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Flashcards in hematological system and diseases Deck (93)
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describe anemia

-deficiency of RBCs
-H&H: women- 11.5/36; men- 12.5/40
-decreased arterial O2 content
-right shift of oxyhgb dissociation curve (increased O2 to tissues)
-increased CO d/t decreased viscosity
-decreased tissue O2 leading to erythropoietin (EPO) stimulation and an increase in RBC production


what are the most common causes of anemia?

-iron deficiency
-chronic disease
-acute blood loss


what causes the oxyhgb dissociation curve to shift left?

-decreased temp (hypothermia)
-decreased 2-3 DPG
-decreased hydrogen ions (alkalosis)


what happens with a left shift of the oxyhgb dissociation curve?

-higher affinity for O2 and hgb binding
-less O2 to the tissues
"hangs on"


what causes the oxyhgb dissociation curve to shift right?

-increased temp (hyperthermia)
-increased 2-3 DPG
-increased hydrogen ions (acidosis)


what happens with a right shift of the oxyhgb dissociation curve?

-less affinity for O2 and hgb binding
-more O2 to tissues
"throws off"


describe the relationship between SaO2 and PaO2

-normal saturation is maintained anywhere within the normal range for PaO2 of 80-100 mmHg
-below 60 mmHg, (or below 90% saturation), saturation levels begin to drop rapidly
*this is the reason 90% is usually considered the lowest acceptable SpO2 reading


what is the minimal acceptable pre op hgb?

-age, chronic disease and anticipated surgical blood loss must be considered (pt. specific)
-hgb of 10 g/dL commonly used


what is considered peak O2 carrying?

hct of 30%
-less than 30%, decreased carrying capacity (anemia)
-more than 30%, increased viscosity


how much more do PRBCs increase hgb in contrast to whole blood?

2x more


how does chronic anemia effect the oxyhgb curve?

-increased 2,3 DPG, causing a right shift
-causing decreased affinity of O2 and hgb binding and more O2 to tissues


how does decreased temperature effect the oxyhgb curve?

-causes a left shift
-increased affinity, decreased O2 to the tissues


when should the anemic pt. be transfused?

-if normovolemic, transfuse when symptomatic
-transfuse with acute blood loss when hgb drops to 7 g/dL (hct 21), esp. with comorbidities
-consider normovolemic hemodilution or cell saver


describe the RBC structure

-bi-concave disc with no nucleus, no mitochondria, 33% hgb
-2, 3 DPG and ATP provide intracellular energy
-life span: 100-120 days
-renal O2 sensors regulate EPO
-EPO stimulates RBC production in bone marrow


name some RBC structure disorders

-hereditary spherocytosis
-hereditary elliptocytosis
-paroxysmal nocturnal hemoglobinuria


describe hereditary spherocytosis and anesthesia implications

-abnormal membrane protein
-most common inherited hemolytic anemia
-1/3 very mild
-5% can have life threatening hemolytic crisis usually d/t infectious illness
-prone to cholelithiasis (gallstones)
*AIs: episodic anemia with infection and cholelithiasis


describe hereditary elliptocytosis and anesthesia implications

-abnormal membrane protein
-prevalent in areas with malaria
-heterozygous is mild
-homozygous can be severe
*AIs: like anemia


describe paroxysmal nocturnal hemoglobinuria and anesthesia implications

-abnormal membrane protein
-increased risk of venous thrombosis
-chronic hemolytic anemia
-life expectancy 8-10 yrs. after diagnosis
*AIs: anemia, hypercoagulability


what are some RBC metabolism disorders?

-glucose-6-phosphate dehydrogenase (G6PD) deficiency
-pyruvate kinase deficiency


describe glucose-6-phosphate dehydrogenase deficiency

-many affected mostly in Asia and the Mediterranean area
-can cause acute, chronic, or very mild hemolytic disease
-precipitated by drugs (forane, sevo, diazepam, lidocaine, prilocaine), infections, fava beans
-therapeutic methylene blue can be life threatening (use in methemoglobinemia, vasoplegic syndrome)
*AIs: dependent on degree of hemolysis; caution w/ pre-op infection and drugs known to precipitate crisis
*infection/sepsis major trigger


describe pyruvate kinase deficiency

-can cause life threatening congenital hemolytic anemia requiring exchange transfusion
-usually chronic with varying hemolysis
-splenectomy may prevent hemolysis
*AIs: dependent on degree of hemolysis; caution w/ pre-op infection and drugs known to precipitate crisis
*infection/sepsis major trigger


describe the hemoglobin molecule

-made up of alpha chains, beta chains, and heme groups
-each heme group binds an O2 molecule
-most disorders r/t amino acid substitution on alpha or beta chains


describe sickle S hgb (hgb SS) disease

-disorder of the beta chain
-membrane distortion causing clumping (sickling)
-homozygous (SS anemia): severe hemolytic anemia, vaso-occlusive crises, splenic and renal infarcts
-leading mortality and morbidity d/.t pulmonary and neuro complications (clots)
-children and adolescents: infarct CVAs
-adults: hemorrhagic CVAs


describe acute chest syndrome associated with hgb SS

-2-3 days post op
-lobular pneumonia-like illness with severe chest pain, fever, tachypnea, cough
-very painful
*tx: transfuse, O2, analgesia, inhaled nitric oxide (vasodilates)


what interventions peri-op can help prevent acute chest syndrome?

-well hydrated
-well oxygenated
*usually bring in the night before and begin to hydrate while NPO and consult hematology to ensure hct is adequate prior to procedure


what are anesthesia implications for hgb SS?

-trait carries no increased risk
-old tx: aggressive intra-op transfusion
-current tx: pre-op transfusion to hct of 30%
-good pain management to decrease sickling/crisis trigger
-may be tolerant to pain meds
***warm, wet, green: normothermia, hydration, oxygenation


what are other pathologies of hgb?

-sickle C hgb
-sickle beta-thalassemia


describe sickle C hgb (hgb C)

-1/4 the prevalence of Hgb SS
-cellular dehydration leads to hemolytic anemia
*AIs: treat like anemia


describe sickle beta-thalassemia

-1/10th the prevalence of hgb SS
-severity depends on hgb A (good hgb) levels (decreased hgb A leads to hgb SS symptoms)


describe miscellaneous hgb pathologies

-greater than 100 identified, most w/o complications
-hgb chain fragments and heme form Heinz bodies which destabilize RBC membrane
-level of Heinz body formation dictates degree of hemolysis
-can have hemoglobinuria and/or renal failure
-splenectomy reduces or eliminates symptoms