Homeostasis Its Effect on the Critically Ill

Homeostasis Defined Homeostasis, according to Nirmalan and Nirmalan (2017), is the propensity for living organisms to maintain relative stability in the internal environment. Homeostasis is made possible through the cooperation of several regulatory mechanisms and separate sub-systems which make up the normal physiology of a living organism (Nirmalan & Nirmalan, 2017). During critical illnesses internal or external stress can make an attempt at interfering with the self-regulation systems beyond what is considered as normal range in physiology.

According to Palaparthi and Med (2017), the word homeostasis is derived from two Greek words i.e. ‘homeo’ (stands for similar) and ‘stasis’ (standing for stable). Homeostasis is the balance, equilibrium and the stability of the body or of the cell (Palaparthi & Med, 2017). Living organisms exhibit this character. The process of maintaining stability in the internal environment necessitates occasional internal adjustments as the environmental conditions continue to change outside and inside the cell. Continuous adjustments are necessary for the achievement of stability or equilibrium.

There are three distinct mechanisms useful in homeostasis regulation and they include Osmoregulation, chemical regulation and thermoregulation (Palaparthi & Med, 2017). There are various body systems responsible for performing these mechanisms such as the respiration system, nervous system, urinary system, reproductive system and the endocrine system. Khan Academy (2018) defines homeostasis as the propensity to oppose changes for the sake of maintaining stability and an internal environment that is relatively constant.

Homeostasis entails loops for negative feedback responsible for counteracting changes in the property of several target values, commonly referred to as the set points (Khan Academy, 2018). The loops for positive feedback, on the other hand, are responsible for amplifying the stimuli for initiation. These loops are responsible for stretching away from the starting point (Khan Academy, 2018). The positive feedback system is not common in the systems of biology (Palaparthi & Med, 2017). The positive feedback functions to quicken the direction that change is taking such as in lactation.

When a child is breastfeeding, mammary glands are massaged, therefore, causing the producing the prolactin hormone from the pituitary gland, where the hormone is secreted. Prolactin release occurs simultaneously in proportion to the act of breastfeeding from the baby. Thermoregulation The loop for negative regulation is a component of thermoregulation. It is the most common phenomena in biological system. In order to homeostasis equilibrium to be maintained the system is responsible for reversing any directional change. This helps to maintain things as they are constantly (Palaparthi & Med, 2017).

For example, when the levels of carbon dioxide are high in the air we breathe internal systems cause the lungs to exhale more carbon dioxide hence resulting to increased respiration. This process helps to maintain the levels of carbon dioxide at balance and also maintain normal lung function. Another example is the rise in body temperature. When the temperature rises the body will automatically cause the hypothalamus to sense the change in temperature. This will trigger some reaction from the brain.

The reaction cause the skin to release sweat and the blood vessels that are closer to the surface of the skin will dilate. This helps to lower the body temperature. The process is known as thermoregulation (Palaparthi & Med, 2017). It is a common phenomenon under the negative feedback system of regulation. Diagram 1 and 2 below is a pictorial representation of the changes that happen during high temperatures.

Source: Khan Academy (2018) Diagram 2 Source: Khan Academy (2018) Osmoregulation Osmosis is a fundamental process that occurs in the body for the purpose of ensuring proper cell function. Osmosis is the process that allows for water movement inside the body (Palaparthi & Med, 2017). The osmotic process takes place through a balancing between the backside and the front sides of cell membrane. This allows the cells’ biochemical process to take place effectively. There are two conditions that are likely to manipulate cell biochemical processes, therefore, resulting to cell death.

First of all when solutes become concentrated beyond what is considered as normal in extracellular fluids a reaction will be triggered. This reaction causes movement of intracellular fluid to the extracellular space, therefore, causing the cell to shrink (Palaparthi & Med, 2017). Secondly, when extracellular fluids solute levels decline a reaction that cause the extracellular fluids to move into the cell is triggered. This causes the cell to sell and eventually rapture when a certain limit is exceeded.

It is fundamental to maintain stability in solute concentration in order to allow for favorable conditions for proper organisms and cell function. This balance is maintained through two homeostasis processes known as diffusion and osmosis (Palaparthi & Med, 2017). Human beings are multicellular with trillions of body cells. Most of these cells are found inside the body of the human being and for this reason most of the cells are unable to interact with the external environment directly. Blood plasma happens to be a component of extracellular fluid inside an organism.

This extracellular fluid is derived from external environment. Body cells will frequently contact this extracellular fluid (Palaparthi & Med, 2017). Chemical regulation The regulation of glucose levels in the blood can be considered a negative feedback process. The level of blood glucose will go up after taking a meal. Insulin will be released from the pancreas after it senses a rise in blood glucose levels. Insulin is responsible for quickening the process of glucose transportation into select tissues from the blood (Palaparthi & Med, 2017).

The levels of blood glucose will consequently go down. This triggers a decline in the stimulus that causes insulin to be released. After the stimulus goes down insulin secretion falls as well (Palaparthi & Med, 2017). Encyclopedia Britannica (2018) compares homeostasis to a thermostat or a temperature regulator. The bimetallic strip on the thermostat is responsible for responding to changes in temperature through disruption or completion of the electric circuit.

When the room temperature goes down the circuit on the thermostat is completed therefore causing the temperature in the room to go up. The circuit is broken causing the furnace to stop heating up at preset level hence lowering the room’s temperature. Biological systems are much more complex than a thermostat. The two systems function to meet similar goals and that is sustaining activity at the range prescribed. It might be maintenance of the thickness of steel rolls or sustenance of circulatory system’s pressure (Encyclopedia Britannica, 2018).

Effects of Critical Illness on Homeostasis Critical illness causes life threatening situations that are characterized by intense metabolic and endocrine alterations (Ingels, Vanhorebeek & Van, 2018). Critical illnesses also disrupt the immune system responses. Overall this adds to the risk of sepsis and nosocomial infections (Ingels, Vanhorebeek & Van, 2018). There are two strategies of metabolism that can be used to alleviate nosocomial infections for critically ill patients. The first one is better control of blood glucose and the second is early restriction of macronutrient (Ingels, Vanhorebeek & Van, 2018).

Hyperglycemia is a common phenomenon among critically ill patients. It is an endocrine metabolism reaction to high stress levels. Hyperglycemia among the critically ill is a sign of poor outcome. Maintaining normal glycemic levels through rigorous insulin therapy is a proven way of reducing mortality and morbidity. Insulin therapy helps in the protection of vital organs from dysfunction. It also helps to prevent severe infections (Ingels, Vanhorebeek & Van, 2018). Insulin therapy helps to produce favorable outcome through the reduction of toxicity levels from high glucose levels in the blood.

Insulin therapy also helps protect the immune and vital organs cells from mitochondrial damage (Ingels, Vanhorebeek & Van, 2018). Hyperglycemia can also impair the burst capacity of the oxidative process and of macrophage phagocytosis. Through restoration of normal glycemic levels normal cell function is restored. The anti-inflammatory impact of insulin therapy can be effective in protecting host tissues from collateral damage as well.

Avoiding the use of parenteral nutrition in the 1st week of intensive care and allowing for deficit in macronutrient levels is an effective way of avoiding prevalence of secondary infections, better recovery and less weakness (Ingels, Vanhorebeek & Van, 2018). The impact of parenteral nutrition can be evidenced from autophagic processes. These processes can cause a compromise on removal of damaged cells and the defense mechanisms of the antimicrobial (Ingels, Vanhorebeek & Van, 2018).

Reduced intake of parenteral nutrition and insulin therapy for the purpose of alleviating infections and further damage to body metabolism processes has opened up an area of research which will allow for better improvement in the comprehension of organ failure, sepsis, and nosocomial infections for the critically ill. Due to the developments enjoyed in critical healthcare patients are now able to survive initial breakdown that causes them to require intensive care. Some intensive care patients remain under intensive care for extended periods otherwise known as prolonged critical illness phase.

This phase consists of acute metabolic and endocrine alterations when the immune system is not under proper regulation. This period is also characterized by suppression of the immune system and by inflammation (Ingels, Vanhorebeek & Van, 2018). The result of the prolonged phase of illness causes muscle weakness which further cause the critically ill patient to continue depending on support. The protracted illness also causes recurrence in sepsis and nosocomial infections. These infections further contribute to dysfunction of multiple organs and can even result to death (Gentile et al., 2012).

Effects of critical illness on homeostasis Intervention for prevention Disrupted immune system responses · Avoiding the use of parenteral nutrition sepsis and nosocomial infections · better control of blood glucose · early restriction of macronutrient Hyperglycemia · rigorous insulin therapy Glucose homeostasis alteration Hyperglycemia has been depicted as one of the endocrine metabolic reactions to stress (Cuesta & Singer, 2012). Hyperglycemia is a condition suffered by almost all patients who are critically ill. Stress hormones are responsible for inducing hyperglycemia. The stress hormones include glucagon, growth hormone, and cortisol etc.

Hyperglycemia drugs are known to worsen the release of stress hormone. Resistance to macronutrients, insulin, glycogenolysis, and gluconeogenesis causes hyperglycemia (Ingels, Vanhorebeek & Van, 2018). Hyperglycemic response has been explained as the adaptation process that occurs automatically to help the critically ill to survive. Hyperglycemia will often cause negative outcomes no matter the level of persistent and pronounced it is. Hyperglycemia is also identified as a sure predictor of mortality in hospitals (Ingels, Vanhorebeek & Van, 2018).

Dysfunction of the immune system for the critically ill Disturbance in the immune system takes place when the critical illness is protracted and acute (Marshall, Charbonney & Gonzalez, 2008). Subject to what stage the illness is at the response to immunity can be hypo-responsive or excessively activated. The adaptive and innate immune processes can be impacted on differently. There are new theories today about the conditions of inflammatory response and anti-inflammatory responses.

One of the theories claims that responses in the anti-inflammatory and pre-inflammatory conditions occur in the early stages and are stimulated after initial insult. If an early response from the pro-inflammatory process is intense it could cause exhaustion. When the initial impact is not dealt with in good time there is a good chance that the adaptive and innate immune systems will fail therefore leading to immune paralysis, immunosuppression and chronic paralysis (Ingels, Vanhorebeek & Van, 2018).

Another theory derived from data of gene expression concerning circulating leucocytes shows that early stimulation of the immune system that is innate beyond the phase of immune-paralysis can cause low inflammation. This will in turn cause mortality due to the irreversible organ damage (Cox, 2012). The causes of the immune variations are not yet properly understood. The reprogramming of leucocytes, acceleration of apoptosis and immune cells exhaustion are considered as possible contributors to damaged immunity.

According to recent proposals immune dysfunction that is acquired can cause impairment of the body defense system due to immune cell failure to take up metabolism of glucose. Immune cells that are in good shape have the capacity to cause glucose conversion for lactation. This is possible even during normal level so f glucose hence boosting production of energy for a strong reaction to inflammation. During secondary infections the metabolic adaptation process fells in WBC circulation.

This is probably as a result of epigenetic changes that take place during critical illness (Angus & Opal, 2016). Sepsis and nosocomial infections susceptibility As a result of the imbalances in the reformulation of the homeostasis mechanisms the critically ill face great danger of getting nosocomial infection. This infection causes mortality and morbidity. It also generates additional costs on the healthcare system (Ingels, Vanhorebeek & Van, 2018).

Moderate and short term hyperglycemia could have some benefits during acute illness or stress since it ensures that glucose supply to the immune cells is sustained. Persistent and severe hyperglycemia is detrimental though (Ingels, Vanhorebeek & Van, 2018). Hyperglycemia induced through stress can cause serious infections because high levels of glucose can negatively impact the fundamental constituents of innate immune reactions. Critical illness can interfere with the path of immunity, therefore, adding to risks of nosocomial infection.

The secondary infection is occasioned by fungi and opportunistic pathogens that come from stimulation of viruses such as cytomegalovirus (Ingels, Vanhorebeek & Van, 2018). Sepsis happens to be a clinical syndrome that is characterized by severe organ dysfunction that threatens life. The organ dysfunction is caused by impaired infection host response. It is a consequence to the malicious or undesirable adjustment to the immune response. Sepsis cause high mortality because of the excessive inflammation levels.

Immunosuppression following the initial stages of pro-inflammation is seen as being responsible for late mortality and morbidity (Hotchkiss, Monneret & Payen, 2013). Research done recently suggests that sepsis can either indirectly or directly result to impairment of every immune cell. Sepsis causes apoptosis acceleration in nearly all the immune cells therefore decreasing the capacity for antigen, cytotoxic levels and diminished cytokine production. Sepsis also causes a reduction in the production of antibodies (Hotchkiss, Monneret & Payen, 2013).

For these reasons sepsis is known to induce dysfunction in both the immune and innate immune reactions therefore contributing to damaged immune system, higher secondary infection risks and microbial challenge. Using Metabolic Processes to Alleviating Infections among the Critically Ill The conventional way or alleviating infection is reducing bacteria exposure among the critically ill. The process entails disinfection, surveillance and absolute hygiene as well as selective decontamination. Recent findings.