Applied Pathophysiology- Test 1 2023 with 2023 with 100% correct questions and answers

Acute Short term; Fast on set Chronic Long term; Slow on set Compensatory Mechanism Physiological response to homeostatic imbalance (Positive or negative feedback mechanism) Congenital Born with Etiology Cause of disease Homeostasis Body natural balance Iatrogenic Unintended affect of treatment Idiopathic Unknown cause of disease Manifestation Signs and symptoms Pathophysiology Development and evolution of disease Predisposing Factors Factors that increase risk of developing a disease Prevetion Trying to keep from occurring Signs Objective (What you observe) Symptoms Subjective (What patient tells you) Syndrome Group of signs and symptoms Active Transport Sodium-potassium pump Facilitated Transport Insulin transporting glucose into cells Osmosis Keeping cells hydrated Diffusion Gas exchange in the lungs Endocytosis Phagocytosis Exocytosis Hormone secreting gland Hypertrophy Increase in the size of cells to meet increased work demand Dysplasia Cells mutate into cells of different size, shape, and appearance; precancerous Metaplasia One adult cell is replaced by another cell type because of chronic irritation & inflammation Atrophy Decrease in the size of cells to conserve energy and resources Hyperplasia Increase in the number of cells usually because of normal stimuli Hypoxia Lack of sufficient oxygen. Most common cause of cell death Ischemia Reduced blood supply. Most common cause of hypoxia Necrosis Cell death from injury. Ischemia is most common cause Benign VS Malignant 1. Benign are slow and malignant are fast growing. 2. Begin DO resemble host and malignant DO NOT 3. Begin DO NOT usually cause death and malignant DO CAUTION C-Change in bowel movement/ bladder habits A-A sore that doesn't't heal U-Unusual bleeding or discharge T-Thickening or lump in breast or elsewhere I-Indigestion or difficulty swallowing O-Obvious change in wart or mole N-Nagging cough or hoarseness Tay-Sach's Disease early onset in life parent of Jewish descent death occurs by age 5 years Neurofibromatosis delayed onset of disease café au lait spots scoliosis Down Syndrome Risk increases with mother's age simian crease, upward slant of eyes increased risk of leukemia Klinefelter's Syndrome XXYsmall penis &testes; gynecomastia increased risk of breast cancer Cleft lip & Cleft palate condition obvious at birth feeding and speech issues increased risk if mom smokes or has diabetes Marfan Syndrome Abraham Lincoln appearance aortic aneurysm & lens displacement late onset Fragile X syndrome Autism spectrum large ears & long narrow face large testes if dad has disease, all daughters are carriers Turner's Syndromes X drooping eyelids & webbed neckgonadal streaks causing infertility Phenylketonuria (PKU) normal at birth but fails to meet milestones screened with heel stick around day 3 enzyme deficiency for phenylalanine Innate Defenses (1st line) Nonspecific- works against any antigen the same way (Reaction is the same regardless of the cause) Distinguishes self from non-self Does NOT distinguish between pathogens (parasite looks same as splinter) Includes: Skin and mucous membranes Chemicals Innate defenses (2nd line) Responds to antigens that penetrate the first line Includes: Inflammatory Response Pyrogens Interferons Complement proteins Inflammatory Responce Vascular reaction- blood response Triggered by mast cells- type of white blood cell (granulocyte) secrete histamine Manifestations include erythema-redness, edema-swelling, and warmth, heat and pain fever and increased wbc count Pyrogens Fever producing molecules Produced and released by macrophages travel to hypothalamus Interferons Proteins released from virus, parasite, and bacteria infected cells Attach to uninfected cells to prevent replication Complement Proteins Blood plasma proteins that enhance antibodies' action Activated by antigens Adaptive Defenses (3rd line) Specific; Develops over time; Uses memory system; Able to recognize antigens Distinguishes self from non-self AND between pathogens Includes: T cells (cell mediated immunity)- cell does work B cells (humoral immunity)- rally troops Work sheet Know all Autoimmune disorders Immune system looses the ability to recognize self Immunodeficiency Diminished or absent immune response General Adaptation Syndrome 1. Alarm 2. Resistance 3. Exhaustion Alarm Initial reaction Sympathetic nervous system Resistance Adaptation (pos or neg) Limit stressor Exhaustion Adaptation failing / coping methods utilized Disease develops (Depression, heart disease, insomnia, anxiety ) Function of Integumentary system 1.Protects the body from pathogen invasions 2.Regulates temperature 3.Senses environmental changes 4.Maintains water balance Contact Dermatitis Acute inflammatory reaction triggered by direct exposure to an irritant or allergen-producing substance Not contagious or life threatening Varies in severity depending on the substance, area affected, exposure extent, and individual sensitivity Usually resolves in 2-4 weeks 2 types: Irritant & Allergic Treatment: identify and remove the causative agent, wet compresses, anti-inflammatory creams (e.g., corticosteroid agents), and systemic anti-inflammatory agents Irritant contact dermatitis Causes: chemicals, acids, and soaps Does not involve the immune system, but triggers the inflammatory response Produces a reaction similar to a burn Manifestations: erythema, edema, pain, pruritus, and vesicles Allergic contact dermatitis Causes: metals, chemicals, cosmetics, and plants. Sensitization occurs on the first exposure, and subsequent exposures produce a type IV cell-mediated hypersensitivity. Manifestations appear 24-48 hours after exposure. Manifestations: same as irritant Atopic Dermatitis (Eczema) Chronic inflammatory condition triggered by an allergen Has an inherited tendency May be accompanied by asthma and allergic rhinitis Most common in infants and usually resolves by early adulthood May affect any area, but typically arms & behind the knees Characterized by remissions and exacerbations Exact cause unknown, but may result from an immune system malfunction Manifestations Red to brownish-gray colored skin patches Pruritus, which may be severe, especially at night Vesicles Thickened (lichenified), cracked, or scaly skin Irritated, sensitive skin from scratching Avoid factors that can worsen: Long, hot baths or showers Stress Sweating Cigarette smoke Certain foods (e.g., eggs, milk, fish, soy, and wheat) Urticaria Raised erythematous skin lesions (welts) Result of a type I hypersensitivity reaction often triggered by food (e.g., shellfish and nuts) and medicine (e.g., antibiotics) May also be a result of emotional stress, excessive perspiration, diseases (e.g., autoimmune conditions and leukemia), and infections (e.g., mononucleosis) Occurs when histamine release is initiated by these substances or conditions Usually short-lived and harmless. Can impair breathing if around the face and progress to anaphylaxis and shock. Manifestations: welts that blanch and pruritus. Treatment: antihistamines, epinephrine, corticosteroids, and maintain respiratory status Psoriasis Common chronic inflammatory condition that affects skin cell life cycle. Cellular proliferation is significantly increased, causing cells to build up too rapidly on the skin's surface. Normally takes weeks, but occurs over 3-4 days with psoriasis. Buildup leads to thickening of the dermis and epidermis because dead cells cannot shed fast enough. The exact cause is unknown, but it is thought to be multifactorial (environmental, genetic, and immunological factors play a role). It can also be a result of an autoimmune process in which T lymphocytes mistake normal skin cells as foreign. A family tendency is observed. Onset is most frequently between 15 and 35 years of age, and may be sudden or gradual. Patient usually experiences remissions and exacerbations. Factors that trigger an exacerbation: bacteria or viral infections, dry air or dry skin, skin injuries, stress, too little or too much sunlight, and excessive alcohol consumption. most often occurs on the elbows, knees, and trunk, No cure Treatment includes topical treatments & sunlight therapy & stress management Bacterial Can be caused by any of the normal flora bacteria. Varies from mild to life-threatening. Staphylococcus and Streptococcus genera are common culprits. Once causative agent identified, treat with antibiotics Examples: Folliculitis Furuncles Impetigo Cellulitis Necrotizing fasciitis Folliculitis Involving the hair follicles Characterized by tender, swollen areas that form around hair follicles, often on the neck, breasts, buttocks, and face Furuncles Also known as boils Begin in the hair follicles and then spread into the surrounding dermis. Most commonly occur on the face, neck, axillae, groin, buttocks, and back. Start as a firm, red, painful nodule that develops into a large, painful mass, which frequently drains large amounts of purulent exudate. Impetigo Common and highly contagious (children 2-5yr) Typically arises from a break in the skin. Lesions usually begin as small vesicles that enlarge and rupture, forming the characteristic honey-colored crust. Can spread throughout the body through self-transfer of the exudate. Spreads to others through direct contact with skin or contaminated objects (towels, clothing, toys) Typically caused by staphylococci, which produce a toxin that attacks collagen and promotes spread. Other manifestations: pruritus and lymphadenopathy. Cellulitis Occurs deep in the dermis and subcutaneous tissue Usually results from a direct invasion of pathogens through a break in the skin, especially those breaches where contamination is likely, or spreads from an existing skin infection Appears as a swollen, warm, tender area of erythema Systemic manifestations: indicators of infection (e.g., fever, leukocytosis, malaise, and arthralgia) Complications: necrotizing fasciitis, septicemia, and septic shock Necrotizing Fasciitis Rare, serious infection, but rates are rising. Typically results from a highly virulent strain of gram-positive, group A, beta-hemolytic Streptococcus that invades through a minor cut or scrape. The bacteria release harmful toxins that directly destroy the tissue, disrupt blood flow, and break down the tissue The first sign may be a small, reddish, painful area that quickly evolves into a painful bronze- or purple-colored patch. The center of the lesion may become black and necrotic; exudate The wound may grow in less than an hour. Systemic manifestations: fever, tachycardia, hypotension, and confusion. Complications: gangrene and shock. Vial Examples: Herpes Simplex I (cold sore) Herpes Zoster (shingles) Verrucae (warts) Herpes Simplex I (cold sore) Typically affects the lips, mouth, and face. Usually begins in childhood. Transmitted by contact with infected saliva. The primary infection may be asymptomatic. After the primary infection, the virus remains dormant in the sensory nerve ganglion to the trigeminal nerve until it is reactivated. Reactivation may be a result of an infection, stress, or sun exposure. When reactivated, causes painful blisters or ulcerations that are preceded by a burning or tingling sensation. The lesions resolve spontaneously within 3 weeks, but healing can be accelerated with administration of oral or topical antiviral agents. Herpes Zoster (shingles) Caused by the varicella-zoster virus. Appears in adulthood years after a primary infection of varicella in childhood. The virus lies dormant on a cranial nerve or a spinal nerve dermatome until it is activated years later. The virus affects this nerve only, giving the condition its typical unilateral manifestations. Manifestations: pain, paresthesia, a red or silvery vesicular rash that develops in a line over the area innervated by the affected nerve, extremely sensitive skin, and pruritic. The rash may persist for weeks to months. Complications: neuralgia and blindness. Treatment: antivirals, antidepressants, and anticonvulsants. Vaccines are available to prevent both varicella and herpes zoster infections. Verrucae (warts) Caused by a number of human papillomaviruses. Can develop at any age and often resolve spontaneously. Transmitted through direct skin contact between people or within the same person. The human papillomavirus replicates in the skin cells, causing irregular thickening. Varying color, shape, and texture depending on type Treatment: laser treatments, cryotherapy with liquid nitrogen, topical antiviral medications, *liver tablets May return after treatment Parasitic Examples Tinea (fungal) Scabies (mites) Pediculosis (lice) Tinea (fungal) Causes several types of superficial fungal infections. These fungi typically grow in warm, moist places (e.g., showers). Typically manifests as a circular, erythematous rash accompanied by pruritus and burning. Tinea capitis: involving the scalp. Common in school-aged children. Hair loss at the site is common. Tinea corporis: involving the body Tinea pedis: involving the feet, especially the toes (athlete's foot) Tinea unguium: involving the nails, typically the toenails Turns nail white and then brown, causing them to thicken and crack Treatment: topical and systemic antifungal agents Scabies (mites) Result of a microscopic human itch mite infestation. Male mites fertilize the females and then die. Female mites burrow into the epidermis, laying eggs over a period of several weeks through a series of tracts. Then the female mites die. Larvae hatch from the eggs and migrate to the skin's surface and burrow in search of nutrients and mature to repeat the cycle. Burrowing appears as small, light brown streaks on the skin. Burrowing and fecal matter left by the mites triggers the inflammatory process, leading to erythema and pruritus. See pink pimples or blisters Mites can only survive for short periods without a host, so transmission usually results from close contact. Treatment: topical treatments multiple times. Not contagious 24 hours post treatment. Pediculosis (lice) Lice infestation: small, brown insects that feed off human blood and cannot survive long without host. Pediculus humanus corpus: body louse. Pediculus pubic: pubic louse. Pediculus humanus capitis: head louse. Females lay nits on the hair shaft close to the scalp. Nits appear as small, white, iridescent shells on the hair. After hatching, the lice bite and suck the host's blood. Bite site develops a highly pruritic macule or papule. Easily transmitted through close contact. Treatment: several topical treatments. Types of Skin Cancer Basal cell carcinoma Most common Develops from abnormal growth of the cells in the lowest layer of the epidermis Rarely metastasizes Squamous cell carcinoma Involves changes in the squamous cells, found in the middle layer of the epidermis Melanoma Develops in the melanocytes Least common type but the most serious Often metastasizes to other areas Skin Cancer Early detection is crucial to positive outcomes. Suspicious features: Asymmetry Border irregularity Color variations Diameter larger than 6 mm Evolving Any skin growth that bleeds or will not heal Any skin growth that changes in appearance over time Diagnosis: history, physical examination, and biopsy. Prevention: limiting or avoiding exposure to UV light. Burns First-degree burns Second-degree burns Third-degree burns: First-degree burns Affect only the epidermis and cause pain, erythema, and edema Second-degree burns Affect the epidermis and dermis and cause pain, erythema, edema, and blistering Third-degree burns Extend into deeper tissues and cause white or blackened, charred skin that may be numb