Vitamins and Lactose

Question 1

Vitamins

general

Answer 1

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

Question 2

Vitamin A

general

metabolism

Answer 2

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

Question 3

Vitamin A Deficiency

general

Answer 3

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

Question 4

Patients with disorders associated with fat malabsorption

Answer 4

Cystic fibrosis
Pancreatic insufficiency
Celiac disease
Cholestatic liver disease
Primary cholangitis
Small bowel Chrohn disease
Short bowel syndrome
Bariatric surgery

Question 5

Vit A deficiency

S/Sx

Answer 5

Night blindness, complete blindness, xerophthalmia
Delayed growth, poor bone growth
Dry Skin, hair
Weakened immune system

Question 6

Vit A deficiency

Tx

Answer 6

In endemic areas, 100,000 – 200,000 IU (30 mg – 60 mg) Retinol, periodic supplementation
Eating foods rich in Vitamin A

Question 7

Vit A

toxicity

Answer 7

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

Question 8

Vitamin B1 (thiamine)

general

Answer 8

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.

Question 9

Question 10

Thiamine deficiency

General

Answer 10

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

Question 11

BeriBeri

infantile
S/sx

Answer 11

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

Question 12

BeriBeri

infantile Tx

Answer 12

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

Question 13

BeriBeri

adult

Answer 13

Adults with two phenotypes “dry” or “wet”

Can happen in adults as complication of weight loss surgery, chronically hospitalized patients

Question 14

BeriBeri- Adult

Dry Sx

Answer 14

symmetrical peripheral neuropathy characterized by both sensory and motor impairments, mostly of the distal extremities

Question 15

BeriBeri Adult

Wet Sx

Answer 15

cardiomegaly, cardiomyopathy, heart failure, peripheral edema, and tachycardia, in addition to neuropathy

Question 16

beriberi

Question 17

Wernicke-Korsakoff syndrome

general

Answer 17

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

Question 18

Wernicke-Korsakoff syndrome

Tx

Answer 18

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

Question 19

Thiamine deficiency in alcoholics

Answer 19

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

Question 20

Patients hospitalized for alcohol withdrawal are at high risk for developing Wernicke encephalopathy

how do we tx?

Answer 20

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

Question 21

Vitamin C (ascorbic acid)

general

Answer 21

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

Question 22

Vitamin C deficiency syndrome/ Scurvy

general
Quantity considered deficient

Answer 22

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)

Question 23

Scurvy

Sx

Answer 23

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

Question 24

Scurvy Presentation

Answer 24

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

Question 25

Scurvy

In the US, deficiency is rare but can happen in

Answer 25

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

Question 26

Scurvy

Tx

peds and adults

Answer 26

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

Question 27

Vitamin D

general
Quantity considered deficit

Answer 27

Fat soluble vitamin
Dermal synthesis is major source
Fewer naturally occurring foods sources that contain vitamin D
Vitamin D sufficiency is defined as a 25(OH)D concentration ≥ 20 ng/mL (50 nmol/L)

anything under 20 is deficient

Question 28

Mechanism of action and pathophysiology of Vitamin D

Answer 28

Dietary vitamin D is incorporated into micelles, absorbed by enterocytes (small intestines), and then packaged into chylomicrons.

Liver & kidneys activate vitamin D into its active metabolite via hydroxylation

Question 29

Vit D

calcium relationship

Answer 29

Vitamin D enhances intestinal absorption of calcium and phosphate. Low concentrations of vitamin D are associated with impaired calcium absorption, a negative calcium balance, and a compensatory rise in parathyroid hormone (PTH), which results in excessive bone resorption.

Question 30

Vitamin D deficiency

Causes

Answer 30

Decreased intake or absorption
Reduced sun exposure
Increased hepatic catabolism
Decreased endogenous synthesis of active form (via decreased 25-hydroxylation in the liver or 1-hydroxylation in the kidney)
End-organ resistance to vitamin D
mutations in the vitamin D receptorrickets despite adequate vitamin D intake

Question 32

Vit D defiency

Sx of prolonged defiency

Answer 32

Reduced intestinal absorption of calcium and phosphorus and hypocalcemia (Secondary hyperparathyroidism)
Demineralization of bones
Osteomalacia in adults and rickets
bone pain and tenderness, muscle weakness, fracture, and difficulty walking

Question 32

Question 32

Vit D defiency

RF

Answer 32

Higher risk patients
institutionalized
obesity
increased skin pigmentation
Higher melanin absorbs less UVR *
malabsorption syndromes (IBD, celiac disease)

Question 32

lactose intolerance

patho

Answer 32

• ingested Lactose is hydrolyzed by Lactase in the intestines and converted into monosaccharides glucose & galactose. These are then taken up into the cells of the small intestine
• In individuals with low lactase activity, ingested lactose, about 75% of it, bypass the SI and goes into the colon where it is converted to short chain fatty acids & hydrogen gas by intestinal bacteria.

Accumulation of lactose & its fermentation causes the symptoms of intolerance

Question 32

vit D

labs and management

Answer 32

Routine lab that is drawn at many wellness/physical exams
25-hydroxyvitamin D (25[OH]D) levels of 12 - < 20 ng/mL do not require any additional evaluation

patients with levels under 20 are at some risk for oseteomalacia

patients under < 12 ng/mL
serum calcium, phosphorus, alkaline phosphatase, parathyroid hormone (PTH), electrolytes, blood urea nitrogen (BUN), creatinine, and tissue transglutaminase antibodies (to assess for celiac disease)

Question 32

lactose intolerance

clin man

Answer 32

Within few hours of ingestion:
Abdominal pain
Crampy, usually periumbilical or to lower quadrants of abdomen
Bloating
Nausea
Diarrhea : More common in children, may be bulky/watery
Flatulence

Question 32

Lactose intolerance

general

Answer 32

A clinical syndrome in which ingestion of lactose or lactose-containing food causes symptoms (abdominal pain, bloating, flatulence, nausea, diarrhea). Lactose intolerance may or may not be associated with lactose malabsorption

• Epidemiology:
  lowest prevalence in Europeans and European Americans
  higher prevalence in African Americans, Asian Americans, and Native Americans

Question 33

lactose intolerance

management

Answer 33

Diet restriction
Avoid completely
Limit milk to 2 cups or less (or its lactose equivalent in cheese and other lactose-containing food items
Take in divided doses
Individuals may start with more strict dietary restriction and then work up to their individually tolerated limit of ingestion of lactose-containing food.
Different foods contain different levels of lactose for example, mozzarella cheese has less lactose than cottage cheese

Vitamin D & Calcium should be supplemented in those who avoid dairy

Lactase enzyme supplementation

Lactaid
Cow’s milk + Lactase; which breaks down the lactose into sugars that are easier to digest