Phys And Pathophys - Red Blood Cells And Disorders

Front 1

how much of the total body weight is blood?

Back 1

6%

Front 2

children develop iron deficiency anemia due to

Back 2

nutritional deficiencies

Front 3

adults develop iron deficiency anemia due to

Back 3

bleeding

Front 4

iron deficiency anemia RBC look like

Back 4

microcytic hypochromic anemia

Front 5

iron supplements need to be continued for

Back 5

1 year to replenish stores

Front 6

most common cause of anemia

Back 6

chronic disease

Front 7

diseases associated with anemia

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infection, cancer, connective tissue disorders, AIDS, ETOH, liver failure, renal failure, diabetes (normal RBC's but fewer)

Front 8

aplastic anemia is

Back 8

when the bone marrow doesn't make enough or any new blood cells

Front 9

causes of aplastic anemia

Back 9

autoimmune disorder, benzene, chloramphenical, phenylbutazone (NSAID), chemotherapeutic agents, viral infections, solvents, radiation

Front 10

anesthetic considerations for aplastic anemia

Back 10

steroids if autoimmune based, blood transfusions, thrombocytopenia (bleeding), prone to infection

Front 11

pernicious anemia is caused by

Back 11

B 12 deficiency

Front 12

pernicious anemia results from

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atrophy of the GI mucosa, decreased intrinsic factor production,

Front 13

pernicious anemia is a type of

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megablastic anemia

Front 14

B-12 or B-9 (folate) deficiency results in symptoms

Back 14

tire easily, weak, short of breath
neuropathy, numbness and tingling in hands
confusion, irritability, depression

Front 15

the body stores how much B12 and B9 in the liver?

Back 15

3-5 years of B12 and several months of folate

Front 16

what surgeries result in B12 or B9 deficiencies

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gastric bypass, short bowels

Front 17

anesthetic considerations for pernicious anemia

Back 17

avoid regional because of neuropathy, avoid nitrous because of further decrease in DNA production because of the inhibition of methionine synthetase

Front 18

most common form of vitamin deficiency

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B9 (folate) deficiency

Front 19

folate is essential for

Back 19

RBC maturation

Front 20

Signs of folic acid deficiency

Back 20

smooth tongue, hyperpigmentation, edema, liver dysfunction, mental depression, megablastic RBC

Front 21

prolonged exposure to nitrous will result in

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megablastic anemia very similar to pernicious anemai

Front 22

conditions leading to hemolytic anemias

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hereditary spherocytosis, glucose 6 dehydrogenase deficiency, pyruvate kindase deficiency, immune hemolytic anemia, thalassemias

Front 23

hemolytic anemias are characterized by

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rapid decrease in HCT and increase in bilirubin

Front 24

side effect of hemolytic anemia

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DIC - free HgB in intravascular space can cause inflammation

Front 25

define hemolytic anemias

Back 25

any condition that causes the RBC to break prematurely or a reduction in the RBC life span

Front 26

hereditary spherocytosis is caused by

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an abnormal RBC membrane that allows sodium to enter causing cells to swell

Front 27

problems from hereditary spherocytosis

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spherical cells can't fold to fit through spleen, frequently tear and are caught in the spleen, splenomegaly

Front 28

lab values for hereditary spherocytosis

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swings in HCT and jaundice, cholelithiasis

Front 29

treatment for hereditary spherocytosis

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splenectomy in over 5 years old, vit B12 and folic acid, blood transfusions

Front 30

the most common inherited RBC enzyme disorder

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Glucose 6 Phosphate Dehydrogenous deficiency

Front 31

G6PD causes

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increase in peroxides that break down the RBC membrane causing cell lysis, precipitation

Front 32

when a person with G6PD is exposed to a trigger, symptoms appear

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2-5 days later

Front 33

treatment for methemoglobinemia by G6PD

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methylene blue (doses less than 7 mg/Kg)

Front 34

pt with G6PD are unable to

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reduce the methemoglobin produced when trigger drugs, like nipride are given

Front 35

G6PD is most commonly found in

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African Americas men (10%)

Front 36

drug triggers for G6PD

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sulfonamides, probenecid, ascorbic acid (large dose), vitamin K, methylene blue (doses > 7 mg/Kg), Quinine, quinidine, prilocaine, nipride, nitroglycerin

Front 37

probenacid is a drug for treatment of

Back 37

gout

Front 38

quinidine is what type of drug

Back 38

antiarrhythmic

Front 39

pyruvate kinase is

Back 39

an enzyme involved in glucose to lactate to pyruvate conversion for ATP production in the RBC

Front 40

pyruvate kinase deficiency mimics what disease

Back 40

hereditary spherocytosis

Front 41

symptoms of pyruvate kinase deficiency

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splenomegaly, cholelithiasis, anemia

Front 42

treatments for pyruvate kinase deficiency

Back 42

transfusion, supportive

Front 43

sickle cell disease is caused by

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a substitution of valine for glutamic acid on the 6th position of the beta chain in the hgb molecule

Front 44

the sickle cell abnormality causes the hgb to

Back 44

clump and form polymer strands leading to the sickle shape

Front 45

life span of a sickle cell RBC

Back 45

12-17 days

Front 46

solubility of Hgb S

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desaturated Hgb S is 50% less soluble than normal Hgb

Front 47

sickling in heterozygous SCA occurs

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in extreme conditions such as low flow and hypoxia

Front 48

what % of Black Americans have SC trait?

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10%

Front 49

sickling occurs at a PaO2 of what in trait

Back 49

20-30 torr

Front 50

what % in SC trait is Hgb S

Back 50

30 - 50%

Front 51

what % of Black Americans have SC disease?

Back 51

1%

Front 52

% of Hgb S in patients with SC disease

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70 - 98%

Front 53

sickling occurs in patients with SC disease at what pressure

Back 53

30 - 50 torr

Front 54

the average P50 value for Hgb S is

Back 54

31 torr

Front 55

children with SC exhibit

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symptoms as their HgbF is replaced by Hgb S, retarded growth, and frequent infections

Front 56

diagnosis of SCA is obtained by

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electrophoresis which detects and measures each Hgb type

Front 57

death from SCA occurs from

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kidney failure or infection

Front 58

Hgb S has higher or lower affinity for O2 than normal Hgb

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lower

Front 59

most common manifestation of SCA is

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pain

Front 60

physiology of pain associated with SCA

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sickled cells adhere more easily to vascular walls which then activates the clotting cascade and inflammatory systems. Flow problems occurs. The cells rupture releasing oxidative substances that prevent NO from being released, causing vasoconstriction

Front 61

Sickle Cell crisis is when

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painful episodes are coupled with life threatening organ events

Front 62

organs prone to infarct in patients with SCA

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kidney, heart, lungs

Front 63

remember with SCA to

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monitor and give fluid

Front 64

sickle cells end up

Back 64

being sequestered in the spleen causing some LUQ pain. Splenectomy may help.