❓Why is insulin recommended when HbA1c is >10%?

1) Severe glucotoxicity
Persistent hyperglycemia suppresses β-cell function and worsens insulin resistance. Insulin rapidly reverses this "glucose toxicity."

2) Relative insulin deficiency
An HbA1c >10% often indicates that endogenous insulin secretion is insufficient. Oral agents alone may not provide adequate glycemic control.

3) Oral medications are not enough
Most oral glucose-lowering drugs reduce HbA1c by 0.5–1.5% and require weeks to achieve their full effect. This is usually inadequate for very high HbA1c levels.

4) Insulin is the most potent
Unlike oral agents, insulin has no fixed maximum glucose-lowering effect and can be titrated to achieve target glucose levels.

5)Prevents catabolism and acute metabolic complications
Patients with HbA1c >10% may have weight loss, dehydration, ketosis, or marked hyperglycemic symptoms. Insulin rapidly suppresses lipolysis and ketogenesis, restores an anabolic state, and relieves symptoms.

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@TheBrainCandy

What is Type 5 Diabetes?

It is diabetes caused by chronic undernutrition, particularly during childhood or adolescence. Long-standing malnutrition impairs pancreatic development and reduces insulin-producing β-cell mass, leading primarily to insulin deficiency rather than autoimmune destruction.
Frequently misdiagnosed as either Type 1 or Type 2 diabetes

Key Clinical Features
-Lean body habitus
-Reduced insulin secretion without autoimmune β-cell destruction
-Little or no significant insulin resistance at presentation
-Negative pancreatic autoantibodies
- Marked hyperglycemia with little or no ketosis, even at very high glucose levels
- High risk of hypoglycemia if treated with insulin doses typically used for Type 1 diabetes

An Important Concept!
As nutritional status improves after prolonged malnutrition, some individuals may develop increasing insulin resistance and their disease can evolve to resemble Type 2 diabetes, reflecting the combined effects of impaired β-cell function and later metabolic changes.

Why does it matter?
Recognizing Type 5 diabetes prevents misclassification and inappropriate treatment. These patients often require careful nutritional rehabilitation and individualized glucose-lowering therapy rather than being managed exactly like patients with Type 1 diabetes.

So!
Not every lean patient with diabetes has Type 1 diabetes.

@TheBrainCandy

This image is a map of a country called Anterior Pituitary.

➮In the remote border regions live the Somatotrophs (GH) and many Gonadotrophs (LH/FSH). These peripheral provinces are the first to suffer when a slowly growing invader arrives.
➮ Near the center sits the capital, home to the Corticotrophs (ACTH)—the emergency command that keeps the whole nation running through cortisol.

When a macroadenoma grows gradually: The outer provinces are compressed first. GH deficiency often appears early, followed by gonadal dysfunction. The capital usually holds out longer.

➮ when disaster strikes suddenly—pituitary apoplexy (hemorrhage or ischemia): The command center may fail abruptly. ACTH secretion can collapse, cortisol levels fall, and the country enters a life-threatening crisis.

In that moment, a new ruler must be appointed immediately: Hydrocortisone.

Delay the coronation, and the kingdom may collapse.

In chronic compression, GH and gonadotropins are often affected first; in acute pituitary apoplexy, secondary adrenal insufficiency is the endocrine emergency that must be treated immediately with glucocorticoids.

May God save our Country ,i mean,pitutary  gland!

@TheBrainCandy

PAD is one of Atherosclerosis cardiovascular disease.
Think of it as equivalent of MI or stroke, even though it is less severe as leg has more collateral vessels and not vital as brain and heart!

The COMPASS trial showed that in patients with stable coronary artery disease or PAD : Rivaroxaban 2.5 mg twice daily + aspirin reduced:
• Major cardiovascular events (CV death, MI, stroke)
• Major adverse limb events (acute limb ischemia and major amputations)

⚠️ The benefit was accompanied by an increased risk of major bleeding.

🗨️
Treat selected PAD patients with low bleeding risk by aspirin 81mg po daily + Rivaroxaban 2.5mg po bid to reduce both cardiovascular and limb events.

@TheBrainCandy

በነገራችን ላይ
"You may be sure you haven't had a heart attack, stroke, or PAD... but are you sure you don't already have silent disease behind them all—atherosclerosis? "

Atherosclerosis begins years—often decades before first heart attack or stroke.

It Is called Subclinical atherosclerosis when silent plaque building up inside the arteries without any symptoms.

Just the silent "evil" growing beneath the surface.

This hidden plaque is the real driver of future myocardial infarction, ischemic stroke, and peripheral arterial disease.

So how can we detect it before it becomes a disaster?

One of the best tools is the Coronary Artery Calcium (CAC) score, a non-contrast CT scan that quantifies calcified plaque in the coronary arteries.

When is CAC useful?

Mainly when your cardiovascular risk is uncertain (borderline/intermediate) and the result would change the decision to start or intensify statin therapy.

Let's find the plaque before the plaque finds the patient.😂

@TheBrainCandy

Growth Hormone(GH) Vs Insulin

GH signals the liver to produce Insulin like Growth Factor-1[IGF-1].

Ok! but...

GH is a counter regualtory hormone for insulin[ i.e. antiInsulin effect]

So the question is if GH is an antiinsulin, why does it make an insulin-like growth factor? 💀

"ምን አልኩህ ዶክተር?!"

New era in HFpEF vs We Ethiopian!

Previously!
The pharmacological management of heart failure with preserved ejection fraction (HFpEF) relied heavily on symptom-focused therapies(diuretics), comorbidity management ( forHTN,Afib... ) , SGLT2i and MRAs.

Despite these medications, obese patients with HFpEF continued to suffer from severe functional limitations.

***
Obesity was viewed as a complicating comorbidity rather than a direct, treatable driver of the underlying HFpEF pathophysiology.

The STEP-HFpEF program and the SUMMIT trial fundamentally altered this view, establishing that targeting the metabolic driver directly improves cardiac endpoints.
In these trials ... GLP1 showed improvment in Quality of life ,functional capacity, risk reduction in CV death.

Now GLP-1 receptor agonists is guideline recommendation for patients presenting with an obese-HFpEF phenotype (LVEF ≥ 45-50% and BMI ≥ 30 kg/m²).

እኔ: "እማማ አንድ መድኃኒት አለ የሚያስፈልገዎት ትንሽ ወደድ ይላል!"
ታካሚ: "ስንት ይሆናል? Dapaውም ተወዶብኛል" አሉ።
እኔ: የአንድ ወር 39ሺህ እስከ 40ሺህ ብር ይሆናል።[በውስጤ:- የእኔ የሁለት ወር ደመወዝ ማለት ነው]

ታካሚ : "ምን አልኩህ ዶክተር?!🙄"

My 2-month Endocrinology attachment is officially done! 🎉

The notes above are just a few pearls collected by a hawk flying over the vast ocean of endocrinology. 🦅🌊

How did you find them?
❤️ Helpful?
🤯 Mind-blowing?
🙄 Confusing?
😑 Useless?

I'd genuinely love your feedback by emojis.
Should I continue sharing notes from my next attachment? 😉

🫁 Did you know?

Healthy people aspirate small amounts of oropharyngeal secretions during sleep surprisingly often. Studies suggest up to 40–50% of healthy adults experience microaspiration while sleeping.
Why don't they develop pneumonia?
Because normal protective mechanisms clear the aspirated material:
✔️ Cough reflex ✔️ Intact swallowing
✔️ Mucociliary clearance ✔️ Alveolar macrophages
✔️ Normal immune defenses

⚠️ When these protective mechanisms fail...
Examples include:reduced consciousness, seizures,GA, Alcohol intoxication, dysphagia,endotracheal intubation, Neuromuscular disease

Aspiration becomes clinically significant.
From here, two different diseases may develop.
1️⃣ Chemical pneumonitis (sterile inflammation)
Usually follows aspiration of acidic gastric contents.
The acid causes chemical injury to the lungs—not infection.
Typical features:
Sudden onset (minutes to hours), Acute hypoxemia, Respiratory distress, Bilateral infiltrates
Fever may occur, but it does not necessarily mean infection
👉 Treatment?
Oxygen
Airway support (HFNC/CPAP/mechanical ventilation if needed)
Suction if appropriate
Supportive care
Treat the underlying cause
🚫 Do NOT rush to antibiotics.
Most patients improve within 24–48 hours with supportive care alone.
Only a minority (about 20–30%) subsequently develop secondary bacterial aspiration pneumonia.

2️⃣ Aspiration pneumonia (infection)
This occurs when aspirated material contains bacteria that establish infection.
Usually develops 24–72 hours after aspiration.

Features:
Persistent or new fever
Leukocytosis
Purulent sputum
Worsening infiltrates
Positive respiratory cultures (when obtained)

👉 This is when antibiotics are indicated.

💊 Antibiotic choice
Choose antibiotics based on where the aspiration occurred:
Community-acquired aspiration pneumonia
Target the usual community respiratory pathogens (and oral flora when appropriate).
Hospital-acquired aspiration pneumonia
Cover hospital-acquired pathogens according to local resistance patterns and HAP/VAP guidelines.

❌ Metronidazole is NOT for everyone
Older teaching suggested routine anaerobic coverage for all aspiration pneumonia.
Current evidence and modern guidelines no longer support this.
Routine addition of metronidazole is generally unnecessary.
Consider anaerobic coverage (e.g., metronidazole or another regimen with anaerobic activity) only when there is strong suspicion of anaerobic infection, such as:
Lung abscess
Empyema
Necrotizing pneumonia
Severe periodontal disease with putrid sputum
Other clinical evidence of anaerobic aspiration

Summary
➡️ Aspiration ≠ antibiotics.
Witnessed aspiration → Think chemical pneumonitis first.
Provide excellent supportive care.
Observe closely over the next 24–48 hours.
Start antibiotics only if bacterial aspiration pneumonia becomes evident or infection is strongly suspected.
Don't prescribe metronidazole routinely—reserve anaerobic coverage for selected situations.
Treat the patient, not the aspiration event.

Hilar LAP is not always from TB!

The hila contain the proximal pulmonary arteries, bronchi, pulmonary veins and lymph nodes.

Hilar enlargement caused by
*enlarged lymph nodes [from different causes]
*enlarged pulmonary arteries[from different causes]
* bronchial masses

@TheBrainCandy