Blood pressure–lowering therapy and treatment targets should be individualized in patients with frailty, a high risk of falls, very limited life expectancy, or symptomatic postural hypotension.
Therapies with strong evidence for delaying chronic kidney disease (CKD) progression include renin–angiotensin system inhibitors (RASi) and sodium–glucose cotransporter 2 inhibitors (SGLT2i). In patients with CKD and heart failure, SGLT2i provide benefits regardless of albuminuria status.
A modest initial decline in estimated glomerular filtration rate (eGFR) is expected following the initiation of hemodynamically active agents such as RASi and SGLT2i. However, a reduction in eGFR of ≥30% from baseline exceeds anticipated variability and should prompt further evaluation.
CKD is not a contraindication to invasive management strategies in patients with acute or unstable cardiac conditions. Similarly, imaging studies are not absolutely contraindicated in patients with CKD; the decision should be based on a careful assessment of individual risks and benefits.
Monitor blood pressure, serum creatinine, and serum potassium levels within 2 to 4 weeks after initiating or increasing the dose of an angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB). ACEi or ARB therapy should generally be continued unless serum creatinine increases by more than 30% within 4 weeks of initiation or dose escalation.
According to FDA recommendations, metformin should not be used in men with a serum creatinine level ≥ 1.5 mg/dL or in women with a level ≥ 1.4 mg/dL, or in individuals over 80 years of age with decreased creatinine clearance. However, treatment with metformin is recommended in patients with type 2 diabetes (T2D), chronic kidney disease (CKD), and an estimated glomerular filtration rate (eGFR) ≥ 30 mL/min/1.73 m².
ADA/KDIGO Consensus Statements:
All patients with type 1 or type 2 diabetes and CKD should be managed using a comprehensive, individualized care plan developed collaboratively between healthcare professionals and the patient. This plan should focus on optimizing nutrition, physical activity, smoking cessation, and weight management. Evidence-based pharmacologic therapies should be implemented to preserve organ function, alongside additional treatments aimed at achieving intermediate targets for glycemic control, blood pressure, and lipid management.
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Myocardial Infarction (MI)
Myocardial infarction is classified into five types based on the underlying etiology and clinical circumstances:
Type 1 MI: Spontaneous myocardial infarction resulting from ischemia due to a primary coronary event, such as plaque rupture, erosion, fissuring, or coronary artery dissection.
Type 2 MI: Myocardial ischemia secondary to an imbalance between oxygen supply and demand. This may occur in the setting of increased demand (e.g., severe hypertension) or decreased supply (e.g., coronary artery spasm, embolism, arrhythmias, or hypotension).
Type 3 MI: Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia and presumed new ECG changes or ventricular fibrillation before biomarkers can be obtained.
Type 4a MI: Myocardial infarction associated with percutaneous coronary intervention (PCI), defined by an elevation in cardiac troponin (cTn) values >5 times the 99th percentile upper reference limit (URL), along with evidence of ischemia.
Type 4b MI: Myocardial infarction associated with documented stent thrombosis.
Type 5 MI: Myocardial infarction occurring in the context of coronary artery bypass grafting (CABG), with cTn elevation >10 times the 99th percentile URL and supporting clinical or imaging findings.
Infarct Location and Clinical Implications
Right Ventricular (RV) Infarction: Most commonly results from obstruction of the right coronary artery or a dominant left circumflex artery. It is characterized by elevated right ventricular filling pressures, which may be accompanied by severe tricuspid regurgitation and reduced cardiac output. RV infarction can significantly impair hemodynamics.
Inferoposterior Infarction: Often leads to some degree of RV dysfunction in approximately 50% of cases and hemodynamic compromise in about 10–15%. In patients with inferoposterior infarction, elevated jugular venous pressure in conjunction with hypotension or shock should prompt consideration of RV involvement. RV infarction in the setting of left ventricular infarction markedly increases mortality risk.
Anterior Infarction: These infarcts are typically larger and are associated with worse outcomes compared to inferoposterior infarctions. They usually result from obstruction of the left coronary artery, particularly the left anterior descending artery. In contrast, inferoposterior infarctions are commonly due to right coronary artery or dominant left circumflex artery occlusion.
Cholangitis
Cholangitis was first defined in 1877 by Jean-Martin Charcot, who described the pathognomonic triad of fever, right upper quadrant pain, and jaundice. Today, cholangitis is defined as the presence of increased hepatic intraductal pressure along with concurrent infection of the obstructed bile ducts.
Chole: Derived from the Greek word “cholÄ“,” meaning bile.The pathogens most commonly identified as causative agents of acute ascending cholangitis are gram-negative and anaerobic organisms. The most common pathogens include Escherichia coli, Klebsiella, Enterobacter, Pseudomonas, and Citrobacter.
Iatrogenic introduction of bacteria often occurs following endoscopic retrograde cholangiopancreatography (ERCP) in individuals with biliary obstruction.
Charcot's Triad: The classical triad (fever, right upper quadrant pain, and jaundice) has high specificity (95.9%) but low sensitivity (26.4%).
Tokyo Guidelines (2018): The sensitivity of the Tokyo guidelines is 100%, with a specificity of 87.4%.
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Thyroid Storm
CAPNOGRAPHY V/S PULSE OXIMETRYCAPNOGRAPHY 
Drainage of the abscess & antibiotic treatment are the cornerstones of treatment.
IV electrolyte replacement can produce life-threatening complications, serious arrhythmias & phlebitis; therefore, supplementation must be carefully monitored. There are multiple underlying factors for electrolyte disorders in adult inpatients, including alterations in absorption, distribution, hormonal, and/or homeostatic mechanisms that can all cause disturbances. Treating the underlying cause and prescribing adequate therapy is essential for repletion. In addition, the intracellular vs. extracellular electrolyte concentrations must be considered. Due to distribution variances, labs may not directly correlate with true electrolyte levels. Therefore, continuous monitoring is essential to properly replete patients.
Immune-mediated: Certain drugs can trigger an immune response that leads to the production of antibodies targeting and destroying platelets. This immune-mediated destruction is a common mechanism of drug-induced thrombocytopenia (DITP). Examples of drugs associated with immune-mediated DITP include specific antibiotics (e.g., penicillins and sulfonamides), nonsteroidal anti-inflammatory drugs (NSAIDs), and some anticonvulsants.
Non-immune-mediated: Other drugs can cause thrombocytopenia through non-immune mechanisms, such as direct toxicity to the bone marrow, where platelets are produced. For instance, chemotherapeutic agents can suppress bone marrow function, resulting in decreased platelet production.
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The
primary bile acids—cholic acid and cheno-deoxycholic acid—are synthesized from
cholesterol in the liver.
The
maximal rate of bile acid synthesis is on the order of 4 to 6 g/day.
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The
isthmus connecting the two renal masses may be positioned in the midline or
laterally resulting in an asymmetric horseshoe kidney, 70% of which are left
dominant.
The
isthmus consists of renal parenchyma in about 80% of cases with the remainder
being composed of a fibrous band.
In
more than 90% of cases, fusion occurs at the lower pole, although fusion may
occur at the upper pole in a small minority of cases.
Higher incidence of UPJ obstructions, nephrolithiasis, and reflux compared to the general population. Increased frequency of some common renal cancers including transitional cell tumors (three to four times more common), Wilms tumor (twice as frequently), and an extremely large increase in very rare tumors such as carcinoid (62 to 82 times).
Multisystem
& progressive disease with cysts formation
Kidney
enlargement with other organ involvement (liver∼ 80%, pancreas
7-36%, spleen)
Intracranial
aneurysms in ∼6% of pts without family history & ∼20%
with a family history (rupture in 65-75%, usually before age 50)
Cardiac
Valve abnormalities in 25-30%
Borders
The above differ from the original description of
Calot’s triangle in 1891 – where the cystic artery is given as the superior
border of the triangle. The modern definition gives a more consistent border
(the cystic artery has considerable variation in its anatomical course and
origin).
Contents
Significance
Supra-physiological dose stimulates the pituitary & releases cortisol from the adrenal cortex, as long as the adrenal cortex has a functional reserve.
Factors
affecting ACTH stim test interpretation:
In females, response to ACTH may be affected OCs which increase CBG levels.
