Tuesday, January 26, 2010

Causes of inflammation



CAUSES OF INFLAMMATION


1. Burn. type of skin injury that may be caused by heat, electricity, chemicals, light, radiation or friction.


2. Physical trauma. refers to physical injury generally of a considerably severe degree.


3. Infection by pathogens. detrimental colonization of a host organism by a foreign specie, the infecting organism seek to utilize the host's resources to multiply, usually at the expense of the host.


Five General Signs of Inflammation


a. rubor(redness)

b. Calor(heat)

c. Dolor(pain)

d. Tumor(swelling/ edema)

e.functio laesa(loss of function)

Anti- inflammatory Medications

ANTI-INFLAMMATORY DRUGS
NSAIDs(non-steroidal anti-inflammatory drugs)- drugs with analgesic, antipyretic and in higher doses with anti inflammatory effects.

most prominent member of this group are as follows: aspirin, naproxen, ibuprofen

  • Aspirin. it releives pain and reduces inflammation and fever. It is the world's most widely used drugs

  • Naproxen. used to reduce inflammation and pain especially in the treatment of arthritis.

  • Ibuprofen. used especially in the tx of arthritis and commonly taken for its antypyretic and anti inflammatory properties.

Mode of action:

NSAIDs acts as a non-selective inhibitor of the enzyme cyclooxygenase inhibiting both cyclooxygenase-1 and 2 isoenzymes. COX catalyzes the formation of prostagladins from arachidonic acid as messenger molecules in the process of inflammation.


Adverse effect:

  • Direct and indirect irritation of the GI tract result in nausesa and vomiting, dyspepsia etc.
  • nephrototoxicity

  • CNS- seizure

Inflammatory disorders

The immune system is often involved with inflammatory disorders.
Some of the disorders associated with inflammation include:

1. Acne Vulgaris. A common human skin disease characterized by areas of skin with multiple non-inflammatory follicular papulesAcne lesions is commonly referred to as pimples. The face and upper neck are the areas which are commonly affected.


Causes:

  • Family/ genetic history
  • hormonal activity
  • stress
  • hyperactive sebaceous gland
  • bacteria in the pores
  • inflammation

2.Asthma. It is a chronic inflammatory disease of thje airways that causes airway hyperresponsiveness, mucosal edema and mucus production. It is the most common chronic disease of the childhood and can occur at any age.

Causes:

  • Environmental
  • Genetic
  • Gene-environmental factors

3. Autoimmune Disease. arise from an overactive immune response of the body againts foreign substances and tissues normally present in the body. The immune system mistakes some part of the body as pathogen and attack it. The tx with autoimmune disease is usually immunosuppression-medication which dereases immune response.

4. Rheumatoid arthritis. a chronic systemic inflammatory disorder that may affect many tissues and organs, but principally attack the joints producing inflammatory sinoviatis that often progresses to destruction of the articular cartilageand ankylosis of the joints.









migration and emigration process



movements of chemical mediators to the injured area





Systemic Effect

An infectious microorganisms can escape the confines of the immediate tissue via the circulatory system where it may spread to other parts of the body.

Systemic effect happens when inflammation overwhelms the host. When it is due to infection the term sepsis is applied.


Systemic inflammation and obesity

With the discovery of interleukins the concepts of systemic inflammation developed. Systemic inflammation is not confined to a particular tissue but involved the endothelium and other organ system.

Systemic response to inflammation

SYSTEMIC RESPONSE TO INFLAMMATION


The inflammatory response is often confined to the site, causing only local s/Sx. However, systemic responses can also occur.

Fever is the most common sign of a systemic response to injury, and it most likely caused by endogenous pyrogens (internal substances that cause fever released from neutrophils and macrophages). These substances reset the hypothalamic thermostat, which controls body temperature, and produce fever. Leukocytosis, an increase in the synthesis and release of neutrophils from bone marrow, may occur to provide the body with greater ability to fight infection. general nonspecific symptoms develop, including malaise, loss of appetite, aching, and weakness.


Local effects:
  • erythema
  • warmth
  • edema
  • pain
  • impaired functioning

Systemic effects:

  • Fever
  • leukocytosis
  • malaise
  • anorexia
  • sepsis

Aspects of disease process

Four Aspects of Disease Process

1. Etiology. Refers to the cause of the disease.

a. Microorganisms.

b. Risk factors.

b.1. Modifiable (diet, lifestyles, vices)

b.2. Non-modifiable (age, gender, heredity)

2.Morphological. In connection to the tissue affected.

3. Physiology.

4. Signs and symptoms.


INFLAMMATORY RESPONSES

Vascular changes
  • Vasodilation
  • Increase capillary permeability
  • Increase blood flow
  • Local tissue congestion
Cellular changes
  • Phagocytosis
  • Increase leukocytes
  • Release of chemical mediators

Inflammation- pathophysiology

PATHOPHYSIOLOGY:
The occurrence of tissue injury promotes vasodilation(can accommodate more blood) therefore more blood flow to the injure area, this leads to rubor(redness) accompanied by callor(heat). As tissue injury is happening cellular permeability(blood) increases that leads to the exudation of CHON this further attracts more water and this results in edema(tumor) accompanying pain due to the pressure exerted to the nerve endings.

Chemical Mediators of Inflammation
Injury initiates the inflammatory response, but chemical substances released at the site induce the vascular changes. Foremost among these chemicals are histamine and kinins.
Hiatamine is present in many tissues of the body but is concentrated in the mast cells. It is release when injury occurs and responsible for the early changes in vasodilation and vascular permeability.
Kinins increase vasodilation and vascular permeability and they also attract neutrophils to the area.
Prostaglandins, another group of chemical substances. are also suspected of causing increased permeability.

2nd and 3rd stage of inflammatory response

SECOND STAGE: EXUDATE PRODUCTION
In the second stage of inflammation the inflammatory exudate is produced, consisting of fluid that escaped from the blood vessels, dead phagocytic cells, and dead tissue cells and products that they release. During this stage the injurious agents is overcome, and the exudate is cleared away by lymphatic drainage.
Major Types of Exudate
Serous- the exudate composition is mainly serous fluid has the consistency of water and clear in color.
Purulent- exudate with the presence or composition of of pus.
Sanguineous- exudate compose of blood, also known as hemorhagic.
THIRD STAGE: REPARATIVE PHASE
This stage involves the repair of injured tissues by regeneration or replacement with fibrous tissue formation. Regeneration is the replacement of destroyed tissue cells by cells that are identical or similar in structure and function. Damaged cells are replaced one by one but also cells are organized so that the architectural pattern and function of the tissue are restored.
When regeneration is not possible, repair occurs by fibrous tissue formation. Damagen tissue are replaced with the connective tissue elements of collagen, blood capillaries, lymphatics and other tissue-bound substances.
In the early stage of this process, the tissue is called granulation tissue appearing pink or red because of the many newly formed capillaries. Later in the process the tissue shrinks and the collagen fibers contract so that a firmer fibrous tissue remains called cicatrix or scar.

Stages of inflammatory response: first stage



STAGES OF INFLAMMATORY RESPONSE

First Stage: Vascullar and Cellular Response




At the start of the first stage of inflammation, blood vessels at the site of injury constrict followed by dilation of small blood vessels. Thus, more blood flows to the injured area. This marked increase in blood supply is referred to as hyperemia and is responsible for the characteristics sign of redness and heat.


Vascular permeability increases at the site with dilation of the vessels in response to cell death, the release of chemical mediators and the release of histamine. Fluids, proteins and leukocytes leak into the insterstitial spaces, and the sign of inflammation swelling and pain appear. Pain is caused by the pressure of accumulating fluid on the nerve endings.


Blood flow slows in the dilated vessels. allowing more leukocytes to arrive at the injured tissues. leukocytes line up along the inner surface of the blood vessels- a process called margination,


then move through the blood vessel wall into the affected tissue spaces , a process called emigration. Leukocytosis happens in response to the exit of leukocytes from the blood.

Introduction. Definition of inflammation

INFLAMMATION


  • a localized respone to a tissue injury.

  • a defensive reaction intended to neutralize, control or eliminate the offending agent and to prepare the site for repair.

  • a nonspecific response that is meant to serve a protective function .
  • occurs in cell injury events like strokes and myocardial infarction.







Types of inflammation
Inflammation is categorized primarily by its duration and the type of exudate produced. It may be acute, subacute or chronic.

1. Acute inflammation. characterized by the local vascular and exudative changes earlier and usually last less than 2 weeks. The response is immediate and serves a protective function, after the injurious agent is removed the inflammation subsides.

2. Chronic inflammation. It develops if the injurious agent persist and the acute response is perpetuated. Symptoms are present for many months or years. A cycle of cellular infiltration, necrosis and fibrosis begins.

3. Subacute inflammation. It falls between acute and chronic inflammation It includes elements of active exudative phase of the acute response as well as elements of repair, as in chronic phase.

Anatomic and Physiologis Barriers


  • intact skin and mucous membranes (skin contains resident bacteria; acidity also inhibits bacterial growth

  • mucous membranes and cilia
  • lungs have alveolar macrophages

  • salive (contains microbial inhibitors such as lactoferrin, lysoyme and secretory IgA

  • Eye produces tears (teras contain lysozyme)

  • GIT (high acidity of the stomach, peristalsis)