Choice “E” is the best answer. This patient has Zollinger-Ellison Syndrome (ZES), which is caused by a gastrin-secreting tumor of the GI tract. The gastrin secretion in turn activates the ECL cells in the stomach. These cells release histamine which stimulates the parietal cells in producing acid. ZES can occur as a part of a genetic syndrome (MEN 1) or sporadically. The offending tumor is located in the duodenum, pancreas, or abdominal lymph nodes. Abdominal pain, heartburn and diarrhea are the most common symptoms in ZES patients. In patients in whom MEN1/ZES is suspected, a history indicative of kidney stones, elevated calcium levels(i.e., hyperparathyroidism), and pituitary disorders (i.e., adenomas) should be sought. The diagnosis of Zollinger–Ellison syndrome is made by a secretin stimulation test, which measures evoked gastrin levels. Fasting gastrin levels, on at least three separate occasions, is another method of diagnosing ZES. Normal basal gastric acid secretion is less than 10 …show more content…
Atrophic gastritis is a chronic inflammation of the gastric mucosa with loss of gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. Abnormally elevated gastrin levels are not found in this condition.
Choice “B” is not the best answer. Chronic gastric outlet obstruction can result in antral dilation which increases acetylcholine levels. Elevated levels of acetylcholine then can cause parietal cells to produce hydrochloric acid and interacts with G-cells to enhance gastrin secretion. However, Gastrin levels typically do not approach those seen in ZES and a secretin stimulation test is negative in these
HPI: MR is a 70 y.o. male patient who presents to ER with constant, dull and RUQ abdominal pain onset yesterday that irradiate to the back of right shoulder. Client also c/o nauseas, vomiting and black stool x2 this morning. He reports that currently resides in an ALF; they called the ambulance after his second episodes of black stool. Pt reports he drank Pepto-Bismol yesterday evening without relief. Pt states that he never experienced similar symptoms in the past. Denies any CP, emesis, hematochezia or any other associated symptoms at this time. Client was found with past history gallbladder problems years ago.
She had a two week history of feeling generally unwell, complaining of tiredness and lethargy. She had no other significant symptoms. Her past history includes well controlled asthma and anxiety. She was a smoker of 20 cigarettes per day. She was taking amitriptyline, Symbicort (budesonide and formoterol inhaler). She had no significant family history of medical illness and had no clinical findings on examination. Blood tests showed corrected calcium of 4.22mmol/L (NR 2.20 -2.60) with suppressed paired PTH of 1.45pmol/L (NR1.60- 6.9). Her renal function was initially impaired, but normalized with rehydration. Her liver function tests, full blood count, vitamin D, myeloma screen and serum ACE levels were all within normal limits. Ultra sound scan (USS) of kidneys, USS of parathyroid and computerized tomography (CT) of thorax, abdomen and pelvis were all reported as normal with no cause found for her
Eisenmenger Syndrome (ES) is a heart defect that was first giving the name in 1897 (Fukushima, 2015). This syndrome happens when the birth defect is not treated before the lungs’ arteries become damaged. Eisenmenger Syndrome is named after Victor Eisenmenger a man who had a patient who showed symptoms such as, breathing complications and skin that was turning a bluish color. The autopsy of this patient lead him to discover a ventricular septal defect [VSD] (El-Chami, 2014), that causes a hole in the wall on the right and left ventricular. This is the defect that begins when signaling for pulmonary artery hypertension, which progresses into more advanced stages of ES. This birth defect eventually causes patients to have various
•Jose symptoms is derived from a disorder called Gastroesophageal reflux disease (GERD) occurring in the digestive system with the consumption of food, irritating the esophagus generally causing notable clinical symptoms such as the following: vomiting, chronic cough, angina, & regurgitation immediately after the consumed food. Jose's experience of the lump in his throat is caused by esophageal sphincter pressure.
Steven-Johnson Syndrome (SJS) is an immune mediated hypersensitivity complex, most often triggered by medications (Foster, 2011). It is characterized by a prodrome of malaise and fever, followed by rapid onset of erythematous or purpuric macules and plaques. The skin lesions progress to epidermal necrosis and sloughing. Mucosal membranes are affected in 92 to 100 percent of patients, usually at two or more distinct sites (High & Nirken, 2012).
Digestive: a sn Irritable Bowel Syndrome This disease affects the muscles in the intestines. It can cause gas, abdominal pain, diarrhea, and constipation. It usually does not lead to further diseases. Most people can control the symptoms through diet, stress management, and medication.
J.P., a 58 year old female, presents to the Emergency Room on March 18th. She has a past medical history of cervical cancer, atheroembolism of the left lower extremity, fistula of the vagina, peripheral vascular disease, neuropathy, glaucoma, GERD, depression, hypertension, chronic kidney disease, and sickle cell anemia. She complains of right lower extremity pain accompanied by fatigue, a decreased appetite, increased work of breathing, burning urination, and decreased urine output for three days. Upon admission, a complete physical assessment was performed along with a blood and metabolic panel. The assessment revealed many positive and negative findings.
A common condition that is associated with GERD and LES problems is having a hiatal hernia. A hiatal hernia is when you have a larger than normal opening in the diaphragm where the esophagus passes through. Since this opening is larger, the stomach begins to enter this opening. When you eat, the stomach and esophagus do not join as they were properly intended and cause malfunctioning of the LES. In some cases, food remains above the LES allowing it to easily travel back up the esophagus.
The patient is a 75-year-old female who is brought to the ER because of some dizziness. She has a very complicated medical history of mitral valve prolapse, uterine fibromas having hysterectomy, a question of Ménière's disease, anxiety, hypertension, asthma, CVA in 1994 with mild right-sided residual weakness, urethral stenosis, recurrent UTIs, pulmonary embolism, and idiopathic afib she did presyncopal developed Equinox, a history of diverticulosis, and diverticulitis. The patient is admitted inpatient. It is to be noted initially there is a question of a syncopal episode. Troponins are negative. She is dehydrated with urinary specific gravity of 10:30, and she has positive nitrates and leukocytes. She was initially placed in the emergency
Gastroparesis is defined as a chronic symptomatic syndrome of delayed gastric emptying without any indications of mechanical obstruction.1 The etiologies for gastroparesis are diverse, but a majority of cases are from idiopathic causes or secondary to diabetes mellitus.2 In a study done of 146 patients with gastroparesis, 36% were suffering from idiopathic gastroparesis, 29% from diabetic gastroparesis and the remaining 35% had a variety of etiologies which included: postgastric surgery, Parkinson’s disease, collagen vascular disorders, intestinal pseudoobstruction and miscellaneous causes.3
Acid is produced naturally in your stomach to help you digest food and to kill bacteria. This acid irritates the stomach lining so our body produces a natural mucus barrier which protects it. Sometimes this barrier may be damaged thus allowing the acid to damage the stomach causing inflammation, ulcers and other conditions. Other times, there may be a problem with the muscular band at the top of the stomach that keeps the stomach tightly closed and this allows the acid to escape and irritate the oesophagus. This is called 'acid reflux' and can cause heartburn and/or oesophagitis. Proton pump inhibitors such as omeprazole stop cells in the lining of the stomach from producing too much acid. This can help prevent ulcers from forming or assist the healing process. By decreasing the amount of acid, they can also help to reduce acid reflux related symptoms such as heartburn.
The intestinal phase of gastric secretion and emptying occurs in the duodenum as a response to arriving chyme and is moderated by hormones ad nervous reflexes. It ensures that the composition and pH of chyme is correct before entering the intestines. Stretching of the duodenum enhances gastric secretion through the production of gastrin which stimulates gastric secretions. Decreased pH and lipids in the duodenum trigger chemoreceptors to send inhibitory signals to the stomach. Chyme in the duodenum also stimulate cells to release messengers that stimulate secretions in the pancreas and gall bladder. The compounds released work to suppress secretion in the gastric system and reduce the stomachs motility. This gives the duodenum time to process its contents before receiving more. The duodenum initially stimulates gastric function but then quickly works to inhibit it. This is a negative feedback system in that the receptors in the duodenum determine control the amount of material entering it through various
This disease is characterized by autoantibodies against intrinsic factor producing cells in the stomach (atrophic gastritis). Intrinsic factor is an important molecule that binds to vitamin B12 in the stomach, allowing the vitamin B12/intrinsic factor complex to become absorbed in the small intestine. Other disorders associated with B12 deficiency include celiac disease and inflammatory bowel disease – this occurs as a result of malabsorption. Individuals that have undergone bowel resection of the stomach or small intestine (e.g., ileum) are also at increased risk.
This was his second episode since 10 days ago where he develop the same pain at his right flank. He suddenly experienced severe pain 8 hours before admission when the pain shifts to his right lower quadrant of his abdomen. The onset is at 6.30 am before worsening at 10 p.m to 2 p.m. He described the pain as continuous sharp pain and gradually increased in severity. There is no radiation of the pain. The pain was exaggerated on movement and touch. There were no relieving factor and he scale the severity as 7/10. He experienced fever for 1 day prior to admission. It was a mild grade continuous fever. He does not experienced chills and rigor. The patient does not experience any nausea or vomiting, no dysphagia, no pain during micturition and no alteration in bowel habit. He experienced loss of appetite but not notice any weight loss.
The patient has experienced fever, chills on body, headaches and anorexia as well as sweating especially during the night. The patient has also been feeling fatigued, muscle aches and nausea as well as vomiting especially after eating (WHO, 2010, p. 117). These symptoms started forty eight hours ago, and the patient has not taken any medication except for some aspirin.