Question

Nursing/homework one paragraph for each question, no hand writing please, require Nursing research, citations and reference

1. Describes the processes of Pulmonary Disease

2. What lines of defense are you enhancing by putting on an antibiotic ointment and covering a wound with a bandaid?

3. What are the inflammatory mediators within white blood cells?

4. Differentiate between vascular response to tissue injury versus cellular response to tissue injury?

5. What does an elevation in leukocytes, sedimentation rate (ESR) or C-reactive protein (CRP) tell you about the location of acute or chronic inflammation?

6. Gastritis is a common disease (acute or chronic). Explain how anti-inflammatory drugs that inhibit prostaglandins can cause or further exacerbate gastritis.

Answer 1

1. Pulmonary Diseases

Lung disease is any problem in the lungs that prevents the lungs from working properly. There are three main types of lung disease:

1. Airway diseases -- These diseases affect the tubes (airways) that carry oxygen and other gases into and out of the lungs. They usually cause a narrowing or blockage of the airways. Airway diseases include asthma, COPD and bronchiectasis. People with airway diseases often say they feel as if they're "trying to breathe out through a straw."
2. Lung tissue diseases -- These diseases affect the structure of the lung tissue. Scarring or inflammation of the tissue makes the lungs unable to expand fully (restrictive lung disease). This makes it hard for the lungs to take in oxygen and release carbon dioxide. People with this type of lung disorder often say they feel as if they are "wearing a too-tight sweater or vest." As a result, they can't breathe deeply. Pulmonary fibrosisand sarcoidosis are examples of lung tissue disease.
3. Lung circulation diseases -- These diseases affect the blood vessels in the lungs. They are caused by clotting, scarring, or inflammation of the blood vessels. They affect the ability of the lungs to take up oxygen and release carbon dioxide. These diseases may also affect heart function. An example of a lung circulation disease is pulmonary hypertension. People with these conditions often feel very short of breath when they exert themselves.

2. Line of Defenses

First Line of Defense

Your body’s first line of defense is like a castle’s moat and walls. It keeps most pathogens out of your body. The first line of defense includes physical(skin), chemical(Mucus, enzymes, Acids etc.), and biological(Normal Flora) barriers.

Second Line of Defense

Did you ever get a splinter in your skin, like the one in Figure below? It doesn’t look like a serious injury, but even a tiny break in the skin may let pathogens enter the body. If bacteria enter through the break, for example, they could cause an infection. These bacteria would then face the body’s second line of defense.

Using antibiotic ointment and covering a wound with a bandaid we prevent the infection in the wound.

in first line of defense body do these things

so, we enhancing the first line of defense.

3. Inflamatory mediators in WBCs

Name	Type	Source	Description
Lysosome granules	Enzymes	Granulocytes	These cells contain a large variety of enzymes that perform a number of functions. Granules can be classified as either specific or azurophilic depending upon the contents, and are able to break down a number of substances, some of which may be plasma-derived proteins that allow these enzymes to act as inflammatory mediators.
Histamine	Monoamine	Mast cells and basophils	Stored in preformed granules, histamine is released in response to a number of stimuli. It causes arteriole dilation, increased venous permeability, and a wide variety of organ-specific effects.
IFN-γ	Cytokine	T-cells, NK cells	Antiviral, immunoregulatory, and anti-tumour properties. This interferon was originally called macrophage-activating factor, and is especially important in the maintenance of chronic inflammation.
IL-8	Chemokine	Primarily macrophages	Activation and chemoattraction of neutrophils, with a weak effect on monocytes and eosinophils.
Leukotriene B4	Eicosanoid	Leukocytes, cancer cells	Able to mediate leukocyte adhesion and activation, allowing them to bind to the endothelium and migrate across it. In neutrophils, it is also a potent chemoattractant, and is able to induce the formation of reactive oxygen species and the release of lysosomal enzymes by these cells.
LTC4, LTD4	Eicosanoid	eosinophils, mast cells, macrophages	These three Cysteine-containing leukotrienes contract lung airways, increase micro-vascular permeability, stimulate mucus secretion, and promote eosinophil-based inflammation in the lung, skin, nose, eye, and other tissues.
5-oxo-eicosatetraenoic acid	Eicosanoid	leukocytes, cancer cells	Potent stimulator of neutrophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation; monocyte chemotaxis; and with even greater potency eosinophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation.
5-HETE	Eicosanoid	Leukocytes	Metabolic precursor to 5-Oxo-eicosatetraenoic acid, it is a less potent stimulator of neutrophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation; monocyte chemotaxis; and eosinophil chemotaxis, lysosome enzyme release, and reactive oxygen species formation.
Prostaglandins	Eicosanoid	Mast cells	A group of lipids that can cause vasodilation, fever, and pain.
Nitric oxide	Soluble gas	Macrophages, endothelial cells, some neurons	Potent vasodilator, relaxes smooth muscle, reduces platelet aggregation, aids in leukocyte recruitment, direct antimicrobial activity in high concentrations.
TNF-α and IL-1	Cytokines	Primarily macrophages	Both affect a wide variety of cells to induce many similar inflammatory reactions: fever, production of cytokines, endothelial gene regulation, chemotaxis, leukocyte adherence, activation of fibroblasts. Responsible for the systemic effects of inflammation, such as loss of appetite and increased heart rate. TNF-α inhibits osteoblast differentiation.
Tryptase	Enzymes	Mast Cells	This serine protease is believed to be exclusively stored in mast cells and secreted, along with histamine, during mast cell activation.

4.

Vascular Response to tissue injury

In the early stages of inflammation, the affected tissue becomes reddened and swollen, due to increased blood flow and to edema fluid. The vascular events of the acute inflammatory response involve three main processes.

• changes in vessel caliber and, consequently, flow

• increased vascular permeability and

• formation of the fluid exudate

Cellular Response to tissue injury

Collectively, you can refer to any injury to the tissue of the body as the inflammatory response. After the tissue is damaged, you'll get chemotaxis of immune cells into the region using chemotactic chemicals. For instance, mast cells produce histamine which causes nearby capillaries to vasodilate and become "leaky" allowing other white blood cells to infiltrate the area. The list of chemicals that can cause chemotaxis is extensive: prostaglandins, kinins, complement, etc. In addition, damaged cells release substance P, which interacts with neurons to send signals to the brain indicating damage, aka pain. This allows the brain to mobilize and send signals modifying the behavior of blood vessels, lymphatic organs, etc. Depending on the type of injury, proteins called fibrins may wall off the damaged tissue to keep the damage from spreading (i.e. a bacterial infection) in a process very similar to blood clotting. White blood cells that infiltrate the area begin determining the type of damage and either prepare for "battle," in the case of infection, or for clean-up, in the case of physical damage like a cut. Once the area has been cleared of pathogens and/or cellular debris, the white blood cells exfiltrate the area or die and are phagocytosed by other white blood cells and a series of regenerative chemicals are released to encourage tissue regrowth. That's where it gets truly complicated as each tissue's regenerative capabilities are different. Some tissues like the liver seem to be able to completely regenerate over time. Others like nervous tissue and skin regenerate with fibrous connective tissue, instead of remaking themselves the way they were before. And the extent of the damage plays a role as well, so other than the basic inflammatory response as a general method for responding to injury, I can't give you any more than that.

5.

C-reactive protein

C-reactive protein has an important role in many parts of the inflammatory process. It is involved in the innate immune response by attaching to microorganisms and damaged cellular components via phosphocholine. This leads to complement activation and phagocytosis. Although C-reactive protein activation of complement increases inflammation and tissue damage, it also has some anti-inflammatory actions, thus it acts as a promoter and down-regulator of inflammation.

C-reactive protein is a useful marker of the acute phase reaction as it responds quickly to the inflammatory process, whether it is an infection, autoimmune disease or tissue necrosis.² C-reactive protein has a doubling time and a decay time of around six hours, and maximal concentrations are reached in less than two days. After the inflammation has resolved, concentrations fall rapidly. Once inflammation and its cause have been identified and treatment is started, there is usually no need for further C-reactive protein measurements.

Erythrocyte sedimentation rate

The erythrocyte sedimentation rate is a surrogate marker of the acute phase reaction. During an inflammatory reaction, the sedimentation rate is affected by increasing concentrations of fibrinogen, the main clotting protein, and alpha globulins. The test mainly measures the plasma viscosity by assessing the tendency for red blood cells to aggregate and ‘fall’ through the variably viscous plasma.

However, the sedimentation rate is often and significantly affected by many factors other than the acute phase reaction. Known influences include:

• plasma albumin concentration

• size, shape and number of red blood cells

• non-acute phase reaction proteins, in particular normal and abnormal immunoglobulins.

Leukocytosis

Leukocytosis is white cells (the leukocyte count) above the normal range in the blood. It is frequently a sign of an inflammatory response, most commonly the result of infection, but may also occur following certain parasitic infections or bone tumors as well as leukemia. It may also occur after strenuous exercise, convulsions such as epilepsy, emotional stress, pregnancy and labor, anesthesia, as a side effect of medication (e.g. Lithium), and epinephrine administration.

There are five principle types of leukocytosis:

1. Neutrophilia (the most common form)
2. Lymphocytosis
3. Monocytosis
4. Eosinophilia
5. Basophilia

6.how anti-inflammatory drugs that inhibit prostaglandins can cause or further exacerbate gastritis

Prostaglandins are found in high concentration in the gastric mucosa and gastric juice. Exogenous prostaglandins inhibit acid secretion, stimulate mucus and bicarbonate secretion, alter mucosal blood flow, and provide dramatic protection against a wide variety of agents which cause acute mucosal damage. The physiological role of prostaglandins is still being elucidated. There is now strong evidence that endogenous prostaglandins modulate acid secretion by blocking the histamine-stimulated increase in cyclic AMP within the parietal cell. This function is probably controlled by intraluminal pH. It is likely that mucus and bicarbonate secretion by both stomach and duodenum are influenced by endogenous prostaglandins. A physiological role of prostaglandins in mucosal protection is less certain. Prostaglandins are released by trivial injury, and this probably serves a defensive function. A mucosa which is prostaglandin-depleted is more susceptible to damage, but does not spontaneously ulcerate. It is conceivable that peptic ulcer disease may be in part caused by an impaired mucosal prostaglandin response to food.

Anti inflamatory drugs inhibit prostaglandins and this results increase acid production in stomach that damage to the stomach wall(mucosa) and cause or exacerbate gastritis.