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Advanced Pathophysiology > WK 2 Chapter 3- hematopoietic function > Flashcards

WK 2 Chapter 3- hematopoietic function Flashcards

1
Q

what are thrombocytes?

A

platelets

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2
Q

what are leukocytes?

A

all the WBCs

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3
Q

what are lymphocytes?

A

a type of leukocytes (type of WBC)

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4
Q

What are erythrocytes?

A

red blood cells

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5
Q

what is the function of erythrocytes?

A

full of oxygen: travel out of tissues–> offload their oxygen–> gather some carbon dioxide–> then come back to the lungs to get more oxygen

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6
Q

what is hemostasis?

A

stoppage of blood flow

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7
Q

what is an example of normal hemostasis?

A

when it seals a blood vessel to prevent blood loss and hemorrhage–> i.e. a cut or damage to vessel

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8
Q

what is an example of abnormal hemostasis?

A

when it causes abnormal clotting (stroke) or it is insufficient to stop blood flow

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9
Q

what is the goal of oxygen getting into the cells?

A

put it into cells with glucose to create energy

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10
Q

what is the function of platelets?

A

help clot areas that are damamged

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11
Q

What are the 5 stages of hemostasis with a cute?

A
  1. vessel spasm (decrease blood loss by slowing blood flow to that area)
  2. formation of platelet plug (now the vessel stops spasming)
  3. blood coagulation (platelet/RBC join onto plug to form more of a clot)
  4. Clot retraction (clot retracts to bring healthy tissue closer together, starts to heal)
  5. Clot Dissolution (clot breaks down, new tissue forms over that area. Macrophages eat debris, fibroblast form new fibers)
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12
Q

Describe the clotting cascades?

A

PROthrombin will turn into thrombin–> thrombin activates fibrinogen to turn into fibrin–> fibrin forms fibers to go over the clot–>platelets and RBCs attach to fibrin & they all cover the cut or damage to form a clot (i.e. thrombus).

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13
Q

what does thrombin do?

A

activates fibrinogen to turn into the active form of fibrin

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14
Q

what is prothrombin?

A

the inactive form of thrombin

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15
Q

what is fibrinogen?

A

the inactive form of fibrin

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16
Q

why do we need inactive and active forms of fibrin?

A

if we only had fibrin floating around in our blood (activated for clotting) we would be forming clots all the time. That is why we need thrombin to activate fibrinogen to turn into fibrin.

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17
Q

what is the short order of the creation of platelet plug?

A

Prothrombin–>thormbin–>fibrinogen–>fibrin

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18
Q

what is leukopenia?

A

decreased levels of WBCs

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19
Q

what is leukocytosis?

A

increased levels of WBCs

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20
Q

what % of blood is neutrophils? what do they do?

A

~70%, fight bacteria

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21
Q

what % of the blood is lymphocytes? what do theydo?

A

~30%, they fight viral infections

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22
Q

what % of the blood is monocytes? what do they do?

A

~7%, they turn into macrophages

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23
Q

what % of the blood is eosinophils? what do they do?

A

~3%, seen in antigen-antibody complexes and parasitic infections

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24
Q

what % of the blood is basophils? what do they do?

A

~1%, release histamine (happens during immune response)

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25
Q

what is the mnemonic for remembering % of types of WBCs?

A

Never Let Monkeys Eat Bananas.— 70, 30, 7, 3, 1

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26
Q

what is the role of capillaries during infection?

A

cells of capillary shirnk, creating space for leukocytes to sneak out of cell and go to site of infection

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27
Q

what are 3 important things to remember about neutrophils?

A
  1. they are a type of leukocytes
  2. they fight bacteria
  3. they are the first to arrive @ the site of infection
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28
Q

what are 7 causes of neutropenia?

A
  1. increased usage
  2. drug suppression
  3. radiation therapy
  4. congenital conditions
  5. bone marrow cancers
  6. spleen destruction
  7. vitamin deficiency
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29
Q

what are manifestations of neutropenia?

A
  1. infections/ulcerations of respiratory tract, skin, vagina, and GI tract
  2. s/s of infection ( fever, malaise, chills).
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30
Q

how do you treat neutropenia?

A

antibiotic therapy, hematopoietic therapy

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31
Q

what happens with mononucleosis?

A

Epstein-Barr Virus (EBV) infects the B cells by killing the B cells or being incorporated into its genome–>The B cells incorporated with EBV produce heterophile antibodies (abnormal antibodies).

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32
Q

what are the manifestations of mono?

what is the onset/incubation, initial and progressive manifestations, and length of course?

A
  1. insidious onset with 4-8 wk incubation
  2. initial=anorexia, malaise, chills
  3. progresses to leukocytosis, fever, chills, sore throat and lymphopathy
  4. acute stage= 2-3 wks, full recovery= 2-3 months
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33
Q

what are lymphomas?

A

cancer of the lymphatic system. most common hematologic CA in the US

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34
Q

what happens on a cellular level with hodgkins lymphoma?

A

solid tumors with reed-sternberg cells (abnormal B lymphocytes which are affected by the lymphoma). They grow to be much larger and they have an owl eye presentation which is how you differentiate between hodgkins/non-hodgkins non-hodgkins dont have reed-sternberg cells…non for no

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35
Q

what are manifestations of hodgkins lymphoma? (7)

A
  1. painless, enlarged nodes
  2. weight loss
  3. fever/ night sweats
  4. pruritis
  5. cough/SOB/chest pain
  6. recurrent infections
  7. splenomegaly
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36
Q

where are cells found in stage I Hodgkin’s lymphoma?

A

in one lymph node or 1 group of lymph nodes, one part of a tissue or an organ

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37
Q

Where are cells found in stage II Hodgkin’s lymphoma?

A

at least 2 lymph node groups on the same side of diaphragm
OR

in one part of a tissue or organ and the lymph nodes near that organ

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38
Q

where are cells found in stage III Hodgkin’s lymphoma?

A
  1. found in lymph nodes above and below the diaphragm.
  2. may be found in one part of a tissue or an organ near these lymph node groups.
  3. also may be in the spleen
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39
Q

where are cells found in stage IV Hodgkin’s lymphoma?

A
  1. cells are found in several parts of one or more organs or tissues
  2. or cells are in an organ and in distant lymph nodes
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40
Q

what is unique about Non-Hodgkin’s Lymphoma? (3 things)

A
  1. More common, worse prognosis
  2. can originate in T cells OR B cells
  3. no reed-sternberg cells
41
Q

what do you get from lymphoid progenerator cells?

A

lymphocytes & their derivatives

  1. B Lymphocytes
  2. T lymphocytes
  3. plasma cells
  4. natural Killer cells
42
Q

what do you get from myeloid progenerator cells?

A

everything except lymphocytes

  1. erythrocytes
  2. mast cells
  3. basophils,
  4. neutrophils
  5. esinophils
  6. monocytes
43
Q

what is leukemia?

what happens on a cellular level with leukemia?

A
  1. cancer of the luekocytes (WBCs)
  2. abnormal proliferation crowds normal blood cells & creates immature WBCs b/c they are made so quickly and pushed into bloodstream before they have a chance to mature
44
Q

what are risk factors for leukemia?

A
  1. exposure to chemical, viral and radiation mutagens
  2. smoking
  3. chemotherapy
  4. DOWN SYNDROME
  5. immunodeficiency disorder
45
Q

Affect, response, and prognosis for Acute Lymphoblastic Leukemia (ALL)?

A
  1. affects primarily children
  2. responds well to tx
  3. good prognosis
46
Q

Affect, response, and prognosis for Acute Myeloid Leukemia (AML)?

A
  1. affects primarily adults
  2. responds fairly well to tx
  3. prognosis somewhat worse than ALL
47
Q

Affect, prognosis, unique fact of Chronic Lymphoid Leukemia?

A
  1. affects primarily adults
  2. responds poorly
  3. it is slow moving so many people live many years after diagnosis
48
Q

affect, response, how Chronic Myeloid Leukemia improves?

A
  1. affects primarily adults
  2. responds poorly to chemo
  3. prognosis improves with allogeneic bone marrow transplant
49
Q

what are manifestations of leukemia? (8)

A
  1. leukopenia
  2. anemia
  3. thrombocytopenia
  4. lymphadenopathy
  5. joint swelling/bone pain
  6. anorexia/wt loss
  7. hepatomeagly/splenomegaly
  8. CNS dysfunction
50
Q

how is leukemia treated?

A

chemo/bone marrow transplant

51
Q

what causes multiple myeloma on a cellular level? what is uniquely excreted?

A
  1. it is plasma cell CA
  2. effects B cells that turn into plasma cells—excessive # of them in bone marrow which crowds other blood forming cells in bone marrow
  3. bence jones proteins excreted via urine
52
Q

what are bence jones proteins?

A

proteins released from B cells that travel through blood stream and are excreted in the urine. * they are abnormal*-they also stress the kidneys/decrease fx

53
Q

what does multiple myeloma destroy?

A

the bones. abnormal plasma cells destroy the bones around them–>multiple dark areas on x-ray

54
Q

what are the manifestations of multiple myeloma? (6)

A
  1. anemia
  2. thrombocytopenia
  3. leukopenia (first 3 from crowded bone marrow)
  4. decreased bone density
  5. bone pain/hypercalcemia
  6. renal impairment
55
Q

what is erythropoiesis? how is it regulated/where does it occur?

A

it is production of erythrocytes (RBCs)

  1. it is regulated by erythopoietin from kidneys
  2. it occurs in bone marrow
56
Q

What causes anemia?

A

decreased # of erythrocytes, leads to reduction of hemoglobin

57
Q

what are general manifestations seen in all anemias? (6)

A
  1. weakness
  2. fatigue
  3. pallor
  4. syncope
  5. dyspnea
  6. tachycardia
58
Q

what is the binding site for oxygen?

A

iron

59
Q

what causes iron-deficiency anemia? why is iron important?

A

decreased iron consumption or absorption, increased bleeding, menstruating women
iron is necessary for hgb production

60
Q

what are manifestations of iron deficiency anemia? (8)

A
  1. cyanosis to sclera
  2. brittle nails
  3. decreased apppetite
  4. headache
  5. irritability
  6. stomatitis (mouth sores)
  7. PICA
  8. delayed healing
61
Q

why is it important to test before supplementing iron deficient anemia?

A

excess iron can be deposited in tissue if not on hgb, free iron is stored in the liver & can damage/scar liver

62
Q

what is pernicious anemia?

A

vitamin B12 deficiency

usual cause is an auto-immune response damaging parietal cells that release intrinsic factor in the stomach

63
Q

why is B12 important? which anemia is B12 associated with? what can it cause?

A

required to DNA synthesis–>defecit leads to decreased maturation and cell division–>leading to myelin breakdown and neuro complications

64
Q

What are manifestations of Pernicious Anemia? (7)

A
  1. bleeding gums
  2. diarrhea
  3. impaired sense of smell
  4. loss of deep tondon reflexes
  5. personality/memory changes
  6. positive babinski sign
  7. paresthesia/unsteady gait
65
Q

how to you diagnose and treat pernicous anemia?

A

B12 levels. INJECTIBLE B12 (bypasses stomach)

66
Q

what causes aplastic anemia?

A

bone marrow depression of all blood cells

67
Q

what causes aplastic anemia? (5)

A

bone marrow depression of all blood cells

  1. idiopathic
  2. autoimmune
  3. medications/medical tx
  4. viruses
  5. genetic abnormalities
68
Q

What are manifestations of aplastic anemia? (3)

A
  1. anemia (weakness, dyspnea, pallor)
  2. leukocytopenia (e.g. recurrent infections)
  3. thromobocytopenia (e.g. bleeding)
69
Q

what causes hemolytic anemia?

A

excessive erythrocyte destruction

70
Q

What causes hemolytic anemia?

A
  • transfusion reactions
  • blood incompatability in neonates
  • autoimmune/genetics
  • infections
71
Q

what are 3 examples of hemolytic anemia?

A
  1. sickle cell anemia
  2. thalassemia
  3. erythroblastosis fetalis
72
Q

what causes sickle cell anemia on a cellular level?

A

Hemaglobin S causes erythrocytes to be abnormally shaped–>these cells carry less oxygen and clog vessels causing hypoxia and tissue ischemia

73
Q

what 2 descents are usually affected by sickle cell anemia? is it genetic?

A

African and Mediterranian. It is co-dominant

74
Q

what is sickle cell trait?

A

heterozygous, less than half of erythrocytes are sickled

75
Q

what is sickle cell disease?

A

homozygous, almost all erythrocytes are sickled

76
Q

what age is sickle cell disease usually noticed?

A

4 months

77
Q

what is sickle cell crisis? How long does it last/what causes pain? what triggers it?

A

painful episodes lasting hours to days. pain is caused by tissue ischemia and necrosis. triggered by dehydration, stress, high altitudes, and fever.

78
Q

how is sick cell crisis managed?

A
  1. oxygen therapy
  2. hydration
  3. pain management
  4. infection control/vaccinations
  5. transfusions
  6. hydroxyurea/bone marrow transplant
79
Q

What causes thalassemia on a cellular level?

A

abnormal hgb on 1 or 2 chains of the 4 chains units

individual doesn’t make proper type of hgb so they don’t carry oxygen well.

80
Q

how is thalassemia inherited/who is most affected?

A

Autosomal Dominant, Mediterranean descent

81
Q

what is polycythemia? What disease is it sometimes seen in?

A

abnormally high erythrocytes (RBCs) causing increased blood volume and viscosity leading to tissue ischemia and necrosis. Sometimes seen in AML

82
Q

What are clinical presentations of polycythemia? (5)

A
  1. cyanotic or plethoric skin
  2. HTN
  3. Tachycardia
  4. dyspnea
  5. headache/visual abnormalities
83
Q

What are complications of polycythemia?

A
  1. Thrombosis
  2. HTN
  3. heart failure
  4. hemorrhage
  5. splenomegaly/hepatomegaly
84
Q

What is hemophilia A? How is it inherited?

A

X linked recessive.

Deficiency or abnormality in clotting Factor VIII (8)

85
Q

what are manifestations of hemophilia A?

A

Bleeding or indications of bleeding (bruising, petechia etc)

86
Q

What is Von Willebrand’s disease?

A

decreased platelet adhesion and aggregation

87
Q

what is Type 1 Von Willebrand’s disease? When is it usually discovered?

A
  • reduced von willebrands factor levels.
  • Usually discovered during trauma or surgery
  • Doesn’t cause spontaneous bleeding
88
Q

What is Type 2 Von Willebrand’s disease?

A

Von Willebrand’s factor building blocks are small than usual or break down easily

89
Q

What is Type 3 Von Willebrand’s disease?

A

no measurable von willebrand’s factor or factor VIII, causes severe bleeding problems

90
Q

what is aquired type Von Willebran’d disease?

A

occurs with Wilm’s tumor, congenital heart disease, systemic lupus erythematosus, and hypothryroidism

91
Q

How does DIC happen?—internal process

A

widespread coagulation which uses up clotting factors, leading to massive bleeding.

92
Q

What is DIC a result of?

A

it is an inappropriate immune response to acute infection

93
Q

What are complications of DIC?

A

shock and multi-system organ failure (b/c they aren’t getting blood supply)

94
Q

what is Idiopathic Thrombocytopenia purpura?

A

hypocoagulation resulting from autoimmune destruction of platelets.

95
Q

who is mostly affected by acute Idiopathic thrombocytopenia purpura? what about chronic ITP?

A

Acute: mostly children, sudden onset
Chronic: Dults 20-50, mostly women

96
Q

what causes ITP? (4)

A
  1. autoimmune disease
  2. immunizations with live vaccine
  3. immunodeficiency disorders
  4. viral infections
97
Q

What is Thrombotic Thrombocytopenic Purpura?

A

Deficiency of enzyme neccessary for cleaving von willebrand’s factor leading to hypercoagulation, which depletes platelet levels.

98
Q

What is Thrombotic Thrombocytopenia Purpura characterized by?

A

thrombosis, thrombocytopenia, and bleeding

Advanced Pathophysiology (4 decks)

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