Definition and Pathophysiology of Shock

Shock is a syndrome of perfusion and cell oxygenation disruptions thoroughly so that tissue metabolic needs are not met. With the disruption of oxygenation results in impaired function of cells or tissues or organs, such as disturbances of consciousness, respiratory function, digestive system, urinary and circulatory system itself. In response to the decrease in oxygen supply, energy metabolism of cells will turn into anaerobic metabolism.

This situation can only be tolerated for a while, and if it continues, the damage of vital organ tissue happens that can lead to death. Shock is not a disease and not always accompanied by the failure of tissue perfusion. Shock can occur at any time to anyone. The handling is based on early right diagnosis.

Pathophysiology of shock

General:

Hypoperfusion in shock leads to the disruption of oxygen supply to cells, resulting in impaired cell metabolism and consequently the formation of ATP is reduced. Hypoperfusion also triggers reflex of sympathetic system activation that increases cardiac output. In addition, there is expenditure of ketokolamin, angiotensin, vasopressin and endothelia which will increase vascular tone so that perfusion pressure can be maintained and enough.

Hypoxia makes the tissue trying to extract O2 as much as possible so that the metabolic needs are met. When all the defense reflexes to the limit of tolerance and hypoxia are not resolved, it will disturb mitochondria, and decrease ATP formation. All systems in the body are not functioning, resulting in complete organ failure, such as brain failure, heart failure, vasoplegia, the buildup of lactic acid, kidney failure, digestive system failure followed by germ and toxic materials transfer into the bloodstream (translocation), and ending with death. Multiple organ failures and death are proportional to the duration and severity of hypoxia.

Specific:

Shock is divided into four types; hypovolemic, obstructive, cardiogenic, and distributive.

According to the value of cardiac output, shock is divided into two; hypodynamic and hyperdynamic shocks. In hypodynamic shock, cardiac output is below normal and central venous pressure is more than normal. Hypovolemic, cardiogenic, and obstructive shocks are included in this type of shock. In hyperdynamic shock, cardiac output value is more than the normal and central venous pressure is less than normal, e.g distributive shock.

Oral Lesions

Lesion is a term that indicates the state of abnormal body tissues. It can occur due to disease process either caused by infection, metabolic problems, autoimmune, or trauma (physical, electrical, chemical).

Oral mucosal lesion:

It is a lesion contained and on the body tissues of oral cavity. The terms used to describe the oral mucosal lesion are:

1. Erosion: the loss of partial surface of epithelium without opening the deeper layers or the connective tissue underneath.

2. Ulcer: The loss of the entire thickness of epithelium and the opening of the tissue underneath.

3. Vesicle: accumulation of clear bounded fluid, having a large diameter, which is more than 5 mm. It can be intraepithelial and singular or plural.

4. Bulla: accumulation of clear bounded fluid, having a diameter of 5 mm. It maybe intraepithelial or sub epithelial and singular or plural

5. Papule: narrow elevated area; clear bounded (the term is more often used to describe cutaneous abnormality of the mucosa lesions)

6. Macula: the area change clear bounded color. It may be small or large and singular or plural.

Wound Healing Phases

Definition of wound is partially lost or damaged body tissue.

Causes of Wound: trauma of sharp or blunt objects, temperature changes, chemicals, explosion, electric shock, or animal bites.

Wound Forms: cuts, puncture wounds, lacerations, abrasions, burns and others.

Wound Healing phases are as follows:

1. Inflammation Phase

It occurs since the injury until about the fifth day. Severed blood vessels in the wound will cause bleeding, and the body tries to stop it with vasoconstriction, shrinkage in broke up vessel edges (retraction), and hemostasis reaction. Hemostasis occurs because platelets out of the blood vessels attach to each other, and together form fibrin net, freeze the blood from the blood vessels. Adjacent platelets will granulate, release chemoattractant pulling inflammatory cells, and activate local fibroblasts and endothelial cells as well as a vasoconstrictor. Meanwhile, the inflammatory reaction happens.

After hemostasis, coagulation process will activate complement cascade, and then it will be released bradykinin and anaphylatoxin. Clinical signs and symptoms of inflammatory reaction become clear, in the form of redness due to dilated capillaries (rubor), warm sense (heat), pain (dolor) and swelling (tumor).

2. Proliferation Phase

It is called fibroplasia phase because the prominent part is proliferation of fibroblast.

It takes place from the end of inflammation phase until about the end of the third week.

Collagen fibers are formed and destroyed again to adjust the tension on the wound which tends to shrink. This trait together with miofibroblast contractile trait cause the pull on the wound edges.

The wound is filled by inflammatory cells, fibroblasts, and collagen, and the formation of new blood vessels (angiogenesis), forming reddish tissue with smooth protruding surface called granulation tissue.

With the covering of the wound surface, fibroplasia process with the formation of granulation tissue will also stop and start the process of maturation in remodeling phase.

3. Remodeling Phase

Maturation process happens which consists of re-absorption of the excess tissue, proper shrinkage according to the gravity, and finally re-formation of new tissue. Body tries to re-normalize all abnormal things because of healing process. Edema and inflammatory cells are absorbed, young cells become mature, new capillaries close and reabsorbed, excess collagen is absorbed and the rest shrinks according to the amount of strain. During this process, it is resulted pale scar tissue, thin, and flexible, and easily moved from the base.

Definition, Purpose and Mechanism of Inflammation

Inflammation is a complex reaction that begins to occur in the blood vessels in response to injury or wound, followed by accumulation of fluid and leukocytes in extravascular tissues. Inflammatory response takes place together with repair process.

Image : en.wikipedia.org

The purpose of inflammation is ruining, dissolving, or limiting the cause of injuries, and this process can in turn be transformed into a series of processes in order to repair the damaged tissue and healing. Repair is begun in the early phase of inflammation and finished when the injury effects are successfully neutralized. During the repair process, the injured tissue, parenchymal cell regeneration and filling the damaged areas by fibroblastic tissue occur.

Inflammation is a protective process to clean or remove the cause of injury (such as toxins or microbes) and the damage (such as cells or necrotic tissue). Without inflammation, infection can occur without control, the wound would not heal, and injured organ will remain sick. However, inflammation and repair processes are still potentially harmful, such as hypersensitivity reaction which can cause life-threatening, such as insect bites, drugs or toxins effects. 

Inflammatory reaction also underlies the development of many chronic diseases, such as atherosclerosis, rheumatoid arthritis, and pulmonary fibrosis. By this basic, it is developed a variety of anti-inflammatory which aims to improve the positive effects of inflammation and control the adverse effects.

The inflammatory response in vascularized connective tissue will involve plasma component, circulating blood cells (such as neutrophils, monocytes, eosinophil, lymphocytes, basophils, and platelets), blood vessels, and cellular components (such as mast cells, fibroblasts, macrophages, lymphocytes) and extracellular (such as collagen, elastin, fibronectin, laminin, etc.) connective tissue. The component parts form strong cellular communication tissues that end by increasing inflammatory response.

Vascular and cellular responses in acute and chronic inflammation are mediated by chemical mediators derived from plasma or cells that induced by inflammatory stimulus.