anemia Flashcards
acute anemia
is a rapid loss of blood (RBC and Hgb)
acute hemmorhagic anemia: severity depends on
site, rate and volume lost
Chronic hemmorhagic anemia: is?
etiology
gradual ongoing loss of blood
(it may not be very noticeabe)
Et:
- prolonged or heavy menses
- bleeding peptic ulcers
- cancerous lesions in GI tract
- hemmorhoids
Tx of hemmorhagic anemia
eliminate cause
what is it: sickle cell anemia
it is a genetic problem.
Recessive homozygous trait
If heterozygous it is sickle cell trait
what are the three types of HB
fetal hemoglobin has a higher affiity for oxygen
adult hemoblogin also exists
sickle cell hemoglobin (in his notes HB S)
It is the globin that varies (the amino acid)
how is HB S differe;nt than HB A
Hb S is 50x less soluble
HB S has valine instead of glutamic acid in the beta chain
what is the problem with HB S
no problem binding to oxygen in lungs
dissociation nthe tissues is normal
the problem occurs after the oxygen dissociation. The HB crystallizes.
How does the HB S change to sickle
the HB S crystallizes on dissociation at low P02->RBC deforms and sickles->chronic hemollysis->vessel occlusion->ischemia->infarction->obstructed capillaries->hypoxia->more sickling
how is SCA lead to a vicious cycle
inc viscosity->impaired circulation->occlusion and further hypoxia->more RBCs sickle->vicious cycle
once the Hb has changed shape and sickled what happens to it
it will have difficulty moving through the capillaries. Because the cells are abnormal the will be destroyed by hemolysis. All problems from hemolytic anemia will apply
in SCA is there a problem in the marrow? how is RBC production affected
no problem there. RBC production wont increase
mnfts of SCA
hemolysis
thrombosis and infarction (nonloacalized)
inc bilirubin
SCA Tx
- supportive (rest, oxygen, analgesics, IV fluids and electrolytes)
- hypertransfusion when pt is at inc risk (eg during surgery, pregnancy) give until pt has 75% donor blood in circulation
- hydroxyurea. Ths is hepatotoxic and toxic to marrow. It is used for cancer but it is also known to cause leukemia. When used in SCA
1. it facilitates the transformation of HB
2. it prevents hemolysis and sickling - marrow or stem cell transplant
what is the most common blood disorder
anemia
whats anemia
hgb or RBC deficiency
etiology of anemia
- defective erythropoiesis
- high hemolysis
- high loss
patho of anemia
abnormal Rbc number, structure or fx which causes dec oxygen carrying capacity and leads to hypoxia
mnfts of anemia
-hypoxia (underying problem that is systemic)
-moderate:
dyspnea (whenver youve hypoxia you will end up with dyspnea which is beneficial, you will also have tachycardia which is beneficial but may cause
palpitations
chronic fatigue
-severe: chronic exhaustion, more palpitations, profound weakness, dizziness & headache (rt the hypoxia), sensitivity to cold (this is because of the lack of energy that would normally be produced in 3 or 4 steps of aerobic cellular respn. 70% of the metabolic heat produced is used to heat the body. the other 30% are for ATP produced
what complications could arise from anemia
potential acidosis
iron deficiency anemia what would you test in the blood
ferritin levels
why does a lack of iron cause anemia
iron is part of the Hb molecule
why is CBC not a useful test for iron def anemia
it will tell you the number of cells and the difffeerential but it doesnt have info abt iron
tx for iron deficiency anemia
underlying cause
iron PO for 4-6 months
folic acid and vitamin b12 deficiency how does this lead to anemia?
-tx?
B12 and folic acid are nec for DNA synthesis and cell division
->abnormal DNA synthesis and cell division-> impaired RBC, WBC and platelets
Tx: vitamin B12 and folic acid
where are erythrocytes produced
how long do they survive
they are produced int he red bone marrow of long bones
survive 120 days
how many RBCs do we produce
180x10^6 per minute (million)
what do RBCs transport and not transport
they transport 02 which is not a nutrient. they dont transport nutrients
Pernicious anemia
what is it
damaged gastric mucosa->no intrinsic factor->poor or no vitamin B12 absorption->RBC rpoduction is impaired
what is intrinsic factor
its a glycoprotein prod by parietal cells of stomach nec for absorption of B12 in the ileum (sm intestine)
what might cause P.anemia
stomach ulcers, infection in stomach,
P. anemia Tx
they used to give small doses and? or? parenterally
now they give high dose of vitamin B12 by mouth
its given IM only if there are neurologic symptoms present
aplastic anemia
all the nec components are present but there is a marrow failure which affects all blood cells
1/3 of the itme it is dt autoimmune issues, radiation, toxic chemicals
2/3 are idiopathic
aplatic anemia tx
mgmt is difficult
underlying cause
transfusions? (cant continuously transfuse)
marrow transplant in severe cases (they would remove the existing marrow and completely replace)
hemolytic anemia is…
Et
premature or excessive hemolysis
1/2 acquired (eg autoimmunity, drugs)
1/2 genetic (eg in thalassemia)
thalassemia
- is an autosomal recessive blood disorder
- affects either the alpha or beta globin chains-> hgb isnt formed properly. There is an enzyme missing
hemolysis process
older RBCs make less ATp and cant maint membrane->fragile->get trapped in narrow vessels of spleen->engulfed by macrophages then get broken into iron, heme, globin.
The globin is reused but the heme and iron are taken to liver and transformed there.
The heme which as transformed into bilirubin can deposit in tissues if theres excess hemolysis.
how does hemolysis present clinically
presents in sclera, skin may be yellow
spleenomegaly and liver inc in size
how do yu Tx hemolyti anemia
underlyiing cause
give oxygen if hypoxic
transfuse
steroids-inhibits hemolysis
renal fx (precipitation in renal tubule dt hemolysis)
splenectomy???-if hemolysis is occurring here
