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Adv Patho > Erythrocytes/Anemias > Flashcards

Erythrocytes/Anemias Flashcards

1
Q

Erythrocyte Function/structure

A
  • About 4-6 million with 120 day lifespan
  • Bi-concave form increases O2 access (main fund to transport O2)
  • Mature RBC - no nucleus or mitochondria
  • Hgb molecules fill RBC cytoplasm
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2
Q

Hgb Molecule

A

Made of alpha & beta chains
Contain 4 heme/globin groups
Each heme carries one O2 molecule via Fe binding site

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3
Q

Erythropoiesis

A

-Stimulated by Renal erythropoeitin in bone marrow
-After age 20, RBC produced in vertebrae, sternum, ribs, and pelvis marrow.
-Expand to more bones in case of anemia.
-Most rbc mature in marrow
-Nucleated RBC in blood indicate disease (infection)
>2% retic count means rapid formation of RBC=infection
-Old RBC lose reversible deformability and removed from circulation.

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4
Q

Reversible Deformability (RD)

A
  • Cells must change shape as they pass capillaries/microcirculation.
  • Ability to change back to biconcave shape
  • Spleen is testing ground for RBC RD
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5
Q

Erythrocyte Destruction

A
  • Hgb phagocytized by macrophages et broken down to heme, iron, and glob in.
  • Heme - degraded to bilirubin. Unconj in blood, conj in liver.
  • Iron - in blood as transferrin, TIBC, stored in liver or sk. muscle. Overload in liver/spleen called hemosiderin.
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6
Q

Body Responses to Anemia - true for all anemias

A
  • Increased erythropoeitin & hematopoeitin
  • Extramedullary hematopoeisis
  • Blood shift to brain/heart
  • Tachycardia (increased heart workload)
  • Fatigue, weakness, dyspnea
  • Tissue hypoxia
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7
Q

Morphological Classification of Anemia - know

A
  • Normocytic, normochromic- decreased cell #
  • Microcytic, hypochromic - abnormal hgb production, missing components
  • Macrocytic, normochromic- large cells (juvenile,nucleated)
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8
Q

Definitions - know

A

Poikilocytosis - alteration in cell shape
Anisocytosis- “ “ size
Hemoglobinemia - hgb in plasma
Hemoglobinurea - urine exertion of hgb
Hemosideriuria - iron excretion via urine (brown)
Hemosiderosis - increased iron storage in kidneys, spleen, liver.

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9
Q

Normocytic Anemia - etiology

A
  • Loss of RBCs - hemorrhage
  • Increased destruction of RBCs (intra or extravascular hemolysis - premature lysis of erythrocytes in circulation) called hemolytic anemia
  • Decreased production of RBCs (aplastic or chronic disease anemia)
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10
Q

Normocytic -Intravascular hemolysis

A

Intravascular hemolysis- breakdown in circulating blood (mechanical injury, transfusion reaction, exogenous factors)

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11
Q

Normocytic -Intravascular hemolysis- clinical manifestation

A 
marked erythropoeisis
hemoglobinemia
hemoglobinuria
hemisiderinuria
hemisiderosis
hyperbilirubinemia
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12
Q

Normocytic -Extravascular hemolysis

A

Defective rbcs trapped in spleen.

Anemias associated Hereditary spherecytosis, G6DP, sickle cell.

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13
Q

Normocytic - Extravas hemolysis -Hereditary Spherocytosis

A
  • Etiology -autosomal genetic disorder
  • Patho - gene mutation causing deficiency in Spectrin (alpha or beta) which is protein on cell surface.
  • RBC membrane instability through tight spaces is compromised and becomes spherical. Unable to fit through spleen circulation therefore; destroyed.
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14
Q

Normocytic - Extravas hemolysis - Hereditary Spherocytosis- clinical manifestation

A

-Aplastic crisis
-Splenomegaly and jaundice
-Blood smear - anisocytosis, spherocytes, Howell-Jolly bodies
-Increased hematopoiesis
-Increased reticulocytes
Treatment - splenectomy

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15
Q

Normocytic - Extravas Hemolyisi - Glucose-6-Phosphate Dehydrogenase Deficiency G6DP

A
  • Common in African Americans/Mediterranean/Males
  • Etiology- mutation to G6DP gene
  • Patho - G6DP deficiency - enzyme required for glutathione production (antioxidant)
  • Lack of glutathione (deal with free radicals) results in oxidative stress damage to RBCs.
  • -Older cells vulnerable, infections and drugs increase oxidative stress.
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16
Q

Normocytic, Extravas Hemolysis - G6DP clinical manifestation

A
  • Hemolytic anemia - more severe in mediterraneon form
  • Hemoglobinemia
  • Hemoglobinuria
  • Blood smear - spherical cells (poikilo and anisocytosis) and Heinz and bite cells.
17
Q

Normocytic - Extravascular Hemolysis -Sickle Cell

A
  • Epi - 1 in 500 Afr. Americans with 8% carrying the cell trait. Also occurs in Mid. Eastern and S. Asian countries.
  • Etiology - mutation in beta globulin gene of hgb molecule
18
Q

Normocytic - Ex. Hemolysis - Sickle cell path

A
  • transforms hgbA (HbA) into hgb S.(HbS) Sickle cell disease = all hgbS (HbS)
  • Decreased PaO2, pH, volume, dehydration and cold cause Hbs to sickle.
  • Sickling - beta chaings in Hbs turn into viscous gel stretching into sickle shape.
  • Initially reversible but eventually irreversible.
19
Q

Normocytic - Ex. Hemolysis - sickle cell clinical manifestation

A
  • Vaso-occlusive cirisis causing tissue hypoxia and pain (bones, liver, lung, brain, spleen, rhabdomyolysis).
  • Sequestration crisis (RBCs pool in spleen, chronic hemolysis, decreased blood volume)
  • Aplastic crisis - very few RBCs in circulation - erythrocyte survival rate to 10-20 days, infection prone)
  • Blood smear - elevated retic count due to increase RBC production)
  • Bone marrow hyperplasia and extramedulary hematopoiesis.
20
Q

Normocytic - Extravas Hemolysis - Sickle cell treatment

A
  • Hydroyxurea forces RBCx to make fetal hgbjj which does not sickle
  • NO decreases platelet aggregation
  • Symptom support (O2, IV fluids, pain mgmt)
21
Q

Normocytic anemias -Decreased RBC Production -

Aplastic Anemia

A

Failure or suppression of myeloid stem cells (pancytopenia)

Etiology - idiopathic (immune mediated suppression), acquired (drugs/chemicals/radiation)

22
Q

Normocytic anemias -Decreased RBC Production - Aplastic Anemia clinical manifestation

A

pancytopenia (anemia, neutropenia, thrombocytopenia)
No splenic enlargement
Bone marrow hypo cellular
Treatment - immunosuppressants if idiopathic. If acquired, remove offending source.

23
Q

Normocytic Anemias - Decreased RBC Production - Anemia of Chronic Disease

A

-Epi - common in hospitalized pts.
-Patho - production of TNFa, IL-1, IL-6, IL10
Inflammation alters normal iron metabolism, decreased iron for erythropoiesis leads to decreased RBC production.

24
Q

Normocytic Anemias - Decreased RBC Production - Anemia of Chronic Disease - clinical manifestation

A
  • mild anemia
  • low serum iron
  • reduced tibc
  • high serum ferritin
  • low erythropoietin levels
25
Q

Microcytic Anemias

A
  • RBC cytoplasm primarly composed of Hgb.
  • Insufficient hgb (microcytic, hypochromic)
  • A and B Thalassemias (common in Mediterranean, Africa, SE Asia)
  • Iron deficiency anemia
26
Q

Microcytic Anemias -Decreased RBC Production - B Thalassemia

A 
Etiology = mutation of Bhemoglobin genes
Patho- Reduced synthesis of Bglobulin
Absence of Bglobulin,
Few B chains lead to fewer hgb molecules
Free globulin chains for upstage aggregates
Apoptosis of defective RBC precursor
Lysis of RBCs containing aglobin chains
27
Q

Microcytic Anemia - Decreased RBC Production - B Thalassemia - clinical manifestation

A
  • Anemia
  • Blood smear - aniso/poikilocytosis, increased retic, normoblasts
  • Spleno and hepatomegaly (due to extra medullary hematopoiesis)
  • Osteoporosis (bone marrow expansion)
  • Hemosiderosis
28
Q

Microcytic Anemia -Decreased RBC Production - A Thalassemia

A

-Etiology - Aglobin gene loci deletion
-Patho - Deletion leads from reduction to total absence of aglobin chains
-Clinical manifestations - silent carrier (single gene deletion) to mild/severe anemia (2-3 gene deletion) to fetal death (absence of all 4 genes)
B aggregates may cause less membrane damage leading to less lysis.

29
Q

Microcytic Anemia - Iron Deficiency Anemia

A

Insufficient iron to form Hgb molecule (formed by A & B chains). Has iron molecule to bind O2 in each chain.
Epi - most common anemia worldwide
Etiology - low iron intake, impaired absorption, increased requirements (pregnancy or chronic blood loss).

30
Q

Microcytic Anemia - Iron Deficiency Anemia - when all iron stores are depleted

A

Patho - deficiency interrupts heme synthesis leads to globin synthesis inhibition
Clinical manifestation - Anemia (hypochromic, microcytic, aniso/poikilocytosis) Pale due to low O2.
Decreased retic
Pica & poor physical development in children
Low ferretin
High TIBC

31
Q

Macrocytic Anemia

A

RBCs very large due to impaired erythropoiesis synthesis.
RBC never able to mature past megaloblast.
Macrocytic, normochromic
Types of anemia:
-Vit B12 deficiency
-Pernicious Anemia
-Decreased folic acid

32
Q

Macrocytic Anemia - Vit B12 Deficiency

A

Vit B12-Cobalamin (folic acid)
Vit B12 required for DNA synthesis during erythropoiesis
Etiology - decreased intake, malabsorption (gastrectomies, ileum resections) , increased requirements.

33
Q

Macrocytic Anemia -Pernicious Anemia

A

Etiology - autoimmune in origin

Epi - Scandinavian, ages 50 and over

34
Q

Macrocytic Anemia - Pernicious Anemia

A

Pathology - Antibodies to parietal cells.
Antibodies to intrinsic factor.
Parietal cells release gastric acid and intrinsic factor et both needed for B12 absorption.

35
Q

Macrocytic Anemia - Pernicious Anemia - clinical manifestations

A
  • Anemia
  • Low serum B12 levels (Schilling test)
  • Bone marrow biopsy (lg ovoid megaloblasts)
  • Blood smear - few retic, Howell-Jolly bodies
  • GI cytology - parietal cell atrophy, glossitis
  • B12 required for neuronal function/myelination (numbness, tingling, loss of balance, dementia)
    Immunological (antibodies to intrinsic factor and parietal cells.
36
Q

Macrocytic Anemia - Folic Acid

A
  • Require for DNA synthesis for normal erythropoeisis

- Etiology - decreased intake increased demand, impaired absorption, folate antagonist like methotrexate.

37
Q

Macrocytic Anemia - Decreased Folic Acid - clinical manifestation

A
  • Blood smear - few retic, nucleated RBCs, anisocytosis
  • Large, ovoid megaloblasts in marrow biopsy
  • Low serum folate
  • NO neurologic changes or gastric atrophy here.
38
Q

Polycythemia/Erythrocytosis

A
  • Men >18.5
  • Women > 16.5
  • Decreased plasma volume
  • Increased RBC mass (primary-gene mutation causes abnormal proliferation of myeloid stem cells, secondary - increased erythropoietin levels from hypoxia).

Adv Patho (11 decks)

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