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Diabetes affects 18% of people over the age of 65, and approximately 625,000 new cases of diabetes are diagnosed annually in the general population. Rationale: Provides ongoing estimate of volume replacement needs, kidney function, and effectiveness of therapy. Rationale: Provides the best assessment of current fluid status and adequacy of fluid replacement.
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Hypersensitivity (or allergy) literally defines an exagerated response of the immune system to antigenic challenge, harmful to the organism itself.
The Gell and Coombs classification (see Table Gell and Coombs classification of hypersensitivity) distinguishes four types of reactions based on antibody (I-III) or cell-mediated (IV) effector mechanisms. There is a significant difference between Type I hypersensitivity and the other types of hypersensitivity caused by antibodies (Type II and III), namely the fact that Type I reactions occur only in a proportion of the subjects exposed to the agent in question (atopic individuals).
Antigens causing type I hypersensitivity reactions (or immediate-type hypersensitivity) are defined as allergens and induce the formation of antibodies of the IgE isotype in certain individuals.
The tissue response caused by type I hypersensitivity reactions is now well understood and is determined by the binding of IgE antibodies to a high affinity receptor which binds the Fc portion of IgEs with subnanomolar affinity and is located on the membrane of mast cells and basophils. The IgE-antigen reaction occurring on the surface of basophils and mast cells leads to receptor cross-linking and degranulation, ie release of vasoactive amines (histamine and serotonin) and other agents (heparin, eosinophil and neutrophil chemotactic factors, platelet-activating factor, a variety of cytokines and prostaglandins and leukotrienes) from the cytoplasmic granules, which collectively cause contraction of smooth muscle cells, vasodilation, increased vascular permeability and platelet aggregation and degranulation.
Unlike Type I reactions, Type II hypersensitivity is caused by direct antibody-mediated cell damage or lysis. There are systemic forms of type III hypersensitivity reactions, such as serum sickness, a disease which is now of pure historic interest but was a common occurrence in patients receiving repeated injections of anti-diphteric horse serum and in which immune complex deposition occurred in a variety of tissues and organs leading to fever, generalised vasculitis with edema and erhytema, arthritis and glomerulonephritis. There are also local forms of immune complex diseases, such as the Arthus phenomenon discussed in an early lecture of this Course. The prototypical type IV (or delayed-type hypersensitivity, DTH) tissue reaction is Koch's phenomenon discussed in an earlier lecture in this Course. Upon re-encounter with antigen, in the so-called effector phase, the antigen-specific TH1 clones undergo further clonal expansion and secretion of a variety of effector molecules.
Thus DTH is ultimately mediated by the macrophages recruited and activated by the products of antigen-specific TH1 clones (see Fig Pathogenesis of Type IV hypersensitivity).
As indicated above, Type I hypersensitivity reactions are involved in a number of diseases that have become remarkably common in Western societies, namely food allergies, eczema, hay fever and, above all, asthma.
The actual causes for the increase in prevalence of these diseases remains a matter of debate but here three points will suffice: (i) environmental factors have clearly driven the change in disease prevalence that has occurred over a relatively short period of time, (ii) a genetic, polygenic predisposition to such diseases (atopy) is involved and, (iii) an IgE-dependent immunological mechanism is ultimately responsible for tissue damage. Asthma is an inflammatory disease of the airways defined by hypersecretion of mucus by bronchial epithelial cells, eosinophil infiltration, bronchial smooth muscle cells (ASM) hyperplasia causing airway hyperresponsiveness (AHR) and bronchospasm (see Fig The pathology of asthma). An intense research effort is underway in order to understand the immunological mechanisms that lead to an IgE type response in subjects with asthma and major advances have been made. Separate and major advances that have occurred in recent years in our understanding of the pathogenesis of asthma have resulted from studies in the mouse as a result of the availability of inbred strains and gene knock-out and knock-in technologies and will be outlined below. Parallel mouse genetic studies have led to the discovery of two important asthma-susceptibility genes (C5 and TIM1).
The gene encoding the C5 component plays a central role in the formation of the membrane attack complex and regulation of the complement system (see lecture on Complement). While mouse genetics played a major role in the discovery of the C5 and Tim1 genes, the asthma-suceptibility gene ADAM33 gene was discovered on the basis of a genome-wide screen which defined chromosome 20p13 as a region linked to asthma.
How do the asthma-related genes recently identified affect the pathogenesis of the disease ?
While some people might say that kind of skill should require 13 years of preparatory school, four years of college, four years of medical school and a specialty in cardiac electrophysiology, I say…Pshaw!  It’s  not rocket science! As a warm up for the rest of this article, you might want to take a gander at Today I Found Out‘s article: “How The Heart Works”. An EKG is a graph (thusly named an electrocardiograph) tracing the strength and direction of this electrical signal. The “PR Interval” segment represents a delay in the signal at another grouping of cells called the AtrioVentricular Node.  This delay allows time for the atria to completely deliver their bounty into the Ventricles. The journey causing this second contraction through the ventricles is represented by the QRS portion of the EKG.
However, anything outside of the normal range is analyzed along with the patient’s symptoms to create a working diagnosis. To bastardize the words of Leo Tolstoy, who seemed to know a thing or two about the heart, “Happy [hearts] are all alike; every unhappy [heart] is unhappy in its own way”. It is very rare, but possible for an EKG to show a flat line, called asystole, when in fact the heart is still beating and producing a pulse.  It is because of this that it’s common practice to confirm death in a patient by looking for asystole in more than one lead. Conversely it is also possible, and more common, to have an EKG show heart activity, and even normal sinus rhythm, after a person has died and their heart is no longer pumping blood.  This is called a PEA, pulseless electrical activity, and shows what is left of the heart’s intact electrical system after the muscle itself has failed. The coffee stimulated brains of two nerdy paramedics with way too much time on their hands. I’m delighted you have cracked one of the greatest myths of all time, namely that medicine is not rocket science at all.


Not to knock Doctors and their education, I am an EMT, and I would question how many Doctors could Actually pass an exam to become a Paramedic.
Then your heart is firing backwards, which would hurt a lot because your basically having a heart attack. Does anyone know if you have had a avib await ion if that would effect a major surgery like colon resection.
Can I just say I loved the way this was written, because it was a lot more light hearted and not so serious with a quirky comment here and there keep me interested I picked this up quite fast, cardiac rehab exam is going to be a breeze!. Even in Scott’s “very simplified” but enlightening explanation of the heart and its function, it is readily apparent that such a complex design of instrument and operation could never have just evolved. Hi, I went to the doctor and he did a EKG and said my T was bad and walked over to a Cardiologist. Find Us On YouTube!Subscribe today to check out our free Daily Knowledge Youtube video series! There are several scoring systems which have been devised as methods of identifying high-risk patients presenting with acute coronary syndrome (ACS).
The Braunwald Classification of unstable angina pectoris (UAP) stratifies patients according to both the type of anginal pain and the underlying cause of the pain.
The GRACE model has been shown to be predictive of in-hospital mortality for patients presenting with ACS. License: All Rights ReservedShort: NASA Root Cause Analysis Safety Moment Steve Gordon February 9, 2010 Why perform Root Cause Analysis (RCA)?
Without treatment an acute attack of gout will usually resolve in 5 to 7 days however 60% of people will have a second attack within one year.
Rosacea – symptoms usually include facial flushing and persistent central facial redness.
Ocular surface inflammation leading to conjunctivitis and ulceration of the cornea (marginal keratitis). It is important that this routine – warmth, massage and clean - should be done regularly until the symptoms have cleared. Demonstrate adequate hydration as evidenced by stable vital signs, palpable peripheral pulses, good skin turgor and capillary refill, individually appropriate urinary output, and electrolyte levels within normal range. Note: Potassium phosphate may be drug of choice when IV fluids contain sodium chloride in order to prevent chloride overload. Although the basic phenomenology of most types of hypersensitivity reactions was established at the end of the 19th century and in the early years of the 20th century (Koch's phenomenon, Richet and Portier's anaphylaxis, Arthus' phenomenon and serum sickness) , it was only in 1963 that Patrick Gell and Robin Coombs produced a comprehensive classification of hypersensitivity reactions according to their underlying immune effector mechanism.
Since the original classification, our understanding of the molecular and cellular immune reactions has considerably developed and several attempts have been made to revise or re-interpet the scheme, one of which is listed below under Further Readings.
As a result, a significant fraction of the IgE produced following initial contact with antigen, becomes 'fixed' on the surface of these cells and, in case of a second contact with antigen, the antigen-antibody reactions occurs not only in solution but also or predominantly on the mast cell and basophil membrane (see Fig Pathogenesis of Type I hypersensitivity).
These reactions can affect a single tissue or organ (as in asthma, hay fever or eczema) or multiple ones (as in generalised anaphilaxis) depending on local or general re-exposure to the allergen.
This occurs for example in the haemolytic disease of the newborn (HDN) caused by Rh incompatibility. When significant quantities of such immune complexes are formed, they can deposit in tissues and lead to a tissue reaction which is initiated by complement activation and leads to mast cell degranulation, leukocyte, predominantly neutrophil, chemotaxis and an inflammatory reactions caused by the activation of these cells (see Fig Pathogenesis of Type III hypersensitivity and time course of serum sickness). In both systemic and local forms of type III hypersensitivity reactions, the emergence as well as the resolution of the tissue lesions and clinical symptoms follow strictly the formation of the immune complexes, the cause of tissue damage (see Fig). Type IV hypersensitivity reactions are caused by activated TH1 cells that are activated by intracellular pathogens, including bacteria, fungi and protozoa, as well certain chemicals ( hair dyes, nickel salts) leading to clonal expansion and differentiation of antigen-specific cells into TH1 clones. These include both cytokines (such as IFN-gamma, TNF-beta, IL-2 and IL-3) and chemokines such as IL-8, monocyte chemotactic and activating factor (MCAF) and a migration inhibiting factor (MIF) that collectively lead to macrophage activation and to the development of a local tissue reaction. Unlike type I, II and III reactions that can be transferred by serum (ie serum antibodies), passive transfer of type IV requires the transfer of antigen-specific TH1 clones that orchestrate the macrophage response. Individual knock-out experiments have clarified that IL4, IL5 and IL9 are primarily responsible for esosinophil infiltration whereas IL13 is responsible for ASM hyperplasia, AHR and IgE production and thus is the major disease-causing signal.T he nuocytes recently discovered by Andrew McKenzie are a major source responsible for IL13 production. These two genes were discovered on the strength of classic mouse genetics (the availability of inbred strains displaying susceptibility or resistance to disease) combined with the availability of mouse and human genome data. It was not expected, however, that the C5 gene could play a major role in the pathogenesis of asthma. For this a asthma-susceptible strain (characterised by bronchial hyper responsiveness and high levels of IL-4, a cytokine essential for IgE class-switch recombination) and a asthma-resistant strain were used for the derivation of congenic (co-isogenic) strains. This region is homologous to human 5q23-35, which had been identified in separate studies in humans as a region containing one or more asthma-related genes.
This region contains 40 genes and was dissected by single nucleotide polymorphism (SNPs), by transmission disequilibrium tests (TDTs) and finally by lung-specific expression studies leading to ADAM33. The C5 gene appears to induce expression of IL-12 by dendritic cells which is required for the development of the TH1 subpopulation and thus affects the balance between the TH1 and the TH2 subpopulations . Several of the key genes have been identified and, just as importantly, it is apparent that the strategies employed appear not only up to the task but also applicable to the analysis of other complex genetic diseases. EKGs are simpler still, being a moving real time map of the “wires” part and how they conduct electricity.  Reading EKGs only seems hard because most cardiologists use long (expensive) words. Or, to make a long story short, most healthy hearts pump blood through the body when stimulated by an electrical signal that travels along predetermined pathways.  This causes the cardiac cells to contract in just the right order, resulting in a magical four chambered pumping action.
This signal then travels through the atria (the smaller and upper two chambers of the heart) causing them to contract and push blood in to the larger and more powerful ventricles below.


With perfect timing this signal continues through the Bundle of His.  The signal splits and speeds along down the left and right bundle branches, making its way to the Purkinje fibers and turning north again. The larger T wave which then finishes off our heartbeat is the repolarization of the ventricles.  I know what you’re thinking, either “what in the what now goes where?” or hopefully, “what wave represents the repolarization of the atria”?  Well, the repolarization of the atria is buried in the larger signal of the QRS and therefore not visible on the graph. For example, my boyfriend is very fit and has a *huge* R wave (hands off his big left ventricle ladies, it’s all mine!  And don’t get me started on his early repolarization…and no…being early in this case is definitely not a bad thing). Willhelm Einthoven in 1903, for which he received the Nobel Prize in 1924.  More impressively, he also had a triangle named after him. I’d say you have some flawed thinking to assume you have learned everything there is about the EKG in a day. Such intelligent design could not have ‘just happened’ at once or over a series of efforts. It has also been validated as a tool for 30-day risk stratification of patients presenting to the emergency room with chest pain.[4] It is very likely the most commonly used tool for risk-stratification as it is the easiest to understand and use of those listed. If you interesting in "NASA Root Cause Analysis" powerpoint themes, you can download to use this powerpoint template for your own presentation template. Vitamin C intake of 1,500 mg per day decreases the risk of gout by 45% compared to 250 mg per day. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, renal and cardiovascular disease and thus at increased risk of death. As blepharitis is a chronic condition the symptoms can also recur and it is advised that lid hygiene be practised as part of your daily routine to prevent any further flare ups.
Presence of infectious process results in fever and hypermetabolic state, increasing insensible fluid losses.
To this time, however, the Gell and Coombs classification remains the most valid and useful framerwork for understanding hypersensitivity. For example haemolytic transfusion reactions (HTR) occur whenever a blood transfution between ABO incompatible individuals is carried out, the haemolytic disease of the newborn occurs whenever a mother Rh- produce an antibody response to Rh+, foetal RBC and serum sickness occurs whenever repeated and substantial doses of foreign serum is injected in patients for therapeutic purposes, as it occurred in the early days of serotherapy.
Atopic individuals thus are susceptible to either generalised anaphylaxis or local tissue reactions that involve a similar pathogenetic mechanism, namely asthma, hay fever, eczema or food allergies.
The principal mechanism responsible for tissue damage as a result of deposition of immune complexes is mediated by complement components, mainly the C3a and C5a anaphylotoxins, that attract phagocytes and mast cells and, following binding to complement receptors on the surface of such cells, lead to degranulation causing a local inflammatory reaction (vasodilation, increased vascular permeability, etc). Two strains of mice, one resistant and one susceptible to asthma were crossed and the F1 was backcrossed to the asthma-susceptible strain. This approach is the one which was first developed by George Snell in the late forties and which led him to the derivation of mouse strains (coisogenic or congenic resistant strains) that differed by only a single or a few closely linked histocompatibility gene (see lecture on Transplantation).
Tim1 (and perhaps the human PHF11 gene as well) also appear to be involved in the development of TH2 cells. This stimulates those Ventricular beefcakes to contract and deliver their payload to the lungs and body (if hearts had biceps, the left ventricle would be the proverbial “gun show”….it’s such a glory hog!). Even a slight shift in any of the complexes, the time, the distance, can mean so many things.
And to think that the heart and its operation is only a singular part of an organism with a myriad of other such amazements which all work together leads one to think that there must have been an exceptionally intelligent Designer of this thing called the human body when the first one was created a living being.
For viewing only, you can play with our flash based presentation viewer instead of downloading the ppt file.
This may be partly due to its association with insulin resistance, obesity but some of the increased risk appears to be independent. DKA is a life-threatening emergency caused by a relative or absolute deficiency of insulin.
The common feature of Type I, II and III is that in all cases the antibody reactions induce cell or tissue damage (hence it appears justified that Gell and Coombs define all these reactions Hypersensitivity) but in the majority of Type II and III reactions there is no individual susceptibility or exagerated response and, in the case of the HTR due to ABO incompatibility, there is not even a first sensitisation phase. Genetic linkage studies on the backcross defined a region on chromosome 2 containing the susceptibility gene(s) and the region was narrowed down to a smaller one through microarray expression analysis in the lung (see Fig C5 as a asthma susceptibility gene).
These linkage studies defined a region of chromosome 11 from which three genes (Tim1, 2 and 3) were cloned and named after the fact that the genes in question appeared to be homologous to Kim1, a gene that encodes the human receptor for the hepatitis A virus. In contrast ADAM33 (a membrane-bound mettaloproteinase) appears to be involved in tissue remodelling. This sure makes it difficult if not impossible to deny something like an all-knowing God had a very significant role in this, doesn’t it?
C5 appeared to be the only gene differentially expressed in the asthma-resistant and susceptible strains and located in the relevant region of chromosome 2.
Further evidence implying the Tim1 gene in asthma was also obtained from association studies in humans which demonstrated that a variant Tim1 gene inhibits the development of TH2 lymphocytes and asthma suceptibility. The genius method of the EKG is quite simple; however, it takes much more practice to be able to determine the many different cardiac pathologies by the reading of an EKG. Molecular cloning of the C5 gene from the asthma-susceptible strain demonstrated a 2 bp insertion which resulted in a truncated transcript and a non-functional gene product. Doctors have an absurb amount of education and trust me when I say we know a lot more then you guys in most aspects.Even an EM doc failing a paramedic exam does not matter. Correlating what you see from the 12 leads to a full understanding of cardiac physiology, in coordination with the rest of human physiology of concern is what takes many years.



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