantholysis.
•Dermatitis Herpetiformis:
•Rare, very itchy small papules, vesicles, occassional bullae.
Males, associated with celiac disease (gluten sensitivity).

63. BULLOUS PEMPHIGOID
•Tense large bulla
•Intact epithelium.

64. BULLOUS PEMPHIGOID
82 year old nursing home, dementia, gastrostomy tube, treated for urinary tract infection

65. BULLOUS PEMPHIGOID
Hemorrhagic blisters
annular arrangement 
in bullous pemphigoid

66. BULLOUS PEMPHIGOID
Antibody against
bullous pemphigoid
antigen in basement
membrane causing
subepidermal
separation
Type II
hypersensitivity
reaction.

67. BULLOUS PEMPHIGOID
Eosinophils at the
DE junction.
Subepidermal bulla

68. BULLOUS PEMPHIGOID - histology
Subepidermal
blister
Inflammation
characterized by
eosinophils
Intact acanthocytic
layer.

69. BLISTERING DISEASES
•Pemphigus :
•vulgaris most common (80%) other variants (vegetans,
foliaceus, erythematosus) are rare
•40-60y, mucosa & skin.
•scalp, face, axilla, groin, trunk.
•Autoimmune, IgG against desmosomes.
•acantholysis, intraepidermal blister, loose cells inside bulla.
•Bullous pemphigoid:
•Elderly, Autoimmune (subepidermal Anchoring proteins).
•thighs, flexor surface of forearms, axilla, groin, 30% oral.
•Large, Tense, Subepidermal bullae, no acantholysis.
•Dermatitis Herpetiformis:
•Rare, very itchy small papules, vesicles, occassional bullae.
Males, associated with celiac disease (gluten sensitivity).

70. Dermatitis Herpetiformis
•Extremely pruritic, small vesicles
•Associated with Celiac disease.
•IgA Anti-gluten Ab cross react with
basement membrane proteins.
•Microabscess – papillae
•Subepidermal blister.
•Granular IgA deposits.

71. Dermatitis Herpetiformis:
•Gross: Intense Itchy, small, erythematous,
pappules, small blisters in groups. (sub epithelial)
•Micro: supepidermal, neutrophilic microabscesses
in dermal papilla.

72. PEMPHIGUSPEMPHIGUS PEMPHIGOIDPEMPHIGOID DHDH
age mid - older elderly 30-40
antibody IgG IgG IgA
locationSuprabasilarSubepidermal subepidermal
inflammati
on
mixed eosinophils neutrophils
Site of
dysfunctio
n
Desmosomes
Basement
membrane and
hemidesmosome
s
Anchoring fibrils
Antibody
against:
Desmoglein
Bullous
pemphigoid
antigen
reticulin
Immuno “fish net”
Linear basement
membrane
Dermal tip

73. "When you speak, speak the truth;
perform when you promise; discharge
your trust... Withhold your hands from
striking, and from taking that which is
unlawful and bad...“
- - APJ Abdul Kalam, President of India.

74. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Chronic Eczema,
•Psoriasis,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Seborrheic Keratosis.
•Actinic Keratosis,
•Malignant:
•SCC, BCC, Melanoma.

75. Skin Tumours Incidence:
•Most Common: (no count, ?disease ….! )
•Moles, Nevi, Freckles,
•Skin Tags & Cherry angioma
•Common:
•Benign: Warts, Seborrheic & Actinic keratosis,..
•Malignant: Carcinoma (Basal, Sq, Melanoma)
•Rare: (less but not uncommon..!)
•Many… Epithelial, adnexal, con. tissue, others.
•Adenoma, fibroma, lipoma, cylindroma… etc..

76. Benign: Nevus/nevi:
•Commonest *
•Congenital / after birth
•Stable, permanent.
•Uniform, symmetrical
suggest benign.
•Irregular, varying
color or growth -
malignancy.
•Rarely grow.
•Changes suggest
malignant
transformation (rare).

77. Nevi types & Pathology:

78. Junctional Nevus:
•Small, flat, symmetric, uniform lesions.
•Cluster of melanocytes at DE junction. (arrow)

79. Compound Nevus:
•Small, raised, dome shaped, symmetric, uniform.
•Cluster of melanocytes in dermis & DE junction.
(arrow)

80. Dysplastic Nevus:
1.Pigmented raised lesion with central darker shade (arrow).
2.Junctional cluster of irregular melanocytes (arrow)
1
2

81. Progression of dysplastic nevus:
A.Lentiginous melanocytic hyperplasia.
B.Lentiginous junctional nevus.
C.Lentiginous compound dysplastic nevus
D.Early melanoma,
E.Advanced melanoma (vertical growth)
Melanoma
Nevus

82. SEBORRHEIC KERATOSIS
•Very common in elderly, Face.
•Round, flat, velvety plaques,
•?arrest in epidermal maturation.
•May be pigmented, Appear
“stuck on” skin.
•Treatment only if inflammed.
•Sudden crop of lesions occur in
internal cancers (Sign of Leser-
Trelat)
•No malignant potential.

83. SEBORRHEIC KERATOSIS

84. SEBORRHEIC KERATOSIS

85. Seborrheic Keratosis:

86. Seborrheic Keratoses: Microscopy
•Thick
hyperplastic
epidermis
above the
surrounding
level.
•Keratin cysts
1
2

87. Seborrheic Keratoses:
Exophytic (outward)
growth of Epidermal
hyperplasia

88. ACTINIC KERATOSIS
•Aged, sun exposure areas.
•Red or tan, Irregular, scaly plaques
•Pre-cancerous skin growth
•Sun-exposed skin
•Hyperkeratosis
•Inflammation
•ulceration
•Crusting
•Dysplasia
•Premalignant

89. Actinic Keratosis
•Lymphoid
infiltrate
•Epithelial atypia.
•Hyperkeratosis,
parakeratosis
•Sun damaged
dermis - Solar
elastosis.

90. ACTINIC KERATOSIS - histology
Parakeratosis
Atrophy
Basilar atypia

91. ACTINIC KERATOSIS - histology
Parakeratosis, atypical basal layer, solar elastosis
Note: atypical cells “spare” hair follicle epithelium.

92. Actinic Keratosis – Horn / Ca.

93. "Thinking is progress. Non-thinking is
stagnation of the individual, organisation
and the country. Thinking leads to right
action. Knowledge without action is
useless and irrelevant. Knowledge with
action, converts adversity into
prosperity.”
- - APJ Abdul Kalam, President of India.

94. SQUAMOUS CELL CARCINOMA
•Common cancer on
sun-exposed skin in
older people.
•Industrial carcinogens
•Arsenic, tobacco, Beetle
nut chewing.
•UV, Ionizing radiation
•Squamous epithelial
cells
•Microscopy:
dyskeratosis. Epithelial
pearls –
Keratin Pearl

95. SQUAMOUS CELL CARCINOMA

96. Epithelial (Keratin) pearl in SCC:
Keratinized – ep. pearl
Dysplastic ep. cells

97. BASAL CELL CARCINOMA
•Relatively common
•Slow growing
•Rarely metastasize
•Occur on sun-exposed
skin
•Pearly papule with
telangectasia
•Large tumors may
ulcerate (rodent ulcer)

98. Basal Cell Carcinoma:
Type •Features Picture
Nodular BCC •Most common
•Small, shiny, pink lump
•Prominent BV network.
Superficial BCC •Often multiple
•Pink or red scaly
irregular plaques
Morphoeic BCC •sclerosing BCC
•scar-like
•(perineural spread)
Pigmented BCC •Brown, blue or grey
•Like melanoma
•Nodular or superficial
Basisquamous BCC •Mixed BCC & SCC
•more aggressive

99. Gross appearance:
•Round, nodular,
pearly/shiny.
•Prominent blood
vessels over the
tumor.
•Shiny Crust over the
lesion.

100. BASAL CELL CARCINOMA
•Note central ulcer
& prominent blood
vessels around.

101. BASAL CELL CARCINOMA

102. Basal Cell Carcinoma:
Squamous cells
(malignant)
extending deep
breaking through
basement
membrane
Squamous
eddies or “ep.
pearls”

103. BASAL CELL CARCINOMA

104. BASAL CELL CARCINOMA
Cords and islands of
basaloid cells
Hyperchromatic nuclei
Peripheral palisading
Clefting between tumor
and stroma
Mucinous stroma

105. Melanoma:
•Nests of atypical
melanocytes
•Melanin
pigment.
•Mitotic figure.

106. Melanoma Clinical Features: note ABCD..

107. Melanoma Types:
•Lentigenous: Flat superficial
basal layer – sun damage.
•Superficial Spreading: Early
stage. Upper layers.
Commonest.
•Nodular: Tumor growing
deep. advanced (all types)
•Acral – Palm/sole,
lentigenous or nodular.
•Subungual: Nail bed,
nodular.

108. Melanoma :

109. Melanoma :
ABCD..
Multiple Nevi one of
them changing
recently  Melanoma

110. Melanoma Types:
Nodular Melanotic
↓ Nodular Amelanotic
Lentigo 
Nodular

111. Melanoma : Histopathology
Tumor cells
extend from
epidermis to
invade the
dermis. Focal
brown
melanin
pigment in
some tumor
cells.

112. Melanoma : Histopathology
•Clusters of
malignant cells.
Clear cytoplasm.
Large pleomorphic
nucleus.
•focal melanin
pigmentation.

113. Melanoma : Histopathology
•Tumor in
dermis.
•focal
melanin
pigmentati
on.
•Inflammato
ry cells
around.

114. Melanoma Staging: Clark’s levels

115. "If you always put limit on everything you do,
physical or anything else it will spread into your
work and into your life. There are no limits. There
are only plateaus, and you must not stay there, you
must go beyond them."
- - Bruce Lee
1940-1973, Martial Artist and Actor

116. Dermatopathology: MD3020 curriculum
1.Acute Inflammations:
•Urticaria,
•Acute Eczema,
•Erythema Multiforme.
2.Chronic Inflammations:
•Chronic Eczema,
•Psoriasis,
•Lichen planus.
3.Infections
•Bacterial (Impetigo),
•Fungal(tinea) &
•Viral(warts).
1.Blistering Diseases
•Pemphigus,
•Pemphigoid,
•Dermatitis herpetiformis.
5. Neoplastic:
•Benign:
•Nevi,
•Seborrheic Keratosis.
•Actinic Keratosis,
•Malignant:
•SCC, BCC, Melanoma.

117. Psychodermatosis

118. Study Tips:
•Preparation:
•Read Lecture notes, attend lecture*.
•Read Robbins Pathology (Basic).
•“Study Images” Gross & Microscopic.
•Make short notes for each condition,
•List 3* clinical features.
•Etiology, Pathogenesis
•List 3* gross features.
•List 3* microscopic features.
•Self Assessment:
•Case studies.
•Questions & Answers.
Test your commitment,
Get ready for Exam tomorrow.....!

119. “Fixing your goal is like identifying
the North Star. You sight your
compass on it and then use it as the
means of getting back on track
when you tend to stray”
--Marshall Dimock
1.What I want to be? Am I going there?
2.What is the best use of my time right now?
Stick this on the wall in your room... !