Chapter 4 Skin and Body Membranes Body Membranes Functions of body membranes Cover body surfaces Line body cavities Form protective sheets around organs Classified according to tissue types Body Membranes Two major categories Epithelial membranes Cutaneous membranes Mucous membranes Serous membranes Connective tissue membranes Synovial membranes Epithelial Membranes Epithelial membranes are simple organs Also called covering and lining membranes These membranes contain both: Epithelial tissue layer Connective tissue layer Epithelial Membranes Cutaneous membrane = skin Dry membrane Outermost protective boundary Consists of two layers Epidermis is composed of keratinized stratified squamous epithelium Dermis is mostly dense (fibrous) connective tissue Epithelial Membranes • Mucous membranes (mucosae) • I Moist membranes Some mucosae secrete protective, lubricating mucus Line all body cavities that open to the exterior body surface • Adapted for absorption or secretion • ' Consists of two layers • Epithelium type depends on site • Loose connective tissue (lamina propria) Epithelial Membranes Serous membranes (serosae) Line compartments in the ventral body cavity that are ciosed to the exterior of the body Occur in pairs, separated by serous fluid, with a visceral and parietal layer Consists of two layers Simple squamous epithelium Areolar connective tissue Epithelial Membranes Specific serous membranes Peritoneum Cover organs in the abdominal cavity Pleurae Surround the lungs Pericardia Surround the heart Connective Tissue Membranes Synovial membranes Loose areolar connective tissue only (no epithelial tissue) Line fibrous capsules surrounding joints Line bursae Line tendon sheaths Secrete a lubricating fluid to cushion organs moving against each other during muscle activity Integumentary System Integumentary system consists of the: Skin (cutaneous membrane) Skin appendages Sweat glands Oil glands Hair Nails Functions of the Integumentary System Insulates and cushion deeper body organs Protects the entire body from: Mechanical damage (bumps and cuts) Chemical damage (acids and bases) Thermal damage (heat or cold) Ultraviolet (UV) radiation (sunlight) Microbes (bacteria) • Water loss Functions of the Integumentary System Regulates heat loss as controlled by the nervous system Acts as a mini-excretory system; sweat aids in the loss of Urea Salts Water Synthesizes vitamin D Secretions create a protective acid mantle Structure of the Skin Two kinds of tissue compose the skin Epidermis Dermis Subcutaneous tissue (hypodermis) Anchors the skin to underlying organs Not technically part of the integumentary system Composed mostly of adipose tissue Serves as a shock absorber and insulates deeper tissues Structure of the Skin Epidermisouter layer Composed of stratified squamous epithelium Most cells are keratinocytes which produce a fibrous protein called keratin Keratinization makes the epidermis tough Desmosomes connect keratinocytes together Avascular Composed of five layers (strata) Structure of the Skin Summary of strata (layers) of the epidermis from deepest to most superficial Stratum basale Stratum spinosum Stratum granulosum Stratum lucidum (thick, hairless skin only) Stratum corneum Structure of the Skin Stratum basale (stratum germinativum) Deepest layer of epidermis Lies next to dermis Wavy borderline with the dermis anchors the two together Cells undergoing mitosis Daughter cells are pushed upward to become the more superficial layers Stratum spinosum Cells become increasingly flatter and more keratinized Structure of the Skin Stratum granulosum Stratum lucidum Formed from dead cells of the deeper strata Occurs only in thick, hairless skin of the palms of hands and soles of feet Stratum corneum Outermost layer of epidermis Shingle-like dead cells are filled with keratin (protective protein prevents wat loss from skin Structure of the Skin Melanin Melanin is a pigment produced by melanocytes Melanocytes are mostly in the stratum basale of the epidermis Color is yellow to brown to black Structure of the Skin Epidermal dendritic cells Alert and activate immune cells to a threat (bacterial or viral invasion) Merkel cells Associated with sensory nerve endings Serve as touch receptors called Merkel discs Structure of the Skin Dermis Connective tissue Underlies the epidermis Two regions Papillary Reticular Structure of the Skin Two regions of the dermis Papillary layer (upper dermal region) contain projections called dermal papillae Areolar connective tissue Indent the epidermis above Many projections contain capillary loops, and others house pain and touch receptors On palm and sole surfaces, papillae increase friction and gripping ability Fingerprints are identifying films of sweat Structure of the Skin Two regions of the dermis Reticular layer (deepest skin layer) Dense irregular connective tissue Blood vessels Sweat and oil glands Deep pressure receptors (lamellar corpuscles) Structure of the Skin Other dermal features Cutaneous sensory receptors Phagocytes Collagen and elastic fibers Blood vessels I Nerve supply Skin Color • Three pigments contribute to skin color 1. Melanin • Yellow, reddish brown, or black pigments 2. Carotene • Orange-yellow pigment (also found in some vegetables) 3. Hemoglobin Red coloring from blood cells in dermal capillaries Oxygen content determines the extent of red coloring Skin Color Redness (erythema) due to embarrassment, inflammation, hypertension, fever, or allergy Pallor (blanching) due to emotional stress (such as fear), anemia, low blood pressure, impaired blood flow to an area Jaundice (yellow cast)-indicates a liver disorder • Bruises (black and blue marks)-hematomas Appendages of the Skin Cutaneous glands are all exocrine glands Sebaceous glands Sweat glands Hair and hair follicles Nails Appendages of the Skin Sebaceous (oil) glands Located all over the skin except for palms and soles Produce sebum (oil) Makes skin soft and moist Prevents hair from becoming brittle Kills bacteria Most have ducts that empty into hair follicles; others open directly onto skin surface Glands are activated at puberty with increased androgens Appendages of the Skin Sweat (sudoriferous) glands Produce sweat Widely distributed in skin Two types of sudoriferous glands Eccrine glands Apocrine glands Appendages of the Skin Eccrine glands More numerous, located all over the body Open via duct to sweat pores on the skin's surface Produce acidic sweat Water, salts, vitamin C, traces of metabolic waste Function in body temperature regulation Appendages of the Skin Apocrine glands Ducts empty into hair follicles in the armpit and genitals Begin to function at puberty Release sweat that also contains fatty acids and proteins (milky or yellowish color) • Play a minimal role in body temperature regulation Appendages of the Skin Hair Located body-wide except for palms, soles, nipples, lips Produced by hair follicle Root is enclosed in the follicle Shaft projects from the surface of the scalp or skin Consists of hard keratinized epithelial cells Melanocytes provide pigment for hair color Hair grows in the matrix of the hair bulb in stratum basale Appendages of the Skin Hair anatomy Central medulla Cortex surrounds medulla Cuticle on outside of cortex Most heavily keratinized region of the hair Melanin provides color Appendages of the Skin Associated hair structures Hair follicle Composed of an inner epithelial root sheath andan outer fibrous sheath Dermal region provides a blood supply to the hair bulb (deepest part of the follicle) Arrector pili muscle connects to the hair follicle to pull hairs upright when we are cold or frightened Appendages of the Skin Nails Heavily keratinized, scalelike modifications of the epidermis Stratum basale extends beneath the nail bed, which is responsible for growth Lack of pigment makes nails colorless Appendages of the Skin Parts of a nail Free edge Body is the visible attached portion Nail folds are skin folds that overlap the edges of the nail; the cuticle is the proximal edge Root of nail is embedded in skin Growth of the nail occurs from nail matrix of nail bed Homeostatic Imbalances of Skin Infections and allergies Athlete's foot Caused by fungal infection (Tinea pedis) Itchy, red peeling skin between the toes Boils (furuncles) and carbuncles Caused by inflammation of hair follicles Carbuncles are clusters of boils caused by bacteria Cold sores (fever blisters) Caused by human herpesvirus 1 Blisters itch and sting Homeostatic Imbalances of Skin Infections and allergies Contact dermatitis Caused by exposure to chemicals that provoke allergic responses Itching, redness, and swelling of the skin Impetigo Caused by bacterial infection Pink, fluid-filled raised lesions around mouth/nose Psoriasis Triggered by trauma, infection, hormonal changes, or stress Red, epidermal lesions covered with dry, silvery scales that itch, burn, Crack, or sometimes bleed Homeostatic Imbalances of Skin • Burns Tissue damage and cell death caused by heat, electricity, UV radiation, or chemicals Associated dangers Protein denaturation and cell death Dehydration and electrolyte imbalance Circulatory shock Result in loss of body fluids and infection from the invasion of bacteria Homeostatic Imbalances of Skin Extent of a burn is estimated using the rule of nines Body is divided into 11 areas for quick estimation Each area represents about 9 percent of total body surface area The area surrounding the genitals (the perineum) represents 1 percent of body surface area Homeostatic Imbalances of Skin . First-degree burn (superficial burn) Only epidermis is damaged Skin is red and swollen Second-degree burn (superficial partial-thickness burn) Epidermis and superficial part of dermis are damaged Skin is red, painful, and blistered Regrowth of the epithelium can occur Homeostatic Imbalances of Skin Third-degree burn (full-thickness burn) Destroys epidermis and dermis; burned area is painless Requires skin grafts, as regeneration is not possible Burned area is blanched (gray-white) or black Fourth-degree burn (full-thickness burn) Extends into deeper tissues (bone, muscle, tendons) Appears dry and leathery Requires surgery and grafting May require amputation Homeostatic Imbalances of Skin Criteria for deeming burns critical (if any one is met): Over 30 percent of body has second-degree burns Over 10 percent of the body has third-or fourth-degree burns Third-or fourth-degree burns of the face, hands, feet, or genitals Burns affect the airways Circumferential (around the body or limb) burns have occurred Homeostatic Imbalances of Skin Skin cancer Most common form of cancer in humans Most important risk factor is overexposure to ultraviolet (V) radiation in sunlight and tanning beds Cancer can be classified two ways Benign means the neoplasm (tumor) has not spread Malignant means the neoplasm has invaded other body areas Concept Link Recall that mitosis gone wild is the basis for cancer (Chapter 3, pp. 82-83). These cells lack normal control of cell division and divide quickly, resulting in errors during DNA replication, mitosis, or both. Cells experiencing rapid, uncontrolled growth become cancerous and can metastasize (spread) to other parts of the body. Homeostatic Imbalances of Skin . First-degree burn (superficial burn) Only epidermis is damaged Skin is red and swollen Second-degree burn (superficial partial-thickness burn) Epidermis and superficial part of dermis are damaged Skin is red, painful, and blistered Regrowth of the epithelium can occur Homeostatic Imbalances of Skin Third-degree burn (full-thickness burn) Destroys epidermis and dermis; burned area is painless Requires skin grafts, as regeneration is not possible Burned area is blanched (gray-white) or black Fourth-degree burn (full-thickness burn) Extends into deeper tissues (bone, muscle, tendons) Appears dry and leathery Requires surgery and grafting May require amputation Homeostatic Imbalances of Skin Criteria for deeming burns critical (if any one is met): Over 30 percent of body has second-degree burns Over 10 percent of the body has third-or fourth-degree burns Third-or fourth-degree burns of the face, hands, feet, or genitals Burns affect the airways Circumferential (around the body or limb) burns have occurred Homeostatic Imbalances of Skin Skin cancer Most common form of cancer in humans Most important risk factor is overexposure to ultraviolet (V) radiation in sunlight and tanning beds Cancer can be classified two ways Benign means the neoplasm (tumor) has not spread Malignant means the neoplasm has invaded other body areas Concept Link Recall that mitosis gone wild is the basis for cancer (Chapter 3, pp. 82-83). These cells lack normal control of cell division and divide quickly, resulting in errors during DNA • One or more of the ABCD characteristics is evolving Developmental Aspects of Skin and Body Membranes Lanugo, a downy hair, covers the body by the fifth or sixth month of fetal development but disappears by birth Vernix caseosa, an oily covering, is apparent at birth Milia, small white spots, are common at birth and disappear by the third week Acne may appear during adolescence Pimples, scales, and dermatitis are more common with aging skin Developmental Aspects of Skin and Body Membranes In youth, skin is thick, resilient, and well hydrated With aging, skin loses elasticity and thins Skin cancer is a major threat to skin exposed to excessive sunlight Balding (alopecia) and/or graying occurs with aging; both are genetically determined other factors that may contribute include drugs and emotional stress

Pearson | A&P - Erin C. Amerman 3rd Edition: Chapter 20 Practice Test

MI 263- Fluoro Part 1- Anatomy (erin) & pathology

ehrn to or not to use an article

Ehri's Phase of Word Reading

Study Guide Module 2 MODULE 2 STUDY GUIDE The Integumentary System ⸻ CHAPTER 1: OVERVIEW OF THE INTEGUMENTARY SYSTEM Components of the Integumentary System The integumentary system consists of: * Skin * Hair * Nails * Sweat glands * Sebaceous glands The skin is the largest organ in the body. Functions of the Integumentary System 1. Protection 2. Sensation 3. Thermoregulation 4. Vitamin D synthesis 5. Communication ⸻ CHAPTER 2: LAYERS OF THE SKIN The skin has two major layers: Epidermis * Superficial layer * Keratinized stratified squamous epithelium * Avascular Dermis * Deeper layer * Connective tissue * Contains blood vessels, nerves, glands, and hair follicles Hypodermis * Not technically part of the skin * Also called subcutaneous layer * Contains adipose tissue Functions: * Energy storage * Cushioning * Insulation * Anchoring skin ⸻ CHAPTER 3: EPIDERMIS Cell Types Keratinocytes * Most abundant cells * Produce keratin Melanocytes * Produce melanin * Protect against UV radiation Tactile (Merkel) Cells * Touch receptors Dendritic Cells * Immune defense * Phagocytize pathogens ⸻ EPIDERMAL LAYERS Deep → Superficial Stratum Basale * Deepest layer * Single layer of cuboidal cells * Contains stem cells * Contains melanocytes * Contains tactile cells * Site of mitosis Stratum Spinosum * 8–10 layers thick * Contains dendritic cells * Connected by desmosomes Stratum Granulosum * 3–5 layers * Keratinization begins * Cells flatten * Organelles begin breaking down Stratum Lucidum * Only in thick skin * Palms and soles * Dead transparent cells Stratum Corneum * 15–30 layers * Dead keratinized cells * Protection from abrasion * Prevents dehydration ⸻ THICK VS THIN SKIN Thick Skin Found on: * Palms * Soles Contains: * Stratum lucidum Thin Skin Found everywhere else Does not contain: * Stratum lucidum ⸻ EPIDERMAL WATER BARRIER Located between: * Stratum spinosum * Stratum granulosum Functions: * Waterproofing * Prevents dehydration * Prevents excess water entry Components: 1. Filaggrin 2. Lamellar proteins 3. Lamellar lipids 4. Tight junction proteins ⸻ CHAPTER 4: DERMIS Made of connective tissue. Papillary Layer Contains: * Areolar connective tissue * Dermal papillae * Capillaries * Tactile corpuscles (Meissner corpuscles) Function: * Light touch sensation Reticular Layer Contains: * Dense irregular connective tissue * Hair follicles * Sweat glands * Sebaceous glands * Arrector pili muscles * Lamellated (Pacinian) corpuscles Function: * Deep pressure * Vibration sensation ⸻ DERMAL FIBERS Collagen Provides: * Strength * Support * Water retention Elastin Provides: * Elasticity * Stretching ability ⸻ CHAPTER 5: PIGMENTATION Melanin Produced by: * Melanocytes Functions: * Skin color * UV protection Effects of UV Exposure UV stimulates: * Keratinocytes * Melanocytes Result: * Increased melanin production * Tanning ⸻ Disorders of Pigmentation Albinism Cause: * Lack of melanin production Effects: * Pale skin * Light sensitivity * Increased skin cancer risk Vitiligo Cause: * Loss of melanocyte activity Effects: * White patches on skin ⸻ CHAPTER 6: FUNCTIONS OF THE SKIN Protection Protects against: * Microorganisms * Chemicals * UV radiation * Water loss * Physical trauma Dermicidin: * Antimicrobial substance in sweat ⸻ Sensory Function Skin detects: * Touch * Pain * Temperature * Pressure * Vibration Receptors Meissner Corpuscles * Light touch Pacinian Corpuscles * Deep pressure * Vibration Tactile Cells * Touch Hair Root Plexus * Detects hair movement ⸻ Thermoregulation When Body Is Hot Blood vessels: * Dilate Sweat glands: * Increase secretion Result: * Cooling When Body Is Cold Blood vessels: * Constrict Result: * Conserves heat Can lead to: * Frostbite ⸻ Vitamin D Synthesis UV exposure stimulates vitamin D production. Vitamin D helps: * Calcium absorption * Bone health * Immune function Deficiency causes: Rickets Children Osteomalacia Adults ⸻ Communication Examples: * Facial expressions * Goosebumps * Sweating * Hair patterns ⸻ CHAPTER 7: HAIR Hair Structure Hair Shaft Visible portion Hair Root Embedded portion Hair Follicle Surrounds root Hair Bulb Growth region Hair Matrix Mitotic cells Hair Papilla Blood supply ⸻ Hair Layers 1. Medulla 2. Cortex 3. Cuticle ⸻ Hair Functions * Protection * Thermoregulation * Sensation * Communication ⸻ Hair Growth Average: * 0.3 mm/day Normal loss: * About 50 hairs/day ⸻ Hair Color Determined by: * Melanin Gray hair: * Reduced melanin production ⸻ Arrector Pili Muscle Functions: * Causes goosebumps * Helps retain heat Controlled by: * Sympathetic nervous system ⸻ Alopecia Definition: * Hair loss Pattern baldness: * Hormonal and genetic ⸻ CHAPTER 8: NAILS Functions: * Protection * Support for grasping Structures: * Nail body * Nail root * Nail matrix * Nail bed * Lunula * Cuticle (eponychium) * Hyponychium ⸻ CHAPTER 9: GLANDS Eccrine Sweat Glands Location: * Most of body Functions: * Thermoregulation Secrete: * Water * Salt * Waste products ⸻ Apocrine Sweat Glands Location: * Armpits * Genital regions Characteristics: * Empty into hair follicles * Produce odor after bacterial breakdown ⸻ Sebaceous Glands Produce: * Sebum Functions: * Lubricates skin * Waterproofs skin * Prevents drying * Antibacterial effects ⸻ CHAPTER 10: SKIN CANCER Basal Cell Carcinoma Origin: * Stratum basale Characteristics: * Most common * Least likely to metastasize ⸻ Squamous Cell Carcinoma Origin: * Stratum spinosum Characteristics: * More aggressive * Can metastasize ⸻ Melanoma Origin: * Melanocytes Characteristics: * Most deadly * Highly metastatic ABCDE Rule A = Asymmetry B = Border irregularity C = Color variation D = Diameter > 6 mm E = Evolving ⸻ CHAPTER 11: SKIN DISORDERS Eczema Symptoms: * Dry skin * Itching * Rash * Inflammation Treatment: * Moisturizers * Corticosteroids ⸻ Acne Cause: * Excess sebum * Keratin buildup * Bacterial infection Common locations: * Face * Chest * Back ⸻ CHAPTER 12: WOUND HEALING Steps: 1. Clot Formation Stops bleeding 2. Scab Formation 3. Fibroblast Activity Produces collagen 4. Capillary Growth 5. Epidermal Repair ⸻ CHAPTER 13: BURNS First-Degree Burn Damage: * Epidermis only Symptoms: * Redness * Pain ⸻ Second-Degree Burn Damage: * Epidermis + part of dermis Symptoms: * Blisters * Swelling * Pain ⸻ Third-Degree Burn Damage: * Epidermis * Dermis * Hypodermis Characteristics: * Nerve destruction * Often painless initially * Requires grafting ⸻ Rule of Nines Head and neck = 9% Each arm = 9% Each leg = 18% Trunk = 36% Genitalia = 1% ⸻ CHAPTER 14: SCARS Scar Tissue Produced by: * Fibroblasts Contains: * Collagen Lacks: * Hair follicles * Sweat glands * Sebaceous glands ⸻ Keloid Raised scar due to excessive collagen Atrophic Scar Sunken scar Examples: * Acne scars * Chickenpox scars ⸻ CHAPTER 15: PRESSURE AND FRICTION INJURIES Bedsores Cause: * Prolonged pressure Result: * Reduced blood flow * Tissue death ⸻ Stretch Marks Cause: * Rapid growth * Pregnancy * Weight gain ⸻ Calluses Cause: * Repeated friction Result: * Thickened epidermis ⸻ Corns Specialized calluses ⸻ Blisters Cause: * Friction Result: * Fluid accumulation between skin layers ⸻ CHAPTER 16: AGING AND THE INTEGUMENTARY SYSTEM Changes: Epidermis * Thinner * Slower cell division Dermis * Less collagen * Less elastin * Slower healing Hypodermis * Fat redistribution * Less cushioning Hair * Thinner * Grayer Nails * Slower growth * More brittle Glands * Less sweat * Less sebum Skin * Wrinkles * Sagging * Dryness ⸻ HIGH-YIELD EXAM FACTS Epidermal Layers Basale → Spinosum → Granulosum → Lucidum → Corneum Touch Receptors * Meissner = Light touch * Pacinian = Pressure/Vibration Pigment Cell * Melanocyte Immune Cell * Dendritic Cell Touch Cell * Merkel (Tactile) Cell Cancer Origins * Basal Cell Carcinoma = Stratum Basale * Squamous Cell Carcinoma = Stratum Spinosum * Melanoma = Melanocytes Sweat Glands * Eccrine = Cooling * Apocrine = Odor Burn Depths * 1st = Epidermis * 2nd = Epidermis + Dermis * 3rd = Epidermis + Dermis + Hypodermis Vitamin D Deficiency * Rickets * Osteomalacia This should cover essentially all of the major concepts from the four readings and is the type of material most likely to appear on a Module 2 Anatomy & Physiology exam

1. Cell Transport Brownian Movement Definition: Random movement of particles caused by their inherent kinetic energy. Occurs above freezing temperatures. Passive process (requires no energy/ATP). Responsible for constant molecular motion. Diffusion Definition: Movement of molecules or ions from an area of higher concentration to lower concentration. Passive transport Moves down the concentration gradient No energy required Facilitated Diffusion Definition: Diffusion through a selectively permeable membrane using membrane proteins. Passive transport High → Low concentration Only certain substances can pass Filtration Definition: Movement of water and dissolved substances through a membrane from higher pressure to lower pressure. Driven by pressure differences Dialysis Definition: Separation of small molecules from larger molecules. Used in dialysis machines Not a normal transport process in the body 2. Active Transport Active Transport Definition: Transport requiring cellular energy (ATP). Endocytosis ("Into the Cell") Phagocytosis Cell Eating Engulfs solid particles Example: White blood cells engulfing bacteria Pinocytosis Cell Drinking Engulfs fluids Exocytosis Definition: Movement of substances out of the cell. 3. Epithelial Tissue Characteristics Covers body surfaces Lines organs and cavities Cells are tightly packed High mitotic rate Connected to connective tissue by a basement membrane Classification by Shape Shape Name Flat Squamous Cube-shaped Cuboidal Tall/elongated Columnar Classification by Layers Layers Name One layer Simple Two or more layers Stratified Example: Simple Columnar Epithelium = One layer of elongated cells 4. Connective Tissue Components Connective tissue contains: Cells Fibers Ground substance Fibers + Ground Substance = Matrix Loose Connective Tissue Areolar Tissue Supports organs Widely spaced fibers Adipose Tissue Fat tissue Insulation Energy storage Reticular Tissue Found in lymph nodes and spleen Acts as a filtering framework Dense Connective Tissue Dense Regular Fibers run in one direction Found in: Tendons Ligaments Aponeuroses Dense Irregular Fibers run in multiple directions Found in: Dermis of skin Elastic Connective Tissue Allows stretching Found in: Walls of arteries Elastic structures 5. Cartilage Hyaline Cartilage Found in: Articular cartilage (joint surfaces) Costal cartilage (ribs) Fibrocartilage Strongest cartilage Found in: Intervertebral discs Pubic symphysis Meniscus of knee Elastic Cartilage Provides flexibility Found in: External ear 6. Skin (Integumentary System) Epidermal Cells Keratinocytes Produce keratin Waterproofing protein Melanocytes Produce melanin Protect from UV radiation Langerhans Cells Immune defense Fight infection Merkel Cells Touch receptors 7. Layers of the Epidermis Deepest → Most Superficial Stratum Basale Stratum Spinosum Stratum Granulosum Stratum Lucidum (only thick skin) Stratum Corneum Thick Skin Found on: Palms Soles Contains: Stratum Lucidum Dead Layers Stratum Lucidum Stratum Corneum Filled with keratin. 8. Skin Glands Sudoriferous Glands Sweat glands Eccrine glands Apocrine glands Sebaceous Glands Produce sebum (oil) Ceruminous Glands Produce earwax Mammary Glands Modified sweat glands Produce milk 9. Skeletal System Upper Extremity Humerus Arm bone Radius Lateral forearm bone Thumb side Ulna Medial forearm bone Forms elbow joint Carpals Wrist bones 8 bones Metacarpals Hand bones Phalanges Finger bones Thumb: 2 phalanges Other fingers: 3 phalanges Pelvis Ilium Superior portion Pubis Anterior portion Ischium Posterior/inferior portion "Sit bones" Lower Extremity Femur Thigh bone Tibia Shin bone Medial Fibula Lateral lower leg bone Tarsals Ankle bones Metatarsals Foot bones Phalanges Toe bones Big toe: 2 phalanges Other toes: 3 phalanges High-Yield Exam Questions 1. What is Brownian movement? Random movement of particles caused by kinetic energy. 2. Does diffusion require energy? No. It is passive transport. 3. Difference between diffusion and facilitated diffusion? Facilitated diffusion requires a selectively permeable membrane protein. 4. What is phagocytosis? Cell eating (engulfing solids). 5. What is pinocytosis? Cell drinking (engulfing fluids). 6. Which epithelial tissue has one layer of column-shaped cells? Simple columnar epithelium. 7. What is the matrix of connective tissue? Fibers + ground substance. 8. Which cartilage is found in intervertebral discs? Fibrocartilage. 9. Which epidermal cells produce melanin? Melanocytes. 10. What are the five epidermal layers? Basale → Spinosum → Granulosum → Lucidum → Corneum. 11. Which bone is on the thumb side of the forearm? Radius. 12. Which bone forms the shin? Tibia. 13. What are the wrist bones called? Carpals. 14. What are the ankle bones called? Tarsals. 15. What are the hand and foot bones called? Metacarpals and Metatarsals. Quick Memorization Tips Pino = Sip → Pinocytosis = cell drinking Phago = Eat → Phagocytosis = cell eating Radius = Radio to Thumb → Radius is lateral Simple = One Layer Stratified = Many Layers Melanocytes = Melanin Keratinocytes = Keratin Sebaceous = Sebum (Oil) Sudoriferous = Sweat Carpals = Wrist Tarsals = Ankle This covers the major concepts your instructor specifically reviewed for the exam

Epains

class commands-Erin Duffy

class commands- Erin Duffy

ephidrine

Question 1: Methodology and Logical Deduction A researcher identifies a specific epiRIL (Epigenetic Recombinant Inbred Line) of Arabidopsis that exhibits significantly delayed flowering compared to the wild-type parent, despite being genetically identical at the DNA sequence level. • Task: Outline how you would use bisulfite sequencing to identify the molecular cause of this phenotype. • Logic Challenge: If the sequencing reveals a Differentially Methylated Region (DMR) in the promoter of the FWA gene, but the DNA sequence itself matches the wild-type, what does this suggest about the stability of the trait over eight generations of selfing?

BIO 114- Plant Identification Images: Elphin Forest

Erin- Professional Practice Final

S8 EPIN U4 TEORÍA DE LA UNIDAD

NeuroLab Ephys Exam

NURS 348 — EXAM 4 STUDY GUIDE Hypertension Definition & Overview • Persistent elevation of BP ≥130/80 mmHg (systolic at/greater than 130 OR diastolic at/greater than 80) on at least 2 separate visits, 2+ weeks apart. • Primary (Essential): No identifiable cause, most common (90–95% of cases). • Secondary: Caused by another condition or adverse effects of medications. Etiology/Pathophysiology • ↑ Peripheral resistance and/or ↑ cardiac output → ↑ blood pressure → When blood vessels get narrower (increased resistance) or the heart pumps more forcefully (increased output), pressure inside the vessels rises “like squeezing a hose while water is running” → Over time, this high pressure damages the vessel walls and heart muscle, increasing the risk for atherosclerosis, heart attack (myocardial infarction), and stroke. • ↑ Increased peripheral resistance (arteriolar constriction) → ↑ afterload → left ventricular hypertrophy → heart failure → The heart pushes against more resistance (afterload), making the heart muscle thicker (hypertrophy). Over time, it becomes weaker and can lead to heart failure. • Kidneys retain sodium and water → ↑ circulating volume → The kidneys hold onto extra salt and water, adding more fluid to the blood. More fluid means higher pressure—like overfilling a water balloon. • Activation of renin–angiotensin–aldosterone system (RAAS) = vasoconstriction + fluid retention. RAAS is like the “blood pressure booster” → When this system turns on, blood vessels tighten and the kidneys save even more salt and water, both of which raise blood pressure. Risk Factors: • Primary: family history, ↑ sodium intake, Obesity (BMI >25), African-American ethnicity, smoking, hyperlipidemia, diabetes mellitus, and stress. • Secondary: kidney disease, Cushing’s, pregnancy, pheochromocytoma, medic (steroids, OCPs). Clinical Manifestations (S/S) • Often asymptomatic (“silent killer”)!!! • Headache, dizziness, fainting, vision changes • Retinal damage on exam (cotton wool spots, papilledema). • Note: if blood pressure reading is elevated then take in both arms; pt legs uncrossed, and arms above heart; correct cuff Diagnostics (Dx)/Labs • Multiple BP readings (both arms, sitting and standing) • ECG → Left-Ventricular hypertrophy. evaluates cardiac function. • Labs → ↑ BUN/creatinine (kidney disease), lipids, glucose, cortisol (Cushing’s) Nursing Care / Nursing Interventions • Monitor pt BP regularly and accurately, check both arms/correct cuff • Put on DASH diet (Dietary Approach to Stop Hypertension) Medications • ⭐️Diuretics (first-line): excess fluids, they need to remove; increase urine • Thiazides (hydrochlorothiazide) inhibits water & sodium reabsorption and increases potassium excretion • Side effects/SE: hypokalemia; monitor potassium(K⁺) levels • Loop (furosemide) decreases sodium reabsorption & increase potassium excretion– SE: hypokalemia; monitor potassium(K⁺) levels • Potassium-sparing (spironolactone) – SE: hyperkalemia; monitor potassium levels. EKG: peaked T waves • Also watch out for muscle weakness, irregular, pulse, and dehydration. • ⭐️Calcium channel blockers (verapamil, amlodipine, and diltiazem) Calcium channel blockers relax and widen blood vessels by preventing calcium from entering muscle cells, leading to lower blood pressure (vasodilation) • SE: constipation; take fiber for verapamil, and all can ↓HR • Avoid grapefruit juice ➡️ toxicity, hypotensive effects Calcium= contract • ⭐️ACE inhibitors (lisinopril, enalapril): prevents angiotensin II → vasodilation • SE: - hypotension; monitor BP and pulse HR -hyperkalemia; monitor potassium levels -erectile dysfunction -⭐️cough linked to angioedema (swollen tissue under the skin around lips, tongue, and glottis); report swelling & discontinue med • ⭐️ARBs (valsartan, losartan): for ACE-intolerant pts from cough/hyperkalemia. ARBs lower blood pressure by blocking angiotensin II from binding to its receptors, preventing vasoconstriction, and reducing fluid retention. • SE: angioedema, heart failure, hyperkalemia • Change position, slowly, report, angioedema, edema, and avoid foods that are high in potassium (bananas, potatoes, apricots, spinach, beans); monitor potassium levels • Aldosterone-receptor antagonists (eplerenone, spironolactone): blocks aldosterone action. • SE: kidney damage, hypertriglyceridemia, hyponatremia, and hyperkalemia; monitor kidney function, triglycerides, sodium, and potassium levels • Avoid Grapefruit juice and St. John’s wort, salt substitutes, and potassium rich foods • ⭐️Beta blockers (metoprolol, atenolol): blocks beta receptors (adrenaline/epinephrine) ➡️reduces heart rate, cardiac output, and blood pressure ↓HR, ↓CO; use cautiously in diabetics • SE: -⭐️erectile dysfunction, -Fatigue, weakness, depression -hypoglycemia • Monitor heart rate (hold if HR is less than 60) and do not suddenly stop taking med (cause rebound hypertension); and don’t give to pts with asthma, airway disease (cause bronchospasms) • Central Alpha-2 agonists (clonidine): calm the nerves that raise blood pressure, letting blood vessels, relax, and BP go down, ↓SNS tone • SE: sedation, orthostatic, hypotension, and sexual dysfunction/impotence • Monitor BP and pulse • Alpha-adrenergic blockers (prazosin, doxazosin): vasodilator= relaxed BP; give at night to avoid first-dose hypotension. Start with low dose. • SE: postural hypotension; make sure patient rises slowly and caution. • Monitor BP 2 hrs after initiation Complications • Hypertensive Crisis: usually when patients do not follow the medication regimen • BP >180/120 → organ damage (encephalopathy, renal failure) • S/S: severe headache, dizziness, blurred vision, confusion, epistaxis • Treat: IV antihypertensives (nitroprusside, nicardipine, labetalol); the goal is to lower BP gradually by 20-25% in first hour. Not less than 140/90. Monitor BP every 5-15 mins Patient Education • Adhere to medication regimen, don’t abruptly stop even when you feel better • Change positions slowly • Encourage DASH diet (low sodium, high fruits/veggies, low-fat dairy) ex: grilled salmon, brown rice, steamed broccoli, and low-fat milk • Avoid high-sodium foods. Consume less than 2.3 g/day • Monitor BP at home • Report signs or symptoms of electrolyte imbalances • Encourage Weight loss, exercise 3x weekly • Encourage Smoking cessation • Encourage Limit alcohol (≤2/day men, ≤1/day women) • Manage stress • Report persistent cough or swelling (ACE inhibitor red flag) Peripheral Venous Disorders(PVD) Patho: problems with veins where Deoxygenated blood can't get back to the heart Oxygenated blood pools in the extremities. The valves are preventing backflow. • Venous Thromboembolism (VTE): blood clot that starts in a vein. -Two types: deep vein thrombosis (DVT) and pulmonary embolism (PE) • Venous insufficiency: Improper functioning of the veins. Veins aren’t able to push back blood to the heart which results in swelling, venous stasis ulcers, or cellulitis. Blood can go down into the veins just fine but cannot come back up. a. VTE ex: Deep Vein Thrombosis (DVT) Pathophysiology • Thrombus (Blood clot) forms in deep veins (usually in legs) → can embolize (travel and block vessel) its way to lungs (PE). • Caused by Virchow’s triad: venous/blood flow stasis, endothelial injury, hypercoagulability. Risk Factors • Surgery (hip, knee, prostate) • Immobility • Heart failure • Pregnancy • Family hx • Oral contraceptives or hormone therapy • Cancer • COVID-19 (elevated D-dimer) • Central venous catheters Clinical Manifestations • Note that clients can be asymptomatic • Calf/groin pain (dull/achy), tenderness, warmth, edema • Unilateral swelling • Shallow, irregular shaped wounds • Too much blood, brown/yellow discoloration • Sudden SOB and sharp chest pain → suspect PE • Positioning: “Elevate Veins”, position up in “V” shape, above heart. Worsens: if dangling, sitting/dangling for long periods of time. Diagnostics • ⭐️Venous duplex ultrasonography = gold standard; it’s an ultrasound of Leg to see blood clot/blood flow through the vessel. • ⭐️D-dimer ↑ = clot breakdown evidence • Venogram/MRI if ultrasound inconclusive Nursing Interventions • Bed rest until anticoagulation started • Elevate leg slightly above heart (no knee gatch). Positioning: “EleVate Veins”, think V as veins are up, to keep the veins open. • Warm compresses • DO NOT massage leg • Compression stockings (after swelling ↓) • Encourage early ambulation when safe • SCDS Medications/Procedures (Anticoagulants) stops blood from clotting, another nurse must be with you • Unfractionated heparin (given IV): prevents clots and growth of existing clot; monitor platelets, and aPTT (how long it takes blood to clot) (1.5–2× normal). Must be given in facility. MUST MONITOR CLOSELY • Antidote: protamine sulfate • Low-molecular-weight heparin (Lovenox/enoxaparin): given SubQ, weight-based, prevention and treatment of DVT, given twice daily, can be used in home setting. Don’t need labs. Monitor for bleeding, and take bleeding precautions (Electric razor, soft toothbrush, environment safety) • Warfarin (Coumadin): oral, inhibits vitamin K clotting factors overlaps; combined with heparin 3–4 days until INR 2–3 (takes awhile to kick in; therapeutic affect) • Antidote: vitamin K • Avoid high vitamin K foods (green leafy veggies) • Monitor PT (range: 11-13.5 secs), INR (must know range: 2–3) • Factor Xa inhibitors (fondaparinux; SubQ) (rivaroxaban, apixaban; oral): Prevents development of Thromboses; transitional medication; initial labs are PT and PTT; not routinely • Direct thrombin inhibitors (dabigatran): directly prevents growth of thrombus Formation, given sub Q ; initiate initial lab values only for PT and APTT. • Antidote: idarucizumab • Thrombolytics (tPA): for massive DVT/PE, directly infused into clot, start within 24hrs- 5 days of clot formation; monitor for bleeding, neuro status, dizziness, headache. Take bleeding precautions, pt must use electric razor and, brush teeth with a soft toothbrush. • Inferior vena cava filter: prevents embolus from reaching lungs (PE), inserted in femoral vein; catches blood clot. Used when pt is unresponsive to other treatments. Monitor: bleeding, hematoma, infection, PE (dyspnea, chest pain, tachycardia). Nursing actions: assess circulation and encourage leg exercises/ambulation early, have patient not sit for too long Anticoagulant Therapy Nurse’s Role • Verify labs,;Double-check with another RN for IV heparin, Assess for bleeding (bruises, gums, stools) and Monitor vitals, mental status (signs of intracranial bleed) Reversal Agents • Heparin → protamine sulfate • Warfarin → vitamin K • Dabigatran → idarucizumab Patient Education • Avoid contact sports • Soft toothbrush, electric razor • Avoid sudden diet changes (vitamin K) Complications (anticoagulants) • ⭐️Pulmonary embolism: sudden dyspnea, chest pain, SOB, anxiety, tachypnea → emergency; sit, patient in high Fowlers, and administer oxygen and anticoagulants • ⭐️Ulcer formation(venous): often formed over the medial malleolus, chronic, hard to heal, can reoccur. Can lead to amputation/death. Neuropathic patients might not feel this. Nursing care: Dressing is left 3–7 days; wound vacuums, diet: high in zinc, protein, iron, and vitamins A and C, debride necrotic tissue so wound can heel. Patient Education(Anticoagulants) • Bleeding precautions (soft toothbrush, electric razor) • Report bruising or black stools • Avoid prolonged sitting/crossing legs • Wear compression stockings b. Venous insufficiency Pathophysiology • Valves and legs are damaged due to prolong venous HTN Our previous blood clot Risk factors: • Sitting/standing in one position for a long period of time • Obesity • Pregnancy • Thrombophlebitis Clinical manifestations: • Status dermatitis(brown discoloration along ankles) • Edema • Stasis ulcers around ankles Labs/DX • D-dimer ↑ = clot breakdown evidence, detects clot Nursing interventions: Elevate legs to increase venous return (20 mins, 4-5/day), position: legs above heart, “Elevate Veins”, Apply stockings, and monitor for cellulitis Patient education: avoid sitting/standing still for too long, change positions often, avoid crossing legs, tight clothing. Apply stockings before getting out of bed in the morning Peripheral Arterial Disease (PAD) : affects blood vessels that carry blood away from the heart; artery carries blood away from heart but has difficulty going down to extremities. Pathophysiology • Atherosclerosis in lower extremities → decreased blood flow to tissues. Risk Factors • Smoking, DM, hypertension, hyperlipidemia, obesity, age, sedentary lifestyle. Clinical Manifestations • Intermittent claudication: leg pain with exercise, relieved by rest; not enough oxygen makes the tissue suffer = pain; ischemia • Pain(sharp) that is only relieved when resting in dependent position • Cool, pale, cyanotic skin • Loss of hair on legs, thick toenails • Weak/absent pedal pulses; dorsalis pedis; Doppler(verify), +1 • Numbness, burning at night • No blood and no edema due to an adequate blood flow • Note: think “A” in PAD as Antarctica, where it’s cold! For cold, pale skin! Diagnostics • ⭐️ABI < 0.9 = PAD; ankle pressure compared to break your pressure; expected finding is 0.9–1.3; less than is PAD • ⭐️Arteriography for visualization of occlusion/decreased arterial flow with contrast injection on a x-ray. Monitor for bleeding, hemorrhage, marked, pedal pulses • Doppler studies → decreased flow in DM patients • ⭐️Exercise tolerance testing → decreased pressure in lower limbs, read the workload of the heart/circulation, and clarification during exercise. May use treadmill or meds (dipyridamole, adenosine). Finding of a BP/pulse waveform = arterial disease. Monitor vitals before, during, and after. Stop test if chest pain or symptoms are severe. Nursing Interventions • Encourage graded exercise until pain, rest, repeat • Avoid elevating legs above heart (impairs flow) • Avoid cold, caffeine, nicotine, tight clothing • Keep extremities warm (no heating pad), they can’t feel • Foot care: inspect daily, no bare feet, toenails straight Medications • Antiplatelets: (aspirin, clopidogrel) reduces blood viscosity and increases blood flow and extremities. Monitor: bleeding, abdominal pain, black, tarry stools. • Statins: (atorvastatin, simvastatin). Relieved manifestations like intermittent claudication. • Pentoxifylline: improves RBC flexibility (claudication). Monitor for bleeding, abdominal pain, black tarry stools. Procedures • Angioplasty (balloon/stent). Opens and helps, maintain the patency of the vessel, however, laser vaporizes atherosclerosis plaque. Monitor for bleeding, vital signs, pulses, cap Refill. As patients rest limbs are straight for 2-6 hrs before ambulation. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Atherectomy rotation, device removes, arterial plaque. Monitor for bleeding and distal pulses. rest limbs are straight for 2-6 hrs. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Arterial revascularization bypass surgery • Used for clients at risk for losing a limb, severe claudication, or limb pain at rest. It reroutes the circulation around the arterial occlusion. • Post-op: ⭐️ maintain adequate circulation in repaired artery, mark pedal/dorsalis pulses(compare both), monitor color/temp, pain, cap refill, blood pressure (HTN= risk for bleeding; Hypotension=clot risk). • Complications: for these notify provider first -graft occlusion: acute blockage of bypass graft within 24 hr(absent pulse, cold foot, increased pain) -compartment syndrome: tissue pressure restricting blood flow; causing ischemia (numbness, tingling, edema, worsening/passive pain) -infection: infection of site (warm, tenderness, elevated, WBC, purulent drainage, use sterile technique) Patient Education • Walk until pain → rest → walk more • Stop smoking • Avoid crossing legs • Diet low in cholesterol and fat Postoperative Care – Peripheral Bypass/Revascularization Priorities • Assess extremity: color, temperature, cap refill, sensation, pulses q15min ×1hr • Mark pedal pulses before surgery • Maintain adequate BP (avoid hypo or hypertension) • Do not flex hip/knee excessively • Encourage ambulation when ordered • Report sudden pain, loss of pulse, pale/cool extremity = graft occlusion Complications • Graft occlusion, Compartment syndrome, Wound infection Arterial vs. Venous Ulcers Feature Arterial Ulcer Venous Ulcer Location Toes, feet, lateral ankle Medial ankle Appearance Pale, dry, round “punched out”, no drainage Irregular, leaky/moist, brown discoloration Pain Severe, worse with elevation Achy, relieved with elevation Skin Cool, shiny Warm, thickened Treatment Improve arterial flow Compression therapy, elevate legs Valvular Heart Disease OVERVIEW Overview • Stenosis = narrowed opening/thickening and hardening • Regurgitation = backflow of blood • Causes: rheumatic fever, degenerative calcification, endocarditis Diagnostics • Chest X-ray → chamber enlargement • ⭐️ECG → hypertrophy • Echo → valve dysfunction • TEE → direct view of valves ⭐️ Medications overview • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine); ACE inhibitors (-pril); angiotensin–receptor blockers (-artan); vasodilators (hydralazine]): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Inotropic agents (digoxin): increases contractility, improves cardiac output. Hold medication if pulse rate (abnormal) is less than 60/min or greater than 100/min. Take medication same time every day, avoid combining with antacids (2hrs). Monitor: toxicity such as weakness, confusion, visual changes, low appetite. • Anticoagulants: reduces risk of thrombus. Monitor: stroke, PT, INR, bleeding/bruising. Procedures • Valvuloplasty (balloon dilation) • Valve replacement • Mechanical = lifelong anticoagulants • Tissue = replace every 7–10 years Patient Education • Prophylactic antibiotics before dental procedures • Good oral hygiene • Daily weights • Sodium restriction • Avoid caffeine/alcohol • Report HF signs (weight gain, edema, SOB) • Avoid alcohol, epinephrine, and ephedrine= can cause dysrhythmias THE 4 VALVULAR DISORDERS Mitral Stenosis Etiology/Pathophysiology: Narrowed mitral valve obstructs blood flow from left atrium (LA) → left ventricle (LV), increasing LA pressure and pulmonary congestion → right-sided heart failure. Often caused by rheumatic fever. Clinical Manifestations: Dyspnea on exertion, orthopnea, pitting edema, fatigue, palpitations, hemoptysis, apical diastolic murmur. Risk Factors: Rheumatic heart disease, aging, congenital malformations. Labs/Diagnostics: Echocardiogram (valve narrowing, pressure gradient), ECG (A-fib), chest X-ray (LA enlargement). Medications/Management: • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Anticoagulants: reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgical: Balloon valvuloplasty or valve replacement. NCLEX Tip: Rheumatic fever is the most common cause. Mitral Insufficiency Etiology/Pathophysiology: Incomplete closure of mitral valve causes blood to leak back into LA during systole → LV dilation and hypertrophy. Clinical Manifestations: Fatigue, dyspnea, orthopnea, palpitations, holosystolic murmur at apex, pitting edema, S3 sounds Risk Factors: Mitral valve prolapse, rheumatic disease, MI, endocarditis. Labs/Diagnostics: Echocardiogram (regurgitant volume), ECG (A-fib), BNP (HF indicator). Medications/Management: • Beta-blockers (-lol); ACE inhibitors (-pril); ARBS/angiotensin–receptor blockers (-artan): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: manage fluid overload. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Anticoagulants if A-fib present; reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgery for severe cases. NCLEX Tip: Afterload reduction decreases regurgitant flow. Aortic Stenosis Etiology/Pathophysiology: Narrowed aortic valve → obstructed LV outflow → ↑ LV pressure → hypertrophy → ↓ cardiac output. Clinical Manifestations: Triad: angina, syncope, dyspnea (heart failure); systolic murmur radiating to carotids. Risk Factors: Aging (calcification), congenital bicuspid valve, rheumatic fever. Labs/Diagnostics: Echocardiogram (valve area), ECG (LV hypertrophy), cardiac cath (pressure gradient). Medications/Management: • Avoid nitrates/vasodilators (can cause hypotension). • Use beta-blockers (-lol) cautiously. reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Surgical aortic valve replacement (definitive). NCLEX Tip: Do not aggressively lower preload; maintain perfusion. Aortic Insufficiency Etiology/Pathophysiology: Incomplete closure of aortic valve → backflow of blood into LV → volume overload → dilation and LV hypertrophy. Clinical Manifestations: Dyspnea, palpitations, fatigue, bounding (“water hammer”) pulse, wide pulse pressure, diastolic murmur. Risk Factors: Rheumatic fever, endocarditis, Marfan syndrome, trauma. Labs/Diagnostics: Echocardiogram (backflow volume), ECG (LV enlargement), chest X-ray (cardiomegaly). Medications/Management: • Calcium channel blockers (-dipine); ACE inhibitors (-pril); vasodilators (hydralazine]): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics for volume management. • Surgical valve replacement when severe. NCLEX Tip: Bounding pulse and wide pulse pressure are hallmark findings. General Nursing & Exam Focus • Best diagnostic test: Echocardiogram (for all). • Monitor for A-fib in mitral disorders. • Valve replacement (mechanical): Lifelong anticoagulation. • Daily weights & fluid balance: Detect early HF. • Positioning: High-Fowler’s for dyspnea, low-sodium diet. Inflammatory Heart Disorders (Endocarditis, Pericarditis, Myocarditis, Rheumatic Carditis) Risk Factors • IV drug use, valve replacement, streptococcal infection, immunosuppression, lower socioeconomic status Pericarditis: inflammation of the pericardium (sac around heart) -RF: heart attack, lupus, rheumatoid arthriti -Clinical manifestations: Chest pain (relieved when leaning forward), coughing, Pericardial friction rub, fever, dysrhythmias, and SOB -Labs/DX: • High WBCs, EKG showing ST or T spiking, echocardiogram (inflamed heart) -Nursing care/Intervention: address pain/inflammation, and monitor for cardiac tamponade, position, patient upright, leaning forward, and monitor ECG - Medications: NSAIDs, corticosteroids, anti antibiotics for bacterial • Ibuprofen/NSAIDs for inflammation (pericarditis). Avoid if patient has peptic ulcer, monitor for G.I. bleeding, platelets, liver/kidney function. Must be taken with food, avoid alcohol. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. -Complication: cardiac tamponade → muffled heart sounds, paradoxical pulse, JVD, hypotension (Beck’s triad) Myocarditis: inflammation of the myocardium (heart muscle itself) -RF: viral (covid, Coxsackie), fungal, or bacterial infection; autoimmune disorder -Clinical Manifestations: Tachycardia, chest pain, murmur, friction rub, dysrhythmias, peripheral swelling, cardiomegaly. -Labs/Dx: ECG, echocardiogram, high troponin, CK – MB, ESR in CRP for inflammation/injury -Nursing Care/interventions: monitor for heart failure, and dysrhythmia’s, provide rest and activity restriction -Medication: • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. Endocarditis: bacterial infection that leaves inflammation of the endocardium (inner layer of the heart); bacterial or fungal Infection of endocardial tissues that leads to necrosis and embolization of growth -RF: congenital/valvular heart disease, prosthetic valve, IV drug use -Clinical Manifestations: janeway lesions, Fever, murmur, petechiae, splinter hemorrhages (red streaks under nail beds), Osler’s nodes -labs/dx: positive blood culture, echocardiogram -nursing interventions/care: administer IV antibiotics, antipyretics for fever, and anticoagulants, patient should use soft toothbrush, and prophylactic antibiotics before dental/invasive procedures -medication: • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. Rheumatic Carditis/heart disease: infection of endocardium due to complication of rheumatic fever; GABHS triggers, rheumatic fever leading to inflammatory lesions in the heart -RF: children, Follows untreated strep infection -Clinical Manifestations: tachycardia, Fever, rash(trunk/extremities), joint pain, murmur, chest pain, muscle spasms, friction rub -Labs/Dx: throat culture (strep infection), positive ASO titer, echocardiogram -Nursing care/Interventions: administering antibiotics to stop strep infection, and promote rest, monitor for heart failure, and encourage life on prophylactic antibiotics. -Medications: antibiotics, valve replacement/repair • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. Nursing Interventions (Overview for Inflammatory disorders) • Monitor for tamponade & HF • Administer antibiotics (penicillin) • Pain relief (NSAIDs for pericarditis) • Bed rest • Emotional support • Auscultate heart sounds; murmur or friction rub • Collab with cardiologist and physical therapists Procedures (Overview for Inflammatory disorders) • Pericardiocentesis for fluid removal, then sent to laboratory; monitor for recurrence of cardiac tamponade. ( pericarditis.) • Valve surgery if damaged Complications (Overview for Inflammatory disorders) • Cardiac tamponade: medical emergency resulted from fluid accumulation in pericardial sac. S/S: dyspnea, dizziness, tightness in chest, restlessness. Administer IV fluids, notify the provider, obtain chest, x-ray or ECG Cardiac Diagnostics & Vascular Access (Ch. 28) Transesophageal Echocardiography (TEE) Provides clear heart images via probe in the esophagus to detect valve disease, thrombi, or heart failure. NPO 4–6 hr, monitor VS, ECG, and sedation; check gag reflex before eating post-procedure; keep HOB 45°. Stress Testing (Exercise or Pharmacologic) Assesses heart’s response to stress for angina, HF, MI, or dysrhythmia. NPO 2–4 hr, avoid caffeine/tobacco, wear comfortable clothes; stop test for chest pain, SOB, dizziness. Post: monitor ECG & BP until stable. Coronary Angiography (Cardiac Catheterization) Identifies coronary artery blockages using contrast dye via femoral, radial, or brachial artery. NPO 4–6 hr, assess renal function, allergies (iodine/shellfish), and hold metformin 48 hr before/after. Post: monitor VS and site for bleeding, hematoma, or thrombosis, keep limb straight, maintain bedrest. Complications: cardiac tamponade (↓BP, JVD, muffled heart sounds), embolism, hematoma, AKI—notify provider. Teach: report chest pain, bleeding, SOB, avoid lifting >10 lb, and take antiplatelets as prescribed if stent placed. Vascular Access Devices (VADs) Provide reliable central access for fluids, meds, TPN, or blood. Verify tip placement via x-ray before use. PICC: up to 12 mo use, insert in basilic/cephalic vein → SVC; no BP/venipuncture in that arm, keep dressing dry. Tunneled Catheter: long-term use, subcutaneous tunnel prevents infection; no dressing once healed. Implanted Port: long-term chemo access; access with Huber needle, flush with heparin after use. Complications: • Phlebitis: redness, pain, warmth—maintain sterile technique. • Occlusion: flush gently with 10 mL syringe; never force. • Mechanical issues: swelling or pain at port site = dislodgement → notify provider

UNIT 9: ETHINIC GROUPS(P2)

Ethinicity internal

erin brockovich