Module 2 2024 Final Thursday AM Sept 26.2024 Student Version (1) PDF

Module 2 Disorders of the Integumentary System Sept 25/26th 2024  Overview Time Topic Duration 10:00-10:15 Check in and Module 1 quiz review 15 min 10:15-10:40...

Module 2 Disorders of the Integumentary System Sept 25/26th 2024  Overview Time Topic Duration 10:00-10:15 Check in and Module 1 quiz review 15 min 10:15-10:40 Structure and function of the skin, Skin lesions 20 minutes 10:40-11:00 Clinical consult -Understanding Measles and the Importance of 15 minutes + 5 min Vaccination- discussion Priyantha Kodithuwak 11:05-11:25 Clinical consult- Systemic Lupus Erythematosus 15 minutes + 5 min Ravkiran Sandhu discussion 11:25-11:30 Wrap up 5 minutes 11:30-11:45 Break 11:45-12:10 Inflammatory Skin disorders, Papulosquamous, Bacterial, Viral, Fungal 25 min Lesions 15 min 12:10-12:25 Benign Tumors and Skin Cancer 12:25-12:50 Practice quiz 15 min 12:50-13:00 Wrap up 10 min 2 Module 1 Quiz 3  Textbook material Structure and Function of the Skin Layers of the Skin The skin is formed of three major layers: 1. A superficial, or outer, layer of epidermis; 1. A deeper layer of dermis (the true skin); and 1. The subcutaneous layer (hypodermis), the lowest lying layer of connective tissue that contains macrophages, fibroblasts, fat cells, nerves, fine muscles, blood vessels, lymphatics, and hair follicle roots (Fig. 46.1). Each skin layer contains cells that represent progressive stages of skin cell differentiation and function. These are summarized in Table 46.1. (next slide) FIG. 46.1 Structure of the Skin. (A) Cross section showing major skin structures 4  Function of the Skin (lecture slide) What are the 4 cells in the epidermis? Lecture video slides 6  Textbook material Layers of the Epidermis Layers of the Epidermis Each skin layer contains cells that represent progressive stages of skin cell differentiation and function. These are summarized in Table 46.1. (next slide) A, From Kumar V, et al. Robbins & Cotran pathologic basis of disease, 10th edition. Philadelphia: Saunders; 2021. B, From Gawkrodger D, Ardern-Jones M. Dermatology, 5th edition. Philadelphia: Churchill Livingstone; 2012. 7  https://www.youtube.com/watch?v=ZiB9mrfQOUs Layers of the Epidermis 7 minutes 8  https://www.youtube.com/watch?v=ZiB9mrfQOUs Layers of the Epidermis 7 minutes 9 https://www.youtube.com/watch?v=-i28L2tMQlw 10  Structure and Function of the Skin- the Dermis Dermis The dermis is 1 to 4 mm thick Composed of three types of connective tissue: (1) Collagen, (2) Elastin, and (3) Reticulin. The haphazard arrangement of connective tissue allows the skin to be mobile and to stretch and contract with body movement. Contents: Hair follicles, sebaceous glands, sweat glands, blood vessels, lymphatic vessels, and nerves. Cells 1. Fibroblasts secrete the connective tissue matrix and collagen. 2. Mast cells release histamine and play a role in hypersensitivity reactions in the skin. 3. Macrophages are phagocytic and participate in immune responses. The conelike projections of the papillary dermis interface with the epidermis. The papillae provide texture to the surface of the skin by forming rete pegs. 11 Dermis Papillary and Reticular layers Papillary layer (thin) Reticular layer (thick) Directly underneath the epidermis Tight network of connective tissue Loose network of connective (collagen, elastin, reticulin) tissue (collagen, elastin, reticulin) Contains capillaries, lymph vessels, Contains (endings of) capillaries, histocytes, sensory neurons lymph vessels, macrophages, mast (sweat glands, hair follicles, cells, sensory neurons. sebaceous glands) Fun fact: The papillary layer of the dermis is responsible for your finger print! Fun fact: Goose bumps are from the contraction of the arrector pili muscles around the hair follicles. Memory tip: Papillary layer is Loose; Reticular layer is Thick Or: Papillary is Petite and Reticular is Robust Dermis https://www.youtube.com/watch?v=-i28L2tMQlw 10 minutes 13  Hypodermis (Subcutaneous) https://www.youtube.com/watch?v=-i28L2tMQlw 14 https://www.youtube.com/watch?v=-i28L2tMQlw 15 10 minutes  Simple explanation of the dermis (but doesn’t mention 2 layers within the dermis) 13 minutes https://www.youtube.com/watch?v=Y8qbLFCjSRI https://www.youtube.com/watch?v=p4hnFf_jmvU  Learning Outcomes Describe common primary and secondary skin lesions using Primary and appropriate terminology. Secondary Skin Lesions Some material covered in the lecture video 18 Primary and Secondary Skin Lesions Disruptions of the skin integrity may be precipitated by trauma, abnormal cellular function, infection, immune responses, inflammation, and systemic diseases. Many skin disorders are benign and self-limiting, whereas others are severe and life-threatening. Secondary lesions Primary lesions Skin lesions that develop from a: 1. Change in a primary lesion (e.g., itching, Changes in your direct injury (e.g. scab from scratching the skin that are not insect bite, scar following surgical incision), associated with any or other conditions 2. Skin lesion that is part of a more complex, (e.g. sunburn, underlying condition (e.g., ulcer secondary acne, insect bite) to vascular condition)  Types of Primary and Secondary Skin Lesions Primary Lesions Secondary Lesions Macule Nodule Atrophy Lichenification Patch Tumor Erosion Scale Papule Cyst Excoriation Scar Pustule Vesicle Fissure Ulcer Plaque Wheal Keloid Telangiectasia Note: Textbook Tables 46.3 and 46.4 describe and illustrate primary and secondary lesions of the skin  Skin Lesion Quiz Name that Lesion! 12 Questions  1 Q. What is this primary skin lesion? Response options: A. Macules B. Papules C. Vesicles D. Wheals Elevated, irregular shape of cutaneous edema, solid, transient, variable diameter E. Plaques What can cause this skin lesion? F. Tumors  1 R. What is this primary skin lesion? Response options: A. Macules B. Papules C. Vesicles D. Wheals Elevated, irregular shape of cutaneous edema, solid, transient, variable diameter E. Plaques What can cause this skin lesion? F. Tumors Insect bite, Urticaria (hives), allergic reaction 2 Q. What is this primary skin lesion? Response options: A. Macule B. Papule C. Vesicle Elevated, firm, rough lesion with flat top surface, > 1mm in diameter D. Wheal What can cause this primary skin lesion? E. Plaque F. Tumor  3 Q. What is this primary skin lesion? Response options: A. Macule B. Papule C. Vesicle D. Wheal A flat, circumscribed area that is a change in the color of the E. Nodule skin; less than 1 cm in diameter F. Tumor What can cause this primary skin lesion? Primary Skin Lesions- Vascular Skin Lesions Primary Skin Lesions- Vascular Skin Lesions Telangiectasia Hemangioma  4Q. What is this primary skin lesion? Response options: An elevated, firm, circumscribed area less than 1 cm in diameter A. Macule B. Papule C. Vesicle D. Wheal E. Nodule Examples: Wart (verruca), elevated moles, lichen planus, fibroma, insect bite F. Tumor 5Q. What primary skin lesion can look like a papule, but is larger and deeper? Response options: A. Macule B. Nodule C. Tumor D. Vesicle E. Pustule  6 Q. What is this primary skin lesion? Response options: A. Macule B. Nodule C. Tumor D. Vesicle Elevated, circumscribed, superficial; does not extend into dermis; filled with serous fluid; less than 1 cm in diameter E. Pustule What conditions may cause this skin lesion? F. Bulla 7Q. What do you call a Vesicle that is more than 1 cm in diameter? Response options: A. Tumor B. Cyst C. Pustule D. Bulla E. Nodule 8Q. What do you call a lesion that is similar to a vesicle, but filled with purulent fluid? Response options: A. Tumor B. Cyst C. Pustule D. Bulla E. Nodule Primary Skin Lesion- Cyst 9Q. What is this secondary skin lesion? 9Q. What is this secondary skin lesion? Response options: A. Keloid B. Hypertrophic Scar C. Atrophy D. Fissure E Scale F. Erosion  Secondary Skin Lesions Hypertrophic Scar Keloid Thin to thick fibrous tissue that replaces normal Irregularly shaped, elevated, progressively enlarging scar; skin after injury or laceration to the dermis grows beyond boundaries of wound; caused by excessive collagen formation during healing  10 Q. What is this secondary skin lesion? Response options: Loss of part of the epidermis; depressed, moist, glistening; follows rupture of a vesicle or bulla or A. Vesicle chemical injury B. Ulcer C. Excoriation D. Scale E Erosion F. Fissure  Secondary Skin Lesions-Excoriation and Fissures Excoriation Fissure Loss of epidermis; linear, hollowed- Linear crack or break from the epidermis out, crusted area to the dermis; may be moist or dry Examples: Abrasion or scratch, scabies Examples: Athlete's foot, cracks at the corner of mouth, anal fissure, dermatitis  11 Q. What is this Secondary Skin lesion? Response options: Loss of epidermis and dermis; concave; varies in size A. Vesicle B. Ulcer C. Excoriation D. Scale E Erosion F. Fissure What are some conditions that may cause this skin lesion?  Stages of Pressure Injury Text book Stage 1: Non-blanchable erythema of intact skin usually over a bony prominence; darkly pigmented skin may appear differently; color changes do not include purple or maroon discoloration. Stage 2: Partial-thickness skin loss with exposed dermis (erosion or intact or ruptured blistering) involving epidermis or dermis presenting as a shallow open ulcer with a red-pink, viable wound bed, without slough. Deeper tissues are not visible. Stage 3: Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend to, but not through, underlying fascia. Adipose tissue visible in the ulcer, granulation tissue and rolled wound edges (epibole) are often present. Stage 4: Full-thickness skin and tissue loss with exposure of muscle, bone, or supporting structures (tendons or joint capsules); can include undermining and tunneling. 40  12 Q. What is this Secondary Skin Lesion? Response options: A. Lichenification B. Ulcer C. Excoriation D. Scale E Erosion F. Fissure Heaped-up, keratinized cells; flaky skin; irregular shape; thick or thin; dry or oily; variation in size Secondary Skin Lesion-Lichenification Rough, thickened epidermis secondary to persistent rubbing, itching, or skin irritation; often involves flexor surface of extremity Example: Chronic dermatitis Clinical Consult Vaccination Strategies Stacie Seaman- Bantin 43 Clinical Consult Systemic Lupus Erythematosus Ravkiran Sandhu 44 Break Time pm 45  Learning Explain the pathophysiological mechanisms Outcomes underlying the development of inflammatory skin disorders, including contact dermatitis and atopic dermatitis. Inflammatory Compare and contrast the clinical Disorders of manifestations of contact dermatitis and the Skin atopic dermatitis. Material covered in the lecture video 46  Which are the immune cells of the epidermis? Langerhans cells act as cellular transducers, transmitting signals encountered at the epidermal surface, including ultraviolet radiation (UVR), chemicals, cosmetics, pathogens, and medicines, as well as signals from the microenvironmental compartment in control of immune homeostasis. In disease state, Langerhans cell function can be modified by the aberrant signaling from both the environment and the microenvironment, resulting in altered immune regulation in inflammatory disorders. Clayton et al. 2017  Acute/Chronic Type I Hypersensitivity Reactions Atopic dermatitis: Chronic inflammation Relapsing and remitting Accompanied by asthma, allergies – the AAA Mediated by IgE 48 Kim et al. 2019  Inflammatory Skin Disorders Remember “AAA” – Atopic dermatitis – Allergies – Asthma – Family History one of the strongest predictors Bjerg et al. 2007  Delayed/Cell-Mediated Type IV Hypersensitivity Reactions The molecule responsible for initiating type IV hypersensitivity from poison ivy is considered a hapten. This molecule is too small to be antigenic on its own and must bind to host proteins before Can be challenging it can cause clinically to find the trigger! sensitization or activate -allergy testing hypersensitivity -elimination diet reaction upon second -fabric softener a big one! exposure 50  Learning Explain the pathophysiology of papulosquamous skin disorders, Outcomes including: Psoriasis, Papulosquamous Acne rosacea, Skin Disorders Acne vulgaris and Lichen planus. Material covered in the lecture video 51  Papulosquamous Disorders Conditions associated with A series of disorders that papulosquamous disorders: are associated with – Psoriasis development of: – Pityriasis Rosea – Papules – Lichen Planus – Scales – Acne Vulgaris – Plaques – Acne Rosacea – Erythema – Lupus Erythematosus Bolded conditions included in learning outcomes 52  Plaque Psoriasis. Plaque psoriasis is characterized by well-demarcated and erythematous plaques with silvery scale Psoriasis on the Plaque trunk, marked by psoriasis on confluent red, well- the elbow demarcated, scaly plaques Psoriasis on the dorsal foot and Psoriasis in the metatarsophala postauricular ngeal joint with area (common psoriatic nails spot) showing dystrophy Kim et al. 2017 Slide and material covered in the Lecture Video Slide and material covered in the Lecture Video Keratinocyte hyperproliferation Rapid epidermal turnover  Mapping out Psoriasis DC migration to Antigenic Trigger? lymph node DC presentation of antigen to Dendritic cell (DC) uptake of unknown antigen CD4 (MHC II) and CD8 (MHC I) DC activation resulting in T-cell activation T cells (mainly CD4) migrate to skin (epidermis) Further production of cytokines Recruitment of & chemokines Neutrophils and T cells release cytokines (mainly by T-cells & Monocytes to skin (IL-1, IFN-gamma, TNF-alpha) and Macrophages) chemokines (CCL27, CXCL14) Keratinocyte Clinical manifestations of psoriasis Chronic hyperplasia scalp, elbows, knees Inflammation ”extensor surfaces”  Based on the pathophysiology of psoriasis, what are possible treatment strategies targeting inflammation? More recently, IL-23/17 have been shown to play an important role in psoriasis, primarily involved in promoting Th17 cells to produce IL-17, leading to increased keratinocyte hyperplasia. Acne Rosacea vs Acne Vulgaris https://www.youtube.com/watch?v=ybU5SGmZbr0 Acne Rosacea 13 min https://www.youtube.com/watch?v=z8Z3z6d1v1M  No Comedones https://www.youtube.com/watch?v=z8Z3z6d1v1M Slide and material covered in the Lecture Video https://www.youtube.com/watch?v=Jm6RvAuIhEw 8 min https://www.youtube.com/watch?v=Jm6RvAuIhEw https://www.youtube.com/watch?v=9Ln11esYb48  Identify causative microorganisms of Learning common bacterial skin infections Outcomes including: Folliculitis, Bacterial Skin Cellulitis and Impetigo. Infections Describe the clinical manifestations of common bacterial skin infections. Material covered in the lecture video 65  Folliculitis Folliculitis is an inflammation of the hair follicle and is typically infectious, caused by bacteria, viruses, parasites, or fungi; S. aureus is a common culprit. Non-infectious causes include trauma or plugging of the follicle. The infection develops from proliferation of the microorganism around the opening and inside the follicle. Inflammation is caused by the release of chemotactic factors and enzymes from the bacteria. The lesions appear as papules or pustules with a surrounding area of erythema. Furuncle of the Forearm. (Courtesy Lesions are most prominent on the scalp and extremities but can occur on Department of Dermatology, University of any hair-bearing area. Prolonged skin moisture, occlusive clothing, topical Utah School of Medicine, Salt Lake City, agents, skin trauma (e.g., shaving facial hair), and poor hygiene are UT.) associated contributing factors to the development of folliculitis. Cleaning with soap and water and topical antibiotics are effective textbook 66 treatments.  Lecture slide Folliculitis 67  Cellulitis Lecture Video slide 68 Impetigo Lecture Video slide 69  Explain the pathophysiology of Learning common viral skin infections caused Outcomes by the: Varicella-zoster virus, Viral Skin Herpes simplex virus, and Infections Human papilloma virus. Describe the clinical manifestations of common viral skin infections. Varicella Zoster, Herpes Simplex covered in the Lecture Video 70 Human Papilloma Virus https://www.youtube.com/watch?v=Qn45Ekp5twE 9 min https://www.youtube.com/watch?v=Qn45Ekp5twE Learning Outcomes Explain the pathophysiology of tinea infections and candidiasis Fungal Skin Describe the clinical manifestations of Infections tinea infections and candidiasis. Material covered in the lecture video 76 Fungal Disorders of the Skin Tinea infections: fungal infections of the skin cause by dermatophytes Dermatophytes: Fungi that thrive on keratin and cause superficial lesions Candidas: fungal infection (Candida Albicans) of mucous membranes on skin, vagina, penis, or mouth C. albicans penetrates the epidermal barrier more easily than other microorganisms because of its keratolytic proteases, other enzymes, and evasion of neutrophil killing.  Fungal Infections Lecture Video Slide https://www.youtube.com/watch?v=qAjfOuTIWC I https://www.youtube.com/watch?v=qAjfOuTIWCI  Describe the relationship between benign Learning skin tumours, including actinic keratosis and Outcomes nevi, and skin cancers.. Compare and contrast basal cell carcinoma, squamous cell carcinoma and melanoma Benign based on underlying pathophysiology and Tumours and clinical manifestations. Skin Cancer Discuss the role of ultraviolet radiation in skin cancer. Material covered in the lecture video 81 Melanocyte Activity- Moles and Freckles  Actinic Keratosis Symptoms, Treatment, and Causes High risk of developing into squamous cell carcinoma https://www.youtube.com/watch?v=ffcHWDpKZqQ 2 min https://www.youtube.com/watch?v=8g3qlIZ5BuY 6 minutes  Lecture Video Slide The term "in situ" added on the end tells us that this is a surface form of skin cancer. SCC in situ is also known as Bowen's disease after the doctor who first described it almost 100 years ago. SCC in situ is usually a red, scaly patch.“ Invasive" squamous cell carcinomas are the type that grow inward and may spread. Lecture Video Slide Lecture Video Slide Lecture Video Slide Lecture Video Slide Lecture Video Slide Lecture Video Slide Lecture Slide Blacks tend to be diagnosed later in the disease and thus can have poorer outcomes  Cancer Development Over Time https://www.youtube.com/wat ch?v=qyTws_GbSps Time last video of the 3 lesions 1 minute 93 https://www.youtube.com/watch?v=YWppfk2Np6A https://www.youtube.com/watch?v=YWppfk2Np6A https://www.youtube.com/watch?v=YWppfk2Np6A Supplementary information https://www.youtube.com/watch?v=MwgrgsLXBsQ Practice Questions- Module 2  Wrap up- Thurs am Lecture These slides are intended to be an additional Video Slide resource to support your learning- supplemental information that extends beyond your learning objectives and not part of test material. Module 2 test – opens Thursday, Sept 26th afternoon and closes by 5 pm October 9th Clinical consults October 10th