nutritional disorders Flashcards
anemia
risk factors
pathogenic classification of rbc production
[Hb] lower than reference value
risk: age, gender, ethnicity, pregnancy, other disease
- decreased rbs production (nutrients, hormones , bone marrow, chronic disease, renal insufficiency)
- increased destruction of RBC
blood loss
morphological classification
complete blood cell count
- Hb, RBC, WBC.
hematocrit = how much of total volume = rbc
mean corpuscular volume (MCV) = hematocrit/RBC
- microcytic (small cell, low rbc count) normocytic, macrocytic (large cell)
mean corpuscular hemoglobin concentration (MCHC) [hemoglobin/hematocrit] - chromicity = low value = fewer Hb , more pale.
iron metabolism
Fe2+ bioactive, absorbable. Fe3+ is not. ferritin stored in cells. bound to transferrin in blood to be transfer.
taken to bone marrow to make rbc. hb taken to macrophage to breakdown, or iron taken to hepatocyte/muscle to store.
iron deficiency anemia (IDA)
no iron = cant make rbc
- limited supply of iron - malabsorption or malnutrition.
- increased loss - bleeding, phlebotomy (drawing too much blood in hospital)
clinical presentation of IDA
fatigue, pallor, weak, dizzy, increase HR, breathing, impaired immune, reduced cognitive and physical performance
microcytic anemia & iron
lack of iron - unstable rbc, smaller than normal.
low MCV, low MCHC
test: iron test isnt great because it fluctuates.
t-sat: transferrin saturation = how much iron bound at any given time
TIBC - total iron binding capacity = max amount of iron bound.
treating iron deficiency
oral iron therapy - nutrients and meds to influence bioavailability. vit C - good, antacids, calcium = bad.
parenteral iron - may cause anaphylactic reaction
recombinant human erythropoietin (EPO) - in patient w chronic kidney disease
blood transfusion - immediate
vit b12
cobalamin
water-soluble vitamin
sources: microbial synthesis, meat, dairy
vit b12 metabolism
bound to food, released by pepsin &HCl. haptocorrin binds b12, travels to small intestine. intrinsic factor interacts w b12 to allow recognition and absorption by enterocyte in small intestine. transferred to transcombalamin then as b12 into blood.
stored in liver or excreted thru urine..
bio actions of vit b12
co-enzyme carries out its actions with folate for cell grwoth, DNA syntehsis, RBC production, neuro function.
helps in methionine and succinyl coa production. their precursors (homocysteine & methylmalonyl coA will be high in vitb12 deficient
causes of anemia of b12
deficiency of IF - pernicious anemia (autoimmune)
decreased GI absorption - crohn’s
inadequate intake - vegetarians
prolonged medication use - proton pump inhibitor
rare congenital disorder - transporter deficiency
clinical presentation of b12 deficiency
neuropsychioatric - development delay, hypotonia, cognitive impair
GI - feeding difficulty, decreased appeptite
macrocytic anemia and b12
impaired DNA synthesis = increase RBc growth without cell division.
high MCV, inadequate RBC production
- low serum b12, high homocysteine, methylmalonic acid. anti-IF/parietal cell = pernicious anemia. liver and thyroid function - rule of other disease causing b12 anemia.
treatment of b12 deficiency
supplements intramuscular injection (when cant absorb naturally)
bone remodeling
balance btw bone form (osteoblasts) and bone resorption (osteoclasts)
bone metabolism
regulation of vit D, calcium & other hormone, mineral, unmineralized matric and mineralized matrix
absorption of vit D - derived from cholesterol, carried by binding protein, cleared from liver.
ca 2+ dependent on vit Dto be absorbed. then can be transferred to bone where stored and calcified.
endocrine regulation of calcium
PTH - regulated by negative feedback loop to maintain Ca2+ levels in body. released when low Ca2+ levels. = increased reabsorption in kidney (phosphate follows), vit D reabrsorption from kidney, absorption from gut.
hypercalcemia
high Ca2+
moans, bones, groanes, stones
hypocalcemia
muscle pain
seizure
tetany
arrythmia
risk factor for bone disease
lifestyle malabsorption increased demands aging ethnicity, sun exposure endocrine disorder rheumatological disorder drugs obestity
rickets and ostomalacia
- deficient mineralization of growth plate (rickets) or bone matric (osteomalacia)
cause: nutritional deficiency
vit d resistance
renal phosphate wasting
osteoporosis
systemic skeletal disorder.
compromised bone strength
osteoclasts break down too much bone before it can be replaced by osteoblasts
osteoporosis diagnosis
personal history of fragility fracture
measurement of bone mineral density.
osteoporosis t-score
osteoporosis treatment
balance diet, smoking alcohol cessation. exercise, calcium vit D supplement. drugs for bone or menopause
