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BI 122 > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

What is blood

A

blood is a connective tissue with a liquid groud substance called plasma

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2
Q

Blood volume

A

average adult= 5 liters

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3
Q

Plasma

A

55% volume of blood

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4
Q

Blood composition

A

water- 92%
amino acids
proteins
carbohydrates
lipids
vitamins
hormones
electrolytes
cellular waste
antibodies

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5
Q

formed elements

A

45% volume of blood

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6
Q

Packed cell volume

A

measure of the proportion of blood that is made up of cells

RBC= 99.9%
WBC= 0.1%
Platelets= 0.1%

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7
Q

Hematocrit (HCT)

A

red blood cell volume

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8
Q

buffy coat

A

WBC’s and platelets

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9
Q

Hemocytoblasts

A

stem cells that mature into all blood cell types and platlets via colony stimulation factors and interleukins.

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10
Q

Characteristics of RBC’s

A

biconcave discs (increase surface area for diffusion and allow folding)
33% by vol hemoglobin (bond with oxygen to yield oxyhemoglobin)
mature cells lack nuclei and organelles (increase of space for hemoglobin)

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11
Q

Oxygenated blood

A

blood with oxyhemoglobin (bright red)

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12
Q

deoxygenated blood

A

blood with deoxyhemoglobin (dark red)

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13
Q

hypoxia

A

low blood oxygen

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14
Q

cyanosis

A

hypoxia leads to the increase of deoxyhemoglobin turning the skin and mucous membranes blue

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15
Q

Causes of cyanosis

A

suffocation, poisonous gases, vasoconstriction of surface vessels due to cold

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16
Q

sickle cell disease

A

an incorrect amino acid causes hemoglobin to sickle (crystallize in decreased oxygen conditions) causing damming in small capillaries: tissue hypoxia

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17
Q

Erythropoiesis

A

red blood cell production

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18
Q

prepartum RBC production

A

yolk sac, liver, spleen

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19
Q

postpartum RBC production

A

red bone marrow

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20
Q

life span of a RBC

A

120 days ish

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21
Q

stimulus for production of RBC’s

A

low oxygen leves caused by the release of the hormone erythropoietin by kidneys and liver

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22
Q

Action of erythropoietin

A

stimulates red marrow to produce and release RBC’s into circulation

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23
Q

Where does damage of RBC’s occur?

A

in capillaries in liver and spleen

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24
Q

What happens to damaged RBC’s

A

phagocytized by macrophages

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25
Q

Hemoglobin components recycled

A

globin chains (polypeptide)
heme groups

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26
Q

what are the heme groups broken down into?

A

iron and bilepigments billiverdin and billirubin. Pigments are then released into the gall bladder.

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27
Q

Bruises

A

subdermal hematomas (ruptured capillaries). They degrade from purple (whole blood) to green (billiverdin) to yellow (bilirubin)

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28
Q

Jaundice

A

excess bile pigments (billiverdin and billirubin) accumulate in the blood resulting in a yellowing of sclera, skin and nails

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29
Q

Factors that affect Erythropoiesis

A
  1. altitude (as blood oxygen decreases, erythropoietin secretion increases causing erythropoiesis
  2. B complex vitamins (B12 and folic acid required for DNA synthesis and erythropoiesis)
  3. minerals (iron is required for hemoglobin synthesis)
  4. Pregnancy (blood volume increases during pregnancy due to water retention. But hematocrite decreases. The imbalance is corrected by erythropoiesis.)
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30
Q

pernicious anemia

A

low dietary levels of B12 or folic acid inhibit hemopoiesis as does an inability to absorb B12 due to the lack of intrinsic factors secreted by stomach cells.

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31
Q

Anemia

A

RBC or hemoglobin deiciency- a reduced oxygen carrying capacity of the blood

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32
Q

Characteristics of WBC’s

A
  1. fight disease
  2. transported in circulation system
  3. leave circulation system and enter tissues to work
  4. formed in red marrow. Lymphocytes also formed in lymphatic organs
  5. possess nucleus
  6. short life span (12 hours) except lymphocytes (several years
  7. comprise <0.1% of PCV/Formed elements
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33
Q

Classifications of WBC’s

A
  1. size
  2. cuclear size and shape
  3. granulation of cytoplasm
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34
Q

Granulocytes

A

neutrophils (phagocytize bacteria, fungi, and some viruses… most important for fighting bacteria)
esosinophils (moderate allergic reactions, fight parasitic worms)
basophils (travels to damaged tissue and releases histamin… promotes inflammation and swelling and heparin… prevents clotting)

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35
Q

Agranulocytes

A

monocyte (matures into macrophages that phagocytize bacteria, dead cells and debris. Fuses in the skeleatl system to produce osteoclasts and also function as microglial cells i nthe nervous system)
lymphocyte (two forms, fight monoclucleusus)

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36
Q

forms of lymphocytes

A

T lymphocyte (mature in thymus): directly attacks tumor cells and foreign cells, like transplants)
B lymphcyte: produces antibodies (gamma globulin proteins) that attack foreign cells, and foreign proteins

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37
Q

HIV

A

reproduces in T cells resulting and their death and compromising the immune system

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38
Q

Never Let Monkeys Eat Bananas

A

Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils

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39
Q

How WBC’s fight infection

A
  1. exit through cappillary walls
  2. WBC’s guided to site of infection via leukocyte trafficking
  3. move through interstitial spaces via ameboid motion
  4. WBC’s perform function at infection site
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40
Q

Pus

A

local accumaltion of leukocytes and microorganism and associated fluids

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41
Q

Sepsis, Septicemia, Bacteremia, and Viremia

A

Sepsis: infection of tissues
Septicemia: infection of the blood
Bacteremia: caused by bacteria
Viremia: caused by viruses

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42
Q

Leukemia

A

cancer of leukocytes
Myeloid leukemia (abnormal granulocytes and monocytes)
Lymphoid leukemia (abnormal lymphocytes)

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43
Q

Leukemia results

A

too many immature leukocytes
too few RBC’s and platelets due to marrow crowding by WBC’s

Symptoms: fatigue, infection, hemophilia, decreased healing of cuts, bruises.

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44
Q

Characteristics of platelets

A
  1. formed in red marrow
  2. result of fragmented megakaryocytes
  3. important in clotting and platelet plug response (stick to damaged vessel surfaces, cause contraction of vessel smooth muscle)
  4. live 10 days
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45
Q

Characteristics of plasm

A
  1. 92% water
  2. 8% organic and inorganic compounds
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46
Q

function of plasma

A
  1. transport RBC WBC and platelets
  2. transport nutrients( amino acids, simple sugars, nucleotides, lipids)
  3. transport gases (nitrogen oxygen and carbon dioxide)
  4. transport vitamins
  5. transport wastes
  6. transport hormones
  7. pH balance
  8. Thermoregulation
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47
Q

Albumin (plasma protein)

A

maintains osmotic pressure in vessels

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48
Q

Edema

A

low serum albumin: fluid enters tissues causing fluid accumulation in the edema of the abdominal cavity. Caused by low protein diet or starvavion: resulting in hypoprotinemia

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49
Q

Globulin (plasma protein)

A

Alpha and beta globulins transport lipds and fat soluble vitamins
Gamma globulin function as antibodies

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50
Q

fibrinogen (plasma protein)

A

blood coagulation

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51
Q

Plasma lipoproteins

A

lipids bond with proteins in plasma to make lipoproteins (proteins in lipoprotein increase= density increase)

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52
Q

Low Density Lipoproteins (LDL)

A

high cholesteral, low protein
(functions is to transport cholesteral to misc. cells)

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53
Q

High Density Lipoproteins (HDL)

A

decrease lipds, increase protein
(function is to transport cholesteral to liver for relase in bile)

54
Q

Phases of Hemostasis

A
  1. vascular phase- smooth muscle in vessel wall constricts
  2. Platelet Phase- platelets stick to torn walls and each other. Platelet factors released to stimulate clot formation and platelet derived growth factor to promote vessel repair
  3. Coagulation Phase- biochemical cascade with serveral dozen clotting factors that changes fibrinogen into fibrin fibers that sticks to formed elements producing a clot
55
Q

Hemophilia

A

deficiency in a clotting factor (VIII or IX) resulting in reduced ro no clotting

56
Q

Clotting initiating mechanisms

A
  1. extrinsic (clotting initiaed by chemicals release from damaged tissues or turbulence from a thrombus)
  2. Intrinsic (clotting initiated by chemicals within blood)
57
Q

Platelet derived growth factor

A

after clot formation platelets release growth factor that stiumulates vessel repair

58
Q

Thrombus

A

stationar clot in vells that decreses or prevents blood flow causing a trhombosis

59
Q

Embolus

A

Thrombus that breaks away and moves downstream. Lodges as vessel narrows causing embolism

60
Q

infarction

A

when a trhombus or embolus stops vlood flow to an area (myocardial infarction)

61
Q

Cerebral vascular accident (Stroke)

A

a thrombus or embolus indeced infarction in the brain

62
Q

Transient ischemic attack

A

temporary blockage in a small artery caused by embolus.

63
Q

angina pectoris

A

a thrombus or embolism that reduces blood flow to myocardium

64
Q

Clot Prevention

A
  1. Rapidly flowing blood (decreased accumulation of clotting factors)
  2. smooth vessels (decreased sites for clot formation)
  3. Aniticoagulants ( natural= heparin, Synthetic= coumadin, aspirin)
65
Q

Hemocompatability

A

RBC’s possess membrane surface antigens that serve in cell recognition

66
Q

Blood type that is the universal donor in emergency

A

Type O- no antigens but anti A and ani B antibodies

67
Q

Blood types that is the universal recipient in an emergancy

A

Type AB: A and B antigens but ot anitbodies

68
Q

Erythroblastosis fetalis

A

When Rh- woman carries an Rh+ baby, fetal blood enters her circulation system at birth when placenta tears causing formation of Rh antibodies. Blood fo second Rh+ baby will be attacked by Rh antibodies.

69
Q

Reducing Transfusion Reactions

A
  1. Use packed cells
  2. infuse whole blood slowly to dilute and decrease chance of agglutination
70
Q

Blood replacement

A
  1. whole blood- contains all components
  2. packed RBC’s
  3. packed platelets
  4. packed WBC
  5. plasma
  6. Artificial blood
71
Q

Components of Cardiovascular system

A

heart and blood vessels

72
Q

Heart location

A

medial

73
Q

Pericardium

A

covering over heart and proximal ends of vessels

74
Q

Pericardial sac

A

fibrous- outer layer
parietal- middle layer
visceral (epicardium)- serous inner layer against heart
Pericardial cavity- serous fluid-filled space between visceral and parietal layers

75
Q

Pericarditis

A

layers of pericardium stick together due to bacterial or viral infection

76
Q

Cardiac Wall structure

A

epicardium- serous lubrication, and energy storage
Myocardium- cardiac muscle tissue, pumps blood through chambers
Endocardium- connective and epithelium, lining of all heart structures; decrease friction and infection

77
Q

Endocarditis

A

bacterial infection of the endocardium

78
Q

Coronary flow of myocardium

A

obtains blood from its own vascular supply and not via atria or ventricles

79
Q

Hypoxia and necrosis

A

caused by compromised flow to the myocardium, treated with coronary bypass surgery or placement of stents

80
Q

Mitral Valve Prolapse

A

one or both of the cusps stretches into the atrium during ventricular contraction causing a back flow of blood

** MVP patients must receive antibiotics prior to dental work to decrease chances of streptococcus from the mouth entering blood and doing further damage to the bicuspid valve (endocarditus)

81
Q

angina pectoris

A

a thrombus or embolism that reduces blood flow to myocardium

** if blood flow is stopped then myocardial infarction occurs

82
Q

Fetal circulation

A

There is no need for pulmonary flow in untero- have fossa ovale (hole between ventricles) and ductus arteriosis (where ligamentum arteriosum will eventually be)

83
Q

Systole

A

chamber contraction

84
Q

diastole

A

chamber relaxation

85
Q

lubb

A

closing of A-V valves during ventricular systole

86
Q

dubb

A

closing of pulmonary and aortic valves during ventricular diastole

87
Q

impulse nodes and bundles

A

strands of non-contractile cardiac muscle that initiate and or conduct impulses

88
Q

sinoatrial node (pacemaker)

A

initiate impulse, impulses spread through both atrial myocardium.

89
Q

atrioventricular node

A

conduction pathway between both atrial and ventricular myocardium

90
Q

AV bundle

A

muscle fibers that conduct impulse towards ventricular myocardium. Divides into Left and Right branches.

91
Q

Purkinje fibers

A

deliver impulse to myocardial fibers

92
Q

Electrocardiograms

A

P wave, QRS complex, T wave

93
Q

p wave

A

depolarization of atrial fibers (atrial ocntraction/ systole)

94
Q

QRS complex

A

depolarization of ventricular fibers (bentricular contraction/ systole)

95
Q

T wave

A

Repolarization of ventricular fibers (ventricular relaxation. diastole)

96
Q

arhythmia

A

absence of normal cardiac rhythm

97
Q

fibrilation

A

uncoordinated contraction of myocardium
A. atrial- not fatal
B. ventricular- fatal- results in cardiac arrest.

98
Q

Flutter

A

rapid contraction of a single atrium

99
Q

Bradycardia

A

abnormally slow beat

100
Q

tachycardia

A

abnormally fast beat

101
Q

sudden cardiac arrest

A

failure to contract. Death within minutes if not treated with automated electronic defibrillator

102
Q

Blood vessel hierarchy

A

heart>arteries>arterioles>metarterioles>capillaries>venules>veins>heart
or
heart>arteries>arterioles>metarterioles>venules>veins>heart

103
Q

arteries and arterioles

A

carry blood away from heart to capillaries under cardiac pressure

104
Q

artery layers

A

tunica interna- endothelim that reduces friction and produces anticoagulants
tunica media- smooth muscle to maintain blood pressure
tunica externa- elastic connective that attahces vessel to adjoining tissues

105
Q

atherosclerosis

A

deposits of plaque line artery lumen and decrease blood flow resulting in increased blood pressure and increased chance of thrombus formation

106
Q

dystrophic calcification

A

trauma to vessel that causes calcium deposition on lumen walls

107
Q

arteriosclerosis

A

arterial walls thicken and lose their elasticity: increased blood pressure and increased chance of aneurysm

108
Q

aneurysm

A

a ballooning of the arterial wall

109
Q

Risk factors of Atherosclerosis

A

high saturated fat diets, smoking, sedentary life,obesity, high blood pressure, emotional, genetics

110
Q

angioplasty

A

process of using an inflatable probe to enlarge the lumen of an artery

111
Q

capillaries

A

continuation of arteriole endothelium. No smooth muscle or connective tissue

112
Q

Precapillary sphincter

A

controls blood flow into capillaries- direct flow into arteriovenous shunts

113
Q

diffusion

A

movement down a concentration gradient

114
Q

filitration

A

movement through pores and slits or membrane due to blood pressures (^ to Low)

115
Q

Movement across capillary membrane

A

diffusion and filtration

116
Q

venules and veins

A

smae tissue construction as arteries with less smooth muscle
major veins below heart contain valves to prevent backflow
larger lumens that an corresponding artery

117
Q

What happens if the ventricles are unable to expel blood as fast as it is received?

A

blood backs up in veins. causes tissue edema since fluids are not being removed as fast as are accumalted

118
Q

varicose veins

A

are over-dilated veins due to increase blood back pressure as aresult of gravity from standing

119
Q

Phlebitis

A

common inflammation of vein caused by bacteria, surgery or injury. if clots are formed and detach, they move through the heart and lodge in lung causing pulmonary embolism

120
Q

Vasomanipulation

A

sympathteic branches of the autonomic nervous system innervate the arterial smooth muscle (vasoconstriction, vasodilation)

121
Q

vasoconstriction

A

increase blood pressure and heat conservation

122
Q

vasodilation

A

decrease blood pressure and heat radiation

123
Q

Systolic BP

A

max pressure prduced by ventricular contraction

124
Q

distolic BP

A

min pressure at time of ventricular relaxation

125
Q

pulse

A

alternating expansion and contraction of arterial wall as result of systole and diastole

126
Q

Factors affecting BP

A
  1. cardiac output (stroke vol x bpm)
  2. blood volume (as vol increases BP increases)
  3. peripheral resistance (as resistance increases, BP increases
  4. viscosity (resistance to flow) as vscosity increases BP increases
  5. salt consumption- nypertrophy
127
Q

hypertrophy

A

as left ventrical works to pump blood at a high blood pressure, myocardium thickens and heart enlarges

128
Q

Congestive heart failure

A

if coronary arteris cannont support increased mass, muscle cells die and heart becomes fibrous and eventually dies

129
Q

Forces of vessel curculation

A
  1. cardiac pressure (BP prodcued by contraction of heart only present on arterial side fo system)
  2. muscle contraciton (BP produced by contraction of skeletal muscle compressing veins and venules)
  3. respiration (BP prodcued by movement of diaphragm against abdominal viscera forcing blood up into throacic veins and into heart
  4. venoconstriction
  5. gravtiy
130
Q

Exercise and the Cardiovascular system

A
  1. increase myocardial mass
  2. increase stroke volume
  3. decrease blood pressure
  4. decrease heart rate
  5. increase hemoglobin and myoglobin
  6. increase blood volume
131
Q

Circulation paths

A
  1. pulmonary circuit
  2. systemic circuit
  3. Cerebral arterial circle (circle of willis)- provides redundancy to cerebral arterial flow
132
Q

Life span changes

A
  1. cardiac output remains same in absence of diseas
  2. decreas in number of myocardial cells- replaced by adipose and connective tissue
  3. heart valves thicken or calcify, becoming more rigid
  4. conduction system does not degenerate
  5. arterioles decrease ability to vasomanipulate
    6.blood presure increases as elasticity and aretery diameter decreases
    7.arterial plaque deposition
  6. number of capillaries decreases.

BI 122 (4 decks)

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