Nov. 4, 2019 Flashcards

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1
Q

What is the role of Fe in the blood?

A

Binds o2

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2
Q

Inadeq intake of Fe results in..?

A

Defective Hgb synth

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3
Q

Why is CBC not the diagnostic test of choice for IRON DEFICIENT ANEMIA?

A
  • RBC count may be normal

- Doesn’t actually measure Fe

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4
Q

What test should you run for IRON DEF AN?

A

Ferritin test

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5
Q

Treatment of IRON DEF AN is..?

A

Treat the cause by supplementing Fe

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6
Q

How long should you supplement Fe for?

A

4-6 months

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7
Q

Adverse affect of excess Fe:

A
  • Toxicity

- Constipation

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8
Q

What are Vit B12 and folic acid needed for?

A

Cell division

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9
Q

What is an adverse affect of inadeq Vit b12 and folic acid?

A

Abn DNA synth and cellular material resulting in defective B cells

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10
Q

What is the Tx of B12 and folic acid deficiency?

A

Supplement

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11
Q

T or F:

PERNICIOUS ANEMIA is from a deficiency of B12 in diet

A

F, it is from deficiency in secretion of INTRINSIC FACTOR

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12
Q

What might result in a deficiency in secretion of INTRINSIC FACTOR?

A

Damage to gastric mucosa

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13
Q

Adverse effects of PERNI AN?

A
  • Poor to no B12 absorption

- Impaired cell synth

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14
Q

What is the Tx of PERNI AN?

A
  • High dose of B12 PO

- If presenting w more symptoms, give B12 IM

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15
Q

Should you supplement INSTRIN FACT in PERN AN?

A

No

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16
Q

What cells are involved in APLASTIC AN?

A

RBCs

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17
Q

The “A” in APLASTIC AN refers to what?

A

A = lack of

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18
Q

What is APLASTIC AN caused by?

A

Marrow (stem cell) failure

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19
Q

How does marrow faiure affect RBCs?

A

Causes defective hematopoiesis

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20
Q

What is the Et of APLASTIC AN?

A

65% idiopathic

35% Autoimmune, radiation, toxic chemicals

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21
Q

Tx of APLASTIC AN

A
  • Transfusions

- Marrow transplant in extreme situations

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22
Q

WHat is the avg lifespan of RBCs?

A

120 days (~4 months)

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23
Q

What removes old RBCs?

A

The spleen

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24
Q

Where are RBCs recycled?

A

In the liver

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25
Q

What causes HEMOLYTIC AN?

A

Premature or excessive HEMOLYSIS

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26
Q

What might cause HEMOLYTIC AN?

A
  • May be d/t genetics (eg THALASSEMIA)

- Acquired (eg autoimmune, drugs)

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27
Q

Define THALASSEMIA

A

Genetic, causes abn form or inadeq amounts of Hgb

28
Q

Mnfts of HEMOLYTIC AN

A
  • The ones from other ANs
  • Jaundice
  • Splenomegaly (enlarged spleen)
  • Hepatomegaly (enlarged liver)
29
Q

Why does JAUNDICE occur in HEMOLYTIC AN?

A

If liver is not working properly, bilirubin will accum in the liver, go through circulation, and deposit in tissues

30
Q

Why does SPLENOMEGALY occur in HEMOLYTIC AN?

A

Spleen is under enormous pressure and enlarges in an attempt to meet the additional workload

31
Q

Why does HEPATOMEGALY occur in HEMOLYTIC AN?

A

Liver is under enormous pressure and enlarges in an attempt to meet the additional workload

32
Q

What is the Tx for HEMOLYTIC AN?

A
  • o2 for hypoxia
  • Steroids
  • Transfusion
  • Splenectomy if extreme
33
Q

Define ACUTE HEMORRHAGIC AN

A
  • Rapid onset

- severity based on site, rate, and vol

34
Q

Define CHRONIC HEMOR AN

A
  • Gradual bleed

- Subtle, concealed

35
Q

4 things that may result in HEMOR AN:

A

1) Peptic ulcer disease (PUD)
2) Tumor
3) Heavy menses
4) Hemorrhoids

36
Q

How does PUD mnft?

A

As occult blood in stool

37
Q

What are hemorrhoids?

A

Varicose veins in rectal area

38
Q

What is the Tx of HEMOR AN?

A

Treat the cause

39
Q

Is SICKLE CELL AN ACUTE or CHRONIC?

A

CHRONIC

40
Q

What kind of GENETIC DISEASE is SI CELL AN?

A

Recessive

41
Q

In SI CELL AN, what GENE is mutated?

A

The GENE that codes for Hgb

42
Q

T or F:

In SI CELL AN, HbA is created instead of HbS

A

F, other way around

43
Q

How many affected ALLELES in SI CELL TRAIT?

A

1

44
Q

If someone hase the SI CELL AN TRAIT, would that be considered homozygous or heterozygous?

A

hetero

45
Q

What is GLUTAMIC ACID?

A

HbA

46
Q

What is VALINE?

A

HbS

47
Q

Explain the relationship between HbA, HbS, and SI CELL AN?

A

HbS replaces HbA in the beta hemoglobin chain

48
Q

T or F:

Loads at high pCO2, dissociates at low pCO2

A

T, but I don’t know what it means…?

49
Q

Why are HbSs lysed?

A

Because the body doesn’t recognize them and they are therefore destroyed

50
Q

What happens when the SI CELLS are lysed?

A

The crystals inside of them are released

51
Q

What happens to the B as a result of crystals being released?

A

The viscosity of the B is increased

52
Q

Why does SI CELL AN cause obstructed flow?

A

Because their shape is not ideal for flowing easily through BVs

53
Q

What is caused by uncontrolled ISCHEMIA?

A

INFARCTION

54
Q

When the vessels are obstructed, what is caused?

A

HYPOXIA

55
Q

In someone with SI CELL AN, HYPOXIA leads to..?

A

More sickeling

56
Q

WHy does HYPOX lead to more sickeling?

A

HYPOXIA lowers the pO2, which causes more dissociating

57
Q

Is SI CELL AN a local or systemic disease?

A

systemic, affects any tissue requiring O2

58
Q

What are 4 mnfts of SI CELL AN?

A
  • HEMOLYSIS
  • Inc BILIRUBIN
  • THROMBOSIS
  • INFARCT
59
Q

Why do many components of SI CELL AN end up in the KIDNEYS?

A

Because the LIVER cannot handle it all

60
Q

Tx for SI CELL AN?

A
  • Supportive
    • Rest, O2, pain control, fluids, lytes
  • Hypertransfusion
    • Give donor B until they have 50% donor B with HbA
  • Hydroxyurea
    • used rarely
    • can cause leukemia,
    • hepatotoxic
    • toxic to marrow
    • Facilitates production of fetal Hgb
    • Limits hemolysis of sickle cells
  • Marrow transplant
61
Q

Define HYPERFX:

A

Endocrine gland secretes too much of a hormone

62
Q

Define HYPOFX:

A

Endo gland secretes little to no hormone

63
Q

What might cause HYPERFX?

A

Inc tropic stimulation (you need negative feedback to keep control of this)

64
Q

What might result in HYPOFX?

A
  • No tropic stimulation (leads to atrophy)
  • Receptor defect
  • Immune disorder
  • Suppressive Tx
  • Lack of iodine in diet (needed for thyroid Fx)
  • Metb deficiency
65
Q

What is the leading ENDO DISEASE?

A

DIABETES MELLITUS (DM)

66
Q

DM is caused by a deficiency of INSULIN in either ________ or ________

A

Quality, action

67
Q

2 other causes of DM?

A

1) Compromised glucose homeostasis

2) Widespread metb problems