Normal and abnormal fluid distribution and function

Published April 15, 2013 by niniebulabula3161743

Normal functioning of cells and tissues is not only dependant on circulation of nutrients but also on normal fluid balance. In this blog i will be giving my insight on normal and abnormal fluid distribution and function, based on what i have learn’t during my lectures and from a couple of other sources. The different processes that I will be referring to are FLUID AND ELECRTROLYTE BALANCE, OEDEMA, HYPERAERMIA AND CONGESTION, HAEMORRHAGE, SHOCK, THROMBOSIS AND EMBOLISM, ISCHAEMIA AND INFARCTION.
FLUID AND ELECTROLYTE BALANCE
This module outlined the basics of fluid ditribution, such as the distribution of body water. I am now well aware that 2/3 of water are in the cells and 1/3 is in the extracellular compartment.(1.JJ RIPPEY 1994). If the balance of the fluid in the body is disrupted, different mechanisms are triggered such as thirst or urine loss (these are just simple examples, there are many more other mechanisms). Electrolyte imbalance is also to be considered in such a case, because it is most likely to be associated with the fluid imbalance. A simple example I can think of is during an episode of my intense exercise routines. I exercise 5 days a week, which 2 of those days I do vigorous exercise which consist mainly of cardiovascular exercise. I noticed that during these workout sessions i sweat more and my sweat is highly salty, my thirst becomes excessive, my breathing accelerates and my body heats up. This is my body’s response to loss of water and sodium(electrolyte) through sweating caused by heat generation in the body, this causes increased thirst signaling that I should replace the lost water by water intake. One would think sodium loss is not a big deal, i certainly did not think so before studying this module. A source stated that “low sodium levels can cause muscle cramping, dehydration and hyponatremia (dangerously low sodium levels in the blood.)”.(2.R.Morris, Are you a salty runner). After reading this statement it occured to me i had suffered the first two signs during exercise, i now know that it is due to low sodium levels.
The link below is for viewing a video about fluid and electrolyte balance in the body.
http://www.youtube.com/watch?v=_DDLTSwxzwg

figure1.
OEDEMA
Oedema is increased fluid in the interstitial tissue spaces or it is a fluid accumulation in the body cavities in excessive amount.(3.M Bezabeh 2004). Before studying this module the only knowledge I had about oedema is that its caused by fluid retension in the tissues, and it is manifested in kwashiorkor. Oedema can be generalised or localised.( JJ RIPPEY 1994). Example of localised oedema is pulmonary oedema : ” this usually occurs in left ventricular failure, it may occur in adult respiratory distress syndrome, the lung increases 2.3 times its normal weight”.(M Bezabeh 2004). An example of generalised oedema also known as anasarca is: “reduction of albumin due to excessive loss or reduced synthesis caused by liver cirrhosis, mulnutrition and protein-losing enteropathy.”( M Bezabeh 2004). For generalised oedema in the case of liver cirrhosis i deduce that this can be caused by by the effect of long term alcoholism. liver cirrhosis being the death of liver cells is bound to cause impaired liver functioning. Ascites is the edema in the peritoneal space.( JJ RIPPEY 2004). This phenomenon occurs in the liver during liver cirrhosis leading to abnormal functioning. There are many more types of localised and generalsied oedema besides the examples I have mentioned above.
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figure 2. pitting oedema an example of localised oedema.

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figure 3. oedema in face and eyelids due to renal oedema, an example og generalised oedema
HYPERAEMIA AND CONGESTION

This module was new knowledge for me, i did not know anything about hperaemia or congestion prior to studying this module. Both of them are a local increase in blood volume in particular tissue. Like oedema which is accumulation of fluid in particular tissue. So this is the common ground between these two modules, which made me understand this module easily.

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figure 4. this figure shows the normal flow of blood, hyperaemia and congestion.

Hperaemia – increased blood flow due to ateriole and artery dilation

Congestion – reduced venous drainage causing increased deoxygenated hemoglobin in blood.( JJ RIPPEY 1994)

During exercise hyperaemia is also manifested. “During exercise, skeletal muscle contractions induce an increase in blood flow (hyperaemia), proportional to the metabolic demand of tissue”. (4. P. Branney 2010). In case of congestion cardiac failure became apparent to me, with the congestion of the veins, the heart loses its ability to pump enough blood to the body’s tissue, therefore the tissues do not receive enough oxygen to function properly.

HAEMORRHAGE

This is the escape of blood from blood vessels, implying that there has been a damage to the vessel.( JJ RIPPEY 1994)

The most simple example of a hemorrhage would be a cut which leads to bleeding. The blood vessel has been damged, blood moves out externally. This is due to physical trauma. Another cause could be inadequate blood clotting due to too few or decreased platelet functioning or low amount of clotting factors in the blood.

subconjunctival hemorrhage

figure 5. A subconjuctival hemorrhage. blood vessel of the eye has been damaged causing bleeding into conjuctiva.

SHOCK

Before study of this module, i only associated the word  ‘Shock’ with horror or a disturbed emotional state. ” the term SHOCK can be regarded as a clinical description of a patient who is pale,  has clammy skin, a rapid thready pulse, low blood pressure and rapid respiration”. (JJ Rippey1994) I realised that my knowledge of the word ‘shock’ was not so far off the clinical term because when some one is ‘shocked’ they do show some of the clinical signs such as a cold sweat and rapid pulse. There are different types of shock

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Table 1. this table shows the different types of shock and how they effect the blood.

The first example of shock that came into mind after going through my notes is suicide attempt by wrist cutting or cutting as self mutilation. During these episodes the individual cuts themselves blood is lost, and if it is continuous bleeding it results in a state of cardiac arrythmia which would lead to hypovolaemic shock. In some cases this leads to death.

THROMBOSIS AND EMBOLISM

Thrombosis is defined as the formation of a solid or semisolid mass from the
constituents of the blood within the vascular system during life. ( M . Bezabeh 2004). I now know that thrombosis is due to haemostasis ( process that causes bleeding to stop). In a nut shell thrombosis is the clotting of blood in response to hemorrhage as a way of restoring homeostasis. the pathogenesis of thrombosis is endothelial injury, stasis or turbulence of blood flow and  blood coagulability. A typical example of thrombosis that I have come to know is Deep vein thrombosis (DVT). During this process blood clots in a vein of the leg, blood is not able to move through the vein as normal because of the block caused by the clot. the blood pressure in the vein increases causing swelling and pain. This swelling caused by blood can be referred to as edema. the video below shows how the process of thrombosis occurs in DVT. How deep vein thrombosis (DVT) forms

Thrombosis can lead to the fate of embolism. Embolus is a travelling thrombus, it travels from one part of the vascular system to another.” An arterial ebolism may be caused by one or more clots, which get stuck in the artery and block blood flow”.(5. DC .Dugdale 2012) In my first blog I discussed cell injury, ischaemia being one of the causes of injury which leads to necrosis( cell death). Since embolism causes a block in blood flow necrosis is due to take place. Hence embolism can lead to infarction.

ISCHAEMIA AND INFARCTION

As I have mentioned in blog 1 that infarction is due to necrosis, causing tissue to die . This is all due to reduced blood flow ( Ischaemia). ” Nearly 99% of all infarcts result from thrombotic or embolitic events” ( M. Bezabeh 2004). i found this fact very interesting, this showed how much of a big role thrombosis and embolism played in disease development. This shows how important normal blood flow through the body is. A healthy lifestyle will save you from all these damaging processes. The video below depicts the process of myocardial infarction due to thrombosis, and the risk factors that can lead to these processes.

http://www.youtube.com/watch?v=BL92vtuj9nc

CONCLUSION

The common ground between these modules is that they they fall under hemodynamic disorders. They involve blood movement in the circulation. In a case of each of these processes the body tries to alter the disorder by trying to achieve homeostasis. The body will produce signs and symptoms and different disease states in particular tissue as a way of maintaining balance. This helps to identify when an internal disorder takes place. For example: during edema, the abnormal accumulation of ECF in ICF tissue, the body alerts you of the disruption by producing swelling of the affected tissue.  With hyperaemia the body can manifest erythema, or in a case of congestive heart failure, shortness of breath, leg swelling and exercise intolerance can occur. In a case of hemorrhage seeing blood externally is not normal besides menstruation. Shock comes with its symptoms which i mentioned earlier on which are abnormal manifestations of the body. Thrombosis and embolism too are shown as disruptions during episodes of stasis blood in different tissues, resulting in edema. And infarctions due to ischaemia will show in the weakening of tissue as the tissue cells die and lose function.

REFERENCES

1. JJ Rippey, General pathology, 1994, Witswatersrand, pg 65, 75, 83, 89, 93.

2.R Morris,2013,Are you a salty sweater, http://www.runningplanet.com/training/salty-sweater.html.  21 March 2013.

3. M Bezabeh, General pathology, 2004, Jimma University, pg 61, 64, 72, 78.

4. P Branney, 2010, What causes exercise hyperaemia?, http://www.livestrong.com/article/333853-what-causes-exercise-hyperemia/  . 21 March 2013

5.DC Dugdale, 2012, Arterial ebolism, http://www.nlm.nih.gov/medlineplus/ency/article/001102.htm . 21 March 2013.

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