Showing posts with label Nutrition. Show all posts
Showing posts with label Nutrition. Show all posts

Friday, June 21, 2019

Understanding Refeeding Syndrome

Refeeding syndrome is a life-threatening metabolic complication of - stay with me - refeeding. It can happen via any route after prolonged starvation.

Who are at risk?
They’re patients with prolonged artifical feeding [parenteral or enteral], malignancy, anorexia and alcoholism.

Why does it happen?
During starvation, the body uses fat and protein for energy. There’s no carbs so there’s little to no insulin.

After refeeding, carbohydrate load causes a spike in insulin level.
Now first prof biochemistry tells you, more insulin means more cellular uptake of phosphate.
That’s it. That low serum phosphate level is the main problem.

How does it present?
Non-specifically and catastrophically. Features are rhabdomyolysis, red and white blood cell dysfunction, respiratory insufficiency, cardiac arrhythmias and seizures.
Left unchecked, it can lead to sudden death.

How do I prevent it?
Identify at-risk patients and give high-dose, high-potency Vitamin C and B complex injection, during re-feeding window.
Monitor vitals and labs closely. Close involvement of nutritionist is ideal.

What if it’s already happened? How do I treat it?
The biggest challenge is management of complications.
As regards phosphate, get the levels back up. Administer oral as well as parenteral phosphate, upto 18 mmol per day.

Thank you, that’d be all.
- Ashish Singh.

Saturday, May 18, 2019

History, physiology and medical aspects of fasting

Hello everyone,

My senior resident at JFK Medical Center did a presentation on fasting. I thought of sharing it with you (especially since it is Ramazan/Ramadan).

Thursday, January 3, 2019

Lifestyle modifications for managing hypertension

Hey guys,

Happy New Year!

Let's get started on lifestyle modifications for treating or managing hypertension.

We Decide to Eat less Salt & drink less Alcohol!

Weight loss: Reduce BMI to <25 
DASH: Diet high in fruits and vegetables and low in saturated fat and total fat
Exercise: 30minutes/day for 5-6 days/week
Dietary Sodium: <3 g/day
Alcohol: 2 drinks/day in men and 1 drink/day in women

The effect of these interventions is in descending order, with weight loss having an impact of about 5-20 mmHg lowering per 10 kg weight loss and reducing alcohol intake can lower BP by 2-4 mmHg!

Remember: If a patient's BMI is already lower than 25, you don't have to ask them to reduce weight any further for this therapeutic effect. Instead, you ask them to switch over to DASH diet!

Hope this is helpful!

Stay awesome!

Tuesday, October 16, 2018

Why is the level of Vitamin B12 increased in CML?

Why is the level of Vitamin B12 increased in Chronic Myeloid Leukemia (CML)?

Pathophysiology: The transport of vitamin B12 in the blood as well as hepatic uptake require the presence of transcobalamins (TCBs).

TCB types I (TCB I) and III (TCB III) ensure the binding of ∼80% of circulating vitamin B12.

Monday, April 30, 2018

Conjunctival xerosis mnemonics

Conjunctival Xerosis

Hello everyone today let's discuss the causes and treatment of conjunctival xerosis.

So basically there are two types of conjunctival xerosis.
a. Epithelial xerosis
b. Parenchymatous xerosis

Epithelial xerosis.
The most common example is Xerophthalmia i.e. Vitamin A deficiency.

Let us discuss Xerophthalmia.

The cause of vitamin A deficiency is mostly its dietary deficiency or defective absorption.

The new WHO classification of Xerophthalmia

XN:   Night Blindness
X1A: conjunctival xerosis
X1B: bitots spots
X2:   corneal xerosis
X3A: keratomalacia <1/3rd of cornea
X3B: keratomalacia >1/3rd of cornea   
XS: corneal scar
XF: fundal changes – known as Uyemura spots, these are defects in the Retinal
Pigment Epithelium.

It consists of local ocular therapy with artificial tears along with vitamin A therapy.
Schedule for vitamin A is as follows :

>1 year of age – 1lakh IU i.m. given on 0 1 14 days
 2lakh IU orally given on 0 1 14 days

<1 year of age – half the dose.

This has to be carried along with treatment of underlying causes like malnutrition or other disorders like diarrhoea dehydration.

Other causes of night blindness:
1. High myopia
2. Late stage of angle closure glaucoma
3. Oguchi syndrome
4. Gyrate atrophy of choroid
5. Retinitis pigmentosa

Parenchymatous Xerosis
It mainly involves the adenoid layer of the conjunctiva.
It can take place due two main reasons     holla! We have a mnemonic here
1. Due to cicatrizing disorders  (cicatrizing disorders turn conjunctiva reasonably shrivelled)
2. Due to over exposure to atmosphere ( marked exposure causes parenchymatous xerosis)

Cicatrizing disorders
1. Cicatricial phemphigoid
2. Diptheric membranous conjunctivitis
3. Trachoma
4. Chemical burns
5. Radiotherapy
6. Stevens-johnson syndrome

Overexposure to atmosphere
1. Marked proptosis
2. Ectropion
3. Coma (lack of blinking)
4. Palsy of cranial nerve 7 (facial palsy)

That’s all for now,
Stay Awesome!
Keep calm and keep studying!

- Ashish G. Gokhale

Wednesday, February 21, 2018

Thiamine and Beri-Beri: A Summary

  • Vitamin B1 is Thiamine.

(TCA = TriCarboxylic Acid cycle aka Kreb's cycle ; LDH = Lactate Dehydrogenase ; PDH = Pyruvate Dehydrogenase ; TPP = Thiamine PyroPhosphate)
  • Peripheral neuropathy in dry beri-beri is symmetric, sensorimotor, distal > proximal and non-inflammatory demyelinating type.
  • Wernicke's syndrome is reversible early while Korsakoff psychosis is reversible in only 20% cases.
  • Wernicke-Korsakoff syndrome has typical damage to dorsomedial nucleus of thalamus and mamillary bodies.
  • Clinical manifestations of B1 deficiency is worsened by glucose load! As seen in pathophysiology, excess of glucose with relative or absolute deficiency of B1 - as TPP - causes diversion from the preferred PDH pathway (linked to TCA), to the LDH pathway causing life-threatening lactic acidosis. Hence, in a patient with alcohol intoxication/ chronic alcoholism a B1+glucose cocktail is given as they usually are deficient in B1.
Biochemistry pearl: Other co-factors in PDH pathway alongside TPP are Lipoic acid, Coenzyme A, FAD(H) and NAD(H).


Clinical diagnosis with confirmatory lab work - that includes:
  • Diagnostic - Blood or RBC transketolase activity and increase after intramuscular B1 administration
  • Supportive - Blood thiamine, pyruvate and lactate levels

You give what the patient lacks. An acceptable regimen is:

Injection B1 100 mg intramuscular for 1 week
followed by
Tablet B1 10 mg once-daily per-oral for 1 month.

Let me know if anything needs clarification. Happy studying!
--Ashish Singh.

Sunday, October 8, 2017

High tHcy associated with mortality from acute stroke!

Hey Awesomites

Various prospective studies in the past years have concluded that high levels of total Homocysteine ( tHcy ) are an independent risk factor for increased mortality from ischemic stroke, after adjustment of confounding factors!

This association is only significant in the large vessel atherosclerosis stroke subtype, and is relatively not significant in small vessel occlusion subtype.

The question that now arises is - Do elevated plasma tHcy levels cause more serious strokes or is it that more serious strokes result in higher tHcy levels?

Studies have found that elevated tHcy levels induce oxidative injury to vascular endothelial cells and impair the production of NO, thus increasing the arterial pressure and risk of stroke.
Also, tHcy enhances platelet adhesion to endothelial cells, promotes the growth of vascular smooth muscles, and is associated with higher levels of prothrombotic factors such as Beta- thromboglobulin, tissue plasminogen activator, and factor VII C.

Whether the more serious strokes increase  levels of tHcy and the changes in the levels before and after the acute episode needs further studies for clarification.

Note : High tHcy is not a cause of stroke and is not associated with stroke severity. Patients in the highest tHcy quartile ( >18.6 umol/L ) with Acute ischemic stroke  in large vessels of brain are in increased risk of Long - term mortality.

Therapy to control and lower tHcy levels with vitamin B supplements has been shown to reduce the risk of stroke and other acute cardiovascular events.
Metabolic B12 deficiency is present in 30% of vascular patients over the age of 70 years, while higher doses of B12 are required in elderly people than younger ones.
However, renal function tests should be done before starting the supplementation because high doses of cyanocobalamine increase cyanide levels in patients with renal impairment ( GFR <50 ml/min ).

Source  )
That's all
- Jaskunwar Singh

Thursday, August 10, 2017

Factors increasing iron absorption in the intestine mnemonic

Hello! Long time, no see!

Did you know a number of dietary factors influence iron absorption?

Ascorbate (vitamin C) and citrate increase iron uptake in part by acting as weak chelators to help solubilize it in the duodenum.

Monday, June 19, 2017

More than what you know about vitamins!

Hello! :)

These were the questions asked during my pharmacology vivas. And I found it fascinating after studying. I have never studied these points about vitamins before! 

Q. Which vitamin deficiency is related with lowering of seizure threshold?

Ans. Pyridoxine Vitamin B6. 

Why? As it is associated with synthesis of neurotransmitter GABA. Therefore, it is indicated during isoniazid induced convulsions. :)

Q. Why laropiprant (20mg) + Niacin (1g) is used in combination?

Ans. Nicotinic acid (a derivative) results in flushing of face.

Why? Vasodilation of cutaneous vessels.

Therefore, we combine it with specific anti-flushing drug called laropiprant.

Q. In hyperemesis gravidarum, what do you give for associated Wernicke's encephalopathy following hyperemesis? 

Ans. I thought of anti-emetics at first but the answer is vitamin B1. (Wernicke's encephalopathy doesn't always result from alcohol :P )

That's for today.
Take care. :)
-Upasana Y.

Thursday, June 1, 2017

Pathophysiology of anorexia in chronic kidney disease

Normal appetite regulation: Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide.

What happens in CKD?

Monday, May 22, 2017

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?

Saturday, May 13, 2017

Research update : Genetic locus of Anorexia nervosa revealed

Hey Awesomites

A Research landmark study led by UN school of medicine has found the first genetic locus for the perplexing illness, anorexia nervosa. Previously it was known that this eating disorder runs in families with genetic and environmental factors both playing their role and there is ten - fold risk in first -degree relatives, but no particular association with a genetic locus was provided.

Thought to be associated with psychiatric disorders like neuroticism and schizophrenia, it has also been positively correlated with underlying metabolic abnormalities including body - mass index (BMI) and insulin - glucose metabolism. Genome - wide association studies ( GWAS ) have revealed a significant locus for anorexia nervosa on chromosome 12, in a region previously shown to be associated with type -1 diabetes mellitus and autoimmune disorders. This means that this eating disorder shares common roots with metabolic and psychiatric traits !!

These results may help in reconceptualizing the underlying aetiology and pathogenesis of such a lethal disorder and also coming up with new treatment interventions to cure the disease.

Thats all
- Jaskunwar Singh

Monday, May 1, 2017

Vitamin B3 and pellagra mnemonics


This post is all about niacin aka vitamin B3 and it's deficiency with loads of mnemonics. Who is excited?

1. How to remember Niacin is vitamin B3:

- You can remember the three vowels in nIAcIn, so it's vitamin B three.
- N has 3 strokes, so Niacin is B3
- NIA - B3

2. Vitamin B3 deficiency, Pellagra, is clinically manifested by photosensitive dermatitis, diarrhea, dementia.

Pellagra mnemonic:
"B3 causes D3"
Diarrhea, Dermatitis, Dementia.

3. Pellagra tends to occur in areas where people eat maize (or corn, the only grain low in digestible niacin) as a staple food.

Mnemonic: Corny people can't be nice. (Corn can't have niacin)

People - Pellagra. PP!

Corny people can't be nice and amazing! Get it? A-maize-ing! Hahahahha! I'm so pun-ny and funny!

4. The amino acid tryptophan is needed to make niacin, serotonin and melatonin.
Mnemonic: Have a nice trip to serotonin land (Serotonin rhymes with Melatonin).

Why is this fact clinically significant?
Carcinoid syndrome leads to excess production of serotonin, which depletes  tryptophan. There's not enough tryptophan to produce niacin, resulting in pellagra.

5. Isoniazid (INH) use can cause vitamin B3.

Mnemonic: INH has 3 letters. B3 deficiency!
Also, isoNIAzid. For NIAcin deficiency.

6. Lastly, you should know about Hartnups disease which is due to defective neutral amino acid transporter on renal and intestinal epithelial cells 

Here's a mnemonic by usmle1mikmonics:
Renal (also intestinal) / Recessive
Transporter defect / Tryptophan deficiency
Neutral amino acids / Niacin deficiency / Nicotinamide supplements (Treatment)
Urine (Tryptophan lost in urine)
Pellagra / high Protein diet (Treatment)
D’s - Dermatitis, Dementia, Diarrhea

That's all!

Monday, April 17, 2017

Mnemonico diagnostico : Vitamin D deficient Rickets

Hey Awesomites

The clinical features specific for Rickets due to vitamin D deficiency are : Vit D BHP RICKETS

V - Visceroptosis ( due to ligament laxity )
D - DEXA scan / low bone Density
B - Bossing of skull
H - Harrison's groove
P - Ping pong ball sensation
R - Rachitic rosary
I - Iron deficiency and other anemias
C - Coxa vara
K - Kyphosis
E - Eruption of teeth ( delayed )
T - Thoracolumbar ( Lordosis )
S - Sternum and ribs protrusion ( Pigeon chest )

Thats all
- Jaskunwar Singh

Friday, March 17, 2017

Facts and Fallacies: Vitamin D link to cancer

Hey Awesomites

Vitamin D has been shown beneficial for a variety of disorders and diseases. Recent studies now suggest that those deficient in vitamin D are at a  higher risk of developing cancer compared to those with adequate levels.

Thursday, March 9, 2017

Amiodarone- induced thyroid dysfunctions


Amiodarone, a potent class III anti- arrhythmic drug is contraindicated in thyroid patients or those with subclinical disease. The reason lies in the pharmacokinetic profile of this drug.

The drug has a structural resemblance to triiodothyronine (T3) and thyroxine (T4). In the body, it is metabolized by dealkylation to Desethylamiodarone (DEA), the intrathyroidal concentration of which is higher than the parent drug.

Normal daily recommended intake of iodine for adults is approx. 0.15mg (150mcg).  Each 200mg tablet of amiodarone contains about 74.4mg of iodine with 7.4mg (10%) being released as free form. This is roughly 50- fold higher than the normal. Therefore, total body stores may remain increased for upto 9 months after stopping the drug.

High iodine content of this drug inhibits  local type-1 5'- deiodinase activity (blocking conversion of T4 to T3) and type- II 5'- deiodinase activity in the pituitary. As a result, TSH is increased initially (mild elevation) and then return to normal or may even decrease in euthyroid patients after weeks, while T4 is normal or raised, and T3 levels decrease.

The increased delivery and uptake of iodine by the thyroid gland may cause increase in hormone production and release, a condition called type-1 Amiodarone- induced thyrotoxicosis (AIT) . In other cases, excessive thyroid tissue destruction due to destructive thyroiditis may lead to type-2 Amiodarone- induced thyrotoxicosis. These are hyperthyroid states!!
Discontinuation of the drug is recommended, if not, then high doses of thioamides and corticosteroids may work in AITs.

Amiodarone may also cause hypothyroidism (AIH) in  patients depending upon the iodine status of individuals and prior thyroid disease. Wolff- chaikoff effect is shown by thyroid cells due to failure of thyroid hormonogenesis. Levothyroxine is the drug of choice.

Thats all
- Jaskunwar Singh

Saturday, March 4, 2017

Facts and Fallacies: Almonds for Migraine


Some people who suffer from migraine are found to be deficient in magnesium and certain  vitamins. This proves to be one of the factor for causing such attacks!

Almonds are rich in magnesium and vitamin B2 ( riboflavin ) and contain salicin, an anti-  inflammatory agent and ingredient in aspirin. So 10- 12 almonds a day, equivalent to 2 aspirins helps in preventing acute attacks of migraine.

However, for those who are allergic to salicin, almonds may even trigger migraine attacks! Therefore prior testing is important in such cases.

Many recent updates and drugs have become available to treat the attacks but no single one is effective in long- term. For those deficient in magnesium and allergic to salicin,  infuse magnesium sulfate solution i.v.  over 3- 5 minutes.

That's all
- Jaskunwar Singh

Thursday, March 2, 2017

Fact of the day: Multi- vitamin supplements beneficial for schizophrenics


Recent studies suggest that high- doses of vitamin B help in reducing the symptoms of schizophrenic patients and those with other neuropsychological disorders, when added to the normal treatment in early stages. (Source)

- Jaskunwar Singh

Monday, February 27, 2017

Fish oil for treatment of asthma


Asthma is a chronic, exaggerated and allergic inflammatory response in the respiratory airways to certain allergens that vary according to seasons.

Omega- 3 fatty acids in high- quality fish oils and other products reduce the inflammation by regulating B- cell function. IgE production is reduced, which otherwise acts to cause asthma symptoms and allergic reactions in patients with mild form of asthma.

The fatty acids are used up by the cells in the lining of respiratory passages to produce hormones that tend to "turn- off" certain factors responsible for attracting white blood cells to the site of inflammation such as leukotrienes, interleukins, and other cytokines.

However, these oils are less effective in severe forms of the disease and in the majority of patients taking corticosteroids.

According to a study, prenatal exposure to fish oils (mainly in third trimester) reduces the risk of wheeze and asthma in children.

Thats all
- Jaskunwar Singh