Vitamin deficiency (A, B, C, D, E, K) Flashcards
Which foods contain vitamin A?
liver, milk, eggs and fish-liver oils
Beta-carotene found in green leafy and orange/yellow vegetables can be converted to vitamin A by the body.
What is the aetiology of vitamin A deficiency?
Inadequate intake of Vit A - esp when rice is the main food
Inadequate absorption of Vit A in conditions such as…
- Coeliac disease.
- Crohn’s disease.
- Giardiasis - an infection of the gut (bowel).
- Cystic fibrosis.
- Diseases affecting the pancreas.
- Liver cirrhosis.
- Obstruction of the flow of bile from your liver and gallbladder into your gut.
What are the risk factors for vitamin A deficiency?
- Absorption problems
- Weight reduction surgery
- Taking orlistat
- Vegan diets
- Alcoholism
- Other liver disease - Vit A is stored in the liver
- Toddlers living in poverty
- Recent immigrants/refugees from low-income countries
How common is vitamin A deficiency?
Unusual in high income countries but very common in low income countries where it often develops because of intestinal infections and worms, and protein-energy malnutrition.
Complete the phrase:
Vitamin A deficiency is the biggest cause of X X in children worldwide.
It is the most common X X in the world.
Vitamin A deficiency is the biggest cause of preventable blindness in children worldwide.
It is the most common nutritional deficiency in the world.
Why can liver disease cause Vit A deficiency?
Why can taking orlistat reduce Vit A absorption?
Vit A is fat-soluble vitamin, thus deficiency is likely if there is fat malabsorption.
Vit A is stored in the liver so liver disease –> deficiency
Where is Vitamin A absorbed?
Small intestine
What are the signs and symptoms of Vitamin A deficiency?
Mild - no symptoms OR..
- Fatigue
- Infections
- Delayed growth
- Infertility
- Miscarriage
Severe forms:
Eye and vision problems - night blindness, keratomalacia (thinning and ulceration of cornea), xerophthalmia (conjunctival and corneal dryness), Bitot’s spots (foamy patches on sclera), cornea perforation, damage to retina causing visual impairment
Skin and hair problems - dry skin, dry hair, pruritus
Name a deficiency syndrome associated with Vit A deficiency.
Xerophthalmia
This vitamin a deficiency syndrome is a big cause of blindness in the Tropics. Conjunctivae become dry and develop oval/triangular spots (Bitôt’s spots). Corneas become cloudy and soft.
Give vitamin a. Get special help if pregnant: vitamin a embryopathy must be avoided. Re-educate and monitor diet.
What investigations would you do for Vitamin A deficiency?
Bloods:
- Serum retinol (<0.7mg/L) and serum RBP (retinol binding protein)
- Zinc - zinc deficiency interferes with RBP production
- Iron panel - Fe deficiency can affect Vit A metabolism
- Albumin - indirect measure of Vit A
- FBC - ?ddx anaemia, infection, sepsis
- U&Es and LFTs for nutritional and volume status
Other:
Dark adaptation threshold can be tested
How do you treat vitamin A deficiency?
Men need 0.7mg and women 0.6mg daily
Easily prevented through consumption of a balanced diet - vitamin A–rich foods, such as liver, beef, chicken, eggs, fortified milk, carrots, mangoes, sweet potatoes, and leafy green vegetables.
For syndromes, supplements are given - 3000mcg for adults
What is the prognosis with Vit A deficiency?
Good if mild deficiency is corrected
In severe forms, there may be permanent loss of vision if treatment not taken early enough. Severe generalised malnutrition in low income countries often leads to death.
What are the 4 most common vitamin B deficiencies?
Thiamine - B1
Niacin - B3
Folate - B9
Cobalamin - B12
- (Riboflavin - B2)*
- (Pyridoxine - B6)*
How common is thiamine deficiency?
0.8-2.8% of population
Mostly in alcoholism - 12.5%
Up to 80% of those with WE who survive will progress to KS
Beriberi is more common in Asian countries where there is large scale consumption of thaimine-depleted polished rice
What are the causes of B1 deficiency?
- Inadequate nutrition
- Reduced absorption
- Impaired utilisation
- Excess thiamine use
Alcoholism - alcohol increases thiamine utilisation and reduces GI uptahe and impairs phosphorylation of thiamine.
Non-alcoholism - poor nutrition, prolonged parenteral nutrition, GI disease, malignancy, diarrhoea, liver disease, hyperemesis gravidarum, haemodialysis.
Genetic causes - rare
What is the difference between wet and dry beriberi?
Dry - peripheral nervous system disorder associated with peripheral neuropathy
Wet - cardiovascular disorder associated with cardiac manifestations and oedema secondary to congestive heart failure
sometimes infantile beriberi can occur secondary to inadequate thiamine in mother’s breastmilk
What are the signs and symptoms of B1 deficiency?
Early non-specific - fatigue and muscle pains
Wernicke encephalopathy - triad of ataxia, altered mental status and ocular abnormalities (ophthalmoplegia/nystagmus)
Korsakoff syndrome - as above + antero/retrograde amnesia, disorientation, lack of insight, confabulation, apathy
Dry beriberi - symmetric sensorimotor polyneuroptahy with decreased sensation , reduced distal reflexes, muscle weakness.
Wet beriberi- high-output cardiac failure, peripheral oedema, pulmonary oedema, orthopnoea
What investigations would you do for B1 deficiency?
Erythrocyte thiamine pyrophosphorylate - reduced; sample should be taken before treating thiamine deficiency. Good indicator if thiamine stores as thiamine depletes at same rate in erythrocyte as other tissues.
ABG - metabolic acidosis
Lactate - elevated
TFTs - to rule out thyrotoxicosis - elevated free T4/T3 and suppressed TSH in thyrotoxicosis
Imaging;
MRI brain - for wernicke’s encephalopathy (increased T2 signal in paraventricular regions of thalamus, mamillary bodies, hypothalamus, periaqueductal region, fourth ventricle floor and midline cerebellum.
How do you treat vitamin B1 deficiency?
IV thiamine - 3 times a day 500mg for 3 days for acute symptomatic adults
What are the complications and prognosis with vitamin B1 deficiency?
- Anaphylaxis from thiamine replacement
- Low-output cardiac failure with thiamine replacement
- Korsakoff’s psychosis
Prognosis: depends on how quickly it is treated. 20% of pts with untreated Wernicke’s will die and of those who survive many progress to Korsakoff’s. Wet Beriberi if untreated can cause death; otherwise significant improvement within first 24hours of therapy. Dry beriberi can take weeks to months to resolve esp if there is coexisting neuropathy e.g. alcohol abuse/diabetes.
What is vitamin B2? Where is it absorbed? What are the associated deficiency syndromes?
Vitamin B2 = riboflavin
Absorbed in the proximal small intestine
Syndromes: angular stomatitis, cheilitis(lips), glossitis
What are good sources of vitamin B3?
Lean meat, poultry, fish, and peanuts are rich in vitamin B3 (niacin); milk and eggs are rich sources of tryptophan, the precursor of niacin.
Deficiency of vitamins B2 (riboflavin) and/or B6 (pyridoxine) reduces the synthesis of niacin from tryptophan and may lead to secondary vitamin B3 deficiency.
What is B3 required for in the body? What is the deficiency syndrome?
- Essential component of NAD and NADP, which are coenzymes required for oxidation-reduction reaction in Krebs’ cycle
- These are essential in all cells for energy production, metabolism, and DNA repair.
- Niancin is also called nicotinic acid
Severe deficiency results in pellagra, which is a combined deficiency of both niacin and its precursor, tryptophan. The symptoms of deficiency are primarily dermatitis, diarrhoea, and dementia. Death results if the condition is untreated.
What are the causes of B3 deficiency?
Marginal deficiency - Dietary history is indicative of a diet marginally and chronically deficient in niacin, without the development of signs and symptoms.
Primary (endemic) pellagra - Severe niacin deficiency resulting in dermatitis, dementia, and diarrhoea as a result of a diet deficient in niacin and/or tryptophan.
Secondary pellagra - Deficiency associated with an underlying condition, such as chronic alcohol abuse, anorexia nervosa, cancer/carcinoid syndrome, vitamin B2 and B6 deficiencies, and medications (e.g., isoniazid).
Risk factors:
- Malnutrition - Consumption of a corn-based, low-protein diet, or a vegan diet (no animal products) with few niacin sources
- Chronic ETOH abuse - can lead to pellagric encephalopathy
- Vit B2 and B6 deficiency - they are coenzymes in the conversion of tryptophan to niacin
- Malabsorption
- Eating disorders
- Drugs - pyrazinamide, ethionamide, fluorouracil, mercaptopurine, hydantoins, phenobarbital, chloramphenicol, oestrogen-containing oral contraceptives, antidepressants, and penicillamine
- Alzheimer’s and Parkinson’s
- Age >65 years
What are the signs and symptoms of B3 deficiency?
Pellagra is classically characterized by “the three Ds”: dermatitis, diarrhea, and dementia.
Pellegrous encephalopathy is characterized by confusion, apathy, depression, impaired memory, abnormal gait, and spastic quadriplegia in severe cases.
What investigations would you do for B3 deficiency?
- Serum tryptophan - low if diet low in tryptophan
- Urinary N-methylnicotinamide - urinary metabolites of niacin would be low - excretion of niacin: 20-30% of intake as N-methylnicotinamide and 40-60% as N-methyl-2-pyridone-5-carboxamide
- Urinary 2-pyridone/N-methynicotinamide ratio - <1 (mg/g creatinine)
- Skin biopsy - confirmatory diagnostic test
- Photosensitivity testing - erythema, swelling, blistering of skin to minimal UV light
- FBC - microcytc anaemia in Fe def, macrocytiv in Vit b12 def, elevated MCV in alcohol abuse
- Serum albumin/proteins - low in malnutrition
- gamma-GT - elevated in alcohol abuse
How do you treat Vit B3 deficiency?
Nicotinamide +/- multivitamin
What is the prognosis/complications of niacin deficiency?
Complications:
- Peripheral neuropathy
- Alcoholic pellagra encephalopathy
- Carcinogenesis - niacin status has an influence on DNA repair, genomic stability, and the immune system. This in turn has an impact on cancer risk and on the adverse effects of chemotherapy
Prognosis:
Shoudl recover fully with vitamin supplementation (most after 2 weeks. Continued supplementation is suggested in some long lasting conditions.
How do you treat vitamin C deficiency?
Vit C replacement - ascorbic acid
Summarise the production of vitamin D in the body.
- UVB on the skin forming Vit D3 in liver (cholecalciferol)
- or Vit D2 from diet (ergocalciferol)
- These are converted in the kidney to Calcitriol by 1-ALPHA-HYDROXYLASE (which is regulated by PTH)
What investigations would you do for vit D deficiency?
Bloods:
Serum 25-hydroxyvitamin D - major circulating form of vitamin D - deficiency: <50 nM/L (<20 ng/mL); insufficiency: between 52-72 nM/L (21-29 ng/mL)
Serum alkaline phosphate - normal or elevated but high in rickets and osteomalacia
Serum Ca - normal in 2o hyperparathryoidism which mobilises calcium from skeleton and conserves Ca in kidney to maintain normal serum Ca
Fasting serum phosphate - low-normal or rarely low in 2o hyperparathyroidism causing phosphaturia
Imaging:
X-ray of knees and wrists - cupping, splaying, and fraying of the metaphysis; Looser’s zone (pseudofracture)
