भिटामिन डी के हो? भिटामिन डी बारे जान्नै पर्ने कुरा मुख्य १० हरु २०८२

Table of Contents

भिटामिन डी बारे यस भित्र:

  • भिटामिन डी को स्रोत के हो?
  • हाम्रो शरीरमा भिटामिन डी को काम के हो? हामीलाई भिटामिन डी किन चाहिन्छ?
  • भिटामिन डी को दैनिक आवश्यकता के हो?
  • भिटामिन डी को कमी के कारणले हुन्छ ?
  • भिटामिन डी को कमी को लक्षणहरु के के हुन्?
  • भिटामिन डीको कमीले के कस्ता जटिलताहरू हुन्छन्?
  • भिटामिन डीको कमीबाट कसरी बच्ने ?
  • भिटामिन डी को कमी कसरी उपचार गर्ने?…
  • हाम्रो शरीरमा भिटामिन डी कसरी परीक्षण गर्ने?
  • भिटामिन डी पूरक को खुराक के हो?
  • के हामी भिटामिन डी को अधिक मात्रा गर्छौं?
  • यदि मलाई भिटामिन डी को कमी छ जस्तो लाग्छ भने मैले के गर्ने?

भिटामिन डी भनेको के हो?

भिटामिन डी एक आवश्यक सूक्ष्म पोषक तत्व हो जुन विभिन्न खाद्य स्रोतहरूमा पाइन्छ। भिटामिन डी बोसोमा घुलनशील हुन्छ, र केहि खानाहरूमा प्राकृतिक रूपमा भिटामिन डी पाइन्छ। फ्याटी माछाको कलेजो बाहेक, अन्य खानाहरू भिटामिन डीको कमसल स्रोतहरु हुन्। हड्डी स्रवस्थ राख्न र शरीरमा क्याल्सियम सन्तुलनको लागि भिटामिन डी आवश्यक हुन्छ।

भिटामिन डी को स्रोतहरु के के हुन?

छालामा भिटामिन डी को संश्लेषण मानव लागि भिटामिन डी को मुख्य स्रोत हो। छालामा रहेको भिटामिन डी
छालामा पराबैंगनी किरणको प्रभावले 7-डिहाइड्रोकोलेस्टेरोललाई प्रोभिटामिन D3 मा रूपान्तरण गरेर बनाउँछ। यो त्यसपछि तापमान निर्भर पुनर्व्यवस्था द्वारा cholecalciferol मा रूपान्तरण हुन्छ। अनुहार र हातमा सूर्यको
एक्सपोजरले भिटामिन डी प्रति दिन 200 IU (अन्तर्राष्ट्रिय एकाइहरू. (International Units) मात्र उत्पादन गर्दछ।
फ्याटी फिश कलेजो अर्को प्रमुख स्रोत हो। अन्य स्रोतहरुमा दूध, मासु र जनावरको कलेजो, अण्डा, केही तरकारीहरू र च्याउ पर्छन्।

हाम्रो शरीरमा भिटामिन डी को काम के हो? हामीलाई भिटामिन डी किन चाहिन्छ?

छालामा उत्पादन गरेपछि, वा खानाबाट भिटामिन डी (D2 वा D3) लिएपछि, हाम्रो रगतलाई 25-हाइड्रोक्सिभिटामिन D र त्यसपछि 1,25-हाइड्रोक्सिभिटामिन Dमा मृगौलामा परिणत हुन्छ। यो भिटामिन डी को सक्रिय रूप हो। 

भिटामिन डी को कार्यहरु निम्न छन्:

  • क्याल्सियम होमियोस्टेसिस
  • हड्डी चयापचय (Metabolism)
  • फास्फोरस चयापचय (Metabolism)
  • मांसपेशी बल
  • क्यान्सर बाट रोकथाम
  • उच्च रक्तचाप र हृदयघात जस्ता हृदय रोगको रोकथाम
  • अन्य endocrine रोगहरु र मधुमेह को रोकथाम
  • प्रतिरक्षा प्रणाली बढाउँदै
  • मस्तिष्क विकास र संज्ञानात्मक कार्य गिरावट को रोकथाम मा मद्दत
  • मानसिक रोगहरु बाट रोकथाम

भिटामिन डी को दैनिक कति आवश्यक हुन्छ ?

भिटामिन डी को दैनिक आवश्यकता  RDA निम्नानुसार छ:

  • १२ महिना सम्मको उमेर: 400 IU प्रति दिन (=10 mcg)
  • १-१८ वर्षका बालबालिका, ७० वर्षसम्मका व्यक्तिहरू: प्रति दिन 600 IU (=15mcg)
  • ७० वर्ष भन्दा माथिका मानिसहरू: 800 IU (=20mcg) प्रति दिन

मानिसहरूमा प्रायः भिटामिन डीको मात्रा कम हुन्छ, र धेरैजसो मानिसहरूमा भिटामिन डीको कमी हुन्छ। धेरै मानिसहरूलाई कमीको पर्याप्त जोखिम हुन्छ। तसर्थ, सबै उच्च जोखिममा रहेका मानिसहरूलाई भिटामिन डीको नियमित पूरकको लागि सिफारिस गरिन्छ। अहिले भिटामिन डी सहितको दुधको फोर्टिफिकेसनले पनि यो आवश्यकता पूरा गर्न थालेको छ ।

मालाब्सोर्पसन (Malabsorption) भएका मानिसहरूलाई प्रति दिन 40000 IU सम्म भिटामिन डी को उच्च थप मात्रा चाहिन्छ।

भिटामिन डी को कमी के कारणले हुन्छ?

विश्वव्यापी रूपमा, अरबौं मानिसहरूमा भिटामिन डीको कमी छ। तल उल्लेख गरिएका केही कारकहरूले हाम्रो शरीरमा

भिटामिन डीको कमी वा प्रतिरोधी हुन सक्छ:

  • सूर्यको किरणको कम जोखिम
  • कम आहार सेवन
  • कम बोसो सेवन
  • मालवशोषण विकार वा सिन्ड्रोम
  • कम घाम लाग्ने क्षेत्रहरूमा बसोबास
  • निष्क्रिय भिटामिन डी (कलेजो वा मृगौला रोग) को प्रयोग गर्ने शरीरको क्षमता कमजोर हुनु
  • हाम्रो शरीरमा पाइने भिटामिन डीलाई कार्य गर्न शरीरको प्रतिरोध
  • वृद्ध उमेर
  • स्टेरोइड औषधि सेवन को उच्च खुराक

भिटामिन डी को कमी को लक्षण के हो?

  • अधिकांश मानिसहरू सुरुमा लक्षणविहीन हुन्छन्
  • हड्डी दुखाइ र कोमलता (Tenderness)
  • मांसपेशी कमजोरी
  • फ्र्याक्चर
  • हिँड्न गाह्रो हुनु

भिटामिन डी को कमीको जटिलताहरु के के हुन?

  • हड्डी  खिइने (Increase bone loss)
  • ओस्टियोपेनिया र ओस्टियोपोरोसिस
  • क्याल्सियम मात्रामा कमी
  • पोटासियम मात्रामा कमी
  • माध्यमिक हाइपरपेराथाइरोडिज्म ( Secondary hyperparathyroidism)
  • फास्फेटुरिया (Phosphaturia)
  • ओस्टियोमलेसिया
  • मांसपेशी कमजोरी
  • क्यान्सर
  • रोग प्रतिरोधात्मक क्षमता कम वा अटोइम्यून रोगहरु
  • दम
  • उच्च रक्तचाप,
  • एमआई
  • मधुमेह
  • गर्भावस्था खरावि परिणाम

भिटामिन डीको कमीबाट कसरी बच्ने ?

  • प्रत्यक्ष सूर्यको प्रकाशमा पर्याप्त एक्सपोजर पाउनुहोस्, विशेष गरी बिहान (१० बजे देखि २ बजे) जब सूर्यको
  • किरणमा पर्याप्त एकाग्रता र UV प्रकाशको ब्यान्ड हुन्छ।
  • भिटामिन डी भएको माछा र माछाको कलेजो खाने
  • अण्डा, मासु र जनावरको कलेजो खानुहोस्
  • फोर्टिफाइड दूध वा भिटामिन डी भएको जुस खानुहोस्

भिटामिन डी को कमी कसरी उपचार गर्ने?

भिटामिन डी को कमी को उपचार मौखिक वा इंजेक्शन द्वारा भिटामिन डी को पूरक द्वारा गरिन्छ।

भिटामिन डी पूरकका दुई रूपहरू छन् जुन पूरकको लागि निन्दनीय रूपमा उपलब्ध छन्। Cholecalciferol (D3) र ergocalciferol (D2)। यी पूरकहरू 400, 600, 800, 1000, 2000, 5000, 10000, 50000, 60000 IU क्याप्सुल, पाउडर वा ट्याब्लेटहरू जस्ता विभिन्न खुराकहरूमा उपलब्ध छन्। केही देशहरूमा तिनीहरू इन्जेक्टेबल फारममा पनि उपलब्ध छन्।

हाम्रो शरीरमा भिटामिन डी परीक्षण कसरी गर्ने?

सीरम भिटामिन डी (25-हाइड्रोक्सिभिटामिन डी) स्तर भिटामिन डी को कमी को लागि पुष्टि गर्न वा स्क्रिन गर्न
रक्त परीक्षण द्वारा मापन गर्न सकिन्छ। सामान्य बुझाइ भनेको ३० एनजी/एमएल (नैनोग्राम प्रति मिलिलिटर) वा ७५ एनएमओएल/एल धेरै व्यक्तिहरूको लागि पर्याप्त छ। यद्यपि, सन्दर्भ दायरा जनसंख्या र सहमतिको आधारमा फरक हुन सक्छ। सीरम पीटीएच (प्याराथाइरोइड हर्मोन) स्तर सीरम भिटामिन डी स्तरसँग उल्टो सम्बन्धित छ त्यसैले यसलाई भिटामिन डीको कमीको जाँच गर्न पनि मापन गर्न सकिन्छ।

भिटामिन डी पूरक को खाना के हो?

भिटामिन डीको कमीलाई रोक्नको लागि पर्याप्त आहार र व्यवहारिक उपायहरूको बावजुद, मानिसहरूमा कमी हुन सक्छ र क्लिनिकल अभिव्यक्तिहरू पनि हुन सक्छ।

भिटामिन डी पूरकका दुई रूपहरू छन् जुन पूरकको लागि निन्दनीय रूपमा उपलब्ध छन्। Cholecalciferol (D3) र ergocalciferol (D2)। यी पूरकहरू 400, 600, 800, 1000, 2000, 5000, 10000, 50000, 60000 IU क्याप्सुल, पाउडर वा ट्याब्लेटहरू जस्ता विभिन्न खुराकहरूमा उपलब्ध छन्। केही देशहरूमा तिनीहरू इन्जेक्टेबल फारममा पनि उपलब्ध छन्।

भिटामिन डी सप्लिमेन्टेसन बिरामी कारणहरू जस्तै गम्भीरता, बिरामीको पाचन क्षमता, बानि वा रोगको नाम रअवस्था हेर्दै निम्न मध्ये कुनै पनि तरिकाद्वारा गर्न सकिन्छ:

  • सुरुमा 6-8 हप्ता (लगभग 2 महिना) हप्तामा एक पटक D2 वा D3 को 60000 IU त्यसपछि प्रति दिन
  • 800 IU प्रति दिन D2 वा D3 को 1000 IU D2 वा D3 को 600-800 IU प्रति दिन
  • पाचन संबन्धि रोगहरूको malabsorption  लागि प्रति दिन 10000 देखि 60000 IU
  • malabsorption को गम्भीरता र कमीको आधारमा केहि अवस्थामा, भिटामिन डी को कमी को उपचार को लागी क्याल्सिडियोल (Calcidiol) वा calcitriol वा dihydrotachysterol जस्तै भिटामिन डी मेटाबोलाइटहरू प्रयोग गर्न सकिन्छ।
  • भिटामिन डी को कमी को उपचार को अर्को मोडालिटी UVB (अल्ट्राभायोलेट बी) प्रकाश को कृत्रिम एक्सपोजर हो। भिटामिन डी को पूरक संग क्याल्सियम पूरक पनि आवश्यक हुन सक्छ।

के भिटामिन D3 भिटामिन D र 25 हाइड्रोक्सिभिटामिन D3 एउटै हो?

25-हाइड्रोक्सिभिटामिन D3 भिटामिन डी को निष्क्रिय रूपहरु मध्ये एक हो जुन रगतमा पाइन्छ र यसको मूल्य

(Value) भिटामिन डी को कमी को लागी मापन गरिन्छ।

भिटामिन डी D3 वा D2 जस्तै हो? Vitamin D3 vs D2

भिटामिन डी दुई प्रकारका हुन्छन्, भिटामिन D2 र डी D3। भिटामिन D3 को स्रोत छाला र जनावरहरूको खाना हो जहाँ भिटामिन D2 वनस्पति स्रोतहरूमा पाइन्छ।

के हामी भिटामिन डी को अधिक मात्रा प्रयोग गरिरहेका छौ?

भिटामिन डी पूरकको विषाक्त खुराक स्पष्ट छैन यद्यपि सहन योग्य माथिल्लो सीमा सेट गरिएको छ। 9 वर्ष भन्दा माथिका बालबालिका र वयस्कहरूका लागि, सबैभन्दा ठूलो माथिल्लो सीमा प्रति दिन 4000 IU (100mcg) हो, जबकि बच्चाहरूको लागि यो कम हुन्छ।

भिटामिन डीको विषाक्तता वा ओभरडोज भएमा निम्न लक्षणहरू देखिन सक्छन्:

  • भोक कम हुनु
  • तौल घट्नु
  • अनियमित मुटुको चाल

यदि मलाई भिटामिन डीको कमी छ जस्तो लाग्छ भने मैले के गर्नुपर्छ?

यदि तपाईंलाई लाग्छ कि तपाईंसँग भिटामिन डीको कमी छ भने तपाईंले आफ्नो डाक्टरलाई भेट्न आवश्यक छ र उहाँले तपाईंलाई भिटामिन डीको कमीको लक्षण र लक्षणहरू बारे केही प्रश्नहरू सोध्नुहुनेछ। उसले तपाईमा भिटामिन डीको कमी छ कि छैन भनेर पुष्टि गर्न केही परीक्षणहरू अर्डर गर्न सक्छ। रिपोर्टहरू पछि उसले धेरै कारकहरू र तपाईंको लागि व्यक्तिगत उपचार योजनाको आधारमा यसको उपचार गर्नेछ। उसले तपाईंलाई कमीको सुधार, लक्षणहरूको राहत, र भविष्यमा समान अवस्थाको रोकथाममा मद्दत गर्नको लागि फलो-अपको लागि सोध्नेछ। भिटामिन डी स्तरको दोहोर्याइएको जाँच सामान्यतया 3-4 महिना पूरक सेवन पछि गर्न सकिन्छ।

यो लेख लेखककै अङ्रेजि लेख बाट उल्था गरिएको हो!

Vitamin D – Quick Notes

  • Definition: A fat-soluble vitamin essential for bone health, immune function, and calcium absorption.
  • Types:
    • Vitamin D2 (Ergocalciferol) – Found in plant sources and fortified foods.
    • Vitamin D3 (Cholecalciferol) – Found in animal sources and synthesized in skin via sunlight.
  • Sources:
    • Sunlight – UVB rays help synthesize Vitamin D in the skin.
    • Foods – Fatty fish (salmon, mackerel), egg yolks, fortified dairy products, mushrooms.
    • Supplements – Used for deficiency or inadequate sun exposure.
  • Functions:
    • Regulates calcium & phosphorus levels for bone health.
    • Prevents rickets (children) & osteomalacia (adults).
    • Supports immune system, muscle function, and cardiovascular health.
  • Deficiency:
    • Causes: Lack of sunlight, poor diet, malabsorption, kidney/liver disorders.
    • Symptoms: Weak bones, muscle weakness, fatigue, depression, increased risk of fractures.
  • Recommended Daily Intake:
    • Infants: 400 IU (10 mcg)
    • Children & Adults: 600-800 IU (15-20 mcg)
    • Elderly: 800-1000 IU (20-25 mcg)
  • Toxicity:
    • Excess intake (>4,000 IU daily) can cause hypercalcemia, kidney damage, nausea, and confusion.
  • Testing & Diagnosis: Blood test measuring 25-hydroxyvitamin D levels.

Causes of vitamin D defeciency

Comparing pitting oedema and non-pitting edema (table of differences, grading, pathophysiology)

Pitting Edema Vs Non-Pitting Edema

Table of Contents(toc)

Pitting Edema

Pitting edema occurs due to an increase in interstitial fluid volume, which
can be displaced when external pressure is applied. This results in t
he
formation of a temporary depression (pit) that persists for a few seconds to
minutes before the fluid redistributes. The severity of pitting edema is often
graded based on the depth of the pit and the time taken for it to resolve
(e.g., 1+ to 4+ scale).

Pathophysiology:

Pitting edema is primarily caused by increased capillary hydrostatic pressure,
decreased oncotic pressure, or increased capillary permeability. The excess
interstitial fluid is primarily composed of water with minimal protein
content, making it easily compressible.

Common Causes:

  1. Cardiac Causes – Congestive
    heart failure (CHF) leads to increased venous pressure and fluid retention.
  2. Renal Causes – Nephrotic
    syndrome or acute kidney injury causes hypoalbuminemia, reducing oncotic
    pressure and leading to edema.
  3. Hepatic Causes – Liver
    cirrhosis causes reduced albumin synthesis, leading to fluid accumulation.
  4. Venous Insufficiency
    Chronic venous stasis results in poor venous return, causing fluid leakage
    into tissues.
  5. Malnutrition – Low
    protein intake leads to decreased plasma oncotic pressure, favoring fluid
    extravasation.

Non-Pitting Edema

Non-pitting edema does not leave an indentation when pressure is applied. It
is typically caused by an accumulation of high-protein fluid or
mucopolysaccharides within the interstitial space, leading to fibrosis and
increased tissue firmness.

Pathophysiology:

Non-pitting edema results from conditions that impair lymphatic drainage,
increase interstitial protein concentration, or induce tissue fibrosis. The
fluid accumulation in these cases is often rich in proteins, leading to
chronic inflammation, fibroblast activation, and skin thickening.

Common Causes:

  1. Lymphedema – Lymphatic
    obstruction due to congenital anomalies (primary lymphedema) or acquired
    causes like filariasis, malignancy, surgery, or radiation therapy.
  2. Myxedema – Seen in
    hypothyroidism due to the deposition of mucopolysaccharides in the dermis,
    leading to thickened, doughy skin.
  3. Lipedema – A disorder
    of fat distribution, primarily affecting women, where the lower limbs
    become symmetrically enlarged without true fluid retention.
  4. Chronic Inflammatory States
    – Conditions such as scleroderma and cellulitis can lead to fibrosis,
    resulting in non-pitting edema.
  5. Medication-Induced
    Certain drugs like calcium channel blockers and corticosteroids can cause
    non-pitting edema due to capillary leak or altered fluid dynamics.

Key Differences in Management:

  • Pitting edema is
    often treated by addressing the underlying systemic cause (e.g.,
    diuretics for CHF, albumin correction in nephrotic syndrome).
  • Non-pitting edema
    requires a different approach, such as lymphatic drainage, thyroid
    hormone replacement (for myxedema), or avoiding triggers in lipedema.
Feature Pitting Edema Non-Pitting Edema
Definition Edema that leaves a temporary dent (pit) when pressed with a finger. Edema that does not leave a dent when pressed.
Cause Fluid accumulation in the interstitial space. Accumulation of proteins, mucopolysaccharides, or lymphatic obstruction.
Common Causes Heart failure, liver disease, kidney disease, venous insufficiency,
malnutrition.
Lymphedema, myxedema (hypothyroidism), lipedema, chronic inflammation.
Appearance Soft and depressible swelling. Firm, thick, and tight swelling.
Response to Elevation Improves with limb elevation. Little or no improvement with limb elevation.
Effect of Diuretics Usually responsive to diuretics. Poor response to diuretics.
Associated Symptoms May have signs of systemic fluid overload (e.g., breathlessness, weight
gain).
Often associated with skin thickening or fibrosis.

Grading of Pitting Edema

Pitting edema is graded based on the depth of the indentation and the time it
takes for the skin to rebound after applying pressure. The most commonly used
scale is the
4-point grading system:

Grade Depth of Pit Rebound Time Clinical Description
1+ < 2 mm Immediate Barely detectable indentation. No visible swelling.
2+ 2-4 mm Few seconds (~15 sec) Slight indentation. Mild swelling.
3+ 4-6 mm Several seconds (~30 sec) Noticeable deep indentation. Marked swelling.
4+ 6-8 mm Prolonged (>30 sec) Deep pit lasting a long time. Severe swelling, possibly affecting
mobility.


Grading of Non-Pitting Edema

Non-pitting edema does not have a universally accepted grading system like
pitting edema. However, it can be assessed based on
severity and functional impact:

  1. Mild: Minimal swelling,
    no significant functional impairment.
  2. Moderate: Noticeable
    swelling, some skin thickening, minor mobility issues.
  3. Severe: Significant
    swelling, skin hardening, fibrosis, and potential ulceration or infection
    risk.
Severity Clinical Features
Mild Minimal swelling, no significant functional impairment.
Moderate Noticeable swelling, some skin thickening, minor mobility issues.
Severe Significant swelling, skin hardening, fibrosis, and potential ulceration
or infection risk.

For lymphedema, a
specific International Society of Lymphology (ISL) Staging System is used:

Stage Clinical Features
Stage 0 (Latent) No visible swelling, but lymphatic damage is present.
Stage I (Mild) Reversible swelling; pitting may be present. Elevation reduces swelling.
Stage II (Moderate) Irreversible swelling, tissue fibrosis begins. No pitting.
Stage III (Severe, Elephantiasis) Severe fibrosis, skin thickening, warty overgrowth, and functional
impairment.

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Commonly asked important Fractures

Commonly Asked Fractures

Table of Contents(toc)

In this article we have commonly asked questions and points regarding orthopedics and fractures.

Upper Limb Fractures

  • Aviator’s Fracture: Neck of Talus
  • Boxer’s Fracture: Neck of 5th Metacarpal
  • Bennett’s Fracture: (Intra-articular) Base of 1st Metacarpal
  • Rolando’s Fracture: (Extra-articular) Base of 1st Metacarpal
  • Chauffeur’s Fracture: Radius above the Styloid Process
  • Galeazzi’s Fracture: Distal Radius with Dislocation of the Distal Radioulnar Joint
  • Monteggia’s Fracture: Proximal Ulna with Dislocation of the Head of the Radius
  • Smith’s Fracture: Reverse of Colles Fracture

Spinal Fractures

  • Chance Fracture: Horizontal Fracture through Vertebrae due to Sudden Deceleration
  • Clay Shoveler’s Fracture: Spinous Process of T1
  • Jefferson’s Fracture: Burst Fracture of Atlas (C1)
  • Hangman’s Fracture: Fracture of Axis (C2)

Lower Limb Fractures

  • Cotton’s Fracture: Trimalleolar Fracture
  • Pott’s Fracture: Bimalleolar Ankle Fracture
  • Jones Fracture: Base of the 5th Metatarsal
  • March Fracture: Stress Fracture of the Second Metatarsal
  • Masonne’s Fracture: Neck of Fibula
  • Toddler’s Fracture: Spiral Fracture of Tibia
  • Crescent Fracture: Iliac Bone with Sacroiliac Disruption

Stress Fracture

Occurs due to repetitive minor trauma to healthy bone. Common locations:

  • Metatarsals (e.g., after long hikes)
  • Tibia & Fibula (in regular athletic activities)

Stress Fracture Question

Q: Stress fracture occurs in:
a) Diseased bone
b) Normal bone of a healthy person ✅
c) Commonly in the humeral shaft
d) Always requires operative treatment

Answer: (b) Normal bone of a healthy person

Solution & Explanation

  • A simple fracture has a single fracture line.
  • A comminuted fracture has multiple fracture lines with bone fragments.
  • An open fracture has a wound where the bone protrudes through the skin.
  • A closed fracture has no external wound.
  • Pathological fractures occur in elderly patients with osteoporosis or in patients with metabolic bone diseases or tumors.
  • Greenstick Fracture: Fracture of the shaft of long bones in children where the outer cortex breaks while the inner cortex bends.

Notes on Erb’s and Klumpke’s palsy

Erb’s Palsy:

Table of Contents (toc)
erbs palsy


Question 

a. Occurs typically usually after breech delivery of smaller babies
b. Is due to injury of C5 and C6 nerve roots
c. All fingers muscles are paralysed
d. There may be unilateral Horner’s syndrome
Ans: ‘b’

Solution

Injury to upper trunk of Brachial plexus (C5, C6, C7) leads t60 Erb’s palsy.

Erb’s palsy

Brachial plexus may be injured when person falls from a height on the side of
head and shoulder whereby the nerves of the plexus are violently stretched.
(upper trunk of the plexus injured).
Paralysis of Ms Deltoid, biceps, brachialis, intraspinatus and spinator.
The position of limb is characteristic i.e., the arm hanges by the side
medially rotated and the forearm is extended and pronated (Policeman’s lip).

Klumpke’s paralysis

Caused by injury in lower trunk of brachial plexus (CB, T₁) characterized by
paralysis of intrinsic hand Ms & CB/T1 dermatome distribution numbness.

Comparing Erb’s Palsy and Klumpke’s Palsy

Here’s a table comparing Erb’s Palsy and Klumpke’s Palsy
Feature Erb’s Palsy Klumpke’s Palsy
Nerve Roots Affected C5-C6 (sometimes C7) C8-T1
Cause Excessive traction on the neck during delivery or trauma (e.g., shoulder
dystocia, fall on the shoulder)
Hyperabduction of the arm (e.g., breech delivery, catching oneself while
falling from a height)
Paralyzed Muscles Deltoid, supraspinatus, infraspinatus, biceps brachii, brachialis Intrinsic muscles of the hand (lumbricals, interossei), flexors of the
wrist and fingers
Clinical Presentation “Waiter’s Tip” posture (arm adducted, internally rotated, elbow
extended, forearm pronated, wrist flexed)
“Claw Hand” deformity (hyperextension at MCP joints, flexion at PIP &
DIP joints)
Sensory Loss Lateral arm and forearm (C5-C6 dermatome) Medial forearm and hand (C8-T1 dermatome)
Reflexes Affected Absent biceps and brachioradialis reflex Intact biceps reflex, but absent grasp reflex
Associated Syndrome Horner’s Syndrome (if sympathetic fibers of T1 are affected: ptosis,
miosis, anhidrosis)
Prognosis Good with early physiotherapy, mild cases recover within months Poorer prognosis if there is nerve root avulsion; may require nerve
grafting

Vitamins and their deficiencies detailed

Vitamins, Sources, Deficiency Diseases, Symptoms, and Signs

Table of Contents(toc)

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Vitamins, Sources, Deficiency Diseases, Symptoms, and Signs
Vitamin Sources Deficiency Disease Symptoms Signs
Vitamin A Liver, carrots, sweet potatoes, leafy greens Night Blindness Poor vision in dim light Dry eyes, Bitot’s spots, keratomalacia
Vitamin B1 (Thiamine) Whole grains, pork, legumes, seeds Beriberi Fatigue, irritability, confusion Muscle weakness, peripheral neuropathy, heart failure
Vitamin B2 (Riboflavin) Dairy, eggs, lean meats, green vegetables Ariboflavinosis Sore throat, swollen tongue Cracks in lips, angular cheilitis, glossitis
Vitamin B3 (Niacin) Poultry, fish, whole grains, peanuts Pellagra Diarrhea, dementia, dermatitis Scaly skin, inflamed mucous membranes
Vitamin B5 (Pantothenic Acid) Eggs, avocado, whole grains Burning Feet Syndrome Fatigue, depression Numbness, burning sensation in feet
Vitamin B6 (Pyridoxine) Poultry, bananas, potatoes, fortified cereals Neuropathy, Anemia Depression, irritability, confusion Seizures, cracks in the lips, swollen tongue
Vitamin B7 (Biotin) Egg yolks, nuts, seeds, liver Biotin Deficiency Fatigue, thinning hair Scaly rash, brittle nails
Vitamin B9 (Folate) Leafy greens, legumes, fortified cereals Megaloblastic Anemia Fatigue, irritability Pale skin, tongue swelling
Vitamin B12 (Cobalamin) Meat, dairy, fortified cereals Pernicious Anemia Memory loss, fatigue Pale skin, shortness of breath, neurological issues
Vitamin C Citrus fruits, strawberries, bell peppers Scurvy Fatigue, depression Swollen gums, bruising, poor wound healing
Vitamin D Fatty fish, fortified dairy, sunlight Rickets (Children), Osteomalacia (Adults) Bone pain, muscle weakness Bowed legs, skeletal deformities
Vitamin E Nuts, seeds, spinach, sunflower oil Neuromuscular Disorders Weakness, coordination problems Loss of reflexes, muscle deterioration
Vitamin K Leafy greens, broccoli, Brussels sprouts Bleeding Diathesis Easy bruising, excessive bleeding Prolonged clotting time

Sources and references:

  • Harvard T.H. Chan School of Public Health – Vitamins and their functions
  • National Institutes of Health (NIH) – Vitamin deficiency and symptoms
  • World Health Organization (WHO) – Micronutrient deficiencies

Questions:

The triad of glossitis, angular fissure, and corneal vascularization is due to deficiency of:

a. Riboflavin
b. Thiamine
c. Niacin
d. Pantothenic acid

Ans: (a) Riboflavin

Solution and facts about Vitamins:

  • Vitamin B2 (Riboflavin) deficiency causes:

    • Cheilosis (inflammation of lips, scaling, and fissures at the corners of the mouth)
    • Corneal vascularization
  • Vitamin B1 (Thiamine) deficiency causes:

    • Dry Beriberi – Wasting, polyneuritis, symmetrical muscle weakness
    • Wet Beriberi – High-output cardiac failure (dilated cardiomyopathy), edema
    • Wernicke-Korsakoff Syndrome – Confusion, ophthalmoplegia, ataxia (classic triad), confabulation, personality changes, memory loss (permanent)
  • Vitamin B3 (Niacin) deficiency causes:

    • Glossitis
    • Pellagra (3Ds) – Diarrhea, Dermatitis, Dementia
  • Vitamin B5 (Pantothenic Acid) deficiency causes:

    • Dermatitis
    • Enteritis
    • Alopecia
    • Adrenal insufficiency
  • Vitamin B6 (Pyridoxine) deficiency causes:

    • Convulsions
    • Hyperirritability
    • Peripheral neuropathy
    • Sideroblastic anemia
  • Vitamin B7 (Biotin) deficiency causes:

    • Dermatitis
    • Alopecia
    • Enteritis
  • Vitamin B9 (Folate) deficiency causes:

    • Macrocytic megaloblastic anemia
    • Glossitis
    • No neurologic symptoms
  • Vitamin B12 (Cobalamin) deficiency causes:

    • Macrocytic megaloblastic anemia
    • Subacute combined degeneration

ESR Vs CRP Video


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Most Common Complication of High Myopia

Most Common Complication of High Myopia

Table of Contents(toc)


Most Common Complication of High Myopia





The Most Common Eye Problem Is





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Myopia, or nearsightedness, and hyperopia, or farsightedness, are both common refractive eye conditions that blur vision. 

Complications of Myopia:

  • Myopic crescents (on the temporal side)
  • Posterior staphyloma
  • Patchy choroidal atrophy within the posterior pole
  • Vitreous syneresis
  • Breaks in Bruch’s membrane with accompanying choroidal atrophy (lacquer
    cracks)
  • Subretinal neovascular membrane with overlying retinal pigment epithelial
    hyperplasia (Foster-Fuchs spot)
  • Retinal detachment

Key Concepts on vision:

  • Physiological myopia is the
    most common eye disorder worldwide.
  • In myopia, parallel rays of
    light focus
    in front of the retina.
  • In hypermetropia, parallel
    rays of light focus
    behind the retina.
  • A 1 mm change in axial
    length leads to a
    3D change in refraction.
    • Shortening causes
      hypermetropia
    • Lengthening causes
      myopia
  • A 1 mm change in corneal
    curvature can lead to
    6D hypermetropia.
  • At birth, the eye is normally hypermetropic.
  • Optical treatment:
    • Myopia → Concave lens
    • Hypermetropia →
      Convex lens
  • Presbyopia: Physiological
    insufficiency of accommodation due to loss of elasticity of the lens capsule
    (age-related).
  • Astigmatism: Unequal
    refractive error in two eyes.
  • Aniseikonia: Unequal
    image shape/size in the visual cortex.
  • Aphakia: Absence of the
    crystalline lens.
    Treatment of choice
    Posterior chamber IOL implantation.
  • The most common eye disorder worldwide is physiological myopia, a refractive error.
  • The most common cause of blindness worldwide: Cataract (more than refractive error and aphakia blindness).
  • The most common cause of irreversible blindness worldwide: Glaucoma.

Differences : Papillitis and Papilledema

Differences Between Papillitis and Papilledema

Table of Contents(toc)
Papillitis Vs Papilledema


Papillitis Vs Papilledema

Here is a detailed table comparing
Papillitis (Optic Neuritis) and
Papilledema:


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Feature Papillitis (Optic Neuritis) Papilledema
Usually Affects Unilateral (U/L) Bilateral (B/L)
Onset Sudden Insidious/Chronic
Loss of Vision Marked, painful Negligible, gradual
Pain with Eye Movement Present Absent
Tenderness Present at the insertion of MR & SR Absent
Other Symptoms Usually not seen Headache, nausea, vomiting (↑ ICP)
Swelling (Edema) of Disc 2-3D swelling >3D swelling, marked blind spot enlargement
Visual Field Defect Centrocecal scotoma Enlarged blind spot
Color Vision Reduced (Dyschromatopsia) Normal
Pupillary Reflex (RAPD) Present (Positive) Absent
Posterior Vitreous Fine opacities present Clear
Cause Optic neuritis, Multiple sclerosis, infections Increased intracranial pressure (tumor, hydrocephalus, meningitis)
Management Steroids (IV Methylprednisolone) Treat underlying cause (reduce ICP)

Papillitis Vs Papilledema


MCQs on Vision and Optic Pathology

  1. What is the most common cause of papilledema?
    a) Optic neuritis
    b) Increased intracranial pressure
    c) Glaucoma
    d) Retinal detachment

  2. Which of the following is NOT a feature of papilledema?
    a) Bilateral involvement
    b) Enlarged blind spot
    c) Sudden painful vision loss
    d) Absence of RAPD

  3. A patient with optic neuritis is likely to have which of the following?
    a) Unilateral sudden vision loss
    b) Marked papilledema
    c) Gradual vision loss
    d) Normal pupillary reflexes

  4. The presence of a relative afferent pupillary defect (RAPD) suggests:
    a) Glaucoma
    b) Optic neuritis
    c) Retinal detachment
    d) Conjunctivitis

  5. What is the primary treatment for optic neuritis?
    a) Acetazolamide
    b) Intravenous steroids
    c) Antibiotics
    d) Antihypertensives

  6. Which condition is associated with a centrocecal scotoma?
    a) Papilledema
    b) Papillitis
    c) Retinitis pigmentosa
    d) Diabetic retinopathy

  7. Which of the following is NOT a common cause of increased intracranial pressure?
    a) Brain tumor
    b) Hydrocephalus
    c) Optic neuritis
    d) Meningitis

  8. What visual defect is classically seen in papilledema?
    a) Central vision loss
    b) Enlarged blind spot
    c) Peripheral scotoma
    d) Homonymous hemianopia

  9. A 25-year-old female with multiple sclerosis presents with unilateral painful vision loss. What is the most likely diagnosis?
    a) Glaucoma
    b) Papilledema
    c) Papillitis (Optic neuritis)
    d) Retinal detachment

  10. The presence of dyschromatopsia (impaired color vision) is most commonly associated with:
    a) Papillitis
    b) Papilledema
    c) Cataract
    d) Age-related macular degeneration


Answer Key:

  1. b
  2. c
  3. a
  4. b
  5. b
  6. b
  7. c
  8. b
  9. c
  10. a

Trachoma – Key Points

Trachoma – Key Points

Table of Contents(toc)


Introduction

  • Definition: A chronic
    infectious eye disease caused by
    Chlamydia trachomatis.
  • Transmission: Spread
    through direct contact with infected secretions, contaminated objects, and
    flies.
  • Symptoms: Eye redness,
    irritation, discharge, photophobia, and progressive corneal scarring.
  • Complications: Corneal
    opacity, trichiasis (inward-growing eyelashes), and blindness.
  • Epidemiology: Leading cause
    of infectious blindness globally, prevalent in poor hygiene and low-income
    regions.

Stages of Trachoma (WHO Grading System)

  1. TF (Trachomatous Inflammation – Follicular): Presence of five or more follicles (>0.5 mm) in the upper tarsal
    conjunctiva.
  2. TI (Trachomatous Inflammation – Intense): Thickened, inflamed upper tarsal conjunctiva with pronounced redness.
  3. TS (Trachomatous Scarring):
    Visible scarring of the tarsal conjunctiva.
  4. TT (Trachomatous Trichiasis): Inturned eyelashes rubbing against the eyeball.
  5. CO (Corneal Opacity):
    Opacity leading to significant visual impairment or blindness.

SAFE Strategy for Trachoma Control
(WHO)

  1. S – Surgery: For
    trichiasis to prevent corneal damage.
  2. A – Antibiotics: To treat
    active infection and reduce transmission.
  3. F – Facial cleanliness:
    Encouraging hygiene to prevent spread.
  4. E – Environmental improvement: Ensuring clean water supply and sanitation.

Antibiotics for Trachoma

  1. Azithromycin (preferred
    drug)

    • Dose:
      • Adults: 1 g orally, single dose
      • Children: 20 mg/kg (maximum 1 g), single dose
    • Duration: Single-dose treatment, repeated annually in endemic areas.
  2. Tetracycline (1%) ophthalmic ointment

    • Dose: Apply to both eyes twice daily
    • Duration: 6 weeks
  3. Erythromycin
    (alternative to azithromycin)

    • Dose:
      • Adults: 500 mg orally twice daily
      • Children: 12.5 mg/kg orally four times daily
    • Duration: 14 days

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“@type”: “Question”,
“name”: “What are Stages of Trachoma and mnemonic?”,
“acceptedAnswer”: {
“@type”: “Answer”,
“text”: “TF (Trachomatous Inflammation – Follicular): Presence of five or more follicles (>0.5 mm) in the upper tarsal conjunctiva.
TI (Trachomatous Inflammation – Intense): Thickened, inflamed upper tarsal conjunctiva with pronounced redness.
TS (Trachomatous Scarring): Visible scarring of the tarsal conjunctiva.
TT (Trachomatous Trichiasis): Inturned eyelashes rubbing against the eyeball.
CO (Corneal Opacity): Opacity leading to significant visual impairment or blindness.
Mnemonic is FISTO.”
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“text”: “S – Surgery: For trichiasis to prevent corneal damage.
A – Antibiotics: To treat active infection and reduce transmission.
F – Facial cleanliness: Encouraging hygiene to prevent spread.
E – Environmental improvement: Ensuring clean water supply and sanitation.”
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Contraindications of Tooth Extraction

Contraindications of Tooth Extraction

Table of Contents(toc)


Introduction

Tooth extraction is a medical procedure that may not be suitable for all patients, especially those with certain health conditions. Below is a categorized list of general, local, absolute, and relative contraindications.

1. General Contraindications

These are conditions where tooth extraction should be avoided due to overall health concerns:

  • Cardiac Diseases:

    • Valvular, Rheumatic, or Ischemic heart disease
    • Congestive heart failure
    • Hypertension
    • Patients on anticoagulation therapy
  • Blood Diseases:

    • Severe anemia
    • Leukemia
    • Hemophilia
    • Agranulocytosis
  • Addison’s Disease

  • Patients on Corticosteroids:

    • Requires dose adjustment
  • Liver Diseases:

    • Jaundice and liver disease
    • Vitamin K deficiency
    • Blood clotting factor deficiencies (Prothrombin, Fibrinogen)
  • Diabetes Mellitus:

    • Poor wound healing due to decayed healing processes
  • Thyrotoxicosis

  • Pregnancy:

    • Especially during the first and third trimesters
    • Risks of abortion, premature delivery
    • Gravid uterus causing discomfort
    • Reduced stamina for opening the mouth
  • Very Old Age:

    • Decreased physiological response
    • Non-healing tissues and increased risk of infection
  • Epileptic Patients

  • Presence of Fever:

    • Infections can complicate healing
  • Debilitating Diseases:

  • Psychosis/Neurosis:

    • Mental health conditions affecting cooperation
  • Allergy to Local Anesthetics (LA)

  • Incorporative Patients:

    • Conditions where patient cooperation is compromised
  • During Menstruation:

    • Hormonal changes may affect healing and tolerance

2. Local Contraindications

These are conditions that affect the immediate area of the tooth that may cause complications:

  • Acute Infections:

    • Presence of infection at the extraction site
  • Malignancy:

    • Growth may spread rapidly after the procedure
  • Irradiated Jaw:

    • Risk of acute osteoradionecrosis due to lack of blood supply (endarteritis obliterans)

3. Absolute Contraindications

Certain conditions make tooth extraction entirely inappropriate:

  • Hemangioma:

    • Increased risk of bleeding
  • Arteriovenous Malformation (AV Malformation):

    • Bleeding that cannot be controlled
  • In the case of such conditions, if extraction is necessary:

    • Place the tooth back in the socket and apply pressure to control bleeding

4. Relative Contraindications

These are conditions where tooth extraction may be performed with caution or special consideration:

  • Diabetes Mellitus:

    • May require special management due to healing concerns
  • Valvular Heart Disease:

    • And other similar conditions where dental management requires careful planning and monitoring
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