“It is easier to find men who will volunteer to die, than to find those who are willing to endure pain with patience.”
“It is easier to find men who will volunteer to die, than to find those who are willing to endure pain with patience.”
‘This is potentially a very important discovery which may go a long way to explain the marked differences in pain sensitivity and chronicity between women and men.”
says James McRoberts, a pain researcher at the University of California-Los Angeles
“When a loved one dies, you might be faced with grief over your loss again and again — sometimes even years later. Feelings of grief might return on the anniversary of your loved one’s death, birthday or other special days throughout the year. This is called anniversary reaction, its not a set back. You’re reflecting memories and that this loved one was important to you. To continue on the path toward healing, know what to expect — and how to cope with reminders of your loss.”
Losing someone or something you love or care deeply about is very painful. You may experience all kinds of difficult emotions and it may feel like the pain and sadness you’re experiencing will never let up. These are normal reactions to a significant loss. But while there is no right or wrong way to grieve, there are healthy ways to cope with the pain that, in time, can renew you and permit you to move on.
For me personally I lost an old friend this year and last year; and anyone out their who has had a loss recently I can relate with providing my deepest condolences to you but know you can move on. Like I told so many last year when my friend Karen died that she is in the next world including a friend Ken this year. Both are in a better world and both are so much happier out of misery but it is us on earth in misery but it will heal in time like a wound. The other thing to know is that both have never left us. They are both with old and new loved ones that they saw all the time and some rarely. They will never leave us helping us get through this rough time just like my father was there in 1999 when he died of cancer but never left me. I know my friends are so much happier, no longer ill and Karen is with her sister who she missed terribly with others she hasn’t seen for a long time. I know she is happier and no longer ill keeping a close eye on all loved ones she had in her life. As long as she is better off I know that is for the better which overrides my misery. Being a RN over 25 years seeing so many types of patients including being a oncology nurse loss of a loved one might be easier for me in dealing with than some but trust me I still have feelings like everyone else in this world. Karen what kills me the most is we reconnected this the year she died and planned to hangout more but God has his reasons for her to leave this world and we couldn’t do more time with each other in this world. I am very thankful I got to see her again last year and was there for her in getting through her few days left.
Grief is a natural response to loss. It’s the emotional suffering you feel when something or someone you love is taken away. The more significant the loss, the more intense the grief will be. You may associate grief with the death of a loved one—which is often the cause of the most intense type of grief—but any loss can cause grief, including: Divorce, loss of health, loss of a job, loss of financial stability, retirement, loss of a friendship, loss of a cherished dream (ex. spouses in their own business, planning to get married that never happens, loss of a mortgage on a new home, a loss of a baby, etc…).
The more significant the loss, the more intense the grief. However, even subtle losses can lead to grief. For example, you might experience grief after moving away from home, graduating from college, changing jobs, selling your family home, or retiring from a career you loved.
Grieving is a personal and highly individual experience. How you grieve depends on many factors, including your personality and coping style, your life experience, your faith, and the nature of the loss. The grieving process takes time. Healing happens gradually; it can’t be forced or hurried—and there is no “normal” timetable for grieving. Some people start to feel better in weeks or months. For others, the grieving process is measured in years. Whatever your grief experience, it’s important to be patient with yourself and allow the process to naturally unfold.
Dr Elisabeth Kübler-Ross pioneered methods in the support and counselling of personal trauma, grief and grieving, associated with death and dying. She also dramatically improved the understanding and practices in relation to bereavement and hospice care. This is quite aside from the validity of her theoretical work itself, on which point see the note, right.
Her ideas, notably the five stages of grief model, the model was first introduced by American Psychiatrist Elisabeth Kübler-Ross in her 1969 book, On Death and Dying, and was inspired by her work with terminally ill patients but simply a significant loss can experience these steps as well. They are: 1.) Denial 2.) Anger 3.) Bargaining 4.) Depression 5.) Acceptance . You go through all these steps in a loss and repeat them and not in order for all. Contrary to popular belief, you do not have to go through each stage in order to heal. In fact, some people resolve their grief without going through any of these stages. And if you do go through these stages of grief, you probably won’t experience them in a neat, sequential order, so don’t worry about what you “should” be feeling or which stage you’re supposed to be in.Kübler-Ross herself never intended for these stages to be a rigid framework that applies to everyone who mourns. In her last book before her death in 2004, she said of the five stages of grief: “They were never meant to help tuck messy emotions into neat packages. They are responses to loss that many people have, but there is not a typical response to loss, as there is no typical loss. Our grieving is as individual as our lives.”
While loss affects people in different ways, many experience the following symptoms when they’re grieving. Just remember that almost anything that you experience in the early stages of grief is normal—including feeling like you’re going crazy, feeling like you’re in a bad dream, or questioning your religious beliefs.
Symptoms of Grief: Shock and disbelief – Right after a loss, it can be hard to accept what happened. Sadness – Profound sadness is probably the most universally experienced. Guilt – You may regret or feel guilty about things you did or didn’t say or do. Anger – Even if the loss was nobody’s fault, you may feel angry and resentful. If you lost a loved one, you may be angry with yourself, God, the doctors, or even the person who died for abandoning you. You may feel injustice has been done to you. Fear – A significant loss can trigger a host of worries and fears. You may feel anxious, helpless, or insecure. You may even have panic attacks. You may feel fears of how do I live without this person. Physical Symptoms – We often think of grief as a strictly emotional process, but grief often involves physical problems, including fatigue, nausea, lowered immunity, weight loss or weight gain, aches and pains, and insomnia.
Coping with grief and loss is one get support.
The single most important factor in healing from loss is having the support of other people. do not grieve alone. Connecting to others will help you heal.
Finding support after a loss
Article is all from the Mayo clinic Nov 2012
“Sepsis is the systemic response to infection and is defined as the presence of SIRS (systemic inflammatory response syndrome) in addition to a documented or presumed infection.”
Part 3 talks to you about the multi-hit theory of SIRS with Inflammatory Cascade of SIRS and lastly the coagulation process in SIRS. It also tells you an extensive amount of infectious and non-infectious causes of SIRS. Lastly the key antidote to SIRS.
A multi hit theory behind the progression of SIRS to organ dysfunction and possibly multiple organ dysfunction syndrome (MODS). In this theory, the event that initiates the SIRS cascade primes the pump. With each additional event, an altered or exaggerated response occurs, leading to progressive illness. The key to preventing the multiple hits is adequate identification of the ETIOLOGY or CAUSE of SIRS and appropriate resuscitation and therapy.
Trauma, inflammation, or infection leads to the activation of the inflammatory cascade. Initially, a pro-inflammatory activation occurs, but almost immediately thereafter a reactive suppressing anti-inflammatory response occurs. This SIRS usually manifests itself as increased systemic expression of both pro-inflammatory and anti-inflammatory species. When SIRS is mediated by an infectious insult, the inflammatory cascade is often initiated by endotoxin or exotoxin. Tissue macrophages, monocytes, mast cells, platelets, and endothelial cells are able to produce a multitude of cytokines. The cytokines tissue necrosis factor–alpha (TNF-α) and interleukin-1 (IL-1) are released first and initiate several cascades.
The release of certain factors without getting into medical specific terms they ending line induces the production of other pro-inflammatory cytokines, worsening the condition.
Some of these factors are the primary pro-inflammatory mediators. In research it suggests that glucocorticoids may function by inhibit-ing certain factors that have been shown to be released in large quantities within 1 hour of an insult and have both local and systemic effects. In studies they have shown that certain cytokines given individually produce no significant hemodynamic response but that they cause severe lung injury and hypotension. Others responsible for fever and the release of stress hormones (norepinephrine, vasopressin, activation of the renin-angiotensin-aldosterone system).
Other cytokines, stimulate the release of acute-phase reactants such as C-reactive protein (CRP) and pro-calcitonin.
The pro-inflammatory interleukins either function directly on tissue or work via secondary mediators to activate the coagulation cascade and the complement cascade and the release of nitric oxide, platelet-activating factor, prostaglandins, and leukotrienes.
High mobility group box 1 (HMGB1) is a protein present in the cytoplasm and nuclei in a majority of cell types. In response to infection or injury, as is seen with SIRS, HMGB1 is secreted by innate immune cells and/or released passively by damaged cells. Thus, elevated serum and tissue levels of HMGB1 would result from many of the causes of SIRS.
HMGB1 acts as a potent pro-inflammatory cytokine and is involved in delayed endotoxin lethality and sepsis.
Numerous pro-inflammatory polypeptides are found within the complement cascade. It is thought they are felt to contribute directly to the release of additional cytokines and to cause vasodilatation and increasing vascular permeability. Prostaglandins and leukotrienes incite endothelial damage, leading to multi-organ failure.
Polymorphonuclear cells (PMNs) from critically ill patients with SIRS have been shown to be more resistant to activation than PMNs from healthy donors, but, when stimulated, demonstrate an exaggerated micro-bicidal response (agents that kill microbes). This may represent an auto-protective mechanism in which the PMNs in the already inflamed host may avoid excessive inflammation, thus reducing the risk of further host cell injury and death.
The correlation between inflammation and coagulation is critical to understanding the potential progression of SIRS. IL-1 and TNF-α directly affect endothelial surfaces, leading to the expression of tissue factor. Tissue factor initiates the production of thrombin, thereby promoting coagulation, and is a proinflammatory mediator itself. Fibrinolysis is impaired by IL-1 and TNF-α via production of plasminogen activator inhibitor-1. Pro-inflammatory cytokines also disrupt the naturally occurring anti-inflammatory mediators anti-thrombin and activated protein-C (APC).
If unchecked, this coagulation cascade leads to complications of micro-vascular thrombosis, including organ dysfunction. The complement system also plays a role in the coagulation cascade. Infection-related pro-coagulant activity is generally more severe than that produced by trauma.
What the causes of SIRS can be:
The etiology of systemic inflammatory response syndrome (SIRS) is broad and includes infectious and noninfectious conditions, surgical procedures, trauma, medications, and therapies.
The following is partial list of the infectious causes of SIRS:
“SIRS can be incited by ischemia, inflammation, trauma, infection or a combination of several “insults”. SIRS is not always associated with infection. While not universally accepted, some have proposed the terms “severe SIRS” and “SIRS shock” to describe serious clinical syndromes that are not infectious in nature and thus cannot be labeled according to the various sepsis definitions”
Steven D. Burdette M.D. (Infectious Disease Medicine M.D.– Wright State Physicians in Dayton, Ohio – http://www.healthgrades.com/physician/dr-steven-burdette-yhfgy)
“The idea behind defining SIRS was to define a clinical response to a nonspecific insult of either infectious or noninfectious origin. In 1992, the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) introduced definitions for systemic inflammatory response syndrome (SIRS), sepsis, severe sepsis, septic shock, and multiple organ dysfunction syndrome MODS).”
It is the body’s response to an infectious or noninfectious insult. Although the definition of Systemic Inflammatory Response Syndrome (SIRS) refers to it as an “inflammatory” response, it actually has pro- and anti-inflammatory components. SIRS is a serious condition related to systemic inflammation, organ dysfunction, and organ failure. It is a subset of cytokine storm, in which there is abnormal regulation of various cytokines. Cytokines are this, the term “cytokine” is derived from a combination of two Greek words – “cyto” meaning cell and “kinos” meaning movement. Cytokines are cell messaging or signaling molecules that aid cell to cell communication in immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma.
Cytokines exist in peptide, protein and glycoprotein (proteins with a sugar attached) forms. The cytokines are a large family of molecules that are classified in various different ways due to an absence of a unified classification system. Protein is acidic as opposed to being alkalinic.
Examples of cytokines include the agents interleukin and the interferon which are involved in regulating the immune system’s response to inflammation and infection.
SIRS, independent of the etiology/cause, has the same pathophysiologic properties, with minor differences in inciting cascades. Many consider the syndrome a self-defense mechanism. Inflammation is the body’s response to nonspecific insults that arise from chemical, traumatic, or infectious stimuli. The inflammatory cascade is a complex process that involves humoral and cellular responses, complement, and cytokine cascades. Best summarized in the relationship between these complex interactions and SIRS is it is in the following 3-stage process. Here is a simple explanation in what occurs without taking pages in explaining the stages to you.
Following an insult to the body, cytokines are produced at the site. Local cytokine production incites an inflammatory response, thereby promoting wound repair and recruitment of the reticular endothelial system. This process is essential for normal host defense homeostasis and if absent is not compatible with life. Local inflammation, such as in the skin and subcutaneous soft tissues occurs.
What occurs is rubor or redness at the site that reflects local vasodilation of vessels. What is caused by release of local vasodilation of the vessels at the area of where the insult starts in the body is substances like nitric oxide (NO) and prostacyclin get released=Acidic.
Tumor or swelling occurs due to vascular endothelial (layer of the skin) tight junction disruption and the local extravasation of protein-rich fluid into the interstitium (layer of the skin), which also allows activated white blood cells to pass from the vascular space (blood stream) into the tissue space to help clear infection and promote repair.
Dolor is pain and represents the impact inflammatory mediators have on local somatosensory nerves. Presumably, this pain stops the host from trying to use this part of his or her body as it tries to repair itself.
The increased heat primarily due to increased blood flow occurs but also increased local metabolism as white blood cells become activated and localize to the injured tissue.
Finally, the loss of function, a hallmark of inflammation and a common clinical finding of organ dysfunction with the infection is isolated to a specific organ (ex. pneumonia—acute respiratory failure; kidney—acute kidney injury. pancreatitis– inflammation of the pancreas).
Importantly, on a local level, this cytokine and chemokine release by attracting activated leukocytes to the region may cause local tissue destruction (ex. abscess) or cellular injury (ex. pus), which appear to be the necessary byproducts of an effective local inflammatory response. Local infection signs & symptoms= puss, swelling. skin temperature hot, pain and redness to the where the insult of the body is.
Ending line what happens is an insult occurs in the body, there is local cytokine production with the goal of inciting an inflammatory response thereby promoting wound repair and recruitment of the reticular endothelial system. Your body is compensating in reacting normally to this insult.
Small quantities of local cytokines are released into the circulation, improving the local response. This leads to growth factor stimulation and the recruitment of macrophages and platelets. This acute phase response is typically well controlled by a decrease in the pro-inflammatory mediators and by the release of endogenous antagonists; the goal is homeostasis. At this stage, some minimal malaise (general weakness)and low-grade fever may become show.
Putting it simple what occurs here is small quantities of local cytokines are released into circulation to improve the local response. This leads to growth factor stimulation and the recruitment of macrophages (cells eating up toxins to the body) and platelets (that are cells the coagulate-cause clotting). This acute phase response is typically well controlled by a decrease in the proinflammatory mediators and by the release of endogenous antagonists. The goal is homeostasis – the body still trying to compensate and react productively to this insult to the body.
If homeostasis is not restored and if the inflammatory stimuli continue to seed into the systemic circulation, a significant systemic reaction occurs. The cytokine release (acidic) leads to destruction rather than protection. A consequence of this is the activation of numerous humoral cascades and the activation of the reticular endothelial system and subsequent loss of circulatory integrity. The body at this stage is decompensating and not productively fighting off this insult to the body and this leads to end-organ dysfunction.
Tune in tomorrow to part 3 of SIRS the conclusion of this topic (extensive noninfectious and infectious causes with more on coagulation and multi cascading reactions in the body due to SIRS).