Pathophysiology Unit 1 Notes PDF
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These notes cover the basics of the concept of pathophysiology. It details the study of changes in cells and tissues in response to injury or disease. It also provides descriptions of disease, and defines key terms such as etiology and nosocomial.
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Pathophysiology Topic 1.1 Introduction to Pathophysiology Pathology - Study of changes in cells & tissues as a result of injury or disease Physiology - The mechanisms of human body functioning Study of underlying changes in body physiology that result from a disorder or disease Looks at s...
Pathophysiology Topic 1.1 Introduction to Pathophysiology Pathology - Study of changes in cells & tissues as a result of injury or disease Physiology - The mechanisms of human body functioning Study of underlying changes in body physiology that result from a disorder or disease Looks at signs & symptoms Refers to alterations in structure & function Disease - Impairment of cell, tissue, organ, or organ system functioning - Results from altered body functions & poses a challenge to homeostasis - Marked by specific signs & symptoms - Identified through lab / diagnostic tests Pathophysiology: Concepts - Clusters current knowledge about health and disease - Organizes knowledge into meaningful & useful ideas - Functional alteration in health - Impossible to detail every disease condition Health- Illness Continuum - Physical - Emotional - Psychological - Spiritual well-being Pathophysiology: Interdependence Anatomy - How the body is put together - Structure Physiology - How the components work together - Function Pathophysiology - Relies on a thorough understanding of anatomical structure & function Pathogenesis - Pattern of tissue changes associated with the development of disease Components - Risk factors (modifiable / non modifiable) - Precipitating factors (triggers) - Etiology (cause) bs diagnosis - Mechanism, progression & resolution of disease Pathophysiology: Risk Factors What are risk factors? - Vulnerabilities that are present to increase the chances that a disease may occur. Example - Obesity-risk factor associated with coronary artery disease Define the following terms Etiology -- exact cause of disease Idiopathic -- when etiology is unknown (the exact cause of disease is unknown) e.g. failing heart because of weak muscle -- cause of muscle weakness not known Nosocomial -- originates while patient is hospitalized e.g. pneumonia bacteria in hospital Iatrogenic -- disease is a by-product of medical diagnosis or treatment e.g. bladder infection after catheter is inserted E.g. antibiotic that damages the client's hearing Putting it all together Etiology is the precise cause of disease. Sometimes the etiology is identifiable, as with the inhalation of a viral microorganism that causes influenza in the airways. If the etiology is unknown, the disease is said to be idiopathic. For example, if a patient has a failing heart because of a weak heart muscle and the cause of the weakness cannot be identified, the patient can be said to have idiopathic cardiomyopathy. If the disease is a by-product of medical diagnosis or treatment, it is said to be iatrogenic. For example, if a patient develops a bladder infection after a catheter is inserted into the urinary bladder, the patient is said to have iatrogenic cystitis. Finally, if a disease originates while a patient is hospitalized, it is described as nosocomial. For example, a form of pneumonia caused by the Staphylococcus bacterium is commonly hospital acquire. Diagnosis Define Diagnosis - Investigation or analysis of the cause or nature of a condition What is Syndrome - A group of symptoms that occur together (recognisable pattern) What is Prognosis - Expected outcome of a disease Etiology vs Diagnosis - Which is the etiology? Which is the diagnosis? Allergy - A hypersensitive reaction, can be inherited Pneumonia - Inflammation of the lungs, can be bacterial in nature Complications & Sequelae Complication - Disease that develops in a person coping with an existing disorder e.g. Secondary bacterial infection Sequelae - Consequence of previous disease or injury - Unwanted outcome - It can be due to disease or treatment - E.g.) ototoxic drugs causing deafness - CVA resulting in paralysis - Scar after burnt Clinical Manifestations - The presence or absence of disease is often marked by specific signs & symptoms Signs - observable or measurable Symptoms - reported / subjective Local vs Systemic Asymptomatic vs symptomatic Clinical Course Acute - abrupt onset, short duration Chronic - develops slowly, symptoms may last a lifetime Remission - symptoms disappear Exacerbations - increase in symptoms Epidemiology Incidence - Rate of occurrence - Number of new cases of a disease in a population over a specific period of time - E.g. increase in number of new syphilis cases among young Canadians Prevalence - Number of people who have the disease in a population over a specific time period Endemic / Epidemic / Pandemic Endemic - The expected or normal incidence to a population or geographical area Epidemic - Dramatic increase in a condition to a large number of people at the same time in a geographical area Pandemic - High numbers of a disease in various regions / across continents Morbidity -- Mortality Morbidity - Disease rates within a group - Condition of suffering from a disease Co-morbidity - Having more than 1 disease at a time Mortality - Deaths that result from a particular disease in a population - E.g. Death rate due to TB Define homeostasis and explain how it relates to pathophysiology Homeostasis is the process by which living organisms maintain a stable internal environment despite external changes. This involves the regulation of various physiological parameters, such as temperature, pH, fluid balance, and electrolyte levels, to ensure that the body functions optimally. Homeostasis is crucial for survival and is maintained through a complex network of feedback systems and physiological processes. Key Concepts of Homeostasis 1\. Dynamic Equilibrium: Homeostasis does not mean a static state but rather a dynamic equilibrium where physiological variables fluctuate within a narrow, acceptable range. For instance, body temperature might vary slightly throughout the day but remains within a range that supports normal function. 2\. Feedback Mechanisms: \- Negative Feedback: Most homeostatic processes use negative feedback loops. In these systems, a change in a physiological variable triggers a response that counteracts the initial change, returning the system to its set point. For example, if body temperature rises, mechanisms such as sweating and vasodilation help cool the body down. \- Positive Feedback: Less common, positive feedback amplifies a change rather than reversing it. This type of feedback is usually found in processes that need to be driven to completion, such as childbirth, where the release of oxytocin increases contractions during labor. 3\. Regulatory Systems: \- Nervous System: Detects changes in the internal environment and sends signals to appropriate effectors (e.g., muscles or glands) to initiate a response. \- Endocrine System: Uses hormones to regulate long-term processes and maintain homeostasis, such as growth, metabolism, and stress responses. Relation to Pathophysiology Pathophysiology is the study of how normal physiological processes are altered by disease or abnormal conditions. It bridges the gap between the physiological functions of the body and the clinical manifestations of disease. Homeostasis is a central concept in pathophysiology because: 1\. Disease Disruption: Many diseases and conditions result from the disruption of homeostasis. For example: \- Diabetes Mellitus: Involves a disruption in glucose homeostasis due to insulin deficiency or resistance, leading to elevated blood glucose levels. \- Hypertension: Results from impaired regulation of blood pressure homeostasis, often due to dysfunctional mechanisms in the cardiovascular system or kidneys. 2\. Compensatory Mechanisms: When homeostasis is disrupted, the body often tries to compensate. Pathophysiology examines these compensatory mechanisms and their efficacy. For example: \- Heart Failure: The body may retain fluid and increase heart rate to compensate for reduced cardiac output, but these mechanisms can eventually exacerbate the problem. 3\. Disease Progression: Understanding how homeostasis is disrupted helps explain the progression of diseases and their symptoms. For instance: \- Chronic Kidney Disease (CKD): Progressive loss of kidney function disrupts fluid and electrolyte balance, leading to symptoms like edema and hypertension. 4\. Treatment Strategies: Therapeutic interventions often aim to restore or support homeostatic processes. For example: \- Antihypertensive Drugs: Used to help regulate blood pressure and restore homeostasis in patients with hypertension. \- Insulin Therapy: Used to manage blood glucose levels and restore homeostatic balance in individuals with diabetes. Summary Homeostasis is the body\'s ability to maintain a stable internal environment through various feedback mechanisms and regulatory systems. Pathophysiology explores how disruptions to homeostasis contribute to disease processes, how the body attempts to compensate for these disruptions, and how treatments can help restore balance. Understanding homeostasis is essential for diagnosing, managing, and treating various health conditions. Cellular Pathophysiology Topic 1.2 Cellular Adaptations Severe or long-term stressors to cells can lead to: - The cell drawing on it's reserves to keep functioning (adaptation through change) or cell death Atrophy - Decrease/shrinkage in cell size Causes: Physiologic atrophy - Aging (decrease in muscle mass can lead to dehydration) - Early development; genetics Atrophy Causes: Pathologic atrophy: - Disuse - Ischemia - Decrease hormonal stimulation - Malnutrition Hypertrophy - Increase in cell size Causes: Physiologic Hypertrophy - Increase trophic signals - Increase demand Hypertrophy Pathologic Hypertrophy - Cardiac Hypertrophy Hyperplasia - Increased number of cells mass increased cell division = enlarged tissue mass - Hypertrophy & hyperplasia are seen together Causes Compensatory Hyperplasia - Occurs with organ regeneration - Occurs in epidermal & bone marrow cells Hyperplasia -- Causes Hormonal Hyperplasia - Occurs with estrogen dependent organs (uterus / breast) Pathologic Hyperplasia - Abnormal proliferation from excessive hormonal stimulation (endometrium & prostate) Compensatory Hyperplasia - Can occur with damaged tissue e.g. hepatocytes after liver damage Metaplasia - Replacing a mature cell with an immature cell - This is the cells attempt to survive a stressful environment Pathologic metaplasia - Chronic irritation & inflammation e.g. smoking produces changes to the lung cells Dysplasia (atypical hyperplasia) - Changes to cell size / shape / uniformity / arrangement structure Causes Pathologic dysplasia - Persistent severe injury or irritation - E.g. epithelial tissue of cervix (e.g. HPV) Classified as mild, moderate, or severe (low grade / high grade) Cellular Injury & Death Causes of injury - Physical - Mechanical - Thermal - Chemical Mechanisms of death - Apoptosis - Necrosis Cellular Injury & Death - Cell injury occurs if cell cannot maintain homeostasis - Cell injury can be reversible or irreversible - If changes occur to the cell nucleus & membranes are altered = irreversible injury & death What are some causes of cell injury Causes of cell injury & death - Hypoxic injury (most common) - ROS (reactive oxygen species) & free radicals - Chemical injury - Infectious agents - Immunologic & inflammatory injury Hypoxic Injury - Most common cause of cell injury Causes - Decrease oxygen in the air - Loss of hemoglobin - Decrease in RBC production - Respiratory or CV disease - Asphyxial injury - Results in ischemia (decrease blood) -- less oxygen to organs Cell Injury -- Critical Thinking - After heart attack ischemia can develop - Blood flow & oxygen can be re-established - Reperfusion cell injury to myocyte Hypoxia is number 1 cause of cell injury Cell Death Mechanisms of death Apoptosis - Cellular suicide (normal programming of old cells (RBC's) Necrosis - Death of cells related to cell injury e.g. heart attack can lead to cell injury & cell death Ischemia -- reperfusion injury - Tissue damage occurs from re-oxygenation - Restoration of oxygen causes inflammation & oxidative damage Free Radicals & ROS - Free radical (e.g. hydrogen peroxide) - Uncharged molecule with an unpaired electron - Unstable molecule ROS -- Reactive Oxygen Species - Toxic oxygen molecule formed by the reaction between oxygen and water during mitochondrial respiration - E.g. peroxides, superoxide, hydroxyl radical, singlet oxygen Chemical Injury - Interaction between a toxic substance & cells plasma membrane Includes - Drugs (medical & street) - Pollutants - Herbicides / insecticides - ETOH - Poisons -- lead / CO Infectious Injury - Injury from pathogens such as bacteria, viruses, fungi - Virulence of pathogen determines the degree of injury Immunologic & Inflammatory Injury - Components of the immune system & inflammatory system can injure cells Includes - Histamine, Antibodies - Complement system - Phagocytic cell Manifestations of cell injury Infiltrates (cellular accumulations) Accumulation of normal cellular substances such as - Water - Proteins - Lipids - Carbohydrates Or Accumulation of abnormal substances such as - Infectious agents - Inflammatory mediators Water Accumulation - Shifting of ECF into cells - May cause organ to increase in size & become pale This all can cause swelling of cells Progressive Changes in Cells - When faced with a stressor a cell can use adaption - If stressor is too harmful the cell may have irreversible injury Cell Injury & Death Once a cell is affected by injury the following processes occur: - ATP depletion - Free Radicals - Increased Cellular Calcium - Non-selective Membrane Permeability Irreversible Injury Irreversible injury results in either apoptosis or necrosis Apoptosis -- cell suicide - Programmed cell death - Cellular self-destruction Causes: - Damaged genetics / old age - Hormone changes - Severe injury to cell - Viral Infections Irreversible Injury Necrosis - Pathological cell death - Rapid loss of plasma membrane, swelling of organelles & dysfunction of mitochondria - Necrotic cells leak contents = inflammation in surrounding tissue - Breakdown of organelles & autolysis Necrosis -- pathological cell death 5 types of necrosis 1. Coagulative -- kidneys, heart, adrenal glands, caused by severe ischemia, protein denaturing albumin change from gelatinous to firm opaque 2. Liquefactive -- ischemic injury to neurons and gila cells in brain, dead brain tissue, cells digested by other cells, tissue becomes soft, liquefies forming cysts 3. Caseous -- pulmonary infections, tissue resemble clumped cheese 4. Fat -- cellular dissolution caused by powerful enzyme lipase, occur in breast, pancreas, tissue appears opaque & chalk white 5. Gangrenous -- death of tissue from severe hypoxia injury to large areas, classified as dry, wet or gas gangrene Apoptosis vs Necrosis Apoptosis = prolonged cell death - Cells that die produce chemicals that recruit phagocytes to engulf the remains of the dead cell - This reduces inflammation Necrosis - Cells that die swell, burst & spill their contents - This triggers the inflammatory response Pathophysiology Topic 1.3 ECF & ICF Homeostasis - Cells Require Adequate - Oxygen & Nutrient Supply - Waste Removal - For Metabolic & Cellular Activities To Occur, Fluid, & Electrolyte Balance Must Be Maintained - Fluid Volume - Distribution - Acid-base Balance Nomenclature Examples, Sodium, Potassium Sodium - Na - Hypernatremia - Hyponatremia Potassium - K - Hyperkalemia - Hypokalemia Body Fluids - Distributed in functional components - Waster moves freely & regulated by osmotic & hydrostatic pressure - Total body water (TBW) = sum of all fluids Intracellular fluid (ICF) - 2/3 of body's water Extracellular fluid (ECF) - 1/3 of body's water Two main compartments of ECF: 1. Interstitial fluid 2. Intravascular fluid 3. Blood plasma Other ECF - Lymph - Transcellular fluids e.g. saliva, sweat, urine, synovial, etc. Aging & Fluid - Total body water decreases with age - Due to: decrease muscle mass, increase fat, decrease kidney function Aging & Distribution of Body Fluids - Total body water (TBW) - Older Adults: % declines with age - Men have greater percentage of body water compared to women - A leaner person has more water than someone who is obese Total body water (TBW) changes with age Infants 70-80% of body weight is TBW TBW (%) in relation to body weight Body build TBW Male TBW Female TBW Infant Normal 60 50 70 Lean 70 60 80 Obese 50 42 60 Distribution of Fluids Water moves between ECF & ICF by osmosis - Sodium balances ECF - Potassium balances ICF Water moves between plasma & interstitial fluids via - Hydrostatic pressure - Oncotic pressure Regulators of fluid balance Thirst -- Indicates fluid needed Sodium -- Promotes water retention Protein (Albumin) -- Promotes fluid retention ADH -- Secreted with ECF deficit -- promotes water reabsorption Aldosterone -- Promotes sodium reabsorption Renin -- Promotes BP & release of aldosterone Lymphatics -- Moves water & proteins back into intravascular space Lungs -- Excrete 500ml of water through normal respirations Kidneys -- Excrete 1200-1500ml daily Fluid Imbalances Edema Excessive accumulation of fluid within interstitial spaces Pathophysiology - Increase in hydrostatic pressure from venous obstruction, sodium and water retention - Decrease oncotic pressure (colloid osmotic) from loss of albumin (e.g. patients with liver failure) - Increase capillary permeability from inflammation - Lymphatic obstruction from tumors or infection, leads to lymphedema Clinical Manifestations of Edema - Classified as localized, generalized, dependent (pitting) - Increase tissue pressure can decrease capillary blood flow = ischemia - Weight gain, swelling & puffiness Alterations in Water Movement: Edema Treatment - Elevate edematous limbs - Use compression stockings or devices - Avoid prolonged standing - Restrict salt intake - Take diuretic agents Electrolytes Chemical substances that carry an electrical charge (ions) Positive charged ions are Cations - Na^+^ - K^+^ - Ca ^2+^ - Mg ^2+^ Negative charged ions are Anions - Cl ^-^ - HPO~4~^-^ These electrolytes are involved in metabolic activities They are essential to the normal function of cells Alterations in Sodium & Water Balance - Sodium excess & deficits both affect fluid tonicity - Imbalance can lead to states of hypovolemia or hypervolemia as ECF water balance shifts - If kidneys retain sodium, less urine, more blood volume - Sodium imbalances are referred to as hypernatremia or hyponatremia - Chloride will follow the movement of sodium Sodium (**(Na^+^)** **Source** - Chief cation in ECF - Associated with Cl- Function - Regulates extracellular volume - Influences blood volume and pressure - Required for nerve muscle function - Prime hormone regulator is Aldosterone Hypernatremia - Increase serum sodium Na+ \>145 mEq/L Etiology - Increased sodium intake - Water deficit Leads to hypertonic fluid state Causes - Can be caused by a gain in sodium (Na+) or loss of water - Inadequate water intake - Inappropriate administration of hypertonic saline solution - Over secretion of aldosterone Signs & Symptoms Results in dehydration the the cells & hypervolemia - Thirst - Hypertension when caused by diet - Edema - Weight Gain - Bounding Pulse - Confusion - Tachycardia = tachyarrhythmia = increased heart rate Imbalance: Hyponatremia - Low Serum Sodium - Results In Swelling of Cells Etiology - Inadequate intake - Diuretics - Water excess Can lead to a hyptonic fluid state Signs & Symptoms - Edema - Lethargy - Hypotension, Tachycardia - Muscle Weakness - Impaired Nerve Conduction - Mental confusion, altered LOC - Seizures Other Electrolytes - Potassium K+ - Magnesium - Calcium (**Ca^2+^)** - Phosphate Potassium (K+) Source - Major intracellular cation Function - Nerve impulse conduction - Maintains cardiac rhythm - Contraction of skeletal & smooth muscle - Aldosterone - Acid / Base Balance - Kidneys Hyperkalemia - Patients with hyperkalemia may have diarrhea - Potassium affected by diarrhea and vomiting Hypokalemia - Risk factor -- overuse of laxatives - Chronic diarrhea can lead to metabolic acidosis, hypokalemia Calcium (**Ca^2+^)** Source - Extracellular cation found in bones and teeth - 40% is in the free form Function - Regulates Neuromuscular Activity - Necessary for Blood Clotting - Smooth, skeletal & cardiac function Balance is maintained by - Parathyroid Gland - PTH & Calcitonin - Vitamin D Hypocalcemia - Low calcium can lead to increase blood coagulation time - Malabsorption syndrome can lead to hypoglycemia-leading to tingling / muscle spasm / intestinal cramping Phosphate (**(HPo~4~^-^)** - Located primarily in bone - Helps to regulate acid-base balance - Provides energy for muscle contractions - Levels are opposite of calcium Regulated by - PTH - Vitamin D Magnesium **(mg ^2+^)** - Intracellular cation - Majority is stored in muscle and bone - Needed for intracellular enzyme reactions, protein synthesis & neuromuscular excitability - Role in smooth muscle contraction and relaxation - Increase or decrease levels mimic calcium Regulated by small intestine and kidneys - Absorbed by intestine - Eliminated by kidneys Hypomagnesemia Low serum magnesium level Etiology - Malnutrition - Malabsorption syndromes - Alcoholism - Water diuretics (loop and thiazides) Hypermagnesemia Elevated serum magnesium level Etiology - Renal failure - Mg2+ containing antacids Symptoms mimic hypercalcemia - Muscle contractions - Weakness - Loss of deep tendon reflexes - Bradycardia & hypotension - Nausea, Dysrhythmia - Respiratory depression - Drowsiness / lethargy Acid -- Base Balance A category of Electrolytes Terminology Tachycardia -- increase in heart rate -100/min Tachyarrhythmia -- increase in heart rate, irregular Bradycardia -- slow heart rate Arrhythmias -- problem with heart rate of rhythm Dysrhythmias-- abnormality in a physiological rhythm of heart & brain Hypervolemia / hypovolemia -- blood volume Ph Overview Measurement of acidity or alkalinity of the blood Inversely proportional to the \# of hydrogen ions Normal PH 7.35-7.45 A H+ increases Ph decreases = Acidosis (Ph lower than 7.35) As H- decreases Ph increases = Alkalosis (Ph higher than 7.45) By product of cellular metabolism is CO2 Excess CO2 combines -- forms carbonic acid - ~H~^+^ ~+\ CO2\ =\ H2CO3~ - ~PaO2\ levels\ --\ 80\ --\ 100\ mmHg\ (no\ real\ role)~ - ~PaCO2\ levels\ --\ 35\ --\ 45\ mmHg~ - ~\45\ =\ hypoventilation~ ~Acid\ Base~ ~Acid~ - ~Substances\ that\ release\ H~^+^ ~ions\ into\ solution~ - ~An\ acid\ is\ a\ H~^+^ ~"giver"~ ~Base~ - ~Substances\ that\ combine\ with\ a\ H~^+^ ~ion~ - ~A\ base\ is\ a\ H~^+^ ~"taker"~ - ~Common\ base\ in\ body\ HCO3~ ^-^ ~Ph\ Changes~ ~Blood\ pH\ is\ balanced\ by\ maintaining\ a\ 1:20\ ratio\ of\ carbonic\ acid\ to\ bicarbonate\ base\ (major\ plasma\ buffering\ system)~ ~Buffering\ mechanisms\ compensate\ for\ changes\ in\ pH~ ~Protein\ Buffering~ ~Plasma\ proteins\ respond\ in\ seconds\ to\ an\ acid-base\ imbalance~ ~Proteins\ function\ either\ as\ an\ acid\ or\ base\ (accept\ or\ donate\ H~^+^~)~ ~This\ is\ achieved\ by\ combining\ with\ Hb\ to\ form\ HHb\ (Deoxyhemoglobin)\ or\ HHbCO2\ (Carbaminohemoglobin)~ ~Respiratory\ Buffer\ System~ ~Respiratory\ system\ is\ responsible\ for\ ↑\ or\ ↓\ respiratory\ rate\ to\ regulate\ CO2~ ~System\ occurs\ within\ minutes\ to\ hours~ - ~In\ acidemia\ ↑\ H~^+^ ~results\ in\ an\ ↑\ rate\ of\ ventilation\ =\ ↓\ CO2\ levels~ - ~In\ alkalemia\ ↓\ H~^+^ ~results\ in\ ↓\ rate\ of\ ventilation\ =\ ↑\ CO2\ levels~ - ~Blood\ pH\ changes\ according\ to\ the\ level\ of\ carbonic\ acid~ - ~pH\ ↓\ Resps\ ↑\ ↑\ Excretion\ Of\ CO2~ - ~pH\ ↑\ Resps\ ↓\ Retention\ Of\ CO2~ ~Renal\ Buffer\ System~ ~Kidneys\ are\ responsible\ for\ excreting\ hydrogen\ (H~^+^~)\ or\ retaining\ (HCO3~^-^~)to\ produce\ either\ more\ acidic\ or\ alkaline\ urine~ ~Responses\ last\ &\ is\ more\ efficient~ - ~Uses\ the\ tubular\ buffer\ system~ - ~Combining\ H+\ with\ ammonia\ (NH3)\ to\ form\ ammonium\ (NH4+)~ - ~Ammonium\ is\ then\ eliminated\ by\ the\ kidneys~ - ~System\ occurs\ within\ hours\ to\ days~ ~Potassium\ /\ hydrogen\ exchange\ buffer~ ~In\ order\ to\ maintain\ acid-base\ balance\ K~^+^ ~&\ H~^+^ ~can\ move\ across\ the\ cell\ membrane~ ~In\ **acidosis\ K**~**^+^** ~will\ move\ out\ of\ the\ cell\ to\ allow\ H~^+^ ~to\ enter\ this\ ↓\ the\ amount\ of\ H~^+^ ~allowing\ for\ an\ adjustment\ of\ pH~ ~Acidosis\ vs\ Alkalosis~ **~Acidosis~** - ~Due\ To\ Amount\ Of\ Acid\ (H~^+^~)\ Or~ - ~Amount\ Of\ Base~ - ~End\ Result:~ - ~Ph\ (\7.45)~ - ~Can\ Be\ **Respiratory**\ Or~ **~Metabolic~** ~Respiratory\ or\ Metabolic~ - ~Any\ respiratory\ disorder\ can\ cause\ respiratory\ acidosis\ or\ alkalosis~ - ~Primary\ Compensator:\ Kidneys~ - ~Any\ other\ type\ of\ disorder\ [other\ than\ respiratory]\ can\ cause\ metabolic\ acidosis\ or\ alkalosis~ - ~Primary\ Compensator:\ Respiratory\ System~ ~Metabolic\ Alkalosis~ - ~↑\ Bicarbonate\ levels\ or\ ↓\ metabolic\ acid~ **~Causes:~** - ~Vomiting~ - ~Gastric\ suctioning~ - ~Bicarb\ intake~ - ~Diuretics~ **~Clinical\ manifestations~** - ~Usually\ reflective\ of\ electrolyte\ imbalances~ **~Include:~** - ~Muscle\ weakness,\ cramping~ - ~Parasthesias,\ tetany~ - ~Resps\ shallow\ &\ slow~ - ~Dysrhythmias~ ~↑\ non-carbonic\ acid\ levels\ or\ ↓\ bases\ from\ ECF~ - **~Causes:~** - ~Renal\ failure~ - ~↑\ Lactic\ acid\ formation~ - ~↑\ Ketones\ from\ lack\ of\ insulin~ ~Compensate\ by\ decreasing\ respiratory\ rate~ - ~Clinical\ manifestations\ are\ reflective\ of\ electrolyte\ imbalances~ **~Include:~** - ~Rapid\ respirations\ (hyperventilation)~ - ~Anorexia,\ nausea,\ vomiting,\ diarrhea~ - ~Dysrhythmias~ ~Respiratory\ Acidosis~ ~Due\ to\ alveolar\ hypoventilation\ production\ of\ CO2~ **~Etiology;~** - ~Depression\ of\ resp\ centre~ - ~Paralysis\ of\ resp\ muscles~ - ~Disorders\ of\ lung\ parenchyma~ - ~Clinical\ manifestations\ are\ related\ to\ the\ severity\ of\ the\ PaCO2\ levels~ **~Include:~** - ~Changes\ to\ resp\ patterns~ - ~Headache,\ restlessness~ - ~Lethargy~ - ~Muscle\ twitching~ - ~Tremors,\ Convulsions~ ~Respiratory\ Alkalosis~ - ~Due\ to\ alveolar\ hyperventilation\ ↓\ plasma\ concentration\ of\ CO2~ - **~Etiology:~** - ~High\ altitudes~ - ~Pulmonary\ disease,\ Heart\ failure~ - ~Fever,\ Anemia~ - ~Anxiety\ or\ panic\ disorders~ ~Compensation\ --\ Decreased\ bicarbonate\ reabsorption~ ~Clinical\ manifestations\ are\ related\ to\ the\ effect\ on\ the\ CNS\ &\ PNS~ **~Include:~** - ~Changes\ to\ resp\ pattern~ - ~Dizziness~ - ~Confusion~ - ~Parasthesias~