Final Exam 393 - Biology PDF

Date of Final: Mon. 12/2 9am Room #1014 Final Exam 30% of grade From the Final Exam Blueprint Genetics, Protein Production, & Cell Communication Explain DNA replication, transcription, and translation, and relate these to protein production Describe the functional and structural roles pro...

Date of Final: Mon. 12/2 9am Room #1014 Final Exam 30% of grade From the Final Exam Blueprint Genetics, Protein Production, & Cell Communication Explain DNA replication, transcription, and translation, and relate these to protein production Describe the functional and structural roles proteins play in cell, organ, and organ system function Compare and contrast the structure and function of ligand-gated ion channel receptors, G-protein coupled receptors, enzyme-linked protein receptors, and intracellular receptors Identify the key ANS receptors and their effects in target organs/tissues Explain DNA replication, transcription, and translation, and relate these to protein production Definitions DNA Replication: DNA makes a copy of itself during cell division Transcription: mRNA is synthesized from single stranded DNA template Translation: mRNA directs synthesis of proteins DNA Replication Occurs in Nucleus of Eukaryotic cells and Cytoplasm of Prokaryotic cells during Synthesis phase Helicase: Unzipper enzyme Polymerase: Adds correct nucleotides, Proofreads Mutations: Wrong pairing or sequence Related to Protein Production: DNA replication ensures that the genetic information is accurately copied before cell division, so the same instructions for protein production are passed on to new cells. Transcription Occurs in Nucleus of the cell mRNA is synthesized from single stranded DNA template RNA polymerase: Separates, matches, proofreads Similar to Replication, U replaces T in mRNA Relation to Protein Production: Transcription converts the DNA sequence into mRNA, which serves as the blueprint for protein synthesis in the next step, translation. Translation Occurs in the Cytoplasm of cell mRNA interacts with ribosomes Ribosomes read sequence tRNA assembles amino acids into proteins Once again, possibility for errors Relation to Protein Production: Translation uses the mRNA to assemble amino acids into a protein, based on the genetic instructions encoded in the DNA. Describe the functional and structural roles proteins play in cell, organ, and organ system function Function Description Example Why it’s an example Structure Provide support and shape Elastin, Collagen Both provide structural to cells and tissues. support: Collagen strengthens tissues, and Elastin allows stretch. Antibodies Help protect the body by Immunoglobulin Infusion Immunoglobulin contains binding to harmful antibodies that fight off invaders like viruses and infections by targeting bacteria. foreign invaders. Enzymes Speed up chemical Helicase, Polymerase Helicase unwinds DNA, reactions in cells, such as and Polymerase helps replication, transcription, build DNA and RNA, and translation. speeding up genetic processes. Messengers Transmit signals to help Insulin, Oxytocin, Growth These hormones act as regulate and coordinate Hormone messengers that regulate biological processes. blood sugar, childbirth, and growth, respectively. Transport and Storage Bind and carry small Hemoglobin Hemoglobin carries molecules and atoms oxygen in the blood, within cells and the body. transporting it from lungs to tissues. Structural Roles of Proteins: Proteins help give cells and tissues their shape and strength. For example, collagen strengthens tissues, while elastin lets them stretch. Hemoglobin keeps red blood cells in shape while carrying oxygen. Functional Roles of Proteins: Proteins also help with important tasks in the body. Enzymes speed up reactions, antibodies fight off germs, and hormones like insulin send signals to control things like growth and blood sugar.  Compare and contrast the structure and function of ligand-gated ion channel receptors, G-protein coupled receptors, enzyme-linked protein receptors, and intracellular receptors Receptor Type Structure Function Primary Secondary Key Feature Messenger Messenger Ligand-Gated Ion Protein with a Opens to let ions Ligand (e.g., None (direct ion Direct ion flow when Channel pore in the into the cell when neurotransmitters) flow) ligands bind. membrane. the ligand binds. (Transmembrane) G-Protein Coupled Protein with 7 Activates a Ligand (e.g., cAMP, Calcium, etc. Uses a second Receptor parts in the G-protein inside hormones, messenger to send membrane. the cell to start a neurotransmitters) signals. (Transmembrane) signaling pathway. Enzyme-Linked Protein with a Activates an Ligand (e.g., None (direct enzyme Activates an enzyme Receptor built-in enzyme. enzyme inside the growth factors) action) directly when ligand cell when the binds. (Transmembrane) ligand binds. Intracellular Receptor Inside the cell, Binds to ligands Ligand (e.g., None (direct gene Affects gene expression often in the that can cross the steroid hormones) regulation) directly. (Cytoplasmic & nucleus. cell membrane Nuclear) and affects gene expression. Ligand-gated ion channels let ions in directly when the ligand binds. GPCRs and enzyme-linked receptors use secondary messengers to pass signals inside the cell. Intracellular receptors affect gene expression directly by binding ligands inside the cell. Transmembrane Receptors - Work by interacting with ligands outside the cell. Examples → Ligand-gated ion channels lets ions in, GPCRs activate secondary messengers, and enzyme linked receptors activate enzymes Intracellular Receptors - Work inside the cell, affecting gene expression after the ligand enters the cell. Example → Cortisol binds to a receptor in the cytoplasm and changes gene activity Identify the key ANS receptors and their effects in target organs/tissues PARASYMPATHETIC RECEPTORS Receptor Type Location Neurotransmitter Effect on Target Organ/Tissue Nicotinic Receptors Skeletal muscles, Acetylcholine (ACh) Opens ion channels, Autonomic ganglia causing muscle contraction or nerve signal transmission. Muscarinic Receptors Smooth muscles, Glands, Acetylcholine (ACh) M2 receptors: Slow heart Heart rate. M3 receptors: Increase digestion, smooth muscle contraction, and gland secretion. SYMPATHETIC RECEPTORS Receptor Type Location Neurotransmitter Effect on Target Organ/Tissue Alpha-1 Adrenergic Blood vessels, Smooth Epinephrine, Causes vasoconstriction, Receptors muscle Norepinephrine increasing blood pressure and directing blood to vital organs. Alpha-2 Adrenergic Nerve terminals Epinephrine, Inhibits the release of Receptors Norepinephrine norepinephrine, reducing further sympathetic activity Beta-1 Adrenergic Heart Epinephrine, Increases heart rate and Receptors Norepinephrine contractility, boosting cardiac output. Beta-2 Adrenergic Lungs, Blood vessels, Epinephrine, Causes bronchodilation Receptors Liver Norepinephrine (opens airways), vasodilation, and stimulates glucose release for energy. Parasympathetic receptors use acetylcholine to regulate body functions like digestion and heart rate. Sympathetic receptors use epinephrine and norepinephrine to trigger the fight or flight response, increasing heart rate, blood pressure, and energy release.  From the Final Exam Blueprint Pharmacokinetics Describe common routes for drug administration Compare benefits and disadvantages associated with common routes of administration Describe pharmacokinetic (PK) processes of absorption, distribution, metabolism, and excretion (ADME) Identify common pharmacokinetic parameters associated with PK processes. (e.g., half-life, volume of distribution, etc.) Describe factors that influence PK processes (ADME): Compare how different drugs are handled by the body & Identify potential for drug interactions based on PK Describe how genetic variants can alter metabolism Describe common routes for drug administration Enteral Routes (oral, rectal) go through the GI tract and may be partially broken down in the liver, reducing the drug’s effect. Parenteral Routes (IV, IM, SC) skip the GI tract, allowing the drug to be absorbed faster and more reliably, with IV having the fastest effect and 100% availability Route of Administration Characteristics Examples of First-Pass Effect Onset of Action Benefits/ Disadvantages Drug Types metabolism of a drug in the The time it takes for a drug to liver before it reaches produce its effect after systemic circulation, administration. reducing its effectiveness Oral Most convenient, Tablets First-pass effect Slow (depends on Benefits: Convenient, easy (Enteric - via GI tract) inexpensive, (metabolism in food) to use, inexpensive, non-sterile Capsules liver) non-sterile, and can be self Takes time for the administered Liquids Drug is absorbed in drug to be absorbed the intestines, then and processed in the Disadvantages: Slow onset, Chewables metabolized by the GI tract. first-pass effect (reduces liver before drug effectiveness), may entering have food interactions circulation, reducing effectiveness. Rectal Erratic Suppositories Less first-pass Moderate Benefits: Useful when oral (Enteric - via GI tract) absorption Rectal effect than oral administration isn't possible, solutions Absorbed through bypasses some first-pass Some of the drug the rectum, but metabolism bypasses the liver, absorption can be but still undergoes erratic. Disadvantages: Erratic partial first-pass absorption, uncomfortable, metabolism. less predictable onset Sublingual/Buccal(Enteric Absorbed under Tablets Bypasses first-pass Rapid Benefits: Fast onset, - via GI tract) the tongue or in Lozenges bypasses first-pass cheek Films Drug enters the Drug is absorbed metabolism, easy to use bloodstream directly into the directly, avoiding bloodstream via Disadvantages: liver metabolism. mucous membranes May be difficult for some under the tongue or patients to use, not all drugs  cheek. are effective in this form Route of Administration Characteristics Examples of First-Pass Effect Onset of Action Benefits/ Disadvantages Drug Types metabolism of a drug in the The time it takes for a drug to liver before it reaches produce its effect after systemic circulation, administration. reducing its effectiveness Intravenous (IV) Directly into Infusions Bypasses first-pass Very rapid Benefits: Irreversible once (Parenteral - outside GI bloodstream, administered, requires tract) reliable, rapid Injection Drug is delivered Drug enters directly medical supervision, onset solutions directly into into the bloodstream, potential for complications circulation without leading to almost (infection, vein irritation) liver metabolism. immediate effect. Disadvantages: Irreversible once administered, requires medical supervision, potential for complications (infection, vein irritation) Intramuscular (IM) Injected into Injections Bypasses first-pass Moderate Benefits: Painful, (Parenteral - outside GI muscle tissue unpredictable onset, risk of tract) Direct absorption Absorption is faster muscle damage or irritation into bloodstream than oral but slower without liver than IV, depending Disadvantages: Painful, metabolism.s on the muscle site. unpredictable onset, risk of muscle damage or irritation Subcutaneous (SC) Injected under Injectable Bypasses first-pass Slower than IM Benefits: Slower onset than (Parenteral - outside GI the skin solutions IV, smaller volume, may tract) Like IM, it avoids Absorption is slower cause local irritation Insulin pens liver metabolism due to smaller before reaching injected volume and Disadvantages: Slower onset Auto injectors circulation.s tissue distribution. than IV, smaller volume, may cause local irritation Inhalation Breathing in drug Aerosols Bypasses first-pass Very rapid Benefits: Irritation to (Parenteral - outside GI as gas or aerosol respiratory system, requires tract) Inhalers Direct entry into Drug enters the proper technique, limited the bloodstream lungs and quickly drug types can be inhaled Nebulizers avoids liver reaches the metabolism. bloodstream, often Disadvantages: Irritation to with immediate respiratory system, requires effects. proper technique, limited drug types can be inhaled Route of Administration Characteristics Examples of First-Pass Effect Onset of Action Benefits/ Disadvantages Drug Types metabolism of a drug in the The time it takes for a drug to liver before it reaches produce its effect after systemic circulation, administration. reducing its effectiveness Transdermal Absorbed Patches Bypasses first-pass Slow, prolonged Benefits: May cause skin (Parenteral - outside GI through the skin irritation, slow onset, tract) (e.g., patches) Drug enters Drug is absorbed limited to certain drugs circulation directly through the skin and through the skin.s released over time. Disadvantages: May cause skin irritation, slow onset, limited to certain drugs Topical Applied directly Creams Very limited Variable Benefits: Limited to external (Parenteral - outside GI to skin, eyes, systemic absorption conditions, may not tract) ears, nose, etc. Ointments Depends on the site penetrate deeply enough for Minimal systemic and type of drug; some treatments Gels absorption, so little typically slower for to no first-pass localized effects. Disadvantages: Lotions effect. Limited to external conditions, may not penetrate deeply enough for some treatments Describe pharmacokinetic (PK) processes of absorption, distribution, metabolism, and excretion (ADME) Four Basic Pharmacokinetic Processes: Absorption, Distribution, Metabolism, Excretion  A Absorption Drug moves from site of Factors affecting admin to systemic circulation Drug Form & Characteristics: How the drug is made (tablet, liquid) and its chemical properties (how it dissolves and whether it’s charged). Body Conditions: Things like food in the stomach, blood flow, and surface area in the intestines (like villi) affect how well the drug absorbs. Transport & Time: P-glycoprotein (Pgp) can pump drugs out, and conditions like diarrhea can reduce contact time, affecting absorption. D Distribution Drug moves from Factors affecting systemic circulation to tissues Drug & Body Characteristics: Drug’s ability to cross membranes and characteristics like size and charge. Blood Flow & Barriers: How well blood circulates and if there are barriers like the blood-brain barrier. Body Conditions: Factors like obesity, hydration, or protein levels (albumin) that can affect where and how much of the drug is distributed. M Metabolism Biotransformation Factors affecting Metabolite is the product Drug & Body Characteristics: Drug’s chemical structure (e.g., of biotransformation size, charge) affects how it interacts with enzymes. Blood Flow & Barriers: Liver blood flow and enzyme activity can influence how quickly and efficiently drugs are metabolized. Body Conditions: Factors like liver health, age, or disease (e.g., liver damage, obesity) can impact metabolism speed and effectiveness. E Excretion Removal of drug or drug Factors affecting metabolites from the body Drug & Body Characteristics: Drug’s solubility and size impact how easily it’s filtered out of the body. This can occur in the Blood Flow & Barriers: Blood flow to kidneys and other kidneys, GI tract (bile), excretion sites (like lungs) affects how quickly the drug is lungs, skin, and breast removed. milk Body Conditions: Kidney function, age, hydration, and other health factors can influence the rate of excretion. Note: Elimination is the removal of drug from the body which includes the metabolism and excretion. Identify common pharmacokinetic parameters associated with PK processes. (e.g., half-life, volume of distribution, etc.) Half-Life: Time for the drug's effect to decrease by half (influenced by metabolism and excretion). Bioavailability: How much of the drug reaches circulation after administration. Volume of Distribution: How widely the drug spreads throughout the body. Clearance: The rate at which the drug is removed from the body. Cmax & Tmax: Peak concentration and time to reach it. AUC: Total drug exposure over time. First-Pass Effect: Drug loss during absorption due to metabolism in the liver. (PK) parameters associated with the different processes (Absorption, Distribution, Metabolism, and Excretion) PK Parameter Description Associated PK Process Half-Life (t1/2) Time it takes for the drug's plasma Elimination → Metabolism, concentration to decrease by half. Excretion Affects dosing frequency. Bioavailability (F) The percentage of the drug that Absorption enters systemic circulation after administration (related to absorption). Volume of Distribution (Vd) The apparent volume in which the Distribution drug is distributed throughout the body. Higher values = more widespread distribution. Clearance (Cl) The rate at which the drug is Elimination → Metabolism, eliminated from the body (includes Excretion metabolism and excretion). Cmax Maximum plasma concentration of Absorption, Distribution the drug after administration. Indicates the peak level of the drug. Tmax Time it takes to reach the maximum Absorption plasma concentration. Area Under the Curve (AUC) The total exposure of the drug in Absorption, Distribution, the bloodstream over time. Helps Metabolism, Excretion understand bioavailability and drug exposure. Clearance (Cl) Measures the efficiency of the body Elimination → Metabolism, in eliminating the drug through Excretion metabolism and/or excretion. First-Pass Effect The reduction in drug concentration Absorption, Metabolism due to metabolism in the liver before it reaches systemic circulation. Describe factors that influence PK processes (ADME): Compare how different drugs are handled by the body & Identify potential for drug interactions based on PK PK Factor Description How different drugs are handled by the Potential for drug body interactions Absorption How drugs get into your Oral drugs go through the digestive system Drugs can change how bloodstream after you take and may lose some effectiveness well others are absorbed. them. (first-pass effect). Liquid drugs get in For example, antacids can faster. Lipid-soluble drugs are absorbed reduce absorption of some easily. drugs, and food can change how much is absorbed. Distribution How drugs spread through Fat-soluble drugs, like diazepam (Valium), Drugs that bind to proteins the body after entering the can pass into the brain easily. Drugs that can interact by displacing bloodstream. are highly protein-bound, like warfarin, other drugs, increasing free can interact with others. drug levels, which can cause side effects. Metabolism How the liver breaks down Some drugs need the liver to activate them CYP450 enzymes are key drugs, often into active or (e.g., codeine turns into morphine). Some, here. One drug can boost inactive forms. like acetaminophen, can become toxic. or slow down the breakdown of others, changing their effectiveness or causing toxicity (e.g., grapefruit juice or rifampin). Excretion How drugs are removed Water-soluble drugs leave through urine Other drugs can affect how from the body, mostly (e.g., metformin). Fat-soluble drugs may quickly the kidneys through urine but get excreted in bile. If the kidneys aren't remove drugs. For sometimes bile or breath. working well, drugs stay in the body example, NSAIDs can longer. reduce kidney function, which can slow down how other drugs are cleared. Drug How one drug affects the Drugs can change each other's absorption, Drugs that affect CYP450 Interaction action of another drug. metabolism, or how fast they're cleared. enzymes can cause issues. For example, antacids lower the absorption Some drugs slow down the of some meds, and antifungals can slow breakdown of others (e.g., down the breakdown of drugs like fluconazole and statins), or warfarin. speed up their breakdown (e.g., phenytoin and birth control). Describe how genetic variants can alter metabolism Genetic variants can affect how the body metabolizes drugs, mainly through differences in enzymes like CYP450. Slow Metabolizers: Some genetic variations make enzymes work slower, causing drugs to stay in the body longer, which increases the risk of side effects or toxicity. Example: Slow metabolism of clopidogrel due to CYP2C19 leads to reduced drug effectiveness. Fast Metabolizers: Other variations cause faster metabolism, reducing drug levels and potentially making the drug less effective. Example: Rapid metabolism of codeine due to CYP2D6 leads to reduced pain relief. Intermediate Metabolizers: Some people have a normal metabolism but can metabolize a drug slightly faster or slower than average. Example: CYP2D6 variations may cause changes in beta-blocker or opioid effectiveness. Impact on Dosing: Genetic tests can help determine the best drug dose for individuals based on their metabolizer type, reducing risks of side effects or treatment failure. In short, genetic variants influence drug metabolism, affecting effectiveness and safety, and genetic testing can help personalize treatment. From the Final Exam Blueprint Pharmacodynamics Describe how regulations affect drug development and use in the United States Describe how drugs interact with receptors as to produce therapeutic & adverse effects Define the terms agonist and antagonist Describe characteristics of the dose response curve Compare efficacy and potency for two drugs Identify potential for drug interactions based on pharmacodynamics Contrast therapeutic, adverse, and side effects of drugs Describe how genetic variants can alter pharmacodynamic response Pharmacodynamics are the actions of a DRUG on the BODY "D" for "Drug" does something to the "Body" Pharmacokinetics are the actions of the BODY on a DRUG "K" for "Kinetics" relates to "K"ontrol by the "Body" Describe how regulations affect drug development and use in the United States Regulations, such as the Food, Drug, and Cosmetic Act (1938), require safety testing Kefauver-Harris Amendments (1962) added effectiveness testing for new drugs The Controlled Substances Act (1970) classifies drugs by their abuse potential Hatch-Waxman Act (1984) promotes generic drugs Note: Drugs must go through preclinical and clinical trials before being approved, with ongoing post-marketing surveillance for safety. Describe how drugs interact with receptors as to produce therapeutic & adverse effects A ligand is a molecule that binds to a receptor, which is a large protein, to cause an effect in the body. Drugs can either imitate natural ligands to activate receptors or block them to stop the effect. Define the terms agonist and antagonist Agonist is a drug that binds to a receptor and activates it, mimicking the action of a natural ligand. An antagonist is a drug that binds to a receptor but does not activate it. It produces pharmacological effects by blocking the action of the natural ligand or agonist. A partial agonist has moderate intrinsic activity, producing a lower max effect than a full agonist, often used in medication-assisted therapy for opioid use disorder. Drugs that don’t work via a receptor → Antacid, osmotic laxatives, chelating agents (resins) Describe characteristics of the dose response curve The dose-response curve shows how the drug's effect increases with the dose. S- shape Response increases with dose Steepest part of curve → Small increases in dose lead to large changes in the response Efficacy: The maximum effect a drug can produce, which is reflected in the level where the curve levels off. Dose-dependent: The response increases as the dose increases up to a point, beyond which it levels off. Levels off because the receptors become saturated. Once all the receptors are occupied by the drug, increasing the dose further does not increase the response. Steeper slope: More potent drug, small dose increase causes large response. Flatter slope: Less potent drug, dose increases cause gradual response. Safer: Flatter slope is safer, as the effect increases more slowly, reducing overdose risk Compare efficacy and potency for two drugs Define Potency: Amount of drug needed for a specific response. More potent = lower dose required. Think: Potent = Powerful at Petite dose Define Efficacy: Maximum effect a drug can produce, regardless of dose. Higher efficacy = greater max response. Think: Efficacy - End result, the End goal of effect Example Drug A lowers bp to 120/80 mmHg at 10mg Drug B lowers bp to 120/80 mmHg at 500mg Compare Potency: Drug A is more potent. It achieves the same effect (lowering bp) at a lower dose. Compare Efficacy: Both drugs have similar efficacy because they both reduce bp to the same level. Identify potential for drug interactions based on pharmacodynamics Receptor Interactions Additive: Drugs have combined effects (2 bp meds) Synergistic: One drug enhances another drugs effect (morphine + diazepam) Antagonistic: One drug blocks (reduces) another’s effect (opioid + antagonist blocking opioids) Receptor Sensitivity Agonists (drugs that activate receptors): Can cause tolerance (making them less effective over time) Antagonists (drugs that block receptors): Prevent receptors from being activated by other substances (like natural chemicals or agonists). Dose-dependent: More likely to occur as the dose increases Idiosyncratic: Unpredictable responses, often due to genetic factors Special Toxicity Risks: QT Prolongation: Some drugs increase risk of arrhythmias Narrow Therapeutic Index: Drugs with small differences between effective and toxic doses need close monitoring to avoid toxicity. Example → Warfarin. Contrast therapeutic, adverse, and side effects of drugs Therapeutic Effect: Desired or intended effect of the drug. Examples → Pain relief, blood pressure reduction Adverse Effect: Unintended harmful effects of the drug at normal doses, which can range from mild to severe Example → Nausea from antibiotics Side Effect: Nearly inevitable secondary effects that occur at therapeutic doses, often mild and not harmful but can be bothersome Example → Drowsiness from antihistamines Describe how genetic variants can alter pharmacodynamic response Genetic variants: People’s genes can cause them to respond differently to drugs, affecting how well the drug works and whether it causes side effects Pharmacodynamics ( "D" for "Drug" does something to the "Body"): Changes in receptors (the parts of the body the drug targets) can make the drug stronger or weaker Example → A gene that increases the number of receptors can make the drug work stronger Pharmacokinetics ( "K" for "Kinetics" relates to "K"ontrol by the "Body"): Genes can affect how fast the body breaks down or removes the drug, which can change its effectiveness or cause toxicity Example → A gene that slows down drug breakdown can cause too much of the drug to build up, leading to toxicity Genetic testing: Tests that help doctors predict how a person will respond to a drug, so they can choose the right medication and dose From the Final Exam Blueprint ANS/Neurotransmitters Describe the four parts of a neuron Understand how neurotransmitters are released and bind in neuronal synapses Discuss the effects of the following neurotransmitters: glutamate, serotonin, norepinephrine, epinephrine, GABA, dopamine, acetylcholine, oxytocin, histamine, substance P & nitric oxide Understand the general role of neurotransmitters in movement arousal/sleep, appetite, cognition, mood/emotion, & pain Describe the four parts of a neuron Dendrites: Receive signals from other neurons Cell Body (Soma): Processes incoming signals and contains the nucleus Axon: Carries the electrical signal away from the cell body to the synapse Axon Terminals: Release neurotransmitters to communicate with other neurons Understand how neurotransmitters are released and bind in neuronal synapses Neurotransmitter Release: Released from the presynaptic neuron (axon terminal) into the synapse Binding: Neurotransmitters bind to receptors on the postsynaptic neuron Reuptake: Neurotransmitters are either taken back up by the presynaptic neuron or broken down by enzymes Discuss the effects of the following neurotransmitters: glutamate, serotonin, norepinephrine, epinephrine, GABA, dopamine, acetylcholine, oxytocin, histamine, substance P & nitric oxide Understand the general role of neurotransmitters in movement arousal/sleep, appetite, cognition, mood/emotion, & pain Transmitter Role Clinical Implications Acetylcholine Muscle contraction Affected in Alezhemers disease Cognition Movement Activation of muscles and Arousal Attention Dopamine Movement Low levels → Parkinsons Drive for movement and Desire Motivation High levels → Schizophrenia Reward Movement Appetite Mood/Emotion GABA Inhibitory Neurotransmitter Low levels → anxiety, seizures Gamma-Aminobutyric Acid Reduces Anxiety Movement Gently inhibits activity Promotes Muscle Relaxation Arousal/Sleep Goes against excitement Mood/Emotion Pain Glutamate Excitatory Neurotransmitter Too much can cause excitotoxicity (cell Growth and Glory in learning Involved in learning and damage), involved in neurodegenerative memory diseases. Pain Histamine Wakefulness Sleep disorders, allergies Hypes you up Immune response Arousal/Sleep Allergic reactions Norepinephrine Arousal Low levels linked to depression Nudges you into action Focus High levels linked to anxiety Fight-or-Flight Response Arousal/Sleep Appetite Mood/Emotion Serotonin Mood Regulation Low levels → depression, anxiety Serene mood, sleep, and appetite Sleep Arousal/Sleep Appetite control Appetite Mood/Emotion Oxytocin Bonding Aka “Love Hormone” involved in Opens emotional bonding Childbirth maternal behaviors and social bonding Lactation Movement Arousal/Sleep Appetite Mood/Emotion Pain  Substance P Pain transmission Involved in chronic pain conditions, Sends pain signals migraine, fibromyalgia Pain Nitric Oxide Vasodilation Important for memory Nurtures blood flow Neurotransmission Cardiovascular health Regulating blood flow Mood/Emotion Movement Arousal/Sleep Appetite Mood/Emotion Pain From the Final Exam Blueprint Pregnancy Discuss hormone changes in pregnancy Understand the formation, function, and flow of blood through the placenta Describe the response of the body to pregnancy Describe anatomical changes that contribute to common complaints during pregnancy Describe the actions of specific vitamins, minerals, and dietary supplements to support pregnancy and fetal development Describe US regulation that addresses safety of drugs in pregnancy Define FDA pregnancy categories Identify nursing actions to support safe use of drugs in pregnancy Discuss hormone changes in pregnancy hCG - Human Chorionic Gonadotropin Produced by embryo and placenta Prevents corpus luteum from regressing, keeps progesterone and estrogen levels high Basic for pregnancy test Example of positive feedback loop Estrogen Produced by corpus luteum and placenta Stimulates growth of uterus, breasts, and external genitalia Relaxes pelvic ligaments Progesterone Produced by corpus luteum and placenta Supports early embryo nutrition (before placenta is formed) Decrease uterine contractility to prevent premature labor Understand the formation, function, and flow of blood through the placenta Formation: Develops from trophoblast cells after blastocysts implants in the endometrium. It forms in the uterus after a fertilized egg implants and it continues to grow throughout pregnancy. Function: Nutrient and gas exchange between maternal and fetal blood; hormone production (estrogen, progesterone) Blood flow: Maternal blood from uterine arteries fills intervillous spaces. Oxygen and nutrients diffuse to the fetus, waste products move from fetus to maternal blood. Describe the response of the body to pregnancy Weight Gain: approx 25-35 lbs including fetus, placenta, and extra blood volume Metabolism: BMR increases by 15% in the second half or pregnancy Respiratory: Increased oxygen use (20% more), uterus presses diaphragm Circulatory: Blood volume increases, maternal blood pressure can decrease Kidney: Increased plasma volume, water retention Breast: Development due to estrogen, progesterone, prolactin, oxytocin Describe anatomical changes that contribute to common complaints during pregnancy Uterus: Enlarges to accommodate a growing fetus, causing back pain and pressure on bladder Breasts: Tender, enlarged, and may cause discomfort GI System: Slower motility (constipation), heartburn due to pressure on stomach Circulatory System: Increased blood volume can lead to varicose veins, swelling Describe the actions of specific vitamins, minerals, and dietary supplements to support pregnancy and fetal development Folic Acid Essential for DNA synthesis, prevents neural tube defects 🩸🩸 400-800 mcg/day, start before conception and during 1st trimester Iron Needed for increased RBC mass and fetal development RDA: 27mg/day; can cause constipation and nausea Calcium 𐂯𐂯 Important for fetal skeletal development (3rd trimester) RDA: 1000mg/day ✗ Avoid: High-dose vitamin A (may cause teratogenicity), alcohol, smoking, illicit drugs Describe US regulation that addresses safety of drugs in pregnancy Dec. 2014 FDA Labeling: Replaced letter categories with detailed labeling. Includes pregnancy and lactation risks and information on reproductive potential. Drug registries to track pregnancy outcomes. Define FDA pregnancy categories A No risk in controlled human studies B Animal studies show no risk, or risk found in animals but not confirmed in humans. C Animal studies show fetal harm, but no human studies available. D Positive evidence of fetal risk, but potential benefits may outweigh risks in serious situations. X Fetal abnormalities confirmed; contraindicated in pregnancy. Identify nursing actions to support safe use of drugs in pregnancy Risk vs. Benefit: Always weigh risks of drug use against untreated condition risks. Avoid: Teratogens (e.g., isotretinoin, thalidomide). Education: Inform women of childbearing age about medication safety. Use Alternatives: If possible, choose drugs with a safer pregnancy profile. Monitor: Drug interactions, side effects, and adjust as needed. From the Final Exam Blueprint Fetal and Pediatric Development Discuss the major events of basic embryology including: – Embryonic Period (conception – week 8), including tissue formation – Fetal Period (weeks 9-40), including fetal lung & circulatory development Understand the general patterns involved in pediatric growth and development Identify factors which influence pediatric growth and development Describe the actions of specific vitamins, minerals, and dietary supplements to support pediatric development Predict common age-related effects on PK process of absorption, distribution, metabolism, and excretion Discuss the major events of basic embryology including: – Embryonic Period (conception – week 8), including tissue formation – Fetal Period (weeks 9-40), including fetal lung & circulatory development Stage Timeline Image Key Events Conception Fertilization Fertilization of egg with sperm Cleavage and Week 1-2 Inner Cell Mass → Forms Embryo Blastocyst Trophoblast → Forms placenta Blastocyst hangs in uterus  Implantation Day 7-8 Trophoblast adheres to the uterine wall Post-Fertilization Epiblast → Amniotic sac Hypoblast → Yolk sac Germ Layer Week 3-4 Ectoderm → Skin, nervous system. Formation Mesoderm → Muscles, bones, circulatory system. Endoderm → GI tract, lungs. Embryonic Conception - Week Major organs form (heart, lungs, Period 8 kidneys, GI system) Fetal Period Week 9 - Week 40 Organ growth and maturation. Lungs: Final development for birth. Circulatory System: Shunts blood away from fetal liver and lungs (ductus venosus, foramen ovale, ductus arteriosus). Hemoglobin & 12 Weeks Bone marrow produces RBCs Blood Fetal hemoglobin can carry 20-50% more oxygen than maternal hemoglobin Understand the general patterns involved in pediatric growth and development Growth → Increase in physical size (height/weight/head circumference) Development → Milestones that increase function and complexity (motor skills/cognitive development) Patterns of Growth Cephalocaudal: Development from head to toe Proximodistal: Development from center of body outward 🐇 Growth Pace 🐌 Rapid: Birth - 2yrs, Puberty - 15yrs Slower: Ages 2 to puberty, 16-20yrs Identify factors which influence pediatric growth and development Factor Image Influence Critical/Sensitive Periods Key periods for development where external factors can significantly impact outcomes (e.g., teratogens, nutrition) Genetics Inherited traits that affect growth and development Environment Physical (nutrition, toxins) and psychosocial (emotional support, family dynamics) Culture Cultural practices that influence growth and behavior (e.g., diet, child-rearing) Health Status Chronic illnesses, nutrition, and overall health affect growth Family Family structure and socio-economic factors impact development (e.g., access to healthcare, emotional support) Describe the actions of specific vitamins, minerals, and dietary supplements to support pediatric development Vitamin/Mineral/Dietary Function Sources Extra Info Supplement Folic Acid Crucial for DNA Leafy greens RDA: 400-800 mcg/day synthesis and neural tube Fortified cereals to reduce neural tube development (especially defects in early pregnancy) Iron Essential for RBC Especially important in AE: GI discomfort, production and oxygen infants, toddlers, and constipation transport pregnant women Calcium Important for bone and Dairy, fortified plant milk, RDA: 1,000 mg/day for dental development leafy greens pregnant/lactating women; 1,300 mg/day for adolescents Vitamin D Supports calcium Sunlight, fortified foods, Deficiency → Can lead to absorption and bone fatty fish rickets in children health Omega-3 Fatty Acids Supports brain Fish oil, flaxseeds, development and walnuts cognitive function Vitamin A Supports vision and Carrots, Sweet potatoes, Can cause toxicity, immune function spinach especially during pregnancy Predict common age-related effects on PK process of absorption, distribution, metabolism, and excretion PK Process Effect with Age Absorption Neonates/Infants: Slower gastric emptying, altered pH, delayed enzyme activity. Older Children: Absorption improves to adult levels. Distribution Neonates/Infants: Higher body water content, lower fat content, immature blood-brain barrier. Older Children: Distribution more like adults. Metabolism Neonates/Infants: Immature liver enzymes (CYP450), slower drug metabolism. Older Children: Metabolic rate increases, approaches adult levels. Excretion Neonates/Infants: Reduced renal function, slower drug clearance. Older Children: Kidney function improves, similar to adults. Note: Infants and neonates have slower metabolism and excretion, requiring adjusted drug dosing. Older children generally have faster metabolism compared to adults. From the Final Exam Blueprint Aging and Dying Discuss the physiologic and psychosocial aspects of normal human development from transition to adulthood to healthy aging Relate the physiologic and psychosocial aspects of aging to health risks Describe and identify nursing considerations associated with common physiologic changes that occur in a dying person Predict common age-related effects on PK processes of absorption, distribution, metabolism, and excretion Discuss the physiologic and psychosocial aspects of normal human development from transition to adulthood to healthy aging Physiologic Skin: Thinning, less elastic, more prone to injury Musculoskeletal: Decreased muscle mass, bone density, joint flexibility. Cardiovascular: Reduced cardiac output, increased blood pressure, stiffened blood vessels. Respiratory: Reduced lung elasticity, decreased alveolar function. Neurologic: Slower reaction times, memory changes, reduced cognitive function. Endocrine: Hormonal changes, decreased thyroid function, menopause. Renal: Decreased renal function, slower filtration rate. Psychosocial Psychological Changes: Memory decline, reduced sensory abilities, possible depression or anxiety. Social Changes: Retirement, loss of loved ones, social isolation. Cultural: Cultural attitudes toward aging can influence mental health and quality of life. Health Risks: Loneliness, depression, chronic disease, cognitive decline. Relate the physiologic and psychosocial aspects of aging to health risks Physiologic Changes Associated Health Risks Image Reduced skin elasticity Risk for pressure ulcers, skin teas Decreased muscle mass Risk for falls, decreased mobility Decreased bone density Increased risk for fractures, osteoporosis Reduced cardiac output HTN, Heart failure, poor circulation Reduced lung function COPD, pneumonia, SOB Decreased renal function Renal failure, electrolyte imbalances Cognitive decline Alzheimer's disease, dementia, depression Psychosocial Health Risks: Social isolation, depression, financial insecurity, caregiver stress Describe and identify nursing considerations associated with common physiologic changes that occur in a dying person Physiologic Change Nursing Considerations Fatigue & Weakness Allow rest, adjust the environment to minimize effort, assist with hygiene Decreased Oral Intake & Impaired Swallowing Educate family on mouth care, consider non-oral meds, provide comfort Decreased Cardiac Output Monitor for hypotension, tachycardia, peripheral cooling; provide comfort. Neurologic Changes Medication review, allow more sleep, monitor for terminal delirium. Secretions in Airways Positioning, mouth care, consider scopolamine patch, provide oxygen, avoid suctioning. Loss of Sphincter Control Incontinence care, maintain dignity, assist with positioning. Inability to Close Eyes Use ophthalmic lubricants or artificial tears. Predict common age-related effects on PK processes of absorption, distribution, metabolism, and excretion Absorption Changes: Decreased gastric acidity, Effect: Slower absorption rate; slowed GI motility, delayed gastric medications may take longer to emptying. have an effect. Distribution Changes: Increased body fat, Effect:Altered drug distribution, decreased lean body mass and total possible drug accumulation in fat body water, reduced serum tissues or altered plasma protein albumin, decreased cardiac output. binding. Metabolism Changes: Decreased hepatic blood Effect:Slower metabolism of drugs, flow, liver size, and enzyme activity potentially leading to accumulation and increased risk of adverse effects. Excretion Changes: Reduced renal blood flow, Effect:Drug accumulation due to decreased glomerular filtration rate impaired kidney function, leading (GFR), fewer nephrons. to toxicity. Common Adverse Drug Reactions in the Elderly Causes: Polypharmacy, drug accumulation, multiple chronic conditions Risks: Drug interactions, adverse effects, higher mortality rates from drug-related issues. Theories of Aging Molecular Level: Gene regulation, cellular senescence, telomere shortening, reactive oxygen species (ROS) damage. Systemic Theories: Neuroendocrine Theory: Aging is the body’s decreased ability to handle stress, with the HPA axis being central to regulating physiological responses. Immune System Decline: Reduced immune function with aging, increased susceptibility to infections and diseases. Summary Aging is not a disease, but a process involving gradual physiologic changes and psychosocial shifts. Health risks in aging are due to combined physiologic decline and psychosocial factors like isolation and depression. Nursing care for dying patients focuses on symptom management (fatigue, pain, secretions) and comfort measures (positioning, mouth care, non-oral meds). Age-related pharmacokinetic changes necessitate dose adjustments and close monitoring to prevent toxicity. From the Final Exam Blueprint Fluids, Electrolytes, Acid/Base Homeostasis Describe homeostatic control of fluid balance Understand how fluids are distributed throughout the body Describe how fluid moves in and out of a cell via osmosis Describe the effects of isotonic, hypertonic, and hypotonic extracellular fluid states on intracellular fluid movement & cells Describe the forces involved in filtration and reabsorption Understand the role and normal ranges of the following cellular electrolytes: sodium, potassium, calcium, magnesium, and phosphate Discuss how chemical, renal, and respiratory buffering systems maintain a constant pH of body fluids Analyze simple blood gasses to determine acidosis/alkalosis Describe homeostatic control of fluid balance Hypothalamus: Stimulates thirst and releases ADH (antidiuretic hormone) to conserve water Kidneys: Through RAAS (Renin-Angiotensin Aldosterone System), kidneys increase sodium and water reabsorption, raising blood pressure. Baroreceptors: In heart and kidneys detect blood pressure changes and trigger fluid retention or excretion SNS: Activation leads to dry mouth and a sensation of thirst The body maintains fluid balance by monitoring blood concentration and volume. When dehydration occurs, the hypothalamus triggers thirst and releases ADH to help the kidneys reabsorb more water. If blood pressure drops, the kidneys release renin, which activates the RAAS, leading to increased blood pressure and water retention. Additionally, baroreceptors detect changes in blood pressure and signal the body to adjust fluid levels accordingly. Understand how fluids are distributed throughout the body Fluid Distribution in the Body Total Body Water (TBW) Infants: 70-80% of body weight Adults: 55-65% of body weight Elderly: 50-55% of body weight Fluid Compartments Intracellular Fluid (ICF): ⅔ of TBW, inside cells Extracellular fluid (ECF): ⅓ of TBW, includes interstitial space and plasma Describe how fluid moves in and out of a cell via osmosis Osmosis: Water moves across semipermeable membranes to balance solute concentrations Isotonic: Equal solute concentration inside and outside the cell. Water moves equally. Hypotonic: Lower solute concentration outside the cell, causing cells to swell Hypertonic: Higher solute concentration outside the cell, causing cells to shrink Describe the effects of isotonic, hypertonic, and hypotonic extracellular fluid states on intracellular fluid movement & cells Isotonic: When the extracellular fluid has the same solute concentration as the intracellular fluid, water moves in and out of the cell at equal rates, so the cell stays the same size. Hypertonic: If the extracellular fluid has a higher solute concentration than the inside of the cell, water moves out of the cell to balance the concentration, causing the cell to shrink. Hypotonic: If the extracellular fluid has a lower solute concentration than the cell, water moves into the cell, causing it to swell and possibly burst. Describe the forces involved in filtration and reabsorption Filtration: This is the movement of fluid from the blood (in the capillaries) into the surrounding tissues (interstitial space). Hydrostatic pressure (a "push" force) in the capillaries forces fluid out of the blood vessels into the interstitial space. Capillary hydrostatic pressure is generated by the pressure of the blood flowing through the capillaries. Reabsorption: This is the movement of fluid from the interstitial space back into the blood vessels. Oncotic pressure (a "pull" force) created by proteins, mainly albumin, in the blood draws fluid back into the capillaries. Capillary oncotic pressure pulls water into the capillaries from the surrounding tissues. Describe the forces involved in filtration and reabsorption Filtration: The movement of fluid from the blood into the tissues. - Hydrostatic pressure (the "push" force) in the capillaries pushes water and solutes out of the blood into the surrounding tissue. Reabsorption: The movement of fluid from the tissues back into the blood. - Oncotic pressure (the "pull" force) created by proteins like albumin in the blood draws water back into the capillaries from the interstitial space. Filtration → Hydrostatic Pressure (pushing fluid out) Reabsorption → Oncotic Pressure (pulling fluid in) Understand the role and normal ranges of the following cellular electrolytes: sodium, potassium, calcium, magnesium, and phosphate Name Role Normal Range Sodium (Na⁺) Sodium is the primary extracellular 135-145 mEq/L cation. It helps regulate fluid balance, blood pressure, and nerve function. Potassium (K⁺) Role: Potassium is the main Normal Range: 3.5-5.0 mEq/L intracellular cation. It is essential for nerve impulses, muscle contractions, and maintaining cell function. Calcium (Ca²⁺) Calcium is involved in bone 9-10.5 mg/dL formation, muscle contraction, blood clotting, and nerve signaling. Magnesium (Mg²⁺) Magnesium is important for enzyme 1.5-2.3 mEq/L function, muscle relaxation, and maintaining normal heart rhythm. Phosphate (PO₄³⁻) Phosphate is involved in energy 2.5-4.5 mg/dL production, bone health, and cell metabolism (part of ATP). Discuss how chemical, renal, and respiratory buffering systems maintain a constant pH of body fluids Chemical Buffers (Immediate Response) Bicarbonate-Carbonic Acid Buffer: Low pH (acidic): Carbonic acid releases H⁺ to raise pH. High pH (alkaline): Bicarbonate absorbs H⁺ to lower pH. Protein & Phosphate Buffers also help in cells and kidneys. Respiratory Buffering System (Fast Response) The respiratory system adjusts the level of carbon dioxide (CO₂) in the blood, which influences pH: If the blood is too acidic (low pH) → Body breathes faster and deeper, expelling more CO₂, which lowers H⁺ concentration and raises pH. If the blood is too alkaline (high pH): The body breathes slower to retain CO₂, which increases H⁺ concentration and lowers pH. This system responds within minutes to hours Renal Buffering System (Slow but Long-Lasting Response) The kidneys regulate pH by excreting or reabsorbing hydrogen ions (H⁺) and bicarbonate (HCO₃⁻): If the blood is too acidic: The kidneys excrete more H⁺ into the urine and reabsorb more bicarbonate, which buffers the acid. If the blood is too alkaline: The kidneys excrete more bicarbonate and retain more H⁺. This system is slower but can help regulate pH over hours to days. Analyze simple blood gasses to determine acidosis/alkalosis pH: Acidosis: pH < 7.35 Alkalosis: pH > 7.45 pCO₂ (Carbon Dioxide): Acidosis: High pCO₂ → Respiratory acidosis Alkalosis: Low pCO₂ → Respiratory alkalosis HCO₃⁻ (Bicarbonate): Acidosis: Low HCO₃⁻ → Metabolic acidosis Alkalosis: High HCO₃⁻ → Metabolic alkalosis From the Final Exam Blueprint Inflammation & Immunity, Wound Healing Describe the three lines of defense State the benefits of inflammation Understand the three components of the inflammatory process Describe the end effects of complement, kinin, and clotting plasma protein systems Relate the inflammatory process to physical examination findings Understand the role of histamines, prostaglandins, leukotrienes, bradykinin, cytokines, and leukocytes in the inflammatory process Describe systemic manifestations of inflammation Describe the three phases of wound healing Describe the use of immunizations to prevent disease Describe the three lines of defense 1st Line: Physical Barriers → Innate Immunity Skin, mucous membranes, cilia, and normal flora prevent pathogen entry Non-specific, no memory, constant defense 2nd Line: Inflammation (Innate Immunity) Response to tissue injury or infection Involves vasodilation, leukocyte recruitment, and phagocytosis Non-specific, no memory, immediate response 3rd Line: Adaptive Immunity Humoral (B-cells) and Cell-mediated (T-cells) immunity Specific response, delayed (4-7 days), memory for faster response on re-exposure Activated by antigens from pathogens or toxins State the benefits of inflammation Prevents infection, limits damage, and prepares tissues for healing Involves vascular changes (vasodilation, increased permeability) and immune cell activation  Understand the three components of the inflammatory process Vasodilation & Vascular Permeability: Increased blood flow and permeability allow immune cells and proteins to reach the site of injury Leukocyte Recruitment: Neutrophils and other immune cells are recruited to the site via chemotaxis and emigration Phagocytosis: Pathogens and debris are engulfed and digested by immune cells like neutrophils and macrophages Describe the end effects of complement, kinin, and clotting plasma protein systems End Effects → Kinin System Bradykinin Production: This peptide causes vasodilation, increases vascular permeability, and induces pain –helping recruit immune cells to the site of injury End Effects → Coagulation (Clotting) System Clot Formation: Prevents excessive blood loss and provides a scaffold for tissue repair. Leukocyte Migration: Directs immune cells to the injured area (chemotaxis). Increased Vascular Permeability: Facilitates the movement of immune cells and proteins into the tissues for healing. Relate the inflammatory process to physical examination findings Finding Cause Image Clinical Significance Redness (Erythema) Vasodilation (when blood vessels Skin or mucous membranes expand to increase blood flow) over the inflamed area appear triggered by the release of mediators red and warm, indicating like histamine and prostaglandins. increased blood supply to the area as part of the inflammatory response. Heat (Warmth) Vasodilation and increased blood Often seen in superficial areas, flow lead to a rise in local this reflects active temperature. inflammation and increased metabolic activity in the affected tissues. Swelling (Edema) Increased vascular permeability (due Soft, puffy tissue around the to bradykinin, histamines, and site of inflammation is a sign of prostaglandins) leads to fluid leakage fluid accumulation (exudate) in from blood vessels into the response to injury or infection. surrounding tissue. Pain (Dolor) Release of pain mediators like Pain at the site of inflammation bradykinin and prostaglandins, which is often a cardinal sign of tissue sensitize nerve endings, and pressure injury and chemical mediator from swelling. release. Loss of Function Pain, swelling, and the inflammatory Limited movement or function response may impair the normal in the inflamed area (e.g., joint functioning of the affected tissue or stiffness, difficulty swallowing) organ. can be an important finding, especially in severe or chronic inflammation. Understand the role of histamines, prostaglandins, leukotrienes, bradykinin, cytokines, and leukocytes in the inflammatory process Term Function Key Points Histamines Cause vasodilation (widen blood vessels) and increase vascular Vasodilation permeability, leading to redness, heat, and swelling. Increased Permeability Swelling Prostaglandins Promote vasodilation, pain, and fever; also increase vascular Pain permeability and support tissue healing. Fever Vasodilation Healing Leukotrienes Function: Involved in chemotaxis (attracting immune cells) and Chemotaxis increasing vascular permeability, contributing to swelling and Increased Permeability immune cell recruitment. Swelling Bradykinin: Function: Causes vasodilation, increases vascular permeability, and Vasodilation triggers pain at the site of injury. Permeability Pain Cytokines Signaling molecules that regulate immune responses; stimulate Immune Signaling leukocyte production, activate inflammation, and coordinate immune Leukocyte Activation cell activities. Leukocytes White blood cells (like neutrophils, macrophages, and lymphocytes) Immune Cells that fight infection, clean debris, and promote healing. Infection Defense Healing Describe systemic manifestations of inflammation Fever Cause: Cytokines (e.g., IL-1, TNF) trigger the hypothalamus to increase body temperature. Effect → Helps fight infection by raising the body’s temperature to inhibit pathogen growth. Leukocytosis Cause: Increased production of white blood cells (especially neutrophils) in response to infection or injury. Effect → Elevated white blood cell count in the blood, indicating an immune response. Increased Acute Phase Reactants Cause: The liver produces proteins like C-reactive protein (CRP) and fibrinogen during inflammation. Effect → These proteins act as markers of inflammation and contribute to immune defense. Erythrocyte Sedimentation Rate (ESR) Cause: Increased levels of acute phase proteins (like fibrinogen) cause red blood cells to settle faster. Effect → An elevated ESR indicates ongoing inflammation or infection. Describe the three phases of wound healing Inflammation (Days 1-3) Goal: Control bleeding, prevent infection, and prepare the wound for healing. Key Actions: Blood clot forms, immune cells clean the wound. Proliferation (Days 3-14) Goal: Control bleeding, prevent infection, and prepare the wound for healing. Key Actions: Blood clot forms, immune cells clean the wound. Remodeling/Maturation (Weeks - 2yrs) Goal: Strengthen and finalize the tissue repair. Key Actions: Collagen is deposited, wound contracts, tissue becomes stronger. Describe the use of immunizations to prevent disease Goal: Immunizations help prevent specific diseases by stimulating the immune system. How it Works: Vaccines introduce a harmless version of a pathogen (e.g., killed or weakened virus) to the body. The immune system responds by producing antibodies and memory cells Benefits: Prevents illness in individuals. Protects the population through herd immunity (if enough people are vaccinated, the disease cannot spread easily). Eradicates diseases (e.g., smallpox, polio) when vaccination rates are high From the Final Exam BluePrint Pain & Analgesics Understand the 4 phases of nociception: transduction, transmission, perception, and modulation Discuss the role of the following neurotransmitters in nociception: glutamate, GABA, substance P, endogenous opioids Differentiate between the following types of pain: acute, chronic, neuropathic, ischemic, and referred Describe treatment modalities that target specific phases of nociception Relate the physiology of drug dependence, tolerance, and addiction to the signs and symptoms of each Describe the mechanism of action, effects of, and uses for major classes of OTC analgesics Predict common adverse effects associated with OTC analgesics Identify prototype drug(s) for categories of OTC analgesics Describe nursing considerations related to the appropriate and safe use of analgesic medications: Acetaminophen/ Ibuprofen/Morphine/Oxycodone  Understand the 4 phases of nociception: transduction, transmission, perception, and modulation (1) Transduction Stimulus: Tissue damage → activates nociceptors (pain receptors). Mediators: Histamine, bradykinin, prostaglandins, etc. (2) Transmission Pathway: Pain signal travels from injury site to the spinal cord and brain. Fibers: Alpha-delta fibers (sharp, well-localized pain) and C-fibers (dull, aching pain). Neurotransmitters: Glutamate, substance P. (3) Perception Awareness: Brain interprets pain (location, intensity, emotional response). Factors: Pain threshold, tolerance, learned behavior. (4) Modulation Alteration: Pain signals can be amplified or dampened. Neurotransmitters: Substance P, histamine (excitatory); GABA, serotonin, opioids (inhibitory). Interventions: Pharmacological (medications) and non-pharmacological (massage, heat/cold). Discuss the role of the following neurotransmitters in nociception: glutamate, GABA, substance P, endogenous opioids Glutamate: Major excitatory neurotransmitter, amplifies pain. GABA: Inhibitory neurotransmitter, reduces pain transmission. Substance P: Promotes pain transmission, contributes to chronic pain. Endogenous Opioids: Endorphins, enkephalins reduce pain by inhibiting pain signals. Differentiate between the following types of pain: acute, chronic, neuropathic, ischemic, and referred Type of Pain Duration Symptom(s) Cause Treatment Signs Example Acute < 3 months Sharp, Tissue Injury Short-term pain Increased HR, BP, Broken bones, Short-term localized pain relief (opioids, RR, sweating, cuts, burns, NSAIDs) nausea, pallor post-surgery Chronic > 3 months Dull, aching, Peripheral/central Multimodal Decreased mobility, Fibromyalgia low Long-term persistent pain nervous system therapies (pain muscle tension, sleep back pain changes. clinics, opioids, disturbance osteoarthritis antidepressants, physical therapy). Neuropathic Pain Long-term Burning, Nerve damage or AntidepressantsAn Numbness, tingling, Diabetic (months to shooting, dysfunction (e.g., ticonvulsantsNerv muscle weakness, neuropathy, years) tingling pain diabetes, shingles) e blocks altered sensation post-herpetic neuralgia Ischemic Pain Variable Aching, Loss of blood flow Restore blood Cold, clammy skin, Heart attack, (short-term to burning, (e.g., heart attack, flow sweating, pallor angina, bowel long-term, tingling pain angina) (nitroglycerin, infarction depending on bypass surgery) cause) Referred Pain Variable Pain in an area Pain felt in a Treat underlying Pain radiating, Shoulder pain (depends on distant from distant area from cause (e.g., heart tenderness in from heart attack, underlying injury the site of injury attack treatment) non-injured areas jaw pain from cause) (e.g., heart attack) tooth infection  Describe treatment modalities that target specific phases of nociception Phase of Nociception Treatment Modality Goal Transduction NSAIDs, Local Anesthetics, Heat/Cold Block the initiation of pain at the injury site Transmission Opioids, Antidepressants, TENS Prevent the transmission of pain signals Perception Opioids, Antidepressants, Cognitive Therapy Alter how pain is perceived in the brain Modulation Opioids, Antidepressants, TENS, Acupuncture Modify or block pain signals along the nervous system Relate the physiology of drug dependence, tolerance, and addiction to the signs and symptoms of each Term Definition Physiology Signs & Symptoms Example Drug Physical state where the Chronic use of a drug Withdrawal Symptoms: Opioid withdrawal (e.g., from Dependence body adapts to the presence alters brain chemistry, Anxiety, irritability, sweating, morphine, oxycodone) can of a drug, and withdrawal leading to a need for nausea, shaking. cause shaking, sweating, and symptoms occur if the drug the substance to avoid nausea. is stopped abruptly. withdrawal Physical Dependence: Body symptoms. "expects" the drug to function normally, and sudden cessation disrupts homeostasis. Tolerance The need for increasing Repeated exposure to Increased Dose: Patients may A patient on opioids (e.g., amounts of a drug to a drug leads to require higher doses to feel the morphine) for pain may need achieve the same effect due downregulation of same level of relief. higher doses over time to to repeated use. receptors or other achieve the same level of adaptive mechanisms Decreased Sensitivity: Less pain relief. in the brain, reducing intense effects with the same the drug's dose. (Tolerance) effectiveness over time. Addiction A behavioral condition Involves the brain's Compulsive Use: Uncontrolled A person addicted to opioids marked by compulsive drug reward system (e.g., craving, repeated use despite may continue using even if it use despite harmful the dopamine negative effects on life (e.g., leads to harm (e.g., loss of consequences, including a pathway), leading to health, relationships). job or relationships), due to strong craving for the compulsive intense cravings and substance. drug-seeking Psychological Dependence: compulsive use. behavior. Strong urge to use the substance, sometimes without physical withdrawal symptoms. Behavioral Changes: Lying, secretive behavior, neglecting responsibilities.  Describe the mechanism of action, effects of, and uses for major classes of OTC analgesics Class Mechanism of Action Effects Uses Adverse Effects NSAIDs Inhibit COX-1 and COX-2 Analgesic, Pain relief, GI upset, renal damage enzymes Anti-inflammatory, Inflammation, Fever with long-term use Antipyretic Acetaminophen Inhibits prostaglandins Analgesic, Mild pain, fever Liver toxicity (overdose (analgesic and (mainly in the brain) Antipyretic reduction risk) antipyretic drug) Aspirin Irreversibly inhibits COX-1 Analgesic, Pain relief, GI irritation, bleeding (NSAID class) and COX-2 Anti-inflammatory, Cardiovascular risk, Reye's syndrome Antipyretic, prevention (children) Antiplatelet COX-2 Inhibitors Selectively inhibit COX-2 Analgesic, Arthritis, acute pain, Cardiovascular risks, (second-generation enzyme Anti-inflammatory, inflammation renal issues NSAIDs) Antipyretic Predict common adverse effects associated with OTC analgesics OTC Analgesic Common Adverse Effects Special Considerations NSAIDs (e.g., Ibuprofen, GI ulcers/bleeding, renal damage, Use cautiously in elderly, Naproxen) cardiovascular issues kidney/heart issues Acetaminophen (Tylenol) Liver toxicity, possible renal damage Limit to 4g/day, be cautious with combo meds Aspirin GI irritation/bleeding, renal issues, allergic Avoid in children (Reye's reactions syndrome) C