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Flashcards in hematological system and diseases Deck (93)
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1

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

2

what are the most common causes of anemia?

-iron deficiency
-chronic disease
-acute blood loss

3

what causes the oxyhgb dissociation curve to shift left?

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

4

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"

5

what causes the oxyhgb dissociation curve to shift right?

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

6

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

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

7

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

8

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

9

what is considered peak O2 carrying?

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

10

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

2x more

11

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

12

how does decreased temperature effect the oxyhgb curve?

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

13

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

14

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

15

name some RBC structure disorders

-hereditary spherocytosis
-hereditary elliptocytosis
-paroxysmal nocturnal hemoglobinuria

16

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

17

describe hereditary elliptocytosis and anesthesia implications

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

18

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

19

what are some RBC metabolism disorders?

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

20

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

21

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

22

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

23

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

24

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)

25

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

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

26

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

27

what are other pathologies of hgb?

-sickle C hgb
-sickle beta-thalassemia
-misc

28

describe sickle C hgb (hgb C)

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

29

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)

30

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