Anemia Flashcards
anemia is _______ blood disorder
most common
anemia is the deficiency of
RBCS and hemoglobin
deficiency of RBCs and hemoglobin due to
- problems with erythropoiesis
- increased/excessive loss of RBCS (bleeding)
- increased hemolysis: breakdown prior to usual time (aprox 120 days)
Patho of anemia
- abnormal number, structure or function of RBC
- decrease in oxygen carrying capacity
- hypoxia
what is the primary manifestation that underpins all other complications of anemia
Hypoxia
Iron deficiency anemia
- need iron to make hemoglobin
- inadequate intake or increased loss of iron
- iron binds to oxygen molecules for transport
- impaired hemoglobin synthesis
what are the manifestations of severe anemia
- chronic exhaustion
- excessive palpitations
- profound weakness & dizziness
- headache (brain will be hypoxic too)
- sensitivity to cold (no 02, not able to carry out anaerobic metabolism, not able to carry heat)
you need iron to make
hemoglobin
Treatment of iron deficient anemia
- treat underlying cause
- iron supplements, Fe p.o. for 4-6m
iron deficiency usually because not taking enough
dietary iron
test to find out if iron deficient
measure iron concentration (NOT A CBC)
Vitamin b12 & Folic acid deficiency
- responsible for DNA synthesis, invovled in cell division, DNA replication
- abnormal DNA synthesis & cell maturation – imparied RBC, WBC & platelets (cells will not mature)
Treatment of Vitamin b12 & folic acid deficiency
- vit B12 & folic acid (supplemental) (dietary deficiency)
- could have a deficiency in one or both
Pernicious anemia
- damaged gastric mucosa
- no intrinsic factor (intrinsic factor produced in mucosa of stomach)
- poor B12 absorption (RBC PRODUCTION IS IMPAIRED)
pernicious anemia is often in people who have had
gastric surgery
Treatment of pernicious anemia
- high dose of vit b12 p.o. (if high dose, some of b12 absorbed without intrinisic factor needed)
- IM b12 injection (only if neuro symptoms present) (IM does through without passing through stomach)
Aplastic anemia (no cell anemia)
- marrow (stem cell failure) – defects exists in marrow
- all blood cells affected
Aplastic anemia Treatment
- Transfusions
- immune suppression
- marrow transplant (get rid of everything in marrow, donor marrow complex severely compromised when eradicating)
Aplastic anemia is from
- 1/3 autoimmune, radiation, toxic chemicals
- 2/3 are idiopathic
Hemolytic anemia
- premature or excessive hemolysis (rupture or destruction of RBCS)
- accquired type (eg. autoimmunity, drugs) targeting erythrocytes
- genetic type (eg. in thalassemia)
Thanlassemia
genetic type of hemolytic anemia
-defective synthesis of hemoglobin putting together doesn’t happen normally
Manifestations of hemolytic anemia
same as general plus:
- Jaundice: excessive bilirubin-bilirubin gets in blood stream, liver can’t keep up to excrete
- Splenomegaly: spleen expands to meed demand of excretion, increase # of cells there also causes it to enlarge
- Hepatomegaly: demand, size and lots of material causes enarlged liver
Treatment of hemolytic anemia
- underlying cause
- 02 for nypoxia
- transfusion
- steroids (to halt hemolysis) (cant use long term, can cause damaging side effects)
- Renal function (precipitation in renal tubule d/t hemolysis)
- Spleenectomy (if too many rbcs being removed, some fxs can be taken over by liver -individual can fx without spleen, have to know hemolysis is happening in spleen)
Acute Hemorrhagic Anemia
rapid loss of blood (RBCS, hemoglobin, Fe) whole blood
-severity based on site, rate & volume lost
Chronic Hemorrhagic Anemia
gradual ongoing blood loss (less easily detected and persists for longer time
Major causes of chronic hemorrhagic anemia
- prolonged or heavy menses
- Bleeding peptic ulcers: bleeding happening in upper GI tract, occult blood will not know there is blood in stool)
- Cancerous lesions of GI tract
- hemorrhoids (frank blood)
Frank blood is
blood from hemorrhoids can see in the toilet bowl
Treatment of Hemorrhagic anemia
-eliminate cause
Sickle cell anemia is
genetic, homozygus recessive
what is homozygus recessive
two matched defective alleles
-matched means they have to be coding for the same thing
Both parents have to be carrier
If heterozygus (sickle cell)
it is sickle cell trait (no manifestations or mild manifestations not fully fledged)
sickle cell anmeia has HBS (hemoglobin sickle cell)instead of
Hba (hemogolbin adult)
mnfts of sickle cell anemia:
all in general +
- hemolysis
- thrombosis & infarction
- increase in bilirubin
sickle cell anemia has valine instead of
glutamic acid
Glutamic acid
acid is normal amino acid needed
with sickle cell has valine and this causes a different form of _______
Hemogolobin (sickle cell hemoglobin)
Path of sickle cell anemia
- Hbs instead of Hba
- Hbs crystallizes on dissociation at low P02
- Rbc deforms & sickles
- chronic hemolysis
- vessel occlusion
- ischemia
- infarction
- obstructed capillaries
- hypoxia
- more sickling
Treatment of sickle cell anemia
- supportive (02, analgesics, IV fluids & electrolytes)
- Hypertransfusion in increased risk (eg. SX, preganacy
- Hydroxyurea (used sparingly, only if needed side effects can can cause leukemia)
- marrow, stem cell transplant (not easy)
Sickle cell breakdown becomes viscous causing
- increase in viscostiy
- impairs circulation
- occlusion & further hypoxia
- more RBC’s sickle viscous cycle
Hbs is 50X less soluble than
Hba, this is not a problem if stays in erythrocyte but if it comes out into blood it is
Sickle cell cannot
move through blood vessel properly
what are the two reasons to use hydroxureya
- increases production of fetal hemoglobin
- tends to breakdown erythrocytes before they sickle
