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DPT 724 Pathophysiology > Lecture 7: Hematologic System > Flashcards

Lecture 7: Hematologic System Flashcards

1
Q

Hematologic System

A

-the form and structure of blood and blood-forming tissues

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2
Q

Blood Components

A
  • plasma

- cellular components: erythrocytes, leukocytes, thrombocytes

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3
Q

Plasma

A
  • clear straw colored fluid
  • carries Abs and nutrients to tissues and carries waste away
  • consists of proteins, albumin, globulin, and fibrinogen and other components and products of metabolism (urea, uric acid, creatinine, and lactic acid)
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4
Q

Erythrocytes

A
  • RBC production called erythropoiesis and you need erythropoietin to do this
  • life span ~120 days
  • developed from stem cell: requires B12, folic acid, and minerals (especially iron)
  • carries oxygen to tissues and removes CO2 from them
  • hemoglobin gives RBC its oxygen carrying ability: iron is component of Hb and vital to oxygen carrying capacity-absorbed iron is transported to bone marrow for Hb synthesis, unused iron is stored as ferritin (and hemosiderin in reticuloendothelial cells)
  • lack of oxygen stimulates formation and release of erythropoietin (activates bone marrow to produce RBCs-primarily made in kidneys)
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5
Q

Leukocytes

A
  • WBCs
  • protect against bacteria and infection
  • varied life spans (hours to months)
  • 5000-10000 microliters
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6
Q

Thrombocytes

A
  • platelets
  • essential to normal clotting along with coagulation factors in plasma
  • small, colorless, cells produced by giant cells in bone marrow called megakaryocytes
  • lifespan is 7-10 days
  • functions: constrict damaged BVs, form hemostatic plugs, provide substances to accelerate blood clotting (clotting factors and platelet factor 3)
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7
Q

SIFTT for Hematopoietic System

A
  • exercise can induce blood volume expansion: immediately with plasma volume, and over a period of time with new blood cells
  • blood doping: use exogenous erythropoietin (risk for increasing blood viscosity and thrombosis)
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8
Q

Aging and Hematopoietic System

A
  • blood composition changes little with age
  • percentage of bone marrow space occupied by hematopoietic issue declines progressively as does total serum iron
  • there is increased platelet adhesiveness, increased plasma membrane fragility, red cell rigidity, etc
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9
Q

Blood Dyscrasias

A
  • abnormal or pathologic condition of blood
  • bone marrow and precursor cells are vulnerable to physiologic changes: can affect cell production, because these cells produce rapidly and have short life spans
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10
Q

Classification of Blood Dyscrasias

A
  • primary: problem within blood itself
  • secondary: results from cause other than a defect in blood
  • quantitative: increased or decreased cell production or cell destruction
  • qualitative: from intrinsic cell abnormalities or plasma component dysfunction
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11
Q

Causes of Blood Dyscrasias

A
  • trauma
  • chemo
  • cirrhosis
  • surgery
  • malnutrition
  • drugs
  • toxins
  • radiation
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12
Q

RBC Disorders

A
  • anemias: decreased bone marrow production

- polycythemia: increased production of bone marrow components

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13
Q

WBC Disorders

A
  • leukopenia: decreased components

- leukemia: increased components

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14
Q

Platelet Disorders

A
  • thrombocytopenia: decreased components
  • thrombocytosis: increased components
  • dysfunctional: thrombocytopathy-usually results from disease
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15
Q

RBC, WBC, and Platelet Disorder

A

-all three decreased results in pancytopenia

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16
Q

Disseminated Intravascular Coagulation (DIC)

A
  • widespread activation of clotting cascade (clotting all the time) then as process consumes platelets and clotting factors clotting is disrupted and results in severe bleeding
  • thrombotic disease caused by over activation of coagulation and fibrinolysis: usually acute, but may be chronic in cancer patients
  • etiology: 5 major precipitating causes-1. infection 2. obstetric complications 3. neoplastic disease 4. disorders that produce necrosis 5. massive insult
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17
Q

Pathogenesis of DIC

A
  • causes small BV blockage, organ damage, depletion of circulating clotting factors and platelets, and fibrinolysis: can lead to severe paradoxical hemorrhage occurring simultaneously within the vascular system
  • diffuse or widespread clotting occurring within arterioles and capillaries all over the body: accelerated clotting results in generalized activation of prothrombin and a consequent excess of thrombin
  • thrombin catalyzes transformation of fibrinogen into fibrin which catalyzes clotting
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18
Q

Clinical Manifestations and Medical Management of DIC

A
  • abnormal bleeding
  • cutaneous oozing of serum
  • petechiae or blood blisters
  • bleeding from GI tract
  • epistaxis: bloody nose
  • sudden bruising
  • dx: decreased platelet count and fibrinogen levels; increased prothrombin time (>15s)
  • tx: may use heparin therapy; aminocaproic acid to inhibit fibrinolysis
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19
Q

SIFTT of DIC

A
  • patients require bedside care
  • avoid dislodging clots or causing new bleeding
  • monitor serial blood study results, esp. Hb, hematocrit and coagulation times
  • bed rest until bleeding episodes is required
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20
Q

Pathophysiology of DIC

A
  • coagulation system triggered
  • excess fibrin is formed (triggered by thrombin) and becomes trapped in microvasculature
  • blood flow to tissues decreases
  • both fibrinolysis and antithrombotic mechanisms lead to anticoagulation
  • platelets and coagulation factors are consumed…massive hemorrhage may ensue
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21
Q

Thromboctopenia: Overview and Pathogenesis

A
  • decreased number of platelets (less than 150,000/mm^3)
  • can prevent hemostasis (steady state)
  • most common cause of hemorrhagic disorders
  • common complication of leukemia or metastatic cancer and aggressive cancer chemotherapy
  • patho: may be congenital or acquired (more common), decreased or defective platelet production in bone marrow, increased destruction outside marrow caused by underlying disorder, blood loss
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22
Q

Thrombocytopenia: Clinical Manifestations and Medical Management

A
  • sudden onset of petechiae in skin
  • bleeding into any mucous membrane
  • general weakness
  • may also lead to tachycardia, SOB, LOC, and death
  • dx: platelet count and bleeding time and bone marrow studies
  • tx: depends on cause but may include plasmapheresis (takes out antiplatelet Abs) or transfusion when platelet count is less than 15,000/mm^3; corticosteroids to increase platelet production; folate to stimulate bone marrow production of platelets; splenectomy if disease is caused by platelet destruction-acts as primary site for platelet removal and Ab production
  • prognosis: excellent if drug-induced
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23
Q

SIFTT of Thrombocytopenia

A
  • be alert for obvious skin or mucous membrane symptoms of thrombocytopenia
  • teach patients to: watch for signs (severe bruising, external hematomas, petechiae), and to apply ice and pressure to site of bleeding
  • strenuous exercise or any exercise that involves straining or bearing down could precipitate a hemorrhage especially in eyes or brain
  • use blood pressure cuff with caution
  • only thigh high compression stockings, no knee high
  • mechanical compression with pneumatic pump and soft tissue mobilization are contraindicated unless approved by MD
  • avoid aspirin and aspirin-containing compounds unless prescribed (could help induce bleeding)
24
Q

The Anemias

A
  • reduction in oxygen carrying capacity of blood owing to abnormality in quantity or quality of erythrocytes
  • WHO defined in terms of Hb level: below 14 g/100 mL in men and below 12 g/100 mL in women
  • not a disease but symptom of many other disorders: dietary deficiency, acute or chronic blood loss, congenital defects of Hb, exposure to industrial poisons, diseases of bone marrow, chronic inflammatory, infectious, or neoplastic diseases
  • SIFTT: exercise for any anemic person should be approved by MD
25
Q

Folic Acid Deficiency Anemia

A
  • insufficient folic acid intake or malabsorption
  • folic acid essential for formation and maturation of RBCs and synthesis of DNA
  • due to water solubility and heat labile properties easily destroyed when cooking
  • deficiency inhibits RBC growth: usually occurs within 4 months (liver stores depleted), only a few deformed RBCs are produced with shortened life spans (weeks instead of months)
  • clinical manifestations: anorexia, SOB, weakness, irritability, nausea, glossitis
  • risk factors: alcohol abuse, poor diet, prolonged drug therapy, pregnancy and breastfeeding (increased demands for folate needed in DNA synthesis), malignant or intestinal diseases
26
Q

Iron Deficiency Anemia

A
  • disorder of oxygen transport in which Hb synthesis is deficient
  • affects 10-30% of adults in US
  • etiology: inadequate intake of iron or malabsorption, pregnancy, blood loss secondary to drug-induced GI bleeding
  • patho: supply of iron too low for optimal RBC production, results in smaller (microcytic) cells that contain less color; when iron stores used up concentration of transferrin (binds and transports oxygen) decreases which leads to smaller than normal RBCs with lower Hb concentration
  • CM: fatigue, DOE, HA, inability to concentrate, pallor, listlessness, susceptibility to infection, palpitations
  • increased CO and tachycardia
  • spoon-shaped thin nails (koilonychia)
  • sore, red, burning tongue (glossitis)
  • sore dry skin in corners of mouth (angular stomatitis)
  • blue tinge to sclera
  • dx: low Hb levels, bone marrow biopsy
  • tx: replacement therapy
27
Q

Pernicious Anemia

A

-most common type of megaloblastic anemia (usually large erythroblasts associated with vitamin B12 deficiency)
-typically occurs between ages 50 and 60
-etiology: low B12 causes anemia-usually an absorption problem, not diet (can’t be produced by human diet)
-patho: decreased production HCL in stomach acid and deficiency of IF which binds to B12 to absorb it so loss of absorption ability (only absorbed in small intestine after binding to IF), IF is secreted by the parietal cells; deficiency inhibits RBC growth and impairs myelin formation –> neurologic damage –> fewer deformed RBCs that have lower than normal Hb concentration; produce macrocytic RBCs (larger than normal with decreased Hb)
CM: GI-nausea, vomiting, anorexia, weight loss, flatulence, diarrhea, and constipation from disturbed digestion
-neurologic: neuritis and weakness in extremities, peripheral numbness and paresthesia, disturbed position sense, lack of coordination, ataxia, and impaired fine finger movement, positive babinski’s and romberg’s signs, lightheadedness, altered vision, loss of B&B control, impotence, irritability, poor memory, HA, depression and delirium
-CV: low Hb leads to palpitations, dyspnea, orthopnea, tachycardia, heart failure
-dx: low Hb levels, bone marrow biopsy
-tx: replacement therapy with high dose oral supplements that can be absorbed by normal intestine

28
Q

The Leukemias

A
  • malignant neoplasm of blood forming cells, specifically replacement of bone marrow by malignant clone of lymphocytic or myelogenous cells
  • classification: lympho- for leukemias involving lymphoid or lymphatic system; myelo- for leukemias of myeloid or bone marrow origin; -blastic and acute for leukemia involving immature cells; -cytic and chronic for leukemia involving mature cells
  • all are fatal if left untreated
  • SIFTT: usual precautions for thrombocytopenia and infection control must be strictly followed, strict hand washing technique, very alert to S&S of infection and report any potential site of infection, arthralgia is common
29
Q

Acute Leukemia-ALL vs. AML

A
  • accumulation of neoplastic, immature, or myeloid cells in bone marrow and peripheral blood (blast cells)-blocks development of normal cells
  • ALL (acute lymphocytic leukemia) diagnosed more frequently in children; bone marrow unable to undergo normal hematopoiesis
  • AML (acute myelogenous leukemia) most common in adults-average survival time 1 year after diagnosis, history usually reveals sudden onset of high fever and abnormal bleeding; pancytopenia: reduction in all cell lines which reflects leukemic cell replacement of bone marrow; leukemia cells may infiltrate skin
30
Q

Acute Leukemia

A
  • etiology: exact cause unknown; 40-50% have mutations in chromosomes
  • patho: immature hematopoietic cells undergo abnormal transformation, which gives rise to leukemic cells-these cells multiply and accumulate crowding out other cells, which prevents normal production of RBCs and WBCs which leads to pancytopenia
  • CM: infection, bleeding, anemia, malaise, fever, lethargy, paleness, weight loss, night sweats
  • dx: blood counts and LP (meningeal involvement)
  • tx: chemotherapy and other drugs
31
Q

Chronic Leukemia: CML

A
  • chronic myeloid leukemia
  • etiology: originates in hematopoietic stem cell and involves overproduction of myeloid cells
  • patho: overproduction of neoplastic granulocytes that circulate into peripheral circulation infiltrating spleen and liver
  • contain distinct philadelphia chromosome: chromosome 22 translocates to chromosome 9 which may be caused by radiation exposure; deadly disease
  • CM: fever, weight loss, weakness, fatigue, bruising, joint pain, heat, intolerance, splenomegaly
  • dx: chromosome studies and serum analysis
  • tx: control leukocytosis and thrombocytosis
32
Q

Chronic Leukemia: CLL

A
  • chronic lymphocytic leukemia
  • etiology: unknown may be genetic
  • patho: progressive accumulation of monoclonal B-lymphocytes
  • CM: infection, fever, fatigue, splenomegaly, weight loss, night sweats, enlargement of lymph nodes
  • dx: lymph node biopsy and routine blood tests
  • tx: chemotherapy
33
Q

Sickle Cell Disease (SCD): Overview and Pathogenesis

A
  • autosomal recessive disorder that affects primarily persons of African and Mediterranean descent
  • provides selective advantage against certain forms of malaria
  • cells only last 10-20 days so RBCs can’t be replaced fast enough
  • patho: results from substitution of aa valine for glutamic acid in Hb S gene-becomes insoluble during hypoxia, as a result RBCS become rigid, rough and elongated forming a sickle shape which causes hemolysis, vasoocclusion results making blood more viscous, normal circulation is impaired causing pain, tissue infarctions, and swelling
34
Q

Sickle Cell Disease: Clinical Manifestations, Diagnosis, Treatment, and SIFTT

A
  • CM: S&S don’t occur until after 6 months: fetal Hb protects infants for first few months after birth; anemia, tachycardia, cardiomegaly, chronic fatigue, unexplained dyspnea, hepatomegaly, irritability, fever, jaundice, pain
  • dx: all infants screened
  • tx: bone marrow transplant cures SCD, not widely used due to availability and risks
  • SIFTT: know signs of chest syndrome and stroke; patients will have lower exercise tolerance and oxygen consumption ability; during crisis pain control may be needed (avoid overexertion, dehydration, smoking, cryotherapy); joint effusion and septic arthritis common; watch for S&S of aseptic necrosis of femoral head (persistent thigh, buttock, or groin pain)
35
Q

How Sickle Cell Disease Happens

A
  • sickle cell transports oxygen normally, but after releasing oxygen, it sticks to the other sickle cells forming long, rods or tubules inside RBCs
  • when sickle cell reoxygenation, cell resumes normal shape but after repeated cycles of sickling and unsickling the erythrocytes is permanently damaged and hemolyzes
  • sickled cells become stiff and sticky and clog small BVs
36
Q

Myeloproliferative Disorders

A
  • uncontrolled production of all bone marrow elements
  • all may progress to acute myelogenous leukemia
  • polycythemia vera
  • essential thrombocythemia
37
Q

Polycythemia Vera

A
  • aka erythrocytosis
  • disorder of bone marrow stem cell primarily affecting production of RBCs
  • CM: increased [RBCs] cause increased blood viscosity and blood volume and may result in HTN and neurologic symptoms (erythromelalgia)
  • classic symptom is itching
38
Q

Essential Thrombocythemia

A
  • increased number of platelets > 600,000/microliter
  • occurs in middle aged to older adults
  • visual disturbances, HA, burning sensation of hands and feet, and skin changes
  • usually asymptomatic until platelet count exceeds 1 million/mm^3
  • may also observe erythromelalgia
39
Q

Hodgkins Lymphoma

A
  • painless, progressive enlargement of lymph nodes, spleen, and other lymphoid tissue
  • number of cells increases as disease progresses
  • peaks at ages 15-35 and again after 50
  • FHx increases likelihood
  • etiology: unknown, may involve previous infection with EBV or exposure to herbicide and other chemicals
  • patho: lymphoid neoplasm characterized by presence of reed-sternberg cells: cells are part of tissue macrophage system and have twin nuclei and nucleoli (owl eye appearance); starts in one group of lymph nodes and spreads to other chains
  • CM: painless swelling in nodes, face, and neck, anemia, jaundice, nerve pain, fatigue, night sweats, fever, pruritus (itching)
  • dx: lymph node biopsy confirms reed-sternberg cells, chest x-ray, bone scans, hematologic tests
  • tx: chemotherapy and radiation
  • prognosis: most curable form of cancer but fatal if untreated
40
Q

Non-Hodgkin’s Lymphoma

A
  • all other lymphoma’s that do not have reed-sternberg cells
  • usually caused by exposure to benzene-comes from cigarette smoke, gasoline, automobile emissions, and industrial pollution; polychlorinated biphenyls (PCBs)-found throughout food chain esp in meats, dairy products, and fish
  • B-cell abnormalities common
  • painless lymphadenopathy is often first symptom
  • rx: radiation or chemo and radiation
  • if patient is taking methotrexate (for RA Rx) and they have back pain and enlarged lymph nodes, send them to physician
41
Q

Multiple Myeloma

A
  • aka plasma cell myeloma
  • primary malignant neoplasm of plasma cells arising mostly in bone marrow-essentially eats bone away
  • mostly seen in older people
  • unknown cause-linked to genetic factors, viral infection, chemical exposure
  • patho: unknown factor stimulates B lymphocytes to turn into malignant plasma cells-increases rate of cell division of plasma cells produced in bone marrow
  • CM: infection is common complication (pneumonia), vision disturbance, HA, somnolence, irritability, confusion, cold intolerance, bone pain, renal impairment, SOB, fatigue, increased urination
  • dx: CBC, urine studies, bone marrow biopsy
  • rx: elimination of malignant plasma cells (chemo)
  • prognosis: incurable
42
Q

Disorders of Iron Absorption-Hemochromatosis

A
  • autosomal recessive hereditary disorder characterized by excessive iron absorption by SI
  • remains asymptomatic until development of iron overloading onset of symptoms at 40-60
  • equal prevalence between men and women, but men experience symptoms 5-10x more often
  • iron is slowly deposited in cells, especially liver, pancreas, heart
  • Sx: weakness, chronic fatigue, abdominal pain, jt pain, hepatomegaly, elevated Hb and liver enzymes
  • dx: blood tests; liver biopsy is definitive with measurement of iron stores
  • monthly monitoring required
  • tx: therapeutic phlebotomy 1-2 times/week
43
Q

3 Groups of Leukocytes

A
  • granulocytes…
  • basophils
  • eosinophils
  • neutrophils: main type aka PMN, not found in healthy tissue
  • all contain lysing agents capable of digesting foreign materials
  • monocytes: largest circulating blood cells, form macrophages once migrated into tissue
  • lymphocytes: secrete cytokines; produce Abs
44
Q

Leukocytosis

A
  • increase in number of leukocytes in blood
  • develops 1-2 hours after onset of acute hemorrhage
  • characterizes many infections diseases when count of more than 10,000/mL
45
Q

Leukopenia

A
  • decrease in number of leukocytes below 5000/mL

- risk for infection increases

46
Q

Basophilia

A
  • high number of basophils
  • have high heparin and histamine content
  • in presence of bacteria or other infectious agents erupt and distribute chemicals that lead to inflammatory and allergic response
47
Q

Eosinophilia

A
  • high number of eosinophils
  • migrate into tissue areas that have contact with external environment
  • usually result of allergic reaction (drugs, hay fever, etc)
  • do not normally participate in fighting most infections, but can be recruited to areas of inflammation by Abs and interleukins
  • weaker than neutrophils
  • able to defend against parasitic infections
48
Q

Neutrophilia

A
  • high number of neutrophils
  • term used to describe early stages of infection or inflammation
  • most plentiful of granulocytes
  • first phagocytic cells to reach infected area-tag them with monocytes
49
Q

Neutropenia

A
  • low number of neutrophils
  • less than 2500/mL
  • acquired: result of toxicity to neutrophil precursors in bone marrow (drugs or infectious agents); lung, breast, prostate and stomach carcinoma; malignant hematopoietic disorders
  • congenital
50
Q

Lymphocytosis

A
  • high number of lymphocytes
  • rare in acute bacterial infections
  • seen in acute viral infections esp. Epstein Barr virus
51
Q

Lymphocytopenia

A
  • low number of lymphocytes

- may be acquired or congenital

52
Q

Monocytosis

A
  • high number of monocytes

- seen in chronic infections

53
Q

Disorders of Hemostasis

A
  • arrest of bleeding after BV injury and involves interaction along BV wall, platelets, and plasma coagulation proteins
  • primary and secondary: primary involves formation of platelet plug at site of vascular injury; secondary: triggered when vascular damage exposes tissue factor
  • platelet count 150,000 to 450,000/mm^3 needed for hemostasis
  • initiated by exposure of blood to tissue factor: tissue factor converts prothrombin into thrombin in first step of coagulation; thrombin promotes conversion of fibrinogen into fibrin in second step
  • von Willebrand Disease
  • Hemophilia
54
Q

Von Willebrand Disease

A
  • most common inherited bleeding disorder
  • dysfunction of vWF; function is to bind collagen fibrils and platelets to form platelet plug
  • platelet disorders characterized by mucosal and skin bleeding (petechiae), purpura, and prolonged oozing after trauma or surgery
55
Q

Hemophilia

A
  • sex-linked autosomal recessive trait: on X chromosome so males most often affected (females carry)
  • caused by abnormality of plasma-clotting proteins for blood coagulation
  • two types: A and B
  • A: classic 80% of all cases (lack CF VIII)
  • B: 15% of all cases (lack CF IX)
  • level of severity listed as % of clotting factor: mild (6-30%): spontaneous hemorrhages are rare; moderate (15%) spontaneous hemorrhage is not usually a problem, but major bleeding episodes can occur after minor trauma; severe (60%) may bleed spontaneously or with only slight trauma
  • can damage joints with hemarthrosis (blood in joint irritates synovium)
  • transmissible diseases: before 86 50% of people with hemophilia seroconverted to HIV+, since 86 no further HIV transmission has occurred; 70-90% who go transmissions before 86 got hep C
  • tx: no known cure or prenatal tx; factor replacement therapy given IV is mainstay
  • aspirin or derivatives must be used with caution
56
Q

SIFTT of Hemostasis Disorders

A
  • regular exercise (including sports, strengthening, and stretching): protects joints, enhances jt fx and beneficial for decreasing frequency of bleeds; although some bleeding may result from participation in a sport, fewer bleeding episodes occur when children engage in regular exercise compared to sedentary individuals
  • jt that requires multiple infusions to stop bleeding or persistent synovitis is not likely to withstand stresses of sport that relies on that joint
  • therapy should include: strengthening ex, coordination ex, methods to reduce and prevent deformity, methods to influence abnormal muscle tone and pathologic patterns of movement, techniques to decrease pain, functional training for ADLs, special techniques like manual traction and mobilization
  • aquatic therapy is excellent modality esp for chronic arthropathy d/t buoyancy, resistive force, hydrostatic pressure
  • never use heat on jt bleed
  • as soon as active bleeding stops, isometric muscle exercise should be initiated to prevent muscular atrophy
  • when pain and edema diminish, begin gentle AROM followed by slowly progressing strengthening ex when joint is pain free through full range
  • preadolescents should avoid high-weight strengthening
  • with severe hemophilia, infusion (with clotting factor) prior to strengthening is usually needed
57
Q

Effects of Aspirin and Other NSAIDS on Platelet Function

A
  • inactivate platelet cyclooxygenase
  • enzyme required for production of thromboxane A2, a potent inducer of platelet aggregation and constrictor of arterial smooth muscle
  • a single dose of aspirin can suppress normal platelet aggregation for 48 hours or longer

DPT 724 Pathophysiology (18 decks)

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