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BIOL 2200 > module 4: blood disorders > Flashcards

module 4: blood disorders Flashcards

1
Q

Define anemia and describe two potential causes

A
  • a decrease in the oxygen-carrying capacity of the blood
  1. the number of red blood cells
  2. the amount of hemoglobin in the red blood cells are low
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2
Q

Fill in the blanks with the following terms: hypoxia, anemia, hypoxemia

___________________ produces ___________________ which produces ___________________

A
  • anemia
  • hypoxemia
  • hypoxia
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3
Q

what is hypoxemia?

A

a reduction in the oxygen content of the blood

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4
Q

what is hypoxia?

A

abnormally low oxygen content in the tissues

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5
Q

what may be analyzed when diagnosing anemia?

A
  • hemoglobin
  • hematocrit
  • RBC count
  • reticulocytes
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6
Q

Describe the general signs and symptoms associated with anemia.

A
  • fatigue
  • dizziness and headaches
  • breathing rate and depth increases
  • shortness of breath
  • rapid and pounding heartbeat
  • vasodilation
  • decrease in blood viscosity (thickness
  • pale lips, nail beds, mucous membranes
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7
Q

why is fatigue a general sign/symptom of anemia?

A

lower aerobic cell respiration = lower ATP

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8
Q

why are dizziness and headaches a general sign/symptom of anemia?

A

lower ATP in CNS

  • nerve tissue especially sensitive
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9
Q

why do breathing rate and depth increase with anemia?

A

body’s attempt to correct hypoxemia: respiratory center response to increase the diffusion rate of oxygen in the lungs

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10
Q

why is shortness of breath a general sign/symptom of anemia?

A
  • cannot get sufficient oxygen to tissues to supply their demands
  • generally happens with more activity because you are trying to gasp in as much air as you can
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11
Q

why is rapid and heart beat a general sign/symptom of anemia?

A

body’s attempt to correct hypoxemia:

  • cardiac centre response increases heart rate and SV to increase blood flow to lungs and tissues
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12
Q

why is vasodilation a general sign/symptom of anemia?

A
  • hypoxia releases signaling molecules like nitric oxide = local vasodilation of tissue capillaries
  • local vasodilation of tissue capillaries = decrease TPR
  • decrease TPR = increase venous return
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13
Q

why is a decrease in blood viscosity a general sign/symptom of anemia?

A
  • reduction in number of blood cells while the body maintains total volume of blood
  • effect is to lower TPR = increase venous return to heart
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14
Q

why are pale lips, nail beds, and mucous membranes a general sign/symptom of anemia?

A

blood less oxygenated = less bright red

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15
Q

Discuss iron deficiency anemia by addressing the following: etiology (cause)

A
  • chronic blood loss
  • lack of sufficient iron in diet
  • reduced ability to absorb iron
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16
Q

Discuss iron deficiency anemia by addressing the following: populations at risk and treatments available

A
  • population at risk:
    • poverty
    • women
    • children
    • elderly
  • treatment:
    • replace lost iron
    • identify and treat condition causinf loss
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17
Q

Discuss iron deficiency anemia by addressing the following: pathogenesis

A
  1. iron stores deplete
  2. fewer RBCs (low hematocrit) with reduced cell volume (mean cell volume - MCV) and low hemoglobin content (mean cellular hemoglobin content- MCHC) produced
  3. theses “anemic” blood cells gradually replace older blood cells
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18
Q

Discuss iron deficiency anemia by addressing the following: histological characteristics

A

the anemic blood cells in iron deficiency are distinctive:

  • microcytic = very small RBC
  • hypochromic = pale RBC due to lack of iron
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19
Q

Describe pernicious anemia by addressing the following: pathology (include: why do we need vitamin B12? what is it used for?)

A
  • atrophic gastritis = gastric mucosa atrophy
  • results in lack of intrinsic factor
  • produces B12 deficiency
    • essential for DNA synthesis/mitosis in RBC and myelination of nerves/nerve function
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20
Q

Describe pernicious anemia by addressing the following: etiology

A
  • autoimmune destruction of gastric mucosa
  • heavy alcohol ingestion, cigarette smoking
  • other causes of B12 deficiency
    • gastrectomy, malabsorption, aging
  • slow pathogenesis (20-30 years)
    • undetected progression of gastritis
    • slow depletion of B12 stores in liver
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21
Q

Describe pernicious anemia by addressing the following: histological characteristics

A
  • megaloblastic RBCs
    • macrocytic = large RBC
    • normochromic = normal colour
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22
Q

Describe pernicious anemia by addressing the following: signs and symptoms

A
  • general symptoms of anemia
  • low serum B12 levels
  • neurologic complications of B12 deficiency:
    • paresthesias in hands/feet (tingling/numbness)
    • depression
    • dementia (sometimes)
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23
Q

Describe pernicious anemia by addressing the following: treatment

A

vitamin B12 injections

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24
Q

Describe folate deficiency anemia by addressing the following: why do we need folate? what is it used for?

A
  • folic acid = vitamin B9 is essential for nucleic acid synthesis within RBC and cell growth and mitosis
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25
Q

Describe folate deficiency anemia by addressing the following: etiology

A
  • malnutrition
  • diets low in green vegetables and meat
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26
Q

Describe folate deficiency anemia by addressing the following: histological characteristics

A

similar features to pernicious anemia

  • megaloblastic (large) and normochromic (normal colour)
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27
Q

Describe folate deficiency anemia by addressing the following: signs and symptoms

A
  • mouth ulcers (stomatitis)
  • watery diarrhea
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28
Q

Describe folate deficiency anemia by addressing the following: at risk population and treatment

A
  • at risk:
    • elderly
    • children
    • alcoholism
    • pregnancy
  • treatment:
    • folic acid supplements
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29
Q

Define polycythemia and name the two types

A
  • polycythemia = too many erythrocyte presence (too many RBC)
  • types:
    • relative polycythemia
    • absolute polycythemia
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30
Q

describe relative polycythemia

A
  • blood cell number is fine, but low fluid
  • brought about through dehydration
  • minor consequences and easily fixes
  • blood becomes very viscous due to low amount of fluids
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31
Q

describe absolute polycythemia

A
  • produces too many RBC
  • 2 forms:
    • primary (polycythemia vera) = rare non-malignant condition where there is an overabundance of bone marrow stem cells
    • secondary = due to hypoxia, which results in overproduction of erythropoietin in compensation for low oxygen levels
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32
Q

what is primary polycythemia?

A

“polycythemia vera”

  • rare non-malignant condition where there is an overabundance of bone marrow stem cells
33
Q

what is secondary polycythemia?

A
  • due to hypoxia
  • results in overproduction of erythropoietin in compenation for low oxygen levels
34
Q

Describe the manifestations of polycythemia

A

variable and related to an increase in RBCs, haemoglobin level, and hematocrit with creased blood volume and viscosity

  • splenomegaly
  • depletion of iron
  • disrupted cardiac output
  • hypertention
  • decreased cerebral blood flow
  • venous stasis
  • thromboembolism
35
Q

what is splenomegaly?

A

spleen is really big due to processing RBC and working overtime to try to get rid

36
Q

what is venous stasis?

A

blood so thick, it starts to pool

37
Q

describe leukocytosis vs leukopenia

A
  • leukocytosis = when WBC count is higher than normal
    • can be normal response to stressors such as infection, surgery, pregnancy, etc.
  • leukopenia = when WBC count is lower than normal
    • never normal response, risk of infection increases dramatically
38
Q

Describe neutrophilia vs neutropenia vs agranulocytosis

A
  • neutrophilia = an early response to infection (shift to left)
  • neutropenia = decrease due to not being able to keep up with production
  • agranulocytosis (granulocytopenia) = extremely low counts of granulocytes
39
Q

Describe lymphocytosis vs lymphocytopenia.

A
  • lymphocytosis = usually produced through viral infection since their job is to attack viruses (adaptive immune response)
  • lymphocytopenia = immune deficiencies, neoplasia, drugs, no known cause
40
Q

Discuss infectious mononucleosis to include the following: cause

A
  • acute infection of B lymphocytes by Epstein-Barr virus (EBV)
    • too many B cells
  • heterophile antibodies are detected = bind to a number of different antigens and can deplete cells
41
Q

Discuss infectious mononucleosis to include the following: Age groups typically become infected? Why?

A

individuals 15-19 years old because they tend to share more food/drinks, etc. and kiss.. lol

42
Q

Discuss infectious mononucleosis to include the following: signs and symptoms

A
  • fever
  • sore throat
  • cervical lymph node enlargement
  • can progress to more serious symptoms
43
Q

Discuss infectious mononucleosis to include the following: usually self-limiting (which immune cells are responsible?)

A
  • cytotoxic T cells
  • natural killer cells
44
Q

Define leukemia

A

a malignant disorder of the blood and blood-forming organs

45
Q

Define pancytopenia. How does it occur?

A
  • pancytopenia = a reduction in all cellular component of the blood as the end result
  • cells start repilicating and get huge expansion of immature cells (malignant leukocytes) = crowds out bone marrow
  • crowds out bone marrow = unable to get mature cells
46
Q

What are some common features of leukemic cells?

A
  • are immature and poorly differentiated (divide rapidly and does not become fully functioning)
  • proliferate rapidly and have a long life span
  • do not function normally
  • interfere with the maturation of normal blood cells
  • circulate in the bloodstream
  • cross the blood-brain barrier
  • infiltrate many body organs
47
Q

Describe some risk factors associated with the development of leukemia.

A
  • can reapperar in families and is associated with other hereditary abnormalities (ex: down syndrome)
  • increased risk has been linked to cigarette smoke, ionizing radiation, infections with HIV or HCV, some drugs
48
Q

What information is used to classify the different kinds of leukemia?

A
  • which type of cell line is affected (lymphocytic or myelogenous)
  • the progression of the disease (acute or chronic)
49
Q

Describe acute leukemias to include: general description

A
  • rapid growth of immature blood cells
  • abrupt onset of disease: short survival time if untreated
50
Q

Describe acute leukemias to include: difference between ALL and AML

A
  • acute lymphocytic (ALL) = concerns lymphycytes
    • vast majority (85%) of all are problems with B cell line
    • least common type overall, but most common type in children
    • accounts for 3 out of 4 cases of childhood cancer
  • acute myelogenous (AML) = concerns any cells except lymphocytes
    • tends to occur more in older adults, but is also seen in children and younger adults
51
Q

Describe acute leukemias to include: manifestations

A
  • fatigue caused by anemia- not fully mature RBC
  • bleeding caused by thrombocytopenia - no functioning platelets
  • infections and fever - no functioning WBC
  • anorexia liver, spleen, lymph node enlargement, neurological/CNS manifestations
  • bone pain - overproduction of cells on bones
  • SOB & tachycardia - anemia compensation
  • swollen lymph nodes - overworking
  • weight loss
52
Q

Describe acute leukemias to include: evaluation and treatment

A
  • difficult to detect early since symptoms are so general
  • blood test and bone marrow biopsy reveal how to diagnose it
  • chemotherapy is typical treatment, along with blood transfusions, and antimicrobial agent
53
Q

Describe chronic leukemias to include: general description

A
  • slow growth of more mature (differentiated) cells which do not function normally
  • onset is gradual: longer survival times. symptoms appear very slowly
54
Q

Describe chronic leukemias to include: CLL

A
  • chronic lymphocytic leukemia (CLL) = accounts for ½ of all leukemias, generally in older people (72)
  • transformation of primarily B cells- refuse apoptosis and accumulate while also becoming inactive = no antibody production
  • supression of normal antibody production = increase in infections
  • causes anemia, thrombocytopenia, and neutropenia
  • can be slow or very aggressive
55
Q

Describe chronic leukemias to include: CML

A
  • chronic myelogenous leukemia
  • clinical manifestations:
    • disease of older people (average age = 67)
    • affect stem cells (exessive amounts of marrow granulocytes, RBC precursos, and megakaryocytes)
  • 3 phases
    • chronic
    • accelerated
    • terminal blast
56
Q

Describe chronic leukemias to include: the 3 phases of CML

A
  • chronic
    • lasting 2-5 years
    • may be asymptomatic
  • accelerated
    • lasting 6-18 months
    • primary symptoms develop, more immature cells in bone marrow and blood
    • enlargement of spleen and liver, infections, weight loss, and fever
  • terminal blast phase
    • lasting 3-6 months
    • more blast cells in blood
    • increase in severity of symptims
    • resembles AML
    • prognosis poor at this point
    • philiadelphia chromosome is observed in 95% of those with CML
57
Q

What is a Philadelphia chromosome?

A
  • chromosomes 9 and 22 exchange parts of long ends
  • the new protein that has been made allows the cell to bypass controls of normal cell growth and differentiation
58
Q

Describe chronic leukemias to include: evalutation and treatment

A
  • blood tests and bone marrow biopsy
  • combined treatments
    • bone marrow transplant - deplete bone marrow and replace it
    • biologic response modifiers - increase body’s immune response
    • combination chemotherapy
59
Q

Describe thrombocytopenia to include the following: general description

A
  • can be alteration in number or quality of platelets
  • too few platelets
60
Q

Describe thrombocytopenia to include the following: risks associated with bleeding

A

risk of hemmorrhage with minor trauma if numbers fall too low

61
Q

Define petechiae and purpuric spots

A

numbers can fall sufficiently low that spontaneous bleeding can occur without ant trauma

  • petechaie = smaller than 2 mm
  • pupuria = larger
62
Q

Describe thrombocytopenia to include the following: etiology

A
  • results from decreased platelet production, increased consumption (over using platelets), or both
  • usually due to increased platelet consumption
63
Q

what are 2 examples of thrombocytopenia?

A
  1. heparin induced
  2. immune thrombocytopenic purpura
64
Q

what is a heparin induced thrombocytopenia?

A
  • IgG bind to platelets and antibodies stick to form clots/clumping of cells
  • most common drug induced condition
65
Q

what is immune thrombocytopenic purpura thrombocutopenia?

A
  • antibodies bind to platelet membrane and clumps together, then phagocytosis happens since they are more susceptible
66
Q

Describe thrombocythemia to include the following: general description

A

too many platelets

67
Q

describe primary thrombocythemia

A
  • receptors does not recognize thrombopoietin, so body always has this hormone in the blood stream because it does not bind to platelets = more platelet production
  • negative feedback effect
68
Q

describe secondary thrombocythemia

A
  • something happens to cause more platelet production (ex: disease)
  • would occur with any disease state that stimulates thrombopoietin production
69
Q

TRUE or FALSE: Individuals have a high risk of large-vessel thrombosis and ischemia in the extremities.

A

true

70
Q

Impaired platelet function is characterized by:

A
  • increased bleeding time in the presence of a normal platelet count
71
Q

Describe inherited vs acquired causes of impaired platelet function.

A
  • inherited = rare
  • aquired
    • drugs decreases platelet aggregation (ex: aspirin, NSAIDs)
    • secondary to leukemia (cowding out effect) = low quality platelets produced
72
Q

Describe the general cause of coagulation disorders.

A

defects of deficiences in one or more of the clotting factors

73
Q

Distinguish between inherited vs acquired coagulation disorders.

A
  • inherited = mutation in genes and don’t make functional clotting factors
    • ex: hemophilia
  • aquired = a result of deficient synthesis of clotting factors by the liver, or due to dietary deficiency or vitamin K
74
Q

Describe the effects of coagulation disorders.

A
  • turbulent or reduced blood flow
  • tissue factor induced
75
Q

describe turbulent or reduced blood flow in the effect of inappropriate coagulation

A

triggers clotting cascade

  • get innapropriate activation of clotting factors
76
Q

describe the tissue factor induced effect of inappropriate coagulation

A

Tf (thromboplastin) released from damaged or inflamed, or dead tissues

  • start cascade of blood clotting
77
Q

what is important to remember with the effect of inappropriate coagulation?

A

not only do you start making emboli/thrombosis, you also lead to uncontrolled bleeding

  • as you start making inappropriate blood clots, you deplete the number of available clotting factors = uncontrolled bleeding
78
Q

Describe disseminated intravascular coagulation to include: general description

A

aquired clinical syndrome characterized by widespread activation of coagulation

  • blood clots all around your body/tissues = block smaller blood vessels/embolus

BIOL 2200 (12 decks)

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