Discussion 2 - Keeping the pH just right! 4949 unread replies.4949 replies. Our bodies are amazing! At any given time, t

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Discussion 2 - Keeping the pH just right!
4949 unread replies.4949 replies.
Our bodies are amazing! At any given time, there are thousandsof different chemical reactions happening in the background of ourbodies to make sure that we are able to function "normally". Ourbody also has many chemical protections built in to make sure thatincoming chemicals don't take us out of normal conditions. One ofthese protections are acid/base buffers.
Buffers are solutions that help keep their environment at acertain pH range. Different parts of your body need to be atdifferent pH's in order to function properly. Your stomach needs tokeep a pH between 1.5 and 3.5 (very acidic) in order to help breakdown food. Your intestines, however, have to have a pH between 5.7and 7.4. When food passes from the stomach to the intestines, thepH needs to drastically so that your intestines don't get hurt. Thepancreas helps to neutralize the pH by adding some bicarbonate(baking soda). Amazing!
Another important part of the body where the pH is buffered isyour blood. Your blood needs to stay between 7.35 and 7.45, sothere is a complex buffering solution to help keep it there.
Even though our bodies are typically really good at keeping thepH where it should be, there are times when these solutions beginto fail. Please read the following case study and thenpost your thoughts on it, along with another example that youindependently find in which acids and bases are causing problems.Unlike last discussion, the example you post can be medical, butyou are also free to find something environmental, industrial, orany other source. Additionally, you need to find two other postsand comment on them in order to receive full credit.
Life-threatening Metabolic Acidosis -
T. Umeda, T. Bartolomei et.al.
Case Description: In health, blood pH ismaintained within a narrow reference range, 7.35-7.45. Medical texts discussing general aspects of acid-base disturbancefrequently include the observation that pH <6.8 is inevitablyfatal. However, there are individual case reports of survivaldespite this degree of extreme acidosis. One such is recentlyreported in which the patient made an apparent full recoveryfollowing an arterial blood pH of just 6.57. The case concerns a 57-year-old lady with type 2 diabetes whosediabetes treatment comprised the blood-glucose-lowering drugmetformin along with daily insulin injections. She also had ahistory of hypertension and peripheral vascular disease thatnecessitated long-term prescription of other drugs, including astatin, aspirin and an angiotensin-converting-enzyme (ACE)inhibitor. The lady presented to the emergency department (ED) of her localhospital with a 3-day history of severe watery diarrhea, nausea andvomiting. Her mental status had deteriorated; she was evidentlydisorientated and confused. She was found to be hypoglycemic (bloodglucose 47 mg/dL, 2.6 mmol/L) and given glucagon.Soon after arrival at ED the patient, who was acutely hypotensive(blood pressure 70/39 mmHg), suddenly became unresponsive andsuffered cardiopulmonary arrest. Following 3 minutes of CPR sheregained spontaneous circulation and was transferred to intensivecare with shock-induced (type 4) acute respiratory failure thatnecessitated intubation and mechanicalventilation. Administration of epinephrine restored blood pressure somewhat(98/37 mmHg) but blood gas analysis at this time revealed severe,high-anion-gap metabolic (lactic) acidosis: pH 6.57, bicarbonate 2mmol/L (2 mEq/L), anion gap 30 mmol/L, and lactate 16.3 mmol/L.Raised creatinine (8.07 mg/dL, 713 µmol/L) confirmed acute kidneyinjury (AKI); her baseline creatinine recorded 1 month earlier wasnormal (0.86 mg/dL, 76 µmol/L).Differential diagnosis of the high-anion-gap lactic acidosisincluded: severe sepsis (septic shock), acute coronary event(cardiogenic shock) and metformin toxicity. In the event, metformintoxicity due to impaired renal clearance of the drug consequent onAKI, aggravated by the ACE inhibitor drug the lady had beenprescribed, was considered the most likely cause.Metformin was withdrawn and urgent renal replacement therapy in theform of intermittent hemodialysis was started. Soon afterinitiation of hemodialysis, the severe acidosis resolved andhemodynamic state gradually started to improve so that the dose ofepinephrine and vasopressin that had been necessary to maintainblood pressure could be reduced. The lady’s condition continued to improve and on admission day 4both epinephrine and vasopressin were withdrawn and on day 6 shewas extubated and able to breathe independently. She was dischargedfrom intensive care 9 days after admission, and from hospital 6days later without any neurological consequence of the cardiacarrest she had suffered. Normal renal function was eventuallyrestored.During her stay in intensive care, investigations revealed noevidence that the severe lactic acidosis was caused by eitherinfection or an acute coronary event, and justification for thediagnosis of metformin toxicity came on day 7 (6 days after thestart of hemodialysis) when serum metformin concentration was foundto be 42 µg/mL (therapeutic range 1-2 µg/mL). Discussion: Acidosis: In discussion of thiscase history the authors explain that metformin-associated lacticacidosis (MALA) is a well-known but relatively rare adverse effectof metformin use; it usually only occurs in those with reducedrenal function.