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Malignant hyperthermia (MH) is a rare genetic disorder that affects the skeletal muscle and causes a fast rise in body temperature, severe muscle contractions and metabolic acidosis in response to exposure to certain anesthetic gases and depolarizing muscle relaxants during general anesthesia. It is caused by a mutation in the ryanodine receptor gene that regulates calcium ion release from the sarcoplasmic reticulum in muscle cells. During an MH episode, excess calcium causes muscle rigidity and a dangerous increase in metabolism that can lead to multiple organ failure and death if not properly treated with dantrolene.
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Malignant hyperthermia
Malignant hyperthermia is a serious, life-threatening condition caused by a genetic defect in the ryanodine receptor or calcium channel that makes individuals susceptible to triggering agents like volatile anesthetics and succinylcholine. When exposed to these agents, calcium is released from the sarcoplasmic reticulum in muscle cells, increasing metabolism and causing symptoms like fever, muscle rigidity, and acidosis. Diagnosis involves testing for genetic mutations or abnormal responses to caffeine and halothane. Treatment requires discontinuing triggers, dantrolene administration, supportive care, and cooling to reduce fever and its complications.
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Malignant hyperthermia
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Medical terminology is a vocabulary for accurately describing
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Medical terminology is a vocabulary for accurately describing
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Rhabdomyolysis is the destruction or disintegration of striated muscle resulting in the leakage of intracellular contents into circulation. It has many causes including trauma, compression injuries, exertion, drugs, infections, and metabolic disorders. The pathophysiology involves an influx of extracellular sodium, water and calcium into muscle cells and an efflux of intracellular potassium and myoglobin. Diagnosis is based on markedly elevated creatine kinase and presence of myoglobin in urine. Treatment focuses on aggressive fluid resuscitation, urine alkalinization, and renal replacement therapy if acute kidney injury develops to prevent complications.
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The document provides an overview of endocrine emergencies including adrenal crisis, diabetic ketoacidosis, and hypoglycemia. It describes the endocrine system and its functions. Adrenal crisis occurs when the adrenal glands cannot produce adequate hormones in response to stress. Diabetic ketoacidosis results from insulin deficiency and excess stress hormones, causing a buildup of ketones in the blood. Assessment, diagnostic testing, nursing diagnoses, and treatment approaches are outlined for these conditions. The goal is to stabilize vital signs and correct fluid, electrolyte, acid-base, and blood glucose imbalances.
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Rhabdomyolysis .-dr.-osama-2017
Rhabdomyolysis is the destruction or breakdown of skeletal muscle fibers that results in the release of intracellular contents into the bloodstream. The document discusses various causes of rhabdomyolysis including physical trauma, excessive exertion, infections, drugs, toxins, and metabolic disorders. It also describes the pathophysiology involving decreased ATP production and increased intracellular calcium levels leading to muscle cell damage. Diagnosis involves elevated creatine kinase and presence of myoglobin in urine or blood. Treatment focuses on aggressive fluid resuscitation to prevent acute kidney injury from myoglobin toxicity, along with urine alkalinization and potentially mannitol diuresis.
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This document provides an overview of fever in the ICU setting. It defines fever and discusses the causes, timing, and workup based on suspected source. Key points include:
- Fever in the ICU is typically defined as a temperature over 38.3°C.
- Fever can be caused by infection, inflammation, or antigen-antibody complexes which induce pyrogenic cytokines like IL-1, IL-6, and TNF.
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Cell Therapy Expansion and Challenges in Autoimmune Disease
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
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English class
- 2. ID the body system affected is a disease that causes a fast rise in body temperature and severe muscle contractions when someone with the disease gets general anesthesia. It is passed down through families. Hyperthermia means high body temperature. This condition is not the same as hyperthermia from medical emergencies such as heat stroke or infection.
- 3. Pathology In a large proportion (50–70%) of cases, the propensity is due to a mutation of the ryanodine receptor (type 1), located on the sarcoplasmic reticulum(SR), the organelle within skeletal muscle cells that stores calcium.RYR1 opens in response to increases in intracellular Ca2+ level mediated by L-type calcium channels, thereby resulting in a drastic increase in intracellular calcium levels and muscle contraction. RYR1 has two sites believed to be important for reacting to changing Ca2+ concentrations: the A-site and the I-site. The A-site is a high affinity Ca2+ binding site that mediates RYR1 opening. The I-site is a lower affinity site that mediates the protein's closing. Caffeine, halothane, and other triggering agents act by drastically increasing the affinity of the A-site for Ca2+ and concomitantly decreasing the affinity of the I-site in mutant proteins.
- 4. Mg2+ also affect RYR1 activity, causing the protein to close by acting at either the A- or I-sites. In MH mutant proteins, the affinity for Mg2+ at either one of these sites is greatly reduced. The end result of these alterations is greatly increased Ca2+ release due to a lowered activation and heightened deactivation threshold. The process of sequestering this excess Ca2+ consumes large amounts of adenosine triphosphate (ATP), the main cellular energy carrier, and generates the excessive heat (hyperthermia) that is the hallmark of the disease. The muscle cell is damaged by the depletion of ATP and possibly the high temperatures, and cellular constituents "leak" into the circulation, including potassium, myoglobin, creatine, phosphate and c reatine kinase.
- 5. Symptons Symptoms include: Bleeding Dark brown urine Muscle ache without an obvious cause, such as exercise or injury Muscle rigidity and stiffness Rise in body temperature to 105°F (40.6°C) or higher
- 6. Diagnosis Tests for the condition may include: Blood clotting studies (PT, or prothombin time; PTT, or partial thrombloplastin time) Blood chemistry panel, including CPK (creatinine phosphokinase, which is higher in the blood when muscle is destroyed during a bout of the illness) Genetic testing to look for defects in the genes that are linked with the disease Muscle biopsy Urine myoglobin (muscle protein)
- 7. Treatmen During an episode of malignant hyperthermia, a medicine called dantrolene is often given. Wrapping the person in a cooling blanket can help reduce fever and the risk of serious complications. To preserve kidney function during an episode, the person may receive fluids through a vein.
- 8. Advantages & Disadvantages Advantages only it affects patients who received general anesthesia. It is inherited. Disadvantages limits the options for anesthesia can cause metabolic acidosis cause myopathy kills