Disorders of blood part 1 Flashcards by Samborg Thedestroyer

Anemia definition

Reduction in total number of circulating erythrocytes hematocrit <38% OR
Decrease in quality or quantity of hemoglobin
M13.5 - 18.0 g/dl
F 12.0-16.0 g/dl

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Hematocrit

Proportion by volume of RBCs

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Hemoglobin

Protein in RBCs that carries oxygen

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Anemia is classified by

Etiology ( 2 groups) morphology (4 groups)

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Etiology 1st group anemia

Decreased production

iron deficiency
pernicious anemia (b12 from altered DNA synthesis)
stem cell dysfunction (aplastic anemia) bone marrow infiltration (carcinoma, lymphoma)

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Etiology classification of anemia 2nd group

Increase destruction
Blood loss acute or chronic hemorrhage
Hemolysis intracorpuscular (sickle cell)
Hemolysis extracorpuscular (malaria, immune mechanism)

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Morphology anemia classification

A combination of RBC size (cytic) normo, micro, macro
and hemoglobin content (chromic) normo,hypo
Normocytic, normochromic
Microcytic, hypochromic etc

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Blood loss anemia

Acute is a decrease in RBCs and remaining ones will be normal
Chronic depletes iron, depletes hemoglobin which causes microcytic/hypochromic
RBCs take 5 days to differentiate from stem cells

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Inherited (membrane) anemia.

A type of hemolytic anemia

Called spherocytosis.
Gene for spectrin (cytoskeleton protein) is defective. RBC loss of shape, destroyed in spleen
Causes Jaundice, Splenomegaly, bilirubin gallstones

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Sickle cell anemia

A type of hemolytic anemia

RBC has abnormal shape and hemoglobin synthesis
RBC is susceptible to damage, lysis and phagocytosis.
Multiple infarcts in various organs with S&S of chronic anemia

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Thalassemia

A type of hemolytic anemia

Alpha and Beta each have major and minor forms. Genetic.
Pathophysiology is defective B HGB precipitates in bone marrow which damages membrane and creates lysis
Microcytic/Hypochromic anemia

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Inherited (Enzyme) a type of hemolytic anemia

Glucose-6-phosphate dehydrogenase deficiency
Males manifest bitches carry
350 variants
African, asian, mediterranean
Defect makes Hb more subjective to oxidative agents such as oxidant drugs, acidosis, ingesting fava beans or infection.
Once oxidized Hb loses ability to maintain it’s affinity for O2 and can lead to hemolysis

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Acquired hemolytic anemia

Toxins and drug (G6PD) infection, trauma/burns/autoimmune DIC

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Types of impaired RBC production anemia

Iron deficiency
Megaloblastic
Aplastic
Other

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Iron deficiency (impaired RBC production)

Dietary intake, blood loss, increased demand.
Microcytic/hypochromic hemoglobin with changes in shape.
Shape changes lead to splenic breakdown, jaundice, bilirubin gallstones

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Megaloblastic (impaired RBC production) pernicious anemia causes

Defective GI secretion of intrinsic factor needed to absorb (autoimmune destruction of gastric mucosa)
Lack of B12 (alcoholics/malnourished)
Intestinal disorder (Chron's or infection)

Megaloblastic (impaired RBC production) pernicious anemia

B12 for DNA synthesis of cells and formation of myelin sheaths
Leads macrocytic/normochromic
Highly injurious (used to be fatal)
Neurologic symptoms are common from myelin sheath deficits

Megaloblastic (impaired RBC production) pernicious anemia S&S

Infection
Mood alterations
GI problems
Cardiac/renal dysfunction
Hb reaches 7-8 classic S&amp;S of anemia
Death from heart failure

Types of hemolytic anemias

Inherited spherocytosis
Sickle Cell
Thalassemia
G6PD deficiency
Acquired

Folic acid (megalosblastic impaired RBC production)

Also involved in DNA synthesis (like pernicious anemia) commonly caused by decreased dietary intake with similar S&S to pernicious anemia but no neurologic S&S

Aplastic anemia (impaired RBC production)

Affects all hematopoietic products (RBC’s WBC’s and platelets anemia, neutropenia, thrombocytopenia-low platelets)
From radiation, chemo, infection, drugs, toxins, autoimmune

A plastic anemia S&S

Anemia S&S and increase infection susceptibility and coagulative disorders

Other causes of impaired RBC production

Inflammation –> cytokines
Renal failure –> EPO
Cancer –> Iron deficiency/leukemia

Clinical manifestations of anemia

Pale skin/membranes/nail beds and lips from reduced hB
CNS = Pissiness, vertigo, syncope
Tachycardia
SOB
Stomatitis and glossitis (mucous membrane/gum inflammation)
Period problems
Delayed healing

Unique S&S to hemolytic anemia

Splenomegalia and jaundice | infarctions (sickle cell)

Polycythemia

Erythrocytosis or increased RBC hB over 15.5g/dl Hematocrit over 55%

Primary polycythemia

Neoplastic disorder of bone marrow Increase in WBC RBC and platelets Increased viscosity Decreased iron stores

Secondary polycythemia

Increased EPO from prolonged hypoxia (high altitude, COPD, heart disease) or Blood doping or Renal disease or neoplasms secreting EPO

Polycythemia S&S

Viscous blood High tendency to clot Hypertension Dark, flushed face, headaches, vision problems, neurologic symptoms and splenomegaly

Non neoplastic altered leukocyte function causes

Leukopenia, leukocytosis, Mono

Leukopenia

Rare, low WBC count. Neutropenia is most common form.

Neutropenia

Most common form of leukopenia, may be congenital or acquired Three forms - autoimmune, infection, and drug induced S&S are related to increased susceptibility to infections, particularly of GI tract and skin

Autoimmune Etiology

RA and Systemic Lupus Erythremia cause formation of auto-antibodies which attack neutrophils

Drugs Etiology

Certain drugs act as antigens (haptens) which stimulate production of antibodies which attack neutrophils, most common are chemo drugs and DMARDS

Leukocytosis

Increased number of WBC (>10,000/microliter) May be an increase in all or some forms Can occur in response to acute infection, allergies, skin diseases, parasitic infections, TB etc. Usually benign May be assosicated with splenomegaly and lymph node enlargement

Infection mononucleosis

Mono or lymphocytosis Generally acute infection of B lymphocytes by Epstein-Barr virus Affected B cells produce antibodies against virus, and T cells attack virus directionly

More fun mono facts

Fever, malaise, pharyngitis, headaches, lymphadenopathy (swollen lymph nodes) and possibly splenomegaly and hepatitis Disease usually self-limiting 2 weeks, can be fatal or result in malignant lymphoma