Nutrition Flashcards
What are the common nutritional deficiencies of alcoholics?
thiamine, pyridoxine, folate (from fresh produce), vitamin A&C, PEM (protein-energy malnutrition)
Do we store vit B12 in our bodies?
Yes
We have about a 5 year supply in our livers
How is malnutrition defined?
Often by BMI less than 16 (normal 18.5-25)
What is marasmus?
PEM due to starvation
Deficient in all calories
Catabolize somatic protein (skeletal muscle) for energy
Decreased arm circumference
Leptin decreased
Look emaciated–broomstick extremities, large head
Serum albumin is normal or slightly reduced
Anemic, vitamin deficient
Immune deficient => infection => death
Lethargic, if prolonged, short stature
Should re-feeding of marasmus people include milk?
No, marasmus patients are uniformly lactose intolerant
What is Kwashiorkor and some causes in the US?
Malnutrition due to reduction in protein. Diets where most calories are carbs.
Can occur in US from protein loss:
Chronic diarrhea
Protein-losing enteropathy
Nephrotic syndrome loss of albumin through the urine
Extensive burns, trauma, sepsis
Maladaptive and more severe than marasmus
Clinical manifestations of kwashiorkor
Weight loss masked by edema (anasarca–generalized edema)
Sparing of subQ fat and muscle, loss of visceral protein
Fatty liver because can’t make the apoproteins needed to remove triglycerides
Tend to die from low immunity => infection
Depigmentation of the skin because can’t make melanin (also seen in marasmus)
Anemia, small intestine villous atrophy, flaky paint appearnace, alternating pale and dark hair from pigment loss, irritability
Angular cheilitis from B vit deficiency.
Hypoalbuminemia
Why does the liver get fatty during starvation?
Liver can’t produce the proteins needed to export fat from the liver so it builds up and accumulates.
What are some major complications to malnutrition?
Delayed wound healing
Risk infection and sepsis
Increased postop death
General info on Bulimia
Behavioral disorder
Involves bingeing and purging in one way or another–this can include excessive exercise
Generally onset in adolescence and in women
Weight kept near normal
Patient is bulimic and vomits often, presents with hematemesis that resolves spontaneously, what is going on?
Repeated retching causes Mallory-Weiss tears that are longitudinal tears in the esophagus that heal spontaneously
Bulimia complications
Vomiting => hypokalemia => cardiac arrhythmias Pulmonary aspiration => pneumonia Mallory-Weiss tears => Boerhave Syndrome Parotid gland hyperplasia => increased serum amylase Dental erosion Russell sign Amenorrhea uncommon Anemia
General info on Anorexia Nervosa
Considered a Psych problem involving body image and perceptual disturbances
Highest death rate of any psych disease
Anorexia nervosa clinical signs
Amenorrhea
Sick Euthyroid= act hypothyroid without measuring hypothyroid because of reverse T3. Causes cold intolerance, bradycardia, constipation, changes in skin and hair (lanugo)
Low bone density => osteoporosis
Anemia
Hypokalemia
Loss of gray matter
May still purge or exercise excessively
GI: early satiety, pancreatic fibrosis, malabsorptive diarrhea on refeeding
CV: thinning left ventricle, hypotension, sudden death from arrhythmia
What are the fat soluble vitamins?
ADEK
These are deficient in any condition that causes steatorrhea
How many water soluble vitamins are there?
9
Endogenous synthesis of vitamins
Vit D from precursor steroids
Vit K from biotin from intestinal flora
Niacin from tryptophan
Remainder must be ingested!
Which vitamins are energy releasing?
Thiamine–B1
Riboflavin–B2
Niacin–B3
Which vitamins are hematopoeietic?
Folic acid
Vit B12
Vit A types and sources
Vit A can come from 2 sources: meat where it is preformed, and vegetables in the form of carotenes and pro-vit-A that must be converted to retionoids
How is Vit A taken up and stored in the body?
Absorbed through the gut as a fat soluble vitamin. Taken up by Ito cells and stored in the liver (6 month supply). RBP (Retinol Binding Protein) transports retinol
Functions of Vit A
Maintains normal vision (every time a photon hits rhodopsin retinol is lost and must be replaced)
Signals cell growth and differentiation via RAR/RXR receptor
Activates osteoclasts
Aids host in resistance to infection
Binding activates nuclear receptors for drug metabolism
Vit A deficiency causes
General malnutrition
Malabsorption of fats:
-bile and pancreatic enzyme deficiencies
-Celiac, crohn, surgical resection of intestine
Depletion during infection–kids
Elderly: use of mineral oil laxative
Orlistat therapy for obesity (prevents fat absorption)
Signs of Vit A deficiency
Night Blindness
Higher death rate from measles, pneumonia, diarrhea
Squamous metaplasia => corneal ulcers, bitot spots in conjunctiva (tangles of keratin mixed with gas-forming bacteria), keratomalacia (corneal lesions), lung cancer, pancreatic duct problems, urinary tract stones, follicular hyperkeratosis of skin
Acute Vit A toxicity
Retinoid-induced cerebral hypertension causing symptoms suggestive of a brain tumor:
- Headache, vomiting
- Stupor
- Papilledema
Carotemia acute and chronic:
- reversible yellowing of the skin
- resembles jaundice but doesn’t affect the sclerae
Chronic Vit A toxicity
From overdose with Vit A retinoids from Fish oils, and liver oils
Symptoms: weight loss, N/V, dryness of lips, epistaxis, bone and joint pain with hyper ostosis, fractures, hepatomegaly with fibrosis
Increased circulating lipids
Hypercalcemia from osteoclast activity
Elevated Liver enzymes: AP and GGT from hepatic injury
Sources and functions of Vit D
Sources: sun converts 7-dehydrocholesterol to Vt D, all dairy in US is fortified, deep-sea fish, ergosterol grain
Acts on osteoclasts to break down bone and produce calcium, also acts in intestines to induce absorption of Ca and Phosphate
Reduces risk of colon cancer
Modulates the immune system
Enhances macrophages
Vit D deficiency causes
Low intake, low sunlight, using sunblock, frequent pregnancies and breast feeding, Impaired fat absorption, diseases of small intestine, deranged metabolism
Vit D deficiency effects
Low vit D => low Ca and Phosphate uptake from intestines => low serum Ca and P => increased PTH => Ca mobilization from bone => poor bone mineralization
Fracture risk
Rickets
Osteomalacia
Hypocalcemic tetany
Signs of hypocalcemic tetany
Blood pressure cuff on arm causes carpal spasm = Trousseau’s sign
Chvostok’s sign = contraction of facial muscles when tap on fascial nerve at parotid gland
Osteopenia types
Osteopenia is deficiency in bone
1) Osteomalacia is deficiency in Ca in the bone, shows with thickened, poorly mineralized trabeculae!
2) Osteoporosis is deficiency in osteoid in bone
Common fractures in osteomalacia
Ribs, hips, wrists, vertebra
kyphoscoliosis
Signs of osteomalacia
Microfractures of weak bone
Skeletal deformations from loss of rigidity
Enlargement of epiphiseal and osteochondral junctions
Signs of Rickets in a preambulatory child
Bones of head soft => squared-head
Rachitic Rosary = increased size of costoshondral junction
Pigeon breast deformity
Signs of rickets in ambulatory kids
bowing of legs because they are weak
expansion of epiphises
Effects of Vit D besides skeleton
Increased synthesis of cathelicidin that helps kill M tuberculosis
Can help reduce incidence of cancers
Vit D toxicity
Hypercalcemia
Metastatic calcifications
Nephrolithiasis
What is abetalipoproteinemia?
Autosomal recessive disorder where lack certain apolipoproteins needed for chilomicron formation and VLDL formation leading to decreased fat absorption and decreased fat soluble vit absorption
Causes of Vit E deficiency in US
Fat malabsorption
Low birth weight infants with immature guts
Abetalipoproteinemia
Vit E deficiency states
Neurologic disease: spinocerebellar degeneration
- absent deep tendon reflexes
- ataxia
- loss of position and vibration sense
- loss of pain sensation
- impaired vision, disordered eye movements
Vit E toxicity
Interferes with absorption of Vitamins A & K and the manufacture of K dependent procoagulants
Where does Vit K come from?
Synthesized by endogenous bacteria
Also conserved in the healthy liver
What factors depend on vit K for synthesis?
Factors VII, IX, X, II
Also, proteins S & C
Consequences of low Vit K
Prolonged PT–factor VII affected first
Bleeding diathesis: gums, heamturia, melena, purpura, hematomas
Neonates: bleeding from many sites, intracranial hemorrhage, prophylaxis with injection at birth
Thiamine actions
Synthesis of ATP
Maintains neural membranes and nerve conduction
Found in the brown part of brown rice
Thiamine disease related deficiencies
Alcoholics!!!
Intractable vomiting of pregnancy
Vomiting or Diarrhea
Refeeding or IV glucose in chronically malnourished (must give them Thiamine supplements)
Tea and coffee reduce thiamine absorption
Thiamine deficiency states
Dry beriberi: polyneuropathy (muscle weakness, loss of sensation and reflexes)
Wet beriberi: CV disease (high output heart failure, peripheral edema and vasodilation, globular heart with thin walls causing thrombi)
Wernicke-Korsakoff syndrome: CNS disease due to severe, chronic deficiency, ataxia, apathy, confusion, nystagmus, ophthalmoplegia, confabulation
Thiamine maintains myelination. Long nerves affected first => foot and wrist drop
What does riboflavin do?
Oxidation reduction reactions
Mitochondrial enzyme
Sources of riboflavin
meat, dairy, vegetables
Causes of riboflavin deficiency
Chronic alcoholism
Advanced cancer
Anorexia nervosa
Milk Avoidance
Riboflavin deficiency presentations
Angular cheilitis
Glossitis
Interstitial keratitis
Bone marrow hypoplasia (anemia)
Niacin (B3) functions and sources
Participates in metabolism of fat, CHO, amino acids
From grains, legumes, seed oils, unavailable in corn, synthesized from tryptophan
Niacin deficiency causes
Corn based diets alcoholics Protracted diarrhea Deficiency in protein Long term administration of isoniazid
Niacin deficiency
4 D’s
Dermatitis: (Pellegra gauntlet) mainly on exposed skin, but vaginal, oral, mucosa become red, thickend, rough, scaling and desquamation with fissures
Diarrhea: from intestinal atrophy, inflammation, ulceration
Dementia: brain, spinal cord neuronal degeneration
Death!
When to take pyridoxine-B6
A cofactor in metabolism of lipids and amino acids
Found in all foods
Deficient in Alcoholics, pregnancy, long term use of isoniazid, estrogen and penicillamine
Pyridoxine-B6 deficiency signs
Like many other B vitamins
Unique in cause of convulsions!
Adverse effects of B-Vitamins
Adverse effects infrequent
Water soluble so pee out what don’t need
Niacin: flushing, headache in high dose
B6/B12: Roseacea skin condition
Vitamin C (ascorbic acid) functions
Scavenges free radicals with vit E
In Scurvy, hydroxyproline-rich collagen lacks tensile strength, rate of synthesis of pro-collagen peptides suppressed => fragile blood vessel walls, defective collagen of wounds
Sources of vit C
Fruits and veggies: citrus, tomato, green peppers highest
Milk, Fish, liver
Causes of scurvy
Poor diet
Alcoholics
Milk-fed infants
Elderly
Childhood scurvy
Hemorrhages due to weak vessel walls
Skeletal changes from abnormal osteoid
Scorbutic Rickets! bowing of bones, widening epiphyses, depression of sternum
Bone problems because bone formation depends on rich blood supply but is disrupted by weak vessels
What is osteoid
the unmineralized organic component of bone
Scurvy symptoms
Loose teeth: gingival swelling and hemorrhage, bacterial periodontal infection
Peri-follicular Rash
Impaired wound healing
Anemia due to blood loss and deficient iron absorption
What can happen if take too much vit C?
Uricosuric can => kidney stones
Increases iron absorption so well may cause iron overload
