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61 Cards in this Set

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  • Back
hematological (blood/vascular) disorders s/s
- edema (fluid) & congestion (blood)
- thrombus & embolus
- infarction
- lymphedema
- shock
- anemia
- polycythemia
- leukocytopenia & leukocytosis
saddle embolus
embolus that straddles the bifurcation in an artery
- 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)
- RBC count falls significantly
reduction in hemogloin and ability of blood to carry oxygen to the organs an tissues
-- fatigue, heart murmur
- too many RBC
- cause viscosity increase of blood and congrestion
- significant reduction in totol white boold cell count
- vulnerable to infection
- blood disorder in which immature white blood cells accumulate
= leukemia
hematopoietic system aging
- decrease in red bone marrow
- decrease:
-total serum iron
-iron-binding capacity
-intestinal absorption of
- 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
blood transfusion candidates
- surgery & b leeding, trauma, burns, disease states
blood transfusion compications
- ABO incompatibilitu
- type II hyperimmune reaction
- air embolism
- circulatory overload
blood transfusion s/s
- fever & chills
- rash
- jaudice
- hematuria
- transuion related acute lung injury (resembles Adult Respiratory Distress
blood transfusion types
- autologous transfusions
- recombinant human erythropoietin (rHuEpo)
- usually in blood in inactive form
- converted to active form by erythropoeitic factor produced by kidneys
- activaed erythropoietin stimulates bone moarrow & promotes hematopoiesis
blood transfusion complications
- usually related to ABO imcompatibility
- a result of Type II hyperimmune reaction
- resulting in destruction of RBCs & intervascular clotting
possible negative outcomes from blood transfusion
- transmission of disease: HBV, HCV, air embolism, & circulatory overload
- reactions may not occur for several days - result of undetected RBC antibody
- 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
iron accumulation in large amounts may result in
- causes tissue damage
- arthropathy
- liver damage & cirrhosis
- cardiomyopathy
- diabetes mellitus
- pulmonary disease
- sterility
hemochromatosis s/s
- abdominal pain
- weakness
- fatigue
- arthralgia
- hepatomegaly
- abnormal darkened skin ( rusty colored w/ constant itch)
- accumulations of porphyrins
- porphyrins needed to form hemoglobin
- accumulated in tissues (ie. CNS)
Porphyria s/s
- seizures
- behavior changes
- port wine urine (passing aromatic compounds)
complete blood count (CBC)
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)
other indicies included in blood count
- 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)
forms of hemoglobin
( over 300 variants)
- HbA: normal adult hemoglobin
- HbF: fetal hemoglobin (destroyed as soon as born)
- HbS: HbC, HbMemphis; hemoglobin found in sickle cell disease
- 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]
causes of anemia
- disease processes that result in exccessive blood loss
- destruction of erythrocytes
- decreased production of erythrocytes
anemia s/s
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
normocytic, normocytic anemia
- from excessive blood loss
- most common
- associated w/:
--long term use of aspirin/non-steroid anit-inflammatory agents
--excessive bleeding from menstration
- RBC are normal size and shape
- normal Hgb concentration
anemias caused by destruction of RBCs
- congenital or acquired
- congenital include: sickle cell disease
-acquired include: autoimmune hemolytic anemia, malaria, hypersplenism
macrocytic, normochromic anemia
- 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
Perniciou anemia
- occures due to vit B12 dificiency
- type of macrocytic, normochromic anemia
microcytic, hypochromic
- RBCs smaller than normal
- Hgb concentration per RBC is below normal
- insufficient heme synthesis (iron deficient states
- insufficent globin synthesis (thalassemia)
aplasic anemia
- life-threatening illness
- bone marrow supressed -> insufficient production of all blood cells (RBC, WBC & platelets)
- cause: congenital, idopathic or acquired (viruses, antibodies, certain chemicals)
- myeloproliferative disorder
- too many RBC
- inc blood volume & inc blood viscosity
- inc WBC & platelets may also occur
primary pohycythemia
- 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
secondary polycythemia
- 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
- "shift to the left"
- inc # of neutrophils (PMNs)
- occurs during periods of stress, after violent exercise & infection
other WBC inc in response to disorder
- monocytosis: during chronic inflammation
- eosinophilia: in allergy
- basophilia: in certain malignacies
- lyphocytosis: in hepatitis, mumps, malignant lymphomas, infectious mononucleosis
leukocytopenia & agranulocytopenia
- occur in certain viral infections & in bone marrow depression
- this can be very serious if not fatal
acute leukemia
2 types:
- acute lylmphoblastic (ALL): common in children
- acute myeloblastic (AML): 80% of acute leukemia in adults
clinical manifestations of AML
- present w/
--weight loss & malaise
--infection & /or bleeding
--tachycardia & tachypnea
- 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)
treatment of AML
- combination chemothereapy produces remission in 70% of patients
- ~25% achieve 5-year survival

- w/o treatment: fatal in 3-6 months
clinical manifestations of ALL
- 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)
AML & ALL onset & prognosis
- 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)
chronic myelogenous (granulocytic) leukemia (CML)
- primarly in middle aged
- slow onset
- granulocytes high
- chromosome abnormality: Philadelphia chromosome -> translocation from C22 t0 C9
CML s/s
- fatigue
- weight loss
- diaphoresis (sweating)
- heat intolerance
- hyperspenism
CML progression
- stabilization can be achieved via numerous chemotherapies
- generally progresses to an acute myeloblastic stage w/ death occurring shortly there after
- ~ 5-6 year survival
chronic lymphocytic leukemia (CLL)
- in older adults
- proliferation of small, immature lymphocytes
- B-lymphocytes involved in most cases -> decc in antibody production
CLL s/s
- similar to CML
- progression to hepatomegaly & lymphoadenopathy
- platelet count falls -> bleeding
- WBC count reduction -> prone to pneumonia & infections
CML progression
- may survive 10 years +
- may develop aggressive formation of immature lymphocytes & severe thrombocytopenia -> shorter survival rate
- may also develop autoimmune hemolytic anemia
variant of B cell leukemia
Hairy cell leukemia
- 5:1 adult male predominacne
- microscopic projects on lymphocytes
- splenomegaly
- fatigue
- series of steps that form a platelety & fibrin clot for purpose of limiting hemorrhage
1. transient vasoconstriction
2. platelet aggregation
3. activation of clotting factor
4. formation of fibrin clot (fibrin mesh)
- 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
laboratory tests
extrinsic pathway -> prothrombin time (how fast prothrombin converted to thrombin

intrinsic pathway -> partial thromboplastin time
- blood thinning therapy
- substitutes to produce vit K
- inhibits clotting
- small blood vessels are destroyed
- purpura (bruising - typically on dorsum of hand & arms)
hereditary hemorrhagic purpura
- Osler-Weber-Rendu: collagen disease allowing skin to stretch & hypermobility of joints
- Erlos Danlos syndrome
- allergic purpura
hereditary forms of purpura
-> 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
- causes purpura & internal hemorrhage
- side effect of cancer that has metastasized to bone marrow, cancer treatment, & aplastic anemia
idopathic thrombocytopenia (ITP)
- 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
disseminated intravascular coagulation (DIC)
- 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
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