Medicine in a minutes

📌 52 years old female patient with diabetes mellitus on oral treatment, presented with bilateral foot and peri orbital edema .

📌 no Hx of CVD , nor Hx peripheral arterial disease.

📌 DM is poorly controlled, and no dietary restriction

✅ Examination : bilateral piiting leg edema grade III , vitally stable , mild peri ocular edema . soft abdomen.

✅ Investigation.. unremarkable RFT , LFT ,TFT ,CBC ,CRP ,ESR , abdominal Us .

but when we sent urinary albumin creatinin ratio interestingly, results as shown above .

🖍diabetic nephropathy is one of commonest nephropathy, when albuminuria is Hallmark of early damage.

🖍if expect that , do urinary albumin creatinin ratio test , that detect early renal insult.

Did you know that the Heart failure treatments you are reading 🔴
And the treatments are referred to as improves prognosis
Such as
ACEI , beta blockers,spironolactone,SGLT2,ARNI,ARBS
She is special to :
Heart failure with reduced ejection fraction (HFrEF)
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🔴Or heart failure with reserved EF
There is no treatment that reduces mortality
But recently it was reported that
SGLT2 can improve prognosis in HFpEF
To become a necessary treatment for all these patients
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Recurrent attacks of this condition
Sometimes triggered by dental procedures, or minor trauma
DX?
Non allergic angioedema (bradykinin mediated)

Diagnosis: Chilaiditi Sign.
Reasoning: The air pocket under the right diaphragm clearly demonstrates haustra (the segmented appearance typical of the large intestine). This confirms that the air is contained within the bowel, rather than being free air in the abdominal cavity. The colon has simply migrated superiorly to sit between the liver and the diaphragm.
Clinical Note: If the patient is asymptomatic, this is simply an anatomical curiosity called Chilaiditi Sign.
Clinical Note: If the patient has abdominal pain, nausea, or respiratory distress, this is termed Chilaiditi Syndrome.

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How the respective patterns of subendocardial (B) and subepicardial (C) experimental injuries are generated according to the theory that the normal ECG pattern (A) is the result of the sum of subendocardial and subepicardial transmembrane action potentials (APs). (B) The example explains the pattern in the case of subendocardial experimental work and also for subendocardial clinical ischemic. (C) This shows the case of experimental subepicardial ischemia. In the clinical setting (D), the ischemic is transmural, never only subepicardial. Therefore, the ST elevation in the clinical setting may be explained by the sum of low‐quality APs of the ischemic zone + normal AP of rest of left ventricle.