Vitamins and Lactose Flashcards
(39 cards)
Vitamins
general
Organic substances that cannot be synthesized by the human body.
Essential to be ingested in our diets in small quantities to facilitate normal metabolism
Vitamins are divided into two categories
Fat soluble vitamins
Vitamin A, D, E, K
Water soluble vitamins
B vitamins & vitamin C
Vitamin A
general
Subclass of lipid soluble compound called retinoic acids. Vitamin A is found in plants in form of provitamins (B-carotene) and in preformed vitamins (retinols; more active form) in animal sources.
Actions:
Eye
Cell-Differentiation
Maintenance of skin, mucus membranes
Key nutrient for fetal development during pregnancy
Vitamin A Deficiency
general
Vitamin A deficiency is rare in USA or in other resource rich countries
serum retinol levels (< 20 micrograms/dL [0.7 micromol/L] suggest deficiency
Can sometimes be seen in bariatric patients who have had procedures. These patients are routinely supplemented with multivitamins.
Biliopancreatic diversion
Gastric Bypass
Vitamin A deficiency is higher among other places of the world
approximately 30 percent among children under age 5 worldwide
Nearly 50 percent in young children in South Asia and sub-Saharan Africa1
Patients with disorders associated with fat malabsorption
Cystic fibrosis
Pancreatic insufficiency
Celiac disease
Cholestatic liver disease
Primary cholangitis
Small bowel Chrohn disease
Short bowel syndrome
Bariatric surgery
Vit A deficiency
S/Sx
Night blindness, complete blindness, xerophthalmia
Delayed growth, poor bone growth
Dry Skin, hair
Weakened immune system
Vit A deficiency
Tx
In endemic areas, 100,000 – 200,000 IU (30 mg – 60 mg) Retinol, periodic supplementation
Eating foods rich in Vitamin A
Vit A
toxicity
Very rare to have from excess ingestion
Acute toxicity occurs in adults when a single dose of > 660,000 IU of vitamin A ingested
Symptoms: nausea, vomiting, vertigo, blurry vision, malaise, drowsiness
Vitamin B1 (thiamine)
general
Acts as a catalyst for converting Pyruvate to Acetyl CoA (from Crebs cycle)
Thiamine has an unidentified role in the initiation of nerve impulse propagation that is independent of its coenzyme functions.
Absorbed in the small intestines. Passes through the intestines into the blood and is then phosphorylated into its active form. Thiamine then enters the target cells via active transport or passive diffusion.
The highest concentrations are found in the skeletal muscles, the liver, the heart, the kidneys, and the brain.
Thiamine deficiency
General
Deficiency may develop in as little as 3 to 14 days
Normal level ranges from 70 -180 nmol/L (3.0 to 7.7 mcg/dL)
Thiamine deficiency in the diet causes two clinical phenotypes:
Beriberi (infantile and adult)
Wernicke-Korsakoff syndrome
BeriBeri
infantile
S/sx
Infantile
Mainly in breastfed infants from moms who do not have sufficient thiamine in diet
Symptoms
Fulminant cardiac syndrome: cardiomegaly, tachycardia, a loud piercing cry, cyanosis, dyspnea, vomiting and pulmonary hypertension
Older infants: neurologic symptoms resembling aseptic meningitis, including agitation, an aphonic (soundless) cry, vomiting, nystagmus, purposeless movements, altered consciousness, and seizure, with no abnormalities on cerebrospinal fluid analysis
BeriBeri
infantile Tx
IV Thiamine 100 to 200 mg TID x 2-3 days, followed by maintenance therapy PO:5-30 mg once daily until no longer at risk for deficiency
BeriBeri
adult
Adults with two phenotypes “dry” or “wet”
Can happen in adults as complication of weight loss surgery, chronically hospitalized patients
BeriBeri- Adult
Dry Sx
symmetrical peripheral neuropathy characterized by both sensory and motor impairments, mostly of the distal extremities
BeriBeri Adult
Wet Sx
cardiomegaly, cardiomyopathy, heart failure, peripheral edema, and tachycardia, in addition to neuropathy
beriberi
Wernicke-Korsakoff syndrome
general
Neurologic complication of thiamine deficiency
Wernicke encephalopathy (WE) is an acute syndrome requiring emergency treatment to prevent death and neurologic morbidity.
nystagmus, ophthalmoplegia, ataxia, and confusion
Korsakoff syndrome refers to a chronic neurologic condition that usually occurs as a consequence of WE.
Reported in those with chronic alcohol use disorder and as a consequence of bariatric surgery
Wernicke-Korsakoff syndrome
Tx
IV Thiamine 200-500 mg TID x 2-7 days, followed by 250 mg QD 3 to 5 days, followed by maintenance therapy, 100 mg QD until no longer at risk for deficiency
Thiamine deficiency in alcoholics
Alcoholics may develop a thiamine deficit because ofimpaired thiamine absorption from the intestine.
Alcohol damages the lining of the intestines
Nutritional thiamine deficiency can occur due to poor eating habits.
Foods that are high in carbohydrates and low in vitamins
Metabolism of carbohydrates are thiamine requiring enzymes
Patients hospitalized for alcohol withdrawal are at high risk for developing Wernicke encephalopathy
how do we tx?
Patients hospitalized for alcohol withdrawal are at high risk for developing Wernicke encephalopathy
Usually treated with IV or PO 100 - 200 mg Thiamine QD x 3-5 days as preventative
Those with clinical signs of malnutrition, liver disease, daily alcohol consumption
PO thiamine 100mg tid, as ongoing supplementary therapy
Vitamin C (ascorbic acid)
general
Water soluble vitamin
Ascorbic acid is absorbed in the distal small intestine through an energy-dependent active transport process. Usual dietary doses of up to 100 mg/day are almost completely absorbed
Blood concentrations of ascorbic acid are regulated by renal excretion.
Ascorbic acid is a reversible biologic reducing agent (electron donor), which is important to maintain the activity of several enzymes that include iron and copper
Involved in many biological processes: fatty acid transport, collagen synthesis, neurotransmitter synthesis, prostaglandin metabolism, nitric oxide synthesis
Historical Context
Captain James Cook
Vitamin C deficiency syndrome/ Scurvy
general
Quantity considered deficient
Largely due to impaired collagen synthesis and disordered connective tissue.
Symptoms of scurvy generally occur when the plasma concentration of ascorbic acid is less than 0.2 mg/dL (11 micromol/L)
Scurvy
Sx
Symptoms noticeable after 3 months of deficiency
cutaneous signs (petechiae, perifollicular hemorrhage, and bruising)
Gingivitis
Arthralgias
Limping in children/refusal to walk
Impaired wound healing
Scurvy Presentation
Scurvy presentation
-follicular hyperkeratosis and perifollicular hemorrhage, with petechiae and coiled hairs
-Other common symptoms include ecchymoses, gingivitis (with bleeding and receding gums and dental caries)
-Sjögren’s syndrome, arthralgias, edema, anemia, and impaired wound healing