MSK 3 Flashcards

1
Q

What is the pathogenesis of Xeroderma pigmentosum?

A

There is defective nucleotide excision repair of DNA damaged by UV light, causing accumulation of pyrimidine nucleotides and other carcinogenic adducts. Chronic damage leads to skin atrophy, telangiectasias, and hypo/hyperpigmented areas.

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2
Q

What infections is Erythema multiforme most commonly associated with?

A

HSV and mycoplasma are commonly associated w/ erythema multiforme, w/c is a cell-mediated inflammatory d/o involving predominantly CD8+ T cells reacting to antigens deposited in the skin. Target lesions may be found along extremities, face, trunk, and neck.

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3
Q

What is the pathogenesis for Gout?

A

Hyperuricemia leads to monosodium urate crystal deposition in joints. Neutrophils phagocytose the crystals and release cytokines and other inflammatory mediators that further neutrophil chemotaxis and activation.

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4
Q

How do you diagnose a patient for Gout?

A

> Synovial fluid analysis would indicate an increase in WBCs.

>Needle-shaped negatively bifringent crystals.

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5
Q

What is the treatment for gout?

A

NSAIDs are first line.

Colchicine is given if the patient is contraindicated for NSAIDs.

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6
Q

What is the pathogenesis of Staphylococcal Scalded Skin Syndrome?

A

Exfoliative exotoxin produced by staphylococci acts as an epidermolytic that cleaves desmoglein in desmosomes. This results in epidermal necrolysis and the slipping off of skin w/ gentle pressure (Nikolsky’s sign).

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7
Q

How does long-term use of Proton Pump Inhibitors contribute to osteoporotic fractures?

A

Insoluble calcium needs an acidic environment for absorption, and PPIs suppress acid production. Risk of fracture increases in patients w/ advanced age, low body weight, tobacco use, and family hx.

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8
Q

What disease is Dermatitis herpetiformis strongly associated with?

A

DH is strongly associated w/ Celiac disease. IgA antibodies form against gliadin or tissue transglutaminase in the intestine. These antibodies can cross-react w/ epidermal transglutaminase.

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9
Q

What is the Trendelburg gait?

A

The hip drops down as the ipsilateral foot is lifted. This is due to an injury to the CONTRALATERAL superior gluteal nerve or to the gluteus medius muscle. Injections to the superomedial quadrant of the butt have high probability of injuring the superior gluteal nerve.

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10
Q

What are the cutaneous side effects of using Topical corticosteroids?

A

Along w/ being anti-inflammatory, Topical corticosteroids also decrease ECM collagen and glycosaminoglycans. There will be dermal atrophy, drying, cracking, and tightening of skin.

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11
Q

What is the Psoas sign?

A

The Psoas sign is pain exacerbated by movements that cause he psoas to be stretched or extended, such as extension of the hip.

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12
Q

What is the MOA of Colchicine?

A

Colchicine binds to intracellular tubulin and inhibits its polymerization into microtubules, thus disrupting cytoskeletal functions like chemotaxis and phagocytosis. It’s useful for neutrophil activity in acute gout.

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13
Q

In a young competitive athlete presenting with acne, what may be suspected?

A

The athlete may be misusing anabolic steroids. After conversion to DHT, androgens promote both follicular epidermal hyperproliferation and excessive sebum production.

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14
Q

What conditions may Xanthelasma be associated with?

A

Any conditions w/ hyperlipidemia can predispose to xanthelasma. Cholestatic conditions like primary biliary cirrhosis are a potential cause for hypercholesterolemia.

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15
Q

What does a biopsy of a blood vessel look like in Leukocytoclastic vasculitis?

A

A cutaneous small vessel vasculitis involving perivascular inflammation of small blood vessels w/ fibrinoid necrosis, and a predominance of neutorphils and fragmented neutrophilic nuclei. This may follow a pathogen (Hep B, C) or drug exposure (Pen, cephalosporins, phenytoin, sulfonamides).

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16
Q

Osteoarthritis vs. Rheumatoid arthritis

[Joint involvement, morning stiffness, systemic ssx]

A

> OA: osteophyte formation leading to bony enlargement of DIP and PIP joints; brief morning stiffness, no systemic ssx.
RA: morning stiffness w/ systemic ssx; symmetric arthritis of MCP and PIP joints; active synovitis w/ warmth and spongy swelling.

17
Q

What cytokine is essential for fibroblast activation in wound healing?

A

TGF-beta stimulates connective tissue synthesis and ECM remodeling, along w/ PDGF. It increases in proliferative phase of wound healing and decreases during maturation phase (fibrosis, scarring).

18
Q

Where is the Common peroneal nerve most vulnerable to injury? Ssx?

A

Because the nerve courses around the fibular neck, fibular neck fractures can injure it and cause weakness upon dorsiflexion and eversion of the foot, as well as loss of sensation over the dorsum of the foot.

19
Q

How may patients w/ Femoral neuropathy present?

A

Weakness involving quadriceps muscle, loss of patellar reflex, and loss of sensation of anterior and medial thigh and medial leg. Patients complaint of difficulty w/ stairs and frequent falling due to “knee buckling.”

20
Q

How does congenital hypothyroidism arise? Ssx?

A

Mom’s T4 that passes transplacentally prevents neonates from having ssx. When mom’s T4 wanes, the impaired metabolism of proteins, carbs, and lipids is marked by slow physical and mental activity. Build up of substances leads to puffy face (edema), umbilical hernia, protruding tongue, and large anterior fontanelle. There is also risk of irreversible intellectual disability.

21
Q

Why are some patient’s given Succinylcholine at risk of arrhythmias?

A

The nicotinic ACh receptor is a nonselective cation channel, so its opening allows for both Na influx and K release. Succinylcholine can cause significant K release and life-threatening arrhythmias in patients high-risk for hyperkalemia (burns, myopathies, crush injuries, denervating injuries).