Non-cardiogenic shock is caused by a circulatory collapse in the body that is not due to problems originating in the heart. Shock is commonly caused by hypo-perfusion though the blood vessels due to lack of blood in the vessels causing low blood pressure and rapid heartbeat. Besides cardiogenic shock‚ there are three other types that cause shock for non-cardiogenic reasons‚ obstructive shock‚ disruptive shock‚ and hypovolemic shock. Obstructive shock results from an obstruction that prevents blood
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Diuretics Hypertension‚ Congestive Heart Failure ‚ Diabetes‚ Cirrhosis and Renal Failure Objectives I. Review renal structure and function II. Neurohumoral regulation of water (ECF) & electrolyte balance III. Pharmacotherapy that acts at the kidney A. Loop diuretics B. Thiazide diuretics C. Carbonic Anhydrase Inhibitors D. K+- sparing diuretics E. Osmotic diuretics F. Others IV. Therapeutic uses I. Structure/Function Germann and Stanfield Fig. 19.2 The Nephron: Tubular Component
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chemical messeges‚ while postsynaptic toxins affect the places nerve signals are interpreted such as muscles and other nerves. Hemotoxic venom destroys tissues in different ways. Many hemotoxins cause problems such as cardiac arrest‚ kidney failure‚ edema‚ necrosis‚ and intense pain. These effects are cause by hemotoxins anticoagulation effects. Enzymes are found commonly in both hemo-and neurotoxins‚ and enzymes play a crucial role in snake
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Man with the Swollen Kidneys Mr. Newman is a 49 year old male who has hematuria‚ fever and severe flank pain. He also has bilateral lumbar tenderness‚ bilateral renal enlargement‚ liver enlargement‚ ankle and facial edema‚ skin pallor‚ and lung sounds suggest pulmonary edema. His vital signs are as follows: BP 172/100‚ heart rate 92 beats per minute‚ and a temperature of 102.2 F. There have been some labs done. His red blood count is 3.1 million cells‚ white blood count is 22‚000 cells‚ potassium
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activity Denies pain chest Ankles swollen Objective Data Vital signs: T 37‚ P 112‚ R 18‚ BP 110/54 Lungs: bilateral lower lobe crackles O2 sat: 94% Skin: cool to touch CV: heart rate regular‚ positive peripheral pulses ECG: no changes +2 edema bilateral ankles Medications: metoprolol 20 mg per day‚ aspirin 325 mg per day Answer the questions and submit via Dropbox
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to pump blood. This results in a reduction of blood supply to the kidneys‚ which then begin to lose their ability to excrete salt and water. This lessened function of the kidney causes the body to retain more fluid. The fluid build-up then leads to edema or congestion of tissues (Fundukian‚ 2011). Incidence Congestive heart failure is a serious condition with significant morbidity and mortality. In the United States‚ African Americans significantly have a
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is used to treat high blood pressure. She is also on Lasix (furosemide)‚ which is a loop diuretic that prevents ones body from absorbing too much salt‚ by allowing the salt to pass through the urine instead. Lasix is used to treat fluid retention (edema) in people with congestive heart failure and it also treats
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creatinine which is indicative of his acute kidney injury. He will continue with a fluid restriction and his kidney function will be monitored. He will see wound care regarding the wounds on his extremities. As his fluid imbalance improves the edema will decrease and the weeping will
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came to clinic today complaining of DOE that began 6 months ago. Currently he developed edema on his low extremities‚ and he gained 13 lbs recently. His LVEF is less than 20%. His SOB is worsening in last 4 days‚ which he has a difficulty to breathe after 30 feet of walking. According to the ACC/AHA guidelines‚ his hemodynamic subset is class II‚ which he has a warm and wet due to his sign and symptoms of edema‚ ascites‚ and hypertension. Also‚ he is currently NYHA FC IV‚ as he can’t breathe regularly
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exhibited marked pedal edema bilaterally. She is being treated with digitalis‚ furosemide (Lasix)‚ KCl‚ and sublingual nitroglycerin. Discussion Questions 1. Which type of heart failure (left or right sided) is usually associated with dyspnea? What other clinical findings are likely to be present with left-sided heart failure? 2. What compensatory mechanisms are likely to be operative in A.O. to enhance cardiac output? 3. What is the most likely cause of A.O.’s pedal edema? 4. What is the cause
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