The two layers of the skin consist of the epidermis and dermis. The epidermis is the uppermost part of the skin, which we can see all over our bodies. The epidermis and dermis are composed of their own layers, which we will discuss in a bit. Below the dermis is the hypodermis, which consists of adipose tissue. Below the hypodermis is the subcutaneous layer, which is the location site for many of our injectable drugs, such as insulin. Between the layers there are many hair follicles, which make up the pilosebaceous unit, consisting of hair, sebaceous gland, apocrine and eccrine sweat glands, and the arrector pili muscle. The pilosebaceous unit is particularly important in thermoregulation and electrolyte homeostasis - sweat glands function to release NaCl and H2O from the body, producing a cooling effect and maintaining electrolyte balance.
Before we get into the functions of the skin, I will go back and summarize the various layers in the epidermis and dermis. The epidermis is composed of 5 or 6 layers, depending on the type of skin. These layers include (from bottom up): Stratum basale, spinosum, granulosum, lucidem (only on thick skin - soles of feet, palms of hands), and the stratum corneum. These sit on the basement membrane, which connects the dermis to the epidermis. The stratum basale consists of merkel cells and cuboidal cells. The stratum spinosum contains melanocytes, responsible for color of the skin, and langerhans cells, which are antigen-presenting cells involved in the immune response. The stratum corneum, the uppermost layer, is also the thickest layer of the skin.
The dermis is made up of many types of cells: fibroblasts, which make up the extracellular matrix, including collagen, mast cells, sensory nerve fibers, and capillaries. The dermis is the area of the skin containing the nerves and blood supply for the skin. Different sensations which are felt on the skin are pressure, pain, and temperature.
The functions of the skin are as follows: 1)protection/barrier for the underlying tissues, 2)wound healing, 3)vitamin D synthesis, 4)sensation, 5)thermoregulation, and 6)secretion. The skin acts as a barrier for bacteria (by secreting its own antimicrobials), UV light, and injury. The skin is extremely efficient at wound healing, as evidenced by the quick healing of superficial cuts and scrapes. Vitamin D synthesis occurs when the sun causes the conversion of 7-dehydrocholesterol to cholecalciferol and eventually into active vitamin d, which is crucial in the regulation of calcium. The skin also detects sensations, as mentioned above, pain, temperature, and pressure. The skin also secretes sweat, antimicrobials, and sebum. Sweat helps to regulate temperature, antimicrobials help to prevent bacterial infection on the skin, and sebum acts as a lubricant and fat secretor.
Pharmacologically, the skin conditions which are included in NAPLEX prep are: acne, cold sores, dandruff, alopecia, eczema, hyperhidrosis, fungal infections, diaper rash, hemorrhoids, pinworm, lice/scabies, minor wounds, burns, poison ivy/oak/sumac, inflammation/rash, and sunscreens. I will be delving deeper into these subjects individually throughout the duration of this APPE rotation. Please refer to this GoogleDoc Folder for all NAPLEX review of skin:
https://drive.google.com/drive/folders/1fS5RbT9WIJHUFy1TrVuWnd4XeQHT7LOT?usp=sharing
Drug-induced rashes are among the most common dermatologic adverse reactions encountered in both inpatient and outpatient settings. While the majority of these rashes are benign and self-limited, some can serve as early signs of more serious hypersensitivity reactions, making prompt recognition and evaluation critical. Cutaneous drug reactions account for approximately 2% to 3% of all adverse drug events and can range from simple morbilliform eruptions to serious immune-mediated conditions such as urticaria, vasculitis, or early manifestations of Stevens-Johnson Syndrome (SJS) or Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS).
The most commonly implicated drug classes include antibiotics (like penicillins, sulfonamides, and cephalosporins), anticonvulsants, NSAIDs, and allopurinol. Morbilliform (maculopapular) eruptions are the most frequent presentation and typically occur 7 to 14 days after drug initiation, often beginning on the trunk and spreading symmetrically. These are generally self-limiting and resolve within days to weeks after discontinuing the offending agent. In contrast, urticarial drug reactions present more acutely with raised, pruritic wheals and are often IgE-mediated. They can be associated with systemic anaphylaxis, particularly when accompanied by angioedema or respiratory compromise.
As pharmacists, we must be able to differentiate between benign cutaneous reactions and early signs of severe hypersensitivity syndromes. Rash characteristics, onset of symptoms, distribution, and associated symptoms (fever, mucosal involvement, lymphadenopathy, eosinophilia) are essential clues. For example, a symmetric maculopapular rash without systemic symptoms may only warrant discontinuation and symptomatic management, whereas a similar rash accompanied by systemic findings should prompt consideration of DRESS or other serious reactions.
In clinical practice, pharmacists contribute significantly to medication safety by assisting in differential diagnosis, identifying the most likely causative agent and guiding appropriate drug discontinuation and allergy documentation. In outpatient settings, pharmacists can educate patients on when to seek medical attention and help differentiate transient, mild rashes from those requiring urgent evaluation. In inpatient care, pharmacists can assist providers in assessing the need for alternative therapies, antihistamines, corticosteroids, or further diagnostic work-up, including dermatology referral if indicated.
Bigby M. Rates of cutaneous reactions to drugs. Arch Dermatol. 2001;137(6):765–770. doi:10.1001/archderm.137.6.765
Romano A, Atanaskovic-Markovic M, Barbaud A, et al. Towards a more precise diagnosis of hypersensitivity to beta-lactams. Clin Exp Allergy. 2020;50(8):805–826. doi:10.1111/cea.13688
Husain Z, Reddy BY, Schwartz RA. Drug-induced urticaria: an update. Am J Clin Dermatol. 2013;14(5):383–395. doi:10.1007/s40257-013-0034-6
Cho YT, Yang CW, Chu CY. Drug reaction with eosinophilia and systemic symptoms (DRESS): an interplay among drugs, viruses, and immune system. Int J Mol Sci. 2017;18(6):1243. doi:10.3390/ijms18061243
Ariza A, Torres MJ, Fernandez J, et al. Diagnosis of immediate allergic reactions to NSAIDs. Clin Exp Allergy. 2011;41(1):1–11. doi:10.1111/j.1365-2222.2010.03638