Exam 1 Prep-2 PDF

MODULE 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PHARMACOLOGY Review terms Cellular responses to diseases injury Pathophysiologic processes Causes of cellular injury Manifestations of disease Signs and symptoms PHARMACOLOGY: drug properties Characteristics of an ideal drug - Effectiveness - Safe...

MODULE 1: INTRODUCTION TO PATHOPHYSIOLOGY AND PHARMACOLOGY Review terms Cellular responses to diseases injury Pathophysiologic processes Causes of cellular injury Manifestations of disease Signs and symptoms PHARMACOLOGY: drug properties Characteristics of an ideal drug - Effectiveness - Safety - Selectivity Additional properties: Reversible action, predictability, ease of administration, lack of drug interactions, cost Nursing process ADPIE 1. Assessment: pre-admission data, high-risk patients 2. Analysis/Diagnosis: potential adverse effects, knowledge deficit 3. Planning: Identify specific interventions directed at solving or preventing 4. Implementation: administrations (routes, etc.) 5. Evaluation: monitors (therapeutics, adverse events, interactions, toxicities) Medication administration Electronic health record · Digital chart · Evidence-based · Real time · Patient centered · Improved outcomes Legislation Medication rights of administration Right drug  Right patient Right dose Right route Right time Right documentation Right assessment Right evaluation Right of education Right of refusal Right of reason—Demonstrated critical thinking Medication safety Medication reconciliation Step 1. Create a list of current medications. For each drug, include the name, indication, route, dosage size, and dosing interval. For patients entering a hospital, the list would consist of all medications being taken at home, including vitamins, herbal products, and prescription and nonprescription drugs. Step 2. Create a list of all medications to be prescribed in the new setting. Step 3. Compare the medications on both lists. Step 4. Adjust medications based on the comparison. For example, the prescriber would discontinue drugs that are duplicates or inappropriate and would avoid drugs that can interact adversely. Step 5. When the next transition in care occurs, provide the updated, reconciled list to the patient and the new provider. By consulting the list, the new provider will be less likely to omit a prescribed medication, commit a dosing error, prescribe a new medication that may duplicate or negate the effects of a current medication, or prescribe a new medication that may interact with a current medication to cause a serious adverse event. Side and adverse effects - Side effects – most likely to occur (mild) unavoidable secondary drug effects at therapeutic doses. Ex: drowsiness caused by antihistamines or gastric irritation caused by aspirin - Adverse effect - unintended effect occurring at normal drug doses Patients who are Most susceptible to adverse effects: - Comorbidities - Genetics - Age - Diet  Medication errors - Any preventable event that may cause or lead to inappropriate medication use or patient harm while the medication is in the control of the healthcare professional, patient, or consumer - Beginning with workers in the pharmaceutical industry, followed by people in the healthcare delivery system, and ending with patients and their family members. - Although it does go through a long list of people before the nurse administers, because the nurse is the last person who can catch mistakes made by others and because no one is there to catch mistakes the nurse might make, the nurse bears a heavy responsibility for ensuring patient safety. Principles of pharmacodynamics and kinetic pharmacogenomics, Pharmacokinetics: The movement of drug through the body and what happens to the drug as it moves through the body Four processes: - Absorption: drug’s movement from its site of administration into the blood. - Distribution: drug’s movement from the blood to the interstitial space of tissues and from there into cells. - Metabolism: the enzymatically mediated alteration of drug structure - Excretion: the movement of drugs and their metabolites out of the body. - EXTRA Elimination: The combination of metabolism plus excretion is called elimination. Drug – food interactions Drug toxicity - Theophylline and caffeine which can result in excessive CNS excitation - Potassium-sparing diuretics and salt substitutes can result in dangerously high potassium levels Drug action - Warfarin and foods rich in vitamin K, Vitamin K reduces the effects of warfarin because warfarin inhibits vitamin K- dependent clotting factors Timing of drug administration - Some drugs are better tolerated on an empty stomach - Others should be taken with food, especially for nausea Drug – drug interactions With pharmacokinetic interactions, the basic mechanisms of drug-to-drug interactions are: Altered absorption  Altered distribution Altered renal excretion Altered metabolism P-glycoprotein Drugs and special populations (lifespan) MODULE 2: ONCOLOGY Colon cancer reading– Review terms Neoplasia or ‘New growth’ : tissue that exceeds normal growth patterns - Neoplasm= tumor Cell differentiation: The process whereby proliferating cells become progressively more specialized cell types - Benign proliferation: well differentiated cells that appear in a mass. - Malignant proliferation: less differentiated cells that can travel from the site of origination to remote sites. THEY CAN BREAK LOOSE which is what makes it deadly because it invades other systems in the body Benign vs metastatic Cancer growth properties - Normally, the number of cells produced = the number of cells that die. - Therefore, the total number of cells in the body remains constant. - In cancer, growth fraction (dividing:resting cells) increases and doubling time decreases. Cell cycle: The cell cycle consists of four major phases: G1, S, G2, and M. - G1: cell prepares to make DNA by synthesizing histones - S phase: DNA synthesis actually takes place - G2: prepares for mitosis (cell division) - M: mitosis occurs Resulting daughter cells have two options: enter G1 and repeat cycle or enter G0 which is when they become mitotically dormant so they do not replicate for days,weeks, or even years, Cancer associated genes: Transformation of healthy cells chart starts with a carcinogenic agent moving to the normal cell. From there, DNA damage occurs and when DNA repair start, the DNA repair genes can reverse the effects and make it into a normal cell again. If not, after DNA damage there is a failure of DNA repair and activation of growth-promoting oncogenes, inactivation of tumor-suppressor genes happens, and alterations in genes that control apoptosis occurs. After that, unregulated cell differentiation and growth occurs and the cell becomes a malignant neoplasm. Proto-oncogenes: - normal genes that can mutate into cancer causing genes - These genes code for normal cell proteins and growth factors, growth factor receptors, transcription factors, etc. Oncogenes: - Proto-oncogenes mutate to oncogenes. - Oncogenes are cancer causing genes.  - Insertions, deletions, translocations increased or activated - Examples: Philadelphia chromosome and chronic myelocytic leukemia; HER-2/neu gene and breast cancer. Tumor suppressor genes - inhibit cell division and suppress cancer formation - Tumor suppressor genes reduce cancer growth. - Mutations to this gene remove the inhibition to cancer genesis. - So if it runs in your family (genetics) or environmental factors that can cause these tumor suppressor genes to to become less active which allows for the formation of cancer in the body The types of genes involved in cancer are numerous, with the two main categories being the proto-oncogenes, which control cell growth and replication, and tumor suppressor genes, which are growth-inhibiting regulatory genes Stages of cancer genesis Stages of Carcinogenesis: The process by which carcinogenic (cancer-causing) agents cause normal cells to become cancer cells is hypothesized to be a multistep mechanism that can be divided into three stages: 1. Initiation: Exposure to carcinogenic agents. DNA damage and initial mutation occurs. - Carcinogenic agent can be chemical, physical biological and produce irreversible changes in the genome of the normal cell 2. Promotion: Mutated cells are stimulated to divide. Is reversible if promoter substance is removed. 3. Progression: Tumor cells compete with one another and develop more mutations which make them more aggressive, resulting in invasion and metastasis. Host and environmental factors - More than likely cancer occurs bc of multiple interactions of risk factors or exposure to a angle carcinogenic agent - Inheritance of genes – breast cancer, ovarian cancer, prostate, and pancreatic cancers are associated with BRCA-1, BRCA-2 - Reproductive hormones – Women (breast and ovary), Men (prostate and testis) - Obesity and higher cancer mortality rates: Obese people tend to produce increased amounts of androgens, a portion of which is converted to the active form of estrogen in adipose tissue, causing a functional state of hyperestrogenism. Because of the association of estrogen with postmenopausal breast cancer and endometrial cancer, the relation is stronger among women than among men.  - Immune system can assist in resistance to cancer through surveillance. This is supported by the use of immunotherapy as cancer treatment. - Traditional risks (HOST): hereditary, hormonal factors, immunologic mechanisms - Immune system plays a central role in resistance against the development of tumors.5, - Environmental agents: chemicals, radiation, cancer causing viruses, alcohol use Effects and manifestations of cancer Local Effects of Tumor Growth on tissue integrity - Compression of adjacent structures - Hollow organs – compression of the viscera and production of obstructions -Blood vessel invasion—Bleeding, hemorrhage - Effusions – production of fluid into body spaces - Sites: Pleural (lung), pericardial (heart), peritoneal (abdomen) - Manifestations based on the site of the effusion Manifestations of Cancer - Site of the cancer determines many of the clinical manifestations. - Example: Lung cancer produces manifestations of pulmonary dysfunction. - Once there is metastasis, other symptoms develop based on the site of metastasis. Systemic Manifestations of Cancer - Anorexia – cachexia syndrome: Lack of appetite (anorexia) with weight loss and protein wasting. More common in children and elderly. The syndrome worsens as cancer advances. - Fatigue and sleep disturbances – most common side effects in cancer patient. Fatigue is not improved with rest. Sleep disturbances include poor sleep quality and night time waking. - Anemia – Low red blood cell counts related to blood loss, lack of red blood cell production, and nutritional issues. Chemotherapy can affect blood counts. Metastasis  The primary tumor is a group of cells with a metastatic subclone using intravasation to enter the bloodstream. The cells then have interaction with lymphocytes and become a tumor cell embolus with platelets attached to the outside. Those then go through extravasation and leave the stream and become a metastatic tumor with angiogenesis holding them to the outside of the stream. Cancer diagnosis IMPORTANT: BIOPSY Study the cell to see what is going on with the cell that is the FIRST THING to do when initial finding to make sure they are ACTUAL cancer cells Tumor markers: - detect antigens produced by or as a response to a tumor - Not as effective in screening for cancers, but more effective to monitor progression. - PSA prostate-specific antigen, and CA125 for ovarian cancer - Some substances, such as hormones and enzymes, that are produced normally by the involved tissue become overexpressed as a result of cancer. - Other tumor markers, such as oncofetal proteins, are produced during fetal development and are induced to reappear later in life as a result of benign and malignant neoplasms - Extremely elevated levels of a tumor marker can indicate a poor prognosis or the need for more aggressive treatment. - The level of most cancer markers tends to decrease with successful treatment and increase with recurrence or spread of the tumor. Cytologic studies - examine tissue and cells microscopically for abnormal cells. - Pap (Papanicolaou) test for cervical cancer: The usefulness of the Pap test relies on the fact that cancer cells lack the cohesive properties and intercellular junctions that are characteristic of normal tissue. Tissue biopsy - removal of tissue for microscopic examination  - Fine needle aspiration for palpable tumors such as breast cancer. - Excisional biopsies for ENTIRE tumor removal. Immunohistochemistry - Immunohistochemistry involves the use of antibodies to facilitate the identification of cell products or surface markers - Identification of cell markers on cancer cells is used to determine the original site of a cancer or for treatment options for best success. In cases in which the origin of the metastasis is obscure, immunochemical detection of tissue-specific or organ-specific antigens can often help to identify the tumor source. - Estrogen receptor on breast cancer determine the use of antiestrogen therapy Grading and staging (general information) The two basic methods for classifying cancers are grading according to the histologic or cellular characteristics of the tumor and staging according to the clinical spread of the disease. Both methods are used to determine the course of the disease and aid in selecting an appropriate treatment or management plan. Grading: - Microscopic examination of differentiation and number of mitoses (grades I – IV) I = well differentiated; IV = poorly differentiated - Surgery may be used to determine tumor size and lymph node involvement. Staging: - Clinical, radiographic, surgical examination to determine the extent and spread. Is important for treatment and prognosis. - TNM: Tumor, Node, Metastasis - T 1–4 = tumor size- 4 being progressive increase i n tumor size or involvement - N 0–3 = lymph node involvement- 3 being increasing involvement of regional lymph node - M0–1 = metastasis- 1 being distant metastasis present, specify sites Treatments - The goals of cancer treatment methods fall into three categories: curative, control, and palliative. - Surgery – will be discussed in clinical courses - Radiation therapy – will be discussed in clinical courses - Chemotherapy - Hormone and anti-hormone therapy - Biotherapy- Cancer in children  - Usually hematologic, nervous, soft tissues, or bone. - Incidence is greatest during the first years of life. - No early warning signs or screening tests. - Treatments produce late sequelae in long term survivors - A number of the tumors of infancy and early childhood are embryonal in origin, meaning that they exhibit features of organogenesis similar to that of embryonic development. - Neuroblastomas arise from the primordial neural crest tissue in the sympathetic nervous system and adrenal medulla.It is the second most common solid malignancy in childhood after brain tumors. Colorectal cancer PHARMACOLOGY General principles of chemotherapeutic pharmacology Tissue growth and chemotherapy The growth fraction - Impact of tissue growth fraction on responsiveness to chemotherapy (high growth fraction, more responsive)- - The ratio of proliferating cells to G0 cells is called growth fraction - A tissue with a large percentage of proliferating cells and few cells in G0 has HIGH growth fraction. - If tissue is mostly composed of G0 cells then it has LOW growth fraction Chemotherapy drugs are also more toxic to normal tissue with high growth fraction - Bone marrow - Skin - Hair follicles - Sperm - Gastrointestinal tract - Really understand this to know how chemotherapy will work : As a rule, the most common cancers—solid tumors of the breast, lung, prostate, colon, and rectum—have a low growth fraction, so they respond poorly to cytotoxic drugs. In contrast, only some rarer cancers—such as acute lymphocytic leukemia, Hodgkin’s disease, and certain testicular cancers—have a high growth fraction, so they tend to respond well to cytotoxic drugs. - Sooooooooo, In practical terms, this means that the most common cancers, which do not respond well to drugs, must be managed primarily with surgery. Only a few cancers can be managed primarily with drugs. Solid tumors do not respond well to chemotherapy (low growth fractions). - There are two reasons for low responsiveness. - First, G0 cells do not perform the activities that most anticancer drugs are designed to disrupt.  Second, because G0 cells are not active participants in the cell cycle, they have time to repair drug-induced damage before it can do them serious harm. - The decrease in growth fraction in older tumors is a major reason why therapeutic success is more likely when cancers are detected early. Because the rate of growth declines as a tumor gets larger Obstacles and strategies for chemotherapy - Toxicity to normal cells prohibits the delivery of doses needed to cure. - Cure requires 100% cell kill since any remaining cells can proliferate’ - Early detection is not possible (1 billion cells needed to detect a solid tumor). - Solid tumors do not respond well to chemotherapy (low growth fractions). - Drug resistance can develop. Toxicities - CYTOTOXIC: toxic to normal tissues especially those that have high percentage of proliferating cells - TOXICITY: is major issue when giving out these drugs t Toxicity to normal cells prohibits the delivery of doses needed to cure: - Injury to normal cells occurs primarily in tissues where the growth fraction is high: bone marrow, GI epithelium, hair follicles, and germinal epithelium of the testes. - Why are cytotoxic anticancer drugs so harmful to normal tissues? Because these drugs lack selective toxicity - To make a cytotoxic drug that is truly selective, the target cell must have a biochemical feature that normal cells lack (think about it like this to better understand why we havent found cure for cancer — By way of illustration, let’s consider penicillin, which kills bacteria by disrupting the bacterial cell wall. Because our cells don’t have cell walls, penicillin cannot hurt us) - MODULE 3: INFECTION Fever patterns: - Intermittent fever pattern: returns to normal at least once in a 24 hr period - Remittent fever: does not return to baseline - Sustained fever: Little variation and no return to baseline - Relapsing fever: Normal for several days before return of fever  Fever mechanisms in five steps: 1. Release of PGE2 or fever-producing cytokines from inflammatory cells. 2. Resetting thermostatic set point in the hypothalamus. 3. Temperature-raising responses: Vasoconstriction, shivering, piloerection, increased metabolism with fever. 4. Core body temperature reaches new set point. 5. Temperature-reducing responses: Vasodilation, sweating, increased ventilation. Manifestations of fever - Prodromal – headache, fatigue, malaise - Chill – sensation of chilling with shaking - Flush – vasodilation with warm skin - Defervescence – sweating Lifespan and fever: Fever in children - decreased immune system - Most due to infection – lethargy seen - Must be watched carefully for development of serious infection Fever in older adults - Lower baseline - May have no or little elevation of temperature - Change in mental status Mechanisms of infectious disease: Prions - Small modified infectious proteins - No genome (RNA or DNA) - Abnormally shaped versions of your own proteins - Cause normal proteins to change shape and become new prions - Can clump together and damage cells - Cause degenerative disease in the central nervous system (e.g., ‘mad cow’ disease) Infection vs colonization; - “Infection” means presence and multiplication. Infection can be identified by areas of redness, tenderness, pain, and frequently with fever - “Colonization” means establishing a presence. Colonization examples: The skin is colonized with bacteria (frequently staphylococcus) on the surface; the GI system is colonized with various bacteria that aid in digestion; microflora are colonizes and are present on the surface of the body Microorganisms make someone ill if there is injury or damage produced Basic characteristics of viruses and bacteria and fungi: Viruses - Cause infectious diseases and malignancies (oncogenic viruses ) - Protein coat surrounding nucleic acid core - DNA or RNA (retroviruses, e.g., HIV) - Cannot reproduce without a host - Use the host cells to make new viruses Bacteria - Autonomously replicating unicellular organisms - Classified as prokaryotes—cells without nuclei and other membrane-bound organelles - Bacteria are classified by shape and staining properties - Shapes: Cocci, bacilli, or spirilla - Gram stain: Positive or negative bacterium based on cell membrane/wall characteristics. - Use hosts for food and shelter - Bacteria shapes Fungi  - Eukaryotic microorganisms - yeasts and molds - Cell walls different from bacteria. - Most require a cooler temperature than human core body temperature. - Most infections are on the surface of the body (ringworm, athlete’s foot) - Systemic fungal infections are serious infections. - Fungi—Yeasts and Molds Portals of entry and sources: Virulence factors: Make an infection more likely to cause disease. These include: - Toxins: Alter a host’s cells producing damage to normal function. - Adhesion factors help the infective organism adhere to and infect the host. - Evasive factors help keep the immune system from killing the infective agent. Toxins - Produced by some bacteria, fungi, protozoans Two main types: Bacterial Endotoxins - Released from parts of the gram-negative bacterial cell wall - Cause host immune inflammatory reactions Bacterial Exotoxins - Released by bacteria and activate clotting, bleeding, inflammation, hypotension, fever. - Damage or kill host cells through endotoxic shock. Stages of infection and diagnosis: - Incubation stage – active replication without producing symptoms - Prodromal stage – initial symptoms (may be vague) as pathogen continues to replicate - Acute stage – pathogen is multiplying and disseminating (most symptoms) - Convalescent stage – resolution of symptoms as pathogen is contained - Resolution stage – pathogen eliminated Effect of antibiotics on microorganisms: How microorganisms develop resistance: Delaying Emergence of Drug Resistance - Treat infections, not contamination  - Treat infections, not colonization - Vaccinate! - Know when to say “No to vanco” - Stop treatment when infection is cured or unlikely - Isolate the pathogen - Break the chain of contagion MRSA: MRSA – Methicillin Resistant Staphylococcus Aureus - Colonized on the skin - Produce infections of skin and soft tissue - Community acquired and hospital acquired - Serious infections of the blood and lungs - Resistance developed in the 1960’s - Genetic mutation – low affinity for penicillins and cephalosporins - Spread by person-to person contact - Careful use of antibiotics (limit use of vancomycin) C. diff: Clostridium Difficile (Bowel infection caused by antibiotic use – Clostridium Difficile (Box 89-1) - Gram positive anaerobic bacillus - Preceded by antibiotic use which kills normal gut flora infects the bowel - Spread through the ingestion of C. diff spores (fecal shedding) - Spread on the hands of health care workers (spores can survive weeks on inanimate objects) - Can produce severe symptoms – shock and death - Oral metronidazole or vancomycin are typical treatmen MODULE 3: PAIN Pathophysiology of pain: What is pain? Unpleasant sensory and emotional experience associated with actual or potential tissue damage (Norris p. 350) Influenced by anxiety, culture and past experience  The most reliable method of assessing pain is to have the patient describe his or her experience Pain is inherently personal and subjective Who defines pain? The patient! Somatosensory system Provides information about touch, temperature, body position, and pain The experience of pain is transmitted via the nervous system and is organized by: ○ Three levels (orders) of neurons leading to the brain (nociceptive pain) ○ Spinal nerves (dermatomes) ○ Nerve fibers specific to pain - type A and type C. Theories of pain: Specificity theory ○ Special pain receptors detect pain (nociceptors). Pattern theory ○ Sensory receptors are shared by other modalities (temperature, touch, etc.) but pain produces specific patterns that are recognized as pain. Gate control theory (Melzack and Wall) ○ Pain can be modulated (regulated) at the level of the spinal cord. Activation of ‘touch’ fibers can block pain impulses. ○ Therefore, tactile stimulation can ‘close the gate’ and block pain. Neuromatrix theory (Melzack) ○ The brain identifies pain as a multi component phenomenon. Pain includes sensory, affective, and cognitive components. Nerve Fires associated with pain (first, second, and third order): A fibers ○ Large, myelinated fibers ○ Impulses travel quickly; “fast pain” C fibers ○ Small, unmyelinated ○ Impulses slower; “slow-wave pain” First order: ○ Nerves Detects the sensation and transmits to the dorsal root ganglion in the spinal cord. Second order: ○ in the spinal cord; transmits message to the thalamus Third order: ○ from the thalamus to the sensory cortex (brain). Type of pain: Duration – ○ Acute: shorter duration that ends when pathology is resolved (surgery, trauma, etc.) ○ Chronic: longer than expected (typically 6 months) and sustained by pathophysiologic factors that are remote from the causation; a detailed pain history should be obtained ○ Treatment approaches will differ Location – ○ Cutaneous (superficial) ○ Deep/visceral Referred – (IMPORTANT TO KNOW FOR EXAM) ○ Pain is perceived at a site different than the origin site (cardiac refers to the shoulder/back/neck; appendicitis often refers to the umbilicus) Think of it like when you feel pain in one area it might not actually be where the pain is actually stemming from. Neuropathic pain – ○ disorder of the peripheral nerve causing sensory disturbances. Can be caused by diabetes, alcohol abuse, hypothyroidism. ○ Phantom limb pain is thought to be due to nerve damage with amputation. Neuralgia – ○ severe brief attacks of pain ○ Trigeminal neuralgia (tic douloureux) – pain from damage to the trigeminal nerve (face) ○ Postherpetic neuralgia – constant or intermittent severe pain after resolution of herpes zoster (shingles). Pain management: Interventions/management  ○ Nonpharmacologic interventions ○ Pharmacologic treatment ○ Surgical treatment Management Strategy ASK about pain regularly: Assess pain systematically BELIEVE the patient and family in their reports of pain and what relieves it CHOOSE pain control options appropriate for the patient, family, and setting DELIVER interventions in a timely, logical, coordinated fashion EMPOWER patients and their families. Enable patients to control their treatment to the greatest extent possible The Joint Commission Pain Management Standards Purpose is to make assessment and management of pain a priority in healthcare The institution is responsible for the management of patient pain Compliance is mandatory (institution can lose accreditation). Standards focus on: ○ Patient’s rights for assessment and management of pain ○ Interdisciplinary teams use a systematic approach to pain management Pain sensitivity: Hyperalgesia: increased painfulness Hypoalgesia/analgesia: reduced/lost pain sensation Allodynia: pain after non-noxious stimulus Headaches: Common reason to seek care from providers Multiple causes Primary or secondary causes Most concerning – sudden onset, accompanied by neurologic symptoms, exertional headaches, headaches in pregnant women or with a history of cancer Migraine – run in families. Influenced by estrogen and diet. ○ Major subtypes: With and without aura (an aura precedes the headache) ○ Symptoms: Throbbing head, nausea, light sensitivity, ○ Triggers: Stress, hormone fluctuations, sleep disturbances Cluster – more men than women. Headaches ‘cluster’ over time followed by headache free time.  ○ Symptoms: Burning or stabbing pain around the eye or temple ○ Triggers: cigarette smoking and alcohol Tension type – most common, does not interfere with daily activity ○ Symptoms: a tight or squeezing sensation around the head ○ Trigger: Stress, intense emotions, fasting Chronic daily – 15 days a month Pain assessment and evaluation: Assessment should include a variety of information including onset, nature, severity, location, radiation ○ May use various formats (PQRST, OLD CARTS, etc.). ○ Be consistent. Pain assessment tools ○ Numeric pain intensity/rating (0-10) ○ Verbal descriptor (none, slight, mild, moderate, severe) ○ Visual analog scale – line that is 10 cm long, patient marks a point on the line to represent pain Assessment and Ongoing Evaluation Comprehensive initial assessment with chronic or cancer pain ○ Intensity and character of pain ○ Physical and neurologic examination ○ Diagnostic tests ○ Psychosocial assessment ○ Pain intensity scales Barriers: Inaccurate reporting by patient Underreporting by patient Language and cultural barriers Physical/psychosocial interventions: Physical interventions Heat Cold Massage Exercise  Acupuncture and transcutaneous electrical nerve stimulation Psychosocial interventions Relaxation and imagery Cognitive distraction Peer support groups Special populations: Decreased respiratory reserve (asthma, emphysema) – will compromise respirations Labor and delivery – respiratory depression in the neonate Head injury – Use with caution. Elevates ICP. Other precautions – infants, geriatric patients, hepatic disease, hypotension. Patient education: Family education – Family should never operate the pump Terms: Nociceptive – injury in the peripheral tissues ○ Nociceptive pathways are the first, second and third order neurons Neuropathic – direct injury to the sensory axons of the nerves Physical dependence: State in which an abstinence syndrome will occur if the dependence-producing drug is abruptly withdrawn; it is NOT equated with addiction Abuse: Drug use that is inconsistent with medical or social norms Addiction: Behavior pattern characterized by continued use of a psychoactive substance despite physical, psychologic, or social harm Hyperalgesia: increased painfulness Hypoalgesia/analgesia: reduced/lost pain sensation Allodynia: pain after non-noxious stimulus PHARMACOLOGY Terminology: Opioid ○ A general term that is defined as any drug, natural or synthetic, that has actions similar to those of morphine Opiate ○ A term that applies only to compounds present in opium Opioid Receptors  Three main classes of opioid receptors and the responses to receptor activation. Opioids react mainly with the mu receptors, weakly with kappa receptors and no reaction with delta. ○ Mu receptors: Analgesia, respiratory depression, euphoria, sedation, and physical dependence ○ Kappa receptors: Analgesia and sedation; kappa activation may underlie psychotomimetic effects seen with certain opioids ○ Delta receptors Pure Opioid Agonists Activate mu receptors and kappa receptors Can produce analgesia, euphoria, sedation, respiratory depression, physical dependence, constipation, and other effects Morphine, fentanyl: Strong opioid agonists Codeine, hydrocodone: Moderate to strong agonists Pure Opioid Antagonists Naloxone [Narcan]: Prototype of the pure opioid antagonists Antagonist at mu and kappa receptors Do not produce analgesia or any of the other effects caused by opioid agonists Used for reversal of respiratory and central nervous system (CNS) depression caused by overdose with opioid agonists Opioid receptors (agonist, antagonists): Agonist (activate receptors) Antagonist (prevent receptor activation) Dosing guidelines: Dosage determination ○ Opioid analgesics must be adjusted to accommodate individual variation ○ The prescriber adjusts doses or will provide ranges for nurses to follow Dosing schedule ○ As a rule, opioids should be administered on a fixed schedule for the first 24 hours Avoiding withdrawal - if taking for more than 20 days (taper over 3-10 days) Patient Controlled Analgesia (PCA) pumps: Patient-controlled analgesia (PCA) Patient-controlled analgesia devices  ○ Limits placed on total dose delivered each hour and how often dosing can occur. Morphine is most commonly used opioid Research shows improved patient outcomes with patient-controlled analgesia versus traditional intramuscular therapy ○ Multiple intramuscular injections: Painful to the patient; cause negative side effects, including bruising and hematoma formation AHA statement on COX inhibitors: American Heart Association Statement on COX Inhibitors American Heart Association (AHA) recommends a stepped-care approach to pain ○ Step 1: Non-drug approach ○ Step 2: Acetaminophen or aspirin ○ Step 3: Non-selective NSAIDSn ○ Stop 4: Selective Cox II inhibitors Most COX inhibitors, especially COX-2 inhibitors, increase the risk for MI and stroke