anemia Flashcards
anemia is the most common
blood disorder
it is a deficiency of
RBC and Hgb deficiency
normally how many RBCs made per min
180 million RBcs per min life span 120 days
RBCs are removed by
the spleen
hemoglobin=
a protein within RBC that transports oxygen in blood
- molecule comprised of 4 subunits, each containing an iron Fe bound to a heme group
- oxygen binds to the Fe atom on the hgb
alpha and beta globuins=
proteins
etiology of anemia
- defective erythropoiesis (formation of RBCs less than 180million/min
- excessive hemolysis (more than 180million/min being removed)
- excessive loss (hemorrhage, loss of whole blood)
patho of anemia?
-abnormal rbc number, structure, or function= decreased O2 carrying capacity= hypoxia
manifestations of anemia?
HYPOXIA causes ALL signs and symptoms
mild anemia—>
not even detected often
moderate anemia—>
chronic fatigue, dyspnea, palpitations
severe anemia—>
chronic exhaustion, profound weakness, excessive palpitations, dizziness, headaches, sensitivity to cold
why do u get cold with severe anemia?
-normally ETC chain produced ATP (40%) and gives off heat (60%) to warm up body, d/t hypoxia, anaerobic metabolism commences, ETC chain does not produce this heat
explain iron deficiency anemia
- high prevalence
- oxygen binds to iron atom in Hgb, so if deficiency in Fe—> less oxygen-carrying capacity of Hgb
- could be due to inadequate intake of iron or excessive loss of iron
- CBC is not enough, need a ferritin test
- treat UNDERLYING cause and (supplemental fe with oral pills 4-6mo)
explain vit b12 and folic acid deficiency
folic acid= vitamin essential for body to make DNA, RNA, and metabolize amino acids
—-> cannot be made by body, found in diet in dark greek leafy veg
vitamin b12= water-soluble vitamin required for normal functioning of CNS and metabolism of every cell in body (including RBCs)—> cannot be made by body, found in animal products/ supplements
deficiency in either= ABNORMAL DNA synthesis—> impaired RBC/WBC and platelets
treat w: vit b12 and folic acid supplements/increased in diet
explain pernicious anemia
- damaged gastric mucosa—> no intrinsic factor produced
- IF must bind with vitamin 12 for vitamin to be absorbed, IF production decreases with age and alcohol
- poor or no it b12 absorption: impaired RBC production
- TREAT with HIGH doses of vitb12 PO (if large amt consumed, body cant help but to absorb it even if IF is absent- passive absorption)
- IM fe is given if neuro problems present
explain aplastic anemia
bone marrow (stem cell failure)---> not making new cells---> deficiency of ALL blood cells etiology: 1/3 autoimmune, radiation, toxic chemicals -can manage autoimmune with drugs, withdraw chemical and radiation 2/3 idiopathic: treatment with transfusions, immune suppression (steroids) or bone marrow transplant
explain hemolytic anemia
premature or excessive hemolysis of RBCs
etiology: acquired (autoimmunity, drugs)
or genetic (eg. thalassemia- decrease of hgb synthesis- distorts shape, recognized as defective, wiped out)
manifestations: jaundice- bilirubin build up d/t excessive breakdown of RBCs
-splenomegaly (increased workload on spleen)
-hepatomegaly (increased workload on liver)
treatment: underlying cause, treat hypoxia, transfusion, monitor renal function, hepatic function, steroids, spleenectomy??
why does jaundice occur in hemolytic
rbcs broken down, globin, heme and iron are recycled
iron is stored n liver and reused to make hemoglobin
-globin broken down into a.as to make proteins
heme is broken down to biliruibin excreted in urine and feces
bilirubin is changed in liver into excretable form
bilirubin in excess- liver cannot cope and deposits in tissues, it is yellow/green, so yellow-ish skin
what is hemorrhagic anemia?
- acute= rapid loss of whole blood (RBC, Hbg, fe)—> shock
- severity depends on site, rate, vol lost
- more life threatening, but quick to dx and treat
- chronic= gradual, ongoing blood loss (hard too diagnose/treat)
- OCCULT in UPPER, BRIGHT in LOWER GI
etiology: prolonged menses, bleeding peptic ulcers, CA lesions in GI tract, hemorrhoids
treatment: treat the bleed! eliminate the causewhat
etiology of sickle cell anemia?
genetic-autosomal recessive
- homozygous: two defective alleles
- heterozygous- one defective
pathology of sickle cell anemia?
-HbA (normal adult hemoglobin) in sickle cell, one A.A is substituted within beta chain—> valine AA instead of glutamic acid, so it is HbS (sickle)
HbS crystallizes after dossociation of Hb at low PO2—> RBC deforms and sickles (forms a crescent shape)—-> body recognizes deformed RBCs and kills them off—-> chronic hemolysis—-> increased viscosity —-> vessel occlusion and impaired circulation —-> ischemia —-> infarction and further hypoxia—–> more sicklig
VISCOUS CYCLE because cycle cells cause hypoxia but are also formed because of hypoxia
loading and offloading of O2 in sickle cell?
is FINE but the altered shape and hemolysis causes ISSUES!!!
manifestations of sickle cell anemia?
- signs and symptoms of regular anemia
- hemolysis overwhelms kidney/liver
- congestion of dead RBCs in vessels—-> thrombosis —-> infarction
- liver overwhelmed —-> juandice
