Nutritional Diseases Flashcards
What is primary vs secondary malnutrition?
Primary malnutrition - a deficiency of ingesting enough nutrients
Secondary malnutrition - deficiency for other reasons, such as inadequate absorption, impaired use / storage, excess loss, or increased demand
Are water-soluble or fat vitamins generally stored extensively, and what is required for proper absorption of fat soluble vitamins?
Generally fat soluble vitamins are stored in excess.
Need effective pancreatic enzyme (lipase) and biliary function to absorb fat-soluble vitamins properly
What are the normal ways in which vitamin A exerts its effect, and what tissues are highly dependent in light of this?
- It binds nuclear hormone DNA-binding receptors (RAR / RXR heterodimers) to influence gene expression
- > most critical for differentiation of mucus-secreting epithelium - Also is a component of Rhodopsin which is needed for seeing in low light
- Immune system -> increased susceptibility to infection
Where in the liver is vitamin A stored?
Cells of Ito -> in the space of Disse, these are also fat-storing cells (explains why they hold vitamin A)
What vision problem does vitamin A deficiency cause? Include the medical term?
Nyctalopia - night blindness due to decreasd rhodopsin in rods / cones
What eye epithelium changes can occur due to vitamin A deficiency?
Keratomalacia - Corneal ulceration
Xerophthalmia - dry eye due to squamous metaplasia of secretory epithelium
What is the corneal clouding which is due to buildup of keratin debris called?
“Bitot’s spots”
What does vitamin A squamous metaplasia cause in other tissues?
Follicular hyperkeratosis
-> secretory epithelium dysfunction, i.e. upper airway, urinary tract, adnexal ducts
What are the four general stages of vitamin deficiency and when must we treat to prevent permanent damage?
- Depletion of vitamin stores
- Loss of cellular metabolism
- Appearance of clinical signs (treat now)
- Morphological defects
Briefly outline the synthesis pathway of vitamin D? How does this relate to possible conditions resulting in deficiency?
7-DHC -> D3 in skin, sunlight
D3 -> 25 D3 in liver
25 D3 -> 1,25 D3 in kidney
1,25 D3 = calcitriol, active form
Underexposure to light, liver disease, or renal disease can result in deficiency
What is the normal physiologic function of vitamin D?
Increases small intestinal absorption of calcium / phosphate via calcium binding proteins.
- Stimulates reabsorption of calcium and phosphate in the kidney
- Increases bone mineralization and resorption to increase bone turnover
What causes vitamin D-dependent rickets?
Inherited defects of the hydroxylase enzymes
What happens to the weight-bearing longbones as a result of rickets (aside from bowing)? Why does this occur?
Since vitamin D is not present (in children), long bones bend since they are formed from non-mineralized osteoid
Overgrowth of osteoid and cartilage at epiphyseal plates produces irregular masses of tissue (in attempt to support increasing weight)
What is another one of the bone deformities in rickets (earliest sign of rickets)?
Rachitic rosary - rib cage popping out on the sides where the cartilage is growing
What is osteomalacia and how does it differ from osteoporosis?
Osteomalacia - caused by vitamin D deficiency in adults, causes soft bones due to excess osteoid relative to mineralization, increasing susceptibility to microfractures. Mineral deformity relative to rickets since bones are totally formed.
Osteoporosis - occurs in old age due to increased breakdown of bone (both osteoid and mineralization decrease) -> bones are brittle and break
What is the function of vitamin K, and where do you get it?
Serves as a cofactor for gamma-carboxylation of clotting factor proteins (2, 7, 9, and 10 + proteins C/S) so they can have two negative charges needed to hold their Ca+2
-> synthesized by intestinal bacteria (B12) and in leafy greens / vegetables
What form of vitamin K is active / inactive and what blocks this?
Vitamin K hydroxyquinone form is active
y-carboxylation yields the Vitamin K epoxide form, which must be re-reduced by Vitamin K epoxide reductase (blocked by warfarin)
What can vitamin K deficiency in neonates cause and why does this happen?
Hemorrhagic disease of newborn
-> due to absence of gut flora (makes vitamin K) and poor placental transportation of vitamin
Where does vitamin E normally sit, and what is the pathway involved in its recycling?
Normally sits in the membrane as an antioxidant
-> deficiency is rare because it is efficiently oxidized by vitamin C / glutathione as reducing agents
What are the deficiency syndromes involving vitamin E? Include one adult and one neonatal syndrome.
- Degeneration of long peripheral axons, dorsal column, and spinocerebellar myelin degeneration (neuropathy appearing similar to B12 deficiency)
- Hemolysis / anemia -> especially infants exposed to oxidative stress of oxygen therapy as newborns
What three major enzymes is thiamine (B1) a cofactor for? What other function does it have?
Think ATP
A: alpha-ketoglutarate dehydrogenase (TCA cycle)
T: Transketolase - pentose phosphate pathway
P: pyruvate dehydrogenase (along with flavin and NAD, 1-2-3)
Also plays a role in neural condition (WK syndrome)
What are the two forms of B1 deficiency that is not WK syndrome and what causes each of them?
Dry beriberi - due to impaired glucose metabolism -> peripheral polyneuropathy with myelin degeneration and symmetrical numbness / muscle wasting
Wet beriberi - abnormal ATP synthesis affects cardiac function -> peripheral vasodilation and high output myocardial failure (dilated cardiomyopathy) causing peripheral edema
What is Wernicke vs Korsakoff syndrome / classic triad and what causes that?
Wernicke encephalopathy - triad of ataxia, confusion, and ophthalmoplegia
Korsakoff psychosis - irreversible, retrograde / anterograde amnesia due to damage to mammillary bodies, thalamus, and periventricular gray matter
What types of reactions and B2, B3, and B6 used for?
B2 - riboflavin: Prosthetic molecular group in flavoproteins (FMN, FAD)
B3 - niacin: Component of NAD / NADP
B6 - pyridoxine: cofactor for transamination / decarboxylation reactions, glycogen synthesis, and synthesis of melanin / monoamine neurotransmitters, and heme synthesis (ALA synthase)
What is the rationale for what tissues are likely to manifest symptoms of B2, B3, and B6 deficiency?
Tissues with rapid turnover or high cellular metabolism (i.e. epithelial cells or nervous system which has a high energy demand)
-> epithelium which are skin-exposed and must turn over the most are the most effective
What syndrome is caused by B3 deficiency?
3 D's of B3 (niacin) Pellagra: Diarrhea - GI epithelium Dermatitis - skin epithelium Dementia - nervous system
