Pathophysiology Notes PDF

Module 1: Introduction to Pathophysiology (Ch 1, 26) 1. Define pathophysiology and outline the need for the practical nurse to understand pathological processes (p.1) ➡ Pathophysiology: study of functional and physiological changes in the body related to disease processes ➡ Disease: deviation form...

Module 1: Introduction to Pathophysiology (Ch 1, 26) 1. Define pathophysiology and outline the need for the practical nurse to understand pathological processes (p.1) ➡ Pathophysiology: study of functional and physiological changes in the body related to disease processes ➡ Disease: deviation form the normal structure or function of any part, organ, system(s); deviation from state of well-being; develops when homeostasis cannot be maintained without intervention ➡ Implications for LPN -​ Be aware of new information, research, diagnostic tests, and therapies that are constantly emerging -​ Understanding pathology will help with informed clinical decision-making, assessment, planning and implementing care promptly -​ Patient education on treatment options, managing condition and modifications to lifestyle ​ 2. Identify and define the terms used to characterize a disease (p.6) Pathogenesis Development of disease; sequence of events involved in the TISSUE changes to the specific disease process Onset (of disease) A) ACUTE: Onset may be sudden and obvious Ex. vomiting, diarrhea, cramps B) INSIDIOUS: Gradual progression; vague and very mild signs Acute (disease) Short-term illness that develops quickly with marked Ex. Acute Appendicitis signs such as fever or severe pain Chronic (disease) Persists over a longer period of time; often milder and Ex. Rheumatoid arthritis gradually develops; often causes permanent tissue damage Subclinical state Pathological changes occur but patient presents no Ex. Kidney damage may obvious signs or manifestations (may be due to large progress to advanced renal reserve capacities of some organs) failure before symptoms are manifested Latent stage “Silent” stage; no clinical signs are evident; may be referred to as “incubation period” in infectious diseases Incubation period Time between exposure to the microorganism and the first appearance or onset of signs + symptoms; can last for one day or prolonged for days or weeks; disease may be communicable (infectious) during this period Prodromal period Early development of disease; changes are occuring in *Lab tests are negative during the body but the signs are non-specific (ex: fatigue, loss this period making it difficult to of appetite, headache) confirm diagnosis Manifestations (of disease) Clinical evidence/effects, signs + symptoms of disease; Local: redness, swelling, may be local (site of problem) or systemic (entire body) localized pain Systemic: fever (pyrexia), malaise, hypotension, tachycardia Signs Objective indicators of disease that are obvious and observable; may be local or systemic Symptoms Subjective feelings or statements made by the affected Ex: pain and nausea individual Lesion Describes a specific local change in the tissue; Microscopic: damaged liver microscopic or highly visible cells Visible: pimple, blister, Syndrome Collection of signs + symptoms; often affecting more than one organ and occurs together in response to a certain condition Diagnostic Tests Lab tests that assist in the diagnosis of a specific disease; may be used for monitoring the response to treatment or progress of disease Remission Period or condition in which the manifestations of the disease subside (permanently or temporarily) Exacerbation Worsening in the severity of the disease or in its signs + Ex. COVID exacerbating symptoms COPD Precipitating factor Conditions that triggers an acute episode Ex. Angina attack triggered by shoveling snow; seizures in epileptics; pollen worsens asthma Therapy Therapeutic interventions; treatment measures used to Ex. Surgeries, promote recovery or slow progress of the disease pharmacotherapy, PT, CBT, alternative medicine and therapies, pain management Sequelae Potential unwanted outcomes of the primary condition Ex. Paralysis following recovery from stroke Convalescence/rehabilitation Period of recovery and return to normal healthy state; may last for several days or months ➡ DISEASE PROGNOSIS (p. 7) Prognosis: the probability or likelihood for recovery or other outcomes Morbidity Disease rates within a group Mortality Relative number of deaths resulting from disease Autopsy Post-mortem examination; determines cause of death Epidemiology The study of tracking patterns and occurrence of disease Data collection centers (WHO, CDC) Occurrence of disease Tracked by two factors: Prevalence # > Incidence # 1.​ Incidence: # of new cases in given population within given time period 2.​ Prevalence: # of new, old, existing cases within a given population + time period Epidemics Higher number of expected cases of infectious disease within an area Pandemic Higher number of infectious diseases in many regions globally Communicable disease Infectious disease that can spread from person to person Notifiable/reportable disease Must be reported by physician to designated authorities; intended to prevent further spread of the disease 3. Outline common predisposing risk factors for disease (p. 6) ➡ Characteristics that make an individual more susceptible to developing a disease, disorder or health condition -​ Indicates a HIGH RISK for the disease but not certain development: Age Ex: Older adults more susceptible to osteoporosis due to age-related bone density loss Gender Ex: Men have higher risk for heart disease; women have higher risk for lupus Genetics Ex: Family history of breast cancer Lifestyle Ex: Smoking, drinking, poor nutritional habits, poor oral hygiene, sedentary lifestyle Medical conditions Ex: People with diabetes have higher risk of developing infections and delayed wound healing Environmental factors Ex: Exposure to air pollution can cause respiratory complications, asthma Socioeconomic factors Ex: Low income and limited access to healthcare services = untreated, poor health outcomes Stress Ex: Can predispose individuals to mental health disorders and hypertension 4. Explain the cellular adaptations most common in health disruption (p. 8) ➡ Cells can adapt their growth + differentiation to altered condition in the body: -​ Ex: increase in breast and uterine tissue during pregnancy (normal adaptations) -​ Reversible once stimuli is removed ➡ Tissues may be modified due to hormonal stimulation (pregnancy) or environmental stimuli (irritation) ➡ Disease develops when cell structure/function change + homeostasis cannot be maintained ➡ Irreversible changes in a cell signal a change in DNA structure or function ➡ Common (Abnormal) Cellular Growth Patterns (p. 9): Atrophy Decrease in SIZE of cells; ex: muscle atrophy = immobility issues Hypertrophy Increase in SIZE of cells; ex: pregnancy Hyperplasia Increase in NUMBER of cells Metaplasia One mature cell is REPLACED by a different mature cell type Dysplasia Increase in ABNORMAL cell growth; precancerous state Anaplasia Loss of differentiation + structure in cells; often seen in most malignant tumors Neoplasia “New growth” (malignancy) Neoplasm AKA TUMOR Two types of tumors: ➡ Benign: do not typically become cancerous; non life-threatening unless found in certain areas ➡ Malignant: cancerous 5. Explain the causes of cell injury (p. 10) ➡ Ischemia: decreased supply of oxygenated blood to tissues or organs (insufficient blood flow) -​ Leads to CELL DEATH  ➡ Hypoxia: reduced oxygen in the tissue -​ Interferes with ATP production -​ Brain, heart, kidneys are high demand + quickly affected ➡ Physical damage: excessive heat, cold, radiation ➡ Mechanical damage: pressure or tearing of tissue ➡ Chemical toxins: ➡ Exogenous: from environment ➡ Endogenous: from inside the body (ex. Ruptured appendix) ➡ Microorganisms: bacteria and viruses ➡ Abnormal metabolites: -​ Genetic disorders -​ Inborn errors of metabolism -​ Altered metabolism ➡ Nutritional deficits ➡ Imbalance of fluids or electrolytes 6. Describe the process of cell damage and necrosis (p. 10) ➡ Apoptosis: programmed cell death and normal occurrence in the body (may not affect surrounding cells) ➡ Pyroptosis: results in lysis, releasing lysosomal enzymes into tissue, causing nearby inflammation, damage and reduced function of cell ➡ Necrosis: AKA CELL DEATH -​ Group of cells die + cause further damage due to cell disintegration -​ Process of cell death varies with cause of damage: Liquefaction Necrosis Dead cells liquefy due to release of certain enzymes ➡ Occurs when brain tissue dies or certain bacterial infections Coagulative Necrosis Cell proteins are altered or denatured ➡ Typically occurs in heart attacks (cell death caused by ischemia) Coagulation, clotting, blockage Fat Necrosis Fatty tissue broken down into fatty acids in the presence of infection or certain enzymes ➡ May cause inflammation Caseous Necrosis Form of coagulation necrosis ➡ Thick, yellowish, “cheesy” substance forms ➡ Develops in tuberculosis (TB) Infarction Area of dead cells resulting from lack of oxygen = significant loss of function ➡ Less than 10 minutes before brain death ➡ Myocardial infarction AKA heart attack Gangrene Area of necrotic tissue that has been invaded by bacteria ➡ High risk for infections + diabetics ➡ Can be wet or dry (depending on location) ➡ WET GANGRENE: -​ Result of liquefaction causing tissue to be cold, swollen + black ➡ DRY GANGRENE: -​ Caused by coagulative necrosis where tissue dries, shrinks + blackens ➡ Two Stages of Cell Damage: 1.​ Initial cell damage: (Refer to Q5: ischemia, mechanical, physical, chemical etc.) -​ Functional changes + possibly reversible if damaging factor is able to be removed 2.​ Irreversible cell damage: -​ Cell death (necrosis, gangrene etc.)  -​ Cell swells + ruptures, membrane affected -​ Large number of cells dying = inflammation = enzymes -​ May undergo lysis; enzymes released from death cells diffuse into blood (helpful for blood work) -​ Nearby cells are damaged 7. Identify the difference between acute and chronic illnesses (p. 6) Acute Illness Chronic Illness ➡ Short-term illness that develops quickly ➡ Develops gradually + persists for a longer period of -​ Marked signs: high fever + severe pain time -​ Sudden + obvious onset -​ Typically milder -​ Vomiting, cramps, diarrhea -​ Can cause more permanent tissue damage -​ May involve intermittent acute episodes ➡ Ex. Acute appendicitis ➡ Ex. Rheumatoid arthritis 8. Analyze the impact stress has on health (p. 615) ➡ Stress: Occurs when individual’s status is altered by their reaction to stressor -​ Considered a precipitating + exacerbating factor for many chronic disorders ➡ Distress: If person cannot adapt/cope - harmful effects may result from stress ➡ Stress Response: Generalized or systemic response to a change (stressor) - internal or external -​ Homeostasis: Body’s compensation to minor changes in needs or environment -​ GAS = General Adaptive System = fight/flight response -​ Stressor: Factor that creates significant change in body function ➡ Three stages in STRESS RESPONSE (GAS/ General Adaptive System) (p. 616) 1.​ Alarm Stage ➡ Body’s defenses are immobilized by activation of: -​ Hypothalamus -​ Sympathetic nervous system -​ Adrenal glands 2.​ Resistance Stage ➡ Elevation of hormonal levels ➡ Peak operation of essential body systems 3.​ Exhaustion Stage ➡ Occurs when body is unable to respond further or damaged by increased demands ➡ SIGNIFICANT EFFECTS of Stress Response: -​ Bronchodilation + increased ventilation -​ Elevated BP + increased HR -​ Arousal of CNS -​ Decreased inflammatory + immune responses -​ Increased blood glucose levels: -​ Glycogenolysis -​ Gluconeogenesis (liver) -​ Protein catabolism (muscle) -​ Lipolysis ➡ Potential Effects of Prolonged Stress (p. 618) a)​ Renal failure: Prolonged severe VASOCONSTRICTION + ISCHEMIA causes cell damage b)​ Stress ulcers: Vasoconstriction + glucocorticoids, decrease in mucosal regeneration + production  c)​ Infection: Depression of inflammatory + immune responses d)​ Delayed healing: Following trauma or surgeries -​ Increased secretion of glucocorticoid - reduction in protein synthesis + oxygen to tissue e)​ PTSD: Serious consequence of major disaster or personal threat -​ Typically occurs within 3 months of event -​ May cause symptoms years later -​ HIGH RISK of developing drug/alcohol dependence ➡ Interventions/Coping with Stress (p. 619) a)​ Adequate rest + healthy diet b)​ Changing lifestyle habits, goals c)​ Use creative solutions to minimize + quickly adapt to stressors d)​ Regular moderate exercise (releases muscle tension) e)​ Engage in activities f)​ Counselling, therapies, support services g)​ Relaxation techniques Module 2: Inflammation and Healing (Ch 5) 1. Describe the body defenses for the prevention of disease (p. 66) ➡ Phagocytosis: process by which neutrophils (leukocytes) + macrophages randomly engulf + destroy bacteria, cell debris or foreign matter -​ Final stage of acute inflammatory process First Line of Defense Second Line of Defense Third Line of Defense ➡ NON SPECIFIC DEFENSE ➡ NON SPECIFIC DEFENSE ➡ SPECIFIC DEFENSE -​ Physical barrier ➡ Phagocytosis: -​ Production of antibodies or -​ (Unbroken) skin -​ Neutrophils cell-mediated immunity -​ Mucous membranes -​ Macrophages -​ B + T cells -​ Secretions: tears, gastric -​ Inflammation -​ Memory cells juices, sweat, normal flora, -​ Fever -​ Vaccinations pH changes 2. Describe the physiology of inflammation (p. 67) ➡ Inflammation/Inflammatory Response -​ Protective mechanism + important basic concept in pathophysiology -​ NORMAL + NON SPECIFIC defense mechanism in response to injury -​ Disorders ending in “it is” = inflammation (ex. Bronchitic, appendicitis, cystitis etc.) -​ Intended to localize + remove injurious agent -​ Signs + symptoms of inflammation are WARNING signs of a problem (observable or hidden within body) -​ NOT THE SAME AS INFECTION, however infection is one cause of inflammation ➡ Causes of Inflammation a)​ Physical damage - cuts, sprains b)​ Caustic chemicals - acids, alkali c)​ Ischemia or infarction d)​ Allergic reactions e)​ Extreme heat or cold f)​ Foreign matter - splinters, glass g)​ INFECTION ➡ STEPS OF INFLAMMATION (p. 67-68) 1. Injury to tissue cells BRADYKININ (triggers nociceptors) + HISTAMINE (vasodilation) are released from injured cells 2. Activation of pain receptors Triggered by the release BRADYKININ 3. Sensation of pain Stimulates mast cells + basophils to release HISTAMINE 4. Capillary dilation Caused by HISTAMINE + BRADYKININ -​ Results in increased blood flow -​ Increased capillary permeability -​ Form exudate 5. Bacteria enters tissue Original injury, break in skin, allows for bacteria to enter tissue -​ Migration of NEUTROPHILS + MONOCYTES to site of injury 6. Neutrophils Phagocytize the bacteria 7. Macrophages Mature monocytes leave the bloodstream + phagocytize microbes 3. Differentiate between local and systemic effects of inflammation (p. 70) ➡ CHARACTERISTICS OF ACUTE INFLAMMATION Local Effects of Inflammation Systemic Effects of Inflammation ➡ Cardinal signs: ➡ General manifestations: a)​ Redness (erythema): increased blood flow to a)​ Fever (pyrexia): injury by vasodilation -​ Common if inflammation is extensive b)​ Swelling (edema): increased capillary -​ Results from release of pyrogens* permeability, shifts protein + fluid into interstitial (released from WBCs or macrophages + space stimulate hypothalamus to increase body c)​ Pain: increased pressure of fluid on nerves; temp) release of chemical mediators (bradykinin + -​ If cold = cutaneous vasoconstriction = histamine) body trying to reduce heat loss d)​ Loss of function: b)​ Malaise (feeling unwell) c)​ Fatigue ➡ Exudate: collection of interstitial fluid formed in d)​ Headache inflamed area, characteristics vary with cause of trauma: e)​ Anorexia (loss of appetite) a)​ Serous: Watery, consists of fluid with small amounts of protein + WBC (Ex. allergic reactions or burns) b)​ Fibrinous: Thick + sticky, high cell + fibrin content -​ Increased risk of scar tissue c)​ Purulent: Thick, yellow-green color, more leukocytes, cell debris + microorganisms -​ INFECTION d)​ Abscess: Localized pocket of purulent exudate or pus in a solid tissue (Ex. around tooth or in brain) e)​ Hemorrhagic: may be present if blood vessels are damaged 4. Compare and contrast the effects of chronic and acute inflammation (p. 70-72) Acute Inflammation Chronic Inflammation ➡ Process of inflammation is the same regardless of ➡ Follows the acute episode of inflammation cause + timing varies ➡ Less swelling + less exudate ➡ Chemical mediators: histamine + bradykinin ➡ Presence of MORE lymphocytes, macrophages, ➡ Injury occurs + chemical mediators affect blood vessels fibroblasts + nerves in the damaged area: ➡ Leads to continued tissue destruction a)​ Vasodilation: relaxation of smooth muscles, ➡ Fibrous scar tissue develops due to increased collagen increasing diameter of arterioles in area b)​ Hyperemia: increased blood flow to injured area ➡ Granuloma may develop around foreign object c)​ Increased capillary permeability: increased fluid -​ Small mass of cells covered with connective in area (leaky vessels) tissue -​ Increased movement of plasma proteins into interstitial area = diluting toxic ➡ Example: cardiovascular disease, neurological material disease, autoimmune disease, rheumatoid disease, -​ Globulin = antibodies cancer, lupus, fibromyalgia -​ Fibrinogen = fibrin mesh localize injurious agent -​ Blood clot = blocks off area d)​ Chemotaxis: attracts cells of the immune system -​ Increased leukocytes in area -​ 1st neutrophils, 2nd monocytes, 3rd macrophages = leads to phagocytosis ➡ Example: infection, chemicals irritants, allergic reaction, trauma/injury, burns, wounds, lacerations 5. Describe the purposes and procedures of the common diagnostic tests for inflammation Diagnostic Test Purpose Blood Test C-Reactive protein -​ Marker of acute inflammation produced by liver in response to inflammatory cytokines -​ High levels = active inflammation Erythrocyte Sediment Rate (ESR) -​ Measures rate at which RBC settle at the bottom of test tube -​ Faster rate = inflammation WBC count -​ Elevated levels (leukocytosis) = inflammatory response due to infection Procalcitonin -​ Elevated in bacterial infections -​ Differentiates bacterial from viral causes of inflammation Cytokine Panel Measures the levels of specific inflammatory cytokines -​ interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) Imaging Studies X-ray Ultrasound  MRI + CT scans Biopsy Sample of affected tissue may be examined to identify cell infiltration, tissue damage, granulomas 6. Outline common medical treatments for inflammation (p. 74) a)​ Drugs Acetylsalicylic acid (ASA) ➡ Anti-inflammatory effects ➡ Analgesic effects (reduces pain) Example: Aspirin ➡ Antipyretic effects (reduces fever) Acetaminophen ➡ Analgesia effects (reduces pain) ➡ Antipyretic effects (reduces fever) Example: Tylenol Nonsteroidal ➡ Anti-inflammatory effects anti-inflammatory drugs ➡ Analgesic effects (reduces pain) (NSAIDs) ➡ Antipyretic effects (reduces fever) Example: Ibuprofen (Advil, Motrin) Glucocorticoids ➡ Anti-inflammatory -​ Extremely valuable for short term treatment but significant adverse effects that Example: hydrocortisone may interfere care b)​ First Aid / ‘RICE’ approach (p. 76) 1.​ Rest 2.​ Ice 3.​ Compress 4.​ Elevate ​ ➡ Cold applications useful in early stages of acute inflammation 7. Describe the types of healing (p. 76) Resolution ➡ Minimal tissue damage ➡ Cell recovers + back to normal Regeneration ➡ Damaged tissue replaced with cells that are functional through mitosis ➡ If complex tissue is altered, may not be functional Replacement ➡ Functional tissue replaced by scar tissue (connective, fibrous tissue) ➡ Cells are incapable of mitosis (brain or heart) ➡ Loss of function First Intention Second Intention Tertiary Intention ➡ Wound is clean, free of ➡ Large break in tissue, more ➡ Wound intentionally left open debris/necrotic tissue inflammation ➡ No approximation ➡ Edges are well approximated ➡ Longer healing ➡ Longer healing time (close together) ➡ More scar tissue ➡ Infected abdominal wound  ➡ Surgical incisions ➡ Compound fractures, large wounds with missing tissue ➡ Complications of Scar Formation a)​ Loss of function -​ Hair follicles -​ Nerves -​ Receptors b)​ Contractures + Obstructions -​ Scar tissue is nonelastic -​ Restricts range of movement c)​ Adhesions -​ Bands of scar tissue joining two surfaces that are normally separated d)​ Hypertrophic Scar Tissue ​ ➡ (Hypertrophy = increase in cell SIZE) -​ Overgrowth of fibrous tissue -​ Leads to hard ridges of scar tissue or keloid formation e)​ Ulceration -​ Blood supply may be impaired around scar -​ Results in further tissue breakdown + ulceration in future 8. Discuss the classifications and effects of burns (p. 80) ​ ➡ Burns are classified by depth of skin damage and % of body surface involved ​ ➡ Many burn injuries are mixed burns, consisting of partial or full-thickness burns First-degree Second-degree Third-degree ➡ Superficial burns ➡ Partial thickness-burns ➡ Full-thickness burns -​ Damage to epidermis + may -​ Destruction of epidermis + -​ Destruction of all skin layers + involve part of dermis part of dermis underlying tissues + nerves -​ Red, painful -​ Red, swollen, blistered, (4th degree) -​ Heal readily without scar sensitive to touch, painful -​ Deep tissue damage tissue during inflammatory stage -​ Require skin grafts as no cells -​ Severe cases: waxy, are available to produce new ➡ Sunburns, mild scald sloughing of dead skin skin cells -​ Easily infected ➡ Most severe cases of electrical, ➡ Severe sunburn, contact burns, scalding, chemical, radiation burns chemical burns, scald injuries (hot liquids) ➡ Effects of Burn Injury (p. 82) a)​ Local + systemic b)​ Dehydration + swelling (inflammatory response) c)​ Shock -​ No bleeding occurs -​ Shifts of water, protein + electrolytes -​ Decreased blood volume -​ Low blood pressure + hypovolemic shock -​ Prolonged shock = kidney failure or damage to organs d)​ Respiratory problems -​ SOB, wheezing, shallow breathing, coughing -​ Inhalation of toxins or fumes, CO2 binds to hemoglobin, replacing oxygen  e)​ Pain f)​ Infection g)​ Increased metabolic needs -​ Heat loss until skin is restored -​ Increased need for protein + carbs -​ Exudate loss -​ Erythrocytes damaged -​ Decreased function of bone marrow + reduced production of blood cells 9. Outline treatments for patients with burns ​ ➡ Hypermetabolism occurs during healing period -​ Increase protein + carbs -​ Heat loss is a problem until skin is restored ​ ➡ Immediate covering of a clean wound -​ Prevents infection -​ Non-stick dressings ​ ➡ Scar tissue develops ​ ➡ Skin grafting -​ Pig skin or cadaver skin, rejected over time but temporary fix ​ ➡ Physiotherapy + Occupational therapy ​ ➡ Surgery -​ May be needed to release restrictive scar tissue ​ ➡ Biosynthetic or synthetic skin substitutes -​ Scar-free wound healing 10. Identify the complications that can occur with burns ​ ➡ Severe burns require long-term treatment as complications are frequent ​ ➡ Length of treatment can impact burn survivor: -​ Psychological + practical effects on job, physical appearance, function, family etc. 11. Discuss the implications of the inflammatory process to the Spheres of Caring Conceptual Framework Module 3: Neoplasms and Pain (Ch 4, 20) 1. Discuss the causes and types of pain (p. 53-60) ➡ Causes of Pain (p. 53) -​ Infection -​ Inflammation -​ Ischemia -​ Necrosis of tissue -​ Stretching of tissue -​ Chemicals, burns, muscle spasms ​ ➡ Characteristics of Pain (p. 56) -​ Location of pain ➡ Referred pain -​ Pain may be perceived at site distant from source -​ Example: heart attack or ischemia in heart ➡ Phantom pain -​ Common in chronic pain or following amputation -​ Does not respond to therapies -​ May resolve within weeks to months  -​ Phenomenon not fully understood -​ Descriptive term -​ Aching, dull, sharp, throbbing, widespread, cramping, constant, periodic, unbearable, mild, moderate, severe etc. -​ Timing of pain -​ Association with activity -​ Observable evidence of pain -​ Pallor, sweating, high blood pressure, tachycardia -​ Signs + symptoms of pain (subjective + objective data) -​ Nausea, vomiting, fainting, dizziness, fear, anxiety, clenched fists, restlessness etc. ➡ Types of Pain (p. 58-60) Acute pain -​ Onset of pain is sudden, severe + short-term -​ Localized or generalized -​ Vomiting may occur -​ Strong emotional, verbal, facial response indicators -​ Subsides once treated Chronic pain -​ More difficult to treat, pain is generalized -​ Decreased quality of life, unemployment, personal relationships -​ Leads to fatigue, irritability, depression, insomnia, weight loss/gain -​ Exacerbations of acute pain -​ Reduced intolerance t Headache -​ Common type of pain (textbook) -​ Types of headaches associated with different causes + locations: -​ Sinus headaches -​ Nasal congestion, eyestrain -​ Typically manageable but can be severe -​ Tension headaches -​ Muscle spasm from emotional stress, prolonged periods of time in one position -​ Dull, constant ache in occipital area -​ Persists for days to weeks -​ Migraines -​ Related to abnormal changes in blood flow + metabolism in brain -​ Temple area -​ Precipitating factors: stress, menstruation, nutrition, hunger may affect severity + duration -​ Pain is throbbing, severe -​ Dizziness, visual sensitivity, nausea, abdominal discomfort, fatigue Neuropathic pain -​ Caused by trauma or disease to somatosensory nerve pathways (no (powerpoint + textbook) beneficial effect) -​ Varies from tingling, burning, or severe sharp/shooting pain -​ Movement + injured nerves can stimulate this type of pain A)​ Peripheral pain -​ Example: diabetic neuropathy, post-herpetic neuralgia B)​ Central pain -​ Caused by dysfunction or damage to brain or spinal cord -​ Example: post-stroke pain, sharp pains, tumors, abscess, direct injuries Nociceptive pain -​ Activation of pain receptors  (powerpoint) -​ Protective - warns of potential or actual injury A)​ Somatic pain (voluntary) -​ Sensory fibers -​ Sharp pains -​ Example: bones, joints, connective tissue, muscles B)​ Visceral pain (involuntary) -​ Originates in organs -​ May be acute or chronic -​ Dull pain, aching -​ Example: heart, liver, gut etc. Ischemic pain -​ Profound, sudden loss of blood flow to to an organ or tissue (textbook) -​ Results in hypoxia leading to tissue damage -​ Acute or chronic -​ Aching, burning, prickling, sharp, shooting pain Cancer-related pain -​ Chronic pain (textbook) -​ Caused by disease progression or treatment of disease 2. Describe the physiology of pain pathways (p. 53) ​ ➡ Afferent: from body to CNS (response) ​ ➡ Efferent: from CNS to body (reaction) ​ ➡ Nociceptors (pain receptors) -​ Free from sensory nerve endings -​ May be stimulated by: ​ ​ ➡ Temperature ​ ​ ➡ Chemical (mediators) -​ Bradykinin -​ Histamine -​ Prostaglandin ​ ​ ➡ Physical/mechanical -​ Pressure ​ ➡ Afferent Pain Fibers -​ Sensory neurons, carry nerve impulses from sensory stimuli towards CNS + brain 1.​ Myelinated A delta fibers (“A” for ACUTE pain) -​ Acute pain = sudden, sharp, localized -​ Transmit impulses rapidly 2.​ Unmyelinated C fibers (“C” for CHRONIC pain) -​ Chronic pain = diffuse, dull, burning, aching sensation -​ Transmit impulses slowly ➡ PAIN PATHWAYS (p. 54) -​ Stimulus travel along a nerve pathway -​ Different places + ways to disrupt pathway for PAIN RELIEF A)​ Dermatome -​ Area of skin supplied by specific spinal nerve -​ Somatosensory cortex: corresponds to source of stimuli -​ As seen in sciatica, shingles B)​ Reflex response (efferent response) -​ Involuntary muscle contraction away from pain source + guards against movement C)​ Spinothalamic bundle (spinal cord) -​ Connect with reticular formation of brain -​ “N” before “P” explains why we feel sharp pain before persistent throbbing/ache 1.​ Neospinothalamic tract = fast impulses (acute pain)  2.​ Paleospinothalamic tract = slow impulses (chronic, dull pain) ➡ OVERVIEW OF PAIN PATHWAY 1.​ Stimulus 2.​ Nociceptor 3.​ Peripheral nerve - afferent pain fibers 4.​ Synapse 5.​ Spinal discussion (cross-over) 6.​ Lateral spinothalamic tract (pain) 7.​ Spinothalamic tracts connect with reticular formation in brainstem - awareness 8.​ Thalamus - sensory relay station 9.​ Somatic sensory area in cerebral cortex (parietal lobe) - perception/locate pain 10.​ Hypothalamus - stress response 11.​ Limbic system - emotional response 12.​ Communication with other regions in brain to integrate responses 13.​ Reflex response - efferent impulse ​ 3. Outline the gate control theory of pain (p. 54) ​ ➡ Gate Control Theory -​ Controls systems, “gates” built into normal pain pathways -​ Modifies pain stimuli conduction + transmission in CNS ​ ​ ➡ Gates open -​ Pain impulses transmitted from periphery to brain -​ Pain perceived ​ ​ ➡ Gates close -​ Reduces or modifies passage of pain impulses 4. Identify factors that influence the pain experience (p. 58) ​ ➡ Pain threshold -​ Level of pain stimuli required to elicit pain response -​ Typically does not vary among individuals ➡ Pain tolerance -​ Degree of pain (intensity or duration) that is endured before person takes action -​ Culturally related -​ May be increased by endorphin release -​ May be reduced by fatigue or stress ​ ➡ Pain perception + response are subjective + varies among individuals ➡ Factors: -​ Age -​ Culture, family, jobs, gender norms -​ Personality -​ Prior unpleasant experiences with pain -​ Anxiety, anticipatory fear of pain -​ Stress 5. Identify the purpose of analgesics in the management of pain (p. 60) ​ ➡ Removes cause of pain ASAP ​ ➡ Analgesic medications -​ Oral -​ Parenterally (injection) -​ Transdermal patch -​ Classified by ability to relieve mild, moderate and severe pain ​ ​ Mild pain Moderate pain Severe pain ASA* Codeine Morphine Acetaminophen Oxycodone Demerol NSAIDs* Percocet Methadone Vicodin Meperidine Oxycodone 6. Describe the role of anesthesia in the control of pain (p. 62) Local anesthesia Spinal/regional General anesthesia Neuroleptanesthesia anesthesia ➡ Injected or applied to ➡ Blocks pain from legs or ➡ Causes loss of ➡ Patient can respond skin or mucous membranes abdomen consciousness via gas or ➡ Relatively unaware of ➡ Removal of skin lesion, ➡ Labor/delivery injection procedure + no discomfort tooth extraction ➡ General surgery ➡ Lidocaine ➡ Epidural ➡ Nitrous oxide (gas), IV ➡ Diazepam 7. Outline the pathological processes contributing to the development of cancer ➡ Terms to know Differentiation ➡ Each cell type differentiates + carries out particular functions ➡ Structure reflects function of the tissue Mitosis ➡ Part of cell cycle ➡ Requires genetic control - DNA + RNA Mutation ➡ DNA in parent cell is altered + passed on to daughter cells that carry on the mutation Apoptosis ➡ Programmed cell death ➡ Controlled by genetic elements Neoplasm ➡ TUMOR ➡ Cell growth no longer responds to normal genetic controls ➡ Continues to reproduce without need for them to reproduce ➡ Characteristics of tumor depend on: -​ Type of cell + location where the tumor came from -​ Unique structure + growth pattern Carcinogenesis ➡ Process where normal cells are transformed into cancer cells Oncology ➡ Study of cancer - diagnosis, treatment, prevention ➡ PATHOLOGICAL PROCESS 1.​ Tumor manifests as large mass composed of more primitive or dysplastic cells 2.​ Normal organization, growth inhibition, functions, cell-cell communication are ABSENT 3.​ Mass tends to compress nearby blood vessels 4.​ Malignant cells DO NOT adhere to each other or metastasize 5.​ Tumor cells secrete enzymes (collagenase) = breaks down surround tissue + helps tumor spread  6.​ Inflammation + loss of normal cells = reduced organ functions 7.​ Necrosis can further inflammation + infection 8.​ SOME cancer cells secrete growth factors = stimulate angiogenesis = promotes tumor development ➡ HOW CANCER SPREADS Invasion Seeding Metastasis ➡ Local spread ➡ Spread of cancer cells in body ➡ Spreads to distant sites via ➡ Tumor cells grow in adjacent fluids or along membranes blood or lymph of other body fluids tissues -​ Type of cancer -​ Aggressiveness -​ Location of primary tumor -​ How long has it been present in body 8. Compare and contrast the characteristics of benign and malignant tumors Benign Tumors Malignant Tumors Cells ➡ Similar to normal cells ➡ Varies in size + shape w/ large nuclei ➡ Differentiated cells that reproduce at higher ➡ Undifferentiated cells rate than normal ➡ Increased and atypical mitosis rate ➡ Normal mitosis Growth ➡ Slow, expanding mass ➡ Rapid growth ➡ ENCAPSULATED* (main difference) ➡ NO CAPSULE ➡ Abnormal shape + size ➡ Does not adhere to each other + detaches easily Spread ➡ Localized ➡ Invades surrounding tissues ➡ Metastasizes to distant sites via blood or lymph vessels Systemic effects ➡ Rare ➡ Often present ➡ Tissue damage Life-threatening ➡ Only in certain locations (ex. Brain) ➡ Yes by tissue destruction + spread of tumors ➡ GRADING/STAGING CANCER -​ Used to estimate PROGNOSIS: -​ Cancer-free state after 5 year survival without recurrence -​ Remission = no clinical signs of cancer (client may experience several remissions) -​ Most common system = TMN system* ​ ➡ T = Tumor size ​ ➡ M = Metastasis (spread) of tumor ​ ➡ N = Nodes (involvement of lymph nodes) Stage Tumor Metastasis Nodes Stage 1 (Early stage) Small, localized None None Stage 2 Larger None Limited spread  Stage 3 Large, invasive None Regional spread Stage 4 (Late stage) Any size Distant metastasis, Any lymph node status advanced spread 9. Describe the systemic and localized effects of cancer on the body Localized Effects Systemic Effects a)​ Pain a)​ Weight loss + cachexia -​ May be absent until late stages -​ Anorexia, fatigue, pain, stress -​ Occurs when tumor is well advanced -​ Increased demands on body from tumor -​ Severity depends on type of tumor cells b)​ Obstruction b)​ Anemia -​ Tumor compresses duct or passageway -​ Caused by blood loss at tumor site -​ Blood supply or lymphatic flow restricted -​ Nutritional deficits = reduced production of -​ GI tract hemoglobin -​ Airflow in bronchi c)​ Severe fatigue c)​ Necrosis + ulceration -​ Caused by inflammatory changes, -​ Bleeding or infection around tumor anorexia, cachexia, anemia -​ Stress of treatment schedule -​ Psychological factors d)​ Effusions -​ Fluid build up in body cavities due to inflammation e)​ Infections -​ Frequently occur as resistance declines f)​ Bleeding -​ Tumor cells may erode blood vessels g)​ Paraneoplastic syndrome -​ Associated w/ certain types of tumors -​ Tumor cells release substances that affect neurological function -​ Hormonal effects 10. List common warning signs of cancer 1.​ Unusual bleeding or discharge anywhere in body 2.​ Change in bowel or bladder habits (ex. Prolonged diarrhea, discomfort) 3.​ Change in wart or mole (size, color, shape) 4.​ A sore that does not heal 5.​ Unexplained weight loss 6.​ Anemia, low hemoglobin, persistent fatigue 7.​ Persistent cough or hoarseness without reason 8.​ A solid, often painless lump, in breast or testes* or anywhere on body ➡ Risk Factors for Developing Cancer Genetic Factors Viruses Radiation Chemicals Biological Factors ➡ Oncogenes that ➡ Oncoviruses alter ➡ Ultraviolet rays ➡ Organic solvents ➡ Chronic irritation + regulate ALL growth host cell DNA ➡ X-rays, gamma ➡ Asbestos inflammation rays ➡ Heavy metals ➡ Age ➡ Radioactive ➡ Formaldehyde ➡ Diet isotopes ➡ Chemotherapy ➡ Lifestyle habits ➡ Increased risk with ➡ Hormones, higher dosage hormone therapy ➡ Family history ​ 11. Describe common screening methods for early detection of cancer ​ ➡ Routine screening -​ Essential for early detection -​ Following treatment to detect any further tumors ​ ➡ Self-examination -​ Early detection if consistent (breast, testes, skin) ​ ➡ Blood tests -​ Measures blood cell levels during treatment -​ May detect tumor markers (ex. PSA test) 12. Describe the purposes and procedures of the common diagnostic tests for cancer detection Lab Tests Medical Imaging Procedures ➡ Cytology: ➡ X-ray ➡ Bone marrow Bx -​ Surgery, fluid sample, pap ➡ Mammogram ➡ Lumbar puncture test ➡ Ultrasound ➡ Bronchoscopy ➡ Blood tests: ➡ MRI, CT scan, PET scan ➡ GI scopes -​ Baselines -​ Tumor markers 13. Outline common treatments for cancer ​ ➡ Surgery -​ Removal of tumor + surrounding tissue -​ Laparoscopic + several small incisions (minimizes tissue damage + improves recovery time) -​ Removal of adequate surrounding tissue may result in function changes -​ Radiofrequency ablation (RFA) -​ Alternative surgery for small, single tumors in solid or fluid-filled organs -​ Lungs are exempt from this ​ ➡ Radiation therapy -​ Used alone or combined with other treatments -​ Causes mutations or alterations in target DNA ➡ destroys rapidly dividing cells -​ Most effective in rapidly dividing cells -​ Some cancers are resistant to radiation -​ May be used prior to surgery to shrink tumor ​ ➡ Chemotherapy -​ Antineoplastic drugs -​ Combination of 2-4 drugs -​ Alkylating agents, antimitotics, antimetabolites, antibiotics -​ Interferes w/ DNA replication + protein synthesis -​ Used alone or combined w/ surgery or radiation ​ ➡ Immunotherapy ​ ➡ Stem Cell transplant ​ ➡ Hormones ​ ➡ Gene therapy ​ ➡ Supportive management 14. Discuss the implications of the cancer process as it relates to the Spheres of Caring Conceptual Framework Module 4: Fluid and Electrolyte Disorders (Ch 2) 1. Review the anatomy and physiology of fluid and electrolytes within the body ➡ Major component of body is WATER -​ Essential to homeostasis -​ Metabolic reactions -​ Transportation system -​ Facilitating movements ➡ Prefixes Inter ➡ between Intra ➡ within Extra ➡ outside of Iso ➡ the same Hyper ➡ high, higher Hypo ➡ low, lower ➡ FLUID COMPARTMENTS a)​ Intracellular compartment (ICF) -​ Fluid INSIDE cells b)​ Extracellular compartment (ECF) -​ Fluid OUTSIDE cells -​ Intravascular fluid, interstitial fluid, cerebrospinal fluid, transcellular fluid, secretions -​ Plasma protein ➡ ALBUMIN ➡ MOVEMENT OF WATER -​ Fluid circulates body via FILTRATION + OSMOSIS -​ Depends on membrane permeability -​ Water moves between compartments via: ➡ HYDROSTATIC PRESSURE “Push” ➡ OSMOTIC PRESSURE “Pull” -​ Amount of water intake = Amount of water output ➡ Fluid intake: ingestion of solid foods or fluids ➡ Fluid output: urine, feces, perspiration, exhaled air -​ Concentration of solutes in fluid affects fluid shift ➡ OSMOLARITY Filtration Osmosis Diffusion Active Transport ➡ Passive transport ➡ Passive transport ➡ Passive transport ➡ Requires ATP ➡ Movement of water + ➡ Movement of water from ➡ Movement of solutes ➡ Movement of solutes solutes from HIGH to LOW area of LOW SOLUTE from areas of HIGH to AGAINST concentration or pressure gradient concentration to area of LOW concentration pressure gradient HIGH SOLUTE concentration ➡ Hypertonic solution: water moves out of cell = cell shrinks (high osmolarity) ➡ Hypotonic solution: water moves into cell = cell swell/burst (low osmolarity) ➡ Isotonic solution: no movement = normal ➡ BALANCE OF WATER + ELECTROLYTES Thirst Antidiuretic Hormone Aldosterone Hormone Atrial Natriuretic Peptide (ADH) (ANP) + B-Type Natriuretic Peptide ➡ Osmoreceptors ➡ Reabsorption of water ➡ Reabsorption of sodium ➡ Synthesized by (hypothalamus) from kidney tubules + water from kidneys myocardial cells ➡ Reduced salivation ➡ Sodium affected ➡ Sodium affected  ➡ Water consumption ➡ Released in response to occurs increased pressure within cardiac chambers ➡ Regulates fluid, sodium + potassium levels 2. Describe the diagnostic tests used to evaluate fluid and electrolyte imbalances ​ ➡ Renal panel/Serum electrolytes ​ ➡ Serum osmolarity ​ ➡ Urinalysis = urine osmolarity ​ ➡ Urine specific gravity (SG) ​ ➡ Liver panel/Serum albumin 3. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: a. edema and dehydration EDEMA DEHYDRATION Effects ➡ Excessive amount of fluid in INTERSTITIAL ➡ Insufficient body fluid: compartment -​ Inadequate intake, excessive loss OR both -​ Swelling or enlargement of tissue -​ Loss effects the ECF first -​ Localized/widespread ➡ Fluid loss -​ Measured by change in weight ➡ More serious in infants + older adults -​ Lack fluid reserves ➡ Water loss may be followed by loss of electrolytes + proteins Causes 1. Increased CAPILLARY HYDROSTATIC 1. Vomiting + Diarrhea PRESSURE -​ Loss of electrolytes + nutrients -​ Result of high BP or blood volume -​ Forces excess amount of fluid out of 2. Excessive sweating capillaries + into tissues -​ Loss of water + sodium -​ Prevents return of fluid from interstitial compartment 3. DIABETIC KETOACIDOSIS* -​ Loss of fluid, electrolytes + glucose in urine 2. Loss of PLASMA PROTEINS (ALBUMIN) -​ Decreased plasma osmotic pressure 4. Inadequate water intake -​ Mostly in older adults or unconscious 3. Obstruction of LYMPHATIC CIRCULATION persons -​ Localized edema -​ Restricts return of excess fluid + protein 5. Use of concentrated formula (in infants) 4. Increased CAPILLARY PERMEABILITY -​ Localized edema -​ May result from bacterial toxins or large burn wounds ➡ widespread edema Signs + ➡ Swelling or enlargement of tissue ➡ Dry mouth Symptoms ➡ Painful, redness, paleness ➡ Reduced skin elasticity or turgor  ➡ Headache (cerebral edema) ➡ Lower BP, weak pulse, fatigue ➡ Localized or widespread throughout body ➡ Increased HEMATOCRIT (% of RBC in blood) ➡ Impaired tissue perfusion, arterial circulation ➡ Decreased brain function, confusion, loss of ➡ Impaired functions consciousness Treatment ➡ Restrict fluid intake ➡ Cold compression b. electrolyte imbalances of: ➡ SODIUM IMBALANCE HYPONATREMIA HYPERNATREMIA Role of Na+ ➡ Blood volume, BP, fluid balance ➡ FLUID balance, blood volume + BP ➡ Normal range: 135-145 mEq/L ➡ Normal range: 135-145 mEq/L ➡ Extracellular cation Na+ ➡ Extracellular cation Na+ Causes “Where did the soDDDDium go?” “The MODEL of Hypernatremia” ➡ Diuretics ➡ Medications, meals (too much Na) ➡ Diarrhea ➡ Osmotic diuretics ➡ Dehydration ➡ Diabetes Inspidus -​ Inadequate salt intake, sweating ➡ Excessive H20 loss ➡ Drains ➡ Low H20 intake -​ NG tubes, fistulas, suctioning Signs + “SALT LOSS” “The model is FIRED” Symptoms ➡ Stupor/Coma ➡ Fever (low grade), flushed skin ➡ Anorexia, N&V ➡ Increased fluid retention + BP ➡ Lethargy ➡ Restless, irritable ➡ Tendon reflexes reduced ➡ Edema (peripheral + pitting) ➡ Limp muscles (weakness) ➡ Decreased urine output, dry mouth ➡ Orthostatic hypotension ➡ Seizures / headache ➡ Stomach cramping Treatment ➡ POTASSIUM IMBALANCE HYPOKALEMIA HYPERKALEMIA Role of K+ ➡ HEART + muscle function, fluid balance + BP ➡ Heart/muscle function, fluid balance, BP ➡ Normal range: 3.5-5 mEq/L ➡ Normal range: 3.5-5 mEq/L ➡ Intracellular cation K+ ➡ Intracellular cation K+ Causes “The body is trying to DITCH K+” “The body CARED too much for K+” ➡ Drugs: loop diuretics furosemide, laxatives, ➡ Cellular movement of K+ from intracellular to glucocorticoids, hydrocortisone extracellular (burns, tissue damage) ➡ Inadequate K+ consumption ➡ Acidosis, Adrenal insufficiency ➡ Too much water intake ➡ Renal failure  ➡ Cushing Syndrome (kidneys excreting too ➡ Excessive K+ intake much K+) ➡ Drugs “K-BANK” ➡ Heavy fluid loss -​ K+ supplements -​ Beta blockers -​ Ace inhibitors + ARBSs -​ NSAIDS -​ K+ sparing diuretics Signs + “7 L’s of laying in ditch” “MURDER” Symptoms ➡ Lethargy ➡ Muscle weakness + muscle cramps ➡ Low shallow respirations = failure ➡ Urine output abnormalities ➡ Lethal cardiac dysrhythmias ➡ Respiratory failure (due to muscle weakness) ➡ Lots of urine (frequent + large) ➡ Decreased cardiac contractility (weak HR) ➡ Leg cramps ➡ EKG changes (Tall peaked T waves) ➡ Limp muscles (weakness) -​ Cardiac rhythm changes = death* ➡ Low BP ➡ Reflex changes, twitching Treatment ➡ CALCIUM IMBALANCES HYPOCALCEMIA HYPERCALCEMIA Role of ➡ Neuron stability, BONES, HR, clotting factors ➡ Neuron stability, bones, HR, clotting factors Ca2+ ➡ Normal range: 8.5-10.5 mEq/L ➡ Normal range: 8.5-10.5 mEq/L ➡ Extracellular cation Ca2+ ➡ Extracellular cation Ca2+ *Ca2+ hates phosphate Causes “Cats are MAAD” “HI CHIMPS” ➡ Malabsorption syndrome ➡ Hyperparathyroidism ➡ Albumin deficiency ➡ Increased intake of Vitamin A + D ➡ Alkalosis = High pH ➡ Calcium supplements, Cancer ➡ Decreased parathyroid, hypoparathyroidism ➡ Hyperparathyroidism ➡ Immobilization, stress on bone = demineralization ➡ Milk-alkali syndrome, Medications ➡ Parathyroid hyperplasia or adenoma ➡ Sarcoidosis Signs + “CATS BLEED” “Chimps have BACKME” Symptoms ➡ Convulsions, confusion, Chvostek Sign ➡ Bone pain ➡ Arrhythmia ➡ Arrhythmia ➡ Tetany, tingling fingers, Trousseau Sign ➡ Cardiac arrest ➡ Spasms ➡ Kidney stones ➡ Blood clotting factors ➡ Muscle weakness ➡ Excessive urination, thirst Treatment ➡ MAGNESIUM IMBALANCES  HYPOMAGNESEMIA HYPERMAGNESEMIA Role of ➡ Muscle relaxation, immune system, blood ➡ Muscle relaxation, immune system, blood Mg++ glucose, bones glucose, bones ➡ Normal range: 1.3-2.1 mEq/L ➡ Normal range: 1.3-2.1 mEq/L Causes “This is HARRDD” “RENAL” ➡ Hyperthyroidism, hyperaldosteronism ➡ Renal failure ➡ Alcoholism ➡ Exogenous load (toxins from outside body) ➡ Results from malabsorption or malnutrition ➡ Necrosis ➡ Diabetic ketoacidosis ➡ Adrenal insufficiency ➡ Diuretics ➡ Lithium intoxication Signs + “Let’s PAINT” “HEY LADD” Symptoms ➡ Personality changes ➡ Lethargy ➡ Arrhythmia, increased HR ➡ Arrhythmia ➡ Insomnia ➡ Depressed neuromuscular function ➡ Neuromuscular hyperirritability ➡ Decreased reflexes ➡ Tremors or chorea (involuntary repetitive movements) Treatment ➡ ACID-BASE BALANCE ​ ➡ To maintain serum pH within normal range ➡ NORMAL RANGE ➡ 7.35 to 7.45 -​ IF pH BELOW 6.8 or ABOVE 7.8 = death ​ ➡ Ratio of bicarbonate ion to carbonic acid (carbon dioxide) MUST be 20:1 -​ Acid-base balance essential to homeostasis ➡ BUFFER SYSTEMS 1.​ Chemical buffer systems ➡ respond to pH changes immediately (HCO3) ➡ Bicarbonate Ion Buffer 2.​ Respiratory regulation ➡ alter carbonic acid levels to change pH (CO2) 3.​ Kidney/renal regulation ➡ modify excretion rate of acids + absorption of bicarbonate ions to regulate pH -​ Most significant but SLOWEST mechanism ➡ BASES Phosphate Chloride ➡ Bone + tooth mineralization ➡ Major extracellular cation ➡ Important in metabolism - ATP ➡ Cl- levels related to Na+ levels ➡ PHOSPHATE BUFFER SYSTEM - acid-base balance ➡ Cl- and bicarbonate ions shift in response to acid-base ➡ Integral part of cell membrane imbalances ➡ Reciprocal relationship w/ serum Ca2+ ➡ HYPERCHLOREMIA ➡ HYPOPHOSPHATEMIA -​ Usually alkalosis -​ High Ca2+ -​ Vomiting, loss of hydrochloric acid -​ Malabsorption syndromes, diarrhea, excess anatacids ➡ HYPERCHLOREMIA -​ Excessive sodium chloride intake ➡ HYPERPHOSPHATEMIA -​ Renal failure, low Ca2+ ➡ ACID-BASE IMBALANCES ​ ➡ ACIDOSIS -​ Increased H+ -​ Decrease in pH ➡ acidic ​ ➡ ALKALOSIS -​ Decreased H+ -​ Increase in pH ➡ basic ➡ TYPES OF ACID-BASE IMBALANCES Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis ⬇ LOWER pH ⬆ HIGHER pH ⬇ LOWER pH ⬆ HIGHER pH ⬇ decreased HCO3 ⬆ increased HCO3 ⬆ increased CO2 ⬇ decreased CO2 ⬆ increased acid ⬇ decreased acid ⬆ increased acid ⬇ decreased acid ⬆ increased base ⬇ decreased base ➡ “ROME” R = Respiratory O = Opposite ​ ➡ High pH = Low CO2 (ALKALOSIS) ​ ➡ Low pH = High CO2 (ACIDOSIS) M = Metabolic E = Equal ​ ➡ High pH = High HCO3 (ALKALOSIS) ​ ➡ Low pH = Low HCO3 (ACIDOSIS) Module 5: Infection and Immunity (Ch 6,7) 1. Explain the relationship between microorganisms and infectious diseases ➡ Microbiology: study of microorganisms ➡ Microorganisms include bacteria, fungi, protozoa + viruses a)​ Non-pathogenic ➡ usually do not cause disease, beneficial, normal flora b)​ Pathogenic ➡ capable of causing disease 2. Describe the characteristics of microorganisms (bacteria, virus, fungi, protozoa) most commonly associated with infectious diseases in humans BACTERIA VIRUS FUNGI PROTOZOA Cell Wall Yes No Yes No Intracellular No Yes, requires host for No Some independent, parasite replication some require living host DNA or RNA Yes No Yes Yes  Drug Treatment Antibacterial Antiviral Antifungal Selective Notes ➡ Unicellular, varies in ➡ Non-living organism ➡ Eukaryotic, contains ➡ Pathogens are shape, size, form ➡ Mutates frequently nucleus usually parasites ➡ Do not require living ➡ DNA/RNA take over ➡ Found throughout cells to survive control of host cell environment (plants, ➡ Some secrete toxic animals, humans) substances ➡ Grows under wide -​ Exotoxins (from range of conditions bacteria) = ➡ Few are pathogenic vomiting etc. -​ Endotoxins (bacterial cell wall) = serious effects ➡ septic shock ➡ Can form endospores ➡ Survive in adverse conditions + heat 3. Differentiate between infectious and non-infectious microorganisms INFECTIOUS MICROORGANISMS NON-INFECTIOUS MICROORGANISMS ➡ Pathogenic ➡ microorganisms capable of causing ➡ Non-pathogenic ➡ do not typically cause disease + disease in host may be beneficial like normal flora -​ Due to pathogens + extrinsic factors -​ Caused by other factors other than pathogens -​ Transmitted from one person to another -​ Due to intrinsic factors -​ Transmission via direct contact or indirect contact, -​ Does not spread from person to person water, air, vectors (insects, animals) -​ Hereditary transmission -​ Hand hygiene + infection control can reduce occurence 4. Identify the location of resident flora on body sites ➡ Normal Flora -​ Common, resident bacteria that is present within body + essential to immune system -​ Supports mucosal immune system (innate immunity) by improving function for defense ➡ PRESENT in: -​ Skin -​ Nose, pharynx -​ Mouth -​ Colon, rectum -​ Vagina -​ Urethra ​ ➡ STERILE in: -​ Areas in our body that LACK microbes ➡ Lungs, brain, blood, bladder, kidneys 5. Explain the term nosocomial infection ➡ Nosocomial infections occur in health care facilities (hospitals, nursing homes etc.) 6. Compare and contrast the local and systemic signs of infection (p. 107) ➡ Local signs -​ Swelling -​ Erythema (redness) -​ Pain, tenderness -​ Lymphadenopathy (swollen lymph nodes) -​ Exudate, purulent ➡ Systemic signs -​ Pyrexia (fever) -​ Malaise (weakness), fatigue, anorexia -​ Leukocytosis -​ Headache, arthralgia -​ Elevated erythrocyte sedimentation rate 7. Recognize sepsis as life-threatening organ dysfunction caused by a dysregulated immune response ➡ SEPSIS (Septicemia) ➡ “sepsis” or “going septic” -​ Multiplication of pathogens in the blood + the cause of sepsis, a toxic inflammatory condition arising from spread of microbes ➡ SEPSIS is an infection that has spread into systemic circulation ➡ Results in SEPTIC SHOCK due to release of large amounts of inflammatory chemical mediators ​ ➡ Systemic vasodilation = MEDICAL EMERGENCY! ➡ Results in: -​ High fever -​ Altered mental state -​ Hypotension (Systolic BP of 100mmHg or less) -​ Tachycardia/tachypnea (Rate of 22/min or greater) -​ Increased WBC 8. Outline the diagnostic tests and common medical treatments for infection (p. 107) ➡ DIAGNOSTIC TESTS 1.​ Culture + staining techniques -​ Specific clinical specimens -​ Drug sensitivity test ➡ Culture and Sensitivity (C&S) -​ Sample taken from specimen -​ “Culture” ➡ Determines type of bacteria -​ “Sensitivity” ➡ Effectiveness of antibiotic on bacteria -​ ➡ If antibiotic kills bacteria ➡ susceptible -​ ➡ If antibiotic fails to kill ➡ resistant 2.​ Blood tests -​ Variations in # of leukocytes ➡ LEUKOCYTOSIS: High WBC ➡ Bacterial infection ➡ LEUKOPENIA: Low WBC ➡ Viral infection 3.​ Differential count 4.​ C-reactive protein + Erythrocyte Sedimentation Rate (ESR) -​ Inflammation 5.​ Immunological testing of body fluids -​ Antigen identification -​ Antibody titer (measure) 6.​ Latex agglutination tests -​ Identifies presence of methicillin-resistant Staphylococcus aureus (MRSA) ➡ TREATMENTS ➡ Classifications of antimicrobials: 1.​ Antibiotics: Derived from organisms or made synthetically 2.​ Antimicrobial: Antibacterial, Antiviral, Antifungal 3.​ Bactericidal: Drug destroys bacteria 4.​ Bacteriostatic: Inhibit reproduction of bacteria 5.​ Broad spectrum: Effective against BOTH gram-positive + gram-negative organisms 6.​ Narrow spectrum: Effective against either gram-positive or gram-negative 7.​ 1st & 2nd generation drugs: Original drug class or later version ​ ➡ Guidelines: -​ Drugs should be administered + taken as ordered -​ Antimicrobials should be taken until completely gone or until new prescription -​ If symptoms continue, call prescriber or physician -​ Do not share drugs -​ If drug resistance is known to occur with infection, multidrug therapy prn 9. Review the anatomy and physiology of the bone marrow, the lymphatic system, and the immune response (p.117-119) ➡ THIRD LINE OF DEFENCE ➡ Specific immunity BONE MARROW THYMUS LYMPHATIC SYSTEM IMMUNE RESPONSE ➡ Produces blood cells ➡ Large in children, ➡ Filters pathogens, ➡ Detect + destroy foreign including WBCs involved in decreased size in adults facilitates immune cell materials immune responses ➡ Maturation + proliferation circulation ➡ Non-specific immunity + ➡ Source of stem cells, of T lymphocytes specific immunity leukocytes, maturation of B ➡ T-cells “cell mediated ➡ Antibodies, T-cells, lymphocytes immunity” B-cells, memory cells ➡ B-cells “humoral immunity” ➡ IMMUNE RESPONSE 1.​ Primary response -​ Occurs with first exposure to antigen -​ Antibodies takes 1-2 weeks to form 2.​ Secondary response -​ Occurs on second exposure to the same antigen -​ Response is intense + sudden with higher antibody levels than primary response ➡ CLASSES OF IMMUNITY ACTIVE IMMUNITY PASSIVE IMMUNITY ➡ Body develops antibodies, T cells + memory B cells 1.​ Natural Passive: maternal antibodies 1.​ Natural Active: antibodies, T cells etc 2.​ Artificial Passive: getting antibodies from 2.​ Artificial Active: T cells + antibodies against another person or animal disease following vaccination 10. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: Multiple Myeloma Acute Leukemia Chronic Leukemia Aplastic Anemia Causes Increased production of Uncontrollable ➡ High ratio of mature ➡ Results from bone plasma cells (mature B multiplication of WBCs WBC proliferation marrow impairment or cells) in bone marrow in bone marrow failure to produce blood ➡ replace bone marrow ➡ High ratio immature cells ➡ bone destruction WBC proliferation Radiation, drugs, ➡ impaired blood cell + ➡ Blood cancer environmental factors antibody production ➡ Signs + Anemia, affected kidney Fatigue, fever, Milder symptoms Anemia, leukopenia Symptoms function, bleeding, pain excessive bleeding or Fatigue, weakness, (low WBC), recurrent even at rest bruising, infections, infections infections, pallor, pain weakness, thrombocytopenia (low platelets) Treatment Chemotherapy, Chemotherapy, Bone marrow analgesics, blood radiation, bone marrow transplant, transfusions transplant chemotherapy, radiation, immunosuppressants, blood transfusions Course Progressive Sudden onset Slow progression May be temporary or Poor life expectancy Rapidly fatal without Better prognosis permanent Malignancy well advanced treatment before diagnosis 11. Describe and compare the diagnostic tests to evaluate hypersensitivity reactions and immune system disorders ➡ Skin tests (allergens) ➡ Blood tests (IgE levels) ➡ Biopsies (autoimmune conditions) ➡ ELISA, Western Blot (HIV diagnosis) 12. Examine the etiology and effects of immunodeficiency (p.131) ➡ IMMUNODEFICIENCY ➡ compromised or absent immune response ➡ Classification of deficits 1.​ PRIMARY DEFICIENCIES -​ Basic developmental failure somewhere in the body -​ Genetic defects -​ May affect other organs 2.​ SECONDARY DEFICIENCIES -​ Acquired immunodeficiency -​ Loss of immune response resulting from specific causes ➡ Chemotherapy, malnutrition, HIV/AIDS, infections, drugs ​ ➡ Effects of immunodeficiency -​ Increased risk for opportunistic infections ​ 13. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: ➡ HYPERSENSITIVITY REACTIONS TYPE 1 TYPE 2 TYPE 3 TYPE 4 Anaphylaxis Cytotoxic Immune Complex Cell Mediated / Delayed Allergic reactions (mild to ABO blood incompatibility Autoimmune disorders Allergic skin rash / contact severe) Cell lysis + phagocytosis Inflammation, vasculitis dermatitis Immediate inflammation + Response to incompatible Immune systems attacks Delayed inflammation blood transfusion itself Transplant rejection pruritus ➡ Lupus, rheumatoid Direct contact with Release of histamine + chemical, dyes, soaps, arthritis chemical mediators metals, poison ivy S+S: Hay fever, rashes, ➡ TB test, contact hives, vomiting, dermatitis, latex anaphylaxis, cough, tingling, fainting, panic, edema, severe hypoxia, low BP Treatment: antihistamines, epinephrine, glucocorticoids ➡ SYSTEMIC LUPUS ERYTHEMATOSUS -​ Autoimmune disorder -​ Chronic inflammatory disease affects multiple organ systems causing inflammation + necrosis -​ Primarily affect young women -​ Signs + symptoms ➡ Face rash across nose + cheeks, butterfly rash ➡ Vasculitis (inflammation of blood vessels) ➡ Warning signs of exacerbation: increased fatigue, rash, pain, fever, headache -​ Treatment ➡ Rheumatologist ➡ Glucocorticoids, NSAIDs ​ ➡ HIV/AIDS 1.​ Human immunodeficiency virus (HIV) -​ HIV Type 2 ➡ primarily in Africa -​ HIV Type 1 ➡ major cause of AIDS -​ HIV+ individual ➡ virus is known to be present in body but no evidence of immunosuppression -​ HIV destroys helper T cells ➡ loss of immune response -​ If pt presents w/ unusual infection or cancer with no pathology ➡ presence of active HIV infection ➡ Transmission via body fluids (blood, semen, vaginal secretions) 2.​ Acquired immunodeficiency Syndrome (AIDS) ➡ Encephalopathy ➡ any disease that alters or affects brain function or structure -​ Final stage with marked signs of numerous serious complications -​ General manifestations of HIV infection -​ Pneumonia -​ GI effects -​ Neurologic effects -​ Secondary infections ➡ primary cause of death -​ Cancer ➡ LYMPHOMAS -​ Cancer of the lymphatic system ➡ Blood cancers that involve lymphocytes + lymph nodes -​ Signs + symptoms -​ Swollen lymph node -​ Two main types 1.​ Hodgkin (rare) -​ Initially involves single lymph node in neck area -​ Localized -​ Spreads to adjacent node -​ Recurrent infections 2.​ Non-Hodgkin (common) -​ Multiple lymph nodes -​ Harder to treat -​ Associated with HIV infections -​ Develops at any age but more common in ages 50+ ➡ LYMPHEDEMA -​ Obstruction of lymphatic vessels ➡ accumulation of lymph fluid -​ Signs + symptoms ​ ➡ Swelling, swollen area is soft ​ ➡ May become firm, painful, unresponsive to treatment ​ ➡ Frequent infections, chills, fever -​ Treatments ➡ Bed rest, diuretics, massage area to promote drainage