📚 Question Bank

In a patient with a coracoid fracture, the action of the long head of triceps muscle is not hindered. It attaches to the infraglenoid tubercle on the lateral border of the scapula and not the coracoid process.

Coracoid process attachements:

• Origin: 2 muscles - Coracobrachialis (medially) and short head of biceps (laterally)
• Insertion: 1 muscle - Pectoralis minor
• 3 ligaments:
• Coracoacromial
• Coracoclavicular
• Coracohumeral

In the given scenario, forceful contraction of the subscapularis muscle has caused the isolated avulsion fracture of the lesser tubercle of the humerus.

The subscapularis muscle is inserted on the lesser tubercle of the humerus. Forceful contraction of subscapularis muscle to resist the abduction and external rotation of the shoulder may cause the isolated avulsion fracture of the lesser tubercle.

Rotator cuff muscles

Muscle

S: Supraspinat us

I: Infraspinatu s

T: Teres Minor

S: Subscapular is

Insertion

Greater tubercl e

Lesser tubercle

The above image shows a characteristic peripheral palisading of tumor cells which is seen in basal cell carcinoma.

The tumour cells resemble cells of stratum basale that have grown into the dermis. This cluster of cells is surrounded at the periphery by perpendicularly arranged cells. It also has a well-organised stroma surrounding it.

Nodular type is the commonest type of basal cell carcinoma. Telengiectasia and cystic areas may be present. Some areas may be pigmented.

Histopathological patterns of basal cell carcinoma include:

• Superficial
• Nodular
• Infiltrative
• Micronodular
• Pigmented.

PUVA therapy, HPV infections, surgical scar and iatrogenic infections are risk factors for basal cell carcinoma.

The following are the risk factors for basal cell carcinoma:

• Solar radiation
• Psoralen-UVA Therapy (PUVA)
• Human Papilloma Virus infections
• Iatrogenic infections
• Surgical scar
• UV-B rays
• Ionising radiation
• Photosensitising drugs
• Previous history of basal cell carcinoma

Basal cell carcinoma typically has no premalignant stage.

The typical basal cell carcinoma runs a slowly progressive course of peripheral extension. The pearly translucent nodule with surface telangiectasia undergoes central necrosis resulting in rodent ulcer with a rolled-out margin.

Metastasis is extremely rare in basal cell carcinoma.

The above image shows malignant cells resembling normal squamous epithelial cells with individual cell keratinization and nests of keratin pearls suggestive of squamous cell carcinoma. Keratoacanthoma is considered a form of well-differentiated squamous cell carcinoma, not a premalignant condition.

Option A: Actinic keratosis is characterized by hyperkeratotic lesions that have a low risk of progression to invasive squamous cell carcinoma(SCC).

Option B: Cutaneous horns are hard conical projections from the skin, made of compact keratin. They arise from benign, premalignant, or malignant skin lesions. Approximately 9 showed SCC pathological features at the base.

Option C: Arsenical keratosis: A cornlike, punctate keratosis caused by arsenic, characteristically affecting the palms and soles, which may progress to squamous cell carcinoma.

The above image is suggestive of actinic keratosis which is associated with mutation of the TP53 gene.

Actinic keratoses are hyperkeratotic lesions occurring on chronically lightexposed adult skin that carry a low risk of progression to invasive squamous cell carcinoma.

Lesions are usually multiple and comprise either macules or papules with a rough scaly surface resulting from disorganized keratinization and a variable degree of inflammation. It is more common in the elderly. Human papillomavirus (HPV) is present in significant numbers in actinic keratosis.

Histopathology is characterized by solar elastosis and disordered epidermal keratinocyte maturation with cytological atypia. The typical lesion shows hyperkeratosis, parakeratosis, and hypergranulosis.

Bowen's disease has a low potential for invasive malignancy.

It is an intraepidermal squamous cell carcinoma that is characterized by a persistent, nonelevated, red, scaly, or crusted plaque with a small potential for invasive malignancy. Histologically, it is characterized by full-thickness epidermal dysplasia.

It usually grows progressively but sometimes undergoes spontaneous partial resolution. It can occur anywhere, but it occurs more in the head and neck region.

Human papilloma virus infection is associated with it.

Image: Red scaly plaque seen on the finger, in an 81-year-old woman with Bowen’s disease.

The above image shows exophytic verruciform growth suggestive of verrucous carcinoma which is a well-differentiated squamous cell carcinoma.

It is slow-growing and rarely metastasizes. The etiology of verrucous carcinoma is unknown but it can develop in areas of chronic inflammation. Human Papillomavirus (HPV) has been associated with this tumor and specifically HPV types 11 and 16 have been described in plantar lesions.

Muir-Torre syndrome is an autosomal-dominant inherited condition and has multiple sebaceous tumors with multiple visceral malignancies like colorectal carcinoma. Other internal malignancies include carcinoma of the endometrium, stomach, small bowel, genitourinary tract, breast, ovary, pancreas, liver, and kidney.

Option A: Cowden syndrome- mucocutaneous lesions, facial trichilemmomas, acral keratosis, papillomatous lesions, and mucosal lesions. The mucosal lesions comprise a warty, ‘cobblestone’ hyperplasia of the tongue and buccal mucosal surfaces. Multiple hamartomatous lesions of ectodermal, endodermal, and mesodermal origin occur.

Option C: Gorlin syndrome or nevoid basal cell carcinoma- an autosomal dominant familial cancer syndrome in which affected individuals are predisposed to the development of multiple BCCs at an early age, characteristic facies, and various skeletal abnormalities.

Option D: Gardner Syndrome- a variant of familial adenomatous polyposis (FAP), is an autosomal dominant disease characterized by gastrointestinal polyps, multiple osteomas, and skin and soft tissue tumors.

Gorlin syndrome, also known as nevoid basal cell carcinoma syndrome, has an autosomal dominant inheritance with mutation of PATCHED (PTCH1) gene.

It consists of the following features:

• Multiple Basal cell carcinomas
• Highly characteristic facies (with large forehead)
• Bifid or misshapen ribs
• Vertebral and other skeletal anomalies
• Pits of the skin of the palms and soles
• Dysgenesis of the corpus callosum
• Calcification of the falx cerebri (at an earlier age than is seen in nonaffected individuals)
• Macrocephaly.

Option A: Muir-Torre syndrome- defect in DNA mismatch repair genes (MLH-1 or MSH-2) and microsatellite instability

Option C: Rombo syndrome- autosomal dominant syndrome with basal cell carcinoma as prominent feature; defective gene unidentified

Option D: Cowden syndrome- PTEN (phosphatase and tensin homologue) mutation

The above image shows melanonychia with the pigmentation of proximal nail fold which is called the Hutchinson's sign. It is seen in subungual melanoma.

In benign nail pigmentation due to drugs (eg. minocycline) or injury (hematoma), the colour stays within the margins of the nail plate and doesn't extend to nail folds.

Option A: Frank's sign - diagonal crease in the earlobes of adults has been associated with an increased risk for atherosclerotic heart disease.

Option B: Fitzpatrick sign (Dimple sign) - squeezing the skin adjacent to a dermatofibroma causes a dimpled appearance on its surface. It is also termed a positive pinch sign or dimple sign.

Option D: Pastia's sign - linear petechial eruption in the skin folds especially on the ante-cubital fossa and axillary fold seen in streptococcal scarlet fever.

Superficial spreading type is the most common type (70) of melanoma, usually arising in pre-existent nevus.

The growth is slow at first and later becomes rapid. Types of melanoma:

• Superficial spreading melanoma
• Lentigo maligna melanoma
• Acral lentiginous melanoma
• Nodular melanoma

The above image depicts melanoma. Only about 20–25 of melanomas arise from pre-existing nevus others arise de novo. The number of naevi will be proportional to the risk.

Risk factors for melanoma are as follows:

• Family history- a positive family history is associated with a two-fold increased risk of
• melanoma
• Melanocytic nevus- may be congenital nevus or atypical/dysplastic nevus
• Genetic mutations- mutations of CDKN2A gene (major susceptibility), MC1R gene (moderate susceptibility), TYR gene (low susceptibility)
• Skin pigmentation and tanning abilities- skin type I in Fitzpatrick’s classification has two-fold increased risk as compared to type IV.
• Sun exposure- intermittent sun exposure during childhood is considered to be an important risk factor.
• Artificial sources of UV- sunbeds and therapeutic UV increase the relative risk for the development of melanoma.

The above image shows a flat, brownish, irregularly shaped lesion suggestive of melanoma. The cyclindependent kinase (CDK) inhibitor 2A gene (CDKN2A), located on chromosome 9p21, is the best established highrisk locus for melanoma susceptibility.

CDKN2A mutations are found in approximately 40 of individuals with familial melanoma.

In melanoma, tumor suppressors that play a protective role against melanoma are mutated. CDKN2A encodes via alternative splicing for two proteins involved in cell cycle regulation:

p16/Ink4a and p14/Arf, both act as tumor suppressors through the Rb and p53 cancer pathways, respectively.

Tumor thickness or Breslow index is the best prognostic factor of melanoma.

It is the distance in millimeters (mm) between the epidermal granular layer and the deepest level of invasion of the primary lesion.

Thicker tumors have a higher metastatic potential. Image: Breslow Depth

The image shown above depicts a nevus. Diameter gt;6 mm is the diagnostic clue for the transformation of a nevus to a melanoma.

The above scenario is suggestive of cylindroma or turban tumor or Spiegler’s tumor which is a tumor of the sweat gland. Trichoblastoma is a tumor of the germ cells of the hair follicle and commonly develops within naevus sebaceous.

Cylindroma is familial, inherited as an autosomal dominant disorder, due to the loss of the cylindromatosis gene, CYLD on chromosome 16q12-13, and have been reported to follow radiotherapy epilation of the scalp.

The lesions are frequently multiple, smooth, firm, pink to red, and somewhat pedunculated. They are mostly seen on the scalp. Histologically, it contains mosaiclike masses - a jigsaw appearance. Malignant transformation is very rare.

Surgery is the treatment of choice.

Pinch purpura is diagnostic of primary systemic amyloidosis.

Purpuric macules and ecchymoses, especially in the periorbital area, develop with minor trauma due to fragility from amyloid deposition around cutaneous vessels.

The common feature of these diseases is the production of monoclonal immunoglobulins of mostly light chains (isotypes κ and λ) serving as amyloid precursors (AL = light chain type/Bence

˜ones amyloid).

Amyloid precipitation within the oral cavity mucosa may present as macroglossia. The given image below shows macroglossia associated with amyloidosis.

Sclerodactyly and Raynauds phenomenon are seen in scleroderma (not scleredema).

The symptoms of scleredema are due to a thickened dermis, deposition of mucin, and replacement of subcutaneous fat with coarse collagen fibers.

The dermis is 3–4 times thicker than normal due to an increase of type 1 collagen synthesis by dysfunctional fibroblast. However, fibroblast proliferation is not seen. Erythema and a peau d’orange appearance of the skin are commonly observed. The hands and feet are characteristically spared.

Diabetic scleredema is the most common type. Here, the accumulation of collagen may be due to irreversible nonenzymatic glycosylation of collagen and resistance to degradation by collagenase. It can also occur post-streptococcal infections.

The image shows scleredema in a diabetic patient with firm nonpitting edema and induration on the upper back, neck, and shoulders on an erythematous background.

The given clinical scenario and the findings shown- blistering, hypo, and hyperpigmented lesions over the sun-exposed areas (seen in panels A-C), and the absence of similar lesions on non-sun exposed areas (back) are suggestive of porphyria which presents with cutaneous features. Acute intermittent porphyria presents with acute abdominal pain, psychosis with no cutaneous features.

The common porphyrias are:

• Cutaneous disease only:
• Porphyria cutanea tarda (PCT)
• Congenital erythropoietic porphyria (CEP)
• Erythropoietic protoporphyria (EPP)
• Cutaneous disease and acute attacks:
• Hereditary coproporphyria (HC)
• Variegate porphyria (VP)
• Acute attacks only - Acute intermittent porphyria.

Porphyria cutanea tarda (PCT) is the commonest porphyria.

It results from the deficiency of uroporphyrinogen decarboxylase (UROD). This causes an accumulation of uroporphyrin and other highly carboxylated porphyrins

It is usually acquired (75, sporadic) and is often associated with liver disease. It does not cause acute attacks.

Patients notice increased fragility on lightexposed skin, particularly the backs of the hands and forearms, with minor trauma shearing the skin away to leave sharply marginated erosions that crust and resolve over few weeks leaving atrophic scars, milia, and often mottled hyper or hypopigmentation. Hypertrichosis on the upper face and forehead is common

Pink or coral-red fluorescence of urine is seen under Wood's light.

The image given below is of porphyria cutanea tarda: erosions, blisters, pigmentary changes, and scarring.

The given image shows xanthelasma palpebrarum. They are seen in:

• Familial hypercholesterolemia
• Type III hyperlipoproteinemia (broad beta disease)
• Primary biliary cirrhosis (chronic cholestasis)

They are not seen in type I hyperlipoproteinemia (familial chylomicronemia).

Xanthelasmas most commonly affect the upper eyelids and the area around the medial canthus. They are relatively soft on palpation and range from pale yellow to yelloworange in color.

Painless, linear, yellow, lipid deposition along the palmar creases and flexor creases of the wrist are descriptive of xanthomata striata palmaris. It is pathognomonic of type III hyperlipoproteinaemia.

The image given below shows xanthomata striata palmaris.