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Anatomy and Phyisology > HLTH module 4: blood and lymphatic > Flashcards

HLTH module 4: blood and lymphatic Flashcards

1
Q

hematocrit

A

is the proportion of blood cells (primarly RBCs) in blood and this indicates the viscocity of the blood; males typically have higher levels than females do

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2
Q

serum

A

the fluid and solutes remaining after the cells and fibrinogen have been removed from the plasma

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3
Q

where do all blood cell originate from?

A

bone marrow of the flat and irregular bones

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4
Q

what is the cellular component of blood?

A

erthyrocytes, leukocytes, and thrombocytes

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5
Q

function of RBCs

A

to transport O2 and sometimes CO2 through binding to hemoglobin

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6
Q

how are RBCs made

A

when O2 levels are low, erthryopoitein is released by the kidneys to stimulate the bone marrow to produce more EBCs

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7
Q

hemoglobin structure

A

consists of two pairs of amino acid chains and four heme groups that each contain an iron molecule that O2 binds to

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8
Q

dyscrasia

A

refers to pathologic conditions of the blood that are disorders associated with teh cellular components

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9
Q

what is another name for WBCs?

A

leukocytes

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10
Q

leukopoiesis

A

the production of WBCs which is stimulated by colony stimulting factors which are produced by macrophages and T lymphocytes

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11
Q

agranulocytes

A

lymphocytes and monocytes

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12
Q

lymphocytes

A

make up 30-40% of WBCs and have B or T types; involved in the immune response

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13
Q

T lymhocytes

A

natural killer cells

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14
Q

B lymphocytes

A

produce antibodies

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15
Q

monocytes

A

can develop into macrophages

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16
Q

granulocytes

A

includes neutrophils, basophils, and eosinophils

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17
Q

neutrophils

A

first responders for immune response and function as phagocytes

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18
Q

what is the most common leukocyte

A

neutorphils

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19
Q

eosinophils

A

tend to combat the effects of histamine and are increased during allergic reactions

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20
Q

basophils

A

migrate from blood to become mast cells and release histamine and heparin

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21
Q

what do mast cells release?

A

histamine and heparin

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22
Q

differential count meaning

A

the proportion of specific types of WBCs in the blood and this assists in making diagnoses

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23
Q

thrombocytes

A

aka platelets; these are essential for clotting through creating a platelet plug that seals small breaks in blood vessels

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24
Q

hemostatsis

A

term for blood clotting

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25
Q

what do platelets develop from?

A

megakaryocytes

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26
Q

what is plasma composed of?

A

proteins, water, and other substances like amino acids, carbohydrates, lipids, vitamins, enzymes, hormones, electrolytes, and waste products

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27
Q

3 types of plasma proteins

A

albumin, globulins, and fibrinogen

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28
Q

what does albumin function for?

A

maintains osmotic pressure

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29
Q

what does globulin function for?

A

antibodies

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30
Q

what does fibrinogen function for?

A

the formation of blood clots

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31
Q

hypoxia

A

low oxygen levels

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32
Q

what does the lymphatic system compose of?

A

lymphatic vessels and lymphoid tissue (this contains palatine and pharyngeal tonsils, lymph nodes, spleen, and the thymus gland

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33
Q

what is the function of the immune system?

A

to return excess interstital fluid and proteins to the blood, to filter and destroy any unwanted material, and to initate an immune response

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34
Q

flow of vessels in lymphatic system

A

vessels begin as small blind end capillaries > branches > trunks > ducts which empty into subclavian veins

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35
Q

differences between blood vessels and lymphatic vessels

A

lymphatic vessels are thinner, contain more valves, and form nodes at certian points

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36
Q

what do conditions that affect the lymphatic system return impact?

A

impacts the protein concentration of blood as well as osmotic pressure

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37
Q

how do lymph nodes offer immune protection?

A

by removing foreign or unwanted matierals form the lymph fluid before they enter the circulation

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38
Q

what do lymph nodes contain?

A

lymphocytes and macrophages

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39
Q

what structures does lymphoid tissue make up?

A

the palatine and pharygneal tonsils, lymph nodes, and thymus gland

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40
Q

how do palatine and pharyneal tonsils offer immune protection?

A

through protectign against bacterial infection as a first line of defence; however, this makes them suspecticle to infections

41
Q

functions of the spleen

A

functions releated to defence (through macrophages), hemaotpoiesis, and RBC or platelet destruction

42
Q

where is the thymus located?

A

in the mediastimun

43
Q

function of the thymus gland

A

the final site for lymphocyte development before birth and secretes hormones after birth; allows lymphocytes to develop into mature T cells

44
Q

composition of lymph

A

a clear, watery, isotonic fluid that closely resembles interstital fluid but with a lower protein concentration; also resembles blood plasma

45
Q

3 steps of hemostatis

A

vasospasm, platelet plug, and coagulation

46
Q

what do surronding cells release during a vascular injury?

A

collagen

47
Q

clotting factors present in the blood

A

prothrombin and fibrinogen

48
Q

3 steps of the platelet plug

A

platelet adhesion, platelet release action, and platelet aggravation

49
Q

what does anemia mean?

A

reduced O2 transport in the blood due to decreased hemoglobin content

50
Q

what are anemias classifed on?

A

size/ shape (morphology) and etiology (the types of anemias)

51
Q

what are the effects of low O2?

A

less energy produced by cells (reduces cell metabolism and reproduction), tachycardia, peripheral vasoconstriction, fatigue, pale face, increased effort to breath, inflamed GI tract, inflamed and cracked lips, skin and hair degeneration, and chest pain during stressful situations

52
Q

different types of anemia

A

iron deficiency, pernicious, aplastic, hemolytic, sickle cell, and thalassemia

53
Q

what kind of cells does iron-deficent anemia result in?

A

small cells (microcytic) and less colour (hypochromic)

54
Q

what can iron-deficent anemia occur as a result of?

A

decreased iron intake, chronic blood loss, hemorrhoids, cancer, excessive menstrual flow, impaired iron absorption, and some infections and cancers

55
Q

signs of iron-deficient anemia

A

pale skin, fatigue, cold intolerance, brittle hair and nails, inflammation of tongue, menstrual irregularities, tachycardia and fainting

56
Q

how is iron-deficiency anemia diagnosed?

A

blood tests that look for low hemoglobin, hematocrit, ferritin, and transferrin or through microscopic examination of cells

57
Q

treatment for iron-deficiency anemia

A

iron rich food or iron supplements

58
Q

pernicious anemia

A

aka megaloblastic anemia; b12 deficiency

59
Q

another name for vitamin B12

A

cyanocobalamin

60
Q

risks of pernicious anemia

A

can create a risk for neurological abnormalities due to the spinal cord; dangerous for pregnant women to impact the fetus

61
Q

what does pernicious anemia result from?

A

a decreased production of intrinsic factor (this helps with B12 absorption in the gastric mucosa)

62
Q

lack of B12 effects

A

causes the bone marrow to produce megaloblastic erythrocytes that end up being destroyed prematurely, essentially causing low RBC and hemoglobin count

63
Q

what is caused by megaloblastic erythocytes?

A

large hypersegmented neutrophils

64
Q

how does pernicious anemia impact the nervous system?

A

demyelination of the peripheral nerves and eventually the spinal cord occurs; this interferes with the conduction of nerve impulses

65
Q

causes of pernicious anemia

A

usually due to autoimmune disorders that impact intrinsic factor production, or from gastrectomy procedures

66
Q

signs of pernicious anemia

A

enlarged sore, red, and shiny tongue; digestive discomfort, neurological symptoms like tingling and burning sensations, and sometimes a loss of muscle control or coordination

67
Q

tests for pernicious anemia

A

blood tests that look for low B12 levels and microscopic tests that look for megaloblastic and nucleated RBCs, as well as large granulocytes

68
Q

treatment for pernicious anemia

A

b12 injections or supplements

69
Q

aplastic anemia

A

results from impairment of failure of bone marrow resulting in a loss of stem cells and decreased numbers of the cellular content in the blood

70
Q

pancytopenia

A

decreased numbers of erythrocytes, leukocytes, and platelets in the blood

71
Q

result of aplastic anemia to the bone marrow

A

more fatty tissue and less cell components

72
Q

causes of aplastic anemia

A

middle age, immunotoxins like radiation, drugs, or chemicals, hep C, autoimmune disorders, and genetic abnormalities

73
Q

signs for aplastic anemia

A

usually are gradual but are weakness, pale skin, recurrent infections, and hemorrhages on the skin

74
Q

diagnosis for aplastic anemia

A

bone marrow biopsies or blood counts

75
Q

treatment for aplastic anemia

A

bone marrow suppressants, blood transfusions, or bone marrow transplants

76
Q

hemolytic anemia

A

results from excessive destruction of RBCs or hemolysis, resulting in low RBC count and total hemoglobin

77
Q

2 types of hemolytic anemias

A

sickle cell and thalassemia

78
Q

sickle cell anemia

A

abnormal hemoglobin shape called HbS that occurs when one amino acid in the pair of beta-globin chains changes

79
Q

what are the adverse effects of the sickle cell shape?

A

it causes damage to the cell membrane, leading to hemolysis, as well as the obstruction of small blood vessels, leading to thrombus formation or tissue necrosis

80
Q

when does the sickle cell shape occur?

A

when O2 levels are low

81
Q

what is the HbS formation caused by?

A

a recessive gene

82
Q

signs of sickle cell anemia

A

pale skin, weakness, tachycardia, yellowish colour of eye, gallstones, spleen enlargement, organ damage, strokes, lung infection, blood vessel damage, late puberty and congestive heart failutre

83
Q

tests for sickle cell anemia

A

looking for the defective gene through blood test or DNA analysis of blood

84
Q

treatment for sickle cell anemia

A

is still being developed but includes the use of hydroxyurea, folic acid supplements, and avoidance of high stress activity or high altitudes

85
Q

thalassemia

A

results from a genetic defect in which one or more genes for hemoglobin and missing or variant

86
Q

what does the genetic mutation in thalassemia result in?

A

it interferes with the globin chains and therefore the amount of hemoglobin being created; it also causes extra chains to accumulate, leading to hemolysis

87
Q

2 types of thalassemia

A

thalassemia alpha and thalassemia beta

88
Q

in what individuals in thalassemia alpha more common in?

A

indian, chinese, and southeast asians

89
Q

in what individuals in thalassemia beta more common in?

A

mediterranean countries

90
Q

signs of thalassemia

A

impaired growth and development, fatigue, abnormal skeletal development, and heart failure

91
Q

tests for thalassemia

A

looks for increased RBC levels, increased iron levels, and small or less colour in RBCs

92
Q

treatment for thalassemia

A

blood transfusions, folate supplements, and sometimes iron chelation therapy

93
Q

primary polycthemia

A

increased production of RBC, granulocytes, and thromobytes in the bone marrow; increased blood viscosity causes blood vessels to swell and for flow to be sluggish

94
Q

what does primary polycythemia result in?

A

thromboses, hemorrhages, infractions throughout the body and elevated blood pressure

95
Q

secondary polycythemia

A

an increase in RBCs that occurs in response to prolonged hypoxia and increased erythorpoietin secretion

96
Q

signs of primary and secondary polycythemia

A

deep bluish, red tone of the skin, an enlarged liver, itchiness, increased blood pressure, headaches, visual disturbances, and high levels of uric acid

97
Q

testing for polycythemia

A

looks for hypercellular bone marrow, along with red marrow replacing yellow marrow

98
Q

treatment for polycythemia

A

drugs or radiation that suppress the activity of bone marrow, or removal or blood

99
Q
A

Anatomy and Phyisology (94 decks)

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