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20% of the mass of adrenal gland. It is made up of interlacing cords of cells known as chromaffin cells. Chromaffin cells are also called pheochrome cells or chromophil cells. These cells contain fine granules which are stained brown by potassium dichromate. Types of chromaffin cells Adrenal medulla is formed by two types of chromaffin cells: 1. Adrenaline-secreting cells (90%) 2. Noradrenaline-secreting cells (10%). „ HORMONES OF ADRENAL MEDULLA Adrenal medullary hormones are the amines derived from catechol and so these hormones are called catecholamines. Catecholamines secreted by adrenal medulla 1. Adrenaline or epinephrine 2. Noradrenaline or norepinephrine 3. Dopamine. „ PLASMA LEVEL OF CATECHOLAMINES 1. Adrenaline : 3 μg/dL 2. Noradrenaline : 30 μg/dL 3. Dopamine : 3.5 μg/dL „ HALF-LIFE OF CATECHOLAMINES Half-life of catecholamines is about 2 minutes. „ SYNTHESIS OF CATECHOLAMINES Catecholamines are synthesized from the amino acid tyrosine in the chromaffin cells of adrenal medulla (Fig. 71.1). These hormones are formed from phenylalanine also. But phenylalanine has to be converted into tyrosine. Stages of Synthesis of Catecholamines 1. Formation of tyrosine from phenylalanine in the presence of enzyme phenylalanine hydroxylase 2. Uptake of tyrosine from blood into the chromaffin cells of adrenal medulla by active transport 3. Conversion of tyrosine into dihydroxyphenylalanine (DOPA) by hydroxylation in the presence of tyrosine hydroxylase 440 Section 6tEndocrinology FIGURE 71.1: Synthesis of catecholamines. DOPA = Di- hydroxyphenylalanine, PNMT = Phenylethanolamine-N- methyltransferase. 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase 5. Entry of dopamine into granules of chromaffin cells 6. Hydroxylation of dopamine into noradrenaline by the enzyme dopamine beta-hydroxylase 7. Release of noradrenaline from granules into the cytoplasm 8. Methylation of noradrenaline into adrenaline by the most important enzyme called phenylethanolamine- N-methyltransferase (PNMT). PNMT is present in chromaffin cells. „ METABOLISM OF CATECHOLAMINES Eighty five percent of noradrenaline is taken up by the sympathetic adrenergic neurons. Remaining 15% of noradrenaline and adrenaline are degraded (Fig. 71.2). FIGURE 71.2: Metabolism of catecholamines. COMT = Catechol-O-methyltransferase, MAO = Monoamine oxidase. Stages of Metabolism of Catecholamines 1. Methoxylation of adrenaline into meta-adrenaline and noradrenaline into metanoradrenaline in the presence of ‘catechol-O-methyltransferase’ (COMT). Meta-adrenaline and meta-noradrenaline are together called metanephrines 2. Oxidation of metanephrines into vanillylmandelic acid (VMA) by monoamine oxidase (MAO) Removal of Catecholamines Catecholamines are removed from body through urine in three forms: i. 15% as free adrenaline and free noradrenaline ii. 50% as free or conjugated meta-adrenaline and meta-noradrenaline iii. 35% as vanillylmandelic acid (VMA). „ ACTIONS OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline stimulate the nervous system. Adrenaline has significant effects on metabolic functions and both adrenaline and noradrenaline have significant effects on cardiovascular system. „ MODE OF ACTION OF ADRENALINE AND NORADRENALINE – ADRENERGIC RECEPTORS Actions of adrenaline and noradrenaline are executed by binding with receptors called adrenergic receptors, which are present in the target organs. Chapter 71tAdrenal Medulla 441 Adrenergic receptors are of two types: 1. Alpha-adrenergic receptors, which are subdivided into alpha-1 and alpha-2 receptors 2. Beta-adrenergic receptors, which are subdivided into beta-1 and beta-2 receptors. Refer Table 71.1 for the mode of action of these receptors. „ ACTIONS Circulating adrenaline and noradrenaline have similar effect of sympathetic stimulation. But, the effect of adrenal hormones is prolonged 10 times more than that of sympathetic stimulation. It is because of the slow inactivation, slow degradation and slow removal of these hormones. Effects of adrenaline and noradrenaline on various target organs depend upon the type of receptors present in the cells of the organs. Adrenaline acts through both alpha and beta receptors equally. Noradrenaline acts mainly through alpha receptors and occasionally through beta receptors. 1. On Metabolism (via Alpha and Beta Receptors) Adrenaline influences the metabolic functions more than noradrenaline. i. General metabolism: Adrenaline increases oxygen consumption and carbon dioxide removal. It increases basal metabolic rate. So, it is said to be a calorigenic hormone ii. Carbohydrate metabolism: Adrenaline increases the blood glucose level by increasing the glycogenolysis in liver and muscle. So, a large quantity of glucose enters the circulation iii. Fat metabolism: Adrenaline causes mobilization of free fatty acids from adipose tissues. Catecholamines need the presence of glucocorticoids for this action. 2. On Blood (via Beta Receptors) Adrenaline decreases blood coagulation time. It increases RBC count in blood by contracting smooth muscless
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„ INTRODUCTION Medulla is the inner part of adrenal gland and it forms 20% of the mass of adrenal gland. It is made up of interlacing cords of cells known as chromaffin cells. Chromaffin cells are also called pheochrome cells or chromophil cells. These cells contain fine granules which are stained brown by potassium dichromate. Types of chromaffin cells Adrenal medulla is formed by two types of chromaffin cells: 1. Adrenaline-secreting cells (90%) 2. Noradrenaline-secreting cells (10%). „ HORMONES OF ADRENAL MEDULLA Adrenal medullary hormones are the amines derived from catechol and so these hormones are called catecholamines. Catecholamines secreted by adrenal medulla 1. Adrenaline or epinephrine 2. Noradrenaline or norepinephrine 3. Dopamine. „ PLASMA LEVEL OF CATECHOLAMINES 1. Adrenaline : 3 μg/dL 2. Noradrenaline : 30 μg/dL 3. Dopamine : 3.5 μg/dL „ HALF-LIFE OF CATECHOLAMINES Half-life of catecholamines is about 2 minutes. „ SYNTHESIS OF CATECHOLAMINES Catecholamines are synthesized from the amino acid tyrosine in the chromaffin cells of adrenal medulla (Fig. 71.1). These hormones are formed from phenylalanine also. But phenylalanine has to be converted into tyrosine. Stages of Synthesis of Catecholamines 1. Formation of tyrosine from phenylalanine in the presence of enzyme phenylalanine hydroxylase 2. Uptake of tyrosine from blood into the chromaffin cells of adrenal medulla by active transport 3. Conversion of tyrosine into dihydroxyphenylalanine (DOPA) by hydroxylation in the presence of tyrosine hydroxylase 440 Section 6tEndocrinology FIGURE 71.1: Synthesis of catecholamines. DOPA = Di- hydroxyphenylalanine, PNMT = Phenylethanolamine-N- methyltransferase. 4. Decarboxylation of DOPA into dopamine by DOPA decarboxylase 5. Entry of dopamine into granules of chromaffin cells 6. Hydroxylation of dopamine into noradrenaline by the enzyme dopamine beta-hydroxylase 7. Release of noradrenaline from granules into the cytoplasm 8. Methylation of noradrenaline into adrenaline by the most important enzyme called phenylethanolamine- N-methyltransferase (PNMT). PNMT is present in chromaffin cells. „ METABOLISM OF CATECHOLAMINES Eighty five percent of noradrenaline is taken up by the sympathetic adrenergic neurons. Remaining 15% of noradrenaline and adrenaline are degraded (Fig. 71.2). FIGURE 71.2: Metabolism of catecholamines. COMT = Catechol-O-methyltransferase, MAO = Monoamine oxidase. Stages of Metabolism of Catecholamines 1. Methoxylation of adrenaline into meta-adrenaline and noradrenaline into metanoradrenaline in the presence of ‘catechol-O-methyltransferase’ (COMT). Meta-adrenaline and meta-noradrenaline are together called metanephrines 2. Oxidation of metanephrines into vanillylmandelic acid (VMA) by monoamine oxidase (MAO) Removal of Catecholamines Catecholamines are removed from body through urine in three forms: i. 15% as free adrenaline and free noradrenaline ii. 50% as free or conjugated meta-adrenaline and meta-noradrenaline iii. 35% as vanillylmandelic acid (VMA). „ ACTIONS OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline stimulate the nervous system. Adrenaline has significant effects on metabolic functions and both adrenaline and noradrenaline have significant effects on cardiovascular system. „ MODE OF ACTION OF ADRENALINE AND NORADRENALINE – ADRENERGIC RECEPTORS Actions of adrenaline and noradrenaline are executed by binding with receptors called adrenergic receptors, which are present in the target organs. Chapter 71tAdrenal Medulla 441 Adrenergic receptors are of two types: 1. Alpha-adrenergic receptors, which are subdivided into alpha-1 and alpha-2 receptors 2. Beta-adrenergic receptors, which are subdivided into beta-1 and beta-2 receptors. Refer Table 71.1 for the mode of action of these receptors. „ ACTIONS Circulating adrenaline and noradrenaline have similar effect of sympathetic stimulation. But, the effect of adrenal hormones is prolonged 10 times more than that of sympathetic stimulation. It is because of the slow inactivation, slow degradation and slow removal of these hormones. Effects of adrenaline and noradrenaline on various target organs depend upon the type of receptors present in the cells of the organs. Adrenaline acts through both alpha and beta receptors equally. Noradrenaline acts mainly through alpha receptors and occasionally through beta receptors. 1. On Metabolism (via Alpha and Beta Receptors) Adrenaline influences the metabolic functions more than noradrenaline. i. General metabolism: Adrenaline increases oxygen consumption and carbon dioxide removal. It increases basal metabolic rate. So, it is said to be a calorigenic hormone ii. Carbohydrate metabolism: Adrenaline increases the blood glucose level by increasing the glycogenolysis in liver and muscle. So, a large quantity of glucose enters the circulation iii. Fat metabolism: Adrenaline causes mobilization of free fatty acids from adipose tissues. Catecholamines need the presence of glucocorticoids for this action. 2. On Blood (via Beta Receptors) Adrenaline decreases blood coagulation time. It increases RBC count in blood by contracting smooth muscles of splenic capsule and releasing RBCs from spleen into circulation. 3. On Heart (via Beta Receptors) Adrenaline has stronger effects on heart than nor- adrenaline. It increases overall activity of the heart, i.e. i. Heart rate (chronotropic effect) ii. Force of contraction (inotropic effect) iii. Excitability of heart muscle (bathmotropic effect) iv. Conductivity in heart muscle (dromotropic effect). 4. On Blood Vessels (via Alpha and Beta-2 Receptors) Noradrenaline has strong effects on blood vessels. It causes constriction of blood vessels throughout the body via alpha receptors. So it is called ‘general vasoconstrictor’. Vasoconstrictor effect of noradrena- line increases total peripheral resistance. Adrenaline also causes constriction of blood vessels. However, it causes dilatation of blood vessels in skeletal muscle, liver and heart through beta-2 receptors. So, the total peripheral resistance is decreased by adrenaline. Catecholamines need the presence of glucocor- ticoids, for these vascular effects. 5. On Blood Pressure (via Alpha and Beta Receptors) Adrenaline increases systolic blood pressure by increasing the force of contraction of the heart and cardiac output. But, it decreases diastolic blood pressure by reducing the total peripheral resistance. Noradrenaline increases diastolic pressure due to general vasoconstrictor effect by increasing the total peripheral resistance. It also increases the systolic blood pressure to a slight extent by its actions on heart. The action of catecholamines on blood pressure needs the presence of glucocorticoids. TABLE 71.1: Adrenergic receptors Receptor Mode of action Response Alpha-1 receptor Activates IP3 through phospholipase C Mediates more of noradrenaline actions than adrenaline actions Alpha-2 receptor Inhibits adenyl cyclase and cAMP Beta-1 receptor Activates adenyl cyclase and cAMP Mediates actions of adrenaline and noradrenaline equally Beta-2 receptor Activates adenyl cyclase and cAMP Mediates more of adrenaline actions than noradrenaline actions IP3 = Inositol triphosphate 442 Section 6tEndocrinology Thus, hypersecretion of catecholamines leads to hypertension. 6. On Respiration (via Beta-2 Receptors) Adrenaline increases rate and force of respiration. Adrenaline injection produces apnea, which is known as adrenaline apnea. It also causes bronchodilation. 7. On Skin (via Alpha and Beta-2 Receptors) Adrenaline causes contraction of arrector pili. It also increases the secretion of sweat. 8. On Skeletal Muscle (via Alpha and Beta-2 Receptors) Adrenaline causes severe contraction and quick fatigue of skeletal muscle. It increases glycogenolysis and release of glucose from muscle into blood. It also causes vasodilatation in skeletal muscles. 9. On Smooth Muscle (via Alpha and Beta Receptors) Catecholamines cause contraction of smooth muscles in the following organs: i. Splenic capsule ii. Sphincters of gastrointestinal (GI) tract iii. Arrector pili of skin iv. Gallbladder v. Uterus vi. Dilator pupillae of iris vii. Nictitating membrane of cat. Catecholamines cause relaxation of smooth muscles in the following organs: i. Non-sphincteric part of GI tract (esophagus, stomach and intestine) ii. Bronchioles iii. Urinary bladder. 10. On Central Nervous System (via Beta Receptors) Adrenaline increases the activity of brain. Adrenaline secretion increases during ‘fight or flight reactions’ after exposure to stress. It enhances the cortical arousal and other facilitatory functions of central nervous system. 11. Other Effects of Catecholamines i. On salivary glands (via alpha and beta-2 receptors): Cause vasoconstriction in salivary gland, leading to mild increase in salivary secretion ii. On sweat glands (via beta-2 receptors): Increase the secretion of apocrine sweat glands iii. On lacrimal glands (via alpha receptors): Increase the secretion of tears iv. On ACTH secretion (via alpha receptors): Adrenaline increases ACTH secretion v. On nerve fibers (via alpha receptors): Adrenaline decreases the latency of action potential in the nerve fibers, i.e. electrical activity is accelerated vi. On renin secretion (via beta receptors): Increase the rennin secretion from juxtaglomerular apparatus of the kidney. „ REGULATION OF SECRETION OF ADRENALINE AND NORADRENALINE Adrenaline and noradrenaline are secreted from adrenal medulla in small quantities even during rest. During stress conditions, due to sympathoadrenal discharge, a large quantity of catecholamines is secreted. These hormones prepare the body for fight or flight reactions. Catecholamine secretion increases during exposure to cold and hypoglycemia also. „ DOPAMINE Dopamine is secreted by adrenal medulla. Type of cells secreting this hormone is not known. Dopamine is also secreted by dopaminergic neurons in some areas of brain, particularly basal ganglia. In brain, this hormone acts as a neurotransmitter. Injected dopamine produces the following effects: 1. Vasoconstriction by releasing norepinephrine 2. Vasodilatation in mesentery 3. Increase in heart rate via beta receptors 4. Increase in systolic blood pressure. Dopamine does not affect diastolic blood pressure. Deficiency of dopamine in basal ganglia produces nervous disorder called parkinsonism (Chapter 151). „ APPLIED PHYSIOLOGY – PHEOCHROMOCYTOMA Pheochromocytoma is a condition characterized by hypersecretion of catecholamines. Cause Pheochromocytoma is caused by tumor of chromophil cells in adrenal medulla. It is also caused rarely by tumor of sympathetic ganglia (extra-adrenal pheochromocytoma). Chapter 71tAdrenal Medulla 443 Signs and Symptoms Characteristic feature of pheochromocytoma is hyper- tension. This type of hypertension is known as endocrine or secondary hypertension. Other features: 1. Anxiety 2. Chest pain 3. Fever 4. Headache 5. Hyperglycemia 6. Metabolic disorders 7. Nausea and vomiting 8. Palpitation 9. Polyuria and glucosuria 10. Sweating and flushing 11. Tachycardia 12. Weight loss. Tests for Pheochromocytoma Pheochromocytoma is detected by measuring meta- nephrines and vanillylmandelic acid in urine and Cathecolamines in olasma
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Unit 1: Psychology’s History and Approaches Big Idea: Psychology is the scientific study of behavior and mental processes. This unit asks: Why do people think, feel, and behave the way they do, and how do psychologists study it? 1. Early Schools of Thought Structuralism Focused on breaking conscious experiences into smaller parts. Example: Describing every taste, smell, and feeling while eating pizza. Functionalism Focused on WHY behaviors and thoughts exist. Example: Fear exists because it helps humans survive danger. Connection: Structuralists asked “What are thoughts made of?” Functionalists asked “What purpose do thoughts serve?” 2. Major Psychological Perspectives Biological Perspective Behavior comes from the brain, genetics, and hormones. Example: Depression connected to serotonin levels. Behavioral Perspective Behavior is learned through rewards and punishments. Example: A dog learns tricks because it gets treats. Cognitive Perspective Focuses on thinking, memory, and problem-solving. Example: Why students remember some facts better than others. Humanistic Perspective Humans naturally strive for growth. Example: Trying to achieve goals and improve yourself. Psychodynamic Perspective Unconscious conflicts affect behavior. Example: Getting unusually angry because of hidden stress. Evolutionary Perspective Behaviors developed because they helped survival. Example: Humans naturally fearing dangerous animals. Sociocultural Perspective Behavior is shaped by culture and society. Example: Different cultures have different expectations for personal space. 3. Research Methods Experiment Used to determine cause and effect. Independent Variable What the researcher changes. Dependent Variable What the researcher measures. Example: Studying whether sleep affects test scores. * Amount of sleep = IV * Test score = DV Correlation Shows relationship between variables. Important: Correlation does NOT equal causation. Example: Ice cream sales and drowning both rise during summer. Random Assignment Participants randomly placed into groups. Helps reduce bias. Double-Blind Procedure Neither researchers nor participants know who receives treatment. Prevents expectations from affecting results. BIG AP EXAM CONNECTION The AP exam loves asking: * Which perspective best explains this behavior? * Which research method should be used? * Why doesn’t correlation prove causation? Example: A psychologist studies how rewards affect studying. → Behavioral perspective + experiment Unit 2: Biological Basis of Behavior Big Idea: Your brain, nervous system, hormones, and genetics all shape behavior. The whole unit asks: How do your body and brain create thoughts, emotions, and behavior? 1. Nature vs. Nurture = Who You Are Main Idea: Your behavior comes from BOTH: * Nature = genetics/heredity * Nurture = environment and experiences Example: Someone may inherit anxiety tendencies but stressful experiences can make anxiety stronger. 2. Nervous System Central Nervous System Brain + spinal cord. Peripheral Nervous System Nerves outside the brain and spinal cord. Sympathetic Nervous System Activates during stress. Example: Heart racing before giving a speech. Parasympathetic Nervous System Calms the body afterward. 3. Neurotransmitters Dopamine Reward and pleasure. Example: Social media likes feel rewarding. Serotonin Mood and sleep. Low levels linked to depression. Acetylcholine Movement and memory. Linked to Alzheimer’s disease. GABA Calms nervous system. Low GABA linked to anxiety. 4. Brain Structures Frontal Lobe Decision-making and personality. Occipital Lobe Vision. Temporal Lobe Hearing and memory. Hippocampus Memory formation. Amygdala Fear and aggression. BIG AP EXAM CONNECTION A student panicking before a test: * amygdala activates fear * sympathetic nervous system increases heart rate * adrenaline releases Unit 3: Sensation and Perception Big Idea: Sensation detects information. Perception interprets information. This unit asks: How does the brain create your experience of the world? 1. Sensation Absolute Threshold Smallest amount of stimulation needed to notice something. Example: Hearing a quiet text notification. Difference Threshold Smallest noticeable difference between stimuli. Example: Noticing the TV volume changed. Sensory Adaptation Becoming less aware of constant stimulation. Example: Not noticing your hoodie after wearing it awhile. 2. Vision Rods Help see in dim light. Cones Detect color. Blind Spot Area without receptors. 3. Hearing Frequency Determines pitch. Amplitude Determines loudness. 4. Perception Gestalt Principles The brain organizes pieces into meaningful wholes. Example: Seeing a complete logo even with missing parts. Depth Perception Ability to see distance in 3D. Example: Catching a volleyball. Perceptual Set Expectations affect perception. Example: Misreading a word because you expected something else. BIG AP EXAM CONNECTION The exam often gives optical illusions or perception scenarios. Example: A person stops noticing a strong smell after 10 minutes. → sensory adaptation Unit 4: Learning Big Idea: Behavior changes because of experience. This unit asks: How do humans and animals learn behaviors? 1. Classical Conditioning Learning through association. Pavlov’s Dogs Dogs learned to associate a bell with food. Unconditioned Stimulus Naturally causes response. Conditioned Stimulus Previously neutral stimulus causing learned response. Example: Feeling hungry when hearing the microwave beep. 2. Operant Conditioning Learning through rewards and punishments. Positive Reinforcement Adding something good to increase behavior. Example: Getting money for good grades. Negative Reinforcement Removing something unpleasant. Example: Seatbelt alarm stopping. Punishment Decreases behavior. 3. Observational Learning Learning by watching others. Example: Kids copying influencers online. BIG AP EXAM CONNECTION The AP exam loves reinforcement examples. Example: A student studies harder after praise from parents. → positive reinforcement Unit 5: Cognitive Psychology Big Idea: Humans think, remember, solve problems, and use language. This unit asks: How does the mind process information? 1. Memory Process Encoding Getting information into memory. Storage Keeping information over time. Retrieval Getting information back. 2. Types of Memory Sensory Memory Very brief memory. Short-Term Memory Temporary limited storage. Long-Term Memory Relatively permanent storage. Working Memory Actively using information. Example: Doing math in your head. 3. Forgetting Proactive Interference Old information disrupts new information. Retroactive Interference New information disrupts old information. Example: Forgetting old password after learning a new one. 4. Problem Solving Algorithm Step-by-step method. Heuristic Mental shortcut. Confirmation Bias Looking for information supporting beliefs. Example: Only reading opinions you already agree with. BIG AP EXAM CONNECTION A student mixes up Spanish vocabulary from last year with current vocabulary. → proactive interference Unit 6: Developmental Psychology Big Idea: Humans develop physically, mentally, and socially across life. This unit asks: How do people change from infancy through adulthood? 1. Piaget’s Cognitive Development Sensorimotor Stage Babies learn through senses and actions. Object Permanence Understanding objects still exist when hidden. Example: Babies searching for hidden toys. Preoperational Stage Children use language but think egocentrically. Egocentrism Difficulty understanding another perspective. Example: A child assuming everyone sees exactly what they see. Concrete Operational Stage Logical thinking develops. Formal Operational Stage Abstract thinking develops. Example: Thinking about hypothetical situations. 2. Attachment Strong emotional bond with caregivers. Secure Attachment Healthy trust and comfort. 3. Parenting Styles Authoritative Strict but supportive. Usually healthiest. Authoritarian Strict with little warmth. Permissive Warm but few rules. BIG AP EXAM CONNECTION A teenager exploring identity and future goals. → Erikson’s identity vs role confusion stage Unit 7: Motivation, Emotion, and Personality Big Idea: Motivation drives behavior, emotions affect actions, and personality shapes how people interact. 1. Motivation Drive-Reduction Theory People act to reduce discomfort. Example: Eating when hungry. Maslow’s Hierarchy Basic needs come before higher goals. Example: Someone struggling financially may focus on survival before self-esteem. 2. Emotion Theories James-Lange Theory Physical response first. Example: Heart races THEN fear is felt. Cannon-Bard Theory Emotion and physical response happen together. Schachter Two-Factor Theory Emotion depends on physical arousal plus interpretation. 3. Personality Trait Theory Personality made of stable characteristics. Big Five Traits * openness * conscientiousness * extraversion * agreeableness * neuroticism BIG AP EXAM CONNECTION A student interpreting sweaty palms before a game as excitement. → Schachter two-factor theory Unit 8: Clinical Psychology Big Idea: Psychological disorders affect thoughts, emotions, and behaviors. This unit asks: How are disorders identified and treated? 1. Anxiety Disorders Generalized Anxiety Disorder Constant excessive worry. Phobias Irrational fears. OCD Obsessions and compulsions. 2. Mood Disorders Major Depressive Disorder Persistent sadness and loss of interest. Bipolar Disorder Extreme mood swings. 3. Schizophrenia Disordered thinking and perception. Hallucinations False sensory experiences. Delusions False beliefs. 4
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VHS Study Guide Psychology WEEK 1: Psychology as a Science The goal of this week is to distinguish between "Pop Psychology" (myths) and "Empirical Science" (facts). 1. The Philosophical Roots & "Big Names" Wilhelm Wundt: Established the first psychology lab (1879). He used Structuralism, trying to map the "structure" of the mind through Introspection (having subjects report every tiny sensation they felt). Sigmund Freud: Founded Psychoanalysis. He believed behavior is driven by the Unconscious mind and childhood traumas. He used dream analysis and "free association." Behaviorism (Watson & Skinner): They rejected Freud. They argued psychology must be an Empirical Science, meaning we only study what we can see and measure. Watson: Famous for the "Little Albert" study (fear conditioning). Skinner: Focused on how rewards/punishments shape behavior (Operant Conditioning). Ivan Pavlov: A physiologist who discovered Classical Conditioning (associating a neutral stimulus, like a bell, with a natural reflex, like drooling). Maslow’s Hierarchy of Needs: A Humanist theory. It’s a pyramid starting with basic survival (food/water) and moving up to Self-actualization (reaching your full potential). 2. The "Brain Traps" (Critical Thinking & Myths) Word-of-Mouth: We believe things just because we’ve heard them a lot (e.g., "We only use 10% of our brain"—FALSE). Desire for Easy Answers: People prefer a "quick fix" (like a 5-minute cure for anxiety) over complex scientific reality. Selective Perception: We only notice things that confirm our existing beliefs. Post Hoc, Ergo Propter Hoc: "After this, therefore because of this." The logical error of assuming that because Event B followed Event A, Event A must have caused it. Inferring Causation from Correlation: The most common exam trap. Just because two variables move together (like heat and crime), it doesn't mean one causes the other. Reasoning by Representativeness: Stereotyping. Thinking a person "looks like" a certain role, so they must be that role (the "Finance Bro" vest example). WEEK 2: Scientific Inquiry and Research This is the "How-To" of psychology. You need to know the difference between just watching people and running a real experiment. 1. Research Methods Naturalistic Observation: Watching subjects in their natural habitat without interfering. High "real world" accuracy, but you have zero control. Case Study (Clinical): An intensive, detailed look at one unique individual (e.g., a person with a rare brain injury). Great for detail, but you can't apply the results to everyone. Archival Research: Looking at old records, newspapers, or medical files to find patterns. Longitudinal vs. Cross-Sectional: Longitudinal: Following the same group of people for 20+ years. (Expensive, but shows true change). Cross-Sectional: Comparing different ages at the same time (e.g., testing 10-year-olds and 50-year-olds today). 2. The Experimental Design (The "Gold Standard") Inductive vs. Deductive: Inductive: Starting with observations $\rightarrow$ forming a theory (Bottom-up). Deductive: Starting with a theory $\rightarrow$ testing it with an experiment (Top-down). Independent Variable (IV): The variable the researcher manipulates (The "Cause"). Dependent Variable (DV): The variable being measured (The "Effect"). Control vs. Experimental Group: The experimental group gets the "treatment"; the control group gets a placebo or nothing. Random Assignment: Every participant has an equal chance of being in either group. This prevents Bias. Single-Blind vs. Double-Blind: Single: Participants don't know which group they are in. Double: Neither the participants nor the researchers know. This prevents the researcher from accidentally giving "cues." WEEK 3: Biology and Behavior The "Hardware" section. How the physical brain creates the "Pink Slime" experience. 1. The Nervous System Map Central (CNS): Brain and Spinal Cord. Peripheral (PNS): Everything else. Somatic: Voluntary movements (walking). Autonomic: Involuntary (heartbeat). Sympathetic: "Fight or Flight" (Eyes dilate, heart speeds up, digestion stops). Parasympathetic: "Rest and Digest" (Calms the body down). 2. The Neuron (The Building Block) Dendrites: Receive messages. Soma (Cell Body): Process info. Axon: Sends the electrical signal. Myelin Sheath: Fatty tissue that speeds up the signal. Synapse: The tiny gap between neurons where chemicals travel. Neurotransmitters: Agonist: A chemical that mimics a neurotransmitter (enhances the effect). Antagonist: A chemical that blocks a neurotransmitter. 3. Brain Tools & Anatomy EEG: Measures electrical brain waves (good for sleep studies). MRI vs. fMRI: MRI shows structure (a picture); fMRI shows function (where blood is flowing). PET Scan: Uses radioactive "tracer" sugar to see which parts of the brain are active. The Endocrine System: Uses Hormones (slow-acting chemicals) released into the bloodstream by Glands (like the Adrenal or Pituitary). 4. The "Hidden" Biological Details (Week 3) Refractory Period: After a neuron fires, it needs a tiny "recharge" break before it can fire again. Think of it like a camera flash or a toilet flushing—you can't do it twice in a split second. Broca’s Area vs. Wernicke’s Area: * Broca’s: Controls Speech Production (Frontal Lobe). If damaged, you know what you want to say but can't get the words out. Wernicke’s: Controls Language Comprehension (Temporal Lobe). If damaged, you can speak, but it's "word salad"—it makes no sense. WEEK 4: Consciousness Consciousness is your awareness of yourself and your environment. It’s not an "on/off" switch; it’s a spectrum. 1. Processing Levels Conscious Processing: Tasks that require focused attention (e.g., learning a new TikTok dance or solving a math problem). Automatic Processing: Tasks we do "without thinking" once they are learned (e.g., walking or an experienced driver steering a car). 2. Altered States Hypnosis: A state of extreme self-suggestion where a person is highly open to direction. Meditation: A practice of focused attention to achieve mental clarity and emotional calm. Daydreaming: A shift in attention away from the current task toward internal thoughts and "mental movies." 3. Psychoactive Drugs (The "Drug Cabinet") Depressants (Alcohol, Barbiturates): Slow down the Central Nervous System (CNS). They decrease heart rate and reaction time. Stimulants (Caffeine, Nicotine, Cocaine, ADHD meds): Speed up the CNS. They increase heart rate and energy. Opiates (Heroin, Morphine, Vicodin): Specifically target pain receptors. They mimic Endorphins to stop pain and create euphoria. Hallucinogens (LSD, Marijuana, Psilocybin): Distort perceptions and evoke sensory images in the absence of sensory input. WEEK 5: Sleep and Dreams Sleep is a biological necessity, not a luxury. Your brain is incredibly active during this "downtime." 1. Stages of Sleep (The Cycle) Stage 1 (NREM-1): Light sleep. You might experience "hypnagogic sensations" (feeling like you are falling). Stage 2 (NREM-2): Deep relaxation. Characterized by Sleep Spindles (bursts of rapid brain activity). Stage 3 & 4 (NREM-3): Deepest sleep. This is when the body repairs itself. If you wake up here, you’ll feel very groggy. REM (Rapid Eye Movement): The "Dream Stage." Your brain waves look like you are awake, but your motor cortex is blocked—meaning your body is paralyzed so you don't act out your dreams. 2. Dream Theories (Why do we dream?) Freud’s Wish Fulfillment: Dreams are a "safety valve" for unacceptable feelings. Manifest Content: The actual storyline of the dream (e.g., being chased by a giant Pink Slime). Latent Content: The hidden psychological meaning (e.g., you are running away from your final exam stress). Activation-Synthesis: The brain's attempt to make sense of random neural static. The brain "synthesizes" a story from random "activation." Information Processing: Dreams help us sort out the day's events and consolidate memories. Threat Simulation Theory: Dreaming allows us to "practice" surviving dangerous situations in a safe environment. WEEK 6: Thinking and Processing This is about "Cognition"—how we use our "Pink Slime" to solve problems and make decisions. 1. Building Blocks of Thought Concepts: Mental groupings of similar objects (e.g., the concept of "Dogs"). Prototype: The best example of a category. (If I say "Bird," you probably think of a Robin, not a Penguin. The Robin is your prototype). Schemata (Schema): A mental framework that helps us organize and interpret information (e.g., your "School Schema" includes desks, teachers, and bells). 2. Problem-Solving Tactics Trial-and-Error: Trying random solutions until one works. (Slow and inefficient). Algorithms: A step-by-step, logical rule that guarantees a solution. (e.g., a math formula or checking every single aisle in a store to find milk). Heuristics: A mental shortcut or "rule of thumb." It's faster than an algorithm but can lead to errors. (e.g., looking at the signs above the aisles to find the milk). 3. The Biases (Why we make mistakes) Confirmation Bias: Searching for information that supports our preconceptions and ignoring everything else. Hindsight Bias: After an event occurs, believing we "knew it all along." Anchoring Bias: Getting "stuck" on the very first piece of information offered. (e.g., if a shirt is "on sale" for $50 down from $100, you think $50 is a deal, even if the shirt is only worth $10). Availability Heuristic: Estimating the likelihood of events based on how easily they come to mind. (e.g., being afraid of a plane crash because you saw one on the news, even though car crashes are more common). Mental Set: The tendency to approach a problem in one particular way, often a way that has worked in the past but may not work now. WEEK 7: Memory Memory is the persistence of learning over time. 1. The Three Stages of Memory Encoding: Getting information into our brain. Semantic Encoding: Encoding the meaning of words (Deepest processing). Visual Encoding: Encoding images. Acoustic Encoding: Encoding sounds. Storage: Retaining that information. Retrieval: Getting the information back out. 2. Types of Storage Short-Term Memory (STM): Holds about 7 items (plus or minus 2) for about 20 seconds. Long-Term Memory (LTM): Unlimited capacity and can last a lifetime. Explicit (Declarative): Facts and experiences (Semantic = facts; Episodic = your life stories). Implicit (Procedural): Skills (like riding a bike or typing). 3. Memory Sins & Failures Schacter’s Seven Sins: Includes Transience (fading over time), Absent-mindedness (forgetting your keys), and Persistence (unwanted memories that won't go away). Amnesia: Anterograde: You can't form new memories. Retrograde: You can't remember the past. 4. Enhancement Techniques Chunking: Organizing items into familiar, manageable units. Spaced Repetition: Studying small amounts over a long time rather than cramming. Mnemonic Devices: Memory aids like "PEMDAS" for math. 5. The "Subtle" Memory Sins (Week 7) The Serial Position Effect: You are most likely to remember the beginning of a list (Primacy Effect) and the end of a list (Recency Effect), but you’ll probably forget the middle. Pro-Tip: This is why you should study the "middle" weeks (Week 4, 5, 6) extra hard! Misinformation Effect: This is why eyewitness testimony is shaky. If someone asks, "How fast was the car going when it smashed into the pole?" you will remember the car going faster than if they said "hit." WEEK 8: Lifespan Development Developmental psychology examines how we change physically, cognitively, and socially from "womb to tomb." 1. Cognitive Development (Jean Piaget) Piaget believed children think differently than adults and move through four stages: Sensorimotor (0–2 years): Exploring the world through senses. Key milestone: Object Permanence (realizing things still exist even if you can't see them). Preoperational (2–7 years): Symbolic thought (make-believe) but lacks logic. Key trait: Egocentrism (thinking everyone sees the world exactly as they do). Concrete Operational (7–11 years): Logical thinking about physical objects. Key milestone: Conservation (understanding that volume stays the same even if the shape of the glass changes). Formal Operational (12+ years): Abstract reasoning and hypothetical "what if" thinking. 2. Psychosocial Development (Erik Erikson) Erikson focused on "crises" we face at each age. Trust vs. Mistrust (Infancy): Is the world safe? Identity vs. Role Confusion (Adolescence): "Who am I?" (This is the most common exam question). Integrity vs. Despair (Late Adulthood): Looking back on life with satisfaction or regret. 3. Moral Development (Lawrence Kohlberg) Pre-conventional: Doing the right thing to avoid punishment or get a reward. Conventional: Doing the right thing because it's the law or to fit in. Post-conventional: Doing the right thing based on universal ethical principles (even if it breaks the law). 4. Parenting Styles Authoritative: High warmth, high rules. (The "Goldilocks" style—best outcomes). Authoritarian: Low warmth, high rules. ("Because I said so!"). Permissive: High warmth, low rules. (More like a friend than a parent). Uninvolved: Low warmth, low rules. (Neglectful). WEEK 9: Learning Learning is a relatively permanent change in behavior due to experience. 1. Classical Conditioning (Ivan Pavlov) Learning by association (connecting two stimuli). Unconditioned Stimulus (UCS): The natural trigger (Food). Unconditioned Response (UCR): The natural reflex (Drooling for food). Neutral Stimulus (NS): A trigger that means nothing yet (A Bell). Conditioned Stimulus (CS): The bell after it has been paired with food. Conditioned Response (CR): Drooling for the bell alone. 2. Operant Conditioning (B.F. Skinner) Learning by consequences (Rewards and Punishments). Positive Reinforcement: Adding something good to increase behavior (A gold star for working). Negative Reinforcement: Removing something bad to increase behavior (The car stops beeping when you buckle your seatbelt). Positive Punishment: Adding something bad to stop behavior (A speeding ticket). Negative Punishment: Taking away something good to stop behavior (Taking away your phone). 3. Observational Learning (Albert Bandura) Learning by watching others. Famous study: The Bobo Doll Experiment, where kids imitated adults punching a doll. 4. The "Fine Print" of Learning (Week 9) Spontaneous Recovery: After a behavior has been "extinct" (gone away) for a while, it suddenly reappears out of nowhere. (Like Pavlov's dog suddenly drooling at a bell weeks after he stopped). Generalization vs. Discrimination: Generalization: Fearing all dogs because one bit you. Discrimination: Only fearing the specific dog that bit you. WEEK 10: Social Influences This is the study of how the "situation" and "group" overpower the individual. 1. The Stanford Prison Experiment (Zimbardo) Demonstrated the power of Social Roles and Scripts. Ordinary students became abusive "guards" or submissive "prisoners" simply because of the role they were assigned. 2. Influence & Conformity Normative Social Influence: Conforming to fit in and be liked (Dressing like your friends). Informational Social Influence: Conforming because you think the group has more info than you (Following the crowd in a new city). Obedience (Milgram): Following orders from an authority figure, even if it hurts someone else. 3. Group Dynamics Social Loafing: Working less hard in a group than when alone (The "Billy" effect). Deindividuation: Losing self-awareness and self-restraint in a large crowd or behind an anonymous screen. Group Polarization: When group discussion leads to more extreme opinions. Bystander Effect: People are less likely to help if others are around due to a Diffusion of Responsibility. 4. Thinking Patterns Fundamental Attribution Error: Blaming someone's personality for their behavior while ignoring the situation. Cognitive Dissonance: The "icky" feeling when our actions don't match our beliefs (e.g., you hate lying, but you just lied to your mom). We usually change our beliefs to match our actions to feel better. 5. Social Psych "Secret" Terms (Week 10) Self-Serving Bias: When we succeed, we take the credit ("I'm a genius"). When we fail, we blame the situation ("The test was unfair"). Foot-in-the-Door vs. Door-in-the-Face: Foot-in-the-Door: Ask for something tiny first, then the big thing. Door-in-the-Face: Ask for something HUGE (get rejected), then ask for the smaller thing you actually wanted. They are more likely to say yes because it feels like a "compromise." WEEK 11: Multiculturalism & Diversity This is the study of how culture, identity, and group values shape our behavior and how we interact with others. 1. Cultural Values Individualism: Cultures that value personal independence and "Me" goals (e.g., USA). Success is based on personal achievement. Collectivism: Cultures that value group harmony and "We" goals (e.g., Latin America, Asia). Success is based on doing what is best for the family or community. 2. Acculturation (How we adapt to new cultures) Integration: The "Best of Both Worlds." Keeping your original culture while participating in the new one. Assimilation: Giving up your original identity to fully "blend in" with the new culture. Separation: Keeping your original culture and avoiding the new one. Marginalization: Feeling like you don't belong to either culture (The "lonely" state). 3. Metaphors for Society The Melting Pot: The old idea that everyone should blend together and lose their differences to become one "American" identity. The Salad Bowl: The newer idea where cultures live together but stay distinct. You can see the "tomatoes" and the "lettuce"—everyone keeps their unique flavor. 4. Social Barriers Microaggressions: Small, daily slights or "backhanded compliments" toward marginalized groups (e.g., "You’re so articulate for someone from your neighborhood"). Prejudice vs. Discrimination: Prejudice is the thought/feeling (pre-judging), while Discrimination is the action (treating someone differently). WEEK 12: Stress & Health This is the study of how our brain's "appraisal" of the world affects our physical and mental health. 1. The Appraisal Process (Lazarus) Primary Appraisal: Judging if a stressor is a Threat (harmful) or a Challenge (potential for growth). Secondary Appraisal: Evaluating your tools. "Do I have the resources to handle this?" If yes, stress stays low. If no, panic sets in. 2. The Body’s Response (Selye’s GAS) General Adaptation Syndrome (GAS): The three stages of how your body reacts to stress: Alarm: Fight-or-Flight. Heart races, adrenaline hits. Resistance: Staying on "high alert" to cope. This is where you grind through the week. Exhaustion: Your battery dies. Your immune system crashes, and you get sick (The Cohen Cold Study). 3. Types of Stress Eustress: "Good stress." The kind that motivates you to finish a project or perform well in a game. Distress: "Bad stress." Chronic pressure that leads to burnout, fatigue, and health problems. 4. Coping Strategies Problem-Focused Coping: Attacking the problem directly. (Example: Time-Blocking your homework so it isn't overwhelming). Emotion-Focused Coping: Managing the feelings. (Example: Going to the Gym or meditating to stop feeling anxious). 5. Stress "Secret" Terms Cortisol: The primary stress hormone. Great for emergencies, but too much of it "eats" your memory and weakens your heart. Psychoneuroimmunology: The fancy word for the study of how your brain (stress) talks to your immune system. WEEK 13: Mental Wellness & The Science of Happiness The goal of this week is to identify the psychological frameworks and empirical studies that explain how humans build resilience and long-term well-being. 1. The Three Dimensions of Happiness (Module 14.5) According to the textbook, happiness is an enduring state consisting of joy and contentment. It is built through three "lives": The Pleasant Life: Attaining and savoring daily pleasures that add joy to the moment (e.g., the aroma of coffee or the feeling of sunshine). The Good Life: Identifying your unique skills and using them to enrich your life. This is where you find the state of Flow—being so "in the zone" that you lose track of time. The Meaningful Life: Using your talents and efforts in the service of the greater good or to help others, which provides a deeper sense of fulfillment than pleasure alone. 2. The Four Pillars of Well-Being (Wellness Studies) Based on Dr. Richard Davidson’s research, well-being is a "trainable skill" rather than a fixed trait. It is built on: Awareness: Noticing what your mind is doing in the present moment (meta-awareness). Connection: Cultivating kindness and healthy social relationships, which are the #1 predictor of long-term health. Insight: Having curiosity about how your own mind works and not believing every negative thought as a "fact." Purpose: Having a clear sense of direction or a "life compass" that guides your daily actions. 3. Empirical Evidence: The Creswell et al. Study (2014) This study provided scientific proof that mental training has biological effects: The Setup: An experimental design where students were randomly assigned to either a mindfulness group or an analytic control group. The Independent Variable: Brief 3-day mindfulness meditation training (25 mins/day). The Dependent Variable: Biological stress markers (Cortisol levels) and self-reported stress. The Result: The mindfulness group showed significantly lower cortisol levels, proving that meditation fosters biological resilience to stress. 4. Scientifically Proven Benefits of Gratitude Research shows that gratitude is a powerful "reset" for the nervous system: Physical: Improved sleep quality and duration; fewer reported aches and pains. Psychological: Reduces "toxic" emotions (envy, resentment) and increases mental strength. Studies of 9/11 survivors showed gratitude was a major factor in preventing PTSD. Social: Encourages "pro-social" behavior, making people more likely to form and maintain new relationships. 5. Mindfulness vs. Meditation (The State vs. The Practice) It is critical to distinguish between these two often-confused terms: Mindfulness: A state of being. It is the quality of being fully present, aware of where we are and what we’re doing, without being overly reactive or overwhelmed. Meditation: The formal practice or "mental gym" used to train the brain. It is the intentional time set aside to practice techniques that eventually lead to a consistent state of mindfulness. 6. Key Terminology & Cognitive Traps Affective Forecasting: The human tendency to overestimate how much future events (both good and bad) will affect our long-term happiness. We assume milestones like "perfect grades" will provide permanent joy, but they usually don't. Optimism & Resilience: Optimism is the general tendency to expect good outcomes. It is the "engine" of resilience—the ability to "bounce back" from major life stressors (like those listed on the SRRS). Problem-Focused vs. Emotion-Focused Coping: * Problem-Focused: Dealing with the stressor directly (e.g., studying for the test). Emotion-Focused: Managing the feelings associated with the stressor (e.g., taking a nap or exercising)
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NURS 348 — EXAM 4 STUDY GUIDE Hypertension Definition & Overview • Persistent elevation of BP ≥130/80 mmHg (systolic at/greater than 130 OR diastolic at/greater than 80) on at least 2 separate visits, 2+ weeks apart. • Primary (Essential): No identifiable cause, most common (90–95% of cases). • Secondary: Caused by another condition or adverse effects of medications. Etiology/Pathophysiology • ↑ Peripheral resistance and/or ↑ cardiac output → ↑ blood pressure → When blood vessels get narrower (increased resistance) or the heart pumps more forcefully (increased output), pressure inside the vessels rises “like squeezing a hose while water is running” → Over time, this high pressure damages the vessel walls and heart muscle, increasing the risk for atherosclerosis, heart attack (myocardial infarction), and stroke. • ↑ Increased peripheral resistance (arteriolar constriction) → ↑ afterload → left ventricular hypertrophy → heart failure → The heart pushes against more resistance (afterload), making the heart muscle thicker (hypertrophy). Over time, it becomes weaker and can lead to heart failure. • Kidneys retain sodium and water → ↑ circulating volume → The kidneys hold onto extra salt and water, adding more fluid to the blood. More fluid means higher pressure—like overfilling a water balloon. • Activation of renin–angiotensin–aldosterone system (RAAS) = vasoconstriction + fluid retention. RAAS is like the “blood pressure booster” → When this system turns on, blood vessels tighten and the kidneys save even more salt and water, both of which raise blood pressure. Risk Factors: • Primary: family history, ↑ sodium intake, Obesity (BMI >25), African-American ethnicity, smoking, hyperlipidemia, diabetes mellitus, and stress. • Secondary: kidney disease, Cushing’s, pregnancy, pheochromocytoma, medic (steroids, OCPs). Clinical Manifestations (S/S) • Often asymptomatic (“silent killer”)!!! • Headache, dizziness, fainting, vision changes • Retinal damage on exam (cotton wool spots, papilledema). • Note: if blood pressure reading is elevated then take in both arms; pt legs uncrossed, and arms above heart; correct cuff Diagnostics (Dx)/Labs • Multiple BP readings (both arms, sitting and standing) • ECG → Left-Ventricular hypertrophy. evaluates cardiac function. • Labs → ↑ BUN/creatinine (kidney disease), lipids, glucose, cortisol (Cushing’s) Nursing Care / Nursing Interventions • Monitor pt BP regularly and accurately, check both arms/correct cuff • Put on DASH diet (Dietary Approach to Stop Hypertension) Medications • ⭐️Diuretics (first-line): excess fluids, they need to remove; increase urine • Thiazides (hydrochlorothiazide) inhibits water & sodium reabsorption and increases potassium excretion • Side effects/SE: hypokalemia; monitor potassium(K⁺) levels • Loop (furosemide) decreases sodium reabsorption & increase potassium excretion– SE: hypokalemia; monitor potassium(K⁺) levels • Potassium-sparing (spironolactone) – SE: hyperkalemia; monitor potassium levels. EKG: peaked T waves • Also watch out for muscle weakness, irregular, pulse, and dehydration. • ⭐️Calcium channel blockers (verapamil, amlodipine, and diltiazem) Calcium channel blockers relax and widen blood vessels by preventing calcium from entering muscle cells, leading to lower blood pressure (vasodilation) • SE: constipation; take fiber for verapamil, and all can ↓HR • Avoid grapefruit juice ➡️ toxicity, hypotensive effects Calcium= contract • ⭐️ACE inhibitors (lisinopril, enalapril): prevents angiotensin II → vasodilation • SE: - hypotension; monitor BP and pulse HR -hyperkalemia; monitor potassium levels -erectile dysfunction -⭐️cough linked to angioedema (swollen tissue under the skin around lips, tongue, and glottis); report swelling & discontinue med • ⭐️ARBs (valsartan, losartan): for ACE-intolerant pts from cough/hyperkalemia. ARBs lower blood pressure by blocking angiotensin II from binding to its receptors, preventing vasoconstriction, and reducing fluid retention. • SE: angioedema, heart failure, hyperkalemia • Change position, slowly, report, angioedema, edema, and avoid foods that are high in potassium (bananas, potatoes, apricots, spinach, beans); monitor potassium levels • Aldosterone-receptor antagonists (eplerenone, spironolactone): blocks aldosterone action. • SE: kidney damage, hypertriglyceridemia, hyponatremia, and hyperkalemia; monitor kidney function, triglycerides, sodium, and potassium levels • Avoid Grapefruit juice and St. John’s wort, salt substitutes, and potassium rich foods • ⭐️Beta blockers (metoprolol, atenolol): blocks beta receptors (adrenaline/epinephrine) ➡️reduces heart rate, cardiac output, and blood pressure ↓HR, ↓CO; use cautiously in diabetics • SE: -⭐️erectile dysfunction, -Fatigue, weakness, depression -hypoglycemia • Monitor heart rate (hold if HR is less than 60) and do not suddenly stop taking med (cause rebound hypertension); and don’t give to pts with asthma, airway disease (cause bronchospasms) • Central Alpha-2 agonists (clonidine): calm the nerves that raise blood pressure, letting blood vessels, relax, and BP go down, ↓SNS tone • SE: sedation, orthostatic, hypotension, and sexual dysfunction/impotence • Monitor BP and pulse • Alpha-adrenergic blockers (prazosin, doxazosin): vasodilator= relaxed BP; give at night to avoid first-dose hypotension. Start with low dose. • SE: postural hypotension; make sure patient rises slowly and caution. • Monitor BP 2 hrs after initiation Complications • Hypertensive Crisis: usually when patients do not follow the medication regimen • BP >180/120 → organ damage (encephalopathy, renal failure) • S/S: severe headache, dizziness, blurred vision, confusion, epistaxis • Treat: IV antihypertensives (nitroprusside, nicardipine, labetalol); the goal is to lower BP gradually by 20-25% in first hour. Not less than 140/90. Monitor BP every 5-15 mins Patient Education • Adhere to medication regimen, don’t abruptly stop even when you feel better • Change positions slowly • Encourage DASH diet (low sodium, high fruits/veggies, low-fat dairy) ex: grilled salmon, brown rice, steamed broccoli, and low-fat milk • Avoid high-sodium foods. Consume less than 2.3 g/day • Monitor BP at home • Report signs or symptoms of electrolyte imbalances • Encourage Weight loss, exercise 3x weekly • Encourage Smoking cessation • Encourage Limit alcohol (≤2/day men, ≤1/day women) • Manage stress • Report persistent cough or swelling (ACE inhibitor red flag) Peripheral Venous Disorders(PVD) Patho: problems with veins where Deoxygenated blood can't get back to the heart Oxygenated blood pools in the extremities. The valves are preventing backflow. • Venous Thromboembolism (VTE): blood clot that starts in a vein. -Two types: deep vein thrombosis (DVT) and pulmonary embolism (PE) • Venous insufficiency: Improper functioning of the veins. Veins aren’t able to push back blood to the heart which results in swelling, venous stasis ulcers, or cellulitis. Blood can go down into the veins just fine but cannot come back up. a. VTE ex: Deep Vein Thrombosis (DVT) Pathophysiology • Thrombus (Blood clot) forms in deep veins (usually in legs) → can embolize (travel and block vessel) its way to lungs (PE). • Caused by Virchow’s triad: venous/blood flow stasis, endothelial injury, hypercoagulability. Risk Factors • Surgery (hip, knee, prostate) • Immobility • Heart failure • Pregnancy • Family hx • Oral contraceptives or hormone therapy • Cancer • COVID-19 (elevated D-dimer) • Central venous catheters Clinical Manifestations • Note that clients can be asymptomatic • Calf/groin pain (dull/achy), tenderness, warmth, edema • Unilateral swelling • Shallow, irregular shaped wounds • Too much blood, brown/yellow discoloration • Sudden SOB and sharp chest pain → suspect PE • Positioning: “Elevate Veins”, position up in “V” shape, above heart. Worsens: if dangling, sitting/dangling for long periods of time. Diagnostics • ⭐️Venous duplex ultrasonography = gold standard; it’s an ultrasound of Leg to see blood clot/blood flow through the vessel. • ⭐️D-dimer ↑ = clot breakdown evidence • Venogram/MRI if ultrasound inconclusive Nursing Interventions • Bed rest until anticoagulation started • Elevate leg slightly above heart (no knee gatch). Positioning: “EleVate Veins”, think V as veins are up, to keep the veins open. • Warm compresses • DO NOT massage leg • Compression stockings (after swelling ↓) • Encourage early ambulation when safe • SCDS Medications/Procedures (Anticoagulants) stops blood from clotting, another nurse must be with you • Unfractionated heparin (given IV): prevents clots and growth of existing clot; monitor platelets, and aPTT (how long it takes blood to clot) (1.5–2× normal). Must be given in facility. MUST MONITOR CLOSELY • Antidote: protamine sulfate • Low-molecular-weight heparin (Lovenox/enoxaparin): given SubQ, weight-based, prevention and treatment of DVT, given twice daily, can be used in home setting. Don’t need labs. Monitor for bleeding, and take bleeding precautions (Electric razor, soft toothbrush, environment safety) • Warfarin (Coumadin): oral, inhibits vitamin K clotting factors overlaps; combined with heparin 3–4 days until INR 2–3 (takes awhile to kick in; therapeutic affect) • Antidote: vitamin K • Avoid high vitamin K foods (green leafy veggies) • Monitor PT (range: 11-13.5 secs), INR (must know range: 2–3) • Factor Xa inhibitors (fondaparinux; SubQ) (rivaroxaban, apixaban; oral): Prevents development of Thromboses; transitional medication; initial labs are PT and PTT; not routinely • Direct thrombin inhibitors (dabigatran): directly prevents growth of thrombus Formation, given sub Q ; initiate initial lab values only for PT and APTT. • Antidote: idarucizumab • Thrombolytics (tPA): for massive DVT/PE, directly infused into clot, start within 24hrs- 5 days of clot formation; monitor for bleeding, neuro status, dizziness, headache. Take bleeding precautions, pt must use electric razor and, brush teeth with a soft toothbrush. • Inferior vena cava filter: prevents embolus from reaching lungs (PE), inserted in femoral vein; catches blood clot. Used when pt is unresponsive to other treatments. Monitor: bleeding, hematoma, infection, PE (dyspnea, chest pain, tachycardia). Nursing actions: assess circulation and encourage leg exercises/ambulation early, have patient not sit for too long Anticoagulant Therapy Nurse’s Role • Verify labs,;Double-check with another RN for IV heparin, Assess for bleeding (bruises, gums, stools) and Monitor vitals, mental status (signs of intracranial bleed) Reversal Agents • Heparin → protamine sulfate • Warfarin → vitamin K • Dabigatran → idarucizumab Patient Education • Avoid contact sports • Soft toothbrush, electric razor • Avoid sudden diet changes (vitamin K) Complications (anticoagulants) • ⭐️Pulmonary embolism: sudden dyspnea, chest pain, SOB, anxiety, tachypnea → emergency; sit, patient in high Fowlers, and administer oxygen and anticoagulants • ⭐️Ulcer formation(venous): often formed over the medial malleolus, chronic, hard to heal, can reoccur. Can lead to amputation/death. Neuropathic patients might not feel this. Nursing care: Dressing is left 3–7 days; wound vacuums, diet: high in zinc, protein, iron, and vitamins A and C, debride necrotic tissue so wound can heel. Patient Education(Anticoagulants) • Bleeding precautions (soft toothbrush, electric razor) • Report bruising or black stools • Avoid prolonged sitting/crossing legs • Wear compression stockings b. Venous insufficiency Pathophysiology • Valves and legs are damaged due to prolong venous HTN Our previous blood clot Risk factors: • Sitting/standing in one position for a long period of time • Obesity • Pregnancy • Thrombophlebitis Clinical manifestations: • Status dermatitis(brown discoloration along ankles) • Edema • Stasis ulcers around ankles Labs/DX • D-dimer ↑ = clot breakdown evidence, detects clot Nursing interventions: Elevate legs to increase venous return (20 mins, 4-5/day), position: legs above heart, “Elevate Veins”, Apply stockings, and monitor for cellulitis Patient education: avoid sitting/standing still for too long, change positions often, avoid crossing legs, tight clothing. Apply stockings before getting out of bed in the morning Peripheral Arterial Disease (PAD) : affects blood vessels that carry blood away from the heart; artery carries blood away from heart but has difficulty going down to extremities. Pathophysiology • Atherosclerosis in lower extremities → decreased blood flow to tissues. Risk Factors • Smoking, DM, hypertension, hyperlipidemia, obesity, age, sedentary lifestyle. Clinical Manifestations • Intermittent claudication: leg pain with exercise, relieved by rest; not enough oxygen makes the tissue suffer = pain; ischemia • Pain(sharp) that is only relieved when resting in dependent position • Cool, pale, cyanotic skin • Loss of hair on legs, thick toenails • Weak/absent pedal pulses; dorsalis pedis; Doppler(verify), +1 • Numbness, burning at night • No blood and no edema due to an adequate blood flow • Note: think “A” in PAD as Antarctica, where it’s cold! For cold, pale skin! Diagnostics • ⭐️ABI < 0.9 = PAD; ankle pressure compared to break your pressure; expected finding is 0.9–1.3; less than is PAD • ⭐️Arteriography for visualization of occlusion/decreased arterial flow with contrast injection on a x-ray. Monitor for bleeding, hemorrhage, marked, pedal pulses • Doppler studies → decreased flow in DM patients • ⭐️Exercise tolerance testing → decreased pressure in lower limbs, read the workload of the heart/circulation, and clarification during exercise. May use treadmill or meds (dipyridamole, adenosine). Finding of a BP/pulse waveform = arterial disease. Monitor vitals before, during, and after. Stop test if chest pain or symptoms are severe. Nursing Interventions • Encourage graded exercise until pain, rest, repeat • Avoid elevating legs above heart (impairs flow) • Avoid cold, caffeine, nicotine, tight clothing • Keep extremities warm (no heating pad), they can’t feel • Foot care: inspect daily, no bare feet, toenails straight Medications • Antiplatelets: (aspirin, clopidogrel) reduces blood viscosity and increases blood flow and extremities. Monitor: bleeding, abdominal pain, black, tarry stools. • Statins: (atorvastatin, simvastatin). Relieved manifestations like intermittent claudication. • Pentoxifylline: improves RBC flexibility (claudication). Monitor for bleeding, abdominal pain, black tarry stools. Procedures • Angioplasty (balloon/stent). Opens and helps, maintain the patency of the vessel, however, laser vaporizes atherosclerosis plaque. Monitor for bleeding, vital signs, pulses, cap Refill. As patients rest limbs are straight for 2-6 hrs before ambulation. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Atherectomy rotation, device removes, arterial plaque. Monitor for bleeding and distal pulses. rest limbs are straight for 2-6 hrs. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Arterial revascularization bypass surgery • Used for clients at risk for losing a limb, severe claudication, or limb pain at rest. It reroutes the circulation around the arterial occlusion. • Post-op: ⭐️ maintain adequate circulation in repaired artery, mark pedal/dorsalis pulses(compare both), monitor color/temp, pain, cap refill, blood pressure (HTN= risk for bleeding; Hypotension=clot risk). • Complications: for these notify provider first -graft occlusion: acute blockage of bypass graft within 24 hr(absent pulse, cold foot, increased pain) -compartment syndrome: tissue pressure restricting blood flow; causing ischemia (numbness, tingling, edema, worsening/passive pain) -infection: infection of site (warm, tenderness, elevated, WBC, purulent drainage, use sterile technique) Patient Education • Walk until pain → rest → walk more • Stop smoking • Avoid crossing legs • Diet low in cholesterol and fat Postoperative Care – Peripheral Bypass/Revascularization Priorities • Assess extremity: color, temperature, cap refill, sensation, pulses q15min ×1hr • Mark pedal pulses before surgery • Maintain adequate BP (avoid hypo or hypertension) • Do not flex hip/knee excessively • Encourage ambulation when ordered • Report sudden pain, loss of pulse, pale/cool extremity = graft occlusion Complications • Graft occlusion, Compartment syndrome, Wound infection Arterial vs. Venous Ulcers Feature Arterial Ulcer Venous Ulcer Location Toes, feet, lateral ankle Medial ankle Appearance Pale, dry, round “punched out”, no drainage Irregular, leaky/moist, brown discoloration Pain Severe, worse with elevation Achy, relieved with elevation Skin Cool, shiny Warm, thickened Treatment Improve arterial flow Compression therapy, elevate legs Valvular Heart Disease OVERVIEW Overview • Stenosis = narrowed opening/thickening and hardening • Regurgitation = backflow of blood • Causes: rheumatic fever, degenerative calcification, endocarditis Diagnostics • Chest X-ray → chamber enlargement • ⭐️ECG → hypertrophy • Echo → valve dysfunction • TEE → direct view of valves ⭐️ Medications overview • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine); ACE inhibitors (-pril); angiotensin–receptor blockers (-artan); vasodilators (hydralazine]): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Inotropic agents (digoxin): increases contractility, improves cardiac output. Hold medication if pulse rate (abnormal) is less than 60/min or greater than 100/min. Take medication same time every day, avoid combining with antacids (2hrs). Monitor: toxicity such as weakness, confusion, visual changes, low appetite. • Anticoagulants: reduces risk of thrombus. Monitor: stroke, PT, INR, bleeding/bruising. Procedures • Valvuloplasty (balloon dilation) • Valve replacement • Mechanical = lifelong anticoagulants • Tissue = replace every 7–10 years Patient Education • Prophylactic antibiotics before dental procedures • Good oral hygiene • Daily weights • Sodium restriction • Avoid caffeine/alcohol • Report HF signs (weight gain, edema, SOB) • Avoid alcohol, epinephrine, and ephedrine= can cause dysrhythmias THE 4 VALVULAR DISORDERS Mitral Stenosis Etiology/Pathophysiology: Narrowed mitral valve obstructs blood flow from left atrium (LA) → left ventricle (LV), increasing LA pressure and pulmonary congestion → right-sided heart failure. Often caused by rheumatic fever. Clinical Manifestations: Dyspnea on exertion, orthopnea, pitting edema, fatigue, palpitations, hemoptysis, apical diastolic murmur. Risk Factors: Rheumatic heart disease, aging, congenital malformations. Labs/Diagnostics: Echocardiogram (valve narrowing, pressure gradient), ECG (A-fib), chest X-ray (LA enlargement). Medications/Management: • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Anticoagulants: reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgical: Balloon valvuloplasty or valve replacement. NCLEX Tip: Rheumatic fever is the most common cause. Mitral Insufficiency Etiology/Pathophysiology: Incomplete closure of mitral valve causes blood to leak back into LA during systole → LV dilation and hypertrophy. Clinical Manifestations: Fatigue, dyspnea, orthopnea, palpitations, holosystolic murmur at apex, pitting edema, S3 sounds Risk Factors: Mitral valve prolapse, rheumatic disease, MI, endocarditis. Labs/Diagnostics: Echocardiogram (regurgitant volume), ECG (A-fib), BNP (HF indicator). Medications/Management: • Beta-blockers (-lol); ACE inhibitors (-pril); ARBS/angiotensin–receptor blockers (-artan): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: manage fluid overload. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Anticoagulants if A-fib present; reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgery for severe cases. NCLEX Tip: Afterload reduction decreases regurgitant flow. Aortic Stenosis Etiology/Pathophysiology: Narrowed aortic valve → obstructed LV outflow → ↑ LV pressure → hypertrophy → ↓ cardiac output. Clinical Manifestations: Triad: angina, syncope, dyspnea (heart failure); systolic murmur radiating to carotids. Risk Factors: Aging (calcification), congenital bicuspid valve, rheumatic fever. Labs/Diagnostics: Echocardiogram (valve area), ECG (LV hypertrophy), cardiac cath (pressure gradient). Medications/Management: • Avoid nitrates/vasodilators (can cause hypotension). • Use beta-blockers (-lol) cautiously. reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Surgical aortic valve replacement (definitive). NCLEX Tip: Do not aggressively lower preload; maintain perfusion. Aortic Insufficiency Etiology/Pathophysiology: Incomplete closure of aortic valve → backflow of blood into LV → volume overload → dilation and LV hypertrophy. Clinical Manifestations: Dyspnea, palpitations, fatigue, bounding (“water hammer”) pulse, wide pulse pressure, diastolic murmur. Risk Factors: Rheumatic fever, endocarditis, Marfan syndrome, trauma. Labs/Diagnostics: Echocardiogram (backflow volume), ECG (LV enlargement), chest X-ray (cardiomegaly). Medications/Management: • Calcium channel blockers (-dipine); ACE inhibitors (-pril); vasodilators (hydralazine]): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics for volume management. • Surgical valve replacement when severe. NCLEX Tip: Bounding pulse and wide pulse pressure are hallmark findings. General Nursing & Exam Focus • Best diagnostic test: Echocardiogram (for all). • Monitor for A-fib in mitral disorders. • Valve replacement (mechanical): Lifelong anticoagulation. • Daily weights & fluid balance: Detect early HF. • Positioning: High-Fowler’s for dyspnea, low-sodium diet. Inflammatory Heart Disorders (Endocarditis, Pericarditis, Myocarditis, Rheumatic Carditis) Risk Factors • IV drug use, valve replacement, streptococcal infection, immunosuppression, lower socioeconomic status Pericarditis: inflammation of the pericardium (sac around heart) -RF: heart attack, lupus, rheumatoid arthriti -Clinical manifestations: Chest pain (relieved when leaning forward), coughing, Pericardial friction rub, fever, dysrhythmias, and SOB -Labs/DX: • High WBCs, EKG showing ST or T spiking, echocardiogram (inflamed heart) -Nursing care/Intervention: address pain/inflammation, and monitor for cardiac tamponade, position, patient upright, leaning forward, and monitor ECG - Medications: NSAIDs, corticosteroids, anti antibiotics for bacterial • Ibuprofen/NSAIDs for inflammation (pericarditis). Avoid if patient has peptic ulcer, monitor for G.I. bleeding, platelets, liver/kidney function. Must be taken with food, avoid alcohol. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. -Complication: cardiac tamponade → muffled heart sounds, paradoxical pulse, JVD, hypotension (Beck’s triad) Myocarditis: inflammation of the myocardium (heart muscle itself) -RF: viral (covid, Coxsackie), fungal, or bacterial infection; autoimmune disorder -Clinical Manifestations: Tachycardia, chest pain, murmur, friction rub, dysrhythmias, peripheral swelling, cardiomegaly. -Labs/Dx: ECG, echocardiogram, high troponin, CK – MB, ESR in CRP for inflammation/injury -Nursing Care/interventions: monitor for heart failure, and dysrhythmia’s, provide rest and activity restriction -Medication: • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. Endocarditis: bacterial infection that leaves inflammation of the endocardium (inner layer of the heart); bacterial or fungal Infection of endocardial tissues that leads to necrosis and embolization of growth -RF: congenital/valvular heart disease, prosthetic valve, IV drug use -Clinical Manifestations: janeway lesions, Fever, murmur, petechiae, splinter hemorrhages (red streaks under nail beds), Osler’s nodes -labs/dx: positive blood culture, echocardiogram -nursing interventions/care: administer IV antibiotics, antipyretics for fever, and anticoagulants, patient should use soft toothbrush, and prophylactic antibiotics before dental/invasive procedures -medication: • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. Rheumatic Carditis/heart disease: infection of endocardium due to complication of rheumatic fever; GABHS triggers, rheumatic fever leading to inflammatory lesions in the heart -RF: children, Follows untreated strep infection -Clinical Manifestations: tachycardia, Fever, rash(trunk/extremities), joint pain, murmur, chest pain, muscle spasms, friction rub -Labs/Dx: throat culture (strep infection), positive ASO titer, echocardiogram -Nursing care/Interventions: administering antibiotics to stop strep infection, and promote rest, monitor for heart failure, and encourage life on prophylactic antibiotics. -Medications: antibiotics, valve replacement/repair • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. Nursing Interventions (Overview for Inflammatory disorders) • Monitor for tamponade & HF • Administer antibiotics (penicillin) • Pain relief (NSAIDs for pericarditis) • Bed rest • Emotional support • Auscultate heart sounds; murmur or friction rub • Collab with cardiologist and physical therapists Procedures (Overview for Inflammatory disorders) • Pericardiocentesis for fluid removal, then sent to laboratory; monitor for recurrence of cardiac tamponade. ( pericarditis.) • Valve surgery if damaged Complications (Overview for Inflammatory disorders) • Cardiac tamponade: medical emergency resulted from fluid accumulation in pericardial sac. S/S: dyspnea, dizziness, tightness in chest, restlessness. Administer IV fluids, notify the provider, obtain chest, x-ray or ECG Cardiac Diagnostics & Vascular Access (Ch. 28) Transesophageal Echocardiography (TEE) Provides clear heart images via probe in the esophagus to detect valve disease, thrombi, or heart failure. NPO 4–6 hr, monitor VS, ECG, and sedation; check gag reflex before eating post-procedure; keep HOB 45°. Stress Testing (Exercise or Pharmacologic) Assesses heart’s response to stress for angina, HF, MI, or dysrhythmia. NPO 2–4 hr, avoid caffeine/tobacco, wear comfortable clothes; stop test for chest pain, SOB, dizziness. Post: monitor ECG & BP until stable. Coronary Angiography (Cardiac Catheterization) Identifies coronary artery blockages using contrast dye via femoral, radial, or brachial artery. NPO 4–6 hr, assess renal function, allergies (iodine/shellfish), and hold metformin 48 hr before/after. Post: monitor VS and site for bleeding, hematoma, or thrombosis, keep limb straight, maintain bedrest. Complications: cardiac tamponade (↓BP, JVD, muffled heart sounds), embolism, hematoma, AKI—notify provider. Teach: report chest pain, bleeding, SOB, avoid lifting >10 lb, and take antiplatelets as prescribed if stent placed. Vascular Access Devices (VADs) Provide reliable central access for fluids, meds, TPN, or blood. Verify tip placement via x-ray before use. PICC: up to 12 mo use, insert in basilic/cephalic vein → SVC; no BP/venipuncture in that arm, keep dressing dry. Tunneled Catheter: long-term use, subcutaneous tunnel prevents infection; no dressing once healed. Implanted Port: long-term chemo access; access with Huber needle, flush with heparin after use. Complications: • Phlebitis: redness, pain, warmth—maintain sterile technique. • Occlusion: flush gently with 10 mL syringe; never force. • Mechanical issues: swelling or pain at port site = dislodgement → notify provider
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7.2: adrenaline
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Hormones
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Adrenaline/Epinephrine
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Adrenaline (Epinephrine)
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Adrenaline
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