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Patho Exam 2 > Hematologic > Flashcards

Hematologic Flashcards

1
Q

what is blood composed of

A

RBCs, WBCs, and platelets

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2
Q

what are pluripotent stem cells

A

precursor cells of all blood cells they can become hematopoietic stem cells

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3
Q

list the 3 categories of WBCs

A
  1. monocytes (w/ granules)
  2. lymphocytes (b cells or t cells)
  3. granulocytes (neutrophils, basophils, eosinophils)
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4
Q

how much of WBCs do monocytes/macrophages make up (%)?

A

monocytes make up approximately 3-7% of all WBCs

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5
Q

how much of WBCs do lymphocytes make up (%)?

A

lymphocytes make up approximately 20-35% of all WBCs

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6
Q

how much of WBCs do neutrophils make up (%)?

A

neutrophils make up approximately 60-70% of all WBCs

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7
Q

neutrophils are also known as what?

A

PMNs = polymorphonuclear leukocytes

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8
Q

what is the difference between segs and bands (these are neutrophils)?

A
  • segs are mature neutrophils that are segmented

- bands are immature neutrophils, they are elevated during infection or severe inflammation

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9
Q

when are bands released?

A

neutrophil bands are released from the bone marrow when the segs have been exhausted
= aka neutrophilia, the increased # of bands

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10
Q

what is the range of neutrophils found in the blood?

A

neutrophils = 4,100 - 10,900 cells/microliter (uL)

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11
Q

how many uL of WBC deem the person to have leukocytosis?

A

above 11,000 uL

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12
Q

what is a leukemoid reaction?

A

this is leukocytosis w/ WBC greater than 50,000 uL, typically from leukemia
- there is an excess of normal early neutrophil precursors

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13
Q

in leukemia, there is a predominance of cancerous and immature WBCs called ______?

A

in leukemia, there is a predominance of cancerous and immature WBCs called BLASTS

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14
Q

how many uL of WBC deem the person to have leukopenia?

A

WBC count below 4,000 uL

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15
Q

how many uL of WBC deem the person to have neutrophilia?

A

in a WBC of 11,000 cells/uL, there are more than 7,700 uL of neutrophils

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16
Q

how many uL of WBC deem the person to have neutropenia?

A

a lack of neutrophils below 1,000 is considered severe and the s/s of inflammation are diminished

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17
Q

what is myelodysplastic syndrome (MDS)

A

this is a disorder affecting the bone marrow (all or some of it) = resulting in a decreased number of at least of the following:

  1. WBC
  2. RBC
  3. Platelets
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18
Q

what are the possible causes of myelodysplastic syndrome (MDS)?

A
  1. exposure to radiation
  2. exposure to benzene
  3. exposure to industrial solvents (like plastics, lubricants, rubbers)
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19
Q

secondary MDS can be caused by what?

A

toxic effect of cancer treatments

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20
Q

s/s of MDS

A

depends on what type of blood cells are affected!

  1. if RBC = s/s of anemia
  2. if WBC = s/s of infection
  3. if platelets = bleeding tendencies
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21
Q

describe leukemia

A

a malignancy in the blood, cancer of the immature WBCs in the bone marrow

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22
Q

describe lymphoma

A

a malignancy in the lymph nodes

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23
Q

name the 2 types of neoplasms

A
  1. leukemia

2. lymphoma

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24
Q

describe the etiology of neoplasms in the blood

A
  1. DNA damage
  2. associated with gene abnormality particularly Philadelphia chromosome (Phc)
  3. associated with changes to the whole chromosome as trisomy (3 vs 2) or monosomy (1 vs 2)
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25
Q

risk factors of developing neoplasms of the blood(6)

A
  1. intense radiation
  2. benzene
  3. some viruses like Epstein Barr or HIV
  4. pesticides/herbicides
  5. chemotherapy/radiation as treatment
  6. repeated/chronic infection with H. pylori (peptic ulcers)
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26
Q

describe the pathway of how blood stem cells (hematopoietics) mature

A
  1. myeloid stem cell
  2. RBC, platelet or myeloblast
  3. if myelobast = granulocyte
  4. granulocyte = neutrophil, basophil, eosinophil

OR

  1. lymphoid stem cell
  2. lymphoblast
  3. B cell, T cell, natural killer cells
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27
Q

what is the common pathologic feature of leukemia

A

uncontrolled proliferation of malignant leukocytes

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28
Q

describe myelocytic leukemia

A

malignant leukocytes arising from the myeloid lineage within the bone marrow

= either (1) acute myelogenous leukemia or (2) chronic myelogenous leukemia

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29
Q

describe lymphocytic leukemia

A

malignant leukocytes arising from the lymphoid lineage within the bone marrow

= either (1) acute lymphocytic leukemia or (2) chronic lymphocytic leukemia

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30
Q

which lymphocytic leukemia is more fatal

A

acute lymphocytic leukemia

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31
Q

where can leukemic cells infiltrate/disperse in the body

A
  1. liver, spleen, lymph nodes = causing enlargement
  2. cross the BBB = affect the brain
  3. any other body organ
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32
Q

what is the most common type of cancer in the US

A

lymphoma

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33
Q

name the 2 categories of lymphoma

A
  1. Hodgkin’s lymphoma (HL)

2. non-Hodgkin’s lymphoma (NHL)

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34
Q

HL vs NHL have similar s/s but how do they vary under microscopic examination?

A
  • HL develops abnormal from B-cells
  • NHL can develop from either B-cells or T-cells

1 difference is the presence of mononuclear tumor cells (Reed-Sternberg cells) in HL this is the hallmark diagnostic abnormality

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35
Q

what is the first sign of lympoma

A

painless enlarged lymph nodes in the neck, groin, or under the arms

s/s are secondary to the uncontrolled lymphoid tissue growth and bone marrow involvement

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36
Q

describe anemia

A

insufficient delivery of oxygen in RBC/Hgb to the tissues = cellular hypoxia and lack of cellular energy

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37
Q

RBC are also known as

A

erythrocytes

38
Q

what is the normal range for RBC in men

A

4.5 - 5.5 x 10^6 cells/cubic millimeter

39
Q

what is the normal range for RBC in women

A

4.0 - 4.9 x 10^6 cells/cubic millimeter

40
Q

describe the process of a pluripotent stem cell becoming a RBC

A
  1. pluripotent stem cell
  2. becomes erythroblast w/ aid from erythropoietin
  3. becomes normoblast
  4. develops into reticulocyte in the bone marrow
  5. fully matures into erythrocytes (bi-concave and non-nucleated)
41
Q

if there is increased blood loss at which step will RBCs be released prior to fully maturing?

A

once it becomes a reticulocyte, the bone marrow will release it into the blood stream = an increase in immature RBCs

42
Q

what influence does hypoxia have

A

major stimulus for erythropoiesis, a decreased level of oxygen at the tissue level like cyanosis

43
Q

what organ secretes erythropoietin?

A

the kidneys

44
Q

what does Hgb do?

A

Hgb carries oxygen to cells and takes carbon dioxide from the cells to the pulmonary circulation = oxygenated again

45
Q

what is the normal range of Hgb for men?

A

13-18 gm/dl

46
Q

what is the normal range of Hgb for women?

A

12-16 gm/dl

47
Q

what is the hematocrit

A

the percentage of blood that contains only RBCs

48
Q

what is the normal range of hematocrit (RBC) for men (%)?

A

45 - 52%

49
Q

what is the normal range of hematocrit (RBC) for women (%)?

A

37 - 48%

50
Q

why is iron important in the RBC

A

its is important in the synthesis of Hgb

51
Q

what are the causes of anemia

A
  1. acute blood loss
  2. chronic blood loss
  3. nutritional: lack of iron, B12, folate
  4. hemolysis
52
Q

how can we benefit anemia through nutrition?

A

intake of animal products (B12) and fresh fruits/veggies, beans, nuts and eggs (folate)

53
Q

what is hypovolemia

A

decreased blood and plasma volume

54
Q

describe the path from acute blood loss to the production of more RBCs

A
  1. acute blood loss
  2. hypovolemia and hypoxia
  3. triggers SNS
  4. increased HR, in attempt to deliver more blood and oxygen to the body

5a. hypovolemia triggers renin-angiotensin-aldosterone system (RAAS)
6a. increase in fluid reabsorption, in attempt to raise the blood volume and BP and less urinary output
&
5b. hypoxia triggers the kidney to produce erythropoietin
6b. stimulates bone marrow to produce more RBCs

55
Q

describe acute blood loss via overt vs covert

A
  • overt = gushing blood

- covert = internal bleeding

56
Q

describe chronic blood loss

A

body loses small amount of blood slowly over a period of time,
- the body can replace the volume lost BUT the body is unable to synthesize healthy RBCs, b/c they require iron, B12 and folate since they slowly became exhausted
= RBCs become iron deficient and now more prone to anemia here on out

57
Q

what is the end result of anemia

A

tissue hypoxia in the heart muscles and brain

58
Q

s/s of anemia

A
  1. pallor
  2. weakness and fatigue
  3. tachycardia and palpitation
  4. chest pain and dizziness (not as important)
59
Q

describe hemolytic anemia

A

occurs when RBC destruction is greater than RBC synthesis

60
Q

what is a special kind of hemolytic anemia

A

sickle cell anemia (SCA)

61
Q

who is sickle cell anemia typically found in

A
  1. African
  2. Middle Eastern
  3. Mediterranean
62
Q

what causes sickle cell anemia

A

abnormal Hgb called Hgb S, RBCs shape become distorted upon exposure to hypoxia or severe stress
= cells are less effective in delivering oxygen and more fragile = sickled RBCs are destroyed by the immune system
= HEMOLYSIS

63
Q

describe the path if sickled RBCs occlude capillaries

A
  1. sickled RBCs occlude capillaries
  2. ischemia in various organs
  3. vaso-occlusive crisis, commonly in chest, abdomen, long bones, joints

= SEVERE PAIN

64
Q

what are common triggers of vaso-occlusive crisis

A
  1. stress
  2. exposure to cold weather
  3. hypoxia
  4. infection
  5. dehydration
  6. high exertion
  7. pregnancy
65
Q

bleeding disorders are related to which blood type

A

platelets

66
Q

what is the normal range of platelets? (no difference between different genders)

A

150,000 - 400,000 per microliter

67
Q

what is a immature platelet and where is it found?

A

megakaryocytes in the bone marrow are immature platelets

68
Q

what composes platelets

A

contain procoagulant substances but lack a nucleus, DNA, and are unable to synthesize proteins

69
Q

what organ stimulates platelet formation?

A

the liver synthesizes thrombopoietin = platelet formation

70
Q

lifespan of platelets

A

7-10 days

71
Q

describe the path of platelets stimulating coagulation

A
  1. injury to the vessel
  2. platelets are drawn to the area
  3. platelets in the area are activated by exposed collagen and von Willebrand factor (vWF)
  4. activated platelets stimulate coagulation factors
    glycoprotein (GP) IIb / IIIa receptors
  5. activated platelets release adhesive proteins and growth factors to further cause aggregation, draw more platelets to the site and facilitate clot formation
  6. thrombus is stabilized by fibrin
72
Q

what does fibrin do

A
  • fibrin strengthens the platelet plug from the primary hemostasis
  • while secondary hemostasis is the formation of thrombus to prevent excessive blood loss requires the activation of coagulation factors, ultimately forming fibrin
73
Q

what are the 2 pathways of the coagulation cascade

A
  1. intrinsic pathways

2. extrinsic pathways (aka tissue factor/TF)

74
Q

describe the extrinsic pathway of coagulation

A
  1. trauma to blood vessel
  2. factor VII (7) is activated and comes in contact w/ fibroblasts or leukocytes in the site = form TF-factor VII (7)
  3. TF-factor VII (7) activates factor X (10)
  4. factor Xa (10a) and factor V (5) form a complex
  5. complex activates prothrombin to thrombin
  6. conversion of fibrinogen to fibrin
  7. thrombin activates XIII (13) / XIIIa (13a)
  8. forms a stable fibrin clot
75
Q

how is clotting time for extrinsic pathway measured?

A

prothrombin time

76
Q

describe the intrinsic pathway of coagulation

A
  1. stasis of blood or tissue damage due to inflammation or atherosclerosis
  2. factor XIII (13) –> factor XI (11) –> factor IX (9) are all activated
  3. the three of them activate factor X (10) (extrinsic pathway comes in)
  4. factor X (10) and factor V (5) activate the conversion of prothrombin to thrombin (extrinsic pathway)
77
Q

how is clotting time for intrinsic pathway measured?

A

activated partial thromboplastin time (aPTT) when someone is on Heparin, a blood clot inhibitor

78
Q

describe clot dissolution

A

begins shortly after a clot forms, allows blood flow to be reestablished and tissue repair to take place

79
Q

what is fibrinolysis

A

the process by which a blood clot is dissolved

80
Q

what is plasminogen

A

proenzyme for fibrinolytic process
- this is present in the blood in its inactive form
- this is converted into plasmin by the plasminogen activator
= plasmin digests fibrin strands of the clot

81
Q

what is hypercoagulability

A

this problem is characterized by increased platelet activity or there is an enhanced formation of coagulation factor

82
Q

what are the causes of hypercoagulability

A
  1. increased platelet activity such as:
    - atherosclerosis
    - diabetes mellitus
    - hypercholesterolemia
    - increased number of platelets (like critically ill)
    - smoking
    - splenectomy
  2. enhanced formation of coagulation factor such as:
    - atrial fibrillation
    - use of oral contraceptives
    - immobility
    - pregnancy/post-partum
83
Q

what is the concern with DVT (a type of hypercoagulability)

A

it can travel to the IVC and reach the pulmonary artery

= pulmonary embolism

84
Q

once you have been diagnosed with a DVT, what is now contraindicated?

A

NEVER use TED stockings! b/c the clot can dislodge and move throughout the body

only use TED stockings after a surgery to prevent a DVT

85
Q

describe how a DVT can cause a stroke

A
  1. artial fibrillation
  2. heart is not contracting properly
  3. clot formation
  4. clot travels to the aorta
  5. then to brachiocephalic artery
  6. then to common carotid artery
  7. then to cerebral artery and lodge itself
    = stroke
86
Q

what is disseminated intravascular coagulation (DIC)

A

DIC is both a disorder of clot formation and bleeding episodes usually found among critically ill patients

87
Q

what is the main issue with DIC for both severe coag and severe bleeding

A
  1. uncontrolled synthesis of thrombin
  2. suppression of anticoagulation mechanisms
  3. abnormal fibrinolysis
    = together all lead to fibrin deposition to small and mid-seized BV’s
  4. obstruct blood flow of major organs like lungs, kidneys and brain
  5. organ failure

when bleeding too much:

  1. persistent activation of coagulation process
  2. depletion of clotting factors and platelets
  3. bleeding
88
Q

causes of DIC

A
  1. obstetric conditions (abruptio placenta; pre-eclampsia/eclampsia)
  2. cancer
  3. severe infection
89
Q

s/s of DIC

A
  1. initial phase: micro emboli
    - can obstruct BVs
    = ischemia / infarction of kidneys, heart, lungs, brain
  2. later phase: bleeding
    - petechia
    - purpura
    - oozing from puncture sites
    - severe hemorrhage
    - cardiovascular shock
90
Q

what is petechia

A

clots that are smaller sizes, small red or purple discoloration or spots due to bleeding into the skin (less than 2mm)

91
Q

how large are purpura

A

larger than 2mm

92
Q

what is the treatment of DIC

A

treat the underlying cause and provide supportive care, can administer heparin but it is controversial

Patho Exam 2 (3 decks)

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