Lab Rats In Lab Coats
اني ليش مدوخ روحي ومدوخكم بهاي التفاصيل؟ لأن شفت مريضة مشخصيها على أنها SLE وهي (بشهادة الطبيب اللي مشخصها) ما عدها غير 2 من أصل 11 من الـ ACR criteria اللي هي الـ immunological والـ arthritis، وحتى ذني مو أكيدات. بس الطبيب من شاف الـ anti-dsDNA +ve جزم بأنها…
Update:
راحت لأطباء روماتو ثنين، وعادت التحاليل مرتين، مرة طلعت نفس النتيجة (anti-dsDNA +ve in low titer والـ ANA هالمرة +ve). والتحليل الثاني طلع -ve. وبعدها ما عدها علامات سريرية للمرض. بالنتيجة اعتبروا أنّ ما عدها SLE (الطبيبة الثانية نصحتها تاخذ الأدوية prophylactically and just in case) بس المريضة رفضت خوفًا من الأعراض الجانبية. ورح تعيد التحليل بعد 6 أشهر.
راحت لأطباء روماتو ثنين، وعادت التحاليل مرتين، مرة طلعت نفس النتيجة (anti-dsDNA +ve in low titer والـ ANA هالمرة +ve). والتحليل الثاني طلع -ve. وبعدها ما عدها علامات سريرية للمرض. بالنتيجة اعتبروا أنّ ما عدها SLE (الطبيبة الثانية نصحتها تاخذ الأدوية prophylactically and just in case) بس المريضة رفضت خوفًا من الأعراض الجانبية. ورح تعيد التحليل بعد 6 أشهر.
To make things even more complicated, SLE patients can have +ve serology two to one year prior to clinical manifestations. Which is why it's advicable to redo the tests a few months later (granted the lab is trustworthy).
T3 & T4 hormones lead to increased cardiac output (CO) and a decrease in systemic vascular resistance (SVR). They also exert a positive inotropic effect on the myocardium.
That's why hyperthyroidism causes wide pulse pressure and systolic hypertension (because of the increase in CO with the simultaneous decrease in SVR).
Hypothyroidism, on the other hand, causes diastolic hypertension by decreasing CO while increasing SVR.
Unfortunately, many of the antiarrhythmic agents are known to have dangerous proarrhythmic actions—that is, to cause arrhythmias.
When the underlying cause of the lactic acidosis can be remedied, blood lactate will be converted to HCO3− and may result in an overshoot alkalosis if excess NaHCO3 has been administered excessively.
In general, NaHCO3 is not indicated in metabolic acidosis except when the pH < 7.1. Even then, it shouldn't be used to normalize the pH, but merely to reduce severity (raising pH to ~7.2)
Consider AKI in anyone with acute illness aged >65y, a history of kidney disease, those on nephrotoxic drugs, and patients who are systemically unwell (e.g. with sepsis).
If it is unclear whether a patient has worsening of their chronic kidney disease (CKD) or AKI, treat as the latter.
Lab Rats In Lab Coats
https://youtu.be/KlKB69DfrUM?si=Fydz3oORxAmAOdqC
Mixing sodium bicarb (NaHCO3) with calcium chloride (CaCl2) would give us CaCO3, that's chalk... Your patient will have chalk sludging in his vessels.
You also shouldn't give
Ceftriaxone & calcium products simultaneously or in the same IV line (especially for pediatric patients, even more especially for neonates). The calcium will crystalize and accumulate particularly in the lungs and kidneys. Guidelines differ, but it's safest to wait for about 48 hours before giving the other substance.
Ceftriaxone & calcium products simultaneously or in the same IV line (especially for pediatric patients, even more especially for neonates). The calcium will crystalize and accumulate particularly in the lungs and kidneys. Guidelines differ, but it's safest to wait for about 48 hours before giving the other substance.