Biol 2200 Unit 4

anemia

a decrease in the oxygen carrying capacity of the blood that happens as a result of either reduction in red blood cell count or amount of hemoglobin

oxygen carrying capacity

holds oxygen; determined by number of red blood cells and amount of hemoglobin in the cells

progression of anemia

anemia produces hypoxemia, which produces hypoxia

hypoxemia

a reduction in the oxygen content of the blood

hypoxia

abnormally low oxygen content in the tissues

manifestations of anemia

fatigue and lethargy, dizziness and headaches, shortness of breath, increased breathing rate and depth, pounding heart rate, vasodilation, decrease in blood viscosity, pallor (such as pale nailbeds and lips), impaired healing, numbness, nausea, GI symptoms, and low grade fever

fatigue and lethargy from anemia

happens as a result of less available oxygen for aerobic respiration to occur, causing less ATP being formed

dizziness and headaches from anemia

happens as a result of less ATP in the central nervous system

shortness of breath from anemia

happens as a result of insufficient oxygen in the tissues that leads to a strain and demand for more oxygen

increased breath rate from anemia

happens due to the respiratory center compensating by trying to speed up and increase diffusion rate

pounding heart beat from anemia

happens as a result of the cardiac centers’ response to fix hypoxemia by increasing stroke volume and heart rate

vasodilation from anemia

happens due to hypoxia releasing signaling molecules that increase local vasodilation

decrease in blood viscosity from anemia

happens from reduction of blood cells while body maintains total blood volume, which results in lower total peripheral resistance and more venous return

causes of anemia

variety of causes; includes blood loss, iron deficiency, pernicious, folate, red bone marrow disorders, sickle cell, thalassemia, aplastic anemia, lead exposure, liver disease, destruction of red blood cells

anemia through blood loss

slow or chronic blood loss from a secondary condition, such as menorrhagia, ulcerative colitis, bleeding gastric ulcers, hemorrhoids, medications (e.g. aspirin), bleeding from cancer, excess blood loss in childbirth, or acute bleeding; results in an iron deficiency

iron storage

80% of iron is bound to hemoglobin in red blood cells, and 20% is bound to storage protein ferritin in cells or transferrin in plasma

iron deficiency anemia

based on hemoglobin production, which depends on amount of available iron; when iron is not available, it creates red blood cells not reaching full size; most common worldwide anemia; results from chronic blood loss, lack of sufficient iron from diet, or reduced ability to absorb iron (e.g. inflammatory bowel disease, genetics)

risk groups for iron deficiency anemia

poverty, elderly, women, children

treatment for iron deficiency anemia

replace lost iron and treat underlying cause

pathogenesis of iron deficiency anemia

iron storages deplete, which means less red blood cells with reduced cell volume and low hemoglobin are produced, and the “anemic” blood cells gradually replace older blood cells

histology of iron deficiency anemia

described as microcytic and hypochromatic

microcrytic

small red blood cell

hypocromatic

pale coloured red blood cells

chronic blood loss

causes anemia; may occur due to excessive menstruation, ulcers, hemorrhoids, gastritis, cancers of the gastrointestinal tract, wounds, childbirth or excessive use of NSAIDs

vitamin B12 anemia

caused by vitamin B12 deficiency

pernicious anemia

a form of vitamin B12 deficiency anemia with an autoimmune etiology; gastric parietal cells are destroyed via a type II hypersensitivity reaction that results in a deficiency of intrinsic factor

parasthesia

numbness and tingling

vitamin B12

essential for DNA synthesis and red blood cell mitosis, as well as myelination of of nerves; comes from a diet of fish, meat, and dairy; intrinsic factor from gastric mucosa allows for absorption of this vitamin

causes of vitamin B12 anemia

diet, autoimmune destruction of gastric mucosa, chronic alcohol ingestion, cigarettes, gastrectomy, malabsorption of the vitamin, aging

manifestations of vitamin B12 anemia

megaloblastic RBCs, low B12 serum levels, paresthesia in hands or feet, depression, confusion, dementia, fatigue, vertigo, sore tongue

normochromic

normal blood cell amount of hemoglobin and normal red colour

macrocytic

larger than normal macrocytic red blood cells

treatment of vitamin B12 anemia

vitamin B12 injections

folate deficiency anemia

type of anemia that lack of folic acid in the body

vitamin b9

needed for nucleic acid synthesis within red blood cells, cell growth, and mitosis, as well as red blood cell maturation

causes of folate deficiency anemia

malnutrition, poor diet

manifestations of folate deficiency anemia

megaloblastic RBCs peripheral neuropathies, neural tube defects in the fetus, mouth ulcers, watery diarrhea

risk group for folate deficiency anemia

elderly, children, alcoholics, pregnant people

polycythemia

excessive erythrocyte production due to erythropoietin overproduction

two types of polycythemia

relative polycythemia and absolute polycythemia

relative polycythemia

high count of red blood cells that happens from dehydration; usually temporary

absolute polycythemia

severe excessive amount of red blood cells; two types called primary and secondary

primary absolute polycythemia

a rare non-malignant condition where there is an overabundance of bone marrow stem cells

secondary absolute polycythemia

happens as a response to hypoxia; an overproduction of erythropoietin to compensate for low oxygen levels from the environment; common in smokers, higher altitudes, and people with coronary heart failure

manifestations of polycythemia

splenomegaly, depletion of iron, hypertension, disrupted cardiac output, decreased brain blood flow (results in problems with sight, hearing, or focus), venous stasis (slow blood flow in veins), thromboembolism

splenomegaly

enlarged spleen caused by polycythemia; when red blood cells go through it, it starts to enlarge due to accumulation

leukocytosis

higher than normal count of leukocytes, or excessive leukocyte production; a normal response to infection, surgery, pregnancy, or hormones; abnormal when caused by malignancies (e.g. leukemia) or blood disorders

leukocytopenia

low count of leukocytes in the body; never a normal response; can be the result of radiation, chemotherapy, or an autoimmune disease (e.g. aplasia anemia, lupus)

causes of granulocytes

increases in basophils, neutrophils, and eosinophils happen due to particular types of infection; decreases can be due to production falling behind when granulocytes are needed

neutrophilia

elevated neutrophil count; an early response to infection

shift to the left

a large release of immature neutrophils in the blood seen in blood tests

neutropenia

lack of neutrophils; happens due to severe and prolonged infections require high demand of neutrophils so production can’t keep up with forming mature neutrophils; causes include starvation, HIV infections, chemotherapy

agranulocytosis (or granulocytopenia)

extremely low counts of granulocytes, especially neutrophils, which are nonexistent; lead to high risk of viral or bacterial infection; can be caused by chemotherapy, aplastic anemia, autoimmune destruction of neutrophils

lymphocytosis

too many lymphocytes in the blood; usually occurs as a result of viral infection (e.g. Epstein Barr virus infection)

lymphocytopenia

lack of lymphocytes; usually due to immune deficiencies (e.g. HIV), neoplasia, drugs (e.g. carbamazepine), and no known cause

infectious mononucleosis (MI)

the acute infection of B lymphocytes by Epstein-Barr virus; transmission happens through saliva

heterophile antibodies

antibodies produced by infectious mononucleosis; can destroy all types of blood cells

pathogenesis of infectious mononucleosis

the EBV invades tissue of the oropharynx, nasopharynx and salivary epithelial cells, which gets deposited into lymphoid tissues and B cells

manifestations of infectious mononucleosis

includes heterophile antibodies, lymphocytosis, fever, sore throat, cervical lymph node enlargement, and extreme fatigue; can progress to more serious symptoms, including enlargement of the spleen

leukemia

cancer of the blood and blood-forming cells (i.e. bone marrow); anaplastic cells accumulate and spill over from the bone marrow into the blood stream, and can infiltrate other organs; common symptom is pancytopenia

pancytopenia

the significant reduction in the number of almost all blood cells, due to the uncontrolled proliferation of malignant leukocytes, which crowd out the bone marrow and force production of other cell types to cease

leukemic cells

anaplastic, immature cells that proliferate rapidly and have a long lifespan; interfere with the maturation of normal blood cells; circulates in the bloodstream and cross the blood-brain barrier to infiltrate many body organs

risk factors for leukemia

associated with other hereditary abnormalities (e.g. Down syndrome); there is an increased risk has been linked to cigarette smoke, ionizing radiation, infections with HIV or HCV, and exposure to some drugs (e.g. chloramphenicol and chemotherapies)

4 classes of leukemia

classified into cell line affected (lymphocytic or myelogenous) and progression of disease (acute or chronic)

formation of blood cells

starts with pluripotent stem cells, then divides to myeloid stem cell or lymphoid stem cell

lymphocytic leukemia

caused by abnormal lymphoid stem cells, leading to abnormal B cells and T cells

myeloid leukemia

result of abnormal myeloid stem cells, resulting in abnormal RBCs, granulocytes (e.g. neutrophils), monocytes, or platelets

acute leukemia

the rapid growth of immature blood cells and abrupt onset of disease; short survival time; can be diagnosed by blood tests and bone marrow biopsy; difficult to detect early

acute lymphocytic leukemia

concerns most of lymphocytes; least common type overall, but most common type in children

acute myelogenous leukemia

concerns any cells except lymphocytes (i.e., neutrophils, platelets,
erythrocytes); tends to occur more in older adults, but is also seen in children and younger adults

manifestations of acute leukemia

fatigue caused by anemia, leukopenia, shortness of breath, tachycardia, bleeding, infections, fever, anorexia, weight loss, swollen lymph nodes, liver and spleen enlargement (hepatosplenomegaly), cachexia, bone pain

manifestations of chronic leukemia

tends to have milder symptoms and longer survival times compared to acute leukemias

treatment of leukemia

induction chemotherapy, blood transfusions and antimicrobial agents, with bone marrow transplant as last resort

chronic leukemia

the slow growth of mature cells that do not normally function; onset tends to be gradual; accounts for majority of adult cases (especially over 40); can be diagnosed with blood tests and bone marrow biopsy

chronic lymphocytic leukemia

involves transformation of primarily B cells, which refuse apoptosis commands and become inactive so no antibody production; there is higher infection due to low antibodies; can be slow or fast

chronic myelogenous leukemia

disease of excessive amounts of marrow granulocytes, RBC
precursors, and megakaryocytes; Philadelphia chromosome is observed and often causes this disease; 3 different phases of the disease called chronic, accelerated, and terminal blast phase

chronic phase of chronic myelogenous leukemia

usually lasts 2-5 years; may be asymptomatic

accelerated phase of chronic myelogenous leukemia

lasts 6-18 months; primary symptoms develop, resulting in more immature cells in bone marrow and blood; manifestations include infections, weight loss, fever, and enlargement of spleen and liver

terminal blast phase of chronic myelogenous leukemia

lasts 3-6 months; more blast cells in the blood, and an increase in
severity of symptoms; resembles acute myelogenous; prognosis is very poor

Philadelphia chromosome

a genetic change where chromosomes 22 and 9 exchange parts of long ends; the protein formed from this mutation allows cells to bypass controls of normal cell growth

treatment for chronic leukemias

combination chemotherapy; increase in body’s immune response (e.g. interferon alpha); bone marrow transplant

thrombocytopenia

too little platelets; results from decreased platelet production, increased consumption, or both; two types are primary and secondary

manifestations of thrombocytopenia

increased hemorrhage risk from minor trauma, spontaneous bleeding can occur without any trauma (e.g. petechiae, purpuric spots); bleeding can be fatal if in the GI tract, respiratory tract or
CNS

heparin-induced thrombocytopenia (HIT)

most common drug-induced condition; happens when heparin (an anticoagulant) is given with surgery; this causes IgG antibodies to produce against a heparin/platelet factor complex, causing aggregation of platelets and increased clot formation, leading to stroke, pulmonary embolism, myocardial infarction, etc

immune thrombocytopenic purpura (ITP)

an autoimmune attack on platelets; antibodies complexes with compounds in the platelet membrane, making them more susceptible to phagocytosis in the spleen; type II hypersensitivity

thrombocythemia

too many platelets; two types called primary and secondary; characterized by increased bleeding time despite a normal platelet count

primary thrombocythemia

happens as a result of inherited defects; defective thrombopoietin receptors on platelets stop negative feedback effect since defective receptor cannot adequately bind and removes thromobopoietin from the blood, thus keeping levels of the hormone high, resulting in more platelet production

secondary thrombocythemia

occurs with any disease state that stimulates thrombopoietin
production, including surgery, infection, cancer and chronic
inflammation

causes of thrombocythemia

includes inherited causes, such as Von Willebrand disease, and acquired causes, such as drugs (aspirin, NSAIDs) and leukemia

clotting factors

specialized proteins in blood plasma that act as a protector to stop bleeding when injured

coagulation disorders

caused by defects or deficiencies in one or more of the clotting factors

causes of coagulation disorders

includes inherited disorders (e.g. hemophilia) and acquired disorders (e.g. deficient synthesis of clotting factors by the liver)

hemophilia

genetic bleeding disorder where the blood does not clot properly because of low levels of vital proteins called clotting factors

inappropriate coagulation

happens due to turbulent or reduced blood flow (e.g. triggering of clotting cascade) or induced tissue factor; problematic because it uses up clotting factors and results in uncontrolled bleeding

disseminated intravascular coagulation

an acquired clinical syndrome; characterized by widespread activation of coagulation, which results in fibrin clots in blood vessels across the body; widespread clotting may lead to blockage of blood flow to organs, leading to multiple organ failure and overconsumption of platelets and clotting factors, leading to severe bleeding; can range from severe, life-threatening to a chronic, low-grade condition

causes of disseminated intravascular coagulation

trauma, obstetric complications, bacterial infection (most frequent cause), and tumours

manifestations of disseminated intravascular coagulation

varies; can include bleeding at the eyes, nose (epistaxis), gums, or at three or more unrelated sites; infarctions of kidney, lungs, heart, or brain that leads to renal failure

treatment of disseminated intravascular coagulation

eliminate the underlying cause, controling thrombosis, replace clotting components (e.g. plasma transfusions), or correct hypovolemia