Hematological & immunological Flashcards
causes of anemia
- blood loss
- immunosuppressant drugs: cyclosporine
- lack of Fe, B12
s/s of anemia
- SOB, dizziness, pallor
- tiredness, fatigue
what are effects of anemia on the circulatory system
- hemodilution: less viscous
- leading to decreased peripheral resistance
- leading to more blood returning to the heart
- results in murmur
severe anemia and increased cardiac workload can lead to HF
normal hemoglobin range
- normal 12+
- bad: 8-9
- less than 7 = send to heaven
normal hematocrit level
- normal 36+
- mod anemia <30%
- severe anemia <20%
normal platelet count
- normal 150,000-450,000
- severe thrombocytopenia <50,000
what is normal absolute neutrophil count (ANC)
- normal: 1,500-8,000
- severe: <500
what condition is considered:
- decreased RBC production
- increased RBC loss
- increased RBC destruction
- decreased production: nutritional deficiency, bone marrow failure (aplastic anemia)
- increased loss: bleed
- increased destruction: sickle cell dx, thalassemia, chemo/radiation
causes of iron deficiency anemia in mothers
- diet low in: meat, fish, and poultry
- gastric bypass surgery
- pregnancy: fetus stores iron and depletes mom of Fe
- Pica: consume non-nutritious foods such as dirt, chalk
iron deficiency anemia causes in infants and children
- premature birth
- insufficient oral intake
- excessive intake of cow’s milk >24oz
- vegan diet
premature infants and adolescents are at risk
treatment for iron deficiency anemia
- diet in iron: meats, fish, poultry, dark leafy veg, whole grains
- fortified cereal introduced around 6M
- high vit C help Fe absorption, but take at diff time
- ferrous sulfate (oral), iron dextran (IV/IM): dark stools expected
take 1hr before other meds, if GI symptoms take with food - packed RBC 2-3mL/kg
what is normocytic anemia
- RBC are normal but are low in numbers and may not function properly
- due to destruction or decreased production of RBCs
causes of normocytic anemia
- parvo
- HIV
- infection
- leukemias
- renal disease
- autoimmune dx
what is sickle cell anemia
- genetic mutation causing moon-shaped RBCs: abnormal hemoglobin S
- fragile RBCs, shorter lifespan (10-20days vs. 120days)
- rigid -> hard to pass through small blood vessels
- can’t carry enough O2 -> ischemia
what is the leading cause of death in young children with sickle cell anemia
- bacterial infection due to immunocompromise (asplenia: nonfunctional spleen)
spleen is often the first organ affected by sickle cell anemia, what is the function of the spleen
- removes old and damaged RBCs
- regulates & stores WBC, RBC, platelets
- produce WBC
- stores iron
what are factors that can contribute to sickle cell crisis
Anything that increases need for O2 or alters the transport of O2
- trauma
- infection, fever
- physical and emotional stress
- dehydration: increased blood viscosity
- hypoxia: hypoventilation, hypothermia -> vasoconstriction
vaso-occlusive crisis (sickle cell anemia)
ischemia -> infarction -> extreme pain
- unilateral weakness -> suspect** stroke**
- swelling of feet and hands (dactylitis) 1st sign in infants
- new or sudden are key words
most common
sequestration crisis (sickle cell anemia)
sickle-cells pooling in spleen or liver
- life-threatening: decreased blood volume -> hypovolemic shock, hypotension
aplastic crisis (sickle-cell anemia)
- lower RBC production & destruction of RBCs
- typically triggered by viral infection or decreased folic acid
- results in anemia
diagnosis for sickle-cell disease
- Hgb electrophoresis
- DNA analysis
treatment for sickle cell crisis
- IVF
- bedrest: lower energy expenditure
- pain control: PCA pump, methylprednisolone
- apply heat to promote vasodilation
- O2 to decrease hypoxia & decreased sickling
- electrolyte replacement: hypoxia results in metabolic acidosis
- blood exchange transfusion (erythrocytapheresis)
- abx for infections
- hydroxyurea: decreases sickling by increasing HgB
what is thalassemia
- genetic autosomal recessive disorder
- results in deficiencies in the rate of production of specific globin chains in hemoglobin -> leading to hemolysis & abundance of RBCS to compensate
diagnostics for thalassemia
- CBC
- Hgb electrophoresis
treatment for thalassemia
- blood transfusion: maintain Hgb around 9.5g/dl
what are the 5 treatment goals for thalassemia
- improved physical and mental well-being
- decreased cardiomegaly & hepatosplenomegaly
- fewer bone changes
- normal or near normal G&D until puberty
- fewer infections
potential complications with thalassemia & their treatments
- hemosiderosis: too much Fe
mineral can’t be eliminated, so deposited in body tissues
treated with Fe-chelating agents - splenomegaly: splenectomy
- bone marrow transplant
treatment for hemosiderosis secondary to thalassemia
iron-chelating agents: deferoxamine, deferasirox, deferiprone: binds excess iron for excretion by kidneys
s/s of thalassemia prior to diagnosis
- anemia: pallor
- hypoxemia
- unexplained fever
- poor feeding, failure to thrive
- enlarged spleen or liver
s/s of progressive thalassemia leading to chronic hypoxia
- headache
- chest and bone pain
- decreased exercise tolerance
- anorexia
- small stature (failure to thrive)
- delayed sexual maturation
what is aplastic anemia
- bone marrow production failure: lower WBC, RBC, platelets
causes of aplastic anemia
- congenital: Fanconi anemia (autosomal recessive)
- acquired: autoimmune dx, viral (hepatitis, parvo, HIV), radiation
leading to pancytopenia (reduction of WBC, RBC, platelets)
s/s of aplastic anemia
- petechiae
- purpurpa
- bloody stools
- infection (fever)
- general s/s anemia
diagnostics for aplastic anemia
- anemia <4.5 x 10^6
- leukopenia <4,500
- thrombocytopenia <150,000
treatment for aplastic anemia
- immunosuppressive therapy
cyclosporine
antithymocyte globulin (ALG)
tacrolimus
cyclophosphamide - enhance bone marrow production
colony stimulating factor (CSF) - stem cell transplant
what is hemophilia
- X linked recessive: males are affected, females can by carriers
- absence of specific coagulation proteins or factors
may bleed for longer periods but not at a faster rate
hemophilia A vs. B
- A (more common): factor 8 deficiency (produced by the liver)
- B: factor 9 deficiency
what is the most common form of internal bleeding from hemophilia
hemarthrosis
- bleeding into joint cavities, esp. in knees, elbows, and ankles
what are s/s of hemarthrosis from hemophilia
- stiffness, tingling, decreased movement in joint
- increased warmth, redness, swelling, severe pain in joint
how to manage hemarthrosis
- elevate & immobilize joints when bleeding
- ice, pain meds
- ROM after bleeding stops to prevent contractures
- physical therapy
- avoid obesity to minimize joint stress
diagnosis for hemophilia
- factor VIII (8) and factor IX (9) assay
- prolonged PTT time >35secs
- genetic testing
normal platelet count, PT, fibrinogen
what should you do if a pt with hemophilia is bleeding
- apply pressure for at least 15 mins and ice to vasoconstrict
- transfuse factor replacement
treatment for hemophilia
- factor 8 or 9 concentrates from genetic engineering or pooled plasma
- DDAVP (vasopressin): treatment for factor 8 activity and mild hemophilia
- corticosteroids for hematuria, acute hemarthrosis, chronic synovitis
- AVOID aspirin and NSAIDs
- physical activity: strengthens muscles around joints to decreased bleed episodes
s/s of hemophilia
- prolonged bleed
- hemorrhage from minor traumas (i.e. tooth eruption, circumcision, sx, fall at home, injections)
- excessive bruising
- subq & IM hemorrhages
- hemarthrosis (bleed into joints) -> limited ROM
- hematomas
- spontaneous hematuria
what is immune thrombocytopenia
also known as idiopathic thrombocytopenic purpura (ITP)
- acquired hemorrhagic disorder typically after a viral infection: thought to be autoimmune
- characterized by: thrombocytopenia (destruction of platelets), prolonged bleeding,and purpura
s/s of immune thrombocytopenia (ITP)
- easy bruising
- bleeding mucous membranes:** epistaxis**, gums
- internal hemorrhage
diagnosis for immune thrombocytopenia (ITP)
- platelet count < 20,000
- increased bleed times
normal is 150,000-450,000
management of immune thrombocytopenia
- restricted activity
- decrease autoimmune responses:
anti-D immunoglobin: prolonged survival of platelets
IVIG
prednisone - NO NSAIDs
- splenectomy
what is disseminated intravascular coagulation (consumption coagulopathy)
- triggered by activation of the coagulation system: i.e. trauma, infections, vascular disorders
- excessive clotting, then depletion of clotting factors -> both thrombosis & hemorrhage
- thrombosis leads to ischemia -> multi-organ dysfunction: kidneys, lungs, brain, liver
what are the possible causes for disseminated intravascular coagulation
- hypoxia
- acidosis
- shock
diagnostics for disseminated intravascular coagulation
- prolonged PT, aPTT, PTT
- increased D-dimer: increased clot formation and breakdown
- very low platelet count
- fragmented RBCs on blood smear (schistocytes)
- depleted fibrinogen
treatment for disseminated intravascular coagulation
- treat the primary reason first, it’s always secondary to something
- supportive therapy
fresh frozen plasma
cryoprecipitate: fibrinogen if levels <100
platelet transfusions
blood transfusions
may require heparin with careful watch
s/s of disseminated intravascular coagulation
- petechia, purpura, bleeding
- bleeding from umbilicus or trachea (newborn)
- GI bleed
- hypotension
- organ dysfunction from infarction and ischemia
what are s/s of incompatible blood transfusion leading to hemolytic reactions
- sudden, severe headache
- chills, fever
- pain at IV site
- N/V
- tightness in chest
- red or black urine
- flank pain
- shock or renal failure
what are nursing responsibilities for hemolytic reactions from blood transfusion
- transfuse blood slow for first 15-20mins or initial 2mL/kg
- save donor blood to recrossmatch with pt blood
- monitor for shock & kidney failure
- urinary catheter for strict I/Os
- monitor for DIC
what are s/s of allergic reaction to donor blood during transfusion
- urticaria (hives)
- flushing
- pruritus
- asthmatic wheezing
- laryngeal edema
what to do if pt has allergic rxn to blood transfusion
- stop immediately
- administer epinephrine
s/s of circulatory overload from too rapid or excessive blood transfusion
- chest pain
- dyspnea
- rales
- cyanosis
- dry cough
- distended neck veins
- HTN
what position to place the pt if they experience circulatory overload from blood transfusion
- semi-fowler to high fowler with legs lower than level of the heart
s/s of air emboli when blood is transfused under pressure
- sudden difficulty in breathing
- sharp pain in chest
what type of fluid to use with blood transfusions
NS only
how long do you have to use blood before it expires
30 mins
you should infuse the blood transfusion within what time range
within 4 hrs
what do you do if any reaction is noted with blood transfusion
- take VS
- maintain patent IV line with NS and new tubing
- notify PCP
