Vitamin Deficiencies Flashcards

1
Q

Vitamin K

A

-fat soluble
-plays a role in coagulation
-controls the formation of coagulation factors 2, 7, 9, 10 (these are made in liver)
-participate in the complex reactions that activate factors 10 and 2
-deficiency affects hemostasis -> if deficient you will bleed

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2
Q

vitamin K sources and deficiency

A

Vitamin K sources:
-Leafy vegetables
-Endogenously from synthesis by intestinal bacteria in colon

Vitamin K deficiency:
-Poor diet
-Malabsorption of fat soluble vitamins
-Broad-spectrum antibiotics suppressing colonic flora that synthesize it in the colon

-Treatment- subcutaneous vitamin K 15mg single dose -> corrects
-Prognosis- Excellent

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3
Q

Vitamin K deficiency labs

A

-prothrombin time (PT) is prolonged
-PTT, Fibrinogen level, thrombin time, and platelet count are not affected

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4
Q

differential diagnosis of vitamin k deficiency

A

-Hepatic coagulopathy- pts can have bleeding if they have liver disease -> Can be distinguished from hepatic coagulopathy only by assessing the response to vitamin K therapy
-if hemostasis is restored with vitamin K therapy -> vitamin K deficiency
-Surreptitious warfarin use- can cause bleeding indistinguishable from vitamin k deficiency bc warfarin causes vitamin k deficiency!!
-Laboratory features indistinguishable from those of vitamin K deficiency
-disseminated intravascular coagulation (DIC)- excess clotting
-decreased platelet count and fibrinogen levels with DIC -> different from vit K deficiency

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5
Q

thiamine (B1) deficiency

A

-Thiamine is a water-soluble
-Absorbed in the jejunum
-Body can’t produce it
-mostly concentrated in skeletal muscles (but also in brain, heart, kidney, liver)
-5mg absorbed in small intestine and is sitting
-30mg storage in tissues (not much!)
-Most thiamine deficiency in US is due to alcoholism -> poor dietary intakes, Impaired B1 absorption from alcohol, metabolism, and storage
-other causes of deficiency- malabsorption, dialysis, and other causes of chronic protein-calorie undernutrition
-deficiency can happen in pts with marginal thiamine status (they have just enough) with intravenous dextrose solutions
-thiamine is required for glucose metabolism -> if someone is starved or malnutrients and you give dextrose you must also supplement thiamine

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6
Q

food sources of thiamine

A

-Whole-grain foods
-Meat/fish/poultry/eggs -> usually removed with processing -> they put it back in
-Milk and milk products
-Vegetables (ie, green, leafy vegetables; -beets; potatoes)
-Legumes (ie, lentils, soybeans, nuts, seeds)
-Orange and tomato juice

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7
Q

symptoms of thiamine deficiency

A

-Early manifestations of deficiency-a norexia, muscle cramps, paresthesias*, and irritability
-paresthesias is tell tale sign its getting bad

-Advanced deficiency primarily affects-
-Cardiovascular system (“wet beriberi”)
OR
-Nervous system (“dry beriberi”)
-heart and nervous system are more sensitive to thiamine deficiency bc of the oxidative metabolism that occurs

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8
Q

wet beriberi

A

-Thiamine deficiency leads to increased metabolic demand and increased need for blood flow.
-Marked peripheral vasodilation and increase in blood volume resulting in high-output heart failure
-vasodilation tricks kidneys into thinking youre volume depleted -> retains Na and water -> fluid over load -> high output heart failure
-Dyspnea, tachycardia, chest pain, cardiomegaly, and pulmonary and peripheral edema

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9
Q

dry beriberi

A

-Involves both the PNS and CNS
-Peripheral nerve involvement- Symmetric motor and sensory neuropathy with pain, paresthesias, and loss of reflexes -> involves LEGS > arms
-it then can progress to…
-CNS involvement- Results in Wernicke–Korsakoff Syndrome

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10
Q

wenicke’s encephalopathy (WE)

A

-ACUTE syndrome
-Encephalopathy, oculomotor dysfunction, gait ataxia
-horizontal nystagmus** and palsy
-Requires emergent treatment to prevent progress to korsakoff’s syndrome (KS) -> death and neurologic morbidity
-tx- thiamine
-COAT- confusion, opthalmoplegia, ataxia, thiamine deficiency

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11
Q

Korsakoff’s syndrome (KS)

A

-chronic neurologic condition that usually occurs as a consequence of longstanding wenicke’s encephalopathy (WE)
-Amnesia, confabulation(pt has fake memories), and impaired learning
-if you give thiamine at this point only half pts will improve
-RACK- retrograde amnesia, antegrade amnesia, confabulation, korsakoff

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12
Q

Wernicke–Korsakoff Syndrome dx and tx

A

-Erythrocyte thiamine transketolase (ETKA)
-Empiric thiamine therapy and response is used to support a diagnosis of B1 deficiency
-Treated with large parenteral doses of thiamine B1
-always put thiamine in glucose solutions for hydration
-Therapeutic doses of other water-soluble vitamins given as well -> if your deficient in one you are probably deficient in many
-prognosis- Complete resolution in half of patients (especially before beriberi) -> Other half obtain only partial resolution or no benefit

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13
Q

niacin

A

-B3
-Niacin is a generic term for nicotinic acid.
-Unlike most other vitamins, niacin can be synthesized from the amino acid tryptophan*
-Niacin is an essential component of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP), which are involved in many oxidation-reduction reactions -> produce ATP

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14
Q

niacin food sources and deficiency

A

-Food sources:
-Protein foods containing tryptophan
-Numerous cereals (fortified in cereals), vegetables, and dairy products
-tuna, beef, liver, chicken

-Deficiency:
-Most commonly due to alcoholism and nutrient–drug interactions.
-Inborn errors of metabolism

-Therapeutic:
-Nicotinic acid is used therapeutically for the treatment of hypercholesterolemia and hypertriglyceridemia
-it does not treat niacin deficiency (NIACINAMIDE DOES)

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15
Q

early and advanced deficiency of niacin

A

-Early manifestations of niacin deficiency are nonspecific:
-Anorexia, weakness, irritability, mouth soreness, glossitis, stomatitis, and weight loss

-Advanced deficiency:
-Pellagra**: dermatitis, diarrhea, and dementia
-Dermatitis- symmetric, sun exposed areas, dark scaly patchy lesions
-Diarrhea- severe, malabsorption, atrophy to intestinal villi, dehydrated
-Dementia- insomnia, irritable apathy, psychosis, memory loss

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16
Q

diagnosis of early and advanced niacin deficiency

A

-Early deficiency- diagnosis requires a high index of suspicion:
-Niacin metabolites (urine)
-Serum and red cell levels of NAD and NADP are also low but nonspecific
-Advanced cases- clinical diagnosis
-Treatment: Oral niacin -> niacinamide (NOT B3 NICOTINIC ACID)

17
Q

vitamin C deficiency

A

-Body cannot synthesize Vitamin C
-water soluble vitamin
-Sources: fruits and vegetables -> citrus - ascorbic acid
-At risk:
-Poor, the elderly, and chronic alcoholics -> Dietary inadequacy
-Chronic illnesses pts have a higher need so they can become deficient (ie. Ca, chronic renal failure)
-Malabsorbers
-Smokers

18
Q

early, advanced and late stage presentation of vitamin C deficiency

A

-Early manifestations -malaise and weakness

-Advanced stages -> scurvy* develops: BLEEDING
-Perifollicular hyperkeratotic papules with surrounding hemorrhage , petechiae, purpura
-Splinter hemorrhages (bleeding under nails), bleeding gums (if no teeth does not have this sign), hemarthroses, and subperiosteal hemorrhages
-Anemia
-Poor wound healing

-Late stages: Edema, oliguria (less urine), neuropathy, intracerebral hemorrhage*, and death

19
Q

diagnosis and treatment for scurvy

A

-Diagnosis of Scurvy:
-Clinically, on the basis of the skin lesions
-Atraumatic hemarthrosis highly suggestive (if not trauma) **
-Confirmation: decreased plasma ascorbic acid levels

-Treatment:
-300–1000 mg of ascorbic acid per day
-Improvement typically occurs within days
-ascorbic acid in large amounts can cause gastritis, farting, diarrhea, or oxalate stone formation (not really seen as much) -> can cause false neg dx tests specifically fecal hemocult cards

20
Q

vitamin A deficiency

A

-common particularly in developing countries
-MC cause of blindness
-Occurs most commonly in the elderly who abuse mineral oil as a laxative and urban poor
-In the US usually due to fat malabsorption syndromes or mineral oil laxative abuse

21
Q

which vitamins are fat soluble

A

-E,D,K, A
-deficiency can be caused by pancreatic abnormalities -> not enough lipase -> cant absorb fat soluble vitamins

22
Q

early and late manifestations of vitamin A deficiency

A

-Early Manifestations:
-Night blindness* is earliest symptom
-Dry conjunctiva (xerosis)
-Small white patches on the conjunctiva (Bitot’s spots)

-Late Manifestations:
-Ulceration and necrosis of the cornea (keratomalacia)
-Perforation, endophthalmitis (purulent inflammation of intraocular fluids), and blindness
-Xerosis and hyperkeratinization of the skin
-Loss of taste

23
Q

diagnosis and treatment of vitamin A deficiency

A

-Diagnosis
-Abnormalities of dark adaptation are strongly suggestive
-Serum levels below 30–65 mg/dL

-Treatment
-Night blindness, poor wound healing, and other signs of early deficiency - Oral vit A 30,000 IU daily for 1 week
-Advanced deficiency with corneal damage- 20,000 IU/kg orally for at least 5 days (WEIGHT BASED)

24
Q

vitamin D

A

-essential for bone mineral metabolism through its role in calcium absorption and osteoclast activity
-levels decrease with increasing age
-very common to be deficient bc we are outside less and wear sunblock
-Supplementation reduces rate of all fractures in the elderly
-deficiency decreases intestinal absorption of calcium
-MC cause of osteomalacia
-Plays a role in osteoporosis
-Causes: Insufficient sun exposure, malnutrition, or malabsorption

25
Q

causes of vitamin D deficiency and high risk populations

A

-Causes:
-Malabsorption: not enough pancreatic lipase (fat soluble), IBD, surgery to small bowel, celiac
-Medications: Anticonvulsants (phenytoin) and Cholestyramine (this binds bile salts - also binds vit D -> excrete it rather than absorb)
-Rickets type 1 or 2
-High Risk: Elderly and Sunlight deprived individuals

26
Q

Rickets type 1

A

-rickets type 1:
-genetic
-Rare autosomal recessive defect in renal synthesis of 1,25(OH)2D (active form of vitamin D)
-Presents in childhood with rickets and alopecia
-Responds to oral calcitriol

-rickets type 2:
-Genetic defect in the 1,25(OH)2D receptor (for active form)
-Variable response to oral calcitriol at very high doses

27
Q

prevention and treatment of vitamin D deficiency

A

-NOF (nation osteoporosis foundation) recommends 800 to 1,000 IU/day for adults age 50 and older.
-Goal:
-Serum 25(OH)D concentration ≥ 30 ng/ml (75 nmol/L)
-In addition to food sources (barely helps), dermal synthesis is the major natural source of the vitamin.
-Sunshine: the face, arms, hands, or back
-Sun exposure without sunscreen for 15 minutes at least twice weekly.

28
Q

vitamin D sources

A

-Surprisingly few foods contain vitamin D unless it’s added to the food.
-There are a few vitamin D super foods:
-Salmon, tuna, mackeral, swordfish
-Mushrooms (exposed to ultraviolet light-increases vitamin D)
-pure cod liver oil

29
Q

food label?

A

-based on 2,000 calories diet
-8oz serving gives 25% of daily vitamin D

30
Q

vitamin D treatment

A

-Sunlight-deprived individuals
-1000 IU daily
-Give prophylactically
-Long-term phenytoin (anti-seziure med) therapy may be treated prophylactically with vitamin D, 50,000 IU orally every 2–4 weeks
-Most adults (>50):
-1200 mg of elemental calcium (total diet plus supplement) + vitamin for bone health
-800-1000 IU of vitamin D daily
-also important for females in 20s to lay down base bone density

31
Q

vitamin D with osteoporosis

A

-Many patients with osteoporosis will need more than the general recommendation of 800-1,000 IU/day.
-Vitamin D3 (cholecalciferol) is the preferred oral supplement -> more active
-The safe upper limit for vitamin D intake for the general adult population was increased to 4,000 IU per day in 2010

32
Q

frank vs insufficiency vitamin d treatment

A

-Frank vitamin D deficiency (<20ng/ml):
Cholecalciferol (D3), 50,000 IU orally once or twice weekly for 6–8 weeks -> then 800-1000 IU daily

-Vitamin D Insufficiency (20 to 30 ng/mL):
800 to 1000 (up to 2,000) international units of vitamin D3 by mouth daily

-All patients receive supplemental oral calcium (eg, calcium citrate or calcium carbonate)

33
Q

water soluble vitamins

A

-B1 (thiamine), B3 (niacin), C
-deficiency seen with alcoholism
-body cannot synthesize C or B1 (thiamine)
-it CAN synthesize niacin (B3) from tryptophan