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
Hemoglobin components recycled
globin chains (polypeptide) heme groups
26
what are the heme groups broken down into?
iron and bilepigments billiverdin and billirubin. Pigments are then released into the gall bladder.
27
Bruises
subdermal hematomas (ruptured capillaries). They degrade from purple (whole blood) to green (billiverdin) to yellow (bilirubin)
28
Jaundice
excess bile pigments (billiverdin and billirubin) accumulate in the blood resulting in a yellowing of sclera, skin and nails
29
Factors that affect Erythropoiesis
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.)
30
pernicious anemia
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.
31
Anemia
RBC or hemoglobin deiciency- a reduced oxygen carrying capacity of the blood
32
Characteristics of WBC's
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
33
Classifications of WBC's
1. size 2. cuclear size and shape 3. granulation of cytoplasm
34
Granulocytes
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)
35
Agranulocytes
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)
36
forms of lymphocytes
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
37
HIV
reproduces in T cells resulting and their death and compromising the immune system
38
Never Let Monkeys Eat Bananas
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils
39
How WBC's fight infection
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
40
Pus
local accumaltion of leukocytes and microorganism and associated fluids
41
Sepsis, Septicemia, Bacteremia, and Viremia
Sepsis: infection of tissues Septicemia: infection of the blood Bacteremia: caused by bacteria Viremia: caused by viruses
42
Leukemia
cancer of leukocytes Myeloid leukemia (abnormal granulocytes and monocytes) Lymphoid leukemia (abnormal lymphocytes)
43
Leukemia results
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.
44
Characteristics of platelets
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
45
Characteristics of plasm
1. 92% water 2. 8% organic and inorganic compounds
46
function of plasma
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
47
Albumin (plasma protein)
maintains osmotic pressure in vessels
48
Edema
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
49
Globulin (plasma protein)
Alpha and beta globulins transport lipds and fat soluble vitamins Gamma globulin function as antibodies
50
fibrinogen (plasma protein)
blood coagulation
51
Plasma lipoproteins
lipids bond with proteins in plasma to make lipoproteins (proteins in lipoprotein increase= density increase)
52
Low Density Lipoproteins (LDL)
high cholesteral, low protein (functions is to transport cholesteral to misc. cells)
53
High Density Lipoproteins (HDL)
decrease lipds, increase protein (function is to transport cholesteral to liver for relase in bile)
54
Phases of Hemostasis
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
Hemophilia
deficiency in a clotting factor (VIII or IX) resulting in reduced ro no clotting
56
Clotting initiating mechanisms
1. extrinsic (clotting initiaed by chemicals release from damaged tissues or turbulence from a thrombus) 2. Intrinsic (clotting initiated by chemicals within blood)
57
Platelet derived growth factor
after clot formation platelets release growth factor that stiumulates vessel repair
58
Thrombus
stationar clot in vells that decreses or prevents blood flow causing a trhombosis
59
Embolus
Thrombus that breaks away and moves downstream. Lodges as vessel narrows causing embolism
60
infarction
when a trhombus or embolus stops vlood flow to an area (myocardial infarction)
61
Cerebral vascular accident (Stroke)
a thrombus or embolus indeced infarction in the brain
62
Transient ischemic attack
temporary blockage in a small artery caused by embolus.
63
angina pectoris
a thrombus or embolism that reduces blood flow to myocardium
64
Clot Prevention
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
Hemocompatability
RBC's possess membrane surface antigens that serve in cell recognition
66
Blood type that is the universal donor in emergency
Type O- no antigens but anti A and ani B antibodies
67
Blood types that is the universal recipient in an emergancy
Type AB: A and B antigens but ot anitbodies
68
Erythroblastosis fetalis
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
Reducing Transfusion Reactions
1. Use packed cells 2. infuse whole blood slowly to dilute and decrease chance of agglutination
70
Blood replacement
1. whole blood- contains all components 2. packed RBC's 3. packed platelets 4. packed WBC 5. plasma 6. Artificial blood
71
Components of Cardiovascular system
heart and blood vessels
72
Heart location
medial
73
Pericardium
covering over heart and proximal ends of vessels
74
Pericardial sac
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
Pericarditis
layers of pericardium stick together due to bacterial or viral infection
76
Cardiac Wall structure
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
Endocarditis
bacterial infection of the endocardium
78
Coronary flow of myocardium
obtains blood from its own vascular supply and not via atria or ventricles
79
Hypoxia and necrosis
caused by compromised flow to the myocardium, treated with coronary bypass surgery or placement of stents
80
Mitral Valve Prolapse
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
angina pectoris
a thrombus or embolism that reduces blood flow to myocardium ** if blood flow is stopped then myocardial infarction occurs
82
Fetal circulation
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
Systole
chamber contraction
84
diastole
chamber relaxation
85
lubb
closing of A-V valves during ventricular systole
86
dubb
closing of pulmonary and aortic valves during ventricular diastole
87
impulse nodes and bundles
strands of non-contractile cardiac muscle that initiate and or conduct impulses
88
sinoatrial node (pacemaker)
initiate impulse, impulses spread through both atrial myocardium.
89
atrioventricular node
conduction pathway between both atrial and ventricular myocardium
90
AV bundle
muscle fibers that conduct impulse towards ventricular myocardium. Divides into Left and Right branches.
91
Purkinje fibers
deliver impulse to myocardial fibers
92
Electrocardiograms
P wave, QRS complex, T wave
93
p wave
depolarization of atrial fibers (atrial ocntraction/ systole)
94
QRS complex
depolarization of ventricular fibers (bentricular contraction/ systole)
95
T wave
Repolarization of ventricular fibers (ventricular relaxation. diastole)
96
arhythmia
absence of normal cardiac rhythm
97
fibrilation
uncoordinated contraction of myocardium A. atrial- not fatal B. ventricular- fatal- results in cardiac arrest.
98
Flutter
rapid contraction of a single atrium
99
Bradycardia
abnormally slow beat
100
tachycardia
abnormally fast beat
101
sudden cardiac arrest
failure to contract. Death within minutes if not treated with automated electronic defibrillator
102
Blood vessel hierarchy
heart>arteries>arterioles>metarterioles>capillaries>venules>veins>heart or heart>arteries>arterioles>metarterioles>venules>veins>heart
103
arteries and arterioles
carry blood away from heart to capillaries under cardiac pressure
104
artery layers
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
atherosclerosis
deposits of plaque line artery lumen and decrease blood flow resulting in increased blood pressure and increased chance of thrombus formation
106
dystrophic calcification
trauma to vessel that causes calcium deposition on lumen walls
107
arteriosclerosis
arterial walls thicken and lose their elasticity: increased blood pressure and increased chance of aneurysm
108
aneurysm
a ballooning of the arterial wall
109
Risk factors of Atherosclerosis
high saturated fat diets, smoking, sedentary life,obesity, high blood pressure, emotional, genetics
110
angioplasty
process of using an inflatable probe to enlarge the lumen of an artery
111
capillaries
continuation of arteriole endothelium. No smooth muscle or connective tissue
112
Precapillary sphincter
controls blood flow into capillaries- direct flow into arteriovenous shunts
113
diffusion
movement down a concentration gradient
114
filitration
movement through pores and slits or membrane due to blood pressures (^ to Low)
115
Movement across capillary membrane
diffusion and filtration
116
venules and veins
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
What happens if the ventricles are unable to expel blood as fast as it is received?
blood backs up in veins. causes tissue edema since fluids are not being removed as fast as are accumalted
118
varicose veins
are over-dilated veins due to increase blood back pressure as aresult of gravity from standing
119
Phlebitis
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
Vasomanipulation
sympathteic branches of the autonomic nervous system innervate the arterial smooth muscle (vasoconstriction, vasodilation)
121
vasoconstriction
increase blood pressure and heat conservation
122
vasodilation
decrease blood pressure and heat radiation
123
Systolic BP
max pressure prduced by ventricular contraction
124
distolic BP
min pressure at time of ventricular relaxation
125
pulse
alternating expansion and contraction of arterial wall as result of systole and diastole
126
Factors affecting BP
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
hypertrophy
as left ventrical works to pump blood at a high blood pressure, myocardium thickens and heart enlarges
128
Congestive heart failure
if coronary arteris cannont support increased mass, muscle cells die and heart becomes fibrous and eventually dies
129
Forces of vessel curculation
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
Exercise and the Cardiovascular system
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
Circulation paths
1. pulmonary circuit 2. systemic circuit 3. Cerebral arterial circle (circle of willis)- provides redundancy to cerebral arterial flow
132
Life span changes
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 8. number of capillaries decreases.