Vitamin deficiency (A, B, C, D, E, K)

Question 1

Answer 1

Question 2

Question 3

Which foods contain vitamin A?

Answer 3

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.

Question 4

What is the aetiology of vitamin A deficiency?

Answer 4

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.

Question 5

What are the risk factors for vitamin A deficiency?

Answer 5

• 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

Question 6

How common is vitamin A deficiency?

Answer 6

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.

Question 7

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.

Answer 7

Vitamin A deficiency is the biggest cause of preventable blindness in children worldwide.

It is the most common nutritional deficiency in the world.

Question 8

Why can liver disease cause Vit A deficiency?

Why can taking orlistat reduce Vit A absorption?

Answer 8

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

Question 9

Where is Vitamin A absorbed?

Answer 9

Small intestine

Question 10

What are the signs and symptoms of Vitamin A deficiency?

Answer 10

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

Question 11

Name a deficiency syndrome associated with Vit A deficiency.

Answer 11

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.

Question 12

What investigations would you do for Vitamin A deficiency?

Answer 12

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

Question 13

How do you treat vitamin A deficiency?

Answer 13

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

Question 14

What is the prognosis with Vit A deficiency?

Answer 14

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.

Question 15

What are the 4 most common vitamin B deficiencies?

Answer 15

Thiamine - B1

Niacin - B3

Folate - B9

Cobalamin - B12

• (Riboflavin - B2)*
• (Pyridoxine - B6)*

Question 16

How common is thiamine deficiency?

Answer 16

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

Question 17

What are the causes of B1 deficiency?

Answer 17

• 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

Question 18

What is the difference between wet and dry beriberi?

Answer 18

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

Question 19

What are the signs and symptoms of B1 deficiency?

Answer 19

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

Question 20

What investigations would you do for B1 deficiency?

Answer 20

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.

Question 21

How do you treat vitamin B1 deficiency?

Answer 21

IV thiamine - 3 times a day 500mg for 3 days for acute symptomatic adults

Question 22

What are the complications and prognosis with vitamin B1 deficiency?

Answer 22

• 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.

Question 23

What is vitamin B2? Where is it absorbed? What are the associated deficiency syndromes?

Answer 23

Vitamin B2 = riboflavin

Absorbed in the proximal small intestine

Syndromes: angular stomatitis, cheilitis(lips), glossitis

Question 24

What are good sources of vitamin B3?

Answer 24

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.

Question 25

What is B3 required for in the body? What is the deficiency syndrome?

Answer 25

* 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.

Question 26

What are the causes of B3 deficiency?

Answer 26

**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

Question 27

What are the signs and symptoms of B3 deficiency?

Answer 27

_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.

Question 28

What investigations would you do for B3 deficiency?

Answer 28

1. _Serum tryptophan_ - low if diet low in tryptophan 2. _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 3. _Urinary 2-pyridone/N-methynicotinamide ratio_ - \<1 (mg/g creatinine) 4. _Skin biopsy_ - confirmatory diagnostic test 5. _Photosensitivity testing_ - erythema, swelling, blistering of skin to minimal UV light 6. _FBC_ - microcytc anaemia in Fe def, macrocytiv in Vit b12 def, elevated MCV in alcohol abuse 7. _Serum albumin/proteins_ - low in malnutrition 8. _gamma-GT_ - elevated in alcohol abuse

Question 29

How do you treat Vit B3 deficiency?

Answer 29

Nicotinamide +/- multivitamin

Question 30

What is the prognosis/complications of niacin deficiency?

Answer 30

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.

Question 31

What is Vitamin B6? Where is it absorbed? What are the associated syndromes?

Answer 31

Vitamin B6 - pyridoxine Absorbed in the small intestine (as the rest, except B2 which is proximal small intestine and B12 which is terminal ileum) Syndrome: polyneuropathy

Question 32

What part of the brain does thiamin deficiency affect?

Answer 32

WE and KS affect: * Bilateral mamillary bodies * Medial hypothalamus * Thalamus * Periaqueductal gray matter * Floor of fourth ventricle Dry beriberi affects peripheral NS

Question 33

Which part of the brain does cobalamin deficiency affect ?

Answer 33

Demyelinating disorder of the spinal cord

Question 34

What part of the brain does niacin deficiency affect?

Answer 34

Primarily neurons in the brainstem, cerebellar dentate nucleus and spinal cord

Question 35

What part of the CNS does folate deficiency affect?

Answer 35

Demyelinating disorder or the spinal cord

Question 36

What kind of environment do B vitamins require for absorption?

Answer 36

Alkaline - they are water-soluble

Question 37

Which vitamin deficiency is a concern for vegans?

Answer 37

B12 because it is not readily found in plant products

Question 38

What syndrome is associated with Vitamin C deficiency?

Answer 38

Scurvy - life-threatening condition due to dietary vitamin C deficiency. Those affected are mostly refugees or victims of famine, older people, individuals with a history of alcohol misuse or an atypical diet, or children with autism or idiosyncratic behavioural abnormalities.

Question 39

How common is Vitamin C deficiency?

Answer 39

Scurvy thought to be rare but 13% of US is still Vit C deficient Epidemics in refugee camps in Africa occurred from 1982 to 1994, with a prevalence as high as 44%

Question 40

What is the aetiology of vitamin C deficiency?

Answer 40

Always due to inadequate dietary intake of Vitamin C There may be genetic variability of haptoglobin and conditioned scurvy (may occur due to hypermetabolism of vit C after cessation of supratherapeutic doses or megadoses of vit C)

Question 41

What is the pathophysiology of vitamin C deficiency causing scurvy?

Answer 41

* Vitamin C is essential for collagen synthesis as a co-factor for hydroxylation of proline to hydroxyproline in the formation of procollagen. * Without this step collagen triple helix cannot assemble * Existent collagen breaks down over time with insufficient replacement with new collagen, blood vessel walls lose integrity leading to perivascular oedema, erythrocyts extravasation and frank haemorrhage * Vitamin C typically increases intestinal absorption of iron x2-6 fold and sometimes more and may explain why iron deficiency is seen as a concomitant illness

Question 42

What are the signs and symptoms of Vitamin C deficiency?

Answer 42

* Constitutional symptoms - arthralgia, myalgia, weakness, lethargy, nausea, emesis, weight loss, dry skin, depression, dyspnoea. * Easy bruising or bleeding * Gait impairment/leg pain * Pedal oedema * Petechial and perifollicular haemorrhages (legs and feet) * Poor wound healing * Bruising and nodular or black ecchymoses at non-traumatic sites * Joint swelling * Oral mucosal petechiae * Coiled hairs * Follicular hyperkeratosis * Tooth loss * Gingival discoloration * Gum swelling Can lead to conjunctival and subconjunctival haemorrhage. Other: dysphagia, alopecia, siccia-like or Sjogren's like syndrome, nail clubbing, peripheral neuropathy, cardiac faiulre, haemorrhagic pleural effusion, osteoporosis.

Question 43

What investigations would you do for vitamin C deficiency?

Answer 43

**FBC and peripheral blood smear** - normocytic anaemia (expected); microcytic or megaloblastic anaemia if other nutritional deficiencies are present **serum/leukocyte/whole blood ascorbic acid** - high risk if deficient **X-ray of knee and wrist** - corner fraction sign, a ground-glass appearance, trabecular atrophy, Pelkan's sign, Frankel's sign

Question 44

How do you treat vitamin C deficiency?

Answer 44

Vit C replacement - ascorbic acid

Question 45

What are the complications of Vit C deficiency?

Answer 45

* Intracerebral haemorrhage - *intracranial haemorrhage signs and symptoms are as follows: headache (upon lying flat, awakening, increasing with change in position); nausea and vomiting; change in alertness; visual changes; decreased sensation; difficulty speaking, swallowing, or reading and writing; weakness; and seizure* * Endocardial haemorrhage * Neck pain * Back pain

Question 46

What is the prognosis with vitamin C deficiency?

Answer 46

_Short-term_ Within days of treatment, most of the major signs and symptoms of scurvy will begin to improve. New signs and symptoms should not appear shortly after treatment starts. If symptoms are not treated promptly, a risk of death is high, so rapid treatment is imperative. _Long-term_ Provided no major haemorrhagic complications occur (i.e., stroke), patients having experienced scurvy should expect full recovery.

Question 47

What is Vitamin D deficiency?

Answer 47

To maximise vitamin D effects on the skeleton and on calcium metabolism, serum 25-hydroxyvitamin D level should be \>75 nanomoles/L (\>30 nanograms/mL). Therefore, vitamin D deficiency is defined as a serum 25-hydroxyvitamin D level of \<50 nanomoles/L (\<20 nanograms/mL), whereas vitamin D insufficiency is regarded as a 25-hydroxyvitamin D level of between 52-72 nanomoles/L (21-29 nanograms/mL).

Question 48

Where is vitamin D absorbed? What is the associated deficiency syndrome?

Answer 48

Vitamin D - absorbed in the jejunum as free vitamin Syndrome - rickets, osteomalacia

Question 49

How common is vitamin D deficiency? Why is it important?

Answer 49

In US/Europe more than 40% of the adult population aged \>50yrs is vitamin-D deficient. However, vitamin D deficicency serum 25-hydroxyvitamin D levels have also been reported in 48% pre-teen girls, 52% adult hispanics/black children, 32% young healthy adults. Mostly in the setting of limited sunlight exposure, even when foods are fortified. **_Why is it important?_** * Vit D deficiency increases risk of chronic disease e.g. cancer, AI, T2DM, CVD, hypertension, cognitive dysfunction, infectious disease, osteoarthritis. * E.g. A study in Finland found that infants who had received 2000 IU of vitamin D per day for the first year of life reduced their risk of type 1 diabetes by 78% 31 years later

Question 50

What is the cause of vitamin D deficiency?

Answer 50

Lack of sun exposure * Avoiding sun exposure * Heavy sunscreen use (e.g. SPF 8 reduces vit D production by 92.5%) * Season, latitude, time of day * Skin pigementation - due to sun screening action of melanin * Ageing - ability of skin to produce vit D with age decreases Inadequate dietary and supplemental Vit D e.g. in infants * Malabsorption syndromes e.g. Coeliac, cystic fibrosis, rohn's disease, Whipple's disease, or short bowel syndrome, as well as those who have undergone gastric bypass surgery. * Using glucocorticoids, antiepileptics, antiretroviral therapy, rifampicin etc --\> activation of steroid and xenobiotic receptors --\> activation of enzymatic machinery destroying 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D. Organ dysfunction * Severe liver failure - associated with fat malabsorption so reduces vit D absorption when more than 90% of liver fails (bc it is not capable of producing 25-hydroxvitamin D). * CKD - inability to produce enough 1,25-dihydroxyvitamin D to regulate calcium metabolism * Vit D deficiency syndrome - e.g. pseudovitamin D-deficiency rickets, vitamin D-resistant rickets, X-linked hypophosphataemic rickets, benign or malignant tumour may produce excessive amount of FGF-23 --\> severe hypophosphytaemia, low levels of serum 1,25-dihydroxyvitamin D and oncogenic osteomalacia.

Question 51

Why do obese people need 2-3 times more vit D intake?

Answer 51

Vitamin D is fat-soluble: when it is ingested or produced in the skin, most of it is initially incorporated into the body fat. For adults with a BMI \>30 the fat sequesters vitamin D; therefore, obesity increases the risk for vitamin D deficiency. This is the rationale behind the recommendation that obese adults require two to three times more vitamin D to both treat vitamin D deficiency and prevent recurrence

Question 52

Summarise the production of vitamin D in the body.

Answer 52

* 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)

Question 53

What are the signs and symptoms of Vit D deficiency?

Answer 53

Rickets: * bowing of legs * chest deformity - pectus carinatum, thoracic assymmetry * rachitic rosary * frontal bossing - increase in bone formation and flattening of forehead * widening of ends of long bones (in children there is poor mineralisation of the epiphyseal plates) * delayed tooth eruption and early dental caries * head sweating - due to increase in neurommuscular activity * localised or generalised bone tenderness - osteomalacia * proximal muscle weakness - getting up from sitting poistion. * waddling gait - due to osteomalacia. Other: * failure to thrive * delayed achievement of motor milestones * fatigue and malaise * symptoms of hypocalcaemia

Question 54

What are the risk factors for vit D defciency?

Answer 54

* Inadequate sunlight exposure * Increased skin pigmentation * Age \>50years * Inadequate dietary and supplemental vit D intake * Malabsorption * Obesity * Medication use * Genetic mutation * Tumour * CKD * Granulomatous disorders - *sarcoidosis and TB due to inceased destruction of vit D* * Primary hyperparathyroidism * Hyperthyroidism

Question 55

What investigations would you do for vit D deficiency?

Answer 55

_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)

Question 56

How do you treat vitamin D deficiency?

Answer 56

* Vitamin D * Sensible sun or UV-B radiation exposure * Calcium _In disorders of Vit D metabolism:_ vit D + sensible sun exposure + 1,25-hydroxyvitamin D3/active analogue + calcium + phosphate

Question 57

What are the complications of vit D deficiency?

Answer 57

* Rickets * Other chronic diseases - * Osteopenia and osteoporosis * Falls and fractures * Treatment-related vitamin D intoxication

Question 58

What is the prognosis with vit D deficiency?

Answer 58

**Asymptomatic vit D deficiency** - most children and adults have no symptoms. Treatment can correct it within 2-3 months ,as long as there are no additional risk factors or disease states that prevent the absorption of vitamin D or metabolism of vit D to 25-hydroxyvitamin D **Symptomatic vit D deficiency** - the earlier the intervention the more favourable the prognosis., with resolution of skeletal malformations of rickets. Especially true for leg deformities. Physical examination findings revert to normal within 3-6 months.

Question 59

What is Vitamin E deficiency?

Answer 59

Serum concentration of less than 12 µmol/L.

Question 60

Where is vitamin E absorbed? What is the associated deficiency syndrome?

Answer 60

Small intestine Hameolysis; neurological deficit

Question 61

Where is Vitamin E found?

Answer 61

nut oils, sunflower seeds, whole grains, wheat germ, and spinach

Question 62

What are the uses of Vitamin E in th body? (3)

Answer 62

1. **Antioxidant effect** - prevents oxidation of saturated fatty acids therefore preventing atheroscleorosis (because oxidised LDLs are more readily taken uo by macrophages --\> foam cells) 2. **Immunomodulation** - Vit E enhances lymphocyte proliferation and decreases immunosuppressive PGE2 and serum lipid peroxidases. 3. **Antiplatelet effect** - inhibits platelet adhesion preventing heart disease

Question 63

What is the aetiology/risk factors of vitamin E deficiency?

Answer 63

RARELY DUE TO DIET LOW IN VIT E. _Malabsorption:_ Absorption depends on normal pancreatic and biliary secretion, micelle formation and penetration across intestinal membranes. * Cystic fibrosis, * abetalipoproteinemia - inability to fully absorb dietary fats, cholesterol and fat-soluble vitamins. * chronic cholestatic hepatobiliary disease, * short-bowel syndrome, and * isolated vitamin E deficiency syndrome (chr 8q) ...are all potential causes of a deficiency state. *Vitamin E overdose is difficult to achieve and, thus, is extremely uncommon.*

Question 64

What is the typical presentation of vitamin E deficiency?

Answer 64

**Neurological and neuromuscular problems:** * Decreased vibratory sense * Distal muscle weakness * Night blindness * Hyporeflexia * Ataxia * Upward gaze nystagmus/dissociated nystagmus * Diffuse muscle weakness * Visual-field constriction * Severe: complete blindness, cardiac arrhythmia, dementia. **Haemolyic anaemia**: - due to oxidative dmage to RBC **Retinopathy** **Impairment of the immune response** _Examination_: Finger-to-nose and rapid, alternating movement tests, are notably affected in vit E deficiency. After treatment, patients' ability to perform such tests may remain somewhat impaired but should improve.

Question 65

What investigations would you do for vitamin E deficiency?

Answer 65

serum alpha-tocopherol level is useful.

Question 66

What is the treatment of vitamin E deficiency?

Answer 66

Oral Vit E supplementation.

Question 67

Where is vitamin K absorbed? What is the deficiency syndrome?

Answer 67

Small intestine Bleeding disorders

Question 68

What foods contain vitamin K?

Answer 68

* green leafy vegetables and oils, * such as olive, cotton seed and soya bean. * green peas and beans, * watercress, * asparagus, spinach, broccoli, * oats and whole wheat. ## Footnote **Vitamin K is also synthesised by colonic bacteria**

Question 69

What are the uses of vitamin K in the body?

Answer 69

Vitamin K is changed to its active form in the liver by the enzyme Vitamin K epoxide reductase. Activated vitamin K is then used to gamma carboxylate (and thus activate) certain enzymes involved in coagulation: Factors II, VII, IX, X, and protein C and protein S. Inability to activate the clotting cascade via these factors leads to the bleeding symptoms

Question 70

How common is vit K deificiency?

Answer 70

Vit K deficiency without bleeding may occur in 50% of infants in US so it is recommended that 0.5-1mg vit K1 to be administered to all newborns shortly after birth Sometimes can be caused by insufficient vit K producing bacteria in gut by insufficient colonisation in first 5-7 days of life (e.g. by lack of breastfeeding or antibiotic therapy)

Question 71

What is the aetiology of vit K deficiency?

Answer 71

* Disrupted intestinal uptaje - bile duct obstruction * Therapeutic/accidental intake of vit K1 antagonists e.g. warfarin * Rarely nutritional Vit K1 deficiency --\> (Gla-residues are inadequately formed and Gla proteins are insufficiently active)

Question 72

What are the risk factors for Vit K deficiency?

Answer 72

* Excessive anticoagulation * Liver disease * Malabsorption * Biliary tract disease * Dietary deficiency * Drugs - colestyramine, salicylates, rifampin, isoniazid and barbiturates are associated with vitamin K deficiency. * Diseases with endogenously produced coagulation inhibitors (eg, lupus anticoagulant and antithrombins) * Miscellaneous - massive transfusion, DIC, polycythaemia vera, nephrotic syndrome, cystic fibrosis, leukaemia.

Question 73

What is the typical presentation of vitamin K deficiency?

Answer 73

* Bleeding to minor trauma * Epistaxis * Petechiae * haematoma * GI bleeding * Menorrhagia * Haematuria * Bleeding from gums Other: cartilage calcification; and severe malformation of developing bone or deposition of insoluble calcium salts in the walls of arteries

Question 74

What investigations would you do for vitamin K deficiency?

Answer 74

* PT and aPTT - all elevated * Antibody test for DCP protein (des-gamma-carboxy prothrombin) - present in vit K absence * Plasma vit K level

Question 75

How do you manage Vit K deficiency?

Answer 75

**FFP** - if life threatening bleeding **Then Vit K -** available as phytomenadione (vit K) and as synthetic water soluble analogue menadiol sodium diphosphate. IV injections should be given slowly as fast IV injection can cause bronchospasm and peripheral vascular collapse. IM injections can lead to severe haematoma formation at injection site if clotting is impaired.

Question 76

What is the prognosis with Vit K deficiency?

Answer 76

Very good prognosis if recognised early and treated properly but severe bleeding can be fatal.