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Patho I: Exam 3 > Hematopoietics: RBC and Platelets > Flashcards

Hematopoietics: RBC and Platelets Flashcards

1
Q

Hematopoietic Stem Cells (HSC)

A

the most common origin of the formed elements of blood- red cels, granulocytes, monocytes, platelets, and lymphocytes

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2
Q

Hematopoiesis

A

the development process of blood

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3
Q

The most active marrow in adults?

A

vertebrae, sternum, and ribs

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4
Q

the most active marrow in children?

A

long bones

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5
Q

composition of blood

A

5.5L; 90% water and 10% solutes

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6
Q

Plasma

A

50-55% of blood volume; contains organic and inorganic elements

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7
Q

Formed Elements

A

Blood cells and Platelets (~45%)

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8
Q

Serum

A

Part of blood which is similar in composition with plasma but exclude clotting factors of blood

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9
Q

Red Blood Cells

A

Transports oxygen and carbon dioxide; lifespan 120 days

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10
Q

Neutrophils

A

Phagocytize bacteria; lifespan 6 hr - few days

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11
Q

Eosinophils

A

Phagocytize antigen antibody complex; attacks parasites; lifespan 8-12 days

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12
Q

Basophils

A

Releases histamine during inflammation; lifespan a few hours- a few days

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13
Q

Monocyte

A

Phagocytize bacteria, dead cells, and cellular debris; lifespan of many months

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14
Q

Lymphocyte

A

Involved in immune protection, either attacking cells directly or producing antibodies; lifespan of many years

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15
Q

Platelets

A

Key roles in blood clotting; lifespan of 5-10 days

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16
Q

Anemia

A

A reduction in the oxygen transporting capacity of blood, resulting from a decrease in the red cell mass to subnormal levels

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17
Q

Diagnostic Features of Anemia

A
  • Decreased Hematocrit
  • Decreased Hemoglobin Concentration
  • Correlate with the red cell mass except when there are changes in plasma volume caused by fluid retention or dehydration
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18
Q

Clinical Features of Anemia

A
  • Pale appearance
  • Weakness
  • Malaise
  • Easy fatiguability
  • Low O2: dyspnea on mild exertion. Hypoxia can cause fatty change in liver, myocardium, and kidney
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19
Q

Microcytic anemia

A

Iron deficiency

EX: thalassemia

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20
Q

Macrocytic anemia

A

Folate or Vitamin B12 deficiency

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21
Q

Normocytic anemia

A

Abnormal shapes

-hereditary spherocytosis, sickle cell disease

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22
Q

Acute Blood loss anemia

A

> 20% blood loss, hypovolemic shock

  • if patient survives: hemodilution
  • normocytic; normochromic anemia
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23
Q

Chronic Blood loss anemia

A

Iron store depletion

-i.e menstruation

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24
Q

Hemolytic Anemia Features

A
  • A shortened red cell life span below the normal 120 days
  • Increased Erythropoietin: Erythroid Hyperplasia and Reticulocytosis
  • Accumulation of hemoglobin degradation productd
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25
Q

Extravascular Hemolysis

A
  • Caused by defects that increase the destruction of RBCs by splenic macrophages
  • Degradation of hemoglobin: hyperbilirubinemia and Jaundice
  • Splenomegaly from “work hyperplasia” of pahgocytes
  • Cholelithiasis
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26
Q

Intravascular Hemolysis

A
  • Severe Injury: red cells burst within circulation

- result from either mechanical force (defective heart valve) or biochemical or physical agents (fixation of complement)

27
Q

Consequences of Intravascular Hemolysis

A

Hemoglobinemia, Hemoglobinuria, and Hemosiderinuria

-Iron deficiency

28
Q

Hereditary Spherocytosis

A
  • Mutations resulting in insufficient membrane skeletal components (spectrin, anykyrin) resulting in reduced stability of RBC membrane
  • partial Splenectomy can correct anemia
29
Q

Clinical Features of Hereditary Spherocytosis

A
  • Anemia, Splenomegaly, and Jaundice
  • Spherical shape- osmotic fragility
  • Generally stable course: parvovirus B19 infection which leads to aplastic crisis, leads to rapid worsening of the anemia and will need blood transfusions
30
Q

G-6-PD deficiency

A
  • Reduced glutathione (GSH) required to neutralize compounds such as H2O2
  • X linked recessive (more affected males)
  • 2-3 days after drug expsoure leads to Hemolysis
  • GSH -> oxidants “attack” of Hb -> Hb denatures and precipitates -> Heinz bodies -> intravascular hemolysis
  • other cells with lesser damage -> extravascular hemolysis
31
Q

Causes G-6-PD deficiency

A
  • Infectious (viral heaptitis, pneumonia)
  • Antimalarials (primaquine), sulfonamides, nitrofuratoin, phenacetin, aspirin, and vitamin K derivatives (fava beans)
  • Oxidants cause both IV an EV hemolysis in G6PD deficient people
32
Q

The reaction that results in oxidative injury and hemolysis

A

G6PD -> oxidative injury -> hemolysis

33
Q

Sickle Cell Disease

A

Glutamate –> Valine

-Chronic hemolysis, microvascular occlusions, and tissue damage

34
Q

Clinical features of Sickle cell disease

A
  • Moderately severe hemolytic anemia: Reticulocytosis, Hyperbilirubinemia, irreversibly sickled cells
  • Vaso- occlusive crisis (pain in bones, lungs, liver, and brain)
  • acute chest syndrome, priapism, stroke. retinopathy/blindness, “autosplenectomy”
  • Chronic hypoxia
  • altered splenic function
35
Q

SCD: Protective factor and rate and degree of sickling

A

-Protection against falciparum malaria
Rate and Degree of Sickling:
-Mean cell hemoglobin concentration (MCHC)
-Intracellular pH
-Transit time of Red Cells through microvascular beds

36
Q

Vaso-occlusive crisis

A

Pain crisis (bones, lungs, liver, brain)

37
Q

Autosplenectomy

A

A negative outcome of disease and occurs when a disease damages the spleen to such an extent that it becomes shrunken and non functional

38
Q

Thalassemia

A

It is caused by inherited mutations that decrease the synthesis of either alpha or beta globin chains that compose adult hemoglobin

39
Q

Thalassemia mechanism

A
  • Decreased HbA formation -> microcytic, hypochromic red cells
  • accumulation of unpaired alpha globin chains -> toxic precipitates that severely damage membranes of red cells and erythroid precursors -> ineffective erythropoiesis
40
Q

Clinical features of Thalassemia

A
  • manifests 6-9 months after birth
  • PBS: microcytic, hypochromic RBCs with anisocytosis (variable size)
  • Extramedullary hematopoiesis
  • cause of death from cardiac disease from iron overload and secondary hemochromatosis
41
Q

Balance between hepcidin and iron

A

Decreased Hepcidin means theres an Overload of Iron from excessive absorption of dietary iron

42
Q

Iron deficiency Anemia

A

Most common nutritional disorder in the world

  1. Dietary lack
  2. Impaired absorption
  3. Increased Requirement
  4. Chronic blood loss
43
Q

Features of Iron Deficient Anemia

A
  • Severe cases: weakness, listlessness, and pallor

- Chronic Anemia: Abnormalities of fingernails (thinning, flattening, and spooning)

44
Q

Transferrin

A

Synthesized in the liver and transports iron; delivers iron to cells, including erythroid precursors

45
Q

DMT 1 (Divalent Metal Transporter 1)

A

When ferrous iron is reduced by ferric reductase, DMT 1 transports it across the apical membrane

46
Q

Ferroportin

A

Moves iron from the cytoplasm to plasma across the basolateral membrane

47
Q

Diagnostic Criteria for Iron Deficiency

A
  • Hypochromic and Microcytic Anemia
  • Low serum ferritin and iron levels
  • Low transferrin saturation
  • increased total iron binding capacity
  • response to iron therapy
48
Q

Causes of Vitamin B12 deficiency

A
  • Achlorhydria (impairs vitamin B12 release from R binders)
  • Gastrectomy (causes loss of IF)
  • Ileal resection (or diffuse ileal disease)
  • Malabsorption syndromes (increased requirements)
49
Q

Clinical Features of B12 deficiency

A
  • Easy fatigability, dyspnea, CHF
  • ineffective Erythropoiesis (mild jaundice)
  • Megaloblastic changes (Beefy red tongue)
  • increased risk of development of gastric carcinoma
  • Neurologic lesions: symmetric numbness, tingling, burning feeling in feet or hands, unsteady gait and loss of position
50
Q

Folate Deficiency

A
  • Inadequate intake (chronic alcoholics)
  • Malabsorption syndromes (Sprue)
  • Increased demand (pregnancy, infancy, disseminated cancer)
  • folate antagonists
  • boiling, steaming, or frying greens for 5-10 minutes destroys 95% of folate
  • Onset: insidious; associated with weakness and easy fatigability
  • NO neurological abnormalities
51
Q

Sources of folate

A

Green vegetables (lettuce, spinach, etc)

52
Q

Causes of Anemia of Chronic Diseases

A
  1. Chronic microbial infections (osteomyelitis, IE, and lung abcess)
  2. Chronic Immune Disorders (rheumatoid arthritis)
  3. Neoplasms
    - high levels of hepcidin
    - chronic inflammation - decreases EPO synthesis in kidney which decreases RBC
    - Red cells may be slightly hypochromic and microcytic
53
Q

Aplastic Anemia

A
  • Multipotent myeloid stem cell suppression -> chronic primary heamtopoietic failure leads to pancytopenia (anemia, neutropenia, and thrombocytopenia)
  • Idiopathic
  • chemicals and drugs, irradiation, viral infections, telomerase mutations
54
Q

Aplastic Anemia Pathogenesis

A

Extrinsic: Immune mediated suppression of marrow progenitors
Intrinsic: Abnormality of stem cells

55
Q

Aplastic Anemia Clinical Features

A
  • Pancytopenia
  • Anemia (progressive weakness, pallor, dyspnea)
  • Thrombocytopenia (Petechiae and ecchymosis)
  • Neutropenia (sudden onset of chills, fever, prostration)
  • Reticulocytopenia
  • Splenomegaly
56
Q

Polycythemia

A

Abnormally high red cell count which increases hemoglobin level

57
Q

Relative Polycythemia

A
  • Dehydration

- Excessive Use of Diuretics

58
Q

Absolute Polycythemia

A
  • 1st degree (intrinsic abnormality of HSCs)

- 2nd degree (progenitors are responding to increased levels of erythropoietin)

59
Q

Most common type of polycythemia

A

Polycythemia Vera

-mutations resulting in erythropoietin independent growth of red cell progenitors

60
Q

Thrombocytopenia

A
  • <100,000/uL: causes bleeding
  • 20,000 to 50,000/uL: aggravate post traumatic bleeding
  • less than 20,000/ uL: spontaneous (non traumatic) bleeding
61
Q

Causes of Thrombocytopenia

A
  • Decreased platelet production
  • Decreased platelet survival
  • Sequestration (too much accumulation in spleen)
  • Dilution
62
Q

Chronic Immune Thrombocytopenic Purpura (ITP)

A
  • Caused by autoantibody mediated destruction of platelets

- Markedly improved by splenectomy (spleen in a major site of removal of opsonized platelets, source of autoantibodies)

63
Q

Clinical features of Chronic Immune Thrombocytopenic Purpura

A
  • Most commonly in adult women <40 yrs
  • bleeding into skin and mucosa
  • H/O easy bruising, nosebleeds, gum bleeding, hemorrhages into soft tissues from minor trauma
  • Manifests first with melena, hematuria, or excessive menstrual flow

Patho I: Exam 3 (4 decks)

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