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Hematemesis Melena Pathophysiology

A history of dyspepsia, peptic ulcer is the initial allegations. So is a history of recurrent vomiting who initially did not bleed, excessive alcohol consumption leads to the suspicion of gastritis and peptic ulcer disease. A history of recurrent vomiting who initially did not bleed more towards Mallory-Weiss. Excessive alcohol consumption leads to allegations of gastritis (30-40%), peptic ulcer disease (30-40%), or sometimes varicose veins. Weight reduction leads to the suspicion of malignancy. Heavy bleeding accompanied by a clot and refractory shock treatment increases the likelihood of varicose veins. A history of previous abdominal aortic surgery increases the likelihood of fistula aortoenterik. At the young age of patients with a history of upper gastrointestinal bleeding brief repeated (often accompanied by hemodynamic collapse) and a normal endoscopy, should be considered Dieulafoy lesion (a submucosal artery, usually near the heart, which can cause intermittent gastrointestina
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Pathophysiology of Coronary Artery Disease

This condition is chronic and begins when a person is an adolescent and then it slowly progresses throughout their life. Coronary artery disease pathophysiology revolves around a few theories. One widely accepted theory is that this condition occurs when the body is trying to heal itself as a result of endothelial injury. Inflammation is also beginning to be accepted as a critical component of potential plaque instability and atherosclerosis activity. Patients who have been diagnosed with established coronary artery disease and have several of the causes and/or risk factors as well are at a much higher risk of experiencing a cerebrovascular accident, myocardial infarction, and other vascular events in the future. Elevated C-reactive protein levels, and other elevated biochemical markers, indicate a higher risk of experiencing a vascular event in the future and it indicates an increased likelihood of vascular inflammation. This marker may also indicate the need for aggressive prevent
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Pathophysiology of Diabetes MellitusType 1

Insulin is essential to process carbohydrates, fat, and protein. Insulin reduces blood glucose levels by allowing glucose to enter muscle cells and by stimulating the conversion of glucose to glycogen (glycogenesis) as a carbohydrate store. Insulin also inhibits the release of stored glucose from liver glycogen (glycogenolysis) and slows the breakdown of fat to triglycerides, free fatty acids, and ketones. It also stimulates fat storage. Additionally, insulin inhibits the breakdown of protein and fat for glucose production (gluconeogenesis) in both liver and kidneys. Hyperglycemia (ie, random blood glucose concentration more than 200 mg/dL or 11 mmol/L) results when insulin deficiency leads to uninhibited gluconeogenesis and prevents the use and storage of circulating glucose. The kidneys cannot reabsorb the excess glucose load, causing glycosuria, osmotic diuresis, thirst, and dehydration. Increased fat and protein breakdown leads to ketone production and weight loss. Without insuli
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Pathophysiology of Typhoid Fever

Typhoid fever , also known as Typhoid , is a common worldwide illness, transmitted by the ingestion of food or water contaminated with the feces of an infected person, which contain the bacterium Salmonella enterica enterica, serovar Typhi. The bacteria then perforate through the intestinal wall and are phagocytosed by macrophages. The organism is a Gram-negative short bacillus that is motile due to its peritrichous flagella. The bacterium grows best at 37°C / 98.6°F – human body temperature. This fever received various names, such as gastric fever, abdominal typhus, infantile remittant fever, slow fever, nervous fever, pythogenic fever, etc. The name of "typhoid" was given by Louis in 1829, as a derivative from typhus . Pathophysiology of Typhoid Fever Transmission of Salmonella typhi can be transmitted through various ways, which is known with 5 M of the Food Fingers, Fomitus (vomiting), Fly, and through Faeces. Faeces and vomiting in patients with typhoid salmonel
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Pathophysiology of Meningitis

Pathophysiology of Meningitis Predisposing factors include upper airway infection, otitis media, mastoiditis, sickle cell anemia and other hemoglobinopatis, a new neurosurgical procedure, head trauma and immunological effects. Venous channels through the posterior nasopharynx, middle ear and mastoid tract to the brain and the veins near the channel meningen; all of these links that support the growth of bacteria. Organisms enter the bloodstream and cause an inflammatory reaction in the meningen and under the cortex, which can cause thrombus and decreased cerebral blood flow. Cerebral tissue due to impaired metabolism meningen exudate, vasculitis and hypoperfusion. Purulent exudate may spread to the base of the brain and spinal cord. Inflammation also spread to the wall membrane of the cerebral ventricles. Bacterial meningitis associated with intracranial physiological changes, which consisted of increased permeability of the blood, the defense area of the brain, cerebral edema an
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Pathophysiology of Hallucination

Pathophysiology of Hallucination Various theories have been put forward to explain the occurrence of hallucinations. When psychodynamic (Freudian) theories were popular in psychiatry, hallucinations were seen as a projection of unconscious wishes, thoughts and wants. As biological theories have become orthodox, hallucinations are more often thought of (by psychologists at least) as being caused by functional deficits in the brain. With reference to mental illness, the function (or dysfunction) of the neurotransmitters glutamate and dopamine are thought to be particularly important. The Freudian interpretation may have an aspect of truth, as the biological hypothesis explains the physical interactions in the brain, while the Freudian deals with the origin of the flavor of the hallucination. Psychological research has argued that hallucinations may result from biases in what are known as metacognitive abilities. These are abilities that allow us to monitor or draw inferences from o
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Pathophysiology of COPD

COPD, or chronic obstructive pulmonary disease, is a progressive inflammatory disease connecting the airways, lung parenchyma, and vasculature. It causes the damage and remodeling of the airways and lung tissue. Proper functioning of lungs is rejected continuously by COPD. Over a period of time, these changes result in more severe conditions such as pulmonary hypertension and right heart failure. The precise pathophysiology of COPD is unidentified. The inflammatory process is a driving aspect in the pathophysiology of COPD. Recent verification suggests that the inflammatory response results in a number of effects, including an arrival of inflammatory cells such as macrophages, neutrophils and lymphocytes. Thickened airways and structural changes such as increased smooth muscle and fibrosis may also be manifested. Cigarette smoking causes an inflammatory response in the lungs. This response does not cease with the removal of the stimulus, but progresses for an unlimited period of time
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