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NRSG 2300
Stephan Wood

Madeleine Bernstein Pathophysiology Exam 1 Acids & Bases • Acid o characteristics & properties  Contain Hydrogen  In aqueous environment: lose an electron  become proton donors  Release H+ ions = proton donor (+)  Conc. Of protons and ability to dissociate determines strength of acid  Strong acids completely dissociate in water; weak acids DO NOT  Stength depends on how many ions it gives away  H+ & H 3 don’t really exist in solutions b/c H is bonding o Biological Functions of Acids  Hydrochloric acid present in stomach aids in digestion by breaking down large and complex food molecules • Breaks down proteins/ food  Amino acids/ fatty acids are required for synthesis of proteins required for growth and repair of our body tissues.  Nucleic acids are important for the manufacture of DNA and RNA  Carbonic acid is important for maintenance of pH equilibrium in the body o Pathophysiology of Acids  Anaerobic metabolism of glucose  Glucose is a 6-carbon sugar broken down to ATP in a multi-step process  Glycolysis, Krebs Cycle, Electron Transfer  Most of these processes are AEROBIC, meaning they require oxygen  In ANAEROBIC situations, there can be a buildup of organic acids  This shifts the body pH towards ACIDOSIS • Bases o Proton acceptors  take up H+ ions o NaOH è Na + OH è OH + H è H O + 2 o Important biological bases: NH3, HCO3 • pH: Logarithmic scale representing conc. of H+ o role in biological systems  living system sensitive to change  ionic “trapping: of macromolecules  protein folding o metabolic acidosis  Acid production out paces buffering system  Accumulate organic acids  pH decreases + + - -  Anion gap = ( [Na ]+ [K ]) - ( [Cl ]+[HCO3] )  Causes  Treatment o Metabolic alkalosis: Increase loss of organic acids  Excessive Vomiting: loss of Cl ions, Kidneys retain HCO 3  Causes: vommitting/ diarhea  Signs and Symptoms  Treatment: o Respiratory acidosis  Alveolar hypoventilation  Hypercapnia: build up of CO2 (EX asthma)  Causes: inability to get oxygen in or CO2 out  Signs/ Symptoms: tickhypnia, short of breath, bluish nailbeds/ mouth  Treatment: reverse the cause, replace lost oxygen, inhibation o Respiratory Alkalosis  Hypocapnia: a state in which the level of carbon dioxide in the blood is lower than normal; can result from deep or rapid breathing  Causes: hyperventilation, severe metabolic stress (fever, pulmonary embolism)  Signs/symptoms: tickhypnic  Treatment: “paper bag” can reinhale CO2 but may miss bigger problem o Blood Gas  pH: below 7.34 bad  PaCO2 & HCO3: respiratory (35-45) & metabolic (22-26) • buffers: allow homeostatis of acid/ base balance o able to absorb and thereby resist large changes in pH o system of regulation: carbonic acid – bicarbonate in blood/ kidney  oxygen in; Co2 out  converted by carbonic anhydrase to carbonic acid  Shocklease principle: system that experiences a change in conc. And pressure will counteract that change to maintain equilibrium o Respiratory: more CO2 you have, more carbonic acid you’ll make  Will become acidonic  respiratory rate will increase (AH!) o Proteins: some amino acids can be buffers at physiological pH o Histidine has closed pKa to plasma pH and is most important buffer o Hemoglobin contains many histidine residues and is important buffering system in blood Fluids and Liquids Water • compartments of water o intracellular o extracellular  Interstitial: in between the cells  Intravascular:  Synovial: w/in joint space  Lymph  CSF: made in ventricles of brain  Urine  Intraoccular: occulus humor  Intestinal: in lumen  pericardial/pleural: lining of heart/ lungs • hydostatic pressure: pressure exerted due to weight of fluid • oncotic pressure: opposing force of hydrostatic pressure, pressure exerted by solutes of that liquid o albumin protein (solute) draws fluid into vascular space  w/o fluid can leak out • Starling’s forces: movement of fluid secondary to filtration • Filtration: movement of things across a selective membrane o not all capillaries equal b/c some soluble to proteins moving back and forth • gradients: determines water movement, different gradients determines smoothness in movement o capillary hydrostatic pressures: o capillary oncotic pressure o intersitial hydrostatic o interstitial oncotic • aquaporins: come in and out (up/down regulation), proteins embedded in the cell membrane that regulate the flow of water • sodium: water follows sodium, dehydration, major extracellular ion • potassium: mostly inside cell and helps to maintain resting membrane potential • proteins: EX albumin, filtration changes with pop of proteins • regulated by ADH: anti-direuretic hormone holds on to water  alc inhibitor of ADH o released w/ dec intrvascular pressure or inc intravascular osmolality o acts on distole tubles in kidney • osmoreceptors: detects osmolality of blood (amount of solute w/in solution) • baroreceptors: detects pressure (EX low pressure against aortic wall  secrete ADH • regulation of MOA: • edema: o Movement of fluid into the interstitial space o Decreased plasma oncotic pressure o Increased capillary hydrostatic pressure: forces fluid out o Increased capillary permeability: membranes exposed to cytokines/ prostoglandins which increases permeability  EX sepsis (severe infection), burns/ trauma o Lymphatic channel obstruction: EX lympodema  lymphs recylce water, obstruction allows leakage in interstitial space o EX Hypoxia (lower levels of oxygen at 8200 ft) cause constriction of arteries (pulmonary artery), inc pressure leads to cerebral edema, confusion Sodium • Sodium: Alkali metal, sixth most abundant metal in earth’s crust • Accounts for 90% of ECF cations • Regulates osmotic forces and water balance • Serum Na: 135 – 145 mEq/L & Pa 3.5-4.5 • Hormonal control - Aldosterone • Hypernatremia/ Hyponatremia: high/ low sodium levels  EX diabetes (hyper) o Symptoms: lethargy, fatigue, muscle weakness, sometimes edema Potassium • Hypokalemia o Decrease intake: easier for cells to excite  can lead to cardiac arrythmias o Excessive loss: big peaking waves o Signs and Symptoms: weakness, lethargy, irritability o EKG: lower = harder to excite o Treatment: loss = albuterol, Ca chloride Calcium • Maintained 8.5-10.5 g/dL • Calcitonin regulates calcium • Hypocalcemia o EX parathyroid glands out, chronic renal disease o Ca is gate keeper for other ions in/ out of cell + involved in actin/myosin contraction process  tetany happens w/ lack of Ca • Hypercalcemia o STONES (renal stones), BONES (Ca stored in bones), GROWNS (helps grow), THRONES (toilet), & PYSCHIATRIC OVERTONES o EX crushes • Aside Vit D Innate Immunity • HIV o Mutates all the time: hard to target with vaccine • Lyme Disease o Tick born illness: American Deer tick o Causes different infections, fever, muscle aches, joint aches o Treatment: antibiotics • Rhinovirus: common cold • Resistance o Antibiotics prescribed when not needed • Innate immune system: not specific, general defense system o Physical barriers  Skin: tightly junctioned epithelial cells  Gi tract: stomach = inhospitable environment  Nose: cilia/ hairs  Eyes: tears w/ immunoglobulin o Identification of antigents o Activation of complement: specialized network of proteins that help to identify antigens and stimulate immune response o Recruitment of inflammatory mediators: cytokines, interleukins, etc.  Help to activate adaptive immune system o Activation of the adaptive immune response o Biochemical barriers  Normal flora: bacteria in body  Gi tract: antibiotics eliminate  Lacto bacillus: part of vaginal normal flora, creates lower ph  less inviting for pathogenic bacteria (causing uti’s etc) • Antimicrobial peptides o Cathelicidins & defensins: utilizes by macrophages and neutrophils  Low levels may cause disease o Polypeptides: neutralize charge on bacterial cell membrane o Macrophages/ neutrophils: white blood cells  carry positively charged polypeptides and attracted to negatively charge bacteria on cell walls o membrane disruption: allow for macrophages and neutrophils (natural antibiotics) to approach
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