Nutritional Anaemia Flashcards
What is Anaemia
RBC number + O2 carrying-capacity insufficient to meet physiological needs
What does insufficient O2 C-C result in
↓[Hb] (w/insuff. RBC)
Anaemia cause
Lack of ingredients body acquires from food = iron, B12 + folate deficiency
Erythropoiesis requires what
Erythropoiesis, requires B12, folic acid, DNA, iron, hg synthesis
Erythropoiesis process
Process, decr. O2 detected by kidneys
EP secreted + binds to receptors that will become RBC
Haemocytoblast (stem cell) to proerythroblast to erythroblast (polychromatic) by EP stim
Then normoblast, nucleus expelled to form reticulocyte = erythrocyte in circulation
Anaemias due to what - 3 categories
= 1. failure of prod. - hypoproliferation (not enough RBC, BM present) = reticulocytopenia
- ineffective erythropoiesis
- Decreased survival = blood loss, haemolysis, reticulocytosis = if anemic, BM will be trying to catch up so early RBCs will be pushed out – if not enough RCyte, BM can’t produce enough RBCs
What is iron and describe its uses
Iron = most abundant trace element, needed for O2 transport
Iron excretion description
No natural excreting method for iron, take in vitamin C, body uses what it needs then excretes it out,
If you take in too much, body has no natural way of losing it = blood loss and desquamation
Iron composition
Ferric = 3+, ferrous = 2+, most iron in body as circulating Hb.
Remainder as storage/transport proteins = ferritin + hemosiderin (cells of liver, spleen + BM)
Describe iron absorption
Iron absorption = regulated by GI mucosal cells and hepcidin,
duodenum & proximal jejunum via ferroportin receptors on enterocytes +
transferred into plasma and binds to transferrin then binds to transferrin receptors on RBC precursors in BM,
if excess = ferritin, iron deficiency = incr. transferrin and decr. in ferritin stores
Reticulocyte count use
Adds further clue as to failure of production or increased losses
What effects absorption levels
Ferrous ions best absorbed + other foods
GI acidity
State of iron storage levels
BM activity
Hepcidin function
Ferroportin internalization and degradation =
↓ iron transfer into blood plasma from duodenum,
↓ in macrophages in recycling senescent erythrocytes
↓ iron-storing hepatocytes
Hepcidin regulation
[iron] in plasma/liver + by erythropoietic demand for iron
What is ferritin
Primary storage protein & providing reserve, Water soluble
What is transferrin saturation
Ratio of serum iron and total iron binding capacity – % of transferrin binding sites occupied by iron
What is transferrin
Glycoprotein made by liver,
Production inversely proportional to Fe stores. Vital for Fe transport.
What is total iron binding capacity
Measurement of the capacity of transferrin to bind iron
Indirect measurement of transferrin
Lab results in iron deficiency anaemia
Ferritin = low
TF sats = low
TIBC = high
Serum iron = low/normal
Iron deficiency causes
Causes = diet, malabsorption, incr. phys needs, blood loss, menstruation, GI tract loss, parasites
Iron deficiency investigations
FBC: Hb, MCV, MCH, Reticulocyte count
Iron Studies: Ferritin, Transferrin Saturation
Blood film
Description of stages in development of IDA
Percentage sats of transferrin w/iron and free erythrocyte protoporphyrin values do not become abnormal until tissue stores are depleted of iron
↓in the [Hb] occurs when iron is unavailable for haem synthesis
MCV/MCH is not abnormal for several months after tissue stores are depleted of iron
Hypochromic microcytic anemia
Red cells that are in general much smaller than a neutrophil, with marked anisocytosis (variation of the red cell size) and hypochromia (area of central pallor of red cells that is larger than normal, indicating a low MCHC).
Microcytosis = size defnining
Hypochromia = colour
Hypochromic microcytic anemia
Iron deficiency anaemia symptoms
Fatigue, lethargy, and dizziness
Iron deficiency anaemia signs
Pallor of mucous membranes, Bounding pulse, Systolic flow murmurs, Smooth tongue, koilonychias (spoon nails)
Macrocytic Anaemia = Hb, MCV, MCHC
Low Hb and high MCV with normal MCHC
Megaloblastic macrocytic anaemia cause
Vitamin B12/Folic acid deficiency
Drug-related
(interference with B12/FA metabolism)
Nonmegaloblastic macrocytic anaemia cause
Alcoholism Hypothyroidism Liver disease Myelodysplastic syndromes Reticulocytosis (haemolysis)
B12/folate needed for
Final maturation of RBC and DNA synth.
Thymidine triphosphate synthesis
Megaloblastic vs. non megaloblastic
M = anemia results from inhibition of DNA synthesis during red blood cell production (can’t move to M phase)
N = are those in which no impairment of DNA synthesis occurs
Folate function
Folate necessary for DNA Synthesis:
Adenosine, guanine and thymidine synthesis
Folate deficiency causes - 3 categories w/examples
Increased demand = Pregnancy / Breast feeding, infancy and growth spurts, Haemolysis & rapid cell turnover: e.g. SCD, disseminated cancer, urinary losses: e.g. heart failure
Decreased Intake = diet, age, chronic alcohol intake
Decreased absorption = medication (folate antagonists), coeliac, jejunal resection + tropical sprue
Effect of alcohol on bone marrow
Alcohol 2 way effect on BM – direct toxin (macrocytosis) or interferes w/folate pathway = make pt’s folate def.
B12 function
Essential co-factor for methylation in DNA and cell metabolism
Intracellular conversion to 2 active coenzymes necessary for the homeostasis of methylmalonic acid (MMA) and homocysteine
What does B12 require
Requires the presence of Intrinsic Factor for absorption in terminal ileum
IF made in Parietal Cells in stomach
Transcobalamin II and Transcobalamin I transport vitB12 to tissues
Can’t absorb B12 w/out it
B12 deficiency causes - 5 categories w/examples
Impaired absorption: Pernicious Anaemia Gastrectomy or ileal resection Zollinger-Ellison syndrome Parasites
Decreased intake:
Malnutrition
Vegan diet
Congenital causes:
Intrinsic factor receptor deficiency
Cobalamin mutation = C-G-1 gene
Increased requirements: Haemolysis HIV Pregnancy Growth Spurts
Medication: Alcohol NO PPI, H2 antagonists Metformin
Haematological consequences
MCV = Normal or raised
= Megaloblastic anaemia, Ineffective erythropoiesis
Hb = Normal or low
RetCount = low
LDH = raised = intramedullary haemolysis
Blood film = Macrocytes, ovalocytes, hypersegmented neuts
BMAT = Hypercellular, megaloblastic, giant metamyelocytes = Unusual to need
MMA = increased = not standard lab test
Effect on cells when B12 low
Fragmented cells
Clinical consequences of nutritional anaemia
Brain: cognition, depression, psychosis Neurology: myelopathy, sensory changes, ataxia, spasticity (SACDC) Infertility Cardiac cardiomyopathy Tongue: glossitis, taste impairment Blood: Pancytopenia
Pernicious anaemia features
Autoimmune disorder
Lack of IF
Lack of B12 absorption
Pernicious anaemia mechanism
Develops AB against IF – against cells or IF itself = consequence same = no IF
Why is oral B12 ineffective for pernicious anaemia
Even if oral B12 administered = cant absorb, injections needed to overcome that pathway
Treatments for anaemia
Treat the underlying cause **
Iron – diet, oral, parenteral iron supplementation, stopping the bleeding
Folic Acid – oral supplements
B12 – oral vs intramuscular treatment
Diagnosis if normal/low MCV
If high ferritin = acute/chronic illness
If low ferritin = iron deficiency, GI/gynae blood loss
Diagnosis if high MCV
If high B12 = MPD+
If normal B12 = alcohol = liver
If low B12 = GPC (anti-gastric parietal cell antibody/IF antibodies = pernicious anaemia
If low B12/folate = dietry deficiency = malabsorbtion
