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Red Blood Cells Flashcards

1
Q

Anemia Classifications
Size (3) Hemoglobin (2) Shape (2)
Measurements (4)

A

Normocytic, Microcytic, Macrocytic

Normochromic, Hypochromic

Poikilocytic, Non-Poikilocytic

Mean Cell Volume
Mean Cell Hemoglobin
Mean Cell Hemoglobin Concentration
Red Cell Distribution Width

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2
Q 
Acute Blood Loss
Compensatory Changes (4)
A 
Increased CFU-E cells (RBC progenitors)
Become Reticulocytes (5 days)

Leukocytosis and Thrombocytosis also occur

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3
Q

Hemolytic Anemias

Extravascular (2) Intravascular (6) Unique Characteristics

A

Extravascular:
Splenomegaly
Caused by decreased RBC deformability

Intravascular:
Hemoglobinemia, Hemoglobinuria
Caused by mechanical injury to normal cells
Also caused by toxins, parasites and complement

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4
Q

Hemolytic Anemias

Common Clinical Features (3) Lab Features (3) Blood Smear (2)

A

Anemia
Jaundice
Cholelithiasis

Decreased Haptoglobin
Unconjugated bilirubinemia
Hemosiderinuria

Increased normoblasts
Reticulocytosis

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5
Q

Hereditary Spherocytosis

Pathogenesis (3) Diagnosis (2) Presentation (3) Crisis Syndromes (2)

A

Mutated cell membrane proteins ankyrin and spectrin
Cells become spheroid and less deformable
Spleen traps and destroys RBCs

Increased sensitivity of RBCs to osmotic lysis (osmotic fragility test)
Increased mean cell hemoglobin concentration

Anemia, Splenomegaly, Jaundice

Aplastic Crisis: caused by Parvovirus destruction of RBC progenitors

Hemolytic Crisis: caused by increased splenic RBC destruction

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6
Q

G6PD Deficiency

Pathogenesis (2) Morphology, Presentation (4) Worse Variant

A

Decreased NADPH causes decreased protection against oxidative stress
ROS cause intra/extravascular hemolysis

Heinz Bodies

Episodic Hemolysis:
Following Infection, Drugs, Fava beans

Mediterranean variant shows worse hemolysis

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7
Q

Sickle Cell Disease

Pathogenesis (4) Blood Smear (3) Complications (4)

A

Point mutation of beta-globin
Glutamate to Valine substitution creates HbS
Increased MCHC, decreasaed pH and slow blood flow increase sickling
Mononuclear cells phagocytose sickled cells causing extravascular hemolysis

Irreversibly sickled cells
Target cells
Howell-Jolly bodies in RBCs

Autosplenectomy
Priapism
Stroke
Retinopathy

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8
Q

Vaso-Occlusive Sickle Cell Crises
Pathogenesis, Examples with Descriptions
Hand-Foot, Acute Chest (2)

A

Hypoxic injury and infarction

Hand-Foot Syndrome: bone pain in kids
Acute Chest Pain: caused by lung infection, life threatening

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9
Q

Non-Occlusive Sickle Cell Crisis Descriptions

Sequestration (3) Aplastic

A

Sequestration Crisis: in kids, entrapment of RBCs in spleen, can cause life threatening shock

Aplastic: Parvovirus B19 RBC progenitor infection

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10
Q

Thalassemia Syndromes

Genetics (4) General Pathogenesis and Presentation

A

Genetics:
Beta - Point mutations of single Beta-globin gene on Chromosome 11
Alpha - Deletions of a pair of Alpha-globin genes on Chromosome 16

Anemia caused by decreased RBC production and lifespan

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11
Q

Beta-Thalassemia

Pathogenesis (2) Secondary Complication, Blood Smear (4)

A

Anemia caused by two mechanisms:
Decreased HbA synthesis
Imbalanced alpha-beta synthesis causes membrane damage that decreases RBC survival (EV hemolysis)

Secondary Hemochromatosis from ineffective erythropoiesis

Anisocytosis (varying size)
Poikilocytosis
Hypochromia
Microcytosis

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12
Q 
Beta-Thalassemia Major vs Minor
Clinical Features (5/2) Lab Values (1/1) Major Treatment (3)
A

Major Clinical:
Anemia starting 6-9 months after birth (HbA needed)
Growth retardation and death at early age
Enlarged bones
Hepatosplenomegaly
Cardiac failure from hemochromatosis

Minor Clinical:
Usually asymptomatic
Mild anemia

Lab values
Major: Elevated HbF
Minor: Elevated HbA2

Treat Major with Iron chelation and blood transfusions
May cure with hematopoietic stem cell transplant

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13
Q

alpha-Thalassemia
Types with Descriptions
Silent Carrier (2) a-Thalassemia Trait (3) HbH Disease (4) Hydrops Fetalis (4)

A

Silent Carrier:
Missing one alpha-globin gene
Asymptomatic

Trait:
Missing two alpha-globin genes
Minimal microcytic anemia
If both deleted from one chromosome, can cause symptomatic a-Thalassemia in offspring

HbH Disease:
Missing three alpha-globin genes
Forms Beta tetramers
Tissue hypoxia disproportionate to level of HgB
Can cause Sequestration Crisis

Hydrops Fetalis:
Caused by four missing alpha-globin genes
Formation of Hemoglobin Barts (gamma tetramers)
Fetus shows edema, hepatosplenomegaly, pallor
Lifelong chelation and transfusion dependence

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14
Q

Paroxysmal Nocturnal Hemoglobinuria

Genetics (2) Pathogenesis (3) Complications (3) Diagnosis, Treatment

A

Phosphatidylinositol glycan complementation group A (PIGA) gene mutation
Only hemolytic anemia caused by acquired defect

Mutation causes GPI-linked protein deficiency
RBCs susceptible to lysis via C5b-C9 MAC
Causes intravascular hemolysis

Hemosiderinuria causing iron deficiency
Venous thrombosis (leading cause of death)
Acute myeloid leukemia or myelodysplastic syndrome

Diagnose with flow cytometry

Treat with Eculizumab

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15
Q

Warm Antibody Immunohemolytic Anemia
Etiologies: Primary/Secondary (3) Pathogenesis (3)
Drug-Induced Mechanisms (2)

A

Primary idiopathic
Secondary - Lupus, Drugs, Lymphoid neoplasms

IgG coats RBCs
Phagocytes remove membrane, forming spherocytes
Spleen destroys spherocytes

Drug Antigens bind RBCs and are attacked
Drugs induce the production of auto-Abs against RBCs

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16
Q

Cold Agglutinin Immunohemolytic Anemia

Etiologies: Acute (2) Chronic (2) Pathogenesis (3) Presentation (2)

A

Acute: mycoplasma pneumoniae, mononucleosis
Chronic: idiopathic, lymphoid neoplasms

IgM binds RBCs in cold periphery
C3b deposited on RBCs
Phagocytes destroy RBCs in liver/spleen/BM

Raynaud phenomenon
Cyanosis in extremities

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17
Q

Cold Hemolysin Immunohemolytic Anemia

Etiology, Pathogenesis (2)

A

Post-Viral infection (in kids)

IgG binds P antigen on RBCs in cold periphery
Once in warm areas, complemented-mediated hemolysis

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18
Q

RBC Trauma Hemolytic Anemia

Etiologies (2) Pathogenesis (2) Blood Smear (4)

A

Cardiac Valve Prosthetics (artificial mechanical)
Microangiopathic disorders: DIC

Microvascular lesion causing fibrin/platelet deposition
Luminal narrowing increases shear forces on RBCs

Shistocytes (RBC fragments)
Burr cells
Helmet cells
Triangle cells

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19
Q

Megaloblastic Anemias

Etiologies (2) Blood Smear (5)

A

Vit B12 deficiency
Folate Deficiency

Macro-Ovalocytes
Nuclear Hypersegmentation of Neutrophils
Hypercellular bone marrow
Giant Metamyelocytes
Band cells
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20
Q

Normal B12

Metabolism (4) and Functions (4)

A

Pepsin breaks B12 from natural binding protein
Haptocorrin picks B12 up and carries to SI
Proteases break B12 from Haptocorrin
Intrinsic Factor picks B12 up and sends it to blood in Ileum

Helps synthesize methionine
Important for Folate synthesis and then Thymidine

Helps synthesize Succinyl CoA
Important for proper synthesis of neuronal lipids

21
Q

Pernicious Anemia

Pathogenesis (3) Morphology (2) Complications (2) Clinical Diagnostic Features (4) Treatment

A

T cell mediated AI damage of gastric epithelium
Triggers formation of auto-Abs
Abs destroy intrinsic factor secreting cells, blocking B12 absorption

Fundic gland atrophy
Stomach metaplasia (intestinalization)
Atrophic glossitis (beefy, shiny tongue)
Demyelination of dorsal and lateral spinal tracts

Megaloblastic anemia
Leukopenia with hypersegnmentation
Low serum B12
Elevated homocysteine and methymalonic acid

Can treat megaloblastic anemia with Folate supplementation (does not treat demyelination)

22
Q

Non-Pernicious Anemia Causes of B12 Deficiency (4)

A

Decreased Pepsin
Ileal resection
Gastrectomy (decreased IF)
Tapeworms

23
Q 
Folate
Normal Functions (3) Causes of Deficiency (3) Presentation
A

Purine synthesis
Converts homocysteine to methionine
dTMP synthesis (Thymidine)

Decreased intake (alcoholics)
Increased requirements (pregnancy, cancer, anemias)
Impaired utilization (Methotrexate)

Megaloblastic anemia identical to B12 deficiency

24
Q

Iron Physiology

Distribution (2) Transport, Absorption Regulation (2)

A

Most iron is in heme and enzymes
About 20% is stored as ferritin

Free iron is toxic, Transferrin used to transport instead

Absorption decreased by hepcidin
In response to elevated intrahepatic iron

25
Iron Deficiency Anemia | Etiologies (4) Morphology, Clinical Features (4) Labs (4) Associated Syndrome with Presentation (3)
``` Dietary lack (infants, elderly, impoverished) Impaired absorption (sprue, chronic diarrhea) Increased demand (children, pregnancy) Chronic blood loss (most common) ``` Hypochromic Microcytic anemia Koilonychia (spoon nails) Fatigue Alopecia Glossitis Elevated Total Iron Binding Capacity (TIBC) Decreased HCT, Ferritin, Hepcidin Plummer Vinson Syndrome: Esophageal webs, anemia, glossitis
26
Anemia of Chronic Disease | Etiologies (3) Pathogenesis (3) Labs (6)
Chronic Microbial Infections: osteomyelitis, endocarditis Chronic Immune Disorders: Rheumatoid Arthritis Neoplasms Chronic inflammation causes increased IL-6 IL-6 causes increased hepcidin Increased hepcidin decreases iron absorption and decreases ferroportin function Decreased TIBC, serum iron, EPO Elevated Ferritin, Hepcidin, Macrophage Iron
27
Aplastic Anemia | Etiologies (5) Pathogenesis (2) Diagnosis, Clinical Features (5) Prognosis
``` Acquired - Idiopathic Chemicals - Chemo drugs Physical Agents - Viral infections Whole body Irradiation Inherited: Telomerase Defects, Fanconi anemia ``` Extrinsic immune mediated suppression of marrow progenitors Intrinsic abnormalities of hematopoietic stem cells "Dry" bone marrow tap devoid of hematopoietic stem cells (hypocellular) ``` Pancytopenia: Reticulocytopenia** Macrocytic Normochromic Anemia Petechiae and Ecchymoses (thrombocytopenia) Frequent Infections (neutropenia) ``` Good prognosis with bone marrow transplant
28
Pure Red Cell Aplasia | Etiologies (3) Clinical Feature
Thymoma Large Granular Lymphocytic Leukemia Parvovirus Infection (can persist if immunocompromised) Primary bone marrow disorder causing only loss of RBCs
29
Myelophthisic Anemia | Etiologies (2) Pathogenesis, Blood Smear (2)
Most often from Metastasis Myeloproliferative disorders Space occupying lesions replace normal bone marrow elements Leukoerythroblastosis Teardrop shaped RBCs
30
Chronic Diseases Associated with Anemia (3)
Chronic Renal Failure Hepatocellular disease Hypothyroidism
31
Polycythemia Clinical Description (2) Relative vs Absolute Primary vs Secondary
Abnormally high red blood cell count Increased Hgb level Relative: caused by dehydration that decreases plasma volume Absolute: caused by increased hematopoietic progenitor cells Primary: Polycythemia vera EPO-independent growth of RBC progenitors Secondary: compensatory of pathologic increase in EPO
32
Excessive Bleeding | Causes (3) and Tests with Descriptions (4)
Increased vessel fragility Platelet deficiency or dysfunction Coagulation issues Prothrombin Time: Extrinsic, Common coagulation paths Partial Thromboplastin Time: Intrinsic and Common Platelet counts Platelet Function Tests: thrombin, vWf tests
33
Vessel Wall Defects Causing Bleeding | Examples (6)
Infections: meningococcemia Drug Reactions: hypersensitivity reactions Collagen Defects: Scurvy, Ehlers Danlos Immune Complex Deposition: Henoch Schonlein Hereditary Hemorrhagic Telangiectasia Perivascular Amyloidosis
34
``` Thrombocytopenia Lab Values (3) Causes (4) ```
<100,000 is thrombocytopenia <20,000 can cause spontaneous bleeding Normal PT/PTT Decreased Production: Bone Marrow defects, HIV Decreased Platelet Survival: Immune-Mediated, DIC, Thrombotic Microangiopathies Sequestration: Splenomegaly Dilution: Blood transfusions
35
Chronic Immune Thrombocytopenic Purpura | Pathogenesis, BM/Blood Findings (2) Clinical Features (4) Treatment
IgG autoantibodies opsonize membrane glycoproteins IIb/IIa or Ib/IX Spleen removes opsonized platelets Increased megakaryocytes Megathrombocytes in peripheral blood Petechiae Ecchymoses Melena Hematuria Glucocorticoids
36
Acute Immune Thrombocytopenic Purpura | Pathogenesis (2) Clinical Features (2)
IgG autoantibodies opsonize membrane glycoproteins IIb/IIa or Ib/IX Spleen removes opsonized platelets Occurs in Kids after viral illness Spontaneously regresses
37
``` Heparin Induced Thrombocytopenia Type I (2) and Type II (4) ```
Type I Occurs right after initiation of therapy Spontaneously resolves ``` Type II Occurs 5-14 days after heparin started Causes arterial/venous thromboses Caused by auto-Abs to Heparin-PF4 complexes Complexes activate platelets ```
38
Thrombotic Thrombocytopenic Purpura | Pathogenesis (2) Clinical Pentad
ADAMTS13 deficiency vWF multimers accumulate and activate platelets ``` Fever Thrombocytopenia Microangiopathic Hemolytic Anemia Transient Neurological Defects Renal Failure ```
39
``` Hemolytic Uremic Syndrome Typical Pathogenesis (2) Atypical Pathogenesis (3) Common Pathologic Feature, Presentation (5) ```
Shiga-like toxin absorbed into circulation Toxin alters endothelial cells which activates platelets Atypical HUS Defects in Complement Factor H, CD46 or Factor I Both types characterized by excessive activation of complement ``` Bloody diarrhea followed by: Fever Thrombocytopenia Renal Failure Microangiopathic Hemolytic Anemia ```
40
Defective Platelet Function Bleeding Inherited Etiologies with Examples (3) Acquired Etiologies (2)
Defective Platelet Adhesion: Bernard Soulier - glycoprotein Ib-IX defect Defective Platelet Aggregation: Glanzmann Thrombasthenia - glycoprotein IIb-IIIa defect Defective Platelet Secretion (storage pool disorders): Defective TxA2 and ADP release Aspirin/MSAID induced Uremia
41
Clotting Factor Deficiencies Clinical Features (2) Most Common Inherited Deficiencies (3) Acquired Deficiencies (2)
Large Post-traumatic ecchymoses or hematomas Prolonged bleeding after any laceration ``` Factor VIII (hemophilia A) Factor IX (hemophilia B) von Willebrand Factor ``` Vitamin K Deficiency (impaired II, VII, IX, X and Protein C) Disseminated Intravascular Coagulation
42
von Willebrand Disease Presentation (3) Lab Values (2) Type 1 (2) Type 2 (2) Type 3 (3)
Mucosal bleeding Excessive wound bleeding Menorrhagia Prolonged PTT and Bleed Time Reduced ristocetin cofactor activity Type 1: Autosomal dominant point mutations Mild deficiency in vWF Type 2: Missense mutations cause defective multimer formation Type 3: Autosomal recessive deletions/frameshift Very low vWF and severe bleeding
43
Hemophilia A | Pathogenesis (3) Lab Value, Diagnosis, Clinical Features (3)
X linked recessive Factor VIII mutations X inversion causes most severe deficiency May develop antibodies to Factor VIII Prolonged PTT Factor VIII assays Most common cause of life threatening bleeding Spontaneous hemorrhage Hemarthroses
44
``` Hemophilia B (Christmas Disease) Pathogenesis, Lab Value, Diagnosis, Clinical Features (2) ```
X linked recessive Factor IX mutations Prolonged PTT Factor IX assays Spontaneous hemorrhage Hemarthroses
45
Disseminated Intravascular Coagulation | Etiologies (4) Pathogenesis (2) Complications (5) Lab Values (4) Associated Syndromes (2)
Obstetric complications Sepsis (endotoxins) Malignancies Major trauma Release of tissue factor that combines with Factor VII Endothelial cell injury which increases tissue factor and decreases anticoagulant thrombomodulin ``` Hypoxia (fibrin deposition) Microangiopathic hemolytic anemia (fibrin deposition) Hemorrhage (platelets consumed) Widespread thrombi in organs Bilateral renal cortical necrosis ``` Prolonged PT and PTT Low fibrinogen Elevated D Dimer Waterhouse Friderichsen Syndrome (N meningitidis) Kasabach-Merritt Syndrome (giant hemangiomas)
46
Febrile Non-hemolytic Reaction | Etiology, Clinical Features (3) Pathogenesis
Most common adverse reaction to blood transfusion Fever Chills Dyspnea Caused by inflammation from donor leukocytes
47
``` Blood Transfusion Allergic Reactions Associated Deficiency (2) Urticaria (2) ```
IgA deficiency predisposes reaction Caused by IgG-mediated reaction to donor IgA Urticarial reaction seen if IgE recognizes allergens in donor blood Responds to antihistamines
48
Hemolytic Transfusion Reactions Acute: Pathogenesis (2) and Presentation (5) Test Delayed: Pathogenesis (2) Prognosis
Acute IgM mediated complement attack on donor RBCs Caused by ABO incompatibility Fever, shaking, chills, flank pain (severe causes DIC) (+) Coombs test Delayed IgG mediated attack on previously sensitized Ags Sensitized from prior blood transfusions Complement activation can be fatal
49
Transfusion Related Acute Lung Injury | Pathogenesis (3) Clinical Features (4)
Two Hit Hypothesis: Primer causes sequestered, sensitized neutrophils in lung microvasculature Neutrophils activated by MHC I Abs in donor blood More likely with donations containing high levels of Abs such as fresh frozen plasma and platelets Sudden onset respiratory failure Diffuse bilateral lung infiltrates Hypoxemia Hypotension

SBL Block 1 (6 decks)

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