My experience Flashcards
Diverticulitis/Diverticulosis
in which pouches within the large bowel wall become inflamed.[1] Symptoms typically include lower abdominal pain of a sudden onset. [1] The onset of symptoms, however, may also occur over a few days. [1] In North America and Europe pain is usually on the left side, while in Asia it is often on the right.[2][4] There may also be fever, nausea, diarrhea or constipation, or blood in the stool.[1] Repeated attacks may occur.
The causes of diverticulitis are uncertain.[1] Risk factors may include obesity, lack of exercise, smoking, a family history of the disease, and nonsteroidal anti-inflammatory drugs (NSAIDs). The role of dietary fibre is unclear.
Diverticulitis typically presents with left lower quadrant abdominal pain of sudden onset.[1] There may also be fever, nausea, diarrhea or constipation, and blood in the stool.[1]
In complicated diverticulitis, an inflamed diverticulum can rupture, allowing bacteria to subsequently infect externally from the colon. If the infection spreads to the lining of the abdominal cavity (the peritoneum), peritonitis results. Sometimes, inflamed diverticula can cause narrowing of the bowel, leading to an obstruction. In some cases, the affected part of the colon adheres to the bladder or other organs in the pelvic cavity, causing a fistula, or creating an abnormal connection between an organ and adjacent structure or other organ (in the case of diverticulitis, the colon and an adjacent organ).
Losartan
Losartan is a selective, competitive angiotensin II receptor type 1 (AT1) antagonist, reducing the end organ responses to angiotensin II. Losartan administration results in a decrease in total peripheral resistance (afterload) and cardiac venous return (preload). All of the physiological effects of angiotensin II, including release of aldosterone, are antagonized in the presence of losartan. Reduction in blood pressure occurs independently of the status of the renin-angiotensin system. As a result of losartan dosing, plasma renin activity increases due to removal of the angiotensin II feedback.Although clinical evidence shows calcium channel blockers and thiazide-type diuretics are preferred first-line treatments for most patients (due to both efficacy[citation needed] and cost), an angiotensin II receptor antagonist such as losartan is recommended as first-line treatment in patients under the age of 55 who cannot tolerate an ACE inhibitor
MOA: when your body detects low blood pressure, body produces angiotensin II which travels throughout the body. Many parts of bodies have special receptor sites. When it does it tells the body to increase blood pressure. Losartan blocks the receptor. 1 tablet taken per day and taken with or without food. Increases potassium in blood.
Colonic angiodysplasia
Angiodysplasia is the most common vascular lesion of the gastrointestinal tract, and this condition may be asymptomatic, or it may cause gastrointestinal (GI) bleeding. [1] The vessel walls are thin, with little or no smooth muscle, and the vessels are ectatic and thin
Angiodysplasia is a degenerative lesion of previously healthy blood vessels found most commonly in the cecum and proximal ascending colon. Seventy-seven percent of angiodysplasias are located in the cecum and ascending colon, 15% are located in the jejunum and ileum, and the remainder is distributed throughout the alimentary tract. These lesions typically are nonpalpable and small (< 5 mm).
Angiodysplasia is the most common vascular abnormality of the GI tract. After diverticulosis, it is the second leading cause of lower GI bleeding in patients older than 60 years. Angiodysplasia may account for approximately 6% of cases of lower GI bleeding. It may be observed incidentally at colonoscopy in as many as 0.8% of patients older than 50 years. The prevalence for upper GI lesions is approximately 1-2%.
What is a worry of SIADH? And what is something to worry about for treatment?
Severe hyponatremia can lead to coma. Physicians currently recognize that central pontine myelinolysis occurs inconsistently as a complication of severe and prolonged hyponatremia, particularly when corrected too rapidly.
Central pontine myelinolysis is a concentrated, frequently symmetric, noninflammatory demyelination within the central basis pontis. In at least 10% of patients with central pontine myelinolysis, demyelination also occurs in extrapontine regions, including the mid brain, thalamus, basal nuclei, and cerebellum. The exact mechanism that strips the myelin sheath is unknown.
One theory proposes that in regions of compact interdigitation of white and gray matter, cellular edema, which is caused by fluctuating osmotic forces, results in compression of fiber tracts and induces demyelination. Prolonged hyponatremia followed by rapid sodium correction results in edema. During the period of hyponatremia, the concentration of intracellular charged protein moieties is altered; reversal cannot parallel a rapid correction of electrolyte status. The term osmotic myelinolysis is more appropriate than central pontine myelinolysis for demyelination occurring in extrapontine regions after the correction of hyponatremia
What are the two most common causes of peptic ulcers
PGE1 -housekeeping and thrombosis
PGE2- inflammatory
- Taking NSAIDs - Both PGE1, PGE2 are produced by COX-1. SO although you are trying to inhibit PGE2, you are also getting housekeeping of Gut mucosa. Prostaglandins are natural chemicals that serve as messengers to promote inflammation. By inhibiting the body’s production of prostaglandins, NSAIDs decrease inflammation and the symptoms and signs of inflammation, such as pain, tenderness, and fever. However, certain prostaglandins also are important in protecting the stomach lining from the corrosive effects of stomach acid as well as playing a role in maintaining the natural, healthy condition of the stomach lining. These protective prostaglandins are produced by an enzyme called Cox-1. By blocking the Cox-1 enzyme and disrupting the production of prostaglandins in the stomach, NSAIDs can cause ulcers and bleeding. Some NSAIDs have less effect on prostaglandins in the stomach than others, and, therefore, may have a lower risk of causing ulcers but the increased risk of ulcers still exists.
- H. pyelori
H. pylori also neutralizes the acid in its environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. These react with the strong acids in the environment to produce a neutralized area around H. pylori. H. pylori harms the stomach and duodenal linings by several mechanisms. The ammonia produced to regulate pH is toxic to epithelial cells, as are biochemicals produced by H. pylori such as proteases, vacuolating cytotoxin A (VacA) [this damages epithelial cells, disrupts tight junctions and causes apoptosis, and certain phospholipases. Cytotoxin associated gene CagA can also cause inflammation and is potentially a carcinogen.
Colonization of the stomach by H. pylori can result in chronic gastritis, an inflammation of the stomach lining, at the site of infection. Helicobacter cysteine-rich proteins (Hcp), particularly HcpA (hp0211), are known to trigger an immune response, causing inflammation. Chronic gastritis is likely to underlie H. pylori-related diseases.[46]
Ulcers in the stomach and duodenum result when the consequences of inflammation allow stomach acid and the digestive enzyme pepsin to overwhelm the mechanisms that protect the stomach and duodenal mucous membranes. The location of colonization of H. pylori, which affects the location of the ulcer, depends on the acidity of the stomach. In people producing large amounts of acid, H. pylori colonizes near the pyloric antrum (exit to the duodenum) to avoid the acid-secreting parietal cells at the fundus (near the entrance to the stomach).[13] In people producing normal or reduced amounts of acid, H. pylori can also colonize the rest of the stomach.
The inflammatory response caused by bacteria colonizing near the pyloric antrum induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to parietal cells in the fundus.[48] Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen, and over time increases the number of parietal cells, as well.[49] The increased acid load damages the duodenum, which may eventually result in ulcers forming in the duodenum.
When H. pylori colonizes other areas of the stomach, the inflammatory response can result in atrophy of the stomach lining and eventually ulcers in the stomach. This also may increase the risk of stomach cancer.
Wolf Parkinson White syndrome
is a disorder due to a specific type of problem with the electrical system of the heart which has resulted in symptoms. About 40% of people with the electrical problem never develop symptoms.Symptoms can include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely cardiac arrest may occur.[1] The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.[1]
The cause of WPW is typically unknown. A small number of cases are due to a mutation of the PRKAG2 gene which may be inherited from a person’s parents in an autosomal dominant fashion. The underlying mechanism involves an accessory electrical conduction pathway between the atria and the ventricles.[1] It is associated with other conditions such as Ebstein anomaly and hypokalemic periodic paralysis.[1] Diagnosis is typically when an electrocardiogram (ECG) show a short PR interval and a delta wave.[3] It is a type of pre-excitation syndromes.[3]
WPW syndrome is treated with either medications or radiofrequency catheter ablation.[4] It affects between 0.1 and 0.3% in the population.[1] The risk of death in those without symptoms is about 0.5% per year in children and 0.1% per year in adults.[5] In those without symptoms ongoing observation may be reasonable.[5] In those with WPW complicated by atrial fibrillation, cardioversion or the medication procainamide may be used.
Individuals with WPW have an accessory pathway that communicates between the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent. This accessory pathway does not share the rate-slowing properties of the AV node, and may conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to contract at 300 beats per minute. Extremely rapid heart rates such as this may result in hemodynamic instability or cardiogenic shock. In some cases, the combination of an accessory pathway and abnormal heart rhythms can trigger ventricular fibrillation, a leading cause of sudden cardiac death.
Diagnosis: WPW is commonly diagnosed on the basis of the electrocardiogram in an asymptomatic individual. In this case, it is manifested as a delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex are actually the impulse making it through to the ventricles prematurely (across the accessory pathway) without the usual delay experienced in the AV node.
