Week 1 - Introduction to Pathophysiology PDF
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Rohan Shammi
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This document provides an introduction to pathophysiology, focusing on medical and traumatic emergencies. It covers the body's response to disease and injury and touches on various biological concepts.
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Medical & Traumatic Emergencies Week 1 – Introduction to Pathophysiology PARA 1503 Rohan Shammi Pathology + Physiology = ? Pathophysiology is the study of the body’s response to disease & injury Pathology is...
Medical & Traumatic Emergencies Week 1 – Introduction to Pathophysiology PARA 1503 Rohan Shammi Pathology + Physiology = ? Pathophysiology is the study of the body’s response to disease & injury Pathology is the laboratory study of cell & tissue changes associated with disease Physiology is the branch of biology that deals with the normal functions of living organisms Highly relevant to any healthcare practitioner, but especially for those in pre-hospital medicine Physiological changes can be incredibly obvious or extremely subtle Remember that in the pre-hospital environment you will not have access to diagnostic imaging, lab work, etc. Disease or injury may be defined as any deviation from the ‘normal’ state of health or wellness As paramedics we may not always have the luxury to treat all aspects of health, but a holistic approach considers an individual’s physical, mental, & social well-being Basics of Human Biology Human body is a collection of organ systems with the cell as its fundamental unit Organs are made up of various tissues / Tissues are made up cells 4 Types of Tissue: Connective – Supports other tissues & binds them together (bone, blood, lymph) Epithelial – Provides a covering or lining (skin, internal linings of the respiratory/GI tracts) Muscle – Including skeletal, smooth, & cardiac muscle tissues Nervous – Allows for transmission of signals from and to the various parts of the body Cellular Respiration – Cells are constantly undergoing this energy releasing process Transforms glucose (simple carbohydrate) & oxygen (O2) into energy in the form of ATP Carbon dioxide (CO2), water (H2O), & heat are byproducts of this reaction ATP is used to power processes from electrolyte transport, muscle contraction, nerve impulse transmission, chemical synthesis, etc. Basics of Homeostasis Homeostasis refers to a relatively constant or stable internal environment Disease develops when significant changes lead to a state in which homeostasis cannot be maintained As paramedics our goal is to: Identify these changes & their likely causes Respond to them with rapid treatment(s) if applicable Rapid transport them to the most appropriate receiving facility (as/when appropriate) There are an incredible network of complex systems that regulate: Energy production & use (ie: aerobic & anaerobic cellular respiration) Fluid & electrolyte balance (ie: diffusion & kidney function) Blood pressure, body temperature, etc. These systems are constantly responding to minor changes & ensuring that ‘compensatory mechanisms’ maintain a state of homeostasis We are rarely consciously aware of these mechanisms As you develop your understanding of anatomy & physiology, patterns emerge that allow you to identify when specific organs & body systems are injured Importance of Fluid & Electrolytes Regulation of fluid/electrolytes is critical for cells Water helps maintain normal body temperature, lubricate & cushion joints, protect the brain/spinal cord, acts as the ultimate biological solvent Electrolytes are essential for maintaining electrical gradients responsible for nerve transmission & muscle contraction Fluid accounts for 60% of total body weight of an adult Intracellular Fluid (ICF) VS Extracellular Fluid (ECF) ICF contains 66% of body’s water, ECF contains remaining 33% Within the ECF there are 2 compartments: Intravascular Fluid (IVF) & Interstitial Fluid (ISF) IVF has 25% of ECF compartment’s water (as plasma within the blood vessel) ISF has 75% of ECF compartment’s water Movement of Fluid & Electrolytes Cell wall is semi-permeable Some things pass freely (ie: water), others cannot (ie: hormones, etc.) Diffusion & Osmosis Passive (requires no energy) Follows natural concentration gradient Osmosis is the diffusion of water specifically Facilitated Diffusion Passive (no energy), but requires transmembrane proteins Think of them as channels or roads that have no entry fee or toll Glucose entry into the cell is an example Active Transport Requires energy (may go against natural gradient) A ‘toll’ in the form of ATP must be paid Na/K pump is the most famous example Tonicity Tonicity – Refers to the capability of a solution to modify the volume of cells placed within them Cells volume changes based on the net movement of water into or out of the cell Isotonic – When a cell is placed in an isotonic solution there will be NO net movement of water out of the cell The cell’s volume remains the same Hypertonic – When a cell is placed in a hypertonic solution there will be a net movement of water OUT of the cell The cell shrivels as water leaves Hypotonic – When a cell is placed in a hypotonic solution there will be a net movement of water INTO the cell The cell swells as water enters As Ontario paramedics we will ONLY ever provide isotonic crystalloid fluids like Normal Saline (0.9% NaCl) Isotonic crystalloid fluids move equally into the ICF & ECF Colloidal fluids are hypertonic and draw water from the ICF to the ECF Fluid Pressure Regulation RoleAnti-Diuretic of the Kidneys Hormone (ADH) Receptor notes water volume low (increased tonicity) Hypothalamus (creates perception of thirst) and stimulates pituitary ADH is released and kidneys retain water Vasopressin Large amount of ADH released all at once Potent vasoconstrictor (increases BP) Renin Angiotensin Aldosterone System Juxtaglomerular apparatus senses decreases in flow (or↓Na) Kidney releases Renin Renin meets Angiotensinogen (made by liver, present in blood at all times) Renin converts angiotensinogen into angiotensin I Angiotensin Converting Enzyme (ACE, present in lungs) changes angiotensin I to angiotensin II Angiotensin II is a potent vasoconstrictor AND stimulates release of ADH and stimulates release of Aldosterone Aldosterone ↑Na reabsorption in distal tubule of kidney and water follows Na (concentration gradient) leading to reabsorption of water Atrial Natriuretic Hormone Simple peptide released by the atria (upper chamber of heart) Counteracts ADH/RAAS. If blood volume/BP is too high (sensed by the stretching of the chamber itself), ANH is relased to ↓Na reabsorption (water will follow) and inhibit the secretion of aldosterone Dehydration in Detail Dehydration is a reduction in the total volume of water in the body ECF compartment (which includes the blood & interstitial fluid) typically loses fluid first It’s most exposed to environmental changes & is responsible for maintaining blood pressure/volume required for organ perfusion As water is lost from the ECF a concentration gradient is created, because the ECF is hypertonic relative to the ICF This results in a fluid shift from the ICF to the ECF causing cellular dehydration 4 systems responsible for homeostasis in dehydration: Thirst mechanism – Perception of thirst encourages replacement of lost fluid volume Important that patient rehydrates with water containing appropriate electrolyte levels (ie: NOT hyponatremic fluids such as distilled water) ADH release – Encourages reabsorption of water within the kidneys RAAS activation – Encourages vasoconstriction & fluid/sodium reabsorption Sympathetic Nervous System (SNS) activation Assessment of Dehydration Important that the paramedic has a strong understanding of the causes & clinical manifestations of dehydration Causes of Dehydration Often the cause is obvious as in heat stroke, physical exhaustion, or severe nausea/vomiting /diarrhea (n/v/d), etc. If dehydration is known/suspected without obvious etiology, explore for gastrointestinal losses and changes in urination (ie: reduced output) Physical Assessment of Dehydration Explore for changes in level of awareness (LOA), including use of tools like the Glasgow coma scale (GCS) Even a mild change in LOA such as confusion or dizziness may indicate moderate dehydration Skin should be assessed for turgor, look for dry lips/mucous membranes, and in neonates/ infants assess for sunken fontanelles, etc. HR, both pulse and ECG should be assessed with tachycardia or elevated HR often being an early sign of mild to moderate dehydration As dehydration worsens heart rhythm will trend towards irregularity RR should be assessed for tachypnea or increased RR (as a consequence of acidosis) and in severe stages for a trend towards irregular respiratory rhythms Clinical Manifestations of Poor Fluid Regulation Fluid Overload causes Edema Ascites (edema noted at the stomach/belly) Peripheral (edema of the feet/ankles or hands) Lungs (pulmonary edema causes respiratory distress and crackles on auscultation) Lack of Fluid causes Dehydration Decreased skin turgor Increased thirst/dry mouth Lethargic/Altered LOA Increased HR/RR/BP Other Consequences of Dehydration Dehydration often leads to electrolyte imbalances, especially involving Na & K If Na levels in the ECF rise (hypernatremia) or K levels drop (hypokalemia) the Na/K pump is compromised, which is vital for maintaining the membrane potential that allows electrical signals in the nervous and muscular systems to function (including the heart and brain) Hypo/Hypernatremia – Na / Sodium Hypo presents with n/v, fatigue, gen weakness, while Hyper presents with profound thirst, muscle twitching, S/C/D Hypo/Hyperkalemia – K / Potassium Important to paramedics as hyperkalemia is treatable pre-hospital Hypo presents with muscle twitches, cramps, gen weakness while Hyper presents with characteristic ECG changes (peaked/tall T waves, widening QRS) Hypo/Hypercalcemia – Ca / Calcium Hypo presents with muscle spasms, tetany, S/C/D while Hyper presents with thirst, frequent urination, gen weakness/fatigue Impaired Glycolysis, Disruption of Mitochondrial Function, & Hypoperfusion ICF water losses alters the chemical composition of the cytoplasm leading to inefficiencies in the first step of cellular respiration ECF water losses lead to decreased perfusion to the vital organs & ultimately a shock state Mitochondria (where the majority of ATP is generated) requires a stable environment, changes in electrolyte and water levels lead to reduced ATP production and potential cell death pH imbalances – Acidosis Inadequate oxygen delivery caused by hypoperfusion from decreased blood volume leads to an increase in anaerobic cellular respiration, far less efficient at generating ATP and resulting in production of lactic acid which contributes to decreasing pH/increasing acidosis Environmental Emergencies Refers to an event or condition related to exposure to temperature extremes, which can include emergencies involving heat and cold Heat exhaustion presents with temperature 40C Active cooling with wet sheets or in cases of heat stroke placement of cold packs to the head/neck, axilla, & groin should be initiated Pre-Hospital Treatment of Dehydration Airway Management Risk of seizure is high in cases of severe dehydration, keeping the airway patent/ protected and preparing for seizure activity before it occurs is critical Ensure patient in adequate position for good air entry, consider tools like OPA/NPA Ensuring Adequate Oxygenation Ensure oxygen provided in accordance with BLS standards, provide high flow O2 early if required & consider tools like BVM ventilations IV (or oral) Fluid Replacement Paramedics should attempt to cannulate large bore peripheral IV and provide isotonic, crystalloid fluid replacement via an infusion of normal saline according to ALS standards Oral fluid requires a completely unaltered pt as risk of aspiration is high Rapid Transport & Addressing Environmental Concerns Patient in an inhospitable environment (such as in hot environment/direct sunlight) should be extricated to cool environment (ie: ambulance) as early as possible Remove excess clothing, especially if tight/restrictive & initiate active cooling if req. Rapid transport is always a critical, life-saving treatment in the pre-hospital environment