anemia Flashcards
(119 cards)
1
Q
3 reasons we could have anemia
A
-defect in production of RBCs so we don’t have enough
-excess destruction of RBCs
-blood loss
2
Q
lower than normal hemoglobin and fewer that normal circulating erythrocytes
A
anemia
3
Q
what does hemoglobin do?
A
carries oxygen from lungs to rest of body
4
Q
what r typical labs you’d see in anyone with anemia ?
A
low RBCs and low H and H
5
Q
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
A
mean corpuscular volume (MCV)
6
Q
measures weight of hemoglobin in individual RBCs
A
mean corpuscular hemoglobin (MCH)
7
Q
average concentration of hemoglobin in erythrocytes
A
mean corpuscular hemoglobin concentration (MCHC)
8
Q
hyperchromic
A
dark color
9
Q
normochromic
A
normal color
10
Q
hypochromic
A
pale color
11
Q
macrocyte
A
large cell
12
Q
normocyte
A
normal size cell
13
Q
microcyte
A
small cell
14
Q
can help visualize cells
A
peripheral smear
15
Q
a reflection of the stored iron
A
ferritin
16
Q
a protein needed to bind the iron
A
transferrin level
17
Q
vitamin B12 and Folate
A
both are nutritional anemias and r necessary for making healthy RBCs
18
Q
toxic to the bone marrow and could interfere with RBC production
A
lead levels
19
Q
a protein that binds with free floating hemoglobin
A
haptoglobin
20
Q
let’s us know if there’s a defect in RBC production
A
Bone marrow aspiration
21
Q
what medicine might we not give to a patient getting a bone marrow aspiration
A
anticoagulants, anti platelets
22
Q
defect in RBC production/low producing type of anemia is
A
hypoproliferative anemia
23
Q
what r the different types of hypoproliferative anemias
A
-iron deficiency anemia
-megaloblastic anemias
-VIT B12 deficiency
-pernicious anemia
-folic acid deficiency
-aplastic anemia
-anemia in renal disease
-anemia of inflammation
24
Q
clinical manifestations of hypoproliferative anemias
A
25
most common type of anemia
iron deficiency
26
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
27
what type of things can interfere with absorption of iron in iron deficiency anemia?
antacids
bariatric surgery
28
weakness, fatigue, malaise, pallor, brittle, spoon shaped nails, smooth red tongue, angular cheilosis, pica, restless leg syndrome
iron deficiency anemia
29
hypoproliferative anemias have high or low reticulocyte count ?
low because our body is not producing enough immature RBCs
30
RBCs low, H/H low, reticulocyte count low, iron level low, ferritin low, transferrin high
iron deficiency anemia
31
pale, small, irregular size, irregular shaped cells
iron deficiency anemia
32
who is at risk for iron deficiency anemia?
children, premature infants, vegans
33
associated with vit B12 (cobalamin) and Vit B9 (folate) deficiency
megaloblastic anemia
34
what 2 things r always on an alcoholics MAR?
thiamine and folic acid
35
what meds can cause vit B12 deficiency?
PPIs, H2 blockers, antacids, Metformin
36
Pallor; smooth, sore, red tongue; mild diarrhea; weight loss; neurological symptoms: confusion, paresthesias, unsteady gait
vitamin B12 deficiency
37
low H/H, low RBC, low reticulocyte count, low B12 level, MCV elevated
vit b12 deficiency
38
what do cells look like in vitamin B12 deficiency?
large and irregular shaped
39
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
40
pregnant patients need more
folic acid
41
commonly caused by a lack of folic acid in the diet
folic acid deficiency anemia
42
Smooth, sore, red tongue, mild diarrhea, pale skin- specifically mucous membranes
folic acid deficiency anemia
43
low H/H, low RBC, low reticulocyte count, low folate level, elevated MCV
folic acid deficiency anemia
44
what do the cells look like in folic acid deficiency anemia
large, irregular shaped
45
foods high in folic acid
dark leafy greens, liver, fortified cereals
46
decreased erythropoietin production causes what anemia
anemia in renal disease
47
what do the cells in renal disease anemia look like?
normal shape and size just not enough production
48
if we sense low oxygenation we increase the secretion of
erythropoietin
49
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
50
infection, fatigue, pallor, dyspnea, purpura (unexplained bruising), lymphadenopathy, splenomegaly, retinal hemorrhages,
aplastic anemia
51
Low RBCs, Low WBCs, low platelets
(pancytopenia)
aplastic anemia
52
said to sometimes cure aplastic anemia
HSCT ( bone marrow transplant)
53
what are three inherited hemolytic anemias?
- thalassemia
-G6pd
-sickle cell anemia
54
protein that binds with free floating hemoglobin and removes it from the body
haptoglobin
55
low RBCs, low H/H, low haptoglobin, low MCV, elevated bilirubin, elevated reticulocyte count
hemolytic anemias
56
what do cells look like in hemolytic anemias?
hypochromic, microcytic, fragile
57
thalassemia cells look like
hypochromic, microcytic
58
thalassemia is classified into 2 major groups
alpha thalassemia
beta thalassemia (more common)
59
occur in ppl of southeast asian and eastern mediterranean descent
alpha thalassemia
60
occurs in this of african descent
beta thalassemia
61
severe anemia. frequent transfusions are required to live
thalassemia major
62
frequent blood transfusions can lead to what issue?
iron overload (hemochromatosis)
63
low RBC, low H/H, low MCV, elevated iron levels, elevated bilirubin levels, elevated reticulocyte count
thalassemia major
64
target cells (bull’s eye appearance), hypochromic, small (microcytic)
thalassemia major
65
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
66
primary hemochromatosis
is inherited
67
secondary hemochromatosis
result of too much iron from supplementation
68
bronze colored skin
cbc normal, elevated ferritin
hemochromatosis
69
medical management for iron overload
therapeutic phlebotomy: removes excess blood
chelation: iv or sub q Deferoxamine (desferal)
70
education for iron overload
-avoid and be careful with iron intake
-avoid vit c
-avoid iron supplements
-recommend having frequent monitoring
71
what side effects r common in chelating agents
vision changes
72
-most patients r asymptomatic
-post exposure may develop pallor, hemoglobinuria, and jaundice
-elevated reticulocyte count
-cells will have heinz body
G6-PD
73
G6PD medical management
identify and remove the cause
74
meds that can lead to G6PD
-sulfadiazine
-nitrofurantoin
-trimethoprim-sulfamethoxazole
-moxifloxacine
-chloramphenicol
-anti-malarials
-NSAIDS
75
foods that can lead to G6PD
fava beans, menthol, tonic water
76
-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
77
fatigue, dizziness, jaundice
splenomegaly, hepatomegaly, lymphadenopathy
immune hemolytic anemia
78
low H/H, elevated reticulocyte count, elevated bilirubin, low haptoglobin
positive coombs test (detects antibodies)
immune hemolytic anemia
79
what do the cells look like in immune hemolytic anemia
microcytic spherocytes
80
medical management for immune hemolytic anemia
-discontinue any offending meds
-corticosteroids
-folic acid supplementation
-blood transfusions
-splenectomy
-immunosuppressive therapy
-monoclonal antibodies
81
patient is anemic due to blood loss
blood loss anemia
82
acute blood loss can be due to
trauma, hemorrhage, surgery
83
chronic blood loss can be due to
gastric ulcer, tumor, polyp, menorrhagia, heavy menses
84
weakness, fatigue, malaise, pallor, dizziness, lightheadedness, SOB, tachycardia, tachypnea
blood loss anemia
85
low RBC, low H/H, elevated reticulocyte count
blood loss anemia
86
cells in blood loss anemia
cells normal shape and size
87
medical management for blood loss anemia
-identify and control cause
-transfusion of rbcs
-increasing iron in diet
-iron transfusion
-iron supplements
88
how many hours do u have to transfuse blood after picking it up
4 hours
89
most common transfusion reaction
febrile non hemolytic reaction
90
clinical manifestations of a febrile non hemolytic reaction
fever, chills
91
medical management for febrile non hemolytic reaction
antipyretics like acetaminophen
92
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
93
-mild reaction
-caused by reaction to a plasma protein in the blood
-urticaria
-pruritus
-flushing
-medical management is diphenhydramine
allergic reaction
94
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
95
medical management for TACO
mild cases: slow down transfusion
severe cases: oxygen and a diuretic
96
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
97
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
98
DX and management for TRALI
-ABG, chest x ray
-aggressive supportive therapy: oxygen, intubation, fluid resuscitation
99
what meds r contraindicated in TRALI
-corticosteroids
-diuretics
100
-occur 14 days post transfusion
- caused by increase in antibodies leading to hemolysis
-fever, anemia, jaundice
delayed hemolytic reaction
101
nursing management for reactions
stop
assess
notify
return
treat
102
-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
103
most common sickle cell crisis and requires hospitalization
acute vaso-occlusive crisis
104
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
105
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
106
clinical manifestations of sickle cell
107
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
108
-chemotherapeutic agent
-increases levels of fetal hemoglobin
-makes the RBCs bigger, rounder, more flexible, and less likely to take on sickle shape
hydroxyurea
109
SE of hydroxyurea
dizziness, headache, rash, erythema, anorexia, N/V, stomatitis, bone marrow depression, cancer
110
most common complication from sickle cell also most common cause of death for sickle cell
acute chest syndrome
111
causes of acute chest syndrome
-atypical bacteria (chlamydia pneumonia, mycoplasm pneumonia)
-viruses (respiratory syncytial virus and parvovirus, influenza)
-pulmonary infarction, pulmonary thromboembolism
112
fever, respiratory distress; tachypnea, cough, wheezing, new infiltrate on chest x ray
acute chest syndrome
113
can progress to acute respiratory distress syndrome and death
acute chest syndrome
114
medical management for acute chest syndrome
blood transfusion
antibiotics
bronchodilators
mechanical ventilation
115
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
116
diagnosis for sickle cell
health history and physical
review of systems
pain assessment
lab data
117
medical management for anemia in renal disease
erythropoietin stimulating agents
-epoetin alpha (most common)
-darbpoetin alfa
-methoxy polyethylene
118
why is there elevated iron levels in thalassemia major?
because of the frequent transfusions to live
119
baseline hemoglobin for someone with sickle cell
5-11
