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61 Cards in this Set
- Front
- Back
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hematological (blood/vascular) disorders s/s
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- edema (fluid) & congestion (blood)
- thrombus & embolus - infarction - lymphedema - shock - anemia - polycythemia - leukocytopenia & leukocytosis |
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saddle embolus
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embolus that straddles the bifurcation in an artery
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shock
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- BP falls so low that perfusion of organs can't occur -- followed in some cases by organ failure
- hypovolemic - caradigenis (heart failing) - obstructive (of bowel due to cancer/tumor, stule) - spetic (blood born infection - neurogenic (CNS injury) |
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anemia
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- RBC count falls significantly
reduction in hemogloin and ability of blood to carry oxygen to the organs an tissues -- fatigue, heart murmur |
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polycythemia
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- too many RBC
- cause viscosity increase of blood and congrestion |
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leukocytopenia
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- significant reduction in totol white boold cell count
- vulnerable to infection |
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leukocytosis
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- blood disorder in which immature white blood cells accumulate
= leukemia |
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hematopoietic system aging
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- decrease in red bone marrow
- decrease: -total serum iron -iron-binding capacity (Ferritin) -intestinal absorption of iron - increase RBC fragility - increased fibrinogen & platelet adhesiveness (primary clotting factors) - decreased hemoglobin & hematocrit - decreased vitamin B21 absorption (pernicious anemia) - decreased number/size of lymph nodes - decreased cellular immunity/T-cell function |
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blood transfusion candidates
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- surgery & b leeding, trauma, burns, disease states
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blood transfusion compications
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- ABO incompatibilitu
- type II hyperimmune reaction - HBV HCV, HIV - air embolism - circulatory overload |
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blood transfusion s/s
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- fever & chills
- rash - jaudice - hematuria - transuion related acute lung injury (resembles Adult Respiratory Distress |
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blood transfusion types
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- autologous transfusions
- recombinant human erythropoietin (rHuEpo) |
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erythropoietin
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- usually in blood in inactive form
- converted to active form by erythropoeitic factor produced by kidneys - activaed erythropoietin stimulates bone moarrow & promotes hematopoiesis |
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blood transfusion complications
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- usually related to ABO imcompatibility
- a result of Type II hyperimmune reaction - resulting in destruction of RBCs & intervascular clotting |
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possible negative outcomes from blood transfusion
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- transmission of disease: HBV, HCV, air embolism, & circulatory overload
- reactions may not occur for several days - result of undetected RBC antibody |
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hemochromatosis
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- autosomal recessive disorder
- excessive iron absorbtion from sm intestine - unable to remove iron that is absorbed in excess so accumulation occurs in organs & tissues (heart, pancreas, liver, skin...) - men8 > women1; ages 50 - 60 |
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iron accumulation in large amounts may result in
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- causes tissue damage
- arthropathy - liver damage & cirrhosis - cardiomyopathy - diabetes mellitus - pulmonary disease - sterility |
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hemochromatosis s/s
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- abdominal pain
- weakness - fatigue - arthralgia - hepatomegaly - abnormal darkened skin ( rusty colored w/ constant itch) |
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Porphyria
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- accumulations of porphyrins
- porphyrins needed to form hemoglobin - accumulated in tissues (ie. CNS) |
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Porphyria s/s
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- seizures
- behavior changes - port wine urine (passing aromatic compounds) |
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complete blood count (CBC)
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consists of:
- totol RBC count/mm3 - total WBC count/mm3 - differenetial white cell count(ie. % agranulocytes - moncytes, lymphocytes) - total platelet count/mm3 - hemoglobin total/100 ml blood - hematocrit (packed cell volume) |
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other indicies included in blood count
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- reticulocytes count (immature RBCs)
- mean corpuscular volume (MCV) (volume of RBCs) - mean corpuscular hemoglobin concentration (MCHC) (proportion of RBC that is hemoglobin) - mean copuscular hemogolobin (MCH) (# of hemoglobin per RBC) |
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forms of hemoglobin
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( over 300 variants)
- HbA: normal adult hemoglobin - HbF: fetal hemoglobin (destroyed as soon as born) - HbS: HbC, HbMemphis; hemoglobin found in sickle cell disease |
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anemia
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- reduction in oxygen carrying capacity of blood
- due to abnormality in quantity & quality of RBC - ind has low RBC count [CDC: <14 gms/100ml males & <12 gms/100ml females] |
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causes of anemia
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- disease processes that result in exccessive blood loss
- destruction of erythrocytes - decreased production of erythrocytes |
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anemia s/s
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1. pallor: caused by dec blood volume, dec hemoglobin, & vosoconstriciton to max O2 delivery to major organs
2. tachycaraida 3. cardiac murmurs: cuased by in velocity of blood flow 4. angina 5. dyspnea, fatiuge, headache, dizziness, syncope, tinnitus, anorexia, constipation/diarrhea, stomatitis (sore tongue/oral mucous membranes |
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normocytic, normocytic anemia
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- from excessive blood loss
- most common - associated w/: --cancer --long term use of aspirin/non-steroid anit-inflammatory agents --excessive bleeding from menstration - RBC are normal size and shape - normal Hgb concentration |
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anemias caused by destruction of RBCs
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- congenital or acquired
- congenital include: sickle cell disease -acquired include: autoimmune hemolytic anemia, malaria, hypersplenism |
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macrocytic, normochromic anemia
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- caused by dec produciton of erythocytes
- RBCs enlarged - Hgb concentration normal - MCH, MCHC normal - MCV inc - occurs when DNA synthesis interfered with - vit B12 &/or folic acid deficiency states - during cancer chemotherapy |
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Perniciou anemia
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- occures due to vit B12 dificiency
- type of macrocytic, normochromic anemia |
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microcytic, hypochromic
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- RBCs smaller than normal
- Hgb concentration per RBC is below normal MCH, MCHC, MCV dec - insufficient heme synthesis (iron deficient states - insufficent globin synthesis (thalassemia) |
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aplasic anemia
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- life-threatening illness
- bone marrow supressed -> insufficient production of all blood cells (RBC, WBC & platelets) - cause: congenital, idopathic or acquired (viruses, antibodies, certain chemicals) |
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polycythemia
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- myeloproliferative disorder
- too many RBC - inc blood volume & inc blood viscosity - inc WBC & platelets may also occur |
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primary pohycythemia
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- polycythemia vera
- bone marrow overproduces blood cells - affects older men - progressive - rust-colored skin, eyes blood shot, headaches w/ fullness in head, dizziness & fatigue - vessel thrombosis common |
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secondary polycythemia
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- acquired form
occurs when either: 1. ciruculating volume of plasma dec (ie. dehydration) 2. # RBC inc due to external cause (ie. smoking) - treatment: remove underlying cause |
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neutrophilia
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- "shift to the left"
- inc # of neutrophils (PMNs) - occurs during periods of stress, after violent exercise & infection |
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other WBC inc in response to disorder
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- monocytosis: during chronic inflammation
- eosinophilia: in allergy - basophilia: in certain malignacies - lyphocytosis: in hepatitis, mumps, malignant lymphomas, infectious mononucleosis |
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leukocytopenia & agranulocytopenia
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- occur in certain viral infections & in bone marrow depression
- this can be very serious if not fatal |
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acute leukemia
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2 types:
- acute lylmphoblastic (ALL): common in children - acute myeloblastic (AML): 80% of acute leukemia in adults |
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clinical manifestations of AML
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- present w/
--weight loss & malaise --lethargy --infection & /or bleeding --fever/chills --tachycardia & tachypnea --splenomegaly - commonly get gout from inc uric acid - WBC counts high - cytoplasm contains Auer rods (rod shaped bodies of immature granulocytes) -> risk for infection - RBC & platelet counts low (so bleeding problematic) |
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treatment of AML
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- combination chemothereapy produces remission in 70% of patients
- ~25% achieve 5-year survival - w/o treatment: fatal in 3-6 months |
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clinical manifestations of ALL
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- s/s similar to AML
- on occasion WBC counts may be normal or low but w/ high lymphocytes count - lymph nodes enlarged - hepatoslenomegaly - weight loss - night sweats - fever (Pale-Epstein: cycling fever) - children w/ ALL more likely to experience bone & joint pain + CNS effects (hdache, seizures) |
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AML & ALL onset & prognosis
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- both have rapid onset
- both have high fatality rate - improved treatment for children w/ ALL have ~90-95% chance for remission - adult chances ~80% -> bone marrow transplantation key (along w/ chemotherapy & physical & occupational therapy) |
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chronic myelogenous (granulocytic) leukemia (CML)
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- primarly in middle aged
- slow onset - granulocytes high - chromosome abnormality: Philadelphia chromosome -> translocation from C22 t0 C9 |
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CML s/s
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- fatigue
- weight loss - diaphoresis (sweating) - heat intolerance - hyperspenism |
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CML progression
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- stabilization can be achieved via numerous chemotherapies
- generally progresses to an acute myeloblastic stage w/ death occurring shortly there after - ~ 5-6 year survival |
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chronic lymphocytic leukemia (CLL)
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- in older adults
- proliferation of small, immature lymphocytes - B-lymphocytes involved in most cases -> decc in antibody production |
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CLL s/s
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- similar to CML
- progression to hepatomegaly & lymphoadenopathy - platelet count falls -> bleeding - WBC count reduction -> prone to pneumonia & infections |
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CML progression
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- may survive 10 years +
- may develop aggressive formation of immature lymphocytes & severe thrombocytopenia -> shorter survival rate - may also develop autoimmune hemolytic anemia |
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variant of B cell leukemia
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Hairy cell leukemia
- 5:1 adult male predominacne - microscopic projects on lymphocytes - splenomegaly - fatigue |
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coagulation
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- series of steps that form a platelety & fibrin clot for purpose of limiting hemorrhage
STEPS: 1. transient vasoconstriction 2. platelet aggregation 3. activation of clotting factor 4. formation of fibrin clot (fibrin mesh) |
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clotting
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- occurs thru activation of an extrinsic & intrinsic pathway -> initiated by factors of plasma
- clot resolution provided by plasminogen: --in active form (plasmin) breaks down & dissolves fibrin in clot --plasminogen proactivators act to convert plasminogen to plasmin |
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laboratory tests
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extrinsic pathway -> prothrombin time (how fast prothrombin converted to thrombin
intrinsic pathway -> partial thromboplastin time |
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Warfarin-Coumdin
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- blood thinning therapy
- substitutes to produce vit K - inhibits clotting |
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vasculitis
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- small blood vessels are destroyed
- purpura (bruising - typically on dorsum of hand & arms) |
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hereditary hemorrhagic purpura
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- Osler-Weber-Rendu: collagen disease allowing skin to stretch & hypermobility of joints
- Erlos Danlos syndrome - allergic purpura |
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hereditary forms of purpura
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-> hemophilia
-bleeding disorder -males; sex-linked recessive -Hemophilia A: missing clotting facator VIII -Hemophila B: lack clotting factor IX (christmas factor) -> von Willebrand's disease -most common -males = females -plateletes don't adhere to collagen in blood vessels -tendency to bleed very easily -plasma protein - von Willebrand's factor - facilitates platelet adherence to vessel walls -factor missing in this disease |
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thrombocytopenia
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- causes purpura & internal hemorrhage
- side effect of cancer that has metastasized to bone marrow, cancer treatment, & aplastic anemia |
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idopathic thrombocytopenia (ITP)
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- autoimmune disorder
- can cause purpura 7 hemorrhage - thrombosis can occur causing intravascular clumping & clotting -> primary thrombsis: myelphroliferative disorder from over-production of platelets -> secondary thrombosis: removeal of speen, inflammation & malignancy causes |
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disseminated intravascular coagulation (DIC)
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- hypercoagulation disorder
- occurs sometimes in cancer, following trama, in ostetrical situations (ie. premature birth), following sepsis, & in severe burns - clotting mech is stimulated by releasle of cytokines - widespread clotting occurs in sm blood vessels - clotting is paradoxical -> clotting factors used at such fast rate that none are available = massive hemorrhaging |
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splenomegaly
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diseases that can result in splenomegaly:
- cysts - primary tumors - vascular occlusion of venous system - tumor at other sites (ie. Hodgkin's Disease) - ind w/ anemia - removal of spleen often beneficial |
