Pathophysiology of Chronic Gastritis

Chronic gastritis can be classified as type A or type B.

Type A (often referred to as autoimmune gastritis) resulting from changes in parietal cells, leading to atrophy and cell infiltration. It is associated with autoimmune diseases, such as pernicious anemia and occurs in the fundus or corpus of the stomach.

Type B (sometimes referred to as Helicobacter pylori, also known as H. pylori) is associated with the bacteria H. pylori, dietary factors such as heat or spicy drink, use drugs and alcohol, smoking or reflux of intestinal contents into the stomach. H. Pylori includes bacteria that are not acid resistant, but this kind of bacteria are able to secure himself in the mucosal lining of the stomach. The presence of this bacterium in gastric mucosa of the stomach lining causing weakening and brittle so that stomach acid can penetrate the layer. Thus both gastric acid and the bacteria causing wound or ulcer. The immune system will respond to bacterial infection H. Pylori by sending beads of leukocytes, killer T cells, and other infection-fighting. However, it is not able to fight infection H. The reason pylori can not penetrate the stomach lining. But also can not be removed so that the immune response continues to increase and grow. Polymorph die and release of superoxide radicals damaging compounds in the cells lining the stomach. Extra nutrients are sent to strengthen the leukocyte cells, but nutrition is also a source of nutrients for H. Pylori. Finally, the state of the damaged epithelium of the stomach, forming a superficial ulceration and can cause hemorrhage (bleeding). Within a few days gastritis and even peptic ulcers are formed.

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Pathophysiology of Pharyngitis

Pathophysiology of Pharyngitis

Transmission is by droplet. Germs infiltrate the epithelial layer, then the epithelium is eroded, then the superficial lymphoid tissue inflammatory reaction occurs with the damming of polymorphonuclear leukocyte infiltration. In the early stages there is hyperemia and edema and increased secretions. Serous exudate at first, but tends to become thickened and dry and can be attached to the pharyngeal wall. By hyperemia, blood vessel walls of the pharynx to the width. Blockage forms a yellow, white, or gray present in follicles or lymphoid tissue. It appears that the lymphoid follicles and blotches on the posterior pharyngeal wall or located more laterally to become inflamed and swollen causing inflammation of the throat or pharyngitis.

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Pathophysiology of Scoliosis

Pathophysiology of Scoliosis

Deformity of the spine called scoliosis, originated from the nerves of weak or even paralyzed attractive segments of the spine. This serves to keep the pull of the vertebrae are in the normal lines of its shape like a ruler or straight. But for some reason, such as the habit of sitting the oblique, make the most of the work to be weak nerves. If this continues over and over becomes a habit, then the nerve will even die. This results in an imbalance of pull on the vertebrae. Therefore, suffering from scoliosis of the spine is curved like the letter or the letter S or C.

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Pathophysiology of Acute Otitis Media

Pathophysiology of Acute Otitis Media

Acute otitis media is often preceded by respiratory tract infections such as sore throats / colds that spread to the middle ear through the eustachian channel.

When the bacteria through the eustachian, the bacteria can cause infections of the channel. So that there was swelling around the channel, channel blockage, and the coming of the white blood cells to fight bacteria.

White blood cells will fight the bacterial cells at the expense of their own, at least to form pus in the middle ear. Tissue swelling around the eustachian cells causes mucus produced when cells multiply mucus and pus, hearing can be impaired because the eardrum and small bones connecting the ear drum with the hearing organ in the inner ear to move freely. Too much fluid, finally able to tear the eardrum because of the pressure.

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