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NUR 326: exam 1 (resp + hematology) > anemia > Flashcards

anemia Flashcards

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1
Q

hemoglobin

A

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

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2
Q

how is carbon monoxide poisoning treated?

A

100% O2 –> possible ventilation, as well

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3
Q

what happens if there are high levels of CO in the environment?

A

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

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4
Q

what else can Hgb bind to?

A

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

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5
Q

HbO2 –> HbO8

A

refers to how many O2 are bound (at the iron site) to the Hgb
more O2, the more red/saturated

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6
Q

diseases of RBCs

A

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)

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7
Q

plasma

A

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.)

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8
Q

cellular components in blood

A

45% total blood volume
Buffy coat: WBC ~7000-9000, platelets ~250,000
RBC: ~5,000,000

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9
Q

absolute anemia

A

reduced RBCs (# is smaller)

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10
Q

relative anemia

A

(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

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11
Q

polycythemia

A

too many RBC’s
decrease amount of plasma

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12
Q

causes of anemia

A

iron deficiency
maturation disorders
hemolytic anemias
acute bleeding
marrow damage (decrease RBC, WBC, platelets)
inflammation
neoplasia
chronic disease

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13
Q

hemolytic anemia

A

autoimmune disease where antibodies attack our own RBC & destroy them

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14
Q

how does kidney disease affect anemia

A

kidneys no longer secrete erythropoietin, thus bone marrow is not stimulated to produce RBC’s

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15
Q

S/S of anemia

A

pallor, fatigue, impaired cognition/memory, SOB, increased HR and RR, coldness, leg cramps, dizziness, low BP, depression, malaise (general feeling of discomfort)

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16
Q

S/S of severe anemia

A

chest pain/angina
heart attack
worsening CHF
fainting

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17
Q

clinical manifestations of mild anemia

A

may have no symptoms or not be recognized

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18
Q

clinical manifestations of mild-moderate anemia

A

fatigue (decrease O2 to tissues –> decreased ATP –> increase lactic acid)
weakness
tachycardia
dyspnea

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19
Q

clinical manifestations of moderate-severe anemia

A

increases HR, RR
hypotension, pallor, faintness
cardiovascular symptoms (esp w/ exertion)

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20
Q

trend with anemia and its effect: oxygen to muscles

A

trend: decreased
effect: weakness

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21
Q

trend with anemia and its effect: energy production

A

decreased
fatigue

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22
Q

trend with anemia and its effect: peripheral circulation (to skin)

A

blood is redistributed (compensatory) to vital organs
pallor

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23
Q

trend with anemia and its effect: cardiac output

A

increased (compensatory)
increased HR, palpitations

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24
Q

trend with anemia and its effect: secretion of erythropoietin

A

increased
bone pain

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25
trend with anemia and its effect: cardiac muscle
hypoxia chest pain, heart failure
26
trend with anemia and its effect: overall oxygenation
hypoxia dyspnea, increased RR
27
ideal Hct levels for male and females
male: 45-52 female: 37-48
28
abnormal hemoglobin diseases
~count may be normal but shapes are irregular sickle cell disease thalassemia
29
sickle cell disease
hgb becomes distorted d/t stress hypoxia, infection, dehydration or anything that can cause stress can distort cells
30
thalassemia
genetic disorder - causes defective hgb defective cells are destroyed in bone marrow or spleen lot of hemolysis
31
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
32
someone with sickle cell disease may have to...
limit sports avoid traveling to high altitudes or places with low O2 be cautious of dehydration
33
anemia
abnormal Hgb (sickle cell) decreased hgb content (loss of iron and key nutrients) decreased # of circulating erythrocytes (decreased production, increased destruction)
34
decreased Hgb can cause...
iron, B12 and folate deficiency
35
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
36
vitamin B12 + folate
necessary for DNA synthesis
37
MCV <80
microcytic anemia
38
MCV 80-100
normocytic anemia
39
MCV >100
macrocytic anemia
40
causes of iron deficiency
decreased: intake, absorption increased demand excessive loss (GI/occult bleeding or menstruation)
41
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
42
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 ***
43
vit B12 and folate pathway
vit B12 converts inactive folate to active folate then DNA synthesis and normal maturation of erythrocytes + other cells
44
folate deficiency
not a problem with absorption decreased intake: alcoholism, diet, cirrhosis increased need: pregnancy inadequate DNA synthesis --> glossitis (inflammation of tongue)
45
vitamin B12 deficiency
pernicious anemia needs to combine with IF to be absorbed in the terminal ileum
46
how and where is the intrinsic factor secreted?
by the gastric parietal cells in the stomach
47
conditions that reduce IF or inhibit absorption
gastric bypass gastrectomy bowel resection
48
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
49
anemia of chronic kidney disease
caused by impaired erythropoietin (RBC) production Hgb+Hct correspond with degree of kidney insufficiency s/s: typical anemic symptoms
50
aplastic anemia
primary condition of bone marrow stem cells body stops producing enough new blood cells decrease in: RBC, WBC, platelets
51
types of aplastic anemia
congenital acquired
52
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)
53
where do RBCs come from?
stem cells, which are produced by bone marrow *also where WBC and platelets come from
54
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
55
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
56
acquired hemolytic anemia
premature destruction of RBCs caused by some external agent
57
causes of hemolytic anemia
autoimmune attack blood incompatibilities drug reactions (NSAIDS, cephalosporins, penicillins)
58
what happens with hemolytic anemia?
when RBCs are destroyed faster than they are replaced formation of immune complexes (antibodies and antigens) lysis (cell death)
59
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)
60
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
61
S/S of 10% of blood loss (500mL)
s/s are rare possibly syncope (fainting/passing out)
62
S/S of 20% of blood loss (1000mL)
no s/s at rest increase HR with exercise
63
S/S of 30% of blood loss (1500mL)
increase HR with exercise flat neck veins when supine decrease BP with sitting/standing
64
S/S of 40% of blood loss (2000mL)
increase HR decrease BP when supine air hunger cool/clammy skin
65
S/S of 50% of blood loss (2500mL)
shock and death
66
chronic blood loss
slow/insidious body has time to compensate
67
causes of chronic blood loss
GI bleed, GI erosions, bleeding deiverticulum (artery bleeds onto colon)
68
what type of anemia does chronic blood loss typically result in?
iron-deficiency anemia
69
complications of chronic blood loss
heart: angina or heart attack lungs: SOB brain: confusion kidneys: decreased perfusion, decreased urine output

NUR 326: exam 1 (resp + hematology) (11 decks)

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