Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

anemia Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

how is carbon monoxide poisoning treated?

A

100% O2 –> possible ventilation, as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cellular components in blood

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

absolute anemia

A

reduced RBCs (# is smaller)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

polycythemia

A

too many RBC’s
decrease amount of plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hemolytic anemia

A

autoimmune disease where antibodies attack our own RBC & destroy them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does kidney disease affect anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

S/S of severe anemia

A

chest pain/angina
heart attack
worsening CHF
fainting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

clinical manifestations of mild anemia

A

may have no symptoms or not be recognized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

clinical manifestations of mild-moderate anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical manifestations of moderate-severe anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

trend with anemia and its effect: oxygen to muscles

A

trend: decreased
effect: weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

trend with anemia and its effect: energy production

A

decreased
fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

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

A

blood is redistributed (compensatory) to vital organs
pallor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

trend with anemia and its effect: cardiac output

A

increased (compensatory)
increased HR, palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

trend with anemia and its effect: secretion of erythropoietin

A

increased
bone pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

trend with anemia and its effect: cardiac muscle

A

hypoxia
chest pain, heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

trend with anemia and its effect: overall oxygenation

A

hypoxia
dyspnea, increased RR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

ideal Hct levels for male and females

A

male: 45-52
female: 37-48

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

abnormal hemoglobin diseases

A

~count may be normal but shapes are irregular
sickle cell disease
thalassemia

29
Q

sickle cell disease

A

hgb becomes distorted d/t stress
hypoxia, infection, dehydration or anything that can cause stress can distort cells

30
Q

thalassemia

A

genetic disorder - causes defective hgb
defective cells are destroyed in bone marrow or spleen
lot of hemolysis

31
Q

when cells become in the sickle shape, what happens?

A

oxygen cannot bind, and increases the chances of blocking blood flow –> leads to pain ischemia
*common areas: liver, spleen, heart, kidneys, retina

32
Q

someone with sickle cell disease may have to…

A

limit sports
avoid traveling to high altitudes or places with low O2
be cautious of dehydration

33
Q

anemia

A

abnormal Hgb (sickle cell)
decreased hgb content (loss of iron and key nutrients)
decreased # of circulating erythrocytes (decreased production, increased destruction)

34
Q

decreased Hgb can cause…

A

iron, B12 and folate deficiency

35
Q

iron

A

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
Q

vitamin B12 + folate

A

necessary for DNA synthesis

37
Q

MCV <80

A

microcytic anemia

38
Q

MCV 80-100

A

normocytic anemia

39
Q

MCV >100

A

macrocytic anemia

40
Q

causes of iron deficiency

A

decreased: intake, absorption
increased demand
excessive loss (GI/occult bleeding or menstruation)

41
Q

risk factors for iron deficiency

A

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
Q

clinical manifestations of iron deficiency

A

s/s of anemia
brittle hair/nails
koilonychia:spoon shaped nails**
smooth tongue
mouth sores
dysphagia
PICA: craving non food **
pagophagia: ice cravings ***

43
Q

vit B12 and folate pathway

A

vit B12 converts inactive folate to active folate
then DNA synthesis and normal maturation of erythrocytes + other cells

44
Q

folate deficiency

A

not a problem with absorption
decreased intake: alcoholism, diet, cirrhosis
increased need: pregnancy

inadequate DNA synthesis –> glossitis (inflammation of tongue)

45
Q

vitamin B12 deficiency

A

pernicious anemia

needs to combine with IF to be absorbed in the terminal ileum

46
Q

how and where is the intrinsic factor secreted?

A

by the gastric parietal cells in the stomach

47
Q

conditions that reduce IF or inhibit absorption

A

gastric bypass
gastrectomy
bowel resection

48
Q

S/S Vitamin B12 deficiency

A

anemia: fatigue, exercise intolerance, weakness, dyspnea, tachycardia, glossitis

neurological: depression, paranoia, confusion, anger/irritability, anxiety, balance and gait issues, memory loss

49
Q

anemia of chronic kidney disease

A

caused by impaired erythropoietin (RBC) production
Hgb+Hct correspond with degree of kidney insufficiency

s/s: typical anemic symptoms

50
Q

aplastic anemia

A

primary condition of bone marrow stem cells

body stops producing enough new blood cells
decrease in: RBC, WBC, platelets

51
Q

types of aplastic anemia

A

congenital
acquired

52
Q

what are problems a patient with aplastic anemia may have?

A

at risk for anemia (decrease in RBC)
at risk for infection (decrease in WBC)
at risk for bleeding (decrease in platelets)

53
Q

where do RBCs come from?

A

stem cells, which are produced by bone marrow

*also where WBC and platelets come from

54
Q

causes of aplastic anemia

A

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
Q

increased destruction of RBCs is caused by

A

abnormal Hgb:
- sickle cell- decreased lifespan of RBC
- thalassemia - absent/decreased production of normal Hgb - alpha or beta
-acquired hemolytic anemia

56
Q

acquired hemolytic anemia

A

premature destruction of RBCs caused by some external agent

57
Q

causes of hemolytic anemia

A

autoimmune attack
blood incompatibilities
drug reactions (NSAIDS, cephalosporins, penicillins)

58
Q

what happens with hemolytic anemia?

A

when RBCs are destroyed faster than they are replaced
formation of immune complexes (antibodies and antigens)
lysis (cell death)

59
Q

what do you look for in a patient with hemolytic anemia?

A

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
Q

blood loss anemia

A

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
Q

S/S of 10% of blood loss (500mL)

A

s/s are rare
possibly syncope (fainting/passing out)

62
Q

S/S of 20% of blood loss (1000mL)

A

no s/s at rest
increase HR with exercise

63
Q

S/S of 30% of blood loss (1500mL)

A

increase HR with exercise
flat neck veins when supine
decrease BP with sitting/standing

64
Q

S/S of 40% of blood loss (2000mL)

A

increase HR
decrease BP when supine
air hunger
cool/clammy skin

65
Q

S/S of 50% of blood loss (2500mL)

A

shock and death

66
Q

chronic blood loss

A

slow/insidious
body has time to compensate

67
Q

causes of chronic blood loss

A

GI bleed, GI erosions, bleeding deiverticulum (artery bleeds onto colon)

68
Q

what type of anemia does chronic blood loss typically result in?

A

iron-deficiency anemia

69
Q

complications of chronic blood loss

A

heart: angina or heart attack
lungs: SOB
brain: confusion
kidneys: decreased perfusion, decreased urine output

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions