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Block 7 Week 2 > Drug Rashes-Buxton > Flashcards

Drug Rashes-Buxton Flashcards

1
Q

What are the most common causes of cutaneous drug reaction rashes?

A

cumulative toxicity, overdoes, photosensitivity and drug-drug interactions

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2
Q

Drugs and their metabolites act as (blank) making some proteins immunogenic inducing either a cell-mediated or humoral response.

A

haptens

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3
Q

What is this:
A drug substance that is capable of reacting with a specific antibody but cannot induce the formation of antibodies unless bound to a carrier protein or other molecule.

A

haptan

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4
Q

WHat are other names for haptens?

A

incomplete antigen, or partial antigen

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5
Q

How do you make a hapten?

A

1) nonreactive drug taken up by host cell
2) activated by phase I metabolism
3) detoxified by phase 2 enzyme or conjugated with host cell protein
4) conjugation forms hapten

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6
Q

What happens if the active form of a nonreactive drug escapes ?

A

reacts w/ soluble host protein and makes soluble hapten-> taken up by APC-> peptide-hapten conjugate -> associates with MHC protein

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7
Q

What is the B pathway for hapten formation?

A

chemically reactive xenobiotics bind to host cell proteins w/out metabolic activation to form haptens

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8
Q

What is a type I hypersensitivity reaction caused by?

A

the formation of drug/antigen-specific IgE that cross-links with receptors on mast cells and basophils leading to immediate release of chemical mediators, including histamine and leukotrienes.

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9
Q

What are the clinical features of a type I hypersensitivity reaction?

A

pruitis, urticaria, angio-oedema and less commonly, bronchoconstriction and anaphylaxis.

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10
Q

The drugs most commonly responsible for type I hypersensitivty are (blank, blank, and blank)

A

aspirin, opioids, and pencillins

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11
Q

Type II or cytotoxic reactions are based on (blank) or (blank) mechanisms

A

IgG or IgM-mediated

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12
Q

Describe type II hypersensitivity reaction mechanisms?

A

binding of antibody to cells w/in subsequent binding of complement and cell rupture

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13
Q

What mechanisms accounts for blood cell dyscrasias such as hemolytic anemia and thrombocytopenia?

A

type II reaction

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14
Q

What is type II or cytotoxic reactions caused by?

A

aspirin, chloroquine, primaquine (antimalarial), dapsone (leprosy), methyldopa (HBP), levodopa

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15
Q

TYpe III reactions are mediated by (Blnak) that arise when ug antigen and antibodies, usually of (blank) or (blank) class, are both present in the circulation, with the antigen present in excess.

A

Intravascular

IgG, IgM

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16
Q

What is this:
Slow removal of immune complexes by phagocytes leads to their deposition in the skin and the microcirculation of the kidneys, joints and gastrointestinal system.

A

type III reactions

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17
Q

Serum sickness and vasculitis are examples of type (blank) reactions

A

III

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18
Q

What drugs cause type III hypersensitivity reactions?

A

penicillin, cephalosporin, sulfonamide, loop and thiazide-type diuretics, phenytoin and allopurinol

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19
Q

type (Blank) reactions are mediated by T cells causing “delayed” hypersensitivity reactions.

A

IV

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20
Q

What are typical examples of Type IV reactions?

A

contact dermatitis

delayed skin tests to TB

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21
Q

Drug-related delayed-type hypersensitivity reactions include (blank) and (blank)
……..These are Type IV reactions

A

Stevens–Johnson syndrome and toxic epidermal necrolysis (TEN).

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22
Q

What drugs cause a type iV hypersensitivity reaction?

A

sulfonamides, nonsteroidal anti-inflammatory drugs,allopurinol, methotrexate

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23
Q

The clinical manifestations of drug hypersensitivity depend on various factors, including…..?

A
  • The chemical or structural features of a drug
  • The genetic background of the affected individual
  • The specificity and function of the drug-induced immune response.
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24
Q

Different types of (blank) can produce diverse clinical patterns of hypersensitivity reaction

A

immune effector mechanism

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25
Q

Penicillins, are the classic drugs acting as haptens, but are reported to cause (blank) (immediate-type) hypersensitivity reactions as well as non-IgE mediated reactions, including morbilliform eruptions, erythema multiforme and Stevens–Johnson syndrome.

A

type 1 IgE mediated

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26
Q

T or F

10% of patients with drug hypersensitivity reactions react to more than one structurally distinct compound.

A

T

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27
Q

The term (blank) has been used to describe patients who have a propensity to react against different, chemically unrelated drugs.

A

multiple drug allergy syndrome

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28
Q

There is a high incidence of hypersensitivity reactions in patients with altered (blank), for example due to viral infections

A

immune status

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29
Q

A well-documented example of drug hypersensitivity with altered immune status is the increased risk of (bank) hypersensitivity in HIV patients.

A

trimethoprim/sulfamethoxazole

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30
Q

Some types of skin rash are very rarely drug induced for example (blank)

A

eczema

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31
Q 
What do these have in common Antacids					Muscle relaxants
Antihistamines (oral)			Nitrates
Atropine					Nystatin 
Benzodiazepines				Oral contraceptives
Corticosteroids				Propranolol
Digoxin 					Spironolactone 
Ferrous sulphate				Theophylline
Insulin					Thyroid hormones
Laxatives				Vitamins
Local anaesthetics  (other than topical)
A

drugs that rarely cause cutaneous eruptions

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32
Q

if a patient taking both demeclocycline and chlorpromazine develops a photosensitivity reaction the chances are that (blank) is the cause, although both drugs are capable of producing the reaction.
However, if the patient develops skin hyperpigmentation then (blank) is more likely to be implicated.

A

demeclocycline

chlorpromazine

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33
Q

The timing of skin reactions is a useful diagnostic tool. In general, the onset occurs (blank) after the introduction of the causative drug.

A

soon

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34
Q

Hypersensitivity reactions to (blank) can occur several weeks after the drug has been discontinued.

A

penicillins

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35
Q

(blank) can also cause very late reactions.

A

Gold

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36
Q

What are signs suggestive of a severe reaction?

A 
mucous membrane involvement
blisters or skin detachment
high fever
angio-edema or tongue swelling
facial edema
skin necrosis
lymphadenopathy
dyspnoea.
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37
Q

In most cases drug eruptions are (blank), resolving gradually after the causative drug is withdrawn.

A

reversible

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38
Q

(blank), may be due to sensitivity to excipients. If this type of reaction is present, it is worth noting the proprietary (brand) names of medicines taken as well as the generic name.

A

Urticaria

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39
Q

What shoud you ask the patient if you suspect a drug reaction?

A

history of drug sensitivity, contact dermatitis, connective tissue disease or atopic disease with asthma or eczema.

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40
Q 
What are these:
Acetaminophen 
Allopurinol
Antimicrobials: cephalosporins, penicillins, chloramphenicol, erythromycin, gentamicin, amphotericin, antituberculous drugs, nalidixic acid, nitrofurantoin, sulfonamides
Antifungals (allylamine type: Terbinafine)
Barbiturates
Captopril
Carbamazepine
Furosemide 
Gold salts 
Lithium 
Phenothiazines 
Phenylbutazone 
Phenytoin
Thiazides
A

drugs causing exanthematous reactions

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41
Q

(blank) (also called morbilliform or maculopapular drug eruptions) are the most common drug-induced eruptions. They are a type of idiosyncratic, T-cell-mediated, delayed (type IV) hypersensitivity reactions.

A

Exanthematous drug eruptions

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42
Q

(blank) present as a widespread, symmetrically distributed rash composed of pink-to-red macules and papules that may coalesce to form plaques.

A

Exanthematous eruptions

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43
Q

Tell me about acetaminophen.

A

well tolerated

  • rash maybe, allergy, erythematous or urticarial
  • serious: drug fever/ mucosal lesions.
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44
Q

Patient who show hypersensitivity reactions to the salicylates only rarely exhibit sensitivity to (blank)

A

acetaminophen

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45
Q

the use of (blank) has been associated ANECDOTALLY with neutropenia, thrombocytopenia, pancytopenia, hemolytic

A

acetaminophen

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46
Q

What organs may be damaged with acetaminophen overdose?

A

kidney damage, liver damage

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47
Q

A fixed drug eruption is due to drugs or chemicals as the (blank) cause

A

SOLE

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48
Q

What is this:
It consists of erythematous round or oval lesions of a reddish, dusky purple or brown color, sometimes featuring blisters.
Initially, one lesion appears, although others may follow.
The patient may complain of itching or burning, but systemic
involvement is usually absent.

A

Fixed Drug eruptions

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49
Q

What is a fixed drug eruption?

A

eruption due to drugs or chemicals

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50
Q

When does a fixed drug eruption appear?

A

within a day to a few weeks

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51
Q

Where are common places to see fixed drug eruptions?

A

hands, feet, tongue, penis, perianal areas

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52
Q

The site of the eruption is fixed, i.e whenever the individual takes the causative drug the eruption occurs …..?

A

within hours at exactly the same site

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53
Q

How long does it take for a fixed drug eruption to heal?

A

7-10 days after causative drug is stopped, although residual hyperpigmentation may be slow to resolve

54
Q

(blank), (blank), and (blank) are frequently implicated in fixed drug eruptions

A

Sulfonamides, tetracycines, and NSAIDs

55
Q

How can you reduce intensity of fixed drug eruption?

A

topical corticosteroids

56
Q 
what do these cause:
ACE inhibitors
Allopurinol
Antimicrobials: co-trimoxazole, sulfonamides, tetracyclines, cephalosporins, penicillin, clindamycin, trimethoprim, metronidazole
Barbiturates
Benzodiazepines
Calcium channel blockers: amlodipine, diltiazem
Carbamazepine
Dextromethorphan
Diltiazem
Fluconazole
Lamotrigine
NSAIDs, including aspirin
Paclitaxel
Paracetamol
Phenolphthalein
Proton pump inhibitors: omeprazole, lansoprazole
Quinine
Salicylates
Terbinafine
A

Fixed drug eruptions

57
Q

(blank) is the second most common form of cutaneous drug reaction after exanthematous reactions.

A

Drug-induced urticaria

58
Q

Urticaria is seen in association with (blank) (blank) and (Blank)

A

anaphylaxis, angioedema or serum sickness.

59
Q

The clinical appearance of drug-induced urticaria is indistinguishable from that from other causes, but is often more severe and may be accompanied by ……?

A

hypotension, breathing difficulties, shock, and even death

60
Q

(blank), sometimes known as nettle rash or hives, present as raised, itchy, red blotches or wheals that are pale in the center and red around the outside.

A

Urticarial lesions

61
Q

Drug-induced urticaria may occur after how many exposures to a drug?

A

after the first exposure to a drug or after many previously well-tolerated exposures.

62
Q

With urticaria, the onset is (blank) than with other drug eruptions. lesions usually develop within 36 hours of initial drug exposure.

A

more rapid

63
Q

Individual urticarial lesions rarely persist for more than a (blank), however on rechallenge, lesions may develop within (blank)

A

day

minutes

64
Q

Urticaria is characterized as acute when it lasts (blank) or less and chronic when it persists.

A

6 weeks

65
Q

(blank) is a vascular reaction resulting in increased permeability and fluid leakage, leading to edema of the deep dermis, subcutaneous tissue or submucosal areas.

A

Angio-oedema

66
Q

T or F

angioedema is rarer than urticaria.

A

T

67
Q

What is generally affected in angioedema?

A

The tongue, lips, eyelids or genitalia are generally affected, and the edema may be either unilateral or symmetrical.

68
Q

Angioedema of the upper respiratory tract can result in serious (blank)

A

acute respiratory distress, airway obstruction and death

69
Q

(blank) inhibitors are one of the most common causes of angioedema.

A

Angiotensin-converting enzyme (ACE)

70
Q

If a patient on ACE demonstrate angioedema, should you take them off of it?

A

yeah duh

71
Q

The mechanism of ACE-inhibitor-induced angioedema is thought to involve increased levels of (blank) which can directly cause vascular permeability.

A

bradykinin

72
Q

(blank), which theoretically do not affect bradykinin, should not present a risk for patients who had this complication while taking ACE inhibitors.

A

Angiotensin-II receptor antagonists

73
Q

What are the dual vasodiatory actions of angioedema and ACE inhibitors?

A

blocks renin-angiotensin mediated vasoconstriction

prevents breakdown of bradykinin leading to formation of NO and prostacycline

74
Q

How can antibiotic cause urticaria?

A

Drugs acting through IgE receptors to the drug on mast cells triggering degranulation

75
Q

How do opoids and codeins and stuff cause urticaria?

alsoatropine, hydralazine, pentamidine, quinine, radiocontrast media, vancomycin, dextran, tubocurarine

A

Drugs that cause mast cell degranulation

76
Q

How does aspirin, NSAIDS, ACE inhibitors, and monoclonal antibodies cause urticaria?

A

drugs that pharmacologically promote or exacerbate urticaria

77
Q

How doe pencillin, sulfonamides, thiouracils, cholecystopgraphic dyes, and aminosalicylic acid cause urticaria?

A

Immune complex formation precipitation and activation of complement

78
Q

How does benzoid acit, butylated hydroxytoluene, sulfites, aspartame, tartrazine, preservatives cause urticaria?

A

excipients in the medication that provoke allergic or pseudoallergic reactions

79
Q

The term (blank) is applied to drug eruptions that resemble acne vulgaris.

A

acneiform

80
Q

What are the common inplicated drugs in acne (papulopustular lesions)?

A

Corticotropin (ACTH), corticosteroids, androgens (in females), oral contraceptives, haloperidol, isoniazid, phenytoin and lithium

81
Q

What causes psoriasis?

A

lithium (can cause it in 1 month)

82
Q

How do you trat psoriasis?

A

topical corticosteroid or calcipotriol cream

83
Q 
What are these:
ACE inhibitors 
Beta-blockers
Chloroquine and hydroxychloroquine 
Digoxin 
Granulocyte colony-stimulating factor (G-CSF) 
Interferons
Lithium
NSAIDs
Penicillamine
Terbinafine
Tetracyclines
TNF-alpha antagonists
Gold
A

Drugs that can cause psoriasis

84
Q

(blank) describes small cutaneous extravasations of blood. It is an occasional feature of drug-induced skin eruptions, and in some cases it is the main characteristic.

A

Purpura

85
Q

Main causes of purpura?

minor causes?

A

thromobcytopenia/platelet dysfunction

drug-related damage to small blood vessesl

86
Q

What are the drugs associated with non-thrombocytopenic purpura?

A

aspirin, quinine, sulfonamides, atropine, penicillin

87
Q

What causes vasculitis?

A

type III hypersensitvity w/ immune complex deposition in postcapilary blood vessels

88
Q

Cutaneous vasculitis commonly presents with raised (blank) on the legs, ranging in size from a pinpoint to several cm. margins are irregular or stellate

A

purpuric lesions

89
Q

How can treat vasculitis?

A

corticosteroids and immunosuppressants

90
Q

(blank) is associated with a hypersensitivity syndrome that typically manifests as a vasculitis involving one or more organ systems.

A

Propylthiouracil

91
Q

How long does it take an agent to cause vasculitis?

A

1 week to several years

92
Q

Most affected patients recover quickly from vasculitis when the drug is withdrawn, but some require prolonged treatment with high-dose (blank) and immuno-suppressants.

A

corticosteroids

93
Q

Involvement of the mucosa is common, so the mouth, eyes and genitalia may be affected, when the condition is usually called (blank)

A

steven johnson syndrome

94
Q

What is this:
Non-urticarial drug eruptions typically occur 7-14 days after initiation of treatment
Incidence is between 1/1000 and 1/3000
Any patients with either disease should be removed from the drug and rechallenge avoided

A

Stevens-Johnson syndrome, Toxic Epidermal Necrolysis

95
Q

(bank) are the major cause of toxic epidermal necrolysis

A

drugs

96
Q

What are common drugs implicated in TEN?

A

antibiotics, antiepileptic drugs, nonsteroidal anti-inflammatory drugs (NSAIDs), ampicillin, allopurinol, corticosteroids (topical and systemic), and the antiretroviral drugs nevirapine and abacavir.

97
Q

(blank) comprises fever, malaise, myalgia, arthralgia, and extensive erythema multiforme of the trunk and face.
It is frequently drug induced. There may be skin blistering and mucosal erosion covering up to 10% of the body surface area.

A

stevens-johnson syndrome

98
Q

(blank) denotes a reaction occurring when a photosensitising agent in or on the skin reacts to normally harmless doses of ultraviolet or visible light.

A

Photosensitivity

99
Q

Photosensitivity may be due to what kind of drugs?

A

topical or systemic

100
Q

Some drugs may induce photosensitivity by precipitating (Blank) or (blank)

A

porphyria

lupus

101
Q

What are some thigns that can cause photoallergic reactions?

A

sunscreens, frangrances, soaps

102
Q

A widespread eruption suggests exposure to a (blank), whereas a localized eruption indicates a reaction to a locally applied (blank)

A

systemic photosensitizing agent

topical photosensitizer.

103
Q

The photosensitivity eruption is usually evident withint (blank) hours of exposure and resembles exaggerated sunburn with erythema, edema, blistering, weeping and desquamation.

A

5-20

104
Q

In photosensitivity reactions The rash is confined to areas exposed to light. (blank) may remain after other features have subsided.

A

Hyperpigmentation

105
Q

(blank) is associated with a 30-50% incidence of photosensitivity

A

amiodarone

106
Q

Amiodarone causing photosensitivity causes symptoms that will develop within (blank) hours of sun exposure as a burning sensation followed by erythema. A small number of affected patients develop slate-grey pigmentation on light-exposed area

A

2 hours

107
Q

light sensitivity may persist up to (blank) months after the drug is stopped

A

4

108
Q

cutaneous pigmenation slowly fades after (blank) is stopped, but may persist for months to years

A

amiodarone

109
Q

(blank) may cause a phototoxic response when given in high doses. THe reaction is characterized by a burning, painful, erythema within minutes of exposure to sunight either directly or through windows.

A

Chlorpromazine (thorazine)

110
Q

WHen causing a photosensitivity reaction with use of chlorpromazine, Erythema may persist for more than (blank) occasionally a golden brown or slate-grey pigmentation predominantly of exposed sites, may be seen.

A

24 hours

111
Q

Drug-induced alteration in skin color may result from increased (blank), increased (blank), or cutaneous deposition of drug-related material.

A

melanin synthesis

lipofuscin synthesis

112
Q

A brown patchy pigmentation on light-exposed areas may be a result of prolonged administration of (blank) . It occurs in about 10% of patients, and women are more likely to be affected.
The pigmentation is similar to chloasma, affecting mainly the face, neck and arms.

A

phenytoin

113
Q 
What do these cause:
Amiodarone (slate grey)
Chloroquine (blue-grey or brown)
Chlorpromazine (blue-grey)
Cytotoxic agents
Gold (blue-grey) 
Hydroxychloroquine
Imatinib
Mepacrine (yellow) 
Minocycline
Oral contraceptives (brown) 
Phenytoin (brown)
A

hyperpigmentation

114
Q

Drugs that induce hair loss may be classified according to the phase of the (blank) that is affected.

A

hair follicle cycle

115
Q

In anagen effluvium (hair loss), drugs induce an abrupt cessation of active anagen growth and the hairs are shed within (blank), with tapered and broken roots.

A

days or weeks

116
Q

Anagen hair loss is an expected pharmacological effect of (blank) and is often dose related

A

cytotoxic chemotherapy

117
Q

Alopecia is associated with (blank) such as cyclophosphamide, cytotoxic antibiotics such as bleomycin, vinca alkaloids, and platinum compounds.

A

alkylating agents

118
Q

How should you treat hair loss?

A

scalp hypothermia

119
Q

(blank) is an excessive growth of coarse hair with masculine characteristics in a female.

A

Hirsutism

120
Q

This is a consequence of androgenic stimulation of hormone sensitive hair follicles. Drugs commonly responsible include (blank) .

A

testosterone, danazol, corticotropin, anabolic steroids and glucocorticoids

121
Q

Patients with drug-induced (blank) may also present with other dermatological signs of virilization, such as acne.

A

hirsutism

122
Q

(blank) is the growth of terminal and/or vellus hair on areas of the body where the hair is usually short, such as the forehead and cheeks.

A

Hypertrichosis

123
Q

Hair gain is usually dose related and is (blank) after drug withdrawal

A

reversible

124
Q

(blank) may produce hypertrichosis in 50% of transplant recipients, with the excess growth being most marked on the face and upper back.

A

Cyclosporine

125
Q 
What do these cause:
Androgens 
Cyclosporine 
Diazoxide 
Methoxsalen 
Minoxidil
Nifedipine
Penicillamine
Phenytoin
Verapamil
A

hypertrichosis

126
Q

Angioedema is a known adverse effect of (blank)

A

ACE Inhibitors

127
Q

If you have intense angioedema with respiratory symptoms should be given (blank)

A

epinephrine, antihistamines, and corticosteroids

128
Q

T or F

angiotensin II receptor antagonists appear to be much less likely to cause angioedema

A

T

129
Q

(blank) are a known cause of photosensitivty reactions.

A

NSAIDS
and
Oral Contraceptives

130
Q

How do you manage photosensitivity?

A

antihistamines and topical steroids

131
Q

What is the most commonly implicated herb in photosensitivity?

A

St. John’s Wort

Block 7 Week 2 (10 decks)

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