Do You Know These Skin Problems In Dermatology Quiz

1. Pt comes for routine check up and you notice several subcutaneous bumps attached to Achilles tendons. Best initial test?

Perform a skin biopsy of the subcutaneous bumps.

*Check Blood Cholesterol levels as xanthomas are associated with hyperlipidemia/LYMPHOPROLIFERATIVE DISORDERS.* Pt has tendinous xanthomas (yellow nodules composed of "lipid" laiden histiocytes in the dermis, these macrophages have FOAMY Cytoplasm which has lot's of TG,Phospholipids,Cholesterol, these macrophages can also be surrounded by inflammatory cells+ FIBROTIC stroma) while xanthelemas(Periorbital plaques/papules that are yellow because foam cells=lipid laden macrophages are lcoated in superficial dermis) usually aren't surrounded by fibrotic tissue,inflammation.also know:*Pale Xanthomas(linear lesions in skin folds that are strongly associated with Primary Billiary Cirrhosis)*Eruptive Xanthomas-Yellow papules which appear when plasma TG and Lipids increase)

Prescribe topical corticosteroids to reduce the size of the bumps.

Order an MRI of the lower extremities to evaluate the bumps.

Tendinous xanthomas are strongly associated with hyperlipidemia and lymphoproliferative disorders, therefore checking blood cholesterol levels would be the best initial test to investigate further. Ordering an MRI, performing a skin biopsy, or prescribing topical corticosteroids would not provide information on the underlying cause of the subcutaneous bumps.

Explanation

Tendinous xanthomas are strongly associated with hyperlipidemia and lymphoproliferative disorders, therefore checking blood cholesterol levels would be the best initial test to investigate further. Ordering an MRI, performing a skin biopsy, or prescribing topical corticosteroids would not provide information on the underlying cause of the subcutaneous bumps.

2. Which layer of the skin contains Desmosomes, Stem cells, and Keratin?

Dermis

*Desmosomes(Located in Statum Spinosum between Stratum granulosum and Statum Basale),Stem cells(in Startum Basale=DEEPEST layer of EPIDERMIS),Keratin(stratum Corneum-Outermost layer) are all located in EPICdermis.*Remember layers of epidermis from outside to inside:Corneum,Lucidum,Granulosum,Spinosum,Basale< after this layers of epidermis then comes Dermis(Blood vessels are located here) and after that Subcutaenous fat.

Muscle

Subcutaneous fat

All three components are located within different layers of the epidermis, which is the outermost layer of the skin.

Explanation

All three components are located within different layers of the epidermis, which is the outermost layer of the skin.

3. Why loss of E-cadherin would promote metastases?

Loss of E-cadherin inhibits cell proliferation and tumor growth

Metastatic dissemination is not affected by changes in E-cadherin levels

*Because cadherins(Calcium dependent adhesion proteins) is where Actin(Microfilament) Cytoskeletons of of cells attach and make up components of Adherent Junctions(bElt desmosome,Zonula Adherens) which normally would connect adjacent epithelial cells>Metastatic dissemination.*Don't confuse this Belt desmosomes with Spot desmosomes(Macula adherens) which provide structural support trough stabilization of INTERMEDIATE filament communications between cells.(In Pemhigus Vulgaris we have igG autoantibodies against Desmoglein3component of Desmosomes(MACULA ADHERENS) which is btw also a Cadherin protein, as we remember desmosomes are located in SPINOsum, thus this type of 2 hypersensitivity leads to destruction of epithelial junctions of these region )

E-cadherin is not involved in cell-cell adhesion processes

E-cadherin is a crucial adhesion molecule in maintaining cell-cell junctions in epithelial tissues. Its loss disrupts these junctions, allowing cancer cells to detach and spread to distant sites, promoting metastases.

Explanation

E-cadherin is a crucial adhesion molecule in maintaining cell-cell junctions in epithelial tissues. Its loss disrupts these junctions, allowing cancer cells to detach and spread to distant sites, promoting metastases.

4. How is the integrity of basolateral membranes of epithelial cells maintained?

By secreting mucus on the apical surface to act as a protective barrier.

*Trough Integrins which are membrane proteins that can bind to laminin and collagen(type IV) in Basement membrane.

By direct interaction with neighboring cells through tight junctions.

Through active transport of ions across the membrane to maintain osmotic balance.

Integrins play a crucial role in maintaining the integrity of basolateral membranes by binding to specific proteins in the basement membrane, rather than through direct cell-cell interactions, mucus secretion, or ion transport.

Explanation

Integrins play a crucial role in maintaining the integrity of basolateral membranes by binding to specific proteins in the basement membrane, rather than through direct cell-cell interactions, mucus secretion, or ion transport.

5. Why is Bullous Pemphigoid Nikolsky Negative while Pemphigus vulgaris is Nikolsky Positive?

Nikolsky Negative means that rubbing of the skin will result in Exfoliation of the outermost layer of the skin which is a characteristic of Pemphigus vulgaris.

*Nikolsky Negative means that rubbing of the skin won't result in Exfoliation of outermost layer of the skin(Upper Epidermis won't separate from basal layer which is also part of epidermis, as vesicle is Subepidermal between basal layer and basement membrane).* +Sign makes sense in Pemphigus where Bullae are thin walled and rupture easily making shallow erosions with dried crust. Acantholysis(Separation of epidermal cells) here results in SUPRAbasal intraepidermal bullae(Due to destruction of Desmosomes between epithelial cells in Spinosum_layer), while in Bullous pemhigoid you have autoantibodies against HEMIdesmosomes which connect Keratin in Basal cells with Basement membrane underneath it, thus defect is in deeper layer and Subepidermal Nonacantholytic bullae has THICKER wall and is tense, thus superficial rubbing won't be able to exfoliate skin, robbin hood tells us that antibodies are directed against Type 17 collagen as a component of HEMIdesmosomes,on skin biopsy of Bullous Pemhigoid you would see separation of basement membrane from basal cells.*You would see Lineaar pattern of Immunofluorecence, + remember that TENSE bullae in Bullous pemhigoid contains eosinophils.(Complement activation with neutrophil recruitment is also involved in tissue damage)*Remember that Pemhigus vulgaris is MORE dangerous with potential for DEATH, due to MUCOSAL involvement and risk of infection(Blisters rupture easy so skin can't protect from pathogens)

Both Bullous Pemphigoid and Pemphigus vulgaris are Nikolsky Positive due to their similar pathogenesis.

Nikolsky Positive indicates a lack of bullae formation in the skin which is true for both Bullous Pemphigoid and Pemphigus vulgaris.

6. Desmosomes use Desmoplakin and cytokeratin to provide structural support via Intermediate filament interactions in which layer of epidermis?

Stratum BASALE

Stratum LUCIDUM

*Desmosomes(Macula adherens,Spot desmosomes) use Desmoplakin and cytokeratin to provide structural support via Intermediate filament interactions, Desmosomes are located in Stratum SPINOSUM of epidermis, Desmoplakins communicate with cytokeratins in respective cells and themselves they come together to create junction between cells.*Autoantibodies agianst desmolgein component are mechanism of acantholysis in Pemhigus vulgaris, these autoandibosies create Fish net/reticular pattern of immunofluorescence = IgG surrounding keratinocytes.*Intraepithelial vesicles in PV are suprabasal, while basal cells resemble a row of tombstones.*As we have Suprabasal vesicles due to destruction of spinosum layer (located between basales and granulosum) there is + nikolsky sign(Outer epidermis separates from Basal layer with Minimal pressure).*THEY WANT YOU TO KNOW THAT PG INVOLVES ORAL MUCOSA(patient can present with Poor appetite due to dysphagia) and that it can be DEADLY without treatment(Corticosteroids,MTX,Azathioprine)

Stratum GRANULOSUM

Desmosomes are located in Stratum SPINOSUM of epidermis. They provide structural support using Desmoplakin and cytokeratin.

Explanation

Desmosomes are located in Stratum SPINOSUM of epidermis. They provide structural support using Desmoplakin and cytokeratin.

7. Examples of macule(Flat lesion with well-circumscribed change in skin color < 1 cm)?

Psoriasis(red, scaly patches on the skin)

*Example of macules include:*Freckles(small flat brown marks arising on the face and other sun exposed areas,esp common in people with red-hair)*Labial Macule(flat dark well-circumscribed spot on lips)*Don't confuse macule with large birthmark(Congenital Nevus) which is basically macule which is larger than 1 cm) and is called PATCH.*Sattar realllllllly wants you to know the mechanism of Freckle(ephelides) is:increased number of melanosomes without altering Number of melanocytes, while Poppie wants you to contrast this with Increase in Number of MelanoCYTES in Solar Lentigo(Brown macules in elderly,Not precancerous and doesn't need treatment, don't confuse with Lentigo maligna melanoma).

Hemangioma(benign tumor made up of blood vessels)

Keloid(an overgrowth of scar tissue)

Macules are flat lesions with well-circumscribed changes in skin color that are less than 1 cm in diameter. Freckles and labial macules are examples of macules as they fit this description. Hemangiomas, psoriasis, and keloids are not examples of macules as they do not meet the criteria mentioned.

Explanation

Macules are flat lesions with well-circumscribed changes in skin color that are less than 1 cm in diameter. Freckles and labial macules are examples of macules as they fit this description. Hemangiomas, psoriasis, and keloids are not examples of macules as they do not meet the criteria mentioned.

8. Elevated solid skin lesion < 1 cm is called?

Nodule, examples include Lipoma and Dermatofibroma

Plaque, examples include Psoriasis and Lichen Planus

*Papule, examples include Acne and Mole(Nevus).*If papule is larger than 1 cm in size it is plaque which is characteristic of psoriasis(Salmon-colored PLAQUE with silvery scales, check pic).*EY everyone knows that psoriasis loves elbows,knees,lumbosacral area, but it can also involve GLANS PENIS(Some uw action)*Note psoriasis has association with specific HLA(Cw-0602)+Poppie wants you to know that sudden onset of psoriasis is highly suggestive for HIV(so they might ask you for which ifnectious agent you should test them), he also wants you to know that Psoriasis commonly is preceded by Strep.pharyngitis.*While UW loves to show psoriatic plaques and ask you association with Joint deforming disease(Psoriatic arthritis) and its association with nail changes(thickening,crumbling,pitting, brown-yellow discoloration)

Vesicle, examples include Herpes and Varicella

The correct term for an elevated solid skin lesion

Explanation

The correct term for an elevated solid skin lesion

9. What structure of virus causes a small fluid-containing blister < 1 cm?

PUSTULE

*Small fluid-containing blister < 1 cm is VESICLE.*Enveloped,DS,Linear,DNA virus which is known as VZV with primary infection it causes Chickenpox(Varicella-presents with multiple crops of lesions in various stages from vesicles to crusts) but VZV can remain latent in dorsal root ganglia and on reactivation(Stress,immunosupression) it can cause Shingles(Zoster, DERMATOMAL distribution of vesicles which manifest with pain/burning sensation,can be disseminated over other regions too).*Now Both chickenpox and Shingles are characterized by formation of VESICLES(small fluid-containing blister<1cm), rupture of vesicles>ulcers that crust in a few weeks and patient is contagious untill lesions are dry.*With VZV infections we have + Tzank smear(+for mutlinucleated giant cells in base of scrapped ulcer) with Eosinophilic Inclusion bodies in MULTINUCLEATED Giant Cells and keratinocytes on light microscope.*Leukocytoclastic vasculitis(Hypersensitivity angiitis)=Small vessel vasculitis along with dermal inflammatory infiltrate can be present (Some UW action :)

MACULE

PAPULE

Vesicle is the correct term for a small fluid-containing blister

Explanation

Vesicle is the correct term for a small fluid-containing blister

10. What is the term for transient smooth raised small/large elevated skin lesions that are hypersensitivity reactions?

*Transient smooth papule/plaque which is itchy is known as wheal(Single unit of urticaria(Hives), often seen with type 1 hypersensitivity in response to allergen, IgE cross linking on mast cells Or DIRECT effect of drugs like Opiates>Degranulation of mast cells, characterized by SUPERFICIAL DERMAL EDEMA+LYMPHATIC CHANNEL DILATION+Excess TRANSUDATE(hypocellular,low protein) NO CHANGES in EPIDEMRIS.*UW also wants you to know that monocytes and eosinophils can be found immediately around dermal venules.

*Vesicle

*Pustule

*Petechiae

The correct answer specifies the characteristics of transient smooth raised skin lesions that are hypersensitivity reactions, known as wheals, in contrast to vesicles, petechiae, and pustules.

Explanation

The correct answer specifies the characteristics of transient smooth raised skin lesions that are hypersensitivity reactions, known as wheals, in contrast to vesicles, petechiae, and pustules.

11. Flaking of which layer of the skin is characteristic of scale, and what conditions might you think about when seeing a patient with scale?

Stratum basale; Lupus, Vitiligo, Dermatitis

*Flaking of Stratum CORNEUM(Outermost layer of epidermis) is characteristic of scale.*Think of SCC,Eczema,Psoriasis(Silvery scales component)

Stratum lucidum; Melanoma, Acne, Rosacea

Stratum granulosum; Basal cell carcinoma, Hives, Impetigo

When a patient presents with scale, it indicates flaking of the stratum corneum, the outermost layer of the epidermis. Conditions such as squamous cell carcinoma (SCC), eczema, and psoriasis with its silvery scales component should be considered.

Explanation

When a patient presents with scale, it indicates flaking of the stratum corneum, the outermost layer of the epidermis. Conditions such as squamous cell carcinoma (SCC), eczema, and psoriasis with its silvery scales component should be considered.

12. A crust with dry exudate, especially in a child, should make you think of?

Scabies

*Honey-colored crusting is characteristic of impetigo Impetigo caused by strep.pyogenes(group A strep), know that baby has risk of developing Post Streptococcal glomerulonephritis(Contrast this with Rheumatic fever which only follows strep.pharyngitis)*Note: if impetigo is characterized by bullae(Large fluid containing blister>1cm), than causative agent is most likely S.aureus.*Impetigo is very contagious and can be transmitted trough skin contact or even by touching objects that came into contact with infected skin.

Chicken pox

Ringworm

Impetigo is a highly contagious bacterial skin infection that commonly affects children. While chicken pox, ringworm, and scabies can also present with skin lesions, they do not typically produce honey-colored crusting like impetigo does.

Explanation

Impetigo is a highly contagious bacterial skin infection that commonly affects children. While chicken pox, ringworm, and scabies can also present with skin lesions, they do not typically produce honey-colored crusting like impetigo does.

13. How would you describe epidermis histologically in a patient with psoriasis?

*Hyperkeratosis(Thickened Stratum Corneum with retention of nuclei in keratinocytes reflecting incomplete keratinization<normal process only in Mucous membranes)+Parakeratosis(Retention of Nuclei) with mitotic activity above basal layer +THINNING or ABSENCE of Stratum GRANULOSUM(layer between lucidum and spinosum), while spinosum layer gets thicker due to HYPERPLASIA(And can have Neutrophilic infiltrates)*CARDINAL SIGN:MUNRO Abscesses(Neutrophils from papillary dermis infiltrating Stratum corneum )+Elongation of rete ridges(which are epidermal thickenings that extend downward between dermal papillae)*Hyperkeratosis(thickening of stratum corneum)alone is characteristic of lot's of other conditions like Callus(callus would refer to thickened stratum corneum in response to mechanical forces, such as the hands of a carpenter working with tools, or the soles of the feet of a child going barefoot)*Sattar wants you to know PUVA combo(UVA + psoralen, Psoralen increases UVA absorbtion, while UVA will destruct proliferating keratinocytes and thus decrease Hyperkeratosis) can be used for treatment of psoriasis Corticosteroids(usually main treatment)and immune therapy can be used(As it is of autoimmune origin)

B. Acantholysis with presence of Clear Cells in the Epidermis

C. Hypergranulosis with absence of Inflammatory Infiltrates

A. Hypokeratosis with thickening of Stratum Granulosum

The correct answer describes the histological findings in epidermis of patients with psoriasis, which includes hyperkeratosis, parakeratosis, thinning or absence of Stratum Granulosum, elongation of rete ridges, MUNRO Abscesses, and hyperplasia in Stratum Spinosum. Option A is incorrect as it describes hypokeratosis instead of hyperkeratosis. Option B is incorrect as acantholysis and presence of clear cells are not characteristic of psoriasis. Option C is incorrect as hypergranulosis is not seen in psoriasis and the presence of inflammatory infiltrates is a common feature in the condition.

Explanation

The correct answer describes the histological findings in epidermis of patients with psoriasis, which includes hyperkeratosis, parakeratosis, thinning or absence of Stratum Granulosum, elongation of rete ridges, MUNRO Abscesses, and hyperplasia in Stratum Spinosum. Option A is incorrect as it describes hypokeratosis instead of hyperkeratosis. Option B is incorrect as acantholysis and presence of clear cells are not characteristic of psoriasis. Option C is incorrect as hypergranulosis is not seen in psoriasis and the presence of inflammatory infiltrates is a common feature in the condition.

14. Which layer of skin is affected in Lichen Planus within the Epidermis?

Stratum spinosum

* Lichen planus is directly a result of hypergranulosis(Thickening of stratum granulosum)**LYMPHOCYTES at dermal-epidermal junction is common histologic finding.(Making sawtooth appearance)*Hep C has association with lichen planus.(So test them for hepatitis C virus)*usually lesions are self-limiting but chronic lesions can increase risk of SCC.*Lesions develop in areas of scratching(Koebner phenomenon)

Stratum basale

Stratum lucidum

Lichen Planus primarily affects the stratum granulosum layer of the Epidermis.

Explanation

Lichen Planus primarily affects the stratum granulosum layer of the Epidermis.

15. What is the condition characterized by epidermal accumulation of edematous fluid in intercellular spaces?

Rosacea

Psoriasis

*Patient likely has Eczematous dermatitis, characterized by spongiosis(Epidermal accumulation of edematous fluid in intercellullar spaces).*Acantholysis(Loss of cohesion between keratinocytes in epidermis/adnexal structures).*Allergic contact dermatitis(Type4 hypers. in response to poison ivy in woods,Nickel in earrings)Irritant contact dermatitis(in response to Laundry detergent)are xamples of spongiotic dermatitis.*Eventually edema can become so prominent that it can result in intraepidermal vesicles due to destruction of desmosomes(MACULA ADHERENS)*Perivascular infiltration with eosinophils and lymphocytes is possible, this infiltrate is confined to superficial dermis if eczematous dermatitis is due to CONTACT with superficial antigen, while if eczematous dermatitis is caused by SYSTEMIC exposure to antigen(like in response to drugs)it can extend to deeper vessels. (UW wants you to know these:)

Impetigo

Eczematous dermatitis is characterized by spongiosis, which is the accumulation of edematous fluid in intercellular spaces. Psoriasis, Rosacea, and Impetigo are not characterized by this feature.

Explanation

Eczematous dermatitis is characterized by spongiosis, which is the accumulation of edematous fluid in intercellular spaces. Psoriasis, Rosacea, and Impetigo are not characterized by this feature.

16. What is the mechanism of albinism and what should patients with albinism be frequently screened for?

Autoimmune destruction of melanocytes; Eye diseases

*Decreased Tyrosinase activity or defective tyrosine transport, that should help you to understand that patholphysiologic basis of the disease is defective/DECREASED melanin production and NOT decreased melanocyte number contrast this with Vitiligo where we have AUTOIMMUNE DESTRUCTION of Melanocytes that leads to IRREGULAR areas of COMPLETE depigmentation, histologically areas of epidermis affected by these circumsciribed macules/patches would be characterized by loss of melanocytes and COMPLETE absence of melanin.*Patients with albinism should be frequently screened for skin cancer(BCC,SCC,Melanoma), while patients with vitiligo are likely to have other Autoimmune disease(Hashimoto's thyroditis,Hypoparathyroidism,Grave's disease)

Increased melanocyte number; Autoimmune diseases

Increased melanin production; Cardiovascular diseases

Albinism is characterized by defective/decreased melanin production due to decreased Tyrosinase activity or defective tyrosine transport. Patients with albinism should be frequently screened for skin cancer (BCC, SCC, Melanoma), as they are at higher risk. It is important to differentiate albinism from conditions like vitiligo, where there is autoimmune destruction of melanocytes leading to irregular areas of complete depigmentation.

Explanation

Albinism is characterized by defective/decreased melanin production due to decreased Tyrosinase activity or defective tyrosine transport. Patients with albinism should be frequently screened for skin cancer (BCC, SCC, Melanoma), as they are at higher risk. It is important to differentiate albinism from conditions like vitiligo, where there is autoimmune destruction of melanocytes leading to irregular areas of complete depigmentation.

17. During infancy, a baby had a pruritic eruption on the face with increased serum IgE levels and asthma. As he grows older, what region is most likely to be affected by these eruptions?

Scalp

Palms and soles

Back

*Antecubital fossa is commonly affected and generally these PRURITIC erruptions which are often weeping and crusting papules and plaques, often erupting in response to certain environmental triggers(Like food) Note that this pruritic rash usually appears on face,scalp,EXTENSOR surfaces and usually appears in babies less <5 years, in Older children AD usually presents with LICHENIFICATION(Thickening of outer layer often due to scratching) that appears on skin flexures(Neck,wrist,popliteal,antecubital fossae).*Baby has Atopic dermatitis(Eczema) which is type 1 hypersensitivity and is associated with atopic diseases(Food allergy,asthma,allergic rhinitis)*Contrast this with Type4 hypersensitivity which is basis for CONTACT dermatitis, where Neomycin(topical aminoglycoside),Nickel(metal in belt buckle,cheap jewelry),poison ivy(Plant in Woods) which causes Itchy rash on CONTACT sites.*uw also wants you to know that AD can be due to Mutations affecting proteins like Filaggrin and other components of epidermis>Compromising barrier function of epidermis.also uw wants you to know that along with peripheral eosinophilia, High levels of cAMP phosphodiesterase is characteristic in Leukocytes of patients affected by AD(Common in children)

Atopic dermatitis commonly affects the antecubital fossa due to its characteristic pruritic, weeping, and crusting papules and plaques. This condition is associated with elevated serum IgE levels and asthma.

Explanation

Atopic dermatitis commonly affects the antecubital fossa due to its characteristic pruritic, weeping, and crusting papules and plaques. This condition is associated with elevated serum IgE levels and asthma.

18. What is the pathophysiology and treatment for acne in teenagers?

Acne is a genetic condition passed down through families and can only be treated with surgical intervention.

*First we need to make Comedone(plugging of outlet of hair follicle by keratin debris basically, it is open it is Blackhhead if it is closed it is whitehead) which is result of sebum,keratin obstructing Pilosebacous follicles, add Propionbacterium Acnes with inflammation and you can get Papules,Pustules,Nodules,Cysts.*Treatment can involve Benzoyl peroxide,Retinoids,Antibiotics.*Remember this bug is aerotolerant anaeorbic Gram+,rod.*Teens get it as Androgen receptors on hair follicles can stimulate increased sebum production in response to testosterone.*Abnormal keratinization can play role(Retinoids decrease follicular keratinization and sebum production,they also decrease bacterial count)

Acne is a viral infection that spreads through skin contact and can be treated with antiviral medications.

Acne is caused by overhydration of the skin leading to clogged pores and can be treated with increased water consumption.

19. How can you differentiate between Intradermal nevi and Junctional nevi? Which one can be pre-malignant?

Both Intradermal nevi and Junctional nevi are always benign and not at risk for malignancy.

Junctional nevi are raised and solid, while Intradermal nevi are flat and well-circumscribed.

Intradermal nevi are flat macules and Junctional nevi are papular lesions.

* Intradermal nevi are papular(Raised,solid<1cm) lesions.*Junctional nevi are flat macules (Flat,well-circumscibred<1cm), characterized by nests of nevus cells along Basal cell layer, at dermal-epidermal junction.*BOTH can be premalignant if atypical/congenital and can Progress to melanoma(MC Killer of all skin cancers) so they should get these lesions checked out often.*But mainly Melanocytic Nevus is BENIGN and is known as MOLE among normal humans :)*But poppie wants you to know that Mole(Nevocellular nevus) is benign tumor of neural crest-derived nevus cells(Modified MelanoCytes), frequently contains hair and this can help you to differ it from melanoma(Cancer wouldn't skip skin around hair follicles)*Poppie also wants you to know that junctional nevus(common in kids)can develop into a compound nevus(Common in adults) where nevus cells can extend into Superficial dermis and obviously both junctional/intrapidermal components are present, he also wants you to know that intradermal nevus develops when compound nevus looses its junctional component.

20. What histologic findings will you see in a patient with nail pitting, arthritis, papules and plaques with silvery scaling on knees and elbows, and a +Auspitz sign?

Decrease in thickness of Stratum Spinosum and Increase in granulosum, Psoriasiform hyperplasia with Spongiosis, Pautrier microabscesses with lymphocytic infiltrates in dermis

*Increase in thickness of Stratum Spinosum(Thus layer between Granulosum and basale) and Decrease in granulosum(Thus layer between Spinosum and Lucidum)*We would also see Acanthosis with Parakeratotic Scaling(Nuclei still stays in cells of Stratum Corneum)*NEVER forget about MUNRO's Microabscesses NEUTROPHILIC infiltrates in Stratum corneum from papillary dermis<Not present in Seborrheic Dermatitis(Hypersensitivity to fungus)

Thinning of Stratum Basale and Thickening of Stratum Granulosum, Lichenoid infiltration with Civatte bodies, Pautrier microabscesses with eosinophilic infiltrates in dermis

Normal thickness of Stratum Spinosum and Epidermal atrophy, Hyperkeratosis with Corneocyte retention, Civatte bodies with apoptotic keratinocytes in epidermis

Histologic findings in psoriasis typically include increased in thickness of Stratum Spinosum alongside other key features such as Acanthosis, Parakeratotic Scaling, Munro's Microabscesses, and neutrophilic infiltrates in the Stratum corneum.

Explanation

Histologic findings in psoriasis typically include increased in thickness of Stratum Spinosum alongside other key features such as Acanthosis, Parakeratotic Scaling, Munro's Microabscesses, and neutrophilic infiltrates in the Stratum corneum.

21. A guy who gets facial flushing in response to external stimuli (alcohol, heat) and has erythematous papules/pustules with no comedones was diagnosed with rosacea. What if he also developed Rhinophyma?

*Bulbous deformation of nose(rhinophyma) is characteristic of Phymatous rosacea.*Goljan wants you to know that mite(demodex folliculorum) has association with acne rosacea and that Sebacous gland hyperplasia is mechanism of Rhinphyma.

Sebaceous gland hypoplasia is a mechanism of rhinophyma.

Demodex folliculorum is associated with erythematotelangiectatic rosacea.

Rhinophyma is characteristic of papulopustular rosacea.

Rhinophyma is a specific manifestation of phymatous rosacea, characterized by the bulbous deformation of the nose. It is important to understand the associations between Demodex folliculorum and acne rosacea, as well as the mechanism of sebaceous gland hyperplasia in rhinophyma.

Explanation

Rhinophyma is a specific manifestation of phymatous rosacea, characterized by the bulbous deformation of the nose. It is important to understand the associations between Demodex folliculorum and acne rosacea, as well as the mechanism of sebaceous gland hyperplasia in rhinophyma.

22. What is a seborrheic keratosis and when should you worry about it?

Seborrheic keratosis is a highly aggressive skin cancer that requires immediate surgical removal.

Seborrheic keratosis is a type of contagious skin condition that can spread through direct contact with an affected individual.

*Generally you don't worry about Seborrheic KERATOSIS as this is mostly Benign NEOPLASM(characterized by pigmented Basaloid cells surrounding keratin-filled cysts) in older people, note:scales of these pigmented papules/plaques are easily rubbed off and this benign tumor can present as coin-like,macular to raised verrucoid lesion.*BUUT if you have Sudden onset of multiple seborrheic keratosis(Leser-Trélat sign) than you should definitely screen patient for GI,Lymphoid and other malignancies.*Robbin hood wants you to know FGFR3 mutations are characteristic for seborrheic keratoses.

Seborrheic keratosis is a type of autoimmune disorder that attacks the nervous system.

23. Skin biopsy would show?

Dermal fibrosis and inflammation

Presence of melanocytes

Absence of any cellular abnormalities

*Epidermal hyperplasia, hyperkeratosis, and koilocytosis(Epithelial cell>Koilocyte with hyperchromatic nuclei,Perinuclear halo,irregular nuclear membrane,usualy present in premalignant lesions caused by HPV)*Perinuclear halo is due to Pyknosis(Irreversible chromatic condensation , nuclear shrinkage that is a sign of irreversible cell death,like apoptosis/necrosis)*Genital Warts are mainly caused by HPV6,11 while 1,2 subtypes are most common skin warts on hands and feet.*HPV16,18 are associated with Cervical cancer.*Condylomata accuminatum can be sometimes described as exophytic lesions in the anogenital region that have keratotic papillary appearance.

Skin biopsy in the context of verrucae/condyloma accuminatum caused by HPV would typically show epidermal changes such as hyperplasia, hyperkeratosis, and the presence of koilocytosis.

Explanation

Skin biopsy in the context of verrucae/condyloma accuminatum caused by HPV would typically show epidermal changes such as hyperplasia, hyperkeratosis, and the presence of koilocytosis.

24. How can you differentiate bacillary angiomatosis from kaposi sarcoma in patients with AIDS?

*Bacillary angiomatosis will likely have NEUTROPHILIC infiltrate(remember causative agent is Bartonella Henselae which is gram Negative rod, patients often get it from cat scratch)*Contrast this Benign Capillary skin papules with Kaposi sarcoma which would Have LYMPHOCYTIC infiltrate and is Endothelial malignancy of mainly Skin but which also can be found in Mouth,GI tract,even RESPIRATORY tract, remember Kaposi sarcoma is caused by HSV8(DS,DNA,linear,enveloped) but you need to be HIV +(Retrovirus with diploid RNA genome),check pic for Kaposi,bacillary is likely to have more solitary/darker lesions with individual lesions being larger.

Kaposi sarcoma presents with darker and larger lesions, while bacillary angiomatosis has more solitary lesions.

Kaposi sarcoma is mainly found in the respiratory tract, while bacillary angiomatosis is mainly localized on the skin.

Bacillary angiomatosis is caused by HSV8, while Kaposi sarcoma is caused by Bartonella Henselae.

Bacillary angiomatosis and Kaposi sarcoma are two distinct conditions that can affect patients with AIDS. It is important to differentiate between them based on histopathological features and causative agents.

Explanation

Bacillary angiomatosis and Kaposi sarcoma are two distinct conditions that can affect patients with AIDS. It is important to differentiate between them based on histopathological features and causative agents.

25. Is cherry hemangioma (usually presents as papular lesions) bad?

Well it is a BENIGN growth whose frequency increases with age it is not dangerous but well it will NOT go away actually it is Likely to INCREASE in size.(if they ask you about it, it is likely about reversal)*Contrast this Cherry hemangioma with Strawberry hemangioma-Benign capillary hemangioma of infancy which appears in newborns in first weeks of life, initially GROWS RAPIDLY but it regresses spontanenously by 5-8 years of age(Don't write poor prognosis just because it looks scary, prognosis is good)

Cherry hemangioma is a malignant growth that requires immediate intervention.

Cherry hemangioma is contagious and can spread to others through physical contact.

Cherry hemangioma is a self-limiting condition that disappears on its own over time.

26. Why does a patient with Turner's syndrome have a webbed neck which can present as a neck mass on MRI?

As a result of excess fat tissue accumulation in the neck area.

Because of abnormal thyroid gland development.

Due to enlarged lymph nodes in the neck region.

*Due to Cystic hygroma which is Cavernous LYMPHangioma(Not hemangioma)

Patients with Turner's syndrome often develop a cystic hygroma, which is a type of cavernous lymphangioma causing the webbed neck appearance.

Explanation

Patients with Turner's syndrome often develop a cystic hygroma, which is a type of cavernous lymphangioma causing the webbed neck appearance.

27. What type of lesion can ulcerate and bleed, with presentation in females possibly being associated with pregnancy and trauma?

Actinic Keratosis

Dermatofibroma

*Description feets Pyogenic granuloma which has been associated with pregnancy, can be due to trauma.

Seborrheic Keratosis

Pyogenic granuloma is a vascular lesion that can ulcerate and bleed. It has been associated with pregnancy and trauma. Actinic Keratosis, Dermatofibroma, and Seborrheic Keratosis are different types of skin lesions with distinct characteristics.

Explanation

Pyogenic granuloma is a vascular lesion that can ulcerate and bleed. It has been associated with pregnancy and trauma. Actinic Keratosis, Dermatofibroma, and Seborrheic Keratosis are different types of skin lesions with distinct characteristics.