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Medical World Dr Rana Sanjay, Dr Rana S P Singh, Patna (2025)

05/10/2025

31st ANNUAL CONFERENCE
CARDIOLOGICAL SOCIETY OF INDIA , BIHAR CHAPTER

🤔Asymptomatic severe aortic stenosis ( ) refers to a serious heart condition where the aortic valve is significantly narrowed but the patient doesn't experience symptoms, a situation now understood to carry a high risk of mortality. While historically treatment was delayed until symptoms appeared, recent evidence suggests a more proactive approach, with interventions like aortic valve replacement (AVR) possibly being beneficial to prevent adverse outcomes and irreversible cardiac damage. The decision for early intervention is complex and requires careful, individualized risk assessment, considering factors beyond just the valve stenosis severity.
👍Why it's a concern:
High Risk of Sudden Death: The transition from asymptomatic to symptomatic severe AS is often abrupt and associated with poor survival rates, with a significant risk of death in untreated severe AS.
Irreversible Cardiac Damage: Delaying intervention allows for further damage to the heart's left ventricle and other structures, which may not be reversible even after valve replacement.
High Prevalence: It is a common condition, particularly among older adults, and is a leading cause of valvular heart disease globally.
👌Shift in Management Strategy:
🫵From Conservative to Proactive: Traditional guidelines recommended close monitoring until symptoms or left ventricular dysfunction developed. However, newer studies and trials like the EASY-AS trial are exploring early intervention, such as TAVR or AVR, to potentially improve outcomes.
🫵Risk Stratification is Key: Identifying patients who may benefit from early intervention involves a deeper dive into their individual risk factors.
Specific High-Risk Characteristics: Indicators for potential early intervention include:
Very high peak aortic jet velocity (often >5 m/s).
Presence of significant myocardial fibrosis.
Valvulo-arterial impedance.
Global longitudinal strain and global myocardial work.
🫵Decision-Making Process:
Shared Decision-Making: The choice between early intervention and continued conservative management is a complex decision made in partnership between the patient and the heart valve team.
🫵Personalized Approach: Factors like the patient's age, comorbidities, and overall clinical status are crucial in determining the best course of action.
🫵Ongoing Research: There is ongoing debate and research, including large clinical trials, to determine the optimal timing and modality for intervention in patients with asymptomatic severe aortic stenosis.
🤔What is the survival rate for severe aortic stenosis?
🫵According to the British Medical Journal, after symptoms appear, patients with severe aortic stenosis have a survival rate as low as 50% at 2 years – and 20% at 5 years – without aortic valve replacement. So timely treatment is critical if you exhibit symptoms.
🤔What is aortic stenosis?
🫵Aortic valve stenosis (or aortic stenosis) describes an aortic valve in your heart that’s narrowed or blocked. This interferes with the normal blood flow out of your heart. Because this condition restricts blood flow, it also limits how much oxygen your body gets. This can cause chest pain, shortness of breath and fainting. Aortic stenosis can cause heart damage, major health problems and even death.
One of four valves in your heart, your aortic valve is the last one that blood flows through before going out to your body. Your aortic valve has three flaps (leaflets) that open to let blood pass through and then seal shut to keep blood from flowing backward into the last heart chamber.

A problem with this valve can be concerning. But today, there are more options than ever to treat aortic stenosis.
🤔What are the symptoms?
👉Aortic stenosis symptoms (progressing from less severe to more severe) include:

Fatigue, which can disrupt your normal activities.
Heart palpitations (being unpleasantly aware of your own heartbeat).
Swelling in your feet, ankles or lower legs.
Chest pain (angina). This can also feel like squeezing, pressure or discomfort and can extend to your neck, jaw, arm or abdomen.
Shortness of breath.
Dizziness, lightheadedness or fainting.
Your primary care provider may refer you to a cardiologist (heart doctor) if they suspect you have aortic stenosis.
🤔What causes aortic stenosis?
👉Aortic stenosis in adults has three main causes:

Wear and tear due to age: Over time, calcium can build up on your valve, limiting blood flow. This type of stenosis happens most commonly after age 65.
Damage from infections: When bacteria from untreated infections reach your bloodstream, they can accumulate on your heart valves. This causes your immune system to damage the valve itself. This is most likely to happen with strep throat or scarlet fever, which, when untreated, can cause rheumatic fever. This disease, which can damage your heart valves, happens most often in those over 50. It may take years or decades before the damage to your heart valves becomes apparent.
Other inherited or chronic conditions: Other rare conditions that can cause aortic valve stenosis are Paget’s disease of the bone, kidney failure and familial hypercholesterolemia. Aortic stenosis is also linked to autoimmune or inflammatory diseases like lupus and rheumatoid arthritis.
🤔What are the risk factors for aortic stenosis?
👉Risk factors for aortic valve stenosis include:
Being male.
Being older than age 65.
Having high cholesterol (hyperlipidemia).
Having high blood pressure.
Using to***co products.
🤔What are the complications of aortic stenosis?
👉When you have aortic stenosis, it takes more effort to move blood through your aortic valve. Your heart works harder than it should to push the blood through. This can lead to a heart attack, heart failure or sudden cardiac death.

People with aortic valve stenosis may also get pulmonary hypertension, bleeding or infective endocarditis.
🤔How is aortic stenosis diagnosed?
👌A cardiologist will typically diagnose this condition based on your symptoms (if you have them) and one or more of the following diagnostic tests:

👉Physical exam. Your provider may look for swelling in your lower legs and ankles, and will also listen to your heart. Providers can often hear a heart murmur, a key sign of aortic stenosis, using a stethoscope.
👉Electrocardiogram (ECG or EKG). This measures your heart’s electrical activity.
👉Chest X-ray, angiography or cardiac CT scan. Each of these uses X-rays to see inside your body.
👉Echocardiogram. This test uses ultrasound waves to create a picture of the inside of your heart.
👉Exercise stress testing. This test measures your heart function while you’re active.
👉Cardiac catheterization. A provider uses a catheter threaded through your arteries to see inside your heart.
👉Heart MRI (magnetic resonance imaging): Using a powerful magnetic field, this provides detailed scans of your heart.
🤔How is aortic stenosis treated?
👌If you have stenosis but no symptoms, your healthcare provider may advise you to simply monitor the issue with follow-up visits and tests. If you develop symptoms, your provider can offer you aortic stenosis treatment options, including:

💊Medication: Providers treat milder cases of aortic valve stenosis with medications. These may include blood thinners, diuretics and other medicines to treat heart rhythm disorders, high blood pressure or heart failure. Medications help with symptoms but can’t keep stenosis from getting worse.
🫀Valve repair: This involves either surgery or balloon valvuloplasty. During aortic valve surgery, a surgeon makes an incision in your chest to directly reach and repair the valve. If you have limited damage and little blood leakage, a provider may use balloon valvuloplasty. This widens your narrowed aortic valve and may improve symptoms until you can have a valve replacement.
🫀Valve replacement: Valve replacement offers several options for people who can’t have a valve repair. Aortic valve surgery replaces the valve with a donor valve (usually from a cow or pig), a mechanical valve or a bioprosthetic valve. Another option is a Ross procedure, which uses your own pulmonary valve to replace your damaged aortic valve. A provider then uses a donor valve to replace your pulmonary valve. Finally, a transcatheter aortic valve replacement (TAVR) allows for the replacement of an aortic valve without surgery. This procedure involves inserting a catheter-based device into an artery and then threading it to your heart.

✒️🩺 Lion DR RANA SANJAY PRATAP SINGH( Dr Rana SP Singh senior physician Patna Bihar 🇮🇳 India )
🥇DC 👉FIRST AID EDUCATION AND EMERGENCY RELIEF⚡ LIONS CLUB INTERNATIONAL DISTRICT 322E

04/10/2025

31st ANNUAL CONFERENCE
Cardiology society of india,venue: Ashoka Hall Maurya, Patna

🤔 , or low blood sodium, is common in heart failure (HF) due to the body's attempt to compensate for reduced cardiac output by activating the hormone vasopressin (AVP), which increases water reabsorption and dilutes sodium levels. Treatment depends on the type: fluid restriction and loop diuretics for dilutional hyponatremia from fluid overload, and sometimes isotonic saline or potassium/magnesium for sodium-depleting forms caused by diuretics. Vasopressin antagonists are a potential treatment for the persistent water retention seen in HF.
Why Hyponatremia Occurs
🫵Reduced Cardiac Output: A weakened heart can't pump enough blood, leading to decreased effective blood volume.
🫵Hormonal Response: This triggers the release of vasopressin (AVP) to try to preserve blood volume and pressure.
🫵Increased Water Reabsorption: AVP increases the kidneys' ability to reabsorb water, which dilutes the blood and lowers sodium concentration.
🫵Diuretic Use: The diuretics used to treat heart failure symptoms can also cause sodium loss, leading to a different type of hyponatremia.
Types of Hyponatremia in Heart Failure
🫵Dilutional Hyponatremia: This is the more common type in heart failure and occurs when the body retains too much water, diluting the remaining sodium. This is often a result of increased AVP and fluid overload.
🫵Depletional Hyponatremia: This type is caused by the excessive use of certain diuretics, which can deplete the body of sodium.
Treatment Approaches
The treatment depends on the specific type of hyponatremia:
👍For Dilutional Hyponatremia:
🫵Fluid Restriction: Limiting fluid intake helps to reduce the excess water in the body.
🫵Loop Diuretics: These medications increase the excretion of free water, helping to reduce the dilution of sodium.
🫵Vasopressin Antagonists: Drugs like tolvaptan are designed to block AVP's effects, promoting water excretion.
For Depletional Hyponatremia:
🫵Isotonic Saline: Administering isotonic (normal) saline can help replace the lost sodium.
Electrolyte Replacement: If potassium or magnesium levels are low due to diuretic use, replacing these can also be helpful.
🤔Why It Matters
Hyponatremia in heart failure is not just a lab finding; it is associated with worse outcomes. It can increase the risk of falls, fractures, and longer hospital stays. Correcting hyponatremia, when appropriate, can potentially lead to better clinical outcomes.
🤔How to treat hyponatremia in congestive heart failure?
👉Highly symptomatic hyponatremia is uncommon in CHF; however, if it occurs it should be treated with hypertonic saline with established diuresis.
🤔Which are two signs of worsening heart failure?
👉Two significant signs of worsening heart failure are a sudden increase in difficulty breathing or the need to use more pillows to sleep comfortably, and rapid weight gain due to fluid retention, often accompanied by swollen legs, feet, or abdomen. These symptoms indicate the heart is struggling more to pump blood and that fluid is building up in the body.
Breathing Difficulties:
Shortness of breath: This may be particularly noticeable when lying down, requiring you to prop yourself up with pillows at night to breathe easier.
Coughing or wheezing: You may experience a persistent cough or wheezing, sometimes with white or pink, frothy sputum, a sign of fluid in the lungs.
Fluid Buildup and Swelling:
Rapid weight gain: Gaining a few pounds in a day or two can be a sign of excess fluid in your body.
Edema: Noticeable swelling (edema) in your ankles, feet, or abdomen is a common indicator of fluid retention.
Increased need to urinate: Worsening heart failure can lead to needing to urinate more frequently, especially at night.
Other signs to watch for:
Fatigue: Extreme tiredness or weakness that worsens over time can signal a decline in heart function.
Confusion or memory loss: A reduced blood flow to the brain, a result of the heart's decreased pumping ability, can lead to confusion or disorientation.
Loss of appetite or nausea: Digestive problems can arise because the body is prioritizing blood flow to vital organs, leading to a feeling of fullness or nausea.
If you experience these signs, it's crucial to contact your healthcare provider immediately to get treatment and prevent complications.
✒️🩺 Lion DR RANA SANJAY PRATAP SINGH ( Rana SP Singh senior physician Patna Bihar 🇮🇳 India)
🥇DC 👉 FIRST AID EDUCATION AND EMERGENCY RELIEF ⚡LIONS CLUB INTERNATIONAL DISTRICT 322E
#स्वास्थ्य

25/09/2025

मैं लायन डॉ राणा संजय प्रताप सिंह उर्फ डाॅ राणा एस पी सिंह वरिष्ठ फिजिशियन पटना बिहार आपको Virus H3N2 पर विस्तृत जानकारी देता हूँ:🔬 1. परिचय

इन्फ्लूएंजा A वायरस का एक सबटाइप है।

"H" = Hemagglutinin (HA) और "N" = Neuraminidase (NA) surface glycoproteins होते हैं।

H3N2 की पहचान पहली बार 1968 के Hong Kong Flu Pandemic में हुई थी।

आज भी यह हर साल मौसमी फ्लू के एक मुख्य कारण के रूप में जिम्मेदार है।
🦠 2. संरचना व वर्गीकरण

Family: Orthomyxoviridae

Genome: Negative-sense, single-stranded, segmented RNA virus

Subtype: H3 (Hemagglutinin type 3), N2 (Neuraminidase type 2)

HA व NA antigenic drift व shift के कारण बार-बार नए वेरिएंट बनते रहते हैं।

📈 3. महामारी विज्ञान (Epidemiology)

हर साल Seasonal flu epidemics में H3N2 का बड़ा योगदान।

भारत सहित दुनिया भर में यह शरद व शीत ऋतु (Oct–Feb) में अधिक सक्रिय रहता है।

WHO surveillance के अनुसार, H3N2 अक्सर बच्चों, बुजुर्गों और इम्यूनोकॉम्प्रोमाइज्ड मरीजों में गंभीर रोग करता है।

1968–69 में H3N2 से विश्वभर में ~10–40 लाख मौतें हुईं।

🤧 4. क्लिनिकल लक्षण (Clinical Features)

Incubation period: 1–4 दिन

अचानक बुखार

खाँसी (dry cough)

गले में खराश

सिरदर्द, मांसपेशियों में दर्द (myalgia)

थकान, कमजोरी

कुछ मामलों में निमोनिया, ब्रोंकाइटिस, अस्थमा की worsening

⚠️ High-risk groups:

> 65 वर्ष

20/09/2025

Management: From BP to GFR — Q&A
🤔Q: Why is blood pressure (BP) tightly linked to kidney function ( )?
👉A: Hypertension damages small renal arteries/arterioles, leading to nephrosclerosis and reduced renal perfusion. This lowers the glomerular filtration rate (GFR). Conversely, impaired kidneys activate the RAAS (renin–angiotensin–aldosterone system), further raising BP. Thus, BP and GFR form a feedback loop in hypertension.
🤔Q: What BP targets are used in relation to kidney protection?
👉A:General hypertensive patients: 300 mg/day): ≤130/80 mmHg is recommended.
without proteinuria: some guidelines allow

19/09/2025

Infection-related Glomerulonephritis ( ): The Double-Faced Monster in Diabetics

🤔Q1. What is infection-related glomerulonephritis (IRGN)?
👉IRGN is a form of glomerulonephritis triggered by bacterial, viral, or fungal infections, commonly seen after Staphylococcus aureus, Streptococcus, or Gram-negative infections.

It is characterized by immune complex–mediated glomerular injury, typically presenting with hematuria, proteinuria, hypertension, and renal dysfunction.
🤔Q2. Why is it called a "double-faced monster" in diabetics?
👉Face 1 – Infection susceptibility:
Diabetics have impaired immunity (neutrophil dysfunction, reduced cytokine response, poor vascular supply).
They are more prone to recurrent skin, soft tissue, urinary tract, and respiratory infections.

Face 2 – Renal vulnerability:
Diabetics often already have diabetic nephropathy (proteinuria, reduced GFR).
Superimposed IRGN worsens kidney function, leading to rapid decline in renal reserve.
The prognosis of IRGN in diabetics is worse than in non-diabetics.
🤔Q3. What are the typical clinical features in diabetic patients with IRGN?
👉Fever, skin/soft tissue infection, pneumonia, or UTI preceding renal symptoms.
Hematuria (gross or microscopic).
Proteinuria (often nephrotic range in diabetics).
Acute kidney injury (rise in serum creatinine).
Hypertension and edema.
🤔Q4. What is the pathogenesis?
👉Infection → circulating immune complexes → deposition in glomeruli.
Complement activation (low C3 levels commonly).
In diabetics, preexisting glomerular damage + microvascular compromise → more severe injury and poor recovery.
🤔Q5. How is IRGN diagnosed?
👉History: Recent or ongoing infection.
Lab findings:
Low C3, normal/low C4.
Hematuria, proteinuria, RBC casts.
Elevated creatinine.
Biopsy findings: Endocapillary proliferative GN, neutrophil infiltration, subepithelial “hump”-like deposits (on EM).
🤔Q6. How is it managed in diabetics?
👉Eradicate infection: Prompt antibiotics, source control.

Supportive care: Blood pressure control, diuretics, dialysis if needed.

Glycemic control: Essential for recovery and preventing further infections.

Immunosuppression: Generally avoided (unless crescentic GN with rapid progression, and infection controlled).
🤔Q7. What is the prognosis in diabetics with IRGN?
👉Non-diabetics: Usually self-limiting with good renal recovery.
Diabetics: Poorer outcomes → higher risk of progression to chronic kidney disease or ESRD due to:
Older age, comorbidities.
Preexisting diabetic nephropathy.
Recurrent/persistent infections.
🤔Q8.What is infection-related glomerulonephritis?
👉Infection-related glomerulonephritis is an immunologically mediated glomerular injury after an infection. Glomerulonephritis may occur with the infection or after a variable latent period. Poststreptococcal glomerulonephritis (PSGN) is the prototype of infection-related glomerulonephritis.
🤔Q9.How to treat post-infectious glomerulonephritis?
👉Post-infectious glomerulonephritis treatment focuses on supportive care to manage symptoms like high blood pressure and fluid retention, including salt and fluid restriction, diuretics, and antihypertensive medications. While antibiotics treat the underlying infection, they don't prevent the condition but help prevent its spread. Immunosuppressants are generally not indicated unless there is evidence of severe, progressive kidney damage.
👌Supportive Care
🥗Dietary & Fluid Restriction: You may need to restrict sodium, fluids, and sometimes protein intake to help control blood pressure and fluid buildup (edema).
💦Diuretics: These medications can increase urine output to reduce fluid overload and lower blood pressure.
🫀Antihypertensives: Medications like calcium channel blockers or angiotensin-converting enzyme inhibitors may be used to manage high blood pressure that isn't controlled by diuretics.
🔬Dialysis: In cases of severe kidney failure, dialysis may be necessary to remove waste products from the blood.
💉Antimicrobial Therapy
💊Antibiotics: A course of antibiotics, such as penicillin, is used to eliminate any remaining bacteria, like group A strep, and prevent spread to others. However, this is generally not effective in preventing the development of the glomerulonephritis if given after the infection has set in.
🫵Special Considerations
👉Immunosuppressive Therapy: Steroids and other immunosuppressive agents are typically not recommended. However, they may be considered for a short course in patients with rapidly progressive kidney failure and crescent formation on a kidney biopsy.
👉Prognosis: Most children with post-infectious glomerulonephritis recover fully with no long-term problems. Adults are more likely to have residual kidney impairment.
👉Important Note: Always consult a healthcare professional for a proper diagnosis and treatment plan.
✅ Key Point for Informatics:
In diabetics, IRGN is a “double-faced monster” because infections both trigger the disease and worsen an already vulnerable kidney, making prevention, early recognition, and aggressive infection control crucial.
✒️🩺 Lion DR RANA SANJAY PRATAP SINGH ( Dr Rana SP Singh senior physician and diabetologist Patna Bihar 🇮🇳 India 🪷)
🦺DC 👉 FIRST AID EDUCATION AND EMERGENCY RELIEF🦁 LIONS CLUB INTERNATIONAL DISTRICT 322E
🦺DIABETES CHAIRPERSON 👉 LIONS CLUB OF PATLIPUTRA ASTHA

15/09/2025

🤔 -prone type 2 diabetes ( ) is a severe form of type 2 diabetes where patients present with diabetic ketoacidosis ( ) or severe ketosis at diagnosis but are not truly insulin-dependent like in type 1 diabetes. Initially, these patients often require insulin to treat the ketosis, but aggressive management of hyperglycemia and improved insulin sensitivity can lead to a state of insulin independence within months. KPD is common in people of African and Hispanic descent, shares risk factors with classical type 2 diabetes (such as obesity and family history), but lacks the autoimmune markers of type 1 diabetes.
Characteristics of KPD.

🤔Common warning signs:
🫵Excessive Thirst and Urination: You may find yourself feeling very thirsty and needing to urinate more often than usual.
🫵Nausea, Vomiting, or Abdominal Pain: These symptoms are often associated with DKA.
🫵Fatigue and Weakness: Feeling extremely tired or weak can be a sign of DKA.
🫵Fruity-Smelling Breath: Your breath may have a distinct fruity or sweet odor, similar to nail polish remover.
🫵Confusion or Difficulty Concentrating: Cognitive changes, such as confusion or trouble focusing, can occur.
🫵Dry Skin and Mouth: Dehydration can lead to a dry mouth and skin.
🫵Rapid, Deep Breathing: You might find yourself breathing more deeply or rapidly than normal.
🫵Flushed Face: A flushed or red face can be a symptom.
👉Severe Insulin Deficiency at Onset:
Patients experience severe hyperglycemia and often diabetic ketoacidosis (DKA) at diagnosis.
👉Absence of Autoimmune Markers:
Unlike type 1 diabetes, individuals with KPD do not have autoantibodies to islet cells, suggesting the cause isn't autoimmune.
👉Prognosis for Insulin Independence:
With proper aggressive diabetic management, beta-cell function and insulin sensitivity can improve, allowing many patients to discontinue insulin within a few months.
👉Distinct Clinical Features:
While the initial presentation can mimic type 1 diabetes, the long-term progression and features align more closely with type 2 diabetes.
👉Risk Factors:
KPD is frequently seen in obese individuals with a strong family history of diabetes, particularly within African and Hispanic populations.
Pathogenesis and Beta-Cell Dysfunction
👉Unique Beta-Cell Dysfunction:
KPD is characterized by distinct beta-cell dysfunction features that differentiate it from both type 1 and type 2 diabetes.
👉Glucose Toxicity:
Progressive hyperglycemia, a risk factor for ketotic relapses, can lead to glucose toxicity, which impairs beta-cell function and insulin sensitivity.
👉Potential Genetic Factors:
Some research suggests a potential monogenic etiology involving genes responsible for beta-cell development and function in certain KPD patients.

💉💊Treatment and Management
🫵Treatment for ketosis-prone type 2 diabetes (KPT2D) begins with an initial episode of diabetic ketoacidosis (DKA) management, including insulin, intravenous fluids, and electrolyte replacement. After DKA resolution, some patients may regain beta-cell function and can transition to lifestyle modifications and oral medications, while others may require long-term insulin therapy. Ongoing management involves regular monitoring of blood glucose, lifestyle changes like diet and exercise, and potentially adding oral antidiabetic agents to maintain control and prevent relapse.
Initial Treatment for DKA Episodes
👉1. Insulin Therapy:
Intravenous (IV) insulin is essential to reverse DKA and bring down high blood glucose levels.
👉2. Fluid and Electrolyte Replacement:
Intravenous fluids are administered to correct dehydration, and lost electrolytes like potassium are replaced.
Post-DKA Management and Transition
👌Beta-Cell Assessment:
After the DKA has resolved, a doctor will assess the patient's beta-cell functional reserve.
👌β- (Beta-cell deficiency): If beta-cell function is severely impaired, the patient will likely require long-term insulin therapy.
👌β+ (Beta-cell reserve): If the patient has preserved beta-cell function, they may be able to discontinue insulin.
👌Transition to Oral Medications:
Once blood glucose levels are controlled, a percentage of patients with KPT2D can be managed with lifestyle modifications (diet, exercise) and oral antidiabetic medications, such as metformin or sulfonylureas.
👌Monitoring for Relapse:
Patients who stop insulin therapy require close monitoring for at least two years to detect any signs of relapse, as progressive hyperglycemia can lead to a return of ketosis.
Long-Term Management
👌Lifestyle Modifications:
A combination of appropriate diet, regular exercise, and weight management (if applicable) is crucial for long-term control.
👌Oral Medications:
Insulin-sensitizing agents and other oral antidiabetic drugs are often used to control blood sugar levels.
👌Continued Monitoring:
Regular follow-up appointments are necessary to assess blood glucose control, monitor for potential relapses, and adjust treatment as needed.
✒️🩺 Lion DR RANA SANJAY PRATAP SINGH alias Dr Rana SP Singh, Senior physician and diabetologist Patna Bihar 🇮🇳 India 🪷
🥇DC 👉FIRST AID EDUCATION AND EMERGENCY RELIEF ⚡LIONS CLUB INTERNATIONAL DISTRICT 322E

Medical World Dr Rana Sanjay

05/10/2025

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