Candy Final Exam PDF

Pathophysiology Final Exam 12/16 10:15 am 70 Questions, 2 hours, Matching columns, 4 select all that apply Benign versus malignant Benign Tumors Malignant Tumors - Well-differentiated; resembles tissue - Range...

Pathophysiology Final Exam 12/16 10:15 am 70 Questions, 2 hours, Matching columns, 4 select all that apply Benign versus malignant Benign Tumors Malignant Tumors - Well-differentiated; resembles tissue - Range from well-differentiated to of origin poorly differentiated. Poorly - Rate of Growth: progressive, slow differentiated; does not resemble - Remain localized: Cohesive cells, tissue of origin well-demarcated from surrounding - Rate of Growth: Erratic, slow tissue - Invasive and infiltrating/destructive - Not invasive, does not destroy to surrounding normal tissue surrounding tissue, and do not break - Lack adhesion to the tumor mass and away or travel from the tumor cell easily break free to travel to distant mass sites in a process called metastasis. - No metastasis - Travel via the lymphatic system or bloodstream - Frequent metastasis Malignant tumors can be staged Stage I: localized Stage II: Early locally advanced Stage III: late locally advanced Stage IV: Metastasized (to another area) Apoptosis Genetically programmed degenerative change that results in cell death - Example: Ovaries undergo apoptosis in female age 55 (menopause) - Example: WBCs undergo apoptosis after their participation in an inflammatory reaction Failure in Apoptosis - Give rise to certain cancers, tumors, and detrimental hyperplastic cell changes - Example: Prostate cancer is theorized to arise from cells that lose their apoptotic function Excessive Apoptosis  - Some disorders are associated with increased cellular apoptosis, which results in excessive cell death rates. - Example: Certain degenerative neurological diseases, such as spinal muscular atrophy, are thought to arise from nerve cells that undergo increased apoptotic rates and, consequently, die prematurely. Changes in the cell Atrophy: A decrease or shrinkage in size - Disuse or diminished workload. Lack of nerve stimulation (paralysis) - Loss of hormonal stimulation. Inadequate nutrition. Decrease blood flow (ischemia), Aging Muscle Hypertrophy: Increase in cell size - Example: The heart hypertrophies in response to hypertension (greater workload because of greater peripheral resistance) - Example: Weightlifters develop hypertrophied muscles because of increase workload and use *Hypertrophy: An increase in size usually due to an increased workload (ventricular hypertrophy) Changes in cell growth *Hyperplasia: Increase in the number of cells - May be compensatory, hormonal or pathologic - Examples: BPH (Benign Prostate hypertrophy), Gingival hyperplasia -> causes: pregnancy, medication, strength trainers Metaplasia: Reversible replacement of one type of cell with another in response to injury - Example: Barrett’s Esophagus: In the esophagitis, the cells of the lower esophagus change to be able to cope with the stomach acid that constantly irritates the cells in GERD -> replacement of the normal stratified squamous epithelium lining of the esophagus by simple columnar epithelium with goblet cells Dysplasia : Abnormal changes in size, shape and organization of mature cells - May be irreversible - Disorder cells, cells that have lost normal architectural arrangement: a PRECANCEROUS condition - A chronic stressor in the cell environment like (carcinogen) can be a cause - Must be watch carefully because very often will develop in NEOPLASIA Neoplasia: New growth - Malignant or benign - Keep dividing uncontrollably -> Lack normal cell function; they do not work  - Lack adhesiveness to other cells (malignant cancer cells break away and travel) - Invasive and destructive to surrounding cells - Abnormal structure and architecture - Secretes inappropriate enzymes, hormones, clotting substances, tumor angiogenesis factor Anaplasia : Poor cellular differentiation - Reversion of cells to simpler and less differentiated form - Hallmark of malignant cells - Not reversible - genetic damage has occurred to cells 1st week first 10 slides vocab definitions: role of nurse, s&s Pathophysiology: - study of disease process *Roles of the nurse: - Prevention of disease: Advocate for the patient. Early case findings. Minimizing impact of illness. Promoting healing and preventing more problems. Maximizing patients potential *Sign: - Objective and measurable. Something I can detect even if the patient is unconscious *Symptom - What the patient is feeling. Something only the patient knows about Pathogenesis - The sequence of cellular and tissue events that take place from the time of initial contact with an etiologic agent until the ultimate expression of a disease. Describes how the disease process evolves Etiology - What sets the disease process in motion Idiopathic - When cause and effect is unknown Risk Factors - The contributions that increase the chance that a certain disease will occur. Common risk: age, alcohol, drug abuse, ethnicity, smoking, exposure Disease - interruption, cessation or disorder of a body system or organ structure. Abnormal functioning occurs - “disease, then, is something an organ has” Illness:  - comes with having a disease, it is the subjective experience - “illness is something a man has” Prognosis - prediction about the outcome of a disease. It is all contingent upon disease, patient factors, environment, resources, ect. Sequelae (Plural for sequela) - Subsequent injuries related to the disease process Complications: new problems in addition to the original disease process CDC: stands for centers for disease control and prevention Morbidity: is the # of ill per 100,00 Mortality: is the # who died per 100,00 Incidence: # of new cases Epidemic: rapid increase in incidence noted - located in a certain area Ex: Ebola, Zika, HIV outbreak… Stages of Disease and Illness Sub-clinical or preclinical: stage where the disease is present, but the patient is unaware *Prodromal stage: vague and non specific manifestations. The patient may feel that something is wrong, but the specific disease is not fully manifest Clinical stage : The disease is evident and identifiable. A diagnosis is clear Fetal alcohol syndrome - Alcohol is a teratogen throughout all of pregnancy - Infants with FAS are born with retarded physical growth, intellectual disabilities cardiac defects, and musculoskeletal abnormalities - Born smaller than normal in length, weight, and head circumference - Facial abnormalities may not be present in all children with FAS, but thin upper lips, a flat midface, a low nasal bridge, a short upturned nose, and an elongated philtrum (space between the nose and lips) - Children with FAS have lifelong health problems with failure to thrive, poor coordination, and low cognitive skills. Inflammation Chapter Specific versus Nonspecific Immunity  Specific Immunity (adaptive immune Nonspecific Immunity (Innate immune system) system) - Final line of defense Nonspecific immunity is composed of successive - Effective against a certain lines of defense. agent only The first line of defense: - Involves B cells (which - Barriers (Skin, mucous membranes, produce antibodies) and T body secretions) cells (which destroy infected - Body reflexes (sneezing, Coughing, cells or help coordinate the Vomiting, Diarrhea) immune response) Second line of defense: Internal nonspecific responses - Inflammatory reaction: Heat, redness, swelling, pain Cells release histamine, Leukocytes enter tissue(Granulocytes, macrophages, mast cells), Leukocytes and plasma produce, inflammatory exudate, Pus is produced, Lymph nodes enlarge - Phagocytosis: White blood cells take in and destroy waste and foreign material ( Neutrophils, Macrophages) - Natural Killer Cells (NK) : Type of lymphocyte found in lymph nodes, spleen, bone marrow, blood. Recognizes body cells with abnormal membranes and secretes protein that breaks down cell membranes. Natural vs. Passive immunity Natural - Active: Contact with the disease - Passive: Placenta, Mother's milk Artificial - Active: Vaccine: Killed, Attenuated, Toxoid, Componented, Recombinant DNA - Passive: Immune Serum Shift to the left An elevated WBC count indicates an acute inflammatory process is occurring - When a high number of bands(immature neutrophils) are present, clinician often use the phase “shift to the left,” indicating an increase in newly formed neutrophils What is Autoimmune disease Occurs when the body’s immune system mistakenly attacks its own healthy cell, tissues, or organs. (antibodies against its own tissues) - These autoantibodies trigger inflammation in organs. In the endocrine system, autoimmunity can cause either hypofunction or hyperfunction of the gland. Hypofunction - HIV, hypothyroidism (underactive thyroid), Addison’s disease (adrenal insufficiency), or type 1 diabetes (where the immune system attacks the insulin-producing cells in the pancreas) Hasimoto’s Disease (immune system produces autoantibodies that attacks the thyroid gland) Hyperfunction - Graves' disease (where the immune system stimulates the thyroid, leading to hyperthyroidism) Cushing Disease (secondary) Cushing's SYNDROME (PRIMARY Cushing's DISEASE hyperadrenalism) SECONDARY Def: endocrine disorder causing excessive cortisol Def: tumor on pituitary producing excessive ACTH secretion (steroids) secretion → excessive cortisol Occurs from: - Adrenal adenoma, carcinoma, hyperplasia - ACTH secretion from lung tumors or other cancers - Exogenous steroid administrations Signs & Symptoms: Weight apple, apple shaped fat distribution, moon face & hump, stretch marks, hirsutism, easy bruising, poor wound healing, skin ulcers, osteoporosis - Effects of High Cortisol Levels (BIHI) - Insulin resistance: Leads to glucose intolerance and hyperglycemia (high blood sugar). - Bone problems: Inhibits bone formation, leading to osteopenia and osteoporosis. - Immunosuppression: Weakens the immune system, increasing the risk of infections. - Hypertension: High cortisol can lead to high blood pressure. Diagnosis Dexamethasone Suppression Test & Salivary Cortisol Test Cardinal signs of Inflammation (RHELP) Redness (Rubor) Heat (Calor) Edema (tumor) Loss of function (Functio laesa) Pain (Dolor) Lab Tests Indicative of Inflammation C-reactive protein (CRP)- determines presence of inflammation Erythrocyte sedimentation rate (ESR)- measure of the rate of sedimentation of RBCs over a Calor specified period of time. CBC with differential to assess for leukocytosis (high WBC count) Persons Enduring Acute Inflammation Experience Systemic Responses Fever, Pain, General malaise (a general feeling of poor health), Lymphadenopathy (swollen lymph nodes), Anorexia, Sleepiness, Lethargy, Anemia, Weight loss Inflammatory The purpose of the inflammatory response is to prepare the injured area for healing. This requires: 1. Leukocytes (neutrophils & macrophages) to remove debris and provide growth factors. 2. Nutrients (proteins, glucose, vitamins) provide the building blocks for cells. 3. Clotting factors and platelets to limit damage. Electrolytes main function: K Potassium, Na Sodium, Calcium and magnesium (matching) CL Sodium (Na+) Potassium (K+) Calcium (Ca+) Magnesium (Mg+) Norm 135-145 mEq/L 3.5-5.0 mEq/L 8.5 – 10.5 mg/dL (total) 1.6- 3.0 mEqL al Range 4.5 – 5.6 mg/dL (ionized) Target Brain Heart Skeletal muscles Heart Organ Regul 1. Kidneys Kidneys Thyroid (Calcitonin) & Kidney ating 2. GI parathyroid Organ 3. Skin Main Fluid & electrolyte Smooth muscle & heart Bone development Maintain intracellular Functi Regulation electrical K on contractions Blood clotting Enzyme reactions Smooth muscle contraction Protein & DNA synthesis Most foods & some Bananas Dairy products Legumes Foods meds Orange Green leafy vegetables Nuts Salts, bacon,cheese Alvocado Juice Lentils Raisins Potatoes Interc K+ Na+ Mg+ Ca+ hange able & phosphate B/c compete for the binding Relati sights onshi p w/ When one is high other is low Notes *MOST ABUNDANT Hypocalcemia: Excessive = decrease AND IMPORTANT *Paresthesias around muscle ELECTROLYTE the mouth, hands, and Deficient = increase feet muscle Prisoner of the cell → stays inside cell *Muscle spasms – ***Vitamin D majority of time Trousseau (hand) & facilitates the Chvostek (face) absorption of calcium  Laryngeal spasm, Tetany, Seizures, Hypotension, Arrhythmias – particularly heart block and V fib Chronic hypocalcemia causes bone pain and fragility, dry skin and hair, cataracts, depression, and dementia. Ketosis, forming ketones Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes that occurs when the body doesn't have enough insulin to use blood sugar for energy - Ketosis or ketoacidosis is a metabolic process that occurs when the body breaks down fat for energy instead of carbohydrates, resulting in a buildup of ketones. - Ketones are water-soluble molecules produced by the liver when there's not enough glucose to fuel the brain - If urine is positive for ketones, the body is burning fat - Ketone body odor – fruity odor - Ketosis = ketone accumulation in the blood - Occurs bc fatty acids accumulate then converts to ketones - Cells start burning fat instead of glucose (think keto diet) - DKA = when there’s no glucose entering the cells bc of either (1) lack of insulin or (2) insulin resistance → cells go into starvation mode → life threatening condition in T1DM Causes of Diabetes Type 1 and 2 Gestational Type 1 Type 2 Any degree of glucose (autoimmune reaction) Cellular insulin resistance → intolerance that occurs during immunological destruction of pancreas overworks to pregnancy ONLY insulin-secreting beta cells compensate to produce more within islets of Langherans of insulin → pancreas is exhausted pancreas. Happens early in life. Placenta with hormones (Immune Mediated) working in opposition to insulin. Cells are insensitive to insulin All women get screened during 90% of T1DM pts have the effects & don’t allow glucose to the second trimester. immune mediate form enter Greater adiposity ⇒ greater insulin resistance Polydipsia (excessive thirst), DKA is often the 1st sign & only Polyuria (excessive urination), occurs in T1DM Polyphagia (increased appetite) Chronic high sugar Hyperosmolar hyperglycemia NO DKA What is Hypoglycemia - Low levels of glucose ( acidotic If pH is greater than 7.45 -> alkalotic **ROME** Respiratory acidosis Respiratory alkalosis pH < 7.35 6 pH > 7.45 PCO2 > 45 PCO2 < 35 Low pH, High CO2 High pH, Low CO2 Metabolic acidosis Metabolic alkalosis pH < 7.35 pH > 7.45 HCO3- < 22 HCO3- > 26 Low pH, Low bicarb (HCO3) High pH, High bicarb Respiratory Acidosis Respiratory Alkalosis Etiology failure of the respiratory system to loss of CO2 from lungs faster than is remove or exhale CO2 as fast as it is produced by cells produced by cells Causes any interference with breathing breathing too fast (anxiety, (ex: COPD, asthma, respiratory hyperventilation, pneumonia) muscle weakness/depression, suffocation) Lab Results PCO2 > 45 mm Hg PCO2 < 35 mm Hg Blood pH < 7.35 Blood pH > 7.45 Patients @ Risk *COPD Anxiety Emphysema Physical exercise Pneumonia Fear Apnea Pneumonia  Atelectasis (collapsed parts of the lungs) Clinical Cyanosis Lightheaded (faint) manifestations Shallow or labored breathing Paresthesias Disorientation Altered consciousness Dysrhythmias muscle spasms Compensation Kidneys attempt to REABSORB Kidneys attempt to REABSORB HCO3- (base) and EXCRETE H+ (acid) maximum H+ and EXCRETE HCO3- Medical (1) Intubation (2) Mechanical Administer sedative & rebreathing Intervention ventilation to increase RR to mask to decrease RR to increase CO2 decrease CO2 Metabolic Acidosis Metabolic Alkalosis Etiology an abnormal accumulation of results from a loss of H+ or an addition acids OR abnormal loss of bases of base to body fluid Causes lactic acidosis, ketoacidosis of Vomiting, of excess gastric acid diabetes, renal failure --> acid Postcode excess bicarb iv waste buildup Excess bicarb ingestion diarrhea with loss of bicarb Lab Results Arterial pH < 7.35 Arterial pH > 7.45 Bicarb < 22 Bicarb > 26 Patients @ Risk Diarrhea Severe vomiting Renal failure Excessive GI suctioning Shock Diuretics Diabetic ketoacidosis Excessive NaHCO3 Clinical Kussmaul’s breathing (deep rapid Lightheaded (faint) manifestations respirations Paresthesias Disorientation, coma Dysrhythmias Dysrhythmias Hypokalemia Hypotension Compensation Lungs increase RR to blow off CO2 Lungs decrease RR to hold CO2 Medical IV bicarb IV NS or IV DIAMOX --> excrete bicarb Intervention and retain K+ Administer KCL or mild acidic IV solution Compensation - An imbalance of pH caused by one system will be made up for by another system after a period of time. - Respiratory(lungs) will assist to regulate metabolic imbalance. - Metabolic(kidney) will assist to regulate respiratory imbalance - If pH is too low in metabolic acidosis, the respiratory center increases the rate of respirations by “blowing off” CO2, which raises pH. - In metabolic alkalosis, the pH is too high: breathing slows, allowing CO2 to accumulate, and pH drops. How do you know the body is compensating? - If the pH is normal but the other levels are not normal than the body has compensated - If the value that is not in alignment with the pH is in the normal column, there is no compensation - Complete compensation = pH is normal. CO2 is abnormal. HCO3 is abnormal. What system would compensate for what system: Respiratory Acidosis Compensation - The kidneys will attempt to to reabsorb HCO3 and excrete H+ Respiratory Alkalosis Compensation - The kidneys will attempt to reabsorb maximum H+ and excrete HCO3- Metabolic Acidosis Compensation  - The lungs will try to blow off CO2 increasing respiratory rate; however, the lungs can increase the ventilatory rate so much Metabolic Alkalosis Compensation - The lungs attempt to retain CO2 by decreasing the rate of respiration; breathing is slowed Hyponatremia - Fewer than 135 mEq/L - Can occur in low blood volume; hypovolemic hyponatremia - Can occur in high blood volume; dilutional hyponatremia Recommended - low sodium diet consisted of fewer than 1,500mg of sodium per day for pt with hypertension and heart failure Symptoms: Headache, Lethargy, Apathy, Confusion, Nausea, Vomiting, abdominal cramping What is Diabetes Insipidus? What are patients at risk for? The body can't properly regulate water balance due to a lack of antidiuretic hormone (ADH) or the kidneys' inability to respond to it. This results in excessive diluted urination and extreme thirst. Risks for Patients: - Dehydration due to excessive fluid loss, Electrolyte imbalances: low sodium (dry mouth, low blood pressure, and dizziness) - Low blood pressure (hypotension) - Polyuria – Large amounts of dilute urine. - Polydipsia – Persistent and intense thirst due to dehydration. - Hypernatremia – which can cause confusion, agitation, or even seizures. Signs and symptoms polyarthritis - 5+ joints are affected by arthritis at the same time. - Joint pain, Stiffness, Swelling, Warmth or redness, Decreased range of motion, Tenderness near a joint - Increase WBC in urine - Blood in urine - Pain Risk factors for heart disease - Female (pst menopause) and males  - Old (65+ yr old) - Family history & genetics - African American - Obese - Diabetes - Ischemic hewart disease - HTN - Life style: smoking, drinking, stress, physical activity Most common signs and symptoms Myocardial infarction - Diaphoresis - Dyspnea - Extreme anxiety - Levine’s sign (fist to chest) - Pallor - Retrosternal crushing chest pain that radiates to shoulder, arm, jaw, or back - Weak pulses S&S left vs right side heart failure Left Right - Dyspnea & Orthopnea - Jugular vein distension ( JVD) - Cough - Ascites - Crackles in the lungs - Hepatosplenomegaly (enlarged spleen - Paroxysmal nocturnal dyspnea & liver) - Ankle or sacral edema aortic aneurysm - First manifestation of an aortic aneurysm is a pulsatile mass - HTN weakens the walls of the arteries, which increase development of bulges in the arterial walls - Cause turbulent blood flow and then may rupture - You can hear brewery over the aneurysm Role of Cortisol  - Cortisol is released when the body experiences stress, "stress hormone" Process for wound healing ***Stages of wound Healing (matching questions) Hemostasis - initial response - bleeding - clot - vasoconstriction, platelet aggregation, leukocyte migration Inflammation - usually last up to 5 days- neutrophil, chemoattractant release, Proliferation and New Tissue Formation - week until maximum strength achieved. May involve regeneration or repair with scar tissue but loss of function Wound Contraction and Remodeling can take up to 2 years Factors Affecting Healing Oxygenation - reduced in COPD, atherosclerosis Circulation - reduced in elderly, CHF, DM, MI Hydration Status - reduced in illness Nutrition - Albumin (protein) Age - accelerated in young, reduced in elderly Immunity - reduced in immunocompromised patient, infection, stress Medications - cortisone, chemotherapy Wound Healing Processes Occur simultaneously 1. Macrophages - dissolve clots, clear debris, add a) TGF-B: (Transforming Growth Factors-Beta) stimulates collagen precursor procollagen b) VEGF: (Vascular Endothelial Growth Factor) stimulates angiogenesis c) MMPs: (Matrix Metalloproteinases) remodel collagen and fibrin 2. Collagen lattice forms 3. Granulation tissue fills in wound 4. Hypertrophic scar tissue overfills the wound 5. Cicatrization (maturation) of the wound may take 1-2 years. Collagen contracts and the scar becomes lighter and smoother. Primary Intention - A clean laceration that requires simple re-epithelialization when edges are approximated - No gap in the tissue - Example: surgical laceration Secondary Intention - A wound with a large gap in tissue; some of the tissue has been gouged out - Prolonged healing involving generation of granulation tissue - Example: decubitus ulcer Tertiary Intention - A wound with a large gap of missing tissue that has been contaminated and needs a drainage tube while healing - Sometimes called delayed primary intention - It is a combination of primary and secondary closure. This type of closure is often preferred when a wound is heavily contaminated to reduce the risk of the wound becoming infected. The wound is cleansed and is watched closely for several days. When the wound appears to be clean and on its way to healing, it is closed surgically. When there is tissue loss, such as might occur in an avulsion injury (portion of the skin and sometimes other soft tissue is partially or completely torn away), wound closure is often delayed to control wound debris and necrotic tissue. Certain types of injuries almost always become infected (i.e. dog bite injuries); these types of injuries are frequently left open and are closed only when infection is controlled Labile Cells - Labile cells continually divide and replicate throughout life, replacing cells that are constantly eliminated. Examples - Skin, hair, nails, oral mucosal cells, gastrointestinal mucosal lining cells, and genitourinary mucous membrane cells: in addition, bone marrow is continuously active as it synthesizes blood cells. - Cancers cells are considered labile cells because they are constantly dividing Stable Cells - Stable cells are cells that are in resting stage until stimulated, when they then enter the cell cycle Examples - bone cells and hepatocytes. Both kinds of cells require major stimuli to enter the cell cycle, undergo mitosis, and regenerate Permanent Cells - Permanent cells cannot regenerate and therefore do not enter the cell cycle - Neurons and cardiac myocytes are considered permanent cels that do not undergo mitosis and have lost the ability to proliferate - Adult “stem cells” can be stimulated to regenerate permanent cells Possible Complications of Wound Healing - Keloid: hyperplasia of scar tissue  - Contractures: inflexible shrinkage of wound tissue that pulls the edges toward the center of the wound - Dehiscence: opening of a wound’s suture line - Evisceration: opening of wound with extrusion of tissue and organs - Stricture: an abnormal narrowing of a tubular body passage from the formation of scar tissue - Fistula: an abnormal connection between two epithelium-lined organs or vessels - Adhesions: internal scar tissue between tissues or organs Dysfunction during Inflammation - Hemorrhage - Fibrous adhesions - Decreased blood volume - Lack of nutrients, Infection Signs and symptoms for infection in wound Wounds may become infected and more tissue damage may result - Abscess – a walled off pocket of infection - Sinus tract – a narrow tunnel forms - Cellulitis - infection - Necrosis and gangrene may occur Role of the Macrophage - Ingest and destroy foreign material, such as pathogens, dead cells, and debris - In chronic inflammation, macrophages can aggregate to form a granuloma, which is a cluster of macrophages that transform into epithelioid cells (macrophages that resemble epithelial cells). These epithelioid cells are surrounded by lymphocytes, fibroblasts, and connective tissue. This structure forms as part of the body's attempt to contain and isolate foreign substances that cannot be easily removed. Lymphatic organs functions, focus on thymus - Thymus Produce and mature T lymphocytes (T cells), which are crucial white blood cells that play a vital role in the immune system by identifying and fighting off foreign invaders like bacteria and viruses - The thymus, located in the mediastinum, is where immature T lymphocytes travel from the bone marrow to the outer cortex. Here, they mature and divide, protected from blood antigens. As they move toward the medulla, they interact with other lymphoid cells, learning to distinguish between self and foreign cells. Once trained, they are released into the bloodstream. - The tissues and organs of the lymphatic system—the lymph nodes, thymus, tonsils, spleen, and red bone marrow—produce various cells to produce the immune response. Primary versus secondary lymphoid tissue Primary Lymphoid Tissue - Bone marrow: produces WBC, RBC and platelets, B cells mature here - Thymus: matures T cells Secondary lymphoid Tissues - Lymph nodes: filter and fight bacteria - Spleen: stores WBCs and RBCs - Lymphoid tissue: protects membranes – Tonsils - Peyer’s patch Functions of the spleen - Highly vascular organ, the “graveyard of RBCs” and an organ of immunity. - It sequesters abnormally shaped and hemolyzed RBCs and destroys them. - Splenomegaly occurs when there is a large amount of RBC breakdown occurring in the body - The spleen removes aged, lysed, and dead RBCs from circulation. - In the spleen, RBCs are broken down into their component parts, which are recycled to make new RBCs. Alarm Stage of Stress - Body's immediate response to stress, often referred to as the "fight or flight" response. - When you encounter a stressor, your body releases hormones like adrenaline and cortisol to prepare you for action Sympathetic nervous system - The body releases norepinephrine which triggers increased heart rate and blood pressure. Hormonal Responses - The brain releases corticotropin-releasing hormone (CRH). - This stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH). - ACTH then prompts the adrenal glands to release epinephrine (adrenaline), cortisol, and aldosterone. Posterior Pituitary: The posterior pituitary releases antidiuretic hormone (ADH), which helps conserve water by reducing urine output. Wound healing - why would a person feel pain from injury A person feels pain from an injury because chemicals like histamine and prostaglandins are released at the wound site during the inflammatory response, which directly stimulate nerve endings, causing a pain sensation; essentially, these chemicals "signal" the body that there is damage, leading to the perception of pain. Why would someone develop a fever Caused by specific cytokines (endogenous pyrogens) to fighting off an infection Polycythemia  - a blood disorder that occurs when there are too many red blood cells in the body Pyelonephritis - Increase WBC in urine - Blood in urine - Pain over flank and kidney Lab test following a heart attack - potassium change , Troponin test - EKG, Damage to muscle Elevated white blood cell count - inflammatory response, such as an infection Roll of the hypothalamus during inflammation - hypothalamus plays a key role by releasing corticotropin-releasing hormone (CRH), which then signals the pituitary gland to release adrenocorticotropic hormone (ACTH), ultimately leading to the release of cortisol from the adrenal glands - a crucial part of the body's stress response to inflammation. ***End Result of All Theories of Pathophysiological Mechanism: Endothelial Injury - Regardless of the etiologic mechanism, chronic hyperglycemia in diabetes is known to cause endothelial injury which, in turn, activates inflammation. Inflammation brings WBCs, inflammatory mediators, and platelets to the site of endothelial injury. - Lipid and macrophage deposition within the injured area causes the eventual formation of foam cells, precursors to atherosclerotic plaque. - Simultaneously, in response to injury, endothelial membranes secrete endothelin. Endothelin inhibits arterial vasodilation and promotes vascular smooth muscle proliferation. This narrows the diameters of arterial vessels. ***HIGH BLOOD SUGAR - BODY PICKS UP AS INFLAMMATORY -> BODY HELPS BY SENDING WBC PLATELETS TO ENDOTHELIAL INJURY SITE -> LIPID AND MACROPHAGE DEPOSITION TURNS IN FOAM CELLS AND PLAQUE -> NARROWS Hepatitis A (internet searched definition; couldn’t find in ppts) Acute & highly contagious liver infection (causes inflammation) - preventable by vaccine - spreads from contaminated food or water, or contact with someone who is infected Absorption and Transport: virus absorbed in intestines>bloodstream>liver. Infection of Liver Cells: Once in liver, it infects liver cells and replicates Immune Response and Inflammation: The immune system detects the infected cells and responds to virus. This immune reaction causes inflammation and liver cell damage. Liver Dysfunction: The inflammation disrupts the liver's ability to process bilirubin, leading to jaundice Contact precautions Preventative cancer screening = early detection important! - Genetic screening - Get biopsy done Diagnosis of breast cancer - Histological examination of lymph nodes: Breast cancer staging is dependent on its spread to axillary lymph nodes & metastasis - Individuals w/ fam history of breast cancer should get genetic screening Purpose for cord blood samples “Who should be offered Prenatal screening” - Women 35 y/o > who’re pregnant or planning to become pregnant - Abnormal ultrasound findings - Couples who are close blood relatives, such as first cousins - Women who have a condition, such as diabetes, that can be associated with an increased risk of fetal problems - Ethnicity - Unexplained or multiple miscarriages - Family history of an inherited condition, intellectual disability, or birth defects Passive diffusion - Movement of water or air particles from high to low concentration without energy Prenatal testing (purpose of taking blood samples from umbilical cord) Tests include: 1. Chorionic villus sampling (CVS) 10 to 12 weeks  2. Amniocentesis 15 to 18 weeks 3. Ultrasound 4. Percutaneous umbilical cord blood sampling (PUBS): check baby’s health & diagnose genetic disorders Diagnosis of aortic valve on ultrasound or X-ray - An aortic valve is most accurately diagnosed using an ultrasound Aortic Sclerosis - Arteriosclerotic calcification of heart valves caused by aging is also common. - Caused by a narrowed, calcified aortic valve often presents as a new heart murmur in an aged adult. - Common cause of aortic stenosis Aortic Insufficiency - Aortic valve is thickened and shortened, which prevents proper closure during systole. - As a result, after the left ventricle pumps its blood volume into the aorta, there is backflow of blood into the left ventricle from the incompetent aortic valve. - When aortic insufficiency is severe, the regurgitant backflow of blood can cause volume overload in the left ventricle. - As left ventricular end-diastolic volume increases, the left ventricle become dilated and loses contractile ability; heart failure can then develop Cyanosis - A bluish coloration of the skin and mucous membranes caused by hypoxia (deficiency of oxygen)