anemia

Question 1

anemia is the most common

Answer 1

blood disorder

Question 2

it is a deficiency of

Answer 2

RBC and Hgb deficiency

Question 3

normally how many RBCs made per min

Answer 3

180 million RBcs per min life span 120 days

Question 4

RBCs are removed by

Answer 4

the spleen

Question 5

hemoglobin=

Answer 5

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

Question 6

alpha and beta globuins=

Answer 6

proteins

Question 7

etiology of anemia

Answer 7

• defective erythropoiesis (formation of RBCs less than 180million/min
• excessive hemolysis (more than 180million/min being removed)
• excessive loss (hemorrhage, loss of whole blood)

Question 8

patho of anemia?

Answer 8

-abnormal rbc number, structure, or function= decreased O2 carrying capacity= hypoxia

Question 9

manifestations of anemia?

Answer 9

HYPOXIA causes ALL signs and symptoms

Question 10

mild anemia—>

Answer 10

not even detected often

Question 11

moderate anemia—>

Answer 11

chronic fatigue, dyspnea, palpitations

Question 12

severe anemia—>

Answer 12

chronic exhaustion, profound weakness, excessive palpitations, dizziness, headaches, sensitivity to cold

Question 13

why do u get cold with severe anemia?

Answer 13

-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

Question 14

explain iron deficiency anemia

Answer 14

• 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)

Question 15

explain vit b12 and folic acid deficiency

Answer 15

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

Question 16

explain pernicious anemia

Answer 16

• 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

Question 17

explain aplastic anemia

Answer 17

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

Question 18

explain hemolytic anemia

Answer 18

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??

Question 19

why does jaundice occur in hemolytic

Answer 19

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

Question 20

what is hemorrhagic anemia?

Answer 20

• 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

Question 21

etiology of sickle cell anemia?

Answer 21

genetic-autosomal recessive

• homozygous: two defective alleles
• heterozygous- one defective

Question 22

pathology of sickle cell anemia?

Answer 22

-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

Question 23

loading and offloading of O2 in sickle cell?

Answer 23

is FINE but the altered shape and hemolysis causes ISSUES!!!

Question 24

manifestations of sickle cell anemia?

Answer 24

• signs and symptoms of regular anemia
• hemolysis overwhelms kidney/liver
• congestion of dead RBCs in vessels—-> thrombosis —-> infarction
• liver overwhelmed —-> juandice

Question 25

treatment of sickle cell anemia?

Answer 25

• supportive (o2, analgesic, IV)
• hypertransfusion in increased risk (surgery, preeg)= until pt has 50% donor blood
• hydroxurea (drug prevents hemolysis, also causes creation of fetal Hbg
• steroids and analgesics
• marrow and stem cell transplant