Context: Hypercalcemia is a commonly encountered clinical problem. In the majority (90%) of the cases it is either due to malignancy or primary hyperparathyroidism and is rarely due to granulomatous disease.
Case Description: We report the case of a muscular sarcoidosis in a 41 year old Caucasian woman with background history of well controlled asthma and anxiety. She presented with lethargy and she had a raised calcium level of 4.2mmol/L. She had no other significant clinical history and her examination findings were normal. She underwent extensive investigations for the cause of her hypercalcemia. Her PTH levels were suppressed. A full body CT scan was performed to exclude underlying malignancy. As part of the ongoing investigation for rarer causes of hypercalcemia, repeated ACE levels were found to be normal. The only diagnostic clue for granulomatous disease was an elevated 1, 25 hydroxy vitamin D level. The
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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
The risk factors that Jessica presented with are a history that is positive for smoking, bronchitis and living in a large urban area with decreased air quality. The symptoms that suggest a pulmonary disorder include a productive cough with discolored sputum, elevated respiratory rate, use of the accessory respiratory muscles during quite breathing, exertional dyspnea, tachycardia and pedal edema. The discolored sputum is indicative of a respiratory infection. The changes in respiratory rate, use of respiratory muscles and exertional dyspnea indicate a pulmonary disorder since there is an increased amount of work required for normal breathing. Tachycardia may arise due to the lack of oxygenated blood available to the tissue stimulating an increase in heart rate. The pedal edema most probably results from decreased systemic blood flow.
How does this history of high blood pressure demonstrate the problem description and etiology components of the P.E.R.I.E. process? What different types of studies were used to establish etiology or contributory cause?
Hyperplasia is the early stage development of cells to cancer cells. It increases in cells that have the capability to proliferate at a fast rate. Often times, hyperplasia is correlated with the increase in proliferation and the speed of mitosis. The increase in the number of cells with hyperplasia means that the proliferation is happening at a faster rate than normal. Hyperplasia is considered to be the early stage of dysplasia, though not all hyperplasia leads to dysplasia.
Hypercholesterolemia is the presence of high levels of cholesterol in the blood. Cholesterol is a waxy fat-like substance and is a major class of lipid, so it gets into the blood by lipoproteins [1]. A high level of lipoproteins is unhealthy. A high level can result in an elevated risk of atherosclerosis and coronary heart disease [2]. The high levels of lipoproteins are often influenced by a combination of genetic and environmental factors such as obesity or dieting habits [2]. High cholesterol can be caused by mutations in the following genes: APOB, LDLR, LDLRAP1, and PCSK9 [3]. Mutations in the LDLR gene are responsible for causing familial hypercholesterolemia, which is the most commonly seen form of inherited high cholesterol [3]. The LDLR gene contains instructions for making LDL receptors or low-density lipoprotein receptors. LDL receptors play critical roles in regulating levels of cholesterol in the blood by removing low-density lipoproteins from the bloodstream. Mutations in the LDLR gene can make the amount of LDL receptors produced less than normal or affect their job of removing the low-density lipoproteins in the blood [4]. People who have these mutations will have higher levels of cholesterol. There are many ways that the environment can affect the levels of cholesterol in the blood. Reducing the amount of dietary fat you consume lowers the total amount of cholesterol in the blood [5]. Sucrose and fructose can raise the amount of LDL in the blood. Reducing fatty foods will however lower the amount of LDL [5]. Having a healthy body and maintaining physical exercise plays a key role in keeping your cholesterol at a healthy level. If you are overweight or obese you can lower your cholesterol levels by simply losing ...
The following presentation will help this class in the teaching of a patient with hypothyroidism. The expected outcome of this presentation for the patient will be as follows:
On admission, a complete physical assessment was performed along with a blood and metabolic panel. The assessment revealed many positive and negative findings. J.P. was positive for dyspnea and a productive cough. She also was positive for dysuria and hematuria, but negative for flank pain. After close examination of her integumentary and musculoskeletal system, the examiner discovered a shiny firm shin on the right lower extremity with +2 edema complemented by severe pain. A set of baseline vitals were also performed revealing a blood pressure of 124/80, pulse of 87 beats per minute, oxygen saturation of 99%, temperature of 97.3 degrees Fahrenheit, and respiration of 12 breaths per minute. The blood and metabolic panel exposed several abnormal labs. A red blood cell count of 3.99, white blood cell count of 22.5, hemoglobin of 10.9, hematocrit of 33.7%, sodium level of 13, potassium level of 3.1, carbon dioxide level of 10, creatinine level of 3.24, glucose level of 200, and a BUN level of 33 were the abnormal labs.
My patient who is a 57 year old male who has a past history of Hypertension, takes Accupril to help with his high blood pressure. Is complaining of chest and lest arm pain. He has a blood pressure of 140bpm a high heart rate, and on the ECG showing significant ST elevation and Sinus Tachycardia.
The thyroid gland is found in the front of the neck and produces two main hormones. The hormones are called thuroxine (T4) and Triiodothyronine (T3). Together these hormones regulate the body’s metabolism by increasing energy use in cells, regulate growth and development, help to maintain body temperature and aid in oxygen consumption. These two hormones are regulated by hormones produced by the hypothalamus and pituitary gland. The hypothalamus senses changes in body’s metabolic rate and releases a hormone known as thyropin-releasing hormone (TRH). This hormone then flows through connecting vessels to the pituitary gland which signals it to release another hormone. This hormone is known as thyroid-stimulating hormone (TSH). TSH then makes its way to the bloodstream until it reaches the thyroid where it is then signaled to activate T3 and T4 production [1]. This mechanism is controlled by a negative feedback loop meaning that when there is a sufficient amount of thyroid hormones in the blood stream, this will signal back to stop production of thyroid stimulating hormones. Complications occur when the thyroid hormones keep increasing even though there is already a sufficient amount of T3 and T4 in the blood stream. This process of over expression of thryroid hormones is known as hyperthyroidism. Hyperthyroidism is a general term that includes any disease that has a consequence of an overabundance of thyroid hormones. Hyperthyroidism is a general term but there are many variant diseases that are in the hyperthyroidism category. These diseases include diffuse toxic goiter, Basedow’s disease, thyrotoxicosis, Parry’s and Graves’ disease.
Dr. Ally, a 49-year-old professor, has been diagnosed with essential hypertension 12 years ago and was on antihypertensive drugs. However, he did not take his medications last year because he was feeling just fine. In addition, he was very busy with work. Nevertheless, he felt tired after work and developed dyspnea while climbing the stairs. Recently, he had a bout of epistaxis (severe nose bleed) with dizziness and blurred vision. He went to the doctor for a check up. His blood pressure was 180/110, and the doctor found rales or crackles on his chest upon auscultation. The doctor ordered rest and asked him to start his medication again.
Vicki is a 42-year-old African American woman who was diagnosed with Hypertension a month ago. She has been married to her high school sweetheart for the past 20 years. She is self-employed and runs a successful insurance agency. Her work requires frequent travel and Vicki often has to eat at fast food restaurants for most of her meals. A poor diet that is high in salt and fat and low in nutrients for the body and stress from her job are contributing factors of Vicki’s diagnosis of hypertension. This paper will discuss the diagnostic testing, Complementary and Alternative Medicine treatments, the prognosis for hypertension, appropriate treatment for Vicki, patient education, and potential barriers to therapy that Vicki may experience.
Schepis, Carmelo, Donatella Greco, and Corrado Romano. "Cardiofaciocutaneous (CFC) Syndrome." Australasian Journal of Dermatology 40.2 (1999): 111-13. Print.
Methemoglobinemia is an uncommon but possible reason for cyanosis. Methemoglobinemia is significant because the disease is fairly rare and consequently most physicians do not consider it as a cause when diagnosing a patient with cyanosis. Regrettably, patients often get misdiagnosed and sometimes treated for the wrong disorder as a result. A two fold dilemma occurs when the patient is treated for an incorrect disorder. The first part of the dilemma includes the patient experiencing all of the negative side effects of the wrong treatment, and gaining no benefit. The second part of the dilemma is that the patient’s actual medical condition is not being treated, and is getting worse with time. The higher the level of methemoglobin in the blood the higher the patient’s chances of dying are. Another thing for doctors to acknowledge is when methemoglobinemia is not considered a valid diagnosis; numerous unnecessary laboratory tests are performed. When unneeded laboratory tests are performed the medical laboratory technologist’s time is wasted when they could be running another patient’s samples. Also running unnecessary laboratory tests costs a great deal of money. During the analysis of cyanosis, physicians should consider methemoglobinemia as a valid diagnosis.
The purpose of this paper is to analyze, diagnose, and to determine a proper treatment plan to work toward the beneficial prognosis for the individual indicated within the case study.
Among these disorders are hypothyroidism and hyperthyroidism. Hypothyroidism is a disorder in which one is diagnosed for having and underactive thyroid. The probability for women over the age of sixty to develop an underactive thyroid is higher than those of other individuals. If left untreated it can potentially lead to obesity, joint pain, heart disease, and other health complications. On the contrary, hyperthyroidism is a disorder in which a person is diagnosed for having an overactive thyroid. This can cause nervousness and anxiety, hyperactivity, unexplained weight loss, and swelling of the thyroid gland which causes a noticeable lump to form on throat (known as a
MEDICAL DIAGNOSIS: Empyema, Hemoptysis, Necrotizing pneumonia, Aspergillosis (Aspergillus fumigatus) cachexia secondary to malnutrition/infection, hypothyroidism, Diabetes Type II melitius , and...