Vitamin Deficiencies Flashcards
Vitamin K
-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
vitamin K sources and deficiency
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
Vitamin K deficiency labs
-prothrombin time (PT) is prolonged
-PTT, Fibrinogen level, thrombin time, and platelet count are not affected
differential diagnosis of vitamin k deficiency
-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
thiamine (B1) deficiency
-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
food sources of thiamine
-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
symptoms of thiamine deficiency
-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
wet beriberi
-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
dry beriberi
-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
wenicke’s encephalopathy (WE)
-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
Korsakoff’s syndrome (KS)
-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
Wernicke–Korsakoff Syndrome dx and tx
-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
niacin
-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
niacin food sources and deficiency
-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)
early and advanced deficiency of niacin
-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
diagnosis of early and advanced niacin deficiency
-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)
vitamin C deficiency
-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
early, advanced and late stage presentation of vitamin C deficiency
-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
diagnosis and treatment for scurvy
-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
vitamin A deficiency
-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
which vitamins are fat soluble
-E,D,K, A
-deficiency can be caused by pancreatic abnormalities -> not enough lipase -> cant absorb fat soluble vitamins
early and late manifestations of vitamin A deficiency
-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
diagnosis and treatment of vitamin A deficiency
-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)
vitamin D
-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
