A&C Final Exam 1 PDF

A&C Final 11/30/24 2:16 PM Exam 1: Inflammation, Healing Process & Immunity Vascular Response: (1st response) 1. Cellular injury 2. Brief transient vasoconstriction 3. Release of chemical mediators like histamine causes vasodilation and increased capillary permeabi...

A&C Final 11/30/24 2:16 PM Exam 1: Inflammation, Healing Process & Immunity Vascular Response: (1st response) 1. Cellular injury 2. Brief transient vasoconstriction 3. Release of chemical mediators like histamine causes vasodilation and increased capillary permeability 4. Vasodilation and capillary permeability are responsible for redness, heat, and swelling 5. Inflammatory exudates made of serous fluid containing plasma proteins and albumin Clinical Manifestations of Inflammation **Cardinal signs of inflammation: Swelling, Heat, Loss of function, Redness, Pain Cellular Response: (2nd response) ○ White blood cells (WBC’s) move from circulation to the site of injury using chemotaxis using the process of § Margination – cells line up against the endothelium § Rolling – close contact with and roll along the endothelium § Adhesion – connecting to the endothelial wall § Diapedesis – cells move through the vessel wall § Chemotaxis – the directional migration of white blood cells (WBC’s) to the site of injury (Messanger Process) Types of WBC: (Never Let Monkeys Eat Bananas) 3 sec, decreased or absent peripheral pulses of lower extremities, Parathesis, Cool shiny skin w/ hair loss & ulcers, Pallor, Claudication ○ DX: Health history, Physical examine, Ankle Brachial Index, Angiography ○ TX: lifestyle, tx hyperlipidemia, ACE inhibitors, antiplatelets, Catheter procedure Acute Arterial Ischemia ○ Causes: A sudden interruption in the arterial blood supply to tissue caused by embolism, thrombosis of an atherosclerotic artery, or trauma ○ CM: 6 P's § Pulselessness, Paresthesia, Paralysis (late sign and signals death of nerves) Poikilothermia, Pallor, and Pain ○ TX: Heparin, Catheter procedure Buerger’s disease ○ Causes: Tobacco use, Inflammatory process of the vessel wall ○ CM: Intermittent claudication, pain ○ TX: Tobacco cessation, avoid cold, avoid caffeine Raynaud’s Phenomenon ○ Causes: Vasospasm of small veins ○ CM: color changes, coldness or numbing, throbbing or pain ○ TX: Tobacco cessation, avoid cold, avoid caffeine Venous Thrombosis ○ Superficial veins thrombosis (SVT) Greater or lesser saphenous ○ Deep vein thrombosis (DVT) Iliac and femoral ○ Venous thromboembolism (VTE) Preferred terminology Spectrum from DVT to Pulmonary Embolism (PE) ○ Causes: Formation of thrombus with vein inflammation. Most common vein disorder. § 3 key factors called Virchow’s Triad Venous Stasis: Occurs when the valves are dysfunctional, or the muscles of the extremities are inactive Damage of the endothelium: Direct or indirect injury that stimulates platelet activation and starts the coagulation cascade Hypercoagulability of the blood: Excessively easy clotting of blood ○ CM: Swollen tender leg, pain, edema, discoloration, dull achy ○ DX: Ultrasound ○ TX: Anticoagulation § Heparin lab value: apTT, antidote- protamine sulfate § Coumadin (Warfarin) lab value: PT/INR, Antidote- vitamin k Anemia Bone Marrow Yellow ○ Preserve fat for energy production and develop bone, cartilage, muscles, and fat cells ○ Long bones, skull, scapula, sternum (flat bones) Red ○ Actively makes blood cells Plasma (Serum minus clotting factors) Composed mainly of water Contains proteins, electrolytes, gases, nutrients (glucose, lipids, amino acids), and waste. Blood Cells (Formed elements) Erythrocytes (RBCs) ○ O2 and CO2 transportation, Leukocytes (WBCs) ○ Fight infection Thrombocytes (Platelets) ○ Coagulation What is anemia? A deficiency in Number of erythrocytes (red blood cells [RBCs]) Quantity or quality of hemoglobin (Hgb) Volume of packed RBCs (hematocrit) CM: Pallor, Glossitis, Fatigue TX: Correct the cause, blood transfusion, drug therapy, supplemental oxygen, rest, nutrition Iron Deficiency Anemia ○ Causes: Most common is inadequate nutrition, malabsorption, blood loss, hemolysis ○ NN: Effects very young, poor diets, and reproductive women ○ CM: Pallor, Glossitis, Cheilitis, Headache, paresthesia, burning sensation of the tongue ○ DX: CBC ○ TX: correct cause, nutritional therapy, oral iron supplements, transfussion of packed RBC's Thalassemia Do not give iron! Types: Alpha Thalassemia – alpha globulin is missing or mutated, 4 genes involved Occur most often in Southeast Asia, the Middle East, China, and African descent Beta Thalassemia – affects the production of the beta globin protein, 2 genes involved Occur most often in Mediterranean origin Genetic Link: Autosomal recessive genetic basis One thalassemic gene: Thalassemia minor – receives the faulty gene from only one parent Two thalassemic genes: Thalassemia major – receive the faulty gene from both parents Clinical manifestations Thalassemia minor: Doesn't need tx, the body adapts. ○ Often asymptomatic ○ Symptoms of Mild to Moderate anemia ○ Microcytosis (small cells) ○ Hypochromia (pale cells) ○ Mild splenomegaly ○ Bronzed color of skin Thalassemia major: Blood transfusions, chelating therapy, splenectomy. ○ Life-threatening ○ Pale and displays general symptoms of anemia ○ Physical and mental growth often slowed ○ Jaundice is prominent ○ Cranial Thickening ○ Pronounced splenomegaly, Hepatomegaly, and Cardiomyopathy ○ Endocrine problems: diabetes, growth retardation, hypogonadism ○ Symptoms develop in childhood by 2 years of age Cobalamin Deficiency: Macrocytic Anemia ○ Causes: a production problem. B12 isn't being absorbed in the stomach and small intestines. Most commonly caused by pernicious anemia (caused by lack of intrinsic factor). This factor is needed for B12 absorption. ○ NN: Lethal if not treated. ○ CM: Sore, red, beefy, and shiny tongue, Anorexia, N/V, abdominal pain ○ TX: Administer B12 and IF, if lacking. Aplastic Anemia ○ Causes: Disease in which the patient has pancytopenia (Decreased RBC, WBC, Platelets) and hypocellular bone marrow. Typically autoimmune ○ CM: General signs of anemia, neutropenic, cardiovascular and cerebral responses. ○ DX: Bone marrow biopsy ○ TX: supportive care, bone marrow transplant and immunosuppressive therapy. Sickle Cell Disease ○ Causes: inherited autosomal recessive disorder causing abnormal Hgb (Hgb S), stiff elongated sickle shape. ○ NN: Episodes are triggered by low O2 such as high altitude, infection, stress, dehydration, and blood loss. Reversible for a while then become irreversible. ○ CM: Typically asymptomatic with main anemic symptoms. During a sickling episode: SEVERE pain, jaundice, cholelithiasis. Starts to effect all body systems due to lack of oxygen. Pneumonia is major complication. ○ DX: Blood smear ○ TX: hydration, oxygen, rest, transfusions is severe. Exam 3: Fluid & Electrolyte Imbalances Body Fluid Compartments Intracellular space (28L): 2/3 of body water Extracellular space: 1/3 of body water ○ Interstitial fluid (10L): Fluid between cells ○ Intravascular (3L) : Plasma, liquid component of blood. Types of ions Cations: positively charged ○ Sodium (𝐍𝐀! ), Potassium (𝐊 ! ), Calcium (𝐂𝐀𝟐! ) and Magnesium (𝐌𝐆𝟐! ) Anions: negatively charged ○ Bicarbonate (𝐇𝐂𝐎$ $ 𝟑$ 𝟑 ), Chloride (𝐂𝐥 ), Phosphate(𝐏𝐎𝟒 ), most proteins Movement of Ions across concentrations Diffusion: The movement of molecules from an area of higher concentration to an area of lower concentration, aiming for equilibrium without energy expenditure. Facilitated Diffusion: The movement of molecules across cell membranes through protein channels, moving from a higher to a lower concentration, without the need for energy (ATP). Active Transport: The movement of molecules across a membrane against the concentration gradient (from lower to higher concentration), which requires energy in the form of ATP. ○ Solute: Salt ○ Solvent: Water ○ Solution: Salt Water ○ Hypotonic: Weak- water moves into the cell. Results in cellular edema. ECF-> ICF ○ Hypertonic: Strong- water moves out of cell. Dehydrated Cells. ICF-> ECF Osmosis: The movement of water molecules through a semi-permeable membrane from an area of lower solute concentration to an area of higher solute concentration, aiming to balance solute concentrations on both sides. Osmotic Pressure: The pressure required to prevent the movement of water by osmosis across a semi-permeable membrane. ○ Osmolarity: The concentration of solutes per liter of solution (Osm/L), often used to measure the concentration of bodily fluids. (More in chemistry, don't really worry about this one) ○ Osmolality: The concentration of solutes per kilogram of solvent (Osm/kg), commonly used in clinical settings to assess body fluids. Concentration of my solution. Normal concentration is 280-295. § Greater than 295: Solute is too high, or too little water= solution too strong(Hypertonic). Cellular dehydration § Less than 280 is too little solute or too much solvent= solution is too weak (Hypotonic). Cellular edema Osmotic Movement: The movement of water across a membrane due to differences in osmolarity between solutions. ○ Isotonic: A solution with the same osmolarity as body fluids, causing no net movement of water into or out of cells. ○ Hypotonic: A solution with lower osmolarity than body fluids, leading to water moving into cells, causing them to swell. ○ Hypertonic: A solution with higher osmolarity than body fluids, causing water to move out of cells, leading to cell shrinkage. Hydrostatic Pressure (Pushing pressure): The pressure exerted by a fluid in a closed system, such as blood pressure within blood vessels, pushing fluid out of capillaries. Oncotic Pressure (Colloid Osmotic Pressure)(Pulling Pressure): The pressure exerted by plasma colloids (proteins, primarily albumin) in blood plasma, which pulls water into the circulatory system. Fluid Spacing Used to describe the distribution of body water ○ First Spacing: normal distribution of fluid in the ICF and ECF ○ Second Spacing: Abnormal accumulation of fluid in interstitial space (i.e. edema) ○ Third Spacing: Excess fluid collects in the nonfunctional areas of the cells; difficult or impossible for fluid to move back into cells or blood vessels. Ex: ascites or peritonitis Nursing Management: Fluid Volume Imbalances Fluid Volume Imbalance: ○ Fluid Volume Deficit: A condition where there is a loss of fluid, either due to decreased intake or excessive loss, leading to hypovolemia. ○ Dehydration: The loss of water without the loss of sodium, leading to hypernatremia and reduced water in the cells. Fluid Volume Excess: A condition characterized by an excess of fluid, often due to excessive intake or retention, leading to hypervolemia and edema. ○ ISO Tonic: 280-295 ○ Hypertonic: >295, Solute increase, Solvent decrease = Cellular Dehydration ○ Hypotonic: 145) Cellular dehydration Causes: Diabetes Insipidus, dehydration, excess sodium intake, primary aldosteronism. CM: Dry mucous membranes, Oliguria, Thirst, lethargy, agitation, seizures, coma, impaired LOC, postural hypotension. TX: correct cause, IV 5%DW or oral water, low sodium diet. Hyponatremia: (5) Dietary intake: Fruits and vegetables such as bananas, oranges, prunes, raisins, and cooked spinach Causes: Massive intake, Kidney Disease, burns CM: cardiac irregularities, weakness, nausea, diarrhea, irritability. TX: Administer K+ free fluids, dialysis, diuretics, kayexalate, insulin, glucose Hypokalemia: (< 3) Abnormal losses of K+ via the kidneys or gastrointestinal tract Causes: diarrhea, vomiting, diuretics CM: Loss of muscle tone, vomiting, cardiac dysrhythmia's, Abdominal distention TX: Increase dietary intake, Iv KCL ○ IV Infusion ○ IV Infusion rate should not exceed 10 mEq/hr ○ IV KCl must always be diluted ○ Never give KCl via push or bolus ○ Invert IV bags several times to ensure dilution ○ Do not add KCl to a hanging IV bag to prevent giving a bolus dose ○ IV KCl must be given by infusion pump Hypercalcemia (> 10.5) Causes: 2/3 of persons: Hyperparathyroidism. 1/3 of persons: Cancers, Kidney, hematologic, breast, lung, Prolonged immobility is a risk factor. CM: Flank pain, deep bone pain, relaxed muscles, Increased BP, Heart blocks TX: Correct primary problem, increasing weight bearing, Biphosphates, IV isotonic Hypocalcemia (< 8.5) Causes: Removal of parathyroid glands, chronic alcohol use CM: tingling of extremities, cramps, convulsions, prolonged QT interval, tetany: Chvostek's- Poke cheek excitability Trousseau's- BP flex-hand excitability Tx: PO/IV replacement calcium gluconate, dietary ACID-BASE BALANCE Acid-Base Regulation 3 mechanisms to regulate pH between 7.35-7.45 ○ Buffer system (1st line of defense) Carbonic Acid-Bicarbonate system § Primary regulator of acid-base balance § Fastest, react immediately ○ Respiratory system (2nd line of defense) § Minutes, reaches maximum effectiveness in hours § Increase respiration and depth (hyperventilation) ○ Decreased CO2 leading to ALK § Decrease respiration and shallow breathing (hypoventilation) ○ Increased CO2 leading to AC ○ Renal system (3rd line of defense) § Hours to days § Long-term acid-base control § Depends on kidneys to reabsorb and conserve all the Bicarbonate (HCO3-) & Excrete acids (H+) ○ Acidemia (reduced blood pH) Increased H+ § Enters the cell in exchange for K+ § May result in hyperkalemia (K+ moves into ECF) ○ Alkalemia (increased blood pH) Decreased H+ § Enters plasma in exchange for K+ § May result in hypokalemia (K+ moves into the ICF) Alterations in Acid-Base Balance Respiratory: Changes in carbonic acid concentration (CO2 Metabolic: Affect the base Respiratory Acidosis: Excess CO2 levels, caused by HYPOventilation, Asthma attacks or COPD. Pneumonia & pulmonary edema, Respiratory failure, Looks like a Narcotics OD pt ○ Increase in carbonic acid ○ CM: Rapid Shallow Breathing, Decreased BP, Cyanotic/Pallor, Drowsiness, Dizzy, Hyperkalemia ○ TX: Bronchodilators, steroids, Bi-pap, Increase RR Metabolic Alkalosis: Excess HCO3 levels, caused by excess NG suction & Vomiting, loss of acids from stomach, diuretics. ○ Increase in base (HC03-) ○ CM: Confusion, hypoventilation, dizzy, increased irritability, n/v/d, muscles tremors, cramps, hypokalemia. ○ TX: Address underlying cause, Increase CO2, Iv fluids Respiratory Alkalosis: Decreased CO2, caused by HYPERventilation, hypoxia, brain injury ○ Decrease in carbonic acid ○ CM: seizures, deep rapid breathing, numbness & tingling, light headedness, n/v, anxiety ○ TX: Breathe into a bag, decrease RR, address anxiety, decrease HCO3 Metabolic Alkalosis: Decreased HCO3, caused by DKA, renal failure, severe diarrhea. ○ Decrease in base (HC03-) ○ CM: Headache, drop in BP, warm flushed skin, n/v/d, Kussmal Respirations (Compensatory Hyperventilation) ○ TX: Fix underlying cause, Increase Bicarbonate IV, increase RR HYPERventilation: blow off CO2, caused by pain, anxiety, stimulant, DKA S/S: Light headedness, CP, numbness & tingling, twitching, vision changes, fainting Correction: Decrease RR/Depth HYPOventilation: Retaining CO2, caused by alcohol, narcotics, head injury, COPD, Alititude S/S: Fatigue, headache, cyanosis, confusion, hypoxia Correction: Increase RR/Depth In general: ○ In acidosis H+ move into cells while K+ moves out; making room for H+ - serum K+ levels rise. (hyperkalemia) ○ In alkalosis cells release hydrogen ions into the blood to increase the acidity of the blood; K+ moves into cells and serum K+ levels fall. (hypokalemia) SaO2: 95% to 100% PaO2: 80 100mmHg, under 80 is Hypoxemia Practice! https://abg.ninja/abg Diabetes Mellitus Pancreas ○ Alpha cells secrete glucagon ○ Beta cells secrete insulin and amylin ○ Delta cells secrete somatostatin ○ F cells secrete pancreatic polypeptide Glucose Storage ○ Excess glucose is converted into glycogen which is stored in the liver, fat, and muscles Function ○ Supplies energy to the brain, heart, muscles, and every other organ DM Diagnostic Studies 1. A1C of 6.5% or higher 2. Fasting plasma glucose (FPG) level of 126 mg/dL or greater. 3. A 2-hour plasma glucose level of 200 mg/dL or greater. Somogyi Effect and Dawn Phenomenon Somogyi effect: hyperglycemia in the morning ○ High doses of insulin causes a decline in blood glucose levels during the night. As a result, counterregulatory hormones are released, rebound hyperglycemia ○ Checking blood glucose between 2:00 and 4:00am will help determine. Dawn phenomenon: hyperglycemia present in the morning Two counterregulatory hormones are released early in the morning hours ○ Affects many people with diabetes and is most severe in adolescence and young adult (Growth hormone peak) Hypoglycemia (< 70) Low BS, excess insulin. CM: Shakiness, excess hunger, palpitations, nervousness, diaphoresis, anxiety, hunger, pallor, cold, confusion, coma, tachycardia. TX: Rule of 15, Glucagon injection or IV 50%Dextrose. Hyperglycemia High BS (Normal range 70-120mg/dL) CM: Polydipsia, polyuria, polyphagia, drowsiness, dry mouth, blurred vision, n/v TX: Insulin Type 1 DM Body attacks the insulin-producing cells of the pancreas Caused by genetic factors, autoimmune disease, or environmental factors CM: Polyuria, polydipsia, polyphagia (Classic symptoms), Weakness, fatigue, weight loss, Can present to ER in DKA if untreated Diabetic Ketoacidosis (DKA) Acute Lack insulin and cannot uptake glucose for energy Fat metabolism (Ketogenesis) for energy and causes accumulation of ketones Liver produces more glucose in response ○ Increases serum glucose even more Osmotic diuresis leads to sodium, potassium, chloride, phosphate, and magnesium depletion Untreated, becomes comatose from dehydration, electrolyte imbalance, and acidosis ○ Complications include shock, renal failure, and death CM: Hyperglycemia, ketosis, acid-base, Kussmal respirations, dehydration DX: CBC, Ketones, urinalysis TX: IV fluids, IV Insulin, IV dextrose to keep BS from dropping significantly, monitor for edema and hypokalemia. Type 2 DM Characterized by inadequate insulin secretion and insulin resistance ○ Not able to make enough insulin or does not use it effectively or both CM: Nonspecific, May have the poly's, recurrent infections, prolonged wound healing, vision problems, neuropathy, obesity. TX: Insulin Macrovascular complications (medium to large vessels) ○ Cerebrovascular ○ Cardiovascular ○ Peripheral vascular ○ Screening: Lipid management, smoking cessation, antiplatelets Microvascular complications (small vessels) ○ Retinopathy ○ Nephropathy ○ Neuropathy ○ Screening: BP and BS management Hyperosmolar Hyperglycemia Syndrome (HHS) This condition is characterized by hyperglycemia, hyperosmolarity, and dehydration without significant ketoacidosis who make enough insulin to prevent DKA. HHS usually presents in older patients over 60 y/o age with type 2 DM Causes of HHS ○ UTI, Pneumonia, Sepsis, Newly diagnosed type 2 DM, Acute illness, and Impaired thirst sensation and/or functional ability to replace fluids More severe neurological manifestations ○ Coma, seizures, hemiparesis and aphasia Glucose levels greater than 600 mg/dl and marked increase serum osmolality Ketone bodies are absent or minimal ○ Has enough circulating insulin so that ketoacidosis does not occur Management is similar to DKA IV administration of insulin and IV fluids (0.9 or 0.45%) Usually requires large volumes of fluid replacement Once blood glucose drops to about 250mg/dl ○ IV fluid containing dextrose are given to prevent hypoglycemia Hypokalemia is not as significant compared to DKA Vision Disorders Eye trauma Causes: Blunt/penetrating, chemical burn, thermal burn, foreign bodies, falling or fights. CM: Pain, redness, swelling, ecchymosis, tearing. Photophobia, blood/fluid drainage vision changes, prolapsed globe TX: Correct cause, stabilize the eye and DO NOT remove the object, irrigation, HOB 45 degree, NPO just incase of surgery Eye infection Sty (External hordeolum) ○ Infection of the meibomian glands in the lid margin, caused usually by Staphylococcus aureus ○ Treat: Apply warm, moist compresses 4x daily Blepharitis ○ Chronic bilateral inflammation of the lid margins can be caused by bacteria or inflammation ○ Treat: Gentle cleansing practices, antibiotic ointment if bacterial to avoid keratitis (inflammation of cornea) Conjunctivitis ○ Inflammation or infection of the conjunctiva ○ Treat: § Bacterial- Self-limiting (antibiotics shorten course), handwashing &avoiding infected individuals □ Chlamydial - Antibiotic therapy § Viral- Self-limiting, cool compresses, prevent the spread § Allergic- avoid allergen, artificial tears, antihistamines Cataracts Opacity of the lens (unilateral or bilateral) Age related CM: Gradual vision decline, abnormal color perception, glare worse at night. TX: increase prescription & light, surgery. Retinopathy Microvascular damage to the retina caused by diabetes and hypertension Diabetic retinopathy Nonproliferative § Common form characterized by capillary microaneurysm, retinal swelling, and hard exudates Proliferative § Advance disease where new blood vessels grow and are fragile that can leak Hypertensive retinopathy Blockages in retinal blood vessels Retinal detachment Detachment of the sensory retina from the pigmented epithelium with fluid accumulation in between the two layers Almost always results in blindness if untreated CM: Detaching retina: Photopsia, Floaters, “cobweb” or “hairnet” in the vision field Retina has detached Vision loss “like a curtain” Vision loss that is inverse to detachment Age-Related macular degeneration (AMD) Dry: Macular cells atrophy, leading to slow but progressive vision loss More common type of AMD, SMOKING CESSATION! Wet: Rapid onset vision loss caused by abnormal angiogenesis in or near the macula; new vessels leak fluid and bleed, scar tissue develops over macula More severe type of AMD CM: Scotomas (blind spots in the visual field), Metamorphosia (distorted vision), Loss of central vision Glaucoma Second leading cause of permanent blindness in US and the leading cause of blindness among blacks Incidence increases with age Group of eye disorders characterized by increased intraocular pressure ○ Primary open-angle glaucoma (POAG) ○ Outflow of aqueous humor is decreased in the trabecular meshwork and drainage becomes clogged ○ Most common type; drainage out of the eye is decreased (slowed) so pressure builds within the eye ○ Angle closure glaucoma (ACG) ○ Reduction in the outflow of aqueous humor ○ Lens bulging occurs with aging causing the iris-corneal angle to close, the lens bulging forward ○ TX: Miotics drops- carbachol (miostat) Exam 4:Musculoskeletal Disorders Strains and Sprains Pathophysiology: Injury to muscles/Tendons (sTrain) or ligaments (sprain) from overstretching or tearing. Diagnosis: Physical examination, imaging (X-ray or MRI) for severe cases. Manifestations: Pain, swelling, bruising, limited movement, muscle spasms. Treatment: ○ RICE: § Rest: Limit weight-bearing activities. § Ice: Apply intermittently in the first 24-48 hours to reduce swelling. § Compression: Use bandages to minimize swelling. § Elevation: Keep the injured area elevated to reduce edema. Types Closed (simple) ○ Skin is intact Open (compound) ○ Skin is broken and bone is exposed Complete or incomplete: Break goes all the way or only partially through the bone. Displaced or non-displaced: the alignment of the bone after the break. Directional: Linear, oblique, transverse, longitudinal, and spiral fractures. Types of fractures. (A) Transverse fracture: the line of the fracture extends across the bone shaft at a right angle to the longitudinal axis. (B) Spiral fracture: the line of the fracture extends in a spiral direction along the bone shaft. (C) Greenstick fracture: an incomplete fracture with 1 side splintered and the other side bent. (D) Comminuted fracture: a fracture with more than 2 fragments. The smaller fragments appear to be floating. (E) Oblique fracture: the line of the fracture extends across and down the bone. (F) Pathologic fracture: a spontaneous fracture at the site of a diseased bone. (G) Stress fracture: occurs in bone that is subject to repeated stress, such as from jogging or running. Fracture Healing (A) Fracture hematoma (w/in 72 hours) Bleeding creates hematoma (B-C) Granulation tissue (3-14 days) Hematoma converts to granulation tissue (new blood vessels, fibroblasts, and osteoblasts) (D) Callus formation (14 -28 days) New bone matrix that is an unorganized network of bone is formed and removal of dead bone by osteoclasts (D)Ossification (3 wks-6months) Continual callus formation (D) Consolidation (6months-1year) distance between bone fragments decreases and eventually close (E) Remodeling (complete union) Excess bone is resorbed, gradual return to the preinjury state. Bone remodels in response to physical loading stress (Wolf’s law) Nursing Care for Fractures Closed reduction: nonsurgical manual realignment of bone fragments. Open reduction: Correction of bone alignment through a surgical incision. Traction: Application of a pulling force. **Important to immobilize the joint above and below the injury. Immobilization cures a majority of the initial pain **Tetanus shot for open fractures. Casts Temporary use Immobilizes the joint above and below a fracture Assess color, temp, cap refill, pulses, edema-especially distal to cast, paresthesia, or decrease sensation External fixation: Metal pins and wires inserted into bone and attached to external rods Internal fixation: Pins, plates, rods, and screws are surgically inserted Compartment Syndrome Indirect complication of fractures. Ischemia can occur after 4-8 hours after onset 6 P's: Pain, Pressure, Paresthesia, Pallor, Paralysis, Pulselessness Do Not elevate or apply cold compresses Hip Fracture Most common cause is falls. Occurs in the proximal 1/3 of the femur. CM: external rotation of hip, muscle spasms, shortening of the affected extremity, pain & tenderness. TX: Surgery, closed reduction. Know common do's after surgery (no low seats or toilets, don't cross legs or chairs without arms) Congenital Hip Dysplasia Pathophysiology: Abnormal hip joint development in infants. S/S: Asymmetric thigh and gluteal folds; shortening of the limb on the affected side Diagnosis: Clinical examination (Ortolani and Barlow maneuvers), Xray. ○ Ortolani test ○ abducting (Out) the thighs and placing anterior pressure at the hip to see if the femoral head slips forward into the acetabulum ○ Barlow test ○ the thigh is adducted (In), and light pressure is applied to see if the femoral head can be felt to slip posteriorly out of the acetabulum. Treatment: Pavlik harness, spica cast or surgery for severe cases. Nursing Care: Monitoring hip position, ensuring proper fit of devices, skin care. Clubfoot Pathophysiology: Congenital Foot adduction, supination deformity with foot turned inward. Diagnosis: Physical examination, sometimes X-rays. Treatment: Casting (Ponseti Method: Serial Casting) bracing, or surgery. Nursing Care: Educating parents that tx begins ASAP after birth, monitoring circulation, and preventing skin breakdown. Scoliosis Pathophysiology: Lateral curvature of the spine, often idiopathic. Rib asymmetry. Diagnosis: Screening during adolescence, X-rays. Treatment: ○ Bracing & Exercise: To halt progression in growing children. ○ Surgery: Spinal fusion for severe cases. Nursing Care: Post-op care, pain management, mobility exercises. Osteoarthritis Pathophysiology and Etiology: Slow, progressive, non-inflammatory disorder of the synovial joints. Degenerative joint disease causing cartilage breakdown. Manifestations: ○ Heberden’s nodes: Bony swellings at distal interphalangeal joints. ○ Bouchard’s nodes: Bony swellings at proximal interphalangeal joints. Treatment: ○ Tylenol: First-line pain relief. ○ NSAIDs: For pain and inflammation. ○ Corticosteroids: For severe inflammation. Rheumatoid Arthritis Pathophysiology & Etiology: Chronic, systemic autoimmune characterized by inflammation of synovial joints. Autoimmune inflammatory disorder affecting joints system-wide. Manifestations: Symmetric joint swelling, stiffness, fatigue. Complications: ○ Felty’s syndrome: Enlarged spleen, decreased white blood cell count. Diagnostic Studies: Blood tests, X-rays. ○ Positive RF, ESR, CRP ○ Antibodies to citrullinated peptide (anti-CCP) § More specific than RF Treatment: ○ DMARDs: Disease-modifying anti-rheumatic drugs. ○ Methotrexate: Commonly used DMARD. ○ Other Medications: Biologics and immunosuppressants. Typical deformities of RA. A: Ulnar drift. B: Boutonnière deformity. C: Hallux valgus. D: Swan neck deformity. Gout Pathophysiology & Etiology: Elevation in uric acid (Hyperuricemia). Causes Uric acid crystal deposits in joints due to metabolic imbalance. Manifestations: Acute joint pain, redness, swelling. Treatment: ○ Avoid Purine foods (organ meats and red meat) and alcohol. ○ Colchicine: Anti-inflammatory specifically for gout. ○ NSAIDs: For pain and inflammation. ○ Allopurinol: Reduces uric acid production. Muscular Dystrophy Pathophysiology and Etiology: Genetic disorder causing progressive muscle weakness.X- linked; males are affected. No neurologic involvement Manifestations: Gradual loss of muscle function. Duchenne muscular dystrophy most common and severe Muscle weakness appears in early childhood and worsens rapidly Becker muscular dystrophy Muscle weakness appears later in childhood and worsens slower Complications: Respiratory issues, cardiac involvement. Adjusting to a Chronic Illness: Emphasis on physical therapy, assistive devices, and support. Disc Degeneration/Back Pain Pathophysiology & Etiology: Degeneration or damage to intervertebral discs, often due to aging or injury. Manifestations: Chronic back pain (lower most common), numbness, weakness in limbs. Treatment: ○ Pain Management: Using various medications and physical therapy. ○ Muscle Relaxants: To relieve muscle spasms. ○ Physical Therapy: Strengthening and flexibility exercises. ○ Heat and Cold: For symptomatic relief. ○ Surgical Options: For severe, persistent cases. IMMOBILIZATION Benefits of Bedrest: decrease oxygen needs of the body and reduce cardiac workload. Consequences of Bedrest: Disuse atrophy, loses muscle (3% a day), systemic effects. Metabolic effects ○ Decreased appetite, constipation, & breakdown ○ Calcium Resorption: calcium is lost from the bones and released into circulation. ○ Deficient in proteins: resulting in a Negative Nitrogen Balance Integumentary System Effects: ○ Pressure Ulcers: Skin breakdown from prolonged pressure. ○ Shear: Tissue damage from skin sliding over surfaces. ○ Friction Injury: Skin irritation due to rubbing. ○ Excoriation: removal of skin by abrasion or scratching ○ Maceration: Skin breakdown due to moisture. Problem: Impaired skin integrity. Cardiovascular System Effects: ○ Cardiac Deconditioning: Weakened cardiovascular function from inactivity. ○ Increased Workload on Heart: Due to blood distribution changes resulting in increased HR, Co, & increased stroke volume to compensate. Valsalva maneuver is contraindicated. ○ Orthostatic Intolerance and Hypotension: Blood pressure drops upon standing, leading to dizziness or fainting. ○ Thrombus formation: Blood Stasis and DVT: Pooling of blood in lower extremities, raising the risk of deep vein thrombosis (DVT). Pulmonary Embolus: Blood clot migrating to the lungs. Problem: Decreased cardiac output and risk of coagulation issues. Respiratory System Effects of Immobility Effects: ○ Hypoventilation: Shallow breathing due to inactivity. ○ Atelectasis: Partial or complete lung collapse. ○ Stationary Secretions: Increased risk of infection from pooled secretions. ○ Altered Gas Exchange: Reduced oxygen and carbon dioxide exchange. ○ Diminished Cough and Hypostatic Pneumonia: Risk of respiratory infection. Gastrointestinal System Effects of Immobility Effects: ○ Slowed Basal Metabolic Rate: Reduced energy expenditure. ○ Slowed Motility and Delayed Gastric Emptying: Causes constipation and discomfort. ○ Anorexia: Decreased appetite, potentially leading to malnutrition. ○ Increased Storage of Fat and Carbohydrates: Weight gain due to inactivity. ○ Negative Nitrogen Balance: Due to protein breakdown for energy. Problem: Risk for imbalanced nutrition, constipation, and deficient fluid volume. Genitourinary Effects of Immobility Effects: ○ Urinary Stasis: Pooling of urine in bladder, raising infection risk. ○ Urinary Retention: Incomplete bladder emptying. ○ Renal Calculi: Increased risk of kidney stones. ○ UTIs: Increased risk of urinary tract infections. Problem: Risk for infection. Developmental Changes Infants, Toddlers, and Preschoolers Immobilized usually because of trauma or the need to correct the congenital skeletal abnormality May affect gross motor skills, intellectual development, and musculoskeletal development Adolescents Social isolation is a concern Adults All physiological systems are at risk Role of adult often changes in regard to the family or social structure Older Adults Often experience functional status changes Increase physical dependence on others Neurological Disorders Stroke (Cerebral vascular Accident) Ischemic Stroke: Blockage of blood vessels-> lack of blood flow to affected area (87% of ALL strokes) Thrombotic: Happens from an injury to a blood vessel wall and the formation of a blood clot happens ○ Most common cause of stroke ○ Lumen becomes narrowed. If completely occluded: infarction occurs ○ Often related during sleep or after sleep ○ Common in older adults especially with high cholesterol, atherosclerosis, diabetes, hypertension, and history of TIA Embolic: blood clot that came from somewhere else in the body, but found its way to the brain and then lodged into an appropriately sized artery ○ Occludes the cerebral artery resulting in infarction and edema of the area ○ Second most common cause of stroke ○ Often related during activity ○ Most originate in the endocardial layer of the heart when a plaque breaks off in conditions of atrial fibrillation, MI, endocarditis, and valvular heart prostheses Hemorrhagic Stroke: a ruptured artery that had a weak wall or an aneurysm (Accounts for 13% of strokes) Intracerebral: bleeding within the brain ○ Poor prognosis ○ Hypertension is the most common cause, coagulation disorders, anticoagulant drugs, trauma, or brain tumors ○ Sudden onset of symptoms that progress from minutes to hours ○ Often related to activity Subarachnoid hemorrhage: bleeding into the CSF space between the arachnoid and pia mater ○ Silent killer, do not have warning signs or symptoms until rupture has occurred ○ Often caused by rupture of a cerebral aneurysm (congenital or acquired), cocaine use ○ Often related to head trauma Transient Ischemic Attack (TIA) Transient episode of neurological dysfunction without acute infarction of the brain. Symptoms are short-term and increases the chance of stroke. Circle of Willis: Most common location for infarctional aneurysms to occur. Signs of Stroke (FAST) Face drooping Arm weakness Speech difficulties Time As well as: Confusion, numbness, sever headache, Trouble sleeping, instability Stroke is DX: CT scan non-contrast. Stroke TX: Recombinant tissue plasminogen activator (tPA) if ischemic and given within 3-4.5 hours. Antiplatelet drugs, Anticoagulants, Statin's, stents. Stroke NN: Assess airway, promote mobility, assess neuro/cardiac status, #1 risk is aspiration pneumonia. Seizures (Epilepsy) Sudden abnormal, excessive electrical discharge of neurons that interrupts normal function Clinical Manifestations of Seizures Tonic Clonic ○ Loses consciousness and falls to ground, if upright; body stiffens (tonic) for 10 to 20 seconds and extremities jerk (clonic) for another 3o to 40 seconds. ○ Cyanosis, excessive salivation, tongue or cheek biting, and incontinence Atonic ○ Tonic episode or loss of muscle tone; suddenly falling to the ground lasting less than 15 seconds. Stays conscious and resumes normal activity immediately; risk for head injury Typical absence ○ Brief staring spell that last less than 1o seconds; unresponsive when spoken to Atypical absence ○ Staring spell with eye blinking or jerking movements of the lips that last more than 10 second Myoclonic absence ○ Rhythmic arm abduction leading to progressive arm elevation that lasts 10 to 60 seconds Focal awareness ○ Conscious and alert but have unusual feelings or sensations of joy, anger, sadness, and nausea and may hear, smell, taste or see things less than 2 minutes Focal impaired awareness ○ Loss of consciousness or change in awareness, producing a dream-like state. May make movements and do things that can be dangerous that last 1 to 2 minutes Drug therapy: Phenytoin, carbamazepine, phenobarbital, lorazepam, diazepam Trigeminal Neuralgia (TN) TN1 is the most common and is typically caused by compression of the trigeminal nerve by the superior cerebral artery. TN2 is less common and is caused by an underlying disease like MS. Present with lower level of pain and does not subside completely! Clinical Manifestations: Sudden, stabbing, unilateral facial pain. Facial twitching, grimacing, facial sensory loss, attacks are brief and only last seconds to minutes. Drug Therapy (TN1=antiseizure meds) (TN2= analgesics or opioids) & Surgery. NN: Assess pain, response to drug therapy, decrease triggering stimuli, psychosocial, nutrition and oral care. Bell’s Palsy Acute, usually temporary facial paresis (palsy) from damage/trauma to facial nerve (CN VII). Cause is unknown, but maybe viral. CM: Unilateral muscle facial weakness, Pain around and behind the ear, Drooping of the eyelid, Drooling, Facial twitching and numbness, Altered taste and hearing TX: mild analgesics, moist heat, PT & electric stimulation, facial exercises, eye protection, nutrition, and psychosocial. Meningitis Acute inflammation of the meningeal tissues surrounding the brain and spinal cord Causes: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae S/S: Fever, Severe Headache, N/V, Nuchal Rigidity, Photophobia, Decreased LOC, Seizures & Rashes NN: Intracranial pressure is most common complications DX: CT scan, Blood culture TX: Antibiotics if bacterial, Symptomatic care, mannitol Renal and Urological Problems Etiology & Pathophysiology of UTI E coli is most common cause Risk factors: Aging, DM, foreign bodies, BPH, catheters, stones Upper UTI ○ Pyelonephritis (Inflammation of renal parenchyma and collecting system) Kidney and Ureters- considered complicated more sick and high fever in younger and elderly population. Lower UTI ○ Cystitis (Inflammation of bladder) ○ Urethritis (Inflammation of urethra) Urosepsis ○ Systemic infection arising from a urologic source, leads to ICU stays because it leads to shock and death. CM of UTI: Emptying: Dysuria, Hesitancy, postvoid dribbling, or incomplete emptying. Storage: Incontinence, nocturia, urgency, urinary frequency Abdominal pain, back pain, fever, cloudy urine or bacteria, sepsis, confusion in elderly. DX: Nitrites, WBC, Leukocyte's, clean catch for UA TX: COLLECT CULTURE BEFORE TX, Increase FL, Trimethoprim/Sulfamethoxazole (TMP/SMX), Phenazopyridine (Pyridium): causes orange urine. NN: Empty bladder every 3-4 hours, bladder is sterile. Elderly less like to show typical signs, have more complicated UTI's. Acute Pyelonephritis Causes: Upper UTI bacterial infection. CM: Fever/chills, nausea/vomiting, malaise, flank pain (CVA pain), dysuria, urgency and frequency DX: H&, UA, checking for sepsis/ severe infection signs TX: Increase FL, fluoroquinolones (more for men or bad infections), TMP/SMX NN: early TX and sign of UTI Urinary Tract Calculi Nephrolithiasis (Kidney stone disease) Calculus = stone Lithiasis = stone formation S/S: ○ Sharp in the flank area, back or lower abdomen, NEVER DULL PAIN! ○ Groin pain ○ Renal colic pain: the stone is most painful when stuck at the junctures, comes and goes. ○ Nausea and vomiting Causes: Several- crystals when in a supersaturated concentration, precipitate and unite to form a stone Types of Urinary Stones Calcium oxalate (most common): Hypercalciuria Calcium phosphate Cystine Struvite Uric Acid DX: CT scan is the gold standard. TX: Lithotripsy (Shock waves to break stone), Surgical NN: May give tamsulosin (Flomax): Alpha blocker to help relax the smooth muscle of the ureter. 4 mm or less in size stones to pass spontaneously. Adequate hydration (3L/day) and dietary changes Benign Prostatic Hyperplasia (BPH) Prostate gland increases in size Disrupts the outflow of urine Develops in the inner part of the prostate (transition zone) CM: obstructive symptoms (decreased urinary stream, difficulty starting, intermittency, dribbling) and irritative symptoms (nocturia, frequency, urgency, dysuria, bladder pain) with potential incontinence. DX: history, physical exam (DRE for prostate size/symmetry), urinalysis, PSA blood test, and further imaging (TRUS, pelvic MRI) if abnormalities are found, with uroflowmetry to assess urine flow rate and duration. TX: 5α-Reductase Inhibitors (block the 5α-reductase type 1 and 2 isoenzymes) Finasteride (Proscar): More common- Decreases size of prostate. □ Women should not touch tablets due to the potential risk to the male fetus Dutasteride (Avodart) Side Effects: Decreased libido α-Adrenergic Receptor Blockers (block α1-adrenergic receptors) Tamsulosin (Flomax) Doxazosin (Cardura) Prazosin (Minipress) Alfuzosin (Uroxatral) Side Effects: Retrograde ejaculation: Semen goes up but doesn't come out. NN: Post-Op care for TURP: indwelling catheter, yearly appt for prostate, avoid straining, blood clots expected for first 24-36 hours, may have incontinence for several weeks, daily cleaning if discharged home with catheter, Observe signs of infection- HIGH RISK Prostate cancer Tumor of the prostate gland Most common cancer in men Slow growing androgen (male hormones)-dependent cancer Develops in the peripheral Zones!!!!!!!! CM: pain in hips or lumbar, similar to BPH, no early symptoms DX: Screenings, rectal exam, biopsy to confirm. TX: Surgical therapy and radiation therapy, chemo, Androgen receptor drugs Gastrointestinal Disorders Gastroesophageal Reflux (GERD) Primary factor causing GERD incompetent lower esophageal sphincter (LES) Other factors causing GERD Delayed gastric emptying Impaired esophageal motility Decrease LES pressure (ex: alcohol, chocolate, drugs, fatty foods, nicotine, peppermint, caffeine, smoking) CM: Pyrosis (most common), Dysphagia, CP, Regurgitation, dyspepsia, hoareseness, sore throat, dental erosion Complications: Barrett's esophagus (BE)- increases risk of throat cancer, ulcers, resp complications. DX: Based on symptoms & response to drugs, endoscopy TX: Lifestyle changes is most effective, smoking cessation, weight loss, PPI's & H2 inhibitors, Nissen fundoplication to tighten LES Peptic Ulcer Disease (PUD) Erosion of the GI mucosal tract by HCl and pepsin Types of PUD ○ Acute ulcer § Superficial erosion and minimal inflammation § Short duration and resolves quickly when the cause is removed ○ Chronic ulcer § Eroding through the muscular wall and formation of fibrous tissue § Long duration and present continuously for many months or intermittently through person’s lifetime § More common than acute ○ Location of ulcer § Gastric: more prevalent in women over the age of 50, occur most often in the antrum, mortality higher § Duodenal: 80 % of all peptic ulcers, incidence higher between 35 and 45 years of age, first 1-2cm of duodenum increased by stress due to increase in acid Causes: H. Pylori, NSAIDs, Stress, smoking, alcohol CM: ○ Gastric Ulcer Discomfort 1-2 hours after meal high in the epigastrium Pain described as burning or gaseous Food tends to worsen the pain ○ Duodenal Ulcer Discomfort 2-5 hours after meals and midmorning, midafternoon, middle of the night across midepgastrium May have back pain Pain described as burning or cramp-like Periodic and episodic pain ○ Other manifestations Nausea, vomiting and feelings of fullness ○ Complications are hemorrhage or perforation, obstruction DX: Biopsy is gold standard to confirm is H. pylori is the cause TX: Antibiotics if H. pylori infection, typically combination therapy. 2!!!! ○ Either: § PPIs § H2 receptor blockers § Bismuth medication: Like pepto. Lifestyle changes Appendicitis Inflammation of the appendix Common cause is obstruction of the lumen by a fecalith Obstruction leads to distension, venous engorgement, and accumulation of mucus and bacteria which can lead to gangrene, perforation and peritonitis= BAD! Sepsis then die. CM: Dull pain followed by n/v, persistent pain in the RLQ, fever, muscle guarding, rebound tenderness. DX: CT scan: non-contrast, McBurney’s Point: halfway between the umbilicus and right iliac crest NN: keep them NPO, antibiotics, get them to surgery Gastroenteritis Inflammation of the mucosa of the stomach and small intestine Viruses are the most common cause Norovirus: foodborne Other causes, bacterial, parasites Clinical Manifestations Sudden diarrhea accompanied by nausea, vomiting, fever and abdominal cramping Self-limiting Conservative treatment Oral fluid replacements: Frequent small sips Antidiarrheal agents short-term use Diverticulitis Inflammation of 1 or more diverticula Diverticula Saccular dilations or outpouchings of the mucosa Diverticulosis Multiple noninflamed diverticula Etiology and Pathophysiology Common in the left descending and sigmoid colon High fiber diets, avoid nuts/corn CM: Left lower quadrant pain, abdominal distension, decrease or absent bowel sounds, nausea, vomiting, and systemic symptoms of infection (fever and leukocytosis with a shift to the left) DX: CT scan with oral contrast TX: managed at home, antibiotic therapy, high fiber diet! Ulcerative Colitis (Colon Only, continuous) Crohn’s Disease (any part of the GI tract- mouth to anus, bad spots/good spots) No known cause: may be autoimmune, genetic, lifestyle Risk Factors Smoking, stress, high intake of refined sugar, total fats and eating fewer raw fruits, vegetables and dietary fiber CM: Crohn’s Abdominal pain that is cramping Watery diarrhea Fever Weight loss Cobblestoning of the mucosa Entire thickness of the bowel wall is involved with areas of health tissue (skip lesions) Perianal abscess, fistulas, and strictures Ulcerative Abdominal pain that is severe constant Bloody diarrhea Fever during acute attacks Mucosa of the bowel is involved that is continuous Pseudopolyps Toxic megacolon DX: CBC, Imaging, H&P TX: no cure, nutrition & lifestyle changes, Drug therapy, surgical Aminosalicylates: Decrease inflammation by suppressing cytokine storms Antimicrobials: prevent secondary infection Corticosteroids: Decrease inflammation. Immunomodulators: Suppress immune response. Biologic: Help prevent flares by decreasing immune response Celiac Disease Autoimmune disease that causes damage to the small intestinal mucosa CM: Foul-smelling diarrhea, steatorrhea (excessively large, pale, oily, frothy stools) abdominal pain, flatulence, abdominal distension, and malnutrition DX: H&P, histological evidence is gold standard. TX: Gluten free diet: most likely the rest of their lives Bone density screening every 2 to 3 years Foods to avoid Barley, wheat, flour, oats, pasta, rye, cookies, cakes, pies, CAN EAT corn Short Bowel Syndrome Condition in which the small intestine does not have enough surface are to absorb nutrients Causes: Surgical removal of too much small intestines and congenital defects Clinical Manifestations: Dehydration, weight loss, diarrhea, vitamin deficiencies and electrolyte imbalances, abdominal pain, flatulence, and steatorrhea TX: Fl and electrolytes, nutrition, bowel resection, dietician, antidiarrheal. Hirschsprung Disease (Congenital Aganglionic Megacolon) Congenital anomaly resulting in mechanical obstruction from inadequate motility Absence of ganglion cells in the affected area resulting in loss of rectosphincteric reflex CM: Abdominal distention, constipation: Short and diarrhea: long, not passing meconium. DX: H&P, biopsy confirms dx TX: surgery to remove aganglionic portion of bowel. NN: May need colostomy (self-esteem issues in teens), meticulous skin care Hypertrophic Pyloric Stenosis Occurs when the circumferential muscle of the pyloric sphincter becomes thickened resulting in elongation and narrowing of the pyloric canal. Cm: Nonbilious vomiting in the early stages: everything they eat, they projectile vomit 80% of what they just ate, not getting digested. Gastric peristalsis may be visible on examination and an olive-shaped mass may be palpated in the epigastrium just to the right of the umbilicus DX: H&P, ultrasound TX: Pyloromyotomy Intussusception Most common cause of intestinal obstruction in children between 3 months and 6 years old Cause unknown Proximal segment of bowel telescopes into a more distal segment pulling the mesentery with it CM: Bilious vomiting and lethargy Passage of red, currant jelly like stools Tender and distended abdomen Palpable sausage shaped mass in upper right quadrant DX: ultrasound TX: gas enema, surgery Last module: Disorders of the Integumentary System which safe sun practices would be included in teaching plan for pt who has photosensitivity: avoid exposure 10am-2pm, greater than 15 SPF, apply sunscreen often and after swimming Drugs that cause photosensitivity: antibiotics such as tetracycline, doxycycline, diuretics such as lasix, hctz, and antidepressants such as amitriptyline, Effexor Skin Cancer is the most diagnosed cancer. Risk factors: fair skin, blonde hair blue eyes, sunbathing or tanning beds, outdoor occupation, near the equator, family history Actinic keratosis (Nonmelanoma) Also known as solar keratosis, Precancerous skin lesions Clinical Manifestations Irregularly shaped, flat, slightly erythematous, indistinct borders with overlying hard scale or horn Treatment and Prognosis Cryosurgery Topical application of fluorouracil Biopsy Basal Cell Carcinoma (Nonmelanoma) Locally invasive cancer arising from the epidermal basal cells Most common type of skin cancer, the least deadly Most occur in the head and neck (sun-exposed areas) Clinical Manifestations Nodular and Ulcerative ○ Small, slowly enlarging papule ○ Borders are semitranslucent or “pearly” with overlying telangiectasia Erosion, ulceration, and depression of the center (Ulcerative) Superficial Erythematous, pearly, sharply defined, barely elevated plaques Treatment and Prognosis Surgical excision with biopsy, cryosurgery, radiation therapy Fluorouracil and imiquimod for non invasive Slow-growing tumor that invades local tissue Metastasis rare, High cure rate Squamous Cell Carcinoma Squamous Cell Carcinoma (Nonmelanoma) Arising from the keratinizing epidermal cells Aggressive and has the potential to metastasize Most common on sun-exposed areas of hands and face Clinical Manifestations Superficial ○ Thin, scaly erythematous plaque without invasion into the dermis Early ○ Firm nodules with indistinct borders, scaling and ulceration Late ○ Covering of lesion with scale or horn from keratinization, ulceration Treatment and Prognosis Surgical excision with biopsy, cryosurgery, radiation therapy Fluorouracil and imiquimod for non invasive High cure rate with early detection and treatment Skin Cancer Melanoma Clinical Manifestations Use ABCDE ○ A-Asymmetry – one half unlike the other half ○ B-Border – irregular border, edges are ragged, notched or blurred; flat or elevated; eroded or ulcerated ○ C-Color – varied pigmentation; shades of tan, brown, black, gray or white ○ D-Diameter – 6 mm or more ○ Evolving – changing appearance over time Treatment and Prognosis Surgical excision with biopsy and possible lymph node evaluation Adjuvant therapy Poor prognosis unless diagnosed and treated early Spreading by local extension, regional lymphatic vessels and bloodstream Cellulitis Inflammation of the subcutaneous tissue Can be caused by staphylococcus aureus and streptococci Clinical Manifestations ○ Hot, tender, erythematous and edematous area with diffuse borders ○ Chills, malaise, and fever Treatment and Prognosis ○ Topical § Moist heat, immobilization and elevation of the area ○ Systemic Manifestations § Systemic antibiotic therapy § Hospitalization § Complications to gangrene if untreated Impetigo A bacterial infection due to an imbalance between host and microorganism change ○ Staphylococcus aureus ○ Group A beta-hemolytic streptococci Associated with bad hygiene and contagious Clinical Manifestations ○ Pruritic, vesiculopustular lesions, thick, honey-colored crust surrounded by erythema most common on face Treatment and Prognosis ○ Topical § Warm saline soaks followed by soap and water removal of crusts § Application of topical antibiotics such as mupirocin ○ Systemic manifestations § Oral antibiotics such as cephalosporins and amoxicillin Pediculosis Head-lice CM: pruritis, nits and eggs attached to hair shaft TX: Permethrin cream, manual removal, wash all clothing and linens Scabies Mite that penetrates stratum corneum and deposit eggs Allergic reaction to eggs, feces, and mite parts causes inflammatory response intense itching at night can indicate what type of mite infestation Clinical manifestations ○ Severe itching, especially at night ○ Presence of burrows especially interdigital webs, flexor surfaces of wrists, genitalia and anterior axillary folds ○ Erythematous papules, possible vesiculation, interdigital web crusting Treatment and Prognosis ○ 5% permethrin topical lotion overnight with 2nd application after 1 week Allergic Conditions of Skin: Dermatitis ○ Absorbed agent acts as an antigen ○ Sensitization occurs after one or more exposures ○ Appearance of lesions 2-7 days after contact with allergen Clinical Manifestations Red papules and plaques Sharply circumscribed with occasional vesicles Usually pruritic and area of dermatitis often take shapes of causative agent Treatment and Prognosis Avoid causative agent Topical or oral corticosteroids Psoriasis Autoimmune chronic dermatitis that involves extremely rapid turnover of epidermal cells defined plaques covered with silvery scales Clinical Manifestations Sharply demarcated silvery scaling plaques on reddish skin, Pruritis, Burning, pain Often located on the scalp, elbows, knees and can be localized, generalized, intermittent or continuous Treatment and Prognosis No cure, but control is possible Topical treatment ○ Corticosteroids and immunomodulators Systemic treatment ○ Natural or artificial UVB ○ Immunosuppressant and Biologic