Bullous pemphigoid


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Bullous pemphigoid

Integumentary system

Pigmented skin disorders



Acneiform skin disorders

Acne vulgaris



Hidradenitis suppurativa

Papulosquamous and inflammatory skin disorders

Contact dermatitis

Atopic dermatitis

Lichen planus

Pityriasis rosea


Seborrhoeic dermatitis


Keratotic skin disorders

Actinic keratosis

Vesiculobullous skin disorders

Epidermolysis bullosa

Bullous pemphigoid

Pemphigus vulgaris

Desquamating skin disorders

Erythema multiforme

Stevens-Johnson syndrome

Skin integrity disorders

Pressure ulcer




Skin infections




Necrotizing fasciitis

Human papillomavirus

Varicella zoster virus

Poxvirus (Smallpox and Molluscum contagiosum)


Herpes simplex virus


Malassezia (Tinea versicolor and Seborrhoeic dermatitis)

Pediculus humanus and Phthirus pubis (Lice)

Sarcoptes scabiei (Scabies)

Human herpesvirus 6 (Roseola)

Parvovirus B19

Varicella zoster virus

Measles virus

Rubella virus

Skin neoplasms

Vascular tumors

Human herpesvirus 8 (Kaposi sarcoma)


Skin cancer

Hair and nail disorders

Alopecia areata

Telogen effluvium


Integumentary system pathology review

Pigmentation skin disorders: Pathology review

Acneiform skin disorders: Pathology review

Papulosquamous and inflammatory skin disorders: Pathology review

Vesiculobullous and desquamating skin disorders: Pathology review

Skin cancer: Pathology review

Bacterial and viral skin infections: Pathology review

Viral exanthems of childhood: Pathology review


Bullous pemphigoid


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USMLE® Step 1 questions

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High Yield Notes

4 pages


Bullous pemphigoid

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USMLE® Step 1 style questions USMLE

of complete

A 70-year-old man comes to the office because of severe generalized pruritus and blisters. The pruritus began a month ago, followed by multiple tense blisters over his body two weeks later. Some of the blisters ruptured, causing moist erosions. Past medical history is significant for Parkinson disease and hypertension. Current medications include levodopa/carbidopa and lisinopril. Vitals are within normal limits. Physical examination shows multiple 1 to 3 cm tense bullae as shown:  

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Which of the following histological findings will be seen in this patient?  

External References

First Aid








Bullous pemphigoid p. 487, 493

autoantibody p. 113

type II hypersensitivity p. 110

IgG antibodies p. 103

bullous pemphigoid p. 493



Stefan Stoisavljevic, MD

Evan Debevec-McKenney

Justin Ling, MD, MS

Bullous pemphigoid is an autoimmune skin disease that causes the skin to form bullae or blisters.

Now, the skin is divided into three layers--the epidermis, dermis, and hypodermis.

The epidermis forms the thin outermost layer of skin.

Underneath, is the thicker dermis layer, and finally, there’s the hypodermis that anchors the skin to the underlying muscle.

The epidermis itself is made of multiple layers of developing keratinocytes - which are flat pancake-shaped cells that are named for the keratin protein that they’re filled with.

Keratinocytes start their life at the lowest layer of the epidermis called the stratum basale, or basal layer which is made of a single layer of stem cells, called basal cells that continually divide and produce new keratinocytes.

The stratum basale also contains another group of cells called melanocytes, which secrete melanin.

Melanin is a pigment protein, or coloring substance.

Below the epidermis is the basement membrane which is a thin layer of delicate tissue containing collagen, laminins, and other proteins.

Basal cells are attached to the basement membrane by hemidesmosomes, a protein complex that stems from the bottom of the basal cells.

Just like an anchor digs into the seafloor and holds a boat in place, hemidesmosomes dig into the basement membrane and hold basal cells in place.

The exact cause of bullous pemphigoid is unclear, but it’s thought that in a person with a genetic precondition, it can be triggered by medications like furosemide, captopril, penicillamine, non steroid anti-inflammatory drugs (or NSAIDs), and antibiotics.

Bullous pemphigoid is a type II hypersensitivity reaction, which is when the immune system produces antibodies that bind to the body’s own cells.

Immune cells called B cells produce IgG antibodies, which are Y shaped molecules with 2 regions, an antigen binding fragment region - or Fab region, and fragment crystallizable region or Fc region.


  1. "Robbins Basic Pathology" Elsevier (2017)
  2. "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
  3. "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
  4. "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
  5. "Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects" Autoimmunity Reviews (2015)
  6. "Assessment of Diagnostic Strategy for Early Recognition of Bullous and Nonbullous Variants of Pemphigoid" JAMA Dermatology (2019)
  7. "Interventions for bullous pemphigoid" Cochrane Database of Systematic Reviews (2010)
  8. "Bullous pemphigoid: Etiology, pathogenesis, and inducing factors: Facts and controversies" Clinics in Dermatology (2013)

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