VITAMINS AND MALABSORPTION Flashcards
1
Q
what are vitamins
A
- 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
2
Q
vitamin a
A
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.
* Metabolism
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3
Q
vitamin a actions
A
- Eye
- Cell-Differentiation
- Maintenance of skin, mucus membranes
- Key nutrient for fetal development during pregnancy
4
Q
vitamin a deficiency
A
- 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
- 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
- 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
5
Q
sx vitamin a deficiency
A
- Night blindness, complete blindness, xerophthalmia
- Delayed growth, poor bone growth
- Dry Skin, hair
- Weakened immune system
6
Q
Vitamin A Deficiency Treatment and
Toxicity
A
- Treatment
- In endemic areas, 100,000 – 200,000 IU (30
mg – 60 mg) Retinol, periodic
supplementation - Eating foods rich in Vitamin 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 - Accutane
- Teratogenic effects
7
Q
Vitamin B1
(thiamine)
A
- Acts as a catalyst for converting Pyruvate
to Acetyl CoA - 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.
8
Q
Signs and
Symptoms of
Thiamine deficiency
A
- 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
9
Q
BeriBeri
A
- 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 - Treatment
- 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
- IV Thiamine 100 to 200 mg TID x 2-3 days,
10
Q
beriberi wet v dry
A
- Adults with two phenotypes “dry” or “wet”
- Can happen in adults as complication of weight loss surgery,
chronically hospitalized patients - Dry
- symmetrical peripheral neuropathy characterized by both sensory and motor
impairments, mostly of the distal extremities - Wet
- cardiomegaly, cardiomyopathy, heart failure, peripheral edema, and tachycardia, in
addition to neuropathy
11
Q
Wernicke-Korsakoff syndrome
A
- 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 - Treatment
- 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
12
Q
Thiamine deficiency in alcoholics
A
- Alcoholics may develop a thiamine deficit because of impaired 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 - 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
13
Q
Vitamin C (ascorbic acid)
A
- 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
14
Q
Vitamin C deficiency syndrome known as
Scurvy
A
- 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)
- 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
15
Q
Scurvy
A
- In the US, deficiency is rare but can happen in
- drug and alcohol use disorders
- bariatric surgery
- living in poverty or on diets devoid of fruits and vegetables
- Institutionalized
- Chronically ill
- Children with autism with highly selective diets devoid of fruits/vegetables
- Treatment
- Peds
- 100 mg ascorbic acid TID (PO, IM or IV) x 7d, then QD for several weeks until the patient is fully recovered
- Adults
- 300-1000mg QD x 1 month
