anemia Flashcards
3 reasons we could have anemia
-defect in production of RBCs so we don’t have enough
-excess destruction of RBCs
-blood loss
lower than normal hemoglobin and fewer that normal circulating erythrocytes
anemia
what does hemoglobin do?
carries oxygen from lungs to rest of body
what r typical labs you’d see in anyone with anemia ?
low RBCs and low H and H
is a measure of the average volume of RBCs. If it’s elevated we would have large cells and if it’s decreased we would have small cells
mean corpuscular volume (MCV)
measures weight of hemoglobin in individual RBCs
mean corpuscular hemoglobin (MCH)
average concentration of hemoglobin in erythrocytes
mean corpuscular hemoglobin concentration (MCHC)
hyperchromic
dark color
normochromic
normal color
hypochromic
pale color
macrocyte
large cell
normocyte
normal size cell
microcyte
small cell
can help visualize cells
peripheral smear
a reflection of the stored iron
ferritin
a protein needed to bind the iron
transferrin level
vitamin B12 and Folate
both are nutritional anemias and r necessary for making healthy RBCs
toxic to the bone marrow and could interfere with RBC production
lead levels
a protein that binds with free floating hemoglobin
haptoglobin
let’s us know if there’s a defect in RBC production
Bone marrow aspiration
what medicine might we not give to a patient getting a bone marrow aspiration
anticoagulants, anti platelets
defect in RBC production/low producing type of anemia is
hypoproliferative anemia
what r the different types of hypoproliferative anemias
-iron deficiency anemia
-megaloblastic anemias
-VIT B12 deficiency
-pernicious anemia
-folic acid deficiency
-aplastic anemia
-anemia in renal disease
-anemia of inflammation
clinical manifestations of hypoproliferative anemias
most common type of anemia
iron deficiency
how is iron deficiency anemia caused
-most often caused by bleeding, commonly GI bleeds like ulcers, tumors,polyps, hemorrhoids, heavy menses
-poor dietary intake
-malabsorption of iron
what type of things can interfere with absorption of iron in iron deficiency anemia?
antacids
bariatric surgery
weakness, fatigue, malaise, pallor, brittle, spoon shaped nails, smooth red tongue, angular cheilosis, pica, restless leg syndrome
iron deficiency anemia
hypoproliferative anemias have high or low reticulocyte count ?
low because our body is not producing enough immature RBCs
RBCs low, H/H low, reticulocyte count low, iron level low, ferritin low, transferrin high
iron deficiency anemia
pale, small, irregular size, irregular shaped cells
iron deficiency anemia
who is at risk for iron deficiency anemia?
children, premature infants, vegans
associated with vit B12 (cobalamin) and Vit B9 (folate) deficiency
megaloblastic anemia
what 2 things r always on an alcoholics MAR?
thiamine and folic acid
what meds can cause vit B12 deficiency?
PPIs, H2 blockers, antacids, Metformin
Pallor; smooth, sore, red tongue; mild diarrhea; weight loss; neurological symptoms: confusion, paresthesias, unsteady gait
vitamin B12 deficiency
low H/H, low RBC, low reticulocyte count, low B12 level, MCV elevated
vit b12 deficiency
what do cells look like in vitamin B12 deficiency?
large and irregular shaped
treatment for vit b 12 deficiency and pernicious anemia:
oral cobalamin or cyanocobalamin for regular vitamin B12 deficiency
Sub Q for pernicious because they can’t absorb it
pregnant patients need more
folic acid
commonly caused by a lack of folic acid in the diet
folic acid deficiency anemia
Smooth, sore, red tongue, mild diarrhea, pale skin- specifically mucous membranes
folic acid deficiency anemia
low H/H, low RBC, low reticulocyte count, low folate level, elevated MCV
folic acid deficiency anemia
what do the cells look like in folic acid deficiency anemia
large, irregular shaped
foods high in folic acid
dark leafy greens, liver, fortified cereals
decreased erythropoietin production causes what anemia
anemia in renal disease
what do the cells in renal disease anemia look like?
normal shape and size just not enough production
if we sense low oxygenation we increase the secretion of
erythropoietin
defect in RBCs is caused by damage of stem cells or marrow cells in bone marrow. Not only r we not producing RBCs, but also WBCs and platelets (neutropenia and thrombocytopenia)
aplastic anemia
infection, fatigue, pallor, dyspnea, purpura (unexplained bruising), lymphadenopathy, splenomegaly, retinal hemorrhages,
aplastic anemia
Low RBCs, Low WBCs, low platelets
(pancytopenia)
aplastic anemia
said to sometimes cure aplastic anemia
HSCT ( bone marrow transplant)
what are three inherited hemolytic anemias?
- thalassemia
-G6pd
-sickle cell anemia
protein that binds with free floating hemoglobin and removes it from the body
haptoglobin
low RBCs, low H/H, low haptoglobin, low MCV, elevated bilirubin, elevated reticulocyte count
hemolytic anemias
what do cells look like in hemolytic anemias?
hypochromic, microcytic, fragile
thalassemia cells look like
hypochromic, microcytic
thalassemia is classified into 2 major groups
alpha thalassemia
beta thalassemia (more common)
occur in ppl of southeast asian and eastern mediterranean descent
alpha thalassemia
occurs in this of african descent
beta thalassemia
severe anemia. frequent transfusions are required to live
thalassemia major
frequent blood transfusions can lead to what issue?
iron overload (hemochromatosis)
low RBC, low H/H, low MCV, elevated iron levels, elevated bilirubin levels, elevated reticulocyte count
thalassemia major
target cells (bull’s eye appearance), hypochromic, small (microcytic)
thalassemia major
medical management for thalassemia
HSCT- can cure it
blood transfusions
iron chelation therapy: removes excess iron from the transfusions so our organs don’t get damaged
primary hemochromatosis
is inherited
secondary hemochromatosis
result of too much iron from supplementation
bronze colored skin
cbc normal, elevated ferritin
hemochromatosis
medical management for iron overload
therapeutic phlebotomy: removes excess blood
chelation: iv or sub q Deferoxamine (desferal)
education for iron overload
-avoid and be careful with iron intake
-avoid vit c
-avoid iron supplements
-recommend having frequent monitoring
what side effects r common in chelating agents
vision changes
-most patients r asymptomatic
-post exposure may develop pallor, hemoglobinuria, and jaundice
-elevated reticulocyte count
-cells will have heinz body
G6-PD
G6PD medical management
identify and remove the cause
meds that can lead to G6PD
-sulfadiazine
-nitrofurantoin
-trimethoprim-sulfamethoxazole
-moxifloxacine
-chloramphenicol
-anti-malarials
-NSAIDS
foods that can lead to G6PD
fava beans, menthol, tonic water
-exposure of erythrocytes alloantibodies
-our body is attacking its own RBCs
-RBC destruction because of an igG antibody (type 2 hypersensitivity reaction)
immune hemolytic anemia
fatigue, dizziness, jaundice
splenomegaly, hepatomegaly, lymphadenopathy
immune hemolytic anemia
low H/H, elevated reticulocyte count, elevated bilirubin, low haptoglobin
positive coombs test (detects antibodies)
immune hemolytic anemia
what do the cells look like in immune hemolytic anemia
microcytic spherocytes
medical management for immune hemolytic anemia
-discontinue any offending meds
-corticosteroids
-folic acid supplementation
-blood transfusions
-splenectomy
-immunosuppressive therapy
-monoclonal antibodies
patient is anemic due to blood loss
blood loss anemia
acute blood loss can be due to
trauma, hemorrhage, surgery
chronic blood loss can be due to
gastric ulcer, tumor, polyp, menorrhagia, heavy menses
weakness, fatigue, malaise, pallor, dizziness, lightheadedness, SOB, tachycardia, tachypnea
blood loss anemia
low RBC, low H/H, elevated reticulocyte count
blood loss anemia
cells in blood loss anemia
cells normal shape and size
medical management for blood loss anemia
-identify and control cause
-transfusion of rbcs
-increasing iron in diet
-iron transfusion
-iron supplements
how many hours do u have to transfuse blood after picking it up
4 hours
most common transfusion reaction
febrile non hemolytic reaction
clinical manifestations of a febrile non hemolytic reaction
fever, chills
medical management for febrile non hemolytic reaction
antipyretics like acetaminophen
most dangerous potentially life threatening reaction
caused by incompatibility of donor and recipient blood
signs
-fever and chills
-low back pain
-nausea
-chest tightness
-dyspnea
-anxiety (impending sense of doom)
-hemoglobinuria
acute hemolytic reaction
-mild reaction
-caused by reaction to a plasma protein in the blood
-urticaria
-pruritus
-flushing
-medical management is diphenhydramine
allergic reaction
caused by too much blood being transfused too quickly
-hypervolemia
-dyspnea
-orthopnea
-tachycardia
-increase in BP
-sudden anxiety
sever cases: severe dyspnea, JVD, crackles, pulmonary edema
-sometimes they’ll be premeditated with diuretic to avoid this
TACO
medical management for TACO
mild cases: slow down transfusion
severe cases: oxygen and a diuretic
can occur during procurement, processing or transfusion
-can occur if blood is not transfused in 4 hours
-fever, chills, hypotension
medical management
-IVF, antibiotics
bacterial contamination
most common cause of transfusion related death
-caused by human leucocyte antigen (HLA) or human neutrophil antigen (HNA)
signs
-acute dyspnea, hypoxia, hypotension, fever, pulmonary edema
-usually occurs 2-6 hours after transfusion
TRALI
DX and management for TRALI
-ABG, chest x ray
-aggressive supportive therapy: oxygen, intubation, fluid resuscitation
what meds r contraindicated in TRALI
-corticosteroids
-diuretics
-occur 14 days post transfusion
- caused by increase in antibodies leading to hemolysis
-fever, anemia, jaundice
delayed hemolytic reaction
nursing management for reactions
stop
assess
notify
return
treat
-inherited RBC disorder
-african descent
-child inherits hemoglobin S gene from from both parents, the cell changes shape when it’s exposed to low oxygenation or oxidative stress
sickle cell disease
most common sickle cell crisis and requires hospitalization
acute vaso-occlusive crisis
caused by infection (human parvo virus), the hemoglobin levels fall so quickly eventually leading to an absence of reticulocyte at all, the body can’t keep up at all
aplastic crisis
the buildup of sickle cells, this can happen in organs and can lead to organ dysfunction, organ infarction, in children can happen in the spleen and in adults in the liver and lungs
sequestration crisis
clinical manifestations of sickle cell
managing sickle cell pain
A: assess the pain
B: believe the patients report of pain
C: complications or cause of pain
D: drugs and distraction
E: environment
F: fluids
-chemotherapeutic agent
-increases levels of fetal hemoglobin
-makes the RBCs bigger, rounder, more flexible, and less likely to take on sickle shape
hydroxyurea
SE of hydroxyurea
dizziness, headache, rash, erythema, anorexia, N/V, stomatitis, bone marrow depression, cancer
most common complication from sickle cell also most common cause of death for sickle cell
acute chest syndrome
causes of acute chest syndrome
-atypical bacteria (chlamydia pneumonia, mycoplasm pneumonia)
-viruses (respiratory syncytial virus and parvovirus, influenza)
-pulmonary infarction, pulmonary thromboembolism
fever, respiratory distress; tachypnea, cough, wheezing, new infiltrate on chest x ray
acute chest syndrome
can progress to acute respiratory distress syndrome and death
acute chest syndrome
medical management for acute chest syndrome
blood transfusion
antibiotics
bronchodilators
mechanical ventilation
commonly seen in patients with sickle
vasoocclusion of the microvasculature, leads to an increase in pulmonary artery pressure and that’s what leads to ______
can be difficult to diagnose because we wouldn’t see it on Xray
can lead to death
pulmonary HTN
diagnosis for sickle cell
health history and physical
review of systems
pain assessment
lab data
medical management for anemia in renal disease
erythropoietin stimulating agents
-epoetin alpha (most common)
-darbpoetin alfa
-methoxy polyethylene
why is there elevated iron levels in thalassemia major?
because of the frequent transfusions to live
baseline hemoglobin for someone with sickle cell
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