Pathologies Flashcards
Radial Nerve Injury
MOA: Can be caused by radial groove of the humerus fracture or Saturday Night Palsy (pressure on radial nerve)
Clinical Presentation: Wrist-Drop Sign. Paralysis of the triceps, brachioradialis, supinator and extensor muscles of the writs and digits. Loss of sensation in the dorsum hand and digits
Musculocutaneous Nerve Injury
Clinical Presentation: Paralysis of coracobrachialis, biceps, and brachialis. Weakened forearm flexion and supination. Loss of sensation on the lateral surface of the forearm
*Commonly caused by weapons
Pronator Syndrome
Clinical Presentation: Pope’s Hand Sign/Sign of Benediction (ring and pinky can bend, but pointer and middle stay straight) Pain and tenderness in the proximal anterior forearm
MOA: Median nerve injury from compression of 2 heads of Pronator Teres muscle
Cubital Tunnel Syndrome
Clinical Presentation: Claw Hand Sign (pinky and ring finger stick up when making a fist). Numbness and tingling of the medial part of the palm and medial 1.5 fingers. Reduced/impaired adduction of fingers. When flexing wrist, hand is drawn to the lateral
MOA: Ulnar nerve compressed by flexor carpi ulnaris at proximal attachment site where 2 heads form a tunnel
Occlusion/Laceration of brachial artery
Leads to ischemia involving forearm flexor muscles
Fracture/dislocation of the proximal humeral epiphysis
Happens to children or adolescents when the arm or shoulder is directly hit by a blow
Rupture of the tendon of the biceps
Clinical Presentation: Popeye deformity (muscle balls near the center of the distal part of the anterior aspect of the arm)
MOA: wear and tear of inflamed tendon (older athletes), excessive forceful flexion of the arm (weight lifting)
Dislocation of the tendon of the long head of the biceps
Clinical Presentation: May notice popping or catching sensations
MOA: Tendinitis and traumatic separation of the proximal epiphysis of the humerus
*associated with rotator cuff injuries 70% of the time
Biceps Tendinitis
Clinical Presentation: tenderness and crackling sound (crepitus) in the region
MOA: repetitive micro trauma from certain motions such as throwing or using a racquet
*tends to have similar pain levels whether actively or passively moved
Ulnar Nerve Injury
Claw Hand Sign (pinky and ring finger stick up when making a fist). Numbness and tingling of the medial part of the palm and medial 1.5 fingers. Reduced/impaired adduction of fingers. When flexing wrist, hand is drawn to the lateral
MOA: Direct hit against hard object or fracture of the medial epicondyle of the humerus
*locations: posterior to medial epicondyle & uncommonly the canal of Guyon
Surgical neck of humerus fracture
MOA: Caused by a fall on an outstretched hand. Causes axillary nerve damage
Clinical Presentation: Pt can still move the injured arm passively with little pain. Dx’d by XR or CT
*common in elderly (trouble abducting after 15 degrees)
Distal end of the humerus fracture
can damage the median nerve
Erb’s Palsy
Clinical Presentation: Waiter’s Tip Position (injured limb hands in medial rotation), loss of sensation on the lateral aspect of the upper limb (deltoid, biceps, brachialis, and brachioradialis)
MOA: Damage to C5 and C6 of brachial plexus from excessive separation of the head and neck
*superior part injury
*common in motorcycle accidents and shoulder dystocia
Backpacker’s Palsy
Clinical Presentation: Sensory deficits in musculocutaneous nerve and radial nerve. Sometimes muscle spasms
MOA: microinjury of the superior trunk of the brachial plexus
*superior part injury
*caused by carrying a heavy backpack
Klumpke’s Palsy
Clinical Presentation: Claw Hand Sign (Pinky and ring finger stick up when making a fist)
MOA: Damage to C8 and T1 of brachial plexus from sudden pulling of the arm superiorly
*inferior part injury
*causes could be grasping a tree branch to stop a fall or pulling of the arm during delivery
Painful Arc Syndrome
aka: Supraspinatus tendonitis, subacromial bursitis and calcification
MOA: inflammation and calcification of the supraspinatus tendon, inflammation of subacromial bursa
Clinical Presentation: pain during the abduction in the 50 - 130 degree range
Rotator Cuff injuries
Clinical Presentation: pain in the anterosuperior part of the shoulder. Shoulder joint dislocation
MOA: Throwing a ball hard, shoulder joint dislocation, or avoiding crushing into and object using your arm
Test: ask patient to lower a fully abducted arm slowly and when reaches 90 degrees it will drop
Thoracodorsal Nerve Injury
Clinical Presentation: Pt is unable to use axillary crutch or do pullups b/c or lack of innervation and thus tension in the latissimus dorsi muscle
*can be injured in surgical operation
Paralysis of Serratus Anterior
MOA: Injury to long thoracic nerve
Clinical Presentation: Winged scapula. Arm cannot abduct above the horizontal position
Fracture of the clavicle
MOA: Indirect forces transmitted through bones of the arm and forearm or falls directly onto the shoulder
Clinical Presentation: medial fragment will elevate (b/c sternocleidomastoid) and lateral will depress (b/c weight of shoulder/arm). Shoulder drops
*70% in the middle 1/3 of the clavicle. relatively common
Avulsion fracture of the greater tubercle of the humerus
MOA: fall on the shoulder of hand
Clinical Presentation: proximal end pulled superio-posterio-laterally by supraspinatus and infraspinatus. Distal end pulled and rotated medially by subscapularis
*common in middle aged and elderly
Transverse fracture of the body of the humerus
Proximal end is pulled laterally by deltoid. Distal end is pulled upward by biceps. Arm is shortened and fracture ends overlap
Supracondylar fracture of the humerus
Distal fragment may be displaced either anteriorly or posteriorly and pulled upward causing the arm to shorten
Colles’ Fracture
MOA: complete transverse fracture of the radius and sometimes ulna within the distal 2 cm. commonly from forced dorsiflexion
Clinical Presentation: dinner form appearance (distal fragment displaced dorsally and proximally. Normal relationship between the radial and ulnar styloid processes is changed and the radial styloid process is moved proximally
Olecranon Fracture
MOA: fall on the elbow
Clinical Presentation: Olecranon is pulled upward by triceps
Fracture of the scaphoid
MOA: Fall onto the palm while hand os abducted
Clinical Presentation: pain when pressing on anatomical snuff box. Poor blood supply to the proximal part of the scaphoid causes slow bone union/avascular necrosis of proximal fragment
*most frequently fractured and most common injury of the wrist
Fracture of the metacarpals
boxer’s fracture from punching
*4th and 5th metacarpals most vulnerable
Dislocation of the epiphysis of the femoral head
MOA: acute trauma or repeated microtrauma
Clinical Presentation: may result in coxa vara. Initial symptom is hip discomfort that may be referred to the knee
*children age 10-17
Tibial fracture
MOA: direct for to the tibia
Clinical Presentation: “boot-top fracture” “bumper fracture” at the middle to distal 1/3 junction
*easily become compound fractures. Can bone graft using fibula
Fibular fracture
MOA: forced inversion or eversion of the foot
*commonly occurs in 2-6 cm proximal to the distal end of the lateral malleolus and often associated with dislocation of ankle joint
Medial epicondylitis
“golfer’s elbow”. painful shaking hands, swinging of a golf club etc.
Tx: RICE
Osteopetrosis
No secondary marrow cavity. Lead weighted long bones
Charcot Joints
Clinical Presentation: peripheral neuropathy, loss of feeling leads to loss of proprioception leading to microfractures, Ca2+ deposits, and abnormal growth b/c the bones can’t respond to normal forces and changes in position
*complication of NIDDM and IDDM most commonly in lower extremities b/c they are weight bearing
Lipoma
Clinical Presentation: soft, mobile, painless mass on the proximal extremities and trunk
MOA: Tumor of adipose tissue. BENIGN.
Histo: well encapsulated/ circumscribed mass of mature fat cells with no pleomorphism
* most common soft tissue tumor of adulthood. Cured by excision
Liposarcoma
MOA: tumor of adipose tissue, MALIGNANT. Arises in the deep soft tissues of the proximal extremities and retroperitoneum.
*occurs in mid-late adulthood. One of the most common sarcomas of adulthood. Aggressive types can metastasize via blood and lymph.
Variants:
- well-differentiated (indolent): amplification of MDM2 oncogene, binds and inactivates p53
- Myxoid/round cell (intermediate in behavior) = chromosomal abnormality/translocation
- Pleomorphic (aggressive, can metastasize)
Nodular Fasciitis
Tumor-like lesion of fibrous tissue
MOA: Self-limited, reactive pseudosarcomatous proliferations in deep dermis, subcutis, or muscle. Nodular and poorly defined
Clinical Presentation: several week history of a solitary,, rapidly rowing, and sometimes painful mass, often on the volar aspect of the forearm, chest, and back`
Superficial Fibromatoses
tumor of fibrous tissue. BENIGN
MOA: fibroblastic infiltrative proliferations
Dupuytren contracture: palmar fibromatosis
Peyronie’s disease: penile fibromatosis
*not called a fibroma b/c not well-defined
Deep Fibromatoses
tumor of fibrous tissue. BENIGN
MOA: mutation in beta-catenin genes present in most
Clinical Presentation: in abdominal wall or muscles of trunk and extremities
*most often in the teens to 30s
Fibrosarcoma
tumor of fibrous tissue. MALIGNANT
*rare, most commonly affects retroperitoneum, thigh, knee, and distal extremities
Slow growing and often present for serveral years at Dx
Can metastasize hematogenously, usually to lungs
Benign Fibrous Histiocytoma (Dermatofibroma)
Fibrohistiocytic tumor. BENIGN
MOA: Uncertain pathogenesis. painless, slow-growing, firm small, mobile nodule in dermis and subcutaneous tissue, well circumscribed
Malignant Fibrous Histiocytoma (MFH)/Undifferentiated Pleomorphic Sarcoma (UPS)
Fibrohistiocytic tumor. MALIGNANT.
In proximal extremities and retroperitoneum
Gross: large gray-white unencapsulated masses
Rhabdomyoma
Tumor of skeletal muscle. BENIGN
extremely rare
Rhabdomyosarcoma
Tumor of skeletal muscle. MALIGNANT.
Histo: “strap cell”. Stains positive for actin, desmin, and myoglobin. Can manifest as soft grapelike masses in mucosal surfaces.
*most common soft tissue of childhood and adolescence < age 20
*most occur in head/neck or GU tract
3 types:
1. Embryonal: most common. develops in the wall of hollow mucosal lined organs
2. Alveolar: deep musculature of the extremities, poor prognosis. Unique cytogenic abnormalities - PAX3 or PAX7 w/ FOXO1a. Causes dysregulated skeletal muscle differentiation. Characteristic histological pattern resembles lungs.
3. Pleomorphic
Leiomyoma
Tumor of smooth muscle. BENIGN
MOA: often arises in uterus (aka fibroids)
*can cause infertility
Leiomyosarcoma
Tumor of smooth muscle. MALIGNANT.
MOA: most develop in the skin, deep soft tissues of the extremities, and retroperitoneum
*must use smooth muscle stain to differentiate from fibrosarcoma and MFH
*more common in females
Hemangioma
Vascular tumor. BENIGN.
MOA: increased number of normal or abnormal vessels filled with blood
3 types:
1. Capillary hemangioma: skin, subq, mucous membranes. “strawberry type” common
2. Cavernous hemangioma: dilated/spongy, larger, more frequently involve deep structures (ex. liver). Doesn’t usually indicate a problem, but could bleed out if traumatized and large enough
3. Pyogenic granuloma (aka lobular capillary hemangioma): exophytic nodule on skin, gingiva, or oral mucosa. No aggregates of histiocytes, but often traumatized/erupted, becomes ulcerated and covered w/ pus
Kaposi Sarcoma
Vascular tumor, low to intermediate grade. MOA: Transmitted sexually. Regardless of clinical subtype, 95% of KS are infected with HHV-8, also known as KSHV. *stain for HHV-8 4 types: 1. Classic/European 2. African/Endemic 3. Transplant associated 4. AIDS associated
Angiosarcoma
Vascular tumor. MALIGNANT.
MOA: most commonly involving skin, soft tissue, breast, and liver
Hepatic - associated arsenic, thorotrast, polyvinyl chloride
Breast - associated with radiation
Synovial Sarcoma
Tumor of uncertain histiogenesis. biphasic tumor with both epithelial and mesenchymal components
MOA: most occur in deep soft tissue around large joints of extremities. characteristic chromosomal translocation (x;18)
*occurs in young adults 20-40
*may metastasize to lung
Nevus
MOA: mole, BENIGN neoplasm of melanocytes
Epidemiology: congenital, present at birth
Clinical Presentation:
Junctional: epidermis, forms nests of melanocytes in the rete ridges, flat mole, fade with age, reticular pigment
Dermal: melanocytes in dermis only, exophytic mole, globular pigment
Compound: dermis + epidermis, raised mole
Melanoma
MOA: malignant neoplasm of melanocytes characterized by two growth phases, (1) radial growth horizontally along epidermis/dermis and (2) vertical growth into deep dermis
Clinical Presentation: Asymmetry, Border Irregularity, Color Variation, Diameter >5mm, Evolving
*most common type of cancer in women (mid-20s), 1/50 people, mostly de novo
Solar Lentigo
MOA: liver spots, tumor of pigmented keratinocytes
Clinical Presentation: found on face/hands of fair skin due to sun damage
*older adults
Seborrheic Keratosis
MOA: BENIGN squamous proliferation comprised of basaloid and squamoid keratinocytes
Clinical Presentation: Leser-Trelat Sign (sudden onset of multiple seborrheic keratosis –> GI carcinoma), warty surface, stuck on plaques, on hair-bearing skin
Histo: horn cysts and lamellated keratin
*common, older adults
Actinic Keratosis
MOA: precursor lesion of squamous cell carcinoma
Clinical Presentation: red scaly papule, sandpaper feel due to sun, found on fair skin on face, back or neck
* older adults. 0.1% progress to SCC
Squamous Cell Carcinoma
MOA: MALIGNANT proliferation of squamous cells arising on sun damaged skin
Clinical Presentation: can occus anywhere on skin, firm flesh color to reddish growth with indistinct border, scaly surface or ulceration, often LOWER LIP
Histo: Keratin pearls
Risk Factors: UVB- induced DNA damage, prolonged exposure to sunlight
Keratoacanthoma
MOA: well-differentiated SCC originating from pilosebaceous glands
Clinical Presentation: cup-shaped tumor filled with keratin debris, develops rapidly and regresses spontaneously
Bowen’s Disease
MOA: SCC in-situ often progressing or coinciding with invasive SCCs
Clinical Presentation: thin, erythematous, scaling plaques
Basal Cell Carcinoma
MOA: malignant proliferation of basal cells of epidermis
Clinical Presentation: elevated nodule with central, ulcerated crater surrounded by dilated vessels (telangiectasia) pink pearlescent papule, often on UPPER LIP
*most common tumor in caucasians
Epidermoid Cysts
MOA: occluded hair follicles fill with loose keratin, aka epidermal inclusion or sebaceous cyst
Histo: granular layer in cyst wall
Pilar Cysts
Clinical Presentation: often on scalp, but can be found on any hair-bearing skin
Histo: dense pink compact keratin with no granular layer
Mycosis Fungoides
MOA: cutaneous T-cell lymphoma caused by malignant CD4+ Th cells
Clinical Presentation: favors sun-protected areas, 5cm+ patches/thin plaques, erythroderma/tumors = more severe
*1/300,000
Mastocytosis
MOA: localized mast cell collection, aka urticaria pigmentosa
Clinical Presentation: brown oval plaque. Darier sign: scratching lesion forms hives
Histo: “fried egg” appearance
*kids
Skin Tag
MOA: pedunculated papilloma
Clinical Presentation: neck, eyelids, trunk, groins, axillae
Histo: outer keratinizing squamous epithelium, inner fibrovascular core; no adnexa
Risk Factors: Weight gain, pregnancy, diabetes
Dermatofibroma
Clinical Presentation: red-brown firm nodule, dimple sign, lower extremities (itchy)
Histo: hemosiderin deposits, CD34-, spindle cell proliferation
*middle-aged adults
Dermatofibrosarcoma Protuberans
MOA: locally aggressive, bulky irregular tumor
Clinical Presentation: trunk
Histo: swiss cheese growth pattern CD34+
*middle-aged adults
Ichthyosis Vulgaris
MOA: deficiency in profilagrin causes abnormal retention of corneocytes
Clinical Presentation: fine scales, lower extremities, itchy
Histo: Diminished granular layer
*autosomal dominant, 1/250
Oculocutaneous Albinism
MOA: defect in tyrosinase which is important in forming melanin pigment
Clinical Presentation: diffuse hypopigmentation, eye problems
Histo: melanocytes and keratinocytes without melanin
*autosomal recessive 1/20,000
Allergic Contact Dermatitis (Eczema)
MOA: caused by exposure to potent external allergen such as poison ivy, nickel, balsam of peru, neomycin, irritant chemicals
Clinical Presentation: pruritic, erythematous, oozing rash with vesicles and edema; typically localized to the point of contact
Atopic Dermatitis (Eczema)
MOA: caused by Langerhan’s cells being too high in the spinous layer of the epidermis. They can easily contact antigens.
Clinical Presentation: Pruritic erythematous, oozing rash with vesicles and edema; often involves face and flexor surfaces
*Birbeck Granules EM
*Type 1 hypersensitivity
Lichen Planus
MOA: exposure to hep C virus, medication, contact allergen leads to self-antigens on basal keratinocytes; T-cells induce death via apoptosis
Clinical Presentation: pruritic, purple, polygonal papules, Wickham striae (oral involvement)
Histo: inflammation of dermal-epidermal junction with “saw-tooth” appearance, dead reds
Lupus Erythematosus
MOA: autoimmune systemic disease with anti-DNA antibodies
Clinical Presentation: butterfly pattern malar erythema
Histo: scales, mucin, positive ANA
*F>M, AA>Caucasian
Bullous Pemphigoid
MOA: IgG Ab against BM of collagen causes destruction of hemidesmosomes between basal cells and underlying BM
Clinical Presentation: subepidermal blisters of skin, oral mucosa spared; tense bullae do not rupture easily
*Ab to BP180, BP230; older adults
Pemphigus Vulgaris
MOA: IgG Ab against desmoglein causes destruction of desmosomes between keratinocytes
Clinical Presentation: upper trunk, painful skin and oral mucosa bullae, thin-walled bullae rupture easily (Nikolsky sign)
Histo: row of tombstones, suprabasilar blister, immunofluorescence-IgG surrounding keratinocytes in “fish net” patterns
*45-55y.o.
*type 2 hypersensitivity
Dermatitis Herpetiformis
MOA: Autoimmune deposition of IgA at tips of dermal papillae, form antigliadin Abs when gluten is consumed
Clinical Presentation: pruritic papules on knees, elbows, lower back, and scalp
Histo: immunofluorescence-granular deposition of IgA in dermal papillae
*strong association with celiac disease
Verruca Vulgaris
MOA: caused by physical transmission of HPV 1, 2, and 4 at site of abrasion
Clinical Presentation: warty, keratotic papules with rough grayish surface, common on hands/feet
Histo: hyperkeratosis, thick granular layer, papillary hyperplasia, KOILOCYTES
*20% school children
Molluscum Contagiosum
MOA: caused by physical transmission of MC virus, a pox virus
Clinical Presentation: waxy, umbilicated papules up to 1cm
Histo: cytoplasmic inclusion (molluscum bodies)
*children/sexually active adults
Pityriasis Rosea
MOA: might be caused by viral infection
Clinical Presentation: occurs in spring/fall, Christmas tree pattern, starts hearld plaque with trailing scale then many lesions
Impetigo
MOA: superficial bacterial skin infection caused by Staph Aureus
Clinical Presentation: erythematous macules that progress to pustules on face/extremities, results in erosions with honey-colored crusts
Histo: staph bacterial colonies, neutrophils
Tinea (ringworm)
MOA: caused by Trichophyton rubrum infection
Clinical Presentation: annular plaques with central clearing and scaly erythematous borders, transmission by direct contact
Histo: fungal hyphae with PAS , neutrophils in pustule
Scabies
MOA: caused by sarcoptes scabei
Clinical Presentation: direct transmission, pruritic papules in fingers, webs, axillae, umbilicus, areolas, genitalia, itching is worse at night
Psoriasis
MOA: excessive keratinocyte proliferation due to genetic predisposition and external trigger, possibly autoimmune associated with HLA-C
Clinical Presentation: salmon-colored plaques with silver scale on scalp, elbows, knees, sacrum; pitting of the nails
Histo: acanthosis parakeratosis, munro’s microabcesses, Auspitz sign (longer rete ridges makes epithelial arcs look thinner)
Acne Vulgaris
MOA: abnormal retention of follicular squames and sebum with infection by Propionibacterium acnes, causing chronic inflammation
Clinical Presentation: face/back/chest with papules/pustules/comedones, worse with stress
Rosacea
MOA: abnormally pronounced vasodilation to a variety of stimuli
Clinical Presentation: facial erythema, telangiectasias, WC Fields rhinophyma, exaggerated blushing, papules, skin thickening
Urticaria
MOA: mast cells release histamine, causing vasodilation and plasma exudation, transient skin swelling due to infection, drug, physical trauma, or autoimmune disease
Clinical Presentation: wheals, individual lesion < 24 hours duration