WorksheetsPharmacology Week 4 Part 2
Total questions: 50
Worksheet time: 25mins
The adult epinephrine auto-injector dose is typically:
0.3 mg for patients ≥30 kg
0.15 mg for patients ≥30 kg
1 mg for any adult
0.01 mg/kg for any adult
Proper counseling for epinephrine auto-injector use includes:
Inject into the deltoid
Inject into the anterolateral thigh
Delay until symptoms fully progress
Carry one injector only
After using an epinephrine auto-injector, the patient should be advised to:
Avoid emergency care if symptoms resolve
Seek emergency medical care
Start ketoconazole
Apply topical clobetasol
If anaphylaxis symptoms persist, repeat epinephrine dosing is recommended:
Every 1–2 hours
Every 5–15 minutes
Once daily
Only after 24 hours
Angioedema is characterized by:
Localized swelling with increased vascular permeability and vasodilation
Painless petechiae from thrombocytopenia
Follicular pustules with fever
Chronic scaling plaques only
Common drug causes of angioedema include:
Macrolides and tetracyclines
ACE inhibitors and ARBs
SSRIs and benzodiazepines
Loop diuretics only
ACE inhibitor or ARB angioedema is best described mechanistically as:
IgE-mediated classic allergy
Anaphylactoid reaction, not IgE-mediated
Type I hypersensitivity confirmed by skin testing in most cases
COX-1 inhibition driven
A key management nuance after stopping an ACE inhibitor due to angioedema is:
Start sacubitril/valsartan immediately
Wait 36 hours before starting sacubitril/valsartan
Wait 12 hours before starting sacubitril/valsartan
Never restart any antihypertensive
Angioedema assessment priorities include:
Only checking temperature
Airway involvement and facial/oropharyngeal swelling
Skin biopsy first
Platelet function assay
A patient develops flushing during a rapid vancomycin infusion. Best interpretation and management?
IgE-mediated allergy, give epinephrine only
Vancomycin flushing syndrome from histamine release, slow infusion
Stevens-Johnson syndrome, discontinue and start methotrexate
COX-1 reaction, add aspirin
Vancomycin flushing syndrome (Red Man Syndrome) is:
A true IgE-mediated allergy
Not an allergic reaction and due to histamine release from rapid infusion
Caused by beta-lactam cross-reactivity
Prevented only with ketoconazole
Penicillins and cephalosporins share:
A common beta-lactam ring
A sulfonamide group
A steroid nucleus
A calcineurin inhibitor backbone
Structural difference noted between the beta-lactam rings is:
Penicillins have a 6-member ring, cephalosporins a 5-member ring
Penicillins have a 5-member ring, cephalosporins a 6-member ring
Both have identical 7-member rings
Neither contains a ring
Cross-reactivity between penicillins and cephalosporins is primarily related to:
Similarities in R1 and R2 side chains
Similarities in gastric pH
CYP enzyme inhibition
COX-1 inhibition
Penicillin allergy is best described as:
Rarely reported
Frequently overreported and about 90% are not true IgE-mediated
Always lifelong and IgE-mediated
Confirmed by symptoms alone without testing
Penicillin skin testing:
Detects presence of IgE
Detects leukotriene overproduction
Detects CYP inhibition capacity
Is positive in almost all adults after 10 years
Regarding penicillin allergy over time:
Reactivity increases with time
Reactivity declines; fewer than 20% remain positive after 10 years
Reactivity stays constant for life
Reactivity disappears within 24 hours in all patients
Sulfonamides typically cause:
Immediate IgE-mediated reactions only
Delayed hypersensitivity reactions
Vancomycin flushing syndrome
Mineralocorticoid excess
Cross-reactivity between antibiotic and non-antibiotic sulfonamides is:
High due to identical metabolism
Low due to structural and metabolic differences
Guaranteed in all patients
Impossible to assess clinically
Best general management for a suspected true drug allergy is:
Continue the agent and add a moisturizer
Discontinue the offending agent
Switch to a higher dose of the same drug
Only use H2 blockers
NSAID and aspirin reactions are often:
IgE-mediated and confirmed by skin testing
Not IgE-mediated and related to COX-1 inhibition with increased leukotrienes
Caused by beta-lactam rings
Due to adrenal insufficiency
Atopic dermatitis is best described as:
Acute bacterial skin infection
Chronic inflammatory skin disease with pruritus as hallmark
Autoimmune blistering disorder
A condition defined by absence of itching
The atopic triad includes:
Atopic dermatitis, allergic rhinitis, asthma
Psoriasis, asthma, urticaria
Contact dermatitis, COPD, eczema herpeticum
Acne, allergic rhinitis, urticaria
First-line pharmacologic therapy for atopic dermatitis is:
Topical corticosteroids
Oral methotrexate
Ketoconazole
Biologic response modifiers
Second-line therapy for atopic dermatitis includes:
Topical calcineurin inhibitors
Oral acitretin
Apremilast
IV ketoconazole
First-line therapy for contact dermatitis is:
Vitamin D analogs
Topical corticosteroids
TNF-alpha inhibitors
Systemic ketoconazole
Systemic corticosteroids are used for contact dermatitis when:
Any facial rash is present
Greater than 20% body surface area is involved
It is mild and localized
Only if there is fever
First-line options for mild to moderate psoriasis include all EXCEPT:
Topical corticosteroids
Vitamin D analogs
Retinoids
Oral ketoconazole
Which moisturizer type reduces transepidermal water loss and is most effective for atopic dermatitis?
Emollients
Humectants
Occlusives
Retinoids
Humectants:
Increase water-holding capacity and may sting on open skin
Are the most occlusive topical form
Smooth skin surface and are most effective moisturizers
Cause skin atrophy
Emollients are best described as:
Increase water-holding capacity the most
Smooth skin surface and are least effective moisturizers
Reduce transepidermal water loss the most
Must be avoided in atopic dermatitis
Which topical formulation is most occlusive?
Lotion
Cream
Ointment
Gel
Which formulation is least occlusive?
Ointment
Cream
Lotion
Paste
Topical corticosteroids are:
Second-line agents for most inflammatory dermatoses
First-line agents with risk of skin atrophy
Only used systemically
Contraindicated in all psoriasis
Choosing topical steroid potency should consider:
Hair color
Age, area, and severity
ABO blood type
Serum sodium
Which topical potency match is correct?
Hydrocortisone 0.25–1% is very high potency
Triamcinolone 0.1% is medium potency
Clobetasol 0.05% is lowest potency
Triamcinolone 0.5% is lowest potency
Which topical steroid listed is very high potency?
Hydrocortisone 1%
Triamcinolone 0.1%
Triamcinolone 0.5%
Clobetasol 0.05%
Topical calcineurin inhibitors are advantageous because they:
Commonly cause skin atrophy
Do not cause skin atrophy and are suitable for face and skin folds
Are first-line for severe anaphylaxis
Require weekly LFT monitoring
A major warning associated with topical calcineurin inhibitors is:
Nephrolithiasis
Lymphoma and skin malignancy
Tendon rupture
Aortic dissection
A common adverse effect with topical calcineurin inhibitors is:
Profound hypotension
Transient burning sensation
Cushingoid facies after 2 days
Severe hepatotoxicity
Psoriasis severity using the Hand Rule: 1% BSA is approximately:
The patient's forearm
The patient's palm
The patient's head and neck
Both legs
Mild psoriasis is defined as:
Under 3% BSA
3–10% BSA
Over 10% BSA
Exactly 10% BSA
Moderate psoriasis is defined as:
Under 3% BSA
3–10% BSA
Over 10% BSA
Over 20% BSA
Severe psoriasis is defined as:
Over 10% BSA
3–10% BSA
Under 3% BSA
Over 1% BSA only
For mild to moderate psoriasis, topical steroids are considered:
Not recommended
Gold standard
Only adjuncts after biologics
Reserved for pregnancy only
For Class 1 (highest potency) topical steroids, recommended limit of continuous use is:
2–4 weeks
2–4 months
10–12 weeks
No limit
After failure of topical calcineurin inhibitors in psoriasis, the next step discussed is:
Immediate TNF-alpha inhibitor
Phototherapy
Ketoconazole
Hydrocortisone replacement
Which sequence reflects the stepwise escalation for psoriasis treatment?
Biologics → systemic → phototherapy → topicals
Topicals → phototherapy → systemic → biologics
Phototherapy → topicals → biologics → systemic
Systemic → topicals → phototherapy → biologics
Calcipotriene is best characterized by:
Rapid onset with severe atrophy
Slower onset with mild irritation
Contraindicated in all adults
Requires weekly LFT monitoring
Tazarotene is:
Safe in pregnancy
Contraindicated in pregnancy
A TNF-alpha inhibitor
Used only for anaphylaxis adjunct therapy
