NUR 315 Pathophysiology (RATED A+) Study Guide. Download To Score An A

Pathophysiology What is the patho (what is the disease) how does it happen and how does it show up in the pt? (Not need know how to treat a disease process). Know power points (under units) mainly and book is just if something is not clear. Use Emedicine (they are same authors as WebMD). Can’t memorize, must understand the concept bc way say in class might not be as ask on test. Assignments- not graded, optional. ABG and EKG practice really evaluate how to interpret blood gasses and EKGs. Def do these worksheets bc if not do well on them here, won’t do well on test. Syllabus- Room 407. Class is 8am-11am. 3 exams and then final exam during finals week- accumulative. Will get study guide for final exam except some new content and is 25%. Other 4.5% is weekly online quizzes- do whole week. She drops one lowest quiz grade. Posted usually by Monday Afternoon or Tuesday morning latest have until Sunday night 10pm to take quiz- 1 hour to do ten items, open book. Under Quiz section in BB. Hour before exam if sick need health care provider clearance to reschedule exam as for other classes. If miss exam on Monday other instructors told and need clearance to go to class. Student health clinic here on campus. Exam be rescheduled and can be in dif format. No makeup for online quizzes. Next week Joseph on Monday and Tuesday will teach 304 at this time slot. The following week caspi teaches in her spot Monday and Tuesday. Do have lecture content after exams. Exam is 1.5 min per item, so 60-75 questions usually so about 2.5 hours to do the test. Bet 9:30 and 10am is twenty min break. Pass around sheet to sign in after break. Good email response time- contact thru email. She will stress what’s important for testing. Review A&P and do reading for quizzes which delves into the patho. Chapter 2 Body tissues-embryonic origin and differentiate into many cells mainly ectoderm (..) and epithilu (over and into organs) A&P of cell. Cell metabolism- know when not receive enough perfusion oxygen etc what happens. Not tested on cell metabolism but know it for other things. Energy, metabolism- carbs and protein into energy for cell function. Get glucose and metabolize it to use as energy. If no oxygen- anaerobic metabolize the glucose, turn into pyruvate and then lactic acid which builds up and is detrimental. Without oxygen get lactic acidosis. With aerobic can use energy more efficiently but in terms of inflammatory and shock, if not get adequate oxygen flow lots of problems occur. Membrane transport mechanism- diffusion of molecules thru cell walls into cell tissues using transport protein- active transport as a carrier. Interchange ions and fluids thru membranes. KNOW: adaptive cellular response to stress Atrophy- shrinkage of the cell size (pt immobilized, not walking around fully ambulating within a week the muscles shrink in size) this is a way to adapt to lack of simulation and use Hypertrophy- increase in cell size, want it for when working out to stretch muscle and become bigger. Also when heart enlarges- most of time it does not do so on its own. It enlarges bc there is a dysfunction and heart trying to compensate Hyperplasia- increase in number of cells, breast enlarge when pregnant to breast feed. When woman has baby and stops feeding they go back to normal. Metaplasia- replace one mature cell by another. Happens when pt exposed to noxious irritant like a smoking pt the lungs scar and cells change and don’t have same efficient function as normal cell. This is compensatory to stress, irritants and toxins. Dysplasia- abnormal changes in size shape and organization of mature cell. See by virus or irritation like cancer. neoplasm- overt change. Just affect of stress. Neoplasms- altered cell differentiation and growth- not act like a normal cell. Sometimes doesn’t die, sometimes spreads, sometimes grows abnormally. Benign- tissue dies, abnormal cell but doesn’t invade other cells. Malignant- does invade other cells, metastasis, appearance and functions differently. Why cells die/injure? Phys agents- mechanical forces, electrical burns. Radiation Chemical- lead Biological- viruses Nutritional- malabsorption, etc. Free radical injury- general idea of it. Area of tissue not getting enough perfusion hypoperfusion- reactive species break away and free radicals form. Body has way to rid of byproducts of oxidation or stress- antioxidants like vitamin c and vitamin e that scavenge the free radicals and help rid of them bc if too overwhelming cause havoc. Local area of infection not getting enough oxygenated bloodflow and get free radicals its okay to be there but if blood pressure goes up and increase flow and free radicals get on systemically thru circulation they cause vessels to dilate and bp drop and crash to hypotensive. Not worry about formation of free radicals but when recirculate that blood. Any pt that had injurious dead tissue removal stroke, or heart attack means lack of good flow to certain organs but when flow to them get subsequent dropout- the free radicals went systemic and caused circulatory collapse. Reperfusion injury. Free oxygen species jump on and systemically cause reperfusion injury (steal electrons from other molecules and that causes physiological derangement in blood vessels to dilate and cause hypotensive episode and drop blood pressure.) KNOW: hypoxia and ischemia Hypoxia- low oxygen to cells, resulting in ischemia Ischemia- when hypoxia is prolonged not have enough nutrients, oxygen delivery and waste removal. If not have enough oxygen to cell not have enough glucose nutrients and energy to remove waste products. Hypoxia causes ischemia and ischemia is how lack of oxygen shows up in the body. Hypoxia for three minutes get resuscitated and fine but if not good resuscitation and down 10 min then hypoxic brain injury and death of brain cells. (global ischemia can turn into multi-organ failure. Kidneys half hour no good flow get injured. Brain within 5 minutes. Heart 20 min. gut longer like 4 hours. (if hypoperfusing then get free radicals and hypoperfusing get lactic acid building up). Ischemia can be reversible depending on the amount of time in that state. Consequences- anaerobic metabolism, lactic acid. Heart not like lactic acid bc changes in cells in myofibrils and heart not work. Bad byproducts of anaori meta and lactic acidosis. KNOW: apoptosis- Programmed cell death. Helps body filter out not so good cells. If clean them out cant become neoplastic and turn into cancers. Apoptosis eliminates old or injured cells that can cause havoc to a person. In cancer apoptosis is impaired and cells programmed not to die but to mutate and change. Apoptis occurs normally in cell tissues and during embryonic processes so no webbed feet. Endometrial cells during menses also to clean out uterus of cells that can be problematic. Breast tissue regression after breast feeding. In als lou gehrigs/alz and parkinsons implicated in these disorders. Necrosis- cell death in organ tissue that is still alove. Gangrene. When tissues die and become necrotic the tissue will self digest. They trigger an inflamm response. Types- liquefication etc not need know specifically. but if have wound with pus (debris of WBCs accumulating at area of infection) can be liquefied. Infarction not enough blood lfow to tissue and area around ischemic area dies off. Blockage in coronary artery n heart no flow there if not reverse quicly goes from ischemic to necrotic. Might be able to reperfuse or dies (necrotic, infracted) cant get back. Stroke- artery in brain blocked off area of ischemia try to resupply flow to but if not permanently dead tissue, infracted. Not from infection but lack of flow to that tissue bed. Gangrene- mass of tissue undergoing necrosis. Smoking pts constrict the vessels and flow not go thru so they lose their limbs. Young men in 30s have multiple amputations. Diabetes damage vessles and lack of flow. Dry gangrene- dead tissue sometimes chop off or falls off, black. Wet gangrene- due to infection it dies. Gas gangrene- anaerobic bacteria- bubbles and malodor coming from the site. (necrosis caused by many causes- dead tissue from infection, hemorrhage or inflame response. Infarction only because of lack of flow). Genetic disorders- Chromosomes footprint of individuals, info in chromosomes is genotype and phenotype way it is associated. Single gene inheritance- traits determinded by single gener. Multifactorail- controlled by a few generes or different places on same gene Autosomal dominant- male or female addected equally. If one parent affected 50 and if both 75% chance. Dominat so only takes one to be expressed in the offspring. Autosomal recessive- both parents need to have for kid to expres it. KNOW: auto rec if both parents unaff but are carries each offspring has 25% if being affected. Sex linked inheriatenc- if female and x link inheritance the double x protects her so not expressed, if male gets it bc xy then he expresses the disease. X link dominant- only one parent need be affted. May be lethal in males x linked dominant. X linked recesiive – KNOW HEMOPHELIA as example. Daughters of affected mael be carriers but sons be affected. Unaffected males of female carrier not give over. How many chromosome 22 pairs of 44 and then sex chromosomes 46 KNOW Female givers x male gives x or y. Dom rec traits- brown over green kids mostly get brown eyes. Genetic disorders- (patho how it shows up really know) Autosomal dominant MARFAN SYNDROME, KNOW males with long torso and anguinal hernia outpouching of intestine disease affecting connective tissue. Inherited disease fo connective tissue causing dysfunction on gene that codes for that connective tissue (connec tissue in joints but also muscles to ligaments in eyes, joints and heart valves.) Cardiovascular anomalies. Connec tissue in aorta blood vessels that can constrict and dilate. Marfan syndrome can affect many organs and affect males or females easily. Some have mild form and some severe. Can affect many organs. Depends how express itself in the dna. Diagnosis based on physical and family history. Many years they thought Lincoln has marfan syndrome. Offspring has 50% getting it. Know how it shows up. Retinal detachment- myopia. Joint hypermobility (loose joints, basketball player). Spinal deformities. Heart valve prolapsed sinking in of the valve. Aortic valve disease when aorta lining gets a tear (dissecting) separating from its lining. Aorta vessels has three layers, if dissects and opens too much then ruptures. KNOW SIGNS AND SYMPTOMS. Autosomal recessive- cystic fibrosis most common disorder. KNOW. Both parents must be carriers for offspring to get disease. If parents are carriers than 50% child is a carrier… defect in chloride transport chain. Sweating- method of transporting chloride and sodium and water follows sodium (sodium couples with chloride). In blood stream the sweat gland, sweats have chloride trapped bet skin supposed to be excreted with sodium. When sweat get rid of NaCL and cool off by losing water. But with cys fib defect in chloride transport and so increasing absorption of sodium and water into the tissues and not getting rid of it. Affects lungs, pancreas and found in the sweat. In sweat gland is increase in chloride bc cant reabsorb it into the bloodstream. The transport mechanism not allow it to be reabsorbed into blood and when reabsorb nacl hold onto water. With infections to get out need to cough out stuff and if cant (not loose) and stays in lungs turns into lower resp infection so bc of chloride transport mechanism cant reabsorb normally nacl but instead foes out of the body so water not be reabsorbed and so cant thin your secretions- spec at lungs and pancreas (not happen systemically, drinking water not help) the pancreatic juices and enzymes cant transport easily to duodenum and cant reabsorb nutrition. (can put a person on pancreatic enzyme, but lungs be chronically infected). Defect in transport of chloride back into the bloodstream (reabsorption). Lungs covered and have outlets for secretions to trachea and out of mouth, can cough em up- at this local level mechanism the chloride transport defective and cant thin our secretions. They test the sweat content see elevated chloride level bc not reabsorbed into blood stream and not where need to for secretion of lungs to be thinned and expectorated. Anything stay in body not supposed to be there gets infected and scars the lungs and eventually need lung transplant. Pt presents with lots of phlegm not cough up, problem is when chronic infections of secretion buildup. Supposed to reabsorb into blood but goes into skin. Increase in chloride in sweat and then cant thin out secretions (water doesn’t get reabsorbed) bc in pancreas, lungs and sweat glands. Very young have lots of infections and mucus, wet cough and shortness of breath. Causes an increase in congestion and mucus bc of failed chloride transport mechanism. Phenylketonuria (know the patho!) Child very fair. Defect in amino acid metabolism phenylalanine. Body cant convert this amino acid to tyrosine the precursor to melanin responsible for skin pigmentation. The brain cannot clear this and is toxic to brain and if not d diagnose quickly then accumulation causes mental retardation toxicity and cognitive problems. Light color hair and skin. Diet restriction of phenylalanine day 2 of birth mandatory blood test. Once feed infant see accumulation of phenylalanine and show signs of disease. Tay Sachs- Enzyme break fatty waste in brain cells and accumulations cause toxicity in all organs but mostly in brain. Spinal cord seizures blindess, death occurs by 2-5 years. Normal at birth but within 6-10 months show lack of attention and responsiveness and die within first years of life. Predomin in eastern hews. Carriers are screened bc death is inevitable, no treatment. Cherry red spot on retina is indicative of tay sachs- accumulation of the fatty waste products on the retina itseld. Chromosomal disorders- alter chromosome bc infection inflation or mutation. Downs syndrome- extra chromosome not 21 wide range of expressivity. Most common chrom disorder. KNOW RISK FACTOR- INCREASE IN MATERNAL AGE. Normal age mother less than 35 1 in 700 births and then over 35 Is 1 in 25 births. Maybe old eggs or more exposure to external factors not sure exactly why. Protruding tongue, flat nasal bridge, small ears, single palmar crease. Mental retardation, heart problems. Turner syndrome- x chromosome disorder, partial or ottal inactivation of x chrom. Spontaneous abortions. Diagnosed when girl go into puberty bc inability to have secondary sex characteristics. Degree of inactivation of x express differently. Shprt stature and webbing of neck, aorta is narrowed at point where suppl rest of body with bloo. Bicuspid affected- aortic valve is tricuspid but theirs is bicuspid. Absent ovaries amenorrhea. Normal intelligence but difficulty driving nonverbal problem solving, math. COA coarctation of aorta so narrows and not supply rest of body with blood. May need heart valve and surgery to fix that. Teratogenic agents- produce abnormalities during embryonic or fetal development. 2 months of preg without knowing it and many of these can occur based on timing and exposure. Maternal health also affect. Toxoplasmosis- exposure to cat feces, undercooked meat, others- varicella, zika, ● T-Toxoplasmosis ● O-Others (Varicella, listeriosis, leptospirosis, EBV) ● R-Rubellas ● C-Cytomegalovirus ● H-Herpes ● Can cause microcephaly, hydrocephalus, eye/hearing problems Chapter 3 Inflammation: Some content tested but inflam going to affect any pts who have had surgery have inflame- any pt with infection have inflame. Response to cell injury. If have infection, cut, injury, it will help trigger the immune inflammatory response it triggers mediator to get to area and clean it up. Phagocytise to remove damaged cell and tissue and increase blood flow to the area to help regrow tissue and heal. Like a papercut- tiny but hurts. Cut damaged tiny capillary vessels and trigger inflame response- trigger platelets to get there and trigger clotting cascade, clump and call fibrin and trigger clotting mechanism. Also trigger immune response macrophages to clean up debris- trigger WBCs to defend the host. Pulse on area of cut is opening vessels cause some capillary dilation and allowing mediators to cross over area of injury. As a result of that dilation (capillary permeability) it gets swollen, itchy, red and hot, causes pain but not bc of the cut but bc of the swelling, some exudates (drainage) to allow plasma mediators to get to area of damage. Neutralize toxins from the paper. Granulocytes- a white blood cell with secretory granules in its cytoplasm, e.g., an eosinophil or a basophil. Neutrophils are most abundant, then there are eosinophils, basophils and mast cells. They leave the blood and go to site of infection. Neutrophils use phagocytosis to destroy enemies. Eosinophils granules have toxic things that kill enemies. Basophils release histamine that triggers an immune response. Mast cells also have histamine and help with healing process. Agranulocytes-…Agranulocytes, also known as mononuclear leukocytes, are white blood cells with a one- lobed nucleus. They are characterized by the absence of granules in their cytoplasm, which distinguishes them from granulocytes. Two types are lymphocytes and monocytes. When monocytes leave circulation they turn into macrophages. Lymphocytes are three kinds- B cell, T cell and natural killer cell. B cells make antibodies that bind to pathogens and destroy them. T cells coordinate the immune response. (they remember past diseases and recognize them to fight them again). Normal inflammatory response- vasodilation, capillary permeability, leukocyte migration, phagocytosis SIRS KNOW!! System inflammatory response,, all capillaries open up vasodilate. Systemic inflammatory response syndrome to a major insult. (not just infection, could be inflame pancreas without infection, a clean surgery such as broken foot getting pins) all post-surgical pts have SIRS response. Heart rate compensate bc need more blood flow to area of insult- whole body responds. Respiratory rate higher- they breathe faster, temperature increases most of the time. Pt becomes febrile bc boosting up inflame response to defend the host. If pt in prolonged SIRS response the temp can be low, cant generate high temp and that’s a bad sign. Older pts might not generate high temp gets hypo. Some infections trigger sirs and make pt hypothermic (yeast in the blood is one example). WBCs usually shoot up higher than normal to help if for too long not enough to generate can be low. Low is for chronically ill or elderly. Most population increase in temp and wbcs. SIRS is systemic response to an insult manifesting in abnormal ways for body to compensate for what it sees as an attack (permeability- tiny capillary opens up and allows plasma to seep thru and in plasma is the mediators). KNOW: (identify and talk about dif cascades with SIRS to MODS) Sirs response not clean, will happen about 24-48 hrs after surgery or nay type of insult. It comes and goes on its own. But if sirs response is bc they have a bug bacteria, virus, organism, yeast, fungus- the damage becomes greater and pt considered SEPTIC. Bug or infection and heart rate higher, resp rate higher, wbc high get sepsis. Sepsis costs millions of dollars and bug problem in healthcare. Sirs + invading organism= sepsis. Severe sepsis= sepsis + organ dysfunction. Wait an extra hour to see if goes down. If because of infection- pt has nasty wound and has this criteria think sepsis. If pt has organ dysfunction- mental status gets funky, get agitated or confused maybe need more oxygen. Organ not working well and cant compensate bc of sepsis is severe sepsis. Vasodilating not making as good urine made now. Dysfunction in baseline, mental status and urination. Any so long a person can breathe 40 times a minute or 40 * Celsius temp before damage. If all vessels opened up then blood pressure drops. Bp think as garden hose and water the flower bed, and need hose over somewhere farther out, need to constrict hose that increase pressure and then can profuse a farther out distance. Normal. If vasodilate and open up garden hose and floods up close the father out place not get perfusion. Organs fail. To increase flow to farther out try to constrict and to supply to farther out need to give more fluid, fill up. If pt becomes hypotensive- vasodilated and no pressure in arteries to get flow farther out gives out fluid 2-3 liters, only have 5 liters of cardiac output at once give hald blood flow over there so blood pressure goes up, if still hypotensive after giving 2-3 litrers then in septic shock bc organs not get their perfusion. The brain kidneys heart gut then lastly skin. SIRS + bug + mental status SEPSIS+ hypotensive despite fluid replacement (if regular give fluid and back) now add constrictors/compressors. Powerful medication only get in ICU. If have fluid and vasocontricting with pressors and still not get flow the kidneys etc get ischemia and go into MODS multiorgan dysfunction syndrome- 2 or more organs down. Pt gets agitated then one system and if fluid given then kidneys affected if still not reach, the nephrons die- third system. Gut shuts down right away without blood flow no motility no abdominal sounds, cant tolerate getting fed. 4-5 systems have 80% mortality. KNOW: Mediators triggered to defend host (increase hr, rr, temp, and wbcs) when enemy comes. The blood vessel vasodilates to allow more leakage. The vessel wall getting permeable and the breaks in capillaries there so losing vessel wall integrity, gets damaged. Platelets triggered to come there and activated so SIRS cascade also triggers clotting cascade by platelets to clump at area of vessel wall damage. High risk for clotting- not such good perfusion bc losing fluid as vasodilate and can clot. When bacteria there and wall permeable the bacteria damages the vessels ability to vasoconstrict and vasodialte (autoregulatue) in septic shock. Not only that capillaries open up to try to help defend thehost, the septic shock the walls cant auto regulate. Give lots of fluid that seaps out into tissues and pt looks very swollen head to toe (periorbital edema skin around eye bulge, testicles size of watermelon, no folds In skin they breakdown, tongue bulge out, pt looks unrecognizable. Cant open eyes conjunctival edema) all fluid shifts into tissues. Organs fail then bc not get the perfusion. 60% mortality in septic shock. Most time prevent bc giving pt many times infections by not proper handwashing. (if fix and kidneys work there will be tons of fluid coming out after). Fever mechanisms: If bug cross hypothalamus try to reset temperature trigger SIRS (increase metabolic rate, fight the infection). Vasulcar stage- casofialation permeability, fluid shift into tissues. Cellualr- wbcs eneter injured tissue and destroy infections with tocins. Kinds of exudates (not test on it but might be a descriptor in a question): drianiage Serous- plasma like. Very thin yellow and clear, a little sticky. Oozes from any type of small cut. Hemorrhagic or sengounous is blood- frank red blood, dark. Fibrinous- stringy and usually tissue trying to regenerate. Membranous/pseudo- covers tonsils, membranes Purulent/suppurative- pus thicker, yellowish, whitish it is wbc debris collecting at site of infection needs to be cleaned out and may be a source of infection. (purulent wound think most likely infection behind it wbc clean out at a serious site that s infected.) 2/6/17 Chapter 8 Fluids & Electrolytes Edema vs third spacing Kknow as part of a clinical picture. Edema is fluid in insterstitial spaces (in tissues where not supposed to be) Dependent edema- when on feet all day. Ridge around ankles. Fluid shifts into a particular area. Third spacing is the shifting of fluid throughout the whole body- generalized edema. Swollen everywhere (conjunctiva, lips, periorbital, scrotum, arms, legs swollen). Third spacing is more of a systemic edema. The vessels are not holding in their fluid appropriately. In septic shock the capillaries dilate and become more permeable and fluid shifts from tight bound vessels to opening up and shift into tissues from head to toe. Electrolytes- substances that dissociate in soln to form ions. Os- pos or neg charged Cation + Anion – KNOW ELECROLYTE NORMAL RANGES (might see dif numbers in the book but know these) Na+ 135-145 mEq/L K+ 3.5-5.0 ** very strict bc incremental changes matter Cl- 95-105 Ca++ 8.5-10.5 mg/dl Mg++ 1.8-3.0 Phos 2.4-4.1 Serum osmolality 280-300 mOsm/Kg H20 Tiny differences isn’t a big deal Fluid and electrolyte shifts occur through: Diffusion- movement of particles across semipermeable membrane depending on size of molecules and concentration of soln. body strives to balance these. Sodium travels across! Though water follows sodium- we talking about normal. Abnormalities occur when too much water and not enough particles or too much particles and not enough water. With enough water to balance everything is a normal situation. If take away water the particles go up in conc bc not enough water to balance them. If body can compensate it will do that and then wont be a problem. In our class we focus on the PROBLEM. We focurs on ABNORMALITIES. Osmosis- water following conc of solute. Higher the osmolality, the more concentration the soln is. The conc of solute in fluids is the osmolality. Water moves to that higher conc of solute to balance. The compartments. Pt Is dehydrated not enough water to equal it out their osmolality goes up. If fluid overloaded then more water to solutes so osmolality goes down. Osmotic pressure: pulling power of soln to draw water across a semipermeable membrane. Isotonic soln- iso=same, a soln that has same osmolality, number of solutes, as body fluids. Nice hydrated cells. The fluid would stay in vascular space and not move in or out of cell. Stay where you put it. Pt with low bp- cuff on artery and compress it and measure pressure it takes to ill artery back up so very dependent on volume. Iv in a vein (vessel) fill isotonic fluid in there should stay in vessel so when check bp again it should go up. Good for bp hydration. Normal saline same number of solutes as plasma so stays in vascular space. Lactated ringers- has potassium and other solutes that it is isotonic- same osmolality conc of blood and stays in vascular space. Can give isotonic soln a lot to rehydrate the pt and give push for heart to perfuse organs. Hypertonic- has more solutes than plasma. Acts as mechanism to draw fluid out of cells and go into the vascular space. It is a pulling power from the cells and the cells become dehydrated and be like a raisin. You start to pee more bc increase fluid in vascular space. Someone with brain edema give them hypertonic soln to pull fluid from brain tissue and dump in urine. Hypotonic- has less solutes than plasma. D5w less osmolality then plasma so water shift into cells and rehydrate the cells. If rehydrate too much and too fast in can cause edema and can burst the cell. (5% dextrose in bag is isotonic but when body uses it it breaks down sugar and is just water and becomes hypotonic soln in water. Basically giving water which is a hypotonic soln) If drink hypotonic solution it can shift into your brain Not too much too quick cant bolus quickly for hypotonic (over permeates the cells)/hypertonic soln (really dehydrate). Can only quickly bolus isotonic. Pressure in cell- plasma protein albumin is a colloid (large molecule) Hydrostatic pressure- amount of pressure in vascular space pushing fluid into vessels towards the tissues and organs. What propels the fluids is the left ventricle of the heart to aorta. Pressure exerted on walls of the vessel usually bc of the pump the aorta. Oncotic pressure- pressure in vessles by big molecules like albumin and RBCs, plasma that maintain the fluid in the vascular space. They balance the pressure in the vessels and the hydrostatic pressure that’s pushing the flow to the end organs. The reason why tissues not flooded with fluid is bc have colloid pressure in the vascular space. If heart starts to fail the blood flow congests the heart (congestive heart failure), pump ot work then heart drowns and immediately the lungs suffer bc back up into lungs and into right side. Blocks breathing and oxygenation. If hydrostatic pressure not great enough to feed tissues then drown heart. If alcoholic and liver cant synthesize albumin all fluid go to tissues and fill up belly, cause edema and end organs suffer but fluids shift bc protein not being synthesized to keep fluid in the vascular space. If missing either colloid pressure or pump not working then have problems. Bad when both. Oncotic pressure- biggest component is Albumin. (hydrostatic pressure exerted on vessels towards organs and tissues. oncotic pressure keeps the fluid in the vascular space.) Filtration- fluid moves across.. Active transport- need carrier like sodium-K+ pump. Balanced as well. Sodium mostly INSIDE the cell. When give blood sample and send for electrolyte sampling and get normal lab values- they spin the sample and the RBCs float to bottom and plasma stay on top. Plasma is extracellular that’s what’s sampled for electrolyte balance, sampling extracellular not testing inside the cell. Get sodium mostly from what’s outside the cell. Water balance- have enough circulating volume to perfuse the tissues. Mechanisms to increase volume- Thirst Adh Raas cascade A & B KNOW the mechanisms! ADH and raas cascade going to be now, in cardiovasc, and renal. ADH: Normal water regulation- hypothalamus senses increase in osmolality. It senses when solutes are elevated or not as the blood flow goes across it. When raised osmolality it signals pituitary gland to release anti-diuretic hormone making you hold onto volume and not pee. Alchohol makes myou pee bc blocks adh production. Too many solutes so releases adh- makes kidneys holds onto water, increases blood pressure bc holds onto fluid. Now returning osmolality back to normal. Thirst happens before adh. If too much adh then the sodium level drops!! Too diluted. Bc holds onto water and then dilutes the sodium (not lose sodium, just diluted)!!! RAAS rennin-angiotensin aldosterone- kidney is very sensitive to fluid and volume. (rennin triggered by glomural) The kidney senses a decrease in perfusion pressure, blood pressure, blood flow, circulation and signals rennin to be released. Rennin is an enzyme that works on angiotensin a plasma protein that floats around inactive. Renin activates angiotensinogin 1 and triggered by Ace enzyme makes it 2 to hold onto sodium and water in the lungs and by doing this cascade in normal functioning kidney- angiotensin 2 is very potent vasoconstrictor. Vasoconstrictor increases blood pressure. If increase perfusion pressure raises bp and triggers ALDOSTERONE in the adrenal glands which works on sodium retension. Aldosterone holds onto sodium in the kidneys and also therefore water. 2 mechanisms activate by raas bc of decrease blood flow to kidney 1. Sodium retention 2. Vasoconstriction. Hopefully these cause kidneys to get more blood flow/perfusion. This happening in kidneys. If thirsty adh triggered. If thirsty and bp drops then RAAS kicks in. holds onto sodium and hopefully enough water in there to not be dehydrated. When thirsty not drink enough not pee a few hours now bp drops and kidney hypoperfused then RAAS takes over. Many drugs based on raas cascade. Increawe blood volume and then systemic vasoconstriction bc if go to core then not feed anything else. Aldosterone holds onto sodium (hopefully water, but wastes potassium so may need to replace it)!! Sodium is balanced with potassium so if hold onto sodium then excrete potassium. Normal ph is 6 in urine. Range 4.6-8.0. normal gavity how much sodium to water in the pee 1.005 to 1.030 greater than 1.030 means more concentration of solutes. Less than 1.030 is overloaded with fluids. if pt dehydrated kidney not enough water so increase in urine spec gravity. ANP and BNP- To oppose RAAS is atrial and b-type natriuretic peptide living in atria and ventricle of the heart. These peptides respond to stretching. If atria or ventricle stretch then too much fluid stretching them therefore the peptide is released and will oppose rennin and raas cascade. This effects volume status by getting rid of fluid (raas holds onto sedum, water and increase bp), if heart overstretch peptide released and start dumping urine. Worry more about B-type of left ventricle which perfuses organs (a does atria). Can measure level of dluif (crackles when listening to lungs and chest x-ray) and measure b type 1000s an d not 400 bc stretched ventricle and need to give diuretic to make them pee. Heart failure in low 1000s, 3 4 5 000 is really bad be in icu and intubated. Increase glomerular filtration rate bc vasodilate glomerular membrane in kidney causing you to make more urine. BNP shows up in pt high level excretion someone whose heart overloaded with fluid when trying to oppose rennin it was activated. Disorders of thirst and ADH Hypodipsia- not able to sense thirst. Elderly and dementia and infants cant tell/sense thirst. Stroke and hypothalamus damaged may not be able to enact thirst sensation Polydipsia- drinking to much water. There is psych disorder to drink a ton and throws electrolyte off. Di and SIADH from brain problems Disorders of water and sodium- fluid volume deficit Not have enough water= Pt is hypovolemic, losing water and electrolytes. Vomiting a lot in short amount of time, diaphoresis- excess sweating, polyuria (metabolite disorder and making a ton of urine), fever making sweat, nasogastric suction (sucking out large volume of flid)/ abnormal drainage, wound lossess need ccs/ml amount losing, (burns more third space losses, fluid shifts). Insufficenient intake- Anorexia, nauseas, impaired swallowing, confsuin, depression (not taking in enough fluid) KNOW CORRELATE HOW FLUID VOLUME DEFICIT SHOWS UP/CLINICAL MAIFESTATIOSN: (not need know percentages) 2% loss- mild fvd 8%= sever fvd Decrease tissue turgor- decreased elastcitiy, pinch skin on top of bony prominence it stays tented, Dry mucous menbranes Sunken eyeballs Decreased tearing Postural hypotension – change in bp from laying down to sitting or standing, changing position. Blood vessels uppoesd to tighten up but not enough volume in vascural space and perfusing brain which is why almost pass out. Hematocrit- excess when in fluid volume deficit URINE OUTPUT- hypovolemic, decreased urine output. Hypervolemia- too much volume, high bp. Body retains both water and sodium. Excess intake of sodium. Impaired fluid balance regulation- if pump not working, we want normal 2 L water intake a day but these pts even on 1 L /2 of what want still ion fluid volume excess. If heart week cant handle even 1 liter sometimes. Heart would get congested and go into lungs and not breather. Not activate RAAS cascade. Fluid serosis- albumin keeps fluid in the vascular space. Pts fluid can go into tissues and overflow the tissues. Also with liver have aldosterone levels off. Clinical manifestations- KNOW Weight gain – very sensitive indicator. Weigh the pt. Edema Hyptertension Adventitious breathe sounds – crackles** sound can auscultate over lung fields sounds like crackling JVD- jugular veinous distension. If laying 30 degrees in bed elevated. And juglar vein should be flat at 30 degrees if not talking. If at 30 deg see bulging of jugular vein then too much fluid in them, fluid volume overload. Blood count/hematocrit- amount of RBCs per volume. Percent of RBCs to volume normal is 35-45 or so, we go by hemoglobin usually. If hematocrit is component of volume and fluid volume overloaded then rbcs percentage is lower and becomes diluted and decreased in fluid volume excess. More concecntrated in fluid volume deficit. Serum osmolality – measure solute conc. Increase in solutes shows fluid volume deficit- not enough water to balance. Decreased serum osmolality shows too much water, fluid volume excess. Mechanisms that cause EDEMA: Fluid overload. Heart failure increases hyperstatic presure0 too much fluid cant pump out goes into tissues and causes edema. If heart not pumping out tissues cant get what need so kidney cant either and wants to activate RAAS. That’s where kidney can kil you bc fluid overloaded but not getting any so activate raas and go further into heart failure and edema. Increase membrane permeability- septic shock, burns, cause shifts- vasodilation. Out of capillaries they shift out and go into tissues. Need albumin to hold onto fluid in vessels and if not squishes tissues. If pt has oncotic fluid shifting into tissues- oncotic PULLS more fluid to the tissues which can cause further increase in edema. Lymph filters blood and gets overloaded and cant clear those proteins bc overworking. Oncotic protein not going where need to, shifting fluid, failure to remove sodium and water bc heart failing or vasodilating effect that causes fluid to shift into tissues. KNOW normal sodium but know key is NERVE FUNCTION/NERURO TRANSMISSION. Coupled with cl and Bicarbonate hco3 and water follows it. Low sodium less than 135 can be bc maybe too much water onboard which washes out sodium, if hypotonic holding on too much water, washed out sodium and cant concentrate urine so spec gravity is low bc sodium is dilute. Causes of hyponetremia- too low sodium Excess sweating Gi suction Salt free diets Adrenal insufficiency bc holds onto sodium Head injury stroke affects adrenal glands Diuretic therapy if lose too much water also lose electrolytes. KNOW SIGNS AND SYMOTOMS Malaise and muscle cramps MENTAL STATUS CHANGES, Headache, confusion, lethargy Nauseas vomiting, diarrhea Headache Convulsions and coma Apprehension- get figity, more agitated. If sodium is low bc water is high and can hurt brain- make coma and seizures Hypernatremia- Extra sodium, water loss, increased osmotic pressure carses fluid to move out of cells into the ecf Cell become dehydrated Plasa sodium aboce 145 Not have enough water on board to balance it out usually. The blood going to be bad flow and more concentrated and more prone to BLOOD CLOTTING. Hypovalemia and hypernatremia make blood more viscous and sluggish and clot easily. KNOW Clincal- Pt is thrisyu Dry mucous membranes Hypotension Rapid pulse for heart trying to compensate Not enough urine bc notenough volume Hypotension Confsion and lethargy Concentrated urine MENTAL status Potassium: INSIDE THE CELL- 3.5-5.0 normal Major cation of ICF Dietary source if too much banana avocado tomato etc, Regulated by kidneys. Potassium not stored well in the body. So if not good diet not have enough potassium. Aldosterone eliminates potassium. Insulin pushes potassium into the cell. Acid bas balance Exercise- muscle contraction triggers K+ release. Need healthy kidney to excrete potassium appropriately. If kidneys too much potassium need dialysis to filter them. Responsible for osmotic integrity fo cells with sodium pot pump Conduction of nerve impulse EFFECT ON CARDIAC MUSCLE- cardiac smooth muscle excitability in action potential. If K+ low: Muscle weakness and leg cramps ver common Fatigue Anorexia and nausea vomiting Decrease bowel sounds CARDIAC ARRYTHMIAS (changes depolarization of cardiac cycle)- cant stabilize cardiac contraction og the muscle HYpokolemia-inadequate intake Excess loss thru gi, kidney and diuretics … Hyperkalemia- KNOW Also cause cardiac arrhythmias Potassium relaxes cardiac muscle as well but too much relaxes too much at 6 seeing cardiac changes. At 7 the pt can arrest. Paresthesias Muscle and resp weakness Causes: Renal insuffiency- Ckd chronic kidney disease Autoimmune nephropathy- affects kidneys Acidosis Adrenal insufficiency if not enough aldosterone cant rid of K+ ACEI/ARBs (ace inhibitors and angio tensin blockers Potassium-sparing diuretics Icf to ecf Too much K+ administration RBC destruction- massive infection or trauma and RBCs break down they spill their contents which is mostly potassium so see it goes up and pt becomes very acidodic. Calcium 8.5-10.5 Stored in bone and ecreted by kidneys Found in icf regulated by pth … HYPOCALCEMIA If poor aborption in GI tract Pancrease grabs calcium and decreases it in blod Vitamin d helps to absorb calcium Renal failure Hypoparathyroidism hyperphosphatemia- with phosphate opposite so if calcium down then phosphate up KNOW SIGNS AND SYMPTOMS Bc of nerve transmission it will affect in dif ways- Tetany- the locking of jaw Trousseau sign when put bp cuff over arm and inflate it causes a spasm Chvostek sign- pain shooting down jaw when tap facial nerve Prolonged st and qt (arrhythmia not need to know) Laryngeal stridor- the larynx can become bc lack of neurotransmission tightens and cause threat to airway Impaired clotting- free floating activated calcium in blood is a clotting mechanism, if calcium low then cant clot Hypotension-arrest: cardiac conduction so makes pt hypotensive or cardiac arrest Hyeprcalcemia- Due to increase in porous bone release of calcium . higher blood conc of calcium and makes bone thin and break easily. Immobility: walking or running causes bone to become more dense and stronger and allows calcium to go into bone and make harder. Immobility does oppos Hypophosphatemia- makes phosphate low when calcium high Hyperparathyroidism- too much activate thyroid Increased GI absorption Clinical: Decreased LOC Ekg changes Av blocks See renal calculi- kidney stones usually of calcium deposition. Lots of dairy products/calcium will deposit in kidneys Bones thin so break- bone pain fractures Calcification- deposits of calcium on organs Band Keratopathy- deposits of calcium on the eyes Magnesium not stored well in body (like potassium) so must intake Helps with myocardial contraction Contracts the myocardium HYPOMAGNESEMIA- Due to malabsorption, gi tract infection/disease or not eating like alcoholics- most not eat Diuretics- rid of electrolytes with water KNOW PRESENTS: Cardiac arrhythmias Hyperreflexia Dysrythmias- forsaads form od cardiac arrest instead of shock and meds give magnesium bc alcoholic or suspect mag deficiency Helps calcium transport so can also have trousseau and chvotek but really for calcium Similar to hypocalcemia Hypermagnesemia- not see much. Only pts with kidneys not work have overload of magnesium Renal failure Cuases Slow resp rate Bradycardia (causes relaxation) Hyporeflexia Decreased loc Phosphate: 2.5-4.5 Anion fond most in icy In boe and teeth Component of atp Acid base Nerve and muscle activity Hyperphosphatemia is low calcium hypocalcemia trousseau chvotek Renal failure Excess intake Hypoparathroidism Hypocalcemia KNOW PRESENTS: Hyperreflexia s/s of hypocalcemia phosphate deposits in joints Hypophosphatemia- Absorption iissues Starvation Alcoholism Malabsorption Hyperparathyroidism Renal phosphate wasting If replace phosphate too quickly then calcium drops- NURSING INTERVENTION REPLACE PHOSPHATE SLOWLY OVER 4-6 HOURS bc if give quickly and calcium drops and pt goes into cardiac arrest its bad. KNOW presents: Dyspnea Muscle weakness Confusion Decreased cardiac contractility Sodium, pot, raas cascade ACID BASE BALANCE- Due assignment after lecture and study do worksheet. Know arterial gasses. KNOW YOUR NORMALS 7.35-7.45 normal in blood Acid olecule can dissociate and relase H+. base can accept or combine with H+ As H+ goes up in blood the ph goes down. Body cells sensitive to ph and can affect normal cell function. Ph is measure of relative balance bet acids and basis in soln. ot is neg log of H+ in mEg/L. Acids added to soln ph goes down 7.35 When base added to soln ph will go up 7.45 Sample of arterial blood and evaluate the gasses in it- can tell the pt true acid-base balance before blodometabolized in liver and messed up. Can tell what goes on in lungs but not metabolized by liver. 1 acid: 20 bases. Primary acid is CO2 and primary base bicarbonate HCO3. We talk about CO2 end product from lungs by clear CO2. If get venous smaple already metabolized. Areteriole not metabolized by liver just worked on by lungs and is co2 not hco3. Greater than 7.45 is alkalosis is ecll derangement/death. Lower than 7.35 is acidosis and also cell derangement/death. Chemical buffer system: 1. Bicarbonate buffer Kidneys can conserve or form new bicarbonate as needed if working. If pt is too acidodic the kidneys can hold onto more bicarb or synthesize more to make it more alkalotic bcbicarb is a base 2. Hydrogen-potassium exchange system. K+. hydrogen ions go into cell if too acidodic and kick out potassium too compensate. They switch plaes to compensate e for acidosis or alkalotic. To help buffer th blod. 3. Protein buffer system Acidosis- H+ diffuses into cells and drives out k+can stop heart, drive out k+ elevates k+ hyperkalemic. Alkalosis- h+ out of cells and k+ in but blood is hypokalemic. Give several scenarios and interpret whats going on. Kidneys can hold on or get rid of bicarb to help regulate. Lungs also can rid of co2 or hold onto co2. If alkalotic then hold onto co2 (co2=acid!!) if acidodic then rid of CO2. How? Control resp rate. Blow off co2 is rid of acid. By retaining co2 breathing less holding on to acid. When sleeping involuntary breathing- co2 starts to climb and central resp centers sense increase in co2 and say take deep breathe too let out more. Nrain stem and peripheral chemorecceptors in carotid branch and in central sense co2 level and respond to it. The only prolem is pts with lung disease- respond to low o2 levels to breathe more. Smokes, copd, have lung disease have dif mechanism. Can alter resp rate. Normal co2 level is 35 to 45 mm Hg! Can blow off more by breathing faster or decrease resp rate to retain co2. Kidneys also regulate ph by rid of h+ in urine if pt is acidodic can reabsorb bicarb into blood as well and make new bicarb from ammonia. Arterial blood gasses to get ph values. From artery to see how co2 elimnated and bicarb eliminated. Might see co2 and bicarb level on electrolyte panel- venous samples metabolized by liver and so dif numbers, Basic metabolic panel or complete metabolic panel. Here bmp and cmp and they not meant to indicate resp status or ph. Arterial blood gasses. Ph, acidosis, alkalosis Paco2 35-45 Bicarb 21-28 kidney working hold on or dump as needed and this is normal range Metabolic acidosis- Initially have low ph bc acidodic 7.35. metabolic reason for kidneys not doing job not resp. maybe anaerobic, or dead tissue somewhere so making more h+ ions maybe kidney not working, maybe loosing bicarbonate fluid via the gi tract- diarrhea (fluid from belly button down) so become acidotic, not need chloride. Too much acid ot losing too much bicarb Diabetic ketoacidosis too much h+ ions bc not feeding tissue sufficiently. Starvation ketocacidosis- breaking down ketones and become acidodic. Anaerobic metab Overdose if acids Renal failure/uremia Loss of bicarn Diarrhea Pancreatic … Imbalance so lungs okay bc metabolic problem. What lungs do? Can increase resp rate to blow off co2. So increase resp rate greater than 20 (greater than normal in adults) hypertachybnic to blow off more co2. Can also gave lactate containing soln like lactated ringer which is isotonic to replace bicarb stores. Really need to fix underlying cause. Kidney failure so need dialysis. If infection rid of it and perfuse those organs.. Metabolic alkalosis:high ph Too much bicarb or lose too much acid. Rid of fluid above bell button- vomiting. Increase bicarb levels Alkalosis- Excess base: Too much antacids Too much lactated ringers Lungs: can slow down resp rate to retain co2 too compensate for excess base. Breathing in a bag. Respiratory acidosis: Increase in co2 they initially try to breathe fast and then when sitting breathe too fast for long not enough energy feel lightheaded and dizzy bc blowing off co2 and vasodilate bp drops and you crash. Exhausting to breathe really fast for two min. Very quickly stop breathing and buld up co2. Gone past ability to compensate by blowing off co2. Caused by Acute disorders of ventilation- which pt not triggered to breathe bc have impaired function of medulla, brain stem injury (can’t breathe on won)and OVERDOSE pt. narcotic overdose stops the trigger of breathing and holds onto co2. Lung disease- copd cant compensate Chest injury Weakness of resp muscles- cant enervate diaphragm so cant breathe properly Airway obstruction Chronic disorders of ventilation: COPd- uses low o2 not high co2 as trigger to breathe. COPD has scarred lungs and have held onto co2 for a while by then. Body used to it. So not trigger them to breathe. They use low oxygen/hypoxia as trigger to breathe. If a pt needs oxygen and are copd you want to give lowest amount of o2 possible bc if give high levels may knock out trigger to breathe. Everyone else use high co2 as trigger to breathe but for copd use low o2 and go up sa needed. Pulmonary fibrosis- scarring of lung tissue and cant exchange gas properly accumulate co2 Increases oco2 production- Hypermetabolic they produce more co2. What can kidneys do? Take a while to hold onto h+ ions from blood so cant rely on for resp acidosis bc take too long. Resp alkalosis- Dece pco2 and increase ph. Caused by hyperventilation (rid of too much co2) Overstimulate resp center Not need third.. Pt usually in hypermetabolic state like Anxiety Pregnant Any infection Sepsis Febrile Exephalitis Makes them breathe daster, Hypoxemia can trigger increased resp rate. Deceased bicarb- decrease h+- high ph and can respond by dumping bicarb???? Mixed acidosis or alkalosis. Resp and metabolic acidosis or resp and metabolic alkalosis. Worst problem leads ph in that direction. Renal failure + narcotic induced resp depression= needs dialysis and ods so decreased resp rate and kidney cant dump H+ ions. Pt with copd gets gi bug cant compensate- resp acidosis and metabolic acidosis dumping bicarb. Gotta fix. T They cannot compensate. Some pts compensate with opposite . only compensated if ph is normal. Not treat number but the pt. opd ph normal but co2 high don’t fix number. If pt dropped to 7.31 acidodic then put on ventilator bc cant compensate. Pt not compensated unless ph is in normal range. Partial compensation exists as well. Get your normal values memorized. 1.Last name first Name abnormal acidosis or alkalosis, Determine if resp or metabolic problem 2. evaluate what going on in lungs 3. biacrb action Ph= 7.30 (7.35-7.45) paCO2=50 (35-45) HCO3 =24 (22-26) Acidodic, acidodic, normal Co2 (less than alk and greather is acid. Bicarb less than 22 is acid and greater than 26 is alk) ACID think resp, bicarb is normal. Respiratory acidosis. If bicarb going really alkolotic 32 that would be partial compensation bc kidneys trying to fix resp problem but there isn’t here so no compensation. 7.48, co2 44, bicarb alkolytic 32 Metabolic Alkalosis, normal, w/ no compensation 7.26 Acidosis, co2 normal bicarb acidodic Metabolic acidosis Lungs not trying to help Metabolic= bicarb Resp= co2 Kidneys- bicarb Lungs- co2 7.10 acidosis, c02 acidic (more co2=more acid), bicarbonate 15 is acidic MIXED bc kidney sdumping bicarbonate and going in acidic direction and so is co2 more present so more acidic. Metabolic and resp acidosis 7.54 Alkalosis, Co2= 20, alkalosis Bicarb 25- alkalosis towards. Mixed so metabolic and resp acidosis. (she wont use 26) 7.33, acidosis, co2- 25 alkalosis, co3- 20 acidosis Metabolic acidosis with partial compensation the alkalytic co2 trying to compensate. Sue two of the same and the other one is compensation. If ph was in normal range then be compensated- not normal but coimpensated so not call resp or metabolic problem. For compensated the numbers out of range but ph normal. 7.28 acidosis, 54 co2 acidosis, 20 hco3 acidosis Metabolic and respiratory acidosis. MIXED. 7.52 ALKALOSIS, co2- 48 is acid and hc03- 36 alk compensate Metabolic alkalosis with partial compensation (hco3 trying to fix but cant) Example of pt with resp rate 35 (breathing heavy) light headed and blood gas would suspect ph 7.49 in resp alkalosis. Can give directions of numbers this is high and this is low. Or give sample of numbers and you determine what it is. HW sheet use as a guide. Clinical example know also. 2/7/17 For Exam 1: Inflame and injury, genes, fluid and electrolytes and neuro on test. Most is what is the patho: not super cellular just basically. How does the disease show up/clinical manifestations: must understand the slides not memorize. Study by making sure not confuse different diseases. Do disease, the patho and how it shows up, the dif electrolytes. Neuro don’t confuse ms and mg- see how different. Memorize- electrolyte values and blood gas values. Use medscape and emedicine and webmd. Must comprehend. Follow the guides given in lecture- whatever she emphasized know and what she didn’t, just be glossed over, don’t bog down on it. Review lectures after class. 10% are pick all that apply bc on nclex at least 10% are pick all that apply. Bet 60-80 questions. 1.5 min for each item. The action potentials is how neurons communicate with each other. All based on interplay of potassium and sodium receptors (review!!). Spinal cord organization, cerebrospinal fluid. Pathologies- What makes pain subjective? Gate control theory: there are several factors involved in individual’s perception and tolerance of pain. Some factors are when have an injury there are emotional factors, cognitive factors (if understand what happened feel pain less), emotional factors, distracted from pain may feel it less. These things we talk about for pain in pt not just meds but distracting them playing music, a massage on dif part of body to distract nerve impulses. Someone cognitively impaired not understand the pain may feel it more. Medicine subscribes to this if affect the other factors can make pain felt less Pain threshold: point at which stimulus perceived as pain. Very subjective. Some people with a small cut ruins their day and others not really notice it Pain tolerance: point at which pain too unbearable. Very subjective. Some people higher pain tolerance than others. Nociceptive pain: pain activated by peripheral tissue injury Neuropathic pain: neuropathic/nerve bundle pain KNOW KINDS OF PAIN: Cutaneous pain: pain related to injury to skin and subcutaneous tissues Deep somatic pain: pain down to muscles and tendons like sprained ankle or joint pain Visceral pain: distension or eschemia of a body organ. If have gall bladder pain or gi bug and colon is inflamed (at the site) Referred pain: pain perceived at a different site than the actual organ that is involved. Gall bladder obstruction they get right shoulder pain. Pancreatitis can go to right shoulder or back KNOW DIF BETWEEN ACUTE AND CHRONIC PAIN! Acute pain: serves a purpose, telling the body something is not right, it indicates a problem. Signals the body there is injury or tissue damage Chronic pain: greater than 6 months in duration and doesn’t serve a purpose. TYPES OF HEADACHES KNOW!! Migraine: happens more commonly in women, about 18% of headaches are migraines. Can be genetic, can be hormonal related. Migraines have an aura attached to them- a feeling that it is going to come on can be hours or days before. They can be associated with other symptoms like nausea, vomiting and photophobia Cluster: more uncommon, men get them more often, pain behind one eye is the hallmark, usually lasts for a few days and goes away Tension-type: dull aching, more common and hat band distribution goes around the head Temporomandibular joint pain (TMJ): headache by imbalance in temporomandibular joint A headache you’ve never had before is most concerning, severe and never go away that is a dif pattern bc indicates something going on in the brain. KNOW TYPES OF MOTOR DISFUNCTION Plegia- stroke or paralysis Paresis- weakness Mono- one limb Hemo- both limbs one side Di/para- both upper Quadric/tetra- all 4 limbs Some involve upper or lower motor neurons. Upper send to lower and they said to nerves that enervate the muscles. Skeletal muscle problems: DISUSE ATROPHY- muscles shrink and lose ability to contract bc of immobilization and disuse (nothing patho wrong. Foot drop for immobilized if not contract foot they have permanent foot that cant contract. Use multipotus foot that keeps it flexed and extended appropriately. Denervation atrophy- no enervation of contraction. Typical of spinal cord injury pts bc not enervated for contractiokn MUSCULAR DYSTROPHY- genetic disorder damages muscle fibers bc absence of dystrophin a protein that maintains integrity of the muscle and so the muscle cannot contract. There is a spectrum of disorders for md Myasthena Gravis: Autoimmune disease- the body creates antibodies against certain tissues and attacks itself. No one knows why. Disorder of muscular junction that affects the motor neurons and muscle cells. Destruction of acetylcholine receptors bc of the antibodies that destroy them and block binding of acetylcholine. Acetylcholine helps muscle to contract so without the ability to use it at those junctions the muscle cant contract. Associated with thymus tunmor awhere antibodies are created or hyperplasia of the thymus gland (in adults the thymus atrophies so sometimes they just remove it). Women usually get more often in early adulthood. Gradual development of weakness proximal to distal portions of the body, if diaphragm is affected which is a muscle that drives respirations than have resp compromise. Only where skeletal muscle involved not cardiac or smooth uscle! Signs and symptoms: KNOW!! Insidious- out of nowhere. Smaller muscles affected first and then can get worse and become wheelchair bound. Muscle fatigue and progressive weakness. Muscle of eyes face mouth throat and neck affected first. DIPLOPIA or PTOSIS- double vision and drooping eyelid bc the EOMS are affected and levator muscle in keeping eyelids up. Cand have difficulty swallowing chewing choking and aspiration. When diaphragm affected ventilation in compromised. There is a spectrum. Autoimmune triggered by stress (alcohol, drugs etc) Periods of flare-ups/exacerbations and remissions, there is some ability to control with lifestyle changes but not easy. Usually younger individuals are involved. Stress, pregnancy, alcohol can cause crises. Use medication to conserve as much acetylcholine as possible in the body. Myasthena crises: stress event or not on meds can get severe muscle weakness, quadriplegia and resp insufficiency and extreme difficulty swallowing and risk for resp. Biggest problem would be not being able to swallow/breathe. Cholinergic crises: too much medication on board, caused by drug toxicity of cholinesterase drugs which prohibit breakdown of ach. SLUDGE: salivation lacrimation urination defacation gi upset and emesis: these signs and symptoms. Smooth muscle hyperactivity and excessive parasympathetic like activity. Bradycardia and increase sweating. Will be asked abt med- tensilon is a hallmark med for MG bc they diagnose MG. pt with symptoms give shot of Tensilon- very short acting to give increase uptake of acetylcholine- when they respond with improved symptoms in the office it’s a way to diagnose MG. Electromyogram- stimulate nerve bundle with electricity and see how it responds. Use dif labs to see as well. Treatment not need know- for all autoimmune bc its in inflammatory state use an immune-depressant med like steroids. Even chemo meds like cytozan is immune suppressant med. Plasmaphoresis- some pts hospitalized with myasthenia crises- filter plasma and filter out antibodies and throw away plasma. Filter the blood. If works it works within a week- usually pts with resp compromise and myasthenia crises. Peripheral nerve injury: ▪ Damage to LMN cell bodies in the spinal cord ▪ Damage to axons in the spinal or peripheral nerves ▪ Damage to myelin sheath (demyelination) ▪ Mononeuropathies ▪ Damage to one peripheral nerve ▪ For example, carpal tunnel syndrome ▪ Polyneuropathies ▪ Damage to many peripheral nerves ▪ For example, Guillain-Barre syndrome Guillain Barre Syndrome Demyelinating disorder but NOT autoimmune disorder, its caused by a virus/infection that triggers this event. Humoral and cell-mediated immune reaction directed at the peripheral nerves. Attacks peripheral nerves. A strep throat or any virus and not recover, instead the virus triggers inflammatory immune rxn to peripheral nerves. It affects longest axon first- ASCENDING PARALYSIS from lower limbs up! Motor paralysis Pt get out of bed then cant walk, in few hours paralyzed from bottom and goes up. When hits diaphragm they cant breathe and are on ventilator. When get over it its done and out of your system. Anyone can get it, not common though. SIGNS AND SYMPTOMS KNOW: Had to have infection 1-3 weeks before Ascending paralysis from bottom up Priority big concern- resp (airway breathing circulation) Treatment: Put pt on ventilator, plasmapheresis and iv immune globulin administration. Parkinson’s Disease KNOW PATHO: Degenerative disorder of the basal ganglia and the dopaminergic nigrostriatal pathway- the part of the brain that supplies dopamine. Dopamine depletion. Happens over time- degenerative not sure why but theoretically repetitive head injuries and concussions but also can be hereditary influence but cant say truly linked. Start in 40s and peak in 50s- prevalent in males. Dopamine inhibit movement in muscle fibers and ach is excitatory. Imbalance of dopamine and acetylcholine so have excess muscle contraction bc lacking the inhibitory influence of dopamine. SIGNS AND SYMPTOMS: Tremor at rest Rigidity (too much contraction it spasms, not flaccid/limp) Bradykinesia/akineasia- slowness in movement ntil cant walk at all Forward leaning gait as walk Dysphagia- muscles of throat and tongue become rigid Speech problems Dementia- in late stages only Depression Constipation- late stages Urinary retention- late stages Not true paralysis bc can send nerve impulses to muscles just lack of dopamine. Bilateral symptoms but usually stat on one side. Evaluation/Treatment: History of pt helps to diagnose, rule out secondary parkinsonism- brain tumor pressing on basal ganglia and stroke to basal ganglia and other meds could effect, no spec tests available Drugs for akinesia and deep brain stimulation- can implant in brain but not for everyone for deep brain stimulation. Amyotrophic Lateral Sclerosis/Lou Gehrig Disease: Degenerative disorder that involves BOTH UPPER AND LOWER MOTOR NEURONS resulting on progressive muscle weakness. No inflammation. Onset at any time from the fourth decade. More in males before menopause. Suspicion glutamate toxicity is involved to cause neuron degeneration theoretically though some meds of glutamate decrease symptoms SIGNS AND SYMPTOMS: Weakness may begin in any or all muscles of body Paralysis can occur with progressive muscle atrophy No mental sensory or autonomic symptoms preset. Have normal intellectual and sensory functions until death. Life expectancy 5 yrs after get symptoms. Evaluation/Treatment: See how much muscles respond to signals. Eventually need resp support bc diaphragm muscle not work. Stephen hawking the miracle of expected als. Multiple Sclerosis Demyelinating and IS autoimmne disorder inflammatory destruction of CNS myelin sheath. Onset bet 20-40 yrs. Female more prevalent. Some genetic association More common whites. T-cells attack myelin sheath and cause inflammation- inflammatory response. Plaques form with demyelination and axons do degenerate over time. The plaques that form cause a loss of nerve conduction and decrease in transmission of nerve impulses. This occurs with flare ups/exacerbations and remissions. SIGNS AND SYMPTOMS: Fatigue Parastheisia- numbeness of fingers and toes Optic nerve- visual field affected Ocular motor nerve- loss of eye movement cerebellum- loss of motor movements, Cerebellum system: loss of motor movements, feel weakness, loss of coordination and balance Evaluation: History and phys exam with mri Ct scan Treatment: Treat exacerbations and progressions Use immunosuppression drugs Use anti-inflammatory drugs to treat exacerbations Treat symptoms of pain, depression, bladder problems weakness (have problem with adl activities of daily life) Spinal Cord injury ▪ 7800 to 10000 persons each year ▪ Most are men between the ages of 16 and 30 years Injury to tissues thru forces that cant handka. Vertebral injurues compress the tissues Bones ligaments and joints may be damaged through fracture, dislocation or noth. Classified: ▪ Flexion ▪ Extension ▪ Compression KNOW: FIRST COMES SPINAL SHOCK, OCCURS AT TIME OF INJURY, LOSS OF RELEX FUNCTION BELOW THE LEVEL OF THE INJURY. Spinal cord injry at T3 pretty high may not be ale to send messages down and messages cant come up thru nervous system but peripheral nerves still work and activated by acetylcholamine. Initially lose peripheral reflexes below level of injry. Transection is where spinal cord injured through and through Reflex fintion lost below lesion Flaccid paralysis- loss of sensation Loss of bladder and rec