module 4 review questions Flashcards by Jade Harper

By what is the oxygen carrying capacity of the blood determined? (2 things)

The number of red blood cells

The amount of hemoglobin in the red blood cells

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Define anemia, hypoxemia and hypoxia. Which produces which?

Anemia: A decrease in the oxygen carrying capacity of the blood

Hypoxemia: a reduction in the oxygen content of the blood

Hypoxia: abnormally low oxygen content in the tissues

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Describe and explain the general signs and symptoms of anemia. (eight things – all to do with breathing, heart rate, blood vessels/blood, lack of ATP)

Fatigue -> decrease aerobic cell respiration = decrease ATP

Dizziness, headaches -> decrease ATP in CNS

Breathing rate and depth -> body’s attempt to correct hypoxemia: respiratory centre response to increase the diffusion rate of O2 in lungs

Shortness of breath -> cannot get sufficient O2 to tissues to supply their demands

Rapid and pounding heart beat -> body’s attempt to correct hypoxemia: cardiac centre response, increased HR & increased stroke volume to increase blood flow to lungs & tissues

Vasodilation: increases demand on heart -> hypoxia releases signalling molecules like nitric oxide, which causes local vasodilation of tissue capillaries, which decrease total peripheral resistance > increase venous return to heart

Decrease in blood viscosity -> reduction in # of blood cells, while the body maintains total volume of blood. Effect is to decrease TPR > increase venous return

Pale lips, nail beds, mucous membranes -> blood less oxygenated = less bright red

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The production of what molecule is affected by iron deficiency? What are the three main causes and pathogenesis (how the disease develops) of iron deficient anemia?

Hemoglobin production is dependent on iron availability

Causes: chronic blood loss, lack of sufficient iron in diet, reduced ability to absorb iron – genetic predisposition, type of diet, IBD

Pathogenesis: iron stores deplete, fewer RBCs produced (low hematocrit) with reduced cell volume (MCV) & low hemoglobin content (MCHC), these “anemic” blood cells gradually replace older blood cells

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Describe pernicious anemia as a cause of vitamin B12 deficiency. What are other means of becoming B12 deficient?

Caused by vitamin B12 deficiency due to atrophic gastritis, an immunologically driven destruction of the gastric mucosa. This stops the production of intrinsic factor, which is required to absorb vitamin B12

Other means: removal of stomach, damage/disease of ileum, diet (strict vegans), malabsorption, age

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For what is vitamin B12 essential?

DNA synthesis / mitosis in RBC & myelination of nerves / nerve function

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Describe the effects of B12 deficiency. Include the appearance of erythrocytes, symptoms and treatment.

Megaloblastic RBCs: macrocytic (large) & normonchromic (normal colour due to normal amount of hemoglobin)

Signs and symptoms: general symptoms of anemia, low serum B12 levels, neurologic complications of B12 deficiency: paresthesias in hands/feet, depression, dementia

Treatment: vitamin B12 injections or supplements (depending upon cause of deficiency)

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Describe folate deficiency anemia and how this relates to the appearance of erythrocytes. Include what folic acid is essential for, causes, risk factors and clinical manifestations. What birth defect can be caused by folic acid deficiency?

Folic acid (vitamin B9) essential for nucleic acid synthesis within RBC & cell growth and mitosis

Similar features to B12 anemia, including appearance of RBC, but no tingling/sensation loss. Deficiency in pregnant women can cause neural tube defects in fetus

Common in malnutrition, diets low in green vegetables and meat

At risk: elderly, children, alcoholism, pregnancy

Other symptoms: mouth ulcers, watery diarrhea

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Define polycythemia.

Excessive erythrocyte presence

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Describe the two forms of polycythemia.

Relative: brought about through dehydration – minor consequence and easily fixed

Absolute: also exists in 2 forms:
Primary: rare non-malignant condition where there is an overabundance of bone marrow stem cells
Secondary: due to hypoxia, which results in overproduction of erythropoietin in compensation for low oxygen levels. Can occur in those living at higher altitudes, smokers and those with COPD and/or coronary heart failure

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Identify to what the manifestations of polycythemia are due, and be able to relate these to specific manifestations.

Variable and related to an increase in RBCs, hemoglobin level, and hematocrit with increased blood volume and viscosity: Splenomegaly, Depletion of iron, Disrupted cardiac output, Hypertension (increase blood viscosity), Decreased cerebral blood flow, Venous stasis (slow blood flow in veins), Thromboembolism

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Define leukocytosis and leucopenia, and outline common causes for each, including which condition can be either pathological or normal, and which condition is always pathological.

Leukocytosis: when WBC count is higher than normal. Can be normal response to stressors such as infection, surgery, pregnancy, hormones, or pathological when caused by malignancies or blood disorders

Leukopenia: when WBC count is lower than normal. Never normal response. When count falls to <1000/mm3, the risk of infection increases dramatically. Can occur as result of radiation (can cause aplastic anemia), autoimmune disease

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Define neutrophilia, neutropenia and agranulocytosis, and outline common causes for each.

Neutrophilia: an early response to infection (shift to left)

Neutropenia: with severe prolonged infections, production can’t keep up with demand. Other causes include aplastic anemia, starvation, autoimmune disorders. HIV, chemotherapy

Agranulocytosis: extremely low counts of granulocytes. Can be caused by chemotherapy

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What does “shift to the left”mean?

Increase in the number of immature neutrophils among blood cells

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Define lymphocytosis and lymphocytopenia and outline common causes for each.

Lymphocytosis: increase of peripheral blood lymphocytes (usually produced through viral infection)

Lymphocytopenia: blood doesn’t have enough white blood cells (lymphocytes) (immune deficiencies, neoplasia, drugs, no known cause)

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Identify the infective agent, transmission, pathophysiology and manifestations of infectious mononucleosis.

Epstein – Barr virus (EBV)

Transmission: commonly through saliva, but can occur with other body fluids

Manifestations: fever, sore throat, cervical lymph node enlargement. Can progress to more serious signs, including enlargement of the spleen (rupture is most common cause of death)

Virus initially invades tissue of the oropharynx, nasopharynx and salivary epithelial cells, then spreads to lymphoid tissues and B cells. Virus infects B cells, multiplying inside them

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What are heterophil antibodies?

Heterophile antibodies are endogenous antibodies in human serum/plasma that may interfere with immunoassays resulting in false elevation, or rarely false depression of measured values.

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Describe leukemia and leukemic cells, in general.

Leukemic cells: Are immature and poorly differentiated, proliferate rapidly and have a long life span, do not function normally, interfere with the maturation of normal blood cells, circulate in the bloodstream, cross the blood-brain barrier, infiltrate many body organs

Malignant disorder of the blood and blood-forming organs.

What is the common pathological feature of all leukemias?

Common pathological feature of all leukemias is uncontrolled proliferation of malignant leukocytes, which “crowd out” bone marrow, causing production of other cell lines to cease, resulting in “pancytopenia” (a reduction in all formed element components of the blood)

Be familiar with typical risk factors for leukemia.

Can reappear in families, and is associated with other hereditary abnormalities (down syndrome)

Increased risk has been linked to cigarette smoke, ionizing radiation, infections with HIV or HCV, some drugs (chloramphenicol, some chemotherapies)

Describe the basis upon which leukemias are broken down into 4 general classes.

Which type of cell line is affected (lymphocytic or myelogenous) and the progression of the disease and type of cell affected:

Acute – rapid onset with short survival time (if untreated)/ very immature cells (“blasts”)

Chronic – longer onset with longer survival time (if untreated) / more mature cells

Define the type of cells that have become malignant in ALL and in AML

Acute lymphocytic (ALL) - concerns lymphocytes (85% from B cell line)

Acute myelogenous (AML) - concerns any cells except lymphocytes (neutrophils, platelets, erythrocytes)

Which of the above tend to be manifested in children / older individuals?

ALL – children

AML - older

Be able to explain the characteristic clinical manifestations, the evaluation and treatment of acute leukemias, in general.

Clinical manifestations: fatigue, shortness of breath, tachycardia, bleeding and bruising, infections and fever, liver spleen and lymph node enlargement, neurological / CNS manifestations, bone pain, anorexia

Difficult to detect early, as symptoms are so general. Blood tests and bone marrow biopsy (reveal presence of many immature WBC 60-100% of cells).

Chemotherapy is usual treatment, along with blood transfusions and antimicrobial agents

Define the type of cells that have become malignant in chronic leukemias.

Slow growth of more mature (differentiated) cells which do not function normally

Describe characteristic clinical manifestations of chronic leukemias, in general.

Chronic lymphocytic leukemia: suppression of normal antibody production = increase in infections, anemia, thrombocytopenia and neutropenia, enlargement of liver, spleen and lymph nodes, weight loss, and fever Chronic myelogenous leukemia: affects stem cells such that there is excessive amounts of marrow granulocytes, RBC precursors and megakaryocytes

What type of cells are primarily affected in CLL, and what are the results?

Transformation of primarily B cells. They become inactive (won’t transform into plasma cells. Refuse apoptosis commands, so accumulate useless B cells)

Which of the leukemias can be sufficiently slow such that an individual may die of an unrelated disease?

CLL

What type of cells are affected in CML?

Affects stem cells such that there is excessive amounts of marrow granulocytes, RBC precursors and megakaryocytes

Describe the 3 phases of CML (you don’t need to memorize the % of blasts cells for each).

Chronic, lasting 2-5 years – may be asymptomatic Accelerated, lasting 6-18 months – primary symptoms develop: enlargement of spleen and liver, infections, weight loss and fever Terminal blast phase, lasting 3-6 months – increasing in severity of symptoms. Resembles AML, prognosis poor at this point

Describe the production of the Philadelphia chromosome and explain its effect.

Chromosomes 9 & 22 exchange parts of long ends. The much smaller 22 that results is known as the Philly chromosome and the new protein that is made allows the cell to bypass controls of normal cell growth and differentiation

Describe the evaluation and treatment of chronic leukemias.

Blood tests and bone marrow biopsy Combined treatments: bone marrow transplant & biologic response modifiers: increase the body’s immune response & combination chemotherapy

Define thrombocytopenia, its manifestations, causes and two examples.

Thrombocytopenia: too few platelets Causes: by decreased platelet production, increased consumption, or both 2 examples: Heparin induced thrombocytopenia (HIT): occurs when heparin (anticoagulant) is given with surgery. The heparin can complex with platelet factor 4 (a compound released by platelets). When this happens, in some people IgG antibodies are produced against this complex. The combination then actually activates platelets, causing increased clot formation. This decreases the platelet count, but the real problem is the produced clots, leading to stroke, pulmonary embolism Immune thrombocytopenic purpura: in some people, antibody complex with compounds in the platelet membrane, making them more susceptible to phagocytosis in spleen

Describe the causes of primary and secondary thrombocythemia.

Primary: platelet production increases, due to defects in the thrombopoietin receptor on platelets (negative feedback effect). The defective receptor cannot adequately bind & remove thrombopoietin from the blood, thus keeping levels of the hormone high in the blood, resulting in more platelet production Secondary: would occur with any disease state that stimulates thrombopoietin production, including surgery, infection, cancer and chronic inflammation

What is the overall effect on individuals of thrombocythemia?

High risk of large vessel thrombosis (ischemia in extremities is common)

By what is impaired platelet function characterized?

Increased bleeding time in the presence of a normal platelet count

Identify one inherited cause and three acquired causes for impaired platelet function.

Inherited: Von Willebrand disease (inability to produce factor that causes aggregation) Acquired: drugs (aspirin) - decreases platelet aggregation, systemic conditions – chronic renal disease leads to build up of urea which is toxic to platelets, secondary to leukemia: “crowding out” effect -> low quality platelets produced

What usually causes a coagulation disorder?

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

What usually causes a coagulation disorder?

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

Identify one inherited and two acquired causes of a coagulation disorder.

Inherited: hemophilia - deficiency in one of the clotting factors Acquired: result of deficient synthesis of clotting factors by the liver, or due to dietary deficiency of Vitamin K

Describe two causes of inappropriate coagulation and explain why this may lead to uncontrolled bleeding.

Turbulent or reduced blood flow: triggers clotting cascade Tissue factor induced: TF released from damaged or inflamed or dead tissues When inappropriate clotting is stimulated, not only is there the problem of emboli/thrombosis, but this also uses up clotting factors and platelets, leading to uncontrolled bleeding

Define and describe DIC and two major problems that it can cause.

Acquired clinical syndrome characterized by widespread activation of coagulation (which is designed to act in a relatively limited area), resulting in formation of fibrin clots in medium and small vessels throughout body Widespread clotting may block blood flow to organs, leading to multiple organ failure & magnitude of clotting may cause consumption of platelets and clotting factors, leading to severe bleeding

Describe three causes and what they result in that causes DIC.

Bacterial infection: most frequent cause particularly involving sepsis Trauma Tumours: widespread inflammatory damage to endothelium Results in uncontrolled activation of extrinsic and intrinsic clotting pathways -> thrombin -> fibrin

Outline the main manifestations of DIC and how it can be treated.

Can present in a variety of ways, depending upon the cause: Appearance of small hemorrhages in the skin (petechiae, purpura), Bleeding at the eyes, nose, gums, three or more unrelated sites, Infarctions of kidney, lungs, heart, brain -> renal failure, respiratory failure -> coma -> death Treatment: Eliminating the underlying cause, Replacing clotting components (plasma transfusions), Control of thrombosis – e.g. heparin with care, Correcting loss of fluid