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pathophysiology > 2 - hematologic function > Flashcards

2 - hematologic function Flashcards

1
Q

red blood cells:

purpose

A

carry oxygen and CO2

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2
Q

red blood cells:

characteristics

A

round with dent

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3
Q

red blood cells:

building blocks

A

iron, B12, folic acid and others

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4
Q

red blood cells:

lab values

A
  • hemoglobin: 120-180 g/L

- hematocrit: % of blood that is RBCs

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5
Q

Anemia

A
  • low levels of RBC
  • reduction in the total number of erythrocytes in the circulating blood or decrease in the level of hemoglobin
  • decreased oxygen-carrying capacity
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6
Q

anemia - needs

A

02, hemoglobin and functioning heart to be clear of anemia

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7
Q

anemia - effects and manifestations

A
  • vary depending on body system, degree and ability to compensate
  • fatigue
  • weakness
  • dyspnea
  • pallor (pale)
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8
Q

anemia - etiology

A
  1. impaired production
  2. blood loss or increased destruction of rbc’s
  3. combination of above
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9
Q

anemia - size

A

identified by terms that end in “cystic”

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10
Q

microcytic

A

small

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11
Q

macrocytic

A

large

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12
Q

normocytic

A

normal

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13
Q

anemia - color

A
  • hemoglobin

- identified by terms that end in “-chromic”

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14
Q

anemia due to inadequate production

A
  • iron deficiency anemia
  • pernicious anemia
  • folate deficiency anemia
  • anemia due to chronic disease
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15
Q

iron deficiency anemia - cell

A
  • lacking iron

- RBC will be microcytic and hypochromic

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16
Q

iron deficiency anemia

A
  • most common type
  • nutritional iron deficiency
  • pregnancy, continous blood loss
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17
Q

iron deficiency anemia - clinical manifestations

A
  • fatigue, weakness, dyspnea, pallor
  • spoon-shaped nails
  • glossitis (red, sore and painful tongue)
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18
Q

iron deficiency anemia - treatment

A
  • treat cause

- iron supplements

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19
Q

pernicious anemia

A
  • caused by a lack of intrinsic factor from the gastric parietal cells
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20
Q

pernicious anemia - intrinsic factor

A
  • required for vitamin B12 absorption
  • lack of B12 leads to anemia
  • cells are large and microcytic
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21
Q

pernicious anemia - clinical manifestations

A
  • fatigue
  • weakness
  • dyspnea
  • nerve demyelination
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22
Q

nerve demyelination

A
  • parenthesis of feet
  • loss of position sense
  • confusion and dementia
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23
Q

pernicious anemia - treatment

A
  • lifelong B12 supplement
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24
Q

Folate deficiency anemia

A
  • folate deficiency
  • poor absorption of folate
  • increased requirement of folate (pregnancy)
  • produces RBC’s similar tot hose of pernicious
  • Large RBC “macrocytic”
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25
Q

folate foods

A
  • green leafy vegetables
  • fruits
  • cereals
  • meats
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26
Q

folate deficiency anemia - clinical manifestations

A
  • fatigue
  • weakness
  • dyspnea
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27
Q

folate deficiency anemia - treatment

A
  • dietary adjustments

- supplements

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28
Q

folate deficiency also linked to

A
  • neural tube defects (mother doesn’t have enough folic acid)
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29
Q

anemia due to chronic disease

A
  • pathologic mechanisms

- associated with systemic lupus erythematous, rheumatoid arthritis and chronic renal failure

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30
Q

pathologic mechanisms

A
  • inadequate production of erythropoietin
  • ineffective bone marrow response to erythropoietin
  • decreased erythrocyte life span
  • depletion of iron stores
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31
Q

erythropoietin made in

A

the kidney

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32
Q

anemia due to increased loss or destruction

A
  • blood loss anemia

- hemolytic anemia

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33
Q

blood loss anemia

A
  • can be acute or chronic
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34
Q

blood loss anemia - acute

A

symptoms are usually related to blood loss e.g. hypotension

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35
Q

blood loss anemia - chronic

A

use up iron stores which lead to iron deficiency

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36
Q

hemolytic anemias

A
  • premature destruction
  • sickle cell disease
  • hemolytic disease of the newborn
  • venoms, infections, mechanical heart valves
37
Q

sickle cell anemia

A
  • characterized by the production of abnormal hemoglobin
  • an autosomal recessive disorder
  • most common in persons of african ancestry but also those who live near the equator
  • estimated that 1 in 10 african americans
38
Q

sickle cell pathophysiology

A
  • due to a mutation in hemoglobin molecule
  • sickle crises triggered by dehydration and hypoxemia
  • HbS can revert to normal or can become irreversibly sickled
39
Q

sickle cell - 2 major consequences

A
  • chronic hemolytic anemia

- blood vessel occlusion

40
Q

chronic hemolytic anemia

A

premature destruction by spleen

41
Q

blood vessel occlusion

A
  • pain

- organ failure

42
Q

alterations in leukocytes

A
  • increased white blood cells

- decreased white blood cells

43
Q

increased white blood cells are called

A
  • leukocytosis

- may be a normal protective physiologic response to physiologic stressors

44
Q

decreased while blood cells are called

A
  • leukopinea
  • NEVER normal
  • radiation, immune deficiencies
45
Q

neoplasia of white blood cells

A
  • leukemia
  • lymphoma
  • both caused by malignancies of white blood cells
46
Q

leukemia

A
  • starts in the bone marrow
  • malignancy of precursors to white blood cells
  • immature white blood cells (leukaemia blasts)
  • leukemia blast crowd out bone marrow and causes pancytopenia
  • infiltrate spleen, liver etc.
47
Q

pancytopenia

A

decreased cellular proliferation of all typed of blood cells

48
Q

leukemia - types

A
  • acute lymphocytic leukaemia
  • acute myelogenous leukemia
  • chronic lymphocytic leukemia
  • chronic myelogenous leukemia
49
Q

leukemia - incidence (more of an FYI)

A

estimate more than 6000 Canadians - 2nd leading cause of death

50
Q

leukemia - cause

A

unknown but likely a combo of environment and genetic condition

51
Q

leukemia - risk factors

A
  • down syndrome
  • previous exposure to chemo and radiation
  • smoking
  • family genetics
52
Q

leukemia - manifestations

A
  • recalling the manifestations of neoplasm
  • pale
  • weakness/fatigue
  • bruising
  • bleeding
  • risk for infections
  • bone pain
  • enlarged liver and spleen
53
Q

leukemia - acute

A
  • sudden onset
  • rapid deterioration
  • rapid progression
54
Q

leukemia - chronic

A
  • slower onset
  • slower deterioration
  • slow progress
55
Q

leukemia - diagnosis

A

measurement of WBC and bone marrow biopsy

56
Q

leukemia - treatment

A

chemotherapy and supportive measures (blood transfusions, fluid replacements etc)

57
Q

lymphatic system

A
  • links immune and hematological systems

- site where various WBC can mature and function

58
Q

lymphatic system - primary structures

A

thymus and bone marrow

59
Q

lymphatic system - secondary structures

A

lymph nodes, spleen, tonsils and intestinal tract

60
Q

lymphadenopathy

A
  • enlarged lymph nodes that become palpable and tender

- can be local or generalized

61
Q

local lymphadenopathy

A

typically due to infection

62
Q

generalized lymphadenopathy

A

typically due to malignancy

63
Q

lymphoma

A
  • proliferation of malignant lymphocytes in the lymphatic system
64
Q

lymphoma - 2 major categories

A
  • hodgkins lymphoma

- non-hodgkin lymphoma

65
Q

hodgkin lymphoma

A
  • cause is unknown although could be genetic or immune
  • bimodal: two separate age groups (15-40 and >55 yrs)
  • 5 year survival is 83%
66
Q

non hodgkin lymphoma

A
  • generic term for neoplasms of B-cells, T-cells, NK-cells
  • impairment of immune system and infectious agents
  • incidence has almost doubled since 1970
  • usually in people > 50 yrs of age
  • 5 year survival is 55-60%
67
Q

lymphoma - manifestations

A
  • lymphadenopathy
  • fever
  • night sweats
  • fatigue
  • weight loss
68
Q

lymphoma - diagnosis

A
  • lymph node biopsy

- reed-sternberg cells in lymph tissue for hodgkin lymphoma

69
Q

lymphoma - treatment

A

chemo and radiation

70
Q

platelets (thrombocytes) - purpose and normal

A
  • to help with clotting

- 140-450x10^9/L

71
Q

platelet disorders

A
  • thrombocytopenia

- thrombocytosis

72
Q

thrombocytosis

A

higher platelet count than normal

73
Q

thrombocytopenia

A
  • lower than normal platelet count
74
Q

thrombocytopenia - cause

A
  • decreased production
  • increased breakdown or consumption
  • or both
75
Q

thrombocytopenia - types

A
  • immune thrombocytopenia
  • heparin induced thrombocytopenia
  • other
76
Q

immune thrombocytopenia purpura (ITP)

A
  • also known as idiopathic thrombocytopenia purpura
  • IgG antibody coats platelets
  • antibody -platelet combination removed from circulation by the spleen
  • acute or chronic
77
Q

immune thrombocytopenia purpura (ITP) - causes

A
  • following an infection

- autoimmune

78
Q

immune thrombocytopenia purpura (ITP) - manifestations and diagnosis

A
  • petechiae purpura
  • purpura
  • brusing
79
Q

immune thrombocytopenia purpura (ITP) - treatment

A

corticosteroids for suppression or removal of spleen

80
Q

petechiar purpura

A

tiny dots

81
Q

purpura

A

a little bit bigger dots

82
Q

bruising

A

big spots

83
Q

heparin-induced thrombocytopenia

A
  • adverse drug reaction to unfractionated heparin
  • platelets are used
  • thrombocytopenia about 5-10 days after heparin
84
Q

bleeding disorders due to genetics

A
  • von Hillebrand disease
  • hemophilia A
  • hemophilia B
  • hemophilia C
85
Q

von Hillebrand disease

A
  • factor VIII (8) deficiency
  • autosomal dominant
  • 20 variants
86
Q

hemophilia A

A
  • factor VIII (8) deficiency

- x-linked autosomal recessive

87
Q

hemophilia B

A
  • factor IX (19) deficiency

- x-linked autosomal recessive

88
Q

hemophilia C

A

factor XI (11) deficiency

89
Q

bleeding disorders affect

A
  • joints
  • skin
  • muscle
  • mouth/gum
  • urine/stool
  • nosebleeds

pathophysiology (16 decks)

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