anemia Flashcards
hemoglobin
RBC’s contain several hundred hgb which transport oxygen
oxygen binds to heme on hgb
reversibly binds oxygen and CO2 for transport
*can also bind carbon MONoxide - hgb binds more tightly to CO and won’t let go of it easily
how is carbon monoxide poisoning treated?
100% O2 –> possible ventilation, as well
what happens if there are high levels of CO in the environment?
oxygen will be displaced off the hgb and molecules will become saturated with carbon monoxide –> people can asphyxiate (deprive/die from lack of O2) bc can’t get O2 onto Hgb
what else can Hgb bind to?
can bind to other substances because of the protein
glucose permanently binds to hgb –> HgbA1C: avg over 3 months bc RBC life is 120 days, so gives us idea of glucose control
HbO2 –> HbO8
refers to how many O2 are bound (at the iron site) to the Hgb
more O2, the more red/saturated
diseases of RBCs
less oxygen is able to be transported to the tissues, which means cells cannot function normally
if decreased O2 supply continues for prolonged period of time –> reduced O2 levels & tissues can begin to die (need O2 for energy)
plasma
55% total blood volume
91% water
7% blood proteins (fibrinogen, albumin, globulin)
2% nutrients (amino acids, sugars, lipids) - hormones (erythropoietin, insulin, etc.) - electrolytes (Na, K, Ca, etc.)
cellular components in blood
45% total blood volume
Buffy coat: WBC ~7000-9000, platelets ~250,000
RBC: ~5,000,000
absolute anemia
reduced RBCs (# is smaller)
relative anemia
(aka dilutional anemia)
increase in plasma without a change in RBCs
plasma volume is increased, so it looks like there are less RBC
OR
decrease in plasma volume, makes it appear like more RBC’s
polycythemia
too many RBC’s
decrease amount of plasma
causes of anemia
iron deficiency
maturation disorders
hemolytic anemias
acute bleeding
marrow damage (decrease RBC, WBC, platelets)
inflammation
neoplasia
chronic disease
hemolytic anemia
autoimmune disease where antibodies attack our own RBC & destroy them
how does kidney disease affect anemia
kidneys no longer secrete erythropoietin, thus bone marrow is not stimulated to produce RBC’s
S/S of anemia
pallor, fatigue, impaired cognition/memory, SOB, increased HR and RR, coldness, leg cramps, dizziness, low BP, depression, malaise (general feeling of discomfort)
S/S of severe anemia
chest pain/angina
heart attack
worsening CHF
fainting
clinical manifestations of mild anemia
may have no symptoms or not be recognized
clinical manifestations of mild-moderate anemia
fatigue (decrease O2 to tissues –> decreased ATP –> increase lactic acid)
weakness
tachycardia
dyspnea
clinical manifestations of moderate-severe anemia
increases HR, RR
hypotension, pallor, faintness
cardiovascular symptoms (esp w/ exertion)
trend with anemia and its effect: oxygen to muscles
trend: decreased
effect: weakness
trend with anemia and its effect: energy production
decreased
fatigue
trend with anemia and its effect: peripheral circulation (to skin)
blood is redistributed (compensatory) to vital organs
pallor
trend with anemia and its effect: cardiac output
increased (compensatory)
increased HR, palpitations
trend with anemia and its effect: secretion of erythropoietin
increased
bone pain
trend with anemia and its effect: cardiac muscle
hypoxia
chest pain, heart failure
trend with anemia and its effect: overall oxygenation
hypoxia
dyspnea, increased RR
ideal Hct levels for male and females
male: 45-52
female: 37-48
abnormal hemoglobin diseases
~count may be normal but shapes are irregular
sickle cell disease
thalassemia
sickle cell disease
hgb becomes distorted d/t stress
hypoxia, infection, dehydration or anything that can cause stress can distort cells
thalassemia
genetic disorder - causes defective hgb
defective cells are destroyed in bone marrow or spleen
lot of hemolysis
when cells become in the sickle shape, what happens?
oxygen cannot bind, and increases the chances of blocking blood flow –> leads to pain ischemia
*common areas: liver, spleen, heart, kidneys, retina
someone with sickle cell disease may have to…
limit sports
avoid traveling to high altitudes or places with low O2
be cautious of dehydration
anemia
abnormal Hgb (sickle cell)
decreased hgb content (loss of iron and key nutrients)
decreased # of circulating erythrocytes (decreased production, increased destruction)
decreased Hgb can cause…
iron, B12 and folate deficiency
iron
iron is essential to normal Hgb production
stored in liver
iron is reused when RBC’s die
CANNOT make Hgb without iron
*gradual development of anemia
vitamin B12 + folate
necessary for DNA synthesis
MCV <80
microcytic anemia
MCV 80-100
normocytic anemia
MCV >100
macrocytic anemia
causes of iron deficiency
decreased: intake, absorption
increased demand
excessive loss (GI/occult bleeding or menstruation)
risk factors for iron deficiency
demographic: elderly, teen, female, immigrant, widower
dietary: low iron/heme iron, low vitamin C, excess tea/coffee, fad diets
social/physical: depression, poor detention, poverty, ETOH abuse, GI disease
clinical manifestations of iron deficiency
s/s of anemia
brittle hair/nails
koilonychia:spoon shaped nails**
smooth tongue
mouth sores
dysphagia
PICA: craving non food **
pagophagia: ice cravings ***
vit B12 and folate pathway
vit B12 converts inactive folate to active folate
then DNA synthesis and normal maturation of erythrocytes + other cells
folate deficiency
not a problem with absorption
decreased intake: alcoholism, diet, cirrhosis
increased need: pregnancy
inadequate DNA synthesis –> glossitis (inflammation of tongue)
vitamin B12 deficiency
pernicious anemia
needs to combine with IF to be absorbed in the terminal ileum
how and where is the intrinsic factor secreted?
by the gastric parietal cells in the stomach
conditions that reduce IF or inhibit absorption
gastric bypass
gastrectomy
bowel resection
S/S Vitamin B12 deficiency
anemia: fatigue, exercise intolerance, weakness, dyspnea, tachycardia, glossitis
neurological: depression, paranoia, confusion, anger/irritability, anxiety, balance and gait issues, memory loss
anemia of chronic kidney disease
caused by impaired erythropoietin (RBC) production
Hgb+Hct correspond with degree of kidney insufficiency
s/s: typical anemic symptoms
aplastic anemia
primary condition of bone marrow stem cells
body stops producing enough new blood cells
decrease in: RBC, WBC, platelets
types of aplastic anemia
congenital
acquired
what are problems a patient with aplastic anemia may have?
at risk for anemia (decrease in RBC)
at risk for infection (decrease in WBC)
at risk for bleeding (decrease in platelets)
where do RBCs come from?
stem cells, which are produced by bone marrow
*also where WBC and platelets come from
causes of aplastic anemia
idiopathic - IDK cause
high dose exposure to toxic agents - radiation, chemicals/toxins (benzene [industry], insecticides, chemo)
autoimmune mechanisms - complication of infection (viral hep, mono) - body begins attacking own cells
increased destruction of RBCs is caused by
abnormal Hgb:
- sickle cell- decreased lifespan of RBC
- thalassemia - absent/decreased production of normal Hgb - alpha or beta
-acquired hemolytic anemia
acquired hemolytic anemia
premature destruction of RBCs caused by some external agent
causes of hemolytic anemia
autoimmune attack
blood incompatibilities
drug reactions (NSAIDS, cephalosporins, penicillins)
what happens with hemolytic anemia?
when RBCs are destroyed faster than they are replaced
formation of immune complexes (antibodies and antigens)
lysis (cell death)
what do you look for in a patient with hemolytic anemia?
low hgb
increased reticulocyte count ( immature RBC)
mild jaundice
hemoglobinuria (tea color)
decreased haptoglobin (marker of RBC destruction; made by liver and attaches to hgb)
blood loss anemia
occult (hidden) or gross (seen)
rate is important:
acute/fast - body unable to compensate, GI bleed, shock
slow - body can begin to compensate by shifting fluids, signaling increase need for RBC
S/S of 10% of blood loss (500mL)
s/s are rare
possibly syncope (fainting/passing out)
S/S of 20% of blood loss (1000mL)
no s/s at rest
increase HR with exercise
S/S of 30% of blood loss (1500mL)
increase HR with exercise
flat neck veins when supine
decrease BP with sitting/standing
S/S of 40% of blood loss (2000mL)
increase HR
decrease BP when supine
air hunger
cool/clammy skin
S/S of 50% of blood loss (2500mL)
shock and death
chronic blood loss
slow/insidious
body has time to compensate
causes of chronic blood loss
GI bleed, GI erosions, bleeding deiverticulum (artery bleeds onto colon)
what type of anemia does chronic blood loss typically result in?
iron-deficiency anemia
complications of chronic blood loss
heart: angina or heart attack
lungs: SOB
brain: confusion
kidneys: decreased perfusion, decreased urine output
