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AS - N935 Advanced Patho II > Hematologic Pathophysiology Anemias > Flashcards

Hematologic Pathophysiology Anemias Flashcards

(46 cards)

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1
Q

Erythrocyte

A

Red blood cell (RBC)
1° function to transport hemoglobin
Transport oxygen to tissues
Contains carbonic anhydrase - enzyme that catalyzes reaction b/w CO2 & H2O to form carbonic acid H2CO3
Produced in the bone marrow
Lifespan 120 days
Individual erythrocyte contains ≈ 300 million Hgb molecules

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2
Q

Reticulocyte

A

Immature erythrocyte

Day 1 or 2 in the bloodstream

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3
Q

Anemia

A 
↓RBCs 
Reduced number circulating RBCs
Adverse effect ↓oxygen-carrying capacity
Hgb <12g/dL 
Pregnancy - physiologic anemia d/t ↑plasma volume
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4
Q

Mean Corpuscle Volume

A

Size

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5
Q

Normocytic

A

Normal sized cells

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6
Q

Microcytic

A

Smaller than normal size cells

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7
Q

Macrocytic

A

Larger than normal size cells

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8
Q

Hemoglobin

A

Four folded globin chains
2 alpha α
2 beta β

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9
Q

Hemolytic anemia

A

Abnormal hemolysis (RBC breakdown)

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10
Q

Erythropoetin

A

Glycoprotein
Formed in the kidneys
Epo stimulated when any condition ↓oxygen transport to tissues

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11
Q

Erythropoesis

A

Red blood cell production
Pluripotent hematopoietic stem cell → proerythroblast → erythroblast (Hgb synthesis begins) → reticulocyte → erythrocyte
Erythroblast loses nucleus
Reticulocyte loses remaining organelles

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12
Q

Polycythemia

A 
↑circulating RBCs
Adverse effect ↑blood viscosity
Slows blood flow ↓oxygen delivery
Significant when Hct >55-60%
- Threatens organ perfusion
- Risk venous/arterial thromboses
Relative polycythemia - dehydration, diuretics, vomiting
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13
Q

Anemia Causes

A

Blood loss - acute or chronic
↑destruction (thalassemia, hemolytic anemia, sickle cell)
↓production (iron deficiency or autoimmune)
Infectious (malaria, babesia, parvovirus)

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14
Q

Polycythemia Causes

A

Sustained hypoxia results in compensation
↑RBC mass ↑Hct

Cancer
COPD (not enough O2)
High altitude adaption

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15
Q

Acute Blood Loss

A

Body replaces plasma fluid portion in 1-3 days leaving low RBC concentration
RBC concentration usually returns to normal w/in 3-6wks

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16
Q

Chronic Blood Loss

A

Unable to absorb enough Fe (via GI) to make Hgb as rapidly as lost
RBCs produced smaller & have little Hgb inside - microcytic hypochromic anemia

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17
Q

Blood Transfusion Thresholds

A

10/30 rule
Hgb <10g/dL
Hct <30%

*Hgb <6g/dL clear benefit from transfusion

EBL <15% no intervention
30% replace w/ crystalloids/albumin
30-40% RBC transfusion
>50% massive transfusion 1:1:1 RBC / FFP / Plt

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18
Q

Transfusion Risks

A

Viral illness transmission (Hep B/C or HIV)
Bacterial infections
TRALI or TACO
Hemolytic transfusion reactions

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19
Q

Iron Deficiency Anemia

Causes

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A 
Nutritional Fe deficit 
- Lower income 
- Pica
Fe stores depletion
- Chronic GI bleeds of menstruation
Pregnancy ↑RBC mass required during gestation
20
Q

Iron

Study These Flashcards
A

Iron required for hemoglobin synthesis
Fe deficiency impairs RBC maturation & diminishes RBC production
Produces microcytic hypochromic anemia
Small & pale RBCs ↓O2 delivery

21
Q

Iron Deficiency Anemia

Treatment

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A 
Fe supplements
Elective surgery postpone 2-4mos PO supplements to correct deficiency
Continue at least 1yr after corrected
Urgent surgery IV w/in few weeks
RBC transfusion
22
Q

Hemolytic Anemia

Study These Flashcards
A 
Accelerated RBC destruction/hemolysis
Immune disorders
Lifespan <120 days
↑immature erythrocytes (reticulocytes)
Unconjugated hyperbilirubinemia
↑lactate hydrogenase
↓haptoglobin
23
Q

Sickle Cell Anemia

Study These Flashcards
A

Autosomal recessive disorder caused by single amino acid substitution in β globin that creates sickle hemoglobin (HbS)
β globin mutation leads to HbS polymerization into long stiff chains when deoxygenated → elongated sickle shape
Returns to normal shape when oxygenated
Most common familial hemolytic anemia
Protective against malaria in heterozygotes

24
Q

HbA

Study These Flashcards
A

Normal hemoglobin

25
HbF
Fetal hemoglobin | Newborns w/ sickle cell anemia are asymptomatic until ↓HbF at 5-6mos
26
Sickle Cell Crisis →
Chronic hemolytic anemia Ischemic tissue damage Spleen auto infarction
27
Chronic Hemolytic Anemia
Repeat sickling damages the RBC membrane | Eventually producing irreversible sickled cells that are removed from circulation
28
Ischemic Tissue Damage
Localized microvasculature obstruction → acute chest syndrome, joints, stroke(s), retinal damage
29
Spleen Auto Infarction
↑sepsis risk w/ encapsulated bacteria
30
Sickle Cell Treatment
Hydroxyurea ↑HbF levels Anti-inflammatory ↓rate acute chest syndrome & blood transfusions 50% Stem cell transplants
31
Autoimmune Anemia
Autoimmune hemolytic anemia (AIHA) IgG & IgM antibodies directed against RBCs RBC lifespan severely decreased
32
Autoimmune Anemia | Causes
Idiopathic Leukemia Infectious (mononucleosis) Drug-induced (PCN or Quinidine)
33
Autoimmune Anemia | Treatment
Immunosuppression & steroids
34
Newborn Hemolytic Disease
Incompatibility b/w mother & fetus - Erythroblastosis fetalis Fetus inherits RBC antigenic determinants from father that are foreign to the mother Mother Rh¯ Father Rh+ Baby Rh+ Fetal RBC enter maternal circulation during 3rd trimester & childbirth (fetomaternal bleed) - Sensitizes mother to paternal RBC antigens leading to IgG anti-D antibodies that cross the placenta & cause fetal RBC hemolysis 2nd pregnancy Rh antibodies attack Rh+ fetus RBCs causing Rh disease (RBC lysis)
35
Rh
Rhesus factor Protein found on RBC surface Genetically inherited Factor refers to Rh (D) antigen only - most immunogenic all non-ABO antigens
36
Rho(D) Immune Globin
Rh disease preventable w/ modern antenatal care RhoGAM IgG anti-D antibody injections 1st antigen-incompatible pregnancy does not produce disease bc mother does not produce anti RBC IgG antibodies (cross the placenta) before delivery When any incompatibility detected mother often receives an injections at 23wks gestation & birth to prevent antibody development towards the fetus
37
G6PD Deficiency
Glucose-6-Phosphate Dehydrogenase X-linked genetic disease G6PD metabolic enzyme involved in the pentose phosphate pathway (important to RBC metabolism) Erythrocyte half-life ≈ 60 days Hemolysis occurs d/t inability G6PD deficient RBCs to protect self from oxidative damage
38
What precipitates G6PD deficiency?
Infection DKA Medications Fava beans
39
G6PD Deficiency Peripheral Smears
Bite cells - RBCs w/ severely damaged membranes that have portions bitten off by macrophages to remove patches associated w/ Hgb precipitates known as Heinz bodies leading to intravascular hemolysis
40
Oxidative Stress
Hemolysis often transient even w/ persistent infection or drug exposure Older cells lysis leaves younger cells w/ ↑G6PD levels that are resistant to oxidant stress
41
G6PD Deficiency Treatment
``` No cure Avoid triggers Treat hemolytic episodes - Hydration - Blood transfusions ```
42
Physiologic Polycythemia
Natives who live at altitude 14,000-17,000 feet Low atmospheric oxygen ↑RBC 30% Heritable genetic adaption
43
Polycythemia Vera
PCV Stem cell or myeloproliferative disorder Hct 60-70% JAK2 gene mutation - does not stop RBC production when too many present Excess erythrocytes Platelets & leukocytes potentially also increase S/S appear 60-70s
44
PCV S/S
Cyanosis, headache, dizziness, GI symptoms, hematemesis, & melena ↑total blood volume Common presenting sign hepatic, coronary, & cerebral thrombosis 30% patients fatal thrombolytic complications 30% mortality r/t leukemia Viscous & engorged vessels Blood passes sluggishly through capillaries ↑amount deoxygenated resulting in bluish/ruddy skin appearance Marrow fibrosis in 10% patients (marrow replaced by fibroblasts & collagen)
45
PCV Treatment
W/o treatment death d/t vascular complications w/in mos Minimize thrombosis risk Phlebotomy helps extend survival 10yrs Myelosuppressive drugs (Hydroxyurea)
46
Polycythemia | Anesthesia Management
Thrombosis risk Reduce Hct prior to surgery - phlebotomy & hydration Hydration NPO status vs. IV fluids Continue hydroxyurea (cytoreductive agent)

AS - N935 Advanced Patho II (20 decks)

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