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WorksheetsPharmacology Week 4 Part 1
Total questions: 50
Worksheet time: 25mins
In anaphylaxis, which epinephrine action most directly reverses capillary leak and edema?
Beta-2 mediated bronchodilation
Beta-1 increased contractility
Alpha-adrenergic vasoconstriction
H2 receptor blockade
Which epinephrine effect most directly improves hypotension in anaphylaxis?
Alpha-adrenergic vasoconstriction
Beta-2 decreased mediator release
Beta-1 increased heart rate
H2 decreased gastric acid
A patient in anaphylaxis has severe bronchospasm. Which receptor action of epinephrine best addresses this?
Alpha-1
Beta-2
Beta-1
H2
In anaphylaxis, epinephrine decreases mediator release primarily by acting on:
Beta-2 receptors
Alpha receptors
Beta-1 receptors
H2 receptors
Which set of anaphylaxis problems is directly counteracted by epinephrine’s combined alpha and beta effects?
Fever, rash, arthralgia
Hypotension, bronchospasm, mucosal edema
Bradycardia, constipation, urinary retention
Hyperglycemia, leukocytosis, osteoporosis
Histamine is best described as:
Synthesized from tyrosine and stored in platelets
Stored in mast cells and basophils and released in hypersensitivity reactions
Released only during bacterial infections
Produced by hydroxylation of tryptophan
Histamine is produced via:
Decarboxylation of histidine
Hydroxylation of phenylalanine
Methylation of lysine
Transamination of tyrosine
H1 receptors are located in all EXCEPT:
Bronchioles
Blood vessels
Intestinal smooth muscle
Sensory nerves
A patient develops wheal and flare with itching after allergen exposure. This is most consistent with activation of:
H1 receptors
H2 receptors
M3 receptors
Beta-1 receptors
Which is a classic manifestation of H1 activation?
Increased gastric acid secretion
Bronchoconstriction
Marked sustained tachyarrhythmia
Profound decrease in cardiac contractility
H1 antihistamines work by:
Preventing histamine synthesis
Inhibiting histamine release from mast cells
Competitively blocking H1 receptors
Irreversibly antagonizing H1 receptors
Which statement about H1 antihistamines is correct?
They prevent mast cell degranulation directly
They do not inhibit histamine release
They increase capillary permeability
They primarily reduce gastric acid secretion
First-generation H1 antihistamines cause more sedation because they:
Have minimal lipid solubility
Do not cross the blood brain barrier
Have high lipid solubility and cross the blood brain barrier
Selectively bind only peripheral H1 receptors
A patient taking a first-generation H1 antihistamine reports dry mouth and urinary retention. These effects are due to:
Alpha-adrenergic agonism
Anticholinergic adverse effects
H2 receptor blockade
Beta-2 agonism
Which adverse effect is most associated with first-generation H1 antihistamines?
Nephrotoxicity
Skin atrophy
Constipation
Weekly LFT monitoring requirement
Second-generation H1 antihistamines are less sedating primarily because they:
Increase CNS penetration
Lower lipid solubility with minimal CNS penetration
Are irreversible antagonists
Also block H2 receptors strongly
H2 receptors are located primarily on:
Bronchiolar smooth muscle
Gastric parietal cells
Sensory nerves
Vascular endothelium only
The main clinical effect of H2 activation is:
Bronchodilation
Increased gastric acid secretion
Decreased capillary permeability
Increased mucus viscosity
H2 receptor antagonists:
Increase gastric acid secretion
Reduce gastric acid secretion and increase gastric pH
Cause significant bronchodilation
Are first-line monotherapy for anaphylaxis
In anaphylaxis, H2 blockers are used primarily to:
Replace epinephrine
Reduce histamine effects in the GI tract and vasculature
Provide immediate relief of bronchospasm
Prevent IgE formation
Glucocorticoids are:
Peptide hormones from the pituitary
Steroid hormones produced by the adrenal cortex
Synthesized in the thyroid
Only exogenous medications
The primary endogenous glucocorticoid is:
Aldosterone
Cortisol (hydrocortisone)
Epinephrine
Fludrocortisone
A major mechanism of glucocorticoids is:
Direct DNA degradation
Regulation of gene transcription
Competitive inhibition of IgE
Opening calcium channels in mast cells
Which is a key anti-inflammatory action of glucocorticoids?
Increased capillary permeability
Increased cytokine production
Inhibition of leukocyte migration
Increased mediator release from basophils
Glucocorticoids reduce inflammation in part by:
Stabilizing lysosomal membranes
Increasing histamine synthesis
Increasing leukocyte adhesion to endothelium
Increasing prostaglandin production
Which metabolic effect is expected with systemic glucocorticoids?
Decreased gluconeogenesis
Increased gluconeogenesis
Increased bone formation
Decreased protein catabolism
Glucocorticoids can cause all EXCEPT:
Lipolysis
Protein catabolism
Increased gluconeogenesis
Increased aldosterone synthesis
A core general prescribing principle for glucocorticoids is:
Highest dose for longest duration
Lowest effective dose for shortest effective duration
Use only at night
Avoid switching agents because equivalence is irrelevant
Adverse effects of glucocorticoids are best described as:
Unrelated to dose or duration
Dose- and duration-dependent
Only dependent on route, not duration
Only immediate and never delayed
When switching systemic corticosteroids, the prescriber must account for:
Histamine receptor selectivity
Dose equivalence
COX-1 inhibition
Beta-lactam cross-reactivity
Which dose equivalence is correct (anti-inflammatory potency)?
Hydrocortisone 20 mg ≈ Prednisone 20 mg
Prednisone 5 mg ≈ Hydrocortisone 20 mg
Dexamethasone 5 mg ≈ Hydrocortisone 20 mg
Methylprednisolone 20 mg ≈ Prednisone 0.75 mg
Which equivalence pairing is correct?
Methylprednisolone 4 mg ≈ Prednisone 5 mg
Triamcinolone 40 mg ≈ Hydrocortisone 20 mg
Betamethasone 4 mg ≈ Hydrocortisone 20 mg
Prednisone 0.75 mg ≈ Hydrocortisone 20 mg
Dexamethasone and betamethasone are characterized by:
Low anti-inflammatory potency and high mineralocorticoid activity
About 25 times hydrocortisone potency with zero mineralocorticoid activity
Strong mineralocorticoid activity with minimal glucocorticoid effect
Equivalent potency to prednisone and strong mineralocorticoid activity
Fludrocortisone is best described as:
Extremely high anti-inflammatory potency
Minimal to no anti-inflammatory activity with very high mineralocorticoid activity
Zero mineralocorticoid activity with high anti-inflammatory effect
A first-line drug for acute anaphylaxis
Which special population concern is correctly matched?
Pediatrics: cataracts and growth suppression
Diabetes: hypoglycemia
Osteoporosis: decreased fracture risk
Immunocompromised: decreased infection risk
Which adverse effect is a known risk of systemic glucocorticoids?
Leukopenia
HPA axis suppression
Bradycardia
Renal tubular acidosis
Which adverse effect pair is most consistent with glucocorticoid therapy?
Hyperglycemia and osteoporosis
Hyponatremia and thrombocytopenia
Severe ototoxicity and nephrolithiasis
Photosensitivity and tendon rupture
Anaphylaxis is best defined as:
Localized rash without systemic involvement
Acute, life-threatening, multi-organ reaction
Chronic inflammatory skin disease
Delayed hypersensitivity reaction only
Which symptom is part of the clinical presentation of anaphylaxis?
Dysphonia (hoarseness)
Chronic lichenification only
Isolated acneiform eruption
Purpura without pruritus
GI symptoms that may occur in anaphylaxis include:
Constipation only
Nausea, vomiting, diarrhea
Hematemesis only
Painless jaundice
First-line pharmacologic treatment for anaphylaxis is:
IV methylprednisolone
IM epinephrine
Oral famotidine
Inhaled albuterol alone
Adult IM epinephrine dosing for anaphylaxis is:
0.03–0.05 mg IM
0.3–0.5 mg IM
3–5 mg IM
0.01 mg/kg IM
Pediatric IM epinephrine dosing for anaphylaxis is best stated as:
0.1–0.3 mg regardless of weight
0.01 mg/kg IM, typically 0.1–0.3 mg
1 mg/kg IM
0.3–0.5 mg IM
Which is an immediate priority in anaphylaxis management?
IV glucocorticoids for immediate relief
Epinephrine and airway management
Start biologic therapy
Topical corticosteroids
If hypotension persists during anaphylaxis despite epinephrine, the next immediate supportive step is:
IV fluids
Oral antihistamine only
Methotrexate
Stop all moisturizers
Anaphylaxis adjunctive therapy for bronchospasm includes:
Inhaled beta-2 agonist (albuterol)
H2 blocker only
Topical calcineurin inhibitor
Ketoconazole
Which adjunctive medication is NOT effective for immediate relief of anaphylaxis symptoms but may reduce biphasic reactions?
IM epinephrine
IV methylprednisolone
Oxygen
IV fluids
Which statement is correct regarding adjuncts in anaphylaxis?
Antihistamines replace epinephrine if symptoms improve
Adjunctive therapies do not replace epinephrine
Steroids are first-line because onset is fastest
H2 blockers are the only necessary medication
EpiPen Jr delivers:
0.3 mg epinephrine
0.15 mg epinephrine
0.01 mg/kg epinephrine
1 mg epinephrine
EpiPen Jr is indicated for patients:
Under 10 kg
Under 30 kg
At least 30 kg
Over 60 kg
