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Bio 252- atherosclerosis > Anemia > Flashcards

Anemia Flashcards

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Biology 101 flashcards
1
Q

anemia is _______ blood disorder

A

most common

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2
Q

anemia is the deficiency of

A

RBCS and hemoglobin

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3
Q

deficiency of RBCs and hemoglobin due to

A
  • problems with erythropoiesis
  • increased/excessive loss of RBCS (bleeding)
  • increased hemolysis: breakdown prior to usual time (aprox 120 days)
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4
Q

Patho of anemia

A
  • abnormal number, structure or function of RBC
  • decrease in oxygen carrying capacity
  • hypoxia
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5
Q

what is the primary manifestation that underpins all other complications of anemia

A

Hypoxia

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6
Q

Iron deficiency anemia

A
  • need iron to make hemoglobin
  • inadequate intake or increased loss of iron
  • iron binds to oxygen molecules for transport
  • impaired hemoglobin synthesis
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7
Q

what are the manifestations of severe anemia

A
  • chronic exhaustion
  • excessive palpitations
  • profound weakness & dizziness
  • headache (brain will be hypoxic too)
  • sensitivity to cold (no 02, not able to carry out anaerobic metabolism, not able to carry heat)
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8
Q

you need iron to make

A

hemoglobin

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9
Q

Treatment of iron deficient anemia

A
  • treat underlying cause

- iron supplements, Fe p.o. for 4-6m

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10
Q

iron deficiency usually because not taking enough

A

dietary iron

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11
Q

test to find out if iron deficient

A

measure iron concentration (NOT A CBC)

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12
Q

Vitamin b12 & Folic acid deficiency

A
  • responsible for DNA synthesis, invovled in cell division, DNA replication
  • abnormal DNA synthesis & cell maturation – imparied RBC, WBC & platelets (cells will not mature)
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13
Q

Treatment of Vitamin b12 & folic acid deficiency

A
  • vit B12 & folic acid (supplemental) (dietary deficiency)
  • could have a deficiency in one or both
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14
Q

Pernicious anemia

A
  • damaged gastric mucosa
  • no intrinsic factor (intrinsic factor produced in mucosa of stomach)
  • poor B12 absorption (RBC PRODUCTION IS IMPAIRED)
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15
Q

pernicious anemia is often in people who have had

A

gastric surgery

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16
Q

Treatment of pernicious anemia

A
  • high dose of vit b12 p.o. (if high dose, some of b12 absorbed without intrinisic factor needed)
  • IM b12 injection (only if neuro symptoms present) (IM does through without passing through stomach)
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17
Q

Aplastic anemia (no cell anemia)

A
  • marrow (stem cell failure) – defects exists in marrow

- all blood cells affected

18
Q

Aplastic anemia Treatment

A
  • Transfusions
  • immune suppression
  • marrow transplant (get rid of everything in marrow, donor marrow complex severely compromised when eradicating)
19
Q

Aplastic anemia is from

A
  • 1/3 autoimmune, radiation, toxic chemicals

- 2/3 are idiopathic

20
Q

Hemolytic anemia

A
  • premature or excessive hemolysis (rupture or destruction of RBCS)
  • accquired type (eg. autoimmunity, drugs) targeting erythrocytes
  • genetic type (eg. in thalassemia)
21
Q

Thanlassemia

A

genetic type of hemolytic anemia

-defective synthesis of hemoglobin putting together doesn’t happen normally

22
Q

Manifestations of hemolytic anemia

A

same as general plus:

  • Jaundice: excessive bilirubin-bilirubin gets in blood stream, liver can’t keep up to excrete
  • Splenomegaly: spleen expands to meed demand of excretion, increase # of cells there also causes it to enlarge
  • Hepatomegaly: demand, size and lots of material causes enarlged liver
23
Q

Treatment of hemolytic anemia

A
  • underlying cause
  • 02 for nypoxia
  • transfusion
  • steroids (to halt hemolysis) (cant use long term, can cause damaging side effects)
  • Renal function (precipitation in renal tubule d/t hemolysis)
  • Spleenectomy (if too many rbcs being removed, some fxs can be taken over by liver -individual can fx without spleen, have to know hemolysis is happening in spleen)
24
Q

Acute Hemorrhagic Anemia

A

rapid loss of blood (RBCS, hemoglobin, Fe) whole blood

-severity based on site, rate & volume lost

25
Q

Chronic Hemorrhagic Anemia

A

gradual ongoing blood loss (less easily detected and persists for longer time

26
Q

Major causes of chronic hemorrhagic anemia

A
  • prolonged or heavy menses
  • Bleeding peptic ulcers: bleeding happening in upper GI tract, occult blood will not know there is blood in stool)
  • Cancerous lesions of GI tract
  • hemorrhoids (frank blood)
27
Q

Frank blood is

A

blood from hemorrhoids can see in the toilet bowl

28
Q

Treatment of Hemorrhagic anemia

A

-eliminate cause

29
Q

Sickle cell anemia is

A

genetic, homozygus recessive

30
Q

what is homozygus recessive

A

two matched defective alleles
-matched means they have to be coding for the same thing
Both parents have to be carrier

31
Q

If heterozygus (sickle cell)

A

it is sickle cell trait (no manifestations or mild manifestations not fully fledged)

32
Q

sickle cell anmeia has HBS (hemoglobin sickle cell)instead of

A

Hba (hemogolbin adult)

33
Q

mnfts of sickle cell anemia:

A

all in general +

  • hemolysis
  • thrombosis & infarction
  • increase in bilirubin
34
Q

sickle cell anemia has valine instead of

A

glutamic acid

35
Q

Glutamic acid

A

acid is normal amino acid needed

36
Q

with sickle cell has valine and this causes a different form of _______

A

Hemogolobin (sickle cell hemoglobin)

37
Q

Path of sickle cell anemia

A
  • Hbs instead of Hba
  • Hbs crystallizes on dissociation at low P02
  • Rbc deforms & sickles
  • chronic hemolysis
  • vessel occlusion
  • ischemia
  • infarction
  • obstructed capillaries
  • hypoxia
  • more sickling
38
Q

Treatment of sickle cell anemia

A
  • supportive (02, analgesics, IV fluids & electrolytes)
  • Hypertransfusion in increased risk (eg. SX, preganacy
  • Hydroxyurea (used sparingly, only if needed side effects can can cause leukemia)
  • marrow, stem cell transplant (not easy)
39
Q

Sickle cell breakdown becomes viscous causing

A
  • increase in viscostiy
  • impairs circulation
  • occlusion & further hypoxia
  • more RBC’s sickle viscous cycle
40
Q

Hbs is 50X less soluble than

A

Hba, this is not a problem if stays in erythrocyte but if it comes out into blood it is

41
Q

Sickle cell cannot

A

move through blood vessel properly

42
Q

what are the two reasons to use hydroxureya

A
  • increases production of fetal hemoglobin

- tends to breakdown erythrocytes before they sickle

Bio 252- atherosclerosis (37 decks)

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