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Patho 2 > 3 - Blood Physiology > Flashcards

3 - Blood Physiology Flashcards

1
Q

RBCs can concentrate hemoglobin in the cell fluid up to:

A

34g/100ml of CELLS
This is the metabolic limit of the cell’s hemoglobin-forming mechanism

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2
Q

In normal people, the percentage of hemoglobin is almost always:

A

the maximum percentage (34% of cells, which equates to 14-15g/dL)

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3
Q

How does hemoglobin circulate in humans?

A

INSIDE RBCs (not bound to the outside)

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4
Q

How much oxygen can be carried by hemoglobin in 100ml of blood?

A

Each g of Hgb can bind with 1.34ml O2, which means
19-20ml O2/100ml blood

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5
Q

Where are RBCs produced in utero? After birth?

A

Liver
Bone Marrow

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6
Q

When do long bones stop producing RBCs?

A

Around 20 years old

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7
Q

RBCs in adults are produced in which bones?

A

membranous bones: vertebrae, ribs, sternum, ilia

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8
Q

All cells in circulating blood are derived from which cell?

A

multipotential hematopoetic stem cell

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9
Q

How is the supply of multipotential hematopoetic stem cells maintained?

A

Every time one is triggered to reproduce, it produces another stem cell in addition to the other cells it multiplies into

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10
Q

Which growth inducer promotes growth and reproduction of virtually all the different types of committed stem cells?

A

Interleukin-3

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11
Q

What differentiates a reticulocyte from a full grown erythrocyte?

A

still contains a small amount of basophilic material (remnants of unnecessary organelles)
These organelles disappear over 1-2 days

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12
Q

The principal stimulus for RBC production in a low oxygen state is:

A

circulating erythropoietin

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13
Q

On a cellular level, how do the kidneys trigger RBC production in hypoxemic states?

A

Renal tissue hypoxia leads to high levels of Hypoxia-Inducible Factor 1 (HIF-1)
HIF-1 is a transcription factor, increasing transcription and production of erythropoietin

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14
Q

If erythropoietin is produced in the kidneys, why do RBC levels increase if other parts of the body are hypoxemic, even if the kidneys are not?

A

Somehow other tissues are able to send signals to the kidney

Circulating NE, Epi, and prostaglandins also stimulate erythropoietin

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15
Q

If someone’s kidneys are both removed or dead, how much erythropoietin can they make?

A

About 10% of normal, which is the percentage usually made by the liver

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16
Q

In hypoxic states, erythropoietin is produced within minutes. How long does it take for new RBCs to appear?

A

About 5 days
Erythropoietin stimulates growth, but it also increases the RATE of RBC production

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17
Q

Which two vitamins are essential to the final maturation of RBCs?
Why?

A

Vitamin B12 and Folic Acid

Required for formation of thymidine triphosphate, which is a building block of DNA

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18
Q

What are the characteristics of blood cells formed with deficient Vitamin B12 and/or Folic Acid?

A

Large RBCs (macrocytes)
flimsy membranes
Irregular shapes
they can carry oxygen, but have live about half or 1/3 as long d/t fragility

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19
Q

Vit B12/Folic Acid deficit anemia is called:

A

maturation failure anemia

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20
Q

Why is intrinsic factor necessary for B12 absorption?

A

Binds tightly with B12, and the binding protects from digestion by secretions

IF ferries it to the brush border and transports it into the blood via pinocytosis

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21
Q

Where is B12 stored?

A

Liver

Released in response to bone marrow levels

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22
Q

How long does abnormal B12 absorption have to take place to cause anemia?

A

Takes about 3-4 years to work through all the B12 stored in the liver

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23
Q

Besides deficient intrinsic factor, what else can cause B12/folic acid deficiency?

A

Any sort of malabsorption syndrome (sprue)

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24
Q

The most common form of hemoglobin in adults is:

A

Hemoglobin A

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25
Q

Every hemoglobin molecule is comprised of:

A

Four heme prosthetic groups

Four hemoglobin chains

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26
Q

Every molecule of hemoglobin can carry _____ atoms and _____ molecules of oxygen

A

8

4

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27
Q

On a cellular level, what causes sickle cell anemia?

A

One of the amino acids on the hemoglobin’s beta chains is substituted

When it’s exposed to low oxygen, it forms elongated crystals inside the RBC, making it almost impossible for the cell to pass through tiny capillaries

Moreover, the crystals can rupture the cell membrane, leading to hemolysis

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28
Q

Why does O2 dissociate so easily from hemoglobin?

A

It binds very loosely with the iron atom via a coordination bond

the oxygen doesn’t become ionic when it’s bound, it remains a molecule

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29
Q

What percentage of iron in the body exists as hemoglobin?

A

65%

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30
Q

What is hypochromic anemia?

A

RBCs with much less hemoglobin than normal

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31
Q

When there is more iron in the body than can be stored as ferritin, what happens?

A

It is stored in the cells as hemosiderin

Unlike ferritin, hemosiderin forms large clusters inside the cell and can be seen on a microscope

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32
Q

Describe the process of iron absorption:

A
  1. liver secretes apotransferrin into bile
  2. apotransferrin binds with free iron and iron compounds in the gut, forming transferrin
  3. Transferrin binds to receptors in intestinal epithelial cells
  4. Released into the blood stream as plasma transferrin
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33
Q

How quickly does iron absorption occur?

A

Extremely slowly

Maximum rate of a couple mg per day

You can’t fix an iron deficiency quickly with diet

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34
Q

Which organelles do RBCs have?

A

They DON’T have a nucleus, mitochondria, or ER

The do have cytoplasmic enzymes that can metabolize glucose and form small amounts of ATP

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35
Q

Which cells are responsible for breaking down hemoglobin?

A

Macrophages in the intestines (Kupffer cells), spleen, and bone marrow

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36
Q

What is anemia?

What are the two broad causes?

A

A deficiency of hemoglobin in the blood

can be caused by too few RBCs or too little Hgb within those RBCs

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37
Q

After a hemorrhage, how long does it take for plasma cells to replenish? RBCs?

A

1-3 days

3-6 weeks

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38
Q

Why does chronic blood loss result in microcytic hypochromic anemia?

A

The body can’t absorb enough iron from the intestines to form Hgb as rapidly as it’s being depleted, so the RBCs are smaller and contain less Hgb

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39
Q

What causes aplastic anemia?

A

Bone marrow aplasia of some kind.

Idiopathic in 50% of cases

Other causes: radiation, toxic chemicals, lupus (immune system attacks bone marrow stem cells)

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40
Q

What is megaloblastic anemia?

What causes it?

A

Large RBCs with odd shapes

pernicious anemia, total gastrectomy, intestinal sprue

41
Q

What is hemolytic anemia?

A

fragile RBCs with short life spans that are destroyed faster than they can be formed

42
Q

What is hereditary spherocytosis?

A

RBCs are small and spherical, can’t withstand any compression (get ruptured in the spleen)

43
Q

Sickle cell anemia is caused by an abnormal types of Hgb called:

A

Hgb S

44
Q

What is erythroblastosis fetalis?

A

Rh-positive RBCs in fetus attacked by antibodies from Rh-negative mother

45
Q

What is secondary polycythemia?

A

Increased RBCs in response to hypoxia

Can either be caused by pathological causes or living at a higher elevation

46
Q

What is polycythemia vera?

A

blast cells don’t stop producing RBCs even when too many cells are already present

Usually causes excess amounts of platelets and WBCs too

47
Q

How is cardiac output effected in polycythemia vera?

A

blood viscosity decreases preload, and increased blood volume increases preload

The two pretty much neutralize each other, and CO is often normal

48
Q

What are the two types of antigens involved in blood typing?

A

The ABO system and the Rh system

49
Q

What are agglutinogens?

Which ones are found on human RBCs?

A

antigens that cause RBC agglutination

A and B antigens

50
Q

Type O blood contains which agglutinogens?

A

Neither A nor B

The type O allele is pretty much inert and causes no agglutination

51
Q

What are the frequencies of the blood types?

A

O: 47%

A: 41%

B: 9%

AB: 3%

52
Q

What are agglutinins?

A

IgG and IgM immunoglobulins

when type A agglutinogen is NOT PRESENT in the RBCs, they develop anti-A agglutinins

53
Q

Why do agglutinins cause clumping?

A

When anti-A agglutinins are mixed with blood that contains A agglutinogens, the agglutinins attach themselves to the RBCs

BUT the agglutinins have multiple binding sites, so they attach multiple RBCs, and clumps form

54
Q

In blood transfusion reactions, what mediates acute hemolysis?

Delayed hemolysis?

A

Acute: activation of the complement system and formation of membrane attack complexes

Delayed: clumping due to agglutination

55
Q

Is immediate or delayed hemolysis more common?

A

Delayed

56
Q

What factors must align for an immediate hemolysis to occur with a blood transfusion?

A

A very high titer of antibodies

different types of antibodies, primarily IgM, called hemolysins

57
Q

How many Rh antigens are there?

Which one is most prevalent?

A

6

D

58
Q

Someone who is called “Rh Negative” does not have ______

A

type D Rh antigen

59
Q

What skin color has the highest rate of Rh negative?

A

Whites! 85% Rh positive

Everyone else is over 95%

60
Q

How long does it take to form Anti-Rh agglutinins?

A

2-4 months

61
Q

In most cases of erythroblastosis fetalis, the mother is Rh ____ and the father is Rh _____

A

negative

positive

62
Q

How can erythroblastosis fetalis be treated?

A

Infusing Rh-negative blood to the infant while removing Rh -positive blood

By the time the infant produces its own Rh-positive blood cells again, the mother’s macrophages are dead

63
Q

Why do neonates who survive erythroblastosis fetalis often have brain damage?

A

Kernicterus

64
Q

How does Rhogam work?

A

Binds to the D antigen on the fetus, preventing detection by maternal macrophages

Somehow inhibits B lymphocyte antibody production in the expectant mother

65
Q

Why do hemolytic transfusion reactions cause kidney failure?

A
  1. toxins released from hemolysis cause renal vasoconstriction
  2. decreased RBCs + toxins = circulatory shock and decreased RBF
  3. if free hemoglobin is greater than the amount of haptoglobin, the rest leaks into the glomerular membranes and clogs up the tubules
66
Q

Define:

Autograft

Isograft

Allograft

Xenograft

A

Auto: from same person

Iso: from identical twin

Allo: from one person to another

Xeno: from nonhuman animal to human

67
Q

What is the difference between serum and plasma?

A

Serum is plasma that has been allowed to clot in the lab to remove fibrinogen and other clotting factors

68
Q

Where are immunoglobulins produced?

A

by plasma cells in the lymph nodes and other lymphoid tissues

69
Q

The other name for platelets is:

A

thrombocytes

70
Q

Why do RBCs have such a limited lifespan?

A

They can’t undergo mitosis

71
Q

WBCs are categorized by structure into ___ or _____

And by function into ____ or _____

A

granulocytes or agranulocytes

phagocytes or immunocytes

72
Q

What gives granulocytes their name?

A

Contain membrane-bound granules with digestive enzymes and inflammatory mediators

73
Q

How are granulocytes transported to sites of injury?

A

They move themselves, like amoebas!!

Called diapedesis

74
Q

What is the most numerous granulocyte?

A

Neutrophil

60% of WBCs

75
Q

Once neutrophils are activated, how long do they live?

A

1-2 days

Their death (and release of granules) causes debridement

76
Q

List the four granulocytes:

A

Neutrophils

Eosinophils

Basophils

Mast cells

77
Q

Describe the granular actions of the four granulocytes (what do they eat/produce?)

A

Neutrophils - digestive enzymes for large microorganisms/debris

Eosinophils - digestive enzymes for antigen-antibody complexes and viruses

Basophils - chemical mediators and anticoagulant (think IgE)

Mast cells - chemical mediators (particularly vasoconstriction)

78
Q

What are the three agranulocytes?

A

monocytes

macrophages

lymphocytes

79
Q

_____ and ____ make up the mononuclear phagocyte system

A

monocytes

macrophages

80
Q

What is the difference between monocytes and macrophages?

A

Monocytes are immature or undifferentiated macrophages

81
Q

Platelets have a _____ cell type

A

They really aren’t cells!

Just irregularly shaped cytoplasmic fragments that help with coagulation

82
Q

What are the primary lymphoid organs?

A

Thymus and bone marrow

83
Q

What are the secondary lymphoid organs?

A

spleen, lymph nodes, tonsils, peyer patches

84
Q

What are the sequelae of spleen removal?

A
  1. Leukocytosis
  2. increased circulating iron
  3. Diminished IgM response
  4. Increased # of defective RBCs and platelets
  5. Thrombocytosis, thrombosis
85
Q

______ are the primary site for the first encounter between antigens and lymphocytes

A

lymph nodes

86
Q

How do lymphocytes get into lymph nodes?

A

diapedesis across the epithelial membrane!

87
Q

The typical human requires ______ new blood cells each day

A

100 billion!

88
Q

Where does hematopoiesis occur in adults? In a fetus?

A

bone marrow

liver and spleen

89
Q

____ and ____ mature differentiate fully before entering the blood

____ and ____ continue to mature in the blood and secondary lymph organs

A

erythrocytes and granulocytes

monocytes and lymphocytes

90
Q

What is extramedullary hematopoiesis?

A

blood cell production in tissues other than the bone marrow

91
Q

Which cytokines stimulate hematopoiesis?

A

Colony-stimulating factors

92
Q

What are the two pools of hematopoiesis?

A

the stem cell pool (maintains the number of pluripotent stem cells)

The bone marrow pool (cells that are actively proliferating and maturing)

93
Q

What is the marginating storage pool?

A

In blood vessels, neutrophils are stored by adhering to the endothelium until needed for an inflammatory response

94
Q

What is the most significant side effect of exogenous r-HuEPO?

A

Hypertension

95
Q

_____ iron can bind and release oxygen. ____ Iron cannot

A

Fe2+ (Ferrous)

Fe3+ (Ferric)

96
Q

What is deoxyhemoglobin and oxyhemoglobin?

A

Binding of oxygen to ferrous iron creates oxyhemoglobin

Release of oxygen reduces iron back to ferrous iron (deoxyhemoglobin)

97
Q

What is methemoglobin?

Why is it problematic?

A

Hemoglobin whose iron has not been reduced

In order for oxyhemoglobin to once again become deoxyhemoglobin (which can bind with oxygen), the ferric iron (Fe3+) has to be reduced back to ferrous iron (Fe2+) by methemoglobin reductase

Methemoglobin cannot bind with O2

98
Q

Which is more common: folate deficiency or Vit B12 deficiency?

A

Folate

the body only contains a couple months’ worth of folate, vs years of B12

Patho 2 (24 decks)

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