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Patho II > E2: Hematologic disorders > Flashcards

E2: Hematologic disorders Flashcards

1
Q

erythrocytes are what kinda cells

A

RBC

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2
Q

erythrocytes are doughnut shaped why

A
  • increases surface are a it can carry more O2
  • very flexible
  • can flatten and squeeze through capps
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3
Q

function of erythrocytes

A

transports o2 via hemoglobin to the cell and carries CO2 to the lungs

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4
Q

what is hemoglobin

A

molecule in cytoplasm of RBC that the O2 attaches to

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5
Q

What are Leukocytes

A

WBC

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6
Q

function of leukocytes

A

defend against infections and remove debris

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7
Q

what are the two agranulocytes

A
  1. macrophages

2. Lymphocytes

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8
Q

what do neutrophils do

A

function first 2 days of inflammation (granulocytes)

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9
Q

normal level of neutrophils

A

55-70%

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10
Q

segmented neutrophils

A

mature

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11
Q

proliferation of cells

A

rapid reproduction of cells (not normal)

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12
Q

band neutrophils

A

immature neutrophils

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13
Q

basophils

A

anti-parasitic granulocytes

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14
Q

eosnophils

A

controls inflammatory/allergic responses (granulocytes)

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15
Q

normal level for basophils

A

.5-1%

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16
Q

eosinophils normal level

A

1-4%

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17
Q

lymphocytes

A

primary cells of immune response

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18
Q

thrombocytes

A

platelets

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19
Q

hematopoiesis

A

production of blood cells in the bone marrow

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20
Q

function of platelets

A

blood coagulation and control of bleeding

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21
Q

what is thrombocytopenia

A

platelet count less than 100,000

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22
Q

what is the lifespan for RBC

A

3-4 months

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23
Q

lifespan of leukocytes

A

7-21 days

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24
Q

thrombocyte life span

A

5-9 days

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25
Q

what forms with minor injuries that have vasoconstriction

A

platelet plug

26
Q

how does hemostasis stop bleeding with minor injuries

A
  • vasoconstriction

- formation of platelet plug

27
Q

how does hemostasis stop bleeding with major injureis

A

clot formation (coagulation cascade)

28
Q

what are the 3 causes of thrombocytopenia

A
  1. autoimmune disorder (IS destroys platelets)
  2. complication of heparin therapy (HIT)
  3. blood loss
29
Q

clinical mani of thrombocytopenia

A
  1. Decreased platelets
  2. hemorrhage
    - epistaxis
    - petechiae
    - hematuria
    - bleeding gums
    - ecchymosis (bruising)
30
Q

disseminated intravascular coagulation (DIC)

A

sequence of events resulting from abnormal, diffuse activation of:

  1. coagulation
  2. fibrinolysis (clot digestion)
31
Q

what causes DIC

A
  1. burns
  2. trauma
  3. shock
  4. cancers- termal
  5. emboli
    6 sepsis (most common cause)
32
Q

what causes DIC

A
  1. burns
  2. trauma
  3. shock
  4. cancers- termal
  5. emboli
    6 sepsis/septicemia- (most common cause)
33
Q

what is hemostasis

A

arrest of bleeding (stops bleeding)

34
Q

what are the two ways that the coagulation cascade start

A

intrinsic pathway

extrinsic pathway

35
Q

intrinsic pathway starts with what

A

blood vessel injury

36
Q

extrinsic pathway starts with what

A

tissue injury

37
Q

coagulation cascade patho chain

A

after intrensic and extrensic is activated:
aggregation of platelet at site of injury-> prothrombin converts to thrombin->thrombin makes fibrinogen which converts to fibrin-> fibrin becomes fibrin clot which is broken down by FDP

38
Q

why is septicemia cause DIC

A

bacteria breaks down which releases endotoxins which act as procoagulants (activates DIC)

39
Q

what is the patho chain of DIC

A

activation (usually sepsis)->release of procoags (stimulates clotting)-> overstimulation of coag system->excess fibrin formation-> disseminated (systemic) intravascular clotting->THEN increased consumption of platelets and clotting factors->decreased platelets and clotting factors->hemorrhage
->OR fibrin deposits in microcirculation “log jam”-> ischemia and infarction (widespread organ hypoperfusion)->clotting

40
Q

how do they diagnose DIC

A

increase D-Dimer which measures the rate of fibrin clot breakdown

41
Q

microvascular clinical mani of DIC

A

CNS- decreased LOC

Skin- Ischemia leading to gangrene

Kidney-oliguria, RF

lungs-SOB, PE

GI-acute ulcerations, necrosis

42
Q

hemorrhage clinical mani of DIC

A
  1. CNS- intracranial bleeding
  2. skin-petechiae, echymosis
  3. mems- gingival bleeding
  4. kidney- hematuria
  5. Gi- bleeding
43
Q

mortality rate of DIC

A

high, depends on cause

44
Q

disorder of coagulation

A

DIC

45
Q

multiple myeloma

A

malignant disorder characterized by proliferation of abnormal plasma (b lymphocytes) in the bone marrow

46
Q

incidence of multiple myeloma

A

peaks in the 6th decade of life

47
Q

etiology of multiple myeloma

A

UNKNOWN

  • genetics
  • viruses
  • bacteria
  • chemicals
48
Q

patho chain of multiple myeloma

A

excess number of abnormal plasma cells (b lymphs) infiltrate the bone marrow-> develop into tumors-> destroy bone-> invade lymph nodes, liver, spleen, kidneys

49
Q

abnormal plasma cells produce

A

myeloma (M) protein
(test for this during diagnosis)
(is a large protein=renal failure)

50
Q

clinical mani of multiple myeloma

A
  1. frequent infections
  2. anemia/bleeding
  3. bone pain/fractures
  4. renal insufficiency/failure
51
Q

lymphoma

A

malignant disease of the lymphoid tissues (thymus, bone marrow, lymph nodes, spleen)

52
Q

where is the majority of the disease located in lymphona

A

90% in the lymph nodes

53
Q

etiology of lymphoma

A

UNKNOWN

  • chromosome abnormality
  • virus
  • immunosuppression
54
Q

incidence of lymphoma

A
  • Hodgkin’s peaks at 20-30

- non-hodgkins at 50+

55
Q

patho of lymphoma

A

normal lymph node or tissue lymph structure is destroyed by excessive (abnormal) proliferation of lymphocytes

56
Q

onset of myeloma

A

insidious and slow

57
Q

hodgkin’s signs

A

reed-sternberg cells in lymph nodes

58
Q

non-hodgkin’s signs

A
  • bone marrow involvement occurs more often than hodgkins

- may different types of cells seen

59
Q

clinical mani of lymphoma

A
  • enlarged, painless, lymph nodes

- night sweats, fever, weight loss

60
Q

cure rate for hodgkins

A

complete remission if treated in early stages one and two

61
Q

cure rate for non hodgkins

A

varies

can be slowly developing or agressive and rapidly fatal

Patho II (23 decks)

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