Skin And Drugs

Front 1

First fat soluble vitamin discovered?

Back 1

Vitamin A

Front 2

Where are fat soluble vitamins stored?

Back 2

Liver

Front 3

Hormone-like vitamin?

Back 3

Vitamin A

Front 4

Fat soluble vitamins?

Back 4

A,D,E & K

Front 5

Vitamin A is synthesized in the body. True or false?

Back 5

False

Front 6

List the 4 forms of Vitamin A.

Back 6

Retinol
Retinal
Retinoid
Retinyl esters

Front 7

Form of Vitamin A stored and transported in the body?

Back 7

Retinol

Front 8

Form of Vitamin A required for vision?

Back 8

Retinal

Front 9

Biologically active form of Vitamin A Responsible for mediating the effects of vitamin A in the body?

Back 9

Retinoic acid

Front 10

Form of Vitamin A ingested as food or supplement?

Back 10

Retinyl esters

Front 11

List the pro-Vitamin A carotenoids converted to Vitamin A by the body?

Back 11

α-carotene
β-carotene
γ-carotene
Cryptoxanthin

Front 12

Pro-Vitamin A carotenoid best converted to Vitamin A and absorbed by the body?

Back 12

β-carotene

Front 13

Name 3 sources of retinyl esters from animals?

Back 13

Palmitic acid
Myristic acid
Dodecanoic acid

Front 14

Vitamin that stimulates epitheleal mucous production?

Back 14

Vitamin A

Front 15

Short-term dermatological effect of Hypervitaminosis A?

Back 15

Desquamation

Front 16

Short-term ophthalmic effects of Hypervitaminosis A?

Back 16

Papilledema
Scotoma
Blind spots
Photophobia

Front 17

Teratogenic Effects of Retinoid drugs?

Back 17

Craniofacial
Neural tube
Urogenital
Musculoskeletal

Front 18

How do carotenoids enter the enterocytes from the GI lumen?

Back 18

Passive diffusion

Front 19

Where are carotenoids transformed into usable retinol?

Back 19

In the enterocytes

Front 20

Where are retinyl esters transformed to retinol?

Back 20

In the GI lumen

Front 21

What type of enzyme transforms retinyl esters to retinol in the GI lumen?

Back 21

Hydrolases

Front 22

How does retinol in the GI lumen enter the enterocytes?

Back 22

Through facilitated diffusion

Front 23

What happens to retinol once it enters the enterocytes?

Back 23

Retinol is esterfied and transferred to the liver for storage

Front 24

Name the intercellular proteins that function in the transport of retinol.

Back 24

Cellular Retinoic Binding Proteins (CRBPs)

Front 25

What are the 4 functions of Cellular Retinoic Binding Proteins (CRBPs)?

Back 25

Transport retinol. Present retinols to appropriate enzymes for esterification.
Protect retinols from enzymes and environment. Control concentrations of free retinol in cell.

Front 26

In what for are retinols stored in the body?

Back 26

As esters

Front 27

Where does esterfication of retinol occur?

Back 27

In the enterocytes

Front 28

Which enzyme esterfies retinol after presentation by CRBPs?

Back 28

LRAT – Lecithin-retinol acyltransferase

Front 29

Which enzyme is upregulated in the enterocytes when retinol levels reach excessive levels?

Back 29

ARAT – Acylcoenzyme A retinol acyltransferase

Front 30

What lipoproteins transport retinol to the liver?

Back 30

Chylomicrons

Front 31

How to chylomicrons move from the small intestine to the liver?

Back 31

They leave the small intestine through the lymphatic system and enter circulation at subclavian vein.

Front 32

Retinyl esters are hydrolyzed to retinol in hepatocytes and then bound to RBPs (retinol binding proteins). Where are the retinol binding proteins found?

Back 32

In the endoplasmic reticulum (ER) of hepatocytes.

Front 33

Which liver cells actually store the Retinol-RBP complexs?

Back 33

Liver stellate cells

Front 34

What happens to retinol in the liver stellate cells if the body does not require its immediate use?

Back 34

Retinol is bound to CRBP and re-esterified for storage by ARAT or LRAT.

Front 35

What happens when the body requires stored retinol?

Back 35

Retinyl esters are hydrolyzed.
Retinol is released into circulation.
Retinol is transported in a complex with RBP

Front 36

What happens when the Retinol-RBP complex travels to cell surface?

Back 36

The complex interacts with transthyretin (TTR), a plasma protein that helps mediate retinol transfer to cell surface receptors for transport into the cell.

Front 37

What else does TTR bind?

Back 37

Thyroxine

Front 38

Which protein transfers retinol from systemic circulation into the cell?

Back 38

Transthyretin (TTR)

Front 39

RBP and TTR enter the cell along with retinol. True or false?

Back 39

False

Front 40

What happens to the retinol once it enters the cell where it will be used?

Back 40

Retinol binds again to CRBP, which delivers it to appropriate site for conversion to active form

Front 41

What is the rate limiting step in the conversion of retinol -> retinal -> retinoic acid?

Back 41

RoDH: Retinol dehydrogenase

Front 42

Name the protein that serves as retinal’s body guard in the cytoplasm of the cell?

Back 42

CRABP: Cellular Retinoic Acid Binding Protein

Front 43

Where does retinoic acid mediate its action?

Back 43

In the cell nucleus

Front 44

How does retinoic acid mediate its action?

Back 44

By binding to nucleur receptors and acting as a transcription regulator

Front 45

Name the two distinct forms of retinoic acid that are biologically active?

Back 45

All-trans-retinoic acid
9-cis-retinoic acid

Front 46

What does all-trans-retinoic acid bind to in the cell nucleus?

Back 46

RA binds to RARs (Retinoic Acid Receptors), a, b, and g

Front 47

What does 9-cis-retinoic acid bind to in the cellular nucleus?

Back 47

9-cis-RA binds to RXRs (Retinoic Acid X Receptors), alpha, beta and gamma

Front 48

RARs and RXRs can homo-dimerize with their own kind, but can the hetero-dimerize with each other?

Back 48

Yes, RARs and RXRs can homo and hetero-dimerize.

Front 49

Where to the dimers bind to regulate gene transciption?

Back 49

They bind to DNA response elements

Front 50

Which retinoic acid receptors are predominant in the skin?

Back 50

RAR alpha and beta

Front 51

How is retinol metabolized in the body?

Back 51

Through glucuronidation and enterohepatic cycling. Unchanged retinol is normally not excreted.

Front 52

How is retinoic acid metabolized in the body?

Back 52

Through decarboxylation and glucoronide formation and excretion in the urine and feces. There is no specific carrier in the blood for retinoic acid.

Front 53

With respect to medicinal chemistry, which part of the retinoid structure is absolutely required for receptor activity?

Back 53

The cyclical β-ionone ring.

Front 54

All-trans-retinol?

Back 54

Retinol

Front 55

All-trans retinoic acid?

Back 55

Tretinoin (Retin-A)

Front 56

13-cis-retinoic acid?

Back 56

Isotretinoin (Accutane) 1st generation retinoid

Front 57

9-cis-retinoic acid?

Back 57

Alitretinoin (Panretin) 1st generation retinoid

Front 58

Second Generation Retinoids – Aromatic Retinoids?

Back 58

Etretinate (Tegison)
Acitretin (Soriatane)

(Etretinate removed due to birth defects)

Front 59

Third Generation Retinoids - Arotinoids

Back 59

Tazarotene (Tazorac)
Bexarotene (Targretin)
Adapalene (Differin)

Front 60

Which class of retinoids is most specific for retinoic acid receptors?

Back 60

The third generation.

Front 61

Why are third generation retinoids more specific for retinoid acid receptors?

Back 61

Reduced flexibility of the side chain.

Front 62

What is the trade name for Tazarotene?

Back 62

Tazorac

Front 63

What is the trade name for Bexarotene?

Back 63

Targretin

Front 64

What is the trade name for Adapalene?

Back 64

Differin

Front 65

Glands that produce most sweat and are concentrated in the palms, forehead and soles of feet?

Back 65

Ecrine glands

Front 66

Odorous glands of the axillary and anogenital areas?

Back 66

Apocrine glands

Front 67

Ceruminous glands and mammary glandsare frequently considered to be modified sweat glands. What category to these glands belong to?

Back 67

Ecrine

Front 68

Enlarged and plugged hair follicles?

Back 68

Comedos

Front 69

Glands that secrete sebum to lubricate skin and hair, slow water loss and act as bactericidal agents?

Back 69

Alveolar glands

Front 70

Accumulation of sebum that blocks sebaceous gland ducts and causes inflammation?

Back 70

Acne

Front 71

Mechanism of action of Retin-A (all-trans retinoic acid)?

Back 71

Reduces the hyperkeratinization that leads to comedone formation.
Decreases adhesion of corneocytes.
Increases shedding and prevents blockage of gland openings.

Front 72

Systemic retinoids?

Back 72

Accutane (Isotretinoin)
Soriatane (Acitretin)

Front 73

Some retinoids remain teratogenic even after discontinued use. Explain this prolonged teratogenic effect?

Back 73

Acitretin and Ecetretin sequester in fat cells

Front 74

Topical retinoids?

Back 74

Retin-A
Tazorac (Tazarotene)
Differin (Adapalene)

Front 75

Topical retinoid prodrug selective for RAR-b and RAR-gamma?

Back 75

Tazorac (Tazarotene)

Front 76

Topical retinoid that binds with RARs but will not bind RXRs or CRABPs?

Back 76

Differin (Adapalene)

Front 77

Topical retinoid with anti-inflammatory effects?

Back 77

Differin (Adapalene)

Front 78

Non-Retinoid Keratolytics?

Back 78

Salycylic acid
Benzoyl peroxide
Propylene glycol

Front 79

Non-retinoid keratolytic that is converted to lactic acid and pyruvic acid, removes hyperkeratotic debris and increases water content of stratum corneum?

Back 79

Propylene glycol

Front 80

Significance of the 4,5 double bond and 3-keto group on ring A of steroid drugs?

Back 80

Glucocorticoid and mineralocorticoid activity

Front 81

Significance of 11β-hydroxyl group on ring C of steroid drugs?

Back 81

Glucocorticoid activity

Front 82

Significance of the 17α-hydroxyl group on ring D of steroid drugs?

Back 82

Optimal potency

Front 83

Addition of double bond on 1,2 position of ring A of steroid drugs?

Back 83

Increases glucocorticoid activity and slows metabolism

Front 84

Fluorination at 9α on ring B of steroid drugs?

Back 84

Enhanced activity

Front 85

C16 subsitutions on ring D of steroid drugs?

Back 85

Elimination of mineralocorticoid activity

Front 86

Adverse effects spcifically related to fluorinated steroid drugs?

Back 86

Perioral dermatitis and Rosacea

Front 87

Augmented betamethasone dipropionate (Diprolene) ?

Back 87

Very high potency steroid

Front 88

Fluocinonide(Lidex, Lidex-E) 0.05%

Back 88

High potency steroid

Front 89

Mometasone furoate (Elocon) 1.0%

Back 89

Medium potency steroid

Front 90

Which potency of steroids causes skin blanching the fastest under the Vasoconstrictor Assay

Back 90

High potency

Front 91

Clobetasol propionate (Cormax, Embeline, Embeline E, Temovate, Olux, Clobex, Clobevate)?

Back 91

Very high potency steroid

Front 92

What keeps glucocorticosteroid receptors inactive inside the cell?

Back 92

Heat check (IP) proteins

Front 93

Steroid receptors enter the cell nucleus and dimerize when activated, where the bind _________?

Back 93

DNA response elements (GREs)

Front 94

Diflorasone diacetate (ApexiCon E cream, Florone cream, Psorcon E) 0.05%

Back 94

High potency steroid

Front 95

Fluticasone propionate (Cutivate) 0.05%

Back 95

Medium potency steroid

Front 96

Betamethasone valerate 0.1%

Back 96

High potency steroid

Front 97

Diflorasone diacetate (ApexiCon) 0.05%

Back 97

Very high potency steroid

Front 98

Fluocinonide (Vanos) 0.1%

Back 98

Very high potency steroid 0.1%

Front 99

Halcinonide (Halog)

Back 99

High potency steroid

Front 100

Amevive?

Back 100

Alefacept (T-Cell modulator)

Front 101

Raptiva

Back 101

Efalizumab (T-Cell modulator)

Front 102

Enbrel

Back 102

Etanercept (T-Cell modulator)

Front 103

Infliximab

Back 103

Remicade (T-Cell modulator)

Front 104

Dimeric fusion protein combination of human LFA-3 and human IgG1 that binds CD2 to induce apoptosis of memory-effector T cells and inhibit cutaneous T-cell activation and proliferation?

Back 104

Alefacept (Amevive)

Front 105

T-cell modulator that requires weekly IM injections?

Back 105

Alefacept (Amevive)

Front 106

Monoclonal antibody (IgG1) against CD11-α integrin subunits of LFA-1 on T-cell surface molecule involved in T-cell activation? Inhibits T-cell migration into skin and cytotoxic T-cell function?

Back 106

Efalizumab (Raptiva)

Front 107

Antibody portion that determines type of Ig?

Back 107

FC

Front 108

T-Cell modulator requiring weekly SC injection?

Back 108

Efalizumab (Raptiva)

Front 109

Genetically engineered fusion protein that combines TNF-α receptor with human IgG1? Binds Tumor Necrosis Factor α (TNF-α) and prevents TNF- α from binding to its receptor? Administered SC.

Back 109

Etanercept (Enbrel)

Front 110

Chimeric monoclonal antibody (IgG1) that binds free and membrane bound TNF- α and prevents binding of TNF- α to its receptor? Requires IV infusion.

Back 110

Infliximab (Remicade)

Front 111

Most common class of drugs that cause drug induced skin reactions?

Back 111

Antibiotics (mostly -cillins)

Front 112

Immunologic skin reactions frequently caused by penicillin (PCN) and other related drugs that occurs in minutes to days due to the mast cell release of chemical mediators that cause edema and vasodilation?

Back 112

IgE-dependent reactions

Front 113

Immunologic skin reactions commonly caused by PCNs, sulfonamides, phenytoin and aminosalicylic acid. Symptoms typically appear six + days after exposure and are due to antigen-antibody complexes?

Back 113

Serum sickness

Front 114

Nonimmunologic skin reactions?

Back 114

Activation of effector pathways
Phototoxicity
Exacerbation of existing disease
Inherited enzyme or protein deficiencies
Alterations of immunologic status

Front 115

Key factor in the diagnosis IgE mediated skin reactions?

Back 115

Onset of minutes to days after exposure

Front 116

Drug induced skin reaction characterized by fever and arthritis?

Back 116

Serum sickness

Front 117

Pruritic, red wheals that rarely last more than 24 hours?

Back 117

Urticaria

Front 118

Urticaria with swollen dermal and subcutaneous tissues?

Back 118

Angioedema

Front 119

Drug mechanism of action that causes urticaria and/or angioedema?

Back 119

IgE-dependent reactions, serum sickness, or activation of effector pathways

Front 120

Common drug causes of urticaria and/or angioedema?

Back 120

Non-steroidal anti-inflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors, radiographic dyes

Front 121

Common drug causes of photosensitivity eruptions?

Back 121

fluoroquinolones and doxycycline

Front 122

Common drug causes of pigmentation changes?

Back 122

Oral contraceptives → melasma
Long-term minocycline → blue/grey pigmentation
Amiodarone → purple pigmentation
Long-term high-dose phenothiazine → grey-brown pigmentation (sun exposed areas)
Chemotherapeutic agents

Front 123

Purpuric lesions that develop 7- 10 days after initiation of drug; usually caused by propylthiouracil, allopurinol, thiazides, sulfonamides, PCN, and some NSAID.

Back 123

Vasculitis

Front 124

Mechanism causing vasculitis

Back 124

Serum sickness

Front 125

Erythematous eruption that may become purpuric and/or lichenoid that is often accompanied by fever, facial edema, and hepatitis and usually begins 2-8 weeks after drug administration.

Back 125

Hypersensitivity syndrome

Front 126

Mechansim causing hypersensitivity syndrome?

Back 126

Idiosyncratic, genetic inability to detoxify toxic metabolic products

Front 127

Most common drug(s) associated with hypersensitivity syndrome?

Back 127

Phenytoin. Others include lamotrigine, minocycline, dapsone, allopurinol, sulfonamides, abacavir, and zalcitabine

Front 128

Sharply demarcated, erythematous lesions that are indurated and purpuric and may progress to hemorrhagic bullae? Mostly seen in women 3-10 days into treatment

Back 128

Warfarin necrosis of the skin

Front 129

Mechanism explaining Warfarin Necrosis of Skin?

Back 129

Warfarin causing a decrease in protein C that leads to hypercoagulability which causes necrosis

Front 130

Other causes of drug induced necrosis of the skin?

Back 130

Heparin, probably due to heparin-induced platelet aggregation occluding blood vessels

Front 131

Skin rash marked by symmetric erythematous macules that often start on the trunk and eventually become confluent? These eruptions are classified as early (few hours to 3 days after administration) or late (≤ 9 days after exposure.

Back 131

Morbilliform Reactions

Front 132

Mechanism explaining drug induced morbilliform reactions?

Back 132

Unknown

Front 133

Drugs known to cause morbilliform reactions?

Back 133

PCNs and sulfonamides.
1% of patients using PCN have cutaneous reaction; 85% of those are morbilliform

Front 134

Skin reaction marked by one or more sharply demarcated erythematous lesions with acute inflammation followed by hyperpigmentation? Lesion recurs in the same location upon re-challenge.

Back 134

Fixed drug eruptions

Front 135

Mechanism explaining fixed drug eruptions?

Back 135

Mechanism unknown, although genetic susceptibility may play a role

Front 136

Drugs known the cause activation of effector pathways leading to nonimmunlogical skin reactions?

Back 136

Opiates, polymixin-B and radio contrast media

Front 137

Drugs that commonly cause fixed drug eruptions?

Back 137

Sulfonamides, tetracyclines, phenylbutazone, NSAIDs, and barbiturates

Front 138

Skin reactions marked by small groupings of shiny, polygonal papules known as Wickham’s Striae?

Back 138

Lichenoid Drug Eruptions

Front 139

Mechanism explaining lichenoid drug eruptions?

Back 139

Thought to be immunologic

Front 140

Common drug causes of lichenoid drug eruptions?

Back 140

Gold salts and antimalarials

Front 141

Skin rash marked by small pustules overlying erythematous skin that coalesce and lead to ulceration? This reaction presents with fever lesions that appear 1-3 weeks after drug exposure.

Back 141

Acute generalized exanthematous pustulosis (AGEP)

Front 142

Mechanisim explaining Acute generalized exanthematous pustulosis (AGEP)?

Back 142

Mechanism unknown

Front 143

Common drug causes of acute generalized exanthematous pustulosis (AGEP)?

Back 143

Antibiotics, lithium, glucocorticoids, and phenytoin

Front 144

Skin reaction characterized by “butterfly” rash on cheeks and nose with photosensitivity and slightly raised erythemous rash? Systemic symptoms present most of the time and 90% of cases occur in women of childbearing years.

Back 144

Systemic Lupus Erythematosus (SLE)

Front 145

Mechanism explaining SLE

Back 145

Autoimmune response

Front 146

How is drug induced SLE distinguished from idiopathic SLE?

Back 146

Drug induced most prevalent in Caucasians; idiopathic most prevalent in African-Americans.
Drug induced less prevalent in females.
Drug induced usually resolves in several weeks; idiopathic remission is rare.
No kidney or CNS problems in drug induced.

Front 147

Drug induced rash marked by blisters and epidermal detachment resulting from epidermal necrosis? This reaction usually presents with fever (above 102.2°F), sore throat and visual impairment.

Back 147

Stevens Johnson Syndrome (SJS)

Front 148

Mechanism explaining Stevens Johnson Syndrome (SJS)?

Back 148

Drug induced epidermal apoptosis

Front 149

Common drug causes of Stevens Johnson Syndrome?

Back 149

Sulfonamides, lamotrigine, aromatic anticonvulsants and -oxicam NSAIDs.
Also associated with Antiepileptic Hypersensitivity Syndrome (AHS).

Front 150

Stevens johnson syndrome with >30% detachement?

Back 150

Toxic Epidermal Necrolysis (TEN)

Front 151

Reason for recommendation of genetic testing prior to treatment with carbamazepine?

Back 151

SJS, TEN, and AHS are strongly associated with HLA-B* 1502, found almost exclusively in people of Asian decent.
Risk= one to six per 1,000 new Asian users.
HLA-B* 1502 positive patients are also at increased risk with other antiepileptic drugs.

Front 152

Most common of all drug induced skin reactions?

Back 152

Morbilliform Reactions

Front 153

Treatment for drug induced immunologic skin reactions when discontinuation does not lead to remittance?

Back 153

Systemic glucocorticoids. Severe cases may require epinephrine

Front 154

Drug induced pruritis can be treated with?

Back 154

Oral antihistamines, emollients and soothing baths

Front 155

Only cutaneous reaction where drugs are the sole cause?

Back 155

Fixed drug eruptions

Front 156

Treatment for warfarin necrosis of the skin?

Back 156

Vitamin K and heparin
Protein-C for protein-C deficient patients

Front 157

Where do the lesions occur in fixed frug eruptions?

Back 157

Lips, hand, genitalia, face and oral mucosa

Front 158

How do you distinguish phototoxicity vs.
photoallergy in photosensitivity reactions?

Back 158

Phototoxicity- nonimmunologic reaction caused by drugs or chemicals.
Photoallergy- immunologic reaction to an excited-state photosensitizer.

Front 159

Treatment for photosensitivity eruptions?

Back 159

Avoid exposure to ultraviolet light.
Use high-potency sunscreens that block UV-A light

Front 160

What are Wickham’s Striae

Back 160

Permanent white lines around the papules caused by lichenoid drug eruptions.

Front 161

Desoximetasone (Topicort)

Back 161

High potency topical steroid

Front 162

Topical steroid that appears on the high potency and very high potency list?

Back 162

Diflorasone diacetate (ApexiCon)

Front 163

Aromatic anticonvulsants most likely to cause Stevens Johnson Syndrome?

Back 163

Phenytoin, phenobarbital and carbamazepine

Front 164

Halobetasol propionate (Ultravate)?

Back 164

Very high potency topical steroid

Front 165

Difference between Stevens Johnson Syndrome and Antiepileptic Hypersensitivity Syndrome (AHS)?

Back 165

The skin does not actually peel in Antiepileptic Hypersensitivity Syndrome (AHS)

Front 166

Topical steroid that appears in the medium and high potency list?

Back 166

Triamcinolone acetonide