Skin: Pathology

Front 1

Common finding in adults.

Back 1

Solar lentigo. (liver spots)

Front 2

Targets. What is this?

Back 2

Erythema multiforme. Hypersensitivity reaction commonly caused by mycoplasma or HSV

Front 3

What causes this?

Back 3

Tinea versicolor. The Malassezia furfur. Fungus acid inhibits melanosomes.

Front 4

Gluten-sensitive enteropathy.

Back 4

Dermatitis herpetiformis. IgA-anti-IgA complexes deposit subdermal

Front 5

Compare the terms:
macula vs patch
papule vs. nodule
vesicle vs. bulla
wheal vs. angioedema

Back 5

Macule: flat, circumscribed area of skin discoloration. Patch > 1 cm macula.
Papule: circumscribed elevation of the skin < 5 mm diameter. Nodule > 5 mm.
Vesicle: colleciton of fluid < 5 mm. Bulla > 5 mm.
Weal: cutaneous edema, angioedema: dermis edema.

Front 6

Define the terms.
Maceration:
Lichenification:
Excoriation:

Back 6

Maceration: surface softening due to constant wetting.
Lichenification: thickening of the skin secondary to scratching.
Excoriation: secondary, superficial ulceration due to scratching

Front 7

Define the histological terms.
Hyperkeratosis:
Parakeratosis:
Acantholysis:
Acanthosis:
Exocytosis:

Back 7

Increased thickening of stratum corneum.
Persistence of nuclei in stratum corneum layer.
Loss of cohesion between keratinocytes.
Hyperplasia of the stratum spinosum.
Exocytosis: infiltration of the epidermis by inflammatory or circulating blood cells.

Front 8

What are the cell layers of the skin?

Back 8

Stratum basalis: dividing stem cells (50 day turnover). Stratum spinosum: contain desmosomes. Stratum granulosum: contain keratohyaline granules. Stratum lucidum: only in thick skin. Stratum corneum: anucleated cells with keratin.

Front 9

How does the basement membrane of the skin remain attached to the superficial dermis and the dermis?

Back 9

BM is attached to keratinocytes via hemidesmosomes. BM is attached to dermis via anchoring fibrils (type IV collagen).

Front 10

Describe the function of melanocytes and where they are located?

Back 10

Melanocytes are derived from neural crest cells and are located in the stratum basalis (whites) or in all layers (blacks). They synthesize melanin in melanosomes which are passed to keratinocytes. Tyrosinase converts tyrosine to DOPA. DOPA is converted to melanin.

Front 11

What causes albinism?

Back 11

Melanocytes cannot produce melanin (absence in tyrosinase or inability to uptake tyrosine).

Front 12

Vitiligo is associated with what disorders?

Back 12

Hypoparathyroidism and hashimoto's. Autoimmune destruction of melanocytes causes the depigmentation.

Front 13

What is an ephilis?

Back 13

A freckle. Increaseed amounts of melanin pigment.

Front 14

Is solar lentigo a result of increased number of melanoctyes or an increased production of melanin by the melanocytes?

Back 14

Solar lentigo occurs in elderly individuals with sun damage in sun exposed areas. The result is macules due to an increase in the number of melanocytes.

Front 15

What causes Ritter's disease?

Back 15

Staphylococcal scalded skin syndrome (Ritter's) is causes by S. aureus which releases an exotoxin (exfoliatin) that cleaves desmoglobin that holds together the spinosum and granulosum layers.

Front 16

Hidradenitis suppurative is an infection of what gland?

Back 16

Hidradenitis suppurativa is a chronic condition characterized by swollen, painful, inflamed lesions in the axillae, groin, and other parts of the body that contain apocrine glands.

Front 17

What is this child suffering from?

Back 17

Impetigo, which is a contagious superficial infection. Staph aureus causes the bullous type while strep pyogenes causes the non-bollous type. Impetigo appears as pustules that rupture to form honey-colored, crusted lesions.

Front 18

What pathogen causes this characteristic skin lesion?

Back 18

Moluscum contagiosum caused by poxvirus (dsDNA) Picture shows a small bowl-shaped lesion with an umbillication.

Front 19

Patient presents to your office with a fever, conjunctivitis, runny nose, a cough, otitis media and Koplik spots on the buccal mucosa. How will the patient present in the near future?

Back 19

A patient with rubeola measels (ssRNA paramyxovirus, - , env) will develop a maculopapular rash after Koplik spots disappears. Complications in this patient can include acute appendicitis in children and giant cell pneumonia.

Front 20

40 year old male presents with polyarthritis, a maculopapular rash, and painful postauricular lymphadenopathy. What pathogen caused these symptoms?

Back 20

Rubella (German measels, RNA togavirus, +, Env).

Front 21

Patient presents with a slapped face appearance on his cheeks. The maculopapular rash also spreads to the trunk. What virus caused this and what other disorders are caused by this virus?

Back 21

The patient has erythema infectiosum caused by parvovirus B19 (ssDNA). Parvo also causes aplastic anemia in chronic hemolytic diseases. Pregnant mothers exposed to a child with this infection may abort the fetus.

Front 22

What is the disease caused by HHV-6 that causes febrile convulsions?

Back 22

Roseola infantum. Maculopapular rash occurs 3-7 days after a high fever.

Front 23

Although clinically obvious, varicella (chickenpox) can also be diagnosed with a positive Tzanck test (scraping + culture). What are some complications of this DNA herpesvirus?

Back 23

Reye syndrome. Pneumonia. Remains latent in cranial and thoracic sensory ganglia. Reemerges as shingles (zoster): painful vesicles following sensory dermatomes.

Front 24

What is Reyes syndrome?

Back 24

Reye syndrome is characterized by acute noninflammatory encephalopathy and hepatic failure. Typically occurs after a viral illness, particularly an URTI, influenza, varicella, or gastroenteritis, and it is associated with the use of aspirin during the illness.

Front 25

Patient recovering from rubeola develops a low grade fever, non-productive cough and flu-like symptoms. What cells may a pathologist find in the lungs of this patietn?

Back 25

Some patients will develop pneumonia as a sequela to measles. Histologically, a unique cell can be found in the paracortical region of hyperplastic lymph nodes in patients affected with this condition. This cell, known as the Warthin-Finkeldey cell, a multinucleated giant cell with eosinophilic cytoplasmic and nuclear inclusions

Front 26

What disease in newborns and children is caused by coxsackie and the clinical features include: small grey vesicles with a halo of erythema on hands/feet, fever, sores, rash with blisters, and buccal mucosa is studded with erosions?

Back 26

Hand, foot, and mouth disease.

Front 27

Where are lesions present in HSV-1 and HSV-2?

Back 27

HSV-1: cold sores on lip and face.
HSV-2: sores in genital region.

HSV-1,2 can be located in both sites, but are most commonly associated with the sites above.

Front 28

You notice a row of painful vesicles on a patient. You determine this rash is secluded to a distribution pattern along the T8 dermatome. What test can you use to diagnose this disease?

Back 28

Tzanck test. This is herpes zoster causing shingles. This DNA herpesvirus remains latent in cranial and thoracic sensory ganglia. Flair ups can result in shingles.

Front 29

What skin lesions can Staph aureus cause?

Back 29

Furunculosis (deep infection of a hair follicle), carbuncle (deep infection of a group of adjacent hair follicles), bollous type impetigo, Hidradenitis suppurativa (apocrine gland infection), Ritters/scalded skin

Front 30

Patient presents with a desquamating, sandpaper-like erythematous rash. He also has a strawberry tongue appearance. The rash spares the patients face. Diagnosis?

Back 30

Streptococcus pyogenes. Increased risk for developing poststreptococcal glomerulonephritis.

Front 31

Name the two types of leprosy and the causitive agent.

Back 31

Mycobacterium leprae.
Tuberculoid type: granulomas with few acid-fast bacteria. Intact cellular immunity.
Lepromatous type: absence of granulomas. Lack of cellular immunity.

Front 32

What bacteria cause acne vulgaris?

Back 32

Propionibacterium has lipases that breakdown the lipids in sebum into fatty acids. These FA cause local irritation and inflammation.

Front 33

Whats the underlying pathophysiology of the rhinophyma that is seen in acne rosacea?

Back 33

Sabaceous gland hyperplasia.

Front 34

Describe the two test used for diagnosing dermatophytoses: Wood's lamp and KOH-treated skin scrapings.

Back 34

Wood's: ultraviolet A light detects fluorescent metabolites produced by organisms.
KOH: identify yeasts and hyphae in the stratum corneum of hair shafts.

Front 35

What is the bacteria that causes syphillis and what are the stages of diseased cause by this STI?

Back 35

Treponema pallidum.
Primary – chancre: painless ulcer (punched out).
Secondary – rash on palms and soles, condyloma latum (painless, wart-like lesion).
Latent.
Tertiary (6-40 years later) – gummatous syphilis, cardiovascular syphilis, neurosyphilis.

Front 36

What type of leprosy will produce:
1) + lepromin test
2) Granulomas
3) Classic leonine facies
4) Autoamputation of digits

Back 36

1) Tuberculoid type
2) Tuberculoid type
3) Lepromatous type
4) Tuberculoid type

Front 37

What causes this disease?

Back 37

This is a characteristic rash caused Borrelia burgdorferi (transmitted by the Ixode tick) which causes Lyme disease. May progress to meningitis and cranial nerve palsies

Front 38

What is the pathogenesis of acne vulgaris?

Back 38

Chronic inflammation of the pilosebaceous unit. Abnormal keratinization. Increased sebum production (androgen-mediated). Propionibacterium acne produces irritating fatty acids.

Front 39

What does acne rosacea cause?

Back 39

Rhinophyma.

Front 40

Tinea capitis is most commonly caused by what two pathogens?

Back 40

Trichophyton tonsurans: negative wood's lamp.
Microsporum canis: positive wood's lamp.

Front 41

Tinea corporis (body), tinea pedis (foot), tinea cruris (groin), and tinea unguium (nail) are most common caused by _______.

Back 41

Trichophyton rubrum.

Front 42

What is intertigo and what causes it?

Back 42

Intertigo is an erythrematous rash in body folds and it is caused by candida albicans.

Front 43

Where is seborrheic dermatitis distributed on the body in adults?

Back 43

Face, scalp. Scaly, greasy on scalp leading to dandruff. Caused by Malassezia furfur.

Front 44

Sarcopes scabiei causes scabies and transfered from person to person via mites. What are the clinical features of scabies?

Back 44

Mites burrow into corneum. Allergic reaction to mites: pruritis, eczematized or urticarial papules.

Front 45

What is the pathogenesis of the most common skin disorder (autosomal dominant)?

Back 45

Ichthyosis is characterized by dry, rough skin with marked scaling but no inflammation. There is a defect in production of filaggrin (keratohyalin granules): defect in keratinization. There is an increased thickness of the stratum corneum, absent granulosum, and hyperkeratotic, dry palms, soles, extensor areas.

Front 46

What is the most common cause of dry skin and pruritus in the elderly (due to decreased skin lipids)?

Back 46

Xerosis.

Front 47

Eczema = dermatitis. Lymphocytes damage e-cadherins (desmosomes) to disappear. What are the clinical features of eczema?

Back 47

Wheepy, vesication, crusting, chronic lichenification (thickening of skin due to itching). Acutely: erythrematous, papules, swelling. Chronic: mores scaly and lichenification.

Front 48

Name some types of dermatitis (eczema).

Back 48

Atopic dermatitis - type I hypersensitivity (latex gloves).
Contact dermatitis: allergic contact (type IV) or irritant (poison ivy, nickel).
Discoid – associated with chronic stress.
Seborrhoeic – involves hairy areas.
Gravitational (stasis) – due to venous insufficiency.
Asteatotic - dry skin (old age).

Front 49

What test can be used to differentiate pemphigus vulgaris and bullous pemphigoid?

Back 49

Pemphigus vulgaris: IgG against desmosomes (type II) , intraepithelial vesicles/bullae – positive Nikolsky sign.

Bullous pemphigoid: IgG’s against basement membranes (type II), vesicles are subepidermal – negative Nikolsky sign.

Front 50

Farmer presents to you with a hyperkeratotic, pearly gray-white skin lesion in a sun exposed area. What is it?

Back 50

Actinic (solar) keratosis: precursor to squamous cell carcinoma and is associated with chronic UV exposure.

Front 51

Intensely pruritic, scaly, violaceous, flat-topped papules with the potential of progress to SCC are ______.

Back 51

Lichen planus.

Front 52

Describe two clinical signs in psoriasis.

Back 52

Koebner phenomenon – scratching leaves a streak of skin lesions.

Auspitz’s sign: blood vessels rupture to cause bleeding. Extension of papillary dermis close to the surface of epithelium.

Front 53

Back 53

Psoriasis: hyperproliferation of keratinocytes. 30% are genetically linked. Well demarcated erythematous plaques with silver scales. Normally occur on extensor surfaces.

Front 54

Christmas tree distribution rash that spontaneously remits after 2-10 weeks: ___________.

Back 54

Pityriasis rosea.

Front 55

Define urticaria.

Back 55

Urticaria: Pruritic elevation of the skin due to mast cell release of histamine (type I).

Front 56

What is the chronic inflammatory dermal disorder associated with diabetes mellitus?

Back 56

Granuloma annulare.

Front 57

Acanthosis nigricans: verrucoid, pigmented skin lesion in axilla. What can this skin lesion indicated?

Back 57

Gastrointestinal adenocarcinoma.

Front 58

What is the skin distribution:
atopic ezcema
adult acne
psoriasis
erythema nodosum

Back 58

Flexor surfaces.
Face/back.
Extensor surfaces.
Anterior shins.

Front 59

What is the pathogenesis of erythema nodosum?

Back 59

Panniculitis – inflammation of the subcutaneous fat.
Immune reaction elicited by various fungi, bacteria, viral infections, malignancies, drugs, etc. Common in sarcoidosis.

Front 60

Name some melanocytic lesions.

Back 60

Ephelis
Lentigines
Acquired melanocytic nevi
Common mole
Blue nevus
Cellular blue nevus
Spindle and epithelioid nevus of Spitz
Halo nevus
Dysplastic nevus

Front 61

Increased pigment production or increase in melanocyte:
Ephelis
Solar lentigo/lentigo simplex
Dysplastic naevi
Melanocytic naevi
Melasma

Back 61

Pigment
Melanocytes
Melanocytes
Melanoctyes
Pigment

Front 62

Is this benign or malignant?

Back 62

Seborrheic keratosis: coin like macular to raised lesion that occurs in individuals older than 50.

Front 63

What is Leser-Trelat sign and what is it an indicator of?

Back 63

Leser trelat sign: rapid increase in the number of keratoses. This can be a paraneoplastic syndrome of stomach adenocarcinoma.

Front 64

Is a keratocanthoma benign or malignant?

Back 64

Benign skin neoplasm that rapidly develops. It mimics SCC, but will heal spontaneously with scarring.

Front 65

Name the four histologically different melanocytic naevi (aka benign neavi, common mole).

Back 65

Junctional: macule; nested proliferation that occurs along the basal cell layer.
Compound: pigmented papillomatous surface; nested proliferation extends into dermis.
Intradermal naevi: often hairy; no epidermal nest; entirely dermal.
Dysplastic naevi:

Front 66

Describe the microsopic and macroscopoic appearance of a dysplastic neavi.

Back 66

Micro: dysplasia - abnormal architecture, mitosis, nuclei:cytoplasm ratio, hyperchromasia. Shoulders (junctional nests on either side), loss of melanin, and linear fibrosis surrounding the epidermal rete ridges.

Macro: diameter greater than 6 mm, irregular borders, irregular distribution of melanin.

Front 67

What is the acronym ABCDE stand for when using it to observe a skin lesion?

Back 67

A - asymmetry
B - border (irregular)
C - color (multicolor, changes)
D - diameter (>10 mm, changes)
E - elevation

Front 68

What are the 7-point checklist (major and minor) used to determine if a skin lesion could be malignant?

Back 68

Major: change in size, shape, color

Minor: diameter >6mm, inflammation, bleeding/oozing, and mild itch or altered sensation

Front 69

What are the risk factors for developing melanoma?

Back 69

Excessive sunlight at a young age, chronic sun exposure, and intermittent sun burning.
Family history (1st, 2nd relatives).
Dysplastic naevi syndrome (autosomal dominant).
Light complexion (+ red/blond hair).
Xeroderma pigmentosum (autosomal recessive, defect in DNA repair).

Front 70

What scale would you use to determine the prognosis of a patient with this lesion?

Back 70

This is a malignant melanoma. Breslow's depth is measured from the granular layer of the epidermis down to the deepest point of invasion. < 0.76 mm invasions: do not metastasize. > 1.7 mm invasions have potential for lymph node metastasis.

Front 71

What are the steps in tumor progression of a melanoma?

Back 71

Atypical melanocyte hyperplasia.
In situ melanoma.
Invasive radial growth phase: no metastatic potential.
Invasive vertical growth phase: malignant cells penetrate the underlying reticular dermis.

Front 72

What are the four common types of melanoma?
Which is the most common?

Back 72

Superficial spreading: (70%), ass. w/ sunburn, may contain areas of regression, extremities/back.
Lentigo maligna: (4-10%), long radial growth phase, flat, on face.
Nodular: (15-30%), no radial growth, directly invasive, poor prognosis.
Acral lentiginous: (2-8%), palm/sole/subungual, most common melanoma in blacks.

Front 73

This is Hutchinson's sign. What is this?

Back 73

Acral lentiginous melanoma. Account for 2-8% of meloma cases. It is the most common melanoma in blacks and commonly found on soles of feet, palms, and subungual. This cancer has a poor prognosis.

Front 74

Patient presents with a skin lesion. You describe it as a pearly, telangiectatic nodule. It is most likely this is the most common malignant skin tumor. How would this nodule look on a histological slide?

Back 74

Basal cell carcinoma which arises from the basal cell layer of the epidermis. Risk factor: chronic sun exposure. On a slide it will appear blue and have palisading nuclei. BCC does not metastasize.

Front 75

Which is SCC and BCC?

Back 75

Left: BCC. Pearly, telangectatic nodule.

Right: SCC. Scaley nodule that is often ulcerated.

Front 76

What are some risk factors for SCC?

Back 76

Excessive exposure to UV light (damage to DNA or damage to (Langerhan’s)), actinic keratosis, lichen planus, Bowen’s disease – SCC in situ, arsenic exposure, scar tissue in a third-degree bird, chronic ulcers and draining osteomyelitits, immunosuppressive therapy, xeroderma pigmentosum, HPV, tobacco (oral cavity), leukoplakia.

Front 77

What tumor is this?

Back 77

SCC. Note the keratinized pearl and the pink staining.

Front 78

What are the three phases of hair growth?

Back 78

Anagen - growth.
Catagen - resting phase.
Telogen - shedding?

Front 79

What is the most common cause of hair loss in 20-40 year old women?

Back 79

Postpartum. Other: oral contraceptive pills, stress, chemo.

Front 80

What disease/syndrome is associated with these nail changes;
1) Nail pitting
2) Koilonychia (spoon)
3) Splinter hemorrhages
4) Mees' lines (white lines)
5) Subungual hematoma

Back 80

1) Psoriasis
2) Iron deficiency
3) Infective endocarditis and trichinosis
4) Arsenic poisoning and systemic illness
5) Blood clot due to trauma