Lecture 14 Part 1
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Questions and Answers

What is the primary cause of Coumadin necrosis?

  • Depletion of protein C causing thrombosis (correct)
  • Concurrent use of heparin
  • Increased levels of procoagulant factors
  • Direct skin exposure to Coumadin

Which demographic is at the greatest risk for developing Coumadin necrosis?

  • Obese men
  • Children under 10
  • Elderly patients
  • Overweight women (correct)

What condition leads to a transient hypercoagulable state when initiating Coumadin therapy?

  • Excessive vitamin K intake
  • Depletion of protein S
  • Depletion of protein C (correct)
  • Increased platelet count

What prevents Coumadin necrosis during the initiation of Coumadin therapy?

<p>Concurrent heparin therapy (B)</p> Signup and view all the answers

Which anatomical areas are most affected by Coumadin necrosis?

<p>Skin overlying subcutaneous fat (D)</p> Signup and view all the answers

What is a characteristic time frame for the onset of DRESS after starting the medication?

<p>2-6 weeks (A)</p> Signup and view all the answers

Which of the following symptoms is commonly associated with DRESS?

<p>Facial edema with erythema (C)</p> Signup and view all the answers

Which organ system is least likely to be affected by DRESS?

<p>Gastrointestinal (C)</p> Signup and view all the answers

What laboratory finding is almost always present in cases of DRESS?

<p>Eosinophilia (A)</p> Signup and view all the answers

What is one common group of drugs that are known to cause DRESS?

<p>Aromatic anticonvulsants (C)</p> Signup and view all the answers

Which of the following metabolic deficiencies is often associated with DRESS caused by aromatic anticonvulsants?

<p>Epoxide hydrolase deficiency (D)</p> Signup and view all the answers

What is the primary treatment approach for managing DRESS?

<p>Quickly diagnosing and stopping the relevant medication (B)</p> Signup and view all the answers

Which of the following statements about slow acetylators in the context of DRESS is accurate?

<p>They accumulate toxic metabolites leading to DRESS. (A)</p> Signup and view all the answers

What are common initial findings on physical examination that may indicate a systemic drug reaction?

<p>Lymphadenopathy, skin blisters, and target lesions (A)</p> Signup and view all the answers

Which laboratory studies should be ordered for patients with suspected drug reactions?

<p>Complete blood count, liver function studies, and urinalysis (D)</p> Signup and view all the answers

What is a characteristic feature of Acute Generalized Exanthematous Pustulosis (AGEP)?

<p>Erythema in groin and axillae with tiny pustules (A)</p> Signup and view all the answers

What is the primary cause of AGEP according to the provided information?

<p>T-cell mediated cytokine response (C)</p> Signup and view all the answers

What type of medications are the most common causes of AGEP?

<p>β-lactam antibiotics and macrolides (C)</p> Signup and view all the answers

What significance does the timing of rash onset have in AGEP diagnosis?

<p>It usually starts within 1-2 days after medication initiation (D)</p> Signup and view all the answers

What are potential complications if AGEP treatment does not involve stopping the causative medication?

<p>Fluid management issues and possible vasculitis (A)</p> Signup and view all the answers

How should AGEP be managed in clinical practice?

<p>Stop the suspected medication if possible (B)</p> Signup and view all the answers

What is the primary difference in the percentage of skin sloughing that distinguishes SJS from TEN?

<p>SJS is ≤10% sloughing, TEN is ≥30% sloughing (C)</p> Signup and view all the answers

Which medication is least likely to be associated with TEN/SJS?

<p>Beta-blockers (A)</p> Signup and view all the answers

What percentage of skin sloughing defines SJS/TEN overlap?

<p>10% to 30% (B)</p> Signup and view all the answers

Which of the following best describes the mechanism of action of FasLigand in TEN/SJS?

<p>FasLigand binds Fas on keratinocytes, initiating apoptosis (C)</p> Signup and view all the answers

What is the recommended high-dose treatment for TEN/SJS delivered early in the disease?

<p>Intravenous immunoglobulin (IVIG) (C)</p> Signup and view all the answers

What role does the accumulation of toxic drug metabolites play in TEN/SJS?

<p>It leads to immune activation and overexpression of FasLigand (C)</p> Signup and view all the answers

In cases of TEN, what other anatomical structures can experience sloughing besides the skin?

<p>Esophageal lining and trachea lining (C)</p> Signup and view all the answers

How does erythema multiforme primarily differ from SJS and TEN?

<p>It typically affects less than 10% of body surface area with minimal mucosal involvement (D)</p> Signup and view all the answers

What common characteristics define a typical drug rash?

<p>Pink-to-red macules, papules, and plaques without scale (D)</p> Signup and view all the answers

Which demographic factors increase the incidence of typical drug rashes?

<p>Increasing age and increasing numbers of medications (C)</p> Signup and view all the answers

What is the mechanism by which the typical drug rash occurs?

<p>Antigen presenting cells internalizing the drug-protein complex and initiating an immune response (B)</p> Signup and view all the answers

When does a typical drug rash usually begin after medication exposure?

<p>1-14 days after the first dose of the medication (B)</p> Signup and view all the answers

What should be done with medications identified as potential causes of a drug rash?

<p>Stop if safe to do so and consider alternatives (A)</p> Signup and view all the answers

Which of the following is NOT a common causative drug class for typical drug rashes?

<p>Beta-blockers (A)</p> Signup and view all the answers

What symptom should be evaluated in a patient with a suspected drug rash to rule out systemic hypersensitivity?

<p>Dark colored urine (B)</p> Signup and view all the answers

What kind of treatments are typically used for managing a typical drug rash?

<p>Symptomatic treatment with oral antihistamines and topical steroids (B)</p> Signup and view all the answers

What is the typical duration for resolving the syndrome caused by toxic metabolites?

<p>2-6 weeks (A)</p> Signup and view all the answers

What is the recommended treatment if the disease is limited to skin involvement and peripheral eosinophilia?

<p>Topical steroids (D)</p> Signup and view all the answers

What is a significant consequence for patients who experience DRESS due to an aromatic anticonvulsant?

<p>All aromatic anticonvulsants are strictly prohibited for life. (A)</p> Signup and view all the answers

What should be monitored in patients who have experienced DRESS several months after the episode?

<p>Thyroid function studies (B)</p> Signup and view all the answers

What is the rarity of Toxic Epidermal Necrolysis (TEN) and Stevens-Johnson Syndrome (SJS)?

<p>About 1 case per million people per year (D)</p> Signup and view all the answers

What common condition increases the risk of developing TEN and SJS?

<p>Immunosuppression (C)</p> Signup and view all the answers

What characterizes the rash associated with TEN and SJS?

<p>Begins as painful erythematous macules (C)</p> Signup and view all the answers

How long after starting the causative medication do TEN and SJS typically manifest?

<p>1-3 weeks (C)</p> Signup and view all the answers

Flashcards

Typical Drug Rash

A common skin reaction in hospitalized patients often triggered by medications like antibiotics, sulfa drugs, and anticonvulsants. It presents as pink-to-red spots, bumps, and patches without scaling, causing itchiness.

Exanthematous Drug Rash

A type of drug rash that typically occurs within 1-14 days after the first dose of a medication. It can last for up to 14 days after the medication is stopped.

Maculopapular Drug Rash

A type of drug rash characterized by flat, red, and raised patches of skin, often seen during a drug reaction.

T-cell-mediated Drug Rash

An immune response in which the body's immune system reacts to a drug or its metabolites. It typically involves T-cells recognizing the drug-protein complex and triggering an immune reaction.

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Symptomatic Management of Drug Rash

A treatment approach for drug rashes that aims to relieve symptoms. It often involves using antihistamines to reduce itching and topical steroids to reduce inflammation.

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Treating Through

The process of stopping a medication suspected to be causing a drug rash while carefully monitoring the patient for signs of worsening or systemic reactions.

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Medication List Review

A list of medications a patient is currently taking, noting when each medication was started and if any were stopped. This is crucial for identifying possible causes of a drug rash.

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Evaluating for Systemic Hypersensitivity Reaction

Examining a patient for potential signs of a systemic reaction to a drug rash, including fever, sore throat, shortness of breath, and dark urine.

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Acute Generalized Exanthematous Pustulosis (AGEP)

A serious skin reaction that can be triggered by medications. It's characterized by a widespread rash with tiny pus-filled bumps, fever, and high neutrophil count in the blood.

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Lymphadenopathy, purpura, mucous membrane abnormalities

A common sign of systemic drug hypersensitivity, characterized by swollen lymph nodes, bruises, and sores in the mouth, eyes, or genitals.

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Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)

A serious cutaneous drug reaction that can manifest as a rash, fever, and elevated white blood cell count.

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β-lactam antibiotics

A medication family known to trigger AGEP. Examples include penicillin, amoxicillin, and cephalexin.

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Macrolide antibiotics

A medication family known to trigger AGEP. Examples include erythromycin, azithromycin, and clarithromycin.

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Calcium-channel blockers

A medication family known to trigger AGEP. Examples include nifedipine, amlodipine, and verapamil.

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Stopping the causative medication

The most crucial step in managing AGEP. It involves immediately discontinuing the causative medication.

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Treating through AGEP

This may be considered in AGEP only when the causative drug is absolutely essential and stopping it would be life-threatening.

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Toxic Epidermal Necrolysis (TEN)

A serious skin reaction characterized by widespread blistering and peeling of the skin, usually caused by a medication.

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Stevens-Johnson Syndrome (SJS)

A less severe form of TEN, with less skin involvement.

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Epidermal Death in TEN and SJS

Both TEN and SJS are characterized by the death of the epidermis, leading to blisters and peeling of the skin.

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Initial Rash in TEN and SJS

The rash usually begins as painful red patches, typically on the trunk and palms and soles.

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Rash Progression in TEN and SJS

The rash spreads to involve other areas such as the trunk, extremities, face, and neck.

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Epidermal Sloughing in TEN and SJS

As the rash progresses, affected areas become dusky, and the epidermis begins to peel off.

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Mucous Membrane Involvement in TEN and SJS

TEN and SJS often involve the mucous membranes of the eyes, nose, mouth, and genitals.

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Frequency of TEN and SJS

Both TEN and SJS are rare conditions, affecting about 1 in a million people each year.

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What is DRESS Syndrome?

A severe drug reaction typically starting 2-6 weeks after medication initiation, characterized by fever, widespread rash, facial swelling, and organ involvement.

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What is Coumadin Necrosis?

Coumadin necrosis is a rare complication of coumadin therapy that occurs within the first week of treatment, primarily affecting obese women. It involves thrombosis of small vessels in subcutaneous fat, leading to pain, erythema, purpura, and potentially necrosis.

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How does the rash in DRESS present?

DRESS is a serious drug reaction featuring a distinctive rash that begins with a typical drug rash, but later develops into widespread, confluent erythema with skin swelling.

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What are the common symptoms of DRESS?

DRESS commonly presents with a fever and a rash, often accompanied by swollen lymph nodes, facial swelling, and a sore throat.

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Why does Coumadin cause necrosis?

Coumadin necrosis occurs because coumadin therapy initially depletes protein C, an anticoagulant, faster than the procoagulant factors (II, VII, IX, X), leading to a transient hypercoagulable state.

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What are the common lab findings in DRESS?

Eosinophilia, elevated liver enzymes (AST/ALT), and potentially kidney, muscle, heart, lung, thyroid, or CNS involvement.

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What makes Coumadin necrosis more likely?

People with inherited partial deficiency of protein C are at higher risk of developing Coumadin necrosis because their hypercoagulable state is more severe and develops faster.

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How is Coumadin necrosis prevented?

Coumadin necrosis is prevented by initiating heparin therapy along with coumadin. Heparin prevents clot formation until coumadin becomes effective, balancing the coagulation factors.

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What are the most common drugs that cause DRESS?

Aromatic anticonvulsants (phenytoin, carbamazepine, phenobarbital) and sulfonamides are the most common drug classes associated with DRESS.

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How long should heparin be used for Coumadin necrosis prevention?

Patients who are at risk of Coumadin necrosis should remain on heparin until coumadin becomes therapeutic, meaning the depletion of procoagulant factors outweighs the initial depletion of protein C.

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What is the proposed mechanism for DRESS with aromatic anticonvulsants?

Patients with DRESS often have a deficiency in the enzyme epoxide hydrolase, leading to accumulation of toxic drug metabolites, resulting in the delayed onset of the reaction.

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What is the proposed mechanism for DRESS with sulfonamides?

Individuals with DRESS from sulfonamide drugs often have a slower acetylation process, leading to the buildup of toxic metabolites that trigger the reaction.

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What is the most important treatment for DRESS?

Stopping the offending medication is the most important factor in treating DRESS. Early diagnosis and intervention are crucial to prevent further complications.

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Erythema Multiforme

A blistering skin reaction with a bulls-eye target appearance. Only affects less than 10% of the body surface area.

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Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

A severe drug reaction that causes inflammation of various organs, including the skin.

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FasLigand

A protein that triggers cell death.

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Keratinocytes

A type of immune cell that plays a role in cell death.

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Intravenous Immunoglobulin (IVIG)

A treatment for autoimmune disorders that uses antibodies from donated blood.

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Non-steroidal Anti-inflammatory Drugs (NSAIDs)

A drug that reduces inflammation.

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Study Notes

Cutaneous Drug Reactions

  • Divided into limited cutaneous, systemic, and serious reactions
  • Drug rash/limited cutaneous reactions are common in hospitalized patients, increasing with age and number of medications, and more common in females.
  • Characterized by pink-to-red macules, papules, plaques without scaling, often itchy.
  • Frequently described as exanthematous or maculopapular, but specific descriptions (e.g., 1-3 cm pink plaques, covering 60% body, accentuated in warm areas) are preferred.
  • Commonly caused by beta-lactam antibiotics, sulfa drugs, and anticonvulsants.
  • Rash onset can range from 1-14 days after the first dose and last up to 14 days after stopping the medication.
  • T-cell-mediated processes; drug binds to protein, complex is internalized by antigen-presenting cell, then presented to drive immune reaction.
  • Treatment is symptomatic with oral antihistamines and topical steroids. Any drug started within two weeks prior to rash onset should be considered as a possible cause, even if stopped. Substitute with safe alternative if possible.
  • Evaluating for fever, sore throat, shortness of breath, dark urine are crucial for systemic drug hypersensitivity suspicion.
  • Physical examination should include lymphadenopathy, purpura, mucous membrane abnormalities, blisters, and target lesions.

Acute Generalized Exanthematous Pustulosis (AGEP)

  • Less common than typical cutaneous drug reactions.
  • Characterized by erythema, often in the groin, axillae, or inner thighs, with tiny pustules (1 mm) visible on close inspection.
  • Pustules and erythema can spread rapidly over the body. Spiking fevers and elevated neutrophil counts are common.
  • Commonly caused by beta-lactam antibiotics, macrolides, and calcium-channel blockers.
  • Onset of rash and fever usually within 1-2 days of starting offending drug.
  • T-cell mediated reaction, likely mediated by neutrophils.
  • Treatment involves stopping the causative drug, which was started within 3 days of rash onset.

Drug Rash with Eosinophilia and Systemic Symptoms (DRESS)

  • About as common as AGEP but far less than regular drug rashes.
  • Onset later than other drug eruptions (2-6 weeks after starting drug).
  • Initially appears similar to typical drug rash, but quickly develops widespread, confluent erythema with skin swelling. Face and neck often involved first.
  • Facial edema with erythema and sore throat, and significant lymphadenopathy are strongly suggestive of DRESS.
  • Treatment focuses on stopping the causative medication.

Toxic Epidermal Necrolysis (TEN) and Stevens-Johnson Syndrome (SJS)

  • Rare, related diseases caused by medication adverse reactions.
  • Characterized by epidermal death and sloughing, differing only in the extent of skin involvement.
  • TEN affects at least 30% of skin, while SJS affects less than 10%
  • TEN and SJS typically emerge 1-3 weeks after initiating the drug.
  • Rash begins as painful, erythematous macules on the trunk and/or palms progressing to dusky erythema with sloughing of epidermis, blister or sheet-like.
  • Mucous membranes are often involved.
  • Treatment involves immediate cessation of causative agent and supportive care.

Coumadin Necrosis

  • Uncommon adverse reaction to coumadin therapy.
  • Often affects overweight women.
  • Starts with pain, followed by erythema progressing to purpura and necrosis, frequently in skin overlying fat (breast, thighs, buttocks).
  • Caused by thrombosis in small vessels of subcutaneous fat due to a transient hypercoagulable state. Temporary depletion of anticoagulants (protein C, etc) precedes the clotting.
  • Prevention involves initiating heparin therapy before starting coumadin to prevent the temporary coagulopathies.

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Description

This quiz covers cutaneous drug reactions, including limited cutaneous, systemic, and serious types. Explore the characteristics, common causes, and treatment options for drug-related rashes, with emphasis on T-cell-mediated processes. Assess your understanding of the specific descriptions and treatments associated with these reactions.

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