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EA, 52 y/o F (Mitochondrial Encephalopathy: decreased protein synthesis…
EA, 52 y/o F
Mitochondrial Encephalopathy: decreased protein synthesis may ultimately lead to the observed decrease in respiratory chain activity by reduced translation of UUG-rich genes such as ND6
Patient currently in respiratory failure. On ventilator: A/C Mode. PEEP 5, Flow rate: 1.0 l/min, FiO2 21, BPM 20, LVol 0.45, peak flow 60 L/min
Last ABGs: pH 7.446, O2 83.8, CO2 35.8, HCO3 24.1. Values are technically normal but edge toward alkalosis
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L-carnitine
Monitor BG, may cause hyperglycemia
Thiamine
Monitor for GI bleed, pulmonary edema, angioedema
Unspecified seizures: Paroxysmal discharges from groups of neural cells, which arise as a result of excessive excitation or loss of inhibition.
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Lacosamide
Monitor for bradycardia, or Afib
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Type II Diabetes: Peripheral insulin resistance and inadequate insulin secretion by pancreatic beta cells
Primary risk factors: high BMI, high carbohydrate intake over many years, smoking, genetic factors, old age
Educate patient and family on lifestyle changes and management. Patient reportedly had poor control over T2D, and was even mentioned (by son) to be sharing lancets with someone else (!)
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Hypoglycemia protocol for BG > 70: glucose tabs, IM glucagon. Monitor BG Q 15 minutes
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MELAS: Mitochondrial Encephalopathy, Lactic acidosis, and Stroke-like episodes. Rare genetic disorder. A heteroplasmic A-to-G point mutation in the dihydrouridine loop of the transfer RNA Leu gene at base pair 3243, leads to the disruption of the global process of intramitochondrial protein synthesis.
2014: first similar episode and exacerbation. Genetic testing confirmed diagnosis. Unknown to what extent disease may be inherited, however, patient has no family history on file. Obtaining family history was not possible this week as patient was unconscious and family did not visit
Pt was prescribed "mitochondrial cocktail" to prevent exacerbation, not to cure
Pt stopped taking medications as she (and family) believed they were supposed to be curative and "didn't work"
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Lactic Acidosis: Mitochondria are unable to continue creating ATP at a rate sufficient to meet the cell's energy needs, causing systemic build-up of lactic acid
Mitochondrial cocktail treatment (e.g. creatine, CoQ-10, etc.)
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Stroke-like symptoms: Nitric oxide can bind the cytochrome c oxidase–positive sites in the blood vessels present in the CNS, displacing heme-bound oxygen and resulting in decreased oxygen availability in the surrounding tissue and decreased free nitric oxide.
Admitted 2/14/2020 with suspected stroke. Tachycardic, hypokalemic, and hypernatremic. Imaging shows no evidence of CVA.
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Non-traumatic rhabdomyolysis: Skeletal muscle cell damage leading to the release of toxic intracellular material into the blood circulation.
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Sinusitis: Aggregates of extracellular matrix and interdependent microorganisms infiltrate the epithelium of sinus tissue.
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