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Pathophysiology > 6.1 RBC & Disorders > Flashcards

6.1 RBC & Disorders Flashcards

1
Q

Red Blood Cells

A

Erythrocyte - Shape allows red blood cell to increase surface area for oxygen diffusion and change shape without rupturing.
Hemoglobin - Facilitates oxygen transportation
Erythropoiesis - Creation of red blood cells from bone marrow

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2
Q

Erythopoiesis

A
  • Number of RBC is maintained by feedback mechanism called Erythropoietin, hormone produced in kidneys.
  • From here it goes to Bone Marrow where it matures
  • Erythropoietin is stimulated by decreased population of RBC, increased tissue oxygen consumption, decreased hemoglobin synthesis, hemorrhage.
  • MAIN STIMULUS FOR RBC PRODUCTION IS HYPOXIA
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3
Q

Erythropoiesis phases

A

Stem Cell - Undifferentiated and may become erythroblast, myeloblast, lymphoblast.
Committed Cell - Immature erythrocyte with nucleus (Erythroblast)
Normoblast - Cell stuffed with hemoglobin and loses nucleus
Reticulocyte - Immature newly produced RBC. Increase in number reflects increase bone marrow activity
Mature RBC

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4
Q

Hemoglobin Synthesis

A
  • Hemoglobin storage/synthesis begins in early erythroblast stage.
  • Contains more than 250 million hemoglobin
  • Lack of iron decreases hemoglobin in RBC
  • Iron comes mainly from dietary intake (duodenum)
  • Iron combines with apotransferrin to form transferrin
  • Transferrin carried in plasma and stored as ferritin
  • Transferrin can also be delivered to developing RBC’s in bone marrow and used for heme synthesis
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5
Q

Iron Cycle

A
  • Most iron is contained and bound to Heme (red pigment in hemoglobin) in erythrocytes and muscle
  • Remained is bound to ferritin/macrophages/hepatic parenchymal cells.
  • When RBC’s are destroyed iron is recycled
  • Iron absorption goes up when stores decrease, and excretion is accelerated when Iron is increased
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6
Q

Erythrocyte Life Cycle

A
  • Released from bone marrow and enter blood stream
  • RBC destroyed by splenic macrophages (phagocytic)
  • Broken down into Heme and Globin molecule
  • Heme releases iron and bilirubin for recycling
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7
Q

Bilirubin Cycle

A
  • Aged RBC’s are destroyed in spleen via macrophages
  • Iron is recycled to make new hemoglobin
  • Transferrin (glycoprotein) makes recycle possible
  • Bilirubin is produced in RBC breakdown and transported to the liver to be excreted in bile
  • Failure of this process results in Jaundice
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8
Q

Anemia

A
  • Decrease in total RBC’s in circulation or decrease in quality and quantity of hemoglobin
  • Caused by impaired RBC production, acute/chronic blood loss, increased RBC Destruction
  • Symptomatic Anemia (< 8 g/dL)
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9
Q

Anemia (cont)

A

Classification - Either by Etiology or Morphology
Etiology
Decreased/Defective production of erythrocytes or increased destruction of erythrocytes

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10
Q

Anemia Morphology (RBC Indices)

A

Mean Corpuscular Volume (MCV) - Size of cell
Mean Corpuscular Hemoglobin (MCH) - Quantity of hemoglobin in RBC
Mean Corpuscular Hemoglobin Concentration (MCHC)
Amount of hemoglobin per cell volume
Size
Macrocytic/Microcytic
Hemoglobin Content
Hyperchromic (Increased MCHC/Darker Color)
Hypochromic (Decreased MCHC/Paler Color)

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11
Q

Hematology Normal Ranges

Important

A

Check document

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12
Q

Manifestation of Anemia (Categories)

A
  • Decreased oxygen transport resulting in compensatory mechanisms.
  • Decrease in RBC indices and hemoglobin level
  • Signs/Symptoms associated with pathologic process associated with anemia
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13
Q

Signs/Symptoms of Anemia

A
  • Weakness
  • Fainting
  • Pallor
  • Tachycardia
  • Angina (Pressure/tightening/pain in chest)
  • Heart failure
  • Hemolytic (rupture) - Anemia
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14
Q

Iron Deficiency Anemia (Etiology/Pathophysiology)

A
  • Most common type of Anemia
    (Microcytic - Hypochromic)

Etiology
Decreased iron intake, Iron loss (Blood Loss), Increased bodily demands (pregnancy, infancy, adolescence)

Pathophysiology
- Deficiency in iron leading to hemoglobin and defect in oxygen carrying capacity

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15
Q

Iron Deficiency Anemia (Diagnostic Studies)

A
  • Decreased hemoglobin and hematocrit
  • Decrease in Ferratin (indicates iron stores)
  • TIBC (Total Iron Binding Capacity) elevated
  • Elevated serum transferrin (body’s attempt to harvest more iron from intestines)
  • Tested via Endoscopy/colonoscopy to reveal marrow stores of hemoglobin
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16
Q

Iron Deficiency Anemia (Clinical Manifestations)

A

Microcytic/Hypochromic Anemia (Pale, Small RBC’s)

  • Fatigue
  • SOB
  • Epithelial Atrophy
  • Tachycardia
17
Q

Iron Deficiency Anemia (Nursing Management)

A
  • Treat source of blood loss
  • Oral replacement of Iron
  • IM Replacement (Not preferred, Z Track method)
  • IV Replacement (Iron Sucrose or Iron Dextan)
18
Q

Iron Deficiency Anemia (Nutritional Therapy/Patient Education)

A

Animal Protein - Heme Iron
Plant Protein - Non-Heme Iron

  • Take oral iron with full meal and glass of water. Stool softeners because constipation may be an issue, stool becomes dark and tarry when taking iron, vitamin C helps body absorb iron, should not lie down for 1 hour after taking iron
19
Q

Aplastic Anemia

A
  • Rare (Failure of bone marrow to replace RBC)
    Lack of all 3 Blood cells (WBCs, RBCs, Platelets)
    Etiology
  • Radiation/chemotherapy, toxins, idiopathic
    Most cases are idiopathic
    Pathophysiology
  • Bone Marrow Hypocellularity
20
Q

Aplastic Anemia (cont)

A

Clinical Manifestations
- Increased Infections, Fatigue, Pallor, Weakness, Petechia, Ecchymoses (bruising), bleeding
(Normocytic, Normochromic Anemia)
Management
- Blood transfusion, bone marrow stimulation medications, immunosuppressants, bone marrow transplant, stem cell transplant

21
Q

Pernicious Anemia

A
  • Macrocytic and Normochromic Anemia
  • Lack of intrinsic factor from parietal cells to absorb vitamin B12. (B12 deficiency)
    Clinical Manifestations
  • Typical Anemia, Nerve Demyelination, Difficulty Walking, jaundice, splenic enlargement, loss of appetite, abdominal pain.
22
Q

Pernicious Anemia (cont)

A

Testing
- Serum Parietal and Intrinsic Factor Antibodies
- Gastric Biopsy (achlorhydria)
- Schilling Test - Urine excretion of B12 (Rarely Done)
Treatment
- Parental, sublingual, high oral dose of Vitamin B12

23
Q

Folate Deficiency Anemia

A
  • Macrocytic and Normochromic anemia with B12 deficiency

Pathogenesis
- Malabsorption of folate (occurs in upper small intestines)

Clinical Presentation
- Similar to Pernicious Anemia except neurologic manifestations are not seen. Fissures of lips (cheilosis) ulcers in buccal mucosa and tongue

24
Q

Folate Deficiency Anemia (cont)

A

Diagnosis
- Folate and B12 Levels
Treatment
- Oral folate 1mg/day

25
Q

Sickle Cell Anemia

A
  • Presence of abnormal structure of globin chain
    Normochromic (no iron deficiency and hemolytic)

Disorders
Sickle Cell Trait - Inherit Hgb A from one parent and Hgb S from another parent (Does not normally sickle)
Sickle Cell Disease - Inherit Hgb S from both parents

26
Q

Sickle Cell Anemia (Pathogenesis)

A
  • Caused by Autosomal Recessive Mutation
  • Hypoxia, Acidosis, Dehydration, Cold Exposure can cause RBC’s to change their configuration
  • Cells stretch into sickle shape, and become dense and rigid
  • RBC’s are more prone to lysis
  • Slows down blood flow
  • Clot formations are common
  • Patient experiences ischemia injuries
27
Q

Sickle Cell Anemia (Clinical Presentation)

A

Acute - Hemolytic Anemia, Enlarged Spleen, Pulmonary Hypertension, DVT, Stroke Risk, Increased Risk of Infection
Chronic - Persistent Anemia, Avascular Necrosis, Organ Damage (Renal Ischemia/Renal Failure)

28
Q

Sickle Cell Anemia

A
  • Severity relates directly to proportion of HbS in RBC
    Diagnosis
  • Newborn Screening (Sickledex) - Cannot distinguish sickle cell disease from sickle cell trait
  • Presence of sickling in peripheral smear
  • Hemoglobin electrophoresis and high performance liquid chromatography identifies different types of Hgb
29
Q

Sickle Cell Anemia Treatment

A
  • Correct precipitating factor
  • Reverse hypoxemia
  • Hydration
  • Pain Medication
  • Hydroxyurea - Medication that increases fetal hemoglobin (HbF) which reduces Hemoglobin S polymerization
30
Q

Polycythemia

A
  • Overproduction of RBC’s (erythrocytosis)
31
Q

Polycythemia Vera

A
  • Abnormality of stem cells in blood marrow
  • Increased blood volume and viscosity (risk of thrombosis)
    Diagnosis - Bone marrow biopsy
    Treatment - Phlebotomy (removal of blood), Hydroxyurea, Pegylated INF (slow RBC production)

Pathophysiology (18 decks)

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